flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article unilateral traumatic hemorrhage of the basal ganglion and bihemisferic cerebral infarction luis rafael moscote-salazar, willem guillermo calderon-miranda, andres m. rubiano, amit agrawal colombia, mexico, india doi: 10.1515/romneu-2017-0063 romanian neurosurgery (2017) xxxi 3: 391 393 | 391 doi: 10.1515/romneu-2017-0063 unilateral traumatic hemorrhage of the basal ganglion and bihemisferic cerebral infarction luis rafael moscote-salazar1, willem guillermo calderonmiranda2, andres m. rubiano3, amit agrawal4 1neurosurgery, critical care unit, university of cartagena, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia 2universidad nacional autonoma de mexico, mexico city, mexico 3neurosurgery, director of neurotrauma research, el bosque university, bogotá, colombia 4department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: among the various injuries caused by the cerebral tramatic lesion are trau matic brain contusions. hemorrhagic contusions of the basal ganglia are unusual. different injuries such as cranial fractures, epidural hemorrhage, subdural hematoma, subarachnoid hemorrhage among others may be associated with brain contusions. in some cases traumatic brain injury arises. we present a case of a patient with unilateral cerebral contusion associated with bihemispheric cerebral infarction. key words: basal ganglia hematoma, bilateral, neurotrauma introduction cerebral ischaemia is an important contributor to morbidity and mortality in patients with traumatic brain injury. cerebral infarction in patients with cranial lesions is mainly related to cerebral herniation, compressive effects of intracranial hematomas, cerebral edema, vasospasm, direct vascular injury, fatty embolism and cortical lesions due to cranial fractures. we present the case of a patient with bihemispheric infarction associated with gangliobasal contusion as an illustration of the heterogeneity of the traumatic brain injury. case report a 30-year-old male patient is taken to our emergency department after to present cranial trauma following a vehicular accident. upon admission, the hemodynamically stable patient, glasgow coma scale 4, was performed tac brain showing the unilateral traumatic hemorrhage of the basal ganglion and bihemisferic cerebral infarction. the patient was transferred to an intensive care unit receivingc onservative managemtn. no cerebral angiography was performed. the patient presented a drowsy evolution and died at 48 hours. 392 | moscote-salazar et al traumatic hemorrhage of the basal ganglion and cerebral infarction figure 1 a and b cerebral ct showing a unilateral traumatic hemorrhage of the basal ganglion and bihemisferic cerebral infarction discussion cerebral trauma is associated with posttraumatic cerebral infarction in up to 2% of cases.there are several hypotheses that may explain the pathophysiology of cerebral ischemia. participation has been proposed mechanisms of intravascular thrombosis as an etiology for cerebral infarctions in traumatic brain injury. the above situations may occur in the context of dissections, thrombi or vasoespasmo. in a multivariate prospective analysis, the presence of low systolic blood pressure was one of the statistically significant risk factors for the development of posttraumatic brain injury infarction. mirvis et al reported the prevalence of postrauma cerebral infarction at 1.9% and tomberg et al reported a prevalence of 3.3%. the tian et al study which included the severity of the trauma moderate and severe injuries increasing the prevalence in 11.9% (42/353). hirata et al reported the case of a patient with cerebral infarction and multiple lesions associated with shock, in this way arise the episodes of severe hypotension as causality of cerebral ischemic lesions. (6). patterns of brain injury in post-traumatic infarcts include cortical injury in borderline areas, arterial territories, multiple focal cerebral infarcts. on the other hand, the development of decompressive craniectomies has increasingly increased the presentation of infarcts associated with the procedure, especially in the areas where post-surgical herniation occurs, a compression of veins and arteries occurs in the dural margins of the duraplasty. it has been hypothesized that a rapid reduction of intracranial pressure by surgical compression causes a shearing of the tissues that finally end in infartar the zone. this type of lesion should be carefully studied in future studies. romanian neurosurgery (2017) xxxi 3: 391 393 | 393 the presence of lesions associated with cerebral infarctions, such as contusions and hematomas may occur, in our case the presence of a gaangliobasal hemorrhage was evidenced. our case illustrates the heterogeneity of the traumatic brain injury and the importance of the individualization of each patient. correspondence luis rafael moscote-salazar email: mineurocirujano@aol.com references 1.stein sc, graham di, chen xh, smith dh. association between intravascular micro thrombosis and cerebral ischemia in traumatic brain injury. neurosurgery 2004; 53 : 687-91 2.dharker sr, mittal rs, bhargava n. ischemic lesions in basal ganglia in children after minor head injury. neurosurgery 1993; 33:863-865 3.mirvis se, wolf al, numaguchi y, corradino g, joslyn jn. posttraumatic cerebral infarction diagnosed by ct: prevalence, origin, and outcome. ajr am j roentgenol 1990;154:1293-8 4.tomberg ta, tikk aa. traumatic cerebral infarct. zh vopr neirokhir im n n burdenko 1989;mar-apr:23-6. 5.tian hl, geng z, cui yh, hu j, xu t, cao hl, et al. risk factors for posttraumatic cerebral infarction in patients with moderate or severe head trauma. neurosurg rev 2008;31:431-7 6.hirata j, ohya m, marukawa s, kumon k .posttraumatic cerebral infarction caused by hemodynamic shearing stress following hemorrhagic shock crit care & shock (2014) 1:16-20 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 413 416 | 413 iatrogenic lumbar pseudomeningocele: a case report and review of literature s.v. rege, harshad patil department of neurosurgery, sri aurobindo medical college and pg institute, indore, madhya pradesh, india abstract: lumbar pseudomeningocele is an uncommon complication of lumbar spine surgeries. this occurred due to extradural encapsulated cerebrospinal fluid collection after accidental durotomy or un-repairable dural tear. on review of literature only 58 cases have been reported so far. magnetic resonance imaging is the investigation of choice for diagnosis of pseudomeningocele. herein author has described a case of iatrogenic pseudomeningocele after lumbar spine surgery and its management. key words: pseudomeningocele, lumbar laminectomy, complication, accidental durotomy introduction iatrogenic lumbar pseudomeningocele is an extradural cystic collections of cerebrospinal fluid (csf) without dural covering which result from a breach in the dura. this is a rare complication mostly occurred due to accidental dural tear during laminectomy in lumbar spine surgery. it also occurred due to lumbar puncture, myelography and intrathecal catheter placement. iatrogenic pseudomeningocele was first reported by hyndman and gerber in 1946[1] and since then only 58 cases have been reported so far. herein we describe a case of iatrogenic pseudomeningocele which was occurred after lumbar spine surgery. case report a 45 years old male admitted in our institute with chief complaint of swelling and pain over operative site for last 15 days and right lower limb radiating pain since 10 days. the patient had undergone a l4-l5 laminectomy and discectomy one month back in another institution. after operation patient was asymptomatic for 15 days. patient developed backache and swelling over operative site. the intensity of pain and swelling increased progressively. patient also experienced a severe radiating pain over the right lower limb. on examination there was swelling over operative site which increased on straining and standing (figure 1). magnetic resonance imaging (mri) lumbo-sacral (ls) spine was done which revealed 4x3 cm csf intensity cystic collection at l4-5 region. the sac arising from l4-5 dura was hypointense on t1w and hyperintense on t2w images (figures 2, 3). 414 | rege, patil iatrogenic lumbar pseudomeningocele figure 1 fluctuating swelling at operative site figure 2 t1w sagittal image showing a hypointense lesion and t2w sagittal image showing a hyperintense cystic lesion located posteriorly at l4-5 level figure 3 t2w axial image of the cystic lesion based on clinical and radiological findings, diagnosis of pseudomeningocele was made. in view of symptoms patient was taken up for surgery. intraoperatively greyish white thick walled sac was found, arising from l4-5 dural defect. on opening the sac, a root was seen entering the cavity through the dural defect. the root was adherent to the defect, adhenolysis was done and root was reduced into the thecal sac after enlargement of the dural defect. excess sac was excised and dura was closed in watertight fashion with overlying fat graft (figure 4). post-operatively the patient’s back pain, swelling and radicular symptoms subsided dramatically (figure 5). romanian neurosurgery (2016) xxx 3: 413 416 | 415 figure 4 intraoperative image: after dural repair and overlying fat graft figure 5 postoperative image after removal of sutures discussion postoperative pseudomeningocele was first reported by hyndman and gerber in 1946 [1]. pseudomeningocele also called as “meningocele spurious”, “pseudocyst” or “false cyst” [2]. miller et al. in 1968 reported three types of pseudomeningocele congenital, iatrogenic and traumatic [2]. most pseudomeningoceles are usually associated with neurofibromatosis and marfan syndrome, and are congenital in origin. congenital pseudomeningoceles tend to occur in the thoracic or thoracolumbar area [3]. traumatic pseudomeningoceles are rare, and more common in the cervical region but it can also occur in the lumbosacral region after a severe distraction injury. the incidence of pseudomeningocele after laminectomy ranges from 0.068% to 2% [4]. postoperative pseudomeningoceles may result from accidental tear in the dural mater and pia arachnoid which is left open during surgery. if the dural mater and pia arachnoid are torn, csf extravasates into the paraspinal soft-tissue space. the csf may be absorbed initially but, after progressive reactions in the connective tissue of the surrounding tissue, csf is absorbed less readily, resulting in pseudomeningocele formation [2, 4]. most of the patients are asymptomatic but some patients present with postural headache, localized back pain and radiculopathy. nerve roots may subsequently herniate through the dural and arachnoid tears. strangulation of the nerve roots within the cyst may lead to radicular pain and motor deficits. some pseudomeningoceles may present as fluctuating mass, enlarging with valsalva maneuver [5]. both these findings were present in our case. mri is the investigation of choice in pseudomeningocele. it can accurately assess the size and location of pseudomeningocele. 416 | rege, patil iatrogenic lumbar pseudomeningocele the cyst content is of low intensity in t1 weighted and with high signal intensity in t2weighted images. this csf-containing cyst is located posterior to the dural sac, although it might rarely grow into the intervertebral disc space [6]. the treatment of pseudomeningocele is controversial, particularly in case of asymptomatic patients. small pseudomeningoceles associated with minimal symptoms can be managed conservatively. early symptomatic pseudomeningoceles associated with a csf fistula can be treated with spinal drainage [7]. symptomatic pseudomeningoceles weeksto-months after initial surgeries may be treated with surgical dural repair. large dural defects may be closed with patch techniques using autologous tissue, dural allografts, or fibrin glue along the suture line. release of cord or root is necessary if adherent to the dura [7]. lumbar shunt or percutaneous subarachnoid drainage can be used in case of dural cutaneous fistulas and early pseudomeningoceles. this procedure can help to create a seal at the leakage site and promote healing by csf diversion [8]. conclusion a pseudomeningocele should be considered as a diagnosis in patients with recurrent back pain, radicular pain, or a persistent headache with background of spinal surgery. wide opening of the cyst, identification of the dural breach and its repair are the key steps of pseudomeningocele surgery. accidental dural tear with csf leakage during lumbar laminectomy and discectomy should be handled properly to prevent development of iatrogenic pseudomeningocele. correspondence dr. harshad patil e-mail: dr.harshadpatil@gmail.com contact no.: +919893894242 address: department of neurosurgery, sri aurobindo medical college and pg institute, indore, madhya pradesh, india references 1.hyndman or, gerber wf. spinal extradural cysts, congenital and acquired; report of cases. j neurosurg. 1946 nov; 3(6):474-86. 2.miller pr, elder fw jr. meningeal pseudocysts (meningocele spurius) following laminectomy. report of ten cases. j bone joint surg am. 1968 mar; 50(2):268-76. 3.sutterlin ce, grogan dp, ogden ja. diagnosis of developmental pathology of the neuraxis by magnetic resonance imaging. j pediatr orthop. 1987 may-jun; 7(3):291-7. 4.teplick jg, peyster rg, teplick sk, goodman lr, haskin me. ct identification of postlaminectomy pseudomeningocele. ajr am j roentgenol. 1983 jun; 140(6):1203-6. 5.hadani m, findler g, knoler n, tadmor r, sahar a, shacked i. entrapped lumbar nerve root in pseudomeningocele after laminectomy: report of three cases.neurosurgery. 1986 sep; 19(3):405-7. 6.murayama s, numaguchi y, whitecloud ts, brent cr. magnetic resonance imaging of post-surgical pseudomeningocele. comput med imaging graph. 1989 jul-aug; 13(4):335-9. 7.mccormack bm, zide bm, kalfas ih: cerebrospinal fluid fistula and pseudomeningocele after spine surgery. spine surgery, techniques, complication avoidance and management edward c, benzel ec 2005, 2:2033-2042 8.aoki n. lumboperitoneal shunt for the treatment of postoperative persistent collection of subcutaneous cerebrospinal fluid (pseudomeningocoele). acta neurochir (wien). 1989; 98(1-2):32-4. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article where is the contre-coup? atypical localization of occipital brain contusion a.i. cucu, claudia florida costea, r.a. sascau, b. dobrovat, i. poeata, turliuc serban, dana mihaela turliuc romania doi: 10.2478/romneu-2018-0003 romanian neurosurgery (2018) xxxii 1: 25 28 | 25             doi: 10.2478/romneu-2018-0003 where is the contre-coup? atypical localization of occipital brain contusion a.i. cucu1, claudia florida costea1,2, r.a. sascau2,3, b. dobrovat1,2, i. poeata1,2, turliuc serban², dana mihaela turliuc1,2 1"prof. dr. n. oblu" emergency clinical hospital, iași, romania 2"grigore t. popa" university of medicine and pharmacy, iași, romania 3"george i. m. georgescu" institute of cardiovascular diseases, iasi, romania abstract: most traumatic brain injuries with occipital impact cause frontal and temporal contre-coup lesions, while patients with coagulopathies are more susceptible to such lesions. we present the case of a chronic ethylic patient with thrombocytopenia, who was treated for ethanol withdrawal syndrome at a psychiatric service. the head ct scan revealed an occipital contusion with atypical localization and the absence of frontotemporal contre-coup lesions. in conclusion, it is recommended a head ct scan to chronic alcoholic patients with psychiatric manifestations, especially in the context of systemic coagulopathies related to excessive alcohol consumption. in the case of chronic ethylic patients that frequently display systemic coagulation disorders, the head ct scan is necessary at the first psychiatric manifestations. key words: atypical occipital contusion, brain injury, coagulopathy introduction traumatic brain injuries represent a major cause of morbidity and mortality worldwide (13). traumatic parenchymal mass lesions are a common sequel of traumatic brain injury (tbi), with an incidence of up to 8.2% of all tbi (6) cases and 13-35% of all severe tbi cases (1). out of these, brain contusions are one of the most common forms of tbi, and they occur most frequently in areas where the sudden deceleration of the head causes brain damage to bony prominences such as the frontal, temporal and occipital poles, in a manner known in literature as coup and contre-coup brain contusions. originally described in the 17th century by french surgeon jean louis petit (1674-1750) (9), our knowledge of these injuries was completed in 1766 by another french surgeon, antoine louis (1723-1792), who presented the results of his research at académie nationale de médecine (4). two years later, in 1768, coup and contrecoup lesions were better understood by the military surgeon of the same origin as his predecessors, louis sebastian saucerotte (1741-1814), thanks to the experiments that he carried out on 28 dogs (12). 26 | cucu et al atypical localization of occipital brain contusion             short case report we present the case of a 55-year-old chronic ethylic patient hospitalized in the department of neurosurgery of "prof. dr. n. oblu" emergency clinical hospital, who was transferred from a psychiatric service due to neurological aggravation (gcs 13). the patient was admitted to the 24-hour psychiatric service for ethanol withdrawal syndrome with delirium. the anamnesis failed to identify, but allowed to suspect the existence of a minor tbi. at the time of admission, the patient presented a gcs of 13 and petechiae at the level of the anterior and posterior thorax as well as on the limbs (figure 1a) the performed head ct scan revealed a left occipital contusion associated with an occipital hemorrhage (figure 1b, c and figure 2a, b red arrows) and a left hemispheric acute subdural haematoma (figure 1c and figure 2a, b blue arrows). the patient also had thrombocytopenia (65,000/mcl), elevated liver enzymes (tgp 100 u/l, tgo 117 u/l, ggt 307 u/l), as well as dyselectrolymia. surgery was performed, by evacuating the left occipital hemorrhage and the right subdural hemispheric haematoma through a left parietal-occipital approach (figure 2c, d). figure 1 petechiae at the level of anterior thorax (a); occipital brain contusion and hemorrhage (b) and left hemispheric acute subdural haematoma (c). coup and counter-coup injuries in tbi with occipital impact (d) (personal collection of authors) romanian neurosurgery (2018) xxxii 1: 25 28 | 27             figure 2 preoperative (a) and postoperative (b) imaging aspects discussions in terms of brain contusions, clinical observations have indicated that in the absence of a skull fracture, most cerebral contusions occur in the frontal and temporal lobes, in the case of occipital impacts, and on the same side in most frontal impacts (2). in tbi with occipital impact, the pattern of brain contusions varies depending on the location of the impact. in the case of midline occipital impacts, contre-coup lesions consist in localized bilateral frontal and temporal lobe contusions (figure 1d). in the case of tbi with lateral occipital impact, contralateral contrecoup contusions are localized at the frontal and temporal lobes on the opposite side of the impact. practically, in the case of tbi with occipital impact, these contre-coup lesions are more severe due to the rough edges of the sphenoid wings and the floor of the frontal anterior fossa, compared to occipital lobe injuries (8). usually, in the case of occipital impacts, contre-coup contusions are localized in the frontal and temporal lobes, whereas the coup contusions are primarily in the cerebellum, without affecting the occipital lobes. when occipital impacts fracture the occipital bone, the lesion distribution changes and coup lesions are predominant, being associated with the occipital lobes, while contre-coup lesions are smaller, although they have the same fronto-temporal localization (7). it is well-known that coagulopathies, within or outside the context of a tbi, lead to intracranial hemorrhage, including thrombocytopenia induced by alcohol or liver disease, which are directly caused by the toxic effects of alcohol on the bone marrow and associated folate deficiency. in the case of our patient, his pre-existing biological context (coagulopathy due to alcoholic hepatopathy) favored, even in the case of a minor tbi, the bleeding of microvessels fractured at the time of primary injury, causing extravasation of blood with occipital hemorrhage. in addition to that, a number of hemostasis abnormalities are present in alcoholic patients, including numerous functional deficits in the platelets such as decreased platelet aggregation (5, 11) associated with disturbances in the ultrastructural morphology (3). conclusion head ct scan is mandatory even for chronic alcoholics known for psychiatric disorders, especially in case that, in the context 28 | cucu et al atypical localization of occipital brain contusion             of their condition, they are predisposed to contusions and cerebral haemorrhages as a consequence of minor trauma or even in the absence of such tbi. correspondence claudia florida costea "prof. dr. n. oblu" emergency clinical hospital, iași, romania e-mail: costea10@yahoo.com references 1.bullock mr, chesnut r, ghajar j, et al. surgical management of traumatic parenchymal lesions. neurosurgery. 2006; 58:s25-s46. 2.chu cs, lin ms, huang hm, lee mc. finite element analysis of cerebral contusion. j biomech. 1994; 27:187194. 3.cowan dh. effect of alcoholism on hemostasis. semin hematol. 1980; 17:137-147. 4.finger s. origins of neuroscience: a history of explorations into brain function. oxford university press, new york. 2001. p 429. 5.haut mj, cowan dh. the effect of ethanol on hemostatic properties of human blood platelets. am j med. 1974; 56:22-33. 6.mandera m, zralek c, krawczyk i, et. al. surgery or conservative treatment in children with traumatic intracerebral haematoma. childs nerv syst. 1999; 15:267269. 7.overgaard j. traumatic injuries of the planum occipitale and posterior fossa brain parenchyma. in samii m, brihaye (eds). traumatology of the skull base: anatomy, clinical and radiological diagnosis operative treatment. springer, berlin. 2012. p 88-93. 8.parker rs. concussive brain trauma: neurobehavioral impairment and maladaptation, crc press, boca raton. 2016. p 217. 9.petit jl. oeuvres completes de jean-louis petit. chapoulaud f., 1837. 10.quinones-hinojosa a, gulati m, singh v, lawton mt. spontaneous intracerebral hemorrhage due to coagulation disorders. neurosurg focus. 2003; 15:e3. 11.salem ro, laposata m. effects of alcohol on hemostasis. am j clin pathol. 2005; 123 suppl:s96-105. 12.saucerotte ls. mélanges de chirurgie neapoli, gay, italy. 1801. 13.turliuc d, cucu a. management of mild and moderate head injuries in adults. romanian neurosurgery. 2010; 17:421-431. 03 03cucuai_where flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 379 382 | 379 thoracic cavernoma with intraosseous and extradural component mimicking metastasis: case presentation umit kocaman1, mehmet haluk ozer1, muhammet bahadir yilmaz1, hakan yilmaz2 1university of izmir of medicine, department of neurosurgery, izmir, turkey 2duzce ataturk state hospital, department of neurosurgery, duzce, turkey abstract: spinal epidural cavernomas are quite rare lesions and only 5% of all cavernomas are located in the spine. the lesions are most commonly localized in the thoracic region. the differential diagnosis includes neurogenic tumors, lymphoma, schwannoma, meningioma, multiple myeloma, ewing's sarcoma and metastasis. a 40year-old male patient presented with paraplegia and mr images revealed an epidural soft tissue constricting the right posterolateral of the cord at the t6 level. pathology showed cavernous hemangioma. a literature search revealed no other case that so closely mimicked metastasis by invading all components of the thoracic vertebra and also expanding to the epidural distance. we therefore present the case emphasizing these features. key words: cavernoma, epidural, thoracic vertebra introduction spinal epidural cavernous angiomas (cavernomas) are quite rare lesions (2). they are most commonly located in the thoracic area in the spinal region (5). the differential diagnosis of spinal masses includes many pathologies. cavernomas should be considered in the differential diagnosis. a literature review revealed no other thoracic cavernoma case invading all components of the thoracic vertebral bone (corpus, pedicle, lamina, facet joints, spinous process), compressing the epidural distance from both the dorsal and anterior aspects, resulting in a moderate depression of the corpus, and creating an appearance of metastasis. we therefore found the case suitable for presentation. case presentation a 40-year-old male presented to our outpatient department with symptoms of weakness, loss of sensation in the legs and difficulty walking for the last 10 days. the medical history of the patient revealed nothing of significance besides smoking 1 pack per day for 20 years. the examination revealed proximal and distal 3/5 muscle strength on the right and proximal and distal 3-4/5 muscle strength on the left lower extremity. 380 | kocaman et al cavernoma of the thoracic vertebra bilateral sensory loss was present with a level at t6. lower extremity deep tendon reflexes were hyperactive and the babinski sign was bilateral positive. the patient could only stand up with bilateral support and had significant difficulty while taking steps. there was no urinary or fecal incontinence or retention. systemic examination revealed no pathology except coarsening of respiratory sounds. contrast-enhanced dorsal mr investigation was requested. the radiology report revealed that the posterior elements of the t6 vertebra were affected by the medullary bone lesion that expanded to the pedicle, more prominently on the right. a large number of medullary bone lesions causing signal increase were present in the t11, t12 and l1 on postcontrast series. metastasis was primarily considered as there were multiple lesions. the interaction of the pedicles and contrast enhancement in an expansile character were most marked at t6. there was less contrast enhancement and expansion at the other levels. a paravertebral soft tissue component was also present at t6. there was significant pressure from to the dural sac and spinal cord from the posterior together with pedicle involvement at the t6 level (figure 1, figure 2, figure 3). a spinal metastasis was primarily considered with these findings. the lesion was causing significant pressure on the spinal cord from the dorsal aspect and especially from the right side at the t6 level. emergency decompression was planned for this region. thepatient was prepared for surgery and preoperative steroids were administered. the patient underwent t6 total laminectomy and flavectomy. a highly vascular and fragile mass with prominent borders that compressed the spinal cord in the anterior direction and was consistent with a cavernoma was found in the epidural distance. the lesion was dissected from the dura was totally excised. the material was sent for pathology evaluation. the pathology result was cavernous hemangioma (figure 4). post-operative examination of the patient revealed proximal and distal muscle strength of 4-5/5 in both lower extremities. the patient was mobilized on the 2nd post-operative day with unilateral support. he was discharged to outpatient follow-up later on. figure 1 figure 2 romanian neurosurgery (2016) xxx 3: 379 382 | 381 figure 3 figures 1, 2, 3 axial and sagittal mr images shows an epidural soft tissue constricting the right posterolateral of the cord at the t6 level figure 4 pathology showed cavernous hemangioma. x20 showing variety size dilated vascular spaces containing erythrocyte, lined by a single layer of endothelium discussion spinal epidural cavernous hemangiomas (cavernomas) are quite rare lesions. they form 8-15% of developmental cerebrovascular malformations. about 80% of cavernomas are supratentorial, 15% are infratentorial and only 5% are localized in the spinal region while 51% of spinal cavernomas are extradural. they are most commonly located in the thoracic region and vertebral column and can also extend to the epidural space (2, 5). spinal epidural cavernomas are most commonly seen between the ages of 30 and 50 years. although their histological characteristics are not different than other cavernomas, they have no capsule in contrast to similar lesions at other locations (1). extradural spinal cavernomas can present with symptoms and signs such as mass effect, bleeding, local pain, acute spinal cord pressure and radiculopathy depending on the location (5). the differential diagnosis of epidural spinal cavernomas includes neurogenic tumors, metastasis, lymphoma, meningioma, multiple myeloma, extraosseous ewing's sarcoma, disc fragment and epidural angiolipoma (3). li ty et al reported a series of 14 spinal epidural cavernomas where 1 lesion each was predicted to be a meningioma, a schwannoma and an arachnoid cyst during the preoperative evaluation but turned out to be a cavernoma on pathology (4). çağıran et al reported a patient with significant sciatalgia who was preoperatively diagnosed as disc hernia but found to have spinal epidural cavernoma during surgery (1). manish s. et al have reported that spinal epidural cavernomas are most commonly confused with schwannoma (6). surgical excision by experienced surgeons provides a cure for spinal epidural cavernoma. 382 | kocaman et al cavernoma of the thoracic vertebra adjuvant stereotactic radiosurgery can be used for residual lesions (6). there is currently no literature reference to a spinal epidural cavernoma creating an appearance of metastasis. all components of the thoracic vertebra including the corpus, pedicles, lamina, facet protrusions and spinal process were invaded with the lesion in our case. there was an epidural mass creating a significant pressure on the cord from the dorsal aspect. a moderately depressed corpus fracture was observed. the presence of an active smoking habit and involvement of the dorsal vertebral corpus indicated metastasis. another interesting feature was the invasion of all vertebral components by the cavernous hemangioma. conclusion spinal cavernomas should be considered in the differential diagnosis of spinal masses. predicting the pathology in these cases can influence the surgical preparation and approach. the history, physical examination, and radiology and laboratory values of the patient should be reviewed in this regard. correspondence hakan yilmaz duzce ataturk state hospital, department of neurosurgery, duzce, turkey e-mail: dr_hakanyilmaz@hotmail.com tel: +90 5066211829 references 1. cagiran i, cagiran e, pestilci z, akinturk n, sari mf: spinal epidural cavernoma mimicing lumbar disc hernia: case report. journal of neurological science (turkish). 30(4): 791-795, 2013 2. jang d, kim c, lee sj, ryu yj, kim j: pure spinal epidural cavernous hemangioma with intralesional hemorrhage: a rare case of thoracic myelopathy. korean j spine 11(2): 85-8, 2014 3. khalatbari mr, abbassioun k, amirimshidi a: solitary spinal epidural cavernous angioma: report of nine surgically treated cases of the literature. eur spine j 22(3): 542-7, 2013 4. li ty, xu yl, yang j, wang j, wang gh: primary spinal epidural cavernous hemangioma: clinical features and surgical outcome in 14 cases. j neurosurg spine 22(1): 39-46, 2015 5. menekse g, okten ai, ozdol c, atay of, guzel e, guzel a: extradural sacral cavernoma: a case report. türk nöroşirürji dergisi 23(1): 96-99, 2013 6. sharma ms, borkar sa, kumar a, sharma mc, sharma bs, mahapatra ak. thoracic extraosseous, epidural, cavernous hemangioma: case report and review of literature. j neurosci rural pract 4(3): 309-312, 2013 microsoft word _6.formatat_sorensen.doc romanian neurosurgery vol. xv nr. 1 35 development of international spinal cord injury data sets fin biering-sørensen executive committee of the international sci standards and data sets presented at the 6th congress of the romanian society of neurosurgery 26.09-30.09.2007 bucharest the purpose of the core data set is to standardize the collection and reporting of a minimal amount of information necessary to evaluate and compare results of published studies. the data are included in the core data set, and are recommended, as a descriptive table in most publications including individuals with sci. the core data set is available at www.iscos.org.uk, and www.asia-spinalinjury.org, including training cases. keywords: bony vertebral injury, spinal cord injury, spinal surgery common international sci data sets should be collected on individuals with sci to facilitate comparisons regarding injuries, treatments, and outcomes between patients, centres and countries. it is found increasingly important to have comparable data elements so that the services affecting worldwide outcome of sci can be assessed and compared. an overall structure and terminology has been developed following the format of the international classification of function (icf) [1]. the core data set was the first one to be developed [2]. the purpose of the core data set is to standardize the collection and reporting of a minimal amount of information necessary to evaluate and compare results of published studies. at minimum, published studies should include information on the gender and age of the study population at the time of injury, the current age of the study population if different from age at injury, the length of elapsed time after injury when data are being collected, the calendar time frame during which the study was conducted, the causes of spinal cord lesion, and the neurologic status of the study population according to the international standards for neurological classificaiton sci. in addition, studies of health services and rehabilitation outcomes should also contain information on the total number of days hospitalized, whether a bony vertebral injury or associated injuries was present, whether spinal surgery was performed, whether patient was ventilator-dependent, and the place of discharge from inpatient care. these data are included in the core data set, and are recommended, as a descriptive table in most publications including individuals with sci. inclusion of more detailed information will depend on the research topic. this information should be provided in either table or text format for the overall study population and for each study group. it is extremely important that data be collected in a uniform manner. the core data set is available at www.iscos.org.uk, and www.asia-spinalinjury.org, including training cases. basic question this is a question, which with an affirmative answer implies that it is possible to go on to one or more specific data set(s) with more detailed information on the particular topic. there will not be such questions for all data sets. examples of basic questions: fin biering-sørensen romanian neurosurgery vol. xv nr. 1 36 bony vertebral injury: yes/no/unknown (from the core data set), if yes ? bony vertebral injury basic sci data set etiology of lesion: sports/ assault/ transport/ fall/ other traumatic/ non-traumatic (from the core data set), if traumatic ? etiology module (sci version of international classification of external causes of injury (iceci) [5]) pain: have you had any pain during the last seven days including today: yes/no, if yes ? pain basic sci data set basic sci data set. this is the minimal number of data elements, including the possible basic question, which together should be collected in daily clinical practice for a particular topic. this mean that the various basic sci data sets in the future may be the basis for a structured record in centres worldwide caring for persons with sci. examples of basic sci data sets: bony vertebral injury basic sci data set spinal surgery basic sci data set lower urinary tract function basic sci data set urodynamic basic sci data set urinary tract imagine basic sci data set bowel basic sci data set pain basic sci data set expanded sci data set. this is a more detailed data set, which may be used as optional for a topic, but may be recommended for specific research studies within the particular area. examples of possible expanded sci data sets: lower urinary tract function expanded sci data set bowel expanded sci data set pain expanded sci data set iceci (international classification of external causes of injury) for sci [5]. module a module may consist of a basic question, a 2-level data set: basic and expanded sci data sets, and other data (e.g. specific scoring-systems), which are appropriate for the particular module. possible examples of modules: urological module: lower urinary tract function basic sci data set lower urinary tract function expanded sci data set urodynamic basic sci data set urodynamic expanded sci data set urinary tract imagine basic sci data set urinary tract imagine expanded sci data set pain module: basic pain question (included in the pain basic sci data set) pain basic sci data set pain expanded sci data set pain scoring international sci data sets developments for development of further data sets the executive committee for the international sci standards and data sets create topic-specific expert working groups. the establishment of working groups in the various areas is done in cooperation with relevant international societies and organizations working with the respective topics. initially, priority has been given to the development of basic questions and data sets within the following areas: bony vertebral injury spinal surgery non-traumatic spinal cord lesions etiology/prevention, based on the who international classification of external causes of injury [3] urology bowel sexual function pain activity, participation and well-being. for each data set a syllabus including definitions, coding schemes, and instructions on how to collect each data item are developed. organization the executive committee for the international spinal cord injury standards and data sets is a steering committee for the specific working groups created for development of international spinal cord injury data sets romanian neurosurgery vol. xv nr. 1 37 developing of specific topic modules and data sets. international organizations and societies within the fields of spinal cord injury, neurosurgery, orthopaedic surgery, rehabilitation and others are being invited to appoint members to join the review process for the creation and evaluation of the best possible international sci data set. process for approval of international sci data sets. a process for approval of the data sets has been established following the points below: 1. the particular sci data set working group itself finalise the data set. 2. the executive committee of the international sci standards and data sets review the data set. 3. comments from the committee are discussed in the particular sci data set working group and a response is made and possible adjustments of the data set performed. 4. iscos scientific committee and asia board review the data set. 5. comments from the committee/board are discussed in the particular sci data set working group and a response is made and possible adjustments of the data set performed. 6. relevant and interested (international) organisations and societies and persons review the data set and iscos and asia websites. 7. comments are discussed in the particular sci data set working group and responses are made and possible adjustments of the data set performed. 8. iscos scientific committee, council and asia board review the data set for final approval. 9. iscos and asia general meetings have the data set for final approval. 10. endorsement of the data set by relevant (international) organisations and societies. data set presentation as soon as a new international sci data set is developed in this iterative manner, consensus has been obtained, and the final draft has been approved together with an appropriate training program, they will be disseminated at meetings, and published în international journals and through the web sites of iscos (www.iscos.org.uk), and asia (www.asiaspinalinjury.org). training programs. for each developed data set training cases will be created and made accessible through the iscos and asia web sites, from which the data guidelines will be freely available. the training cases should preferable precede download of the particular data set. this training will provide examples on how to code the data set and will give a minimal introduction to those using the data sets in their own environment. all new data sets approved will be made available with a data collection syllabus at the web sites of iscos (www.iscos.org.uk), and asia (www.asiaspinalinjury.org). references 1. biering-sørensen f, charlifue s, devivo m, noonan v, post m, stripling t, wing p. international spinal cord injury data sets. spinal cord 2006 sep;44(9):530. 2. devivo m, biering-sørensen f, charlifue s, noonan v, post m, stripling t, wing p. international spinal cord injury core data set. spinal cord 2006 sep;44(9):535-40. 3. http://www.iceci.org/ 19praveenkumar_large subgaleal romanian neurosurgery | volume xxx | number 4 | 2016 | october december article large subgaleal hematoma producing turban head in 10 year boy with cerebral palsy: rare case report with review of literature praveen kumar tripathi, vardan kulshreshtha, gaurav jaiswal, tarun kumar gupta india doi: 10.1515/romneu-2016-0091 562 | tripathi et al large subgaleal hematoma in child doi: 10.1515/romneu-2016-0091 large subgaleal hematoma producing turban head in 10 year boy with cerebral palsy: rare case report with review of literature praveen kumar tripathi, vardan kulshreshtha, gaurav jaiswal, tarun kumar gupta departments of neurosurgery, rnt medical college, udaipur, rajsthan, india abstract: subgaleal hematomas (sghs) are not uncommon. because the subgaleal space has no anatomical boundaries, sghs usually involve a large space and are typically limited to the parietal region. cases of sghs involving whole of head are relatively rare. in this study we report a rare case of massive enlargement of head after sgh causing severe pain and giving an appearance of turban. a 10 year old, male patient with cerebral palsy presented with progressive enlargement of head attaining a size of turban due to habitual head banging and self-punching overhead. sgh drainage and hematoma aspiration were performed and the patient’s head size was restored. key words: subgaleal hematoma (sgh), cerebral palsy (cp) introduction subgaleal hematoma is a potentially lifethreatening extracranial bleed that occurs most commonly in neonates after difficult instrumental deliveries (1). its occurrence beyond the neonatal period is rare and is often associated with head trauma involving tangential or radial forces applied to the scalp causing emissary veins traversing the subgaleal space to be ruptured (2). subgaleal hematoma (sgh) is a common clinical disease, largely because the subgaleal space is relatively loosely defined. the vast majority of sghs are gradually absorbed. for cases exhibiting difficulties in absorption, puncture with aspiration or incision followed by drainage can achieve satisfactory outcomes (3). large subgaleal hematoma due to trivial head trauma in a cerebral palsy patient habitual of head banging and self-punching with no reported literature is interesting to describe. case report a 10 year old boy was admitted in our ward with cheif complaint of progressive enlargement of head for 20 days. history was suggestive of initial swelling over frontal and parietal region which later involved whole of head. there was history of habitual head banging and self-punching overhead. patient romanian neurosurgery (2016) xxx 4: 562 – 565 | 563 was a diagnosed case of cerebral palsy with paraparesis. perinatal history was suggestive of vaginal delivery with meconium aspiration syndrome. on examination patient was mentally retarded with spastic paraparesis with speech abnormality and inablity to hold head. head was enlarged with head circumference 134 cm with multiple soft, fluctuant, transilluminant, tender boggy swellings over frontal, bilateral parietal and occipital region of scalp. pallor was present without lymph node enlargements or other manifestations of bleeding tendency such as purpura or ecchymosis. ncct brain revealed multiple pockets of extracalvarial fluid collection with internal septations in subgaleal region of scalp suggestive of subgaleal hematoma involving both sides without any intracranial hemorrhage, midline shift or skull fractures. the screening coagulation tests revealed normal coagulation profile with decreased haemoglobin (7.0 gm/dl). since it was a huge collection with multiple septations, aspiration of sgh in multiple stages was done with application of pressure bandage. a closed suction drain kept in right parietal region which had largest pocket. a total of approximately 400 ml blood stained fluid drained. paediatrician opinion sought and patient was discharged after 15 days after complete resolution of subgaleal hematoma with advice to avoid head banging and head punching and to follow in pediatric and neurosurgery opd. patient was followed after 1 & 3 months of discharge, no recurrence noted. figure 1 massive subgaleal hematoma invoving whole of scalp mimicking turban 564 | tripathi et al large subgaleal hematoma in child figure 2 ncct brain of the patient at admission figure 3 resolved subgaleal hematoma after aspiration and closed drain placement discussion the subgaleal space is located between the periosteum and the epicranial galea and comprises loose connective tissue; vessels connecting the scalp vein and skull diploe vein as well as the intracranial venous sinus are located within this space. external shear force during trauma may result in the rupture of the vessels, causing a large amount of blood to flow into the subgaleal space to form an sgh. the subgaleal space is not bounded by suture lines; therefore, an sgh can involve massive swelling of the entire scalp (4, 5). nontraumatic sgh is very rare. the cause of nontraumatic sgh is sometimes associated with aneurysms of the sta, scalp avf, and coagulation disorders (6, 7). davis et al. reported on the diagnosis and management of neonatal subgaleal hemorrhage, and described it to be caused by a rupture of the emissary veins, which are connections between the dural sinuses and the scalp veins (8). kashino et al. reported that an angiographic examination of three out of four cases of atraumatic sgh showed a well-developed sta on the surface of the sgh, and one case had shown similar findings from the early stage of the development of the hematoma (9). raffini et al reported a von willebrand disease case of sgh (10). cerebral palsy is commonly associated with a spectrum of developmental disabilities, including mental retardation, epilepsy, and visual, hearing, speech, cognitive, and behavioral abnormalities. very impaired children with cerebral palsy, especially those with mental retardation, can have self-abusive romanian neurosurgery (2016) xxx 4: 562 – 565 | 565 behavior such as biting, head banging, or scratching. in the present patient, sgh developed due to self-abusive behavior of patient while the blood coagulation and platelet aggregation functions were normal. no definitive therapeutic strategy has yet been established for sgh. therefore, there are various opinions concerning the treatment of hematoma. falvo et al. elected surgical evaluation and pressure dressings to shorten the period of blood resorption and decrease the risk of infection, calcification, and blood reaccumulation (11). faber noted that aspiration may set the stage for infection or may be followed by recurrent bleeding and suggested that the extravasation itself may act as a tamponade to prevent further bleeding (12). beauchamp et al. noted that hematoma aspiration was unnecessary unless severe pain, impending necrosis of the overlying scalp, or evidence of infection was present (13). in present case there was a huge subgaleal hematoma with multiple septations causing severe pain and discomfort to the patient, aspirated and pressure bandage applied. to the best of our knowledge, this is the first case to be reported with large subgaleal hematoma involving the entire scalp caused by self-abusive behavior of patient with cerebral palsy. an excellent response to treatment with surgical aspiration and compression bandage can be achieved followed by behavior therapy and rehabilitation. references 1.benaron da. subgaleal hematoma causing hypovolumic shock during delivery after failed vaccum extraction: case report. j perinatol. 1993;13:228–31. 2.vu tt, guerrera mf, hamburger ek, klein bl. subgaleal hematoma from hair braiding.case report and literature review. pediatr emerg cure. 2004;20:821–3. 3.strowitzki m, eymann r, schleifer j and steudel wi. vertex epidural hematoma with communicating bifrontal subgaleal hematomas treated by percutaneous needle aspiration. pediatr neurosurg 2001; 35: 1-4 4.panigrahi s, mishra ss, das s and patra sk. large subgaleal hematoma as a presentation of parahemophilia. j neurosci rural pract 2013; 4: 240-242. 5.kichari jr and gielkens h. massive traumatic subgaleal haematoma. emerg med j 2013; 30: 344. 6.rohyans ja, miser aw, miser js. subgaleal hemorrhage in infants with hemophilia: report of two cases and review of the literature. pediatrics 1982;70:3067. maruki c, nakajima m, tsunoda a, ebato m, ikeya f. a case of giant expanding cephalhematoma: does the administration of blood coagulation factor xiii reverse symptoms? surg neurol 2003;60:138-41. 8.davis dj. neonatal subgaleal hemorrhage: diagnosis and management. can med assoc j. 2001; 164 (10): 14521453. 9.kashino s, takuji t, nagai h. a study on diffuse subgaleal hematoma in childhood. nerv syst child. 1988; 13(14): 319-323. 10.raffini l, tsarouhas n: subgaleal hematoma from hair braiding leads to the diagnosis of von willebrand disease. pediatr emerg care. 2004; 20(5): 316-318. 11.falvo ce, san filippo ja, vartany a, et al. subgaleal hematoma from hair combing. pediatrics. 1981; 68: 583 584. 12.faber m. massive subgaleal hemorrhage: a hazard of playground swings. clin pediatr. 1976; 15: 384-385. 13.beauchamp cj, metcalf mb. subgaleal hemorrhage. pediatrics. 1983; 72: 912-913. romanian neurosurgery (2019) xxxiii, 1: 74-76 doi: 10.33962/roneuro-2019-015 www.journals.lapub.co.uk/index.php/roneurosurgery toddler with repeated fall frequently visiting hospital presented with acute subdural hematoma on readmission with ultra-rapid evolution: surgical management strategy guru dutta satyarthee1 1 department of neurosurgery, neurosciences centre, aiims new delhi, india abstract repetitive fall producing head injury in children may lead to development of intracranial hematoma. the course of evolution may be rapid in case of repeated fall due to induction of sub-clinical coagulopathy caused by repetitive cranial injury. the awareness of such possibility is highly desired among the pediatrician and neurosurgeon and emergency team and quick diagnosis and pertinent imaging study is of immense value and appropriate surgical management for prompt and expediting the evacuation of intracranial hematoma evacuation should be attempted to preserve good neurological outcome. authors reports a case, who had rapid neurological worsening, managed surgically with good neurological outcome, further various surgical management options along with pertinent literature are briefly reviewed. introduction traumatic brain injury is a global epidemic affecting all age group and producing cognitive, emotional, psychological, and economic burden and various disability and huge cost to society on care of acute phase of head injury extending to the rehabilitative phase. author presents a case, who had repeated fall in house due to carelessness and previously also visited hospital for fall, at current admission had rapid neurological worsening due to acute subdural hematoma. he was managed successfully. case illustration author presents a case of twoyear old male child with history of r e pe at ed f al ls. p at ie n t ha d fa ll f rom fi rst f loo r wi th l oss of consciousness. patient presented to trauma emergency, on evaluation gcs was e4v5m6 with no focal neurological deficit. computed tomography head did not reveal presence of fracture or intracranial haematoma and discharged satisfactorily after observation. (fig-1) however, due carelessness of parents, the child had again fell down and brought to emergency in unconscious state after three days after discharge from hospital following previous admission. on examination at current admission, vitals were stable with gcs was e3v3m5. his keywords repeated fall, cranial injury, acute subdural hematoma, surgery corresponding author: guru dutta satyarthee department of neurosurgery, neurosciences centre, aiims new delhi duttaguru2002@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 75 toddler with repeated fall… pupils were asymmetric, left pupil was dilated and not reacting to light. urgent repeat computed tomography scan head was done, showed presence of acute subdural hematoma extending over the left frontotemporal with midline shift with subfalcine herniation. (fig-2). baby had further neurological deterioration while awaiting admission at emergency to e2v2m4 and hence taken up for emergency surgical evacuation of acute sdh under general anaesthesia. dura was tense and following opening the dura, thick dark coloured blood clot was observed in the subdural space. post operatively child was electively ventilated for two days and then extubated and continued to receive decongestant therapy, antibiotics and antiepileptic medication continued. following emergency evacuation of acute subdural hematoma, pupil anomaly improved. at the time of discharge, child was e4v5m6, accepting orally and playing actively with mother. discussions figure 1. cranial computed tomography scan following fall at previous admission showing no evidence of fracture or presence of extra-axial or intra-axial hematoma. figure 2. computed tomography showing presence of large acute subdural hematoma over left frontotemporal region with associated mass effect and subfalcine herniation, at current admission. figure 1. non contrast computed tomography after six months following surgical evacuation of acute subdural hematoma. discussion traumatic brain injury constitutes leading causes of acquired disability and death in the infants as well as children1. subdural hematoma is most common intracranial pathology observed in neurosurgical practice following traumatic brain injury2,3. falls and motor vehicle accidents are common non-inflicted causes, while child abuse among infants and young children are unfortunate inflicted causes of traumatic brain injury2. the pathomechanism of fall from a short height in the very young children impart a predominantly linear force to the head. these forces can cause local deformity of skull or in cases forces being sufficient enough to produce skull fractures, and extradural hematomas. subdural hematomas development commonly results from displacement of the brain relative to the dura, and may associated with rupture of the bridging veins courses from the brain's surface to the overlying larger draining venous sinuses4,5. however, extradural hematomas is commonly associated with 76 guru dutta satyarthee focal impact injuries, but subdural hematoma almost always results from angular head deceleration, in which the brain continues to rotate relative to the more stationary skull and dura, associated with diffuse parenchymal damage. management of traumatic brain injury primary aims for limiting the progression of the primary brain injury and minimizing secondary brain injury6-11. surgical management is the mainstay of management of acute subdural hematoma with mass effect. however, in acses with rapid neurological deterioration, surgical decompression needs to be expedited and, in many resource, scarce centre, operation theatre may not be available, larger burr hole craniostomy with evacuation of subdural hematoma with subdural drain placement can offer an option with burr hole being placed at the site of thickest component9,11. satyarthee et al. reported burrhole evacuation of acute subdural haematoma is considered as a novel technique to reverse the worsening neurological state of patient7,8. other traditional approach include craniotomy with evacuation of subdural hematoma, decompressive craniectomay and management of associated intracerebral hematoma. decompressive craniectomy or other major intracranial procedure for evacuation of acute subdural hematoma can be done if patient gcs and neurological status remains stable8-13. conclusion a child with repeated fall may develop larger haematoma, although previous cranial ct scan may not show presence of any intracranial hematoma, and depending on history, detailed clinical assessment, appropriate neuroimaging study is advocated and further early and rapid neurological deterioration, emergent surgical management is must. awareness of rare but important pathology is highly recommended for pediatrician, neurologist, neurosurgeon and emergency care team. references 1. parslow rc, morris kp, tasker rc, forsyth rj, hawley ca. uk peadiatric traumatic brain injury study steering group, epidemiology of traumatic brain injury in children receiving intensive care in the uk. arch dis child 2005; 90:1182-7 2. ewing-cobbs l, prasad m, kramer l, louis pt, baumgartner j, fletcher jm, et al. acute neuroradiologic findings in young children with inflicted or noninflicted traumatic brain injury. childs nerv syst 2000; 16:25-33 3. vinchon m, defoort-dhellemmes s, desurmont m, dhellemmes p. accidental and nonaccidental head injuries in infants: a prospective study. j neurosurg 2005; 102:3804. 4. meservy cj, towbin r, mclaurin rl, myers pa, ball w. radiographic characteristics of skull fractures resulting from child abuse. ajr am j roentgenol 1987; 149:173-5. 5. vance bm. ruptures of surface blood vessels on cerebral hemispheres as a cause of subdural hemorrhage. ama arch surg 1950; 61:992-1006 6. gennarelli ta, thibault le. biomechanics of head injury. in: wilkins rh, rengachary ss, editors. neurosurgery. 1 st ed. new york: mcgraw hilb; 1985. p. 1531-36. 7. satyarthee gd, chouksey p., singh p., agrawal d, gurjar h. emergent burr-hole drainage of traumatic acute subdural haematoma with drain placement in pre-existing coagulopathy showing rapid neurological deterioration: a novel technique, indian j neurotrauma 2015;12:19-22 8. motohashi o: single burr hole evacuation of traumatic asdh of posterior fossa in emergency room, j neurotrauma. 2002; 19:993-938. 9. youichi yanagawa, toshihisa sakamoto: results of single burr hole drainage for acute subdural hematoma with non-reactive pupil. turk neurosurg 2012; 22(2):196-9. 10. sinha s, raheja a, garg m, moorthy s, agrawal d, gupta dk, satyarthee gd, singh pk, borkar sa, gurjar h, tandon v, pandey rm, sharma bs. decompressive craniectomy in traumatic brain injury: a single-center, multivariate analysis of 1,236 patients at a tertiary care hospital in india. neurol india. 2015 ;63(2):175-83. 11. alvis-miranda hr, m rubiano a, agrawal a, rojas a, moscote-salazar lr, satyarthee gd, calderon-miranda wg, hernandez ne, zabaleta-churio n. craniocerebral gunshot injuries; a review of the current literature bull emerg trauma 2016; 4 (2) 65-74 12. verma sk, borkar sa, singh pk, tandon v, gurjar hk, sinha s, satyarthee gd, gupta d, agarwal d, sharma bs. traumatic posterior fossa extradural hematoma: experience at level i trauma center. asian j neurosurg. 2018 apr-jun;13(2):227-232. 13. satyarthee gd. ideally, how early should cranioplasty be performed-days, weeks, or months following decompressive craniectomy surgery to label as "optimal early cranioplasty"? big enigma. world neurosurg. 2018; 112:302-303. 11kocamanumit_intrasphenoidal romanian neurosurgery | volume xxx | number 4 | 2016 | october december article intrasphenoidal rathke's cleft cyst: case presentation and review of the literature umit kocaman, muhammet bahadir yilmaz, hakan yilmaz turkey doi: 10.1515/romneu-2016-0083 520 | kocaman et al intrasphenoidal rathke's cleft cyst doi: 10.1515/romneu-2016-0083 intrasphenoidal rathke's cleft cyst: case presentation and review of the literature umit kocaman1, muhammet bahadir yilmaz1, hakan yilmaz2 1university of izmir of medicine, department of neurosurgery, izmir, turkey 2usak state hospital, department of neurosurgery, usak, turkey abstract: rathke's cleft cyst is a benign lesion of embryological origin with sellarsuprasellar localization. it is found in 12-33% of normal pituitary glands in autopsy series. although it is mostly asymptomatic, it can cause symptoms by compressing surrounding neural and pituitary tissues. the most common symptoms are endocrine problems, visual problems and headache. uncommonly, the lesion can present with apoplexy. it is rarely reported outside sellar-suprasellar sites, such as the cerebellopontine angle, prepontine cistern, and intrasphenoidal locations. we present an intrasphenoidal rathke's cleft cyst found during investigation of a headache and operated on. we discussed the case with literature review and two similar reported cases. key words: cyst, intrasphenoidal, rathke cleft, sellar-suprasellar introduction rathke's cleft cyst (rcc) is a benign, intrasellar, epithelial cystic lesion with mucoid content (6, 9). it is found in 12-33% of normal pituitary glands in autopsy series (9). it is thought to originate from rathke's pouch remnants. although these sellar and suprasellar lesions are usually asymptomatic, they can also cause symptoms due to pressure on surrounding neural tissues and the pituitary gland (6). the most common symptoms are endocrine problems, visual problems and headache. rarely, the lesion can present with apoplexy (6, 10). a few case presentations have reported in places other than sellar and suprasellar locations. two cases with pure intrasphenoidal localization were reported in the literature (4, 9). we present our intrasphenoidal case and discuss the case with literature review. case presentation a 28-year-old female patient presented with headache extending to the left eye. investigations revealed an isointense lesion filling the sphenoid sinus and eroding the planum sphenoidale and with contrast enhancement at the periphery on t1-weighted images. the sella base, the pituitary gland and stalk was intact (figures 1 and 2). the examination of the patient revealed no romanian neurosurgery (2016) xxx 4: 520 – 525 | 521 neurological deficit. no abnormality was present on laboratory analyses. the patient was operated through the transnasal transsphenoidal route. fluid with the viscosity of motor oil discharged from the cystic structure filling the sphenoid sinus. then the cyst wall was totally excised. pathology preparation showed cytokeratin (+), s100 (-), cd1a (-), and cd68 (+) in the cyst epithelium. the pathology report was rathke's cleft cyst accompanied by xanthogranulomatous inflammation (figure 3). the patient’s headache resolved in the postoperative period. postoperative 1st year follow-up mri and paranasal sinus tomography revealed no contrast enhancing lesion (figures 4 and 5). figure 1 preoperative brain mri images reveal an isointense lesion filling the sphenoid sinus and extending to the ethmoids with contrast enhancement of the periphery on t1-weighted images. the pituitary gland and stalk are seen to be intact 522 | kocaman et al intrasphenoidal rathke's cleft cyst figure 2 preoperative paranasal sinus tomography reveals a cystic lesion with inthesphenoid sinus, mostly on the right, eroding the planum sphenoidale and extending to the ethmoids figure 3a he x 20 with mucous and ciliated cyst epithelium. 3b: squamous metaplasia of cyst epithelium he x 20. 3c: xanthogranulomatous inflammation at cyst wall he x 20. 3d: cd68 (+) histiocytes at the wall dab x 10 romanian neurosurgery (2016) xxx 4: 520 – 525 | 523 figure 4 postoperative 1st year mri follow-up reveals no cystic lesion in the sphenoid sinus figure 5 postoperative 1st year paranasal sinus tomography reveals no cystic lesion in the sphenoid sinus 524 | kocaman et al intrasphenoidal rathke's cleft cyst discussion rccs usually have an anterior sellar or anterior intrasellar-suprasellar localization. a couple of cases located at the pontocerebellar angle (3, 12) or prepontine cistern (5) have been reported. an intrasphenoidal symptomatic rcc was reported only in 2 cases in the literature (4, 9). a pure sphenoidal location can be explained with the lesion's embryological origin (9). rccs originate fromrathke's pouch remnants (9). this pouch develops from the ceiling of the stomodeum coated with epithelial cells of ectodermal origin as a diverticulum towards the diencephalon in the 4th gestational week (9). the infundibulum develops from the neuroepithelium of the diencephalon origin in the same period. it migrates towards the craniopharyngeal canal. while the hypophyseal diverticulum is extending in the 5th week, the part connected to the oral ectoderm narrows and then closes and degenerates in the 6th week. the infundibulum andrathke's pouch become in contact again at the 5th week. the adenohypophysis and neurohypophysis develop in this way (9). this embryological process indicates that rcc's can be found at any location in the craniopharyngeal canal (9). rcc lesions are usually small and asymptomatic. the presenting signs may be hormonal problems, apoplexy, hypophysitis, abscess, hypothalamic dysfunction, sphenoid sinusitis, oculomotor involvement, metabolic encephalopathy or visual problems depending on the location (1, 6, 7, 10, 11). chronic cephalgia can also be seen with rcc. acute and severe headache can develop in patients with rcc due to bleeding inside the cyst, chemical meningitis, increased sellar pressure or local inflammation (6, 8). the first intrasphenoidal rcc in the literature was presented by megdichebazarbacha et al (9). headache and diplopia were present in a 41-year-old male patient in this case. the symptoms disappeared after spontaneous rhinorrhea but the headache and left visual loss recurred 4 months later. radiological analyses revealed an intrasphenoidal lesion compressing the pituitary gland and optic chiasm. the patient was operated with the transrhinoseptal approach and the symptoms resolved postoperatively (9). the second case in the literature was presented by kalina et al (4). a lesion that could be an intrasphenoidal rathke's cleft cyst was found during investigations performed for seizures in a 13year-old male patient in their case presentation. mucocele, meningocele and craniopharyngioma wereconsidered in the differential diagnosis. it was decided that the lesion was rcc and endoscopic fenestration was performed. the lesion had disappeared on 3rd month follow-up investigations (4). radiological rcc diagnosis has become more common with the start of mri use. an rcc can be seen as a well-delineated lesion that is hyper/iso/hypointense on t1-weighted and hyperintense on t2-weighted mri images depending on the amount of cholesterol, mucopolysaccharide and protein inside the cyst (2, 9). there is usually no contrast enhancement or circular enhancement may be present. cct shows hypodense lesions romanian neurosurgery (2016) xxx 4: 520 – 525 | 525 without contrast enhancement. the pituitary gland is usually around or below the cyst (9). the differential diagnosis mainly includes bleeding craniopharyngioma and adenoma. while rcc is usually not calcified, craniopharyngiomas become calcified and can be detected on cct. microscopically, rcc is covered with ciliated columnar or cuboidal epithelium and craniopharyngioma with squamous cells. the cyst content of rcc resembles motor oil. calcification is usually not seen in rcc cases. most rccs are asymptomatic and radiological preliminary diagnosis and differentiation from craniopharyngioma are therefore important. while the treatment aim for craniopharyngiomas is total excision, cyst drainage through the transsphenoidal route and limited excision of the cyst wall can be enough for rcc patients (9). preliminary consideration of rcc radiologically will therefore determine how aggressive surgery will be (9). written informed consent of the patient was obtained. correspondence hakan yilmaz, usak state hospital, department of neurosurgery, usak, turkey. e-mail: dr_hakanyilmaz@hotmail.com tel: +90 5066211829 references 1.albini ch, macgillivray mh, fisher je, et al. triad of hypopituitarism, granulomatous hypophysitis, and ruptured rathke’s cleft cyst: neurosurgery 1988; 22: 133136 2.brassier g, morandi x, tayar e. rathke’s cleft cyst: surgical-mri correlation in 16 symptomatic cases. j neuroradiol 1999;26: 162-171 3.fan j, qi s, peng y, et al. an isolated primary rathke's cleft cyst in the cerebellopontine angle. j neurosurg 2014; 121(4): 846-850 4.kalina p, rykken j. pediatric sphenoidal rathke’s cleft cyst. journal of pediatric neuroradiology 2012; 1: 313– 316 5.kim e.a. case of ectopic rathke's cleft cyst in the prepontine cistern. j korean neurosurg soc 2012; 52(2): 152-155 6.kim e.a. rathke's cleft cyst presenting with apoplexy. j korean neurosurg soc. 2012;52(4): 404-406 7.komatsu f, tsugu h, komatsu m, et al. clinicopathological characteristics in patients presenting with acute onset of symptoms caused by rathke’s cleft cysts. actaneurochir (wien) 2010; 152: 1673-1678 8.kurisaka m, fukui n, sakamoto t, et al. a case of rathke’s cleft cyst with apoplexy. childs nerv syst 1998, 14 : 343-347 9.megdiche-bazarbachah, ben hammouda k, aicha ab, sebai r, et al. intrasphenoidal rathke cleft cyst. ajnr am j neuroradiol 2006; 27(5): 1098-100 10.pawar sj, sharma rr, lad sd, et al. rathke’s cleft cyst presenting as pituitary apoplexy. j clin neurosci 20012; 9: 76-79 11.rosales my, smith tw, safran m. hemorrhagic rathke’s cleft cyst presenting as diplopia. endocr pract 2004; 10: 129-134 12.zhou l, luo l, hui x, et al. primary rathke's cleft cyst in the cerebellopontine angle associated with apoplexy. childs nerv syst 2010; 26(12): 1813-1817 microsoft word 1apetreica_paediatric romanian neurosurgery (2018) xxxii 2: 183 186 | 183             doi: 10.2478/romneu-2018-0024 paediatric brain monitoring with information technology (kidsbrainit) era-net neuron grant c.a. apetrei1, c. gheorghita2, a. tascu3,4, a.st. iencean1, tsz-yan milly lo5, ian piper6, st.m. iencean1,7 1neurosurgery, "prof. dr. n. oblu" clinical emergency hospital iasi, romania 2neurosurgery, "sf. maria" children clinical emergency hospital iasi, romania 3neurosurgery, "bagdasar-arseni" clinical emergency hospital bucharest, romania 4neurosurgery, "carol davila" university of medicine and pharmacy bucharest, romania 5university of edinburgh (child life & health) / royal hospital for sick children (paediatric critical care medicine), uk 6brainit group co-ordinator, principal health care scientist, neuro-intensive care monitoring research, uk 7neurosurgery, "grt popa" university of medicine and pharmacy iasi, romania abstract: the complete name of this era-net neuron grant is “paediatric brain monitoring with information technology (kidsbrainit). using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety”. the project coordinators are ms. dr. tsz-yan milly lo (consultant paediatric intensivist and research lead in paediatric critical care medicine ) and ian piper from university of edinburgh, uk and the partners are: prof. bart depreitere and his team from neurosurgery & intensive care research group, university hospitals leuven, belgium; prof. juan sahuquillo and his team from department of neurosurgery, vall d’hebron university hospital, barcelona, spain and the romanian team with doctors ca apetrei, c gheorghita and a tascu as principal investigators in three different hospitals. this material is based on the scientific project proposal with the basic project data. the aim of this grant is to test two clinically relevant hypotheses: after sustaining traumatic brain injury (tbi), paediatric patients with a longer period of measured cerebral perfusion pressure (cpp) maintained within the calculated optimal cpp (cppopt) have an improved global clinical outcome and better tolerance against raised intracranial pressure (icp). paediatric tbi patients requiring intensive care are recruited from more contributing centres in 4 different countries. their anonymised routinely collected bedside physiological monitoring data in minute-resolutions linking with anonmyised clinical and outcome data are exported 184 | apetrei et al paediatric brain monitoring with information technology (kidsbrainit)             and archived in the central kidsbrainit data-bank. cppopt is calculated and icp dose-response analyses are performed on the kidsbrainit dataset and their correlations with global outcome at 6 months are determined. the final aim of this study is to improve the treatments of the abnormal physiology insults: increase pressure from brain swelling (raised icp) and brain perfusion pressure (cpp). key words: cerebral perfusion pressure, children brain trauma, intracranial pressure, paediatric brain monitoring introduction as we have already mentioned this material is based on the scientific project proposal with the basic project data, made by dr. tsz-yan milly lo. traumatic brain injuries in children represent a major cause of morbidity and mortality worldwide and it is the main cause of death in children older than one years of age. as shown in the project proposal the “majority of children who survives a life threatening brain trauma have new disabilities that affect how they function throughout the rest of their lives. this also has great impact on their carers and societies. currently the best option to improve survival and recovery of children with life threatening brain trauma is to improve their early hospital treatments including intensive care because none of the new experiemental therapies tested in the laboratory is useful in clinical practice.” also we find that “the current best therapeutic option to improve paediatric tbi outcome is to optimise physiological support in the intensive-care to minimise secondary physiological insults which are proven to negatively affect outcome. however therapeutic thresholds for abnormal physiology vary between units and are implemented clinically without validation. to give these patients the best possible recovery, we urgently need clinically relevant and readily translatable research that optimises paediatric brain trauma treatment and reduces inequality between different centres.” secondary ischaemic injury from reduced brain perfusion is the main insult neurointensive care management aims to prevent and we need to monitor cerebral blood flow (cbf) and metabolism continuously to prevent brain ischaemia. “intact cerebrovascular autoregulation means having the ability to maintain a stable brain perfusion for varying mean arterial blood pressure (map). in clinical practice, we know cerebrovascular autoregulation is intact when a patient retains the pressure active pattern while considering the relationship between map and icp. optimal cpp (cppopt) is the cpp level that maintains the pressure active pattern. cerebrovascular autoregulation is known to be impaired after severe tbi and the degree and range of this dysfunction vary between patients and over time within the same patient. continuous real-time physiological monitoring is a recognised standard in tbi intensive-care romanian neurosurgery (2018) xxxii 2: 183 186 | 185             management and icp-lowering therapy is recommended when icp is elevated above 20 mmhg or more, but this treatment threshold is only based upon clinical experience.“ we hypothesize that having measured cpp within calculated cppopt provide better tolerance to raised icp and improve recovery in childhood brain trauma. methodology patient recruitment: children aged 2 to 16 years who require intensive care management after sustaining accidental tbi are eligible for inclusion. the contributing units ( uk, belgium, spanish, and romanian centres) have similar treatment protocols, which include: ‐ defined raised icp treatment guidelines using osmo-diuretics as a first line medical treatment; ‐ using intravenous infusions of vasopressive drugs (noradrenaline infusion being the first choice) to drive mean arterial blood pressure to achieve a target cpp; ‐ sedation and muscle relaxant protocol; ‐ mechanical ventilation to control paco2 to low normal values; ‐ actively controlling core body temperature to normothermia. data collection: patients’ anonymised clinical data are collected; it includes the cause and nature of injury, age, glasgow coma score (gcs) on admission and after acute non-surgical resuscitation, pupillary responses, initial radiological and computerized tomography (ct), operative and other treatment details. each patient’s anonymised clinical data is linked to their physiological and outcome data in the kidsbrainit data-bank using an anonymous study id. routinely measured physiological data in minute-resolutions are captured from the bedside monitors prospectively. all physiological data are anonymised prior to exporting, and then stored in the kidsbrainit central data-bank outcome assessments are performed by each local team. data analyses cppopt calculation and icp doseresponse visualisation analyses are performed to test our hypotheses and determine if tbi patients with favourable outcome have longer periods of measured cpp within the calculated cppopt ranges and an enhanced tolerance of raised icp. figure 1 correlation of cerebro-vascular autoregulation and raised icp 186 | apetrei et al paediatric brain monitoring with information technology (kidsbrainit)             the accordance between cppopt and actual cpp is calculated to evaluate the association with survival (gos > 1) and favorable outcome (gos >3): ‐ the percentage of time for which the actual cpp is within the recommended cppopt range; ‐ the average difference between actual cpp and cppopt; ‐ the average absolute difference between actual cpp and cppopt; ‐ the average absolute difference when actual cpp is outside cppopt range; ‐ the average difference where actual cpp is below cppopt; ‐ the average difference where actual cpp is above cppopt; and ‐ the previous criteria are used in a multivariate logistic regression model. conclusions the findings from our study and any treatment target recommendations are directly transferable back to a wider clinical audience because no special equipment or software is required beyond that is currently used for the routine minute-by-minute physiological bedside monitoring. acknowledgments this work is within the grant: “paediatric brain monitoring with information technology (kidsbrainit): using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety”, grant: cofund-neuron iii eranet kidbrainit, funding no.2 / 01/06/2017. correspondence: a. tascu, "carol davila" university of medicine and pharmacy bucharest, romania e-mail: tascu_alexandru@yahoo.com references 1. tsz-yan milly lo. paediatric brain monitoring with information technology (kidsbrainit): using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety. proposal application form era-net neuron, 2016 2. guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents (second edition). pediatr crit care med 2012. 13, no 1 (suppl.) 3. chambers ir, jones pa, lo tym et al. critical thresholds of intracranial pressure and cerebral perfusion pressure related to age in paediatric head injury. j neurol neurosurg psychiatry 2006. 77(2): 234240. 4. depreitere b, güiza f, van den berghe g, schuhmann m, maier g, piper i, meyfroidt g. pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in severe traumatic brain injury patients based on minute-by-minute monitoring data. j. neurosurgery 2014 jun; 120(6): 1451-1457. 5. güiza f, meyfroidt g, lo tym, jones pa, greet van den b, depreitere b. continuous optimal cpp based on minute-by-minute monitoring data: a study on a pediatric population. acta neurochir 2015. 6. guiza f, depreitere b, piper i et al. visualizing the pressure and time burden of intracranial hypertension in adult and paediatric traumatic brain injury. intensive care medicine 2015. 41(6): 1067-1076. 7. hutchison js, frndova h, lo tym et al. impact of hypotension and low cerebral perfusion pressure on outcomes in children treated with hypothermia therapy following severe traumatic brain injury: a post hoc analysis of the hypothermia pediatric head injury trial. dev neurosci. 2010; 32(5-6): 406-12 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article cystic meningioma: unusual entity with review of literature vikas maheshwari, maneet gill, amit narang, m.n. swamy india doi: 10.1515/romneu-2017-0086 romanian neurosurgery (2017) xxxi 4: 551 554 | 551 doi: 10.1515/romneu-2017-0086 cystic meningioma: unusual entity with review of literature vikas maheshwari, maneet gill, amit narang, m.n. swamy department of neurosurgery, armed forces medical college, pune, india abstract: cystic meningioma is a relatively rare condition, radiological appearance of the cystic-solid components of the mass may create a diagnostic dilemma. the presence of a cyst is not a common imaging feature and this makes it difficult to differentiate it from hemangioblastoma, craniopharyngioma, metastasis and gliomas. cystic meningiomas are present more commonly in children. we present a 60 year old male who presented with seizures and frontal lobe signs. the lesion was suspected as glioma however, postoperative histopathological examination demonstrated as meningioma. patient showed remarkable recovery after surgery. complete cyst resection should be considered if it is technically feasible and safe. key words: cystic meningioma. cystic brain tumor, meningioma introduction meningiomas account for nearly 15% of all intracranial tumors and are the common extra-axial tumors as well as the most common intracranial non glial tumors. most of them are benign, although atypical and malignant forms of meningiomas also exist.(5) cystic meningioma is a relatively rare condition accounting for 2% to 4% of all intracranial meningiomas. (8) meningiomas with cystic component mimic metastatic lesions or malignant gliomas often causing diagnostic dilemma. the presence of a cyst is not a common imaging feature and this makes it difficult to differentiate it from hemangioblastoma, craniopharyngioma, metastasis and gliomas. (10) the other confounding feature is the presence of peri tumoral edema. we hereby report a case of cystic meningioma, along with review of literature.case history 60 year male, with no comorbidities presented with history of frontal headache, memory disturbances of six months and behavioural changes in the form of agitation, irrelevant talks and use of abusive language of four months duration. there were two episodes of generalized tonic clonic seizures. no h/o blurring of vision or vomiting. on examination patient was hemodynamically stable. neurologically his gcs was e4v4m6 with no cranial nerve involvement. there 552 | maheshwari et al cystic meningioma were no motor or sensory deficits. his mini mental score was 8/30 mri brain fig (1a &1b) showed solid cystic mass lesion measuring 42.3 x 60.9 x 43.7 mm in the right superior and middle frontal gyrus. solid component was hypointense in t1w, mildly hyperintense on t2w with presence of perilesional edema. contrast mri showed enhancement of solid part with septal enhancement of cystic component. there was thick, smooth dural enhancement of the frontal lobe. the lesion was abutting lateral wall of anterior 1/3rd of superior saggital sinus (fig 1-b & c). mrs showed increased choline to creatine ratio. patient underwent rt fronto-temporal craniotomy with gross total excision of tumor. intraoperativaly lesion had well defined tumor brain interface. cystic component was in posterolateral aspect. the tumor was moderately vascular non suckable with base infiltrating convexity dura. a thin sleeve of tumor over the anterior 1/3rd of superior saggital sinus was cauterized. post op cemri brain (fig 2a & 2b) showed minimal residual tumor along the wall of superior sagittal sinus. postoperative recovery was uneventful and patient discharged on 8th post op day. mmse score improved to 27/30 at the time of discharge. patient is on regular follow up and doing well. histopathology showed meningothelial meningioma who grade-1. figure 1 – contrast mri brain (a) axial cut(white arrow) showing solid and cystic componant. (b) coronal & (c) sagital cut (white arrow) lesion abutting superior sagital sinus romanian neurosurgery (2017) xxxi 4: 551 554 | 553 figure 2 post operative contrast mri a(axial) & b (sagital)– showing complete excision of the tumor discussion the term “cystic meningioma” has been used to describe meningiomas having cysts intratumoral or peritumoral. (5) rengachary et al. described two varieties 1) intratumoural cysts and 2) peritumoural cysts, based on meningothelial cell lining of the cyst. (8) these are more common in paediatric patients than in adults. in adults, cystic components are found in only about 3-7 % of cases as was seen in our patient.(12) the most common location is the frontoparietal region. (4) large cystic meningiomas are usually difficult to differentiate from gliomas, intracranial abscesses, hemangioblastomas and metastatic lesions. (13) the underlying mechanism of cyst formation remains unclear. penfield was the first to describe cyst formation in a meningioma. according to fortuna et al. (1) intratumoral cysts are the outcome of cystic degeneration, ischemic necrosis, or hemorrhage within the tumor. in addition, transudation or secretory changes within the meningioma may also lead to the formation of cysts.(7) a peripheral cyst, on the other hand, may represent either peripheral degeneration or an arachnoid cyst.(2) nauta et al. in 1979 described four types of relationship between cyst and tumor in cystic meningiomas: (6) a)a centrally located intratumoral cyst that is surrounded by macroscopic tumor throughout, b)a peripherally situated intratumoral cyst c) a peritumoral cyst that actually lies within the adjacent brain d) peritumoral cyst at the interface of tumor and brain. worthington et al (11) then added a fifth type to the nauta classification: type v, in which the cysts enclosed the tumor nodule with the neoplastic cells on the cystic wall. our case was probably a nauta type ii as had a peripherally situated intratumoural cyst. patients of cystic meningioma have a clinical presentation similar to classical meningiomas. symptoms can vary from features of raised intra cranial tension, seizures, headache or neurological deficits. since most of the meningiomas are of extra axial origion, preoperative cemri brain 554 | maheshwari et al cystic meningioma remains the gold standard for diagnosis. fdg pet though useful in differentiating atypical meningiomas from low grade meningiomas , has a little role in diagnosis of cystic meningioma.(9) notably, atypical meningiomas have the tendency to form a cyst, as opposed to other subtypes of meningioma. the most frequent histological subtype has been found to be the meningothelial subtype. our case also had similar histology. (10) treatment and prognosis depend on a various factors, such as histological subtype, tumor location, age of the patient, and comorbidities. patients can be followed with serial mri to assess for growth of tumor if the tumor is small and patient is asymptomatic.(5) most of the benign meningiomas, depending up on location and accessibility, can undergo a safe total resection. in cases of malignant meningiomas, in addition to resection, combination of radiation and chemotherapy (adriamycin and dacarbazine or ifosfamide and mesna) as adjuvant therapy has shown to increase median survival up to 3 years. (3) conclusion some of meningiomas are associated with diagnostically confusing cysts. cystic meningiomas are present more commonly in children. in spite of the various mr imaging features, cystic meningioma may present with diagnostic dilemmas. their differentiation from the more common gliomas, abscesses, hemangioblastomas and metastases is sometimes difficult. it is advisable to excise it completely as leaving behind cystic components can lead to recurrence of a potentially curable tumor. correspondence dr. vikas maheshwari email drvikas08@rediffmail.com, armed forces medical college, pune – india – 411040 phone +91 9545638380 references 1.an hy, yu ik, kim ms, kim sm, kim hk. angiomatous meningioma: ct and mr imaging features. j korean soc radiol 2011;64:429-34. 2.buetow mp, buetow pc, smirniotopoulos jg. typical, atypical, and misleading features in meningioma. radiographics 1991;11:1087-106 3.falavigna a, santos ja, chimelli l, ferraz fa,bonatelli ad ade p. anaplastic meningioma: case report. arq neuropsiquiatr 2001 4.j. cho, j. gagliardi, and s. chadda, “cystic meningioma,” applied radiology, pp. 29–30, 2009. 5.mittal a, layton kf, finn ss, snipes gj, opatowsky mj. cystic meningioma: unusual imaging appearance of a common intracranial tumor.proc (bayl univ med cent). 2010 oct;23(4):429-31 6.nauta hjw, tucker ws, horsey wj, bilbao jm, gonsalves c. xanthochromic cysts associated with meningioma. j neurol neurosurg psychiatry 1979;42:529-35. 7.odake g. cystic meningioma: report of three patients. neurosurgery. 1992;30:935–940. 8.tatli m ,guzel a , gokselh h m. cystic meningiomas: report of three cases turkish neurosurgery 2006, vol: 16, no: 4, 185-188 9.valotassiou v, leondi a, angelidis g, psimadas d, georgoulias p. spect and pet imaging of meningiomas. the scientific world journal. 2012;2012:1-11 10.wang p, han s, liu n, yu c, qi x, zhu m, zhang x, wang li, yan c. peritumoral cystic meningioma: areport of two case and review of literatureexp ther med. 2016 mar;11(3):904-908. 11.worthington c, caron jl, melanson d, leblanc r. meningioma cysts. neurology. 1985 dec;35(12):1720-4 12.zhang d, hu lb, zhen jw, zou lg, feng xy, wang wx et al. mri findings of intracranial cystic meningiomas. clin radiol 2009;64:792-800 13.zhao x, sun jl, wang zg, zhang tg, wang cw, ji y. clinical analysis for an unusual large cystic meningioma: case report and review of the literature. clin neurol neurosurg. 2008;110:605-8. microsoft word _6.formatata_seferis.doc romanian neurosurgery vol. xvi nr. 1 29 gamma-knife: radiosurgery in greece efficiency of the method for patients with vestibular schwannomas (clinical assessment) ch.a. seferis gamma knife department, hygeia hospital, athens, greece vestibular schwannomas are histologically benign tumours which arise from the schwann cells in the acoustic division of the 8th cranial nerve. it is important to distribute the lowest possible dose during the "visual" route of the facial nerve around the ventricular part of the tumour, as the latter is located at the pontomedullary junction on the anterior margin of the internal auditory duct. we can note that using doses of gamma irradiation we can satisfactorily control the volume of the lesion, as is confirmed by the patients' bi-annually follow-up appointments while there is a low percentage of adverse events that involve the cranial nerves. keywords: gamma-knife, radiosurgery, vestibular schwannomas introduction based on the findings of gamma-knife radiosurgery performed at hygeia hospital to treat patients with vestibular schwannomas, we can present the clinical and neuro-otological behaviour of these spaceoccupying lesions in 79 patients within a two-year follow-up period after treatment. presentation vestibular schwannomas are histologically benign tumours which arise from the schwann cells in the acoustic division of the 8th cranial nerve. thanks to the latest technological advancements in neuro-imaging methods and neurophysiological techniques, there is an increase in incidence rate of vestibular schwannoma patients in the general population. nevertheless, despite these new techniques (monitoring of the 8th cranial nerve, evoked acoustic potentials during microsurgical procedure), the operation cannot eliminate morbidity and mortality. based on the features of the tumour, we can apply several types of treatments beyond the conventional surgical approach. one of these non-invasive techniques to treat vestibular schwannomas is radiosurgery using gamma radiation (photons) or "gamma-knife", as it is more widely known. this study describes the findings of radiosurgery in patients with vestibular schwannomas who have been treated over the last four years at the gamma-knife unit of hygeia hospital. material and method over the last four years, 79 cases of vestibular schwannomas have been treated at the gamma-knife unit of hygeia hospital. of these patients, 23 had already undergone a surgical operation and afterwards they chose to use this method as a supplementary treatment of the residual lesion. there are available audiograms performed upon 18 patients within two years after treatment while audiograms for other patients are still pending. of the 79 patients who underwent the treatment, one passed away within four years after treatment (due to pre-existing heart problems), four patients lost to follow-up and have not reported on the response of the lesion to the gamma ch.a. seferis romanian neurosurgery vol. xvi nr. 1 30 knife radiation, while twelve patients have not provided a pre-operation audiogram as requested before the treatment. two of the patients said that "their life quality deteriorated after the treatment", and one of them has also reported deterioration in hearing. to analyze the effect of radiation, patients were recommended to comply with a follow-up schedule that included appointments on months 6, 12, 18, 24 after gamma-knife treatment and provide medical reports of recent brain mri and audiogram. the objective of the follow-up was to be monitoring the vestibular schwannoma volume and any change in hearing acuity obtained through gamma-knife treatment. the used gy dose and the isodose curve of radiation were also measured in terms of their effect on the progress of vestibular schwannomas. the mean age distribution was 55 years (range 27 74 years). of the 79 patients, 9 had intracanalicular tumours only, 19 had both intracanalicular and cisternal tumours, and 51had simple tumours in the pontocerebellar cistern. the mean volume (μv) was4,79 cm3 (range 0.20-19.3 cm3). features of the gamma-knife treatment gamma-knife radiosurgery utilises the following four principles: (i) locate the "target" using neuro-imaging techniques with a stereotactic head frame and a computer to record and edit data, (ii)determine the volume (v) of the lesion. (iii)determine distribution of radiation dose and finally (iv)treat using photons. during the treatment, the mean isodose curve used was 48,2 % ranged between 40% 54 %. it is very important to locate the target and thus exclude significant brain structures from gammaradiation, such as the cranial nerves surrounding the tumour, the cerebellum and of course the brain stem. at this point we should note that when defining important brain structures the facial nerve constitutes a major problem, mainly because it can be dislocated by the lesion (facial paresis is a common complication of the surgical treatment). consequently, when using neuro-imaging techniques, we should mainly be concerned about protecting the facial nerve and preventing complications that may be caused by radiation. for this, it is important to distribute the lowest possible dose during the "visual" route of the facial nerve around the ventricular part of the tumour, as the latter is located at the pontomedullary junction on the anterior margin of the internal auditory duct. during the treatment, the mean dose was 12,09 gy (range 11 14 gy) and the mean maximum dose was 19,83 gy (range 20,5gy – 29,9 gy). the mean volume of the radiated schwannomas was 4,72 cm3 (range 0.2 cm3 -19.3 cm3). to follow the international literature and to protect non-defined segments of the facial and trigeminal nerves that may be included in the lesion area, we administered to these areas doses that did not exceed 13 and 15 gy, respectively, while the dose administered to 2 patients having a tumour with a space-occupying effect on the brain stem did not exceed 10 gy. all patients responded well to the treatment and all of them discharged from the hospital the next morning after the end of the treatment. no one reported problems, such as epileptic attacks during their hospitalization, while severe headache was reported by 12 patients as the only adverse event, probably due to the stereotactic frame. to treat headaches, analgesic medication was administered for a short time period (2-3 days) and after discharge. follow-up and clinical assessment with the exception of one case, all patients had an mri test within six months after treatment. six of them did not attend follow-up appointments of month 12 and eleven of them did not undergo an audiogram within the two-year period (reporting as an excuse that they had fully regained their hearing). the rest of them have not yet completed two years since the gamma-knife treatment. the clinical assessment included: α) hearing evaluation β) effect of radiation on the surrounding cranial nerves. gamma-knife: radiosurgery in greece romanian neurosurgery vol. xvi nr. 1 31 based on these facts, we evaluated the progress of the patients' life quality depending on how they appreciated it after the gamma-knife treatment. we also asked them whether the treatment was worth it. results the mean follow-up period was 24 months (1-51 months). 84.2% of the patients provided at least the first mri (at the 6-month follow-up appointment). functionality of the surrounding cranial nerves no one of our patients who underwent gamma-knife surgery as their first choice for treating their vestibular schwannoma developed any functional disturbances of the facial nerve or sensory disturbances of the trigeminal nerve immediately after treatment or later during the follow-up period. patients who had developed a house-brackmann grade iii-iv facial paresis before radiosurgery did not show any significant change. changes in hearing most of the patients who underwent radiosurgery using a gamma-knife system have not reported any significant change in the hearing acuity they had before treatment although we should take into account that most of them did not comply with the follow-up and audiogram schedule, despite repeated recommendation. nevertheless, those who provided preand post-treatment audiograms (only patients who belonged to gardner-robertson scale class i and ii were evaluated) showed improvement in hearing ("gain" in db) until their second follow-up appointment both at 2 khz and 4 khz, from 5 to 45 db and from 4 to 20 db, respectively. only one woman patient showed a 10 db decrease in hearing acuity at 2 khz at the 12month follow-up. changes in clinical state most of the patients, who underwent gamma-knife treatment and developed neurological symptoms before radiosurgery, say that they experienced improvement or even complete regression of symptoms (nausea, dizziness, tinnitus, drowsiness etc.) only one woman patient reported deterioration of symptoms and 3 other patients did not report any significant change of symptoms. conclusion as a conclusion of this study on vestibular schwannoma cases treated at hygeia hospital, we can note that using doses of gamma irradiation as low as those firstly applied at karolinska and pittsburgh institutes (lower than those used when the treatment was initially applied at hospitals on abroad), we can satisfactorily control the volume of the lesion, as is confirmed by the patients' bi-annually follow-up appointments while there is a low percentage of adverse events that involve the cranial nerves. using stereotactic mri imaging and a schedule of multiple doses seems to mainly contribute to this outcome. according to the international bibliography, the method may fail if the doctor chooses not to partially exclude lesions located within the upper size limit of the treated area. the "acoustic gain" in db is also a notable point of interest, although most patients cannot perceive it as a significant change in their hearing. references 1.henzel m, hamm k, sitter h, gross mw, surber g, kleinert g, engenhart-cabillic r. comparison of stereotactic radiosurgery and fractionated stereotactic radiotherapy of acoustic neurinomas according to 3-d tumor volume shrinkage and quality of life. strahlenther onkol. 2009;185(9):567-73. 2.liscak r, vladyka v, urgosik d, simonova g, vymazal j. repeated treatment of vestibular schwannomas after gamma knife radiosurgery.acta neurochir (wien). 2009;151(4):317-24; 3.lobato-polo j, kondziolka d, zorro o, kano h, flickinger jc, lunsford ld. gamma knife radiosurgery in younger patients with vestibular schwannomas.neurosurgery. 2009;65(2):294-300 4.mann w, gouveris ht. diagnosis and therapy of vestibular schwannoma. expert rev neurother. 2009;9(8):1219-32. 5. pollock be. stereotactic radiosurgery of benign intracranial tumors. j neurooncol. 2009;92(3):337-43. 6. silk ps, lane ji, driscoll cl. surgical approaches to vestibular schwannomas: what the radiologist needs to know. radiographics. 2009;29(7):1955-70. 7.verma s, anthony r, tsai v, taplin m, rutka j. evaluation of cost effectiveness for conservative and active management strategies for acoustic neuroma. clin otolaryngol. 2009;34(5):438-46. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article high lumbar disc herniation coexisting with thoracic meningioma – an issue of differential diagnostic m. dabija, v. dorobăţ, alina paiu romania doi: 10.1515/romneu-2017-0047 romanian neurosurgery (2017) xxxi 3: 289 293 | 289 doi: 10.1515/romneu-2017-0047 high lumbar disc herniation coexisting with thoracic meningioma – an issue of differential diagnostic m. dabija1,2, v. dorobăţ3, alina paiu3 1“grigore t. popa” university of medicine and pharmacy iaşi, romania 2emergency clinical hospital “prof. dr. n. oblu’’, iaşi, romania 3resident in neurosurgery, emergency clinical hospital, “prof. dr. n. oblu’’, iaşi, romania abstract: meningiomas involving the spinal compartment are relatively rare compared to the intracranial ones representing between 7,5% and 12,5% of all cns meningiomas, most of them being located in the intradural compartment respecting the pial layer of the spinal cord. affecting ten times more often women rather than men, especially in the 5th and 6th decade of life, they pose a difficult diagnostic setting despite modern neuroimagistic techniques. the matter of correct differential diagnosis becomes even more doubtful, most of the patients of that age having also associative degenerative disorders, e.g. lumbar disc herniation. in this case proper neurological examination is the key as we will furthermore demonstrate the mri exam being targeted on the level of the sensorial dysfunction and not on the most common region which gives according pathology. the following case presentation can be considered “classic” representing a patient with all the criteria mentioned above including a long history of rheumatologic and chronic back pain medication for pain relief .we used the frankel scale for grading the preand postoperative neurological status. acute neurological deterioration (under 24 hours) is an important criteria for admission in emergency unit with around the clock exploration followed by microsurgical operation for the best possible outcome. coexisting chronic lesions may be left behind and kept under surveillance, operated only when clear signs of health disorder appear. because there are reported cases of thoracic meningiomas discovered after hernia disc operation and even cases of paraplegia due to a missed lesion, the aim of this article is to emphasize the importance of proper neurological examination preceding any mri exploration. key words: spinal meningioma, high lumbar disc herniation, tumor resection, acute neurological deterioration 290 | dabija et al high lumbar disc herniation coexisting with thoracic meningioma background spinal meningiomas are relatively rare compared to the intracranial ones, representing only 1% of all meningiomas involving the nervous system(1). this is why, despite the advances and the availability of modern neuroimagistic methods nowadays, it is still a problem of missed diagnosis. being a rare condition, one has to “light a bell” when coming across specific symptoms listed below. it is always frustrating when you receive a patient with a long history of treatment for a lumbar degenerative disorder, and a simple babinski sign can make the difference. that is because spinal meningiomas are slow growing tumors and therefore their onset of symptoms is often insidious with unspecific back pains and the signs of spinal cord compression appearing late in the evolution(2). when you encounter associated pathology which can explain this clinical picture, it is even more difficult. on the other hand, degenerative disorders are very common and their concomitance with spinal tumors is a frequent fact. the two diseases – degenerative and tumoral may involve the same vertebral segment, and that is a favorable case because imaging for one will comprehend both of them, but there are cases when the two conditions appear in different regions, and a wrong indication for mri may pass over the other . in the current paper we present the case of a woman of 60 years old which presents with severe back pains with a long history of medical treatment and severe paraparesis – frankel c – motor function evaluated 3/5. she was already investigated mri – lumbar region – and diagnosed with lumbar disc herniation l1-l2. case presentation we present the case of a 60 year-old woman which was admitted in june 2017 in our center in emergency with severe paraparesis – frankel c with motor function 3/5 on the right and 4/5 on her left leg. low back pain was present during the last years, with a long history of medical treatment. in the last two months the patient experienced a gait disturbance with rapid aggravation in the last 24 hours. the neurologic examination revealed the paraparesis with bilateral babinski sign, spasticity, hyperreflexia, clonus and urinary difficulties. sensibility was depressed under t7 territory. on admittance the patient presented herself with an mri of the lumbar region which evidenced a lumbar disc herniation at the l1-l2 level with spinal cord compression at the cone level. (figure 1) figure 1 –t2weighted sagittal image confirmed a disc herniation at the l1-l2 level romanian neurosurgery (2017) xxxi 3: 289 293 | 291 figure 2sagittal magnetic resonance image extramedullary mass located between d7-d8 vertebral level, spinal cord displacement and compression.t1weighted images and important enhancement after gadolinium injection because of the high level of sensory dysfunction an mri of the thoracic region was performed in emergency and this one revealed an intradural extramedullary spinal tumor with homogenous enhancement at the t7-t8 level – most likely a meningioma – with obvious displacement and compression of the spinal cord. (figures 2, 3). figure 3 sagittal, axial and coronal mr image showing extramedullary mass on right lateral and anterior part of the spinal canal at the t7-t8 level with spinal cord dorsal displacement and compression 292 | dabija et al high lumbar disc herniation coexisting with thoracic meningioma the very next day the patient was operated, we performed a microsurgical resection of the extraaxial tumor which was indeed a meningioma with a large and calcified dural insertion in the anterior lateral part of the canal with resection of the dentate ligament and coagulation of the insertion. the histological examination confirmed a meningothelial meningioma. the postoperative evolution was favorable, the patient managed to walk without assistance after one week from surgery. the intensity of the low back pain decreased after the surgery and the patient preferred not to operate the lumbar disc herniation, resting it under our surveillance. discussion we are in this paper in front of two different types of pathological conditions: one, the lumbar disc herniation, which is very common (3), representing for many neurosurgeons and orthopedists the major part of their activity, and perhaps that is why it comes first to the mind of the practitioner, so they will furthermore explore the patient in this direction. on the other hand we have a very rare condition – spinal meningioma – which may have an insidious evolution that can mimic other degenerative or neurological diseases. spinal meningiomas are intradural extramedullary slow growing tumors, with insidious onset of symptoms, often only unspecific back pain, previous rheumatologic and back pain medical treatment being almost always present in the history of that disease. our patient also had a long period of antiinflammatory, muscle relaxant, antalgic and neurotrophic treatment, with time intervals of remission in symptomatology, but with continuous deterioration of her gait disturbances. finally she shows up in the emergency unit in a poor neurological status, with severe neurological deficit – frankel c with motor function evaluated 3/5, with clear signs of spasticity, hyperreflexia, clonus and urinary difficulties, cutaneous hypoesthesia with a superior level on t7. she already had a lumbar mri which showed a lumbar herniation on l1-l2 level, with spinal cord compression at the cone level, and she was sent for emergency neurosurgical treatment of this pathology. a conus medullaris syndrome has a clinical presentation that include loss of bladder reflex – urinary retention, paraparesis, hyperreflexia. what can make the difference? a meticulous neurological examination which in our case showed the level of sensitivity on t7 level and put the indication for thoracic spine mri imaging. the neurologic aggravation appeared in less than 24 hours so we considered our patient an emergency, exploring her the same day, and operating the next day, the result being favorable. the third day following surgery, we managed to raise the patient and she was able to walk some steps, and one week after that, she was able to walk without assistance. the postoperative evolution in spinal meningiomas is often associated with a good outcome even in the patients with neurological deficits or in elder ones (4). we did not perform any surgery on the l1-l2 disc herniation because the low back pain, apparently the only symptom related to this pathology, improved, and we shall surveil this condition. romanian neurosurgery (2017) xxxi 3: 289 293 | 293 there are other reported cases of patients operated for lumbar degenerative disorders with thoracic meningiomas discovered after the lumbar surgery was performed, even cases of paraplegia due to a missed thoracic lesion following lumbar surgery (5, 6, 7). we consider that is possible to avoid this type of error by giving more time to the neurological examination of our patients. this examination has to include motor, sensory and autonomous function tests in order to avoid missed diagnosis which can have a poor ending. conclusion spinal meningiomas are often benign lesions and a proper diagnostic and meticulous microsurgical resection will have in the outmost of cases good results. the concomitance of other spinal disorders, in particular these very frequent degenerative ones, may be a source of confusion and we emphasize, even if not necessary, the importance of a scrupulous neurological examination. acute neurological deterioration has to be treated in an emergency manner. from our experience, we have to do any effort to operate as soon as possible, desirably in the first 24 hours, in order to obtain better results. correspondence dabija marius e-mail: mariusdabija.md@gmail.com references 1. gottfried on, gluf w, quinones-hinojosa a, kan p, schmidt mh. spinal meningiomas: surgical management and outcome. neurosurg focus. 2003;14:e2. doi: 10.3171/foc.2003.14.6.2. 2. solero cl, fornari m, giombini s, lasio g, oliveri g, cimino c, pluchino f. spinal meningiomas: review of 174 operated cases. neurosurgery. 1989;25:153–160. doi: 10.1097/00006123-198908000-00001. 3. choi ys. “pathophysiology of degenerative disc disease”. asian spine journal 3.1 (2009): 39-44. 4. roux fx, nataf f, pinaudeau m, borne g, devaux b, meder jf. intraspinal meningiomas: review of 54 cases with discussion of poor prognosis factors and modern therapeutic management. surg neurol 1996;46:458—63 [discussion 63—4]. 5. takeuchi a, miyamoto k, hosoe h, shimizu k. thoracic paraplegia due to missed thoracic compressive lesions after lumbar spinal decompression surgery. report of three cases. j neurosurg 2004;100(1 suppl. spine):71—4 6. ko sb, lee sw, shim jh. paraplegia due to missed thoracic meningioma after laminotomy for lumbar spinal stenosis: report of two cases. asian spine j 2011;5:253—7. 7.knafo s, lonjon g, vassal m , bouyer b spinal cord compression due to undiagnosed thoracic meningioma following lumbar surgery in an elderly patient: a case report, orthopaedics & traumatology: surgery & research (2013) 99, 983—986 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article extracranial internal carotid artery aneurysm: case illustration marco zenteno, liliana escobar, angel lee, hernando raphael alvis-miranda, willem guillermo calderon-miranda, luis rafael moscote-salazar mexico, colombia doi: 10.1515/romneu-2017-0079 romanian neurosurgery (2017) xxxi 4: 517 521 | 517 doi: 10.1515/romneu-2017-0079 extracranial internal carotid artery aneurysm: case illustration marco zenteno1, liliana escobar1, angel lee1, hernando raphael alvis-miranda2, willem guillermo calderon-miranda3, luis rafael moscote-salazar2 1national institute of neurology and neurosurgery “dr. manuel velasco suarez” mexico city, mexico 2department of neurosurgery, university of cartagena, cartagena de indias, colombia 3national autonomous university of mexico, mexico city, mexico abstract: extracranial internal carotid artery aneurysms (eicaa) are uncommon lesion. these aneurysms can be classified as true or false aneurysms, atherosclerotic, dysplastic, infectious, posttraumatic and iatrogenic aneurysms. the most common presentation is central neurologic dysfunction, either a stroke or a transient ischemic attack. the rupture of these aneurysms can lead to severely impairment and can affect the quality of life of the patients or even may lead to death. management of these lesions is required in most cases to prevent complications, however there is no treatment guideline or expert consensus for the management. we present a case of an unusual eicaa, associated with kinking of the affected vessel and review the literature. key words: extracranial internal carotid artery; cerebral aneurysm; carotid kinking; endovascular therapy introduction extracranial carotid artery aneurysms are rare, with estimated incidence between 0.1%2% of all angiographical diagnostic procedures in large series; and up to 3.7% of all carotid procedures; and between 0.4 – 4% of all peripheral artery aneurysms.(1) a review of the literature conducted by the vascular group of the cleveland clinic foundation identified only 12 total reported cases, including 8 at their own facility, over a 17-year period. they can be classified according to their physiopathology as true or false aneurysms, according to their etiology in atherosclerotic, dysplastic, infectious, posttraumatic and iatrogenic aneurysms. extracranial internal carotid artery aneurysms (eicaa) generally are asymptomatic, but neurological symptoms are the most frequent. despite its rarity, these 518 | zenteno et al extracranial internal carotid artery aneurysm aneurysms are of interest because of their diverse etiology, and the need for correct choices of diagnostic and therapeutic strategies. they can severely affect the quality of life of the patients or even may lead to death if they are not recognized and treated. (2) it can give rise to serious complications like haemorrhage due to rupture, stroke and thromboembolism. we present the case of a patient with angiographical diagnostic compatible with an unusual eicaa. case report a 40-years-old female patient was admitted to the emergency department with presence of a pulsatile mass located in the right lateral cervical region. the mass was not associated with any pain, there was no history of trauma. occasionally she had complains of dysphagia. auscultation does not reveal any pathological murmur. cerebral and cervical vessels panangiography showed presence of one aneurysm of 20mm x 20mm, located in the right cervical internal carotid artery, in the bulbar portion, immediately distal to a severe kinking. (fig 1,2 3). the a1 portion of the ipsilateral anterior cerebral artery was hypoplastic, and the pressure sequence is negative, being discarded collaterals. the left internal carotid artery was completely normal. the medical board decided to perform endovascular therapy. maneuvers of microcatheter, guides, microguides, and stent navigation were performed with the road mapping. figure 1 3d angioct scan: lateral viev of the right carotid axis figure 2 3d angioct scan: lateral viev of the right carotid axis romanian neurosurgery (2017) xxxi 4: 517 521 | 519 figure 3 angioct scan: lateral viev of the right carotid axis the initial planning was to perform embolization through exclusive stent application, thus, a guide is navigated distal to the lesion, trying repeatedly to navigate the stent in the vessel and coating the aneurysm ostium. kinking rectification maneuvers (cervical hyperextension, cephalic limb contralateral rotation, apnea in maximum inspiration, buddy wire technique with guide 0.014, and hydrophilic terumo® guide) were failed. because of the risk of dissection secondary a forced maneuver in a patient without collateral circulation, it was decided to engage the maneuver and proceed to the coils placement. the coils were deployed according to the usual technique, covering the entire aneurysm sac without complications. a marked diminution in the filling of the aneurysm was observed immediately. the selective catheterization of the left vertebral artery (lva), produced a dissection in the v1-v2 union, which was not feasible to correct, because the microguide not able to navigate distal to the dissected portion. the collaterals from the right vertebral artery were satisfactory, taking both vertebral territories, renouncing to perform angioplasty. in controls was observed that lva was never completely occluded. full-dose antiplatelet is maintained, turning to orally antiplatelet posteriorly. the patient was discharged without any complications. discussion eicaa are rare vascular problems with a great potential for lethal thromboembolic episodes.(5) associated kinking of the artery is futher rare. the most frequent cause is atherosclerosis (46%–70%), followed by fibromuscular dysplasia, trauma, iatrogenic lesions, congenital defects, irradiation arteritis, or infection of the parapharyngeal space extending to the vessel wall. some authors suggest that it is of great importance to distinguish the etiology of the aneurysms because atherosclerotic eicaa might have a greater risk of early complications than dysplastic ones. it is important to establish if there is associated kinking of the artery. ilic et al suggest that degenerative aneurysms usually are associated with tortuosity of the artery unlike dysplastic aneurisms, which can usually be mistaken for a kinked artery. (5) due to enlargement of the saccular aneurysm, 520 | zenteno et al extracranial internal carotid artery aneurysm concomitant kinking of the ica may be present, as in our patient, adding further risk of cerebral events. furthermore, dysplastic aneurysms are localized below the kinked artery and are much complicated for surgical reconstruction as a result of its fragile and thin wall.(5) just for remember isolated major abnormalities in the cervical segment of the ica occur near of its origin or at the distal portion, at level of the atlas or axis. weibel after performing 1438 angiographies of neck vessels, found that 75% of ica kinks were placed at 2-4 cm of the carotid bifurcation. these aneurysms may be asymptomatic or present as a cervical pulsatile mass and provoke symptoms of adjacent neurovascular structure compression. the most common presentation is central neurologic dysfunction, either a stroke or a transient ischemic attack. (3) extracranial carotid aneurysm is equivocally diagnosed by palpation and visual inspection; however, ct scans and mri are useful diagnostic methods, but they cannot always be performed immediately. for the diagnosis, color doppler ultrasonography is very useful because realtime pictures of the aneurysm can be obtained noninvasively. there is no treatment guideline or expert consensus for the management of eicaa till today, but management is required in most cases to prevent complications. the therapy includes resection of the aneurysm and restoration of flow with venous, arterial, or prosthetic graft or endovascular stenting or end to end primary anastomose, depending on the size, location, and anatomic relation to surrounding structures. (4) diverse surgical procedures have been reported: aneurysmectomy with end-to-end anastomosis, vein graft or dacron interposition, anastomosis between the external and internal carotid artery, or even arterial ligation in emergency cases of aneurysm rupture. endovascular interventions require conductive anatomy and a skilled provider armed with the correct equipment to facilitate successful treatment via this modality. using this approach one must also be concerned with the possibility that the vessel of the patient may continue to undergo age-related growth or dilation around the inserted device. it should be considered the fact that there exists no significant experience with the use of endovascular techniques in the treatment of this kind of aneurysms. recent experience suggests that endovascular stenting is an emerging alternative treatment with promising results and a revolution from operative to endovascular intervention. due to paucity of data and lack of large series, limited knowledge of its safety and efficacy is available, as mentioned previously. other authors consider that endovascular stenting is technically feasible with high procedure success and relatively low complication rate in patients with eicaa, with both shortand mid-term outcomes appearing to be favorable. it is necessary when deciding in favour of endovascular therapy to evaluate for some circumstance that difficult the choice of endovascular repair such as fragile wall and narrow lumina of the altered artery. (5). romanian neurosurgery (2017) xxxi 4: 517 521 | 521 conclusion eicaa is a very rare occurrence that needs urgent management, the advanced imaging and surgical techniques used in the treatment of this patient avoided potential negative outcomes. regard endovascular therapy there exists no significant experience in the treatment of this kind of aneurysms, but in selected patients, can be an excellent option, with satisfactory outcomes. references 1. welleweerd jc, moll fl, de borst gj. technical options for the treatment of extracranial carotid aneurysms. expert rev cardiovasc ther [internet]. 2012 jul [cited 2013 nov 2];10(7):925–31. available from: http://www.ncbi.nlm.nih.gov/pubmed/22908925 2. garg k, rockman cb, lee v, maldonado ts, jacobowitz gr, adelman ma, et al. presentation and management of carotid artery aneurysms and pseudoaneurysms. j vasc surg [internet]. 2012 jun;55(6):1618–22. available from: http://www.sciencedirect.com/science/article/pii/s07415 21411031028 3. yoneyama t, kawashima a, sugiura m, yamaguchi k, itou k, namioka a, et al. technical options for the surgical management of extracranial carotid artery aneurysms. three case reports. neurol med chir [internet]. 2012 jan [cited 2013 nov 1];52(4):208–12. available from: http://www.ncbi.nlm.nih.gov/pubmed/22522332 4. rosset e, albertini jn, magnan pe, ede b, thomassin jm, branchereau a. surgical treatment of extracranial internal carotid artery aneurysms. j vasc surg [internet]. 2000 apr [cited 2013 nov 2];31(4):713–23. available from: http://www.ncbi.nlm.nih.gov/pubmed/10753279 5. ilic n, koncar i, dragas m, markovic m, kostic d, davidovic l. aneurysm of the kinked extracranial internal carotid artery: extraordinary union. [internet]. am. surg. 2010. p. e214–e215. available from: http://ezproxy.unicartagena.edu.co:2048/login?url=http: //search.ebscohost.com/login.aspx?direct=true&db=a9h &an=64471265&lang=es&site=ehost-live romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article conus medullaris dermoid tumour. uncommon presentation of conus medullaris dermoid as an exophytic mass lesion guru dutta satyarthee, ashwini kumar, luis rafael moscote-salazar india, colombia doi: 10.1515/romneu-2017-0015 romanian neurosurgery (2017) xxxi 1: 97 – 100 | 97             doi: 10.1515/romneu-2017-0015 conus medullaris dermoid tumour. uncommon presentation of conus medullaris dermoid as an exophytic mass lesion guru dutta satyarthee1, ashwini kumar1, luis rafael moscote-salazar2 1department of neurosurgery, neurosciences centre, aiims new delhi, india 2neurosurgeon-critical care, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia abstract: authors report an extremely uncommon case dorsally exophytic conus dermoid in a threeyears old boy, who underwent meningocele repair locate at lumbosacral region at an age of one month. the boy presented with low backache and difficulty in passing urine. magnetic resonance imaging evaluation of spine revealed presence of a large exophytic mass located dorsally in the conus and the features suggestive of dermoid. he underwent surgical intervention during surgery lesion was dorsally exophytic containing cheesy material with hairs, excision of dermoid along capsule was carried our successfully. pertinent literature and management of exophytic conus dermoid is discussed briefly. key words: conus dermoid, barrel gun like mass, conus mass, exophytic, signet ring introduction dermoid represent the rare midline tumors and constitute about 1-2% of the spinal tumors [1]. dermoid are thought to arise from ectopic ectodermal tissue inclusion during embryonic cns development [2]. dermoids are usually extramedullary tumors and mostly occurs during the first and second decade of life. the most common location for spinal dermoid is conus medullaris. our case is rare as the dermoid was intramedullary and had exophytic growth. the lumbosacral region spina bifida may be associated with intradural spinal dermoid tumours. however exophytic dermoid is very uncommon occurrence. was present, the patient was operated and the intra op findings were consistent with dermoid. histopathological examination confirmed the diagnosis. case illustration a-3-year boy, delivered at term of nonconsaguinous marriage presented with history of insidious onset slowly progressive low backache and difficulty in micturition with progressive paraparesis of lower limbs. significant history include surgery for 98 | satyarthee et al conus medullaris dermoid tumour             lumbosacral meningocele at age of two months. on examination the patient was conscious and alert with grade one power in both lower limbs. a graded sensory loss below umbilicus. presence of transverse scar at lower lumbar region of previous surgery was present. he had no past history of trauma or meningitis. signs were present mri of dorsolumbar spine revealed presence of a single large exophytic mass located dorsally at l1-l3 level (figure 1) and cauda equina roots were pushed anteriorly and existing nerve root exiting ventral to the conus mass lesion large dorsally helophytic tumor in the conus). and the features suggestive of dermoid, showing hypointense signal on t1 weighted image (figure 2 and hyperintense signal on t2 weighted image (figure 3), sagittal section image showing the tumour. he underwent d12 to fourth lumbar vertebral level re-exploration of wound, after lamina removal, bulging dura was observed .midline durotomy was done (figure 4). a large cyst like gun barrel was seen, pushing cauda equina nerve roots anteriorly along spinal cord. a midline myelotomy was made and dermoid cyst decompression started and complete removal was carried out. filum terminate was also divide, dermoid tumour was removed; it consisted of hair interspersed in the cheesy material. the cyst wall was thin. histopathological examination of the resected specimen revealed typical feature of dermoid. postoperative period was uneventful. at the last follow-up after three month following surgery, with improvement of power in lower limbs was noticed, he was playing and attending school. figure 1 magnetic resonance imaging t2 weighted dorsolumbar spine, sagittal section image showing large hyperintense intramedullary conus lesion like gun barrel appearance figure 2 magnetic resonance t1 weighted dorsolumbar spine, axial section image of three-yearboy showing large hyperintense intramedullary conus lesion like signet ring appearance romanian neurosurgery (2017) xxxi 1: 97 – 100 | 99             figure 3 magnetic resonance imaging t2 weighted dorsolumbar spine, axial section image showing large hyperintense intramedullary conus lesion like signet ring appearance figure 4 intraoperative photograph showing conus dermoid after dural opening discussion dermoid are the midline tumors can occur anywhere along neurospinal axis. dermoid can be congenital as well as acquired in origin. they account for about 1.1% of the spinal tumors [3]. they are slowly growing tumor and usually present in second decade of life [4]. mostly these tumors are intra spinal and rarely occur intramedullary. dermoid represent the rare midline tumors and constitute about 1-2% of the spinal tumors [1]. intracranial dermoid cysts are uncommon, it accounts for about 0.1 to 0.7 % of all intracranial tumours [5]. the intracranial dermoid cyst arises from ectoderm, probably derived from cell nest included during the closure of neural tube. the cyst wall is lined with stratified squamus epithelium and mixed appendages of ectodermal origin including sebaceous gland, sweat gland, and hair follicles. the cyst content is mixture of decomposed epithelial cells containing keratin, glandular secretion, lipid metabolites, and cholesterol. rarely dental enamels are also observed [7]. dermoid cysts are found in supratentorial and infratentorial compartment and within the spinal canal [8]. the commonest location of intracranial dermoid cyst is posterior fossa. the more common supratentorial tumours are located on skull base, frontal or temporal or suprasellar region. it can present at any age, but most common at 2nd and 3rd decades, of life. the clinical symptomatology is variable rarely it may be detected incidentally [9]. however, most patients presents with seizure, longstanding headache [7], [8]. it may present with cyst rupture, meningiomas, vasospasm, increased intracranial pressure, dementia and possible focal neurological deficits. death can be consequence of rupture of dermoid cyst [8]. intracranial dermoid cyst can be associated with complete or incomplete sinus tract, usually ending in an intracranial location of dermoid [6]. patient may even present with repeated episodes of meningitis 100 | satyarthee et al conus medullaris dermoid tumour             or cerebellar abscess [5]. x-ray of spine may show widening of spinal canal with thinning of lamina. calcification and rarely fat-fluid level. a spinal computed tomography may show associated bone defect, spina bifida, vertebral body abnormality or associated bony spur. however, ct scan is usually not advised unless a suspicion of co-existing bony spur is suspected. the mri spine clearly delineates soft tissue with size shape, relation to conus, shift of spinal cord and cauda equina nerve roots and thickening of filum terminale or lipoma, calcification if present have shell like appearance. the management of this associated pathology should be based on pathology causing neurological deficit [10] [11] [12] [13] [14] conclusion the patient presenting with cervical spine fusion anomaly, the imaging of posterior fossa is advised to exclude congenital posterior cranial fossa dermoid cyst and associated congenital craniovertebral junction anomaly. the aim of surgery should be directed to pathology, which is symptomatic. however, the surgical management has to tailored for individual patient. correspondence guru dutta satyarthee, e-mail: drguruduttaaiims@gmail.com references 1. rapoport rj, flanders ae, tartaglino lm. intradural extramedullary causes of myelopathy. semin ultrasound ct mr 1994; 15(3):189-225. 2. netsky mg. epidermoid tumors. review of the literature. surg neurol 1988; 29:477-83. 3. lunardi p, missori p, gagliardi fm, fortuna a. longterm results of the surgical treatment of spi¬nal dermoid and epidermoid tumors. neurosurgery 1989; 25:860-4. 4. egelhoff jc. pediatric head and neck imaging. in: haaga jr, editor. ct and mr imaging of the whole body. 4th ed. london: mosby; 2003. p.696. 5. diekmann-guiroy b, huang ps. kippel-feil syndrome in association with a craniocervical dermoid cyst presenting as aseptic meningitis in adult: a case report. neurosurg 1989; 25: 625-655. 6. schijman e, monges j, cragnaz r. congenital dermal sinuses, dermoid and epidermoid cysts of the posterior fossa. child’s nerv syst 1986; 2: 83-89. 7. smith as, benson je, blaser si, mizushim a, tarr rw, balon em. diagnosis of ruptured intracranial dermoid cyst: value of mri over ct. ajnr 199; 12: 175180. 8. lunardi p, missori p. supratentorial dermiod cysts. j neurosurg 1991; 75: 262-266. 9. hamer j. diagnosis by computerize tomography of intradural dermoid with spontaneous rupture of dermoid cyst. acta neurochir 1980; 51; 219226. 10. sivrioglu ak, kara k, tutar s, sönmez g. pedicle thinning finding on x-ray imaging of the lumbar spine: a case of spinal conus dermoid cyst. spine j. 2016 jun;16(6):e395-6. 11. sharma m, mally r, velho v.ruptured conus medullaris dermoid cyst with fat droplets in the central canal [corrected]. asian spine j. 2013 mar;7(1):50-4 11. de maio pn, mikulis dj, kiehl tr, guha a. airp best cases in radiologic-pathologic correlation: spinal conus dermoid cyst with lipid dissemination. radiographics. 2012 ; 32(4):1215-21. 12. liu h, zhang jn, zhu t. microsurgical treatment of spinal epidermoid and dermoid cysts in the lumbosacral region. j clin neurosci. 2012;19(5):712-7. 13. klekamp j. tethered cord syndrome in adults. j neurosurg spine. 2011 sep; 15(3):258-70. 14. falavigna a, righesso o, teles ar. concomitant dermoid cysts of conus medullaris and cauda equina. arq neuropsiquiatr. 2009; 67(2a):293-6. 15. tufan k, cekinmez m, sener l, erdogan b. infected lumbar dermoid cyst presenting with tetra paresis secondary to holocord central lesion. j child neurol. 2008 aug; 23(8):934-7. 16. muthukumar n, srisaravanan j. intramedullary dermoid in a low lying conus tethered by a fatty filum embryological implications. acta neurochir (wien). 2007 nov;149(11):1173   romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article a case report on result of posterior fossa decompression on syringomyelia in a case of chiary type i malformation asheesh kumar gupta, avdhesh shukla, anand sharma, s.n. iyengar india doi: 10.2478/romneu-2018-0020 160 | kumar et al posterior fossa decompression on syringomyelia doi: 10.2478/romneu-2018-0020 a case report on result of posterior fossa decompression on syringomyelia in a case of chiary type i malformation asheesh kumar gupta, avdhesh shukla, anand sharma, s.n. iyengar department of neurosurgery g.r. medical college gwalior, india abstract: the prime objective in the surgical treatment of chiari malformation (cm) and/or syringomyelia (sm) is based on the restoration of the normal cerebrospinal fluid (csf) dynamics at the craniovertebral junction through the creation of a large artificial cisterna magna. in this case a patient came to our hospital with type 1 chiary malformation having large syrinx which underwent posterior fossa decompression by midline sub occipital craniectomy with subpial cerebellar tonsillar resection which after one year of follow up we have found significant resolution of syrinx radiologically. key words: syringomyelia sm, chiary malformation type 1 cmi, foramen magnum decompression fmd introduction the pathophysiology of syrinx formation and progression is important for surgeons in their selection of a surgical approach for syringomyelia (sm) secondary to chiari malformation type i (cmi). there is broad consensus on the role of mechanical blockage of cerebrospinal fluid flow at the craniocervical junction in the pathogenesis of sm secondary to cmi [1, 2]. posterior fossa decompression (pfd) is currently preferred by most surgeons as the standard surgical option in the treatment of sm secondary to cmi [3– 6]. this results in decompression of the cerebellar tonsil restores the normal cerebrospinal fluid flow [7]. in addition, a wide variety of surgical procedures as adjuvants to standard pfd, including syringosubarachnoid shunting, obex plugging and resection of the cerebellar tonsil, have been advocated in previous studies, which potentially induce bias with respect to the evaluation of syrinx resolution. to date, few reports have quantitatively evaluated syrinx resolution after pfd or identified predictive factors for better improvement. in addition to occipital pain and vertigo, dissociative sensory loss is one of the most frequent clinical presentations in children and adolescents with cmi. in this case we have done posterior fossa decompression by midline sub occipital craniectomy with subpial cerebellar tonsil resection in a patient of chiary malformation type 1 with syringomyelia then after one year of follow up there was resolution of syrinx was found radiologically. romanian neurosurgery (2018) xxxii 1: 160 163 | 161 case report a 45 year old female presented to our neurosurgery opd with the chief complaints of occipital headache since two years, weakness bilateral upper limb since six months, difficulty in holding objects since six months on examination there was dissociative sensory loss as decrease in pain and temperature sensations up to c7 dermatome with preservation of pressure and joint position sense, power was -4/5 on bilateral upper limb with bilateral hand grip weakness, reflexes were exaggerated on both upper and lower limbs and planter reflex was extensor. on mri cervical spine showed there was chiary type 1 malformation with large syrinx over crevico dorsal region (figure 1). patient was planned for routine surgery and posterior fossa decompression by midline suboccipital craniectomy with subpial resection of cerebellar tonsil and decompression of the cervical cord was done in sitting position. after one year of follow up now patient have relieved occipital headache with no sensory loss but grip of both hand was weak till now, on mri cervical spine there was significant reduction in the syrinx was found (figure 2). radiographic evaluation the severity of cerebellar tonsillar descent and features of the syrinx were evaluated via measurement of the following indices on the t1-weighted sagittal mri: the distance of cerebellar tonsillar descent (mm), the configuration of the syrinx, the maximal syrinx/cord (s/c) ratio and length of the syrinx. the extent of cerebellar tonsillar descent was further classified into three grades [14]: grade i, in which the tonsil descended beyond the foramen magnum but did not reach the c-1 arch; grade ii, in which the tonsil reached the c-1 arch; and grade iii, in which the tonsil descended beyond the c-1 arch. syrinx configuration was categorized into distended, moniliform, slender, and circumscribed types [14]. the maximal anteroposterior diameter of the syrinx (s) divided by the anteroposterior diameter of the spinal cord (c) at the same level provided the maximal s/c ratio [15]. syrinx length was defined as the number of vertebral segments spanned by the syrinx. syrinx resolution was defined as any demonstrable decrease in maximal s/c ratio or length. any postoperative decrease in the maximal s/c ratio or syrinx length divided by the preoperative value was calculated as a radiographic improvement rate. significant improvement of syrinx was defined as any more than 20% decrease in maximal s/c ratio or length on follow-up mri, and complete resolution was used to describe the syrinx disappearing after pfd. in our case preop parameters of patient was grade ii tonsillar herniation was found, syrinx was moniliformed, syrinx length was 13 vertebra, s/c ratio was 0.86, after operation and 1 year of follow up parameters were no cerebellar tonsils herniation syrinx was slender with length of 13 vertebra, s/c ratio was 0.46. so there was significant improvement in syrinx with radiographic improvement rate was 46.5%. 162 | kumar et al posterior fossa decompression on syringomyelia pre op mri post op mri after 1 year follow up discussion the outcome of pfd for the treatment of sm secondary to cmi has varied widely in previous studies in terms of maximal s/c ratio and syrinx length. hida et al. [8] reported that 30 of 33 patients with sm secondary to cmi exhibited obvious syrinx resolution after pfd. depreitere et al. [16] reported that 80% of patients (16/20) showed a favorable result consisting of complete syrinx resolution in 8 patients and obvious syrinx reduction in another 8. wetjen et al. [12] documented the time course of syrinx resolution after pfd and found that the syrinx resolved significantly over a short period of time after decompression. significant improvement was also reported in 7 of 7 patients in a study by feldstein and choudhri [17] and 11 of 12 in a study by ghanem et al. [18]. however, low rates of significant improvement have also been reported. in studies by caldarelli and colleagues and mcgirt and colleagues, syrinx resolution after pfd was found only in 50 and 62% of patients, respectively [10,19]. this discordance may be related to broad age range, different surgical procedures, or variability in the definition of significant improvement. in general, pediatric patients have a better response to pfd than adults. we found significant syrinx improvement after pfd in patients with cmi, particularly within the initial several months after surgery. romanian neurosurgery (2018) xxxii 1: 160 163 | 163 correspondence dr. asheesh kumar gupta m.ch. resident department of neurosurgery g.r. medical college gwalior. addressroom no. 39 senior boys hostel g.r. medical college gwalior mobile no.7828832632 emailasheesh_gsvm@yahoo.com references 1.milhorat th, nishikawa m, kula rw, dlugacz yd. mechanisms of cerebellar tonsil herniation in patients with chiari malformations as guide to clinical management. acta neurochir (wien) 2010;152:1117– 1127. doi: 10.1007/s00701-010-0636-3. [pmc free article] [pubmed] [cross ref] 2. mcgirt mj, atiba a, attenello fj, wasserman ba, datoo g, gathinji m, carson b, weingart jd, jallo gi. correlation of hindbrain csf flow and outcome after surgical decompression for chiari i malformation. childs nerv syst. 2008;24:833–840. doi: 10.1007/s00381-0070569-1. [pubmed] [cross ref] 3. tubbs rs, lyerly mj, loukas m, shoja mm, oakes wj. the pediatric chiari i malformation: a review. childs nerv syst. 2007;23:1239–1250. doi: 10.1007/s00381-0070428-0. [pubmed] [cross ref] 4. durham sr, fjeld-olenec k. comparison of posterior fossa decompression with and without duraplasty for the surgical treatment of chiari malformation type i in pediatric patients: a metaanalysis. j neurosurg pediatr. 2008;2:42–49. doi: 10.3171/ped/2008/2/7/042. [pubmed] [cross ref] 5. navarro r, olavarria g, seshadri r, gonzales-portillo g, mclone dg, tomita t. surgical results of posterior fossa decompression for patients with chiari i malformation. childs nerv syst. 2004;20:349–356. doi: 10.1007/s00381-003-0883-1. [pubmed] [cross ref] 6. xie j, wang y, zhao z, zhang y, si y, yang z, liu l, lu n. one-stage and posterior approach for correction of moderate to severe scoliosis in adolescents associated with chiari i malformation: is a prior suboccipital decompression always necessary? eur spine j. 2011;20:1106–1113. doi: 10.1007/s00586-011-1717-6. [pmc free article] [pubmed] [cross ref] 7. hankinson tc, klimo p, jr, feldstein na, anderson rc, brockmeyer d. chiari malformations, syringohydromyelia and scoliosis. neurosurg clin n am. 2007;18:549–568. doi: 10.1016/j.nec. 2007.04.002. [pubmed] [cross ref] 8. hida k, iwasaki y, koyanagi i, sawamura y, abe h (1995) surgical indication and results of foramen magnum decompression versus syringosubarachnoid shunting for syringomyelia associated with chiari i malformation. neurosurgery 37:673–678 (discussion 678–679) [pubmed] 10. caldarelli m, novegno f, vassimi l, romani r, tamburrini g, di rocco c. the role of limited posterior fossa craniectomy in the surgical treatment of chiari malformation type i: experience with a pediatric series. j neurosurg. 2007;106:187–195. [pubmed] 12. wetjen nm, heiss jd, oldfield eh. time course of syringomyelia resolution following decompression of chiari malformation type i. j neurosurg pediatr. 2008;1:118–123. doi: 10.3171/ ped/2008/1/2/118. [pmc free article] [pubmed] [cross ref] 12. ono a, ueyama k, okada a, echigoya n, yokoyama t, harata s (2002) adult scoliosis in syringomyelia associated with chiari i malformation. spine (phila pa 1976) 27:e23–e28 [pubmed] 14. qiu y, zhu zz, wang b, yu y, qian bp, zhu f. radiological presentations in relation to curve severity in scoliosis associated with syringomyelia. j pediatr orthoped. 2008;28:128–133. doi: 10.1097/bpo.0b013e31815ff371. [pubmed] [cross ref] 16. depreitere b, calenbergh f, loon j, goffin j, plets c. posterior fossa decompression in syringomyelia associated with a chiari malformation: a retrospective analysis of 22 patients. clin neurol neurosurg. 2000;102:91–96. doi: 10.1016/s0303-8467(00)00073-1. [pubmed] [cross ref] 17. feldstein na, choudhri tf. management of chiari i malformations with holocord syringohydromyelia. pediatr neurosurg. 1999;31:143–149. doi: 10.1159/000028850. [pubmed] [cross ref] 18. ghanem ib, londono c, delalande o, dubousset jf (1997) chiari i malformation associated with syringomyelia and scoliosis. spine (phila pa 1976) 22:1313–1317 (discussion 1318) [pubmed] 19. mcgirt mj, attenello fj, atiba a, garces-ambrossi g, datoo g, weingart jd, carson b, jallo gi. symptom recurrence after suboccipital decompression for pediatric chiari i malformation: analysis of 256 consecutive cases. childs nerv syst. 2008;24:1333–1339. doi: 10.1007/ s00381-008-0651-3. [pubmed] [cross ref] 20 20kumarguptaasheesh_a case report microsoft word 11florianmedial.doc i.st. florian et al medial temporal avm 93 medial temporal arterio-venous malformation case report i.st. florian1,2, c. abrudan1, c. matei2 1university of medicine and pharmacy “iuliu hatieganu “ clujnapoca, romania, neurosurgical department 2cluj county clinical emergency hospital, neurosurgical department abstract we introduce an uncommon case of small arterio-venous malformation (avm) on a critical location. a young woman with left anterior medial temporal avm was referred to our department in comatose state. we decided to treat this case by open surgery. secondary hydrocephalus occurred and a ventriculo-peritoneal shunt was inserted. the postoperative course was with no complications, and the patient was discharged in good state and six months later she resumed her activity. the case is of interest in the light of the decision-making process, and the techniques and surgical skills for the surgery of arterio-venous malformations on this critical location. keywords: arterio-venous malformations, intraventricular hemorrhage, temporal lobe, microsurgery introduction the surgical treatment of large or critically located arterio-venous malformations (avms) of the brain tests the technical skills of even the most accomplished neurosurgeons. medial temporal avms constitute a special group. avms of the medial temporal lobe frequently involve the basal ganglia and the thalamus, and for this reason they are commonly judged to be inoperable [4]. medial temporal avms are anterior, midtemporal and posterior or paratrigonal [1,2,3]. anterior lesions are supplied from the anterior choroidal branches, the anterior temporal branches of the middle and posterior cerebral arteries and branches of the posterior communicating artery. venous drainage is usually into the basal vein of rosenthal, but there might be outflow into the sphenoparietal sinus, medial sylvian vein or the vein of labbé [4]. in patients who present with intracranial hemorrhage form an avm, the risk of recurrent hemorrhage and progressive neurologic deficit would argue strongly in favor of surgical intervention in most of the cases. we present a case of medial temporal avm treated by open surgery, through pterional approach. 94 romanian neurosurgery (2010) xvii 1: 93 98 case report a previously healthy, 22-year-old woman experienced a sudden onset of headache, nausea and vomiting, in the morning of october 15th 2006 at three o’clock, during sleep. at seven o’clock the attack reoccurred and she lost consciousness. she was admitted in our department on the same day with comatose state, having gcs (glasgow coma scale) 8, right hemiparesis, left oculomotor complete palsy (strabismus, midryasis, ptosis) and meningism. the admission ct scan showed diffuse subarachnoid, and a more important intraventricular hemorrhage, in the left lateral ventricle, with a left medial temporal lobe hematoma. an underlying small (< 3 cm) avm was seen on mri angiography and left carotid angiogram (figure 1). its feeding arteries were posterior communicating artery, choroidal artery and posterior cerebral artery. venous drainage was into the vein of rosenthal. in the 3rd day after admission she was taken into the operating room. a standard neuroansthesia induction with pentobarbital, fentanyl and muscle relaxant was used. anesthesia was maintained with nitrous oxide, isoflurare and narcotic. standard physiologic monitoring was performed during surgery. spinal drainage was instituted and mannitol administrated before surgery. the patient was positioned supine with the neck extended and the head turned 30 degrees to the right. the avm was approached via left pterional craniotomy with microsurgical splitting of the anterior part of the sylvian fissure (figure 2). the whole malformation was resected using microsurgery principles. due to prior intraventricular hemorrhage, we left in place an external ventricular drainage for five days, when ct-scan follow up revealed the resolution of the intraventricular hemorrhage and no hydrocephalus (figure 3). the postoperative course was uneventful with regained consciousness and the ct-scan follow up showed complete resection of the avm, and no others lesions. the patient was discharged in very good condition: she was alert, with no neurological deficits except the left oculomotor palsy which has been partly solved, and mild memory disturbances. 6 weeks later the patient experienced a cognitive decline, her memory disturbances worsened, impairment of affection and gait disturbances. a ct scan examination was obtained which revealed communicating hydrocephalus. she was readmitted in our department, and underwent surgery for a ventriculoperitoneal drainage. the postoperative course was with no complications and she was discharged with general and neurological status improved. at 6 months follow-up the patient was in a good state presenting a mild degree of ptosis on the left eye, and she resumed her activity, poetry. i.st. florian et al medial temporal avm 95 figure 1 preoperative imaging study: a, b, preoperative ct-scan which revealed left medial temporal haematoma, intraventricular and subarchnoid hemorrhage; c, d, mri study and e, angiography mri, and f, right carotid angiography with small avm, supplied from posterior communicating artery, choroidal artery and posterior cerebral artery 96 romanian neurosurgery (2010) xvii 1: 93 98 a b figure 2 intraoperative aspects, a, the posterior communicating artery (pcoa) serves as a useful guide towards the malformation, black arrow head avm, arrow pcoa, b, the avm is totally resected, white head arrow oculomotor nerve and arrow pcoa figure 3 ct scan 3 days follow up revealed the resolution of hemorrhage and no hydrocephalus discussion cerebral arterio-venous malformations are one of the most difficult challenges for neurosurgeons either from the decision-making process or the techniques and surgical skills for this surgery. medial temporal avm are a special group in the medial hemispheric avm. in one series of 300 surgically treated avms of the brain, 55 lesions were located in the medial aspect of the hemisphere and seven lesions were located in the anterior medial temporal lobe [3]. the natural history of these lesions in not fully known yet. moreover, available evidences indicate that patients with avm, who are left untreated frequently, die prematurely or are left incapacitated. these may occur, because the main presentation of an avm is with rupture and hemorrhage. the risk of hemorrhage is 4% per year, and the annual mortality rate is 1% [4]. this dismal prognosis encourages the surgery approach of these lesions. anterior medial temporal avms are supplied from the anterior choroidal arteries, the anterior temporal branches of the middle, and posterior cerebral arteries and branches of the posterior communicating artery. venous drainage is usually into the basal vein of rosenthal, but there might outflow into the sphenoparietal sinus, medial sylvian vein or the vein of labbé. treatment planning for avms depends on the risk of subsequent hemorrhage, which is related to prior hemorrhage, smaller avm size, deep venous drainage, and relatively high arterial feeding pressures [2]. all of these were present in our case. we had a comatose young patient with ruptured small medial temporal avm with intraparenchimatous temporal haematoma and deep venous drainage, so we decided to treat this case by open surgery. emergent intracerebral haematoma evacuation can be performed i.st. florian et al medial temporal avm 97 with or without avm resection. we are advocates of an early surgery, and based on accurate preoperative planning we decided to resect the malformation at the same time. there are surgeons, who suggest that it is preferable to wait several weeks for the associated edema to reduce, for the haematoma to liquefy, and for the brain to regain the autoregulation, because the risk of rebleeding during this time is low [4]. also, the repeated angiography, after a few weeks, showed a new configuration of the avm, which was altered by the haematoma and hypertension. regarding the size of critical located malformations, stereotactic radiosurgery, microsurgical resection or embolization (if multiple hemorrhages) are the options for small (< 3 cm diameter) arteriovenous malformations [4,5]. radiation therapy does not represent a first line approach of the avms, especially of the ruptured ones [3, 5]. malformations that are located on the medial aspects of hemispheres are generally not suitable for preoperative embolization therapy. these malformations are supplied by distal branches of the choroidal arteries, posterior communicating arteries, which have a small intraluminal diameter and arise from the parent vessel at right angle. these factors make embolization hazardous and therefore it is not usually indicated for malformations in this location [3]. surgical resection is the mainstay of definitive treatment and it is the most effective in order to prevent rebleeding. arterio-venous malformations of the medial temporal lobe are usually resected through subtemporal-transcortical approaches that provide a trajectory that is perpendicular to the plane of the avm [1]. the pterional approach and orbitozygomatic approach are also recommended for these lesions. based on our experience we performed the resection of avm via pterional approach with microsurgical splitting of the anterior part of the sylvian fissure. this approach allows the visualization of the supraclinoid carotid artery and its branches that lead back to the malformation on the medial side of the temporal lobe [3]. the anterior choroidal artery or posterior communicating artery serves as a useful guide back into choroidal fissure and to the substance of the malformation. malformations in this location involve the uncus and the amygdala as well as portions of the anterior hippocampal formation. these regions are amenable to resection when involved by the avm. arterio-venous malformations of the medial temporal lobe which involve the basal ganglia and the thalamus are commonly judged to be inoperable. in order to prevent hydrocephalus due to the presence of ventricular and subarchnoid hemorrhage, we operated with spinal drainage, and after surgery we left in place an external ventricular drainage for five days, when ct-scan follow up revealed a normal postoperative aspect. despite all, after six weeks the patient developed a communicating hydrocephalus, which was treated by ventriculo-peritoneal drainage. subarachnoid and intraventricular hemorrhages favor the development of 98 romanian neurosurgery (2010) xvii 1: 93 98 hydrocephalus, which may occur in 1015% of patients. this is caused by the scarring of the arachnoid granulations and alterations in csf [2]. typically, late hydrocephalus is a communicating type and develops 10 or more days after subarachnoid hemorrhage, and the treatment is ventriculoperitoneal shunt. conclusions cerebral arterio-venous malformations are one of the challenges for neurosurgeons either from the decision-making process or the techniques and surgical skills for this surgery. medial temporal avm are a special group in the medial hemispheric avm. the advantages of surgery are the immediate elimination of the hemorrhage and of the risk for rebleeding, and the improvement in seizure control if the avm itself is generating seizures. in our experience pterional approach represents the best way in order to treat these lesions because allows the visualization of the supraclinoid carotid artery, and its branches that lead back to the malformation on the medial side of the temporal lobe and permits the resection of the uncus and the amygdala as well as portions of the anterior hippocampal formation, when necessary. references 1.du rose, young wl, lawton mt, yasargil mg, abdulrauf si, gonzalez lf, spetzler rf) tangential resection of medial temporal lobe arteriovenous malformations with the orbitozygomatic approach neurosurgery 54(3): 645–652, 2004 2.heros rc arteriovenous malformations of the medial temporal lobe. surgical approach and neuroradiological characterization j neurosurg 56(1): 44-52 1982 3.solomon ra, stein mb in wilkins rh and rengachary ss neurosurgery 2nd ed. mcgraw-hill professional publishing 241: 2448-2454 1995 4.steinberg gk, stoodley ma in schmidek and sweet operative neurosurgical techniques 4th ed. w.b. saunders company 100: 1363–1391 2000 5.steinberg gk, fankant jl, marks mp stereotactic heavy-charged particle bragg peak radiation for intracranial arteriovenous malformations n engl j med 323: 345–353 1990 romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0051 article  medico-legal implications of c1 vertebral fractures. case report tatiana iov, diana bulgaru-iliescu, simona damian, a. knieling, mădălina maria diac, d. tabian, sofia david romania      404 | iov et al medico-legal implications of c1 vertebral fractures             doi: 10.2478/romneu-2018-0051 medico-legal implications of c1 vertebral fractures. case report tatiana iov2, diana bulgaru-iliescu1, simona damian1, a. knieling1, mădălina maria diac1, d. tabian2, sofia david1 1“grigore t. popa” iași university of medicine and pharmacy, institutute of legal medicine iași 2institute of legal medicine iasi, romania abstract: introduction: the upper c1-c2 column is the subject of several erroneous diagnostics. the most common mechanisms of injuries include fall from high-impact skulls, car accidents, etc. vertebra c1 can also be injured by mild trauma. the japanese show that atlas fractures occur in about 2-13% of the cervical spine fractures and about 1.3% of the total spinal cord injuries. it is underlined that ct examination is the most useful diagnostic method. the czechs show that the atlas lesions appear in 1-2% of the cervical spine lesions. americans reported fracture of the atlas in 7% of the cervical spine fractures. even if ct has shown its value, lateral radiography is recommended in c1-c2 fractures. when victims are children or people injured in high-speed car crashes, the reported mechanisms were the fall from a high level and the impact on the tip of the flexed skull. the italians mention that the c1-c2 area is the most exposed diagnostic area with errors. material and methods: given the difficulty of establishing a diagnosis of c1 type fractures, we present in this paper such a case. we highlight the value of a ct scan. the victim is a 26-year-old woman with a trauma from the wall. the main issue in this case is that the diagnosis made by the radiologist seems to be wrong, the electronic and imprinted copies are of inferior quality. a second opinion revealed a very fine fracture that seemed to come from an older date than the date when the victim claimed she was assaulted. the better the lesions, the more misleading the interpretations. any imaginary imaging lesion, especially if it is obvious in electronic reconstructions, must be brought to the attention of the physician if they are taken into account by "image". the axial ct sections may omit some lesions under certain conditions, for example at the upper and lower poles of a spherical, ovoid or cubic structure, such as the atlas lateral mass. conclusions: the diagnostic solution in this case is the reconstruction of the axial sections in several planes. the crack can be highlighted, in the case of a reconstructed image, only after stacking the axial images. the mechanism could be through sudden romanian neurosurgery (2018) xxxii 3: 404 408 | 405             compression, during a sudden head movement, uninitiated and uncontrolled by the neck muscles, when a movement occurs over the degree of elasticity of the occiput-atlas joint, the occipital condyles compressing abruptly, unilaterally one of the atlas masses. in such clinical cases, we experience pain, muscle contraction and torticollis, on a normal neurological background. key words: c1 fracture, diagnosis, injury mechanism literature data the upper cervical vertebral spine (c1-c2) is the most predisposed area for an erroneous diagnosis. the most frequent mechanisms in such injuries are fall from a height with cranial impact, active hitting of the skull, traffic accidents. the c1 vertebrae can also be injured in minor trauma, often miss looked. the japanese studies show that atlas fractures are encountered in 2-13% of all cervical spine injuries and approx. 1,3% of all vertebral injuries. also, it highlights the importance of the ct examination in the diagnosis of cervical fractures. (1) czech studies reveal that atlas injuries account for 1-2% of all vertebral fractures and 7% of all cervical fractures. atlas fractures are either isolated or associated with axis or occipital condyle injuries (2). the americans show that atlas fractures make up for 10-10,7% of all cervical fractures. although the ct examination if, usually, superior to the x-ray, in case of c1-c2 fractures it’s recommended a lateral incidence x-ray investigation. in children, the reports of c1 isolated fractures only involved the anterior arch. as a mechanism of injury in children, there are mentions of falling from a height with vertex impact, while the cervical area in flexed or after high-speed traffic accidents (3, 4). the italians mention the upper cervical area (c1-c2) is the topographical are most predisposed to an erroneous diagnosis. missing if such fractures in x-ray examination involves neurological complications for the patients and subsequent medico-legal involvement of the physician. diagnosis error may occur due to a confusion with osteoporosis or to the poor quality of radiological examination. suspicions of c1-c2 injuries can be clarified after ct examination (5). aim of the paper we report such a case due to its rarity and to accentuate the utility of correct interpretation of the ct scan in order to avoid juridical errors. material and method a 26 years-old female patient suffered an injury after being hit against a wall. she is examined 7 days later in the medico-legal cabinet, presenting philadelphia cervical collar. the medical documents mention, at the moment of the initial examination, spontaneous and pressure pain in the upper cervical spinous processes (c1-c3) and right occipital epicranial hematoma. the cervical xray didn’t reveal any obvious fractures, and correct alignment of the anterior and posterior 406 | iov et al medico-legal implications of c1 vertebral fractures             wall. the axial ct examination (performed immediately after the injury), reveal a vertical fissure, with no displacement, of the right lateral mass of c1 vertebrae. in the c1-c7 segment, there are no other obvious posttraumatic changes and no signs of medullar compression (figure 1). the therapeutical attitude involved philadelphia cervical collar for a month and recommended control ct examination after this interval. due to suspicions on the correctitude of the diagnosis, the ct images (both printed and electronical) were reinterpreted by another specialist, who concludes that the initial diagnosis (“vertical fracture (fissure) with no displacement, involving the right lateral mass of the c1 vertebrae”) has no correspondent in the axial sections, on the sp 3 spinal slice, where the is no cortical interruption; however, the evaluation may have been limited by the limited visualization capacity of the “windows”. also, it was mentioned that neither the printed or electronical copies of the ct examination, didn’t have diagnostic quality, especially when it comes to subtle injuries. the diagnosis of such injuries has to be performed on the ct workstation, with special diagnostic software. 18 days after the injury, due to the discordance of the two diagnostics, a new examination was requested, with a higher performance apparatus. the investigation revealed a cortical fracture involving the internal spongious mass of the right lateral mass of c1 vertebrae (incomplete fracture of the lateral mass) (figure 2). figure 1 ct image immediately after trauma romanian neurosurgery (2018) xxxii 3: 404 408 | 407             figure 2 ct scan after 18 days the conclusion was that the patient had a stabile injury, which doesn’t need immobilization in more aggressive contention systems (halo-vest or casted minerva), philadelphia collar being enough for both antalgic purpose in for prevention of vicious consolidation. due to the incertitude, the two ct images were compared and discussed in the neurosurgery service, concluding that they weren’t conclusive for the diagnosis of right lateral mass fracture. it was recommended a classic tomographical examination (not computer tomography) centered on the assumed injury. results even if the x-ray may omit traumatic injuries, especially fissure-type, there would be no contradiction for the ct examination which would suggest a fracture (10). spiral ct is the most performant current examination, the first choice in cervical spine injuries. in hospitals in which this technology is available, it should be applied from the beginning, with no preceding x-ray. planning the ct examination, as far as number of sections, finesse and interval goes, depends on the clinical recommendation (actually, no radiological examination shouldn’t be performed in the absence of clinical indication). a clinically unoriented examination or excessively detailed can subject the patients to an unjustified large radiation dosage. the examination protocol is configured for revealing the injuries who’s reporting may essentially change the therapeutical attitude and not for minimal injuries, in which case the number of injuries may increase if the examination is very detailed. conclusions the subtler the injuries, the more frequent are the interpretation errors. any injury imagistically “assumed”, especially if it’s obvious during electronic reconstructions (computer composed images may be a source of false images – artefacts, unlike classical radiological images which are more subjective) has to be subjected to the clinician’s attention, which has to corroborate the results with the clinical picture. the clinical attitude should consider clinically confirmed injuries and not images. on the other hand, if we limit the right of the radiologist to report all imagistic “anomalies”, we convert the radiological act 408 | iov et al medico-legal implications of c1 vertebral fractures             into “judicial” practice and not a diagnostic one (mal-praxis cases in the western world show this tendency of the medical system of working for the lawyers, not for the patients). axial ct slices may miss some injuries, in certain conditions as the superior and inferior extremities of a spherical, oval or cubical structure, as the lateral mass of the atlas – case in which the solution is multiple plan reconstruction of the axial slices. a fissure can be identified, in case of retroreconstructed image, only after stack-addition of the axial images. the injury, in this case, is limited to the bone spongious area, with no cortical interruption (young bones are elastic and can host such injuries, without cortical interruption). the mechanism could involve sudden compression during a sudden movement of the head, uninitiated and uncontrolled by the neck muscles, when there is a movement exceeding the elasticity limit of the occipital-atlas articulation, the occipital condyles determining a one-sided, sudden compression of the one of the atlas lateral masses. in such case, we can encounter pain, muscle spasm and torticollis, with a normal neurological exam. correspondence diana bulgaru bulgarudiana@yahoo.com references 1. shirasaca a., endoh m, matsuzawa y, sugihara e, sakai n, ninchoji t, uemura k. isolated fracture of the lateral mass of the atlas. department of neurosurgery, shida general hospital of fujieda, japan, no shinkei geka 1989;17(7):679-82 2. stulik j, krebec m. injuries of the atlas. acta chirr orto traumat. 2003;70(5):274-8. 3. cusmano f, ferrozzi f, uccelli m, bassi s. upper cervical spine fracture:sources of misdiagnosis. radiol med (torino). 1999 oct; 98 (4): 230-5. 4. de coster ta, cole hc. atlanto-axial dislocation in association with rheumatic fever. spine. 1990;15:591-595. 5. o’laoire sa, thomas dgt. transoral approaach to the cervical spine. report of four cases. j. neurol. neurosurg. psychiat.1982;45:60-63. 6. mirvis se, geisller fh, jelinek jj. acute cervical spine trauma. evaluation with 1,5 t-rmn. radiol. 1988;166:807-816. 5. bremer am, ngaun to. internal metal plate fixation combined with anterior interbody fusion in cases of cervical spine injury. neurosurg. 1983;12:649-653. 7. goffin j, plets c, van den bergh r. anterior cervical fusion and osteosynthetic nstabilization according to caspar. neurosurg. 1989;25:865-871. 8. maiman dj, barolat g, larson sj. management of bilateral locked fecets of the cervical spine. neurosurg. 1986;18:542-547. 9. angelescu n. tratat de patologie chirurgicală. vol ii. editura medicala. bucuresti. 2001, p 2390-2392. 10. popescu i.: tratat de chirurgie.vol ii. editura academiei române. bucureşti. 2007, p167. microsoft word 12hozsamer_the new generation romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article the new generation iraqi neurosurgeons' armamentarium to gain the nobel prize, an overview of the planning and expectation for the future samer s. hoz, mohammed maan abdul azeez, ali adnan dolachee, osama m. al-awadi, luis rafael moscote-salazar iraq, colombia doi: 10.2478/romneu-2018-0012 romanian neurosurgery (2018) xxxii 1: 105 109 | 105             doi: 10.2478/romneu-2018-0012 the new generation iraqi neurosurgeons' armamentarium to gain the nobel prize, an overview of the planning and expectation for the future samer s. hoz1, mohammed maan abdul azeez2, ali adnan dolachee3, osama m. al-awadi4, luis rafael moscote-salazar5 1neurosurgeon, neurosurgery department, neurosurgery teaching hospital, baghdad, iraq 2medical student, college of medicine, baghdad university, iraq 3neurosurgeon, department of neurosurgery, college of medicine, al-qadisiyah university, iraq 4neurosurgeon, neurosurgery department, nursing-home hospital, baghdad, iraq, president of the association of neurological surgeons in iraq 5neurosurgeon, cartagena neurotrauma research group, universidad de cartagena, cartagena, colombia introduction nobel prizes are among the most famous and most prominent scientific awards worldwide (1). since the first nobel prizes were awarded in 1901, the recipients have captured the interest of the world’s scientific, literary, and political communities (2). the four science nobel prizes (physics, chemistry, medicine/physiology, and – since 1969 – economics) have performed extremely well as a method of recognizing the highest level of achievement (3). the nobel prize in physiology or medicine is closely related to human diseases, for which it is paid more attention (4). although originally awarded to individuals, the science prizes are now awarded a maximum of once a year to a maximum of three laureates, which makes a maximum total of only 12 laureates annually (3). no one has so far won the nobel prize in physiology or medicine twice in a lifetime (4). the average intelligence quotient (iq) in iraq is 87 which represents the 20th of the world ranking (5) which is as an average will be the best starting point for astonishing future. richard lynn and tatu vanhanen argue that differences in national income are correlated with differences in the average national iq. these results are controversial and have caused much debate, they must be interpreted with extreme caution (5). every now and then it is important to update and, if necessary, adjust our ways of operationalizing and valuing excellence (6). it would be useful in developing new algorithms for guiding the individual’s and the 106 | hoz et al iraqi neurosurgeons' armamentarium to gain the nobel prize             community’s contribution to science (7). by singling out individual scientists as paragons of scientific achievement in their fields, the nobel prize seems to endorse the “archetypical” idea of a solitary researcher making his or her one great discovery or invention, to the benefit of mankind, as it is stated in alfred nobel’s will (6). analyzing citation impact, it was shown by bornmann and leydesdorff that countries such as usa, u.k., and germany, having a high population number and a well-working economy, lead in science (8,9). when exploring biographical and historical accounts of these communities, it was apparent that much greater interconnectedness existed among scientific communities than is reflected by doctoral mentor-mentee relationships (7). in short, science in the big science era has become an activity that is more complicated even than playing simultaneous chess. it might be compared to playing a variety of different games on different boards simultaneously, with each game having its own standards of excellence, its own morale (6). planning discussion five levels are the ladder to the doctor in general (and for the neurosurgeon in specific) to be a world-class scientist and then will be ready for the competition on nobel prize nomination. these are 1. personal level. 2. local institution level. 3. national level. 4. international level. 5. world-class level (figure 1). figure 1 new generation iraqi neurosurgeons' armamentarium to gain the nobel prize (levels and transfer points requirements) level 1 the personal level focuses on the basic individual characteristics, theoretical knowledge and the practical aspect. the basic personal characteristics which include 2 main elements a. the knowledge and passion for learning anatomy and/or physiology and/or radiology. b. technical skills required for surgery in general. these characteristics should be as perfect as possible and it will determine future direction based on your confidence in them. romanian neurosurgery (2018) xxxii 1: 105 109 | 107             the theoretical knowledge of neurosurgery requires a thorough studying of different resources (textbooks, notes and cases books, q and a books, websites, youtube channels and even mobile applications). the studying of these resources must be in 3 ways, the first is a general appreciation of the topics then you must read them focusing on the exam style requirements and the final way is to read the topics with an interest-oriented way (i.e.: focusing on the topics you are more interested in to build up ideas and to comprehend the defect in the current literature for future directions). the personal level should include focusing on the practical side and to spend as much time as possible in the operation room whether observing or scrubbing as that will improve your personal abilities to be more patient, delicate and oriented during surgery, that's why the operations record is always important and represents a critical point in the curriculum vitae of any neurosurgeon. transfer point1 (from the personal level to the local institute level): the dedication and appreciation of your job is the only requirement to get access to the next level. you can't be distinguished from your coworkers unless you have an extradedication and passion for your daily job as compared with your colleagues. level 2 the local institute (hospital or college): four ideas should be delivered and enhanced during your daily work in your institution to fulfill this level, these include 1. show respect to every person in your institute, happily obey your up-line commands and always try participate in an active team work. 2. active participation in all the cme (continuous medical education) events and with the time make an effort to suggest new directions or new events to force yourself for continuous studying and being oriented about the updates in your field. 3. try to add new innovative points in each of the usual daily activities in your work even the simple one like patient examination or preparation for surgery or medical records. 4. try to build up your own style as a surgeon, this requires an equilibrium between being different and being safe surgeon. transfer point2 (from the local institution level to the national level): two critical requirements for this transfer, being a really oriented person (oriented about your job) and the ability to import an international ideas or activities or projects into your country. level 3 national level: five phases needed to do a recognized activity at the national level, these include: 1. attending, active participation and even organizing conferences at the national level. 2. arrange research groups to conduct multi-center or national studies. 3. participate and support the national association or society. 4. start new national scientific project fundamentally created to fit your country needs. 5. coaching younger colleagues and even medical students interested in neurosurgery and support them as much as possible as they will be your team in the future or they may be the next nobel laureates.   108 | hoz et al iraqi neurosurgeons' armamentarium to gain the nobel prize             transfer point 3: (from national level to the international level) six points desired for this transfer, 1. selfconfidence. 2. flexibility in the method of thinking, in the ideas and even in the lifestyle. 3. certification and validation of your previous work. 4. a real team spirit and work. 5. ability to export your national and local experience or projects to the international scientific community. 6. finally and the most important is to have the vision and expectations of the next steps for the upcoming future. level 4 the international level: 4 stages should be optimized to reach this level: 1. attending of international conferences, workshops and even online conferences as a participant and then as a speaker to present your work and the current status of neurosurgery in your institution or country. 2. participate or start an international research project. 3. participate in an international book chapter or even write your own. 4. be in contact with the international organizations, societies or association and try to be involved in their projects to be a dynamic fellow and then a member of their international authorities. all these will support your chances to build your personal relationships and to enrich your scientific social network which is the foremost goal not only a way to promote your career at that esteemed level. transfer point 4: (from the international level to the world-class level) four imperative facets are useful here, 1. honesty with yourself, your patients and your colleagues is a huge step that builds up people trust and pushes you toward your target. 2. having the ability to invent ideas, projects and achievements sharing will maximize your productivity. 3. a particular topic directing (like your real interest in a specific disease) during the whole carrier will increase your opportunity to invent a new idea, treatment option or surgical technique about it. 4. finally, the luck in choosing opportunities will have a great impact on your global influence. obtaining nobel awards clearly constitutes a crucial challenge for nations worldwide, as they are a significant determinant of a country’s prestige and a reliable index of the efficiency of its scientific policy (1). still, for many scientists, it is difficult to imagine that virtual proximity could ever be a satisfying replacement for the day-to-day personal interaction found in a positive mentoring relationship (7). acknowledgement should stay as our basic desire, fueling creativity and perseverance, even under hazardous conditions, and science continues to rely on individuals who are willing to display this behavior (6). nobel awards are central indicator of a country’s scientific achievement, which includes the number of publications and research expenditure (1), so having the vision and the insightful thinking will promote the next generation iraqi neurosurgeon to attain more recognized position and high qualification and that may render them as future nominees for the nobel prize.   romanian neurosurgery (2018) xxxii 1: 105 109 | 109             references 1.doi h, heeren a, maurage p (2014) scientific activity is a better predictor of nobel award chances than dietary habits and economic factors. plos one 9(3): e92612. 2.lichtman ma. alfred nobel and his prizes: from dynamite to dna. rambam maimonides med j 2017;8 (3):e0035. review. doi:10.5041/rmmj.10311 3.charlton b. why there should be more science nobel prizes and laureates – and why proportionate credit should be awarded to institutions. medical hypotheses. 2007;68(3):471-473. 4.ye s, xing r, liu j, xing f. bibliometric analysis of nobelists’ awards and landmark papers in physiology or medicine during 1983 2012. annals of medicine. 2013;45(8):532-538. 5.davies c. iq and global inequality by richard lynn and tatu vanhanen. economic affairs. 2007;27(3):104-105. 6.zwart h. the nobel prize as a reward mechanism in the genomics era: anonymous researchers, visible managers and the ethics of excellence. journal of bioethical inquiry. 2010;7(3):299-312. 7.chariker j, zhang y, pani j, rouchka e. identification of successful mentoring communities using networkbased analysis of mentor–mentee relationships across nobel laureates. scientometrics. 2017;111(3):1733-1749. 8.bornmann l, leydesdorff l. the validation of (advanced) bibliometric indicators through peer assessments: a comparative study using data from incites and f1000. journal of informetrics. 2013;7(2):286-291. 9.schlagberger e, bornmann l, bauer j. at what institutions did nobel laureates do their prize-winning work? an analysis of biographical information on nobel laureates from 1994 to 2014. scientometrics. 2016;109(2):723-767. doi: 10.33962/roneuro-2021-023 the stent-assisted coil-jailing technique for very small intracranial aneurysm treatment a. chiriac, n. dobrin, georgiana ion, z. faiyad, i. poeata romanian neurosurgery (2021) xxxv (2): pp. 148-151 doi: 10.33962/roneuro-2021-023 www.journals.lapub.co.uk/index.php/roneurosurgery the stent-assisted coil-jailing technique for very small intracranial aneurysm treatment a. chiriac1,2, n. dobrin2, georgiana ion2, z. faiyad2, i. poeata1 1 "grigore t. popa" university of medicine and pharmacy, iasi, romania 2 “prof. dr n. oblu” clinic emergency hospital, iasi, romania abstract the stent-assisted coil-jailing technique was initially introduced as an effective and secure method in the treatment of large wide-necked intracranial aneurysms. later on, this technique has proved its efficiency in the safety and optimal treatment of very small aneurysms. in this article, we will present the successful treatment of a very small middle cerebral artery aneurysm using the stent-assisted coil-jailing technique and review the current trends in this type of treatment. introduction with the advances in endovascular technologies, endovascular coil embolization of ruptured cerebral aneurysms has become the first efficient treatment option. nevertheless, endovascular coiling of very small aneurysms remain controversial. most of these particular vascular lesions are conformational characterized by a small dome and large-neck. the technical difficulties are represented by the high risk of procedure-related rupture and coil migration due to a very limited aneurysm volumes and structural restriction of embolization coils. stent-assisted coil-jailing technique is a very popular endovascular method that could be feasible and effective for such structural complicated aneurysms. however, the technique should be used carefully and above all, its usage must be safe and lead to good clinical results with regard to aneurysm occlusion. in this report, we describe a successfully treated very small middle cerebral artery aneurysm using the stent-assisted coil-jailing technique in order to provide a more comprehensive view of this challenging endovascular treatment and eventually to offer helpful clinical information for the management of such cases [8]. case presentation a 50-year-old woman presented with a sudden-onset headache for which she addressed the emergency department at a local hospital. a keywords very small aneurysm, stent-assisted coil-jailing technique corresponding author: a. chiriac “prof. dr n. oblu” clinic emergency hospital, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 149 the stent-assisted coil-jailing technique for very small intracranial aneurysm treatment head ct-scan investigation was performed immediately and showed a lenticular hematoma and mild subarachnoid haemorrhage in the left sylvian fissure. due to the suspicion of an aneurysmal cerebral hemorrhage, the patient was immediately transferred to our hospital for further diagnosis and treatment. at admission she was confused and with right hemiparesis. her past medical history included hypertension with no regular treatment. the brain ct angiography raised the suspicion of an aneurysmal dilatation on m1 segment of left middle cerebral artery. a subsequent subtraction catheter cerebral angiography confirmed a very small aneurysm at the origin of left charcot artery. due to the very small dimension of the aneurysm (2.3 mm × 2.0 mm) and relatively large neck a stent-assisted coil-jailing technique was proposed for the occlusion of the lesion. a (left) b (right) c d e f g h i j k figure 1. a, b – diagnostic cerebral ct and angio-ct images; c, d, e, f, g, h, i – intraprocedural dsa images; postprocedural cerebral ct images. the intervention performed the next day on a biplane angiography system (infinix, toshiba, canon medical system) under general anesthesia by our neurosurgical team with many years of experience in neuroendovascular interventions. written informed consent was obtained prior to the treatment. commercially available 6f introducer sheath from merit medical was placed into the right femoral artery. a 6f chaperon guiding catheters (microvention) was carefully advanced over 0.035 glidewire up to the proximal segment of the left internal carotid artery. using the 3d-ct images analysis a favourable working angle roadmap for the target aneurysm was obtained. a prowler 10 microcatheter (codman j&j) was then very carefully advanced over a 0.014 transed microwire (boston 150 a. chiriac, n. dobrin, georgiana ion et al. scientific) and positioned into the aneurysm sac. keeping the microcatheter in this fixed position a second prowler select plus microcatheter (codman j&j) was inserted up to the m1 / m2 bifurcation level of the left middle cerebral artery. with its help a 4/16 mm enterprise 2 intracranial stent (codman j&j) is deployed over the aneurysm neck and the first microcatheter in a jailed configuration. after the prowler select plus microcatheter withdraws, two galaxy g3 mini microcoils (cerenovus johnson&johnson) were then inserted and detached into aneurysm. the coils placement was done very slowly, and gentle handling of the microcatheter was used to avoid tension build-up in the aneurysm and to allow the coil loop to form inside the aneurysm. after detaching the last coil, the microcatheter is carefully retracted so as not to cause any movement of the stent. a dsa acquisition is performed to check the permeability of all vessels and complete occlusion of the aneurysm. finally, the entire guiding system is retracted with a compressive dressing of the femoral puncture site. the patient was placed into intensive care and received 75mg clopidogrel and 100mg aspirin daily. a cerebral ct scan was performed 7 days postoperatively and showed the lenticular hematoma resorption. the patient was discharged home after 3 days in good neurological condition. discussions the literature reports that very small intracranial aneurysms (≤3 mm) represent 13.2%–15.1% of all intracranial aneurysms. on the other hand, according to isuia study only 0.1% (per year) of small aneurysms (<5 mm) of the anterior circulation will manifested by rupture. there have been also several particular studies that have reported incidences of small aneurysms of up to 7% of all ruptured aneurysms[s]. in this clinical situation an emergency treatment must be initiated. endovascular coil embolization or microsurgical clipping of ruptured very small cerebral aneurysms are still challenging methods due to distinctive technical difficulties [t,x,s]. if in the case of endovascular treatment the very small size of the aneurysmal dome frequently associated with a wide neck make it difficult to place a coil safely, in the case of microsurgical treatment the thin-walled and too small neck make it difficult to accept a clip without narrowing or tearing the parent artery [3,6,9]. the stent-assisted coiling technique represents an efficacious adjuvant technique for treating widenecked aneurysms. the advent of these adjuvant techniques has made possible the endovascular occlusion of an increasing number of very small aneurysms. the stent-assisted coil-jailing technique has become often considered as the most efficient option for the embolization of very small aneurysms. this technique allowed, not only to provided the necessary support to achieve a stable coil arrangement, but also solved the problem of overestimating the coil length in small aneurysms. by this technique, if the coil is too long for a small aneurysm, the remaining coil segment (tail) could be purposely left and jailed between the stent and the parent artery wall at the end of the embolization procedure. the main complication reported in very small aneurysms was intraprocedural rupture. if the first studies reported significantly higher rates of procedural rupture, with the continuing development of endovascular devices and greater operator experience, the last ones did not show a significant association between very small aneurysms and intraprocedural rupture. it seems that the preferred use of stent-assisted coil-jailing technique might explain the evolution of the previously mentioned results. obtaining a stable position of the microcatheter by fixing it between the arterial wall and the stent, as well as the possibility of coils insertion into aneurysm with the tip of the microcatheter in its neck area, without the need of navigation in the aneurysmal sac caused a significant reduction in the risk of intraprocedural rupture in very small aneurysms [1,3,6,9] another complication described in very small aneurysms was that of thrombemolism. because of a restricted intra-aneurysmal space and an improper dome/neck ratio, coil migration and coil loop protrusion may frequently occur in very small aneurysms embolization. the thromboembolic complications rate for such events has been reported in the literature as varying between 2.1%– 12%. the new designs of the intracranial stents and development of the assisted coil techniques have allowed the significant reduction of these complications by their ability to prevent the herniation of the coils and at the same time to fix outside the blood flow the possible oversized coils. these have also simplified the procedure and 151 the stent-assisted coil-jailing technique for very small intracranial aneurysm treatment prevent possible complications caused by the replacement of the coils [2,4,6]. the recurrence rates of previously coiled vary small intracranial aneurysms in early published reports were variably, in a range approximately similar to those of larger intracranial aneurysms (range from 21% 15%) [s,t,x].with the increasing use of the jail technique in cases of embolization of very small aneurysms, new studies have reported much lower recurrence rates in these vascular lesions (range from 7.5 % 1.5%.) [3.5.6.9].this technique has proven useful for the dense packing of the very small aneurysm and avoiding the recoiling of an inappropriate aneurysm occlusion. conclusions the stent-assisted coil-jailing technique has been proven as an efficient approach for the treatment of very intracranial aneurysms with excellent and safety profiles. this technique allowed us both to support the coil loops in the aneurysmal sac by stabilizing the microcatheter and to solve the problem related to the possible oversizing of the length of a coil. references 1. beuing, o., lenz, a., donitza, a., becker, m., serowy, s., & skalej, m. (2020). stent-assisted coiling of broad-necked intracranial aneurysms with a new braided microstent (accero): procedural results and long-term follow-up. scientific reports, 10(1), 1-8. 2. jindal, g., miller, t., iyohe, m., shivashankar, r., prasad, v., & gandhi, d. (2016). small intracranial aneurysm treatment using target (®) ultrasoft (™) coils. journal of vascular and interventional neurology, 9(1), 46–51. 3. kim, s. m., lee, h. g., choi, b. s., kim, j. s., lee, s. j., kim, h. y., ... & jin, s. c. (2018). recurrence of small cerebral aneurysms (< 4 mm) treated endovascularly using target® nano™ coils. journal of cerebrovascular and endovascular neurosurgery, 20(2), 106. 4. van rooij wj, keeren gj, peluso jp, sluzewski m. clinical and angiographic results of coiling of 196 very small (< or = 3 mm) intracranial aneurysms. (2009) ajnr am j neuroradiol. apr;30(4):835-9.. 5. rong-bo q, hua j, kai w, ze-lin s. stent-jail technique in endovascular treatment of wide-necked aneurysm. turk neurosurg. 2013;23(2):179-82.. 6. li, c. h., su, x. h., zhang, b., han, y. f., zhang, e. w., yang, l., ... & gao, b. l. (2014). the stent-assisted coil-jailing technique facilitates efficient embolization of tiny cerebral aneurysms. korean journal of radiology, 15(6), 850. 7. zhang y, yang m, zhang h, zhang x, li y, jiang c, liu j, yang x. stent-assisted coiling may prevent the recurrence of very small ruptured intracranial aneurysms: a multicenter study. world neurosurg. 2017 apr;100:22-29. 8. zhou y, peng q, wu x, zhang y, liu j, yang x, mu s. endovascular treatment of tiny aneurysms with lowprofile visualized intraluminal support devices using a "compressed" stent technique. front neurol. 2020 dec 18;11:610126. 9. wang, j. w., li, c. h., tian, y. y., li, x. y., liu, j. f., li, h., & gao, b. l. (2020). safety and efficacy of endovascular treatment of ruptured tiny cerebral aneurysms compared with ruptured larger aneurysms. interventional neuroradiology, 26(3), 283-290. 10. xue, g., zuo, q., tang, h., zhang, x., duan, g., feng, z. & liu, j. (2020). comparison of low-profiled visualized intraluminal support stent-assisted coiling and coiling only for acutely ruptured intracranial aneurysms: safety and efficacy based on a propensity score-matched cohort study. neurosurgery, 87(3), 584-591. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article angiography procedure and endovascular treatment. retrospective analysis in neurosurgery department of “prof. dr. n. oblu” clinic emergency hospital iasi georgiana ion, a. chiriac, n. dobrin, i. poeată romania doi: 10.1515/romneu-2017-0071 444 | ion et al angiography procedure and endovascular treatment doi: 10.1515/romneu-2017-0071 angiography procedure and endovascular treatment retrospective analysis in neurosurgery department of “prof. dr. n. oblu” clinic emergency hospital iasi georgiana ion1, a. chiriac, n. dobrin1, i. poeată “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: a retrospective analysis of the cases admitted, investigated and treated in “prof. dr. n. oblu” clinic emergency hospital from the beginning of activity in the angiography laboratory from 2008 to june 2017. key words: angiography, aneurysm, fistula, tumor, procedure, treatment introduction cerebral and spinal angiography is a procedure of diagnosis for patients with a neurologic disease that can be completed by a treatment maneuver. pathology that can be explored and treated through neuroangiography is extensive: spinal avm or fistula, extracranial carotid or vertebral stenosis or dissection, cerebral tumors, cerebral avm or fistula ,aneurysms, sah, nontraumatic parenchymal cerebral hemorrhage, carotid-cavernous fistula, cerebral spasm, stroke, cerebral vasculitis, cerebral venous thrombosis, etc. regarding the treatment procedure, in this department the situation is at the level of international specialized centers. in neurosurgery department of “prof. dr. nicolae oblu” emergency hospital the angiography procedure through seldinger catheterization it started in 2007, when it was a learning period for the neurosurgeons dedicated for this pathology (dr. faiyad ziyad, dr. chiriac alexandru, dr. dobrin nicolae with the support of prof. dr. poeata ion). after the introduction of angiography in the neuroradiological diagnosis, soon after it was used also in neurosurgery hospital from iasi by senior neurosurgeons. direct puncture of the carotid artery or vertebral artery with a trocar and direct injection of contrast substance has been heavily used with the purpose of diagnostic for tumors, intracerebral haemorrhage or vascular abnormalities, when the computer tomography or mri were not available. materials and methods starting the year 2008 the main procedures which were conducted in the laboratory of romanian neurosurgery (2017) xxxi 4: 444 454 | 445 angiography were: diagnostic angiography, endovascular treatment of aneurysms, av fistula, avms, percutaneous angioplasty with stent or balloon and more recently, intraarterial injection of nimotop or thrombolysis and tumor embolization. it must to be noted that carotid-cavernous fistulas were included in the category of avm/avf. in the lower table are represented the main procedures conducted from january 2008 to june 2017. procedure first of all, a patient's preparation must be carried out with some blood tests (urea, creatinine, blood cell count, coagulation) an electrocardiogram, a neurologic examination and a review of available imaging. if the patient is following treatment with antiplatelet or anticoagulants, medication in continue on the day of the procedure. regarding the patient preparation, this should not eat or drink for 12 hours before the procedure, the inghinal region should be sterilely preparedand at least one peripheral access catheter. the family and the pacientare advised about the stages and alsothe risks and benefits of the procedure and they must to sign the consent. the patient is brought in the angiography room in an disposable costume with a saline solution 0,90% nacl perfusion and is positioned on the angiography table in supine. 446 | ion et al angiography procedure and endovascular treatment the inguinal region is discovered and sterilized with betadine. monitoring of the patient during the procedure is made through heart rate, blood pressure and electrocardiographic. sedation and general anesthesia are used for the cases when treatment is required or in patients who are unable to cooperate. otherwise, they are advised of the possible heat sensation that may occur when injecting the contrast substance and the need not to move during the procedure. after the positioning, the patient is covered with sterile disposable fields over which the necessary tools are placed (disposable). local anesthesia with lidocaine 1% is performed at the puncture site and a standard 18 g needle is used for the access for a 5f sheath (in case of diagnostic angiography), a 6f or an 8f sheath (in case of treatment). all the instruments are washed with heparinized saline solution before use. in general, the right common femoral artery is the main access path. the catheterization is made with a catheter of varying sizes and shapes, depending of aortic arch anatomy and the tortuosity of the vessels, the most common being an 5fangled catheter of 90-cm length. during the advancement, a guidewire (hydrophilic 0.035-inch wire) is advanced into the catheter under fluoroscopic monitoring. the catheter should be handled with care, especially in the case of very tortuous vessels, when sufficient forward guidewire can straighten them. a stopcock is used for contrast injection or for continuous saline flush. contrast injection into the selective internal carotid artery, external carotid artery or vertebral artery highlights the cerebral vascular tree. in cases when is needed the catheterization of the smaller vessels (from vertebral arery, distal eca) or suprapetrous segment of the internal carotid artery, a microcatheter and microwire are used under the protection of a continuous heparinized saline infusion. the basic positions purchased are lateral, anteroposterior and oblique (45 degree) or three-dimensional rotation and 3d reconstruction of the vascular tree. after the procedure patients rest in dorsal decubitus for at least 8 hours under careful supervision in neurosurgery department or in neurointensive care units. among contraindications of this procedure are counting coagulopathy, iodine contrast allergy or renal insufficiency, all of which being relative contraindications. among the complications of the vascular catheterization are to be retained the dissection, spasm of the artery or embolus with distal occlusion. results starting in 2008 endovascular procedures were more limited to diagnostic procedure, 2 cerebral avms treated and 9 ruptured aneurysms embolization. in the next year were made 152 angiographies, 4 avms treated and romanian neurosurgery (2017) xxxi 4: 444 454 | 447 10 aneurysms. in 2010 the number of diagnostic procedure decreased to 109, with 9 aneurysms treated, 2 avms and 1 percutaneous angioplasty with stent. regarding the year 2011, the activity was more intense, with 166 diagnosis, 13 aneurysms treated, 5 avms and 9 carotid artery stenosis treated. in the following year it was the first tumor embolization (pedicle from eca with glue and coils), 256 diagnostic procedures, 20 aneurysms treated, 15 avms and 26 stent procedure. regarding the year 2013, the procedures were similar (282 diagnosis angiography, 40 aneurysms treated, 22 avms, 3 tumors and 26 stent procedures). in 2014, the main procedures are represented in the chart below (274 diagnosis, 23 stent, 27 aneurysms, 37 avms and 2 tumor embolization). a similar a trend is observed in 2015, with 252 diagnostic angiography, 44 aneurysms treated endovascular, 18 avms, 2 tumors and 4 percutaneous angioplasty with stent. regarding 2016, the number of percutaneous endovascular explorations were 294, 14 stent procedures, 45 aneurysms treated, 20 avms and 4 tumor pedicle closure. from january 2017 to june 2017 were made 226 procedures of diagnostic, 42 aneurysms, 15 stent application (of which 4 percutaneous angioplasty with balloon), 21 avms and 5 tumor embolization. it must be noted that the mean age of patients investigated and treated endovascular was 56 years old (varies between 12 and 83 years), with a slight predominance of the male gender. representative cases endovascular embolization of tumors case1 m. 57y epicranian formation vertex and right hemiparesis (crural predominant). 448 | ion et al angiography procedure and endovascular treatment pre/post sta, mma, oa closure with glue case 2: f, 12y, 1 year progressive visual field disorder; bilateral papillary edema. figure 2.1. cerebral mri with contrast figures 2.2. & 2.3. a. of tentorium cerebelli figure 2.4. pedicular injection of pcoma and pca precocious and tardive contrast injection pre/post coils closure of the tentorial branch of vertebral romanian neurosurgery (2017) xxxi 4: 444 454 | 449 case 3 f, 16y. right cervicobrahialgia followed by progressive tetraparesis (4/5). figure 3.1. cervical mri figures 3.2., 3.3. & 3.4. tumoral blush injected from tyrocervical trunk figures 3.5 & 3.6. thyrocervical trunk closure with glue figures 3.7. & 3.8. pre-post glue injection aneurysms case 4: f, 54y, sah, h&h=3, day 1, ruptured pcoma and achoa aneurysms. figure 4.1. angio-ct 3d reconstruction figure 4.2. dsa after clipping the 2nd rupture figure 4.3. coils partial occlusion 450 | ion et al angiography procedure and endovascular treatment case 5 m, 34y, right hemiparesis, dysphagia for 3 months. figures 5.1., 5.2. & 5.3. basilar trunk aneurysm figure 5.4. left vertebral artery closure with coils figure 5.5. right va figure 5.6. stent assisted coiling figure 5.7. dsa after 3 months romanian neurosurgery (2017) xxxi 4: 444 454 | 451 case 6 f, 34y, sah, h&h=3 figures 6.1. & 6.2. diagnosis angio ct figures 6.3. & 6.4. vertebral artery at admission and after 19 days figure 6.5. endovascular closure with coils avms and fistula case 7 f, 43y, motor facio-brachial seizures for 24 h, headache. figures 7.1., 7.2. & 7.3. left ica onyx closure 2 pedicle left aca 452 | ion et al angiography procedure and endovascular treatment case 8 f, 53y, sudden headache and vomiting, sleepiness. pre/post closure one pedicle –distal right pca with glue case 9 f, 40y, chemozis, right exophthalmia, severe cranial trauma 5 months ago figure 9.1. right carotid-cavernous fistula figures 9.2. & 9.3. pre/post balloon inflation romanian neurosurgery (2017) xxxi 4: 444 454 | 453 case 10 f, 85y, right third nerve paresis, exophthalmia figures 10.1. & 10.2. right ica catheterization figure 10.3. gdc closure of the cc fistula case 11 m.13, gtc seizures figure 11.1. mri venous ectasia figure 11.2. right va figures 11.3. & 11.4 closure of the fistula with coils a complete and comparative graph is shown below, from 2008 to 2017. 454 | ion et al angiography procedure and endovascular treatment discussion angioct scan and angioirm are useful tools in the diagnosis of neurological and neurosurgical pathology, but with a lower sensitivity and specificity than angiography. is observed that, after less than 3 years of practice, the number of proceedings made in iasi angiography laboratory has increased significantly. after the year 2012 the diagnostic angiographies made remain relatively constant, but the number of aneurysms treated endovascular(coiling, stent assisted coiling or flow diverter) has increased ,as well as the number of tumors combined treated (presurgical closure of pedicles from eca,ica or vertebral artery with glue or coils). the number of stent or balloon angioplasties is relative constant during the almost 10 years of activity. in the last year protocols for stoke and endovascular treatment have been established, and the first trombaspiration was experienced in a case of carotid dissection. in case when vascular spasm is present during or after the embolization, nimodipine injection (5ml dissolved in 15 ml of saline solution) is often effective, even in segmental vasospasm. it was observed that, patients who benefit from intraarterial injection of nimotophave a better evolution during the first 21 days. conclusions diagnosis and endovascular treatment is indispensable to any neurosurgical center, because the pathology involved is more and more diverse and numerous. every few year’s new devices and substances are being developed that increase the efficiency of this procedure. during this years an increasing efficiency was observed both as procedure, duration, resultsand impact on the patient. but, the most important, is that this team is complete (regardingthe possibility of treating both surgically and endovascular) and is made up of neurosurgeons with a vast experience of over 10 years. references 1.sun ho ahn, md1 ethan a. prince, md1 gregory j. dubel, md1;basicneuroangiography: review of techniqueand perioperative patient care;semininterventradiol 2013;30:225–233 2.tratat de chirurgie vol. vi – neurochirurgie, ioan st. florian, ion poeata, academieiromane 2015 3.http://neuroangio.org/neuroangiotopics/introductory-brain-angiography/ 4.masaaki shojima, md; marie oshima, phd; kiyoshi takagi, md, phd; ryo torii, phd;motoharuhayakawa, md, phd; kazuhiro katada, md, phd;akio morita, md, phd; takaakikirino, md, phd;magnitude and role of wall shear stress oncerebral aneurysmcomputational fluid dynamic study of 20 middle cerebralartery aneurysms ; stroke. 2004;35:2500-2505 5.timothy j. kaufmann, md, john huston, iii, md, jay n. mandrekar, phd, cathy d. schleck, bs, kent r. thielen, md, and david f. kallmes, md; complications of diagnostic cerebral angiography: evaluation of 19 826 consecutive patients;radiology;june2007,volume 243, issue 3 6. richard e. latchaw; guidelines for diagnostic neuroangiography: a model to emulate from neuroradiologist's perspective; american journal of neuroradiology january 2000, 21 (1) 44-45. 7.neil m. borden, md, 3d angiographic atlas of neurovascular anatomy and pathology, cambridge university press,2006 microsoft word 19guptaasheesh kumar_epidemiological 340 | gupta et al epidemiological study of thoracolumbar pott’s spine             doi: 10.2478/romneu-2018-0042 epidemiological study of thoracolumbar pott’s spine at a tertiary care hospital in north india asheesh kumar gupta, aditya srivastava, r.l.s. sengar department of neurosurgery g.r. medical college gwalior, india abstract: the vertebral column is involved in less than 1% of all the cases of tuberculosis. it can associated with major neurological deficits due to compression of adjacent neural structures with significant deformity of spinal column. therefore, early diagnosis and management of spinal tb has special importance in preventing these serious complications. in order to extract current trends in diagnosis and medical or surgical treatment of spinal tb we performed a review with patients admitted to our hospital between 2016 and 2017. although the development of more accurate imaging modalities such as magnetic resonance imaging and advanced surgical techniques have made the early diagnosis and management of spinal tb much easier, these are still very challenging topics. in this review we aim to discuss the diagnosis and management of spinal tb based on studies with acceptable design, clearly explained results and justifiable conclusions. key words: cobb’s angle, pott’s spine introduction tuberculosis is a very common disease in developing countries affecting a large proportion of population. it is a major cause of mortality and morbidity in india. there are large number of cases having extrapulmonary tuberculosis. vertebral column is a common site for extra-pulmonary tuberculosis. the entity is called as pott’s spine. pott’s disease, described by sir percival pott, is one of the oldest demonstrated diseases affecting humans [1,2]. the thoracolumbar spine is the most commonly affected, with less frequent involvement of the cervical and sacral spine [3]. tuberculous spondylitis is diagnosed in the second, third, or fourth decade of life in developing nations, with a male to female ratio ranging from 1.3 : 1 to 1.7 : 1 [2,3,4–6]. neurologic deficits with or without kyphotic deformities are a frequent sequelae of serious disease [7]. material and methods the study was conducted in the department of neurosurgery, g. r. medical college and jay arogya hospital, gwalior, romanian neurosurgery (2018) xxxii 2: 340 346 | 341             m.p. india, over a period of one years. of all patients with thoracolumbar pott’s spine admitted in the hospital during the study period were included. patients of all age groups and both sexes were included in the study. these cases were analyzed for age, sex incidence, location and histopathological diagnosis. statistical analysis was done by calculating the numbers and percentage for computing the incidence in various age groups, in sexes, location. study design: a meta analysis ethical approval: the study was undertaken after consent and clearance by the ethical committee of g.r. medical college gwalior. inclusion criteria: of all patients admitted with thoracolumbar pott’s spine during the period 2016 – 2017 were included. exclusion criteria: patients with cervical pott’s were excluded. sample size: fifty patients methodology: age, sex, location, presenting complaints were studied. statistical analysis: it was done by calculating number and percentage for computing the incidence in various age groups, in sexes, location and also comparison with other studies. observation the present study comprises of 50 patients of thoracolumbar pott’s spine admitted in the department of neurosurgery, g.r. medical college gwalior & j.a. group of hospitals, gwalior from feb 2016 to aug 2017. table 1 age wise distribution of patients age in years no of patients percentage up to10 4 8% 11-20 4 8% 21-40 20 40% 41-60 17 34% >60 5 10% the mean age of patients in the study was 38.24 years. table 2 sex wise distribution of patients sex number of patients percentage male 25 50% female 25 50% 342 | gupta et al epidemiological study of thoracolumbar pott’s spine             table 3 distribution according to location of disease location of disease number of patients percentage upper dorsal spine d1-4 7 14% mid dorsal spine d4-8 11 22% lower dorsal spine d8-12 23 46% lumbar spine l1-5 9 18% in the present study we have found that dorsal spine was most commonly affected (72%) while lumbar spine was affected in only 18% of the cases. table 4 clinical features sign and symptoms number of patients percentage backache 50 100% motor weakness in lower limb (paraparesis) 45 90% paraplegia 5 10% sign and symptoms number of patients percentage sensory deficits 43 86% autonomic disturbances (bowel and bladder involvement) 18 36% immobility 44 88% in the present study back pain is the most common presenting symptom and found in all the patients taken in the study while motor weakness in form of paraparesis or paraplegia was the second most common symptom noted. discussion it is estimated that almost six billion people are infected with tb and over nine million new cases of active tb occur annually with two to three million deaths. extra pulmonary tb accounts for about 15–20% of all cases and nearly 1–3% of patients suffering from tb have involvement of the skeletal system. the present study has been carried out in the department of neurosurgery, g.r. medical college, gwalior on the patients of romanian neurosurgery (2018) xxxii 2: 340 346 | 343             the thoracolumbar pott’s spine during february 2016 to august 2017. total 50 cases of thoracolumbar pott’s spine were studied . in present study patients have found that thoracolumbar pott’s spine presented in age group ranging from 4 years to 68 years, with mean age of 38.24 years. in present study we have found that there were 25 (50%) male and 25 (50%) female patients. on comparison with various studies we found a near similar age and sex incidence. table 5 age and sex wise distribution of the patients s.n study age group (years) mean age (years) sex ratio (m:f) 1 present study 4-68 38.24 50:50 2 m. ehasei et al. (8) 5-80 42.5 48:52 3 park et al. (9) 10-76 44 50:50 4 kenyon et al. (10) 14-65 29 47:53 5 su et al. (11) 10-88 44.5 50:50 6 barriere et al. (12) 20-76 42 56:44 7 alothman et al. (13) 15-80 53 53:47 8 solagberu et al. (14) 2-70 27 48:52 location wise distribution in this study, out of fifty patients with pott's disease of the spine, thoracic spine was the most affected levels of the spine; where in 34 patients (68%) was found to be affected with tuberculosis. in 7 cases (14%) the disease affected the thoracolumbar vertebrae (d12-l1) and in 9 cases (18%) it was in the lumbar spines. table 6 location wise distribution s.n. study thoracic (%) thoraco lumbar (%) lumbar (%) 1 present study 68 14 18 2 m. ehsaei et al. (8) 46 10 33 3 park et al. (9) 78 11 20 4 kenyon et al. (10) 65 41 5 su et al. (11) 33 17 42 6 barriere et al. (12) 48 0 21 7 alothman et al. (13) 55 36 8 solagberu et al. (14) 24 24 44 clinical features among the 50 patients studied the most common symptom was back pain 50 (100%), fever detected in 12(24%), malaise in 9(18%) and weight loss in 25(50%) of cases. in neurologic examination 45(90%) had paraparesis. 43(86%) had sensory loss, 18(36%) of patients complained of sphincter problem, and immobility 44(88%) cases. table 7 clinical features s.n. study back pain parapares is sensory loss autonomic disturbance s 1 present study 100 90 86 36 2 m. ehsaei et al. (8) 85 64 45 30 3 elbashir g ahmed et al. (15) 66 72 70 4 fam et al. 100 344 | gupta et al epidemiological study of thoracolumbar pott’s spine             s.n. study back pain parapares is sensory loss autonomic disturbance s (16) 5 pertuiset et al. (17) 97 6 leibert et al. (18) 100 7 puigdeng olas et al. (19) 100 table 8 type of operation performed operative procedure number of patients percentage decompression alone 25 50 decompression with instrumentation 25 50 table 9 comparison of effectiveness between both procedure after 6 month sign & symtoms patients got relieved by decompression alone % patients got relieved by decompression with instrumentation % p value pain relief 96 80 0.831 improvement in power 77 78 0.977 improvement in sensation 71.5 91 0.598 improvement in autonomic system 25 50 0.466 mobility 77 91 0.716 improvement in cobb’s angle 28 84 0.0312 post op xray of patient operated for d4-5 pott’s spine by decompression with instrumentation intra op images showing decompression with instrumentation and decompression alone. romanian neurosurgery (2018) xxxii 2: 340 346 | 345             following conclusions were derived from the study:  the incidence of disease was equal in both males and females.  mean age was 38.24 years and ranging from 4 years to 68 years.  dorsal spine was most commonly involved and in dorsal spine lower dorsal spine is involved most commonly.  backache was the most common presenting symptom (100%) and patient came to the hospital with motor weakness in 90% cases.  all the cases were proven histologically to be tubercular in origin.  no death was recorded in the present study.  decompression with instrumentation group is the surgical procedure of choice for thoracolumbar pott’s spine as this is simple, safe procedure with improved stability of spine and improved and early mobility on long term follow up. correspondence: dr. asheesh kumar gupta m.ch. resident department of neurosurgery g.r. medical college gwalior, india addressroom no. 39 senior boys hostel g.r. medical college gwalior mobile no.7828832632 emailasheesh_gsvm@yahoo.com references 1. taylor gm, murphy e, hopkins r, rutland p, chistov y. first report of mycobacterium bovis dna in human remains from the iron age. microbiology 2007; 153:1243–1249. 2. lifesorm,weaverp,hardereh.tuberculous spondylitis in adults .amj bone joint surg 1985; 67:1405–141. 3. gorse gj, pais mj, kusske ja, cesario tc. tuberculous spondylitis: a report of six cases and review of the literature. medicine (baltimore) 1983; 62:178–193. 4. five-year assessments of controlled trials of ambulatory treatment, debridement and anterior spinal fusion in the management of tuberculosis of the spine. studies in bulawayo (rhodesia) and in hong kong. sixth report of the medical research council working party on tuberculosis of the spine. j bone joint surg br 1978; 60:163–177. 5. a 10-year assessment of a controlled trial comparing debridement and anterior spinal fusion in the management of tuberculosis of the spine in patients on standard chemotherapy in hong kong. eighth report of the medical research council working party on tuberculosis of the spine. j bone joint surg br 1982; 64:393–398. 6. a 10-year assessment of controlled trials of inpatient and outpatient treatment of plaster-of-paris jackets for tuberculosis of the spine in children on standard chemotherapy. studies in masan and pusan, korea. ninth report of the medical research council working party on tuberculosis of the spine. j bone joint surg br 1985; 67:103–110. 7. jain ak, kumar s, tuli sm. tuberculosis of spine [c1–d4]. spinal cord 1999; 37:362–369. 8. m. ehasei et al (medical journal of the islamic republic of iran.vol. 23, no. 4, february, 2010. pp. 200206). 9. park dw. outcome and management of spinal tuberculosis according to the severity of disease: a retrospective study of 137 adult patients at korean teaching hospitals. spine (phila pa 1976) 2007;32:e130– e135. 346 | gupta et al epidemiological study of thoracolumbar pott’s spine             10. kenyon pc, chapman al. tuberculous vertebral osteomyelitis: findings of a 10-year review of experience in a uk centre. j infect. 2009;59:372–373. 11. su sh, tsai wc, lin cy, lin wr, chen tc, lu pl, et al. clinical features and outcomes of spinal tuberculosis in southern taiwan. j microbiol immunol infect. 2010;43:291–300. 12. barriere v, gepner p, bricaire f, bletry o, caumes e. current aspects of spinal tuberculosis: apropos of 16 case reports. ann med interne (paris) 1999;150:363–369. 13. alothman a, memish za, awada a, al-mahmood s, al-sadoon s, rahman mm, et al. tuberculous spondylitis: analysis of 69 cases from saudi arabia. spine (phila pa 1976) 2001;26:e565–e570. 14. solagberu ba, ayorinde ro. tuberculosis of the spine in ilorin, nigeria. east afr med j. 2001;78:197– 199. 15. ahmed eg, elbadawi nee, ibrahim ek, mohammed mm (2013) clinical presentation of pott’s disease of the spine in adult sudanese patients. j med microb diagn 2: 120. 16. fam ag, rubenstein j. another look at spinal tuberculosis. j rheumatol. 1993;20:1731–1740. 17. pertuiset e, beaudreuil j, lioté f, horusitzky a, kemiche f, richette p, et al. spinal tuberculosis in adults. a study of 103 cases in a developed country, 1980–1994. med (balt) 1999;78:309–320. 18. leibert e, schluger nw, bonk s, rom wn. spinal tuberculosis in patients with human immunodeficiency virus infection: clinical presentation, therapy and outcome. tuber lung dis. 1996;77:329–334. 19. puigdengolas x, iranzo d, pol m, perez r, ubierna mt, olive a, et al. tuberculous spondylodiscitis. retrospective study of 14 cases. rev esp reumatol. 1993;20:151–154. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article pre-hospital care: data profile from traumatic brain injury registry ranjan kumar jena, amit agrawal, m. ashok, b.v. subrahmanyam india doi: 10.1515/romneu-2017-0055 romanian neurosurgery (2017) xxxi 3: 339 343 | 339 doi: 10.1515/romneu-2017-0055 pre-hospital care: data profile from traumatic brain injury registry ranjan kumar jena1, amit agrawal1, m. ashok2, b.v. subrahmanyam3 1department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 2national institute of epidemiology (icmr), chennai, india 3department of forensic medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: introduction: there are multiple factors from injury spot till patient reach trauma unit, which affect their outcome. the literature of same from developing country is mere. the present study investigates primary care, mode of transportation and emergency management among tbi patients visiting a tertiary institute. methods: the data of 337 patients was selected from a trauma registry. the data of tbi patients visiting emergency were entered in standard computer interface after obtaining their consent. the standard proforma was developed by filemaker pro advanced 13 (copyright © 1994-2015, filemaker, inc) and web data entry interface drupal cms. data was analyzed using stats direct version 3.0.150. results: seventy five percent of patients were from rural setup. about 67% of patients visiting emergency had undergone first aid from both rural and urban setup. forty percent of patients came directly, only about 5% were referred from other hospitals. majority of patients were accompanied by relatives (87%) followed by spouse (8.6%). non ambulance mode (31%) was more than ground ambulance (25%) to reach emergency setup. emergency management of airway, breathing and circulation was significant with outcome at discharge (p<0.001). conclusion: the study reports that majority of patients had undergone first aid before reaching trauma unit. non ambulance mode of transportation is more. the study emphasis for detail study on pre hospital care variables with larger sample size. key words: first aid, bystander, transportation, ambulance, airway, breathing, circulation introduction traumatic brain injury (tbi) is a lead cause of neurological disability in india. (1) in our country most of injury control strategies focus on primary prevention that is adopting safety measures and following appropriate road rules. only few metropolitan cities have adopted these guidelines, but not completely. 340 | kumar et al data profile from traumatic brain injury registry (2) the secondary prevention is by providing adequate medical response to manage and thereby minimise harm following an injury. (2) for injury per se immediate handling in emergency and in time transportation to health care is very crucial for early management care that prevents long term consequences. (3) unfortunately, the well trained staff capacity to provide this basic level of medical care does not exist in all the parts of our country. (3) the current study estimates the primary aid, transportation and early life support that tbi victims are engrossing in current medical setup. methods the current study data is selectively selected from a trauma registry data that is in first phase. the data collection was carried out at narayana medical college and hospital, nellore, andhra pradesh (india). the center has exclusive emergency trauma care. the study was approved by institute ethical board. all participants or their by standers consent was obtained before enrolling in to the study. the data was collected on a predesigned proforma that is compatible with computerized management system. the electronic data entry interface was developed by filemaker pro advanced 13 (copyright © 1994-2015, filemaker, inc) and web data entry interface drupal cms (http://www.neuropractices.com/node/add/tb i-registry). the trauma registry proforma constitutes core data variables that are important for trauma patients as suggested by utstein template (4). for the present study mainly focusing on pre hospital care we have selected variables like; primary aid, referral centre, by stander (person assist trauma victim), transportation and early basic life support measures. statistical analysis analysis of data was done using stats direct version 3.0.150 (statsdirect ltd. statsdirect statistical software. http://www.statsdirect.com. england: statsdirect ltd. 2015.). for the categorical data, frequencies and percentages were calculated and for continuous variables, mean and standard deviation was determined. significance among categorical data was evaluated using chi square test with significance level of lesser than 0.05. results during study period 337 head injury patients’ data was documented. from 2013, 2014, 2015 there were 77 (22.8%), 220 (65.2%) and 40 (11.8%) patients, respectively. the mean age was 36.26±15.86 years. males were four times more than females. the details of patient’s first aid, referral, by stander and transportation are described in table 1. only one victim worn helmet and car seat belt was inserted by one individual. the hospital advance life support like airway, breathing and circulation was significant with outcome at discharge. refer table 2 for more details. in circulation category cardiopulmonary resuscitation was performed in three patients and all were expired. twenty four (7.12%) patients expired during study period. romanian neurosurgery (2017) xxxi 3: 339 343 | 341 table 1 shows frequency and percentages of safety measures, referral, by stander and transportation frequency percent first aid no 110 32.6 yes 227 67.4 referral details patient bought directly to trauma centre 137 40.6 private hospital 12 3.6 government hospital 6 1.8 not available 182 54 patient brought by relatives 296 87.8 spouse 29 8.6 self 2 0.6 friend 1 0.3 unknown 1 0.3 missing 8 2.4 transportation ambulance 86 25.6 public vehicle 106 31.4 police vehicle 2 0.6 not available 143 42.4 discussion the study result reports that only one victim had taken safety measure by wearing helmet and securing seat belt. about two third patients were given first aid before appearing to tertiary emergency centre. forty percent of patients approached emergency by themselves. majority of patients accompanying person was patients relative (87%), followed by spouse (8.6%). transportation by public vehicle (31%) was more than ground ambulance transportation (25%). emergency life support approaches like airway, breathing and circulation was significant with discharge outcome. table 2 depicts advanced trauma life support with alive or death outcome at discharge sl no. variables outcome p value alive dead 1 airway <0.001 clear 194 6 incubated 90 13 adjunctive 70 1 obstructed 4 0 2 breathing <0.001 spontaneous, adequate 189 5 mechanical ventilation 61 16 spontaneous, insufficient 41 2 unknown 4 0 3 circulation <0.001 intravenous fluids 285 20 cardio pulmonary resuscitation 0 3 no specific treatment 20 1 the present study deals with tbi patient’s data from a tertiary emergency centre. about three forth of patients are from rural setup and remaining is from urban area. from the results it is obvious that patients did not take any safety precautions while travelling in vehicle. patients from urban area did not take any safety precautions then from rural setup it is difficult to expect. this shows that victims are either negligent or violating the rules. the world health organization (who) reports that middle and low income countries 342 | kumar et al data profile from traumatic brain injury registry especially from asia reports with very low percentage of helmet usage. (5) in spite of implementing strict guidelines and adopting preventive strategies for vehicle users, still they are unaware or negligent in using safety precautions. the present study reports that 70% of patients from rural and 60% of patient from urban have undergone first aid before reaching tertiary centre. victim sustaining head injury will be generally shifted to nearest local hospital where general evaluation will be done. further any requirement of ct scan or sensorium deterioration or non-availability of neurosurgeons the patient will be shifted to tertiary hospital. a study from a metropolitan city reports that 87% of patients had first aid before reaching referral trauma centre. (6) mild head injuries constitutes majority of tbi population and majority of patients may suffer from post-traumatic symptoms in multi spectrum which causes them to worry and meet the concerned specialist especially during acute and sub-acute phase of injury. (7, 8) this may be the possible reason for patient them self to approach treating doctor. injured patient accompanied to emergency by a person is very important. (9) the literature on same is insufficient. the present study reports that majority of patients were accompanied by relatives followed by spouse. in trauma circumstances, injured victim should be transported to hospital or trauma unit as early as possible. mode of transportation had an significant effect on patient outcome. (9, 10) studies from lower and middle income strata, reports that a substantial number of emergencies were transported by non-ambulance vehicles. (9, 11) a study from mumbai found about 35% of trauma patients were transported to the main trauma center via ambulance. (12) our study reports patients from both rural and urban areas, where bulk of transportation is by private vehicle and followed by ground ambulance. pre hospital care during early phase of injury is very crucial as it has potential effect on outcome of injured patient. (13) our country with huge rural setup has limited access to basic life support. the first responder with basics of managing emergencies by non-invasive method has a potential fruitful avenue. the care of airway, oxygen supplementation, cardiopulmonary resuscita¬tion, and stopping of the external bleeding, immobilization of the fractures at accident spot and careful transportation without further damage is very important. (14) but these facilities are lagging in our setup. most of the private hospitals at both rural and urban refer tbi patients to tertiary trauma unit. the availability of well-trained basic life support staff is deficient in most part of our country especially in rural areas. the present study reports that airway and breathing management at emergency is significant with outcomes at discharge. limitation the study has chosen few variables from trauma registry that is specific for the paper. the variables are not complete for pre hospital care. the deficient variables will be upgraded in next phase of data collection. the study has focused on only few variables but however the romanian neurosurgery (2017) xxxi 3: 339 343 | 343 variables have much impact on outcome of tbi and of public interest. conclusion the pilot study reports that majority of tbi patients had undergone first aid and private transportation is most common mode of transportation to reach trauma unit. the emergency management of airway, breathing and circulation has significant effect on discharge outcome. detail studies with larger sample and multi hospital level should be planned to get better overview of pre hospital care in our country. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 references 1.das a, botticello al, wylie gr, radhakrishnan k. neurologic disability: a hidden epidemic for india. neurology 2012;79:2146-2147. 2.gururaj g. epidemiology of traumatic brain injuries: indian scenario. neurological research 2002;24:24-28. 3.ramanujam p, aschkenasy m. identifying the need for pre-hospital and emergency care in the developing world: a case study in chennai, india. japi 2007;55. 4.ringdal kg, coats tj, lefering r, et al. the utstein template for uniform reporting of data following major trauma: a joint revision by scantem, tarn, dgu-tr and ritg. scandinavian journal of trauma, resuscitation and emergency medicine 2008;16:7. 5.peden m. world report on child injury prevention: world health organization, 2008. 6.pruthi n, ashok m, shiva kv, jhavar k, sampath s, devi bi. magnitude of pedestrian head injuries & fatalities in bangalore, south india: a retrospective study from an apex neurotrauma center. indian j med res 2012;136:1039. 7.iverson gl. outcome from mild traumatic brain injury. current opinion in psychiatry 2005;18:301-317. 8.arciniegas db, anderson ca, topkoff j, mcallister tw. mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. neuropsychiatr dis treat 2005;1:311-327. 9.agrawal a, coronado vg, bell jm, et al. characteristics of patients who died from traumatic brain injury in two rural hospital emergency departments in maharashtra, india, 2007-2009. international journal of critical illness and injury science 2014;4:293-297. 10.yattoo gh, tabish sa, afzal wm, kirmani a. factors influencing outcome of head injury patients at a tertiary care teaching hospital in india. int j health sci (qassim) 2009;3:59-62. 11.nielsen k, mock c, joshipura m, rubiano am, zakariah a, rivara f. assessment of the status of prehospital care in 13 lowand middle-income countries. prehosp emerg care 2012;16:381-389. 12.roy n, murlidhar v, chowdhury r, et al. where there are no emergency medical services-prehospital care for the injured in mumbai, india. prehospital and disaster medicine 2010;25:145-151. 13.dash hh. prehospital care of head injured patients. neurol india 2008;56:415-419. 14.sampalis js, boukas s, lavoie a, et al. preventable death evaluation of the appropriateness of the on-site trauma care provided by urgences-santé physicians. the journal of trauma 1995;39:1029-1035. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article spinal schwannomatosis of the cauda equina in the absence of neurofibromatosis: case report and treatment strategies dana turliuc, a. cucu, r. sandu, gabriela dumitrescu, claudia costea romania doi: 10.1515/romneu-2017-0007 romanian neurosurgery (2017) xxxi 1: 47 – 53 | 47             doi: 10.1515/romneu-2017-0007 spinal schwannomatosis of the cauda equina in the absence of neurofibromatosis: case report and treatment strategies dana turliuc1,2, a. cucu2, r. sandu2, gabriela dumitrescu2, claudia costea1,2 1“grigore t. popa” university of medicine and pharmachy of iaşi, romania 2“prof. dr. n. oblu” emergency clinical hospital of iaşi, romania abstract: schwannomatosis is a rare tumor syndrome characterized by the presence of multiple benign non-vestibular, non-intradermal schwannomas and by the absence of neurofibromatosis type 1 or 2 syndromes. multiple schwannomas are clinically and genetically distinct from neurofibromatosis, and the main treatment in case of symptomatic lesions is represented by surgical resection. in case of asymptomatic lesions, the indicated treatment is neuroimaging follow-up (mri). we are presenting the case of a patient with three schwannomas of the cauda equina, as well as the treatment strategy in the case of this rare pathology. key words: spinal schwannomatosis, multiple schwannomas, treatment introduction schwannomatosis is a syndrome characterized by the existence of multiple schwannomas at the level of the spinal cord, cranial or peripheral nerves, but without the presence of vestibular schwannomas, ependymomas, meningiomas, or astrocytomas, which are encountered in neurofibromatosis type 2 (nf2) (15, 22, 25, 27, 28). nonetheless, infrequently, the existence of meningiomas or ependymomas has been reported within schwannomatosis (3, 9). schwannomatosis was reported for the first time in 1973, as neurofibromatosis type 3 (18), and even though some researchers considered it to be an incomplete form, or a subcategory of nf2 (7), the subsequent genetic and molecular studies have shown that schwannomatosis is a separate genetic and clinical syndrome (13, 20, 24). schwannomatosis represents 3-5% of the patients with schwannomas (11, 23, 24). short case report we are presenting the case of a 59 year old female patient who was hospitalized for the 48 | turliuc et al spinal schwannomatosis of the cauda equina             first time in 2011, at “prof. dr. n. oblu” clinical emergency hospital of iaşi, for long standing low back pain and bilateral sciatica with insidious onset 10 months previously, as well as paraparesis with insidious onset 5 months previously. the imaging explorations carried out in 2011 revealed three lumbar spinal schwannomas located at the level of the cauda equina (figure 1). moreover, the head and spine mri did not detect the existence of other schwannomas. surgery was performed with the complete resection of the symptomatic schwannoma (the bigger schwannoma) (figure 2). the subsequent anatomopathological examination was of schwannoma with antoni a and b regions (figure 3), and the postoperative evolution was favourable, without neurological deficits or residual radicular pain. even though the patient did not have clinical symptoms, she was monitored every year through spine mri neuroimaging, which did not identify significant increases in the volume of the tumors. in 2016, the patient was admitted again in our neurosurgery unit for the occurrence of an important long standing low back pain and left side sciatica about 6 months before. the lumbar spine mri performed (2016) revealed the increased size of one of the two tumors, in comparison with the previous imaging explorations (2011) (figure 4). both tumors were resected (figure 5), and the postoperative evolution was favourable. moreover, the anatomopathologic diagnosis of the two tumors was of schwannoma with antoni a and b areas. figure 1 t1-weighted (sagittal, coronal and axial) gadolinium-enhanced mri images (2011) in which the 3 schwannomas of the cauda equina can be noticed romanian neurosurgery (2017) xxxi 1: 47 – 53 | 49             figure 2 preoperative (a) and postoperative (b) gadolinium-enhanced mri images (2011) figure 3 the tumour had a biphasic feature as it was made up of hypercellular areas (antoni a) composed of a haphazard arrangement of bland cells with spindled and oval nuclei, and myxoid hypocellular areas (antoni b) with large irregularly spaced vessels (hematoxylin-eosin, x100 figure 4 t1-weighted (axial) gadolinium-enhanced mri images (2011/2016) highlighting the increased size of one of the schwannomas 50 | turliuc et al spinal schwannomatosis of the cauda equina             figure 5 intraoperative appearance of the two schwannomas (a, b), postoperative appearance (c) and their correspondence in mri neuroimaging (d) (the bigger schwannoma – red arrow, the smaller schwannoma – blue arrow) table i maccollin’s diagnostic criteria for schwannomatosis (16) definitive schwannomatosis possible schwannomatosis age >30 years and two or more non-intradermal schwannomas, at least one with histologic confirmation and no evidence of vestibular tumor of high-quality mri scan and no known constitutional nf2 mutation age <30 years and two or more non-intradermal schwannomas, at least one with a histologic confirmation and no evidence of a vestibular tumor on a high-quality mri scan and no known constitutional nf2 mutation or or romanian neurosurgery (2017) xxxi 1: 47 – 53 | 51             one pathologically confirmed nonvestibular schwannoma plus a first-degree relative who also meets the above criteria age >45 years and two or more nonintradermal schwannomas, at least one with histologic confirmation and no symptoms of 8th nerve dysfunction and no known constitutional nf2 mutation or radiographic evidence of a non-vestibular schwannoma and a first degree relative also meeting the criteria for definite schwannomatosis discussion spinal schwannomas are benign tumors that develop from the schwann cells of the nerves and represent approximately one third of all benign primary spinal tumors (17). the majority of schwannomas are solitary lesions that can affect one or several nerves (5, 10), but they can also be multiple, suggesting the presence of syndromes, the most frequent of which is nf2. spinal schwannomas unassociated with neurofibromatosis was reported for the first time in 1993 by the american daras m., at the metropolitan hospital from new york (5). the schwannomatosis diagnosis is supported by the anatomopathological diagnosis which, apart from the antoni a and antoni b regions (26), also highlights other histological findings, such as: nerve oedema, intraneural growth pattern and myxoid stroma (21). like in nf2, the schwannomas are growing slowly and do not turn into malignant lesions (2). the genetics of schwannomatosis is complex and not yet fully understood (14), given that over 90% of the sporadic cases and 50% of the familial cases of schwannomatosis do not have an identified genetic mutation (19, 20). an associated germline mutation inactivating the smarcb1 gene is encountered in only 40-50% of the familial forms, and in less than 10% in the sporadic cases (20). moreover, the family history is present only in 15-25% of the cases (20). the first clinical sign of patients who are suffering from schwannomatosis is pain on the tract of the implied nerve (8, 12, 16), unlike patients suffering from nf2, who seek medical care for the occurrence of neurological deficit, which is represented in 95% of the cases by hearing impairment (6). in our patient’s case, the onset symptomatology was represented by long standing low back pain and bilateral sciatica, followed by the insidious onset of neurological deficit. the age of onset of schwannomatosis is represented by the fourth decade (1, 11, 24), 52 | turliuc et al spinal schwannomatosis of the cauda equina             unlike patients with nf2, who seek medical care at an earlier age (5). even though some criteria for diagnosing schwannomatosis have been proposed, they are currently unclear. in 1997, jacoby et al. proposed as a criterion for schwannomatosis the presence of 2 or more schwannomas, in the absence of vestibular schwannomas, in patients over the age of 18 (13). later on, in 2005, maccollin et al. also enumerated several criteria: the presence of 2 or more non-intradermal schwannomas, over 30 years of age, the absence of mri-detectible vestibular schwannomas, as well as the absence of constitutional mutations encountered in nf2 (table 1) (16). the treatment indicated in schwannomatosis is the surgical removal in symptomatic cases (4) and follow-up in non-symptomatic cases. moreover, in our patient’s case, the biggest schwannoma which was actually symptomatic, was initially resected (figure 1, figure 2). for the other two smaller, nonsymptomatic schwannomas (figure 5), a conservative follow-up treatment was decided upon. five years after the initial surgery, the patient was hospitalized for the occurrence of pain, due to the increased size of the second schwannoma. thus, surgery with the complete resection of the two tumors was performed, having a favourable postoperative evolution. conclusions in the case of multiple spinal schwannomas, head neuroimaging (mri) and audiological testing must also be taken into consideration in order to exclude nf2. in spite of the similarities between nf2 and schwannomatosis, they are two distinctive entities, both genetically and clinically, which can pose diagnosis problems. the maccollin criteria can be useful to differentiate between these two syndromes. in the case of patients with spinal schwannomatosis, we recommend surgical treatment in the case of symptomatic tumors, and conservative follow-up treatment in case nonsymptomatic tumors. correspondence andrei cucu “prof. dr. n. oblu” emergency clinical hospital iasi, romania e-mail: andreiucucu@yahoo.com references 1.antinheimo j, sankila r, carpén o, pukkala e, sainio m, jääskeläinen j. population-based analysis of sporadic and type 2 neurofibromatosis-associated meningiomas and schwannomas. neurology. 2000; 54:71-76. 2.bhattacharyya ak, perrin r, guha a. peripheral nerve tumors: management strategies and molecular insights. j neurooncol. 2004; 69:335–349. 3.boyd c, smith mj, kluwe l, balogh a, maccollin m, plotkin sr. alterations in the smarcb1 (ini1) tumor suppressor gene in familial schwannomatosis. clin genet. 2008; 74(4): 358-366. 4.conti p, pansini g, mouchaty h, capuano c, conti r. spinal neurinomas: retrospective analysis and long-term outcome of 179 consecutively operated cases and review of the literature. surg neurol. 2004; 61(1):34-43, discussion 44. 5.daras m, koppel bs, heise cw, mazzeo mj, poon tp, duffy kr. multiple spinal intradural schwannomas in the absence of von recklinghausen's disease. spine. 1993; 18(16): 2556-2559. 6.evans dg, huson sm, donnai d, neary w, blair v, newton v, harris r. a clinical study of type 2 neurofibromatosis. q j med. 1992; 84:603-618. 7.evans dg, mason s, huson sm, ponder m, harding ae, strachan t. spinal and cutaneous schwannomatosis is a variant form of type 2 neurofibromatosis: a clinical romanian neurosurgery (2017) xxxi 1: 47 – 53 | 53             and molecular study. j neurol neurosurg psychiatry. 1997; 62:361-366. 8.govind m, radheyshyam m, achal s, ashok g. intradural extramedullary spinal cord tumors: a retrospective study at tertiary referral hospital, romanian neurosurgery. 2016; xxx (1):106-112. 9.hadfield kd, newman wg, bowers nl, wallace a, bolger c, colley a, mccann e, trump d, prescott t, evans dg. molecular characterisation of smarcb1 and nf2 in familial and sporadic schwannomatosis. j med genet. 2008; 45(6):332-339. 10.halliday al, sobel ra, martuza rl. benign spinal nerve sheath tumours: their occurrence sporadically and in neurofibromatosis types 1 and 2. j neurosurg. 1991; 74:248-253. 11.huang jh, simon sl, nagpal s, nelson pt, zager el. management of patients with schwannomatosis: report of six cases and review of literature. surg neurol. 2004; 62:353-361. 12.iacob g. spinal meningiomas. personal experience and review of literature, romanian neurosurgery. 2014; xxi (2):146-160. 13.jacoby lb, jones d, davis k et al (1997) molecular analysis of nf2 tumour suppressor gene in schwannomatosis. am j hum genet 61:1293–1302. 14.koontz na, wiens al, agarwal a, hingtgen cm, emerson re, mosier km. schwannomatosis: the overlooked neurofibromatosis? ajr am j roentgenol. 2013; 200: w646–w653. 15.maccollin m, woodfin w, kronn d, short mp. schwannomatosis: a clinical and pathologic study. neurology. 1996; 46:1072–1079. 16.maccollin m, chicocca ea, evans dg friedman jm, horvitz r, jaramillo d, lev m, mautner vf, niimura m, plotkin sr, sang cn, stemmer-rachamimov a, roach es. diagnostic criteria for schwannomatosis. neurology. 2005; 64:1838-1845. 17.mautner vf, tatagiba m, lindenau m, funsterer c, pulst sm, baser me, kluwe l, zanella fe. spinal tumors in patients with neurofibromatosis type 2: mr imaging study of frequency, multiplicity, and variety. ajnr am j roentgenol. 1995; 165(4):951-955. 18.nimura m. neurofibromatosis. rinsho derma. 1973; 15:653-663. 19.piotrowski a, xie j, liu yf, poplawski ab, gomes ar, madanecki p, fu c, crowley mr, crossman dk, armstrong l, babovic-vuksanovic d, bergner a, blakeley jo, blumenthal al, daniels ms, feit h, gardner k, hurst s, kobelka c, lee c, nagy r, rauen ka, slopis jm, suwannarat p, westman ja, zanko a, korf br, messiaen lm. germline loss-of-function mutations in lztr1 predispose to an inherited disorder of multiple schwannomas. nat genet. 2014; 46: 182-187. 20.plotkin sr, blakeley jo, evans dg, hanemann co, hulsebos tjm, hunter-schaedle k, kalpana gv, korf b, messiaen l, papi, l, ratner n, sherman ls, smith mj, stemmer-rachamimov ao, vitter j, giovannini m. update from the 2011 international schwannomatosis workshop: from genetics to diagnostic criteria. am j med genet a. 2013;161a:405-416. 21.poliani pl, desantis s, bettensky ra et al. defining histologic criteria for the diagnosis of schwannomatosis, aspen, co, 2005. 22.purcell sm, dixon sl. schwannomatosis. an unusual variant of neurofibromatosis or a distinct clinical entity. arch dermatol. 1989; 125: 390-393. 23.radek m, tomasik b, wojdyn m, snopkowskawiaderna d, błaszczyk m, radek a., neurofibromatosis type 2 (nf 2) or schwannomatosis?--case report study and diagnostic criteria. neurol neurochir pol. 2016; 50(3):219-225. 24.seppala mt, saino ma, haltia mj, kinnunen jj, setälä kh, jääskeläinen je.. multiple schwannomas: schwannomatosis or neurofibromatosis 2. j neurosurg. 1998. 89:36-41. 25.shin kh, moon sh, suh js, jahng js. multiple neurilemomas. a case report. clin orthop. 1998; 357: 171-175. 26.wippold fj 2nd, lubner m, perrin rj, lämmle m, perry a. neuropathology for the neuroradiologist: antoni a and antoni b tissue patterns. ajnr am j neuroradiol. 2007; 28(9):1633-1638. 27.wolkenstein p, benchikhi h, zeller j, wechsler j, revuz j. schwannomatosis: a clinical entity distinct from neurofibromatosis 2. dermatology. 1997; 195: 228-231. 28.yamamoto t, maruyama s, mizuno k. schwannomatosis of sciatic nerve. skeletal radiol; 2001; 30: 109-113. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article outcome of surgically treated head injury in unattended patients at neurosurgery department in tertiary care centre an institutional study praveen kumar tripathi, vardan kulshreshtha, gaurav jaiswal, tarun kumar gupta india doi: 10.1515/romneu-2017-0039 romanian neurosurgery (2017) xxxi 2: 233 239 | 233 doi: 10.1515/romneu-2017-0039 outcome of surgically treated head injury in unattended patients at neurosurgery department in tertiary care centre an institutional study praveen kumar tripathi, vardan kulshreshtha, gaurav jaiswal, tarun kumar gupta department of neurosurgery, r.n.t medical college, udaipur, rajasthan, india abstract: this is a prospective study, carried out at our department. many patients with history of trauma with head injury, whose identity cannot be ascertained, are admitted in our hospital. the management of these unattended patients from pre-hospital till discharge, rehabilitation or death is full of difficulties especially when surgical intervention has to be done. we conducted a prospective study by enrolling 11 consecutive unattended patients in whom neurosurgical procedures performed at our hospital. out of 11 patients, 9 (82%) were male, most were in the age group of 21-30 years. the mean age was 30 years. mean duration of hospital stay was 11.27 days. the cause of head injury was road traffic accident in all patients. majority of the patients 10 (90%) had glasgow coma scale less than 8 on admission. two patients 2 (18%) died in hospital, 7 (63%) patients had good recovery. during the course of treatment identity of all 11 patients was established and 8 (72%) patients who survived were discharged to home. all discharged patients were followed at interval of 1 month and 3 months. four (50%) & 5 (62%) patients showed good recovery (gos) at 1 month & 3 month respectively key words: anonymous patient; head injury; nameless patient; outcome; unknown patients; unidentified patient introduction the total number of deaths in road accidents in india was 169107 during 2014 (1). the incidence of road traffic accident in rajasthan in 2014 was 24639 and out of which the total number of deaths in road accidents in rajasthan was 10287 during 2014, which was 6.08% of the total number of deaths in road accidents in india during the year (1). in india, the incidence of head injury is steadily increasing with urbanization and increasing number of vehicular population (2). among the road traffic accidents 70% have head injury, among road accident deaths 70% are 234 | kumar tripathy et al surgically treated head injury in tertiary care centre due to head injury. majority of deaths occur during first 72 hours. recently, number of fatal accidents has increased in india. every minute there is an accident and every eight minute there is a death (3). attempts to systematize care of patients with severe tbi have culminated in evidence-based guidelines issued by the joint task force between the brain trauma foundation and the american association of neurological surgeons (4, 5). our institute which is a tertiary care center of a developing country and a lot of severe head injury patients are being referred to us. many such patients are often brought by policemen and bystanders and their identities are not known at the time of admission. these patients present a unique challenge in management. in this background we conducted prospective study in this group of patients who underwent neurosurgical procedure(s) for understanding their mode of injury, presentation, treatment and outcome and factors affecting outcome after surgery of head injury. methodology this was a prospective study, conducted at department of neurosurgery, maharana bhupal government hospital, rnt medical college, udaipur, rajasthan. from march 16, 2015, until march 30, 2016, out of 118 consecutive patients unattended patients admitted in our department with history of head injury, eleven (11) patients who underwent neurosurgical procedure(s) were enrolled in the study. we analysed demography, mode of injury, clinical presentation, and condition at admission, treatment given, hospital stay, outcome and factors affecting outcome of the patients. all patients were clinically evaluated by a team comprising of doctors from surgical, medical and orthopaedics specialties in the emergency department and subsequently admitted and treated at neurosurgery. complete primary evaluation was done. ncct brain and whenever necessary, x-rays, ct scan of spine, usg abdomen, mri spine or contrast ct (abdomen/chest) were carried out to rule out other injuries. results out of 11 patients, 9 (82%) were male, and only 2 (18%) were female (table 1). none of patients was less than 20 yrs of age, while the most patients 5 (45%) were in the age group of 20-29 years, while only 4 (36%) patients were of 30-39 year age group . none were > 60 years of age group (table 2). road traffic accident was the only cause of injury in all 11 cases. table 1 demography (gender) of head injury in unknown patients underwent neurosurgery: (n=11) demography no. of patients percentage gender male female 9 2 82 18 total 11 romanian neurosurgery (2017) xxxi 2: 233 239 | 235 table 2 demography of head injury in unknown patients underwent neurosurgery: (n=11) demography no.of patients percentage mean age(years) age group <20 20-29 5 45 30-39 4 36 40-49 2 18 50-59 >60 total 11 at the time of admission glasgow coma scale (gcs) score of less than 8 was seen in 9 (82%) cases. gcs between 8 and 12 was seen in 2 (18%) cases. plain ct scan of head revealed edh in 6 (54%) patients, 4 (36 %) had sdh and 1 (9%) patient had depressed fracture (table 3). associated injuries were seen in total 3 (27%) patients. one patient (9%) had chest injury, 2 (18%) had limb fracture. table 3 clinical characteristic and type of lesion in head injury of unknown patients treated surgically: (n=11) number of patients percentage cause of head injury road traffic accident other 11 11 100 100 glasgow coma scale at admission 13-15 12-8 <8 2 9 18 82 type of brain injury (major component) extradural haematoma (edh) subdural haematoma(sdh) cerebral contusion depressed fracture diffuse axonal injury(dai) subarachnoid haemorrhage(sah 6 4 1 55 36 09 other injury chest injury abdominal injury limb fracture 1 2 09 18 other emergency surgical speciality procedure 1 icd insertion for chest injury 09 236 | kumar tripathy et al surgically treated head injury in tertiary care centre table 4 surgical procedures performed (n=11) type of surgery no. of patients percentage decompressive craniectomy craniotomy depressed fracture elevation burr hole evacuation 6 4 1 54 37 9 total 11 100 these 11 patients who needed surgical intervention where decompressive craniectomy was carried out in 6 (54%), craniotomy was in 4 (37%), 1 patient (9%) underwent depressed facture elevation (table 4). during treatment, 3 patients (27%) had pneumonia, 1 (9%) had wound infection (table 5). mean stay at hospital in these patients was 11 days with longest stay of 20 days in one patient. at the time of discharge, 3 patients (27%) had gcs of 13-15 and 5 (45 %) had gcs score 12-8, only 1 patient had gcs less than 8 at time of discharge. according to glasgow outcome scale (gos) of these patients, 3 (27%) had good recovery, 4 (36%) had moderate disability, 1 (09%) had severe disability, and 3 (27%) died during treatment. during the course of treatment identity of all the 11 (100%) patients was identified and 8 (73%) patients who survived were sent home with relatives. all patients who were discharged followed at 1month and 3 month intervals. 4 (50%) & 5 (62%) patients showed good recovery (gos) at 1 month & 3 month respectively. none of the discharged patients lost to follow up at 3 months. table 5 complications during treatment of the patients (n-11) complications no. of patients percentage pneumonia meningitis septicemia wound infection csf leak -hydrocephalus 3 1 27 9 total 4 table 6 outcome and destination of patients during discharge (n=11) outcome no. of patients percentage glasgow outcome scale good recovery moderate disability severe disability vegetative state death 3 4 1 3 27 36 09 27 glasgow coma scale at discharge 13-15 8-12 < 8 3 5 27 45 discharged location home destitute home 11 0 100 0 romanian neurosurgery (2017) xxxi 2: 233 239 | 237 table 7 outcome during follow up of patients after discharge (n-08) outcome after 1 month n=08 after 3 month n=08 glasgow outcome scale good recovery moderate disability severe disability vegetative state death 4 4 5 3 lost to follow 0 0 table 8 average hospital stay in unattended patients (n-11) longest stay period longest icu stay period mean stay 20 days 13 days 11days discussion in a study by ahmad fu et al. 2006, out of 325 unidentified patients, there were 9 (3%) patients in the pediatric age group and 16 (5%) patients were above 60 years of age. of these, 193 (65%) could be identified during the hospital stay (6). an additional 40 (13%) patients were sent home after they regained memory of their addresses. forty seven patients (15%) died without their identities being established. seventeen (6%) patients remained unknown and were sent to rehabilitation/poor homes with the help medical social worker (6). in study of wanger etal, approximately one third of patients with moderate head injury and half of patients with severe head injury were operated, most of them being for cerebral contusions and/or subdural hematomas (7). mortality following head injury has been reported to be in the range of 39-51% (8, 9). study by liew bs et al. showed both known and unknown head injury patients, among 72 patients of head injury eleven patients (15%) died during hospitalization (10). there were only sixty one (85%) patients were discharged from hospital, where by twenty nine (40%) with good outcome (gos 4 and 5) while the remaining thirty two (44%) patients were with either severe disability or vegetative state. only one patient continued to suffer severe disability, while the rest had moderate or good recovery (10). in another study there were twelve patients (17%) under the age of twenty years, only 5 patients (7%) were above 60 years. twenty patients (29%) were treated by surgery, most often for cerebral contusion (33 patients 47%) (11). till date no prospective study has been conducted to assess outcome of such unidentified patients who underwent neurosurgical procedures. in our study 11 patients who needed surgical intervention where decompressive craniectomy was carried out in 6 (54%), craniotomy was in 4 (37%), 1 patient (9%) underwent depressed facture elevation. mean hospital stay in these patients was 11 days with longest duration of 20 days. among these patients, 3 (27%) had good recovery, 4 (36%) had moderate disability, 1 (09%) had severe disability, and 3 (27%) died during treatment. during the course of treatment identity of all 11 (100%) patients was identified and 8 (72%) patients who survived were sent home with relatives. these unidentified patients with unknown identities present considerable challenges in 238 | kumar tripathy et al surgically treated head injury in tertiary care centre their management. they are usually found lying on road in unconscious state and brought to hospital by policemen or by passers who are ill equipped and often ignorant in handling patients with severe injuries. their prehospital management is usually improper and lack of proper transfer facilities, in ambulances, further aggravates their condition. we receive many such patients from peripheral hospitals, because of lack of proper facilities there. very often such patients are destitute and their injuries are compounded by presence of debility because of poor nutrition, other medical conditions like diabetes, hypertension, substance abuse and mental illnesses. therefore, it is imperative that these patients be evaluated with a very high index of suspicion for above conditions. during their hospital stay, the role of paramedical staff is of paramount importance; their daily nursing care in absence of a relative is a challenging task. it needs a team of trained and empathetic nursing staff along with a physiotherapist, dietician, psychologist, and social worker who can help and rehabilitate them. performing neurosurgical procedures in such patients is not devoid of difficulties ranging from consent to rehabilitation. existing infrastructure and much trained staff, enthusiastic multidisciplinary team, social workers and media personals help many unidentified patients with severe head injury in rehabilitation. it is highly gratifying for the treating team to see such patients return back to our outpatient department with their relatives. we believe that there is an urgent need to sensitize the general public and police about the transportation and prehospital management of such severe head injury patients. our peripheral hospitals need to be well equipped for treatment of such patients. treatment of such unknown patients can entail a huge expenditure and therefore, every hospital should allocate funds for the above purpose and only those patients who are in need of higher medical care should be referred to higher center. the role of social media and general media also has a capacitive role in spreading awareness and rehabilitating unidentified patients. conclusion unidentified head injury patients are posed with challenges. outcome of these patients is comparable to patients who are accompanied by their relatives. their management from prehospital to treatment and discharge from hospital is quite challenging especially in icu and meeting nutritional standards. there mean hospital stay is sometimes longer in comparison to similar patients as they may remain unidentified. they need special care for which staff should be well trained and hospital must have economic resources. hospital should have a protocol system to deal with such patients especially when they require neurosurgical interventions. a good network of social workers and active involvement of media helps in identification and rehabilitation of these patients. references 1. http://ncrb.gov.in/statpublications/maps-2014/adsi2014%20maps/adsi-2014-accidentsroadaccidentcases.pdf 2. report of road safety cell: ministry of transport govt of india, january 1993. romanian neurosurgery (2017) xxxi 2: 233 239 | 239 3. head injuries: a neglected field in india. national medical journal 1991; 4:53-44. 4. guidelines for the management of severe head injury. the brain trauma foundation. the american association of neurological surgeons, the joint section on neurotrauma and critical care. j neurotrauma. 1996;11:641–734. 5. the brain trauma foundation. the american association of neurosurgical surgeons. the joint section on neurotraumaand critical care. trauma systems. j neurotrauma. 2000;17:457–627. 6. ahmad fu, mahapatra ak, mehta vs. outcome of unknown head injury patients at a tertiary care neurosurgical centre: neurology india 2006; 54:73-4. 7. wanger ak, sessere hc, hammond fm, et al. international traumatic brain injury: epidemiology and risk factors associated with severity and mortality. j trauma 2000; 49:404-10. 8. lannoo e, van rietvelde f, colardyn f, et al. early predictors of mortality and morbidity after severe closed head injury. j neurotrauma 2000;17:403-14. 9. bulger em, nathens ab, rivara fp, et al. brain trauma foundation: management of severe head injury: institutional variations in care and effect on outcome. crit care med 2002; 30:1870-6. 10. liew bs, johari sa, nasser aw, abdullah j. severe traumatic brain injury: outcome in patients with diffuse axonal injury managed conservatively in hospital sultanah aminah, johor bahruan observational study. med j malaysia 2009; 64: 280-8. 11. outcome of head injury in unknown patients at level1 apex trauma centre nath, haradhan deb et al. the indian journal of neurotrauma , volume 8 , issue 1 , 11 15 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article efficacy of electromyography and nerve conduction velocity monitoring in surgical management of terminal lipoma in children ashraf el badry, mohamed elsaeed, ahmed abdel khalek, azza abdelazeez egypt doi: 10.1515/romneu-2017-0030 romanian neurosurgery (2017) xxxi 2: 191 196 | 191 doi: 10.1515/romneu-2017-0030 efficacy of electromyography and nerve conduction velocity monitoring in surgical management of terminal lipoma in children ashraf el badry1, mohamed elsaeed2, ahmed abdel khalek3, azza abdelazeez4 1assistant professor of neurosurgery department 2assistant professor of neurology department 3professor of radiology department 4assistant professor of pathology department faculty of medicine, mansoura university hospital, egypt abstract: background: the prognosis of terminal lipomas is better than that of other sites and pathology especially their management nowadays became clearer with better surgical outcome due to advancement of surgical tools and neurophysiology study. objective: to assess the outcome of excision of terminal lipomyelomeningocele and reconstruction of the neural tube. methods: from 2002 to 2016, 32 cases of terminal lipomyelomeningocele in mansoura university hospital, insurance hospital and el ahrar specialized center, the age of the cases ranged between 10 days and 4,3 years underwent surgical management of total or near-total lipoma excision and neural tube reformation with minimum follow up of 6 months. results: according to system which applied to show the success of the operations, of the 32 patients, 9 cases represent (28.1%) showed total excision of the lipoma; 17 patients represent (53.1%) had 25 mm3 of lipoma or less and 6 patients represent (18.75%) had 26 mm3 of fat or more. the neurological and urological complications was about 25%, while other complications like cerebrospinal fluid leak, wound disruption and infection was 9.4%. the surgical morbidity was comparable with the published papers. conclusion: the excision of terminal lipomyelomeningocele and recreation of the neural tube by monitoring throughout emg & ncv with low surgical morbidity and better results than leaving them without management or surgical interference without neurophysiological monitoring. key words: terminal lipomyelomeningocele, lipoma, reconstruction of neural placode. abbreviations: drez, dorsal root entry zone; mri, magnetic resonance imaging, csf, cerebrospinal fluid. 192 | el badry et al electromyography in surgery of terminal lipoma patients and methods patients the prognosis terminal (caudal in chapman 3) lipomas had better than that of other types and locations of spinal lipomas, their surgical management established with no debate of its benefit (1, 4, 5, 15, 21). the principle of its management includes total/gross total excision of the lipoma; with separation of neural placode from the dura and reformation of neural tube. from 2002 to 2016, 32 cases of terminal lipomyelomeningocele in mansoura university hospital , insurance hospital and el ahrar specialized center included in the study their age varied from 10 days to 4,3 years with a mean age of 3.5 months had total or gross total excision guided microscopically and with nerve stimulator, with minimum follow up of 6 months... there were 15 males and 17 females. in the literature the lipomyelo – meningocele defined as a part of the distal conus and the fat protrudes outside through the dorsal bony defect, with sac filled by cerebrospinal fluid (csf). (1, 15) figure 1 lipomyelomeningocel a, b mri 1 tisla sagittal and axial cuts t1 w show lipoma, cerebrospinal fluid surround part of the conus protrude out of the spinal canal through a dorsal defect surgical technique embryological important notes in the literatures in embryology of the spinal cord, mclone and his colleagues suggested that the gap present due to defect between the cutaneous and neural ectoderms during early separation, which lead to the paramedian mesenchyme to fill the space between neural folds and invade the central canal. (15, 17, 18) as known the dorsal root ganglions generated from neural crest cells at the outer surface of the neural fold then its roots grow ventrolateraly but never traverse, the lipomatous stalk. (4, 8, 9) surgical principle this technique guided by principles which described by pang who was one of the leaders in management of spinal lipomas with its verities but modified according to facilities and learning curves (11, 12, 13), longitudinal skin and soft-tissue incision then sharp dissection separating the subcutaneous lipoma from the skin and subcutaneous tissue till reaching the defect in the bony spinal canal and excision of the lipoma till the bony defect. the dissection begin one level above the rostral periphery of the lipoma, to move from normal anatomy to disturbed one which gives us better orientation of the last normal nerve root and drez before starting excision of lipoma. the lower extent not the same important like the upper one then we made wide laminectomy to give full view till the lateral edges of the dura sac. romanian neurosurgery (2017) xxxi 2: 191 196 | 193 then: excision of the lipoma and separating it from the inner surface of the dura, opening the dura at upper end of the lipoma in the midline let us take better view and our dissection will be more skillful. the dural edges are retracted by sutures. next, the white fibrous band between lipoma and the tethered cord is identified. the drez and dorsal nerve roots are lateral to this line. then dissection according to this line and more in the side of lipoma guided also by position of the drez and the neural placode. we began excision of the lipoma at the proximal end where the normal anatomy present between lipoma, drez and nerve root then dissection along the white fibrous line. cauterization usage is applied minimally to avoid injury to the drez and postoperative dysesthesia may appear. after total resection of the lipoma and detaching of the placode from the inner dura we rule the placode on itself by suture to decrease adhesion between it and inner dura by making the contact surfaces smooth. the closure was by interrupted 6–0 nylon sutures without force. figure 2 a surgical exposure of lumbosacral lipoma, b lateral dissection of the lipoma figure 3 reconstruction of the placode and closure of the wound results to achieve the success of the operations we must assess three elements: 1) the amount fat left 2) the state of reformation of neural tube and 3) presence of complications to these operations, according to the amount of fat left: the amount fat left was assessed by postoperative magnetic resonance imaging (mri) or c.t sagittal reformatting at 3 months. the results of the 32 patients was as follow, 9 cases represent (28.1%) showed complete removal of the lipoma with no residual; 17 patients represent (53.1%) showed 25 mm3 or less of fat left postoperatively, these cases showed multiple nerve fibers entangled with fat; and last 6 patients represent (18.75%) showed the amount of fat left was more than 26 mm3 of fat left due to the lipoma on the ventral surface or entangled with the neural placode. the reformation of the neural tube and placode reconstruction is achieved the cord from the lipoma and inner dura with rolling it raw edges on itself to get smooth surface and the close the dura in water tight fashion. 194 | el badry et al electromyography in surgery of terminal lipoma figure 4 postoperative (a) sagittal mri t1 w and postoperative (b) sagittal reformat ct of a lipomyelomeningocele revealing a blunty stump of the terminal conus after excesion of the lipoma table 1 show complications of total/gross total resection of lipomyelomeningocele complication no. of cases % loss of sensation 4 12.5 new weakness 3 9.4 voiding dysfunction 2 6.25 csf leak 2 6.25 pseudomeningocele 3 9.4 wound infection 2 6.25 overall complications 16 50.05 with obeying this principle the cord-sac ratio, represent free movement of the placode inside the created dural pouch which approved untethering of the cord on postoperative axial mri or ct at the widest portion of neural tube reformation. so the 32 cases grouped in three categories: lower than (<30%) in the widest reformatted dural sacs, medium (between 30% and 60%) medium category, and high (>60%) in most tight sacs. 20 cases represent (62.5%) had ratio between cord and the sac less than 30%, 7 cases represent (21.9%) had ratios between 30% and 60%, and 5 cases represent (15.6%) had ratio more than 60%. complications table 1 showed nine cases represent (28.1%) experienced neurological complication from surgery. only 3 patients (9.4%) developed motor weakness and 4 patients (12.5%) suffered sensory loss. 2 patients with had bladder dysfunction beside motor weakness. csf leak or pseudomeningocele were seen in five cases, we reoperated in 3 cases of them. so overall surgical complication rate for our surgeries represent 50.5%. discussion the study by kulkarni from neckerenfants malades, paris in 2004, showed without any doubt that asymptomatic lipomas will be deteriorating by 43% in 10 years follow up 10-year (11). the white plane which compact collagen fibers between the lipoma and neural placode is the crucial point in excision of terminal lipoma through it we can do dissection safe with aid of microscope and micro scissors. inspite of arai and his colleagues (1) and chapman (4), postulated that lipo myelo meningocele carry poor prognosis, on the other hand we found it carry better prognosis if we dissect carefully and along the white line from the extra spinal lipoma extended to the intra spinal part guided by nerve stimulator to separate the lipoma form the cord. one of the most important goals in this surgery is untethering of the cord from inner romanian neurosurgery (2017) xxxi 2: 191 196 | 195 dural surface with failure to accomplish this goal lead to recurrence of symptoms (4, 5, 14). pierre-kahn and his colleagues. 14 and xenos and his colleagues (5) were pioneers in surgically managing the lipomyelomeningocele reported failure of untethering the cord in 20% of their cases which lead to worse neurological condition of the cases as nerve roots entangled with fat but we overcome this obstacle by stressing on following the white line between fat and the cord and the nerve stimulation which let us know the good functioning roots from nonfunction one which we can cut it without worry about increase neurological deficit. reformation of the neural tube and reconstruction of the neural placode as done by mclone and his colleagues (15) we realized the presence of smooth surface of the placode by rolling its raw edges on itself making smooth surface between the cord and the inner dura made the untethering was accomplished and decrease the rate of recurrence. in literature of pierre-kahn and his colleagues (4) showed only neurulation in 17% of the cases due to failure of total excision of the lipoma in most cases, and others (16) also had same results. in our partial resection group, we cannot made complete neurulation due to failure of getting raw edges of the neural placode on itself as consequence of incomplete excision of the lipoma. on the other hand, we were able reformation of neural placode and neural tube in 81.6% of our case due to complete or near complete lipoma excision. we found autologous fascia graft good alternative if needed, as pierre-kahn and his colleagues (15) did. the result also less successive than described by pang who spent more than 20 years in this subject (11, 13) may be due to less experience of using nerve stimulator and less experience with this surgical approach which built up from case to another. in discussing the complications, most of papers in this subject showed partial excision as the safest policy to decrease the neurological complication which reported as 4% who had weakness; but most common was neuropathic pain by heat from electrical cautery near the drez and dorsal roots. we saw to decrease this complication by controlling the minor bleeding by oxidized cellulose or gel foam which worked as tamponade and lastly by low currant electro cautery if needed in very limited situation. csf leaks (6.25%) and wound complications (6.25%) in our series was comparable with those in the published papers of the same issue which verified csf leak range from 2% to 47% (4, 5, 6, 15, 16, 17, 18) and wound dehiscence and infection represented from 2% to 26% (5, 6, 7, 8, 15, 16), our strong point to decrease these complication was: good bony exposure cephalic and caudal so we could dissect from normal to abnormal anatomy with preservation of the dura to close the sac water tight then good anatomical closure with muscle flap if needed to strengthen the closure of the defect, fibrin glue was used in some cases but because it was not standardized in all cases we did not represent it as one of the main factors in decrease wound disruption and csf leak. 196 | el badry et al electromyography in surgery of terminal lipoma conclusion the excision of terminal lipomyelomeningocele and recreation of the neural tube by monitoring throughout emg & ncv with low surgical morbidity and better results than leaving them without management or surgical interference without neurophysiological monitoring. correspondence ashraf el badry, m.d., ifaans address: department of neurological surgery mansoura university hospital, egypt email address: ashrafbadry@hotmail.com or ashrafbadry@mans.edu.eg phone: +201111300033 or +201223477444 references 1. arai h, sato k, wachi a: surgical management in 81 patients with congenital intraspinal lipoma. child nerv syst,1992,8:171. 2. caldarelli m, mclone dg, colins ja, suwa j, knepper pa: vitamin a induced neural tube defects in a mouse. concepts pediatr neurosurg , 1985,6:161–171. 3. chapman ph: congenital intraspinal lipomas: anatomic considerations and surgical treatment. childs brain, 1982, 9:37–47. 4. chapman ph, davis kr: surgical treatment of spinal lipomas in childhood. pediatr neurosurg, 1993,19:267– 275. 5. cochrane dd, finley c, kestle j, steinbok p: the patterns of late deterioration in patients with transitional lipomyelomeningocele. eur j pediatr surg, 2000,10 [suppl 1]:13–17. 6. hoffman hj, taecholarn c, hendrick eb, humphreys rp: management of lipomyelomeningoceles. experience at the hospital for sick children toronto. j neurosurg , 1985,62:1–8. 7.james he, williams j, brock w, kaplan gw, u hs: radical removal of lipomas of the conus and cauda equina with laser microneurosurgery. neurosurgery, 1984,15:340–343. 8. kanev pm, lemire rj, loeser jb, berger ms: management and long-term follow-up review of children with lipomyelomeningocele, 1952-1987.j neurosurg, 1990,73:48–52. 9. koyanagi i, iwasaki y, hida k, abe h, isu t, akino m: surgical treatment supposed natural history of the tethered cord with occult spinal dysraphism. child nerv syst, 1997, 13:268–274. 10. kulkarni hv, pierre-kahn a, zerah m: conservative management of asymptomatic spinal lipomas of the conus. neurosurgery, 2004,54:868–875 11-pang d: tethered cord syndrome: newer concepts, in wilkins rh, rengachary ss (eds): neurosurgery update ii. new york, mcgraw-hill, 1991, pp 336–344. 12. pang d: spinal cord lipomas, in pang d (ed): disorders of the pediatric spine. new york: raven, 1995, pp 175–201. 13. pang d: spinal cord lipoma, in batjer hh, loftus c (eds): textbook of neuro -logical surgery. baltimore, lippincott williams &wilkins, 2002, pp 896–915. 14-pierre-kahn a, lacombe j, pichon j, giudicelli y, renier d, sainte-rose c, perrigot m, hirsch j: intraspinal lipomas with spina bifida: prognosis and treatment in 73 cases. j neurosurg , 1986,65:756–761. 15. pierre-kahn a, zerah m, renier d, cinalli g, sainterose c, lellouch-tubiana a, brunelle f, le merrer m, giudicelli y, pichon j, kleinknecht b, nataf f: congenital lumbosacral lipomas. child nerv syst, 1997,13:298–335. 16. la marca f, grant ja, tomita t, mclone dg: spinal lipomas in children: outcome of 270 procedures. pediatr neurosurg, 1997, 26:8–16. 17. mclone dg, suwa j, collins ja, poznanski s, knepper pa: neurulation: biochemical and morphological studies on primary and secondary neural tube defects. concepts pediatr neurosurg, 1983, 4:15– 2910. 18. mclone dg, naidich tp: spinal dysraphism: experimental and clinical, in holtzman rnn, stein bm (eds): the tethered spinal cord. new york, thieme, 1915, pp 14–28. 19. mclone dg, naidich tp: laser resection of fifty spinal lipomas. neurosurgery, 1986,18:611–615. 20. sutton ln: lipomyelomeningocele. neurosurg clin n am, 1995,6:325–338. 21. xenos c, sgouros s, walsh r, hockley a: spinal lipomas in children. pediatr neurosurg, 2000, 32:295– 307. microsoft word 11maraby-salgadojohana_brain romanian neurosurgery (2018) xxxii 2: 283 289 | 283             doi: 10.2478/romneu-2018-0034 brain abscess and dental infections: a review johana maraby-salgado1, samer s. hoz2, alexis narvaez-rojas4, guru dutta satyarthee5, loraine quintana-pajaro1, alfonso pacheco-hernandez, luis rafael moscote-salazar3 1cartagena university, cartagena de indias, colombia 2department of neurosurgery, neurosurgery teaching hospital-baghdad, iraq 3department of neurology, division of neurosurgery, cartagena university, cartagena de indias, colombia 4universidad nacional autonoma de nicaragua, managua 5all india institute of medical science, new delhi, india abstract: odontogenic infections may cause brain abscesses. although infrequent, infections can lead to development of aggressive brain lesions that may be lifethreatening for patients. with the advent of new antibiotic treatments, dental abscesses appear to be under control but all patients with high risk of brain abscess should be assessed and treated properly. hereby, we present an overview of the information available in the literature of the relationship between brain and dental abscesses. key words: brain abscess; dental infection; neurosurgery introduction dental abscess and facial cellulitis put dentists on alert for potentially lifethreatening conditions such as sepsis or airway obstruction, but the risk of a brain abscess is a complication of odontogenic infection that dentists rarely consider. [1] untreated odontogenic infections can advance to osteomyelitis, cellulitis, myofascial space abscess, lymphadenitis, bacteremia, or sepsis, all of which can be extremely dangerous. brain abscesses, which are rare, are also a potential type of infection that could arise. these are suppurative infections of the brain parenchyma that are surrounded by a vascularized capsule. in the united states, there are only 1,500 to 2,500 brain abscess cases each year [2,3]. central nervous system (cns) infections and their sequelae still constitute a major source of morbidity. [4,5] in the recent past, the introduction of newer broad spectrum antibiotics, improved imaging technology, and intensive care facilities have significantly altered the natural history of cns infections. [6] brain abscess (ba) is a universal health problem with a high morbidity and mortality rate; thus, the disease today presents a leading public health 284 | maraby-salgado et al brain abscess and dental infections             problem and a major burden on health care facilities all around the world. [6,7] ba is a dynamic focal form of intracranial suppuration and a serious life‑threatening emergency. [7] they begin as a localized area of cerebritis and develop into an encapsulated collection of pustular materials presenting as a mass‑like lesion, similar to the abscess in other sites. bacterial brain abscesses have three main etiologies. the most common cause is contiguous spread of infection from the oropharynx, middle ear, and paranasal sinuses. brain abscesses can also arise from hematogenous dissemination of bacteria. previous cranial trauma and neurosurgical procedures can also cause brain abscesses. [810] however, in up to 15%–30% of cases, the cause of brain abscesses is unknown. the majority of brain abscesses arise from the direct spread of infection through the facial planes, and often originate in the paranasal sinuses, middle ear and mastoid área [1]. history over the years, there have been a number of case reports of brain abscess, in which the microorganisms were thought to have arisen from a dental source. there are few reports of brain abscesses of odontogenic origin [11,12]. corson et al. [13] reviewed 17 reports from the 1940s to the 1990s, in which the mortality rate was 30 % (6/20). antunes et al. [12] described the location of brain abscesses and their treatment in 11 cases from the 1960s to the 1980s, and in five cases from 2001 through 2007. a systematic review by moazzam et al. [11] included 60 individual cases, 40 of which were published since 2000. they reported the precipitating dental pathology or procedures, the pathogenic microorganisms, the locations of cns infections, and clinical outcomes [11]. the mortality rate of patients with intracranial bacterial infections of oral origin in that study was improved to 8.3 % (5/60) [11]. ewald et al. [14] reported six cases of pyogenic infection of the cns secondary to dental infection. they indicated that there was no definable origin for intracerebral or intraspinal infection in up to 25 % of cases, and these are termed ‘‘cryptic abscesses’’ [14], [6]. they noted that a dental focus should always be considered in the evaluation and treatment of ‘‘cryptic’’ cns infections, and recommended clinical evaluation by a dentist and oral pantomogram [6]. in the report described by neidert et al. [15] regarding the suspected origin of infection, most cases could be linked to an oral/dental source (23%) followed by sinusitis (14%) or a cardiac source (14%), and no specific origin of infection could be determined in other cases (43 %). [16] mechanism of infection to determine the oral origin of intracranial infections, oral surgeons should know the underlying mechanism of oral bacterial spread into the cns. hematogenous spread via bacteremia is probably a more common route tan direct venous drainage. therefore, there appears to be no predilection for the location of odontogenic foci. there may be no apparent past history or symptoms of acute inflammation caused by odontogenic foci or dental procedures prior to romanian neurosurgery (2018) xxxii 2: 283 289 | 285             development of brain abscess. microbes can spread as a result of acuteinfection with a large number of involved pathogens or highly virulent microorganisms, as well as chronic infection with recurrent bacteremia [16]. the oral cavity is well recognised as being home to a rich and abundant microflora. [13] in particular, dental plaque contains one of the most concentrated accumulations of microorganisms in the human body, with approximately 350 different bacterial strains isolated in marginal periodontitis and 150 in endodontic infections. bacteria gaining access to the blood stream may then spread to distant sites and there has long been an association between oral bacteria, in particular a-haemolytic streptococci, and bacterial endocarditis. dental procedures alleged to have caused a brain abscess are very wide ranging, and include extraction, operative dentistry, periodontal therapy, dental local anaesthetic injection and dental prophylaxis [17]. this would suggest that the mechanism esponsible for the production of the bacteraemia is not as critical as the host response. in this case report there was no apparent history of an acute dental infection or dental procedure prior to development of the brain abscess. however it would appear that from very mild manipulations of the mouth, bacteria can transfer into the blood stream. one study in children found a transient bacteraemia in 38.5% of episodes of tooth brushing, while procedures such as dental extraction, produce a massive shower of organisms into the blood stream [18]. within 1 min of a dental procedure, microorganisms may have reached the heart, lungs and peripheral capillary system. in most individuals the reticuloendothelial system eliminates these microbes in a matter of minute [13]. this is not the case in immunocompromised populations, for example, organ transplant patients and those with aids where there has been a reported increased incidence of brain absces. [6] although certain underlying brain pathologies such as a previous stroke [13] or underlying neoplasm [13] may serve as a nidus for abscess formation, in most cases there is no apparent predisposing brain lesion. epidemiology brain abcess (ba) is one of the most serious diseases of the cns. this condition is more common among men twice to three times, and morbidity rate is highest in fourth decade of the life [3,25] brain abcess is still associated with high morbidity, including seizures (up to 80%), persistent altered mental status, and focal motor deficits. [26] brain abscess continues to be a significant problem in the developing world due to large scale poverty, illiteracy, and lack of higiene. a ba may be developed from three sources and one of these is through from pericranial contiguous focus in 25-50% of cases (such as the sinuses, middle ear, or dental infection), interestingly dental infections, ethmoid or frontal sinusitis (usually spreads to the frontal lobe), and subacute or chronic otitis media or mastoiditis (preferentially spreads to the inferior temporal lobe and cerebellum). [4] 286 | maraby-salgado et al brain abscess and dental infections             etiology ba are frequently polymicrobial, from oral cavity, hemathogenous spread (intra‑ abdominal/ pelvic infections), and from otorhinolaringeal infections the commonest organisms isolated are anaerobic pathogens (streptococci, bacteroides spp., prevotella melaninogenica, propionibacterium, fusobacterium, and actinomyces and aerobic gram‑negative rods, like morganella morganii) [4,19-21] there are reports that e. faecalis was also found in a case of brain abscess secondary to odontogenic procedures in a patient with teleangiectasia, although its occurrence is rare and infrequent, since it is usually a nosocomial pathogen [22] e. faecalis is an infrequent causative agent of brain abscess. this organism is usually a nosocomial pathogen, and its presence in the central nervous system (cns), rarely if ever as a cause of meningitis, has been associated with anatomic defects, prior neurosurgery and trauma, or high-grade bacteremia and immunodeficiency [22,23]. common portals of entry for enterococcal bacteremia are the urinary tract and sites of intra-abdominal and pelvic sepsis [22-24]. however, recently, literature provided evidence that due to its ability to produce biofilms, e. faecalis is often involved in endodontic infections [23], rendering sites of dental work a potential portal of enterococcal bacteremia. [22] a literature review revealed four cases of brain abscess involving pus from which e. faecalis was isolated [22, 25, 26] there have also been reports of aggregatibacter actinomycetemcomitans, which is recognised as one of the major pathogens in destructive periodontal disease. a cerebral abscess linked to a dental source is a rare occurrence, since in most individuals the blood-brain barrier, along with the immune response, will exclude bacteria. [27] a. actinomycetemcomitans has been also described as a cause of meningitis, brain abscess, endophthalmitis (with and without concomitant endocarditis), soft tissue infections, septic arthritis, osteomyelitis, and endocarditis. it may be part of the endogenous flora of the mouth and can be recovered from about 20% of healthy teenagers and adults it is normally found in dental plaque, periodontal pockets and gingival sulcus, and is one of the major pathogens in adult and juvenile forms of periodontitis. it is present in more than 50% of adults with refractory periodontitis and 90% of patients with localised aggressive periodontitis. [27, 28] clinical presentation ba can be primarily present in four basic syndromes, viz. focal mass expansion, intra‑ cranial hypertension, diffuse destruction, and focal neurological deficit. [29] in most cases, predisposing risk factors, such as congenital heart disease, decreased immunity, or the presence of a septic focus, can be identified. [4] the clinical presentation of intracranial abscess is dependent on the origin of infection, site, size, number of lesions, specific brain structures involved, the neighborhood romanian neurosurgery (2018) xxxii 2: 283 289 | 287             anatomy disturbances involving cisterns, ventricles, and the dural venous sinuses, and any secondary cerebral injury. [30] frequently patients present with symptoms of increased intracranial pressure (headache, nausea/vomiting, and altered mental status), focal neurologic deficits, and fever (although fever can be absent in 30-76% of cases). nathoo et al. [7] reported that headaches, fever, and nuchal rigidity were the commonest clinical presentation. the duration of symptoms ranged from 1 day to 8 weeks (average 11.4 ± 10 days; p = 0.7). [4]. this is generally present in patients with brain abscess, secondary to periodontal infections. diagnosis neuroimaging, usually a computed tomography (ct) scan with contrast, is essential to diagnose a ba. the typical finding on ct scan or mri is a hypodense lesion with a contrast‑enhancing ring. [26] ct facilitates early detection, exact localization, and accurate characterization, determination of number, size and staging of the abscess, diagnosing the microbiological source of any infection must be based on sound microbiological methodology. bacteria isolated from the distant abscess must represent that found within the oral cavity. an array of molecular fingerprinting techniques based upon nucleotide sequencing can now be applied to provide supportive evidence for the identification of isolates from different sources. such techniques should be utilized to further our understanding as to whether oral sources of infection can give rise to brain abscess. [13] the differential diagnosis between ba and brain tumors is of extreme importance. rahmat-langendoen et al. explores difficult.their similarity and shows that the symptoms are similar that makes the diagnosis of ba of dental origin extremely. [28] treatment recently, mouren et al, described in a case report a patient with brain abscess secondary to odontogenic injection using metronidazole, vancomycin, and cefotaxime [31]. although ba is essentially a surgical pathology, arlotti et al. [32] recommend that choice of patients for a medical approach must be made on an individual basis. these authors consider best candidates for medical treatment to be those with a small abscess (<2.5 cm), in good initial clinical condition, glasgow coma scale (gcs) > 12, and for whom the etiology is well ‑known (microorganism isolated from material other than the abscess pus) recommendation grade c; or in the case of multiple abscesses, after surgery of abscesses >2.5 cm or surgery of abscesses that cause a mass effect, or in patients at serious risk of operation even if in these, the final decision must consider that the prognosis is often bad in any case recommendation grade d. [4] for muzumdar et al. [29], there are no pragmatic rules for treatment of brain abscess and each case must be individualized and treated on its own merits. the main stay of the treatment includes prompt action and 288 | maraby-salgado et al brain abscess and dental infections             institution of antibiotic therapy. penicillin and chloramphenicol have long been used until we have opted for cefotaxime/ ceftriaxone/ceftazidime, vancomycin, and metronidazole, and this is in agreement with the treatment administered to the patient. steroid administration should be generally avoided unless the patient demonstrates signs of meningitis or disproportionate cytotoxic edema posing a life threatening problem. legg advocated anticonvulsant therapy for 5 years to all patients with cerebral abscess. discontinuation of antiepileptic drugs can be considered when patient is seizure-free for at least 2 years after surgery and electroencephalogram. [29] bacteroides, peptostreptococcus, and fusobactrium are common anaerobes and are sensitive to metronidazole. staphylococcus is common in post-traumatic and postoperative cases; in infants and neonates, post‑ meningitic abscess is caused by gram‑ negative organisms. [17] sulpha drugs are most effective in nocardia and vancomycin against staphylococcus. [4] conclusions a cerebral abscess linked to a dental source is a rare occurrence and its clinical features are often nonspecific. it is worth noting that this latter component calls upon dental clinicians to pay more attention in the identification and treatment of oral and odontogenic sources for brain abscesses. correspondence dr. luis rafael moscote-salazar e-mail: mineurocirujano@aol.com references 1. christine e. hibberd tdn. brain abscess secondary to a dental infection in an 11-year-old child: case report. j can dent assoc 2012;78:49. 2. sung yong park dws, chul min park, min seok oh, dong-kun lee. brain abscess due to odontogenic infection: a case report. j korean assoc oral maxillofac 2014;40:147-51. 3. mamelak an mt, obana wg, rosenblum ml. improved management of multiple brain abscesses: a combined surgical and medical approach. neurosurgery 1995;36:76-85. 4. alvis-miranda h, castellar-leones s, elzain m, moscote-salazar l. brain abscess: current management. journal of neurosciences in rural practice. 2013;4(5):67. 5. muzumdar d. central nervous system infections and the neurosurgeon: a perspective. international journal of surgery. 2011;9(2):113-116. 6. mathisen ge jj. brain abscess. clin infect dis. 1997;25:76379. 7. nathoo n ns, narotam pk, van dellen jr. . brain abscess: management and outcome analysis of a computed tomography era experience with 973 patients. world neurosurg 2011;75:716-26. 8. xiao f tm, teng lj, tseng hm, tsai jc. brain abscess: clinical experience and analysis of prognostic factors. surg neurol 2005;63:442-9. 9. tseng jh tm. brain abscess in 142 patients: factors influencing outcome and mortality. . surg neurol 2006;65:557-62. 10. tonon e sp, gallucci m, vaglia a. brain abscess: clinical aspects of 100 patients.. int j infect dis 2006;10:103-9. 11. moazzam aa rs, sedghizadeh pp, zada g, habibian m. intracranial bacterial infections of oral origin. j clin neurosci 2015. 12. antunes aa dss, de carvalho rw, avelar rl, pereira cu, pereira jc brain abscess of odontogenic origin. j craniofac surg. 2011;22:2363–5. 13. ma corson kp, ra seymour. are dental infections a cause of brain abscess? case report and review of the literature. oral diseases 2001;7:61–5. 14. ewald c ks, kalff r pyogenic infections of the central nervous system secondary to dental affections—a report of six cases. neurosurg rev 29:. 2006;29:163–6 (discussion 6–7). romanian neurosurgery (2018) xxxii 2: 283 289 | 289             15. neidert mc kk, actor b, regli l, bozinov o, burkhardt jk preoperative c-reactive protein predicts the need for repeated intracerebral brain abscess drainage. . clin neurol neurosurg 2015;131:26–30. 16. masaya akashi kt, junya kusumoto, shungo furudoi, kohkichi hosoda, takahide komori. brain abscess potentially resulting from odontogenic focus: report of three cases and a literature review. j maxillofac oral surg. 2016. 17. schuman nj tj. brain abscess and dentistry: a review of the literature. quintessence int. 1994;25:411–3. 18. roberts gj hh, sury mrj et al dental bacteraemia in children. paediat cardiol 1997;18:24–7. 19. w. m. pyogenic infective diseases of the brain and spinal cord. 1893. 20. beller aj sa, praiss i. brain abscess.review of 89 cases over a period of 30 years. j neurol neurosurg psychiatry 1973;36:757-68. 21. bhatia r tp, banerji ak. brain abscess‑an analysis of 55 cases. int surg 1973;58(565-8). 22. eleni mylona cv, vasilios papastamopoulos and athanasios skoutelis. brain abscess caused by enterococcus faecalis following a dental procedure in a patient with hereditary hemorrhagic telangiectasia. j clin microbiol 2012;50(5):1807. 23. moellering r, jr. enterococcus species, enterocuccus bovis and leuconstoc species. principles and practice of infectious diseases 2010. 24. fisher k pc. the ecology, epidemiology and virulence of enterococcus. microbiology 2009;155:1749 –57. 25. inamasu j ea. brain abscess developing at the site of preceding intracerebral hemorrhage. j neurol 2002;249:221–3. 26. siatouni a ea. brain abscess following intracerebral haemorrhage. j clin neurosci 2007. ;14:986 –9. 27. brady p, bergin, sarah, cryan, bartley, flanagan, oisin. intracranial abscess secondary to dental infection. journal of the irish dental association. 2014;60 (1):32-4. 28. marcelo rodrigues azenha gh, idelmo rangel garcia jr. multiple brain abscess from dental origin: case report and literature review. oral maxillofac surg 2012;16:393–7. 29. muzumdar d js, goel a. brain abscess: an overview. int j surg 2011;9:136-44. 30. arlotti m gp, pea f, tomei g, vullo v, de rosa fg, et al. consensus document on controversial issues for the treatment of infections of the central nervous system: bacterial brain abscesses. int j infect dis 2010;14(4):7992. 31. marouene ben hadj hassine lo, amine derbel, nabiha douki. cerebral abscess potentially of odontogenic origin. case reports in dentistry. 2015;1:1-4. 32. arlotti m gp, pea f, tomei g, vullo v, de rosa fg, et al. consensus document on controversial issues for the treatment of infections of the central nervous system: bacterial brain abscesses. int j infect dis. 2010;14(4):7992. microsoft word 9matmusaevmaruf_highflow 262 | matmusaev et al high flow bypass for cavernous carotid aneurysms             doi: 10.2478/romneu-2018-0032 high flow bypass for cavernous carotid aneurysms maruf matmusaev1, temur duschanov2, yasuhiro yamada3, katsumi takizawa4, tsukasa kawase3, riki tanaka3, miyatani kyosuke3, yoko kato3, ahmed ansari3 1republican specialized scientific and practical medical center of neurosurgery, tashkent, uzbekistan 2department of neurosurgery, republican research center of emergency medicine, tashkent, uzbekistan 3department of neurosurgery, banbuntane hotokukai hospital, fujita health university, nagoya, japan 4department of neurosurgery, asahikawa red cross hospital, hokkaido, japan abstract: introduction and objective: high flow extracranial to intracranial (hf ec–ic) cerebral revascularisation may be necessary in the management of complex skull base tumours and intracranial aneurysms. bypass grafting can be considered high flow when a radial artery or the saphenous vein is interposed between the extracranial carotids arteries and intracranial vessels. the decision as to whether to use a low flow or high flow bypass is determined by the anticipated cerebral blood flow needed and the availability of a supply source. in this study, we have used this method to bypass for two cases of giant aneurysms of the cavernous sinus part of the ica. methods: two cases of giant ice aneurysm not amenable to clipping or coiling were taken since 2016. patients were treated in neurosurgery department of fujita health university banbuntane hotokukai hospital, nagoya, japan. during bypass surgery, intraoperative methods were used to determine the patency of the graft artery: doppler sonography and indocyanine green (icg) dual-image videoangiography (diva). results: two patients with symptomatic large and giant cavernous carotid aneurysms were evaluated as not amenable for clipping or endovascular treatment due to location and size of the aneurysm and associated high morbidity risk with these treatment options. in both cases radial artery graft was used for high-flow ec-mca bypass and proximal internal carotid artery was ligated. additionally, for high-flow bypass was performed superficial temporal artery (sta) to middle cerebral artery (mca) bypass. diva, icg and doppler sonography were used multiple times to assess the patency of graft artery. in one case there was not complete ligation of the ic after postop dsa, the next day was romanian neurosurgery (2018) xxxii 2: 262 271 | 263             performed reintervention to completely ligate ic. postoperative course was uneventful, there were no mortality or morbidity. follow-up showed good recovery and postoperative ct and dsa showed complete occlusion of ligated ic and patent functioning arterial graft. conclusions: cavernous carotid aneurysms (cca) are rare and pose considerable challenges in management. a bypass procedure before parent artery occlusion, preferable to reduce the risks of postocclusion stroke. intraoperative doppler sonography and diva makes it easy to check the patency of the graft. diva is superior over doppler or icg in terms of better visualization of related anatomical structures. key words: high flow bypass, cavernous carotid aneurysm, radial artery graft introduction cavernous carotid aneurysms (cca) are rare and pose considerable challenges in management. high flow extracranial to intracranial (hf ec–ic) cerebral revascularisation may be necessary in the management of complex skull base tumors and intracranial aneurysms [1]. bypass grafting can be considered high flow when a radial artery or the saphenous vein is interposed between the extracranial carotids arteries and intracranial vessels. the decision as to whether to use a low flow or high flow bypass is determined by the anticipated cerebral blood flow needed and the availability of a supply source.the risks and benefits of treatment of cca should be carefully considered because ccas are not a common pathology, and there are no definite guidelines for treatment currently. furthermore, data about the natural history and pathogenesis of cca is limited. indications for treatment of cca are summarized in table 1.[2,3] table 1 indication of surgical intervention for cavernous part of ica giant aneurysms asymptomatic aneurysms symptomatic aneurysms  extension of aneurysm into subarachnoid space  origin from anterior genu of cavernous carotid  radiographic enlargement of aneurysm  subarachnoid hemorrhage  unbearable ipsilateral face or retro‑orbital pain  progressive ophthalmoplegia  sudden, severe ophthalmoplegia objective of this study is to evaluate effectiveness and surgical techniques of hf ef – ic bypass as appropriate choice of surgical treatment for giant aneurysms of cavernous sinus part of internal carotid artery. materials and methods this study was conducted on two cases with giant aneurysms of the cavernous sinus part of the ica that treated with high flow bypass techniques using radial artery (ra)in our practice at neurosurgery department of fujita health university banbuntane 264 | matmusaev et al high flow bypass for cavernous carotid aneurysms             hotokukai hospital, nagoya, japan since 2016. preoperative evaluation was done with digital subtraction angiography(dsa) and 3d-ct angio. balloon occlusion test was not perform on these patients, because of atherosclerotic vessels.it is essential to evaluate collateral supply of both intracranial vessels and arteries of non-dominant upper limb using non-invasive fusion or dsa. during surgical procedure that has been done by us, doppler sonography (ds), indocyenine green (icg) and dual-image videoangiography (diva) were used to determine the patency of the graft artery. case report 77-year-old female was admitted to our hospital with complains of 3 months history of headache and dizziness. pre operative 3dct, mri and dsa showed a giant aneurysm on the right cavernouspart of internal carotid artery (ica) that is why diagnosis was a giant right aneurysm of the cavernous portion. illustration of procedure (a) trapping (cervical internal carotid artery ligation withclipping of c3 segment of internal carotid artery, just proximal toophthalmic artery origin) of cavernous carotid aneurysm with high‑flowbypass. (b) cervical internal carotid artery ligation with high‑flowbypass. both techniques result in the complete aneurysm thrombosis.first segment of anterior cerebral artery (a1), anterior choroidalartery, first segment of middle cerebral artery (m1), second segmentof middle cerebral artery (m2), ophthalmic artery (opha), posteriorcommunicating artery (pcoa), and radial artery graft (rag)[4,5]. surgical procedure first, anastomose the sta to m4 (peripheral part of the m2 to which ra is anastomosed).in the supine position with raisedand turnedhead to the opposite side. due to presence of many procedures, two operation teams carry out operation by using two microscopes to shorten operation time at the same time. team for radial graft preparation identifies and confirms collateral circulation using dsa. if there is good collateral circulation ra graft can be obtained at least 18 cm in length but it is effective to get longer as much as possible because the diverging from the brachiocephalic trunk is the limit of removal on the proximal side, so the distal side is removed as long as possible. during or some time before obtaining ra graft, to let sta-mca bypass precede for the assist bypass both parietal branch and frontal branch of sta is dissected. it is important to note that the main disadvantage of ra graft is the potential for vasospasm following harvest, which may lead to total occlusion of the vessel and therefore vasospasm is prevented by using pressure distention technique. a b romanian neurosurgery (2018) xxxii 2: 262 271 | 265             normal parieto-temporal craniotomy is enough, but removing the bones of middle cranialfossa should be appropriate for the ra graft. as for the common artery, it is not necessary to expose a long segment, yet the external carotidartery that becomes the anastomosis of ra is to be exposed to as high position as possible to choose the anastomotic part. to occlude the central of the ica, two 1.0 silk threads are put throughthe internal carotid beforehand and identify the posterior belly of the digastric muscle and hypoglossal nerve.choose the submandibular root as the graft root. as for this root, the length of this graft becomes theshortest, and thus the influence such as the pressure of graft can be avoided. however, pay much attention whether there is not possibilities for torsion or kinking of the graft in the blind part to be occurred. making tunnel for graft by using merkmal consists of following stages; insertion of forefinger from the interval of posterior belly and thehypoglossal nerve from the cervical side till styloid process and then towards the upper front. when it reaches cranial side by kelly forceps that is inserted in front part of the zygomatic bone from the interval of the temporal muscle and the temporale bone it reaches to cranial side fromthe neck. on the cranial side, ra graft is anastomosed to the silk thread in the chest tube.by pulling out the silk thread to the neck side, the ra graft can be indwelled from the head to the neck, after the final confirmation following the anastomosis of the ra graft to m2 by the 9.0 nylon suture because of the big vascular size and solid wall of ra, remove the chest tube.first, anastomose the sta to m4 (peripheral part of the m2 to which ra is anastomosed). as for sta performend-toside anastomosis by 10.0 nylon suture. the purpose of this bypass is to prevent the ischemia complications at thetime of ra-m2 anastomosis that calls for the longer-time temporary blockade (assist bypass) and to monitor the brainsurface mca pressure to evaluate the patency of ra graft that was completed finally in real time during the operation and in this stage anastomosis process is finished. after that temporary clip in ra in the region close to the anastomosis is done so as to prevent retrograde flows of blood into the graft.finally,due to the wide vascular diameter proximal part of ra-eca end-to-side anastomosis can be performed by continuous suture of 7.0 prolene.before blood flow is restored to the brain, the distal end of the cca and the proximal side of the ica are clamped, then the proximal side of the eca and the distal clamp of the conduit are opened, which allows air to vent through the superior thyroid artery. ds, icg and diva are used during operation after proximal native ica clamping to demonstrate graft patency and to evaluate the anastomotic sites. after all proximal ica is ligated and anticoagulation reversed with protamine. in the case of giant aneurysm at the cavernous portion, the parent vessel is not ligated distally, as all of the aneurysm is still thrombosed. 266 | matmusaev et al high flow bypass for cavernous carotid aneurysms             dissecting the ra while applying appropriate tension with vascular tape pressure distension technique is performed to prevent vasospasm prepped recipient artery. arrow: m2 for the ra graft, arrow head: m4 for the sta ica permanently occluded by double ligation with a 1.0 silk suture icg and diva demonstrates that there is not blood flow into ica after occlusion of ica (previous stage) a b dopler sonography of mca (a) and ra graft (b) after anastomosis. final image of ra graft bypass. (proximal view) icg and diva illustration of blood flow restoration after anastamosis romanian neurosurgery (2018) xxxii 2: 262 271 | 267             patient was treated with radial artery (ra) graft technique and ica occlusion. postoperative 3d-cta and confirmed disappearance of the aneurysm and the ra graft patency. a,d,c: preoperative 3d-cta and dsa shows a giant aneurysm on the right intracavernous internal carotid artery (ica). f,g,h,i: postoperative 3d-cta confirmed disappearance of the aneurysm and the ra graft patency. h,i:, arrow: radial artery graft results two patients with symptomatic large and giant aneurysms of cavernous partof icawere evaluated as not amenable for clipping or endovascular treatment due to location and size of the aneurysm and associated high morbidity risk with these treatment options. in both cases radial artery graft was used for high-flow ec-mca bypass and proximal internal carotid artery was ligated. additionally, for high-flow bypass was performed superficial temporal artery (sta) to middle cerebral artery (mca) bypass. diva, icg and doppler sonography were used multiple times to assess the patency of graft artery. in one case there was not complete ligation of the ic after postop dsa, after one month was performed reintervention to completely ligate ic. postoperative course was uneventful, there were no mortality or morbidity. follow-up showed good recovery and postoperative ct and dsa showed complete occlusion of ligated ic and patent functioning arterial graft.   a b c d gf i e   h 268 | matmusaev et al high flow bypass for cavernous carotid aneurysms             discussion tarr et al. and origitano et al. think that the cumulative risks of not performing revascularization in patients who tolerate ica balloon occlusion (risk of bto itself 3.7–7% false negative rate of bto 7–22%) exceed the surgical risk of revascularization (3–7%). murai et al. reported in 17 bypass surgeries cranial nerve dysfunction (iii and vi) caused by altered blood flow from the ica after occlusion was the most common complication (three cases in cca) and typically was temporary. houkin et al.[4] reported in 36 patients with giant or largeaneurysms located at the cavernous portion of the ica postoperative angiography showed patencyof bypass graft in 97% of cases. aneurysms disappeared and thrombosed on postoperative angiography and magnetic resonance imaging, respectively. houkin et al and kamiyama reported that most of the aneurysms would spontaneously thrombose after proximal ligation without the distal outflow occlusion. [4,5] in addition, endovascular techniques have been developed to treat cca, which included intra‑aneurysmal coil embolization with or without stent or balloon‑assist, and flow‑ diverting stent. performed intra‑aneurysmal coil embolization in seven patients with large or giant symptomatic cca. after the operation, one patient improved the symptoms of aneurysmal mass effect, two patients unchanged and four patients deteriorated. they concluded that intra‑ aneurysmal coil embolization is not an effective treatment option for large or giant cca. [6] according to a recent report, a flow diverting stent has been developed for the effective treatment of an unruptured giant symptomatic cca;[7] however, early,[8] and delayed [9,10] rupture of the aneurysm after treatment has been described. the incidence delayed ruptured of an aneurysm after the stent is 0.6–1%, but was not reported for early rupture. the risk factor is aneurysm size 10 mm or larger.[9] in cases of a ruptured aneurysm with flow divertingstent treatment, the blood flow entered the aneurysm saccontinuously without intra‑aneurysmal pressure reductionimmediately after device deployment. furthermore, it wasnecessary to use the antiplatelet agent during the perioperativeperiod after stenting. therefore, prompt prevention of theaneurysmal re‑ rupture could not be obtained.[11] hasegawa et al reported in cases with direct ccf (carotid cavernous fistula) due to ruptured however, endovascular management was not always available on an urgent basis in some institutes and was not always successful, in which case direct surgical trapping of the lesion and distal bypass might be indicated. [12] little et al.[13] reported 15 cases of symptomatic cca weretreated with different methods of ica occlusion withouthigh‑flow bypass. good results were achieved in most cases,but delayed ipsilateral cerebral ischemia was found in twocases (13%), and partial retrograde filling of the aneurysmwas demonstrated in three cases. postoperative complications of six case series are summarized in table 2. [13,4,14,15,17,16] romanian neurosurgery (2018) xxxii 2: 262 271 | 269             table 2 list of complications ischemic stroke cranial nerve palsy ruptured acom aneurysm de novo aneurysm formation delayed re‑ enlargement of cca epilepsy due to hyperperfusion syndrome 2/15 cases (13%) one case for sta‑mca bypass with selverstone clamp occlusion one for ica ligation) *mean follow‑up period 5.6 years cn3, cn5 palsy 2/15 cases no no no no 1/36 cases (2.8%) ra graft occlusion *mean follow‑up period 7.2 years no no no no no 3/11 cases (27.3%) early 1 case delayed 2 cases *mean follow‑up period 13.9 years no ruptured acom aneurysm (1 case) (2 cases, contralateral cca and acom) delayed re‑ enlargement of cca (2 cases) no 0% *mean follow up period 5.2 years cn3,6 palsy (3/13 cases) no no no no 2/12 cases (16.7%) both are embolic stroke one case is asymptomatic cn2 (1 case) cn3,4 (2 cases) cn3,4,6 (1 case) cn6 (1 case) no no no no 1/8 cases (12.5%) a small ipsilateral frontal ischemia (transient dysarthria and gait disturbance) *mean follow‑up period 3.15 years cn4 (1 case) no no no epilepsy due to hyperperfusion syndrome (1 case) conclusions cavernous carotid aneurysms (cca) are rare and pose considerable challenges in management. a bypass procedure before parent artery occlusion, preferable to reduce the risks of postocclusion stroke. for cca with mass effect, high‑flow bypass with proximal occlusion of ica (without trapping) seems to be the first choice treatment for large and giant cca because of the high rate of aneurysm thrombosis. in our case series, the ra proved to be a useful graft for cerebral revascularization. its long-term patency has been demonstrated in the surgical management of giant aneurysms of the cavernous and paraclinoid icas. the 270 | matmusaev et al high flow bypass for cavernous carotid aneurysms             ra has a lumen that closely approximates that of the m2 segment, and it has the advantage of being a physiological conduit for arterial blood. unlike venous grafts, the ra lacks valves and varices, and is technically easier to harvest because of its consistent anatomical location and size. more resistant to kinking than the sv, the ra is preferable to this vein, whose flow mismatch can lead to subsequent flow turbulence and graft thrombosis. the ra grafts can better tolerate intermittent temporary occlusion when compared with vein grafts, whose valves and endothelium can promote thrombosis in lowflow states [18,19]. intraoperative doppler sonography and diva makes it easy to check the patency of the graft. diva is superior over doppler or icg in terms of better visualization of related anatomical structures. references 1. sheau fung sia, michael kerin morgan. high flow extracranial-to-intracranial brain bypass surgery. journal of clinical neuroscience. volume 20, issue 1, january 2013, pages 1-5 2. russell sm, jafar jj. microsurgical treatment of intracavernous carotid artery aneurysms. in: le roux pd, winn rh, newell dw, editors. management of cerebral aneurysms. philadelphia: saunders; 2004. p. 711‑29. 3. linskey me, sekhar ln, hirsch wl jr., yonas h, horton ja. aneurysms of the intracavernous carotid artery: natural history and indications for treatment. neurosurgery 1990;26:933‑7. 4. houkin k, kamiyama h, kuroda s, ishikawa t, takahashi a, abe h.long‑term patency of radial artery graft bypass for reconstruction ofthe internal carotid artery. technical note. j neurosurg 1999;90:786‑90. 5. kamiyama h. bypass with radial artery graft. no shinkei geka1994;22:911‑24. 6. morita k, sorimachi t, ito y, nishino k, jimbo y, kumagai t, et al. intra‑aneurysmal coil embolization for large or giant carotid artery aneurysms in the cavernous sinus. neurol med chir (tokyo) 2011;51:762‑6. 7. szikora i, berentei z, kulcsar z, marosfoi m, vajda zs, lee w, et al. treatment of intracranial aneurysms by functional reconstruction of the parent artery: the budapest experience with the pipeline embolization device. ajnr am j neuroradiol 2010;31:1139‑47. 8. turowski b, macht s, kulcsár z, hänggi d, stummer w. early fatal hemorrhage after endovascular cerebral aneurysm treatment with a flow diverter (silk‑stent): do we need to rethink our concepts? neuroradiology 2011;53:37‑41. 9. lin lm, colby gp, jiang b, pero g, boccardi e, coon al. transvenous approach for the treatment of direct carotid cavernous fistula following pipeline embolization of cavernous carotid aneurysm: a report of two cases and review of the literature. bmj case rep 2014;2014. pii: bcr2014011235. 10. kallmes d, boccardi e, bonafe a, cekirge s, fiorella d, hanel r, et al. o‑009 safety of flow diversion: results from a multicenter registry. j neurointerv surg 2013;5 suppl 2:a6. [abstr]. 11. schneiders jj, vanbavel e, majoie cb, ferns sp, van den berg r. a flow‑diverting stent is not a pressure‑ diverting stent. ajnr am j neuroradiol 2013;34:e1‑4. 12. hasegawa h, inoue t, tamura a, saito i. urgent treatment of severe symptomatic direct carotid cavernous fistula caused by ruptured cavernous internal carotid artery aneurysm using high‑flow bypass, proximal ligation, and direct distal clipping: technical case report. surg neurol int 2014;5:49. 13. little jr, rosenfeld jv, awad ia. internal carotid artery occlusion for cavernous segment aneurysm. neurosurgery 1989;25:398‑404. 14. niiro m, shimozuru t, nakamura k, kadota k, kuratsu j. long‑term follow‑up study of patients with cavernous sinus aneurysm treated by proximal occlusion. neurol med chir (tokyo) 2000;40:88‑96. 15. murai y, teramoto a, mizunari t, kobayashi s, kamiyama h. treatment of complex internal carotid artery aneurysm using radial artery grafts. surg cereb stroke 2007;35:387‑93. 16. murai y, mizunari t, umeoka k, tateyama k, kobayashi s, teramoto a. radial artery grafts for romanian neurosurgery (2018) xxxii 2: 262 271 | 271             symptomatic cavernous carotid aneurysms in elderly patients. neurol india 2011;59:537‑41. 17. shimizu h, matsumoto y, tominaga t. parent artery occlusion with bypass surgery for the treatment of internal carotid artery aneurysms: clinical and hemodynamic results. clin neurol neurosurg 2010;112:32‑9. 18. surdell dl, hage za, eddleman cs, gupta dk, bendok br, batjer hh. revascularization for complex intracranial aneurysms. neurosurg focus 2008;24:e21. 19. kocaeli h, andaluz n, choutka o, zuccarello m. use of radial artery grafts in extracranial‑intracranial revascularization procedures. neurosurg focus 2008;24:e5. 03_paper romanian neurosurgery | volume xxx | number 4 | 2016 | october december article when flow diverters fail: short review and a case illustration of a device failure marco zenteno1, angel lee1, jennifer lorena herrera bejarano2, guru dutta satyarthee3, hernando raphael alvis-miranda2,luis rafael moscote-salazar2 1mexico, 2colombia, 3india doi: 10.1515/romneu-2016-0075 romanian neurosurgery (2016) xxx 4: 467 – 474 | 467 doi: 10.1515/romneu-2016-0075 when flow diverters fail: short review and a case illustration of a device failure marco zenteno1, angel lee2, jennifer lorena herrera bejarano3, guru dutta satyarthee4, hernando raphael alvis-miranda5, luis rafael moscote-salazar6 1“manuel velasco suarez” national institute of neurology and neurosurgery, ciudad de mexico, mexico 2hospital angeles inn universidad, ciudad de mexico, mexico 3physician, universidad del rosario, colombia 4associate professor of neurosurgery, all india institute of medical sciences, new delhi, india 5resident of neurosurgery, universidad de cartagena, cartagena de indias, colombia 6red latino, latin american trauma & intensive neuro-care organization, bogota, colombia abstract: the ultimate aims of treatment of the intracranial aneurysms are reconstruction the vessel wall and correcting the hemodynamic disturbance. a flow diverter (fd) is a stent placed inside lumen of the parent artery with aim to blood flow reduction into the aneurysms sac to the extent of almost stagnation leading to gradual onset of progressive thrombosis and neointimal lining of arterial wall remodeling to maintain blood outflow into perforators the side and branches. flow diverter is considered as an effective treatment for fusiform, wide-necked, large and giant intracranial unruptured aneurysms. however, fd implantation may also be associated with growth and rupture of residual aneurysms. the most frequent complication of endovascular aneurysms management is thromboembolic events and less common are intra and postoperative hemorrhagic aneurysmal rupture. authors report a case where a lack of operation of the device as illustration is presented to demonstrate the shortcomings of this new type of devices. key words: flow diverter device, aneurysms, neuro-intervention introduction the treatment of intracranial aneurysms (ia) is based on principle of isolating aneurysm from parent vessels, occluding blood flow into the aneurysm and to restore the physiological flow. the aneurysm treatment can be accomplished by surgical clipping of aneurysm at neck allowing definitive and complete aneurysm isolation 468 | zenteno et al flow diverter device failure but carries a high risk of complications such as cerebral edema, arterial vasospasm, and infarction. a large variety of new devices for the treatment of ia are popping up in recent years with the aim to improve the prognosis of patients , however, the understanding of local hemodynamics is not still incomplete. flow diverter devices (fd) are device, which is similar to the stent, designed with aim to achieve normal vessel reconstruction, and causing blood flow diversion along the anatomical course and sparing out of the flow vector of the neck and dome of the aneurysm. recent publication show successful use of flow in the management of intracranial aneurysm, but these may fail also. [1–4] hemodynamic factors are considered to play the biggest factor in the progression and rupture of ia. recently several cases of fd failure are reported. [1, 2] authors reports an additional case of fd device and hence these devices should be considered for experimental use. according to the proposed goal in the treatment of intracranial aneurysms, fd is designed in a way to ensure complete management of ia and preventing possible associated post-treatment complication [5] i.e. bleeding, reconstruction of the vessel wall and correction of the hemodynamic flow abnormality [1]. flow diverters represents a new generation of stents as a superior new alternative treatment for ia. [4, 10, 11, 1216]. flow diverters are a stent, placed inside the lumen of the main artery to reduce blood flow to the aneurysm causing stasis and gradually progressive thrombosis and subsequent remodeling of the inner layers of the blood vessel wall [4, 11, 13, 15]; keeping and maintaining normal blood flow [1] into the branches of the main artery. the ability of a stent to accomplish these goals is dependent on the amount of metal on its surface, the rigidity of fd, and bioactivity of the stent material [15]. additionally, the placement of the flow diverters could change vessel anatomy, aneurysm and finally flow to brain regions [1, 10]. hemodynamic studies suggest stent with a porosity above 50-70 % , can cause significant reduction of the flow rate to the aneurysm sac [1, 9, 10, 12, 13, 14], leading to progressive formation of thrombus and this finally causing total occlusion [3, 4, 10, 13, 14, 16]. however, clinical results of flow diverters can be varied [4] and also dependent on morphology of aneurysm, size of neck and presence of branching vessel originating from fundus. in addition to the flow diverters, other treatment options of ia include coil embolization and surgical clipping [3]. the middle cerebral artery aneurysms were evaluated in the study of international cohort subarachnoid aneurysms (isat) observed required two complementary procedures including surgical approaches and endovascular for the complete occlusion of the aneurysm [6, 15]. the surgical aneurysm clipping of has been considered for the treatment of middle cerebral artery aneurysms after endovascular therapy as presence of branches growing from where the aneurysm arises or the same within are always considered as risk factors [6]. bracard et al. analyzed 140 patients with middle cerebral artery aneurysms, 73 had unruptured aneurysms. all cases received as romanian neurosurgery (2016) xxx 4: 467 – 474 | 469 embolization coil treatment without any other adjuvant technique [12]. thromboembolic complications were noted in 8.5%, a high incidence of these complications was evident in ruptured cases 13.7% versus 3.8% unruptured aneurysms [6, 9]. however, most frequent criticisms associated with coil embolization therapy are high rate of aneurysm recurrence after treatment, incomplete occlusion and the presence of remnants of the aneurysm [6]. description of flow diverters: the pipeline embolization device (ped) is a mesh made tube like, composed of platinum (25%) and rest 75% of the alloy of cobalt and nickels (fig. 1) [1, 11]. it can provides a coverage of 30-35% of the vessel in question and the common diameter of pore is 0.02 to 0.5 mm2 [1, 14]. the coverage area provided by the ped is about three times of intracranial stent [1, 11]. once the device is positioned through the segment of the aneurysm is released, beginning to expand and rotate for clockwise [1]. flow diverters with a low degree of porosity but a high pore density can achieving a further reduction of flow within the aneurysm sac [3, 4, 5, 10, 11]. the blood flow into the aneurysm is influenced by the geometry, the surrounding vasculature, the size and position of the aneurysm [4, 9, and 13]. the aneurysm diameter also plays a very important role in predicting a possible rupture of intracranial aneurysm [4, 9, and 13]. the theoretical advantage of this technique is based on reconstruction of the main vessel, thrombosis of aneurysm sac of any morphology regardless of the aneurysm neck diameter [6]. these are important considerations which play a role in making a proper decision during treatment and influencing its possible outcomes [4]. bleeding complications of flow diverters: bleeding complications with the use of ped device are estimated to be 1.75%, with of 0.75% morbidity and approximately 1%mortality [1, 8]. among the most frequent complications include ipsilateral parenchymal hemorrhage and subarachnoid hemorrhage [1]. complications usually occur between 2135 days after implantation of the device [1]. the inflow of blood in the residual aneurysm during post-implantation is considered a risk factor [1]. furthermore, leukocytes contained in the process of thrombus formation, activity of lytic enzymes such as elastase with increased activity and presence in the thrombi of red blood cells in white cell; which leave an organized formation of these thrombi [15] which could explain the subsequent breaking of intracranial aneurysms [1]. wan et al. reported three patients treated with flow diverters which showed massive stroke after device implantation and bleeding during the procedure [2]. thromboembolic complications: among the most frequent risks of endovascular treatment the hemorrhagic aneurysm rupture is among them, intraoperative and postoperative level [7]. thromboembolic complications are much more common [7]. the frequency of thromboembolic complications may vary, it was 7% in unruptured aneurysms cases in the 470 | zenteno et al flow diverter device failure athena study by and in 12.5% of cases showed thromboembolic complications e clarity study [7]. morbidity and mortality occurred in 3.8% of cases [7]. the stents use leads to increase in the perioperative stroke risk and usually occurs within the first 48 postoperative hours in 10% of cases [7]. the risk factors for thromboembolic events are size and length of aneurysms [7]. the increased frequency of thromboembolic events may also be associated with the development of subarachnoid hemorrhage [7]. the use intra and post-operative anticoagulants and antiplatelet have been proposed to reduce the frequency and severity of thromboembolic events [7, 9]. use of heparin: heparin is recommended during interventions due to intravascular use of multiple tools and prolonged duration of procedure lasting up to many hours [7] prolonging the rest period the patient during surgery. heparin should be initiated with a bolus of 3000-5000 iu followed by a dose of 20-40 iu / kg / h continuously monitored blood thinners to keep clotting times between 200 and 300 seconds [7]. this is used to manage irrigation thromboembolic and hemorrhagic of flow diverters. world and interventional neuroradiology federation and therapeutics (wfitn) bolus administration recommends use of 500-1000 iu / h continuously, with monitoring of clotting times around the 200s [7]. it is not possible to determine the concentrations of heparin in the blood during surgery. usually it carried out prior monitoring of clotting times in order to see the effectiveness of this drug before shifting the patient to surgery [7]. doses of 70-80 u / kg have been proposed in protocols using heparin in cardiac care obtaining an effective anticoagulation [7]. after administration of boluses of 70 u / kg continues with an adjustment in the dose of 18u / kg / h and the levels of clotting times [7]. the wfitn do not recommend the use of postoperative anticoagulation [7]. no clutch, published clinical results have not been convincing, finally from a biological perspective seems more relevant the use of antiplatelet agents [7]. furthermore it should be noted patients usually remain long period for resting on the bed during recovery time favoring venous stasis and possible thrombotic event; ray et al. justified the use of low molecular weight heparins in the postoperative prophylactic doses in [7]. antiplatelets: treating an aneurysm with the use of a foreign body within a vascular lumen, having of high velocity blood flow and the possibility of being associated with injuries in the vessel wall. [7] these leads to platelet aggregation thus justifying the use of antiplatelet agents to prevent and treat intra and postoperatively thromboembolic complications [7, 8]. a study in which, protocol based use of antiplatelet are reviewed in three stages: treatment is not only in the post-operative and post-operative yamada et al. [7] reported thromboembolic complications rates of 16%, 2.3% and 1.9% respectively [7]. they also report a reduction in the rate of angiographically visible blood clots in patients who received antiplatelet pre-procedure compared with those who did not receive [7]. romanian neurosurgery (2016) xxx 4: 467 – 474 | 471 the commonly used antiplatelets are acetylsalicylic acid, clopidogrel, prasugrel, among others [7]. schemes: unruptured aneurysms: treatment should be simply coil embolization or remodeling ball when needed [7]. the use of anticoagulants and antiplatelet agents increases the risk of bleeding during the procedure [7]. the use of intraoperative heparin is recommended after surgery infusions of heparin should be stopped [7]. simple antiplatelet therapy: 75 mg of aspirin only for long-necked aneurysms in accordance with the recommendations of the wfitn [7]. should be given a loading dose of clopidogrel 600 mg two hours before surgery and inject 250 mg of aspirin immediately after the other possibility is to inject antagonists of the glycoprotein iib / iiia after the aneurysm has assured [7] . coil embolization and stent placement: the patient should be prepared with 75 mg / day of aspirin and 75 mg / day clopidogrel for 4-7 days prior to surgery [7], a loading dose of 600 mg of clopidogrel could be administered two hours before stent placement [7]. management of thromboembolic complications: intraoperative management of thromboembolic events demand a constant verification of clinical and biological parameters of each patient e.g. blood pressure and the degree of anticoagulation requirement [7]. clotting times should be kept greater than 250 seconds, if below, additional bolus administration of 2000 iu [7] is recommended. to reduce the risk of embolisms one flow diverter telescoping functioning as a bypass this provides an “incarceration “clot is used. [13] the device expands distal to proximal opening a new road and catching the clot that is occluding against the vessel wall; thus can prevent distal embolization [13]. when clots are accessible in the proximal artery thrombectomy could be considered as part of the approach [7]. case illustration a 56-years-old female patient reported to the endovascular therapy service at the “manuel velasco suarez” neurology and neurosurgery national institute, for presenting headache with red flag symptoms. as precedents, various months earlier she was treated of giant carotid aneurysm with a fd (pipeline®) in a hospital from usa. (figure 1) during initial evaluation she had power 4/5 in left upper extremity, while the rest of the motor balance was within normal range. she underwent imaging study including mri brain, dynamic cranial ct angiography, showed which evidenced of residual aneurysmal flow and the presence of recent thrombus, associated with significant perilesional edema with mass effect. the patient is advised to undergo repeat mri and cerebral magnetic resonance angiography after two weeks showing the findings (figure 2). the management was conservative. review subarachnoid hemorrhage is a devastating disease, whose treatment depends at time interval following ictus, needs advice of 472 | zenteno et al flow diverter device failure various specialties i.e. neurosurgery, neurology, intensive care, and neuroradiology and to various forms of treatment for complication are medical or endovascular vasospasm treatment, surgical clipping / embolization). the concept of flow diverters for aneurysm occlusion is not new and almost since past ten years, it was studied in dogs to assess the effects of flow dynamics in experimental aneurysms of the carotid arteries. (15, 16, 17, 18). filling the aneurysm and blocking or deflecting the inflow may promote thrombosis, preserving the parent vessel. turowski et al [5] reported a – 69yearold patient, who required the placement of a fd silk-stent, for a large par ophthalmic aneurysm, she developed fatal subarachnoid hemorrhage. author proposes that a reduction in the strength of the aneurysm walls can act in conjunction with the residual flow as a weak point for mechanical rupture. this case demonstrates that fd is a technology to be tested in future, for its effectiveness, despite series showing good results, although such complications are also reported in the literature with unfavorable outcomes. figure 1 digital subtraction angiography showing the micro-guide navigability through the internal carotid artery (ica); also showing the stent measurements (a and b). stent unfolding, through the eluting balloon insufflations (c and d). total exclusion of the aneurysm (e). no alteration on the venous phase (f). intracranial vasculature is intact (h) ba g e dc h f romanian neurosurgery (2016) xxx 4: 467 – 474 | 473 figure 2 three-dimensional reconstruction, in which is appreciated complete absence of the aneurysm, with appropriate visualization of the proximal and distal stent markers (a and b). – dynamic ct angiography coronal and sagittal sections, where appropriate stent patency and showing minimal filling of the aneurysm (c, d, e and f) conclusions endovascular reconstruction using flow diverters although represent an effective treatment option for fusiform, long, giant, wide-necked aneurysms, but associated with 5-10% of morbidity and mortality [1]. flow diverters stents assisted therapy of aneurysm proposes a new method of endovascular reconstruction of complex aneurysms, using a fine mesh placed outside the aneurysm sac reducing the flow within it subsequently cause thrombosis [16]. the results of the next studies could answer the question of how to prevent complications, if flow diverters could replace coil embolization or when it would certainly indicated the use of flow diverters [1]. flow dividers could reduce the risk of embolization associated with recanalization following endovascular treatment of aneurysms [20, 21, 22]. treatment with a single stent can alter hemodynamic of aneurysm creating the right conditions making more favorable flow thrombus formation [14, 15]. the most important goal should be complete elimination of the risk of post-procedural aneurysmal rupture, can be achieved with use of a single technique that does not produce alteration of the hemodynamic flow [20, 21, 22]. recent reports of multiple stent implantations through aneurysm neck could improve the effectiveness of flow diverters against reduction of blood flow to the aneurysm sac [20, 21, 22]. correspondence dr. luis rafael moscote-salazar e-mail: mineurocirujano@aol.com references 1. darsaut te, rayner-hartley e, makoyeva a, salazkin i, berthelet f, raymond j. aneurysm rupture after endovascular flow diversion: the possible role of persistent flows through the transition zone associated with device deformation. interv neuroradiol. 2013; 19(2):180-5. 2. cebral jr, mut f, raschi m, scrivano e, ceratto r, lylyk p, et al. aneurysm rupture following treatment with flow-diverting stents: computational hemodynamics b c c d e f a d 474 | zenteno et al flow diverter device failure analysis of treatment. ajnr am j neuroradiol 2011; 32:27–33. 3. clarençon f, di maria f, biondi a, chiras j, sourour n-a. distant and delayed (>7 days) hemorrhage after treatment by flow-diverter stents in intracranial aneurysms: a rare but potentially serious complication. ajnr am j neuroradiol 2013; 34:e81–2. 4. raymond j, salazkin i, georganos s, guilbert f, desfaits a-c, gevry g, et al. endovascular treatment of experimental wide neck aneurysms: comparison of results using coils or cyanoacrylate with the assistance of an aneurysm neck bridge device. ajnr am j neuroradiol 2002; 23:1710–6. 5. turowski b, macht s, kulcsár z, hänggi d, stummer w. early fatal hemorrhage after endovascular cerebral aneurysm treatment with a flow diverter (silk-stent): do we need to rethink our concepts? neuroradiology 2011; 53:37–41. 6. wong g, kwan m, ng r, yu s, et al. flow diverters for treatment of intracranial aneurysms: current status and ongoing clinical trials. journal of clinical neuroscience 2011; 18: 737-740. 7. wong g. why current evidence is against flow diverters for treatment of carotid blowout syndrome. european journal of radiology 2013; 82: 191. 8. karacozoff a, shellock f, wakhloo a. a next generation, flow diverting implant used to treat brain aneurysms: in vitro evaluation of magnetic field interactions, heating and artifacts at 3-t. magnetic resonance imaging. 2013; 31: 145-149. 9. wu yo, yang pe, shen j, huang q et. al. a comparison of the hemodynamic effects of flow diverters on widenecked and narrow-necked cerebral aneurysms. journal of clinical neuroscience. 2012; 19: 1520-124. 10. wong g, ponn w.s. current status of computational fluid dynamics for cerebral aneurysms: the clinician’s perspective. journal of clinical neuroscience 2011; 18: 1285-1288. 11. machi p, lobotesis k, vendrell jf, riquelme c, eker o, costalat v, bonafe a endovascular therapeutic strategies in ruptured intracranial aneurysms. eur j radiol. 2013 oct; 82(10):1646-52. 12. bracard s, barbier c, derelle al, anxionnat r. endovascular treatment of aneurysms: pre, intra and post-operative management. eur j radiol eur j radiol. 2013; 82(10):1633-7. 13. bendok b, aoun s. flow diversion for intracranial aneurysms: optimally defining and envolving a new tool and approach. world neurosurgery 2011; 76 (5): 401-404. 14. sfyroeras et al. flow diverting stents for the treatment of arterial aneurysms. journal of vascular surgery (2012) 840-845. 15. anzai h et al. optimization of flow diverters for cerebral aneurysms. journal of computational science 2012; 3:1-7. 16. duffis ej, et al. recent advances in neuroendovascular therapy. clin neurol neurosurg (2013) 1-6. 17. j.e. cohen et al. the use of flow diverter stents in the management of traumatic vertebral artery dissections. journal of clinical neuroscience 2013; 20: 731-734. 18. j.e. cohen et al. the use of telescoped flow diverters as an endovascular bypass in the management of symptomatic chronic carotid occlussion. journal of clinical neuroscience 2012; 19: 1026-1028. 19. chalouhi n, jabbour p, tjoumakaris s, strake rm, dumont as, liu h, rosenwasser r, el moursi s, fernando gonzalez l. treatment of large and giant intracranial aneurysms: cost comparison of flow diversion and traditional embolization strategies, world neurosurgery (2013) 1-25. 20. tremmel m et al. alteration of intraaneurysmal hemodinamics for flow diversion using enterprise and vision stents. world neurosurgery (2010) 1-10. 21. zhang y, chong w, qian y. investigation of intracranial aneurysms hemodynamics following flow diverter stent treatment. medical engineering & physics 35 (2013) 608-615. 22. mangiafico s, et al. endovascular strategy for unruptured cerebral aneurysms. eur j radiol (2012) 1-8. doi: 10.33962/roneuro-2021-051 awake focussed craniotomy for oedematous/large brain lesions. a pilot study for safety and feasibility jitin bajaj, sharad narayan sharma, gopal maravi, aamir iqbal, y.r. yadav, ankur shrivastav, ketan hedaoo, ambuj kumar, mallika sinha, shailendra ratre, vijay parihar, narayan swamy romanian neurosurgery (2021) xxxv (3): pp. 309-315 doi: 10.33962/roneuro-2021-051 www.journals.lapub.co.uk/index.php/roneurosurgery awake focussed craniotomy for oedematous/large brain lesions. a pilot study for safety and feasibility jitin bajaj1, sharad narayan sharma2, gopal maravi2, aamir iqbal3, yr yadav1, ankur shrivastav1, ketan hedaoo1, ambuj kumar1, mallika sinha1, shailendra ratre1, vijay parihar1, narayan swamy1 1 department of neurosurgery, nscb govt. medical college, jabalpur, india 2 department of anesthesiology, nscb govt. medical college, jabalpur, india 3 department of surgery, nscb govt. medical college, jabalpur, india abstract aim: awake craniotomy has been proven to be safe and effective. it has generally been used for non-edematous conditions. if done in edematous states, large craniotomies are advised. here, we report the combined use of techniques of awake anaesthesia and focussed craniotomy for dealing with large/edematous brain lesions. materials and methods: this was a prospective single-centre study from may to october 2019. included were adult cooperative patients presenting with edematous brain lesions. a completely awake cycle was used using ring scalp block, dexmedetomidine loading, and maintenance infusion, and use of midazolam and fentanyl. the dural flap was lifted limited to the lesion, and sometimes in stages to tackle the bulging brain. data was collected for resection volume, pain scores using visual analogue scale (vas) during the surgery, seizures, complications, new deficits, blood loss, duration of surgery, icu, and postoperative hospital stay. results: fifteen patients underwent the procedure. pathologies were high-grade gliomas (7), low-grade gliomas (3), tuberculoma (2), metastasis (1), ependymoma (1), and meningioma (1). fourteen patients underwent total, and one underwent subtotal excision. brain bulge could be handled with the staged opening of the dura and intratumoral decompression. no patient required postoperative ventilatory support. intraoperative pain scores ranged from 2-3. the duration of surgery ranged from 60280min. blood loss ranged from 75-300ml. postoperative stay varied from 3-20 days. there were two intraoperative seizures (managed), two csf leaks, and two infections. two patients developed transitory motor deficits. conclusion: awake focussed craniotomy was found safe and effective for large/edematous brain lesions in appropriately selected patients. keywords anaesthesia, awake craniotomy, brain tumour, keyhole surgery corresponding author: jitin bajaj department of neurosurgery, nscb govt. medical college, jabalpur, india bajaj.jitin@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 310 jitin bajaj, sharad narayan sharma, gopal maravi et al. introduction awake craniotomy (ac) has been proven to be safe and effective in several conditions, including lowgrade gliomas, epilepsy surgeries, and vascular diseases.2,12,13 it provides several advantages over craniotomy done under general anesthesia (ga). firstly, it gives the ability to use intraoperative monitoring of eloquent regions, including speech, motor, and visual areas. secondly, pulmonary complications due to intubation, ventilation, etc., that can occur with ga can be avoided. thirdly, positional complications like ulcers, spinal torsions, etc. can also be prevented. since the level of sedation is lesser than ga, the ac is essentially more physiological. the use of newer drugs like dexmedetomidine has proved to be safe and effective in awake craniotomies, perioperative, and icu situations.1,3. ac has been generally used in non-edematous conditions, possibly due to the apprehension of intraoperative brain bulge. if done in edematous states, large craniotomies have been advised.4 also, for the lesions with midline shift, the asleep-awakeasleep cycle has been used, and the data regarding the size of craniotomy is missing.5 small craniotomies are associated with lesser operative time, blood loss, wound complications, etc. than large craniotomies. we have reported minicraniotomy and endoscopic-assisted excision of deep-seated brain tumors and hematomas in the past.8,9 in this article, we report the combined use of techniques of awake and focussed craniotomies for dealing with large or edematous brain lesions. materials and methods this was a prospective study done at a single center from may 2019 to october 2019. institutional ethics committee permission was taken. the trial was registered under the clinical trials registry of india with reference number ctri/2019/05/019338. patient inclusion criteria were adult cooperative patients presenting with large or edematous brain lesions defined as either the tumor volume 30 cc3, or edema volume 60 cc3, or the total volume of tumor + edema 60 cc3. patient denying taking part in the study, or with cardiac or respiratory illnesses were excluded from the study. karnofsky status and minimental status examination (mmse) were calculated both before and after the surgery. anesthesia protocol patients were explained about the procedure and habituated with the types of questions to be raised before the surgery. once in the operation theatre, glycopyrrolate 0.2mg, fentanyl 100mcg, and ondansetron 4mg were administered intravenously, and an oxygen mask (o2) was applied. monitoring included an electrocardiogram, pulse oximetry, blood pressure (bp), end-tidal co2, and urine output. ring scalp block was performed with 20 ml of 0.5 percent bupivacaine. the infiltration was given in the territories of supraorbital, supratrochlear, zygomaticotemporal, auriculotemporal, lesser occipital and greater occipital nerves. the incision site was again infiltrated with 2% lignocaine and 1:100,000 adrenaline. infusion of dexmedetomidine (1ug/kg/hr) was then started and stopped 10 minutes before the neurocognitive testing. the level of sedation was assessed by the ramsay sedation score and was maintained between a score of 3 to 5 until neurocognitive testing was started. bispectral index monitoring was not available at our center and was not used in any of the cases. figure 1. shows the patient positioning. an 'l' shaped rod allows the surgeon to work in a sterile field and anesthetist to have face accessible for interacting with the patient and emergency airway management if the need arises. surgical protocol: we defined focussed craniotomies as bone opening not more than 1 cm and dural opening not more than 0.5 cm of tumor edges. all surgeries were done by the same surgeon. a preoperative dose of antibiotic (ceftriaxone) and 4mg of dexamethasone was given in every case. patients were placed supine with neck tilt in order to make the surgical trajectory as perpendicular to the ground as possible. a three-pin mayfield head clamp was applied for immobilization. patients were 311 awake focussed craniotomy for oedematous/large brain lesions allowed to move their limbs within the limits of safety. an l-shaped stand was placed right across the patient’s face, and draping was done in a way to have the face always accessible to the anesthetist (figure 1). the scalp flap was elevated according to the need, and a small craniotomy was lifted depending upon the lesion. the deeper the lesion, the smaller the craniotomy was made, according to the inverse funnel-shaped principle of keyhole surgeries. the brain bulge, if anticipated, was tackled with the initial small opening of dura, tumor decompression and later rest of the dural opening if needed. the bipolar cautery settings were used at the minimum. cold saline was always kept ready to abort the seizure if it happens. the lesions were resected with the standard bimanual dissection technique. cortical mapping with direct cortical stimulation was done in the last five cases. it was initially assessed over the exposed surface, and the absence of the eloquent region allowed the resection. mapping was repeatedly done during the procedure, along with the clinical testing. there was no difficulty in achieving the hemostasis in any of the cases. stopping the dexmedetomidine raised blood pressure to be normal, and asking the patient to cough confirmed the hemostasis. dura was closed, the bone was reposited, and standard closure techniques were followed in all the cases. table 1. demographic details of the patients. s. no. age in years / gender loc. side diagnosis tumor vol. (cc3) edema vol. (cc3) hydro cephalous resection intraope --rative brain bulge blood loss (ml) duration of surgery (min) procedure related complication 1. 55/m pf right metastasis 5.4 60 absent total present 100 60 intraoperative seizure 2. 25/f af left recurrent hgg 36.6 66.32 absent total present 200 120 csf leak, infection 3. 30/m ap left tuberculoma 14.4 75 absent total present 75 60 none 4. 32/m pf right recurrent hgg 40 100 absent subtotal present 150 200 csf leak, infection 5. 45/m mf left tuberculoma 37.63 67.32 absent total present 100 150 none 6. 53/m pf right convexity meningioma 22.8 110.7 absent simpson grade 1 present 200 120 none 7. 40/m af right hgg 38.5 22 absent total present 200 150 none 8. 34/m af left ependymoma 42.75 20.4 absent total present 200 280 none 9. 45/m pf right hgg 40.1 21 absent total present 180 200 none 10. 24/m pf left hgg 44.5 23.2 absent total present 300 180 transient speech slurring 11. 30/f ap right hgg 40.2 21.1 absent total present 250 210 none 12. 40/m pf right lgg 38.5 24.5 absent total present 250 180 intraoperative seizure 13. 22/m ap right lgg 40.2 23.1 absent total present 250 150 transient shoulder weakness 14. 29/m ap left hgg 30.5 40.2 absent subtotal present 250 200 none 15. 42/f mf left lgg 41.2 21.2 absent total present 200 220 none postoperative care postoperatively, they were given iv antibiotics for three days, and oral antibiotics for five more days. dexamethasone, anticonvulsants, and analgesics were given for a minimum of one week and tapered thereafter. surgical resection the resection was termed as gross total resection (gtr) (100% removal), near-total (91-99% removal), subtotal (str) (51-90% removal), and tumor biopsy (<10% removal). these were determined based on a comparison of preoperative and postoperative imaging volumetrically. the duration of surgery was calculated from the time of incision to the last stitch. subtracting the amount of irrigation fluid from the drain fluid and weighing the gauges after surgery calculated blood loss. 312 jitin bajaj, sharad narayan sharma, gopal maravi et al. pain score patients were asked to rate the degree of maximum pain during the surgery on the visual analog scale (from 0-10, where 0 means no pain, and 10 means life-threatening pain). results fifteen adult patients (12 males, 3 females) ranging from 22-55 years were operated in the study period. the diagnosis included high-grade gliomas (7), lowgrade gliomas (3), tuberculoma (2), metastasis (1), ependymoma (1) and meningioma (1). three gliomas were previously operated and were recurrences. all tumors were located either cortically or subcortically. seven patients had a history of seizures before the surgery. the demographic details, including the location of tumors, are given in table 1. neurological status and deficits the preoperative mmse of the patients ranged from 22-30 (mean = 27.26 2.49). postoperatively at six weeks mmse ranged from 28-30 (mean = 29.38 0.76). the preoperative karnofsky status of the patients ranged from 50-100 (mean = 77.33 15.79), and it improved to range from 80-100 (mean = 91.53 8.98) at six weeks. there were four patients with prior hemiparesis. one of them had an increase in shoulder weakness that resolved in six weeks. another patient had new speech slurring, which resolved in four weeks. for these two patients, the surgery had to be stopped after the new deficit. none of the patients had a permanent new neurological deficit. figure 2. a & b shows the t2 weighted mri with a large left parafalcine mass arising from the ventricle approached with awake minicraniotomy. c shows the 3cm sized bone opening. d-e shows the postoperative scan of the patient showing complete tumor excision. the red bracket shows the minicraniotomy on the scan. tumor volume and perilesional edema lesion volume ranged from 5.4cc3 to 44.5 cc3. the mean tumor volume was 34.21 11.30 cc3. perilesional edema volume ranged from 20.40 cc3 to 110.7cc3 with a mean of 46.4 31.2 cc3. surgical resection the dura was opened in a limited manner over the tumor or just more than the tumor. fourteen patients underwent total, and one underwent subtotal excision of the masses (due to tumor invasiveness). focussed craniotomies were lifted based on the methodology described. figure 2 shows a parafalcine mass arising from the ventricular wall (ependymoma) approached through an awake frontal minicraniotomy. one of our patient (case 4) had a significant bulging brain and for it staged dural opening and tumor resection was carried out. in the end, the brain was lax (figure 3). one patient (recurrent grade iii glioma) had a previous large craniotomy. going through it needed resection of a wedge of normal brain tissue to tackle the bulging brain. therefore a new minicraniotomy with a direct trajectory was planned that allowed us to hit the tumor only and prevent the venous compression of the normal brain (figure 4). there was no difficulty in achieving hemostasis in any of the cases. figure 3. 'a’ is the preoperative mri of a large recurrent glioma grade iii. 'b' shows the postoperative scan of the patient. the dura was opened in a staged manner with the tumor resection to tackle the bulging. the mass could be excised subtotal due to its invasion into the surrounding eloquent region. blood loss and duration of surgery average blood loss was 146.66 57.37 ml. although 313 awake focussed craniotomy for oedematous/large brain lesions no direct objective comparison was made with the cases done under ga, the blood loss was found subjectively equal to them. the mean duration of surgery was 131.33 61.86 min, and similar was observation for it. figure 4. a shows the preoperative scan of the patient with a large mass. it shows the prior site of craniotomy (i) and a newer approach (ii). b shows a 3 cm size width dural opening. c shows the postoperative scan of the patient with a newer minicraniotomy site visible and total resection of the mass. intraoperative vitals mean blood pressure fell by 12.66 4.16 mm hg, and the mean pulse fell by 13.06 5.79/min after the bolus dose of dexmedetomidine. pain score postoperatively, patients were asked to rate their maximum level of pain on a score of 1-10 (1minimum, 10-maximum as possible). the pain score for all the patients ranged from 2-3, with the mean score being 2.6 0.63. postoperative hospital stay all patients could be discharged without any new neurological deficit with a mean hospital stay of 7 4.08 days ranging from 3-20 days. complications there was one event of intraoperative focal faciobrachial seizure, which possibly occurred due to the high value of bipolar coagulation. it was managed with pouring cold saline over the brain and giving 1.5mg midazolam intravenously. on reducing the value of bipolar coagulation, there was no other seizure. one case (recurrent gbm) developed a cerebrospinal fluid leak, which was controlled with the resuturing of the wound. another patient (recurrent glioma grade iii) developed a wound site infection, which required prolonged antibiotics. we believe both the latter complications should not be attributed to the ac since they were recurrent cases and can happen with craniotomies under ga also. there was one case of speech slurring (recovered in 6 weeks) and one case of shoulder weakness (recovered in 2 weeks). neuromonitoring in the speech slurring case was not done, while in the shoulder weakness case didn’t show the localization of the shoulder area. there was no procedurerelated permanent morbidity or mortality. no case of any pressure-related injury or cautery burns etc. happened. follow-up one patient of metastasis (case 1metastasis from melanoma) succumbed to his illness one month later. another patient tuberculoma with tbm (case 3), also died one month later due to basal infarcts. rest patients were neurologically intact, having a follow-up of 3-6 months. discussion ac has been done for a long time.6,7 however, the safety and efficacy of small craniotomies in edematous brain lesions have not been described before. traditionally, for ac, a large bone flap has been recommended to avoid brain compression at the edges.4 the present set of technology with the newer concept of keyhole surgery allows us to explore in this direction.10,11 this study is probably the first one in the literature to report the safety and feasibility of focussed ac for large or edematous brain lesions. we found that small craniotomies were beneficial in large or edematous lesions, contrary to the previous observation.4 the reasons may be the usage of principles of keyhole surgery. we found three things to be required for awake focussed craniotomies. 1. patient selection: all patients were adults and cooperative, as is required for all awake surgeries. 2. proper positioning: patients were positioned to make the operative site highest and trajectory perpendicular to the ground. this made the surrounding brain to fall apart and pushed the tumor out towards us. we used a mayfield head clamp to make these positions. it also inhibited any untoward movement of the patient. 3. small craniotomy: this avoided the compression of the surrounding brain and veins between 314 jitin bajaj, sharad narayan sharma, gopal maravi et al. tumor and dural edges. points 2 & 3 are explained in figure 5. figure 5. shows the technique through which small craniotomy works. 'a' is the preoperative mri of the patient showing a small metastasis with significant perilesional edema. if proper positioning is made with the tumor at the highest position, the edematous forces (red arrows) will aid in forcing it out. since the site of the craniotomy is near to the tumor, no brain tissue/veins get compressed between the edges of the tumor and dura. 'b' shows the marker ct depicting a radioopaque marker at the site of the mass. 'c' shows the postoperative scan with a small craniotomy. note the surrounding cortex expands and takes space of the tumor. the face was always accessible to the anesthetist that provided the ability to use non-invasive ventilation or laryngeal mask airway ventilation if the need arise, although we didn't need them in any of the cases. the duration of the action of bupivacaine is 4-8 hours and this allowed us to perform the surgery with minimal pain. dexmedetomidine decreased the blood pressure and pulse rates mildly but these were always under control. this drug also has an analgesic effect which allowed the procedure to be performed for the convexity meningioma and parafalcine mass (cases 6 and 8). the cases in our series were heterogeneous with tumor size ranging from 5.4 cc3 to 44.5 cc3, and edema volume ranging from 20.40 cc3 to 110 cc3. this showed that the procedure was safe in cases with high intracranial pressure, in lesions of various etiologies, and with a variable amount of tumor size and edema. the ga helps in decreasing the intracranial pressure (icp) by deep sedation. however, during its reversal, it also makes the patient susceptible to a sudden rise in icp, bp, pulse rate, etc. which can create postoperative complications like hematomas. we believe that awake surgeries are more physiological than the surgeries done under ga. the level of sedation, heart rate, bp, icp, etc. are close to the baseline in the awake state, while all of these vary a lot in the ga state. although there were cases of operative site hematoma in taylor et al. series,13 we found none in our series. we believe that after tumor removal, the stoppage of dexmedetomidine leading to the restoration of bp and asking the patient to cough helped in confirmation of hemostasis, which carried to the postoperative state. the average blood loss and operative duration were similar to the personal experience of the surgeon. a direct objective comparison was not possible with surgeries done under ga due to the variability of the diagnosis and vascularity of the tumors operated. there was no procedure-related complication apart from one intraoperative seizure, which was easily controlled with cold saline and midazolam. the costs of the procedures done under awake conditions are less due to the lack of need of anesthesia gases, endotracheal tube, and postoperative icu stay. the cost of dexmedetomidine with midazolam is very less compared to the anesthesia gases and ventilatory support. these factors play a very important role in resource-limited settings. limitations of our study include small sample size and a single team’s experience, which may create bias. a multicenter randomized controlled trial between craniotomies under awake and ga conditions will be better to show its superiority/inferiority for the rates of the degree of surgical resection, duration, blood loss, and brain bulge. the intraoperative seizure is a critical limitation of ac, but these can be managed as mentioned. all tumors were located near the surface in our series, and safety and efficacy in deeper lesions need to be established. however, despite these limitations, this study shows the safety and feasibility of awake focussed craniotomies in large or edematous brain lesions. conclusion awake focussed craniotomy was found safe and effective for large or edematous brain lesions in appropriately selected patients. references 1. bekker ay, kaufman b, samir h, doyle w: the use of dexmedetomidine infusion for awake craniotomy. anesth analg 92:1251–1253, 2001 2. gamble aj, schaffer sg, nardi dj, chalif dj, katz j, dehdashti ar: awake craniotomy in arteriovenous malformation surgery: the usefulness of cortical and 315 awake focussed craniotomy for oedematous/large brain lesions subcortical mapping of language function in selected patients. world neurosurg 84:1394–1401, 2015 3. kaur m, singh pm: current role of dexmedetomidine in clinical anesthesia and intensive care. anesth essays res 5:128–133, 2011 4. khu kj, ng wh: intraoperative swelling leading to neurological deterioration: an argument for large craniotomy in awake surgery for glioma resection. j clin neurosci off j neurosurg soc australas 16:886–888, 2009 5. ouyang mw, mcdonagh dl, phillips-bute b, james ml, friedman ah, gan tj: does midline shift predict postoperative nausea in brain tumor patients undergoing awake craniotomy? a retrospective analysis. curr med res opin 29:1033–1038, 2013 6. penfield w: combined regional and general anesthesia for craniotomy and cortical exploration: part i. neurosurgical considerations. anesth analg 33:145–155, 1954. 7. penfield w: combined regional and general anesthesia for craniotomy and cortical exploration: part i. neurosurgical considerations. int anesthesiol clin 24:1– 11, 1986. 8. ratre s, yadav n, parihar vs, dubey a, yadav yr: endoscopic surgery of spontaneous basal ganglionic hemorrhage. neurol india 66:1694–1703, 2018. 9. ratre s, yadav yr, parihar vs, kher y: microendoscopic removal of deep-seated brain tumors using tubular retraction system. j neurol surg part cent eur neurosurg 77:312–320, 2016. 10. 1reisch r, perneczky a, filippi r: surgical technique of the supraorbital key-hole craniotomy. surg neurol 59:223– 227, 2003. 11. reisch r, stadie a, kockro ra, hopf n: the keyhole concept in neurosurgery. world neurosurg 79:s17.e9s17.e13, 2013. 12. sitnikov ar, grigoryan ya, mishnyakova lp: awake craniotomy without sedation in treatment of patients with lesional epilepsy. surg neurol int 9:177, 2018. 13. taylor md, bernstein m: awake craniotomy with brain mapping as the routine surgical approach to treating patients with supratentorial intraaxial tumors: a prospective trial of 200 cases. j neurosurg 90:35–41, 1999. doi: 10.33962/roneuro-2021-014 intracranial hydatid disease. our experience at peripheral tertiary care centre in india and review of literature s.n. gautam, jigmisha acharya, banesh jain, piyush kumar panchariya romanian neurosurgery (2021) xxxv (1): pp. 85-93 doi: 10.33962/roneuro-2021-014 www.journals.lapub.co.uk/index.php/roneurosurgery intracranial hydatid disease. our experience at peripheral tertiary care centre in india and review of literature s.n. gautam, jigmisha acharya, banesh jain, piyush kumar panchariya government medical college, kota, rajasthan, india abstract background: echinococcosis also known as hydatid disease is an endemic zoonotic disease with growing public health concern with an estimated financial burden of us dollars 193,539,740 annually. its definitive host being carnivores and man being an accidental intermediate host. the most common organ affected is the liver, the brain is involved in about 2% of cases. intracranial hydatid carries high morbidity owing to pressure effect and a slow-growing hence the diagnosis is often delayed. surgery is the mainstay of treatment; medical management being reserved for selected cases. materials and method: a retrospective analysis of all the cases of intracranial hydatid disease managed at our department was done from 2013 to 2020 and data were analysed. results: a total of 6 cases were found with an incidence of 1.33% of all intracranial space-occupying lesions during the study period with male to female ratio of 5:1, mean age at presentation 21.2 years, 4 out of 6 patient in the pediatric age group, cyst localised mainly in middle cerebral artery territory, mostly solitary but multiple in one case, all cases managed surgically with preoperative rupture in one case, recurrence noted in another one, albendazole was given to cases only with rupture or recurrence. conclusions: intracranial hydatid disease should be suspected in all non-enhancing cystic brain lesions especially in endemic regions and all patients should have preferably surgical excision using the “dowling technique” with medical management reserved for inaccessible lesions, patients unfit for surgery, rupture and recurrent cases. its high time when public health strategies should also be focussed on prevention and control of disease with appropriate measure at the community level. introduction hydatid is a greek word meaning “a drop of water” [23]. hydatid disease also known as echinococcosis is an endemic zoonotic disease, with studies showing it to be an increasing public health concern and can be regarded as emerging or re-emerging disease [22] with an estimated annual financial loss of us dollars 193,539,740 [4]. it is known to occur in all continents and in at least 100 countries with much more frequency in south america, australia, middle east, and parts of north africa than in europe and north america [31]. the highest prevalence keywords intracranial hydatid, echinococcosis, zoonosis, dowling’s technique, albendazole corresponding author: piyush kumar panchariya government medical college, kota, rajasthan, india drpiyushpanchariya@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 86 s.n. gautam, jigmisha acharya, banesh jain et al. of human hydatid disease in india has been reported from andhra pradesh, saurashtra, and tamil nadu [25]. about 60-75% of affected patients are from paediatric age group [31]. echinococcosis is caused by infestation of larvae of taenia echinococcus. the definite host in the life cycle are carnivores commonly dog and humans being the accidental intermediate hosts who are infected by the feco oral route or by direct contact. liver is most commonly affected organ followed by lungs. the brain is involved in less than 2% of cases [20], and incidence of hydatic among all intracranial space occupying lesions is 1-2% only [29]. intracranial echinococcosis is treated primarily by surgery using “dowling technique” with proctoscolicidal drugs used to sterilize the cyst, decrease the chances of anaphylaxis, decrease the tension in the cyst wall, reducing the risk of spillage during surgery and the recurrence rate, recurrent cysts, multiple inaccessible cysts [12]. we present here a case series of 6 consecutive case of intracranial hydatid disease successfully treated at our institute and literature about intracranial echinococcosis is reviewed. materials and methods we retrospectively analysed six cases of intracranial echinococcosis managed at department of neurosurgery, government medical college, kota from 2013 to 2020. a detailed recording of demographic profile of patients, presenting factors, risk factors, investigations, surgical procedure and its outcome, other treatment modalities and their follow up was made. observation and results an overall 6 cases of intracranial echinococcosis reported to our centre over the period and a total of 450 intracranial space occupying lesions operated during this period representing an incidence of 1.3% among all intracranial space occupying lesions. the details of patients recording are as given in table 1. table 1. case details of patients with intracranial hydatid cyst. age/ sex presentation and duration of symptoms location and number management recurrence intra operative rupture albenda zole risk factor 12y/ f headache, seizures, right hemiparesis; 6 months left temporoparietal , single surgery no no no history of contact to pets. 14y/ m headache, vomiting, left hemiparesis; 3 months right temporoparietal , single surgery no no no no documented risk factor. 8y/ m headache, vomiting, seizures ; 1 month left temporoparietal, multiple surgery yes no yes [after surgery for recur-ence] history of contact to pets. 31y/ m headache, vomiting reduced vision in right eye; 3 months right mastoid region, single surgery no no no no documented risk factor 5y/ m headache, vomiting, left hemiparesis; 3 months right lateral ventricle, single surgery no no no no documented risk factor 60y/ m headache, right hemiparesis; 5 months left parietal, single surgery no no no no documented risk factor 87 intracranial hydatid cyst: literature review the mean age of presentation was 21.2 years and a total of 4 out of 6 [66.6%] patients were below 16 years. the mean duration of symptoms was 3.5 months. there was a male to female ratio of 5:1. two of the patients had history of contact with pets. all patients came from rural area of rajasthan. the commonest presentation was headache present in all cases [100%] followed by vomiting and hemiparesis being present in 4 out of 6 patients [66.66%], seizures in 2 out of 6 patients [33.33%] and reduced visual acuity in one patient [16.66%]. the commonest location of cysts were in temporoparietal region with single cases each of intraventricular and infratentorial locations [figure 1]. [a] [b] [c] [d] [e] [f] figure 1. pre-operative scans showing location of intracranial hydatid cyst [a] to [d] left temporoparietal, [e] right intraventricular location, [f] multiple intracranial hydatid cysts. 88 s.n. gautam, jigmisha acharya, banesh jain et al. figure 2. delivery of intracranial hydatid cyst using dowling’s technique. figure 3. post operated scans showing complete excision of cyst. figure 4. recurrence in patient after 6 month of primary surgery. figure 5. histopathological microphotograph [40x] showing laminated ectocyst, scolex and inflammatory infiltrate. only one patient [16.66%] presented with multiple cysts [figure 1f] . all patients were undergone a plain ct brain followed by an mri brain to exactly localise the cyst, looking for consistency, number and status of surrounding brain parenchyma. the search of cyst located in other body organs using x ray chest and usg abdomen revealed no other associated cyst. all patient underwent craniotomy and cyst excision after routine investigations and anaesthesia clearance. we did not carry out serological investigations to test presence of antigen as it has less probability to be positive in intracranial hydatid disease and adds no significance to the management. all patients received a peri operative coverage of steroids for the risk of intraoperative rupture and dissemination . an adequate craniotomy was made as per the location of cyst, cyst was approached via corticectomy of size at least three fourth of size of cyst. the cyst was delivered through dowling’s technique dissecting peri cystic plane using hydro dissection and lowering the head end of table [figure 2]. there was an intraoperative rupture of cyst in one case. complete excision of cyst were achieved in all cases [figure 3]. no intraoperative anaphylaxis was noted in any case. one patient developed extradural hematoma at craniotomy site in post operative period which was successfully managed conservatively. all excised cysts were subjected to histopathological confirmation which were consistent with hydatid cyst. there had been recurrence reported after 6 months of primary surgery in one case who was then operated at some other centre for recurrence but developed recurrence again after second surgery and later operated again at our centre only [figure 4]. cases who had rupture during surgery and recurrence following surgery were given tablet albendazole in divided doses of 10 mg/kg/day for a 28 days cycle followed by 14 days drug free interval upto 4 cycles. there has been a constant and good recovery of neurological symptoms in all cases. all the cases have been in follow up over a variable period of 6 months to seven years, we have a protocol of having post operated ct brain in immediate post operated period, an mri brain at three months and one years of follow up. 89 intracranial hydatid cyst: literature review discussion and review of literature hydatid disease is an emerging zoonotic parasitic disease, cases have been reported in all continents and across 50 countries around the globe. the countries with higher prevalence included mediterranean countries, middle east countries, russia, australia, new zealand, france, china, india [1]. the worldwide incidence of echinococcosis has been estimated to be 100,000 – 3,00,000 cases annually but only about 2-3% cases are of intracranial echinococcosis which actually may be higher but underreported [25, 12]. guesnar reported first case of cerebral hydatid [9]. intracranial hydatid forms about 1-2 % of all intracranial space occupying lesions [21], the ratio in our series reported to be 1.33% of all brain space occupying lesions operated during this period. the majority of cases about 6580% found in paediatric age group possibly because of patent ductus arteriosus [9,14], in our series 4 out of 6 patients [66.66%] were under 15 years of age. no patent ductus arteriosus was found in any of our patient. there has been a male preponderance which was seen in present series also. in indian context, lot of single case reports are there on intracranial hydatid cyst, we found two case series of nine cases by tanki etal [29] and five cases by gupta etal [14] and compared the results with present series [table 2]. table 2. comparison of results of case series by tanki etal [29] , gupta etal [14] and current series tanki etal [2009-2015] gupta etal [1984-1997] current series [2013-2020] number of cases 9 5 6 incidence in terms of percentage of total intracranial space occupying lesion 0.06% 0.05% 1.13% mean age of presentation 11.5 years 13.4 years 21.2 years paediatric patients 9/9 [100%] 4/5 [80%] 4/6 [66.66%] duration of symptoms 1 month to 2 years 1 month to 2 years 1 months to 6 months male : female ratio 5:4 3:2 5:1 risk factors 1) contact to pets 2) rural location 7/9 8/9 2/5 3/5 2/6 6/6 symptoms seizures [most common], hemiparesis, vomiting and headache hemiparesis [most common], seizures headache [most common], hemiparesis, vomiting, seizures location of cyst four parietal solitary cysts, two frontal solitary, one parietooccipital solitary, two parietal multiple cysts one patient each with frontal, lateral ventricle, parietal. two patients with multiple cysts in parietal and temporoparietal region. two patients each with temporoparietal solitary cyst, one with lateral ventricle, one parietal, one mastoid, one with multiple temporoparietal cysts intraoperative rupture 3 cases 2 cases 1 case 90 s.n. gautam, jigmisha acharya, banesh jain et al. anaphylaxis following rupture nil nil nil recurrence two cases; one year of surgery two cases; six month to one year after primary surgery one case, 6 months following surgery albendazole to all patients following surgery, 10 mg/kg for two months to two patients following recurrence, 10 mg/kg for one month two patients, one with rupture another with recurrence, 10mg/kg upto 4 cycles follow up period 6 months to five years six months to eight years six months to seven years echinococcosis is caused by larvae [metacestode] of cestode species of the genus echinococcus like e. granulosus [cystic echinococcosis], e. multilocularis [alveolar], e. vogeli or e. oligarthus [polycystic echinococcosis]. the two most common affecting humans are granulosus which has a limiting membrane and multilocularis with no limiting membrane and hence grow aggressively [23,25]. at least 7 of 9 strains of e. granulosus are found to be infective in humans with g5 strain responsible for most cases globally while g1 and g5 causes most infections in india [25]. humans being the accidental intermediate host, get infected through the faeco oral route by ingestion of food or milk contaminated by dog faeces containing ova of the parasite or by direct contact with dogs. the eggs loose their enveloping layer in the stomach, releasing the embryos. the embryos pass through the wall of the gut into the portal system and are carried to the liver where most larvae get entrapped and encysted. some may reach the lungs and occasionally, some may pass through the capillary filter of the liver and lungs and get entry into the systemic circulation. these may even reach the brain. commonly affected organs include liver, lungs, brain, spleen, kidney, orbit, musculoskeletal system [23,11,13] . contact to pets may or may not be always present, it was there in two of our patients. all the patients of our series were from rural area where there are large open areas and contamination of soil with stray dog’s faeces is a common occurrence which is in accordance with the hypothesis of significant environmental contamination where in parasite eggs can survive longer in conditions of high humidity [32]. intracranial hydatid cyst may be primary [single] with multiple scolices and broods capsule hence fertile with a risk of recurrence following rupture while secondary [multiple] thought to arise from multiple scolices released from left side of heart or cyst rupture in heart, lacks broods capsule hence non fertile with negligible risk of recurrence following rupture[12,1,14,26]. in cerebral tissue most common location of hydatid disease is in territory of middle cerebral artery which was also seen in our series where 4 out of 6 locations were in territory of terminal branches of middle cerebral artery [23,12,14]. intraventricular location is now being reported in literature more and more as has been reported by sharad et al [23], we had one patient with lateral ventricle hydatid cyst and contrary to common supratentorial locations [12,14] we had one patient with hydatid cyst located in right mastoid region. other locations of intracranial echinococcosis reported in literature are orbit, skull bones, pons, basal ganglia [10,27]. the usual clinical presentation may be signs of raised intracranial pressure more common in paediatric population or focal neurological deficits common in adults [12,14]. headache was commonest presentation in present series in all cases followed by vomiting, hemiparesis and seizures. the diagnosis of intracranial hydatid relies on radiological investigations. on ct head, there is hypodense non contrast enhancing oval homogenous cystic mass lesion with thin walls and smooth margins usually in territory of middle cerebral artery with pressure effect on surrounding brain parenchyma as per the size of lesion with no surrounding edema [10,30]. usually upon diagnosis the lesions are of considerable size before symptoms appear as intracranial hydatid cyst is a slow growing lesion although a variable growth rate of 1-10 cm/ year has been documented in literature [23,9,14,28]. on mri brain, cyst wall has low signal intensity on both t1 and t2 imaging with no enhancement, daughter cysts or hydatid sand may be visible on mri, no rim enhancement is a differentiating feature from cystic high grade tumours or abscess [10,30]. infiltrating margin and surrounding edema may be a 91 intracranial hydatid cyst: literature review feature of echinococcus multilocularis. mrs and diffusion weighted imaging has now being used to further aids to diagnosis. chand et al [7] demonstrated mildly elevated choline, depressed creatine and naa, and a large peak of lactate, pyruvate and acetate. pyruvate has been considered a specific in vivo marker for cestodal, in particular hydatid cysts [7,19,17,35]. all patient underwent ct brain followed by mri brain in current series and pre op diagnosis of hydatid cyst was considered in all cases was considered based on consistent radiological findings. no patient in current series was subjected to mrs. the various differential diagnosis to be considered on radiology should include cystic tumours, porencephalic cysts, arachnoid cysts, epidermoid cysts, neurocysticercosis, toxoplasma [23,30,5]. among serological tests immunoblot test is the test of choice targeting the specific arc 5 antigen present in hydatid fluid of e.granulosus. the sensitivity and specificity of test is 91% and 98% respectively. it may show cross reaction with taenia cysticercosis. casoni’s test is of little significance in cerebral hydatid disease [23, 22]. no patient in current series was subjected to any laboratory investigation to ascertain hydatid disease pre operatively as radiological findings were typical of disease. the treatment of choice for intracranial hydatid disease is surgical excision of cyst without rupture [16]. the preferred technique includes the dowling technique later modified by arana iniguez and san julian. the essential steps include creation of a large flap; careful handing during all operative steps to avoid monopolar coagulation; opening the atrophic cortex overlying the cyst over an area with a diameter no less than three quarters of the diameter of the cyst; and allowing the cyst to fall out by just lowering the head of the operating table and flushing warm saline between the cyst and surrounding brain [6,2]. in case of multiple cyst , largest one is targeted first. no technique can be applied to all the cases as a general rule and there should be an approach pre operatively identified for each case [16]. we got a complete resection of cyst in all the cases under microscopic guidance, although rupture was there in one case but no anaphylaxis was seen. there have been reports of irrigating the cavity with hypertonic saline to prevent recurrence specially after inadvertent intra operative cyst rupture [26,33]. there may be post operative cerebral edema, sub dural effusions, hydrocephalus, loss of autoregulatory mechanisms following cyst excision and decompression which should be suspected and diagnosed timely [23,15]. no such complication was seen in our series. although an underlying edh at craniotomy site was seen in one case which was successfully managed conservatively. the pathological character of cyst consists of three layers the endocyst which has inner germinal layer, scolices, brood capsule which proliferate by internal budding. in e. multilocularis there is external budding and hence infiltrating margins are there. the ectocyst the outer laminated layer, the host inflammatory capsule pericyst which has blood vessels to supply nutrition to the parasite[23,9,14]. all cases were subjected to histopathological confirmation in current series with confirmation of all the layers in the specimen. [figure 5] the medical management consists of protoscolicidal agent albendazole in divided doses with a total dose of 10 mg/kg/day. it is parasiticidal and acts by blocking the uptake of glucose by larvae and adult parasites [18]. albendazole results in disappearance of up to 48% of cysts and a substantial reduction in size of the cysts in another 28% [26]. praziquantel increases the serum concentration of albendazole four fold and hence a combination of drugs is more effective than either alone [23,26]. the use of drugs is limited to patient not fit for surgery, inaccessible cyst, history of intraoperative rupture, recurrence. the drugs are given over a 28 days cycle with 14 days drug free interval upto 4 to 6 cycles[12,15] . although isolated case reports of medical management of intracranial echinococcosis are there in literature[24,8]. in the current series two patients one with recurrent disease and another with intraoperative rupture of cyst were put on albendazole upto 4 cycles after surgical excision and no recurrence has been documented till now in regular follow up. hydatid disease is an emerging and remerging public health problem where surgical and medical management of individual cases is just a palliation and a public heath strategy to control and prevent the disease is reasonable approach. each country need to identify the prevalent strain, definitive and intermediate host in her geographical location and derive policies accordingly. as far as india is concerned, checking the population of stray dogs, surveillance of dogs, periodic stool testing and 92 s.n. gautam, jigmisha acharya, banesh jain et al. accordingly treatment, preventing direct access to raw offal at slaughter house and farms should be implemented. many countries such as new zealand, australia, and china have been successful in this regard and india is yet to catch up [31,34]. despite a silent but constantly growing public health concern and growing number of intracranial hydatid disease, there has been a need of more and more literature to better manage the cases of intracranial echinococcosis and also to address this entity on community level also. through this series we have shared our experience of successful management of intracranial echinococcosis and also adds on to a complete literature review over this under reported cerebral disease. conclusions hydatid disease should be suspected in all cystic non enhancing mass lesions specially in endemic regions and goal of treatment should be complete surgical excision with no rupture of cyst while reserving albendazole for selected cases, alongside addressing this condition on community level also with incorporation of carefully drafted public health policies. declarations financial support: nil conflict of interest: nil consent: proper consent has been taken from all patients and their legal guardian to use their data for academic publication with assurance of non-disclosure of identity to the best of the extent. references 1. ali nemati , ahmad kamgarpour , murtaza rashid , sahar sohrabi nazari. giant cerebral hydatid cyst in a childa case report and review of literature, british journal of medical practitioners, september 2010; 3 (3) : a338 2. arana-iniguez r, san julian j: hydatid cyst of the brain. j neurosurg 12:323–335, 1955 3. bhattacharya d, bera ak, bera bc, das sk. molecular appraisal of indian animal isolates of echinococcus granulosus. ind j med res 2008;127:383-7. 4. budke, c. m., deplazes, p., & torgerson, p. r. (2006). global socioeconomic impact of cystic echinococcosis. emerging infectious diseases, 12(2), 296–303 5. bükte y, kemaloglu s, nazaroglu h, ozkan u, ceviz a, simsek m. cerebral hydatid disease: ct and mr imaging findings. swiss med wkly 2004;134:459 67 6. carrea r, dowling e jr, guevera a: surgical treatment of hydatid cyst ts of of the central nervous system in the pediatric age (dowling’s technique). childs brain 1:4–21, 1975 7. chand k, kanodia ak, manpreet g, et al. in vivo proton magnetic resonance spectroscopy in a known case of intracranial hydatid cyst. neurol india 2005;53:337–8. 8. chen s., li n., yang f., wu j., hu y., yu s. etal medical treatment of an unusual cerebral hydatid disease. bmc infectious diseases (2018) 18:12 9. dharker sr, vikram m : hydatid disease. in : text book of neurosurgery, third edition. eds.ramamurthi b, tandon pn. jaypee brothers medical publishers (p) ltd, new delhi 2012; 794-798 10. diren hb, ozcanli h, boluk m, kilic c. unilocular orbital, cerebral and intraventricular hydatid cysts: ct diagnosis. neuroradiology 1993;35:149 50. 11. garcia ls, bruckner da. tissue cestodes: larval forms. in: diagnostic medical parasitology. 4th ed. washington, dc: asm press; 2001. p. 387 403 12. gautam s, sharma a. intracranial hydatid cyst: a report of three cases in north-west india. j pediatr neurosci. 2018;13(1):91-95. doi:10.4103/jpn.jpn_141_17 13. geramizadeh b. unusual locations of the hydatid cyst: a review from iran. iran j med sci 2013;38:2 14. 14. gupta s, desai k, goel a. intracranial hydatid cyst : a report of five cases and review of literature.neurol india 1999;47:214 15. guzel a, tatli m, maciaczyk j, altinors n. primary cerebral intraventricular hydatid cyst: a case report and review of the literature. j child neurol 16. izci y., tuzun y., secer h.i., enzil g., cerebral hydatid cysts: technique and pitfalls of surgical management. neurosurgery focus 24 (6):e15, 2008 17. jayakumar pn, srikanth sg, chandrashekar hs, et al. pyruvate: an in vivo marker of cestodal infestation of the human brain on proton mr spectroscopy. j magn reson imaging 2003;18:675–80 18. kalaitzoglou i, drevelengas a, petridis a, palladas p. albendazole treatment of cerebral hydatid disease: evaluation of results with ct and mri. neuroradiology 1998;40:36‑9. 19. kohli a, gupta rk, poptani h, et al. in vivo proton magnetic resonance spectroscopy in a case of intracranial hydatid cyst. neurology india 1995;45(pt 1):562–4. 20. luo k, luo dh, zhang tr, wen h. primary intracranial and spinal hydatidosis: a retrospective study of 21 cases. pathog glob health. 2013; 107(2):47–51 21. mala r, ananth ml, nagaraju bn, rao cv. intracranial hydatid cysts-some rare presentations of cases. j ntr univ health sci 2014;3:263-6. 22. miabi z, hashemi hm, ghaffarpour h, ghelichna h, media r. clinicoradiological findings and treatment outcome in patients with intracranial hydatid cyst. acta med iran 2005;43:359 64 23. pandey s, pandey d, shende n, sahu a, sharma v. cerebral intraventricular echinococcosis in an adult. surg neurol int 2015;6:138. 93 intracranial hydatid cyst: literature review 24. ramosaço e., kolovani e., ranxha e, vyshka g., primary multiple cerebral hydatid cysts in an immunocompetent, low-risk patient. idcases 21 (2020) e00882 25. rao ss, mehra b, narang r. the spectrum of hydatid disease in rural central india: an 11-year experience. ann tropmed public health 2012 ;5:225-30. 26. reddy d r. managing cerebral and cranial hydatid disease. neurol india 2009;57:116-8 27. rivierez m, el azhari a, el tantaoui m, alaoui m. hydatid cyst of the cavernous sinus. a case. neurochirurgie 1992;38:46 9. 28. sierra j, oviedo j, berthier m, leiguarda r. growth rate of secondary hydatid cysts of the brain. case report. j neurosurg 1985;62:781 2. 29. tanki h, singh h, raswan us, et al. pediatric intracranial hydatid cyst: a case series with literature review. pediatr neurosurg 2018;19:1–6. 30. taslakian b., darwish h., intracranial hydatid cyst: imaging finding of a rare disease. bmj case rep 2 august , 2016. 31. tuzun y, kadioglu hh, izci y, suma s, keles m, aydin ih. the clinical, radiological and surgical aspects of cerebral hydatid cysts in children. pediatr neurosurg. 2004;40:155–60 32. veit p, bilger b, schad v, schäfer j, frank w, lucius r. influence of environmental factors on the infectivity of echinococcus multilocularis eggs. parasitology 1995;110:79-86. 33. wang j, cai b, you c. surgical treatment options for cerebral alveolar echinococcosis: experience in six patients. neurol ind 2009;57:157-61 34. world health organization: report of who working group meeting on echinococcosis research and control. china-12th october. beijing:1993. p. 3. 35. yadav vk, sudhakar sv, panwar j. pathognomonic mri and mr spectroscopy findings in cerebral hydatid cyst. acta neurol belg 2015. doi: 10.33962/roneuro-2021-058 gastroparesis as a complication in the patient with traumatic brain injury sandra marcela mass-ramirez, ivan david lozada-martinez, josé bohorquez-rivero, ezequiel garcia-ballestas, diego bustos, ingrith tatiana poveda-castillo, raúl david delgado-marrugo, víctor julián daza-martínez, andrés david sastre -martínez, michael gregorio ortega-sierra, tariq janjua, maría paz bolaño-romero, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (3): pp. 345-351 doi: 10.33962/roneuro-2021-058 www.journals.lapub.co.uk/index.php/roneurosurgery gastroparesis as a complication in the patient with traumatic brain injury sandra marcela mass-ramirez1, ivan david lozada-martinez1,2,3,4, josé bohorquez-rivero5, ezequiel garcia-ballestas6, diego bustos6, ingrith tatiana poveda-castillo7, raúl david delgado-marrugo8, víctor julián dazamartínez9, andrés david sastre-martínez10, michael gregorio ortega-sierra11, tariq janjua12, maría paz bolaño-romero1, luis rafael moscotesalazar2,3,4 1 medical and surgical research centre, university of cartagena, colombia 2 colombian clinical research group in neurocritical care, university of cartagena, colombia 3 latin american council of neurocritical care, cartagena, colombia 4 globan neurosurgery committee, world federation of neurosurgical societies 5 school of medicine, universidad del sinú, cartagena, colombia 6 center for biomedical research, university of cartagena, colombia 7 school of medicine, fundación universitaria juan n corpas, bogotá, colombia 8 school of medicine, universidad militar nueva granada, bogotá, colombia 9 school of medicine, corporacion universitaria remington, medellín, colombia 10 school of medicine, fundacion universitaria sanitas, bogotá, colombia 11 school of medicine, corporación universitaria rafael nuñez, cartagena, colombia 12 department of intensive care, regions hospital, minnesota, usa abstract patients with acute neurological diseases (traumatic brain injury, hemorrhagic or ischemic stroke, spinal cord injury or tumour) may present with various systemic alterations such as changes in cardiovascular and r espiratory response, gastrointestinal function disorders, metabolic and endocrinological abnormalities, coagulopathies, among others. head injury increases the risk of malnutrition due to multiple factors related to nutrient intake, abnormalities in energy expenditure, eating behaviour disorders, gastrointestinal changes, and medication side effects. keywords traumatic brain injury, gastrointestinal tract, gastroparesis, delayed gastric emptying corresponding author: ivan david lozada-martínez medical and surgical research centre, university of cartagena, colombia ilozadam@unicartagena.edu.co copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 346 sandra marcela mass-ramirez, ivan david lozada-martinez, josé bohorquez-rivero et al. gastrointestinal conditions include gastroparesis, which is defined as a delay in gastric emptying in the absence of mechanical obstruction. these patients often report nausea, vomiting, pain, postprandial fullness and abdominal swelling. although the exact mechanism by which it occurs in traumatic brain injury is not known, it is related to complications such as intracranial hypertension, so it is most often seen in cases of severe trauma. therefore, the objective of this review is to expose basic and practical concepts about gastroparesis and its approach. introduction traumatic brain injury (tbi) is one of the most frequent acute brain pathologies that constitute a serious public health problem worldwide due to its high mortality and number of cases of permanent disability after its occurrence [1]. the most recent data provided by the centers for disease control and prevention (cdc) estimates that for the year 2019 there were about 61,000 tbi-related deaths in the united states, which is approximately166 deaths every day [2]. this condition can be caused by a blow, jolt or penetrating head injury that disrupts the normal functioning of the brain [2]. tbi, especially severe tbi (glasgow coma scale < or equal to 8), is associated with many consequences, the most common being altered consciousness, coma, movement and gait disorders, memory impairment learning, among others; however, the occurrence of gastrointestinal dysfunction in patients, such as gastroparesis, has been reported days after traumatic brain injury [3]. the incidence of gastroparesis (gp) in tbi ranges around 45-50%, and is closely related to the severity of trauma and intracranial hypertension [4]. gp is a well-documented finding among patients with severe tbi [5]. gp is defined as delayed gastric emptying in the absence of mechanical obstruction [6-8]. in these patients, a temporal profile of delayed emptying has been described during the first 2 weeks post-trauma with subsequent improvement [4]. although the exact cause of gp in tbi is unknown, altered nerve signaling to the stomach appears to be a factor [9]. other factors that promote its onset are inflammation, sepsis, hydroelectrolytic alterations (hypokalemia, hypomagnesemia), hyperglycemia, frequently used drugs (opioids, furosemide, hydantoin, antacids, corticosteroids, among others), renal and hepatic dysfunction, and liver dysfunction [4,6]. considering the relevance of this topic in the care of the neurocritical patient and the lack of current evidence to know the impact of this condition, the objective of this review is to present basic concepts related to the pathophysiological process, general approach and future perspectives of gastroparesis in patients with traumatic brain injury. general information on gastroparesis in patients with tbi it has been shown that more than 50% of patients with severe traumatic brain injury do not tolerate enteral feeding, which presents itself in the form of vomiting, abdominal distension, delayed gastric emptying, esophageal reflux and decreased intestinal peristalsis [10]. the above suggests that gastrointestinal dysfunction is a frequent entity following tbi and that the association between the severity of brain injury and enteral feeding intolerance appears to be related to the existence of a link between the central nervous system and the non-functioning gut [10]. as mentioned above, one of the factors involved in such intolerance consists of delayed gastric emptying or gastroparesis [11]. gastroparesis and altered gastric accommodation are the result of a neuromuscular dysfunction of the stomach. kao et al [11] conducted a study where they evaluated the half-time of gastric emptying of liquid meals in patients with moderate to severe tbi, finding that head trauma can cause significantly prolonged gastric emptying [11]. other studies have shown that tbi can also induce a decrease in both intestinal contractility and transit and an increase in inflammation in intestinal smooth muscle, which may indicate that motility is inhibited in the small intestine due to inflammatory damage secondary to brain injury [10]. on the other hand, delayed gastric emptying has been frequently observed in patients with intracranial hypertension (ih). increased intracranial pressure (icp) causes a large increase in sympathetic activity, which is responsible for several of the systemic and peripheral gastrointestinal symptoms [12]; this increase in turn can lead to changes in gi motility and in water and electrolyte absorption. similarly, madroszkiewicz et al [13] conducted a study to evaluate the effects of acute and chronic icp on gastric myoelectric activity and found that the most significant changes in gastric activity were 347 gastroparesis as a complication in the patient with traumatic brain injury observed in patients after severe traumatic brain injury with acute ih. pathophysiological aspects under normal conditions, food is liquefied in the stomach by the digestive action of gastric acid and antral contractions [14]. these antral contractions, essential for the crushing of solid food and gastric emptying, are mediated by extrinsic vagal innervation (gastric branches from the anterior and posterior vagal trunks) and intrinsic cholinergic neurons [14,15]. nitrergic neurons mediate intrinsic inhibitory mechanisms, which facilitate pyloric relaxation and intragastric peristalsis. these neurons are essential for gastrointestinal (gi) muscle relaxation prior to contraction, and are responsible for downstream inhibition prior to upstream contraction, which is induced by excitatory neurons (cholinergic neurons) [14]. these inhibitory and excitatory neuronal effects are transmitted through interstitial cells of cajal (icc), fibroblast-like cells (positive for platelet-derived growth factor receptor α pdgfrα), and smooth muscle cells of gi muscles. this causes the muscular layer of the stomach to behave like a multicellular electrical syncytium so that coordinated contractions, which are initiated in the proximal stomach and involve the entire circumference of the stomach, can propagate into the antropyloric region [14,16,17]. pdgfrα-positive iccs and fibroblast-like cells are considered to be the pacemaker cells of the gastrointestinal tract and possess the ability to transmit electrical signals (figure 1) [17]. in gastroparesis, delayed gastric emptying is associated with decreased antral motility and, in some patients, pyloric sphincter dysfunction due to neuromuscular dysfunction [14]. on the other hand, after traumatic brain injury, primary tissue damage (somatic and axonal) induced by mechanical damage to the brain causes the release of intracellular and intraaxonal contents, as well as the extravasation of blood products [18]. in response to this tissue damage, local activation of microglia occurs. at the same time that the local microglial inflammatory response occurs, brain infiltration and accumulation of peripheral immune cells is generated, which enter due to alterations in the blood-brain barrier after tbi [19]. these cells mediate inflammatory processes through the production of a variety of inflammatory cytokines, chemokines, adhesion molecules, reactive oxygen and nitrogen species, among others [18]. figure 1. mechanisms of antral motility, accommodation and gastric emptying. created by authors with biorender. some studies have shown reductions in the number of icc in the stomach body of patients with gastroparesis [20,21]. this reduction in icc could impair conduction of electrical activity through the electrical syncytium and thus interfere with coordinated gastric electrical rhythms, peristalsis and gastric emptying [14]. both the decrease in the number and damage of iccs in the stomach of some patients with gastroparesis have been associated with a decrease in the number of m2 antiinflammatory macrophages, which express the mannose receptor (cd206) and heme oxygenase 1 (ho1) and are responsible for mediating cellular repair. in this way, m2 macrophages protect neural tissue against the effects of oxidative stress and inflammation [14,20]. thus, a possible explanation for the occurrence of gastroparesis as a complication of an episode of tbi is that a decrease in the number or damage of icc in patients with a reduced number of m2 antiinflammatory macrophages would generate a deficiency in the protection of neural tissue against the effects of oxidative stress and inflammation. ultimately, these events could result in gastric intrinsic neural dysfunction, which would be the cause of gastroparesis 348 sandra marcela mass-ramirez, ivan david lozada-martinez, josé bohorquez-rivero et al. clinical and diagnostic considerations gp manifests itself through a wide array of signs and symptoms, including nausea (predominant symptom), vomiting, pain (burning or burning), early satiety, postprandial fullness, abdominal distension, bloating, and upper abdominal discomfort. gpassociated pain is mainly located in the epigastrium, is described as persistent or nocturnal, and is often reported after a meal (food-induced pain) [8,9]. the severity of gastroparesis is assessed by the degree of nutritional impairment or weight loss or by the degree of delayed gastric emptying (e.g., the proportion of food retained in the stomach for a given number of hours), which will be influenced by the method and foods used to test overall stomach function. similarly, there are several symptom severity scales to assess clinical signs and symptoms [14]. in the neurocritical patient with enteral feeding by nasogastric tube (ngt), increased gastric residuals and intolerance to enteral feeding are typically reported [9]. this delays adequate nutrition, favors aspiration of gastric contents and pneumonias, thus prolonging hospital stay, increasing medical costs and contributing to a higher risk of mortality [4, 6, 9]. diagnosis the diagnosis of gp is based on the presence of signs and symptoms and the demonstration of delayed gastric emptying. it should be emphasized that, before assessing gastric motor activity or emptying rate, it is necessary to exclude other possible causes of symptoms. generally, people in whom gp is suspected require upper endoscopy to exclude mechanical obstruction or ulcer disease. while endoscopy is often normal in patients with delayed gastric emptying, in severe cases, endoscopy may reveal food debris in the stomach, the so-called bezoarslaboratory tests should rule out water and electrolyte disorders, and glycemia and thyroid function should also be requested. subsequently, gastric motor function tests can be considered [8,9]. as previously mentioned, documentation of delayed gastric emptying is essential for a definitive diagnosis. the evaluation of gastric emptying includes a variety of methods [22-24]. currently, scintigraphy is the most widely used diagnostic technique and is considered the gold standard for documenting delayed gastric emptying; using this technique, a radioactive substance is administered and two-dimensional images show the emitted radiation [7, 24, 25]. carbon 13 (13c)-octanoic acid or 13c-acetic acid breath analysis is used in some institutions, but requires more time than the 1or 2hour scintigraphy tests [6, 8]. other diagnostic methods include ultrasound but depend on a specialized operator [6]. when gastric emptying tests are inconclusive, particularly in those patients with pronounced postprandial fullness or early satiety, measurements of gastric accommodation can also be estimated by validated methods such as positron emission tomography (pet/ct) and magnetic resonance imaging (mri), or by screening tests such as proximal stomach size on gastric scintiscan (taken immediately after ingestion of a radiolabeled meal) or by a water or nutritive drink loading test [26]. in the intensive care setting, the most commonly used method for assessing gastric emptying is the measurement of gastric residual volume (grv) [24,25], which can be accomplished by connecting a 50 ml syringe to an ngt and aspirating the residual contents. another way to measure vgr is to connect a drainage bag to the end of an ngt and lower the bag below chest level for 10 minutes [27]. delayed gastric emptying is often designated when the grv is 250 ml or more. however, factors such as patient position (low or high elevation from the head of the bed), feeding port tube location (deeper in the body of the stomach or near the gastroesophageal junction), and the internal diameter of the feeding tube (narrow or wide) may affect the grv [23,24]. therapeutic approach to gastroparesis in the setting of tbi the treatment of gp focuses on 2 pillars: 1) restoration of water and electrolyte balance, glycemic control, suspension of drugs that alter gastric motility (pro-gastroparasitics) and modifications in the diet provided, which should be low in volume and lower in calories, but with shorter intervals between servings [28]. higher kcal and weight meals are associated with longer emptying times. the diet should preferably be liquid and fat-free; fat intake releases cholecystokinin which can further delay gastric emptying. high fiber foods are recommended to prevent the formation of bezoars [6]. in patients with tbi, actual energy needs can be up to 60% higher than expected values [29]. therefore, it has been emphasized that, in terms of 349 gastroparesis as a complication in the patient with traumatic brain injury complications and survival, nutritional support is beneficial for neurocritical patients [30]. enteral nutrition instead of parenteral nutrition is generally the preferred means of nutritional support. it is indicated for maintaining and restoring electrolyte balance, in addition to providing nutritional [31]. enteral nutrition can be instituted through many routes, such as ngt and nasoenteric tubes, or by gastrostomy or jejunostomy that simultaneously decompresses the stomach and allows enteral nutrition [32]. particularly in patients with tbi, gp makes oral nutritional support difficult. to overcome the difficulties associated with gp, transpyloric placement of the feeding tube has been recommended [9, 33]. however, tube displacement and difficulties in passing the tube through the pylorus are common problems. in addition, the need for transpyloric feeding has been questioned, as it does not result in a significant decrease in complications [34]. therefore, strategies have been developed to improve gastric motility with intragastric enteral feeding. 2) the administration of drugs to stimulate and improve gastric emptying and reduce nausea and vomiting. several prokinetic agents have been shown to achieve this goal. these drugs increase antral contractility, correct gastric arrhythmias, and improve coordination of antroduodenal movements [6,28]. with recent advances in research on prokinetic agents, the following three categories of drugs are frequently used in gp patients. dopamine antagonists: metoclopramide is a dopamine antagonist with both central and peripheral activity [6]. it acts on dopaminergic (d2) and serotonergic (5-ht3) receptors, and stimulates the release of acetylcholine in myenteric plexus neurons [28]. in addition to its antiemetic effect, it has prokinetic activity [6]. it is more effective in shortterm treatments, no longer than 15 days [8]. the usual dose is 10 mg iv 3 or 4 times a day and the dose may be doubled in severe cases. although frequently used, it may cause neurological symptoms with longterm use [28]. side effects are related to central dopaminergic blockade causing sporadic acute dystonic reactions, facial spasms, parkinsonian symptoms and asthenia [6, 8, 28]. domperidone is another dopamine antagonist, but with peripheral activity only [6]. it has a prokinetic and antiemetic action and has a particularity, it does not cross the blood-brain barrier, therefore, it does not produce extrapyramidal side effects [28]. superior efficacy and tolerability have been suggested for domperidone over metoclopramide [35, 36]; therefore, it has been considered as the drug of choice. the dose is 10 mg distributed in 4-6 daily intakes [28]. like metoclopramide, it can produce hyperprolactinemia [6]. substituted benzamides: cisapride facilitates acetylcholine release from myenteric plexus neurons through a 5-ht4 receptor-mediated effect [6]. superior efficacy and tolerability have been suggested for cisapride over metoclopramide [37]. however, due to the increased risk of qt interval prolongation with cardiac arrhythmias, its use in routine clinical practice has been restricted [1]. cinatapride is another non-antiemetic prokinetic. it is a 5-ht4 receptor agonist. it facilitates the release of acetylcholine. unlike its predecessor cisapride it does not produce qt interval prolongation or severe cardiac arrhythmias. the usual dose is 1 to 2 mg distributed in two daily doses [28]. antibiotics: erythromycin is a macrolide that stimulates gastroduodenal motilin receptors. it is the most potent prokinetic, with a significant improvement in gastric emptying. however, it has no antiemetic action [6]. the dose is 300-750 mg/day distributed in 3-4 intakes, preferably iv [28]. due to its antibiotic properties, long-term use may lead to the induction of resistant strains. there are other possible side effects such as ototoxicity and pseudomembranous colitis, which limits long-term use in patients with gastroparesis. in addition, the problem of tachyphylaxis makes long-term use less attractive. concomitant hyperglycemia may interfere with or block its prokinetic property [28]. future perspectives traumatic brain injury remains a major cause of mortality, morbidity and economic burden worldwide, and will always be a frequent entity in neurocritical care settings, since its main causes are falls and motor vehicle accidents, which are events that occur on a daily basis in our environment [38,39]. in first world countries, there has been a trend towards reducing tbi incidences driven by 350 sandra marcela mass-ramirez, ivan david lozada-martinez, josé bohorquez-rivero et al. public health interventions such as seat belt legislation, helmet use, and workplace health and safety standards [38]. in underdeveloped countries, as is the case in latin america, these established prevention standards are not complied with by the majority of their inhabitants, which leads to a higher number of tbi cases in emergency departments. therefore, the appropriation and acquisition of knowledge on this subject is fundamental. knowing the pathophysiological aspects and degrees of severity would help to understand the mechanisms by which different complications occur after tbi, as well as to evaluate the good or bad prognosis of functional recovery and to anticipate the rehabilitation needs of patients. gastrointestinal alterations, in this case gastroparesis, as a complication associated with severe tbi is no exception, since there are large gaps in knowledge, its pathophysiology and inconsistencies among published studies on this subject. for this reason, neurogastroenterological research, which aims to improve the understanding of the physiology and pathophysiology of the digestive neurological subsystems from which functional symptoms arise, has aroused great interest within the scientific community. similarly, research on the relationship between gastroparesis and intracranial hypertension should be expanded, as it has been suggested that correction of these gastric abnormalities may facilitate the recovery of patients with brain lesions. on the other hand, neuronutrition is also a line of research that has gained strength in recent years, due to the importance of nutrition in patients with neurological disorders; it is necessary for the proper functioning of respiratory muscles, cardiac function, the balance of the coagulation cascade, electrolyte and hormone balance, and renal function, as well as influencing functional recovery and the overall cost of medical care. the need to identify and treat the patient with malnutrition or impaired gastrointestinal function is a critical aspect of patient management [40]. the above explains why research on gastroparesis in the context of tbi is essential to improve specific and overall patient outcomes with general involvement, and thus reduce the rate of secondary complications such as pulmonary aspiration or malnutrition, overall morbidity, mortality, and disability. conclusion traumatic brain injury remains a pathological condition with a considerable burden of disease worldwide. gastroparesis is a complication that substantially influences morbidity, mortality and disability in the traumatic brain injury patient by intervening in the nutrition process, among many others. although its pathophysiology is not clearly known, early treatment of its symptoms can substantially improve the prognosis. references 1. capizzi a, woo j, verduzco-gutierrez m. traumatic brain injury: an overview of epidemiology, pathophysiology, and medical management. med clin north am. 2020; 104(2):213-238. 2. traumatic brain injury and concussion. 2021. available at: https://www.cdc.gov/traumaticbraininjury/get_the_fa cts.html. accessed june 21, 2021. 3. cederberg d, hansson ha, visse e, siesjö p. antisecretory factor may reduce icp in severe tbi-a case series. front neurol. 2020; 11:95. 4. ott l, young b, phillips r, mcclain c, adams l, dempsey r, et al. altered gastric emptying in the head-injured patient: relationship to feeding intolerance. j neurosurg. 1991; 74(5):738-42. 5. altmayer t, o'dell mw, jones m, martin v, hawkins hh. cisapride as a treatment for gastroparesis in traumatic brain injury. arch phys med rehabil. 1996; 77(10):1093-4. 6. masaoka t, tack j. gastroparesis: current concepts and management. gut liver. 2009; 3(3):166-73. 7. stanghellini v, tack j. gastroparesis: separate entity or just a part of dyspepsia? gut. 2014; 63(12):1972-8. 8. parkman hp, hasler wl, fisher rs. american gastroenterological association technical review on the diagnosis and treatment of gastroparesis. gastroenterology. 2005; 127(5):1592–622. 9. frazer c, hussey l, bemker m. gastrointestinal motility problems in critically ill patients. crit care nurs clin north am. 2018; 30(1):109-121. 10. keshavarzia z, afsharic ar, mohammadzadehd n, mohebbie m, mohebbie m, mollazadeh h. traumatic brain injury and the gastrointestinal tract: the role of female sexual hormones. j endocrinol metab. 2017; 7(6):163-171. 11. kao ch, changlai sp, chieng pu, yen tc. gastric emptying in head-injured patients. am j gastroenterol. 1998; 93(7):1108-1112. 12. mcallister tw. neurobiological consequences of traumatic brain injury. dialogues clin neurosci. 2011; 13(3):287-300. 13. madroszkiewicz d, thor p, moskała m, madroszkiewicz e, gościński i. effects of intracranial hypertension on gastric myoelectrical activity evaluated by using clinical and 351 gastroparesis as a complication in the patient with traumatic brain injury radiological symptoms. neurol neurochir pol. 2005; 39(1):41-8. 14. camilleri m, chedid v, ford ac, haruma k, horowitz m, jones kl, et al. gastroparesis. nat rev dis primers. 2018; 4(1):41. 15. lucena af, tibúrcio rv, vasconcelos gc, ximenes jd, cristino filho g, graça rv. influence of acute brain injuries on gut motility. rev bras ter intensiva. 2011; 23(1):96-103. 16. sanders km, ward sm, koh sd. interstitial cells: regulators of smooth muscle function. physiol rev. 2014; 94(3):859-907. 17. wood jd. neuropathophysiology of functional gastrointestinal disorders. world j gastroenterol. 2007; 13(9):1313-32. 18. mcginn mj, povlishock jt. pathophysiology of traumatic brain injury. neurosurg clin n am. 2016; 27(4):397-407. 19. habgood md, bye n, dziegielewska km, ek cj, lane ma, potter a, et al. changes in blood-brain barrier permeability to large and small molecules following traumatic brain injury in mice. eur j neurosci. 2007; 25(1):231-8. 20. bernard ce, gibbons sj, mann is, froschauer l, parkman hp, harbison s, et al. association of low numbers of cd206-positive cells with loss of icc in the gastric body of patients with diabetic gastroparesis. neurogastroenterol motil. 2014; 26(9):1275-84. 21. stein dm, feather cb, napolitano lm. traumatic brain injury advances. crit care clin. 2017; 33(1):1-13. 22. nursal tz, erdogan b, noyan t, cekinmez m, atalay b, bilgin n. the effect of metoclopramide on gastric emptying in traumatic brain injury. j clin neurosci. 2007; 14(4):344-8. 23. camilleri m, parkman hp, shafi ma, abell tl, gerson l; american college of gastroenterology. clinical guideline: management of gastroparesis. am j gastroenterol. 2013; 108(1):18-37; quiz 38. 24. kar p, jones kl, horowitz m, chapman mj, deane am. measurement of gastric emptying in the critically ill. clin nutr. 2015; 34(4):557-64. 25. adike a, quigley em. gastrointestinal motility problems in critical care: a clinical perspective. j dig dis. 2014; 15(7):335-44. 26. orthey p, yu d, van natta ml, ramsey fv, diaz jr, bennett pa, et al. intragastric meal distribution during gastric emptying scintigraphy for assessment of fundic accommodation: correlation with symptoms of gastroparesis. j nucl med. 2018; 59(4):691-697. 27. kuppinger dd, rittler p, hartl wh, rüttinger d. use of gastric residual volume to guide enteral nutrition in critically ill patients: a brief systematic review of clinical studies. nutrition. 2013; 29(9):1075-9. 28. godoy d, panhke p, piñero g, videtta w, aguilera s. cuidados intensivos en trauma craneoencefálico grave. neuroc colomb. 2016; 23(3):193-234. 29. moore r, najarian mp, konvolinka cw. measured energy expenditure in severe head trauma. j trauma. 1989; 29(12):1633-6. 30. hadley mn, grahm tw, harrington t, schiller wr, mcdermott mk, posillico db. nutritional support and neurotrauma: a critical review of early nutrition in fortyfive acute head injury patients. neurosurgery. 1986; 19(3):367-73. 31. pesce m, borrelli o, saliakellis e, thapar n. gastrointestinal neuropathies: new insights and emerging therapies. gastroenterol clin north am. 2018; 47(4):877-894. 32. quigley em, o'mahony s, heetun z. motility disorders in the patient with neurologic disease. gastroenterol clin north am. 2011; 40(4):741-64. 33. thor pj, gościński i, kolasińska-kloch w, madroszkiewicz d, madroszkiewicz e, furgała a. gastric myoelectric activity in patients with closed head brain injury. med sci monit. 2003; 9(9):cr392-5. 34. spain da, deweese rc, reynolds ma, richardson jd. transpyloric passage of feeding tubes in patients with head injuries does not decrease complications. j trauma. 1995; 39(6):1100-2. 35. dumitrascu dl, weinbeck m. domperidone versus metoclopramide in the treatment of diabetic gastroparesis. am j gastroenterol. 2000; 95(1):316-7. 36. patterson d, abell t, rothstein r, koch k, barnett j. a double-blind multicenter comparison of domperidone and metoclopramide in the treatment of diabetic patients with symptoms of gastroparesis. am j gastroenterol. 1999; 94:1230–1234. 37. feldman m, smith hj. effect of cisapride on gastric emptying of indigestible solids in patients with gastroparesis diabeticorum: a comparison with metoclopramide and placebo. gastroenterology. 1987; 92:171–174. 38. khellaf a, khan dz, helmy a. recent advances in traumatic brain injury. j neurol. 2019; 266(11):2878-2889. 39. suchner u, senftleben u, eckart t, scholz mr, beck k, murr r, et al. enteral versus parenteral nutrition: effects on gastrointestinal function and metabolism. nutrition 1996; 12:13-22. 40. slone ds. nutritional support of the critically ill and injured patient. crit care clin. 2004; 20(1):135-57. microsoft word _3.formatata_iencean.doc romanian neurosurgery vol. xv nr. 2 13 vascular intracranial hypertension pathogenesis and treatment st.m. iencean1, a.v. ciurea2, i. poeata3 1neurosurgery, “prof dr nicolae oblu” hospital, iasi, romania 2clinical emergency hospital "bagdasar arseni” bucharest, the university of medicine and pharmacy “carol davila”, bucharest, romania 3clinical emergency hospital “prof dr nicolae oblu” iasi the umph “gr.t. popa”, iasi, romania intracranial hypertension can occur in cerebral-vascular illnesses due to sanguine, cerebral or extra-cerebral circulatory disorders, which modify the dynamics of the intracranial fluids and cause the intracranial pressure increase. the volume of the cerebral parenchyma increases due to the modifications occurred at the level of the cerebral sanguine capillaries, which leads to: the occurrence of the extracellular brain edema and cerebral congestive edematization with an increase in the volume of the cerebral parenchyma by vascular dilatation. the vascular types of intracranial hypertension have characteristic etiologies and they occur in thrombophlebites and cerebral venous thrombosis, in hypertensive encephalopathy and during the ischemic stroke. keywords: cerebral venous thrombosis, hypertensive encephalopathy, intracranial hypertension, ischemic stroke introduction intracranial hypertension can occur in cerebralvascular illnesses due to sanguine, cerebral or extracerebral circulatory disorders, which modify the dynamics of the intracranial fluids and cause the intracranial pressure increase. there are disorders in the auto-regulation of the cerebral hemodynamics and the cerebral parenchyma volume continues to increase due to the brain edema or to the increase in the cerebral sanguine volume (brain swelling ) with the secondary increase in the intracranial pressure. [4, 15, 26] the volume of the cerebral parenchyma increases due to the modifications occurred at the level of the cerebral sanguine capillaries, which leads to: the occurrence of the extracellular brain edema due to the increased quantity of interstitial fluid: extracellular edema produced by a hydrostatic mechanism (ultra-filtration) in severe arterial hypertension, extracellular edema with oncotic induction (vasogenic edema) due to an increased permeability of the brain blood barrier (open brain-blood barrier) cerebral congestive edematization with an increase in the volume of the cerebral parenchyma by vascular dilatation. the vascular types of intracranial hypertension have characteristic etiologies and they occur by: slowing down or decreasing the intracranial venous flux in thrombophlebites and cerebral venous thrombosis, the decrease in the venous flux at the level of the superior longitudinal sinus (sls) directly in compressive lesions (hollowing fracture, etc.) or in sls shunting by an intracranial arterial-venous malformation, or the extra-cranial illnesses that block the returning venous circulation at the cervical level, reduce the cerebral venous drainage and cause the decrease in the absorption of the cranial-spinal fluid and then the occurrence of the brain edema. st.m. iencean romanian neurosurgery vol. xv nr. 2 14 in hypertensive encephalopathy, when the hydrostatic brain edema occurs (by ultra-filtration), as well as a brain swelling (by vasodilatation). the cerebral ischemia or the ischemic stroke reduces the arterial sanguine contribution and causes an ischemic brain edema, which is a mixed brain edema, both a cellular edema (cytotoxic) and an extracellular brain edema with oncotic induction (vasogenic). [26, 27, 46, 49] cerebral venous thrombosis the cerebral venous drainage is slowed-down or even stopped in illnesses that influence the intracranial venous circulation or on extra-cranial conditions that may interest the great vessels at the level of the throat, usually by compression from vicinity. [5, 6, 7, 8, 26] the cerebral venous circulation is reduced in: cerebral thrombophlebites and superficial venous thrombosis, thrombosis of dural sinuses, thrombosis of the profound venous system, and thrombosis of the cavernous sinus. [11, 12, 16] the thrombotic venous occlusion is more frequent in the following etiological situations: infections (usually, the local infections are: otitis, sinusitis, etc., also in the case of meningitis). mastoiditis may produce the thrombosis of the venous sinuses with a syndrome of secondary intracranial hypertension, an entity that symonds describes as “otitic hydrocephalus”, tumor lesions at the level of the sinus, with its infiltration and obstruction (especially in meningiomas), when the tumor development is not responsible for the occurrence of ich, traumatic brain injury, pregnancy and puerperium, etc. the calcifications of the sinus extended scythe have a reduced incidence (figure). the frequency of the impacts on the dural sinuses and of other cerebral veins is as follows: the thrombosis of the sagittal sinus and of the lateral sinuses is happens in 75 – 85 % of cases the thrombosis of the superficial cortical veins occurs in approximately 10 – 15 % of cases, the thrombosis of the profound cerebral veins occurs in approximately 5 – 10 % of cases, and the thrombosis of the cavernous sinus occurs in less than 5 % of cases. cerebral venous thrombosis reduce the returning venous circulation from the brain and the skull, a venous stasis is produced and the cerebral sanguine circulation is slowed down. there are areas of cerebral hypo-anorexia concomitantly to areas of venous congestive edematization, and the cellular cerebral (cytotoxic) edema occurs, as well as the oncotic extracellular (vasogenic) edema, which evolves to a mixed brain edema. [20, 21, 22, 32, 33] the venous sinuses also ensure the resorption of the cerebrospinal fluid, and the thrombosis of the venous sinuses leads to a diminished drainage of the cerebrospinal fluid. therefore, a progressive intraventricular accumulation of cerebrospinal fluid occurs, with a pressure increase in the ventricular system and the occurrence of the hydrocephalic brain edema. these phenomena happen slowly, in varied successions, but the evolution is progressive towards an intracranial pressure increase. the iatrogenic thrombosis of the internal jugular veins is quoted in cases of prolonged use of the jugular catheters for the intravenous administration of medication. in such cases, the same pathogenic processes occur, and the ich syndrome may appear. the symptomatology is caused by the initial causal lesion, after which neurological focal symptoms may occur related to the progression of the venous thrombosis, as well as symptoms caused by the intracranial pressure increase. a venous infarct often happens, which is associated to a cerebral hemorrhage, which also aggravates the neurological clinical presentation. usually, the clinic evolves to an incomplete or complete syndrome of intracranial hypertension. [34, 37, 39, 41, 42, 52] the main characteristics of the intracranial pressure increase in cerebral venous thrombosis are: -a slow increase in the intracranial pressure up to the normal limit value of 20 mm hg, usually during a period of a few days, vascular intracranial hypertension romanian neurosurgery vol. xv nr. 2 15 -over the value of 20 mm hg, the icp increase continues to be progressive, and it may reach maximum values of approximately 30 mm hg in a few hours or days. this gradual increase allows the compensating mechanisms to act more efficiently, and also for the applied therapy to encourage the intracranial pressure decrease and the improvement of the cerebral sanguine circulation. the maximum values that may be reached in cases of intracranial hypertension syndrome are of approximately 3035 mm hg (sometimes the maximum values may be of 40 mm hg) and the pathological pressure values may last for several weeks, with a slow return to normal pressure values and period of intermittent increases, usually, there is a recurrence to intracranial pressure values of about and above 20 mm hg, which causes the persistency of a prolonged attenuated symptomatology. the treatment of the venous thrombosis with an ich syndrome is as follows: etiological and pathogenic for the vascular disorder, when possible, pathogenic for the intracranial hypertension syndrome. a particular pathogenic mechanism is the reduction of the venous flux at the level of the superior longitudinal sinus (sls) with an important blockage of the cerebrospinal fluid resorption: in the case of arterial-venous malformations with the excitation of the galien vein (galien vein aneurisms), when there is a sls shunting by malformation and the cerebrospinal fluid resorption is diminished by the occurrence of the hydrocephalus. in infants and small children, the dominating symptomatology is the cardiac disorder due to the increased venous return, while the ich syndrome also occurs in older children. in the case of a median intrusive cranial fracture, which interests the third posterior part of the sls. at children with craniostenoses, there may be anomalies of the venous drainage, which interests the sigmoid sinus and the jugular vein, which may cause a venous hypertension, with a diminished drainage of the cerebrospinal fluid and the increase in the intracranial pressure. usually, the phenomenon occurs up to the age of 6 years old, after which a collateral venous drainage is developed by the stylomastoid plexus, leading to the normalization of the intracranial pressure. fig. 1 cranial pressure increase in cerebral venous thrombosis: to = start of the cerebral venous thrombosis t1 = the moment when the normal limit value of 20 mm hg is reached t2 = after the progressive increase in the intracranial pressure, the maximum values of approximately 30 – 35 mm hg are reached t3 = the moment when, after a varied period of increased pressure values, the icp begins to decrease progressively, usually after treatment ∆ t1 = t1 – to: the period of intracranial pressure increase up to the normal limit value of 20 mm hg, which usually lasts for a few days ∆ t2 = t2 – t1: the icp increase period up to the maximum value, which may last for several hours to several days ∆ t3 = t3 – t2: the period of time of maximum intracranial pressure values, which usually last for several weeks. st.m. iencean romanian neurosurgery vol. xv nr. 2 16 a b c fig. 2 calcifications at the level of the brain scythe (a), extended towards the superior longitudinal sinus (b), bilateral (c), with a slowing-down of the venous drainage, a decreased resorption of the cerebrospinal fluid and an ich syndrome hypertensive encephalopathy high blood pressureis the most important predisposing factor for cerebral-vascular illnesses, and the most frequent complication is the cerebral hemorrhage. the exaggerated increase in the values of the systemic blood pressure also causes disorders of the cerebral circulation auto-regulation, with other secondary cerebral suffering. hypertensive encephalopathy is defined in the clinical presentationof induced intracranial hypertension by an acute episode of arterial hypertension. [4, 15, 26] 1. the acute hypertensive encephalopathy is caused by the acute blood pressure increase in: severe high blood pressure, uncontrolled/untreated high blood pressurein pregnancy (eclampsia), high blood pressure in glomerulonephritis, pheochromocytoma, etc. the acute increase in the sanguine pressure values leads to the inefficiency of the cerebral vascular autoregulation, a generalized cerebral vascular dilatation occurs and/or there is an increased permeability of the cerebral capillaries. the increased permeability in the brain blood barrier has been constant more frequently at the level of the gray matter. therefore, the increase in the volume of the cerebral parenchyma is caused by: brain swelling by vasodilatation, hydrostatic extracellular brain edema, by ultrafiltration when the brain blood barrier is intact (close brain-blood barrier) oncotic (vasogenic) extracellular brain edema by an injury of the brain blood barrier (open brain-blood barrier). the posterior reversible encephalopathy syndrome (pres) or the reversible posterior leucoencephalopathy syndrome (rpls) with a hypertensive etiology is included in the acute form of vascular etiopathogeny ich. the clinical presentationis typical and the dwi exploration shows an extracellular brain vascular intracranial hypertension romanian neurosurgery vol. xv nr. 2 17 edema by the increase in the water mobility with a posterior bilateral location, and a sub-cortical interest in the white matter too. the treatment consists of decreasing the systemic blood pressure. [26, 27, 31, 53] 2. the chronic hypertensive encephalopathy (binswanger encephalopathy) is a rare cerebralvascular illness with a chronic extracellular brain edema: hydrostatic brain edema combined with the oncotic brain edema. the intracranial pressure increase in acute hypertensive encephalopathies are characterized by: the relatively high speed with which the intracranial pressure reaches the normal threshold value in approximately a few hours the icp continues to increase above the normal values for a period that is usually shorter than the previous interval, of few hours only the maximum values that the icp may reach are of 30 50 mm hg and the period with pathologic intracranial pressure values is usually of several hours, rarely of several days. the anti-hypertensive treatment improves the clinical condition. the unmonitored hypertensive patients, or those who are incompletely treated may present repeated episodes of hypertensive encephalopathy, or they may suffer from the most frequent complication, which is the cerebral hemorrhage. the clinical evolution of hypertensive encephalopathy is up to an incomplete syndrome of intracranial hypertension, and it has a regressive aspect. in the pathogeny of the syndrome, there is an auto-limiting mechanism: the intracranial pressure increase caused by the increase in the sanguine blood pressure and by occurrence of the cerebral vasodilatation generated the collapse of the walls of the intracranial sanguine vessels, and, to a certain extent, to a diminished cerebral sanguine volume. the mechanism consists of the direct action of the increased intracranial pressure over a functional disorder that is secondary to the exceeded autoregulation of the cerebral circulation, and it has a limited value. the treatment of the hypertensive encephalopathy is both etiologic and pathogenic: the treatment of the hypertensive episode, as an etiologic aspect, and the pathogenic treatment of the intracranial hypertension syndrome. fig. 3 intracranial pressure increase in hypertensive encephalopathy: to = beginning of the increase in the sanguine blood pressure t1 = the moment when the normal icp limit value is reached t2 = the moment when the icp has the maximum value t3 = beginning of the decrease in the intracranial pressure values ∆ t1 = t1 – to: period of icp increase up to the normal limit; it lasts for several hours ∆ t2 = t2 – t1: the icp increase period to the maximum values, lasting for several hours ∆ t3 = t3 – t2: the period when the pathologic icp values are maintained, usually of a few hours; it is rarely prolonged to a few days; the causal treatment of the high blood pressureis efficient. ischaemic stroke the cerebral ischemia is caused by the cerebral circulatory insufficiency, which may be chronic or acute. [1, 2, 3, 9, 11] the acute cerebral circulatory insufficiency or the ischemic stroke can manifest itself as: transitory ischemic stroke, progressive ischemic stroke, regressive ischemic stroke, st.m. iencean romanian neurosurgery vol. xv nr. 2 18 complete ischemic stroke or the cerebral infarct. the cerebral infarct can be of a thrombotic or embolic nature. the ischemic stroke represents 85 % of the cerebral-vascular illnesses. the large ischemic cerebral lesions are accompanied by the brain edema with cerebral herniation (sub-falciform) and by the intracranial pressure increase. [13, 14, 15, 17] there are multiple causes of the ischemic cerebral vascular accidents: vascular illnesses: carotid atherosclerosis, infectious arteriopathies, posttraumatic occlusions of internal carotid arteries, of vertebral arteries or of middle cerebral arteries, arterial compressions at the cervical level, various vasculopathies, cerebral embolism of a cardiac nature – which represents approximately 60 70 % of the cerebral embolism cases: in the case of a mitral illness with atrial fibrillation, coronary thrombosis, paradoxical embolisms, infectious endocardites, etc. there may be rare cases of: hyper-coagulability, policitemia vera, etc. the extended cerebral ischemic infarct with phenomena of intracranial hypertension is caused by the occlusion or stenosis of a great cerebral artery: the internal carotid artery or a terminal branch that irrigates a vast territory, such as the middle cerebral artery. the extended ischemic infarct of the sylvian artery occurs in approximately 10 % of the patients with acute cerebral circulatory insufficiency, and it has been designated as the malign infarct of the sylvian artery due to the increased mortality, of up to 80 % of cases, despite the therapeutic means used. [1, 17, 18, 19, 24, 25] the massive cerebellum ischemic infarct can cause the collapse of the 4th ventricle with the occurrence of an acute obstructive hydrocephalus and an acute ich syndrome, and it has a direct compressive effect on the brainstem with the manifestation of vegetative disorders. in the case of the cerebral hemispheric ischemic stroke, the decreased sanguine flow in the territory of the middle cerebral artery leads to the occurrence of certain ischemic metabolic disorders at the level of the affected cerebral parenchyma. the permeability of the cerebral capillaries increases (open brain-blood barrier) and the extracellular oncotic (vasogenic) edema occurs. the evolution is usually a rapid one, with the extension of the brain edema, the increase in the intracranial pressure and the occurrence of the subfalciform cerebral hernia (median line movement towards the unaffected cerebral hemisphere). although the intracranial pressure increasing mechanism is based on the cerebral ischemia with a hypoxic brain edema, which is characteristic for the parenchymatous lesions, while the etiology is represented by the impacts on a great cerebral artery, and it includes the ischemic stroke on vascular intracranial hypertension. [26, 28, 29, 30, 35] since the moment of the arterial occlusion, the intracranial pressure increase is: rapid until it reaches the normal pressure limit of 20 mm hg, by the progression of the brain edema and the surpassing of the pressure compensating possibilities, with a duration of up to several hours above the normal pressure values, the icp increase is also a rapid one, and the maximum values are reached within a short interval of time: half an hour – several hours the maximum values of the intracranial pressure are of approximately 40 – 50 mm hg and the duration of these pathological values is of several days and it corresponds to the intensive care period. fig. 4 malign infarct of left sylvian artery with important ischemic brain edema and sub-falciform cerebral herniation (by cardiac rhythm disorder) vascular intracranial hypertension romanian neurosurgery vol. xv nr. 2 19 fig. 5 complete infarct of left sylvian artery (traumatic occlusion at the level of the throat, strangulation) the evolution is rapid towards the decompensation of the intracranial hypertension with almost 80% unfavorable results despite the applied treatments. there is an attempt in using the etiological treatment of the arterial obstruction and the pathogenic treatment for the ich syndrome. during the first three hours from the beginning, there may be an intravenous administration of recombined tissue plasminogen activator (rtpa) in a dose of 0.9 mg/kg, maximum 90 mg; the administration of streptokinase or of other thrombolytic agents does not have the same efficiency as rtpa. the brain edema receives a pathogenic treatment with osmotic diuretics (mannitol), and hyperventilation if there is an imminent decompensation of intracranial hypertension and the production of a brain herniation etc. [1, 35, 36, 38, 40, 43, 47]. sometimes, there is an attempt of a surgical intervention: decompressive craniectomy of posterior cerebral fosse and of evacuation of a cerebellum infarct with a compressive effect on the brainstem, perhaps with a ventricular drainage, decompressive craniectomy and the evacuation of a cerebral hemispheric massive infarct, which may diminish the intracranial hypertension, but the surviving patients is left with major neurological deficits. a particular case of generalized cerebral ischemia is met in the post-resuscitation syndrome when the sanguine flux disorder includes the entire brain, with a complete ischemia throughout the stroke, followed by reperfusion disorders.[26, 48, 50, 51, 54, 55] the consequence of this cerebral circulatory failure, primary – before and during cardiopulmonary resuscitation, and secondary ischemic damage, during reperfusion is the development of the mixed brain edema: both cytotoxic and vasogenic, concomitantly to the production of the glial-neuronal necrosis. the hyperemic reperfusion may exacerbate the brain edema. the mixed brain edema accentuates the elevated intracranial pressure and it exacerbates the brain injury. the treatment is complex and the results do not compensate the efforts. fig. 6 characteristics of the intracranial pressure increase in the ischemic stroke: to = the moment when the arterial occlusion happens t1 = the moment when the normal icp limit value is reached t2 = the moment when the icp value is at maximum, of approximately 40 – 50 mm hg t3 = the moment when the icp begins to decrease; the icp value diminishing is rare in the sylvian malign ischemic stroke ∆ t1 = t1 – to: the icp increasing period up to the maximum normal value; it lasts for several hours ∆ t2 = t2 – t1: the period when icp reaches the maximum values, lasting for a half an hour – one hour ∆ t3 = t3 – t2: the period when the pathological icp values are maintained; it may last for several days. the table below includes a comparative presentation of the three forms of vascular intracranial hypertension. st.m. iencean romanian neurosurgery vol. xv nr. 2 20 table 1 etio-pathogenic and evolutionary characteristics of the various forms of vascular ich cerebral venous thrombosis hypertensive encephalopathy ischemic stroke cerebral vascular pathology: thrombosis of dural sinuses thrombosis of cortical veins cerebral vascular pathology: dilatation of cerebral arteries cerebral vascular pathology: infarct of sylvian artery massive cerebellum infarct cerebral blood flow : reduced venous outflow cerebral blood flow : increase arterial inflow cerebral blood flow : reduced arterial inflow pathogenesis: venous dilatation; open bbb and vasogenic brain edema and diminished csf drainage with hydrocephalic brain edema pathogenesis: dilatation of cerebral vessels; closed bbb and hydrostatic brain edema, and increased vascular permeability with open bbb and vasogenic brain edema pathogenesis: ischemic increased capillary permeability; open bbb and vasogenic brain edema icp increase: slow to the normal limit slow above the normal limit icp increase: rapid to the normal limit slow above the normal limit icp increase: rapid to the normal limit rapid above the normal limit sub-acute and chronic evolution possible decompensation acute and sub-acute evolution rarely decompensation acute evolution usually decompensation pathogenic treatment pathogenic and etiologic treatment etiologic and pathogenic treatment, decompressive craniectomy references 1. albers gw, bates ve, clark wm, bell r, verro p, hamilton sa. intravenous tissue-type plasminogen activator for treatment of acute stroke: the standard treatment with alteplase to reverse stroke (stars) study. jama. 2000; 283: 1145–1150. 2. alberts mj, hademenos g, latchaw re, et al. recommendations for the establishment of primary stroke centers: brain attack coalition. jama. 2001; 283: 3102–3109. 3. asil t, uzunca i, utku u, berberoglu u. monitoring of increased intracranial pressure resulting from cerebral edema with transcranial doppler sonography in patients with middle cerebral artery infarction. j ultrasound med. 2003;22(10):1049-53 4. bateman ga. vascular hydraulics associated with idiopathic and secondary intracranial hypertension. am j neuroradiol. 2002; 23(7):1180-6. 5. bergui m, bradac gb. clinical picture of patients with cerebral venous thrombosis and patterns of dural sinus involvement. cerebrovasc dis. 2003;16(3):211-6. 6. biousse v, tong f, newman nj. cerebral venous thrombosis. curr treat options neurol. 2003;5 (5):409-420. 7. brandt t, pessin ms, kwan es, caplan lr. survival with basilar artery occlusion. cerebrovasc dis. 1995; 5: 182–187. 8. brandt t, von kummer r, muller-kuppers m, hacke w. thrombolytic therapy of acute basilar artery occlusion: variables affecting recanalization and outcome. stroke. 1996; 27: 875–881. 9. brott t, bogousslavsky j. treatment of acute ischemic stroke. n engl j med. 2000; 343: 710–722. 10. brown mm. surgical decompression of patients with large middle cerebral artery infarcts is effective: not proven. stroke. 2003;34(9):2305-6. 11. carter bs, ogilvy cs, candia gj, rosas hd, buonanno f. one-year outcome after decompressive surgery for massive nondominant hemispheric infarction. neurosurgery. 1997; 40: 1168–1175. 12.chopko bw, kerber c, wong w, georgy b. transcatheter snare removal of acute middle cerebral artery thromboembolism: technical case report. neurosurgery. 2000; 40: 1529–1531. 13.christou i, alexandrov av, burgin ws, et al. timing of recanalization after tissue plasminogen activator therapy determined by transcranial doppler correlates with clinical recovery from ischemic stroke. stroke. 2000; 31: 1812–1816. 14.coull bm, williams ls, goldstein lb, et al. anticoagulants and antiplatelet agents in acute ischemic stroke. stroke. 2002; 33: 1934–1942. 15.cruz j, minoja g, okuchi k. major clinical and physiological benefits of early high doses of mannitol for intraparenchymal temporal lobe hemorrhages with abnormal pupillary widening: a randomized trial. neurosurgery. 2002;51(3):628-37. 16.cumurciuc r, crassard i, sarov m, valade d, bousser mg.headache as the only neurological sign of cerebral venous thrombosis: a series of 17 cases. j neurol neurosurg psychiatry. 2005; 76(8):1084-7. 17.demchuk am, burgin ws, christou i, et al. thrombolysis in brain ischemia (tibi) transcranial doppler flow grades predict clinical severity, early recovery, and mortality in patients treated with intravenous tissue plasminogen activator. stroke. 2001; 32: 89–93. vascular intracranial hypertension romanian neurosurgery vol. xv nr. 2 21 18.demchuk am, tanne d, hill md, et al. predictors of good outcome after intravenous tpa for acute ischemic stroke. neurology. 2001; 57: 474–480. 19.diener hc, ringelstein eb, von kummer r, et al. treatment of acute ischemic stroke with the low-molecular-weight heparin certoparin: results of the topas trial: therapy of patients with acute stroke (topas) investigators. stroke. 2001; 32: 22–29. 20.eckstein hh, schumacher h, dorfler a, et al. carotid endarterectomy and intracranial thrombolysis: simultaneous and staged procedures in ischemic stroke. j vasc surg. 1999; 29: 459– 471. 21.farb ri, vanek i, scott jn, mikulis dj, willinsky ra,et al idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis. neurology. 2003 13;60(9):1418-24. 22.ferro jm, canhao p, bousser mg, et al cerebral vein and dural sinus thrombosis in elderly patients. stroke. 2005;36(9):1927-32 23.ferro jm, lopes mg, rosas mj, et al delay in hospital admission of patients with cerebral vein and dural sinus thrombosis. cerebrovasc dis. 2005;19(3):152-6. 24.fraser jf, hartl r. decompressive craniectomy as a therapeutic option in the treatment of hemispheric stroke. curr atheroscler rep. 2005;7(4):296-304. 25.hajat c, hajat s, sharma p. effects of poststroke pyrexia on stroke outcome: a meta-analysis of studies in patients. stroke. 2000; 31: 410–414. 26.iencean st m a new classification and a synergetical pattern in intracranial hypertension. medical hypotheses, 2002;58(2):159-63. 27.iencean st m vascular intracranial hypertension, j med sciences 2004. 4, 4 : 276 – 281 28.jansen o, schellinger p, fiebach j, hacke w, sartor k. early recanalisation in acute ischaemic stroke saves tissue at risk defined by mri. lancet. 1999; 353: 2036–2037. 29.kakinuma k, ezuka i, takai n, yamamoto k, sasaki o. the simple indicator for revascularization of acute middle cerebral artery occlusion using angiogram and ultra-early embolectomy. surg neurol. 1999; 51: 332–341. 30.kalafut ma, schriger dl, saver jl, starkman s. detection of early ct signs of >1/3 middle cerebral artery infarctions: interrater reliability and sensitivity of ct interpretation by physicians involved in acute stroke care. stroke. 2000; 31: 1667–1671. 31.kanazawa m, sanpei k, kasuga k. recurrent hypertensive brainstem encephalopathy.j neurol neurosurg psychiatry. 2005;76(6):888-90. 32.kasper gc, wladis ar, lohr jm, et al. carotid thromboendarterectomy for recent total occlusion of the internal carotid artery. j vasc surg. 2001; 33: 242–250. 33.kidwell cs, saver jl, mattiello j, et al. thrombolytic reversal of acute human cerebral ischemic injury shown by diffusion/perfusion magnetic resonance imaging. ann neurol. 2000; 47: 621 34.king jo, mitchell pj, thomson kr, et al: cerebral venography and manometry in idiopathic intracranial hypertension. neurology,45:2224–2228, 1995 35.von kummer r, nolte pn, schnittger h, thron a, ringelstein eb. detectability of cerebral hemisphere ischaemic infarcts by ct within 6 h of stroke. neuroradiology. 1996; 38: 31–33. 36.kuo jr, lin cl, chio cc, wang jj, lin mt. effects of hypertonic (3%) saline in rats with circulatory shock and cerebral ischemia after heatstroke. int care med. 2003;29(9):1567-73. 37.linskey me, sekhar ln, hecht st. emergency embolectomy for embolic occlusion of the middle cerebral artery after internal carotid artery balloon test occlusion: case report. j neurosurg. 1992; 77: 134–138. 38.mathew p, teasdale g, bannan a, oluoch-olunya d. neurosurgical management of cerebellar haematoma and infarct. j neurol neurosurg psychiatry. 1995; 59: 287–292. 39.mccormick pw, spetzler rf, bailes je et. al thromboendarterectomy of the symptomatic occluded internal carotid artery. j neurosurg. 1992; 76: 752–758. 40.melgar ma, rafols j, gloss d, diaz fg. postischemic reperfusion: ultrastructural blood-brain barrier and hemodynamic correlative changes in an awake model of transient forebrain ischemia. neurosurgery. 2005;56(3):571-81. 41.owler bk, besser m. extradural hematoma causing venous sinus obstruction and pseudotumor cerebri syndrome. childs nerv syst. 2005;21(3):262-4. 42.owler bk, parker g, halmagyi gm, pseudotumor cerebri syndrome: venous sinus obstruction and its treatment with stent placement. j neurosurg. 2003;98(5):1045-55. 43.oyelese aa, steinberg gk, huhn sl, wijman ca. paradoxical cerebral herniation secondary to lumbar puncture after decompressive craniectomy for a large space-occupying hemispheric stroke: case report. neurosurgery. 2005;57(3):e594 44.phatouros cc, higashida rt et al. endovascular stenting of an acutely thrombosed basilar artery: technical case report and review of the literature. neurosurgery. 1999; 44: 667–673. 45.rajpal s, niemann db, turk as. transverse venous sinus stent placement as treatment for benign intracranial hypertension in a young male: case report and review of the literature. j neurosurg. 2005;102(3 suppl):342-6. 46.santarius t, menon dk. images in clinical medicine. carotidartery thrombosis secondary to basal skull fracture. n engl j med. 2003 , 31;349(5):e5. 47.schlaug g, benfield a, baird ae, et al. the ischemic penumbra: operationally defined by diffusion and perfusion mri. neurology. 1999; 52: 1528–1537. 48.schwab s, hacke w. surgical decompression of patients with large middle cerebral artery infarcts is effective. stroke. 2003;34(9):2304-5. 49.sindou m, auque j, jouanneau e. neurosurgery and the intracranial venous system. acta neurochir suppl. 2005;94:167-75. 50.steiger h-j. outcome of acute supratentorial cerebral infarction in patients under 60: development of a prognostic grading system. acta neurochir. 1991; 111: 73–79. 51.suh dc, sung kb, cho ys, et al. transluminal angioplasty for middle cerebral artery stenosis in patients with acute ischemic stroke. am j neuroradiol. 1999; 20: 553–558. 52.tamimi a, abu-elrub m, shudifat a et al. superior sagittal sinus thrombosis associated with raised intracranial pressure in closed head injury with depressed skull fracture. pediatr neurosurg. 2005;41(5):237-40. 53.tsumoto t, miyamoto t, shimizu m, et al. restenosis of the sigmoid sinus after stenting for treatment of intracranial venous hypertension: case report. neuroradiology. 2003;45(12):911-5. 54.walters bb, ojemann rg, heros rc. emergency carotid endarterectomy. j neurosurg. 1987; 66: 817–823. 55.yoshimoto y, kwak s. superficial temporal artery-middle cerebral artery anastomosis for acute cerebral ischemia: the effect of small augmentation of blood flow. acta neurochir. 1995; 137: 128–137. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article postraumatic pneumorrhachis: report of three cases and classification proposal huber s. padilla-zambrano, jessica amaya-quintero, ramos-villegas yancarlos, luis rafael moscote-salazar, willem guillermo calderon-miranda, joulen mo-carrascal, johanna maraby, amit agrawal colombia, mexico, india doi: 10.1515/romneu-2017-0064 394 | padilla-zambrano et al postraumatic pneumorrhachis doi: 10.1515/romneu-2017-0064 postraumatic pneumorrhachis: report of three cases and classification proposal huber s. padilla-zambrano1, jessica amaya-quintero1, ramosvillegas yancarlos1, luis rafael moscote-salazar2, willem guillermo calderon-miranda3, joulen mo-carrascal1, johanna maraby1, amit agrawal4 1university of cartagena, cartagena, colombia 2neurosurgery, universidad de cartagena, colombia 3resident of radiology, national autonomous university of mexico, mexico city, mexico 4department of neurosurgery, narayna medical college hospital, chinthareddypalem nellore, andhra pradesh, india abstract: the pneumorrhachis is the presence of air at the level of the spinal canal. it can have several causes among which are: traumatic, iatrogenic among others. clinical cases: we present three cases of male patients handled by our neurosurgery service with traumatic pneumorrhachis patients, which were managed in a conservative manner, with control images. conclusions: pneumorrhachis has traditionally been classified as internal if air is present in the subdural or subarachnoid space and external if the air is located at the epidural level. we propose a classification in degrees (moscote-agrawalpadilla) which is more practical from the clinical and radiological point of view. key words: pneumorrhachis, spinal neurotrauma, spinal cord introduction the term pneumorrhachis (pr) refers to the presence of air in the spinal canal, is a rare phenomenon with a varied etiology, being the posttraumatic pr the least frequent. (1) in most cases, it is asymptomatic, but may have symptoms that are related to its cause. (2) they are usually diagnosed incidentally in imaging studies such as computed tomography and magnetic resonance imaging. (3) pr has been described in various pathologies. knowledge of this is critical for the emergency physician and neurosurgeon. we present three cases and make a proposal of tomographic classification. illustrative cases case report 1 a 30-year-old male patient, with no relevant history, received a gunshot wound in the cervical region. a cervical ct scan revealed romanian neurosurgery (2017) xxxi 3: 394 398 | 395 the presence of c4 fracture and cervical pneumorrhach. the patient presented complete spinal cord injury. it was handled conservatively, did not present cerebrospinal fluid fistula or neuroinfection (figure 1). case report 2 a 28-year-old male patient, who presented during a fight, trauma with sharp object at the dorsal level. presenting neurological deficit at the t6 sensitive level, with loss of sphincters and paraplegia that is interjected as a complete medullary section. ct scan of the cervical, dorsal and lumbar spine is evidenced by p pneumorrhachis at t5 level (figure 2). the patient did not improve clinically. handled conservatively, without cerebrospinal fluid fistula. he was sent home at 20 days, continues to receive intensive rehabilitation. case report 3 a 40-year-old male patient with no morbid history. presenting trauma in the lumbar region with forceful object, evaluated by neurosurgery, is performed lumbar ct scan that as a pathological finding was observed lumbar spine ct scan showing evidence of pneumorrhachis at the level of l3 (figure 3). the patient was managed conservatively. he was sent home at 48 hours. figure 1 cervical spine ct scan showing pneumorrhachis at the height of c7 figure 2 dorsal spine ct scan showing evidence of pneumorrhachis at t5 figure 3 lumbar spine ct scan showing pneumorrhachis at the height of l3 396 | padilla-zambrano et al postraumatic pneumorrhachis discussion the pneumorrhachis pr is a condition characterized by the presence of air in the spinal canal, either in the epidural, subdural or subarachnoid space. (3, 4) initially it was described in 1977 by gordon et al. under various terms such as: intraspinal pneumocele, spinal, subdural or subarachnoid pneumatosis; spinal and epidural emphysema, air myelogram, among others. (4, 5) but the term "pneumorrhachis" was coined by newbold et al. in 1987. (2, 6) this is classified as intradural and extradural considering the anatomical location of the air within the spinal canal. (2, 3, 5) extradural pr is generally harmless, whereas intradural pr is associated with major trauma, and is considered a marker of serious injury. (3, 7) various conditions may directly or indirectly produce pr, including trauma, respiratory complications, factors that produce high intrathoracic pressure and barotraumas, or may occur spontaneously. in some cases, the conditions and lesions caused by pr are not detectable. (5, 8) accordingly, pr can be etiologically classified as iatrogenic, non-traumatic, and traumatic. among the causes for iatrogenic lesion are: surgical interventions, anesthetic and diagnostic techniques; non-traumatic causes may include: violent coughing due to bronchial asthma or acute bronchitis, cardiopulmonary resuscitation, foreign body airway obstruction, physical exertion, or drug abuse by inhalation. (7) pr secondary to trauma is uncommon in the literature, and may occur due to causes such as: traumatic brain injury, cervical, thoracic, abdominal, and pelvic injuries and may result from penetrating spinal cord injuries by a firearm or sharpener. (3, 7, 9) air can enter the spinal canal directly or indirectly, the first mainly of traumatic or penetrating origin; and the second by dissection of the soft paraspinals by a unidirectional valve mechanism until reaching the spinal canal. (4) generally, this air within the cord does not migrate and is spontaneously reabsorbed into the bloodstream for several days without relapse. (3, 7) there have been reports of air bubbles isolated in the spinal canal, whose locations according to their frequencies are organized as follows: thoracic, cervical, lumbosacral, cervico-thoracic, cervico-lumbar and thoracolumbar regions. in the internal pr, this distribution may depend on the site of dissection, velocity, and air volume; on the other hand, in external pr, air is generally concentrated in the posterior epidural space. (5, 10) pr can be of primary or secondary origin, being associated with the presence of air distributed in other cavities such as: thorax, mediastinum, pericardium, subcutaneous tissue and intracranial cavity. (5, 7) in addition, for this classification, it is necessary to consider whether intraspinal air is the cause and the origin or result of the associated appearance of air in the body. (5) generally, pr is usually asymptomatic but rarely presents associated symptoms such as discomfort, pain and neurological deficiencies; in addition it can also produce meningism and alteration of consciousness (4, 5), which is why the diagnosis is mainly radiographic and not clinical. among the most used tools we find: simple radiographic that is useful for the early detection of associated lesions and the romanian neurosurgery (2017) xxxi 3: 394 398 | 397 detection of large amounts of intraspinal air; computed tomography (ct) is the tool of choice, but it is difficult to differentiate between intradural and extradural pr, which is why it is necessary to use magnetic resonance imaging. (4, 5) adequate differentiation of the intraspinal air and spinal gases caused by degenerative, malignant, inflammatory and infectious diseases must be performed, since ct does not allow this differentiation to be made clearly, which is why this similarity must be considered in the differential diagnosis. (2, 5, 10) there is no specific treatment for the management of pr, this usually focuses on the associated lesions. air as such is not usually dangerous, but its presence is fundamental to identify underlying pathologies. (4, 6, 11) classification proposal based on a literature review of available cases, we propose to classify ptsd in grades depending on their size on ct scans, in grades i, ii and iii. grade i would be the pr which is located towards the periphery in the spinal canal and occupies no more than 30%, grade ii occupying up to 60% and grade iii occupying more than 60% (figure 4). on the other hand, the pr will later be assigned to the anatomical region where it is identified. figure 4 scheme of the proposal classification moscote-agrawal-padilla conclusions post-traumatic pr is a rare condition but its timely diagnosis is important. although rp is usually self-limited and without other therapeutic consequences, it is essential to define the cause and extent of the injury. in view of this, the treating specialist should thoroughly evaluate the pathologies that may cause the presence of air in the spinal canal to determine a suitable treatment for the patient. correspondence dr. luis rafael moscote-salazar universidad de cartagena, cartagena de indias, colombia e-mail: mineurocirujano@aol.com references 1. gill m, sreenivas m, beniwal rs. post-traumatic cervical pneumorrhachis a rare entity. british journal of neurosurgery. 2011;251:134–5. 2. el-halabi d, alkandari t, yaktien mm. traumatic air in spinal canal pneumorrhachis. anaesthesiology intensive therapy. 2012;44:25–7. 3. kim ky, kang jh, lee mh, han y, choi dw. atypical traumatic pneumorrhachis accompanied by paraparesis. ann rehabil med. 2014;383:410–4. 4. segura ds. caso 3-2015 : masculino 19 años con neumorraquis post-traumático. revista clínica de la escuela de medicina ucr hsjd. 2015;52:1–3. 5. oertel mf, korinth mc, reinges mht, krings t, terbeck s, gilsbach jm. pathogenesis, diagnosis and management of pneumorrhachis. eur spine j. 2006;15suppl 5:s636–43. 6. hadjigeorgiou gf, singh r, stefanopoulos p, petsanas a, hadjigeorgiou fg, fountas k. traumatic pneumorrachis after isolated closed head injuries: an upto-date review. journal of clinical neuroscience. 2016;34:44–6. 7. gelalis id, karageorgos a, arnaoutoglou c, gartzonikas d, politis a, georgakopoulos n, et al. traumatic pneumorrhachis: etiology, pathomechanism, diagnosis, and treatment. spine journal. 2011;112:153–7. 398 | padilla-zambrano et al postraumatic pneumorrhachis 8. derner m, drugová b, hořejší l, skvára d, druga r. massive pneumorrhachis, pneumocephalus and pneumoopticus following thoracic trauma and avulsion of the brachial plexus: case report and review of the literature. prague medical report. 2011;1121:56–66. 9. luh ht, kuo mf, lai dm, chen cm, xiao f, yang sh. traumatic pneumorrhachis associated with pulmonary herniation into spinal canal. spine journal. 2014;145:853–4. 10. dwarakanath s, banerji a, chandramouli b. posttraumatic intradural pneumorrhachis : a rare entity. indian journal of neurotrauma. 2009;62:151–2. 11. mcintosh se, salcedo-dovi h, cortes v. air in the spinal canal associated with trauma. the journal of emergency medicine. 2006;311:33–5. microsoft word template_first page romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article clinical diagnosis versus autopsy diagnosis in head trauma andreea-alexandra velnic, bianca hanganu, valentin petre ciudin, dragoș crauciuc, irina smaranda manoilescu, beatrice gabriela ioan romania  doi: 10.1515/romneu-2017-0072 microsoft word _7.formatata_iliescu.doc romanian neurosurgery vol. xvi nr. 1 32 bilateral optic malignant astrocytoma in a 3 year old child with nfi – case presentation bogdan iliescu1, m. vukic2, ziyad faiyad1, ramona filipescu*, ion poeata1 13rd neurosurgery department, “prof. dr. n. oblu” clinical emergency hospital 2department of neurosurgery, medical school university of zagreb, zagreb, croatia *neurosurgery department, “st mary” children’s hospital we present a rare case of a 3 year old child with a fast-growing bilateral exophtalmus in the context of neurofibromatosis type 1. we analyze the particularities of the clinical and imagistic aspects of the case, and discuss them in the light of pathological diagnosis (malignant astrocytoma) and imagistic follow-up. keywords: malignant astrocytoma, neurofibromatosis type 1, optic nerve, optic chiasm introduction neurofibromatosis type 1(nf i) is a common autosomal dominant condition that affects about 1 in 5000 people. optic nerve glioma is one of the landmark lesions characterizing this disease. they usually occur in children during the first decade of life and are seen in 11–30% of patients with nf i. when associated with nf1, the tumors are more often benign, can be multifocal and bilateral, and are usually found within the optic nerves although they can occur anywhere along the optic pathway, all the way to the visual cortex. although the unilateral occurrence is a finding quite common in this population (up to 30%) bilateral involvement of the optic nerves is rare. further, the optic gliomas in nf1 are self-limiting lesions with a very slow growth (which stops in adolescence). as a result exophtalmus is a very rare finding and they require surgical intervention in a very small number of cases. case report a 3 year old boy was addressed to our department for a fast-growing, grotesque exophtalmus, bilateral but more prominent on the left side. from apparently normal to present status the evolution occurred during a period of roughly 6 months (as documented by family photographs. he lost vision in both eyes 8 months before presentation, after a short period of amblyopia with a rapid course (7 days). the clinical exam revealed café-au-lait spots of various sizes and locations (trunk and limbs) and important of left eye conjunctiva. both eyes were deviated from the normal position towards inferior left corner. no other clinical sign was apparent. a brain and orbit mri exam was ordered with contrast enhancement. axial t1-weighted magnetic resonance images showed isointense masses developing within both optic nerves, occupying most of the retro-ocular orbit and extended to the optic chiasm. both lesions enhanced homogeneously after contrast administration. decision was made to remove both tumors in order to restore facial cosmetics and to prevent further deterioration of the eyes (the left eye was already affected by a severe conjunctivitis). the two gliomas were approached in one surgery through a bifrontalleft pterional approach, orbit ceiling perforation, dural flap and complete tumor removal. the desired cosmetic result was achieved, but third day bilateral optic malignant astrocytoma romanian neurosurgery vol. xvi nr. 1 33 postoperatively the patient developed high fever, vomiting and presented signs of meningeal irritation. lumbar puncture revealed a high concentration of white blood cells (5100/ml) and immediate antibiotic therapy was started with vancomycin. the initial microscopic pathological exam indicated the two tumors as being pilocytic astrocytoma and suggested further investigation through immunohistochemistry. the suggestion was followed and the second exam revealed the tumors to be malignant astrocytomas with a ki67 index of 12%. at three months postoperatively a mri follow-up was performed. the new scan revealed a mass occupying lesion within the optic chiasm with the same characteristic as the previous optic nerve tumors. the lesion was, visible on the initial scan, showed an accelerated growth reaching 1,6 cm in diameter. the patient was addressed to gamma-knife center for radiosurgery. discussion although optic nerve glioma represents a common finding in patients with type 1 neurofibromatosis, either unilateral or bilateral, our case posed a clinical challenge from the start as to the reasons behind a very fast growth rate (from normal to massive exophtalmus in about 6 months). the classic tumor found in nfi is known to be a slow growing tumor that has a self-limiting evolution with variable influence on visual function. our patient lost vision in both eyes in a very short period (7 days). furthermore, the mri aspect of both optic nerve tumors didn’t present any particular characteristics to set them apart form the usual optic nerve glioma or to suggest malignancy. although the initial surgery removed successfully the optic nerve tumors to a good cosmetic result the immunohistochemical diagnostic, the rapid clinical course, and the imagistic documentation of a relapse of the disease at the level of optic chiasm all concur to a reserved vital prognostic. we believe that this case is illustrative for the need to put together all the available data in diagnosing, treating and counseling a case with salient tumors in the context of nfi, never overseeing the most rare possibilities. a) b) fig. 1 clinical aspect in a) november 2008, and b) february 2009 bogdan iliescu romanian neurosurgery vol. xvi nr. 1 34 fig. 2 café-au-lait spots on runk and limbs bilateral optic malignant astrocytoma romanian neurosurgery vol. xvi nr. 1 35 fig. 3 a) fig. 3 b) fig. 3 comparative mri aspects in a) november 2008, and b) february 2009, native and after contrast enhancement on the left and right images respectively bogdan iliescu romanian neurosurgery vol. xvi nr. 1 36 fig. 4 ct control 1st day postop fig. 5 mri aspects at 3 months postoperatively romanian neurosurgery (2019) xxxiii, 1: 77-79 doi: 10.33962/roneuro-2019-016 www.journals.lapub.co.uk/index.php/roneurosurgery middle cerebral artery stroke following massive hornet sting: a case report gopal sedain1, gentle sunder shrestha2 1 neurosurgery, alka hospital, jawalakhel, lalitpur, nepal 2 anaesthesiologist and critical care physician, alka hospital, jawalakhel, lalitpur, nepal abstract hornet stings are frequently encountered in practice in nepal. majority of patients sustain minor illness. however, complications like anaphylactic shock and the rare acute kidney injury, multiple organ dysfunction and acute myocardial infarction have been reported. ischemic stroke following hornet stings has been reported infrequently in scientific publications. we report a case of fatal right middle cerebral artery territory ischemic stroke and acute kidney injury in a 40-year farmer. introduction human encounter with hornets has been found in plantation, cultivation and forest areas. they are aggressive upon disturbance and attack in swarms causing victims to sustain multiple stings. the sting is excruciatingly painful and the insect leaves the stinger. unlike typical bees, hornets and wasps do not die after stinging because their stingers are not barbed and are not pulled out of their bodies. hornet stings are more painful to humans than typical wasp stings because hornet venom contains a large amount (5%) of acetylcholine. hornets, like many social wasps, can mobilize the entire nest to sting in defense, which is highly dangerous to animals and humans. the attack pheromone is released in case of threat to the nest. the majority of sufferers recover with minor illness. but fatal and non-fatal complications that arise from such stings include anaphylaxis, acute kidney injury (8), multiple organ dysfunction (7), myocardial infarction (3) and ischemic stroke (1,2,5,6). vasoactive, inflammatory, and thrombogenic peptides and amines, including histamine, leukotrienes, and thromboxane are responsible for the end organ complications. the allergenic proteins such as phospholipases which elicit ige responses, resulting in mast cell activation, underlie the anaphylaxis. case report a 40-year-old patient was referred to the emergency department for decreased consciousness after sting by a swarm of hornets. the keywords hornet, sting, middle cerebral artery stroke corresponding author: gopal sedain alka hospital, jawalakhel, lalitpur, nepal newron79@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 78 gopal sedain, gentle sunder shrestha previously healthy farmer from the dang valley in western nepal was stung by around 100 hornets when he was collecting maize crops in his field. he was immediately taken to local hospital where he received chlorpheniramine (antihistamine) and hydrocortisone. the patient had fall in sensorium for which he was referred to our center. the family’s medical history did not reveal thromboembolic disease or significant neurological and autoimmune rheumatoid disease. upon arrival, his gcs was poor (6/15). physical examination revealed multiple stings in his body including his face and scalp. (fig 1) he had acute kidney injury (creatinine level 9.5mg%). his serum ldh was 5211(normal range: 225-450) and cpk of 3652 (normal <170u/l). he had severe metabolic acidosis with bicarbonate level of 15meq/l. his ct head revealed a large mca (middle cerebral artery) ischemic stroke with mass effect and midline shift. (fig 2) he underwent dialysis for acute kidney injury, however patient succumbed to his illness. figure 1: hornet sting induced local erythematous changes in the forearm. figure 2: plain ct head revealing large right mca infarct with mass effect discussion hornet venom contains vasoactive, inflammatory, and thrombogenic peptides and amines, including histamine, leukotrienes, and thromboxane. the venom also contains allergenic proteins such as phospholipases which elicit an ige response, resulting in mast cell activation which is the hallmark of anaphylaxis. pain, wheal, flare, edema and swelling, which are generally self-limiting, constitute local disease. multiple stings can lead to vomiting, diarrhea, generalized edema, dyspnea, and hypotension. severe systemic complications include anaphylaxis which constitutes the leading cause of death, acute kidney injury, multiple organ dysfunctions, disseminated intravascular coagulation, myocardial infarction, rhabdomyolysis and neurological disease. numerous neurological complications include ischemic stroke, venous sinus thrombosis, ocular myasthenia gravis and thrombotic thrombocytopenic purpura. the proposed underlying mechanism of early ischemic stroke includes hypotension of anaphylaxis and vasospasm due to treatment with adrenaline. the delayed phenomena leading to infarctions appear to be spasms caused by vasoactive substances and thrombosis induced by thrombogenic factors in venom (1). the other neurological complications of stings which have been reported are individual case reports of ocular myasthenia gravis, optic neuritis, limb numbness, trigeminal neuralgia and encephalopathy. postulated mechanisms include both toxic effect of venom and hypersensitivity to venom (6). in the case of acute myocardial infarction following hornet stings, the postulated mechanism is a combination of coronary vasoconstriction and platelet aggregation secondary to mediators released after wasp sting, aggravated by exogenous adrenaline given as part of the treatment. 79 middle cerebral artery stroke following massive hornet sting: a case report in our patient, we postulate that the systemic immune mediated reaction to the bee sting caused vasoconstriction and a prothrombotic state with subsequent ischaemia leading to stroke. conclusions insect stings can lead to neurological complications and can be fatal. timely intervention is required to prevent these. references 1. bhat r, bhat kr, pais r.bilateral haemorrhagic cerebellar infarction following honeybee sting. j assoc physicians india 2002; 50:721–2. 2. day jm. death due to cerebral infarction after wasp stings. arch neurol 1962; 7:184–186 3. levine hd. acute myocardial infarction following wasp sting. report of two cases and critical survey of the literature. am heart j 1976 ;91: 365-374 4. paudel b, paudel k. a study of wasp bites in a tertiary hospital of western nepal. nepal med coll j 2009;11: 52-56. 5. riggs je, ketonen lm, bodensteiner jb, benesch cg. wasp sting-associated cerebral infarction: a role for cerebrovascular sympathetic innervation. clin neuropharmacol 1993; 16: 362-365. 6. sachdev a, mahapatra m, d’cruz s, kumar a, singh r. wasp sting induced neurological manifestations. neurol india 2002 ;50: 319-321 7. watemberg n, weizman z, shahak e, aviram m, maor e. fatal multiple organ failure following massive hornet stings. j toxicol clin toxicol 1995 ;33: 471-474. 8. xuan bh, mai hl, thi tx, thi mt, nguyen hn. swarming hornet attacks: shock and acute kidney injury--a large case series from vietnam. nephrol dial transplant 2010 ;25: 1146-1150 12moscote-salazarluisrafael_acutesubdural romanian neurosurgery | volume xxx | number 4 | 2016 | october december article acute subdural hematoma as a complication of diagnostic lumbar puncture: case report luis rafael moscote-salazar1, andres m. rubiano1, hernando raphael alvis-miranda1, nasly zabaleta-churio1, willem guillermo calderón-miranda2, gabriel alcalá-cerra1, jorge aquino-matus2 1colombia, 2mexico doi: 10.1515/romneu-2016-0084 526 | moscote-salazar et al acute subdural hematoma as a complication of diagnostic lumbar puncture doi: 10.1515/romneu-2016-0084 acute subdural hematoma as a complication of diagnostic lumbar puncture: case report luis rafael moscote-salazar1, andres m. rubiano2, hernando raphael alvis-miranda3, nasly zabaleta-churio4, willem guillermo calderón-miranda5, gabriel alcalá-cerra6, jorge aquino-matus7 1neurosurgeon, red latino, latin american trauma & intensive neuro-care organization bogota, colombia 2universidad el bosque, meditech foundation, neurosurgeon, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia 3resident of neurosurgery, universidad de cartagena, cartagena de indias, colombia 4nurse, red latino, latin american trauma & intensive neuro-care organization, colombia 5resident of radiology, national autonomous university of mexico, mexico d.f, mexico 6neurosurgeon, universidad de cartagena, colombia 7physician, universidad de san carlos de guatemala, national autonomous university of mexico, mexico d.f, mexico abstract: background: intracranial hemorrhagic complications are unusual after diagnostic lumbar puncture. case report: a diagnostic lumbar puncture was performed in a 55 year-old male for acute bacterial meningitis workup. immediately after the procedure he developed intense headache and a head computed tomography (ct) was done which identified an acute subdural fluid collection. no surgical management was offered and conservative medical follow-up was indicated. conclusion: the occurrence of a headache with red flags after a lumbar puncture may suggest the possibility of an acute subdural hematoma. key words: complications, subdural hemorrhage, intracranial hematoma, lumbar puncture introduction lumbar puncture is a diagnostic and therapeutic procedure in patients with a focal neurologic clinical picture in whom infections or cerebral aneurism rupture is suspected. nonetheless, even performed under expert hands, it is not extent of complications such as romanian neurosurgery (2016) xxx 4: 526 – 529 | 527 spinal or intracranial hemorrhages. acute subdural hematoma complicating a lumbar puncture is rare. few reports have been published about rare complications, including spinal anesthesia among others. (1, 2, 3, 4). the clinical case and literature review of an acute subdural hematoma after lumbar puncture is reported. physiopathological findings are discussed. clinical case a 50 year-old male presented to our private clinic with a 4 hour history of dysarthria. past medical history was relevant for hypertension. upon admission he was alert and cooperative with slurred speech. on neurological examination, no alteration in cranial nerves was detected and no other neurological deficit was documented. a brain ct scan (figure 1a and b) was negative. over the next 24 hours he developed headache, fever and nuchal rigidity, and a diagnostic lumbar puncture was done reporting normal laboratory test results (not shown). twelve hours after the procedure he developed intense headache refractory to analgesics and a brain ct scan revealed a right parietal hyperdense lesion compatible with an acute subdural hematoma with little mass effect. no surgical management was offered and underwent medical treatment and observation. clinical course was eventful and 8 days after the procedure he was discharged home with no neurological deficit. figure 1 (a, b) non-contrast brain ct scan on admission with no relevant findings 528 | moscote-salazar et al acute subdural hematoma as a complication of diagnostic lumbar puncture figure 2 (a, b) non-contrast brain ct scan showing a right subdural parietal hematoma after lumbar puncture discussion subdural hematoma is a rare complication after lumbar puncture in medical literature. (5, 6, 7). a proposed mechanism relates to traction and tear of the intracranial subdural veins under a low pressure gradient secondary to the extraction of cerebrospinal fluid (csf). an excessive loss of csp of about 250 cc may cause displacement of the intracranial structures. (8, 9, 10) risk factors for the formation of subdural collections are: cerebral atrophy, cerebral aneurisms, and blood dyscrasias including platelet anti-aggregation drugs, arteriovenous malformations, pregnancy, dehydration and fenestrations from previous punctures. also, technical difficulties have been associated with neuroaxial hematomas. this risk may be reduced performing an atraumatic lumbar puncture technique with fine needles (11, 12). intraparenchymal hemorrhage has been described in less frequency and usually associated with rapid onset or transitory high blood pressure. (13) conclussion the true incidence of subdural hematoma secondary to a lumbar puncture is unknown and it is possible that many patients are treated without any imaging studies. treatment of this type of complications may be surgical or conservative as in the case presented. complementary imaging studies are recommended for patients with new onset of mild symptoms after a lumbar puncture. romanian neurosurgery (2016) xxx 4: 526 – 529 | 529 correspondence dr. luis rafael moscote-salazar red latino, latin american trauma & intensive neuro-care organization, bogota, colombia e-mail: mineurocirujano@aol.com references 1. bjarnhall m, ekseth k, bostrom s, vegfors m. intracranial subdural haematoma: a rare complication following spinal anaesthesia. actaanaesthesiolscand 1996; 40:1249-1251. 2. acharya, r., chabra, s.s., ratra, m., sehgal, a.d.: cranial subdural haematoma after spinal anaesthesia. br j anaesthesia 2001; 86: 893-895. 3. loo cc, dahlgren g, irestedt l. neurological complications in obstetric regional anaesthesia. int j obstetanesth 2000; 9:99-124. 4. alemohammad s, bouzarth wf. intracranial subdur¬al hematoma following lumbar myelography. j neurosurg 1980;52:256-258 5. lavie f1, hervé d, le ber i, brault jl, sangla s, de broucker t. bilateral intracranial subdural hematoma following lumbar puncture: report of a case. rev neurol (paris). 1998 oct;154(10):703-6. vos pe1, de boer wa, wurzer ja, van gijnj.subdural hematoma after lumbar puncture: two case reports and review of the literature. clinneurolneurosurg. 1991;93(2):127-32. 6. gaucher dj jr1, perez ja jr. subdural hematoma following lumbar puncture. arch intern med. 2002 sep 9;162(16):1904-5. 7. reynolds f. dural puncture and headache. avoid the first but treat the second. br med j 1993; 306: 874-876 8. acharya r, chhabra ss, ratra m, sehgal ad. cranial subdural haematoma after spinal anaesthesia. br j anaesth 2001; 86: 893-895. 9. van de kelft e, bosmans j, parizel pm, van vyve m, selosse p. intracerebral hemorrhage after lumbar myelography with iohexol: report of a case and review of the literature. neurosurgery. 1991;28(4):570–574. 10. de la linde c. complicaciones de la anestesiaespinal. act anestreanim (madrid) 1997; 7: 15-26. 11. pryle bj, carter ja, cadoux-hudson t. delayed paraplegia following spinal anaesthesia. anaesthesia 1996; 51: 263-267. 12. peiró cm, caballer n, errando cl, moliners.spinal and cerebral hematoma following diagnostic lumbar puncture with fatal course.revespanestesiolreanim. 2003 nov;50(9):481-5. spanish romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article state of the art neurosurgical op theater necesity, not option! răzvan onciul, andrei marinescu, georgeta popa, a.v. ciurea romania doi: 10.2478/romneu-2018-0004 romanian neurosurgery (2018) xxxii 1: 29 34 | 29 doi: 10.2478/romneu-2018-0004 prof. md. msc a.v. ciurea: “brain is life!” january 2018 state of the art neurosurgical op theater necesity, not option! răzvan onciul1, andrei marinescu1, georgeta popa2, a.v. ciurea3,4 1student, “carol davila” umph, bucharest, romania 2neuroradiology department, sanador hospital, bucharest, romania 3neurosurgery department, sanador hospital, bucharest, romania 4neurosurgery department “carol davila” umph, bucharest, romania abstract: cerebral activity is extremely complex and requires a super diagnosis investigation there is no limit to this super investigation, especially in the case of expansive tumor or non-tumoral le-sions. modernization of the diagnosis in these lesions has gained science fiction aspects. adapting to those changes, operatory blocks and neurosurgeons all around the world have been improved to the same extent in order to obtain the most perfect results with keeping the quality of life. the modern slogan of neurosurgery is “maximal safe resaction". continu-ing on this theme we can state that the equipment of the surgical apparatus is very special and extremely expensive. complex but in accordance with one of the most exquisite agglomeration of atoms in the entire known universe, the human brain! key words: neurosurgery, mri, op theather, neuronavigation, operating microscop, hibryd op room, robotic surgery, future, science-fiction introduction inicidence of intracranial or intrarahidian lesion processes have lately increased. on one hand, more and more complex investigative means have appeared, and on the other hand, the number of primary and secondary neurosurgical disease in the whole european pathology has increased. in these conditions, the smallest neurology, ophtalmologic and ent signs should be considered taking a proper clinical examination and carrying out paraclinical investigations: mri with all facilities-native, contrast, angio and flair, stir, dti etc. 30 | onciul et al state of the art neurosurgical op theater material after complete diagnosis of expansive lesion in the nervous system we must intervene quickly because there is no place for expansion in the intracranial space and the intracahidian space. in fact, the current name in all such situations is intracranial expansive (peic) or intrara-hidian process. neurosurgical intervention should be done in a timely manner with all possible facilities to achieve a good result with restitutio ad integrum. a modern neurosurgical room needs a proper operating table for special operator procedures – maquet – plus the right external illuminators. the patient’s head must be secured in the mayfield device to prevent any movement during craniotomy maneuvers and laso to allow intracranial injuries to be tackled in the most dificult locations. (figure 1) a b figure 1 marker for neuronavigation and mayfield fixator (a, b) neuronavigation is used for accurate lesion delineation and targeted opening based on neuronavigation data from previous mri and ct-scan. of particular importance are the neuroanesthesia conditions that have to be perfect: hypnosis, sedation, analgesic medication, brain relaxation through depletion treatment. intraoperative and postoperative mri are a routine in most medical centers of civilized countries. neurosurgical approach is done minimally invasive under the operator microscope with avoidance of elocvent areas, which is done by obtaining data from functionally mri correlated with neuronavigation. the technology behind the operating microscopes romanian neurosurgery (2018) xxxii 1: 29 34 | 31 has improved a lot, reaching major performances (ex: pentero 900). currently in bucharest there are 7 pentero microscopes with an individual value of 260.000 euros (fig. 2). they bring a major benefit to both the surgeon and the patient: the operations are made easier, more elegant and comfortable for the neurosurgical team and with fewer risks for the patient due to the visualization of both the lesion and the surrounding vasculopathy structures. the exerezis of the expansive process is extremely slow, careful, with the exact delimitation of the lesional entity to normal brain tissue. the exeretion must be made as complete as possible, but with the preservation of the quality of life. hemostasis is performed very carefully in order not to leave intracerebral hemorrhagic areas, then try to restore csf pathways, open the arachnoid spaces and basal cisterns. (figure 3) the cerebral substance is continuously irrigated with "warm" (at body temperature) saline solution. after that, the total ablation of the lesion is made, with the application of hemostatic substances on the surface based on human fibrins autologous (afs) – thereby stopping any kind of diffuse bleeding. microneurosurgical instrumentation must be of the highest quality, of course titanium, perfectly adapted to neurosurgical procedures that require a finesse imposed by the complex and sophisticated brain structures. (figure 4) a b figure 2 operating theatre (pentero 900 microscope) (a, b) 32 | onciul et al state of the art neurosurgical op theater a b figure 3 tumor mass (meningioma) completely removed it must be used watertight closer of dura mater or without dural plastia or artificial dura, again applying the afs product for stoping the rest of csf. reimplantation and perfect fixation of the bone calvaria it is an impotant element for cerebral neural volumetry and physiology. closure in perfect anatomical planes is necessary to restore the adjacent structures. all of these surgical procedures other than patient benefit recognized in all publications are also an element of neurosurgical training. (1) a b figure 4 microsurgical instruments (a, b) ideally, every surgical operation in the operating theater must be video recorded to be reviewed later, from a forensic point of view, but especially used as material in the education process, helping to speed up the learning curve. regarding vascular pathology this involves for the future an interdisciplinary angio suit in which the angiographic diagnosis is completed with the open microsurgical approach (clipping) and also with the current endovascular procedures (coils). (2) always present in the modern or must be: the special neurosurgery kits for craniocerebral or spinal interventions, cranial nerve romanian neurosurgery (2018) xxxii 1: 29 34 | 33 monitoring devices, hydrocephalic drainage kit, lumbar csf drainage kit, etc. neuroendoscopy is also a very important point to achieve in minimally invasive intraventricular interventions. this is necessary to restore csf circulation and to resect injuries at the cerebral ventricular structures level. (3) curently the biggest improvement of a neurosurgical theather is the hybrid operating room in witch u can add to the standard or other devices such as: surgical angiography, carms, intraoperative/postoperative ct scan or even intraoperative/postoperative mri. (figure 5) figure 5 hybrid operating room a hybrid operating room is a major investment; only the purchase cost is between 1 and 2 million euros; added to these are the high costs of remodeling and maintenance. however, the economic benefit is reflected in the increasing demand for complicated surgeries. the surgical act become less time consuming with shorter periods of hospitalization for patients due to more accessible methods of intervention. in addition, intraoperative imaging also facilitates immediate quality assurance that leads to a reduction in errors. perspectives the future is the robotic surgery which is being attempted to be implemented in the field of functional neurosurgery (involuntary movements) (4, 5, 6). robotic systems are not widely used in neurosurgery compared to other areas of medicine such as urology, cardiology and gastroenterology. this is due to the anatomical challenges of such a complex and space-limited organ and to the fact that the brain includes extremely sensitive tissue. (figure 6) (7). 34 | onciul et al state of the art neurosurgical op theater figure 6 neuroarm (univestity of calgary, alberta, canada) all these very costly elements are necessary for a better outcome and restitution of the patient’s quality of life. at least, in neurosurgery science-fiction technology in the operating theater is not an option, it is a necessity! conclusion it is impossible to predict the future evolution of neuroimaging diagnosis in cerebral lesions, in particular. technological developments compete for the development of this complex chapter. accordingly, the entire operator palette with all the devices included is constantly adapting to operating results as perfect as possible with patient integration into family, professional and, of course, social work. the evolution of the entire technology in op theather is extremely fast and adapted to the latest acquisitions of neuroanatomy, neurophysiology, neuroscience and especially neuroimaging. abbreviations csf= cerebro spinal fluid mri= magnetic resonance imaging ct= computed tomography sf= science-fiction or= operating room afs= autologous fibrin solution flair=fluid attenuation inversion recovery stir= short t1 inversion recovery dti = diffusion tensor imaging references 1.dammann p. breyer t. wrede k. h., stein k. p., wanke i., grams e., gizewski r. e., schlamann m., forsting m., sandalcioglu e.. “treatment of complex neurovascular lesions: an interdisciplinary angio suite approach.” therapeutic advances in neurological disorders 7.1 (2014): 60–70. 2.konakondla s., reginald f, and schirmer c.m.. “simulation training in neurosurgery: advances in education and practice.” advances in medical education and practice 8 (2017): 465–473. 3.rohde v. behm t., ludwig h. wachter d. “the role of neuronavigation in intracranial endoscopic procedures.” neurosurgical review 35.3(2018): 351–358. 4.madhavan k.,kolcun j.p.g., chieng l. o.,wang m. y., “augmented-reality integrated robotics in neurosurgery: are we there yet?,” neurosurgical focus (2017), 42, no. 5, 5.de benedictis a., palma p.,amante p., rizzi m., marras c. f., trezza a., carai a., genovese e., procaccini e., messina r., randi f., cossu s., esposito g., “robotassisted procedures in pediatric neurosurgery,” neurosurgical focus (2017) , 42, no. 5, 6.benabid al, hoffman d, seigneuret e, chabardes s. robotics in neurosurgery: which tools for what? acta neurochir suppl. 2006;98:43–50. 7.amirabdollahian f., livatino s.,vahedi b., gudipati r., sheen p., gawrie-mohan s., and vasdev n., “prevalence of haptic feedback in robot-mediated surgery: a systematic review of literature,” journal of robotic surgery, 12, (2018) isue 1, 11-25 04 04onciulrazvan_state flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article odontoid process fracture in 2 year old child: a rare case report prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, yadav kuldeep india doi: 10.1515/romneu-2017-0080 522 | hanuman prasad et al odontoid process fracture in 2 year old child doi: 10.1515/romneu-2017-0080 odontoid process fracture in 2 year old child: a rare case report prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, yadav kuldeep department of neurosurgery, dr rml ims lucknow uttar pradesh, india abstract: in small childrens spine injuries are rare. in this age group upper cervical spine is commonally affected. odontoid process fracture involve only a subset of cervical spine fractures. in small childrens, this fracture typically involves the cartilaginousplate that separates the odontoid process from the body of the axis. odontoid processfracture is rare in children less than 7 years of age. key words: odontoid process, fracture, 2 years of age, management introduction cervical spine injuries in small children are rare with a reported incidence of 0.2 to 0.5% of all fractures or dislocations and 1.5 to 3% of all lesions in the spine [1]. in younger children upper cervical spine is commonaly affected, with over 50% of spinal injuries in small children affecting this region. this relates to the child's greater head-to body ratio,and horizontal orientation of the facet joints where more forces are centered around the junction between the large head and the smaller body[2].in small children, dens fracture typically involves the cartilaginous plate that separates the odontoid process from the body of the axis. the cartilaginous end plate between the dens and the body of c2 does not ossify until the child is 5 to 7 years old[3]. therefore, odontoid synchondrosis fractures are common in young children less than 7 years of age [4,5].odontoid process fracture are rare in small children only few cases are reported in the literature. the current literature reports that these fractures can be successfully treated with nonoperative management including cervical spine immobilization as well as operative interventions ranging from closed reduction and external fixation to posterior fixation or fusion of c1/c2 [6]. we present a case of odontoid process fracture in a 2-year-old patient managed by surgery. case report a 2 year-old female child was brought with history of road traffic accident followed by quadriparesis and inability to hold the neck. romanian neurosurgery (2017) xxxi 4: 522 525 | 523 examination revealed a conscious child with a gcs score of 15/15. the tone was increased in all four extremities with child moving all 4 limbs but was not able to stand. plain ct cervical spine (figure 1a and 1b) and plain xray cervical spine (figure 2b) revealed fracture of the odontoid process with anterior subluxation of c1 over c2. patient was immobilized with a philadelphia collar. 1a 1b figure 1a and 1b odontoid process fracture figure 2a preoperative x-ray shows anterior subluxation of c1over c2 figure 2b postoperative x-ray in view of the presence of significant neurological deficits and the posterior displacement of the fractured odontoid fragment, it was felt that conservative treatment with external immobilization might not be helpful. hence, c1, c2 posterior 524 | hanuman prasad et al odontoid process fracture in 2 year old child fixation (sontag method) done. after posterior wire fixation good reduction achieved (figure 2b). in postoperative period patient was kept on philadelphia collar. postoperative period was uneventful. three months after surgery, patient was able to walk and hold the neck. discussion in small children, c2 vertebral body is divided by the paired neurocentral synchondrosis between the neural arches and the body of axis and the subdental synchondrosis between the dens and the body of axis [7]. fusion of this synchondrosis usually takes place by 7 years of age. most cases of odontoid fractures in children less than 7 years of age are odontoid synchondrosis fracture. odontoid process fracture in children below 7 years of age are rare, only few cases are reported in literature. management of such fractures in the pediatric population remains unclear. after reviewing the literature, we found only one other case report describing the management of a displaced type 2 odontoid process fracture in a small children. in this publication, bhagat and coauthors described operative intervention of a displaced type 2 odontoid process fracture in a 2-year-old girl [8]. although they did not describe when union occurred, they noted marked remodeling of the fracture over a 30-month period. with such paucity of literature on this topic, it is unknown whether operative intervention aids fracture union and functional outcome in the small children. there are various options available for management of odontoid process fracture.(1) external immobilisation (2) posterior c1-c2 sublaminar wiring(3)c1-c2 transarticular screw(4) odontoid screw fixation.odontoid screw fixation is controversial in small children. in small children most odontoid synchondrosis fractures is often treated by external immobilization. approximately 96% fusion rate is expected with external immobilization alone [9]. however, surgery does have a role in selected patients with odontoid fractures [10]. generally, surgery is an option in patients who fail conservative treatment. recent literature shows that certain characteristics of odontoid fractures are associated with high failure rate with external immobilization alone[10].fulkerson et al.[10] reported that a significant displacement of the odontoid of 11% to 100%, angulation greater than 30 degrees, clinical evidence of upper cervical spinal cord injury were indications for surgical intervention. in our patient, there was posterior displacement of the odontoid more than 11% with clinical as well as clinical evidence of upper cervical cord injury and hence our patient had the necessary indications for surgical fixation. the fact that our patient showed significant improvement with surgical treatment indicates that in selected patients with odontoid fractures surgical fixation is a viable option. in our patient, posterior wire fixation was chosen because the fracture fragments were displaced posterioly and causing compression over cord. post operatively patient was placed on philadelphia collar and patient condition gradually improved. romanian neurosurgery (2017) xxxi 4: 522 525 | 525 our case illustrates that certain odontoid process fractures in small children can be successfully managed with c1-c2 posterior wire fixation and postoperatively philadelphia collar. conclusion most of the odontoid fracture in small children is odontoid synchondrotic fracture but odontoid process fracture is a rare event. most patients with odontoid fracture can be treated by external immobilization alone. however, selected patients with this condition will benefit from surgical fixation as illustrated in this case report. correspondence dr. hanuman prasad prajapati address: department of neurosurgery, dr rml ims lucknow uttar pradesh (india) mobile no.: 07727934104 email: pushpa84.dhp@gmail.com references 1. patel j c, tepas j j iii, mollitt d l, pieper p. pediatric cervical spine injuries: defining the disease. j pediatr surg. 2001;36(2):373–376. [pubmed] 2. fesmire f m, luten r c. the pediatric cervical spine: developmental anatomy and clinical aspects. j emerg med. 1989;7(2):133–142. [pubmed] 3. sherk hh, nicholson jt, chung sm. fractures of the odontoid process in young children. j bone joint surg am. 1978;60:921–924. [pubmed] 4. blauth m, schmidt u, otte d, krettek c. fractures of the odontoid process in small children : biomechanical analysis and report of three cases. eur spine j. 1996;5:63– 70.[pubmed] 5. odent t, langlais j, glorion c, kassis b, bataille j, pouliquen jc. fractures of the odontoid process : a report of 15 cases in children younger than 6 years. j pediatr orthop.1999;19:51–54. [pubmed] 6. mueller o m, gasser t, hellwig a, dohna-schwake c, sure u. instable cervical spine injury in a toddler: technical note. childs nerv syst. 2010;26(11):1625–1631. [pubmed] 7. garton hj, park p, papadopoulos sm. fracture dislocation of the neurocentralsynchondroses of the axis.case illustration. j neurosurg. 2002;96(3 suppl):350. [pubmed] 8. bhagat s, brown j, johnston r. remodelling potential of paediatric cervical spine after type ii odontoid peg fracture. br j neurosurg. 2006;20(6):426–428. [pubmed] 9. fassett dr, mccall t, brockmeyer dl. odontoid synchondrosis fractures in children. neurosurg focus. 2006;20:e7. [pubmed] 10. fulkerson dh, hwang sw, patel aj, jea a. open reduction and internal fixation for angulated, unstable odontoid synchondrosis fractures in children : a safe alternative to halo fixation? j neurosurgpediatr. 2012;9:35–41. [pubmed] romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article haemangioblastomas of the central nervous system in von hippel lindau syndrome involving cerebellum and spinal cord v.a. kiran kumar, vissa shanti, yaswanth sandeep, jatinder kumar mittal, amit agrawal india doi: 10.2478/romneu-2018-0021 164 | kumar et al haemangioblastomas of the central nervous system in von hippel lindau syndrome doi: 10.2478/romneu-2018-0021 haemangioblastomas of the central nervous system in von hippel lindau syndrome involving cerebellum and spinal cord v.a. kiran kumar1, vissa shanti2, yaswanth sandeep1, jatinder kumar mittal1, amit agrawal1 narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 1department of neurosurgery; 2department of pathology key words: cerebellar hemangioblastoma, spinal hemangioblastoma, von hippellindau disease von hippel-lindau (vhl) disease is a multisystem familial syndrome of autosomal dominant inheritance characterized by retinal, cerebellum and spinal cord hemangioblastomas, renal cell carcinomas, adrenal pheochromocytomas, angiomatous or cystic lesions of the kidneys, pancreas, and epididymis. (1) a 41 year old female patient presented with headache from 2 years, one episode of seizure generalised tonic clonic type, two episodes of vomiting. on examination cerebellar signs were positive on right side. mri brain (plain & contrast) was suggestive of well-defined non enhancing hypodense lesion of size 41x28mm, with eccentric enhancing nodule seen in right cerebellar hemisphere with mild perilesional edema and the lesion is causing mass effect with the shift of cerebellar vermis & 4th ventricle to the left side s/o right cerebellar hemangioblastoma (figure 1) she underwent right suboccipital craniectomy and excision of the tumour) (figure 2). as the patient also had neck pain and paresthesias in both upper and lower limbs and urgency of micturition, patient was evaluated with mri cervical spine (plain and contrast) (figure 3) which was suggestive of heterogenous cystic lesion extending with in central canal from c5-d4 level ,with intense heterogenous enhancement noted involving solid portion of lesion at c7&d1 segments. usg abdomen was s/o multiple pancreatic cysts ,one in tail region 8.6x7.1cm, polycystic kidney disease, a cystic lesion in right adrenal gland of size 4.1x2.8cm and the lesion showing internal vascularity on colour doppler flow imaging. opthalmologic examination visual acuity was 6/9 in both eyes; the intraocular pressure was within normal limits, did not reveal any retinal angiomas. this patient underwent laminectomy and excision biopsy of the lesion. (figure 4) romanian neurosurgery (2018) xxxii 1: 164 167 | 165 histopathological examination (hpe) showed anastomosing network of capillary vessels interspersed with nests of stromal cells with moderate amount of pale pink cytoplasm suggestive of haemangioblastoma (figure 5). figure 1 ct scan of the brain plain and contrast images showing cystic lesion with enhancing nodule in the left cerebellar hemisphere figure 2 mri of the brain contrast image showing cystic lesion with enhancing nodule in the left cerebellar hemisphere figure 3 mri of the brain contrast image showing cystic lesion with enhancing nodule in the left cerebellar hemisphere and cervical spinal cord figure 4 mri of the brain contrast image showing cystic lesion with enhancing nodule in the left cerebellar hemisphere and cervical spinal cord 166 | kumar et al haemangioblastomas of the central nervous system in von hippel lindau syndrome figure 5 (a and b) (a) vascular tumor with tumor cells having vacuolated cytoplasm and hyperchromatic nuclei (h&e, x100), and (b) the tumour was composed of anastomosing capillary network with interspersed vacuolated stromal cells (h&e; 400x) the prevalence of vhl has been estimated to be between 1:35,000-1:40,000. (2, 3) a family history of retinal or central nervous system hemangioblastoma (hb), only one hb or visceral lesion (renal tumours,pancreatic cysts or tumours, pheochromocytoma, papillary cystadenomas oftheepididymis) is required to make the diagnosis of vhl. (4) for isolated cases without a clear family history, two or more hb or one hb and a visceral manifestation is required. (5) although hemangioblastomas commonly involve cerebellum, spine and medulla; however when the lesions are multiple the outcome is poorer. (5) as it is obvious the clinical features depend on the location and multiplicity of the lesions. midline lesions of the cerebellum cause truncal ataxia, laterally situated tumour lesions commonly present with dysmetria. (6-8) the imaging technique of choice for hemangioblastomas is contrast enhanced mri of the brain and spinal cord. this will show the characteristic lesions cystic lesions with a solid enhancing mural nodule. (9) the definitive treatment of these lesions is complete surgical removal of symptomatic lesions including removal of the mural nodule. (10, 11) gamma knife radio surgery has been reported as effective against the solitary small or medium sized mural nodule of haemangioblastoma while the cystic component requires repeated evacuation. (12) needless to say that the management of hemangioblastomas is more challenging for patients with vhl syndrome as there is presence of multifocal tumour which require high index of suspicion and multiple surgeries. correspondence dr amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.hamid da, abdullah j, ariff ar, muhamad m, madhavan m. cerebellar hemangioblastoma in a patient with von hippel-lindau disease: a case report. the malaysian journal of medical sciences: mjms 2000;7:43. 2.maher er, iselius l, yates jr, et al. von hippel-lindau disease: a genetic study. journal of medical genetics 1991;28:443-447. 3.neumann hph, wiestler od. clustering of features of von hippel-lindau syndrome: evidence for a complex genetic locus. the lancet 1991;337:1052-1054. 4.memon kl, rosen sw. lindau's disease. am j med 1964;36:595-617. 5.bhargava s, rao a, mishra a. a case of von hippel lindau disease. med j armed forces india 2007;63:302304. 6.gumprecht h, lumenta cb. multifocal hemangioblastoma in a young woman with hippel romanian neurosurgery (2018) xxxii 1: 164 167 | 167 lindau syndrome. zentralblatt fur neurochirurgie 1997;59:181-184. 7.richard s, martin s, david p, decq p. von hippellindau disease and central nervous system hemangioblastoma. progress in genetics and clinical management. neuro-chirurgie 1998;44:258-266. 8.weinberg ra. tumor suppressor genes. science 1991;254:1138-1146. 9.quadery fa, okamoto k. diffusion-weighted mri of haemangioblastomas and other cerebellar tumours. neuroradiology 2003;45:212-219. 10.lonser rr, heiss jd, oldfield eh. tumor devascularization by intratumoral ethanol injection during surgery. j neurosurg 1998;88:923-924. 11.salomé f, colombeau p, fermeaux v, et al. renal lesions in von hippel-lindau disease: the benign, the malignant, the unknown. european urology 1998;34:383392. 12.niemelä m, lim yj, söderman m, jääskeläinen j, lindquist c. gamma knife radiosurgery in 11 hemangioblastomas. j neurosurg 1996;85:591-596. 21 21kirankumarva_haemangioblastomas flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article white cerebellar sign a grave prognostic indicator saurabh jain india doi: 10.1515/romneu-2017-0056 344 | jain white cerebellar sign doi: 10.1515/romneu-2017-0056 white cerebellar sign a grave prognostic indicator saurabh jain department of neurosurgery, gbh american hospital, udaipur, rajasthan, india key words: white cerebellar sign, head injury, prognosis, glasgow coma scale, resuscitation introduction a white cerebellar sign is a classic yet uncommon sign. an early recognition is required to prognosticate the patient. initially it was described with child abuse (1) and perinatal hypoxia, but later on its implications were broadened to the traumatic brain injury too. due to unknown reasons this sign is exclusively limited to pediatric population only. case presentation a two year old female child brought to emergency department after an episode of fall from 12 feet height while playing. on examination her glasgow coma scale was three( e1v1m1). very shallow respiration and pupils were not reacting. after initial intubation and ventilation, she was subjected to ncct head. the ncct head suggested multiple calvarial fractures, multiple contusions with sub arachnoid haemorrhage involving whole of cerebrum with generalised hypodensity of supratentorial compartment (figures 1, 2, 3). the patient was kept in critical care unit. inspite of best efforts the clinical condition continued to deteriorate and she died after 36 hours of hospital admission. discussion generalised hypodensity in supratentorial compartment gives an illusion of hyperdense cerebellum, that’s why it is also termed as white cerebellar sign or reversal sign. initially it was described with perinatal hypoxia and child abuse but later on described in traumatic injury. lot of case reports and review articles are available in medical literature (1-6), narrating this sign. almost all of them describes very bad outcome except chalela et al whose patient made a remarkable recovery (2). the exact cause and mechanism is yet to decipher. the work of myers is considered as a milestone who suggested that preservation of central structures is due to transtentorial herniation in stage of acute oedema. though his observations were based on animal models (3). in his another work myers suggested that elevated serum glucose secondary to anoxia, ischemia is the probable cause of this rampant process (4).while bird et al hypohesised that distension of deep medullary vein secondary to obstruction in venous outflow in elevated intracranial pressure is the principle cause of this grave sign(5). romanian neurosurgery (2017) xxxi 3: 344 345 | 345 figure 1 axial ncct head showing multiple contusions and sah and calvarial fractures figure 2 axial ncct head depicting hypordensity of supratentorial compartment conclusion generalised hypodensity in supratentorial compartment is suggestive of severe raise in intracranial pressure so much that it hampers the blood supply in bilateral cerebral hemisphere. this is seen as white cerebellar sign and associated with very bad prognosis usually in terms of mortality of sever morbidity. figure 3 axial ncct head depicting hypordensity of supratentorial compartment correspondence dr. saurabh jain 203, the garnet, 33 b new fatehpura, udaipur, rajasthan, india email: drsaurabh_jain@rediffmail.com mobile: +91 7746885699 references 1. harwoodnash dc. abuse to pediatric central nervous system. ajnr am j neuroradiol 1992;13:569-75. 2. neurocrit care. 2013 jun;18(3):398-9. the white cerebellum sign: an under recognized sign of increased intracranial pressure. chalela ja1, rothlisberger j, west b, hays a. 3. myers re. experimental models of perinatal brain damage: relevance to human pathology. in : gluck l (ed), intrauterine asphyxia and the develop brain. yearbook med: chicago; 1977. p. 37-97 4. myers re, de courten myers gm. metabolic principles of patterns of perinatal brain injury, in: crawford jw, ed. risks of labour. wiley: new york; 1985. p. 119-46. 5. bird cr, drayer bp, gillies fh. pathophysiology of reverse edema in global cerebral ischemia. ajnr am j neuroradiol 1989;10:95-8. 6. malik v, murthy tv, raj v, vyas s, mehar us. ‘white cerebellar sign’ in immediate post-partum period. [last accessed on 2014 feb 10]. 11moscote-salazar_aninternational_ romanian neurosurgery (2016) xxx 3: 383 386 | 383 an international based survey about preferences in neurosurgical irrigation fluids in neurotrauma procedures luis rafael moscote-salazar1, amit agrawal2, willem calderonmiranda3, andres rubiano4, jorge aquino-matus5 1neurosurgery department, red latinolatin american trauma & intensive neuro-care organization, bogotá, colombia 2department of neurosurgery, mm institute of medical sciences & research maharishi markandeshwar university mullana, ambala, haryana, india 3department of radiology, universidad nacional autonoma de mexico, hospital general "dr. manuel gea gonzález", mexico 4department of neurosurgery, universidad el bosque, red latino latin american trauma & intensive neuro-care organization, bogotá, colombia 5internal medicine, universidad nacional autonoma de mexico hospital general "dr. manuel gea gonzález", mexico abstract: background: traumatic brain injury surgery is the most frequently performed by neurosurgeons. the use of 0.9% saline solution (normal saline) irrigation and other solutions during neurosurgical procedures has been considered a cause of neural tissue injury. the normal saline has been used for many years, but at cellular level it may cause harmful changes. the emergence of new solutions, such as artificial cerebrospinal fluid and ringer's lactate, seem to produce less damage effects on brain tissue. the aim of this study is to evaluate the trends in use of irrigation solutions in traumatic brain injury surgeries. materials and methods: this study was conducted through a web-based survey sent to 40 neurosurgeons worldwide. results: over the period of the study data was collected from the 40 physicians and the 100% of the respondents used any type of irrigation solution during neurosurgery. conclusion: the use of normal saline in brain surgery is a widespread practice worldwide, despite the negative effects on neural tissue as it may contribute to further damage. the conception of new irrigation solutions for neurosurgery, especially in traumatic brain injury, may be a useful alternative for future studies and to expand our knowledge on this topic. key words: traumatic brain injury, neurosurgery, neurosurgical irrigation solution, harmful effects, physiological saline, ringer’s lactate solution, artificial cerebrospinal fluid introduction the routine use of various solutions such as 0.9% saline (normal saline), ringer's lactate and others have been routinely used to replenish cerebrospinal fluid leaks during neurosurgical procedures. it was established 384 | moscote-salazar et al neurosurgical irrigation fluids in neurotrauma procedures that the composition of the fluids is one of the factors associated with the development of cerebral edema. there are few published reports in the literature regarding irrigation solutions in neurosurgery (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12), but to date there is no published study focused on neurotrauma. in order to assess the current state of international trends on the use of irrigation solutions for traumatic brain injury surgery, an international webbased survey was conducted among neurosurgeons. materials and methods the primary endpoint was to determine how neurosurgeons use irrigation solutions in traumatic brain injury surgery. we developed an international web-based structured survey with real time results through an online survey creator (http://www.encuestafacil.com). the survey invitations were sent by e-mail, and aimed neurosurgeons who manage patients with traumatic brain injury to meet their management techniques in relation to national and international guidelines on head trauma (6–8), during the months of september and october 2015. for ethical considerations, no institution affiliation was requested. we used dichotomous choice questions, and multiple choice questions with a single answer. among the variables evaluated were: experience, occupation, type solutions, and the use of irrigation solutions in various traumatic brain injury surgeries. answers from the survey were compiled and entered into an excel database (microsoft®, redmond, washington, usa). each answer to a question was placed in a corresponding category and the frequencies of each category were computed. the data were analyzed by spss software 17.0 (chicago, illinois, usa). results forty neurosurgeons and residents worldwide completed the survey. most of the respondents had between 5 and 20 years of experience (5-10 years with 30% [n=12] and 10-20 years with 27.5% [n=11]). only 22.5% (n=9) had 0-5 years and 20% (n=8) had more than 21 years of experience. when asked about occupation, 30 (75%) were neurosurgeons and 10 (25%) were resident of neurosurgery. when asked about preferences of irrigation of solutions more frequently used during craniotomies, 82.5% (n=33) used normal saline solution, 12.5% (n=5) used ringer's lactate, and 5% (n=2) used other type of solution. in regard to irrigation solutions used frequently during traumatic brain injury surgery, 82.5% (n=33) used normal saline, 10% (n=4) used ringer's lactate, and 7.5% (n=3) used other type of solution. when asked about the solution used more frequently during decompressive craniectomy, 80% (n=32) used normal saline, 10% (n=4) used ringer's lactate, and 10% (n=4) used other type of solution. when considering irrigation temperature, 55% (n=22) used solutions with corporal temperature, 5% (n=2) used cold solutions, and 40% (n=16) used solutions at room temperature. the use of irrigation solutions was based on institutional policy (20%; n=8), personal preferences (47.5; n=19), and both (32.5; n=13). romanian neurosurgery (2016) xxx 3: 383 386 | 385 discusion in neurosurgical practice, very little attention has been given to deleterious effects of the solutions used for irrigation, despite the increase in the cerebral edema. in traumatic brain injury surgery it is crucial to understand the physiopatholgy of secondary posttraumatic cerebral edema, and therefore limiting additional injury to neural tissues. (13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24). in 1949, elliott reported the first artificial cerebrospinal fluid, known as elliot's solutions a and b. today its use is restricted because of the high costs. other potentially useful fluids developed in japan as artcereb show potential clinical uses at cellular level. (30) the presence of cerebral edema is well known to be a risk factor for morbidity and mortality in post-operative neurosurgery patients. some surveys have studied trends in irrigation fluids in neurosurgery (29). in this study also it was also determined that the artificial cerebrospinal fluid is mainly used in the united states, canada and japan. our results confirm data from the literature concerning that the election of irrigation solutions depends mainly on the surgeon's preference. in other tissues such as in the peritoneal cavity, it was shown that normal saline causes loss of fibrinolytic activity. (25, 26, 27, 28, 31). among the characteristics that differentiate normal saline to cerebrospinal fluid are the ph, osmolality, concentration of inorganic salts, and the absence of glucose, protein, cholesterol and others. conclusion although a web-based survey does not represent the general population of neurosurgeons worldwide, it was designed in a simplistic fashion to facilitate the ease of answer. we conclude that it is necessary to improve the state of knowledge on irrigation solutions for traumatic brain injury surgery in order to limit post-operatory cerebral edema and cellular damage. future work in the area is recommended. correspondence dr. luis rafael moscote-salazar e-mail: mineurocirujano@aol.com references 1.pople, i.k., ettles, e.d. the role of endoscopic choroids plexus coagulation in the management of hydrocephalus. neurosurgery. 1995;36:698–702. 2.uchida, k., yamada, m., hayashi, t., mine, y., kawase, t. possible harmful effects on central nervous system cells in the use of physiological saline as an irrigant during neurosurgical procedures. surg neurol. 2004;62:96–105. 3.choi, s., mccomb, j.g., levy, m.l., gonzalez-gomez, i., bayston, r. use of elemental iodine for shunt infection prophylaxis. neurosurgery. 2003;52:908–913. 4.dubey, p.k., singh, a.k. venous oxygen embolism due to hydrogen peroxide irrigation during posterior fossa surgery. j neurosurg anesthesiol. 2000;12:54–56. 5.milhorat, t.h. cerebrospinal fluid physiology. hydrocephalus and the cerebrospinal fluid. williams and wilkins, baltimore; 1972 (p. 1–41). 6.doi, k., kawano, t., morioka, y., fujita, y., nishimura, m. various irrigation fluids affect postoperative brain edema and cellular damage during experimental neurosurgery in rats. surg neurol. 2006;66:565–571. 7.elliott, k.a.c., jasper, h.h. physiological salt solutions for brain surgery: studies of local ph and pial vessel reactions to buffered and unbuffered isotonic solutions. j neurosurg. 1949;6:140–152. 8.lewis, r.c., elliott, k.a.c. clinical uses of an artificial cerebrospinal fluid. j neurosurg. 1949;6:256–260. 386 | moscote-salazar et al neurosurgical irrigation fluids in neurotrauma procedures 9.hansson, e., vällfors, b. a study of irrigation fluids for neurosurgery on brain primary cell cultures. cell mol life sci. 1980;36:64–65. 10.vällfors, b., rosengren, l.e., persson, l.i. exposure of the cat brain surface to neurosurgical irrigation fluids, hydrogen peroxide and air. quantitative assay of blood–brain barrier dysfunction. acta neurochir. 1982;64:225–232. 11.vallfors, b., hansson, h.a., belghmaidi, m. mesothelial cell integrity of the subdural and arachnoid surfaces of the cat brain after exposure to neurosurgical irrigation fluids and air: a scanning electron microscopicstudy. neurosurgery. 1983;12:35–39. 12.sakatani, k., ohtaki, m., morimoto, s., hashi, k. isotonic mannitol and the prevention of local heat generation and tissue adherence to bipolar diathermy forceps tips during electrical coagulation. technical note. j neurosurg. 1995;82:669–671. 13.enomoto, r., tatsuoka, h., komai, t., sugahara, c., takemura, k., yamauchi, a. et al, involvement of histone phosphorylation in apoptosis of human astrocytes after exposure to saline solution. neurochem int. 2004;44:459–467. 14.fujita, y., doi, k., harada, d., kamikawa, s. modulation of physiological hemostasis by irrigation solution: comparison of various irrigation solutions using a mouse brain surface bleeding model. j neurosurg. 2010;112:824–828. 15.nishimura, m., doi, k., naito, s. pharmacological assessment of artcereb irrigation and perfusion solution for cerebrospinal surgery based on glucose incorporation activity in primary cultures of rat brain cells. yakugaku zasshi. 2010;130:127–130. 16.salvador, l., valero, r., carrero, e., caral, l., fernández, s., marín, j.l. et al, cerebrospinal fluid composition modifications after neuroendoscopic procedures. minim invasive neurosurg. 2007;50:51–55. 17.el-dawlatly, a.a. blood biochemistry following endoscopic third ventriculostomy. minim invasive neurosurg. 2004;47:47–48. 18.derbent, a., erşahin, y., yurtseven, t., turhan, t. hemodynamic and electrolyte changes in patients undergoing neuroendoscopic procedures. childs nerv syst. 2006;22:253–257. 19.oka, k., yamamoto, m., nonaka, t., tomonaga, m. the significance of artificial cerebrospinal fluid as perfusate and endoneurosurgery. neurosurgery. 1996;38:733–736. 20.yamamoto, m., jimbo, m., ide, m., tanaka, n., umebara, y., hagiwara, s. perioperative antimicrobial prophylaxis in neurosurgery: clinical trial of systemic flomoxef administration and saline containing gentamicin for irrigation. neurol med chir (tokyo). 1996;36:370–376. 21.ziai, w.c., lewin, j.j. improving the role of intraventricular antimicrobial agents in the management of meningitis. curr opin neurol. 2009;22:277–282. 22.smith, s.v., forman, d.t. laboratory analysis of cerebrospinal fluid. clin lab sci. 1994;7:32–38. 23.weed, l.h., wegeforth, p. experimental irrigation of the subarachnoid space. j pharmacol exp ther. 1919;4:317–334. 24.hansson e, vällfors b. a study of irrigation fluids for neurosurgery on brain primary cell cultures. experientia. 1980 jan 15;36(1):64-5. 25.vällfors b, hansson ha, belghmaidi m. mesothelial cell integrity of the subdural and arachnoid surfaces of the cat brain after exposure to neurosurgical irrigation fluids and air: a scanning electron microscopic study.neurosurgery. 1983 jan;12(1):35-9. 26.połubinska a1, winckiewicz m, staniszewski r, breborowicz a, oreopoulos dg. time to reconsider saline as the ideal rinsing solution during abdominal surgery.am j surg. 2006 sep;192(3):281-5. 27.breborowicz a1, oreopoulos dg. is normal saline harmful to the peritoneum? perit dial int. 2005 apr;25 suppl 4:s67-70. 28.połubinska a1, breborowicz a, staniszewski r, oreopoulos dg. normal saline induces oxidative stress in peritoneal mesothelial cells. j pediatr surg. 2008 oct;43(10):1821-6. 29.shiobara, r., ohira, t., onozuka, s., & kawase, t. (2005). a study on the use of irrigation fluids in neurosurgery. japanese journal of neurosurgery, 14(5), 323-330. 30.elliot ka, jasper hh (1949) physiological salt solutions for brain surgery; studies of local ph and pial vessel reactions to buffered and unbuffered isotonic solutions. j neurosurg 6: 140-152. 31.kazim sf1, enam sa, shamim ms. possible detrimental effects of neurosurgical irrigation fluids on neural tissue: an evidence based analysis of various irrigants used in contemporary neurosurgical practice. int j surg. 2010;8(8):586-90. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article intracranial foreign body in a child luis rafael moscote-salazar, amit agrawal, marticela cabeza-morales, nasly zabaleta-churio, willem guillermo calderon-miranda, alfonso pacheco-hernandez, gabriel alcala-cerra, andres m. rubiano colombia, india, mexico doi: 10.1515/romneu-2017-0088 560 | moscote-salazar et al intracranial foreign body in a child doi: 10.1515/romneu-2017-0088 intracranial foreign body in a child luis rafael moscote-salazar1, amit agrawal2, marticela cabezamorales3, nasly zabaleta-churio4, willem guillermo calderonmiranda5, alfonso pacheco-hernandez6, gabriel alcala-cerra7, andres m. rubiano6 1neurosurgery, red latino, organización latinoamericana de trauma y cuidado neurointensivo, bogota, colombia; 2department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh, india; 3university of cartagena, cartagena de indias, colombia; 4nurse, universidad popular del cesar, valledupar, colombia; 5department of radiology, universidad nacional autonoma de mexico, ciudad de mexico, mexico; 6neurosurgery, red latino, organización latinoamericana de trauma y cuidado neurointensivo, bogota, colombia; 7neurosurgery, hospital universitario cari, barranquilla, colombia abstract: intracranial foreign bodies are rare events that occur accidentally and depending on the extent and involvement of the brain parenchymal, generate focal neurological deficit, bleeding and even long-term complications. in present article we describe a case of 4 year child and discuss the approach, management and prognosis. key words: head injuries, penetrating; craniocerebral trauma; complications introduction the presence of intracranial foreign bodies is a rare event. it occurs more frequently in men under 30 years of age (1), with children and adults being more prone to intoxication (2) within these events, a variety of modalities have been reported, some more unusual than others (3-5). the main risk of these is the generation of brain damage, which in many cases will depend on the speed with which the object enters the skull and the depth it reaches. (2). case report a 4-year-old boy attending the emergency department of the hospital de arauca for presenting a 4-hour clinical presentation consisting of a low-velocity intracranial penetrating lesion with a punctured foreign body in the temporal region. on physical examination, hemodynamic parameters were stable, glasgow 15/15, both the pupils were normal in size and reacting well to light, there was mild left brachiocrural hemiparesis. there was profuse bleeding from the scalp wound. xrays revealed a foreign body that was romanian neurosurgery (2017) xxxi 4: 560 563 | 561 penetrating the cranial vault (figure 1) and compromises part of the cerebral parenchyma in the right temporal region. in the computerized axial tomography, there is an intracranial fragment (not available). this is followed by surgery to remove a foreign body, and a right temporal craniotomy, foreign body removal, and duroplasty. postoperative the child recovered well without any neurological deficits. figure 1 a and b intracranial foreign body before surgery discussion intracranial penetrating lesions present a variety of clinical pictures, approaches and prognoses, depending on the nature and extent of the injury to the cranial vault (table 1) (1). in our case a low speed injury caused the injury, with mainly penetrating force of the object. many objects have been described as causing these pictures, from knives, pencils, nails (4-9), to umbrellas. (1) the penetration of these elements into the skull will depend on several factors, however to penetrate the skull the exerted forces must be > 522 n in the temporal region, ie. he fontanelles and the natural foramina (orbits, foramen magno, nostrils, and oral cavity) (1, 10) the temporal zone is also considered a vulnerable region because it is thinner and requires a shorter distance to cross the vital brain structures and the vasculature (1), when these lesions are directed towards the posterior region, they present with a worse prognosis. (1) the extent of these lesions does not depend only on the type, but also on the impalement trajectory (it refers to lesions where the subject in motion is impacted with the object in the form of a rod, generating a longitudinal canal) (2) and vascular lesions. (15) the diagnosis of these lesions is evident when the foreign body is observed in situ, and the ideal is not to remove it without having made an assessment of the compromised structures. (1) these patients can enter with hemodynamic alterations depending on the presence or absence of vascular lesion and according to the involved vessel. (3) the ideal is to keep the patient hemodynamically stable, 562 | moscote-salazar et al intracranial foreign body in a child with a permeable airway, until the following behavior is determined. (1) physical examination may suggest from asymptomatic pictures to paralyzes of cranial nerves (mainly iii-vi), dysphasias and hemiparesis. (1) rapid assessment is required because the patient may enter subdural and extradural hematomas, cerebral edema, cerebral contusion, pneumocephalus, hydrocephalus, and fractures, which require early attention to avoid irreversible damage. (1) the evaluation of these lesions is done through imaging studies, depending on the center of attention, radiographs and / or ct scan are used as the main studies, the latter being the one that allows a better evaluation of the adjacent structures affected. (1, 2, 11, 12) in turn the effectiveness of these will depend on the material of the object, since elements such as wood because of its low density are difficult to identify (1) and usually require the use of other aids such as magnetic resonance imaging (mri). if you suspect vascular injury, an angiogram is recommended. (1, 13) the medical treatment of these patients consists of early anticonvulsive treatment (which continues at least one week after the injury), accompanied by antibiotic (1) and if indicated anticonvulsant prophylaxis. (6) after performing the above measures the foreign body must be removed, the approach for its extraction depend on the anatomical location, compromised intracranial structures and surgeon preference. (3) in contrast to the rest of the body, the extensive area of debridement and irrigation is not recommended; on the contrary, it should be sought to preserve as much brain tissue as possible (1), and bleeding control after extraction. (1) it is recommended if there is no intracranial vascular alteration, nor associated lesions, no craniotomy after extraction. (13) some authors recommend post-surgery, leaving a subarachnoid lumbar drainage to avoid an increase in intracranial pressure. (3) when these objects are not removed early, there are remains or inadequate antibiotic coverage, there are infectious pictures that may even lead to brain abscesses in the following months. (3) in fact the post-event infection rates are higher than 40% in children. (1) among the complications are arteriovenous fistulas, occlusion (7), vasospasm, vascular transection (1) and even death in patients due to cerebral ischemia and edema secondary to arterial injury. (3) for follow-up of the patient, if penetration into the brain tissue is suspected, angiography should be repeated within 2 to 4 weeks, regardless of the method of removal used, in order to detect intracranial hemorrhage or pseudoaneurysm formation, a potentially fatal complication. (13) additionally, follow up with imaging studies. (2) conclusion the presence of intracranial objects is uncommon and requires a high index of suspicion and proper management, to prevent major neurological injuries, sepsis and unfavorable outcome. correspondence luis rafael moscote-salazar e-mail: rafaelmoscote21@gmail.com romanian neurosurgery (2017) xxxi 4: 560 563 | 563 references 1.caldicott dge, pearce a, price r, croser d, brophy b. not just another ‘head lac’… low-velocity, penetrating intra-cranial injuries: a case report and review of the literature. injury 2004;35:1044-1054. 2.orszagh m, zentner j, pollak s. transorbital intracranial impalement injuries by wooden foreign bodies: clinical, radiological and forensic aspects. forensic science international 2009;193:47-55. 3.arunkumar mj, selvapandian s, rajshekhar v. penetrating intracranial wooden object: case report and review of ct morphology, complications, and management. surg neurol 1999;51:617-620. 4.shahpurkar vv, agrawal a. fatal orbitocranial injury by fencing and spectacle sidebar. indian journal of ophthalmology 2008;56:345-346. 5.agrawal a, pratap a, agrawal cs, kumar a, rupakheti s. transorbital orbitocranial penetrating injury due to bicycle brake handle in a child. pne 2007;43:498-500. 6.ali m, usman m, alam i, ishaq m. an unusual cause of traumatic brain injury in khyber pakhtunkhwa: a case report. journal of postgraduate medical institute (peshawar-pakistan) 2012;26. 7.balasubramanian c, kaliaperumal c, jadun ck, dias ps. transorbital intracranial penetrating injury-an anatomical classification. surg neurol 2009;71:238-240. 8.srivastava c, singh sk, ojha bk, chandra a. intracranial penetrating glass injury: a case report. the indian journal of neurotrauma 2012;9:64-66. 9.suleiman ao, afolabi oa, alabi bs. an unusual penetrating stab injury in a child: case report. international journal of pediatric otorhinolaryngology extra 2013;8:119-121. 10.johnson dg, condon vr. foreign bodies in the pediatric patient. current problems in surgery 1998;35:271273-271379. 11.can m, yildirim n, ataç gk. dissecting firearm injury to the head and neck with non-linear bullet trajectory: a case report. forensic science international 2010;197:e1317. 12.türkçüoğlu p, aydoğan s. intracranial foreign body in a globe-perforating injury. can j ophthalmol 2006;41:504-505. 13.rosenson j, mantuani d. self-inflicted orbital and intracranial pencil. j emerg med 2012;43:490-491. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article rare case of multiple meningiomas in nonneurofibromatosis patient at unusual locations vikrant setia, deepashu sachdeva, shrinivas odugoudar, pravin borde, daljit singh india doi: 10.1515/romneu-2017-0040 240 | setia et al multiple meningiomas in non-neurofibromatosis patient doi: 10.1515/romneu-2017-0040 rare case of multiple meningiomas in nonneurofibromatosis patient at unusual locations vikrant setia1, deepashu sachdeva1, shrinivas odugoudar2, pravin borde1, daljit singh3 1senior resident, department of neurosurgery, g.b. pant institute of post graduate medical education and research, new delhi, india 2formerly: senior resident, g.b. pant institute of post graduate medical education and research 3head of neurosurgery department, g.b. pant institute of post graduate medical education and research, new delhi, india abstract: multiple meningioma is a condition in which more than one intracranial lesion is seen in different location and these lesions may occur with or without signs of neurofibromatosis. incidence of multiple meningioma range from 1 to 10% in different series. we report a case of multiple meningioma in a 33 years old female who had 14 intracranial lesions both supratentorially and infratentorially, and underwent surgery for large right lateral intraventricular meningioma. she had two meningiomas located in posterior fossa associated with supratentorial meningioma, which has been rarely reported. key words: meningioma, non-neurofibromatosis, supratentorially introduction the incidence of multiple meningioma is 1 to 2% of all meningioma cases in cushing and eisenhardt series.(1) inspite of multiple intracranial lesions prognosis remains almost same as solitary lesion and in one-third of cases there is occurence of different grades of malignancy simultaneously. the purpose of this case report presentation is to elicit the varied manifestation of multiple meningioma along with its management. case report a 33 years old female patient presented with to us with worsening headache and vomiting of 7 days duration, gradually progressive hearing loss in both ears for past 8 years and difficulty in balance and gait for past 2 years. on examination, patient had features suggestive of raised intracranial pressure with papilledema on bilateral fundus examination. patient had no signs of neurofibromatosis. she had bilateral sensory-neural hearing loss and ataxia. contrast enhanced ct scan and mri romanian neurosurgery (2017) xxxi 2: 240 243 | 241 revealed fourteen contrast enhancing intracranial lesions supratentorially and infratentorially, largest located in right lateral ventricle (figures 1a & 1b). the screening of spine was negative for any tumor. chromosome analysis revealed normal female karyotype and no numerical or structural anomalies detected at 450-550 banding resolution. patient underwent right temporoparietal craniotomy and excision of right lateral ventricle tumor (simpson grade ii) (figure 2a). histological examination was suggestive of grade i transitional meningioma (figure 2b). post-operative period was uneventful and patient was followed up for a period of 1 year, however patient refused further treatment and interventions. figures 1a and 1b mri scan showing location of meningiomas at various location with the largest being right intraventricular in location (1) and two infratentorial lesions (2 & 10) 242 | setia et al multiple meningiomas in non-neurofibromatosis patient figures 2a and 2b post op ct demonstrating excision of rt intraventricular tumor and histopathology showing features suggestive of transitional meningioma (who grade 1) discussion meningiomas arise from arachnoid cap cells and account for 13-19% of all intracranial neoplasms. (2,3) although most of the meningiomas are benign, 6% are atypical and 1-2% are frankly malignant.(2)most meningiomas occur sporadically and are of unknown etiology. genes associated with meningiomas are nf2 on chromosome 22 and dac-1 on chromosome 18. there is higher frequency of meningiomas in women and progesterone receptors found in 80% of meningiomas. multiple meningiomas are defined as atleast two spatially separated meningiomas occurring at same time, or more than two meningiomas arising sequentially from 2 clearly distinct regions. (4) the term ‘multiple meningiomas’ was first described by cushing and eisenhardt to denote the occurence of multiple tumors in absence of neurofibromatosis or acoustic neuromas. (1) pathogenesis of multiple meningiomas has two distinct hypothesis. the first hypothesis suggest tumor arise independently in different location and the second hypothesis suggest that a single transforming event occurs and the original clone of cells spread throughout the meninges in formation of multiple clonally related tumors. (2, 3) in locatelli et al series of 10 cases, a total of 227 intracranial meningiomas were reported from 1977 to 1984 and all 10 patients were female.(5) galabert-gonzdez et al(6) reported 13 cases of multiple mengiomas between 1983 and 2003 and none of the patient had manifestations of neurofibromatosis. after the advert of ct, domericulli et al (2) detected multiple meningioma in 4-5 % of romanian neurosurgery (2017) xxxi 2: 240 243 | 243 cases. the most common location of all was supratentorial convexity and parasagittal falx. multiple meningiomas occurring in posterior fossa are very rare. (7) in our case review we had two tumors located in posterior fossa one at cp angle and the other one in the central tentorium. about 80-90% of multiple meningiomas are benign and are who grade i. (8) tomita et al, described fibrous and anaplastic type of histology in multiple meningiomas. (9) however, in one-third of cases, simultaneous occurence of different grades of malignancy in the lesion is observed. surgery is the treatment of choice for multiple meningiomas and prognosis does not differ from solitary benign meningiomas. surgical decision is based on the following characteristics. symptomatic meningioma, asymptomatic meningioma greater than 3 cm in size and surgically accessible and symptomatic expanding tumor. (10, 11) our patient had one tumor which was removed surgically, whereas the other lesion was left to be followed up at frequent interval. the one in cp angle is planned subsequently in second admission. conclusion multiple meningiomas are rare and are seen more commonly in females. this condition is more commonly associated with neurofibromatosis. psammomatous, fibroblastic, menigothelial and transitional types are the most common histological subtypes. surgery is the treatment of choice for symptomatic lesions. prognosis of multiple meningioma is good and may be same as for solitary meningiomas. correspondence dr. pravin borde, senior residentg.b. pant institute of post graduate medical education and research. email: bordepravin26@gmail.com address: senior resident, g.b. pant institute of post graduate medical education and research; department of neurosurgery; 1, jln marg; new delhi-02 phone no: 9718599360 references 1. cushing h., and eisenhardt l., meningiomas: their classification, regional behavior, life history, and surgical end results. charles c. thomas, springfield, iii, usa, 1938. 2. domenicucci m, santoro a, d'osvaldo dh, delfini r, cantore gp, guidetti b. multiple intracranial meningiomas. j neurosurg. 1989;70:255-60 3. whittle ir, smith c, navoo p, colile d. meningiomas seminar. lancet 2004;363:1535-43. 4. spallone a, neroni m, giuffre r. multiple skull base meningiomas: case report. surg neurol 1999;51:274-80. 5. locatelli d., bottoni a., uggetti c., and gozzoli l. multiple meningiomas evaluated by computed tomography; neurochirurgia, vol. 30, no. 1, pp. 8–10, 1987 6. gelabert-gonzalez m., leira-muino r., fernandezvilla j.m. et al., “multiple intracranial meningiomas,” revista de neurologia, vol. 37, no. 8, pp. 717–22, 2003. 7. kim t. s. , park j. k., jung s. et al., “multiple intracranial meningiomas,” journal of korean neurosurgical, vol. 26, no. 12, pp. 1685–91, 1997. 8. gruber t, dare ao, balos ll, lele s, fensttermaker ra. multiple meningiomas arising during long-term therapy with progesterone agonist megerostrol acetate, j neurosurg 2004; 100:328-31 9. tomita t, kurimoto m, yamatani k y, et al. multiple meningiomas consisting of fibrous meningioma and anaplastic meningioma. journal of clinical neuroscience 2003; 10:622-24. 10. salvati m, caroli e , ferrante l, zentralbl neurochir, 2004, vol.65 (04), pp.180-4 11. sheehy jp, crockard ha. multiple meningiomas: a long-term review. j neurosurg 1983; 59:1-5. 20kulshreshthavardan_traumaticcerebellar romanian neurosurgery | volume xxx | number 4 | 2016 | october december article traumatic cerebellar hematoma in paediatric patient – a case report and review of literature vardan kulshreshtha, praveen tripathi, gaurav jaiswal, tarun kumar gupta india doi: 10.1515/romneu-2016-0092 566 | kulshreshtha et al traumatic cerebellar hematoma in paediatric patient doi: 10.1515/romneu-2016-0092 traumatic cerebellar hematoma in paediatric patient – a case report and review of literature vardan kulshreshtha, praveen tripathi, gaurav jaiswal, tarun kumar gupta rnt medical college, udaipur, india abstract: paediatric trauma is common emergency in emergency departments of hospitals worldwide. one of the uniqueness is the trauma sustained mostly in household areas and even the mode of injury is often subtle. paediatric head injury is the one of the common reasons for children visiting the emergency department. expert management and gentle care is an essential requirement in paediatric head injury cases. the management of the paediatric traumatic brain injury certainly depends upon the clinical conditions of patient and computed tomography {ct} findings. most of the traumatic brain injuries can be managed conservatively but at times the surgical management has to be undertaken. a 6 month old child admitted with the history head injury. ncct head revealed cerebellar hematoma with overlying subdural haemorrhage. initially the child was managed conservatively but as the sensorium deteriorated the surgical evacuation was performed. the paediatric post fossa traumatic haemorrhage is a relatively uncommon and the management also needs to be individualized as per the patient’s condition. key words: pediatric head injury, traumatic cerebellar hematoma introduction trauma has become a global burden over the society in terms of mortality and morbidity world over. the adults as well as children both are affected in traumatic injuries but the scenario is worse with the children. the spectrum of injuries is sometimes different in paediatric population. the deficits happen even after minor injuries yet extraordinarily more noteworthy deficits occur after serious head trauma. head injury in children represents a huge amount of emergency department visits and hospital visit every year and continues to be a major cause of mortality and disability in patients above one year of age. falls are the most frequent kind of injury, followed by road traffic accident.1 traumatic brain injury (tbi) is a leading source of childhood injury, with the centre for disease control (cdc) stating that in the usa alone, almost half a million romanian neurosurgery (2016) xxx 4: 566 572 | 567 (473,947) emergency department (ed also referred to as accident and emergency departments) visits for tbi are made annually by children aged 0 to 14 years. the children of 0-4 years were the commonest population amongst these subset of patients. (2) the fact that most are sustained in the home of the child itself is an interesting fact. in india over 40 % populations is under 15 year age. mahapatra et al in 1995 found that 30% head injury subjects were in paediatric population under the 15 years age. (3) the various modes of injury in children are fall from height, road traffic accidents, sports injuries, assault, objects falling over head, battered children. an observation of the head injuries in children from aiims delhi is detailed as under (table 1). (3) table 1 various modes of injuries in children, aiims observation of 183 patients mode number fall from a height 101 road traffic accidents 71 assault 09 sports injury 02 the paediatric tbis need an expert management. the importance of gentle nature of care given to a paediatric patient cannot be overemphasised. the initial management of the patient is same as for others emergencies includes abc protocol, assessment of consciousness and non-contrast computerized tomography [ncct]. the consciousness is assessed using modified glasgow coma scale (gcs) {table 2}. traumatic posterior fossa haemorrhages are relatively rare entity in children. the incidence of cerebellar hematoma is even rarer. we here report a case of child of 6 month with head injury resulting in cerebellar hematoma and overlying subdural haematoma (sdh) admitted in our institution. case report a 6 month baby was admitted in neurosurgical ward of our institute with the history of sustaining head injury due to falling of television set overhead. on admission the modified gcs for the child was 14/15. the ncct head was done as per the protocol. it was suggestive of the right cerebellar hematoma of 1.0 cm with overlying thin sdh with overlying subgaleal hematoma and linear fracture of the ipsilateral occipital bone (figures 1, 2). the conservative management was started. the sensorium of the patient deteriorated six hours later and the decision for the operative intervention was undertaken. right suboccipital craniectomy was performed. the cerebellar hematoma with subdural hematoma was evacuated. the child was postoperatively shifted to icu and extubated later. the child was discharged on 4th postoperative day uneventfully. on two months follow up child presented with refusal to feed and episodes of vomiting, ncct head was suggestive of the hydrocephalus (figure 3). the ventriculoperitoneal shunt was performed (figure 4). the child was discharged on 2nd postoperative day after shunt. on six month follow up the child was fine with no neurological deficits. 568 | kulshreshtha et al traumatic cerebellar hematoma in paediatric patient figure 1 ct head showing cerebellar hematoma with sdh with occipital bone fracture figure 2 ct head showing cerebellar hematoma with sdh figure 3 follow up ct head showing postoperative hydrocephalus figure 4 ct head post vp shunt discussion the scenario of a child presenting to the emergency departments with the history of trauma is common. amongst these visits the incidence of head injury are the commonest. in the study of 2100 children under 13 years of romanian neurosurgery (2016) xxx 4: 566 572 | 569 age or younger the most frequent kind of injury noted was head injury in 84.3% of cases. out of 2100 patients 161 succumbed to the injuries and 145 out of 161 died because of head injury alone. (4) the modes of the injury are mostly fall, hit with heavy object, sports activity, road traffic accidents. battered baby is a serious mode of injury and the clinicians should keep the possibility of this in mind on attending the child with polytrauma. while the traffic injuries are more common in western hemisphere the fall from height is still the leading cause of injury in our india. (5, 6) in the evaluation of 297 children in a series the incidence of head injury was found to be 22%. fall from height accounted for 67% and road traffic accidents accounted for 24.4% of the injuries. (7) in india, children between 1 and 15 years from about 35% of the total population. (3) the presentation of the child may be widely varying in cases of head injury. the child may be in shock because of losing blood intracranially which is relatively uncommon in adult population. the cranial vault in children is not rigid so the relative rise in intracranial pressure may be less severe in children as compared with adults. the processes of evaluating a child with head injury are airway, breathing, circulation, disability evaluation, exposure and evaluation of other injuries and fluid resuscitation. the proper following of these steps is mandatory for successful and effective management of the patients. it should be remembered that a child who seems to be normal may not have a score of 15/15. the best responses for the various ages have been summarised below (table 3) and should be born in mind while assessing a child. table 2 glasgow coma scale for children score response eye opening 4 spontaneous 3 to sound/speech 2 to pain 1 none verbal 5 appropriate for age 4 crying but consolable 3 irritable/restless 2 lethargic 1 none motor 6 spontaneous/obeys 5 localises 4 withdraws 3 abnormal flexion 2 abnormal extension 1 none table 3 best age matched gcs score age best motor best verbal best overall 0-6 months 2 or 3 2 9 6-12 months 4 3 11 12-24 months 4 4 12 2-5 years 4 or 5 4 13 >5 years 5 5 14 570 | kulshreshtha et al traumatic cerebellar hematoma in paediatric patient lack of physical signs can not specify that there is no intracranial pathology. (g) the difference among the clinical status and ncct findings has also been noted. sometimes it becomes difficult to correlate the ncct findings with the clinical status of patients. (8, 9, 10) the various manifestations of paediatric brain injury in children are edh, diffuse brain injury, brain contusions, depressed fractures and intraparenchymal hematoma. the various ncct findings in paediatric patients from a series of aiims 3, delhi (table 4) are as follows: table 4 ncct findings from a series of aiims, delhi type of lesion number of patients extradural hematomas 15 subdural hematomas 29 cerebral contusions 85 cerebral hematomas/ oedema 37 diffuse axonal injury 14 intraventricular haemorrhage 5 brainstem hematoma 6 cerebral infarction 8 normal scan 31 the incidence of traumatic cerebellar hematomas in the adults is quite uncommon. takeuchi et al reported in their series of 4315 patients 17 (0.4%) had cerebellar hematoma. (11) d. avella et al reported and incidence of 0.54% (18/3290). (12) sato et al reported in their series of 1176 patients 8 patients had cerebellar hematomas (0.7%). (13) the incidence of the traumatic cerebellar hematoma in children is relatively rare. this is usually followed by the direct occipital injury or as an associated manifestation of the countercoup injuries. schneider et al reported four cases of cerebellar hematoma in children (14). fisher reported 2 cases which were fatal for the patients. (15) gurdijan reported two cases of such patients with traumatic cerebellar hematomas. (16) wright et al (17) reported six cases. tsai (18) reported 14 patients of cerebellar hematoma out of which 2 were child. the management depends upon the ncct head abnormalities and the clinical condition of the patient. the ct scan is the first and most important investigation. it delineates the presence of the hematoma, size/location of hematoma, cisternal status, presence of hydrocephalus, presence of bone fractures and the status of the brainstem. mri of brain is generally not needed because of good imaging with ct head. zuccarello et al. reported five cases of cerebellar injury in their series of ten cases of traumatic posterior fossa haemorrhage in children. (19) the various possible mechanism of injury may be: 1. occipital blow with occipital bone fracture with underlying cerebellar hematoma 2. blow from front such as frontal blow and a countercoup injury 3. acceleration-deceleration injury the management as suggested initially by buczek et al was that all intracerebellar hematomas should be evacuated. (20) currently the opinions have shifted towards the conservative approach as suggested by the romanian neurosurgery (2016) xxx 4: 566 572 | 571 size of the hematoma, other associated findings, clinical status of the patients, absence of signs of raised intracranial pressure and the availability of the frequent ct scans facility. treatment may be subdivided into two categories. 1. conservative 2. surgical conservative management is employed when the patient is fully conscious and the hematoma is superficially located and size is less than 3 cm or volume less than 15 ml. however these patients should always be followed up clinically and radiologically for the expanding hematomas, obstruction of 4th ventricle or basal cisterns. surgical management is employed in the patients with size of hematoma more than 3 cm, larger hematoma causing obstructive hydrocephalus and effacement of cisterns, associated subdural or extradural hematomas. the above mentioned management may be outlined in the following algorithm. algorithm showing management of cerebellar hematoma the outcome of these patients depends upon the various factors as outlined below. (20) 1. initial gcs 2. location of hematoma 3. associated other haemorrhages {edh/ sdh} 4. status of ventricles and cisterns 5. hematoma size and volume 6. presence of subarachnoid haemorrhage 7. associated supratentorial lesions. 572 | kulshreshtha et al traumatic cerebellar hematoma in paediatric patient conclusion traumatic cerebellar hematoma is rare in children. the management should be focused over these entities as they can be potentially life threatening in children. the conservative management should be undertaken carefully as the potential for the clinical deterioration is high and urgent evacuation is the key to successful management of these hematomas. however the standard treatment protocols need to be formulated. references 1.adirim, t.a., wright, j.l., lee, e., lomax, t.a., & chamberlain, j.m. (1999). injury surveillance in a paediatric emergency department. american journal of emergency medicine, 17, 499-503. 2.centre for disease control, cdc (2010). traumatic brain injury, in the united states. emergency department visits, hospitalizations and deaths. cdc. united states. 3.mahapatra, a.k., & kamal, r. (2001). a textbook of head injury. modern publishers: new delhi. 4.schutman, s.a., barnes, p., duhaime, a.c., et al. (2001). evaluation and management of children younger than two years old with apparently minor head trauma: proposed guidelines. paediatrics, 107, 983-93. 5.venes, j.l., & collins, w.f. (1975). bifrontal decompressive craniectomy in the management of head trauma. journal of neurosurgery, 42, 429-33. 6.bharti, p., nagar, a.m., bharti, s., et al. (1995). evaluation of paediatric head injury patients in last five years. neurology india supplement, 43(171). 7.greenes, d.s., & schutzman, s.a. (1998). occult intracranial injury in infants. annals emergency medicine, 32, 680-6. 8.dietrich, a.m., bowman, m,j., ginnpease, m.e., et al. (1993). paediatric head injuries: can clinical factors reliably predict an abnormality on computed tomography? annals emergency medicine, 22, 1535-40. 9.quayle, k. s., jaffe, d.m., kupperman, n., et al. ( 1997). diagnostic testing for acute head injury in children: when are heads computed tomography and skull radiographs indicated? paediatrics, 99, e11. 10.ratan, s.k.., kulshreshtha, r., & pandey, r.m. (1999). predictors of post traumatic convulsions in head injured children. paediatric neurosurgery, 30, 127-31. 11.takeuchi, s., takasato, y., masaoka, h., & hayakawa, t. (2011). traumatic intra-cerebellar haematoma: a study of 17 cases. british journal of neurosurgery, 25, 6267. 12.d’avella, d., cacciola, f., angeleri, f.f., et al. (2001). traumatic intracerebellar haemorrhage contusions and hematomas. journal of neurosurgery science, 45, 29-37. 13.sato, k., hinokuma, k., matsuzawa, y. et al. (1987). clinical study of traumatic cerebellar contusion. no shinkei geka, 15, 1285-1289. 14.schneider, r. c. (1955). craniocerebral trauma. in correlative neurosurgery, kahn, e.a., bassett, r.c., schneider, r.c., crosby, e.c. (eds). pp275-326. springfield: charles c thomas. 15.fisher, r.g., kim, j.k., & sachs, e. (1958). complications in posterior fossa due to occipital trauma their operability. jama, 167, 176-182. 16.gurdjian, e.s., surgical treatment of patients with head injury. presented at 14th annual meeting of congress neurological surgeons, bal harbour, florida, november 18, (1964) 17.wright, r.l. (1966). traumatic haematomas of the posterior cranial fossa. journal of neurosurgery, 25, 402409. 18.tsai, f.y., teal, j.s., itabashi, h.h., huprich, j.e., hieshima, g.b., & segall, h.d. (1980). computed tomography of posterior fossa trauma. journal computer assisted tomography, 4, 291-305. 19.zuccarello, m., andrioli, g.c., fiore, d.l., longatti, p.l., pardatsher, k., & zampieri, p. (1982). traumatic posterior fossa haemorrhage in children. acta neurochir (wein), 62, 79-85. 20.buczek, m., jagodzinski, z., kopytek, m., & dabrowska, e. (1989). conservative treatment of posttraumatic intracerebellar hematoma. wiad lek, 42, 550555 microsoft word 13dabijamgiantfrontal.doc m. dabija, n. ianovici giant epidermoid cyst 103 giant frontal and cerebellopontine angle epidermoid cyst. case report m. dabija, n. ianovici neurosurgery, university of medicine and pharmacy “gr.t. popa” iasi abstract we present the case of a 38-years old woman presenting in a state of unconsciousness, (glasgow coma scale score 7), with right hemiparesis, the onset of symptoms being acute, after 3 consecutive convulsive crisis, in a patient with no previous neurological sign, except progressive aggravating headaches. cranial computed tomography reveal an enormous hypodense lesion in the left frontal and temporal lobe, frontal horns of the ventricular system and prepontine and cerebellopontine angle regions. the patient underwent emergent surgical intervention, the evacuation of the content and partial removal of the capsule of the giant epidermoid cyst was achieved by frontal craniotomy. the diagnosis was presumed by the classical aspect of the content of the cyst and it was confirmed by histological examination. the immediate postoperative evolution was good with regression of hemiparesis and comatose state, with one complication in the third day after surgery; she developed the symptoms of mollaret meningitis, with nearly normal csf parameters, who responded well at the treatment with dexamethasone. keywords: epidermoid cyst, aseptic meningitis introduction epidermoid cysts, also known as "pearly tumors” because of their bright white appearance at intraoperative resection, developed from epithelial inclusions in basal cisterns, diploe of the skull and, very rarely in the intrinsic brainstem or pineal region, during neural tube closure or formation of secondary cerebral vesicles. they are not really tumors, their growth is due to the continuous formation of the keratohyalin from continued desquamation by the epithelium tissue. their growth is very slow, so the onset of their clinical manifestations is variable between 20 and 40 years in most of the cases. we present our experience with a patient who has a giant epidermoid cyst in the frontal area with infratentorial extension in the prepontine and cerebelopontine angles with surgical resection of the lesion. we report these very rare case and we made a short discussion with reviews of the literature. case report we present our experience with the case of a 38 years old woman who presented in the emergency room in a comatose state, with right hemiparesis, right facial central nerve paresis, generalized hypertonic state with neck stiffness and bilateral babinsky sign. it was in fact a post epileptic condition, the patient suffered 5 consecutive crisis with no free interval between them. the 104 romanian neurosurgery (2010) xvii 1: 103 107 mother of the patient reported a history of chronic headaches with a progressively aggravated evolution, which was, especially in the last two month, intractable to non-narcotic analgesics, associated occasionally with nausea, dizziness and vomiting. a ct-scan was performed in emergency and it revealed an extremely large well circumscribed hypodense lesion, which occupied the anterior left cranial fossa, the temporal pole, involved the both frontal horns with infratentorial extension in the prepontine and cerebellopontine cisterns. the formation was slightly hyperdense when compare to the csf and it had a heterogeneous appearance. no enhancement was noticed after contrast administration. figure 1 preoperative image of the frontaltemporal cyst figure 2 the lesion involves the frontal horns of the lateral ventricles figure 3 prepontine extension of the epidermoid cyst m. dabija, n. ianovici giant epidermoid cyst 105 figure 4 right cerebellopontine extension of the lesion the patient was hospitalized in the intensive care unit and the evolution was favorable with the recovery of the state of conscience but with a mild confusion and somnolence and persistence of the right hemiparesis and dysphasia. the very next day the patient underwent the surgical intervention. we performed a fronto-temporal craniotomy and, after the incision of the dura we discovered the specific aspect of the pearly-white desquamated keratin flakes which was removed and the dissection of the capsule was performed. this capsule was very adherent especially at the level of the sylvian and carotid vessels and at the level of the optic nerve and even at the cortical level in some points, therefore we was forced to make only a subtotal excision. we demanded a histological exam of the capsule and that one confirmed a stratified squamous epithelium. the postoperative ct_scan revealed a remnant of the epidermoid material at the level of the ventricular system, especially in the right (contra lateral) one. because of the very low growing rate of the lesion we decided to survey these remnants and those of the posterior fossa. figure 5 postoperative image at 24 hours figure 6 postoperative image at 48 hours 106 romanian neurosurgery (2010) xvii 1: 103 107 figure 7 postoperative image: ventricular residual epidermoid material the postoperative evolution was very good in the first two days with complete recovery of the preoperative mild hemiparesis, but, in the third day, the patient accused severe headaches, nausea, vomiting, and fever (temperature between 38 and 39,5°c). we performed a lumbar puncture and that one revealed no meningitis aspects, wbc count of 0/mm³, glucose was 50mg/dl, the proteins was 76 mg/dl and we found 2560 red cells/mm³. the aseptic mollaret meningitis was very probable the cause and the evolution was good with the remission of the symptoms in three days under the treatment with dexamethasone. in the fourth and fifth postoperative days the patient installed two right jacksonian crisis and we start a treatment with depakine chrono 1500mg/day. the patient was discharged with no neurological deficits and no other accuses in the 14-th postoperative day. discussions epidermoid tumor was first reported in 1683 by duverney(7) and their first epidermal origin description and their nomination as “epidermoid” was in 1854 by remak(8). epidermoid is a term who means “epiderm like” and it clearly suggests that their content is made of the tissues normally present in the skin. the capsule of these lesions is, in fact, a keratinizing stratified squamous epithelium that resembles the keratinizing epidermis of the skin and the fibrous capsule is a dermal connective tissue (1). the interior is formed by a “pearly” white, waxy tissue, formed by concentric lamellar deposits of keratin rich in cholesterol crystals, secreted by the basal cuboidal germinative stratus of the peripheral epidermal tissue (2). their origin is in ectopic inclusions of epithelial cells during neural tube closure (3) or as a dysembriogenesis of the gastrulation with a secondary disruption of the neural tube continuity in the third to fifth week of gestation (4). the location of the epidermoid cysts includes the diploic region of the calvaria, ventricular system, cerebellopontine angle, optic chiasm and parapituitary region, pineal area and the collicular plate. they can displace or envelope neural or vascular structures and they may have a thick capsule witch can be very adherent to the surrounding brain tissue, vessels and nerves. due to their very slow growth, their mean age of clinical manifestations and hospital admission is 35 years and they occur more often in women (5). the dermoid cysts, witch contains also hair follicles and sebaceous glands, tend to reveal by more precocious symptoms, because their content, more heterogeneous, increase more rapidly. one of the most common initial symptoms is the severe headache due to the raised intracranial pressure but, very often, to the aseptic meningitis, explained by the leakage of the cholesterol in the m. dabija, n. ianovici giant epidermoid cyst 107 cerebrospinal fluid and chemical irritation (6). that may be the case of our patient who suffered intractable headache with nausea and vomiting in the last two month before the presentation. the symptoms are not specific and depend on the location of the cyst. the clinical picture developed insidiously due to the slow keratin formation but there are also described acute evolutions by rupture of the cysts (spontaneous, traumatic, or iatrogenic) or by cystic hemorrhage. the rupture of the cyst can produce also the aseptic meningitis or mollaret meningitis. mollaret described that type of recurrent, aseptic and selflimited meningitis in 1944 in a patient with an spinal thoracic epidermoid lesion. he described also the mollaret cells, a type of leucocytes larger then the common pmns with round or kidney shape and deep situated nucleus, presented in the blood tests of that patient (9). our patient installed that type of meningitis in the postoperative period, with violent headaches, nausea, vomiting, fever, neck stiffness photophobia and nearly normal constants in the csf analysis. the symptoms responded well to corticoid therapy. ventricular involvement, with both frontal horns occupied by the epidermoid material may play a role in the preoperative violent headaches and postoperative mollaret meningitis. conclusions epidermoid cyst is a rare condition, and the predilection for the ventricular system or cerebellopontine angle is well known, but we present a case which associated the two previous locations with the frontal temporal location, an extremely rare one. the onset of symptoms with progressive aggravating headaches, nausea and vomiting is the common one, but the presentation of the patient with 5 consecutive generalized crises, with hemiparesis and mild dysphasia might be a rare debut. postoperative evolution was good with complete recovery and absence of any symptoms at the discharge from the hospital and in the next 2 years of our neurological surveillance. the postoperative aseptic meningitis is a common complication and is due to the chemical irritation of the csf and the subarachnoid space by the collagen rich content of the cyst. references 1. robert h. wilkins, setti s. rengachary: neurosurgery, vol.1, part vi, neuro-oncology: an overview, section e, epidermoi and dermoid tumors, pp 655-661; 2. fornari m, solero c l: surgical treatment of intracranial dermoid and epidermoid cysts in children, childs nervous system, 6: 66-70, 1990; 3. gormley w, tomecek f, qureshi n: craniocerebral epidermoid and dermoid tumors: a review of 32 cases, acta neurochirurgica (wien) 128; pp1115-1121, 1994; 4. dias m, walker m: the embryogenesis of complex dysraphic malformations: a disorder of gastrulation? pediatric neurosurgery 18: pp229-253, 1992; 5. winn r, dacey r: youmans neurological surgery, fifth edition, saunders, volume 1, section ii, part 6, 68 epidermoid, dermoid and neurenteric cysts, 12231231, 2004 6. desouza c, desouza r, da costa s: cerebellopontine angle epidermoid cysts: a report on 30 cases, journal ofneurology, neurosurgery, and psychiatry;52:986-990, 1989; 7. ji young jeon, jae min kim: epidermoid cyst of the fourth ventricle, journal of the korean neurosurgery society 38: 478-480, 2005; 8. remak r : ein beitrag zur entwicklungsgeschichte der krebshaften geschwulste. dtsch arch klin med. 6: 170, 1854; 9. baoqin gao, jun yang: mollaret meningitis associated with an intraspinal epidermoid cyst, pediatrics 120;e220-e224, 2007; romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article surgery in cervical disc herniation: anterior cervical discectomy without fusion or with fusion andrei stefan iencean romania doi: 10.1515/romneu-2017-0008 54 | iencean surgery in cervical disc herniation             doi: 10.1515/romneu-2017-0008 surgery in cervical disc herniation: anterior cervical discectomy without fusion or with fusion andrei stefan iencean phd student, “grigore t. popa” university of medicine and pharmacy iasi, iasi, romania department of neurosurgery, “n. oblu” emergency hospital iasi, romania abstract: the study included a group of anterior cervical microdiscectomy without fusion performed at one level (either c5-c6 level or at the c6-c7 level) and a second group of patients with same single-level of anterior cervical discectomy with fusion. the kinematic analysis included the range of motion, anteroposterior translation and disc height assessed for the cervical functional spinal units at the operated level and adjacent levels. at the operated level the range of motion and the translation were minimal in the anterior cervical discectomy without fusion group, both for the c5-c6 and c6-c7 levels, and absent in the cervical discectomy with fusion group. the superior adjacent levels translations were greater in the acdf group compared with the acd group. the clinical results of both types of cervical discectomy were comparable. in cervical microdiscectomy without fusion the elastic fibrous intradiscal scar at the operated level allows a small degree of mobility and the adjacent cervical levels are not overstressed. no need for anterior cervical discectomy with fusion to trait a single level cervical disc herniation than in selected cases. key words: anterior cervical discectomy without fusion, anterior cervical discectomy with fusion, elastic fibrous intradiscal scar, postoperative intervertebral translation introduction cervical disc herniation is a common pathology of the cervical spine and the surgical treatment lead to the decompression of compressed neural elements and the stability of the cervical spine, without abnormal movements. anterior cervical discectomy without fusion (acd) and anterior cervical discectomy with fusion (acdf) are common approaches among spine surgeons for most cervical herniated discs. most spinal surgeons consider that the results of these two types of approaches (acd and acdf) are comparable both in terms of the decompression and the cervical stability. we tried to determine the biomechanical differences of anterior cervical discectomy without fusion versus anterior cervical discectomy with fusion in this study. romanian neurosurgery (2017) xxxi 1: 54 – 58 | 55             material and methods we present a comparative study of patients undergoing one level anterior cervical discectomy without fusion versus anterior cervical discectomy with fusion. the study included forty patients operated at either c5c6 level or at the c6-c7 level: a group of anterior cervical microdiscectomy without fusion performed at one level on 20 consecutive patients was matched to a second group of 20 patients with single-level of anterior cervical discectomy with fusion based on level, age and sex. inclusion criteria for the acd and acdf groups: patients included for the acd and acdf groups presented with clinical symptoms due to one level herniated cervical disc; patients had preoperative complete general and neurological examination, all patients had preoperative mri and plain radiographs of the cervical spine anterioposterior, lateral neutral, flexion and extension obtained preoperatively. as exclusion criteria: the patients with clinical or imagistic evidence (mri, x-rays) of additional diseased cervical spine, history of cervical spinal injury were excluded from the study. also the patients with cervical instability at the level of disc herniation, which need a possible fusion and fixation, were excluded from the group of acd patients. the study selection criteria and outcome measures were identical, with the exception being the surgical technique: anterior cervical microdiscectomy without fusion and anterior cervical discectomy with fusion. figure 1 preoperative mri of c5-c6 disc herniation and postoperatively mri after anterior cervical microdiscectomy without fusion the biomechanical analysis included the intervertebral angulations, antero-posterior translation and disc height assessed for the cervical functional spinal units at the operated level and adjacent levels. the measurements of preoperative and postoperative anterior-posterior translation of the operated level and of the superjacent levels were compared between the groups of acd and acdf. thus the translations of c3c4 level and c4c5 level were compared for the c5c6 operated level with the same level translation between the groups of acd and acdf. the intervertebral translations were measured in millimeters on the converted digital radiographies using dicom viewer software. these parameters were studied in the matched patients from both groups using the statistical averages, standard deviations, the paired student's t-test and p-value for statistical significance. 56 | iencean surgery in cervical disc herniation             figure 2 intervertebral translation during cervical flexion and axtension results the demographic data of these patients are presented in table 1. the distribution of patients by age, sex and level of disc herniation is not significant because the cases were selected to match according to the type of surgery. the clinical results of these two types of approaches were comparable. at the operated level the range of motion and the translation were present in the acd group, for operated level, c5-c6 and c6-c7 and were absent in the acdf group. the statistical averages of the preoperative intervertebral translations of c3-c4 and c4c5 levels for operated c5-c6 level were equal each level for both type of surgery and also they are very similar for operated c6-c7 level in acd and acdf. the statistical analysis using student's t-test of these postoperative intervertebral translations of superjacent levels of operated level by these two types of surgery found a p-value <0.01, therefore a very good statistical significance as shown in table 2. the comparison of superjacent translations for the fusion at c5-c6 and c6-c7 levels found that the inferior level fusion (c6c7) produced a higher increase in the c3-c4 level translation. table i demographic data of patients for each group of discectomy (in pairs) table ii the mean values of the postoperatively intervertebral translations during cervical flexion and extension for operated c5-c6 / c6-c7 disc herniation (in mm). (p<0.01) age 35-39 40-49 50-58 total acd / acdf c5-c6 m f 2 1 2 1 2 2 6 4 acd / acdf c6-c7 m f 1 1 2 2 2 2 5 5 operated levels measured level acd acdf δ normal (mean) c5-c6 c3 c4 2.4 2.6 0.27 2.1 c4 c5 2.3 2.4 0.10 2.5 c5 c6 0.5 0 2.2 c6-c7 c3-c4 2.1 2.4 0.34 2.1 c4-c5 2.2 2.4 0.2 2.5 c5-c6 1.54 1.67 0.13 2.2 c6-c7 0.14 0 1.3 romanian neurosurgery (2017) xxxi 1: 54 – 58 | 57             the range of motion and the translation were greater at superjacent levels in the acdf group compared with the acd group. discussion in this study we determined the differences in the intervertebral translations one year postoperatively after anterior cervical microdiscectomy without fusion versus anterior cervical discectomy with fusion in two groups in pairs, each of 20 patients. the comparison of our results with the normal data showed the translation was present in the acd group and the translation was absent in the acdf group at the operated level. the absence of intervertebral translation at the operated level is explained by intervertebral fusion in the acdf group. the presence of lower values of intervertebral translation at the operated level in the acd group is normal and is not a spinal instability. the healing at the operated level after the acd consists of an intradiscal fibrous scar and not a real bone fusion because the cartilaginous endplates should be left intact. this elastic fibrous intradiscal scar ensures the cervical stability and allows a small degree of mobility at the operated level in the acd group. in the acd group the means of the intervertebral translation were close to normal values at superjacent levels and in the acdf group the intervertebral translation was greater compared with the normal values and with the acd group. the comparison of superjacent translations found that the c6-c7 level fusion produced a higher increase in the c3-c4 level translation than the c5-c6 level fusion, therefore the range of motion is higher at a more distant level where the amplitude of movement may be higher. these results may explain why acdf may lead to acceleration of degenerative changes at immediately overstressed superjacent discal levels secondary to abnormal spinal motion. the results of this study and the review of the literature show that acd has comparable clinical results with acdf in single level cervical disc herniation and acd ensures postoperatively a very good cervical stability. conclusions the clinical results of anterior cervical microdiscectomy without fusion and anterior cervical discectomy with fusion were comparable. in anterior cervical microdiscectomy without fusion the elastic fibrous intradiscal scar at the operated level allows a small degree of mobility and the adjacent cervical levels are not overstressed. anterior cervical discectomy with fusion may lead to acceleration of degenerative changes at immediately overstressed adjacent discal levels secondary to greater intervertebral translation at these adjacent levels. we believe that there is no need for anterior cervical discectomy with fusion to trait a single level cervical disc herniation than in selected cases with preoperative instability at same level. anterior cervical microdiscectomy without fusion is a valid option in patients with one level cervical disc herniation without local instability. references 1.gebremariam l, koes bw, peul wc, huisstede bm.evaluation of treatment effectiveness for the 58 | iencean surgery in cervical disc herniation             herniated cervical disc: a systematic review. spine 2012; 37:e109-118. 2. caruso r, pesce a, marrocco l, wierzbicki v. anterior approach to the cervical spine for treatment of spondylosis or disc herniation: long-term results. comparison between acd, acdf, tdr. clin ter 2014; 165: e263-270. 3. song kj, choi by. current concepts of anterior cervical discectomy and fusion: a review of literature. asian spine j 2014; 8: 531-539. 4. yang j, hai y, pang c, li h, zu d, zhu g, xia x, pei b. biomechanical study on the effect of the length of cervical anterior fusion on adjacent levels. zhonghua wai ke za zhi 2014; 52: 692-696. 5. xia lz, zheng yp, xu hg, liu p. effect of anterior cervical discectomy and fusion on adjacent segments in rabbits. int j clin exp med 2014; 7: 4291-4299. 6. oktenoglu t, cosar m, ozer af, iplikcioglu c, sasani m, canbulat n,sarioglu ac. anterior cervical microdiscectomy with or without fusion. j spinal disord tech 2007; 20: 361-368. 7. rosenthal p, kim kd. cervical adjacent segment pathology following fusion: is it due to fusion? world j orthop 2013;4: 112-113. 8. wu sk, kuo lc, lan hc, tsai sw, chen cl, su fc. the quantitative measurements of the intervertebral angulation and translation during cervical flexion and extension. eur spine j 2007; 16: 1435-1444 9. lundine km, davis g, rogers m, staples m, quan g. prevalence of adjacent segment disc degeneration in patients undergoing anterior cervical discectomy andfusion based on pre-operative mri findings. j clin neurosci 2014;21: 82-85. 10. rihn ja, lawrence j, gates c, harris e, hilibrand as. adjacent segment disease after cervical spine fusion. instr course lect 2009; 58: 747-756. 11. sheth jh, patankar ap, shah r. anterior cervical microdiscectomy: is bone grafting and in-situ fusion with instrumentation required? br j neurosurg 2012; 26: 12-15. 12. nandoe tewarie rd, bartels rh, peul wc. longterm outcome after anterior cervical discectomy without fusion. eur spine j 2007; 16: 1411-1416. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article multilevel “fish vertebrae” in a patient with tumor-induced osteomalacia d. adam, d. iftimie, gina burduşa, cristiana moisescu romania doi: 10.1515/romneu-2017-0048 294 | adam et al multilevel “fish vertebrae” in a patient with tumor-induced osteomalacia doi: 10.1515/romneu-2017-0048 multilevel “fish vertebrae” in a patient with tumorinduced osteomalacia d. adam1,2, d. iftimie1, gina burduşa1, cristiana moisescu1 1department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania abstract: background and importance: “fish vertebra” is an uncommon anomaly of vertebral body shape, consisting of central depression of the superior and inferior vertebral surfaces. it has been associated with various conditions: osteoporosis, osteomalacia, hyperparathyroidism, paget disease, sickle cell disease, multiple myeloma and systemic lupus erythematosus. clinical presentation: a 29-year-old male patient, previously treated for ankylosing spondylitis (with nsaids and tnfα inhibitor), without any clinical improvement, was admitted to our neurosurgical department. he complained of difficult gait, possible only with the aid of a cane, low back pain and bilateral hip pain, but without leg pain. he denied any history of recent trauma. neurological examination was normal. plain thoracic and lumbar spine x-rays revealed multilevel “fish vertebrae”. lumbar spine mri and contrast thoraco-abdominal ct scan showed fractures of multiple structures: left l4 pedicle, right l4 lamina and pars interarticularis, right ii-vii costal arches, left i-v costal arches and bilateral sacral alae. we performed extensive laboratory tests that detected low seric phosphorous and pth levels, with increased alkaline phosphatase, indicating a possible endocrinological cause for this condition. subsequently, we decided to transfer the patient to an endocrinological department. a diagnosis of hypophosphatemic osteomalacia was established and increased fgf23 levels, later determined, suggested it was tumorinduced osteomalacia. whole-body mri was unable to locate the tumor, but gallium-68 dotatate pet/ct revealed a small (15 mm in diameter), hyperfixating mass in the head of the right femur. the patient was treated with oral calcitriol and phosphate, with alleviation of symptoms. surgical excision of the tumor was recommended, but the patient decided to postopone the operation. conclusion: modern medical imaging and biochemical testing have made the leap from merely observing vertebral biconcavities to diagnosing their cause and, consequently, the possibility to adequately treat uncommon causes of “fish vertebra”, such as neuroendocrine tumor-induced osteomalacia. key words: fish vertebrae, hypophosfatemic osteomalacia, tumor-induced osteomalacia (tio), multiple fractures, fgf23, gallium-68 dotatate pet/ct romanian neurosurgery (2017) xxxi 3: 294 301 | 295 clinical presentation a 29-year-old male, former cocaine user (until 2010), with a negative family history for neoplasia or osteomalacia, was previously diagnosed with ankylosing spondylitis at an university hospital in great britain, approximately a year prior to his presentation at our neurosurgical department. he had been treated with nsaids and subsequently tnfα inhibitor (adalimumab), without alleviation of symptoms. at that time, a contrast thoraco-abdominal ct scan revealed modified thoracic and lumbar vertebral bodies, with a biconcave aspect and no other focal bone lesions, an aspect suggestive for a congenital metabolic or endocrine disorder. at admission to our department, he presented a difficult gait, possible only with the aid of a cane, low back pain, bilateral hip pain, but without leg pain. he mentioned a fall from approximately 2,5 meters approximately 7 years ago, but denied any history of recent significant trauma. general physical examination revealed a patient with normal weight, generalized muscle atrophy, thoracolumbar kyphoscoliosis and rigidity of thoracic and lumbar spine. neurological examination was normal. plain lumbar and thoracic spine x-rays revealed a symmetrical biconcave deformity of all visualized vertebral bodies, an aspect also known as “fish vertebrae” (figures 1a, 1b). lumbar mri confirmed the “fish vertebra” appearance of lumbar vertebral bodies (figure 2a) and additionally showed a recent left l4 pedicle fracture (figure 2b). however, lumbar vertebral alterations suggestive for ankylosing spondylitis were absent. a b figure 1 lumbar (a) and thoracic (b) spine x-ray revealing a symmetrical biconcave aspect of all vertebral bodies (“fish vertebrae”) figure 2 (a): lumbar mri (t2-weighted) confirming the “fish vertebrae” appearance of vertebral bodies. (b): axial slice (t2-weighted) of lumbar mri showing a recent left l4 pedicle fracture a b 296 | adam et al multilevel “fish vertebrae” in a patient with tumor-induced osteomalacia we performed a thoraco-abdominal contrast ct scan, which revealed the “fish vertebra” aspect of all thoracic and lumbar vertebral bodies (figure 3.a, 3.b) and, in comparison with the previous ct scan and lumbar mri, fractures of multiple additional structures: •right l4 lamina and pars interarticularis; type a0 spinal fractures according to the ao spine classiffication (figure 3.c), •right ii-vii costal arches and left i-v costal arches •bilateral sacral alae the patient’s routine blood tests were unremarkable. therefore, we performed extensive laboratory test in order to determine the cause of the patient’s “fish vertebra” and multiple spontaneous fractures. inflammation markers were within normal ranges. we ruled out sickle cell disease because the patient’s hemoglobin levels and peripheral blood smear were normal. available tests for autoimmune diseases, such as hla-b27, rheumatoid factor, anti-ro, anti-dsdna, c-anca, p-anca, anti-mitochondrial antibodies, were also within normal ranges. the abnormalities that caught our attention were the low blood phosphate and parathyroid hormone (pth) levels, with an increased alkaline phosphatase (table i). we strongly suspected an endocrinological condition and therefore decided to transfer the patient to an endocrinology department of a neighboring hospital. figure 3 coronal (a) and sagittal (b) ct slices of the thoraco-lumbar spine showing the multilevel “fish vertebrae” aspect. (c): sagital ct image revealing a l4 lamina and pars interarticularis fracture a b c romanian neurosurgery (2017) xxxi 3: 294 301 | 297 table i blood test anomalies that suggested an endocrinological condition endocrinologists continued investigations, revealing osteoporosis on dxa scan, increased bone turnover markers (β-crosslap and p1np) suggestive for increased bone resorbtion, low 25-hydroxy-vitamin d, hyperphosphaturia, proteinuria and glycosuria (tabel ii). they established the diagnosis of hypophosphatemic osteomalacia with adult onset, considering that the differential diagnosis should be made between acquired fanconi syndrome, congenital hypophosphatemic rickets with adult onset and tumor-induced osteomalacia. table ii additional tests performed by endocrinologists the patient was treated with oral calcitriol and phosphates (potassium dihydrogenphosphate/sodium monohydrogenphosphate dihydrate) under phosphatemia control and recommended a dairy-rich diet. one month later, he presented slight alleviation of symptoms and partial correction of hypophosphatemia. fgf-23 levels (a test not widely available), later determined, were increased (383 pg/ml, with a normal range of 26-110 pg/ml), highly suggestive for oncogenic osteomalacia. the next step was locating the causative tumor. the patient underwent a whole body mri that was unable to detect a tumor, showing only bone alterations compatible with osteomalacia. however, a gallium-68 dotatate pet/ct subsequently performed revealed a small, hyperfixating lesion in the right femoral head (15 mm in diameter), with a high expression of somatostatin receptors, which suggested a neuroendocrine tumor (figure 4a, 4b). investigation result normal range seric phosphorus 1,43 2.7 – 4.5 mg/dl pth 9,83 15 – 65 pg/ml alkaline phosphatase 335 35 – 129 ui/l investigation result normal range seric phosphorus 1,7 2,3 – 4,7 mg/dl alkaline phosphatase 306 38 – 129 ui/l 24-hour urine phosphorous 1,54 0,3 – 1 g/24 h 24-hour urine glucose 5.8 0 – 0,5 g/24 h dxa lumbar spine t = -4,3 osteoporosis = t≤ -2,5 dxa left hip t = -3,9 osteoporosis = t≤ -2,5 298 | adam et al multilevel “fish vertebrae” in a patient with tumor-induced osteomalacia figure 3 coronal (a) and axial (b) slices of the gallium-68 dotatate pet/ct, showing a small (15 mm in diameter) hiperfixating lesion located in the right femoral head surgical excision of the tumor was recommended, but the patient decided to postpone surgery. his symptoms continued to alleviate under treatment. unfortunately, due to a lack of histopathological analysis of the tumor, a definitive diagnosis could not be established. discussion classical radiological investigations and modern imagistic techniques of the spine can reveal vertebral bodies with altered shape. an uncommon type of modified vertebral body is called “fish vertebra”. these particular vertebrae present a biconcave aspect determined by the depression of the central area of the superior and inferior vertebral surfaces. the changes in normal vertebral body shape can be limited to a single vertebra or extend to several levels. biconcave vertebrae, an abnormal shape for human vertebrae, were called “fish vertebrae” due to the resemblance with the normal vertebrae of fish, described by albright, resnick or rexroad in codfish, tuna or salmon, respectively. the biconvex appearance of the disc between two “fish vertebrae” is similar to a fish mouth, hence the alternative term of “fish mouth vertebrae”. (1, 2) the earliest reports of this spinal anomaly were published in the first half of the 20th century, on the basis of their radiological appearance. the first description of a biconcave vertebra belongs to schmorl. in 1926, he reported it in a patient with osteomalacia, stating that the vertebra resembled “the silhouette of a fish vertebra”3. the intraosseous herniation of the intervertebral disc causes disruption of the subchondral bone. “fish vertebrae” are most prominent in the lower thoracic and upper lumbar regions of the spine. this biconcave aspect of vertebrae has been described in various conditions: osteoporosis, a b romanian neurosurgery (2017) xxxi 3: 294 301 | 299 osteomalacia, hyperparathyroidism, paget disease, sickle cell disease, multiple myeloma and sle (lupus). (1, 2, 4–7) “fish vertebrae” have been frequently encountered in patients with age-related osteoporosis. a single vertebral body can be affected with an unequal concavity of the superior and inferior surface of the vertebra. furthermore, an emphasis of the subchondral bone and of the vertical trabecular pattern can be seen on plain spine x-ray. however, the most frequent shape alteration of an osteoporotic vertebra is represented by a compression fracture, with the characteristic wedge-vertebra aspect. in the case of osteomalacia, all vertebral bodies can present a “fish vertebra” aspect with the two endplates equally depressed. in 1932, leivy (8) first described the biconcave appearance of vertebrae in patients with sickle cell disease (scd), considering it pathognomonic for this condition. due to the fact that the same radiological aspect also appears in other diseases, distinctive radiological features (for the cup-like depression of vertebrae in patients with scd) were searched. caroll et al (9) considered that “cupping of the vertebral end plates… is manifest in about 30% of the adults with this blood dyscrasia”. this form of endplate distortion is considered to be a defect in development and not an acquired lesion, as in the case of osteoporosis. in the case of patients with sickle cell disease, the floor of central depression is flat, not rounded, and the concavity of the two vertebral surfaces is almost identical in shape and depth, i.e. simetrical. the development of these shape alterations is caused by stasis of regional circulation, anoxia and ischemia associated with this chronic hemolytic anemia. (10) the cartilaginous endplate is the equivalent of the growth cartilage of long bones, the metaphysis. ischemia manifests itself significantly more in the middle portion because the periphery is also vascularized by short perforating vessels from the periosteal circulation. thus, the central part of the vertebral growth plate is the one predominantly affected by circulatory alterations, determining a local inhibition of bone growth. pathological changes appear in the first year and continue throughout the patient’s life, but the radiological features become apparent in their teens. the first descriptions of “fish vertebra” using classical radiological examinations only noted that the sign appears in several conditions. speculations were made regarding the mechanism of similarly development of this particular shape in such different disorders. although the “fish vertebra” aspect has attracted the attention of radiologists, rheumatologist and endocrinologists, there are only a small number of published cases. modern imagistic techniques have allowed not only the confirmation of biconcave vertebral bodies, but also establishing the causes of these alterations. in our patient, ct and mri scans revealed the uncommon fish vertebra aspect, but also multiple fractures that impaired his locomotion and were an explanation for his pain. 300 | adam et al multilevel “fish vertebrae” in a patient with tumor-induced osteomalacia absence of family history, blood test markers and radiological changes associated with autoimmune diseases (such as ankylosing spondylitis) were suggestive for a different type of disorder. the correlation between hypophosphatemia and hyperphosphaturia with a dxa test positive for osteoporosis oriented the differential diagnosis to osteomalacia, possibly caused by an endocrine tumor, i.e. oncogenic osteomalacia. this diagnosis was supported by high levels of fgf23, which is secreted by osteocytes in response to elevated calcitriol levels and overproduced by some types of tumors, such as benign mesenchymal neoplasms. (11, 12) tumor induced osteomalacia is considered a paraneoplastic syndrome. (13) the main role of fgf23 is the regulation of plasmatic phosphate concentration. it decreases the reabsorption and increases excretion of phosphate in the proximal renal tubule. also, it inhibits production and stimulates the breakdown of calcitriol. tumors secreting fgf23 are often small and difficult to find with conventional imaging. (14) in our case, a whole body mri was unable to detect the tumor. gallium (68ga) dota-tate (gatate) was used for tumor diagnosis with pet/ct. (15) dotatate is an amide of the acid dota which acts as a chelator for a radionuclide and (tyr3)-octreotate, a derivation of octeotride, which binds to somatostatin receptors found on the cell’s surface of some neuroendocrine tumors. thus, the tumor was found in the right femoral head, presenting a diameter of only 15 mm. conclusion “fish vertebra” or biconcave vertebra represents an uncommon anomaly of the vertebral body, initially revealed by roentgenologic investigation. it is associated with several conditions (osteoporosis, osteomalacia, sickle cell disease etc.), with minor variations in aspect of the concavities. modern medical imaging and biochemical testing have made the leap from merely observing vertebral biconcavities to diagnosing their cause and, consequently, the possibility to adequately treat uncommon conditions such as neuroendocrine tumorinduced osteomalacia. references 1. resnick dl. fish vertebrae. arthritis rheum. 1982;25(9):1073-1077. http://www.ncbi.nlm.nih.gov/pubmed/7126291. accessed march 13, 2017. 2. murphy wa, divito dm. fuller albright, postmenopausal osteoporosis, and fish vertebrae. radiology. 2013;268(2):323-326. doi:10.1148/radiol.13122478. 3. schmorl cg. die pathologische anatomic der wirbelsäule. verh dtsch ges ortho. 1926;21:3–41. 4. huang c, zehrer t, mueller l, michie c. “step vertebrae”, “fish mouth vertebrae” or “h vertebrae” in sickle cell disease. west lond med j. 2013;6(1):19-22. 5. ntagiopoulos pg, moutzouris d-a, manetas s. the "fish-vertebra" sign. emerg med j. 2007;24(9):674-675. doi:10.1136/emj.2006.039131. 6. ozaki d, shirai y, nakayama y, yoshihara k, huzita t. multiple fish vertebra deformity in child with systemic lupus erythematosus -a case report-. j nippon med sch. 2000;67(4):271-274. doi:10.1272/jnms.67.271. 7. reynolds j. a re-evaluation of the “fish vertebra” sign in sickle cell hemoglobinopathy. am j roentgenol. 1966;97(3):693-707. doi:10.2214/ajr.97.3.693. romanian neurosurgery (2017) xxxi 3: 294 301 | 301 8. leivy fe, schnabel tg. abdominal crises in sickle-cell anemia. am j med sci. 1932;183(3):381-391. 9. carroll ds. roentgen manifestations of sickle cell disease. south med j. 1957;50(12):1486-1490. http://www.ncbi.nlm.nih.gov/pubmed/13495701. accessed march 13, 2017. 10. cockshott wp. dactylitis and growth disorders. br j radiol. 1963;36(421):19-26. doi:10.1259/0007-1285-36421-19. 11. yamashita t, yoshioka m, itoh n. identification of a novel fibroblast growth factor, fgf-23, preferentially expressed in the ventrolateral thalamic nucleus of the brain. biochem biophys res commun. 2000;277(2):494498. doi:10.1006/bbrc.2000.3696. 12. fukumoto s. physiological regulation and disorders of phosphate metabolism--pivotal role of fibroblast growth factor 23. intern med. 2008;47(5):337-343. http://www.ncbi.nlm.nih.gov/pubmed/18310961. accessed march 13, 2017. 13. zadik y, nitzan dw. tumor induced osteomalacia: a forgotten paraneoplastic syndrome? oral oncol. 2012;48(2):e9-e10. doi:10.1016/j.oraloncology.2011.09.011. 14. clifton-bligh rj, hofman ms, duncan e, et al. improving diagnosis of tumor-induced osteomalacia with gallium-68 dotatate pet/ct. j clin endocrinol metab. 2013;98(2):687-694. doi:10.1210/jc.2012-3642. 15. hofman ms, kong g, neels oc, eu p, hong e, hicks rj. high management impact of ga-68 dotatate (gatate) pet/ct for imaging neuroendocrine and other somatostatin expressing tumours. j med imaging radiat oncol. 2012;56(1):40-47. doi:10.1111/j.17549485.2011.02327.x. 4mostarchidbrahim_spontaneous romanian neurosurgery | volume xxx | number 4 | 2016 | october december article spontaneous regression of a lumbar disc herniation: case report brahim el mostarchid, cherkaoui mandour, el azami el hassani abdelilah morocco doi: 10.1515/romneu-2016-0076 romanian neurosurgery (2016) xxx 4: 475 – 478 | 475 doi: 10.1515/romneu-2016-0076 spontaneous regression of a lumbar disc herniation: case report brahim el mostarchid, cherkaoui mandour, el azami el hassani abdelilah department of neurosurgery, military hospital, rabat, morocco abstract: lumbar disc herniation is a common disease that induces back pain and radicular pain. some cases require conservative treatment or at times relived spontaneously. spontaneous regression of disc herniation is an atypical clinical presentation, and it has been recognized with the advancement of recent advances in imaging techniques. we present a 35-year-old woman presented a spontaneous regression of a lumbar disc herniation with good outcome after intensive physical therapy program. spontaneous regression of disc herniation is thought to occur via an inflammatory reaction with molecular mechanisms of phagocytic processes. key words: herniated disc, regression, spontaneous introduction lumbar disc herniation is a common cause of lower leg radiculopathy. it’s widely accepted that conservative treatment must be done first exceptionally in neurological deficit, severe unremitting leg pain despite conservative measures, and repeated time loss from work, and equina syndrome signs. the prognosis is generally good. spontaneous regression of herniated discs in patients treated non-operatively has been reported in the literature in the past. it involves virtually all spinal compartments i.e. cervical, thoracic, and lumbar (1-4) and becomes clinically present in a variety of ways, including myelopathy and radiculopathy. recent advances in imaging techniques: computed tomography (ct) and magnetic resonance imaging (mri) have facilitated the precise documentation of this fact (2). however, the underlying mechanism remains unclear. here we present a case of lumbar radiculopathy due to a sequestered herniated disc at the l5-s1 level in which neurological improvement coincided with a significant diminution in the size of the extruding disc fragment documented on serial ct scans. the possible mechanism of sequestered fragment disc resorption is discussed. case report a 35-year-old moroccan woman was admitted with progressive low back and right leg pain along the l5 dermatome with no appearance cause. one admission she was in good healthy. body mass index was normal. somatic 476 | mostarchid et al spontaneous regression of a lumbar disc herniation examination showed no abnormality. on examination the straight-leg-raising test was positive on the right side (40°). neurological examination showed no sensory impairment or cauda equina symptoms. the lumbar ct scan showed a herniated disc with inferior migration and sequestered fragment on l5-s1 level (figure 1). the patient was treated conservatively with bed rest, muscle relaxants, and nonsteroidal anti-inflammatory drugs for 20 days. after that period he participated in a physical therapy program during one month: (3 times one week). 40 days after the onset of pain the patient returned to daily activities. he was symptom-free and the serial ct scan performed 4 and 9 months showed spontaneous and almost complete regression of the sequestered fragment on l5-s1 level (figure 2). our patient presented a spontaneous regression of a lumbar disc herniation with good out come after intensive physical therapy program. figure 1 ct scan of lumbar axial (a-b) and sagittal (c-d) view on the l5-s1 intervertebral level showing image herniated disc with inferior migration and sequestreted fragment romanian neurosurgery (2016) xxx 4: 475 – 478 | 477 figure 2 follow-up ct image at the same location one year later. note the almost complete disappearance of the herniated disc fragment seen in figure 1 discussion this event is rare. recent advances in imaging techniques (ct, mri) have facilitated the precise documentation of this fact (2-5). however, the underlying mechanism remains unclear. although the phenomenon of spontaneous disappearance of decrease in size of herniated disc fragments is well known, the exact mechanism underlying this process remains unclear. three possible explanations for disc regression are discussed in the literature: retraction into the intervertebral space, dehydration/shrinkage, and resorption due to inflammatory reaction. researchers have brought forward three possible explanations which could provide a satisfactory answer (1, 2, and 3). the first, the theory of dehydration, states that the herniated disc fragment disappears due to gradual dehydration and shrinkage. the second hypothesis, the theory of resorption, the most experimentally studied one, supports the idea of cartilaginous tissue resorption through enzymatic degradation and phagocytosis as a result of an inflammatory reaction and neovascularization. the inflammatory reaction could be the result of an autoimmune response developed when the disc contents extrude into the epidural space and are recognized as “foreign” (3). studies have revealed neovascularization at the periphery of the sequestrated disc and the presence of macrophages and t cells in the vascularized areas. anti-interleukin-1, intracellular adhesion molecule-1, lymphocyte functionassociated antigen, and basic fibroblast growth factor are also expressed on most of the mononuclear cells. furthermore, the cell infiltration is more prominent in the nucleus pulposus than in the annulus fibrosus. finally, blood vessels in the extruded tissue are formed either through metaplasia of undifferentiated mesenchymal cells or they are derived from blood vessels that have invaded the annulus fibrosus as a result of disc degeneration. according to the third 478 | mostarchid et al spontaneous regression of a lumbar disc herniation explanation, the theory of retraction, the herniated disc retracts back into the intervertebral space. this is the case if the disc protrudes through the annulus fibrosus but at the same time is not separated from it. it is possible, though, that all three proposed mechanisms play a role in the diminution process. it is also noted that larger fragments are more frequently observed to diminish than smaller ones, possibly because of their larger water content (dehydration, resorption). (6) extruded material exposed to the epidural space may be resorbed more quickly than that beneath the ligament. vascular supply probably plays a role in the mechanism of resorption. in our previous reported case of posterior migration of lumbar sequestered disc fragment, a mri showed a peripheral enhancement mimicking a space occupying lesion. the epidural fat is vascular; the presence of fragment in this space will induce an inflammatory response with granulation tissue and neovascularization around the extruded tissue, causing a ring enhancement with gadolinium in the mri scan. (7). this finding supported the third explanation of spontaneous regression of a lumbar disc herniation (5). in addition, radiographic changes often follow clinical improvement (relief of pain). studies have shown maximal clinical improvement within one year, but the reduction in disc size continued thereafter. this phenomenon is explained first by a progressive decrease in the pressure exerted by the fragments on neural structures and second by gradual amendment of the inflammatory response (4). conclusion the regression of sequestered large lumbar disc is very rare but well documented. spontaneous regression was observed in the sequestration-type lesions. vascular supply probably plays a role in the mechanism of resorption. correspondence 1. brahim el mostarchid e-mail: mostarchid@yahoo.fr gsm: 212 06 61 29 68 62 2. cherkaoui mandour e-mail: mandour1978@hotmail.com gsm: 212 06 53 42 12 25 3. el azami el hassani abdelilah e-mail: elazami@yahoo.fr gsm: 212 06 61 25 66 60 references 1. sei a, nakamura t, fukuyama s et al: spontaneous regression of lumbar hernia of the nucleus pulpus. follow-up study of 4 cases by repeated magnetic resonance imaging. rev chir orthop reparatrice appar mot, 1994; 80: 144–49 2. birbilis ta, matis gk, theodoropoulou en. spontaneous regression of a lumbar disc herniation: case report. med sci monit. 2007; 13(10): 121-123 3. mochida k, komori h, okawa a, muneta t, haro h, shinomiya k. regression of cervical disc herniation observed on magnetic resonance images. spine. 1981; 23(9):990-5. 4. saal ja: natural history and nonoperative treatment of lumbar disc herniation. spine, 1996; 21: 2s–9s 5. slavin kv, raja a, thornton j, wagner fc jr: spontaneous regression of a large lumbar disc herniation: report of an illustrative case. surg neurol, 2001; 56: 333-36 6. doita m, kanatani t, harada t, mizuno k: immunohistologic study of the ruptured intervertebral disc of the lumbar spine. spine, 1996; 21:235–41 7. el mostarchid b, el-asri a. c., belhachmi a, akhaddar a, gazzaz m, boucetta m. posterior epidural migration of a sequestrated lumbar disc fragment. neurosciences 2008; 13 (2) 199-200 romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article incidence, hospital costs and in-hospital mortality rates of surgically treated patients with traumatic cranial epidural hematoma ibrahim burak atci, hakan yilmaz, mehmet yaman, oguz baran, okan türk, bilgehan solmaz, ümit kocaman, nuriye guzin ozdemir, nail demirel, ayh an kocak turkey doi: 10.2478/romneu-2018-0013 110 | atci et al incidence, hospital costs and in-hospital mortality rates doi: 10.2478/romneu-2018-0013 incidence, hospital costs and in-hospital mortality rates of surgically treated patients with traumatic cranial epidural hematoma ibrahim burak atci1, hakan yilmaz2, mehmet yaman1, oguz baran1, okan türk1, bilgehan solmaz1, ümit kocaman3, nuriye guzin ozdemir1, nail demirel1, ayh an kocak1 1istanbul research and training hospital, department of neurosurgery, istanbul, turkey 2usak university hospital, department of neurosurgery, usak, turkey 3izmir cigli research and training hospital, department of neurosurgery, izmir, turkey abstract: background: in this study, the patients who were operated in two clinics due to traumatic cranial epidural hematoma (edh) were assessed retrospectively and the factors that increase the costs were tried to be revealed through conducting cost analyses. methods: the patients who were operated between 2010 and 2016 with the diagnosis of edh were assessed in terms of age, sex, trauma etiology, glasgow coma scale (gcs) at admission, the period from trauma to hospital arrival, trauma-related injury in other organs, the localization of hematoma, the size of hematoma, length of stay in the intensive care unit (icu), length of antibiotherapy administration, number of consultations conducted, total cost of in-hospital treatments of the patients and prognosis. results: distribution of gcs were, between 13-15 in 18 (36%) patients, 9-13 in 23 (46%) patients and 3-8 in 9 (18%) patients. the reasons for emergency department admissions were fall from high in 29 (58%) patients, assault in 11 (22%) patients and motor vehicle accident in 10 (20%) patients. the average cost per icu stay was 2838 $ (range=343-20571 $). the average cost per surgical treatment was 314 $. icu care was approximately 9 times more expensive than surgical treatment costs. the mortality rate of the study cohort was 14% (7 patients). conclusion: the prolonged period of stay in the icu, antibiotherapy and repeat head cts increase the costs for patients who are surgically treated for edh. key words: antibiotherapy, cost analysis, epidural hematoma, traumatic introduction epidural hematoma (edh), which was defined for the first time by hutchinson in 1867, is a common type of traumatic brain injury (tbi) in which blood accumulation occurs between the dura mater and the romanian neurosurgery (2018) xxxii 1: 110 115 | 111 cranium due to trauma. it is 4 times more common in men than in women. although middle meningeal artery is responsible in 85% of the analyzed case series, life-threatening hemorrhages can also be observed as a result of venous hemorrhages. the mass effect of the blood results in pupillary anomalies, neurological deficits, loss of consciousness and high mortality. the mortality rates vary between %5-45 and immediate surgical intervention is of the utmost importance in required cases [1-3]. in this study, the medical records of 50 patients with edh who were surgically treated in 2 clinics were assessed retrospectively and the factors for increased patient costs were analyzed. methods the patients who were surgically treated for traumatic edh in two clinics between january 2010 and january 2016 were included in this retrospective study. the assessed data were as follows: age, gender, trauma etiology, glasgow coma scale at admission, the period from trauma to hospital arrival, traumarelated injury in other organs, the localization of hematoma, the size of hematoma, length of stay in the intensive care unit (icu), length of antibiotherapy administration, number of consultations conducted, total cost of inhospital treatments of the patients and prognosis. all statistical analyses were performed using statistical package for the social sciences version 15 (spss inc., chicago, usa). the results were expressed as mean±standard deviation or frequency (%). the student’s ttest was used to determine the significance of the differences among groups. a p value of<0.05 was considered statistically significant. results of all patients, 46 (92%) were men and 4 (8%) were women.the mean age of the patients was 35.4±5.6 years (range=7 months68 years). regarding admission gcs, the scores ranged between 13-15 in 18 (36%) patients, 9-13 in 23 (46%) patients and 3-8 in 9 (18%) patients. the most common reason for emergency department admissions was fall from high (58%), followed by assault (22%) and motor vehicle accident (mva) (20%)(table 1). forty-two (84%) patients were admitted to the emergency department within 4 hours of trauma. the concomitant systematic injuries were as follows: extremity fractures in 10 patients, lung contusion in 4 patients, liver laceration in 3 patients, retroperitoneal hemorrhage in 2 patients and non-significant spinal fractures in 8 patients. besides concomitant systematic injuries, 35 patients had concomitant cranial pathologies. there were linear skull fracturesin 44 patients, depression fractures in 5 patients, subdural hematoma in 4 patients, and intracerebral hematoma in 2 patients. all patients were diagnosed with computed tomography (ct) scans. the intraoperative evaluation revealed that the most common localization of edh was temporal (36%), followed by temporoparietal (24%) and frontal (14%) (table 2). the thickness of epidural hematoma was between 10-15 mm in 10 (20%) patients, 15-30 mm in 32 (64%) patients and >30 mm in 8 (16%) patients. 112 | atci et al incidence, hospital costs and in-hospital mortality rates thirty-eight (76%) patients were taken to icu post-operatively, and 12 (24%) patients were taken to neurosurgery clinic beds. the average length of stay in the icu was 8.6 days (range=1-60 days). the daily average cost of icu was 343 $ and the average cost per icu stay was 2838 $ (range=343-20571 $) (table 3, figure 1). the average cost per surgical treatment was 314 $. icu care was approximately 9 times more expensive than surgical treatment costs. during icu followup, an average of 3.8 (range= 2-13) neurosurgery consultations was performed per patient. seven patients died in the icu and the mortality rate of the study cohort was 14%. the admission gcs values of these 7 patients were below 6. besides, all these 7 patients had other concomitant intracranial pathologies and they were operated within 4 hours following the trauma. thirty-one patients were taken to service beds following icu follow-up. the average length of service bed stay was 5.7 days (range=1-28 days) for the remaining 43 patients. the average cost per service bed stay was 2057 $ (range=1285–3428 $). during service stay, patients had undergone an average of 3.7 (range=2-10) repeat head cts. except for the post-operative early control ct, none of the other control cts demonstrated a surgical pathology and affected the treatment. all patients in this study received prophylactic ceftriaxone treatment. during icu follow-up, following pathologic agents were cultivated in serum, urine, feces and tracheal samples: methicillin-resistant staphylococcus aureus (mrsa) in 4 samples, acinetobacter baumannii in 2 samples, enterococcus faecalis in 3 samples, and klebsiella pneumonia in 2 samples. double or triple antibiotherapy was administered to these cases for an average of 10 days. double antibiotherapy was applied and continued for 7 days in another group of 10 patients due to fever although no pathologic agent could be cultivated and their white blood cells (wbc) were within normal ranges. to sum up, double or triple antibiotherapy was administered to 21 patients and these treatments continued for 7-10 days. the total cost of antibiotics constituted 15% of total cost of stay. the total cost of patients who stayed in the icu for ≥10 days and who had double antibiotherapy were significantly higher than the total cost of other patients (p<0.05) (table 4). regarding glasgow outcome scale (gos), thirty-five patients were discharged with low disability (gos 5), four patients with moderate disability (gos 4), three patients with severe disability (gos 3), and one patient with persistent vegetative state (gos 2) (morbidity rate=16%) (table 5). all the patients who were discharged with gos 3 and 2 were ≥50 years of age. when gcs is correlated with cost analysis, a gcs value of ≤8 was statistically significantly correlated with cost (p<0.05). table 1 trauma etiology etiology patient number and percentage falling from high 29 (%58) assault 11 (%22) traffic accident 10 (%20) romanian neurosurgery (2018) xxxii 1: 110 115 | 113 table 2 the localization of epidural hematoma localization patient number and percentage temporal 18 (%36) temporoparietal 12 (%24) frontal 7 (%14) parietal 6 (%12) occipital 5 (%10) posterior fossa 2 (%4) table 3 the daily average cost of icu department icu icu mean charge % of total blood processing 21.26 $ 6.2% central supply 45.27 $ 13.2 pharmacy without antibiotics 35.32 $ 10.3 antibiotherapy (average) 51.45 $ 15 icu physician 6.86 $ 2 labaratory 116.96 $ 34.1 radiology 33.95 $ 9.9 inhalation theraphy 31.89 $ 9.3 total 343 $ 100 table 4 antibiotic use, total financial effects and ct application rates of these patients antibiotic use double or triple anti biotherapy double anti biotherapy single anti biotherapy period of antibiotic use (average) 10 days 7 days 5 days reproduction status 4 mrsa 3 enterococcus 2 acinetobacter 2 klebsiella no reproduction (high wbc, fever) no reproduction total 11 patients (%22) 10 patients (%20) 29 patients (%58) total cost (%) %40 %28 %32 ct application (average: 3.7) 6 4.6 2.5 table 5 distribution of patients according to gos results at discharge gos number % 1 7 14 2 1 2 3 3 6 4 4 8 5 35 70 discussion acute edh constitutes 2.7-11% of tbis. it is frequently seen in men and young adults. regarding analyzed cases, it was seen on lateral surfaces of hemispheres having 70% frequency for central pterion. the most commonly reported causes in the literature are falls, mvas, and assaults. the incidence is lower in children and elderly, as there is close relationship between the dura and the osseous skull [2, 3]. there were linear fractures in 60% of the skull x-rays in our study group and standard diagnostic procedure was cranial ct. compared to x-rays, linear fractures or complicated compression fractures are more frequently observed at the level of hemorrhage in cranial cts. there is not a consensus to decide which patients will be a candidate for surgical procedure, but a close neurologic and radiologic follow-up is required for foreseeing hematoma growth. generally, symptomatic edhs should be correlated with gcs, and surgery should be planned in cases when the thickness of hematoma exceeds 15 mm [4-7]. in the literature, the most important determinant for prognosis and outcome is gcs. although the general mortality rate is 20-55%, it is 5-10% in early diagnosed and 114 | atci et al incidence, hospital costs and in-hospital mortality rates intervened cases [4, 7]. in our study, it was observed that mortality rate decreased and prognosis was better in younger patients and patients with higher gcs values. since brain injuries frequently include multiple trauma and multiple organ injuries, they require icu follow-up and treatment. many patients are also followed up by anesthesia physicians in icus during the postoperative period. immobile patients become susceptible to infections in the icus. it was found that the cost increased incrementally with prolonged stay in the icu. the reasons for increased costs were analyzed in our study. daily price for icu standard bed is determined by the ministry of health. however, this standard price can be surpassed quite often with costs of examination, treatment and imaging studies, and the institution can experience financial losses. the main reasons for high costs are infection prophylaxis, and broad spectrum combined antibiotics administered to infected cases. the period before an infectious disease clinic consultation and antibiotherapy application is 3 days at maximum particularly in patients who are brought to icu intubated during the postoperative period because of low gcs. the reason for this is pulmonary infections, which occurs following air passage to bronchi after ventilation and passing through physiological ways. central nervous system (cns) infection is not frequent in edhs as they are usually in the form of closed fractures. nevertheless, cns infection rates increase in patients with skull base involvement, and pneumocephalus, rhinorrhea or otorrhea. in these situations, short-term prophylactic antibiotherapy can be applied in selected cases. besides, the risk for atelectasis increases in postoperatively immobile patients andcombined antibiotherapy is applied rapidly due to increased body temperature and leukocytosis. usually prophylactic administration is performed before the results of cultures. the most important factors that can reduce costs, and mortality and morbidity rates in these patients are shortening icu stay, weaning from mechanical ventilation within the shortest time possible, and mobilization. furthermore, another factor that increases the costs is the prophylactic antibiotherapy with the prediagnosis of cns infection or pulmonary infection. in our study, the costs of antibiotherapy constituted 15% of the total costs. the antibiotherapy costs of patients who stayed in the icu for 10 or more days and who had double or triple antibiotherapy were significantly higher than other patients. another postoperative cost increasing factor is frequently performed neuroimaging studies. cranial ct is the most frequently used imaging modality during the preand postoperative periods in edh. the follow-up is made with frequent cranial cts in unoperated patients [8, 9]. in our study, the mean number of ct scans for the follow-up of edh was 3.7. however, ct scans in icu follow-up of patients with longer stays can range between 7-8. yet, the data analysis revealed that ct scans, except for postoperative control brain cts, did not affect our treatment choice. frequent cranial cts in the post-operative period increase the cost and also expose the patient to radiation. close follow-up with neurological examination following ct scan romanian neurosurgery (2018) xxxii 1: 110 115 | 115 in the postoperative early period can decrease both the costs and the risk of radiationinduced comorbidities. conclusion in conclusion, the length of stay in the icu, double or triple antibiotherapy, and frequent head cts increase the costs for patients undergoing surgery for edh. though human life is a sacred phenomenon over all kinds of cost calculation, we believe institutions and patients will benefit from reduction of unnecessary antibiotherapy and limitation of frequent head cts. what is known about this topic •epidural hematoma, which was defined for the first time by hutchinson in 1867, is a common type of traumatic brain injury (tbi) in which blood accumulation occurs between the dura mater and the cranium due to trauma. •patients with epidural hematoma requires icu follow-up and treatment. what this study adds •the prolonged period of stay in the icu, antibiotherapy and repeat head cts increase the costs for patients who are surgically treated for edh. correspondence ibrahim burak atci. istanbul research and training hospital, department of neurosurgery; istanbul, turkey. telephone: +90 212 459 60 88 cellphone: +90 505 773 31 55 fax: +90 212 459 62 30 e-mail: drburakatci@hotmail.com references 1. sahuquillo-barris j, lamarca-ciuro j, vilalta-castan j, rubio-garciae, rodriguez-pazos m. epidural hematoma and diffuse axonal injury. neurosurgery. 1985;17(2):378379 2. rivas jj, lobato rd, sarabia r, cordobés f, cabrera a, gomez p. extradural hematoma: analysis of factors influencing the courses of 161 patients. neurosurgery. 1988;23(1):44-51 3. cheung ps, lam jm, yeung jh, graham ca, rainer th. outcome of traumatic extradural haematoma in hong kong. injury. 2007;38(1):76-80 4. deniz fe, türk cc, ismailoğlu o, bozkurt g, ozcan oe. rapid spontaneous resolution of epidural hematoma: a case report. ulus travma acil cerrahi derg. 201;16(3):280-282 5. chen ty, wong cw, chang cn, lui tn, cheng wc, tsai md, lin tk. the expectant treatment of "asymptomatic" supratentorial epidural hematomas. neurosurgery. 1993;32(2): 176-179 6. bejjani gk, donahue dj, rusin j, broemeling ld. radiological and clinical criteria for the management of epidural hematomas in children. pediatr neurosurg. 1996;25(6):302-308 7. bezircioğlu h, erşahin y, demirçivi f, yurt i, dönertaş k, tektaş s. nonoperative treatment of acute extradural hematomas: analysis of 80 cases. j trauma. 1996;41(4):696-698 8. ding j, yuan f, guo y, chen sw, gao ww, wang g, cao hl, ju sm, chen h, zhang pq, tian hl. a prospective clinical study of routine repeat computed tomography (ct) after traumatic brain injury (tbi). brain inj. 2012;26(10):1211-1216 9. shin ds, hwang sc, kim bt, jeong jh, im sb, shin wh. serial brain ct scans in severe head injury without intracranial pressure monitoring. korean j neurotrauma. 2014; 10(1):26-30 13 13burakatciibrahim_incidence doi: 10.33962/roneuro-2021-054 fibrous dysplasia of sphenoid bone presenting as a case of loss of vision abhishek katyal, daljit singh romanian neurosurgery (2021) xxxv (3): pp. 327-329 doi: 10.33962/roneuro-2021-054 www.journals.lapub.co.uk/index.php/roneurosurgery fibrous dysplasia of sphenoid bone presenting as a case of loss of vision abhishek katyal1, daljit singh2 1 senior resident (post mch). department if neurosurgery. g.b pant institute of postgraduate medical education & research, maulana azad medical college, delhi university, india 2 director, professor & head. department of neurosurgery. g.b pant institute of postgraduate medical education & research, maulana azad medical college, delhi university, india abstract background: fibrous dysplasia is a fibro-osseous lesion of unclear aetiology wherein normal bone is replaced by abnormal fibrous tissue and immature bone. fibrous dysplasia is associated with a defect in osteoblastic differentiation and maturation that originates in the mesenchymal precursor of the bone & is well documented to affect craniofacial structures. case description: a case of the lesser sphenoid wing fibrous dysplasia is described which presented with symptoms of pressure effects on the optic nerve, managed subsequently with microsurgical decompression of the nerve. conclusion: craniofacial fibrous dysplasia is an uncommon entity which can present with loss of vision, wherein the visual prognosis depends upon timed & adequate surgical intervention. introduction fibrous dysplasia is associated with a defect in osteoblastic differentiation and maturation where normal medullary bone is replaced with a variable amount of abnormal and structurally weak fibrous and osseous tissue. it is of particular interest to neuroophthalmologist as it can affect craniofacial bones wherein encroachment on the paranasal sinuses, orbit, and foramina of the skull can produce variety of ophthalmological symptoms. here in a case is described of fibrous dysplasia of lesser sphenoid wing presenting with optic nerve compression & visual loss. case report a 45-year-old female housewife presented with holocranial headache for 1 year which was dull aching, moderate intensity, and gradually progressive, non-pulsatile, no specific aggravating factors, relieved on medication. there was no history of vomiting, seizures, trauma, aura and photophobia, facial pain & anosmia. she also complained of keywords fibrous dysplasia, sphenoid wing, orbit corresponding author: abhishek katyal department if neurosurgery. g.b pant institute of postgraduate medical education & research, maulana azad medical college, delhi university, india ak.neurosx.47@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 328 abhishek katyal, daljit singh blurring of vision followed by gradual progressive painless, visual deterioration in right eye for 2 months. there was no history of painful movements of eyeball, reddening/ congestion, diplopia, proptosis, epiphora/ glare. she didn’t complain of tunnelling of vision & had no history suggestive of hormonal changes. examination revealed the visual acuity in right eye as 6/60 & left eye 6/12 unchanged with pinhole, pupillary response was normal in left eye whereas relative afferent pupillary defect was present in right eye. on perimetry, paracentral scotoma was observed on right side while left side was normal. fundus examination, extraocular movements & conjunctiva were normal on both sides. on ct scan of brain, orbit & skull base, diffuse expansion of medullary cavity with ground glass bone matrix with no contrast enhancement & intact cortices was noted involving bilateral greater & lesser wing of sphenoid, bilateral anterior clinoid processes & pterygoid plates with orbital wall & roof thickening on both sides causing narrowing of bilateral optic canals (right more than left) (fig.1). blood investigations were normal. figure 1. based on imaging findings, a provisional diagnosis of fibrous dysplasia was made. right frontal craniotomy was performed and optic nerve decompression was achieved by drilling of right anterior clinoid process and orbital roof. intra-operatively right sphenoid wing , frontal bone, anterior clinoid process and orbital roof was found to be thickened and bone was spongy and vascular while the optic nerve seemed to be compressed in optic canal, with thinning of intracanalicular portion. optic nerve decompression was done till orbital apex (fig 2a &2b). histopathological examination revealed irregular trabeculae of woven bone within fibrous tissue which lacked osteoblastic rimming suggestive of fibrous dysplasia. post operative ct scan showed significant drilled out bony portion at right orbital roof thus demonstrating decompression of the optic nerve as compared to preoperative scans (fig 3 & 4). visual acuity in right eye as assessed at the end of 1 month & 2 months of follow up period was 6/36 & 6/24 respectively, hence showing betterment; along with improvement in headache. figure 2a. figure 2b. figure 3. 329 fibrous dysplasia of sphenoid bone presenting as a case of loss of vision figure 4. discussion fibrous dysplasia was first recognized by von recklinghausen in 1891 and further characterized and named by lichtenstein in 1938. it is one of the most common benign skeletal disorders and can affect any bone in the body [2]. it is most common in adolescents and young adults, and progression decreases after puberty [2]. there are three types of fibrous dysplasia: monostotic (the most common, accounting for 70% of cases), polyostotic, and mccune-albright syndrome. mccune-albright syndrome is characterized by polyostotic fibrous dysplasia, endocrine hyperfunction (which can lead to precocious puberty in female patients), café au lait pigmentation of the skin, and other extraskeletal abnormalities [1]. fibrous dysplasia has a predilection for the skull base; particularly the ethmoid (most common) followed by sphenoid, frontal, maxilla bones & orbits [5]. consequently, patients with fibrous dysplasia may exhibit local cosmetic deformity (the most common manifestation), headaches, proptosis, impaired ocular movement, and loss of visual acuity [2]. based on radiographic features, fibrous dysplasia is classified into 3 types, the pagetoid, or “groundglass,” pattern is the most common (56% of all cases); it appears as a mixture of dense and radiolucent areas of fibrosis. the sclerotic pattern (23% of cases) is uniformly dense. the cystic pattern (21%) is characterized by an spherical or ovoid lucidity surrounded by a dense bony shell.[3] involvement of the orbit leading to visual loss is the most feared complication, and surgical decompression may be warranted in acutely or progressively symptomatic patients (or in both) [1,2]. radiotherapy and chemotherapy have no role in the treatment of fibrous dysplasia, and the former may increase the risk for malignant degeneration (most commonly osteosarcoma) [3,4]. fibrous dysplasia may be complicated by aneurysmal bone cyst formation [1]. malignant degeneration occurs in 4% of cases of fibrous dysplasia and is more common with the monostotic type. the interval between the diagnosis of fibrous dysplasia and evidence of sarcomatous degeneration is long, with a mean of 15 years. close imaging follow-up with serial ct and mri is essential in patients with known fibrous dysplasia. worsening pain, development of a soft tissue mass, or elevation of alkaline phosphatase levels should raise concern for malignant degeneration [2]. conclusion fibrous dysplasia of the sphenoid bone, although not a common entity, can present with symptoms of visual loss. timely intervention & adequate microsurgical decompression of the optic nerve results in good postoperative visual outcome and is of prognostic significance. references 1. dumont as, boulos pt, jane ja jr. cranioorbital fibrous dysplasia: with emphasis on visual impairment and current surgical management. neurosurg focus. 2001;10(5):6. 2. g. eric, clair st., mccutcheon ian e. skull tumors. in: winn hr. youmann & winn’s neurological surgery, 7th ed. philadelphia, elsevier publishers; 2017. vol 2, pg 1341-42. 3. liakos gm, walker cb, carruth ja. ocular complications in craniofacial fibrous dysplasia. br j ophthalmol. 1979 sep;63(9):611-6. 4. lustig lawrence r, holliday michael j, mccarthy edward f, nager george t. fibrous dysplasia involving the skull base and temporal bone. arch otolaryngol head neck surgery 2001; 127: 1239-47. 5. singh harjitpal, c mohan. indian j. fibrous dysplasia of sphenoid bone. otolaryngol. head neck surg. 2007; 59: 157-59. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article commonly available ct characteristics and prediction of outcome in traumatic brain injury patients anil kumar, umamaheswara reddy v., vasuki pratyusha, ashok munivenkatappa, ranabir pal, kishore v. hegde, ranjan jena, satish kumar s., amit agrawal india doi: 10.1515/romneu-2017-0016 romanian neurosurgery (2017) xxxi 1: 101 – 110 | 101             doi: 10.1515/romneu-2017-0016 commonly available ct characteristics and prediction of outcome in traumatic brain injury patients anil kumar1, umamaheswara reddy v.2, vasuki pratyusha3, ashok munivenkatappa4, ranabir pal5, kishore v. hegde6, ranjan jena7, satish kumar s.8, amit agrawal9 1resident of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 2assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 3department of biostatistics and epidemiology, national institute of mental health and neurosciences, bangalore, india 4mbbs, phd: scientist c, vrdl project, national institute of epidemiology, icmr, chennai – 77, tamil nadu, india 5department of community medicine, andaman and nicobar islands institute of medical sciences, port blair – 744104, india 6professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 7assistant professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 8associate professor of emergency medicine, department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 9professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: background: acute computerized tomography (ct) characteristics are used widely and most accepted for prediction of outcome among traumatic brain injury (tbi). the commonly available and simple combinations of existing and unexplored ct parameters may be more useful in prediction of outcome. the present study explores commonly available ct characteristics by possible combinations based on anatomical basics. methods: abnormal ct sign was considered with any cranial lesion. based on anatomical locations of cortical lobes, nine possibilities were made that include individual and combinations of mentioned lobes. the laterality was either right or left or bilateral. the outcome was favourable or unfavourable based on discharge glasgow outcome scale (gos). binary logistic regression was used to predict outcome. 102 | kumar et al commonly available ct characteristics             results: 452 patients were recruited in the present study. there was significant risk of unfavourable outcome among patients with location of sub dural haemorrhage (sdh) in parietal + temporal region (or=10,p<0.001); cerebral contusion in temporal region (or=3,p=0.03), frontal + temporal region(or=16,p=0.001), frontal + parietal + temporal region (or=18.7,p<0.001). patients with four abnormal ct signs had worst outcome. presence of sdh on right side (or=4.5,p<0.001) and bilateral cerebral contusion (or=4.5,p=0.003) was at the risk of unfavourable outcome. conclusion: the present study based on anatomical classification has shown that location and laterality of lesion can significantly predict tbi outcome. key words: ct characteristics, locations, laterality, cortical regions, prediction, outcome introduction computerized tomography (ct) examination remains the investigation of choice in the acute phase of traumatic brain injury (tbi). ct characteristics not only widely accepted for descriptive purposes, but also increasingly being used as major predictor of outcome in tbi. following tbi the pathological findings on ct scan that is represented by scoring system is oriented in predicting prognification of outcome (2, 4, 12, 13). various studies and the international guidelines on prognosis include the ct scoring system as a major outcome predictor13. several predicting models in terms of scoring had been developed for tbi prognostication. few models are validated and few are not accurately validated (12). the current available ct scoring systems based on abnormal ct characteristics do not provide details that are best suited for prediction. possibly there are other very simple combinations of ct parameters that may be more appropriate for this specific purpose that has not been investigated in detail. the aim of the present study is to examine the possible available ct characteristics with simple combinations based on anatomical location and distribution. methods inclusion and exclusion criteria inclusion criteria for the study were patients with history of tbi and having abnormal ct signs. any age group and both the genders were considered, very importantly willing to participate in study. the study was approved by institute ethical committee; the purpose of the study was explained in patients own language and willing patient/relative written consent was taken before enrolling into the study. abnormal ct signs patient’s emergency ct scan showing any cranial abnormality was considered as abnormal ct signs. abnormal cranial ct signs were intra cerebral haemorrhage (ich), cerebral contusion, sub arachnoid haemorrhage (sah), extra dural haemorrhage (edh), sub dural haemorrhage (sdh) and skull fracture (figures 1-4). romanian neurosurgery (2017) xxxi 1: 101 – 110 | 103             figure 1 ct scan brain plain showing left parietoocciptal extradural hematoma with scalp swelling and right frontal polar contusion figure 2 ct scan brain plain showing left frontotemporo-parietal acute subdural hematoma with mass effect and midline shift figure 3 ct scan brain plain showing left temporal contusion with mass effect and perilesional oedema figure 4 ct scan brain plain showing right temporal thin acute subdural hematoma and coalescing contusion causing formation of intracerebral hematoma with peri-lesional oedema and mass effect 104 | kumar et al commonly available ct characteristics             location based on location of abnormal ct signs on different lobes of brain it was categorized into nine groups. that includes frontal, temporal, parietal, occipital, frontal + temporal, frontal + parietal, parietal + temporal, temporal + occipital, frontal + parietal + temporal. further each patient either having edh or sdh or ich or cerebral contusion or skull fracture, abnormal ct signs were grouped into one with either of one mentioned, two with combination of two abnormal signs, three combinations of three abnormal signs and four with combination of four abnormal signs. laterality the laterality of abnormal ct signs was categorized into left hemisphere, right hemisphere and bilateral hemisphere. outcome the discharge outcome was evaluated using glasgow outcome scale (gos). the scale was categorized into favourable that includes good and moderate recovery and unfavourable that includes persistent state, severe disability and death. statistical analysis the collected data was analyzed using spss software ibm spss version 22. percentages were calculated for categorical data, and mean, standard deviation was calculated for continuous data. logistic regression model binary logistic regression was used to identify the possible risk factors responsible for discharge outcome favourable or unfavourable (dependent variables). the variables that included in logistic regression model are; edh, sdh, cerebral contusion, ich, skull fracture, sah, location and laterality of abnormal ct signs. significance level was considered with p value of ≤0.05. results during study period 452 patients were explored with mean age of 39.39 ± 15.08 years. victims from male gender were four times (79%) higher than female group (21%). patients with favourable and unfavourable outcome were 84% and 16% respectively. location of abnormal ct signs distribution of edh, sdh, ich, cc and skull fracture at nine different location mentioned elsewhere are detailed in table 1. location of edh at temporal region is 1.2 times at the risk; occipital region at 6 times at the risk; frontal + parietal region at 2 times at the risk of unfavourable outcome, however none were significant. sdh at parietal + temporal region was significantly (p<0.001) 10 times at the risk of unfavourable outcome. presence of cerebral contusion was at temporal region was 3 times at the risk (p=0.03); frontal + temporal region was 16 times (p=0.001) at the risk; frontal + parietal + temporal region was 18.7 times (p<0.001) at the risk of unfavourable outcome. for details refer table 2. majority of patients had one abnormal ct sign that is 271(60%), followed by two 146(32%), three 31(7%) and four (1%) abnormal findings. patients with one, two and three abnormal ct findings were at lesser risk of unfavourable outcome with reference to four abnormal ct findings (table 2). romanian neurosurgery (2017) xxxi 1: 101 – 110 | 105             laterality of abnormal ct signs distribution of abnormal ct signs (edh, sdh, cerebral contusion, sah) either on left or right or bilateral hemispheres are shown in table 3. majority of patients has abnormal ct signs (edh, sdh, cerebral contusion, sah) on right side 215 (48%), followed by left side 151 (33%) and bilateral 86 (19%). sdh on right side is significantly (p<0.001) 4.5 times at the risk of unfavourable outcome. bilateral cerebral contusion is significantly (p=0.003) 4.5 times at the risk of unfavourable outcome. presence of bilateral abnormal ct sign is significantly (p=0.005) 2.4 times at the risk of unfavourable outcome. table i distribution of abnormal ct findings in different anatomical lobes of brain location abnormal ct signs n (%) extra dural haemorrhage sub dural haemorrhage intra cranial haemorrhage cerebral contusion skull fracture none 348 (77) 292 (65) 446 (98.8) 174 (38.5) 326 (72) frontal 27 (6) 40 (9) 2 (0.4) 113 (25) 50 (11) temporal 30 (7) 18 (4) 2 (0.4) 79 (17.5) 60 (13) parietal 16 (3.5) 7 (1.5) 0 27 (6) 3 (0.7) occipital 7 (1.5) 6 (1) 1 (0.2) 1 (0.2) 5 (1) frontal + temporal 1 (0.2) 0 0 12 (2.7) 2 (0.4) frontal + parietal 14 (3) 6 (1) 1 (0.2) 9 (2) 0 parietal + temporal 1 (0.2) 19 (4) 0 20 (4) 7 (0.3) temporal + occipital 7 (1.5) 64 (14) 0 1 (0.2) 7 (0.3) frontal + parietal + temporal 0 0 0 16 (3.5) 0 total 452 (100) 452 (100) 452 (100) 452 (100) 452 (100) table ii outcome prediction based on location of ct characteristics abnormal ct sign location significance odds ratio 95% ci lower upper extra dural haemorrhage* temporal 0.83 1.2 0.22 6.50 occipital 0.06 6 0.88 40.43 frontal + parietal 0.36 2 0.41 10.96 106 | kumar et al commonly available ct characteristics             sub dural haemorrhage* frontal 0.47 1.6 0.40 6.85 parietal 0.40 2.3 0.31 17.38 frontal + temporal 0.11 5.4 0.64 44.93 parietal + temporal <0.001 10.2 4.25 23.89 cerebral contusion* frontal 0.11 2.1 0.84 5.28 temporal 0.03 3 1.10 8.58 parietal 0.21 2.6 0.56 12.30 frontal + temporal 0.001 16.2 3.29 80.29 frontal + parietal 0.76 1.5 0.11 18.38 parietal + temporal 0.24 2.5 0.54 11.42 frontal + parietal + temporal <0.001 18.7 4.86 71.87 skull fracture* frontal + temporal 0.53 2.9 0.10 79.45 parietal + temporal 0.39 5 0.13 186.39 number of abnormal ct signs$ one 0.10 0.18 0.02 1.37 two@ 0.10 0.18 0.02 1.39 three@ 0.13 0.19 0.02 1.70 * reference is no abnormal ct sign; $reference is presence of four abnormal ct sign; @ combination of either extra dural haemorrhage or sub dural haemorrhage or intra cranial haemorrhage or cerebral contusion or skull fracture table iii distribution of abnormal ct findings based on laterality laterality abnormal ct signs n (%) extra dural haemorrhage sub dural haemorrhage cerebral contusion sub arachnoid haemorrhage none 350 (77.4) 272 (60) 181 (40) 404 (89.3) left hemisphere 47 (10.4) 68 (15) 95 (21) 16 (3.5) right hemisphere 51 (11.2) 104 (23) 127 (28.2) 23 (5) bilateral hemisphere 4 (1) 8 (2) 49 (11) 9 (2.2) total 452 (100) 452 (100) 452 (100) 452 (100) romanian neurosurgery (2017) xxxi 1: 101 – 110 | 107             table iv outcome prediction based on distribution of ct characteristics laterality of abnormal ct signs significance odds ratio 95% ci lower upper extra dural haemorrhage* bilateral 0.59 2.1 0.13 34.01 sub dural haemorrhage* left 0.32 1.5 0.64 3.66 right <0.001 4.5 2.20 9.16 bilateral 0.85 1.2 0.14 10.55 cerebral contusion* left 0.28 1.6 0.68 3.72 right 0.30 1.5 0.70 3.10 bilateral 0.003 4 1.60 9.31 sub arachnoid haemorrhage* left 0.94 1.1 0.21 5.16 bilateral 0.37 2.1 0.39 11.83 laterality of abnormal ct signs@ left 0.70 0.88 0.47 1.64 bilateral 0.005 2.4 1.29 4.38 p<0.05; *reference is no abnormal ct sign; @reference is right side discussion the present study summarize that there is significant risk of unfavourable outcome among patients with sdh in parietal + temporal region; cerebral contusion in temporal, frontal + temporal, & frontal + parietal + temporal regions and also patients presenting sdh on right sided and bilateral cerebral contusion. patients with ≤ three abnormal ct signs are having favourable outcome as compared with four abnormal ct signs. presence of bilateral abnormal ct sign is significantly having unfavourable outcome as compared with right side. among brain injury patients, early diagnosis and aggressive management is very crucial to prevent further complications of ongoing injury process. identification of anatomical site of injury is essential for taking appropriate measures to reduce morbidity and mortality (1). in acute settings imaging helps in accurate localization of any cerebral damage. during first 24 hours of injury conventional ct scan is considered to be imaging modality of choice because of its availability, lesser imaging time, able to perform on disturbed patients and cost effective (2). ct scan is superior in detecting any bony damage and bleeding in brain parenchymal or meninges or spaces (3). ct characteristics not only provide details of devastating site but also provide base for 108 | kumar et al commonly available ct characteristics             interpreting outcome (4). brain injury is affected by multiple factors and heterogeneous in manifestation because of which identifying variables specific for outcome prediction is challenging. in present armamentarium individual or combination of ct characteristics scoring system has remained vital entity in prognostication of tbi patients. the scoring systems have incorporated ct characteristics like cisterns, midline shift, volume of mass lesions, blood in brain spaces, and density of lesion (5, 6). many studies have detailed and verified these scoring systems in predicting outcome. the scoring systems are not without limitations. prediction of tbi outcome may be better with individual or combination of location and/or laterality of abnormal ct signs (4, 8, 9, 10). the locations of abnormal imaging characteristic either focal or diffuse are also important in predicting outcome (10). but localization of imaging characteristic in specific brain lobes (either single or combination) may also be useful in outcome prediction, because brain lesions in different anatomical areas are heterogeneous in manifestation (10). a study on paediatric tbi predicted outcome based on location of brain lesions. in the study the brain were distinguished into three zones: zone a (cortical structures); zone b (basal ganglia, corpus callosum, internal capsule, and thalamus); and zone c (brainstem). the magnetic resonance imaging (mri) fluidattenuated inversion recovery (flair) hyperintense lesions in mentioned zones were correlated with gos. the study reported that patients with lesion in all three zones were 4.4 times at the risk of unfavourable as compared to lesions only in zone a or both in zone a & b (10). in the present study only cortical areas are evaluated based on standard anatomical demarcation that is frontal, parietal, temporal and occipital lobes. our study reports that the patients with abnormal ct signs in one or two or three lobes were having favourable outcome with reference to abnormal ct signs in four brain lobes. the injury to brain in multiple areas predicts worst outcome as reported from our study and literature. the type of ct characteristics that include sdh, edh, sah, ich and intra ventricular haemorrhage (ivh) plays a significant role in prediction of outcome (7, 8). the anatomical locations of mentioned ct characteristic also have significance in outcome prediction (8, 9). a study from china correlated daily living activities (as assessed by barthel index) with location of brain lesions among tbi patients. the study reveals that cerebral contusion in temporal, parietal, frontal and occipital lobes among moderate to severe tbi patients were showing significant difference with outcome. the current study reports that cerebral contusion in temporal, frontal + temporal, & frontal + parietal + temporal region and sdh in parietal + temporal region are at the risk of unfavourable outcome. laterality of brain injury has significant role in prediction of outcome (11). a study evaluated occupational profile of unilateral tbi patients. the study reported that patients with left hemispheric tbi manifest with poorer functional independence, ability, participation and the quality of performance of everyday activities. the study suggested romanian neurosurgery (2017) xxxi 1: 101 – 110 | 109             that patients with left hemispheric brain lesion need intensive treatment for better improvement (11). the current study reported that patients with bilateral abnormal ct signs have unfavourable outcome as compared with right sided lesions. the abnormal ct characteristics like sdh on right sided and cerebral contusion on bilateral distribution were having worst outcome. limitation; posterior fossa abnormality is not incorporated in the present study, as posterior fossa has significant effect on outcome (10). our study is restricted only to cortical areas, but sub cortical and brain stem regions are also affected in brain injury as evidenced in literature (10). in the study unfavourable outcome number is lesser than one forth of favourable outcome. the present study had not grouped severity of injury, grouping was important because mild injury may not have significance with location of brain lesions and outcome (8). ich and cerebral contusion is taken as two different entities. in spite of these limitations our study provides clue that very commonly available ct findings provide higher prediction value for tbi outcome. conclusion the study endow that anatomical distributions of ct findings have potential inference in predicting of tbi outcome. further studies should include these variables with appropriate anatomical distribution into existing scoring system and look for any higher predictive values in interpreting tbi outcome. correspondence dr amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com mobile+91-8096410032 references 1. lee b, newberg a. neuroimaging in traumatic brain imaging. neurorx. 2005 apr;2(2):372-83. 2. glauser j. head injury: which patients need imaging? which test is best? cleve clin j med 71:353–357, 2004. 3. yealy dm, hogan de. imaging after head trauma. who needs what? emerg med clin north am 9:707– 717, 1991. 4. maas ai, steyerberg ew, butcher i, dammers r, lu j, marmarou a, mushkudiani 4. na, mchugh gs, murray gd. prognostic value of computerized tomography scan characteristics in traumatic brain injury: results from the impact study. j neurotrauma. 2007 feb;24(2):303-14. 5. marshall lf, marshall sb, klauber mr, clark mvb, eisenberg hm, jane ja, luerssen tg, marmarou a, foulkes ma: a new classification of head injury based on computerized tomography. j neurosurg 75:s14–s20, 1991. 6. maas ai, hukkelhoven cw, marshall lf, steyerberg ew. prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. neurosurgery. 2005;57(6):1173–1182. 7. azian aa, nurulazman aa, shuaib l, mahayidin m, ariff ar, naing nn, abdullah j. computed tomography of the brain in predicting outcome of traumatic intracranial haemorrhage in malaysian patients. acta neurochir (wien). 2001;143(7):711-20. 8. zhang yg, li cx, guan gf, chen xr, fang hm, wang z, chen xp. correlation of daily living activities with location and severity of traumatic brain injury. fa yi xue za zhi. 2014 dec;30(6):434-6. 110 | kumar et al commonly available ct characteristics             9. sharda p, haspani s, idris z. factors prognosticating the outcome of decompressive craniectomy in severe traumatic brain injury: a malaysian experience. asian j neurosurg. 2014 oct-dec;9(4):203-12. 10. smitherman e, hernandez a, stavinoha pl, huang r, kernie sg, diaz-arrastia r, miles dk. predicting outcome after pediatric traumatic brain injury by early magnetic resonance imaging lesion location and volume. j neurotrauma. 2016 jan 1;33(1):35-48. 11. huertas-hoyas e, pedrero-pérez ej, águilamaturana am, gonzález-alted c. study of the preand post-treatment functionality of unilateral acquired brain injuries. rev neurol. 2014 apr 16;58(8):345-52. 12. gao j, zheng z. development of prognostic models for patients with traumatic brain injury: a systematic review. int j clin exp med. 2015 nov 15;8(11):19881-5. 13. chesnut rm, ghajar j, maas ar: guidelines for the management and prognosis of severe traumatic brain injury part ii: early indicators of prognosis in severe traumatic brain injury. j neurotrauma 17:556–627, 2000. microsoft word 12temkarprasad_isthere 290 | temkar et al cfd in neurovascular compression syndrome             doi: 10.2478/romneu-2018-0035 is there a role for computational fluid dynamics (cfd) in neurovascular compression syndrome? prasad temkar1, yoko kato2, yasuhiro yamada2, ahmed ansari2 1apollo institute of neurosciences, apollo speciality hospitals, chennai, india 2department of neurosurgery, fujita health university, banbuntane hotokukai hospital, japan abstract: introduction – cfd uses complex algorithms to predict flow of fluids through a tube & also predicts its impact on walls. it is increasingly being used for prediction of aneurysmal wall thickness, flow, wall shear stress and to decide clip strategy. this is an experimental study, which analyses use of cfd in neurovascular compression syndrome and probable future applications. we analysed cfd findings in 12 cases retrospectively to know fluid dynamics of vessels and its implications. methodology – twelve patients – 7 cases of trigeminal neuralgia and 5 of hemifacial spasm who were to be treated by mvd, were enrolled. cfd i.e. wssv (wall shear stress vector), wssm (magnitude), sl (stream line) and pressure, was done in all prospectively. results – cfd of superior cerebellar artery, anterior inferior cerebellar artery and vertebral artery was done in each case at the contact site and immediate pre + post contact location. comparitively high wssm correlated maximally at nerve vessel contact junction (nvcj) and also high sl at the nvcj comparing with nerve vessel contact proximal (nvcp), wssv showed wide variations and pressure change was in-conclusive. conclusion – at contact site, the high wssm& sl might be a reliable indicator of a neurovascular conflict zone. to conclusively validate the findings we need large number of patients and control group. key words: computational fluid dynamics, neuralgia, nerve vessel contact. introduction dandy was the first to report vascular compression of the trigeminal nerve, since then the concept of neurovascular compression syndrome for trigeminal neuralgia and hemifacial spasm (hfs) developed. (1) the pathophysiology being pulsatile compression of the offending artery over the affected nerve at the root entry zone(rez). microvascular decompression still remains the mainstay for treatment. precise assessment of the complex nervevessel relationship at the root entry zone of the trigeminal nerve is useful for planning romanian neurosurgery (2018) xxxii 2: 290 296 | 291             microvascular decompression in patients with idiopathic trigeminal neuralgia.2 recently a fusion imaging technique for 3d mr cisternography and angiography by compositing a 3d mr cisternogram and a coregistered 3d mr angiogram in a single 3d image, has been described to provide a reliable assesment of the same. (3) computational fluid dynamics (cfd) uses complex algorithms to predict flow of fluids through a tube & also predicts its impact on walls. it is increasingly being used for prediction of aneurysmal wall thickness, flow, wall shear stress and to decide clip strategy. (5) this is an experimental study, which we use of cfd to analyze the hemodynamics in offending arteries of neurovascular compression syndrome. materials and methods data was collected retrospectively from 12 patients (7 tgn, 5 hfs; women, men; age range, 34 – 87 years; mean, 63.9 years) with neurovascular compression syndromes (table 1). the offending arteries as seen on preoperative imaging and intraoperative findings were (sca, pica, va). in all cases mvd was done via the retrosigmoid approach. all patients were imaged by means of 3d mr cisternography, 3d mr angiography (mra) and 3d ct angiography (cta). a 3d fusion image was created by superimposing the obtained images & neurovascular conflict at the root entry zone was visualized. surgical simulation images were prepared before surgery and were compared with the intraoperative surgical field image. cfd analysis done of contrast enhanced multi detector cta images with post processing done on ziostation 2 software. the offending vessel was isolated & shape was reconstructed. cfd analysis was done using hemoscopev1.5(ebm, tokyo) and values for wall shear stress(wssm), wall shear stress vector((wssv), streamline flow velocity(sl), & circumferential pressure was calculated. after confirmation intraoperatively, site of neurovascular conflict (nvcj), proximal (nvcp) and distal (nvcd) to it was marked in hemoscope. the relative ratio`s of nvcj to ncvp and nvcj to nvcd were calculated. results the 3d fusion image created before surgery was compared with intraoperative locali-zation of compression at rez. these respective zones were marked as nvcj (junction), nvcp (proximal) & nvcd (distal). the values of wssm, sl, pd are variable according to systolic and diastolic cardiac cycles6. hence, their comparitive ratio’s were used to remove the bias and equated to less than 1, if low or more than 1 if high. if the comparision was relatively close then it was equated to one. detailed results of each patient and their respective comparision values of wssm, sl & pd have been presented in table 2. the wssv has been represented as presence (+) or absence (-) of change of linearity at a particular junction. the generalized patient population data on terms of age, sex, offending artery, side of symptoms, comorbidities & drugs used have been presented in detail in table 1. 292 | temkar et al cfd in neurovascular compression syndrome             wssm comparing nvcj/nvcp was high (>1) in 8 cases, 2 cases were almost equal, low in 2 cases; nvcj/nvcd was high in 9 cases, low in 1 case, equal in case. sl comparing nvcj/nvcp was high(>1) in 9 cases, 3 cases were almost equal, never low; nvcj/nvcd was high in 9 cases, low in 2 cases, equal in 1 cases. pressure loss comparing nvcj/nvcp was high(>1) in 3 cases, 1 case was almost equal, low in 7 cases; nvcj/nvcd was high in 6 cases, low in 5 cases, equal in case. wssv showed variation in direction at nvcj in 7 cases, at nvcp in 4 cases, at nvcd in 2 cases. table 1demographics of the affected patients in the study. nvc syndrome side age sex comorbids artery tgn left 73 f htn,dm sca hfs right 40 f aica tgn left 70 m dm sca tgn left 35 f htn,dm sca tgn right 74 m htn sca hfs left 72 f dm va tgn left 77 f htn sca hfs left 74 f aica hfs left 73 m aica tgn right 66 f htn sca tgn left 61 f htn,dm sca hfs right 47 m aica table 2 summary of patients data and comparision of hemodynamic charcteristics with cfd hfs >1 >1 >1 >1 <1 <1 tgn 1 >1 1 >1 <1 <1 lt tgn >1 >1 >1 >1 <1 <1 rt tgn >1 >1 >1 >1 >1 <1 lt hfs >1 >1 >1 >1 <1 >1 lt tgn >1 <1 >1 >1 <1 <1 lt hfs 1 >1 1 >1 <1 >1 lt hfs >1 >1 1 1 <1 >1 rt tgn >1 >1 1 >1 lt tgn >1 >1 >1 <1 tgn trigeminal neuralgia, hfs hemifacial spasms; nvcpproximal nvc region, nvcjjunction nvc site, nvcd distal nvc region, fvflow velocity, wssmwall shear stress magnitude, wssv wall shear stress vector, pdpressure loss. as it is comparision study ratio’s were averaged with following values >1high; <1 low; 1both values approximately equal. wssv variations; (+) present, (-) absent   romanian neurosurgery (2018) xxxii 2: 290 296 | 293             representative cases case 1: a 64 years lady with no comorbidities complained of typical lancinating pain in the right v1 distribution, on carbamazepin (max dosage) for last 3 months without resolution of symptoms and depression. mri showed neurovascular conflict at rez of vth nerve by superior cerebellar artery(sca); she underwent transposition of the sca with good relief of symptoms immediate post operatively. figure 1clockwise from top: a) 3d cta with 3d mra recon.; b)intraop view; c)wssm; d)pressure: e)streamline flow velocity; f)wssv after superimposing 3d cta over 3d mra, the vessel was reconstructed on ziostation. cfd analysis of the pica with attention near the area of neurovascular conflict was done in vcfd of hemosopev1.5. cfd analysis of the sca with attention near the area of neurovascular conflict was done. wssm was higher at nvcj than both nvcp or nvcd. pressure was lower at nvcj compared to nvcp but higher than nvcd. sl also was higher at nvcj as compared to both nvcp&nvcd. wssv showed some variation in direction at nvcj site but was almost linear at nvcp&nvcd. patient had come for follow up after 6 months with good pain relief & completely off medications. case 2: a 77 year old hypertensive, diabetic lady presented with left sided persistant recurring hemifacial spasms which interfered with her way of life. she was on clonazepam for 6 months without any relief. mri showed a tortuous anterior inferior cerebellar artery(aica) compressing the 7th nerve anteriorly and posteriorly. she was evaluated with 3d cta, 3d mr cisternography and 3d mra. she underwent transposition of pica at first without relief and was re-operated with re transposition of aica and teflon padding all around. 294 | temkar et al cfd in neurovascular compression syndrome             after superimposing 3d cta over 3d mra, the vessel was reconstructed on ziostation. cfd analysis of the pica with attention near the area of neurovascular conflict was done in vcfd of hemosopev1.5 .wssm was higher at nvcj than both nvcp or nvcd. pressure was lower at nvcj compared to nvcp but higher than nvcd. sl also was higher at nvcj as compared to both nvcp&nvcd. wssv showed some divergant vectors iatnvcj site but were almost linear at nvcp&nvcd. patient had come for follow up after 6 months with good pain relief & completely off medications. discussion neurovascular conflict (compression) syndromes viz., hfs &tgn, usually produce discomforting symptoms which prevent individuals from having a normal life. microvascular decompression is the only permanent solution. they have a high recurrence rate if not treated correctly. hence there is a need for precise evaluation of the conflict zone to plan course of surgery. the primary pathology is the nerve being compressed by a pulsatile artery and vice versa. hence it is postulated that some hemodynamic changes would be seen at the site6. recently role of cfd in analysing the growth of unruptured aneurysms has been studied extensively [9,10]. also the perianeurysmal& intra aneurysmal hemodynamics have been studied using cfd & increasingly being used in prediction of aneurysmal wall thickness, flow, wall shear stress and accordingly clip strategy is decided. [7,8] therefore the interest in analysing the hemodynamics of offending vessel at the site of compression. cfd uses complex mathematical algorithms requiring high end computer softwares making it difficult to apply in daily use. it also provides a lot of cfd parameters, evaluation of analysis result and that the value is also not constant. hence we used a dedicated software hemoscope-v1.5 to analyse the blood flow at the site of neurovascular conflict. from the medical images information (dicom data) of the patient, the blood vessel shape in 3d is created with ziostation 2. next, in hemoscope-v1.5,vessel module the vessel inlet ,nvcj is marked & with vcfd module analysis module fv, sl, wp, wssv, were obtained. romanian neurosurgery (2018) xxxii 2: 290 296 | 295             wall shear stress (wssm) results from friction between blood flow and the vessel wall, creating a tangential force exerted on the wall. high wssm meant that flow is fast near endothelium & low wssm meant slow flow near endothelium – usually seen proximal to stenotic areas leads to plaque formation. in our series also we concur with the above as ratio of nvcj/nvcp was high in most of our findings. sato et al have also reported similar findings in their study on hemifacial spasm.6wssv indicates the direction of shear stress at wall. usually parallel vectors are seen in straight vessel.while convergent and divergent vectors are found at turn or branching or stenotic (thick) or dilated areas (thin). change in the direction of vector in straight vessel could be due to external factors like compression/traction of vessel. we noted some change in direction of vectors at the nvcj in many cases but sometimes also at nvcp or ncvd. so this evidence was not substantial to qualify the above. pressure is the force of blood column on the arterial wall circumferentially leading to stretching/stress on all wall layers. at higher pressures the intima is affected leading to remodeling of vessel wall or atherosclerotic changes. in our series pressurewascomparitively lower at nvcj but did not show significant p value to confirm the association. streamline flow velocity(sl) is the measurement of blood flow velocity at a given point. at low velocity the flow was streamline or linear, whereas at turns or stenotic areas it showed turbulent flow with high velocity. in our series, we have a good correlation of high sl at nvcj compared to nvcp. we think it may be due to the stenosis caused by compression, and also where it was equal may be due to remodeling of the intima in some cases having long duration of symptoms. limitations of the study the cfd analysis was done at a cardiac cycle common to a single study but could not be generalized in every case as done by sato et al.; butcomparision was made within one study to remove the bias. the compressed vessels are sometimes very thin and may not be able to be reconstructed correctly. also overlying vessels or bone may add artifacts while recreating vessel shape. the software hemoscope-v1.5(tokyo) was primarily made to asses perianeurysmal environment and we have applied it to smaller arteries.6 conclusions comparatively high wssm and high sl at nvcj to nvcp correlates well with area of neurovascular conflict. due to lack of sufficiently large number of cases, its validity remains a question. but this study certainly provides hope that the role of cfd in neurovascular syndromes is certainly the future. future applications may involve use of cfd analysis postoperatively after complete resolution or recurrence of symptoms and compare with preoperative values. references 1. neurovascular compression (conflict)]. slavik ee1, djurovićbm et-al;actachiriugosl. 2008;55(2):161 2. satoh t, onoda k, date i: preoperative simulation for microvascular decompression in patients with idiopathic trigeminal neuralgia: visualization with threedimensional magnetic resonance cisternogram and 296 | temkar et al cfd in neurovascular compression syndrome             angiogram fusion imaging. neurosurgery 60: 104-14, 2007 3. satoh t, onoda k, date i: preoperative simulation for microvascular decompression in patients with idiopathic trigeminal neuralgia: visualization with threedimensional magnetic resonance cisternogram and angiogram fusion imaging. neurosurgery 60: 104-14, 2007 4. satoh t, omi m, nabeshima m, et al: severity analysis of neurovascular contact in patients with trigeminal neuralgia: assessment with the inner view of the 3 d mr cisternogram and angiogram fusion imaging. ajnr am j neuroradiol 30: 603-7, 2009 5. shojima m, oshima m, takagi k, et al: magnitude and role of wall shear stress on cerebral aneurysm: computational fluid dynamic study of 2 0 middle cerebral artery aneurysms. stroke 35: 2500-5, 2004 6. toru satoh, keisuke onoda et al: local hemodynamics of compressed blood vessels in neurovascular compression site of unilateral facial spasm using numerical fluid dynamics (cfd) 7. janiga g, sugiyama k, kono k, et al: the computational fluid dynamics rupture challenge 2013phase 1: prediction of rupture status in intracranial aneurysms． ajnr am j neuroradiol 30:530-6, 2015 8. hassan t, timofeev ev, saito t, et al: proposed parent vessel geometry-based categorization of saccular intracranial aneurysms: computational flow dynamics analysis of the risk factors for lesion ruptur.jneurosurg 103:662-80, 2005 9. shojima m, oshima m, takagi k, et al: magnitude and role of wall shear stress on cerebral aneurysm: computationalfluid dynamic study of 2 0 middle cerebral artery aneurysms. stroke 35: 2500-5, 2004 10. sforza dm, putman cm, tateshima s, et al: effects of perianeurysmal environment during the growth of cerebral aneurysms: a case study. ajnr am j neuroradiol 3 3 :1115-20, 2012 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article management of subdural chronic hematoma in colombia: national survey marticela morales-cabeza, amit agrawal, gabriel alcala-cerra, huber s. padilla-zambrano, andres m. rubiano, alfonso pacheco-hernandez, luis gabriel moscote-salazar, hernando alvis-miranda, luis rafael moscote-salazar colombia, india, venezuela doi: 10.1515/romneu-2017-0031 romanian neurosurgery (2017) xxxi 2: 197 202 | 197 doi: 10.1515/romneu-2017-0031 management of subdural chronic hematoma in colombia: national survey marticela morales-cabeza1, amit agrawal2, gabriel alcala-cerra3, huber s. padilla-zambrano1, andres m. rubiano4, alfonso pacheco-hernandez5, luis gabriel moscote-salazar6, hernando alvis-miranda1, luis rafael moscote-salazar5 1university of cartagena, cartagena de indias, colombia 2department of neurosurgery, narayna medical college hospital, chinthareddypalem, andhra prades, india 3e.s.e hospital universitario cari, barranquilla, colombia; department of neurological research, health sciences and neurosciences (cisneuro) research group, university of cartagena, cartagena de indias, colombia 4hospital universitario de neiva-fundacion meditech, neiva, universidad el bosque, bogota, colombia 5department of neurological research, health sciences and neurosciences (cisneuro) research group, university of cartagena, cartagena de indias, colombia 6hospital universitario de maracaibo, universidad del zulia, maracaibo, venezuela abstract: chronic subdural hematoma is a growing neurological pathology, especially in older people. thus, describing how this entity is approached in colombia is of great importance because it allows to evaluate and contrast this approach with that of other countries, comparing the techniques used, therapeutic management and additional measures. in this study, this comparison was carried out using a self-administered survey with 16 multiple-choice items. the results were evaluated in microsoft excel, determining measures of central tendency accompanied by frequencies and percentages. as an initial management, 75.5% preferred to use 1burr hole and, in cases of recurrence, craniotomy is the choice in 50% of cases. regarding the placement of drainage, its use was estimated to be 83.3%, especially the subdural system closed to external drainage, with a preference of 85.2%, and without use of corticosteroids as adjuvant therapy in 88.9 % of respondents. these data are consistent with the results of studies in other countries regarding the management of this pathology. key words: chronic subdural hematoma; craniotomy, neurosurgery 198 | morales-cabeza et al management of subdural chronic hematoma in colombia introduction chronic subdural hematoma (hsc) is one of the most common neurological pathologies (1-4), with an incidence of 3.4 per 100,000 population in patients younger than 65 years of age and 8-58 per 100,000 in older adults. 65 years (5, 6), being more frequent in the male sex, (7) people with risks of falls, convulsions, alcohol abuse, coagulation disorders (2, 8) and associated medicines (9). its origin begins from the formation of acute hematomas, which may resolve spontaneously or increase in size and continue to enlarge, generating rupture of small veins as it expands, further increasing the amount of blood and thus becoming a hsc8, (10). it is rarely produced as a complication of cuts of unbroken cerebral aneurysms (11). its diagnosis is performed by imaging, mainly ct scan and magnetic resonance imaging (mri). (12) the treatment options include craniotomy, burr hole craniostomy (bhc), twist drill craniostomy (tdc), endoscopic management and medical management; however, there is still no consensus on the technique of choice. (8) on the other hand, the use of preventive measures to reduce recurrence has been implemented, including: use of corticosteroids, angiotensin receptor antagonists, correct positioning of the head postoperatively, continuous subdural irrigation, among others (13). despite this, recurrence rates have been reported from 6.6 to 38% and mortality rates of 3.8% (8). this high recurrence rate, coupled with the prevalence of this condition, raises the need to know how this pathology is approached in colombia, the conditions that could be influencing this method and, at the same time, to evaluate the implications that this may have on the patient. materials and methods a descriptive observational study was performed. we included 54 participants who were part of the medical staff of some colombian institutions. as the only criterion of inclusion, it was necessary that participation should be voluntary, after signing an informed consent. a survey was carried out using a virtual platform (ww.encuestafacil.com), which consisted of 16 multiple-choice questions related to the management of hsc, and had variables such as: academic training (place of training in general neurosurgery and profession), use of surgical techniques (burr hole, twist drill, others), use of drugs (steroids, anticonvulsants, antibiotics), use of devices (drains) and other measures. the data were entered in a database in microsoft excel and analyzed using the same program, using descriptive statistics by means of determination of measures of central tendency, frequency and percentages, according to the options marked in the survey. results socio-demographic characteristics of the 54 participants in the study, 92.6% (50) were men, with a male: female ratio of approximately 13: 1. the countries where neurosurgery was performed were colombia with 43 subjects (79.6%), followed by other countries in central and south america with 8 romanian neurosurgery (2017) xxxi 2: 197 202 | 199 subjects (14.8%), north america with 2 (3.7 %) and another continent 1 subject (1.9%). as for their profession, 77.8% of the respondents were general neurosurgeons and 12.2% had another sub-specialty. surgical aspects as for the initial management of the patient, the technique of choice was 1 burr hole, with a prevalence of 75.5% when compared to the others (figure 1). the technique of choice in cases of recurrence was also evaluated (table 1). the irrigation of the dural cavity during the surgical procedure and the use of drains at the end were reported in high proportions, with values of 85.2% and 83 % respectively. figure 1 technique of preference in the initial management of hsc table 1 technique of choice in the management of recurrent hsc number of patients (%) twist drill 1 1,9 1 burr hole 18 33,3 2 burr hole 7 13 subdural peritoneal shunt 1 1,9 craniectomy 27 50 total 54 100 use of medicines regarding the management of patients in whom there were no seizures, 88.9% of the participants did not use anticonvulsants, and 11.1% used them, administered for less than 1 day (1.9%) or 7 to 5 days (9.3%). the use of antibiotics was also investigated, evidencing a significant use of these in a preoperative (83.3%) and postoperative (64.8%), with a predominance of 82.7% for cephalosporins, 17% for others types (except for fluoroquinolones and penicillin, of which no use was reported by specialists in the management of this pathology). another of the drugs evaluated was the use of systemic steroids as one of the measures for the management of patients with hsc, evidencing that 48 (88.9%) of the respondents deny their use compared to only 6 (11.1%) that allow you to use it. other measures the implementation of other additional measures for the management of hsc, such as the use of the head in zero degrees in the 24 hours post-surgical were studied, reporting that 70.4% of the respondents use this measure, compared to 29.6% who refrain from using it. the use of drains was also evaluated, revealing that 46 of the participants (85.2%) prefer a subdural system closed to external drainage, 2 (3.7%) prefer a closed subgaleal system to external drainage, while 6 of them (11.1%) did not use any drains. regarding the perception about the importance of age as a determinant of the surgical decision, 77.8% considered that it is not a determining parameter when deciding to intervene, while the other 22.2% consider it important. 200 | morales-cabeza et al management of subdural chronic hematoma in colombia discussion the hsc is one of the neurological pathologies that is reported more frequently (1). its handling must be in charge of a trained professional. in the present study, 77% of the participants who perform the approach of these patients are general neurosurgeons, compared to 22% who have a subspecialty, which reflects that due to the high frequency of this pathology, the management by a general neurosurgeon is more frequent, having all the capacities and training to be able to offer him of equal way, an adequate attention to the patient, without that this has negative repercussion in the morbidity and mortality. the training country of the majority of the participants was colombia; a fact that can be explained by the lack of opportunities for specialization abroad, personal preferences or socioeconomic issues. determining the cause of this result would require another study that is not the subject of this article. the variety of surgical techniques to intervene to these patients, generates controversy about the procedure of choice; (burr-hole 1, 8 of these (15.1%) 2 burr-hole and only 5 (9.4%) the craniectomy. these data coincide with those observed in countries like nigeria (14) and other studies where the first two techniques are of choice (15) mainly due to the low rates of recurrence reported (826%). irrigation of the subdural space in a systematic way (2, 14, 16) and that in our country is reported in 85.2% of cases. regarding the procedure of choice in cases of recurrence, the most used was the craniotomy, followed by the 1 burr hole, 2 burr hole, and tdc, which contrasts with other studies where bhc occupies the first place, followed by the tdc, the latter considered advantageous because it can be performed at the patient's bedside with the use of local anesthesia, together with cost and time saving (8). this difference could be given by the population studied, places of training and access to certain materials and procedures. therefore, the technique of choice may vary depending on where the intervention is performed, without representing malpractice or prejudice to the patient. the use of antibiotics is one of the main measures used in any type of surgery and has been shown to be largely used prophylactically in the preand postoperative phase to treat hsc (83.3% and 64, 8% respectively). however, there is little information in the literature about its use, dosage, duration and types of recommended antibiotics. in most scenarios where they are used, it is a way of intervening for an existing infection (17). within the medication given to the patient, the anticonvulsants have been routinely used in the post-surgical period, based on the concept that after the intervention, patients may frequently exhibit some extent of the underlying traumatic brain injury, thus establishing a risk factor for seizures. (6) although the data indicate that 88.9% do not use them, 9.7% use it for 5 to 7 days and 1% use it only in the first hours. despite this, its use is not yet considered as a routine or standardized practice (14). the role of inflammation as a determinant in the pathophysiological process of hsc has been known for several years. despite this, the use of steroids as additional therapy is limited in many countries (14) romanian neurosurgery (2017) xxxi 2: 197 202 | 201 including colombia, due to limited clinical evidence of its effectiveness and cost-benefit relationship (18, 19). in countries like canada, abstention from its use occurs in more than 80% of neurosurgeons (18). after surgery, most neurosurgeons place a subdural system closed to external drainage. it has been shown that its use after the evacuation of a hsc can accelerate the washing of inflammatory and fibrinolytic factors confined within the subdural cavity, thus decreasing its recurrence (2, 13, 20). in spite of this, the use of subdural drainage is not a systematic practice in all countries. in the present study, 83.3% place a drainage at the end of the surgical procedure, and in countries such as nigeria, the use is 42.8%, (14) whereas a survey in the united kingdom and the republic of ireland showed that only 11% of neurosurgeons always place a drain (11). concern for surgical risk is one of the main reasons why some neurosurgeons avoid their use, due to the fear of: perforation of the cortex, generation of a subdural hematoma or the formation of a subdural empyema bacterial (12). with respect to prognosis and conceptions about the intervention, more than 70% of the participants consider that age is not a determining factor when evaluating a possible intervention, which indicates that the majority of patients who enter and are not candidates for medical treatment, will have the opportunity to be managed surgically to seek the final resolution of your picture. this generates higher cure rates and is consistent with other countries (1). despite this, there are reports that young patients tend to have a better outcome. (21) but despite this controversy, this should not be a reason to delay or deny intervention in older patients and more so because they are the first group affected. after the surgical intervention, the adoption of measures such as variation in the position on the stretcher, have been considered as support tools. although 70.4% of the participants use the head in zero degrees; in other places, tredenlenburg position is used in order to increase cerebrospinal fluid (csf) pressure and help brain reexpansion. despite this, the results are considered contradictory, and the role of the positions as stimulants or inhibitors of recurrence has not been determined. (14) regarding the limitations of the study, it should be clarified that equal proportions of respondents from each of the participating hospital centers were not taken into account, which would make it ideal to carry out another study that includes a greater number of professionals from other regions of the country. country, to confirm if the results obtained are similar or consistent with those of the present study. in addition, the fact that the majority of participants presented their training in this country could have influenced the results obtained. conclusion chronic subdural hematoma is a pathology that in colombia is approached mainly by the general neurosurgeon, and whose treatment agrees with most measures adopted in other countries at the intervention level of choice, medication use and additional measures. 202 | morales-cabeza et al management of subdural chronic hematoma in colombia correspondence dr. luis rafael moscote-salazar email: mineurocirujano@aol.com references 1.lo w-l, lee t-c, fang p-s, huang y-h. chronic subdural hematoma in patients under age 65 years: a comparative study of age cohort. formosan journal of surgery 2013;46:10-14. 2.bellut d, woernle cm, burkhardt j-k, kockro ra, bertalanffy h, krayenbühl n. subdural drainage versus subperiosteal drainage in burr-hole trepanation for symptomatic chronic subdural hematomas. world neurosurg 2012;77:111-118. 3.santarius t, qureshi hu, sivakumaran r, kirkpatrick pj, kirollos rw, hutchinson pj. the role of external drains and peritoneal conduits in the treatment of recurrent chronic subdural hematoma. world neurosurg 2010;73:747-750. 4.singla a, jacobsen wp, yusupov ir, carter da. subdural evacuating port system (seps)-minimally invasive approach to the management of chronic/subacute subdural hematomas. researchgate 2012;115. 5.aspegren op, åstrand r, lundgren mi, romner b. anticoagulation therapy a risk factor for the development of chronic subdural hematoma. clin neurol neurosurg 2013;115:981-984. 6.ducruet af, grobelny bt, zacharia be, et al. the surgical management of chronic subdural hematoma. neurosurg rev 2012;35:155-169. 7.marshman lag, manickam a, carter d. risk factors for chronic subdural haematoma formation do not account for the established male bias. clin neurol neurosurg 2015;131:1-4. 8.singh sk, sinha m, singh vk, et al. a randomized study of twist drill versus burr hole craniostomy for treatment of chronic subdural hematomas in 100 patients. the indian journal of neurotrauma 2011;8:83-88. 9.vladila a-m, mitrea d-a, nica s, et al. chronic subdural hematoma: a case report and review of the literature. romanian journal of neurology 2014;13:35. 10.kumar p, kiran u. management of chronic subdural haematoma: single burr-hole drainage and irrigation using the technique of “syringing”. the indian journal of neurotrauma 2013;10:105-108. 11.inamasu j, watabe t, ganaha t, et al. clinical characteristics and risk factors of chronic subdural haematoma associated with clipping of unruptured cerebral aneurysms. journal of clinical neuroscience 2013;20:1095-1098. 12.ahmed s, agrawal d, kale ss, mahapatra ak. a comparative study of treatment of chronic subdural hematoma — burr hole drainage versus continuous closed drainage. the indian journal of neurotrauma 2011;8:17-23. 13.alcalá-cerra g, young amh, moscote-salazar lr, paternina-caicedo a. efficacy and safety of subdural drains after burr-hole evacuation of chronic subdural hematomas: systematic review and meta-analysis of randomized controlled trials. world neurosurg 2014;82:1148-1157. 14.rabiu tb. chronic subdural hematoma: a survey of neurosurgeons' practices in nigeria. surg neurol int 2013;4:58. 15.smith md, kishikova l, norris jm. surgical management of chronic subdural haematoma: one hole or two? international journal of surgery 2012;10:450-452. 16.adachi a, higuchi y, fujikawa a, et al. risk factors in chronic subdural hematoma: comparison of irrigation with artificial cerebrospinal fluid and normal saline in a cohort analysis. plos one 2014;9:e103703. 17.aslan a, eser o, coşar m, albayrak r. salmonellainfected chronic subdural hematoma. researchgate 2009;39:139-142. 18.santarius t, lawton r, kirkpatrick pj, hutchinson pj. the management of primary chronic subdural haematoma: a questionnaire survey of practice in the united kingdom and the republic of ireland. researchgate 2008;22:529-534. 19.berghauser pont lme, dirven cmf, dippel dwj, verweij bh, dammers r. the role of corticosteroids in the management of chronic subdural hematoma: a systematic review. eur j neurol 2012;19:1397-1403. 20.santarius t, kirkpatrick pj, ganesan d, et al. use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial. lancet 2009;374:1067-1073. 21.sarma p, indira devi b, shukla dp, bhat di. subacute and chronic subdural hematoma in young population less than 40 years. the indian journal of neurotrauma 2014;11:1-4. ansaria_rolesertraline romanian neurosurgery (2016) xxx 3 role of sertraline in insomnia associated with post traumatic brain injury (tbi) depression ahmed ansari1, akhilesh jain2, r.s. mittal3, achal sharma4, anand sharma5, i.d. gupta6 1mch neurosurgery, sms medical college, jaipur, rajasthan, india 2md psychiatry, head of dept., esi hospital, jaipur, rajasthan, india 3mch neurosurgery, professor and head, sms medical college, jaipur, rajasthan, india 4mch neurosurgery, professor, sms medical college, jaipur, rajasthan, india 5mch neurosurgery, consultant, artemis hospital, delhi 6professor psychiatry, sms medical college, jaipur, rajasthan, india abstract: traumatic brain injury (tbi) is a major cause of disability (1, 2). sleep disturbances, such as insomnia, are very common following traumatic brain injury and have been reported in frequencies from 40% (3) to as high as 84% (4). sleep disruption can be related to the tbi itself but may also be secondary to neuropsychiatric (e.g., depression) or neuromuscular (e.g., pain) conditions associated with tbi or to the pharmacological management of the injury and its consequences. post-tbi insomnia has been associated with numerous negative outcomes including daytime fatigue, tiredness, difficulty functioning: impaired performance at work, memory problems, mood problems, greater functional disability, reduced participation in activities of daily living, less social and recreational activity, less employment potential, increased caregiver burden, greater sexual dysfunction, and also lower ratings of health, poor subjective wellbeing. these negative consequences can hamper the person’s reintegration into the community, adjustment after injury, and overall qol. (5) the connection between depression and insomnia has not been investigated within the post tbi population to a great extent. for the general population, clinically significant insomnia is often associated with the presence of an emotional disorder (6). fichtenberg et al. (2002) (7), in his study established that the strongest relationship with the diagnosis of insomnia belonged to depression. given the high prevalence of depression during the first 2 years following tbi (8), a link between depression and insomnia among tbi patients makes innate sense. the present study aims at assessing role of sertralline in post tbi insomnia associated with depression. introduction traumatic brain injury (tbi) is a major cause of disability (1, 2). sleep disturbances, such as insomnia, are very common following traumatic brain injury and have been reported in frequencies from 40% (3) to as high as 84% (4). sleep disruption can be related to the tbi itself but may also be secondary to ansari et al role of sertraline in insomnia associated with post tbi depression neuropsychiatric (e.g., depression) or neuromuscular (e.g., pain) conditions associated with tbi or to the pharmacological management of the injury and its consequences. post-tbi insomnia has been associated with numerous negative outcomes including daytime fatigue, tiredness, difficulty functioning: impaired performance at work, memory problems, mood problems, greater functional disability, reduced participation in activities of daily living, less social and recreational activity, less employment potential, increased caregiver burden, greater sexual dysfunction, and also lower ratings of health, poor subjective wellbeing. these negative consequences can hamper the person’s reintegration into the community, adjustment after injury, and overall qol. (5) the connection between depression and insomnia has not been investigated within the post tbi population to a great extent. for the general population, clinically significant insomnia is often associated with the presence of an emotional disorder6. fichtenberg et al. (2002) (7), in his study established that the strongest relationship with the diagnosis of insomnia belonged to depression. given the high prevalence of depression during the first 2 years following tbi (8), a link between depression and insomnia among tbi patients makes innate sense. the present study aims at assessing role of sertralline in post tbi insomnia associated with depression. materials and methods the study was carried out in neurosurgery ward and opd of sms medical college and group of hospitals, rajasthan, a 3000 bedded superspeciality tertiary care centre. sample was recruited through the follow up in neurosurgery opd and indoor. being the largest medical institute in the state of rajasthan, it caters the health needs of entire state as well as neighboring states. a total of 250 male traumatic brain injury patients with mild to moderate severity were screened initially. eighty patients were found to have depression on assessment with phq-9 and subsequent interview with psychiatrist. out of these eighty patients, fiftysix were found to have insomnia, who finally constituted the study sample size. the study was further divided randomly in to two groups, consisting of twenty eight patients in each group. one group designated as intervention group (cases) was given 50 mg sertralline daily po. the other group was not given any medication and served as control group. the nature and purpose of the study was explained to the participants and written informed consent was obtained either by the participant himself or his next of kin. the study was limited to male participants only to ensure the homogeneity of the group with regard to the interactions of demographic variables, disease characteristics, and social stresses. the study protocol was approved by the institution`s ethical committee. all the participants were evaluated initially after two week interval for first 4 weeks and at the end of 6 months. to be eligible to participate in study, the patients had to be 18 years or older, should have had at least two weeks old injury, have a romanian neurosurgery (2016) xxx 3 history of tbi with a documented loss of consciousness or other evidence of a tbi (i.e., pathology on neuroimaging), and be able to comprehend or answer verbal or written questionnaires. participants were excluded from the study if they were known 1. to have a serious medical illness, 2. to have a current substance abuse disorder using dsm-iv criteria, 3. to have mass brain lesions or other neurologic diagnoses other than tbi, 4. to have a history of current or past psychosis or mania, mdd or any other mental disorder except current depression using dsm-iv criteria, or 6. to have a history of clinically significant liver or renal disease. at the initial assessment, demographic characteristics of the cases and controls were assessed on a self-designed semi structured proforma by interviewing the participants with additional information on injury characteristics of the cases by exploring the medical records and neuroradiological investigations. severity of tbi was assessed by gcs. initially cases and controls were assessed on insomnia severity scale for insomnia. at the end of six months, both cases and controls were assessed on isi to measure improvement in sleep. measures in this study, the interview was focused on assessment of severity of tbi, depression and insomnia using gcs, phq-9 and insomnia severity scale (iss). gcs (9), an extensively used clinical scale for assessing the depth and duration of impaired consciousness and coma. three aspects of behavior are independently measured—motor responsiveness, verbal performance, and eye opening. these can be evaluated consistently by doctors and nurses and recorded on a simple chart which has proved practical both in a neurosurgical unit and in a general hospital. the scale facilitates consultations between general and special units in cases of recent brain damage, and is useful also in defining the duration of prolonged coma. depression was assessed by administering the nine-item phq-9, a self-report version of prime-md11 which assesses the presence of major depressive disorder using modified diagnostic and statistical manual, fourth edition (dsm-iv) criteria. there is good agreement reported between the phq diagnosis and those of independent psychiatry health professionals (for the diagnosis of any one or more phq disorder, kappa = 0.65; overall accuracy, 85%; sensitivity, 75%; specificity, 90%) (17, 18). in this study hindi version of phq-9 was used. it has been validated in indian population and is considered to be reliable tool for diagnosis of depression. the phq-9 is a dual instrument that is used to establish a provisional depressive disorder as well as it provides a symptoms severity score. for the diagnosis of depression, we define clinical significant depression as: a phq-9 score of 8–9 as minor depression, a phq-9 score of 10 or greater as moderate depression; a score of 15 or more and one of the two cardinal symptoms (either depressed mood or anhedonia) as definite major depression (10, 11). we considered ansari et al role of sertraline in insomnia associated with post tbi depression phq 9 score of 10 or more as depression in this study. insomnia was assessed on insomnia severity index (isi) (12). isi is one of the most commonly used disease-specific measures for self-perceived insomnia severity. the isi has 7 items describing insomniarelated health impairments. each item is rated on a 5-point likert scale with scores ranging from 0 to 4, indicting ‘‘none’’, ‘‘mild’’, ‘‘moderate’’, ‘‘severe’’ and ‘‘very severe’’ sleep problems, respectively. the total isi score is calculated by summing the scores from the 7 items, and range from a minimum of 0 to a maximum of 28, with higher scores reflecting more severe sleep problems. in clinical assessments, the isi total summary score falls into 1 of 4 isi categories; with scores 0–7, 8– 14, 15–21, and 22–28 indicating no clinically significant insomnia, sub-threshold insomnia, moderate insomnia and, clinically severe insomnia, respectively. the psychometric properties of the isi have been evaluated in earlier studies and have been reported to have sound measurement quality for measuring perceived insomnia severity and the impact of insomnia in different populations (13, 14). we used hindi version of the insomnia severity index (15) which has a reliability of 0.91 and a corrected item correlation range of 0.56–0.87. hindi version of the insomnia severity index is a valid and reliable tool for the measurement of severity of insomnia. lesion localization was done on the basis of ct scan, conducted as part of the initial work up of the patient. the results were characterized as presence or absence of contusions, intracerebral bleed, subarachnoid, epidural or subdural bleed in various regions, namely, frontal, temporal, parietal and occipital. statistical analysis data were checked for normality, outliers, and missing data. no imputation of missing data was performed. statistical analyses were performed by correlation analyses (pearson and spearman), paired t test and chi-square tests analyses. results a total of 250 male patients of tbi were recruited in this study. 35.6% of the 250 patients were found to have depression (n=89). 9 out of 89 depressive patients dropped out from the study (10.11%). 80 patients (32%) of tbi with depression were evaluated for insomnia. 56 patients (70%) of post tbi depression with insomnia finally constituted the study sample. maximum number (30.4%) of patients with insomnia were found in the age group of 18-24 years (n=17), followed by 26.7% in the age group 25-34 years (n=15). however it was found to be statistically insignificant (p=0.938). insomnia as measured on isi was statistically more common (p=0.04) in mild tbi cases (58.9%) than the moderate tbi (41.1%) patients with depression. majority of the patients (46.43%) who had insomnia sustained injury more than 6 months back (n=26), followed by 23.2% of injury being less than 3 months duration (n=13). although this observation was found to be statistically insignificant (p=0.934). romanian neurosurgery (2016) xxx 3 neuroanatomical localization was also correlated with insomnia in post tbi depression among tbi patients. left side of brain injury was present in the majority (55.35%) of patients. this was followed by right side injury in 39.28% of patients (n=22) and diffuse axonal injury in 5.35% of patients (n=3). it was found insignificant on statistical analysis (p=0.761) [table 1]. cerebral contusion was the most common (32.14%) finding of injury (n=18), followed by multiple injury including contusion in 30.35% (n=17) of the cases. out of these 17 cases, 14 patients had contusion. thus, overall patients with contusion constituted 57.14% (n=32) of the study sample. other findings, like extradural, subdural, subarachnoid hemorrhage and even fractures were also found to be implicated in lesser frequency. we further tried to explore the distribution of cerebral contusion in these patients, and found 14 (57.1%) among 32 contused patients had multiple contusions, although single lobe contusion were also associated with insomnia, but in lesser numbers [table 2]. mean score of isi at the beginning of the treatment was 18.821 with sd 2.091 and 18.643 with sd 3.129 in intervention and control group respectively, and this was found to be statistically insignificant (p=0.802). at the end of the study, significant improvement was observed in isi scores in intervention group (mean=8.464, sd=2.202), as compared to control group (mean=10.786, sd=2.114).this effect was statistically significant (p=0.00018) [table 3]. table 1 demographic characteristics of tbi depressive insomniac patients age in years cases control total 18-24 10 7 17 25-34 7 8 15 x2=0.798 35-44 5 6 11 (p=0.938) 45-54 4 5 9 55-64 2 1 3 65 or more 0 1 1 type of injury rta 22 24 46 x2=0.563 ffh 4 3 7 (p=0.754) assault 2 1 3 others 0 0 0 gcs mild 16 17 33 x2=0.074 moderate 12 11 23 (p=0.786) duration of head injury <3 months 8 9 17 x2=0.136 3-6 mths 7 6 13 (p=0.934) >6 months 13 13 26 localization right side 10 12 22 x2=0.547 left side 16 15 31 (p=0.761) diffuse axonal injury 2 1 3 ansari et al role of sertraline in insomnia associated with post tbi depression table 2 lesion type based on ct scan table 3 statistical analysis of insomnia among tbi depressive patients mean sd se p value iss (at 0 mth) cases 18.821 2.091 0.395 0.802 control 18.643 3.129 0.591 iss(at 6 mth) cases 8.464 2.202 0.416 0.00018 control 10.786 2.114 0.399 discussion our study population was almost close to the age of distribution of tbi in general adult male population. the age range was 18-86 years with a mean age of 31.83 years in the intervention group and 32.95 years in the control group. jain et al. (2) and verma et al. (2007) (16) have also reported similar findings with regard to age and sex distribution in their study on chronic tbi patients evaluated for sleep disorders. insomnia was reported in 70% of post tbi depressive patients. this finding is supported by earlier studies, wherein insomnia has been reported between 15% and 77% in post tbi patients shortly after or well into the future (24). this finding was considerably less than the 77% reported by varney et al. (16), who used dsm-iii criteria. conversely, these findings were considerably more than the 14% reported by deb et al. (18) who relied on icd-10 diagnostic criteria. the correlation between occurrence of insomnia and duration in tbi was found insignificant. insomnia has been reported between 29% and 50%% in post tbi patients during one year after the trauma (19, 20, 21). population-based studies indicate that insomnia occurs in approximately 40% of individuals with a tbi of any severity and is often the most prevalent somatic complaint in this population (27). insomnia in depression was more common in mild tbi patients than those with moderate severity. the reason for this common occurrence in mild tbi could have been that mild tbi patients are more likely to retain their cognitive functions intact, thus are capable of acknowledging their deficits caused by trauma. clinchot et al. (1998) (17) and fichtenberg et al. (2002) (22) showed an inverse relationship and cohen et al. (1992) (23) noted ct scan findingscase control total contusion 8 10 18 multiple injury 9 8 17 edh 1 3 4 sdh 3 2 5 sah 2 0 2 nad/dai 5 4 9 others/foreign body 0 1 1 site of contusions in brain right frontal 1 2 3 left frontal 2 2 4 right parietal 1 0 1 left parietal 0 0 0 right temporal 1 0 1 left temporal 1 2 3 multiple contusions 8 6 14 romanian neurosurgery (2016) xxx 3 increased prevalence with increasing severity of tbi. some researchers have postulated the reason for this paradoxical finding to the fact that the people with severe brain injury are likely to under report and those with milder injury are more aware of their problem and therefore more likely to report about insomnia. verma et al. (2007) (16) looked at the more objective data that can be collected with polysomnography and multiple sleep latency test. their work noted that there was a relationship between severity of tbi and some but not all of the measures of the sleep disorders. in particular more severe tbi was associated with higher percentage of stage i sleep, number of awakening per night and the night spent awake each night. this study has also tried to explore the neuroanatomical localization of injury in respect to insomnia. cerebral contusion was the most commonly implicated area involving multiple lobes, however single lobe involvement was also seen. brain injury secondarily caused by extradural, subdural or intraparenchymal hematoma or involvement of brainstem (with contusion, distortion and hemorrhage) can compromise neurotransmitter release. the raised intracranial pressure during the acute or subacute stages of tbi, either secondarily to cerebral edema or cerebral hyperaemia may contribute indirectly (24). our finding that sertraline is associated with decrease in insomnia symptoms after tbi is consistent with evidence about the neuropathological mechanism that may contribute to the development of major depression following tbi. human post mortem pathologic (25), cerebrospinal fluid (26), and imaging (27) evidence supports a role for serotonin in the depressions of tbi patients. patients who are depressed following mild tbi have blunted prolactin response to buspirone, suggesting altered serotonin function in these patients compared with patients not depressed after mild tbi. hence, it may be argued that the occurrence of insomnia may have been associated with coexisting depression in these patients and improvement in mood symptoms with sertralline may have led to improvement in insomnia as well. fava maurizio et al (28), 2002, conducted a study to assess whether fluoxetine, sertraline, and paroxetine differ in efficacy and tolerability in depressed patients and the impact of baseline insomnia on outcomes. patients (n = 284) with dsm-iv major depressive disorder were randomly assigned in a double-blind fashion to fluoxetine, paroxetine, or sertraline for 10 to 16 weeks of treatment. using the hamilton rating scale for depression (ham-d) sleep disturbance factor score, patients were categorized into low (<4) or high (≥4) baseline insomnia subgroups. changes in depression and insomnia were assessed. safety assessments included treatment-emergent adverse events (aes), reasons for discontinuation, and aes leading to discontinuation. in addition, aes were evaluated within insomnia subgroups to determine emergence of activation or sedation. depression improvement, assessed with the ham-d-17 total score, was similar among treatments in all patients (p = 0.365) and the high (p = 0.853) and low insomnia (p ansari et al role of sertraline in insomnia associated with post tbi depression = 0.415) subgroups. insomnia improvement, assessed with the ham-d sleep disturbance factor score, was similar among treatments in all patients (p = 0.868) and in the high (p = 0.852) and low insomnia (p = 0.982) subgroups. analyses revealed no significant differences between treatments in the percentages of patients with substantial worsening, any worsening, worsening at endpoint, or improvement at endpoint in the ham-d sleep disturbance factor in either insomnia subgroup. treatments were well tolerated in most patients. no significant differences between treatments in the incidence of aes suggestive of activation or sedation were seen in the insomnia subgroups. improvement in overall depression and in associated insomnia was achieved by most patients regardless of baseline insomnia. kathleen brady et al (29), 2000, conducted a twelve-week, double-blind, placebocontrolled trial preceded by a 2-week, singleblind placebo lead-in period. sertraline treatment yielded significantly greater improvement than placebo on 3 of the 4 primary outcome measures including insomnia. sertraline was well tolerated, with insomnia the only adverse effect reported significantly more often than placebo (16.0% vs 4.3%; p=.01). since the isi values also improved in controls over time although less than cases, it is possible that patients get adjusted over a period of time. hence, it may be argued that the drug may not be as effective beyond initial few months after development of insomnia as in the beginning. however, it does not rule out the importance of intervention as compliance to treatment gets affected because of associated insomnia and depression. conclusion there has been an understanding that the psychological consequences especially depression are likely to affect insomnia independently, as it may also lead to poor participation in productive and healthy living, decreased social and leisure activities, reduced sexual interest, poor drug compliance further deteriorating the existing problem. the overall improvement in insomnia in these patients may be explained by the improvement in depression with sertraline treatment. limitations the present study has not taken patients with severely low gcs into consideration. moreover, isi scale used is more of a subjective index which takes into consideration patient`s verbatum. correspondence ahmed ansari mch neurosurgery, sms medical college, jaipur, rajasthan, india e-mail: ahmed.ansari2@gmail.com references 1. langlois ja., rutland-brown w., wald mm: the epidemiology and impact of traumatic brain injury: a brief overview. j head trauma rehabil. 21(5) :375-378, 2006 2. jain a, mittal rs, sharma a, sharma a, gupta id: study of insomnia and associated factors in traumatic brain injury. asian journal of psychiatry 8: 99-103, 2014 3. bushnik t, englander j, wright j: patterns of fatigue and its correlates over the first 2 years after traumatic brain injury. j. head trauma rehabil. 23: 25–32, 2008 4. lew hl, poole j, vanderploeg r, goodrich gl, dekelboum s, guillory sb, et al: program development romanian neurosurgery (2016) xxx 3 and defining characteristics of returning military in a va polytrauma network site. j. rehabil. res. dev. 44: 1027– 1034, 2007 5. zeitzer jm, friedman l, o’hara r: insomnia in the context of traumatic brain injury. j. rehabil. res. dev. 46: 827–836, 2009 6. kim e, lauterbach ec, reeve a, et al: neuropsychiatric complications of traumatic brain injury: a critical review of the literature (a report by the anpa committee on research). j neuropsychiatry clin neurosci. 19(2):106– 127, 2007 7. fichtenberg nl, zafonte rd, putnam s, mann nr, millard ae: insomnia in a post-acute brain injury sample. brain inj. 16: 197–206, 2002 8. jorge re, robinson rg, arndt s: are there symptoms that are specific for depressed mood in patients with traumatic brain injury. j. nerv. ment. dis. 181: 91–99, 1993 9. graham t, bryan j: assessment of coma and impaired consciousness: a practical scale. lancet 304: 81–84, 1974 10. kroenke k, spitzer rl, williams jb. the phq-9: validity of a brief depression severity measure. j. gen. intern. med. 16: 606–613, 2001 11. wittkampf ka, naeije l, schene ah, huyser j, van weert hc: diagnostic accuracy of the mood module of the patient health questionnaire: a systematic review. gen. hosp. psychiatry 29: 388–395, 2007 12. bastien ch, vallieres a, morin cm: validation of the insomnia severity index as an outcome measure for insomnia research. sleep med. 2: 297–307, 2001 13. sierra jc, guillen-serrano v, santos-iglesias p: insomnia severity index: some indicators about its reliability and validity on an older adults sample. rev. neurol. 47: 566–570, 2008 14. yu d: insomnia severity index: psychometric properties with chinese community-dwelling older people. j. adv. nurs. 66: 2350–2359, 2010 15. lahan v, gupta r: translation and validation of the insomnia severity index in hindi language. indian j. psychol. med. 33: 172–176, 2011 16. verma a, anand v, verma np: sleep disorders in chronic traumatic brain injury. j. clin. sleep med. 3: 357– 362, 2007 17. clinchot dm, bogner j, mysiw wj, fugate l, corrigan j: defining sleep disturbance after brain injury. am. j. phys. med. rehabil. 77: 291–295, 1998 18. deb s, lyons i, koutzoukis c, 199:. neuropsychiatric sequelae one year after a minor head injury. j. neurol. neurosurg. psychiatry 65: 899–902, 1998 19. mahmood o, rapport lj, hanks ra, fichtenberg nl: neuropsychological performance and sleep disturbance following traumatic brain injury. j. head trauma rehabil. 19: 378–390, 2004 20. schwab ka, ivins b, cramer g, johnson w, slusstiller m, kiley k et al: screening for traumatic brain injury in troops returning from deployment in afghanistan and iraq: initial investigation of the usefulness of a short screening tool for traumatic brain injury. j. head trauma rehabil. 22: 377–389, 2007 21. clinchot dm, bogner j, mysiw wj, fugate l, corrigan j: defining sleep disturbance after brain injury. am. j. phys. med. rehabil. 77: 291–295, 1998 22. fichtenberg nl, zafonte rd, putnam s, mann nr, millard ae: insomnia in a post-acute brain injury sample. brain inj. 16: 197–206, 2002 23. cohen m, oksenberg a, snir d, stern mj, groswasser z: temporally related changes of sleep complaints in traumatic brain injured patients. j. neurol. neurosurg. psychiatry 55: 313–315, 1992 24. baumann cr, werth e, stocker r, ludwig s, bassetti cl: sleep–wake disturbances 6 months after traumatic brain injury: a prospective study. brain 130: 1873–1883, 2007 25. donnemiller e, brenneis c, wissel j, scherfler c, poewe w, riccabona g et al: impaired dopaminergic neurotransmission in patients with traumatic brain injury: a spect study using 123i-beta-cit and 123iibzm. eur. j. nucl. med. 27: 1410–1414, 2000 26. porta m, bareggi sr, collice m, assael bm, selenati a, calderini g et al: homovanillic acid and 5hydroxyindole-acetic acid in the csf of patients after a severe head injury. ii. ventricular csf concentrations in acute brain post-traumatic syndromes. eur. neurol. 13: 545–554, 1975 27. mobayed m, dinan t: buspirone/prolactin response in post head injury depression. j affect disord 19:237– 241, 1990 28. maurizio f, sharon lh, rajinder aj, joan bk, mary en, jill sg: acute efficacy of fluoxetine versus sertraline and paroxetine in major depressive disorder including effects of baseline insomnia. journal of clinical psychopharmacology 22(2):137-147, 2002 29. brady k, pearlstein t, gregory m a, baker d, rothbaum b, carolyn rs et al: efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial. jama 283(14):1837-1844, 2000 microsoft word _4.formatata_pruna.doc romanian neurosurgery vol. xv nr. 2 22 calcified chronic subdural hematoma – case report viorel pruna md, narcisa bucur md, phd, angela neacsu md, alina voina md, giovani andrei md, aura sandu md, prof. m. gorgan md first neurological clinic, fourth department of neurosurgery, clinic emergency hospital “bagdasar-arseni” bucharest the authors present a case of a female patient, 26 years old, who suffered a craniocerebral trauma 15 years ago, by falling from a different level. she manifested an intracranial hypertension syndrome and seizures at the moment of hospital admission. brain ct scan reveals a large right fronto-parietal calcified subdural mass with left shift of median line. the lesion was isointense on t1 and hyperintense in t2 weighted magnetic resonance imaging (mri). calcified or atypical meningioma, bony tumor and subdural abscess were included in differential diagnosis. she underwent surgery and a calcified chronic subdural hematoma was completely excised, with good postoperative recovery. after two months of follow up, seizures were controlled with a minimal dose of medication, control ct scan showing absence of the hematoma and brain re-expansion. in summary, this uncommon calcified chronic subdural hematoma was successfully excised, resulting in a good recovery. from the literature review and the experience in this patient, authors consider surgical treatment for calcified chronic subdural hematoma as necessary and often results in neurological improvement, especially concerning seizures. keywords: calcification, chronic subdural hematoma, seizures introduction calcified chronic subdural hematoma (ccsh) is relatively common since the first description in 1884 (8). in the elderly, observation is recommended for asymptomatic calcified chronic subdural hematoma without acute or progressive neurological disorders. the incidence of ccsh has been reported to be 0.3% to 2.7% of all chronic subdural hematomas (csh) (8). there are about 100 cases reported in the literature (10). although surgical treatment for the csh is widely accepted, there is still some controversy about whether it should be used. case report the authors present a case of a female patient, 26 years old, who suffered a cranial-cerebral trauma 15 years ago, by falling from a different level. she manifested an intracranial hypertension syndrome and seizures at the moment of hospital admission, which started in january, 2009 and persisted under anticonvulsant treatment (carbamazepine 2/day). brain ct-scan (native and bone window) reveals a large hypodense elliptical right frontal-parietal calcified subdural mass, with left shift of median line (fig. 1a, 1b). the lesion was isointense on t1 and hyperintense in t2 weighted magnetic resonance imaging (mri) and had a volume of 7/6/1,2 cm (fig. 2a, 2b). computerized eeg shows a theta-subtheta lesion of 6 c/s, with right temporal localization, which tend to irradiate controlateral. calcified or atypical meningioma, bony tumor and subdural abscess were included in differential diagnosis. after complete investigation, the patient was proposing for surgery, in attempt to total removal of the compressive mass, to establish a histopathological diagnosis and to eliminate the seizures. the surgery was performed under general anesthesia, with the patient in supine position and the head fixed in mayfield frame, raised at 200 and controlateral rotated at 300. calcified chronic subdural hematoma romanian neurosurgery vol. xv nr. 2 23 a b fig. 1a, 1b preoperative brain ct-scan (native and bone windows) a b fig. 2a, 2b mri cerebral a frontal-parietal flap was made and the dura mater was opened in an arcuate manner, with basal pedicle and then was suspended. an elliptical mass of about 7/6 cm was found, with hard consistence and liquid yellow content (fig. 3a, 3b, 3c). the calcified hematoma was then totally removed (fig. 4). a b c fig. 3a, 3b, 3c intraoperative picture reveal calcified hematoma v. pruna romanian neurosurgery vol. xv nr. 2 24 fig. 4 intraoperative picture after the calcified hematoma was then removed fig. 5 postoperative ct-scan 7 days after surgery hemostasis was achieved by electrocoagulation and surgicel. wax was added to bone. the dura was closed with nylon 3.0. an epidural drainage was applied. the bone flap was reinserted. the skin was closed in anatomical layers. the wound was patched. no complications occurred during the procedure, neither after surgery. postoperative the patient was conscious, cooperative and without motor or sensitive deficits. the drainage was removed 48 h after surgery and the patient was mobilized. anticonvulsant treatment was maintained. control ct scan (fig. 5) was made 7 days after surgery, showing absence of the hematoma and brain re-expansion. at this time surgical threads was suppressed and the patient was checked out with the following instructions: follow up at 2 months, continue anticonvulsant treatment at least 6 months, avoid alcohol, coffee and sun exposure. histopathological examination reveals chronic subdural hematoma with fibrous transformation and large areas of calcification. long term prognosis is excellent. discussion chronic subdural hematoma is usually one of the complications of minor head trauma. disorders such as coagulopathy (therapeutic anticoagulant use, sepsis, liver insufficiency), intracranial hypotension (secondary to overdrainage resulting in bridge veins traction in shunted patients), chronic alcoholism, vascular malformations, and primary and metastatic tumors may also play roles in the etiology of chronic subdural hematoma (7). calcification or ossification is observed at a rate of 0.8% to 10% in patients with chronic subdural hematoma (5). the pathogenesis of calcification in chronic subdural hematomas is not completely clear. however, many authors have suggested that local, metabolic, and vascular factors play a role in the development of calcification and ossification. afra reported that the circulation in the subdural space with absorption and vascular thrombosis may be responsible for the development of calcification (1). most ccshs are located at the convexity and the extent of the calcification varies widely, sometimes involving the entire hemispheric surface. ccshs can be diagnosed by ct or mri (6, 10), and differentiated from the usual csh by imaging studies and gross pathology. ccshs have the following characteristics: (1) elliptical shape with the longest diameter in the frontal-temporal direction; biconvex or flat shape on cross section, (2) the content is gelatinous or clay-like, but not liquefied, (3) the inner membrane is thick and has sinusoidal blood vessels, (4) the inner membrane is partially adhered to and evaginated into the cerebral cortex (2-4). sometimes the ccsh may be confused with other calcified extra-axial space-occupying lesions, such as calcified: • epidural hematoma • calcified subdural empyema • meningioma calcified chronic subdural hematoma romanian neurosurgery vol. xv nr. 2 25 • calcified arachnoid • cyst and • calcified convexity dura mater with acute epidural hematoma, • inherent metabolic tendency to calcification, prolonged existence of the hematoma in the subdural space. the course of the development of calcification in a ccsh is unclear. however, the hematoma may progress gradually from hyalinization to calcification, and finally ossification through irritation of the tissue. after hemorrhage calcification usually takes 6 months to many years to develop (1, 8). it is difficult to understand the mechanisms of the development of a calcified csh, because it takes a long course. poor circulation and absorption into the subdural space and vascular thromboses, inherent metabolic tendency to calcification, prolonged existence of the hematoma in the subdural space, stagnant blood due to sufficient arterial supply and inadequate venous return, thick connective tissue membrane, and other local factors are considered to contribute to the development of calcification of csh (1, 7). one of the most frequent complications that may be observed after chronic subdural hematoma operations is recurrent hemorrhage. it is thought that insufficient brain expansion following hematoma drainage, developing following prolonged compression in recurrent hemorrhage is the basic factor (9). conclusion in summary, this uncommon calcified chronic subdural hematoma was successfully excised, resulting in a good recovery. from the literature review and the experience in this patient, authors consider surgical treatment for calcified chronic subdural hematoma as necessary and often results in neurological improvement, especially concerning seizures. references 1.afra d: ossification of subdural hematoma. report of two cases. j neurosurg 18:393-397, 1961. 2.debois v, lombaert a: calcified chronic subdural hematoma. surg neurol 14:455-458, 1980. 3.granata f, graziussi g, de carlo c, avella f, fucci g: calcified chronic subdural hematoma. a case report. acta neurol (napoli) 32:340-346, 1977. 4.hirakawa t, tanaka a, yoshinaga s, ohkawa m, tomonaga m: calcified chronic subdural hematoma with intracerebral rupture forming a subcortical hematoma. a case report. surg neurol 32:5155, 1989. 5.ide m, jimbo m, yamamoto m, umebara y, hagiwara s: asymptomatic calcified chronic subdural hematoma--report of three cases. neurol med chir (tokyo) 33:559-563, 1993. 6.loh jk, howng sl: huge calcified chronic subdural hematoma in the elderly--report of a case. kaohsiung j med sci 13:272-276, 1997. 7.mori n, nagao t, nakahara a, izawa m, amano k, kitamura k: [a case of huge calcified chronic subdural hematoma]. no shinkei geka 10:1203-1209, 1982. 8.niwa j, nakamura t, fujishige m, hashi k: removal of a large asymptomatic calcified chronic subdural hematoma. surg neurol 30:135-139, 1988. 9.norman ch, jr., dubowy j: chronic calcified subdural hematoma. j natl med assoc 63:3-5, 1971. 10.yan hj, lin ke, lee st, tzaan wc: calcified chronic subdural hematoma: case report. changgeng yi xue za zhi 21:521-525, 1998. microsoft word 20kumarkiran_external romanian neurosurgery (2018) xxxii 2: 347 354 | 347             doi: 10.2478/romneu-2018-0043 external ventricular drainage for intraventricular hemorrhage v.a. kiran kumar1, n.a. sai kiran1, v. anil kumar2, luis rafael moscote-salazar3, amrita ghosh4, ranabir pal5, venkata ramya bola1, amit agrawal1 1department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 2department of anesthesia, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 3neurosurgery-critical care, red latino, organización latinoamericana de trauma y cuidado, neurointensivo, bogota, colombia 4faculty, department of biochemistry, calcutta medical college, 88, college street, kolkata700073, india 5department of community medicine, mgm medical college and lsk hospital, kishanganj 855107, bihar, india abstract: background: intervention to reduce intracranial pressure using external ventricular drain (evd) is a common life saving measure in a neurosurgery intensive care unit(icu). objective: the present study was undertaken to assess the outcome of patients who underwent external ventricular drainage for intraventricular hemorrhage(ivh). methods: the available data of the patients who underwent placement of external ventricular drain from february 2012 to may 2016 for intraventricular hemorrhage (ivh) at narayana medical college and hospital, nellore, was retrieved from the hospital case records and analyzed. results: total of 69 patients were included in this study. mean age was 53.7 ±11.6 years. clinical presentation included altered sensorium in 66 patients (96%), hemiparesis in 62 patients (90%) , vomiting in 40 patients (58%) and seizures in 9 patients (13%). fifty two patients (75%) were known hypertensives and 10 patients (15%) were diabetic. past history of smoking was recorded in 16(23%) patients and alcohol intake in 17 patients (25%). gcs at the time of admission was 3-8 (low) in 39 patients (57%), 9-12 in 23 patients(33%) and 13-15 in 7 patients (10%). at the time of admission, 60 patients ( 87%) had diastolic blood pressure more than 90 mmhg, 63 patients (91%) had systolic blood pressure more than 140 mmhg. major site of hemorrhage was basal ganglia in 24 348 | kumar et al external ventricular drainage for intraventricular hemorrhage             (35%), thalamus in 13 (19%), cerebellum in 5 (7%), brain stem in 3, frontal/temporal in 2 patients. sah with ivh was noted in 12 patients (17%) and only ivh was noted in 10 patients (14%). mean duration of external ventricular drainage was 4.6+1.7 days (range 1-9 days). mean hospital stay was 11.3±7.5 days and mean icu stay was 8+5.4 days. thirty eight patients (55%) died during hospital stay. at the time of discharge, poor out come (glagow out come score 1-3) was noted in 52 patients (75%) and good out come (glagow out come score-4,5) was noted in 17 patients. among various parameters analyzed , poor gcs (3-8) at admission, history of smoking and alcohol intake were found to correlate significantly with poor outcome. none of the other factors like old age, site of bleed, pupillary asymmetry at admission, high blood pressure at admission, past history of hypertension and diabetes were found to correlate with poor outcome. conclusions: majority of the patients with intracranial hematomas with intraventricular extension presented in poor neurological condition (gcs= 3-8). poor neurological condition at the time of admission, past history of smoking and alcohol intake were associated with poor outcome. key words: basal ganglia bleed, thalamic bleed, external ventricular drainage, hydrocephalus, intraventricular hemorrhage, intracerebral hemorrhage, subarachnoid hemorrhage introduction the external ventricular drain (evd), also called as ventriculostomy or extraventricular drain, is often used as an emergency procedure in neurosurgery to manage hydrocephalus and reduce raised intracranial pressure (icp) when there is acute obstruction to the normal flow of cerebrospinal fluid (csf). insertion of an evd help in reduction of icp by draining csf/intraventricular blood, permits introduction of various medications and allow intracranial pressure monitoring. well trained nursing staff are required for managing these cases to ensure appropriate zeroing, maximum sterility, and flawless integrity of the evd collecting system. icp waveform analysis and close monitoring of csf drainage are extremely important and can affect clinical outcomes. 1 evd is required in various conditions like intracranial (basal ganglia/ thalamus/ brainstem) hemorrhage (ich) with intraventricular extension, subarachnoid hemorrhage (sah) with intraventricular hemorrhage, traumatic brain injury (tbi), cerebellar infarct with hydrocephalus, bacterial/tubercular meningitis etc. many of these conditions are associated with intracranial hypertension with intracranial pressure (icp) above 20 mmhg due to obstruction of cerebrospinal fluid (csf) outflow. 2 external ventricular drain (evd) provides temporary cerebrospinal fluid (csf) diversion in these patients. the present study was undertaken to assess the outcome in patients with intraventricular hemorrhage who underwent evd placement. romanian neurosurgery (2018) xxxii 2: 347 354 | 349             methods the present retrospective observational study was carried out at narayana medical college and hospital, nellore. after institutional ethical committee (iec) approval, the data of the patients who underwent placement of external ventricular drainage for intraventricular hemorrhage (ivh) from february 2012 to may 2016 was retrieved from the hospital case records and analyzed. the demographic, clinical, radiological, management and outcome details of the patients were recorded in a predesigned proforma. external ventricular catheter placement was performed in the operation theatre and a standard approach was followed to perform the procedure i.e. kocher's point to insert the ventricular catheter, tunneling of the catheter to reduce infection, fixation of the catheter to the scalp, secure attachment for csf collection and keeping the csf collection bag at appropriate height. the side of the insertion was decided based on the ventricular enlargement and amount of the blood in the lateral ventricles. evd catheter was subcutaneously tunneled for an approximate distance of 5 cm from the ventriculostomy site incision and externalized. all the patients received prophylactic pre-operative antibiotics. after evd insertion, patients were managed in intensive care unit and csf output was closely monitored. csf was regularly monitored for any evidence of infection (cell count, gram staining and culture). once the csf became clear and ventricles were cleared reasonably of blood (particularly disappearance of the blood from the fourth ventricle), the evd catheter was removed. before removing the evd, the drain was raised approximately 20 cm above the external auditory meatus to make sure that the patient is not drain dependent. statistical analysis the study data were collected in a predesigned data collection tool and later entered into the microsoft excel sheet. spss version 24 was used to analyze data and calculate frequency distribution, percentages and descriptive statistics. chi-square / fisher exact test was used to find the significance of study parameters on categorical scale and independent samples t test for parameters on continuous scale. significance is assessed at 5 % level of significance. a probability (p) value of <0.05 was considered significant. results sixty nine patients were included in this study. there were 45 male (65.2%) and 24 female (34.8%) with a male to female ratio of 1.87: 1. mean age was 53.7 ±11.6 years and majority (30) were in the age group of 51-60 yrs [table 1]. fifty two patients (75%) were known hypertensives and 10 patients (15%) were diabetic. past history of smoking was recorded in 16(23%) patients and alcohol intake in 17 patients (25%). clinical presentation included altered sensorium in 66 patients (96%), hemiparesis in 62 patients (90%) , vomiting in 40 patients (58%) and seizures in 9 patients (13%). at the time of 350 | kumar et al external ventricular drainage for intraventricular hemorrhage             admission, 60 patients (87%) had diastolic blood pressure more than 90 mmhg, 63 patients (91%) had systolic blood pressure more than 140 mmhg. pupillary asymmetry was noted in 5 patients. pupillary light reaction was absent in 3 patients. gcs at the time of admission was 3-8 (low) in 39 patients (57%), 9-12 in 23 patients (33%) and 13-15 in 7 patients (10%). mean gcs at admission was 8 ±3. major site of hemorrhage was basal ganglia in 24 (35%), thalamus in 13 (19%) , cerebellum in 5 (7%), brain stem in 3, frontal/temporal in 2 patients. sah with ivh was noted in 12 patients (17%) and only ivh was noted in 10 patients (14%). mean duration of external ventricular drainage was 4.6+1.7 days ( range 1-9 days). mean hospital stay was 11.3±7.5 days and mean icu stay was 8+5.38 days. thirty eight patients died during hospital stay. at the time of discharge, poor out come (glagow out come score 1-dead, 2persistent vegetative state, 3severe disability) was noted in 52 patients (75%) and good out come (glagow out come score 4-moderate disability, independent and 5good recovery, normal life despite minor deficits) was noted in 17 patients (25%). poor gcs (38) at admission was found to significantly correlate with poor outcome ( p value 0.025) [ table 1]. mean gcs at the time of admission in patients with poor out come was 7.4+3 as compared to 9.7+1.8 in patients with good out come (p value 0.001). statistically significant poor outcome was also noted in patients with past history of smoking and alcohol intake [table 3]. poor outcome was noted in 94% (16/17) of patients with past history of alcohol intake as compared to 69% (36/52) in patients without history of alcohol intake (p value0.05). poor outcome was also noted in all the patients ( 16/16) with past history of smoking as compared to 68% (36/53) in patients without history of smoking (p value0.007). none of the other factors like age, gender, site of bleed, pupillary asymmetry/ reaction to light at the time of admission, systolic blood pressure/diastolic blood pressure at the time of admission, past history of hypertension / diabetes mellitus were found to correlate with poor outcome [tables 1,2,3]. table 1 the outcome correlation with age, gender, gcs at admission, pupil size/reaction to light and blood pressure at the time of admission (n=69) poor outcome (gos 1-3) good outcome ( gos 4,5) p value age groupa (yrs) 21-30 4 (100%) 0 (0%) 0.71 31-40 2(100%) 0 41-50 12(80%) 3(20%) 51-60 22(73%) 8(27%) 61-70 8(67%) 4(33%) 71-80 4(67%) 2(33%) romanian neurosurgery (2018) xxxii 2: 347 354 | 351             mean age 52.6+12.1 yrs 57.4+9.5 yrs 0.141 gendera male 35 (78%) 10(22%) 0.15 female 17 (71%) 7(29%) gcsa,b 3-8 34(87%) 5(13%) 0.025 9-12 13(56%) 10 (44%) 13-15 5(71%) 2 (29%) mean gcs 7.4+3.1 9.7+1.8 0.001 pupil sizea,b equal 48 (75%) 16(25%) 0.64 asymmetry 4 (80%) 1 (20%) pupillary light reactiona,b present 49 (74%) 17 (26%) 0.57 absent 3 (100%) 0 systolic blood pressurea,b >140 mm hg 49 (78%) 14 (22%) 0.15 <140 mm hg 3(50%) 3 (50%) mean systolic blood pressurea,b (mm hg) 176+30.9 162+41.8 0.172 diastolic blood pressurea,b >90 mm hg 47(78%) 13 (22%) 0.2 <90 mm hg 5 (55%) 4 (45%) mean diastolic blood pressurea,b (mm hg) 100.6+14.5 94.47+18 0.159 a data for poor and good outcome is given as number of patients (%) b examination findings at the time of admission table 2 location of bleed and patient outcome location of bleed poor outcome (gos 1-3) good outcome ( gos 4,5) p value basal ganglia 20 (83%) 4(17%) 0.371 thalamus 10(77%) 3(23%) cerebellum 2(40%) 3(60%) sah 8(67%) 4(33%) only intraventricular hemorrhage 8(80%) 2(20%) frontal/temporal lobe 1(50%) 1(50%) brain stem 3(100%) 0 data for poor and good outcome is given as number of patients (%) table 3 risk factors and patient outcome risk factors poor outcome (gos 1-3) good outcome (gos 4,5) p value hypertension yes 40 (77%) 12 (23%) 0.747 no 12 (71%) 5(29%) diabetes mellitus yes 8 (80%) 2 (20%) 0.53 no 44(75%) 15 (25%) alcohol intake yes 16 (94%) 1(6%) 0.05 no 36 (69%) 16 (31%) smoking yes 16 (100%) 0 0.007 no 36(68%) 17(32%) data for poor and good outcome is given as number of patients (%) 352 | kumar et al external ventricular drainage for intraventricular hemorrhage             discussion numerous forms of acute brain injury benefit from continuous icp monitoring and cerebrospinal fluid (csf) diversion provided by an evd. after insertion, evd monitoring and maintenance essentially become responsibility of nursing staff and well trained nursing staff are required to prevent evd associated meningitis and for early detection of complications like blockage of evd. [1-9] it has been reported that the occurrence of intraventricular hemorrhage (ivh) ranges from 30% to 50% in cases of spontaneous intracerebral hemorrhage and it frequently results in acute obstructive hydrocephalus. [911] external ventricular drainage is a life saving procedure in these patients. [6,12] evd does help to drain csf, remove ventricular and subarachnoid blood and blood products. evd not only reduce intracranial pressure but also potentially reduce the inflammatory response from blood products which might help in reducing chances of persistent hydrocephalus following ivh. [13] it is difficult to specify the timeline when to remove the evd as it may vary from cases to case. once the purpose of evd is served (either discontinuations of the icp monitoring or resolution of the clot and hydrocephalus) a decision to remove evd can be made. [14,15] evd placement can be associated with many complications like infection (e.g. ventriculitis and meningitis), hemorrhage, disconnection, misplacement, dislodgement or blockage of the catheter. [16-19] reported incidence of evd associated meningitis/ ventriculitis is 0-22%. [2,20] this risk can be reduced by judicious use of prophylactic antibiotics while taking precautions to avoid the risk of the development of resistant organisms. [2,20] in literature evd catheters which are covered with antibiotic impregnated and coated with ionized silver particle have shown to be beneficial, however we did not use these catheters in our series because of the cost involved. [2,20] we followed the standard strategies to reduce the infection rate i.e. proper tunneling of the evd catheter, careful monitoring of the evd dressing site, any evidence of csf leak, keeping the csf collection system in an upright position, less frequent change in the drain tubing and minimizing the duration of the evd. [2,20,21] evd related infections can be prevented by careful surgical technique, tunneling of the ventricular catheter 22 and early removal of the evd (preferably within 5 days). [23,24] in patients with intracranial hematomas, presence of ivh and associated hydrocephalus are associated with poor outcome and mortality independently. [911,25] hypertension, diabetes mellitus, smoking and alcohol intake are reported to be high risk factors for intracranial hematomas. [26-27] the reported mortality from ich (with hypertensive intracerebral hemorrhages) ranges from 60 to 86% similar to 55% noted in our series. [28-32] however in a series it was shown that evd was lifesaving with a survival rate of 67.9% . [15]   romanian neurosurgery (2018) xxxii 2: 347 354 | 353             conclusions majority of the patients with intracranial hematomas with intraventricular extension presented in poor neurological condition (gcs= 3-8). poor neurological condition at the time of admission, past history of smoking and alcohol intake were associated with poor outcome. correspondence dr n a sai kiran (mch), assistant professor of neurosurgery, department of neurosurgery, narayana medical college hospital chinthareddypalem nellore-524003, andhra pradesh (india) emailsaikiransssihms@gmail.com mobile+91-8904779819 references 1. muralidharan r. external ventricular drains: management and complications. surgical neurol int 2015;6:s271-4. 2. dey m, jaffe j, stadnik a, awad ia. external ventricular drainage for intraventricular hemorrhage. curr neurol neurosci reports 2012;12:24-33. 3. lwin s, low sw, choy d, yeo tt, chou n. external ventricular drain infections: successful implementation of strategies to reduce infection rate. singapore med j 2012;53:255. 4. ghani e, zaidi gi, nadeem m, rehman l, noman ma. role of cerebrospinal fluid diversion in posterior fossa tumor surgery. j college physicians surgeons pak 2003; 13: 333-6. 5. poppen jl. ventricular drainage as a valuable procedure in neurosurgery: report of a satisfactory method. arch neurol psychiatr 1943;50:587-9. 6. walker ct, stone jj, jacobson m, phillips v, silberstein hj. indications for pediatric external ventricular drain placement and risk factors for conversion to a ventriculoperitoneal shunt. pediatr neurosurg 2012;48:342-7. 7. gaberel t, magheru c, parienti j-j, huttner hb, vivien d, emery e. intraventricular fibrinolysis versus external ventricular drainage alone in intraventricular hemorrhage. stroke 2011; 42:2776-81. 8. tsang aco, leung gkk. external ventricular drain infections. hydrocephalus: intech, 2012 9. bhattathiri ps, gregson b, prasad ksm, mendelow ad. intraventricular hemorrhage and hydrocephalus after spontaneous intracerebral hemorrhage: results from the stich trial. brain edema xiii 2006:65-8. 10. steiner t, diringer mn, schneider d, et al. dynamics of intraventricular hemorrhage in patients with spontaneous intracerebral hemorrhage: risk factors, clinical impact, and effect of hemostatic therapy with recombinant activated factor vii. neurosurgery 2006;59:767-74. 11. tuhrim s, horowitz dr, sacher m, godbold jh. volume of ventricular blood is an important determinant of outcome in supratentorial intracerebral hemorrhage.critcare med1999;27:617-21 12. bhargava d, alalade a, ellamushi h, yeh j, hunter r. mitigating effects of external ventricular drain usage in the management of severe head injury. acta neurochirurgica 2013; 155: 2129-32. 13. staykov d, huttner hb, struffert t, ganslandt o, doerfler a, schwab s, et al.intraventricular fibrinolysis and lumbar drainage for ventricular hemorrhage. stroke 2009; 40(10):3275-80. 14. leung gkk, ng kb, taw bbt, fan yw. extended subcutaneous tunnelling technique for external ventricular drainage. br j neurosurg 2007;21:359-64. 15. ojo oa, asha ma, bankole ob, kanu oo. improvised external ventricular drain in neurosurgery: a nigerian tertiary hospital experience. j neurosci rural pract 2015;6:304. 16. beer r, pfausler b, schmutzhard e. management of nosocomial external ventricular drain-related ventriculomeningitis. neurocrit care 2009;10:363. 17. narayan rk, kishore pr, becker dp, ward jd, enas gg, greenberg rpintracranial pressure: to monitor or not to monitor? a review of our experience with severe head injury. j neurosurg 1982;56:650-9. 18. paramore cg, turner da. relative risks of ventriculostomy infection and morbidity. acta neurochirurgica 1994;127:79-84. 19. sundbärg g, nordström c-h, söderström s. complications due to prolonged ventricular fluid pressure recording. br j neurosurg 1988;2:485-95. 354 | kumar et al external ventricular drainage for intraventricular hemorrhage             20. nurses aaon. care of the patient undergoing intracranial pressure monitoring/external ventricular drainage or lumbar drainage. glenview (il): am assoc neurosci nurs 2011:1-38. 21. woodward s, addison c, shah s, brennan f, macleod a, clements m. benchmarking best practice for external ventricular drainage. br j nurs 2002;11:4753. 22. rafiq mfa, ahmed n, ali s. effect of tunnel length on infection rate in patients with external ventricular drain. j ayub med coll abbottabad 2011;23:106-7. 23. roitberg bz, khan n, alp ms, hersonskey t, charbel ft, ausman ji. bedside external ventricular drain placement for the treatment of acute hydrocephalus. br j neurosurg 2001; 15: 324-7. 24. wong gkc, poon ws, wai s, yu lm, lyon d, lam jmk. failure of regular external ventricular drain exchange to reduce cerebrospinal fluid infection: result of a randomised controlled trial. journal of neurology, neurosurgery & psychiatry 2002;73:759-61. 25. mayfrank l, lippitz b, groth m, bertalanffy h, gilsbach jm. effect of recombinant tissue plasminogen activator on clot lysis and ventricular dilatation in the treatment of severe intraventricular haemorrhage. acta neurochirurgica 1993;122:32-8. 26. ikram ma, wieberdink rg, koudstaal pj. international epidemiology of intracerebral hemorrhage. current atherosclerosis reports 2012;14:300-306. 27. narayan sk, sivaprasad p, sushma s, sahoo rk, dutta tk. etiology and outcome determinants of intracerebral hemorrhage in a south indian population, a hospital-based study. annals of indian academy of neurology. 2012;15:263-266. 28. douglas ma, haerer af. long-term prognosis of hypertensive intracerebral h32. narayan sk, sivaprasad p, sushma s, sahoo rk, dutta tk. etiology and outcome determinants of intracerebral hemorrhage in a south indian population, a hospital-based study. annals of indian academy of neurology. 2012;15(4):263-266. doi:10.4103/0972-2327.104333. emorrhage. stroke 1982;13:488-91. 29. graeb da, robertson wd, lapointe js, nugent ra, harrison pb. computed tomographic diagnosis of intraventricular hemorrhage. etiology and prognosis. radiology 1982;143:91-6. 30. little jr, blomquist jr ga, ethier r. intraventricular hemorrhage in adults. surgical neurology 1977;8:143-9. 31. pia hw. the diagnosis and treatment of intraventricular haemorrhages. progress in brain research 1968;30:463-70. 32. taheri sa, wani ma, lewko j. external ventricular drainage and passive vs. active neurosurgical intervention in the management of hypertensive intracerebral hemorrhage with rupture into the ventricles. journal of neurosurgical anesthesiology 1989;1:233-40. doi: 10.33962/roneuro-2021-024 endovascular treatment options for carotid-cavernous fistulae roxana codreanu, rares cristian filep, lucian marginean romanian neurosurgery (2021) xxxv (2): pp. 152-158 doi: 10.33962/roneuro-2021-024 www.journals.lapub.co.uk/index.php/roneurosurgery endovascular treatment options for carotid-cavernous fistulae roxana codreanu1, rares cristian filep2, lucian marginean2 1 emergency clinical county hospital, targu mures, romania 2 university of medicine, pharmacy, sciences and technology “george emil palade”, ph.d. school of medicine, targu mures, romania abstract a carotid-cavernous fistula is a pathological shunt between the internal or external carotid arteries and the cavernous sinus (cs). the arteriovenous shunt can be direct, between the internal carotid artery and the cs, or indirect, between meningeal branches from the carotid arteries and the dural coverings of the cs. direct fistulas occur most commonly after craniofacial trauma, while indirect shunts result from various chronic diseases. signs and symptoms depend on the venous drainage routes. exophthalmos, chemosis, and diplopia are caused by venous drainage through the superior and inferior ophthalmic veins. if venous egress is mainly through the inferior petrosal sinus, patients complain of pulsatile tinnitus. cortical venous drainage is the most dangerous route because it can lead to focal neurological deficits and intracerebral haemorrhage. treatment of carotid-cavernous fistulae can be achieved through different endovascular techniques, using detachable balloons, coils, liquid embolic agents, covered stents, and flow-diverters. this paper aims to report three cases with carotid-cavernous fistulae, which were successfully cured using different transarterial and transvenous modalities. introduction carotid cavernous fistula (ccf) refers to an aberrant arteriovenous communication between the carotid arterial system and the venous compartments of the cavernous sinus (cs). based on the arterial feeding source, ccf’s can be direct or indirect.1 according to the barrow classification of ccf’s, a direct, high-flow connection between the internal carotid artery (ica) and the cs is regarded as a “type a” fistula. indirect ccfs, which typically have a low flow, are classified as type b if they are supplied only by the dural branches of the ica, type c by dural branches of the external carotid artery (eca), and type d by both ica and eca dural branches. the majority of type a ccf’s are more commonly a result of blunt or penetrating trauma, accounting for 75% of all ccf cases.1 clinical manifestations of type a fistulas depend on the venous outflow from the cs and include ocular pain, exophthalmos, chemosis, ocular foreign body sensation, visual disturbances, and headaches for an anterior superior ophthalmic venous route. drainage keywords carotid-cavernous fistula, endovascular treatment, transarterial, transvenous corresponding author: rares cristian filep university of medicine, pharmacy, sciences and technology “george emil palade”, ph.d. school of medicine, targu mures, romania raresfilep@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 153 endovascular treatment options for carotid-cavernous fistulae to the posterior venous outflow channels can lead to neurologic symptoms, such as aphasia and confusion.2 digital subtraction angiography (dsa) is the gold standard in the diagnosis of ccf. it must be performed before any potential intervention. endovascular treatment is now the first therapeutic option for ccfs because it is associated with high occlusion and low complication rates.3 depending on the angioarchitecture of the fistula, endovascular obliteration can be achieved by a combination of coils, detachable balloons, liquid embolic agents, and stents.4 this paper aims to present a case series of three patients with ccf’s occluded using different transarterial and transvenous treatment strategies. case descriptions case 1 a 17-year-old female patient was admitted in july 2020 to the emergency department of an outside hospital for craniofacial trauma with multifocal, displaced mandibular fractures, active bleeding in the oral cavity, and marked facial edema after a motor vehicle accident. urgent maxillofacial surgery was performed to stop the bleeding and treat the mandibular fractures. after several days the patient complained of left ocular pain. periorbital edema, chemosis, and exophthalmia developed gradually afterward. ct angiography showed an enlarged left cavernous sinus compared to the contralateral side (fig. 1, a) and a dilated, engorged superior ophthalmic vein. (fig. 1, b, c). five days later, she was transferred to our hospital for further investigations. catheter angiography confirmed a high-flow, type a, left carotid-cavernous fistula with a 4.2 mm direct “communication” between the ica and the cs, located on the horizontal part of the cavernous segment (fig. 1, d, e, f). venous drainage was mainly through the superior ophthalmic vein, markedly enlarged, explaining her main signs and symptoms (fig. 1, e). additionally, drainage occurred in the pterygoid venous plexus, inferior petrosal sinus, and jugular vein, and through the coronary sinus in the contralateral cavernous sinus (fig. 1, d). based on the angioarchitecture of the fistula, a decision was made to occlude the fistula with coils through a transarterial approach using the balloon-remodeling technique. figure 1. axial ct angiogram images in a. enlarged left cs (white arrows), b. engorged left sov (white arrow), c., and left exophthalmia. dsa images in d. frontal projection, the drainage through the coronary sinuses (arrowheads) in the contralateral cs, ips, and internal jugular vein, e. lateral projection, engorged sov (white arrow), f. lateral projection, the “venous pouch” connected to the ica (white circle). cs=cavernous sinus; sov=superior ophthalmic vein; dsa=digital subtraction angiogram; ips=inferior petrosal sinus; ica=internal carotid artery. 154 roxana codreanu, rares cristian filep, lucian marginean on the following day, under general anesthesia, through a right femoral approach, a 6f guiding catheter was placed in the distal cervical ica, followed by navigation of a microcatheter in the cs and a hypercompliant balloon in the carotid siphon (fig. 2, a). while the balloon was inflated over the arterial “tear,” six bare platinum, detachable coils were implanted through the microcatheter into the left cavernous sinus (fig. 2, b). no antiplatelet therapy was used during the procedure. after the first coil was deployed, a bolus of 5000 iu of unfractionated heparin was administered intravenously. after the 6th coil was introduced, complete obliteration of the fistula was obtained (fig. 2, c, d). there were no periprocedural complications. immediately after the procedure, the patient was extubated. her symptoms regressed completely over the following days, and she was discharged four days later. a control angiogram was performed three months later, confirming the total exclusion of the fistula without additional sequelae (fig. 2, e, f). figure 2. a. blank roadmap image shows the inflated balloon in the ica, overlying the coil mass; b. lateral projection fluoroscopy image: the coil mass is better seen; c, d. frontal and lateral projection dsa images immediately after the procedure showing complete obliteration of the fistula; e, f. control angiogram after three months demonstrating cure of the fistula. ica=internal carotid artery, dsa=digital subtraction angiogram. case 2 an 8-year-old boy was admitted to our hospital with exophthalmos and chemosis of the left eye, which developed gradually for the last week before admission. upon neurological examination, the patient was conscious, cooperative, with motor aphasia and right hemiparesis. his neurological deficits resulted from a left hemispherectomy, which he received after significant head trauma during a motor vehicle accident seven months prior. the following day, under general anesthesia, a catheter angiography revealed a left high-flow barrow type a carotid-cavernous fistula (fig. 3 a, b). the fistula was also opacified retrogradely from the vertebral artery (fig. 3 c, d). in addition, due to the high flow, aspiration from the external carotid artery via artery of foramen rotundum was evident (fig. 3, g). a decision was made to cure the fistula by sacrificing the left ica with coils. a 6f guiding catheter was placed in the left ica, followed by navigation of a microcatheter in the supraclinoid segment. two penumbra occlusion devices were deployed distal and proximal to the fistula (fig. 3, e), achieving complete obliteration of the ica and fistula. the 155 endovascular treatment options for carotid-cavernous fistulae enlarged artery of the foramen rotundum was occluded with a 1mm target nano coil (fig 3. g, h). a cure of the fistula was immediately seen upon contrast injection in the vertebral artery (fig. 3, i). chemosis and exophthalmia gradually improved following the procedure, and the patient was discharged three days later. figure 3. dsa images showing a, b. frontal and lateral projections, high-flow fistula with a large venous pouch, draining in the sov; c, d. the fistula is opacified retrogradely through the pcom, during contrast injection in the right va; e, f. two penumbra occlusion devices (white arrows) were deployed in the ica distal and proximal to the fistula, with immediate occlusion of the ica; g, h. aspiration through an enlarged artery of the foramen rotundum (dashed arrow) was interrupted by occluding the artery with a 1mm target nano coil; i. final contrast injection in the va shows no residual filling of the fistula. dsa=digital subtraction angiogram; sov=superior ophthalmic vein; pcom=posterior communicating artery; va=vertebral artery; ica=internal carotid artery. case 3 a 33 years-old male patient was admitted to our hospital with diplopia, ptosis of the left eyelid, exophthalmia, and chemosis of the left eye. the symptoms had a gradual onset in the last two weeks before admission. mri performed at another institution revealed enlarged left cs and sov (not shown). upon admission, his blood pressure and other laboratory findings were within normal limits. neurological examination was also normal. the only significant information that he recalls was an abrupt deceleration from 100km/h, without head trauma, while driving a truck, two weeks before symptom onset. catheter angiogram performed the following day revealed a left, indirect, barrow type d dural ccf, opacified through meningeal branches from the ica and eca (fig. 4 a, b, c, d). venous drainage occurred through the sov and iov. 156 roxana codreanu, rares cristian filep, lucian marginean figure 4. a, b. frontal and lateral projection dsa images showing a left dural, indirect ccf, and venous drainage through the sov and iov; c, d. the fistula is opacified through meningeal branches from the eca; e, f. complete cure of the fistula obtained with transvenous onyx injection. dsa=digital subtraction angiogram; ccf=carotid-cavernous fistula; sov=superior ophthalmic vein; iov=inferior ophthalmic vein; eca=external carotid artery under general anesthesia, super-selective catheterization of the eca and its meningeal branches was performed with a 1.3f headway duo microcatheter (microvention, california, usa) with the goal of occluding the fistula trans arterially (not shown). however, a sufficiently distal position could not be obtained, raising the concern of an incomplete obliteration. therefore, a combined transarterial and transvenous route was chosen to occlude the fistula by injecting a liquid embolic in the cs while preventing its reflux with a compliant balloon inflated in the ica. the left internal jugular vein was punctured under roadmap guidance, followed by the placement of a 6f sheath (fig. 5, a). a scepter c compliant balloon (microvention, california, usa) was navigated in the ica (fig. 5, b) and inflated to prevent reflux of the liquid embolic. a 4f diagnostic catheter was placed at the level of the left ips, which was not visible. after multiple failed attempts to recanalize the ips with a terumo 35 guidewire, we managed to cross the ips and reach the cs with a coronary angioplasty wire, pilot 14 (abbott, chicago, usa) (fig. 5, c, d) and a headway duo microcatheter. superselective contrast injection confirmed the position inside the cs and the enlarged sov (fig. 5, e, f). with the balloon inflated in the cavernous ica, two vials of onyx (medtronic, dublin, ireland) were slowly injected through the headway duo microcatheter until the fistula was no longer visible (fig. 4, e, f). no complications occurred during or after the procedure. symptoms improved almost immediately on the angiographic table. the patient was discharged five days later with residual diplopia. figure 5. a. a 6f sheath was placed in the ijv under roadmap guidance; b. the compliant balloon inflated had the role in preventing reflux of the liquid embolic in the cavernous ica; c, d. frontal and lateral projection roadmap images: a coronary wire was successfully navigated from the ijv through the ips in the cs; e, f. frontal and lateral projection dsa images confirming the microcatheter position in the cs; g, h. frontal and lateral fluoroscopy images showing the final onyx cast. ijv=internal jugular vein; ica=internal carotid artery; ips=inferior petrosal sinus; cs=cavernous sinus; dsa=digital subtraction angiogram. 157 endovascular treatment options for carotid-cavernous fistulae discussion endovascular treatment of carotid-cavernous fistulae can be achieved by transarterial or transvenous approaches. furthermore, multiple devices and occlusion strategies are available. the selection of a treatment strategy depends mainly on the angioarchitecture of the fistula. in the first case presented, transarterial occlusion with coils was, in our opinion, the safest plan due to a good visualization of the shunt and the easy access to the enlarged venous pouch. the treatment strategy in the second case was dictated by the absence of the left hemisphere, such that sacrifice of the ica was deemed the safest and fastest cure possible. transarterial treatment of direct ccf’s using detachable coils was first reported by halbach et al. in 1991.5 since then, this technique has been assessed in multiple retrospective cohort studies. the reported immediate complete obliteration rate was around 70%, and up to 90% after later reinterventions, with no periprocedural morbidity or mortality.5–7 the main reasons behind incomplete obliteration were a large arterial defect or a large aneurysmal dilation of the cavernous sinus.6 to preserve the parent artery and prevent coil herniation in the ica, non-detachable balloons or intracranial stents can be used as reconstructive treatment options.6,8 in addition, incomplete closure of the fistula can lead to a change in hemodynamics, leading to a redirection of blood drainage, e.g., from the sov to cortical cerebral veins, which can rupture and cause an intracerebral hemorrhage. detachable coils have potential disadvantages in the treatment of ccf’s. due to the dense packing needed to occlude the fistula, the coil mass can cause mechanical compression on the nerves that travel in the cs, with subsequent cranial nerve palsy (cnp). worsening or developing new cnp after fistula closure seems to be associated with the total volume of coils used. almost 80% of patients who needed a coil volume larger than 0.2 cm3 developed new or worsening previous cnp. only 70% of these patients recovered completely, requiring a more extended period than patients with lower coil volumes.9 to achieve such a dense packing necessary to cure the fistula, a mean number of 14-22 coils are needed per patient.6,7 this large number of coils increases the cost of the procedure and the irradiation to the patient. if obliteration of the fistula with coils cannot be obtained transarterial, transvenous access is a viable alternative. it can be achieved by a posterior route to the cs through the internal jugular vein and inferior petrosal sinus or an anterior approach through the facial or superior ophthalmic vein.4,9 considering the internal trabecular structure of the cs, using only detachable coils might be partially responsible for the relatively low immediate occlusion rate. consequently, coils can be combined with liquid embolic agents, either as a first-line approach or as a bail-out strategy to achieve complete obliteration.4 this technique requires a combined transarterial and transvenous access. usually, embolic agents are injected into the coil mass. at the same time, a noncompliant balloon is inflated in the ica, covering the laceration to prevent emboli from occluding ica branches. immediate obliteration rates reported for this technique are higher than those for coiling alone, reaching 90%.10 however, care should be taken when injecting liquid embolic in the cs, not to occlude normal draining veins and to cause a hemorrhagic infarct. in the third case reported, the structure of the fistula was so diffuse that we considered coils impossible to position properly. therefore, only liquid embolic was slowly injected into the cs. concomitantly, a compliant balloon was inflated in the cavernous segment of the ica to prevent liquid from refluxing into the artery, causing an ischemic stroke. covered and flow-diverting stents can also occlude the tear in the cavernous segment of the ica while preserving its patency.4 however, covered stents are rigid, not designed for intracranial arteries, making them difficult to navigate and deploy. the first report of a direct ccf, caused by a ruptured aneurysm in a 72 years-old female patient, successfully obliterated with a flow-redirection endoluminal device (fred) flow-diverter, was presented in 2012 at the abc-win, val d’isere meeting by stefanita dima and lucian marginean. since then, other reports have shown that transvenous or transarterial coiling of the cavernous sinus, with simultaneous flow-diverter implantation in the ica, achieves a 100% obliteration rate.11,12 conclusions carotid-cavernous fistulae represent a heterogeneous disease. this heterogeneity is caused by the different angioarchitecture of each fistula. these architectural particularities dictate the best 158 roxana codreanu, rares cristian filep, lucian marginean endovascular treatment modalities. transarterial balloon-assisted coiling is associated with relatively high immediate obliteration rates and a low number of complications. however, due to the large volumes of coils needed to occlude the fistula and their subsequent mass effect, cranial nerve palsies can persist for more extended periods. transvenous occlusion with coils and liquid embolic has a higher cure rate than coiling alone; however, inadvertent reflux of liquid embolic into normal arteries can lead to devastating ischemic complications. as technology evolves, endovascular choices will continue to expand, allowing higher immediate cure rates and shorter recovery intervals. flow-diversion devices are promising adjuncts to the arsenal of devices aimed at carotid-cavernous fistulas. they can promote a faster thrombosis of the fistula, and more importantly, offer a scaffolding surface over the arterial laceration that can serve as a platform for endothelial growth and complete reconstruction of the internal carotid artery. ethical requirements no personal data of the patient is available for identification. conflicts of interest the authors declare that there is no conflict of interest. references 1. barrow, d. l. et al. classification and treatment of spontaneous carotid-cavernous sinus fistulas. j neurosurg 62, 248–256 (1985). 2. thomas, a. j. et al. proposal of venous drainage–based classification system for carotid cavernous fistulae with validity assessment in a multicenter cohort. neurosurgery 77, 380–385 (2015). 3. gemmete, j. j., ansari, s. a. & gandhi, d. m. endovascular techniques for treatment of carotid-cavernous fistula. j neuro-ophthalmol 29, 62–71 (2009). 4. zaidat, o. o. et al. multimodal endovascular therapy of traumatic and spontaneous carotid cavernous fistula using coils, n-bca, onyx and stent graft. j neurointerv surg 3, 255 (2011). 5. halbach, v. v., higashida, r. t., barnwell, s. l., dowd, c. f. & hieshima, g. b. transarterial platinum coil embolization of carotid-cavernous fistulas. ajnr am j neuroradiol 12, 429–33 (1991). 6. bink, a. et al. coil embolization of cavernous sinus in patients with direct and dural arteriovenous fistula. eur radiol 19, 1443 (2009). 7. luo, c.-b. et al. transarterial detachable coil embolization of direct carotid-cavernous fistula: immediate and longterm outcomes. j chin med assoc 76, 31–36 (2013). 8. morón, f. e., klucznik, r. p., mawad, m. e. & strother, c. m. endovascular treatment of high-flow carotid cavernous fistulas by stent-assisted coil placement. ajnr am j neuroradiol 26, 1399–404 (2005). 9. nishino, k. et al. cranial nerve palsy following transvenous embolization for a cavernous sinus dural arteriovenous fistula: association with the volume and location of detachable coils. j neurosurg 109, 208–214 (2008). 10. yu, y. et al. embolization of direct carotid cavernous fistula with onyx and coils under transarterial balloon protection. cardiovasc inter rad 37, 679–685 (2014). 11. nossek, e. et al. use of pipeline embolization devices for treatment of a direct carotid-cavernous fistula. acta neurochir 157, 1125–1130 (2015). 12. baranoski, j. f. et al. flow diverters as a scaffold for treating direct carotid cavernous fistulas. j neurointerv surg 11, 1129 (2019). doi: 10.33962/roneuro-2021-059 a reverse brain herniation (rbh) after ventriculoperitoneal shunt (vp) in posterior fossa tumour with obstructive hydrocephalus. a rare and fatal complication lamkordor tyngkan, avatar singh, abdul rashid bhat romanian neurosurgery (2021) xxxv (3): pp. 352-354 doi: 10.33962/roneuro-2021-059 www.journals.lapub.co.uk/index.php/roneurosurgery a reverse brain herniation (rbh) after ventriculoperitoneal shunt (vp) in posterior fossa tumour with obstructive hydrocephalus. a rare and fatal complication lamkordor tyngkan, avatar singh, abdul rashid bhat abstract the risk of hydrocephalus in posterior fossa tumour is quite high (7190%), cerebrospinal fluid (csf) diversion procedures like ventriculoperitoneal (vp) shunt, endoscopic third ventriculostomy (etv) and external ventricular drainage (evd) are emergency procedures and may improve symptoms like headache and vomiting. however, post-operative deterioration after csf diversion should alert the clinician to the possibility of rbh which is rare (3%) and has a high mortality. we report a case of a 12-year female child with a left cerebellar lesion with hydrocephalus. vp shunt was done and her pupils revert back to normal size, two hours post-surgery her pupils become dilated and not reacting to light, an urgent ct was done which showed reverse brain herniation. reverse brain herniation is a very rare complication after the csf diversion procedure with a poor prognosis. introduction obstructive hydrocephalus secondary to posterior fossa tumour is quite common, occurring in 71–90% of children with posterior fossa tumors.1the optimal management of hydrocephalus in a child with a posterior fossa tumor is a topic of debate.2 the question of whether to place an external ventricular drain (evd), insert a ventriculoperitoneal shunt (vps), perform an endoscopic third ventriculostomy (etv), or defer csf diversion procedures before resective surgery depends on the clinical presentation and individual surgeon practice; there exists no class i evidence to guide management.3cerebrospinal fluid (csf) diversion procedure carry the risk of reverse brain herniation (rbh) which is rare and associated with significant mortality. rbh may aggravate hydrocephalus and cause hemorrhagic infarction of the brainstem and cardiorespiratory disturbance. 4, 5 we report case of left cerebellar lesion with obstructive hydrocephalus that developed fatal reverse brain herniation after ventriculoperitoneal (vp) shunt. keywords posterior fossa tumour, hydrocephalus, reverse brain herniation, ventriculoperitoneal shunt corresponding author: abdul rashid bhat skims srinagar, india seven_rashid@rediffmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 353 a reverse brain herniation (rbh) after ventriculoperitoneal shunt (vp) case report a 12-year female child presented to surgical emergency department with complaints of headache since 2 months and altered sensorium since 2 hours. on examination glasgow coma scale (gcs) was e1v1m2 (4/15), pupils bilaterally dilated not reacting to light, magnetic resonance imaging (mri) showed left cerebellar heterogenous enhancing lesion with hydrocephalus. urgent intubation and right ventriculoperitoneal shunting was done, csf came out under high pressure. post surgery patient pupils revert back to normal size and reacting to light and patient was shifted to neuro icu as she was not extubated. however after 2 hour of surgery her pupils become dilated and not reacting to light again, urgent ncct (non contrast computed tomography) was done which showed decompressed ventricles with shunt tip in situ and revesre brain herniation. surgical decompression of posterior fossa tumours was planned but patient relatives didn’t give consent for surgery and unfortunately patient died after 3 days. discussion to the best of our knowledge only three cases of revesre brain herniation (rbh) after csf diversion procedure in posterior fossa tumour with hydrocephalus has been reported in the literature. obstructive hydrocephalus secondary to posterior fossa tumors is quite common, occurring in 71–90% of children with posterior fossa tumors.1 csf diversion procedures are emergency procedure in these cases; however, post-operative deterioration in the condition of the patient after csf diversion should alert the clinician to the possibility of rbh of the brain. rbh is the least understood of the brain herniation syndromes and is a rare complication of vp shunt with an incidence of 3%.6 cuneo et al. reported that cerebellar mass (65%) is the commonest lesion associated with rbh, followed by lesions of cp angle (13%), the pons (11%), and the fourth ventricle. it usually occurs when the mass originates near the incisura, when drainage of the lateral ventricles relieves obstructive hydrocephalus, or when the opening in the tentorium is large.4 galen's vein lies immediately above the posterior tentorial incisura. herniation of the vermis through the notch displaces galen's vein upward against the splenium and the unyield¬ing free edge of the falx. acute compression of galen's vein may produce hemorrhagic infarction in the diencephalon and the adjacent white matter if venous collateral channels fail.4 direct compression of the brainstem and downward tonsillar herniation may be present. the clinical picture includes signs of pontine compression (obtundation, hyperventilation, decerebrate rigidity, and small fixed pupils), midbrain compression (loss of upward gaze and pupils which may be fixed and dilated). compression of the brainstem nuclei causes severe bradycardia and asystole.4, 5 in our case as tumour was large possible cause of reverse brain herniation (rbh) into the supratentorial compartment, was a sudden decrease in the supratentorial pressure due to the shunt. gurajala i et al. showed that interruption of vp shunt and prompt institution of mechanical ventilation immediately after clinical diagnosis of rbh may have reduced the extent of herniation. even though rbh has significant mortality, surgical decompression should be undertaken as soon as possible even in cases of severe rbh.8 our patient was only mechanically ventilated because patient relatives denied for any surgical intervention. the mortality associated with rbh is significant. in the series by cuneo et al, only seven cases out of a total of 52 reviewed were diagnosed antemortem and the mortality was 100%. cases reported later in the literature had a better outcome. in about 25% of the patients, ventricular drainage is directly responsible for precipitation of the herniation.5, 6, 8, 9 hence, patients who undergo csf diversion should be observed closely for reverse brain herniation (rbh) postoperatively. table 1. reported cases of reverse brain herniation (rbh) after csf diversion in obstructive hydrocephalus secondary to posterior fossa tumour ca se author yea r age / sex location of tumour treatment out -come 1 singha sk et al9 20 09 57/ m midline posterior fossa (involving vermis and both cerebellum) hemangiobl atoma with hydrocepha lus etv + suboccipit al craniecto my and tumor decompre ssion. uneve ntful 354 lamkordor tyngkan, avatar singh, abdul rashid bhat 2 guraja l i et al8 20 12 45/ m right cerebellopo ntine (cp) angle tumours with hydrocepha lus vp shunt + tumour decompre ssion dischar ged with nasoga stric tube 3 marap pan k et al10 20 18 3.5 /f 4th intraventric ular tumour vp shunt not avail -able 4 presen t case 20 21 12/ f left cerebellar lesion vp shunt expired etvendoscopic third ventriculostomy; vp ventriculoperitoneal conclusions ventriculoperitoneal shunt for obstructive hydrocephalus with posterior fossa tumour can be complicated by reverse brain herniation which is a rare complication and can be fatal if prompt diagnosis and intervention is not done. surgical decompression should always be done even in a case of severe rbh. a. b. figure 1. (a) axial cemri image showing left cerebellar lesion with heterogeneously enhancing lesion; (b) coronal mri image showing left cerebellar lesion with hydrocephalus. a. b. figure 2. ncct (a) axial image showing decompressed ventricles with reverse brain herniation; (b) saggittal image showing raised tentorium with revesrse brain herniation. references 1. sainte-rose c, cinalli g, roux fe, maixner r, chumas pd, mansour m. management of hydrocephalus in pediatric patients with posterior fossa tumors: the role of endoscopic third ventriculostomy. j neurosurg 2001; 95: 791-7. 2. schijman e, peter jc, rekate hl, sgouros s, wong tt. management of hydrocephalus in posterior fossa tumors: how, what, when? childs nerv syst 2004; 20: 1924. 3. lam s, reddy gd, lin y, jea a. management of hydrocephalus in children with posterior fossa tumors. surg neurol int 2015; 6: s346-8. 4. cuneo ra, caronna jj, pitts l, townsend j, winestock dp. upward transtentorial herniation: seven cases and a literature review. arch neurol 1979; 36: 618–23. 5. prabhakar h, umesh g, chouhan rs, bithal pk. reverse brain herniation during posterior fossa surgery. j neurosurg anesthesiol 2003; 15: 267–9. 6. raimondi aj, tomita t. hydrocephalus and infratentorial tumors. j neurosurg 1981; 55: 174–82. 7. ecker a. upward transtentorial herniation of the brain stem and cerebellum due to tumor of the posterior fossa with special note on tumors of the acoustic nerve. j neurosurg 1948; 5: 51-61. 8. gurajala i, brahmaprasad v, rajesh a, ramachandran g, purohit ak. reverse brain herniation following ventriculoperitoneal shunt. indian j anaesth 2012; 56: 585-7. 9. singha sk, chatterjee n, neema pk. reverse herniation of brain: a less recognized complication in a patient with midline posterior fossa tumor postendoscopic third ventriculostomy. j neurosurg anesthesiol 2009; 21: 354– 5. 10. marappan k, sankaran a, dejveegan k, ross k. a known complication of posterior fosssa tumour rarely encounteredreverse coning. apollo med 2018; 15: 1835. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article post-traumatic massive acute subdural haematoma in a child following trivial fall amit agrawal india doi: 10.2478/romneu-2018-0022 168 | agrawal post-traumatic massive acute subdural haematoma in a child doi: 10.2478/romneu-2018-0022 post-traumatic massive acute subdural haematoma in a child following trivial fall amit agrawal department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: post-traumatic acute subdural haematomas are rare in children and associated with significant cerebral oedema. there is need to understand pathophysiology in a better way to improve the outcome. we report a case of traumatic acute subdural haematoma in five year old male child because of its rarity and difficulty confronted in the management of this lesion. key words: acute subdural haematoma, pediatric head injury, trauma introduction acute traumatic intracranial hematomas (asdh) in children are rare lesions and account for 2.9% of a total of intracranial hematomas and 0.6% of a total of children with cranio-cerebral trauma. (1) out of these acute post-traumatic subdural haematoms in children are still rarer (1-6) and involve infants, new born and toddlers in order of frequency. (6) we report a case of traumatic acute subdural haematoma in five year old male child because of its rarity and difficulty confronted in the management of this lesion. case report four year old male child presented with the history of fall from bullock-cart after 6 hours of injury. he was in altered sensorium since than and had multiple episodes of vomiting. there was no history of ear, nasal or throat bleed or convulsions. his general and systemic examination was unremarkable. neurologically he was in altered sensorium and his gcs was e1v1m4. pupils were small in size but reacting to light. he was moving all four limbs left side more than right side. his computerized examination (ct scan) examination showed a large acute subdural haematoma over left temporo-parietooccipital region with significant cerebral oedema, mass effect and midline shift (1.5 cm) (figure 1). his blood investigations were normal. he underwent large left temporoparietal craniotomy and evacuation of thick acute subdural blood clot. after evacuation of haematoma brain was very tense and bulging. dura was closed with the help of pericranial graft. child was kept on endotracheal tube and electively ventilatied. he was also started on romanian neurosurgery (2018) xxxii 1: 168 – 169 | 169 high dose of anti-oedema measures and prophylactic anticonvulsant. after 6 hours of surgery child started to develop hyperthermia and fluctuation in pulse rate and blood pressure. he was started on ionotropic support. in spite of these measures he could not be revived and expired. figure 1: large acute subdural haematoma over left temporo-parieto-occipital region with significant cerebral oedema, mass effect and midline shift discussion causes of acute subdural haematomas in children are mainly non-traumatic (parental or familial abuse) and trauma is an uncommon cause of asdh. (3,6) indications for surgical evacuation are based upon clinical and radiological features (4) and correct diagnosis and early surgical intervention combined with therapeutic measures improves cerebral hemodynamics (4) and ensures a favorable outcome in majority of the cases. (1, 4, 5) however in children with asdh there is a high incidence of increased intracranial pressure. (4) these findings of cerebral oedema in children with asdh signifies severe injury and associated poor neurological status further make the outcome worse as in present case. (2) post-traumatic asdhs in children need further evaluation to better understand the pathophysiology for better management and to improve outcome. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.okladnikov gi, nesterenko lkh, svarovskaia vi, aksenov sa, kurov om, potapov iua. [acute traumatic intracranial hematoma in children][article in russian] zh nevropatol psikhiatr im s s korsakova. 1989;89(8):53-5. 2.chung cy, chen cl, cheng pt, see lc, tang sf, wong am. critical score of glasgow coma scale for pediatric traumatic brain injury. pediatr neurol. 2006 ;34(5):379-87. 3.dashti sr, decker dd, razzaq a, cohen ar. current patterns of inflicted head injury in children. pediatr neurosurg. 1999 ;31(6):302-6. 4.meyer pg, ducrocq s, rackelbom t, orliaguet g, renier d, carli p. surgical evacuation of acute subdural hematoma improves cerebral hemodynamics in children: a transcranial doppler evaluation. childs nerv syst. 2005 ;21(2):133-7. 5.spanu g, pezzotta s, silvani v, leone v. outcome following acute supratentorial subdural hematoma in pediatric age. j neurosurg sci. 1985 ;29(1):31-5. 6.gutierrez fa, raimondi aj. acute subdural hematoma in infancy and childhood. childs brain. 1975;1(5):269-90. 22 22agrawalamit_post-traumatic microsoft word 1cuciureanut_intravenous romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article intravenous thrombolysis in acute ischemic stroke – our experience tudor cuciureanu, diana hodorog, iulian dan cuciureanu romania doi: 10.1515/romneu-2017-0021 romanian neurosurgery (2017) xxxi 2: 137 145 | 137             doi: 10.1515/romneu-2017-0021 intravenous thrombolysis in acute ischemic stroke – our experience tudor cuciureanu1, diana hodorog2,3, iulian dan cuciureanu2,3 1phd student, “grigore t. popa” university of medicine and pharmacy, iaşi, romania 2“grigore t. popa” university of medicine and pharmacy, iaşi, romania 3“prof. dr. n. oblu” emergency hospital, iaşi, romania abstract: stroke is a major health problem worldwide and nationally: the second leading cause of death and dementia, the most common cause of epilepsy in the elderly, and a common cause of depression. stroke is associated with an increased rate of morbidity, but it is also the leading cause of long-term morbidity and disability in industrialized countries. thrombolysis by administering intravenous recombinant tissue plasminogen activator (iv-rtpa) is the only treatment method "in the therapeutic window" recognized in international protocols. the benefit-risk ratio should be evaluated on a case-by-case basis, with the neurologist's decision being individual and often difficult. the aim of our study was to analyze the outcome of this procedure in our hospital since 2015. we performed a retrospective clinical study of 77 patients with acute ischemic stroke subjected to iv-rtpa. most patients with ischemic stroke undergoing intravenous thrombolysis did not receive chronic antithrombotictherapy. in most cases (76%) there was a decrease in the nihss score at 24 hours after thrombolysis and especially after 7 days (between 3 and 19 points), reflecting a reduction in poststroke disability in thrombolyzed patients. in the series of patients undergoing i.v. thrombolysis 5 deaths (10%) were recorded, the lowestrate of data/death ratereported in the literature (1418%). key words: stroke, thrombolysis outcome introduction stroke is a bleak reality of the society we live in through its effects on the physical and mental status of the patient and his/her socioprofessional reintegration. it is a major health problem worldwide and nationally: the second leading cause of death and dementia, the most common cause of epilepsy in the elderly, and a common cause of depression. stroke is associated with an increased rate of morbidity, but it is also the leading cause of long-term morbidity and disability in industrialized countries. 138 | cuciureanu et al intravenous thrombolysis in acute ischemic stroke             thrombolysis by intravenous (iv) administration of recombinant tissue plasminogen activator (rtpa) is the only treatment method "in the therapeutic window" recognized in international protocols to which romania adhered through the national program of intervention in acute ischemic stroke. alteplaza is currently the only thrombolytic agent that has proven effective through in international clinical trials, with a real impact on dependence and disability or risk of death after stroke. at the same time, it is not a risk-free therapeutic method, the main risk being the hemorrhagic one, a major risk for elderly patients with elevated blood pressure, diabetes and severe stroke. the benefit-risk ratio should be evaluated on a case-by-case basis, with the neurologist's decision being individual and often difficult. difficulty in dealing with each patient is not only due to medical particularities but also to collateral aspects such as: problems with obtaining informed consent in patients with speech disturbances or confusional syndrome, timely interaction with patient's family, difficulty in communicating essential information in clear and understandable terms to a moderately or poorly informed population under the pressure of the "time is brain" principle. the disability due to ischemic stroke in patients undergoing thrombolysis with iv-rtpa is reduced or absent 3 months after the acute ischemic event, a 30% reduction in this disability not being accompanied by a significant change in mortality [1]. material and method we performed a retrospective clinical study of 77 patients with acute ischemic stroke subjected to thrombolysis with iv-rtpa based on eligibility criteria assessed by neurologists on 24-hour duty between june 2015 and may 2017 at the iasi “prof.dr. n. oblu” emergencyhospital. the data were collected from the medical records, emergency medical records, andintensive care observation charts. the following parameters were assessed: vascular risk factors, prior cardio/cerebrovascular risk prevention therapy (antiplatelet, anticoagulant, statin), severity of neurological deficit assessed with the nihss scale at baseline and in dynamics, aspects radiographic score at stroke onset,time from stroke onset to the initiation of thrombolytic therapy. results the age of enrolled patients ranged from 28 to 92 year. age distribution of patients gender distribution of patients subjected to thrombolysis revealed a female predominance.   romanian neurosurgery (2017) xxxi 2: 137 145 | 139             gender distribution most patients subjected to thrombolytic therapy had one or more vascular risk factors. only 5 patients had an ischemic stroke of undetermined etiology, explained by incomplete laboratory assessment due to the logistic problem (lack of thrombophilia tests, absence of transthoracic or transesophageal echocardiogram, impossibility of holter ecg monitoring). arterial hypertension was the main vascular risk factor in most patients, especially in the group at very high additional risk. atrial fibrillation, chronic ischemic heart disease, dyslipidemias, diabetes mellitus and chronic alcohol abuse were also present in the panoply of vascular risk factors in patients undergoing thrombolysis. vascular risk factors in the patients subjected to thrombolysis most ischemic strokestreated by thrombolysis involved the carotid system territory mainly on the topography of the middle cerebral artery, and only 10% had a vertebrobasilarsystem location. arterial territory the average nihss score was 15 points, reflecting asignificant percentage of cases with severe neurological deficits, most likely a consequence of the long time interval between stroke from to hospital presentation to the hospital, but also of the still long time from presentation to thrombolysis administration. in most cases (76%) a decrease of nihss score (between 3 and 19 points) was recorded at 24 hours and especially 7 days after thrombolysis, which reflects a reduction in poststrokedisability in the thrombolyzed patients. clinical assessment imaging assessment. native cerebral ct scan in emergency revealed a 10-point aspects score in most patients subjected to thrombolysis (80%), only one fifth of patients having an aspects score of 7-10 points. evaluation of the remnant neurologic deficit after thrombolysis therapy was made, according to the protocol, at 3 months for 49 patients who underwent neuromotor 140 | cuciureanu et al intravenous thrombolysis in acute ischemic stroke             rehabilitation using the modified rankin scale (mrs) and the barthel capacity scale. of these, the majority (34 cases) had low mrsscores and high barthel index scores, signifying a reduced severity of the remnant neurologic deficit after stroke. these scores correlated with the decrease of nihss score during acute stroke. assessment at 3 month aspects score time intervals needed for the clinical and laboratory assessment of the patients eligible for thrombolytic therapy were compared with those specified in the national protocol; and international guidelines. the shortest time intervals were recorded for receiving the results of the compulsory tests specified in the thrombolysis protocol and result of imaging assessment, and the interval from presentation to emergency department (ed) to the initiation of thrombolysis was generally longer than recommended. laboratory efficacy to illustrate we present the results of priority action for interventional treatment of patients with acute stroke in accordance with data in the romanian registry of interventional treatment for acute stroke.         romanian neurosurgery (2017) xxxi 2: 137 145 | 141             interval stroke onseted presentation interval ed presentation – brain ct scan interval ed presentation – receiving laboratory test results interval stroke onset –treatment administration interval ed presentation treatment administration 2012-2014 75 30 53 150 75 2014-2015 65 30 44 135 70 2015-2016 86 34 50 165 79 2016 (janaug) 99 31 51.5 175.4 78.7 recommendations in international guidelines 25 45 60 most of the patients undergoing intravenous thrombolytic therapy were not on chronic antithrombotic treatment for secondary prevention at home. home treatment prior to thrombolysis prior statin treatment as to the patients on pre-stroke statin therapy, in only 5 of the 13 patients therapy was targeted at lowering ldl-cholesterol. patients not on pre-stroke statin therapy accounted for the majority of those with high onset nihss score (greater severity of neurological symptoms) and also tended to have lower e aspects scores. in the series of patients subjected to intravenous thrombolysis 5 deaths (10%) were recorded, rate lower than that reported in the literature (14-18%). mortality rate discussions ischemic stroke is produced by thromboembolic or hemodynamic mechanism. the pathogenesis of cerebral infarction is complex and consists of several stages, the processes involved in cellular injury determining an ischemic cascade. a multitude of factors are considered in cell dysfunction 142 | cuciureanu et al intravenous thrombolysis in acute ischemic stroke             and death. seconds to minutes after the loss of glucose and oxygen supply to neurons, the ischemic cascade begins. this is a complex process that starts with the discontinuation of the normal electrophysiological function of neurons. pathophysiologically, the decrease in oxygen and glucose supply leads to inappropriate energy supply and thus tofailureofenergy dependent processes such asion pumping. the result is the disruption of ionic homeostasis, with the influx of ca and water into the cells and lactic acidosis. finally cytotoxic edema occurs. the role of excitatory amino acids (especially glutamate liberated from ischemic cells) is a key element because they bind to nmda receptors and excite neurons, causing an influx of ca and na that activates the enzymatic cascade ultimately leading to irreversible cellular lesions and neuronal death. other events induced by ischemia consist in free radical production, which causes lipid peroxidation and cell membrane rupture. lactic acid accumulation and the consecutive biochemical changes are important in determining the extent of cellular lesions. in terms of anatomopathological lesions, focal cerebral ischemia has two areas: -1.”core ischemic zone" at the center of the ischemic area where, through the depletion of energy reserves (blood flow <12 ml /100 mg /tissue /min), neuronal death (necrosis) occurs. -2. “ischemic penumbra”, present both at the margin of ischemic focus and even within the cerebral infarction for a short period of time contains functionally altered but still viable cerebral tissue supplied with blood by arteries the "luxury perfusion" (bf = 1223ml/100mg /tissue/min) [2]. at this level there is a risk of apoptotic-like cell death. ivrtpa thrombolysis diminishes the extent of the infarct area towards the penumbralzone and also causes an increase of reperfusion processes, as shown by the studies (epithet echoplanar imaging thrombolytic evaluation trial) [3]. ischemic penumbra: -has a limited duration but may persist for over 12 hours after the occurrence of focalization signs due to ischemic stroke -may progress to infarction due to neural lesions secondary to some biochemical cascades with cytotoxic and excitotoxic effects -ion homeostasis and transmembrane potentials are maintained -being a dynamic process, it has potential for reversibility if and reperfusion and neuroprotection therapies are initiated as early as possible. the onset and time course of molecular processes are different. at the level of ischemic focus outbreak, increased excitotoxicity and secondary biochemical reactions cause necrosis in minutes to hours (within the first 24h), while at the level of ischemic peninsula excitoxicity and secondary biochemical reactions cause apoptotic-like cell death which can last hours to days. thus, the earlier the initiation of the therapeutic strategy aimed at restoring blood flow and providing neuroprotection, the higher the percentage of saved penumbral zone with potential for reversibility. imaging assessment by perfusion ct scans and romanian neurosurgery (2017) xxxi 2: 137 145 | 143             magnetic resonance imaging (mri) and determination of diffusion–perfusion mismatch would allow a correct selection of patients who may benefit most from thrombolysis due to accurate quantification of the infarct zone versus potentially reversible ischemic penumbra. the use of these brain imaging techniques also allowed the expansion of the therapeutic window for i.v. thrombolysis from 3 to 4.5 hours [4, 5] revascularization therapy in acute ischemic stroke includes intravenous thrombolysis and endovascular treatment procedures (mechanical thrombectomy, intraarterial thromboaspiration, intra-arterial pharmacological thrombolysis, combined pharmacological and mechanical treatment). patients with acute ischemic stroke within the first 4.5 hours of the onset of neurological deficits may be eligible for systemic thrombolysis with rtpa administered intravenously, the recommended dose in the protocol being 0.9 mg/kg body weight, up to a maximum dose of 90 mg, of which 10% is administered bolus and the remainder is perfused over 1 hour [6]. the narrow therapeutic window, reduced efficacy for large artery occlusion, contraindications to this treatment in patients who associate a higher risk for bleeding complications are elements limiting this type of therapy. the main and most feared postthrombolysis complication is intracerebral hemorrhage. it can be of varying degrees of severity, ranging from simple nonsystematized petechiae to well-defined hematomas with mass effect, and which may be asymptomatic or symptomatic, by clinical deterioration of more than 4 points on the nihss (national institute of health stroke scale). this major complication may occur early or late, more than 24 hours after thrombolytic therapy, and predictive factors are not clearly established. the increased risk of hemorrhage appears to be related to: advanced age, hypertension, diabetes, amyloid angiopathy, leukoaraiosis, severity of signs of early ischemia on ct scan, or cerebral ischemia volume evidenced by diffusion weighted mri. according to some studies, the favorable post-thrombolysis course seems to correlate both with arterial rechanneling and with efficient collateral circulation [7,8, 9,10]. although the therapeutic window for the rtpa treatment was extended to 4.5 hours, studies show that patients in whom thrombolysis was performed within the first 3 hours show a double benefit compared to those in whom this therapeutic intervention is performed within 34.5 hours [11]. that is why it is imperative that all lines of care, emergency services and all involved factors to be maximally effective, so that patients with acute ischemic stroke to have rapid access to clinical and laboratory assessments in order to be eligible thrombolytic therapy. and this means functional collaboration protocols between emergency medical services, ambulance service dispatching system, emergency department medical staff, neurologists and neuroradiology unit. increasing the number of hospitals with stroke and thrombolysis units as well as lines dedicated 24/24 to thrombolysis could lead to an increase in the proportion of patients with thrombolyzed acute ischemic stroke of all 144 | cuciureanu et al intravenous thrombolysis in acute ischemic stroke             stroke cases [12]. other elements to be considered in order to extend the application and increase the benefit of thrombolytic therapy could be: increased number of stroke units, access to modern vascular imaging techniques, and extension of interventional neuroradiology services. another important aspect related to thrombolytic therapy in acute ischemic stroke is informed consent. thrombolysis cannot be initiated without the patient's consent, which in many cases cannot be obtained because of language or understanding problems caused by stroke. obtaining the consent from the patient's relatives may also be difficult, either because they are not present in due time in the hospital unit, or because the information given to them about the benefits vs. risk of thrombolysis is not sufficiently understood. using and disseminating information materials about thrombolysis among the population or through media could shorten the time needed to obtain informed consent in order to save time until the actual initiation of thrombolytic therapy [13, 14, 15]. in conclusion the decision to initiate intravenous thrombolysis therapy in acute ischemic stroke during the therapeutic window remains an individualized and difficult one for the neurologist, because even when observing the indications in the national protocol, a number of decision-making elements remain incompletely clarified: thrombolytic therapy in patients with neurological symptoms occurring in the morning on waking or in elderly patients; use of the best neuroimaging method for assessing eligibility for thrombolysis and optimal benefit-risk assessment, the optimal organization model of structures and services involved in acute stroke management, so as to provide the fastest circuits in view of providing access to thrombolytic therapy for as many patients as possible. correspondence diana hodorog email: diana_hodorog@yahoo.com references 1.thompson robinson, zahidzaheer, and amit k. mistri. thrombolysis in acute ischaemic stroke: an update, theradv chronic dis. 2011 mar; 2(2): 119–131 2.bravo y., martí-fàbregas j., cocho d., rodríguezyáñez m., castellanos m., de la ossa n. pérez, et al. (2008) influence of antiplatelet pre-treatment on the risk of symptomatic intracranial haemorrhage after intravenous thrombolysis. cerebrovas dis 26: 126–133 3.davis s.m., donnan g.a., parsons m.w., levi c., butcher k.s., peeters a., et al. for the epithet investigators (2008) effects of alteplase beyond 3 h after stroke in the echoplanar imaging thrombolytic evaluation trial (epithet): a placebo-controlled randomized trial. lancet neurol 7: 299–309 4. engelter s.t., bonati l.h., lyrer p.a. (2006) intravenous thrombolysis in stroke patients of ≥80 versus <80 years of age—a systematic review across cohort studies. age ageing 35: 572–580 5. european stroke organisation. (2008) eso guidelines for the management of ischaemic stroke, basel: european stroke organisation 6.hacke w., donnan g., fieschi c., kaste m., von kummer r., broderick j.p., et al. (2004) association of outcome with early stroke treatment: pooled analysis of atlantis, ecass, and ninds rt-pa stroke trials. lancet 363: 768–774 7.lees k.r., bluhmki e., von kummer r., brott t.g., toni d., grotta j.c., et al. (2010) time to treatment with intravenous alteplase and outcome in stroke: an updated romanian neurosurgery (2017) xxxi 2: 137 145 | 145             pooled analysis of ecass, atlantis, ninds, and epithet trials. lancet 375: 1695–1703 8.price c.i., clement f., gray j., donaldson c., ford g.a. (2009) systematic review of stroke thrombolysis service configuration. expert rev neurotherap 9: 211–213 9.manuel cappellari, paolo boviet. all. the thrombolysis and statins (thrast) study. neurology. 2013 feb 12; 80(7): 655–661. 10.prinz v, endres m. statins and stroke: prevention and beyond. curropinneurol 2011;24:75–80 11.sacco s, toni d, bignamini aa, et al. effect of prior medical treatments on ischemic stroke severity and outcome. functneurol 2011;26:133–139 12.appelrosp.thrombolysis in acute stroke. lancet, volume 385, no. 9976, p1394, 13.emberson, j, lees, kr, lyden, p et al. effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. lancet. 2014; 384: 1929– 1935 14.wardlaw, jm, murray, v, berge, e, and delzoppo, gj. thrombolysis for acute ischaemic stroke. cochrane database syst rev. 2014; 7: 109–110 15.wardlaw, jm, murray, v, berge, e et al. recombinant tissue plasminogen activator for acute ischaemic stroke: an updated systematic review and meta-analysis. lancet. 2012; 379: 2364–2372 romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0052 article shaken baby syndrome. case report tatiana iov, sofia david, simona damian, a. knieling, mădălina maria diac, d. tabian, diana bulgaru-iliescu romania      romanian neurosurgery (2018) xxxii 3: 409 417 | 409             doi: 10.2478/romneu-2018-0052 shaken baby syndrome. case report tatiana iov2, sofia david1, simona damian1, a. knieling1, mădălina maria diac1, d. tabian2, diana bulgaru-iliescu1 1“grigore t. popa” university of medicine and pharmacy of iași, iasi forensic institute 2iasi forensic institute, romania abstract: recognition of abuse and the treatment of child victims are recent concepts in the history of mankind. increasing the awareness of the need to treat and prevent such abuse is a characteristic of modern society. the beaten child syndrome was described by ambroise tardieu in 1860, and shaken baby syndrome (sbs) was clearly illustrated in medical literature a century later by caffey in 1972. the definition of sbs is based on the association of major intracranial lesions with minimal external lesions and the diagnosis is still difficult to establish. the authors describe a reduced number of 7 cases of pediatric patients addressed for forensic expertise and where suspicion of sbs has arisen. the lesion mechanisms involved in the production of this syndrome are still controversial and are sources of frequent debates in legal medicine. these uncertainties can make legal punishment inoperable. the therapeutic management of these children in neurosurgery is not subject to international consensus, and discrepancies between different clinics impede a comparative cohort assessment. however, sbs is a major public health problem due to severe neurological injuries caused to child victims during brain development. key words: sbs, cerebral injuries literature review the symptoms of the shaken baby syndrome are difficult to identify, and the family usually avoid describing the cranial trauma suffered by the child. nonspecific symptoms like vomiting, crying and irritability are often confused with gastric or intestinal disorders. violent shaking is often repeated, but the one with the highest intensity is the one that causes the death. the macroscopic and microscopic examination of the brain, the examination of the eyes and bones can, in most cases, identify the shaken baby syndrome. the shaken baby syndrome (sbs) is also called head trauma due to child abuse, shaking impact syndrome, or shaken child syndrome (8). the syndrome of the shaken child was defined by dr. caffey, a radiologist, in 1972 (1) as a form of physical abuse to a 1-2 years old child. the most at risk are babies aged between 0 months and 2 years. the head of a baby is 410 | iov et al shaken baby syndrome             relatively heavy compared to his body, and the neck muscles are so weak that they cannot hold the baby's head very well (7). shaking the baby can cause: blindness, brain damage, cerebral palsy, apoplexy attack, epilepsy, loss of hearing, learning difficulties, and later behavioral problems (9). does this syndrome occur only in children aged 1-2 years? no, in the united states, such cases have been reported in children up to 7 years old (2) and each year, about 1300 children are seriously injured or die from cranial trauma due shaking. (3) shaken child syndrome is a major cause of death, accounting for about 25-30% of all sbs children. around 60-75% of the surviving children have mild or severe retardation, paralysis, including tetraplegia, cerebral paralysis, convulsive disorders and blindness. the less serious cases of sbs are difficult to diagnose, especially in infants. a characteristic of the shaken child's syndrome is the absence of external traumatic signs, but the irritability, the slowed down rhythm of the growth, the slowing down of the deglutition reflex, lethargy, vomiting, depression, increase of head size, intracranial hypertension, changes in the respiratory system and dilated pupils are some of the signs. other associated lesions are retinal bleeding, long bone fractures and subdual hematomas. (4, 5) brain injuries of a traumatic nature, in children, without an external head injury, strongly advocate the shaking mechanism. (2, 6) in california, almost all sbs victims who survive are transferred to maternal care after diagnosis. in the united states, there is also a child-shatter prevention project that in the west of new york has reduced the baby's syndrome rate by 55% and it is currently known as a national model. after the birth of the child, all parents were shown in the hospital a video recording about sbs prevention that includes simple information on how to act if the children cry and then they were asked to sign a commitment. this project has been replicated in several countries due to its resounding success. new york state’s laws now require all hospitals to provide this program to all new parents. in recent years, some us states have passed a series of laws on the prevention of sbs (4). etiology sbs is produced by vigorously shaking the child's body through his arms, legs, chest or shoulders. the child's head will thus perform repeated flexion-extension movements. it is a non-impact traumatic association, produced by an indirect whiplash mechanism, with repeated and accelerated decelerations, with snap back and forth head movements. the most dangerous are the rotational movements, which cause uneven and asymmetrical landslides of the cerebral hemispheres relative to each other in relation to the skull. however, there are authors who do not recognize the veracity of this mechanism and who consider that such injuries cannot be produced by simply shaking the baby’s body, in the absence of an even minor impact between the cephalic extremity and a hard body/ surface. obviously, there is also sbs with head impact, but in these cases, the lesions are somewhat specific to classical mechanical trauma mechanisms. nevertheless, most of the literature in this romanian neurosurgery (2018) xxxii 3: 409 417 | 411             domain recognizes and supports the existence of pure sbs without impact. the high sensitivity of children under 1 year old to such movements is due to several factors: the relatively large dimensions and mass of the cephalic extremity comparing to the rest of the body; the immaturity of the neck muscles, which cannot yet support the baby's head, allowing broad movements, which are further amplified by inertia, and without defense reflections to counteract the amplitude of the movements through muscle contractions; the space between the brain and the dura mater is large, allowing the brain to slip more freely in relation to the bone and meningeal structures; high water content of the child's brain compared to an adult’s one; incomplete myelination of the brain nerve substance. pathophysiology and morphopathology because of shaking the baby's body, considering the morphological characteristics of the small child and the rigidity of intracranial fibrous structures (dura mater, falx cerebri, tentorium cerebelli), and the relatively fixed structures (cranial nerves, carotid blood vessels, or vertebrobasilar system) the brain will move inside the skull, with the result of characteristic lesions. external findings are very poor, except when other forms of physical abuse are associated to sbs. however, it is possible to identify ecchymotic patches of the fingers of the aggressor on the victim's anterior and posterior chest, in the positions of hand holding. under the conditions of a usual grip of the aggressor's hands on the child's chest, we may find symmetrical lesions, an oval ecchymosis on each of hemithorax region, anterior (by compression with the thumb) and multiple ecchymosis on the posterior thorax, paravertebral (compression with the other fingers). however, we should not forget that sbs can also be caused by shaking of the upper or lower limbs or shoulders, and can therefore find mild contusion (ecchymosis) at different levels. it is also possible to find external lesions of different age. the internal exam detects some typical lesions, which grouped, define sbs: subdural hematoma is found in over 90% of cases. it occurs by rupture of the bridging veins as a result of the violent shaking, causing the head to snap back and forth on the neck. bilateral and interhemispheric collections are frequently found. in many cases the volume of the hematoma is not very high, in contrast to the patient's severe clinical condition, which makes us to believe that in sbs the subdural hematoma would not be a cause of death. although caffey described chronically subdural hematoma as typical, modern literature reports the highest frequency for the occurrence of acute bleeding. sometimes subdual hematomas of different age may coexist, indicating repeated trauma. geddes mentions the appearance of the intradural hemorrhage as an effect of bridging vein rupture in sbs. in many cases, the subdural hematoma is accompanied by subarachnoid hemorrhages, with elective locations on the convexities of the cerebral hemispheres and their internal faces. 412 | iov et al shaken baby syndrome             retinal hemorrhages are present in 85100% of cases. pre-retinal, intraretinally, and retroretinin hemorrhages, often confusing, are the most common; vitreous hemorrhages are rarely encountered (10%). retinal detachment can appear. in many cases (81-85% of cases with retinal hemorrhages), the lesions are bilateral. it has not been established a relation between the location of retinal hemorrhages (right/left) and subdual hematomas. to explain these injuries, several theories have been issued: optical nerves shearing by the brain that slips inside the skull, for this mechanism advocating the relatively frequent findings of concentric retinal hemorrhages around the papilla of optic nerve; hypertension in the retinal venous system as a result of cerebral edema, but this is rather the pathophysiological explanation of terson syndrome; vascular mechanism: transient stop of blood flow due to compression of the vascular carotid-ophthalmic system during head shaking, or retinal vasospasm; retinal hemorrhages as a result of inertial movements of the vitreous body during acceleration / deceleration cycles mechanism revealed in the small child due to its high vitreous consistency and strong adhesion to the vitreoretinal surface; vascular ruptures due to the slippage of the retinal layers and their disruption; acute thoracic compression with valsalva effect and retinal hemorrhage due to increased intracerebral venous pressure. in the ocular sphere, in the fatal cases, there are necroptic findings of bleeding around the optic nerves and axonal ruptures. probably these lesions are common in sbs, being the cause of evolution with optic nerve atrophy in many cases where victims survive, the necroptic exam of a case revealed bilateral retro-ocular hemorrhages, but they may have been produced by local extension from the optic nerve sheaths presenting bleeding sleeves. parenchymal brain injury. cerebral contusion appears quite rare due to the morphological immaturity of the brain structures, with the lack of myelinization. contusive hemorrhagic lesions can occur in the corpus callosum due to its torsion during movements with the angular accelerator component, the basal faces of the frontal and temporal lobes, by contact with the rumpus surface of the skull base and the upper cerebellum pedunculum by striking the tentorium cerebelli. meningo-cerebral lesions are usually accompanied by moderate brain edema. diffuse axonal rupture is a severe and typical lesion for sbs, possibly involved more than the subdural hematoma in the infaust prognosis of the syndrome. these occur as a result of the rotating movements of the head, which create shear forces. axonal ruptures are largely responsible for the clinical condition of the victim, with varying levels of mental status, and often even by the patient's death. as a technique for identifying these lesions in the histopathology laboratory, 68-kda neurofilament immunoprecipitation and beta amyloid precursor protein (beta-app) have already been established, thus visualizing axonal amputation bulbs in the form of round or oval acidophilus masses. the technique can romanian neurosurgery (2018) xxxii 3: 409 417 | 413             also be used to find axonal lesions in the optic nerves. medullary lesions: subdural hematomas and high cervical medullary contusions are reported due to shaking of the victim's head. axonal lesions were found. periadventitial hemorrhage in the vertebral artery between c1 and c4 was reported by gleckman in a sbs case. there are injuries that occurs through an indirect mechanism of gripping: rib fractures with typical paravertebral localization, scapular fractures, vertebral spine apophyses and long bone fractures in exceptional situations. clinical diagnosis upon reaching the hospital, patients with sbs typically have nonspecific symptoms, varying and sometimes progressive degrees of consciousness, and respiratory disturbances. the glasgow coma scale (gcs) score is one of the most important indicators of the severity of the traumatic brain involvement in sbs. data on the average glasgow score in patients with sbs at the time of the arrival at the emergency unit varies depending on the author, in most cases ranging between 9-12 gcs. thus, there is a correlation between the severity of the gcs and prognosis. gillilanda has made a definition of sbs based on a clinical diagnostic criterion: echimotic compression marks with fingers and/or ribs fractures, subdural and/or leptomeningeal hemorrhage and a history of vigorous shaking. according to this author, if at least two criteria are met, the diagnosis of sbs can be concluded. for ocular lesions, the diagnosis is primarily based on an exam of the bottom of the eye. it must, therefore, enter a mandatory protocol to recommend an ophthalmologic examination to a child under 1 year who presents a subdural hematoma, even in the absence of external signs of violence. a morphometric analysis of the retinal bleeding is also useful, as there has been observed a correlation between the retinal hemorrhage and the reality of sbs and visual prognosis. paraclinical diagnosis the main investigations that contribute to the diagnosis of sbs are: cranio-cerebral computer tomography (ct), nuclear magnetic resonance imaging (mri), high-resolution cranial ultrasound, thoracic radiography (for the diagnosis of possible costal fractures), laboratory blood tests (for the differential diagnosis of hemorrhagic lesions) and lumbar puncture. forensic aspects in case of the survival of the victim, the forensic physician will have to interpret the medical documentation prepared by other specialists (pediatricians, neurosurgeons, ophthalmologists) and in collaboration with them, to make a synthesis and establish the diagnosis of sbs. it should be kept in mind: the presence of lesions considered as specific to the syndrome (subdural hematoma, retinal hemorrhage); the exclusion of other violent or nonviolent causes responsible for causing such injuries; 414 | iov et al shaken baby syndrome             the exclusion of traumatic head injury, following a very careful external examination; a history of violent shaking of the child's body. the time of medical care for healing of sbs is around 45-50 days but, in some cases, it may exceed 60 days, endangering the life of the victim through the existence of the subdural hematoma. the legal framing of the deed is also given by the intentional element, as, in most of cases the perpetrator did not wish to produce these consequences. sometimes he/she did not even know that shaking the child with the intention to make him stop crying can cause such serious injuries. in the case of healing with sequelae, the forensic physician will appreciate the existence of a physical or mental disability, the loss of a function (visual, auditory) and the level of functional deficit created because of the trauma. in cases of death of the victim, the forensic physician will not see, during an external examination, any signs or lesion due to violence, but he will discover serious internal lesions. as a rule, in all cases where a subdural hematoma is identified in a baby child, it is mandatory to examine and collect the eyeballs (through the endocranial orbital approach) for microscopic examination. it is recommended to examine the brain after putting it in 10% formalin for 3 weeks, to better identify the traumatic brain injuries. the examination of the fresh sample and its sectioning are difficult and predisposes to artifacts due to the low consistency of the brain in children of this age. the microscopic examination is mandatory to confirm the macroscopicallyobserved meninges, cerebral and ocular lesions, to diagnose the microscopic traumatic lesions, to attest their vital lesion character and to assess its age. fragments of cerebral substance from all areas with macroscopic lesion will be drawn. for the immunohistochemistry, samples from the white substance of both cerebral hemispheres, cerebellum, cerebral trunk, marrow, optic nerves, will be collected. usually, staining with hematoxylin-eosin is used, but perls staining is also useful in assessing the age of a hemorrhagic lesion because it highlights hemosiderin. the microscopic examination of the cerebral and medullary substance, and of the cranial nerves after immune marker for the beta-amyloid precursor protein (beta-app) or for neurofilament (68-kda neurofilament), positive techniques for axonal ruptures, but still hardly accessible in the forensic services in our country. the eyeballs will be examined after fixation in formalin and sagittal sections will be practiced, one of them continuing with longitudinal sectioning of the optic nerve. case report the emergency sheet revealed that the child was hospitalized for 35 minutes. at the hospital admission the child was having first degree coma, left eye = right eye, fixed mydriasis, corneal and deglutition reflexes were present, free airways, spontaneous breathing, physiological vesicular murmur, absent rales, cardiac sinusal rhythm, 80 beats romanian neurosurgery (2018) xxxii 3: 409 417 | 415             per minute heart rate. the craniocerebral ct scan revealed a parenchymatous hypodensity extended on the entire left hemisphere and also on the right frontal lobe paramedian on the right anterior carotid artery’s territory, significant collapse of the left lateral ventricle, subfalcine engagement of the median line structures, bilateral transtentorial engagement. a copy of the consultation sheet showed that the child was hospitalized for 17 hours and 44 minutes with the diagnosis of” massive cerebral infarct in the territory of the medium carotid artery, posterior carotid artery, left anterior carotid artery and right anterior carotid artery”. the patient’s reason for presentation: third degree coma, bilateral fixed mydriasis. the medical history showed that the child developed consciousness disorders apparently after a trauma through aggression. neurological examination: without active movements, areflexia (hyporeflexia), reactive exclusively to pain. local examination: right frontal localized excoriations at the internal and external angle of the left eye and at the left auricular concha; right laterocervical localized ecchymosis at thighs and buttocks bilateral. from the epicrisis of the observation sheet it turned out that the evolution was unfavorable with the installation of a non-reversible cardiorespiratory arrest at the resuscitation maneuvers and exitus. necroptic exam revealed: there was no investigation data at the time of the necropsy. after a through investigation of social data it appears that the minor was in the care of his grandmother with his other brothers. it also appears that the grandmother repeatedly applied "physical corrections" to him, striking him with the hands or hitting him with a strap. the last correction was applied by taking him to his shoulders and shaking him, then applying several strokes with her hand over baby’s head and body, then hit him with a rubber hose (for household use). immediately after this correction, the minor felt dizziness, lethargic, unable to keep his balance, reason why her grandmother sit him in the bed. six hours after the "correction", the child, who was sitting on the bed, fell aside, fed an insufficiently, drank water, and then fell asleep. two days after the "correction", the condition of the child got worse and the ambulance was announced. the body belongs to a male child, 89 cm in height, age-appropriate constitution, 2 years and 10 months old, with a known identity. macroscopically examination revealed multiple scratches: on the right frontal region, left eye internal and external angle, mandibularleft side, left laterocervical region; multiple ecchymosis with localization on the forearm and left hand, at the buttocks, thighs and calves. internal examination findings were: left hemisphere subdural hematoma 0.4 cm thick; cerebral edema; contusion and cerebral dilaceration at the base of left cerebral hemisphere. the anatomo-pathological microscopic examination establishes the following: focal inflammatory infiltration in leptomeninges, diffuse cerebral contusion, important edema in perivascular and pericelular spaces. due to the absence of high-intensity external cranial marks and the presence of traumatic brain injuries, in the provisional 416 | iov et al shaken baby syndrome             conclusions, the mechanism of production was established as a mechanism for shattering. later on, the mechanism for brain lesions (the subdural hematoma, the contusion and the cerebral dilaceration) was issued: it was possible to produce it most probably by vibrating cerebral substance in the sudden mobilization of the child’s body and head by another person, but it cannot be excluded repeatedly active blows to the head with or by blunt objects, if the investigation demonstrates this mechanism. the grandmother was assessed by forensic experts and psychiatrists. at the examination of the abuser it was concluded that the grandmother suffers from major depressive disorder with anxious phobic elements and preinvolutive background with reactive onset. the grandmother’s behavior creates the constitutive elements of the first degree murder and has been committed with discernment. conclusions the mechanism of producing craniocerebral lesions was most likely a hyperflexion followed by head hyperextension due to trauma to the neck that interested the left carotid artery; clarification of the mechanism was done with neurosurgeon specialists. neurosurgeon specialists have hypothesized about the whiplash injury cranio-cerebral lesion mechanism, which can explain brain contusion lesions associated with cerebral infarction lesions as a result of repeated traumatic lesions of the left carotid artery at the cervical level. because this type of trauma is produced as a result of lack of education in this respect, we appreciate that prevention measures are of paramount importance, with physicians taking the lead in these actions. consequently, even in maternity, doctors and nurses need to inform the parents of the little boy barely come into the world about the adverse consequences of shaking the child. massive campaigns over time in civilized countries, supported by the media, had the motto: "never shake the child!”. guidelines for parents are simple messages that aim to summarize the attitude to adopt in difficult times. because this type of trauma is produced as a result of lack of education in this respect, we appreciate that prevention measures have importance, doctors has the main role in these actions. therefore, even in maternity, doctors and nurses have to inform the parents of the little boy barely come into the world about the adverse consequences of shaking baby. correspondence anton knieling tony_knieling@yahoo.com references 1. caffey j. on the theory and practice of shaking infants. its potential resitual effects of permanent brain damage and mental retardation. am j forensic med pathology. 1972;22:112-122. 2. salehi-had h, brandt jd, rosas aj, rogers kk. findings in older children with abusive head injury: does shaken-child syndrome exist. pedriatics journal. 2006;117:1039-1044. 3. keean h et al. a population-based study of inflicted traumatic brain injury children. jama, the journal of the american medical association. vol. 290. 2006;290(5):621-626. romanian neurosurgery (2018) xxxii 3: 409 417 | 417             4. dias m et al. preventing abusive head trauma among infants and young children: a hospital – based, parent education program. pediatrics: official journal of the american academy of pediatrics. 2005;115(4):470-477/ 5. ioan bg. tanatologie medico-legală – note de curs. editura junimea. iaşi. 2007, p 55-56. 6. grigoriu c. repere în patologia medico-legală. editura junimea. iaşi. 2007, p.135. 7. plăhteanu m, baciu gh, pădure a. aspecte medicolegale lezionale în traumatologia mecanică. editura performantica. iaşi. 2004, p.164. 8. ciurea av, davidescu hb: traumatologie craniocerebrală. editura universitară „carol davila”. bucureşti. 2007, p. 287. 9. bulgaru-iliescu d. anomia microsocială – forme şi consecinţe. editura timpul. 2002, p 117-118. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article spontaneous regression of extruded lumbar disc herniation: case report and its pathogenesis prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmed faran india doi: 10.1515/romneu-2017-0065 romanian neurosurgery (2017) xxxi 3: 399 403 | 399 doi: 10.1515/romneu-2017-0065 spontaneous regression of extruded lumbar disc herniation: case report and its pathogenesis prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmed faran department of neurosurgery, dr rml ims, lucknow, up, india abstract: lumbar disc herniation is a common disease that present with back pain and radicular pain. the most efficient method for the treatment of lumbar disc herniation is still controversial. spontaneous regression of lumbar disc herniation has been recognized with the advancement of radiological diagnostic tools and can explain the reason of spontaneous relief of symptoms without treatment. the proposed hypothesis are; dehydration, retraction of the disc herniation in the annulus fibrosus, enzymatic catabolism and phagocytosis. in this study we present a case with large lumbar disc herniation regressing by itself and the potential mechanisms of disc regression have been discussed. key words: intervertebral disc herniation, spontaneous regression, pathogenesis introduction lumbar disc herniationis a common disease presenting with low back pain and radiculopathy. some cases require surgical treatment due to persistent severe pain however in other cases pain relieved with conservative treatment. this occurs as the result of decrease in pressure exerted from the herniated disc on neighbouring neuro structures and a gradual regression of inflammation. recently with advances in magnetic resonance imaging many reports have demonstrated that the herniated disc has the potential for spontaneous regression. regression coincided with the improvement of associated symptoms. however the exact mechanism for regression is remains unclear. here, we present a cases of lumbar disc herniation with spontaneous regression. we review the literature and discuss the possible mechanisms, the precipitating factors of spontaneous disc regression and the proper timing of surgical intervention. case report a 52 years old female patient presented with 5month history of back pain radiating in the left lower extremity. neurological examination showed no abnormality except a positive left straight leg raising test. mri 400 | prasad et al spontaneous regression of extruded lumbar disc herniation lumbosacral spine revealed a left posterolateral disc extrusion at l5-s1 level (figures 1a and 1b). patient was advised for surgery but she refused. conservative treatment including bed rest, physiotherapy, nonsteroidal antiinflammatory drugs, and analgesics was advised. patient was on regular follow up on opd basis. gradually patient improved within 5-6 months and after 6month repeat mri of lumbosacral spine was done. it showed regression of previously extruded disc at l5-s1 level (figures 2a and 2b). figure 1a mri lumbosacral spine saggital section showing extruded disc at l5-s1 level figure 1b mri lumbosacral spine axial section showing left paracentral disc herniation at l5-s1 level figure 2a repeat mri lumbosacral spine saggital section showing regression of previously extruded disc at l5-s1 level romanian neurosurgery (2017) xxxi 3: 399 403 | 401 figure 2b mri lumbosacral spine axial section showing regression of previous left paracentral disc herniation at l5-s1 level discussion lumbar disc herniation is one of the common cause of low back pain. conservative management including bed rest, oral antiinflammatory drugs, analgesics and physiotherapy is recommended for treatment of lumbar disc herniations [1]. surgical intervention is advised in the absence of resolution of symptom in two months or presence of cauda equina syndrome, motor weakness or progressive deficit while being medically managed [2]. the potential for regression of disc herniation had been occasionally reported and it leads to questioning of the choosing the treatment modality. although extensive documentations are found in the literature, the mechanisms proposed for regression of disc herniation are still incomplete. dehydration within the nucleus pulposus and shrinkage, a mechanical retraction of herniated disc material back into the annulus fibrosus, and enzymatic degradation and phagocytic reduction via immunohistologic mediators are three popular mechanisms assumed in the literature. the second mechanism mechanical retraction of the herniated disc is a theoretical assumption expected to occur when the disc herniation protrudes through the annulus fibrosus by preserving` anatomical relation. third mechanism which has been studied by many authors depends on a series of inflammatory responses of autoimmune system, including neovascularization, production of matrix proteinases, increasing of cytokines levels, enzymatic degradation, and macrophage phagocytosis [3]. pathogenesis histological studies had shown an inflammatory reaction around the herniated nucleus pulposus. local production of tnf alpha by schwann cells, endothelial cells, fibroblasts and mast cells attracts macrophages to the site of injury [4]. neovascularisation had also been reported at the edge of herniated nucleus pulposus. both inflammation and neovascularisation are thought to be required for phagocytosis. macrophage infiltration seems to be prominent in large disc herniations, as sequestrations have 2-3 times more inflammatory cells than extrusion type herniations[5]. neovascularisation is also most abundant in extrusions and sequestrations and is hindered by ligaments and/or annulus fibrosus. therefore it is seen 402 | prasad et al spontaneous regression of extruded lumbar disc herniation that both generalized and localized bulges have the poorest potential to regress. in other type of patients, in addition to mechanical compression, biochemical substances released by the disc, such as phospholipase a2 and nitric oxide, have been thought to play a role in nerve inflammation and pain which may persist after the resolution of disc herniation [6]. neovascularization in the outermost areas of herniated nucleus pulposus (hnp) presenting an enhancing rim in mr images, is thought to be a major determinant of spontaneous regression of hnp. at mr image, the neovascularization is easily detected by contrast enhancement. however the degree of neovascularization is varied. newly developed vessels in and around hnp play an important role in the wound healing process and resorption of hnp. neovascularization was observed at the periphery of the sequestrated discs. enhanced lesion at periphery of herniated disc is considered to represent inflammatory granulation. inflammatory cells are most commonly seen in the sequestrated type hnp. there was prominent infiltration of the inflammatory cells in the periphery of the extruded or sequestrated discs and most of them are macrophages. macrophages are observed only in the periphery of the disc fragments [7]. tumor necrosis factor (tnf)-α was the initiator of the inflammation, following contact between the macrophages and disc tissue. tnf-α could also act to accelerate the cascade of both angiogenesis and matrix degradation [8]. on reviewing the literature we found that thickness of rim enhancement is a more important factor to spontaneous regression than the extent of rim enhancement. when rim enhancement is present on enhanced mr images, there is a possibility of spontaneous regression even though the herniated mass may be located within the intradural space [9]. the ratio of reduction in size of enhancing lesions is even higher in t2 hyperintense herniations. the relatively-high water content can be the expression of soft, well-hydrated disc material or even an edema related to neovascularization and inflammatory reaction [10]. mr images are considered as a useful tool to predict the spontaneous regressive potential of hnp. spontaneous regression of disc is seen occasionally. therefore, non-surgical treatment can be another therapeutic option to treat hnp, when the patients did not want surgical treatment or if there is no neurological deficit. the presenting patient refuse surgical treatment and regression of disc is seen after conservative treatment. conclusion spontaneous regression of hnp is rare condition. conservative treatment may be an option if the patient did not wants surgical treatment and have no motor weakness, bladder symptoms and tolerable pain, even though the size of herniated disc is large. correspondence dr. hanuman prasad prajapati address: department of neurosurgery, dr rml ims, lucknow, up (india) mobile no.: 07727934104 email: pushpa84.dhp@gmail.com romanian neurosurgery (2017) xxxi 3: 399 403 | 403 references 1. macki m., hernandez-hermann m., bydon m., gokaslan a., mcgovern k., bydon a. spontaneous regression of sequestrated lumbar disc herniations: literature review. clinical neurology and neurosurgery. 2014;120:136–141. doi: 10.1016/j.clineuro.2014.02.013. [pubmed] [cross ref] 2. rahmathulla g., kamian k. lumbar disc herniations ‘to operate or not’ patient selection and timing of surgery. korean journal of spine. 2014;11(4):255–257. doi: 10.14245/kjs.2014.11.4.255. [pmc free article][pubmed] [cross ref] 3. guinto f. c., jr., hashim h., stumer m. ct demonstration of disk regression after conservative therapy. american journal of neuroradiology. 1984;5(5):632–633. [pubmed] 4. olmarker k & larsson k .tumor necrosis factor alpha and nucleus-pulposusinduced nerve root injury. spine 1998;23:2538-44. 5. ozaki s, muro t, ito s & mizushima m. neovascularisation of the outermost area of herniated lumbar intervertebral discs. j orthop sci 1999;4:286-92. 6. virri j, gronblad m, seitsalo s, habtemariam a, kappa e & karaharju e. comparison of the prevalence of inflammatory cells in subtypes of disc herniations and associations with straight leg raising. spine 2001;26:2311-5. 7. autio ra, karppinen j, niinimaki j, ojala r, kurunlahti m, haapea m, et al. determinants of spontaneous resorption of intervertebral disc herniations. spine (phila pa 1976) 2006;31(11):1247–1252.[pubmed] 8. ikeda t, nakamura t, kikuchi t, umeda s, senda h, takagi k. pathomechanism of spontaneous regression of the herniated lumbar disc: histologic and immunohistochemical study. j spinal disord. 1996;9(2):136–140. [pubmed] 9. kato t, haro h, komori h, shinomiya k. sequential dynamics of inflammatory cytokine, angiogenesis inducing factor and matrix degrading enzymes during spontaneous resorption of the herniated disc. j orthop res. 2004;22:895–900. [pubmed] 10. splendiani a, puglielli e, de amicis r, barile a, masciocchi c, gallucci m. spontaneous resolution of lumbar disk herniation: predictive signs for prognostic evaluation. neuroradiology. 2004;46:916–922.[pubmed] doi: 10.33962/roneuro-2021-016 the effect of long-term subgaleal drain retention (for 14 days) in preventing cerebro-spinal fluid (csf) fistula development in cases with an insufficiently closed dural defect after craniotomy or craniectomy umit kocaman, hakan yilmaz romanian neurosurgery (2021) xxxv (1): pp. 98-102 doi: 10.33962/roneuro-2021-016 www.journals.lapub.co.uk/index.php/roneurosurgery the effect of long-term subgaleal drain retention (for 14 days) in preventing cerebro-spinal fluid (csf) fistula development in cases with an insufficiently closed dural defect after craniotomy or craniectomy umit kocaman1, hakan yilmaz2 1 izmir cigli region education and research hospital, department of neurosurgery, izmir, turkey 2 university of health sciences, izmir bozyaka education and research hospital, department of neurosurgery, izmir, turkey abstract purpose: our aim was to determine the effectiveness of long-term subgaleal drain retention in preventing csf fistula development that may occur in the wound site when the dura cannot be completely closed after craniotomy or craniectomy. material and method: this study was planned to include the cases of craniotomy and craniectomy performed at bakırcay university cigli training and research hospital during 2017-2021. the study has been made in a retrospective manner to include a subgaleal drain group and a control group. both groups were selected from bakırcay university cigli training and research hospital. a subgaleal drain was placed in 18 cases with a large or multiple defect after craniotomy or craniectomy where the defect could not be completely closed with grafts. it was planned to be kept in place for 14days with free drainage. patients were administered antibiotics for three days after the surgery. patients were monitored for csf fistula and infection development. on the other hand, 12 patients having large dural defect were included in the control group. patients in the control group were determined by a random selection method. patients were followed for 2 days under subgaleal drainage. the control group was also monitored for csf fistula and infection development. both groups statistically were compared with each other in terms of csf fistula and infection development. results: there were 18 cases where the dura was closed insufficiently, long-term subgaleal drainage was performed. the mean age was 66.6 (34-82) years. the surgery performed was craniotomy/craniectomy for cerebellar hematoma drainage in 3 cases, acute subdural hematoma drainage in 5 cases, supratentorial tumour resection in 5 cases, large depression fracture in 4 cases and debridement of cerebral tissue damaged by firearm injury in 1 case. the drain was withdrawn at the end of the 14th day in all patients. a csf fistula did not occur in any of 18 patients (%0) included in the study. in all patients (%100), the wounds were healed without any problems and no signs of local or systemic infection were found. in the control group, the mean age is 62.2 (48-88) years. csf fistula developed in 4 (%33.3) of 12 patients keywords subgaleal drain, csf fistula, dural defect corresponding author: hakan yilmaz university of health sciences, izmir bozyaka education and research hospital, department of neurosurgery, izmir, turkey dr_hakanyilmaz@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 99 long-term subgaleal drain in preventing csf fistula in cases with dural defect after cranial surgery in the control group. we had to apply lumbal external drainage in 2(%50) of 4 patients with csf fistula. central nervous system infection developed in one (% 8.33) patient. conclusion: long-term subgaleal drainage can be used as an alternative to lumbar external drainage. introduction csf leakage is an important risk factor in cranial surgeries where the dura is opened. this risk may increase even further in cases requiring dural patches, those with history of diabetes mellitus, during surgery for meningioma that has invaded the dura and bones, and according to craniotomy localization [1]. csf leakage after craniotomy is directly related to intracranial infections [2]. conventional methods are currently successfully used to minimize csf fistula development. primary tight closure of the dura and patching with galeal graft, lata graft or allograft when necessary and providing support to the dural repair site with biological tissue adhesives are certain precautions that can be taken during the surgery. the most important established method after the development of an csf fistula is the resuturing of the wound area and simultaneous insertion of lumbar drainage [3,4,5]. external ventricular drainage can be used for csf fistula treatment in selected cases and when lumbar drainage is contra-indicated. we think that a subgaleal drain can be safely used as an alternative to lumbar drainage when the dura cannot be closed completely after craniotomy or when leak proof characteristics of the duraplasty are suspect. we share our results from the clinical experinces on this subject. material and method we included cases of craniotomy and craniectomy performed at bakırcay university cigli training and research hospital during 2017-2021 in this retrospective study. cases in which the dura had a large defect and could not be closed were investigated in the study. although duraplasty was performed with the aid of a galeal graft or dural patch, it had not been possible to ensure adequate closure. the subgaleal drain placed during surgery was therefore left for free drainage for 14 days. a 10 ch soft drain with a drainage bag was prefered as the subgaleal drain. the drain was always kept open and below the head level of the patient. daily wound dressing and drain care was performed. hemogram, sedimentation and crp were monitored every 3 days; daily 2x1g cefazolin was administered intravenously during 3 days. on the other hand, 12 patients having large dural defect were include to the control group. patients in control grup were determined by random selection method. the control group was followed for 2 days under subgaleal dranaige. control group was also monitered for csf fistula and infection development. the both groups statistically was compared with each other in terms of csf fistula and infection development. statistical analysis was performed with pearson’s chi-square test. figure 1. a case where the defect dural to firearm injury is too large that duraplasty cannot be made. figure 2. closure of the case using frontal flap and soft subgaleal drainage with 10 ch drainage bag. 100 umit kocaman, hakan yilmaz results there were 18 cases where the dura had a large defect and could not be closed and where subgaleal drainage was planned. the surgery performed was craniotomy/craniectomy for cerebellar hematoma drainage in 3 cases, acute subdural hematoma drainage in 5 cases, supratentorial tumor resection in 5 cases, large depression fracture in 4 cases and debridement of cerebral tissue damaged by firearm injury in 1 cases, the mean age of 18 patients included in the evaluation was 66.6 (34-82) years. there were 11 males and 7 females. duraplasty with a galeal graft had been attempted first, followed by a dural patch if that was not possible. however, adequate dura closure could not be ensured due to reasons such as dural tissue loss, dura maceration, cerebral edema, and damaged dura structure in traumatic cases. long-term subgaleal drainage was planned during operation in these patients. the subgaleal drain was withdrawn and closed with a single suture at the end of 14 days. a csf fistula did notdevelop in any patient (%0). suture removal was at the 7-10 days on average. local or systemic infection were not found in any of the cases (%0). in the control group, mean age is 62.2 (48-88) years. there were 7 males, 5 females. csf fistula developed in 4(%33.3) of 12 patients in control group. we had to apply lumbal external dranaige in 2(%50) of 4 patients with csf fistula. central nervous system infection developed in one (% 8.33) patient. the development of csf fistula is statistically significant in patients with long-term subgaleal drain use compared to the control group (according to pearson’s chi-square test; p:0.018). again, there is no statistically significant difference between the long-term subgaleal drain group and the control group in terms of preventing the development of central nervous system infection due to csf fistula (according to pearson’s chi-square test; p:0.400). discussion long-term subgaleal drainage provides time for wound site healing in cases where duraplasty is not possible due to a large dural defect. the drainage bag was kept just below the head level. we used long-term subgaleal drainage in 18 patients with a dural defect in this study. the lack of a csf fistula in the patients indicates that this is an effective and practical method. a study similar to ours was conducted in patients who underwent spinal surgery and had an iatrogenic dural tear. a subfascial drain was inserted for the patients who had csf leakage despite dura repair and wound healing was allowed. the drain was left for 15 days. none of the patients developed longterm drainage-related complications and no permanent csf fistula was observed [4]. another study evaluated 24 patients who had undergone posterior fossa surgery with a csf fistula. the csf fistula was treated with conservative treatment that required resuturing in only 2 of the patients and lumbar external drainage was used in 20 patients. two patients required ventriculoperitoneal shunt insertion due to hydrocephalus. the importance of lumbar external drainage with resuturing of the wound site in the treatment of a csf fistula was emphasized in that study [5]. we believe that subgaleal drainage could provide an alternative to lumbar external drainage. placing a subgaleal drain during surgery and conducting the follow-up with drainage from the beginning reduces the risk of csf fistula development while we are trying to treat a csf fistula that has already developed with lumbar external drainage. this may be an advantage of subgaleal drainage. there may also be a period of a few days when csf leakage is followedup with sutures while the flow continues after the csf fistula develops in patients with lumbar external drainage. the patient can also suffer from infections during this time. there is no such period with subgaleal drainage. another study compared infection rates in terms of meningoventriculitis development in patients who required lumbar external drainage (led) and external ventricular drainage (evd). the infection rates for evd and led were reported as 7.5 and 24.7 per 1000 evd and led days respectively. the meningoventriculitis rate was highest between the 4th and 9th days. they found evd not to be an important meningoventriculitis risk factor while led was among the major risk factors [3].furthermore, subgaleal drainage may have a lower infection risk as it is less invasive than evd. since both lumbar external drainage and subgaleal drainage are placed under sterile conditions, a significant risk may not occur as long as drainage care is performed regularly. we did not find any significant findings in terms of infection. some articles suggest replacement of external ventricular catheters every 101 long-term subgaleal drain in preventing csf fistula in cases with dural defect after cranial surgery 10 days [6]. a similar study was also conducted in spinal durotomy cases. a subfascial epidural drain was placed after primary repair and left for a mean period of 5.3 days for draining in these patients. a csf fistula did not develop in any patient and no excessive drainage occurred. it should be noted here that daily and careful monitoring of the drainage and wound dressing during long-term subfascial drainage follow-up is very important in terms of reducing the risk of infection. if signs of infection develop, the drain should be withdrawn, appropriate antibiotic treatment should be reviewed and repair with re-exploration considered. another study has reported that the prolonged subgaleal drainage and suture technique used to eliminate csf leakage and wound problems after decompressive craniectomy significantly decreases wound problems [7]. we would like to emphasize that long-term subgaleal drainage may be less invasive and more practical than led. led has several disadvantages. it is contra-indicated in some cases. it cannot be performed following cranial surgery for tumor resection and if there is a residual mass that can cause tonsillar herniation. led after surgery that may interrupt csf flow creates a risk of tonsillar herniation [8]. these risks do not seem to be present with subgaleal drainage. as the biggest disadvantage of the application is that we cannot know in advance whether a patient develops a csf fistula. we decided to extend the subgaleal drainage period in patients with one criteria. this is large dural defect despite duraplasty. our experince has shown that complete dural closure is not possible in some cases. in these cases, prolonging the subgaleal drainage time can give us time for wound healing. led is an invasive procedure. known complications that can develop during or after the procedure include spinal headache, spinal epidural hemorrhage, radiculopathy, epidermoid tumor formation, intracranial subdural hygroma or bleeding, vestibulo-cochlear dysfunction, ocular problems and dural sinus thrombosis [8]. these complications are not encountered with subgaleal drainage in practice. led can also lead to problems during the follow-up. too much drainage can result in serious morbidity and mortality. experienced ancillary healthcare staff are therefore required to monitor the lumbar drainage. the disadvantage of subgaleal drainage is the risk of csf leakage from drain path after the drain itself is removed. we used a compressive dressing after the removal of the drain and no csf fistula occurred in any of our cases. biological tissue adhesive can be applied to the drain route as an alternative as mentioned in the menovsky et al. study [9]. another study has reported biological tissue adhesive applied to sutures after primary dura repair to reduce the risk of csf fistula [1]. our study can clarify the following issue: the development of csf fistula is statistically significant in patients with long-term subgaleal drain use compared to the control group. conclusion long-term subgaleal drainage in preventing csf fistula development in cases with dural defect is a less invasive and more effective alternative to led with practical application and follow-up. there is no risk of infection if the drain is cared for properly. references 1. hutter g, von felten s, sailer mh, schulz m, mariani l. risk factors for postoperative csf leakage after elective craniotomy and the efficacy of fleece-bound tissue sealing against dural suturing alone: a randomized controlled trial. j neurosurg2014;121(3):735-44. 2. shi zh, xu m, wang yz, et al. post-craniotomy intracranial infection in patients with brain tumors: a retrospective analysis of 5723 consecutive patients. br j neurosurg2017;31(1):5-9. 3. scheithauer s, bürgel u, bickenbach j, et al. external ventricular and lumbar drainage associated meningoventriculitis:prospective analysis of timedependent infection rates and risk factor analysis. infection 2010;38(3):205-9. 4. osun a, samancioglu a, aydın t, mutlucan uo, korkmaz m, ozkan u. managing the cerebrospinal fluid leaks after spinal surgery by prolonged subfascial drainage. journal of neurological sciences [turkish] 2013;30(4):748-755. 5. altaf i, vohra ah, shams s. management of cerebrospinal fluid leak following posterior cranial fossa surgery. pak j med sci2016;32(6):1439-1443. 6. gulsen i, ak h, demir n, sosuncu e, arslan m. how frequently external ventricular drainage device should be changed in children with ventriculoperitoneal shunt infection? pak j med sci2015;31(2):435-8. 7. sughrue me, bloch og, manley gt, stiver si. marked reduction in wound complication rates following decompressive hemicraniectomy with an improved 102 umit kocaman, hakan yilmaz operative closure technique. j clin neurosci2011;18(9):1201-5. 8. mark s. greenberg, handbook of neurosurgery. seventh edition, thieme, 2010. 9. menovsky t, de vries j, bloss hg. treatment of postoperative subgaleal cerebrospinal fluid fistulas by using fibrin sealant. technical note. j neurosurg 1996;90(6):1143-5. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 387 390 | 387 acute spontaneous subdural hematomaas unusual complication after tooth extraction willem guillermo calderon-miranda1, nidia escobar hernandez2, luis rafael moscote salazar3, amit agrawal4 1department of radiology, universidad nacional autonoma de mexico, mexico 2department of radiology, neuroradiology, hospital general “dr. manuel gea gonzalez”, mexico 3department of neurosurgery, universidad de cartagena, cartagena de indias, colombia 4department of neurosurgery, mm institute of medical sciences & research, maharishi markandeshwar university, mullana-ambala, haryana, india abstract: background: intracranial bleeding has been reported in the literature associated with tooth extraction. coagulation disorders are often associated with complications after dental extraction. in this case report, we describe a case of spontaneously intracranial subdural hematoma possible after tooth extraction. case description: the patient was a 26-y-old female without any underlying diseases. a computerized tomography scan showed a subdural hematoma 48 hours after the dental extraction. she was managed with a burr hole, good postoperative evolution and discharged to home. conclusion: although rare, the presence of headache with signs of alarm after the extraction of a tooth, we must discard intracranial abnormalities. to the best of our knowledge this is the first report in the literature of a spontaneously intracranial subdural hematoma possible after tooth extraction. key words: subdural hematoma, tooth, bleeding; tooth extraction introduction the intracranial subdural hematomas usually have a history of trauma, rarely described spontaneous bleeding. (1-3) the bleeding episodes associated with tooth extraction have been described in patients with use of anticoagulation. (4, 5) occurrence of spontaneous subdural hematoma following dental extraction has not been reported in the english literature. here, we present a case of spontaneous intracranial subdural hematoma in a young patient after the extraction of a tooth. case report our patient is a 26-year-old female, developed headache of increasing intensity, nausea, and emesis 6hours of evolution. she had undergone a tooth extraction procedure 2 days before the onset of headache. at the time examination in the emergency room the patient was alert, oriented to person, place and date and 388 | calderon-miranda et al subdural hematoma after tooth extraction had no focal neurologic deficits. a computed tomography (ct) scan of the brain showed a left fronto-parietal subdural hematoma (figures 1, 2 and 3). the patient coagulation profile was normal. the patient underwent burr hole evacuation of the subdural hematoma. the patient did well and discharged on post admission day 4. at the time of discharge patient was relieved of headache. figure 1 noncontrast ct of the brain demonstrating a left fronto-parietal subdural hematoma figure 2 contrast ct of the brain demonstrating a fronto-parietal left subdural hematoma with minimal medial enhancement figure 3 – ct angiogram of the brain showing normal blood vessels romanian neurosurgery (2016) xxx 3: 387 390 | 389 discussion we describe an unusual case of subdural hematoma subsequent to the extraction of a tooth. several factors are cited as causes, the most common cause head trauma, chronic alcoholism and anticoagulation. (6-8) in general, we can establish two groups of patients in terms of age, under 65 years and older, representing the age distribution in 20% and 80%, respectively. (6-8) the treatment options for these lesions depend on the clinical presentation and size of the lesions and ranges from observation alone, to the use of different types of drugs and surgical evacuation in symptomatic cases. (6-8) given the pathophysiology possibly the best option is the emptying of the collection. conservative treatment is based on the osmotic theory of formation and growth of hsc, by parenteral administration of hyperosmolar substances, which tend to reduce absorption, the volume of the hematoma. (6, 8) in our case the patient presented with severe headache and responded well to surgical management with good results. in geriatric population, the trauma is most frequent, and become significant if associated with other comorbidities such as diabetes mellitus, end-stage renal disease, hypertension, cerebrovascular disease, neurodegenerative diseases, anticoagulant or antiplatelet therapy; the latter are found much less frequently in patients younger than 65 years, however, consider that these are involved in events traumatic violent, more trivial events, so you might expect a different clinical presentation in both groups. it has been suggested that alcohol chronically by cortical atrophy, coagulopathy secondary to chronic liver damage and most probably favor risk of head trauma injury. in the literature it is present between 10 and 50% of cases. other causes are described primary tumors, metastases or vascular malformations, among others. (9-12) naama et al. (13) reported two cases who presented with acute signs of intracranial hypertension secondary to a spontaneous acute subdural hematoma in which spontaneous bleeding from a small cortical artery was seen during operation. it has also been described subarachnoid hemorrhage after tooth extraction. (14) conclusion intracranial bleeding after dental extractions are rare phenomena and have been described very few cases. we report a patient who developed a spontaneous subdural hematoma possible after the extraction of a tooth, without presenting coagulopathy. our case illustrates the phenomenon of developing an intracranial subdural collection after dental procedures and suggest that any patient with headache and warning signs, it must be studied with complementary imaging tests. correspondence dr. luis rafael moscote-salazar e-mail: mineurocirujano@aol.com references 1.arnold pm, christiano ld, klemp ja, anderson kk. nontraumatic spontaneous acute subdural hematoma in identical teenage twins 1 year apart. pediatr emerg care 2011;27:649-651. 390 | calderon-miranda et al subdural hematoma after tooth extraction 2.chhiber s, singh j. acute spontaneous subdural hematoma of arterial origin: a report of four cases and review of literature. neurology india 2010;58:654. 3.martins wa, teixeira ab, frigeri tm, paglioli e. spontaneous subdural hematoma associated to duret hemorrhage. interdisciplinary neurosurgery 2015;2:13-15. 4.abdullah wa, khalil h. dental extraction in patients on warfarin treatment. clin cosmet investig dent 2014;6:65-69. 5.naganawa t, sakuma k, kumar a, fukuzawa s, okamoto t, ando t. intracranial hemorrhage after tooth extraction in a patient with chronic disseminated intravascular coagulation. journal of oral and maxillofacial surgery, medicine, and pathology 2015;27:854-857. 6.dumont tm, rughani ai, goeckes t, tranmer bi. chronic subdural hematoma: a sentinel health event. world neurosurgery 2013;80:889-892. 7.foelholm r, waltimo o. epidemiology of chronic subdural haematoma. acta neurochirurgica 1975;32:247250. 8.karibe h, kameyama m, kawase m, hirano t, kawaguchi t, tominaga t. [epidemiology of chronic subdural hematomas]. no shinkei geka neurological surgery 2011;39:1149-1153. 9.carter g, goss an, lloyd j, tocchetti r. current concepts of the management of dental extractions for patients taking warfarin. australian dental journal 2003;48:89-96. 10.devani p, lavery km, howell cjt. dental extractions in patients on warfarin: is alteration of anticoagulant regime necessary? british journal of oral and maxillofacial surgery 1998;36:107-111. 11.salam s, yusuf h, milosevic a. bleeding after dental extractions in patients taking warfarin. british journal of oral and maxillofacial surgery 2007;45:463-466. 12.stiefelhagen p. stroke after tooth extraction. mmw fortschritte der medizin 2009;151:17. 13.naama o, belhachmi a, ziadi t, et al. acute spontaneous subdural hematoma: an unusual form of cerebrovacular accident. journal of neurosurgical sciences 2009;53:157-159. 14.mamedov rt, bakhmudov br. subarachnoid hemorrhage occurring as a complication after tooth extraction. stomatologii ͡a 1993;72:81. 13kumarr_thoracic spine romanian neurosurgery | volume xxx | number 4 | 2016 | october december article thoracic spine stab injury with pneumocephalus and pneumorrhachiasis: a unique case report and review of literature rakesh kumar, radhey shyam mittal, ashok gandhi india doi: 10.1515/romneu-2016-0085 530 | kumar et al thoracic spine stab injury with pneumocephalus and pneumorrhachiasis doi: 10.1515/romneu-2016-0085 thoracic spine stab injury with pneumocephalus and pneumorrhachiasis: a unique case report and review of literature rakesh kumar1, radhey shyam mittal2, ashok gandhi3 1assistant professor, department of neurosurgery, king georges medical university, lucknow, uttar pradesh, india 2professor and head of department, department of neurosurgery, sawai man singh medical collage, jaipur, rajasthan, india 3associate professor, department of neurosurgery, sawai man singh medical collage, jaipur, rajasthan, india abstract: trauma to skull base or sinus is the most common cause of pneumocephalus. there are only few published reports of traumatic pneumocephalus secondary to penetrating injury of upper spine, epidural anaesthesia and lumber puncture. till date only one case of pneumocephalus and pneumorrhachiasis after thoracic spine stab injury is reported in available english literature that too associated without any neurological deficit. to our knowledge, this is the first reported case of pneumocephalus and pneumorrhachiasis after thoracic spine stab injury with asymmetrical, incomplete spinal cord injury leading to neurological deficit in the patient. the management protocol of such injuries needs to be individualised for better outcome. key words: stab injury, thoracic spine, pneumocephalus, pneumorrhachiasis, spinal injury introduction stab injury is one of the most common varieties of civilian injuries. pneumocephalus with pneumorrhachiasis and spinal cord injury after spine stab injury is a very rare entity. the subarachnoid space in the brain and spinal cord is continuous, thus air may ascend from the spine into the cranial subarachnoid space producing pneumocephalus. till date only one case of pneumocephalus and pneumorrhachiasis after thoracic spine stab injury is reported in available english literature that too associated without any neurological deficit. (1) the present paper reports a unique case of pneumocephalus and pneumorrhachiasis with spinal cord injury after thoracic spine stab injury associated with neurological deficit romanian neurosurgery (2016) xxx 4: 530 – 535 | 531 along with review of literature. patient was managed conservatively with good recovery. case report a 25 year old gentleman was admitted to the department of neurosurgery with the history of assault. patient had stab injuries over chest and back and developed weakness in lower limbs and retention of urine following this incident. there was no history of loss of consciousness, vomiting or ent bleeding. on physical examination, his vitals were normal. on motor examination there was bilateral foot drop with right ankle and toes power grade zero. in left ankle and toe dorsiflexion was 0/5 and planter flexion was 3/5.rest of the muscle groups power was 5/5. on sensory examination, there was approximate 50% loss of touch, temperature and pain sensation below l 3 dermatome in right and below l 4 dermatome in the left side. there was absent ankle jerks and planter was mute bilaterally. superficial abdominal reflexes were present. there were sutured stab wounds over left anterior chest wall and back at d11 and d12 vertebra level. no csf leak was noticed from the back wound. in initial radiographs of chest and dorsolumbar spine no abnormality was detected. ct scan of chest and abdomen revealed bilateral minimal haemothorax. ct scan of dorsolumber spine revealed mild anterior wedging of d 11 vertebra, fracture of left pars interarticularis and left pedicle of d12 vertebra without any displacement (figure 1a). on detailed observation of axial cuts of ct chest droplets of air were present intradurally at d 12 level suggestive of pneumorrachiasis (figure 1b). for further evaluation of spinal cord injury mri of dorsolumber spine was advised which revealed hyper intense area in spinal cord at upper border of d12 vertebrae and no cord compression. there was no air bubble seen in the mri as contrast to the ct scan presentation which may be due to the resolution of air bubble by day 4 when mri was taken (figure 2). since patient complained of persistent headache and pneumorrachiasis was also present, ct head was done which revealed pneumocephalus with presence of air in prepontine, perimesenchephalic cisterns, left temporal and right frontal horn of lateral ventricle (figure 3a). patient was managed conservatively along with regular chest and limb physiotherapy. broad spectrum antibiotics and anticonvulsants were also administered. patient gradually improved and headache disappeared within 7 days. repeat ct scan of head on 7th day showed resolved pneumocephalus (figure 3b). he was discharged from the hospital with assured follow-up. his motor weakness did not improve during the hospital stay although sensory dysfunction gradually improved and at the time of discharge he had decreased sensation below s1 dermatome. patient sensory deficit improved on four months follow-up. his bladder function and motor power in bilateral lower limbs improved significantly at fourteen months follow-up. the power in bilateral lower limbs at ankle and toes was grade 4/5. patient was able to walk without support. 532 | kumar et al thoracic spine stab injury with pneumocephalus and pneumorrhachiasis figure 1 sagittal spinal ct image revealing undisplaced fracture of parsinterarticularis and pedicle of d12 vertebra (1a) and axial chest ct scan showing intradural droplet of air at d12 vertebra level (1b) figure 2 mri dorsolumbar spine showing hyper intense signal in spinal cord at upper border of d12 level without cord compression romanian neurosurgery (2016) xxx 4: 530 – 535 | 533 figure 3 initial axial plain ct head revealing pneumocephalus with presence of air in basal cistern and left temporal horn of lateral ventricle(3a) and repeat ct scan of head on 7th day showed resolved pneumocephalus(3b) discussion spinal cord injury following stab injury is a rare occurrence. peacock et al (2) ( 1977) in his largest review of 450 cases of spinal stab injuries found knife as most common (84.2%) weapon used and thoracic segments (63.8%) are involved mostly. they found complete spinal cord injury in 20.9% of cases. brownsequard type of hemisection was most common type (55.11%) in incomplete spinal cord injury. (3) lipschitz and block (1962) (4) postulated three mechanism of spinal cord injury in stab injury. the spinal cord may be injured directly or indirectly by indriven bone fragments, by damaging the vascular supply to the spinal cord with resulting edema or by damaging the cord due to concussion or contusion resulting from counter coup spinal cord injury. traumatic pneumorrhachis is a rare finding. the subarachnoid space in the brain and spinal cord is continuous, thus air may ascend from the spine into the cranial subarachnoid space producing pneumocephalus. (1) pneumocephalus develops in about 78% of patients with traumatic pneumorrhachis. (1) three case reports of pneumocephalus following penetrating injury of cervical spine, (3, 5, 6) and one case of pneumocephalus following penetrating injury to lumbar spine are reported in available english literature. (7) till now, only one case of pneumocephalus and pneumorrhachiasis without neurological deficit after thoracic spine stab injury is reported. (1) to our knowledge, this is the first reported case of pneumocephalus and pneumorrhachiasis with spinal cord injury after thoracic spine stab injury associated with neurological deficit. entrance of air into the intracranial subarachnoid space is thought to be due to one of the following two mechanisms, first drop in intracranial pressure causing a vacuum effect which results in an influx of air with 534 | kumar et al thoracic spine stab injury with pneumocephalus and pneumorrhachiasis respiration and coughing or secondly by a valve like effect at the wound site that allows air only to enter into subarachnoid space but not to exit. (3, 5) in the first reported case of a knife stab wound causing pneumocephalus, naseem et al (1986) (6) also proposed that a drop in intracranial pressure from cerebrospinal fluid leak creates a vacuum that subsequently allows the influx of air into the subarachnoid space which causes pneumocephalus. pneumorrhachis is usually asymptomatic and is primarily a radiographic and not a clinical diagnosis. the presentation of pneumocephalus is often vague and nonspecific. the patient may complain of headache, nausea, vomiting, lethargy and altered state of consciousness and may show signs of meningism. the diagnosis of pneumocephalus following spinal stab injury is often unsuspected and made only after a cranial ct scan. the initial management of spinal cord injury caused by stab wound consists of local wound debridement, primary closure of the wound and intravenous administration of antibiotics to prevent cns infection. (8) indications for operative intervention are retained foreign body, persistent csf leakage, and sepsis. stab wounds involving cauda equina roots require special attention and exploratory laminectomy is often indicated in such cases. even after a delay of many years, operations on adherent and partially severed cauda equina roots may sometimes results in useful functional recovery. (9) complete spinal cord injury having poor prognosis, but in partial lesions, especially with brown-sequard syndrome type of injuries good functional neurological recovery occurs usually. (2) in the largest reported series of 450 cases of stab injuries of spinal cord, 65.6% of cases has good recovery, in 17.1% cases recovery was fair and in 17.3% cases there was no significant recovery (2). no empiric guidelines for the treatment of pneumorrhachis and standards of care exist due to its rareness and the different etiopathogenesis. therefore, the conditions causing pneumorrhachis has to be evaluated and the contributing causes have to be appropriately treated. tension pneumorrhachis and pneumocephalus with nervous tissue compression may require intervention. treatment of pneumocephalus depends on the patient condition, the extent and progression of the air collection, and the etiology. careful clinical monitoring and serial ct scanning of the brain following the procedure is recommended. our patient had asymmetrical neurological involvement of the spinal cord without neural compression or cord laceration with small pneumocephalus that is why after thorough examination of the patient and evaluation of the ct and mri scans, he was managed with conservative approach and had good recovery. conclusions stab injuries are one of the most common injuries which we come across in our day to day practice. pneumocephalus and pneumorrachiasis with spinal cord injury following stab injury in thoracic spine is a rare and very unusual presentation. early and romanian neurosurgery (2016) xxx 4: 530 – 535 | 535 accurate diagnosis based on clinical examination and radiology is essential for this rare injury. because of the rareness of the case, management protocol of such injuries must be individualized for better outcome and better recovery of the patient. correspondence dr. rakesh kumar mailing address: 4kh 2,shastri nagar jaipur, rajasthan, india 302016. email address – rksingh2226@gmail.com. phone number – 91 –9984540111, 9667652170. fax number: 0141-2566484 references 1.tejirian t., gabikian p., petrosyan m.,demetriades d. pneumocephalus after penetrating thoracic trauma; case report and review of literature.j.trauma.2009;67:507512. 2.peacock wj, shrosbree rd, key ag. a review of 450 stabwounds of the spinal cord. s afr med j. 1977;51(26): 961-964. 3.bunc g, roskar z, vorsic m. pneumocephalus secondary to a neck stab wound without neurologic injury in a 13 year old girl. peadiatr neurosurg.2001;34:239-241. 4.lipschitz r, block j. stab wound of the spinal cord.lancet,july.1962;28:169. 5.uppot rn, vinay gk, gould sw, hirohiko i. pneumocephalus and brown-sequard’s neurologic injury caused by a stab wound to the neck. ajr.1999:173;1504 6.naseem m. hood jd. devasthali r. traumatic pneumocephalus caused by stab wound to the neck. ajnr 1986;7:174—175. 7.valente ma, bender ea. severe pneumocephalus after penetrating injury to the lumbar spine.ijcri 2012;3(4):23-25. 8.hwan ml, nam hk, chang ii p.spinal cord injury caused by a stab wound-a case report.yonsei med j. 1990;31(3): 280-284. 9.landau b and ransohoff j.journal of neurosurgery.1968;28:257. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article real-time patency verification during clipping aneurysm and sta-mca by-pass with dualimage videoangiography riki tanaka, anton shatokhin, ilya senko, ishu bishnoi, treepob sae-ngow, yasuhiro yamada, daisuke suyama, tsukasa kawase, yoko kato, ahmed ansari japan doi: 10.2478/romneu-2018-0005 romanian neurosurgery (2018) xxxii 1: 35 39 | 35 doi: 10.2478/romneu-2018-0005 real-time patency verification during clipping aneurysm and sta-mca by-pass with dual-image videoangiography riki tanaka, anton shatokhin, ilya senko, ishu bishnoi, treepob sae-ngow, yasuhiro yamada, daisuke suyama, tsukasa kawase, yoko kato, ahmed ansari department of neurosurgery, fujita health university banbuntane hotokukai hospital, nagoya, japan abstract: the dual-image videoangiography (diva) is a new tool which helps identify ves-sels and surrounding structure. this method is based on use of indocyanine green video angiography (icg-va) technology on real time microscopic operative image. in this two case, we report of using diva in sta-mca bypass surgery of 46 years old, female patient of stenosis of right mca. and using diva during clipping ica paraclinod aneurysm of 35 years old, female. during surgery, it helped in identifying temporal and frontal branches of the sta and there careful selection. after anastomosis, diva was used to refine vessel patency and functioning of the anastomosis. diva has the potential to replace icg-va as a tool for checking the patency of graft during bypass procedures and obliteration of aneurysm along with surgical procedures for avm and d-avf. diva allows visualization of vessels against a background of normal brain and has better visualization at greater depth and high magnification. this is particularly important during bypass surgery, which very often is performed in deep surgical fields and high magnification. key words: diva, icg, sta-mca bypass, aneurysm introduction during microvascular surgery, it is of utmost importance to observe blood flow for checking complete occlusion of aneurysm, intact flow through the parent vessels and non-occlusion of perforating arteries, ensuring patency of bypass vessels and understanding the microsurgical anatomy of arteriovenous malformations (avm) and dural arteriovenous fistula (davf) [1–3]. neurovascular surgeon has various modalities in his armamentarium like doppler ultrasonography, indocyanine green video angiography (icg-va), conventional angiography and endoscopic visualization. the latest addition in this field is dual image 36 | tanaka et al patency verification during clipping aneurysm and sta-mca by-pass videoangiography by sato et al.[4]. it enables the simultaneous visualization of both light and near-infrared (nir) fluorescence images of icg-va. we used diva during bypass surgery on a patient with mca arteritis, and during clipping aneurysm on patient with acoa aneurysm, and we evaluated its potentials as an adjunct to conventional icg-va. materials and methods microscope and diva system: the opmi pentero flow 800 intraoperative microscope (carl zeiss meditec, jena, germany) was used for the operations. the near-infrared color camera minirc-2000k (mizuho, japan. 48mm x 48mm x 119mm; 0.3kg) was mounted on the pentero microscope in order to visualize diva during surgery. the operative field was illuminated via an operating microscope by halogen and xenon lamps with a filter to eliminate wavelengths over 780 nm. in the cam-era unit, visible light was filtered to 400– 700 nm and nir fluorescence emission light was filtered to 800–900 nm using a special sensor unit with an optical filter. light and nir fluorescence images were simultaneously visualized on a single monitor. we bolus injected icg 0.3 mg/kg body weight systemically. case report first case 46-year-old female patient was admitted to our department be-cause of a transient ischemic attack with left paresthesia and facial paralysis. the neuroradiological workup as suggestive of mca arteritis (figure 1). she suffered three transient ischemic attacks (tia) involving right mca territory in last one year. ct and mri angiography confirmed stenosis of the right mca. an stamca bypass surgery was therefore scheduled for revascularization of the right hemisphere. she underwent surgery right side sta-mca bypass after informed consent. diva initially was used during surgery to identify temporal and frontal branches of the sta and there careful selection. after the craniotomy, right mca branches (m4) frontal and temporal were identified and prepared. then the two branches of sta were anastomosed with frontal and temporal branches of mca individually. diva was used to refine vessel patency and functioning of the anastomoses. it revealed insufficient blood flow in the arteries of the donor. we did mechanical restoration of blood flow by milking of sta branches without switching off the diva mode (figure 2). postoperatively mri angiography confirmed the patency of anastomoses (figure 3). the patient’s neurological symptoms regressed in the early postoperative period and patient was discharged without any complications. second case 35-year female patient came with complaint of headache. the ct-ag detected unruptured ica paraclinoid aneurysm. she was operated by left pterional craniotomy and transsylvian approach. after distal dissection of lateral fissure, we used diva to visualize ica and optic nerve (figure 4). it helped in identifying relation between aneurysm and left optic nerve. after clipping aneurysm, we used diva again for checking patency of artery and decompression of optic nerve from aneurysm (figure 5). there was no postoperative complication. romanian neurosurgery (2018) xxxii 1: 35 39 | 37 suppl 2: 246–251; discussion 251 figure 1 preoperative 3d ct-ag show stenosis right mca m1 a b figure 2 surgical view icg videoangiography and diva at the time of operation. icg showing black and white color, that’s why the unfilled part of sta branch appears similar to brain i.e. black. while diva is showing unfilled part of sta branch as a normal vessel present over brain, because of ability to show colored anatomical structures figure 3 postoperative mri-ag shows excellent patency of anastomosis and right mca a b figure 4 a real intraoperative image shows left ica paraclinoid aneurysm and optic nerve. b diva image of same aneurysm showing compression of optic nerve by aneurysm (arrow) a b 38 | tanaka et al patency verification during clipping aneurysm and sta-mca by-pass a b figure 5a real intraoperative image shows clipped left ica paraclinoid aneu-rysm. b diva image of same clipped aneurysm showing no flow in aneurysm and decompression of optic nerve (arrow) discussion rabbe et al. described the utility of icg-va for neurovascular surgeries in 2003[1]. subsequently there has been widespread use of icg-va in neurovascular surgeries throughout the world. one drawback of icgva is that we cannot observe the surrounding structures including clip position as icg-va only gives a vision of near infra-red (nir) fluorescence images showing the vessels in a black background. diva as reported by sato et al.[4] gives normal impression of the vessels in original color initially, followed by vessels highlighted in green as the dynamics of blood flow changed from an “inflow” to “washout”. intracerebral bypass microsurgery requires not only advanced technical skills in microsuturing, but also reliable tools in order to evaluate the vessels patency. icg-va is routinely used with this purpose, and has proven to be very useful in supporting the vascular neurosurgeon. apart from the drawback of icg-va mentioned above, the other potential limitations of icgva are suboptimal visualization in deep operative fields and high magnification [5]. also at times, it is difficult to visualize and differentiate the deep located perforators from the aneurysm neck. diva as a combination of tools provides real time simultaneous visualization of vessels and surrounding structures. green color used in diva, serves as a contrast for vessels which are red (arteries) and blue (veins) against a normal brain background, diva makes it easier to understand anatomical relations between intracranial structures. the volume of dye essentially re-mains same as that used for icgva. we have recently started using diva during cerebrovascular surgeries. we concur with the findings of sato et al. that di-va gives better resolution of vessels at depth and under high magnification, courtesy to the highresolution video system and hence is an excellent tool for bypass procedures which is often performed at depth and under high resolution. diva suffers from the same limitation of icg-va, i.e. vascular structures not exposed in the operative field can’t be romanian neurosurgery (2018) xxxii 1: 35 39 | 39 visualized. moreover, it gives a better vision of the depth of field. it can have an impact in decision-making during surgery. conclusion diva has the potential to replace icg-va as a tool for checking the patency of graft during bypass procedures and obliteration of aneurysm along with surgical procedures for avm and d-avf. diva allows visualization of vessels against a background of normal brain and has better visualization at greater depth and high magnification. this is particularly important during bypass surgery, which very often is performed in deep surgical fields and high magnification. references 1. raabe a, beck j, gerlach r, zimmermann m, seifert v. near-infrared indocy-anine green video angiography: a new method for intraoperative assessment of vascular flow. neurosurgery 2003;52:132–139; discussion 139. 2. akdemir h, oktem is, tucer b, menkü a, başaslan k, günaldi o. intraopera-tive microvascular doppler sonography in aneurysm surgery. minim invasive neurosurg min 2006;49:312–6. 3. anegawa s, hayashi t, torigoe r, harada k, kihara s. intraoperative angi-ography in the resection of arteriovenous malformations. j neurosurg 1994;80:73–8. 4. sato t, suzuki k, sakuma j, takatsu n, kojima y, sugano t, saito k.: de-velopment of a new highresolution intraoperative imaging system (dual-image videoangiography, diva) to simultaneously visualize light and near-infrared flu-orescence images of indocyanine green angiography. acta neurochir (wien). 2015 sep;157(8):1295-301. 5. zaidi h.a., abla a.a., nakaji p, chowdhry s.a., albuquerque f.c., spetzler r.f.. indocyanine green angiography in the surgical management of cerebral arteriovenous malformations: lessons learned in 130 consecutive cases. neurosurgery 2014;10 05 05tanakariki_realtime flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article kinked and retained nasogastric tube in polytrauma patient; a case report ashok kumar, vardan kulshreshtha, pavan kumar, gaurav jaiswal, tarun kumar gupta india doi: 10.1515/romneu-2017-0041 244 | kumar et al kinked and retained nasogastric tube in poly trauma patient doi: 10.1515/romneu-2017-0041 kinked and retained nasogastric tube in polytrauma patient; a case report ashok kumar1, vardan kulshreshtha1, pavan kumar1, gaurav jaiswal2, tarun kumar gupta3 1senior residents, 2associate professor, 3professor department of neurosurgery, rnt medical college, udaipur, india abstract: enteral feeding is an important and preferred technique of feeding in head injury patient to provide nutrition. as inadequate nutrition causes decrease in physical ability, neurological impairment and takes a long time for improvement or delayed deterioratation. with our best knowledge kinked and retained nasogastric tube in stomach is a very rare complication of feeding in head injuries patients. predisposing factors that can cause kinking is excess tube length, tube in situ for long time and small bore tube. we are reporting one such case of kinked and retained nasogastric tube in the stomach of a polytrauma patient which was retrieved by upper gi endoscope. key word: nasogastric tube, kinked, retained, g i endoscopy introduction nutritional support constitutes an important issue in intensive care for critically ill patients. however, it is generally neglected and underestimated in the subgroup of tbi population. in the recent most important trials in nutrition, casaer et al. only included 0.6% of patients with neurological diseases (1). enteral nutrition is clearly established as the preferential route of nutrition support for this population verses parenteral nutrition. there appears to be a consensus on early initiation of enteral nutrition. adequate nutritional support in tbi is essential to provide the optimal milieu for neurological and systemic recovery. despite various studies in tbi, “what, when, and how’ of nutritional replacement remains elusive. nutrition therapy should start early within 24 to 48 hours of admission to the intensive care unit. the feeding should be adjusted based on the patient’s nutritional requirements over the next 48 to 72 hours (2). american association of neurological surgeons’ (aans) guidelines the recommended full nutritional replacement to be instituted by the seventh day. cochrane collaboration reviews have suggested that nutrition therapy may improve mortality and neurological outcomes (3). early feeding may be associated with a trend towards better outcomes in terms of survival and disability (4). enteral nutrition has many advantages over total parenteral nutrition (tpn), the latter being associated with several romanian neurosurgery (2017) xxxi 2: 244 247 | 245 complications (5). the weighted average mortality for severe tbi is 39%, and for unfavorable outcome is 60% on the glasgow outcome scale (6). case report a 15 year female patient admitted in department of neurosurgery as a follow up case of head injury with chest injury with blunt trauma abdomen. he sustained injury due to fall from tree 2 month back, at time of admission gcs was e1v1m4 and pupillary anisocoria present, right pupils was 2mm nonreactive and left pupil was 4mm nonreactive, clinically multiple ribs fracture present and surgical emphysema over right side of chest. patient intubated and simultaneously intercostals drainage tube was inserted. after stabilizing the patient cect chest and abdomen and ncct head done, cect chest and abdomen revealed multiple ribs fracture with hemothorax left side, liver laceration, while ncct head revealed a small intracranial hemorrhage in frontal area along the falx and small subdural hematoma at frontal convexity (figure1). patient kept on ventilator and on 2nd day tracheotomy was done. patient was managed conservatively and subsequently weaned from ventilator and tracheostomy decanulated and discharged with satisfactory general condition after 21 days with nasogastric tube in situ with follow up advice. patient presented for follow up after 2 weeks period. we tried to change the nasogastric tube but it was not possible for which pt was shifted to gastroenterology department and upper gi endoscopy done. it revealed kinking of nasogastric tube and densely adhered with its side eyelets (figure 2). distal end of tube was held by grasper and proximal end was pulled, this procedure repeated many time because tube in side stomach was become hard which was causing slippage from grasper, finally it was detached from point of contact at eyelets and was pulled out judicially (figure 3). figure 1 ncct head: frontal ich along the falx and thin sdh along bi-frontal convexity 246 | kumar et al kinked and retained nasogastric tube in poly trauma patient figure 2 kinked and adhered nasogastric tube figure 3 retrieved tube discussion complication of nasogastric feeding is well known, it has been found that nasogastric tube has functional and mechanical complication. the distal portion of ngt has multiple apertures (the weakest part) making it susceptible to kink, coil, and knot. tan m et, al. demonstrated the complications which appeared were: tube dislodgement (48.5%); electrolytic alterations (45.5%); hyperglycemia (34.5%); diarrhea (32.8%); constipation (29.7%); vomiting (20.4%); tube clogging (12.5%); and lung aspiration (3.1%) (7). de aguilar-nascimento and kudsk demonstrated that of 932 blind post pyloric tube placement attempts, (46%) failed and 20 (1.6%) were airway misplacements (8). montejo et, al. found that 251 patients (63%) experienced one or more gi complications during their feeding course. yung-fong tsai et, al. conducted study that insertions using smaller size ngts or softer silicone stomach tubes have more kinking (9). although an apparently innocuous and simple procedure, ngt insertion is essentially an invasive procedure and often needs repetitive attempts which may result in adverse events such as kinking, knotting, bleeding, false passage; sometimes the attempts end in failure. (10) we reported this case to bring this rare presentation of kinked and retained nasogastric tube in such patients. conclusion a multidisciplinary approach should be performed in head injury patients to provide adequate nutrition, energy and electrolyte. kinking of nasogastric tube are rare condition and have been described very few cases. one of the common causes of complication of nasogastric feeding is unawareness and ignorance of tube feeding. nasogastric feeding most widely used for feeding purpose in head injury patients but the great care to be taken to avoid its complication by choosing appropriate tube size, type and positioning by x-rays, irrigation by plane water after each feed and drugs, routine changing of tube. removal and insertion of tube should be romanian neurosurgery (2017) xxxi 2: 244 247 | 247 carried out routinely, and whenever there is difficult to retrieve the tube it should be removed under endoscopic guidance otherwise there may be high possibilities of injury to gastro esophageal junction which may cause bleeding, reflux disease and may leads to death. correspondence ashok kumar, 401 hitawala complex, raghuroop apartment, sardarpura, udaipur, rajasthan, india email: dr.ashokkumar011@gmail.com phone: +919610463977 references 1. casaer mp, mesotten d, hermans g, wouters pj, schetz m, et al. (2011) early versus late parenteral nutrition in critically ill adults. n engl j med 2011 aug 11;365(6):506-17. doi: 10.1056/nejmoa1102662. epub 2011 jun 29 2. cook am, peppard a, magnuson b (2008) nutrition considerations in traumatic brain injury. .nutr clin pract 23: 608–620, sage journal dec 2008. 3. perel p, yanagawa t, bunn f, roberts i, wentz r, pierro a. nutritional support for head-injured patients. cochrane database syst rev. 2006;(4):cd001530. review. 4. borzotta p, pennings j, papasadero b, paxton j, mardesic s, borzotta r. enteral versus parenteral nutrition after severe closed head injury. j trauma. 1994;37:459–66. 5. frost p, bihari d. the route of nutritional support in the critically ill: physiological and economical considerations. nutrition. 1997;13 (suppl):58s–63. 6. rosenfeld jv, maas ai, bragge p, morganti-kossmann mc, manley gt, et al. early management of severe traumatic brain injury. 2012, lancet 380: 1088–1098 7. tan m, zhu jc, yin hh. enteral nutrition in patients with severe traumatic brain injury: reasons for intolerance and medical management br j neurosurgery 2011; feb: 25 (1) 28doi 10.3109/02688697.2010.522745 8. de aguilar-nascimento je, kudsk ka. clinical costs of feeding tube placement. jpen j parenter enteral nutr. 2007;31:269–273. 9. yung-fong tsai, chiao-fen luo, amina illias, chihchung nasogastric tube insertion in anesthetized and intubated patients: a new and reliable method lin, and huang-ping yu, bmc gastroenterlogy 2012;12:99 10. sekhar ranjan basu, sabyasachi das, sujata dolai, santanu ghosh, mohan chandra mandal1, pallab kumar mistri, rajiv roy. comparison of four techniques of nasogastric tube insertion in anaesthetised, intubated patients: a randomized controlled trial. iga214 year: 2014 | volume: 58 | issue: 6 | page: 714-71. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article short same segment fixation versus short segment fixation in postoperative correction of kyphosis and pain reduction in thoracolumbar spine fractures mohamed state, ahmed zaher, nabil ali egypt doi: 10.1515/romneu-2017-0001 romanian neurosurgery (2017) xxxi 1: 3 – 7 | 3             doi: 10.1515/romneu-2017-0001 short same segment fixation versus short segment fixation in postoperative correction of kyphosis and pain reduction in thoracolumbar spine fractures mohamed state, ahmed zaher, nabil ali department of neurosurgery, mansoura university, egypt abstract: introduction: posterior short segment pedicle screw fixation is considered the most common way for management of unstable thoracolumbar spine fracture. this study is aiming to evaluate the efficacy of both posterior short same segment and posterior short segment pedicle screw fixation on postoperative kyphotic angle and pain dense score in thoracolumbar fractures. methods: this is a prospective study of 32 patients with single level thoracolumbar spine fracture between june 2011 and may 2014. patients were divided randomly into 2 groups, one of them was submitted to short same segment posterior pedicle screw fixation with mean age 31.25+9.25ys, while the other group submitted to short segment posterior pedicle screw fixation with mean age 29.18+9.65ys. cobb method and denis work scale were used to assess kyphotic angle and pain score respectively on admission, during follow up period and after one year postoperatively. results: the short same segment type of operation showed improvement in correction in kyphotic angle deformity at the end of follow up period although this improvement was not statistically significant compared to short segment type. the short same segment patients showed statistically significant improvement as regard pain denis score among those patients treated by short segment fixation. conclusion: in this study short same segment posterior pedicle screw fixation is more efficient in postoperative pain reduction than short segment posterior pedicle screw fixation. key word: fracture, kyphotic angle, spine introduction the aim of surgical management of any spine fracture is early ambulation, healing without deformity and minimizing pain (8). spine considered unstable if two or more spinal columns are affected (2).restoring vertebral columns stability and early patient's mobilization are the goals of treatment of thoracolumbar spine fracture (3). posterior short segment pedicle screw fixation is 4 | state et al short segment fixation in postoperative correction of kyphosis             considered the most common way for management of unstable thoracolumbar spine fracture (5). most of burst fractures of spine occurred in thoracolumbar junction because it represents a transitional zone between stiff kyphotic thoracic spine and mobile lordotic lumbar spine (7). progressive kyphosis remain a concern in posterior short segment pedicle screw fixation and lack of anterior column support is the main cause (6). aim of the work evaluation of the efficacy of both posterior short same segment pedicle screw fixation and the posterior short segment pedicle screw fixation on postoperative kyphotic angle and pain dense score in thoracolumbar fractures. patients and methods this is a prospective study including 32 patients with single level thoracolumbar spine fracture. the study was conducted between june 2011 and may 2014 in mansoura emergency hospital. patients were divided randomly into two groups; one of them was submitted to short same segment posterior transpedicular screw fixation with the mean age of 31.25+9.25ys, and the other group was submitted short segment posterior transpedicular screw fixation with mean age of 29.18+9.65ys. radiological examinations were done for all patients and they included lateral view plain x-ray, computed tomography scan (ct) and magnetic resonance imaging (mri) to assess the level of the fracture, admission kyphotic angle, and the neural tissue status. patients with neurological deficits, multiple spine fractures and polytraumatized patients were excluded. cobb method was used to assess the kyphotic angle by drawing two lines perpendicular to other two lines representing superior end plate of the vertebra above and inferior end plate of the vertebra below. the kyphotic angle was classified to minimal form (0-5 degrees) deformity, mild from (6-15 degrees), moderate from (16-20 degrees) and severe (greater than 20 degrees (1)). one half of the patients with fracture spine were fixed surgically by posterior short segment pedicle screw fixation (ss) by fixation of one level above and one level below the fractured level, the other half of the patients were fixed by posterior short same segment pedicle screw fixation (sss) by using additional screws in the fractured level. polyaxial top loading screws were used for all patients. patients were followed up regularly at 3 months intervals. last follow up for final assessment of kyphotic angle and pain dense score was at one year postoperatively. all patients were followed up with plain x-rays and ct scans of dorsolumbar region. denis work scale was used to assess patient's pain status and his ability to return to work denis work scale was classified to five categories (5): •w1: patients back to his previous job. •w2: patient back to previous job but not full time work. •w3: patient unable to return to previous job but can work full time in other job. •w4: patient unable to return to full time job. •w5: patient unable to work (complete disability). romanian neurosurgery (2017) xxxi 1: 3 – 7 | 5             table i demographic characters of the patients characters type of operation test of significance p-value sss n=16 ss n=16 age + sd 31.25+9.85 29.18+9.65 0.62 0.5 gender: no. % no. % chi-square male 12 75 9 56.25 1.25 0.26 female 4 25 7 43.25 mode of trauma: falls 7 43.75 5 31.25 0.62 0.5 motor car accident 2 12.5 3 18.75 motor bicycle accident 7 43.75 8 50 there is no statistically significant difference as regard demographic characters of age, gender and mode of trauma between patients who underwent short same segment and short segment fixation. table ii outcome of kyphotic angle correction and pain dense score following short same segment and short segment posterior transpedicular interbody screw fixation variables type of operation test of significance p-value short same segment fixation n=16 short segment fixation n=16 kyphotic angel at end of follow-up: no. % no. % mild 11 68.75 4 25 4.438 0.085 moderate 4 25 8 50 severe 1 6.25 4 25 pain dense score: w1 3 18.75 0 0 15.813 0.03 w2 9 56.25 5 31.25 w3 2 12.5 4 25 w4 2 12.5 6 37.5 w5 0 0 1 6.25 the short same segment type of operation showed improvement in correction of kyphotic angle deformity at the end of follow up period although this improvement is not statistically significance compared to short segment type. the short same segment patients showed statistically significant improvement in pain dense score than patients treated by short segment fixation. p value is considered statistically significant at p ≥ 0.0 6 | state et al short segment fixation in postoperative correction of kyphosis             a b figure 1 a) preoperative case with lumbar 3 vertebral fracture , b) post-operative short segment fixation at the end of follow up period a b figure 2 a) preoperative case with lumbar 2 vertebral fracture, b) post-operative short same segment fixation at the end of follow up period romanian neurosurgery (2017) xxxi 1: 3 – 7 | 7             discussion the goal of treatment of thoracolumbar spine fractures are restoring spine stability and pain improvement (3). in this study there was no statistically significant difference between patients with short segment and short same segment posterior fixation as regard to age, gender and mode of trauma. these results are in agreement with tezeren and kuru (3). in this study the short same segment operation showed correction of kyphotic angle deformity at end of follow up period, but this improvement was not statistically significant compared to short segment fixation. these results are in agreement with allanay et al. (1) who demonstrated longterm loss of kyphotic correction occurred with short same segment posterior fixation. however, jonathan et al. (4) in their study showed that short same segment fixation provide successful kyphotic correction. our results showed statistically significant improvement of the pain dense score among patients treated by short same segment posterior fixation than those treated by short segment posterior fixation; these results are in agreement with jonathan et al. (4) who reported clinical improvement in pain and disability with short same segment posterior fixation. the improvement of the pain dense score and kyphotic angle correction with short same segment posterior fixation is probably due to increased biomechanical stability and reduction of implantation failure. correspondence mohamed state e-mail: mohamedstate@yahoo.com; phone: (+2)01005004133 ahmed zaher e-mail: azaher2005@hotmail.com; phone: (+2)01001314522 nabil ali e-mail: nabmansali@hotmail.com; phone: (+2)01223920738 references 1. allanay a, aracolu e, yazici m, oznur a and surat a: short segment pedicle instrumentation of thoracolumbar burst fractures: does transpedicular intracoporeal grafting prevent early failure. spine 2001; 26 (2): 213. 2. denis f: spinal instability as defined by the threecolumn spine concept in acute spinal trauma. clin ortho 1984; 189: 65-76. 3. gunduz tezeren and ilhami kuru: posterior fixation of thoracolumbar burst fracture short segment pedicle fixation versus long segment instrumentation. spinal disord tech j 2005; 18 (6): 485-488. 4. jonathan-j, james l, chen md and moris m: short same segment fixation of thoracolumbar burst fractures.journal of medicine and public health,2012; 71. 5. lingwang, jianjun li and hong wan: posterior short segment pedicle screw fixation and tlif for the treatment of unstable thoracolumbar/lumbar fracture. bmc musculoskeletal disorders 2014; 15:40. 6. melain rf, burkus jk and benson dr: segmental instrumentation for thoracic and thoracolumbar fracture prospective analysis of construct survival and five year follow-up. spine j 2001; 1: 310-323. 7. peter g, whang md, alexander r and vaccaro md: thoracolumbar fracture: posterior instrumentation using distraction and ligamentotaxis reduction. j am acad orthop surg 2007; 15: 695-701. 8. yousry eid, mohamed el-shafie, hany morsy and magdy el-dakkakhny: posterior short segment pedicle screw fixation for unstable thoracolumbar fractures. pan arab j 1999; 3 (2): 75-83.   flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article study of predisposing risk factors and etiology of chronic subdural hematoma in clipped patients of unruptured intracranial aneurysms – an institutional experience t. kawase, ahmed ansari, yoko kato, yasuhiro yamada, riki tanaka japan, india doi: 10.1515/romneu-2017-0081 526 | kawase et al risk factors for chronic subdural hematoma in clipped unruptured aneurysms doi: 10.1515/romneu-2017-0081 study of predisposing risk factors and etiology of chronic subdural hematoma in clipped patients of unruptured intracranial aneurysms – an institutional experience t. kawase1, ahmed ansari1,2, yoko kato1, yasuhiro yamada1, riki tanaka1 1neurosurgery, fujita health university, banbuntane hotokukai hospital, nagoya, japan 2neurosurgery, upums, saifai, up, india abstract: introduction: chronic subdural hematoma in clipped patients of unruptured intracranial aneurysms might lead to sudden neurological deterioration and may need emergency evacuation. we studied the effects of various factors in its etiology. materials and methods: a retrospective study of 91operated clipped patients of unruptured aneurysms in the year 2014-2015 was taken. various predisposing factors were studied. results: goreisan use was not associated with any reduction in post operative csdh formation. arachnoidoplasty and reduced post operative dead space contributed in a reduced formation of csdh. conclusion: older male patients with aneurysms who had been treated with anticoagulant drugs should be considered candidates for additive arp to prevent the development of postoperative csdh. key words: goreisan, arachnoidoplasty, anticoagulant, subdural hematoma introduction chronic subdural hematoma (csdh) is one of the most common neurosurgical complications and one of the most under reported complication following clipping of unruptured aneurysms. it may lead to sudden neurological deterioration and might need surgical evacuation. mori and maeda reported that post operative complications of csdh occurred in 5.4% of patients (1). most of the patients of csdh are treated by surgical evacuation, although there are some who have been treated by corticosteroids (2), angiotensin converting enzyme inhibitors (3), hypertonic glucose (4) and mannitol (5). recently, especially in japan, the use of traditional herbal medicine in the prevention of csdh in post operative cases has come into prevalence (6). goreisan is believed to have two important actions-one is the diuretic action and the other is hydrostatic modulating action in which the movement of water molecules is adjusted (7). romanian neurosurgery (2017) xxxi 4: 526 529 | 527 we report our institutional experience with goreisan in operated unruptured aneurysm cases. materials and methods we conducted a retrospective study in the year 2014-2015. all patients of unruptured intracranial aneurysms of any age and sex, with follow up for one year were included in the study. a total of 91 patients were thence enrolled for the present study. different factors were evaluatedage and sex of the patient, anti coagulant use, post operative pneumocephalus, arachnoidoplasty, and goreisan use. 91 clipped patients of unruptured aneurysms who later developed csdh were included in the study. the patients were divided into two groups. in the first group, 21 cases were symptomatic csdh causing either mass effect or deterioration in consciousness and required surgical evacuation. the second group had 70 cases which were asymptomatic or small csdh and managed conservatively. single burr hole evacuation method was deployed for evacuation of csdh. routine follow up of these patients over a period of 1 year was performed. statistical analysis for age comparison, student t-test (unpaired) was used. rest data was qualitative, analysed by chi square test. results table i showing characteristics in groups operated for csdh and those not operated following clipping group 1: 21/91 (23%) group 2: 70/91 (77%) mean age 69.5 years (p<0.015) 64.44 years male:female 11:10 8:62 goreisan use 17/21 48/70 anticoagulant 3/21 (p =0.044) 2/70 dead space 19/21(90.5%) 27/70 arachnoidoplasty 4/21 31/70 528 | kawase et al risk factors for chronic subdural hematoma in clipped unruptured aneurysms figure 1 case illustration of 76 years female with a: left mca aneurysm, b: post operative day 1 ct scan showing bifrontal pneumocephalus, c: 2 months following surgery patient had left csdh causing mass effect, d: following evacuation of the hematoma discussion although the pathogenesis of csdh is not completely understood, various key points need to be highlighted. subdural effusion is believed to be the result of arachnoid tearing by neurosurgical intervention, which causes fluid with or without blood to invade the subdural space and facilitate the formation of outer membrane (8), which then forms internal capillaries or sinusoids. these fenestrated blood vessels allow plasma fluid leakage and the resultant enlargement of the subdural space. repeated bleeding occurs from degenerating endothelium of capillaries which is accompanied by local hyperfibrinolysis. csdh tends to occur in patients in elderly patients of unruptured aneurysms, because brain atrophy tends to cause enlargement of the subarachnoid space and stretching of the bridging veinswhich facilitate the tearing of the arachnoid membrane and leakage of bloody cerebrospinal fluid into subdural space. our series reported a higher incidence of csdh, as all the patients operated were unruptured aneurysms which had a lax brain compared to other series which had a much lower incidence of csdh, due to their clipping in ruptured aneurysms. secondly, with the suctioning of csf from cisterns, the laxed brain in unruptured aneurysms became all the more laxed. we noted a reduced incidence of post operative csdh in male patients, which may be countered by absence of oestrogen, which may cause the blood vessels in the inner dural layer to become more ectatic because of estrogen priming of these vessels and thus more likely to bleed (9). some studies have reported an important role of aquaporin 4 (aqp4) in csdh. utsuki et al reported that aqp4 is expressed in the outer membrane of csdh (10). aquaporins are a family of transmembrane channels that allow rapid movement of water and in some cases small molecules across the plasma membrane, hence playing a critical role in brain edema pathogenesis (11,12). goreisan inhibits aqp4 (13), which is expressed on the outer membrane of csdh. asano et al also described the aqp blocking action of goreisan (14). however, our study did not find any particular benefit with the usage of goreisan. torn arachnoid causes a direct contact between subdural space and the cortex, which romanian neurosurgery (2017) xxxi 4: 526 529 | 529 leads to continued oozing from the capillaries, hence leading to increase formation of csdh. we found that with the use of arachnoidoplasty, the incidence of csdh was overtly reduced in our patients. we recommend that older male patients with aneurysms who had been treated with anticoagulant drugs should be considered candidates for additive arp to prevent the development of postoperative csdh. correspondence ahmed ansari assistant professor neurosurgery, upums, saifai, up, india. ahmed.ansari2@gmail.com references 1. mori k, and maeda m. "surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. neurologia medico-chirurgica 41.8 (2001): 371-381. 2. voelker jl. nonoperative treatment of chronic subdural hematoma. neurosurg clin n am.2000 jul;11(3):507-13. 3. weigel r, hohenstein a, schlickum l, weiss c, schilling l. angiotensin converting enzyme inhibition for arterial hypertension reduces the risk of recurrence in patients with chronic subdural hematoma possibly by an antiangiogenic mechanism. neurosurgery. 2007 oct;61(4):788-92; discussion 792-3. 4. ambrosetto c. post traumatic subdural hematoma. further observations on nonsurgical treatment. arch. neurol 1962;6: 287-292. 5. suzuki j, takaku a. non surgical treatement of chronic subdural hematoma. j. neurosurgery. 1970; 33: 548-553. 6. okamura a, kawamoto y, sakoda e, murakami t, hara t. evaluation of recurrence factors and goreisan administration for chronic subdural hematoma after percutaneous subdural tapping. hiroshima j. med. sci. 2013; 62:77-82. 7. ohnishi n, nagasawa k, yokoyama t.the verification of regulatory effects of kampo formulations on body fluid using mice model. j. trad. med. 2000; 17:131-136. 8. hasegawa m, yamashita t, yamashita j, suzuki m, shimada s. traumatic subdural hygroma: pathology and meningeal enhancement on magnetic resonance imaging. neurosurgery 1992; 31: 580-585. 9. markwalder tm. chronic subdural hematomas: a review. j neurosurg. 1981;54:637–645. 10. utsuki s, oka h, inukai m, abe k, fujii k. role of saireito in postoperative chronic subdural hematoma recurrence prevention. j. trad. med. 2012; 29: 137-142. 11. g. t. manley, d. k. binder, m. c. papadopoulos, a. s. verkman. new insights into water transport and edema in the central nervous system from phenotype analysis of aquaporin-4 null mice. neuroscience. 2004; 129(4): 983–991. 12. s saadoun, m papadopoulos, d davies, s krishna, b bell. aquaporin-4 expression is increased in oedematous human brain tumours. j neurol neurosurg psychiatry. 2002 feb; 72(2): 262–265. 13. kurita, t., k. nakamura, m. tabuchi, m. orita, k. ooshima and h. higashino,, 2011. effects of gorei-san: a traditional japanese kampo medicine, on aquaporin 1, 2, 3, 4 and v2r mrna expression in rat kidney and forebrain.. j. med. sci., 11: 30-38. 14. asano s, watanabe t, shinohara t, fujii n, ogawa a, nakagomi t. medical treatment by goresan only or with other hemostatic agents for chronic subdural hematoma without operations. gazz. med. ital. 2013; 172: 911-915. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article first episode of consciousness loss: setting new standards in acute care management dan iulian cuciureanu, antonia nita, victor constantinescu, tudor cuciureanu romania doi: 10.1515/romneu-2017-0073 romanian neurosurgery (2017) xxxi 4: 465 473 | 465 doi: 10.1515/romneu-2017-0073 first episode of consciousness loss: setting new standards in acute care management dan iulian cuciureanu1,2, antonia nita2, victor constantinescu, tudor cuciureanu3 ¹“prof dr. n. oblu” clinical emergency hospital, iasi, romania ²“grigore t. popa” university of medicine and pharmacy iasi, romania ³institute of gastroenterology and hepatology, iasi, romania abstract: there is a high prevalence of patients addressed to the emergency department presenting a first episode of consciousness loss. the high prevalence of patients admitted to the emergency departments (ed) with a first episode of consciousness loss (ecl) is well established. although there are studies assessing acute management in these patients, there is still need for more data on clinical and paraclinical characteristics which may prompt early etiological diagnosis, especially in countries where integrated medical procedures are lacking and access to specialized medical care is still limited. sudden death syndrome, early cerebral morphological changes emerging in chronic epilepsy is the main motivation for an early diagnosis of epilepsy. the aim of our study was to evaluate demographic, clinical and paraclinical data in adult patients referred to our emergency hospital presenting a first episode of consciousness loss, in order to avoid misdiagnosis (with personal and social high impact) and unnecessary anti-epileptic treatment versus underestimation of epilepsy diagnosis. conclusion: there is a clear need to improve multidisciplinary circuits in patients with a first episode of consciousness loss at a local level, in order to promote accurate and prompt diagnosis. we consider necessary to build a unitary online platform in order to establish an early and complete diagnosis. key words: loss of consciousness, first episode, early diagnosis, multidisciplinary platform. introduction the loss of consciousness represents a condition frequently addressed to the emergency unit. there are numerous possible conditions that can determine the loss of consciousness: cardiac syncope, neurally mediated syncope, orthostatic hypotension, epileptic seizures, psychogenic non-epileptic seizures. yet, in many cases, the etiology of 466 | cuciureanu et al first episode of consciousness loss ecl remains unknown. the place of eeg in routine evaluation of a first ecl has represented a subject of debate. our primary goal was to evaluate the incidence of eeg disturbances in the first days after ecl. material and methods we performed a retrospective observational study over 12 months, between january 2015 and january 2016, in our neurological department that included adult patients addressed for investigating their first episode of consciousness loss. inclusion criteria: adult patients (age>18) with an initial non-syncopal amnestic episode of consciousness loss (transient loss of consciousness, tloc) admitted in our neurological unit for further investigations. epidemiological, clinical and paraclinical (routine eeg in first 24 hours, long-term eeg, cardiological examination, brain imagery) data were assessed. results we included 110 patients (mean age 46.5, s.d ±15.5, female patients 62%) from 4800 patients with different diagnosis (figures 1 and 2). younger patients, both male and female (26 45 years) were more affected (figures 3 and 4). regarding possible etiologies, 16 % of patients did not associate any comorbidities. furthe rinvestigations revealed: cerebral malformations in 7% of patients, cerebral parenchymal sequelar lesion in 30%patients, endocrinological disorders in 5% and psychiatric disturbancies in11 % of investigated patients (figures 5, 6). initial standard eeg monitoring showed epileptiform abnormalities in 20% of patients (figure 7). figure 1 patients age figure 2 patients’ gender figure 3 decade repartition for women romanian neurosurgery (2017) xxxi 4: 465 473 | 467 figure 4 decade repartition for men figure 5 – comorbidities figure 6 age related comorbidities figure 7 standard eeg epileptiform changes figure 8 the incidence of epileptiform changesage group: 18-25 years figure 9 the incidence of epileptiform changesage group: 26-35 years figure 10 the incidence of epileptiform changes age group: 56-65 years figure 11 the incidence of epileptiform changes age group: 86-95 years 468 | cuciureanu et al first episode of consciousness loss the 36-45 years group and 86-95 group had more eeg abnormalities suggesting an epileptiform caracter of loss and no evident correlation with any kind of comorbidities despite the natural history of aging (figures 811). finaly, epilepsy diagnosis, based on electro-clinical and imagery findings was affirmative in 36% of patients. the highest prevalence was in the youngest and the oldest patients with a male predominance especially for generalized seizures (figures 12-14). figure 12 discharge diagnosis according to age groups figure 13 women types of seizures figure 14 men types of seizures figure 15 discharge diagnosis according to standard eeg (without any changes) romanian neurosurgery (2017) xxxi 4: 465 473 | 469 figure 16 discharge diagnosis according to standard eeg with changes discussion according to smith j, the timing of eeg recording may be important: assessment within 24 hours after seizure revealed interictal epileptiformdischarges in 51%, compared with 34% who had later eeg. epileptiform activity is specific, but not sensitive for the diagnosis of epilepsy, as the cause of a t-loc or other paroxysmal event is clinically likely to be epilepsy. we found a great number of patients with epilepsy (72%) having eeg abnormalities while 37% of patients in normal eeg patients (fig 15-16). eeg has relatively low sensitivity in epilepsy, ranging between 25–56%. specificity is better, but variable, ranging between 78– 98%. about 50% of patients with epilepsy show interictal epileptiform discharges (ied) in the first eeg test. and eeg with epileptiform abnormalities is associated with an increased risk of seizure recurrence (level a). (smith j, 2005)l. the transient nature of consciousness loss episode infers a proeminent and critical place in the clinical management of the history and symptom descriptions. to make a diagnosis of the cause of ecl and to determine the prognosis for the person with ecl, represented by the the risk of future adverse events, one should take into consideration the etiology of the sudden event. breen and colleagues (2005) showed that 72% of patients presenting symptoms compatible to first seizure and admited to ed, were offered a first seizure clinic appointment in a university hospital within six weeks of referral. the same authors noted that 9% of patients had a subsequent seizure while awaiting review. the study conclusion was that adults who suffer a first possible epileptic seizure and have no neurological complications can be safely managed on outpatient basis. yet, prompt diagnostic orientation is highly necessary for complete follow-up. a large, multicentric, prospective study showed that out of 1419 patients, 1217 were diagnosed with syncope, whereas 202 were diagnosed of non syncopal ecl, which included 36 cases of ecl caused by epilepsy and 166 caused by diverse or unknown causes (baron-esquivias et al., 2010). ecl associated with seizure opens a differential diagnosis, including convulsivant syncope or first manifestation of an epileptic disorder. the report of the guideline development subcommittee of the american academy of neurology and the american epilepsy society (2015) concerning the management of an unprovoked first seizure in adults, highlighted relevant clinical factors associated with an increased risk of seizure recurrence according to evidence-based 470 | cuciureanu et al first episode of consciousness loss medicine: prior brain insults, epileptiform abnormalities on eeg, nocturnal eeg, which recommend antiepileptic treatment, given the higher risk of recurrent seizure within the first 2 years after a seizure (krumholtz et al., 2015). the combination of wake and sleep records gives a yield of 80% in patients with clinically confirmed epilepsy (smith et al., 2005). eeg place in routine evaluation of ecl should be carefully considered, as epileptic seizure imitators like the loss of postural tone in atonic seizures and cataplexia have misleading clinical similarities. it is estimated that 20–30% of cases are indeed misdiagnosed as epileptic seizures (chadwick & smith, 2002). prolonged interictal sampling using eeg monitoring increases yield by about 20%, and is now more widely available through 24 hour ambulatory multichannel digital eeg. (smith et al., 2005) to differentiate an epileptic from a nonepileptic seizure, the clinician has to rely on his “art of listening.” this is timeconsuming and remains a challenge during a time-limited consultation. protocols should be in place that ensure proper assessment in the emergency department (nice, 2014). a detailed history and witness account are essential for diagnosing and managing episodic altered consciousness 20% of patients labelled and treated as epilepsy have other causes for apparent blackouts (perrig and jallon, 2008). some medical societies recommend that patients with a suspected diagnosis of epileptic seizure should be seen by a neurologist or an epilepsy specialist before the diagnosis is made (scottish intercollegiate guidelines network, 2015). symptoms of panic and dissociation may be common in the prodromal phase, although patients may sometimes avoid to provide a detailed description (stone et al., 2005). more anamnestic and clinical features useful in distinguishing psychogenic non-epileptic attacks (“pseudoseizures”) from epileptic convulsions are needed. psychogenic nonepileptic attacks as part of panic disorders and dissociative disorder are commonly mislabeled (beghi et al., 2015). panic symptoms frequently accompany epilepsy and it has been shown that they may worsen or mimic seizures. it has been inferred that almost 50% of adults admitted to intensive care for “status epilepticus” may have psychogenic attacks and not epilepsy. frontal lobe seizures are easily misdiagnosed as psycho-genic attacks (bourion-bedes et al., 2014). there are also patterns of central nervous system syncope related to brain and spinal cord lesions. data from litterature showed that syncope and psychogenic attacks are the most common reasons for misdiagnosis of epilepsy (petkar et al, 2006). zaidi et al. (2000) performed a head-up tilt test and carotid sinus massage under eeg in 38 patients with uncertain diagnosis and in 47% a diagnosis could be established. in young fainters a common cause of ecl is neurologically mediated reflex syncope, and in particular vasovagal faint. rapid autonomic adjustments also depend on local environmental biochemistry produced by slower endocrine, and local regulatory mechanisms. dysautonomic symptoms are proeminent in ecl dscription, yet there are romanian neurosurgery (2017) xxxi 4: 465 473 | 471 still no clear-cut quantitfiable measures in clinical set-ups to asssess directly and promptly sympatho excitation or vagal symptoms, resulting in circulatory adjustment deficiences reflected in cardiocirculatory changes, adrenal secretion and renovascular adjustments. biosignals such as heart rate or blood pressure show a continuous variability that may be altered if there is autonomic dysfunction. similar to the electrocardiogram, the variability of heart rate can be assessed under resting conditions and during challenge (hilz et al., 2006). there are various parameters of heart-rate variability describe by post-processing of ecg data (task force of the european society of cardiology and the north american society of pacing and electrophysiology, 1996). the standard deviation of the heart rate, the pnn50 (a parameter that indicates the proportion of differences in consecutive rr intervals that are longer than 50 ms), rmssd (the square root of the mean squared differences of successive rr intervals) as time-domain parameters and low-frequncy (lf), high frequency (hf), lf/hf ratio as frequency domain parameters, recorded during 5 min or more, reflect the influence of the parasympathetic and sympathetic system on heart-rate modulation (freeman et al., 1995). schellong test or the tilt-test may reveal orthostatic hypotension defined as a fall in systolic blood pressure of at least 20 mm hg or diastolic blood pressure of at least 10 mmhg (winker et al., 2005). the “subclavian steal syndrome” is rather rare, but can cause ecl due to retrograde blood flow in the vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion (osiro et al. 2012). therefore, when contextual circumstances are in favor of such a haemodynamic phenomena (e.g. effort), ultrasound doppler examination of neck vessels may provide the etiology of the syncope. cardiac causes such as transient polymorphic ventricular tachycardia (vt) in the congenital long qt syndrome may also cause ecl and can easily be misdiagnosed as epilepsy and wrong or delayed management, sometimes leading to cardiac arrest and hypoxic brain damage. the stars (syncope trust and reflex anoxic seizures) medical advisory committee, with european and north american multidisciplinary members, comprising cardiologists, paediatric and adult neurologists and general physicians, defined this issue as a worldwide concern (stars, 2007; fitzpatrick and cooper, 2006). hypoglycaemia and its related causes (including excessive alcohol intake), dismetabolic and endocrine dysfunction (e.g. hypocalcemia, phaeochromocytoma) should also be taken into consideration when investigated a first ecl (smith, 2001). the diagnosis of episodic altered consciousness rests largely with the clinical history,despite the remarkable advances in the technology of imaging and neurophysiology.common reasons for misdiagnosis may be inadequate or missing history—for example, no witnesss, clonic movements or incontinence accompanying syncope or psychogenic attacks, overstatement of family history of epilepsy, overinterpretation of minor 472 | cuciureanu et al first episode of consciousness loss electroencephalography (eeg) abnormalities or normal age specific variants (perrig and jallon, 2008). evidence-based medicine progress infers the need of new standards in management of a first episode of consciousness loss. early and successful interventions are conditioned by existence of multidisciplinary protocols and prompt access to specialist care (beghi et al., 2006; nice, 2016). defensive medicine and patients' tendency to ask for more examinations in a medical system based on rather individualized medical approaches than integrative set-ups may lead to diminished efficacy of initial medical examination and also to potential diagnosis and treatment delay. studies on large populational data have shown that the social and economic burden of delayed or missdiagnosis of ecl episodes is substantial (stokes et al., 2004). furthermore, the sudden unexplained death in epilepsy (sudep) phenomena is a subject of concern among patients experiencing ecl, as studies have shown that some cases of sudep may be due to unsuspected disease and arrythmic syncope (hirsch and hauser, 2004). conclusion therefore, it is a clear need to improve multidisciplinary circuits in patients with a first ecl at a local level, in order to promote accurate and prompt diagnosis of patients who are admitted at emergency department for a first episode of loss of consciousness in a region with rather limited access to multidisciplinary routine protocols.. new issues adressed by the present project proposal are based mainly on the need to highlight new biomarkers accesible in routine and emergency set-ups that allow a prompt differential diagnosis. in this respect, we consider that neuro-vegetative patterns examination (e.g. heart rate variability in a routine test and stand-up test, schellong test) may help the early orientation of the diagnosis, diminishing the percentage of ecl of unknown cases. correspondence dan iulian cuciureanu e-mail: cuciureanu57@gmail.com references 1.breen dp, dunn mj, davenport rj, gray aj. epidemiology, clinical characteristics, and management of adults referred to a teaching hospital first seizure clinic. postgrad med j. 2005 nov; 81(961):715-8. pmid: 16272236 2.baron-esquivias g, martínez-alday j, martín a, moya a, garcía-civera r, paz lópez-chicharro m, martínmendez m, del arco c, laguna p. epidemiological characteristics and diagnostic approach in patients admitted to the emergency room for transient loss of consciousness: group for syncope study in the emergency room (gesinur) study.europace. 2010 jun; 12(6):869-76. doi: 10.1093/europace/euq018. epub 2010 mar 9. pmid: 20215367 3.krumholz a, wiebe s, gronseth gs, gloss ds, sanchez am, kabir aa, liferidge at, martello jp, kanner am, shinnar s, hopp jl, french ja.evidencebased guideline: management of an unprovoked first seizure in adults: report of the guideline development subcommittee of the american academy of neurology and the american epilepsy society.neurology. 2015 apr 21;84(16):1705-13. doi: 10.1212/wnl.0000000000001487.pmid:25901057 4.smith sjm, eeg in the diagnosis, classification, and management of patients with epilepsy. j neurolneurosurg psychiatry 2005;76:suppl 2 ii2-ii7 doi:10.1136/jnnp.2005.069245 5.chadwick d, smith d. the misdiagnosis of epilepsy.bmj. 2002 mar 2;324(7336):495-6. romanian neurosurgery (2017) xxxi 4: 465 473 | 473 6.national institute for health and care excellence (uk), nice. epilepsies: diagnosis and management (cg137), 2016 7.perrig s, jallon p.is the first seizure truly epileptic? epilepsia. 2008;49suppl 1:2-7. doi: 10.1111/j.15281167.2008.01442.x. 8.scottish intercollegiate guidelines network (sign).diagnosis and management of epilepsy in adults. edinburgh: sign; 2015.(sign publication no. 143). [may 2015]. available from url: http://www.sign.ac.uk 9.stone j, carson a, sharpe m. (2005) functional symptoms and signs in neurology: assessment and diagnosis. j neurolneurosurg psychiatry 76:2–12. 10.beghi m, negrini pb, perin c, peroni f, magaudda a, cerri c, cornaggiacm psychogenic non-epileptic seizures: so-called psychiatric comorbidity and underlying defensemechanisms. neuropsychiatr dis treat. 2015 sep 30;11:2519-27. doi: 10.2147/ndt.s82079. ecollection 2015. 11.bourion-bédès s, hingray c, faust h, vignal jp, vespignani h, schwan r, jonas j, maillardl. pitfalls in the diagnosis of new-onset frontal lobe seizures.epilepsybehav case rep. 2013 nov 28;2:1-3. doi: 10.1016/j.ebcr.2013.10.002. ecollection 2014.pmid:25667854 12.petkar s, cooper p, fitzpatrick ap.how to avoid a misdiagnosis in patients presenting with transient loss of consciousness.postgrad med j. 2006 oct;82(972):630-41. 13.zaidi a, clough p, cooper p, scheepers b, fitzpatrick ap. (2000) misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. j am collcardiol 36:181–184 14.hilz mj, dütsch m. quantitative studies of autonomic function. muscle nerve. 2006 jan;33(1):6-20. 15.task force of the european society of cardiology and the north american society of pacing and electrophysiology. heart rate variability: standards of measurement, physiological interpretation, and clinical use. circulation 1996; 93: 1043–1065. 16.freeman r, weiss st, roberts m, zbikowski sm, sparrow d. the relationship between heart rate variability and measures of body habitus. clinauton res 1995; 5: 261–266. 17.winker r, prager w, haider a, salameh b, rüdigerhw.schellong test in orthostatic dysregulation: a comparison with tilt-table testing.wienklinwochenschr. 2005 jan;117(1-2):36-41. 18.osiro s, zurada a, gielecki j, shoja mm, tubbs rs, loukas m.a review of subclavian steal syndrome with clinical correlation.med scimonit. 2012 may;18(5):ra57-63. review.pmid: 22534720 19.fitzpatrick ap, cooper p. diagnosis and management of patients with blackouts. heart. 2006 apr; 92(4): 559–568. doi: 10.1136/hrt.2005.068650. pmcid:pmc1860900. 20.syncope trust and reflex anoxic seizures (stars),international medical advisory committee (mac), 2007, www.stars.org.uk 21.smith sjm. if it’s not epilepsy.jneurolneurosurg psychiatry 2001;70(suppl ii):ii9–ii14 22.stokes t, shaw ej, juarez-garcia a, camossostefinovic j, baker r.clinical guidelines andevidence review for the epilepsies: diagnosis and management in adults and children in primary and secondary care london: royal college of general practitionerslondon: royal college of general practitioners, 2004 23.hirsch lj, hauser wa.can sudden unexplained death in epilepsy be prevented? lancet. 2004 dec 1831;364(9452):2157-8. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article primary sinonasal undifferentiated carcinoma with intracranial extension presenting postoperatively as garcin syndrome: a rare case report and review of literature prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmad faran, chhabra anuj india doi: 10.1515/romneu-2017-0089 564 | prasad et al primary sinonasal carcinoma with intracranial extension doi: 10.1515/romneu-2017-0089 primary sinonasal undifferentiated carcinoma with intracranial extension presenting postoperatively as garcin syndrome: a rare case report and review of literature prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmad faran, chhabra anuj department of neurosurgery, dr rml ims lucknow uttar pradesh, india abstract: sinonasal undifferentiated carcinoma (snuc) is an aggressive malignancy originating in the mucosa lining the walls of the nasal cavity and paranasal sinuses. it is a rare tumor that usually presents in an advanced stage, is highly invasive, and is traditionally reputed to be refractory to even the most radical therapy with an attendant poor prognosis. this is particularly true when it transgresses the cranial base. key words: sinonasal undifferentiated carcinoma,intracranial extention, garcin syndrome introduction snuc was first described in 1986 as a rare and highly aggressive neoplasm arising from the nasal cavity and paranasal sinuses[1]. these tumors tend to be large and expansile, with widespread involvement of the nasal cavity and paranasal sinuses. bone destruction and invasion of adjacent structures such as the orbit, cranial vault, and skull base is frequently seen. the median age of presentation is the sixth decade and men are more commonly affected (male to female ratio of 2.3:1) the vast majority of affected patients present with epistaxis, rhinorrhea, nasal obstruction, and facial pain[2,3]. very rarely these tumour present as garcin syndrome. garcin syndrome consists of unilateral palsies of almost all cranial nerves without either sensory or motor long-tract disturbances and without intracranial hypertension, and it is caused by a malignant osteoclastic lesion at the skull base. the underlying cause of garcin’s syndrome is usually a sarcoma, lymphoma, metastasis, chemodectoma, or carcinoma of the skull base. the literature on garcin’s syndrome is limited, and this makes the present case rare and interesting. the natural history, clinical course and histological features of snuc are poorly understood[4] overall survival of patients with snuc is poor in most reported series. although no clear consensus exists regarding treatment, a multidisciplinary approach combining surgery (craniofacial resection) with chemotherapy and radiation may be used romanian neurosurgery (2017) xxxi 4: 564 567 | 565 to control local disease[2,3]. the extent of disease at diagnosis represents the most sensitive predictor for survival. the purpose of this report is to present a case of snuc and to review the current concepts of diagnosis, differential diagnosis and management of this rare disease. case report 43 years old patient presented to ous with complain of bifrontal headache and nasal obstruction from last 3 month. on examination patient was conscious and oriented to time place and person. his cranial nerve examination was normal except that there was decrease smell sensation on right side. motor, sensory and cerebellar examination was normal and bladder bowel was not involved. patient was investigated properly and mri brain with contrast was done [figure 1, figures 2a and 2b]. patient was planned for surgery and right sided extended frontal craniotomy was done. tumour present in basifrontal ethmoidal region was removed, part of tumour attached to medial wall of orbit was left [figure 3]. dura was repaired and frontal sinus was exteriorized. postoperatively patient was conscious and oriented. on day 5 patient develop headache and on subsequent days right sided ptosis was noticed. initially it was partial ptosis but in 2-3 days it become complete ptosis and it also develop on contralateral side. on examination we found that there is also involvement of 4th and 6th cranial nerve. within next 5-6 days there is also involvement of 5th, 7th, 9th, 10th and 12th cranial nerve on ipsilateral side. patient also develop pain in the back region. inspite of involvement of multiple cranial nerve patient had no motor and sensory impairment and his bladder and bowel was intact. we report this case as snuc is very very rare and involvement of multiple cranial nerve in step by step fashion without impairment of motor and sensory systems (garcin syndrome) is extremely rare. so this case become an interesting case and only few such cases are reported in the literature. a b c figure 1a mri t1w axial image shows hypointence mass present in right frontal region figure 1b mri t2w axial image shows iso to hypointence mass present in right frontal region figure 1c contrast mri axial image shows contrast enhancing mass present in right frontal region a b c figure 2a contrast mri saggital image shows contrast enhancing mass in right basifrontal region with extension into nasal cavity figure 2b contrast mri coronal image image shows contrast enhancing mass in right basifrontal region with extension into paranasal sinuses figure 2c h&e stained sections show a tumour disposed in nests with interspersed lymphocytes and plasma cells. the tumourcells are round to oval with high nuclei-cytoplasmic ratio, hyperchromatic nuclei and scant cytoplasm. numerous mitotic figuresare evident 566 | prasad et al primary sinonasal carcinoma with intracranial extension a b c figure 3a post ope mri t1w axial image shows hyperintence changes in right frontal region figure 3b post ope mri t2w axial image shows iso to hyperintence changes in right frontal region figure 3c post ope contrast mri axial image shows small residual tumour in right frontal region discussion snuc is an aggressive, highly malignant tumor of the mucosal lining of the nasal and paranasal sinuses. it was first described as a distinct and separate entity by frierson et al in 1986 [5].the prognosis of the patient is very poor with high frequency of local recurrence and distant metastasis. these tumour generally present with epistaxis, nasal obstruction and headache. very rarely these tumour present as garcin syndrome. garcin syndrome is an ipsilateral step-by-step deterioration of all 12 cranial nerves, first described in 1927. this rare progressive condition is generally associated with skull based malignant osteoclastic lesions but has also been described with sarcoma, lymphoma, metastasis, chemodectoma, or carcinoma of the skull base. cranial nerves involvement in these tumour occurs in many ways. first, the tumor may extend superiorly through foramen lacerum, which is an unimpeded pathway near the fossa of rosenmuller into the cranium, thus involving the cranial nerves in the middle cranial fossa and cavernous sinus. cancer may break through the pharyngo-basilar fascia and spread along vascular sheaths, that is, facial planes surrounding the jugular vein and carotid artery. lateral and posterior extension of the primary growth itself may involve the lower cranial nerves exiting from jugular and hypoglossal foramina. confirming the diagnosis of snuc at the light microscopic level can be challenging, since the microscopic differential diagnosis include olfactory neuroblastoma, rhabdomyosarcoma, undifferentiated nasopharyngeal carcinoma (lymphoepithelioma), malignant lymphoma, malignant melanoma and neuroendocrine carcinoma. snuc can be differentiated from these other neoplasm by correlating clinical, light microscopic, immunohistochemical and ultrastructural charecteristics. [6] the tumour is positive for pan-cytokeratin, epithelial membrane antigen, cd99, cytokeratin7 with scattered p-40 expression on immunohistochemistry. olfactory neuroblastoma typically present as a polypoidal mass protruding from the roof of nasal cavity. immunohistochemistry demonstrate staining for neuroendocrine markers such as neuron specific enolase (nse), synaptophysin and chromogranin. s100 is usually positive in a sustentacular pattern [7]. differential diagnosis of snuc from olfactory neuroblastoma and neuroendocrine carcinoma may be difficult because a small proportion of snuc may express neuroendocrine markers including nse and romanian neurosurgery (2017) xxxi 4: 564 567 | 567 chromogranin. however snuc lacks s-100 and does not show glandular differentiation or rosettes. snuc has more extensive cytological atypia and necrosis. ultrastructurally neuroendocrine markers tend to be focal and no neurosecretory granules are evident in snuc. [8] melanoma and lymphoma are easily differentiated on the basis of immunohistochemistry. melanoma stain positively for s-100, hmb 45 and melan a, while lymphomas are invariably positive for cd19 and cd20 as well as other b cell lineage markers [9]. due to rarity of the disease the proper diagnostic and management criteria could not be defined. on reviewing the literature we found that we can differentiate this tumour from others by histological and immunohistochemical properties. snuc could be treated by craniofacial resection followed by adjuvant radiotherapy and or combination of chemotherapy. inspite of these multimodality treatment these tumour recur in one year and most of these patient died. [10]. so early diagnosis and prompt treatment can improve the survival of these patient. conclusion sinonasal undifferentiated carcinomas (snuc) are highly aggressive lesions arising in the superior nasal cavity and paranasal sinuses. the differential diagnosis may be wide since a range of similar lesions may present at this site. recently the criteria for diagnosis of snuc has been clarified. on the basis of histological and immunohistochemical charecteristics we can differentiate it from other lesions. correspondence dr. hanuman prasad prajapati address: department of neurosurgery, dr rml ims lucknow uttar pradesh (india) mobile no.: 07727934104 email: pushpa84.dhp@gmail.com references 1. frierson hf jr, mills se, fechner re, et al. sinonasal undifferentiated carcinoma: an aggressive neoplasm derived from schneiderian epithelium and distinct from olfactory neuroblastoma. am j surg pathol 1986;10:771-9. 2. righi pd, francis f, aron bs, et al. sinonasal undifferentiated carcinoma: a 10-year experience. am j otolaryngol 1996;17:167-71. 3. phillips cd, futterer sf, lipper mh, et al. sinonasal undifferentiated carcinoma: ct and mr imaging of an uncommon neoplasm of the nasal cavity. radiology 1997;202:477-80. 4. s.r. smith, p. som, a. fahmy, w. lawson, s. sacks, m. brandwein a clinicopathological study of sinonasal neuroendocrine carcinoma and sinonasal undifferentiated carcinoma laryngoscope, 110 (2000), pp. 1617–1622 5. frierson h f, jr, mills s e, fechner r e, taxy j b, levine p a. sinonasal undifferentiated carcinoma. an aggressive neoplasm derived from schneiderian epithelium and distinct from olfactory neuroblastoma. am j surg pathol. 1986;10:771–779. [pubmed] 6. norleza an,gendeh bs, challenges in the treatment of sinonasal undifferentiated carcinoma: a ray of hope, med j malaysia 2005 aug,60(3) 281-285. 7. taxy jb, bharani nk, mills se, frierson hf jr, gould ve. the spectrum of olfactory neural tumours.a light microscopic, immunohistochemical and ultrastructural analysis.am j surg pathol 1986;10:687-695. 8. smith sr, sem p, fahmy a, lawson w, sacks s,brandwein m. a clinicopathological study of sinonasal neuroendocrine carcinoma and sinonasal undifferentiated carcinoma. laryngoscope 2000;110:1617-1622. 9. franquemont dw, mills se. sinonasal malignant melanoma. a clinicopathologic and immunohistochemical study of 14 cases. am j clin pathol1991;96:689-697. 10. musy p y, reibel j f, levine p a. sinonasal undifferentiated carcinoma: the search for a better outcome. laryngoscope. 2002;112:1450–1455. [pubmed microsoft word _8.formatata_stan.doc romanian neurosurgery vol. xvi nr. 1 37 consideration on hemicraniectomy horatiu stan, bogdan suciu, alexandru iosif, adriana cocis department of neurosurgery, “bagdasar-arseni” emergency hospital, bucharest, romania decompressive hemicraniectomy is a surgical technique used to relieve the increased intracranial pressure. there is no standardized surgical technique to clearly state the minimum area of the cranial vault needed to obtain the best results. the aim of the current paper is to present our surgical technique and experience used in performing hemicraniectomies, technique that we consider optimal for his purpose. our experience consists in 17 operated cases and eleven patients (64,7%) were long term survivors. keywords: cerebral edema, decompressive hemicraniectomy, malignant cerebral infarction, traumatic head injuries introduction decompressive hemicraniectomy is a surgical technique used to relieve the increased intracranial pressure. benefits from hemicraniectomy was reported in ischemic stroke, central venous thrombosis, intracerebral hematoma, head injuries (especially acute subdural hematoma), encephalitis, subdural empiema, aneurismal subarachnoid hemorrhage and even in other rare clinical situations such as reye's syndrome or hepatic failure (7,9). the common pathological aspects of this disease are massive brain swelling with increased intracranial pressure. the overall goal of hemicraniectomy is to increase the volume-buffering capacity of the cranial vault, allowing for centripetal herniation, minimizing centrifugal compression of brain stem structures (9). from historical point of view, cases of hemicraniectomy date back as far as the late 1800s, but the procedure was first described in 1905 by harvey cushing (1,2). however the term “hemicraniectomy“ is frequently derisory and wrongly used for any operations involving a large cranial vault followed by removal of the bone for permitting the brain to enlarge. there is no standardized surgical technique to clearly state the minimum area of the cranial vault needed to obtain the best results. the aim of the current paper is to present our surgical technique and experience used in performing hemicraniectomies, technique that we consider optimal for his purpose. also, we discuss the opportunity of these “saving lifes” operations and the way a satisfactory functional and esthetical recovery occurs. material and methods our experience consists in 17 cases operated by the author in cluj-napoca neurosurgical clinic, romania, between january 2002 and january 2008 (table 1). malignant cerebral infarction count for 7 cases (41,2%), traumatic head injuries count for 9 cases (52,9%), and encephalitis with subdural empiema for one case (5,9%). the same standard surgical procedure was preformed for each of the patients. bifrontal decompressive craniectomies were not included. the indications for hemicraniectomy were based on these head ct-scan characteristics: massive cerebral edema with midline shift (more than 1 cm) with horatiu stan romanian neurosurgery vol. xvi nr. 1 38 disappearance of basal cisterns, correlated with clinical state at admission and neurological evolution of the patients. for malignant cerebral infarction with clear ct criteria, the surgery is indicated before the patient becomes comatose. in posttraumatic hematomas or epidural empiemas with encephalitis, we compare the mass effect on ct with the thickness of the hematoma. hemicraniectomy was preformatted when a large discrepancy of the mass effect was found, even if the patients already develop sign of brain herniation (uncal or subfalxial herniation). surgical technique considerations: the patient is placed with the side of craniotomy upward, head elevated to 15 degree. the line of skin incision is described from posterior to anterior: beginning retro-auricular (to the mastoid), extended in a supero-posterior manner and than reversed to anterior approximately 2 cm parallel to the sagittal line until the widow peak, then reversed infero-basal, respecting the hair line to the preauricular region. care must be taken to preserve the principal ramifications of temporary artery inside de musculocutaneous flaps. the temporalis muscle is reflected basally. the margins and burrholes for hemicraniectomy, described from anterobasal to posterior are: temporo-basal, under the level of ear pina; pterional at the site of the classic keyhole; fronto-basal, above the level of frontal sinus, to expose frontal pole but avoid entry in the frontal air cells sinus; then along the planned paramedial craniectomy margin, 2 cm parasagittal (avoid lesions over saggital sinus and bridging veins), until lambda point; then antero-basal, tangent with lambdoid suture, until 1 cm above the asterion (to avoid lacerations of transverse-sigmoid sinus). the sphenoid wing is fractured and removed. decompression was extended far enough to the floor of the middle fossa to relieve pressure from the herniating mediobasal temporal lobe and up to the midline to avoid compression of the bridging veins (1-2 cm) (10). the dura is opened by a large radial incision to allow the brain to expand outward (11). prophylactic, if the intracranial pressure is not elevated, dural edges are tacked up to bony margins. large duraplasty with extra space for brain to enlarge, using all periostal tissue from the cranial vault is performed. results eleven from 17 patients (64,7%) were long term survivors. six patients (35,3%) died in the first 3 weeks postoperatively. male gender was predominant (65%). median age was 46,8 years for the survivals patients and 60,3 years for the group of deceased patients. in the stroke group median age was 56,7 years. male gender represented 57,1%. right hemisphere was affected in 71,43% of cases. four patients out of 7 (57,1%) were long term survivors (42,9% mortality in stroke group). over 70% of the patients were progressively somnolent, presenting intracranial hypertension and hemiparesis on admission. only 20% of these (representing 1 case who died at 2 weeks postoperative by pulmonary trombembolism) died postoperatory. all patients admitted in coma state (30%) died postoperatory. from the deceased patients in the stroke group, 2 died from pulmonary complications and only one by general state deterioration determined by cerebral herniation. sixty-seven percent (2 cases) from these were admitted in comatous state. in posttraumatic lesions, the group’s median age was 48 years. male gender was predominant (88,9%). the right hemisphere was affected in 86,41% of cases. six patients from 9 (66,7%) were long term survivors (33,3% mortality in posttraumatic group). all the patients with posttraumatic lesions at admission were in medium or high grade coma scale. two patients died by general state deterioration determinated by cerebral herniation and one patient from pulmonary complications. from the deceased patients 66,7% were admitted in grade iv coma state. long term neurological recovery was excellent especially in the cases of posttraumatic lesion. cranioplasty with self bone kept in abdominal fat (placed in right abdominal subcutaneous fat at the time of hemicraniectomy) was made initially in 7 cases (41,2%). the majority of grafts showed some degree of degeneration. two of these cases (28,6%) were complicated by infection and the bone was removed. consideration on hemicraniectomy romanian neurosurgery vol. xvi nr. 1 39 after the infection was cured, cranioplasty with custommade plate was performed. in other two cases direct custom-made cranioplasty was preformed with no complications. silicone rubber mould cast polyethylmethacrylate-hidroxyapatite plate manufractured using rapid prototyping techniques offered us the maximum functional and esthetical recovery (12, 13). we use it now as primary intention technique for large cranioplasty. discussions hemicraniectomy versus medical care. established clinical trials and retrospective study for malignant cerebral infarction show a reduced mortality at hemicraniectomisated patients from 75-80% to 2430%. (5,6,9) much more, the mortality can be further reduced with 10% by undertaking decompression within 24 hours of ictus. (9) in the cases of traumatic hematomas, whitefied and colleagues found in a series of 26 patients the following results: 61% of the patients who underwent decompressive craniectomy attained favorable outcome, compared with 30% in the control group. other recent studies suggest that young patients with gcs greater than 4 may benefit from decompression when the intervention is performed early. young age is a frequently discussed factor for a good outcome for hemicraniectomisated patients. in our study the median age was 46,8 years for the survivors and 60,3 years for the group of deceased patients. surgical indications criteria for the patients with ischemic stroke, ct related criteria for hemicraniectomy are: massive cerebral edema with deviation of the midline shift (more than 1 cm) and lack of basal cisterns. neurological deterioration and cerebral edema are installing progressively in 24-72 hours. ct aspects are also variable during this interval: after 24 hours from stroke, hipodensity of the infracted area may be seen; malignant cerebral edema usually appear only 48 hours after the initial event. however, ct criteria must be correlated with the clinical state at admission and neurological evolution of the patients. if the patient is already in a coma, we think that no good results will be achieved, and the patients have no indication for operation. in our study the mortality was significantly higher in the group admitted in comatous state (100% mortality) compared with the patients who were only somnolent or presenting sign of intracranial hypertension and hemiparesis (20% mortality, representing 1 case who decedate at 2 weeks postoperative by pulmonary trombembolism). these proves there is no need to wait for the patient to become comatose to perform a hemicraniectomy. this is not the case with posttraumatic supraacute epi/subdural hematomas, were life of a high grade coma patient, even with pupillary inequality or recent installed bilateral midriasis, may still be saved by a heroical intervention. in posttraumatic hematomas (with or without subjacent cerebral contusion) and also in epidural empiema with encephalitis, for hemicraniectomy to be indicated the mass effect should be larger than the thickness of hematoma. these make all the difference between the need of hemicraniectomy and the need of a classic cranial vault for evacuation of intracranial collection. although the mortality rate probably will fall after decompressive surgery, it is unclear which groups of patients benefit most from the procedure (4). this type of surgical intervention was wrongly reserved especially for the most critical cases, admitted in high grade coma scale, frequently with constituted neurological sign of cerebral herniation. these cases have anyway a poor outcome, determinates by the advanced of cerebral herniation and the general deterioration. also, frequently these patients, after survival from the postoperative state, remain in vegetative state for a long period of time, dying lastly from bronhopulmonary or systemic complications. in either of the cases, the outcome of these patients was very poor, wrongly inducing the idea that hemicraniectomy is an hopeless operations. the good operative indications, applications of the standardised large hemicraniectomy and favorable evolutions of intensive medical care for comatose patients, will increase the real chances of survival for this patients, reveling finally the importance of this surgical procedure. horatiu stan romanian neurosurgery vol. xvi nr. 1 40 hemicraniectomy versus other types of decompressive vaults. (or “how large should the extension of bone removal be?”) the magnitude of intracranial cerebral pressure reduction correlates with the size of craniectomy and ranges from 15-85%. durotomy further enhances the release of cerebral pressure (9). the need for a radical approach (in terms of extension of bone removal) was recognized by kerr in 1968 in the event of severe posttraumatic cerebral edema. his observation was echoed in the case of massive cerebral ischemia by rieke who found that a few of their initial surgically treated patients harbored a bone defect that was too small, not providing adequate space for decompression and resulting in brain herniation through the skull opening (8). wirtz reveal that an exponential relationship between craniotomy size and gained volume for brain to enlarge. until 6 cm diameter of the cranial vault the decompression is not significant. to obtain a 50 ml gained volume, craniotomy size must have at least 10 cm in diameter (10,11). the real increase in decompression volume is obtained from 12 cm, witch correspond to much over 100 ml buffering volume. to every centimeter in plus over 12 cm, an additional increase of decompression volume of approximately 50 cc is obtained (10). in another study regarding surviving patients, the mean distance to the temporal skull base was less (1.7 ± 1.2 cm) than for those who did not survive (2.3 ± 1.3 cm)(10). conclusions best result in surgical treatment of malignant cerebral edema caused by a variability of pathological lesions (especially malignant cerebral ischemia and supraacute convexital subdural hematoma) depends principally by three thinks: good operative indications, applications of the standardisated large hemicraniectomy and best intensive medical care for these patients. a large hemicraniectomy presumes that the craniotomy vault should have at least 10-12 cm diameter. until 6 cm diameter of the cranial vault the decompression is not significant. good operative indication is based on the ct criteria and clinical state at admission. these make that the operative indication to be different for the principal malignant edema condition. for post ischemic edema ct criteria are massive cerebral edema with deviation of the midline shift and disparities of basal cisterns. from clinically point of view, there are no needs to wait that the patients become comatose to perform a hemicraniectomy. we can anticipate his evolution based on ct aspects and knowledge of natural evolution of the ischemic stroke. patients with ischemic stroke presented in coma state have no benefit from hemicraniectomy. in posttraumatic hematomas and epidural empiema with encephalitis, for the hemicraniectomy to be indicated, mass effect must be large compared with the thickness of hematoma. for this cases, good result can be obtained by a ultra rapid operation despite clinical condition. nr age sex diagnose admision state cranioplasty complicaions and postoperative evolutions 1 61 f right mcat coma grd.iii dead at 11 days postop. by general state deteriorations determinate by post cerebral herniation. 2 47 f right ict somnolent ich hemiparesis at 6 months with self bone kept in abdominal fat no complications 3 53 m right ict somnolent ich hemiparesis at 12 months with custom-made plate. no complications 4 46 m right ict somnolent ich hemiparesis at 6 months with self bone kept in abdominal fat. no complications 5 67 m right mcai somnolent ich hemiparesis dead at 1 week postop. by pulmonary trombembolism. consideration on hemicraniectomy romanian neurosurgery vol. xvi nr. 1 41 6 64 f left mcat coma grd.ii dead at 2 weeks postop. by pulmonary complications. 7 59 m hemoragic stroke somnolent ich hemiparesis at 2 months with self bone kept in abdominal fat. infection of bone with staphilococus aureus. target antibiotherapy with vancomicine was made. the bone was removed at 2 months after the cranioplasty. after the infections was cured, cranioplasty with custom-made plate was made. nr age sex diagnose admision state cranioplasty complicaions and postoperative evolutions 8 61 m right convexital posttraumatic sdh coma grd. ii at 6 months with self bone kept in abdominal fat. no complications 9 37 m right convexital posttraumatic sdh coma grd. iii at 6 months with self bone kept in abdominal fat. no complications 10 21 m right convexital posttraumatic sdh coma grd.iii no complications 11 45 f right convexital posttraumatic sdh coma grd.iv dead at 2 weeks postop. by general state deteriorations determinate by post cerebral herniation. 12 23 m left convexital posttraumatic sdh. coma grd. iii with papillary asymmetry at 2 months with his own cranial vault kept in abdominal fat. infection of cranioplasty bone. the bone was removed and at 6 months after the infection was cured cranioplasty with custom-made plate. 13 67 m left convexital posttraumatic sdh. coma grd.ii at 6 months with self bone kept in abdominal fat. 14 70 m posttraumatic hemorrhagic contusions, sah coma grd.iii dead at 2 weeks postop. by pulmonary complications. 15 53 m right convexital posttraumatic sdh coma grd.iii at 12 months with custom-made plate. no complications. 16 55 m right convexital posttraumatic sdh coma grd. iv dead at 2 weeks postop. by general state deteriorations determinate by post cerebral herniation. 17 48 m epidural empiema with cerebral encephalitis. somnolent ich hemiparesis at 12 months with custom-made plate. no complications. horatiu stan romanian neurosurgery vol. xvi nr. 1 42 references 1.pamela linton. time and space heal head injuries. waine medicine 1999. 2.cushing, h. the establishment of cerebral hernia as a decompressive measure for inaccessible brain tumors: with the description of intermuscular methods of making the bone defect in temporal and occipital regions. surg gynecol obstet 1905; 1 : 297. 3.scarcella, g. encephalomalacia simulating the clinical and radiological aspects of brain tumor; a report of 6 cases. j neurosurg 1956; 13: 278. 4. rishi gupta, md; e. sander connolly, md; stephan mayer, md; mitchell s.v. elkind, ms, md. hemicraniectomy for massive middle cerebral artery territory infarction. a systematic review. stroke, 2004;35:539-543. 5.eric ju¨ttler, md; stefan schwab, md, phd; peter schmiedek, md, phd; andreas unterberg, md, phd; michael hennerici, md, phd; johannes woitzik, md; steffen witte, phd; ekkehart jenetzky, md; werner hacke, md, phd;decompressive surgery for the treatment of malignant infarction of the middle cerebral artery (destiny) a randomized, controlled trial stroke. 2007;38:25182525. 6.hemicraniectomy after middle cerebral artery infarction with lifethreatening edema trial (hamlet). protocol for a randomised controlled trial of decompressive surgery in space-occupying hemispheric infarction jeannette hofmeijer, g johan amelink, ale algra, jan van gijn, malcolm r macleod, l jaap kappelle, h bart van der worp and the hamlet investigators trials 2006, 7:29. 7.christian rainer wirtz, m.d., thorsten steiner, m.d., alfred aschoff, m.d., ph.d., stefan schwab, m.d., holger schnippering, m.d., hans herbert steiner, m.d., werner hacke, m.d., ph.d., and stefan kunze, m.d., ph.d. hemicraniectomy with dural augmentation in medically uncontrollable hemispheric infarction neurosurgical focus 2(5): article 3, 1997. 8.desiree j. lanzino, ph.d., p.t., and giuseppe lanzino, m.d.decompressive craniectomy for space-occupying supratentorial infarction: rationale, indications, and outcome neurosurg focus 8 (5):article 3, 2000. 9.clark chen, edward r.smith, cristopher s.ogily and bob s.carter decompressive craniectomy. physiologic rationale, clinical indications, and surgical considerations.. schmidek & sweet operative neurosurgical techniques: indications, methods, and results. 2006 elsevier inc. pg. 70-81. 10.christian rainer wirtz, m.d., thorsten steiner, m.d., alfred aschoff, m.d., ph.d., stefan schwab, m.d., holger schnippering, m.d., hans herbert steiner, m.d., werner hacke, m.d., ph.d., and stefan kunze, m.d., ph.dhemicraniectomy with dural augmentation in medically uncontrollable hemispheric infarction.. neurosurgical focus 2(5): article 3, 1997. 11.peter hutchinson, ivan timofeev, and peter kirkpatrick .surgery for brain edema. neurosurg focus 22 (5):e14, 2007 12.horatiu rotaru, mihaela bǎciuţ, horatiu stan, simion bran, horea chezan, alexandru iosif, mircea tomescu, seong-gon kim, alexandru rotaru, grigore bǎciuţ. silicone rubber mould casted polyethylmethacrylate-hydroxyapatite plate used for repairing a large skull defect. jouranal of cranio-maxillofacial surgery (2006) 34, 242-246. 13.horatiu rotaru, horatiu stan, horea chezan, doru munteanu, seong-gon kim, alexandru rotaru, grigore baciut, petru berce, cristian dinu, simion bran reconstruction of the calvarial defectsusing custom-made cranioplasty plates. tmj 2007, vol. 57, no. 1 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article intracranial – extracranial meningioma: a case report of a rare entity vuk aleksic, milan spaic, miljan mihajlovic, marko samardzic, igor popovic, nenad zivkovic, aleksandra cvijovic serbia doi: 10.1515/romneu-2017-0049 302 | aleksic et al intracranial – extracranial meningioma doi: 10.1515/romneu-2017-0049 intracranial – extracranial meningioma: a case report of a rare entity vuk aleksic1, milan spaic1, miljan mihajlovic1, marko samardzic1, igor popovic1, nenad zivkovic1, aleksandra cvijovic2 clinical – hospital center zemun, belgarde, serbia 1department of neurosurgery; 2department of radiology abstract: meningiomas are common benign intracranial tumors. however, intracranial meningiomas with extracranial extension are exceedingly rare lesions with only a few reported cases in the literature. we report a case of an 86 years old female patient presented with enlarging mass over left parietal region for last 3 years. besides cosmetic, she had no complaints. head ct scan with bone window showed a large tumor consisting of intracranial and extracranial part, suggestive for meningioma. patient was operated, and both parts of tumor were removed. taking into account surgery indication and patient’s age, bone flap was returned. the postoperative course was uneventful and patient fully recovered. in the case of epicranial tumor attached to the underlying bone, meningioma should be excluded. key words: meningioma, intracranial – extracranial meningioma, epicranial tumor introduction meningiomas accounts for about 20-30% of all intracranial tumors. however, intracranial meningeomas with extracranial extension are exceedingly uncommon lesions with only a few cases reported in literature (1). we report a case of an 86 years old female patient with large intracranial meningioma with extracranial extension. case report a 86 years old female patient referred to our neurosurgery department due to progressive epicranial growth over left parietal region for last 3 years. she had only complaint on cosmetic appearance. patient neurological examination was normal. local status revealed a hard growth over left parietal region with intact overlying skin. patient had a positive history of treated hypertension. brain ct scan with bone window revealed a large tumor romanian neurosurgery (2017) xxxi 3: 302 305 | 303 consisting of intracranial and extracranial parts involving left parietal region (figure 1). the tumor was invading the brain tissue, but there was no significant edema. patient underwent operation and first the extracranial part was removed, after which parietal craniotomy was performed. dura with overlying tumor was cropped and subdural part of tumor was separated from the underlying brain parenchyma. part of tumor attached to bone flap was trimmed and taking account indication of surgery, as well as patient’s age, bone flap was returned to place (figure 2). histopathological study of the removed tumor confirmed the diagnosis of meningioma (who gradus i). the postoperative course was uneventful, and patient fully recovered. the control ct scan showed perfect position of bone flap, without signs of tumor rest (figure 3). patient was discharged on 10th day after surgery. follow up after 6 months was within normal expectations. figure 1 brain ct scan with bone window showing a large tumor consisting of intracranial and extracranial parts involving left parietal region figure 2 intaroperative view showing: (a) extracranial part of the tumor, (b) resection of extracranial part of the tumor, (c) bone flap after removal of extracranial tumor part, (d) resection of dura with intracranial (subdural) part of tumor figure 3 the control brain ct scan discussion meningiomas account for about 20% to 30% of all intracranial tumors (1). the incidence rate of meningiomas is about 2.6/100,000 populations, being more frequent in female patients. meningiomas incidence increases with age. meningiomas typically have benign histological findings (5). this is in accordance with our case, since we presented a female patient with large meningioma which showed benign histopathological finding. 304 | aleksic et al intracranial – extracranial meningioma however, meningiomas with extracranial extension are rare lesions, with only a few cases reported in literature (6, 7). according to study of darweesh alkhawaja et al, the locations of the extracranial meningiomas were: parietal region in 21 cases (31.8%), frontal region in 16 cases (24.2%), temporal area in seven cases (10.6%), occipital area in four cases (6.1%), frontoparietal in 11 cases (16.7%), frontotemporal in three cases (4.5%), temporoparietal in two cases (3.0%), and diffuse in two cases (3.0%) (2). our patient had most usual site of tumor origin because tumor was located in the left parietal region. typically symptoms of meningioma are not specific, and usually are associated with seizures, headache, paresis, personality changes and visual impairment. the diagnosis is made through brain ct or mri scan (3). our patient only had complaint on cosmetic appearance, and her neurological examination was normal. in the case of progressive epicranial tumor growth, clinical exam and neuro-radiological evaluation are necessary even in the absence of neurological deficit or severe clinical symptoms. as mentioned above, extracranial meningiomas are rare neoplasm’s, accounting for less than 2% of all meningiomas, but are most often found in the head. the relative rarity, in addition to inconsistencies in nomenclature, limits the study of these tumors. historically, they have been referred to as extracranial, extradural, extraneuraxial, and ectopic neoplasm’s arising outside of the central nervous system. the most widely used classification of extracranial meningiomas was proposed by hoye et al. (table 1) (4). table 1 the most widely used classification of extracranial meningiomas hoye classification system for extracranial meningiomas delineated based on site of origin (4) type a extracranial extension of meningioma with intracranial origin (secondary) type b extracranial extension of meningioma arising from skull base foramen (primary) type c ectopic tumor without connection to foramen, cranial nerve, or intracranial extension (primary) type d extracranial metastasis with documented intracranial lesion (secondary) in this case, the method of elimination led as to the conclusion that our patient had type a extracranial meningioma. also, the tumor was firmly attached to the dura, with a large base, and thus probable origin of tumor was from this site. taking into account indication of surgery (cosmetic appearance), patients age, as well as assumption that tumor originate from underlining dura, bone flap was returned to place due to better cosmetic appearance without much fear of tumor recurrence from the arachnoid cap cells which can be trapped in the bone flap or cranial sutures. since follow up after 6 months was within normal expectations without signs of tumor recurrence, our hypothesis that patient had romanian neurosurgery (2017) xxxi 3: 302 305 | 305 type a extradural meningioma (extracranial extension of meningioma with intracranial origin) was probably right, but since this neoplasms are slowly growing tumors, further checkups are required. in the case of extracranial meningiomas, surgical resection is the treatment of choice. if there is doubt about complete resection, the lesion should be followed with appropriate neuroimaging studies. in the case of recurrence, inoperability because of medical comorbidities, and in the case of incomplete resection, radiotherapy is recommended. also, in all cases of who grade ii and iii lesions, adjuvant radiotherapy is suggested (2). in our patient gross total resection was achieved without need for adjuvant radiotherapy. in the case of epicranial tumor growth, especially if attached to the underlying bone, meningioma should be excluded even in the absence of severe symptoms or neurological deficit. surgical resection is the treatment of choice with adjuvant radiotherapy in some cases. correspondence vuk aleksic department of neurosurgery, clinical hospital center zemun, belgrade, serbia address: vukova 9, 11000 belgrade, serbia e-mail: aleksicvuk@hotmail.som telephone number: +381 65 220 78 45 references 1.agrawal a, mohan m, shanthi v, reddy u. intracranial-extracranial meningioma mimicking an aggressive skull bone tumor. romanian neurosurgery. 2013;4:389-93. 2.al-khawaja d, murali r, sindler p. primary calvarial meningioma. j clin neurosci. 2007;14(12):1235-9. 3.cech da, leavens me, larson dl. giant intracranial and extracranial meningioma: case report and review of the literature. neurosurgery. 1982;11:694-7. 4.hoye sj, hoar cs, murray je: extracranial meningioma presenting as a tumor of the neck. am j surg. 1960;100:486 5.longstreth wt jr, dennis lk, mcguire vm, drangsholt mt, koepsell td. epidemiology of intracranial meningioma. cancer. 1993;72(3):639-48. 6.morina a, kelmendi f, morina q, morina d, mekaj a. intracranial extracranial huge meningioma: report of a case. turk neurosurg. 2015;25(5):779-82. 7.rojas-marroquín a, palencia hn, curán a, ramírez la. giant intracranial and extracranial meningioma of the falx cerebri: surgical management and case report. open journal of modern neurosurgery. 2015;5:88-92. romanian neurosurgery (2019) xxxiii, 1: 80-86 doi: 10.33962/roneuro-2019-017 www.journals.lapub.co.uk/index.php/roneurosurgery epidemiological study of intracranial meningiomas in a tertiary care hospital avdhesh shukla1, asheesh kumar gupta1, anand sharma1, s. n. iyengar1 1 department of neurosurgery, g. r. medical college gwalior, india abstract meningiomas are tumours that arise from the meningothelial cells. most of these tumours are intracranial; some are intraspinal and few extra cranial. there are many histological variants classified into three grades depending on clinical behaviour. classification is important for determining the modality of treatment. objectives: to study the incidence, location, sex and age predilection, histological variants and grading of meningiomas based on who 2007 classification and recurrence if present. materials and methods: all 200 cases of meningiomas. based on histological features, typing and grading of meningiomas was done as per the who 2007 classification of meningiomas. age, sex incidence, location of meningiomas were studied. results: meningiomas comprised 26.17% of all cns tumours during the study period. of 764 cns tumours, 200 were meningiomas. most of them were intracranial, predominantly involving the convexities of brain, females and the 41 – 50 age group. of these, 180 were benign grade i tumours, 12 were grade ii and 8 were grade iii. the most common histological variant was fibroblastic and meningothelial. grade ii and grade iii tumours commonly recurred. conclusion: meningiomas are slow growing tumours arising from the meningothelial cells accounting for 26.17% of all cns neoplasms showing a variety of histological patterns, more common in women, predominantly grade i tumours. recurrence of tumours depends on histological grade and extent of surgery. introduction a meningioma is a tumour that develops from the specialized meningothelial cell called as arachnoidal cap cells, the membrane that surrounds the brain and spinal cord, and located along the parasagittal sinus, over the cerebral convexity, sphenoid wing, around the pontocerebellar angle and along region of the spinal cord (1). meningiomas constitute approximately a quarter of central nervous system (cns) neoplasms. most meningiomas (90%) are categorized as benign tumours, with the remaining 10% being atypical or malignant. harvey cushing in 1922 coined the name “meningioma” for the most common dural based tumour, accounting for 15-30% of all primary intracranial tumours (2). these tumours can occur in any age, but commonly present in middle age and has a female preponderance, keywords intracranial meningioma, epidemiological study, tertiary care hospital corresponding author: asheesh kumar gupta department of neurosurgery, g. r. medical college gwalior, india asheesh_gsvm@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 81 epidemiological study of intracranial meningiomas in a tertiary care hospital with a female/male ratio of approximately 2:1 intracranial and 10:1 on the spine. genetic factors also play a role in meningioma development and predisposition. type 2 neurofibromatosis (nf2) is an autosomal dominant condition related to a mutation on chromosome 22q12 and is a common condition related to increased risk for developing meningiomas, among other neoplasms (3). ninety percent of meningiomas are benign, 6% are atypical, and 2% are malignant tumours (4). meningiomas vary in their symptoms, cranial meningiomas may cause seizures, headaches, and focal neurological deficits. diagnosis is made by a contrast enhanced ct and/or contrast mri (magnetic resonance imaging) scan. while mris are in some ways superior, the ct-scan can be helpful in determining if the tumour invades the bone, cause hyperostosis of bone. most patients with meningioma undergo resection to relieve neurological symptoms. complete resection is often curative. for incompletely resected or recurrent tumors not previously irradiated, radiotherapy is administered. two of the most important factors that determine the prognosis in patients with meningiomas are the extent of the resection and the tumor’s histological grade (5). although as a group they are considered to be benign, symptoms, variability in recurrence frequency, life expectancy, histological appearance and prognosis exist. material and methods this study is a retrospective study conducted in the department of neurosurgery, g. r. medical college and jay arogya hospital, gwalior, m.p. india, over a period of 5 years. of all cns tumours, only cases of meningiomas during the study period were included. meningiomas in all age groups and both sexes were included in the study. other cns tumours were excluded. these cases were analysed for age, sex incidence, location and histopathological diagnosis. statistical analysis was done by calculating the numbers and percentage for computing the incidence in various age groups, in sexes, location and hpe diagnosis. study design: a meta-analysis ethical approval: the study was undertaken after consent and clearance by the ethical committee of g.r. medical college gwalior inclusion criteria: of all cns tumours, only cases of meningiomas during the period 2012 – 2017 were included. meningiomas in all age groups and both the sexes were included in the study. exclusion criteria: other cns tumours were excluded. sample size: two hundred cases of meningiomas methodology: based on histological features, typing and grading of meningiomas was done as per the who 2007 classification of meningiomas. age, sex incidence, location of meningiomas were studied. statistical analysis: it was done by calculating number and percentage for computing the incidence in various age groups, in sexes, location and also comparison with other studies. observation and results table 1: age wise distribution of patients s.no. age (yrs) no. of patients perce ntage 1. < 20 9 4.5% 2. 20-40 75 37.5% 3. 41-60 96 48% 4. > 60 20 10% table 3: presenting complaints s.no. clinical presentation no. of patients percentage 1. headache 178 89% 2. seizure 96 48% 3. raised icp 80 40% 4. ptosis 20 10% 5. hemiparesis 69 34.5% 6. behaviour problem 15 7.5% 7. memory difficulties 40 20% 8. visual problem 27 13.5% 82 avdhesh shukla, asheesh kumar gupta, anand sharma, s.n. iyengar table 2. gender wise distribution of patients s.no. gender no. of patients perce ntage 1. male 92 46% 2. female 108 54% table 4: distribution of patients according to location of tumour s.no. location of tumour no. of patients perce ntage 1. falx or parasagital 40 20% 2. convexity 80 40% 3. sphenoid wing 20 10% 4. olfactory groove 13 6.5% 5. petroclival 3 1.5% 6. posterior fossa & cp angle 22 11% 7. tentorial 9 4.5% 8. pterional 2 1% 9.. tuberulam sellae 2 1% 10 intraventricular 5 2.5% 11 diploic 2 1% 12 foramen magnum 2 1% table 5. type of craniotomy location of tumour no. of patients perce ntage fronto-temporo-parietal craniotomy 20 10% frontoparietal craniotomy 62 31% frontal 33 16.5% temporo-parietal 19 9.5% tempro-parieto-occipital 9 4.5% bifrontal 15 7.5% parietal 5 2.5% sub-occipital 24 12% parieto-occipital 13 6.5% 83 epidemiological study of intracranial meningiomas in a tertiary care hospital table 6. distribution of patients according to according to surgical excision s.no. simpson grade no. of patients percentage 1. i 30 15% 2. ii 135 67.5% 3. iii 17 8.5% 4. iv 16 8% 5. v 2 1% table 7. distribution of patients according to size of the tumour s.n. size of tumour no. of patients percentage 1 1-3 cm 0 0 2 3-4 cm 138 69 3 4-5 cm 42 21 4 >5 cm 20 10 table 8. distribution of patients according to grade s.no. grade no. of patients perce ntage 1. i 180 90% 2. ii 12 6% 3. iii 8 4% table 9. post op complications s.no. post op complications no. of patients 1. infection 38 2. seizure 23 3. hemiparasis 86 4. visual loss 1 5. behavior change 28 6. memory deficit 43 7. raised (icp) 13 84 avdhesh shukla, asheesh kumar gupta, anand sharma, s.n. iyengar table 10. patient follow up data given as frequency s.no. follow up no. of patie nts with re curre nce % 1. < 2 year 5 2.5% 2. 2-5 years 12 6% figure 1. pre op and post op ct of tuberculum sellae meningioma. figure 2. pre op and post op ct of olfactory groove d figure 3. pre op and post op ct of posterior fossa meningioma figure 4. pre op and post op ct of sphenoid wing meningioma figure 5. pre op and post op ct of frontal convexity meningioma figure 6. pre op and post op ct of para saggital meningioma 85 epidemiological study of intracranial meningiomas in a tertiary care hospital discussion meningiomas constitute 25 30% of all cns tumours and are the most common tumour arising from the meninges (6). in our centre out of 764 cases of cns tumours, meningiomas constituted 200 (26.17 %), similar to studies by ab, shah et al (7), ruberti r f (8), intisar sh patty et al (9), shrilakshmi 25.25% and ejaz butt et al (10). women are more likely to develop a meningioma, (5) as in our study, females were more commonly affected 108 cases (54%) compared to males 92 (46%). a female preponderance for meningioma correlates with an endogenous hormone level and exogenous hormone replacement in postmenopausal women (in whom an increased incidence of meningioma is seen) as compared with postmenopausal women who have not taken exogenous hormone replacement therapy. the present study revealed that the incidence of meningioma was common in the age group 41-60 years 48% of patients. the mean age was 48.54 years. in the studies done by a b shah et al (7), shrilakshmi (2), the most common age group involved were also 40-50 years. meningiomas in children are less common (11), and in our study, there were only 9 cases of meningiomas in children of age group 11-20 years. the intracranial location of meningiomas were distributed as to be the convexities were commonly involved 40%, in which frontal was more common, 45.45%, followed by the parasagittal and falcine meningioma were 20%, 10% were in sphenoid wing, 11% in cp angle and posterior fossa. in a study by shrilakshmi et al, 61.11% of tumours were located in convexity. the clinical presentation of meningiomas, depends on tumour location (12). the symptoms at presentation are rarely precipitous, but often insidious. onset of slowly evolving headache is common and usually not associated with other symptoms suggestive of raised intracranial pressure, reflecting the slow growth of these tumours. a history of partial seizures is common for convexity meningiomas and an insidious personality change that is confused with dementia or depression is common in patients with large inferior frontal meningiomas (4). in our study, the most common clinical symptoms were headache, seizures and vomiting. the common radiological findings were mass lesions with pressure effect on adjacent structures and peritumoral edema. meningiomas divided in wide variety of histological patterns. our present study revealed that the most common histologic type was meningothelial (38.89%), similar to studies by nasrin samadi et al (13) sangamithra et al (14), thomas backer et al (15), followed by atypical meningiomas (16.67%). the other variants were fibroblastic (11.11%), transitional (11.11%), psammomatous variant, angiomatous, lympho-plasmacytic and fibrous (5.56%) each. according to who (5) atypical meningiomas have more than three of the following features – increased cellularity, smaller cells with high n/c ratio, greater than 4 mitotic figures/ 10hpf, prominent nucleoli and geographic necrosis. in our study (16.67%) of atypical meningiomas were reported. singh avninder et al (16) reported that papillary meningiomas and anaplastic meningiomas are rare and constitute 1 – 2.5% of all meningiomas. in the studies done by s hoon et al (17) and gottfried et al. (18) histological analysis reveals that 80–90% of meningiomas are benign [world health organization (who) grade i], 5–15% are atypical (who grade ii) and associated with a marked increase in recurrence. only 1–3% of the cases become anaplasic or malignant (whograde iii), developing a high tendency to invade brain structures, metastasize, and recur. in our study, 16.67% of atypical meningioma was observed. though meningiomas are considered to be benign tumours, recurrence is frequently observed (19). benign meningiomas can recur following incomplete resection, if large and associated with monosomy14 and del (1p36). the extent of surgical resection depends on the size of the tumour, site, and its relation to vital structures. the best accepted system for prediction of recurrence is the simpson grading system for completeness of resection (20), which evaluates the invasion of the venous sinuses, tumour nodules in adjacent dura, and infiltration of unresected bone by meningothelial cells. the recurrence rates that simpson refers to 9% for grade i, 16% for grade ii, 29% for grade iii, 39% for grade iv, and 100% for grade v, respectively. simpson’s scale of grading divides the extent of resection into 5 grades: grade i: complete removal grade ii: complete removal with coagulation of dural attachment 86 avdhesh shukla, asheesh kumar gupta, anand sharma, s.n. iyengar grade iii: complete removal, without coagulation of dural attachment or resection of involved sinus or hyperostotic bone grade iv: subtotal resection grade v: decompression biopsy. for patients with resection grades iv and v, endpoint for recurrence was enlargement of the remaining tumour, shown on mri or ct. in addition, histological characteristics of malignancy such as peritumoral brain edema, cellular pleomorphism, nuclear atypia, presence of macronuclei, atypical mitoses, increase of neovascularization, brain invasion and necrosis, favour recurrence rate of meningiomas (20). the treatment in grade i meningioma is total resection. in grade ii and grade iii meningiomas (2), surgery and adjuvant radiotherapy are the treatment of choice. extent of surgical resection is one of the most important factors in predicting recurrence along with histological grading. bone flap removal was done for 2 cases due to intraoperative brain swelling. immediate complication was haematoma in 2 cases (3.84%), for which reexploration was done. major post-operative complications in our study were convulsions 21.1%, wound infection 17.3%, csf leak in 9.62%, meningitis in 11.53%, of cases. all the patients before surgery were adequately treated with anti-convulsive therapy. postoperatively 15% of cases developed convulsions within 48 hrs after surgery. they were controlled with increase in the dose of anti-epileptics or addition of another antiepileptic drug. the major morbidity in our series was post-operative infection, in the form of wound infection, csf leak, and meningitis. follow-up period was 6 months to 5 years. cases were followed up with ct brain in symptomatic patients. twelve cases of recurrence are noted on follow-up for which incomplete resection was done. anyhow follow-up period was not enough to assess the recurrence as meningiomas are slow growing tumours. references 1. jose carlos, adrian mosquera. an integrative analysis of meningioma tumors reveal the determinant genes and pathways of malignant transformation. frontiers in oncology.2014;(4)147. 2. shrilakshmi.s, meningiomas: a clinicopathological study. int j med res health sci. 2015;4(4):827-831. 3. yangsy, parkck, parksh, kimdg, chungys, junghw. atypical and anaplastic meningiomas: prognostic implications of clinicopathological features. j neurol neurosurgpsychiatry .2008; 79(5):574–80. 4. jason rockhill, maciej mrugala, marc c. chamberlain, intracranial meningiomas: an overview of diagnosis and treatment. neurosurg focus 2007; 23 (4): e1. 5. deborah l. commins, roscoe d. atkinson and margaret e. burnett, review of meningioma histopathology; neurosurg focus 2007; 23 (4): e3. 6. a perry, d. n. louis, b. w. scheithauer. h. budka, a. von deimling: meningiomas in who classification of tumours of the central nervous system, 4th edition, iarc press, lyon 2007; 1:164-72. 7. ab shah, ga muzumdar, ar chitale. meningiomas: a report of a hospital-based registry. indian j pathology and microbiology 2005; 48(4): 468-71. 8. ruberti r f, the surgery of meningiomas: a review of 215 cases. african journal of neurological sciences 2007. 9. intisar s.h patty. central nervous system tumoursa clinicopathological study. j dohuk univ.2008; 11, (1):173 80. 10. m. ejaz butt, saeed a. khan, naseer a. chaudrhy, g.r. qureshi. intra-cranial spaceoccupying lesionsa morphological analysis.biomedica 2005; 21.31-35. 11. nirav mehta, sanatbhagwati, and geetaparulekar; meningiomas in children: a study of 18 cases; j pediatric neurosciences 2009;4(2): 61–65. 12. rutten i, cabay je, withofs n, lemaire c, aerts j, baart v, et al: pet/ct of skull base meningiomas using 2–18f-fluoro-l tyrosine: initial report. j nucl med 48:720–5, 2007. 13. nasrin samadi, seyed ali ahmadi; meningioma: a clinicopathological evaluation. malaysian journal of medical sciences 2007;14(1): 46-52. 14. sashidhar babu, shantveer g uppin, megha s uppin, et al. meningiomas: correlation of ki67 with histological grade. neurology india 2011; 59 (2) 20407. 15. jan regelsberger, christian hagel, pedramemami, thorsten ries, oliver heese, manfred westphal; secretory meningiomas: a benign subgroup causing life-threatening complications; neuro oncology 2009 december; 11(6): 819–24. 16. singh avninder, sarjotvermani, sharma shruti et al. papillary meningioma: a rare but distinct variant of malignant meningioma. diagnostic pathology 2007; 2:3. 17. sang hoonyoon, chun kee chung, and tae ahnjahng.surgical outcome of spinal canal meningiomas.j korean neurosurgsoc. 2007; 42(4): 300–04. 18. oren n. gottfried, wayne gluf, alfredo quinoneshinojosa, peter kan, and meic h. schmidt.spinal meningiomas: surgical management and outcome neurosurg focus 2003; 14 (6): 2. 19. konstantinos violaris, vasileios katsarides, maria karakyriou, pavlos sakellariou, surgical outcome of treating grades ii and iii meningiomas:a report of 32 cases.neuroscience journal 2013; 706481, 4 pages.konstantinos violaris, vasileios katsarides, pavlos 87 epidemiological study of intracranial meningiomas in a tertiary care hospital sakellariou , the recurrence rate in meningiomas: analysis of tumor location, histological grading, and extent of resection. open journal of modern neurosurgery, 2012; 2, 6-10 microsoft word 2adamdanil_recurrencechronic romanian neurosurgery (2018) xxxii 2: 187 204 | 187             doi: 10.2478/romneu-2018-0025 recurrence of chronic subdural hematomas requiring reoperation: could small trephination be a valid alternative to conventional approaches? danil adam1,2, dragos iftimie2, cristiana moisescu2 1„carol davila” university of medicine and pharmacy, bucharest, romania 2department of neurosurgery, „saint pantelimon” clinical emergency hospital, bucharest, romania abstract: background: chronic subdural hematomas (csdhs) are one of the most common intracranial lesions treated in a neurosurgical department. they associate significant morbidity and mortality that increase in the case of recurrences requiring reoperation. despite extensive published literature, there is still significant debate regarding optimal management of csdhs and their potential recurrence. objective: identify factors for recurrence requiring reoperation of csdhs in order to adjust our management strategies. methods: a retrospective review of 64 cases harbouring 71 csdhs that were surgically treated in the neurosurgery department of “saint pantelimon” clinical emergency hospital over a period of two years (january 2016 december 2017). two main surgical techniques were used: small trephine and large bone flap craniotomy, according to the operating surgeon’s preference. ct scans were performed at admission and 24 hours postoperatively. postoperative management was similar in all cases. results: recurrence requiring reoperation (rrr) was encountered in 16 (25%) of the reviewed cases. reoperation was found to be significantly more often encountered in particular preoperative ct characteristics: laminar type (rrr=38,10%, p=0.027) and maximal thickness above 22 mm (43,75%, p = 0,013). surgical technique had a substantial impact on recurrence: in trephinated cases, reoperation was required in only 8 of 51 patients (rrr=15,69%, p = 0.007), while large bone flap craniotomy associated a rrr of 61,54% (p = 0.008), which increased when associated with inner membranectomy (rrr=87,5%, p = 0,007) or subdural drain placement (88,89%, p = 0.007). reoperations not only doubled the neurosurgical hospital length of stay, but also associated higher perioperative mortality rates (18.75% versus 14,58%). conclusions: in our series, surgical technique had a decisive impact on the rate of recurrence. csdh surgery is another example of “in medio stat virtus”, where finding 188 | adam et al recurrence of chronic subdural hematomas requiring reoperation             the right balance between the least and most aggressive technique has the potential of providing the best outcomes, and thus small trephination could be taken into consideration. key words: chronic subdural hematoma, recurrence requiring reoperation, risk factors, small trephination introduction first described by swiss pathologist johann jakob wepfer in 1658 in his treatise on strokes entitled “historiae apoplecticorum”, chronic subdural hematomas (csdhs) nowadays represent a common intracranial lesion treated in a neurosurgical department. the elderly population is more frequently affected by this condition due to a series of predisposing factors, including: increased use of antithrombotic medication, vascular fragility, larger subdural space and susceptibility to frequent mild traumatic brain injuries secondary to same-level falls. [1] the incidence of csdh is estimated at 1.7 to 18 per 100 000 people/year and rises to 58 per 100 000/year in individuals > 65 years of age. [2] as the population > 65 years is expected to double by 2030, an increase in the incidence of csdh in the coming years is also expected. [3] surgical evacuation remains the treatment of choice for symptomatic csdh, with several surgical methods including twist drill craniotomy or burr hole with drainage, and large craniotomy being used. [4,5] despite its high incidence and extensive published literature regarding risk factors, management and outcome, the optimal surgical strategy as well as postoperative management of csdhs continue to attract significant debate. current management of symptomatic csdhs is accompanied by a rather high mortality rate, of 13%, which translates into approximately 4 deaths a year due to this disorder in a typical neurosurgical department. [6,7] in spite of rather simple operative procedures, the recurrence rate is relatively high (up to 33%), as compared with other traumatic brain injuries. [8,9] recurrences requiring reoperation (rrr) lead to an increase of morbidity and mortality rates. they also translate into a prolonged hospital length of stay and, implicitly, into increased financial costs. [10] the aim of the current study was to investigate factors predicting rrr in patients who underwent surgery for csdhs in our department, in an effort to adjust our treatment strategies and consequently improve the surgical outcome. material and methods we retrospectively reviewed data of 70 consecutive patients with csdhs which were surgically treated in the neurosurgery department of “saint pantelimon” clinical emergency hospital over a period of two years, between january 2016 and december 2017. romanian neurosurgery (2018) xxxii 2: 187 204 | 189             patients that, for various reasons, lacked a postoperative 24-hour control ct scan were excluded from the study, resulting in a total number of 64 patients harbouring 71 surgically treated csdhs who met de inclusion criteria. general characteristics patient demographics such as age, sex, medical history and risk factors for csdh were recorded. the specific risk factors that were taken into consideration are represented by alcohol abuse and antithrombotic medication. in all cases included, any pre-existing antiplatelet or anticoagulant therapy was temporarily discontinued upon admission and resumed after hospital discharge. the preoperative glasgow coma scale (gcs) score and relevant neurological findings were also noted, warranting the subsequent choice of surgical management. csdhs were diagnosed by head ct scan on the day of admission and subsequently confirmed by intraoperative findings. hematomas were grouped into 4 types based upon imagistic appearance, as classified by nakaguchi et al. all types included in this classification were found in our cohort (fig. 1): homogeneous, laminar, separated, and trabecular.[11] figure 1 preoperative ct scans of included patients according to the classification of nakaguchi et al.: homogenous hypodense subtype (a), isodense subtype (b), hyperdense subtype (c); laminar type (d); separated type (e), with gradation subtype (f); trabecular type (g) 190 | adam et al recurrence of chronic subdural hematomas requiring reoperation             the preoperative ct scan findings additionally evaluated were: maximum hematoma thickness (assessed in mm), midline shift, and whether the hematoma was unior bilateral. in order to determine hematoma size in bilateral cases, the maximum thickness was considered. surgical management all patients underwent surgery under general anaesthesia and orotracheal intubation. the csdhs were evacuated using two distinct surgical techniques: small trephine (25 mm diameter) craniotomy and 5 or 6 burr-holes bone flap craniotomy. in small trephination cases, a 5 – 6 cm linear scalp incision was performed, followed by a 25 mm craniotomy centred on the maximal thickness of the hematoma and a star-shaped incision of the underlying dura mater. the external membrane of the hematoma was opened in a circular fashion, preserving a 0.5 cm margin from the craniotomy. after hematoma evacuation, this margin was coagulated under visual control, and retracted as far as the craniotomy allowed. the remaining cavity was irrigated with warm saline solution in order to eliminate any residual blood clots. in some cases, a partial inner membranectomy was performed, while in others it was left intact. an epidural or subdural closed-system drainage was placed and maintained for at least 24 h. the bone flap was repositioned and secured with nylon sutures (fig. 2). figure 2 1-month postoperative ct reconstruction after using the small trephination technique and reposition of the bone flap the operative technique used was chosen according to the surgeon’s preference. in cases of bilateral symptomatic csdhs, the operation was performed on both sides in the same manner, during the same operative session. postoperative management a standard procedure was applied in all cases: after surgery, the patients were transferred from the or to the icu for at least 24 h for general monitoring, bed rest and treatment consisting of intravenous hydration with 1000 ml of saline solution and 500 ml 10% glucose solution. antiepileptic prophylaxis with a single loading dose of phenytoin was started during surgery; antiepileptic medication was continued only in the cases of at least one preoperative seizure. low dose heparin was also prophylactically prescribed, in order to prevent vascular occlusive events. in cases of romanian neurosurgery (2018) xxxii 2: 187 204 | 191             pre-existing antiplatelet or anticoagulant therapy, medication was resumed after discharge, depending on indications. neurological status was constantly monitored and logged at least once every day. in all cases, follow – up ct scans were performed in the first postoperative day, comparing residual hematoma thickness and midline shift with the preoperative value. recurrence of csdh requiring reoperation was diagnosed when neurological status did not improve postoperatively, new neurological symptoms occurred or the existing ones worsened, and re-accumulation of a subdural collection on the operated side was visible on follow – up ct scan. general outcome (home discharge, discharge to another hospital or death in hospital), as well as hospital length of stay, were also evaluated. statistical analysis data were described using means (standard deviations) and numbers of patients (percentages) for continuous and categorical variables, respectively. the tests were performed using ibm’s spss statistical analysis software (ibm spss v20). univariate and multivariate linear regression analyses were performed to assess the relationship between risk factors for chronic subdural hematomas, preoperative hematoma thickness, hematoma characteristics based on ct appearance (uni-/ bilateral, type of hematoma based on nakaguchi’s classification) and type of operation, with rrr. in all circumstances a probability (p) value of <0.05 was considered statistically significant and all tests were 2-tailed. results out of the 64 patients included, 16 developed recurrence requiring reoperation, representing 25% of all cases. patients demographics consisting of sex, age, risk factors and gcs score on admission are presented in table 1. table 1 general patient characteristics and associated rate of recurrence characteristics total no (%) nonrecurrent no (%) recurrent no (%) p-value gender  male 47 (73.44) 33 (70.21) 14 (29.79) .03  female 17 (26.56) 15 (88.24) 2 (13.33) age groups  ≥ 65 49 (76.56) 36 (73.44) 13 (26.53) .17  < 65 15 (23.44) 12 (80) 3 (20) risk factors  chronic alcohol abuse 29 (45.31) 22 (75,86) 7 (24.14) .05  antiplatelet 14 (21.88) 9 (64.29) 5 (35.71) .41 192 | adam et al recurrence of chronic subdural hematomas requiring reoperation             medication  anticoagulant medication 9(14.06) 7 (77.78) 2 (22.22) .98 preoperative gcs score  3 – 8 12 (18.75) 9 (75) 3 (25) .53  9 – 12 8 (12.5) 5 (62.5) 3 (37.5) .61  13 -15 44 (68.75) 34 (77.27) 10 (22.73) .40 out of the 64 patients included in the study, 47 (73,44%) were males and 17 (26.56%) were females, with a male-to-female ratio of approximately 2:1. a lower recurrence rate was noted among the female population, male sex being associated with a higher rate of recurrence (p= 0.03) a number of 42 patients (65.5%) have suffered repeated mild traumatic brain injuries before admission, while the rest of the patients (34.5%) could not mention notable head trauma in the past 3 months. age at presentation varied between 45 and 89 years, with an average of 69.56 years and a considerably high percentage (76.56%) 65 years old or older, consistent with the increased incidence of csdhs among the elderly population. however, age did not correlate with recurrence requiring reoperation (p=0.17). regarding risk factors for csdh development, previous antiaggregant treatment associated an increased, yet not statistically significant, rate of hematoma recurrence requiring reoperation (p = 0.41). chronic alcohol abuse, although frequently encountered among our patients (45.31%), did not present a statistically significant association with recurrence. the leading symptoms at admission were headache, dizziness, confusion and motor deficit, with an average gcs score of 12. a recurrence rate above our overall average can be observed in the 9-12 gcs group, although not statistically significant (p =0.61). preoperative ct scan identified 7 cases of bilateral chronic subdural hematomas, 3 of which subsequently required reoperation, with a recurrence rate of 42.86%, higher than 22.81%, associated with the unilateral group, but the association did not prove to be statistically relevant (p = 0.051, table 2). table 2 ct characteristics of csdhs and associated rate of recurrence characteristics total no (%) nonrecurrent no (%) recurrent no (%) p-value unilateral 57 (89.06) 44 (77.19) 13 (22.81) bilateral 7 (10.94) 4 (57.14) 3 (42.86) .051 maximal thickness  ≥ 22 mm 32 (50.00) 18 (56.25) 14 (43.75) .013 romanian neurosurgery (2018) xxxii 2: 187 204 | 193             maximum hematoma thickness was calculated between 9 and 46 mm, with an average of 21,75 mm. the selection of cut-off values for hematoma thickness was based on assessment of roc curves to find the best predictive ability. regarding the roc curve of thickness ≥ 22 mm, the area under the roc curve was 0.712 (95% ci = [0.5840.840], p = 0.013, fig. 3). a cut-off of thickness at 22.50 mm produced a sensitivity of 66% and a specificity of 40%. the probability of no rrr was estimated to be 95% if thickness was below 22.50 mm, and 78% if thickness was above 22.50 mm. regression analysis demonstrated that hematoma thickness ≥ 22 mm represented a significant predictor for csdh rrr (p =0.013). figure 3 roc curve of preoperative thickness ≥ 22 mm all types of chronic subdural hematomas according to the nakaguchi’s classification were encountered in our case series. the laminar type was most frequently found (21 cases), also associating the highest recurrence rate (38.10%). it was also the only type of hematoma with a statistically significant association with recurrence (p=0.027; table 2). homogenous hypoand hyperdense subtypes presented a below average reoperation rate, but it was not found to be statistically significant (p = 0.78 and p = 0.96 respectively; fig. 4).  < 22mm 32 (50.00) 30 (93.75) 2 (6.25) type  homogenous hypodense 8 (12,50) 7 (87.50) 1 (12.50) .78  homogenous isodense 8 (12,50) 6 (75.00) 2 (25.00) .82  homogenous hyperdense 5 (7,81) 5 (100.00) 0 (0.00) .96  laminar 21 (32.81) 13 (61.90) 8 (38.10) .027  separated 14 (21,88) 11 (78.57) 3 (21.43) .56  gradation 4 (6,25) 3 (75.00) 1 (25.00) .67  trabecular 4 (6,25) 3 (75.00) 1 (25.00) .73 194 | adam et al recurrence of chronic subdural hematomas requiring reoperation             figure 4 rate of recurrence in different types of hematomas according to the nakaguchi classification regarding surgical management, there were only 2 types of procedures used for hematoma evacuation, depending on the surgeon’s preference. the majority (79,69%) were operated through a small trephine craniotomy. this approach associated a recurrence rate of 15,69%, lower than the 61,54% encountered when a large bone flap craniotomy was performed. this result proved to be statistically relevant (p =0.008). hematoma inner membrane was partially resected in 39% of cases, while in the remaining patients it was left intact. reoperation was more often encountered after this debatable surgical manoeuvre was performed (40% versus 15,38%). however, when considering the type of approach in association with partial inner membranectomy, the least invasive approach (trephine without membranectomy) presented the lowest recurrence rate (14,71%), while the most aggressive one (bone flap craniotomy and inner membranectomy) presented an unexpectedly high recurrence rate (87,5%, fig. 5). the results proved to be statistically significant (p = 0.007, table 3). romanian neurosurgery (2018) xxxii 2: 187 204 | 195             figure 5 rate of recurrence when considering surgical approach and membranectomy table 3 type of operation and associated rate of recurrence type of operation total no (%) nonrecurrent no (%) recurrent no (%) pvalue small trephine craniotomy 51 (79.69) 43 (84.31) 8 (15.69) .007 large bone flap craniotomy 13 (20.31) 5 (38.46) 8 (61.54) .008 type of operation ± partial inner membranectomy  small trephine craniotomy without membranectomy 34 (53.13) 29 (85.29) 5 (14.71) .52  large bone flap craniotomy without membranectomy 5 (7,81) 4 (80.00) 1 (20.00) .43  small trephine craniotomy with membranectomy 17 (26.56) 14 (82.35) 3 (17.65) .49  large bone flap craniotomy with membranectomy 8 (12.50) 1 (12.50) 7 (87.50) .007 type of operation + epidural/ subdural drainage  small trephine craniotomy + epidural drain 26 (40.63) 22 (84.61) 4 (15.38) .23  large bone flap craniotomy + epidural drain 4 (6.25) 4 (100.00) 0 (0.00) .39  small trephine craniotomy + subdural drain 25 (39.06) 21 (84.00) 4 (16.00) .11  large bone flap craniotomy + subdural drain 9 (14.06) 1 (11.11) 8 (88.89) .007 also, evaluating surgical approach together with drainage placement, regardless of membranectomy, a similar significantly high rate of recurrence (88,89%) can be observed when associating a large bone flap with subdural drainage (p =0.007; table 3). length of hospital stay varied greatly, between 1 and 74 days with an average of 14,31 days. patients that were re-operated spent on average 22 days in our neurosurgical department, almost two times the number of days compared with nonrecurrent cases that were discharged after an average of 11,58 days. overall in-hospital mortality was 15,63%, slightly higher in the recurrent group 196 | adam et al recurrence of chronic subdural hematomas requiring reoperation             (18,75%) compared with the nonrecurrent group (14,58%). causes of death were in all cases associated with comorbidities, especially previous heart conditions. there was however a notable difference regarding number of cases that required transfer to another department and were not immediately discharged home. also, more cases in the recurrent group needed additional medical care in neurological or rehabilitation departments (fig. 6). fig. 6 comparison of outcomes in recurrent and nonrecurrent groups discussion in 1857, virchow (1821 – 1902) described csdh as “pachymeningitis haemorrhagica interna”. at that time, the condition was considered fatal. over the last 150 years, there was a great improvement in outcomes of this disorder, mainly due to better understanding the pathophysiology, introduction of modern imaging, especially the ct scan in the 1970’s, and refinement of operative techniques. although a frequently encountered pathology in neurosurgery, there has been relatively little progress in its management during the past 20 years. this is contrasting the evolution of concepts and surgical techniques in other neurosurgical subspecialties, such as functional, spinal, oncologic or vascular neurosurgery. [12] the poor outcome is directly related to the high risk of recurrence requiring reoperation associated with csdhs. in the last decade, many studies have proposed a series of risk factors that are associated with an increased recurrence rate. relationship between csdh’s rrr and age. there were few sporadic studies that suggested a causality relationship between advanced age and recur¬rence of csdhs requiring reoperation. [13–15] however, most recent studies have demonstrated no correlation between advanced age and an increased rate of recurrence. [11,16] also, in out cohort of 64 surgically treated patients, age over 65 years did not correlate with recurrence. advanced age is however a known risk factor for the development of csdh. this relationship can be explained by the development of cerebral atrophy that is associated with aging, as demonstrated by romanian neurosurgery (2018) xxxii 2: 187 204 | 197             yang et al in a study published in 2012. [17] yang proved his theory by studying previous research regarding the pathogenesis of csdh. considering csdh patients, 29 – 38% of them have no memorable precipitating trauma, unlike acute subdural hematoma cases that are almost always preceded by compelling trauma. [18] this observation was confirmed in our patients, 34% of them having no recollection of previous head trauma. most of csdh patients suffer mild, unremarkable trauma, usually with no loss of consciousness. [19] cerebral atrophy enables minor stress or trauma to determine separation of the dura–arachnoid interface. once these two layers are separated, fibrin, from either serum or exudates, can induce proliferation of granulation tissue on the inner dural surface which leads to formation of a neomembrane and consequent growth of new vessels directly within the subdural space. [20] subsequent studies have proven that csdhs can develop secondary to bleeding from these vessels. [21] it has also been stated that atrophy leads to tearing of bridging veins between the rigidly fixed dura and mobile arachnoid layer. [22] thus, studies assessing the pathogenesis of csdh supported yang’s hypothesis that patients with cerebral atrophy associate a greater risk of developing csdh. this connection between cerebral atrophy and csdh contributes to further understanding why patients older than 65 years, who have a higher incidence of brain atrophy present an increased risk for csdh development. [23] the results of our study support yang’s theory, when considering that more than 70% of patients included were over 65 years. relationship between csdh’s rrr and alcoholism the framingham heart study demonstrated an important correlation between alcoholism and cerebral atrophy. [24] the results suggested that cerebral atrophy may be one characteristic feature of alcoholic patients and thus is a risk factor for csdh development. [18] in this study, a significant number of subjects presented chronic alcohol abuse (45,31%). however, the rate of recurrence requiring surgery for these patients is similar to the general overall reoperation rate. the fact that a considerable proportion of the included patients were represented by elders and chronic alcoholics merely supports results from previous studies, advanced age and alcohol abuse representing risk factors for the development of chronic subdural hematoma, not for its recurrence. relationship between csdh’s rrr and antithrombotic medication the significantly higher prevalence of chronic subdural hematoma among the elderly could also be partially explained by the fact that 41% of them take antithrombotic medication, usually prescribed for prevention or treatment of coronary artery disease.[25] nevertheless, csdh patients under antiplatelet or anticoagulant therapy can pose a serious challenge for the neurosurgeon, generally associating a greater risk of intra and postoperative bleeding. 198 | adam et al recurrence of chronic subdural hematomas requiring reoperation             despite the absence of a definitive protocol, most neurosurgeons prefer to preoperatively discontinue and substitute antithrombotic therapy. once discontinued however, the optimal timing for operation, as well as for resuming antithrombotic medication is unclear. decision making remains a challenge: there is an unknown risk of intracranial re-bleeding when therapy is restarted too early and, simultaneously, a constant risk of vascular thrombotic events under suboptimal anticoagulation. in our study, 35,9% of patients were under antithrombotic or anticoagulant medication which, in all cases, was discontinued and replaced with low dose heparin before surgery. patients were operated after a variable interval, from a few hours up to 10 days, depending on the neurological status and associated conditions necessitating antithrombotic medication. antithrombotic medication was not resumed during hospitalization in the neurosurgical department in any of the aforementioned cases. this decision was made in accordance with recommendations in published literature. [26] concerning recurrence requiring reoperation in these patients, we found a higher recurrence rate in cases with antiplatelet treatment (37,5%), by comparison with the overall rate (25%). relationship between csdh’s rrr and ct characteristics ct scanning of patients with csdh provides a significant amount of information regarding the intracranial status and remains the most important diagnostic investigation for this disorder. numerous ct characteristics traditionally related to csdh recurrence have been reported and widely debated in the literature. these included bilateral site of csdh, preoperative and postoperative haematoma thickness or volume, preoperative and postoperative midline shift, haematoma densities, postoperative presence of air in the csdh cavity, and postoperative persistence of residual csdh space. [18,27,28] however, the influence of these ct features on outcome was not consistent between studies. therefore, we evaluated possible associations between the radiological characteristics of chronic subdural hematomas and their recurrence rate in our series. the imaging appearance of csdhs based on the density changes was assessed using the classification described by nakaguchi et al. into four types: the homogeneous (including hypodense, isodense, and hyperdense subtypes), laminar, separated (including gradation subtype) and trabecular.11 we also evaluated if chronic subdural hematomas were unior bilateral, the pre-and postoperative hematoma thickness, as well as midline shift. we found only two significant predictors for postoperative recurrence: laminar type and preoperative haematoma thickness > 22 mm. isodense, hyperdense, laminar and separated appearances are considered to have a greater tendency towards re-bleeding due to a greater vascularity, compared to homogenous types. [11,29] our data suggested that the laminar type was an important predictor of postoperative romanian neurosurgery (2018) xxxii 2: 187 204 | 199             recurrence, associating a rate of 38,10%, significantly higher than the overall recurrence rate in our cohort (25%). the other types of hematoma: homogenous, separated and trabecular, presented similar associated recurrence rates. these findings generally correspond with some results reported in literature. in 2001, mori et al. reported the outcome of 500 patients with surgically treated csdh and did not find a positive correlation between ct densities of hematomas and the rate of recurrence. [18] more recent studies however have different results. in 2017, stanisic et al proposed a grading system for prediction of chronic subdural hematoma recurrence requiring reoperation called the oslo score, 2 of the 5 maximum possible points being attributed for certain types of the nakaguchi classification (laminar, separated, isodense and hyperdense). [30] in our study we found a much higher reoperation rate (42,86%) associated to bilateral chronic subdural hematomas, compared to the overall 25%. the fact that bilateral csdhs associate a much higher recurrence rate compared to unilateral ones has been confirmed by numerous other studies. torihashi et al. reviewed 343 cases of csdh, including 61 patients who had a recurrence and his analyses showed that a bilateral csdh was an independent predictor for the recurrence of csdh. [31] the correlation seems to be caused by poor brain re-expansion that creates the potential for recurrence of the hematoma. [14] there are numerous reports that evaluated the preoperative volume of csdh on ct scan as a prognostic factor for recurrence. it was included in the oslo score, which considered that a preoperative hematoma volume greater than 130 ml has a significant impact on recurrence. in our study, we evaluated preoperative maximal hematoma thickness on ct scan, a characteristic much less discussed in the literature compared to preoperative volume, but readily available in our standard radiological reports. we found that a preoperative hematoma thickness > 22 mm associated a recurrence rate of 43,75%, in great contrast with a rate of only 6,25% when thickness was lower than 22 mm. based on this difference, it appears that preoperative hematoma thickness greatly influences the recurrence rate. relationship between csdh’s rrr and type of operation the treatment of csdh is an extremely debated topic. in 1925, putnam and cushing suggested craniotomy and removal of the outer membrane as a treatment option. [32] for many years craniotomy has been accepted as the optimal technique in the treatment of csdh despite the high associated surgical mortality rate of 30%. nowadays however, the following techniques have been adopted world-wide for csdh management: (1) two burr holes and irrigation; (2) single “large” burr hole with irrigation and aspiration; (3) single burr hole with placement of a subdural drain, maintained 24-48 hours, (4) twist drill craniotomy with aspirative drainge and (5) large craniotomy with excision of the subdural membrane. [33,34] lega et al. performed in 2009 a “medline search on articles published between january 200 | adam et al recurrence of chronic subdural hematomas requiring reoperation             1966 and september 2006 about csdhs and made a decision analysis”. they suggested that burr hole craniotomy is superior to twistdrill craniotomy and large craniotomy in treating csdhs. [35] regan et al. compared burr hole craniotomy and large craniotomy, proving the superiority of the latter technique when considering reoperation rates [36] also, williams et al. compared burr hole and twist drill craniotomy and found a much higher reoperation rate (64%) associated to the latter procedure and only 11 % reoperation rate associated with burr hole craniotomy. [37] the 64 patients included in the study were operated using two main types of surgical approaches: small trephination applied for the majority of the patients (79%), and large craniotomy used in the rest of the cases (20,31%). when strictly considering the type of the approach, the recurrence rate was significantly higher in cases where a large craniotomy was performed (61,54%), compared to 15,69%, the recurrence rate associated to small trephine craniotomy. another systematically discussed topic throughout the literature is the necessity of internal membranectomy after hematoma evacuation and whether its resection has any influence upon the recurrence rates. many authors have addressed this issue but the conclusions were not altogether consistent, some favouring membranectomy, while others regarding it as a main prognostic factor for recurrence. lee et al compared three different primary surgical methods (burr-holes, enlarged and extended craniectomy with partial membranectomy) in 172 patients with csdh. the rate of re-operation was 16% in the group of burr-hole drainage, whereas it was 18% and 23% in partial membranectomy with enlarged and extended craniectomy, respectively.16 also, khadka et al. reported favourable outcome in 98.6% of 365 patients who underwent single burr-hole drainage, with no membranectomy. [38] on the other hand, kim et al. compared a group of 16 patients who underwent a small craniotomy and another group of 42 patients who underwent a large craniotomy, with partial and extended membranectomy respectively. they concluded that the large craniotomy with extended membranectomy reduced the re-operation rate, compared with the small craniotomy group. [39] in our cohort, there were 25 cases (39,06%) in which a partial internal membranectomy was performed, in the rest of the cases the inner membrane being left intact (60,94%). membrane incision was associated with a significantly increased recurrence rate (40% versus 15,38%). this rate was even higher when associating a large craniotomy with inner membranectomy (rrr=87,5%). a cause for this high recurrence rate after operated csdh via this technique could be the fragile sinusoidal vessels that are present at the junction of inner and outer membranes which had not been adequately coagulated, provoking repeated multifocal hemorrhages. [40] another reason could be stretching and rupturing of bridging veins entering the superior sagittal sinus once brain begins to reexpand. [39] similar results were encountered in balevi’s cohort which included 148 patients romanian neurosurgery (2018) xxxii 2: 187 204 | 201             with surgically treated csdh’s, 28 of them being operated by large craniotomy with inner membrane excision. [41] the latter group associated a recurrence rate of 28.5%, while the reported rate associated to burr hole drainage is 4%–8%. [42] given the high recurrence rate associated with inner membranectomy that we observed, we do not recommend performing this surgical manoeuvre. „to drain or not to drain?” is a disputed question to which santarius et al provided an answer in the lancet in 2008. they conducted a randomized controlled trial in which patients with csdh were assigned to receive a subdural drain or no drain after evacuation. surprisingly enough, the trial was ended prematurely due to a significant reduction of recurrence, morbidity, and mortality at 6 months in patients receiving a drain. recurrence occurred in 10 of 108 (9.3%) patients with a drain, and 26 of 107 (24%) without. [3] in our cohort, a drain was placed in all cases, with a variation regarding its position: epidurally or subdurally. we did not find a significant difference regarding recurrence rate when comparing epidural with subdural drainage following small trephine craniotomy (15,38% versus 16%, respectively). the results are similar to the ones presented by kaliaperumal et al. they compared two types of drainage, subperiosteal drainage and subdural drainage following bur hole, in a cohort of 50 patients with operated csdh, detecting no significant differences between recurrence rates. [43] concerning the considerably more aggressive technique, we found an increase of recurrence rate when associating large craniotomy with subdural drain (88,89%). as a result of a literature data review, it appears that there is a great diversity regarding approaches for csdhs, varying from small, less invasive techniques (twist drill, burr hole) to large sized, more aggressive ones (bone flap). the trephination method that we currently practice can be adequately considered an intermediate technique between the two extremes, clearly leaning towards the less invasive category. when considering small sized approaches, burr hole and small trephine craniotomies are very similar regarding recurrence rates. the exception from this category is the twist drill craniotomy which usually associates higher reoperation rates. small trephine craniotomy, with a 25 mm diameter, offers a good operative field in order to coagulate the external hematoma membrane, as well as the possibility to easily aspirate hematoma content, especially in the trabecular type cases where septa could prevent complete evacuation, or in the cases where hematoma content is not completely liquefied. another advantage consists in the possibility to easily reposition the bone flap, thus avoiding any poor cosmetic results, regardless of trephine positioning. amongst the two extremes represented by small (burr hole, twist drill) and large craniotomies, the approach that we use (small sized trephination) could be considered a valid alternative in csdh surgery. 202 | adam et al recurrence of chronic subdural hematomas requiring reoperation             limitations this is a retrospective, single-centre study so it presents certain limitations and the results presented should be interpreted accordingly. the number of patients is small despite the relatively long inclusion period and high incidence of operated csdh in a typical neurosurgical department. no member of our neurosurgical department used the burr hole or twist drill techniques so, unfortunately, we could not compare it to our small trephination. there were a few patients excluded due to lack of postoperative imaging studies. also, the surgical interventions were performed by different neurosurgeons included in our department, each with certain unquantifiable particularities regarding technique. conclusions certain ct characteristics of chronic subdural hematomas associate a significantly higher rate of recurrence: laminar type and increased thickness (>22 mm). nevertheless, these are nonmodifiable factors. in our series, surgical technique had a decisive impact on the rate of recurrence. while some surgeons might still argue in favour of large bone flap craniotomies, subdural drainage and / or membranectomy, their negative influence on the rate of recurrence is undeniable. csdh surgery is another example of “in medio stat virtus”, where finding the right balance between the least and most aggressive technique has the potential of providing the best outcomes, and thus small trephination could be taken into consideration. ethical approval all procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 helsinki declaration and its later amendments or comparable ethical standards. for this type of study formal consent is not required. references 1. asghar m, adhiyaman v, greenway mw, bhowmick bk, bates a. chronic subdural haematoma in the elderly--a north wales experience. j r soc med. 2002;95(6):290-292. http://www.ncbi.nlm.nih.gov/pubmed/12042376. accessed february 14, 2018. 2. ducruet af, grobelny bt, zacharia be, et al. the surgical management of chronic subdural hematoma. neurosurg rev. 2012;35(2):155-169. doi:10.1007/s10143011-0349-y 3. santarius t, kirkpatrick pj, ganesan d, et al. use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial. lancet. 2009;374(9695):1067-1073. doi:10.1016/s0140-6736(09)61115-6 4. horn em, feiz-erfan i, bristol re, spetzler rf, harrington tr. bedside twist drill craniostomy for chronic subdural hematoma: a comparative study. surg neurol. 2006;65(2):150-153. doi:10.1016/j.surneu.2005.05.030 5. kotwica z, brzeziński j. chronic subdural haematoma treated by burr holes and closed system drainage: personal experience in 131 patients. br j neurosurg. 1991;5(5):461-465. doi:10.3109/02688699108998474 6. wakai s, hashimoto k, watanabe n, inoh s, ochiai c, nagai m. efficacy of closed-system drainage in treating chronic subdural hematoma: a prospective comparative study. neurosurgery. 1990;26(5):771-773. http://www.ncbi.nlm.nih.gov/pubmed/2352594. accessed february 14, 2018. 7. beatty ra. subdural haematomas in the elderly: experience with treatment by trephine craniotomy and not closing the dura or replacing the bone plate. br j romanian neurosurgery (2018) xxxii 2: 187 204 | 203             neurosurg. 1999;13(1):60-64. http://www.ncbi.nlm.nih.gov/pubmed/10492687. accessed february 14, 2018. 8. rohde v, graf g, hassler w. complications of burrhole craniostomy and closed-system drainage for chronic subdural hematomas: a retrospective analysis of 376 patients. neurosurg rev. 2002;25(1-2):89-94. http://www.ncbi.nlm.nih.gov/pubmed/11954771. accessed february 14, 2018. 9. camel m, grubb rl. treatment of chronic subdural hematoma by twist-drill craniostomy with continuous catheter drainage. j neurosurg. 1986;65(2):183-187. doi:10.3171/jns.1986.65.2.0183 10. mellergård p, wisten o. operations and reoperations for chronic subdural haematomas during a 25-year period in a well defined population. acta neurochir (wien). 1996;138(6):708-713. http://www.ncbi.nlm.nih.gov/pubmed/8836286. accessed february 14, 2018. 11. nakaguchi h, tanishima t, yoshimasu n. factors in the natural history of chronic subdural hematomas that influence their postoperative recurrence. j neurosurg. 2001;95(2):256-262. doi:10.3171/jns.2001.95.2.0256 12. weigel r, schmiedek p, krauss jk. outcome of contemporary surgery for chronic subdural haematoma: evidence based review. j neurol neurosurg psychiatry. 2003;74(7):937-943. doi:10.1136/jnnp.74.7.937 13. probst c. peritoneal drainage of chronic subdural hematomas in older patients. j neurosurg. 1988;68(6):908-911. doi:10.3171/jns.1988.68.6.0908 14. robinson rg. chronic subdural hematoma: surgical management in 133 patients. j neurosurg. 1984;61(2):263-268. doi:10.3171/jns.1984.61.2.0263 15. jack a, o’kelly c, mcdougall c, max findlay j. predicting recurrence after chronic subdural haematoma drainage. can j neurol sci / j can des sci neurol. 2015;42(1):34-39. doi:10.1017/cjn.2014.122 16. lee j-y, ebel h, ernestus r-i, klug n. various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? surg neurol. 2004;61(6):523-527. doi:10.1016/j.surneu.2003.10.026 17. yang a il, balser ds, mikheev a, et al. cerebral atrophy is associated with development of chronic subdural haematoma. brain inj. 2012;26(13-14):17311736. doi:10.3109/02699052.2012.698364 18. mori k, maeda m. surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. neurol med chir (tokyo). 2001;41(8):371-381. http://www.ncbi.nlm.nih.gov/pubmed/11561347. accessed february 19, 2018. 19. deci dm. chronic subdural hematoma presenting as headache and cognitive impairment after minor head trauma. w v med j. 100(3):106-107. http://www.ncbi.nlm.nih.gov/pubmed/15384743. accessed february 19, 2018. 20. apfelbaum ri, guthkelch an, shulman k. experimental production of subdural hematomas. j neurosurg. 1974;40(3):336-346. doi:10.3171/jns.1974.40.3.0336 21. fujisawa h, ito h, saito k, ikeda k, nitta h, yamashita j. immunohistochemical localization of tissue-type plasminogen activator in the lining wall of chronic subdural hematoma. surg neurol. 1991;35(6):441-445. doi:10.1016/0090-3019(91)90177-b 22. yamashima t, friede rl. why do bridging veins rupture into the virtual subdural space? j neurol neurosurg psychiatry. 1984;47(2):121-127. http://www.ncbi.nlm.nih.gov/pubmed/6707651. accessed february 19, 2018. 23. decarli c, massaro j, harvey d, et al. measures of brain morphology and infarction in the framingham heart study: establishing what is normal. neurobiol aging. 2005;26(4):491-510. doi:10.1016/j.neurobiolaging.2004.05.004 24. paul ca, au r, fredman l, et al. association of alcohol consumption with brain volume in the framingham study. arch neurol. 2008;65(10):13631367. doi:10.1001/archneur.65.10.1363 25. baechli h, nordmann a, bucher hc, gratzl o. demographics and prevalent risk factors of chronic subdural haematoma: results of a large single-center cohort study. neurosurg rev. 2004;27(4):263-266. doi:10.1007/s10143-004-0337-6 26. kamenova m, lutz k, schaedelin s, fandino j, mariani l, soleman j. does early resumption of lowdose aspirin after evacuation of chronic subdural hematoma with burr-hole drainage lead to higher recurrence rates? neurosurgery. 2016;79(5):715-721. doi:10.1227/neu.0000000000001393 204 | adam et al recurrence of chronic subdural hematomas requiring reoperation             27. matsumoto k, akagi k, abekura m, et al. recurrence factors for chronic subdural hematomas after burr-hole craniostomy and closed system drainage. neurol res. 1999;21(3):277-280. http://www.ncbi.nlm.nih.gov/pubmed/10319336. accessed february 22, 2018. 28. escosa baé m, wessling h, salca hc, de las heras echeverría p. use of twist-drill craniostomy with drain in evacuation of chronic subdural hematomas: independent predictors of recurrence. acta neurochir (wien). 2011;153(5):1097-1103. doi:10.1007/s00701010-0903-3 29. oishi m, toyama m, tamatani s, kitazawa t, saito m. clinical factors of recurrent chronic subdural hematoma. neurol med chir (tokyo). 2001;41(8):382386. http://www.ncbi.nlm.nih.gov/pubmed/11561348. accessed february 22, 2018. 30. stanišić m, pripp ah. a reliable grading system for prediction of chronic subdural hematoma recurrence requiring reoperation after initial burr-hole surgery. neurosurgery. 2017;81(5):752-760. doi:10.1093/neuros/nyx090 31. torihashi k, sadamasa n, yoshida k, narumi o, chin m, yamagata s. independent predictors for recurrence of chronic subdural hematoma: a review of 343 consecutive surgical cases. neurosurgery. 2008;63(6):1125-1129. doi:10.1227/01.neu.0000335782.60059.17 32. putnam tj, cusching h. chronic subdrual haematoma: its pathology its reaction to pachymeningitis haemoragica interna and its surgical treatment. arch surg. 1925;11(3):329-339. doi:10.1001/archsurg.1925.01120150002001 33. ko b-s, lee j-k, seo b-r, moon s-j, kim j-h, kim sh. clinical analysis of risk factors related to recurrent chronic subdural hematoma. j korean neurosurg soc. 2008;43(1):11-15. doi:10.3340/jkns.2008.43.1.11 34. liu y, xia j, wu a, wang y. burr-hole craniotomy treating chronic subdural hematoma: a report of 398 cases. chinese j traumatol = zhonghua chuang shang za zhi. 2010;13(5):265-269. http://www.ncbi.nlm.nih.gov/pubmed/20880450. accessed march 5, 2018. 35. lega bc, danish sf, malhotra nr, sonnad ss, stein sc. choosing the best operation for chronic subdural hematoma: a decision analysis. j neurosurg. 2010;113(3):615-621. doi:10.3171/2009.9.jns08825 36. regan jm, worley e, shelburne c, pullarkat r, watson jc. burr hole washout versus craniotomy for chronic subdural hematoma: patient outcome and cost analysis. plos one. 2015;10(1):e0115085. doi:10.1371/journal.pone.0115085 37. ray williams g, baskaya mk, menendez j, polin r, willis b, nanda a. burr-hole versus twist-drill drainage for theevacuation of chronic subdural haematoma:a comparison of clinical results. j clin neurosci. 2001;8(6):551-554. doi:10.1054/jocn.2000.0926 38. khadka nk, sharma gr, roka yb, et al. single burr hole drainage for chronic subdural haematoma. nepal med coll j. 2008;10(4):254-257. http://www.ncbi.nlm.nih.gov/pubmed/19558065. accessed february 23, 2018. 39. kim j-h, kang d-s, kim j-h, kong m-h, song k-y. chronic subdural hematoma treated by small or large craniotomy with membranectomy as the initial treatment. j korean neurosurg soc. 2011;50(2):103. doi:10.3340/jkns.2011.50.2.103 40. black pm, davis jm, kjellberg rn, davis kr. tension pneumocephalus of the cranial subdural space: a case report. neurosurgery. 1979;5(3):368-370. http://www.ncbi.nlm.nih.gov/pubmed/503299. accessed february 26, 2018. 41. balevi m. organized chronic subdural hematomas treated by large craniotomy with extended membranectomy as the initial treatment. asian j neurosurg. 2017;12(4):598. doi:10.4103/ajns.ajns_8_15 42. okada y, akai t, okamoto k, iida t, takata h, iizuka h. a comparative study of the treatment of chronic subdural hematoma--burr hole drainage versus burr hole irrigation. surg neurol. 2002;57(6):405-9; discussion 410. http://www.ncbi.nlm.nih.gov/pubmed/12176202. accessed february 26, 2018. 43. kaliaperumal c, khalil a, fenton e, et al. a prospective randomised study to compare the utility and outcomes of subdural and subperiosteal drains for the treatment of chronic subdural haematoma. acta neurochir (wien). 2012;154(11):2083-2089. doi:10.1007/s00701-012-1483-1 microsoft word 14martiniuccpolytrauma.doc 108 romanian neurosurgery (2010) xvii 1: 108 113 polytrauma with severe traumatic brain injury. case report c. martiniuc1, gh. dorobat2 1resident in anesthesiology and intensive care, iasi neurosurgery hospital 2professor of anesthesiology and intensive care, umf iasi, dental medicine faculty, head of anesthesia and intensive care unit, iasi neurosurgery hospital abstract the management of polytrauma patients requires a multidisciplinary approach, usually realised by a trauma team, based on trauma protocols. this category of patients should be treated in trauma centers, which are hospitals with extensive human and infrastructure resources. the authors present the case of a 17 years old female, a car accident victim, successfully treated in iasi neurosurgery hospital. as our hospital did not fulfill the requirements of a trauma center, the patient was managed in cooperation with various specialists from other hospitals. after the secondary survey, the patient presented severe traumatic brain injury (glasgow coma scale 5), double fracture of the mandibula, left pulmonary contusion, grade i spleen injury, fracture of the left clavicle and left radius bone, having an injury severity score of 29. during the neurointensive care unit hospitalization, the patient was submitted to multiple neurosurgical interventions. she was mechanically ventilated for 10 days, with complications during the evolution such as acute respiratoy distress syndrome, bacterial meningitis and severe sepsis with hospital aquired microorganisms. during the stay in icu, after an alternating but eventually positive evolution, the rehabilitation therapy was instituted. at discharge, after a lenght of stay (los) of 69 days, the patient was alert and awake with sensory aphasia and right hemiparesis and was referred to a neurologic rehabilitation clinic. keywords: severe traumatic brain injury, polytrauma, severe sepsis, ards introduction polytrauma is a syndrome determined by the action of different powerful agents (e.g. mechanical, chemical) that affect at least two regions of the human body, with at least one of the injury having a lethal potential. the newer definition of polytrauma implies the use of injury severity score (iss) iss must be equal or greater than 17 (2) (table 1). the etiology and seriousness of polytrauma has very much changed in the last century due to the development of mankind (warfare tehniques, car industry) . we report the case of a car accident victim. the patient was admitted in the intensive care unit (icu) of iasi neurosurgery hospital with an iss of 24, having severe traumatic brain injury, chest and abdominal trauma and multiple bone fractures, the brain injury beeing the most severe of all the traumatic injuries. case presentation the patient t.a., female, aged 17, victim of a car accident, without other known associated pathology or drug abuse c. martiniuc, gh. dorobat polytrauma with brain injury 109 history was brought by the ambulance at the emergency department of iasi neurosurgery hospital in deep coma (glasgow coma scale 5 – e1v1m3), intubated, sedated, mechanically ventilated. the neurologic exam revealed spontaneous flexion of both arms and miotic, equally in diameter and reactive pupils. the patient was haemodinamically stable, with breath sounds present equally bilateral and left basal rales. the cerebral native ct-scan revealed bilateral frontotemporal haemorragic contusions, left occipital hematoma and laceration, with diffuse cerebral edema without midline shift and left parieto-occipital cominutive fracture. the patient had received mannitol 1 gram per kilogram in the ambulance. as our hospital did not have the resources of a trauma center and as the cerebral injuries did not require emergent surgical intervention (except for the insertion of a intracranial catheter for intracranial pressure (icp) monitoring, not available in our hospital at that time), the patient had to be sent to the surgery clinic for the diagnosis and treatment of the chest, abdomen and extremity injuries. ais score injury 1 minor 2 moderate 3 serious 4 severe 5 critical 6 unsurvivable the patient returned to our clinic after a few hours, diagnosed with left basal pulmonary contusion, grade i spleen injury, double fracture of the mandibula, fracture of the left clavicle and distal epiphysis of the left radius bone, none of which had necessitated emergency intervention. the patient was admited in the intensive care unit (icu) of the neurosurgery hospital, as the cerebral injuries had the highest severity. she received the standard icu care (vital signs monitoring, cvp monitoring via a central venous line, nasogastric tube, hourly diuresis monitoring). she received analgesia and sedation with fentanyl and propofol, and was mechanically ventilated in ippv autoflow assist mode (intermitent positive pressure ventilation). the ventilator parameters were set to maintain the paco2 (partial pressure of carbon dioxide in arterial blood) between 30 and 35 mm hg (mild hyperventilation). head of bed was raised at 45 degrees. the mean arterial pressure was maintained over 90 mm hg (according to the guidelines 4) without the use of vasoactive drugs. the oxygenation was good pao2 (partial pressure of oxygen in arterial blood) ≥ 100 mm hg at a fio2 (fraction of inspired oxygen) of 0.5. the lab tests on admission (complete blood count, biochemistry, coagulation tests) were normal except for the hemoglobin (8.5 g/dl), hematocrit (25.5%) and white cell count (19800/mm3). serial neurological examinations were performed, as there was no icp monitoring available. enteral nutrition was initiated. after 24 hours of hospitalisation, the patient developed anisocoria (left mydriasis). 110 romanian neurosurgery (2010) xvii 1: 108 113 table 1 the patient’s iss (injury severity score) based on ais (abbreviated injury scale) on icu admission (2) region injury description ais square top three head & neck cerebral contusion 4 16 face double fracture of the mandibula 1 chest left basal pulmonary contusion 2 4 abdomen grade i spleen injury 2 4 extremity fracture of the left clavicle fracture of the distal epiphysis of the left radius bone 1 1 external none 0 injury severity score 24 the ct scan showed, apart from the injuries presented at admission, the augmentation of the cerebral edema, compression of the left lateral ventricle and important midline shift towards right. as the neurological status did not improve after intermitent boluses of mannitol, the surgeons performed an emergent left decompressive craniectomy. after the intervention, the neurological status improved pupils would become equal and reactive with a gcs of 6 (e1v1m4). on the second and third postoperative day, the patient began to present pulmonary rales and fever (≤38,8ºc) (being mechanically ventilated) and hypoxemia despite higher values of fio2. in addition, the chest x-ray showed bilateral lung infiltrates; corroborated with a low hypoxemia score (pao2/fio2 under 200 mmhg), and a suggestive clinical context (pulmonary contusion), all these criteria sustained the diagnosis of acute respiratory distress syndrome (ards) (3). the ventilation mode was switched to bipap (bi-level positive airway pressure), with a lung protective strategy ventilation (low tidal volumes were used). still, the alveolar recruitment measures were impeded by the use of low values of peep (positive end expiratory pressure) because of the cerebral edema.. during the first 2 postoperative days, it was difficult to adapt the patient to the ventilator whilst trying not to aggravate the cerebral edema shown on the postoperative day 1 ct scan (figure 2). this is why we chose to paralyse the patient with atracurium. intermitently we stopped the muscle relaxant for neurologic examinations. the paralysis only slightly improved the hypoxemia score and was stopped after 48 hours. after that, we increased the peep values to 10 – 12 cm h2o, which improved the oxygenation. c. martiniuc, gh. dorobat polytrauma with brain injury 111 in the third postoperative day the bacteriology came positive in the tracheal secretions for pseudomonas aeruginosa, with negative hemocultures, urine and feces cultures. the chest x ray was suggestive for bronchopneumonia; the lab tests showed, apart from the inflammatory syndrome, a severe anemia (hematocrit 19%), but also moderate thrombocytopenia with altered coagulation tests, a low albuminemia and unconjugated hyperbilirubinemia – signs of liver failure. the anemia was hemolytic. the patient became oliguric, with a serum creatinine value of 2.2 miligrams per deciliter. with the procalcitonin test positive, we suspected severe sepsis of pulmonary origin. (surviving sepsis campaign, 2004). at that time, the patient had a sofa (sequential organ failure assessment) score of 14 (6). we performed initial fluid resuscitation (first 6 hours) according the surviving sepsis campaign 2004 guidelines (5). the patient received broad spectrum antibiotics until the positivation of cultures; aftewards, as guided by the antibiogram (the strain had sensibility for imipenem) she also received erytrocite mass, fresh frozen plasma and albumin. for two days we initiated inotrope (dobutamine – 5 µgrams/kilogram/ minute) and vassopressor therapy (dopamine – 6–10 µgrams/kilogram/ minute) because of the hemodynamic instability. we did not have the possibility of inserting a swan ganz catheter, which would have been useful for managing the hemodynamic parameters. figure 1 cerebral ct scan on admission (see text for explanations) the patient responded well to the therapy. gradually, the vasopressors were stopped. the hypoxemia score gradually improved, corelated with the chest x-ray images. still, the patient continued to present pulmonary rales and subfever, which resolved after three days. the renal and livere failure responded well to fluid resuscitation. there was no need for renal replacement therapies. figure 2 ct scan: postoperative day 1. one can observe the brain herniation through the craniectomy space through the seriated neurological evaluations, the patient began to present reactivity at pain stimuli (withdrawal on the left side, right hemiplegia) – gcs – 6. the pupils were equal and reactive. the haemorrhagic cerebral injuries began to resolve, and the ct scan performed at day 4 showed the diminuation of the mass effect as the brain herniated through the craniectomy defect. (figure 3). 112 romanian neurosurgery (2010) xvii 1: 108 113 during the 8th postoperative day, the patient opened her eyes. after a cpap weaning protocol, she was detubated (glasgow coma scale 10). antibiotherapy was continued (imipenem plus levofloxacin). after a period of relative stability, the cultures from the tip of the central venous catheter became positive also for pseudomonas aeruginosa, with sensibility for imipenem. in the meantime, several complications of trauma and surgery developed – hydrocephalus, external csf (cerebrospinal fluid) fistula and after that, meningitis with coagulase-negative staphilococcus susceptible at linezolid and vancomycin. a continuous lumbar drainage was instituted (because of the meningitis, an external ventricular drainage was contraindicated) and vancomycin was added in the therapy. the fistula and meningitis gradually resolved. figure 3 ct scan: postoperative day 4 (see text) after 7 days of continuous lumbar drainage, for the definitive treatment of hydrocephalus a ventriculo-peritoneal shunt was put in place. during the evolution, the haemorrhagic injuries showed resorption, but an ischemic area in the left frontal lobe persisted (see figure 4). figure 4 ct scan: 18 weeks after the accident after 56 days in the icu, the patient was transferred to a maxillo-facial surgery clinic, for the definitive treatment of the mandibula fracture she was sent back after 2 days. during the time spent in the icu, the neurologic rehabilitation therapy was instituted. the patient was discharged with right hemiparesis, sensory aphasia and deglutition disturbances, receiving food via the naso-gastric tube. she was reffered to a neurologic rehabilitation clinic. within one month, the deglutition disturbances ameliorated, and the aphasia partially resolved. after 8 months, the patient returned to our clinic for cranioplasty. discussion the main issues in the management of this patient with severe tbi were the lack of a trauma center in iasi and the lack of c. martiniuc, gh. dorobat polytrauma with brain injury 113 icp monitoring in our hospital. the trauma patient is one of the most critical patients. the management of polytrauma should be realised in a trauma center, by a trained trauma team (1). transportation between different hospitals for diagnosis should be avoided, if possible. still, we had to send the patient for the evaluation of the chest and abdominal injuries, as our hospital was the first medical facility the patient had been brought to. the initial neurologic deterioration took place with the patient being sedated, mechanically ventilated, with the ventilatory parameters corelated with the seriated abgs and with a mean arterial pressure kept above 90 mm hg, but without an icp monitor. despite its controversies, the management of high icp was realised by decompressive craniectomy, which allowed the prolapse of the edematous brain through the edges of the craniectomy defect. the challenges of this case were the management of the combination between severe head trauma and ards, and of the severe sepsis, with msof (multi systemic organ failure) – respiratory, liver, renal failure. in evolution, this case presented multiple septic complications. the postoperative external csf fistula was the cause of the meningitis with a nosocomial bacteria. the patient was hospitalized for 69 days. the hospitalisation costs were around 20000 ron. conclusion the decompressive craniectomy, despite the controversies, proved efficient. the management of ards combined with severe tbi was difficult during the first two postoperative days. severe sepsis was treated according to the latest guidelines. the alternating clinical evolution of the patient was due to the hospital aquired microorganisms, with multiple antibiotic resistance. acknowledgements the authors would like to thank professor ion poeata, dr. bogdan costachescu, dr. cornel balan – neurosurgeons, dr. meda balan – anesthesiology and intensive care specialist, professor corneliu aldescu – head of radiology and computed tomography department of iasi neurosurgery hospital. references 1. 1.american college of surgeons committee on trauma. advanced life support course for physicians.chicago: american college of surgeons, 1997 2.2.baker sp et al, "the injury severity score: a method for describing patients with multiple injuries and evaluating emergency care", j trauma 14:187-196;1974. 3.3.bernard gr, artigas a, brigham kl, carlet j, falke k, hudson l, lamy m, legall jr, morris a, spragg r. the american-european consensus conference on ards. definitions, mechanisms, relevant outcomes, and clinical trial coordination. am j respir crit care med. 1994 mar;149(3 pt 1):818-24. 4.4.brain trauma foundation guidelines for the management of severe traumatic brain injury – 3rd edition – journal of neurotrauma, vol. 4, supplement 1, 2007 5.5.surviving sepsis campaign guidelines for management of severe sepsis and septic shock 2004. crit care med. 2004;32(3):858-873 6.6.vincent jl, moreno r, takala j, willatts s, de mendonça a, bruining h, reinhart ck, suter pm, thijs lg. the sofa (sepsis-related organ failure assessment) score to describe organ dysfunction/failure. on behalf of the working group on sepsis-related problems of the european society of intensive care medicine. intensive care med 1996 jul;22(7):707-10 romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article when hanging caused an intracranial haemorrhage a rare case report vardan kulshreshtha, ashok kumar, gaurav jaiswal, tarun kumar gupta india doi: 10.1515/romneu-2017-0017 romanian neurosurgery (2017) xxxi 1: 111 – 114 | 111             doi: 10.1515/romneu-2017-0017 when hanging caused an intracranial haemorrhage a rare case report vardan kulshreshtha, ashok kumar, gaurav jaiswal, tarun kumar gupta department of neurosurgery, rnt medical college, udaipur, india abstract: depressive illness is a growing health hazard into modern era days. depression may sometimes result in suicidal tendency in a major number of patients. suicidal attempt not only leads to loss of life, but also a significant number of survivors retain various morbidity. we here report a rare case of intracranial haemorrhage (ich) following a suicidal attempt by hanging. key words: suicidal hanging, intracranial haemorrhage introduction depression is a common disorder in modern world. its prevalence is rising and there are a number of reasons behind. the depression is a treatable disorder. a major number of patients with depression present to the physicians with unexplainable vague complaints and this happen mostly in primary care settings. the average national deficit of psychiatrists in india is estimated to be 77% which may be as high as 90% in certain states individually. (1) hence to get proper and timely treatment in indian scenario is rather a difficult task. the depression has been rated as the third leading cause of the global burden of the disease accounting for 4.3% of the disability adjusted life years (daly). it will be a leading cause of disease burden by year 2030. (2, 3) patients often has the tendency to commit suicide in course of their depressive disease. the problem is worse in those suffering from chronic depression. we here report a case of patient of depressive disorder who presented to us with ich immediately following a suicidal attempt by hanging. case report a 30 year old male patient was referred to the department of neurosurgery from department of emergency medicine with alleged history of suicidal attempt by hanging. the patient was a diagnosed case of depression but defaulter on treatment. no history of substance abuse or any chronic drug intake was present. there was a history 112 | kulshreshtha et al iintracranial haemorrhage caused by hanging             of attempted suicide in past also. the vitals were all within normal limits. the glasgow coma scale (gcs) was e2v2m5 with dilated left side pupil. there was right sided hemiparesis noted with left sided facial weakness. there was ligature mark noted around the neck. there were no other external injury marks over the scalp and elsewhere over the body. non contrast computed tomography (ncct) head revealed a large ich in left in thalamoganglionic region with intraventricular haemorrhage with significant mass effect and midline shift of 9 mm to contralateral side. left side frontotemporoparietal (ftp) decompressive craniotomy was done. the ich was evacuated completely and duroplasty performed. the patient was managed postoperatively as per the standard institutional protocols. the patient was discharged in satisfactory condition with advice to review in psychiatry clinics. on 6 month and 1 year follow up the patient was well and independent. figure 1 preoperative ct scan figure 2 photo of patient with ligature mark on neck figure 3 postoperative ct scan discussion recently it has been found that 10-15% patients in their life time suffer a major depressive illness4 and 5% suffer from a major depression in a given year. (5) in indian scenario the overall prevalence of depression is 15.9% roughly similar to the global prevalence. (6) more than half of the depression patients may have suicidal romanian neurosurgery (2017) xxxi 1: 111 – 114 | 113             ideation (7). one of the study from india reported suicidal attempts in 16% patients of depression. (8) further those attempted suicide once had a higher tendency to commit suicide in future too. various modes of attempting suicide are hanging, drowning, poisoning, drug over dosage, self inflicted gun shots/burns etc. as per the national crime records bureau (ncrb) of india, total number of suicides committed in 2014 were 1,31,666. the number of suicides in the country during the decade (2004–2014) has recorded an increase of 15.8% (1,31,666 in 2014 from 1,13,697 in 2004). when a person attempts a suicide he may loose his life or may be saved if timely intervened by some help. the survivors may also end up with various morbidities. hanging is a form of strangulation that involves suspension of body with the ligature tied around the neck. weight of body acts. hangings may be sub classified as complete or incomplete. when the whole body hangs off the ground and the entire weight of the victim is suspended at the neck, the hanging is said to be complete. incomplete hangings imply that some part of the body is touching the ground and that the weight of the victim is not fully supported by the neck. hangings may also be classified by intent (e.g., homicidal, suicidal, autoerotic, accidental).the various injuries that take placed while a person attempts hanging are asphyxia, venous congestion of brain, cerebral ischemia, fracture/ dislocation of cervical vertebra. various changes which have been described in the literature are diffuse cerebral hypoxia, diffuse cerebral oedema, subarachnoid haemorrhage, arterial intimal injury. the hanging causes a form of asphyxia. most of the patients die because of the hypoxic ischemic neuronal damage. there has been to date no case report in the literature of neurosurgery and forensic medicine about development of ich in victim surviving hanging. we report this case to bring this rare presentation of hanging resulting in ich and later on uneventful recovery without any neurological deficit. conclusion: the various manifestations of hanging have been described in literature such as anoxic edema, hypoxic encephalopathy, venous brain congestion. occurrence of ich after hanging should be kept in mind especially in those not gaining consciousness on time or showing focal neurological deficits. timely diagnosis and intervention can be life saving in these patients. correspondence vardan kulshreshtha, 41-b, ambamata scheme , udaipur, rajasthan( india) e-mail: drvardan@gmail.com, +917023334765 references 1. world health organisation. global burden of disease report, 2004 update. available at http.//www.who.in/healthinfo/global_burden_disease/g bd_report_2004update_fullpdf. 2.ostun, t.b., ayuso-mateos, j.l., chatterji, s., mathers, c., murray, c.j.l. global burden of depressive disorder in the year 2000. british journal of psychiartry, 184, 38692, 2004. 3.thirunavukarasu, m., thirunavukarasu, p. training and national deficit of psychiatrists in indiaa critical analysis. indian j psychiatry, 52, 83-8. 2010. 4.bromet, e., andrade, l.h., hwang, i., sampson, n.a., alonso, j., de girolamo, g, et al. crossnational 114 | kulshreshtha et al iintracranial haemorrhage caused by hanging             epidemiology of dsm-iv major depressive episodes. bmc med, 9, 90. 2000 5.murphy, j. m., laird, n,m., monson, r.r., sobel, a.m., leighton, a.h. a 40 year perspective on the prevalence of depression. the sterling county study. arch gen psychiatry, 57, 209-15, 2000. 6. poongothai, s., pradeepa ,r., ganesan, a., mohan,v. prevalence of depression in a large sub urban south indian population. the chennai urban rural epidemiology study (cures-70).plos one2009;4:e7185 7.sokero tp, melartin tk, rytsälä hj, leskelä us, lestelä-mielonen ps, isometsä et.suicidal ideation and attempts among psychiatric patients with major depressive disorder. j clin psychiatry 2003;64:1094-100. 8.srivastava as, kumar r. suicidal ideation and attempts in patients with major depression: sociodemographic and clinical variables. indian j psychiatry 2005;47:225–8. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article primary meningeal sarcoma (fibrosarcoma) of cervical spine in an 11 yr old boy: an extremely rare case report kumar pradeep, verma pawan kumar, das srikant, gupta ashok india doi: 10.1515/romneu-2017-0032 romanian neurosurgery (2017) xxxi 2: 203 206 | 203 doi: 10.1515/romneu-2017-0032 primary meningeal sarcoma (fibrosarcoma) of cervical spine in an 11 yr old boy: an extremely rare case report kumar pradeep, verma pawan kumar, das srikant, gupta ashok department of neurosurgery, sms medical college, jaipur, rajasthan, india abstract: primary meningeal sarcoma is a rare tumor in pediatric age group. here we were reporting an extremly rare case report of an 11 year old boy presented with quadriparesis and bladder involvement. mri revealed a cervical dural based tumor with extension to cord parenchyma and neural foramina involving paravertebral tissue. the histopathology revealed mesenchymal tumor with malignant potential which on immunohistochemical (ihc) study found to be vimentin positive fibrosarcoma. key words: primary meningeal sarcoma, fibrosarcoma, pediatric age, cervical spine introduction primary meningeal sarcomas are rare but highly aggressive tumors predominantly affecting children. primary malignant sarcoma of spine is extremely rare. it is very difficult to diagnose on radiological characteristics which are similar to more common dural based pathology like meningioma, lymphoma, hemangiopericytoma, melanoma, rhabdomyosarcoma and gliosarcoma. even the more common spinal meningioma, like intracranial meningioma, is very rare in paediatric age group. tumor locations also differ from those seen in adult in which more common in dorsal spine while in children more in cervical region. the malignant behaviour can be predicted on radiological characteristics but confirmed only on histopathological examination (hpe) and ihc study. case report an 11year-old boy presented to us in july 2016 with gradually progressive spastic weakness of all four limbs from 3 months starting from lower limbs with bladder incontinence. there was no history of prior radiation or chemotherapy. on clinical evaluation the power in both lower limbs was 0/5, right upper limbs 2/5 and left upper limb 3/5. biceps, triceps, knee and ankle jerks were exaggerated. there was decrease sensation to touch, pain, and temperature below c3 dermatome. on further evaluation we performed mri of cervical spine with screening of brain and whole spine which showed isointense lesion on t1 and heterogenous hyperintense signal on t2 extending from c4-d1 level with intramedullary and extradural extension on right side along c8 nerve root in right paravertebral region (figures 1a, 1b). the 204 | kumar et al – cervical primary meningeal sarcoma in children lesion was associated with marked perilesional edema extend from cervicomedullary junction to d4 region as hyperintense signal. on t1 gd+ the lesion showed heterogenous contrast enhancement (figures 2a, 2b). according to the location and mri features of the tumor, the lesion was pre operatively diagnosed as nerve sheath tumor with neurofibroma, meningioma, ependymoma, sarcoma, lymphoma and melanoma were kept in diffential diagnosis. figure 1 (a) t1 –mri of cervical spine showing isointense lesion, (b) t2-mri showing heterointense signal extending from c4-d1 with perilesional hyperintense signal figure 2 (a) t1 gd+ saggital image showing intense contrast enhancement, (b) axial image showing contrast enhacement with intramedullary and extradural extension on right side along c8 nerve root in right paravertebral region figure 3 histopathology showed spindle cell neoplasm arranged in fascicles and at places in sheets, there is loss of lobular architecture , nucleoli are inconspicuous, necrosis absent, mitoses >4/10 hpf with glial infiltration romanian neurosurgery (2017) xxxi 2: 203 206 | 205 figure 4 (a) spindle cell positive for vimentin (b) mib score> 18% the patient underwent laminectomy. intraoperatively dura was tensed which was incised in the midline. the tumor was firm, moderately vascular firmally adhered to medulla and dura extending along c8 nerve root in right paravertebral region which was resected along with the nerve root. subtotal excision of the tumor was done as the lesion was infiltraring the parenchyma of the cord. histopathology showed spindle cell neoplasm arranged in fascicles and at places in sheets, there is loss of lobular architecture, nucleoli are inconspicuous, necrosis absent, mitoses >4/10 hpf with glial infiltration (figure 3). ihc study reveals spindle cells positive for vimentin (figure 4) and negative for sma, ema, s-100, cd34 and desmin. the mib score was 18% (figure 4b). this confirms the diagnosis of fibrosarcoma and excludes the other tumors. discussion pediatric spinal cord tumors constitute only 5% of tumors of the central nervous system, 25% of which occur in the intraduralextramedullary region [1]. pediatric spinal tumors are very rare with an annual incidence of almost 1 per 1000000 children, presenting 5 to 10% of all central nervous system tumors in children [4]. one to 10% occurs in the intradural-extramedullary region [8]. the meningeal tumors of infancy and childhood has broad category and includes meningioma, hemangiopericytoma, fibrous histiocytoma, meningeal sarcoma and melanotic tumors [5]. meningeal sarcomas are very aggressive tumors with an average 1-year survival rate of 50% after complete tumor resection [7]. the survival depends mainly upon the extent of resection. although intracranial meningeal sarcomatosis with multiple lesion involving spines had been reported as rare case report in literature, however, primary meningeal sarcoma exclusively involving cervical spine is extremely rare. the meningeal sarcoma are tumors arising from mesenchymal tissue thus may arise from the dura, the leptomeninges, or the adventitial fibroblasts of the blood vessels [6]. in general, the etiology is unknown. in adults, however, the intracranial meningeal sarcoma has been documented to occasionally occur following radiation therapy of other brain tumors particularly for radiotherapy of sella for pituitary adenoma [6]. in these cases, they typically arise 2–10 years after irradiation [6]. documentation of a previous trauma followed by proliferation repair and subsequent sarcomatous change is exceptional. meningeal sarcomas can differentiate according to several lines, thus presenting as fibrosarcoma, chondrosarcoma, leiomyosarcoma, rhabdomyosarcoma, osteosarcoma, 206 | kumar et al – cervical primary meningeal sarcoma in children angiosarcoma or malignant fibrous histiocytoma [2]. therefore, immunohistochemical analysis must be performed. on immunohistochemical examination of primary meningeal sarcomatosis, vimentin is usually the only intermediate filament that can be detected which confirms the diagnosis as fibrosarcoma [3]. the investigation of choice remains mri with contrast which delineates the extent of the lesion and degree of meningeal involvement but it can’t differentiate from even more common benign lesions like meningioma or neurofibroma radiologically. however, in our patient, we found no specific imaging criteria to differentiate meningeal sarcoma either from other solid meningeal tumours or from other tumoural and inflammatory meningioses. in order to avoid misinterpretations and delay of therapy, early open biopsy or surgical resection of the lesion should be done. radical tumour resection seems to afford the best prognosis, whereas the benefits of radiation therapy and chemotherapy are still not clear. conclusion meningeal sarcomas are locally aggressive cns tumors with a true metastatic potential in childhood. clinical manifestations are variable depending upon the location of the tumor. they can occur either as circumscribed masses or as diffuse leptomeningeal tumors. cystic structures, heterogeneous contrast enhancement, and connection to the meninges can be indicative of the localized form. on mri, the extent of the lesion and degree of meningeal involvement can be assessed precisely. due to a few number of cases published so far, the biological behavior and clinical management (e.g. postoperative radiation or chemotherapy) of this tumor entity require further research and investigation. correspondence dr. pradeep kumar department of neurosurgery, sms medical college, jaipur, rajasthan, india. 302004 email: dr.pradeepk28@gmail.com mobile: 09828929366 references 1.binning m, klimo jr. p, gluf w, goumnerova l. spinal tumors in children. neurosurg clin n am 2007;18:63158. 2.bruner jm, tien rd, enterline ds. tumors of the meninges and related tissues. in: bigner dd, mclendon re,bruner jm (eds) russel and rubinstein’s pathology of tumors of the nervous system. 6th edn. london: arnold publishers; 1998. p. 67–139. 3.jellinger k, paulus w: mesenchymal, nonmeningothelial tumors of the central nervous system. brain pathol.1991;1:79–87. 4.kumar r, giri pj. pediatric extradural spinal tumors. pediatr neurosurg 2008;44:181-89. 5.malluci cl, parkes se, barber p, powell j, stevens mcg,walsh ar,et al. paediatric meningeal tumors. childs nerv syst 1996:12:582–89. 6.nussbaum es, wen dyk, latchaw re, nelson mj.meningeal sarcoma mimicking an acute subdural hematoma on ct. j comput assist tomogr.1995: 19: 643–45. 7.rueda-franco f, l´opez-corella e. sarcomas in the central nervous system of children. pediatr neurosurg.1995: 22: 49–56. 8.wilson pe, oleszek jl, clayton gh. pediatric spinal cord tumors and masses. j spinal cord med 2007;30 (suppl 1):s15-s20. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article analysis of 30-day unplanned readmissions after degenerative spinal disease surgery d. adam, d. iftimie, gina burduşa, cristiana moisescu romania doi: 10.1515/romneu-2017-0009 romanian neurosurgery (2017) xxxi 1: 59 – 65 | 59             doi: 10.1515/romneu-2017-0009 analysis of 30-day unplanned readmissions after degenerative spinal disease surgery d. adam1,2, d. iftimie1, gina burduşa1, cristiana moisescu1 1department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania abstract: background: degenerative spinal disease surgery is frequently performed in most neurosurgical departments. unplanned 30-day readmissions represent a significant economic burden and have been used in several studies as a tool to evaluate quality of patient care. objective: to review 30-day unplanned readmission rates after degenerative spinal disease surgery in our department, in order to identify their causes and determine strategies aimed at decreasing their frequency. methods: a retrospective analysis was performed on all patients operated in our department for spinal stenosis or disc herniation over a 3 year period (january 2014 – december 2016), evaluating the rate and causes of unplanned readmission in the first month after discharge. complications were divided in medical and surgical. results: out of the 1106 patients included, 33 (2,98%) presented a 30-day unplanned readmission. the percentage was higher after disc herniation surgery (3,40%), compared to spinal stenosis (1,92%). pain management was the most common medical cause for readmission (45,45%), while in the surgical group, csf leaks were the most frequent complication (18,18%). conclusions: the rate of 30day readmissions was low in our series but, even so, they associate significant costs. they could be avoided by applying correct and aseptic surgical technique, proper availability of dural sealing agents and superior patient medical education. key words: degenerative spine disorders, 30-day readmission introduction surgery for degenerative spinal disease is frequently performed in most neurosurgical departments, usually as an elective intervention. several of these patients develop long-term postoperative complications, the so-called failed back surgery syndrome. others are readmitted in the first postoperative month for early complications, either medical or surgical. these unplanned and undesirable readmissions are grounds for patient-doctor conflict and represent a significant economic burden. in the us, a 2008 report showed an 18% rate of 30-day readmissions that 60 | adam et al analysis of 30-day unplanned readmissions after surgery             amounted to over 15 billion dollars in costs (1). there is a difference of opinion regarding 30-day unplanned readmissions. on one hand, the official opinion is depicted as suboptimal patient care. consequently, hospitals with high readmission rates are exposed to financial penalties. on the other hand, from the doctors’ point of view, these readmissions can be explained as a consequence of reduced mortality due to a high quality of care for patients with severe conditions. postoperative complications for patients with spinal stenosis and disc herniation have been extensively studied. the goal of this study is to review 30-day readmissions after spinal stenosis and disc herniation surgery, performed over a 3-year period in our neurosurgical department, in order to identify their causes and develop means to reduce their incidence rate. material and methods patient records were analyzed for all disc herniation and spinal stenosis surgical interventions that were performed in our department, between january 2014 and december 2016. patient characteristics, such as age, sex and comorbidities were evaluated, as well as early medical and surgical postoperative complications that determined readmission in the first 30 days after discharge. lumbar disc herniation surgery was performed using the interlamar approach. regarding spinal canal stenosis, laminectomy was used for decompression, while foraminal spinal stenosis was treated with ipsilateral fenestration and foraminotomy for unilateral symptoms and bilateral for bilateral symptoms. in both cases, the hypertrophic ligamentum flavum was removed and the nerve root was decompressed in the foramen by using partial facetectomy. postoperatively, patients were treated with antibiotics for the first 24 hours, antiinflammatory medication for 3 days and pain medication. patients who resided in the same city were discharged 3 days postoperatively, while the ones that did not were discharged 7 days after surgery. patients were advised to use a lumbar waistband for 1 month. in addition, they received instructions regarding local hygiene. complications that determined readmission in the first 30 days were divided into medical and surgical. the persistence of back pain or radiculopathy was noted, as well as the development of new symptoms, local surgical wound complications (dehiscence, infection, csf leak) or surgical reintervention. results a number of 1106 surgeries for degenerative spine disease were performed in the neurosurgical department of “saint pantelimon” clinical emergency hospital, bucharest, between january 2014 and december 2016. among these patients, 33 were readmitted within 30 days of discharge, resulting in a 30-day readmission rate of 2,98%. only patients that were operated for degenerative spinal disease were taken into account, excluding the ones that were diagnosed and planned for surgery in the nearest future, or did not have surgical indication. romanian neurosurgery (2017) xxxi 1: 59 – 65 | 61             the rate of 30-day readmission was higher for patients operated for disc herniation (3,40%) than for spinal stenosis (1,92%) (table i). a possible explanation for this discrepancy between the two types of surgery may be the increased difficulty of hernia operation due to the supplementary surgical maneuvers of fragmentectomy and discectomy. readmitted patients presented a relatively equal distribution regarding decades of age (table ii). table i 30-day readmissions according to the type of surgery number of patients % of patients degenerative spinal disease surgeries 1106 disc herniation 793 71,70% spinal canal stenosis 313 28,30% 30-day readmissions 33 2,98% after disc herniation surgery 27 3,40% after spinal stenosis surgery 6 1,92% table ii characteristics of patients with 30-day readmission number of patients % of patients sex male 20 60,61% female 13 39,39% age mean age 54,6 20-29 yrs. 1 3,03% 30-39 yrs. 6 18,18% 40-49 yrs. 7 21,21% 50-59 yrs. 6 18,18% 60-69 yrs. 5 15,15% 62 | adam et al analysis of 30-day unplanned readmissions after surgery             70-79 yrs. 7 21,21% 80-89 yrs. 1 3,03% comorbidities diabetes 9 27,27% hypertension 20 60,61% obesity 8 24,24% gastrointestinal disorders 7 21,21% cardiovascular disease 17 51,52% chronic obstructive pulmonary disease 6 18,18% depression 3 9,09% table iii overall complications number of patients % of patients overall complications 33 medical 15 45,45% pain 14 42,42% transient ischemic attack 1 3,03% surgical 18 54,55% wound dehiscence 4 12,12% surgical site superficial infection 3 9,09% csf leak 6 18,18% disc herniations 5 15,15% the most common medical cause for readmission was low back pain and/or leg pain. low back pain was more frequently encountered in spinal stenosis surgery patients and was managed with medication. in this group, pain lasted for 2-3 weeks after surgery. two patients were also diagnosed with coxarthrosis and presented pain exacerbation after discharge. another cause for readmission was cardiovascular disease. a patient presented a transitory loss of consciousness at home and drowsiness at readmission. she had interrupted blood thinners prescribed for her pre-existent atrial fibrillation. cerebral ct scan and neurological examination were romanian neurosurgery (2017) xxxi 1: 59 – 65 | 63             normal and the diagnosis was established as transient ischemic attack. she received adequate medication for stroke prevention. among the surgical causes of readmission, csf leaks were the most frequent. five patients developed this complication after disc hernia surgery, two of them after recurrent herniation surgery and one after lumbar spinal stenosis surgery. after intraoperative acknowledgement of csf leak, the dural sealing techniques consisted of muscle tissue, fat or gelaspon placement that were used due to the lack of other agents’ availability (tisucol, tachosil), proved to be insufficient. in three cases, surgical reintervention was necessary and tachosil application was used. one patient was treated by injecting the surgical wound with autologous blood and another one with the use of closed, external drainage, with remission of leakage after 9 days. patients with csf leaks maintained bed rest for 3 days after initial surgery and received antibiotic treatment. however, two developed surgical wound infection, with staphylococcus aureus and escherichia coli respectively. another three patients presented superficial supraaponeurotic infection due to granuloma. after granuloma resection and wound debridement, per secundam suture was performed and surgical wound closure was achieved in all cases. five patients with foraminal spinal stenosis treated with fenestration and foraminotomy with persistent symptoms after surgery were also readmitted. in these cases, the foraminal stenosis was also caused by a disc protrusion for which no surgical maneuver was initially considered necessary. these patients were reoperated, discectomy was performed without fusion and presented a good postoperative outcome. surgical wound dehiscency occurred in four patients, three of which were operated for disc herniation and one for spinal stenosis. these patients were overweight, with associated diabetes mellitus. wound resuture concluded with healing and good neurological outcome. discussion first-month readmissions after operated spinal degenerative disorders (disc herniation, spinal stenosis) represent a reason of discontent for both the patient and doctor, and simultaneously determine an increase in medical care costs. in our series they represented 2,98% of the entire number of patients operated for disc herniation and spinal stenosis with a higher rate for patients operated for disc herniation (3,40%) than for spinal stenosis (1,92%). literature data, as well as our results reveal that they are the result of a medical or surgical complication during patient care in which, in some cases, comorbidities may also be involved. in a recent study which comprised a diverse neurosurgical pathology, that included a number of 163.743 cases, the general 30-day readmission rate was 8,63% (2), and in particular, 6,92% for lumbosacrat spinal decompression. the readmission rate of neurosurgical patients with diverse neurosurgical pathology was recently reported varying between 6,9% and 11,8% (3, 4). 64 | adam et al analysis of 30-day unplanned readmissions after surgery             in other studies strictly regarding spinal pathology, 30-day readmission rate was reported between 3,84% and 9,1% (5–10). spinal operations are more frequent than other neurosurgical interventions, but although their readmissions rates are lower in comparison with other types of surgery, they occupy third place in taylor’s study (2). this rate can be lowered by avoiding surgical complications. in our study, almost half of readmissions were related to pain management. their high number could have been avoided if patients had respected discharge instructions and had addressed their general practitioner for evaluation and treatment. acute postoperative pain represented 0,5% of early readmissions according to wang et al5. back pain located at the level of the surgical intervention is usually caused by muscular compression and hypoxia, mainly in spinal stenosis patients when surgery is performed at multiple levels. another cause for readmission is surgical wound dehiscency caused by granulomas associated with superficial infection. we consider that this complication can be avoided by respecting the correct superficial layer suture technique and aseptic measures. the subcutaneous suture with a downward oriented knot avoids granuloma formation. csf leakage was the most frequent surgical complication in our series, representing 18,18% among reasons for readmission and 0,54% of the total number of reviewed interventions. when the durotomy was discovered intraoperatively, surgical repair consisting of muscle, fat and gelaspon application was attempted and postoperatively, patients were instructed to maintain bed rest for the following 3 days. although, after suture removal, the surgical wound appeared clean and dry, these patients returned after a few days presenting csf leakage. there were several factors that determined fistula development: the impossibility of dural suture through miniopen approach, periduroradicular fibrosis encountered in patients who had previous surgery at the same level, obesity and diabetes. lack of necessary products for immediate repair of dural tear imposed a second surgical intervention with higher costs compared to the value of the initially required products. the low number of postoperative infections can be explained by the systematic epidural application of 1 gram of vancomycin. ever since we initiated this protocol, postoperative discitis practically disappeared. infections associated with granuloma can be prevented by adopting the downward facing knot subcutaneous suture and enhanced sterile techniques. in some studies, postoperative infections were the most common complication, especially when a device, implant or graft were used5. shah et al4 reported that surgical site infection accounted for 11,2% of readmissions. in mccormack’s study (6), they represented 32% of 30-day readmissions after spine surgery. there are literature reports of nosocomial infections such as urinary tract infections and pneumonia. if, in our series, these nosocomial infections had developed, such patients would romanian neurosurgery (2017) xxxi 1: 59 – 65 | 65             have been admitted in other cities or departments. among readmitted patients, five presented foraminal stenosis for which hypertrophic ligamentum flavum resection and partial facetectomy were performed by using interlamar approach. the intraoperative decision was against the removal of the protruding disc. due to inadequate decompression by removal of hypertrophic ligament without removal of protruding disc, neurological symptoms remained nearly identical as in the preoperative period. the surgeons managing the respective cases decided to perform discectomy through the same interlamar approach. conclusions degenerative spinal disorders are frequent in neurosurgical practice and generally have good postoperative outcomes. readmissions at 30 days after discharge were rare in our series, but still associated significant costs. some of these are avoidable by using correct and aseptic surgical techniques. cases of incidental durotomy could have been resolved during the first surgical intervention if the necessary sealing agents had been supplied, a measure that could prove to be superior, regarding overall cost effectiveness. these measures associated with patient education regarding behavior in the early recovery period can mitigate rehospitalisation for lumbar decompression patients, reduce patient morbidity and medical costs. references 1. medicare payment advisory commission. a path to bundled payment around a rehospitalization, in: report to the congress: reforming the delivery system. washington dc; 2008. 2. taylor bes, youngerman be, goldstein h, et al. causes and timing of unplanned early readmission after neurosurgery. neurosurgery. 2016;79(3):356-369. doi:10.1227/neu.0000000000001110. 3. buchanan cc, hernandez ea, anderson jm, et al. analysis of 30-day readmissions among neurosurgical patients: surgical complication avoidance as key to quality improvement. j neurosurg. 2014;121(1):170-175. doi:10.3171/2014.4.jns13944. 4. shah mn, stoev it, sanford de, et al. are readmission rates on a neurosurgical service indicators of quality of care? j neurosurg. 2013;119(4):1043-1049. doi:10.3171/2013.3.jns121769. 5. wang mc, shivakoti m, sparapani ra, guo c, laud pw, nattinger ab. thirty-day readmissions after elective spine surgery for degenerative conditions among us medicare beneficiaries. spine j. 2012;12(10):902-911. doi:10.1016/j.spinee.2012.09.051. 6. mccormack ra, hunter t, ramos n, michels r, hutzler l, bosco ja. an analysis of causes of readmission after spine surgery. spine (phila pa 1976). 2012;37(14):1260-1266. doi:10.1097/brs.0b013e318245f561. 7. amin by, tu t-h, schairer ww, et al. pitfalls of calculating hospital readmission rates based on nonvalidated administrative data sets. j neurosurg spine. 2013;18(2):134-138. doi:10.3171/2012.10.spine12559. 8. deyo ra, mirza sk, martin bi, kreuter w, goodman dc, jarvik jg. trends, major medical complications, and charges associated with surgery for lumbar spinal stenosis in older adults. jama. 2010;303(13):1259. doi:10.1001/jama.2010.338. 9. kim bd, smith tr, lim s, cybulski gr, kim jys. predictors of unplanned readmission in patients undergoing lumbar decompression: multi-institutional analysis of 7016 patients. j neurosurg spine. 2014;20(6):606-616. doi:10.3171/2014.3.spine13699. 10. schairer ww, carrer a, deviren v, et al. hospital readmission after spine fusion for adultspinal deformity. spine (phila pa 1976). 2013;38(19):1681-1689. doi:10.1097/brs.0b013e31829c08c9. microsoft word 21jaiswalmanish_analysis romanian neurosurgery (2018) xxxii 2: 355 358 | 355             doi: 10.2478/romneu-2018-0044 analysis of traumatic brain injury related to kite flying festival: an institutional study manish jaiswal, somil jaiswal, bal krishna ojha, sunil kumar singh, anil chandra, chhitij srivastava department of neurosurgery, king george’s medical university, lucknow, u.p., india abstract: introduction: makar sankranti or uttarayan is the kite flying festival in india. the festival marks the end of winter and the beginning of summer as the sun moves to the tropic of cancer bringing with it longer and warmer days. but it turns into a difficult day for those who are hospitalised after suffering from kite flying related injuries. aims & objectives: the objective of this cross sectional study was to review the demographics, causes injury, severity, treatment and outcome of traumatic brain injuries in victims of this kite flying festival who were admitted in department of neurosurgery on the occasion this year in january. patients & methods: a total of 46 traumatic brain injured patients was admitted under neurosurgery services that day, out of which 18 cases were related to kite flying related injury. data of these 18 patients were analysed and outcome were measured at discharge. result: kite flying festival related neurotrauma increase 39% more emergency admission burden as compared to routine days in neuro-emergency ward. most common cause of head injury among them was fall from roof. majority of them had mild head injury. associated injuries to other part of body were present in 46% patients. conclusion: children were most affected due to unsupervised kite flying on roof and road side catching of kites. depressed fracture was commonest type of traumatic brain injury. strict attention to safety measures and parental supervision while flying kites can avoid many preventable injuries to life. key words: kite flying injury; traumatic brain injury; festival related trauma   356 | jaiswal et al kite flying festival related traumatic brain injury             introduction any festival having some kind of sport or game on the occasion has certain injuries unique to it, even a seemingly harmless and docile sport like flying a kite. injuries of kite flying activity are commonly sustained by kite-flyers, kite-runners, riders of two wheelers and pedestrians [1,2,3]. the distribution of kite related injuries varies over different locations and regions and is influenced by the local cultures and traditions, like there is an epidemic of kite related injuries during the festival of makar sankranti in the states of gujrat, rajasthan, uttar pradesh and other part of north india in january or the basant festival in peshawar, pakistan [4,5]. while a few articles do speak about the spectrum of kite related injuries [6,7,8], exclusive literature focusing on traumatic brain injuries related to the kite flying festival is seldom found. patients & methods it was a hospital based observational cross sectional study of all cases of traumatic brain injury victims admitted in neurosurgery emergency on the day of kite flying festival (makar sankranti). a total of 46 traumatic brain injured patients was admitted under neurosurgery services that day, out of which 18 cases were related to kite flying related injuries. data of these 18 patients were analyzed for demographic details regarding age and sex of the patients, time since the injury to hospital admission, cause of head injury, severity of traumatic brain injury based on the glasgow coma score, findings on ct scan of the brain, treatment provided and outcome based on the glasgow outcome score. outcome was measured at discharge. results there were 18 (39%) patients who were admitted for traumatic brain injuries related to kite flying festival on that day along with other 28 head injury patient admission unrelated to this kite flying accident. out of 18 patients, there were 17 males (94.5%) and 1 female (5.5%). there were patients of all age groups. most affected age group was 5-15 years. the age distribution of patients is shown in (figure 1). mean age of patients was 11 years (range 5-38 yrs). figure 1 age distribution of kite flying festival related traumatic brain injury patients fall from roof was the commonest cause of injury in 12 patients (67%), followed by a fall on ground and collision with motor vehicles during running on road for catching kites in 4 patients (22%). two patients (11%) sustained an injury due to fall from the tree during kite removal from tree (figure 2). romanian neurosurgery (2018) xxxii 2: 355 358 | 357             figure 2 causes of traumatic brain injury in kite flying related accident 13 (72.22%) had mild head injuries, 4 patients (22.22%) had moderate head injuries and 1 patient (5.5%) had severe head injuries (figure 3). ct scan was normal in 7 patients (38.8%). there were depressed skull fractures in 5 patients (27.7%), extradural hematoma in 2 patients (11.11%), intracranial hematomas in 3 patients (16.6%) and diffuse cerebral edema in 1 patient (5.5%). figure 3 head injury severity in kite flying related trauma eight patients (44.4%) had associated injuries to other parts of the body. 3 patients had spinal injuries, 2 had rib fractures, 2 patients had facial injuries and 1 had abdominal visceral injury. eight patients (44.4%) underwent surgery, which included elevation of depressed fracture, debridement and suturing of large scalp laceration in 4, spinal fixation in 2 patients, craniotomy and evacuation of extradural haematoma in 1 patient & decompressive craniectomy in 1 patient. all associated injuries were treated nonoperatively. mean hospital stay was 9 days (range 3 – 38 days). the outcome was assessed at the time of discharge. at the time of discharge 14 patients (77.7%) had a good recovery, 2 patients (11.1%) had moderate disability, 1 patient (5.5%) had severe disability and one patient died. during the hospital course, one 6 years old child with compound depressed fracture died of meningitis. discussion most of the injuries sustained during kiteflying, reported in literatures were due to falls, cuts, head injuries or fractures [3,4,9]. people were also injured while on streets, riding on motor bikes, children catching wandering cut off kites on the roads [10]. teenagers sustained most injuries due to falls related to kite-flying activities [11]. in traffic accidents the major consequences were fractures and wounds. head injury was the major consequence of falls. kite flying might look like blossom floating in the wind, but it is one of the dangerous sports in the world. every year this gruesome game has left hundreds of people with sustained injuries and disabilities and many others dead in india [4,5,7,9]. among all age groups this is a popular sport in children and young and thus more injuries are observed in younger age groups [12,13]. in this study a decrease was observed in the 358 | jaiswal et al kite flying festival related traumatic brain injury             number of injuries with increase in age. prevention of childhood injuries is of great importance to both individuals and society, but unfortunately, has largely been either excluded from attention or treated in an inappropriate manner. nadir mehmood et al. in their study mentioned falls and head injuries while flying kites to be the most important cause of morbidities [14]. falls while flying kites are a leading cause of the global burden of injury to children resulting in more than 37,000 deaths annually for those aged 15 years [1,3,14]. therefore proper preventive measures, increasing awareness about the possible effects of such a sport and offering social counselling to the families can help to reduce the incidence of injuries in our population. for obtaining this objective, the need is to increase the awareness of the parents and society and to reduce the incidence of such injury; this study is a small part of that investigation. conclusions children were most affected due to unsupervised kite flying on roof and road side catching of kites. depressed fracture was commonest type of traumatic brain injury. strict attention to safety measures and parental supervision while flying kites can avoid many preventable injuries to life. a preventive program, legislations and educational reinforcement should be promoted to decrease the number of kiteflying-related traumatic brain injury. correspondence dr. manish jaiswal assistant professor, department of neurosurgery. king george’s medical university chowk, lucknow, u.p., india-226003 email: manishmlnmc@gmail.com mobile no. 8933816028 references 1. charles m. court-brown, alexander m. wood, stuart aitken. the epidemiology of acute sports-related fractures in adults. injury, int. j. care injured (2008) 39, 1365—1372. 2. chaudhari n. adolescent injuries. indian pediatr1990; 27:1261-1267 3. coggan c, patterson p, brewin m, hooper r, robinson e. evaluation of waitakere community injury prevention project. inj prev 2000;6:130–4. 4. colver a, hutchinson p, judson e. promoting children’s home safety. bmj 1982;285:1177–80. 5. court-brown cm, caesar b. epidemiology of adult fractures: a review. injury 2006; 37: 691-7. 6. guyer b, gallacher ss, chang b, azzara cv, cupples la, colton t. prevention of childhood injuries: evaluation of the statewide childhood injury prevention program (scipp). am j public health 1989;79:1521–7. 7. haddon w, baker sp. injury control. in clark dw, macmohanb, eds.preventive medicine.2 no edn, boston, little brown &company, 1978; 172. 8. kimati vp. childhood accidents in dar-e-salaam. trop. geogr. med. 1971, 29: 91-95. 9. neto jbr, ferreira gc, filho als, fontes mobq, bomfim f, abrantes wl. kiting injuries: report of two cases and discussion. j trauma injury infection crit care 2000;48(2):310. 10. paul cl, sanson-fisher rw, redman s, carter s. preventing accidental injury to young children in the home using volunteers. health promot int 1994;9:241–9. 11. sitaraman s, sharma s, saxena s, sogani kc. accidents in infancy and childhood. indian peditr. 1985, 22:815-818. 12. tendon j.n., karla, a., karla, k., sahu, s.c., nigam, c.b. and qureshi, g.u., 1993. profiles of accidents in children. indian pediatrics 30: 765-769. 13. vineis p, ronco g, ciccone g, gogliani f. home injuries in children: a population-based intervention trial. epidemiology 1994; 5:349 –51. 14. mehmood n, khwaja zh, ramazan s, quddus a. kite-flying associated injuries in rawalpindi. ann pak inst med sci 2010;6:116-9 microsoft word _7.formatate_selected_abstracts.doc romanian neurosurgery vol. xv nr. 1 38 selected abstracts from the 6th national congress of the romanian society of neurosurgery 26 – 30 septembre 2007, bucharest, romania early rehabilitation of higher cortical brain functioning in neurosurgery. how to humanize human skills following acute brain lesions klaus r.h. von wild professor of neurosurgery, medical faculty university of münster, professor of neurorehabilitation and reengineering of brain and spinal cord lesions, international neuroscience institute, hannover, germany in coop. with sascha skudelny1, federico hernández-meyer2 1creative director, media science university of siegen, germany; 2mag. pharmacy, pharmaceutical and medical communications, huétor-vega (granada), spain objectives today, increasingly more patients with brain lesions survive the acute stage, however, suffering from severe impairment of higher cerebral functioning (who-icf). early neurorehabilitation can significantly improve functioning and patients’ reintegration. methods functional rehabilitation is an original task of neurosurgery. impairments refer to loss of structures and functions. disabilities refer to limitations or participating restrictions. functioning is an umbrella term encompassing all body functions, activities and participation. neurorehabilitation needs a multidisciplinary team approach. results the essential aspect in early rehabilitation is the integration of disciplines and consistent goal setting to regard individual patients’ needs. good structural organization of the team, notice of basic communication rules, conflict management and a definite decision making increase productive interdisciplinary working. the movie shows our team approach and the daily work on the special ward. reintegration is demonstrated in two of our patients. discussion obviously the impairment of mental-cognitive and neurobehavioral functioning and not the loss of physical skills will cause patients’ loss of life transactions and final outcome. rehabilitation is possible because of the individuals’ neural plasticity. conclusion functional rehabilitation is a process whereby patients who suffer from impaired higher cerebral functions following injury or disease regain their former abilities or, if full recovery is not possible, achieve their optimum physical, mental, social and vocational capacity. it aims at patients’ reintegration. in order to facilitate such goals neurosurgeons should start with team approach as early as possible and will have to work in close collaboration with the neuropsychologist and all other members of the team day by day. focused beam surgery in central skull base meningiomas involving the parasellar space l steiner, md, phd, d. schlesinger, phd with open-ended follow-up mri in cases with presumed total extirpation of meningiomas, an increasing number of residuals and recurrences are detected that need radiosurgery. little is known about the pathophysiological changes induced by gamma surgery at the cellular level in tumors. division of tumor cells is presumably selected abstracts romanian neurosurgery vol. xv nr. 1 39 inhibited by radiation-induced damage to dna. it has been shown that the gamma beams obliterate the microvascular supply to tumors. it was proposed that the induction of apoptosis by gamma radiation to proliferating cells may be responsible for at least part of the effect of gamma surgery on tumors. also, such contentions may be premature as they may point the direction to future research. between march 1989 and december 2004, steiner treated using the gamma knife 150 patients with central skull base meningiomas involving the parasellar space. of 150 patients, for a variety of reasons 8 patients were lost for follow-up leaving 142 patients available for analysis. there were 102 tumors of 0.4 8 cc (mean 4cc). four tumors disappeared, 64 did shrink, 28 remained unchanged and 6 increased. there was no morbidity or mortality. there were 40 tumors measuring 0.6 36 cc (mean 8cc). two did shrink, 28 remained unchanged and 10 increased. there was no mortality, however, new neurological symptoms occurred in 5 cases. our policies in intracranial meningiomas in patient over 60 years old (experiences of 109 cases) prof. a.v. ciurea1, md, a. tascu1, md, d. talianu1, md, f. stoica2, md, r. rizea1, md, a. gheorghita3, md, arcan ayssa1, md clinic hospital bagdasar-arseni, bucharest, romania 11st neurosurgical dpt., 2gamma knife surgery dpt., 3neuroasthesiological dpt. keywords: intracranial meningiomas, patients over 60 y.o., microsurgery, ct-scan, mri, mra, dsa, simpson scale, gamma knife surgery (gks), gos introduction intracranial meningionas (i.m.) are tumors good bounded, important vascularization, with invasion of dura mater and bones structure. i.m. account for 14,319% for primary intracranial tumors; females are most affected. authors present personal data in i.m. in patients over 60 years old, in connection with all possible complication by associated pathology. method the experience of authors base on a cohort of 578 cases i.m. consecutive admitted & operated and pathological diagnosed in the 1st neurosurgical department, “bagdasar arseni” clinic hospital, in period 1997– 2006 (10 years of experience). over 60 years there are 109 cases (18,8%) with the female preponderance (1,8:1). the most affected group of age. (in our data) was the 5th decade 194 cases (33,5%). the most frequent tumors site are parasagital (26 cases, 24,2%) followed by the convexity (24 cases, 22,2%) and olfactory grove area 21 cases (19,1%). the clinic diagnose is completed with all neuroimagistic armamentarium (ct-scan, mri/ mra, dsa). we excluded of our data the multiple i.m. the clinical features were: headache (68 cases, 98.2 %), increased icp syndrome (47 cases, 67.6 %), visual impairment (42 cases, 61,3 %), seizures (39 cases, 56.8 %), personality changes (27 cases, 38.6 %), cranial nerve palsy i, iii, vi (19 cases, 27.5 %), miscellanies (vomiting, ataxia) (9 cases, 13.6 %). the associated pathology was dominated by: systemic arterial hypertensive (68 cases, 62%) and obesity/hypercolesterolemia (37 cases, 34,1%), followed by ischemic cardiopathy (72 cases, 66%), diabetus mellitus (28 cases, 26%), chronic alcoholism (9 cases, 8%), ischemic stroke (13 cases, 12%), atrial fibrilation (40 cases, 32%), miscellanea (76 cases, 70%, e.g. anticoagulant therapy). results the tumoral removal was totality in 94 cases (86,2 %) of cases in subtotality in 15 cases (13,8%) (skull base meningiomas). no biopsy in our data. in subtotal removal was possible to realize gammaknife surgery (gks). according of simpson scale (1957) the i.m. cases were included in grade ii (59 cases, 54,1%) followed by grade iii (35 cases, 32,1%) and grade iv (15 cases, 13,7%). pathological aspects: the classic bening cases grade i was predominant (95 cases, 87,2%), followed by the atypical meningiomas (7 cases, 6,71%) and anaplastic cases (5 cases, 4,61%) and malignancy meningiomas (2 casers, 1,83%) the giants i.m. (over 6 cm in diameter) was selected abstracts romanian neurosurgery vol. xv nr. 1 40 represented 14 cases (13,1%). the authors advocate on the microsurgical resection with slow decompression of the brain tissue & copios salin solution irrigation for prevention of ischemic cerebral accident. also it is necessary the preservation of arterial and especially venous structure to prevent the brain venous infarct. no intraoperative mortality. the important complications were: seizures (50%), cranial nerve palsy (28,5%), visual impaiment (19,1%), modified neurological deficit (9,1%). in this cohort, the follow-up period was between 6 month to 8 years (medium rage 4,5 years). recurrences were noticed in 16 cases (14,6%); in small cases gks was avaible as first option. the glasgow outcome scale (gos) in i.m. (after 3 month), group studied was: good recovery 57 cases (52,3%), moderate disability 35 cases (31,8%), severe disability 7 cases (6,4%), death 10 cases (9%). majority of deaths is caused by broncho-pulmonary infections, postoperatory myocardium infarction and pulmonary thrombo-embolism. conclusions i.m. are prevalent benigns tumors, slow growing, extraxial location with perfect neuroimagistic diagnosis. in all cases it is necessary the total removal without any injury of vascular and neural structure, especially with caution in patients over 60 y.o., with cerebro-vascular pathology. in these conditions it is pursued avoidance of ischemic cerebral infarct. finally, authors advocate for the best preoperatory preparation concerning of the risk factors (ischemic cardiopathy, arterial hypertension, diabetes mellitus, chronic hepathorenalo-pathy, e.g.) for obtained a good outcome & quality of life and family integration. the challenge of intracranial meningiomas dr. keki e. turel, dr. nootan kumar sharma, dr. shashank joshi bombay hospital institute of medical sciences, mumbai, india meningiomas are the second most common supratentorial tumor of central nervous system (cns). they account for around 15% of the tumors of the cns. 90% of intracranial meningiomas are located supratentorially while less than 10% within the posterior fossa and rest involve the ventricular system. meningiomas arise from arachnoid cap cells, mostly in the vicinity of arachnoid granulations along dural venous sinuses. though exact etiology is unknown, these have also been grown in the region underlying old injury sites. their incidence is two to three folds higher in females. multiple meningiomas are frequent with nf-2. meniningiomas are extraaxial tumors which produce symptoms as result of mass effect. they are usually irritative or paralytic foci. in advanced cases they cause a rise in intracranial pressure or even erode the overlying bone. total surgical excision is the best treatment a neurosurgeon can offer to his patients. it includes excision of main tumor, 1 cm of surrounding dura, involved overlying bone and even dural sinuses if infiltrated by it. while achieving this goal, great care is needed to preserve surrounding brain, cortical veins, dural venous sinuses, and cranial nerves. thus it is a great challenge for a neurosurgeon. owing to their critical situation, some tumors cannot be excised completely. they needed adjuvant therapy like radiosurgery, radiotherapy or gamma knife surgery. despite complete surgical excision, recurrence is a known phenomenon and poses a big challenge even to the most experienced neurosurgeons. molecular biological marker studies are found much useful in predicting recurrence. these are estrogen and progesterone receptors, platelet derived growth factor receptors, tenascin and ki 67 as proliferative marker. in the last 205 consecutive operated cases, supratentorial meningiomas were 141 while infratentorial were 64. location wise distribution of supratentorial were sphenoid wing (42 cases), convexity (36 cases), parasagittal (21 cases), suprasellar (17 cases), falcine (15 cases), olfactory groove (6 cases), intra-ventricular (2 cases), cavernous sinus (1 cases) and diploic (01). infratentorial meningiomas were cp angle (35 cases), petroclival (10 cases), tentorial (7 cases), foramen magnum (5 cases), cerebellar convexity (5 cases), and falcotentorial (2 cases). recurrence has been documented in 15 cases. selected abstracts romanian neurosurgery vol. xv nr. 1 41 detailed analysis of our material will be presented and video clips of representative cases and our techniques will be demonstrated. transbasal subfrontal interhemispheric approach for midline intracranial lesions prof. ibrahim sbeih, mbchb., frcs., frcssn department of neurosurgery, jordan university of science and technology , ibn alhaytham hospital, amman – jordan this approach has been used extensively in our department for the last 15years. it entails low frontal bone entery with or without opening of frontal air sinus. it also entails sectioning of most anterior part of superior sagittal sinus and cutting of falx most anteriorly. it also entails preservation of both olfactory tracts and interhemispheric approach towards anterior fossa, sellar, and suprasellar lesions. we have used this approach for radical total excision of craniopharyngiomas, suprasellar meningiomas, giant invasive pituitary adenomas and clivus chordomas . this pproach has also been used for olfactory groove meningioma, ant. fossa skull base lesions like sinonasal tumors and adenocarcinoma involving paranasal sinuses, among other lesions. the advantage of this approach is that it puts the neurosurgeon in a position of total control over neurovascular structures allowing surgical manouveres on all sides of the tumor thus allowing preservation of blood supply for neural structures and excellent vascular control în cases of bleeding. smell was preserved in more than 70% of cases and minimal complications were encountered; meningitis and csf leak. this approach has advantage over pterional or lateral subfrontal approach in that it allows you to see and control over the far end of the intracranial lesions thus improving upon the surgical results and recurrence rate. intracranial meningiomas: a 6-year’s surgical experience florian i.s., md, phd, oslobanu a. , md, dura l., md, iordache linda, md, tusnea d., md umph “iuliu hatieganu” cluj-napoca & cluj county, emergency hospital, neurosurgical department keywords: meningiomas, preoperative planning, surgical results background the surgical treatment of the intracranial meningiomas is still a challenge for the neurosurgeon, considering that its ultimate goal that of total resection in hope of no future recurrence while avoiding postoperative complications is difficult to obtain in some cases. objectives our aim is to determine relevant epidemiological, clinical, imagistic, surgical and histological particularities, emphasizing the correlations between these case specifics and postoperative results. methods the authors designed a retrospective study of 213 cases with intracranial meningiomas treated surgically between 2001 and 2006. we evaluated the operative indications and techniques by correlating the patients’ general and neurological status at admission, histopathology, location, size and resection grade with postoperative clinical status and imagistic findings. results from 1051 brain tumors operated by the authors in a 6years period, 213 cases of histological confirmed meningiomas were included in the study. the patients’ age, sex, associated diseases, neurological status, ct-scan, mri and cerebral angiography, made up the preoperative evaluation. the most frequent locations were at the convexity (34.5%) and the sphenoid ridge (13.7%). according to histological findings most of the cases were meningothelial (38%), transitional and fibrous meningiomas. the extent of the tumor resection was selected abstracts romanian neurosurgery vol. xv nr. 1 42 graded using the simpson and demonte scales, a grade i or ii tumor removal being performed in 86% of cases. gos and karnofsky scale showed good outcome in 80% of cases, while the medium to longterm value of surgery was established by periodical follow-ups, the screened period varying from 4 months to 6 years. the rate of recurrence was 14%, occurring mostly in malign and subtotal removed tumors. conclusions the immediate outcome of the surgical treatment of meningiomas depends mainly on careful patient selection, rigorous operative planning and extent of resection well correlated with the patients’ clinical status, location of the tumour, and its intraoperative microsurgical aspects. meningioma neurosurgery in conformational radiotherapy era: a series of 79 consecutive cases i. poeata, n. ianovici, a. chiriac, z. faiyad, s. gaivas, m. ivanov, b. iliescu “sf. treime” university hospital, ateneului, nr. 2, iasi total microsurgical removal of meningiomas defined the main goal of tumor surgery for a very long time. as soon as conformational radiotherapy became available in romania (gama-knife si linac), small tumor fragments, in difficult locations can be left on site for radiotherapy. even more, bone infiltration sites and insertions on dural sinuses could also be subject to iradiation. last, but not least, radiotherapy can be used to attack the insertion and tumoral bed of 2nd and 3rd degree meningiomas. to assess the change in the therapeutical view, once complementary radiotherapy isavailable we analyzed a series of 78 consecutive meningioma cases microsurgically removed between april 2004 – april 2007. there were in our series 44 cases of cranial base meningiomas (11 sphenoid wing, 5 pterion, 4 orbit, 3 cavernous sinus, 2 cranio-facial, 2 pituitary body, 7 cerebello-pontine angle), 16 sinus meningiomas (10 sagittal superior sinus, 4 inferior, 2 lateral), 4 falx meningiomas de coasa, 3 tentorial meningiomas, 21 convexity meningiomas. based on their morphopathology there have beem 25 1st grade, 29 2nd grade, and 24 3rd grade. this series contains 4 cases of re-occurrence after initial removals performed in ours or other centers. we present some illustrative cases and intraoperatory images as well as the outcome fo the patients included in this protocol. microsurgical approach was modified, given the availability of conformational radiotherapy in 10% of the cases, incomplete removal of the tumor being considered of a higher risk compared to the risk of radiotherapy. surgery results of 100 petroclival meningiomas mainly operated by the anterior transpetrosal approach takeshi kawase, kazunari yoshida petroclival meningiomas, originated medial to the internal auditory meatus (iam) were subclassified according to the tumor extension : clival type (c) : located medial to the iam, sphenoclival type (sc); with middle fossa extension, petroclival type (pc); with wider attach extended posterior to the iam. the anterior transpetrosal approach (apa) was applied in 76 cases of c or sc type and the combined petrosal or two –staged operation was used in pc type. the surgical results of 100 petroclival meningiomas are presented. results gross total removal was achieved in 60% (71% underwent apa). the patients condition were independent (kps?80) in 88%, temporary dependent in 3 %, permanently dependent (kps?60) in 7%. there was no surgical mortality. during follow-up for av. 8 years, radiosurgery had been done in 24 patients showing tumor residue, and only 9% showed tumor regrowth. the 3 patients underwent reoperation and two died of tumor malignant change or suicide. their morbidity was depended on presence or absence of selected abstracts romanian neurosurgery vol. xv nr. 1 43 perforator injury of the brain stem (5%). permanent double vision occurred in 8 %. facial hypesthesia was common (20%), but patient’s compaint was mild. facial palsy was as low as 5 %, and no complication to the lower cranial nerves. conclusion the apa is a kind of key hole surgery, epidurally accessed to the tumor attachment without exposing the lowere cranial nerves. the benefits are the following 5 points: 1) early access to tumor feeders, 2) removal of middle fossa tumor, 3) low risk of cn vii ? xi injury, 4) low risk of venous complication, 5) hearing preservation. the technique of key hole surgery and the strategy how to avoid such complications will be presented. surgical management of petroclival tumors: defining outcome /resection goals deepak kumar gupta, ashish suri, vaishali suri, bs sharma all india institute of medical sciences, new delhi, india e-mail: dkg_nsurgery@yahoo.co.in keywords: petroclival meningiomas, mib labeling index, vascular endothelial growth factor, outcome, extent of resection aim petroclival tumors are rare and require extensive skull base approaches, associated with high morbidity/mortality owing to location/relationship to adjacent neurovascular structures.materials and methods: 48 cases (mean age: 37±17 yr) of petroclival tumors (36 were meningiomas, 10 chondroma/sarcomas. 2 hemanangiopericytoma) operated over 5 yr period (2001-2005) were analysed. follow up was 3-64 months(mean 33±7mo). immediate outcome assessed by adl grading and long term outcome by kps. slides were reviewed for vegf(vascular endothelial growth factor), mib labeling index and were correlated with brain stem invasion( mri), preop factors and clinical outcome. observations mean tumor size was 3.7cm±0.7cm. giant tumors (>4.5cm) were noted in 27 cases. brain stem compression with t2 signal change was noted in 11/36 petroclival meningiomas(30%). middle fossa extensions and cavernous sinus ext was noted in 65% and 19% cases. preop hydrocephalus noted in 25% cases. extended middle fossa approach was done in 26 cases while combined ( emf with retrosignoid) was done in 12 cases. gross total excision was done in 55% cases.histopathologically, transitional variety was most common. mean mib labeling index in gr i meningioma was2.26%vegf positivity was noted in 4/26 cases. results perioperative morality was 8%. postop chest infection noted in 27% cases,worsening of cr nerve function in14%, culture negative meningitis in 12% cases. in the presence of vegf positivity, median mib index was 8.5 %.vegf positivity and high mib labeling index was noted in patients with brain stem invasion and this correlated with poor outcome. conclusions hydrocephalus, tumor size, brain stem infiltration/peritumoral edema affected surgical outcome. mib , vegf hold promising outcome predictor role.intraop (lack of arachnoid plane, fibrous tumors, vessel encasement) and preop risk variable can help improve neurological outcome. mortality can be further brought down by preventing chest infection to lower cranial nerve deficit. selected abstracts romanian neurosurgery vol. xv nr. 1 44 surgical management of the posterior fossa meningiomas; a study on a number of 142 patients prof. l. danaila, m.d., c. toader m.d., f. stefanescu m.d., d. petrescu m.d., l. gheorghitescu m.d., c. nastase ph.d., c. palade ph.d. second neurosurgycal department; national neurology and neurovascular diseases institute keywords: meningioma, posterior fossa, microsurgycal technique, cerebellopontine angle, tentorial noch, petroclival, foramen magnum, peritorcular, pineal. objective our study has been developed between 1982 and july 31th, 2007. in this period in our department were operated a number of 1183 patients with meningiomas; supratentorial and in the posterior fossa. only 142 of this meningiomas were located in the posterior fossa (pf) space. the porpos is to relevate the diversity of location in pf, importantes anatomical structures surrounding the tumors, the greate diversity of approach and the excelent result obtained by microsurgycal technique. methods this 142 patient have been diagnoticated either with computed tomography (ct) or magnetic resonance imaging (mri). the postoperativ folow-up has taken at six month, one year, three years and five years. our study is a retrospective analyse. results this yielded 63 omen and 37% man; the ratio was 2: 1. the great ratio of incidence was before and after the climacterium. the groupe of age most frequetly afected has been 45 years sice 65 years. the medium average has been 57,8 years. the location of this meningiomas were: cerebellopontine angle 34% man and 23 omen, tentorial noch 4% equal at man and women, transverse sinus 19% man and 16 omen, petroclival region 23% equal at man and women, foramen magnum, equal man and women 3%, peritorcular region 3% at women and one patient, a woman developed tumour in the pineal region. the histopathologicaly results of the pf meningiomas operated in our department were the folowing: meningothelial m. 41%, transitional (mixed) m. 20%, psammomatous m. 8%, microcystic m.6%, secretory m. 6%, chordoid m. 5%, metaplastic m.4%, atypical m.3%, papillary m. 3%, fibrous (fibroblastic) m.2% and clear cell m. 2%. because of the substantial risk of neurological morbidity a gross total resection (gtr) to minimize tumour reccurence rates could not be justified. in our cohort at107 patients have been efectuated gtr and in a number of 35 patient we have been efectuated near total resection (ntr). according to de simpson scale we clasified our patients like this: simpson i: doesn’t patient exists, simpson ii: 72 patients, simpson iii: 35 patients, simpson iv: 25 patients and simpson v: 10 patients. conclusion the micorsurgicaly technique increase the good results that we obtained but intraoperatively defined tumour characteristics played an important role in identifying the subset of patients with an increased risk of postoperative deficits. by selectively pursuing an ntr rather that a gtr, neurological morbidity was reduced significantly without significantly increasing the rate of tumour reccurence. first nerve preservation in olfactory grove meningiomas prof. a.v. ciurea, md1, a. tascu, md1, a. iliescu, md1, r. radulescu, md1, m. lisievici, md2, f. brehar, md1, a. gheorghita3, md 11st neurosurgical department, 2neuropathological department, 3ati department bagdasar-arseni clinic hospital, carol davila medical school, bucharest, românia keywords: olfactory groove meningioma (ogm), mri, simpson scale, gos, gks, olfactory nerve preservation, quality of life background olfactory groove meningiomas (ogm) arise in the anterior cranial fossa at the cribiform plate of the selected abstracts romanian neurosurgery vol. xv nr. 1 45 ethmoid bone. ogm represent 8 10 % of all intracranial meningiomas. ogm is a slow-growing tumors more often bilateral than unilateral, compressing progressively the cerebral frontal lobes and included olfactory nerves. the authors' aim is to reveal the best surgical management, with total removal and also with minimal complications to contribute in improving of quality of life (qol). first nerve preservation is one of our option in obtain the perfect qol in ogm. material and method the authors present a retrospective study on 44 cases of ogm operated on from 1990 to 2006 (16 years, 1st neurosurgical department, neurosurgical clinic, bagdasararseni hospital). the patients’ age range between 20 to 71 years (mean age 52 years) and the gender distribution f:m was 1.5:1. the clinical features were dominated by: headache 40 cases (90.9 %), anosmia 34 cases (77,2 %), personality changes 28 cases (63.6 %), visual impairment 27 cases (61,3 %), increased icp syndrome 25 cases (56.8 %). the size of the tumor was more than 6 cm in diameter (giant) in 31 cases (70.4%). all patients underwent microsurgical resection using bilateral subfrontal (30 cases-68.4%), unilateral subfrontal (10 cases22,7%) or pterional approach (4 cases – 9,1%). results the tumor resection degree (simpson scale, 1957) was: grade i 0 cases (0 %), grade ii -25 cases (56,8 %), grade iii 12 cases (27,3 %) and grade iv -7 cases (15,9 %). no biopsy was done (grade v). regarding of pathological aspects, ogm were: classic benign 41 cases (93,2 %) and atypical 3 cases (6,8 %). the important postoperative complications were: seizures 22 cases (50%), worsening of visual function 6 cases (13.6%), csf fistula 3 cases (6.8%), speech disorders 2 cases (4.5%), etc. postoperative anosmia was noticed in 36 cases (81,8%). the outcome realized six months postoperative was: good recovery 26 cases (59.1%), moderate disability 14 cases (31,8%) and 2 deaths (4.5%) by pulmonary emboli. the recurrence was noticed in 4 cases (9,1 %) which require a second surgical approach. the gks was not available, in our data. fourteen patients were psychological evaluated (six month’s postoperative) and the real improving was noticed after 18 months postoperative. the olfactory nerve was preserved in eight cases (18,1%), only in small and medium size of ogm. conclusion ogm is a benign tumor with silent evolution; the bilateral subfrontal approach is the best method which allows a total removal of ogm. the factors which contribute to improve the qol were: large approach, best visualization of anatomical structures, the gradually tumor debulking, minimal brain retraction, and preserve carefully arterial and visual pathways. the olfactory nerve preservation is possible only in small and medium size of ogm. recurrent meningiomas: an unsolved enigma dr. keki e. turel, dr. nootan kumar sharma, dr. shashank joshi bombay hospital institute of medical sciences, mumbai, india meningiomas are commonest benign tumors affecting central nervous system. microsurgical excision is the best treatment a neurosurgeon can offer to these patients. complete surgical excision (simpson’s grade i) should be the ‘goal’ during first surgery as neurological recovery is guarded during subsequent interventions. despite complete excision, recurrence is a known phenomenon that can frustrate the best of neurosurgeons. histological grading can predict recurrence up to a certain extent. according to pathological behavior, meningiomas can be aggressive, invasive, anaplastic or sarcomatous. malignant (grade iii) meningiomas show recurrence in 50% cases. molecular biological marker studies have shown promise in predicting recurrence. different receptors viz. estrogen receptor (er), progesterone receptor (pr), platelet derived growth factor receptor (pdgfr), and tenascin have been demonstrated on cell membrane of meningioma selected abstracts romanian neurosurgery vol. xv nr. 1 46 cells. ki 67 is a proliferation marker. different chromosomal abnormalities have been found associated with meningiomas. chromosome 22q is principal amongst them and carries tumor suppressor gene for nf-2. other important deletions are 1p and p16. thus prevention of tumor recurrence is a challenge for neurosurgeons. in the last 205 consecutive operated meningioma cases, we have documented 15 cases of recurrence. amongst them, 13 cases were supratentorial meningiomas. recurrence rate was higher in male patients. few of them needed re-surgery while remaining received radiotherapy or watchful monitoring. monitoring included serial clinical neurological examinations followed by contrast enhanced mri. we will also present our techniques of microsurgical excision for prevention and treatment of symptomatic recurrence. detailed analysis of our clinical and data of molecular biological marker studies will also be presented. factors influencing surgical outcome in patients with focal cortical dysplasia kostas n. fountas, md,phd assistant professor of neurosurgery, university hospital of larisa, school of medicine, university of thessaly focal cortical dysplasia (fcd) represents the most common neuronal migrational disorder. this term describes a wide spectrum of neuropathological abnormalities ranging from mild, welldemarcated cytoarchitectural changes to severe and extensive cortical lamination disorders. the association of fcd with epileptogenesis, although not clearly understood, has been well established. in the cases of medically refractory epilepsy secondary to fcd resective (mainly) and nonresective (less commonly) surgery constitutes a valid treatment option. pre-operative work-up of these patients includes detailed neurological examination, meticulous evaluation of seizure semiology, neuropsychological evaluation, surface ictal and interictal eeg, brain mri, proton mr spectroscopy, spect and siscom studies, pet scan, magnetic source imaging (msi) and invasive eeg monitoring. surgical approach is individualized on each patient with lesionectomy, topectomy, and lobectomy being the most commonly performed procedures. multiple subpial transaction (mst) technique is reserved for only those cases that the epileptogenic focus involves eloquent cortex. several parameters have been identified by different clinical investigators as outcome prognostic factors. histological subtype of fcd, severity of pathologic changes, extent of operative resection, patient’s age, existence of dual pathology, anatomic location of dysplastic tissue, and duration of seizures have considered important in predicting surgical outcome among patients of previously published surgical series. the characteristics of these series and the significance of each of these factors will be analyzed. the aim of this communication is to outline those parameters that their presence could favorably influence the surgical outcome of fcd surgical candidates. medulloblastoma c. di rocco neurosurgery, catholic university, medical school-rome, italy medulloblastomas continue to be a subject of great interest to the neurosurgeon. indeed, the surgical respectability of this tumor is coupled with the still persisting uncertainty about the late outcomes following the multimodality treatment which is necessary to cure at least some of the affected children. nowadays, improvements in surgical technique and in intraoperative and post-operative care allow safer and more complete surgical removals. on the other hand, refinements in radiation therapy and chemotherapy assure a better control of eventually residual tumors, consequently arising the question whether the radical excision is still the mandatory goal of the surgical treatment. selected abstracts romanian neurosurgery vol. xv nr. 1 47 unfortunately, this dilemma remains still unsolved. in fact, in spite of the numerous animal models and the promising results of several molecular studies, which have identified new targets for the chemotherapeutic treatment, in the clinical practice the staging of medulloblastoma is still based on traditional biological parameters such as the age of the patient at operation and the extent of the surgical excision. neuroprotection neuroplasticity and vasogenic brain edema hari shanker sharma laboratory of cerebrovascular research, department of surgical sciences, anesthesiology &intensive care medicine, university hospital, uppsala university, uppsala, sweden the microenvironment of the central nervous system (cns) is precisely and meticulously maintained by a set of dynamic physiological barriers located within the cerebral microvessels of the brain (blood-brain barrier) and spinal cord (bloodspinal cord barrier) as well within the epithelial cells of the choroid plexus separating the blood and cerebrospinal fluid (csf) interface (blood-csf-barrier). the physicochemical properties of these cellular barriers are quite comparable to that of an extended plasma membrane. the bbb and the bscb are quite tight to small molecules (12 å, lanthanum ion), whereas bcsfb is less restrictive in nature. on the other hand, the ependymal cell linings of the cerebral ventricles and spinal canal, referred to as csf-brain barrier do not normally restrict passage of several small sized molecules. however, protein transport across these barriers is severely restricted. entry of proteins into the cns microenvironment induces vasogenic edema formation that is primarily responsible for cell and tissue injury. these bloodcns-barriers (bcnsb) are often compromised under a wide variety of psychological, traumatic, metabolic, ischemic, environmental or chemical insults leading to neuronal, glial and axonal damage. opening of the bcsnb to various endogenous or exogenous substances and proteins alters the molecular, cellular, biochemical, immunological and metabolic environment of the cns leading to abnormal neuronal function and brain pathology. this review is focused on current status of the bcsnb breakdown in experimental models of emotional stress, traumatic injuries, psychostimulants as well as key environmental health hazards, i.e., heat and/or nanoparticles exposure. breakdown of the bcnsb in these conditions altered gene expression and induced brain pathology and neurodegeneration. attenuation of the bcnsb disruption with drugs, antibodies or growth factors markedly reduced the development of brain pathology. taken together, these observations strongly indicate that the bcnsb can be considered as a “gateway” to the neurological diseases. spinal cord evoked potentials, a tool to predict spinal cord edema and neuroprotection tomas winkler md, phd, prof. hari shanker sharma institute for neuroscience, uppsala university, sweden the functional loss following acute spinal cord injury (sci) is only partly caused by the initial mechanical trauma. the trauma also initiates realease of different chemical agents which in turn induce further damage, secondary injury (si). with rat experiments we have tried to map which substances are involved in the development of si. after laminectomy spinal cord evoked potentials (scep) are recorded continously with epidurally electrodes placed rostrally and caudally from the laminectomy area, stimulation of sensory nerves in the right hindlimb. sci is induced with a longitudinal inscision in the right dorsal horn of t10t11. with this technique, tracts passing the injury zone is left mechanically unharmed. in untreated animals, rostral scep vanishes within a few seconds after sci and is replaced by a positive injury potential. after 35 h there is sometimes a slight recovery. 5 h after sci there is a pronounced increase selected abstracts romanian neurosurgery vol. xv nr. 1 48 of water content in injured segments. if the animals are pretreated before sci with any of several tested drugs, dorsal sensory tract function is maintained (preserved scep) and edema and histopatological changes 5 h later are less or absent: pcpa (inhibitory on serotonin synthesis), naloxone (opoidreceptor antagonist), indomethacine (inhibitory on prostaglandin synthesis), nimodipine (calciumchannel blocker), diazepam (benzodiazepine ii agonist), ibuprofen (antiinflammatory drug), insulinlike growth factor and nerve growth hormone (local application on the spinal cord), cimetidine (blocking histamin ii receptors), no-syntetase inhibitor. cyproheptadine (blocking serotonin ii receptors) increased sci. some drugs has shown minor effects when applicated locally immediately after injury. our further studies will concentrate on follwing questions: which sustances are involved in later parts of si? is it possible to interfere with these clinically? other ways for adminstration of drugs to the injured parts of spinal cord? are some of these substances also involved in changes during monitoring of spinal cord and brain in the operation theatre? clinical assessment of impaired higher brain functioning after acute tbi. the clinical role of the german coma remission scale (crs) for brain protection klaus von wild professor of neurosurgery and functional neurorehabilitation münster / hannover, germany ojective the extent of persistent handicaps following acute brain damage is essentially the result of cognitive, mental, and neurobehavioral impairments the rehabilitation of brain damaged patients means brain protection during the early and long-term rehabilitation process that comprises the comprehensive, closely intermeshing interdisciplinary therapy of the injured patient from the very start and with the deployment of all available staff and technical resources, with the ultimate aim of enabling the patient to be socially reintegrated as fully as possible. the task of early rehabilitation is to diagnose, minimize, and treat the manifold impairments and secondary complications under intensive care conditions in such a way that the individual potential for recovery is maintained and used and at the same time to enhance the plasticity of the central nervous system (spektrum of rehabilitation)(1). methods our data are based on ten years experience on early neurosurgical rehabilitation of after acute brain damage, predominantly adults, preponderant traumatic brain injured (tbi) that were compared with the results of our prospective hannover münster study on quality management of tbi of all age classes (1-8). the coma remission scale (crs) was published by our own working group in 1993 (2,3,6).crs is based on the gcs , however, we added two items up to 24 points total score to describe cognitive and neurobehavioral functioning and recovery in the early stage when fim, barthel and drs are not applicable and the modified early rehab barthel already starts to work. results the first probe (clemenshospital) is based on the results after early rehabilitation of 252 consecutive patients after different kind of brain lesions that were observed at 6 and 60 months after 7mpact (mean 26 months)(1,3-5). the second probe respects quality management of 258 (3.8%) out of 6.783 tbi that received rehabilitation with one year outcome (7,8) the incidence of tbi is 321/100.000 , thereof 90% mtbi and 5% severe damages. the percentage of concomitant organ lesion (polytrauma) is 70% respectively one third of the rehab. patients, which is important in respect to both the functional impairments and secondary, tertiary complications during the phase of early and late rehabilitation.%0% of he early rehab patients suffered from at least one secondary complication. in hospitals lethality out of all 5.221 selected abstracts romanian neurosurgery vol. xv nr. 1 49 (70.1%) tbi was 19.2% within the first 10 days and 25.3% within the first month. from these figures and our previous studies we may calculate the necessity for neurotraumalogical rehabilitation in a total of 55% of all tbi-patients admitted to the icu. we did not observe an essentially poorer outcome in polytraumatised patients in respect to the gos and the fim. commentary the aim of (early) neurological-neurosurgical rehabilitation is brain protection in respect to the patient’s final social reintegration. frequent secondary and tertiary complications after acute brain damage require careful clinical assessment of impaired functioning during the course of acute (intensive) care and rehabilitation. we recommend the crs assessment tool of choice during early functional recovery, for example in combination with the efbi, disability rating scale (drs), and functional independence measure (fim). crs follow up demonstrates clinical restoration of brain plasticity and impairment of functioning too secondary to numerous impending complications. neuroprotection and neuroplasticity a dualistic vision of a continuous process dafin f. muresanu, professor md phd neurology, umph cluj-napoca, romania neuroprotection and neuroplasticity, processes that are apparently independent, with different control, represent in fact two sequences of the same process. every lesion triggers a neuroprotective endogenous reaction, after a latency period. a reparatory endogenous process (known as endogenous neuroplasticity) follows this answer also. continuously understanding the nature of both forenamed processes, and the manner of switching from neuroprotection to neuroplasticity, will lead to the improvement of specific pharmaceutical strategies. this presentation analyzes, on one hand, the fundamental biological processes that are continuously going on in the nervous system (neuroprotection, neuroplasticity, neurotrophicity and neurogenesis), and, on the other hand, the molecular pathophysiological mechanisms (excitotoxicity, inflammation, misfolding proteins, apoptosis like processes, free radicals, etc.). another goal of this presentation is to present and analyze the perspectives of basic and clinical researches in this field. although there is an increasing number of available treatments, only a very few molecules had some positive outcomes. the causes of the unsatisfactory results of the clinical studies are divided in two major categories: the first category is directly related with the complexity of the pathophysiological cascades that cannot be controlled with a single molecule that targets a single mechanism (wrong strategy). the second category is related with the transfer modality from the experimental research in clinical research and with the incorrect design of the clinical studies. neurotrophic factors are among the few active molecules that positively control both processes. because neurotrophic factors manage to control the sensitive balance of the two named processes, their chances of large-scale applicability as a treatment in different neurological disorders are highly significantly. selected abstracts romanian neurosurgery vol. xv nr. 1 50 3n therapies (neuroprotection, neuroplasticity & neurorehabilitation) important factors to improve the global outcome in intracranial aneurysm prof. a.v.ciurea1, m.d, assoc. prof. d. muresanu4, md, assoc. prof. g. onose, md2, a. iliescu1, md, a. chefneux3, md, r. radulescu1, md, r. rizea1, md 1neurosurgical department, 2neurorehabilitation department, clinical hospital ‘bagdasar-arseni’, bucharest, neurosurgical department, 3iuliu hateganu, neurological department, clujnapoca, românia keywords: intracranian aneurysms, neuroprotection, neuroplasticity, neurorehabilitation subarachnoid hemorrhage, hunt & hess scale, 3d ct angiography microsurgery, embolization, rebleeding, vasospasm, nimotop, 3h therapy background the intracranial aneurysm (i.a.) represent a prevalence between 0,2-7,9% in the literature. the variability depends of hospital referral. neuroimaging findings and autopsy pattern. the pathology of intracranial aneurysm is a dominant element in neurosurgical activity, because of multiple preoperatory and management problems. ia affected prepoderently the active age (40 and 60 years old) and the male sex. the cerebral circulation must be evaluated in totality and aneurysms in particular and the accuracy management is necessary for limitation of important lifethreatring complication (rebleeding and ischemic stroke). therapeutical solution: early neurosurgical approach or endovascular aneurysm obliteration. actually the 3n therapies represent an important steps to improve the global outcome in cerebral vascular aneurysm. material & methods the author present a study about 468 consecutive operated patients with intracranial aneurysms, operated in first neurosurgical department between 1997-2006 – 10 years (30 children and 438 adults). most cases (195 cases-45,5%) were between 41 and 50 years old. the predominant sex is male 291 cases (68%) (2,1: 1). the symptoms were dominated by: headache (98%), stiffneck (94%) and focal neurologic deficit (91%). most patients were hunt and hess 2 (243 cases, 36,7%), hunt and hess 3 (102 cases, 15,4%) at admittance. the associated pathology was: systemic arterial hipertension (321 cases, 75%) and obesity/hypercolesterolemia (146 cases, 34,1%), ischemic cardiopathy (60 cases,16%), diabetus melitus (60 cases,16%), chronic alcoholism (49 cases,13%), ischemic stroke (45 cases,12%), atrial fibrilation (38 cases, 10%), miscellanea (53 cases, 14%, anticoagulant therapy). the main investigations were: ct scan, ds angiography. actually, the most important were 3d ds angiography and 3d ct angiography. the common localization of intracranial aneurysms was the anterior communicating artery 151 cases (35,3 %); the other locations were: medium cerebral artery 127 cases (29,7%), posterior comunicating artery 77 cases (17,9%), internal carotid artery 57 cases, (13,3%), basilar top 8 cases (1,8%) and vertebral artery 8 cases (1,8%). multiple aneurysm represent in our data 40 cases (8,5%). all cases were operated, as soon as possible after the subarachnoid hemorrhage (sah) and ia angiography diagnosis. “early surgery” eliminates the risk of re-bleeding and facilities the treatment of vasospasm which peak is between 6-8 days post sah. from all complications two are very critical for life and morbidity: aneurysm rebleeding and cerebral ischemia. the therapeutical operative measures for intraoperatory aneurysm rupture prevention are: mild hyperventilation (pac02 30-35 mmhg); elevation of the head; deliberate hypotension; temporary clip. the most important intraoperatory aneurysms surgery is the perfect microsurgical approach which realized the perfect aneurysm dissection with all perforates, collaterals and magistral arteries; the clip application on the aneurysm neck is the surgical procedure to cure the vascular malformation (gold standard aneurysm obliteration). also as intraoperative neuroprotective measures we mention: local papaverine solution administration, abundant saline water washing. selected abstracts romanian neurosurgery vol. xv nr. 1 51 during postoperative period we noticed the following complications: vasospasm, obstructive hydrocephalus, seizures, cerebral edema, and general complications. the following neuroprotective measures for postoperative complications preventions are: 3h therapy (hypertensive therapy, hypervolemic, hemodilution). nimotop therapy could be used in preoperative period also, for cerebral ischemia prevention. (3-7 ml/h depends on arterial systemic pressure), but 3h therapy could be applied with maximum efficiency only în postoperative period (after aneurysm clipping). the glasgow outcome scale (gos) in our data (at 6 months postoperator) shows: good recovery 286 cases (66.8%), moderate disability 101 cases (23.6%), severe disability 21 cases (4.9%), persistent vegetative state 5 cases (1.1%), death 15 cases (3.5%). actually, an important number of ia will be treated by endovascular embolization. the guglielmi detachable coils (gdc) represent an electrolytically detachable platinum coils placed via endovascular techniques. this gdc is feet for vertebro-basilar aneurysm in which the open microsurgical approach is difficult. our experience in 1st neurosurgical dpt. consist in 24 cases of embolization. also in this procedure appears many complication: aneurysm rupture, cerebral ischemia, neurological deficit and consciousness status modification. conclusions ia represents an important neurosurgical challenge. also ia by the rupture and complication is the real lifethreatering diseases. complete vascular exclusion is the treatment of choice by open microsurgical approach or endovascular embolization. the important measures to avoid rebleeding and cerebral ischemic stroke in intracranial aneurysms are perfect evaluation and early approach, perfect aneurysm dissection and neuroprotective measures (pre, intra and postoperatory). neuroprotective agents – useful to avoid cerebral ischemic stroke the timing of aneurysm surgery is one of the key of avoidance lifethreatring complication. unruptured cerebral aneurysms presenting with ischemic events michel w bojanowski, md, frcs(c) and nancy mclaughlin, md neurosurgery, centre hospitalier de l’université de montréal, montréal, canada background in rare circumstances an unruptured cerebral aneurysm may present with ischemic events. the goal of this study was to evaluate results following aneurysmal treatment of such patients. methods within the 166 consecutive patients treated for an unruptured aneurysm, 9 presented with ischemic events. potential cardiac, hematologic or extracranial vascular etiology were eliminated. results at admission, all patients were investigated with a cerebral mri and angiography. an acute ischemic lesion in the symptomatic territory was demonstrated in 5 patients. the aneurysm responsible of the ischemic event was located on the internal carotid artery (n=3), the middle cerebral artery (n=4), superior cerebellar artery (n=1) and the basilar artery (n=1). they measured 10mm or less (n=5); 11-20mm (n=2); more than 20mm (n=2). four aneurysms were partially thrombosed on imagery. three patients were treated endovascularly of which two had residual neck and one a recurrent aneurysm. all required a second embolization. five patients were treated surgically. of these, one thrombosed the aneurysm’s parent vessel and two had distal emboli with neurological deficits. the aneurysm was completely excluded in 4/5 operated patients. embolization of the basilar aneurysm was impossible. all treated patients had a favorable prognosis. conclusion aneurysms presenting with ischemic events are often small and located on the anterior circulation. although the risk of thromboembolic events following surgery are high in this series, the functional prognosis is favorable. selected abstracts romanian neurosurgery vol. xv nr. 1 52 multiple intracranial meningiomas with different pathological subtype assoc. prof. gorgan mircea, neacsu angela, bucur narcisa, pruna mihai viorel, calina niki adrian, martin dan, lisievici mihai, vasiliu-bacovia daniel first neurosurgical clinic, fourth neurosurgical department, clinic emergency, hospital “bagdasar-arseni”, bucharest keywords: multiple meningiomas, different pathological subtype, treatment strategy the term “multiple meningioma” is used to describe the simultaneous or sequential appearance of two or more independently situated meningiomas, not necessarily of the same pathological subtype. in the pre-ct (computed tomography) era, the frequency of multiple meningiomas without neurofibromatosis was reported to be less than 3%. since the introduction of ct and mri, the frequency of multiple meningiomas without signs of neurofibromatosis has ranged between 4.5% and 10.5%; nevertheless, the concomitant occurrence of multiple intracranial and spinal meningiomas in the same patient is rare. 15% of cases with multiple meningiomas present different pathological subtypes. authors present the case of a 63 y.o. woman, admitted for left proptosis and hemicrania evolving for three months. at the screening ct scan with contrast were discovered two lesions: a left fronto-temporal mass, intensely contrast enhancing, with peritumoral edema, inserted on the sphenoid wing, extended in the infratemporal fossa and ethmoidal sinus; the other lesion was cystic, located parieto-temporally, in the corticosubcortical area, with a small tumoral nodule located deeply. mri defined the details and the size of the lesions: 63/65/71 mm left solid tumor suggesting a sphenoid wing meningioma, and a 67/62/72 mm right parieto-temporal cystic lesion with moderate mass effect. authors insist on neurosurgical strategy for treatment of multiple intracranial masses with different consistency-solid and cystic. adequate surgical planning was done after mri with contrast examinations, who were strongly suggestive for multiple intracranial meningiomas. surgical approach was done in two steps, according to treat first the cystic lesion because we supposed that is a recent developed lesion with high risk of sudden volume increase followed by neurological deterioration. on another way, attacking first the solid tumor, we could have a high risk to decompensate the cystic lesion. neurological and general evolution after two steps neurosurgery was without incidents with a very good outcome. pathological examination revealed two different types of meningioma: microcystic and transitional. conclusion despite the multiplicity of sites, multiple meningiomas do not differ in prognosis from benign solitary meningiomas. when cystic and solid tumors coexist supratentorial, bilaterally, the first approach is on the cystic lesion that precludes the uneventful complications. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article twist drill craniostomy vs burr hole craniostomy in chronic subdural hematoma: a randomized study somil jaiswal, a.k. chaudhuri, s.n. ghosh, s. ghosh, s.k. saha, pooja jaiswal india doi: 10.1515/romneu-2017-0057 346 | jaiswal et al twist drill craniostomy vs burr hole craniostomy doi: 10.1515/romneu-2017-0057 twist drill craniostomy vs burr hole craniostomy in chronic subdural hematoma: a randomized study somil jaiswal1, a.k. chaudhuri2, s.n. ghosh2, s. ghosh2, s.k. saha2, pooja jaiswal3 1department of neurosurgery, king george’s medical university lucknow, uttar pradesh, india 2department of neurosurgery, ipgmer kolkata, west bengal, india 3department of pathology, iims&r, lucknow, uttar pradesh, india abstract: aim: to compare two most common operative procedures used in patients with chronic subdural hematomas twist drill craniostomy and burr hole craniostomy. material and methods: the study was a prospective randomized controlled trial on patients with chronic subdural hematomas. results: both procedures are comparable with respect to outcome but surgical duration is statistically higher in burr hole craniostomy than twist drill craniostomy. conclusion: twist drill craniostomy is procedure of choice in emergency surgical situation. key words: twist drill craniostomy, burr hole craniostomy, chronic subdural, burrhole drainage, recurrence introduction chronic subdural haematoma (csdh) is one of the most common clinical entities encountered in daily neurosurgical practice with an approximate incidence of 13.1 cases per 100,000 population and mortality rates reported upto 13% (1). it generally occurs in the elderly population in whom age related reductions in brain volume with a corresponding increase in the size of the subdural space increase the vulnerability to this disease. it is common in elderly with the peak incidence in the eighth decade (2, 3) and a male: female ratio of 3:2 (3, 4-7). trauma is probably the most important risk factor which is associated in about two third of patients (3, 8, 9). contemporary surgical treatment options range from twist drill craniostomy (± irrigation ± drainage), burr hole craniostomy (± irrigation ± drainage) and large craniotomies with marsupialisation of haematoma membranes. burr hole craniostomy (bhc) seems to have been the most commonly performed procedure for decompressing chronic subdural haematomas in the past 20 years (20). this procedure shares the advantages of twist drill craniostomy, with its high cure rate and low risk of morbidity and mortality, and the romanian neurosurgery (2017) xxxi 3: 346 355 | 347 advantage of has low risk recurrence similar to craniotomy to with its low risk of recurrence. however, statements in favour of the less invasive twist drill craniostomy is the positive correlation between the degree of invasiveness and the number of non-surgical complications in elderly people and has an added advantage that it can be performed at bedside and allows early mobilization of elderly moribund patients and reduced inpatient hospital stay (25). various aspects of treatment including techniques: twist drill and burr-hole craniostomy versus craniotomy with or without additional irrigation, with or without drainage, position of drain, postoperative nursing of patient, single versus double burrhole technique have been studied so far. evidence based meta-analysis of contemporary surgical treatment of subdural hematoma identified twist drill craniostomy and burr hole craniostomy as the safest methods. burr hole craniostomy has the best cure to complication ratio and is superior to twist drill craniostomy in the treatment of recurrences (19). this study aimed at evaluation of advantages and disadvantages of the two most commonly used methods of treatment by a prospective blinded randomized trial so as to provide class i evidence as to which of these commonly performed surgical treatment of chronic sdh [burr hole craniostomy (bhc) and twist drill craniostomy (tdc)] is better in term of complications, recurrence, cure and hospital stay. material and methods this prospective randomized study, was carried out from february 2012 to september 2013 in the s.s.k.m hospital, i.p.g.m.e.r, kolkata, india. all patients above the age of 18 yrs with unilateral chronic subdural hematoma were a part of study. exclusion criteria were bilateral chronic sdh, unilobar sdh, post craniotomy sdh, hygroma or empyema. consentbefore enrolling patient in the study, written informed consent was obtained in bengali / english/ hindi/ from the patient, or from the blood relative preferably the first degree relative in patients who were comatose or were unable to give consent, explaining both the treatment options i.e. bhc and tdc and need of further studies to prove the superiority of one procedure over the other. ethical approval was taken from the institutional ethics committee. detailed history including history of trauma within last 3 months, use of anticoagulant or antiplatelet drugs in last 1 week, alcoholism, history of hypertension and diabetes was obtained. complete clinical examination was performed and neurological performance of the patients was evaluated using the glasgow coma scale (gcs) and markwalder’s neurological grading system (mgs). the neurological and the general status of each patient on admission and before surgery were assessed by these 2 parameters. routine blood investigations and coagulation profile were obtained. any coagulopathy correction and need of blood or blood product transfusion were noted. ct details of the following parameters: maximum thickness of hematoma, density, midline shift was noted. 348 | jaiswal et al twist drill craniostomy vs burr hole craniostomy randomization the subjects were randomly allocated into two intervention groups, group a (twist drill arm) & group b (burr hole arm) by using the startrek random number generator. total of 79 subjects were recruited, out of which 37 subjects were in bhc group and 42 subjects were in tdc group. surgical technique •patients in group a underwent double (frontal and parietal) twist drill craniostomy (using a twist drill) under local anesthesia. two 5 mm scalp incision with no.11 surgical blade was given over frontal and parietal region and skull openings of 5 mm were made. later, dura was punctured and gradual drainage of hematoma fluid with irrigation of subdural space with isotonic normal saline was done using soft silicon catheter. a closed system silicone drain was placed in frontal subdural space through the frontal opening and tunneled away from the primary scalp incision. single suture was applied at both frontal and parietal sites. •patients in group b underwent surgery under local anesthesia/ monitored analgesia. standard double burr hole craniostomy (>15 mm diameter) at frontal and parietal region was performed. the dura mater was opened with a cruciate incision, and coagulated with bipolar diathermy. similar irrigation of subdural space and insertion of soft silicon drain in frontal subdural space was done. apart from the craniostomy process all other surgical steps were similar. duration of surgery was time of incision to final suturing was noted. drain was connected to a collection bag that was kept in a dependent position for 48-72 hours and then removed. post operative assessment postoperative ct scan was obtained on 7th postoperative day and noted for: residual collection, thickness of subdural collection, density of collection, mid-line shift and associated findings of parenchymal hematoma, acute subdural hematoma, pneumocephalus if present. at the time of discharge neurological status was assessed by gcs and mgs scores. patients of both the groups were assessed by glasgow outcome scale and markwalder grade at 4 weeks & ct scan was obtained. residual hematoma was defined as any residual collection with midline shift on ct scan obtained on 7th post operative day.recurrence was defined as occurrence of symptoms and signs attributable to an ipsilateral subdural residual hematoma seen on a ct scan within 1 month of the original drainage procedure. reoperation was done in all cases of recurrence. morbidity was defined as any procedure related complication (such as parenchymal injury, wound infection, seizures) during or after surgery other than recurrence and mortality. mortality included any death within 30 days of post operative period. cure rate was defined as percentage of patients with complete cure (gos of 5 or mgs o) at one month follow up. primary outcome measure was recurrence rate requiring reoperation, defined as the rate of reoperation to treat recurrent chronic subdural hematoma in patients previously treated with any of the two procedures secondary outcome measures were morbidity, mortality and length of hospital stay. romanian neurosurgery (2017) xxxi 3: 346 355 | 349 statistical analysis statistical analysis was performed with help of epi info (tm) 3.5.3. chi-square (χ2) test was used to test the association of different study variables with the study groups. z-test (standard normal deviate) was used to test the significant difference between two proportions. t-test was used to compare the means. p < 0.05 was considered statistically significant. results 79 patients admitted in sskm hospital neurosurgery emergency were randomly assigned in two groups during the period february 2012 to september 2013 as per the study protocol. out of 79 patients, 37 patients underwent burr hole craniostomy and 42 patients underwent twist drill craniostomy. there was no significant difference between the two groups related to age, gender, predisposing factors, presenting complaints, gcs and mgs at admission, ct scan parametersdensity, thickness and midline shift as shown in table 1. ct scan parameters thickness of hematoma in bhc group were 19.89±4.89mm, 14.41±3.79mm and 0.42±0.32mm vs tdc group were 20.76±4.76 mm, 14.58±3.51 mm and 0.92±0.32 mm at admission, 7th post operative day and at 1 month follow up showed no significant difference between two groups as depicted in table 2. similarly mid line shift and density of hematoma also demonstrated no significant difference between groups at admission, 7th post op day and at 1 month follow up. outcome table 3 depicts that patients with glasgow outcome scale 5 at one month denoted as cured was higher in bhc (94.59%) as compared with tdc (88.10%) showed no significant difference among the group(z=1.63;p>0.05). gos score and mgs score at 1 and 3 months showed no significant difference in two groups. patients with recurrence was higher in tdc group (4.88%) as compared with bhc group (2.78%) demonstrated no significant difference (p>0.05), all three patients were re operated with the previous technique. mean duration of surgery in bhc group 52.13± 7.22 min was significantly higher than that of tdc group 36.66±11.77 min and was statistically significant (p=0.0001).thus tdc was better than bhc with respect to operative time. both groups were no different with respect to mean duration of hospital stay. 34.5% patients in tdc group showed residual collection in post op ct head while it was 30.56% in bhc group and there was no significant difference between the groups(p>0.05). complications there was no significant difference between the two groups related to complications during hospital stay. one patient died in both the group which presented at the time of admission in low gcs (table 3). predictors of outcome gos 5 was found in patients of higher gcs who were of young age group (57.66± 3.44; p<0.01) as significant. similarly male gender and higher gcs at admission showed significant correlation with better outcome. 350 | jaiswal et al twist drill craniostomy vs burr hole craniostomy table 1 bhc (n=37) tdc (n=42) p mean age 56.91 54.59 p>0.05 male/female 33/4 36/6 p>0.05 predisposing factors trauma hypertension diabetes mellitus alcoholism antiplatelet drugs anticoagulants 28 10 7 3 1 4 32 11 7 2 0 4 p>0.05 presenting complaints headache hemiparesis vomiting altered sensorium gait disturbance memory loss urinary incontinence speech disturbance 26 24 11 8 7 7 3 2 28 24 16 8 7 6 4 1 p.0.05 gcs at admission 14-15 9-13 3-8 25 10 2 24 15 3 p>0.05 mgs at admission 0 1 2 3 4 2 10 24 1 0 0 14 26 2 0 p>0.05 ct scan parameters thickness of hematoma mean ± s.d. mid line shift mean ± s.d. density hypodense isodense hyperdense 19.89±4.34 10.70±2.84 18 10 9 20.76±4.51 10.83±3.91 10 13 19 t77=0.87;p>0.05 t77=0.16;p>0.05 χ2=5.96 p>0.05 romanian neurosurgery (2017) xxxi 3: 346 355 | 351 table 2 ct scan parametershematoma thickness radiological features bhc group (n=37) tdc group (n=42) significance of difference thickness at admission mean ± s.d. 19.89±4.34 20.76±4.51 t77=0.87;p>0.05 thickness at 7th post op day mean ± s.d. 14.41±3.79 14.58±3.81 t77=0.19 ; p>0.05 thickness at 1 month mean ± s.d. 0.44±0.32 0.92±0.32 t75=1.58; p>0.05 table 3 outcome variable bhc group (n=36) tdc group (n=41) significance of difference(p) gos at 1 month mean ± s.d. 4.97± 0.16 4.82±0.588 t77=1.40;p>0.05 range 4-5 2-5 mgs at 1 month mean ± s.d. 0.03 ± 0.01 0.17 ± 0.05 t77=0.53;p>0.05 range 0-1 0-3 cure rate cure (gos 5 at 1 month) 35/37 (94.59%) 37/42 (88.10%) recurrence 1(2.78%) 2(4.88%) z=0.47;p>0.05 residual collection 11 (30.56%) 14 (34.15%) z=0.33;p>0.05 mean duration of surgery (in minutes) mean ± s.d. 52.13± 7.22 36.66±11.77 t77=6.97;p=0.0001 range 30-60 20-75 mean duration of hospital stay (in days) mean ± s.d. 7.41±1.46 7.48±1.79 t77=0.18; p>0.05 range 7 – 15 7 17 352 | jaiswal et al twist drill craniostomy vs burr hole craniostomy table 4 comparison of morbidity among two groups complications bhc group (n=36) tdc group (n=41) significance of difference no. % no. % p wound infection 2 5.56 1 2.44 0.71 >0.05 seizures 1 2.78 0 0.00 1.07 >0.05 meningitis/abscess 1 2.78 0 0.00 1.07 >0.05 parenchymal hematoma 0 0.00 1 2.44 1.07 >0.05 morbidity 4 11.11 2 4.88 1.02 >0.05 discussion hamilton et al. (18) compared burr hole evacuation and craniotomy and found no difference between the procedures. svein and gelety (39), robinson (22) and markwalder et al. (15) advocated the use of only burr hole craniostomy for evacuation of hematomas. camel and grubb (26) had achieved an excellent outcome (86%) by using twist drill craniostomy with continuous catheter drainage. in this study highest incidence in men was noted between 40-60 yrs of age and an average age of occurrence of csdh was 53.05 yrs which is similarly seen in studies by markwalder (15), cameron (2), robinson (22) and kaste (23). age is a strong predictor of clinical outcome by gos scale (p<0.01) in our study this is similar to the study by r. ramachandran and t. hegde (23). male to female ratio reported in literature is 3:2 (3, 4, 5, 6, 7) whereas in this study it came out to be 6.9:1. the higher incidence in men can be attributed to higher rates of head injury in males. the major presenting complaints were non-specific headache (63.29%) focal neurological deficit in the form of hemiparesis (55.70%), and symptoms of raised intracranial pressure such as vomiting (34.8%) and altered sensorium (20.25%). similarly headache was the most common complaint in the study by smely et al (17). cameron (2) in his series had limb weakness in 40%, cognitive disturbances in 30% and headache in 20%. history of trauma was obtained in 75.94% of patients in this study with no difference in the two groups. smely et al. (17) has reported 50% cases related to trauma. the two groups in other studies of horn et al (19) and muzii et al. (20) are similar. other predisposing factors in both the groups in my study were similar without any significant difference. pre operative gcs was identified as strong predictor of clinical outcome in gos scale. villagrasa (25) showed that a low gcs at admission had a higher mortality rate. gokmen et al (21) found that pre operative gcs is an important criterion for operative mortality than surgical method. neurological status of patients in mgs score was similar in romanian neurosurgery (2017) xxxi 3: 346 355 | 353 both the groups. this finding is similar to the series of smely et al. (17), gokmen et al (21) and muzii et al. (20) their data in both the groups were similar. pre operative ct scan finding of hematoma density in the two groups of the study showed no significant difference. similarly the other comparative studies had comparable data in their two groups without any significant difference. pre operative ct scan in this study showed no statistically significant difference in hematoma thickness between the two groups. even studies by smely et al. (17) horn et al. (19), muzii et al. (20), gokmen et al. (21) did not show difference in preoperative hematoma thickness in their study groups and their data were comparable. recurrence has been a major problem in the treatment of csdh with significantly increased morbidity and poor outcome. recurrence rates in our study are 4.88% in tdc group and 2.78% in bhc group respectively without any significant difference (p>0.05) in the two groups although favouring bhc group. weigel et el. (12) in their meta analysis have reported 33% (3-76) recurrence in tdc group and 12.1 %( 0-28) recurrence in bhc group with a significant difference in the two groups. gokmen et al. (21) have reported 3% and 7% recurrence respectively in tdc and bhc group. smely et al (17) have reported 18% and 33% reoperation rates respectively. all these study groups have noted no significant difference similar to our study except the meta analysis by weigel et al (12). in our study we had 25 cases of residual collection, out of which 14 cases (34%) of residual collections were in tdc group and 11 cases (30%) in bhc group. other than 3 cases of recurrence in 1 month follow up, rest showed complete resolution. ct scan at 3rd month follow up showed complete resolution in them. difference in the two groups is not statistically significant. this study supports markwalder’s finding in complete resolution of hematoma by 2-3 month following discharge from hospital. cases in which hematoma increases and causes neurological deterioration or persistent or progressive headache, repeated treatment should be considered. average mortality reported in evidence based outcome meta-analysis by weigel et al. (12) 2.9% (0-7.9%) in tdc group and 2.7% (032%) in bhc group. horn et al. (19) has reported 7% and 13%, gokmen et al. (21) 2.6% and 3% whereas muzii et al. (20) has reported no significant difference in two groups. in our study mortality in tdc group was 2.44 % (1 case) and in bhc group was 2.78% (1 case). both the patient died before 7th post operative day assessment. both the patients had low gcs score at the time of admission. this suggests that preoperative gcs is an important predictor of operative mortality than the surgical method. weigel et al. (12) had demonstrated 3% (07.6%) morbidity in tdc group and 3.8% (09%) in bhc group. muzii et al. (20) have reported no difference between the 2 groups. morbidity in this study in tdc group was 2 cases (4.88%) and in bhc group 4 (11.11%). mean duration of hospital stay in tdc group was 7.48 days and 7.41 days in bhc group and difference in not statistically significant although this difference favours 354 | jaiswal et al twist drill craniostomy vs burr hole craniostomy bhc group. muzii et al. (20) reported no difference between the two groups. however gokmen et al. (21) has reported larger hospitalization in tdc group and larger hospitalization was associated with higher overall mortality in his study. minimum duration of hospitalization in our study was kept as 7 days to obtain 1st post operative ct scan of patient. only patients with some complications were not discharged after 7th post-operative day. therefore our duration of hospital stay is biased. the cure rates were 94.59% in bhc group and 88.10 % in tdc group at 1 month follow up. this difference is not significant. similarly the difference in the two groups was not significant in study by horn et al. (19) and gokmen et al. (21). however study by william et al. (15) and decision analysis by lega et al. (14) have proven superiority of bhc over tdc in respect to clinical outcome and complications. all the patients who had shown complete resolution of csdh by 1 month and showed normal ct scan at 3 month follow up in this study. gokmen et al. (21) with a follow up study for up to 6 months suggested three months follow-up was sufficient. conclusion cure rate was higher in bhc group than tdc group, though it was not statistically significant. duration of surgery was significantly higher in bhc group than tdc group. thus tdc is less time consuming procedure and is procedure of choice in emergency situations. burr hole craniostomy and twist drill craniostomy, both the procedures are comparable with respect to residual collection, recurrence, operative complications, morbidity and mortality. reoperation should be considered in cases of residual collection only if there are persistent progressive symptoms with significant post operative subdural collection. age, gender and clinical status at admission are important determinants of clinical outcome after surgery. correspondence dr. somil jaiswal mailing address 15/49 sector 15 indira nagar, lucknow, uttar pradesh, india. email: dr.somil26@gmail.com phone: +91 7755075630 references 1. kudo h, kuwamura k, izawa i, et al: chronic subdural hematoma in elderly people: present status on awaji island and epidemiological prospect. neurol med chir (tokyo) 1992; 32:207 2.cameron mm: chronic subdural haematoma: a review of 114 cases. j neurol neurosurg psychiatry 1978; 41:834 3.ernestus ri, beldzinski p, lanfermann h, et al: chronic subdural hematoma: surgical treatment and outcome in 104 patients. surg neurol 1997; 48:220 4.hennig r, kloster r: burr hole evacuation of chronic subdural haematomas followed by continuous inflow and outflow irrigation. acta neurochir (wien) 1999; 141:171. 5. krupp wf, jans pj: treatment of chronic subdural haematoma with burr-hole craniostomy and closed drainage. br j neurosurg 1995; 9:619. 6. reinges mh, hasselberg i, rohde v, et al: prospective analysis of bedside percutaneous subdural tapping for the treatment of chronic subdural haematoma in adults. j neurol neurosurg psychiatry 2000; 69:40. 7. van havenbergh t, van calenbergh f, goffin j, et al: outcome of chronic subdural haematoma: analysis of prognostic factors. br j neurosurg 1996; 10:35. 8.chen jc, levy ml: causes, epidemiology, and risk factors of chronic subdural hematoma. neurosurg clin n romanian neurosurgery (2017) xxxi 3: 346 355 | 355 am 2000; 11:399 9.sambasivan m: an overview of chronic subdural hematoma: experience with 2300 cases. surg neurol 1997; 47:418. 10.markwalder tm. chronic subdural haematomas a review. j neurosurg 1981;54:637. 11.weigel r, hohenstein a, schlickum l, et al: angiotensin converting enzyme inhibition for arterial hypertension reduces the risk of recurrence in patients with chronic subdural hematoma probably by an angiogenic mechanism. neurosurgery 2007; 61:788. 12.weigel r, schmiedek p, krauss jk. outcome of contemporary surgery for chronic subdural haematoma: evidence based review.j neurol neurosurg psychiatr 2003; 74:937-43 13.rohde v, graf g, hassler w: complications of burrhole craniostomy and closed-system drainage for chronic subdural hematomas: a retrospective analysis of 376 patients. neurosurg rev 2001; 69:40 14.lega bc, danish sf, malhotra nr, sonnad ss, stein sc. choosing the best operation for chronic subdural hematoma : a decision analysis. j neurosurg. 2010;113:615–621 15.gr, baskaya mk, menendez j, polin r, willis b, nanda a. burr-hole versus twist-drill drainage for the evacuation of chronic subdural haematoma : a comparison of clinical results. j clin neurosci. 2001;8:551–554 16. svien hj, gelety je: on the surgical management of encapsulated subdural hematoma. a comparison of the results of membranectomy and simple evacuation. j neurosurg 1964; 21:172 17.smely c, madlinger a, scheremet r: chronic subdural haematoma—a comparison of two different treatment modalities. acta neurochir (wien) 1997; 139:818 18.hamilton mg, frizzell jb, traumer bi. chronic subdural haematomas. the role of craniotomy reevaluated. neurosurgery 1993;33:67 19.horn em, feiz-erfan i, bristol re, spetzler rf, harrington tr: bedside twist drill craniostomy for chronic subdural hematoma: a comparative study. surg neurol 65:150–153, 2006 20.muzii vf, bistazzoni s, zalaffi a, carangelo b, mariottini a, palma l: chronic subdural hematoma: comparison of two surgical techniques. preliminary results of a prospective randomized study. j neurosurg sci 49:41–46, 2005 21.gokmen m, sucu hk, ergin a, gokmen a, bezircio lu h . randomized comparative study of burr-hole craniostomy versus twist drill craniostomy ; surgical management of unilateral hemispheric chronic subdural hematoma. zentrabl neurochir 2008 aug : 69(3):129-33 22. robinson rg. chronic subdural haematoma, surgical management in 133 patients. j neurosurg 1984;61:263 23. kaste m, waltimo o, haiskanen o. chronic bilateral subdural haematoma in adults. acta neurochir 1979;48:231 24. ramachandran r, hegde t-. chronic subdural hematomas—causes of morbidity and mortality. surg neurol 2007; 67:36772. 25. villagrasa j, prat r, diaz jf. analysis of prognostic factors in adults with chronic subdural haematomas. neurologia 1998;13:120 [spanish]. 26.camel m, grubb rl. treatment of chronic subdural haematomas by twist drill craniostomy with continuous drainage. j neurosurg 1986; 65:183 microsoft word 4ungureanugh_giant trigeminal romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article giant trigeminal schwannomas-case report and a short literature review gheorghe ungureanu, ioan stefan florian romania doi: 10.1515/romneu-2017-0024 romanian neurosurgery (2017) xxxi 2: 161 164 | 161             doi: 10.1515/romneu-2017-0024 giant trigeminal schwannomas-case report and a short literature review gheorghe ungureanu, ioan stefan florian cluj county emergency hospital, romania abstract: trigeminal schwannomas (ts) are rare tumors that are located in the posterior and middle cranial fossae in about a quarter of the cases. the presentation pattern is different according to the involved compartment and the goal of surgery is complete removal. we present the case of a 35-year old woman who presented a left sided ts extending from the posterior to the middle fossa and cavernous sinus. we review the relevant literature regarding diagnosis and surgical treatment of these tumors. key words: trigeminal nerve, schwannoma, multiple cranial fossae introduction trigeminal nerve schwannomas (ts) are rare entities, accounting for 1 to 8% of all intracranial schwannomas and less than 0.4% of all intracranial tumors [4]. women seem to be affected more often than men and the majority of cases present in the third or fourth decade of life [2]. the tumors can arise from the trigeminal dorsal root entry zone, the gasserian ganglion or any of the three branches of the vth cranial nerve and this variability in origin can lead to complex tumors, which extend in one or in multiple cranial fossae [3]. the symptomatology is not related to tumor size as most patients usually present with mild facial hypoesthesia, various visual disturbances, and sometimes facial pain [14]. various authors presented their series in the literature, but surgical experience in giant trigeminal schwannomas is still limited. we present a case of a giant trigeminal schwannoma and perform a short review of the current literature. case report a 35-year old woman presented in our department complaining of a 6 months old left-side facial paresthesia, difficulty in chewing, loss of balance, facial pain that was lancinating, alternating from moderate to severe, irradiating to the lower face, aggravated by chewing. the clinical exam revealed a mild left hemifacial spasm, left hemifacial paresthesia and a mild facial asymmetry. cerebellar signs included ataxic gait and dysdiadochokinesia. a gadolinium-enhanced mri was performed and revealed a defined, solid tumor extending from the left posterior fossa to the middle fossa and cavernous sinus (figure 1). the tumor dislocated the brainstem medially and exerted cerebellar compression, and compressed without incorporating the carotid artery. the tumor was hyperintense both on t1 and t2-weighted images and enhanced significantly after contrast injection. based on 162 | ungureanu, florian giant trigeminal schwannomas             the clinical and radiological findings, a provisional diagnosis of trigeminal schwannoma was made and surgery for tumor removal was recommended. the patient was positioned on the left side and a subtemporal craniotomy, with a retrosigmoid extension, was performed. the tumor was solid, showed a good delineation from vascular and nervous elements, and was mildly vascularized. a complete removal was performed. after surgery, the patient has a transient worsening of the facial paresthesia, which remitted in a couple of days. pathology analysis showed spindle-shaped bipolar cells that formed fascicles and palisading appearance. immunohistochemistry of the tumor was positive for s100, cd34, vimentin and confirmed the diagnosis of ts. the postoperative mri showed complete tumor removal and no tumor regrowth was noted on the one and five years mri (figure 2). at the one year control, the patient did not show any neurological deficits and declared she returned to a completely normal life. a b c figure 1 preoperative mri showing a hyperintense tumor in t2-weighted imaging extending from the posterior to the middle fossa and cavernous sinus (a), which compresses the brainstem (b), and has a cystic structure (c) a b c figure 2 postoperative mri at 5 years showing axial (a) and coronal (b) complete tumor removal, with no signs of brainstem compression and a liquid filled area where the tumour was located (c) romanian neurosurgery (2017) xxxi 2: 161 164 | 163             discussions in 1953, jefferson tried to characterize trigeminal schwannomas and designed a classification which divided these tumors into three categories, according to their origin [7]. type a included tumors originating anterior of the gasserian ganglion and located in the middle cranial fossa, type b included tumors in the posterior fossa, originating from the trigeminal root and type c defined tumors located both in the posterior and middle cranial fossae [7]. yoshida and kawase also offered a classification of ts into six categories and divided those that affect multiple cranial fossae [13]. about 25 % of tumors appear in multiple compartments and because of the rarity of ts, these tumors are infrequent and no standard treatment exists [8]. what authors agree on is the fact that complete surgical excision is usually curative and as such, whenever feasible, this should be the goal of surgery [10]. whenever ts arise from the root of the trigeminal nerve, they involve the posterior fossa [5]. because of the fact that they can also appear on any of the nerve branches, these tumors can also grow epidurally into the infratemporal fossa or orbit [5]. pathological findings are usually those of any schwannoma, but it must be considered that in about 1% of cases these tumors are associated with neurofibromatosis and therefore other consecutive tumors or, very rarely, a type of melanotic tumor can occur in the trigeminal nerve [13]. the trigeminal nerve has a mix component, of both sensory and motor fibers. therefore symptoms of decreased facial sensibility or diminished force of mastication can raise the suspicion of a ts [1]. facial hypoesthesia is the initial symptom in 60% of cases, but it must be kept in mind that because of their large size, symptoms related to any other cranial nerve, cerebellar or brainstem symptoms are also possible [9]. radiological appearance plays a pivotal role in diagnosing and planning the surgical treatment of ts. mri is the method of choice. tumors usually appear as hypo or isointense on t1 and as hyperintense on t2-weighted imaging, with high enhancement after contrast administration [1]. a ct scan offers a complementary view of these tumors, as it can demonstrate the existence of bone erosion [14]. usually, contrast enhancement on ct is homogeneous or it can have a circum enhancement in cystic lesions [14]. surgical strategy in ts is generally tailored on the tumor and no definitive recommendations can be made. because of the difference in the classification systems, lack of volumetric studies and report of trigeminal function, there is an inevitable difficulty in comparing different series, the same as in the case of other complex skull base tumors [6, 9]. some authors divide the possible approaches into conventional approaches and skull-base approaches [14]. the conventional approaches include the subtemporal intradural, frontotemporal infratemporal, while the skull base approaches include anterior transpetrosal, zygomatic infratemporal or zygomatic transpetrosal [12, 13]. some authors describe the use of adjuvant technical means, e.g. endoscopy, especially in those tumors that extend into multiple cranial compartments [8, 9, 11]. as previously mentioned, the goal of surgery should be a complete removal, without sacrifice of neurological function. it must be kept in mind that sometimes, transient neurological deficits 164 | ungureanu, florian giant trigeminal schwannomas             can appear after surgery, but these disappear in a few days [12]. in our experience, the use of a conventional approach is sufficient in most cases, in order to achieve complete removal. tumors are usually solid and soft and detachment from ica or nervous structures is performed easily. the preservation of function of the trigeminal nerve is possible in those cases in which the tumor is well delimitated, although this is rarely the case in giant tumors. conclusions our article presents the case of a giant ts and discusses relevant aspects of the neurosurgical literature regarding this aspect. ts are rare tumors and they’re treatment is still not standardized. patients usually present with symptoms related to impaired trigeminal function, but cerebellar and brainstem signs are also possible in the case of ts which invade multiple cranial fossae. complete surgical removal is usually curative and should be the purpose whenever possible without affecting neurologic function. surgery through a modified subtemporal approach is a feasible option in those tumors that do not extend in the infratemporal sinus. correspondence gheorghe ungureanu victor babes, no. 43/7, cluj-napoca, cluj county, romania e-mail: ungureanugeorge@gmail.com references 1. agarwal a (2015) intracranial trigeminal schwannoma. neuroradiol j 28(1):36–41 2. coniglio aj, miller mc, walter ka, crane bt (2013) trigeminal schwannoma with extracranial extension and brainstem compression. otol neurotol 34(6):e42-4 3. fukaya r, yoshida k, ohira t, kawase t (2011) trigeminal schwannomas: experience with 57 cases and a review of the literature. neurosurg rev 34(2):159–170 4. goel a, muzumdar d, raman c (2003) trigeminal neuroma: analysis of surgical experience with 73 cases. neurosurgery 52(4):783–90; discussion 790 5. gupta p, sharma a, singh j (2016) solid cystic trigeminal schwannoma with intraorbital extension causing proptosis and vision loss. asian j neurosurg 11(4):456 6. ioan stefan florian, gheorghe ungureanu, alexandru florian (2016) the role of the basal cisterns in the development of posterior fossa skull base meningiomas. rom neurosurg xxx(3):321–328 7. jefferson g (1953) the trigeminal neurinomas with some remarks on malignant invasion of the gasserian ganglion. clin neurosurg 1:11–54 8. konovalov an, kalinin pl, shimanskii vn, shapirov oi, kutin ma, fomichev d v, kadasheva ba, turkin am, kurnosov ab (2014) [experience of surgical management of trigeminal schwannomas that simultaneously spread to the middle and posterior cranial fossae]. zhurnal vopr nei ̆rokhirurgii im n n burdenko 78(5):23–32; discussion 32 9. raza sm, donaldson am, mehta a, tsiouris aj, anand vk, schwartz th (2014) surgical management of trigeminal schwannomas: defining the role for endoscopic endonasal approaches. neurosurg focus 37(4):e17 10. samii m, alimohamadi m, gerganov v (2014) endoscope-assisted retrosigmoid intradural suprameatal approach for surgical treatment of trigeminal schwannomas. neurosurgery 10 suppl 4(4):565–75 11. samii m, alimohamadi m, gerganov v (2014) endoscope-assisted retrosigmoid intradural suprameatal approach for surgical treatment of trigeminal schwannomas. clin neurosurg 10(4):565–575 12. sharma bs, ahmad fu, chandra ps, mahapatra ak (2008) trigeminal schwannomas: experience with 68 cases. j clin neurosci 15(7):738–743 13. yoshida k, kawase t (1999) trigeminal neurinomas extending into multiple fossae: surgical methods and review of the literature. j neurosurg 91(2):202–11 14. zhang l, yang y, xu s, wang j, liu y, zhu s (2009) trigeminal schwannomas: a report of 42 cases and review of the relevant surgical approaches. clin neurol neurosurg 111(3):261–269 microsoft word _5.formatata_dobrin.doc romanian neurosurgery vol. xv nr. 2 26 semiology of neurosurgical skull base notes irina dobrin1, gr. zapuhlîh2, n. dobrin3, i. poeata4, n. ianovici3, a. chiriac 1military hospital iasi, emergency departament, 2state university of medicine and pharmacy “n. testemitanu” chisinau, moldavia, 3clinical hospital no.3, iasi, neurosurgical departament, 4university of medicine and pharmacy “gr.t. popa”, iasi each lesion in the skull base involve important neural and vascular elements after this we can appreciate, where the lesion is clinically localized. also is very important to do the semiological assessment before and after the surgical approach. keywords: anterior skull base, the central skull base introduction as previously noted endoand exo-skull base as presents from the prior to posterior three compartments: anterior, median and posterior. the petrooccipital suture subdivides along the longitudinal axis of the skull in two lateral regions and a single central aspect (csb, central skull base). fig. 1 skull base and cbs exposure anterior limit of asb, anterior skull base, is defined, as is seen in the figure, the thin posterior wall of frontal sinus which may have various shapes and sizes, and earlier planum clinoidale, sphenoid sinus cavernous ceiling that separates the posterior border of the floor above sets. horizontal portion of the previous base is relatively convex and presents numerous impressions giriforme (2, 9). measurements on cadavers but also on ct or mri explorations showed that ethmoid fovea is generally less than one inch over the horizontal plane of base important thing in surgical approaches (1). the most important anatomical structures in the floor above are orbital and paranasal sinuses. communications with the orbit are often ways of spreading infections or neoplasic processes from the vicinity of orbit with sofand iof fissures (superior respective inferior orbital fissure) entail the involvement of nerve iii, iv, vi, v1, the ophthalmic vein or to the iof impairment of v2, infraorbitare vessels and also are involved elements vasculonervoase of septic infratemporale and pterigomaxilare. lateral portion of the iof is an important milestone in the orbitotomy process side of previous resection of anterior skull base (1, 5, 9). semiology of neurosurgical skull base romanian neurosurgery vol. xv nr. 2 27 clinic skull base lesions is highly polymorphic due to the complexity of nerve vascular lesions that abound in this region. until more modern neurosurgical era of skull base lesions were considered virtually inoperable. in the late nineteenth century began developing techniques for the skull (kraus, haltead, panse) and later as surgeons chusing, dandy, guiot, break barriers to interdisciplinary and put the foundation of what today we call the skull base surgery. in 1992 in hannover occurs first international congress of skull base. in our country in 2002 is held the first congress of skull base surgery with international participation (a.v. ciurea). clinical features of the skull base are grouped in several syndromes depending on the location of the disease process. these syndromes are characteristic of each group of nerves and vessels that run through the skull. thus we define these foramens: cribriform ethmoidale plate with olfactory nerves optic canal with optic nerve superior orbitare fissure with 3, 4, 6, 5i nerves and superior ophthalmic artery and vein foramen rotundum, with 5ii nerve foramen ovale with 5iii nerve and meningeal accesory artery foramen spinosum, with middle meningeal artery internal acoustic pore with 7 and 8 nerves foramenul jugular wit 9, 10, 11,nerves and jugular vein hipoglosal foraman foramen magnum with 11 nerve, medulla spinalis , spinal and vertebral arteries cranial nerves palsies: 3, 4, 5i, 6 pathological preceses wich involve superior orbital fissure and anterior part of cavernous sinus 3, 4, 5i, 5ii , pathologies of posterior cavernous sinus 5, 6 apex pietros 7, 8, internal acoustic meatus 9, 10, 11, foramen jugular 9, 10, 11, 12, and simpathetic plexus (1, 5, 9, 8, 10) superior orbitar fissure syndrome and apex orbitary syndrome this anatomical structure is behind the orbit between the two sphenoid wing and similar to the optical channel contains superior ophthalmic vein, ophthalmic division of trigeminal nerve (lacrimal, frontal, supraorbital, supratrohlear, nasociliar). syndrome is characterized by muscle paralysis extraoculari, disruption of the first divisions of the trigeminal and are frequent involvement of the optic nerve. clinical experience the following issues: ptosis, dry corneal sensation and decrease visual acuity. this protopsului with tear chemozis suggest an intense and expansive process in the orbit. potential causes are trauma, neoformaţii orbit, inflammatory processes and vasculitis (6,7). inflammatory processes can be isolated (nonspecific) or associated with systemic diseases: graulomatoza wegener, poliarterita nodoasă, sarcoidosis, temporal arteritis. fungal infections are a rare case of apex orbit syndrome, most often related to micozele sinus. cavernous sinus extends from the posterior superior fissure to dorsum of the sella. syndrome tolosa hunt is an inflammatory granulomatosis involving the inside of the cavernous sinus, superior orbit fissure and has the following diagnostic criteria: retroorbitare pain oftalmoplegie with or without involvement of the optic nerve and sympathetic plexus, symptoms occur episodically with remission spontaneous imagistical aspects exclud other pathologies this syndrome is usually an exclusion syndrome when eliminated other causes: traumatic, inflammatory, neoplasic . ths syndrome (tolosa-hunt) is responsible for less than 5% cases of ophtalmoplegia painful and affects both sexes equally, most commonly in the decade of your life. pain characteristic pear and retro orbit is very intense and is resolved spontaneously. cause is unknown and presents a good response to corticosteroids. irina dobrin romanian neurosurgery vol. xv nr. 2 28 during the state of skull base lesions predominate intracranial hipertension syndrome with multiple cranial nerve impaired. this characteristic is fosterkennedy syndrome anosmia is present in nerve i damage ipsilateral, optic atrophy and contolateral papillary stasis. a combination of intracranial hypertension syndrome and the cranial nerves is common in olfactory groove meningioma (4, 8). sphenoid fissure syndrome presents impaired nerves ii, iii, iv, v1, and vi of which may be primitive optic atrophy. cavernous sinus syndrome (foix) include palsies of 3,4,6, nerves with trigeminal involvement. top of rock syndrome (gradenigo) involves reaching nerves v and vi are also known as petrous apicitis involved in otitis media, mastoiditis, is manifested by otalgia and paralysis of nerve ipsilaterala vi. paratrigeminal syndrome (raeder) is practically an apex syndrome of rock to which are added claude bernard horner syndrome by involvement of sympathetic pericarotidian plexus. described in 1918 by raeder as oculosimphatetic syndrome, he also reported the absence of anhidrozei in the affected side. internal acoustic meatus syndrome is characterized by internal conduct audutiv nerves vii and viii resulted achieve clinically with peripheral facial palsy, deafness and disorders echilbru. posterior foramen, jugular syndrome, paresis nerves ix, x, xi ipsilaterala ie faringovelolaringiana paralysis, paralysis trapeze and scm, disturbances sensitivity in the territory of pairs x and ix. condilo – posterior foramen syndrome : paralysis of nerves ix, x, xi, in addition with paresis of n. xii. hemibasal syndrome (garcin) include cranial nerve involvement ipsilateral on hemiskull base. this is a very rare syndrome observed in neoplasms of exobasal invasion without affecting endobasal encephalon itself. it may be a manifestation of schminke tumor, a poorly differentiated carcinoma involving lymphoid tissue in the tonsilar region and nasopahrynx. villaret syndrome is characterized by paresis of nerves ix, x, xi, xii, in addition with a syndrome claude bernard horner by lovely periarterial involvement. it is a rare syndrome characteristic of skull base osteomyelitis occurs in immunocompromised patients. besides these syndromes with involvement multiple cranial nerves are described and other congenital syndromes involving the skull base. phace, is an acronym which denotes a combination of syndromes involving skull base , neurocutanate events, posterior fossa haemangioma, abnormal blood various aortic coarctation, cardiac defects, sternal disjunction. the most frequent involvement at the skull base is v1. also present impaired dandy walker type of body calos hypoplasia or agenesis, persistent artery trigeminala, hypo or carotidian agenesis (6,7). other syndromes with anterior skull base involvement craniosinostosis craniosiostosis sunt defined as premature closure of one or more sutures in the skull bones. cause premature closure of the suture skull growth inhibition on a direction perpendicular to that suture. sutures may generate more involvement of intracranial hypertension syndrome. semiology of neurosurgical skull base romanian neurosurgery vol. xv nr. 2 29 fig. 3 ostelysis of the skull base with foramen jugular involvement terminology scafocephaly premature fusion of suture sagital trigonocephaly premature closure of the suture metopes plagiocphaly premature closure of the coronary suture unilaterally brachycephaly premature closure of bilateral coronary suture posterior plagiocephaly lambdoide unilateral premature closure of the suture. besides these types considered classical (non syndrome) are described also syndromic craniosionostosis characterized by craniofacial dismorphism. apert syndrome is characterized by acrocephalosindactilia and brachycephalism and turicefalie, specific provision of orbits down and out, hipertelorism, is massive facial hypoplasia, other aspects are the deafness, speech disorders, acne, intellectual retardation. crouzon syndrome, initially described in 1912 by a french neurosurgeon , is characterized by exorbitism, retrognatism, inframaxilim. patients with this syndrome have a very characteristic facies. premature suture of coronare suture generate oxicephalie brahim. hipertelorismulof the orbit is more common in crouzon than in apert syndrome instead hydrocephalus and mental retardation are not so pronounced as in apertisyndrome. retroposition of the maxilonasal region can cause breathing difficulties. conclusions the clinical trial is vital to any medical activity. consultation, the first impact with the patient must be able to focus on the location of the lesion, so, flair, integration and synthesis is determined on a case history of exploration foe a good treatmen choice. references 1.ciurea a.v., constantinovici a. – ghid practic de neurochirurgie, editura medicala 1998 60-65 2.donald pj. history of skull base surgery. in: donald pj, ed. surgery of the skull base. philadelphia, pa:. lippincottraven;1998:3-14. 3.damasio a.r. l’erreur de descartes. edition odile jacob. 1999 4.derome pj,visot a, monteil jp, et al. management of cranial chordomas.in: sekhar ln, schramm vl jr, eds. tumors of the cranialbase: diagnosis and treatment. mount kisco, ny: futura publishers;1987:607-622. 5.frasin gh. ,cozma n -anatomia capului şi a gatului – curs – umf iaşi 1978 35-42 6.gandour-edwards gl, kapadia sb, barnes l. pathology of skull base tumors. in: donald pj, ed. surgery of the skull base. philadelphia, pa:. lippincott-raven;1998:31-51. 7.gopinath s.p., robertson c.s.: clinical evaluation of a miniature strain gauge transductor for monitoring intracranial pressure, neurosurgery 36:1137-41, 1995 8.lyons bm. surgical anatomy of the skull base. in: donald pj, ed. surgery of the skull base. philadelphia, pa:. lippincottraven;1998:15-30. 9.petrovanu i. , antohe s. – neuroanatomie clinica, editura editdan, iaşi 1999 58-75 10.weber al, curtin hd. imaging of the skull base. in: donald pj, ed. surgery of the skull base. philadelphia, pa:. lippincottraven;1998:87-104. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 426 | kumar dwivedi et al variant of misme syndrome rare variant of misme syndrome – a case report with review of literature ashish kumar dwivedi, shashi kant jain, ashok gandhi department of neurosurgery s.m.s. medical college, jaipur, india abstract: misme syndrome, also known as neurofibromatosis type-2 (nf2), stands for multiple inherited schwannomas, meningiomas, and ependymomas (misme) in the peripheral and central nervous system. it is a rare disorder of autosomal dominant inheritance due to mutations of a tumor-suppressor gene on the chromosome 22q12. clinically, it is characterized by multiple benign tumors arising in both the central and the peripheral nervous system, particularly from the bilateral vestibular nerve in more than 90% of the patients and more than two thirds of them develop spinal tumors. simultaneous occurrence of bilateral vestibular schwanoma with cervical and lumbar ependymoma without neuro cutaneous marker with weakness of limb as initial presentation is rare finding in single patient. here, we are reporting a rare case of misme syndrome harbouring bilateral vestibular schwanoma with cervical and lumbar ependymoma tumors in a 45 year old male patient having no other lesion and neurocutaneous marker with weakness of limb as initial presentation without posterior subcapsular cataract. key words: ependymoma, meningioma, neurofibromatosis type 2, misme syndrome, schwannoma introduction neurofibromatosis (nf) is a syndrome of an autosomal dominant inheritance. nf is divided into two types: nf1 and nf2. nf1, formerly known as von recklinghausen disease, is caused by mutations of neurofibromin gene on the long arm of chromosome 17. nf1 is one of the most common single-gene disorders affecting neurological function in humans (3). nf2, also known as the misme syndrome is caused by mutations of "merlin" gene on the chromosome 22q12. nf2 is a rare genetic disorder with multiple benign nervous system tumors, so as named as misme syndrome (1, 10, 12) although nf1 and nf2 are associated with autosomal dominant inheritance, up to half of nf1 and nf2 patients are due to spontaneous mutation. the incidence is about 1 in 3500 live births for nf1 and 1 in 60,000 for nf2(5). it has no predilection for race, sex and ethnicity (2). although, simultaneous occurrence of the bilateral vestibular schwanoma with cervical and lumbar ependymoma in an individual can be uncommonly encountered, occurrence of romanian neurosurgery (2016) xxx 3: 426 431 | 427 bilateral vestibular schwanoma with cervical and lumbar ependymomas with weakness of limb as initial presentation without posterior subapsular cataract in a single patient is a rare finding. case report a 45 yr old male patient presented to our outpatient department with the chief complaints of upper motor neuron type weakness of left side of upper limb and lower limb for 15 years, which was of insidious onset with initial progression and later non progressive course. his other complaints were hearing loss and tinnitus in the left ear for last 6 years, headache in left sub occipital region for 5 years, hearing loss with tinnitus in right ear for 2 yrs, swaying on either side while walking or difficulty in speech for last 6 months. there is no family history of similar disease which suggests that it is a sporadic case. neurological examination revealed decrease in sensation on left side face with absent corneal reflex on left side left lower motor neuron type seventh cranial palsy(house and brackmann grade 3),and bilateral sensory neural hearing loss(left>right) and left 9th and10th cranial nerve palsies. motor examination revealed increase tone in all four limbs (modified ashworth score -1). power of the left side upper limb and lower limb was 4/5 and in right side upper and lower limb was 5/5 and it is non progressive in last 10 years. deep tendon reflexes are 3+ in all four limbs; planter was extensor bilaterally. sensations of touch and pinprick were decreased by 50% below c3 level. pure tone audiometry was suggestive of bilateral sensory neural deafness more on left side. ophthalmic evaluation revealed bilateral mild papiloedema with no subcapsular lenticular opacities. magnetic resonance imaging (mri) of brain was showing a mass lesion present in left cerebellopontine angle (cp angle) cistern (figure 1a). mass was causing compression of brainstem. there is another smaller lesion on right cp angle cistern (figure 1a). mri of spine revealed a well-defined intramedullary lesion at c3-c4 (figure 1b) and another lesion at l1 region (figure 1c). we performed the microscopic subtotal excision of left cp angle lesion through retrosigmoid sub occipital approach as it was causing significant brainstem compression and planned right cp angle lesion for staged resection at later stage. as cervical and lumbar lesions were not causing progression of symptoms for years, we left it and follow up is planned. histopathology report of left cp angle lesion revealed it was vestibular schwannoma (figure 3). post-operative scan suggestive of near total excision of left cp angle lesion (figure 2). there is no further deterioration of cranial nerve palsies post operatively. figure 1a 428 | kumar dwivedi et al variant of misme syndrome figure 1b figure 1c figure 1a showing mass lesion in both cp angle region with heterogeneous contrast enhancement and brain stem compression on left side. figure 1b and 1c showing mass lesion at c3-c 4 and l1 level figure 2 post-operative image suggestive of near total excision of left cp angle lesion figure 3 histopathology suggestive of schwanoma discussion misme syndrome is synonymous with neurofibromatosis (nf) type 2 neurofibromatosis is a condition with autosomal dominant inheritance characterized by presence of multiple spaces occupying lesion in central and peripheral nervous system. the first probable reported case of neurofibromatosis type 2 was that of romanian neurosurgery (2016) xxx 3: 426 431 | 429 wishart in 1820 (18). this patient had multiple intracranial tumours with no cutaneous features and was, therefore, different to those patients reported by von recklinghausen in 1882 (17), whose principal features were nodular skin lesions with no intracranial tumours. later authors reported cases of neurofibromatosis type 1 with intracranial tumours and neurofibromatosis type 2 with cutaneous features (9, 4). in reporting a large family with neurofibromatosis in 1930, gardner and frazier (6) suggested that bilateral acoustic neuromas represented a separate central form of von recklinghausen neurofibromatosis. nf was classified as two types based on their clinical and pathological features (9). nf 1 caused by defect in neurofibromin gene which is located on long arm of chromosome 17, whereas nf 2 caused by mutations in merlin gene located on long arm of chromosome 22. this merlin gene is a tumor suppressor gene, which maintains cell connection of cytoskeleton with the plasma membrane, there by controls shape, motility of cell as well as growth regulation (5). it has almost 90% clinical penetrance rate. the diagnosis of nf2 usually made in 2nd and 3rd decades of life, mostly 18 to 24 yrs of age (5). diagnostic criteria which confirms diagnosis of nf2 is a) bilateral 8th cranial nerve schwannomas on imaging or b) first degree relative with nf2 and unilateral 8th cranial nerve schwannoma at <30 yrs or any two of following: glioma, neurofibroma, schwannoma, meningioma, juvenile posterior subcapsular lenticular opacity. the criteria for presumptive or probable diagnosis of nf2 are a) unilateral 8th cranial nerve schwannoma <30 yrs and: glioma, schwannoma, meningioma or posterior subcapsular cataract or cortical cataract. b) multiple meningiomas (two or more) and unilateral vestibular schwannoma <30 yrs or at least one of glioma, schwannoma, juvenile posterior subcapsular cataract (7, 14, 15) almost more than 90% cases of nf2 will develop bilateral 8th cranial nerve schwannomas. in literature occurrence of schwannomas from other cranial nerves like trigeminal, occulomotor, trochlear and abducens nerves have been described previously. the most common type of spinal tumor in nf2 is schwannomas. most common site is cervico thoracic region originating from dorsal root. 50 to 75% of nf2 patients develop meningiomas, most commonly in supra tentorial location. histopathologically mostly they are fibroblastic type. in spinal cord, meningiomas are mostly seen in thoracic region. ependymomas are seen in intramedullary location of conus medullaris or cervical region. approximately 90% of nf2 patients had ocular lesions. neurological examination and imaging of craniospinal axis is crucial to establish a diagnosis. mautner et al published a case series of 48 nf2 patients regarding their prevalence of various lesions in 1996(13). he concluded that 46 patients had 8th cranial nerve schwannomas (96%, 43 bilateral and 03 unilateral), 43 patients (90%) had spinal tumors, 30 patients (63%) had posterior subcapsular cataracts, 28 patients (58%) had meningiomas, and trigeminal schwannomas 430 | kumar dwivedi et al variant of misme syndrome were present in 14 (29%) patients. mr imaging of brain and spine with contrast is the investigation of choice in nf2 patients. nf2 patients should be managed by multidisciplinary approach which includes a neurologists, neurosurgeons, neuroradiologists, ophthalmologist, geneticist, audiologists and otologists. every child with family history of nf2 should be screened with imaging of brain and spine as early as possible from 10 to 12 years with annual scans until 4th decade. management in nf2 patients is preservation of function rather cure as they have lifelong tendency to develop new tumors and or recurrences. nf2 related 8th cranial nerve schwannomas are difficult to manage as they are often large by the time they are diagnosed and tend to behave aggressively. symptomatic vestibular schwannomas should be treated early to preserve auditory and other cranial nerve functions. there are various modalities for treatment of vestibular schwannomas in nf2. single or multiple fraction stereotactic radio surgery advocated at some centres with good local control and low incidence of side effect. regardless of approach all centers agree that intervention should be done only if there is documented tumor growth or progressive hearing loss. surgical options include radical resection, partial removal and decompression. we prefer a suboccipital retrosigmoid approach with goal of preserving facial nerve and hearing. there was significant brainstem compression in our case on one side so we did subtotal removal of mass lesion to relive compression from brainstem. we planned staged resection for the contalateral tumor. early surgery is advocated if vestibular tumor is less than 1.5 centimetres (cms) in diameter to preserve hearing and facial nerve function. if size is more than 1.5 cms it is preferred to wait until there is motor dysfunction due to brainstem compression. cochlear implants, hearing aids and auditory brainstem implants are alternative modes of treatment for complete hearing loss (16, 11). menengioma in nf2 are removed for cortical compression causing neurological deficit or seizure activity. surgical removal of intramedullary spinal tumor is recommended only when there are sign of spinal cord compression. hydrocephalus is treated with either direct tumor removal or ventriculoperitoneal shunt before definitive surgery. conclusion misme syndrome, or nf2, is not a curable disease. limited usefulness of adjuvant therapy leaves surgery as primary treatment to alleviate symptoms. surgery should be limited to removal of tumour that are causing symptoms. surgical approaches to tumors of nf2 is generally similar to the approach of same tumor in patients without nf2. however, the decision of when to operate and what level of aggressiveness is required, is often of critical importance in nf. even though the relentless progression of disease may be discouraging many times, ability of neurosurgical procedures to alleviate symptoms and improve quality of life is significant. romanian neurosurgery (2016) xxx 3: 426 431 | 431 references 1.asthagiri ar, parry dm, butman ja, kim hj, tsilou et, zhuang z, et al. neurofibromatosis type 2. lancet 2009; 373(9679):1974-86. 2. baser me, evans dg: lack of sex-ratio distortion in neurofibromatosis 2.am j med genet 2000, 95:292. 3. costa rm, silva aj. molecular and cellular mechanisms underlying the cognitive deficits associated with neurofibromatosis 1. j child neurol 2002; 17(8):622-6; discussion 627-9, 646-51 4. cushing h. tumours of the nervus acusticus and the syndrome of the cerebello-pontine angle. philadelphia, wb saunders, 1917. 5. evans dg. neurofibromatosis type 2 (nf2): a clinical and molecular review.orphanet j rare dis 2009; 4:16. .6.gardner wj, frazier ch. bilateral acoustic neurofibromas: a clinical study and field survey of a family of five generations with bilateral deafness in thirty eight members. arch neurol psychiatr 1930; 23: 266-302. 7.gutmann dh, aylsworth a, carey jc, korf b, marks j, pyeritz re, et al.the diagnostic evaluation and multidisciplinary management of neurofibromatosis 1 and neurofibromatosis 2. jama 1997; 278(1):51-7. 8. harada h, kumon y, hatta n, sakaki s, ohta s. neurofibromatosis type 2 with multiple primary brain tumors in monozygotic twins. surg neurol 1999; 51(5):528-35. 9. henschen f. zur histologie und pathogcnese der kleinhirnbrucken-winkeltumoren. arch psychiatr 1915; 56:21 10. holland k, kaye ah. spinal tumors in neurofibromatosis-2: management considerations a review. j clin neurosci 2009; 16(2):169-77. 11.lustig lr, yeagle j, driscoll cl, blevins n, francis h, niparko jk. cochlear implantation in patients with neurofibromatosis type 2 and bilateral vestibular schwannoma. otol neurotol 2006; 27(4):512-8. 12.mautner vf, baser me, thakkar sd, feigen um, friedman jm, kluwe l. vestibular schwannoma growth in patients with neurofibromatosis type 2: a longitudinal study. j neurosurg 2002; 96(2):223-8. 13.mautner vf, lindenau m, baser me, hazim w, tatagiba m, haase w, et al.: the neuroimaging and clinical spectrum of neurofibromatosis 2. neurosurgery 1996, 38:880-885. 14.mautner vf, tatagiba m, guthoff r, samii m, pulst sm. neurofibromatosis 2 in the pediatric age group. neurosurgery 1993; 33(1):92-6. 15. national institutes of health consensus development conference statement on acoustic neuroma, december 11-13, 1991.the consensus development panel. arch neurol 1994; 51(2):201-7. 16.roehm pc, mallen-st clair j, jethanamest d, golfinos jg, shapiro w, waltzman s, et al. auditory rehabilitation of patients with neurofibromatosis type 2 by using cochlear implants. j neurosurg2011; 115(4):827-34. 17. von recklinghausen f. uber die multiplen fibroma der haut und lhre beziehung zu den multiplen neuromen. berlin: a. hirschwald, 1882 18. wishartjh.case of tumours in the skull, dura mater, and brain. edinburgh med surgj 1982; 18: 393-397 microsoft word 13singhabhay_pituitary romanian neurosurgery (2018) xxxii 2: 297 302 | 297             doi: 10.2478/romneu-2018-0036 pituitary apoplexy in setting of dengue hemorrhagic fever with thrombocytopenia: case report and review of literature abhay singh1, rahul gupta2, gangesh gunjan3, harjinder singh bhatoe4, dhawal sharma4 1general surgery, neurosurgery, fortis hospital, noida, u.p., india 2neurosurgery, additional director neurosurgery, fortis hospital, noida, u.p., india 3consultant neurosurgery, fortis hospital, noida, u.p., india 4neurosurgery, fortis hospital, noida, u.p., india abstract: pituitary apoplexy is an acute clinical syndrome. it may occur spontaneously or as a result of several precipitating factors; one such factor being thrombocytopenia. acute febrile illness accompanying with bleeding tendency is the main clinical feature of dengue. if the diagnosis is made in time, urgent treatment in the form of decompression of optic nerves may help to save vision. according to literature, only seven cases have been reported with pituitary apoplexy in setting of dengue hemorrhagic fever. we report eighth case of pituitary apoplexy in patient having dengue hemorrhagic fever with its management and review of literature. key words: dengue hemorrhagic fever, pituitary apoplexy, thrombocytopenia introduction pituitary apoplexy is an acute clinical syndrome characterized by sudden headache, vomiting, visual disturbances, ophthalmoplegia, altered consciousness, secondary to infarction or hemorrhage within a pituitary tumor or nontumorous pituitary gland. [1,2] the diagnosis is often missed in the early stages. ct and mri of the brain are helpful in making the diagnosis of pituitary apoplexy. pituitary apoplexy may occur spontaneously or as a result of several precipitating factors; one such factor being thrombocytopenia. dengue is an infectious disease which can be seen worldwide. acute febrile illness accompanying with bleeding tendency is the main clinical feature of dengue. [3] dengue hemorrhagic fever (dhf) is characterized by fever, hemorrhagic tendencies, thrombocytopenia, and increased vascular permeability. [4] according to literature, only seven cases have been reported with pituitary apoplexy in setting of dengue hemorrhagic 298 | singh et al pituitary apoplexy in dengue hemorrhagic fever             fever. we report eighth case of pituitary apoplexy in the setting of dengue hemorrhagic fever with its management and review of literature. case report a 48 year old female presented with history of high grade fever 3 days. she was evaluated at local hospital where serology for dengue infection was positive and she had low platelet count. patient was referred to our hospital for further management. there was no history of petechial rash and spontaneous bleeding from mucosal surfaces. on third day of admission she complaint of sudden diminution of vision and severe headache. the platelet count decreased to 17,000. (table 1) table 1 daily platelet count platelets /mm3) on admission day 1 day 2 day 3 day 4 day 5 platelet count 72,000 50,000 22,000 17,000 33,000 131,000 ncct head was done which was suggestive of presence of sellar/suprasellar well defined heterogeneously hyperdense mass (25mm x 20mm x 18mm) with hyperdense area of bleed. (figure 1) figure 1ncct head axial sections: sellar/suprasellar well defined heterogeneously hyperdense mass with hyperdense area of bleed mri brain showed well defined in homogeneously enhancing sellarsuprasellar mass with internal area of bleed. (figure 2, 3 &4) figure 2 mri t2 wi coronal sections: heterogeneously hyperintense signal with presence of areas of bleed figure 3mri flair axial sections: well defined extraaxial mass in sellar / suprasellar region measuring 2.6 x 2.3 x 2 cm in size figure 4 mri contrast enhanced coronal sections: mild to moderate inhomogenous post contrast enhancement with hemorrhagic area the optic chiasm was draped on its superior surface with no visualized area of in romanian neurosurgery (2018) xxxii 2: 297 302 | 299             between planes. on examination patient had bitemporal hemianopia by confrontation method. patient’s hormone profile revealed decreased serum thyroid and prolactin hormone levels [growth hormone (gh) = 2.30 ng/ ml; luteinizing hormone (lh) =2.64 miu/ml; prolactin (prl) =2.23 ng/ml; cortisol = 6.53 μ/dl; follicle stimulating hormone = 5.85 miu/ml; t3 = 47.87 ng/dl; thyroxine (t4) = 4.82 μg/dl; thyroid stimulating hormone (tsh) = 1.220 μiu/ml)] patient underwent several platelet units transfusion and was operated after platelet count reached above 100,000. urgent transnasal transsphenoidal decompression of the pituitary macroadenoma was performed. intraoperatively, there was evidence of bleed inside the tumor post operative period was uneventful and patient was discharged subsequently. histopathology was consistent with pituitary apoplexy with bleed. on three month follow up, patient had hypocortisolemia with no visual defect. discussion pituitary apoplexy may occur spontaneously or as a result of several precipitating factors such as head trauma, dynamic tests to evaluate pituitary function, surgery (mainly cardiac surgery), coagulation disorders, medications including aspirin, estrogens, heparin, and dopamine agonists and some conditions such as chronic systemic hypertension, diabetes mellitus, and radiotherapy. [1, 2, 5, 6] the precipitants of pituitary apoplexy can be classified into 4 categories: (1) reduced blood flow into the pituitary adenoma, resulting in infarction; (2) acute increase in blood flow to the pituitary gland from the hypothalamus portal system because it may increase the intra sellar pressure; (3) stimulation of the pituitary gland, as occurs in any stress inducing states; and (4) thrombocytopenia because of increased risk of bleeding. [5, 7] dengue fever is endemic in tropical countries and can range from a nonspecific febrile illness to dhf, which is characterized by high grade fever, marked thrombocytopenia (<100,000/μl), and increased vascular permeability. [4] in dhf, patients may have episodes of hypotension and hypovolemia, leading to oscillations in blood pressure. [4] because it is an acute systemic illness, there is an increased demand on the pituitary gland and pituitary stimulation. in addition, dhf is characterized by severe thrombocytopenia and increased hemorrhagic tendencies. all these factors combined may have a compounding effect on the risk of pituitary apoplexy in a pre existing pituitary adenoma. however, the association of dhf and pa is exceedingly rare and only few case reports document their co occurrence. [6, 8, 9, 10, 11, 12] other causes of visual deterioration in patients with dengue fever are optic neuropathy, maculopathy, retinal capillary occlusion, foveolitis, and retinal hemorrhage. [8, 13] the review of literature regarding the incidence of pituitary apoplexy in the setting of dhf revealed seven previously reported cases. the summary of these cases along with their comparative features has been described in table 2. (table 2) 300 | singh et al pituitary apoplexy in dengue hemorrhagic fever             table 2 summary of the reported cases of pituitary apoplexy in setting of dengue hemorrhagic fever reference age/ sex clinical feature platelet counts hormonal profile mri findings management follow up kumar et al (2011) 31/f vision loss, h/a, vomiting hypothyroid, rest of the hormonal profile normal low (45,000/m m3) pituitary macroadeno ma (16×22 mm) with acute bleed endoscopic endonasal decompressio n of the tumor residual bitemporal field defects at 3-month f/u wildenberg et al – case 1 ( 2012) 40/m h/a, vomiting, acromegali c features acromegaly; hypogonadotro pic hypogonadism mildly decreased (98,000/m m3) intrasellar lesion s/o – pituitary apoplexy transsphenoi dal surgery 20 days after apoplexy acromegaly persists; other hormones normal wildenberg et al – case 2 ( 2012) 38/m prolactino ma on medical mx, presents with visual field deficits hypogonadism; prolactin decreased on medical management mildly decreased (79,000/m m3) pituitary mass with areas of bleed urgent transsphenoi dal surgery visual field defects improved. hormonal deficits persist tan et al. (2014) 53/m acute-onse t lt third, sixth nerve palsy, rt temporal hemianopi a hyperprolactino ma; thyrotropin and gonadotropin deficiency low (16,000/m m3) 37×24×31 mm hemorrhagic pituitary adenoma with b/l cavernous sinus extension underwent transsphenoi dal surgery for decompressio n (two surgeries) prolactin normal, anterior pituitary deficits and right eye visual defects persist mishra et al (2015) 43/m decreased vision, h/a, vomiting normal hormonal profile low (47,000/m m3) 23×21×20 mm sellar and suprasellar mass with bleed urgent transsphenoi dal decompressio n of tumor visual acuity improved. residual visual field deficits persist balaparames wara rao et al (2016) 45/m severe h/a, vomiting and loc normal hormonal profile low (27,000/m m3) pituitary apoplexy (sellar and suprasellar lesion) and obstructive hydrocephal evds to manage hcp; followed by endoscopic endonasal decompressio n vision normal. anterior pituitary deficits present romanian neurosurgery (2018) xxxii 2: 297 302 | 301             us varma et al (2016) 39 /f fever, melena, vision loss ,altered sensorium hypothyroid, hypogonadotro phic hypogonadism low (11,000/m m3) pituitary adenoma with apoplexy urgent decompresio n of tumor symptoms subsided our case 48/f fever, h/a, vision loss hypothyroidism & hypoprolactino ma low (17,000) pituitary apoplexy (sellar and suprasellar lesion) urgent transsphenoi dal decompressio n of tumor visual acuity improved, hypocortisole mia in our case we had a smooth outcome but as reported by balaparameswara rao et al, it can be strormy i.e. fluid & electrolyte imbalance which can occur in pituitary surgery. in all cases decompresion of the tumour by transpenoidal technique was done and was successful. vision improved in half of the cases. conclusions pituitary apoplexy can occur in setting of dengue hemorrhagic fever. dengue hemorrhagic fever should be considered as a cause of pituitary apoplexy. transsphenoidal decompression of the tumor has good results in these cases. if the diagnosis is made in time, urgent treatment in the form of decompression of optic nerves may help to save vision. correspondence dr. abhay singh – fortis hospital, sec-62, gautambudh nagar, noida, u.p. india 201301 e mailabhaysingh291183@gmail.com mobile no. 8130503451 references 1. möller goede dl, brändle m, landau k, bernays rl, schmid c. pituitary apoplexy: re evaluation of risk factors for bleeding into pituitary adenomas and impact on outcome. eur j endocrinol 2011; 164:37 43. 2. semple pl, webb mk, de villiers jc, laws er jr. pituitary apoplexy. neurosurgery 2005; 56: 65 72. 3. wiwanitkit v. dengue fever: diagnosis and treatment. expert rev anti infect ther 2010; 8:841‑5. 4. simmons cp, farrar jj, nguyen vv, wills b. dengue. n engl j med 2012; 366:1423 32. 5. biousse v, newman nj, oyesiku nm. precipitating factors in pituitary apoplexy. j neurol neurosurg psychiatry 2001; 71:542 5. 6. balaparameswara rao sj, savardekar ar, nandeesh bn, arivazhagan a. management dilemmas in a rare case of pituitary apoplexy in the setting of dengue hemorrhagic fever. surg neurol int 2017;8:4. 302 | singh et al pituitary apoplexy in dengue hemorrhagic fever             7. arafah bm, taylor hc, salazar r, saadi h, selman wr. apoplexy of a pituitary adenoma after dynamic testing with gonadotropin releasing hormone. am j med 1989; 87:103 5. 8. kumar v, kataria r, mehta vs. dengue hemorrhagic fever: a rare cause of pituitary tumor hemorrhage and reversible vision loss. indian j ophthalmol 2011; 59:311 2. 9. mishra ss, panigrahi s, das s. dengue hemorrhagic fever: a rare case of pituitary apoplexy. neurol india 2014; 62:92 3. 10. tan sk, seow cj, tan e, chau yp, dalan r. pituitary apoplexy secondary to thrombocytopenia due to dengue hemorrhagic fever: a case report and review of the literature. endocr pract 2014;20:58 64 11. wildemberg le, neto lv, niemeyer p, gasparetto el, chimelli l, gadelha mr. association of dengue hemorrhagic fever with multiple risk factors for pituitary apoplexy. endocr pract 2012; 18:97 101. 12. varma, harsha sh, reddy, amaresh p, pradeep. a rare case of pituitary apoplexy secondary to dengue haemorrhagic fever. indian j endocrino & metabol 2016; 21:p46-46. 1p. 13. sanjay s, wagle am, au eong kg. optic neuropathy associated with dengue fever. eye. 2008; 22:722–4. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article management of c2-c3 fracture subluxation by anterior cervical approach and c2-c3 transcortical screw placement amit agrawal india doi: 10.2478/romneu-2018-0023 170 | agrawal c2-c3 fracture subluxation and c2-c3 trans-cortical screw placement doi: 10.2478/romneu-2018-0023 management of c2-c3 fracture subluxation by anterior cervical approach and c2-c3 trans-cortical screw placement amit agrawal department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: cervical spine injuries are the major cause of morbidity and mortality in trauma victims. upper cervical spine injuries account for about 24% of acute fractures and dislocations and one third of fractures occur at the level of c2, while one half of injuries occur at the c6 or c7 levels. in contrast to this approach we used the transverse cervical, platysma splitting incision at a lower (c3-c4 disc) to expose the upper cervical spine particularly lower border of c3 (entry point for the screw). key words: cervical spine, dislocation fracture, trauma, upper cervical spine introduction cervical spine injuries are the major cause of morbidity and mortality in trauma victims. (1, 2) upper cervical spine injuries account for about 24% of acute fractures and dislocations 3 and one third of fractures occur at the level of c2, while one half of injuries occur at the c6 or c7 levels (4-6). we discuss a case of c2 fracture with c2-3 subluxation and review the surgical approaches. case report a 17 year old male presented with history of road traffic accident collision with tata magic van while he was going on motor cycle. since then he was altered in altered sensorium. at the time of presentation to emergency room had glasgow coma scale was e2v2m3. he had paucity of movements of all four limbs. pupils were bilateral equal and reacting to light. general and systemic examination was unremarkable. ct scan brain showed subarachnoid hemorrhage and mild cerebral edema. x-ray cervical spine lateral view showed c2 body fracture and posterior subluxation over c3 (figure 1). mri cervical spine showed fracture subluxation of c2 over c3 with cord contusion at the same level (figure 2). the patient was put on cervical traction and it resulted in reduction of the fracture and subluxation (figure 1a). once he was stabilized hemodynamically he underwent anterior cervical approach and fixation of c2 and c3 with screw (figure 3). the patient romanian neurosurgery (2018) xxxii 1: 170 – 173 | 171 underwent right anterior cervical approach though transverse cervical platysma splitting incision. radiographic imaging was used to help guide the pins and subsequent screw placement (figure 3b). follow up x-ray showed good alignment and position of the screw (figure 4). the patient is gradually improving neurologically improving at follow up. figure 1 x-ray cervical lateral view showing (a) c2 body fracture and posterior subluxation of c2 over c3 and (b) almost normal alignment of c2 and c3 after skull traction figure 2 mri cervical spine showing in addition to fracture subluxation there is cord contusion at the level of c2 and c3 figure 3 intra-operative image showing (a) the screw entry point in the lower anterior edge of c3 and (b) intra-operative x-ray image showing restoration of the alignment of c2 and c3 figure 4 post-operative x-ray showing almost normal alignment of c2 and c3 with good position of the screw, please note the fractured anterior half of the c2 body discussion subluxation of the cervical spine in adults usually occurs at c4-c7 segments. (6, 7) the "hangman's fracture," or traumatic spondylolisthesis of c2 characterized by bilateral pars interarticularis fractures, most of 172 | agrawal c2-c3 fracture subluxation and c2-c3 trans-cortical screw placement these fractures result from falls and motor vehicle crashes. 8 based on the mechanism of injury and the characteristics of the displacement effendi et al (8) classified these injuries into type-i fractures: due to axial compression with hyperextension and are characterized by little or no displacement (c2c3 disc is normal), type-ii fractures: result from initial hyperextension with axial compression followed by severe hyperflexion of the neck (c2-c3 disc is disrupted and the body of c2 is displaced in extension, flexion, or anterior listhesis) and type-iii fractures: due to a combination of flexion and compression leading to dislocation of the c2c3 facet joints with anterior displacement of c2 in flexion. (8) c2-c3 fracture subluxation is uncommon and can be due to traumatic (914) and non-traumatic causes (i.e. pathological fracture (15) and grisel's syndrome 16). fracture/subluxation at the c2-c3 level is an uncommon injury. (9, 10, 13) these patients can present with severe neck pain (11, 13 12) with mild neurological symptoms (13) or even without neurological deficits. (11, 12) x-rays and ct of the cervical spine will demonstrated the amount of bony injury and extent of dislocation (13, 14, 16, 17) while mri (as in present case) will help to demonstrate any injury to the spinal cord. management of these fractures in neurologically intact patients with anatomical alignment and/or stable positioning is external stabilization. (14, 16, 18, 19) fractures of c2/c3 with displacement and angulation need either anterior or posterior surgical approaches for fixation after applying skull traction to regain alignment. (8, 10-13, 20-22) the options in anterior cervical approach include anterior c2/3 discectomy with locking plate-screw fixation and fusion 10 surgical exposure of the upper cervical spine is challenging, and for fusion and instrumentation on the upper cervical spine the prevascular extraoral retropharyngeal approach has been described as it allows direct anterior access to c2 and c3 while allowing extension to the lower cervical spine. (10, 23, 24) although this approach is safe, in rare instances there may be permanent dysphagia (due to the injury to the hypoglossal nerve) may be transient dysphagia. (10, 23) in contrast to this approach we used the transverse cervical, platysma splitting incision at a lower (c3-c4 disc) to expose the upper cervical spine particularly lower border of c3 (entry point for the screw). correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com mobile+91-8096410032 references 1.the annual statistical report for the model spinal cord injury care systems. university of alabama at birmingham national spinal cord injury statistical center 2004. 2.scannell g, waxman k, tominaga g, barker s, annas c. orotracheal intubation in trauma patients with cervical fractures. archives of surgery (chicago, ill: 1960) 1993;128:903-905; discussion 905. romanian neurosurgery (2018) xxxii 1: 170 – 173 | 173 3.bohlman hh. acute fractures and dislocations of the cervical spine. an analysis of three hundred hospitalized patients and review of the literature. the journal of bone and joint surgery american volume 1979;61:1119-1142. 4.minigh j. traumatic injuries to the cervical spine. radiologic technology 2005;77:53-68. 5.miller md, gehweiler ja, martinez s, charlton op, daffner rh. significant new observations on cervical spine trauma. ajr american journal of roentgenology 1978;130:659-663. 6.plunkett pk, redmond ad, billsborough sh. cervical subluxation: a deceptive soft tissue injury. journal of the royal society of medicine 1987;80:46-47. 7.ooi ss, wong sv, radin umar rs, azhar aa, yeap js, megat ahmad mmh. mechanisms of cervical spine injuries for non-fatal motorcycle road crash. the medical journal of malaysia 2004;59:146-152. 8.effendi b, roy d, cornish b, dussault rg, laurin ca. fractures of the ring of the axis. a classification based on the analysis of 131 cases. j bone joint surg br 1981;63b:319-327. 9.levine am, edwards cc. the management of traumatic spondylolisthesis of the axis. the journal of bone and joint surgery american volume 1985;67:217226. 10.basu s, chatterjee s, bhattacharya mk, seal k. injuries of the upper cervical spine: a series of 28 cases. indian journal of orthopaedics 2007;41:305-311. 11.madhavan p, monk j, wilson-macdonald j, fairbank j. instability due to unrecognised fracture-subluxations after apparently isolated injuries of the cervical spine. j bone joint surg br 2001;83:486-490. 12.vasan t. circumferential fusion for sub-axial cervical spine fracture—subluxations. the indian journal of neurotrauma 2007;4:65-70. 13.machinis tg, fountas kn, kapsalaki ez, kapsalakis i, grigorian aa. a rare case of complete c2-c3 dislocation with mild neurological symptoms. european spine journal: official publication of the european spine society, the european spinal deformity society, and the european section of the cervical spine research society 2006;15 suppl 5:585-589. 14.mueller dg, mueller k. three case studies involving the use of a noninvasive halo for cervical stabilization. jpo: journal of prosthetics and orthotics 2005;17:40. 15.dang d, baig mn, christoforidis g, chiocca ea, gabriel j. c2/c3 pathologic fractures from polyostotic fibrous dysplasia of the cervical spine treated with percutaneous vertebroplasty. european spine journal : official publication of the european spine society, the european spinal deformity society, and the european section of the cervical spine research society 2007;16 suppl 3:250-254. 16.martínez-lage jf, morales t, fernandez cornejo v. inflammatory c2-3 subluxation: a grisel's syndrome variant. archives of disease in childhood 2003;88:628629. 17.harrington jf, likavec mj, smith as. disc herniation in cervical fracture subluxation. neurosurgery 1991;29:374-379. 18.harris jh. radiographic evaluation of spinal trauma. the orthopedic clinics of north america 1986;17:75-86. 19.novelline ra, rhea jt, rao pm, stuk jl. helical ct in emergency radiology. radiology 1999;213:321-339. 20.verheggen r, jansen j. hangman's fracture: arguments in favor of surgical therapy for type ii and iii according to edwards and levine. surgical neurology 1998;49:253-261; discussion 261. 21.suchomel p, hradil j, barsa p, et al. [surgical treatment of fracture of the ring of axis "hangman's fracture"]. acta chirurgiae orthopaedicae et traumatologiae cechoslovaca 2006;73:321-328. 22.samaha c, lazennec jy, laporte c, saillant g. hangman's fracture: the relationship between asymmetry and instability. j bone joint surg br 2000;82:1046-1052. 23.park sh, sung jk, lee sh, park j, hwang jh, hwang sk. high anterior cervical approach to the upper cervical spine. surgical neurology 2007;68:519-524; discussion 524. 24.tesiorowski m, lipik e, jasiewicz b, kacki w. [surgical treatment of old c2 spinal fracture with c2/c3 subluxation using an anterior retropharyngeal approach-case report]. chirurgia narzadow ruchu i ortopedia polska 2002;67:323-326. 23 23agrawalamit_management of c2-c3 doi: 10.33962/roneuro-2021-053 spinal conditions in geriatric patients in developing countries. a four years institutional experience abdulrahman al-mirza, omar al-taei, tariq al-saadi romanian neurosurgery (2021) xxxv (3): pp. 321-326 doi: 10.33962/roneuro-2021-053 www.journals.lapub.co.uk/index.php/roneurosurgery spinal conditions in geriatric patients in developing countries. a four years institutional experience abdulrahman al-mirza1, omar al-taei1, tariq al-saadi2 1 sultan qaboos university college of medicine, sultanate of omanmuscat, al-khoudh, oman 2 department of neurology & neurosurgery montreal neurological institute, faculty of medicine, mcgill university, qc, canada abstract background: the spinal injury in an elderly patient is associated with higher mortality and an increased frequency of life-threatening complications and specifically spinal cord injuries. the aim of this study is to study the prevalence of geriatric spinal neurosurgical conditions in the neurosurgical department at khoula hospital, muscat, sultanate of oman. results: 171 patients were admitted due to spinal pathologies, which will be the main focus of the present study with an average age of 70.7 years. the male-to-female ratio was (1.5:1). degenerative conditions were the most common spinal diagnosis (90.6%) followed by traumatic accidents (2.9%). most of the patients underwent surgical intervention (78.9%). the majority of the patients (91.2%) of the patients stayed in the hospital for less than 15 days. there was a significant difference between the age of patients above and below 75 years the gender (p=0.003) and between the length of stay and type of intervention (p<0.005). conclusion: spinal cord-related pathologies are a growing cause of mortality and morbidity worldwide, because of the increasing number of elderly people due to an increasingly rising life span worldwide. in the present study, degenerative conditions were the most common spinal diagnosis followed by traumatic accidents. introduction over the past years, the evolution of new medical equipment and enhancing of technology and neuroanesthesia and icu, have expanded the daily neurosurgical practise. (1). the aging population in western civilization places an increase demand on health system in terms of number and special needs. (1). the elderly population is defined as adults aging 65 years or older. (2). within europe, people aged 80 years and older is projected to double from 5% to 9% in 2040. (3). with the increase age, the presence of comorbid conditions probability increase makes the need for specific measures necessarily. (4). elderly population are not exempt from neurosurgical practise. (5). on the other hand, with this population increase, neurosurgeon workload will keywords spinal causes, geriatric, elderly, neurological deficits corresponding author: tariq al-saadi department of neurology & neurosurgery montreal neurological institute, faculty of medicine, mcgill university, canada tariq.al-saadi@mail.mcgill.ca copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 322 abdulrahman al-mirza, omar al-taei, tariq al-saadi involve these patients in greater portions. (5). moreover, an injury in an elderly patient is associated with a higher mortality and an increased frequency of life-threatening complications and specifically spinal cord injuries. (6). as the incidence of traumatic spinal cord injury in elderly rises, neurosurgeons are increasingly faced with difficult discussions regarding management. (7. the most common mechanism of traumatic spinal cord injuries are falls and they occur frequently due to age-related deteriorations. traumatic spinal cord is associated with greater morbidity in elderly (7). a previous study done by alsaadi et al investigating the prevalence of low back pain (lbp) among sultan qaboos university staff in sultanate of oman showed that the prevalence of lbp among them was 44.7% among the included cohort, in which majority (68%) of them were suffering from the pain for more than one year. among those who had lbp for more than one year, 73.5% were less than 50 years old (8). carpal tunnel syndrome one the most comments neuropathies with a peak age of 50-54 and second peak 75-84. (2) the aim of this study is to retrospectively analyse the prevalence of peripheral nerve and spinal cord injuries in sultanate of oman. the traumatic spinal injuries service is shared between the neurosurgery department and the ortho-spine department. the current article dealt only with cases admitted under neurosurgery department. the health care services in oman is considered as having one of the best health care systems in the world according to world health organization reports (9,10). the department of neurosurgery in kh is the main neurosurgical center in the country with average admissions of 1600 patients annually (11,12). in the present study, we chose a cut of age of 65 years and older according to the local definition, taking into account the increase in life span throughout the last few decades and the improvement in the quality of life that results from many changes in all social and health care sectors in the country. methods study group this is a retrospective study conducted at khoula hospital located in muscat, sultanate of oman. the study was approved by the research ethical committee at khoula hospital/ ministry of health (pro122020072). medical records of 171 patients who are above the age of 65 and admitted to the neurosurgical ward and diagnosed with spinal and peripheral nerve conditions, from the period of january 2016 to 31st december 2019 were included. the study includes both omani and non-omani patients. patients with the following features are excluded: • non elderly patient (below 65 years). • non neurosurgical conditions and neurosurgical conditions other than spinal and peripheral nerve diseases. • elderly with spinal conditions admitted under orthospine department. • outside the study period (from 1st january 2016 to 31th december 2019). • patients with missing or incomplete data. • data collection: data was obtained from the health information system included: patient demographics (age, gender), presenting symptom, previous surgical history, preoperative and postoperative glasgow coma scale (gcs), radiological findings, indication for surgery, diagnosis, length of hospital stay (los), length of icu admission and treatment proposed. then the information classified into continues and categorized variables and analyzed accordingly. data analysis research database was analyzed and processed using the statistical package for the social sciences (spss) software (version23). the categorized variables were cross-tabulated using frequency tables and pie charts or bar charts. chi-square test was used to obtain the significance of the association between categorized variables, using a p value of ≤ 0.05 as the cut-off for significance. the numerical variables were summarized by their medians, means, and ranges, and the categorical variables were described by their counts and relative frequencies. all the p values were 2-sided, and a p value < 0.05 was considered to be significant in all the analyses. results table 1 showing demographic characteristics of the included cases in the present study. we have total of 669 patients admitted in neurosurgical department at khoula hospital in muscat the capital city of sultanate of oman in four years’ period (from 2016 to 2019). out of those 669 patients, 171 patients 323 spinal conditions in geriatric patients in developing countries. were admitted due to spinal and peripheral nerve pathologies, which will be the main focus of the present study. fifty-four and four tenths % of the study cohort were more than 75-year-old. male to female ratio was (1.5:1). degenerative conditions were the most common spinal diagnosis (90.6%) followed by traumatic accidents (2.9%). most of the patients underwent surgical intervention (78.9%). majority of the patients (91.2%) stayed in the hospital less than 15 days. table 1. demographic characteristics of the patients number of patients (%) category number of patients admitted each year 202 (30.0%) 2019 172 (25.7%) 2018 154 (23%) 2017 141 (21.3%) 2016 669 total number of admitted neurosurgical cases (2016-2019) 171 total number of spine cases age 93 (54.4%) ≥75 78 (45.6%) < 75 gender 69(40.4%) female 102(59.6%) male spinal diagnosis 155 (90.6%) degenerative conditions 5(2.9%) traumatic 4 (2.3%) infection 7(4.1%) peripheral nerve disease type of interventions 135 (78.9%) surgical 36(21.1%) conservative length of stay (los) 156 (91.2%) ≤ 15 days 15 (8.8%) >15 days figure 1. total number of admitted patients with spinal cases in each year figure 1 represents the total number of admitted patients with spinal diagnosis in each year. as seen in the graph, spinal cases were continuously raising among the study years with the highest number of cases in 2019 (n=53, 31.0%). table 2 showing the association between the age of the patients with spinal pathologies and the gender. it demonstrates that there was significant difference between age of patients above and below 75 years the gender, in which male patients were more commonly found to belong into the older age group (p=0.003). table 2. the association between the age of the patients and other variables (gender and gcs) gender male female age less than 75 46 47 more than 75 56 22 p-value 0.003 table 3. the association between the los (length of stay) of the patients and other variables (age and type of intervention) length of stay (los) age type of intervention < 75years ≥ 75 years surgical conserv -ative less than or equal to 15 days more than 15 days 86 70 129 27 7 8 6 9 p-value 0.530 0.005 324 abdulrahman al-mirza, omar al-taei, tariq al-saadi the association between the los of the patients and other variables (age and type of intervention) is shown in table-3. there was no significant relationship between the age of the patients (more and less than 75 years) and los (15 days as a cut off value), (p=0.530). also it represents that there was a significant difference between los and type of intervention (surgical vs conservative), (p<0.005). discussion increasing life expectancy, along with rising health care related expectations is producing an important workload across all medical fields, considering that most medical diseases increase in frequency with age, more elderly will require neurosurgical care including the spinal cord related diseases. additionally, with the advances in diagnostic and surgical techniques spinal neurosurgical diseases have led more patients to be treated in a better quality and quantity which explains the continuously raising neurosurgical cases generally and spinal cases specifically among the present study years (1,2). one hundred seventy-one patients were admitted due to spinal pathologies, which will be the main focus of the present study. 54.4% of the study cohort were more than 75-year-old (range 65-68). another study done by a gulati et al showed a mean age of 73 years (range 65-88). male to female ratio was (1.5:1). inglis et al. conducted a study that showed was in the same line of our study in which 61% of the cases were males. this can be explained by the fact that males are more predisposed to injuries in their daily life activities, as well as the fact that omani count population states that the male to female ratio in oman is 180.8 males per 100 females (6,13). degenerative conditions were the most common spinal diagnosis followed by traumatic accidents in our study. correspondingly, chibbaro et al conducted a study that demonstrate that degenerative spinal diseases were one of the most common procedures performed in along with cranial procedures for tumour resection, and burr hole for chronic subdural hematoma among elderly patients over the two separate time periods (1983-1985 and 2003-2005) which shows the high incidence of those group of diseases. for traumatic spine injuries, it was reported that most of the injuries were due to falls from less than standing height, which may emphasize the age-related reduced capability of the spine to withstand the mechanical stress as only 13% of traumatic injuries occurs due to violent acts and automobile accidents as reported by devivo et al (14,15). carpal tunnel syndrome (cts) was also reported as it is the most common entrapment neuropathy worldwide and in the present study (2). the few previous studies in the prevalence of peripheral nerve diseases among elderly suggested a bimodal age distribution with a peak between ages 50–54 years, and a second peak between 75–84 years, which is the reason why it’s important to take such group of diseases in consideration among geriatric age group (2). in the current study, most of the patients underwent surgical intervention (78.9%). in contrast, another study shows that 77% of patients were treated conservatively, specifically in traumatic spine injuries (6). treatment decision making in elderly patients in more arguable than younger age, as they are less likely to withstand the physiological and pathological insult of surgery and more likely to develop post-operative complications, additionally, they often have spine instability requiring extensive surgery with a poor neurological prognosis, and consequences of healthcare issues associated with living with more significant neurological deficit (7) we found that, 91.2% of the patients stayed in the hospital less than 15 days. in accordance to our study, chibbaro et al reported a period of stay between 6-8 days, in the other hand, the median hospital stay for patients was 136 days in a study done by a gulati et al. those variations are due to the differences in the type of injury, type of intervention, the pre-existing medical conditions and other related factors (1,6). the lack of a long-term rehabilitation center in the country might be another contributing factor to this. as patients should be cleared for discharge home when the safety of the mobility is guaranteed. the present study also demonstrates that there is significant difference between age of patients above and below 75 years the gender, in which male patients were more commonly found to belong into the older age group. this can due to the fact that increased life expectancy in developing countries in the last few decades, due to better medical scrutiny of the elderly, better knowledge and practice by neurosurgeons and all other associated physicians and surgeons in the elderly patient’s management, which improves the patient’s ability to practice their 325 spinal conditions in geriatric patients in developing countries. daily life and predispose them to more spinal related injuries and their consequences. (2) the current study found that there was no significant relationship between the age of the patients and los. also it represents that there is a significant difference between los and type of intervention (surgical vs. conservative), (p<0.005). osteoporosis and other typical spinal problems of advanced age, multiple comorbidities, and the lessened physical performance that goes along with age are accompanied by markedly heightened expectations on the part of our older patients. thus, the value of different treatment strategies needs to be rationally assessed due the risk of prolonged stay in the hospital (increased los) (3). surgical decision making for this age group is a multifactorial process so its advocated that chronologic age must be evaluated in the light of patient’s clinical status to define eligibility for surgery (16,17). limitations there were several limiting factors in the present study. it was a retrospective, single-centered study over a period of four-years. thus, a number of confounding factors found, for example, the degree of advancement in modern medical technology and the availability of modern diagnostic facilities. cases admitted under the orthopedic department were not included which might present a large number of patients. the follow-up was not included in the data of the present study. additionally, the oncological causes of spinal related disorders were not mentioned and discussed in the present paper, as they will be discussed in a separate paper along with all other neurosurgical tumors. conclusion spinal cord related pathologies are growing cause of mortality and morbidity worldwide, because of the increasing number of elderly people due to an increasingly rising life span worldwide. in the present study, degenerative conditions were the most common spinal diagnosis followed by traumatic accidents. special care must be taken when dealing spinal cases due its potentially high morbid outcomes, especially among geriatric age group due to the age-related reduced capability of the spine to withstand the mechanical stress. abbreviations length of hospital stay (los) carpal tunnel syndrome (cts) availability of data from medical records of patients from the “al-shifa health information system” of ministry of health in sultanate of oman used in khoula hospital. authors contributions am and ot: report writing, data collection and analysis ts: research design, analysis and review. all authors have read and approved the manuscript. references 1. blumenthal, scott, steven herskovitz, and joe verghese. 2006. “carpal tunnel syndrome in older adults.” muscle and nerve 34(1):78–83. doi: 10.1002/mus.20559. 2. chibbaro, salvatore, f. di rocco, o. makiese, g. mirone, m. marsella, a. c. lukaszewicz, e. vicaut, b. turner, s. hamdi, t. spiriev, p. di emidio, r. pirracchio, d. payen, b. george, and d. bresson. 2011. “neurosurgery and elderly: analysis through the years.” neurosurgical review 34(2):229–33. doi: 10.1007/s10143-010-0301-6. 3. maldaner, nicolai, johannes sarnthein, oliver bozinov, luca regli, and marian christoph neidert. 2018. “neurosurgery in octogenarians: a prospective study of perioperative morbidity, mortality, and complications in elderly patients.” world neurosurgery 110:e287–95. doi: 10.1016/j.wneu.2017.10.154. 4. anon. n.d. “neurosurgery_for_the_elderly_.pdf.” 5. gulati, a., c. j. yeo, a. d. cooney, a. n. mclean, m. h. fraser, and d. b. allan. 2011. “functional outcome and discharge destination in elderly patients with spinal cord injuries.” spinal cord 49(2):215–18. doi: 10.1038/sc.2010.82. 6. inglis, tom, dan banaszek, carly s. rivers, dilnur kurban, nathan evaniew, nader fallah, zeina waheed, sean christie, richard fox, jean marc mac thiong, karen ethans, chester ho, angelo gary linassi, henry ahn, najmedden attabib, christopher s. bailey, michael g. fehlings, daryl r. fourney, jérôme paquet, andrea townson, eve tsai, christiana l. cheng, vanessa k. noonan, marcel f. dvorak, and brian k. kwon. 2020. “inhospital mortality for the elderly with acute traumatic spinal cord injury.” journal of neurotrauma 37(21):2332– 42. doi: 10.1089/neu.2019.6912. 7. maurice-williams, r. s. 1994. “neurosurgery in the elderly.” british journal of neurosurgery 8(6):651–53. doi: 10.3109/02688699409101178. 8. al-saadi, tariq, ahmed al kumzari, and mohammed hassan. 2018. “relationship between low back pain and types of office, home and car seats in sultan qaboos 326 abdulrahman al-mirza, omar al-taei, tariq al-saadi university staff.” american journal of medical sciences and medicine 6(1):13–18. doi: 10.12691/ajmsm-6-1-3. 9. the world health report 2000 (health systems: improving performance). who geneva. available at: https://www.who.int/whr/2000/en/. 10. al-kalbani, h., al-saadi, t., al-kumzari, a., & al-bahrani, h. (2020). public’s perception and satisfaction on the health care system in sultanate of oman: a cross-sectional study. annals of the national academy of medical sciences (india), 56(04), 214-219. doi:10.1055/s-00401721554 11. g p mishra, tariq al saadi, neeraj salhotra, samit biniwale, mohammad hadad, mohammad hashim, ali al mashani, qassim al hinai and sharad samson rajmani. brain and spinal tumors incidence annual audit 2017 of dept of neurosurgery khoula hospital muscat oman: a review. american journal of medical case reports. 2018; 6(7):128-131. doi: 10.12691/ajmcr-6-7-2 12. al-saadi t, al sharqi a, alsharqi j, alblushi k, alrasbi a, al-farsi m, al-ghafri s, al-abri s, al-saadi h. leaving against medical advice among patients with brain tumours in the middle east: khoula hospital experience. int clin neurosci j [internet]. 2020sep.28 [cited 2021mar.20];7(4):179-84. available from: https://journals.sbmu.ac.ir/neuroscience/article/view/30 700https://www.ncbi.nlm.nih.gov/books/nbk189784/ta ble/appc.t1/ 13. https://gccstat.org/en/ 14. devivo mj, kartus pl, rutt rd, stover sl, fine pr. the influence of age at time of spinal cord injury on rehabilitation outcome. arch neurol 1990; 47: 687–691. 15. kiwerski je. injuries to the spinal cord in elderly patients. injury 1992; 23: 397–400 16. kalff, rolf, christian ewald, albrecht waschke, lars gobisch, and christof hopf. 2013. “degenerative lumbale spinalkanalstenose im höheren lebensalter.” deutsches arzteblatt international 110(37):613–24. doi: 10.3238/arztebl.2013.0613. 17. dindo d, demartines n, clavien pa. classification of surgical complications: a new proposal with evaluation in a cohort of 6336 patients and results of a survey. ann surg. 2004;240:205-213. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article transsphenoidal surgery in cushing disease: the challenging microadenoma (local experience) wael k. zakaria, ahmed n. taha egypt doi: 10.2478/romneu-2018-0014 116 | zakaria et al transsphenoidal surgery in cushing disease doi: 10.2478/romneu-2018-0014 transsphenoidal surgery in cushing disease: the challenging microadenoma (local experience) wael k. zakaria, ahmed n. taha department of neurosurgery, mansoura university hospital, mansoura, egypt abstract: background: cushing disease is uncommon challenging disease. the adenomas are usually small in size in most case making the disease diagnosis and management is sometimes difficult. in some cases, the tumor cannot be identified on imaging studies and in many cases the adenoma is eccentric in location adding more difficulties to the trans-sphenoid approach for excision of such tricky tumors. object: to evaluate the challenge of diagnosis and trans-sphenoid surgery for acth pituitary microadenomas. methods: 21 patients with acth secreting adenomas were involved in this retrospective study. all cases were operated up on via trans-sphenoid approach during the period from january 2009 till october 2015. all of them were microadenomas. all patients had obvious cushing manifestations. in all cases magnetic resonance (mr) imaging and ct paranasal sinuses were performed. in this study: cases with macroadenomas and recurrent cases after previous trans-sphenoid approach or gamma knife radiosurgery were excluded. results: among the 21 patients; 14 were female and 7 weremale with age ranging from 21 to 44 years. the imaging study was positive for microadenoma in 18 patients while in 3 cases; no tumor was seen on the mri imaging. all were operated via the trans-sphenoid approach (12 patients via the microscopic technique and other 9 patients via the endoscopic technique). the adenoma was successfully removed in 15 out of the 18 patients with evident adenoma on pre-operative mri imaging while partial hypophysectomy were done in 5 cases without an evident adenoma on pre-operative mri study or difficult adenoma identification. in one patient; the procedure was aborted because of sphenoid sinus abnormalities and the tumor was successfully removed via trans-cranial approach. disease remission was achieved in 17 patients. in 4 patients; complete remission was not achieved and gamma knife radiosurgery was done after surgery. disease progression occurred in two patients with initial remission and was treated gamma knife radiosurgery. 13 patients had an acth deficiency after surgery while other hormonal replacement therapy is needed in only 5 cases. csf rhinorrhea occurred in 2 patients and was managed with transient lumbar drain without any subsequent morbidities. transient diabetes insipidus occurred in 6 romanian neurosurgery (2018) xxxii 1: 116 124 | 117 cases and was treated conservatively. conclusions: the transsphenoidal approach acth secreting pituitary microadenomas is considered safe and effective for achieving disease remission despite the challenge of diagnosis and intra-operative tumor identification. key words: adrenocorticotrophic hormone, magnetic resonance, computed tomography, cerebrospinal fluid introduction surgery is considered the golden standard treatment for acth secreting adenomas causing cushing disease. these benign adenomas are mostly microadenoma and easily achievable via the classic trans-sphenoid approach. however, there is still considerable challenges in the disease diagnosis management. in many cases (around 40%), the tumor cannot be identified on the preoperative imaging studies (post-contrast magnetic resonance imaging) and intraoperative identification of the adenoma is dependent on the experience of the surgeon. even if the inferior petrosal sinus sampling is feasible; its accuracy in identification the site of the adenoma is questionable.¹’²’⁹ another challenge is eccentric location of many adenomas is eccentric and despite its small size; it can be very close the carotid artery adding more difficulties to the trans-sphenoid approach for excision of such tricky tumors.⁵’⁷’¹⁰ the goal of surgery shouldn't only to remove the tumor but also to preserve the pituitary function to prevent postoperative hypopituitarism necessitating long term hormonal replacement therapy.³’⁴’⁵’⁸ the aim of this study is to evaluate the challenge of diagnosis and potential difficulties and outcome of the trans-sphenoid approach for acth secreting pituitary adenomas. patients and methods 21 patients with acth secreting adenomas were involved in this retrospective study. all the patient had obvious clinical manifestations of cushing disease. all these cases were operated up on in the neurosurgery department via the trans-sphenoidal approach during the period from january 2009 to october 2015. we evaluated all the medical data and imaging studies to assess all the potential difficulties in the disease diagnosis and the expected surgical challenge and this data was correlated with the operative finding and postoperative outcome particularly the rate of disease remission. data analysis included patient age, gender, clinical manifestations, pre-operative and initial and late postoperative hormonal levels including serum cortisol and acth levels and pre-operative and post-operative imaging studies. in all cases, magnetic resonance (mr) imaging of the sellar region and ct paranasal sinuses were performed. in this study; cases with macroadenomas (greater than one cm in the size) and recurrent cases after previous transsphenoid approach or gamma knife radiosurgery were excluded. outcome assessment was evaluated by improvement of the cushing manifestation, hormonal assessment to ensure biochemical remission and post-operative contrast enhancing magnetic resonance imaging. post-operative cortisol level evaluation was routinely done on 118 | zakaria et al transsphenoidal surgery in cushing disease the first day after the surgery and then after one, three and six months thereafter. then hormonal evaluation was done annually for assessment of any relapse. remission was defined by either normalization of the serum cortisol level or those with low serum cortisol level (≤3 mg/dl) necessitating hormonal replacement therapy. those patients with remaining elevated serum cortisol level were considered treatment failure. post-operative imaging (mri) was done initially after three months to ensure any residual tumor and then annually for five years to detect any recurrence. post-operative morbidities (transient or permanent) were also analyzed. results among the 21 patients; 14 were females and 7 were males with age ranging from 21 to 44 years (mean 33.6). all patients had the clinical manifestation of cushing disease (table 1). headache was manifest in eleven patients, 2 patients had ocular palsy concomitant with his cushing manifestation (figure 1), and in one patient; impotence was his early presentation for cushing disease. in three patients; uncontrolled diabetes was the triggering for the diagnosis of the disease and in one patient refractory hypertension was the initial presentation. depending on the preoperative post-contrast magnetic resonance study; we have 2 categories of patients; those with positive microadenoma (18 patients) and those with negative finding (3 patients). all patients were operated up on via the transsphenoid approach (12 patients via the microscopic endonasal technique and other 9 patients via the endoscopic endonasal technique) (table 2). the technique was exactly like what was widely described in the literature but we have faced with difficulties from mucosal changes rendering it more friable and bloody and difficulties from difficult control of the blood pressure. in one patient with conical shaped sinus; drilling of the bony sinus was performed under image guidance but bleeding was evident and the approach was aborted and the adenoma was removed three weeks later via the trans-cranial approach. table i patients characteristics male 7 female 14 male-female ratio: 1:2 patient sex 21 to 44 years (mean 33.6) age headache: 11 patients diabetes: 12 patients (three of them was the initial presentation) hypertension:13 patients (one of them was the initial presentation) skin changes: 19 patients abnormal fat distribution: 18 patients impotence: 1 patients clinical presentation (cushing manifestation) 9 months 78 months follow up period romanian neurosurgery (2018) xxxii 1: 116 124 | 119 table ii imaging characteristic, treatment plan and outcome of surgery positive for adenoma: 18 patients negative for adenoma: 3 patients pre-operative mri of the sella microscopic trans-sphenoidal approach: 12 patients endoscopic trans-sphenoidal approach: 9 patients technique of surgery adenoma removal: 15 via the trans-sphenoidal approach one via additional trans-cranial approach after aborted tans-sphenoid approach partial hypophysectomy: 5 patients intra-operative finding positive:18 patients negative: 3patients pathological confirmation of adenoma gamma knife radiosurgery: 6 patients 4 patients: treatment failure 2 patients: disease progression after initial remission medical treatment: cortisol replacement therapy:13 patients other hormonal replacement therapy: 5 patients post-operative treatment csf rhinorrhea: 3 patients (transient) transient diabetes insipidus: 6 patients surgery related morbidities table iii disease remission (biochemical markers) disease remission: 17 patients (80.9%) immediate after surgery: 8 patients within 6 months from surgery: 7 patients up to one year from surgery: 2 patients failure to achieve remission: 4 patients (19.1%) disease progression after initial remission: 2 patients (9.5%) remission in relation to pathological confirmation: positive adenoma (15 patients): 14 patients achieved remission mixed adenoma and hyperplasia (3 patients): two achieved remission negative specimen (3 patients): one achieved remission post-operative cortisol level: hypocortisolemia: 13 patients eucortisolemia: 4 patients persistent hypercortisolemia: 4 patients 120 | zakaria et al transsphenoidal surgery in cushing disease the adenoma was successfully removed in 15 out of the 18 patients with evident adenoma on pre-operative post-contrast magnetic resonance study (figure 2) while partial hypophysectomy were done in 5 cases without an evident adenoma on pre-operative mri study or difficult adenoma identification. pathological confirmation for the adenoma was achieved in 15 patients, mixed adenoma and hyperplasia in 3 patients while specimen was negative in three cases. follow up period ranged from 9 months up to 78 months. disease remission (table 3) was achieved in 17 patients (80.9%). in 4 patients (19.1%); complete remission was not achieved and gamma knife radiosurgery was done after surgery. disease progression occurred in two patients (9.5%) after initial remission and was treated with gamma knife radiosurgery. no approach related mortalities occurred. 13 patients had post-operative cortisol deficiency and was maintained on replacement therapy. other hormonal replacement therapy was needed in only 5 cases. csf rhinorrhea occurred in 2 patients and was managed with transient lumbar drain without any subsequent morbidities. also, the case that was operated via the trans-cranial approach after failed trans-sphenoid surgery developed csf rhinorrhea after 2nd surgery and was managed with transient lumbar drain. transient diabetes insipidus occurred in 6 cases and was treated conservatively. discussion cushing disease is uncommon challenging disease. it occurs due to acth secreting adenomas which in majority of cases are microadenomas but many reports showed that macroadenomas can cause up to 13% of cushing disease patients.⁶’⁸’⁹’¹¹’¹³’¹⁴ however, we decided to concentrate in this reports on challenge and outcome of surgery for de novo cases of acth secreting adenomas rather than macroadenomas or previously treated cases to stress on the challenge of treatment and outcome of such small lesion not to involve other potential challenge rather than the adenoma itself.¹’³’⁶’¹¹’¹² the female predominance and age distribution in our study matches with the finding of other reports.¹’²’⁵’⁷’⁹ the challenge of this disease starts with disease diagnosis. several factors are important in the endeavor to obtain satisfactory results. preoperative detection of the acth secreting adenoma is crucial for the surgical outcome, achievement of cure and prevention of surgically induced hypopituitarism.⁸’¹⁰’¹⁵’¹⁶’¹⁷ our 1st problem was with three cases (14.3%) with all manifestation of cushing disease with exclusion with all potential differential diagnosis with negative finding of the postcontrast magnetic resonance of the sella. our incidence of negative imaging is lower than what reported in other studies which may reach up to 40% of cushing microadenomas which mostly due to lack of referral of mri negative patients to our neurosurgical service.⁶’⁷’¹¹’¹²’¹³’¹⁷although inferior petrosal sampling played a role in identification the site of adenoma however we don't have such facility and in many reports, its accuracy is up to 60% in identification the site of adenoma.³’⁴’⁹’¹⁰’¹¹ in such cases our decision was to explore the pituitary gland for the adenoma or do partial hypophysectomy. romanian neurosurgery (2018) xxxii 1: 116 124 | 121 the trans-sphenoid technique is exactly like what have been reported in different series and there was no difference between the microscopic versus the endoscopic approach for addressing such tiny adenomas.¹’²’⁵’⁸’¹⁶’¹⁷ however, in our cases there was a potential challenge in the approach specific to this problem in the form of friable bloody nasal mucosa adding some difficulties to the nasal step of the approach. another problem was the difficult control of the blood pressure during the procedure that increased the bleeding during the nasal phase of the approach. in one case; the sphenoid sinus was conical shaped type and under c arm guidance we tried to drill the bony sinus to reach the sellar floor but due to excessive bleeding and lack of navigation system under our facilities; we decided to abort the procedure and to come back from above via trans-cranial approach and the adenoma was removed. in five patients, no adenoma could be identified during pituitary gland exploration and partial hypophysectomy was performed. many reports addressed the issue of negative exploration of pituitary gland for adenoma and advocated hemi-hypophysectomy of pituitary gland particularly on the side of positive inferior petrosal sampling with reported cases of disease remission even with absence of any pathological confirmation.⁶’⁹’¹⁰’¹¹’¹⁴’¹⁷ the issue of cushing disease remission both clinically and by biological confirmation has been addressed in many reports with overall remission ranging from 59 to 98% in different clinical series.²’⁴’⁵’⁸’⁹ variable factors predict the potential remission rate; the size of adenoma, whether its de novo or recurrent, presence of cavernous sinus invasion and presence or absence of pathological confirmation. remission rate is higher in newly diagnosed microadenomas without cavernous sinus invasion and slightly higher in pathologically proven adenoma rather than those with inconclusive pathological smear.¹’²’⁷’¹²’¹³’¹⁴ we have achieved remission in 80.9% of cases but all of them is microadenomas. in one case; the adenoma was located laterally in close contact with internal carotid artery and despite pathological confirmation of being adenoma; remission wasn't achieved and was sent for gamma knife (figure 1). among our three cases with negative pathological confirmation; only one case (33.3%) showed disease remission and other two cases were sent for gamma knife. figure 1 mri images of case with cushing disease with uncontrolled diabetes presented with ptosis due to 3rd nerve palsy 122 | zakaria et al transsphenoidal surgery in cushing disease figure 2 a case of cushing disease removed via microscopic trans-sphenoid approach. the above image showed her pre-operative picture and that one and three years after surgery with regression of all cushing manifestations and the below image showed her pre-operative and post-operative mri with total removal of her adenoma in another case that post-operative remission wasn't achieved; the pathological smear revealed mixed adenoma and hyperplasia and the patient was also referred for gamma knife treatment. recurrence of disease is not uncommon and it can happen over many years after initial remission hence long term follow up is necessary for those patients. overall recurrence rate ranged from 5 % to 60 % in many case series and it can occur up to 10 years from remission.⁹’¹⁰’¹¹’¹³’¹⁴ recurrence is more expected in cases of macroadenomas, cavernous sinus invasion and with negative pathological confirmations or when the hyperplasia rather than adenoma is the cause of the disease.²’³’⁴’⁸’¹⁷ in our cases; we have two cases (9.5%) of disease progression after initial remission. the pathology in one of them was mixed adenoma and hyperplasia and was advised to have gamma knife treatment. the 2nd case showed recurrent adenoma on postoperative magnetic resonance study but the patient preferred to do gamma knife radiosurgery rather than the advised repeated trans-sphenoid approach. complication after trans-sphenoid surgery for cushing disease is relatively high compared to other pituitary adenomas and it may reach up to 53% in some reports.⁴’⁹’¹¹’¹⁵ also, mortality rate has been reported up to 8.4%. complications could be minor and transient or it may be permeant or even life threatening. reported morbidities romanian neurosurgery (2018) xxxii 1: 116 124 | 123 included epistaxis, pituitary hypofunction, csf leakage, pneuomocephalus, meningitis, visual impairment, ocular motility dysfunction, and occasional deep venous thrombosis and pulmonary embolism.⁵’⁶’⁷’⁸’¹⁴’¹⁶’¹⁷ some reports⁹’¹⁰’¹¹’¹²’¹³ claimed that morbidity was less with endoscopic procedures rather than with microscopic technique but in our study; there was no much difference. our reported morbidities included transient csf rhinorrhea (2 patients), transient diabetes insipidus (6 cases) and hypopituitarism (5 patients). another case that was operated via the transcranial approach after failed trans-sphenoid surgery developed csf rhinorrhea after 2nd surgery and was managed with transient lumbar drain. 13 patients had post-operative cortisol deficiency and was maintained on replacement therapy. conclusions the transsphenoidal approach for acth secreting pituitary microadenomas is considered safe and effective for achieving disease remission despite the challenge of diagnosis and intra-operative tumor identification. both microscopic and endoscopic techniques are of equal safety and efficacy. both pre-operative tumor identification on magnetic resonance imaging of the sella and positive pathological confirmation of removed tissue play a role in achievement of remission. disease progression may occur after initial remission hence long term follow up of those patients is necessary. correspondence wael k. zakaria department of neurosurgery, mansoura university hospital, gomhorria str., mansoura, egypt phone: +2 01229333344 e-mail: drwaelmusa@yahoo.com drwaelmusa@gmail.com references 1. atkinson ab, kennedy a, wiggam mi, mccance dr, sheridan b: long-term remission rates after pituitary surgery for cushing's disease: the need for long-term surveillance. clin endocrinol (oxf) 63:549–559, 2005 2. cappabianca p1, cavallo lm, colao a, de divitiis e.:surgical complication associated with the endoscopic endonasal trans-sphenoidal approach for pituitary adenomas. j neurosurg. aug 97(2):293-298,2002 3. chandler wf, barkan al, hollon t, sakharova a, sack j, brahma b, schteingart de: outcome of transsphenoidal surgery for cushing disease: a singlecenter experience over 32 years. neurosurgery. feb 78(2):216-223, 2016 4. chee gh, mathias db, james ra, kendall-taylor p: transsphenoidal pituitary surgery in cushing’s disease: can we predict outcome?. clin endocrinol (oxf) 54:617– 626, 2001 5. dehdashti ar1, gentili f.: current state of the art in the diagnosis and surgical treatment of cushing disease: early experience with a purely endoscopic endonasal technique. neurosurg focus. 23(3): e9, 2007 6. hassan-smith zk1, sherlock m, reulen rc, arlt w, ayuk j, toogood aa, cooper ms, johnson ap, stewart pm.: outcome of cushing's disease following transsphenoidal surgery in a single center over 20 years. j clin endocrinol metab. apr;97(4):1194-1201, 2012 7. jagannathan j, sheehan jp, jane ja jr.: evaluation and management of cushing syndrome in cases of negative sellar magnetic resonance imaging. neurosurg focus: 23(3): e3, 2007 8. netea-maier rt, van lindert ej, den heijer m, van der eerden a, pieters gf, sweep cg, et al: transsphenoidal pituitary surgery via the endoscopic technique: results in 35 consecutive patients with cushing’s disease. eur j endocrinol 154:675–684, 2006 124 | zakaria et al transsphenoidal surgery in cushing disease 9. patil cg, veeravagu a, prevedello dm, katznelson l, vance ml, laws er jr.: outcomes after repeat transsphenoidal surgery for recurrent cushing’s disease. neurosurgery: 63(2):266-270, 2008 10. pouratian n, prevedello dm, jagannathan j, lopes mb, vance ml, laws er jr: outcomes and management of patients with cushing’s disease without pathological confirmation of tumor resection after transsphenoidal surgery. j clin endocrinol metab 92:3383–3388, 2007 11. prevedello dm, pouratian n, sherman j, et al.: management of cushing’s disease: outcome in patients with microadenoma detected on pituitary magnetic resonance imaging. j neurosurg. 109(4):751-759, 2008 12. semple pl, laws er jr.: complications in a contemporary series of patients who underwent transsphenoidal surgery for cushing’s disease. j neurosurg. aug 91(2):175-179, 1999 13. semple pl, vance ml, findling j, laws er jr.: transsphenoidal surgery for cushing's disease: outcome in patients with a normal magnetic resonance imaging scan. neurosurgery. mar;46(3):553-559, 2000 14. sheehan jm, lopes mb, sheehan jp, ellegala d, webb km, laws er jr.: results of transsphenoidal surgery for cushing’s disease in patients with no histologically confirmed tumor. neurosurgery. 47(1):33-36, 2000 15. starke rm, reames dl, chen cj, laws er, jane ja jr: endoscopic transsphenoidal surgery for cushing disease: techniques, outcomes, and predictors of remission. neurosurgery 72:240–247, 2013 16. wagenmakers ma, boogaarts hd, roerink sh, timmers hj, stikkelbroeck nm, smit jw, et al.: endoscopic transsphenoidal pituitary surgery: a good and safe primary treatment option for cushing's disease, even in case of macroadenomas or invasive adenomas. eur j endocrinol 169:329–337, 2013 17. yap lb, turner he, adams cb, wass ja: undetectable postoperative cortisol does not always predict long-term remission in cushing’s disease: a single centre audit. clin endocrinol (oxf) 56:25–31, 2002 14 14zakariawael_transsphenoidal doi: 10.33962/roneuro-2021-017 safety of surgical management of accessory sinus pericranii in infants mohamed m. elsherbini, hatem badr, amr farid khalil romanian neurosurgery (2021) xxxv (1): pp. 103-107 doi: 10.33962/roneuro-2021-017 www.journals.lapub.co.uk/index.php/roneurosurgery safety of surgical management of accessory sinus pericranii in infants mohamed m. elsherbini, hatem badr, amr farid khalil mansoura university, egypt abstract purpose: to better understand the pathological process of sinus pericranii and the safety of the surgical intervention. methods: patients’ archive review of patients who underwent surgical management for sinus pericranii with a confirmed diagnosis and with follow up period greater than 6 months. results: 6 infants were included; all underwent disconnection surgically with good outcome in all cases. conclusion: disconnection surgery for sinus pericranii is a safe procedure with a good prognosis. introduction sinus pericranii (sp) is first described in 1850, definition evolved over time with better understanding of the pathology, firstly described by stromeyer as a bag of blood 1, later it was described as an outpouch of the dural sinus till 1936 when fevre and modec outlined the communication between intracranial and extra-cranial venous systems. sinus pericranii is a rare extracranial developmental venous anomaly characterized by emissionary vein connecting dural venous sinus to a subgaleal venous varix which may cause skull erosion 2. though the exact pathogenesis is not well understood, a number of posttraumatic cases were reported even if the trauma passed unnoticed at the time 1’3. on the other hand, sp has been associated with congenital conditions like esophygeal atresia, meningocele, craniosinostenosis and other intracranial venous anomalies 4’5’6. another theory adopted by renier and marche proposed sp is linked to increased intracranial pressure, based upon observing sp in patients with hydrocephalus, macrocephaly and craniosinostenosis 7. sp is presented solely as “primary” pathology, or “secondary” to an intracranial vascular malformation. the rarity of the pathology and paucity of observational studies make it challenging to plan for treatment and/or expect the course of the disease, however the natural course of the disease is benign, hemorrhage could be fatal in case of accidental injury. keywords sinus pericranii, scalp swelling, developmental venous anomaly corresponding author: mohamed m elsherbini mansoura university, egypt m_elsherbiny@mans.edu.eg copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 104 mohamed m. elsherbini, hatem badr, amr farid khalil in this study, we report our experience with six cases of sp who were managed surgically, all of them were of infantile group age. patients and methods patients’ archive was reviewed to include patients who were admitted to neurosurgery ward for scalp lump during the years 2018 to 2020 and whose follow up continued for at least 6 months. patients with other extracranial vascular malformations other than sp e.g scalp avm were excluded as well as patients with non-vascular scalp lesions. only patients younger than 2 years were included. medical records were searched for clinical presentation, radiology, associated pathology and management. follow up records in outpatient clinic were obtained for the mentioned period. results study included 6 infants ,4 of them were males. age ranged from 3 to 8 months, with average 4.3 months. four families (67 %) gave history of head trauma, patients were followed up for at least 6 months with average 11.8 months follow up period (table 1). case age (months) sex head trauma radiology surgical maneuver follow up (months) 1 3 m yes ct, mri, mrv disconnection, mass excision 6 2 4 m yes mri, mrv disconnection 17 3 8 f yes mri, mrv disconnection, mass excision 15 4 5 f no mri, mrv disconnection, mass excision 13 5 3 m no ct, mri, mrv disconnection 11 6 3 m yes ct, mri, mrv disconnection 9 table 1. five lesions were midline and one lesion was parasagittal, while all were related to superior sagittal sinus with various patterns of venous drainage but no cases showed significant parenchymal drainage into the varix. pathological examination showed endothelial lining of the varix in five cases, and one case’s pathology report was irrelevant. one case was associated with esophageal atresia, otherwise neither associated pathologies nor intracranial vascular anomalies were reported. surgical technique: all surgeries were performed under general anesthesia, scalp incision directly over the lesion with surgical target to identify the emerging vein to disconnect and excise the subgaleal mass when applicable. outcome: all patients were discharged fully conscious with no neurological deficit either on discharge or during follow up visits. one patient showed superficial wound infection in the first follow up visit (one-week post-operative), which responded to conservative management. discussion sp is presented early in life either with mild symptoms e.g pain and tenderness or severe symptoms related to hemodynamic disturbance e.g bradycardi8, however the most common presentation is non-pulsatile soft scalp swelling (fig 1) which becomes tense on crying and straining, scalp swelling causing cosmetic disfigurement was the main complaint for all the cases in this study, such cases should be clinically and radiologically differentiated from other scalp lumps before proceeding to treatment 8. parents seek medical advice with or without history of head trauma which could be missed as well, majority (67%) of patients in our study gave positive history of trauma. though some cases are strongly linked to head trauma, the frequent association with other cranial vascular anomalies especially developmental venous anomalies supports the congenital theory of the origin of sp such as failure of regression of interperiosteodural venous plexus or non-closure of skull sutures 5’6. figure 1. main presentation of sp as a scalp swelling, usually 105 safety of surgical management of accessory sinus pericranii in infants devoting hair on top when increases in size. related to coronal suture (a), behind the coronal suture (b). both infants with open fontanile. figure 2. mri t2 coronal (a), and axial t1 of two different cases showing midline sp related to sss. ct scan is required to identify skull erosion and enlarged diploic vein. mri (fig 2) is needed to exclude parenchymal lesions and avm’s 9, no cases of coexisting intracranial pathology were encountered in this study, while mrv we found beneficial to classify sp via a non-invasive tool. the necessity of digital subtraction angiography (dsa), though concluded by gandolfo is not indicated in all cases according to our experience. in our study, mrv was sufficient to classify sp into primary and accessory, no dominant cases were encountered in this study. mrv was not among the radiology options for gandolf series 10. we suggest that dsa could be reserved to cases with associated intracranial vascular anomaly or with suspected significant venous drainage into the varix. pathologically sp is categorized into two main groups, dominant where it represents a drainage to the cortex and accessory where part of the cortex or the dural sinus drains directly and solely into the varix 10. another classification suggested by brook et al 11 to categorize sp according to the feasibility of endovascular treatment, a, b, c. where a stands for the dominant variant, b for the accessory variant and c variant in which no parenchymal venous drainage into the varix. type c is the safest for endovascular embolization and type a is an absolute contraindication for. histological classification by nakasu12 listed three different types; a) fibrous architecture with cavernoma like structure, b) venous varix with endothelial lining and c) herniated dural venous sinus. though spontaneous regression of sp through thrombosis had been reported, cases underwent surgery in this series were large and parents decided to undergo surgery 4’13. surgical management includes disconnection of the emissary vein (fig 3) with excision of the mass when applicable, which was performed for all our cases. for three patients in this study (50 %), disconnection of the vein was enough to collapse the mass completely with no actual mass to be excised, for these cases only biopsy of the potential cavity was performed, one of which showed irrelevant sample. some authors reported closure of bone defect with bone wax or cranioplasty for larger defects which was not necessary in this series. serious complication such dural sinus laceration and hemorrhage were reported 14, though not encountered in this study, we believe this complication is liable to happen with nakasu type c which could be excluded preoperatively and intraoperatively with microsurgical microscope. figure 3. surgical management, subcutaneous dissection to identify the connection vein thoroughly (a), identification of the connection vein, skeletonization and cauterization (b). endovascular therapy is a valid means for treatment of sp, it can be performed either via direct puncture, transvenous or combined. endovascular therapy carries the risk of skin sloughing and thromboembolic events, also it is questionable to consider it less invasive than surgery in infantile age group included in this study. in a case report by brook et al 11, nbca was used to embolize the varix however cosmetic outcome is questionable as it initiates an inflammatory reaction which might lead to varix hardening. another case report by kessler et al15 reported good cosmetic result using direct absolute alcohol injection after transvenous endovascular closure of the in/outflow point. the concerns about absolute alcohol leakage into circulation are serious, connection site to systemic 106 mohamed m. elsherbini, hatem badr, amr farid khalil circulation should be confirmed to be sealed before proceeding to injection. also, theoretical assumption that embolization might lead to development of new vascular anomalies in the region surrounding the occluded one is a reasonable concern. although most of cases of pavanello et al series8, the largest to our knowledge, were treated via endovascular techniques, it included only 7 infantile cases which were managed conservatively except for one which was treated surgically during the corrective surgery of the associated craniosynostosis. the same study reported spontaneous resolution of a number of accessory cases, an option was not accepted for all the parents in this study due to the disfigurement at time of presentation. another large study by gandoflo et al 10 included 15 infants, six of which required surgical intervention, four of them were dominant variant, with good outcome for all cases including dominant cases which were managed surgically. these results make the necessity of dsa, which is an invasive maneuver, questionable since categorizing sp via dsa didn’t change the role of surgery, also significant brain parenchymal drainage is diagnosed with mrv (fig 4). figure 4. mrv showing accessory sp, related to sss. with no significant brain parenchymal drainage into the varix. in all means, the extent of treatment depends on the degree of normal brain parenchyma draining into the dva, as a rule no normal parenchymal brain drainage should be compromised. conclusion sp is a rare condition in infants characterized by a subgaleal venous varix connected to intracranial venous system via abnormally enlarged emissary vein(s), surgical management of sinus pericranii in infants is safe method for accessory cases with no significant parenchymal drainage into the varix. abbreviations avm: arteriovenous malformation; ct: computed tomography; dsa: digital subtraction angiography; dva: developmental venous anomaly; mri: magnetic resonance imaging; mrv: magnetic resonance venogram; nbca: n-butyl cyanoacrylate; sp: sinus pericranii. references 1. courville, c. b. & rocovich, p. m. a contribution to the study of sinus pericranii (stromeyer); report of case with some comments on pathology of the lesion. bull. los angel. neuro. soc. (1946). 2. leblanc, i. et al. pericranial sinus. j. neuroradiol. neuroradiol. (1994). 3. david, l. r., argenta, l. c., venes, j., wilson, j. & glazier, s. sinus pericranii. j. craniofac. surg. (1998) doi:10.1097/00001665-199801000-00003. 4. hayakawa, i. et al. spontaneous regression of sinus pericranii. report of a case. neurol. surg. (1978). 5. sakai, k. et al. sinus pericranii associated with a cerebellar venous angioma. neurol. med. chir. (tokyo). (1997) doi:10.2176/nmc.37.464. 6. sherry, r. g., walker, m. l. & olds, m. v. sinus pericranii and venous angioma in the blue-rubber bleb nevus syndrome. am. j. neuroradiol. (1984). 7. renier, d. & marchac, d. craniofacial surgery for craniosynostosis: functional and morphological results. annals of the academy of medicine, singapore (1988). 8. m., p. et al. sinus pericranii: diagnosis and management in 21 pediatric patients. j. neurosurg. pediatr. (2015). 9. manjila, s. et al. a review of extraaxial developmental venous anomalies of the brain involving dural venous flow or sinuses: persistent embryonic sinuses, sinus pericranii, venous varices or aneurysmal malformations, and enlarged emissary veins. neurosurg. focus (2018) doi:10.3171/2018.5.focus18107. 10. gandolfo, c. et al. sinus pericranii: diagnostic and therapeutic considerations in 15 patients. neuroradiology (2007) doi:10.1007/s00234-007-0211-7. 11. brook, a. l., gold, m. m., farinhas, j. m., goodrich, j. t. & 107 safety of surgical management of accessory sinus pericranii in infants bello, j. a. endovascular transvenous embolization of sinus pericranii: case report. j. neurosurg. pediatr. (2009) doi:10.3171/2008.10.peds08267. 12. nakasu, y., nakasu, s., minouchi, k. & handa, j. multiple sinus pericranii with systemic angiomas: case report. surg. neurol. (1993) doi:10.1016/0090-3019(93)90108-d. 13. carpenter, j. s., rosen, c. l., bailes, j. e. & gailloud, p. sinus pericranii: clinical and imaging findings in two cases of spontaneous partial thrombosis. am. j. neuroradiol. (2004). 14. spektor, s., weinberger, g., constantini, s., gomori, j. m. & beni-adani, l. giant lateral sinus pericranii: case report. j. neurosurg. (1998) doi:10.3171/jns.1998.88.1. 0145. 15. kessler, i. m., esmanhoto, b., riva, r. & mounayer, c. endovascular transvenous embolization combined with direct punction of the sinus pericranii: a case report. interv. neuroradiol. (2009) doi:10.1177/159101990901 500410. 14canazgokhan_pituitary romanian neurosurgery | volume xxx | number 4 | 2016 | october december article pituitary adenoma in monozigotic twins with cri du chat syndome: a rare case report gokhan canaz, huseyin canaz, ibrahim alatas turkey doi: 10.1515/romneu-2016-0086 536 | canaz et al pituitary adenoma in monozigotic twins with cri du chat syndome doi: 10.1515/romneu-2016-0086 pituitary adenoma in monozigotic twins with cri du chat syndome: a rare case report gokhan canaz1, huseyin canaz2, ibrahim alatas2 1bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery, istanbul, turkey 2florence nightingale hospital, istanbul bilim university, department of neurosurgery, istanbul, turkey abstract: pituitary adenomas are rare tumours of pediatric population. in etiology, genetic factors are more common than they are in adults. because of the rarity of the cases, there are only a few large case studies in the literature. pituitary tumours in children are often related with syndromes like men type 1, carney complex and mc cune albright, but there is no case in the literature associated with cri du chat syndrome. statisticlly, it has been reported that, pediatric tumours occur more often in twins, in the pediatric population. main treatment for prolactinomas is medical intervention with dopamine agonists, as in adults. surgery is prefered when the tumour is resistant to medical treatment or shows mass effects around sellae. in that situation, as in adults, both transcranial and transsphenoidal approach is possible. key words: pituitary, cri du chat, twins, adenoma introduction pituitary adenomas are rare tumours in children and adolescents. they comprise approximately 3% of all suprasellar pediatric tumors and 2-6% of them can be surgically treated (3, 13). pituitary tumours in children are rarely malignant and secretory. acth secretory adenomas occur more frequent in early childhood but the most common secretory adenomas in elder children are prolactinomas (5, 9, 17). although etiology is uncertain, concordance with genetic syndromes, oral contaseptive use in pregnancy, twining and some malignancies are reported (4). the best known genetic syndromes accompanying pituitary adenomas are multiple endocrine neoplasia type 1 (men 1), carney compex, familial isolated pituitary adenoma (fipa) and mccune albright syndromes. case presentation 14 years old monozygotic twin sisters, who had been diagnosed with cri du chat syndorme, were admitted to hospital with premenarcheal galactorrhea complaint. romanian neurosurgery (2016) xxx 4: 536 – 539 | 537 pituitary magnetic resonance imaging (mri) was performed. both sisters presented with a pituitary lesion of 5.8mm x 3.3mm and a 33 3.4mm x 2.6mm, respectively, with low contrast enhancement, which was compatible with pituitary microadenoma (figures 1, 2). figure 1 mri study showing a 5.8mm x 3.3mm solid lesion with low contrast enhancement in the right portion of the pituitary gland, suggestive for a microadenoma. a. coronal view. b. sagittal view figure 2 mri study showing a 3.4mm x 2.6mm sized cystic lesion with low, peripheral contrast enhancement in theright side of the pituitary gland. a. coronal view. b. sagittal view prolactin levels were respectively 120 μg/l and 70 μg/l (normal range 3.3-26.7 μg/l). laboratory studies revealed no renal dysfunction or hypothyroidism. visual examination appeared suboptimal, although the exam was scarcely reliable because of the 538 | canaz et al pituitary adenoma in monozigotic twins with cri du chat syndome patient mental retardation. surgical intervention was suggested for both patients, but family refused the surgery. patients were directed to the endocrinology department for medical treatment and follow-up. discussion cri du chat syndrome is a hereditary congenital syndrome, caused by a deletion on short arm of 5th chromosome (7). incidence is 1/20.000-50.000 birth (11). microcephaly, round face shape, hypertelorism, micrognathia, low ear line, hypotonia and various psychomotor symptoms and mental retardation are common findings. the main clinical feature is, a high-pitched monochromatic cry, that gives the name to the syndrome (7, 12). 'some studies demonstrated the association between deletions on 5q and neoplasia like acute myeloid leuchemia, myelodisplastic syndrome and crohn disease (14). morphological anormalities of the clivus and sella turcica, but not any pituitary disorders nor increase in the risk of neoplasia has been reported in cri du chat syndrome (6). some studies have reported an increased prevalence of some tumors, i.e. testicular and non-thyroid endocrine cancers in twins. on the other hand, colorectal cancer and leukemia appear to be less frequent in twins. in a study including 3,200 twin cancer patients, the reported frequency of pituitary tumours was two-fold higher than in the general population, but the etiopathological mechanisms remain to be defined (4). pediatric pituitary adenomas are extraordinarily rare tumours in early childhood. frequency is a little bit higher in adolescents but stil very rare relative to adults (9). these tumours in pediatric population are frequently part of a genetic condition. pituitary tumors often present in the context of men type 1, carney complex, fipa and mccune albright syndromes. mutations to oncogens and tumour supressor genes, like gnas, pttg, hmga2, and fgfr-64, have been also identified in sporadic cases of pituitary adenoma (2, 15). in early childhood, acth secretor tumours are the most common functional adenomas although they are very rare. they usually occur as a part of men type 1(8). during adolescent period, rate of prolactinomas and growth hormon secretory tumours evaluated relatively higher (1). beside genetic factors, oral contraseptive use, high parity count and twining also considered among potential risk factors (4). some authors suggest that pituitary adenomas in children are more aggressive than in adults, although this matter is still largely debated' and add references. 50% of all pituitary tumorus are prolactinomas. they occur more often in late childhood and girls (9). two main complaints are headache and visual deficites, due to mass effect, but delayed puberty, amenorrhea and galactorrhea are more characterised complaints in girls. 'the first line treatment for prolactinomas in both children and adults is dopamine agonists. main purpose is to reduce both prolactin levels and tumour size (10). conditions like acute visual deficit, hydrocephaly, csf leakage require emergency surgery. elective surgery should be reserved to cases of resistance to medical treatment (16). romanian neurosurgery (2016) xxx 4: 536 – 539 | 539 conclusion pediatric pituitary adenomas are extremely rare tumors which relationship with genetic syndromes have been revealed. beside known syndromes, their concommitance with different syndromes in some cases, shows the importance of genetic studies. further investigations are necessary to enlight the possible genetic etiology. correspondence gokhan canaz, bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery 34147 bakırkoy/istanbul. tel: +90 212 409 15 15 mobile: +90 536 944 94 39 email: gokhancanaz@gmail.com references 1. abe t, ludecke dk, saeger w. clinically nonsecreting pituitary adenomas in childhood and adolescence. neurosurgery 1998; 42: 744-750; discussion 750-741. 2. alexander jm, biller bm, bikkal h, et al. clinically nonfunctioning pituitary tumors are monoclonal in origin. the journal of clinical investigation 1990; 86: 336340. 3. espay aj, azzarelli b, williams ls, et al. recurrence in pituitary adenomas in childhood and adolescence. journal of child neurology 2001; 16: 364-367. 4. hemminki k, chen b. are twins at risk of cancer: results from the swedish family-cancer database. twin research and human genetics : the official journal of the international society for twin studies 2005; 8: 509-514. 5. kane la, leinung mc, scheithauer bw, et al. pituitary adenomas in childhood and adolescence. the journal of clinical endocrinology and metabolism 1994; 79: 11351140. 6. kjær i. sella turcica morphology and the pituitary gland—a new contribution to craniofacial diagnostics based on histology and neuroradiology. the european journal of orthodontics 2012. 7. lejeune j, lafourcade j, berger r. [crying cat disease (partial deletion of the short arm of the 5 chromosome)]. acquisitions medicales recentes 1966: 217-228. 8. marx sj, agarwal sk, kester mb, et al. multiple endocrine neoplasia type 1: clinical and genetic features of the hereditary endocrine neoplasias. recent progress in hormone research 1999; 54: 397-438; discussion 438-399. 9. mindermann t, wilson cb. pediatric pituitary adenomas. neurosurgery 1995; 36: 259-268; discussion 269. 10. molitch me. management of prolactinomas during pregnancy. the journal of reproductive medicine 1999; 44: 1121-1126. 11. niebuhr e. the cri du chat syndrome: epidemiology, cytogenetics, and clinical features. human genetics 1978; 44: 227-275. 12. overhauser j, huang x, gersh m, et al. molecular and phenotypic mapping of the short arm of chromosome 5: sublocalization of the critical region for the cri-du-chat syndrome. human molecular genetics 1994; 3: 247-252. 13. partington md, davis dh, laws er, jr., et al. pituitary adenomas in childhood and adolescence. results of transsphenoidal surgery. journal of neurosurgery 1994; 80: 209-216. 14. schmutz j, martin j, terry a, et al. the dna sequence and comparative analysis of human chromosome 5. nature 2004; 431: 268-274. 15. spada a, mantovani g, lania a. pathogenesis of prolactinomas. pituitary 2005; 8: 7-15. 16. taskapilioglu mo, yilmazlar s, eren e, et al. transnasal transsphenoidal surgical method in pediatric pituitary adenomas. pediatric neurosurgery 2015; 50: 128-132. 17. webb c, prayson ra. pediatric pituitary adenomas. archives of pathology & laboratory medicine 2008; 132: 77-80. doi: 10.33962/roneuro-2021-060 a rare occurrence of primary basal ganglia germinoma in an adult patient. a case report and literature review ebtesam abdullaa, harleen lutherb, tejal shahc, nisha chandrand romanian neurosurgery (2021) xxxv (3): pp. 355-360 doi: 10.33962/roneuro-2021-060 www.journals.lapub.co.uk/index.php/roneurosurgery a rare occurrence of primary basal ganglia germinoma in an adult patient. a case report and literature review ebtesam abdullaa1, harleen lutherb1, tejal shahc2, nisha chandrand3 1 department of neurosurgery. salmaniya medical complex, manama, bahrain 2 department of radiology. salmaniya medical complex, manama, bahrain 3 department of anatomical pathology. salmaniya medical complex, manama, bahrain abstract background: basal ganglia germinomas (bggs) represent a diagnostic and management neurosurgical dilemma. because of the rarity of these tumors in adults, the management strategies are not well defined. case description: a 24-year-old man was presented with progressive left-sided hemiparesis. cranial computed tomography (ct) and magnetic resonance imaging (mri) demonstrated a heterogeneous lesion with few microcystic nodules, seen involving the right basal ganglia with calcification. a stereotactic brain biopsy (sbb) was obtained. histopathology revealed bgg. the patient received whole-brain radiation therapy (wbrt) and reported marked improvement in symptoms with no recurrence during a follow-up period of four years. conclusion: bgg should be considered a part of the differential diagnosis in young adults presented with hemiparesis and a heterogeneous lesion in the basal ganglia. standard recommendations for the management of such rare lesions in adults are needed. introduction intracranial germinomas represent 0.5 to 3% of all intracranial tumors. [2-4,5,7] they are mostly found in the pineal and suprasellar regions. [17] rarely, they arise from the basal ganglia and are sparsely reported in the literature. [1-7] adults with an established diagnosis of basal ganglia germinoma (bgg) are exceedingly rare. [5] only thirteen cases of primary bgg have been reported to date. bggs are difficult to treat due to their deep anatomical position inside the brain, making them rarely susceptible to total eradication. management practices range from stereotactic brain biopsy (sbb) to partial or more aggressive resections and even empirical radiation without a prior histological diagnosis, plus radiation therapy (xrt) and chemotherapeutic agent administration. [15,7] keywords basal ganglia, germinoma, radiation therapy corresponding author: ebtesam abdulla salmaniya medical complex, manama, bahrain dr.ebtesam@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 356 ebtesam abdullaa, harleen lutherb, tejal shahc, nisha chandrand adult bggs have rarely been investigated in isolation. thus, the natural history remains mostly undefined, and the therapeutic paradigms have not been standardized yet. this article is intended to discuss a good outcome for a young adult diagnosed with bgg, using a minimal intervention strategy. we also provide a review of the relevant literature. case description a previously asymptomatic 24-year-old male was presented to our facility after experiencing five months of isolated progressive left-sided weakness. the vital signs and all other systemic clinical parameters were normal. the neurological evaluation was grossly intact aside from left-sided hemiparesis (grade 4/5 medical research council) and left-sided deep tendon hyperreflexia. his gait pattern was characterized by dragging his left foot while walking. figure 1. preoperative cranial ct scan demonstrates a mildly hyperdense irregular lesion in the right basal ganglia with dense calcification (a) and a heterogenous, moderate enhancement in the postcontrast study (b). initially, a plain and intravenous contrast cranial computed tomography (ct) scan (figure. 1) was performed, showing a mildly hyperdense lesion with moderate post-contrast enhancement and containing an area of calcification in the right basal ganglia. cranial magnetic resonance imaging (mri) demonstrated a heterogeneous signal intensity lesion with few microcystic nodules in the right basal ganglia with calcification on pre-contrast images (figure. 2). the lesion showed mild hypointensity on t1-weighted images (figure. 2a), hyperintensity on t2-weighted images (figure. 2b) and fluid-attenuated inversion recovery images, and moderate heterogeneous patchy enhancement in postcontrast t1-weighted images (figure. 2e). there was evidence of patchy restricted diffusion in diffusion-weighted imaging (figure. 2c). after a negative comprehensive check-up, including spinal mri, whole-body ct scan, hiv serology, ophthalmic examination, and positron emission tomography scan without abnormalities, amongst the differential diagnoses entertained was primary basal ganglia germinoma, followed by other less likely differentials of pilocytic astrocytoma, primitive neuroectodermal tumor, and cryptococcus meningitis. figure 2. preoperative cranial mri demonstrates a right basal ganglia lesion with mild hypointensity on the t1-weighted sequence (a) and heterogeneous hyperintensity with microcystic nodules on the t2-weighted sequence (b). the lesion shows patchy restricted diffusion in the form of a patchy high signal with a high b value of dwi (c) and a low signal apparent diffusion coefficient (d). the lesion shows patchy enhancement in the postcontrast t1-weighted sequence (e). sbb was performed on the patient. histopathological evaluation (figure. 3) revealed nests of neoplastic cells separated by thin fibrous septa. the neoplastic cells were large and polygonal with distinct eosinophilic cytoplasm and a vesicular nucleus with a conspicuous nucleolus. no fibrillary background, trophoblastic cells, rosette formation, or neutrophils were noted. mitosis (2-4/hpf) and large areas of necrosis and hemorrhage were present in the tumor. there were a few scattered lymphocytes. the tumor cells were strongly and diffusely positive for placental alkaline phosphatase (plap), beta-human chorionic gonadotropin (b-hcg), and cd117. however, they were negative for glial fibrillary acidic protein, synaptophysin, chromogranin, isocitrate dehydrogenase 1, oligodendrocyte transcription factor 2, s100, epithelial membrane antigen, 357 a rare occurrence of primary basal ganglia germinoma in an adult patient myogenin, cd 20, and cd 30. the ki-67 index was 4050%, and ini-1 was preserved. a diagnosis of basal ganglia germinoma was made based on histological findings. the blood serum sample showed an elevated bhcg of 563 mlu/ml and a normal alpha-fetoprotein (afp) of 3.5 μg/l. the cerebrospinal fluid (csf) sample showed an elevated b-hcg of 350 mlu/ml and a normal afp of 1.1 μg/l. no atypical cells were detected in the csf sample. the patient received whole-brain radiation therapy (wbrt) using a volumetric modulated arch therapy technique with a total dose of 24 gy in 15 fractions over four weeks, followed by a tumor boost of 16 gy in 10 fractions over two weeks. repeated blood serum, three months post-xrt, showed a normal b-hcg of 0.4 mlu/l. over a four-year followup, the patient significantly improved after xrt and had no tumor recurrence on the mri (figure. 4). discussion adults with primary bggs are uncommon, and their natural history and treatment are rarely the topic of published work.[5] we performed a literature search of the following databases on may 17, 2021: pubmed and google scholar. we included adult patients (age ≥ 19) with germinoma located in the basal ganglia (striatum, pallidum, subthalamic nucleus, and substantia nigra) (table. 1). patients with a tumor mainly located in the thalamus were excluded from the review. adding our case, thirteen patients were diagnosed with pure germinoma, and one patient was diagnosed with germinoma mixed with syncytiotrophoblastic giant cells. six tumors were right-sided, six tumors were left-sided, and two tumors were bilateral. all of the patients were men. the median age at diagnosis was 24.5 years old (the range was 19-31 years) figure 3. histopathology of right basal ganglia germinoma. the lesion shows sheets of cells having abundant eosinophilic cytoplasm, pleomorphic nuclei with prominent nucleoli, 20x, 40x he (a & b). the tumor cells are strongly and diffusely positive for b-hcg (c) and plap (d) immunostain and negative for synaptophysin (e). ini-1 is preserved (f). table 1. clinical characteristics of reported adult cases of primary basal ganglia germinoma source age/sex presentation ich signs ǂ duration (months) afp (s/c) hcg (s/c) elizabeth j et al. 2002 21/m hemiparesis, speech difficulty yes 12 na/na na/na sonoda y et al. 2008 24/m hypokinesia no 6.9 +/na -/na 31/m hemiparesis, hypokinesia no 6.9 -/-/ 29/m di, personality change no 11.4 -/-/ 358 ebtesam abdullaa, harleen lutherb, tejal shahc, nisha chandrand phi jh et al. 2010 19/m hemiparesis no 8 -/na -/na lin jc et al. 2012 24/m bizarre behavior no 0.5 -/na -/na vialatte de pemille c et al. 2016 21/m hemiparesis no nr -/-/ wei x-h et al. 2016 31/m headache yes nr -/na na/na 19/m hemiparesis no nr -/na +/na 21/m hemiparesis, polydipsia no nr -/na -/na 30/m hemiparesis no nr -/na -/na 29/m hemiparesis no nr -/na -/na woo pym et al. 2017 21/m hemiparesis no 24 -/na -/na our case, 2021 24/m hemiparesis no 5 -/+*/+* ǂ ich signs reported: headache, vomiting, dysphagia, papilloedema 6th cranial nerve palsy. *beta subunit of hcg keywords: m: male; ich: intracranial hypertension; nr: not reported; s: serum; c: cerebrospinal fluid; na: not applicable; -: normal level; +: high level, di: diabetes insipidus. table 2. magnetic resonance imaging findings before stereotactic brain biopsy of reported adult cases with primary basal ganglia germinoma source mri findings enhancement mass effect hemorrhage cyst formation calcification dr other elizabeth j et al. 2002 + + + + nr nr multiple lesions sonoda y et al. 2008 + + nr + nr + + nr multiple lesions phi jh et al. 2010 nr bilateral lin jc et al. 2012 + nr + nr nr bilateral vialatte de pemille c et al. 2016 + nr nr nr nr multiple lesions wei x-h et al. 2016 + + + nr nr ca, multiple lesions nr + + nr yes ca, multiple lesions + + nr yes ca, multiple lesions + + nr nr ca, multiple lesions + + + nr nr multiple lesions woo pym et al. 2017 nr + + + nr yes early ca our case, 2021 + + minimal + + patchy none keywords: nr: not reported; dr: diffusion restriction; ca: cerebral atrophy. table 3. treatment protocols and outcome of adult patients with primary basal ganglia germinoma source sbb surgery xrt ctx outcome recur -rence type total (gy) fractions duration (weeks) boost (gy/fractions/weeks) elizabeth j et al. 2002 no tr yes (type nr) nr nr nr nr yes minimal improvem ent no 359 a rare occurrence of primary basal ganglia germinoma in an adult patient sonoda y et al. 2008 yes no lb 60 nr nr nr yes partial response no yes no no yes complete response yes yes no no yes complete response yes phi jh et al. 2010 yes no bg + wv 50.4 + 36 nr nr nr yes complete remission no lin jc et al. 2012 yes no csrt nr nr nr nr yes complete resolution no vialatte de pemille c et al. 2016 yes no csrt 24 nr nr 16/nr/nr no nr nr woo pym et al. 2017 no ntr csrt nr nr nr nr yes complete resolution no our case, 2021 yes no wbrt 24 15 4 16/10/2 no mark improvem ent no keywords: sbb: stereotactic brain biopsy; tr: total resection; lb: local brain; bg: basal ganglia; wv: whole ventricle; ntr: near-total resection; nr: not reported; xrt: radiation therapy; csrt: cerebrospinal radiation therapy; wbrt: whole-brain radiation therapy; ctx: chemotherapy. figure 4. cranial mri of the previously treated basal ganglia germinoma at the last follow-up demonstrates stable disease with surrounding gliosis and post-radiation changes with secondary ex-vacuo dilation of the ipsilateral frontal horn of the lateral ventricle in t1 and t2-weighted images (a & b). no new lesion was detected in the post-contrast t1-weighted image (c). presenting symptoms included hemiparesis (71.4%), hypokinesia (14.2%), psychiatric symptoms (14.2%), diabetes insipidus (14.2%), headache (7.14), and speech difficulty (7.41%). signs and symptoms of increased intracranial pressure such as headache, vomiting, papilledema, dysphagia, and sixth cranial nerve palsy were found in two patients at the initial presentation. diabetes insipidus due to the coexisting suprasellar lesion was evident in two patients. at the onset of symptoms, patients seek medical attention after a median of 9.3 months (range: two weeks to two years). serum afp and hcg were measured in (13/14) cases. elevation of serum afp and hcg was detected in one patient and two patients, respectively. csf testing for afp and hcg was not routinely performed. in all patients, cranial mri was required for radiological diagnosis (table. 2). eight patients had multiple lesions in the internal capsule (4 cases), thalamus (3 cases), frontal lobe (2 cases), septum pellucidum (1 case), pineal (1 case), suprasellar (2 cases), corpus callosum (1 case), frontotemporal gyri (1 case) regions, as well as the basal ganglia. in five individuals, the initial study revealed ipsilateral cerebral hemiatrophy, indicating wallerian degeneration. the patterns seen in the mri were varied and were related to the duration of the disease before admission. the mri patterns ranged 360 ebtesam abdullaa, harleen lutherb, tejal shahc, nisha chandrand from a subtle patchy lesion seen in the t2-weighted sequence with no contrast enhancement to a large lesion with a mass effect and vivid contrast enhancement. some bggs displayed hemorrhagic and cystic components or calcification. hydrocephalus was evident in four cases. reported therapeutic strategies are outlined in (table. 3). sbb was performed in seven cases and craniotomy in two (reported 1 transylvanian approach) patients. postoperative imaging in craniotomy patients revealed one complete resection and one near-total resection. seven patients received xrt (3 craniospinal, 1 whole-brain, 1 basal ganglia with whole-ventricle, and 1 local brain technique). seven cases received platinum-based antineoplastic regimens to mitigate xrt toxicity. however, chemotherapy alone did not seem to improve survival. follow-up imaging (> 3 months) was available for eight patients. while most reported marked improvement in symptoms, some reported poor neurological outcomes. in general, all treated tumors by xrt tend to show no recurrence on subsequent imaging or progression to the contralateral side. our patient, for example, is notable for being: 1. diagnosed in an adult patient, 2. diagnosed in a middle eastern patient, 3. located in the basal ganglia, 4. not associated with ipsilateral cerebral atrophy, and 5. successfully managed with a minimal treatment strategy, 6. showed no recurrence during the follow-up period. as far as we know, such a case has never been described before. conclusion bggs are rare entities, and a high degree of suspicion is needed for their diagnosis, especially in young adults with hemiparesis and a heterogeneous basal ganglia lesion on cranial mri. early detection of such lesions is critical, as a delay in intervention may result in poor neurological recovery. sbb followed by wbrt seems to be a minimal and safer treatment strategy for managing such lesions. references 1. elizabeth j, menon g, bhattacharya rn, radhakrishnan vv.germinoma of the basal ganglia: a case report and review of literature. neurol india 2002;50:84-6. 2. lin jc, ju dt, chen cm, et al. germinoma involving bilateral basal ganglia: a rare case report. journal of medical sciences 2012; 32(1), 43-46. 3. phi jh, cho b-k., kim s-k., et al. germinomas in the basal ganglia: magnetic resonance imaging classification and the prognosis. journal of neuro-oncology 2010; 99(2), 227–236. 4. sonoda y, kumabe t, sugiyama s. , et al. germ cell tumors in the basal ganglia: problems of early diagnosis and treatment. j neurosurg pediatr 2008; 2 (02) 118-124. 5. vialatte de pemille c, bielle f, mokhtari k, kerboua e, alapetite c, idbaih a. basal ganglia germinoma in an adult. world neurosurg 2016;92:584.e511–584.e514. 6. wei x-h, shen h-c, tang s-x, et al. radiologic features of primary intracranial ectopic germinomas. medicine 2016; 95(52), e5543. 7. woo pym, chu ach, chan ky, kwok jck.progressive hemiparesis in a young man: hemicerebral atrophy as the initial manifestation of basal ganglia germinoma. asian j neurosurg 2017;12:65–68. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0053 article computational fluid dynamics as an indicator of offending vessel in trigeminal neuralgia and hemifacial spasms mayur kamath v., yasuhiro yamada, yoko kato japan      418 | mayur et al computational fluid dynamics in trigeminal neuralgia             doi: 10.2478/romneu-2018-0053 computational fluid dynamics as an indicator of offending vessel in trigeminal neuralgia and hemifacial spasms mayur kamath v.1, yasuhiro yamada2, yoko kato2 1department of neurosurgery, kasturba medical college, mangalore & fellow, department of neurosurgery, banbuntane hotokukai hospital, fujita health university, nagoya, japan 2department of neurosurgery, banbuntane hotokukai hospital, fujita health university, nagoya, japan abstract: context: newer imaging tool for diagnosing offending vessel in trigeminal neuralgia (tn) and hemifacial spasms (hfs). aim: to find out if computational fluiddynamics (cfd) can correctly predict the offending vessel in hfs and tn & thus improving the outcome of microvascular decompression) mvd. settings and design: cfd is a relatively new mode of imaging. its application to indicate offending vessel in tn & hfs was tested. materials & methods: retrospectively we studied 13 consecutive patients operated in 2017 for either hfs or tn. preoperatively mri & computed tomography angiogram (cta) were done and the offending vessel identified along with its point of contact with the concerned nerve. cfd was done using hemoscope 2015 software and wall pressure, wall shear stress, vector & streamline flow were obtained in the offending vessel (test) & contralateral vessel (control). results of these were charted on an excel sheet & results analyzed. the postoperativeoutcome were assessed and compared with cfd results. statistical analysis used: small study group hence statistical analysis couldn’t be applied. results: of the 13 patients, offending artery had high wall pressure in 12 and increased wall shear stress innine. among the controls six had high wall pressure and only two had high wall shear stress. conclusion: cfd can be used to determine offending vessel and can predict good outcome following microvascular decompression. key words: trigeminal neuralgia, hemifacial spasms, computational fluid dynamics, microvascular decompression & offending vessel. introduction the diagnosis of hfs & tn are mainly clinical based on patient's symptoms.tn is usually diagnosed based on following symptoms & signs1: unilateral facial pain, no extension beyond trigeminal territory, pain is paroxysmal with intervals of remission. pain occurs spontaneously or more commonly triggered by a stimulus. on examination there is usually romanian neurosurgery (2018) xxxii 3: 418 425 | 419             no hypoesthesia or defective corneal reflex. these patients usually would have responded at least initially to medical management. hfs on the other hand involves sudden involuntary contraction of one side of the face. usually imaging in tn & hfs reveals an offending artery abutting the trigeminal & facial nerve respectively. the most common offending artery in tn is superior cerebellar artery (sca) followed by anterior inferior cerebellar artery (aica)2,3,4,5. the most common offending artery in hfsis aica followed by posterior inferior cerebellar artery (pica) & vertebral artery (va)6. mostly the radiological evaluation for trigeminal neuralgia & hemifacial spasms include high resolution t2 mri which includes constructive interference in steady state (ciss) & fast imaging employed steady state acquisition (fiesta), t1 post gadolinium mri and ct angiography7. computational fluid dynamics (cfd) is the use of applied mathematics, physics and computational software to visualize how a liquid flows – as well as how the liquid affects objects as it flows past8.in case of humans it is blood (liquid) that flows through blood vessels (tube). cfd gives us valuable information of blood flow through the vessels and hence has valuable applications. wall pressure is the force of blood column on the arterial wall circumferentially leading to stretching/stress on all wall layers. wall shear stress is the tangential drag force produced by blood moving across the endothelial surface. it is a function of the velocity gradient of blood near the endothelial surface. its magnitude is directly proportional to blood flow and blood viscosity and inversely proportional to the cube of the radius. wall shear stress regulates arterial wall remodelling. vector and stream line velocity indicate the weather blood flow within the vessels is laminar or turbulent. cfd has had multiple applications in imaging of the cerebral aneurysms in the past. some of cfd in cerebral aneurysm include diagnosing thin walled regions in unruptured aneurysms9, rupture prediction of intracranial aneurysm10, 11. there has been however been some confusion regarding whether high or low wall shear stress leads to rupture with some authors believing both high and low wall shear stress causes aneurysmal rupture12. however cfd was not used in predicting the offending vessel and incriminating it as the cause of trigeminal neuralgia or hemifacial spasms until dr. toru satoh from ryofukai satoh neurosurgical hospital, hiroshima, japan pioneered a study13. however no other articles were published on this regard at the time of writing this paper. trigeminal neuralgia is treated initially with oral anticonvulsants like carbamazepine or oxcarbamazepine14. lamotrigine, clonazepam, gabapentin, pregablin and valproate are other drugs that have beneficial effects in trigeminal neuralgia.15,16,17,18 hemifacial spasms are treated initially with botulinum toxin19. gabaergic drugs and anticonvulsants are less effective when compared to botulinum toxin but are of some benefit in early stages when the contractions are weak & infrequent. microvascular decompression (mvd) is reserved for patients not responding to medical line of management.microvascular 420 | mayur et al computational fluid dynamics in trigeminal neuralgia             decompression for tn & hfs is offered to patients with neurovascular conflict (nvc). mvd is based on the fact the principle that the cause of neuralgia/ spasm is due to compression of the nerve by a vessel & mvd aims at removing that compression by either altering the path of offending vessel i.e. transposition or inserting teflon/ muscle patch between the offending vessel and the nerve at the point of nvc i.e. interposition. mvd has shown excellent results in both trigeminal neuralgia and hemifacial spasms. an analysis of twenty-two papers representing 5,685 patients treated with mvd for hfs found that an average of 91.1% of patients had complete resolution of symptoms over a median 2.9year follow-up period20. another metaanalysis included 8,484 cases of tn who underwent either mvd or gamma knife and concluded that mvd is better than gkrs in treating patients with idiopathic tn, better outcomes in the mvd group is because of immediate post op pain relief&mvd should be offered as first line of surgical intervention if no contraindication for surgery21. however there are reports that even despite of good microvascular decompression there are instances of no pain relief. our study wanted to address such cases so as to improve the overall operative outcome by better preoperative evaluation of offending vessel. aim of the study to find out if computational flow dynamics (cfd) can correctly predict the offending vessel in hemifacial spasms (hfs) and trigeminal neuralgia (tn) & thus improving the outcome of mvd. materials & methods in this retrospective study we studied 13 consecutive patients who underwent mvd procedures in the year 2017. our preoperative workup included a 3d cta and 1.5 t mri including ciss & fiesta sequences. with the help of these images the point of neurovascular conflict is confirmed. once the offending vessel and point of nvc is identified, 3d cta images are used to construct cfd using hemoscope 2015 software. in the hemoscope 2015 software, once the offending vessel is isolated the two points are marked proximal and distal to the nvc and orthogonal are constructed. once this procedure is done the hemoscope 2015 software automatically measures the vessel length, inlet and outlet diameter of the vessel. once the measurements are done we choose the inlet and cfd is run on onsite mode which takes approximately ten to fifteen minutes for completing analysis. once the analysis is complete the wall pressure, wall shear stress, streamline velocity and vector at nvc which serves as test and is charted on an excel sheet. once the data is entered the entire procedure is repeated with normal contralateral vessel which serves as control and data of analysis charted on same excel sheet. similarly, the data of all 13 patients were analyzed bilaterally and charted in the excel sheet. the data was expressed in terms of percentage of the values. microvascular decompression involves patient to be in general anesthesia in lateral position with affected side up and head fixed to a sugita clamp. once the patient is meticulously prepared and draped we use a retroauricular incision and elevation of a subcutaneous flap followed by a small three by romanian neurosurgery (2018) xxxii 3: 418 425 | 421             three centimeter retro sigmoid craniotomy to expose the transverse – sigmoid sinus junction. dura is opened in a y shaped manner. the sharp arachnoid dissection is carried out on the lateral aspect of the cerebellum and csf is released from lateral cerebellomedullary cistern. once the cerebellum is lax, the cerebellum is dissected to expose the lower cranial nerve, seventh eighth complex and the trigeminal nerve. once the nerve is identified sharp dissection is carried out to expose the root entry zone (rez) of the nerve. any vessel in the path of rez is identified by dual image video angiography (diva) & endoscopy. once the offending vessel is identified mvd is carried out either by transposition or by interposition. we always advocate intraoperative nerve monitoring of v, vii & viii cranial nerves. once adequate mvd is achieved the decompression is confirmed with diva& endoscopy that no vessel is abutting the nerve at its rez. after this hemostasis is achieved and dura closed in a watertight fashion and augmented with subcutaneous tissue flap and fibrin glue. the craniotomy defect is corrected by using a mesh of appropriate size& fixed with screws. the wound is closed in three layers i.e. muscle, subcutaneous tissue and skin. postoperatively patient is followed up in terms of immediately post-surgery, one month post-surgery and three months postoperatively. the pain is graded as per barrow neurological institute (bni) pain intensity score22. score pain description i no pain, no medications ii occasional pain, no medications required iii some pain, adequately controlled with medications iv some pain, not adequately controlled with medications v severe pain or no pain relief results of the 13 patients, male: female ratio was five is to eight. the patients ranged from 47 to 77 years with a mean of 63.8 years. of the 13 patients five had hemifacial spasms while eight had trigeminal neuralgia. of the five patients with hemifacial spasms four had it on the left side while one had it on the right. of the eight patient with trigeminal neuralgia six had it on the right side while two had it on the left. on imaging, in five cases of hfs offending vessel was pica in three cases, va pica in one case and aica in one case. these vessels corresponded well to the intraoperative findings. among the eight tn patients seven had sca as the offending artery whereas one case had aica. however intraoperatively we could not find an offending vessel in one of the cases where imaging suggested an sca as an offending vessel. cfd analysis suggested that among the 13 patients, 12 patients (92.3%) had high wall pressure and ten patients (76.9%) had high wall shear stress at nvc on the affected side. however only six patients (46.1%) had high wall pressure &only two patients (15.4%) had high wall shear stress on the normal side. in the one patient we could not find the offending vessel intraoperatively the wall pressure on the cfd analysis was low however 422 | mayur et al computational fluid dynamics in trigeminal neuralgia             the wall shear stress was high. of the five patients with hemifacial spasms, four (80%) had complete relief immediately, at one month &three months follow up whereas one (20%) patient had complete relief immediately &at one month follow up but had recurrence of symptoms at three months follow up that required no treatment. of the eight patients with trigeminal neuralgia, seven (87.5%) patients had good control of pain (bni grade two or less) immediately, one month &three month follow up & required no medication at three month follow up. however one (12.5%) patient had bni grade four at three months follow up despite immediate and one month follow up bni grade of one. patient was treated by trigeminal nerve block. our results of mvd for hfs & tn were comparable with other studies20, 21. table 1 analysis of cfd in 13 patients operated for mvd in 2017 parameter test control wall pressure high 12/13 (92.3%) 6/13 (46.1%) wall pressure low 1/13 (7.7%) 7/13 (54.9%) wall shear stress high 10/13 (76.9%) 2/13 (15.4%) wall shear stress low 3/13 (23.1%) 11/13 (84.6%) table 2: worksheet. wp: wall pressure, wss: wall shear stress. io nvc: intraoperative neurovascular conflict. ip: interposition tp: transposition. tn outcomes in bni pain intensity score. in wp & wss 1 is high, 0 is low. io nvc 1 present, 0 absent romanian neurosurgery (2018) xxxii 3: 418 425 | 423             1a 1b figure 1 representative case depicting high wall pressure and high wall shear stress on affected side(a) whereas low wall pressure and wall shear stress on normal side (b)   high wall pressure & wall shear stress at nvc zone of rt sca in patient with rt tn low wall pressure and wall shear stress on lt sca in patient with rt 424 | mayur et al computational fluid dynamics in trigeminal neuralgia             discussion in day to day practice, we as neurosurgeons face plenty of dilemmas when it comes to nerve compression syndromes & mvd. though most of the patients are treated conservatively at the onset. about 10-25% of the patients develop resistance to the medications. some patients cannot tolerate the medications/ allergies. there are multiple case scenarios wherein we as neurosurgeons are not able to help our patients with their misery. we would like to quote some of the scenarios which we believe all neurosurgeons who have an experience in treating tn & hfs will relate to. case one: young patient with no comorbidities comes with history of classical trigeminal neuralgia. not responding to medicines. mri shows proximity of sca to v nerve but no conflict. patient in severe distress and wants to undergo microvascular decompression despite the fact that he still may not get relief. we operate find sca loop around the rez of v nerve. achieve good mvd. post operatively patient is pain free and has good quality of life without medicines. case two: patient elderly, with underlying heart disease on antiplatelet therapy. classical trigeminal neuralgia initially responding but now not responding to medications. mri shows ‘obvious’ nvc. patient consents for surgery. antiplatelet drugs withheld for 5 days prior to surgery after cardiology consult. on table even with extensive arachnoid dissection we fail to identify any nvc at the rez of v nerve. we handle the v nerve and come out. postoperatively patient still has pain. case three: 47 year old with left hemifacial spasms. no comorbidities. mri suggestive of va pica nvc with vii nerve. offered mvd & accepted. intraoperatively large va pica compression of vii nerve was seen. mvd achieved. patient was free of symptoms on first postoperative day but on second day post operatively symptoms recurred. all these scenarios have one thing in common. we cannot incriminate the offending vessel as the cause for the patients’ symptoms. since blood flow and dynamics within the offending vessel plays an important basis of ncs, we have turned to cfd to predict offending vessel & incriminate it for the patients’ symptoms. microvascular decompression is one of the first line of treatment in patients with failure with medications. mvd yields a good cure rates up to 90 % in cases when there is marked compression on preoperative mri1. we have in our study tried to find ways in which we could predict the offending vessel accurately thereby improving patient selection in future resulting in only selection of cases where the offending vessel seen on imaging is the cause of patients’ symptoms and offering them mvd as treatment of choice. limitations of our study include small sample size and short period of follow up. we recommend that in future a prospective study with more number of patients be done. we also recommend use of postoperative cfd to see for changes in the offending vessel after one year of complete remission of symptoms. conclusion from our results we can safely conclude that cfd canplay an important role in predicting the offending vessel in patients with romanian neurosurgery (2018) xxxii 3: 418 425 | 425             tn & hfs. however greater sample size along with longer follow up period is required. high wall pressure and wall shear stress at nvc zone are features that predict offending vessels in cases of tn & hfs. high wall shear stress along with high wall pressure was more specific than high wall pressure alone in predicting the offending vessel in tn & hfs. references 1. marc sindou, neurosurgical management of trigeminal neuralgia; essential practice of neurosurgery:2nd edition; p 1365 – 66. 2.sekula rf, jr, et al. microvascular decompression for elderly patients with trigeminal neuralgia: a prospective study & systematic review with meta-analysis. j neurosurg. 2011; 114: 172 -179. 3. trucer b, et al. microvascular decompression for primary trigeminal neuralgia: short term follow up results and prognostic factors. j korean neurosurg soc. 2012: 4247. 4. oesman c, et al. long term follow up of microvascular decompression for trigeminal neuralgia. skull base. 2011; 21: 313 – 322. 5. zhang h, et al. the long term predictors of pure microvascular decompression for primary trigeminal neuralgia. world neurosurg 2013may jun; 79(5-6): 756 – 62. 6. chang hyun oh, et al. a case of hemifacial spasm caused by an artery passing through the facial nerve. j korean neurosurg soc. march; 57(3): 221 – 224. 7. marinos kontzialis, et al. imaging evaluation of trigeminal neuralgia. j istanb univ fac dent. 2017; 51 (3 suppl 1): s62 s68. 8. https://whatis.techtarget.com/definition/computatio nal-fluid-dynamics-cfd 9. suzuki t, et al. determining the presence of thin walled regions at high pressure areas in unruptured cerebral aneurysms using computational fluid dynamics. neurosurgery. 2016 oct; 79(4): 589 -95. 10. skodvin to, et al. rupture prediction of intracranial aneurysm: a nationwide matched case-control study of hemodynamics at time of diagnosis. j neurosurg. 2017 nov 3: 1 – 7. 11. zhang y, et al. low wall shear stress is associated with the rupture of intracranial aneurysm with known rupture point: case report and literature review. bmc neurol. 2016 nov 18; 16(1): 231. 12. h. meng, et al. high wss or low wss? complex interactions of hemodynamics with intracranial aneurysm initiation, growth, and rupture: toward a unifying hypothesis. american journal of neuroradiology. july 2014, 35(7) 1254 – 1262. 13. toru satoh.technical aspects of multi-fusion imaging:nvc of trigeminal neuralgia and hemifacial spasm. j neurosurgery ahead of print. 14. zongshi qin, et al. comparative efficacy and acceptability of anticonvulsant drugs for classical trigeminal neuralgia: a bayesian network meta-analysis protocol. bmj open. 2018;8(1): e017392. 15.court je, et al. treatment of tic douloureux with a new anticonvulsant ( clonazepam). j neurol neurosurgery psychiatry 1976; 39:297 – 9. 16. yuan m, et al.efficacy & safety of gabapentin vs carbamazepine in the treatment of of trigeminal neuralgia: a meta-analysis. pain pract 2016;16:1083–91. 17. obermann m, yoon ms, sensen k, et al. efficacy of pregabalin in the treatment of trigeminal neuralgia. cephalalgia 2008;28:174–81. 18. peiris jb, perera gl, devendra sv, et al. sodium valproate in trigeminal neuralgia. med j aust 1980;2:278. 19.lu ay, et al. hemifacial spasms and neurovascularcompressionscientificworldjournal. 2014;2014:349319. 20. l. e. miller and v. m. miller, “safety and effectiveness of microvascular decompression for treatment of hemifacial spasm: a systematic review,” british journal of neurosurgery, vol. 26, no. 4, pp. 438–444, 2012. 21. ian berger, et al. microvascular decompression versus stereotactic radiosurgery for trigeminal neuralgia: a decision analysis. cureus. 2017 jan; 9(1): e1000. 22. riesenburger ri, hwang sw, schirmer cm, et al. outcomes followingsingle-treatment gamma knife surgery for trigeminal neuralgia witha minimum 3-year follow-up. j neurosurg. 2009;112(4):766-771. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 391 396 | 391 re-alignment of operated anterior odontoid screw displaced odontoid type 3 without resurgery: an unusual case report with a brief review of literature ahmed ansari department of neurosurgery, hamdard institute, jamia hamdard, new delhi, india abstract: odontoid fractures are particularly dangerous variety of cervical injury, due primarily to spinal cord trauma. in this article, we describe the re alignment of displaced operated type 3 odontoid # with anterior screw fixation with cervical traction. key words: odontoid fracture, anterior odontoid screw, traction. introduction odontoid fractures comprise 9-20% of all cervical spine fractures. (1, 2, 3, 4) many patients succumb to their injury at the time of accident due to spinal cord trauma, due to the strategic location of these fractures. (5) pain is the most common symptom, followed by neurological deficits in surviving patients. (6) nonunion and delayed myelopathy are the main problems associated with conservative management of these fractures. (7, 8) in this case report, we discuss about realignment of operated anterior odontoid screw displaced #type 3 with traction. case report a 56 year old man presented following road traffic accident after twenty-five days to us with nape of neck pain and qaudriparesis. bilateral increased tone in upper and lower limbs was noted. power in bilateral upper limbs was 3/5 and lower limbs was 4/5. a ct craniovertebral junction (figures 1 and 2) and mri cvj and cervical spine (figure 3) revealed displaced type 3 odontoid # with hyperintense signals at cvj cord with cord compression. the patient was placed on traction, which improved power in his limbs and aligned the displaced odontoid segment. anterior odontoid screw (os) fixation was performedand patient was given philadelphia collar. the patient being highly noncompliant removed his collar on post-op day 1, moving his neck violently. post-op ct cvj (figures 4, 5) revealed displaced odontoid segment. the patient reported a reduction in his limb power. he was again placed on traction, which resulted in an increase in his limb power, signifying instability. repeat radiology (figure 6) revealed alignment of # odontoid segment. he was advised posterior fixation but due to financial constraints, the patient party refused for surgery. he was given four post cervical collar for the stabilisation of # odontoid, after a few days of traction. 392 | ansari re-alignment of operated anterior odontoid screw displaced figure 1 sagittal ct images showing displaced odontoid # type 3 figure 2 coronal ct images showing type 3 odontoid figure 3 sagittal mri image showing cord hyperintense signals with compression figure 4 sagittal ct image showing displaced odontoid segment following anterior os fixation figure 5 coronal ct image following anterior os fixation romanian neurosurgery (2016) xxx 3: 391 396 | 393 figure 6 x-ray cvj with aligned odontoid # segment following anterior os fixation with post op traction discussion goel a., (9) compared odontoid with a typical kolkata hand rickshaw puller. the weight of the entire rickshaw is on the two wheels, and the rickshaw puller primarily has to guide and direct the vehicle without bearing any weight on himself. he can run with the rickshaw for kilometers without feeling any weight on his shoulders. the rickshaw puller may be an old man or may even be injured, but can still carry on his work. this is essentially because the entire weight of the rickshaw is on the two wheels that are also the primary site of movement. moreover, the rickshaw will lose its direction, movement, and even its stability if there is no rickshaw puller or if the rickshaw puller is unable to stand on his feet. on similar lines, the facets are the only true joints in the entire spine. the odontoid process and the intervertebral discs have similar roles of assisting or guiding and providing a purpose to the movements that are initiated and completed in the facets. the concept in the treatment of odontoid fracture is based on the premise that if the odontoid process is injured such that the spinal alignments have altered and dynamic images show evidence of instability, the surgery has to aim at providing stability to the region by fixation of the facets. anderson and d'alonzo (1974) (10) have classified odontoid fractures into type i, ii and iii. based on this universally accepted classification, the type ii and iii odontoid fractures often require some form of stabilization. (11, 12) however the optimum treatment strategy on whether to perform surgery or to continue the patient on conservative management is still mired in controversy. (6, 13, 14) the surgical approaches prevalent for dealing with acute odontoid fractures include either an anterior odontoid screw (os) placement or a posterior fixation (pf). (15, 16, 17, 18, 19) conservative management using a halo brace is associated with variable fusion rates between 53-93%. the associated morbidity is related to its prolonged usage in a recumbent patient. (1, 20, 21) we gave the patient four post cervical collar, as he was highly irritable and non-compliant with halo brace. shetty et al. (22) demonstrated an 84.2% fusion rate with conservative management in stable type ii fractures. literature shows that there is a growing trend towards surgical fixation of these fractures as fusion rates are better and 394 | ansari re-alignment of operated anterior odontoid screw displaced the patients may be mobilized early. (23, 24) anterior os fixation was initially described by nakanishi (17) and bohler (1982). (18) this procedure allows for a more physiological fusion by direct osteosynthesis of the fracture lines and has the advantage of preserving normal rotation at the atlanto-axial joint. many authors have recommended pf as the procedure of choice for the surgical approach in type iia and type iii fractures due to a slightly higher non-union rate associated with os fixation. moon et al., (25) fountas et al., (26) and lee et al. (27) in their series showed fusion rates of 100%, 87%, and 96%, respectively. bhanot et al. (28) reported a 94% fusion rate with one case of non-union and one screw pull-out in their series of 17 type ii odontoid fractures after an anterior screw fixation. shrinivasan et al. (29) could successfully place os in 84.6% type ii fractures with an 82% fusion rate. apfelbaum (2000) (16) and dantas (2002) (30) have advised against the placement of anterior os in fractures with an anterior oblique fracture line due to the high nonunion rates. whenever the angle of the odontoid fracture line is less oblique and screw trajectory across the fractured segments is achievable, os fixation should be the first line management option as it provides for better functional results. sawarkar dp et al, (31) reported a 100% fusion rate with magerl`s technique. this technique may be used as a stand-alone procedure or may be supplemented with a c1c2 sub-laminar wiring. addition of sublaminar wiring, however, did not change results of this technique in our series. this procedure is technically difficult and requires a steep upward trajectory. the three-point rigid fixation and cost-effectiveness of the procedure is responsible for its popularity. the goel/harms technique of c1-c2 fixation is more versatile when compared to the former procedure. they reported fusion rates of 100% in the 14 patients who underwent this form of fixation. there is, however, a risk of 1.3-5.8% (more with magerl technique) of vertebral artery injury in posterior fusion procedures. (32) the biomechanical strength of this fixation is also less than ideal as compared to the magerl or goel/harms procedure (that provides a strong rotational stability). (20) therefore, the c1-c2 sublaminar wiring technique should be used as the last resort. goel et al (33, 34, 35, 36, 37) prefers posterior lateral mass fixation in all cases where surgical treatment for fractured odontoid process is contemplated. the dictum should be that whenever one is in doubt about the stability, one should fix it. any evidence of instability of the region should point at malfunctioning of the facets and the need for fixation. and when one attempts to fix the region, the most versatile and proven method of fixation should be employed. if the surgery is contemplated, it should not be a semifinal surgery; it should be of the type that will result in fixation and fusion of the region. any surgery in the region is major and should be done with all preparedness and precautions. although attempts to fuse the fractured odontoid process and to retain the movements at the facet joints can be successful in some cases, he resorts to fixation-arthrodesis of the atlantoaxial joint and settle the score once and for all. romanian neurosurgery (2016) xxx 3: 391 396 | 395 correspondence dr. ahmed ansari assistant professor, department of neurosurgery, hamdard institute, jamia hamdard, new delhi, india. e-mail: ahmed.ansari2@gmail.com phone: +91-9997456045 references 1. hadley mn, browner c, sonntag vk. axis fractures: a comprehensive review of management and treatment in 107 cases. neurosurgery 1985;17:281-90. 2. ryan md, henderson jj. the epidemiology of fractures and fracture dislocations of the cervical spine. injury 1992;23:38-40. 3. grauer jn, shafi b, hilibrand as, harrop js, kwon bk, beiner jm, et al. proposal of a modified, treatmentoriented classification of odontoid fractures. spine j 2005;5:123-9. 4. rao g, apfelbaum ri. odontoid screw fixation for fresh and remote fractures. neurol india 2005;53:416-23. 5. bucholz rw, burkhead wz, graham w, petty c. occult cervical spine injuries in fatal traffic accidents. j trauma 1979;19:768-71. 6. rizvi sa, fredø hl, lied b, nakstad ph, rønning p, helseth e. surgical management of acute odontoid fractures: surgery-related complications and long-term outcomes in a consecutive series of 97 patients. j trauma acute care 2012;72:682-90. 7. moskovich r, crockard ha. myelopathy due to hypertrophic nonunion of the dens: case report. j trauma 1990;30:222-5. 8. crockard ha, heilman ae, stevens jm. progressive myelopathy secondary to odontoid fractures: clinical, radiological, and surgical features. j neurosurg 1993;78:579-86 9. goel a. treatment of odontoid fractures. neurol india 2015 ;63:7-8 10. anderson ld, d'alonzo rt. fractures of the odontoid process of the axis. j bone joint surg am 1974;56:1663-74. 11. hadley mn, browner cm, liu ss, sonntag vk. new subtype of acute odontoid fractures (type iia). neurosurgery 1988;22:67-71. 12. roy-camille r, saillant g, judet t, de botton g, michel g. factors of severity in the fractures of the odontoid process (author's transl). rev chir orthop reparatrice appar mot 1980;66:183-6. 13. shears e, armitstead cp. surgical versus conservative management for odontoid fractures. cochrane database syst rev 2008:cd005078. 14. ryken t, hadley m, aarabi b, dhall s, gelb d, hurlbert j, et al. management of isolated fractures of the axis in adults. neurosurgery 2013;72:132-50. 15. aebi m, etter c, coscia m. fractures of the odontoid process. treatment with anterior screw fixation. spine (phila pa 1976) 1989;14:1065-70. 16. apfelbaum ri, lonser rr, veres r, casey a. direct anterior screw fixation for recent and remote odontoid fractures. j neurosurg 2000;93:227-36. 17. nakanishi t. internal fixation of the odontoid fracture. cent jpn j orthop trauma surg 1980;23:399406. 18. bohler j. screw-osteosynthesis of fractures of the dens axis (author's transl). unfallheilkunde 1981;84:221-3. 19. bohler j. anterior stabilization for acute fractures and non-unions of the dens. j bone joint surg am 1982;64:1827. 20. julien td, frankel b, traynelis vc, ryken tc. evidence-based analysis of odontoid fracture management. neurosurg focus 2000;8:e1. 21. polin rs, szabo t, bogaev ca, replogle re, jane ja. nonoperative management of types ii and iii odontoid fractures: the philadelphia collar versus the halo vest. neurosurgery 1996;38:450-6. 22. shetty a, kini ar, prabhu j. odontoid fractures: a retrospective analysis of 53 cases. indian j orthop 2009;43:352-60. 23. smith he, vaccaro ar, maltenfort m, albert tj, hilibrand as, anderson dg, et al. trends in surgical management for type ii odontoid fracture: 20 years of experience at a regional spinal cord injury center. orthopedics 2008;31:650. 24. nourbakhsh a, shi r, vannemreddy p, nanda a. operative versus nonoperative management of acute odontoid type ii fractures: a meta-analysis. j neurosurg spine 2009;11:651-8 25. moon ms, moon jl, sun dh, moon yw. treatment of dens fracture in adults: a report of thirty-two cases. bull hosp jt dis 2006;63:108-12. 396 | ansari re-alignment of operated anterior odontoid screw displaced 26. fountas kn, kapsalaki ez, karampelas i, feltes ch, dimopoulos vg, machinis tg, et al. results of long-term follow-up in patients undergoing anterior screw fixation for type ii and rostral type iii odontoid fractures. spine (phila pa 1976) 2005;30:661-9. 27. lee sc, chen jf, lee st. management of acute odontoid fractures with single anterior screw fixation. j clin neurosci 2004;11:890-5. 28. bhanot a, sawhney g, kaushal r, aggarwal ak, bahadur r. management of odontoid fractures with anterior screw fixation. j surg orthop adv 2006;15:38-42. 29. srinivasan us, dhillon cs, mahesha k, kumar v. anterior single lag screw fixation in type ii dens fracture -indian experience. int j neurotrauma (ijnt) 2008;5:8791. 30.dantas fl, prandini mn, caires ac, fonseca ga, raso jl. management of odontoid fractures using anterior screw fixation: analysis of 15 cases. arq neuropsiquiatr 2002;60:823-9. 31. sawarkar d, singh p, siddique s, agrawal d, satyarthee g, gupta d, et al. surgical management of odontoid fracture at level one trauma center: a singlecenter surgical series of 142 cases. neurol india 2015;63:40-8. 32. steltzlen c, lazennec jy, catonné y, rousseau ma. unstable odontoid fracture: surgical strategy in a 22-case series, and literature review. orthop traumatol surg res 2013;99:615-23. 33. goel a, laheri v. plate and screw fixation for atlantoaxial dislocation. (technical report). acta neurochir (wien) 1994;129:47-53. 34. goel a, desai k, muzumdar dp. atlantoaxial fixation using plate and screw method: a report of 160 treated patients. neurosurgery 2002;51:1351-7. 35. goel a. treatment of basilar invagination by atlantoaxial joint distraction and direct lateral mass fixation. j neurosurg spine 2004;1:281-6. 36. goel a, shah a. reversal of longstanding musculoskeletal changes in basilar invagination after surgical decompression and stabilization. j neurosurg spine 2009;10:220-7. 37.goel a. screws, facets and atlantoaxial instability. world neurosurg 2013;80:514-5. microsoft word 16stanhconsideration.doc 122 romanian neurosurgery (2010) xvii 1: 122 124 consideration on hemicraniectomy – part ii h. stan, b. suciu, al. iosif, adriana cocis departament of neurosurgey, medical university of cluj abstract decompressive hemicraniectomy is a surgical technique used to relieve the increased intracranial pressure. the aim of the current paper is to present our surgical technique and experience used in performing hemicraniectomies, technique that we consider optimal for his purpose. our experience consists in 17 operated cases and eleven patients (64.7%) were long term survivors. keywords: decompressive hemicraniectomy, increased intracranial pressure, surgical technique consideration on hemicraniectomy, part i was published in volume xvi, no. 1/2009 of romanian neurosurgery we presented our experience in the field and discussed clinical aspects, indication and outcomes. the part ii of this paper comes to detail our surgical technique with images. surgical technique considerations the patient is placed with the side of craniotomy upward, head elevated to 15 degrees. the line of skin incision is described from posterior to anterior: beginning retro-auricular (to the mastoid), extended in a supero-posterior manner and than reversed to anterior approximately 2 cm parallel to the sagittal line until the widow peak, then reversed infero-basal, respecting the hair line to the preauricular region (figure 1). care must be taken to preserve the principal ramifications of temporary artery inside de musculocutaneous flaps to avoiding devascularisation and necrosis of the incision edge. a large periosteal tissue flap is harvested from the entire exposed area for ulterior duroplasty (figure 2). using a monopolar subperiostal dissection the temporalis muscle is reflected basally. the margins and burr holes for hemicraniectomy, described from anterobasal to posterior are: temporobasal, under the level of ear pina; pterional at the site of the classic keyhole; fronto-basal, above the level of frontal sinus, to expose frontal pole but avoid entry in the frontal air cells sinus; then along the planned paramedial craniectomy margin, 2 cm parasagittal (avoid lesions over saggital sinus bridging veins and arachnoid’s granulations), to lambda point; then antero-basal, tangent with lambdoid suture, until 1 cm above the asterion (to avoid lacerations of transverse-sigmoid sinus) (figure 3). the sphenoid wing is fractured and removed. decompression was extended far enough to the floor of the middle fossa to relieve pressure from the herniating mediobasal temporal lobe and up to the midline to h. stan et al consideration on hemicraniectomy 123 avoid compression of the bridging veins (1-2 cm) (1). the cranial vault is removed. dura is opened by a large radial incision to allow the brain to expand outward (figure 4) (2). prophylactic, if the intracranial pressure is not elevated, dural edges are tacked up to bony margins. large duraplasty with extra space for brain to enlarge, using all periostal tissue from the cranial vault is performed (figure 5). it is important that the duroplasty to have a “sun flower shape”, to permit free enlargement of the brain without damaging the cortical substance. the temporalis muscle is resting on the dural surface. extradural drain is placed. cutaneous flap is sutured in one plane in a donati manner. figure 1 the patient is placed within the side of craniotomy upward, head elevated to 15 degree. the line of skin incision is described from posterior to anterior: beginning retro-auricular (to the mastoid), extended in a supero-posterior manner and than reversed to anterior approximately 2 cm parallel to the sagittal line until the widow peak, then reversed infero-basal, respecting the hair line to preauricular region. to avoid necrosis of the skin incision edge, care must be tacked to preserve the principal ramifications of temporary artery inside de musculocutaneous flaps. figure 2 an large periosteal tissue flaps is recoltated for ulterior duroplasty figure 3 the temporalis muscle is reflected basally. the margins and keyhole for hemicraniectomy, described 124 romanian neurosurgery (2010) xvii 1: 122 124 from anterobasal to posterior are: temporo-basal, under the level of ear pina; pterional aproximatively at the site of the classic keyhole; fronto-basal, above the level of frontal sinus, to expose frontal pole but avoid entry in the frontal air cells sinus; then along the planned paramedial craniectomy margin, 2 cm parasagittal (avoid lesions over saggital sinus and bridging vains), until lambda point; than antero-basal, tangential with lambdoid suture, until aproximatively 1 cm above the asterion (to evoid entry in transversesigmoid sinus). figure 4 the dura is opened by a linear incision extended radial to allow the brain to expand outward. figure 5 large duroplasty with extra space for brain to enlarge, using all periostal tissue recoltated from the cranial vault is made. references 1.hemicraniectomy with dural augmentation in medically uncontrollable hemispheric infarction. christian rainer wirtz, m.d., thorsten steiner, m.d., alfred aschoff, m.d., ph.d., stefan schwab, m.d., holger schnippering, m.d., hans herbert steiner, m.d., werner hacke, m.d., ph.d., and stefan kunze, m.d., ph.d. neurosurgical focus 2(5): article 3, 1997. 2.surgery for brain edema. peter hutchinson, f.r.c.s.(sn), ivan timofeev, m.r.c.s., and peter kirkpatrick, f.r.c.s.(sn). neurosurg focus 22 (5):e14, 2007 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article conus intramedullary pyogenic abscess in a 4years old child: a rare case report and review of literature prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmad faran india doi: 10.1515/romneu-2017-0090 568 | prasad et al conus intramedullary pyogenic abscess in a 4years old child doi: 10.1515/romneu-2017-0090 conus intramedullary pyogenic abscess in a 4years old child: a rare case report and review of literature prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmad faran department of neurosurgery, dr rml ims lucknow uttar pradesh, india abstract: intramedullary pyogenic abscess in the conus medullaris in a young child is an extremely rare condition. it had never been reported in literature. it should be differentiated from other more common pathology like tubercular abscess, dermal sinus, epidermoid and dermoid tumour. early diagnosis and prompt surgical evacuation may lead to good neurological recovery from this rare benign pathology. key words: conus medullaris, intramedullary, pyogenic absess, children introduction intramedullary abscess especially in conus region is an extremely rare condition, only few cases reported in the literature. most of the reported cases shows that these abscess are mainly due to tubercular pathology [1, 2, 3, 4, 5, 6]. some of the reported cases shows that congenital dermal sinus and epidermoid cyst also causes abscess in this region. we report that what we believe to be the first instance of its occurrence within the conus medullaris in a young child. this case study shows the salient clinical, etiopathogenesis, and radiologic features. we also discuss management of this rare entity and review the pertinent literature to the best of the authors’ knowledge, an intramedullary conus pyogenic abscess especially in young child had never been reported in literature. case report a 4 years old female child presented to ous with complain of weakness of both lower limb from last 4month and urinary incontinence, difficulty in walking and intermittent fever from last 1month. patient was taking antibiotic for last 15 days. on examination patient was conscious and oriented. bulk was normal and tone was increased in both lower limb. her power was 3/5 at hip, knee and ankle joint bilaterally. knee and ankle reflex was +3 and there was no clonus. her sensation was diminished in both lower limb below l1 dermatome. there was no any cutaneous stigmata of spinal dysraphism. patient was evaluated with contrst mri dorsolumbar spine with screening of whole spine. on mri t2wi shows well circumscribed, hyperintense, cystic mass at d11 to l1 region. contrast mri shows romanian neurosurgery (2017) xxxi 4: 568 571 | 569 peripheral enhancement of the lesion. patient was planned for surgery. in surgery d11 to l1 laminectomy was done. there was no any dural adhesion or arachnoiditis. a small midline myelotomy done at most bulged part of cord. on myelotomy frank creamy colour pus was coming out. suction irrigation of the cavity was done. pus was sent for afb staining, culture sensitivity and for tb pcr. afb and tb pcr was negative for tuberculosis and no any organism was found on culture. post operatively patient was given antibiotic for 4 weeks. patient improve gradually and she can stand and walk with support. a b c figure 1a mri t2wi of dorsolumbosacral spine, saggital section showing wellcircumscribed, hyperintense lesion at d11-l1 figure 1b contrast mri of dorsolumbosacral spine, saggital section showing peripheral enhancement of the lesion figure 1c contrast mri of dorsolumbosacral spine, coronal section showing peripheral enhancement of the lesion a b figure 2a mri t2wi of dorsolumbosacral spine, axial section showing wellcircumscribed, hyperintense,cystic lesion figure 2b contrast mri of dorsolumbosacral spine, axial section showing peripheral enhancement of the lesion discussion intramedullary spinal cord pyogenic abscess at young age is extremely rare. on reviewing the literature we found that no case of intramedullary pyogenic abscess in conus medullaris was reported in children. only two such case of intramedullary pyogenic abscess in conus medullaris was reported in adult [7,8]. most of the other reported cases of intramedullary abscess in conus medullaris was mostly a tuberculoma or a tuberculous abscess. intramedullary abscess in conus medullaris may be due to bacterial infection, tuberculosis,dermal sinus and or due to 570 | prasad et al conus intramedullary pyogenic abscess in a 4years old child dermoid and epidermoid cyst. there was no history of any tubercular contact, any focus of tuberculosis in the body. intraoperatively there was absolute lack of either dural or arachnoidal adhesions around the conus. this was at variance with the findings of dense arachnoidal adhesions surrounding the involved intramedullary segment noted bymost authors reporting an intramedullary tuberculous abscess [1,6]. on pathological examination tb pcr was negative and no acid fast bacilli was seen on afb staining .so we have ruled out a tubercular abscess in our case. in our case there was no any dermal sinus or dermoid and epidermoid tumour. no history of cutaneous stigmata of spinal dysraphism. intraoperatively frank pus of cream colour was found which suggest pyogenic etiology. although no microorganism was detected on culture sensitivity test.most likely it was due to use of preoperative antibiotics. although the pathogenesis of this primary conus abscess was unknown. a complex sequence of events may have led to the genesis of conus pyogenic abscess. hematogenous spread of bacteria (which was present in subclinical state) obstructed an end artery in the cord substance causing ischemic necrosis.further expansion of the liquid content occurred through osmosis via the virchow robinson spaces within the cord producing the pyogenic abscess. although the conus intramedullary abscess was a rare entity. most of the reported cases of conus intramedullary abscess was due to tuberculosis. conus intramedullary pyogenic abscess was extremely rare condition, only two such case was reported in adult. no such case was reported in children. other pathology causing intramedullary abscess in conus medullaris were also reported in literature. m.f. hassan et al. [7] reported intramedullary pyogenic abscess in the conus medullaris in adult. j lee et al [8] reported nocardia cyriacigeorgica abscess of the conus medullaris in an immunocompetent host. bs koppel et al [9] reported intramedullary abscess in conus medullaris due to dermal sinus.rs mauricewilliums et al. [10] reported intramedullary abscess in conus medullaris due to epidermoid cyst. conclusion to the best of our knowledge, an intramedullary pyogenic abscess located within the conus medullaris in a young child are extremely rare. no such case was reported in the literature. early diagnosis and treatment leads to improved recovery of this rare benign pathology. correspondence dr. hanuman prasad prajapati address: department of neurosurgery, dr rml ims lucknow uttar pradesh (india) mobile no.: 07727934104 email: pushpa84.dhp@gmail.com references 1. cheng km, ma mw, chan cm, leung cl: tuberculous intramedullary spinal cord abscess. acta neurochir (wien) 139:1189-1190, 1997. 2. courson b, brunel m, petit m, tondut a: intramedullary tubercular abscess. bull soc med afr noire lang fr 13:500-503, 1968. 3. devi bi, chandra s, mongia s, chandramouli ba, sastry kv, shankar sk: spinal intramedullary romanian neurosurgery (2017) xxxi 4: 568 571 | 571 tuberculoma and abscess: a rare cause of paraparesis. neurol india 50:494-496, 2002. 4. hanci m, sarioglu ac, uzan m, i°lak c, kaynar my, oz b: intramedullary tuberculous abscess: a case report. spine (phila pa 1976) 21:766-769, 1996. 5. hoda mf, prasad r, singh vp, maurya p, singh k, sharma v: spinal intramedullary tubercular abscess. indian j tuberc 52:211-214, 2005. 6. tacconi l, arulampalam t, johnston fg, thomas dg: intramedullary spinal cord abscess: case report. neurosurgery 37:817-819, 1995. 7. hasan mf, mohamed mb,kalsi.p, sinar ej,bradey n: intramedullary pyogenic abscess in the conus medullaris.br j neurosurg. 2012 feb;26(1):118-9. 8. lee j, whitby m, hall bi: nocardia cyriacigeorgica abscess of the conus medullaris in an immunocompetent host. j clin neurosci. 2010 sep;17(9):1194-5. 9.koppel bs, daras m, duffy kr: intramedullary spinal cord abscess. neurosurgery 1990;26:145-6. 10.maurice-williams rs,pamphilon d,coakham hb. intramedullary abscess-a rare complication of spinal dysraphism. j neurol neurosurg psych 1980;43:1045-8. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article intracranial actinomycosis: case report and review of literature alfonso pacheco-hernandez, jorque aquino-matus, willem guillermo calderon-miranda, jean carlos pinto-angarita, ronsangela ramirez-barranco, katherine gomez-barragan, ernesto jose rocha-reyes, marco antonio blancas-rivera, zyanya patricia carbajal menes, paulo cesar puac polanco, guru dutta satyarthee, luis rafael moscote-salazar colombia, mexico, usa, india doi: 10.1515/romneu-2017-0042 248 | pacheco-hernandez et al intracranial actinomycosis doi: 10.1515/romneu-2017-0042 intracranial actinomycosis: case report and review of literature alfonso pacheco-hernandez1, jorque aquino-matus2, willem guillermo calderon-miranda2, jean carlos pinto-angarita1, ronsangela ramirez-barranco1, katherine gomez-barragan1, ernesto jose rocha-reyes1, marco antonio blancas-rivera2, zyanya patricia carbajal menes3, paulo cesar puac polanco4, guru dutta satyarthee5, luis rafael moscote-salazar1 1universidad de cartagena, cartagena de indias, colombia 2universidad nacional autonoma de mexico, mexico city, mexico 3hospital general dr. manuel gea gonzález; national autonomous university of mexico school of medicine, mexico city, mexico 4neuroradiology section, department of radiology, university of north carolina school of medicine, usa 5department of neurosurgery, neurosciences centre, all india institute of medical sciences, new delhi, india abstract: actinomycosis infection is a slow progressing disease, in which involvment of the central nervous system by actinomyces israelii is uncommon (less than 5%). clinical picture is non-specific and is often misdiagnosed with neoplasia; some clinical clues my arise suspicion. the case of a 59 year-old female is reported who presented headache and focal neurologic signs and in whom a out-of the hospital diagnosis of a neuroepitelial dysembryoplastic tumor was made; nonetheless after careful interview and physical exploration, a spectroscopy magnetic resonance of the brain and hystopathological description of the lesion was made and yielded the definitive diagnosis of intracranial actinomyces infection. treatment and progression were uneventful. key words: actinomycosis, intracraneal, infection, brain, abscess, tumor introduction actinomycosis is a slow progression infection caused by filamentous microaerophilic anaerobic gram positive bacteria from the family actinomycetaceae (1). it has been supposed to be similar to fungi for the similarity in ramification and the formation of a mycelial net; nonetheless the presenece of muraminic acid in the cellular wall and the absence of a nuclei attached to the romanian neurosurgery (2017) xxxi 2: 248 252 | 249 cellular membrane, clearly differentiate them into prokaryotic bacteria (schizomycetes) closely related to mycobacteria. (2). the most common species from the actinomycetes gender are: nocardia, streptomyces and actinomyces; being a. israelii the common among them. (3) actinomycosis is a relatively rare infection that occurs 1 in 300,000 persons per year. men are affected three times more than women (3). the clinical picture and radiologic findings are unspecific, and are similar to any pyogenic abscess (4). actinomycosis infection to the central nervous system is generally secondary to hematogenous disemmination from the primary infection in the lung, abdomen, pelvis or by continuity in a cervical, oral or facial infection, since it is closely related to mycobacteria in the mouth and gastrointestinal tract (5-9). since infection to the cns is not common, it may be misdiagnosed with a cerebral neoplasia (1). therefore, we report the case of a 59 years-old female with csn actinomycosis in the national institute of high technology at monteria, colombia. case presentation a 59 years-old female with past medical history of hypertension under treatment with losartan, type 2 diabetes mellitus under treatment with homeopathy, and previously heavy smoker who had been admitted in the past 6 months with holocraneal headache resistant to analgesics and associated with nausea, vomiting, and loss of vision in the left eye, temporospatial disorientation and blurred speech. she was admitted on may 2016 with an occupying lesion in the brain and a gadolinium-enhanced magnetic resonance imaging (mri) suggested a dysembryonic neuroepithelial tumor (dnet). (figures 1 a and b). a spectroscopy mri reported a lowsignal poorly defined lesion in t1 sequence and high-signal in t2 sequence compromising the amygdala, hippocampus, uncus, left thalamus in its posterior portion and extending to the left occipitotemporal and inferior temporal gyrus. additionaly, some contrast enhanced nodular foci were seen. spectroscopy study reported high levels of choline, creatine and low levels of nacetylaspartate. she underwent a craniectomy with resection of the 100% of the lesion by a left partial temporal lobectomy. postoperative head ct scan reported a hypodensity in the surgical bed with a small left pericapsular hematoma and no mass effect. she persisted disoriented but with no neurological deficit. she was discharged at the 6th day after surgery. nonetheless, she was readmitted and in the er she was found with a cgs 9 points (e2 v2 m5), reactive pupils, right hemiparesis and ipsilateral pyramidal syndrome. brain ct scan was unremarkable and histopathological studies from previous surgery resection were obtained and reported reactive inflammatory changes in glia, mononuclear infiltrate in the perivascular space, mononuclear infiltrate and neuropil edema with presence of filamentous structures compatible with chronic encephalitis corresponding to cerebral actynoimicosis. laboratory workup reported leukocytes in 15.8x10^9/l and sodium in 125 meq/l, which explained neurological deficit that recovered after sodium iv reposition over the next 48 hours. antibiotic therapy was 250 | pacheco-hernandez et al intracranial actinomycosis initiated with penicillin g 2 million iv qid for 10 days followed by penicillin vk 2 grams po/day for 6 months. evolution was uneventful but persisted with temporo-spatial disorientation. a b figures 1 a and b brain irm showing a low-signal poorly defined lesion in t1 sequence and high-signal in t2 sequence compromising the amygdala, hippocampus, uncus, left thalamus in its posterior portion and extending to the left occipitotemporal and inferior temporal gyrus discussion actinomycosis is an infrequent and slow progression infection which originates partially from the normal buccal flora. a crucial step in the development of the infection is the loss of the mucosal barrier. (10) actinomycosis usually produces acute purulent infections which confluent foci may form cavities and cause chronic abscesses. metastasis seldom occurs and it is favored by hematogenous dissemination. (11) sites of infection are in the head and neck (50%), abdomen (20%), thorax (15%), pelvis, heart and brain (15%). central nervous system infection is rare and it occurs in less than 5% of cases. pathogenesis is believed to occur as a direct invasion from head and neck tissues, as well as lower mandible, ears and paranasal sinus, through the fascia and extending through the skull base and meninges. other mechanisms postulated are the perineural extension through the intervertebral spaces and hematogenous dissemination. (3) in cerebral actinomycosis, common clinical features are headache and focal neurological signs (12), and symptoms may be present for a long time and fever may not occur. infection present as brain abscess (67%), meningitis and meningoencephalitis (13%), actinomycoma (7%), epidural or subdural space infection (7%) (13). a distinctive characteristic of cerebral actinomycosis is a chronic indolent phase with presence of solitary or multiple lesions. therefore, diagnosis requires a high clinical suspicion, relying on the chronicity, slow progression, characteristic features on brain romanian neurosurgery (2017) xxxi 2: 248 252 | 251 imaging and refractory/recurrent natural history. (11) nonetheless, actinomyces are underestimated bacteria as cause of infections, and therefore are underdiagnosed. (11) cns actinomycosis must be suspected in patients with previous history of actinomycosis in other sites and presenting with long duration of neurologic symptoms with or without fever. common risk factors include hiv infection, aids, dental procedures, history of head, gastrointestinal, otorhinolaryngologic surgery, cyanotic congenital heart disease and use of intrauterine devices. (6, 13, 14) brain imaging is not helpful into differentiate among other infectious and noninfectious diseases; ct scan or mri may report a irregular o nodular ring-shaped thick wall lesion. (15) ct scan identifies cerebral and cerebellum abscesses which are generally solitary but may be multiple (in combination with a granulomas) and present homogeneous enhancement with a thick wall and perilesional edema (16). mri identifies better lesion in the subdural space, cavernous sinus and inner ear canal in patients with acute purulent meningitis. spectroscopy mar reveal elevation in amino acids, acetate and succinate. (17) there is no serologic or skin test available. microbiologic identification of actinomyces may take up to 3 weeks and has low in sensibility. (18) in cases where culture is positive, the most commonly found associated with cns infection is a. israelii; other species found are a. naeslundii which may cause subdural empyema and a. viscosus (10-21). therefore, diagnosis is usually made with histopathological studies. actinomyces is identified by an outer zone of granulation tissue, a purulent core with azurophilic granules measuring 1-2 mm (associated with a calcium phosphate compounds), and fibrotic walls surrounding a neutrophilic infiltrate. (17). differential diagnosis includes tuberculosis, fungi, nocardiosis, other germs and neoplasia. (11) successful treatment requires drainage of the primary abscess followed by systemic antibiotics. surgical debridement should be aggressive with complete resection of the capsule. (11) penicillin remains the drug of choice but at high doses and during a long course (6 to 12 months). (22). penicilin g (1824 miu/day divided in 6 doses) for 4 to 6 weeks is followed by penicillin vk (1-2 grams/day divided in 4 doses); alternatively, amoxicilin (1.5 grams/day divided in 3 doses for 6 to 12 months) may be used. individualized treatment is always mandatory. other antibiotics that have showed efficacy but with limited experience are imipenen, ceftriaxone, and ciprofloxacin. antibiotics as metronidazole, thrimetoprimsulfametoxazole, ceftazidime, oxacilin, amynoglucosides and fluoroquinolones are not effective but may be used in polymicrobial infections according to antibiotic sensitivity tests. (22) a long course of antibiotic therapy must be completed to assure eradication of infection. treatment must be individualized and if extended beyond clinical remission, risk of recurrence is minimized. ct and mri should be used to monitor treatment response. (22) 252 | pacheco-hernandez et al intracranial actinomycosis references 1. bello y. e, ojeda p, mosquera o. a, martínez f, lozano a. j. actinomicosis del sistema nervioso central: presentación de caso. rev colomb radiol. 2013; 24(4): 3827-31. 2. tsai ms, tarn jj, liu ks, chou yl, shen cl. multiple actinomyces brain abscesses: case report. j clin neurosci off j neurosurg soc australas. 2001 mar;8(2):183–6. 3. van dellen jr. actinomycosis: an ancient disease difficult to diagnose. world neurosurg. 2010 sep;74(23):263–4. 4. riesgo p, orozco m, piquer j, cortés f, botella c, navarro j, cabanes j. absceso cerebral actinornicótico: caso clínico. neurocirugía 1996; 7: 230-234. 5. ewald c, kuhn s, kalff r: pyogenic infections of the central nervous system secondary to dental affections. a report of six cases. neurosurg rev 29:163167, 2006. 6. nithyanandam s, d’souza o, rao ss, battu rr, george s: rhinoorbitocerebral actinomycosis.ophthal plast reconstr surg 17:134-136, 2001. 7. salvati m, ciappetta p, raco a, artico m, artizzu s. primary intracranial actinomycosis. report of a case and review of the literature. zentralblatt für neurochir. 1991;52(2):95–8. 8. corbin d, solaro l, flint g, williams ac: actinomycotic brain abscess following abdominal suppuration. j neurol neurosurg psychiatry 50:1705 1706, 1987. 9. trutnovsky g, tamussino k, reich o: short-term antibiotic treatment of pelvic actinomycosis. int j gynaecol obstet 101:203-204, 2008. 10. roth j, ram z. intracranial infections caused by actinomyces species. world neurosurg. 2010 sep;74(23):261–2. 11. akhaddar a, elouennass m, baallal h, boucetta m. focal intracranial infections due to actinomyces species in immunocompetent patients: diagnostic and therapeutic challenges. world neurosurg. 2010 sep;74(23):346–50. 12. akhaddar a, elmostarchid b, boucetta m. primary subdural empyema after spontaneous vaginal delivery. surg infect. 2009 aug;10(4):363–4. 13. smego ra, jr: actinomycosis of the central nervous system. rev infect dis 9:855-865, 1987. 14. olah e, berger c, boltshauser e, nadal d. cerebral actinomycosis before adolescence. neuropediatrics. 2004 aug;35(4):239–41. 15. soto-hernández jl, morales va, lara giron jc, balderrama bañares j: cranial epidural empyema with osteomyelitis caused by actinomyces, ct, and mri appearance. clin imaging 23:209-214, 1999. 16. adeyemi oa, gottardi-littell n, muro k, kane k, flaherty jp. multiple brain abscesses due to actinomyces species. clin neurol neurosurg. 2008 sep;110(8):847–9. 17. wang s, wolf rl, woo jh, wang j, o’rourke dm, roy s, et al. actinomycotic brain infection: registered diffusion, perfusion mr imaging and mr spectroscopy. neuroradiology. 2006 may;48(5):346–50. 18. desai a, lollis ss, missios s, radwan t, zuaro de, schwarzman jd, duhaime ac: how long should cerebrospinal fluid cultures be held to detect shunt infections?. clinical article. j neurosurg pediatr 4:184 189, 2009. 19. bebrova e, lochmann o, tichy m, nyc o: actinomyces viscosus in subdural empyema. epidemiol mikrobiol imunol 43:21-22, 1994. 20. jamjoom ab, jamjoom zab, al-hedaithy ss: actinomycotic brain abscess successfully treated by burr hole aspiration and short course antimicrobial therapy. br j neurosurg 8:545-550, 1994. 21. hirai t, nunoya t, azuma r: actinomycosis of the brain and temporal bone in a goat. j vet med sci 69:641643, 2007. 22. brook i. actinomycosis: diagnosis and management. south med j. 2008 oct;101(10):1019–23. romanian neurosurgery (2019) xxxiii, 1: 87-89 doi: 10.33962/roneuro-2019-018 www.journals.lapub.co.uk/index.php/roneurosurgery introduction of triage. an experience of a triage nurse in a tertiary centre in japan shinobu tsuge1, takahiro shinagawa1, kumi hara2, akio aihara3 1 icu nurse, icu fujita health university, banbuntane houtokukai hospital, nagoya, japan. 2 icu head nurse, icu fujita health university, banbuntane houtokukai hospital, nagoya, japan. 3 nursing director, nursing director chamber, fujita health univesity banbuntane hotokukai hospital, nagoya, japan. abstract emergency medical treatment in japan is subject to jurisdiction by the fire department. triage, by definition, is a dynamic process, as the patient's status can change rapidly. triage is very important for japan, where emergency patients are on the rise. the role of triage nurse is also important. that will improve the life-saving rate of emergency patients and improve the reversion to society. introduction emergency medical treatment in japan is subject to jurisdiction by the fire department. patients being transported by ambulance will be treated as soon as they arrive at the hospital, japanese ambulance can be requested for free. in recent years, the rate of emergency vehicle dispatch and emergency patients tend to increase year by year.triage was introduced to japan so that medical treatment can be provided to patients who really need urgent. history of triage triage, by definition, is a dynamic process, as the patient's status can change rapidly. patients may enter the triage stream at any point1. urgency scales of the world are being developed in the united states in 1994, australia in 1993 and canada in 19953. since around 2012, operation of jtas became popular, and it was introduced in many hospitals. our hospital is an emerg ency design ated hospital. jtas (japan triage and acuity scale) [4] japan focused on ctas (canadian triage and acuity scale)2 in canada. ctas is a highly credible scale that is progressing in north america, asia and europe. japan developed and introduced jtas based on ctas. emergency patients such as brain surgery diseases and cardiovascular diseases are 8507 in one year in japan [5]. we aimed at improving the keywords emergency, role of triage nurse, tertiary centre in japan corresponding author: shinobu tsuge fujita health university, banbuntane houtokukai hospital, nagoya, japan ahmed.ansari2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 88 shinobu tsuge, takahiro shinagawa, kumi hara, akio aihara the life-saving rate of our hospital. therefore, from 2018 triage was introduced. components of jtas pre-hospital treatment as a pre-hospital treatment, there are doctors, car and doctor helicopter. the emergency system in japan, ambulance and walking patients are treated in the same place. the emergency medical system in japan is different for each facility patients who go to an emergency hospital are patients with mild to severe cases and urgent cases. among them, as many as 1% of the patients who walked into the hospital waiting for a sudden change are hidden. there is a danger of missing the patient's life crisis if you are consulting in order of acceptance. moderate emergency patients are accepted for 24 hours. triage method [6] triage will walk to the patient who come to the hospital, the triage nurse will receive the patient. 1. triage fast touch. after reception, the nurse first responds, at that time, she judges the severity and urgency is necessary or not. if it is an emergency, she starts the treatment immediately. in case of infectious diseases, patients should be isolated. 2. we ask for chief complaints, followed by vital sign measurements, interview, objective findings, etc and the patient is judged according to jtas level. patient is asked to wait in the waiting room or monitoring room if monitoring is necessary. 3.after triage, i will consult the patient, when the turn comes triage nurse a nurse performing a triage is called a triage nurse there are 30 nurses involved in triage. nurses' years of experience ranged from 5 to 30 years. in order to introduce triage, it was necessary to confirm the ability of the nurse. what is sought are medical knowledge, first-aid skills, cooperation with other occupations, judgment. training for triage in introducing triage, i confirmed the triage knowledge of the nurse many nurses do not know hospital triage. depending on the years of experience, there is a difference in ability to do triage. training was given based on: what is triage urgent degree and severity merit by the triage perform in the triage about qsofa [7] (quick sepsis related organ failure assessement) conclusions triage is very important for japan, where emergency patients are on the rise. among the medical staff, fast touch to the patient is triage nurse, who will improve the life-saving rate of emergency patients and improve the reversion to society. table 1 work site job description intensive care type icu intensive care of severely hospitalized patients er type er all emergency medical examination each departmenttype collaborative type from er to ward treatment from initial care to ward table 1 level 1 resuscitation: immediate treatment level 2 emergency: rapid treatment level 3 semi-emergency: first-aid measures may be necessary level 4 low emergency: treatment within 1 hour to 2 hours level 5 non-emergency: no urgency figure 1 fast touch. assessment of severe complaints 89 introduction of triage. an experience of a triage nurse in a tertiary centre in japan figure 2 vital sign measurement medical interview figure 3 medical examination references 1. evolution of triage systems, iain robertson ‐ steelet al, emerg med jv.23(2); 2006 feb. 2. prehospital canadian triage & acuity scale prehospital ctas paramedic guideby joan, burton, 7. 3. health system organization and governance in canada and australia: a comparison of historical developments, recent policy changes and future implications. donald j. philippon et al. 4. a study on the effect of introducing jtas in emergency outpatient (jtas in the emergency room). toru koyama (toru oyama) et al. 5. kyoto university hospital guidanc e 2015. 6. gilboy n, tanabe t, travers d, rosenau am. emergency severity index (esi): a triage tool for emergency department care, version 4. implementation handbook 2012 edition. ahrq publication no. 12-0014. rockville, md. agency for healthcare research and quality. november 2011. 7. utility of quick sepsis-related organ failure assessment (qsofa) to predict outcome in patients with pneumonia. müller m, guignard v, schefold jc, leichtle ab, exadaktylos ak, pfortmueller casendtoplos one. 2017 dec 21;12(12): e0188913. doi: 10.1371/journal.pone.0188913. ecollection 2017. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article hemimegalencephaly without seizures: report of a case and review of literature agrawal atul, dutta gautam, singh daljit, sachdeva deepashu, gupta robin india doi: 10.1515/romneu-2017-0050 306 | agrawal et al hemimegalencephaly without seizures doi: 10.1515/romneu-2017-0050 hemimegalencephaly without seizures: report of a case and review of literature agrawal atul1, dutta gautam1, singh daljit2, sachdeva deepashu1, gupta robin1 department of neuro-surgery, govind ballav pant institute of postgraduate medical education and research (gipmer), new delhi, india 1senior resident, 2professor and head of the department abstract: hemimegalencephaly is a rare malformation of the brain characterized by enlargement of one cerebral hemisphere. the classic clinical triad consists of intractable epilepsy, severe psychomotor delay and hemiparesis. we report a case of a six months old girl, with the radiological features of hemimegalencephaly but with a comparatively benign clinical course. she had mild developmental delay but with no paresis or seizures. literature revealed only two reported cases of hemimegalencephaly without the presence of seizures. we discuss the clinical and radiological findings of this third reported case. key words: brain malformations hemimegalencephaly, seizures introduction hemimegalencephaly (hme) is a rare, sporadic type of congenital brain malformation, characterized by enlargement of one cerebral hemisphere. [1] hme is largely thought to be a malformation due to abnormal neuronal and glial proliferation. [2] this is accompanied by dysplasia of the cerebral cortex along with polymicrogyria, agyria/pachygyria, and white matter heterotopia, which results in intractable epilepsy and profound disabilities. [1] the classical clinical triad described is of epilepsy, severe psychomotor retardation and contralateral hemiparesis. [1,4] which are often severe in nature and associated with a significant mortality in infancy. [1,6] onset of symptoms commonly occurs in the first week of life. [4] early surgical intervention including hemispherectomy, either anatomical or functional is warranted in these patients to achieve a better outcome in the control of epilepsy and to promote psychomotor development. [3] however, there have been isolated reports of milder clinical presentation [4] including only a single case report of a child having hme without any presentation of seizures. [5] in this report, we describe a child who presented to our department for management of lumber meningomyelocele whose further workup revealed hme. romanian neurosurgery (2017) xxxi 3: 306 309 | 307 case report a six months old female child was referred to our neurosurgical department for evaluation and management of a lump in lower back that is present since birth along with macrocephaly. she was product of a fullterm pregnancy of non-consanguineous parents; the prenatal history was normal and the baby cried immediately after birth. height at birth was 48 cm and weight was 2500 g along with a head circumference of 41.2 cm with a flat anterior fontanelle along with lump at lower back. she had extra digits on both feet and had mildly delayed neurological development. she had no clinical evidence of paresis of any limbs neither she ever had a seizure or seizure-like episode as per 6 months of age. on examination, a head circumference over the 99th centile was noted in the child but there was no signs or symptoms of raised intracranial pressure. we plotted the head circumference on a growth chart when she was found to have no crossing of centile lines, consistent with normal growth of the child. she was found to have 6x4cm lumber meningomyelocele. non-contrast ct and mri of the brain and spine was obtained. ct and mri brain of the child demonstrated features typical of hme (figure 1). asymmetrical abnormalities were noted, with the left hemisphere larger in volume than the right. this asymmetry was associated with abnormalities both of grey and white matter. the left hemisphere demonstrated cortical malformation and polymicrogyria, as well as generalized loss of white matter bulk with cortical dysplasia. there was associated asymmetry of the ventricular system. radiological features were consistent with hme. mri spine was suggestive of lumber lipomenigomyelocele. she underwent sac excision and dural repair and postoperative stay was uneventful. the family was informed that the child did not require neurosurgical intervention for hme currently, but that she was at risk of developing epilepsy and should be closely observed for clinical seizures. discussion hme is a rare anomaly and there is a paucity of large series in the literature. in one of the comprehensive reviews, the authors describe 14 cases, examining clinical, radiological and electrophysiological features. [4] in this series, the authors report that one patient did not have seizures. beside this isolated case, extensive medline search revealed only one report where occurrence of hme without seizures was described, making the current case only the third reported. severe epilepsy is a hallmark of the condition, being present in all 10 patients described in another large series. [1] in fact, hme carries a significant mortality risk due to the severity of the epilepsy [6,7] as well as association with significant psychomotor delay and hemiparesis. the current case is unusual in only having one of the clinical triad (developmental delay) and only in mild form. 308 | agrawal et al hemimegalencephaly without seizures figure 1 noncontrast ct (a & b) and t2w mri brain (c & d) showing enlarged left cerebral hemisphere with ventricular dysmorphism, white matter changes, cortical dysplasia and polymicrogyria of the left frontal and parietal lobe hme on brain imaging consists of cortical gray matter almost uniformly abnormal, areas of increased thickness of the cortical gray matter (gm), abnormal gyral patterns, increased signal intensity in the subcortical white matter (wm) on t2-weighted images, blurring of the gm-wm transition, atrophy or hemispheric hypertrophy or demyelination. [8] this patient presented almost all of these mri findings supporting hme. the wm signal change may be consistent with either demyelination or advanced myelination. the ipsilateral ventricle is usually enlarged and dysmorphic, often with extension of the romanian neurosurgery (2017) xxxi 3: 306 309 | 309 posterior horn of the lateral ventricle across the midline. this patient did not have grossly enlarged ventricles but asymmetric. vigevano et al., [4] in their series of 14 patients, divided hme into two groups: a and b. group a was characterized by severe, uncontrollable epilepsy with marked hemiparesis and delay (7/7), whilst group b had more mild clinical features with sporadic seizures and a later onset of epileptic attacks. radiological features were less severe in group b, with no patient having microgyria on their scan. we consider the current case represents “group b”-type child, who is as yet too young to have had her first seizure. the other possibility is that there is a population of “silent” hme, with absent or mild clinical signs but with radiological features of the malformation and that this was an incidental finding when the child was being investigated for unrelated reasons. as availability of mri scanning becomes ever more widespread, it may be that further similar cases are detected as children have brain imaging for various other reasons. conclusion it is important to recognize the abnormal tissue organization to make the correct diagnosis. in children, brain mri is the gold standard diagnostic tool, with brain enlargement and wm changes. different degree of changes in signal intensity revealing the wm abnormalities is the most important and constant sign in hme. regular follow up and close observation is required in scarce cases like the present one who do not manifest seizures on presentation for later development of epilepsy so that early surgical intervention may be undertaken. correspondence dr. gautam dutta, m.ch, senior resident, department of neuro-surgery, govind ballav pant institute of postgraduate medical education and research (gipmer), new delhi110002 phone number: 9968034400 e-mail: gautamblue@hotmail.com references 1.flores-sarnat l. hemimegalencephaly: part 1. genetic, clinical, and imaging aspects. j child neurol. 2002;17:373–84. 2.barkovich aj, kuzniecky ri, jackson gd, guerrini r, dobyns wb. classification system for malformations of cortical development. neurology. 2001;57:2168–2178. 3.di rocco c, battaglia d, pietrini d, piastra m, massimi l. hemimegalencephaly: clinical implications and surgical treatment. child’s nerv syst 2006;22:852–866. 4.vigevano f, fusco l, granata t, fariello g, di rocco c, cusmai r. hemimegalencephaly: clinical and eeg characteristics. dysplasias of cerebral cortex and epilepsy. lippincott-raven, philadelphia. 1996; pp 285–294. 5.greg james, mano shanmuganathan, william harkness. hemimegalencephaly without epilepsy: case report. childs nerv syst. 2014;30:1617-19. 6.vigevano f, bertini e, boldrini r, bosman c, claps d, di capua m, di rocco c, rossi gf. hemimegalencephaly and intractable epilepsy: benefits of hemispherectomy. epilepsia. 1989;30:833–843. 7.bosman c, boldrini r, dimitri l, di rocco c, corsi a. hemimegalencephaly. histological, immunohistochemical, ultrastructural and cytofluorimetric study of six patients. child’s nerv syst. 1996; 12:765–775. 8.barkovich a, moore k, jones b, vezina g, koch b, raybaud c et al. diagnostic imaging pediatric neuroradiology. salt lake city, utah: amirsys-elsevier 2007. section 1: cerebral hemispheres malformations: i1-20. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article surgical management of giant cell tumor of axis vertebra: review of fourteen cases in literature with a case illustration guru dutta satyarthee, luis rafael moscote-salazar, amit agrawal india, colombia doi: 10.1515/romneu-2017-0066 404 | satyarthee et al – surgical management of giant cell tumor involving axis vertebra doi: 10.1515/romneu-2017-0066 surgical management of giant cell tumor of axis vertebra: review of fourteen cases in literature with a case illustration guru dutta satyarthee1, luis rafael moscote-salazar2, amit agrawal3 1department of neurosurgery, neurosciences centre, aiims new delhi, india 2neurosurgery, critical care unit, red latino, latin american trauma & intensive neurocare organization, bogota, colombia 3department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: primary spinal giant cell tumor (psgct) considered as rare primary neoplasm, with predilection for subarticular location and commonly located at knee joint region, sacrum or distal radius, however, spinal involvent is uncommon and comparatively much rarer in the cervical spine. further occurrence of giant cell tumor in the axis vertebra is extremely uncommon and easily misdiagnosed and, thus, treatment is still debated and various treatment modalities and different surgical approaches were utilized during evolution of surgical management. authors could collect only 14 cases of primary giant cell tumor affecting axis vertebra in a detailed pubmed and medline search, out of which 12 cases were primary and rest two case was recurrent. so authors reviewed in total thirteen cases primary giant cell tumor of axis managed surgically, including our case. out of 13 psgct, twelve cases were managed with surgical resection and the rest one case was managed with monoclonal antibody using denosomab monotherapy without any surgical intervention. in the surgical group (n=12), nine cases had two staged surgical procedure, first being posterior fixation followed by anterior approach with resection of tumor while, the rest three had one stage surgical resection including current case. authors reports a unique case of spinal giant cell tumor developing in a38 year male with history of renal transplant , presented with neck pain and difficulty in walking, neuroimaging revealed a osteolytic mass lesion involving body of axis vertebra with extension into right sided lamina , underwent two stage complete surgical intervention. authors describes management of such rare locally recurring primary bony pathology affecting axis vertebra as it is not only interesting and challenging and different management modalities, various, surgical approaches and issue of renal osteodystrophy along with pertinent literature is also reviewed briefly. key words: spinal giant cell tumor of axis vertebra, surgical management, two stage treatment, renal osteodystrophy, management romanian neurosurgery (2017) xxxi 3: 404 413 | 405 introduction the first description of giant cell tumour was put forward by cooper and travers in 1918. (1) the "giant cell tumor” term was coined by bloodgood in 1919. (2) psgct location represent extremely uncommon location, constitute about 5-15 % of all g ct. (3, 4, 5) in psgct, vertebral body is more commonly involved compared to the posterior vertebral elements (6, 7). the management of gct is controversial due to its rarity of occurrence and associated unpredictable behavior. (2-6) in 1940, jaffe et al. (3) made an attempt to clearly define the definitive patological basis for classifying and differentiating giant cell tumor from similar lesions eg. aneurysmal bone cyst, chondrosarcoma, chondro­ myxoma and nonosteogenic fibroma of bone. however, a wide local surgical excision must include adjacent surrounding normal tissue whenever feasible. case illustration a 38 –year male presented with complaints of neck pain for last six months, insidious in onset, which used to get worsened in sitting position and during walking, used to support his head and neck by hand which associated with restriction of neck movement. his significant past medical history included renal transplant in december 2007, at our institute for end stage chronic kidney disease secondary to chronic glomerulo-nephritis associated vasculitis. he was getting regular follow-up with nephrologist and transplant surgery opd clinic and he was advised to continue medication including, tablet prednisolone 5mg daily, capsule tacrolimus 3.5 mg twice a day, along with antihypertensive medications in addition to injection erythropoietin 100 mcg subcutaneous every three week and iron and folic acid supplementation. in march 2008, had graft dysfunction, graft biopsy was suggestive of antibody mediated rejection with evidence of transplant glomerulopathy. he also suffered cytomegalovirus colitis in 2013. routine serum biochemistry revealed blood urea 53 mg/dl and serum creatinine 2.4 mg/dl, while the rest of biochemistry and hemogram were within normal limit. noncontrast craniovertebral junction computed tomography revealed evidence of osteolytic lesion of axis affecting the second cervical vertebra causing expansion of the body with presence of septation and also extending into right side lamina, cortical breach observed on antero-inferior aspect, causing compromise of the spinal canal with secondary cervical canal stenosis. (figures 1, 2, 3) magnetic resonance imaging of craniovertebral junction, sagittal section image demonstrated presence of heterogeneous signal intensity mass lesion affecting vertebral body of axis, measuring 36 x 30 x 22 mm in size, (figures 4 and 5 a, b) causing expansion and destructive the vertebral body and also further extending to involving lamina and producing significant mass effect in form of obliteration and indentation of anterior thecal sac and spinal 406 | satyarthee et al – surgical management of giant cell tumor involving axis vertebra cord indentation as well as displacement at same level. as he had slightly deranged renal function, planned for two stage surgical excision to avoid further renal function compromise. first stage planned was radical decompression, obtaining specimen for histopathological confirmation and posterior occipitocervical fixation and followed by transoral decompression after first surgery depending on renal functional status in the second stage surgery, as deranged renal function precluded prolonged surgery for combined anterior and posterior approach in a single setting. after anaesthesia clearance, he was taken up for surgery under strict guidance and supervision of nephrologist. he was and taken up for surgery in the prone position. an skin incision from inion to c5 level was given, further dissection was carried out along ligamentum nuchae and occipital bone, c1 to c4 lamina were exposed. the anterior arch of c1 was removed, laminectomy of c2 and c3 were carried out. the right lamina showed presence of soft, grayish yellow, moderately vascular mass. the c2 body was entered and gross total microsurgical decompression was carried out under, however, the part of the lesion located central part of axis vertebra was not accessible. after securing hemostasis, posterior occipitocervical fusion was carried out with occipital plate and lateral mass screw fixation of c3 and c4 level. he tolerated surgical procedure well with no fresh neurological worsening or any renal parameters derangement in the post-operative period. x-ray showed implant in proper position. (figure 6) he underwent second stage transoral decompression after seven months following first surgery. histopathological examination of specimen showed numerous osteoblastic giant cells, stroma shows oval to spindle cells and features were compatible with giant cell tumor and also received radiotherapy. he is doing well at last follow up after one year following initial surgery. figure 1 computed tomography scan of craniovertebral junction, sagittal section image, showing osteolytic lesion of vertebral body and fracture lower endplate of axis vertebra romanian neurosurgery (2017) xxxi 3: 404 413 | 407 figure 2 coronal section, computed tomographic scan of cranio-vertebral junction image of 38-year male with renal transplant showing osteolytic lesion of vertebral body involving more to right side egg shell like preserved cortex axis vertebra figure 3 magnetic resonance imaging of craniovertebral junction, coronal section, t1 weighted image showing osteolytic lesion of vertebral body involving more to right side egg shell like preserved cortex axis vertebra figure 4 t1 weighted image isointense lesion involving vertebral body of axis magnetic resonance imaging of craniovertebral junction, sagittal section image showing mass causing compression of cervical cord figure 5a axial section t1 weighted image figure 5b axial t2 weighted image axial section magnetic resonance imaging of craniovertebral junction 408 | satyarthee et al – surgical management of giant cell tumor involving axis vertebra figure 6a axial section image figure 6b sagittal section craniovertebral junction ct scan post-operative computed tomography scan, showing evidence of laminectomy with metallic artifact of implant in situ discussion giant cell tumour is commonly distributed in subarticular location with predilection for knee joint region, sacrum, distal radius and proximal radius, and those located in appendicular regions, usually remain centered in the epiphysis plate and extend eccentrically beyond epiphyseal boundary. (3, 4) however, vertebral column involvement is very rare 9 and overall the cervical region localization accounts for less than 1% of overall occurrence of giant cell tumors. (4) due to unpredictable behavior, in general only a third of total cases ultimately remain truly benign, while the rest two-third cases may progresses ultimately to either become locally invasive or may show metastasis to distant focus. in 1982, fabiani et al (10) did a detailed review could collect a total of 66 cases pspct including their own two cases, which were located in the spinal column and 30 % occurred in cervical spine region, another 45 % in thoracic and 25% in lumbar region respectively. giant cell tumor usually occurs in third or fourth decades of life, with a mean age of 27 years and show slight female preponderances. spinal gct frequently presents with pain over the spinal column, progressive paraparesis or quadriparesis, however sphincter disturbance is less common. authors in a detailed literature search of psgct involving axis vertebra, could find only 12 primary case of psgct in the literature (4, 6, 9, 16, 17, 18, 22) (table 1) and additional another two had recurrent gct 8. (23) radiograph may show selective involvement of vertebral body with soapbubble appearance associated with rarefaction and expansion of the vertebral body are important characteristic feature and may be helpful aid in preoperative diagnosis of the vertebral mass lesion and accordingly surgical intervention can be planned. romanian neurosurgery (2017) xxxi 3: 404 413 | 409 table 1 review of primary giant cell tumor occurring in the axis vertebra s.no. author/ reference no. of cases year age/ sex site of lesion stages of surgical resection surgical approach 1. honma et al.9 2 1989 axis single trans lingual and mandible splitting approach with fusion of spine from the atlas to the third cervical vertebra axis single 2. shirzadi et al. 6 1 2011 15-year/ male odontoid process single stage surgery initial surgery 3 cebula et al.4 1 2012 body and lateral masses of axis vertebra c2 giant cell tumor colonized by aneurysmal bone cyst two stage preoperative embolization with two staged surgical intervention 4. hiromasa et al 16 1 2012 23-year/ female body and vertebral arch of axis vertebra cranial part of c3 vertebra on posterior two stage first posterior fusion with surgical resection and second anterior approach spinal tumor extirpation and anterior fusion 5 chen et al. 18 5 2015 27-year/ male axis vertebra two staged first – posterior occipito-cervical fixation with secondintralesional curettage 36-year/ female axis vertebra two staged, firstposterior fixation second stage intra-lesional curettage 24-year /female axis vertebra two stage first posterior occipito-cervical fixation second intra-lesional curettage 45-year /female axis vertebra two stage first posterior occipito-cervical fixation second stage partial resection 23year /male axis vertebra two stage first posterior occipito-cervical fixation with 2nd stage partial resection 6 mattei et al. 17 1 2014 22 -year/ female vertebral body and odontoid process non-surgical monotherapy with denosumab monoclonal antibody designed to inhibit the receptor activator of nuclear factor kappa-b ligand led to long-term remission 7 bakhsh et al.22 2015 11–year/ male body and odontoid process two staged surgery first posterior decompression and posterior fixation, followed by anterior decompression and fixation current case 1 2017 38–year/ male body of axis and right lamina staged first posterior decompression and posterior fixation, second stage – transoral decompression 410 | satyarthee et al – surgical management of giant cell tumor involving axis vertebra computed tomography clearly delineates the extent of lesion, bony outline and spinal stability, involvement of foramen transeversarium and vertebral artery encasement. the ct angiography may better delineate the course of vertebral artery and delineates its relation to lesion. mri spine is considered as investigation of choice and typically shows hypointense mass lesion on t1 w image, and without significant alteration on t2 w image, also clearly delineates thecal sac and any spinal cord distortion as well as any associated co-existing intradural pathology or myelomalacia or cord signal alteration due to pressure effect. (4, 11) histologically, the giant cell tumour is characterized by well vascularized lesion, uniformally composed of spindle or oval shaped undifferentiated stromal cellswith evenly dispersed numerous large multinucleated giant cells. (2, 3, 5) stromal cells and evenly dispersed numerous giant cell resemble each other in regard to nuclei. however, the giant cell is also found in osteogenic sarcoma, chrondroblastoma, osteoblastoma, fibrous dysplasia, brown tumor and aneurysmal giant cell tumors. but distribution of giant cell may be either focally distributed or very few in number and giant cell size may be small and having few nuclei in these tumors. the natural history of psgct without treatment consist of enormous growth of tumor size, causing pressure effect on adjoining neurovascular structure leading to pathological fracture, malignant transformation and even distant metastasis. management of gct is surgical excision, however, wide surgical excision is not possible in cases of vertebral column lesion because of proximity to critical relation to spinal cords and vertebral artery in a single stage. (3, 5, 7) as single stage surgery involving anterior and posterior approaches produces significant alarming morbidity. (6, 9) the staged surgical approaches are devised and also used to ensure maximum resection of mass lesion with reduction in the morbidity. (4, 16, 17) all cases of psgct involving axis vertebra in literature were subjected for surgical resection (4, 6, 9, 16, 17) except one reported by mattei et al. al (18) without surgical intervention and he was managed with monoclonal antibody using denosomab monotherapy. in the surgical group of psgct, eight cases underwent staged surgical procedure, first stage being posterior fixation followed by anterior approach in the second stage (4, 16, 17) current case was also managed in staged procedure. however, two cases, reported by homnma et al. (9) underwent anterior bases approach utilizing translingual and mandible splitting route with fusion of spine extending from atlas to third cervical vertebra and one caes also reported by shizardi et al. managed with single stage decompression surgery. (6) cases with giant cell tumor often show recurrence and there is wide range of variation depending upon the nature, route of surgical approaches, fixation, expertise of surgical team and extent of surgical decompression. about 20-40 % recurrence rate is observed after simple curettage, however recurrence rate significantly decreases with more radical surgical procedure utilization followed by adjuvant therapy. in staged tumor resection romanian neurosurgery (2017) xxxi 3: 404 413 | 411 surgery, may provide better chances of radical decompression with appropriate fixation and further minimizing morbidity. (9) if tumour recurs, further repeat biopsy of mass lesion is advisable to exclude recent malignant transformation, (8) followed by surgical resection and replacement of bone defects with suitable bone grafting and appropriate bony fixation which may prevent further recurrence. at recurrence, if the histopathological grading of tumour is higher, the lesion usually tends to invade vertebral body as well as posterior elements as compared to those confined to vertebral body alone (20 % versus less than 6 %). (13) periodic regular follow-up with detailed neurological examination with neuro imaging is recommended for five-years. (8) psgct is are generally considered histologically benign; however, can also exhibits locally aggressive behavior with a relatively high local rate recurrence of up to 60%, if treated with curettage but it also carries the potential for distant metastasis, commonest to the lung, noted in upto 4% of cases. (19) bone and mineral disorder may occur frequently in renal transplant recipient and usually carry a high risk of bone fracture and associated morbidity. (20) a spectrum of a bone diseases are observed following the renal transplantation which may include osteoporosis. the pathophysiology of such bone disorders after transplantation results due to complex interplay of factors ie preexisting renal osteodystrophy, immunosuppression and alterations in the parathyroid hormone-vitamin d-fibroblast growth factor 23 axis and altered mineral metabolism. (20) alterations in the metabolism of calcium, phosphorus and magnesium minerals and parathyroid hormone, alkaline phosphatase, vitamin d and can have significant impact. calcineurin inhibitors are linked to development of fresh osteoporosis, steroid therapy may cause additional osteoporosis and varying degrees of occurrence of the osteonecrosis. immunosuppressant may impair osteoblast proliferation and differentiation differentpharmacologic management are suggested withdrawal of steroid therapy, and supplementation of bisphosphonates, vitamin d derivatives, and denosumab are proposed. (21) psgct is locally invasive with variable is relatively a low radiosensitive tumor, so radiotherapy is usually reserved for surgically inaccessible or inoperable cases. however, radiation therapy also carries a risk of occurrence of high grade sarcoma in surrounding tissues. (13) chemotherapy trial with adriamycin has been tried for skull-base gct. recently mattei et al. al (18), reported a 22 year female managed primarily with monoclonal antibody using denosomab without surgery. as surgical fixation in cases, with renal transplantation is double edges sword, as surgical resection without fixation may severely limit the extent of surgical resection and carry a chances of large residual. however, spinal fixation also carry risk of implant failure due to associated osteoporosis, continued therapy with steroid, immunosuppression medication. author advocates a balanced 412 | satyarthee et al – surgical management of giant cell tumor involving axis vertebra intervrention and tailored made therapy should be utilized for treatment in cases with psgct of axis with renal transplantation and more frequent follow-up with neuroimaging to look for stability of implant and early detection of the tumor recurrence is highly important. conclusion early diagnosis and surgical management with spinal stabilization can help in preserving good neurological status, staged surgical procedure represents definitely a viable option for management of primary giant cell tumor affecting axis vertebra. while dealing with osteolytic pathology of axis vertebra, possibility of giant cell should also be considered despite rare occurrence as surgery can provide definitive surgical management along with adjuvant therapy and recently monoclonal antibody therapy is also showing promise for locally invasive and locally recurring primary lesion and neurosurgeons and radiologist must be aware of this pathology. correspondence dr. guru dutta satyarthee associate professor department of neurosurgery room no. 714 neurosciences centre, aiims new delhi e-mail: drguruduttaaiims@gmail.com references 1. cooper, astley, traveres b: surgical essays. vol, i pp i 86-208. london cox and son and longman and co, 1918. 2. bloodgood j c, bone tumors. central (medullary) giant cell tumor (sarcoma) of lower end of ulna, with evidence that complete destruction of bony shell or perforation of the bony shell is not a sign of malignancy. ann surg 1919; 69: 345-359. 3.jaffe hl, lichtenstein l, portis rb; giant cell tumor of bone. its pathological appearance, grading, supposed variants and treatment. arch pathol 1940; 30: -993-103l. 4. cebula h, boujan f, beaujeux r, boyer p, froelich s. [giant cell tumor of the c2 colonized by an aneurismal bone cyst. report of case]. neurochirurgie. 2012 ;58(6):376-81. [ french.] 5. tsuchiya h, kokubo y, sakurada k, sonoda y, saito s, kayama t. [a case of giant cell tumor in atlas]. no shinkei geka. 2005 aug;33(8):817-23. [japanese.] 6. shirzadi a, drazin d, bannykh s, danielpour m. giant cell tumor of the odontoid in an adolescent male: radiation, chemotherapy, and resection for recurrence with 10-year follow-up. j neurosurg pediatr. 2011 oct; 8 (4):367-71. 7. bayar ma, erdem y, gokcek c, koktekir e, kilic c, yasitli u, tekiner a. giant cell reparative granuloma of the axis. turk neurosurg. 2009 oct;19(4):423-7. 8 . razak ma, fazir m. neurological recovery in a patient with recurrent aggressive giant cell tumour of the axis--a case report. med j malaysia. 2000 ; 55 suppl c:97100. 9. honma g, murota k, shiba r, kondo h. mandible and tongue-splitting approach for giant cell tumor of axis. spine (phila pa 1976). 1989 ;14(11):1204-10. 10. fabiani a, brignolio f, favero m, benech f, torta r benign and malignant cranio-spinal giant cell tumours. report of four cases. acta neurochir (wien). 1982;64(12):133-50. 11 van giffen nh, van rhijn lw, van ooij a, cornips e, robben sg, vermeulen a, maza e. benign fibrous histiocytoma of the posterior arch of c1 in a 6-year-old boy: a case report. spine (phila pa 1976). 2003 sep 15;28(18):e359-63. 12. yamada s, oshima k, hamada k, sotobori t, joyama s, hashimoto n, outani h, tanaka y, nakanishi k, araki n. giant cell tumor of the tendon sheath arising from a membrane surrounding the posterior arch of c1: a case report.spine j. 2016 may;16(5):e353-7. 13. gonzález-martínez e, santamarta d, lomas-garcía j, ibáñez-plágaro fj, fernández-fernández jj, ariño tr, garcía-cosamalón j. giant-cell granuloma of the axis. j neurosurg spine. 2012;16(2):191-4. romanian neurosurgery (2017) xxxi 3: 404 413 | 413 14. gołabek w, skwarcz a, warda e. [surgical approach to the atlas and axis]. otolaryngol pol. 1995;49 suppl 20:318-322.[ polish.] 15. gonzález-martínez e , santamarta d, lomas-garcía j, ibáñez-plágaro fj, fernández-fernández jj, ariño tr, garcía-cosamalón j. giant-cell granuloma of the axis. j neurosurg spine. 2012;16(2):191-4. 16. hiromasa k , shin k, seiji a, akihiko k, ryotaro i, morio m, kota w, yorihisa i, kaoru o, taneaki n. transoral anterior approach using median mandibular splitting in upper spinal tumor extirpation. oral surg oral med oral pathol oral radiol. 2012 nov;114(5):e12-6. 17. mattei ta , ramos e , rehman aa , shaw a , patel sr , mendel e . sustained long-term complete regression of a giant cell tumor of the spine after treatment with denosumab. spine j. 2014 jul 1; 14(7):e15-21. 18. chen g, li j, li x, fan h, guo z, wang z. giant cell tumor of axial vertebra: surgical experience of five cases and a review of the literature. world j surg oncol. 2015 ;13:62. 19. carrasco ch, murray ja. giant cell tumors. orthop clin north am. 1989;20:395–405. 20 . bouquegneau a , salam s , delanaye p , eastell r , khwaja a . bone disease after kidney transplantation. clin j am soc nephrol. 2016 jul 7; 11(7):1282-96. 21. kalantar-zadeh k , molnar mz, kovesdy cp, mucsi i, bunnapradist s. management of mineral and bone disorder after kidney transplantation. curr opin nephrol hypertens. 2012 ; 21(4):389-403. 22. bakhsh a, ali siddiqui km, moumneh g, el maghrabi t. giant cell tumor of c2 (axis): a case report and short review of literature. clin cancer investig j 2014;3:102-4 23. bartanusz v, ziu m, jimenez df, crownover rl, langevin am. zoledronic acid therapy for recurrent giant cell tumor of the c2 vertebra in an adolescent. the spine journal. 2015 aug 1;15(8):1886-7. microsoft word _9.formatata_dobrin.doc romanian neurosurgery vol. xvi nr. 1 43 biomechanics and biometry of the anterior skull base irina dobrin1, patrick courtheoux2, n. dobrin3, i. poeata4, n. ianovici4 1emergency military hospital “dr. i. czihac”, emergency departament 2chu-caen, france 3clinical hospital no.3, iasi, neurosurgery departament 4university of medecine and pharmacy “gr.t. popa”, iasi we present here some interesting points of view concerning the biomechanics aspects of the skull base. also several problems are studied concerning the skull base symmetry with some pathological implications. keywords: skull base, skull base symmetry, facial asymmetry introduction in the opinion of the famous anatomist testut, the skull base is similar to a ship. this illustrative image obviously takes into consideration the existence of a bow designed to balance the undulatory movements caused by the c1 – c2 occipital articulations. it’s about the exoskull, which allows through its apophyses the insertion of various muscle groups which ensure the equilibrium of this unstable system at the first sight, should we consider the static equilibrium. the development symmetry of the skull base ensures the motion symmetry, the asymmetric development generating compensatory movements at the level of the calvarium but also in the c0 – c1 – c2 movement system (4, 7, 10). one can notice that the symmetry is given by the sagittal plane on the nasion – opistion direction, while the spheno – occipital articulation is similar to a torsion pushrod whose modification may generate various aspects of asymmetry: -torsion -lateral rotation -front-posterior rotation similarly, a malposition of the temporal bone between the sphenoid and the occipital may generate forms of asymmetry through the difference of the semicircular channels. fig. 1 exobasis showing the insertion muscle groups irina dobrin romanian neurosurgery vol. xvi nr. 1 44 fig. 2 schematic representation of the skull base fig. 3 schematic representation on the longitudinal plane according to some authors (j. p. relier, n. seguin), the origin of the asymmetries of the skull base is found in the embryonary period under the influence of extrinsic factors – infectious diseases, mother’s traumas, but also intrinsic causes such as intra-uterine pressure or various problems during the delivery (2, 3, 10). the modification of the orientation of the solid pyramids following the traction of the insertion musculature which takes part in the cephalic static and especially the sternocleidomastoidian may generate asymmetries at the level of the skull base. during the common practice, most of the clinic doctors meet patients with more or less obvious facial asymmetries. luckily, most of them are nor symptomatic (15). fig. 4 asymptomatic facial asymmetry fig. 5 the importance of the alignment of ocular axes biomechanics and biometry of the anterior skull base romanian neurosurgery vol. xvi nr. 1 45 nevertheless, an efficient anamnesis may show various attitudes of the child in the suckling period, future modifications in the attention disorders during school, dyslexia, dysortographies with the apparition of cervical pain or vertigo during adulthood. as clinical implications, the asymmetry of the front floor of the skull base is most frequently met in the case of craniofacial congenital anomalies and may trigger several effects such as: asymmetry of orbital cones, with the modification of the muscles of the oculomotricity, astigmatism, modification of the visual axes with perturbations of the perception of space (2, 4, 16). the asymmetry of the orbital cones generated by the craniofacial malformations may induce convergence disorders; this is why in certain situations the surgical correction is necessary. notions of biometry of the front floor of the skull base – anterior skull base in the study of ontogenetic and phylogenetic development of the front floor of the skull base it was noticed that this platform which supports the olfactory tracts, the basal part of the front lobes, vascular elements of the fore circulation, does not have a stationary form and structure but changes throughout the course of life. thus, surgical approach of this region raises problems, depending on the individual situation and anatomic particularities of each subject. in the next stage we set out to analyze the various types of front floor of the skull base at the adult and their clinical surgical implications (17). definitions -the angle of the orbital ceilings represents the angle of intersection of the two horizontal parts of the frontal bone which forms the orbital ceilings at the junction place with the ethmoid towards the fovea etmoidalis; it is measured in the coronary plane which passes through the zygomatic apophyses of the frontal (upo). -the depth of the front floor of the skull base (p) – from the horizontal plane tangent to the convexities of the orbital ceilings a perpendicular line descends on the median line at the crista galli level. -the depth of the ethmoidal fovea (pfe) is measured imagistically on ct or rmn and the depth angle of the ethmoidal fovea (up) is defined as the angle set by the horizontal plane tangent to the orbital fossa; it generally passes through the dorsum sellae and the plane which unites the dorsum sellae with the area of maximum declivity of the ethmoidal fovea. -the sub-frontal approach angle (usf) is limited by the plane which passes through the upper margin of the dorsum sellae, namely the area of maximum declivity of the ethmoidal fovea and the plane which passes through the dorsum sellae with the tip of the superior recessus of the frontal aeric sinus (1, 2). fig. 6 t2 irm shows a depth of 2.6 cm. with an upo of 128° irina dobrin romanian neurosurgery vol. xvi nr. 1 46 fig. 7 ct craniocerebral exploration up= 14° and pfe 1.3 cm fig. 8 up=13°, pfe=1.3cm fig. 9 irm exploration for the evaluation of the sub-frontal angle usf=33° biomechanics and biometry of the anterior skull base romanian neurosurgery vol. xvi nr. 1 47 fig. 10 ct exploration with 3d reconstruction, usf=38° the practical importance of these aspects table 1 the table presents the average values of the angles and distances defined above on a lot of 120 patients randomly selected for study from the imagistic archive of the department of neuroradiology p upo usf up pfe b 3.2 128.3 39 14.2 1.5 f 2.8 127.5 36.5 13.4 1.3 p-d-depth upo-oda-orbitary depth angle usf-sfa-subfrontal angle up-ef-ethmoidal fovea pfe-def-depth of ethmoidal fovea other biometric aspects fig. 11 showing various angles modified along the evolution of the skull there was conducted an anatomic study of 65 skull bases on fresh cadaver samples, having in mind the appreciation of various forms of the front floor of the skull base, of the surface. various measurements were made: the thickness of the orbit ceiling, the thickness and height of crista galli, the number of perforations at the level of the cribriform plate. the percentage of the surface of the front floor of the skull base of the total surface of the base was calculated (12, 14). the morphometric aspects of the skull base are considered to be important for various clinical applications, the surgical approaches taking into consideration the various pre-surgical measurements. the dimensional anatomy of the skull base must be irina dobrin romanian neurosurgery vol. xvi nr. 1 48 imagistically appreciated in order to facilitate the exposure of various pathological aspects (4, 6, 12). similarly, the skull base was analyzed in the context of the cranial ensemble and the elements of phylogenetic evolution. conclusions the skull base is the platform on which the encephalon rests, provides support and protection and represents the main transit area of the big blood vessels and nerves. the study of the skull base must be conducted taking into consideration its two sides – the exobase and the endobase, but also the neighboring structures. the human skull has a crucial anatomic and surgical importance. it is considered as the most complex region whose approach implies several specialties, all of them converging towards a nucleus called skull base surgery. the surgical techniques have progressively evolved together with the anesthetic ones, especially since these anatomical areas are filled with vascular and nervous elements of vital importance. the study of the symmetry of the skull base is especially relevant in solving certain pathological aspects and also the appreciation of the approach angles of the skull base facilitates the various procedures of surgical approach. references 1.aldescu corneliu – neuroradiodiagnostic – editura junimea, iaşi, 1982, 56-64 2.aldescu corneliu – radiologie pentru studenti şi medici stomatologi – editura polirom 1999,87-105 3.arseni c. afectiunile neurochirurgicale ale sugarului şi copilului mic, ed. medicala 1979 67-93 4.bajenaru o, pop t orbita. in: rezonanta magnetica nucleara in diagnosticul clinic, sub red. pop t, ed. medicala, bucuresti, 1995 125-147. 5.beals sp, joganic ef. transfacial exposure of anterior cranial fossa and clival tumors. bni quarterly. 1992;8:2-28. 6.bessou p. cours diu posture toulouse janvier 2001 7.bilsky mh, kraus dh, strong ew, et al. extended anterior craniofacialresection for intracranial extension of malignant tumors. 8.am jsurg. 1997;174:565-568. 9.bogousslavsky j. ,leger jean-marc,interpretation des examens complementaires en neurologie , groupe liaisons 2000 10.bourjat p, veillon f pathologie oculo-orbitaire-tdm et irm. in: imagerie radiologique tete et cou, paris, ed. vigot, 1995. 11.bouthillier a, van loveren hr,tew jm jr. anterior approaches tothe clivus: classification and indications. contempneurosurg.1994;16:1-8. 12.ciobanu g.,mihailovici l. , ghid practic de tehnica radiologica cranio-faciala ,editura facla,1986, 93-109 13.halimi r.h.,doyon d., traumatismes maxillo-faciales. 1991 14.housepian em si colab. tumors of the orbit. in: youmans rj (ed), neurological surgery. philadelphia, wb, saunders co. 1990 458-468. 15.hasegawa m,torii s, fukuta k, et al. reconstruction of the anteriorcranial base with the galeal frontalis myofascial flap and the vascularizedouter table calvarial bone graft. neurosurgery. 1995;36:725-731. 16.hildebrand j. – neurooncologie, groupe liaisons, 2000 36-47 17.taveras and ferrucci, radiology on cd diagnosis • imaging • intervention, lippincott williams & wilkins, baltimore, 1999 323-365 romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article spontaneous resolution of large non-traumatic bilateral acute-on-chronic subdural hematoma d. adam, d. iftimie, gina burduşa, cristiana moisescu romania doi: 10.1515/romneu-2017-0002 8 | adam et al spontaneous resolution of large subdural hematoma             doi: 10.1515/romneu-2017-0002 spontaneous resolution of large non-traumatic bilateral acute-on-chronic subdural hematoma d. adam1,2, d. iftimie1, gina burduşa1, cristiana moisescu1 1department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania abstract: background and importance: chronic subdural hematomas are a frequently encountered neurosurgical pathology, especially in the elderly. they often require surgical evacuation, but recent studies have shown good results with conservative treatment in selected cases. clinical presentation: we report the case of a 72-year old patient that developed large, non-traumatic, bilateral, acute-on-chronic subdural hematoma after repeated abdominal surgery for appendicular carcinoma. he presented an abdominal wound infection and good neurological status (gcs score of 14 points), factors that indicated the delay of surgical intervention. subsequent clinical and radiological improvement forestalled the operation altogether and he presented complete spontaneous resolution of subdural hematomas at only 5 months after diagnosis. conclusion: although surgical treatment is performed in the majority of chronic subdural hematomas, in clinically and radiologically selected cases, the operation can be avoided. the hematoma can present resolution, either spontaneously or with the help of conservative treatment. key words: acute-on-chronic subdural hematoma, spontaneous resolution, computer tomography thickness clinical presentation a 72-year-old male with a history of iterative pulmonary embolism for which anticoagulant therapy was prescribed (acenocumarol), arterial hypertension, heart failure and chronic renal disease, was operated for acute appendicitis in a county hospital. histopathological analysis revealed an appendicular carcinoma and subsequently he was admitted to a nearby hospital where a right ileohemicolectomy with right parietal peritoneum and pelvic peritoneum resection and adhesiolysis were performed. over the course of hospitalization, the patient developed clostridium difficile infection that responded positively to oral antibiotic treatment (metronidazole and vancomycin). on the 16th postoperative day, the patient developed impaired romanian neurosurgery (2017) xxxi 1: 8 – 16 | 9             general condition, absence of transit and diffuse abdominal pain. surgeons performed an exploratory laparotomy and established the diagnosis of dynamic bowel obstruction. on the 17th postoperative day (first day after his third surgical intervention), he presented temporospatial disorientation, and the head ct scan revealed bilateral acute-on-chronic subdural hematoma, with a maximum thickness of 26 mm on the right and 24 mm on the left side, and diffuse cerebral edema (figure 1). the patient was transferred to our neurosurgical department and admitted in the intensive care unit. at admission, he presented temporo-spatial disorientation with no other neurological deficits (gcs score = 14 points). the patient had no history of head trauma. local examination revealed five peritoneal drainage tubes and a dehiscent, infected surgical abdominal wound. routine blood tests at admission showed moderate anemia (hb=8,32 g/dl), with a low hematocrit (24.82%), low platelet count (147.000/ul) and an increased inr (1,70). taking into consideration the abdominal wound infection, poor laboratory test results and, most importantly, the good neurological status of the patient, we decided to postpone the surgical intervention. conservative management and close neurological monitoring were performed. abdominal wound cultures were positive for pluri-resistant klebsiella and proteus, sensitive only to tobramycin and colistin; urine culture was positive for pseudomonas susceptible only to colistin and repeated blood cultures were negative. the patient was treated with colistin and daily dressing of the abdominal wound was performed. he later developed a large bilateral pleural effusion that was successfully managed with bilateral pleurostomy. contrast ct scan performed 2 weeks after admission excluded dural or calvarial metastases as a cause for subdural hematomas and showed a reduction of density, as well as size of subdural hematomas (figure 2). the patient maintained a good neurological status throughout the hospitalization period (42 days), with an overall slight neurological improvement (gcs score = 15 points). he was retransferred to the surgical department in order to treat the ongoing postoperative abdominal wound infection, with the recommendation of monitoring the neurological status and repeat ct scan in case of deterioration. at that time, a control head ct scan revealed bilateral chronic subdural hematoma with a tendency towards resorbtion (figure 3). after one week he was sent to a rehabilitation center. at 5-month follow-up, the patient presented a gcs score of 15 points with no neural deficits and a new head ct scan showed the complete resolution of bilateral subdural hematoma (figure 4). 10 | adam et al spontaneous resolution of large subdural hematoma             figure 1 ct scan performed before the transfer to our department that revealed bilateral acute-onchronic subdural hematoma, without midline shift, with a thickness of 26 mm on the left and 24 mm on the right side figure 2 contrast ct scan, performed 2 weeks after transfer showing reduction of density and size of bilateral chronic subdural hematoma; no dural or calvarial metastases were detected romanian neurosurgery (2017) xxxi 1: 8 – 16 | 11             figure 3 control ct scan before retransfer showing bilateral chronic subdural hematoma (homogenously hypodense) with a resolution tendency figure 4 ct scan performed 5 months later, showing complete resolution of subdural hematomas   12 | adam et al spontaneous resolution of large subdural hematoma             discussion definitions a subdural hematoma represents an accumulation of blood between the dura mater and the arachnoid layer. the chronic subdural hematoma consists of liquefied, yellowishbrown, protein-rich, degraded blood, encapsulated in an external, fibroblastic, neomembrane and an internal one, over the arachnoid membrane. the most frequent cause of a chronic subdural hematoma is minor traumatic brain injury in an elderly patient. a subdural hematoma is considered chronic when it is discovered at more than 3 weeks after the initial head trauma, with a hypodense aspect on computer tomographic examination. occasionally, fresh blood can be present within a hypodense subdural hematoma, an entity that can be called acute-on-chronic. history chronic subdural hematoma was initially described by wepfer in a postmortem case, while virchow named this entity “pachymeningitis hemorrhagica interna”. (1, 2) in 1914, trotter (3) emphasized the traumatic origin of chronic subdural hematomas that are caused by tears of the bridging veins, mechanism demonstrated by subsequent studies. (4, 5) causes the incidence of chronic subdural hematomas in senior citizens presents a high degree of variability in published studies, being approximately 8,2/100.000/year (6). for people over 70-years-old, the reported incidence is 58/100.000/year (7), while foelholm and waltimo estimated a rate of 12/100.000/year (8). accidental falls represent the foremost risk factor in asghar’s study (57%), followed by anticoagulation therapy and alcohol abuse6. by analyzing postmortem examinations of cancer patients, graus estimated that subdural hematomas amount to 26% of the 7% of intracranial hemorrhages which occur in these patients (9). the case that we report presented two associated risk factors: appendicular carcinoma and anticoagulant treatment (acenocumarol). furthermore, his prior repeated pulmonary embolisms could have been a complication of his yet undiagnosed malignant tumor due to the associated clotting disorders that can develop because of it. at admission in our department, the patient presented an inr of 1,70. reichman et al considered that an inr of over 1,5 is one of the indicators of coagulopathy (10). the pathophysiology of chronic subdural hematomas has been a constant interest of research, beginning with the old osmotic gradient theory of gardner (11). in recent decades, a new possible mechanism of hematoma expansion was proposed: the rebleeding of sinusoidal capillaries of the parietal membrane which present modified walls (12–15). this rebleeding explains the development of hyperdense areas within chronic subdural hematomas, that justify the label of acute-on-chronic that is commonly used. clinical features after surgical treatment of the patient’s aforementioned appendicular carcinoma, he romanian neurosurgery (2017) xxxi 1: 8 – 16 | 13             developed temporo-spatial disorientation as the sole neurological sign that suggested the benefit of a head ct examination. cognitive function impairment is common among elderly patients. only their sudden onset or rapid neurological deterioration suggest an acute intracranial condition. frequently, a subdural hematoma could be suggested by intracranial hypertension symptoms or focal neurological deficits that appear later in its evolution in the elderly due to their cerebral atrophy. markwalder et al have elaborated a clinical grading scale (table i). (5) investigations head ct scan shows an extracerebral fluid collection, of various thickness, with a density close to that of csf. it can also identify midline shift, if present. in our reported case, the ct scan revealed bilateral chronic subdural hematoma, without midline shift. bilateral subdural hematomas are encountered in approximately 15 to 20% of cases. (16) table i markwalder grading scale of chronic subdural hematoma grade mental status alterations neurological examination 0 absent normal 1 alert + headaches absent or mild neurological deficits 2 drowsy or disorientated hemiparesis 3 stuporous hemiplegia 4 comatose decerebrate/decorticate posturing management the gold standard of chronic subdural hematoma treatment is surgical evacuation, with the help of various techniques, such as burr hole or twist drill craniotomy, followed by drainage of the cavity. these procedures ensure a rapid brain decompression and improvement of neurological symptoms. an increasing number of neurosurgeons have noted that spontaneous resolution of chronic subdural hematomas can occur in some cases, and thus they can be managed conservatively. conservative management of a chronic subdural hematoma is recommended in: • asymptomatic patients or with mild, transitory headache, • reduced thickness with absence of mass effect and midline shift17, • located in the frontal region, with a minimal mass effect and with the presence of a hypodense area between the hematoma and the cerebral cortex, indicating the presence of csf (18). kim et al (19) monitor patients with a chronic subdural hematoma that present volume and thickness of under 43 ml and 13 mm, respectively and a midline shift of under 5 mm on the head ct scan. parlato et al (20) consider that in the case of patients older than 70 years, with altered mental status, brain atrophy and absence of intracranial hypertension signs and symptoms, a “wait and see” strategy should be applied. in some patients, resolution of chronic subdural hematoma was noted under conservative treatment, with the help of corticotherapy, osmotherapy, tranexamic acid, etc. that have the effect of: • inhibition of the inflammatory process 14 | adam et al spontaneous resolution of large subdural hematoma             • inhibition of the hipofibrinolytic activity in chronic subdural hematoma • inhibition of the angiongenic properties of the parietal neomembrane • reduction of the osmotic pressure inside the hematoma’s capsule, this effect thus stopping rebleeding (21–24) the presented case was not treated with any of the aforementioned drugs, and thus their mechanism of action and efficiency will not be thoroughly presented. we emphasize that some chronic subdural hematomas can present resolution over time, in 4 to 15 months after trauma, either spontaneous, or with the help of conservative treatment. recent studies have proposed a grading system based on radiological criteria, that can predict the prognosis of a conservative treatment strategy of chronic subdural hematoma (tabel ii) (25, 26). tabel ii radiological grading system of chronic subdural hematoma for evaluating the potential for success of conservative treatment size based on midline shift small (no midline shift) 0 medium (< 5mm) 1 large (5-10 mm) 2 massive (>10 mm) 3 density based on hounsfiel units on ct scan < 30 0 31 – 40 1 >40 2 *bilateral chronic sdh 1 extra point to be added for patients with a lower score (0-2), conservative treatment has a better chance of success, compared to patients with a higher score. by correlating this radiological grading system with the clinical grading scale described by markwalder, we can state that for patients with chronic subdural hematoma that have a low score (0-2) in both grading systems, the ones that refuse the surgical intervention or are inoperable, conservative treatment can be a potentially successful alternative to the surgical treatment. the patient we reported presented confusion with no focal neurological deficits and his head ct showed a bilateral hematoma with mixed hypo-hyperdensity and no midline shift. according to the markwalder grading system, he had a two point score and as for the radiological grading system, a score of three. the operation could not be performed due to the local infection of the postoperative abdominal wound. in addition, his good neurological status allowed postponing the neurosurgical intervention. repeated head ct scans showed the reduction of density of the acute-on-chronic hematoma and subsequently, its disappearance at 5 months after diagnosis. conclusion although surgical treatment is performed in the majority of chronic subdural hematomas, in clinically and radiologically selected cases, the operation can be avoided. the hematoma can present resolution, either spontaneously or with the help of conservative treatment. romanian neurosurgery (2017) xxxi 1: 8 – 16 | 15             references 1. wepfer j. observationes anatomicae ex cadaveribus eorum quos sustulit apoplexia, cum exercitatione de ejus loco affecto. schaffhusii: impensis o. a waldkirch; 1675. 2. virchow r. das hamatom der dura mater. verh phys med ges wurzbg. 1857;(7):134-142. 3. trotter w. chronic subdural hæmorrhage of traumatic origin, and its relation to pachymeningitis hæmorrhagica interna. br j surg. 1914;2(6):271-291. doi:10.1002/bjs.1800020608. 4. yamashima t, yamamoto s, friede rl. the role of endothelial gap junctions in the enlargement of chronic subdural hematomas. j neurosurg. 1983;59(2):298-303. doi:10.3171/jns.1983.59.2.0298. 5. markwalder tm, reulen hj. influence of neomembranous organisation, cortical expansion and subdural pressure on the post-operative course of chronic subdural haematoma--an analysis of 201 cases. acta neurochir (wien). 1986;79(2-4):100-106. http://www.ncbi.nlm.nih.gov/pubmed/3962738. accessed february 13, 2017. 6. asghar m, adhiyaman v, greenway mw, bhowmick bk, bates a. chronic subdural haematoma in the elderly-a north wales experience. j r soc med. 2002;95(6):290292. http://www.ncbi.nlm.nih.gov/pubmed/12042376. accessed february 13, 2017. 7. kudo h, kuwamura k, izawa i, sawa h, tamaki n. chronic subdural hematoma in elderly people: present status on awaji island and epidemiological prospect. neurol med chir (tokyo). 1992;32(4):207-209. http://www.ncbi.nlm.nih.gov/pubmed/1378564. accessed february 13, 2017. 8. foelholm r, waltimo o. epidemiology of chronic subdural haematoma. acta neurochir (wien). 1975;32(34):247-250. http://www.ncbi.nlm.nih.gov/pubmed/1225014. accessed february 13, 2017. 9. graus f, rogers lr, posner jb. cerebrovascular complications in patients with cancer. medicine (baltimore). 1985;64(1):16-35. http://www.ncbi.nlm.nih.gov/pubmed/3965856. accessed february 13, 2017. 10. reichman j, singer s, navi b, et al. subdural hematoma in patients with cancer. neurosurgery. 2012;71(1):74-79. doi:10.1227/neu.0b013e3182517938. 11. gardner wj. traumatic subdural hematoma. arch neurol psychiatry. 1932;27(4):847. doi:10.1001/archneurpsyc.1932.02230160088009. 12. putnam tj, cusching h. chronic subdrual haematoma: its pathology its reaction to pachymeningitis haemoragica interna and its surgical treatment. arch surg. 1925;11(3):329-339. doi:10.1001/archsurg.1925.01120150002001. 13. ito h, yamamoto s, saito k, ikeda k, hisada k. quantitative estimation of hemorrhage in chronic subdural hematoma using the 51 cr erythrocyte labeling method. j neurosurg. 1987;66(6):862-864. doi:10.3171/jns.1987.66.6.0862. 14. murakami h, hirose y, sagoh m, et al. why do chronic subdural hematomas continue to grow slowly and not coagulate? role of thrombomodulin in the mechanism. j neurosurg. 2002;96(5):877-884. doi:10.3171/jns.2002.96.5.0877. 15. hohenstein a, erber r, schilling l, weigel r. increased mrna expression of vegf within the hematoma and imbalance of angiopoietin-1 and -2 mrna within the neomembranes of chronic subdural hematoma. j neurotrauma. 2005;22(5):518-528. doi:10.1089/neu.2005.22.518. 16. blumberg p. traumatic intracerebral hemorrhage. in: reilly p, bullock r: head injury : pathophysiology and management. 2nd ed. london: hodder arnold; 2005. 17. naganuma h, imai s, yamazaki h, et al. a study of self-resolving chronic subdural hematomas. yamanashi chuo byoin nenpo. 1985;(12):47-51. 18. baldawa ss, nayak n. spontaneous resolution of bilateral chronic subdural hematoma. turk neurosurg. 2015;25(5):835-836. doi:10.5137/1019-5149.jtn.1046614.1. 19. kim hc, ko jh, yoo ds, lee s-k. spontaneous resolution of chronic subdural hematoma : close observation as a treatment strategy. j korean neurosurg soc. 2016;59(6):628-636. doi:10.3340/jkns.2016.59.6.628. 20. parlato c, guarracino a, moraci a. spontaneous resolution of chronic subdural hematoma. surg neurol. 2000;53(4):312-5-7. http://www.ncbi.nlm.nih.gov/pubmed/10825513. accessed february 13, 2017. 21. bender mb, christoff n. nonsurgical treatment of subdural hematomas. arch neurol. 1974;31(2):73-79. doi:10.1001/archneur.1974.00490380021001. 22. sun tfd, boet r, poon ws. non-surgical primary 16 | adam et al spontaneous resolution of large subdural hematoma             treatment of chronic subdural haematoma: preliminary results of using dexamethasone. br j neurosurg. 2005;19(4):327-333. doi:10.1080/02688690500305332. 23. suzuki j, takaku a. nonsurgical treatment of chronic subdural hematoma. j neurosurg. 1970;33(5):548-553. doi:10.3171/jns.1970.33.5.0548. 24. kageyama h, toyooka t, tsuzuki n, oka k. nonsurgical treatment of chronic subdural hematoma with tranexamic acid. j neurosurg. 2013;119(2):332-337. doi:10.3171/2013.3.jns122162. 25. thotakura ak, marabathina nr. nonsurgical treatment of chronic subdural hematoma with steroids. world neurosurg. 2015;84(6):1968-1972. doi:10.1016/j.wneu.2015.08.044. 26. soleman j, noccera f, mariani l. the conservative and pharmacological management of chronic subdural haematoma. swiss med wkly. 2017;147:w14398. doi:smw.2017.14398. doi: 10.33962/roneuro-2021-030 the use of corticosteroids in autoimmune encephalitis. basic and clinical considerations bryan lester nahar-gonzález, ivan david lozada-martinez, yandris arevalo-martínez, loraine quintana-pajaro, silvia prada-soto, teresa pacheco-hernandez, william florez-perdomo, yelson alejandro picón -jaimes, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (2): pp. 192-198 doi: 10.33962/roneuro-2021-030 www.journals.lapub.co.uk/index.php/roneurosurgery the use of corticosteroids in autoimmune encephalitis. basic and clinical considerations b.l. nahar-gonzález1, i.d. lozada-martinez2,3,4, y. arevalomartínez5, l. quintana-pajaro3,5, s. prada-soto6, t. pacheco-hernandez2, w. florez-perdomo3, y.a. picón-jaimes7, l.r. moscote-salazar2,3,4 1 medical and surgical research center, new jersey, usa 2 medical and surgical research center, university of cartagena, colombia 3 colombian clinical research group in neurocritical care, university of cartagena, colombia 4 latin american council of neurocritical care, cartagena, colombia 5 center for biomedical research, university of cartagena, colombia 6 medical and surgical research center, atlanta, usa 7 medical and surgical research center, valencian international university, chile abstract autoimmune encephalitis (ae) is a brain inflammation caused by autoantibodies that target proteins, intracellular and extracellular antigens, triggering damage in the cns; ae is classified in various syndromes caused by various antibodies, it is a diagnosis of exclusion. therefore, it has to be differentiated from multiple causes that could unleash encephalitis. however, its treatment is based primarily on immunotherapy, where corticosteroids as immunosuppressive agents, play a key role in the treatment along with other agents. introduction the immune system, under certain pathophysiological conditions, is capable of producing antibodies against cells, tissues, or organs, triggering known autoimmune diseases [1]. these reactions are often expressed in the central nervous system, for example, autoimmune encephalitis (ad), which is a brain inflammation due to the presence of freely circulating autoantibodies that affect nerve cells [2]. the advent of technologies that have allowed the detection of antibody subtypes, has modified the classification of autoimmune encephalitis, substantially improving the diagnosis, management, and prognosis of these patients [1,2]. however, one of the current challenges consists of keywords encephalitis. autoimmunity. autoantibodies. corticosteroids corresponding author: ivan david lozada-martínez medical and surgical research center, university of cartagena, colombia ilozadam@unicartagena.edu.co copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 193 the use of corticosteroids in autoimmune encephalitis as in early diagnosis and management in low-level hospital institutions, which do not have laboratories or specialized equipment that facilitate this type of exam, so the approach in these cases is general, frequently with the isolated use of corticosteroids [3]. based on the above, the objective of this manuscript is to present evidence on the role of corticosteroids in the treatment of autoimmune encephalitis, highlighting basic and clinical aspects that translate their understanding and usefulness. pathogenesis of autoimmune encephalitis ad is brain inflammation produced by the action of autoantibodies directed against cell surface proteins, intracellular and intracellular antigens [2,4]. various processes such as paraneoplastic syndromes, molecular mimicry, vaccines, or failure of immune tolerance, might trigger the production of autoantibodies against specific antigens that cause disease [1,4]. for this reason, the identification of autoantibodies constitutes a fundamental step to understand the pathophysiological mechanism of autoimmune encephalitis, its complete understanding will allow choosing the appropriate diagnostic tests and treatment [1,4]. autoimmune encephalitis is classified taking into account the pathophysiological mechanism that produces it (figure 1). for this reason, the pathogenesis will be addressed, considering grouping antibodies according to the location of their antigens [5-7]. figure 1. autoimmune encephalitis classification according to the pathogenetic mechanism [2,4,6,7]. paraneoplastic syndromes, in which antibodies "anti-hu" are directed against intracellular antigens, primarily tissue such as temporal lobe, cerebellum, brainstem, dorsal roots, and autonomic nervous system [8-9]. in other autoimmune systemic syndromes such as systemic lupus erythematosus, where there are antibodies against phosphorylated ribosomal p proteins, neurological and/or psychiatric manifestations may occur, such as psychosis, with a positive correlation between antibody levels and severity of symptoms [10,11]. the binding of antibodies to antigens, whether at the intracellular or extracellular level, causes alteration of synaptic interactions and prevents the expression of these receptors; if this happens for a long time, irreversible damage to the central nervous system could be generated [12]. clinical manifestations ad has a wide clinical spectrum in which they can be found from the typical encephalitis with involvement of the limbic system, to complex neuropsychiatric symptoms. these symptoms are related to the type of antibody and the antigen to which it is directed (table 1) [1,2,5]. antigen manifestations nmda psychosis, dystonia, chorea, epilepsy, cognitive impairment, dysautonomia ampa psychosis, limbic encephalitis, aggressiveness, hallucinations, sleep disorders gad 65 stiff man syndrome, dm1, cerebellitis anna 1 cerebellitis gaba psychosis, epilepsy caspr2 neuromyotonia, muscle spasm, fasciculations, insomnia, hallucinations table 1. clinical manifestations related to the type of antigen [2,5]. symptoms despite being variables, in most adolescents and adults evolve in stages, initially, the symptoms may appear similar to a viral infection in which headache and fever are the most common. later, between days and weeks, neuropsychiatric 194 b.l. nahar-gonzález, i.d. lozada-martinez, y. arevalo-martínez et al. symptoms are triggered. these may include psychosis, euphoria, aggression, inappropriate sexual behaviors, fear, panic attacks, and compulsive behaviors, cognitive impairment, seizures (predominantly in pediatric patients) [13], sleep disturbances, developmental and language regression, catatonia, gait instability, and autonomic instability [14,15]. subtypes of autoimmune encephalitis depending on the presence of specific autoantibodies directed against synaptic and neuronal cell surface antigens [2], the following encephalitis subtypes occur: antibodies against intracellular antigens anti-hu encephalitis (anna-1) in anti-hu encephalitis (anna-1), many patients present with sensory neuropathy, cerebellar degeneration, encephalitis, or encephalomyelitis. interestingly, this condition is closely related to small cell lung cancer [5]. other patients with anti-hu present with a pattern of encephalitis with greater involvement of the brainstem [16-18] or limbic system [8,18,19]. antibodies against intracellular synaptic proteins anti-gad65 encephalitis in anti-gad65 encephalitis (glutamic acid decarboxylase 65 kd), the antibody targets the enzyme required for the synthesis of the neurotransmitter gaba [5,20,21]. it is clinically associated with type 1 diabetes mellitus, cerebellar ataxia, stiff man syndrome [22,23] and limbic encephalitis [2,8,18,19]. in the paraneoplastic setting, it is related to paraneoplastic cerebellar degeneration [5]. antibodies against extracellular antigens anti-nmdar encephalitis anti-nmdar (n-methyl-d-aspartate receptor) encephalitis represents 20% of autoimmune encephalitis, being the most frequent [2]. it begins with fever, nausea and diarrhea, 2 weeks later psychiatric and / or neurological symptoms begin, progressing rapidly with a tendency to severity, reaching a comatose phase [14,24,25]. its classic manifestations are: psychosis, agitation, dyskinesias, sleep disorders, mutism, encephalopathy, faciobrachial seizures, dysautonomia, and cognitive impairment [25]. anti-lgi1 encephalitis anti-lgi1 encephalitis (glioma-inactivated leucine-1) is responsible for most cases of encephalitis attributed to vgkc1 antibodies, its most frequent symptoms are myoclonus, seizures, hyponatremia, limbic encephalitis and fascio-brachial dystonic seizures [26-28]. anti-caspr2 encephalitis anti-caspr2 encephalitis is associated with morvan syndrome and isaacs syndrome. it may present with confusion and personality change [5.29]. seronegative autoimmune encephalitis a subgroup of patients, due to their clinical manifestations, presents suspicion of autoimmunity, but the antibody detection test is negative, their main symptoms are of a psychiatric nature, including perceptual alterations, catatonia and agitation [1]. diagnostic approach the diagnosis of ad is made based on the clinical characteristics, so it should be suspected in any adult or child with the previously mentioned manifestations. usually, the diagnosis is accompanied by magnetic resonance imaging, electroencephalography, functional neuro imaging, analysis of systemic tumors, and detection of antibodies. in magnetic resonance, the ea may appear as a completely normal image to an abnormal increase in contrast in the cortical or subcortical area of the brain parenchyma. positron emission tomography, although not performed routinely, can report an increase in frontal-occipital metabolism. this latter finding is related to longstanding [1,2,3,30] disease. the most frequently observed changes in cerebrospinal fluid (csf) are predominantly lymphocytic pleocytosis or oligoclonal bands in the csf. another diagnostic tool is the eeg. in this study, a low frequency of disordered activity can be observed, but epileptogenic activity is rarely evidenced. a unique finding, known as a delta brush, is related to prolonged disease [31]. another useful tool is the detection of autoantibodies in both blood and csf. one of the most frequent antibodies isolated is the igg anti 195 the use of corticosteroids in autoimmune encephalitis nmdar antibody [15]. it should be emphasized that the detection of antibodies in csf has greater sensitivity and specificity than serum detection [32]. in certain cases, the anti-nmdar type iga and igm may be isolated, but these do not have diagnostic value, however, they are associated with chronic diseases such as schizophrenia [33,34]. in the setting of advanced encephalitis, antibodies tend to remain elevated in csf, while their titers may be low in serum due to treatment [30,35,36]. the differential diagnosis of ad includes a broad category of psychiatric disorders such as psychosis or schizophrenia (the most common), malignant catatonia, or viral encephalitis. although not very common, cases of autoimmune encephalitis associated with covid-19 have been reported [3739]. pillars of autoimmune encephalitis therapy there are 2 primary goals in ad therapy: reducing inflammation and slowing the development of the disease, which in turn improves symptoms in patients [1]. a cornerstone of treatment is the early use of immunotherapy when there is a high clinical suspicion of ae, even when the presence of neoplasia or the presence of antibodies has not been identified [40]. however, antibody identification is crucial and that leads to a specific treatment. if there is the presence of tumors, resection this is an important part of treatment [2,3,6]. immunotherapy immunotherapy in ad includes general immunosuppressive agents and others that target phases of pathogenesis [6]. there are 3 lines of treatment; a first-line consisting of steroids, intravenous (iv) immunoglobulin and plasmapheresis (plex), a second containing rituximab and cyclophosphamide, and an alternative therapy that includes agents such as azathioprine, mycophenolate mofetil [1,3,6,41, 42], which are steroid-sparing agents used for maintenance, and tocilizumab for refractory cases [6]. it is important to keep in mind that ae associated with neoplasms has a faster course and is irreversible; in other words, it is difficult for patients to recover even when treatment is started early [43]. in the event of clinical suspicion of ad, empirical treatment should be instituted as quickly as possible, even before the results of antibody tests [40], and may include steroids and/or iv immunoglobulins [5], and if the first-line therapy fails, we should start the second line as quickly as possible. the response to first-line therapy [6] can be observed approximately 2 weeks after starting treatment, so this is the time to take into account for changing therapy, if necessary. however, a significant number of patients with ad will respond to first-line therapy and will have a good outcome within 1–2 weeks after initiation of therapy [3]. table 2 describes the therapeutic lines available for the management of ad. therapy therapeutic target posology children adults first line therapy corticosteroids methylprednisolon e (solumedrol) [5] cytokines, deplete t cells 30 mg / kg up to 1000 mg iv over 3 to 5 days 1 gram per day for 3-5 days iv immunoglobuline antibodies and autoimmune mediators 2 g / kg over 2 days, followed by weekly dose for the next 4 weeks** 0.4 g / kg / day for 5 days plasmapheresis antibodies and autoimmune mediators 1 session every 2 days for 5-7 days second line therapy rituximab cd20 + b cells and short-lived plasma cells 375 mg / m2 iv infusion weekly for 4 weeks cyclophosphamide lymphocytes (alters dna crosslinking) 750 mg / m2 iv monthly *** for 3-6 months [3,6] alternative therapy azathioprine lymphocytes (blocks nucleotide synthesis) initially 1-1.5 mg / kg once daily or divided twice daily, target 2-3 mg / kg / day 196 b.l. nahar-gonzález, i.d. lozada-martinez, y. arevalo-martínez et al. mycophenolate lymphocytes (inhibits imp dehydrogenas e) initially 500mg twice daily, target 1000mg twice daily tocilizumab cytokines initially 4 mg/kg, followed by an increase of 8 mg/kg per month based on clinical response il-2 (aldesleucina) cytokines 1.5 million iu / day, 4 subcutaneous injections 3 weeks apart each other ** if a synaptic antibody/cell surface disorder is detected, administer ivig, plasmapheresis, and/or steroids. if a synaptic / cell surface antibody is determined and significant symptoms are shown, provide first-line therapy if not provided [5]. ** in severe cases, it is given more frequently with the first 2-3 cycles given every 2 weeks [1] *** until improvement is observed [5]. table 2. therapeutic lines for autoimmune encephalitis [1,5,6]. symptomatic treatment it is composed of sedative drugs, to induce and maintain sleep; drugs to manage agitation and emotional instability such as benzodiazepines, clonidine, antiepileptics, choral hydrate, or others, which usually offer benefits [3]. treatment in the presence of seizures must be carried out aggressively with antiepileptics. the majority of patients do not require long-term seizure treatment [44]. corticosteroids and its mechanism of action in encephalitis corticosteroids are the most important first-line agents in ad therapy [3,6], being beneficial in multiple autoimmune disorders [5,6]. although there is no strong evidence for the superiority of corticosteroids over other therapies, they are the first treatment option, followed by intravenous immunoglobulins and plex [6]. mechanism of action corticosteroids are a group of drugs with antiinflammatory characteristics that act on intracellular glucocorticoid receptors [6], interrupting the transcription of multiple pro-inflammatory genes [6,7] that are activated in chronic inflammatory diseases [7] and that encode cytokines, chemokines, adhesion molecules, inflammatory enzymes, receptors, and proteins [6,7]. they influence almost all cytokines, thus depleting t cells, inhibiting th1 differentiation, macrophage dysfunction, and eosinophil apoptosis [6]. in high concentrations, they have activity on the synthesis of anti-inflammatory proteins and induce post-transcriptional or postgenomic effects [6,7]. advantages they penetrate the brain, an advantage it has over other drugs such as rituximab, which does not cross the blood-brain barrier (bbb) [6], so they are given as empirical therapy in suspected ad [45]. in addition, they modulate the bbb [3] restoring its integrity and controlling cerebral edema [6]. goldenholz et al [45] state that corticosteroids as a low-cost therapy could play a role in treatment algorithms for suspected ad cases [45]. similarly, prasad et al [46] that in ad a good response to steroids has been shown even when no confirmed serology suggests an autoimmune basis [46]. disadvantages steroids have low specificity on antibody-mediated immune processes, so their efficacy has been debated in ad since they slightly decrease the number of circulating b cells, not contributing much to antibody titers; in addition, they have been associated with systemic side effects [6]. it should be noted that side effects are more frequent with the use of oral steroids than with intravenous [1]. corticosteroids can also cause or increase the psychiatric symptoms associated with ad, and some clinical studies even suggest neurotoxic and neurodegenerative effects of corticosteroids after chronic exposure [6]. management steroids are administered iv or orally, the former being delivered as “pulse doses” (table 2). this therapy is not standard and there are no clear treatment regimens [1]. nosadini et al [47] carried out a systematic review on immune therapy in ad, with the aim of generating evidence on the use, type of treatment and efficacy, finding that as first-line 197 the use of corticosteroids in autoimmune encephalitis therapy, it is used in the majority of cases (more than 50% of patients with ad) [47]. conclusion autoimmune encephalitis is a syndrome whose pathogenesis involves different immunological pathways against neuronal surface antigens, for which immunotherapy with various immunosuppressive agents has been proposed as treatment; with a relatively accepted answer. corticosteroids are consolidated as first-line agents in the treatment of ad, however, better quality studies are needed to demonstrate their superiority over other therapies, and thus identify the safest and most effective system. references 1. mooneyham glc, gallentine w, van mater h. evaluation and management of autoimmune encephalitis: a clinical overview for the practicing child psychiatrist. child adolesc psychiatr clin n am. 2018; 27(1):37–52. 2. bost c, pascual o, honnorat j. autoimmune encephalitis in psychiatric institutions: current perspectives. neuropsychiatr dis treat. 2016; 12:2775–87. 3. dale rc, gorman mp, lim m. autoimmune encephalitis in children: clinical phenomenology, therapeutics, and emerging challenges. curr opin neurol. 2017; 30(3):334– 44. 4. fukata m, yokoi n, fukata y. neurobiology of autoimmune encephalitis. curr opin neurobiol. 2018; 48:1–8. 5. lancaster e. the diagnosis and treatment of autoimmune encephalitis. j clin neurol. 2016; 12(1):1-13. 6. gonzález torre ja, cruz-gómez áj, belenguer a, sanchissegura c, ávila c, forn c. hippocampal dysfunction is associated with memory impairment in multiple sclerosis: a volumetric and functional connectivity study. mult scler j. 2017; 23(14):1854–63. 7. barnes pj. how corticosteroids control inflammation: quintiles prize lecture 2005. br j pharmacol. 2006; 148(3):245–54. 8. gultekin sh, rosenfeld mr, voltz r, eichen j, posner jb, dalmau j. paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients. brain. 2000; 123 (pt 7):1481-94. 9. sillevis smitt p, grefkens j, de leeuw b, van den bent m, van putten w, hooijkaas h, et al. survival and outcome in 73 anti-hu positive patients with paraneoplastic encephalomyelitis/sensory neuronopathy. j neurol. 2002; 249(6):745-53. 10. bonfa e, elkon kb. clinical and serologic associations of the antiribosomal p protein antibody. arthritis rheum. 1986; 29(8):981-5. 11. koffler d, miller te, lahita rg. studies on the specificity and clinical correlation of antiribosomal antibodies in systemic lupus erythematosus sera. arthritis rheum. 1979; 22(5):463-70. 12. tanaka k. recent update on autoimmune encephalitis/encephalopathy. clin exp neuroimmunol. 2015; 6(1):70–82. 13. wright s, vincent a. pediatric autoimmune epileptic encephalopathies. j child neurol 2017; 32(4):418–28. 14. dalmau j, tüzün e, wu hy, masjuan j, rossi je, voloschin a, et al. paraneoplastic anti-n-methyl-d-aspartate receptor encephalitis associated with ovarian teratoma. ann neurol. 2007; 61(1):25-36. 15. prüss h, dalmau j, harms l, höltje m, ahnert-hilger g, borowski k, et al. retrospective analysis of nmda receptor antibodies in encephalitis of unknown origin. neurology. 2010; 75(19):1735-9. 16. dalmau j, graus f, rosenblum mk, posner jb. anti-hu-associated paraneoplastic encephalomyelitis/sensory neuronopathy. a clinical study of 71 patients. medicine (baltimore). 1992; 71(2):59-72. 17. saiz a, bruna j, stourac p, vigliani mc, giometto b, grisold w, et al. anti-hu-associated brainstem encephalitis. j neurol neurosurg psychiatry. 2009; 80(4):404-7. 18. voltz r, gultekin sh, rosenfeld mr, gerstner e, eichen j, posner jb, et al. a serologic marker of paraneoplastic limbic and brain-stem encephalitis in patients with testicular cancer. n engl j med. 1999; 340(23):1788-95. 19. lawn nd, westmoreland bf, kiely mj, lennon va, vernino s. clinical, magnetic resonance imaging, and electroencephalographic findings in paraneoplastic limbic encephalitis. mayo clin proc. 2003; 78(11):1363-8. 20. kim j, namchuk m, bugawan t, fu q, jaffe m, shi y, et al. higher autoantibody levels and recognition of a linear nh2-terminal epitope in the autoantigen gad65, distinguish stiff-man syndrome from insulin-dependent diabetes mellitus. j exp med. 1994; 180(2):595-606. 21. dalakas mc. stiff person syndrome: advances in pathogenesis and therapeutic interventions. curr treat options neurol. 2009; 11(2):102-10. 22. manto mu, laute ma, aguera m, rogemond v, pandolfo m, honnorat j. effects of anti-glutamic acid decarboxylase antibodies associated with neurological diseases. ann neurol. 2007; 61(6):544-51. 23. alexopoulos h, dalakas mc. a critical update on the immunopathogenesis of stiff person syndrome. eur j clin invest. 2010; 40(11):1018-25. 24. dalmau j, gleichman aj, hughes eg, rossi je, peng x, lai m, et al. anti-nmda-receptor encephalitis: case series and analysis of the effects of antibodies. lancet neurol. 2008; 7(12):1091-8. 25. florance-ryan n, dalmau j. update on anti-n-methyl-daspartate receptor encephalitis in children and adolescents. curr opin pediatr. 2010; 22(6):739-44. 26. irani sr, michell aw, lang b, pettingill p, waters p, johnson mr, et al. faciobrachial dystonic seizures precede lgi1 antibody limbic encephalitis. ann neurol. 198 b.l. nahar-gonzález, i.d. lozada-martinez, y. arevalo-martínez et al. 2011; 69(5):892-900. 27. sen a, wang j, laue-gizzi h, lee t, ghougassian d, somerville er. pathognomonic seizures in limbic encephalitis associated with anti-lgi1 antibodies. lancet. 2014; 383(9933):2018. 28. thompson j, bi m, murchison ag, makuch m, bien cg, chu k, et al. faciobrachial dystonic seizures study group. the importance of early immunotherapy in patients with faciobrachial dystonic seizures. brain. 2018; 141(2):348356. 29. lópez-chiriboga as, klein c, zekeridou a, mckeon a, dubey d, flanagan ep, et al. lgi1 and caspr2 neurological autoimmunity in children. ann neurol. 2018; 84(3):473-480. 30. florance nr, davis rl, lam c, szperka c, zhou l, ahmad s, et al. anti-n-methyl-d-aspartate receptor (nmdar) encephalitis in children and adolescents. ann neurol. 2009; 66(1):11-8. 31. schmitt se, pargeon k, frechette es, hirsch lj, dalmau j, friedman d. extreme delta brush: a unique eeg pattern in adults with anti-nmda receptor encephalitis. neurology. 2012; 79(11):1094-100. 32. gresa-arribas n, titulaer mj, torrents a, aguilar e, mccracken l, leypoldt f, et al. antibody titres at diagnosis and during follow-up of anti-nmda receptor encephalitis: a retrospective study. lancet neurol. 2014; 13(2):167-77. 33. dahm l, ott c, steiner j, stepniak b, teegen b, saschenbrecker s, et al. seroprevalence of autoantibodies against brain antigens in health and disease. ann neurol. 2014; 76(1):82-94. 34. hara m, martinez-hernandez e, ariño h, armangué t, spatola m, petit-pedrol m, et al. clinical and pathogenic significance of igg, iga, and igm antibodies against the nmda receptor. neurology. 2018; 90(16):e1386-e1394. 35. okamoto s, hirano t, takahashi y, yamashita t, uyama e, uchino m. paraneoplastic limbic encephalitis caused by ovarian teratoma with autoantibodies to glutamate receptor. intern med. 2007; 46(13):1019-22. 36. seki m, suzuki s, iizuka t, shimizu t, nihei y, suzuki n, et al. neurological response to early removal of ovarian teratoma in anti-nmdar encephalitis. j neurol neurosurg psychiatry. 2008; 79(3):324-6. 37. monti g, giovannini g, marudi a, bedin r, melegari a, simone am, et al. anti-nmda receptor encephalitis presenting as new onset refractory status epilepticus in covid-19. seizure. 2020; 81:18-20. 38. burr t, barton c, doll e, lakhotia a, sweeney m. n-methyld-aspartate receptor encephalitis associated with covid-19 infection in a toddler. pediatr neurol. 2021; 114:75-76. 39. panariello a, bassetti r, radice a, rossotti r, puoti m, corradin m, et al. anti-nmda receptor encephalitis in a psychiatric covid-19 patient: a case report. brain behav immun. 2020; 87:179-181. 40. graus f, titulaer mj, balu r, benseler s, bien cg, cellucci t, et al. a clinical approach to diagnosis of autoimmune encephalitis. lancet neurol. 2016; 15(4):391-404. 41. shin yw, lee st, park ki, jung kh, jung ky, lee sk, et al. treatment strategies for autoimmune encephalitis. ther adv neurol disord. 2017; 11:1756285617722347. 42. vernino s, o'neill bp, marks rs, o'fallon jr, kimmel dw. immunomodulatory treatment trial for paraneoplastic neurological disorders. neuro oncol. 2004; 6(1):55-62. 43. vedeler ca, antoine jc, giometto b, graus f, grisold w, hart ik, et al. paraneoplastic neurological syndrome euronetwork. management of paraneoplastic neurological syndromes: report of an efns task force. eur j neurol. 2006; 13(7):682-90. 44. dalmau j, lancaster e, martinez-hernandez e, rosenfeld mr, balice-gordon r. clinical experience and laboratory investigations in patients with anti-nmdar encephalitis. lancet neurol. 2011; 10(1):63-74. 45. goldenholz dm, wong vs, bateman lm, apperson m, oskarsson b, akhtar s, et al. treatment of γ-aminobutyric acid b receptor-antibody autoimmune encephalitis with oral corticosteroids. arch neurol. 2012; 69(8):1061-3. 46. prasad p, bhargava a, khichar s, gupta vk. clinical spectrum of autoimmune encephalitis: case series from western rajasthan. j clin diagnostic res. 2017; 11(11): or01-or04. 47. nosadini m, mohammad ss, ramanathan s, brilot f, dale rc. immune therapy in autoimmune encephalitis: a systematic review. expert rev neurother. 2015; 15(12):1391-419. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article unruptured anterior communicating artery aneurysm with co-existing blister aneurysms: case report and review of literature karthikeyan y.r., rashim kataria, virendra deo sinha india doi: 10.1515/romneu-2017-0033 romanian neurosurgery (2017) xxxi 2: 207 – 210 | 207 doi: 10.1515/romneu-2017-0033 unruptured anterior communicating artery aneurysm with co-existing blister aneurysms: case report and review of literature karthikeyan y.r., rashim kataria, virendra deo sinha department of neurosurgery, sms medical college, jaipur, india abstract: blister aneurysms are a separate class of vascular malformations with a unique etiopathogenesis and clinical profile, elusive to radiological imaging and complex to manage. unless identified and managed appropriately they often lead increased morbidity intra and post operatively. they are commonly reported in internal carotid artery. we are reporting a rare case of intraoperatively diagnosed blister aneurysm of the anterior cerebral artery, the management options and the importance of constant vigilance in cases where the aneurysm appears unruptured intraoperatively. key words: anterior communicating artery, unruptured aneurysm, blister aneurysm, a1 segment introduction blister aneurysms (ba) are a relatively common entity seen in the supraclinoidal internal carotid artery (ica). their occurrence in the anterior cerebral artery (aca) is very rare and limited to case reports. bas are etiopathologically different from the berry aneurysms and pose a great challenge in diagnosis and management. we are reporting a very rare case of co-existent anterior communicating artery (a-comm) saccular aneurysm with blister aneurysms of the anterior communicating artery and adjacent a1 segment along with the review of literature and management options of this complex clinical entity. case summary a forty five year old lady presented to us with a history of sudden severe headache and trivial ground level fall. on examination the patient was conscious but drowsy. neurological examination was unremarkable. the initial computed tomography brain showed blood in the basal cisterns and associated intraventricular hemorrhage. emergency ct angiography was performed. [figure 1] it revealed a single saccular anterior communicating artery aneurysm with the dome pointing towards the left and slightly posteriorly. vasospasm was seen in bilateral a2 segment of aca and the neck was 4mm in width. the patient was planned for emergency 208 | karthikeyan et al unruptured anterior communicating artery aneurysm clipping of the aneurysm. right pterional approach was planned. intra operatively, a single a-comm aneurysm with the above mentioned configuration was identified. there were no signs of rupture of the saccular aneurysm such as tit, surrounding hematoma, irregular dome or surrounding adhesions. it appeared unlikely to be the source of bleed. the saccular aneurysm was clipped. on careful evaluation two small blister aneurysms were found, one in the right a1 segment near a-comm and the other on the a-comm. these were surrounded by a small hematoma in the vicinity. [figure 2] we considered this to be the source of bleeding. a small muscle patch was harvested from the temporal muscle and placed over the blister aneurysm and was secured with a fenestrated clip encompassing the right a1 and proximal right a2. postoperative ct angiography brain showed normal distal flow bilaterally. [figure 3] the patient underwent a satisfactory recovery post operatively. discussion blister aneurysms (ba) are typically described as hemispheric aneurysmal bulge protruding from non‑branching sites of the intracranial arteries. the term “blister” was introduced in 1988 by takashi. (1)the most common reported site of ba is aneurysms arising from non-branching sites from the dorsomedial wall of the internal carotid artery (ica). the relative frequencies of bas are ica 91.6%, a-comm 2.8%, middle cerebral artery 1.9%, posterior cerebral artery 1.6%, basilar artery 1.6% and anterior cerebral artery 0.3%. (2) figure 1 a computed tomography (ct) of brain showing intraventricular hemorrhage. b three dimensional ct angiography (right) showing superiorly projecting a comm aneurysm romanian neurosurgery (2017) xxxi 2: 207 – 210 | 209 figure 2 diagrammatic representation of intraoperative view of a-comm aneurysm on the dorsal aspect and the two blisters, one in the right a1 segment near a-comm and the other on the a-comm figure 3 post-operative three dimensional ct angiography showing the clips in-situ and with distal flow in bilateral anterior cerebral artery bas exhibit rapid changes in size and morphology on angiograms. other features characteristic of these aneurysms are preponderance of arterial hypertension, atherosclerosis, ica dissection, younger age and female sex.(3) pathological studies have revealed focal wall defects covered by a thin layer of fibrous tissue and adventitia without any evidence of the usual collagenous layer.(3) the exact pathogenesis of these aneurysms are uncertain but the proposed mechanism is atherosclerotic weakening leading to wall changes, hemodynamic stress and possible dissection. these pathological features not only differentiate them from the routine saccular aneurysms but also explain their unpredictable behavior pre and intra operatively. this predisposes them to a high risk of premature rupture during surgery and associated development of large lacerations on the parent vessel with resultant poor outcome in many of these patients. because of their small size, fragile‑thin wall and a broad‑based neck these aneurysms are a real challenge to manage. patients typically present with acute subarachnoid hemorrhage (sah). the angiographic diagnosis of ba on conventional two dimensional digital subtraction angiography may be difficult because of their small size and irregular morphology. repeat angiography often documents luminal changes or growth of these lesions. their natural history remains unpredictable. bas are often the cause of bleed in sah of unknown etiology. three dimensional digital subtraction angiography remains the gold standard investigation for diagnosis of these notorious lesions. as these aneurysms are etiopathologically different from the saccular aneurysms their management is complicated and controversial. the standard clipping techniques are not 210 | karthikeyan et al unruptured anterior communicating artery aneurysm feasible in most cases and when possible they are risky and require expertise. numerous therapeutic strategies have been used including direct clipping, clipping plus wrapping, wrapping alone, clipping with encircling graft clips, encircling silicone clip application, primary suturing of ica, vascular staple clip closure of ica and trapping with or without extracranial-intracranial bypass. (4) over the past decade significant advances have been made in endovascular techniques (flow diverters, stents) which are gradually becoming the standard of care for the small but complicated aneurysms. gonzales et al systematically reviewed 62 published series and they concluded that bas are more aggressive than saccular aneurysms and have a higher incidence of complications irrespective of the technique used. (5) bas are further complicated by regrowth and rebleeding after treatment. though endovascular techniques have a low morbidity, postoperative antiplatelet therapy remains a major constraint. one has to carefully look for bas in every case where the saccular aneurysms do not show any signs of rupture during the surgery. we would also like to emphasize the importance of various surgical techniques mentioned above for intraoperatively identified bas, which were not visualized in pre-operative imaging specially in facilities which lack the advanced endovascular techniques. constant vigilance for these lesions in all cases of saccular aneurysms, more so in the absence of definite signs of rupture and their prompt management will lead to a better overall outcome. though advanced endovascular techniques have become the procedures of choice, the importance of acquaintance with the open surgical techniques of management cannot be overemphasized. hence the surgical techniques of management of these lesions are still relevant in current day practice. correspondence dr. rashim kataria associate professor neurosurgery department of neurosurgery sms medical college, jaipur mail: rashim_kat@yahoo.com contact: +91 9636261597 references 1. chinchure sd, gupta v, goel g, gupta a, jha a. subarachnoid hemorrhage with blister aneurysms: endovascular management. neurol india 62: 393-399, 2014. 2. gonzalez am, narata ap, yilmaz h, bijlenga p, radovanovic i, schaller k, lovblad ko, pereira vm. blood blister-like aneurysms: single center experience and systematic literature review. eur j radiol 83(1): 197205, 2014. 3. jha an, gupta v. blister aneurysms. neurol india 57(1): 2-3, 2009. 4. peschillo s, cannizzaro d, caporlingua a, missori p. a systematic review and meta-analysis of treatment and outcome of blister-like aneurysms. am j neuroradiol 37(5): 856-861, 2016. 5. sim sy, shin ys, cho kg, kim sy, kim sh, ahn yh, yoon sh, cho kh. blood blister-like aneurysms at nonbranching sites of the internal carotid artery. j neurosurg 105: 400-405, 2006. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article intradural spinal neurocysticercosis: case illustration jorge balderrama, dania elizabeth trinidad arevalo, willem guillermo calderon-mirada, andrei f. joaquim, alfonso pacheco-hernandez, amit agrawal, huber said padilla-zambrano, daniela lopez-cepeda, jessica amaya-quintero, yancarlos ramos-villegas, luis rafael moscote-salazar mexico, brazil, colombia doi: 10.1515/romneu-2017-0082 530 | balderrama et al intradural spinal neurocysticercosis doi: 10.1515/romneu-2017-0082 intradural spinal neurocysticercosis: case illustration jorge balderrama1, dania elizabeth trinidad arevalo2, willem guillermo calderon-mirada3, andrei f. joaquim4, alfonso pacheco-hernandez5, amit agrawal6, huber said padillazambrano7, daniela lopez-cepeda7, jessica amaya-quintero7, yancarlos ramos-villegas7, luis rafael moscote-salazar5 1neuroradiology, national institute of neurology and neurosurgery "manuel velasco suárez", mexico city, mexico; 2national institute of neurology and neurosurgery "manuel velasco suárez", mexico city, mexico; 3department of radiology, national autonomous university of mexico, mexico city, mexico; 4neurosurgeon, state university of campinas (unicamp), campinas-sao paulo and centro infantil boldrini, campinas-sp. brazil; 5neurosurgeon, university of cartagena, cartagena de indias, colombia; 6professor of neurosurgery, mm institute of medical sciences & research maharishi markandeshwar university, mullanaambala, haryana, india; 7university of cartagena, cartagena de indias, colombia abstract: introduction: neurocysticercosis (ncc) is a common parasitic infection of the central nervous system caused by the larvae of the taenia solium. spinal cord involvement is very uncommon. clinical case: a female patient with a history of ncc presented with chronic and recurrent headache associated with motor and sensory deficit, which develops tonic-clonic convulsion, with spatial disorientation. she also had intracranial hypertension syndrome, meningitis syndrome, and pyramidal sygns suggestive of spinal ncc. conclusions: neurocysticercosis usually occurs in developing countries and should be considered as a differential diagnosis of neurological diseases. early diagnosis and treatment are mandatory, as well as education to the community to primary prevention. key words: neurocysticercosis, spine, taenia solium introduction cysticercosis is the most common parasitic disease affecting the central nervous system in under developing countries, caused by the larvae of the taenia solium. neurocystecircosis ncc is unusual form of cysticercosis (1–6), which can be categorized according to its main cns involvement as: parenchymal, leptomeningal, intraventricular or spinal, according to the location of the lesions. spinal ncc accounts for about 0.7 to 0.85% of all cases, and most of these are accompanied by concomitant intracranial involvement (2,7–9); it also may occur with extra-spinal involvement romanian neurosurgery (2017) xxxi 4: 530 535 | 531 (vertebral) or intraspinal (intradural, extramedullary or intramedullary) (4), being the extramedullary-intradural form the most common, with an incidence of almost 80% of the spinal forms (5). case a female patient with a history of ncc diagnosis characterized by intense oppressive headache and periods of amnestic, which had received a peritoneal ventricle bypass system – sdvp because of presenting obstructive hydrocephalus secondary to ncc. prior to the shunt surgery, she developed an uncontrolled convulsive syndrome for the last 2 months. one month later, she presented with a moderate to severe pulsatile headache, irradiated in the frontal region of the evening predominance, triggered by stress factors, which improved with the intake of nsaids. a week later, severe intensity headache (10/10 on the analogue pain scale), which was irradiated to the frontal region of the evening predominance, reappeared, accompanied by nausea, subjective vertigo, and an approximate weight loss of 5 kg. the patient presented progressive weakness in the left lower limb, which then became bilateral. it also refers to frequent falls with inversion of the right foot to ambulation. following this, it presents paresthesias (numbness and cramps) with increased difficulty in walking and sensory deficit. at the initial neurological examination are found the mental functions preserved, the cranial nerves without alterations, strength, tone, trophism and normal sensitivity, neurophatic gait, muscular stretching reflexes +++ are symmetrical and generalized, without data of meningeal irritation. cerebellar examination is normal. there are no pathological or ataxic reflexes. after admission, she performs tonic-clonic convulsive crisis with disorientation in time and place, encountering endocranial hypertension syndrome, meningeal irritation syndrome and pyramidal syndrome. in addition, are the reflexes of hoffman, tromner and palmomental. in the initial ct scan, it was observed enlargement of the ventricular system and a mild right frontal cortical hypodensity, suggestive of ncc, an mri of the lumbar and thoracic spine was performed, as well as csf sample for cytochemical analysis. the glucose was 37 mg/dl, with an increase of proteins levels 49 mg/dl and increase of the number of cells at the expense of lymphocytes, with an elisa test for diagnosis cysticercus positive. spinal myelography was performed, showing altered contrast suggestive of spinal cysticercosis (figure 1). it was decided to start treatment with albendazole. patient is managed on an outpatient basis by family decision. figure 1 spinal myelography showing contrast alteration suggestive of spinal cysticercosis, with many levels of stensosis due to the cysts 532 | balderrama et al intradural spinal neurocysticercosis ncc is a common parasitic infection of the central nervous system cns, being the main cause of acquired epilepsy and other neurological morbidities in many areas of the world, especially in under developed countries (1,10). the peak of incidence is between the 3rd and 4th decade of life (11). this infection is common in central and south america, most of southeast asia, part of china, many non-muslim regional of africa (10). the ncc was first described by paranoli in 1550, and its causative agent, the taenia solium, was recognized by leuckart y kuchenmeister in the 19th century (6,12,13). spinal involvement is rare, and it has been subdivided in extradural, intradural-extramedullary and intramedullary, being the most rare form of presentation, accounting for <20% of all cases (1,4,7,14–16). spinal ncc occurs frequently with a diagnosis of intracranial ncc, these cases are approximately 75%, however, isolated cases of spinal ncc are uncommon (6,11,16). ncc transmission form is fecal-oral. the parasite is the cestode, taenia solium, pigs are the intermediate host and humans are the definitive host (6,9). life cycle starts in pigs, the larvae is encapsulated in muscles, subcutaneous tissues, liver, lungs, and brain, and then in humans starts with the ingestion of cysticercal eggs in food contaminated (6,14,17). in the stomach thanks to gastric acid the larvae is release from the eggs, and then it penetrate the intestinal mucosa and it goes to bloodstream, where is able to migrate to brain, muscle, and the eyes. through small capillaries into the parenchyma or through the choroid plexus into the ventricles, the larvae is disseminated to the subarachnoid space (6,14). inside the human the larvae produce proglottids that contain many eggs, which are expulse in feces and may be ingested by intermediate hosts. also humans can be infected by themselves (17). ncc patients generally experience prolonged periods without symptoms and may present neurological manifestations such as local neurological deficit and seizures (17). in addition, they may present various symptoms such as generalized pain, radoculopathies, paresthesia, numbness, quadriparesis, frank equine tail syndrome, anatomical dysfunction of the intestine and bladder; radicular pain and progressive weakness of the extremities; the latter thow being the most common manifestations (4,14,18,19). in contrast, parenchymal ncc is characterized by epileptic convulsions, subarachnoid ncc manifestations with headache and intraventricular ncc sings as an acute or intermittent syndrome of intracranial hypertension (11). these manifestations are produced by the cyst size, location and degeneration products (14,16). in addition, it triggers pathophysiological mechanisms such as mass effect, which causes compression of the spinal cord and produces myelopathy that causes progressive weakness in patients (20–22); and inflammatory reaction that may lead to the appearance of arachnoiditis, meningitis and obstruction of the subarachnoid pathways (4,14). the intact cyst causes less inflammatory reaction and is easy to surgical excision; on the other hand, degeneration of the cyst when parasite death occurs can cause romanian neurosurgery (2017) xxxi 4: 530 535 | 533 severe symptoms (4,16,23,24). the localization of these is more common at the thoracic level, but can occur in any region of the spine (4). the extradural ncc presented in the lumbar region causes relatively slow symptoms, compared to the presence of an intramedullary ncc in the cervical region that causes a fast and early deterioration (16). three clinical stages of ncc have been defined: active, inactive, and transitory; and 4 pathological stages: vesicular, colloid vesicular, granular nodular and calcified nodular. the vesicular stage is the active form; the nodular and colloidal vesicular granules represent the transitory stage; and the calcified nodular pathological stage is an inactive stage of neurocysticercosis (11,25). differential diagnoses for spinal cystic lesions are spinal tumors, epidermoid tumor, echinococcosis, arachnoid / colloid cyst, hydatid cysts, tuberculosis, sarcoidosis, and meningocele. the diagnosis of ncc is made from neuroimaging, analysis of csf and the detection of antibodies in serum (7,15,16). several criteria have been proposed to facilitate its diagnosis; the major criteria include neuroimaging findings suggestive of ncc (cystic lesions or large calcifications), detection of anticystic antibodies by immunoblotting and resolution of cystic lesions after treatment with albendazole or praziquantel. minor criteria include clinical manifestations suggestive of ncc, positive csf elisa for detection of anticostercer antibodies or cysticercan antigens and presence of cysticercosis outside the cns. epidemiological criteria include residence or travel to an endemic area or exposure to a t. solium carrier. the diagnosis is made with the presence of 2 major criteria plus 1 minor and 1 epidemiological (11,15,16). the imaging study of choice for the detection of spinal lesions is mri, however, it is difficult to detect small calcifications (5,7,15). mri findings vary depending on the stages of the disease. the initial or vesicular stage is characterized by csf isointense lesions that appear hypointense in t1 and hyperintense in t2, without surrounding edema. the colloidal vesicular stage is characterized by the presence of hypointense perilesional edema in t1 and hyperintense in t2, the cyst now appears as a ring, slightly hyperintense in t1 and hyperintense in t2. in the nodular granule stage, the capsule thickens and calcifications begin. in the calcified nodular stage, densely calcified cysts are difficult to visualize in mri, unlike cat scan where they are easily seen (4,14,16). the csf elisa test is useful to confirm the diagnosis of ncc in patients with neurological signs, but in whom neuroimaging findings are inconclusive. the typical histopathological findings of ncc are the presence of dead or active translucent cysts with eosinophilic lining, usually surrounded by clear fluid and chronic inflammatory cells including neutrophils, eosinophils, and giant cells. the presence of calcified cysts can be observed in late and inactive stages (7,15,16). csf examination may show low or normal levels of glucose, increased protein, lymphocytic pleocytosis, and eosinophilia (4). for spinal ncc treatment there are decisive factors as activity of the disease and 534 | balderrama et al intradural spinal neurocysticercosis location of parasites (11,15). a terapy with praziquantel and albendazole (at dosis of 15mg/kg/day for 4 to 6 weeks) are efficient in neurologically stable patients (4,5,11,15–17). antiparasitic treatment, due to the death of parasites, may lead to exacerbation of neurological symptoms (17,26). surgical excision is the treatment of choice in patients with symptoms due to mass compression in the spinal cord, large cystic lesion or acute neurological deterioration during pharmacotherapy, in order to avoid irreversible neurological damage (4,9,11,15– 17). preoperative adjuvant treatment with albendazole allows to improve dissection planes during surgery (4,15). steroid administration as well as extensive irrigation of the spinal canal helps to minimize the postsurgical inflammatory process (9,15,17,26). during the medical management a strict neurological monitoring is vital to avoid the acute neurological deterioration secondary to inflammatory response. to make sure the targered lesion within the planned surgical field, the surgeon should consider recent scan (16). to reduce ncc transmission the best way is by community education on endemic areas and those who wish to travel to areas where ncc prevails (26). outcomes in patients with spinal ncc depend on cyst location, severity of inflammation, chronicity of symptoms and time of treatment (6,16). intramedullary spinal ncc has a poorer outcome than patients with ncc-induced extrinsic spinal cord and cauda equine compression in the absence of severe arachnoidal scarring. a complete improvement can be achieved, however in some cases the symptoms may be continuous or recurrent due to of arachnoid inflammation (6). spinal intradural ncc is a rare variant of cysticercosis, which usually occurs in developing countries with poor practices in food preparation. the early detection of manifestations suggestive of spinal ncc allows the clinician an early diagnosis for a specialized management in the search to prevent permanent neurological complications. disease promotion and prevention practices become an important tool for reducing the incidence of ncc, especially in endemic areas. correspondence dr. luis rafael moscote-salazar, e-mail: mineurocirujano@aol.com references 1. kumar s, handa a, chavda s, tiwari r, abbey p. intramedullary cysticercosis. j clin neurosci. 2010;17(4):522–3. 2. lim bc, lee rs, lim js, cho ky. a case of neurocysticercosis in entire spinal level. j korean neurosurg soc. 2010;48(4):371–4. 3. garcia hh. europe pmc funders group diagnosis and treatment of neurocysticercosis. 2012;7(10):584–94. 4. ganesan s, acharya s, kalra kl, chahal r. intradural neurocysticercosis of lumbar spine: a case report. glob spine j. 2015;5(4):e1-4. 5. surase s, natekar a, bijwe s, velho v, tiwari r, solanke v. intra-medullary primary spinal cysticercosis : a case report. int j surg res. 2015;4(1):7– 9. 6. alsina ga, johnson jp, mcbride dq, rhoten prl, mehringer cm, stokes jk. spinal neurocysticercosis. neurosurg focus. 2002;12(6):e8. 7. yoo m, lee ch, kim kj, kim hj. a case of intraduralextramedullary form of primary spinal cysticercosis misdiagnosed as an arachnoid cyst. j korean neurosurg soc. 2014;55(4):226–9. romanian neurosurgery (2017) xxxi 4: 530 535 | 535 8. salazar noguera em, pineda sic r, escoto solis f. intramedullary spinal cord neurocysticercosis presenting as brown-sequard syndrome. bmc neurol. 2015;15(1):1–4. 9. hansberry dr, agarwal n, sharer lr, goldstein im. minimally manipulative extraction of polycystic cervical neurocysticercosis. eur spine j. 2016; 10. nash te, garcia hh. diagnosis and treatment of neurocysticercosis. nat rev neurol. 2012;7(10):584–94. 11. pant i, chaturvedi s, singh g, gupta s, kumari r. spinal cysticercosis: a report of two cases with review of literature. j craniovertebr junction spine. 2016;7(4):286. 12. agale s v, bhavsar s, choudhury b, manohar v. isolated intramedullary spinal cord cysticercosis. asian j neurosurg. 2012;7(2):90–2. 13. olivia ji, angulo-rivero p. cysticercosis of the nervous system i . introduction and general aspects. 1962; 14. qazi z, ojha bk, chandra a, singh sk, srivastava c, patil t. isolated intramedullary spinal cord cysticercosis. j neurosci rural pr. 2014;5(1):s66–8. 15. jongwutiwes u, yanagida t, ito a, kline se. isolated intradural-extramedullary spinal cysticercosis: a case report. j travel med. 2011;18(4):284–7. 16. gupta s, singh pk, gupta b, singh v, azam a. isolated primary intradural extramedullary spinal neurocysticercosis: a case report and review of literature. acta neurol taiwan. 2009;18(3):187–92. 17. del vecchio rf, rita pinzone m, nunnari g, cacopardo b. neurocysticercosis in a 23-year-old chinese man. am j case rep. 2014;15:31–4. 18. apuzzo ml, dobkin wr, zee cs, chan jc, giannotta sl, weiss mh. surgical considerations in treatment of intraventricular cysticercosis. an analysis of 45 cases. j neurosurg. 1984 feb;60(2):400–7. 19. ahmad fu, sharma bs. treatment of intramedullary spinal cysticercosis: report of 2 cases and review of literature. surg neurol. 2007 jan;67(1):74–7. 20. canelas hm, ricciardi-cruz o, escalante ad. cysticercosis of the nervous system: less frequent clinical forms. iii. spinal cord forms. arq neuropsiquiatr. 1963 jun;21:77–86. 21. cabieses f, vallenas m, landa r. cysticercosis of the spinal cord. j neurosurg. 1959;16:337–41. 22. colli bo, assirati junior ja, machado hr, dos santos f, takayanagui om. cysticercosis of the central nervous system. ii. spinal cysticercosis. arq neuropsiquiatr. 1994 jun;52(2):187–99. 23. kim sk, wang kc, paek sh, hong ks, cho bk. outcomes of medical treatment of neurocysticercosis: a study of 65 cases in cheju island, korea. surg neurol. 1999 dec;52(6):563–9. 24. proano j v, madrazo i, garcia l, garcia-torres e, correa d. albendazole and praziquantel treatment in neurocysticercosis of the fourth ventricle. j neurosurg. 1997 jul;87(1):29–33. 25. sotelo j, marin c. hydrocephalus secondary to cysticercotic arachnoiditis. a long-term follow-up review of 92 cases. j neurosurg. 1987 may;66(5):686–9. 26. rizvi saa, saleh am, frimpong h, al mohiy hm, ahmed j, edwards rd, et al. neurocysticercosis: a case report and brief review. asian pac j trop med. 2016;9(1):100–2. microsoft word 3radup_combined romanian neurosurgery (2018) xxxii 2: 205 210 | 205             doi: 10.2478/romneu-2018-0026 combined telovelar-minimal transvermian approach for a bleeding pontine cavernoma in a 48-year-old patient – case report and literature review r. radu1, g. petrescu1, c. gorgan2, c. cristescu3, f. m. brehar1,4, r.m. gorgan1,4 1neurosurgery department, “bagdasar-arseni” emergency hospital, bucharest, romania 2neurology department, “bagdasar-arseni” emergency hospital, bucharest, romania 3anesthesiology and intensive care department, “bagdasar-arseni” emergency hospital, bucharest, romania 4 neurosurgery department, “carol davila” university of medicine and pharmacy, romania abstract: symptomatic pontine cavernous malformations carry a high risk of recurrent bleeding, which may result in permanent neurological deficit. such lesions require surgical management that can be challenging to the neurosurgeon due to their anatomical location and their proximity to delicate neural structures. an ideal surgical approach should provide maximal surgical resection with minimal morbidity. we present the case of a 48-year-old woman with a pontine cavernoma with repeated spontaneous intralesional hemorrhages, resected using a telovelar approach extended by a minimal incision of the inferior vermis, with good surgical outcome. the telovelar approach provided a good access to the lateral recesses and the foramen of luschka, while the lower vermian incision provided a greater vertical working angle inside the ventricle. key words: cavernous malformation, brainstem, suboccipital, telovelar, transvermian, motor evoked potentials introduction a cavernous malformation is a cluster of thin-walled, angiogenically immature vessels that form blood-filled locules. their prevalence in the general population is estimated at 0.1-0.5% [1,2]. pontine cavernomas account for the majority of brainstem cavernous malformations [3]. it has been reported that infratentorial cavernomas are more dangerous than supratentorial lesions, with one report showing a 30 times greater tendency to bleed [4]. the characteristic lack of tight junctions 206 | radu et al combined telovelar-minimal transvermian approach for pontine cavernoma             between endothelial cells makes these lesions prone to leaking, most of them being surrounded by a complete hemosiderin rim. cavernous malformations exhibit a wide variety of dynamic clinical behaviors, being a relatively common cause of recurrent spontaneous nontraumatic intracranial hemorrhage among young and middle-aged adults [5]. once considered occult lesions due to their extremely low-flow angiographic behavior, without arteriovenous shunting, cavernous malformations are now easily distinguishable on ct and mri. based on their imaging appearance, zabramski described four characteristic types of lesions [6]. type i lesions appear hyperintense on both t1and t2-weighted sequences due to subacute hemorrhage. type ii lesions contain loculated hemorrhages surrounded by a gliotic envelope, presenting as a mixed hyperintense/hypointense signal on both t1 and t2 imaging, with a low signal rim with blooming on t2* sequences. type iii lesions are isoto hypointense, suggesting chronic hemorrhage. type iv lesions are multiple punctate microhemorrhages visible only on t2* sequences. the management of asymptomatic lesions is often observation, while surgical treatment is indicated by most authors after the first symptomatic episode [7-9]. due to the location of most brainstem cavernomas in the pontine and medullary regions, the posterior approaches are generally the most commonly used. these include the suboccipital approach, the supracerebellar infratentorial approach and the retrosigmoid approach. other rare approaches include the telovelar approach, the transvermian approach and the far lateral transcondylar approach [10]. case presentation history a 48-year-old woman with no prior medical history, presented to the emergency room with two weeks of progressive left-sided facial numbness, gait ataxia and intermittent diplopia, which was exacerbated by right lateral gaze. the ct scan showed a hyperdense, homogenous mass with clearly demarcated contour in the right side of the pons (fig. 1). figure 1 cerebral ct scan reveals a hyperdense mass with well-defined borders located in the right side of the pons. mri revealed a single non-contrast enhancing tumoral mass of 18/16/21 mm, located in the right-middle pons, with inhomogenous structure due to t1 hyperintense areas suggestive of acute hemorrhage and a t1, t2 and flair hypointense area (fig. 2). the mass was clearly contoured by a hypointense rim, suggestive of hemosiderin. mri also showed minimal perilesional edema and mass effect on the fourth ventricle. the imaging was evocative of a zabramski type ii lesion. romanian neurosurgery (2018) xxxii 2: 205 210 | 207             figure 2 mr image depicting a 18/16/21 mm mass suggestive of cavernoma. surgical technique the patient was placed in a prone position with the head slightly raised and flexed for a better exposure of the space between the occiput and c1. a linear midline incision was performed at 1-2 cm above the external occipital protuberance down to the level of the c4 vertebra, followed by a median subocccipital craniectomy from below the torcula to the foramen magnum. the dura was opened with a y-shaped flap over the cerebellar hemispheres. the approach was performed using microsurgical techniques. due to the high risk of injury to the pontine nuclei, transcranial stimulation-induced motor and somatosensory evoked potentials were monitored intraoperatively. the tela choroidea was incised at its attachment to the tinea of the fourth ventricle. the inferior medullary velum of the fourth ventricle was subsequently incised to complete the exposure to the foramen of luschka. an additional minimal incision of the inferior vermis expanded the surgical corridor, providing a better vertical working angle inside the fourth ventricle. an area of hemorrhagic effusion was visualized on the superior pontine aspect of the floor of the 4th ventricle. the cavity of the hematoma offered a good surgical corridor to the lesion. resection of the cavernoma proceeded by entering its capsule, followed by evacuation of its content and dissection in circumferential planes, leaving a cavity formed by normal parenchyma (fig. 3). figure 3 – intraoperative view. a – cavernoma surrounded by hemorrhagic effusion. b – piecemeal resection of the cavernoma. c – postresection cavity 208 | radu et al combined telovelar-minimal transvermian approach for pontine cavernoma             postoperative outcome immediate postoperative exam showed no new-onset neurologic deficit and remission of the diplopia and facial numbness. immediate postoperative ct showed gross total resection (fig. 4). the patient was discharged 11 days after surgery with no neurologic deficit (fig. 5). figure 4 postoperative ct scan showing complete resection of the cavernoma. figure 5 – the patient on postoperative day 7 with no neurologic deficit. at the 2-month follow-up, the patient showed normal neurologic status (fig. 6) and complete resection was confirmed by mri (fig. 7). figure 6 – prof. r. m. gorgan with the patient at the 2-month follow-up figure 7 – mri scan at the 2-month follow-up showing complete resection of the cavernoma discussions pontine cavernomas often represent a considerable microsurgical challenge to the operator, mainly because of the location, but also due to the high risk of complications. surgery is indicated after severe or recurrent episodes of bleeding, neurologic worsening or when the cavernoma is exophytic and more accessible for the surgical resection [11,12]. romanian neurosurgery (2018) xxxii 2: 205 210 | 209             complete removal of the lesion is required in order to prevent recurring hemorrhagic events, as rebleeding has been shown to occur in 40% of cavernoma remnants after surgery [13]. although cavernous malformations are now resected using less invasive approaches, it is still believed that exposure and adequate visualization are of utmost importance. abla et al. recommend increased bone removal, within reason, to limit brain retraction and to enhance visibility [14]. the transvermian and telovelar approaches have been frequently reported in literature. the transvermian approach was used to resect the first cavernous malformation described in literature by walter dandy in 1928 [15]. however, recent reports describe transient mutism associated with incision of the vermis which resulted in abandoning this approach in favor of other routes to the fourth ventricle [16]. another disadvantage of the transvermian approach is the risk of neural injury caused by the vermian incision, removal of the vermis or tonsils, and the retraction of two halves of the split vermis [17]. the telovelar and transvermian approaches to the fourth ventricle were compared by tanriover et al [17]. these approaches were performed in 10 cadaveric specimens and the operative angle of approach and the superior, inferior, and lateral exposure for each approach were determined using stealth image guidance with screen capture. the transvermian approach provided slightly better visualization of the medial aspect of the rostral fourth ventricle. the telovelar approach provided better access to the lateral recesses and foramen of luschka without an incision through cerebellum. the study did not determine area of exposure, which is an important consideration when working inside the fourth ventricle. we decided to perfom a telovelar approach combined with an additional minimal linear incision of the inferior vermis. this approach offered an increased exposure of the superior pontine aspect of the fourth ventricle as well as greater working angle in the sagittal plane inside the ventricle compared to the telovelar approach alone while also avoiding the risks of a complete transvermian approach. the good surgical outcome with no intraoperative incidents and no neurological deficits suggests that the vermian incision may be safely performed if needed for a good surgical exposure. conclusions the pons remains a difficult territory to access and mastery of the various surgical approaches is a difficult challenge for neurosurgeons. most pontine cavernomas can be resected via the classically described approaches but it is possible to combine parts of various approaches in order to facilitate the resection of a lesion in its entirety while minimizing morbidity. correspondence brehar felix mircea felixbrehar@yahoo.com 210 | radu et al combined telovelar-minimal transvermian approach for pontine cavernoma             references 1. labauge p, denier c, bergametti f, tournier-lasserve e. genetics of cavernous angiomas. lancet neurol. 2007;6(3):237–44. 2. revencu n. cerebral cavernous malformation: new molecular and clinical insights. j med genet. 2006;43(9):716–21. 3. abla aa, benet a, lawton mt. the far lateral transpontomedullary sulcus approach to pontine cavernous malformations: technical report and surgical results. neurosurgery. 2014;10(3):472–80. 4. porter pj, willinsky ra, harper w, wallace mc. cerebral cavernous malformations: natural history and prognosis after clinical deterioration with or without hemorrhage. j neurosurg. 1997;87(2):190–7. 5. tatlisumak t, cucchiara b, kuroda s, kasner se, putaala j. nontraumatic intracerebral haemorrhage in young adults. nat rev neurol. 2018. 6. zabramski jm, wascher tm, spetzler rf, johnson b, golfinos j, drayer bp, et al. the natural history of familial cavernous malformations: results of an ongoing study. j neurosurg. 1994;80(3):422–32. 7. wang cc, liu a, zhang jt, sun b, zhao yl. surgical management of brain-stem cavernous malformations: report of 137 cases. surg neurol. 2003;59(6):444–54. 8. hauck ef, barnett sl, white ja, samson d. symptomatic brainstem cavernomas. neurosurgery. 2009;64(1):61–70. 9. giovani a, sandu a, neacsu a, gorgan rm. surgical treatment and outcome of cerebral cavernomas – a 10 years’ experience. rom neurosurg. 2014;21(4):395–405. 10. hosainey sam, meling tr. a 34-year-old woman with brainstem cavernous malformation: the anterior transcallosal transchoroidal approach and literature review. j neurol surg reports. 2014;75(2):e236–40. 11. ohue s, fukushima t, kumon y, ohnishi t, friedman ah. surgical management of brainstem cavernomas: selection of approaches and microsurgical techniques. neurosurg rev. 2010;33(3):315–22. 12. abla aa, lekovic gp, turner jd, de oliveira jg, porter r, spetzler rf. advances in the treatment and outcome of brainstem cavernous malformation surgery: a single-center case series of 300 surgically treated patients. neurosurgery. 2011;68(2):403–14. 13. mouchtouris n, chalouhi n, chitale a, starke rm, tjoumakaris si, rosenwasser rh, et al. management of cerebral cavernous malformations: from diagnosis to treatment. scientificworldjournal. 2015;2015:808314. 14. abla aa, turner jd, mitha ap, lekovic g, spetzler rf. surgical approaches to brainstem cavernous malformations. neurosurg focus. 2010;29(3):e8. 15. dandy we. venous abnormalities and angiomas of the brain. arch surg. 1928 nov 1;17(5):715 16. deshmukh vr, figueiredo eg, deshmukh p, crawford nr, preul mc, spetzler rf. quantification and comparison of telovelar and transvermian approaches to the fourth ventricle. neurosurgery. 2006;58(suppl. 2):202–7. 17. tanriover n, ulm aj, rhoton al, yasuda a. comparison of the transvermian and telovelar approaches to the fourth ventricle. j neurosurg. 2004;101:484–98. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article case report: minimal invasive approach in a case of cervical schwannoma raghuvendra kumar, amar c dhal, abhishek kumar india doi: 10.1515/romneu-2017-0018 romanian neurosurgery (2017) xxxi 1: 115 – 121 | 115             doi: 10.1515/romneu-2017-0018 case report: minimal invasive approach in a case of cervical schwannoma raghuvendra kumar, amar c dhal, abhishek kumar department of neurosurgery, ipgme&r kolkata, india abstract: purpose: the purpose of our case report is to present our experience with minimal invasive approach in a case of cervical schwannoma. method: the data of patient treated for cervical schwannoma like site, size and extension of the lesion were obtained by neuroimaging and preoperative neurological status obtained by clinical examination. the postoperative neurological status and radiological image were available. the clinical course was documented by karnofsky score (kps). result: we approached the tumour through interlaminar fenestration in cervical (c1-c2) region. postoperative neuroimaging revealed complete removal of the lesion and no sign of spinal instability. at discharge improvement of kps score and neurological improvement was observed. conclusion: minimal access procedures are increasingly gaining popularity in spine surgery. the aim of the surgical procedure is minimizing the invasiveness and maximizing the efficacy. modern neuroimaging allows adequate preoperative planning and microsurgical techniques provide adequate execution of the surgical act. key words: cervical schwannomas, interlaminar fenestration, minimally invasive technique introduction schwannomas are the most common extramedullary spinal tumors, representing almost one-third of primary spinal neoplasms [16]; they are categorized as spinal nerve sheath tumors (nsts) together with neurofibromas. they affect men and women in equal proportions and are mainly encountered in their 50s; they may cause signs and symptoms related to the radicular and/or spinal cord involvement in the interested spinal level [1, 5]. the majority of schwannomas are located in the lumbar, followed by the thoracic and cervical spine [1, 6, 19]. traditionally laminectomy is used to approach these lesions [9, 18], even if it may cause delayed postoperative spinal instability and deformities [7, 8, 18, 23], thus requiring reconstructive procedures [2, 17]. in order to prevent these complications, many authors have performed and popularized alternative 116 | kumar et al minimal invasive approach in cervical schwannoma             less invasive surgical techniques. in our case we approached the tumour through interlaminar fenestration in cervical c1-c2region as our patient had idem sitiuated in the right anterolateral position. patient case presentation a 50 yr old male with average built and height, govt employee presented with the c/o weakness of all four limbs with tingling and numbness all four limb since 1 yr. history of neck pain since 1 yr. urinary symptoms like hesitancy, frequency and urgency since 3 months. weakness started initally in right lower limb then involving upper limb on same side with involvement of opposite upper and lower limb in a span of 3 month. our patient had ability to carry out normal acitivity and work with kps of 80, with no comorbidities nor any familiy history of genetic diseases. patient used to take pregabalin 75 mg twice a day and pantroprazole 40 mg once a day with minimal relief of symptoms as advised by physician whom patient consulted previously with no history of any drug allergey. patient had mixed dietary habits. on examination patient had increased tone with mrc grade of power 4/5 in all four limbs with exaggerated all deep tendon reflexes bilaterally with b/l plantar extensor and absent superficial reflex with preserved anal tone. patient had decreased all modality of sensation below c5 level. imaging location, size, extent of the lesion, and preoperative neurological status of patient, was obtained by neuroimaging data and clinical examination. postoperative clinical examination and radiological images, including computed tomography (ct) scan and magnetic resonance (mr) imaging, were obtained. mr images (p+c), showing characteristic well marginated inhomogeneous intradural extramedullary lesion at right anterolateral aspect of spinal canal at foramen magnum,c1,c2 level with 25x29x18 mm size, causing compression at cervicomedullary junction…? neurofibroma. surgical procedure after anesthetic fitness, written and informed consent, patient was planned for operation. position-prone with slight neck flexion. incision made from occiput to c3 spinous process. the fascia was dissected free, incised longitudinally in the mid line. muscular insertions were dissected in a subperiosteal way from the spinous processes and from laminae. lamina of c1 and c2 identified. space was increased with the help of small mastoid retractor. partial ligamentum flavectomy of ipsilateral side was done. right sided interlaminar dural incision was made between c1 and c2 space and underlying arachnoid layering the tumor was seen. arachnoidal separation over tumour was done. tumour of approx. 2 x 3 cm, greyish pink, variegated consistency, lying antero lateral to cord with clear plane between tumour and adjacent cord seen. with meticulous surgical dissection tumour was completely removed in total and free flow of csf was seen at the end of surgery. no nerve root was sacrificied to reach or to remove the tumour. water tight dural closure done and confirmed. patient was extubated after procedure and romanian neurosurgery (2017) xxxi 1: 115 – 121 | 117             observed in icu and neurological assesment was done and confirmed to be better than preoperative period except for operative site pain. the mean length of hospital stay was 6 days after the surgical procedure. patient was evaluated before discharge and at follow up for complain of pain and for neurological status. pain was subsided, and there was significant improvement of neurological status. follow up ct scan & mr images were obtained and did not reveal residual tumor. no signs of spinal instability found on ct scan. histological examination confirmed the diagnosis of schwannoma. figure 1 pre-op sagittal t2-mri figure 2 pre-op axial t2-mri 118 | kumar et al minimal invasive approach in cervical schwannoma             figure 3 post-op 3d ct scan romanian neurosurgery (2017) xxxi 1: 115 – 121 | 119             figure 4 post-op t2 mri, axial & coronal section discussion traditionally open posterior laminectomy is used to approach these lesions. multiple risk factors are associated with cervical spine deformity after laminectomy including age (11, 15, 22) location and extension of laminectomy (upper, middle, or lower cervical spine) (3, 11, 22) number of laminae removed, preoperative loss of lordosis (10, 11) intraspinal pathologies (10, 14) degree of facet resection (11). kaptain et al. (10) reported that the risk of postoperative deformities doubled when the spine was deformed preoperatively. fassett et al. (8) noted a 14% incidence of postoperative kyphosis in patients who initially had a lordotic cervical spine, and more than twice the incidence (30%) in patients whose spine was straight (4ᴼ of lordosis or kyphosis) preoperatively. spinal cord lesions alone, without surgical destabilization, can cause spinal deformities in both adults and children (20). extent of laminectomy and then the exposure of dura mater are related to the formation of epidural scar tissue and so to the risk of postoperative spinal-fluid fistulae (13). fibrosis often produces adhesions tethering the nerve root to adjacent tissues, impeding nerve mobility and increasing tension on the nerve during motion, leading to pain, due to local nerve fiber traction, and to nerve injury (4). reduction of the scar formation is associated with clinically better results (21), emphasizing the importance of preventing the formation of epidural fibrosis through devices, such as good sterile technique, meticulous hemostasis, and in particular minimal tissue trauma. in this case, we discuss our surgical experience in the treatment of cervical schwannomas. ability in microsurgical 120 | kumar et al minimal invasive approach in cervical schwannoma             techniques has allowed us to remove spinal tumor. exploiting the wider space between the vertebrae c1 and c2, we performed an interlaminar fenestration, with decreasing iatrogenic trauma. in our patient, no complication was observed. static and dynamic plain radiograph films and ct scan showed no kyphosis and/or instability postoperatively and also during follow-up. postoperative mr images demonstrated complete tumor removal, without epidural fibrosis. clinical and neurological results were good. conclusion minimal access procedures are increasingly gaining popularity in spine surgery. the aim of the surgical procedure is minimizing the invasiveness and maximizing the efficacy. modern neuroimaging allows adequate preoperative planning and microsurgical techniques provide adequate execution of the surgical act. the procedure has to be tailored case by case considering the specific lesional features and the individual anatomical situation. correspondence dr. raghuvendra kumar, department of neurosurgery, institute of postgraudate medical education & research (ipgme&r) kolkata, pin700020, india mobile no: 09007366440, 07238085537 email: dr.raghuvendrakumar@gmail.com references 1.abbasi ss, senoglu m, theodore n et al (1998) microsurgical management of spinal schwannomas: evaluation of 128 cases. j neurosurg spine 9:40–47 2.alexander e jr (1985) postlaminectomy kyphosis. in: wilkins rh, rengachary ss (eds) neurosurgery, vol 3. mcgraw-hill, new york, pp 2293–2297 3. aronson dd, kahn rh, canady a et al (1991) instability of the cervical spine after decompression in patients who have arnold-chiari malformation. j bone joint surg am 73:898–906 4.cemil b, tun k, kaptanoglu e et al (2009) use of pimecrolimus to prevent epidural fibrosis in a postlaminectomy rat model. j neurosurg spine 11:758– 763 5.cerqui a, kim dh, kim sh (2007) surgical approaches to paraspinal nerve sheath tumors. neurosurg focus 22(6):e9 6.conti p, pansini g, mouchaty h (2004) spinal neurinomas: retrospective analysis and long-term outcome of 179 consecutively operated cases and review of the literature. surg neurol 61:35–44 7.deutsch h, haid rw, rodts ge, mummaneni pv (2003) postlaminectomy cervical deformity. neurosurg focus 15(3):e5 8. fassett dr, clark r, brockmeyer dl, schmidt mh (2006) cervical spine deformity associated with resection of spinal cord tumors. neurosurg focus 20(2):e2 9.guidetti b (1974) removal of extramedullary benign spinal cord tumors. in: krayenbuhl ii, brihaje j, loew f (eds) advances and technical standards in neurosurgery, vol 1. springer, new york, pp 173–197 10.kaptain gj, simmons ne, replogle re et al (2000) incidence and outcome of kyphotic deformity following laminectomy for cervical spondylotic myelopathy. j neurosurg 93(suppl 2): 199–204 11.katsumi y, honma t, nakamura t (1989) analysis of cervical instability resulting from laminectomies for removal of spinal cord tumor. spine 14:1171–1176 12.koch wiewrodt d, wagner w, perneczy a (2007) unilateral multilevel interlaminar fenestration instead of laminectomy or hemilaminectomy: an alternative surgical approach to intraspinal space-occupying lesions. neurosurg spine 6:485–492 13.la rocca h, macnab i (1974) the laminectomy membrane. studies in its evolution, characteristics, effects and prophylaxis in dogs. j bone joint surg br 56:545–550 14.lonstein je (1977) post-laminectomy kyphosis. clin orthop relat res 128:93–100 romanian neurosurgery (2017) xxxi 1: 115 – 121 | 121             15.mikawa y, shikata j, yamamuro t (1987) spinal deformity and instability after multilevel cervical laminectomy. spine 12:6–11 16.nittner k (1976) spinal meningiomas, neurinomas and neurofibromas and hourglass tumors. in: vinken pj, bruyn gw (eds) handbook of clinical neurology, vol 20. tumors of the spine and spinal cord. north-holland, amsterdam, pp 177–322 17.raimondi aj, gutierrez fa, di rocco c (1976) laminotomy and total reconstruction of the posterior spinal arch for spinal canal surgery in childhood. j neurosurg 45:555–560 18.schwartz th, mccormick pc (2004) spinal cord tumors in adults. in: winn hr (ed) youmans neurological surgery, vol 4, 5th edn. wb saunders, philadephia, pp 4817–4834 19.seppala mt, haltia mjj, sankila rj, jaaskelainen je, heiskanen o (1995) long-term outcome after removal of spinal schwannomas: a clinicopathological study of 187 cases. j neurosurg 83:621–626 20.sim fh, svien hj, bickel wh et al (1974) swan-neck deformity following extensive cervical laminectomy. a review of twentyone cases. j bone joint surg am 56:564– 580 21.tatsui ce, martinez g, li x, pattany p, levi ad (2006) evaluation of duragenh in preventing peridural fibrosis in rabbits. j neurosurg spine 4:51–59 22.yasuoka s, peterson ha, maccarty cs (1982) incidence of spinal column deformity after multilevel laminectomy in children and adults. j neurosurg 57:441–445 23.yeh js, sgouros s, walsh ar, hockley ad (2001) spinal sagittal malalignment following surgery for primary intramedullary tumors in children. pediatr neurosurg 35(6):318–324 romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article contralateral clipping of bilateral middle cerebral artery aneurysms. case report georgiana ion, alexandru chiriac, ziyad faiyad, ion poeata romania doi: 10.1515/romneu-2017-0010 66 | ion et al contralateral clipping of bilateral middle cerebral artery aneurysms             doi: 10.1515/romneu-2017-0010 contralateral clipping of bilateral middle cerebral artery aneurysms. case report georgiana ion1, alexandru chiriac, ziyad faiyad1, ion poeata “grigore t. popa” university of medicine and pharmacy, iasi, romania 1“prof. dr. n. oblu” clinic emergency hospital, iasi, romania introduction middle cerebral artery aneurysm represent 20% of all intracranial aneurysms, 20%-30% of patients with this pathology have multiple aneurysms. bilateral middle cerebral artery aneurysm clipping can be done unilateral or bilateral, depending on a number of variables. a series of studies were conducted to determine the best method of treatment for this condition by comparing the surgical results of both approaches. morphological features of the aneurysm can determine the choice of the best ways to approach. case report this is the case of a female patient of 47 years old who presented in neurosurgery department for headache episodes and vertigo with onset of 2 years, but these episodes worsened by 2 month with a duration of 4 days. the patient is without significant associated pathology, except ventricular extrasystolic arrhythmia. the cerebral mri scan conducted pointed out two middle cerebral artery aneurysms of which the right one being partially thrombosed and larger with no signs of haemorrhage. mri scan t2, flair, tof, t1 romanian neurosurgery (2017) xxxi 1: 66 – 72 | 67             the 3d reconstruction from the tof acquisitions helped us to better visualize the aneurysm configuration and the branches additional to the aneurysm and confirming the supposition of a partially thrombosed aneurysm. the next step was the digital subtraction angiography for a meticulous viewing of the vascular architecture and to evaluate the possibility of an endovascular treatment. 68 | ion et al contralateral clipping of bilateral middle cerebral artery aneurysms             dsaleft ica, right ica considering the fact that the right bifurcation mca aneurysm is partially thrombosed and the contralateral mca aneurysm has a large neck at the origin of a lateral lentriculostriate artery, then the best treatment option was bilateral clipping via a unilateral craniotomy. the aneurysms were clipped by a right frontotemporal craniotomy. patient was seated in supination, with the head in an easy extension and slightly rotated to the left. a curvilinear skin incision was made starting at the zigomatic arch and extending to the midline behind the hairline. the skin flap was retracted anteriorly and the temporal muscle was retracted laterally. a frontotemporal craniotomy was performed of about 4cm/4cm in two burr holes, one at the pterion and another at the level of the superior temporal line. a part of the lesser wing of the sphenoid bone was removed using a rongeur. the dura was incised in a curvilinear manner and suspended anterior. dissection of the sylvian fissure was performed under the magnification of the microscope. steps: 1. proximal ipsilateral sylvian fissure dissection and retraction of the frontal lobe with visualization of the ipsilateral optic nerve, supraclinoid ica up to the bifurcation after dissection and opening the carotid and optic cisterns. 2. contralateral opticocarotid space dissection and identification of the middle cerebral artery after dissection proximal of the left sylvian fissure. progressive elevation of the medial frontal lobe helped to uncover the left m1 segment. romanian neurosurgery (2017) xxxi 1: 66 – 72 | 69             3. exposure of the contralateral mca bifurcation by progressively increased retraction of the contralateral frontal lobe and dissection of the arachnoid adhesions along the inferior surface of the mca and identification of the aneurysm. 4. aneurysm clipping 5. ipsilateral aneurysm clipping using ultrasound guidance and focused sylvian opening. 6. identification of the bifurcation right mca aneurysm and first clip application after 70 | ion et al contralateral clipping of bilateral middle cerebral artery aneurysms             visualization of the distal m1 segment, m2 frontal, m2 temporal branches. 7. dissection of the dome from the m2 branches and adhesions, application of the second clip and sectioning the aneurysm. postoperatively patient had a good outcome, with no neurological sequelae and was released after 6 days. romanian neurosurgery (2017) xxxi 1: 66 – 72 | 71             postoperatively ct scan discussion microsurgical clipping of the middle cerebral artery aneurysm is still the method of choice for the treatment of these. some advantages it would be efficient and sustainable exclusion from circulation of the aneurysm and the treatment of the complications like intracerebral hematoma associated or the treatment of intracerebral hypertension. location of the aneurysm is very important for preoperative planning especially for aneurysms in the mirror. for aneurysms located at the bifurcation of the mca is mandatory to dissect the aneurysm and both the m2 segments for a good application of the clip with complete occlusion of the aneurysm neck. if this theory is not possible, the best choice is to leave a part of the neck unclipped in order to keep both m2 permeable. another notion that we must take into account is that the lateral lenticulostriate arteries may arise at the bifurcation or even distal. additional steps are required when intraluminal thrombosis, calcifications or giant or a more complex configuration appear. especially in cases when the aneurysm in unruptured, a less invasive approach is chosen like minimizing the craniotomy size, the brain and vessels manipulation and a focused opening of the sylvian fissure. this management may be helped by intraoperatory neuronavigation or ultrasound. classically the proximal sylvian approach is used, when the sylvian fissure is dissected from medial to lateral, this allowing an early proximal control and the neck of the aneurysm is exposed before the dome, but with the risk of injury of vessels of sylvian fissure by extensive dissection. the distal sylvian approach that requires less dissection or superior temporal gyrus approach are less used. new less invasive methods like focused sylvian opening with or without using neuronavigation or ultrasound are more effective by avoiding extensive dissection and minimizing the risk of vasospasm. this method allows viewing the m1 segment proximal to the neck and also the dome and the m2 branches around the aneurysm. among the disadvantages include anatomical 72 | ion et al contralateral clipping of bilateral middle cerebral artery aneurysms             disorientation or there may not be sufficient surgical field to apply more clips. regarding contralateral clipping of mca aneurysm through a unilateral approach is needed for a careful review of the local vascular anatomy. classical theory says that the optimal aneurysm that can be clipped via a contralateral approach is an unruptured mca-m1 segment aneurysm that is projected interior or anterior. in cases when the aneurysm is located at the mca bifurcation, the contralateral approach is feasible if the m1 segment is short, if there is no brain edema after sah, hydrocephalus, or arachnoid adhesions and the aneurysm projection is advantageous. the contralateral frontotemporal approach for anterior circulations aneurysms was described in some series with success, but a microsurgical anatomical corridors for approaching these aneurysms were not determined. from studies published the length of the m1 segment for a safe approach is 14 mm. the rate of obliteration after surgical clipping in between 97%-99% the rest consisting of some cases with residual neck or incomplete obliteration of the aneurysm dome. conclusion a single craniotomy with a contralateral microsurgical approach has a good postoperative outcome with a shorter surgical time but requires a preoperative meticulous analysis of the local anatomy, the distance to the contralateral corridor and aneurysm configuration. references 1. sacular middle cerbral artery aneurysms: state of the art classification and microsurgery, ahmed elsharkawy, university of helsinki, 2014 2. mirror aneurysms: a reflection on natural history, meissner i1, torner j, huston j 3rd, rajput ml, wiebers do, jones lk jr, brown rd jr; international study of unruptured intracranial aneurysms investigators., j neurosurg. 2012 jun; 116 (6):1238-41. 3. contralateral approach to bilateral middle cerebral artery aneurysms: comparative study, angiographic analysis, and surgical results, andrade-barazarte h1, kivelev j, goehre f, jahromi br, noda k, ibrahim tf, kivisaari r, lehto h, niemela m, jääskeläinen je, hernesniemi ja, neurosurgery. 2015 dec; 77(6):916-26 4. contralateral approach to bilateral middle cerebral artery aneurysms: comparative study, angiographic analysis, and surgical results, hugo andrade-barazarte, md juri kivelev, md, phd felix goehre, md behnam rezai jahromi, mb kosumo noda, md tarik f. ibrahim, md riku kivisaari, md, phd hanna lehto, md, phd mika niemela, md, phd juha e. jääskeläinen, md, phd, neurosurgery (2015) 77 (6): 916-926 5. contralateral approaches to bilateral cerebral aneurysms: a microsurgical anatomical study, eric m. oshiro, m.d., david a. rini, m.f.a., and rafael j. tamargo, m.d. department of neurosurgery, the johns hopkins hospital, baltimore, maryland, neurosurgical focus, february 6, 1997. 6. tratat de chirurgie vol. vi – neurochirurgie, ioan st. florian, ion poeata, academiei romane 2015 7. bilateral middle cerebral artery aneurysms: a comparative study of unilateral and bilateral approaches, servet inci, atilla akbay, tuncalp ozgen, neurosurgical review 35(4):505-18 · may 2012 8. unilateral pterional approach to bilateral aneurysms of the middle cerebral artery. de sousa aa1, filho ma, faglioni w jr, carvalho gt., surg neurol. 2005;63 suppl 1:s1-7. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article management of spinal dural arteriovenouse fistula a. chiriac, georgiana ion, n. dobrin, i. poeată romania doi: 10.1515/romneu-2017-0074 474 | chiriac et al management of spinal dural arteriovenouse fistula doi: 10.1515/romneu-2017-0074 management of spinal dural arteriovenouse fistula a. chiriac, georgiana ion1, n. dobrin1, i. poeată “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: spinal dural arteriovenous fistulas are rare vascular lesions whose management is still at high interest between specialists. if microsurgical treatment is still considered as treatment of choice for sdavfs, endovascular treatment is increasingly grow in interest with the development of endovascular techniques and new embolization materials. in this article we made a short discussion about the spinal dural arteriovenous fistulae on aspects related to anatomy, pathophysiology, diagnosis and treatment, with some general conclusions. key words: spinal dural arteriovenous fistulas, endovascular treatment, microsurgical treatment introduction vascular malformation of the spinal cord represents rare clinical condition characterized by a difficult diagnosis and complex management. spinal dural arteriovenous fistulas (sdavf) are the most common injuries in these pathological entities with important clinical implications. these direct communications between radicular artery and medullary vein usually results in myelopathy due to venous hypertension effect. with the advances in neuroimaging, microneurosurgery and neuroendovascular techniques the complete treatment of these pathological situations is very feasible with the possibility of complete remission of clinical symptomatology. endovascular embolization was reported as an effective therapy in the treatment of sdavfs that can be used as singular and definitive intervention in some particular cases. we present a particular case with sdavf treated by endovascular embolization and discuss the treatments possibilities to more fully understand the optimal management of these lesions. vascular anatomy spinal cord vascularisation is provided by the anterior spinal artery (asa) and the paired posterior spinal arteries (psa). the asa consists of the junction of two branches originating from the two vertebral arteries proximal to the vertebrobasilar junction. on its path, it receives contributions from branches of vertebral and ascending cervical romanian neurosurgery (2017) xxxi 4: 474 483 | 475 arteries in the cervical region as well as from intercostal and lumbar arteries at the corresponding levels. the radiculomeningeal arteries are branches of the segmental arteries founded at almost every spinal level supplying the dura in the spinal canal. unlike these, radiculomedullary arteries, which exist only at some levels, are implicated in spinal cord vascular perfusion. the artery of adamkiewicz (great anterior radiculomedullary artery) is the dominant thoracolumbar segmental artery with variable origin from t8 to l1 vertebral segments that connects to asa and supplies the spinal cord. the posterior spinal arteries arise from either the posterior inferior cerebellar or vertebral arteries (v3 or v4 segments) and as they descend on either side of the dorsolateral cord surface they are reinforced by segmental/radicular branches. it anastomoses with its fellow and with the anterior spinal artery [1,6]. epidemiology and pathophisiology sdavf represents 70% of spinal arteriovenous shunts that commonly occur in the thoracic and lumbar spines of middleaged men[4,6]. the majority of sdavfs occur spontaneously, but a post-traumatic etiology cannot be excluded in a significant proportion of them. typically, this disease affects male patients (in 80% of cases) in their 50s and 60s,3 the pathophysiology of sdavf consist in spinal cord venous hypertension due to one or a few small low-flow arteriovenous shunts between a radiculomeningeal artery and a radiculomedullary vein, typicaly located in the intervertebral foramen within the dura[4,6,7]. the retrograde venous drainage circuit in sdavf is represented by a radiculomedullary vein (most frequently dorsal to the cord) into the perimedullary venous system and finally the medullary veins. the venous drainage of the sdavf is slow and expansive, and may reach the cervical spinal canal or cauda equine by ascending or descending blood reflux. because the radiculomedullary veins are not anatomically numerous the presence of sdavf is often associated with their and epidural veins congestion and thrombosis. that explains why the low-flow arteriovenous shunt of sdavf induces a rises of venous pressure (74% of the mean arterial pressure) which leads to decreased arteriovenous gradient, segmental spinal cord edema that may progress to congestive ischemia and necrotizing myelopathy. the caudocranial progression is favorized by a valveless venous system of the cord resulting in ‘arterialization’ of these veins with thickened and tortuous walls. the pressure in the draining vein also varies with arterial pressure and may lead to an accutization of simptoms. because the sdavfs is a slow-flow fistulae, hemorrhage is a rare clinical manifestation. subarachnoid hemorrhage is rarely encountered especially in high cervical localization. [6,7] 476 | chiriac et al management of spinal dural arteriovenouse fistula figure 1 figure 2 classification many classification systems were reported and changed over time in the literature. between 1971 and 2011 seven major classification systems have been enunciated based on the evolution of diagnostic methods and treatments for spinal av shunts. the most used described in 2002 by spetzler and colleagues and divided the vascular spinal lesions in savfs and savms. savfs are further subdivided based on their extradural versus intradural location. the intradural savfs were divided in ventrally or dorsally due to their relation to the spinal cord. in turn, intradural ventral savfs are further divided into types a, b and c depending on the number and size of feeding branches [1,6]. extradural savfs represents direct connection between a branch of a radiculomenigeal artery and the epidural venous plexus (figure 4). these are rare entities characterized by enlargement of epidural veins with medullary venous congestion that may cause compression of the spinal cord or nerve roots. more recently rangel-castilla et al. divided these lesions in type a (savfs drain into both the epidural venous plexus and perimedullary venous plexus) and type b (savfs drain only into batson’s plexus). type b1 lesions compress the thecal sac due to an enlarged epidural venous plexus and type b2 lesions lack such compression [1,6,7]. radicular anterior artery lumbar artery cauda equina artery vertebral artery ascending cervical artery subclavian artery artery of adamkiewicz aorta intercostal/lumbar artery ventral costovertebral artery segmental artery spinal artery ventral radiculomeningeal artery dorsal radiculomeningeal artery muscular branches anterior/posterior radicular artery romanian neurosurgery (2017) xxxi 4: 474 483 | 477 figure 3 figure 4 intradural dorsal savfs are the most common type of spinal vascular malformation consisting in a direct connection between a dorsal radiculomedullary arterie and a medullary vein at the dural nerve root sleeve (figure 3). progression of venous hypertension to the coronal venous plexus leads to venous congestion and progressive myelopathy. intradural ventral savfs are typically high-flow direct fistulas between the asa and coronal venous plexus. the lesions develop in the ventral subarachnoid space and can be further categorized into three subtypes according to their size. type a fistulas are single-feeder lesions with slow blood flow and mild venous hypertension. type b fistulas are progressively high-flow lesions with multiple minor feeders. type c fistulas are usually large fistula with a markedly enlarged venous drainage [1]. clinical symptoms most clinical reports showed a delay between the onset of clinical symptoms and diagnosis of these vascular lesions (between 12 and 44 months) [6]. this is largely due to nonspecific clinical presentation. the presenting symptoms usually include a combination of unilateral or bilateral lower extremity motor weakness that is worsening by intense movements. gait disturbance, sensory symptoms (pain, paresthesias, diffuse or irregular sensory loss, hyperesthesia) and sphincter/bladder disturbances are also seen and commonly lead the clinicians to consider or exclude many other disorders before considering sdavfs. often misleading, mono or polyradiculopathy and low back pain are encountered and contribute to the difficulty of true diagnosis. bowel and bladder incontinence, sexual dysfunction and urinary retention are seen late in the course the disease process. the symptoms are typically progressive and the natural evolution of untreated patients is to sever aggravation over a period of 6 months to 2 years. spontaneous 478 | chiriac et al management of spinal dural arteriovenouse fistula recovery has not been reported so far as sudden worsening has been more and more common [1,7]. misdiagnosis usually includes degenerative spine diseases, spinal cord tumours, neuromuscular diseases, peripheral vasculopathy or neuropathy. imaging diagnosis it is all accepted that the mri is the primary investigation for the evaluation of myelopathy and the first line in diagnosis of sdavfs. the presence of dilated perimedulary serpentine vessels on t2 signal was found to be the most sensitive mri findings in sdavfs. the abnormal shunts are much better outlined after administration of intravenous gadolinium-based contrast agents, increasing the sensitivity and specificity of mri exam for sdavfs diagnosis (figure 5a). the mra sequences permits a better imaging characterization of the abnormal enlarged perimedulary vessels concerning their relative size, number and tuotuasity. mra is a useful tool for planning the surgical treatment and following monitoring (figure 5b). other imaging signs like spinal cord edema, enlargement, gliotic or atrophy were reported depending on the stage of venous hypertension [6]. conventional catheter angiography is the gold standard investigation for the diagnosis and classification of the sdavfs. the selective catheterization and evaluation of each individual segmental arteries at thoracic and lombar level have to be performed for sdavf identification. once an identified fistula, a prolonged angiographic imaging acquisition has to be performed for a complete characterization of the venous drainage (figure 5c). in patients with sever venous hypertension and myelopathy at thoracolumbar area the venous drainage is delayed or even absent. for suspected cervical or lombosacral sdavfs the angiographic investigation of vertebral and ascending cervical arteries or the internal iliac and iliolumbar arteries should be performed. a b c figure 5 sdavf aspects on a mri t2; b mra and c – catheter angiography romanian neurosurgery (2017) xxxi 4: 474 483 | 479 treatment treatment of sdavf must be performed as soon as possible and it could be microsurgical ligation, endovascular obliteration, or both. although the microsurgical treatment is considered the gold standard technique, the endovascular treatment could be a feasible and safe option. the microsurgical approach is performed by a posterior approach with a midline laminectomy one level above and below the fistula origin. the dura is opened in the midline and the radiculo-menigeal artery shunt must be identified extradural. in the case of a fistula with multiple small arterial pedicles, these should be carefully identified by dissection along the dural root sleeve (figure 6). the draining arterialized vein must be exposed and clearly identified against dilated perimedulary veins. the microsurgical technique consists in cauterization and microscissor interruption of the fistula. postoperative angiography is indicated to confirm complete surgical obliteration. most of the studies have reported an improved disability scores and lower recurrence rates after microsurgery treatment compared with endovascular obliteration. surgical management of sdavf was also necessary when an incomplete endovascular obliteration or recanalization were the final results [2,3]. once the improvements in endovascular technique and embolic materials, the endovascular treatment of sdavfs has more largely used. figure 6 microsurgical clipping and disconnection of artery feeder figure 7 endovascular glue injection in artery feeder and proximal radiculomedullary draining vein the success of endovascular treatment was considered when a complete occlusion of the proximal radiculomedullary draining vein and the site of the fistula itself were obtained. the procedure consists in right transfemural access by 6f sheath placement. after the identification of the arterial supply of sdavf a guiding catheter is placed at the ostium of the corresponding segmental artery to offer more support for navigation into the often tortuous feeders. then a microcatheter is advanced under road-mapping over a 480 | chiriac et al management of spinal dural arteriovenouse fistula microwire in order to reach the closest point to the fistula. if the embolization is performed too proximally in the radicular feeding artery, collateral feeders could develop distally and repermeabilized the fistula. a microcatheter angiography is recommended before starting the embolic agent injection in order to ensure if the anterior spinal, posterior spinal or a radiculomedullary artery are not direct connected to fistula. endovascular occlusion is performed by slowly glubran 2 or onix injection into proximal draining vein while occluding the fistula site and feeding arterial vessels (figure 7). finally, control angiography is performed by selective catheterization of the segmental arteries arising at least two levels above and below the sdavf site. if there is no complete obliteration of the fistula usually the patient is addressed for a microsurgical approach as soon as possible. also, if there are doubts concerning the complete occlusion of the proximal radiculomedullary draining vein, a control angiographies are performed at one, three and six months later[2,3,6]. illustrative case case 1 this 62-year-old male presented with progressive gait instability, numbness and dysesthesias in the bilateral lower extremities, as well as increased lower extremity fatigue and urinary incontinence. magnetic resonance imaging and mr angiography of the spine demonstrated diffuse cord edema in the dorsal spine, with multiple abnormal blood vessels surrounding the spinal cord. these findings prompted a referral of the patient to our neurosurgical department for further evaluation and treatment of a suspected sdavf. spinal angiography was performed by selective injection of the right t-10 intercostal artery. the selective angio showed filling of a right radiculomeningeal branch from the region of the nerve root sleeve that filled a fistula (figure 8a, 8b). no other contributions to the spinal sdavfs were identified. the asa was found to arise from the left t-11 intercostal artery with no implication on fistula. the right radiculomeningeal branch is then microcatheterized and after detachment of a gdc-10 coil at its level the feeding branchs were embolized using glubran 2. (figure 8c, 8d) control angiography demonstrated complete obliteration of the sdavf without compromise to the right t-10 intercostal artery. one week following embolization procedure, his gait began to markedly improve and he was discharged to recovery clinic. a b romanian neurosurgery (2017) xxxi 4: 474 483 | 481 c d figure 8 t-10 sdavf a mri t2; b catheter angiography; c – gdc-10 detachment; d – sdavf occlusion case 2 a 61-year-old male was addressed to a neurologic department for progressive gait instability. magnetic resonance imaging of the spine demonstrated multiple abnormal blood vessels surrounding the spinal cord (figure 9a). based on the suspicion of a spine avm the patient was addressed to our neurosurgical department. at admission the neurological examination revealed bilateral lower-extremity motor weakness and sensory deficits, with the left side more severely affected. there was no motor or sensory deficit in the upper extremities. selective spinal angiography at left t-7 intercostal artery showed sdavf supplied by its radiculomeningeal branch and draining into a tortuous proximal radiculomedullary vein (figure 9b). a posterior approach with a midline t7-t8 laminectomy was performed. the dura was opened in the midline, the radiculomenigeal artery shunt was identified and a clip is applied on it. if the collapse of the drainage vein is observed with the change of blood flow arterial arterial to venous, the shunt is cauterized and disconnected (figure 9c, 9d). postintervenion angiography was performed for fistula interruption documentation. the patient was discharged to a local recovery centre. he continued to improve and was almost back to his baseline neurological and ambulatory status at the 6month follow-up. a b 482 | chiriac et al management of spinal dural arteriovenouse fistula c d figure 9 t-7 sdavf a mri – t1/tse/enhancment; b catheter angiography; c – shut identification; d – shunt cauterization and micro scissor disconnection discussion sdavfs were defined as abnormal direct connection between a radicular extradural artery and an intradural vein. most of studies show a predominance of the lesion in the thoracic spine and to male gender. the vast majority of patients presents with different degrees of neurological impairments usually correlated with the level of venous hypertension and its time occurrence. many authors are still considered the surgical obliteration of sdavf to be the gold standard for management of these lesions. however, improvements in endovascular technique and development of new embolic materials have made a greater number of patients with such vascular lesions to be treated for this type of treatment. the literature presents rates of successful endovascular therapy that vary between 25% and 90%[4,7]. the advantages of this treatment have been associated with shorter time hospitalization, minimal procedural morbidity and earlier initiation of rehabilitation programs. contraindication for endovascular occlusion o sdavf are represented by the spinal cord supply from the same arterial trunk as the feeding artery of the fistula, difficulties of a distal catheterization of the feeder artery due to its anatomical particularities, or recanalization of fistula after a previous embolization session. all experts have agreed that the success of endovascular treatment is closely related to the complete occlusion of both the arterial feeder and the proximal radiculomedulary vein. recent comparative studies between microsurgical and endovascular treatment of sdavfs on larger series of patients have shown that there are no statistically significant differences in postinterventional neurological recovery. early diagnosis and successful treatment of the fistula were demonstrated to be strong correlated with improvement in clinical symptoms. it was also found that improvement in motor function after treatment is more likely to occur than improvement in urinary dysfunction. the patients must be postinterventionaly monitored by clinical examination and at least mri imaging. in endovascular treated sdavfs a catheter angiography control is recommended. romanian neurosurgery (2017) xxxi 4: 474 483 | 483 conclusions endovascular treatment of sdavfs represents a good and effective option for management of these vascular lesions. however, some limitations on the possibility of applying this type of treatment have been described. for most cases, surgical treatment is still considered the first intention treatment. references 1. ducruet, a. f., crowley, r. w., mcdougall, c. g., & albuquerque, f. c. (2012). endovascular management of spinal arteriovenous malformations. journal of neurointerventional surgery, neurintsurg-2012. 2. gemmete, j. j., chaudhary, n., elias, a. e., toma, a. k., pandey, a. s., parker, r. a., ... & robertson, f. (2013). spinal dural arteriovenous fistulas: clinical experience with endovascular treatment as a primary therapy at 2 academic referral centers. american journal of neuroradiology, 34(10), 1974-1979. 3. gross, b. a., albuquerque, f. c., moon, k., & mcdougall, c. g. (2016). validation of an ‘endovascular-first’approach to spinal dural arteriovenous fistulas: an intention-to-treat analysis. journal of neurointerventional surgery, neurintsurg2016. 4. koch, m. j., stapleton, c. j., agarwalla, p. k., torok, c., shin, j. h., coumans, j. v., ... & patel, a. b. (2017). open and endovascular treatment of spinal dural arteriovenous fistulas: a 10-year experience. journal of neurosurgery: spine, 26(4), 519-523. 5. lenck, s., bernat, a., bresson, d., labeyrie, m., & saint-maurice, j. (2016). spinal dural arteriovenous fistula. j spine, 5(287), 2. 6. patsalides, a., santillan, a., knopman, j., tsiouris, a. j., riina, h. a., & gobin, y. p. (2010). endovascular management of spinal dural arteriovenous fistulas. journal of neurointerventional surgery, jnis-2010. 7. sivakumar, w., zada, g., yashar, p., giannotta, s. l., teitelbaum, g., & larsen, d. w. (2009). endovascular management of spinal dural arteriovenous fistulas: a review. neurosurgical focus, 26(5), e15; 8.takai, k. (2017). spinal arteriovenous shunts: angioarchitecture and historical changes in classification. neurologia medico-chirurgica, 57(7), 356–365. http://doi.org/10.2176/nmc.ra.2016-0316 9. wakhloo, a. k., patel, n. v., deleo iii, m. j., & shaibani, a. (2006). vascular anatomy of the spine, imaging, and endovascular treatment of spinal vascular diseases. chapter 92,the spine. 5th ed. philadelphia, pa: saunders, 1-23. 24ciureaav_discopatia 174 | cervical vertebral discopathy cervical vertebral discopathy prof. dr. msc. alexandru vlad ciurea pitesti university publishing house – 2017 authors: stud. andrei alexandru marinescu, assoc. prof. stefan iencean, md, phd the monograph published by pitesti university publishing house in 2017 under the coordination of prof. alexandru vlad ciurea md, phd, msc. represents an important step in the study of a frequent contemporary pathology. cervical vertebral discopathy is a polymorphic ailment of the modern society. this pathology became more frequent in the past years due to the modern way of life: incorrect postures, sedentariness, tempestuous physical exercises, bad diet, excessive use of different substances (ex: alcohol, tabaco, etc.) and many other factors. the clinical diagnosis is represented by pain in the cervical region with or without radiation to the upper limbs, in the early stages. the symptomatology can evolve in late stages to uni or bilateral neurological deficits of upper or lower limbs, difficulty or impossibility in walking or standing. in different population studies in usa, the prevalence of cervical vertebral discopathy is around 3.5-4 out of 1000. this frequent ailment of the active population caused the elaboration of clear and concise diagnosis and treatment criteria, precise medical protocols and the modernization of both conservative and surgical treatments. due to increased prevalence of this degenerative pathology in the active population, the authors recorded an increased number of neurosurgical interventions because the decompression of the dural sac and nerve roots is mandatory in most cases. since the publishing of “cervical vertebromedullary pathology” by prof. constantin arseni no other treatise was dedicated to this cervical degenerative pathology alone, until now. today, this polymorphic ailment benefits from a complete and correct clinical and imagistic diagnosis through ct/mri in association with electromyography. the gold-standard investigation is the cervical mri (non-invasive, non-ionizing) which can correctly diagnose the degenerative cervical ailment in all the scanned sequences: romanian neurosurgery (2018) xxxii 1: 174 175 | 175 t1, t2, stir, flair. this investigation can highlight the presence of a cervical vertebral canal stenosis, posterior longitudinal ligament ossification and spondylolisthesis. currently, there exists the possibility of a perfectly curative treatment and controllable evolution through a complex management – do not forget that the cervical region is an extremely fragile region which connects the head to the rest of the body. in the evolution of surgical treatment methods there were different vertebral disc substitution techniques. it started with an osseous graft for the iliac crest, followed by different biomaterials (palacost, pyramesch), and culminated with the insertion of a cervical cage made out of peek (polyeter-eterketon) biomaterial. even more than that, the authors mention an even better solution, which is currently under study: the use of autologous fatty tissue (recent study from 2017 on 300 patients – istanbul – favorable evolution). a cage made out of peek is one of the safest implants in disk hernia treatment. it is a material with no proven cytotoxicity (in vitro studies). this implant has no corrosive, allergenic or carcinogenic properties. it has the same elasticity as the bone and prevents the kyphosis of the cervical region. it is also an mri-compatible material. the authors dedicate an entire chapter to the disk hernia surgical treatment: from incision to closing the patient. the current, most frequent surgical treatment is represented by acdf (anterior cervical discectomy with fusion) and has remarkable postoperative morpho-functional results. the presented treatise covers the subject of cervical vertebral discopathy in a manner adequate for a medical resident or a young specialist in the field of neurosurgery, neurology and medical recovery. the monograph discusses related anatomy, semiology, physiology, physiopathology in a concise manner and offers both conservative and surgical therapeutic solutions. its entire content is based on the complex experience of the authors in the field of degenerative cervical pathology at the neurosurgical department of elias clinical hospital and the neurosurgical department of sanador clinical hospital. the neurosurgical part is discussed based on clinical, imaging and operatory data. the subject of treatment is covered presenting both anterior and posterior surgical approaches. the monograph contains 200 pages filled with rich iconography and a modern bibliography and contains substantial anatomy information related to the cervical region: vertebral column, spinal cord and cervical plexus. microsoft word 14sharmaanand_rectal romanian neurosurgery (2018) xxxii 2: 303 305 | 303             doi: 10.2478/romneu-2018-0037 rectal migration of ventriculo-peritonial shunt: a rare case report anand sharma1, avdesh shukla2, s.n. iyengar2 1gajra raja medical college, india 2department of neurosurgery, gajra raja medical college, india abstract: colonic perforation following ventriculoperitoneal shunt is a rare complication. the common treatment is to remove the perforating catheter and replace with new one. in this case report we reported a rare case of colonic perforation following vp shunt and its anal migration. we have discussed its pathogenesis, management strategy and review of literature. key words: ventriculoperitoneal shunt, anal migration introduction ventriculoperitoneal shunt (vps) is the most common treatment for hydrocephalus, but it can have serious complications. the migration of the distal catheter within the bowel so that it protrudes through the anus is a relatively rare complication, but it can result in a potentially serious infectious complication, sepsis, or even death. we reported a rare case of peritoneal shunt catheter migrated through the anus and its review of literature. case report an 18 – month presented to us with complaints that the child protruded a white tube per anus on defecation for last one day with clear fluid dripping from it (figure 1). the child had undergone the right-sided vp shunt (chhabra-slit-in-spring silicone medium pressure shunt) procedure 8 months back for congenital hydrocephalus. on examination, the child was afebrile, alert and had no neck rigidity, and the abdomen was soft. on rectal examination, there was a white tube coming from beyond the reach of finger. total leukocyte count (tlc) was 7200/cumm. an ultrasonography (usg) abdomen was normal. plain-film radiographs of the abdomen showed the distal catheter within the colonic lumen and traversing the sigmoid colon and rectum (figure 2). the child was operated and the shunt was cut at abdominal surface through a small incision. the rest of the distal tube was extracted per rectum. the proximal tube was taken out as external drainage. on antibiotics, the child improved. the cerebrospinal fluid (csf) culture done after 3 weeks was sterile and so a revision of shunt was done on the left side. the child was asymptomatic at 2 years follow-up. 304 | sharma et al rectal migration of ventriculo-peritonial shunt             figure 1 distal shunt tube protrudes through anus abdomen figure 2 x-ray film of standing discussion vp shunting is a procedure commonly used to treat obstructive or normal-pressure hydrocephalus in neurosurgery. vp shunt placement is often accompanied by various complications such as ventriculitis, meningitis, and sepsis and may cause several rare abdominal complications, including intestinal volvulus, pseudocyst, and extrusion through the scrotum, colon, anus, umbilicus, vagina, bladder, or heart. spontaneous bowel perforation is a rare complication of vp shunt surgery, occurring in only 0.01%–0.07% of cases; however, the mortality rate, which is due to intracranial or intra-abdominal infections, is considerably high at about 15% of all such reported cases [1-3]. the exact pathogenesis of spontaneous bowel perforation is unclear having been first reported by wilson and bertran [4] in two pediatric patients. since the initial report, there have been approximately 90 documented cases in the literature regarding vps-induced bowel perforation. in cases that have warranted surgical intervention, or by autopsy, the authors have described an encasing fibrotic scar anchoring the tubing to an area of the bowel and causing ulceration, and theoretically, eventual perforation”. the possible other factors responsible for bowel perforation are thin bowel wall in children, sharp and stiff end of the vp shunt, use of trocar by operating surgeons, chronic irritation by the shunt, previous surgery, infection and silicone allergy. management of bowel perforation is highly individualized and dependent upon the presenting signs and symptoms of the patient. immediate externalization is necessary to maintain shunt patency, as well as to limit the retrograde spread of bacteria along the shunt system, which can cause ventriculitis or meningitis [5]. if there is a concern of abdominal abscess or peritonitis, laparotomy is the preferred treatment choice to manage the bacterial infection. [6,7] however, in cases where there is no evidence romanian neurosurgery (2018) xxxii 2: 303 305 | 305             of peritoneal involvement and the patient's exam remains benign, it is believed that the fistulous opening should close spontaneously after removal of the catheter[8], as in our case. importantly, when re-shunting a patient, we highly recommend choosing a different terminus outside the abdominal cavity, as there remains the concern that the factors leading to bowel perforation are still present, such as the atrium (as in our case) or pleura. corresponding author: dr anand sharma, mch neurosurgery assistant professor gajra raja medical college ph. +919873190047 dranandsharma100123@gmail.com references 1. birbilis t, zezos p, liratzopoulos n, oikonomou a, karanikas m, kontogianidis k, et al. spontaneous bowel perforation complicating ventriculoperitoneal shunt: a case report. cases j 2009;7:8251.
 2. sami a, ait ben ali s, choukry m, achouri m, naja a, ouboukhlik a, et al. anal migration of ventriculoperitoneal shunt catheter. apropos of 3 cases [article in french]. neurochirurgie 1995;41:315e8. 3. ghritlaharey rk, budhwani ks, shrivastava dk, gupta g, kushwaha as, chanchlani r, et al. trans-anal protrusion of ventriculo-peritoneal shunt catheter with silent bowel perforation: report of ten cases in children. pediatr surg int 2007;23:575e80. 4. wilson cb, bertan v, authors. perforation of the bowel complicating peritoneal shunt for hydrocephalus. report of two cases. am surg. 1966;32:601–3. 5. ibrahim aw, author. e-coli meningitis as an indicator of intestinal perforation by v-p shunt tube. neurosurg rev. 1998;21:194–7. 6. “schulhof la, worth rm, kalsbeck je, authors. bowel perforation due to peritoneal shunt. a report of 7 cases and a review of the literature. surg neurol. 1975;3:265–9. 7. sells cj, loeser jd, authors. peritonitis following perforation of the bowel: a rare complication of a ventriculoperitoneal shunt. j pediatr. 1973;83:823–4. 8. sharma a, pandey ak, radhakrishnan m, kumbhani d, das hs, desai n, authors. endoscopic management of anal protrusion of ventriculo-peritoneal shunt. indian j gastroenterol. 2003;22:29–30.” 5khairkarpraveen_neuropsychiatric aspects romanian neurosurgery | volume xxx | number 4 | 2016 | october december article neuropsychiatric aspects of paediatric brain tumours: an update praveen khairkar, srikanth reddy, amit agrawal india doi: 10.1515/romneu-2016-0077 romanian neurosurgery (2016) xxx 4: 479 – 492 | 479 doi: 10.1515/romneu-2016-0077 neuropsychiatric aspects of paediatric brain tumours: an update praveen khairkar, *srikanth reddy, amit agrawal** associate professor, department of psychiatry, *senior resident, department of psychiatry, mahatma gandhi institute of medical sciences, sevagram, wardha, maharashtra, india **professor, department of neurosurgery, narayna medical college hospital, nellore, india abstract: the diagnosis and treatment of children and adolescents with cancer has a tremendous and lasting effect on the patients, their families, and other individuals in their social network. it carries a host of psychological and neurobehavioral ramifications, from questions of mortality to changes in levels of functioning in multiple domains. childhood cancer remains the leading cause of illness-related death in childhood, but significant advances in survival have been made in the past 40 years. this review looks at the neuropsychiatric presentations, psychosocial and treatment-related issues that arise in children with brain tumors. key words: paediatric brain tumours, neuropsychiatric presentations background psycho-oncology addresses the two major psychiatric and psychological dimensions of pediatric cancer; first, the psychiatric comorbid disorders and psychological responses of children at all stages of illness and their families and, the psychological stresses on health professionals delivering their care; and second the psychological, behavioural, and social factors that influence cancer risk, detection, and survival. (1) though pediatric cancers constitute a very small portion of the total cancers diagnosed, accounting to only 2% of the total cancers, they remain one of the leading causes of illness related death in childhood. (2) brain tumors constitute the second most common tumors in the pediatric age group after the leukemias. (3) pediatric brain tumors are not similar to adult tumors. meningioma, malignant gliomas, schwannomas and pituitary tumors are common in adults; however these tumors are rare in children. (4-5) in children more than 50% of the brain tumours are infratentorial and the common tumours are low grade gliomas and primitive neuroectodermal tumours. (6-7) gliomas represent 45 – 50% of all the pediatric primary brain tumors and are by far the commonest of them. (8) to appreciate the experience of a child who has cancer it is helpful to have an understanding of 480 | khairkar et al neuropsychiatric aspects of paediatric brain tumours the treatments involved. treatment of pediatric cancer may involve chemotherapy, radiation, surgery, or stem cell/bone marrow transplant, or some combination of these modalities. in contrast, children with primary cns malignancies, the second most common cancer of childhood, may have surgery only (eg, children with a pilocytic astrocytoma) or have surgery, radiation, and intensive chemotherapy (eg, children with medulloblastoma). (9) significant advances in treatment of pediatric brain tumors had influenced the survival rate in the past 40 years. the overall 5year survival rate for 0to 16-year-olds diagnosed between 1975 and 1979 was 62.9%, compared with 81.5% in 2005.9-10 much of this progress has come from the collaboration of pediatric oncology researchers and clinicians. the children’s oncology group (cog), supported by the national cancer institute, creates standardized treatment protocols for pediatric cancers and then analyzes the responses to care and disseminates this information to all pediatric cancer providers. (11) the degree of emotional expressiveness in children with brain tumor (s) and its possible effect on prognosis have been the subject of interest of a large body of literature. few descriptive case reports noted shorter survival both in adolescent and adult patients with depressed, resigning attitude compared with patients who were able to express more negative emotions, such as anger. (12) other clinical and epidemiological studies have not supported such an influenced in cancer risk or in cancer mortality. (13) this review looks at the neuropsychiatric presentations, psychosocial and treatmentrelated issues that arise in children with brain. neuropsychiatric presentations: brain tumours can be either supratentorial or infratentorial depending upon whether they arise from above or below the tentorium. the subjects having tumours in the supratentorial space manifest convulsions more frequently, whereas subjects having tumours in the infratentorial space manifest problems related to balance, posture and cranial nerve functions. interestingly, morning headaches, nausea, and lethargy resulting from tumour obstruction of the ventricles and raised intracranial tension are some of the common presentations of both of them. (14) neuropsychiatric presentations in children with brain tumour commonly changes over the course of illness and depends on medical, psychological and social factors: the disease itself (i.e., site, symptoms, clinical course, side effects of chemotherapeutic agents or radiations); prior levels of adjustment; the threat that cancer poses to attaining age appropriate developmental tasks and goals; cultural, religious and spiritual attitude; presence of emotionally supportive persons or caregivers; the potential for psychological and physical rehabilitation; and finally child’s temperament and coping style as well as prior experience with loss. (15) unlike in adults with brain tumours in whom the wide spectrum of neuropsychiatric presentations are being reported the focus in pediatric age group has been largely on issues of adjustment, emotional and mood disorder and cognitive impairment. let us discuss issues related to adjustments. romanian neurosurgery (2016) xxx 4: 479 – 492 | 481 adjustment problems: similar to any other significant stressor, child has problems in adjusting himself to the truth of having a critical illness such as brain tumour. pediatric patients who survive brain tumors cope with the direct physiological insult caused by the tumor itself, the treatments (neurosurgery, chemotherapy, and/or high dose central nervous system irradiation) and treatment related squeal (e.g., impaired health, extensive school absence, familial stress). coping of these psychological problems may be different for children of different age group. in preschool age, the child is mostly occupied with magical thinking and believes that he suffering from any chronic illness is a punishment given to him for some trivial wrong deeds. as the preschool children spend most of the time with their family, separation from them for the purpose of the treatment can be very traumatic to the child. in school, the child may face disrupted functioning and problems with peer relationship. this social squeal can be handled by involving child in activities such as board games, computers etc., and educational help can be provided by offering school tutors. it’s not until adolescence, that the child is able to understand the complexity of the chronic illness. (16) the common distresses that the teenager experiences after being diagnosed of cancer are “loosing hair”, “missing leisure activities”, “fatigue”, “pain from procedures and treatment” and “worry about missing school”. (17) in adolescence, the patients are not able to form intimate relationships as a result of negative self-image and pessimistic attitudes. this adds to their loneliness and restricted availability of coping resources. both of these are challenged during treatment because of feelings of being different and physical appearance changes such as hair loss caused by chemotherapy or weight gain caused by corticosteroids. as a result of low selfesteem and body image concerns expressed by adolescents with cancer, they avoid or are less likely to establish intimate relationships.18 future concerns about fertility, threatened by cancer treatment, is also a prominent issue. semen cryopreservation is available for boys but there are no definitive preservation methods available for girls. (19) these psychological adjustment problems make the children with brain tumors susceptible to various psychiatric illnesses such and mood disorder and anxiety disorder. emotional/ anxiety/mood disorders one might assume that a severe stressor such as a diagnosis of cancer during childhood would overwhelm an individual’s ability to cope emotionally and most if not all children would experience emotional difficulties. however, studies suggest that most children with cancer do not exhibit significant levels of depression or anxiety, although a significant minority do experience marked levels of psychological distress. (20–23) some clinical observations have indicated that a subset of patients exhibit more problems, such as greater difficulty coping. (22) other studies show the emotional well-being of children with cancer currently receiving chemotherapy to be remarkably similar to case-control classroom peers, (23) and initial studies of cancer survivors similarly failed to find increases in social and emotional problems in 482 | khairkar et al neuropsychiatric aspects of paediatric brain tumours children with cancer, (24) although new data on survivors has challenged this view. in assessing a child’s mood, the clinician must be knowledgeable about the side effects of the treatments, which may include fatigue, decreased appetite, and disturbed sleep. if a child does present with clinically significant depressive symptoms, the treatment follows the same course as it would in the physically well child; that is, with psychotherapy such as cognitive-behavioral therapy (cbt) and antidepressant medication as indicated. (25) although no large studies have been conducted in children with cancer, selective serotonin reuptake inhibitor (ssri) medications are the pharmacologic antidepressant treatment of choice, as they are in the population at large. (26) in an uncontrolled pilot study of 15 children with cancer and depression or anxiety, fluvoxamine was well tolerated and effective. (27) in another small study, 7% of children involved in national institutes of health (nih) research trials for cancer were found to have been prescribed antidepressant medication. (28) the investigators of this study noted increasing acceptance for psychopharmacologic treatment of subthreshold psychiatric disorders to improve quality of life, and concluded that in addition to psychological support always being indicated in the setting of anxiety or depression, there is a role for the judicious use of psychotropic medications. the child with cancer often presents to mental health treatment with anticipatory anxiety and/or nausea and vomiting. there are no documented incidence or prevalence studies on particular or specific type (s) of anxiety spectrum disorders developed after brain tumors. however, anticipatory anxiety without nausea or vomiting component is initially addressed with behavioral interventions. the child may feel nauseated or vomit on arriving at the outpatient clinic or hospital. one study reports 59% of children experienced mild to severe anticipatory nausea and vomiting despite the use of ondansetron. (29) in mild cases, the effective behavioral approaches include thought stopping, hypnosis, distraction, and relaxation. (30) more severe cases of such typified presentations in association with postchemotherapy nausea and vomiting may respond to increased use of antiemetics, including higher doses of ondansetron, corticosteroids, and benzodiazepines. there are also some data to support the use of acupuncture in this population. (31) treatment related issues: in the psychiatric evaluation and treatment of children with cancer, several prominent areas of difficulty related to cancer treatment emerge, and include psychiatric effects of chemotherapeutic agents, neurocognitive effects of treatment from chemotherapy and cranial radiation, and issues related to adherence with treatment. for the sake of understanding, the neuropsychiatric adverse effects of most commonly prescribed and reported drugs viz. corticosteroids and interferon are discussed below. corticosteroids corticosteroids are routinely used for the treatment of childhood cancers and their sequelae. in many chemotherapy protocols, including leukemias and lymphomas, romanian neurosurgery (2016) xxx 4: 479 – 492 | 483 corticosteroids play a central role. the appearance of adverse psychiatric symptoms is common in children who are receiving highdose corticosteroids. these symptoms include changes in mood, sleep, and appetite. research in the area of psychiatric adverse effects to corticosteroids is much more extensive in adults than in children. the adult literature supports the role of corticosteroids in causing behavioral changes including depression, mood elevation, irritability, anger, insomnia, and excess talkativeness. (32–34) psychiatric sequelae are usually dose-dependent and studies have reported increased severity of psychiatric symptoms with higher doses of corticosteroids. patients can become severely depressed, manic, psychotic and/or delirious. in the largest study of its type, severe psychiatric reactions were seen in 1.3% of patients receiving prednisone 40 mg per day or less; in 4% to 6% of patients receiving 41 to 80 mg per day; and in 18.4% of patient receiving more than 80 mg per day. (35) the use of corticosteroids in children has been studied in children with renal, pulmonary, and gastrointestinal diseases more commonly than in children with cancer and reviewed extremely well by satel. (36) effects seen in children with cancer are consistent with the behavioral changes seen in children with other illnesses and in the adult population. in children receiving prednisone at a dosage of 60 mg/m2/d for leukemia and lymphoma, increased irritability, argumentativeness, tearfulness, reports of “talking too much,” tiredness, low energy, and night waking were common symptoms, with a trend toward more symptoms in younger children. (37) in children with all, groups receiving prednisone 40 mg/m2/d and 120 mg/m2/d showed adverse changes in attention/hyperactivity, emotionality, sleep disturbance, depressed mood, listlessness, and peer relations, although there was no significant difference between the two steroid groups. (38) in a few cases, the severity of a child’s depression or mania or the development of psychosis requires a reduction or discontinuation of the corticosteroids as well as acute psychopharmacologic intervention. for mild forms of depression, psychotherapeutic strategies can be beneficial. psychoeducation for patients and families that symptoms may be transient and biochemically mediated rather than the result of a sudden giving up or self-pity is essential. (39) neurocognitive deficits apart from adjustment problems and emotional disorders in children, neurocognitive deficits are of a great concern and interest in subjects of brain tumours and their incidence is found to be unacceptably high. the incidence is variable with some reports stating it to be present in more than 50% of paediatric cancers (2), whereas some reports put it at 40% – 100% among long term brain survivors (40) and some go on to state that impaired intelligence is present in 90% of conventionally treated medulloblastoma patients. (41) despite the differences between all and malignant brain tumors, there are significant similarities among the symptoms comprising neurocognitive deficits, particularly with regard to the treatments of brain irradiation and intrathecal chemotherapy. while a considerable body of 484 | khairkar et al neuropsychiatric aspects of paediatric brain tumours evidence has accumulated on the nature of white matter damage from those treatments, variations in tumor pathology and combined treatment protocols over time have made the need for further research necessary. in order to summarize our understanding of the neuropsychological impact of childhood cancers and their treatment, we have chosen to define core deficits, which involve executive functions, processing, and fluid abilities, and secondary deficits, which are knowledge based and oftentimes referred to as crystallized abilities. in the current conceptualization, it is the detrimental effects of cancer and cancer therapy on the biological substrates of core abilities that eventually result in more observable secondary deficits. several excellent reviews are available supporting this approach to understanding neurocognitive deficits among children surviving brain tumors (42), suggesting that children surviving brain tumors are at greater risk for more severe deficits because of the increased aggressiveness of their therapy and, in particular, the continued use of crt. while the late effects of crt typically emerge within 1 to 2 years of administration, there is evidence that brain-damage effects may be delayed up to 7 years. (43) children who survive a brain tumor do appear to be at risk for social difficulties following cessation of treatment, perhaps due to increased severity of neurocognitive injury. (44) these core and secondary symptoms of neurocognitive deficits may also impact other areas of functioning, such as social interactions. the major core neurocognitive deficits and risk factors among children treated for malignant brain tumors. premorbid factors the occurrence of neurocognitive deficits depend on various premorbid factors such as female sex, younger age at treatment, genetic polymorphisms, and population and social risk factors. (45) as compared to older counterparts, a younger age at treatment consistently shows a significantly greater decline in age-adjusted scaled scores of intellectual functioning over time. in couple of the studies by same author, the subjects of medulloblastoma who were younger (<8.85 years) experienced more neurotoxicity, when measured on tests of intellectual functioning, than those who were older at treatment (>8.85 years). (46-470 similar findings were reported demonstrating significantly greater declines in age-adjusted scaled scores of factual knowledge and nonverbal abstract thinking as well as an overall estimate of full-scale iq in younger subjects receiving radiation treatment for medulloblastoma. (48) like younger age, female gender also correlated with poorer neurocognitive functions as compared to males having solid brain tumors when measuring for intellectual and academic functioning, including a test of reading comprehension. (49) moreover in comparison to males, early age of diagnosis and low social economic status were associated with more severe cognitive impairment in females. (50) other pre-morbid factors predicting the neurocognitive deficits in paediatric subjects of brain tumours are genetic polymorphisms, and population and social risk factors. (51-52) romanian neurosurgery (2016) xxx 4: 479 – 492 | 485 sources of neurocognitive deficits neurocognitive deficits can occur by myriad of causes ranging from primary cns tumour effects, neurosurgical squeal, raised intracranial tensions, seizures and antiepileptic treatments, cranio-spinal radiotherapies and systemic and cns focused chemotherapies. (53) the growing tumour as well as the raised intracranial pressure occurring mostly as a result of obstructive hydrocephalus causes compression of tissue at both local and remote sites. hydrocephalus is involved with problems of neurocognitive functioning including memory, attention and perceptual performance. (54) one study demonstrated an association between presence of hydrocephalus and a higher risk for intellectual deficits in paediatric brain tumour subjects. (55) however early correction of hydrocephalus may result in no lasting effect on cognitive functioning. (56) similarly extent of resection in neurosurgery has also been associated with deficits in intellectual functioning with higher decline associated with more extensive resection. (57) posterior fossa syndrome (mutism, ataxia and behavioural changes), developing after surgery has a higher risk for neuropsychiatric squeal. (58, 59) further studies demonstrated that the surgical resection of brain tumours without adjuvant therapy was itself associated with deficits in neuropsychological testing in attention, memory, processing speed, and visuospatial processing, and a variety of behavioral problems. moreover other factors such as shunt infections, meningitis or the need for repeat surgery further increased the risk of cognitive decline. (60, 61) exposure to cranial radiotherapy while getting treated for brain tumours has also shown to be responsible for the cognitive decline. it is postulated to cause greatest damage to developing white matter and as a result has been shown to cause the greatest negative squeal for the developing brain. myelination normally continues after birth into the third decade of life (62) and exposure to crt can disrupt this developmental process, ending in demyelination, and ultimately white matter damage. in addition, immature oligodendrocytes are thought to be more vulnerable to injury than the mature counterparts. (63) treatment with cranial radiotherapy has shown to reduce the iq by 15 to 25 points in children with brain tumors. (64, 65) in view of these findings of significant cognitive decline, efforts are now shifted to develop new protocols having the advantage of decreasing the radiation exposure while maintaining the same cure rate. these efforts involve using early focal radiotherapy and decreasing the target tissue volume and dose of cranial radiation. (66) like radiotherapy, chemotherapy with agents such as methotrexate has also shown to cause neurocognitive deficits though not as severe as the former. methotrexate is known to interfere with folate metabolism resulting in demyelination and other toxic effects on cns thereby leading to cognitive decline. (67) problems that are reported with the use of chemotherapy in treatment of pediatric brain tumors are problems with sustained attention, which correlated with teacher reports of poorer academic performance, particularly in mathematics, increased internalizing 486 | khairkar et al neuropsychiatric aspects of paediatric brain tumours behaviors on the child behavior checklist, a parent report measure of social competence and behavior problems, visual processing, visual-motor functioning, attention and executive functioning, academic performance, verbal abilities, and memory with female gender and young age (particularly less than age 3 years) as risk factors. (68-70) psychopharmacological and palliative care interventions for neurocognitive effects: although the research on the pattern and causes of neurocognitive deficits in pediatric brain tumors has been rapidly progressing over the last few decades, the development of empirically validated treatment for these deficits is still in its infancy. the role of psychiatrists and psychologists in identifying, assessing and dealing with these deficits cannot be underestimated. as in any child with academic difficulties and cognitive impairments, mental health professionals should strive towards educating family members and school personnel about the deficits that are expected to develop as the treatment progresses and also advocating for proper services. the management can be a primary prevention wherein, the cns insult is tried to be reduced in order to prevent development of neurocognitive deficits. as radiotherapy is known to cause the maximum cns insult, protocols are using lower doses of cranial radiation, decreasing the tissue target volume, and postponing radiation in the highest risk groups or using early focal radiotherapy to minimize the cognitive effects. (71) newer forms and techniques for delivering radiation are also being used. for example, proton beam radiotherapy, as opposed to standard photon radiotherapy, may decrease the likelihood of significant neurocognitive decline, because there is no exit radiation dose thereby decreasing the volume of white matter involved. in addition to morbidity-limiting strategies to minimize the neurotoxic effects (particularly cranial radiation), some investigators have examined interventions for neurocognitive effects after they have occurred. (72, 73) as in any child with academic difficulties and cognitive impairments, mental health professionals working with survivors of cancer have a role in educating family members and schools about deficits seen in this population, and advocating for appropriate accommodations and services. studies show that the decline in iq may not be apparent initially and can be progressive over time, highlighting the importance of following children longitudinally. one potentially useful addition to the development of interventions for cognitive deficits has been an appraisal of the influence of the family environment and resources following recovery from traumatic brain injury. the importance of family cohesiveness and stability in recovery from brain injury has long been known. as early as 1958, it was reported that children who suffered a traumatic brain injury and developed psychiatric disturbance had greater degrees of family pathology as those who did not experience a mental disorder. (74) other researchers have further demonstrated the relationship between family pathology and behavioral difficulties among brain injured children. (75, 76) more recently, yeates and colleagues (77) (1997) have documented that romanian neurosurgery (2016) xxx 4: 479 – 492 | 487 chaotic and dysfunctional family environments have a significant adverse impact on neurological and neuropsychological recovery from traumatic brain injury among school-age children. this relationship appears to be valid even when severity of brain injury and other medical factors were experimentally controlled (max et al., 1999). (78) it appears that family burden, characterized by ratings from parents as to the negative impact of the child’s injury on the family, and overall family adjustment are significant predictors of continued neurobehavioral symptoms following childhood traumatic brain injury (yeates et al., 2001). (79) how might these findings be relevant to survivors of childhood cancer having neurocognitive problems? one could speculate that the family environment might be of equal or greater importance in the treatment and recovery of a chronic lifethreatening disease compared with an acute event such as a traumatic brain injury. certainly, educating parents to be advocates for their children by giving them sufficient information and support should be a component of any clinical intervention. whether formal training in special skills would facilitate recovery of function among children treated for traumatic brain injury or cancer is not yet known. adherence adherence a more proactive term than compliance to treatment regimens is a prominent issue with children and adolescents having brain tumors. adolescents consistently show higher rates of non-adherence compared with children and adults in the treatment of cancer and other life-threatening illnesses. (80-84) risk factors for poor adherence with cancer treatment in adolescents have been identified, including low socioeconomic status of the family, (84–86) barriers to communication such as cultural and linguistic differences, (87) and mental illness, including depression in a parent and behavioral disturbances during the patient’s childhood.88 clinically, poor communication between adolescents and their parents around treatment seems to be a significant contributor to poor adherence. it is important to identify non-adherence issues early in treatment. blood levels of a drug or its metabolites have been used to monitor adherence with oral medication regimens, such as 6mercaptopurine in the treatment of all. (85,86) a nonjudgmental inquiry about the patient’s consistency in taking the medication may be just as effective. (84) confusion about appropriate doses or about who is responsible for administering the medication may contribute to unintentional non-adherence. psychological issues at the end of the life although most children with cancer survive, childhood cancer remains the leading cause of illness-related death in childhood and is the second leading cause of death in children, behind accidents. the reality of cancer as a sometimes terminal illness affects patients, families, and caregivers alike. oncology teams utilize the services of social workers, psychologists, psychiatrists, chaplains, and child life specialists to assist the child, family, and staff with the challenges faced at the end of life. these care providers can facilitate family conversations about death 488 | khairkar et al neuropsychiatric aspects of paediatric brain tumours between parents and with the child. (89) conversations about dying and end-of-life care are inherently difficult and often avoided, but data support having open conversations with children. kreicbergs and colleagues (90) found that parents of children with severe malignant disease who had conversations with their children about dying did not regret these conversations. children with cancer experience significant physical and psychological symptoms and suffering at the end of life. (91) despite this, palliative care services are available at only 58% of institutions caring for pediatric oncology patients, highlighting one obstacle to offering optimal care to all children treated for cancer. (92) many of the difficulties encountered in the terminal phase of children with cancer are common to all children at the end of life. see the article by knapp and colleagues elsewhere in this issue for further exploration of this topic. conclusions neuropsychiatric presentations of pediatric brain tumors are both interesting and valuable in the midst of current concerns; interesting because it increases our understanding about presenting patterns and their mechanism of evolvement and useful because of the possibility of learning more and better from previous experiences of clinicians. recent decades have brought about tremendous improvements in survival outcomes for children with cancer. overall, children with cancer are resilient, but they are confronted with several challenges adjusting to their illness, dealing with treatment related effects, and for some facing end-of-life care. children having brain tumours undergo various psychosocial stressors and related psychiatric problems such as mood disorders and neurocognitive deficits which need to be evaluated and assessed longitudinally in every child. these facts make the need that both mental health clinicians and pediatricians should play a critical role in providing the assessment, support, and treatment needed in the childhood cancer population. continued research in this field is imperative. incorporation of systematized psychiatric care in the routine management of paediatric brain tumours can improve the quality of life of the patients and make the oncology treatment complete. continued research in this field is however imperative. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayna medical college hospital nellore, pin-524003 ap, india email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 references 1.rouhani m, holland jc. psychiatric aspects of cancer. in gelder mg, andreasen nc, lopez-ibor jj, geddes jr. new oxford textbook of psychiatry, second edition, oxford university press, new york , 2009 2.national cancer policy board (u.s.), weiner sl, simone jv. childhood cancer survivorship: improving care and quality of life. washington, dc: national academies press; 2003. romanian neurosurgery (2016) xxx 4: 479 – 492 | 489 3.linabery am, ross ja. trends in childhood cancer incidence in the u.s. (1992-2004). cancer 2008;112(2):416–32. 4.horner mj, ries lag, krapcho m. editors. seer cancer statistics review, 1975–2006. based on november 2008 seer data submission. bethesda (md): national cancer institute. available at: http://seer.cancer.gov/csr/1975_2006/, posted to the seer web site, 2009. 5.karajannis m, allen jc, newcomb ew. treatment of pediatric brain tumours. j cell physiol. 2008;217:584–9. 6.pollack if. the role of surgery in pediatric gliomas. j neurooncol. 1999;42:271–88. 7.pollack if. brain tumours in children. n engl j med. 1994;331:1500–7. 8.duffner pk, cohen me, myers mh, heise hw. survival of children with brain tumors: seer program. 1973-1980. neurology. 1986;36:597-601. 9.robertson pl. advances in treatment of pediatric brain tumours. neurorx. 2006;3:276-91. 10.ris md, beebe dw. neurodevelopmental outcomes of children with low-grade gliomas. dev disabil res rev 2008;14:196-202. 11.gottardo ng, gajjar a. chemotherapy for malignant brain tumors of childhood. j child neurol 2008;23:114959. 12.temoshok l. biopsychosocial studies on cutaneous malignant melanoma: psychosocial factors associated with prognostic indicators, progression, psychophysiology and tumor-host response. soc sci med 1985;20:833-40. 13.derogatis, l.r., morrow, g.r., fetting, j. the prevalence of psychiatric disorders among cancer patients. journal of the american medical association. 1983;240:751–7. 14.panigrahy a, bluml s. neuroimaging of paediatric brain tumors: from basic to advanced magnetic resonance imaging (mri). j. chil neurol 2009;24:13431365. 15.forsyth pa, posner jb. headaches in patients with brain tumors: a study of 111 patients. neurology 1993;43:1678-82. 16.kurtz bp, abrams an, psychiatric aspects of pediatric cancer, child adolesc psychiatr clin n am 2010;19:40121. 17.hedstrom m, ljungman g, von essan l. perception of distress among adolescents recently diagnosed with cancer. j pediatr hematol oncol 2005;27:15-22. 18.evan ee, kaufman m, cook ab, zeltzer lk. sexual health and self-esteem in adolescents and young adults with cancer. cancer 2006;107:1672-9. 19.weintraub m, gross e, kadari a, ravitsky v, safran a, laufer n, et al. should ovarian cryopreservation be offered to girls with cancer. pediatr blood cancer 2007;48:4-9. 20.kashani j, hakami n. depression in children and adolescents with malignancy. can j psychiatry 1982;27:474–7. 21.allen l, zigler e. psychological adjustment of seriously ill children. j am acad child psychiatry 1986;25:708–12. 22.patenaude af, kupst mj. psychosocial functioning in pediatric cancer. j pediatr psychol 2005;30:9–27. 23.pai al, drotar d, zebracki k, moore m, youngstrom e. a meta-analysis of the effects of psychological interventions in pediatric oncology on outcomes of psychological distress and adjustment. j pediatr psychol 2006;31:978–88. 24.eiser c, hill jj, vance yh. examining the psychological consequences of surviving childhood cancer: systematic review as a research method in pediatric psychology. j pediatr psychol 2000;25:449–60. 25.march j, silva s, petrycki s, curry j, wells k, fairbank j, et al. fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: treatment for adolescents with depression study (tads) randomized controlled trial. jama 2004;292:807-20. 26.kersun ls, elia j. depressive symptoms and ssri use in pediatric oncology patients. pediatr blood cancer 2007;49:881-7. 27.gothelf d, rubinstein m, shemesh e, miller o, farbstein i, klein a, et al. pilot study: fluvoxamine treatment for depression and anxiety disorders in children and adolescents with cancer. j am acad child adolesc psychiatry 2005;44:1258–62. 28.pao m, ballard ed, rosenstein dl, weiner l, wayne as. psychotropic medication use in pediatric patients with cancer. arch pediatr adolesc med 2006;160:818-22. 29.tyc vl, mulhern rk, barclay dr, smith bf, bieberich aa. variables associated with anticipatory nausea and vomiting in pediatric cancer patients receiving 490 | khairkar et al neuropsychiatric aspects of paediatric brain tumours ondansetron antiemetic therapy. j pediatr psychol 1997;22:45-58. 30.stockhorst u, spennes-saleh s, ko¨rholz d, gobel u, schneider me, steingruber hj, et al. anticipatory symptoms and anticipatory immune responses in pediatric cancer patients receiving chemotherapy: features of a classically conditioned response? brain behav immun 2000;14:198-218. 31.gottschling s, reindl tk, meyer s, berrang j, henze g, graeber s, et al. acupuncture to alleviate chemotherapy-induced nausea and vomiting in pediatric oncology – a randomized multicenter crossover pilot trial. klin padiatr 2008;220(6):365-70. 32.lewis da, smith re. steroid-induced psychiatric syndromes. a report of 14 cases and a review of the literature. j affect disord 1983;5:319-32. 33.kershner p, wang-cheng r. psychiatric side effects of steroid therapy. psychosomatics 1989;30:135-9. 34.wolkowitz om. prospective controlled studies of the behavioral and biological effects of exogenous corticosteroids. psychoneuroendocrinology 1994;19:23355. 35.the boston collaborative drug surveillance program. acute adverse reactions to prednisone in relation to dosage. clin pharmacol ther 1972;13:694-8. 36.satel sl. mental status changes in children receiving glucocorticoids. review of the literature. clin pediatr (phila) 1990;29:383-8. 37.harris jc, carel ca, rosenberg la, joshi p, leventhal bg. intermittent high dose corticosteroid treatment in childhood cancer: behavioral and emotional consequences. j am acad child psychiatry 1986;25:120-4. 38.drigan r, spirito a, gelber rd. behavioral effects of corticosteroids in children with acute lymphoblastic leukemia. med pediatr oncol 1992;20:13-21. 39.schaefer m, engelbrecht ma, gut o, fiebich bl, bauer j, schmidt f, et al. interferon alpha (ifn alpha) and psychiatric syndromes: a review. prog neuropsychopharmacol biol psychiatry 2002;26:731-46. 40.glauser ta, packer rj. cognitive deficits in long-term survivors of childhood brain tumors. child’s nervous system 1991;7:7-12 41.dennis m, spiegler b, hetherington cr, greenberg m. neuropsychological squeal of the treatment of children with medulloblastoma. journal of neuro-oncology 1996;29:91-101 42.ris md, noll rb. long-term neurobehavioral outcome in pediatric brain tumor patients: review and methodological critique. journal of clinical and experimental neuropsychology 1994;16:21-42. 43.brouwers p, riccardi r, fedio p, poplack dg. longterm neuropsychologic sequelae of childhood leukemia: correlation with ct brain scan abnormalities. the journal of pediatrics 1985;106:723-8. 44.vannatta k, gartstein ma, short a, noll rb. a controlled study of peer relationships of children surviving brain tumors: teacher, peer, and self ratings. journal of pediatric psychology 1998;23:279-87. 45.nathan pc, patel sk, dilley k, goldsby r, harvey j, jacobsen c, et al. guidelines for identification of, advocacy for,and intervention in neurocognitive problems in survivors of childhood cancer: a report from the children’s oncology group. arch pediatr adolesc med 2007;161:798-806. 46.mulhern rk, palmer sl. neurocognitive late effects in paediatric cancer. curr probl cancer 2003;27:177-97 47.mulhern rk, kepner jl, thomas prm, armstrong fd, friedman hs, kun le. neuropsychological functioning of survivors of childhood medulloblastoma randomized to receive conventional (3,600 cgy/20) or reduced (2,340 cgy/13) dose craniospinal irradiation: a paediatric oncology group study. journal of clinical oncology 1998;16:1723-8. 48.palmer sl, goloubeva o, reddick we, glass jo, gajjar a, kun l, et al. patterns of intellectual development among survivors of paediatric medulloblastoma: a longitudinal analysis. journal of clinical oncology 2001;19:2302-8. 49.greenberg hs, kazak ae, meadows at. psychologic functioning in 8to 16year-old cancer survivors and their parents. j pediatr 1989;114:488–93. 50.waber dp, carpentieri sc, klar n, silverman lb, schwenn m, hurwitz ca, et al. cognitive sequelae in children treated for acute lymphoblatic leukemia with dexamethasone or prednisone. journal of paediatric hematology oncology 2000;22:206-13. 51.nathan pc, patel sk, dilley k, goldsby r, harvey j, jacobsen c, et al. guidelines for identification of, advocacy for,and intervention in neurocognitive problems in survivors of childhood cancer:a report from the children’s oncology group. arch pediatr adolesc med 2007;161:798–806. romanian neurosurgery (2016) xxx 4: 479 – 492 | 491 52.phipps s, dunavant m, srivastava dk, bowman l, mulhern rk. cognitive and academic functioning in survivors of paediatric bone marrow transplantation. j clin oncol 2000;18:1004–11. 53.fleishman sb, kalash gr. chemotherapeutic agents and neuropsychiatric side effects. in psycho-oncology (ed. j.c. holland), pp. 630–9. oxford university press, new york. 1998 54.scott ma, fletcher jm, brookshire bl. memory functions in children with early hydrocephalus. neuropsychology 1998;12:578-589 55.jannoun l, bloom hjg. long-term psychological effects in children treated for intracranial tumors. international journal of radiation, oncology and physics 1990;18:747-753. 56.ris md, noll rb. long-term neurobehavioral outcome in pediatric brain-tumor patients: review and methodological critique. journal of clinical and experimental neuropsychology 1994;16:21-42. 57.packer rj, meadows at, rorke lb, goldwein jl, d’angio g. long-term squeal of cancer treatment on the central nervous system in childhood. medical and pediatric oncology 1987;15:241-253. 58.levisohn l, cronin-golomb a, schmahmann jd. neuropsychological consequences of cerebellar tumour resection in children: cerebellar cognitive affective syndrome in a paediatric population. brain 2000;123:1041-50. 59.wolfe-christensen c, mullins ll, scott jg, mcnallknapp ry. persistent psychosocial problems in children who develop posterior fossa syndrome after medulloblastoma resection. pediatr blood cancer 2007;49:723-6. 60.steinlin m, imfeld s, zulauf p, boltshauser e, lovblad ko, ridolfi la, et al. neuropsychological long-term squeal after posterior fossa tumour resection during childhood. brain 2003;126:1998-2008. 61.kao gd, goldwein jw, schultz dj, radcliffe j, sutton l, lange b. the impact of perioperative factors on subsequent intelligence quotient deficits in children treated for medulloblastoma/posterior fossa primitive neuroectodermal tumors. cancer 1994;74:965-71. 62.sowell er, thompson pm, holmes cj, jernigan tl, toga aw. in vivo evidence for post-adolescent brain maturation in frontal and striatal regions. nature neuroscience 1999;2:859-861. 63.fern r, moller t. rapid ischemic cell death in immature oligodendrocytes: a fatal glutamate release feedback loop. journal of neuroscience 2000;20:34-42. 64.mulhern rk, kovnar e, langston j, carter m, fairclough d, leigh l, et al. long-term survivors of leukemia treated in infancy: factors associated with neuropsychologic status. journal of clinical oncology 1992;10:1095-102. 65.ris md, noll rb. long-term neurobehavioral outcome in pediatric brain tumor patients: review and methodological critique. journal of clinical and experimental neuropsychology 1994;16:21-42. 66.skowronska-gardas a. a literature review of the recent radiotherapy clinical trials in pediatric brain tumors. rev recent clin trials 2009;4:42-55. 67.buizer ai, de sonneville lm, veerman aj. effects of chemotherapy on neurocognitive function in children with acute lymphoblastic leukemia: a critical review of the literature. pediatr blood cancer 2009;52:447–54. 68.achenbach tm. manual for the child behavior checklist/4-18 and 1991 profiles. burlington (vt): university of vermont department of psychiatry; 1991. 69.campbell lk, scaduto m, sharp w, dufton l, van slyke d, whitlock ja, et al. a meta-analysis of the neurocognitive squeal of treatment for childhood acute lymphocytic leukemia. pediatr blood cancer 2007;49:65-73. 70.anderson fs, kunin-batson as. neurocognitive late effects of chemotherapy in children: the past 10 years of research on brain structure and function. pediatr blood cancer 2009;5:159-64. 71.roman dh, sperduto pw. neuropsychological effects of cranial radiation: current knowledge and future directions. international journal of radiation oncology, biology, physics 1995;31:983-98. 72.butler rw, mulhern rk. neurocognitive interventions for children and adolescents surviving cancer. j pediatr psychol 2005;30:65-78. 73.butler rw, sahler oj, askins ma, alderfer ma, katz er, noll rb. interventions to improve neuropsychological functioning in childhood cancer survivors. dev disabil res rev 2008;14:251-8. 74.harrington ja ,letemendia fjj. persistent psychiatric disorders after head injuries in children. journal of mental science 1958;104:1205-7. 75.lezak md. living with the characterological altered brain injured patient. journal of clinical psychiatry 1978;39:592-8. 492 | khairkar et al neuropsychiatric aspects of paediatric brain tumours 76.worthington j. the impact of adolescent development on recovery from traumatic brain injury. rehabilitation nursing 1989;14:118-22. 77.yeates ko, taylor hg, drotar d, wade sl, stancin t, klein s, et al. pre-injury family environment as a determinant of recovery from traumatic brain injuries in school-age children. journal of the international neuropsychological society 1997;3:617-30 78.max je, roberts ma, koele sl, lindgren sd, robin da, arndt s, et al. cognitive outcome in children and adolescents following severe traumatic brain injury: influence of psychosocial, psychiatric and injury-related variables. journal of the international neuropsychological society 1999;5:58-68. 79.yeates ko, taylor hg, barry ct, drotar d, wade sl, stancin t. neurobehavioral symptoms in childhood closed-head injuries: changes in prevalence and correlates during the first year postinjury. journal of pediatric psychology 2001;26:79-91. 80smith sd, rosen d, trueworthy rc, lowman jt. a reliable method for evaluating drug compliance in children with cancer. cancer 1979;43:169-73. 81.lansky sb, smith sd, cairns nu, cairns gf jr. psychological correlates of compliance. am j pediatr hematol oncol 1983;5:87-92. 82.tebbi ck, cummings km, zevon ma, smith l, richards m, mallon j. compliance of pediatric and adolescent cancer patients. cancer 1986;58:1179-84. 83.festa rs, tamaroff mh, chasalow f, lanzkowsky p. therapeutic adherence to oral medication regimens by adolescents with cancer. i. laboratory assessment. j pediatr 1992;120:807-11. 84.tebbi ck. treatment compliance in childhood and adolescence. cancer 1993;71:3441-9. 85.de oliveira bm, viana mb, zani cl, romanha a. clinical and laboratory evaluation of compliance in acute lymphoblastic leukaemia. arch dis child 2004;89:785-8. 86. lancaster d, lennard l, lilleyman js. profile of noncompliance in lymphoblastic leukaemia. arch dis child 1997;76:365-6. 87.spinetta jj, masera g, eden t, oppenheim d, martins ag, van dongen-melman j, et al. refusal, noncompliance, and abandonment of treatment in children and adolescents with cancer: a report of the siop working committee on phychosocial issues in pediatric oncology. med pediatr oncol 2002;38(2):114-7. 88.die-trill m, stuber ml. psychological problems of curative cancer treatment. in: holland jc, editor. psychooncology. new york: oxford university press;1998. p. 897-906. 89. beale ea, baile wf, aaron j. silence is not golden: communicating with children dying from cancer. j clin oncol 2005;23:3629-31. 90.kreicbergs u, valdimarsdottir u, onelov e, henter ji, steineck g. talking about death with children who have severe malignant disease. n engl j med 2004;351:1175-86. 91.wolfe j, grier he, klar n, levin sb, ellenbogen jm, salem-schatz s, et al. symptoms and suffering at the end of life in children with cancer. n engl j med 2000;342:326-33. 92.johnston dl, nagel k, friedman dl, merza jl, hurwitz ca, friebert s. availability and use of palliative care and end-of-life services for pediatric oncology patients. j clin oncol 2008;26:4646-50. microsoft word _1.formatata_vonwild.doc romanian neurosurgery vol. xv nr. 2 3 academia multidisciplinaria neurotraumatologica brief history klaus von wild kvw@neurosci.de professor of neurosurgery medical faculty university münster, former head clinic for neurosurgery and department for early rehabilitation, clemenshospital münster, and professor of neurorehabilitation and reengineering of brain and spinal cord lesions, ini, hannover, germany world academy for multidisciplinary neurotraumatology, abbreviation amn, was initiated and established in munich on may, 2004. the key goal of amn is the advancement of neurotraumatology all over the world regarding basic molecular and epidemiological research, practical application and teaching concerning pre-hospital, emergency medical, and in-hospital medical care, early neurosurgical and long-term neurologicalneuropsychological rehabilitation and social reintegration, trauma prevention and the social-economic health care aspects. head and spinal cord injuries can happen to everybody, everywhere and at any time. the amn is involved directly and exclusively in non-profit activities. keywords: molecular and epidemiological research, neurotraumatology, trauma prevention introduction the academia multidisciplinaria neurotraumatologica, in english world academy for multidisciplinary neurotraumatology, abbreviation amn, was initiated and established on invitation of klaus von wild in munich on may 19th, 2004 (fig. 1) when giorgio a. brunelli, italy, anwar el etribi, egypt, mario prosiegel, germany, wai s poon, hong kong, motoi shoda, japan, and klaus von wild, germany, appended their signatures to the foundation document. dr. t. kanno, director of fujita health university, toyoake, aichi, japan, has given him good reason to transfer the original philosophy of emn to neuroscientists worldwide when he had been honoured honorary member of the european academy of multidisciplinary neurotraumatology and gained his own experience of our academicians close multidisciplinary cooperation and close friendship since these people were especially interested in challenging fields of neurotrauma. besides academic persons therapists, politicians, social health care people could meet and discuss beyond geographic, cultural and socio-economic boarders in europe. the key goal of amn is the advancement of neurotraumatology all over the world regarding basic molecular and epidemiological research, practical application and teaching concerning pre-hospital, emergency medical, and in-hospital medical care, early neurosurgical and long-term neurologicalneuropsycho-logical rehabilitation and social reintegration, trauma prevention and the socialeconomic health care aspects. head and spinal cord injuries can happen to everybody, everywhere and at any time. one has to keep in mind that lower social income and lower education are the risk factors that count for the major burden of neurotrauma in both developing and developed countries. starting with aid of accident prevention (education) up to the victim’s social reintegration (neuropsychology) mark the beginning and the final target of the ongoing (holistic) chain of our multidisciplinary efforts to finally improve klaus von wild romanian neurosurgery vol. xv nr. 2 4 the patients (and next of kin) health related quality of life (hrqol) after brain and spinal cord injuries and impaired higher cortical and spinal cord functioning in the world. the amn is involved directly and exclusively in non-profit activities. methods the purpose of the world amn is the advancement of neurotraumatology in research, practical application and teaching. this purpose is to be attained by, in particular, 1. the organisation of international congresses as well as participation in such events including regional and national workshops and educational meetings in all fields of neurotraumatology. 2. commitment to excellence in education through organisation of workshops and intensification of cooperation with scientific academies, societies, associations as well as research institutions and companies who are concerned with questions related to neurotraumatology. 3. the communication between national and international academies, societies and associations concerned with neurotraumatology in research, practical applications and education. 4. the goal of the annual/biannual amn congresses would be to bring the best minds we could gather at a single time to focus on a specific problem that resulted in better knowledge and clinical care over a certain problem within the area of neurotraumatology. for this model to be successful, the meetings by necessity would be small and different people would be attending at different times, depending on the focus of the discussion. 5. the goal of amn would be a true continuum of knowledge that could be transferred into a continuum of care. it is also extremely important amn congresses will have a variety of speakers at different levels of their professional development 6. the site of any meeting should be dependent on the scientific value and theme that that meeting will foster. dr. prigatano attempted to establish that tone for the amn phoenix meeting when his focus was clearly on neurosurgical and neuropsychological collaboration in the treatment of tbi patients. future meetings should also have a theme and draw on areas of expertise in the locale in which the meeting will be held (quotes gp prigatano). 7. each meeting should also provide for poster sessions and encourage dialogue between senior and junior colleagues, as well as across disciplines. 8. it is now apparent that intervention has to be based not only on integrated knowledge about anatomical location of lesions, plasticity of the brain, influence of neurobiology and neurochemistry, but mainly on integration of psychological treatment strengthening life transaction (quotes a-l christensen 8. amn academicians welcome for more informal opportunity for interaction with colleagues and the possibility of extended discussion on walks, at dinner or over drinks. something that cannot be easily done when confronted with a huge group of attendees (quotes d. stein). results amn congresses 1st amn brescia, italy, giorgio a. brunelli; 29 – 30 march 2004 main topic:recent advances in neurotraumatology. a multidisciplinary approach in conjunction with 5th international symposium on experimental spinal cord repair and 3rd conference of the wfns committee for neurorehabilitation 2nd amn phoenix, arizona, usa, george p prigatano; 11 – 13. november, 2004 main topic:neuropsychological and neurosurgical collaboration in the treatment of tbi patients 3rd amn nagoya, japan, tetsuo kanno, 10 march, 2005 main topics: prevention and pre-hospital care of tbi and sci; trauma at hyperacute, acute, and chronic stage, surgical neurorehabilitation, psychiatric aspects, quality of life after sci, basic research academia multidisciplinaria neurotraumatologica romanian neurosurgery vol. xv nr. 2 5 4th amn copenhagen, denmark, anne-lise christensen; 18 – 20 may, 2006 topic: mind and brain in neurotrauma 5th amn düsseldorf germany volker hömberg and klaus von wild main topics: neuropsychology in childhood; motor rehabilitation i childhood, pharmacology in rehabilitation; high end imaging in tbi; tbi management; cognition; brain and the art hands on workshop 1-6: 1: evidence based motor therapies in children 2: non invasive assessment of human brain plasticity.3: neurpsychology in pediatric tbi; 4: spinal cord repair, 5: management of epilepsy after tbi.6:management of spasticity after tbi amn board april 2008 president wen-ta chiu, m.d., phd, professor & superintendent taipei medical college, affiliated wanfang municipal hospital taipei medical college, taipei, teiwan 1st past president george p. prigatano, ph.d., neuropsychologist, 3rd amn2004 congress president, professor & newsome chair, department of clinical neuropsychology, barrow neurological institute, st. joseph's hospital & medical center, phoenix, arizona, usa vice president yoichi katayama,m.d.,ph.d., professor and chairman department of neurological surgery, dean of nihon university school of medicine, itabashi-ku tokyo, japan honorary president & secretary general: dr. klaus r.h. von wild, professor of neurosurgery, medical faculty university, former director department neurosurgery clemenshospital, münster, germany, chairman scientific committee donald g. stein, ph.d., emergency medicine brain research laboratory emory university, school of medicine, atlanta, ga,usa treasurer dr. hans tritthart, prof. emeritus of neurosurgery, department of neurosurgery university hospital graz, austria 2nd treasurer mrs. yoko kato, m.d., ph.d., professor of neurosurgery, wfns assistant secretary, department of neurosurgery, fujita health university, toyoake aichi 470, japan secretary wai sang poon mb chb (glasg.)frcs, 7th amn2009 congress president elect, professor and chief devision of neurosurgery, department of surgery prince of wales hospital, chinese university of hong kong, shatin. n.t.hong kong 6th amn2008 congress president dr. alexandru vlad ciurea, professor of neurosurgery, neurosurgical department and neuroimaging department1, clinic hospital, bagdasararseni, president romanian siciety of neurosurgery, second vice-president wfns, bucharest, romnania 6th amn2008 co-congress president dr. dafin muresanu, professor of neurology, chairman department of neurology, dean of the faculty of health sciences, iuliu hateganu university of medicine and pharmacy, secretary general ssnn, cluj-napoca, romania 5th amn2008 congress president dr. volker hömberg, professor of neurology, rehabilitation physician, neuro-electrophysiology, director st mauritius therapieklinik, secretary general wfnr meerbusch ggmbh, meerbusch, germany 4th amn2006 congress president anne-lise christensen, ph.d., neuropsychologist, professor emeritus, founder & former head center for rehabilitation of brain injury, university of copenhagen, denmark 2nd amn2005 congress president tetsuo kanno, m.d., ph.d., professor of neurosurgery, director, fujita health university, toyoake, aichi, japan. 1st amn2004 congress president giorgio a. brunelli, m.d. ph.d., prof. of orthopaedics, director escri, director foundation for research on spinal cord lesions, prof. emeritus and former chairman of the school of specialisation in orthopaedics and traumatology, university of brescia, italy honorary member. klaus von wild romanian neurosurgery vol. xv nr. 2 6 honorary members bazon brock giorgio a. brunelli anne-lise christensen tetsuo kanno joaquin fuster ph.d. professorof psychiatry and biobehavioral sciences neuropsychiatric, institute and brain research institute schoolof medicine los angeles, california usa klaus r.h. von wild commentary summary of 4th world amn congress copenhagen, denmark may 2006, respectfully submitted donald g. stein, ph.d. emory university, atlanta georgia, u.s.a. chair, scientific committee amn one of the major issues facing the field of brain injury rehabilitation is how to bring together the various approaches to patient care and treatment-from the early, acute stage of the injury cascade to the longerterm reintegration of the tbi survivor back into the family and community. thanks to tremendous advances in laboratory technologies and noninvasive imaging of brain activity, considerable progress is being made in understanding the molecular-biological mechanisms initiated by a tbi and the genomic and proteomic changes that unfold over the days and weeks following the primary damage. unfortunately, much of the new work in molecular neuroscience is published in arcane and often obscure journals read only by specialists. new journals appear almost daily, becoming more and more reductionistic, cellular and molecular in their approaches, with little or no discussion of the functional and holistic consequences of the findings and their implications for the treatment of brain-damaged individuals. neuroscientists themselves often disparage translational research in which the end result is the development of a therapy or treatment for a disease condition. in the united states, hardly any graduate students in neuroscience programs ever get to see a patient to understand better the complexities faced by individuals with tbi or other cns disorders, as they try to adapt to their circumstances. many rehabilitation clinicians find it difficult to communicate with their basic science colleagues because their terminology, methods, and perspectives on what is important are so different, and because basic researchers are often dismissive of clinical practice as having no ‘scientific’ base and being unconcerned with ‘mechanism’ -where mechanism means finding a genetic or at least a molecular basis for the condition without regard to psychological implications or outcomes. the academy of multidisciplinary neurotraumatology was founded in recognition of the growing disparity of viewpoints between clinicians and basic researchers in the field of traumatic brain injury. amn exists to bring together medical, neuropsychological and basic neuroscience investigators in a collegial environment in which participants can present and discuss their approaches to improving the lives of people with brain injuries. each year, the two-and-a-half-day meetings focus on a theme. for 2006, this theme was “bridging the gap between brain and mind,” organized and hosted in copenhagen, denmark by drs. anne-lise christensen and frank humle of the university of copenhagen and the center for the rehabilitation of brain injury. the center, the first of its kind in europe, was founded over 21 years ago with dr. christensen as its first director. the copenhagen congress was ambitious in its attempts to address one of the most complex philosophical and practical issues in the field-bridging the gap between mechanistic brain processes and the psychological manifestations of these processes in intact and brain-damaged people. clinical practitioners in neurorehabilitation, medical specialists in neurology, neurosurgery and pediatrics, and students from neurosurgery, neurology and psychiatry came together to discuss a number of sub-themes related to the overall program of what can be done to measure and improve functional outcomes after traumatic brain and spinal cord injuries across the developmental spectrum. several historical presentations traced the development of ideas across the last few centuries and showed that the growing contemporary recognition of more holistic approaches to rehabilitation had been developed early academia multidisciplinaria neurotraumatologica romanian neurosurgery vol. xv nr. 2 7 in the 20th century by advanced thinkers such as alexander luria, kurt goldstein and others who pioneered many of the concepts almost taken for granted in neurorehabilitation training and research today. discussions included how to define “functional outcomes”; dealing with coma and “consciousness”; definitions of consciousness in its various manifestations; and the problems of treating patients as unique individuals in the context of their history, learning experiences, cultural influences and stage of maturational and personal development. there were also sessions on what is currently known in basic research about early ‘physiologic’ intervention in the treatment of tbi-that is, in the first few hours of the injury cascade-and how such early interventions could theoretically impact later rehabilitation and physical and cognitive therapy. in other words, can neuroprotection and neuroregeneration therapies, by preserving nervous tissue in the early stages of the injury cascade, provide for a better matrix to enhance developmental, cognitive and social rehabilitation processes in the later stages of the patient’s recovery? another important question that was discussed was whether there is sufficient evidence to show that early alterations in molecular and physiological changes in damaged brain tissue can be ‘predictive’ of the extent of later deficits or improvements in cognitive and social functions. the meeting ended with a general discussion of goals and strategies for future basic research and clinical practice in neurotrauma and neurorehabilitation. participants agreed that a new, less mechanistic, more holistic, patient-oriented perspective is needed--one that recognizes that many higher cognitive processes have a social basis and that complex cognitive, motor and sensory function can no longer be seen as simply mediated by specific genes, receptors or highly localized brain regions. if acute-stage treatments and later-stage cognitive rehabilitation strategies are to realize their full potential and if molecular neuroscience is to contribute to our understanding of how and under what conditions rehabilitation works, the participants agreed that a better dialog between basic researchers in molecular neuroscience and clinical rehabilitation specialists will be essential. these collegial discussions at amn meetings are only the first step in the development of more effective treatments, but they are an important and critical step in promoting crossdisciplinary teaching, research and progress in finding a “cure” for tbi and its related disorders. microsoft word 22sachidanandgautam_a clinicoradiological scoring romanian neurosurgery (2018) xxxii 2: 359 365 | 359             doi: 10.2478/romneu-2018-0045 a clinicoradiological scoring for management of acute subdural hematoma: a prospective study sachidanand gautam1, anubhav sharma2, s.c. dulara2 1department of neurosurgery, government medical college, kota rajasthan, india 2department of anesthesiology and critical care, government medical college, kota rajasthan, india abstract: background: acute subdural hematoma is the most common type of traumatic intra cranial hematoma accounting for 24% cases of severe head injuries and caries highest mortality. the aim of this study is to analyze the prognostic factors and to propose neuro-clinical and radiological prognostic scoring system on the clinical spectrum and to evaluate the postoperative outcome and validate the same. methods: this is a prospective study which included 100 patients admitted in government medical college, kota, rajasthan from 01st jan 2016 to 30 june 2017 with head injury and were diagnosed to have traumatic subdural hemorrhage. a detailed clinical history, physical examination, computerized tomography scan was performed in all patients and were divided into 2 groups; that is conservative or surgical interventional as per neuro-clinical and radiological prognostic scoring system. results: the maximum patients suffering from subdural hematoma were in the age group of 11-60 years with male predominance 72%. the most common mode of injury was rta with 68 % of incidence. 36 out of 100 cases presented to hospital with gcs <8 while 44 patients showed improvement of gcs after resuscitation. out of 100 cases, surgical approach was considered in 34 patients while remaining patients were managed conservatively. pupillary reaction, hypotension, ct scan findings that is, thickness of hematoma >10mm and midline shift of >5mm, delay in interval between the surgery had greatly affected on outcome of patients. conclusions: according to the results, use of neuro-clinical and radiological prognostic scoring system is very useful in determining early intervention and also avoids unnecessary surgical intervention. key words: clinicoradiological score, neuro intervention, subdural hematoma   360 | gautam et al clinicoradiological scoring for management of acute subdural hematoma             introduction since the first attempts at aggressive neurosurgical intervention for traumatic acute subdural hematoma in the 1930's and 1940's, the rate of mortality from this injury has ranged from 76% to 90%. [7] despite new technology and advent of new neuroradiological techniques and neurointensive monitoring and treatment, traumatic acute subdural hematoma remains one of the most lethal of all head injuries. acute subdural post-traumatic haematoma's (sdh) continue to have a distressingly high morbidity and mortality. clinical factors like presenting gcs, pupils, time to operative interval, hemodynamics and co-morbidities plays a critical factor in overall outcome from acute subdural hematoma. clinical material and methods this is a prospective observational study which included 100 patients admitted in government medical college, kota, rajasthan from 01st jan 2016 to 30 june 2017 with head injury, diagnosed to have traumatic subdural hemorrhage. all cases were analyzed with respect to age, sex, mode of injury, gcs at the time of presentation, post resuscitation gcs, pupillary anisocoria, focal neurological deficit, hemodynamic status, imaging findings of thickness of hematoma, midline shift, simple sdh or complicated sdh, finding on repeat ct after 6 hrs, gcs at the time of discharge and at four weeks. patients were evaluates according to neuro-clinical and radiological prognostic scoring system and were divided into two groups; conservative and operative. criteria for surgical intervention were – 1.neuro-clinical and radiological prognostic score of 1-5 with hemodynamic stable patient and duration of arrival in hospital after trauma of less than 6 hrs with no co-morbid conditions. 2. neuro-clinical and radiological prognostic score of 6-10 with hemodynamic stable patient and duration of arrival in hospital after trauma of less than 6 hrs with no co-morbid conditions and hematoma thickness more than 10 mm. results one hundred cases of acute subdural hematoma out of 854 cases of head injury constituted 11.7%. youngest patient was 4 months old and oldest patient was 88 year old. 82% of patients were in second to sixth decade. this study showed that males are predominant as compared to females. out of 100 cases, males constituted 72% whereas 28% were female (table 1).   romanian neurosurgery (2018) xxxii 2: 359 365 | 361             table 1 age and sex distribution age no. of patients male female 1-10 10 8 1 11-60 82 44 18 >61 8 20 9 total 100 72 28 the most common mode of head injury was found to be road traffic accidents accounting for 68% of total and fall from height and physical assaults being subsequent with 18% and 14% incidence respectively. (table 2) table 2 mode of injury mode of injury no. of patients % rta 68 68 fall from height 18 18 assualts 14 14 looking at the data, glasgow coma scale at time of presentation to hospital was equal in distribution in < 8 and 9-13 groups with 36 patients in each group. patients with gcs range of 9-13 showed significant improvement after post resuscitation (table 3). table 3 glasgow coma scale at the time of presentation to hospital and post resuscitation gcs no. of patients at the time of arrival post resuscitation < 8 36 34 913 36 44 14-15 28 22 comparing others factors like pupillary abnormality, there was a significant (100%) death among patients presented with bilateral pupil dilatation corresponding to 13 patients. patients with normal pupil on presentation were 34 in numbers and out of which only 3 patients had mortality having a 9% distribution (table 4). table 4 pupillary abnormalities pupils no. of patients mortality % normal pupils 34 3 9 unilateral dilated pupil 53 18 34 bilateral dilated pupil 13 13 100 comparing table 5, out of 42 patients who presented with contralateral hemiparesis, 24 patients (57%) had mortality, whereas only 10 patients of 58 died who presented with no neurological deficit. when comparing hemodynamic status, patient had significant mortality when presenting with systolic bp of less than 90 mmhg as compare to more than 90mmhg having 71.42% and 17% mortality in each (table 6). table 5 focal neurological deficit neurological deficit no. of patients mortality % no neurological deficit 58 10 17 contralateral hemiparesis 42 24 57 table 6 hemodynamic status bp no of patients mortality % systolic bp <90mmhg 28 20 71.42 systolic bp >90mmhg 78 14 17.95 362 | gautam et al clinicoradiological scoring for management of acute subdural hematoma             table 7 and 8 shows incidence and mortality of patients as per neuroimaging that is ct scan, while table 7 illustrates mortality on the basis of hematoma thickness on the other hand table 8 explains mortality on the basis of midline shift. majority of patients came with a hematoma thickness of 5-10 mm corresponding to 40 in number with 14% mortality and the highest mortality rate was in patients presenting with more than 10 mm thickness with 19% mortality. looking at table 8, 66 patients of the total cases presented with midline shift of more than 5 mm with a significant mortality rate of 45.45%. table 7 ct scan thickness of hematoma thickness of hematoma no of patients mortality % <5mm 28 01 3.6 5-10mm 40 14 35 >10mm 32 19 59 table 8 midline shift midline shift no. of patients mortality %age <5mm 34 04 11.76 >5mm 66 30 45.45 our study population showed other associated intracranial injury which highest incidence of 32 patients having sdh with sah corresponding to 53.13% on mortality scale on the other hand simple sdh corresponded to 26 cases with a 7.69% of mortality (table 9). table 9 associated intra cranial injury associated injury no of patients mortality % simple sdh 26 02 7.69 sdh with edh 08 01 12.5 sdh with contusion 34 14 41.18 sdh with sah 32 17 53.13 looking at glasglow outcome score at 4 weeks (table 10), patients were divided into 5 grades from 1-5. there was equal distribution among grade 1(34%), grade 5(34%) and between grade 2(8%), grade 3(8%) patients with grade 4 having 16% patients. table 10 glasgow outcome scale at 4 week grade no. of patients % 1 34 34 2 08 08 3 08 08 4 16 16 5 34 34 prognostic criteria was evaluated in all patients using table 11 and patients were given score for each factor from 0 to 1.sum of total score (0 to 10) was calculated and patients were divided into 3 groups with score 1-5 in group 1, 6-8 in group 2 and 9-10 in group 3. out of 42 patients in group 1, 22 patients were kept for conservative management and 20 were operated with 90.9% and 55% mortality in each. in group 2 with score of 6-8 there were total 24 patients out of which 15 patients were kept in conservative group with only 6.66% mortality and 9 patients out of 24 were operated with romanian neurosurgery (2018) xxxii 2: 359 365 | 363             22.2% mortality rate. when comparing group 3 with 9-10, both conservative and operative patients had zero mortality rate having 30 and 4 patients in each. table 11 gautam and sharma clinicoradiological prognostic score (0 to 10) prognostic factors 0 1 gcs on arrival in hospital < /= 8 >9 hematoma thickness (in mm)in ncct head on arrival >5 <5 presence and/ or degree of midline brain shift (in mm) in ncct head on arrival >5 <5 increase in midline shift and thickness of hematoma in repeat yes no ncct head after 6 hrs pupil abnormality yes no age > 60 < 60 availability of ot, neurointensive care,ct and other facilities no yes co-morbidity and associated trauma yes no time to arrival in tertiary centre (in hours) > 6 < 6 drop of gcs in subsequent examination > 2 <2 table 12 management of acute subdural hematoma according to prognostic score score total no of patients conservative operative total mortality % mortality total mortality % mortality score 9-10 34 30 0 0 4 0 0 score 6-8 24 15 1 6.67 9 2 22.2 score 1-5 42 22 20 90.9 20 11 55 discussion morbidity and mortality after an acute subdural haematoma are the highest of all traumatic mass lesions. this poor outcome results largely from associated parenchymal injuries and subsequent intracranial hypertension. [10] of the many variables that have been found to significantly correlate either positively or negatively (age, sex, gcs at the time of presentation, post resuscitation gcs, pupillary anisocoria, focal neurological deficit, hemodynamic status, imaging findings of thickness of hematoma, midline shift, simple sdh or complicated sdh, finding on repeat ct after 6 hrs, gcs at the time of discharge and at four weeks) with morbidity or mortality from acute subdural hematoma, [1,3] only two can potentially be affected by neurosurgical intervention: the time from injury to operative intervention for evacuation of hematoma and the control of icp. prompt surgical intervention for evacuation of traumatic intracranial hematomas has been emphasized in the literature but little hard evidence is available to support its efficacy. as advocated by us we believe that surgery should be performed as early as possible, especially in patients with neuro-clinical and radiological prognostic 364 | gautam et al clinicoradiological scoring for management of acute subdural hematoma             score of 1-5 with hemodynamic stable patient and duration of arrival in hospital after trauma of less than 6 hrs with no co-morbid conditions and in patients with neuroclinical and radiological prognostic score of 6-10 with hemodynamic stable patient and duration of arrival in hospital after trauma of less than 6 hrs with no co-morbid conditions and hematoma thickness more than 10 mm. isolated asdh, acting as a compressive lesion, is an uncommon clinicopathological entity. majority of patients with asdh have associated focal (contusion / laceration / intracerebral haematoma) or global (diffuse axonal injury, subarachnoid haemorrhage) involvement of the brain or both of these. in addition, ischaemia underlying the haematoma and ipsilateral hemispherical brain swelling (? hyperaemic, ? oedematous), which may be self perpetuating, are consistent findings in most patients with surgically significant haematoma. [8,9] kristianson and tandon found 100% mortality when pupils are dilated and fixed, 19% when they are unequal and 14% when pupils are normal3 which is comparable to our study. the factors affecting the prognosis of the patients with asdh were assessed by zhao hong as follows (1) mechanism of injury. the primary causes of asdh were fall (53%), motor vehicle accidents (37%), blunt impact injuries (4%), and other factors (7%). there was no significant difference in mortality and functional recovery rate regardless of injury mechanism. (2) age, significant higher mortality is found in the patients over 65 years old. (3) sex. in spite of a 3-to-1 male predominance, there was no significant difference in the prognosis between males and females. (4) pupillary reflex. bilateral absence of pupillary reflexs was associated with an 88% mortality and a 7% functional recovery rate. and (5) time from injury to operation which is comparable to our study. [11] age is a strong factor influencing both mortality and morbidity, as several authors have identified in their works. in our study confirms this result: there is a significant statistical correlation between age and patient’s outcome. despite some contradictions, most literature supports children faring better than adults who have severe brain injury. gennereli et al found that interval between injury to surgery, hypotension and basal cistern obliteration are the three important factors, which have significant impact on outcome. our study also found these three factors together have significant impact to the extent of 90% mortality. [4] heissler and dietz et al found thickness of haematoma, midline shift are having significant impact on outcome. they found haematoma thickness of >10 mm with midline shift >5mm are having 30% increased mortality than those without. our study showed similar trend with mortality reaching 30%. [4] in 1989, howard, et al [5]., reported extremely favorable results in the management of acute subdural hematoma with the primary discriminating variables being age and clot size. in their patients aged 18 to 40 years, the mortality rate was only 18% with functional survival in 66% as romanian neurosurgery (2018) xxxii 2: 359 365 | 365             compared to rates of 74% and 5%, respectively, in those aged over 65 years. even in young patients with low gcs scores the results were similarly encouraging: 25% mortality and 67% functional recovery which is comparable to our data [6]. conclusions we found that, the following factors are having significant influence on the outcome of acute sub dural hematoma in our study: gautam and sharma clinicoradiological prognostic score of 9-10 have favorable outcome and score 6-8 have good outcome with early intervention if required hypotension and associated intracranial or other injury are another factor which is having significant influence on the outcome after surgery for acute subdural hematoma. this proposed clinicoradiological prognostic score is useful in peripheral neurosurgery centre having limited resources. according to the results, use of neuro-clinical and radiological prognostic scoring system is very useful in determining early intervention and also avoids unnecessary surgical intervention. correspondence dr s.n. gautam, house no 63, shrinathpuram, sector b, kota, rajasthan-324010, india, +919413553530 references 1. braakman r, gelpke gj, habbema jdf, et al: systematic selection of prognostic features in patients with severe head injury. neurosurgery 6:362-370, 1980 2. d’amato, o. piazza:prognosis of isolated acute post-traumatic subdural haematoma j neurosurg sci 2007;51:00-00 3. fell da, fitzgerald s, moiel rh, et al: acute subdural hematomas. review of 144 cases. j neurosurg 42: 3742,1975 4. gennereli ta, et al. influence of the type of intracraniallesion on outcome from severe head injury. j neurosurg 1982;56(1):26-32. 5. howard ma iii, gross as, dacey rg jr, et al: acute subdural hematomas: an age-dependent clinical entity. jneurosurg 71:858-863,1989 6. jack e. wilberger, jr.,mark harri. acute subdural hematoma: morbidity, mortality, and operative timing, j neurosurg 74:212-218, 1991 7. munro d: the diagnosis and treatment of subdural hematoma. a report of sixty-two cases. n engl j med 210: 1145-1158,1934 8. tandon pn : management of head injury: fads, fashions and facts. neurol india 1986; 34 : 1-30. 9. tandon p n. acute subdural haematoma : a reappraisal. neurol india 2001;49:3-10 10. raman ks, ramamurthi b. subdural haematoma. neurol 1970;18:18. 11. zhao hong and bai xiang-jun:influence of operative timing on prognosis of patients with acute subdural hematoma: chinese journal of traumatology 2009; 12(5):296-298 romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article hyperbaric oxygen therapy in the treatment of brain abscess: about a case cherkaoui mandour, miloudi gazzaz, brahim el mostarchid morocco doi: 10.2478/romneu-2018-0015 romanian neurosurgery (2018) xxxii 1: 125 128 | 125 doi: 10.2478/romneu-2018-0015 hyperbaric oxygen therapy in the treatment of brain abscess: about a case cherkaoui mandour, miloudi gazzaz, brahim el mostarchid department of neurosurgery, military hospital mohammed v – rabat, morocco abstract: the management of brain abscess remains a challenging topic usually involving a multimodal concept. the efficiency of hyperbaric oxygen therapy is currently being used in many areas, and has been proven in infections with deep and superficial location. we report our experience with hyperbaric oxygen therapy combined with antibiotics in the treatment of this disease in a children case. the evolution was very favourable; we believe that the hyperbaric oxygen therapy is a reliable adjuvant therapy for brain abscess. key words: brain abscess, hyperbaric oxygen therapy, stereotactic introduction brain abscess continues to constitute one of the most important neurosurgical diseases and the management still presents a challenging problem (3, 5, 6, 11). in recent years, there is increasing tendency to use a safe and effective therapeutic means. we report a case of a child who was treated for a brain abscess with stereotactic aspiration combined with antibiotic and hyperbaric oxygen (hbo) therapy. case report a 17-year-old male, was admitted to the hospital with signs of intracranial hypertension and fever. neurological examination revealed no disturbances of consciousness no motor or sensory deficit. brain magnetic resonance imaging revealed a right frontal abscess (figures 1-2). abscess was treated by stereotactic aspiration combined with hbo and systemic antibiotic therapy. the patient received hbo (100% o2 at 2.5 ata for 90 min) for 30 days and intravenous antibiotics for 4-week. clinical and radiological evolution was very favorable. after one week computed tomography (ct) of brain showed a total regression of the abscesses (figure 3). discussion bacterial brain abscess continues to constitute one of the most important neurosurgical diseases. its management can be done by several methods: antibiotics alone (12, 13) drainage, aspiration, and excision (2, 13). 126 | mandour et al hyperbaric oxygen therapy in the treatment of brain abscess the choice of procedure may be influenced by the age and neurological condition of the patient, location, stage of the abscess and the type of abscess. some surgical management has been revolutionized by the development of image-guided stereotaxy that has proven to be a relatively simple and safe method. figure 1 gadolinium-enhanced axial t1-weighted mri scans showing a right frontal abscess figure 2 gadolinium-enhanced coronal t1weighted mri scans showing a right frontal abscess figure 3 computed tomography (ct) of brain after one week, revealing a complete resolution of the abscess romanian neurosurgery (2018) xxxii 1: 125 128 | 127 antibiotics continue to be an integral part of the treatment of intracranial abscesses (1, 11) and the use of hbo therapy as like as an adjunctive treatment has been approved by the undersea and hyperbaric medical society since 1996 (4). hyperbaric oxygen exerts influence on tissues via a lot of mechanisms: one of the most important effects is stimulation of the bactericidal action of white blood cells (11). it has been reported that the leukocyte bacteria-killing capacity is substantially impaired in hypoxic surroundings (11). hbo therapy increases the oxygen tension in infected tissues, resulting in improvements in phagocytic killing of bacteria direct bactericidal effects on some microorganisms (11). additionally, improved tissue oxygen tensions in ischemic tissues during hbo therapy inhibits the growth of aerobic and facultative anaerobic bacteria by inducing a variety of metabolic effects involved with the synthesis of proteins, nucleic acids and essential cofactors of metabolic reactions (9, 10). a combination of hbo and stereotactic aspiration in the management of brain abscesses is very important because stereotactic aspiration minimize iatrogenic brain damage caused by brain retraction and dissection, it also minimizes operation time and hospital stay (3, 5, 11). on the other hand, hyperbaric oxygen (hbo) has remarkable results in neurosurgical infections (7, 8). conclusion it is believed that hyperbaric oxygen is an important adjunctive traitement in the management of brain abscess, because it can reduce the length of time on antibiotics. correspondence cherkaoui mandour e-mail: mandour1978@hotmail.com telephone: 212 06 53 42 12 25 miloudi gazzaz e-mail: gmilou@hotmail.com telephone: 212 06 48 34 80 05 brahim el mostarchid e-mail: elmostarchid@hotmail.com telephone: 212 06 48 34 89 45 references 1.barlas o, sencer a, erkan k, eraksoy h, sencer s, bayındır c: stereotactic surgery in the management of brain abscess. surg neurol,1999,52:404–410. 2.beller aj, sahar a, praiss i: brain abscess: review of 89 cases over a period of 30 years. j neurol neurosurg psychiatry,1973,36: 757–768. 3.haines ss, mampalam t, rosenblum ml, nagrib mg: cranial and intracranial bacterial infections, in youmans jr (ed): neurological surgery. w.b. 4.hampson nb:hyperbaric oxygen therapy:1999 committe report. kensington, undersea and hyperbaric medical society, 1999, pp 1–82. 5.kole km, rosenblum ml: management of multiple brain abscesses, in batjer hh, loftus cm (eds): textbook of neurological surgery. principles and practice. philadelphia, lippincott williams and wilkins, 2003, pp 3151–3157. 6.kurschel s, mohia a, weigl v, eder hg. hyperbaric oxygen therapy for the treatment of brain abscess in children. childs nerv syst. 2006 jan,22(1):38-42. 7.m. kutlay, a. colak, h. simsek, s. yildiz, k. topuz, s. kaya, a. cetinkal, m. demircan. antibiotic and hyperbaric oxygen therapy in the management of postoperative discitis. undersea and hyperbaric medical society. 2008, vol. 35, no. 6 8.a. larsson • j. uusija¨rvi • f. lind • b. gustavsson • h. saraste. hyperbaric oxygen in the treatment of 128 | mandour et al hyperbaric oxygen therapy in the treatment of brain abscess postoperative infections in paediatric patients with neuromuscular spine deformity. eur spine j (2011) 20:2217–2222 9.lampl la, frey g: hyperbaric oxygen in intracranial abscess, in kindwall ep (ed): hyperbaric medicine practise. arizona, best publishing co., 1995, pp 661–670. 10.mehmet resid onen, sait naderi. role of hyperbaric oxygen therapy in spinal pathologies. world spinal column journal, volume 6 / no: 1 / january 2015 11.murat kutlay, ahmet colak, senol yildiz, nusret demircan, osman niyazi akin stereotactic aspiration and antibiotic treatment combined with hyperbaric oxygen therapy in the management of bacterial brain abcesses.neurosurgery 2005, 57:1140-1146. 12.rosenblum ml, hoff jt, norman d, weinstein pr, pitts l: decreased mortality from brain abscesses since advent of computerized tomography. j neurosurg,1978,49:658–668. 13. rosenblum ml, mampalam tj, pons vg: controversies in the management of brain abscesses. clin neurosurg,1986,33:603–632. 15 15mandourcherkaoui_hyperbaric flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article posttraumatic hydrocephalus: lessons learned from management and evaluation at a tertiary institute with review of literature ashok kumar, pavan kumar, gaurav jaiswal, tarun kumar gupta india doi: 10.1515/romneu-2017-0058 356 | kumar et al posttraumatic hydrocephalus doi: 10.1515/romneu-2017-0058 posttraumatic hydrocephalus: lessons learned from management and evaluation at a tertiary institute with review of literature ashok kumar, pavan kumar, gaurav jaiswal, tarun kumar gupta department of neurosurgery, r n t medical college, udaipur, raj, india abstract: background: post traumatic hydrocephalus (pth) is a commonest treatable complication of severe traumatic brain injury that’s leads to failure of improvement and worsening of the outcome. incidence of posttraumatic hydrocephalus is 0.7%-29% reported in different literature. we have observed the development of pth frequently seen in patients with severe head injury and after decompressive craniectomy (dc). pathophysiology includes inflammatory changes and adhesion of arachnoid granulation, cerebral ischemia and alteration in cerebrospinal fluid (csf) dynamics. we studied 35 cases of pth diagnosed and treated at our institute from may 2008 to may 2017. material and methods: this is hospital based retrospective and prospective study conducted in tertiary center on the basis of neuro-radiological examination of the patient. clinical biodata and radiological profile of the patients was studied at initial presentation with trauma, and when the patient worsened with symptoms of raised intracranial pressure (icp) in state of established pth. these cases were treated by medium pressure ventriculoperitoneal shunt (v.p shunt) and outcome was evaluated. results: incidence of pth in our study is (2.3%). out of 35 cases 24 (68.57%) were male and 11(31.4%) were female. road traffic accident (rta) was the most common mode of injury (82.85%), acute subdural hematoma (sdh) was the most common finding on c.t scan in 15 cases (42.8 %). decompressive craniectomy was performed in 77% at time of initial trauma. pth had favourable outcome with v.p. shunting in 91.42%. conclusion: patients with traumatic brain injury present with many complications but pth is most frequent sequeale that can present in form of various neurological symptoms after trauma and decompressive craniectomy. c.t. scan brain is the investigation of choice for diagnosis of pth. outcome was favourable after v.p. shunt in pth. key words: post traumatic hydrocephalus, severe head injury, v.p. shunting romanian neurosurgery (2017) xxxi 3: 356 363 | 357 introduction post-traumatic hydrocephalus or hydrocephalus following traumatic brain injury (tbi) is not just a ventricular enlargement but an active and progressive disorder of cerebrospinal fluid (csf) accumulation in the ventricular system, causing compression of the brain parenchyma. (1) posttraumatic hydrocephalus is a treatable complication of head injury and can present with several different clinical syndromes. these include obtundation, simple failure to improve; a tetrad of psychomotor retardation, memory loss, gait trouble, and incontinence; and unusual symptoms including emotional disorder. (2) post-hemorrhagic hydrocephalus is the result of extra ventricular obstruction of csf absorption, hence communicating hydrocephalus. ventricular enlargement following head injury is a frequent finding but cases that require shunt operation are relatively rare. (3) patients (pt) developing post traumatic hydrocephalus presents with various types of neurological symptoms with different types of severity. several different neurological sequeale of post-traumatic hydrocephalus (pth) has been recognized since dandy’s report in 1914 and has been recognized as a clinicopathologic entity and the incidence rates of symptomatic pth in the literature, ranging from 0.7% to 29%. (4) the beneficial effect of dc in reducing icp has been well-documented in several studies. there is a wide spectrum of post-traumatic sequeale of traumatic brain injury. the awareness of hydrocephalus acquired as a consequence of head injury lags behind these explanations for neurological plateauing or deterioration. early identification of this condition may lead to early performance of shunting procedures that may dramatically halt or reveres the process. however, failure to identify hydrocephalus is not uncommon and this is especially true when the surgeon has adopted a fatalistic acceptance of an unfortunate outcome. aims and objective to study the various neurological and radiological factor of the patients who were diagnosed with post traumatic hydrocephalus and their outcome after v.p. shunt. material and methods this retrospective and prospective study conducted at tertiary center in neurosurgery department on the basis of neuro-radiological examination of the patient. a total of 1500 patients were evaluated for traumatic brain injury in our hospital from may 2008 to may 2017. detailed of the patient at time to presentation at casualty, and when the patient worsened with symptoms of raised icp were studied. treatment plan either conservative or surgical at initial trauma were also noted. medical records of 35 patients, who had undergone vp shunt for posttraumatic hydrocephalus were analyzed. clinical factors analyzed were the age, sex, mode of injury preoperative c.t. scan, glasgow coma scale (gcs), and radiographic evidence of ventricular dilatation on non-contrast ct scan brain with periventricular lucencies was taken as radiological criteria of hydrocephalus. there were twenty four males and eleven female. the youngest patient was a boy aged 358 | kumar et al posttraumatic hydrocephalus 15 years, while the eldest was 80 year-old female (table 1). twenty nine patients sustained head injury due to rta, while six patients sustained injury due to other cause like fall on ground, strike with heavy object (table 2). ct findings at the time of initial injury in these 35 cases were: sdh was most common finding in 15 patients and the least common finding was ivh seen in 2 patients (table 3). table 1 age distribution age number %age 10-20 4 11.4% 21-30 8 22.8% 31-40 3 8.5% 41-50 10 28.5% 51-60 3 8.5 61-70 5 14.2% 71-80 2 5.7% table 2 mode of injury mode of injury number of patients percentage rta 29 82.85 other cause 6 17.15 table 3 ncct finding after trauma finding no of case percentage sdh 15 42.8% sah 9 25.7% ich 6 17% contusion 3 8.5% ivh 2 5.7% all patients with severe head injury, pt with age group 10 years to 80 years were included in this study while pt with major concurrent medical illness, substance abuse, psychiatric illness, concomitant blunt trauma abdomen, chest injury excluded. decompressive craniectomy was performed in 77% at time of initial trauma. (3) patients those were diagnosed as a posterior fossa contusion developed hydrocephalus within a span of 5 to 7 days and they were improved after vp shunting. all these cases were treated by medium pressure v.p shunt and post operative outcome was evaluated. results in present study out of 35 cases of pth, 24 (68.57%) were male and 11(31.4%) were female. the incidence of pth is 2.3 % in severe head injuries rta was the most common mode of injury (82.85%), acute subdural hematoma was the most common finding on c.t. scan in 15 romanian neurosurgery (2017) xxxi 3: 356 363 | 359 cases (42.8 %). outcome was favourable 91.2% after medium pressure v.p. shunt. in the current study, patients presented with various neurological feature after initial injury. most common finding at time of worsening was conscious impairment in 25 (71.4%) cases, followed by vomiting and headache and least common was incidental finding prior to cranioplasty (table 4). time interval for built up for hydrocephalus was early within 5 days in 3 patients and late in two patients up to two month, while most of the patients developed hcp at the interval of 1 month. table 4 clinical presentation of pth impaired consciousness 25 71.4% vomiting 20 57.1% headache 20 57.1% hemiparesis 10 28.5% dysphasia 14 40%% urinary incontinence 6 17% incidental finding prior to cranioplasty 2 8.5% table 5 time interval for pth time interval number of patients 5 days 3 1 month 18 1-3 month 12 3 month-6 month 2 thirty two patients (91.4%) showed improvement in clinical features after ventriculo-peritoneal shunting. three (11.4%) died. repeat shunt was done in two patients of decompressive craniectomy, because blockage seen at proximal end of the shunt. three patients were died and the cause of death in these patients was ventilator associated pneumonia. figure 1 ncct brain: showing acute sdh, ftp convexity left side with mass effect 360 | kumar et al posttraumatic hydrocephalus figure 2 ct scan of same patient after 4 weeks interval showing hydrocephalus figure 3 resolved hydrocephalus of vp shunt figure 4 ncct brain: acute sdh ftp convexity left side with mass effect figure 5 post op scan after decompressive craniectomy romanian neurosurgery (2017) xxxi 3: 356 363 | 361 figure 6 ncct brain: day 90 incidentally diagnosed pth and gliosis figure 7 scan revealing vp shunt and mesh cranioplasty with resolve hcp discussion criteria given by kishore et al. (5) were used to diagnose hydrocephalus were used in this study: 1) a distended appearance of the anterior horns of the lateral ventricles; 2) enlargement of the temporal horns and the 3rd ventricle; 3) normal or absent sulci; 4) if present enlargement of the basal cisterns and the 4th ventricle; and 5) periventricular decreased density. tian et al, found that traumatic sah is a risk factor for the development of hydrocephalus in head injury patients. (6) risk factors for pth are not yet fully identified but data suggested severity of injury, age, duration of coma, and dc increased the risk. (7) jiao et al. reported that advanced age, subarachnoid hemorrhage (sah), and hygromas (subdural, or interhemispheric) are correlated with the development of hydrocephalus. (8) some authors found that the distance of craniectomy to the midline was a factor associated with hydrocephalus after decompressive craniectomy. they considered that when the skull was removed too close to the midline, the external force compressing the temporal and parietal bridging veins was reduced, and that this might cause an increase in venous blood flow and extracellular fluid absorption and a decrease in brain parenchyma volume, causing a consequent increase in ventricular volume, which resulted in post-operation hydrocephalus. (9) distance from the midline is the only factor associated with hydrocephalus after tbi was reported by de bonis et al. (9) some studies reported that patients with dc whose superior limit was <25 mm from midline had a significant risk factor for development of hydrocephalus (9, 10, 11). waziri et al found no relationship between dc and hydrocephalus through retrospectively analyzing a cohort of consecutive patients. 362 | kumar et al posttraumatic hydrocephalus (12) gudeman et al. reported the incidence of ventricular enlargement after tbi between 1.5% to 29%, when evaluated by ct. (13) cardoso et al. suggested that, post traumatic hydrocephalus may present with various clinical syndromes including altered sensorium, failure to improve, psychomotor retardation, memory loss, gait ataxia and incontinence (14). these cases were treated by v.p shunting and outcome was evaluated. pth commonly occurs in first year post trauma and has been reported as early as within 7 hours of injury. (15) in our study 3 patients were diagnosed on 5th post-trauma day and one as late as 90th post operative day which was accidentally diagnosed during follow up period. higher incidence of pth has been found with extended dc hence; early cranioplasty should lead to restoration of normal intracranial pressure dynamics and spontaneous resolution of hydrocephalus. it has been found that sah is most important pathology leading to the development of pth. (13, 16) while in our study most common finding was sdh in 15 (42.8%) patients and sah in 9 (25.9.%). pth most commonly developed in patients those underwent decompressive craniectomy for acute subdural hematoma sdh. the reason is that out of total head injuries maximum number of patients had sdh at our centre. hematoma may leads to inflammatory changes and adhesion to arachnoid granulation that causes impaired csf circulation and eventually responsible for development of hydrocephalus. shunt surgery was performed in most of the patient within 6 month after trauma. in this study, showed no correlation between interval time and postoperative improvement in those patient who developed pth after decompressive craniectomy while it was a very good results noted following early shunt surgery in patient having posterior fossa hematoma whoever managed conservatively. however, sheffler et al.16 presented a case of pth that improved with a shunting procedure after having clinical symptoms of pth for 11 months after a closed head injury. wood et. al. (17) insisted that patients with clinical symptoms of hydrocephalus for less than 6 months had a better prognosis. decompressive craniectomy that has been found to be associated with development of pth by various mechanism like altering csf flow dynamics, mechanical blockage around convexities, inflammation of arachnoid granulation by post surgical debris. (12, 18) conclusion in present study we have found that pth is commonest sequeale of severe head injury and in those who underwent decompressive craniectomy. however, several other late complications of dc have been reported, including sinking flap syndrome, extra-axial fluid collection and hydrocephalus. hydrocephalus was developed early in patient with posterior fossa sah or contusion in comparison to decompressive craniectomy. csf absorption is meanly dependent on arachnoid granulation function and pressure difference between the subarachnoid space and draining venous supply. hence, decompressive craniectomy results in decreased csf outflow as well its absorption; thus, leading to hydrocephalus. ncct brain romanian neurosurgery (2017) xxxi 3: 356 363 | 363 should perform not only to diagnose pth but also to rule out other causes of delayed deterioration or when patient fails to improve after initial trauma. early diagnosis and performance of shunting procedures may significantly stop or reveres the sequence of worsening. this study showed that most patients with pth were improved after shunt surgery. following the shunt surgery, there was rapid improvement noted in conscious level, headaches and in cognitive functions and outcome of our study was favourable in 92.7% cases. all the cases of pth should be treated by medium pressure v.p. shunt. correspondence dr. ashok kumar 401 hitawala complex, raghuroop apartment, sardarpura udaipur rajsthan, india email: dr.ashokkumar011@gmail.com phone: +919610463977 references 1.choi i, park hk, chang jc, cho sj, choi sk, byun bj. clinical factors for the development of posttraumatic hydrocephalus after decompressive craniectomy. j korean neurosurgery soc. 2008;43:227–231 2. beyerl b, black pm. posttraumatic hydrocephalus. neurosurgery.1984;15:257–261. 3. bret p, hor f, huppert j, lapras c, fischer g. treatment of cerebrospinal fluid rhinorrhea by percutaneous lumboperitoneal shunting: review of 15 cases. neurosurgery. 1985;16:44–47. 4. dandy we, blackfan kd. internal hydrocephalus. an experimental, clinical and pathological study. j neurosurg. 1964;21:588–635. 5.kishor prs, lipper mh, miller jd, girevendulis ak, becker dp, vines fs. post-traumatic hydrocephalus in patients with severe head injury. neuroradiology 1978; 16:261-5. 6. tian hl, xu t, hu j, cui yh, chen h, zhou lf. risk factors related to hydrocephalus after traumatic subarachnoid hemorrhage. surg neurology2008; 69: 241246; discussion 246. 7. chuang k, stroud nl, zafonte r. rehabilitation of patients with traumatic brain injury. in: winn hr, editor. youmans neurological surgery. ed 6.phildelphia, pa: elsevier saunders; 2011. pp. 3516–3534.pp. e3511–e3513. 8. jiao qf, liu z, li s, zhou lx, li sz, tian w, et al. influencing factors for posttraumatic hydrocephalus in patients suffering from severe traumatic brain injuries. chin j traumatol 2007; 10: 159-162. 9. de bonis p, sturiale cl, anile c, gaudino s, mangiola a, martucci m, et al. decompressive craniectomy, interhemispheric hygroma and hydrocephalus: a timeline of events? clinical neurology neurosurg 2013; 115: 13081312. 10. takeuchi s, takasato y, masaoka h, hayakawa t, yatsushige h, nagatani k, et al. hydrocephalus after decompressive craniectomy for hemispheric cerebral infarction. j clin neuroscience 2013; 20: 377-382. 11. wang lp, wu cg, yao j. risk factors of posttraumatic hydrocephalus after decompressive craniectomy for patients with craniocerebral trauma. chin j trauma. 2014;30:307–310. 12. waziri a, fusco d, mayer sa, mckhann gm, 2nd, connolly es., jr postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. neurosurgery.2007;61:489–493. 13. gudeman sk, kishore pr, becker dp, lipper mh, girevendulis ak, jeffries bf, et al. computed tomography in the evaluation of incidence and significance of post-traumatic hydrocephalus. radiology.1981;141:397–402. 14. cardoso er, galbraith s. posttraumatic hydrocephalus — a retrospective review. surg neurol 1985; 23:261-4. 15.takagi h, tamaki y, morii s, ohwada t. rapid enlargement of ventricles within seven hours after head injury. surg neurol 1981; 16:103-5. 16. sheffler lr, ito vy, philip pa, sahgal v. shunting in chronic post-traumatic hydrocephalus: demonstration of neurophysiologic improvement. arch phys med rehabil. 1994;75:338–341. 17. wood jh, bartlet d, james ae, jr, udvarhelyi gb. normal-pressure hydrocephalus: diagnosis and patient selection for shunt surgery. neurology. 1974;24:517–526. 18. foroglou g, zander e. post-traumatic hydrocephalus and measurement of cerebrospinal fluid pressure. acta radiol diagn (stockh) 1972; 13:524-30. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 397 398 | 397 research on post –traumatic neurodegenerative disorders from india ashok munivenkatappa1, amit agrawal2 1national institute of epidemiology (icmr), chennai, india 2department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india traumatic brain injury (tbi) is a major public health burden in our country, due to accelerated urbanization, unprecedented motorization, growing industrialization, changing life styles and absence of safety policies among people. in 2002 it was estimated that 1.6 million indian populations sustain traumatic brain injury with 200,000 deaths (1). tbi continues to pose a serious public health challenge, with numerous deaths at the scene and a large percentage of surviving patients have lifelong disabilities. tbi is a diseases process not an event. any severities of brain injury manifest problems in multi spectrum that lasts for days, months, years, sometimes the post traumatic sequel continues throughout the life. such changes includes cellular and sub cellular inflammation that cause significant effect on patient cognitive, behavioral and personality level. among sensitized individuals the chronic pathological changes can lead to neurodegenerative conditions. dementia is a neurodegenerative condition characterized by progressive memory loss with other mental deficiency. in india there is increase in prevalence and incidence of dementia. as per urban reports from several regions of our country the prevalence of dementia in india ranges from 0.8 to 4.1%. the percentage varies from north, south, east and west due to multi ethnic, multi-cultural and environmental differences (2). a study among kashmiri pandit population from north india has reported that the incidence rate of dementia is 5.34 per 1000 person-years (3). apart from ageing, positive family history, illiteracy, and low socio economic status the non-communicable diseases like stroke and brain injury form a major risk factor for progressive dementia. unfortunately, the published indian literature on post traumatic dementia is still far short of the actual need. studies from developed countries have reported that tbi is an important risk factor for later cognitive decline, which has been linked to development of dementia and chronic neurodegenerative conditions (4-6). delayed progressive persistent neuroinflammation have been demonstrated among tbi cases by both histopathological and neuroimaging studies (7, 8). among chronic neurodegenerative conditions alzheimer’s constitutes about three forth of cases, followed by dementia with levy bodies and vascular type (6). several studies have reported that 398 | munivenkatappa, agrawal post –traumatic neurodegenerative disorders from india patients with moderate to severe tbi are at higher risk of developing alzheimer’s disease (4). recent studies have reported that repetitive mild tbi (also concussion injury) have linked to increased risk for chronic traumatic encephalopathy (cte) a variant of neurodegenerative diseases (9). studies are focussing on exploring possible reason and also any targets that can reduce or completely treat post traumatic progressive neuro inflammation responsible for neuro degenerative diseases. our country has enough resources with respect to both tbi and dementia, but the research in this area is limited. the geriatricians, neuroscientists, and clinicians should integrate to improve the research quality in tbi and neuro degenerative disorders. translation research in this area is very crucial for epidemiological and intervention research that aimed to reduce or prevent the disease condition. correspondence dr. ashok munivenkatappa scientist c, vrdl project, national institute of epidemiology (icmr), chennai – 77 e-mail: ashokmphdns@gmail.com phone: +91-9844250897 references 1. gururaj g (2002) epidemiology of traumatic brain injuries: indian scenario. neurological research 24: 24-28. 2. das sk, pal s, ghosal mk. dementia: indian scenario. neurol india. 2012 nov-dec;60(6):618-24. 3. raina sk, pandita kk, razdan s. incidence of dementia in a kashmiri migrant population. ann indian acad neurol. 2009 jul;12(3):154-6. 4. fleminger s, oliver dl, lovestone s, rabe-hesketh s, giora a. head injury as a risk factor for alzheimer's disease: the evidence 10 years on; a partial replication. j neurol neurosurg psychiatry. 2003 jul;74(7):857-62. 5. gardner rc, burke jf, nettiksimmons j, kaup a, barnes de, yaffe k. dementia risk after traumatic brain injury vs nonbrain trauma: the role of age and severity. jama neurol. 2014 dec;71(12):1490-7. 6. lobue c, wilmoth k, cullum cm, rossetti hc, lacritz lh, hynan ls, hart j jr, womack kb. traumatic brain injury history is associated with earlier age of onset of frontotemporal dementia. j neurol neurosurg psychiatry. 2015 sep 10. [epub ahead of print] 7. farbota kd, sodhi a, bendlin bb, mclaren dg, xu g, rowley ha, johnson sc. longitudinal volumetric changes following traumatic brain injury: a tensor-based morphometry study. j int neuropsychol soc. 2012 nov;18(6):1006-18. 8. johnson b, neuberger t, gay m, hallett m, slobounov s. effects of subconcussive head trauma on the default mode network of the brain. j neurotrauma. 2014 dec 1;31(23):1907-13. 9. gardner rc, yaffe k. epidemiology of mild traumatic brain injury and neurodegenerative disease. mol cell neurosci. 2015 may;66(pt b):75-80. microsoft word 17ienceanbookrew.doc st.m. iencean, a.v. ciurea intracranial hypertension 125 book review intracranial hypertension st.m. iencean and a.v. ciurea nova science publishers, new york, 2009; isbn: 978-1-60741-862-7 the publication of a romanian medical monograph in a prestigious american publishing house represents a medical publishing event and recognition of the value of romanian medicine. the monograph entitled “intracranial hypertension”, written by the romanian neurosurgeons dr. stefan m. iencean and prof av ciurea, was edited in late october 2009 by nova science publishers, a publishing house in new york. in the romanian medical literature the known publications to date are the classic monograph entitled “intracranial hypertension” written by prof c arseni and al i constantinescu in 1972, the chapter on intracranial hypertension from “practical handbook of neurosurgery” written by prof alex constantinovici and av ciurea in 1998 and the paper entitled “intracranial hypertension” published by dr stefan m. iencean in 2006, based on a synthesis of scientific data, imaging investigations, biochemical investigations and modern electrophysiological investigations. the monograph “intracranial hypertension” written by the two romanian authors offers the updated knowledge accumulated to date in the field along with the major individual contributions of the authors. the authors are two well-known romanian neurosurgeons: dr st.m. iencean (iasi) and prof a.v. ciurea (bucuresti). the paper covers the entire theme in 16 chapters, richly illustrated with drawings and original diagrams, all the selected imaging being significant for the clinical situations selected; the bibliography is ample and recent. 126 romanian neurosurgery (2010) xvii 1: 125 127 the merit of this monograph is that it offers the possibility of a complete and systematic understanding of intracranial hypertension, based on the experience and the important contributions of the two authors. the monograph is classically structured: it begins with general considerations about intracranial hypertension, elements of anatomy and physiology and fundamental notions of intracranial hypertension, continuing with the pathology, clinical picture, laboratory explorations and the types of intracranial hypertension. the relationship between intracranial pressure and the mechanisms of increased intracranial pressure are thoroughly discussed and followed by a presentation of the current methods for measuring intracranial pressure. pathogenesis of intracranial hypertension constitutes an important chapter of the monograph and it includes the modifications of the three intracranial components, which contribute separately or together to the development of intracranial hypertension: brain parenchyma, cerebro-spinal fluid and blood circulation. the appearance of an additional intracranial mass induces mechanical effects of compression, displacements of brain substance and afterwards or at the same time biochemical changes emerge in the vascular wall, in glia and in neurons with the development of the brain edema. the changes in cerebrospinal fluid dynamics and in cerebral blood circulation represent a factor of major instability in the pathogenesis of increased intracranial pressure. the most serious consequences of increased intracranial pressure are represented by the effects on the pressure infusion in the brain which causes cerebral ischemia and by the pressure differences between craniospinal compartments, producing brain herniation. presentations of the clinical picture and of decompressed disease symptoms follow, followed then by a chapter about paraclinic explorations which comprises the classic and modern investigations, by selecting the most characteristic imaging situations which present the intracranial hypertension syndrome. the classification of intracranial hypertension highlights the authors’ personal contributions, which have been published in professional journals in the country and abroad: intracranial parenchymatous hypertension, vascular intracranial hypertension, and intracranial hypertension by affecting the cerebrospinal fluid dynamics idiopathic intracranial hypertension. the main characteristics of each syndrome and the elements of clinical and etiological differentiation related to age and clinical stage are discussed. the last chapters deal at large with each type of disease, with the presentation of the specific pathology, of the clinical picture, of the paraclinic explorations and of specific treatment. an important subchapter is intracranial pressure monitoring, which permits the trace of intracranial pressure variations, the determination of brain infusion pressure and the assessment of therapeutic efficiency. st.m. iencean, a.v. ciurea intracranial hypertension 127 intracranial parenchymatous hypertension is discussed in relation to the mode of onset: acute or gradual onset which constitutes an extremely useful approach for the clinician who must detect this pathology. cranio-cerebral traumas represent a significant share of acute forms of disease and their discussion is elaborate, with the prominence of the last acquisitions in intracranial pressure monitoring and therapy. vascular intracranial hypertension is discussed with the three main ethnologies: cerebral thrombosis, hypertensive encephalopathy and ischemic cerebro-vascular disease with its diagnosis features, its evolution and treatment. intracranial hypertension has two etiologic forms when a disorder of csf dynamics occurs: through the disorders of csf dynamics, having an obstructive internal hydrocephalus and through the disorders of csf’s resorption. idiopathic intracranial hypertension is discussed extensively by presenting the possible pathogenic mechanisms whereof the authors had an original contribution. the evolution and the prognosis of the disease and the treatment of intracranial hypertension are the last chapters related to this disease, with the presentation of therapeutic schemes in cerebral edema, in order to maintain the cerebral blood perfusion to normal values in terms of increased intracranial pressure and in order to decrease the secretion and the excess of cerebro-spinal fluid. the principles of emergency treatment of intracranial hypertension syndrome and the treatment schedule of acute traumatic intracranial hypertension are also presented. the last chapter discusses the intracranial hypotension syndrome, which often may have a clinical picture similar to that of intracranial hypertension and which requires recognizing and applying an adequate treatment. the recognition of the romanian authors’ contribution in classifying some aspects of this pathology which is essential in neurosurgery and neurology was also confirmed by them being chosen to develop the “intracranial hypertension” chapter in the international guide “essential practice of neurosurgery” addressed to young neurosurgeons and edited by the world federation of neurosurgical societies. the monograph published by dr. st m iencean and prof av ciurea is a success in the international medical literature and it reaffirms the value of the romanian school of neurosurgery, being a reference book of intracranial hypertension. prof. dr. alexandru constantinovici umf „ carol davila” bucureşti honorary president of the romanian society of neurosurgery flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article leptomeningeal metastasis mimicking chronic subdural hematoma saurabh jain india doi: 10.1515/romneu-2017-0092 romanian neurosurgery (2017) xxxi 4: 575 576 | 575 doi: 10.1515/romneu-2017-0092 leptomeningeal metastasis mimicking chronic subdural hematoma saurabh jain department of neurosurgery, gbh american hospital, udaipur, rajasthan, india abstract: the presentation of leptomeningeal metastasis varies widely. it can also present a condition very similar to chronic subdural hematoma. one should have a low threshold for suspicion while diagnosing such conditions to avoid catastrophic events. introduction chronic subdural hematoma is one of very common neurosurgical disorder. it usually involve older age group people. the management involves ncct head followed by surgery. we encounter a similar patient whose ncct is almost diagnostic for chronic sdh but on detailed examination it was found to be leptomeningeal metastasis from breast. case a 45 year old female came to outpatient department with complaints of headache, giddiness on walking and cognitive impairment. the ncct head (figure 1) is suggestive of hypodense collection in rt frontotemporoparietal region along with the mass effect and midline shift to the right. on first instance it was considered to be a case of chronic sdh but disproportionate edema and mass effect raised a suspicion. on detail reexamination there was a small area of induration found at right breast. patient was subjected to magnetic resonance imaging and biopsy of indurated part. the mri revealed a leptomeningial metastasis (figure 2) probably originating from breast malignancy which is confirmed by local tissue biopsy (adenocarcinoma). patient was transferred to oncology care where she was managed by surgery, chemotherapy and radiotherapy but she succumbed to her illness on 30th day of first consultation. figure 1 ncct head the right frontoparietal mass resembling chronic sdh with cerebral oedema 576 | jain leptomeningeal metastasis mimicking chronic subdural hematoma figure 2 mri brain contrast image deciphering leptomeningeal disease discussion though chronic sdh and leptomeningeal metastasis looks similar in imaging they are altogether different pathology. as per the biggest review article on chronic sdh by yadav et al the annual incidence is variable in different age groups but overall falls in the range of 1-5.3 per 100,000 population (1). the incidence increases when we consider population on anticoagulants, older age and other co-morbid illness. (1, 2, 3). the chronic sdh being the commonest neurosurgical illness the leptomeningeal metastasis is very rare. though the autopsy series claim up to 20% of metastatic death. the incidence is about 5% of all metastatic cancers patients (4, 5, 6). the chronic sdh is benign condition with mortality is less than 2% while the leptomeningeal disease is associated with almost 100% mortality (6, 7, 8). the great difference in these two disease makes it necessary to diagnose exactly the pathology. this case report is basically emphasized the similarity of two altogether different pathology on ncct head, so much that one can misdiagnose the leptomeningeal disease as chronic sdh and end up in catastrophic results. author recommends that every case of chronic sdh should be correlated with thorough clinical examination and least suspicion threshold. the doubts should always be ruled out by appropriate investigation i.e. contrast mr imaging. correspondence dr. saurabh jain 203, the garnet, 33 b new fatehpura, udaipur, rajasthan, india email: drsaurabh_jain@rediffmail.com mobile: +91 7746885699 references 1. yadav yr, parihar v, namdev h, bajaj j. chronic subdural hematoma. asian j neurosurg 2016;11:330-42 2. karibe h, kameyama m, kawase m, hirano t, kawaguchi t, tominaga t. epidemiology of chronic subdural hematoma. no shinkei geka. 2011;39:1149–53. 3. krupa m. chronic subdural hematoma: a review of the literature. part 1. ann acad med stetin. 2009;55:47– 52. 4. kaplan jg, desouza tg, farkash a, et al. leptomeningeal metastases: comparison of clinical features and laboratory data of solid tumors, lymphomas and leukemias. j neurooncol 1990; 9:225. 5 posner jb. neurologic complications of cancer, f.a. davis, philadelphia 1995. 6. kesari s, batchelor tt. leptomeningeal metastases. neurol clin 2003; 21:25. 7. sikahall-meneses e, salazar-pérez n, sandoval-bonilla b. chronic subdural hematoma. surgical management in 100 patients. cir cir. 2008;76:199–203. 8. miranda lb, braxton e, hobbs j, quigley mr. chronic subdural hematoma in the elderly: not a benign disease. j neurosurg. 2011;114:72–6. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article outcome of medial sphenoidal wing meningioma surgery ashraf el badry, azza abdelazeez egypt doi: 10.2478/romneu-2018-0006 40 | el badry et al outcome of medial sphenoidal wing meningioma surgery doi: 10.2478/romneu-2018-0006 outcome of medial sphenoidal wing meningioma surgery ashraf el badry1, azza abdelazeez2 1neurosurgery department; 2pathology department faculty of medicine, mansoura university hospital, egypt abstract: background: sphenoid wing meningiomas among difficult surgery tumours due to involvement of important structures like optic nerve, cavernous sinus or carotid artery. objective: to evaluate outcome and prognostic factors in patients with medial sphenoid wing meningiomas after microsurgery in a series of 47 patients with medial sphenoid wing meningioma. method: this paper includes analysis of 47 patients & their data who underwent surgical management for meningiomas involving the medial sphenoid wing in the period between jan 2008 and february 2016 at mansoura university hospital. results: the most of patients were suffering from visual impairment (59.6%), followed by headaches (38.2%). total tumor resection were achieved in 23 cases, incomplete in 19 cases and partial resection in 5 cases. visual acuity improved or stable in 57.4% of the patients. preoperative neurological deficit remains unchanged postoperative in 35 cases while improved in 4 cases. 8 cases developed permanent 3rd nerve palsy. tumor recurrence was in 7 patients. conclusion: there are many factors influence the prognosis of inner sphenoid wing meningioma including the extent of surgical resection, cavernous sinus invasion, present or absent of peritumoral edema, vascularity of the tumor, size of the tumor, presence or absence of arachnoid plane between the tumor and surrounding neurovascular structures and preoperative neurological condition key words: sphenoid, meningioma, inner wing, surgery introduction the intracranial meningioma presumed to represent about 14 to 18% of all intracranial neoplasms. the sphenoid ridge meningioma account approximately 20% of all supratentorial meningioma, on the other hand the half of it occurred in the medial sphenoid ridge [5]. it was termed for the first time by cushing and eisenhardt, differentiating between two forms: globoid tumors that poses nodular nature & meningioma en plaque variety, which had a flat shape (sheet) and spread alongside the sphenoid wing. the globoid tumours additional divided into three categories (figure 1): medial group, middle group & lateral group. the medial group romanian neurosurgery (2018) xxxii 1: 40 55 | 41 (figure 2) appeared in the segment adjacent to the anterior clinoid process. this particular meningiomas had an inherited surgical difficulties, morbidities & mortalities due to its intimate relations to optic nerve, cavernous sinus, cranial nerves that enter superior orbital fissure and arteries of anterior circulation. [14] on the other hand, the extent of tumours resection still one of major factor influencing the recurrence rate which may alter the long term outcome of those patients making operative procedures a challenge to skull base neurosurgeons all over the world in spite of advancement in microscopes, microsurgical tools and neurosurgery equipment. on the light of this concepts, many neurosurgery preferred to remove these tumours partially or grossly subtotally then refer the patients to radiosurgery. [13,17] figure 1 diagram show the three tires of sphenoid wing meningioma according to the location: medial group (yellow), middle group (orange), lateral group (blue) figure 2 diagram reveal the site of dural base to the medial sphenoid wing meningioma the decision making became more difficult to get balance between surgical morbidity & mortality and recurrent rate by adopting a good microsurgical technique maintaining cranial nerves & skull base vessels integrity. our goals in this paper: to evaluate outcome and prognostic factors in patients with medial sphenoid wing meningiomas after microsurgery & application of current neurosurgical equipment in a series of 47 patients with medial sphenoid wing meningioma retrospectively. patients & method this paper includes analysis of 47 patients & their data who underwent surgical management for meningiomas involving the medial sphenoid wing (the location was defined by preoperative imaging & intraoperative report while the pathology was 42 | el badry et al outcome of medial sphenoidal wing meningioma surgery confirmed by histological assessment) in the period between jan 2008 and february 2016 at mansoura university hospital. all cases that involved middle & lateral two thirds of sphenoid wing were excluded. also, we excluded all meningiomas enplaque in this paper as it is not limited to medial sphenoid wing beside it is specific entity that different from our interest of globoid medial sphenoid wing meningioma (did not obey the three tires classification) and the surgical procedures for these tumors are entirely different. the cases who lost in follow up less than 3 months or incomplete data were also eliminated from our study. the follow-up period varied from 3-60 months (mean 14.7 months). patients’ demographic data 35 women and 12 men, mean age of 51.3 years (vary between 32 to 68 years). the clinical pictures of these cases (table 1) as follow: visual impairment 59.6%, headaches 38.2%, 3rd nerve palsy 8.5%, limb weakness in three cases, proptosis appeared in two cases and epilepsy manifested in two cases. table 1 patients’ demographic data clinical presentation number of cases % visual impairment 28 59.6% headaches 18 38.2% 3rd nerve palsy 4 8.5% limb weakness 3 6.4% proptosis 2 4.26% epilepsy 2 4.26% all patients who were involved in our research had a complete data including:  complete clinical neurological & ophthalmological (visual acuity) examination  computed tomography “thin cuts “on skull base to visualize bony skull base anatomical land marks  mri imaging with its variety: t1we (pre & post contrast ) to delineate the tumor and visualize its relations to the proximate neurovascular structures & optic nerves while t2we determine the integrity of arachnoid plane & gave a rough idea about tumor consistency i.e. hypointense may be associated with tumor firmness  cta, mra or traditional angiography was done to show tumor feeders and to determine the extent of encasement of the internal carotid artery and its branches by the tumor  surgical archives, discharge sheets, histological reports, follow-up records, and post-operative imaging findings. patients’ radiological data: the mean tumor diameter was 5.7 cm (centimeter) and varied between 3.2 cm & 6.1 cm. the peritumoral edema was present in 19 cases (40.4%) while the med line shift was seen in 15 cases (32%). the calcifications appeared in 6 cases (12.8%). 24 cases (51.06%) showed ipsilateral invasion of the cavernous sinus. the involvement of the optic nerve canal was seen in 5 cases (10.6%) the extent of tumor resection was determined according to the simpson grading scale (grade i: total removal with its dural romanian neurosurgery (2018) xxxii 1: 40 55 | 43 attachment, grade ii: total removal with coagulation of dural base, grade iii: subtotal excision...etc.). the post-operative functional outcomes were established according to the kps scale. the patients who had a high rank kps (80-100) who depend on himself to do normal daily activities (4). kps was used to evaluate all patients (pre & post) operatively and in follow-up assessments. [5] surgical techniques: the main objectives of the surgical procedures in our patients were decompression of the optic nerve and complete resection of the tumor intradurally with or without elimination of the intracavernous tumor portion. in our series, pterional approach was applied in 36 cases while orbito-zygomatic approach was performed in 11 patients (1) optimal patient positioning: the patient was placed in supine position. the head was rotated to contralateral side of the procedure with angle ranged from 30o to 60o with elevated head of the bed about 15°. (2) incision: the shape of the scalp incision varied: question mark flap behind the hair line or bi-coronal skin flap but both must reach by sub fascial dissection to the orbital rim anteriorly and zygomatic arch inferiorly (3) bone flap: traditional pterional bone flap, or extended orbito-zygomatic bone flap with added orbital rim & zygomatic arch. (4) sphenoid ridge drilling: we removed the outer and middle portion of sphenoid wing or even to anterior clinoid process if necessary, extradurally using high speed drill. to get space and minimize brain retraction (5) tumor devascularization: through coagulation of the basal dura after elevation of it under microscopic visualization to decrease the external carotid artery tumor feeders. (6) opening the sylvian fissure meticulously (7) early localization, revealing and decompression of the on (optic nerve) and ica (internal carotid artery) (8) tracking the on and ica to the tumor and explore it (9) internal tumor debulking by piece meal or using causa (cavitron ultrasonic surgical aspirator) (10) meticulous extracapsular devascularization and dissection (11) preservation of the adherent/adjacent neurovasculature. we depend on maintain the patency of nutrient feeders to the on after its decompression for achieving a functioning on post-surgery. (12) we de-roofed the optic canal and /or superior orbital fissure if the tumor extend in it to relieve the compression on these nerves (13) if arachnoid plain between (the ica & its branches) and the tumour was intact thus assisting in dissection of these vessels easily peel off the tumour (14) meticulous managing cavernous sinus cs involved part of the tumor by removing it if partial cs involvement or leaving this part if excessive invasion of cs by the tumor to avoid high possibility of cranial nerves destruction. (15) removal of the involved bone and tumor dural base if possible (16) dural reconstruction by fascia late or artificial dura and closure in water tight fashion. (17) closure of the bone flap (18) anatomical closure 44 | el badry et al outcome of medial sphenoidal wing meningioma surgery case illustration 49 years old lady had a complaint of sever persistent frontal headache not responding to medical treatment followed by visual deterioration on right eye. visual premetry revealed enlargement of the left blind spot and left upper inner quadrantanopia. mri images revealed left medial sphenoid wing meningioma iso to hypo intense with homogenous enhancement that encasing rt. ica and compressing the rt. on (figure 3). traditional angiography (figure 4) showed the feeders of the tumor that include: frontal branch of mma (middle meningeal artery) from rt. eca & meningo-hypophyseal a. which is branch of tentorial a. from ica. it did not show any constriction in rt. ica. we adopt pterional approach (figure 5). the surgical technique was as described earlier. through the steps with microscopic tools we removed the tumour totally with peeling off the tumour from rt. ica & rt. on and preserving the nutrient vessels to all the optic apparatus as it is crucial steps to maintain vision. post operatively the vision improved by visual premetry assessment. post-operative ct brain axial cuts reveal complete removal of the tumour. a b c d e f figure 3 pre-operative brain mri images of rt. medial sphenoid wing meningioma that compressing rt, on, encasing rt, ica and extending to the sellar region. a. mri brain t1we axial cut. b. mri brain t2we axial cut that showed iso to hypo intensity of the tumour that indicate some degree of tumour softening. c & d. mri brain t1we coronal cuts. e & f mri brain t1we post contrast axial cuts display homogenous enhancement that indicate high vascularity romanian neurosurgery (2018) xxxii 1: 40 55 | 45 a b c d figure 4 rt. eca & rt. ica angiography images a-d: (a-b) from rt. eca, the frontal of mma feeding the tumor (c-d) from rt. ica, meningo-hypophyseal a. branch of tentorial a. give feeder to the tumour a b c d e f g h figure 5 a intraoperative picture reveal drilled sphenoid wing bone till ant. clinoid and appearance of the whole dural flap. b microscopic picture showed coagulation of the tumour feeders in the tumour dural base by using the bipolar cautery. c. opening the sylvian fissure under the microscope. d. internal debulking of the tumour using cusa under microscope. e .peeling the tumour off the optic nerve. f using the micro-scissor to complete the removal of the tumour that encasing the optic nerve. g. removing the tumour underneath the optic nerve & in the sellar area. h. microscopic picture showed complete tumour excision 46 | el badry et al outcome of medial sphenoidal wing meningioma surgery figure 6 post-operative ct brain axial cut display complete removal of the tumour 2nd case pre & post-operative presented in (figures 7, 8, 9) with complete excision of the tumor: figure 7 second case of medial sphenoid wing meningioma preoperative mri images t1we axial, sagittal and coronal cuts, pre & post contrast figure 8 pre-operative ct brain angiography of 2nd case show encasement of ica & mca (middle cerebral artery) by the tumour and show some tumour calcification figure 9 post-operative 2nd case ct brain axial cut display complete tumour resection romanian neurosurgery (2018) xxxii 1: 40 55 | 47 the last presentation case pre-operative mri brain axial & coronal images in (figure 10), postoperative ct brain axial cuts (figure 11) and post-operative mri brain t1we axial cut display entire tumor removal. figure 10 3rd case pre-operative mri brain axial & coronal images display medial sphenoid wing meningioma figure 11 3rd case post-operative ct brain axial cut show disappearance of the tumour after the surgery figure 12 3rd case post-operative mri brain axial cut show total tumour excision post microsurgical results: about the tumours pathological examination in these cases (table 3) the most common in these cases was mesothelial meningioma (figure 13, 14). the second most common was transitional meningioma then fibrous, angiomatous and the least pathology was atypical meningioma that showed aggressive pathological features like more cellular density, partial spiral structure, vascular hyperplasia, necrosis, mib about 10% and nuclear enlargement (figure 15, 16). table 2 histopathological results of the 47 medial sphenoid wing meningiomas pathology number of cases percentage % mesothelial 23 cases 48.9% transitional 12 cases 25.5% fibrous 7 cases 14.9% angiomatous 2 cases 4.25% atypical 3 cases 6.4% figure 13 100 -h&e stain show mild increased cellular density 48 | el badry et al outcome of medial sphenoidal wing meningioma surgery figure 14 characteristic psammoma bodies for meningioma figure 15 200 -h&e stain increase in cell density, partial spiral structure, vascular hyperplasia, pattern less pattern, necrosis, nuclear enlargement. all of the above indicate atypical variant of meningioma figure 16 mib more than 10% according to the extent of tumours excision: total tumor resection (simpson i-ii) was accomplished in 23 cases (48.9%). on the other hand, (simpson iii) was achieved in 19 cases (40.4%) and the partial resection (simpson iv ) was done in 5 cases (10.6%). the reason for incomplete removal of tumours in the last two categories may be related to firmness of the tumours, absence of clear arachnoid plane between ica & its branches and the tumours leading to adherent of the tumours on the vessels adventitia beside encasement of cranial nerves & optic apparatus which make complete tumor removal possess a very high morbidity. regarding visual acuity post-operative changes: it showed improvement or stable in 27 cases (57.4%). the neurological deficit remained unchanged postoperative in 35 cases (74.5%) while improved in 4 cases (8.5%). the mean karnofsky performance scale (kps) score for the patients in the study was 86.2 (ranged from 60 to 100) at 1 year after surgery, which was 74.5 at 10 days after surgery. our research permanent morbidity represent 17.02% & 3 (6.3%) mortality. all the complication & its prognosis summarized in (table 2) and (figure 17). 13 patients with subtotal resection and 5 patients with partial resection received postoperative radiotherapy. tumor recurrent was present in 7 patients (14.9%). these cases analyzed according to the degree of tumor excision and the results was: a case of complete removal, the 2nd case was incomplete resection and residual 5 cases showed partial removal. the analysis of the same cases in relation to the pathology the results was: 3 cases the pathological investigation was mesothelial in 3 cases, transitional in 1 case, angiomatous in 1 case, atypical in 2 cases (table 3). romanian neurosurgery (2018) xxxii 1: 40 55 | 49 table 3 showed postoperative complications in 47 medial sphenoid wing meningioma cases complications number s percentages (%) outcomes at discharge csf leakage 3 6.4% 2 cured hemiparesis 5 10.6 3 improved, 2 unimproved incomplete aphasia 4 8.5% 2 improved cerebral infarction 2 4.25% permanent epidural hematoma 3 6.4% all cured tumor bed bleeding 6 12.76% all cured oculomotor nerve palsy 9 19.15% 1 cured, 8 not improved 6th n. palsy 2 4.25% 2 cured subcutaneous collection 4 8.5% 4 cured table 4 pathology of recurrent cases pathology number of cases mesothelial 3 cases transitional 1 case angiomatous 1 case atypical 2 cases figure 17 a diagram display the prognosis of complication in our series by statistical analysis we document the influence of many factors on postoperative patient’s conditions & survival: extent of tumor excision (p=0.026), peritumoral edema (p=0.038, vascularity of the tumours ((p=0.005), size of the tumor (p=0.029), presence of arachnoid plane between the tumours and surrounding neurovascular structures (p=0.004), preoperative neurological condition (p=0.005). the factors that did not affect the patient postoperative status include: patients age, sex, duration of symptoms, surgical approach and tumor volume (average 3.7 cm3) range between 2.6 cm3 to 6.1 cm3. 50 | el badry et al outcome of medial sphenoidal wing meningioma surgery discussion medial sphenoid wing meningiomas (mswm) had inherited a difficult surgical challenge due to limited critical location that bounded by on, clinoid process, sphenoid wing, ica and cranial nerves gone through superior orbital fissure. in spite of its narrow site, it represent over than half of all meningiomas that appear in sphenoid wing. [5] in the past decades, the total resection of those tumours was not achieved in most of the cases by reason of high morbidity & mortality related to attempts of radical removal leading the neurosurgeon to prefer partial removal. but the advances in microscopes, microinstruments, modern neurosurgery tools and imaging studies make this goal possible. [4] in our research total tumor resection (simpson i-ii) was accomplished in 23 cases (48.9%). alternatively, (simpson iii) was achieved in 19 cases (40.4%) and the partial resection (simpson iv) was done in 5 cases (10.6%). the main causes for incomplete excision in our research could be correlated to increased firmness of the tumours, lack of clear arachnoid plane between ica & its branches and the tumours leading to adherent of the tumours on the vessels adventitia making total resection impossible without vascular injury that may be fatal beside encasement of cranial nerves & optic apparatus and inability to remove the intra-cavernous part which make complete tumor removal possess a very high morbidity. one of major factors that affect the extent of tumor removal also was blood loss volume.we made all possible ways to decompress the on & all compressed neurovascular structures, maximum intra dural debulking of the tumor (the primary our surgery goals) without burden the patients conditions as we can. these results is comparable to what is mentioned by brotchi & bonnal, nakamura et al and sughrue.[14,17] in spite of the old series showed complete removal of the mswms fluctuated between 23 to 50%.[16]. the improvement of the success rate may be related to adoption of microsurgical techniques, invented micro instruments, neuro anesthesia cumulative experience all over the world and in our series may be also to the learning curves of the surgeons. [5, 4] according to the approach, we did not find any difficulty of meningioma removal because of the selected approach and the approach value in success surgical rate was statistically insignificant. this result opposite to statement by zhang et al. we can explain that by more homogenous features in our surgical group than zhang group. we adopt orbitozygomatic approach to the tumours that creeping in the middle cranial fossa and extend more posteriorly but the traditional pterional approach was selected to tumours that extend upward. this concept was used to get more detailed view of the on which can be localized more accurate through the skull base land marks to avoid injury during tumor removal as conducted by the same author. we agree about early devascularization of meningiomas feeders in the skull bas dura was a critical step in reducing blood loss [19] but still extradural anterior clinoidectomy one of the essential steps in all of our approaches in mswms romanian neurosurgery (2018) xxxii 1: 40 55 | 51 which approved by lee et al [10] and against nakamura et al statement to get more room for dissection and early identification of on. the visual impairment represent the commonest preoperative neurological deficit. in literature the paper in last 10 years show further post-operative vision recovery but did not reach the acceptable level.[4,19] in our series, the vision improved or stable in 27 cases (57.4%). bassiouni et al reported of 106 cases, va (visual acuity) improved in 21 cases (40.4%) and lee et al reported a fair results using a cranial base technique. [3] our results was obtained thanks for meticulous microsurgical technique, preservation of on nutrient feeders and avoidance of cautery whenever possible. li et al gave same explanation in his series. [12] the neurological deficit in our cases remained permanent postoperatively in 35 cases (74.5%) while improved in 4 cases (8.5%). our research morbidity represent 17.02% & 3 cases (6.3%) mortality. al-mefty et al stated morbidity rate of 25% and mortality rate 42.9% in a his series of 24 cases and testified that “while czernicki et al reported a low mortality rate which was 6.7%. the complications after surgery were related with the extent of tumor resection”. [2] while other international authorities conducted a mortality rate that reach 15.4% and the frequency of permanent profound neurological deficit fluctuating between 8.8 % and 60%. [8] our data was comparable to these results. the mortality and morbidity had a very close relation to the cavernous sinus tumor portion beside in ability to dissection of neurosurgical bundles from the tumor, spasm of perforators or /and vascular injury. we minimize this issue by adequate drilling of the sphenoid bone, anterior clinoid removal to get space and early identification of neural & vascular structures to decrease its injury during tumor removal that most of the time may mask its location. the most common complication in our cases was 3rd n. palsy that was in 4 cases (8.5%) preoperative and became 9 (6 total -3 partial) cases (19.15%) immediate postoperative then improved (1 cured -3 total -5 partial ). these results may be higher than some paper of the same interest as zhang et al who stated post-operative 3rd n. palsy in 18.9% but improve in most of the cases and reduced to 4 cases only suffered from 3rd n. palsy[8].this may be as a result thermal injury during drilling the lip of superior orbital fissure (sof) and anterior clinoidectomy, injury of 3rd n. in the meningioma cavernous part [1,3,7,14,18]or/and surgical manipulation or cautery at the tent edge where 3rd n. pass to enter the oculomotor triangle and sof. so it wise to leave adherent cavernous sinus tumor part to decrease postoperative 3rd n. impairment. csf leak recorded in 3 cases in our research which appeared in many extensive skull base approaches. we treat it with lumbar drain for few days then acetazolamide tablets 500mg1000gm according to body weight as oral tablets /per day under umbrella of broad spectrum antibiotic. two of the three cured while the 3rd case developed meningitis and we evd (external ventricular drainage) device and the patient died. nakamura et al mentioned a case of post-operative csf leak 52 | el badry et al outcome of medial sphenoidal wing meningioma surgery who treated by endoscopic endonasal transsphenoid repair [14] and sughrue et al also a case treated conservatively. may be the difference because we did not use fibrin glue in early cases to seal the skull base dura and also we adopt lumbar drain to decrease the incidence of csf leak. 6th n. palsy occurred in 2 patients postoperatively. thus may be related to brain edema postoperative and both patient treated conservatively till the edema subside then the 6th n improved spontaneously as documented by liu d et al who gave the same report. 5 cases suffered from hemiparesis as postoperative condition 3 of them had weakness preoperative after few weeks 3 cases improved. incomplete aphasia occurred in 4 cases (8.5%) 2of them improved we assumed the surgical manipulation around perforator in territory of mca (middle cerebral artery) may trigger spasm in some extent, peritumoral edema was in optimum level postoperative that burden the patients neurological conditions beside the effect of retractors. during the series upgrade we adopt more skull base bone removal to minimize brain retraction, minimize coagulation to reduce the incidence of new neurological deficit. many paper mentioned these complications in similar surgeries for mswm as nakamura et al, czernicki et al, bassiouni et al, hao, liu et al. [3, 7, 8, 11, 14] may be it appeared in ours and in nakamura et al study due to presence of larger tumours that extend posteriorly and superiorly wit adherence to mca or aca perforators or to the mca or aca adventitia [2]. thus also explain the presence of two cases of cerebral infarction which was evident clinically & radiologically. they died few weeks after the surgery and the case of death in patient was massive cerebral edema with massive infarction & the other case was sever chest infection in 67 years old male with history of heavy smokers and bronchial asthma. liu et al conducted 6 patient died due to recurrence or progression of the tumours and 2 died of unrelated diseases [11] there was 3 case of acute epidural haematoma: two case treated surgically and a case managed conservatively. the bleeder was the stem of middle meningeal in two cases due to retraction in foramen spinosum. in 3rd case, the bone sinuses was the source of bleeding. the tumor bed haemorrhage occurred in 6 cases. 5 cases managed conservatively because of there was no midline shift or progressive increasing of the volume may be due to general oozing without identified the source of bleeding while one case treated surgically due to progressive enlargement of the haematoma and the source was small perforator. nakamura testified 2 cases of mortality: a case of mca stroke & haemorrhage in tumor bed and the other because of cerebral edema on the other hand kim et al reported 5 cases of postoperative haemorrhage/infarction (8.5%) without details about the cause or the criteria [9]. the cause of intracerebral tumor bed haematoma the well of the surgeon to minimize and meticulous bleeding control to avoid postoperative strokes and worsening of the patients’ neurological condition. subcutaneous collection appeared in 4 cases (8.5%) three of them treated conservatively and only 1 managed by surgical wound romanian neurosurgery (2018) xxxii 1: 40 55 | 53 revision. sughrue et al reported 4 cases of wound infection and a case of wound dehiscence. [17] we did not have any cases suffered from postsurgical intracranial hypotension, hyponatremia or the syndrome of inappropriate antidiuretic hormone secretion (siadh) as reported by czernicki et al and this might be due to small number of our cases. [7] histopathological examination showed the most common type was who grade i mesothelial meningioma in 23 cases (48.9%) as reported by many authorities.[11,14,17] but we had three cases of atypical meningioma which different from nakamura et al who did not report any cases of atypical meningioma [14] in patients long-term prognosis regarding the quality of life: over all the mean kps score for the patients in the study was 86.2 (ranged from 60 to 100) at 1 year after surgery, which was 74.5 at 10 days after surgery. while abdelaziz et al stated excellent outcomes 38 patients, with a kps score > 90 in 89% of their cases 1 year after surgery [1]and liu et al showed in 120 mswms cases mean kps was 83.5 at 10 days after surgery then improved to be 90.6 as mean kps (ranged from 60 to 100) 12 months after [11].so our results may goes with international data because of advanced microsurgical techniques, learning curve with preservation of perforators whenever possible and appropriate decision making according to patient condition. 13 patients subtotal resection and 5 patients with partial resection received postoperative radiotherapy as we applied benefit of radiotherapy on enhancing the patients survival as approved by pamir et al in his series [15] but we did not notice the radiotherapy problem in follow up and we believed the detailed results of radiotherapy may be is not our research focus. 7 patients (14.9%) showed tumor recurrence. this recurrence have a close relation to the extent of tumor excision (5 cases with previous partial removal, a case of former complete removal, last case had earlier incomplete resection). also it related to involvement of cavernous sinus, grade of meningioma (2 cases with atypical meningioma had recurrence). in the case of complete removal who showed recurrence the tumorous hyperostotic bone & dura may be the nidus for regrowth. nakamura et al reported the high rate of recurrence (27.5%) of clinoidal meningioma related to involvement of cavernous sinus as only cause in comparison to low rate of tumor recurrent in case showed no cavernous sinus involvement (7.7%) [2] while liu et al mentioned the close relation between recurrence in his series and tumor atypia [11] by analyzing the data statistically ,we found the influence of several factors on postoperative patient’s prognosis: extent of tumor excision (p=0.026) and we can explained that by the major effect of residual volume to promote the chance of recurrence as mentioned earlier, peritumoral edema (p=0.038) due to lower blood flow to the brain, limited space for retraction & higher incidence of brain contusion during surgery (we can overcome this by more removing skull base bone as total drilling of sphenoid wing, 54 | el badry et al outcome of medial sphenoidal wing meningioma surgery clinoidectomy). the vascularity of the tumours represent one of the main factors affecting our patients prognosis (p=0.005) especially internal carotid parasitic blood supply that may be difficult to identify & control intraoperative beside its sometimes related to perforators. the size of the tumor (p=0.029) because of major neurovascular involvement, cavernous sinus invasion & rich blood supply internal & external carotid that lead to more blood loss and sometimes limit the surgical excision as conducted by pamiret al& goel et al [15]. the presence of arachnoid plane between the tumours and surrounding neurovascular structures (p=0.004) play also important role in the series results due to its facilitator effect in tumor total excision, reduce the vasospasm by isolating the neurovascular bundles that limiting the surgical manipulation in these vital structures with subsequent reduction of vasospasm & cranial nerves injury. the preoperative neurological condition was (p=0.005) as it was a reflection of invasion & involvement of neurovascular structure like optic nerve on, other cranial nerves and cranial vascular tree. the factors that did not affect the patient postoperative status include: patients age, sex, duration of symptoms, surgical approach. many researchers conducted the importance of some of these factor on patient survival and quality of life like sughrue et al nakamura et al, zhang etal, liu d et al [9,13,11,17,19] but our result disagree with kim et al about age as influencing factor [9] conclusion: there are many factors influence the prognosis of inner sphenoid wing meningioma including the extent of surgical resection, cavernous sinus invasion, present or absent of peritumoral edema, vascularity of the tumor, size of the tumor, presence or absence of arachnoid plane between the tumor and surrounding neurovascular structures and preoperative neurological condition. correspondence ashraf elbadry, m.d., ifaans, osaka university fellow address: department of neurological surgery, faculty of medicine, mansoura university hospital, egypt email: ashrafbadry@hotmail.com; ashrafbadry@mans.edu.eg cell phone: +201111300033 – +201223477444 references 1.abdel-aziz km, froelich sc, dagnew e, jean w, breneman jc, zuccarello m, et al. large sphenoid wing meningiomas involving the cavernous sinus: conservative surgical strategies for better functional outcomes. neurosurgery 2004; 54(6):1375–83. 2.al-mefty o, smith rr: surgery of tumors invading the cavernous sinus. surg neurol 30:370-381, 1988 3.bassiouni h, asgari s, sandalcioglu ie, seifert v, stolke d, marquardt g: anterior clinoidal meningiomas: functional outcome after microsurgical resection in a consecutive series of 106 patients. clinical article. j neurosurg 111:1078-1090, 2009 4.behari s, giri pj, shukla d, jain vk, banerji d: surgical strategies for giant medial sphenoid wing meningiomas: a new scoring system for predicting extent of resection. acta neurochir (wien) 150:865-877, discussion 877, 2008 5.benjamin v, mccormack b: surgical management of tuberculum sellae and sphenoid ridge meningiomas, in schmidek hh (ed): operative neurosurgical techniques: indications, methods, and results. philadelphia, w.b. saunders, 2000, pp 305–315. 6.crooks, v, waller s, smith t, hahn tj: the use of the karnofsky performance scale in determining outcomes romanian neurosurgery (2018) xxxii 1: 40 55 | 55 and risk in geriatric outpatients. j gerontol 46: m139-144, 1991 7.czernicki t, kunert p, nowak a, marchel a. results of surgical treatment of anterior clinoidal meningiomas our experiences. neurol neurochir pol.2015; 49(1):29-35. doi: 10.1016/j.pjnns. 2015.01.003. epub 2015 jan 15. pub med pmid: 25666770. 8.hao s, tian r, wu z, et al. clinical characteristics and prognosis factors analysis for post-operative ptosis of sphenocavernous meningiomas: a single institution study. clin neurol neurosurg 2015; 131:35–41. 9.kim jh, jang wy, jung ty, kim iy, lee kh, kang wd, kim sk, moon ks, jung s.predictive factors for surgical outcome in anterior clinoidal meningiomas: analysis of 59 consecutive surgically treated cases. medicine (baltimore). 2017apr; 96(15):e6594. doi: 10.1097/ md.00000000000065 -94. pubmed pmid: 28403097; pubmed central pmcid: pmc5403094. 10.lee jh, jeun ss, evans j, kosmorsky g: surgical management of clinoidal meningiomas. neurosurgery 48:1012–1019, 2001. 11.liu dy, yuan xr, liu q, jiang xj, jiang wx, peng zf, ding xp, luo dw, yuan j. large medial sphenoid wing meningiomas: long-term outcome and correlation with tumor size after microsurgical treatment in 127 consecutive cases. turk. neurosurg. 2012; 22(5):547-57. doi: 10.5137/1019-5149.jtn.5142-11.1. pubmed pmid: 23015330. 12.li x, liu m, liu y, zhu s: surgical management of tuberculum sellae meningiomas. j clin neurosci 14(12):1150-1154, 2007 13.malik i, rowe jg, walton l, radatz mwr, kemeny aa: the use of stereotactic radiosurgery in the management of meningiomas. br j neurosurg 19(1):1320, 2005 14.nakamura m, roser f, jacobs c, vorkapic p, samii m: medial sphenoid wing meningiomas: clinical outcome and recurrence rate. neurosurgery 58:626–639, 2006 15.pamir mn, belirgen m, ozduman k, kiliç t, ozek m. anterior clinoidal meningiomas: analysis of 43 consecutive surgically treated cases. acta neurochir 2008;150(7):625–35. 16.pompili a, derome pj, visot a, guiot g: hyperostosing meningiomas of the sphenoid ridge: clinical features, surgical therapy, and long-term observations: review of 49 cases. surg neurol 17:411– 416, 1982. 17.sughrue me, rutkowski mj, chen cj, shangari g, kane aj, parsa at, berger ms, mcdermott mw. modern surgical outcomes following surgery for sphenoid wing meningiomas. j neurosurg. 2013 jul; 119(1):86-93. doi: 10.3171/2012.12.jns11539.epub 2013 feb 22. pubmed pmid: 23432379. 18.tobias s, kim ch, kosmorsky g, et al. management of surgical clinoidal meningiomas. neurosurg focus 2003; 14:e5. 19.zhang j, shrestha r, cai bw, zhou pz, li yp, jiang s. management of large medial sphenoid wing meningiomas: a series of 178 cases. turk neurosurg. 2014; 24(5):664-71. doi: 10.5137/1019-5149.jtn.766813.2. pubmed pmid: 25269034. 06 06elbadryashraf_outcome flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article post v-p shunt surgical site edh an uncommon complication: case report manish garg, deepashu sachdeva, ketan patel, anita jagetia, a.k. srivastava india doi: 10.1515/romneu-2017-0043 romanian neurosurgery (2017) xxxi 2: 253 – 256 | 253 doi: 10.1515/romneu-2017-0043 post v-p shunt surgical site edh an uncommon complication: case report manish garg, deepashu sachdeva, ketan patel, anita jagetia, a.k. srivastava department of neurosurgery, gb pant institute of postgraduate medical education and research and maulana azad medical college, new delhi, india abstract: ventriculoparitoneal shunt is well established modality of treatment for hydrocephalous. complication of v-p shunt are also mentioned in literature like shunt infection shunt migration etc [8]. here we are describing a rare complication of vp shunt which barely mentioned in literature. a 22 yr male admitted with complain of headache & vomiting patient was diagnosed to have tubercular meningities with hydrocephalous. patient planned for ventriculoparietoneal shunt surgery and vp shunt was done. on 3rd post-surgery day patient develop weakness in left side of body. urgent ncct head done which showed edh at surgical site. immediate craniotomy and evacuation of hematoma was done patient improved and discharged. thus we are discussing the importance of meticulous surgery for v-p shunt, post op ct scan and treatment. key word: v-p shunt, v-p shunt complication, extradural hematoma introduction ventriculoperitoneal (vp) shunting is a very common procedure done for the treatment of hydrocephalus, and is associated with fewer complications as compared to other methods of ventricular decompression and include shunt obstruction, infection, development of craniosynostosis, microcephaly, and excessive drainage of cerebrospinal fluid (csf) leading to intracranial hematomas (subdural, epidural, and intraventricular) [8, 4]. among the intracranial hematomas, subdural hematomas (sdhs) are more common than extradural hematomas (edhs) [7]. we are reporting a case of postoperative edh following vp shunt placement in an adult patient with a tubercular meningities and hydrocephalous. case report 22 year male admitted with c/o headache and vomiting for 6 month patient was investigated and ct head showed gross dilatation of all ventricles with change of tubercular meningitis. other supporting investigation to confirm the tuberculosis like 254 | garg et al post v-p shunt surgical site edh an uncommon complication esr, mauntaoux test, pcr which confirmed the diagnosis of tbm. patient planned for right v-p shunt (chabra medium pressure slit and spring shunt). under general anesthesia patient was positioned in supine head was tilted left side after painting and draping u shaped incision given at frazier’s point (6 cm above and 4 cm lateral to inion). burr hole made dura coagulated cruciate incision given and shunt ventricular end inserted in first attempt. csf pressure was highly raised and csf was grossly cleared csf sent for culture sensitivity cytology, biochemical study. post operatively patient symptoms got relieved. on 3 rd post-operative day patient became disoriented and developed weakness left side of body. urgent ncct head done which showed right parieto-occipital edh with mass effect and midline shift. immediately patient underwent right parieto-occipital craniotomy and evacuation of extradural hematoma. post operatively patient improved neurologically and discharged with no neurological deficit. he has been under regular follow up and has no neurological deficit. figure 1 preopeartive image showing hydrocephalous figure 2 right parieto-occipital edh with mass effect {coronal cut} figure 3 right parieto-occipital edh with mass effect {axial cut} figure 4 extra dural hematoma at vp shunt site {introperative image} romanian neurosurgery (2017) xxxi 2: 253 – 256 | 255 figure 5 post edh evacuation {axial cut} discussion extra dural hematoma, as a complication of ventriculoperitoneal shunt surgery for the management of hydrocephalus, is a rare condition. it often occurs in young patients, and there are some anatomical regions (parietal and frontal) where the pathology is more frequently found. the theory behind the occurrence of this not clear and many hypothesis given to justify the occurrence of edh post v-p shunt. many author thought that pressure exerted on dura while inserting the ventricular end lead to the separation of dura from inner surface of skull lead to damage of in between vessel which lead to the edh formation. sudden decrease in intracranial pressure post shunt can lead to expansion of edh [7]. multiple attempt for insertion of ventricular end can lead to parenchymal injury which also lead to edh formation. extradural hematoma always develops in a matter of days, weeks or months after surgical procedure [1, 6].contrary in our case patient presented acutely. patients with very high intracranial pressure or with intensive cortical atrophy, in long standing hydrocephalus, are most at risk. perhaps the skull-to-duramater adhesion become altered. the mortality of patients with edh is higher than for those with subdural bleeding. [2] coagulation profile disarrangement also an important factor for edh at operative site [3]. post-operative trauma also a responsible factor. in our case report since patients coagulation profile was normal and there is no history of any trauma in postoperative phase. since we prefer to give small cruciate incision over dura before insertion of ventricular end chance of overstretching of dura ruled out. ventricular end was inserted in first attempt so trauma to parenchyma which lead to edh has also ruled out so in our case sudden decompression of the ventricles and lowering of ict seem to be the cause of edh formation at the operative site. conclusion extradural hematoma though is very rare after shunt surgery but it must be consider as the differential diagnosis of post v-p shunt deterioration of patient. since it can be easily diagnosed and treated ncct should be done to rule it out. we also conclude that meticulous surgery for v-p shunt and routine use of the high pressure systems (90 mm to 120 mm water) to minimize sudden changes[5] and using newer ways to slower the decompression like anti-gravity can prevent such a deadly complication. 256 | garg et al post v-p shunt surgical site edh an uncommon complication correspondence dr. manish gaeg department of neurosurgery gb pant institute of postgraduate medical education and research and maulana azad medical college. full postal address: department of neurosurgery, gb pant institute of postgraduate medical education and research and maulana azad medical college, jln marg i, new delhi, india. pin code: 110002 email: manishgarg11@gmail.com references 1. alappat jp, baiju, praveen, jayakumar k, sanalkumar p. delayed extradural hematoma: a case report. 2. arq neuropsiquiatr epidural hematoma after ventriculoperitoneal shunt surgery 1998;56(3-b):629-632. 3. fujimoto y, aguiar ph, carneiro jd, martins rs, ciquini o, jr, de andrade af, et al. spontaneous epidural hematoma following a shunt in an infant with congenital factor x deficiency. case report and literature review. neurosurg rev. 1999;22:226–9. [pubmed: 10682933]. 4. kalia kk, swift dm, pang d. multiple epidural hematomas following ventriculoperitoneal shunt. pediatr neurosurg. 1993;19:78–80. [pubmed: 8443100]. 5 'o'brien ms. hydrocephalus in children. in: youman jr, ed. neurological surgery, 2nd ed. philadelphia: wb saunders, 1982; vol.3,1409-16. 6. vinay byrappa, shruti redhu, and bhadrinarayan varadarajan j neurosci rural pract. delayed incidental diagnosis of postoperative extradural hematoma following ventriculoperitoneal shunt 2015 janmar; 6(1): 94–96. doi: 10.4103/09763147.143211 pmcid: pmc4244800. 7. wolfsberger s, gruber a, czech t. multiple supratentorial epidural haematomas after posterior fossasurgery. neurosurg rev. 2004;27:128–32. [pubmed: 14652780]. 8. wu y, green nl, wrensch mr, zhao s, gupta n. ventriculoperitoneal shunt complications in california: 1990 to 2000. neurosurgery. 2007;61:557–63. [pubmed: 17881969] doi: 10.33962/roneuro-2021-055 the impact of lockdown on incidence of neurosurgery trauma patients in india ashutosh roy, somil jaiswal, b.k. ojha, chittij srivastava romanian neurosurgery (2021) xxxv (3): pp. 330-333 doi: 10.33962/roneuro-2021-055 www.journals.lapub.co.uk/index.php/roneurosurgery the impact of lockdown on incidence of neurosurgery trauma patients in india ashutosh roy, somil jaiswal, b.k. ojha, chittij srivastava department of neurosurgery, king george’s medical university, lucknow, u.p., india abstract objective: covid19 pandemic challenged the global healthcare system and both developed and developing countries responded with their might to fight this global pandemic. road traffic accidents are a major cause of morbidity and mortality in india and we studied the impact of lockdown on neurosurgery trauma patients in a tertiary care centre in india. methods: indian government announced complete lockdown on 25th march 2020 and india remained in complete lockdown till 31st may 2020. we included the patients admitted from 1st january 2020 to 24th march 2020 in pre lockdown period and25th march to in this cross-sectional study we divided the patients into two groups of pre lockdown and lockdown period and incidence of neurosurgery trauma patients was assessed for road traffic accident, assault, hit by animal and fall from height. result: in our study 491 patients were admitted in pre lockdown and 369 patients were admitted in lockdown period. road traffic accident patients were more in pre lockdown 39.5% (n=194) as compared to lockdown period 31.2% (n=115). however, cases of assaults were more in the lockdown period (14.6%, n=54) as compared to pre lockdown (3.9%, n=19). the death rate in neurosurgery trauma patients reduced significantly in lockdown (7.3%, n=27) as compared to pre lockdown (21.8%, n=107). conclusion: the covid19 pandemic induced lockdown resulted in a decrease in motor vehicle movements which further decreased the incidence of rta and related trauma however incidence of assault-related trauma and cases increased significantly in this period. the overall outcome of such patients improved probably due to better utilization of available health care facilities. introduction the first reports of covid19 disease started to appear from various parts of china and it gradually spread in european nations first and then usa while in india initial cases were reported in january 2020.1 indian government on first announced a public participation lockdown and on 24th march, 2020 ordered an unprecedented nationwide lockdown for 21 days and subsequently extended till 31st may 2020.2 this absolutely indispensable and globally appreciated rigorous lockdown froze the world's largest democracy. this lockdown made everything to stand still in a country of second largest population and keywords assault, india, lockdown, road traffic accidents, trauma corresponding author: ashutosh roy department of neurosurgery, king george’s medical university, lucknow, u.p., india ashutosh27roy@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 331 the impact of lockdown on incidence of neurosurgery trauma patients in india caused significant decrease in motor vehicular activities.3 this resulted in subsequent decrease in the cases of neurosurgery trauma patients. although india has only 1% of the motor vehicles of the world yet nearly 37000 persons died in 2019.4 impact of lockdown on cases of road side accidents and assault cases, their prevalence and the effective healthcare provided to the victims is not assessed properly in world medical literature. we tried to study the impact of lockdown on number of cases and efficacy of treatment provided to the patients admitted in india in our study. aims and objectives to study the impact of lockdown on trauma cases in a hospital in india. to study the quality of health care in terms of operations and survival of the trauma patients during covid19 pandemic and difference in level of care during and without lockdown. materials and methods this was a retrospective cross-sectional study done in our hospital which is the biggest tertiary referral centre of india. all patients who presented with history of trauma during the lockdown between 26th march 2020 to 31st may 2020 were compared with a comparative period of 67 days between 19th january 2020 to 25th march 2020. we included all the patients who presented to our trauma centre. our study was aimed to study the patients with a history of road traffic accidents (rta), fall from height, domestic accidental injuries, injuries, sports-related injuries, assault injures, or injuries caused by animals. we collected data on trauma patients from our hospital's electronic database. the following data were collected on a standard data abstraction sheet: baseline characteristics, mode of injury, type of rta, treatment given and hospital outcome. statistical analysis we analyzed the data by using a statistical package for social sciences for windows (spss inc. released 2007, version 23.0. armonk, ny, usa). dichotomous variables were compared by using the chi-square test. the factors associated with the profile of trauma patients during these two study periods were determined by bivariate logistic regression analysis and their 95% confidence intervals (ci) calculated. a two-sided p-value of less than 0.05 was considered statistically significant. observations and results in this study total 860 patients were enrolled based on inclusion and exclusion criteria. we found in this study that total 491 patients were admitted in pre lockdown and 369 in lockdown. these patients were classified into patients of rta, assault, fall from height and others. the total number of patient admitted in lockdown was less as compared to pre lockdown period in our trauma centre. (table 1) table 1. total patients admitted in pre lockdown and lockdown period (april 2021) percent total number of patients admitted percent prelockdown 491 57.1 lockdown 369 42.9 total 860 100.0 this study suggested that more young patients were reported in our causality trauma centre indicating a more burden of accidental injuries during pre lockdown period as compared to lockdown period. in this study admission of male patients was more during pre lockdown period (n= 373, 76% in pre lockdown v/s n=276, 74.3% in lockdown) as compared to lockdown which suggested that road traffic accidental trauma in males during pre lockdown period. however admission of female patients was slightly more during lockdown period (n=93, 25.2%) as compared to pre lockdown (n=118, 24%). this suggested a rising trend of injuries amongst females during lockdown which we further investigated in our study. we found that more females were subjected to assault (n=54, 14.6% during lockdown v/s n=19, 3.9% in pre lockdown) during pre lockdown period and most cases were of domestic violence. also in this study there was a slight increase in admission of children during lockdown period (n=26, 7%) as compared to pre lockdown period (n=26, 5.3%). (table2) table 2. mode of injury in patients admitted in lockdown and pre lockdown period time period total pre lockdown lockdown mode of injury fall count 66 50 116 % within lockdown 13.4% 13.6% 13.5% hit count 3 2 5 332 ashutosh roy, somil jaiswal, b.k. ojha et al. % within lockdown 0.6% 0.5% 0.6% rta count 194 115 309 % within lockdown 39.5% 31.2% 35.9% assault count 19 54 73 % within lockdown 3.9% 14.6% 8.5% others count 209 148 357 % within lockdown 42.6% 40.1% 41.5% total count 491 369 860 % within lockdown 100.0% 100.0% 100.0% in this study more patients were admitted with history of road traffic accidents (n=194, 39.5%) during pre lockdown period as compared to lockdown (n=115, 31.2%) suggesting a statistically significant fall in incidence of road traffic accidents in lockdown (p value <.05). however the admissions of patients with history of assault was more in lockdown period (n=54, 14.6%) as compared pre lockdown (n=19, 3.9%). there was a statistically significant increase in number of cases of assault in lockdown period reflected in our study. (table3) table 3. outcome of patients in lockdown versus pre lockdown period lockdown total pre post outcome left against medical advise count 72 40 112 % within lockdown 14.7% 10.8% 13.0% deaths count 107 27 134 % within lockdown 21.8% 7.3% 15.6% abscond count 7 3 10 % within lockdown 1.4% 0.8% 1.2% transferred to other departments count 40 33 73 % within lockdown 8.1% 8.9% 8.5% discharges count 265 266 531 % within lockdown 54.0% 72.1% 61.7% total count 491 369 860 % within lockdown 100.0% 100.0% 100.0% in this study the outcome of patients was improved in lockdown period with deaths due to trauma was more in pre lockdown period (n=107, 21.8%) as compared to lockdown period (n=27, 7.3%). similarly discharges were more in lockdown period (n= 266, 72.1%) as compared to pre lockdown period (n=265, 54%). discussion we worked on a hypothesis that lockdown will halt all the motor vehicular activities in the country and will cause significant decrease in cases of road traffic accidents and associated injuries.5 this was also projected in ijcmr by nandkishore m harne et al in 2020.6 as according to our hypothesis, this study also showed that patients admitted due to road traffic accidents were decreased by 8% during lockdown as compared to pre lockdown. this fall in number of road traffic cases was due to reduced vehicle activities and also due to reduced demand and supply ratio of essential commodities during lockdown period. this reduced economic activities and fall in motor vehicle accidents was also observed in other countries like uk.7 during the testing times of covid19 disease this fall in cases of accidents was a breather in terms of burden on already stretched healthcare system. we found a slight increase in pediatric populations admitted with history of trauma in our hospital between the two periods during lockdown period (n=26, 7%) as compared to pre lockdown period (n=26, 5.3%) but not significant statistically. more likely the cause of this finding was children being more at home and hence more prone to injuries and domestic violence in lockdown period.8,9 in this study we found increased incidence of assault and accidental injuries amongst females during lock down period in our study which was suggesting of increased cases of domestic violence and related assault in this section of society.10similar data was found in the studies published in lancet journal suggesting increased incidence of rage and anger during the period of lockdown mainly due to economical constraints and psychological breakdowns. increased incidence of assault has been reported in other parts of world too during lockdown.11 the pan-global lockdown has aptly been described as “the world's largest psychological experiment”.12 a review of multiple studies done on the effect of quarantine published by the lancet shows that quarantine in the past has been associated with increased fear and anger among other emotions that may have perpetrated 333 the impact of lockdown on incidence of neurosurgery trauma patients in india assaults.13 in this study we found a statistically significant difference in outcome of patients admitted with history of trauma. this study suggested that lesser number of admissions during lockdown successfully helped to provide better healthcare to these patients. conclusion this study concluded that during lockdown the number of trauma cases was decreased as compared to pre lockdown period. the cases of road traffic accidents were decreased in our hospital but the incidence of assault was increased during lockdown period. incidence of assault in case of females increased and also there was increase in injuries in pediatrics age group during lockdown period. references 1. cnn hr esha mitra and swati gupta. india places millions under lockdown to fight coronavirus. cnn. accessed may 22, 2021. https://www.cnn.com/2020/03/23/asia/corona virus-covid-19-update-india-intl-hnk/index.html 2. hebbar n. pm modi announces 21-day lockdown as covid-19 toll touches 12. the hindu. https://www.thehindu.com/news/national/pmannounces-21-day-lockdown-as-covid-19-toll-touches10/article31156691.ece. published march 24, 2020. accessed may 22, 2021. 3. gettleman j, schultz k. modi orders 3-week total lockdown for all 1.3 billion indians. the new york times. https://www.nytimes.com/2020/03/24/world/asia/indiacoronavirus-lockdown.html. published march 24, 2020. accessed may 22, 2021. 4. road accidents in india: this is what makes indian roads deadliest times of india. the times of india. accessed may 22, 2021. https://timesofindia.indiatimes.com/in dia/this-is-what-makes-indian-roads-deadliest/articlesho w/78870630.cms 5. lockdown in india: lockdown cuts road deaths by 62%. | india news times of india. accessed may 24, 2021. https://timesofindia.indiatimes.com/india/covid-lockdo wn-saved-nearly-9000-lives-26000-injuries-on-roads/ar ticleshow/76637367.cms 6. harne nm, maraskolhe ds, pandhare ml, rathod bt. lockdown versus epidemiology of orthopedic injuries: our experience at tertiary care center in central india. 2020;7(11):3. 7. uk road travel falls to 1955 levels as covid-19 lockdown takes hold | transport | the guardian. accessed may 24, 2021. https://www.theguardian.com/uk-news/2020/apr/ 03/uk-road-travel-falls-to-1955-levels-as-covid-19lockdown-takes-hold-coronavirus-traffic 8. christey g, amey j, campbell a, smith a. variation in volumes and characteristics of trauma patients admitted to a level one trauma centre during national level 4 lockdown for covid-19 in new zealand. n z med j. 2020;133(1513):81-88. 9. hernigou j, morel x, callewier a, bath o, hernigou p. staying home during “covid-19” decreased fractures, but trauma did not quarantine in one hundred and twelve adults and twenty eight children and the “tsunami of recommendations” could not lockdown twelve elective operations. int orthop. 2020;44(8):1473-1480. doi:10.1007/s00264-020-04619-5 10. jacob s, mwagiru d, thakur i, moghadam a, oh t, hsu j. impact of societal restrictions and lockdown on trauma admissions during the covid-19 pandemic: a singlecentre cross-sectional observational study. anz j surg. 2020;90(11):2227-2231. doi:10.1111/ans.16307 11. hatchimonji js, swendiman ra, seamon mj, nance ml. trauma does not quarantine: violence during the covid-19 pandemic. ann surg. 2020;272(2):e53-e54. doi:10.1097/sla.0000000000003996 12. lockdown is the world’s biggest psychological experiment and we will pay the price. world economic forum. accessed may 24, 2021. https://www.weforum.org/agenda/2020/04/this-is-thepsychological-side-of-the-covid-19-pandemic-that-wereignoring/ 13. brooks sk, webster rk, smith le, et al. the psychological impact of quarantine and how to reduce it: rapid review of the evidence. the lancet. 2020;395(10227):912-920. doi:10.1016/s0140-6736(20)30460-8. https://timesofindia.indiatimes.com/in microsoft word 5cucuai_prognostic romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article prognostic factors in atypical meningioma a.i. cucu, claudia florida costea, i. poeată, dana mihaela turliuc romania doi: 10.1515/romneu-2017-0025 romanian neurosurgery (2017) xxxi 2: 165 171 | 165             doi: 10.1515/romneu-2017-0025 prognostic factors in atypical meningioma a.i. cucu1, claudia florida costea1,2, i. poeată1,2, dana mihaela turliuc1,2 1“prof. dr. n. oblu” emergency clinical hospital of iaşi, romania 2“grigore t. popa” university of medicine and pharmacy of iaşi, romania abstract: atypical meningioma represent an intermediary group between the benign meningioma (grade i) and anaplastic meningioma (grade iii), and are known for high recurrence rate and short life expectancy. after modification of the classification world health organization in 2007, subsequent studies have tried to find prognostic factors for recurrence and survival, which are inconstant from author to author. this paper aims to present a short review of the most important prognostic factors in atypical meningioma. key words: atypical meningioma, prognostic factors, survival, recurrence introduction atypical meningioma (am) represent an intermediate risk group between benign (grade i) and anaplastic meningioma (grade iii), being known for their tendency to relapse after the surgery (42, 54, 66) and increased morbidity and mortality (24, 37, 54, 63). the rarity of am cases and the inconsistent histological criteria in time regarding their definition led to the difficult understanding of the management of these types of tumours, especially of the prognostic factors (2, 10, 20, 40, 43, 47). moreover, in recent years it has been noticed an increase in the number of am diagnostics (13, 48) and that is why, in view of an adequate management, it is necessary to clarify the factors of prognostic in am. incidence intracranial meningiomas represent about one third of the primary brain tumours (13, 34), being the most frequent intracranial primary benign tumours (5, 7, 31). among them, am represents about 4.7-7.2% of all meningioma diagnoses (33). after introducing the classifications of world health organization (who) from 2000 and 2007, the percentage of am increased to 20-30% among all the meningiomas (47, 48, 65). willis et al., in a study on 314 patients for a period of ten years (1994-2003), concluded that if in agreement with who grading system (1993) am represented 5-7%, according to the new criteria who (2000), they represented 20.4% (65). 166 | cucu et al prognostic factors in atypical meningioma             the anatomo-pathological evolution of am the existence of am and malign meningioma was recognized from 1938, when cushing and eisenhardt reported a type of meningioma with mean survival rate of 2.5 years (63). the concept of “atypical grade ii meningioma” was introduced for the first time in 1985 by professor juha jääskeläinen from finland (25). in 1990, mayo clinic group suggested a set of criteria for am, where the absence of anaplasia, an important predicting factor for recurrence was the cerebral invasion (53). three years later, in 1993, who included am (grade ii) as intermediary category between the benign meningioma (grade i) and anaplastic or malign meningioma (grade iii). nevertheless, in 1993 the criteria who were not implemented at large scale (48). even though cushing recognized since the 1930s the malign potential of meningiomas (11), no uniform system of classification was accepted until 2000, when the classification who became more objective and reproducible (34). it was followed by the revision who in 2007, when the criteria of brain invasion became additional criterion in am, even in the absence of anaplasia or atypia (49). in 2016, who upgraded the classification of meningiomas from 2007 (33). according to this new classification (32), based on three histological grades, am were divided into: benign meningioma (grade i), atypical meningioma (grade ii) and malignant meningioma (grade iii). currently, the criteria of diagnostic for am are: clear or chordoid cell histology, brain infiltration, 4 to 19 mitoses per 10 high-power fields, or 3 or more of the following: increased cellularity, necrosis, small cell change, prominent nucleoli and “sheetlike” growth (33). the classification who of meningioma from 2016 reinforced “brain infiltration” as a stand-alone histological feature for am (32, 62). factors of prognostic in am the factors of prognostic in am can be divided into: demographic (age, gender), clinical, factors of prognostic related to the morphology of the tumour (location of tumour, tumour dimensions, anatomopathological characteristics) and prognostic factors related to the degree of surgery resection (table i). i. demographic factors of prognostic (age, gender) age. current studies have proved that the age of the patient with am can be considered a factor of prognostic related to the survival (14, 56, 68). furthermore, some studies have proved that an increased age at diagnosis was a factor of poor prognostic for recurrence (3, 4, 8, 9, 14, 18, 56, 68), some authors mentioning even the age > 65 as being the age limit for poor prognosis (28, 47). zaher et al. has proved that age < 50 is a good factor of prognostic for overall survival (oas) (68), and durand et al. has found as well as a factor of good prognostic the age < 60 (14). on the other hand, aboukais et al. has not found any difference between progressionfree survival (pfs) in relation to the age at diagnostic (1). gender. unlike benign meningiomas that romanian neurosurgery (2017) xxxi 2: 165 171 | 167             seem rather linked to oestrogen levels and thus more frequent in women, am have different gender demographics, mainly larger in men (19, 35, 64, 70). as for gender as factor of prognostic, the studies are inconsistent. if some authors consider that male gender represents a risk factor for a shorter survival (61), others have reported that on the contrary, female gender would represent a predicting factor for recurrence, having a relapse rate twice as bigger that in male gender (69). ii. clinic factors of prognostic (motor deficit, karnofsky performance status scale) related to admission simptoms, zhao et al. concluded that the neurologic deficit (paresis) can be considered a factor of poor prognostic, since these patients had a higher tendency to relapse than the patients with other symptoms (69). also, the karnofsky performance status scale (kps) was taken into account as factor of prognostic. thus, zhao et al. proved that the patients with kps >80 presented a higher pfs comparing with the patients with kps < 80 (69). iii. factors of prognostic related to the morphology of the tumour (tumour location, the dimensions of the tumour, the anatomopathological characteristics) tumor location. am at the level of the cerebral convexity was associated with a longest survival, and it was correlated with the total excision made in case of locating the tumour (45, 55, 68). on the other hand, parasagittal-falcine location of am led to an increase of recurrence, probably because of the residual tumour along the superior sagittal sinus (61). dimensions of the tumour. another factor of prognostic that influences the survival was found the size of the tumour (12, 18). garzonmuvdi et al. noticed that in tumour with dimensions between 50 and 100 mm there is a decrease of survival by the increase of morbidity and mortality (18). anatomo-pathological characteristics. with the classification who in 2007, the relation between the histological grade of the meningioma and the outcome has become even stronger, studies on long series confirming it (22, 53). the proliferative activity of meningiomas is measured with ki-67 labelling index (li), considered as a potential instrument to establish the recurrence of meningiomas (22, 26, 44). the ki-67 index proved in a study as being the strongest distinguishing criterion between atypical and classical and anaplastic meningioma (29). also, the immunohistochemical overstaining for mib-1 antigen, cdk4, cdk6, p53, p16, p21, prb protein, cyclin d1 and mitotic index were proved to be factors of prognostic, showing a statistically higher recurrence rate and also a shorter time of recurrence versus understaining (27, 58, 59, 60). among them, higher mib-1 li proved to be the strongest indicator for poor outcome in am (16, 46, 47, 61). also, other anatomopathological and immunohistochemical factors with role of factors of prognostic were also discovered, mitosis and osteopontin (6, 30). when mitosis is closer to 20 per 10 highpower fields, it reflects biology of tumour more aggressive comparing with low mitosis (6). osteopontin, a protein involved in tumour progression was proved to be correlated with 168 | cucu et al prognostic factors in atypical meningioma             poor clinical outcome and as predictor of am (30). iv. factors of prognostic related to surgery resection the extent of surgery was reported as being the most important predictor of outcome in patients with meningiomas by reducing both the mortality and the recurrence (3, 14, 15, 19, 20, 21, 23, 34, 38, 47, 53, 57, 67, 68). the extent of resection (simpson grading) was proved to be a factor of prognostic also in respect to the oas. thus, survival proved to be significantly higher in patients with gross total resection (gtr) (that most authors consider to be simpson grade 1, 2) than those with subtotal resection (str) (simpson grade 3, 4) (1, 14, 17, 20, 27, 36, 46, 68, 69). also, studies have shown that pfs was better in patients with subtotal resection (simpson grade 3, 4) comparing with biopsy only (simpson grade 5) (28, 45, 56, 68). on the other hand, pasquier et al. concluded in their study that the extent of surgery resection was not a factor of prognostic for the meningiomas of grade ii and iii, but its statistic analysis was done on the whole group, without distinction between the grades (47). related to the bone invasion of the meningioma, even though initially it was not accepted as factor of prognostic in am (41), gabeau-lacet et al. and ho et al. proved that it can be an important predictor of poor treatment outcome (17, 22). prognostic patients with am have a poor prognosis and increased mortality, with a median survival rate lower than 2 years (33). also, patients with secondary am have a risk of recurrence three times higher (69) and a rate of death at 3-5 years twice as higher (50, 51, 52) and about 10-30% of the am undergoing transformation to who grade iii (39, 67). table i prognostic factors in am (recent studies) year author no. cases prognostic factors for survivals prognostic factors for recurrence 2016 endo (16) 45 age, degree of resection, mib1-li age, mib1-li 2015 zhao (69) 89* degree of resection, kps paresis, secondary meningioma, female 2014 hammouche (20) 79 degree of resection 2013 aboukais (1) 167 degree of resection 2013 park (46) 83 age degree of resection mib1-li 2013 zaher (68) 44 degree of resection, age degree of resection 2011 mair (36) 114 degree of resection 2010 vranic (61) 86* male, parasagittal-falcine location brain invasion, parasagittal-falcine location, high mitotic index 2009 durand (14) 166 degree of resection, age degree of resection, age 2009 gabeau-lacet (17) 47 age, bone involvement degree of resection, bone involvement 2008 pasqueir (47) 119* age, kps, high mitotic index kps, high mitotic index *atypical and anaplastic meningioma romanian neurosurgery (2017) xxxi 2: 165 171 | 169             conclusion many of the factors of prognostic for survival or recurrence, as well as the resection extent, histopathological characteristics, age, gender or patient’s symptoms on admission remain still unclear and must be verified in larger cohorts. correspondence claudia florida costea “prof. dr. n. oblu” emergency clinical hospital iasi, romania email: costea10@yahoo.com references 1.aboukais r, baroncini m, zairi f, reyns n, lejeune jp. early postoperative radiotherapy improves progression free survival in patients with grade 2 meningioma. acta neurochir (wien). 2013; 155(8): 1385-1390. 2.aghi mk, carter bs, cosgrove gr, et al. long-term recurrence rates of atypical meningiomas after gross total resection with or without postoperative adjuvant radiation. neurosurgery. 2009; 64(1): 56-60. 3.aizer aa, bi wl, kandola ms, et al. extent of resection and overall survival for patients with atypical and malignant meningioma. cancer. 2015; 121: 4376-4381. 4.aizer aa, arvold nd, catalano p, et al. adjuvant radiation therapy, local recurrence, and the need for salvage therapy in atypical meningioma. neuro oncol. 2014; 16(11): 1547-1553. 5.bondy m, ligon bl. epidemiology and etiology of intracranial meningiomas: a review. j neurooncol. 1996; 29: 197-205. 6.bruna j, brell m, ferrer i, et al. ki67 proliferative index predicts clinical outcome in patients with atypical or anaplastic meningioma. neuropathology. 2007; 27: 114120. 7.cbtrus. statistical report: primary brain tumors in the united states, 1998–2002. central brain tumor registry of the united states, hinsdale. 2005. 8.champeaux c, dunn l. world health organization grade ii meningioma: a 10-year retrospective study for recurrence and prognostic factor assessment. world neurosurg. 2016; 89: 180-186. 9.champeaux c, wilson e, shieff c, et. al. who grade ii meningioma: a retrospective study for outcome and prognostic factor assessment. j neurooncol. 2016; 129(2): 337-345. 10.cleary c, curtin d. giant atypical intraventricular meningioma presenting with visual loss in a child. ir j med sci. 2010; 179: 617-619. 11.cushing hw, eisenhardt l. meningiomas: their classification, regional behavior, life history, and surgical end results. springfield, ill: charles c thomas, 1938. 12.detti b, scoccianti s, di cataldo v, et al. atypical and malignant meningioma: outcome and prognostic factors in 68 irradiated patients. j neurooncol. 2013; 115:421427. 13.dolecek ta, propp jm, stroup ne, kruchko c. cbtrus statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2005–2009. neuro oncol. 2012; 14(5): 1-49. 14.durand a, labrousse f, jouvet a, et al. who grade ii and iii meningiomas:a study of prognostic factors. j neurooncol. 2009; 95: 367-375. 15.dziuk tw, woo s, butler eb, et al. malignant meningioma: an indication for initial aggressive surgery and adjuvant radiotherapy. j neurooncol. 1998; 37: 177188. 16.endo t, narisawa a, ali hs, et al. a study of prognostic factors in 45 cases of atypical meningioma. acta neurochir (wien). 2016; 158(9): 1661-1667. 17.gabeau-lacet d, aghi m, betensky ra, barker fg, et al. bone involvement predicts poor outcome in atypical meningioma. j neurosurg. 2009; 111: 464–471. 18.garzon-muvdi t, yang w, lim m, et al. atypical and anaplastic meningioma: outcomes in a population based study. j neurooncol. 2017; online. 19.goyal lk, suh jh, mohan ds, et al. local control and overall survival in atypical meningioma: a retrospective study. int j radiat oncol biol phys. 2000; 46: 57–61. 20.hammouche s, clark s, wong ah, et al. long-term survival analysis of atypical meningiomas: survival rates, prognostic factors, operative and radiotherapy treatment. acta neurochir (wien). 2014; 156(8): 1475-1481. 21.hardesty da, wolf ab, brachman dg, et al. the impact of adjuvant stereotactic radiosurgery on atypical 170 | cucu et al prognostic factors in atypical meningioma             meningioma recurrence following aggressive microsurgical resection. j neurosurg. 2013; 119: 475-481. 22.ho dm, hsu cy, ting lt, chiang h. histopathology and mib-1 labeling index predicted recurrence of meningiomas: a proposal of diagnostic criteria for patients with atypical meningioma. cancer. 2002; 94: 1538-1547. 23.hug eb, devries a, thornton af, et al. management of atypical and malignant meningiomas: role of highdose, 3d-conformal radiation therapy. j neurooncol. 2000; 48:151-160. 24.iacob g, craciun m. atypical meningioma. romanian neurosurgery. 2012; xix 3: 203-209. 25.jääskeläinen j, haltia m, laasonen e, et al. the growth rate of intracranial meningiomas and its relation to histology. an analysis of 43 patients. surg neurol. 1985; 24: 165-172. 26.karamitopoulou e, perentes e, diamantis i, maraziotis t. ki-67 immunoreactivity in human central nervous system tumors: a study with mib1 monoclonal antibody on archival material. acta neuropathol. 1994; 87: 47-54. 27.kim ms, kim kh, lee eh, et al. results of immunohistochemical staining for cell cycle regulators predict the recurrence of atypical meningiomas. j neurosurg. 2014; 121(5): 1189-1200. 28.kim y, ketter r, henn w, et al. histopathologic indicators of recurrence in meningiomas: correlation with clinical and genetic parameters. virchows arch. 2006; 449: 529-538. 29.kolles h, niedermayer i, schmitt c, et al. triple approach for diagnosis and grading of meningiomas: histology, morphometry of ki-67/feulgen stainings, and cytogenetics. acta neurochir (wien). 1995; 137: 174-181. 30.lin ck, tsai wc, lin yc, hueng dy. osteopontin predicts the behaviour of atypical meningioma. histopathology. 2012; 60: 320-325. 31.longstreth wt jr, dennis lk, mcguire vm, et al. epidemiology of intracranial meningioma. cancer. 1993; 72: 639-648. 32.louis dn, perry a, reifenberger g, et al. the 2016 world health organization classification of tumors of the central nervous system: a summary. acta neuropathol. 2016; 131(6): 803-820. 33.louis dn, ohgaki h, wiestler od, et al. the 2007 who classification of tumours of the central nervous system. acta neuropathol. 2007; 114: 97-109. 34.louis dn, scheithauer bw, budka h, et al. meningiomas. in: khleihues p, cavenee wk (eds) who classification of tumours pathology and genetics tumours of the nervous system. lyon: iarc press, 2000. 35.mahmood a, caccamo dv, tomecek fj, malik gm. atypical and malignant meningiomas: a clinicopathological review. neurosurgery. 1993; 33: 955963. 36.mair r, morris k, scott i, carroll ta. radiotherapy for atypical meningiomas. j neurosurg. 2011; 115(4): 811819. 37.mangubat ez, byrne rw. major intratumoral hemorrhage of a petroclival atypical meningioma: case report and review of literature. skull base. 2010; 20: 469473. 38.marcus hj, price sj, wilby m, et al. radiotherapy as an adjuvant in the management of intracranial meningiomas: are we practising evidence-based medicine? br j neurosurg. 2008; 22: 520-528. 39.mattozo ca, de salles aa, klement ia, et al. stereotactic radiation treatment for recurrent nonbenign meningiomas. j neurosurg. 2007; 106(5): 846-854. 40.mawrin c, perry a. pathological classification and molecular genetics of meningiomas. j neurooncol. 2010; 99: 379-391. 41.miller dc. predicting recurrence of intracranial meningiomas. a multivariate clinicopathologic model interim report of the new york university medical center meningioma project. neurosurg clin n am. 1994; 5(2): 193-200. 42.modha a, gutin ph. diagnosis and treatment of atypical and anaplastic meningiomas: a review. neurosurgery. 2005; 57(3): 538-550. 43.monleon d, morales jm, gonzalez-segura a, et al. metabolic aggressiveness in benign meningiomas with chromosomal instabilities. cancer res. 2010; 70: 84268434. 44.ohta m, iwaki t, kitamoto t, et al. mib1 staining index and scoring of histologic features in meningioma. cancer. 1994; 74: 3176-3189. 45.palma l, celli p, franco c, et al. longterm prognosis for atypical and malignant meningiomas: a study of 71 surgical cases. neurosurg focus. 1997; 2(4):e3. 46.park hj, kang hc, kim ih, et al. the role of adjuvant radiotherapy in atypical meningioma. j neurooncol. 2013; 115(2): 241-247. 47.pasquier d, bijmolt s, veninga t, et al. atypical and romanian neurosurgery (2017) xxxi 2: 165 171 | 171             malignant meningioma: outcome and prognostic factors in 119 irradiated patients. a multicenter, retrospective study of the rare cancer network. int j radiat oncol biol phys. 2008; 71: 1388-1393. 48.pearson be, markert jm, fisher ws, et al. hitting a moving target: evolution of a treatment paradigm for atypical meningiomas amid changing diagnostic criteria. neurosurg focus. 2008; 24:e3. 49.perry a, louis dn, scheithauer bw, et al. meningeal tumours. in: louis dn, ohgaki h, wiestler od, cavenee wk (eds) who classification of tumours of the central nervous system. lyon: iarc press, 2007. 50.perry a. meningiomas. in: mclendon r, rosenblum m, bigner dd (eds) russell & rubinstein’s pathology of tumors of the nervous system. london: hodder arnold, 2006. 51.perry a, gutmann dh, reifenberger g. molecular pathogenesis of meningiomas. j neurooncol. 2004; 70(2): 183-202. 52.perry a. unmasking the secrets of meningioma: a slow but rewarding journey. surg neurol. 2004; 61(2): 171-173. 53.perry a, scheithauer bw, stafford sl, et al. “malignancy” in meningiomas: a clinicopathologic study of 116 patients, with grading implications. cancer 1999; 85(9): 2046-2056. 54.perry a, stafford sl, scheithauer bw, et al. meningioma grading: an analysis of histologic parameters. am j surg pathol. 1997; 21:1455-1465. 55.pisćević i, villa a, milićević m, et al. the influence of adjuvant radiotherapy in atypical and anaplastic meningiomas: a series of 88 patients in a single institution. world neurosurg. 2015; 83: 987-995. 56.sade b, chahlavi a, krishnaney a, et al. world health organization grades ii and iii meningiomas are rare in the cranial base and spine. neurosurgery. 2007; 61: 11941198. 57.simpson d. the recurrence of intracranial meningiomas after surgical treatment. j neurol neurosurg psychiatry. 1957; 20(1): 22-39. 58.smith js, lal a, harmon-smith m, et al. association between absence of epidermal growth factor receptor immunoreactivity and poor prognosis in patients with atypical meningioma. j neurosurg. 2007; 106(6): 10341040. 59.sun sq, kim ah, cai c, et al. management of atypical cranial meningiomas, part 1: predictors of recurrence and the role of adjuvant radiation after gross total resection. neurosurgery. 2014; 75(4): 347-354. 60.sun sq, cai c, murphy rk, et al. management of atypical cranial meningiomas, part 2: predictors of progression and the role of adjuvant radiation after subtotal resection. neurosurgery. 2014; 75(4): 356-363. 61.vranic a, popovic m, cor a, et al. mitotic count, brain invasion, and location are independent predictors of recurrence-free survival in primary atypical and malignant meningiomas: a study of 86 patients. neurosurgery. 2010; 67:1124–1132. 62.wang c, kaprealian tb, suh jh, et al. overall survival benefit associated with adjuvant radiotherapy in who grade ii meningioma. neuro oncol. 2017. online 63.whittle ir, smith c, navoo p, collie d. meningiomas. lancet. 2004; 363: 1535-1543. 64.wiemels j, wrensch m, claus eb. epidemiology and etiology of meningioma. j neurooncol. 2010; 99: 307-314. 65.willis j, smith c, ironside jw, et al. the accuracy of meningioma grading: a 10-year retrospective audit. neuropathol appl neurobiol. 2005; 31: 141-149. 66.yamasaki f, yoshioka h, hama s, et al. recurrence of meningiomas. cancer. 2000. 89: 1102-1110. 67.yang sy, park ck, park sh, et al. atypical and anaplastic meningiomas: prognostic implications of clinicopathological features. j neurol neurosurg psychiatry. 2008; 79: 574-580. 68.zaher a, abdelbari mattar m, zayed dh, et al. atypical meningioma: a study of prognostic factors. world neurosurg. 2013; 80: 549-553. 69.zhao p, hu m, zhao m, et al. prognostic factors for patients with atypical or malignant meningiomas treated at a single center. neurosurg rev. 2015; 38: 101-107. 70.zhou p, ma w, yin s, et al. three risk factors for who grade ii and iii meningiomas: a study of 1737 cases from a single center. neurol india. 2013; 61: 40-44. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 432 | raheja, satyarthee chronic subdural hematoma development in chronic myeloid leukemia spontaneous chronic subdural hematoma development in chronic myeloid leukemia cases at remission phase under maintenance therapy, management strategy a series with literature review amol raheja, guru dutta satyarthee department of neurosurgery, neurosciences centre, all india institute of medical sciences, new delhi, india abstract: chronic subdural hematoma (csdh) is common squeal of trauma and rarely associated with anticoagulant therapy, antiplatelet, chemotherapeutic drugs, arteriovenous malformation, aneurysms and post-craniotomy. however its occurrence is very unusual with systemic haematological malignancy and mostly reported with acute myeloid leukemia; however incidence of sdh occurrence in chronic myelogenous leukemia (cml) is very rare. cml is a haematological malignancy characterized by chromosomal alteration, pathologically represents increased proliferation of the granulocytic cell line without loss of capacity to differentiate. cml has three phases – remission phase, accelerated phase and blast crisis. about 85 % of patients present in remission phase of disease and carries a favorable prognosis. as intracranial, subdural hematoma usually occur in the accelerated phase or blast crisis phase or extremely uncommon during chronic remission phase, although only those affected, who are neglecting therapeutic medication or discontinued therapy or rarely as an adverse effect of medications. however, important role of neurosurgeon lies in early detection and correction of platelet count and associated hematological abnormality as quite sizeable proportion of cases may not need surgical intervention instead can be managed conservatively under regular supervision in association with oncologist colleague, but few cases may need urgent surgical intervention. so, selecting a subgroup of cml cases in the remission phase requiring surgical intervention, presenting with csdh is not only challenging, as failure to make an informed and timely precise decision can lead to catastrophic worse outcome and even mortality. so, purpose of current article is to formulate the management therapeutic plan. authors report three cases of cml in chronic remission phase, receiving treatment under guidance of haemto-oncologist at our institute presented with spontaneous chronic sdh. the mean age was 36 years (range 2944 years), 66% were male, headache was presenting feature in all 100% (n=3), 66% cases were hemiplegic and 33% unconscious each, in 66% cases csdh were located on right fronto-temporal region and 33% had small left sided thin csdh. about were romanian neurosurgery (2016) xxx 3: 432 440 | 433 66% cases (n=2) were managed surgically by burr hole placement and drainage drain placement while 33% case (n=1), who had thin csdh was managed conservatively. favorable outcome was observed in 100% cases (n=3) outcome was favorable in all of our cases. key words: chronic myeloid leukemia, remission phase, chronic subdural hematoma, management introduction chronic subdural hematoma (csdh) is an important cause of morbidity and usually caused by previous trauma, post-craniotomy surgery, thrombocytopenia, chronic alcoholism, radiation induced or intake of various medications including anticoagulants, antiplatelets or following rupture of intracranial aneurysms (1-4, 5), arteriovenous malformations (5) and cocaine drug abuser (8). it is very rarely reported to occur with intracranial neoplasms like meningioma (10), rhabdomyosarcoma (15). association of c sdh is reported with lymphoma (16), choriocarcinoma (18), however, its occurrence is very unusual with systemic haematological malignancy and mostly occurred in association with acute myeloid leukemia. csdh occurrence is extremely uncommon in chronic myeloid leukemia (cml), but few cases are reported in form of isolated case –report, tend to occur only in the accelerated phase of cml authors present three cases of chronic sdh occurrence in chronic remission phase of cml, who were treated at hemato-ontological clinic, were in the remission phase of cml, developed csdh, managed successfully. case illustration one a 35 year male reported with complains of with insidious onset gradually progressive headache, vomiting, left sided hemiparesis and altered sensorium for last two weeks with no antecedent history of trauma, alcohol or oral anticoagulants or antiplatelets intake. he was diagnosed as case of cml, about 18 weeks back. at present, he was in the chronic remission phase receiving maintenance dose of oral tyrosine kinase inhibitor imatinib mesylate. on neurological examination at admission, he was drowsy with glasgow coma score (gcs) of 13 with pupils’ bilaterally normal size and briskly reacting to light. left sided seventh nerve upper motor neuron paresis and spastic hemiparesis along with brisk deep tendon jerks and plantar were bilaterally extensor. haematological investigations were within normal limit with mild leucocytosios. ct scan head, revealed presence of right sided fronto-parietal hypodense chronic sdh, volume were about 60 ml and causing mass effect with 8 mm midline shift to the left (figure 1). a right frontal and parietal burr hole were made and hematoma evacuation was carried out under local anesthesia and intravenous sedation. post-operative ncct head subsidence of mass effect with no residual csdh. he gradually improved clinically and was discharged in stable condition with gcs of 15. he was re-admitted with similar complaints of headache and right sided 434 | raheja, satyarthee chronic subdural hematoma development in chronic myeloid leukemia weakness 6 months later. hemogram and coagulation profile were within normal limits. repeat ncct head, showed mixed density fronto-parietal sdh on contra lateral left side (figure 2). magnetic resonance imaging (mri) was carried out to rule out brain parenchyma lesion which revealed presence of sub-acute subdural hematoma over left frontoparietal region (figure 3). he underwent left sided frontal and parietal burr hole and hematoma evacuation with uneventful recovery. histopathology report and cytopathological analysis of subdural fluid were inconclusive for any malignant infiltration of dura mater or subdural membrane or subdural fluid. he was doing well without any further recurrence; however, maintenance medication for cml was continued in consultation with haematology department. patient was still in chronic phase at twelve months following first surgery. figure 1 pre-operative non-contrast ct scan head showing right sided hypodense chronic sdh, extending over fronto-parietal region causing mass effect (case 1) figure 2 repeat non-contrast ct scan head at six months following first surgical burr hole drainage showing fresh sdh development on contralateral side located overleft fronto-parietal area (case 1 ) figure 3 mri brain, t2wi,axial section at six months follow-up to correlate ct findings, following first surgical evacuation of sdh showing no residual sdh ,but newly developed sdh on contralateral side located overleft frontoparietal region (case 1 ). case illustration two a 44 year male was referred to neurosurgical emergency services from romanian neurosurgery (2016) xxx 3: 432 440 | 435 haematology department with outpatient department with complains of persistent headache and progressive left hemiparesis for one month. no other relevant history or co morbid illness was elicited. he was diagnosed with cml about one year back and presently in chronic remission phase on maintenance therapy. on neurological evaluation, his gcs was 15/15, with left sided upper motor neuron type facial nerve paresis. power in left upper and lower limb was 4/5. haematological parameters were within normal limits. ct scan head revealed presence of chronic sdh in right fronto-temporo-parietal region measuring approximately 45 ml with mass effect and midline shift of 5 mm. he underwent elective burr whole drainage of sdh. intra-operative, altered blood with thickened pseudo-membrane surrounding it. histopathogical evaluation of dural membrane biopsy and cytopathology of subdural fluid was also non-contributory. post-operative ncct head showed nearcomplete evacuation of sdh and relief of mass effect. he had uneventful postoperative phase with recovery of hemiparesis. he tolerated surgical procedure well. at the last followup 6 months following surgery, he was doing well and continuing to receive maintenance therapy of tyrosine kinase inhibitor. case illustration three a 29 year old female reported our outpatient services with gradually worsening headache for 3 weeks. she also had no other significant history except diagnosis of with cml, six months back and currently on in chronic phase on maintenance therapy under supervision of haematologist. neurological examination was unremarkable and haematological investigations showed platelet count and coagulation profile within normal limit. ncct head revealed hypodense left side thin fronto-temporal chronic sdh measuring about 15 ml. (figure 4) the findings were confirmed on mri (figure 4). she responded well to conservative management without further increase in size. she was kept on regular followup on outpatient services basis for six months till her follow up ct scan revealed complete resolution of hematoma. figure 4 non-contrast enhanced mri brain t1wi, axial section hyperintense signal intensity , sdh showing over left side fronto-temporal area (case3) discussion chronic myelogenous leukemia (cml) is a haematological malignancy characterized by chromosomal alteration, typically showing reciprocal translocation between chromosomes 9 and 22, observed approximately in 90% cases. pathologically 436 | raheja, satyarthee chronic subdural hematoma development in chronic myeloid leukemia represents increased proliferation of the granulocytic cell line without loss of capacity to differentiate. the clinical course of cml can be subclassified into three phases – chronic phase, accelerated phase and blast crisis. about 85 % of patients of chronic remission phase carry a favorable prognosis, if kept on longterm tyrosine kinase inhibitors maintenance therapy. however, chronic stage can also progress to either accelerated phase or blast crisis phase accompanying with unfavorable prognosis, if left untreated in chemotherapeutic resistant cases. predominant factor for differentiating among both phases is presence of 10-19 % myeloblasts and greater than 20 % myeloblasts in peripheral blood smear or bone marrow examination in former and latter respectively (7, 20). however, with advent of newer selective tyrosine kinase inhibitors, treatment of cml is revolutionized with improved outcome, 80-90 % longterm survival rates. (12) during course of therapy very few cases may develop major intracranial bleeding, who were receiving medication for cml treatment under combined supervision of haematologist and oncologist. chronic subdural haematoma contains an inner and an outer capsule. the capillary endothelial cells lining of capsules contains cytoplasmic protrusions and fenestrations. mean age in the present series was 36 years (range 29-44 years) compared to 50 years as mean age at presentation, with male to female ratio was 2:1 compared to 1.3: 1 as reported in jonte et al series. (6) patients in chronic phase of disease had favorable outcome with 100% survival rate during short term follow up. authors advocated further evaluated of these cases should be carried to rule out systemic haematological malignancy. (6) spontaneous sdh occurrence in association with solid malignancy may have additional history of precipitating factors like head injury, however such history is usually absent in haematological malignancy specifically acute myeloid leukemia (14); although rare, an only very few cases have been reported in association with other systemic haematological malignancy (1, 2, 3, 9, 11, 17, 19). exact mechanism of sdh occurrence in is still debated, various postulates are put forward including – malignant cell deposits causing occlusion of dural blood vessels, rupture of occluded dural blood vessels into subdural space and tumor necrosis in metastatic deposits, thrombocytopenia secondary to chemotherapeutic agent therapy, development of disseminated intravascular coagulation disorder. even direct secondary dural leukemic deposits are postulated to explain repeated recurring sdh following surgical intervention. our first case had right sided frontotemporal csdh and after six months following evacuation, developed csdh on contralateral side necessitating surgical intervention on that side also. cases with diagnosed case of cml, who are put chemotherapeutic treatment, may carry increased risk of intracranial haemorrhage depending on stage of primary disease. in a study conducted by druker et al, observed incidence of intracranial haemorrhage in cml romanian neurosurgery (2016) xxx 3: 432 440 | 437 patients, who are on medical treatment in the range of – 5 % in blast crisis phases, 1 % in accelerated phase and almost negligible risk of 0.6 % in the chronic remission phase. (4). the occurrence of chronic sdh in chronic phase of disease is extremely uncommon. however, our cases were very unique as all were in chronic remission phase, who were on regular treatment under care of haematologist supervision receiving tyrokinase inhibitor imatinib mesylate or dasatinib, according to optimal requirement in response to therapy. however, histopathological evaluation of biopsy specimen of dural membrane ruled out presence of any malignant cell deposit and further cytopathology of subdural fluid was negative for malignant cells in all our cases. however, mechanism of intracranial bleed remains elusive despite presence of normal haematological parameters i.e., platelet count and coagulation profile, dysfunction of platelet aggregation and reduced α2-plasmin inhibitor factors and even acquired van will brand disease was are also incriminated. (9, 13) giuffrè suggested role hormonal factors, in addition to mechanical, hematogenic and vasogenic factors, could play an important role in the pathogenesis of these hematomas. (21) csdh can either increase in volume size and clinically presents with focal neurological deficit and mass effect or extremely rarely cam even show slowly resolution over time. mechanism of gradual progression in size of the chronic subdural haematomas were attributable to csf passage caused due to osmolarity gradient, which in turn caused by blood degradation products. however, recently proposed mechanism attribute to leaking capillaries causing repeated microhaemorrhgaes taking place into the haematoma cavity. the leaking component may exceed the resorptive capacity of chronic subdural haematomas, leading to its enlargement all of our patients were clinically and haematologically in remission phase with strict supervision and guidance of therapy under haematologist at our institute. all the patients had platelet counts and coagulation profile within normal range. (21) these may be cause of deterioration of our two cases, treatment of subdural hematoma is usually surgical evacuation in symptomatic cases, however, csdh occurring secondary to coagulation disorder or hematological malignancy may even responds to correction of haematological abnormality and with relief of mass effect or resolution of asdh even without any need of surgical intervention. as our two cases needed surgery and 33 % cases responded to conservative treatment. surgical approach of csdh management include burr whole craniostomy with or without drain placement, mini craniotomy or rarely craniotomy and excision of thick membrane in those cases with extremely thick membrane or repeated failure of burr whole craniostomy. in the current study, two out of three cases, required surgical evacuation of sdh and underwent burr whole evacuation by placing frontal and parietal burr holes and irrigation and drain was also kept for three days following surgical procedure. in the postoperative period scan revealed complete evacuation. fortunately third case did not required surgical intervention. our cases had 438 | raheja, satyarthee chronic subdural hematoma development in chronic myeloid leukemia no complication except one case (case1), who during follow-up period, developed new onset csdh on contralateral side at six month following initial surgery, which also required surgical evacuation and all three cases are under regular follow-up on maintenance therapy under hemato oncologist. prognosis of cml associated with csdh in remission phase is definitely better than the blast or crisis phase. in 2015 authors reported development of csdh ma during accelerated phase of chronic myeloid leukemia presented with seizure, who had and rapid progression course and had fatal outcome despite surgical intervention, however, csdh was diagnosed after a delay, accordingly author further recommends timely selection of potential surgical candidate as requirement of asdh is critical in addition to timely surgery to provide for good neurological outcome along with high degree of suspicion is must. (23) table i summary of chronic myeloid leukemia cases, who developed chronic subdural hematoma and management outcome sl. no age (year) /sex clinical features ncct head cml stage/ chemotherapy interval of sdh occurrence followings diagnosis of cml hematologi cal investigation managemen t follow-up remark 1 35/m headache, unconsciousness right frontotemporal chronic remission / yes 4 months within limit right sided burr hole, after 6 months burr hole on left side 2 years doing well fresh chronic sdh on contralateral side 6 month following the first surgery 2 44 /m headache, hemiparesis right frontoparietal chronic remission / yes one year within limit burr hole drainage 18 months well 3 29/ f headache left thin frontotemporal region chronic remission / yes six months within limit conservative 17 months doing well romanian neurosurgery (2016) xxx 3: 432 440 | 439 conclusion chronic subdural hematoma can be associated with recent history of physical trauma, drug intake, coagulation disorder and very rarely haematological malignancy. chronic myeloid leukemia can be predisposing factors especially during blast crisis phase. all our cases were already diagnosed case on maintainace therapy for cml in the chronic remission phase presented with headache and focal neurological deficit. two out of three were managed surgically and rest one responded favorably to medical therapy. it is especially important to select subgroup of patients among all cases, who are potential surgical candidate, otherwise delay in selection and treatment can produce catastrophic event. it is prudent to be vigilant in all case of chronic cml and other hematological malignancy, especially those cases developing headache or focal neurological deficit and haematologist should also be warned about possibility and minimum ct scan head must be carried out at the first suspicion of any developing intracranial pathology mass lesion without wasting golden time. correspondence dr. guru dutta satyarthee, associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: duttaguru2002@yahoo.com references 1. abdulhamid mm, li ym, hall wa. spontaneous acute subdural hematoma as the initial manifestation of chronic myeloid leukemia. j neurooncol. 2011; 101(3):513-6. 2. bromberg je, vandertop wp, jansen gh. recurrent subdural haematoma as the primary and sole manifestation of chronic lymphocytic leukaemia. br j neurosurg. 1998; 12(4):373-6. 3. comănescu a, roşca e, bota m, ninulescu g chronic subdural hematoma in a patient with acute myeloid leukemia and dural metastatic infiltration. rom j morphol embryol. 2008; 49(2):259-62. 4. druker bj, sawyers cl, capdeville r, ford jm, baccarani m, goldman jm. chronic myelogenous leukemia. hematology am soc hematol educ program. 2001:87-112. 5. gelabert-gonzalez m, iglesias-pais m, fernandez-villa j (2004) acute subdural haematoma due to ruptured intracranial aneurysms. neurosurg rev 27: 259-262 6. jonte f, barez a, soto i, rayón c, carrera d, coma a, pérez llanderal j, arribas m. [features of chronic myeloid leukemia at diagnosis. study of a series of 134 cases]. sangre (barc). 1992; 37(5):345-50. 7. karbasian esfahani m, morris el, dutcher jp, wiernik ph (2006). "blastic phase of chronic myelogenous leukemia". current treatment options in oncology 7 (3): 189–199. 8. keller tm, chappell et spontaneous acute subdural hematoma precipitated by cocaine abuse: case report. surg neurol 1997; 47: 12-15 9. kim ms, lee dh, lee yr, kim dk, bae sh, hwang jy, kwon ka, lee s, han jy, kim ku, kim sh. a case of subdural hematoma in patient with chronic myeloid leukemia treated with high-dose imatinib mesylate. korean j hematol. 2010 ; 45(1):73-5. 10. lakshmi prasad g, ramdurg sr, suri a, mahapatra ak. a rare association of meningioma with intratumoral bleed and acute subdural hematoma. neurol india. 2010; 58 (6):977-8. 11. lin ch, hung gy, chang cy, chien jc. subdural hemorrhage in a child with acute promyelocytic leukemia presenting as subtle headache. j chin med assoc. 2005; 68(9):437-40. 12. mandal r, bolt dm, shah bk. disparities in chronic myeloid leukemia survival by age, gender, and ethnicity 440 | raheja, satyarthee chronic subdural hematoma development in chronic myeloid leukemia in preand post-imatinib eras in the us. acta oncol. 2013 ; 52(4):837-41 13. matsue k, aoki t, odawara j, kimura s, yamakura m, takeuchi m. haemorrhagic complications associated with reduced alpha2-plasmin inhibitor during imatinib use in a patient with philadelphia chromosome-positive acute lymphoblastic leukaemia. leuk res. 2009; 33(6):867-9. 14. minette se, kimmel dw. subdural hematoma in patients with systemic cancer. mayo clin proc. 1989 jun; 64(6):637-42. 15. nejat f, keshavarzi s, monajemzadeh m, mehdizadeh m, kalaghchi b. chronic subdural hematoma associated with subdural rhabdomyosarcoma: case report. neurosurg. 2007; 60(4):e774 e775. 16. ohtsuki t, nishimatsu h, mizukami h, ohnishi m, kimura f, motoyoshi k, nagata n malignant lymphoma with subdural effusion. rinsho ketsueki 1992; 33: 841843 17. prasad bc, chandra vv, varaprasad g. dural metastases in chronic myeloid leukemia presenting as subdural hematoma. turk neurosurg. 2012; 22(6):777-8 18. rocque bg, baskaya mk (2008) spontaneous subdural hematoma as the initial presentation of choriocarcinoma: a case report. j med case rep 2: 211 19. song kw, rifkind j, al-beirouti b, yee k, mccrae j, messner ha, keating a, lipton jh. subdural hematomas during cml therapy with imatinib mesylate. leuk lymphoma. 2004 aug; 45(8):1633-6. 20. vardiman j, harris n, brunning r (2002). "the world health organization (who) classification of the myeloid neoplasms". blood 100 (7): 2292–302 21. g i u ffrè r. physiopathogenesis of chronic subdural hematomas: a new look to an old problem. riv neurol 1987; 57:298-304. 22. raheja a, satyarthee guru dutta, mahapatra ashok kumar. chronic subdural hematoma development in accelerated phase of chronic myeloid leukaemia presenting with seizure and rapid progression course with fatal outcome: romanian neurosurgery (2015) xxix 2: 199 202 199 microsoft word _1.formatata_kato.doc romanian neurosurgery vol. xvi nr. 2 5 towards a better future in profession and life for women neurosurgeons and their patients yoko kato department of neurosurgery, fujita health university, japan keywords: neurosurgery, neurosurgeon, women, professional introduction almost 30 years ago, women rarely chose surgery as a profession. even in 1978 when i graduated, 7 or 8 women out of a 100 student group, kept away from surgery, which was considered to be too intense and heavy. they tended to choose ophthalmology, otolaryngology, or pediatrics. at that time, without a doubt, there were many female doctors who were especially interested in surgery, as they were efficient and skillful. however, they didn't know anyone who had managed family, children and housework all together, being primarily a doctor, not even thinking of becoming a neurosurgeon. there were not enough social environments and confidence built to undertake such a career at that time. however, time passes rapidly, and now the percentage of female students and female doctors in europe approaches 70-80%. there are more women-neurosurgeons nowadays, but still female interns tend to avoid tough specialties, and surgery is given a cold shoulder. a national survey of women surgeons in canada11 was undertaken to evaluate their ability to combine career with personal and family care. a 93 item questionnaire was mailed in july 1990 to 459 female surgeons. most surgeons were married. only 6.5% were separated or divorced. 70% of them had at least one child. the most common surgical specialty was obstetrics and gynecology. women surgeons practicing in canada were able to combine productive careers with rewarding family lives and were satisfied with their decision to do so despite the compromises involved. medical science has been dominated by men. there are still very few women researchers in medical science. this science should be developed by both male and female researchers if it is to be equally fair and offer good medical service to female and male patients. thus, gender neutrality in medical research is most desirable. sandrick has given her comments of the residency experience: the woman's perspectives in the journal bull am coli surg. she comments that every surgeon has to go through residency with its long hours, the heavy case loads, the three-in-the-morning emergencies, the probing questions on rounds, the snatches of sleep in the on-call room, and the physical and emotional rigors of the or. many surgeons characterize residency training as brutal, uncompromising, even harassing; it is no different for men or women. female neurosurgeons in japan comprise only 3% of total number of neurosurgeons in japan, while the total number of female doctors will hopefully reach 30% of the total japanese doctors by the end of 2015. however, the present work environment of female neurosurgeons is not so good. the recent tendency amongst the younger generation is to enjoy life and thus to avoid selecting such professions where there i? lot of dedication and hard work demanded, besides a long residency program. the present generation of yoko kato romanian neurosurgery vol. xvi nr. 2 6 female doctors does not want to take up surgical fields, especially the cardiac and neurosurgical fields of surgery where maximum work load and tension exist in the' profession. it is the previous generation who still have to struggle to maintain their positions and to progress ahead of their male counterparts. the social scenario for and aspiring young female doctor to become a professional neurosurgeon in any institution is not favorable. hence, a basic solution lies in making social romance has prevented female neurosurgeons from progressing and proceeding a step ahead of male neurosurgeons in both the research field and clinical practice. the male chauvinistic thinking of females being a weaker sex, whose only role in society is to bear and rear a baby, is an absolute misconception. we see achiever, women in all walks of life, topping their fields of interest, but the situation is not the same for female neurosurgeons as hardly ever do we see a lady neurosurgeon being the president of any neurosurgical institution or a neurosurgical conference. recently there were a series of medical reforms that drastically changed the medical system of education and practice. increased monitoring and control of responsibility in medical practice and higher interest toward the qol (quality of life) among the patients and general public, has shifted the frontline forward. achievement in the treatment of certain illnesses is considered a significant qol improvement. in this new environment, in which female doctors, account for nearly 40% of all doctors in japan, have to work. neurosurgery has aspects that will keep young aspiring physicians away from it: long working hours and many emergencies, and thus increasing numbers of female doctors may therefore stay away from neurosurgery. there is no maternity leave in europe and this states that environment has been arranged for female doctors. i hope that japan will be the same way like europe someday. there are currently 369 female neurosurgeons in japan. as the numbers of female doctors is growing, we are facing lots of problems in neurosurgery. we have just established a "women doctors' bank" and i hope this will give us some kind of solutions. regardless of the mixed responses, pregnancy, delivery and child raising, family problems, inconvenient working time and discrimination have been clearly found. that is the main concern at choosing residency too. the need for social, financial and educational support has been outlined as a recommendation to the institutions regulating the health care labor force. the implementation of a reform is very important and may help the currently practicing women neurosurgeons, however, increasing their number is a process that will be the result of the active intervention of our organizations and supporters to all levels of social interaction-at national, governmental, academic, ngo, informal groups, through media, family support and education, educational institutions. we are certain that the evolution of the japanese society we are witnessing now will provide the highly qualified professionals-women the place they deserve. i am having a hard time trying to envisage how neurosurgery will look in the future and how can i, personally, contribute. let me talk a little bit about myself-1 received enthusiastic congratulations from the media when in april 2006 i became the first female japanese professor in 60 years of neurosurgery, considered as a very male dominated field of surgery. neurosurgery has numerous charms and thrills. this is the only branch where you can get actively in contact with living brain, and i am quite sure this is one of the medical specialties where you are constantly able to refine your skills, as if there is a mistake it can lead to disastrous results. therefore, it was considered a "scared" area in medicine. however, it also means it is stressful, with long hours of surgery, with dedicated care for the patient for prolonged periods, making it a difficult specialty to choose for a woman. as in the proverb "we tend to be good at those things we like," the first priority in choosing your specialty is that you must love it to make it a life-long work. as for myself, i love neurosurgery and this is why i have chosen it. l can not remember regretting my passion toward it because of the hard work. my desire to complete it as my life-long treasure was always bigger than my worries. on the other hand, you may think it would be physically easier in the specialties, such as dermatology or internal medicine. that, however, totally towards a better future romanian neurosurgery vol. xvi nr. 2 7 depends on how you live and how much you are dedicated to your medical professional role and what are you trying to accomplish in medicine. if you think that way, there is no easy choice. at any department of surgery, operations are the daily routine, but in medicine the personal psychological contact with the patients and the beginning i found some families stating they did not like female doctors, but as i built up my confidence after each case, these minute issues became less and less important to me. i felt very strongly that once i built up relations of trust and personal contact with patients, everything should be fine. now in the age of less invasive treatment, neurosurgery will see significant changes in treatment methods. but the important thing is to 'have the spirit of a surgeons and improve your skills, and this is something that should not ever change as time goes by. as said in the old days, "once in doubt, go for it," if you are hesitating, take the challenge, and if any young female doctors have this spirit, step in and go for neurosurgery. if you can pursue that endeavor for the rest of your life or not, depends on your own determination and spirit, and if you are brave enough, people around you will accept you, approve you, and help you improve. when you have those hours of fatigue and desperation, stop for a while and rest, and then start again, to make your dream come true with each step forward you make. if you like neurosurgery, take it seriously, do not hesitate, and take the challenge, and think of it as your future. references 1.mizgala c, mackinnon s, walters b, ferris le. women surgeons. the results of the canadian population study. ann surg 1993; 218: 37-46 2.enker ic, schwarz k, enker j.. the disproportion of femaie and male surgeons în cardiothoracic surgery. thorac cardiovasc surg 1999; 47: 131-135 3.sandrick k. the residency experience: the woman's perspective. bull am coli surg. 1992; 77: 10-17 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article post traumatic vertebro basilar dissection: case report and review of literature karthikeyan y.r., sanjeev chopra, somnath sharma, devendra purohit india doi: 10.1515/romneu-2017-0051 310 | karthikeyan et al post traumatic vertebro basilar dissection doi: 10.1515/romneu-2017-0051 post traumatic vertebro basilar dissection: case report and review of literature karthikeyan y.r., sanjeev chopra, somnath sharma, devendra purohit department of neurosurgery, sms medical college, jaipur, india abstract: posterior circulation territory stroke following mild head injury is a known entity although rarely seen. numerous case reports appear in literature from time to time highlighting this complication. blunt trauma to the head and neck possibly causes injury to the vertebrobasilar system in the form of angiorrhexis, subintimal, intramural and perivascular hemorrhage which causes secondary narrowing of the injured vessel. these processes can be complicated by progressive thrombosis & vascular occlusion. here we are reporting a case of post traumatic vertebra-basilar dissection causing bilateral cerebellar and brainstem infarct. key words: vertebral artery dissection, post traumatic, head injury, posterior fossa infarct introduction blunt cerebro vascular injury (bcvi) encompasses a spectrum of disease processes due to damage of the vertebral and carotid arteries. in the current era of trauma epidemic with increasing number of high velocity motor vehicle accidents, these injuries become more relevant. they may present immediately or in a delayed fashion. high index of suspicion and thorough screening is of utmost importance. here we report one such case with the review of literature. case summary a 50 year old gentleman presented to us with a history of high speed motor vehicle accident. on examination the patient was unconscious, intubated, had no respiratory effort and no motor response to pain. no obvious external injury was seen except for lacerated wound over the forehead. pupils were bilaterally pinpoint and not reacting to light. ncct brain showed large acute infarcts involving bilateral cerebellar hemispheres, medulla, pons and mid brain (figure 1). focal acute infarcts were also seen in the left thalamus and left medial temporal lobe. ct cervical spine showed fracture of the clivus and the occipital bone in the midline extending upto the groove for the vertebral artery bilaterally. fracture of left transverse process of c2 vertebra was also noted. cect chest and romanian neurosurgery (2017) xxxi 3: 310 315 | 311 abdomen was unremarkable. in view of the suspected vascular injury, a four vessel carotid angiography was contemplated. there was no enhancement in v3 and v4 segment of left vertebral artery and almost the entire length of basilar artery sparing its tip suggestive of complete occlusion with a likely possibility of post traumatic dissection.v1 and v2 segments were of normal caliber with no evidence of filling defect suggestive of thrombosis (figure 2 and figure 4). lt vertebral artery was seen to arise from the aortic arch. right vertebral artery was of normal caliber (figure 3). both the common carotids and bilateral internal and external carotids were of normal caliber. the patient was managed conservatively but he succumbed to his condition within 24 hours of admission. figure 1 computed tomography brain showing large acute infarcts involving bilateral cerebellar hemispheres and brain stem 312 | karthikeyan et al post traumatic vertebro basilar dissection figure 2 a: ct angiography brain showing no enhancement in v3 and v4 segment of left vertebral artery and almost the entire length of basilar artery.normal right vertebral artery b: anomalous origin of left vertebral artery from the aortic arch figure 3 normal right vertebral artery figure 4 absent flow in v3,v4 segment of left vertebral artery discussion blunt cerebro vascular injury (bcvi) encompasses a spectrum of disease processes due to damage of the vertebral and carotid arteries. the reported frequency is between 0.5% and 1.55% of all cases of blunt trauma. the common causes of bcvi include motor vehicle collision followed by a fall from height. extensive skull base fracture, cervical fracture, cervical soft tissue hematoma and facial fracture are common high risk factors for bcvi. of great clinical significance is that bcvi can occur even after a minor impact such as cervical traction, contact sports and chiropractic manipulation. neck vessel injury is probably an under diagnosed complication of head or cervical spine trauma. a high index of suspicion followed by early recognition of these romanian neurosurgery (2017) xxxi 3: 310 315 | 313 complications is absolutely essential to prevent poor outcomes. the commonest site of vertebral artery dissection seems to occur at c1-c2. (1) most common fracture patterns described are subluxations, upper c1 to c3 body fractures and transverse foramen fractures, while spinous process fractures of the lower cervical spine are rarely reported. (5) in our patient we found fracture of the left transverse process of c2 vertebra. predisposing conditions include infections, fibromuscular dysplasia, hereditary connective tissue diseases, hyperhomocysteinemia and migraine. dissections are commonly sub-intimal and cause stenosis (48%) or occlusion (35%). subadventitial dissections form pseudo aneurysms (17%), which can rupture intracranially causing sub-arachnoid hemorrhage. (3) posterior fossa infarcts following trauma are often a result of vascular dissections, vertebrobasilar spasm, embolization or systemic hypoperfusion. posterior inferior cerebellar artery (pica) territory is the commonest territory involved followed by superior cerebellar infarcts. (6) the mechanism of injury in patients with blunt trauma is not entirely clear. hyperextension and rotation, direct blows to the neck, intraoral trauma and basilar or other skull fractures have been suggested as possible mechanisms. in a patient with polytrauma, it is often difficult to ascertain the exact mechanism of injury. it seems likely that stretching and twisting of the vessels or impalement against the transverse processes of the vertebral bodies or a fractured bony fragment may result in these injuries. no definite evidence exists to support these hypotheses. whether a local deficiency in elastic fibers or other structural abnormalities may account for the frequent location of blunt injuries in the ica has not been established. (2) in our case the mechanism of injury is most likely to be due to a combination of hyperextension, rotation and direct trauma to the neck secondary to high speed motor vehicle accident. although penetrating injury to the cervical vessels is usually readily suspected, blunt injuries may be elusive. their relative infrequency (3% to 10% of cervical arterial injuries) and their common association with other injuries especially closed head trauma, render their diagnosis more difficult. symptoms of extracranial vertebral dissections may occur at any time from minutes to days after trauma. in some cases the delay may be extended up to six weeks which may confound the diagnosis. delayed onset of detectable neurologic deficits characteristically leads to delay in diagnosis. (2) the denver screening criteria provide a screening protocol for bcvi based on injury mechanisms, injury patterns and symptoms (table i). this protocol can identify trauma patients at risk for bcvi with a sensitivity of 97% and a specificity of 42%. (5) 314 | karthikeyan et al post traumatic vertebro basilar dissection table i the most common aortic arch branching pattern includes three main branches namely brachiocephalic, left common carotid and left subclavian. other branching patterns are formed due to the increased or decreased number of branches and their formation. in some cases, there are two aortic branches. the first branch includes the common trunk of right subclavian, right common carotid and the left common carotid arteries. the second branch is related to the left subclavian artery. this aortic arch branching pattern is called bovine aortic arch. some variations of the aortic arch branches are rare such as the presence of retroesophageal right subclavian artery as the last branch of the aortic arch. in a study in 2006 by nayak et al on 62 human cadavers in india, 94% of the patients had a normal aortic branching pattern and 4.8% of them had a common origin for the carotid arteries. doubled trunk branching and the right subclavian branching from aortic arch were observed in 1.6% of cases. in their study, the left vertebral artery branching from the aortic arch was reported in 1.6% of cases. (1) in our patient the left vertebral artery was seen to arise from the aortic arch. though an incidental and rare finding on angiography, it possibly may have played a role in the etiopathogenesis of the injury due to abnormal long course of the vessel predisposing it traction injury and consequent dissection. here we are reporting a rare case of bcvi which presented with isolated posterior fossa infarct which was associated with an anomalous origin of the left vertebral artery. bcvi is a rare but well-documented clinical entity with a wide spectrum of clinical features. in the current era of trauma epidemic with high velocity trauma the incidence of bcvi denver screening criteria for bcvi • signs/symptoms of bcvi o arterial hemorrhage o cervical bruit o expanding cervical hematoma • focal neurologic deficit o neurologic examination incongruous with head ct scan findings o stroke on secondary ct scan • risk factors for bcvi o high-energy impact with: o leforte ii or iii fracture o cervical-spine fracture patterns: o subluxation, fractures extending into the transverse foramen o fractures of c1-c3 o basilar skull fracture with carotid canal involvement o petrous bone fracture o diffuse axonal injury with gcs score <6 o near hanging with anoxic brain injury romanian neurosurgery (2017) xxxi 3: 310 315 | 315 and its complications are expected to be on the rise. high index of suspicion in appropriate clinical situations is the key to early diagnosis and prompt management to improve clinical outcome. correspondence dr. devendra purohit professor neurosurgery department of neurosurgery sms medical college, jaipur mail: devendrapurohit@rediffmail.com contact: +91 9829190335 references 1.datta sgs. posterior circulation stroke following mild head injury. ind j neurotrauma.2008;.5( 1):47-48. 2.fakhry sm, jaques pf, proctor hj. cervical vessel injury after blunt trauma. j vasc surg. 1988 oct;8(4):501-8. 3.gunasekara h, wijeratne m, arambepola p. posttraumatic vertebral artery dissection. ceylon med j. 2010 dec;55(4):123-4. 4.jalali kondori b, asadi mh, rahimian e, tahsini mr. anatomical variations in aortic arch branching pattern. arch 2016 jan; 19(1):72-4. 5.kobayashi k, imagama s, okura t, yoshihara h, ito z, ando k et al. fatal case of cervical blunt vascular injury with cervical vertebral fracture: a case report. nagoya j med sci. 2015 aug; 77(3):507-14 6.konar s, pandey p, anita m. superior cerebellar artery infract in a case of multiple territory infarct following severe brain injury: a rare occurrence. ind j neurotrauma.2012;9:150-3. 15satyartheeguru_primary romanian neurosurgery | volume xxx | number 4 | 2016 | october december article primary giant myxoma of the temporal bone with major intracranial extension: presenting with hearing impairment and ear polyp guru dutta satyarthee1, luis rafael moscote-salazar2 1india, 2colombia doi: 10.1515/romneu-2016-0087 540 | satyarthee, moscote-salazar primary giant myxoma of the temporal bone doi: 10.1515/romneu-2016-0087 primary giant myxoma of the temporal bone with major intracranial extension: presenting with hearing impairment and ear polyp guru dutta satyarthee1, luis rafael moscote-salazar2 1associate professor, department of neurosurgery, all india institute of medical sciences, new delhi, india 2neurosurgeon-critical care, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia abstract: myxomas are mesenchymal origin, benign tumor, constituting approximately half of the benign cardiac tumors. occasionally, it may also occurs at other locations, though the intracranial location of a myxoma is considered exceptionally rare. only isolated few cases of intracranial myxoma are reported in the literature, almost all were locally confined within the originating bone. the extensive pubmed and medline search yielded only eight cases of primary myxoma arising in the temporal bone with extension into intracranial compartment. however intracranial extension is limited as early detection, however, osterdock et al reported a case also arising from temporal bone with extensive intracranial extension. author report an interesting case of intracranial myxoma in 27yearoldmale, involving the temporal bone associated with extensive bony erosion and also extending into infratemporal fossa, mastoid, and frontoparietal region and a polypoidal mass protruding into external ear. to the best of knowledge of authors, temporal myxoma presenting with external ear polypoidal mass, which underwent successful surgical excision is not reported and represent first case in the world literature. key words: intracranial primary myxoma, temporal bone, surgery, outcome introduction primary intracranial myxoma is an extremely uncommon lesion, however, majority of reported cases represent metastatic intracranial myxoma. [1] it originates from mesenchymal tissue with predilection in the diminishing frequency i e. heart, skin, bone or genitalia. [2, 5-8] primary myxoma is a benign but locally invasive tumour [2,7]. surgical en-block excision of the lesion along with surrounding soft tissue is considered as the treatment of choice. [9-13] incomplete excision may lead to early recurrence and further myxoma is not responsive to radiotherapy. although radical resection is goal but always may not be possible especially in cases of intracranial romanian neurosurgery (2016) xxx 4: 540 – 546 | 541 myxoma and further challenges due to gelatinous consistency, local invasiveness of lesion and nature of neoplasm. case illustration a-27-yearold male presented with 5year history of progressive hearing loss, protruding soft mass through right external acoustic meatus associated with sero-sanguinous discharge . he developed progressive bulging over the right temporal region for last four years, causing cosmetic facial distortion. he also developed slowly progressive worsening headache, which was not associated with vomiting, visual decline or double vision. he consulted otolaryngologist, who advised computed tomography scan of head with bone window view and coronal reconstruction and referred to our neurosurgery outpatient services. on examination, he was of average built and height. the swelling over right temporal and infratemporal region was hard and bony in consistency. a soft fleshy mass with serosanguinous discharge was protruding through external auditory meatus with intact surfaces except raw area at one place. his visual acuity was normal. he had no field defect on confrontation test. the pupils were normal with brisk light reflex. the optic fundi were normal. right sided conductive deafness was also present. other cranial nerves were unremarkable. muscle strength of extremities was good and there were no pathological reflexes. the haematological and biochemical profiles were within normal limits. the cranial computed tomography scan revealed a large heterogeneous calcified mass located in the right middle cranial fossa extending and invading into the petrous and squamus portion of right temporal bone, causing the erosion of middle cranial fossa base with extension into right infratemporal fossa causing swelling in the temporal and infratemporal fossa of, its size was 6x4.5x 5 cm. (figure 1). large inhomogeneous mass lesion of size 6x4.5 x 5cm, with rim of calcification extending and invading the petrous and squamus portion of temporal bone, also causing the erosion of middle cranial fossa base with extension into infratemporal fossa. a large hypodense area with calcified rim was noted that was extending into frontoparietal region and infratemporal region in the bone window view. (figure 2) hrtct of temporal bone also confirmed destruction of squamus and petrous temporal bone (figure 3) along with middle and inner ear and associated extension into the eustachian tube. (figure 4) radiologically, the possible diagnosis of chondrosarcoma was entertained and possibility of other primary skull base tumour was also considered as differentials. he was planned for surgical management. he underwent right-sided frontotemporal craniotomy. the tumour was causing remoulding and expansion of squamus and petrous temporal bone with erosion through outer table and extension into middle ear. it was primarily located extra-durally. it was firmly attached to dura. however, no dural infiltrated was observed during intraoperative period. it had variable consistency, areas of gelatinous consistency corresponding to hypodense areas in the ct scan were present. the rim was solid and more fibrous. gelatinous part was relatively lesser vascular unlike solid part. tumour was also eroded through middle fossa to extend into sub 542 | satyarthee, moscote-salazar primary giant myxoma of the temporal bone temporal region. piecemeal dissection of tumour along with surrounding infiltrated muscle was carried out. external auditory meatus was closed after excision of polypoidal extension. the histopathological examination of resected specimen revealed presence of sparsely cellular tumour consisting of stellate to spindle shaped cells. these cells did not exhibit hyperchromasia, pleomorphism or mitotic activity. no mitosis or necrosis was observed. the bony specimen shows bony trabecullae, no evidence of tumor infiltration was observed. the tumour histopathology was interpreted as benign myxoma. in the postoperative period, cranial ct scan showed excision with subsidence of mass effect and no hematoma in the surgical resected cavity. he was discharged from the hospital on eighth post-operative day. figure 1 non-contrast enhanced computed tomography of head, axial section image showing large inhomogeneous mass lesion of size 6x4.5 x5cm, with rim of calcification extending and invading the petrous and squamus portion of temporal bone, also causing the erosion of middle cranial fossa base with extension into infratemporal fossa figure 2 – computed tomography head, bone window view image showing extra-large mass lesion with irregular rim of calcification causing erosion of middle cranial fossa and extending upto the right internal ear figure 3 non-contrast enhanced computed tomography of head, coronal section image demonstrating large area of hypodense with calcified rim causing destruction of squamous part of the right temporal bone with extension into the infratemporal fossa figure 4 computed tomography head, bone window view, coronal section re-constructed image of 27-year male showing destruction of middle and inner ear with complete loss of mastoid air cells romanian neurosurgery (2016) xxx 4: 540 – 546 | 543 figure 5 post-operative computed tomography scan of head showing excision of temporal myxoma discussion a myxoma is a benign neoplasm, however, biologically it behaves like locally invasive tumour. myxoma originates from tissues of mesenchymal origin. however, most of primary myxoma is commonly located in the heart, skin, genitalia and aponeurotic tissue. although myxoma arising in bone, development begins in bonemarrow, subsequently causes expansion of dipole and ultimately expansion, destruction and remoulding of involved bone caused by aseptic pressure necrosis. primary myxoma of head and neck usually involve maxilla and mandible. [16-22] primary myxoma involving skull base and vault is very rare. primary intracerebral myxoma is not reported; even secondary intracranial myxoma is also uncommon. intracerebral monastic myxoma, which usually originates as a result of metastatic deposit or remobilization from primary cardiac myxoma. only few isolated case report of primary intracranial myxoma is reported. [17, 11-13, 21, 23] the etiology of myxomas occurring in the head and neck region still remains unclear, although postulated about head and neck myxomas, these may arise from the tooth germ cells, because of presence in the maxillary and mandibular region. [22] kleinsasser postulated primitive mesodermal tissue filling the middle ear space in the embryo and in the newborn may give rise to temporal bone myxomas. [17, 18, 23] myxoma can occur at any age and both sexes are at equal risk. radiologically ct scan shows hypodense to isodense mass lesion with variation in pattern of enhancement following contrast administration. even there is variation in degree of bony involvement, extensive bony involvement is considered extremely uncommon and our case was unique having huge intracranial extension, although only one such case was reported by osterdock et al [3]. the management of myxoma is mainly surgical excision with wide margins of surrounding healthy soft tissue. myxomas possess a strong tendency to recurrence, especially in the bones. [24] in cases of temporal bone myxomas, where healthy margins cannot be achieved, drilling and piecemeal removal as much as tissue are possible, can be seen as needs to be adequate. the radical surgery requirement must be evaluated in light of safety and preservation of facial nerve and inner ear function. windfuhr and schwerdtfeger [25] advocated en bloc excision with wide margins is not possible in view of ill-defined margins of tumor and complex anatomy of temporal bone in cases harbouring temporal bone myxomas. therefore, it is wise to operate thoroughly but 544 | satyarthee, moscote-salazar primary giant myxoma of the temporal bone without sacrificing vital structures. regular follow-up is required, both clinically and radiologically, to detect recurrence early. the treatment of myxoma is surgery, although en bloc resection of intracranial myxoma is considered extremely difficult due to presence of important neurovascular structures difficult. [table 1] practically impossible to maintain its intactness during surgical dissection of these tumours, if cannot be excised with surplus surrounding tissue. but it is impossible in cranial skull-base and temporal bone [2, 4]. due to associated danger of en-block resection, in relation to intracranial myxoma, piecemeal removal is preffered. despite operative difficulties, the treatment of myxoma is surgical as myxoid tumours are generally insensitive to radiation therapy. due to its locally invasiveness, complete surgical excision is difficult. charabi et al reported left temporal myxoma which was involving mastoid, antrum and epitympenum but without any intracranial extension [2]. klein et al reported a primary intracranial myxoma located in the posterior fossa without extensive bony involvement and intraoperatively tumour was relatively peeled from cerebellum easily [4]. however, in few cases myxoma grows beyond confines of dipole and extends into adjoining spaces. in these cases with significant intracranial extension and associated with extensive bone destruction, where attempt of radical excision may not be possible. nagatani et al reported a case of primary myxoma of pituitary fossa, which had extensive bone erosion with spread into suprasellar cistern and inferiorly into sphenoid sinus after eroding sellar floor [16]. table i published report of primary intracranial myxoma originating in the temporal bone s. no. series/ (ref. no.) year site intracranial extension 1. richarth & terrache (6) 1969 temporal bone not mentioned 2. bulghov et al (7.) 1980 temporal bone not mentioned 3. charabi et al. (2) 1989 temporal bone no 4. osterdock et al (3 ) 2001 temporal bone extensive 5 hsieh et al. (11) 2006 temporal bone small 6 oruckaptan et al (1) 2010 temporal bone small 7 sareen et al21 2010 temporal bone external auditory canal, middle ear, mastoid antrum nil 8 zhang (15) 2006 lateral skull details not available current case 2016 temporal bone extensive osterdock et al [3] reported a 17year -old male with left temporal bone invading petrous bone myxoma associated with a large intracranial extradural component containing central gelatinous part surrounded by hyperdense rim extending up to frontoparietal region and inferiorly up to posterior fossa. our case also had extensive spread extending to frontoparietal region and posteriorly invading mastoid, middle ear, eustachian tube and polyploidy like extension through middle year after perforating tympanic membrane into romanian neurosurgery (2016) xxx 4: 540 – 546 | 545 external auditory canal. to best of our knowledge this is first case of primary intracranial myxoma with extensive bony erosion, which was also further extending to infratemporal fossa, mastoid, and frontoparietal region with mass protruding into external ear. recurrences are common, up to 25 % case may show recurrence if radical excision was not carried out [9]. the recurrence after surgery can occur as early as months and can delay up to 10 years. mueller et al reported a 12-yeargirl, a case of surgically resected medulloblastoma, received adjuvant radiotherapy, presented with a mass lesion at the left transverse sinus during the follow-up [13]. further added close relation to the radiation field of the posterior fossa medulloblastoma treatment, developed myxoma as a secondary radiation induced neoplasm. conclusion the primary intracranial myxoma although care but important and its possibility of must be kept as one of differentials in all cases, who present with destructive skull base lesions. the primary aim of the treatment is gross total excision, as en-block resection may not be always possible in cases with extensive intracranial extension. further these cases need close monitoring with regular follow-up and screening cranial mri to pick up early recurrences and provide tailored made appropriate treatment to each cases. correspondence guru dutta satyarthee, associate professor, department of neurosurgery, all india institute of medical sciences email: drguruduttaaims @gmail.com references 1. oruckaptan hh, sarac s, gedikoglu g : primary intracranial myxoma of the lateral skull base : a rare entity in clinical practice. turk neurosurg 2010 ; 20 : 86-89 2. charabi s, engel p, bonding p: myxoid tumours in the temporal bone. j laryngol otol 1989; 103: 1206-1209. 3. osterdock rj, greene s, mascott cr, amedee r, crawford be: primary myxoma of the temporal bone in a 17-year old boy: case report. neurosurgery 2001; 48: 945948. 4. klein mv, schwaighoterv bw, sobel df, heselink jr: primary myxoma of the posterior fossa. neuroradiol 1990; 32: 250-251. 5. kawai t, murakami s, nishiyama h, kishino m, sakuda m, fuchihata h: diagnostic imaging for case of maxillary myxoma with a review of the magnetic resonance images of the myxoid tumours. oral surg oral med oral patho oral radiol endo 1997; 84: 449-454. 6. richarth w, terrache k: myxoma of temporal bone. h no, 1969; 17(4): 113-115. 7. bulghov nj, gorokhov aa, likhackev lv: rare tumour (myxoma) of temporal bone. zhurnsl ushnykh, nosovykh i gorlovykh boleznei 1980; 5: 76. 8. peltola j, magnusson b, happonen r-p, barman h: odontogenic myxoma: a radiological study of 21 tumours. br j oral maxillofac surg 1994; 32: 298-302. 9. whitman ra, stewart s, stoopack jg, jerrold tc: myxoma of mandible: report of case. j oral surg 1971; 29; 63-70. 10. funari m, fujita n, peck ww, higgins cb: cardiac tumor assessment with gddtpa enhanced mr imagings. j comput assist tomogr 1991; 15: 9353-9585 11. hsieh dl, tseng hm, young yh. audiovestibular evolution in a patient undergoing surgical resection of a temporal bone myxoma. eur arch otorhinolaryngol. 2006 ;263(7):614-7 12. graham jf, loo sy, matoba a. primary brain myxoma, an unusual tumour of meningeal origin: case report. neurosurgery 1999; 45:166–170 546 | satyarthee, moscote-salazar primary giant myxoma of the temporal bone 13. mueller om, van de nes ja, wieland r, schoch b, sure u. surgical treatment of primary intracranial myxoma in a child following radiotherapy: case report and review of the literature. childs nerv syst. 2010; 26(6):829-34. 14. defatta rj, verret dj, ducic y, carrick k: giant myxomas of the maxillofacial skeleton and skull base. otolaryngol head neck surg 2006; 134: 931-935. 15. zhang lw, zhang ms, zhang jt, luo l, xu zl, li gl, et al. : [myxoma of cranial base: study of 23 cases]. zhonghua yi xue za zhi 2006; 86: 1592-1596. 16. nagatani m, mori s, takimoto n, arita n, ushio y, hayakawa t, gen m, uozumi t, mogami h primary myxoma in the pituitary fossa: case report. neurosurgery. 1987 feb;20(2):329-31. 17.allen pw. myxoma is not a single entity: a review of the concept. ann diagn pathol 2000;4:99-123. 18.stout ap. myxoma: the tumor of primitive mesenchyme. ann surg 1948;127:706-19. 19.canalis rf, smith ga, konrad hr. myxomas of the head and neck. arch otolaryngol 1976;102:300-5. 20.andrews t, kountakis se, maillard aa. myxomas of the head and neck. am j otolaryngol 2000;3:184-9. 21.sareen d, sethi a, mrig s, nigam s, agarwal ak. myxoma of the temporal bone: an uncommon neoplasm. ear nose throat j 2010;89:e18-20. 22.white dk, chen sy, mohnac am, miller as. odontogenic myxoma. a clinical and ultrastructural study. j oral surg 1975;36:901-7. 23.kleinsasser o. osteoblastic myxoma of the ear ("otenchymoma"). hno 1966;14:218-22. 24.andrews t, kountakis se, maillard aj. myxomas of the head and neck. am j otolaryngol 2000;21:184-9. 25.windfuhr jp, schwerdtfeger fp. myxoma of the lateral skull base: clinical features and management. laryngoscope 2004;114:249-54 doi: 10.33962/roneuro-2021-029 upper cervical spine tuberculosis. a case report a. khelifa, l. berchiche, w. bennabi, m. al-zekri, a. morsli romanian neurosurgery (2021) xxxv (2): pp. 189-191 doi: 10.33962/roneuro-2021-029 www.journals.lapub.co.uk/index.php/roneurosurgery upper cervical spine tuberculosis. a case report a. khelifa, l. berchiche, w. bennabi, m. al-zekri, a. morsli neurosurgical department of beo university hospital, algiers, algeria abstract tuberculosis is an infection caused by mycobacterium tuberculosis; mainly affects the lungs; spinal tuberculosis presents 6 % of the extrapulmonary locations; upper cervical spine tuberculosis is a rare condition and counts only 0.3 to 1 % of all spinal tuberculosis; that makes it a rare condition studied by few case reports. we report a case of upper cervical spine tuberculosis of the atlantoaxial facet joint. introduction upper cervical spine tuberculosis is a rare pathology (1,2), although medical treatment is uniformly indicated, surgical management is still debated whether to operate or not patients with poor clinical presentation. case presentation the patient is a 19 years old young man without past medical history who was presenting during 3 months a neck pain with a limitation of the neck movement, there was no neurologic deficit at the admission, the cervical spine ct showed a bone lytic lesion interesting the left hemi body of axis, its pedicle and the left atlantoaxial joint; the lesion was hypo intense t1 wi hyper intense t2 on spinal mri (figure 1); those images were not specific although an infectious origin was suspected, so first the patient was operated by an anterior approach where we performed total removal of the lesion. histological examination was in favor of caseo-follicular tuberculosis; immediately anti tuberculosis chemotherapy was started under the protocol 5 rhze/4 rh (5 months of rifampicin, isoniazid, pyrazinamide, ethambutol and 4 months of rifampicin and isoniazid). in a second time, the patient was operated and via a posterior approach we performed an occipitoc3-c4 fixation. in post-operative there was a pain relief and images showed a progressive reossification of the lytic lesion (figure 2). discussion upper cervical spine tuberculosis is a rare condition and counts only 0.3 to 1 % of all spinal tuberculosis (1,2); it starts frequently unilaterally by involving the cancellous part of the facet of atlas but less frequently keywords tuberculosis, upper cervical spine, atlantoaxial dislocation corresponding author: adel khelifa neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 190 a. khelifa, l. berchiche, w. bennabi et al. as in our case, the cancellous portion of the facet of axis and of the odontoid process (3). the upper level is considered to be the highest mobile region of the cervical spine (1,2) and protects a part of the spinal cord that the aggression could jeopardize major functions and even could be fatal. although progressive, the infectious lesions including tuberculosis cause the same amount of instability as the traumatic lesions (4), and in the most times the lesion itself couldn’t be as dangerous on the neurological structures as the spinal instability caused by the destructions of the main bony and ligamentous stability structures; despite that, the presence of a contralateral healthy joint could limit the clinical presentation to neck pain and torticolis and delays the appearance of neurologic deficit (3). on the other side the ligamentous system appears to be unilaterally incompetent even more the obliquity of the inclination of the facet of atlas in the atlantoaxial joint probably resulted in its lateral subluxation over the facet of axis (3); for that the surgical indication is still debated. other authors proposed classifications based on the presence or not of atlantoaxial dislocation (figure 3) (1), and they propose conservative management in case of minor deficit in absence of atlantoaxial dislocation or an anterior compression due to a large retropharyngeal abscess or granulation destroyed bone (1). figure 1. preoperative images; a: axial ct, b: coronal ct, c: left parasagittal ct passing through the left c2 pedicle, d: sagittal ct, e: sagittal t2 wi mri, and f: axial t2 wi mri; those images show the bone lytic lesion interesting the left hemibody of axis, its pedicle and the left atlanto axial joint; the lesion was hypo intense t1 wi hyper intense t2 on spinal mri. figure 2. 6 years post operative images; a and c : spiane ct, axial and coronal slides passing through c2 showing a total reosification of the lesion (the arrow); b: axial ct showing the screws placement on c3; d: x-rays of the occipito cervical fixation 191 upper cervical spine tuberculosis lifeso classification stage 1 minimal bony or ligamentous destruction; no aad. stage 2 minimal bony or ligamentous destruction; reducible or irreducible aad present. stage 3 significant bony or ligamentous destruction evident. bhagwati et al. grading system grade i merely inflammatory involvement of bony structures of the cvj with formation of granulation tissue and destruction of bone. grade ii formation of a large retropharyngeal abscess with bony changes. grade iii associated subluxation of the atlantoaxial joint, by bony destruction and/or laxity of apical and transverse ligaments. grade iv formation of epidural abscess and compression of the cervicomedullary junction and the upper cervical cord, with neurological defi cits that may be mild or severe. figure 3. grading systems for the tuberculosis of the cranio vertebral junction. aad: atlantoaxial dislocation, cvj: craniovertebral junction (1). conclusion upper cervical spine is a rare location of tuberculosis; it is a serious affection that could lead to neurologic deficit or even fatal. in association with medical treatment, surgery is indicated especially if there is a risk of instability. declarations of interest none. funding this research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. references 1. sanjay behari, namit singhal, suresh nayak, and vijendra k. jain. craniovertebral junction tuberculosis. the craniovertebral junction: diagnosis, pathology, surgical techniques / [edited by] atul goel, francesco cacciola. isbn 978-3-13-149071-1. © 2011 georg thieme verlag. 2. singkat dohar apul lumban tobinga, rendra irawanb, mohammad triadi wijayab,aji antorob, eko setiawanb, rian septian. instability treatment due to upper cervical tuberculous spondylitis. international journal of surgery case reports 61 (2019) 267–270. https://doi.org/10.10 16/j.ijscr.2019.07.044. 3. atul goel & abhidha shah. lateral atlantoaxial facetal dislocation in craniovertebral region tuberculosis: report of a case and analysis of an alternative treatment. acta neurochir (2010) 152:709–712. doi 10.1007/s00701-0090467-2. 4. r. roy-camille. spinal instability. rachis, 1994, vol.6, no 2 pp 107-112. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article ruptured anterior communicating artery aneurysm with spontaneous ventriculitis: an unusual case report with review of literature mayank sinha, ashok gupta, amit pratap singh deora, mukesh vij india doi: 10.1515/romneu-2017-0034 romanian neurosurgery (2017) xxxi 2: 211 214 | 211 doi: 10.1515/romneu-2017-0034 ruptured anterior communicating artery aneurysm with spontaneous ventriculitis: an unusual case report with review of literature mayank sinha1, ashok gupta2, amit pratap singh deora3, mukesh vij1 1neurosurgery department, s.m.s medical college, jaipur, india 2senior professor, s.m.s medical college, jaipur, india 3assistant professor, s.m.s medical college, jaipur, india abstract: ventriculitis is a potentially life-threatening infection, and an early diagnosis is essential for the appropriate treatment of ventriculitis. unsuspected ventriculitis might be a source of persistent infection and therapeutic failure in the management of meningitis. we present a rare case of spontaneous ventriculitis in a patient of acomm aneurysm who was neither immunocompromised nor any intervention was done on him. introduction intracranial aneurysm of infectious origin, are rare and represent 2% to 6% of all intracranial aneurysms. [2]they are more commonly seen in patients with septicemia and hiv/aids and are a particularly wellknown complication of infective endocarditis. intravenous drug abuse and relative immunocompromised state such as diabetes are becoming more commonly associated with cerebral mycotic aneurysm. [3] bacterial ventriculitis or meningitis is a relatively rare but serious complication after neurosurgical intervention. clinically, the diagnosis is often difficult to establish because of its insidious onset and atypical symptoms. [1] pyogenic ventriculitis is uncommonly reported in adults and is almost exclusively seen in patients who have undergone cranial surgery, placement of a drain or shunt, or sustained head trauma. here we present a case of ruptured anterior communicating artery aneurysm (? mycotic) with rare spontaneous ventriculitis in a young male who had not underwent any neurosurgical intervention and was not immunocompromised prior to diagnosis of ventriculitis. no similar case report has been found in available search of literature. case report a 40 years male presented to emergency department with complaints of severe holocranial headache since 2 days. it was associated with dizziness and vomiting 212 | sinha et al ruptured anterior communicating artery aneurysm with spontaneous ventriculitis episodes. on examination, the patient was afebrile, with no neck rigidity and was neurologically intact. his non-contrast ct head was done in emergency, which shown right frontal and anterior interhemispheric intracerebral bleed along with intraventricular extension. suspecting an aneurysmal bleed ct angiography of brain was done. it showed saccular anterior communicating artery aneurysm of size 4.9 mm with narrow neck. a small unruptured right middle cerebral artery bifurcation aneurysm was also found. symptomatic treatment was started and digital substraction angiography was done on next day, which confirmed the finding of ct angiography of brain. next day patient’s condition detoriated with patient having high grade fever and severe neck rigidity with altered sensorium. ct head was done, which shown hydrocephalus with edema around the intra cerebral bleed. patient was shifted to operation theatre for clipping of aneurysm. as as the brain was tense, before opening the duramater, external ventricular drain was inserted through left kochers point, instead of anterior third ventriculostomy for hydrocephalus. purulent material with flakes came out from evd, which was sent to microbiology, which reported pus cells with gram negative bacilli. aneurysmal clipping was abandoned. patient was shifted to intensive care unit with exraventricular drain in situ and started on higher antibiotics. csf picture was suggestive of severe infection. grossly, it was turbid, rbc-numerous, wbc1000-1100cells/cumm, <90% polymorphs.csf protein was305.07mg/dl, csf sugar was low value mg/dl and chloride was 116.6 mmol/l. culture of csf shown klebsiella species. figure 1 t angiography of brain sagittal view showing anterior projecting acomm aneurysm of size 4.9 mm with narrow neck figure 2 figure showing large hyperdense bleed in right parasaggital frontal lobe and anterior interhemispheric fissue patient”s 2-d echocardiography was done, to rule out infective-endocarditis, which showed no vegetations and was grossly normal. patient”s chest x -ray and usg abdomen was also normal. complete blood count and c-reactive protein was also within normal limit. patient”s condition improved after 2 days of antibiotic therapy. but after 3 days patient’s condition detoriated again and he expired. romanian neurosurgery (2017) xxxi 2: 211 214 | 213 discussion mycotic aneurysm represents less than 5% of all intracranial aneurysm. [3] streptococcus viridians and staphylococcus aureus are responsible for 57% to 91% of mycotic aneurysm. [2]more than 80% of patients with infectious aneurysm carry an underlying diagnosis of endocarditis. extravascular infections like meningitis, cerebral abscess, subdural empyema, osteomyeltis of skull or sinus infections can also extend into the arterial wall and cause infectious aneurysm. infectious aneurysms from an extravascular source tend to occur proximally,whereas embolic infectious aneurysms associated with infective endocarditis occur predominantly in distal cerebral arterial regions. [2] in this case, possibility of mycotic aneurysm is very less. the point against mycotic aneurysm are (1) proximal location of aneruysm (2) size and shape of aneurym (3) no predisposing factor (endocarditis or any intervention) (4) immunological status. pyogenic ventriculitis refers to inflammation of the ventricular ependymal lining accompanied by pus in the ventricular system [5]. there can be various predisposing factors including a recent neurosurgical procedure, head injury with csf leakage, meningitis, and brain abscess. [5] pyogenic ventriculitis can complicate central nervous system (cns) infections such as meningitis or brain abscesses and may even occur as a spontaneous infection in significantly immunocompromised patients. the most common organisms associated are coagulase-negative staphylococcus and s. aureus. now a days, gram negative species such as klebsiella pneumoniae, pseudomonas aeruginosa, enterobacter cloacae, and enterobacter aerogenes are becoming increasingly common due to nosocomial infections [6]. ventriculitis is associated with a high mortality, from 30 to 70%. [4] because of the associated high rate of morbidity and mortality, early diagnosis of ventriculitis is crucial. ventriculitis may present insidiously with slow progress or there may be acute hydrocephalus with loss of consiousness. diagnosis of pyogenic ventriculitis is difficult and relies on a high degree of clinical suspicion. early diagnosis is essential to enable appropriate treatment. in this case there can be two possibilities. first, there may be ruptured mycotic aneurysm with intraventricular extension of infection. but as mentioned earlier, this possibility is very less. other possibility, may there be noninfectious ruptured anterior communicating artery aneurysm with spontaneous ventriculitis as no cause of ventriculitis can be detected. it may be due to some nosocomial infection or subclinical septicemia. this case highlights the importance of greater degree of clinical suspicion needed in dealing with hydrocephalus with intraventricular bleed in case of an aneurysm and to rule out ventriculitis even if clinical picture is obscure. 214 | sinha et al ruptured anterior communicating artery aneurysm with spontaneous ventriculitis correspondence dr. mayank: sinha-mksdoc@gmail.com dr. ashok gupta: drashokjp@yahoo.com dr. amit pratap singh deora: dramitdeora@gmail.com dr. mukesh vij: dr.mukeshvij@gmail.com address: neurosurgery department, b.m.r.c buildng, 2nd floor, s.m.s, jaipur, india references 1. berk sl, mccabe wr. meningitis caused by gramnegative bacilli. ann intern med 1980;93:253-260 2. scott a.meyer,joshua bederson.infectious intracranial aneurysms.in:h richard winn.youmans neurological surgery,6th ed:elseviers saunders;2011.p-3972-5 3. retrospective review of cerebral mycotic aneurysms in 26 patients: focus on treatment in strongly immunocompromised patients with a brief literature review.l.m. allen, a.m. fowler, c. walker, c.p. derdeyn, b.v. nguyen, a.n. hasso, b.v. ghodke, g.j. zipfel, d.t. cross iii, and c.j. moran. published october 11, 2012 as 10.3174/ajnr.a3302 4. lozier ap, sciacca rr, romagnoli mf, connolly es jr. ventriculostomy-related infections: a critical review of the literature. neurosurgery 2002;51:170-81. 5. ventriculitis: an unusual cause of sepsis in an elderly patient who presented with persistent fever ahc yuen, fck mok. asian j gerontol geriatr 2006; 1: 49–52 6. ct and mr imaging features of pyogenic ventriculitis melanie b.fukuia, robert l. williamsa, sanjay mudigondaa. american journal of neuroradiology 25memoriam 176 | in memoriam: prof. alexandru constantinovici md., phd. (1929-2018) in memoriam: prof. alexandru constantinovici md., phd. (1929-2018) titular member of the academy of medical sciences yet another distinguished personality of romanian neurosurgery has passed away and left friends and pupils grieving. professor alexandru constantinovici, one of the most proeminent neurosurgeons in postcommunist romania has always been a beacon of fairness and dedication towards the training of neurosurgeons and constant development and evolution of the neurosurgical school in romania. his whole activity lies on the shrine of this extraordinary discipline of neurosurgery as he practically had no time for any other activity or his family. dedication, strength and tenacity are the three keywords of prof. alexandru constantinovici’s life. a symbol of constant dedication and painstaking routine, he always sought to push romanian neurosurgery to the highest level, thus recovering as much lost time as possible since romania cut ties with the west in 1947. after graduating medical school in bucharest in 1952 he began his activity as a surgeon with a prodigal early career at the “colentina” hospital of bucharest. he later embraced the field of neurosurgery becoming a consultant in 1970 and joining the ranks of university lecturers in bucharest. he passed through every academic rank and was appointed professor of neurosurgery in 1991, the same year he was appointed chief of the largest neurosurgical hospital – a challenge passed forward by professor constantin arseni. the scientific and professional activity of professor constantinovici encompassed every possible subspecialty (both in cranial and spinal neurosurgery). he was concerned with introducing novel paraclinical investigations such as the use of radioactive isotopes in fie diagnosis of cerebral and spinal lesions. in this respect he was a vocal promoter of the new field of nuclear medicine and he is credited with the first use of nuclear medicine in neurosurgery in romania. he was the first promoter of trans-sphenoidal surgery for pituitary tumors in romania. the same year he was appointed professor and chief of neurosurgery in bucharest, he was voted president of the romanian society of neurosurgery. after 2 mandates as president he became honorary president and developed a very wide field of scientific activity in country and abroad, thus crucially contributing at the romanian neurosurgery (2018) xxxii 1: 176 178 | 177 construction and development of the romanian journal of neurosurgery – „romanian neurosurgery”. since 1991 professor constantinovici was the first one to adopt english as a mandatory language in the entire romanian neurosurgical meme, thus delicately forcing romanian neurosurgeons to rally to western standards. professor constantinovici participated on behalf of romania at countless conferences, symposiums and international congresses, especially those organized by the european association of neurosurgical societies and the world federation of neurosurgical societies. as one of his closest collaborators i have served under him in 1993 at the wfns congress in acapulco, a vital moment for romanian neurosurgery as worldwide recognition was attained. an essential element in prof. constantinovici’s activity was represented by the international acceptance of the romanian school of neurosurgery through its capability of training neurosurgeons capable of covering the most demanding positions. the scientific activity of prof. alexandru constantinovici md was prodigious, realizing over 200 scientific papers, presented and published in specialized journals. we also mention the 16 monographs/treaties, in which his contribution was major, as the main author or in collective. last but not least, we reveal the opening of the so thorny firelds of pituitary tumors pathology through transfenoidal approach and radioisotopic methods in the diagnosis of nervous system disorders. prof. constantinovici attained numerous distinctions in his activity and developed professional relationships with numerous colleagues throughout the world. his 16 published monographs are present even today in the national neurosurgical heritage. in 1982 he became a corresponding member of the „american academy of neurological surgeons” – the most prestigious neurosurgical society at the time. he was admitted in 1993 in the french speaking neurosurgical society. in 1995 he became a full member of the „romanian academy of medical sciences”. under his leadership romanian neurosurgery gained a new aura, a modern drive and a never stopping lust for knowledge in all possible fields: pituitary diseases, vascular neurosurgery, surgical treatment of epilepsy, neuroendoscopy and last but not least, neurosurgical applications of nuclear medicine. unfortunately, his activity came to a sudden halt in 1999 when, for personal reasons, he decided to pass the torch along – while at full health and professional maturity – choosing to deal with the scientific 178 | in memoriam: prof. alexandru constantinovici md., phd. (1929-2018) constructive issues of neurosurgery and covering less the surgical aspects of neurosurgery. for all those who knew him prof. constantinovici was a symbol of friendship, attachment and dedication in all possible situations ranging from difficult times in the operating room up to issues concerning family life. the authors wish to express their empathy for the mourning relatives. we will never forget his warm smile and his wise words. has passed into eternity a neurosurgical personality, an accomplished colleague, a surgeon who was a trainer and a creator in the neurosurgical field. d. mohan md., phd., bihor county emergency hospital, oradea, romania a.v.ciurea md., phd., msc., dr. h.c. mult., sanador medical center, bucharest, romania romanian neurosurgery (2019) xxxiii, 1: 90-93 doi: 10.33962/roneuro-2019-019 www.journals.lapub.co.uk/index.php/roneurosurgery surgeon specialist branding or what do surgeon specialists need to know about their brand emil zhalmukhamedov1 1 founder of scientissimum medical group, iau com ms 1; volunteer nys emtb, executive marketing board advisor, medical student at international american university college of medicine, st. lucia; founder of scientissimum medical group, walter dandy neurosurgical society medical student member, global neurosurgery advocate, gssa, syrus member, usa abstract as the world has widely adapted the principle of searching for relevant information online, many practicing physicians, especially those who are involved in specialty must pay a close attention to their brand and their reputation on the world wide web. there are numerous web pages available to the general public about particular physician and where he/she practices. most of those pages are either managed by a third-party company or created for promotional use. some physicians are not even aware of this and are found by surprise when their patients bring up the information, they found on them online. physician’s name is a brand that he or she carries throughout entire medical career, and it might make or break the legacy of academic or private physician on the long run. introduction the modern physician leadership skills have tremendously shifted from academia to patient advocacy within the hospital walls. nowadays, modern physician leaders, particularly surgeon specialists are required to have a proper information about their brand online, if they want to actively engage in the patient advocacy, improvement of medical techniques, drive better brand awareness about their practice or ultimately raise a better return on investment for their department. by owning and optimizing physician’s brand image online, physician showcases his/her professionalism exactly the same way, as it would be presented in the real world. a first impression is an exact trademark – how patients as well as colleagues are going to perceive a particular physician, whether it’s online or in-person. method this research publication demonstrated the latest techniques and practices that available for surgeon specialists to implement on their keywords physician branding, physician leadership, healthcare management corresponding author: emil zhalmukhamedov scientissimum medical group, iau com ms 1, usa scientissimum@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ http://www.lapub.co.uk/ 91 surgeon specialist branding or what do surgeon specialists need to know about their brand behalf in order to improve their branding or reputation online. the strategy employed in this paper is widely used by marketing professionals and could be applied to any surgical subspecialty to improve physician’s brand awareness and recognition. basic online search a very first step in identifying your presence online is to perform a simple online search. by searching your name in any popular search engines such as google, bing or yahoo will bring the results associated with your name. by doing so, a physician can see what comes up, what hospitals or educational institutions he or she is associated with, physician ratings and comments, social media profiles etc. this is a very important first step that any physician should take in order to see where he/she stands online, as this helps to understand where the work needs to be done and how to improve or make it better. during a quantitative online research of specialist’s name, it’s advisable to make priority notes on troubling websites and negative reviews that come up on the first 3 pages of search engines. the theory strongly suggests performing a search for up to 3 pages, as less than 10% of people online go beyond 3rd page of google [1]. by creating notes on troubling websites first, a doctor creates a visual picture where he/she needs to do some work. as a rule of thumb, most of the troubling websites where most of the physicians find surprising ratings are on physician rating websites such as google business, yelp, ratemds, vitals, healthgrades, facebook, zocdoc, caredash, angie’s list and more. when we surveyed surgeon specialists whether they were aware of their online reputation score on the rating websites, most of them didn’t even know that their name was associated or mentioned there. that’s why this very first step of identifying your online weakness, is a crucial step in your journey on better branding in general. the next step after identifying your brand vulnerabilities online is to make notes on the websites that provide accurate and positive information about doctor’s name. there will be information that is most likely associated with your residency ties, medical school or current/past employment webpages. if these pages still show up on the first three pages of search engine, it’s a good indicator of brand awareness online. name/brand ownership once the troubled as well as properly informative websites were noted, it’s time to visit those website and understand who owns these websites, what comments prevails there and how you can get a full ownership of the given information. it was interestingly noted, that some websites incorrectly identify physician’s specialty and association with the hospital. those misinforming websites should be contacted directly for correction or reported for misleading information. what every physician needs to understand is, that if his or her information is found online and they do not own it, then somebody else does. if this situation persists and it’s not corrected right the way, it can potentially ruin physician’s reputation, as random negative content could be fed directly to the search engines on daily basis. that’s why it’s very crucial to own your personal information online. dealing with incorrect information and negative reviews once the list of good and bad websites is established, a physician should proactively engage with the bad ones first. generally, every legitimate website should have a “contact us” page where any technical errors could be addressed. this is where you need to email or sometimes-even call to get your information corrected. once it’s done, the next step will be addressing negative reviews. to address negative reviews, a physician should clearly understand why a negative review occurred. on some review websites such as yelp, a doctor can message a reviewer directly about given feedback online, in order to smooth the situation and potentially turn a negative review into a positive. however, there are some situations, where you get no response from the user at all. in this case, it’s advisable to leave a public reply/feedback with thorough explanation why the misunderstanding has occurred. this way a professionalism and constructive criticism should be taken into consideration before leaving a public comment. being professional in person and online is an essential tool for any respected physician of the modern world, this is where a parallel between virtual and real world crosses the path. if physician struggles with the negative reviews online, it’s advisable to fully optimize social media networks. a logical reason to optimize or sometimes 92 emil zhalmukhamedov even create more social media profiles is to push negative websites further down to the 3rd, 4th pages of search engine. social media has one of the highest online traffics out of the entire internet; therefore, social media websites are the ones that usually show up on the top pages of any search engine. by optimizing those social media profiles, physician can create more positive brand awareness, regardless of the prior negative reviews. to support statement on importance of online reviews; a study that was conducted by brightlocal demonstrated that out of all businesses online, 47% of general populations look at the reputation of doctor before making a decision on primary visit (figure 1). figure 1 the anatomy of a good medical brand any reputable healthcare brand online has five main points, these points are: 1. professionally done website optimized for mobile devices. 2. a unified (consistent) high definition profile and cover picture throughout all websites, including social media. 3. academic cv or biography. 4. a website or information website link on how to contact physician. 5. shared relative information associated with physician’s specialty and accepted insurance. ideally, these top 5 points must be present throughout all the active websites where physician’s information is found online. outside of those points, it’s advisable to establish an online physician’s niche, just like a specialty that physician specializes in. whether a physician would like to be found a thought-provoking leader or just share the latest news from the industry or his/her own practice – but it has to be consistent [2]. any physician who is actively engaged with his/her own brand sees a phenomenal potential for growth not only academically but also in the professional world of medicine [3]. an understanding the physician’s strength and capability will certainly create a great brand awareness and recognition for physician’s career on a long run. personal vs. professional use of social media network some physicians who experienced social media probably understand there are 2 main differences between personal and professional use of social media networks. for example, a personal profile on facebook is completely different from business 93 surgeon specialist branding or what do surgeon specialists need to know about their brand profile. this is where many physicians fail to separate two. a business facebook page allows physician to see engagement with audience, advertise a promoted content, see statistics etc [4]. while personal profile is mostly used to connect with friends and family. so, it’s very important to separate these two and the same rule applies to the widely used physician networks such as linkedin and instagram. results optimization and ownership of surgeon specialist’s identity online can make or break the outlook on physician’s long-term career. it’s important to own and correct misleading information online right the way, in order to prevent further damage. a simple research and advocating for your own brand name online, as it was shown here, can tremendously increase surgeon specialist’s reputation in the eyes of the patients and the entire world. discussion in the competitive world of modern healthcare, where physicians take an active role of advocating for their patients or simply would like to be connected with potential patients or colleagues, brand image plays a huge role in the era of internet. a shift from the old-school word of mouth to the new way of searching for information about particular doctor, forced many physicians to pay closer attention to the marketing techniques in order to be properly recognized online for their identity and work. [5,6] with open and free accessibility of the internet [7], any person can now build his or her own brand, however, the same way this brand can be misrepresented or misleading to the general public. any practicing physician should take this particular issue seriously, as it can trigger a multitude of unwanted results in terms of personal branding. a modern surgical specialist should be an active advocate of his or her own brand online as well as inperson. in this research paper we showcased how any surgical specialists can own their brand identity and what steps they should take in order to be successful. there are some limitations to this study, as evolving marketing techniques are constantly changing, however the basic principles of marketing strategy on branding and brand awareness remained the same for the last 5 years. conclusion as internet plays a huge role in everyday life, owning and protecting your brand identity is becoming a crucial step for any well-respected physician specialist. a full optimization and ownership of physician’s brand name showcases a better correlation to a positive image online and drives better return on investment on the long run. surgeon specialists who are actively sought online by patients [8] and professional medical colleagues will have an ability to correctly represent who they are and what they stand for in the most professional and positive way. references 1. 1. c. insights, the value of google result positioning, chitika | online advertising network. (2017). https://chitika.com/2013/06/07/the-value-of-google-resultpositioning-2/ (accessed february 19, 2019). 2. t.l. gaines, 7 tips for branding: what doctors need to know, kevinmd.com. (2018). https://www.kevinmd.com/blog/2018/02/7-tips-brandingdoctors-need-know.html (accessed february 19, 2019). 3. lair d.j., sullivan k., cheney g. marketization and the recasting of the professional self: the rhetoric and ethics of personal branding. manag. commun. q. 2005; 18:307–343. doi: 10.1177/0893318904270744. 4. instagram business account or personal account what's the difference? meetedgar. (2018). https://meetedgar.com/blog/instagram-business-accountwhats-the-difference/ (accessed february 19, 2019). 5. f.-y. chu, y.-x. dai, j.-y. liu, t.-j. chen, l.-f. chou, s.-j. hwang, a doctor’s name as a brand: a nationwide survey on registered clinic names in taiwan, international journal of environmental research and public health. 15 (2018) 1134. doi:10.3390/ijerph15061134. 6. lair d.j., sullivan k., cheney g. marketization and the recasting of the professional self: the rhetoric and ethics of personal branding. manag. commun. q. 2005; 18:307–343. doi: 10.1177/0893318904270744 7. s. gorbatov, s.n. khapova, e.i. lysova, personal branding: interdisciplinary systematic review and research agenda, frontiers in psychology. 9 (2018). doi:10.3389/fpsyg.2018.02238. 8. w.d. evans, j. blitstein, d. vallone, s. post, w. nielsen, systematic review of health branding: growth of a promising practice, translational behavioral medicine. 5 (2014) 24–36. doi:10.1007/s13142-014-0272-1. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article pseudomeningocoele after baclofen pump placement in a child: a case report and preventive measures rahul gupta, abhay singh, gangesh gunjan, harjinder singh bhatoe india doi: 10.1515/romneu-2017-0083 536 | gupta et al pseudomeningocoele after baclofen pump doi: 10.1515/romneu-2017-0083 pseudomeningocoele after baclofen pump placement in a child: a case report and preventive measures rahul gupta1, abhay singh2, gangesh gunjan1, harjinder singh bhatoe3 1neurosurgery; 2general surgery, dnb neurosurgery resident 3neurosurgery, director&hod neurosurgery fortis hospital, noida, u. p. india abstract: intrathecal baclofen therapy is a well-established means of treating intractable spasticity and dystonia in paediatric as well as adult population. complications of baclofen pump placement include infection, malfunctioning and refraction to baclofen. we report a case of eight year child suffering from spasticity due to cerebral palsy, who developed pseudomeningocoele due to peri-catheter leak. steps and precaution pertaining to pump implantation in a child are discussed. baclofen pump insertion in a child needs some extra precautions due to non-availability of pediatric implants and poor built of the pediatric patient to adjust with a bulky device. preventive measures should be taken to prevent peri-catheter csf leak. key words: baclofen pump, csf leak, pseudomeningocoele introduction intrathecal baclofen (gamma-aminobutyric acid analogue) therapy is a well established means of treating intractable spasticity and dystonia in pediatric as well as adult population. a programmable intrathecal pump provides a direct, pattern-controlled delivery of baclofen to the spinal cord. complications of baclofen pump placement include infection, malfunctioning and refraction to baclofen. [2] they can occur at the time of implantation and throughout the life of the implanted system. any complication requiring removal or change of implant can be very expensive. we report a case of pseudomeningocoele after baclofen pump placement in a child and its preventive measures. case history eight year old female presented with cerebral palsy since birth with progressive spasticity in all the limbs. she had severe pain and difficulty in moving the lower limbs. on examination, grade 4 spasticity was noted in both lower limbs according to modified asworth’s grading system. oral baclofen was tried but was not effective. intra-thecal instillation of 25 mcg baclofen, patient showed improvement in spasticity. hence, baclofen (tricumed) pump romanian neurosurgery (2017) xxxi 4: 536 539 | 537 placement was performed by the standard technique. drug dose was increased from 25 mcg/ day to 50 mcg/ day on 3rd day. patient showed significant improvement and physiotherapy was started. patient came to opd after 5 days with soft, fluctuant, nontender swelling at the site of baclofen pump placement. there was no swelling along the track of the tubing or insertion site in the lumbar spine. her limbs were less spastic than before. compressive dressing was done, antibiotics escalated and physiotherapy continued. keeping csf collection in mind, raised icp was ruled out by ct scan of brain. patient again came 4 days later with tense wound bulge which extended along the track of tubing up to lumbar spine (figure 1). the swelling was tapped with 20 g needle and about 50 ml of clear fluid aspirated. gross appearance and laboratory examination suggested it to be csf without any evidence of infection. keeping csf leak in mind, we planned reexploration under general anaesthesia. first abdominal wound was explored and around 100 ml of clear fluid evacuated. connection between the catheter and baclofen pump was found to be intact (figure 2). then, lumbar wound was explored and around 50 ml csf evacuated. active csf leak around the catheter at the entry point into the thoracolumbar fascia was noted. fascia was cut, muscles were separated and catheter was traced up to duramater. l2 partial laminectomy was also performed to create space to inspect the entry point into the duramater. dural leak was noted around the catheter which was due to a long vertical slit in the duramater. meshed muscle with biological glue was kept over duramater around catheter. sutures applied over muscle and fascia (purse string sutures) around the catheter. wound closed in multiple layers with precautions to prevent any kink to the catheter. post operative period was uneventful and patient was discharged after 2 days. there was no wound bulge or csf leak after that. figure 1 swelling in anterior abdominal wall figure 2 connection between catheter and baclofen pump found intact discussion the intrathecal baclofen pump is surgically implanted in the subcutaneous tissue of anterior abdominal wall. baclofen is delivered via a silicone rubber catheter into the lumbar subarachanoid space. 538 | gupta et al pseudomeningocoele after baclofen pump toughy needle (16g) is inserted through the fascia blindly into the thecal sac and catheter is passed through it. though there is a mismatch in the diameter of needle and catheter, we assume that elasticity and strength of tissue shall grasp the catheter surface tightly to prevent any retrograde peri-catheter leak of csf. still, csf leak may occur due to following reason: 1. catheter related problems like dislodgement, migration, fracture, breakage, kinking, occlusion and puncture. 2. duramater is thin and may get torn with tip of needle 3. if the length of catheter surrounded by tissue is not adequate. 4. muscles are less bulky and compression force of soft tissue over the catheter is less 5. disparity in size of puncture needle versus catheter diameter appears to be more significant in a child as sealing property of thin duramater may be less effective. such patients may present with drowsiness, nausea, headache, muscle weakness and lightheadedness due to csf leak or increase in spasticity as a result of the pump delivering an incorrect dose of baclofen. [4] in our case, patient responded well initially, but there was csf collection along the path of baclofen pump and its tubing. we suspected disconnection between catheter and pump; but this was found intact on fluoroscopy and later confirmed on exploration.[3] we did ct scan brain and ruled out hydrocephalous as raised icp may promote peri-catheteric csf leak. on exploration, there was pericatheter dural leak which was due to poor muscle bulk, short length of tubing in soft tissue and a large rent in the duramater. while inserting a lumbar intradural catheter, we depend on body’s natural mechanism to hold the catheter and prevent a csf leak. this patient was a thin built female child who was bedridden for a long time; hence the natural mechanism to grip the catheter was deficient. cases of seroma and pus collection have been reported in the literature. [1, 2, 5, 6] initially, we suspected it to be seroma, so just a compressive dressing was applied. we avoided aspiration fearing that it may introduce infection. we aspirated only when it became tense and bulging. it was csf and infection was ruled out by negative culture examination. hence, we recommend some preliminary measures to be taken: 1. the size of the toughy needle should be smaller for pediatric patients and we recommend that the manufactures’ should design smaller needles. 2. open insertion is not necessary in the adult patients but in children we should dissect up to the duramater and directly insert catheter under vision. we can put biological glue and muscle around the dural puncture site to prevent csf leak. 3. strong purse string suture should be applied around the catheter on the fascia. 4. rule out raised intracranial pressure before pump insertion. conclusion baclofen pump insertion in a child needs many extra precautions due to non availability of pediatric implants and poor built of the pediatric patients to adjust with a bulky device. preventive measures should be taken to prevent peri-catheter csf leak. romanian neurosurgery (2017) xxxi 4: 536 539 | 539 correspondence dr abhay singh fortis hospital, sec-62, gautambudh nagar, noida, u.p. india 201301 e-mail: abhaysingh291183@gmail.com mobile no. 8130503451 references 1. albright al, awaad y, muhonene m, et al. performance and complications associated with the synchromed 10-ml infusion pump for intrathecal baclofen administration in children; j neurosurg: pediatr 2004; 10: 64-68 2. awaad y, rizk t, siddiqui i, et al. complications of intrathecal baclofen pump: prevention and cure. isrn neurolo volume. 2012; 2012: 575168, doi: 10.5402/2012/575168. 3. ilias w, todoroff b. optimizing pain control through the use of implantable pumps; med devices (auckl). 2008; 1: 41–47 4. mohammed i, hussain a. intrathecal baclofen withdrawal syndromea life-threatening complication of baclofen pump: a case report, bmc clin pharmac 2004; 4:6 5. motta f, buonaguro v, stignani c. the use of intrathecal baclofen pump implants in children and adolescents: safety and complications in 200 consecutive cases. j neurosurg: pediatr 2007; 107: 32-35. 6. plassat r, verbe bp, menei p, et al. treatment of spasticity with intrathecal baclofen administration: longterm follow-up, review of 40 patients. spinal cord 2004; 42: 686–693. doi: 10.33962/roneuro-2021-018 endoscopic lumbar discectomy using side viewing conical working tube. an institutional experience mohammad kaif, kuldeep yadav, rakesh kumar, deepak kumar singh romanian neurosurgery (2021) xxxv (1): pp. 108-113 doi: 10.33962/roneuro-2021-018 www.journals.lapub.co.uk/index.php/roneurosurgery endoscopic lumbar discectomy using side viewing conical working tube. an institutional experience mohammad kaif, kuldeep yadav, rakesh kumar, deepak kumar singh department of neurosurgery. “dr ram manohar lohia” institute of medical sciences, lucknow, india abstract objective: the paradigm of surgical therapy for spinal disease especially for lumbar disc herniation has gradually shifted from traditional open surgeries to minimally invasive spinal surgeries. endoscopic discectomy has been performed widely using various devices and techniques. in this study, we present our experience of endoscopic discectomy using a unique device with separate side viewing channel. methods: 26 patients of lumbar disc herniation treated between march 2015 to april 2018 using the unique conical working tube with separate side-viewing endoscopic channel have been retrospectively analysed. their preoperative and postoperative oswestry disability index (odi) and macnab scores were used to evaluate the outcome with a mean follow up of 37.04 months. results: there were 18 males and 08 females with age ranging from 19-72 years (mean-38.4 years). the follow up ranged from 25 months to 60 months with a mean of 37.04 months. the mean preoperative odi score was 72.4 which decreased to a mean of 7.6 and the outcome evaluated by macnab criteria was 65.3% excellent, 19.2 % good, 11.5% fair, 3.8% poor. 1 patient underwent a second surgery. none of the patients had to change their occupation postoperatively. complications occurred were dural tear in 1 patient and transient foot paresis in 1 which improved spontaneously. conclusion: endoscopic discectomy using conical working tube is a safe and effective technique for lumbar disc prolapse. the long-term results are comparable to conventional techniques. introduction endoscopic lumbar discectomy for lumbar disc herniation (ldh) has been an ever-evolving procedure since its inception, because of the benefits it caters over open surgery. open surgical procedures for ldh are associated with greater muscle, nerve roots and dural sac retraction, lamina and facet joint resection, etc. this leads to more muscular injury, epidural scarring, postoperative pain, longer hospital stays and greater blood loss. endoscopic lumbar discectomy overcomes these associated drawbacks of open surgery for ldh but is associated with its own keywords lumbar disc herniation, endoscopic discectomy, side viewing endoscopic device corresponding author: mohammad kaif “dr ram manohar lohia” institute of medical sciences, lucknow, india dr_kaifmohd@yahoo.co.in copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 109 endoscopic lumbar discectomy using side viewing conical working tube difficulties and complications. steep learning curve, endoscopic approach related anatomical limitations and vague tissue differences are few problems associated with endoscopic procedures. various devices have been developed to increase the ease of procedure and reduce the learning curve along with associated complications. kambin and gellman first introduced endoscopic lumbar discectomy in 1973.11 later various devices were introduced like yeung endoscopic spine system (yess), transforaminal endoscopic spine system (tessys), destandau system etc.18,7,4 similarly various authors have reported their experience of endoscopic discectomy using different devices , although many of these lack the literature on long term results of endoscopic surgery.4,5,12,2 in this article we present our institutional experience of endoscopic discectomy using the conical working tube with separate viewing channel. methods study setting: this study was conducted in the department of neurosurgery dr ram manohar lohia institute of medical sciences, lucknow, india. study design and period: it is a retrospective study based on follow up of 26 patients of ldh treated using the conical working tube with side viewing endoscopic channel.9 the hospital records of 38 patients who underwent endoscopic lumbar discectomy using this device between march 2015 to april 2018 were retrieved. only those patients were included in this study who could be contacted on telephone and responded to the odi (oswestry disability index) and macnab score formats. study participants: endoscopic surgery was conducted on patients who presented with low backache along with radicular pain in lower limbs with or without neurological deficit and failed conservative management. patients with segmental instability, no clinico-radiological correlation or evidence of infection were excluded from this study. there were 18 males and 08 females with age ranging from 19 years-72 years (mean-38.4 years). the follow up ranged from 25 months to 60 months with mean of 37.04 months. instrument design: this device comprises of a conical working tube which is passed over coaxial dilators and secured in position by a holding device attached to the operating table. it has a separate side viewing channel for the telescope which is attached to a light source and camera. no special instruments are used for laminotomy and discectomy. (figure 1) operative technique: patient is positioned prone after general anaesthesia on a wilson’s frame or foam bolsters. level is localised using fluoroscopy. incision deep to fascia is given 1 cm lateral to midline. firstly, a dilator is passed with a 5mm trocar up to the lamina and the trocar is removed. a gentle medial to lateral and cranial to caudal sweeping movements are done for the elevation of soft tissue. serial dilators are passed over this first tube followed by the working tube over these dilators which is finally fixed to table after removal of serial dilators. position of the working tube is confirmed under fluoroscopy. a cannula with trocar is passed from the separate side channel through a separate stab incision and locked in the working tube using the locking mechanism. a zero-degree telescope (4 mm diameter and 180 mm length) is passed through this separate channel. the tip of the telescope just reaches up to the inner part of the working tube. the light source and camera is attached to the cannula and the image orientation is done by rotating the camera on scope. (figure 1) figure 1. a instrument design, b instrument setup with telescope and light source, c fluoroscopic view with endoscopic device. medial part of the facet and contiguous lamina are identified. a small hemi-laminotomy and medial facetectomy were done using kerrison rounger. the ligamentum flavum is detached from the under surface of the lamina and removed. traversing nerve root and thecal sac are identified using a ball probe. the nerve root is retracted medially and the disc is removed by entering the disc space through the annular tear or an annulotomy. the disc space is irrigated with normal saline to wash out the loose 110 mohammad kaif, kuldeep yadav, rakesh kumar et al. disc fragments. the nerve root is inspected to ensure adequate decompression. (figure 2) the entire assembly is removed and the fascia is closed with absorbable suture. skin is closed using subcuticular sutures. figure 2. a nerve root, b medial of part facet joint, c disc fragment being excised, d disc space after discectomy. postoperative management: patients were mobilized in the evening of the day of surgery and were discharged on the next postoperative day. in this study the mean hospital stay was 1.6 days. complications: an incidental dural tear was observed in 1 patient. this was managed by sealing the defect by fibrin glue. no postoperative csf leak or pseudomeningocele or any long-term sequelae were observed. the other postoperative complication was transient foot paresis in 1 patient which improved spontaneously. results patients were evaluated using odi score. the score was interpreted as 0% to 20% (minimal disability), 21% to 40% (moderate disability), 41%to 60% (severe disability), 61% to 80% (crippled) and 81% to 100% (bed bound/ exaggerating their symptoms). both the preoperative and postoperative odi were compared and its differences were calculated. the mean preoperative odi score was 72.4 which decreased to a mean of 7.6 postoperatively. the final outcome was evaluated using macnab criteria which was divided into excellent, good, fair and poor categories. as per macnab criteria 65.3% (n=17) had excellent outcome, 19.2 % (n=05) had good, 11.5% (n=03) had fair, 3.8% (n=01) had poor outcome. one patient experienced persistent radicular pain of same intensity and was diagnosed to have a residual disc fragment which was removed later by microsurgery. none of the patients had to change their occupation due to their lumbar disc disease. (table 1) s. no procedural characteristics value 1 outcome (mac nab) excellent good fair poor n=17 ( 65.3% ) n=5 ( 19.2% ) n=3 ( 11.5% ) n=1 ( 3.8% ) oswestry disability index (odi) mean preoperative score mean postoperative score 72.4 7.6 2 complications dural tear transient foot paresis n=1 ( 3.8%) n=1 ( 3.8%) 3 repeated surgery n=1 ( 3.8%) table 1. summary of procedure related data. discussion lumbar intervertebral disc herniation, leading to various symptoms have been catered through multiple operative modalities. the classic discectomy described by mixter and barr14 has undergone a series of modifications to develop into the present day discectomy procedure.15 the classic discectomy required a larger incision, separation and retraction of paraspinal muscles that led to an increase in postoperative morbidity such as increased pain, a delay in resuming activities and a lengthy hospital stay with significant financial burden on patients especially in a developing nation. moreover, the extensive surgery could lead to the instability of spine with due course of time. to overcome the disadvantages and problems 111 endoscopic lumbar discectomy using side viewing conical working tube associated with classic discectomy, various minimal invasive techniques have been developed. in 1978, williams17 described micro discectomy which established as a guide to a lesser invasive approach to lumbar spine. this was the mini variant of conventional discectomy through a much smaller incision as compared to the previous technique. howe and frymoyer8 reported a success rate of 60%–97% with the micro discectomy but it still required the separation of paraspinal muscles from the lamina and spinous process leading to the denervation of the paraspinal muscle complex and causing a delay for the patient in resuming daily activities. endoscopic spinal surgery began as percutaneous endoscopic discectomy. kambin (1973) and hijikata et al. (1975) had attempted the earliest endoscopic surgery in 1970’s.16 since then this technique has got modifications through generations10, in order to improve the patient outcome and increase the domain of indications for endoscopic spine surgery (table 2). various authors have described their results of micro endoscopic discectomy (med) some of which are mentioned in table 3. jensdottir et al in their retrospective study reported a good/excellent outcome of micro discectomy10. casal moro et al in their prospective study reported that med is a safe technique with lesser tissue trauma and comparable results to that of conventional techniques3. bhansare et al reported their experience using the destandau technique with excellent short and long term results1. first generation second generation third generation newer innovation yeung endoscopic spine system interlaminar uniportal endoscopic spine surgery endoscopic decompression endoscopic lumbar interbody fusion surgery percutaneous endoscopic lumbar discectomy interlaminar biportal endoscopic spine surgery endoscopic foraminotomy transforaminal endoscopic lumbar discectomy table 2. generations of endoscopic spinal surgery. author/y ear numb er of patie nts outco me measu res outcome recurre nce complication kulkarn i et al. 2014 188 vas, odi statisticall y significant pain relief 3 (1.5%) 11 (5%) dural tears, 1(0.5%)infec tion, 1(0.5%) wrong level hussein et al. 2014 185 nrs, mcnab odi statisticall y significant pain relief 2 convert ed to open 3 dural tears li et al. 2015 72 vas, odi, mcnab 97% good to excellent 1 no complicatio ns kyung chul choi et al. 2016 20 vas, odi 91.3% good to excellent 1 1 transient neurological deficit sung soo eun et al. 2016 62 vas, mac nab significant pain relief 06 2 dural tears kyung chul choi et al. 2017 149 vas, odi 90.6% good improve ment 04 1 transient neurological deficit kaif et al 2017 66 vas, odi, mac nab 86.36% good to excellent 02 discitis 1, dural tear 2, transient foot paresis 1 hyung sun kim et al. 2018 98 vas, odi 96.1% good to excellent 03 2 neurologica l deficit ziquan li et al. 2019 21 vas, odi significant improve ment 00 2 dural tear 1 dysesthesia chao li et al. 2019 184 vas, odi, mac nab 89.3% good to excellent 14 4 dural tear 1 neurological deficit * vas: visual analogue scale, odi: oswestry disability index. table 2. studies of endoscopic discectomy. 112 mohammad kaif, kuldeep yadav, rakesh kumar et al. our study also reveals the similar results regarding the excellent/good outcome of the patients using our specific side viewing conical working tube. the results with this device were excellent to good in 84.5% of cases after a mean follow up of 37.04 months which is comparable with other studies of all the minimally invasive lumbar discectomy techniques practiced worldwide. casalmoro reported surgical complication rate of 3 to 10 % in various techniques whereas destandau in his series reported 3.5% and 4 of his patients required reoperation18. in our series we experienced 7.7% (n=2) of such complications and 3.8% (n=1) required reoperation. the popular device used for med is the metrx system, which is a serial dilator system utilizing the interlaminar corridor. it has a telescope mounted at the top end edge of the working channel, but as experienced by the senior surgeons this technique causes clutter while working bimanually through the working tube. the other disadvantage is the high cost of the specialized hardware. the destandau system is another popular device with excellent to good long-term results but it has the disadvantage that direct visualization using naked eye or microscope is not possible and also minimally invasive inter-body fusion cannot be performed through this device. the cost of these devices are very high which is one of the major hindrance in expansion of this technique. our system is an indigenous innovation with a very low cost. the freedom of surgical maneuverability is the advantage9. the hardware cost is further reduced as it utilizes the conventional discectomy instruments and same telescope which is used in transcranial endoscopic surgeries. conclusions endoscopic discectomy using this conical working tube is a safe, effective and low cost technique for lumbar disc prolapse. it has the advantage for early mobilization, short hospital stays and lower financial burden. overall outcome is comparable to the conventional techniques. limitation our study has limitations with the retrospective nature of the data collection. small sample size is also a limitation of this study. references 1. bhaisare r, kamble b, patond k: long-term results of endoscopic lumbar discectomy by "destandau's technique" asian spine j. 2016 apr; 10(2): 289–297. 2. bhandari s. early experiences in endoscopic lumbar discectomy by destandau technique for prolapse intervertebral disc. j maharashtra orthop. assoc. 2006; 4:174-79. 3. casal-moro r, castro-menéndez m, hernándezblanco m, bravo-ricoy ja, jorge-barreiro fj. long term outcome after microendoscopic diskectomy for lumbar disk herniation: a prospective clinical study with a 5-year follow-up. neurosurgery. 2011;68(6):1568-75; discussion 1575. 4. destandau j. technical features of endoscopic surgery for lumbar disc herniation: 191 patients. neurochirurgie 2004; 50:6-10. 5. destandau j. a special device for endoscopic surgery of lumbar disc herniation. neurol. res 1999; 21:39-42. 6. findlay gf, hall bi, musa bs, et al: a 10-year follow up of the outcome of lumbar microdiscectomy. spine (phila pa 1976). 1998; 23:1168–1171. 7. hoogland t, schubert m, miklitz b, et al. transforaminal posterolateral endoscopic discectomy with or without the combination of a low-dose chymopapain: a prospective randomized study in 280 consecutive cases. spine (phila pa 1976) 2006; 31: e890-7. 8. howe j, frymoyer jw. the effects of questionnaire design on the determination of end results in lumbar spinal surgery. spine (phila pa 1976) 1985; 10:804-5. 9. husain m, jha dk, agrawal s, husain n, gupta rk. conical working tube: a special device for endoscopic surgery of herniated lumbar discs. neurosurg. j spine. 2005;2(3):265-70. 10. jensdottir m, gundmundsson k, hannesson b et al: 20 year follow up after the first microsurgical lumbar discectomies in iceland. acta neurochir(wein)2007; 149:51-58. 11. li x, hu z, cui j, et al. percutaneous endoscopic lumbar discectomy for recurrent lumbar disc herniation. int j surg 2016; 27: 8-16. 12. lyson t, mariak z, jadeszko m, kochanowicz j, lewko j. results of destandau microendoscopic lumbar discectomy. neurol. neurochir. pol 2008; 42:10511. 13. manyoung kim, hyeun-sung kim, sung woon oh, et al. evolution of spinal endoscopic surgery. neurospine 2019;16(1):6-14. 14. mixter wj, barr js. rupture of the intervertebral disc with involvement of the spinal canal. n engl j med 1934; 211:210-5. 15. smith mm, foley kt. microendoscopic discectomy (med): surgical technique and initial clinical results. proceedings of the thirteen annual meeting of the joint section of disorders of the spine and peripheral nerve of the american association of neurological surgeons; 1997 feb; newport beach, ca. 16. telfeian ae, veeravagu a, oyelese aa, et al. a brief history 113 endoscopic lumbar discectomy using side viewing conical working tube of endoscopic spine surgery. neurosurg focus 2016; 40:e2. 17. williams rw. microlumbar discectomy: a conservative surgical approach to the virgin herniated lumbar disc. spine (phila pa 1976) 1978; 3:175-82. 18. yeung at, tsou pm. posterolateral endoscopic excision for lumbar disc herniation: surgical technique, outcome, and complications in 307 consecutive cases. spine (phila pa 1976) 2002; 27: 722-31. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article single center experience and technical nuances in the treatment of distal anterior cerebral artery aneurysms dorin nicolae gherasim, gabriel gyorki, adrian balasa romania doi: 10.1515/romneu-2017-0003 romanian neurosurgery (2017) xxxi 1: 17 – 24 | 17             doi: 10.1515/romneu-2017-0003 single center experience and technical nuances in the treatment of distal anterior cerebral artery aneurysms dorin nicolae gherasim, gabriel gyorki, adrian balasa department of neurosurgery, targu mures, romania abstract: objective: this study presents the experience of one neurosurgical center in the treatment of 18 consecutive patients with distal anterior cerebral artery (daca) aneurysms during a 10 years period. our aim was to compare treatment outcomes of these lesions with intracranial aneurysms in general, and to present technical nuances in surgical treatment. methods: we analyzed the clinical and radiological data of 18 patients treated between 2005 and 2015. all patients were treated surgically using the microscope. no patients were lost to follow-up. we compared treatment and outcome of ruptured daca aneurysms (n 18) with all consecutive ruptured aneurysms treated in our clinic during the same period (n 446). results: daca aneurysms accounted for 4% of all intracranial aneurysms. they were smaller (median, 5,5 versus 9 mm) we found only one case with associated aneurysms (5,5%). daca aneurysms presented more often with intracerebral hematomas (39% versus 26%) than ruptured aneurysms in general. their microsurgical treatment showed the same complication rates (treatment morbidity, 15%) as for other ruptured aneurysms in literature. their mortality rate was lower (11% versus 24%). conclusion: despite their specific anatomic features, and particular surgical technique, with modern treatment methods, ruptured daca aneurysms have the same favorable outcome and lower mortality as ruptured aneurysms in general. key words: cerebral aneurysm, distal anterior cerebral artery, pericallosal artery, subarachnoid hemorrhage distal anterior cerebral artery aneurysms (daca), frequently referred to as pericallosal artery aneurysms, represent aneurysms that arise distal tot the anterior communicating artery (acoma), most commonly at the origin of the callosomarginal artery. they are uncommon, comprising only 2.7 to 9.2% (mean, 4.4% in 13 large series) of all intracranial aneurysms. (14, 23, 10) their location in the interhemispheric fissure, the association with intracerebral hemorrhage, with multiple aneurysms and with vascular anomalies of the anterior cerebral artery (aca) offer the neurosurgeon 18 | gherasim et al treatment of distal anterior cerebral artery aneurysms             a complex pathology and challenging surgical technique. the complexity of this pathology is completed by the specific anatomic features of daca aneurysms, such as their small size and the broad neck with originating branches at this level (14, 23). anatomy the acoma is normally divided into five segments, a1 through a5 (fig. 1). segments a2 through a5 form the daca. the a2 segment extends from the acoma to the junction between the rostrum and genu of the corpus callosum. the a3 segment courses around the genu of the corpus callosum and ends at the point where the vessel takes a sharp turn posteriorly. the a4 segment runs superior to the corpus callosum, extending to a point just behind the coronal suture. the a5 segment is the portion of the acoma that lies posterior to the coronal suture (10). the literature is lacking detailed studies on the anatomy of daca aneurysms, with the notable exception of the finnish group coordinated by hernesniemi et al which divided daca aneurysms in seven groups, with the genu of the corpus callosum (gcc) as the anatomic landmark for this division (aneurysms at each of these locations require a modified microsurgical approach). 1) frontobasal aneurysms: located on the a2 frontobasal branches. 2) a2 trunk aneurysms: located directly on the a2 segment. 3) inferior a3 aneurysms: located on the proximal part of the a3 segment inferior to the gcc. 4) anterior a3 aneurysms: located on the central part of the a3 segment anterior to the gcc. 5) superior a3 aneurysms: located on the distal part of the a3 segment superior to the gcc. 6) a4 or a5 aneurysms. 7) distal branch aneurysms: located on the distal cortical branches originating from the a3 to a5 segments: the callosomarginal artery (cma) (14, 3). objectives this study presents the experience of one neurosurgical center in the treatment of 18 consecutive patients with ruptured daca aneurysms during a 10years period. our aim was to compare treatment outcomes of these lesions with intracranial aneurysms in general, and to present technical nuances in surgical treatment. material and methods we analyzed the clinical and radiological data of 18 patients treated between 2005 and 2015. all patients were treated surgically by clip ligation using the microscope. no patients were lost to follow-up. we compared treatment and outcome of ruptured daca aneurysms (n 18) with all consecutive ruptured aneurysms treated in our clinic during the same period (n 446). results from the 466 patients treated for ruptured cerebral aneurysms in our department, 18 presented with ruptured daca aneurysms representing 3,8%. mean age was 53 years, and females were twice as frequent than men. we used the classification developed by the finnish group (14), in order to classify those 18 aneurysms, and as a result we observed that the majority of our cases were type 4 located aneurysms – anterior a3 aneurysms (table 1). romanian neurosurgery (2017) xxxi 1: 17 – 24 | 19             table i number of patients according to hernesniemi’ classification of daca aneurysms daca aneurysm classification no of cases (%) type 1 1 (5,5) type 2 1 (5,5) type 3 2 (11) type 4 11 (77,5) type 5 3 (16,5) as seen in table 2, 50% of patients with daca aneurysms in our clinic were admitted in good clinical condition (hunt-hess 1and 2), with only 1 patient being admitted in critical condition (hunt-hess5). table ii clinical (hunt-hess and wfns scores) and imagistic status (fisher scale) at presentation intracerebral or interhemispheric hematoma was seen in 7 patients, representing 38,8% of patients with daca aneurysms (figure 1). from the imagistic point of view, as a protocol, every patient had native head ct scan upon admission. if subarachnoid hemorrhage (sah) or intracerebral hematoma (ich) were present raising the suspicion of ruptured aneurysm, the patient was sent to angio suite, for a 4 vessel cerebral angiography (figure 2). the medium size of daca aneurysms in our series was 6.2 mm (range 4.5-12 mm), and 13 patients harboured daca aneurysms smaller than 7 mm (72.2%). an interesting finding was the fact that from the 18 patients in our series we had only one case with associated unruptured cerebral aneurysm representing only 5,5%. figure 1 non enhanced ct scan of patient with fisher 3 sah figure 2 left aci injection on ds angiography on the same patient revealing a type 3 saccular aneurysm on the left daca nr hunt hess wfns fisher scale 1 1 1 2 2 1 1 2 3 3 3 2 4 1 1 3 5 2 2 4 6 3 4 4 7 3 2 3 8 2 1 2 9 1 1 4 10 1 2 2 11 3 2 4 12 3 4 3 13 3 3 4 14 5 5 4 15 3 4 2 16 3 3 4 17 2 3 2 18 1 1 2 20 | gherasim et al treatment of distal anterior cerebral artery aneurysms             surgical technique our service has an “early surgery” policy, thus 78% of patients were admitted in our service in the first 24h after rupture and 72% underwent early surgery. as a technique, the goal was to identify the parent vessel and to obtain proximal control as soon as possible, so interhemispheric approach and dissection was carried out following interhemispheric cortical arteries which took us as close as possible to the anterior communicating complex on the anterior fossa floor. after identifying the post communicating segment of the anterior cerebral arteries, dissection along their trajectory was realized with the identification of the saccular aneurysm and the emerging branches. there are some particular aspects that need to be considered when performing surgery for daca aneurysms. first the interhemispheric fissure provides a narrow corridor for the approach. there is little csf present in the interhemispheric cisterns, so in order to simplify the approach on a swallowed brain, external ventricular drain (evd) or lumbar drainage can be an option. the arachnoid adhesions make the dissection of interhemispheric cisterns difficult. additionally, parasagittal veins may represent a challenge – but these structures must be preserved. and of course, once the interhemispheric approach is realized, early identification of parent vessel isn’t always easy. figure 3 intraoperative images of a right frontal interhemispheric approach and clipping of type 3 daca aneurysm romanian neurosurgery (2017) xxxi 1: 17 – 24 | 21             outcomes clinical outcome was assessed using the modified rankin scale (mrs) both at discharge and at six months. we considered good outcome an m rs between 0 and 2. as seen in tables 3 and 4 there is a clear relation between the neurological status at admission and the clinical outcome. in the patients group with good neurological status at admission (hunt-hess 1 and 2), n-10, there was only one patient (10%) with poor outcome – m rs-5. table iii clinical outcome of patients with daca aneurysms in our clinic table iv relation between the neurological status at admission and the clinical outcome in the group of patients with poor neurological status at admission (n-8), there were 6 patients (75%) with poor outcome (m rs-3-6). the only patient in this group admitted in critical condition (hunt-hess-5), died one week after surgery. perioperative complications included intraoperative rupture of aneurysm (4 cases – 22,2%), postoperative intracerebral hematoma (1 case-5,5%) and meningitis (1 case – 5,5%). the overall morbidity was 11% (2 cases). discussion clinical outcome the outcomes obtained in this small series are comparable to those of previous reports. we evaluated 18 patients treated for ruptured daca aneurysm. successful clipping was achieved in all of these patients, with no recurrence of sah at 6 months and no need for retreatment (2, 28, 25). good clinical outcome, measured using m rs (m rs 0 2) was achieved in 11 patients (60,5%). in our study, the statistically significant predictor of outcomes in the patients with sah was the presenting hunthess score. patients in a lower hunt-hess grade (i and ii) had a favorable outcome in 90% of cases, compared with 25% of patients in the hunt-hess groups iii, iv and v. these results show that, despite the difficulties associated with aneurysms in this location, good results can be achieved in most patients who have a good clinical grade. poor grade patients remain a significant challenge, particularly those patients with large parenchymal hemorrhages (1, 15, 24, 29). outcome at 6 months favorable (mrs 0-2) 12 cases (67%) unfavourable (mrs 3-6) 6 cases (33%) h-h/mrs 0 1 2 3 4 5 6 i 3 2 1 0 0 0 0 ii 0 1 2 0 0 1 0 iii 0 1 1 3 1 1 0 iv 0 0 0 0 0 0 0 v 0 0 0 0 0 0 1 22 | gherasim et al treatment of distal anterior cerebral artery aneurysms             ohno et al concluded in their analysis that daca aneurysms tend to rupture at a smaller size. in their series, 73% of the patients harbored aneurysms smaller than 5 mm. in pandey et al series, the majority of patients harbored aneurysms smaller than 6 mm. in our series 72% of daca aneurysms treated were smaller than 7 mm with a median size of 6.2 mm. thus, the question of whether unruptured daca aneurysms should be treated at a smaller size compared to the limit of 7 mm set by the isuia trial for anterior circulation aneurysms, seems to be a valid one, and needs further investigation (16, 21, 22). symptomatic vasospasm represents the most important cause of morbidity in patients surviving sah and affects up to 30% of patients presenting with sah caused by ruptured aneurysms in the anterior circulation (6, 8, 17). in our series, only two patients developed clinically significant vasospasm, both with fisher grade iii sah on ct scans. the majority of our patients were in fisher grade ii (50%) and iv (39%) and, thus, would not be supposed to develop vasospasm. it seems that patients with distal aneurysms (daca/mca) have a lower incidence of spasm because most of these patients tend to have localized bleeding instead of the diffuse sah. surgical technique and nuances microsurgical clipping remains the main therapeutic tool, the endovascular treatment being limited by the distal location and complex anatomy of daca aneurysms. (4, 7, 9) nonetheless, surgical clipping of daca aneurysm presents with specific difficulties compared with other locations, as described in previous studies (11, 13, 26, 27). the particularities of daca aneurysms are related to the narrow approach and deep location making the approach less straight forward. as described by the majority of the authors, we utilized a right frontal interhemispheric approach making sure to have proximal control before dissecting and clipping the aneurysm. the approach was adapted to the type of daca aneurysm ranging from frontobasal approaches for type 1 and 2 daca aneurysms to frontoparietal craniotomies for the more distally located aneurysms. although rarely used, neuronavigation can be an important additional tool in the neurosurgeon’s armamentarium, making the approach less invasive and more straight forward. once the approach realized, early identification of parent vessel is of paramount importance because of the lack of anatomic landmarks which makes safe dissection and clipping of daca aneurysm difficult. these factors make these aneurysms more prone to early intraoperative rupture, lehecka et al reporting in their large 501 patients study an incidence of 22% of intraoperative rupture (15). in our study we had similar results, with 5 patients (27,5%) that had early intraoperative rupture. all cases were managed without early or late postoperative complications. the overall rate of complications was 11% (1 case of meningitis, and 1 case of postoperative intracerebral hematoma), and these complication rates are similar to those reported in the literature for the treatment of daca aneurysms (9, 13, 14, 19). romanian neurosurgery (2017) xxxi 1: 17 – 24 | 23             conclusions daca aneurysms are usually small with specific anatomic features such as wide neck and association with anatomic variations of aca. surgical clipping is a safe and effective method of treatment, but it must be adapted to the location of the aneurysm on the aca, and proximal control is of paramount importance. following the actual trend for the treatment of intracranial aneurysms, most of these aneurysms will eventually be treated by endovascular means (5, 12, 18, 20). nonetheless, knowledge of the specific features regarding the microsurgical approach and clipping of these aneurysms and the expected outcomes remain an important skill in the arsenal of vascular neurosurgeons. correspondence dr. dorin nicolae gherasim – md, neurosurgeon, department of neurosurgery, targu mures tel: +40 726 29 26 27 fax:+40 265 210621 e-mail: dorin.gherasim@gmail.com references 1. auguste ki, ware ml, lawton mt, nonsaccular aneurysms of the azygos anterior cerebral artery, neurosurg focus 17 (5): e12, 2004; 2. carter bs, sheth s, chang e, sethl m, ogilvy cs: epidemiology of the size distribution of intracranial bifurcation aneurysms: smaller size of distal aneurysms and increasing size of unruptured aneurysms with age, neurosurgery 58:217–223, 2006. 3. cavalcanti dd, albuquerque fc, silva bf, spetzler rf, preul mc, the anatomy of the callosomarginal artery: applications to microsurgery and endovascular surgery, neurosurgery 66:602-610, 2010 4. chhabra r, gupta sk, mohindra s, mukherjee k, bapuraj r, khandelwal n, khosla vk: distal anterior cerebral artery aneurysms: bifrontal basal anterior interhemispheric approach. surg neurol 64:315–320, 2005. 5. cohen je, rajz g, itshayek e, shoshan y, umansky f, gomori jm, endovascular management of traumatic and iatrogenic aneurysms of the pericallosal artery. report of two cases., j neurosurg 102:555–557, 2005. 6. de sousa aa, dantas fl, de cardoso gt, costa bs: distal anterior cerebral artery aneurysms. surg neurol 52:128–136, 1999. 7. ferroli p, ciceri e, addis a, broggi g, self-closing surgical clips for use in pericallosal artery–pericallosal artery side-to-side bypass. case report, j neurosurg 109:330–334, 2008. 8. inci s, erbengi a, ozgen t: aneurysms of the distal anterior cerebral artery: report of 14 cases and a review of the literature. surg neurol 50:130–140, 1998. 9. gelfenbeyn m, natarajan sk, sekhar ls, large distal anterior cerebral artery aneurysm treated with resection and interposition graft: case report, neurosurgery 64: e1008–e1009, 2009 10. kakou m, destrieux c, and velut s, microanatomy of the pericallosal arterial complex, j neurosurg 93:667– 675, 2000 11. kawashima m, matsushima t, sasaki t, surgical strategy for distal anterior cerebral artery aneurysms: microsurgical anatomy, j neurosurg 99:517–525, 2003 12. keston p, white pm, horribine l, sellar r: the endovascular management of pericallosal artery aneurysms. j neuroradiol 31:384–390, 2004. 13. kim lj, albuquerque fc, mcdougall c, spetzler rf. combined surgical and endovascular treatment of a recurrent a 3 –a 3 junction aneurysm unsuitable for stand-alone clip ligation or coil occlusion, neurosurg focus 18 (2): e6, 2005; 14. lehecka m, porras m, dashti r, niemelä m, hernesniemi ja, anatomic features of distal anterior cerebral artery aneurysms: a detailed angiographic analysis of 101 patients, neurosurgery 63:219–229, 2008; 15. lehecka m, lehto h, niemelä m, juvela s, dashti r, koivisto t, ronkainen a, rinne j, jääskeläinen je, hernesniemi ja, distal anterior cerebral artery aneurysms: treatment and outcome analysis of 501 patients, neurosurgery 62:590–601, 2008 16. lehecka m, niemelä m, seppänen j, lehto h, koivisto t, ronkainen a, rinne j, sankila r, jääskeläinen j, hernesniemi j, no long-term excess 24 | gherasim et al treatment of distal anterior cerebral artery aneurysms             mortality in 280 patients with ruptured distal anterior cerebral artery aneurysms, neurosurgery 60:235–241, 2007. 17. martinez f, spagnuolo e, calvo a: aneurysms of the distal anterior cerebral artery [in spanish]. neurocirugia (astur) 16:333–344, 2005. 18. menovsky t, van rooij wj, sluzewski m, wijnalda d: coiling of ruptured pericallosal artery aneurysms. neurosurgery 50:11–15, 2002. 19. miyazawa n, nukui h, yagi s, et al: statistical analysis of factors affecting the outcome of patients with ruptured distal anterior cerebral artery aneurysms. acta neurochir 142:1241–1246, 2000 20. nguyen tn, raymond j, roy d, chagnon m, weill a, iancu-gontard d, f guilbert, endovascular treatment of pericallosal aneurysms, j neurosurg 107:973–976, 2007 21. ohno k, monma s, suzuki r, masaoka h, matsushima y, hirakawa k. saccular aneurysms of the distal anterior cerebral artery. neurosurgery. 1990;27:907–12. 22. pandey a, rosenwasser rh, veznedaroglu e, management of distal anterior cerebral artery aneurysms: a single institution retrospective analysis (1997–2005), neurosurgery 61:909–917, 2007 23. perlmutter d, rhoton, jr al., microsurgical anatomy of the distal anterior cerebral artery, j neurosurg 49:204-228, 1978 24. ross n, hutchinson pj, seeley h, kirkpatrick pj: timing of surgery for supratentorial aneurysmal subarachnoid haemorrhage: report of a prospective study. j neurol neurosurg psychiatry 72:480–484, 2002. 25. steven da, lownie sp, ferguson gg, aneurysms of the distal anterior cerebral artery: results in 59 consecutively managed patients, neurosurgery 60:227– 234, 2007; 26. traynelis vc, dunker ro, interhemispheric approach with callosal resection for distal anterior cerebral artery aneurysms. technical note, j neurosurg 77:481-483, 1992. 27. türe u, hicdönmez t, elmaci i, peker s: giant pericallosal artery aneurysm: case report and review of the literature. neurosurg rev 24:151–155, 2001. 28. ugur hc, kahilogullari g, esmer af, comert a, odabasi ab, tekdemir i, elhan a, kanpolat y: a neurosurgical view of anatomical variations of the distal anterior cerebral artery: an anatomical study. j neurosurg 104:278–284, 2006 29. yasargil mg, carter p, saccular aneurysms of the distal anterior cerebral artery, j neurosurg. volume 39 february, 1974 romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article sturge weber syndrome: review of literature with case illustration guru dutta satyarthee, manik prabhu, luis rafael moscote-salazar india, colombia doi: 10.1515/romneu-2017-0019 122 | satyarthee et al sturge weber syndrome             doi: 10.1515/romneu-2017-0019 sturge weber syndrome: review of literature with case illustration guru dutta satyarthee1, manik prabhu1, luis rafael moscote-salazar2 1department of neurosurgery, aiims new delhi, india 2neurosurgeon-critical care, red latino. latin american trauma & intensive neuro-care organization, bogota, colombia abstract: sturge-weber syndrome (sws) also called as encephalotrigeminal angiomatosis, is a sporadically occurring rare neuro-cutaneous syndrome, characterized by vascular malformation with capillary venous angiomas involving face, choroidal layer of eye globe and leptomeninges responsible for ophthamological as well as neurological signs and symptoms. authors report an interesting case, a six year old girl, who presented with seizures, facial port wine stain and normal psychomotor development. ct scan showed left cerebral hemiatrophy, left frontal and parieto occipital calcification with cortical calcification in left high frontal convexity. cranial mri scan also confirmed finding of left cerebral hemiatrophy and also revealed presence of gyriform cortical calcification, prominent flow voids seen in left basal ganglia. her seizure is well controlled with antiepileptic medication. the pertinent literature is reviewed and management of such cases is discussed briefly. key words: sturge-weber syndrome, seizure, port wine stain, development introduction sturge-weber syndrome is a rare disorder that occurs with a frequency of 1: 50,000 [1]. sws is sporadic neurocutaneous disease, being characterized by presence of facial portwine stain, ocular glaucoma and choroidal haemangioma in the eye, leptomeningeal angioma often involving occipital and posterior parietal lobes. this syndrome comprises of constellation of symptoms and signs i.e. including facial nevus, seizures, intracranial hemiparesis, calcification and association of mental retardation [2-8]. case illustration a 6-year-old girl presented to our emergency services with history of left focal motor seizure with secondary generalization lasted about five minutes associated with loss of unconsciousness , frothing of mouth and urinary incontinence. she had six episodes of similar seizures over last two years, which were not associated without any post-ictal neurological deficits. for which, she was kept on phenylhydantoin but not controlled, however, with addition of phenobarbitone, seizures are well controlled and she had no romanian neurosurgery (2017) xxxi 1: 122 – 128 | 123             fresh seizure for last one year. parents noticed facial port wine discoloration at birth involving right upper part of face; baby was first issue of nonconsanguineous marriage, delivered normally at full term. perinatal history was unremarkable. she was vaccinated at our institute under supervision of paediatrician, as part of universal immunization programme against diphtheria, pertusis, tetanus and b.c.g. no history of trauma, drug allergy or exanthematous rashes. she had normal psychomotor development. at present patient has no neurological deficit. patient has venous angiomas involving ophthalmic segment of right trigeminal nerve. on physical examination, the pulse rate was 110 per minute, respiratory rate 24 per minutes and blood pressure 96/72 mm hg. there was port-wine stain involving upper half of right upper face. she was incoherent to speech with glasgow-coma scale of 14/15, with presence of left facial port wine venous angiona (figure 1 a) both pupils were briskly reacting but uncooperative for fundus evaluation and rest of neurological examination was unremarkable. a peripheral venous access was made by putting intravenous canula, immediately after her arrival in emergency room. blood sample were taken for blood sugar serum phenytoin level and blood chemistry. seizures were controlled with intravenous midazolam. hematological and biochemical profile carried out in emergency care unit was within normal range. computerized tomography (ct) scan of the head revealed left cerebral hemi atrophy involving left frontal and parieto-occipital lobe with cortical subcortical calcification (figure 1 b, c, d) along with enlargement of left lateral ventricle choroid plexus. progress was satisfactory and her residual neurological speech deficit resolved within after two hours. child was discharged on phenytoin and phenobarbitone. mri scan of brain was carried out during follow-up period revealed, left cerebral hemiatrophy with gyriform cortical calcification, (figure 2) prominent flow voids seen in left basal ganglia. (figur 3) choroid plexus enlargement seen in left lateral ventricle. (figure 4) no diffusion restriction on dwi images. cerebellum and brain stem are normal. hypertrophy of calvarium on left side also noted. (figure 5) ophthalmological evaluation was done, showed no evidence of ocular involvement. she is under our regular follow-up. figure 1 a clinical photograph showing portwine venoios angioma over left side of face 124 | satyarthee et al sturge weber syndrome             b c d figure 1 b, c, d contrast enhanced computed tomography head showing atrophy of left cerebral hemisphere with calvarial thickening in a six-year girl with sturge weber syndrome with calcification figure 2 mri brain axial t2 weighted image showing atrophy of left cerebral hemisphere figure 3 mri brain of six -yearold female with sturge weber syndrome coronal section, t2 weighted image showing atrophy of left cerebral hemisphere romanian neurosurgery (2017) xxxi 1: 122 – 128 | 125             figure 4 mri brain of a six years girl, t2 weighted image showing presence of left cerebral hemispheric atrophy figure 5 mri brain parasagittal section, t2 weighted image t2 weighted image showing atrophy of left cerebral hemisphere with prominent veins in a case of sturge weber syndrome discussion sturge weber syndrome (sws) belongs phakomatosis disorders. sws has constellation of congenital malformation including hamartomatous malformations and lesions involving eye, skin, and central nervous system may be specially affected. in1860, it was first described by schirmer, further detailed specific description was provided by sturge in the year1879. weber, dimitri and wissing described the typical gyriform calcifications observed on plain x ray skull. krabbe is credited for correlating intracortical calcifications with gyriform calcifications on simple x-ray skull and hence also popularly called as krabbe syndrome, sturge weber dimitri syndrome, encephalotrigeminal angiomatosis and encephalofacial angiomatosis [3]. sturgeweber syndrome is a rare neuro cutaneous syndrome with estimated incidence of 1 in 20000 to 1 in 50000 live births [9-16]. the characteristic manifestations of sws are leptomeningeal angiomas, facial port wine venous angioma, and glaucoma. leptomeningeal angiomas typically tends to involve the occipital and posterior parietal lobe, also considered as the hallmark; however, degree of involvement is highly variable and can be either very extensive to involve ipsilateral lobes of ipsilateral or even extending to involve contralateral cerebral hemispheres. cutaneous vascular malformation usually occurs in the face, which is usually in the distribution of ophthalmic division of trigeminal nerve [4, 5]. sturge weber syndrome is classified into three types. the type 1 includes angiomas involving face and leptomeningeal as well as the possibility of presence of glaucoma or choroidal lesions. normally, only one side of the brain is affected. this type represents the commonest type. type 2 involvement includes a facial angioma (port wine stain) with a possibility of glaucoma developing. however, it is not associated with any 126 | satyarthee et al sturge weber syndrome             evidence of brain involvement. the final type-3 typically associated with leptomeningeal angioma involvement but facial angioma is absent and glaucoma tends to occur rarely. this type is only diagnosed via brain scan. [14] sws may be complete type characterized by presence of skin and central nervous system manifestation, but. incomplete types are also reported without associated common facial nevus [6]; current case had complete manifestations with presence of port wine stain over upper half on right side of face as well as central nervous system involvement. age of being clinically getting symptomatic for sturge weber syndrome is highly variable, spanning from immediate after birth in the neonatal period to the adolescence, although delayed diagnosed as late as sixth decade is also reported. it is usually present at birth with a port-wine stain on the forehead and upper eyelid involving only one side of the face, or rarely the whole face. the birthmark colour can vary from light pink to deep purple depending on complexion of rthe cases, caused due to an overabundance of capillaries around the ophthalmic division of the fifth cranial nerve. sturge weber syndrome is also associated with blood vessels malformation of the pia mater on the same side of the head as the facial angioma. this causes calcification of tissue and degeneration loss of neurons in the cerebral cortex. neurological symptoms include seizures, which usually begin in infancy and may worsen with advancing age. there may also be motor deficit or developmental delays and cognitive delays; about 50% cases may suffer with glaucoma. muniz reported a two days old baby with acute life threatening event ,who presented to an emergency department to seek management[7, 8]. focal motor seizures are the most common neurological manifestation in sws patients, usually present by the age of three years. many patients have intractable seizures, which may eventually lead to motor deficits and mental retardation [9]. our patient had normal motor and scholastic performance and had first seizure at age of four year. computed tomography of head typically shows curvilinear and gyriform calcifications presence in atrophic areas of brain and associated thickening of calvarial and contrast study shows leptomeningeal enhancement [10, 11]. characteristic findings observed on cranial mri include cerebral parenchymal atrophy, enlargement of medullary, periventricular veins and the enlargement of choroid plexus. and may have associated leptomeningeal, cortical gyriform abnormal signal or enhancement. current case had, left cerebral atrophy with enlargement of periventricular veins with left lateral ventricle choroid plexus demonstrated on mri brain, while cranial ct scan showed gyriform calcification with left cerebral atrophy and left sided calvarial thickening however other causes of seizure needs exclusion prior to labellling sws as principal cause of seizure disorder. [12-14] romanian neurosurgery (2017) xxxi 1: 122 – 128 | 127             important differential for intracranial calcifications at multiple site, cerebral hemiatrophy and includes cerebral arteriovenous malformation, infective pathology i.e. torch infection, neurocysticercosis, healed cortical infarct, post-radiotherapy induced changes [14-18] gupta et al reported a case of hypothalamic glioma occurring in a 7-yearold child, who presented with seizures and diabetes insipidus, underwent near total decompression of the hypothalamic glioma successfully using subfrontal approach. he had a stormy postoperative course due to status epileptics. he remained symptom and seizure free on antiepileptics at last follow-up after three years following surgery. [14] treatment revolves primarily around seizure control, with surgical resection only indicated rarely in refractory cases. ophthalmological examination is also essential to identify and treat ocular involvement [18, 19] conclusion prompt and aggressive seizure control with medication is usually sufficient to control seizure; however, in cases of medically refractory seizure surgery may be required. further, seizure control is essential for psychological and cognitive well being, long term neurological outcome and quality of life of cases suffering with sturge-weber syndrome. correspondence guru dutta satyarthee e-mail: drguruduttaaiims@gmail.com references 1. thomas-sohl ka, vaslow df, maria bl. sturgeweber syndrome: a review. pediatr neurol 2004; 30: 303-10 2. baselga e. sturge-weber syndrome. semin cutan med surg 2004; 23:87-98. 3. jeevankumar b, devinder mohan thapa, sturge weber syndrome: a report of three cases. indian j dermatol 2001; 46(3):185-87. 4. zaki sa, lad v. sturge-weber syndrome with bilateral facial nevus and early cerebral calcification. j pediatr neurosci. 2011 jul; 6(2):114-5. 5. comi am. pathophysiology of sturge-weber syndrome. j child neurol 2003; 18:509e16 6. moe p, seay ar. neurologic and muscular disorders. in: hay ww,hayward ar, levin mj, sondheimer jm, editors. current pediatric diagnosis and treatment, 16th edn. singapore: mcgraw hill; 2003. p. 717-92. 7. muniz ae. sturge-weber syndrome presenting as an acute life threatening event. pediatr emerg care 2004; 20:610-2 8. ferrari l, coppi e, caso f, santangelo r, politi ls, martinelli v, comi g, magnani g. sturge-weber syndrome with an unusual onset in the sixth decade: a case report. neurol sci. 2012 aug;33(4):949-50 9. sydney ch’ng, swee t. tan. facial port-wine stains e clinical stratification and risks of neuro-ocular involvement. j plast reconstr aes 2008; 61, 889-93. 10. hu et al .mr susceptibility weighted imaging (swi) complements conventional contrast enhanced t1 weighted mri in characterizing brain abnormalities of sturge-weber syndrome. j magn reson imaging. 2008; 28(2): 300–307. 11. akinpar e. the tram track calcifications. radiol 2004; 231:515-6. 12. satyarthee gd, mahapatra ak. seizure as presentation of pituitary adenomas; series of four cases. neurosciences today 2002; 6: 167-169. 13. rishabh pasricha, satyarthee gd. seizure occurrence in spinal dysraphism operated cases: series of four cases with literature review american j clinic neurol neurosurg 2015; 2, : 41-44. 14. gupta dk , satyarthee gd, sharma mc, mahapatra ak . hypothalamic glioma presenting with seizures. a case report and review of the literature. pediatr neurosurg. 2006;42(4):249-53. 128 | satyarthee et al sturge weber syndrome             15. moore gj, slovis tl, chugani ht. proton magnetic resonance spectroscopy in children with sturge-weber syndrome. j. child neurol. 1998; 13 (7): 332-5 16. pascual-castroviejo i, viaño j, moreno f et-al. hemangiomas of the head, neck, and chest with associated vascular and brain anomalies: a complex neurocutaneous syndrome. ajnr am j neuroradiol. 1996; 17 (3): 461-71 17. griffiths pd. sturge-weber syndrome revisited: the role of neuroradiology. neuropediatrics. 1996;27 (06): 284-94. 18. comi am. update on sturge-weber syndrome: diagnosis, treatment, quantitative measures, and controversies. lymphat res biol. 2007;5 (4): 257-64. 19. shirley md, tang h, gallione cj et-al. sturge-weber syndrome and port-wine stains caused by somatic mutation in gnaq. n. engl. j. med. 2013;368 (21): 1971-9. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article broken lumbar pedicle screw – a short report ashish kumar dwivedi, rashim kataria, virendra deo sinha india doi: 10.1515/romneu-2017-0091 572 | kumar dwivedi et al broken lumbar pedicle screw doi: 10.1515/romneu-2017-0091 broken lumbar pedicle screw – a short report ashish kumar dwivedi1, rashim kataria2, virendra deo sinha2 1department of neurosurgery, k.e.m. hospital mumbai, maharashtra, india 2department of neurosurgery, s.m.s. medical college and attached hospital jaipur, rajasthan india abstract: spinal fixation is one of the common surgical procedure performed by spine surgeons. among the various spinal fixation technique, pedicle screw fixation is of paramount importance especially when instability is in dorsolumbar and sacral region of spine. like any surgical procedure, pedicle screw fixation is not devoid of complications. broken pedicle screws are one of the rare complication of this procedure with a great challenge to deal with such situation. we are reporting one of the rare complication of pedicle screw fixation with literature review and our philosophy to deal such complication. introduction pedicle screw fixation is the recommended procedure with strong construct and higher rates of fusion. [1-6] despite providing strong construct and higher rate of fusion, this procedure is not free of complications. [1-6] we are reporting a case of 38-year-old lady who underwent pedicle screw fixation for burst fracture of l2 vertebra two and half years back, now came to us with history of fall followed by implant breakage and wound dehiscence. case report a 38-year-old female underwent pedicle screw fixation for l2 vertebral body fracture two and half year back. she was apparently well until 15 days back when she had fall from height followed by wound dehiscence and severe pain over the operated site. on further examination broken implant was visible from wound dehiscence. there was no neurological deficit on examination. removal of broken implant was planned. we have removed both the rod and few of the screws but some of screw were stuck in the body and could not be removed by any means, thus left as such. [figures 1a and 1b]. patient was free of operated site pain with no neurological deficit at 6-month follow-up. discussion of all the patient underwent pedicle screw fixation, 0.4-24.5% patient present with breakage of pedicle screws. [1,4] incidence of breakage of pedicle screw is 1-11.2% of all the romanian neurosurgery (2017) xxxi 4: 572 574 | 573 inserted screws. [1,4]. pseudo arthrosis may be possible cause of implant failure. [1] caudal screws are subjected to greater axial stress than those of cephalic one. [2] fatigue striation and ductile fracture around the edges are the additional explanation for breakage of pedicle screw. [2] removal of the broken implant is the treatment of choice in such cases. removal of broken rods and broken heads of pedicles are usually achieved easily but removal of the broken pedicle screw is not always easy. figure 1a figure 1b figure 1 showing broken pedicle screws various techniques have been described to remove broken pedicle screws. removal of pedicle screw by creating a deep pilot hole in the centre of the fractured screw and engaging the screw driver to reverse and rotate the screw counter-clockwise is described in literature. [7] removal of broken pedicle screw is also possible by using a high-speed drill with a long bit and making a slot over the top surface of the broken screw to accommodate screwdriver. [4] drilling inside the broken screw is not an easy task and any additional effort can add to the possibility of moving the broken screw further deeper, which may result in devastating complication. [5] although after removal of broken pedicle screw, larger diameter screw can be inserted but whether reinsertion is really needed if breakage of pedicle screws takes place years after the primary procedure, is the controversial. in our opinion spinal fusion is already complete by this prolonged duration and spine is stabilized, impacted broken pedicle screws can be left as such without any untoward sequalae. conclusion although there are various techniques which describe the method of removal of impacted broken pedicle screws, it is not always possible to remove the deeply impacted broken pedicle screws. in such condition, broken pedicle screws can be left in situ with no further complication if the fusion is adequate. 574 | kumar dwivedi et al broken lumbar pedicle screw correspondence dr ashish kumar dwivedi senior registrar, department of neurosurgery k.e.m. hospital mumbai, maharashtra, india email addressdrashishkumardwivedi@gmail.com mobile number9610510564 references 1.lonstein je, denis f, perra jh, pinto mr, smith md, winter rb. complications associated with pedicle screws. j bone joint surg (a) 1999; 81:1519–1528. [pubmed] 2.chen cs, chen wj, cheng ck, jao sh, chueh sc, wang cc. failure analysis of broken pedicle screws on spinal instrumentation. medical engineering & physics. 2005; 27:487–496. [pubmed] 3. di lorenzo n, conti r, romoli s. retrieval of broken pedicle screws by "friction" technique. technical note. j neurosurg. 2000; 92:114–116. [pubmed] 4. duncan jd, macdonald jd. extraction of broken pedicle screws: technical note. neurosurg. 1998; 42:1399– 1400. [pubmed] 5. kaya ah, dagcinar a, celik f, senel a. simple technique for removing broken pedicular screw with plain and serviceable screwdriver. eur spine j. 2008;17:1116–1118.[pmc free article] [pubmed] 6. agrawal a. simple technique for removing broken pedicular screws. malays orthop j. 2014 mar; 8(1):66-67. 7. mcguire ra jr. a method for removal of broken vertebral screws. orthop review. 1992; 21:775–776. [pubmed] romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article the miracle of st. alfege’s hospital and the history of the treatment of myasthenia gravis cristina croitoru, dana turliuc, florentina danciu, a. cucu, claudia costea romania doi: 10.1515/romneu-2017-0011 romanian neurosurgery (2017) xxxi 1: 73 – 79 | 73             doi: 10.1515/romneu-2017-0011 the miracle of st. alfege’s hospital and the history of the treatment of myasthenia gravis cristina croitoru1, dana turliuc1,2, florentina danciu1, a. cucu1, claudia costea1,2 1“prof. dr. n. oblu” emergency clinical hospital iasi, romania 2“grigore t. popa” university of medicine and pharmacy iasi, romania abstract: having a recent history, the neurological condition called myasthenia gravis has raised dilemmas and questions among doctors since it was first discovered in the 16th century and it has not ceased to be a challenge. nowadays, neuroscience researchers from around the world have been striving to perfect a modern treatment of this condition. our paper is an incursion into the past, more precisely into the history of the treatment of this disease, from its origin to date, when immunological therapy has progressed. key words: myasthenia gravis, treatment of myasthenia gravis, history of medicine introduction the myasthenia gravis (mg) condition has had a relatively recent history, given its discovery as late as the 16th century (figure 1). although it is full of misunderstandings and errors, the history of mg has acquired the value of truth later, thanks to neurologists, neuro-psychiatrists and neurosurgeons passionate about science, as they not only tried to understand its pathology, but also to find means of treatment (5). despite these efforts, until as late as the 1930’s, the treatment of mg was empirical and only amount to: bed rest, administration of tonic preparations (iron, quinine, mercury, arsenic and strychnine) and various extracts from animal glands (thymus, ovary, testicle, adrenals), as well as radioactive substance injections and thymus and thyroid irradiations. thus, we can say that the treatment of mg was in most cases ambiguous, which turned into “a source of discouragement to the patient and a cause of nightmare for the physician” (16). the first efficient substance: ephedrine the year 1930 marked an important progress in the history of the treatment of mg, as ephedrine proved to be the first efficient substance in the treatment of mg. this substance is still used as second-line medication in the treatment of this condition. the efficiency of ephedrine in mg was 74 | croitoru et al the miracle of st. alfege’s hospital and myasthenia gravis             discovered by the american chemist harriet isabel edgeworth (1865-1916), who suffered from mg herself and who took ephedrine for menstrual cramps and accidently noticed an improvement in her muscle fatigue (9). in the light of the breakthroughs in the field of muscular contraction, neuroscience researchers focused their attention on creatinine metabolism. thus, dr. walter boothby published, between 1932 and 1936, various papers on the beneficial effect on the symptoms of the disease of the aminoacid glycine combined with ephedrine (4). the miracle of st. alfege’s hospital: physostigmine the year 1934 marked the beginning of a modern approach to the treatment of mg. while treating a patient suffering from mg, the british doctor mary broadfoot walker (1888-1974) (figure 2) discovered the beneficial effect of physostigmine on muscle fatigue and palpebral ptosis. the young doctor noticed that the effect lasted between 2 and 5 hours, depending on the concentration of the physostigmine administered subcutaneously. she published her findings that same year in the prestigious journal lancet: “i think that this effect of physostigmine on myasthenia gravis is important, though it is only temporary, for it improves swallowing and might tide the patient over respiratory crisis. it supports the opinion that fatigability is due to poisoning of the motor end-organs, or myoneural junctions” (31). thus, physostigmine came to be known as “the miracle of st. alfege’s hospital”, named after one of the hospitals where mary walker worked (15). table the main breakthroughs in the history of the treatment of mg, modified after afifi (1) figure 1 possible onset of myasthenia gravis with unilateral left ptosis (pierrot amedeo modigliani, paris-1915) (public domain) year treatment 1930 ephedrine 1932 glycine 1934 physostigmine 1936 first thymectomy 1949 acth 1950s corticotherapy 1966 reintroduced corticotherapy 1967 azathioprine 1973 acetylcholine receptor is autoantigen 1976 plasma exchange 1980 cyclophosphamide 1984 intravenous immunoglobulin 1987 cyclosporine 2000s immunotherapies romanian neurosurgery (2017) xxxi 1: 73 – 79 | 75             mary broadfoot walker alfred blalock douglas fambrough figure 2 contributors to the treatment of myasthenia gravis in addition to physostigmine, dr. mary walker also studied the effects of neostigmine and potassium chloride on mg patients with remarkable yet short-lasting results. she noted an improvement in muscle fatigue and the absence of central side effects of physostigmine (18, 30). due to her pioneering in the treatment of mg, mary walkera still is one of the major contributors to the treatment of mg, with numerous incommensurable achievements: she is the first specialist who suggested the idea of “myasthenic crisis”, the first specialist to have noted that mg is located in the neuromuscular junction and also the first specialist to have discovered the clinical effect which was later called “the mary walker effect”. of all of dr. mary walker’s achievements, the most important is the use of physostigmine as primary therapy. this also stimulated the research of other acetylcholinesterase inhibitors like edrophonium in 1950 by macfarlane (20) or pyridostigmine in 1954 by kermit osserman (23). these are still being used as first-line drugs in the treatment of mg. the use of neostigmine in the treatment of mg may be also credited to the german lazar remen (1907-1974), who published in german literature in 1932, that is 2 years before mary walker, a paper that claimed that the symptoms of a patient with mg improved after she had received neostigmine (26). total resection of the thymus gland in the treatment of mg being aware of ernst ferdinand sauerbruch’s (1875-1951) post-thymectomy 76 | croitoru et al the miracle of st. alfege’s hospital and myasthenia gravis             results, the american surgeon alfred blalock (1899-1964) (figure 2) performed the resection of a post-radiotherapy cystic tumor. the case was of a 19-year old girl with generalized mg, who underwent surgery during the remission period and who was administered prostigmin before and after the surgery. the case was published 3 years later, in 1939, in a paper in which blalock claimed that the myasthenic symptoms were remitted. 21 years later the patient was still alive (3, 13). encouraged by this positive result, in 1941, blalock started to practice thymectomy in mg patients without thymus tumors. thus, he published reports on 6 cases of transsternal thymectomy and noticed that three of them did not subsequently require drug therapy (2). inspired by blalock’s promising results, the english surgeon geoffrey keynes, (18871982) also performed 120 thymectomies between 1942 and 1949 in mg patients, and reported a 65% improvement in his cases (17). the treatment of mg through thymectomy had also crossed the ocean, as the american surgeon oscar theron clagett (1908-1990) and the neurologist lee eaton (1905-1958), from the mayo clinic, had performed 72 thymectomies in mg patients, which they subsequently compared to the 142 mg cases that had not undergone surgery (8). later, that is between 1950 and 1954, there was a difference of opinion between the two continents as concerns thymectomy efficiency in mg patients. on the one hand, the americans clagett and eaton from the mayo clinic, claimed that thymectomy was inefficient, on the other hand, the english keynes argued against. it was later proven that this difference of opinion was due to the fact that most of the patients that had undergone surgery in the mayo clinic had thymus tumors, whereas in england they had thymic hyperplasia (1). this discrepancy was settled in 1955 when clagett and eaton set clear thymectomy criteria: absence of thymus tumors and patients’ age below 50 (7). acth and cortisol wishing to achieve the same effect as thymectomy without the actual surgical procedure, in 1949, the americans clara torda and harold wolff from the new york hospital administered acth to 15 patients suffering from mg. immediately after the administration of 500mg for 5 days, they noted a visible worsening of the symptoms in all the patients, including one dead; yet, they later noted the improvement of the symptoms of 10 out of 15 patients (29). after cortisol had been isolated and discovered in the adrenal glands and its effects had been studied by the chemists edward kendall (1886-1972) and tadeus reichstein (18971996) (14), cortisone started to be administered to mg patients in 1950. neuroscience researchers noted the same effect as in the case of acth, with a significant initial worsening and an improvement after a few days. nevertheless, due to its life-threatening effects, they do not encourage the use of hydrocortisone in the treatment of mg. according to the german neuropsychiatrist friedrich jolly (1844-1904) and the british doctor mary broadfoot walker (thirty nine years later) suggested that in mg romanian neurosurgery (2017) xxxi 1: 73 – 79 | 77             the impairment was located in the neuromuscular junction and that acetylcholine was the mediator involved (5), in 1956 the american david grob et al. shed some more light on the matter by claiming that the seat of mg was at the post-synaptic level (10). a year later, that is in 1957, another neuroscientist, john desmedt, published in the nature journal a study in which he considered the post-synaptic component responsible for muscle fatigue in mg (6), and also suggested a possible acetylcholine depletion in the neuromuscular junction (22). myasthenia gravis......an autoimmune disease? after the neuroscience researchers concluded that in mg the seat of impairment was located in the post-synaptic region, the medical world suggested that mg may be an autoimmune disease, as its association with autoimmune diseases has been noted. thus, in 1954, in a review of 138 cases of systemic lupus erythematosus patients, harvey et al. noted that 3 of them also suffered from mg (12). nevertheless, the first specialist to officially launch in literature the assumption related to the autoimmune nature of mg was dr. smithers dw, in 1958 (1). that same year, kermit osserman, who had studied the effect of pyridostigmine, made a classification of mg and divided it into four groups depending on symptom severity and location (1). smithers’ assumptions were confirmed in 1960 by the scottish doctor john simpson. a review of all 404 cases of mg recorded between 1953 and 1955 enabled simpson to reach three conclusions: that mg patients had thymus abnormalities, that thymectomy has a positive influence of disease prognosis and that there is a connection between mg and several other diseases like rheumatoid polyarthritis, systemic lupus erythematosus, hyperthyroidism, aplastic anemia, pernicious anemia or sarcoidosis. thus, simpson concludes that “myasthenia gravis is a muscular autoimmune response, in which an antibody of the protein in the end-plate can be involved as a reaction to an infection or thymus influenced by the pituitary gland” (27). that same year, i.e. is in 1960, jacques miller proved the immunological function of the thymus, in a series of studies that he published a year later in the lancet (21). in 1968, in his attempt to discover a serum protein able to inhibit neuromuscular transmission, william nastuk et al. focused on the study of the complement in mg. he found correlations between the serum complement level and disease activity and argued that “the levels of complement are decreased during the clinical activity of the disease, while during its remission, they increase. this suggests the possibility that mg is an autoimmune mediated disease” (28). furthermore, in an attempt to identify the generator of these autoimmune reactions – an anti-striated muscle antibody, arthur strauss analyzed the serum of 1139 subjects, of whom: 129 were healthy, 386 had mg and 674 suffered from inflammatory, endocrinological and carcinomatous myopathies, muscular dystrophies and thymomas not accompanied by mg (28). since he discovered that in subjects with mg and thymomas, serum globulins retained the complement, strauss established a certain connection between thymus abnormalities and impulse transmission alteration in the 78 | croitoru et al the miracle of st. alfege’s hospital and myasthenia gravis             neuromuscular junction. thus, once the assumption according to which autoimmunity plays an essential role in mg pathogenesis was accepted, the reintroduction of corticotherapy, which had been abandoned for its life-threatening effects, was supported. initially, cortisol and then prednisone started to be administered for their immunosuppressant functions, in more carefully calculated doses. subsequent studies showed that symptom worsening was temporary and that an obvious disease symptom improvement was visible after 7 to 10 days (1). “by borrowing” from the lymphoma and leukemia therapy, doctors started to focus their attention on other classes of medicines like: immunosuppressants, chemotherapy drugs or cytotoxic drugs. thus, azathioprine started with 1967 to be administered to mg patients in europe and cyclophosphamide since 1980 (14). reference year 1973 1973 is considered a reference year in the history of the treatment of mg, since it marks two essential discoveries in understanding the pathology of this condition and its approaching the current level of knowledge. the first occurred in the johns hopkins hospital, when douglas fambrough (figure 2) noted that acetylcholine receptors were located solely in the postsynaptic component after he had used a radioactively labeled from the cobra venom (alpha-bungarotoxin), with high binding affinity to the acetylcholine receptor (11). the second discovery belongs to jim patrick and jon lindstrom from the salk institute, who identified the acetylcholine receptor as the autoantigen responsible for triggering the autoimmune response (24). lindstrom also isolated acetylcholine receptor antibodies in 1976. he injected rabbits with acetylcholine receptors sampled from electric eels and found that they exhibited flaccid paralysis and breathing difficulties and in addition that the symptoms were partially improved by prostigmin administration (19). the confirmation of the autoimmune pathogenesis and of the existence of acetylcholine receptor antibodies occurred in 1976, when fueron treated three mg patients by plasmapheresis, with certain clinical improvement (25). this is actually the decisive breakthrough marking the transition towards a modern therapeutic approach and continuation of the immunological and genetic research of mg. conclusion having a relatively recent history, the treatment of mg has been a challenge for neuroscientists, and especially for doctors, who were faced with an unknown disease the therapy of which was even more unknown. whereas the first disease description was done in england and the symptoms and name of the disease were later clarified in germany, we can safely say that the treatment and immunopathological grounds originate in the united states. although answers have been found to questions that seemed to have no answer, the complexity of mg is still very much visible nowadays, when the medical world has got involved in a process of continuous exploration, which focuses on the genes involved, on new autoantigenes and also on new immunotherapies of an extremely “complex” condition. romanian neurosurgery (2017) xxxi 1: 73 – 79 | 79             correspondence dana turliuc “prof. dr. n. oblu” emergency clinical hospital iasi, romania e-mail: turliuc_dana@yahoo.com references 1.afifi a k. myasthenia gravis from thomas willis to the present. neurosciences. 2005; 10(1):3-13. 2.blalock a, harvey am, ford fr, lilienthal jl. the treatment of myasthenia gravis by removal of the thymus gland: preliminary report. jama. 1941; 117: 1529-1533. 3.blalock a, mason m f, morgan hj, et al. myasthenia and tumors of the timus gland, report of a case in which the tumor was removed. ann surg. 1939; 110: 554-561. 4.boothby wm, adams m, power mh, et al. myasthenia gravis: second report on the effect of treatment with glycine. mayo clinic proc. 1932; 7: 737-756. 5.croitoru cg, turliuc dm, danciu f, cucu ai, turliuc s,costea cf. myasthenia gravis – a beginning with no end. romanian neurosurgery. 2016; xxx (1): 77-82. 6.desmedt je. nature of the defect of neuromuscular transmission in myasthenic patients. post-tetanic exhaustion. nature. 1957; 179:156-157. 7.eaton lm, clagett ot. present status of thymectomy in treatment of myasthenia gravis. am j med. 1955; 19:703-717. 8.eaton lm, clagett ot. thymectomy in the treatment of myasthenia gravis. results in seventy-two cases compared to one hundred and forty-two cases. jama. 1950; 142: 963-967. 9.edgeworth h. a report of progress on the use of ephedrine in a case of myathenia gravis. jama. 1930; 94:1136. 10.grob d, johns rj, harvey am. studies in neuromuscular function. bull johns hopkins hosp. 1956; 99:153-181. 11.fambrough dm, drachman db, satyamurti s. neuromuscular junction in myasthenia gravis: decreased acetycholine receptor. science. 1973; 182:193195. 12.harvey am, shulman le, tumulty pa, conley lc, schoenrich eh. systemic lupus erythematosus: review of the literature and clinical analysis of 138 cases. medicine. 1954; 33:291. 13.hughes t. the early history of myasthenia gravis. neuromuscular disorders. 2005; 15:878-886. 14.keesey j.c., „ a history of treatments for myasthenia gravis”, seminars in neurology, 2004, 1: 5-16. 15.keesey jc. myasthenia gravis. an illustrated history. roseville (ca): the myasthenia gravis foundation of california, 2002. 16.kennedy fs, moersch fp. myasthenia gravis: a clinical review of eightyseven cases observed between 1915 and early part of 1932. can med assoc j. 1935; 37: 216-223. 17.keynes g. the results of thymectomy in myasthenia gravis. bmj. 1949. 1: 611-616. 18.laurent lpe, walther ww. the influence of large doses of potassium chloride on myasthenia gravis. lancet. 1935; 16:1434-1435. 19.lindstrom jm, seybold me, lennon va, whittinham s, duane dd. antibody to acetylcholine receptor in myasthenia gravis. neurology. 1976, 26: 1054-1059. 20.macfarlane dw, pelikan ew, unna kr. evaluation of curarizing drugs in man. j pharmacol exp ther. 1950; 100:382-392. 21.miller j. immunological function of the thymus. lancet. 1961; 2: 748-749. 22.mimenza-alvarado a, tellezzenteno jf, garciaramos g, estanol b. la historia de la miastenia gravis. los hombres y las ideas. neurologia. 2007; 22. 23.osserman ke, teng p, kaplan li. studies in myasthenia gravis. preliminary report on therapy with mestinon bromide. jama. 1954. 155:961-965. 24.patrick j, lindstrom j. autoimmune response to acetylcholine receptor. science. 1973. 180: 871-872. 25.pinching aj, peters dk. remission of myasthenia gravis following plasma-exchange. lancet. 1976; 2: 13731376. 26.remen l. zur pathogenese und therapie der myasthenia gravis pseudoparalytica. deutsche zeitschrift fur nervenheilkunde. 1932; 128:66. 27.simpson j. myasthenia gravis: a new hypothesis. scott med j. 1960; 5: 419-436. 28.strauss ajl. myasthenia gravis. autoimmunity and the thymus. advances in internal medicine, vol xiv. chicago: year book medical publishers, 1968. 29.torda c, wolff hg. effects on adrenocorticotrophic hormone on neuro-muscular function in patients with myasthenia gravis. proc soc exp biol med. 1949; 71: 432-435. 30.walker mb. case showing the effect of prostigmin on myasthenia gravis. proc roy soc med; 1935; 28: 759-761. 31.walker mb. treatment of myasthenia gravis with physostigmine. lancet. 1934; 1200-1201. 6khairkarpraveen_neuropsychiatric presentations romanian neurosurgery | volume xxx | number 4 | 2016 | october december article neuropsychiatric presentations of pediatrics brain tumors: cases series praveen khairkar, anand kakani, amit agrawal india doi: 10.1515/romneu-2016-0078 romanian neurosurgery (2016) xxx 4: 493 – 497 | 493 doi: 10.1515/romneu-2016-0078 neuropsychiatric presentations of pediatrics brain tumors: cases series praveen khairkar, anand kakani1, amit agrawal2 department of psychiatry, mahatma gandhi institute of medical sciences, sevagram, india 1department of neurosurgery, datta meghe institute of medical sciences, sawangi (m), wardha, india 2department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: brain tumors constitute the second most common tumors in the pediatric age group after the leukemias. symptoms and signs depend on growth rate of tumor, its location in the central nervous system, the extent of peri-tumoral vasogenic edema and the age of the child. most common neuropsychiatric problems reported in children with brain tumor(s) include adjustment problems, anxiety disorder, neurocognitive deficits and depressive disorder as reported by very few case reports and isolated observational data. to the best of our knowledge no similar data or reports are as yet published from india on the similar lines. we wish to report case series of neuropsychiatric presentations in different types of brain tumors observed at our rural tertiary care multi-speciality hospital. key words: neuropsychiatric manifestations, brain tumors, pediatric introduction neoplastic brain tumors may be broadly divided into two types, namely those neoplasms that are primary to the brain and those that represent metastases from systemic cancers such as bone or lungs. brain tumors constitute the second most common tumors in the pediatric age group after the leukemias. (1) pediatric brain tumors are not similar to adult tumors in many ways. childhood brain tumors demonstrate greater histological variation. in addition, meningioma, malignant gliomas, schwannomas and pituitary tumors are common in adults; however these tumors are rare in children. in children more than 50% of the brain tumours are infratentorial and embryonal in origin and the common tumours are low grade gliomas and primitive neuroectodermal tumours. (2-3) gliomas represent 45 – 50% of all the pediatric primary brain tumors and are by far the commonest of them. (4-5) symptoms and signs depend on growth rate of tumor, its location in the central nervous system (cns), the extent of peri 494 | khairkar et al neuropsychiatric presentations of pediatrics brain tumor tumoral vasogenic edema and the age of the child. the overall symptomatology may be divided into following domains: headache; non-focal symptoms, focal signs and symptoms and specific syndromes such as intellectual deterioration or seizures. (6) the treatment of these pediatric brain tumors involve only surgery (eg, children with a pilocytic astrocytoma) or have surgery, radiation, and intensive chemotherapy (eg, children with medulloblastoma). (7,8) the overall 5 year survival rate of pediatric cancers increased from 62.9% in 1970’s to 81.5% in 2001. (9) most common neuropsychiatric problems reported in children with brain tumor(s) include adjustment problems, anxiety disorder, neurocognitive deficits and depressive disorder as reported by very few case reports and isolated observational data. to the best of our knowledge no similar data or reports are as yet published from india. we report cases series of brain tumor with differential neuropsychiatric presentations as seen and illustrated while treating them. case vignettes case 1 9 years old male child presented with insidious onset of dull aching continuous, headache fronto-temporal region, gait disturbance (magnet in type) and two episodes of generalized tonic-clonic seizures lasted for 15-30 seconds associated with urinary incontinence. his t2 weighted mri showed 6 x 7 cm homogenous mass at right frontoparietal region with gadolinium enhancement. on mental state examination child was irritable, sad and pre-occupied with pain and was having cognitive deficit in speech, language and memory domains. he had undergone surgical treatment in the form of ventriculo-peritoneal shunting and removal of large tumor which was found to be meningioma. case 2 a 5 years old girl presented to psychiatric outpatient services with dizziness and hypersomnalance along with excessive eating and weight gain. her bmi was 29.2 and was grossly reluctant to go to school (school phobia). she was brought to emergency department when she sustained two episodes of consecutive days morning omitting and one episode of loss of consciousness precipitated by lip-smacking movements, automatism and hallucinatory behavior. she was found to have 2 cm of non-enhancing mass at temporal lobe with increased signal intensity on t2 weighted image. on mental status examination, she was found to have moderate depressive disorder borderline intelligence and binge type eating disorder. case 3 8 years old female child was incidentally brought to pediatrics department with complaints and difficulty in walking, eye to hand co-ordination, nystagmus, coarse tremors, and speech difficulty, reading and arithmetic problems. on physical examination, cerebellar signs were grossly present. mri brain showed 3 x 4 cm midline cerebral tumor protruding into 4th ventricle suggestive of “medulloblastoma”. her iq was 78. she was referred to neurosurgery for further treatment. romanian neurosurgery (2016) xxx 4: 493 – 497 | 495 case 4 13 years old male child was brought by his parents with presentation of rapid cycling affective disorder (rcad) since last 6-7 moths. his symptoms of excessive eating, excessive sleepiness (18-20 hrs), irritable and labile mood with inability to concentrate on studies, excessive demands for different eatables and withdrawal behavior, becoming aggressive when confronted by family members to restrict his food, sleep or to focus on study. he would remain better spontaneously for 1-2 wks and again continue to have similar semiology of symptoms in the cyclic pattern. he could not go to school during his symptomatic phase. on examination, he was found to have bitemporal hemianopia. his mri brain showed calcified 2 x 2 cm two discrete nodules, one at hypothalamus and other at left anterior cingulated gyrus. his rcad was effectively treated with sodium valporate 600 mg per day, with olanzepine 5 mg per day and was subsequently referred to the department of neurosurgery. case 5 a 6 years old male child was brought to emergency pediatrics department with complaints of acute onset of paroxysmal episodes of 4-5 convulsive seizures began from the right half of the extremity and involved whole body, followed by post-ictal confusion and state of flaccidity. his mri showed left temporo-parietal 65 x 57 mm low intensity non-enhancing homogenous mass. on mental status examination he was found to have fearfulness, forgetfulness, insomnia and perceptuo-cognitive deficit. he underwent craniotomy and histopathology showed grade iii astrocytoma. case 6 12 years old female presented to ent department with complaining of left sided headache, tingling numbness sensations on left half of face, elementary auditory hallucinations, 3-4 episodes of sensory motor seizures without secondary generalizations. her mri brain showed left parietal 32 x 36 mm heterogenous density non-enhancing mass. the diagnosis of organic schizophreniform psychosis secondary to brain tumor was considered. she underwent craniotomy and her histopathology showed that it was indolent gangliocytoma containing both neural and glial elements. case 7 a 9 year old male child was diagnosed as acute lymphoblastic leukemia. he underwent 3 cycles of recommended chemotherapy predominantly intravenous and intrathecal methotrexate. further he received about 1800 cgy cranial irradiation as part of cns prophylaxis. thereafter he had been observed to be in complete remission for about a year. however, he was referred from school to psychiatric services for newly developed problems in reading and arithmetic skills, paroxysms of panic attacks, nightmares and wish to die which were quite prominent and were unlike to his premorbid self. case 8 a 5 year old male child presented to pediatrician with 3-4 month history of morning vomiting, gait disturbance and excruciating headache at occipital region with 496 | khairkar et al neuropsychiatric presentations of pediatrics brain tumor crying spells and insomnia. his headache had not responded to nsaid’s prescribed by local physician. his mri brain showed 4 x 7 cm, homogenous, hyperintensity, non-enhancing mass in cerebellar region involving vermis suggestive of cerebellar astrocytoma. he underwent successful extensive surgical resection. his histology showed pilocytic tumor with biphasic pattern with varying proportions of bipolar cells with rosenthal fibers and loose multipolar cells with microcysts. on day 2 post-operatively he developed delirium, hyperactive type secondary to infection/hypoxemia/anemia. he remained hospitalized in intensive care unit for next two weeks and recovered completely. discussion brain tumour is probably one of the most terrifying diagnoses, a child and his or her loved ones will ever hear. the degree of psychological emotional expressiveness in children with brain tumor (s) and its possible effect on prognosis have been the subject of interest of a large body of literature. few descriptive case reports noted shorter survival both in adolescent and adult patients with depressed, resigning attitude compared with patients who were able to express more negative emotions, such as anger. 10 frontal lobe tumors in children is often accompanied by apathy, dullness and somnolence. (11) tumors of thalamus and hypothalamus may also cause intellectual deterioration along with additional symptoms like hypersomnolence, weight gain or diabetes insipidus. (11, 12) development of dementia or personality changes which is often seen in frontal lobe tumors in adult are not practically possible or documented. mania may uncommonly occur with tumors of mesencephalon, hypothalamus, cingulate gyrus or frontal lobe; similarly psychosis may occur with tumors most commonly of the temporal lobe followed by frontal lobe and corpus callosum. (11, 13) unlike in adults with brain tumors in whom the wide spectrum of neuropsychiatric presentations are being reported; the focus in pediatric age group has been largely on issues of adjustment, emotional and mood disorder and cognitive impairment. (11,14) however, in our case series we observed evolution and persistence of sleep disorders, psychosis, delirium, eating disorder, rapid cycling affective disorder and panic attacks in addition to previously documented presentations. finally, neuropsychiatric presentations in children with brain tumor commonly changes over the course of illness and depends on medical, psychological and social factors: the disease itself (i.e., site, symptoms, clinical course, side effects of chemotherapeutic agents or radiations); prior levels of adjustment; the threat that cancer poses to attaining age appropriate developmental tasks and goals; cultural, religious and spiritual attitude; presence of emotionally supportive persons or caregivers; the potential for psychological and physical rehabilitation; and finally child’s temperament and coping style as well as prior experience with loss. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery romanian neurosurgery (2016) xxx 4: 493 – 497 | 497 narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.national cancer policy board (u.s.), weiner sl, simone jv. childhood cancer survivorship: improving care and quality of life. washington, dc: national academies press; 2003. 2.pollack if. the role of surgery in pediatric gliomas. j neurooncol. 1999;42:271–88. 3.pollack if. brain tumours in children. n engl j med. 1994;331:1500–7. 4.duffner pk, cohen me, myers mh, heise hw. survival of children with brain tumors: seer program. 1973-1980. neurology. 1986;36:597–601 5.robertson pl. advances in treatment of pediatric brain tumours. neurorx. 2006;3:276–91. 6.forsyth pa, posner jb. headaches in patients with brain tumors: a study of 111 patients. neurology 1993;43:1678-83 7.ris md, beebe dw. neurodevelopmental outcomes of children with low-grade gliomas. dev disabil res rev 2008;14(3):196–202. 8.gottardo ng, gajjar a. chemotherapy for malignant brain tumors of childhood. j child neurol 2008;23(10):1149–59 9.horner mj, ries lag, krapcho m, et al, editors. seer cancer statistics review, 1975–2006. based on november 2008 seer data submission. bethesda (md): national cancer institute. available at: http://seer.cancer.gov/csr/1975_2006/, posted to the seer web site, 2009. 10.allen l, zigler e. psychological adjustment of seriously ill children. j am acad child psychiatry 1986;25(5):708–12 11.kurtz bp, abrams an. psychiatric aspects of pediatric cancer. pediatric clinic of north america 2011;58:10031023. 12.beal mf, kleinman gm, ojemann rg et al. gangliocytoma of the third ventricle: hyperphagia, somnolence, and dementia. neurology 1981;31:1224-8 13.murthy p, jayakumar pn, sampath s. of insects and eggs: a case report. j neurol neurosug psychiatry 1997;63:522-3 14.steinlin m, imfeld s, zulauf p, et al. neuropsychological long-term squeal after posterior fossa tumour resection during childhood. brain 2003;126(9):1998–2008. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article current epidemiological trends of brain abscess: a clinicopathological study neha singh, deepak kumar singh, rakesh kumar, hanuman prajapati india doi: 10.1515/romneu-2017-0067 414 | singh et al current epidemiological trends of brain abscess doi: 10.1515/romneu-2017-0067 current epidemiological trends of brain abscess: a clinicopathological study neha singh1, deepak kumar singh2, rakesh kumar2, hanuman prajapati2 “dr. ram manohar lohia” institute of medical sciences, lucknow, india 1department of radiodiagnosis; 2department of neurosurgery abstract: aims: to determine the current epidemiological trends, clinical presentation and commonest organism of brain abscess in this part of the country. material and methods: 104 cases admitted during august 2009 to july 2016 in the department of neurosurgery of dr rmlims lucknow were included in the study. detailed clinical history was taken and detailed neurological examination was done. relevant laboratory investigations were done as needed along with ct scan and /or mri brain. patients were managed by aspiration or surgical excision and aspirated material sent for microbiological examination. results were collected and analyzed. results: chronic suppurative otitis media (csom) was the commonest cause of infection in 54.81% cases. trauma was encountered in 10.58%% cases. other causes were haematogenous spread of infection, dental caries and immunodeficiency. no source could be identified in 23 patients (22.11%). conclusion: chronic suppurative otitis media (csom) is still a major cause of brain abscess in developing country like india which is a benign curable disease and should not be neglected. prompt diagnosis and treatment allows immediate decompression of mass reduces duration of antibiotic stay and minimizes treatment cost. key words: brain abscess, epidemology, management introduction otogenic brain abscess still constitute the major type encountered in developing countries. this is in marked contrast to the reports from western literature of a decline in otogenic brain abscess. the development of brain abscess is similar to the formation of an abscess in other parts of body, the reaction depending upon the virulence of the organism and the resistance of the host. healthy brain tissue is quite resistant to bacterial infection. indeed, this likely explains the predisposition of pyogenic abscess to form in regions of prior infarction, trauma or surgery. however, once an inoculum has taken hold in the brain romanian neurosurgery (2017) xxxi 3: 414 421 | 415 parenchyma, the absence of lymphatics makes it poorly equipped to fight off the infection. once established, a series of events transpires on a generally predictable sequence that is divided into four stages based on imaging as well as neuropathological studies. these are stage i of early cerebritis, stage ii of late cerebritis, stage iii of early capsular formation and stage iv of late capsular stage. tubercular brain abscess (tba) is as rare but serious condition. it resembles a pyogenic brain abscess clinically and radiologically and possesses a problem in diagnosis and treatment. fungal infections of the central nervous system, once a relatively rare occurrence, are increasingly common due to the expansion of immunocompromised populations at risk, and therefore are important to recognize early and manage appropriately. the objective of this study is to find out the incidence of brain abscess in different age group and sex of the population catered by this institution along with the commonest source of infection and type of management needed in most of the cases and overall morbidity and mortality. material and methods the study incorporated all cases of brain abscess treated in department of neurosurgery of dr rml ims lucknow since august 2009 to july 2016. criteria for inclusion all patients with confirmed diagnosis of brain abscess on the basis of clinical data, ct scan and mri were included in this study irrespective of age and sex. workup and management patients were worked up by detailed history of present illness pointing to a septic focus, general and detailed neurological examinations. apart from routine hematological investigations, all patients were subjected to ct scan or mri study. all patients were managed either conservatively or by aspiration (by twist drill, usg guided, stereotactic) or by surgical excision. pus was sent for slide examination (gram staining, z-n staining for afb, indian ink staining) and culture and sensitivity test (aerobes, anaerobes). third generation cephalosporin and metronidazole were given in all patient empirically which were subsequently changed after culture and sensitivity report. treatment for primary focus was also advocated as per direction of concerned department. all patients were followed up for at least three months and observed for recurrence and neurological sequelae. all the relevant data were collected and analyzed. results age and sex distribution: out of a total of 104 patients, 78 were male and 26 were female, thus male and female ratio was 2.71:1 this table showed age wise incidence of the cases. majority of the patients (73.08%) were below 20 years of age. youngest patient was of 2 months of age and the oldest was 63 years old. 416 | singh et al current epidemiological trends of brain abscess table 1 age distribution age group total no. of cases male female 0-10 33 (31.73%) 24 (23.07%) 9 (8.65%) 11-20 43 (41.35%) 33 (31.73%) 10 (9.61%) 21-30 14 (13.46%) 10 (9.61%) 4 (3.84%) 31-40 5 (4.81%) 3 (2.88%) 2 (1.92%) 41-50 3 (2.88%) 2 (1.92%) 1 (0.96%) 51-60 3 (2.88%) 2 (1.92%) 1 (0.96%) 61-70 3 (2.88%) 1 (0.96%) 2 (1.92%) aetiological factors chronic suppurative otitis media was the commonest source of infection. a total of 57 cases (54.81%) developed brain abscess secondary to discharging ear. the duration of ear discharge was from few months to many years. in 10 cases, hematogenous spread of infection from remote area was the cause of brain abscess. cyanotic heart disease was aetiological factor in four cases (figure 1a). in one case the source of infection was dental caries. two cases were associated with hiv infection, among which one case was of fungal origin. trauma was detected as the cause in 11 cases. meningitis was the culprit in 3 cases; one of them of paediatric age group presented with subdural empyema along with parenchymal abscess (figure 1b& 1c). no source was identified in 23 cases and none of abscess developed following paranasal sinus infection. two of our cases were having deficiency in cell mediated immunity (hiv). two cases were found following surgery for head trauma in the post op period (figure 1d). the empyema thoracic was the cause of abscess in one case. figure 1 multiple brain abscesses in a patient of cyanotic heart disease (a). subdural empyema developing in a child as a sequel of meningitis (b). subdural empyema with intraparenchymal abscess in a patient as a complication h. influenze meningitis(c).parietal abscess developing following surgical decompression in a head injury patient (d) clinical presentation majority of cases (88%) reported between 15 to 35 days duration of illness i.e. in the stage of late capsule formation and thus having well defined capsule. at presentation, 85 patients (81.73%) were having symptoms suggestive of raised intracranial pressure i.e. headache and vomiting. there was mild to moderate degree of fever in 61(58.72%). 21 cases (20%) presented with seizure whether focal or generalized. 34 patients had altered sensorium ranging from drowsiness to deep coma. 33 cases (31.80%) had focal neurological deficit in the form of hemiparesis, cranial nerve weakness, dysphasia, and cerebellar signs. romanian neurosurgery (2017) xxxi 3: 414 421 | 417 location of abscess temporal lobe was the site in 27 cases (25.96%) with or without extension to parietal lobe, whereas cerebellum was involved in 16.35% of cases. 21 patients had frontal abscess and 13 had frontoparietal location. multiple abscesses were found in 8 cases and kept in separate group irrespective of intracranial location. 2 patients had thalamic abscess. 6 (5.77%) were associated with either subdural empyema or epidural abscess. in 2 cases, interhemispheric subdural abscess was found (figure 2). figure 2 contrast enhanced ct scan shows well defined ring enhancing lesions with perifocal edema suggesting abscess in left frontal (a) and temporal region (b). axial cuts through posterior fossa showing left cerebellar abscess with subdural empyma (c) well defined abscess in right cerebellopontine cistern with marked mass effect and hydrocephalous (d) microbiological examination pus culture was positive in only 57 cases (54.56%). streptococcus was the commonest offending organism seen in 21 cases followed by staphylococcus (n = 13) and pseudomonas (n = 3). culture was sterile in 47 cases (45.44). anaerobes were found in 6 cases (5.77%) where bacteroides species was the principal isolates. in 9 cases (8.65%) mixed organisms were found. mycobacterium was isolated in 4 cases figure 3a) out of which 2 cases were associated with pulmonary kochs. within 2 fungi cases, candida was associated with hiv infection. management since most of the cases presented in early and late capsular stage, they managed directly by excision of abscess cavity. 78 cases (75.00%) were managed by direct excision. 9 cases (8.65%) were managed by preliminary aspiration followed by excision because of deteriorating consciousness. 12 cases (11.54%) were managed only by repeated aspiration. conservative treatment was given to the abscess in cerebritis stage, multiple abscesses and small solitary abscess. two cases of cerebritis stage were subjected to operation when showed sign of deterioration on conservative treatment. all multiloculated and cerebellar abscesses were managed by surgical excision (figure 3b& 3c). all the cases, irrespective of surgical procedure, received antibiotics either single or in combination. during last 5 to 6 year, a combination of ceftriaxone and metronidazole were started in every case and changed subsequently after culture report. those cases showing sterile culture showed good response to both drugs. 418 | singh et al current epidemiological trends of brain abscess those cases which were managed conservatively, received antibiotics for 4-6 weeks including 2 weeks of intravenous therapy while those cases which were treated by direct excision, received antibiotics only for 3 weeks. figure 3 post contrast axial ct image shows thick walled conglomerated ring enhancing lesions with marked perifocal edema and mass effect in left frontal region suggesting tubercular brain abscess (a). eroded trephine bone flap (b). excised abscess wall (c) outcome overall mortality in this series was 10.58%. patient with cyanotic heart disease and those having multiple abscesses had the highest mortality. those patients who were having low gcs and features of herniation died even after surgery. those cases having gcs below 8 had 62.50% mortality, while mortality was only 1.45% in the patient having gcs between 13 to 15. four cases which were being treated by repeated aspiration died and one died who was put on conservative treatment. three patients died among direct surgical excision group. there were 5 cases of recurrence, three of them were those who did not go for operation for otitis media i.e. eradication of primary focus and two recurrent cases were those which were infected by pseudomonas and had aspiration only. all patients received antiepileptic drug post-operatively and only two cases had generalized seizure in spite of aed. all the patients presented with focal neurological deficit, improved either during post-operative hospital stay or follow up period, except solitary case of pyocephalus who remained in vegetative state till one year of follow up. discussion incidence the incidence of brain abscess depends on geographical location and living standard within a given region. in our study, the incidence among all intracranial space occupying lesion was 20.8% which is much higher than other studies. bhatia et al (1973) [1], menon, bhardwaj et al (2008) [2] reported incidence of brain abscess 8%, 8.2% and 15% respectively .again according to incidence our study highlighted the increase incidence as compared to other studies as mentioned above. this may be due to low socioeconomic status and poor living condition of the population catered by this institute. besides that, improvement in health care delivery system has led to more and more cases coming up for medical advice and being diagnosed by technological advancements. age and sex distribution in our study, there were 76 males and 28 females. male preponderance amongst cases were seen as 2.71:1. this may be due to discrimination in seeking medical advice on the basis of sex by local population and exposure of male population to trauma more romanian neurosurgery (2017) xxxi 3: 414 421 | 419 than female. in other studies also, the incidence of brain abscess is more in male as compared to females. this predilection for males is unexplained in most series. in our study, majority of cases (73.08%) were seen in first two decades of life. the main aetiological factors of abscess in our series, like csom, chd and trauma were mostly found in this very young age group. most other studies like gupta et al (1990) [3], menon and bhardwaj et al (2008) also showed high incidence in first two decades of life as 67.5%. brain abscess in neonates and infants is rare but our study showed higher incidence due to low socio economic status and poor hygiene. aetiological factors the incidence of contiguous spread of infections into brain parenchyma is decreasing in the most parts of the world, especially in advanced countries, with prompt treatment of the initial source of infection. but in most of the large series of brain abscess from developing countries, mastoid infection still remains to be the commonest source of intracranial abscess. the present study encountered large number of intracranial abscess secondary to middle ear infection (58.95%), which probably reflects the gravity of ear infection about which people of this particular area are not aware. similar results have been reported in other study from india (bhardwaj& joshi 1998, lakshmi et al 1993) [4]. this clearly indicates that an ear infection is often neglected and not treated aggressively in developing countries, while in developed countries the incidence of csom had come down to 0.04% of all ear infection (osma et al, 2000) [5]. with the increasing incidence of road accidents, head trauma had become an important predisposing factor of brain abscess. in our series, it was 10.58 %, while morgan et al (1973) [6], gupta et al (1990) and menon& bhardwaj et al (2008) observed it in 13.63%, 16.25% and 8% respectively. we found two cases of brain abscess due to deficiency in cell mediated immunity i.e. aids. in 22.11% of cases in our study no focus of primary infection was found which was comparable with other study. clinical presentation location in our series 55.77% of abscess was located in supratentorial compartment. in most of the other series, the abscess was located mainly in supratentorial region where temporal, frontal and parietal lobes were commonly affected. thus it is well evident that temporal lobe was the commonest site in those series including ours where middle ear infection was the main aetiological factor. microbiology in our series streptococci and staphylocci was the commonest organism isolated. berlit et al, 1996; [7], estivado et al, 1995; [8], malik et al, 1994 also reported these organism as commonest. upon reviewing the literature the overall incidence of pseudomonas as the causative organism has been found to be low. in our series pseudomonas cases were found mostly in otogenic group. multiple drug resistance was found to be the major problem in pseudomonas infection leading to recurrence and mortality. for 47 (45.44%) specimens in this study, no organism was isolated from culture. the high incidence of such cultures may be because the 420 | singh et al current epidemiological trends of brain abscess samples were collected from a tertiary care centre and patients had undergone a treatment of long duration with broad spectrum of antibiotics before they reported to the hospital. it has been previously reported that in 9–63% of primary pus specimens, no organism was isolated upon culture [9]. mycobacterium was found in 4 cases (3.85%) of all brain abscess cases in our study. out of which 2 cases (50%) were associated with pulmonary koch’s in contrast to 1 of 6 cases (16.67%) in raj kumar et al’s series (2002) [10]. the difference may be due to small sample in the study. fungal abscess was found in 2 cases (1.92%); aspergllus species was isolated from one of the hiv infected case which succumbed in long treatment. scully, baden and katz et al (2008) documented similar high fatality of cns aspergellosis. management non-operative management in our series, 3.84% of cases were treated non-operatively which included either abscess in cerebritis stage or deep seated abscess or solitary abscess having diameter less than 2.5 cm. the mortality in this group was 9.09 %. rosenblum et al (1980) [11] documented complete resolution of abscess with medical therapy where abscess was of less than 2.00 cm in diameter. surgical management in this series, we have had better results with excision of capsule either directly or proceeded by aspiration. about 84%of the patients in this series treated by surgical excision of capsule with resultant mortality of about 5.22% while only 11.54% of patients treated by aspiration alone with 33.33% mortality. the aspiration group included most of case of abscess caused by cyanotic heart disease resulting in high mortality. since majority of the cases in this series was having large abscess with well-defined capsule and was showing significant mass effect on ct scan with sign of raised intracranial pressure, excisional surgery was done in them. and all of them received antibiotics only for 3 weeks postoperatively showing no recurrence on the part of antibiotic therapy. thus excision allows immediate decompression of mass and reduces the duration of antibiotic therapy and consequently resulting in shorter hospital stay and low cost of treatment. outcome the most important determinant of the outcome is the neurological condition of the patient at the start of treatment. the other factors that contribute to mortality are the age of the patient, multiplicity of abscesses and the nature of the infection. improvement in microbiological isolation technique, newer and most effective antibiotics have significantly reduced the mortality. the overall morality in present study was 10.58% and a statistically significant association was shown between the age of the patient and mortality. in our series morality was approximately 63.72% in comatose patient. garfield (1969) [12], karandonis et al (1975); [13] bhatia et al (1973) all reported approximately 90% mortality among comatose patient. thus we can see that mortality statistics has not changed significantly since past for comatose patient, which is the important determinant of outcome. we could not find any significant romanian neurosurgery (2017) xxxi 3: 414 421 | 421 association between the causal organism and mortality. in the present study 2 patients (18.18%) who died had multiple abscesses. in this study we did not find significant neurological deficit and disability in cured group. all neurological deficits found at the time of presentation, improved completely in due course of time during follow up. beller et al (1973) [14] reported 50 percent and carey et al (1972) [15] reported 35 percent incidence of permanent neurological sequelae following brain abscess. there was one case of pyocephalus who remained in vegetative state post operatively. conclusion there has been a decrease in mortality due to brain abscesses since 1975, as seen in different studies. this may be due to advances in diagnostic modalities, antibiotic regimens and surgical techniques. paracranial suppuration is still the most common source of intracranial abscesses in india, with no major change in bacteriology. earlier diagnosis and aggressive treatment of these conditions will certainly reduce the incidence of such brain abscesses. correspondence dr. deepak kumar singh professor (jr) & head department of neurosurgery dr ram manohar lohia institute of medical sciences, lucknow, india-226010 mob no+919984014649 email: gkp.deepak@gmail.com references 1. bhatia r, tandon pn, banerji ak. brain abscess: an analysis of 55 cases. int. surg. 58:565, 1973. 2. bharadwaj r, joshi b n. brain abscesses – a study of the causative organisms with special reference to anaerobes. indian j patholmicrobiol 31: 44–48, 1988. 3. gupta sk, mohanty s, tandon sc, et al. brain abscess with special reference to infection by pseudomonas. br j. neurosurgery 4: 279-286, 1990. 4. lakshmi v, rao rr, divakar i. bacteriology of brain abscess. observation in 50 cases. j med microbiol. 38: 187, 1993. 5. osma u, cureoglu s, hosoglu s. the complications of chronic otitis media: report of 93 cases. j laryngolotol 114: 97–100, 2000. 6. morgan h, wood mw, murphy f. experience with 88 consecutive cases of brain abscess. j neurosurgery 38: 698-704, 1973. 7. berlit p, fedel c, tornow k, schmiedeck p. bacterial brain abscess-experiences with 67 patients. fostschr. neurol. psychiatr. 64 (8): 297-306, 1996. 8. estirado de cabo e, arzuaga torre ja, roman garcia f, delpozo garcia jm, perez maestu r, martinez lopez de letona j. cerebral abscess: clinical review of 26 cases. rev clinesp 195 (5): 304-7, 1995. 9. gregory dh, messner r, zinnerman h h. metastatic brain abscesses. a retrospective appraisal of 29 patients. arch internmed 119:25–31, 1967. 10. rajkumar pandey c, bose n, sahay s, et al. tuberculous brain abscess: clinical presentation, pathophysiology and treatment in children. child’s nervous system 18:118-123, 2002. 11. rosenblum ml, hoff jt, norman d et al. nonoperative treatment of brain abscess in selected high-risk patients. j neurosurgery 52: 217-225, 1980. 12. garfield j. management of supratentorial intracranial abscess: a review of 200 cases. br med j 2: 7-11, 1969. 13. karandanis d, shulman ja. factors associated with mortality in brain abscess. arch int medicine 135: 1145, 1975. 14. beller a j, sahar a, praiss i. brain abscess – review of 89cases over a period of 30 years. jneurol neurosurg psychiatry 36:757–768, 1973. 15. carey me, chou sn, french la. long-term neurological residua in patient surviving brain abscess with surgery. j. neurosurg. 34: 652-656, 1971. microsoft word _3.formatata_iencean.doc romanian neurosurgery vol. xvi nr. 2 17 intracranial pressure monitoring study in severe traumatic brain injury and post-traumatic hydrocephalus dr. şt.m. iencean1, prof. dr. n. ianovici2, prof. dr. a.v. ciurea3 1neurosurgery, hospital “prof dr n oblu ”iasi 2university of medicine and pharmacy “gr.t. popa”, hospital “prof. dr. n. oblu” iasi 3university of medicine and pharmacy “carol davila”, emergency clinic hospital ”bagdasar-arseni” bucharest objective. to evaluate patients who developed hydrocephalus following a severe traumatic brain injury in connection with the monitoring of intracranial pressure (icp) during the acute stage of brain trauma. methods. there were studied 25 patients with severe head injuries and gcs score of 7 to 4, age between 20 and 60 years, who underwent icp monitoring and cerebral perfusion pressure (cpp) monitoring. sixteen surviving patients were followed for 12 months and the development of the post– traumatic hydrocephalus was found at five patients. conclusions. the analysis of the data of this study shows some observations: mortality in severe traumatic brain injuries is corelated with a low gcs score, high icp values and arterial hypotension. the favourable outcome is in connection with a high initial gcs score, a decrease of icp and normal values of cerebral perfusion pressure. there were five cases of moderate post-traumatic hydrocephalus and these cases of hydrocephalus have stabilized and did not need a surgical intervention. keywords: post-traumatic hydrocephalus, intracranial pressure, traumatic brain injury post-traumatic hydrocephalus (pth) is a frequent and serious complication that follows a traumatic brain injury (tbi) (1, 3, 4, 9). the onset of pth may vary from 2 weeks to years after tbi and the incidence varies greatly from study to study: 0.7 50%, variation results from underdiagnosis and atypical presentation. mazzini et al , 2003, found that 50% of patients with postacute phase severe tbi had post-traumatic hydrocephalus, but that only 11% required surgery (8). post-traumatic hydrocephalus may present as normal pressure hydrocephalus (nph) or syndrome of increased intracranial pressure. post-traumatic hydrocephalus needs to be distinguished from cerebral atrophy (ie, hydrocephalus ex vacuo) and ventricular enlargement caused by a failure of brain development. this study proposes to evaluate the monitoring of intracranial pressure (icp) and cerebral perfusion pressure (cpp) in the treatment of patients with severe traumatic brain injury (tbi) in connection with the post traumatic hydrocephalus. the patients were followed 12 months post tbi. methods there were studied 25 patients with severe head injuries and gcs score of 7 to 4, age between 20 and 60 years, who underwent icp monitoring and cerebral perfusion pressure (cpp) monitoring (minute-by-minute collection system). a subgroup of 11 patients underwent surgery for intracranial hematomas and another subgroup of 14 patients did not need any surgery. icp monitoring started from the moment of surgery or just after determining the diagnosis by computed tomography (ct), through ventricular catheterism in connection with a spiegelberg-type monitor. şt.m. iencean romanian neurosurgery vol. xvi nr. 2 18 results the group of operated patients included 7 patients with acute intracranial hematoma: 4 cases with gcs score of 6 to 4 and icp remained elevated for 12 hours to 3 days despite of treatments for lowering of icp and with poor results. 3 cases with gcs score of 7 and 6; icp decreased gradually in 6 hours to 2 days, with favourable outcome. one patient had a pre-existing hydrocephalus (probably a stabilized hydrocephalus) without important clinical symptomatology after the surgery. four patients with chronic subdural hematoma (gcs = 7 – 6), where icp decreased gradually in the first 3 to 6 hours after surgery, with a good outcome. there was a moderate ventricular enlargement at one patient after 4 months, but without clinical decompensation and he did not need a surgical treatment. the group of patients without surgery: 5 cases with gcs 5 to 4, and constant high icp values, difficult to correct, with bad outcome; 9 cases with gcs of 7 to 5, with high values of icp which decreased gradually under medical treatment, with a favourable evolution. three patients had an unimportant or moderate ventricular enlargement after 3 to 6 months, with minor clinical symptomptomatology and favourable evolution after medical treatment. (fig. 1 a, b, c) discussion in a study of 1979, jensen and jensen presented a clinical analysis of 160 patients: the patients were studied either by: quantitative isotope ventriculography (qiv) or by lumbar isotope cisternography (lic) and 30 % of them developed post-traumatic hydrocephalus. clinical signs were independent of the icp and of the type of hydrocephalus and the treatment was surgical shunting (6). later beyerl and black (1984) shown that posttraumatic hydrocephalus is a treatable complication of tbi, pth should be treated if lumbar csf pressure > 180 mm h2o and typical symptoms of nph are present (2). in 1996 marmarou, foda et al. found that 44% of head injury survivors may develop ventriculomegaly and posttraumatic hydrocephalus was diagnosed in 20% of survivors and their outcome was significantly worse (7). the studies of last years (tian and xu, 2007; jiao and liu, 2007) have found that risk factors for posttraumatic hydrocephalus are increasing age, low gcs score on admission and intraventricular hemorrhage and severe traumatic subarachnoid hemorrhage; the posttraumatic hydrocephalus have appeared in 11.96 % cases. they said that continuous lumbar drainage of csf can greatly reduce pth (5, 10). the number of cases in our study is of 25 patients, but there were only severe tbi and they had a low gcs score (< 7). the post–traumatic hydrocephalus was found at five patients at sixteen surviving patients followed for 12 months. there were five cases of moderate post-traumatic hydrocephalus and these cases of hydrocephalus have stabilized and did not need a surgical intervention. one patient had a pre-existing hydrocephalus (a stabilized hydrocephalus) without important clinical symptomatology. therefore there were four moderate post-traumatic hydrocephalus after severe traumatic brain injuries. the hydrocephalus patients had minor clinical symptomatology and favourable evolution after medical treatmentand they did not need a surgical treatment. conclusions 1. in the present study there were five cases of moderate hydrocephalus: one case of pre-existing hydrocephalus with an acute intracranial haematoma; one case after a chronic subdural haematoma and three cases after non-surgical severe traumatic brain injury. these cases of hydrocephalus have stabilized and did not need a surgical intervention. 2. there were five types of aspects of icp during the evolution of severe brain injury: a.normal and constant icp; b.initial normal icp and increased icp later caused of a secondary surgical intracranial lesion; intracranial pressure monitoring study romanian neurosurgery vol. xvi nr. 2 19 c.initial normal icp and gradual increased icp in connection with brain edema d.initial increased icp with constant high values of icp; e.initial increased icp that become normal after surgery. 3. mortality in severe traumatic brain injuries is correlated with a low gcs score, high icp values and arterial hypotension. the reduction of icp and the increase of cpp are individual and they require a continuous pressure control. the favourable outcome is in connection with a high initial gcs score, a decrease of icp and with normal values of cerebral perfusion pressure. this study was not found any correlation of the values of icp (during the icp&cpp monitoring) and the later appearance of post-traumatic hydrocephalus. references 1. arseni c, ciurea av. clinicotherapeutic aspects in the growing skull fracture. a review of the literature. childs brain. 1981;8(3):161-72. 2. beyerl b, black pm: posttraumatic hydrocephalus neurosurgery 1984;15 (2):257-61 3. ciurea av, kapsalaki ez, coman tc, roberts jl, et al supratentorial epidural hematoma of traumatic etiology in infants. childs nerv syst. 2007;23(3):335-41. 4. iencean st m pattern of increased intracranial pressure and classification of intracranial hypertension. j medical sciences, 2004 , 4, no 1, ,pp. 5258 5. jiao qf, liu z et al.: influencing factors for posttraumatic hydrocephalus in patients suffering from severe traumatic brain injuries. chin j traumatol. 2007;10(3):159-62. 6. jensen f, jensen ft: acquired hydrocephalus. a clinical analysis of 160 patients studied for hydrocephalus. acta neurochir (wien). 1979; 46 (1-2): 119-337. 7. marmarou a, foda ma et al. posttraumatic ventriculomegaly: hydrocephalus or atrophy? a new approach for diagnosis using csf dynamics. j neurosurg. 1996;85(6):1026-35 8. mazzini l, campini r, angelino e et al posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. arch phys med rehabil. 2003;84(11):1637-41. 9. miki t, nakajima n, wada j, haraoka j. cause of post-traumatic hydrocephalus because of traumatic aqueduct obstruction in two cases. j trauma. 2006;61(4):985-9. 10. tian hl, xu t et al risk factors related to hydrocephalus after traumatic subarachnoid hemorrhage (tsah) surg neurol. surg neurol. 2008;69(3):241-6 doi: 10.33962/roneuro-2021-045 essentials of nimodipine in neurocritical care patients sandra marcela mass-ramirez, carmen sofia sierra-ochoa, ivan david lozada-martinez, b.s. aristizabal-carmona, juan esteban suárez -muñoz, lina marcela ortiz-roncallo, jose david rubiano-buitrago, bryan hernández-nieto, s. antonio-barahona botache, j. eduardo cárdenas-mayorga, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (3): pp. 270-276 doi: 10.33962/roneuro-2021-045 www.journals.lapub.co.uk/index.php/roneurosurgery essentials of nimodipine in neurocritical care patients sandra marcela mass-ramirez1, carmen sofia sierra-ochoa1, ivan david lozada-martinez1,2,3,4, brayan stiven aristizabal-carmona5, juan esteban suárez-muñoz5, lina marcela ortizroncallo6, jose david rubiano-buitrago7, bryan hernández-nieto8, sergio antonio-barahona botache9, julián eduardo cárdenas-mayorga10, luis rafael moscote-salazar1,2,3 1 medical and surgical research centre, university of cartagena, colombia 2 colombian clinical research group in neurocritical care, university of cartagena, colombia 3 latin american council of neurocritical care, cartagena, colombia 4 global neurosurgery committee, world federation of neurosurgical societies 5 school of medicine, fundación universitaria autónoma de las americas, pereira, colombia 6 school of medicine, universidad de la sabana, bogotá, colombia 7 school of medicine, universidad nacional de colombia, bogotá, colombia 8 school of medicine, universidad simón bolivar, barranquilla, colombia 9 school of medicine, universidad surcolombiana, neiva, colombia 10 school of medicine, fundación universitaria juan n corpas, bogotá, colombia abstract nimodipine is a drug belonging to the group of calcium channel blockers, very well tolerated, widely recognized for its central action as a vasodilator preventing vasospasm secondary to aneurysmal subarachnoid haemorrhage. it is currently approved as a drug used in the treatment of this type of haemorrhage, mainly because it is effective in reducing neurological deficits due to delayed cerebral ischemia. in addition, due to its relaxing action on the cerebral vascular musculature and its facility to cross the blood-brain barrier, it has multiple functions in other types of cerebral vascular lesions such as ischemic stroke and other neurological conditions involving stress or cell death. its role as a prophylactic agent in the treatment of migraine and its effect as a neuroprotective agent have also been evaluated. keywords nimodipine, aneurysmal subarachnoid haemorrhage, cerebrovascular disorders, central nervous system diseases, neuroprotection corresponding author: ivan david lozada-martínez medical and surgical research centre, university of cartagena, colombia ilozadam@unicartagena.edu.co copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 271 essentials of nimodipine in neurocritical care patients introduction calcium channel blockers act by blocking the entry of calcium ions into vascular and cardiac smooth muscle cells during membrane depolarization. its inhibition causes essentially relaxation of arterial vessels, because muscle contraction is highly dependent on calcium influx. this is why the main effects of calcium channel blockers are relaxation of arterial and vascular smooth muscle cells, resulting in arterial vasodilatation [1]. in general, they are indicated in the treatment of hypertension and other major cardiovascular disorders; however, their use has also been suggested in the management of cognitive disorders and other neurological disorders [2]. based on the above, the pharmacological effect of vasodilators on cerebral blood flow, such as calcium channel blockers, has been extensively studied and evaluated in different pathological conditions that compromise cerebral vascular integrity. nimodipine, being lipophilic, can cross the blood-brain barrier; in fact, studies have shown that nimodipine is more lipophilic than nifedipine and its volume of distribution in the brain of rats was three times greater than that of nifedipine [3]. early pharmacological studies characterized nimodipine as a potent cerebral vasodilator drug [3]. subsequently, several studies confirmed the cerebral vasodilator activity of nimodipine and mentioned that, in addition to its calcium antagonist action on the smooth muscle of cerebral blood vessels, nimodipine may have direct neuronal effects [3]. thus, different studies were developed to identify its efficacy in different brain alterations that generate some degree of compromise in the cerebral vascular endothelium, such as traumatic brain injury, stroke and migrainea. one of the main complications following a subarachnoid hemorrhagic stroke is arterial spasm, which is caused by the presence of blood in the subarachnoid space [4]. nimodipine plays an important role in inhibiting reflex vasospasm, thus acting as a neuroprotector. it has also been shown that the prophylactic use of nimodipine in patients with aneurysmal subarachnoid hemorrhage reduces the risk of ischemic brain damage, a frequent complication of this event [5,6]. in this review, the essential aspects of nimodipine for the management of patients in the neurocritical state are presented. pharmacological aspects of nimodipine nimodipine (c21-h26-n2-o7) is a drug belonging to the group of second-generation 1,4-dihydropyridine calcium channel blockers [7]. it has been used for various situations since the 1980s, where it was initially implemented in the management of systemic arterial hypertension but later approved by the food and drug administration (fda) for the treatment of vasospasm after aneurysmal subarachnoid haemorrhage [7-9]. it is not widely used, since its use is mainly aimed at the management of patients with this type of stroke [10]. mechanism of action voltage-dependent calcium channels (vdccs) are widely distributed throughout the body and their function is to regulate the excitability and secretion of different cell types. nimodipine binds to the alpha1 subunits containing the voltage sensor and transmembrane pores of l-type vdccs, acting as a negative allosteric modulator of the function of this channel [7,8]. four alpha-1 isoforms have been identified within the l-type class of which cav1.2 or cav1.3 are those that are widely expressed in the cardiovascular system and in neurons, therefore, they are of great importance in the pathophysiology of the central nervous system (cns), because they have a high relationship with cells involved in the regulation of the neurovascular unit [8]. during depolarization of the smooth muscle cells of blood vessels, there is an influx of calcium ions; nimodipine acts by blocking these channels, preventing this influx and causing vasodilatation [7]. in addition, it has a high lipid solubility, so it has a preference for acting on cerebral blood vessels and can cross the blood-brain barrier [7,10]. in this way, it has an effect on cerebral blood flow by having the ability to reverse the persistent pathological activation of l-type channels in cerebral arteries, which are responsible for reflex vasoconstriction in case of injury [8,11]. clinical utility of nimodipine in neurocritical care haemorrhagic stroke nimodipine is an fda-approved drug included in the general treatment of aneurysmal subarachnoid haemorrhage (asah) [12,13]. it has the ability to reduce the risk of cerebral ischemia and improves clinical prognosis. the dose recommended by clinical practice guidelines is 60 mg orally every 4 hours 272 s.m. mass-ramirez, c.s. sierra-ochoa, i.d. lozada-martinez et al. during the first 48 hours after the onset of symptoms or when the patient's hemodynamic status permits, and is maintained for the following 21 days [12,14]. if the enteral route cannot be used, it is recommended to use intravenous nimodipine, gradually increasing up to 2mg/h, avoiding arterial hypotension; it should be switched to the oral route as soon as possible [12]. the most frequent complication of asah is delayed cerebral ischemia, which is believed to be the product of multiple processes such as angiopathic microand macrovasospasm, loss of autoregulation, cortical depolarization, microthromboembolism, and heterogeneity of capillary transit time [8,15,16]. it has been postulated that cortical depolarization propagates from the nucleus and vulnerable regions, causing additional ischemia both adjacent to the core lesion and in distant regions with compromised perfusion due to large vessel vasospasm; when nimodipine is used, cortical depolarization is initiated less frequently and less severely, decreasing the risk of delayed cerebral ischemia [8]. several studies have demonstrated the efficacy of nimodipine in improving neurological status following this type of hemorrhagic event [17,18]. philippon et al [19] conducted a prospective randomized double blind study in patients with asah to determine whether the use of nimodipine reduces the severity of ischemic deficits secondary to vasospasm and found that, although not observed in all cases, nimodipine effectively decreases the occurrence of neurological deficits due to vasospasm. pickard et al [20] conducted a prospective trial with the aim of establishing the effect of nimodipine on the incidence of ischemic events and proven cerebral infarction, and on the reduction of death and severe disability after subarachnoid hemorrhage; it was shown that the use of oral nimodipine 60 mg every four hours is well tolerated, reduces cerebral infarction and improves outcome after subarachnoid hemorrhage. finally, in a similar study, petruk et al [21] concluded that treatment with nimodipine in poor-grade patients with subarachnoid hemorrhage results in an increase in the number of good outcomes and a reduction in the incidence of delayed neurologic deterioration due to vasospasm. the efficacy of nimodipine in the context of subarachnoid hemorrhage has also been evaluated in children. song et al [22] conducted a prospective randomized controlled clinical trial in children with subarachnoid hemorrhage, with the aim of evaluating the effect of prophylactic nimodipine in preventing vasospasm and improving outcomes in this type of patient. as a result, they concluded that prophylactic nimodipine cannot reduce the incidence of vasospasm in children with subarachnoid hemorrhage, but may improve shortterm brain function on the other hand, sriganesh et al [23] evaluated the effect of intra-arterial nimodipine on regional cerebral oxygen saturation (rso2) and systemic hemodynamic indices during therapy for cerebral vasospasm following asah. analysis of the results showed that there was no change from baseline in ipsilateral and contralateral rso2 after administration of intra-arterial nimodipine, but there was a significant decrease in mean arterial pressure and total peripheral resistance index. these latter hemodynamic changes could offset any potential effect of intra-arterial nimodipine to improve rso2. further studies are needed to corroborate this theory several studies have also been conducted comparing the effectiveness of nimodipine with other calcium channel blockers in the treatment of patients with asah. one of these is the study by schmid-elsaesser et al [24] where they evaluated the efficacy of magnesium (nature's physiological calcium antagonist) versus nimodipine to prevent delayed ischemic deficits after asah. they showed that, in the magnesium group, 15% experienced clinical vasospasm and 38% experienced angiographic/transcranial doppler vasospasm, compared to 27% and 33% of patients in the nimodipine group, respectively [24]. the authors conclude that the efficacy of magnesium in the prevention of delayed ischemic neurological deficits in patients with asah is comparable to that of nimodipine and further studies are needed to better define its role in these neurological circumstances and on its combined administration with nimodipine. ischemic stroke most strokes are ischemic, i.e., caused by reduced blood flow with obstruction of small and large vessels. this sudden loss of blood supply is associated with a massive influx of calcium ions into neurons, which is the common pathway leading to 273 essentials of nimodipine in neurocritical care patients cell death [25]. it is proposed that inhibition of calcium entry by the use of calcium channel blockers could protect neurons and reduce neurological deterioration after stroke several studies have investigated the efficacy of nimodipine in improving clinical outcomes after ischemic stroke. steen et al [26] conducted a study in pigtailed monkeys, which were subjected to 17 minutes of complete cerebral ischemia followed by 96 hours of intensive care treatment. they evidenced that the neurological outcome at 96 hours after ischemia was significantly better in nimodipinetreated monkeys than in controls, and a histopathological scoring system yielded a significantly better mean score for the treated group than for the untreated group [26]. in the randomized, double-blind, multicenter clinical trial conducted by the american nimodipine study group, a positive finding was that patients treated with nimodipine had a 30% reduction in the frequency of clinical worsening compared to placebo within 18 hours after stroke [27]. however, the results compared with those of other clinical trials are contradictory. in the study by kaste et al [28], where the hypothesis that nimodipine would improve functional outcome in acute hemispheric ischemic ischemic stroke was tested, no differences in functional outcome were observed between treatment groups. similarly, in a cochrane meta-analysis where randomized controlled trials comparing a calcium antagonist versus a control in people with acute ischemic stroke were included, it was found that calcium antagonists showed no effect on the primary outcome (rr 1.05; 95% ci: 0.98 to 1.13) or on death at the end of followup (rr 1.07, 95% ci 0.98 to 1.17); therefore, the authors concluded that no evidence was found to support the use of calcium antagonists in patients with acute ischemic stroke [29]. further studies are needed to clarify whether the use of nimodipine in ischemic stroke is beneficial or not. uses of nimodipine in other neurological conditions calcium channel antagonists, such as flunarizine, are used as a drug for migraine prophylaxis, so the role of nimodipine in the treatment of this condition has been studied [30]. nimodipine could intervene in the pathophysiology of migraine by blocking the entry of calcium into the smooth muscle cells of cerebral vessels, preventing the vasomotor manifestations of migraine. the possibility of a neurogenic mechanism of action has also been studied [31]. recent case reports have elucidated the efficacy of nimodipine in the treatment of prolonged hemiplegic migraine (hm) linked to the atp1a2 gene mutation [32]. the case was reported by dannenberg et al [32] where a girl diagnosed with mh developed drowsiness, confusion, nausea, vomiting, photophobia, left hemiparesis and unilateral central facial palsy, after two days of headache. initially, levetiracetam and dexamethasone were administered, but due to the persistence of symptoms, nimodipine was added on the sixth day to prevent new spasms [32]. nimodipine infusion rapidly improved the patient's symptoms and was well tolerated, and within 12 hours improved left arm motor function. the authors concluded that nimodipine treatment should be considered for prolonged migraine attacks in patients with atp1a2 mutations. on the other hand, clinical and experimental data have attributed a neuroprotective effect to calcium channel blockers, specifically nimodipine. this is why leisz et al [33] conducted a study with the aim of evaluating the relationship of nimodipine treatment on the in vitro neurotoxicity of various cell types subjected to stress. schwann cell lines, neuronal cells and astrocytes were treated for 24 hours with nimodipine and incubated under osmotic, oxidative and heat stress conditions. the results demonstrated a cell type-independent protective effect of prophylactic treatment with nimodipine, through decreased activation of caspase 3 and 7, and increased activation of creb (cyclic adenosine monophosphate response element-binding protein) and akt (proteinkinase b) signaling. the authors suggest that these investigations should be continued in vivo to determine whether these mechanisms can be transferred to patient tissues. similarly, herzfeld et al [34] analyzed the neuroprotective effects of nimodipine on neuro2a neuroblastoma cells after the application of cell death inducers (surgery-associated stress, such as heat or mechanical stress). the results indicated that nimodipine significantly decreased ethanol-induced cell death by up to 9% at all concentrations tested; in addition, heat-induced cell death was reduced by 2.5% and mechanical treatment-induced cell death was reduced by up to 15%. these findings 274 s.m. mass-ramirez, c.s. sierra-ochoa, i.d. lozada-martinez et al. demonstrated that nimodipine rescues neuro2a cells from stress in a mild but significant manner, adverse effects and limitations of use of nimodipine nimodipine is generally well tolerated, but its use is correlated with some side effects related to its vasodilator property. hypotension is the most frequently reported adverse effect compared to placebo treatment [35]. hajizadeh et al [36] conducted a study with the aim of determining adherence to oral nimodipine administration in patients admitted with asah. they found that 39% of patients who started nimodipine in the neurosciences intensive care unit reduced the dose due to excessive falls in blood pressure, and transient discontinuation occurred in 2% patients [36]. they concluded that most patients with asah did not complete 21 days of nimodipine and hypotension was the main reason for the change or suspension of the dose. however, the hypotensive effect can be minimized by generating control of the blood pressure by reducing the dose given to the patient. other adverse effects of the drug include headache, dizziness, flushing, nausea, diarrhea, edema of the feet, rash and palpitations. an increase in serum liver enzyme concentrations has also been reported in patients on intravenous treatment with nimodipine, but it is reversible and is thought to be due to the ethanol in the intravenous formulation and not to nimodipine [35]. isolated cases of confusion with psychosis and myocardial ischemia during treatment with nimodipine have been reported [35]. intrathecal administration of dihydropyridines has been suggested with the aim of decreasing cerebrospinal fluid (csf) concentrations of these drugs, with lower systemic concentrations and fewer systemic side effects, mainly hypotension [37]. etminan et al [37] reviewed data from intrathecal application of a slow-release nimodipine eg-1962 microparticle system to improve outcome and prevent delayed cerebral ischemia following subarachnoid hemorrhage. given the strong rationale for investigating the effects of eg-1962 in patients suffering from subarachnoid hemorrhage, they initiated two clinical trials on intracisternal and intraventricular application of eg-1962. hänggi et al [38] also described the development of sustained-release nimodipine microparticles that can be administered directly into the subarachnoid space or brain ventricles to improve the outcome of patients with asah. eight injectable formulations of nimodipine microparticles in poly (dl-lactide-coglycolide) (plga) polymers were tested in vitro. their efficacy has been tested and it has been concluded that nimodipine-plga microparticles significantly attenuate angiographic vasospasm. among the contraindications, a history of hypersensitivity reaction to nimodipine is an absolute contraindication, while hepatic insufficiency and hypotension are relative contraindications for its administration. finally, it is relevant to mention that nimodipine is not safe during pregnancy (category c) and should only be used in these circumstances if there is a strong risk-benefit ratio; breastfeeding is also contraindicated while taking the drug due to possible harmful effects on the baby [1]. final recommendations the efficacy of nimodipine in improving outcomes in the treatment of aneurysmal subarachnoid hemorrhage is well established in the literature. its pharmacological approach is aimed at reducing the harmful effects of subarachnoid blood, prevent aneurysm rebleeding, and treatment to reduce the risk of delayed cerebral ischemia or vasospasm [39]. it would be interesting to further investigate the mechanisms by which nimodipine decreases asahassociated complications and whether it has any impact on neurological conditions following the occurrence of the event it is also important to investigate the effects of nimodipine on ischemic strokes, which constitute a large percentage of the events encompassed within the context of acute neurological pathology. as noted above, there is much controversy regarding the possible effects of nimodipine in the management of patients with ischemic stroke and it is essential to clarify these concepts. likewise, future scientific research should be directed to investigate the action of nimodipine not only at the level of the cerebral vasculature, but also in the central nervous system as a whole, since it has been mentioned about the possible neuroprotective effects in other neurological pathologies. finally, further research is needed on microparticulate systems that have a sustained release formulation of nimodipine administered directly into the central nervous system by various 275 essentials of nimodipine in neurocritical care patients routes, such as intraventricular, which have been tested in patients with subarachnoid hemorrhage [40]. it is necessary to establish whether this method of local administration could be more beneficial than the oral presentation of nimodipine, since with the latter the concentrations administered to the vulnerable brain may be very low due to side effects such as systemic hypotension. references 1. livertox: clinical and research information on druginduced liver injury [internet]. bethesda (md): national institute of diabetes and digestive and kidney diseases; 2012–. calcium channel blockers. 2017. 2. godfraind t. discovery and development of calcium channel blockers. front pharmacol. 2017; 8:286. 3. scriabine a, van den kerckhoff w. pharmacology of nimodipine. a review. ann n y acad sci. 1988; 522:698706. 4. reyes g, mendizábal r, acosta r, ayala a, soto j, pérez j, et al. cerebral vasospasm following aneurysmal subarachnoid hemorrhage: diagnostic methods and assessment scales. rev hosp jua mex. 2008; 75(3):206212. 5. maher m, schweizer ta, macdonald rl. treatment of spontaneous subarachnoid hemorrhage: guidelines and gaps. stroke. 2020; 51(4):1326-1332. 6. francoeur cl, mayer sa. management of delayed cerebral ischemia after subarachnoid hemorrhage. crit care. 2016; 20(1):277. 7. m das j, zito pm. nimodipine. 2021 jan 17. in: statpearls [internet]. treasure island (fl): statpearls publishing; 2021. 8. carlson ap, hänggi d, macdonald rl, shuttleworth cw. nimodipine reappraised: an old drug with a future. curr neuropharmacol. 2020; 18(1):65-82. 9. sandow n, diesing d, sarrafzadeh a, vajkoczy p, wolf s. nimodipine dose reductions in the treatment of patients with aneurysmal subarachnoid hemorrhage. neurocrit care. 2016; 25(1):29-39. 10. carlson ap, hänggi d, wong gk, etminan n, mayer sa, aldrich f, et al. single-dose intraventricular nimodipine microparticles versus oral nimodipine for aneurysmal subarachnoid hemorrhage. stroke. 2020; 51(4):11421149. 11. janovák l, turcsányi á, bozó é, deák á, mérai l, sebők d, et al. preparation of novel tissue acidosis-responsive chitosan drug nanoparticles: characterization and in vitro release properties of ca2+ channel blocker nimodipine drug molecules. eur j pharm sci. 2018; 123:79-88. 12. guerrero lópez f, de la linde valverde cm, pino sánchez fi. general management in intensive care of patient with spontaneous subarachnoid hemorrhage. med intensiva. 2008; 32(7):342-53. 13. macdonald rl. origins of the concept of vasospasm. stroke. 2016; 47(1):e11-5. 14. hänggi d, etminan n, mayer sa, aldrich ef, diringer mn, schmutzhard e, et al. clinical trial protocol: phase 3, multicenter, randomized, double-blind, placebocontrolled, parallel-group, efficacy, and safety study comparing eg-1962 to standard of care oral nimodipine in adults with aneurysmal subarachnoid hemorrhage [newton-2 (nimodipine microparticles to enhance recovery while reducing toxicity after subarachnoid hemorrhage)]. neurocrit care. 2019; 30(1):88-97. 15. hänggi d, etminan n, macdonald rl, steiger hj, mayer sa, aldrich f, et al. nimodipine microparticles to enhance recovery while reducing toxicity after subarachnoid hemorrhage. neurocrit. care. 2015; 23(2):274–284. 16. macdonald rl. delayed neurological deterioration after subarachnoid haemorrhage. nat. rev. neurol. 2014; 10(1):44–58. 17. allen gs, ahn hs, preziosi tj, battye r, boone sc, boone sc, et al. cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage. n engl j med. 1983; 308(11):619-24. 18. li k, barras cd, chandra rv, kok hk, maingard jt, carter ns, et al. a review of the management of cerebral vasospasm after aneurysmal subarachnoid hemorrhage. world neurosurg. 2019; 126:513-527. 19. philippon j, grob r, dagreou f, guggiari m, rivierez m, viars p. prevention of vasospasm in subarachnoid haemorrhage. a controlled study with nimodipine. acta neurochir (wien). 1986; 82(3-4):110-4. 20. pickard jd, murray gd, illingworth r, shaw md, teasdale gm, foy pm, et al. effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: british aneurysm nimodipine trial. bmj. 1989; 298(6674):636-42. 21. petruk kc, west m, mohr g, weir bk, benoit bg, gentili f, et al. nimodipine treatment in poor-grade aneurysm patients. results of a multicenter double-blind placebocontrolled trial. j neurosurg. 1988; 68(4):505-17. 22. song y, qian sy, li y, liu j, li z, jia xl, et al. effectiveness and safety of nimodipine in preventing cerebral vasospasm after subarachnoid hemorrhage in children. zhonghua er ke za zhi. 2019; 57(5):338-343. 23. sriganesh k, venkataramaiah s, palaniswamy sr, ramalingaiah ah. effect of intra-arterial nimodipine on cerebral oxygen saturation and systemic hemodynamic indices in patients with cerebral vasospasm: a prospective cohort study. j neurosurg anesthesiol. 2020; 32(2):177-181. 24. schmid-elsaesser r, kunz m, zausinger s, prueckner s, briegel j, steiger hj. intravenous magnesium versus nimodipine in the treatment of patients with aneurysmal subarachnoid hemorrhage: a randomized study. neurosurgery. 2006; 58(6):1054-65. 25. siesjö bk, bengtsson f. calcium fluxes, calcium antagonists, and calcium-related pathology in brain ischemia, hypoglycemia, and spreading depression: a 276 s.m. mass-ramirez, c.s. sierra-ochoa, i.d. lozada-martinez et al. unifying hypothesis. j cereb blood flow metab. 1989; 9(2):127-40. 26. steen pa, gisvold se, milde jh, newberg la, scheithauer bw, lanier wl, et al. nimodipine improves outcome when given after complete cerebral ischemia in primates. anesthesiology. 1985; 62(4):406-14. 27. clinical trial of nimodipine in acute ischemic stroke. the american nimodipine study group. stroke. 1992; 23(1):38. 28. kaste m, fogelholm r, erilä t, palomäki h, murros k, rissanen a, et al. a randomized, double-blind, placebocontrolled trial of nimodipine in acute ischemic hemispheric stroke. stroke. 1994; 25(7):1348-53. 29. zhang j, liu j, li d, zhang c, liu m. calcium antagonists for acute ischemic stroke. cochrane database syst rev. 2019; 2(2):cd001928. 30. takeuchi y. actualización en migraña [update on migraine headache]. acta neurol colomb 2008; 24:s44s52. 31. leone m, frediani f, patruno g, valentini s, bussone g. is nimodipine useful in migraine prophylaxis? further considerations. headache. 1990; 30(6):363-5. 32. dannenberg f, prager c, schmidt f, tietze a, bittigau p, kaindl am. intravenous nimodipine treatment for severe episode of atp1a2 hemiplegic migraine. pediatr neurol. 2020; 112:71-72. 33. leisz s, simmermacher s, prell j, strauss c, scheller c. nimodipine-dependent protection of schwann cells, astrocytes and neuronal cells from osmotic, oxidative and heat stress is associated with the activation of akt and creb. int j mol sci. 2019; 20(18):4578. 34. herzfeld e, strauss c, simmermacher s, bork k, horstkorte r, dehghani f, et al. investigation of the neuroprotective impact of nimodipine on neuro2a cells by means of a surgery-like stress model. int j mol sci. 2014; 15(10):18453-65. 35. langley ms, sorkin em. nimodipine. a review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in cerebrovascular disease. drugs. 1989; 37(5):669-99. 36. hajizadeh barfejani a, rabinstein aa, wijdicks efm, clark sl. poor utilization of nimodipine in aneurysmal subarachnoid hemorrhage. j stroke cerebrovasc dis. 2019; 28(8):2155-2158. 37. etminan n, macdonald rl, davis c, burton k, steiger hj, hänggi d. intrathecal application of the nimodipine slowrelease microparticle system eg-1962 for prevention of delayed cerebral ischemia and improvement of outcome after aneurysmal subarachnoid hemorrhage. acta neurochir suppl. 2015; 120:281-6. 38. hänggi d, etminan n, steiger hj, johnson m, peet mm, tice t, et al. a site-specific, sustained-release drug delivery system for aneurysmal subarachnoid hemorrhage. neurotherapeutics. 2016; 13(2):439-49. 39. peacock sh, james c, turnbull mt, cowart jb, reid jm, freeman wd. pharmacogenomics of cytochrome p450 of nimodipine metabolism after aneurysmal subarachnoid hemorrhage. j neurosci nurs. 2019; 51(5):238-242. 40. carlson ap, alchbli a, hänggi d, macdonald rl, shuttleworth cw. effect of locally delivered nimodipine microparticles on spreading depolarization in aneurysmal subarachnoid hemorrhage. neurocrit care. 2021; 34(1):345-349. doi: 10.33962/roneuro-2021-025 deep cerebral vein thrombosis due to anaemia in a child rajneesh misra, sushil kumar, sandeep sharma romanian neurosurgery (2021) xxxv (2): pp. 159-161 doi: 10.33962/roneuro-2021-025 www.journals.lapub.co.uk/index.php/roneurosurgery deep cerebral vein thrombosis due to anaemia in a child rajneesh misra, sushil kumar, sandeep sharma st. stephens hospital, tis hazari, delhi, india abstract an eighteen-month-old child presented with vomiting, fever and altered sensorium of two days duration. he had anaemia and computed tomography of head revealed hyper-dense internal cerebral veins, vein of galen and inferior sagittal sinus and bilateral thalamic hypo-density. the child improved with anti-coagulants and packed cell transfusion. introduction deep cerebral veins include the internal cerebral vein, vein of galen, basal vein of rosenthal and the straight sinus. approximately 10% of the cases of cerebral venous thrombosis are contributed by deep cerebral venous system, the remainder being that due to superficial system (1). symptoms of deep cerebral venous thrombosis (dcvt) are confusing and non-specific. hence the diagnosis is often delayed. a high index of suspicion can save valuable lives if proper treatment is initiated at an early stage. recently we came across a case of dcvt with anemia which is unusual and hence is being reported. case report an 18-month-old child presented with 3-4 episodes of vomiting since 2 days, fever and tonic posturing of all four limbs since one day. on examination, the child had fever, tachycardia of 150/min, respiratory rate of 44/min. he was in altered sensorium. fundus was normal and the deep tendon reflexes were brisk. the plantar were extensor. investigations revealed hb of 6.34 g/dl, rbc count of 4.43* 106/mm3, wbc 17.6*103/mm3, with a differential count of ne 64.4%, l28.2%, mo. 7.1%, eo 0.3%; hct 23.7%, mcv 53.4fl, mch 14.2pg, mchc 26.6g/dl, platelet count 1236*103/microlitre, mpv 6.4, procalictonin 0.797. peripheral smear showed anisocytosis, hypochromia, microcytosis, poikilocytosis, and target cells. serum electrolytes, lfts, kfts were normal. csf was colorless, clear and on microscopy, contained 22 cells/microlitre with 98% polymorphs, 2% lymphocytes with rbc+ve, gram staining was negative and culture was sterile after 72 hours. computed tomography revealed hyperdensity in the internal cerebral vein of galen and the straight sinus (fig. 1). there were bilateral keywords anaemia, computed tomography, deep cerebral vein thrombosis. corresponding author: rajneesh misra st. stephens hospital, tis hazari, delhi, india misra_rajneesh@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 160 rajneesh misra, sushil kumar, sandeep sharma thalamic hypodensities and hydrocephalus. radiologists were sure of thrombosis of deep cerebral venous system and advised a follow up mri in the follow up period. figure 1. (top row) non-contrast (left) and contrast (right) axial computed tomography scan showing bilateral thalamic hypodensity and hyper-dense deep cerebral venous system (on plain scan). (bottom row) non contrast (left) and contrast(right) sagittal ct showing hyper dense deep cerebral venous system on noncontrast scan which remains as such with contrast. figure 2. (top row) follow up mr showing very small area of infarct (dwi on left) surrounded by a ring of edema and patency of deep venous system demonstrated in mrv (right). (bottom row) follow up mri demonstrating small hypo-intense areas on t(left) and flair (right) in bilateral thalami. the patient was started on acylovir and anticoagulants (enoxaparin). external ventricular drainage was instituted. he had recurrent seizures which were controlled with anti-epileptics. sensorium improved over a period of time and the evd was removed. he was discharged after 20 days of hospitalization in conscious state with power of 4/5 in all limbs with mild hypotonia. investigations for possible thrombophilia were normal. these included cardiolipin antibodies (6.03normal <12 mpl),homocysteine(11.62micromol/lnormal 5.46-16.2), protein c (67-normal 70-140 iu/dl),mhftr mutation(+ve),phospholipid igg(1.52normal <10), phospholipid igm(2.42, normal <10).on follow up, he was ambulant with mild dystonia and mri done at 3 and 9 months revealed recanalization of the deep cerebral venous system (fig. 2). discussion deep cerebral venous thrombosis is a rare cause of stroke in children and may be associated with poor prognosis (2). the diagnosis is often delayed as the symptoms of venous occlusion are varied and nonspecific. children may present with encephalopathy as seen in our case or may have headache, seizures or raised intracranial pressure. in our patient, all the biochemical parameters were normal. hematological investigations revealed microcytic, hypochromic anemia and the diagnosis cerebral dvt was established with a noncontrast computed tomography (ct).ct may be normal in 30% of the cases (2, 3). the thalami only or the basal ganglia may show edema or infarction. at times, the thalamic involvement may be unilateral even with bilateral dcvt (4). sidek et al in 2015 could collect 24 cases of isolated deep cerebral vein thrombosis and added one of their own. out of 25 cases, 15 were bilateral infarctions (5). hyper-density in the deep venous system on ct is suggestive of the diagnosis. mri can serve as a contributory tool by demonstrating hypo-intense lesion on t2wi and hyper-intense image on t1wi(6, 7). though mri appears to be sensitive for detection of cerebral deep vein thrombosis, it could provide additional diagnostic benefit in only two cases of cdvt,where thrombosis could not be suspected on ct(8). hydrocephalus was due of thalami causing occlusion of the third ventricle. recanalization can occur (9) and was seen in our patient as well. our patient was treated with low molecular weight heparin,vitamin k and packed cell transfusion. 161 deep cerebral vein thrombosis due to anaemia in a child clinical outcome was favorable. thrombosis resolved at 5 months. onset may be acute (less than 48 hours), subacute (48hrs to 1 month) and more chronic disease. mortality was reduced from 48% to 13% with the use of heparin, increasing the importance of early diagnosis(10).the predisposing factors include dehydration, hypercoagulable state, states of infection and malignancy(2). acute thrombosis decreases the level of antithrombin, protein c, and protein s. therefore the tests for thrombophilic states should be performed at least 6 weeks after an acute thrombotic event and inr should be maintained between 2-3. investigations for hypercoagulability panel were negative in our patient except anemia. various mechanisms have been postulated to explain iron deficiency leading to csvt.serum iron prevents thrombopoiesis (11) and acts as an inhibitor of thrombocytosis.therefore, iron deficiency leads to increased platelets and results in a hypercoagulable state .increased erythropoietin activity during iron deficiency anemia stimulates megakaryocytosis. microcytosis decreases cell deformability and increases viscosity leading to deranged flow pattern (12). in the presence of infection, increased metabolic demand can create anemic hypoxia with predisposition to venous thrombosis (13). ourpatient, had anemia with occult infection as indicated by high tlc.this, in our opinion was responsible for the dcvt. he did not have any evidence of dehydration or thrombophilic state (cardiolopin antibody was negative and homocysteine, protein c, phospolipid igg and igm levels werereported to be normal). early diagnosis coupled with institution of low molecular weight heparin and blood transfusion resulted in good outcome. references 1. ferro jm, canhao p, stam j, bousser mg, baringarrementaria f. iscvt investigations: prognosis of cerebral deep vein thrombosis: results of international study on cerebral vein and dural sinus thrombosis(iscvt). stroke 2004;34:664-670. 2. spearman mp ,jungreis ca, wehner jj, gerszten pc, welch wc. endovascular thrombolysis in deep cerebral venous thrombosis. am j neuroradiol 1997;18:502-506. 3. bousser mg, ferro jm. cerebral venous thrombosis: an update. lancet neurol 2007;6:167-170. 4. chang k, tariq u, khan rm, nickles tp and lock jr jh. unilateral thalamic venous infarction in an infarct: a rare presentation of bilateral deep cerebral venous thrombosis. case rep radiol 2018oct 24;2018:3618619. 5. sidek s, rahmatk,ramli n. imaging findings. neurology asia 2015;20:191-195. 6. kamal ak, itrat a, shoukat s, khealani a, kamal k.j pak med assoc 2006;56:557-559. 7. hermann ka, sporerb,yousry ta. thrombosis of the internal cerebral vein associated with transient unilateral thalamic edema:a case report and review of literature. ajnr am j neuroradiol2004;25(8):1351-5. 8. crombe d, haven fr, gille m. isolated deep venous thrombosis diagnosed on ct and mr imaging. a case study and literature review.jbr-btr 2003;86:257-261. 9. okamoto k, ito j.quiz case of the month. eur radiol1998;8:319-320. 10. smith ag, cornblath wt, deveikis p. local thrombolytic therapy in deep cerebral venous thrombosis. neurology 1997:48:1613-1619. 11. hartfield ds, lowry nj,keene dl, yager jy. iron deficiency: a cause of stroke in infants and children. pediatrneurol 1997;16:50-3. 12. gold dw, gulati sc. myeloproliferativediseases.in: isselbacher kj, braunwald e, wilson jd, martin jd,fauci as, kasper dl, editors. harrison’s internal medicine.13thed. new york: mcgraw hill; 1994. p.175764. 13. keane s, gallagher a, ackroyd s, mcshane ma, edge ja. cerebral venous thrombosis during diabetic ketoacidosis. arch dis child 2002;86:204-5. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article moyamoya syndrome with contra lateral daca aneurysm: first case report with review of literature ashish kumar dwivedi, pradeep kumar, trilochan shrivastava, shashi kant jain india doi: 10.1515/romneu-2017-0059 364 | kumar dwivedi et al moyamoya syndrome with contra lateral daca aneurysm doi: 10.1515/romneu-2017-0059 moyamoya syndrome with contra lateral daca aneurysm: first case report with review of literature ashish kumar dwivedi, pradeep kumar, trilochan shrivastava, shashi kant jain department of neurosurgery, s.m.s. medical college and attached hospital jaipur, rajasthan india abstract: moyamoya disease is a progressive steno-occlusive disease of bilateral internal carotid artery with the development of fine collateral vessels and is an angiographic diagnosis. concurrent moyamoya disease with intracranial aneurysm had been reported in literature by various authors. moyamoya disease is reported with aneurysm at various locations including basilar tip, anterior choroidal artery, posterior choroidal artery, anterior cerebral artery and middle cerebral artery. after reviewing literature thoroughly there is not a single case report on moyamoya disease with isolated distal anterior cerebral artery aneurysm with the best of our knowledge. here we are reporting a case of moyamoya disease of left petrous and cavernous part of internal carotid artery with contralateral distal anterior cerebral artery aneurysm in a 36-year-old male. key words: digital subtraction angiogram (dsa), moyamoya disease (mmd), moyamoya syndrome (mms), daca aneurysm introduction moyamoya disease (mmd) is a chronic cerebrovascular disease of unknown etiology characterized by progressive occlusion of distal part of internal carotid artery (ica) and circle of willis and development of collateral vessels (moyamoya vessels) close to occlusion. [1] unilateral moyamoya disease is known as moyamoya syndrome (mms). progressive occlusion of ica alters the flow dynamics in unobstructed vessels with compensatory dilatation of moyamoya vessels. this increase flow, result in rise of blood pressure and formation of aneurysm. [2] reported incidence of intracranial aneurysm in mmd is 3.4-14.8 %. [3] cerebral aneurysm with mmd is first reported in 1965. [4] hemorrhagic event in mmd with associated aneurysm is believed to be due to rupture of aneurysm. [5] because of complex pathology and variable anatomy, even in the era of great advancement in micro neurosurgery and interventional neurology, clear guide lines for the management of aneurysm with mmd is lacking. we are reporting a case of mmd of left side petrous and cavernous segment ica and aneurysm of right side distal anterior cerebral artery (daca). romanian neurosurgery (2017) xxxi 3: 364 367 | 365 case report a 36-year-old male patient presented to our outpatient department with complaint of sudden onset severe headache, dizziness and nausea for 6 days with no past history of any systemic medical illness. neurological examination at the time of admission was normal. non-contrast ct shows intraventricular hemorrhage involving lateral, third and fourth ventricle. [figures 1a and 1b] ct angiography revealed right side daca aneurysm. digital subtraction angiogram was suggestive of mmd of left petrous and cavernous segment of ica with aneurysm of pericallosal branch of daca of size 4.6 mm with 2.18 mm neck. [figures 2a and 2b] patient underwent endovascular coiling embolization of the daca aneurysm which was unsuccessful as catheterization of daca was not feasible due to tortuosity of cervical segment of right ica and right anterior cerebral artery (aca). hence, microsurgical clipping was planned but the patient denied for clipping surgery. patient was followed in outpatient department later for 6 months and then he lost the follow-up. figure 1a ct head showing intraventricular haemorrhage figure 1b ct angiography sagittal view showing daca aneurysm figure 2a dsa showing right side daca aneurysm of size 4.6mm with 2.18 mm neck figure 2b dsa showing “puff of smoke’’ appearance characteristics of mmd of left internal carotid artery (petrous and cavernous part) discussion simultaneous occurrence of mmd with intracranial aneurysms is reported by various authors from circle of willis to moyamoya vessels, but posterior circulation aneurysms 366 | kumar dwivedi et al moyamoya syndrome with contra lateral daca aneurysm are the most commonly reported aneurysm with mmd. [6] they are usually classified into two subtypes of mmd with aneurysm of major artery and mmd with aneurysm of peripheral artery. major artery aneurysms are usually saccular aneurysm while peripheral artery aneurysms are pseudo aneurysm resulting from the rupture of fusiform or dissecting aneurysm arising from moyamoya vessels. yeon et al classified aneurysm with mmd into 3 categories, aneurysm at major arteries (circle of willis), distal peripheral artery (anterior and posterior choroidal artery) and moyamoya vessels [7] mmd with associated meningeal artery aneurysm and anastomosis site aneurysm had also been reported in literature. [8] kawaguchi et al reported 23% of anterior circulation aneurysm in his series of 111 patient of aneurysm with mmd. treatment options for the anterior circulation aneurysm in mmd are greatly varied among the reported series and include either surgical clipping or endovascular embolization. [6] over all outcomes of these aneurysm with associated mmd is not satisfactory with significant mortality and morbidity. direct surgical clipping as well as endovascular embolization of ruptured basilar tip aneurysm in mmd is associated with high risk of complication. although recent studies favours the endovascular embolization for basilar tip aneurysm in a patient with mmd, optimal strategy for the treatment is yet to define. treatment of anterior choroidal artery aneurysm in patient with mmd is based on the fact that whether patient will require revascularization procedure or not. in patient requiring revascularization procedure, craniotomy is preferred over endovascular treatment since it treats both the aneurysm and mmd simultaneously. craniotomy and endovascular embolization, both are effective way to treat posterior choroidal artery aneurysm with associated mmd. disappearance of posterior choroidal artery aneurysm following revascularization procedure as well as with conservative treatment has been reported in literature. [9] moyamoya vessel mainly signifies lenticulostriate artery (lsa) and thalamoperforator artery (tpa). there is various treatment option for the treatment of lsa aneurysm in mmd patients including surgical clipping, endovascular embolization and revascularization procedures. each of these procedures has their own merits and demerits. superficial temporal arterymiddle cerebral artery (sta-mca) anastomosis is an effective procedure for management of the ischemic lesion in mmd. increase hemodynamic stress over anastomosis site makes it vulnerable for development of aneurysm. there are case reports on anastomosis site aneurysm which were treated with craniotomy and followed significant complications. iwama et al reported a case of mmd harbouring, three anterior circulation aneurysms located at a1 segment of aca, anterior communicating artery and daca. clipping was performed for all these aneurysms followed by sta-mca bypass. [10] postoperative outcome was satisfactory. this is the only case report of daca aneurysm in patient with mmd available in romanian neurosurgery (2017) xxxi 3: 364 367 | 367 literature. however isolated daca aneurysm in a patient with contra lateral mmd have never been reported in literature. in nutshell, treatment of aneurysm with associated mmd depends on site and hemodynamic characteristic of aneurysm. craniotomy is considered if revascularization procedure is required. endovascular embolization is an alternate to craniotomy as it avoids the risk of craniotomy and risk of disruption of collateral vessels. thus, revascularization surgery is one of the important factors to determine the outcome in aneurysm patient with associated mmd. correspondence dr. ashish kumar dwivedi senior registrar, department of neurosurgery, s.m.s. medical college and attached hospital jaipur, rajasthan, india302004. mobile no. 9610510564 email: drashishkumardwivedi@gmail.com references 1.hashimoto n, et al. guidelines for diagnosis and treatment of moyamoyadisease (spontaneous occlusion of the circle of willis). neurol med chir (tokyo).2012; 52: 245-266. 2.yoshida y, yoshimoto t, shirane r, sakurai y. clinical course, surgical management, and long-term outcome of moyamoya patients with rebleeding after an episode of intracerebral hemorrhage: an extensive follow-up study. stroke 1999; 30: 2272-6. 3.ueki k, meyer fb, mellinger jf. moyamoya disease: the disorder and surgical treatment. mayo clin proc 1994; 69:749-57. 4.maki y, nakata y. autopsy of hemangiomatous malformation of the internal carotid artery at the base of brain. no to shinkei 1965; 17:764-6. 5.tanaka y, ogashiwa m, takeuchi k.the moyamoya phenomenon with accompanying intracranial aneurysm.neuroradiology. 1978; 16: 289-90. 6.kawaguchi s, sakaki t, morimoto t, et al. characteristics of intracranial aneurysms associated with moyamoya disease. a review of 111 cases. acta neurochir (wien). 1996; 138: 1287-1294. 7.yeon j y, kim j s & hong s c. incidental major artery aneurysms in patients with non-hemorrhagic moyamoya disease. acta neurochir (wien). 2011; 153: 1263-1270. 8.park y s, suk j s & kwon j t. repeated rupture of a middle meningeal artery aneurysm in moyamoya disease. case report. j neurosurg. 2010; 113: 749-752 9.kuroda s, houkin k, kamiyama h, et al. effects of surgical revascularizationon peripheral artery aneurysms in moyamoya disease: report of three cases.neurosurgery. 2001; 49: 463-467; discussion 467-468. 10.iwama t, todaka t & hashimoto n. direct surgery for major artery aneurysmassociated with moyamoya disease. clin neurol neurosurg. 1997; 99 suppl 2: s191193. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0054 article parasagittal meningioma surgery ashraf elbadry, azza abdelazeez egypt      426 | elbadry et al parasagittal meningioma surgery             doi: 10.2478/romneu-2018-0054 parasagittal meningioma surgery ashraf elbadry1, azza abdelazeez2 1neurosurgery department; 2pathology department faculty of medicine, mansoura university hospital, egypt abstract: background: meningioma in parasagittal location represent between 20%-30% of meningioma in the cranial cavity. the close relation of it with superior sagittal sinus make its surgical resection is a great challenge to the surgeon to get a good result. patients & method: we collected 23 cases of parasagittal meningioma cases medical records (including pre-& postoperative clinical pictures, images plus operative details and complications post operatively) who admitted to neurosurgery dept., mansoura university hospital and underwent surgical resection in the period that began in 2010 and ended in 2016. we followed up the cases at least for 6 months. results: the patient’s age varied between 64-35 years. 16 female & 7 males. the presenting symptoms was headache (11 patients), fits (6 patients), motor weakness (5 cases), abnormal gait (1 patient) and dizziness (1 case). 15 cases had gross total tumor excision while 8 cases showed partial tumor removal. recurrence rat was in 4 cases (17.4%) plus two mortality cases. conclusion: through our series we could detect cardinal factors in prognosis of these cases which included: tumor size, histology, preoperative identification of the venous collateral and preservation of it in the surgical maneuver. the meticulous microscopic surgical technique can augment this goal. key words: parasagittal, meningioma, intracranial hypertension, superior sagittal sinus introduction the term parasagittal meningioma (psm) applies to those tumors involving the sagittal sinus and the adjacent convexity dura and falx. it comprises approximately 19.5 to 45% of meningiomas in the cranial cavity. the lateral wall of the sss lateral angle and wall may be invaded partially or completely with presence of tumor inside the lumen of sss. or the tumor may grow to partially or completely occlude the sinus. [12] parasagittal meningioma represents a challenge to neurosurgeons all over the world [2] especially if invading the superior sagittal sinus (sss) lumen, bridging vital collaterals encasement or adherence and many of them may be faced by serious vascular sequelae i.e. venus infarction that lead to sever neurological deficit when they operated in such cases. in some cases, even the superficial romanian neurosurgery (2018) xxxii 3: 426 442 | 427             cortical and intra-diploid veins injury led to the same catastrophe because it represents essential part of venous drainage. [18] inspite of cushing was the first neurosurgeon who operated on (psm) 1910 [3] and the contribution of others like olivercrona, poppen, hoessly and logue in addition etc. but still there is no accurate protocol for dealing with these cases [1,15,16]. even there is no general concept letting the surgeon in the light of the pros and cons of radical resection to follow it [4]. on the other hand, many of them prefer subtotal & partial tumor resection followed by many alternative options like expectance, gama knife and radiotherapy to reduce surgical morbidity and mortality [7] the role of well-developed collateral (secondary to complete sss occlusion) play important role in preferring total meningioma removal [8] patients and method we collected 23 cases of parasagittal meningioma cases with variable degrees of sss involvement who admitted to neurosurgery dept., mansoura university hospital in the period that began in 2010 and ended in 2016 were enrolled in this study. we excluded the cases who did not fulfill all essentials for this series like:  incomplete medical records  presentation of other comorbidities  lost follow up early postoperative  the cases who presented to us as a recurrent case with primary surgery outside our department all cases examined neurologically pre-& post-operative, their images (ct scan, mri pre and post contrast, venus mra and in some cases angiography) had been evaluated to estimate the degree of sss invasion and select the operative plan beside pathological reports. we used the sindhu’s classification [18] in assessment of sss invasion by the tumor (figure 1) because we assume it is more practical and simple to follow than other classifications like the merrem-krause's & bonnal–brotchi's categories. they underwent surgical resection. figure 1 sindou's classification in assessment of sss invasion by the tumor: grade i the tumor attached to the sss lateral wall, grade ii the tumor invades the lateral recess, grade iii the tumor invades the sss lateral wall, grade iv the lateral wall in addition to the roof of sss have been invaded by the tumor, grade v the whole sss have been invaded by the meningioma except one of both lateral wall, grade iv the whole sss have been invaded by the tumor. [18] 428 | elbadry et al parasagittal meningioma surgery             surgical procedure we used anatomical landmarks to estimate the position of sss in planning the skin incision and operative flap to minimize sss injury. we did not use any neurophysiological study. all cases monitored intraoperative for air embolism we used central venous catheter to aspirate the air if air embolism occurred intraoperatively. we used mainly two options in reconstruction of the dura layer defect after meningioma removal: galea capitis if the defect is small and fascia lata graft in large dural layer defect.in few cases we used artificial dura mater under endotracheal intubation general anesthesia. the position of the patient on operative table was planned according to the meningioma location: if the tumor in the anterior half of the sinus the patients have been placed in supine position, on the other hand, the patient has been placed in prone position if the meningioma was present in posterior half of the sss. the patient had been held in position by three-point fixation mayfield we used mixture of carbocaine 2% and saline solution for injection sub-dermis and sub-periosteum as first step in galea flap preparation (figure 2). after skin incision, the galea flap did not exceed the superior temporal line laterally. the craniotomy flap was made according to matching the anatomical land marks in the images and the patient. the craniotomy flap was centered in sss with rectangular flap with burr holes on sss both sides (figure 3). the care must be taken in separation of the dura from the bone flap to avoid sss injury. sometimes we saw hypertrophied lacunae as a sequela of hypertrophied venous collaterals. we applied microscope in all cases. its magnification varied from to 10 to 16x. figure 2 show the planned skin incision after sub dermis injection with mixture of carbocaine 2% and saline solution figure 3 revealed the burr holes for craniotomy flap was done figure 4 show the dura opening carefully from lateral to medial to avoid sss injury & visualization of bridging veins romanian neurosurgery (2018) xxxii 3: 426 442 | 429             figure 5 show coagulation of tumor feeders to reduce the bleeding figure 6 show identification of collateral veins that creep on tumor capsule (appeared under the microscope hypertrophied, wide caliber attached to sss) and identifying the tumor brain interface with meticulous dissection figure 7 show freeing the capsule from the surrounding brain tissue figure 8 reveal internal debulking then removing part of psm capsule using causa figure 9 show freeing the last part of the tumor from the bridging veins which drain in sss figure 10 show dissection of the tumor capsule from the feeder in tumor be brain parenchyma 430 | elbadry et al parasagittal meningioma surgery             figure 11 show the final stage after total excision of the brain tumor and hemostasis of psm tumor bed figure 12 sow repairing the dural defect with galea capitis patch figure 13 show water tight suturing the dura mater the dura opened carefully in the lateral dural flap edge (figure 4) from posterior forward then open it from lateral to medial making the dural flap base is the attachment to sss. we began by coagulation the tumor feeders (figure 5) & venus drainage with preservation of collateral veins (that appeared under the microscope hypertrophied, wide caliber attached to sss and run parallel to it) (figure 6) as much as possible by early identification under the microscope. the care must be taken to avoid aggressive brain retraction by working inside the meningioma by piecemeal tumor excision (internal tumor debulking) then freeing the capsule from the brain tissue by identifying the tumor brain interface that represent arachnoid plane to reduce pial and brain vessels injury (figures 7, 8, 9, 10). we applied wet cotton strips in this plane continuously till complete tumor removal we did not apply. the pericallosal and callosomarginal arteries must be visualized and gently dissected from (psm) medial inferior surface then the involved part of the falx could be excised safely. finally, we removed the meningioma part that invaded the sss if possible. the grade of tumor on sindou's classification [18] determined the management of sss involvement: category i there is line of cleavage between the meningioma and the sss leaving it intact, in grade ii we followed the tumor part of the lateral recess then suture the defect in the sss, in grade iii we removed the tumor with simple reconstruction of sss by galea capitis if possible or subtotal tumor excision was applied leaving the tumor remnant that adhered to the sss, in grade iv, v we preferred subtotal resection while in grade vi romanian neurosurgery (2018) xxxii 3: 426 442 | 431             we removed the whole tumor in addition to the sss involved part with occlusion of it preremoval to avoid embolism. we removed the involved part of the falx to reduce the recurrence. we controlled the tumor bed blood oozing by hemostatic materials after blood pressure normalization for at least 10 minutes (figure 11). at the end of the procedure we reconstruct the dural defect by galea capitis flap (figures 12 and 13) if it was small and fascia lata graft if it was large in most cases but few were reconstructed by artificial dura mater, sometimes we used autologous abdominal fat to close the defect also. if we removed the bone that invaded by the tumor (figure 14) we used titanium mesh and mini-screws to cover the bone defect. (figures 15, 16) figure 14 mri of psm cases: a &b tiwi axial cut, c t2wi axial cut, d t1wi axial cut with contrast. e t1wi with contrast coronal cut. f t1wi with contrast sagittal cut. reveal invasion & occlusion of sss and calvarial skull bone erosion over it a c b d e f 432 | elbadry et al parasagittal meningioma surgery             figure 15 ct brain coronal cuts show the titanium mesh covering the bone defect that was invaded by tumor and excised with the tumor figure 16 mri brain sagittal cuts show the mesh covering the bone defect that was invaded by tumor and excised with the tumor we used dexamethasone intraoperatively and for one week postoperative. beside antibiotic, manitol, loop diuretic and phenytoin were routinely administrated to these patients. for all cases, low molecular weight heparin was administered for all patients more than 3 weeks postoperatively; we recommend antiplatelet therapy after hospital discharge. in normal course of the cases we requested mri brain pre-& post contrast plus venus mra after three months (unless complication occurred we requested it earlier) then every 6 months interval. we followed up the cases at least for 6 months clinically and radiologically. we began the patients follow up two weeks after discharge from the hospital then every two months intervals for the first six months. after that we followed them annually. the mean follows up period was 3.2 years. we exclude all cases who did not have adequate follow up file data. presenting cases case 1: 62 years old male presented with persistent headache not respond to simple analgesics followed by seizures, on neurological examination mild right hemiparesis. images showed 3 cm diameter tumor size in the middle third of sss (figure 17) that took feeder from left middle meningeal artery (figure 18) and had multiple venus twigs toward sss which is patent (figure 19) romanian neurosurgery (2018) xxxii 3: 426 442 | 433             figure 17 mri brain: axial (t1wi, t2wi, t1wi with contrast), coronal cut t1wi with contrast and sagittal t1wi with contrast showed middle third sss left parasagittal meningioma grade iii on sindou's classification figure 18 left external carotid angiography revealed prominent feeder from left middle meningeal artery figure 19 left common carotid angiography venus phase revealed prominent multiple venus drainage twigs from the tumor toward sss from left middle meningeal artery 434 | elbadry et al parasagittal meningioma surgery             in the surgery: the patient was placed in supine position head up 20 head median position vertex up 10°, we applied curved skin incision so that the skin flap became about 5 * 5 cm with its center 2 cm behind bregma. the surgical procedure was done under the microscope with coagulation of the tumor feeders from left middle meningeal artery to reduce the bleeding and tumor venous drainage to sss also have been occluded then we peeled the tumor from the sss after internal debulking in piecemeal way. we saw some feeders from aca as a result of arachnoid layer tumor invasion toward brain parenchyma. simpson grade 2 have been achieved in this case (figure 20, 21). case 2: female patient 53 years old presented by headache and progressive left hemiparesis till motor power became grade 3 it worsens in left upper limb followed by left lower one mri brain pre and post contrast revealed showed middle third sss right parasagittal meningioma grade ii on sindou's classification (figure 22). the right internal carotid artery and both external carotid arteries feeding the tumor with high blood flow without sss occlusion (figure 23). figure 20 post operative ct brain scan axial cuts show grossly total excision of the tumor with some pneomocephalous in tumor bed romanian neurosurgery (2018) xxxii 3: 426 442 | 435             figure 21 mri brain scan t1wi with contrast axial cuts show grossly total excision of the tumor with some pneomocephalous in tumor bed a b c d figure 22 mri brain: axial cut t1wi [a], axial t2wi [b], axial t1wi with contrast [c], coronal cut t1wi with contrast [d] showed gross total resection of middle third sss right parasagittal meningioma grade ii on sindou's classification a b c d figure 23 angiography for the same case right external carotid angiography [a], left external carotid angiography [b]. right internal carotid angiography [c] venus phase [d] revealed high feeder flow from right internal carotid artery plus both external carotid also and the sss was not occluded we used supine position for the patient, head was fixed at 3 points in the midline then head tilted to the other side. under the microscope we devascularised the tumor by using electrocautery of the feeders from right eca , right &left ica and tumor draining veins with preservation of brain parenchyma draining veins above the tumor capsule toward the sss then we excised the meningioma internally piecemeal followed by removing the tumor part that adherent to the sss at the end and got simpson grade 2 which appeared in postoperative mri brain images (figure 24) postoperatively the weakness worsen for few days then gradually improved. 436 | elbadry et al parasagittal meningioma surgery             a b figure 24 mri brain: axial t1wi with contrast [a], coronal cut t1wi with contrast [b] showed no apparent residual tumor results 23 patients had parasagittal meningioma underwent surgical tumor resection in neurosurgery dept., mansoura university hospital in the period that began in 2010 and ended in 2016 the patient’s age varied between 64-35 years and the median age was 49,2 years. 16 females & 7 males. right in 12, left in 9 and bilateral involvement in 2 cases. the presenting symptoms are mentioned in table 1. table i presenting symptoms of 24 parasagittal meningioma cases presenting symptom anterior 1/3rd middle 1/3rd posterior 1/3rd total motor weakness 0 4 1 5 epilepsy 3 2 1 6 headache 6 3 1 10 dizziness 1 0 0 1 abnormal gait 1 0 0 1 the meningiomas category in these patients, according to sindou classification, are summarized in table 2. table ii meningioma location category i category ii category iii category iv category v category vi anterior 1/3rd 2 3 2 3 2 middle 1/3rd 3 1 1 2 1 posterior 1/3rd 1 2 total 6 4 3 3 2 5 8 cases had bone hyperostosis and calvarial bone invasion that revealed by images. 15 cases had gross total tumor excision (simpson grade i or ii) while 8 cases showed partial tumor removal (simpson grade iii or iv). the tumor size was estimated by measuring the meningioma three dimensions in the images (modified ellipsoid volume: a*b*c/2). the parasagittal meningioma average volume was approximately 57.2 cm3. the histopathology of these cases of (psm) was grade 1 in 18 cases (78.3%), 3 cases atypical meningioma (13 %) and 2 cases was malignant grade (8.7%) (figures 25, 26, 27) romanian neurosurgery (2018) xxxii 3: 426 442 | 437             a b c figure 25 he films of g 1 psm: a x 40 magnification; b x 100; c x 200 show criteria of meningioma a b c figure 26 immune stain for a case of psm: a ema (+vet); b vimentin (+); c mib-1 (+) 2% figure 27 he of invaded bone film by meningioma cells in cases of psm recurrence appeared in 4 cases (17.4%) plus two mortality cases. our patient’s postoperative complication in relation to meningioma sindou classification is mentioned in table 3. complications category i category ii category iii category iv category v category vi brain swelling 1 2 csf leak 1 1 new neurological deficit 1 2 1 2 hemorrhage 1 1 mortality 2 systemic 1 1 recurrence 2 1 1 438 | elbadry et al parasagittal meningioma surgery             distribution of the complication in relation to the parasagittal meningioma location on sss (table 4). complications anterior 1/3rd middle 1/3rd posterior 1/3rd behavior changes 1 motor weakness 3 visual impairment 1 dysphasia 1 brain edema 1 1 1 infection 1 1 csf leak 2 hemorrhage 1 1 mortality 1 1 recurrence 2 1 1 we observed 5 patients suffered from new neurological impairment: one has behavior changes which was aggressive early postoperative then gradually improved within limit leaving permanent personality changes as a result of venous infarction during anterior 1/3rd sss parasagittal tumor surgical removal. 3 patients with middle sss 1/3rd parasagittal meningioma experienced motor weakness (2 category iv & 1 category vi) one patient who had posterior 1/3rd parasagittal meningioma developed contralateral hemianopia with central vision sparing postoperatively. one patient suffered from dysphasia as a result of parasagittal meningioma on the middle 1/3rd of sss that improved gradually. all of them developed venous infarction due to sss impairment or due to venus collateral injury. aggressive brain edema developed in 3 (1 grade v & 2 grade vi) according to sindou classification but according to the tumor location (1 anterior 1/3rd, 1 middle 1/3rd & posterior 1/3rd) as a result of massive venus infarction caused by collateral veins occlusion or sss impairment. two died within few days in spite of decompressive surgery and the last one lived suffered from serious neurological deficit and permanent sever disability. two patients suffered from hemorrhage post operatively (1 of middle 1/3rd tumor and the other of posterior 1/3rd parasagittal meningioma) the first have been managed surgically and the other passed conservatively the operated meningioma of the sss middle 1/3rd (sss segment between coronal and lambdoid suture) had highest incidence of neurological impairment 4 cases. two of them show some improvement within few weeks. behavior changes was detected on operated meningioma of anterior 1/3rd. the visual impairment as post-operative sequela of operated posterior 1/3rd parasagittal meningioma improved lightly within few months. all of these neurological complications appeared as a result of sss occlusion partially or total and or as a result of sss collateral veins (that creeped on tumor capsule) obstruction due to intraoperative lacerations, coagulation to stop bleeding or romanian neurosurgery (2018) xxxii 3: 426 442 | 439             post-operative block. so, may administration of low molecular weight heparin after 36 hours postoperatively will reduce the venous obstruction complications. the leak of csf was detected in two cases and treated conservatively. infection appeared in one case and treated with i.v. antibiotic till blood culture & swap culture result had been obtained. we switched to appropriate antibiotic. the recurrence was observed in four cases during follow up. discussion the parasagittal meningiomas was first described by cushing and eisenhardt as meningiomas that attached to sss without brain tissue separating it from the sinus. [3] in these cases, the sss might be invaded by the tumor in variable degree. these tumours primary management modality according to the literatures varied between surgical excision and radiosurgery. [2] we adopt operative removal as primary treatment for parasagittal meningioma because many evidences in scientific papers mentioned higher incidence of brain swelling with its sequelae after radiation due to delayed collateral veins blocking. the optimum surgical procedure for parasagittal meningioma to remove it totally with minimum complication still controversy. [14] neurosurgeons like brotchi and sindou recommended putting the patients in semi sitting position to permit a free venus drainage from the head to reduce the brain edema that facilitate the tumor resection with minimal brain parenchymal injury [2,18]. we adopt this technique in addition to use the gravity to get more space for surgical manipulation with minimal brain retraction. the drawback of this position is higher incidence of air embolism. we used a central venus line (cv) & co2 detector to early detection and management of this serious position related complication. we adopt wide craniotomy flap to better visualization of sss both sides in addition to collateral veins that creeping in tumor capsule toward sss which its preservation (particularly those of rolandic brain territory) have a crucial role in post-operative venus infarction avoidance.[9] during surgery it relatively difficult to determine which vessels can be sacrificed safely in addition to misinterpretation of cortical veins size because in large tumours may appeared smaller than its real caliber as a result of the vessels stretch over the tumor capsule. this concept mad us leaving some small tumors parts around the large collateral veins around sss. we used galea capitis patch or fascia lata graft to close the dural defect in most cases as we believed it gave better results with less infection rate and adequate heeling. sometimes we adopt abdominal fat to help in closing and in forcing the defect closure [5,10,11]. the complications in our series was more frequent in surgery of sss anterior 1/3rd meningiomas (9 of 12 cases: one of them died) then middle 1/3rd (8/9 patients) patients and the least was in those of sss posterior 1/3rd. we can have explained that by impairment of essential venus collateral that was well developed in the high grade of sindou classification tumors as a result of extensive sss invasion that lead to massive edema or 440 | elbadry et al parasagittal meningioma surgery             extensive venus infarction. [11,12] and this was opposite to what mentioned by schmidelsaesser who stated that the anterior 1/3rd parasagittal meningioma surgery could be passed well without any consequences. the explanation of our results referred to: anatomical variations of draining brain area by anterior 1/3rd of sss and presence of vital collateral bridging veins [17]. adequate interpretation of preoperative mri t2we & traditional angiography may give vital information about sss patency, tumor relation to bridging veins such as rolandic & labbe and collaterals. the favor of good prognosis after surgery was: complete occlusion of sss by tumor, patent rolandic & labbe veins that did not involve by the tumor plus absence of hypertrophied collaterals. [10,11] we believed that the primary surgery for parasagittal meningioma is highly significant in its progression and that goes with many literatures like what was mentioned by sindou, pradilla et al, raza et al. and alverni even with reconstruction of sss gave good outcome with low mortality and recurrence rate [15,16,18]. while other authorities like dimeco et al [4], black et al. [1] and sughrue et al. [19]. they postulated that the residual small tumor volume which invade sss will not increase in short period because the most common histopathological grade was benign one and if it happened they prefer to shift to radiotherapy. in the light of this concept: the cornerstone cause of tumor relapse is incapability to remove it in the first surgical procedure as mentioned by minimanoff et al [13]. the recurrence in our study discovered in 4 cases (17.4%) which presented in the international series that varied between (32%4%) [1,19]. table 5 below summarized collected data of parasagittal meningioma surgical management results studies. table v showed collected data of parasagittal meningioma surgical management results studies author/year cases mortality (%) recurrence (%) hoessly and olivecrona /1953 196 12.3 6 simpson20/1957 107 19 logue5/1975 91 4.4 11 bonnal and brotchi /1978 21 4.7 14 giombini et al./1984 243 17.7 dimeco et al./2008 108 1.9 13.9 sindou and alvernia /2000 100 3 4 colli et al./2006 53 1.9 32.7 raza et al./2010 61 1.5 11   romanian neurosurgery (2018) xxxii 3: 426 442 | 441             surgical mortality in our (psm) cases was two cases (8.7%). the scientific paper mentioned that the mortality rate was over 40% in old series that reduced to be less than 2% in newest papers and we referring this excellent result to adoption of microscopic techniques, neurophysiological study application, navigator usage and most important cause was early detection in smaller size but in our society may we see these cases with a very large volumes that invade the arachnoid plane and important bridging veins [6] conclusion through our series we could detect cardinal factors in prognosis of these cases which included: tumor size, histology, preoperative identification of the venous collateral and preservation of it in the surgical maneuver. the meticulous microscopic surgical technique can augment this goal. correspondence ashraf elbadry, m.d., ifaans, osaka university fellow address: department of neurological surgery, faculty of medicine, mansoura university hospital, egypt email address: ashrafbadry@hotmail.com ashrafbadry@mans.edu.eg cell phone: +201111300033 – +201223477444 references 1. black pm, zauberman s. parasagittal and falx meningiomas. meningiomas: a comprehensive text. in: palmir mn, black pm, fallbusch r (eds). china: saunders; 2010. p. 349-354. 2. brotchi j. should we pursue superior sagittal sinus grafting in parasagittal meningiomas in 2013? world neurosurg. 2014;82:325–6. 3. cushing h. meningiomas their classification regional behavior. life history and surgical end results. springfield 1938:404-505. 4. di meco f, li kw, casali c, ciceri e, giombini s, filippini g, et al. meningiomas invading the superior sagittal sinus: surgical experience in 108 cases. neurosurgery. 2004;55:1263–72. 5. di vitantonio h, de paulis d, del maestro m, ricci a, dechordi sr, marzi s, et al. dural repair using autologous fat: our experience and review of the literature. surg neurol int. 2016;7(suppl 16):s463–8. [pmc free article] 6. hancq s, baleriaux d, brotchi j. surgical treatment of parasagital meningiomas. semin neurosurg 2003;14:203210. 7. lee jm, jung s, moon ks, seo jj, kim iy, jung ty, et al. preoperative evaluation of venous systems with 3dimensional contrast-enhanced magnetic resonance venography in brain tumors: comparison with time-offlight magnetic resonance venography and digital subtraction angiography. surg neurol. 2005;64:128–33. 8. n, malikov s, fuentes s, pech-gourg g, graillon t, dufour h. superior sagittal sinus reconstruction using a femoral venous graft after total removal of a meningioma. case report. neurochirurgie. 2013;59:43–6. 9. nussbaum es, defillo a, janjua tm, nussbaum la. microvascular repair of an injured cortical draining vein. surg neurol. 2009;72:530–1. 10. mantovani a, di maio s, ferreira mj, sekhar ln. management of meningiomas invading the major dural venous sinuses: operative technique, results, and potential benefit for higher grade tumors. world neurosurg. 2014;82:455–67. 11. mathiesen t, pettersson-segerlind j, kihlström l, ulfarsson e. meningiomas engaging major venous sinuses. world neurosurg. 2014;81:116–24. 12. maxwell re, chou sn. parasagittal and falx meningioma. operative neurosurgery. in: schmidek hh, sweet wh (eds). 2nd edition. orlando: grune stratton; 1988 p. 563-570. 13. minimanoff ro, dosoretz de, linggood rm, ojemann rg, martuza rl: meningioma: analysis of recurrence and progression following neurosurgical resection. j neurosurg 1985; 62:18-24 442 | elbadry et al parasagittal meningioma surgery             14. pires de aguiar ph, aires r, maldaun mv, tahara a, de souza filho am, zicarelli ca, et al. is sagittal sinus resection in falcine meningiomas a factor of bad surgical outcome? surg neurol int. 2010;1:64. 15. pradilla g, solero cl, dimeco f. parasagittal meningiomas. al-mefty’s meningiomas. in: de monte f, mc dermott mw, al-mefty o (eds). new york: thieme; 2011. p. 142-160. 16. raza sm, gallia gl, brem h, wegart jd, long dm, olivi a. perioperative and long tern outcomes from management of parasagittal meningiomas invading the superior sagittal sinus. neurosurgery 2010;67:885-893. 17. schmid-elsaesser r, steiger hj, yousry t, seelos kc, reulen hj. radical resection of meningiomas and arteriovenous fistulas involving critical dural sinus segments: experience with intraoperative sinus pressure monitoring and elective sinus reconstruction in 10 patients. neurosurgery 1997;41:1005-1016 18. sindou m, auque j, jouanneau e. neurosurgery and the intracranial venous system. acta neurochir suppl. 2005;94:167–75. 19. sughrue me, rutkow ski, gopal sg, et al. results with judicious modern neurosurgical management of parasagittal and falcine meningiomas. j neurosurg 2011;114:731-737. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article traumatic spinal cord injuries – epidemiologic and medico-legal issues bianca hanganu, andreea alexandra velnic, valentin petre-ciudin, irina manoilescu, beatrice gabriela ioan romania doi: 10.1515/romneu-2017-0075 484 | hanganu et al traumatic spinal cord injuries doi: 10.1515/romneu-2017-0075 traumatic spinal cord injuries – epidemiologic and medico-legal issues bianca hanganu, andreea alexandra velnic, valentin petre-ciudin, irina manoilescu, beatrice gabriela ioan “grigore t. popa” university of medicine and pharmacy, institute of legal medicine, iași, romania abstract: spinal cord injuries represent a special category of injuries in traumatic pathology, with high morbidity and mortality, which justify their analysis with the aim to identify useful aspects in order to prevent and treat them. we therefore performed a retrospective study on 426 cases in order to analyze epidemiology and medico-legal issues related to spinal cord injuries. the studied items regarded socio-demographic aspects (gender, age, home region), type of lesions (vertebral, spinal cord, association with other trauma), circumstances leading to trauma (cause of the injury, season), data regarding hospitalization (medical condition at the hospital admission, number of days of hospitalization, clinical diagnosis, imaging exploration level) and data resulting from autopsy (diagnosis, toxicological examination). most of our results are consistent with literature data, except for some epidemiological items, which might be explained with cultural differences, life style and inhomogeneous population. based on our results, the general conclusion is the need for prevention campaigns, focusing on road traffic accidents and falls (especially in elderly) as the main causes of spinal cord injuries. key words: spinal cord trauma, death, epidemiology, legal medicine introduction spinal cord injuries represent a special category in traumatic pathology, both regarding the high morbidity and mortality and dysfunctions leading to low quality of patient’s life [4]. mostly important is the cervical region, the most frequently affected [1], as it is associated with head trauma, difficulties in intubation and its major consequence, quadriplegia [5]. the incidence of spinal cord trauma varies largely among reported studies worldwide, mainly because of inclusion criteria, identification procedures and treatment possibilities, both before and after the admission to the hospital or owing to geographical and cultural factors [4]. thus, romanian neurosurgery (2017) xxxi 4: 484 489 | 485 the lowest reported annual incidence was 2.3 per million in canada and the highest 83 per million in alaska [4]. soopramanien in a study conducted in 1994 reported an annual incidence for romania of at least 28.5 per million inhabitants [11]. aim and objectives the aim of our aim was to identify the epidemiological and medico-legal aspects which may be useful in preventing and treating spinal cord injuries. the main objectives are as follows: highlighting the causative and contributing factors in spinal cord trauma, identifying the most common injuries and the most frequent mechanisms of injury. material and methods we performed a retrospective study using the data collected from the autopsy reports issued by the institute of legal medicine of iasi and the medical records during a 6 year time frame. inclusion criteria of the cases were: the presence of spinal cord injury, alone or associated with injuries in other segments of the body and admission to the hospital prior to death, immediately after trauma. the analyzed items were: sociodemographic factors (gender, age, home region), sustained injuries (spinal, spinal cord, association with other injuries), circumstances leading to trauma (cause of trauma, season), data mentioned in the medical files (medical condition at admission, number of days of hospitalization, clinical diagnosis, imaging exploration) and data acquired during autopsy (diagnosis, toxicological examination). results socio-demographic factors we analyzed 426 cases of spinal cord trauma which fulfilled the inclusion criteria mentioned above. analysis of the gender revealed male predominance337 (79%) as opposed to female89 (21%), with male:female ratio 3.5:1. mean age was 55.3 years, most of the cases over 60 years (38% of the cases), while the least were under 20 years (5.1% of the cases). rural to urban ratio revealed almost twice higher the number of cases in rural area than in urban area, respectively 281:145. circumstances leading to trauma seasonal distribution showed a relatively equal distribution in summer (26.5%), autumn (28.6%) and winter (27.9%), the minimum number of cases recorded during spring (16.9%). circumstances leading to trauma correlated with the gender of the victim revealed the first place in women for road traffic accidents (52% versus 37% in male), while the falls hold the first place in male victims (49% versus 31% in female). after 60 years of age the leading circumstances for spinal trauma are the falls (51.5% of these cases), followed by road traffic accidents (36.8% of these cases), while under 20 years of age, the leading circumstance is road traffic accidents (72.72% of these cases), followed by falls (18.18% of these cases). 486 | hanganu et al traumatic spinal cord injuries for 55% of all the victims toxicological analysis revealed the presence of alcohol in the blood samples collected during the autopsy, 21% showing a blood alcohol concentration above 2g%o, this being the case for 15.38% of the road traffic victims and 7.32% of the fall victims. level and type of injuries the most affected was the cervical level, both in isolation (52%) and associated injuries in other segments of the spine, comprising 70%, in one case being affected the entire spine. the most frequent recorded injuries were dislocations, caused by falls (31%) as well as by road traffic accidents (18.2%), followed by simple fractures, produced during road traffic accidents (14.2%) and fall (10.2%). data regarding hospital admission 27.81% of the road traffic accident victims and 43.97% of the fall victims have died in less than 24 hours after admission, while 5.32% of the road traffic accident cases and 26.7% of the fall cases have died after more than 30 days following admission in the hospital. at admission, 17.37% of the victims were in coma (22.48% of the road traffic accident victims and 18.84% of the fall victims), 20.18% of the victims had an influenced state of consciousness (6.5% of the road traffic accident victims and 39.26% of the fall victims), while the remaining victims of the road traffic accidents and falls were conscious (16 cases, 2 of which sustained spinal trauma during road traffic accidents and 14 after a fall). discussions the main objective of our study was to analyze the epidemiological factors in spinal cord trauma which have led to death, in order to identify the most common mechanisms and circumstances of injuries, the risk factors, causative and contributing factors, as well as the people most exposed to be the victims of this type of injuries, in order to prevent and effectively treat them. during the time frame of our study, 426 cases have been identified, most of the victims being in the group over 60 years of age, which could be explained by the degenerative changes characteristic to elderly people [1], with a mean age of 55.3 years. on the contrary, das et al. (2013) identified in their study conducted in india that the most affected age group, with more than 60%, people between 20-39 years of agethe productive age group of a society, highlighting the alteration of the productivity of that country due to spinal cord trauma [1]. shingu et al. (1994) report the main affected age group in japan55.8% as people between 40-69 years [10], so as kamravan et al. (2014) who report the mean age being 37.2±15.9 years [5]. hagen et al. (2012) identified in their review, after analyzing the cases with traumatic spinal cord injuries until 2011, the lowest mean age in turkey26.8 years, and the highest in oklahoma55.5 years, noting also an increase of the incidence for people over 60 yearsfrom 5% to 13% [4]. along with aging, the prognostic becomes poorer, recovery potential decreases and the risk for complications increases [4], specific anatomy romanian neurosurgery (2017) xxxi 4: 484 489 | 487 features concurring to a higher incidence of these injuries in elderly: calcification of the ligaments, decreased elasticity and increased bone demineralization [1]. males are generally more affected than females, male to female ratio in our study being 3.7:1, alike with the results of kamravan et al. 2014, who identified a 3:1 ratio [5] and with another romanian study which identified a 3.35:1 ratio for the southern part of the country [11]. instead, das et al. (2013) identified a higher ratio, of 8.43:1, in a study regarding cervical spinal cord injury in eastern india, this difference being ascribed to the mainly household activity of the women [1]. an equal frequency was identified in studies conducted in taiwan and iran [4]. regarding the circumstances of injury in spinal trauma, in our study prevail road traffic accidents (52% of the women and 37% of the men) and falls (49% of the men and 31% of the women). by comparison, a study made in the south of romania more than 20 years ago revealed the falls from height as the major cause of spinal trauma, 59%with 19% falls from horse-drawn carts, while 13% involved road traffic accidents [11]. comparing these results with the findings of our study we note a marked increase of the road traffic accidents, most probably as a consequence of the general development of the country and road infrastructure and important increase of the road traffic. another study published in the same period of time, i.e. 1994, in japan, reveals the contrarythe predominance of the road traffic accidents in 44.6% of the cases followed by falls in 29.2% of the cases [10]. a different situation is observed in india, where it is seen a lower risk for women to be victims of road traffic accidents as their main activity involves the house [1]. road traffic accidents represented the main cause of spinal injury in the study performed by kamravan et al. (2014), while fredo et al. (2012) identified 60% of the cases being the victims of falls and 21% the victims of road traffic accidents [3]. hagen et al. (2012) identified the highest percent of road traffic accidents related to spinal cord injuries in the west africa89%, and the lowest in greenland4%, pakistan and nepalboth with 7% [4]. regarding the spinal cord injuries produced after falls, data published by hagen et al. (2012) showed the highest percent in pakistan and nepal82% and the lowest in south africa3% [4]. these differences in reported number of cases might be explained by the geographical factors, disparity in defining the terms and methods for data collection [4], as well as differences in the level of development of the countries where the studies were performed [1]. 281 of the total number of cases in our study came from rural areas and 145 from urban area, with a ratio of almost 2:1. dryden et al. (2003) detected a 2.5 times higher risk for spinal cord injuries in people from villages in relation to people from urban areas [2]. hence the risk for spinal trauma is higher in rural regions, where most of the people perform rough activities or farming [11] as opposed to intellectual activities in cities. analysis of seasonal repartition of cases revealed relatively equal frequencies in our study in summer, autumn and winter, with the fewest cases in spring. these results differ 488 | hanganu et al traumatic spinal cord injuries from those reported by karamehmetoglu et al. (1995), who found the highest frequency during springmainly as a result of falls, followed by summermainly road traffic accidents [7]. sharif-alhoseini and rahimimovaghar (2014) reported the repartition of falls and road traffic accidents as follows: summer, spring, autumn and winter, assigning the road traffic accidents more frequently in spring, while the falls in winter [9] and karacan et al. (2000) reported the highest frequency of road traffic accidents during summer [6]. mondal et al. (2011) identified the predominance of road traffic accidents occurring during may-june [8]. the hypothesis of the present study take into account the fact that during winter and summer the spinal trauma might be attributed at least in part to extreme sports. given the fact that cervical injuries are the most frequent causes of death [1] it is justified the high incidence of the injuries in this segment52% isolated injuries and 70% associated with injuries in other segments. however, studies performed in china show only 5% cervical injuries, as opposed to turkey, with 92% of the injuries, the difference being explained either as a consequence of different causal patterns or geographical and financial factors which may contribute to underreporting of spinal injuries [4]. shingu et al. (1994) reported 74.3% of cases involving the cervical segment [10]. the most frequent recorded injury in our study was dislocation, comprising 31% in falls and 18.2% in road traffic accidents, followed by simple fracture in 14.2% of the road traffic accidents and 10.2% in falls. das et al. (2013) reported the prevailing of fractures in combination with dislocation in 53.7% of cases, while simple fractures were recorded for 34.3% and isolated dislocation in 10.8% of cases [1]. data regarding the frequency and level of injuries may contribute for the improvement of the work environment in spinal surgery, both by training the surgeons and adjustment of surgical instruments and techniques [1] and by training specialists from related fields: occupational therapists, physiotherapists and rehabilitation doctors [11]. alcohol ingestion highly influences the occurrence of traumatic injuries. more than half of the victims were under the influence of alcohol at the moment of the trauma, for 21% blood alcohol concentration being more than 2%o, of which 26 were victims of road traffic accidents and 14 victims of falls. shingu et al (1994) reported the presence of alcohol in 32.2% of bicyclists and 8.9% of car accidents victims [10]. alcohol represented a main risk factor for the association of spinal cord injuries with head trauma, as reported by hagen et al. (2012) [4]. conclusions the rate of spinal cord injuries varies largely in the identified studies, although the predominance of cervical segment was a general rule. given the serious consequences of these injuries, it is therefore necessary to provide suitable medical and rehabilitation services, followed by supporting services and appropriate life style which might lead to minimization of the impact these injuries have on the victims and their families. romanian neurosurgery (2017) xxxi 4: 484 489 | 489 differences detected across studies performed in this field regarding circumstances, age and gender may be explained by differences in culture, life style and inhomogeneous study population. however the results of our study as well as those of other similar studies emphasize the need for prevention campaigns especially regarding road traffic accidents and falls (mostly in elderly) and reducing alcohol ingestion. regarding this last aspect, the high incidence of blood alcohol ingestion suggests the need for a moderate ingestion, alerting the people about the risks they expose especially before driving a car or bicycle, or when they need to perform highly risky activities. correspondence andreea alexandra velnic e-mail: andreea.velnic@yahoo.com irina manoilescu e-mail: manoilescuirina@yahoo.com references 1.das s, datta pp, das m, de s, firdoush ka, sardar t, datta d, jana tk, ghosh mk, dutta s, nandy sn, sarkar p, santra s, de c. epidemiology of cervical spinal cord injury in eastern india: an autopsy-based study. n z med j 126:30-40, 2013 2.dryden dm, saunders ld, rowe bh, may la, yiannakoulias n, svenson lw, schopflocher dp, voaklander dc. the epidemiology of traumatic spinal cord injury in alberta, canada. can j neurol sci 30:113121, 2003 3.fredø hl, rizvi sa, lied b, rønning p, helseth e. the epidemiology oftraumatic cervical spine fractures: aprospective population study fromnorway. scand j trauma resusc emerg med 2012;20:85 4.hagen em, rekand t, gilhus ne, gronning m. traumatic spinal cord injuries – incidence, mechanisms and course. tidsskr nor laegeforen 132:831-837, 2012 5.kamravan hr, haghnegahdar a, paydar s, khalife m, sedighi m, ghaffarpasand f. epidemiological and clinical features of cervical column and cord injuries; a 2-year experience from a large trauma center in southern iran. bull emerg trauma 2:32-37, 2014 6.karacan i, koyuncu h, pekel oe, sumbuloglu g, kirnap m, dursun h, kalkan a, cengiz a, yalinkilic a, unalan h, nas k, orkun s, tekeoglu i. traumatic spinal cord injuries in turkey: a nation-wide epidemiological study. spinal cord 38:697-701, 2000 7.karamehmetoglul ss, unal s, karacan i, yflmaz h, togay hs, ertekin m, dosoglu m, ziyat mi, kasaroglu d, hakan t. traumatic spinal cord injuries in istanbul, turkey. an epidemiological study. paraplegia 33:469471, 1995. 8.mondal p, kumar a, bhangale ud, tyagi d. a silent tsunami on indian road: a comprehensive analysis of epidemiological aspects of road traffic accidents. br j med med res 1:14-23, 2011 9.sharif-alhoseini m, rahimi-movaghar v. hospitalbased incidence in traumatic spinal cord injury in tehran, iran. iran j public health 43:331-341, 2014 10.shingu h, ikata t, kaoth s, akatsu t. spinal cord injuries in japan: a nationwide epidemiological survey in 1990. paraplegia 32:3-8, 1994 11.soopramanien a. epidemiology of spinal injuries in romania. paraplegia. 32:715-722, 1994 microsoft word 4turliucdanamihaela_thelionheart romanian neurosurgery (2018) xxxii 2: 211 216 | 211             doi: 10.2478/romneu-2018-0027 the lion heart of a neurosurgeon: the stress during a life of neurosurgery dana mihaela turliuc1,2, claudia florida costea1,2, ş. turliuc2, r.a. sascău2,3, emilia pătrăşcanu2,4, i. poeată1,2, a.i. cucu1 1"prof. dr. n. oblu" emergency clinical hospital, iași, romania 2"grigore t. popa" university of medicine and pharmacy, iași, romania 3"george i. m. georgescu" institute of cardiovascular diseases, iasi, romania 4regional institute of oncology, iasi, romania “a good surgeon must have an eagle’s eye, a lion’s heart and a lady’s hand”. (old english proverb) abstract: neurosurgery is a rewarding career choice in which there are many challenges and stress factors that can lower the level of satisfaction and also increase the levels of burnout. the identification and management of common work-related stressors is important for improving the performance of health-care specialists and also for providing high-quality patient care. introduction it is well-known that surgeons work in a stressful environment due to the multiple surgical challenges, technical requirements and time pressure they have to face on a daily basis [16,53]. they also experience complex crisis situations while performing surgical procedures, which can inevitably lead to acute stress, with direct effects on patient outcomes [19,51]. despite all these stressful factors, neurosurgery was and will always be a rewarding specialization [33]. exhaustion and burnout syndrome in 2015, the american neurosurgeon mcabee et al. published a recent nationwide study from usa where he reported a significant 57% of american neurosurgeons who met the burnout syndrome criteria [33]. this condition is defined as a clinical syndrome characterized by a high degree of emotional exhaustion and depersonalization and a low sense of personal accomplishment with negative consequences on the surgeon’s state of health and on the patient’s postoperative evolution [11,12,13,21,31,32, 33]. also, the burnout syndrome has been 212 | turliuc et al lion heart of a neurosurgeon             included in the international statistical classification of diseases and related health problems 10th revision (icd-10), and its symptoms are: exhaustion, fatigue, cynicism, poor judgment, feelings of ineffectiveness and disconnection with patients and colleagues [10,11,41], but also lower quality of care for patients [52]. the prevalence of burnout is 40% in surgical specialties [5,6,7], being the greatest during the years of training [17], with residents being the most exposed of all doctors [39], as more than half of them are affected [52]. as concerns the field of neurosurgery, the prevalence of the burnout syndrome was estimated to range between 27 and 56.7%, with the highest rate among all surgical subspecialties [27,33]. this is accounted for by the fact that neurosurgery training is long-lasting, competitive, with the longest training programs of all specialties and the third most competitive specialty (76%) after vascular surgery (71%) and orthopedics (75%) [37]. moreover, neurosurgery residents tend to work more than other residents in other specialties, as evidenced by the accreditation council for graduate medical education in the usa with duty hours up to 88h/wk, which is 10% above the 80h limit for the other specialties [34]. the best demographic predictor of burnout syndrome is the number of hours worked per week, although many factors have been taken into account such as: hours slept per night and nights/weekends worked per month [17], number of nights on call per week (8), younger age [28], or even the specialty practice area [5,6,7]. also, the burnout syndrome is associated with substance abuse, suicidal ideation, medical errors, impairment of interpersonal relationships or even desire by young surgeons to retire early [9,14,42,43,49,50], anxiety and depression [5]. also, patients who have been treated by surgeons suffering from burnout are most often unhappy with the level of healthcare received [9]. as far as the level of satisfaction of doctors is concerned, the most unsatisfied surgeons are those who do not have time for their personal life or family [5,6,7,41] or work in private practice [6], and the most satisfied were reported to be those who have enough time for non-patient care activities [5,6,7,28], the eldest [28], those who spend more time in the operating theater [44], or those who teach at university [6]. in this regard, mcbee demonstrated that neurosurgeons who are also academics have a lower rate of burnout than nonacademic neurosurgeons [33], which shows that neurosurgeons feel more satisfied if they are challenged at their work place. in 2015, mcbee et al. demonstrated that factors that increase the satisfaction in a neurosurgeon’s career are: having children, being surgically productive, being intellectually stimulated, and a balance between their neurosurgeon careers and life outside of work [33]. stress in 1936, hines and brown were among the first to assume that mental stress can lead to hypertension, influencing cardiovascular activity by increasing their heart rate (hr) and blood pressure (bp) [20]. another romanian neurosurgery (2018) xxxii 2: 211 216 | 213             research conducted in 2002 industrial workers proved a 2.2 times higher risk of cardiovascular events and mortality in high job stress employees compared to their low job stress colleagues [24]. when individuals are exposed to workplace risk factors, their reaction to stress may be emotional, behavioral, cognitive and physiological [45]. thus, although low levels of stress may enhance alertness and efficiency of tasks [25], excessive and acute stress levels during surgery may affect attention [26], concentration and motor skills [2,3,15], may interfere with manual dexterity [2,3], cognitive functioning [36] and memory retrieval [29]. el cirujano (the surgeon), jan sanders van hemessen. madrid, museo del prado (between 1550-1555) (public domain) this is of major importance, since for the purpose of performing a safe surgical procedure, it is necessary to integrate complex cognitive processes with manual dexterity [4]. studies have shown that all these pathophysiological changes that occur in prolonged stress may lead to anxiety, depression, alcoholism, substance abuse, broken relationships or even suicide, all of which are more common among surgeons and physicians than in other professions [9]. also, with regard to surgical professions, studies have shown that the constant intraoperative fluctuation of bp and hr may increase the risk for coronary events [23], cerebrovascular disease [22], diabetes (35) and impairment of cognitive functioning and structural brain changes [18,38] or depression [47]. a recent study in orthopedic surgeons has shown that the bp of trainees was much higher when they performed surgery alone than when they performed it under supervision [18]. as concerns the high levels of stress during surgery, studies have shown that they are specific, higher in surgical residents and young specialists, and are attributed to the novelty of the procedures [18], and on the other hand, experienced surgeons are accustomed to the stress of surgery under pressure and intraoperative complications [12,13]. cardiovascular disease cardiovascular diseases are among the most common causes of death among doctors, including surgeons. when stress reaction persists for a long time, neurosurgeons may develop cardiovascular disease, chronic fatigue or musculoskeletal disorders due to the activation of the sympathoadrenal system and the hypothalamic-pituitary-adrenocortical axis leading to hyperlipidemia, atherosclerosis, hypertension and hence coronary heart 214 | turliuc et al lion heart of a neurosurgeon             disease [45]. interestingly enough, the cardiovascular response to intraoperative stress differs from that induced by exercise. in this respect, the increased bp incidence (sbp/dbp> 180/90mmhg) was higher during surgery, whereas the tachycardia rate was higher during exercise [45]. the surgeon’s cardiovascular response to surgical procedures undoubtedly varies during the surgical procedures, being higher in more difficult surgical procedures or in the critical phases of the surgery [18,46]. thus, sharma et al. reported higher incidence of abnormal bp elevation episodes during vestibular schwannoma excision and aneurysm clipping surgeries, compared to the rest of neurosurgical procedures on the brain [45]. bunevicius et al. found that during brain aneurysm surgery, if the procedure is divided into seven surgical phases (1 before skin incision, 2 after craniotomy, 3 after dural opening, 4 after aneurysm neck dissection, 5 after aneurysm clipping, 6 after dural closure, 7 after skin closure), the highest hr and bp (systolic, diastolic and mean bp) occurred during and after the aneurysm neck dissection and clipping phases. these were followed by a gradual decline and return to normal levels. interestingly enough, intraoperative cardiovascular and hemodynamic response was independent of the neurosurgeon’s experience [12,13]. conclusion mental stress and work-related stress management in the operating theater has important implications for both the neurosurgeon's health and the safety of the patient. from this point of view, it is important to find factors that increase personal satisfaction and reduce mental stress. in this respect, an alternative found in recent years has been to listen to one’s favorite music in the operating theater [40], which seems that even improves performance and reduces autonomic reactivity [1]. since there have also been studies showing that music in the operating theater may lead to distraction [30,48], further research is required in this direction. correspondence claudia florida costea "prof. dr. n. oblu" emergency clinical hospital, iași, romania e-mail: costea10@yahoo.com references 1. allen k, blascovich j. effects of music on cardiovascular reactivity among surgeons. jama. 1994; 272:882-884. 2. arora s, sevdalis n, nestel d, et al. the impact of stress on surgical performance: a systematic review of the literature. world j surg. 2010; 147:318-330. 3. arora s, sevdalis n, aggarwal r, et al. stress impairs psychomotor performance in novice laparoscopic surgeons. surg endosc. 2010; 24:2588-2593. 4. arora s, sevdalis n, suliman i, et al. what makes a competent surgeon? experts’ and trainees’ perceptions of the roles of a surgeon. am j surg. 2009; 198:726-732. 5. balch cm, oreskovich mr, dyrbye ln, et al. personal consequences of malpractice lawsuits on american surgeons. j am coll surg. 2011; 213:657-667. 6. balch cm, shanafelt td, sloan ja, satele dv, freischlag ja. distress and career satisfaction among 14 surgical specialties, comparing academic and private practice settings. ann surg. 2011; 254:558-568. romanian neurosurgery (2018) xxxii 2: 211 216 | 215             7. balch cm, shanafelt td, sloan j, satele dv, kuerer hm. burnout and career satisfaction among surgical oncologists compared with other surgical specialties. ann surg oncol. 2011; 18:16-25. 8. balch cm, shanafelt td, dyrbye l, et al. surgeon distress as calibrated by hours worked and nights on call. j am coll surg. 2010; 211:609-619. 9. balch cm, freischlag ja, shanafelt td. stress and burnout among surgeons: understanding and managing the syndrome and avoiding the adverse consequences. arch surg. 2009; 144:371-376. 10. balch cm, copeland e. stress and burnout among surgical oncologists: a call for personal wellness and a supportive workplace environment. ann surg oncol. 2007; 14:3029-3032. 11. bittner jg iv, khan z, babu m, hamed o. stress, burnout, and maladaptive coping: strategies for surgeon well-being. bull am coll surg. 2011; 96:17-22. 12. bunevicius a, bilskiene d, macas a, tamasauskas a. hemodynamic response during aneurysm clipping surgery among experienced neurosurgeons. acta neurochir. 2016; 158(2): 221-227. 13. bunevicius a, tamasauskas a. stress during neurosurgery: no need to worry?acta neurochir. 2016; 158: 623-624. 14. campbell da jr, sonnad ss, eckhauser fe, campbell kk, greenfield lj. burnout among american surgeons. surgery. 2001; 130:696-705. 15. flin r, o’connor p, crichton m. safety at the sharp end: a guide to non-technical skills. ashgate, aldershot. 2008. 16. georgiou k, larentzakis a, papavassiliou ag. surgeons' and surgical trainees' acute stress in real operations or simulation: a systematic review. surgeon. 2017; 15(6):355-365. 17. golub js, weiss ps, ramesh ak, ossoff rh, johns mm 3rd. burnout in residents of otolaryngology-head and neck surgery: a national inquiry into the health of residency training. acad med. 2007; 82(6):596-601. 18. gupta ho, gupta s, carter rl, mohammed a, meek rm. does orthopaedic surgical training induce hypertension? a pilot study. clin orthop relat res. 2012; 470:3253-3260. 19. gurman gm, klein m, weksler n. professional stress in anesthesiology: a review. j clin monit comput. 2012; 26:329-335. 20. hines ea, brown ge. the cold pressor test for measuring the reactivity of the blood pressure: data concerning 571 normal and hypertensive subjects. am heart j. 1936; 11:1-9. 21. honkonen t, ahola k, pertovaara m, et al. the association between burnout and physical illness in the general population-results from the finnish health 2000 study. j psychosom res. 2006; 61:59-66. 22. huang y, xu s, hua j, et al. association between job strain and risk of incident stroke: a metaanalysis. neurology. 2015; 85(19):1648-1654. 23 kivimäki m, batty gd, ferrie je, kawachi i. cumulative meta-analysis of job strain and chd. epidemiology. 2014; 25(3):464-465. 24. kivimäki m, leino-arjas p, luukkonen r, et al. work stress and risk of cardiovascular mortality: prospective cohort study of industrial employees. bmj. 2002; 325:857. 25. klein g. sources of power. how people make decisions. mit press, cambridge, ma. 1998. 26. klein g. the effects of acute stress on decision making. in: driskell je, salas e (eds) stress and human performance. lawrence erlbaum associates, mahwah. 1996. 27. klimo p, decuypere m, ragel bt, et al. career satisfaction and burnout among u.s. neurosurgeons: a feasibility and pilot study. world neurosurg. 2013; 80(5):e59-68. 28. kuerer hm, eberlein tj, pollock re, et al. career satisfaction, practice patterns and burnout among surgical oncologists: report on the quality of life of members of the society of surgical oncology. ann surg oncol. 2007; 14:3043-3053. 29. kuhlmann s, piel m, wolf ot. impaired memory retrieval after psychosocial stress in healthy young men. j neurosci. 2005; 25:2977-2982. 30. lee jy, lantz ag, mcdougall em, et al. evaluation of potential distractors in the urology operating room. j endourol. 2013; 27:1161-1165. 31. maslach c, schaufeli wb, leiter mp. job burnout. annu rev psychol. 2001; 52:397-422. 32. maslach cjs, leiter m. maslach burnout inventory manual, consulting psychologists press, palo alto. 1996. 33. mcabee jh, ragel bt, mccartney s, et al. factors associated with career satisfaction and burnout among us neurosurgeons: results of a nationwide survey. j neurosurg. 2015; 123:161-173. 216 | turliuc et al lion heart of a neurosurgeon             34. muscatello mr, bruno a, carroccio c, et al. association between burnout and anger in oncology versus ophthalmology health care professionals. psychol rep. 2006; 99(2):641-650. 35. nyberg st, fransson ei, heikkila k, et al. job strain as a risk factor for type 2 diabetes: a pooled analysis of 124,808 men and women. diabetes care. 2014; 37:22682275. 36. raio cm, brignoni-perez e, goldman r, phelps ea. acute stress impairs the retrieval of extinction memory in humans. neurobiol learn mem. 2014; 112:212-221. 37. rakovec-felser z. professional burnout as the state and process–what to do? collegium antropologicum. 2011; 35(2):577-585. 38. rothwell pm, howard sc, dolan e, et al. prognostic significance of visit-to visit variability, maximum systolic blood pressure, and episodic hypertension. lancet. 2010; 375:895-905. 39. shakir hj, mcpheeters mj, shallwani h, pittari je, reynolds rm. the prevalence of burnout among us neurosurgery residents.neurosurgery. 2017; oct 27. 40. shambo l, umadhay t, pedoto a. music in the operating room: is it a safety hazard? aana j. 2015; 83:43-48. 41. shanafelt t, dyrbye l. oncologist burnout: causes, consequences, and responses. j clin oncol. 2012; 30:1235-1241. 42. shanafelt t, sloan j, satele d, balch c. why do surgeons consider leaving practice? j am coll surg. 2011; 212:421-422. 43. shanafelt td, balch cm, bechamps g, et al. burnout and medical errors among american surgeons. ann surg. 2010; 251:995-1000. 44. shanafelt td, balch cm, bechamps gj, et al. burnout and career satisfaction among american surgeons. ann surg. 2009; 250:463-471. 45. sharma ms, thapa a, chandra sp, et al. intraoperative pulse and blood pressure recordings of neurosurgeons: a pilot study of cardiovascular performance. neurosurgery. 2010; 66:893-899. 46. song mh, tokuda y, nakayama t, sato m, hattori k. intraoperative heart rate variability of a cardiac surgeon himself in coronary artery bypass grafting surgery. interact cardiovasc thorac surg. 2009; 8:639641. 47. stansfeld sa, shipley mj, head j, fuhrer r. repeated job strain and the risk of depression: longitudinal analyses from the whitehall ii study. am j public health. 2012; 102:2360-2366. 48. way tj, long a,weihing j, et al. effect of noise on auditory processing in the operating room. j am coll surg. 2013; 216:933-938. 49. west cp, huschka mm, novotny pj, et al. association of perceived medical errors with resident distress and empathy: a prospective longitudinal study. jama. 2006; 296:1071-1078. 50. williams es, manwell lb, konrad tr, linzer m. the relationship of organizational culture, stress, satisfaction, and burnout with physician-reported error and suboptimal patient care: results from the memo study. health care manage rev. 2007; 32:203-212. 51. wong sw, smith r, crowe p. optimizing the operating theatre environment. anz j surg. 2010; 80:917-924. 52. thomas nk. resident burnout. jama. 2004; 292:2880-2889. 53. turliuc d, turliuc s, cucu a, buraga v, costea cf. claiming dignity while dangling between life and death. romanian journal of artistic creativity. 2015; 1:34-38. microsoft word 15kaifmohammad_longterm 306 | kaif et al long term results of endoscopic lumbar discectomy             doi: 10.2478/romneu-2018-0038 long term results of endoscopic lumbar discectomy using side viewing conical working tube mohammad kaif1, kuldeep yadav, mazhar husain2 1m.ch. (neurosurgery) assistant professor of neurosurgery, “dr ram manohar lohia” institute of medical sciences, lucknow, (up), india 2m.ch. (neurosurgery) chief of neurosurgery, sahara hospital, lucknow, (up), india abstract: object: endoscopic discectomy is a common procure performed worldwide with various devices being used and studies have reported their long term results. in this study we present the long term results of the unique device with separate side viewing channel. methods: 66 patients of lumbar disc herniation treated between march 2009 to april 2012 using the unique conical working tube with separate side viewing endoscopic channel. their preoperative and postoperative oswestry disability index (odi) and macnab scores were used to evaluate the outcome after a minimum follow of 5 years with mean follow up of 76.18 months. results: there were 46 males and 20 females with age ranging from19-72 (mean-38.4 years). the follow up ranged from 61 months to 95 months with mean of 76.18 months. the mean preoperative odi score was 74.7 which decreased to a mean of 7.8 and the outcome evaluated by macnab criteria was 69.69% excellent, 17 % good, 10% fair, 3.03% poor. 2 patients underwent second surgery. none of the patient had to change their occupation due to their lumbar disc disease. complications occurred were dural tear in 2 patients, transient foot paresis in 1 patient and 1 discitis in 1 patient which improved on medical management. conclusion: endoscopic discectomy using thins conical working tube is a safe and effective technique for lumbar disc prolapse. it has the advantage for early mobilization, short hospital stay and low cost. the long term results are comparable to the conventional techniques. key words: endoscopy, discectomy, herniated disc, prolapsed intervertebral disc, lumbar spine introduction surgery for prolapsed lumbar intervertebral disc is one of the most common surgery performed by spinal surgeons. open micro discectomy or endoscopic inter-laminar or transformational lumbar discectomy are preferred modality of romanian neurosurgery (2018) xxxii 2: 306 313 | 307             treatment by most spinal surgeons with proven safety and outcome and each having is advantages and disadvantages. xue-song wang in their meta-analysis concluded that the inter-laminar endoscopic surgery has the advantage of decreased hospital stay and blood loss in comparison to microdiscectomy and with similar results for long term pain control, functional recovery or incidence of complication [32]. various authors have reported their experience ofendoscopic discectomy using different devices with excellent to good long term follow up. in this report with summarize the long term results of endoscopic discectomy using the conical working tube with separate viewing channel. clinical material and methods this is a retrospective study based on long term follow up of 66 patients of lumbar disc herniation treated using the unique conical working tube with side viewing endoscopic channel [14]. the hospital records of 212 patients who underwent endoscopic lumbar discectomy using this device between march 2009 to april 2012 were retrieved. only those patients were included in this study who could be contacted on telephone and responded to the odi and macnab fomat. the indication for surgery was low backache with radicular pain in lower limb with or without neurological deficit and failed conservative management. the patients who had segmental instability, no clinicradiological correlation or evidence of infection were excluded from this study. there were 46 males and 20 females with age ranging from19-72 (mean-38.4 years). the follow up ranged from 61 months to 95 months with mean of 76.18 months.  instrument design: this device consists of a conical working tube which is passed over coaxial dilators and secured in position by a holding device attached to the operating table. it has a separate side viewing channel for the telescope which is attached to light source and camera. no special instruments are used for laminotomy and discectomy. figure 1. figure 1 instruments design. 1a. photograph of the device with its measurements; 1b. device placed in a spine model; 1c. diagrammatic representation of the device with disc forceps in inside the device showing the ease of using regular instruments through the device without clutter  operative technique: after general anesthesia the patient is positioned in prone position on a wilson’s frame or foam bolsters. the level is localised using fluoroscopy and 18-20mm skin incision is given in midline. the fascial incision is made 1 cm lateral to midline. the first dilator is passed with a 5mm trocar upto the lamina and the trocar is removed. a gentle medial to lateral and cranial and caudal sweeping movement is done for 308 | kaif et al long term results of endoscopic lumbar discectomy             elevation of soft tissue. two subsequent dilators are passed over this first tube. finally the working tube is passed over these dilators and fixed to table. the position of the working tune is confirmed using fluoroscopy. a cannula with trocar is passed from the separate side channel through a separate stab incision and locked in the working tube using the locking mechanism. the telescope “0” degree, 4 mm diameter and 180 mm length is passed through this separate channel. the tip of the telescope just reaches upto the inner part of the working tube. the light source and camera is attached to the cannula and the image orientation is done by rotating the camera on scope. figure 2. figure 2 steps of the procedure 2a. 1st dilator with sharp trocar being passed; 2b. 2nd dilator being passed over the 1st dilator; 2c. final working tube being passed; 2d. cannula for telescope being passed through separate channel in the working tube; 2e. telescope being passed; 2f. complete the device assembly in situ and fixed to the operating table the medial part of the facet and contiguous lamina are identified. a small hemiliaminotomy medial facetectomy is made using kerrison rounger. the ligamentum flavum is detached from the undersurface of the lamina above using an angle micro-curette. ligamentum flavum is then removed and the traversing nerve root and thecal sac are identified using ball probe. the nerve root is retracted medially and the disc is removed by entering the disc space through the annular tear or an annulotomy with no 11 surgical blade. the disc space is irrigated with normal saline to wash out loose disc fragments. the nerve root is inspected to ensure adequate decompression. figure 3, figure 4. the entire assembly is removed and the fascia is closed with absorbable suture. skin is closed using subcuticular sutures. figure 3 magnified view through the device 3a. extruded disc; 3b. dissector; 3c. nerve root; 3d. thecal sac; 3e. telescope romanian neurosurgery (2018) xxxii 2: 306 313 | 309             figure 4 endoscopic view 4a. nerve root retractor; 4b. intervertebral disc; 4c. nerve root; 4d. ball dissector; 4e disc forceps holding the disc; 4f. thecal sac; 4g. facet joint postoperative managementpatients were mobilized in the evening of day of surgery after and discharged on the next day. in this study the mean hospital stay was 1.6 days. complications the most common complication was found to incidental dural tear, observed in 2 patients. this was managed by sealing the defect by fibrin glue. no postoperative csf leak or pseudomeningocele or any long term sequelae was observed. the other postoperative complications were transient foot paresis in 1 patient and 1 discitis in 1 patient which improved on antibiotic therapy. results the patients were evaluated using odi score and the total score was calculated. the score was interpreted into 0% to 20% (minimal disability), 21% to 40% (moderate disability), 41%to 60% (severe disability), 61% to 80% (crippled) and 81% to 100% (bed bound/ exaggerating their symptoms). both the preoperative and postoperative odi were compared and its difference was calculated. the outcome at the last visit was evaluated by mcnab criteria in to excellent, good, fair and poor. the follow up ranged from 61 months to 95 months with mean being 76.18 months. the mean preoperative odi score was 74.7 which decreased to a mean of 7.8. the outcome evaluated by macnab criteria was 69.69% (n=46) excellent, 17 % (n=11) good, 10% (n=7) fair, 3.03% (n=2) poor. one patient experienced persistent radicular pain of same intensity was diagnosed to have a residual disc fragment which was removed by microsurgery and the other patient developed recurrence of symptoms 2 years after 1st surgery. he was diagnosed with bony canal stenosis at the same level with instability and underwent intervertebral fusion. none of the patient had to change their occupation due to their lumbar disc disease. discussion the technique of classical discectomy as described by mixter and barr has undergone significant change to minimize the trauma of long incision, extensive muscle dissection and laminectomy leading to prolonged post operative hospital stay, morbidity due pain, scarring around nerve root and instability [27], (table 1). to over these disadvantages microsurgical technique was adopted which has made a siginifinat improvement in the outcome (table 2). 310 | kaif et al long term results of endoscopic lumbar discectomy             table 1 studies of open laminectomy/laminotomy with discectomy author & year no. of patients results excellent/goodfollowup in years atlas et al. 2005 217 69 10 bakhsh et al. 2010 39 79 10 butterman et al. 2004 100 92 2.5 hsu et al. 2011 226 82 2 jansson 2004 22261 78 6 mariconda et al. 2006 201 90 27.8 martinez quinones et al. 2011 142 93 5 table 2 studies of microdiscetomy author & year no. of patients criteria results excellent/good mean followup in years recurrence findlay et al. 1998 79 macnab 83% 10 jensdottir et al. 2007 134 91% 20.7 12.7% moore et al. 1994 100 93% 8.6 10.5% schoeggl et al. 2003 672 prolo 77% 6.3 vik et al. 2001 62 81% 8.5 to further minimise the disadvantages of open surgery foley and smith described microendoscopic discectomy (med) in 1997 for root decompression in cases of lumbar disc disease [12]. varoius authors have described their results of med which is mentioned in table 3. table 3 studies of endoscopic discectomy author & year no. of patients tech outcome measures outcome recurrence complication li et al. 2015 72 il vas,odi, mcnab 97% good to excellent 1 no complications xu et al. 2014 36 il vas excellent 2 patients converted to open none hussein et al. 2014 185 il nrs, mcnab odi statistically significant pain releirf 2 converted to open 3 dural tears kulkarni et al. 2014 188 il vas,odi statistically significant pain releirf 3(1.5%) 11 (5%)dural tears,1(0.5%)infection, 1(0.5%) wrong level kim et al. 2013 224 il vas odi statistically significant pain releirf 5% none yadav et al. 2013 400 il vas, mcnab 90% significant improvement 2(0.5%) 3 facet injuries, 7 dural tears,2 infections,1 persistent paresthesia kim et al. 2012 18 il mcnab 98% complete removal 2 residual 1 duraltera kaushal et al. 2012 300 il mcnab 90% excellent to good 2 nerve root injury kim et al. 2012 30 il significant improvement none chumnanvej et al. 2011 60 il mcnab 91.6% excellent outcome 2 none romanian neurosurgery (2018) xxxii 2: 306 313 | 311             chen et al. 2011 123 il vas, odi significant improvement 3 1 dural tear dezawa et al. 2011 30 il statistically significant improvement 1 persistent radiculopathy wang et al. 2011 30 il vas significant improvement 20% converted to open 4.1% duralteras, 4 nerve root injury, 1 dvt, 1 discitis jhala mistry et al. 2010 kaif et al 2017 100 66 il il mcnab mcnab,odi 91% excellent to good 86.36% excellent to good 4 second surgery in 2 4 discitis, 1 nerve root damage discitis 1, dural tear 2, transiet foot paresis 1 jensdottir et al in their retrospective study reported a good/excellent outcome of micro discectomy after up a mean followup of 20.7 years [17]. casal moro et al in their prospective study reported that med is a safe and reproduce able technique with lesser tissue trauma with comparable results to that of conventional techniques [6]. bhansare et al reported their 10 year experience using the destandau technique with excellent short and long term results [4]. the other technique of minimally invasive lumbar discectomy commonly practiced via the transforaminal route through the kambin’s triangle has been reported with improvement in the japanese orthopedic association score of 76% [34]. the disadvantage of this technique is that the contralateral component of the disc bulge and the diffuse bony canal stenosis are difficult to address. the long term results with this device were excellent to good in 86.36% of cases after a mean followup of 76.18 months which is comparable with the long term studies of all the minimally invasive lumbar discectomy techniques practiced worldwide. none of the patients had to change their profession in this follow up period. casalmoro reported surgical complication rate of 3 to 10 % in various techniques whereas destandau in his series reported 3.5% and 4 of his patients required reoperation [11]. in our series we experienced 6.15 % (n=4) of such complications and 3.03% (n=2) required reoperation. the popular device which is commonly used is the metrx system for the med which a serial dilator system utilizing theinterlaminar corridor. it has a telescope mounted at the top end edge of the working channel but as experienced by the senior surgeon this technique causes clutter while working bimanually through the working tube. the other disadvantage is the high cost of the specialized hardware. the destandau system is the other popular device used worldwide with excellent to good long term result but it has the disadvantage that direct visualization using naked eye or microscope is not possible and also minimally invasive inter-body fusion cannot be performed through this device. the cost of these devices are very high which is a major deterrent in expansion of this technique and as this is an indigenous innovation it has very low cost. the hardware cost if further reduced as it utilizes the conventional discectomy instruments and same telescope which is used in transcranial endoscopic surgeries.   312 | kaif et al long term results of endoscopic lumbar discectomy             conclusions endoscopic discectomy using this conical working tube is a safe and effective technique for lumbar disc prolapse. it has the advantage for early mobilization, short hospital stay and low cost. the long term results are comparable to the conventional techniques. corresponding author dr kuldeep yadav, m.ch. (neurosurgery), assistant professor of neurosurgery, dr ram manohar lohia institute of medical sciences, lucknow,(up), india kuldeepyadavrml@gmail.com references 1. atlas sj, keller rb, wu ya, et al: long-term outcomes of surgical and nonsurgical management of sciatica secondary to a lumbar disc herniation: 10 year results from the maine lumbar spine study. spine phila pa. 1976;2005:30:927–935. 2. bakhsh a: long-term outcome of lumbar disc surgery: an experience from pakistan. j neurosurg spine 2010; 12: 666–670. 3. bhaisare r, kamble b, patond k. long-term results of endoscopic lumbar discectomy by "destandau's technique". asian spine j. 2016;10(2):289-97. 4. bhaisare r, kamble b, patond k: asian spine j. 2016 apr; 10(2): 289–297. long-term results of endoscopic lumbar discectomy by "destandau's technique" 5. buttermann gr: treatment of lumbar disc herniation: epidural steroid injection compared with discectomy. a prospective randomized study. j bone joint surg 2004;86: 670–679. 6. casal-moro r, castro-menéndez m, hernándezblanco m, bravo-ricoy ja, jorge-barreiro fj. long-term outcome after microendoscopic diskectomy for lumbar disk herniation: a prospective clinical study with a 5-year follow-up. neurosurgery. 2011;68(6):1568-75;discussion 1575. 7. chen h. t., tsai c.h., chao s. c. et al., “endoscopic discectomy of l5-s1 disc herniation via an interlaminar approach: prospective controlled study under local and general anesthesia,” surgical neurology international. 2011; 2(93). 8. chumnanvej s., kesornsak w., sarnvivad p. and kuansongthum v., “full endoscopic lumbar discectomy via interlaminar approach: 2-year results in ramathibodi hospital,” journal of the medical association of thailand. 2011; 94(12):1465– 1470. 9. destandau j. technical features of endoscopic surgery for lumbar disc herniation: 191 patients. neurochirurgie. 2004;50(1):6-10. 10. dezawa a. and sairyo k., “new minimally invasive discectomy technique through the interlaminar space using a percutaneous endoscope,” asian journal of endoscopic surgery. 2011;4(2):94–98. 11. findlay gf, hall bi, musa bs, et al: a 10-year followup of the outcome of lumbar microdiscectomy. spine (phila pa 1976). 1998; 23:1168–1171. 12. foley kt, smith mm. microscopic discectomy. tech neurosurg 1997;3:301-307 13. hsu wk, mccarthy kj, savage jw, et al: the professional athlete spine initiative: outcomes after lumbar disc herniation in 342 elite professional athletes. spine j. 2011; 11: 180–186 14. husain m, jha dk, agrawal s, husain n, gupta rk. conical working tube: a special device for endoscopic surgery of herniated lumbar discs. neurosurg j spine. 2005;2(3):265-70. 15. hussein m., abdeldayem a. and mattar m. m. m., “surgical technique and effectiveness of microendoscopic discectomy for large uncontained lumbar disc herniations: a prospective, randomized, controlled study with 8 years of follow-up,” european spine journal, 1992–1999, 2014: 23(9). 16. jansson ka, nemeth g, granath f, et al: surgery for herniation of a lumbar disc in sweden between 1987 and 1999. an analysis of 25,576 operations. j bone joint surg br. 2004; 86b:841–847. 17. jensdottir m, gundmundsson k, hannesson b et al:20 year follow up after the first microsurgical lumbar discectomies in iceland. acta neurochir(wein) 2007;149:51-58. 18. jhala a. and mistry m., “endoscopic lumbar discectomy: experience of first 100 cases,” indian journal of orthopaedics. 2010;44(2):184–190. 19. kaushal m. and sen r., “posterior endoscopic discectomy: results in 300 patients,” indian journal of orthopaedics. 2012;46(1):81–85. romanian neurosurgery (2018) xxxii 2: 306 313 | 313             20. kim c. h., chung c. k. and woo j. w., “surgical outcome of percutaneous endoscopic interlaminar lumbar discectomy for highly migrated disc herniation,” journal of spinal disorders and techniques, 2012. 21. kim c. h., chung c. k., woo j. w., “surgical outcome of percutaneous endoscopic interlaminar lumbar discectomy for highly migrated disc herniation,” journal of spinal disorders and techniques, 2012. 22. kim h. s. and park j. y., “comparative assessment of different percutaneous endoscopic interlaminar lumbar discectomy (peid) techniques,” pain physician. 2013;16(4):359–367. 23. kulkarni a. g., bassi a., and dhruv a., “microendoscopic lumbar discectomy: technique and results of 188 cases,” indian journal of orthopaedics, 2014: 48(1) 81–87. 24. li z.-z., hou s.-x., shang w.-l., song k.-r. and zhao h.-l., “the strategy and early clinical outcome of full-endoscopicl5/s1 discectomy through interlaminar approach,” clinical neurology and neurosurgery, 2015;(133) 40–45. 25. mariconda m, galasso o, secondulfo v, et al: minimum 25-year outcome and functional assessment of lumbar discectomy. spine (phila pa. 1976, 2006; 31: 2593–2599. 26. martinez quinones jv, aso j, consolini f, et al: long-term outcomes of lumbar microdiscectomy in a working class sample (in spanish). neurocirugia 2011; 22: 235–244. 27. mixter wj, barr js: rupture of intervertebral disc with involvement of spinal the canal. n eng j med. 1934;211:210-215. 28. moore aj, chilton jd, uttley d: long-term results of microlumbar discectomy. br j neurosurg. 1994;8:319– 326. 29. schoeggl a, reddy m, matula c: functional and economic outcome following microdiscectomy for lumbar disc herniation in 672 patients. j spinal disord tech. 2003;16:150–155. 30. vik a, zwartz ja, hulleberg g, et al: eight year outcome after surgery for lumbar disc herniation: a comparison of reoperated and not reoperated patients. acta neurochir (wien). 2001;143:607–611. 31. wang b., l¨u g., patel a. a., ren p. and cheng i., “an evaluation of the learning curve for a complex surgical technique: the full endoscopic interlaminar approach for lumbar disc herniations,” spine journal. 2011;11(2): 122–130. 32. xue-song w: a meta-analysis of interlaminar minimally invasive discectomy compared to conventional microdiscectomy for lumbar disk herniation: clinical neurology and neurosurgery. 2014; 127:149-147. 33. yadav y. r., parihar v., namdev h., agarwal m., and p. r. bhatele, “endoscopic interlaminar management of lumbar disc disease,” journal of neurological surgery part a: central european neurosurgery. 2013; 74(2); 77–81. 34. yoshimoto m, iwase t, takebayashi t, ida k, yamashita t. microendoscopic discectomy for far lateral lumbar disk herniation: less surgical invasiveness and minimum 2-year follow-up results. j spinal disord tech. 2014 ;27(1):e1-7. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 399 404 | 399 solitary plasmocytoma of the skull: case report and review of the literature luis rafael moscote-salazar1, hernando raphael alvis-miranda2, willem guillermo calderon-miranda3, zenen antonio carmona meza4, nidia escobar hernandez5, marco antonio blancas-rivera6, amit agrawal7 1neurosurgeon, universidad de cartagena, cartegena de indias, colombia; 2resident of neurosurgery, universidad de cartagena, cartagena de indias, colombia; 3resident of radiology, universidad nacional autonoma de mexico, hospital general doctor manuel gea gonzalez, mexico; 4chief research, universidad de cartagena, cartagena de indias, colombia; 5chief of radiology, hospital general doctor manuel gea gonzalez, mexico; 6physician, universidad nacional autonoma de mexico, mexico; 7professor of neurosurgery, mm institute of medical sciences & research, maharishi markandeshwar university, mullanaambala, haryana, india abstract: solitary plasmacytoma and extramedullary plasmocytoma are tumors of malignant character composed of plasma cells, with a mean age of onset at 60 years. they can appear anywhere where the reticuloendothelial system is present. usually these tumors lead to the development of multiple myeloma in a period of time ranging from 3 to 5 years. we present a rare case handled in our neurosurgery service associated with an unusually long period of evolution. key words: solitary plasmacytoma, plasmocytoma, forehead mass introduction multiple myeloma (mm) is defined as neoplastic proliferation of plasma cells that make monoclonal protein in most cases. the paraprotein can be found in serum or urine. these lesions extend to extramedullar areas where bone destruction occurs. one of the entities that may arise in the context of mm is plasmacytoma, correlating with a more aggressive course of the disease. diagnosis is based on clinical symptoms, imaging findings, serum immunoglobulin electrophoresis, and lab studies demonstrating end organ damage (hypercalcemia, anemia, and renal insufficiency). diagnosis is confirmed by histopathologic analysis following tissue biopsy or bone marrow aspirate. we present the case of a patient with a giant frontal lesion, which was consistent with a plasmacytoma associated with long period of evolution. case report male patient, 47-yo, from rural area, with history of been working in palm oil production, 400 | moscote-salazar et al solitary plasmocytoma of the skull fishing and construction for several years. is admitted to our institution referred from a first level care center, because of the presence of a large frontal lesion associated with head trauma 30 years ago, which was gradually increasing in size. the patient referred dyspnea on moderate exercise and fatigue. on examination, the patient was in regular conditional, afebrile, hydrated, hemodynamically compensated, normal vital signs, a lesion protrude in the medial frontal region, 15 x 15 cms (figures 1a and b) soft at touch; no lymphadenopathy, cardiopulmonary, abdomen and extremities were normal. it was decided to perform skull radiography, head ct-scan (figures 2, 3a, 3b). images were evaluated, and we decided to perform frontal craniotomy with tumor resection. patient developed mediate and immediate satisfactory postoperative course. during icu stance the patient status declines, developing hyperazoemia. the pathology report was consistent with a lesion composed of plasma cells. the nephrology service establishes the diagnosis of renal failure; the patient progressed without improvement and died from respiratory complications. figure 1 head deformation; a. lateral view and b. frontal view of the patient head, showing a large, oval frontal lesion figure 2 lateral plain cranial radiography showing multiple bone lesions in the frontal area of the skull romanian neurosurgery (2016) xxx 3: 399 404 | 401 figure 3 head ct-scan, a. axial slides showing a large, circular lesion located on the frontal pole, compromising frontal hemispheres bilaterally, but also the frontal bone, protruding through it, and bulking the scalp. b. bone window, showing the large bone defect caused by the tumor discussion plasmocytoma is a rare entity that arises from malignant proliferation of b-cell line (non-hodking lymphoma). malignant plasma cell tumors include: extramedullary plasmocytoma (ep); solitary plasmocytoma of the bone (spb); multifocal form of multiple myeloma; mm; and plasmablastic sarcoma. unlike mm, spb is a localized disease of plasma cells in bone formation without systemic complications. intracranial plasmocytoma account for only 4% of all primary plasma cell tumors, with a conversion rate to mm occurring in approximately 50% of reported cases, (1) and in those patients with diagnosis of mm, intracranial ep as metastatic spread of mm occurs in 1% of reported cases. (2) spb comprises 4% of all plasma cell malignancies, they are characterized by bone erosion, and ep arises in submucosal layer of tissues without bone involvement. plasma cell neoplasms can histologically mimic a large variety of tumors (e.g., carcinomas, lymphomas, leukemia, plasma cell granulomas, sarcomas and histiocytic lesions). in fact, they are cytologically and immunophenotypically identical. the distinction between the various plasma cell neoplasms is based on clinical and radiological features. (3) immunocytochemical study with antibodies to κ and λ light chains is a useful evaluation tool for a suspected plasmacytoma to distinguish it from a reactive proliferation. (3) the diagnosis of spb or ep is made by the presence of a single plasmacytoma in the bone or the soft tissue and the absence of clinical, histologic, and radiological evidence of multiple myeloma; (4) they have a mean age of presentation of about 10 years younger than those who develop mm. (4) most patients with plasma cell neoplasms present initially with vague symptoms, such as bone pain, anemia, or fatigue. the first rational approach for differential diagnosis of the spb or ep is the exclusion of other plasma cell dyscrasias and, particularly dissemination of the disease into mm. this evaluation 402 | moscote-salazar et al solitary plasmocytoma of the skull requires complete blood count with white cell differential, erythrocyte sedimentation rate, serum calcium, phosphorous, blood urea nitrogen, creatinine, serum and urine protein electrophoresis, bone marrow biopsy, chest radiograph, and a radiographic skeletal survey. (5) skeletal survey may detect lytic lesions, compression fractures (pathological), and osteopenia in areas with hemopoietically active bone marrow (vertebrae, ribs, femur, humerus, pelvis, sternum, and skull). (4–6) bone marrow biopsy is required to detect malignant, plasmacytosis >10% is suggestive of mm.6 regard the serum protein electrophoresis, it shows a sharp spike called the m component (m for monoclonal). when present, elevation of creatinine and uric acid is indicative of impaired renal function due to blockage of renal tubules by paraproteins and increased tumor load. the systemic search must persist for at least a year after the discovery of an intracranial plasmacytoma, especially if the mass is located in the skull base. (7) treatment some difficulties limit the correct approach of treatment for these patients, especially for the small number of patients and the lack of controlled trials with statistically significant results, making that treatment of choice stills doubtful. radiotherapy is the most accepted therapeutic strategy; other treatment choices are surgery, the combination of radiotherapy and surgery, and chemotherapy. (5) spb and ep are optimally treated with complete surgical resection plus external radiation therapy. (7) local control of solitary ep in the head and neck seems to be improved when the dose to the clinical target volume is <45 gy, a minimum dose of 45 gy should be recommended. (8) chemotherapy forms the mainstay of treatment of mm. the employment of chemotherapy (cyclophosphamide, vincristine, adriamycin, and dexamethasone) in combination with autologous peripheral blood stem cell transplant and interferons provides good quality of life, almost for 5 to 7 years. (9) for refractory or relapse cases while undergoing the above regimens, thalidomide and dexamethasone or high-dose dexamethasone is used. surgical treatment is limited to adjuvant therapy and bone complications. currently there are supported minimally invasive procedures for prophylactic fixation of fractures, spinal cord decompression when indicated, and treatment of pathological fractures. (10) gong et al., (11) reported the similar case of spb in skull. ct scan revealed an 8 cm × 9 cm osteolytic lesion on the scalp of skull with a well demarcated margin. a cakelike mass was revealed at ct soft tissue window. the mass was completely excised. the level of response to treatment, and in particular, the complete response, is associated with better long-term results. these patients should be followed every three months to assess the appearance of new signs or symptoms of disease; and note that survival solitary plasmacytoma is longer than multiple myeloma patients in the absence of diffuse abnormalities in the bone marrow, kidney lesions and calcium metabolism. romanian neurosurgery (2016) xxx 3: 399 404 | 403 the main prognostic indicator for spb and ep is the progression to mm, being the cranial base location the strongest predictor for that progression. (7) tumoral recurrence varies between 10% and 22%. (12) factors associated with high risk for local recurrence are the initial size of tumor (diameter >5 cm), age of patient (>60 years), the incompleteness of treatment, and an initial increase of serum proteins. (5) conclusions plasmatic cell tumors are a rare disease, representing less than 1% of tumors of the head and neck. usually they come from the brain parenchyma, or from dural or bone infiltration. sometimes this type of injury is associated with mm. this last fact is the rationale for differential diagnosis of the spb or ep is the exclusion of other plasma cell dyscrasias. unlike mm, spb and ep are localized disease of plasma cells without commitment systemic complications such as renal failure, hematological disorders, neurological and immunological. pain and bone destruction with pathological fractures represent the most common clinical signs of this disease; therefore sometimes lab results are similar to mm as calcium disorders, renal dysfunction and increased beta-2 microglobulin; plasmacytoma therefore has a better prognosis than mm. correspondence luis rafael moscote-salazar, m.d. neurological surgery, university of cartagena e-mail: mineurocirujano@aol.com cartagena de indias, colombia references 1. cerase a, tarantino a, gozzetti a, muccio cf, gennari p, monti l, et al. intracranial involvement in plasmacytomas and multiple myeloma: a pictorial essay. neuroradiology [internet]. 2008 aug [cited 2014 sep 23];50(8):665–74. available from: http://www.ncbi.nlm.nih.gov/pubmed/18516599 2. fassas ab-t, muwalla f, berryman t, benramdane r, joseph l, anaissie e, et al. myeloma of the central nervous system: association with high-risk chromosomal abnormalities, plasmablastic morphology and extramedullary manifestations. br j haematol [internet]. 2002 apr [cited 2014 sep 23];117(1):103–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/11918539 3. singh ad, chacko ag, chacko g, rajshekhar v. plasma cell tumors of the skull. surg neurol [internet]. 2005 nov [cited 2014 sep 23];64(5):434–8; discussion 438–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/16253694 4. nofsinger yc, mirza n, rowan pt, lanza d, weinstein g. head and neck manifestations of plasma cell neoplasms. laryngoscope [internet]. 1997 jun [cited 2014 sep 23];107(6):741–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/9185729 5. abemayor e, canalis rf, greenberg p, wortham dg, rowland jp, sun nc. plasma cell tumors of the head and neck. am j otolaryngol [internet]. 1988 dec [cited 2014 sep 23];17(7):376–81. available from: http://www.ncbi.nlm.nih.gov/pubmed/3230611 6. singh ad, chacko ag, chacko g, rajshekhar v. plasma cell tumors of the skull. surg neurol [internet]. 2005 nov 1 [cited 2014 sep 23];64(5):434–8; discussion 438–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/10 7. schwartz th, rhiew r, isaacson sr, orazi a, bruce jn. association between intracranial plasmacytoma and multiple myeloma: clinicopathological outcome study. neurosurgery [internet]. 2001 nov [cited 2014 sep 23];49(5):1039–44; discussion 1044–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/11846895 8. tournier-rangeard l, lapeyre m, graff-caillaud p, mege a, dolivet g, toussaint b, et al. radiotherapy for solitary extramedullary plasmacytoma in the head-andneck region: a dose greater than 45 gy to the target volume improves the local control. int j radiat oncol biol 404 | moscote-salazar et al solitary plasmocytoma of the skull phys [internet]. 2006 mar 15 [cited 2014 sep 23];64(4):1013–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/16343803 9. segeren cm, sonneveld p, van der holt b, baars jw, biesma dh, cornellissen jj, et al. vincristine, doxorubicin and dexamethasone (vad) administered as rapid intravenous infusion for first-line treatment in untreated multiple myeloma. br j haematol [internet]. 1999 apr [cited 2014 sep 23];105(1):127–30. available from: http://www.ncbi.nlm.nih.gov/pubmed/10233375 10. jagannath s, kyle ra, palumbo a, siegel ds, cunningham s, berenson j. the current status and future of multiple myeloma in the clinic. clin lymphoma myeloma leuk [internet]. 2010 feb [cited 2014 sep 24];10(1):28–43. available from: http://www.ncbi.nlm.nih.gov/pubmed/20223727 11. gong j-s, kang w-y, zhu j, xu j-m. a hole in the skull: ct manifestations of a solitary plasmacytoma in skull. quant imaging med surg [internet]. 2012 mar [cited 2014 sep 23];2(1):61–2. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3496502&tool=pmcentrez&rendertype=abstract 12. weber dm. solitary bone and extramedullary plasmacytoma. hematol am soc hematol educ progr [internet]. 2005 jan [cited 2014 sep 23];373–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/16304406 microsoft word 24srinivasm_referral romanian neurosurgery (2018) xxxii 2: 377 383 | 377             doi: 10.2478/romneu-2018-0047 referral pattern to neurosurgeons in a tertiary care teaching hospital m. srinivas1, s. satish kumar1, venkata ramya bola2, ranabir pal3, radhika gorantla4, m. jahnavi5, b.v. subramanyam6, luis rafael moscote-salazar7, r. lakshman kumar5, amrita ghosh8, amit agrawal5 1department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, ap, india 2department of management information system, narayana medical college hospital, chinthareddypalem, nellore, ap, india 3department of community medicine, esic medical college and hospital, faridabad, india 4department of hospital administration, narayana medical college hospital, chinthareddypalem, nellore, ap, india 5department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, ap, india 6department of forensic medicine, narayana medical college hospital, chinthareddypalem, nellore, ap, india 7cartagena neurotrauma research group, university of cartagena, cartagena de indias, colombia 8department of biochemistry, medical college, calcutta abstract: background: due to lack of pre-hospital care, direct admission of traumatic brain injury (tbi) patients to dedicated neurosurgical department remains difficult in many parts of world. objective: the present pilot study was conducted to understand the referral pattern of patients to the neurosurgery department and to develop an algorithm to stratify the spectrum of cases as per the severity of condition and possibility of direct neurosurgical care. materials and methods: details of referral patterns, demographic and clinical profile, management and outcome of consecutive tbi cases admitted in the department of neurosurgery were collected with predesigned proforma. results: of total 55 cases, 40 (73%) were males; 26 (47%) between 36-55 years age; 26 (47%) referred directly to the center; 24 (44%) self-referred; 34 (62%) referred from emergency department; mostly (32, 58%) admitted after 12pm; 22 (40%) admitted for 16-30 days. in the analysis of investigations, 37(67%) cases had ct, 378 | srinivas et al referral pattern to neurosurgeons             15 (27%) had mri, 4 (7%) had x-ray, 1 (2%) undergone all three investigations, while 8 (15%) didn’t have any; mostly (42, 76%) cases were referred for the management of tbi and 38 (69%) required operative interventions. conclusion: our findings strongly suggest that referral of tbi cases need improvement in this part of country where hindrances delay tbi cases to reach dedicated neurological intensive care leading to delay of committed care and optimization of strategy for reduction of case fatality. key words: head injury, referrals, neurosurgical management, tertiary care hospital introduction road traffic accidents remain the single biggest cause of injuries and injury-related mortality, accounting for a quarter of all injury deaths. [1] worldwide, an estimated 1.3 million people die on roads each year and as many as 78.2 million get injured. projections indicated that these figures will increase by about 65 percent over the next 20 years, unless there is a new commitment to prevention initiated. this effect of projected increases will be greater in lowand middleincome countries, as they currently account for over 90 percent of all road traffic injury deaths. [2] the problem of road trauma and its growing trend in the lowand middleincome countries is not a new problem and it has previously been described as a neglected global epidemic. [3] worldwide road traffic accidents account for an estimated 50 million injuries. [4] all over the world about 59 percent of road traffic deaths occur among productive age group i.e. young adults between 15 and 44 years. [5] our center narayana medical college hospital, nellore, andhra pradesh, india, continues to play a pivotal role in the management of head and spinal cord injuriesin this region. many patients with acute or chronic neurological problems often get admitted under general medicine and other departments. some with other primary diagnosis may also develop neurological complication due to course of illness or as a part of complication. this is a descriptive cross-sectional study of a head injury (hi) registry was conducted with the aim of establishing the pattern of referrals of hi for neurosurgery dept. the findings of this study hopefully will provide insights for the neurosurgical management of hi in the dedicated tertiary care teaching hospitals in south india. materials and methods this is a prospective study of consecutive hi patients managed in a neurosurgical dept. at the narayana medical college hospital (nmch), nellore, andhra pradesh, india between march to october 2017. nmch, the centre of excellence is a 1420 bedded tertiary care teaching hospital committed to provide exemplary care to meet or exceed the patient expectations. each of the referred patients was examined by the neurosurgeon who attended the referral. the patients were diagnosed clinically with proper history, examination with the help of investigations in required cases. information regarding the demographic and clinical profile were gathered through a pretested questionnaire. romanian neurosurgery (2018) xxxii 2: 377 383 | 379             the research protocol was reviewed and accepted by the institutional ethical committee, nmch. our study population included 55 trauma patients whose case sheets of head injury were examined for the referral patterns. firstly, the cases of head injury presenting primary referral and selfreferral and to the nmch were sorted. selfreferral was defined as the cases of head injury that presented directly at the neurosurgery department and the primary referral was defined as those cases examined initially in another health facility before presenting in nmch were labeled the primary referral ones. the sources of referrals of the latter were noted including types of health facilities (private, general hospitals or other tertiary facilities) from which they were referred for neurosurgical care, and the place of origin in nellore where the trauma occurred. the number of health facilities (one, two and more) earlier visited before arrival in nmch, nellore, as well as whether there was any in-house neurosurgical service in any of these facilities was also noted. the reason for the inter-hospital transfers from the other centers was also noted from the referral letters whenever available. statistical analysis the clinical profile of the cases was transferred to an electronic spreadsheet, and analyzed using the spss version 24 (the spss inc, ii, usa) and presented here in descriptive statistics including frequencies and proportions, means (standard deviation, sd), 95% confidence, ci, median (range). categorical variables were explored for associations with the chi-squared test. an alpha value of <0.05 was deemed significant for associations. the referral pattern of the neurosurgical cases represented as follows: results fifty five (55) neurosurgery referral cases managed at this tertiary care center were taken up in this study and their clinical data is captured in the registry over period of eight months. in the demographic details, of these 55 cases, 73% are males and 27% were females. only 2% are less than 18 years of age, 16% are in the age group 18-35years, 47% are under the age group 36-55years and 35% are above 55 years (table 1).   380 | srinivas et al referral pattern to neurosurgeons             table 1 demographic profile of the neurosurgery referral cases gender frequency percent f 15 27% m 40 73% age group <18 years 1 2% 18-35 years 9 16% 36-55 years 26 47% >55 years 19 35% time of admission am 20 36% pm 32 58% na 3 5% length of stay 1-15 days 14 25% 16-30 days 22 40% 31-55 days 16 29% na 3 5% primary ref direct 26 47% referred 17 31% na 12 22% self ref no 11 20% yes 24 44% na 20 36% emd no 8 15% yes 34 62% na 13 24% most of the cases (47%) are referred directly to the tertiary care hospital while 31% are referred from the primary health care centers and 22% referral is not available. while 44% are self-referred to the neurosurgery dept. 62% are referred from emergency to neurosurgery dept. mostly (58%) cases are admitted after 12pm, while 36% are admitted before 12pm and time of admission for 6% cases is not available. most of the patients (40%) stayed 16-30 days in the hospital (los) while 25% stayed for 1-15 days, 29% stayed 31-55 days and los for 6% of cases is not available. [table 1] of these 55 referrals, 67% undergone ct.27% underwent mri, 47% cases underwent x-ray investigations. it is observed that 2% undergone all the three i.e., ct, mri and xray radio diagnosis while 15% dint undergo ct, mri and x-rays. most of the cases 76% are brain injuries, 15% are spinal cord injuries, 5% are both brain and spinal cord injuries while data of 4% cases is not available. 69% are managed surgically in the neurosurgical dept. while 20% are managed medically and management of the 11% cases is not available. [table 2] table-2 clinical details of the neurosurgery referral cases ct frequency percent yes 37 67% no 18 33% mri yes 15 27% no 40 73% x rays yes 4 7% no 51 93% case romanian neurosurgery (2018) xxxii 2: 377 383 | 381             brain 42 76% spinal cord 8 15% both 3 5% na 2 4% investigations ct 37 67% mri 15 27% x rays 4 7% all 1 2% none 8 15% management medical 11 20% surgical 38 69% na 6 11% discussion the data of our study strongly support an urgent need for awareness in the public sector for direct referrals to the neurosurgery dept. within the golden hour and platinum minutes and educating the public with development of a dedicated network of telemedicine using all sorts of gadgets including android phones for an effective surgical management of the trauma cases from pre-hospital care to reaching early to the tertiary care teaching hospital or well-equipped center of excellence in neurosurgery and neurosciences. road trauma is an emergent global issue. there is huge disparity between the population affected by road trauma and the resource allocation. if the current trend continues, a predicted extra five million lives will be lost in this decade and in the younger age groups. india is yet to establish an effective system of delivering trauma care and emergency services to a majority of its citizens despite its economic success. [6] we have to prepare ourselves urgently as 90 percent of global trauma mortality occurs in low-and-middle-income countries (lmics). [7] in high income countries (hics), trauma mortality has steadily declined, but a similar trend is not seen in lmics. [8] in india, the trend of in-hospital trauma mortality has remained unchanged in the past decade, despite advances in imaging and medical equipment. [9] in addition, india’s 30-day trauma mortality rate is twice that of comparable patients admitted to trauma centers in hic settings. the reasons for the high rates and unchanging trends remain unknown and unexplored. [10] high clinical load [11], low-resources, and high out-of-pocket expenditures [12] are commonly named as barriers to improving trauma care in india. [13] however, several studies have demonstrated that low-cost interventions can improve trauma care outcomes. [7,14] report on road accidents in india 2016, published by transport research wing under ministry of road transport & highways, government of india, has revealed that rtas record at least 413 people died every day in 1,317 road accidents which means that at least 17 deaths occurred in road accidents in 55 accidents every hour in the given time period15 i.e., there is one death on the indian road every six-eight minutes and this is expected to escalate to one death every three minutes by 2020. [15] though the neurosurgeons are available in the tertiary care trauma centers, many head injury patients are initially evaluated and 382 | srinivas et al referral pattern to neurosurgeons             treated in the primary care centers or nontrauma care centers. it is beyond any discussion that all patients who clearly need a neurosurgical intervention should be transferred as early as possible. however, the inter-hospital referral of trauma case is another complex concern which is to be solved. the decision to transfer a patient to another hospital might definitely influence the decisions in treatment priorities and even the mode of treatment. the patient demographic profile reflects that most of the trauma victims 47% are middle aged group 36-55 years and are males 73% and shows the high prevalence of injuries while attending their duties. educating and creating awareness regarding the hospital referrals and the importance of timely transfer to the specialized tertiary care trauma centers like nmch can result in better evaluation, earlier treatment and best outcomes. there is need to educate health care workers about the quality of care for head and spinal cord injury victims and to ensure early and ongoing neurosurgical care provided in nmch and other health care centers. efforts need to be made at the prehospital level to get victims to the traumatic care centers with in golden hour and provide initial care for which introduction and educating the public with telemedicine appears to be boon with the team of doctors, nurses, technicians, supporting staff and equipment to be provided to execute the concept of telemedicine. to reduce the burdens of the traumatic injuries, the injury prevention strategies regarding road traffic safety, work place safety, improvement in referral patterns, and implementation of protocol for traumatic registry, quality improvement in pre-hospital, primary health care centers, emergency, neurosurgery, and rehabilitation care are essential. strengths and limitations we had done health service research on referral of tbi cases that need holistic approach in this part of country where impediment delay tbi cases to reach devoted neurosurgical intensive care to optimize reduction of case fatality, morbidity and disability. we had several limitations. we had to study referral pattern with a small sample in a single center in the infrastructure poor set up in south-india. conclusions the study addresses that majority of tbi patients were referred from the site of injury and emergency department depending on time of accident that determined the subsequent investigations and interventions. the analysis strongly suggests that improvement of care for patients with severe head injury represents the best strategy for reduction of case fatality in those hospitalized after blunt trauma and that neurological intensive care intervention is central to such a strategy. the results support an urgent need for awareness in the public sector for direct referrals to the neurosurgery dept. within the golden hour and platinum minutes and educating the public with telemedicine for an effective surgical management of the trauma cases in the tertiary care teaching hospital which is a center of excellence in neurosurgery and neurosciences. romanian neurosurgery (2018) xxxii 2: 377 383 | 383             correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com mobile+91-8096410032 references 1. peden m, hyder a. road traffic injuries are a global public health problem. bmj 2002;324:1153-1153. 2. bhalla k, shotten m, cohen a, et al. transport for health: the global burden of disease from motorized road transport2014. 3. nantulya vm, reich mr. the neglected epidemic: road traffic injuries in developing countries. bmj: british medical journal 2002;324:1139. 4. organization wh. global status report on road safety: time for action: world health organization, 2009. 5. who. road traffic injuries [online]. available at: http://www.who.int/mediacentre/factsheets/fs358/en/. accessed 2017-12-13 04:30:54 6. mcintosh b, sheppy b, rane s. an indian tragedy, an indian solution: perspective of managing service quality in emergency medical services in india. the journal of global health care systems 2012;2. 7. chandran a, hyder aa, peek-asa c. the global burden of unintentional injuries and an agenda for progress. epidemiologic reviews 2010;32:110-120. 8. mock c, joshipura m, arreola-risa c, quansah r. an estimate of the number of lives that could be saved through improvements in trauma care globally. world journal of surgery 2012;36:959-963. 9. gerdin m, roy n, dharap s, et al. early hospital mortality among adult trauma patients significantly declined between 1998-2011: three single-centre cohorts from mumbai, india. plos one 2014;9:e90064. 10. roy n, gerdin m, ghosh s, et al. 30-day in-hospital trauma mortality in four urban university hospitals using an indian trauma registry. world journal of surgery 2016;40:1299-1307. 11. stelfox ht, joshipura m, chadbunchachai w, et al. trauma quality improvement in low and middle income countries of the asia–pacific region: a mixed methods study. world journal of surgery 2012;36:1978-1992. 12. kumar ga, dilip tr, dandona l, dandona r. burden of out-of-pocket expenditure for road traffic injuries in urban india. bmc health services research 2012;12:285. 13. stewart bt, quansah r, gyedu a, ankomah j, donkor p, mock c. strategic assessment of trauma care capacity in ghana. world journal of surgery 2015;39:2428-2440. 14. hashmi zg, haider ah, zafar sn, et al. hospitalbased trauma quality improvement initiatives: first step toward improving trauma outcomes in the developing world. journal of trauma and acute care surgery 2013;75:60-68. 15. desk ew. road accidents in india, 2016: 17 deaths on roads every hour, chennai and delhi most dangerous. 2017. 26gentlemandisappeared romanian neurosurgery (2018) xxxii 1 | 179 a gentleman disappeared dr. claudiu gh. savu dear colleagues, dear friends, unfortunately, time becomes an enemy from the moment we were born. and the flow of sand from the hourglass is even fiercer ever since you became a neurosurgeon. from that moment on, you live in a whirlwind of the profession: breaks, bleeding, clips, complications, csf fistula, relapses, suppurations, etc. a whirlpool that often adds to the dysfunctions of the medical world, those of colleagues or even family. it's not easy at all! often, the battle to succeed in this noble profession resembles the struggle for survival in who knows what, hot, jungle. victory means to heal, but it also means to progress. we forget too easily that we are part of one of the most respected medical specialties. without false modesty, i say: neurosurgeons are an elite. unfortunately, it is happening more and more often to blame ourselves on our own physicians’ condition. or, if we do not do it, to be unnaturally silent in the face of mass media outbursts. i do not mean we do not have our own colleagues at least with imperfections. but the mistakes of one or the other must not hit the community around our profession. equally, we have to say that we had, and still have, patterns of behavior and attitude. ladies and gentlemen in the true sense of the word. one of these exceptional gentlemen was neurosurgeon claudiu gh. savu. it does not matter when and where it was born, where it grew up, or whether it was a member of a party or not. he had an extraordinary education. he was our colleague, assistant professor at the clinic of professor constantin arseni. he was head of one department at bagdasar-arseni hospital when led by professor alexandru constantinovici. no one could ever blame him for anything. he did not use ugly / heavy words, he was never aggressive and he did not criticize his colleagues. he always helped his collaborators, behaved civilized, and was a model for the young neurosurgeons he had formed. it was an example of professionalism and balance in clinic 1 of neurosurgery in bucharest. doctor claudiu savu was a behavioral model for romanian neurosurgery. at one point, he left bucharest at the neurosurgical center in baia mare. he continued to be the same valuable neurosurgeon and the same man of humanity and vast cultural respiration. maramures appreciated him both as a primary neurosurgeon and as a medical director at a private center. but it also recognized him as a man who gave spirit, culture and a dignified and decent attitude towards others. what's left behind? the most important for a doctor an impressive number of healed patients. a large number of colleagues who have known his professionalism. and the image of a doctor with a warm smile and a gentleman's attitude... god rest his good soul! prof. md. msc a.v. ciurea flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article giant subgaleal cerebrospinal fluid leakage: an unusual complication of chronic subdural hematoma surgery luis rafael moscote-salazar, hernando raphael alvis-miranda, amit agrawal, willem calderon-miranda, alfonso pacheco-hernandez colombia, india, mexico doi: 10.1515/romneu-2017-0052 316 | moscote-salazar et al giant subgaleal cerebrospinal fluid leakage doi: 10.1515/romneu-2017-0052 giant subgaleal cerebrospinal fluid leakage: an unusual complication of chronic subdural hematoma surgery luis rafael moscote-salazar1, hernando raphael alvis-miranda2, amit agrawal3, willem calderon-miranda4, alfonso pachecohernandez5 1neurosurgery, critical care unit, red latino organización latinoamericana de trauma y cuidado neurointensivo, bogotá, colombia 2resident of neurosurgery, universidad de cartagena, cartagena de indias, colombia 3neurosurgery, mm institute of medical sciences & research maharishi markandeshwar university mullana ambala, haryana, india 4resident of radiology, universidad nacional autonoma de mexico, mexico d.f, mexico 5universidad de cartagena, cartagena de indias, colombia abstract: we report a rare case of chronic subdural hematoma complicated with a giant subgaleal cerebrospinal fluid leakage. physical examination was performed with no alteration in mental status and no focal neurological disorder. the subdural hematoma was drained and two weeks later, patient was admitted to our hospital with a giant scalp swelling. physical examination revealed a left parietal subcutaneous collection. the patient was reoperated with a correction in the fistula, he presented a satisfactory postoperative evolution. to our knowledge, this is the first report in literature of a chronic subdural hematoma with a complicated giant subgaleal cerebrospinal fluid leakage. key words: chronic subdural hematoma, subgaleal cerebrospinal fluid leakage, surgery, neurotrauma introduction chronic subdural hematoma is an encapsulated collection of blood, located below the dura, essentially characterized by the presence of a membrane. usually, it occurs in the elderly (> 65 years), and is considered to be a sentinel event. a ct brain scan is the current method of choice for the diagnosis of this entity. it should especially be suspected in patients presenting dementia, and although it’s less frequent, investigation should be performed in patients with transient neurologic deficit. there is still no consensus regarding the ideal surgical modality, however, the recommended procedure is considered to romanian neurosurgery (2017) xxxi 3: 316 318 | 317 be closed suction drain through drill holes. it has been debated whether intraoperative collection improves results. we report the case of a man of 75-years-old who presents scalp swelling, a week after the operation of chronic subdural hematoma. to our knowledge, this is the first case reported of giant scalp swelling in literature. case report a 75-year-old male patient without any relevant clinical record, presented holocraneal headache for 1 month, and was transferred from a local hospital that does not have access to neurosurgical care. the patient was admitted to our emergency department with a glasgow coma scale (gcs) score of 14. cranial ct revealed a 12 mm left frontoparietal csdh with 10 mm mid-line shift. we decided to perform surgical evacuation of subdural hematoma with placement of a closed drainage system. the postoperative period was unremarkable, and at 1 month follow-up, the patient was in gcs 15. postoperative tc documented brain reexpansion and resolution of the subdural collection. five weeks later, he was taken to our neurosurgery department for a giant scalp swelling. (figures 1 and 2). we performed the drainage of a subgaleal collection with hemorrhagic content. the drain was placed in the subgaleal region, in the hole trepanation zone; a bandage was held for 7 days. the subgaleal drainage was removed in the second postoperative day. a week later, the patient was discharged, and during the month of monitoring, the presence of the subgaleal collection had disappeared. figure 1 giant scalp swelling figure 2 preoperative cranial ct showing a left giant subgaleal cerebrospinal and adjunct the bur hole discussion the progressive growth of the hsc is related to a late clinical appearance due to old age as well as brain adaptation. as a result of an approximate 200g weight reduction, there’s been an increase of 6 and 11% in the extracerebral space, thus, causing the growth of the subdural collection to create space problems. the clinical presentation in the elderly is varied. in 20-50% of times, a dementia syndrome is described, which can be 318 | moscote-salazar et al giant subgaleal cerebrospinal fluid leakage mistaken for senile dementia. it is thus recommended that research through computed tomography (ct) be done in all patients with cerebral qualitative consciousness disorder regardless of their age. headaches, speech disturbances, hemiparesis, seizures, etc. may also occur as a transient neurological deficit. typically, the hsc occurs in male patients over 60 years of age, who have alcoholic tendencies or suffer from blood dyscrasias and frequent falls. these individuals complain of a progressive clinical syndrome characterized by a motor, which adds to the evolution signs and symptoms of intracranial hypertension. predisposing factors such as, altering coagulation (blood dyscrasias, anticoagulation, alcoholism), risk factors for arterial degenerative disease (diabetes mellitus, hypertension), and development of pressure gradients (hydrocephalus, epilepsy, spinal tap, drain csf, brain atrophy) should be considered. we must remember that the bilateral hsc is frequently smaller, which can confuse diagnosis and delay management. complications occur between 3-28%. rohde et al. reported a complication rate of 20.5% in a series of 376 patients operated by craniotomy burr hole. (5). complications include convulsions, subdural empyema, subdural hematoma, intracerebral hematoma and a case of subdural hematoma complicated with fistula subgaleal reported in a child with an arachnoid cyst. our case is an adult consisting of the first described in the literature. correspondence dr. luis rafael moscote-salazar e-mail: mineurocirujano@aol.com references 1. menovsky t, vries j, bloss hg. treatment of postoperative subgaleal cerebrospinal fluid fistulas by using fibrin sealent. j neurosurg 1999;90:1143-1145 2. karavelioğlu e, eser o, boyac mg. a rare complication of chronic subdural hematoma surgery; subgalea cerebrospinal fluid leakage. case report. pam tıp derg 2013;6(3):158-161 3. maxwell ja, goldware si. use of tissue adhesive in the surgical treatment of cerebrospinal fluid leaks: experience wit isobutyl-2-cyanoacrylate in 12 cases. j neurosurg 1973;39:332-6. 4. tse dt, panje wr, anderson rl. cyanoacrylate adhesive used to stop csf leaks during orbital surgery. arch ophthalmol 1984;102(9):1337-9. 5. rohde v, graf g, hassler w. complication of burrhole craniostomy and closed-system drainage for chronic subdural hematomas: a retrospective analysis of 376 patients. neurosurg rev 2002;25:89-94. doi: 10.33962/roneuro-2021-033 primary calvarial cavernous haemangioma in a child. a case report adel khelifa, walid bennabi, lakhder berchiche, abdelhalim morsli romanian neurosurgery (2021) xxxv (2): pp. 207-209 doi: 10.33962/roneuro-2021-033 www.journals.lapub.co.uk/index.php/roneurosurgery primary calvarial cavernous haemangioma in a child. a case report adel khelifa, walid bennabi, lakhder berchiche, abdelhalim morsli neurosurgical department of beo university hospital, algiers, algeria abstract a wide variety of bone lesions is encountered on the skull and usually with poor clinical presentations and non-specific radiological features. primary cavernous hemangioma is one of these rare calvarial lesions that the symptoms are limited to a simple subcutaneous mass frequently neglected by the patient. although seen in all ages from neonate to elderly; few cases were reported in the literature of patients in the first decade of life. we report a case of four years old boy with primary calvarial cavernous hemangioma in order to help to understand this pathology and to urge physicians to explore any chronic subcutaneous mass at any age. introduction skull hemangioma is a rare pathology with minimal clinical presentation and non-specific images. the first known description of this lesion in literature was in 1845 by toynbee [1]. skull hemangiomas are classified into capillary and cavernous types; with cavernous type being more frequently seen [1,2,3,4,5,6]. we present a case of four years old boy with primary calvarial cavernous hemangioma. case presentation the patient is a four years old boy with trisomy 21. the parents consulted for the appearance of a right fronto parietal subcutaneous mass; of barely 1 cm of diameter. a brain ct was performed objectified an extra axial right fronto parietal lesion of 42 x 29 mm; isodense, with intense homogenous enhancement after contrast injection, and bone destruction from where the lesion get through to the subcutaneous region; there was also a circumferential osteophytic bone reaction (figure 1). the patient was operated and the lesion was totally removed through a frontoparietal bone flap. in post-operative there were no complications. pathology study was in favor of bone cavernous hemangioma. no supplementary management was necessary. control images performed nine years later, showed no residual tumor or recidivism (figure 2). keywords hemangioma, bone tumours, skull tumours corresponding author: adel khelifa neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 208 adel khelifa, walid bennabi, lakhder berchiche et al. figure 1. preoperative brain ct; a: before injection; b: after injection; c: bone window. the images objectify an extra axial right fronto parietal lesion; it appears spontaneously isodense (a, horizontal arrow), with intense homogenous enhancement after contrast injection (b, horizontal arrow), and bone destruction from where the lesion get through to the subcutaneous region (c, horizontal arrow). there was also a circumferential osteophytic reaction from the inner calvarial bone (a and c, vertical arrows). figure 2. nine years post-operative mri showing no tumor recidivism. a: axial flair sequence; b: axial t1 injected image. discussion primary calvarial hemangiomas (pchs) are rare lesions; they account of 0.2 % of all bone neoplasm [1,3,5,6,7,8]. yang et al. reviewed 93 cases of pch reported in the literature from 1845 to 2015; according to this paper most patients were in the fourth and the fifth decade [1,2]. only 0.9 % of pchs were seen in the first decade of life as in our case [2]. frontal bone is a predilection location for pchs with 44.1% of all cases [1,2]. clinical presentation depends on the topography of the lesion. subcutaneous mass and headaches were the most frequent reasons for consultation [1,2]; neurologic deficit is rarely seen [1,2,4,5,6,7,8]. proptosis, impaired vision, facial nerve paralysis, tinnitus, and hearing loss are seen in orbital and skull base locations [1,2]. bleeding from the lesion may be seen in the epidural or subarachnoid spaces [1,3,7]. on plane x-rays and on ct scan, pch is a lytic lesion with sclerotic rim; after contrast injection the enhancement is constant it could be heterogeneous or homogenous as in our case [2,3]. for us those finding were sufficient to indicate the surgery and to plan the resection strategy. although not specific, mri affords supplementary information about the relation of the lesion with the underlying dura, parenchyma, and vascular structures; it shows hypo to iso intense mass on t1 weighted images, hyperintense on t2 weighted images and on flair sequences; there is a large enhancement after gadolinium injection [1,3]. pchs are accessible lesions for surgical resection, thus total removal with acceptable margin is the treatment of choice [1]; this could be achieved through a skin incision and craniectomy centered on the lesion. in adult the bone defect is correct usually with cranioplasty. as in our case the management of many other pediatric cases in the literature was limited to lesion removal without bone correction due to the young age face to future skull changing [4,8]; other teams preferred cranioplasty [6] or remodeling [5]. conclusion subcutaneous mass could underestimate deep infiltrating and brain compressive lesion. this is the case of rare lesions like calvarial cavernous hemangioma which is seen in any age. this lesion is associated with the best prognostic if totally removed. 209 primary calvarial cavernous haemangioma in a child conflicts of interest none. references 1. yang y, guan j, ma w, li y, xing b, ren z, et al. primary intraosseous cavernous hemangioma in the skull. medicine march 2016; 95 (11). doi:10.1097/md.0000000000003069. 2. cervoni l, artico m, delfini r. intraosseous cavernous hemangioma of the skull. neurosurg. rev 1995; 18: 6164. 3. politi m, romeike b. f.m, papanagiotou p, nabhan a, struffert t, feiden w, et al. intraosseous hemangioma of the skull with dural tail sign: radiologic features with pathologic correlation. ajnr am j neuroradiol september 2005; 26: 2049–2052. 4. cosar m, eser o, aslan a, korkmaz s, boyaci g, aktepe f. intradiploic cavernous hemangioma of the skull in a child: a case report. childs nerv syst 2008;24: 975–977. doi:10.1007/s00381-008-0638-0. 5. martínez-lage j f, torroba m a, pérez b c, almagro m j, lópez-guerrero a l, rosa p. cavernous hemangiomas of the cranial vault in infants: a case-based update. childs nerv syst 2010; 26: 861–865. doi 10.1007/s00381-0101151-9. 6. vural m, acikalin m f, adapinar b, atasoy m a. congenital cavernous hemangioma of the calvaria. neurosurg pediatrics 2009; 3: 41-45. doi: 10.3171/2008.10.peds08161. 7. gottfried o n, gluf w m, schmidt m h. cavernous hemangioma of the skull presenting with subdural hematoma. neurosurg focus 2004 oct 15; 17(4): ecp1. doi:10.3171/foc.2004.17.4.7. 8. yoshida d, sugisaki y, shimura t, teramoto a. cavernous hemangioma of the skull in a neonate. child’s nerv syst 1999; 15: 351–353. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 441 445 | 441 epidermoid cyst in anterior, middle & extension of posterior cranial fossa: rare imaging with review of literature vivek kumar kankane1, gaurav jaiswal2, tarun kumar gupta2 neurosurgery, r.n.t. medical college & m.b. hospital, udaipur, rajasthan, india 1resident; 2department of neurosurgery abstract: epidermoid cysts are benign slow growing more often extra-axial tumors that insinuate between brain structures, we present the clinical, imaging, and pathological findings in 35 years old female patients with atypical epidermoid cysts which was situated anterior, middle & posterior cranial fossa. ncct head revealed hypodense lesion over right temporal and perisylvian region with extension in prepontine cistern with mass effect & midline shift and mri findings revealed a non-enhancing heterogeneous signal intensity cystic lesion in right frontal & temporal region extending into prepontine cistern with restricted diffusion. patient was detoriated in night of same day of admission, emergency fronto-temporal craniotomy with anterior peterousectomy and subtotal resection was done. the histological examination confirms the epidermoid cyst. the timing of ectodermal tissue sequestration during fetal development may account for the occurrence of atypical epidermoid cysts. key words: epidermoid cyst, anterior, middle, posterior cranial fossa, prepontine cistern introduction epidermoid cysts are benign, slow growing extra-axial tumors that account for 1% of all intracranial tumors (10). embryologically, they are derived from ectodermal inclusions during neural tube closure from the third to the fifth weeks of embryogenesis (10, 8). they frequently occur at the cerebellopontine angles and parasellar regions, insinuating between brain structures. conversely, epidermoid cysts in intraparenchymal or intradiploic locations are very rare, accounting for less than 5% of all intracranial epidermoid cysts (1). here, we reported rare cases of 35 years old female demonstrated an extra-axial epidermoid cyst which was situated in anterior, middle as well as posterior cranial fossa. case report we reported a clinical case concerning a 35 years old female who presented convulsions during 5 years, headache & ataxia during 5 months, slurring of speech during 3 months & diminished of vision in both eyes during 2 months. the clinical examination found lower motor neuron type grade iv facial nerve palsy 442 | kankane et al epidermoid cyst in anterior, middle & extension of posterior cranial fossa on right sided with ataxia & vision of bilateral eyes is only perception of light with right sided occulomotor nerve & lateral rectus palsy. the ncct head (figure 1) show hypodense lesion over right temporal and perisylvian region with extension in prepontine cistern with mass effect & midline shift. mri brain (figure 2) with contrast showed heterogeneous signal intensity cystic lesion in right frontal & temporal region extending into the prepontine cistern with mass effect and midline shift. the lesion appears hypointense on t1w and hyperintense on t2w sequence and showing restriction on diffusion weighted images. patient was detoriated in night of same day of admission so underwent emergency surgey via fronto-temporal approach with anterior peterousectomy and subtotal resection. a solid part of the tumor and the capsule were deliberately left due to adhesions to the neurovascular structure. it was a pearly tumor. the histological examination (figure 2) confirms the epidermoid cyst. figure 1 ncct head showed right temporal lobe and perisylvian region hypodense lesion with extension in prepontine cistern, mass effect & midline shift romanian neurosurgery (2016) xxx 3: 441 445 | 443 figure 2 a, b, c mri brain with contrast showed heterogeneous signal intensity cystic lesion in right frontal & temporal region extending into the prepontine cistern with mass effect and midline shift. the lesion appears hypointense on t1w and hyperintense on t2w sequence and showing restriction on diffusion weighted. d, e h & e 40 &10 magnification histopathological finding shows an epidermoid cyst lined by maturing and keratinizing stratified squamous epithelium and sqames, which is formed from degenerative keratinocyte 444 | kankane et al epidermoid cyst in anterior, middle & extension of posterior cranial fossa discussion epidermoid cysts can occur throughout the neuroaxis, most commonly in the cerebellopontine angles (40–50%) and the parasellar region (10). conversely, atypical epidermoid cysts are rare, with intra-axial epidermoid cysts accounting for less than 1.5% of all intracranial epidermoid cysts (1) and intradiploic epidermoid cysts (including congenital cholesteatomas) accounting for approximately 3% (6, 7). in our case is 1st reported case in world’s literature, in which epidermoid cysts involving anterior, middle as well as post fossa. occasionally the epidermoid found in pineal gland (9) or the brainstem (11). the proposed embryological pathogenesis of the typical epidermoid cyst involves trapped ectodermal components travelling along the otic vesicles during neural tube closure, thus accounting for the propensity for its location at the cerebellopontine angles (2). cell entrapment from the mesectodermal origin of the neural crest within the primitive cerebral hemisphere may lead to the formation of such rare intracerebral lesions (5). along this line of reasoning, intraparenchymal epidermoid are thought to arise when the ectodermal inclusion occurs before the third week of embryogenesis (when the primary cerebral vesicle is being formed), while intradiploic epidermoid cysts originate from aberrant ectodermal remnants that become trapped after neural tube closure (1, 6, 2). the radiological differential diagnoses of an epidermoid cyst include an arachnoid cyst, dermoid cyst, abscesses, metastasis, or slow growing brain tumors. flair and dwi sequences (4) have been proposed as useful discriminator in differentiating an arachnoid cyst from the typical epidermoid cyst, in which the signal intensity of the arachnoid cyst follows csf signal without restricted diffusion. a dermoid cyst is usually at a more central location with foci of calcifications which could be differentiated from epidermoid cyst (12). abscesses show typical rim of the contrast enhancement, metastasis is usually multiple with known primary tumor and heterogeneous contrast enhancement, and cystic neoplasm usually shows solid component with enhancement. current debate is ongoing regarding the optimal treatment for an epidermoid cyst. on the one hand, gross total resection of epidermoid cysts offers a definite treatment with prevention of its occurrence or aseptic meningitis (7). conversely, epidermoid is often located in close proximity to neurovasculature and vital brain parenchyma, and thus a conservative resection can be considered given the slow growing nature of this tumor, with a linear growth rate similar to normal epithelial cells (one generation per month)(3). conclusion epidermoid presented in anterior, middle and posterior cranial fossa is extremely rare case with unusual location. this is a first case reported in world’s literature. accurate preoperative diagnosis can be very difficult due to the radiological similarities to other common intracerebral cysts (e.g., astrocytomas or gliomas). magnetic resonance imaging (mri) studies, especially with romanian neurosurgery (2016) xxx 3: 441 445 | 445 diffusion-weighted images, allow greater accuracy in the preoperative differential diagnosis. radical surgical removal should be attempted, but a less aggressive surgical strategy should be considered if there is strong adherence between the tumor capsule and the neurovascular structure of brain tissue, particularly in eloquent areas. correspondence vivek kumar kankane neurosurgery resident, r.n.t. medical college & m.b. hospital, udaipur, rajasthan, india. email: vivekkankane9@gmail.com address: c/o dr. h.l, khamesara 59 sardarpura, udaipur, rajasthan, india, pincode 313001 mobile no. 8955337812 references 1. aribandi m and wilson nj; ct and mr imaging features of intracerebral epidermoid—a rare lesion. the british journal of radiology 81: 97–99, 2008 2. berhouma m, bahri k, jemel h, and khaldi m: intracerebral epidermoid tumor: pathogenesis of intraparenchymal location and magnetic resonance imaging findings. journal of neuroradiology 33: 269– 270, 2006 3. collins vp, loeffler rk, and tivey h: observations on growth rates of human tumors. the american journal of roentgenology, radiumtherapy, and nuclear medicine 76: 988–1000, 1956 4. hakyemez b, aksoy u, yildiz h, and ergin n: intracranial epidermoid cysts: diffusion-weighted, flair and conventional mr findings. european journal of radiology 54: 214–220, 2005 5. iaconetta g, carvalho ga, vorkapic p, samii m: intracerebral epidermoid tumor: a case report and review of the literature. surg neurol 55(4): 218-222, 2001 6. ichimura s, hayashi t, yazaki t, yoshida k, and kawase t: dumbbell-shaped intradiploic epidermoid cyst involving the dura mater and cerebellum. neurologia medico-chirurgica 48: 83–85, 2008 7. khan an, khalid s, and enam sa: intradiploic epidermoid cyst overlying the torcula: a surgical challenge. bmj case reports, 2011 8. kurosaki k, hayashi n, hamada h, hori e, kurimoto m, and endo s: multiple epidermoid cysts located in the pineal and extracranial regions treated by neuroendoscopy—case report. neurologia medicochirurgica 45: 216–219, 2005 9. mackay ci, baeesa ss, and ventureyra ecg: epidermoid cysts of the pineal region. child’s nervous system 15: 170–178, 1999 10. osborn ag and preece mt intracranial cysts: radiologicpathologic correlation and imaging approach. radiology 239: 650–664, 2006 11. sari a, ozdemir o, kosucu p, and ahmetoglu a: intra-axial epidermoid cysts of the brainstem. journal of neuroradiology 32: 283–284, 2005 12. smirniotopoulos jg and chiechi mv: teratomas, dermoids, and epidermoids of the head and neck. radiographics 15: 1437–1455, 1995 16harishapn_giant osteoma romanian neurosurgery | volume xxx | number 4 | 2016 | october december article giant osteoma of the skull vault: a rare case of mixed variety p.n. harisha, harneet singh ghotra, amit agrawal india doi: 10.1515/romneu-2016-0088 romanian neurosurgery (2016) xxx 4: 547 – 551 | 547 doi: 10.1515/romneu-2016-0088 giant osteoma of the skull vault: a rare case of mixed variety p.n. harisha, harneet singh ghotra, amit agrawal department of neurosurgery, narayana medical college, nellore, andhra pradesh, india abstract: osteoma is the most common primary bone tumor in the craniofacial skeleton. however, most of these are small, asymptomatic and arise from the facial bones or in relation to the paranasal sinuses. cranial vault osteomas, that too giant and symptomatic are much rarer. we report a case of sixty year-old gentleman presented with a very slowly increasing, painless, hard swelling on the left side of his head. computerized tomography scan showed the left parietal calvarial tumor to be having large exostotic and enostotic components. he underwent an en-bloc excision of the tumor and cranioplasty. giant, symptomatic cranial vault osteoma with concurrent exostotic and enostotic components is extremely rare. these lesions can be safely and completely excised with careful planning and attention to detail. key words: cranial osteoma excision, enostotic, exostotic, giant osteoma, skull tumor introduction osteoma is the most common primary bone tumor in the craniofacial skeleton, reported to affect 0.43% of the population. (7) however, most are small and asymptomatic, arising in the paranasal sinuses and facial bones. cranial vault osteomas, that too giant and symptomatic are much rarer. even when found, these tumors have been described to grow either extracranially (exostotic) or intracranially (enostotic). a tumor with both exostotic and enostotic components has not been described so far. such a tumor poses a unique set of challenges for surgical management. we report the first case of a giant, symptomatic cranial vault osteoid osteoma of mixed variety (with giant exostotic and enostotic components) and discuss the nuances of its safe and complete surgical excision. case report a sixty year-old gentleman presented with a very slowly increasing, painless, hard swelling over the left parietal region over the past 10 years. the swelling had now attained a very large size and he had holocranial headache over the last 2 months and a feeling of clumsiness and fatigability in the right hand. he did not have swellings anywhere else in the 548 | harisha et al giant osteoma of the skull vault body, nor did any of his family members have similar complaints. on examination, a large swelling was noted over the left parietal region, measuring about 16cmx13cm, having a smooth surface. the swelling extended from just behind the coronal suture to the iniomastoid line anteroposteriorly and from 2 cm off the midline to 2 cm short of the base of the mastoid mediolaterally. (figures 1 and 2) it was nontender and bony hard to palpation. his neurological examination revealed papilloedema and a pronator drift in the right upper limb. the deep tendon reflexes were brisk on the right side. a computerized tomography (ct) scan showed the lesion to be having a large enostotic component, in addition to the clinically obvious exostotic component. the enostotic component was extending further more anterior and medial than the limits of exostotic component. the former was causing mass effect on the underlying brain, resulting in a midline shift of >10mm to the right. (figure 3) a diagnosis of giant left parietal osteoma was made. he underwent complete excision of the tumor and cranioplasty with polymethyl methacrylate. a large left temporo-parieto-occipital squarescalp flap based inferiorly was raised, leaving the pericranium on the tumor. several burr holes were placed all around the tumor and on either side of the sinuses to be exposed during craniotomy. after careful separation of underlying dura and sinuses, burr holes were connected with craniotome. the free bone flap containing the entire tumor was elevated while dissecting the underlying dura adherent to the enostotic component with fine periosteal elevators. the dissection was started anteriorly, progressing medially and posteriorly. the superior sagittal sinus, left transverse sinus and finally the torcula were carefully separated and the entire tumor, along with a margin of >1cm was excised en-bloc (figure 4). there was no dural breach by the tumor. the venous ooze from the exposed sinuses was controlled with gelfoam and the bleeding from dural vessels controlled by generous use of bipolar coagulation. cranioplasty was performed with acrylic, placing multiple dural hitch stitches. the histology of resected tumor confirmed features of osteoid osteoma. wound drain was removed after 5 days. but he developed subgaleal collection under the skin flap which was treated with aspiration, antibiotics and application of crepe bandage (figure 5). subsequently, the wound healed well. by three months, he had been relieved of headache, right hand weakness had completely improved and normal skull contour had returned. he continues to be asymptomatic at one year follow-up (figure 6). figure 1 romanian neurosurgery (2016) xxx 4: 547 – 551 | 549 figure 2 figure 3 figure 4 figure 5 figure 6 discussion osteoma is the most common primary benign tumor in the craniofacial skeleton. a vast majority of these arise in relation to the paranasal sinuses or mandible. (7) cranial osteomas have been classified by haddad fs et al. into four types: 1 intraparenchymal, 2 dural, 3 skull base and 4 skull vault. the skull vault osteomas are further subdivided into two types: exostotic (arising from outer table) and enostotic (arising from inner table 550 | harisha et al giant osteoma of the skull vault and growing intracranially). (4) although not frequently described in literature, exostotic osteomas are believed to be much more common but most often asymptomatic. (5) enostotic and symptomatic osteomas are rare. to our knowledge, an osteoma having both exostotic and enostotic components has not been reported so far. this is the first such report with giant exostotic and enostotic components in a symptomatic cranial vault osteoma. the symptomatic tumors have been reported to present with headache, seizures, visual symptoms (when orbit is involved), pneumocephalus, mucocele and abscess (when paranasal sinus is involved) and even hydrocephalus due to superior sagittal sinus involvement. (2, 4, 5) our patient presented with headache and right pyramidal signs probably due to direct compression of motor cortex by the enostotic component of tumor. previously, the term “large” osteoma has been used for a tumor greater than 3cm and the term “giant” reserved for those larger than 6 cm. (5) the tumor in our patient was much larger, with the greatest dimension being 16cm. only one skull vault osteoma previously described, has been slightly larger (17.5cm). (3) surgical management of these benign tumors is most often simple and curative. however, management of the large ones with involvement of paranasal sinus and/or orbit is more complicated and has been well described by other workers. (1, 6) the giant tumors involving the vault, especially when containing both exostotic and enostotic components, present a different set of challenges. the planning of craniotomy requires careful surface marking of the enostotic component apart from the obvious exostotic component. where facilities are available, use of neuronavigation at this stage can be helpful. after disconnecting the bone flap containing the tumor from the surrounding bone, care has to be taken to separate the dura from the enostotic component. a lesion as large as the one in our patient is likely to be overlying one or more venous sinuses and utmost care has to be exercised in dissecting the tumor from them. in our patient there was no dural breach. but lesions with mushroom-like growth can breach the dura and haddad fs et al. have described disconnecting the overlying bone flap in three separate pieces before dissecting the enostotic tumor off the underlying brain and blood vessels. (4) during cranioplasty it is important to place multiple dural hitch stitches to obliterate the large epidural dead space. it is probably appropriate to excise the excess and redundant skin prior to closure. it was not done in our patient and led to persistent wound collection under the redundant skin flap, although eventually wound healed well without any major consequences. conclusion giant, symptomatic cranial vault osteoma with concurrent exostotic and enostotic components is very rare. a safe and total excision of these lesions is possible, with careful planning and attention to detail. surgical excision provides complete cure, with excellent outcome. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery romanian neurosurgery (2016) xxx 4: 547 – 551 | 551 narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1. adeleye ao. a giant, complex fronto-ethmoidal ivory osteoma: surgical technique in a resource-limited practice. surgical neurology international 2010;1:97. 2. corriero g, maiuri f, giamundo a, cirillo s, briganti f. giant osteoma of the cranial vault with acromegaly and hydrocephalus. a case report. journal of neurosurgical sciences 1985;29:331-334. 3. fan kl, ghadjar k, yuan jt, lazaref j, wilson l, bradley jp. giant cranial osteoma: successful staged excision of the largest reported. the journal of craniofacial surgery 2012;23:e480-482. 4. haddad fs, haddad gf, zaatari g. cranial osteomas: their classification and management. report on a giant osteoma and review of the literature. surgical neurology 1997;48:143-147. 5. izci y. management of the large cranial osteoma: experience with 13 adult patients. acta neurochirurgica 2005;147:1151-1155; discussion 1155. 6. secer hi, gonul e, izci y. surgical management and outcome of large orbitocranial osteomas. journal of neurosurgery 2008;109:472-477. 7. smith me, calcaterra tc. frontal sinus osteoma. the annals of otology, rhinology, and laryngology 1989;98:896-900. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article successfully treated multiple brain abscess in a newborn: a case report aleksic vuk, mihajlovic miljan, zivković nenad, misela raus, marko samardzic, stanic milenko serbia doi: 10.1515/romneu-2017-0026 172 | vuk et al successfully treated multiple brain abscess in a newborn doi: 10.1515/romneu-2017-0026 successfully treated multiple brain abscess in a newborn: a case report aleksic vuk1, mihajlovic miljan1, zivković nenad1, misela raus2, marko samardzic1, stanic milenko1 1department of neurosurgery, clinical hospital center zemun, belgrade, serbia 2department of neonatology, university children’s hospital tiršova, belgrade, serbia abstract: multiple brain abscesses are exceedingly uncommon in newborns and represent a serious medical problem associated with high morbidity and mortality. treatment is also controversial issue, and can require surgery, abscess aspiration, antibiotic therapy, and eradication of the primary source. we report a case of successfully treated multiple brain abscess in a newborn with combined therapy which consisted of abscess aspiration and prolonged antibiotics. patient developed hydrocephalus as late complication which was also successfully treated with ventriculoperitoneal shunt. key words: multiple brain abscesses, neonates, infants introduction brain abscess in newborns is a very rare disease and despite advances in neurosurgical, neuroradiological, and microbiological techniques, as well as the availability of new antibiotics, still remains a serious medical problem associated with high mortality and clinically significant neurological morbidity (1, 2). brain abscess represents cerebral infection that started as a localized area of cerebritis, after which becomes a pus collection surrounded by well vascularized capsule (1). cerebral abscess can be single or multiple (3). treatment of brain abscess is controversial issue, and can require surgery, abscess aspiration, antibiotic therapy, and eradication of the primary source. young patients, especially infants with multiple or large abscesses have unfavorable outcome (4). we present a case of successfully treated newborn with multiple cerebral abscesses. case report we present a case of male infant, referred to our neonatology department, 24 days after birth, from another clinic for further treatment of suspected multiple brain abscesses. the infant was delivered vaginally as a fourth child from healthy father and mother with previous medical history of hypothyroidism treated with ptu and highgrade fever for 10 days before delivery. apgar romanian neurosurgery (2017) xxxi 2: 172 177 | 173 scores at 1 and 5 minutes were 8 and 9 respectively. patient had a history of admission to the neonatal intensive care unit in another hospital the second day after birth due to lethargy and fever (38.3c). at that time, laboratory findings showed polycythemia (hb >225 g/dl, hct >68% in capillary blood sample) and unconjugated hyperbilirubinemia (280 micromol/l), so phototherapy was started. during the 6 day of life he was still adynamic and presented shortness of breath and chest discomfort. he was cyanotic and blood oxygen saturation maintained around 78% and 82%. the anterior fontanel was prominent and suture lines were widened. patient had septic appearance. the sepsis screen showed leukopenia (total leukocyte count 4200/mm, absolute neutrophil count 1450/mm) and raised c-reactive protein (84 mg/dl). chest xray and echocardiography showed normal findings. results of cerebrospinal fluid study were suggestive of bacterial meningitis (wbc 1890/mm3, hypoglycorrhachia 1,8 mmol/l, proteinorrhagia 34 g/l), and empiric antibiotic therapy (ceftriaxone, amikacin, amplicillin) was initiated. during the next day patient had focal epileptic seizure with secondary generalization. blood and csf culture were sterile. however, urine culture was positive for proteus mirabillis, and antibiotics were changed to meropenem and ciprofloxacin due to antibiogram. on the same day, the cranial ultrasonogram showed multiple bilateral cystic formations with blurred content, indicative for brain abscesses. also, diffuse brain edema was noted. the brain computed tomography (ct) showed multiple wellcircumscribed mass lesions with surrounding edema, with the midline shifting to the right, which was consistent with multiple brain abscesses (figure 1). following the ct result, neurosurgery consultation was performed in our hospital, which resulted in the decision of abscesses drainage, which was immediately performed under ultrasound guidance. the microbiological examination and culture of obtained cysts material were sterile. in the following period, the patient was well with no neurological abnormalities. however, on the 30th day after birth, patient become febrile again (38,2c) and the sepsis screening showed increased crp (72 mg/l). the patient’s head circumference was 36 cm. control lumbar puncture was not performed because the patient was receiving an antibiotic regimen and there was a risk of brain shift. urine culture again revealed proteus mirabilis, so the same antibiotic therapy was continued. on day 34, the neurological examination was normal. antibiotic therapy was continued for six weeks, and oral cefalexin was prescribed upon discharge. the patient’s neurological examination was normal at discharge. a cranial mri performed at 4 months revealed multiple bilateral abscesses in recovery, but with significant lateral and third ventriculomegaly. since hydrocephalus was diagnosed, following the mri result, a neurosurgery consultation resulted in ventriculo-peritoneal shunt insertion. antibiotic therapy was also continued. postoperative control ct scan showed regression of brain abscesses (figure 2). ultrasonographic follow-up was performed weekly, and lesions became cystic and decreased after day 50. on the last check-up patient had no neurological deficit. 174 | vuk et al successfully treated multiple brain abscess in a newborn figure 1 brain ct scan showing multiple brain abscesses with the midline shifting to the right figure 2 control ct scan discussion cerebral abscesses are uncommon in infants and the treatment of such brain lesions is still in debate, despite many advances in neuroimaging, neurosurgical and microbiological techniques, as well as the availability of new antibiotics (4, 5). high morbidity and mortality of cerebral abscesses necessitates finding appropriate diagnostic and therapy methods (6). in the study of sharma et al, mortality in patients with multiple pyogenic brain abscesses is 32% (7). we reported a good outcome in patient treated with antibiotics and ultrasound guided aspiration with full neurological recovery, without seizures or infections after hospital discharge. control mri performed at the end of the second year showed no signs of any abscesses recurrence. although similar to other space-occupying lesions (like neoplasm), brain abscesses symptoms tend to be more rapidly progressive. infants usually present with combination of poor feeding, vomiting, irritability or lethargy, seizures, prominent fontanel and sometimes enlarging head circumference with widening of suture lines (8). in our case, clinical presentation was in accordance with mentioned symptoms. however, our patient had early respiratory discomfort with an oxygen saturation drop. although often described as late onset complication (9), respiratory discomfort can be present at the early stage of disease, as seen in our case. most common cause of brain abscess in neonates are meningitis and septicemia. in the romanian neurosurgery (2017) xxxi 2: 172 177 | 175 study of reiner et al. which included 30 patients, brain abscess was found in 20 patients with meningitis, and 13 patients with septicemia (6). rarely abscess can be a complication of head trauma, congenital heart disease, or shunt surgery. multiple abscesses are more frequent in immunocompromised patients. most common causes of meningitis and abscess in infants are proteus mirabillis and seratia marcescens (10-12). in our case blood, csf and aspiration material culture were sterile, but urine culture was positive for proteus mirabillis, so antibiotics were given according to this results. according to many authors, ct and mri are the best diagnostic procedures in patients with multiple brain abscesses (13). however, according to anca et al, ultrasound examination seems to be more effective tool than ct and mri, and they strongly suggest that all patients under 6 months of age with suspected or diagnosed bacterial meningitis undergo ultrasound transfontanelar examination followed by ct and/or mri (9). also, besides being excellent tool for initial diagnosis, it is recommended for follow-ups (9, 14, 15). in our case, clinical presentation raised suspicion of central nervous system involvement, and ultrasound examination indicated presence of brain abscesses, and definitive diagnosis was confirmed with ct and mri afterwards. taking into account the ease of use and its high accuracy, we propose ultrasound examination as the first diagnostic tool in infants with suspected bacterial meningitis or brain abscess, followed with mri as a second imagistic tool. however, since differentiation between an ischemic lesion and an abscess in the early phase of development is sometimes difficult with ultrasound, and if clinical data and findings are not sufficient for diagnosis, ct scan should be performed (16). treatment of this rare and devastating condition still remains a challenge. the majority of authors agree that combined therapy with surgical drainage or aspiration with specific antibiotics is basic treatment protocol (17, 18). mamelak et al, suggest the aggressive surgical drainage of all abscesses larger than 25 mm in diameter, combined with 6 – 8 weeks of antibiotics (17). also the indications of surgery, as well as the type of surgery are still subject of much debate among neurosurgeons (19). the choice of procedure can be influenced by many factors such as: age, neurological condition, location and number of lesions, and stage of the abscess. minimally invasive methods are mainly done in easy accessible or deep lesions. this methods (single burr hole aspiration or transfontanelar aspiration) achieve fast and safe drainage of abscess material, produce minimal brain tissue damage, and provide immediate reduction of intracranial pressure. additionally, rapid evacuation of pus allows a more favorable local environment in which antibiotics function more effectively (19, 20). on the other hand, some authors consider formal craniotomy equal to minimally invasive aspirational procedures. however, multiple abscesses are not amenable to craniotomy excision. today, craniotomy is recommended in children older than 3 years of age with well-formed brain abscess, traumatic and mycotic abscesses, multiloculated abscesses, as well in traumatic abscesses with foreign bodies (19, 21). in our 176 | vuk et al successfully treated multiple brain abscess in a newborn case we used combined therapeutic approach. antibiotics were initial therapy, followed by ultrasound guided aspiration of cystic material. since definitive microbacterial diagnosis was not obtained, antibiotics were firstly given ex juvantibus, but were later replaced by the finding of urine culture, positive for proteus mirabilis. since there are no precise guidelines for treatment of brain abscesses, individualized and personalized medical approach must be considered, taking into account the factors mentioned above. hydrocephalus is a common complication of brain abscesses, and may occur as a result of abscess drainage or surgery. also, lowering of intracranial pressure and decompression of structures in one hemisphere can result in relative enlargement of the contra lateral ventricular system. in cases with the absence of signs of elevated intracranial pressure, shunt surgery is not required. also, infection is probably still present even though surgical procedures are completed, and thus ventriculoperitoneal shunt may be hazardous. so, the distinction between hydrocephalus and ventriculomegaly is crucial for shunt surgery indication (19, 22). although our patient significantly improved on received therapy, and there were no clinical signs of increased intracranial pressure, we decided to perform ventriculoperitoneal shunt surgery since mri finding was very indicative of active hydrocephalus. in conclusion, despite huge progress of neurosurgical and neuroradiological techniques, as well as introduction of new antibiotics, brain abscesses still represent difficult medical problem with many possible complications, so personalized medical approach still remains the best choice. references 1.senapati sb, mishra ss, satapathy mc. large brain abscess in a newborn. j pediatr neurosci. 2015;10(2):193-4. 2.sutton dl, ouvrier ra. cerebral abscess in the under 6 month age group. arch dis child. 1983;58(11):901-5 3.makhoul ir, epelman m, kassis i, daitzchman m, sujov p. escherichia coli brain abscess in a very low birthweight premature infant. isr med assoc j. 2002;4(9):727-8. 4.krajewski r, stelmasiak z. brain abscess in infants. chils nerv syst. 1992;8:279-280. 5.moss sd, mclone dg, arditi m, yogev r. pediatric brain abscess. pediatr neurosci. 1988;14:291-296 6.renier d, flandin c, hirsch e, hirsch jf. brain abscesses in neonates. j neurosurg. 1988; 69: 877–82. 7.sharma bs, khosla vk, kak vk, gupta vk, tewari mk, mathuri a. multiple pyogenic brain abscesses. acta neurochir (wien). 1995;133:36-43. 8.britt rh. brain abscess. in: wilkins rh, rengachary ss (eds): neurosurgery. new york: mcgraw-hill, 1985, pp: 1928-1956 9.anca ai, jugulete g, brezan f, luminos m, horhoianu ai, cinteza e, acs b. transfontanelar ultrasound diagnosis of brain abscesses in two neonates. medical ultrasonography. 2009;11(4):77-82. 10.carre m, sarlangue j, baronnet rr, nicolau a, demarquez jl. cerebral abscess caused by proteus mirabilis in the neonatal period. arch fr pediatr 1987;44(10):871-4 11.hervas ja, ciria l, henales v, lopez p, de la fuente a, del valle jm. nonsurgical management of neonatal brain due to proteus mirabilis. helv paediatr acta. 1987;42(56):451-6. 12.sakata h, marauyama s. serratia marcescens brain abscess in newborn. kansenshogaku zassh. 1988;72(8):845-8. 13.sommer f, aldini r, kolodziejczyk d. systemic antibiotic therapy on multiple intracerebral abscesses of unknown origin. acta neurochir (wien). 1998;140(10):1095-6. 14.basu s, mukherjee kk, poddar b, et al. an unusual case of neonatal brain abscess following klebsiella pneumonia septicemia infection 2001;29:283-285. romanian neurosurgery (2017) xxxi 2: 172 177 | 177 15.de oliveira rs, pinho vf, madureira jf, machado hr. brain abscess in a neonate: an unusual presentation. childs nerv syst 2007;23:139-142 16.frazier jl, ahn es, jallo gi. management of brain abscesses in children. neurosurg focus 2008;24:e8 17.mamelak an, mampalam tj, obana wg, rosenblum ml. improved management of multiple brain abscesses: a combine surgical and medical approach. neurosurgery. 1995;36:76-85. 18.voloshchuk si. the treatment of multiple brain abscesses. lik sprava. 1998;8:134-136. 19.erdogan e, izci y, dizer u, baysefer a. multiple brain abscesses in a baby: case report and review of the literature. annals of neurosurgery. 2002;2(5):1-6. 20.skrap m, melatini a, vassallo a, sidoti c. stereotactic aspiration and drainage of brain abscesses. experience with 9 cases. minim invasive neurosurg. 1996;39(4):108-12. 21.hagan re. early complications following penetrating wounds of the brain. j neurosurg. 1971;34(2 pt 1):132-41. 22.piatt jh. hydrocephalus; trearment. in wilkins rh. rengachary ss (eds): neurosurgery. new-york: mcgraw-hill 1996, pp: 3633-3643 romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article morphometric analysis of the arteries of willis polygon huseyin canaz, murat arslan, husniye hacıoglu, mehmet tokmak, gokhan canaz, safiye cavdar turkey doi: 10.2478/romneu-2018-0007 56 | canaz et al morphometric analysis of the arteries of willis polygon doi: 10.2478/romneu-2018-0007 morphometric analysis of the arteries of willis polygon huseyin canaz1, murat arslan2, husniye hacıoglu3, mehmet tokmak4, gokhan canaz5, safiye cavdar6 1florence nightingale hospital, istanbul bilim university, department of neurosurgery, istanbul, turkey 2istanbul forensic science institute, morgue department, istanbul, turkey 3marmara university school of medicine, department of anatomy, istanbul, turkey 4istanbul medipol university, department of neurosurgery, istanbul, turkey 5bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery, istanbul, turkey 6koc university school of medicine, department of anatomy, istanbul, turkey abstract: objective: willis polygon forms the basis of the arterial circulation of the cerebrum. willis polygon is a vascular structure whom variations are not rare. knowledge of the anatomy and preservation of its integrity is crucial for performing neurovascular surgery and intracranial tumour surgery. because of the important vascular and neurological structures, approaches to this region are considered extremely risky. one of the main variations in-person basis is the diameter differences of the arteries, which forms willis polygon, between the left and right hemispheres. about structure and variations, studies of rhoton and yasargil had formed the touchstone. our aim is to contribute to the literature and clinical studies, to be done in the future, by comparing our results with previous studies about variations and morphometric features of willis polygon. methods: arteries of 30 fresh cadaver brains were examined during autopsies in t.c. ministry of justice istanbul forensic science institute. bilaterally anterior cerebral artery a1 segment lengths, distance between anterior communicating artery-callosomarginal artery outputs, posterior cerebral artery p1 segment lengths were measured using a digital calliper. after dissections and measures, photos of the region were taken and vascular anatomy and variations noted. from every single cerebrum samples were obtained from bilaterally a1, a2, callosomarginal artery, middle cerebral artery, posterior communicant artery, p1 and basilar artery. samples were fixed by using 10% buffered-formalin. taken samples were transported to marmara university faculty of medicine, department of anatomy laboratory. samples were examined and interior diameters were measured under the microscope. results: our results with artery diameters and lengths were similar with literature. different from literature, in anterior cerebral artery a1 segment, posterior cerebral artery p1 segment and posterior romanian neurosurgery (2018) xxxii 1: 56 64 | 57 communicant artery no aplasia were noted. in 50% of the samples, callosomarginal artery were originate from a2 segment. in one case, we observed left and right pericallosal arteries were joined together at the end of the a2 segment and continued as a single pericallosal artery. we could not find any information about this variation in the literature. conclusion: before surgical operations, detailed knowledge of willis polygon and evaluation of the pre-op cerebral angiography considering possible variations, reduce mortality and morbidity ratios. in addition, because of the role of flow gradients of willis polygon in aneurysm formation, and in terms of better understanding the collateral circulation which is important in vascular occlusive diseases and vascular surgery, we believe, more anatomic studies about this region needed. key words: willis polygon, circle of willis, morphometric analysis introduction willis polygon forms the basis of the arterial circulation of the cerebrum (figure 1). willis polygon is a vascular structure whom variations are not rare (1, 3). knowledge of the anatomy and preservation of its integrity is crucial for performing neurovascular surgery and intracranial tumour surgery. because of the important vascular and neurological structures, approaches to this region are considered extremely risky (16). one of the main variations in-person basis is the diameter differences of the arteries, which forms willis polygon, between the left and right hemispheres (5). about structures and variations, studies of rhoton and yasargil had formed the touchstone (10, 16). our aim is to contribute to the literature and to the clinical studies, to be done in the future, by comparing our results with previous studies about variations and morphometric features of willis polygon. material and method to evaluate the morphological characteristics of the willis polygon and its constituent arteries in the turkish population, arteries of 30 fresh cadaver brains (60 hemispheres) were examined during routine autopsies in t.c. ministry of justice istanbul forensic science institute. all the protocols were conducted with the consent of t.c. ministry of justice istanbul forensic science institute, board of science. for the study, cadavers aged between 25 – 50 years old, without head injury were selected. during routine autopsies, after calvarium removal, cerebrums were removed with caution by preserving vessels. on removed cerebrums, arteries of willis polygon were dissected macroscopically and examined (figure 2). bilaterally anterior cerebral artery (aca) a1 segment lengths, distance between anterior communicating artery (acoma)callosomarginal artery (cma) outputs, posterior communicating artery (pcoma), posterior cerebral artery(pca) p1 segment lengths were measured using digital calliper. after dissections and measurements, vascular anatomy and variations were documented by taking photos of the region. from every single cerebrum, samples were obtained from bilaterally a1, a2, cma, middle cerebral artery (mca), pcoma, p1 and basilar artery (ba). samples were fixed by using 10% 58 | canaz et al morphometric analysis of the arteries of willis polygon buffered-formaldehyde. taken samples were examined and interior diameters were measured under a microscope in marmara university faculty of medicine, department of anatomy laboratory (figure 3). statistical evaluations were made using the statistical package for social scienses (spss) 22.0 (chicago, il). all continuous variables were reported as median±standart deviations (sd). figure 1 illustration of arteries that form willis polygon. aca: anterior cerebral artery, acoa: anterior communicating artery, mca: middle cerebral artery, pcoa: posterior communicating artery, pca: posterior cerebral artery, ba: basilar artery figure 2 arteries of willis polygon. aca: anterior cerebral artery, acoa: anterior communicating artery, mca: middle cerebral artery, pcoa: posterior communicating artery, pca: posterior cerebral artery, ba: basilar artery figure 3 microscopic image of an artery sample results in our study, we used 30 cadaver cerebrums with no head trauma (14 female, 16 male). a1 segment a1 segment diameters on the right were measured as maximum 2104.593 µ, minium 1039.152 µ and median was 1540.092±366.9 µ. on the left, maximum 2699.584 µ, minimum 1247.152 µ and median was 1841.398±355.0 µ (table 1). a1 segment lengths on the right were measured as maximum 18mm, minimum 10mm and median was 13.56±2.25mm. on the left, maximum 17mm, minimum 10mm and median was 13.76±1.87mm (table 1) (figure 4). a2 segment a2 segment diameters on the right were measured as maximum 2185.284 µ, minimum 1627.145 µ and median was 1860.174±129.5 µ. on the left, maximum 2148.649 µ, minimum 1699.004 µ and median was 1841.061±14.6 µ (table 1). a2 segment lengths on both right and left were measured as maximum 25mm, romanian neurosurgery (2018) xxxii 1: 56 64 | 59 minimum 14mm. median on the right was 18.83±3.81mm and on the left was 18.73±3.02mm (table 1) (figure 4). posterior communicating artery pcoma diameters on the right were measured maximum 1394.94µ, minimum 638.17µ and median was 881.377±170.9µ. on the left, maximum 1410.156µ, minimum 648.95µ and median was 892.247±201.4µ. posterior communicant artery lengths on the right were measured as maximum 26mm, minimum 11mm and median was 15.63±3.39mm. on the left, maximum 24mm, minimum 11mm and median was 15.9±3.24mm (table 1). p1 segment p1 segment diameters on the right were measured as maximum 2529.639 µ, minimum 902.703µ and median was 1807.549±402.42µ. on the left, maximum 2548.47µ, minimum 948.29µ and median was 1809.082±350.05µ (table 1). p1 segment lengths on the right were measured as maximum 11mm, minimum 5mm and median was 7.033±1.44mm. on the left, maximum 10mm, minimum 5mm and median was 6.933±1.2mm (table 1) (figure 5). middle cerebral artery mca diameters on the right were measured maximum 3017.994µ, minimum 2645.399µ and median was 2819.351±101.01µ. on the left, maximum 2992.678µ, minimum 2649.495µ and median was 2819.284±94.18µ. basilar artery basilar artery diameters were maximum 3040.072µ, minimum 1939.17µ and median was 2722.276±247.57µ (figure 5). callosomarginal artery cma diameters on the right were measured as maximum 1489.14µ, minium 836.447µ and median was 1232,402±152,51µ. on the left, maximum 2805.314µ, minimum 932.184µ and median was 1267,75±361,99µ (figure 6). cma was observed in 3 cases only on the right side and in 1 case, only on the left side. in two case bilaterally cma was absent. the origins of cma were, left a3 in 10 cases, left a2 in 15 cases and right a3 in 12 cases, right a2 in 15 cases. in 11 cases, cma were originated from different segments. table 1 diameter and length measurements of arteries of the willis polygon as mean, minimum and maximum blood vessels mean min. max. a1 diameter (µ) right 1540.092±366.9 1039.153 2104.593 diameter (µ) left 1841.398±355.0 1247.152 2699.584 length (mm) right 13.56±2.25 10 18 length (mm) left 13.76±1.87 10 17 60 | canaz et al morphometric analysis of the arteries of willis polygon a2 diameter (µ) right 1860.174±129.5 1627.145 2185.284 diameter (µ) left 1841.061±14.6 1699.004 2148.649 length (mm) right 18.83±3.18 14 25 length (mm) left 18.73±3.02 14 25 pcoma diameter (µ) right 881.377±170.9 638.17 1394.94 diameter (µ) left 892.247±201.4 648.95 1410.156 length (mm) right 15.63±3.39 11 26 length (mm) left 15.9±3.24 11 24 p1 diameter (µ) right 1807.549±402.42 902.703 2529.639 diameter (µ) left 1809.082±350.05 948.29 2548.47 length (mm) right 7.033±1.44 5 11 length (mm) left 6.933±1.2 5 10 mca diameter (µ) right 2819.351±101.01 2645.399 3017.994 diameter (µ) left 2819.284±94.18 2649.495 2992.678 ba diameter (µ) 2722.276±247.57 1939.17 3040.072 cma diameter (µ) right 1232,402±152,51 836.447 1489.14 diameter (µ) left 1267,75±361,99 932.184 2805.314 figure 4 a1 and a2 segments of aca figure 5 p1 segment of pca and ba romanian neurosurgery (2018) xxxii 1: 56 64 | 61 figure 6 cma: callosomarginal artery discussion the blood circulation of the cerebrum is formed by 4 arteries as two internal carotid arteries and two vertebral arteries. internal carotid arteries form the anterior system and vertebral arteries form the posterior system. at the base of the cerebrum, the vascular web that creates the connection between these two systems is named as the “circle of willis”, or “willis polygon” (1, 10) vessels participating the structure of the polygon are two ica’s, two aca’s, acoma, two pcoma’s, two pca’s, ba and two mca’s (1, 9). willis polygon provides collateral circulation between vertebrobasilar system and carotid system, and in-between cerebral hemispheres. direction of flow inside the polygon is determined by vessel diameters and pressure gradient. the efficiency of this collateral circulation is the main determinant of the degree of neurological deficits, in case of stenosis or occlusion in one of the main feeder arteries (2, 6). many variations in the anatomy of the willis polygon had been shown and the configuration which could be described as normal is seen in only 50% of the population (6, 9, 11). approaches to this region are frequently caused by tumours, endovascular interventions and vascular pathologies such as aneurysms and arteriovenous malformations. with better understanding of the region anatomy, lower complication and rates better outcomes would be achieved. besides differences in configuration, variations in willis polygon are also caused by differences in vessel diameters and lengths (11). in our study, in 19 (63%) cadavers left a1 inner diameters were measured wider and in 11 (37%) cadavers right a1 inner diameters were wider. differences were significant in 15 (50%) cadavers for the left a1 and 8 (26.6%) cadavers for the right a1. in 13 cases (43%), left a1 were longer than right a1 and in 9 cases (30%) vice versa. in 8 cases (27%) bilaterally a1's were the same length. diameter differences between a1 segments have great value on formation mechanisms of acoma aneurysms. as a general rule, in case of diameter difference between a1 segments, acoma aneurysms were originated from the wider side. if the left and right a1 diameters were equal then acom aneurysms more likely to originate from the middle portion (14, 15). it is reported that, in 10%, a1 segment could be one sided hypoplastic or aplastic (12). a1 hypoplasia is associated with anterior communicating artery aneurysms in 85% of cases. this is the only known variant which is correlated with cerebral aneurysm localization and formation (9). in our study, we did not observe any hypoplastic or aplastic a1 segment. a1 segment aneurysms forms 1.4% of all intracranial aneurysms (15). ipsilateral fronto-temporo-sphenoidal craniotomy were 62 | canaz et al morphometric analysis of the arteries of willis polygon suggested as most suitable approach for aneurysms of this area (15). in 19 cadavers (63%) right a2 inner diameter was wider than left a2. in 10 cadavers (33%) left a2 was wider but the difference was not significant. in one case we observed that after acoma, left aca was ended with branching on the medial surface of left hemisphere. the right aca was continuing as the only pericallosal artery, and then in the beginning of a3 divided and continued as two pericallosal arteries. in literature it is reported that pericallosal arteries might origin from single log, but no ratio was reported (12). in our study, occurance rate of this variation were 3.3%. in addition, in one case we observed that left and right pericallosal arteries were joined together at the end of a2 and continued as one single pericallosal artery. we could not find any information about this variation in the literature. in yasargil’s series, pericallosal artery aneurysms are reported as 5.6% of acoaaca aneurysms, and as 2.3% of the all intracranial aneurysms (15). pericallosal artery aneurysms are mostly seen on a2 segment (4). in our literature research, we noted that on proximal side of cma and frontopolar artery, aneurysms were more frequent (1, 15). interhemispheric approach, following paramedian frontal craniotomy, has been been using for pericallosal artery aneurysms (15). distal aca aneurysm surgeries have its own difficulties. because of interhemispheric fissure and callosal cistern are narrow areas, lumbar drainage would be helpful to widen the workspace. falx depth could be low and consequently there might be adhesions between both cingulate gyruses. aneurysms of this area are often large based and sclerotic, and frequently involve the vessels which branch from here. sclerosis could occur on both aneurysm fundus and contralateral pericallosal artery, as a result adhesions between these two structures may occur. this can cause difficulties during dissection. some of the time, it is hard to tell, from which aca, the aneurysm was originated and angiography would not be clear. dome of the aneurysm can be adhered to piamater over cingulate gyrus or it could be buried inside the cingulate gyrus. for all of these, retraction of frontal lobe should be done minimal and with extreme caution. (15). acoa is the artery, where the most of the variations observed in willis polygon (7). it can be as a single line or lines or as a vascular web (10). in our study, in 21 cadavers (70%) acoa was as a single line; in 2 cadavers (6.6%) it was as a conjoint of both aca’s; in 4 cadavers (13.3%) it was formed by 3 or 4 thin vessels; in 3 cadavers (10%) it was web-formed. because of the large number of studies about acoa and it is a detailed, deep subject; morphological analysis of this artery was not conducted. in 12 of the cadavers (40%) left pca inner diameter was wider than right pca. in 18 cadavers (60%) right pca was wider. there were significant differences on 7 cases (4 left pca (13.3%), 3 right pca (10%)). in 18 cadavers (60%) we measured the left pca longer than right, and in 12 cadavers (40) right pca was longer. basilar artery starts with two vertebral arteries joining together in pontomedullary romanian neurosurgery (2018) xxxii 1: 56 64 | 63 sulcus area and continues through prepontine cistern. with age, basilar artery may become more twisted, longer and the bifurcation may be positioned at a higher level (16). 15% of the saccular aneurysms occur in vertebrobasilar system, and 63% of them occur on basilar bifurcation. the concomitance of anomalies such as hypoplastic pca or pca, with basilar bifurcation aneurysms, is significantly high (8). in 3 of the cadavers (10%), only left callosomarginal artery were missing. right callosomarginal artery was missing in only one cadaver (3,3%). in 2 cadavers (6,6%) bilaterally callosomarginal arteries were absent. in rhoton’s series, it is reported that callosomarginal artery were missing in 20% of the examined hemispheres (8)(66). in our study, among 60 hemispheres, the callosomarginal artery was absent in total 8 hemispheres. callosomarginal artery is the largest branch of the pericallosal artery and mostly takes origin from the a3 segment, but it can also take origin from a2 or a4 (9). in our study, callosomarginal artery was taking origin from left a3 in 10 cases, left a2 in 15 cases, right a3 in 12 cases and right a2 in 15 cases. in 11 cases, callosomarginal arteries origins were different segments. in total 60 hemispheres, 22(36.6%) of the callosomarginal artery were originated from a3 segments and 30 of the arteries (50%) were originated from a2 segments. we saw no significant relationship between artery lengths and diameters. in our study, our results were consistent with the literature most of the time. it is reported that a1, p1 and pcoa segments could be aplastic in 10%; but we did not encounter this variation in any of our cases. conclusion flow strength, intravascular pressure, turbulent flow and artery wall disorders in bifurcation areas takes part in aneurysm pathophysiology (13). willis polygon, which provides a collateral circulation between carotid and vertebrobasilar system, is a place that intracerebral aneurysms frequently take place. the gold standard treatment of the intracranial aneurysm is still the clipping. mastering the anatomy of willis polygon and pre-operative analyses of angiography, considering possible variations, is crucial to decrease mortality and morbidity of this serious operations. in terms of better understanding the collateral circulation which is important in vascular occlusive diseases and vascular surgery, we believe, more anatomic studies about this region needed. correspondence gokhan canaz, bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery 34147 bakırkoy/istanbul. tel: +90 212 409 15 15 mobile: +90 536 944 94 39 email: gokhancanaz@gmail.com references 1alpers bj, berry rg, paddison rm. anatomical studies of the circle of willis in normal brain. ama archives of neurology and psychiatry 1959;81:409-418. 2arnold u, lehmann r, kursawe h-k, lückel w. hypoplasia of vertebrobasilar arteries; in du boulay g, molyneux a, moseley i (eds): proceedings of the xiv 64 | canaz et al morphometric analysis of the arteries of willis polygon symposium neuroradiologicum: london, 17–23 june 1990. berlin, heidelberg, springer berlin heidelberg, 1991, pp 426-427. 3bouthillier a, van loveren hr, keller jt. segments of the internal carotid artery: a new classification. neurosurgery 1996;38:425-432; discussion 432-423. 4cinnamon j, zito j, chalif dj, gorey mt, black ks, scuderi dm, hyman ra. aneurysm of the azygos pericallosal artery: diagnosis by mr imaging and mr angiography. ajnr american journal of neuroradiology 1992;13:280-282. 5morris p. practical neuroangiography. lippincott williams & wilkins, 2007. 6mumenthaler m, toole jf, patel an, caffi j, iff-knopf k. zerebro-vaskuläre störungen: mit kapiteln über angewandte embryologie, anatomie der gefäße und physiologie des gehirns und des rückenmarks. springer berlin heidelberg, 2013. 7nathal e, yasui n, sampei t, suzuki a. intraoperative anatomical studies in patients with aneurysms of the anterior communicating artery complex. journal of neurosurgery 1992;76:629-634. 8rhoton al, jr. aneurysms. neurosurgery 2002;51:s121158. 9rhoton al, jr. the supratentorial arteries. neurosurgery 2002;51:s53-120. 10rhoton al, jr., saeki n, perlmutter d, zeal a. microsurgical anatomy of common aneurysm sites. clinical neurosurgery 1979;26:248-306. 11saeki n, rhoton al, jr. microsurgical anatomy of the upper basilar artery and the posterior circle of willis. journal of neurosurgery 1977;46:563-578. 12schünke m, schulte e, schumacher u. prometheus lernatlas der anatomie: kopf, hals und neuroanatomie ; 115 tabellen. thieme, 2009. 13toole jf, murros k, veltkamp r. cerebrovascular disorders. lippincott williams & wilkins, 1999. 14ujiie h, liepsch dw, goetz m, yamaguchi r, yonetani h, takakura k. hemodynamic study of the anterior communicating artery. stroke 1996;27:20862093; discussion 2094. 15yaşargil mg. microneurosurgery. georg thieme verlag, 1984. 16yaşargil mg. microneurosurgery vol.1. georg thieme verlag, 1984. 07 07canazhuseyin_morphometric romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article retrieval of a retained broken scalpel blade from lumbar intervertebral disc space a case report yogesh agrawal, somnath sharma, sanjeev chopra, devendra kumar purohit india doi: 10.1515/romneu-2017-0020 romanian neurosurgery (2017) xxxi 1: 129 – 132 | 129             doi: 10.1515/romneu-2017-0020 retrieval of a retained broken scalpel blade from lumbar intervertebral disc space a case report yogesh agrawal, somnath sharma, sanjeev chopra, devendra kumar purohit department of neurosurgery, sawai man singh medical college and hospital jaipur, rajasthan, india abstract: lumbar diskectomy is a common procedure in neurosurgery, besides the common complications broken scalpel blade during disc removal is a rare event. usually retrieval of such sharp retained fragments in same sitting is difficult and to prevent further complications another session is warranted [1]. we report a case of broken scalpel blade during l1-l2 lumbar intervertebral disc removal and successful surgical retrieval of that tip of knife with the help of operative microscope under fluoroscopic guidance during same sitting before any hazardous complications develop. key words: broken scalpel, fluoroscopy, retrieval introduction lumbar diskectomy is being done in increasing frequency worldwide, one such risk associated with this procedure is breaking of the surgical knife blade during disc removal. the complications caused by iatrogenic foreign bodies are well known, but cases are rarely published because of the medico legal implications [2], early identification and removal of a foreign body can prevent hazardous and detrimental complications [3]. however in a few cases, surgeon's attempts might be successful but most of the broken blades could not be retrieved during the initial surgery because it is lost in disc space and attempt to remove cause further descent of fragment so procedure is terminated [1], this retained foreign body in the disc space may remain clinically silent [4] or migration of such foreign body during ambulation might have lead to hazardous complications [3] and removal of such sharp fragment to prevent further complications, another session is warranted usually [1], literature regarding this issue is scarce, and there are no unique guidelines to address these complications. we are reporting a case in which scalpel blade broken during lumber intervertebral disc removal and successful surgical retrieval of that tip of knife blade done in same sitting with the help of microscope under fluoroscopic guidance before any hazardous complication develop. 130 | agrawal et al retrieval of a retained broken scalpel blade             case summury a 29 year male presented with complain of back pain for last 6 month and sudden weakness in bilateral lower limb with urinary and fecal incontinence for last 10 days. imaging confirm significant compression of thecal sac and b/l neural foraminas at l1/l2 vertebra level due to intervertebral disc herniation (figure 1) hence l1 laminectomy and l1/l2 disc removal was planned, while removing the intervertebral disc the tip of no. 15 scalpel blade (figure 4) snapped off and was jammed in the disc space, attempts to retrieve the tip resulted in a further descend of the knife into the disc space, fluoroscopy revealed that knife was still in the disc space (figures 2, 3). owing to the risk of migration further attempt of blind removal was stopped and by using microscope under fluoroscopic guidance we catch the tip and exteriorized successfully before any hazardous complication develop. figure 1 – saggital t2w mri of dorso-lumbar region showing l1/l2 inter-vertebral disc protrudion with thecal sac compression romanian neurosurgery (2017) xxxi 1: 129 – 132 | 131             discussion among common complications that occur during intervertebral disc removal, retained foreign body like broken scalpel blade are rare, very few cases are reported in literature. first case series of four cases on retained foreign body (broken knife) within the disc space and migration towards abdominal cavity and viscera was published by amirjamshidi et al in 1994. the no 15 knife blade with narrow junction is more prone to break during cutting of firm and calcified annulus and posterior longitudinal ligament. the broken fragment may be seen within disc space and can be removed in same setting. however attempts to remove it, can cause further descent of fragment in deep disc space and fluoroscopy and better illumination is required for removal of such fragment ,if such facility in operative room is not available, surgeon should close the wound and refer the patient to center where these facilities are available. in that cases patient should be informed and kept under close observations. retrieval of a broken knife blade buried in the intervertebral disc space can be a challenge and even impossible to achieve despite hours of attempts hence second surgery is recommended in most of case [1]. 132 | agrawal et al retrieval of a retained broken scalpel blade             migration these foreign bodies during intra-operative surgical manipulation or ambulation in postoperative period could led to serious complications and the clinical manifestation of these foreign body depends upon their locations and vicinity to the vital structures, anterior migration of the knife could cause gut and retroperitoneal viscera injury or vascular complications like injury to large vessels ,on the other hand posterior migration into the spinal canal could cause injury to spinal cord and neurological deficit [1, 3, 5]. complications due to broken scalpels and migration into the blood circulation or heart has been described by herbert de praetere at al (5). a broken sharp scalpel left in an intervertebral space and slipped to pelvic cavity during an operation of intervertebral disc also reported by le wang at al [6] in our case we need to respond the question whether the object should be retrieve or not ?, conservative treatment is an option in asymptomatic foreign bodies without associated risks, particularly if they are small, smooth, rounded, blunt and minimal contaminated and embedded in and paraspinal muscles. patients in whom the blade is within a collapsing disc space or is pointing towards the vertebral body secondary intervention can be postponed [1]. intervention is necessary if symptomatic, irrespective of their location or asymptomatic patients with sharp foreign body with associated risk factors and possible complications [5]. owing to the risk of hazardous complications, removal was the only option in our case and blind procedure was not appropriate due to the nature of the object. therefore successful localization under fluoroscopic guidance and removal of tip of knife was done with the help of operative microscopic in our patient in same sitting. conclusion because of the potential hazards of migration and late serious complications, removal of sharp retained fragment in same or another session is recommended and we have to be cautious while using 15 no surgical knife in narrow disc space. correspondence dr. yogesh agrawal mbbs, ms, 3rd year mch resident address: department of neurosurgery, sawai man singh medical college and hospital jaipur, rajasthan, india phone: 08955560199 e-mail: agrawaly_2k@yahoo.co.in references 1. amirjamshidi a, mehrazin m, abbassioun k, ketabtchi e. retained broken knife blades within the disc space. spine 1994;19:981-4. 2. karcnik tj, nazarian ln, rao vm, gibbons ge jr. foreign body granuloma simulating solid neoplasm on mr. clin imaging 1997;21:269-72 3. alexander ph chan, km sieh,sm leung ,ky cheung, ky fungextacorporeal foley catheter spring device mimicking an intervertebral foreign body in transforaminal lumbar interbody fusion surgery.hongkong med j vol no. 5,oct 2009 4. okten ai, adam m, gezercan y. textiloma: a case of foreign body mimicking a spinal mass. eur spine j 2006;15 suppl 5:626s-629s. 5. migration of a broken scalpel into the heart after spine surgery herbert de praetere, caroline vanden eycken, bart meuris, and paul herijgers interact cardiovasc thorac surg. 2014apr;18(4): 527–529 6. a broken sharp scalpel left in an intervertebral space and slipped to pelvic cavity during an operation of intervertebral disc displacement h li, w wang, a he hunan yi ke da xue xue bao hunan yike, 1997 europepmc.org   doi: 10.33962/roneuro-2021-010 volumetric threshold of pituitary macroadenoma as a predictor to visual impairment. clinical correlation mohamed elsherbini, mahmoud saad, mohamed deniwar romanian neurosurgery (2021) xxxv (1): pp. 66-70 doi: 10.33962/roneuro-2021-010 www.journals.lapub.co.uk/index.php/roneurosurgery volumetric threshold of pituitary macroadenoma as a predictor to visual impairment. clinical correlation mohamed elsherbini, mahmoud saad, mohamed deniwar mansoura university hospital, elgomhoreya st., mansoura, egypt abstract purpose: in this study, we aimed at correlating the curve of visual impairment against pituitary macroadenoma size. method: in this study, we retrospectively analyzed the visual correlation between the volume and dimensions of pituitary adenoma and the degree of visual impairment on patients’ examination. 35 patients with no history of eye or refraction disorder were included in the study. spearman correlation test was used to validate the correlation. results: 57 % of pituitary macroadenoma patients suffer from visual impairment, even if not the primary presentation. macroadenomas greater than 5 cm³ in volume and/or 2 cm height are more likely to cause various degrees of visual impairment, this correlation is not linear beyond these values. conclusion: visual impairment due to pituitary adenomas is more frequent than the presentation, the threshold volume is 5 cm³ and height is 2 cm, bigger adenomas behaviour is more multifactorial than the only size. introduction pituitary gland lesions are commonly associated with visual manifestations at different levels, either as the primary presentation, or as a finding during neurological examination. these manifestations are explained by the intimate relationship between the pituitary gland and the visual pathway. the pituitary gland is covered superiorly by the diaphragma sellae; a fibrous dural layer with a small opening called the diaphragmatic hiatus through which the infundibulum courses. the suprasellar cistern is located above the diaphragma sellae and separates it from the optic chiasm. the suprasellar cistern is first compressed by pituitary tumors before their growth proceeds to compress the optic chiasm. the size of the pituitary gland varies along life and differs from male to female; at birth it weights around 100 mg, while in adulthood it reaches up to 500 mg with tendency to be bigger in females especially during puberty, pregnancy and lactation. in adults it measures around 8-10 mm and reaches 12 mm in females during lactation. (cox and elster 1991). keywords visual impairment, optic compression, pituitary, macroadenoma corresponding author: mohamed elsherbini mansoura university hospital, elgomhoreya st., mansoura, egypt m_elsherbiny@mans.edu.eg copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 67 volumetric threshold of pituitary macroadenoma as a predictor to visual impairment pituitary adenomas, when increase in size, may lead to visual impairment via direct optic pathway compression which leads to neuronal injury via blocking axonal conduction, blocking axoplasmic flow or/and demyelination. (munoz negrete and rebolleda 2002) chronic optic pathway compression leads to optic atrophy which is irreversible, this is more noted in non-functioning pituitary adenoma patients since secretory lesions tend to present earlier by hormonal imbalance. (jagannathan, dumont et al. 2005). direct optic pathway compression, though a primitive explanation, is not the only mechanism for visual impairment in patients with pituitary macroadenoma. the course of visual deterioration in relation to volume and height of the tumor is an important key to understanding the pathological process since the size of the tumor is the best predictor for visual recovery. (monteiro, zambon et al. 2010). patients and methods patients data data of patients admitted to mansoura university hospital with sellar lesion between 2017 and 2019 were reviewed and analyzed. only patients with lesions larger than 10 mm in at least one dimension were included, patients with incomplete medical reports were excluded. visual acuity visual acuity is recorded in decimal method where values are obtained on snellen’s chart, while severe visual impairment values are given according to grover et (grover, fishman et al. 1999) al ; 0.0025 for cf “counting fingers”, 0.002 for hm “hand movement”, 0.0016 for “light perception” (lp), and 0.0013 for nlp “no perception of light”. values from both eyes are summed giving each patient a single value representing visual acuity in both eyes. patients with history of eye surgeries and/or other local eye pathologies were excluded. measurement dimensions of the lesions are measured on mri t1 with contrast axial, coronal and sagittal to obtain largest horizontal, vertical and ap diameters respectively. the volume of the tumor was calculated using the traditional geometric formula; ½ (length x width x height), patients with recurrent lesions were excluded since according to chi-cheng chuanf (chuang, lin et al. 2017) the traditional formula is not applicable for recurrent cases while it proves high degree of accuracy for primary lesions. pathology lesions were classified into functioning and nonfunctioning according to patients’ pre-operative serum hormonal levels. histopathological examination reports were reviewed, patients with lesions other than pituitary adenomas were excluded. statistical analysis spearman correlation test was used to compare visual acuity values to adenoma volume and each dimension individually. prism graphpad version 5 software was used to perform statistical analysis. results 35 patients were included in the study, 18 of them were males (51 %), mean age was 46.3 years which ranged from 23 to 75 years. most common primary presentation is hormonal related symptoms, collectively, in 15 patients, followed headache in 13 patients, while visual impairment was the primary presentation for only 7 patients (20 %). (table 1). number, % gender: male female 18 (51.4 %) 17 clinical presentation: endocrinal headache visual 15 (42.9 %) 13 (37.1 %) 7 (20 %) visual acuity: intact mean visual acuity 7 (20 %) 0.77 tumor size: min max mean 0.6 cm³ 40 cm³ 12.3 cm³ pathology: non-secretory gh secreting acromegaly impotence prolactin secreting amenorrhea accidentally discovered 16 (45.7 %) 7 (20 %) 6 1 10 (28.6 %) 4 4 68 mohamed elsherbini, mahmoud saad, mohamed deniwar galactorrhea impotence acth secreting (cushing) 1 1 2 visual impairment was the secondary complaint in 13 patients (37 %) and on examination only 7 patients (20%) showed intact visual acuity (2/2). 19 adenomas were secretory, 15 of these patients’ primary presentation was hormonal related symptoms and 4 were accidentally discovered during pre-operative lab assessment. acromegaly was the most common hormonal presentation in 6 patients (31.5 %), amenorrhea in 4, cushing in 2, male sexual dysfunction in 2 and galactorrhea in one patient. pathologically, among the 19 secretory adenomas prolactin secreting was of the highest incidence in 10 patients, gh secreting in 7 and acth secreting in 2 patients. male sexual dysfunction was the primary presentation for both prolactin and gh secreting adenomas, one patient each. visual acuity mean is 0.77 for the sum of both eyes, ranged from no pl in one eye to intact vision (2). mean tumor volume was 13.3 cm³, ranged from 0.6 to 40 cm³. mean ap diameter, width and height were 2.57, 2.65 and 2.86 cm respectively. according to spearman correlation test, visual acuity impairment is negatively correlated to lesions greater than 5 cc in volume (r – 0.67, p < 0.001, fig 1) and greater than 2 cm in height (r – 0.6, p < 0.001, fig 2), beyond these values visual acuity impairment was not in a linear relationship neither to tumor volume nor height. 0 10 20 30 40 50 0.0 0.5 1.0 1.5 2.0 2.5 volume (cm³) v is u a l a c u it y figure 1. representing visual acuity to tumor volume (cm³) correlation, showing just 2 patients with visual impairment with lesions less than 5 cm³, while strong negative correlation right to the 5 cm³ value (r – 0.67), but not linear. 0 2 4 6 0.0 0.5 1.0 1.5 2.0 2.5 height (cm) v is u a l a c u it y figure 2. representing visual acuity to tumor height (cm) correlation, showing just 2 patients with visual impairment with lesions less than 2 cm, while strong negative correlation right to the 2 cm value (r – 0.6), but not linear. illustrative cases case 1 41 years old male presented with acromegalic features and sexual dysfunction. hormonal assay showed elevated serum growth hormone level. radiologically detected 3 x 3.5 x 3 cm lesion with severe chiasm displacement and stretch, fig 3. visual acuity was 0.67 and 0.33 for right and left eyes respectively. figure 3. case 1, coronal mri with contrast showing 3 x 3.5 x 3 cm lesion with severe chiasm displacement and stretch (red arrow). case 2 33 years old female lady presented with typical cushing syndrome, elevated serum cortisol, no significant visual affection, mri with contrast showed pituitary lesion 1.1 x 0.5 x 0.3 cm with no chiasm compression, fig 4. typical hormonal presentation prior optic compression. figure 4. case 2, coronal mri with contrast showing lesion 1.1 x 0.5 x 0.3 cm with no chiasm compression (red arrow). 69 volumetric threshold of pituitary macroadenoma as a predictor to visual impairment case 3 55 years old post-menopausal lady presented with visual impairment; hormonal assay showed elevated serum prolactin which was not the primary presentation as the patient was postmenopausal; amenorrhea. lesion dimensions were 2.5 x 3.8 x 2.5 cm with severe chiasmatic compression and corresponding visual acuity npl and hm in right and left eye respectively, fig 5. figure 5. case 3, coronal mri with contrast showing lesion 2.5 x 3.8 x 2.5 cm with severe chiasmatic compression and stretch. case 4 40 years old lady presented with visual impairment, examination showed visual acuity of hm and cf in right and left eye respectively. dimensions of the lesion in mri were 2x2.2x2.7 cm with severe optic compression, fig 6. figure 6. case 4, coronal mri with contrast showing a 2x2.2x2.7 cm lesion. discussion pituitary adenomas are the most common tumor of the sellar region representing 10-15% of all intracranial neoplasm, they are classified according to size into microadenomas and macroadenomas; greater than 10 mm(asa and ezzat 2009). macroadenomas start confined to the sella, the earliest extra-sellar extension is the upward growth into suprasellar cistern, this is anatomically explained by the hard-bony relationship in other directions. less commonly macroadenomas are seen extending into the sphenoid sinus downwards, or laterally encasing the ica within the cavernous sinus. (ouyang, rothfus et al. 2011) headache is the most common presentation of pituitary adenoma (kim, jin et al. 2019), in this study headache was the first primary presentation if hormonal presentations are separately listed, while hormonal presentation, in total, are of higher incidence. it’s noted that patients with secretory adenomas seek medical advice in early stages due to hormonal related symptoms prior to visual pathway compression, except when amenorrhea is masked by menopause, case 3. though it’s not the most common presentation, optic pathway compression is eventual when the tumor volume exceeds certain limit, functioning adenomas tend to present early with hormonal manifestations prior to visual presentation, this was also concluded by brada et al (brada, rajan et al. 1993) who reported visual compression in 73 % of non-functioning adenoma patients, while only in 44.7 % in functioning ones. in the current study, examination showed 28 patients (80%) of patients were found to have various degrees of visual impairment, taking in consideration that patients with history of errors of refraction and/or eye pathology were excluded, the incidence of visual impairment due to pituitary macroadenoma is higher than presentation which in this study was (20 patients, 57 %); with either main or secondary complaint. visual acuity deficits due to optic pathway compression by pituitary tumors are studied in several publications (kim, jin et al. 2019) (kasputyte, slatkeviciene et al. 2013) (wang, sun et al. 2008), as well as explained by the anatomical relationship of the pituitary gland to the optic pathway. in this study, the threshold of optic compression regarding volume and height of the tumor is identified. various anatomical factors may affect the degree of optic pathway compression including site of the chiasm and the capacity of suprasellar cistern which anatomically ranges from 8 – 13 mm (rhoton 2002), this may explain the discrepancy between case 1 where the adenoma is greater in size and height than case 3 and yet shows radiologically less optic compression and clinically less visual impairment. the volume of the pituitary tumor can be accurately measured via the traditional equation ½ (length x width x height). this method was validated by chi-cheng chuang et al (chuang, lin et al. 2017) , where the equation was proven to be accurate for pre-operative assessment, but not valid for residual and hence recurrence, recurrent cases where excluded in this study based on that conclusion. similar to our results, h wang et al (wang, sun et al. 2008) reported significant visual impairment in 70 mohamed elsherbini, mahmoud saad, mohamed deniwar patients with hardy’s grade above b, with no significant difference between the groups b, c and d. these results raise the debate regarding various factors affecting chiasm compression course, as for 2 cm height i.e hardy grade b is the threshold for optic manifestations, lack of significant difference among greater sizes may be attributed to other factors including tumor consistency, growth rate and vascular interruption to the optic pathway. anatomical reserve capacity and individual variation of cistern size should be taken in consideration. visual field deficits, though not included in this study, are strongly associated with visual impairment in the majority (76 %) of cases. (wang, sun et al. 2008) unlike previous studies, in this study, visual acuity of both patients’ eyes were summed giving each patient a single value representing visual acuity, authors believe this is a more accurate assessment of overall visual impairment than listing each eye individually, since decussation of optic fibers takes place in optic chiasm which is the most common site of compression. visual acuity impairment is seldomly significant in pituitary microadeoma patients (less than 1 cm) which are usually contained within the sella, while significant visual impairment starts beyond 2 cm height which can be explained by the growth into the supra-sellar cistern i.e transformation to hardy grade b(rilliet, mohr et al. 1981). according to monteiro et al (monteiro, zambon et al. 2010), tumor size was the best predictor for postoperative visual recovery, the author reported that visual acuity is serviceable before optic atrophy develops hence the importance of correlating tumor volume to clinical visual impairment. conclusion pituitary macroadenomas with height greater than 2 cm and/or volume greater than 5 cc are significantly associated with visual acuity impairment, behavior beyond these values (hardy groups b,c and d) is not linear and its course can neither be predicted nor explained by tumor size solely, to predict visual impairment due to pituitary macroadenomas, further multi-factorial studies are encouraged. declarations ethical approval: n/a, retrospective analysis of archive. consent for publication: n/a. availability of data and materials: please contact the author for data requests. competing interests: the authors declare that they have no competing interests. funding: no fund was received for this study. authors’ contribution: me: principle investigator, data collection, statistics and contribution to writing. ms: data collection, revision. md: data collection, contribution to writing, revision and amendments. authors’ information: all authors are staff members of neurosurgery department in mansoura faculty of medicine and its affiliated hospital; mansoura university hospital. references 1. asa, s. l. and s. ezzat (2009). "the pathogenesis of pituitary tumors." annu rev pathol 4: 97-126. 2. brada, m., b. rajan, et al. (1993). "the long-term efficacy of conservative surgery and radiotherapy in the control of pituitary adenomas." clin endocrinol (oxf) 38(6): 571578. 3. chuang, c. c., s. y. lin, et al. (2017). "different volumetric measurement methods for pituitary adenomas and their crucial clinical significance." sci rep 7: 40792. 4. cox, t. d. and a. d. elster (1991). "normal pituitary gland: changes in shape, size, and signal intensity during the 1st year of life at mr imaging." radiology 179(3): 721-724. 5. grover, s., g. a. fishman, et al. (1999). "visual acuity impairment in patients with retinitis pigmentosa at age 45 years or older." ophthalmology 106(9): 1780-1785. 6. jagannathan, j., a. s. dumont, et al. (2005). "genetics of pituitary adenomas: current theories and future implications." neurosurg focus 19(5): e4. 7. kasputyte, r., g. slatkeviciene, et al. (2013). "changes of visual functions in patients with pituitary adenoma." medicina (kaunas) 49(3): 132-137. 8. kim, t. g., k. h. jin, et al. (2019). "clinical characteristics and ophthalmologic findings of pituitary adenoma in korean patients." int ophthalmol 39(1): 21-31. 9. monteiro, m. l., b. k. zambon, et al. (2010). "predictive factors for the development of visual loss in patients with pituitary macroadenomas and for visual recovery after optic pathway decompression." can j ophthalmol 45(4): 404-408. 10. munoz negrete, f. j. and g. rebolleda (2002). "[automated perimetry and neuro-ophthalmology. topographic correlation]." arch soc esp oftalmol 77(8): 413-428. 11. ouyang, t., w. e. rothfus, et al. (2011). "imaging of the pituitary." radiol clin north am 49(3): 549-571, vii. 12. rhoton, a. l., jr. (2002). "the sellar region." neurosurgery 51(4 suppl): s335-374. 13. rilliet, b., g. mohr, et al. (1981). "calcifications in pituitary adenomas." surg neurol 15(4): 249-255. 14. wang, h., w. sun, et al. (2008). "the pattern of visual impairment in patients with pituitary adenoma." j int med res 36(5): 1064-1069. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article large armored bridging over fractured vertebra with intraspinal tumor mimicking bony mass caused by migrated fragments of burst cervical vertebra presenting with severe cervical myelopathy guru dutta satyarthee, luis rafael moscote-salazar india, colombia doi: 10.1515/romneu-2017-0035 romanian neurosurgery (2017) xxxi 2: 215 221 | 215 doi: 10.1515/romneu-2017-0035 large armored bridging over fractured vertebra with intraspinal tumor mimicking bony mass caused by migrated fragments of burst cervical vertebra presenting with severe cervical myelopathy guru dutta satyarthee1, luis rafael moscote-salazar2 1department of neurosurgery, neurosciences centre, aiims new delhi, india 2neurosurgeon-critical care, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia abstract: vertebral body may get displaced anterior or posteror with elements of rotation. however, burst cervical spine vertebral fracture may migrate anteriorly and posteriorly simultaneously. however anterior displaced fragment forming armor like mass is very rare. similarly, the posteriorly propelled fragments migrating caudally and posterolaterally producing a large osseous mass inside spinal canal mimicking bony tumour causing severe cervical canal stenosis and presenting with marked myelopathy is extremely rare. to the best knowledge of authors, association of such traumatic dual pathology represents first of its kind in western literature, who was neglected early medical advice and presenting with marked compressive cervical myelopathy. she underwent successful surgical decompression with gradual recovery of spastic limb weakness and recovery of sensation. authors also highlights the importance of early resuscitation and adequate maintainace of mean arterial pressure following acute spinal cord injury. pertinent literature is briefly reviewed. key words: axial loading, cervical burst fracture, armor like mass, intraspinal large bony mass introduction the unstable cervical spinal injury and its subsequent management is challenging as early diagnosis can be difficult, but a missed spine injury can be associated with devastating long-term consequences. [1] as a dictum spinal column injury is presumed to occur until it is excluded. in a case with suspected cervical spine injury, the neck movement should be minimized and should be transported on a backboard with a semi-rigid collar, with the neck stabilized on the sides of the head with sand bags or glass bottles, taped from side to side of the board. in cases of 216 | satyarthee, moscote-salazar posttraumatic severe cervical myelopathy suspected spinal mal-alignment, skeletal traction with tongs is applied at the earliest even if clinically no evidence of neurologic deficit exists. [2, 3] detailed neuroimaging evaluation is indicated in patient with myelopathy features, altered sensorium from head injury or intoxication with severe neck pain or tenderness or patients of poly-trauma [4, 5, 6] case illustration a 21 – year -old female college student had road traffic accident six months back developed spastic quadriparesis immediately following injury, however, showed gradual improvement over the next three months but again noticed worsening of neurological symptom, which mainly involved difficulty in walking and occasional incontinence of urine. on admission, examination revealed healthy female with stable vitals, neurological evaluation revealed hypertonia of all four limbs with power of 4/5, x-ray cervical spine revealed fracture of the sixth cervical vertebra with presence of a large armor like mass placed anteriorly to verbral body and getting attached at lower part of anterior surface of the fifth cervical vertebra and extending across the sixth and finally attaching to anterior surface of the seventh cervical vertebra. (figure 1). ct cervical spine, sagittal section clearly demarcated the fracture of sixth cervical vertebra with presence of armored mass and also revealed posterolateral migration of vertebral body fragments and disc against posterior surface of upper part c7 body and c6 level into the adjoining spinal canal forming intraspinal large osseous tumor mass producing significant secondary spinal canal stenosis. (figures 2, 3) mri cervical spine, t1 weighted image, revealed presence of intraspinal large mass, probably formed due to migration of vertebral fragments in the postero-lateral and caudal direction in acse of axial loading, producing an osseous mass, which was extensively projecting into the spinal canal at c6 and c7 levels mimicking osseous neoplasms, producing significant secondary canal stenosis with displacement and indentation of thecal sac and also delineated armor like osseous. (figures 4, 5, 6) figure 1 x-ray cervical spine, lateral view showing collapse of sixth cervical vertebra (small arrow head) with arched large bony mass like an armored fused with fifth vertebra (horizontal large arrow) romanian neurosurgery (2017) xxxi 2: 215 221 | 217 figure 2 ncct cervical spine, axial section image at seventh cervical vertebral body showing caudal migrated posterolateral fragment causing formation of an intraspinal large mass producing severe canal stenosis (large arrow head) figure 3 ncct cervical spine, sagittal section showing fracture of sixth cervical vertebra with posterolateral migration of disc against c7 body (arrow head) and cranial migrating and fused with fifth cervical forming large armor extending across the collapsed sixth cervical vertebra figure 4 mri sagittal section, t1 weighted image, showing intraspinal large bony mass lying against seventh cervical body a (small arrow head) and also armored like mass anterior bridging over collapsed sixth cervical vertebra (large arrow) figure 5 mri sagittal section, t2 weighted image, showing fracture of sixth cervical vertebra with postero-lateral and caudal migration of disc fragment lying against seventh cervical body (arrow head) 218 | satyarthee, moscote-salazar posttraumatic severe cervical myelopathy figure 6 mri axial section t2weighted image showing fracture fragments of sixth cervical vertebra with postero-lateral migration and lying against c7 she underwent surgery through anterior cervical approach and corpectomy of sixth cervical vertebra along with c5-6 and c67 discectomy was carried out. removal of anteriorly placed large armor like bony mass, which was covering fifth and most of sixth vertebral body was completely drilled out using midas diamond drill. intraoperative, presence of a large intraspinal space occupying bony mass lesion was noted, which was producing marked canal stenosis, under microscopic assistance meticulous drilling was also carried out with mida’s rex cutting and diamonds drill very patiently. the consistency of armored mass and intraspinal fragments were very hard and extremely vascular, while the latter was adherent to posterior longitudinal ligaments. adequate thecal sac decompression was finally achieved, posterior osteophyte of c5 and c7 level was also removed and adequate removal of posterior longitudinal ligament was carried out intraoperatively, however, no dural breach was noted. at the end of surgery, thecal sac was lax and nicely pulsating. after achieving adequate hemostasis, appropriate sized iliac crest graft harvested and placed in corpectomy space and stabilized using anterior cervical plating and bi-cortical anterior cervical screws. discussion the cervical spine fractures may cause collapse of vertebral body and fragmentation, which may either lie at same level in the anterior or posterior displaced or can even show migration in the cranial or caudal direction, and in association with other osteoligamentous disruption produces significant motor, sensory, autonomic neurological deficit. nature of injury could be flexion injury, flexion-rotation injury, extension injury or vertical axial compression injury or complex type of cervical spine injury. [7, 8, 9] the basic biomechanics of burst fracture of the cervical vertebral body usually occurs with downward transmission of compressive force to lower cervical spine levels, the vertebral body can get shatter circumferentially and typically producing typically burst vertebral body fracture and cause disruption of the anterior and middle vertebral columns, with a variable degree of posterior protrusion of the middle column into the spinal canal producing spinal canal stenosis. [1] romanian neurosurgery (2017) xxxi 2: 215 221 | 219 on xray cervical spine and ct scan shows presence of a vertical fracture line and with further loading degree of further comminution and protrusion of the vertebral body fragments can occur anteriorly and posteriorly or even caudal or cranial migration with respect to the contiguous vertebra in a different permutation and combination can occur. reduction of vertebral body height, displacement of disco-ligamentous complex may enter spinal canal producing spinal canal stenosis. [6] the origin, position and size, direction of displacement fragments are usually related to the mechanism of genesis and vector of impact forces leading to vertebral fracture. [1] however, anteriorly propelled vertebral fragment may fuse with upper vertebral body and forming big armored mass and providing natural stability, while the posteriorly displaced fragment may enter into canal and in association with extruded disc can cause severe canal compromise causing severe cervical myelopathy feature, necessitating early diagnosis and early surgical intervention should be carried out to provide good neurological outcome. unfortunately current case could not seek early advice, may be due to poverty tried to delay and presented to us after a delay of six month following accident. the cartilaginous inter-space that underlies the dural origin of a nerve root of c5, c6 and c7 is the inter-space of an uncovertebral articulation. it is interposed between the central core cartilage of the disc and the nerve root originating from dura. [2, 3] a cervical nerve roots do not lies in contact with the interspace of intervertebral disc between dural origin to intervertebral foramina. a cartilage fragment originating from disc may compress intradural segment of the nerve root by migrating within the epidural space, but entry to area near the origin of the nerve root covered in a dural sheath is blocked by uncovertebral joint interface filled with fibrocartilage. [2] early evacuation of patient from site of injury, proper stabilization, early resuscitation, with aim to maintain adequate circulation and breathing, monitoring of mean arterial pressure augmented blood pressure even with support of vasopressor drugs , care and monitoring in the critical care unit and early surgical intervention may offers the chances of improved neurological recovery. these cases may require anterior stabilization, or in addition may need posterior fixation or 360 degree circumferential fusion depending upon degree of spinal instability, clinical feature and progressive neurological deterioration, extent of neural canal compromise, degree of loss of vertebral height, facetal dislocation, rotational component, associated fracture of lamina and associated systemic injury. [8-12] an intensive resuscitation and maintainace of adequate blood pressure under vasopressor support with a mean arterial pressure of 85 mm hg should be maintained for at least seven days following acute spinal cord injury need to highlighted to improve the neurological outcome,. as in resource starved centres, inadequate infrastructure not only delay in referral to hospital and many of these cases does not get adequate treatment and monitoring in the intensive care unit. 220 | satyarthee, moscote-salazar posttraumatic severe cervical myelopathy witiw et al observed current advancement of knowledge of early secondary phases of spinal cord injury pathophysiological processes led to development of targeted medical management with emphasis on improving tissue perfusion and oxygenation by induction of hypertension, avoidance of hypotensive episodes and also noted earlier surgical decompression of traumatic spinal cord injury improves neurological recovery. [9] vale et al. observed early aggressive medical management is important factor and can optimizes the potential for enhanced neurological recovery of patients suffering with traumatic acute spinal cord injuries. [10] readdy et al. conclude after analysis of 34 cases with acute traumatic central cord syndrome, who were administered vasopressor agents to maintain targeted mean arterial pressure, definitely led to improvement in neurological status in all the treated patients. [11] catapano et al. highlighted an important social issue and tried to explore the widely prevalent biased attitude of physician as well as paramedical staff towards spinal cord injury victims, especially those with complete neurological deficit while providing resuscitation or inside the hospital care and called for immediate and radical social change on humanitarian approach . further, such patient should also be helped to get social inclusion. [12] care of associated injury is of paramount importance. however, rehabilitation and social inclusion are also important steps towards managing cases of spine injury suffers. [4, 6, 8] conclusion authors advocate early surgical management can lead to development of advanced spinal deformity and severe neurological deficits. management of spine injury should start from the site of accident and prehospital care, adequate resuscitation and continued care is paramount importance. meanwhile adequate care of air way and breathing and proper circulation is highly important in the early first week following acute spinal cord injury, neglected cases may develop spinal deformity, which is not east y technically and highly challenging. however, presence of armored like mass in association with intraspinal migrate fragment forming large mass is extremely rare, and although rare, possibility of such condition should be considered in neglected cervical spine cor injury sustain axial loading with burst fracture. correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi, india e-mail: drguruduttaaiims@gmail.com references 1. lee c, kim ks, rogers lf. triangular cervical vertebral body fractures: diagnostic significance ajr am j roentgenol. 1982 jun;138(6):1123-32. 2. browne km . the anatomy, spatial relationships, and role of uncovertebral articulations as the source of posterolateral cervical cartilage sequestrations. j neurosurg spine. 2010 mar;12(3):270-4. 3. ailawadhi p, agrawal d, satyarthee gd, gupta d, sinha s, mahapatra ak. use of o-arm for spinal surgery romanian neurosurgery (2017) xxxi 2: 215 221 | 221 in academic institution in india: experience from jpn apex trauma centre. neurol india. 2011 ; 59(4):590-3. 4. verma sk, singh pk, agrawal d, sinha s, gupta d, satyarthee gd, sharma bs. o-arm with navigation versus c-arm: a review of screw placement over 3 years at a major trauma center. br j neurosurg. 2016 dec;30(6):658-661 5. sawarkar dp, singh pk, siddique sa, agrawal d, satyarthee gd, gupta dk, sinha s, kale ss, sharma bs. surgical management of odontoid fractures at level one trauma center: a single-center series of 142 cases. neurol india. 2015 jan-feb;63(1):40-8. 7. garg k, satyarthee gd, singla r, sharma bs extensive long-segment cervicothoracic traumatic spinal epidural hematoma with avulsion of c7, c8, and t1 nerve roots. j neurosci rural pract. 2014 oct;5(4):414-6. 8. lalwani s, punia p, mathur p, trikha v, satyarthee g, misra mc. hospital acquired infections: preventable cause of mortality in spinal cord injury patients. j lab physicians. 2014 jan;6(1):36-9. 9. witiw cd , fehlings mg. acute spinal cord injury. j spinal disord tech. 2015 jul;28(6):202-10. 10. vale fl , burns j, jackson ab, hadley mn. combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management. j neurosurg.1997 ;87(2):239-46. 11. readdy wj, whetstone wd, ferguson ar, talbott jf, inoue t, saigal r, bresnahan jc, beattie ms, pan jz, manley gt, dhall ss. complications and outcomes of vasopressor usage in acute traumatic central cord syndrome. j neurosurg spine. 2015 ; 31:1-7. 12. catapano js , john hawryluk gw , whetstone w , saigal r , ferguson a , talbott j , bresnahan j , dhall s , pan j , beattie m , manley g . higher mean arterial pressure values correlate with neurologic improvement in patients with initially complete spinal cord injuries. world neurosurg. 2016 ;96:72-79. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article do acute ischemic stroke patients receive the right treatment in non-stroke units? d. adam, gina burduşa, d. iftimie romania doi: 10.1515/romneu-2017-0044 romanian neurosurgery (2017) xxxi 3: 263 271 | 263 doi: 10.1515/romneu-2017-0044 do acute ischemic stroke patients receive the right treatment in non-stroke units? d. adam1,2, gina burduşa1, d. iftimie1 1department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania abstract: background: modern treatment of acute ischemic stroke includes thrombolysis and thrombectomy performed for eligible patients in specialized stroke centers. however, a number of patients are admitted in neurosurgical or intensive care departments of emergency hospitals, units where routine treatment strategies are applied. objective: to evaluate the management of patients admitted in these departments that do not benefit from thrombolytic or endovascular treatment. methods: a retrospective analysis was performed, including all patients admitted to the neurosurgery department and intensive care unit (icu) of the “st. pantelimon” clinical emergency hospital with the primary diagnosis of acute ischemic stroke in the year 2016. the following data was retrospectively collected: patient age and sex, comorbidities, risk factors for ischemic stroke, level of consciousness at admission, neurological deficits, stroke location, blood glucose levels, interval from stroke onset to admission, treatment and discharge status. results: in 2016, 63 patients with primary diagnosis of acute ischemic stroke confirmed by head ct scan were admitted in our hospital. none presented indication for decompressive craniectomy. over a half of them (57,14%) were comatose. the majority of patients admitted to the icu (76,47%) received glucose 10% infusions in the first 24 hours from admission, despite increased blood glucose levels at admission. a number of 38 (60,32%) of these patients died. conclusions: patients with acute ischemic stroke should be treated in stroke units with proper equipment and specialists. national public health institutions should take the necessary measures in order to ensure that patients get to the best facility in order to receive the right therapy in the right amount of time. key words: ischemic stroke, hyperglycemia, glucose 10% infusion introduction stroke is the third cause of death and the first cause of neurological disability worldwide (1). in the european union, 1 million people develop an ischemic stroke yearly and it is estimated that in 2020 the total prevalence will be 6,2% of the total population. over 4,7 million strokes occur worldwide every year. 264 | adam et al do acute ischemic stroke patients receive the right treatment in non-stroke units? during their lifetime, approximately 1 in 6 individuals will develop a stroke (2). the management of ischemic stroke has evolved from treatment of risk factors and management of complications, to i.v., i.a. thrombolysis or thrombectomy for eligible patients, which could be supplemented in the future with neuroprotective and stem cell treatment. current treatment options are performed in units specialized in endovascular treatment, considered “standard of care” for patients with ischemic disabilitating stroke. these new therapies are performed by neurologists and neurointerventional radiologists during the opportunity window of up to 6 hours from stroke onset or from time last seen well. not all patients with ischemic stroke are admitted to medical centers specialized in their treatment and only a part of them arrive during the therapeutic time window. in our emergency hospital, patients with neurological deficits arrive by ambulance in the emergency department, where they are diagnosed and admitted to the neurosurgical department or intensive care unit (icu). the aim of this study is to evaluate the management of patients admitted in these departments that do not benefit from thrombolytic or endovascular treatment. material and methods this study encompasses all patients admitted to the neurosurgery department and icu of the “st. pantelimon” clinical emergency hospital in the year 2016 with the primary diagnosis of acute ischemic stroke. all patients were brought in by ambulance to the emergency department and were admitted with the diagnosis of acute ischemic stroke, based upon the neurological examination and emergency head ct scan. if the initial head ct scan was inconclusive, the investigation was repeated after 12-24 hours. conscious patients were hospitalized in the neurosurgical department while the ones that were comatose or presented decompensated comorbidities were admitted in the icu. all patients’ medical records were reviewed and the following data was collected: patient age and sex, comorbidities, risk factors for ischemic stroke, level of consciousness at admission, neurological deficits, stroke location, blood glucose levels, interval from stroke onset to admission, treatment and discharge status. in our hospital, thrombolytic or endovascular treatment is not available. in the case of comatose patients, management goals were sustaining vital functions, stabilization of paraclinical parameters and treatment of risk factors and comorbidities. we have particularly evaluated the outcome of patients and the treatment they received during hospitalization. patients with a favorable neurological evolution, meaning alleviation or stabilization of motor deficits were transferred to a neurological recovery department or discharged at home. results in the year 2016, 63 patients with a primary diagnosis of acute ischemic stroke confirmed romanian neurosurgery (2017) xxxi 3: 263 271 | 265 by head ct scan arrived in the emergency room and were admitted in our hospital. the majority of patients were over 60 years old (58 cases, 92,06%), without a significant difference regarding gender distribution (table 1). regarding comorbidities, most patients presented high blood pressure (55; 87,3%), atrial fibrillation (47; 74,6%) and diabetes mellitus (24; 38,1%). at time of presentation 36 patients were comatose (57,14%) and the remaining 27 (42,86%) were conscious (gcs≥9). on the basis of neurological deficits (hemiparesis, aphasia, seizures), 52 (82,54%) developed an ischemic stroke in the anterior circulation, while vertigo and balance disorders suggested the stroke’s location in the posterior circulation in 16 cases (25,39%). the presumptive diagnosis of ischemic stroke and its location were confirmed by cerebral ct scan that showed loss of greywhite matter differentiation, an area of hypodensity and/or hyperattenuation of a blood vessel. tabel i patient characteristics number percentage total number 63 gender male 29 46,03% female 34 53,97% age group 30-39 1 1,59% 40-49 2 3,17% 50-59 2 3,17% 60-69 16 25,40% 70-79 22 34,92% 80-89 14 22,22% 90-99 6 9,52% comorbidities high blood pressure 55 87,30% atrial fibrillation 47 74,60% diabetes mellitus 24 38,10% congestive heart failure 22 34,92% hypercholesterolemia and obesity 13 20,63% gcs at presentation 266 | adam et al do acute ischemic stroke patients receive the right treatment in non-stroke units? 3 8 36 57,14% 9 15 27 42,86% admission department neurosugery 19 30,16% intensive care unit 44 69,84% neurological deficits hemiparesis 35 55,56% aphasia 17 26,98% balance disorders 16 25,39% coma 36 57,14% seizures 3 4,76% stroke location anterior circulation 52 82,54% • unilateral mca 40 63,49% • bilateral mca 7 11,11% • terminal ica 2 3,17% posterior circulation 13 20,63% evolution discharged at home 16 25,40% transfered to neurological recovery department 9 14,28% deceased 38 60,32% in only 29 patients the time interval between the stroke onset to admission could be established. out of these, only 7 were admitted in less than 6 hours from symptoms’ onset. although only 24 patients were previously diagnosed with diabetes mellitus, initial blood sugar levels were above the normal range in 53 patients of which 15 were admitted in the neurosurgery department and 38 in the intensive care unit. the 38 cases in the icu with increased blood glucose levels, in addition to support of vital functions, routinely received glucose 10% infusion in 26 cases in the first day of hospitalization (76,47%), 5 (14,71%) from the second day, 2 (5,88%) from the third day and 1 (2,94%) from the fourth. out of the 63 admitted patients, a number of 38 (60,32%) patients died (12 male and 26 female). out of the 44 patients admitted in the icu, of which 36 were comatose (gcs 3=12, gcs 4=7, gcs 5=2, gcs 6 = 9, gcs 7 = 4, gcs 8 = 2) and 38 had increased blood sugar levels, 34 received treatment with glucose 10% and 38 died. romanian neurosurgery (2017) xxxi 3: 263 271 | 267 only 6 patients from to the intensive care unit group survived, that presented normal blood sugar levels on admission. among the 25 patients admitted in the neurosurgery department, only 5 received treatment with glucose initiated in the third and fourth day of hospitalization. all these patients presented a favorable evolution and were transferred to neurological recovery departments. patients that died in the icu were in critical condition at admission (various degrees of coma). none of these cases presented indication for decompressive craniectomy. discussion stroke is defined as an acute disruption of cerebral function of a presumed vascular cause that produces a neurological deficit which lasts more than 24 hours or leads to death in the first 24 hours. ischemic stroke is caused by absence of blood flow in a part or the entire brain, that induces nerve cells’ deprivation of glucose and oxygen. the most frequent cause of ischemic stroke is occlusion of a cerebral artery, but it can also be induced by deprivation of oxygen only (in the case of a cardio-respiratory arrest) or glucose deprivation only as, in the case of diabetic patients treated with insulin overdoses. patients with ischemic stroke present, on admission to hospital, in up to two thirds of cases, increased blood sugar levels. (3) hyperglycemia is defined as a blood glucose concentration greater that 115 mg/dl (6,1 mmol/l). between 20% and 50% of acute stroke patients presented with hyperglycemia at admission in the studies of gray and toni (4, 5). hyperglycemia in these cases can be the result of: •previously diagnosed diabetes mellitus patients, that represent 8-20% of stroke patients, with poor glycemic control •patients with undiagnosed diabetes mellitus represent 5-28% (6, 7) •as a result of early hormonal response to cerebral ischemia (stress response) (8, 9). hyperglycemia enhances acidosis and ischemic neuronal damage by facilitating free radical formation, activating ph-dependent endonucleases, enhancing glutamate release and excessive influx of calcium, with the end result of neuronal death (10). hyperglycemia accelerates the ischemic process in stroke. in stroke patients, hyperglycemia is associated with larger infarct volumes, poor functional outcome, increased stroke mortality independent of age, stroke severity or stroke type. (11–13) our in-hospital mortality is very high (60.32%), by comparison with 7,8% reported by ihara in a recent study performed in japan (14). the majority of admitted stroke patients were outside the opportunity window for thrombolysis/thrombectomy and already in critical condition (comatose), which can explain the high rate of in-hospital mortality. in addition, most of them received a potentially harmful treatment, consisting of glucose 10% infusions administered in the first 268 | adam et al do acute ischemic stroke patients receive the right treatment in non-stroke units? 24 hours from stroke onset, to patients that were already hyperglycemic. in stead et al’s study, ischemic stroke patients with hyperglycemia were 2,3 times more likely to be dead within 90 days, by comparison with those with normal glucose levels (15). in diabetic patients with ischemic stroke, the 30-day mortality rate is 2 fold higher. (11) hyperglycemia has been suggested as an independent risk factor for the hemorrhagic conversion of stroke after administration of thrombolytic therapy. in the setting of stroke, euglycemia should be the clinical goal. glucose levels should be tested repeatedly and if it is higher than 140180 mg/dl, treatment with insulin is indicated (1). insulin is administered subcutaneously because intravenous administration increases the risk of hypoglycemia. scott et al (3) infused 500 ml of 10% dextrose with 16 u insulin and 20 mmol potassium chloride (gki) in mild to moderate hyperglycemia following acute stroke and considered it a pragmatic intervention which effectively lowers plasmatic glucose levels within the normal range. however there is limited evidence as to whether reduction of glucose levels in acute ischemic stroke improves patient outcome. european stroke initiative (eusi) guidelines consider that routine use of insulin infusion regimes in patients with moderate hyperglycemia and acute ischemic stroke cannot be recommended. (16) blood glucose levels exceeding 180 mg/dl have to be reduced. maintaining a blood glucose level of 140 mg/dl seems to be reasonable, as more aggressive targets may worsen outcome. (17) the use of intravenous saline and avoidance of glucose solutions in the first 24 hours after stroke is common practice in stroke units. (18) in our study, 36 patients were in a critical condition at presentation (gcs<8) and 38 presented hyperglycemia. the administration of 10% glucose to ischemic stroke patients with hyperglycemia in the first 24 hours is harmful to nerve cells, hastens the expansion of the stroke’s core in the penumbra, enlarges the infarction zone and increases the rate of mortality. a decompressive craniectomy could have been considered only in the case of two patients with malignant infarction, but their critical condition contraindicated the potential surgical intervention. stroke care has entered into a new era. in order to prevent persistent brain damage in an acute ischemic stroke, early restoration of cerebral blood flow is necessary. in 1996 the us fda approved intravenous thrombolysis with rt-pa for treatment of acute ischemic stroke. intravenous rt-pa has become the “holy grail” of acute stroke treatment and is still the standard treatment for eligible stroke patients presenting within 4,5 hours after symptom onset. however, it may produce recanalization and reperfusion in 5-10% of patients. reperfusion rates are higher in the m2 segment of the mca, in small vessels and in microvascular structures. in contrast, it is ineffective in the majority of patients with large thrombi and in patients with large vessel occlusions. romanian neurosurgery (2017) xxxi 3: 263 271 | 269 intravenous thrombolysis has a limited effectiveness in large vessel occlusion. mechanical thrombectomy determined high rates of recanalization in proximal artery occlusion. when a cerebral vessel is obstructed, there are two compartments in its respective territory: core and penumbra. inside the core, brain tissue is already dead, while in the penumbra neurons are structurally intact, only their functionality being affected. the goal of stroke treatment is to save the penumbra because the center of the infarction extends in the penumbra, while the latter shrinks progressively until the entire vascular territory becomes infarcted. the infarction’s evolution is dependent on the occlusion time and the state of collateral blood flow. in some patients with poor collateral circulation, the progression is faster, while in the case of good collateral flow, the progression is slower (19). khartri et al state that every 30 minutes of reperfusion delay is associated with a relative 10% reduction of good outcome probability (mrs = 0-2) (20). endovascular mechanical thrombectomy is an important advance for those patients with large vessel occlusion and stroke located in the anterior circulation. the criteria presented in the new guidelines for mechanical thrombectomy are: •pre-stroke mrs score = 0-1 •acute ischemic stroke that received i.v. tpa within 4,5 hours of symptom onset. •causative occlusion of the internal carotid artery or proximal (m1) middle cerebral artery (mca) •age of 18 years or older •nihss score ≥ 6 •alberta stroke program early ct (aspects) score ≥ 6 •treatment that can be initiated within 6 hours of symptom onset (21) selection of patients for endovascular treatment of acute ischemic stroke can be performed with the help of ct or mri imaging. diffusion weighted magnetic resonance imaging is the gold standard for estimating the ischemic core. it provides full brain coverage and detects smaller lesions (22). perfusion ct evaluates cerebral blood volume and cerebral blood flow, but does not provide any information in cases with critical blood flow in preceding hours, that remitted with subsequent reperfusion. the continued evolution of various therapies and technologies (such as aspiration and stent retrievers) will play an important role in the successful treatment of stroke patients. stroke patients have to be treated as quickly as possible. today, the time windows has been extended beyond 6 hours from time last know well. the dawn trial has shown a 73% reduction in disability in stroke patients treated within 24 hours. (23) conclusions a part of patients with ischemic stroke are admitted to emergency hospitals in neurosurgical or intensive care departments, units that are not all specialized in performing thrombolysis or thrombectomy. 270 | adam et al do acute ischemic stroke patients receive the right treatment in non-stroke units? in this retrospective study we have analyzed the treatment received by these patients, that frequently included glucose 10% infusions, indicated from the first day of hospitalization even in the case of hyperglycemia and we have found a high rate of mortality in these cases. raising awareness upon the fact that glucose infusions administered to hyperglycemic patients in the first 24 hours after stroke onset could have a negative effect on their outcome and should not be prescribed routinely is of significant importance. this could be achieved with the help of cme courses for all physicians that are currently involved in the management of stroke patients. patients with acute ischemic stroke must be treated in stroke units, with proper equipment and specialists, where they should arrive in good time in order to benefit from a modern, efficient treatment provided by neurologists or neurointerventional radiologists. an increase in number and capacity of these medical units specialized in the treatment of ischemic stroke is imperative. results of our analysis are intended to correct routine treatment strategies of stroke patients and to raise the awareness of national public health institutions. the necessary measures should be taken in order to ensure that patients get to the best facility in order to receive the right therapy in the right amount of time. references 1. mcelveen wa, alway d. ischemic stroke and transient ischemic attack – acute evaluation and management. in: stroke essentials for primary care. totowa, nj: humana press; 2009:9-33. doi:10.1007/9781-59745-433-9_2. 2. kaste m. strategies for increasing access to mechanical thrombectomy in the us and worldwide. in: international stroke conference, 22-24 february 2017. houston, usa. 3. scott jf, robinson gm, french jm, o je, alberti k, gray cs. glucose potassium insulin infusions in the treatment of acute stroke patients with mild to moderate hyperglycemia the glucose insulin in stroke trial (gist). http://stroke.ahajournals.org/content/strokeaha/30/4/79 3.full.pdf. accessed july 31, 2017. 4. gray cs, french jm, bates d, cartlidge ne, venables gs, james of. increasing age, diabetes mellitus and recovery from stroke. postgrad med j. 1989;65(768):720724. http://www.ncbi.nlm.nih.gov/pubmed/2616396. accessed july 27, 2017. 5. toni d, sacchetti ml, argentino c, et al. does hyperglycaemia play a role on the outcome of acute ischaemic stroke patients? j neurol. 1992;239(7):382-386. http://www.ncbi.nlm.nih.gov/pubmed/1403020. accessed july 27, 2017. 6. oppenheimer sm, hoffbrand bi, oswald ga, yudkin js. diabetes mellitus and early mortality from stroke. br med j (clin res ed). 1985;291(6501):1014-1015. http://www.ncbi.nlm.nih.gov/pubmed/3931771. accessed july 27, 2017. 7. gray cs, taylor r, french jm, et al. the prognostic value of stress hyperglycaemia and previously unrecognized diabetes in acute stroke. diabet med. 1987;4(3):237-240. doi:10.1111/j.14645491.1987.tb00870.x. 8. candelise l, landi g, orazio en, boccardi e. prognostic significance of hyperglycemia in acute stroke. arch neurol. 1985;42(7):661-663. http://www.ncbi.nlm.nih.gov/pubmed/4015462. accessed july 31, 2017. 9. van kooten f, hoogerbrugge n, naarding p, koudstaal pj. hyperglycemia in the acute phase of stroke is not caused by stress. stroke. 1993;24(8):1129-1132. http://www.ncbi.nlm.nih.gov/pubmed/8342185. accessed july 27, 2017. 10. li pa, shuaib a, miyashita h, he qp, siesjö bk, warner ds. hyperglycemia enhances extracellular glutamate accumulation in rats subjected to forebrain ischemia. stroke. 2000;31(1):183-192. romanian neurosurgery (2017) xxxi 3: 263 271 | 271 http://www.ncbi.nlm.nih.gov/pubmed/10625736. accessed july 31, 2017. 11. capes se, hunt d, malmberg k, pathak p, gerstein hc. stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients. stroke. 2001;32(10). http://stroke.ahajournals.org/content/32/10/2426.long. accessed july 27, 2017. 12. weir cj, murray gd, dyker ag, lees kr. is hyperglycaemia an independent predictor of poor outcome after acute stroke? results of a long-term follow up study. bmj. 1997;314(7090):1303-1306. http://www.ncbi.nlm.nih.gov/pubmed/9158464. accessed july 31, 2017. 13. bellolio mf, gilmore rm, ganti l. insulin for glycaemic control in acute ischaemic stroke. in: bellolio mf, ed. cochrane database of systematic reviews. chichester, uk: john wiley & sons, ltd; 2014. doi:10.1002/14651858.cd005346.pub4. 14. iihara k. comprehensive stroke care capabilities in japan. neurosurgery. 2015;62:107-116. doi:10.1227/neu.0000000000000806. 15. stead lg, gilmore rm, bellolio mf, et al. hyperglycemia as an independent predictor of worse outcome in non-diabetic patients presenting with acute ischemic stroke. neurocrit care. 2009;10(2):181-186. doi:10.1007/s12028-008-9080-0. 16. ringleb pa, bousser mg, ford g, et al. ischaemic stroke and transient ischaemic attack. in: european handbook of neurological management: second edition. vol 1. oxford, uk: wiley-blackwell; 2010:101-158. doi:10.1002/9781444328394.ch9. 17. hyperglycemia and hypoglycemia in stroke: practice essentials, overview, hyperglycemia in stroke. http://emedicine.medscape.com/article/1162340overview. accessed july 31, 2017. 18. gray cs, hildreth aj, sandercock pa, et al. glucosepotassium-insulin infusions in the management of poststroke hyperglycaemia: the uk glucose insulin in stroke trial (gist-uk). lancet neurol. 2007;6(5):397-406. doi:10.1016/s1474-4422(07)70080-7. 19. jovin t. mechanical thrombectomy treatment: when does the clock run out? in: international stroke conference 17-19 february 2016, los angeles, usa. 20. khatri p, yeatts sd, mazighi m, et al. time to angiographic reperfusion and clinical outcome after acute ischaemic stroke: an analysis of data from the interventional management of stroke (ims iii) phase 3 trial. lancet neurol. 2014;13(6):567-574. doi:10.1016/s1474-4422(14)70066-3. 21. bhole r, goyal n, nearing k, et al. implications of limiting mechanical thrombectomy to patients with emergent large vessel occlusion meeting top tier evidence criteria. j neurointerv surg. 2017;9(3):225-228. doi:10.1136/neurintsurg-2015-012206. 22. albers g. mri for imaging salvageable tissue: simply the best. in: international stroke conference 17-19 february 2016, los angeles, usa. 23. jovin tg, nogueira rg. dawn in full daylight (dwi or ctp assessment with clinical mismatch in the triage of wake up and late presenting strokes undergoing neurointervention). in: 3rd european stroke organisation conference, 16-18 may 2017, prague. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article burr hole site acute extradural hematoma after ventriculoperitoneal shunt surgery: a rare case report and its pathogenesis prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmed faran, chhabra anuj india doi: 10.1515/romneu-2017-0068 422 | prasad et al burr hole site acute extradural hematoma after ventriculoperitoneal shunt surgery doi: 10.1515/romneu-2017-0068 burr hole site acute extradural hematoma after ventriculoperitoneal shunt surgery: a rare case report and its pathogenesis prajapati hanuman prasad, singh deepak kumar, singh rakesh kumar, ahmed faran, chhabra anuj department of neurosurgery, dr rml ims lucknow uttar pradesh, india abstract: ventriculoperitoneal (vp) shunt, a common neurosurgical procedure, has a long list of known complications associated with it. a rare but dangerous complication of vp shunt procedure is extradural hematoma (edh). it can be diagnosed and managed easily before it turns into a catastrophic complication. key words: extradural hematoma, ventriculoperitoneal shunt, pathogenesis introduction ventriculoperitoneal (vp) shunt is a commonly performed neurosurgical procedure, also has the longest list of postoperative complications. the most common site of edh is on fronto-parietal region. this may be due to loose fixation of the dura to the cranial vault at this region [1]. vp shunt causes sudden decompression of the brain that can lead to either subdural hematoma (sdh) or edh formation. formation of edh is relatively rare in comparison to sdh. very few cases of post-vp shunt edh formation have been reported in the literature. we report this case to spread awareness of this relatively rare complication of a very common neurosurgical procedure, which, in some cases, can be avoided, and, in all cases, can be diagnosed and managed easily before it turns into a catastrophic complication. case report a 12 years old patient presented to ous with complain of headache, vomiting and imbalance while walking from last 6months.headache and vomiting become severe from last 10 days. on examination patient was conscious and oriented his cranial nerve, motor and sensory system examination was normal. cerebellar signs was positive on both side. ct brain was suggestive of fourth ventricle mass with obstructive hydrocephalus. right sided medium pressure ventriculoperitoneal shunt was done post operatively patient was relieved from headache and vomiting. on third post op day patient again develop headache mri brain with contrast was done mri brain shows fourth ventricle mass with right fronto parietal acute edh with right romanian neurosurgery (2017) xxxi 3: 422 425 | 423 sided shunt in situ. patient was planned for surgery and right fronto parietal craniotomy with suction evacuation of acute edh was done. after two weeks patient was planned for definitive surgery. figure 1 figure 2 discussion ventricular shunting to treat hydrocephalus is a very common neurosurgical procedure worldwide. complications such as obstruction of the device and infection are more frequent than bleeding [2, 3, 4]. after shunt surgery, development of sdh are more common than edh. development of edh after shunt surgery are very rare and only few cases are reported in literature. on reviewing the literature we found that there are various mechanism described for post shunt surgery edh formation, but the exact mechanism is not clear. the most proposed mechanism for hematoma formation after ventricular decompression is sudden lowering of intra-cranial pressure, which results in a suction force on structures between the cortex and the inner table of the skull [5]. sdh develop because of tearing of cortical bridging veins and meningeal vessels tearing leads to formation of edh. in case of edh, detaching the collagenous fixation of the dura from the inner table of the skull may initially cause the dural and diploic veins to bleed into the epidural space. as the hematoma enlarges and the distance between the dura and the bony arterial channels increases, the dural arteries may also tear. second mechanism is that the traction exerted on the dura mater during insertion of shunt causes a displacement and make the vessels between the membrane and the skull to be torn. this is supported by the fact that most reported cases occur in children, in whom the dura is less tightly adhered to the skull than in adults. in case of edh directly adjoining the burr hole site of vp shunt, excessive coagulation of dura of the burr hole before dural incision, in some cases, may cause enough shrinkage to result in dural separation from the skull and edh formation. this dural separation is further aided by rapid lowering of intracranial pressure. once bleeding has begun by any mechanism, arterial bleeding into the resulting pocket creates a hydraulic “water press” effect, progressively stripping away the dura from the skull and widening the perimeter of the hematoma. 424 | prasad et al burr hole site acute extradural hematoma after ventriculoperitoneal shunt surgery edh developing post operatively usually causes symptoms during or immediately after surgery. however, the diagnosis may be delayed in a case with vp shunt insertion because of a reduction in csf volume in the ventricles via a properly functioning shunt [6]. the most common initial symptom is a headache, and there may be seizures in delayed cases [6]. post-shunt edh can be managed surgically and conservatively. the choice between a surgical or a non-surgical treatment of post-shunt edh requires the evaluation of various factors: volume, thickness, midline shift and amount of fresh blood present on ct scan, and the clinical picture. in our case, because the patient was symptomatic with mri brain findings of mass effect and midline shift, we considered the patient for surgical intervention. right fronto parietal craniotomy with suction evacuation of edh done. after two weeks patient was planned for definitive surgery. minimal csf spillage at the time of ventricular catheter insertion, meticulous surgical technique, use of highor mediumpressure valves or differential pressure valves, slow return to upright position and close follow-up even including a postoperative ct scan help to minimize the bleeding complications after vp shunting [7]. use of valve-regulated shunt systems has lowered the incidence of sdh and edh after ventricular drainage. there are only 18 cases of epidural hematomas after valve-regulated shunt placement in the literature [8]. most of these cases had acute hematomas, and only five of them had chronic calcified/ossified hematomas. these patients were 15-35 years old. edh contralateral to the vp shunt has been also described [9]. the largest case series of epidural hematoma after ventricular decompression, from odake and matsumoto[9], includes not only ventriculoperitoneal shunt but also other procedures for draining cerebrospinal fluid: ventricular puncture, ventriculography, ventriculoatrial shunts leading to development of edh after the procedure. we suppose that in our case, the mechanism appears is sudden decompression of the dilated ventricles, stripping the dura from the bone and leading to the acute epidural hematoma. furthermore, the long hydrocephalus associated with lower thickness of the left brain parenchyma, have contributed to the event. conclusion edh as a complication of ventriculoperitoneal shunt is a rare but dangerous complication which, in some cases, can be avoided, and, in all cases, can be diagnosed and managed easily before it turns into a catastrophic complication. correspondence dr. hanuman prasad prajapati department of neurosurgery, dr rml ims lucknow, uttar pradesh (india) email: pushpa84.dhp@gmail.com references 1. higazi i. epidural hematoma as complication of ventricular drainage: report of a case and review of literature. j neurosurg. 1963;20:527–528. [pubmed] romanian neurosurgery (2017) xxxi 3: 422 425 | 425 2. louzada pr, requejo pr, barroso mv, vaitsman rp, machado al, paiva ms, salame jm. bilateral extradural haematoma after acute ventricular over-drainage. brain injury. 2012;26:95–100. [pubmed] 3. driesen w, elies w. epidural and subdural haematomas as a complication of internal drainage of cerebrospinal fluid in hydrocephalus. acta neurochir (wien) 1974;30:85–93. [pubmed] 4. chen gm, cai t. clinical analyses of complications after ventriculoperitoneal shunt in 125 cases. di yi jun yi da xue xue bao. 2004;24:1078–1079. [pubmed] 5. wolfsberger s, gruber a, czech t. multiple supratentorial epidural haematomas after posterior fossa surgery.neurosurg rev. 2004;27:128–32. [pubmed] 6. seyýthanoglu h, guzey fk, emel e, ozkan n, aycan a. chronic ossified epidural hematoma after ventriculoperitoneal shunt insertion: a case report. turk neurosurg. 2010;20:519–23. [pubmed] 7. yue cp, mann ks. fluid chronic epidural haematoma. a rare complication of ventriculoperitoneal shunt. j neurol neurosurg psychiatry. 1985;48:953–5. [pmc free article] [pubmed] 8. paiva ws, oliveira am, de andrade af, brock rs, teixeira mj. remote postoperative epidural hematoma after subdural hygroma drainage. case report med 2010. 2010:417895. [pmc free article] [pubmed] 9. jain sk, sundar iv, sharma v, arora r, prasanna kl. chronic ossified extradural hematoma on the opposite side of the ventriculoperitoneal shunt procedure: a rare case report. saudi j health sci. 2012;1:159–61. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article giant frontoethmoidal osteoma with orbital involvementa rare case report with review of literature pankaj gupta, arvind sharma, jitendra singh, tarun ojha india doi: 10.1515/romneu-2017-0084 540 | gupta et al giant frontoethmoidal osteoma doi: 10.1515/romneu-2017-0084 giant frontoethmoidal osteoma with orbital involvement a rare case report with review of literature pankaj gupta1, arvind sharma2, jitendra singh1, tarun ojha2 1department of neurosurgery, mahatma gandhi medical college, jaipur, india 2department of neurosurgery, sawai man singh medical college, jaipur, india abstract: osteomas are benign tumours that involve paranasal sinuses more than other parts of body. frontal sinus is most common while sphenoid is least one. they are usually asymptomatic and diagnosed incidentally on imaging for other reasons. giant variety of frontoethmoid osteoma is very rare and only few cases are described in literature. orbital involvement in giant frontoethmoid osteoma is even rarer. due to threat to vision, this variety is an indication for surgical intervention followed by reconstruction of defect. as these tumours are very large, endoscopic approaches are less indicated and there is no clear consensus which open surgical approach is better. we are reporting such a rare case of giant frontoethmoid osteoma causing proptosis and restriction of eye movement that was treated with open surgical approach. key words: giant, osteoma, frontoethmoid introduction osteomas are rare benign bony mesenchymal tumours. they commonly involve craniofacial bony skeleton and jaw bones (12). they constitute about 1% of all bone tumours & 11% of all benign bone tumours (2). they are slowgrowing, often asymptomatic & incidentally detected in 1% of skull x-ray and 3% of the cranial computed tomography (ct) scans. these tumours involves frontal, ethmoid, maxillary & sphenoid sinus in decreasing order of frequency. giant frontoethmoidal osteomas are very rare and patient usually present early as there is limited anatomical space (14,15,16). orbital and skull base involvement is very unusual in ethmoidal osteoma and can produce neurologic and ophthalmic manifestation hence surgical intervention is required in these patients(14,16). ct scan remains the gold standard to diagnose this pathology and surgery remains the treatment of choice for symptomatic frontoethmoidal osteomas. we are reporting such a rare case of frontoethmoidal osteoma that was treated surgically with special focus on various surgical options. romanian neurosurgery (2017) xxxi 4: 540 544 | 541 case report a 14 year male child referred from otolaryngology department with chief complains of insidious onset, slowly progressive nasal blockage with difficulty in nasal breathing since last 4 years. patients often had off and on mild headache for that he takes oral analgesic and his headache was relived after taking these medications. gradually his mother notice broadening of his nasal bridge with deviation and bulging of his left eyes. ct scan of pns showed a large frotoethmoidal osteoma. patient further evaluated in neurosurgery department. he was conscious and oriented. his vitals were within normal range. on neurologic examination, his higher mental status was normal. there were no cranial nerve deficits nor any deficit in sensory or motor system. his cerebellar examination was normal. position of his right eye was normal but his left eyes was slightly bulging and deviated to left & there was slight restriction of left eye movement on superiomedial direction. there was no relationship of proptosis with bending forward. visual acuity & fundus examination of both eyes was normal. on palpation, swelling was bony hard in consistency. a ct scan of the brain with pns (figure 1) revealed a hyperdense giant mss of approximately 7.2 cm of size occupying the left supraorbital region, frontoethmoid region. figure 1 preoperative ct scan showing giant frontethmoid osteoma figure 2 – post-operative scan showing complete removal of osteoma surgical intervention was advised and possible complications and outcomes were explained to them in detail. after taking written and informed consent patient taken to operation theatre. patient put on supine position with a bolster placed below the shoulder so that neck remains in extension. bicoronal skin incision given and skin flap raised with pericranium lifted separately. supraorbital bifrontal craniotomy done. as soon as dura separated from anterior cranial base, ivory white osteoma visualized. frontoethmoidal part of osteoma taken out with orbital part removed separately. reconstruction of the anterior cranial base performed using pericranial patch. this was further reinforced by tissue glue. in post 542 | gupta et al giant frontoethmoidal osteoma operative patient did well. there was no csf leak from the nose and his proptosis was resolved with no diminution in vision. postoperative ct scan (figure 2) showed complete removal of osteoma. histopathological examination confirmed the diagnosis of benign osteoma. discussion osteomas are rare benign bony tumours. they invovles paranasal sinuses (13) most common, & found in the frontal sinus (71.8%) and less often in the ethmoid sinus (16.9%), maxillary sinus (6.3%) or sphenoid sinus (4.9%) (11). osteomas of the other bony regions are also reported. osteomas affect less than 1% of population with slight male preponderance (17). 95% of the patients having osteoma remain asymptomatic (11). the average reported size of osteoma involving paranasal sinuses is less than 2 cm (12) but when the size exceeds more than 3cm they are termed as giant (4). most of osteomas are sporadic but few cases may have genetic predisposition like gardener syndrome (3). the pathogenesis of osteoma formation is not very clear and there are different theories (10,11,15). traumatic theory of gerber states that injuries suffered during puberty may cause the growth of osteoma from bone sequestra. inflammatory theory which states that chronic sinusitis of paranasal sinuses can stimulate osteoblastic cell hence there is formation of osteoma. most recent theory is embryologic theory which states that osteoma arises from the remains of persistent embryologic cells located at the junction of the ethmoid and frontal sinuses. traumatic and embryologic theories are most accepted one. symptomatology of osteomas depends upon the location. overall most common symptoms is headache (10). sometimes osteoma may involve anterior cranial base and patients may have cerebrospinal fluid leak, meningitis, pneumatocele (5) and brain abscess (8). as the orbit is very close to ethmoid sinus, giant osteoma of frontoethmoidal region may involve the orbit and can produce proptosis, diplopia and other ocular symptoms (16). very rare complications like amourosis (18) and orbital emphysema is also reported in frontoethmoidal osteoma. there are three different types of osteoma viz. ivory, mature and mixed (12). this is very crude classification. each osteoma has all these kind of cells but proportion of each cell varies. more mature cells migrate from the centre and align themselves to periphery and this is the reason that there is no recurrence after leaving some peripheral part of the osteoma (17). ct scan of the paranasal sinuses is the investigating modality of choice. it can exactly delineate which part of the craniofacial skeletal is involved but it lacks the sensitivity and specificity of mri for soft tissue detail like optic nerve involvement. radionuclide scan can be performed that shows more radionuclide uptake in active growing lesions. osteoblastoma, osteoid osteoma (19), fibrous dysplasia, ossifying fibroma and chondroma (9) are major differential diagnosis of osteoma. there is no need for active management for osteoma except sphenoid osteoma (11) that threaten orbital romanian neurosurgery (2017) xxxi 4: 540 544 | 543 apex or optic canal and a giant frontoethmoidal osteoma with involvement of orbit. there is no clear consensus among surgeons that which surgical treatment is better for frontoethmoidal osteoma. open and endoscopic surgical approaches can be used to treat these pathologies. the choice of surgical approach is based upon tumor location, dimension, extension and experience of surgeon. there is rapid expansion in endoscopic technology and now a day’s endoscopic approaches are more commonly performed in small and medium size osteomas (13). less morbidity, less blood loss, no operative scar, close and direct visualization of tumor and less hospital stay are usual benefits of endoscopic approach (13). long learning curve, huge instrument cost, difficult intraoperative control of bleeding, inability of bony reconstruction and non-familiarity with endoscopic anatomy of paranasal sinuses are usual drawbacks of endoscopic approach. open surgical approaches remains treatment of choice for giant frontoethmoidal osteoma. the osteoplastic flap technique, anterior surgical exposure (craniofacial, transcoronal, and transcutaneous paranasal approaches), external fronto-ethmoidectomy, and lateral rhinotomy have all been described in the literature as possible techniques in the resection of giant osteomas that extends beyond the ethmoid sinus (6,7,14,21). recurrent sinusitis, cranial nerve injury, ptosis, ophthalmic complication, meningitis, postoperative csf leak and bleeding are the most common complications after open surgical procedures (1,20). in our case it was huge frontoethmoidal osteoma with involvement of orbit & requires post-operative reconstruction that renders endoscopic approach less favorable. the goal of surgery is complete excision of lesion. during surgery of frontoethmoidal osteoma with orbital involvement, nearby vital structures may got damaged like cribiform plate, optic nerve, eye globe, anterior and posterior ethmoidal arteries. good aesthetic outcome is also important as far as possible (16). tumours should be removed enbloc as far as possible and if surgeon is not able to do so than central hard part of osteoma should be drilled out and peripheral thinned rim of tissue should be taken out separately (4). same technique should apply to orbital osteomas. in our case we first approach anterior skull base intracraniallyextradurally & removed frontoethmoidal part of osteoma enbloc. orbital part removed separately. postoperative defect after removal of giant frontoethmoidal osteoma should repair as far as possible. small defect can be repair using pericranial patch or galeal-pericranial patch. large defect should be repair using autologus calvarial bone graft, as this graft provides natural cranial contour. synthetic implants can also be used for correction of postoperative defect. we offered reconstruction of bony defect but due to financial constrains, patient and his parents refused for the same. post-operative recurrence of osteoma is very unusual but few case reports are described of rapid recurrence (2). csf leaks, meningitis, post-operative bleeding, and injury to vital structures like optic nerve and lacrimal apparatus injury are the common postoperative complications. 544 | gupta et al giant frontoethmoidal osteoma conclusion giant frontoethmoidal osteomas with orbital invasion are very rare lesions. most of the existing literature on this pathology is in the form of case reports or small case series hence no definitive approach is superior. in today’s era both surgical and endoscopic approaches can be used. in case of giant osteomas due to invasion of nearby structures like orbit, endoscopic approaches are less useful. our case is very unique and adds a rich knowledge to the existing literature and reaffirms the open surgical procedure as preferred modality of treatment in case of giant frontoethmoidal osteoma. references 1.benatiya i, andaloussi, touiza e, bhallil s et al., “orbital osteoma: three case reports,” bulletin de la soci´et´e belge d’ophtalmologie 2006; 300: 73–9. 2.grayeli ab, redondo a, and sterkers o, “anterior skull base osteoid osteoma: case report,” british journal of neurosurgery 1998;12:173–75. 3.haddad fs, haddad gf, zaatari g, “cranial osteomas: their classification and management. report on a giant osteoma and review of the literature,” surgical neurology 1997; 48: 143–47. 4.izci y, “management of the large cranial osteoma: experience with 13 adult patients,” acta neurochirurgica2005; 147:1151–55. 5.johnson d, tan l. intraparenchymal tension pneumatocele complicating frontal sinus osteoma: case report. neurosurg 2002;50:878-80. 6.karapantzos i, detorakis et, drakonaki ee, ganasouli dl, danielides v, kozobolisvp, “ethmoidal osteoma with intraorbital extension: excision through a transcutaneous paranasal incision,”actaophthalmologica scandinavica2005; 83: 392–94. 7.karbassi e, arabi mianroodi a, shamsadini a, “orbital extension of a giant ethmoidal sinus osteoma in a 30-yearold female,” iranian journal of otorhinolaryngology 2013; 25: 119–22. 8.koyuncu m, belet u, sesen t. huge osteoma of the frontoethmoidal sinus with secondary brain abscess. auris nasus larynx 2000;27:285-7. 9.livaoĝlu m, cakir e, karaçal n. large orbital osteoma arising from orbital roof: excision through an upper blepharoplasty incision. orbit 2009;28:200-2. 10.ma’luf rn, ghazi ng, zein wm, et al. orbital osteoma arising adjacent to a foreign body. opthal plast reconstr surg 2003;19:327-30. 11.mansour am, salti h, uwaydat s, et al. ethmoid sinus osteoma presenting as epiphora and orbital cellulitis: case report and literature review. surv ophthalmol 1999;43:413-26. 12.mchugh jb, mukherji sk, lucas dr. sino-orbital osteoma. a clinicopathologic study of 45 surgically treated cases with emphasis on tumors with osteoblastoma-like features. arch pathol lab med 2009;133:1587-93. 13.miman mc, bayindir t, akarcay m, et al. endoscopic removal technique of a huge ethmoido-orbital osteoma. j craniofac surg 2009;20:1403-6. 14.muderris t, bercin s, sevil e, kiris m, “endoscopic removal of a giant ethmoid osteoma with orbital extension,” acta informatica medica2012; 20:266–68. 15.naraghi m , kashfi a, “endonasal endoscopic resection of ethmoido-orbital osteoma compressing the optic nerve,”american journal of otolaryngology: head and neck medicine and surgery2003; 24, 408–12. 16.pons y, blancal jp, v´erillaud b et al., “ethmoid sinus osteoma: diagnosis and management,” head & neck 2013;35: 201–4. 17.selva d, white va, o’connell jx, et al. primary bone tumors of the orbit. surv ophthalmol 2004;49:328-42. 18.siboni p, shindo m. orbital osteoma with gaze-evoked amaurosis. arch ophthalmol 2004;122:788. 19.sires bs, benda pm, stanley rb jr, rosen ce. orbital osteoid osteoma. arch ophthalmol 1999;117:414-5. 20.wei la, ramey na, durairaj vd et al., “orbital osteoma: clinical features and management options,” ophthalmic plastic and reconstructive surgery 2014; 30: 168–74. 21.yiotakis i, eleftheriadou a, giotakis e, manolopoulos l, ferekidou e, kandiloros d, “resection of giant ethmoid osteoma with orbital and skull base extension followed by duraplasty,” world journal of surgical oncology 2008;. 6; 110 romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article endovascular coil oclusion of spontaneous ruptured vertebral artery dissecting aneurysm a. chiriac, georgian ion, n. dobrin, z. faiyad, i. poeata romania doi: 10.1515/romneu-2017-0004 romanian neurosurgery (2017) xxxi 1: 25 – 31 | 25             doi: 10.1515/romneu-2017-0004 endovascular coil oclusion of spontaneous ruptured vertebral artery dissecting aneurysm a. chiriac, georgian ion1, n. dobrin1, z. faiyad1, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi, romania 1“prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract: spontaneous dissecting aneurysm of vertebral artery is known as a rare pathological condition causing a subarachnoid hemorrhage in the posterior circulation. the treatment of ruptured vertebral artery dissecting aneurysms is still an important subject of debates in the literature. we present a particular case of ruptured vertebral artery dissecting aneurysms that was treated by only endovascular guglielmi detachable coils occlusion. a brief review of technical possibilities of treatment of these types of vascular lesions, with their advantages and disadvantages are discussed. key words: vertebral artery dissecting aneurysm, endovascular coil occlusion introduction spontaneous ruptured vertebral artery dissecting aneurysms are rare condition but with a higher incidence risks of re-rupture, morbidity and mortality. however, these aneurysms are now being reported more frequently with increasingly use of advanced neuroimaging techniques. a clinical and autopsy series research reported a 3 to 5% of intradural vertebral artery dissection of patients with subarachnoid hemorrhage. only 11% of spontaneous vertebral artery dissection appears in the intracranial segment of vertebral artery [5, 6]. due to their high incidence of rebleeding compared with classic saccular aneurysms a more rapid initiation of treatment of these lesions is indicated. the treatment can be carried out either open surgery or endovascular embolization. the deep location and close relationship to lower brain stem and lower cranial nerves of these vascular lesions made the endovascular techniques as the first intention treatment. we present a case of spontaneous vertebral artery dissecting aneurysms addressed with a subarachnoid hemorrhage and discuss the technical aspects of treatment of these vascular lesions. we will focus on the endovascular coil technique which is very rare reported in this pathological situation. 26 | chiriac et al endovascular coil oclusion of vertebral artery dissecting aneurysm             case report a 67 years old female was addressed to our neurosurgical clinic for a sudden episode of headache followed by a short episode of loss of consciousness which started two days ago. initially the patient was evaluated with grade 3 on hunt and hess scale and recovered to grade 2 at admission. computerized tomogram (ct) scan performed to the addressing department have showed a subarachnoid hemorrhage localized in perimedullary cistern and left cerebellopontine angle and forth ventricle (figure 1a). ct angiography revealed large dissecting aneurysm at proximal portion of intracranial vertebral artery (v4 segment) (figure 1b, d, e, f, g) [1]. the digital substraction angiography (dsa) performed in our department confirmed the cta diagnosis and decision for an immediately endovascular treatment with coils was taken (figure 1h). the procedure was performed with the patient under general anesthesia. an introducer sheath of 6fr was used to access the right femoral artery. a 6 fr guiding catheter was placed at the v2 segment of the left vertebral artery using an angled hydrophilic guide 0.035 (terumo). repeated angiographic imaging acquisitions were performed for clear exposure of aneurysmal neck. after obtaining an optimum working position, an excelsior sl-10 microcatheter (stryker) was placed inside the aneurysm by using a transend 0.014 micro-guidewire (boston scientific) slightly curved on top. a gdc-10 3d coil with a diameter as close as possible to the aneurysmal sac was chosen and introduced, to obtain a more stable anchorage configuration at both aneurysmal sac and at its neck level. subsequently they were successively introduced and detached another more 9 coils gdc-10 with complete occlusion of the aneurysm, and without any coil loop protrusion into the lumen of the carrying artery. the stable configuration of coil construction was maintained after the withdrawal of the microcatheter from the aneurysm. repeated control angiographic exposures were performed in various angulations (figure1i). the whole guiding system was then retracted with local compressive bandage application. during the procedure 2500 ui heparin were given after placing the first coil and another 5000 ui at the end of the procedure. post-operative ct showed no signs of hydrocephalus or cerebral infarction (figure 1c). the clinical evolution was very good and the patient was discharged home after 19 days. romanian neurosurgery (2017) xxxi 1: 25 – 31 | 27             a  b  c  d  e  f  28 | chiriac et al endovascular coil oclusion of vertebral artery dissecting aneurysm             figure 1 a axial ctproved sah in the perimedullary cistern; b,d,e: mpr images with cta revealing a left-sided vada; f three dimensional computed tomography (3d ct) angiography showing a left vada and g schematic representation[1]; h,i: dsa images with the leftside vada before and after coil embolization discussion vertebral artery dissecting aneurysm (vada) is a rare condition caused by successive phenomena represented by disruption of the internal elastic lamina, leukocyte and macrophage infiltration, endothelial coverage followed by neointima formation. continuous hemodynamic stress on this thin layer of intradural adventitia will result in a subarachnoid hemorrhage. the reported incidence of sah in the literature was between 67% and 86% [7, 8]. the etiology of spontaneous vada is still discussed and various predisposing factors like collagen abnormalities, fibromuscular dysplasia or arterial hypertension were attributed to its pathophysiology. clinical g  h  i  romanian neurosurgery (2017) xxxi 1: 25 – 31 | 29             manifestation varies and patients can present with headache, ischemic stroke, subarachnoid haemorrhage, or symptoms associated with mass effect, mostly on the brainstem or low cranial nerves. unlike traumatic vada, ruptured spontaneous vada have been reported with an unfavourable clinical outcome due to their high incidence of rebleeding within 24 hours. emergency treatment initiation is mandatory to prevent the fatal rebleeding. the two main concept of vada treatment are represented by deconstructive and reconstructive techniques of the parent vessel. both techniques could be applied by surgical or endovascular procedures (figure 2). open surgical techniques are represented by proximal parent artery clipping, dissection segment trapping, dome clipping, circumferential wrapping and vertebral arterial reconstruction. the firs surgical procedure consisting in proximal occlusion of the vertebral artery close to dissection was reported by yonas et all in 1977. for about a decade this procedure was considered as standard surgical technique for this vascular condition [ 5, 6, 7, 8]. figure 2 a, b, c, d: schematic representation of deconstructive and reconstructive techniques for treatment of vada first endovascular treatment for vada by proximal occlusion of vertebral artery using detachable balloon or coils was considered the safest techniques. this technique was indicated especially in patients with vada involving posterior inferior cerebellar artery (pica). reports showing refilling of the aneurysm from the opposite vertebral artery and repeated haemorrhage caused the search of new treatment options. thus, the strategy of endovascular treatment changed from proximal occlusion to trapping by complete occlusion of arterial dissection segment with detachable coils. even if this endovascular procedure has been reported in many series of cases as the most efficient treatment of ruptured vada, especially in acute phase, it is not indicated in situation of pica or spinal artery involvement at the site of arterial dissection. this procedure was also reported to be limited by antegrade recanalization of the aneurysm from contralateral vertebral artery. incomplete coil occlusion of the entry to dissecting aneurysm or detachable coil occlusion of the false lumen followed by true lumen dilatation to the normal diameter simultaneously with false lumen collapsing could be the explanations of this unfavourable evolution. for lesion involving the origin of pica or spinal artery iiahara et all [5, 6] reported a therapeutic planning to minimize the risk of treatement-releated morbidity based on balloon test occlusion followed by internal trapping of the dissected site [7, 8, 9, 10]. more recent reconstructive endovascular techniques such as coil occlusion, stent 30 | chiriac et al endovascular coil oclusion of vertebral artery dissecting aneurysm             placement or stent-supported coil embolization were successfully reported. the only coil occlusion technique is feasible in case of o saccular dome configuration of arterial dissected wall. this will offer the possibility to obtain a stable coil arrangement with or without a balloon assisted technique. the stenting or stent-supported coil embolization are still debated especially due to need of major anticoagulation in the acute sah phase. multimodal approaches in the context of a combined treatment (endovascular and microsurgical) have been also mentioned in the literature. additional anastomotic surgical revascularization was proved helpfully and effective after endovascular occlusion. autoexpandable stent placement followed by subsequent surgical circumferential wrapping of the aneurysm was also reported as multimodal treatment [3, 4, 11]. nevertheless, treatment of spontaneous ruptured vadas is not without some complication. kitanaka et all reported that a very high rate of postoperative complication with major causes of disability were attributable to lower cranial nerve palsy and associated condition as prolonged intubation and tube feeding [2, 5, 6]. vertebral artery recanalization by antegrade flow, coil compactation, coil loop migration, intra-stent thrombosis and distal thrombembolism have been also reported as complications of endovascular treatments. intermittent headache episodes accompanied by vertiginous syndrome were mentioned to some patient with unilateral vertebral artery occlusion due to hemodynamic stress caused by enlarging diameter of opposite vertebral artery. conclusions despite discussions regarding optimal treatment of spontaneous ruptured vadas it is a common practice to treat immediately the patients presented with sah. most patients with subarachnoid haemorrhage undergo surgical or endovascular treatment to prevent rebleeding. major reports showed that endovascular techniques appear to be the safe and effective method especially in critical condition. also, follow-up angiographic studies are needed due to unpredictable evolution of these lesion and some related technique complications. references 1. cloud g.c., . markus h.s; diagnosis and management of vertebral artery stenosis. qjm 2003; 96 (1): 27-54. doi: 10.1093/qjmed/hcg003. 2. hamada, j. i., kai, y., morioka, m., yano, s., todaka, t., & ushio, y. (2003). multimodal treatment of ruptured dissecting aneurysms of the vertebral artery during the acute stage. journal of neurosurgery, 99(6), 960-966. 3. heit, j., dodd, r., do, h., steinberg, g., chang, s., & marks, m. (2016). e-023 patient outcomes, aneurysm occlusion, and cerebral infarction following endovascular treatment of dissecting vertebral artery aneurysms. journal of neurointerventional surgery, 8(suppl 1), a57-a57. 4. hernández-durán, s., & ogilvy, c. s. (2014). clinical outcomes of patients with vertebral artery dissection treated endovascularly: a meta-analysis. neurosurgical review, 37(4), 569-577. 5. iihara, k., sakai, n., murao, k., sakai, h., higashi, t., kogure, s., ... & nagata, i. (2002). dissecting aneurysms of the vertebral artery: a management strategy. journal of neurosurgery, 97(2), 259-267. 6. lee, j. w., jung, j. y., kim, y. b., huh, s. k., kim, d. i., & lee, k. c. (2007). spontaneous dissecting aneurysm of the intracranial vertebral artery: management strategies. yonsei medical journal, 48(3), 425-432. romanian neurosurgery (2017) xxxi 1: 25 – 31 | 31             7. nakagawa, k., touho, h., morisako, t., osaka, y., tatsuzawa, k., nakae, h., ... & karasawa, j. (2000). long-term follow-up study of unruptured vertebral artery dissection: clinical outcomes and serial angiographic findings. journal of neurosurgery, 93(1), 19-25. 8. prabin, s., shigeyuki, s., masaaki, s., yoshihiro, k., takahito, o., kazuhiko, s., & kaoru, k. (2009). endovascular coil occlusion of ruptured vertebral artery dissecting aneurysm: a case report. neurology asia, 14(2). 9. sano, h., kato, y., okuma, i., yamaguchi, s., ninomiya, t., arunkumar, r., & kanno, t. (1997). classification and treatment of vertebral dissecting aneurysm. surgical neurology, 48(6), 598-605. 10. shin, g. w., & jeong, h. w. (2015). endovascular treatment of intracranial vertebral artery dissecting aneurysms: follow up angiographic and clinical results of endovascular treatment in serial cases. neurointervention, 10(1), 14-21. 11. wang, y., zhao, c., hao, x., wang, c., & wang, z. (2014). endovascular interventional therapy and classification of vertebral artery dissecting aneurysms. experimental and therapeutic medicine, 8(5), 14091415. doi: 10.33962/roneuro-2021-080 reperfusion injury in brain stroke sabrina rahman, moshiur rahman romanian neurosurgery (2021) xxxv (4): pp. 475-477 doi: 10.33962/roneuro-2021-080 www.journals.lapub.co.uk/index.php/roneurosurgery reperfusion injury in brain stroke sabrina rahman1, moshiur rahman2 1 department of public health, independent universitybangladesh, dhaka, bangladesh 2 department of neurosurgery, holy family red crescent medical college, dhaka, bangladesh abstract the occlusion of a cerebral artery by a thrombus accounts for about 80% of strokes. reperfusion can save hypoperfused brain tissue from early cerebral blood flow restoration (cbf), thus limiting neurological impairment. the most successful treatments for stroke care have proven to be reperfusion techniques. one of the key drawbacks of these treatment methods is that early ischemic brain tissue reperfusion can lead to adverse effects, including blood-brain barrier breakdown, which can lead to cerebral oedema, haemorrhage of the brain, or both. haemorrhages are especially devastating after reperfusion and are associated with exceptionally high morbidity and mortality. fear of haemorrhage-related reperfusion greatly restricts the use of stroke therapies. reperfusion injury, a mechanism that further damages brain cells, the ischemic arterial wall, and the microvasculature, is due to the deleterious effects of early restoration of cerebral blood flow following stroke. it seems clear that the brain will benefit from therapies to restore cbf to an ischemic region. the brain's reliance on normal cbf levels is underlined by the sensitivity of the brain to relatively short ischaemic cycles. experimental and clinical data, however, suggests that tissue damage can be aggravated by organ reperfusion. [1] studies have failed to prove that infarct size is increased by reperfusion. reperfusion can aggravate the formation of oedema and lead to abnormal blood flow patterns and microvascular lesions within the reperfused areas. focal cerebral ischemia – reperfusion injury it is characterized by a thick infarction center surrounded by a peripheral zone of penumbra-called potentially viable tissues. [2] this is a crucial region for the dissemination of ischemic lesions. ischemiareperfusion induces a cascade of molecular events that cause neuronal death that range from immediately to several days later in time. [3] two different mechanisms of cell death are displayed by post-ischemic neurons: necrosis and apoptosis. during ischemia-reperfusion injury, several events occur, including ca21-induced protease activation, glutamate toxicity, free radical development, receptor-mediated death signals, and altered pro -apoptotic and anti -apoptotic protein expression, eventually triggering the morphological result that can be either necrosis or apoptosis. [4] apoptosis is spread predominantly in the penumbra. in focal or incomplete cerebral ischemia, propofol has keywords reperfusion injury, brain stroke, neurosurgery corresponding author: moshiur rahman holy family red crescent medical college dhaka, bangladesh dr.tutul@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published october 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 476 sabrina rahman, moshiur rahman been shown to be effective in preventing cerebral injury. [5] but the propofol therapeutic window was not well explored. in focal cerebral ischemia, infarction in the reperfused brain can extend into the peripheral region, and the degree of this expansion may be due to the penumbra cell outcome. [5] the acute penumbra is evanescent and deteriorates steadily, ultimately subsuming within the ischaemic heart. [2] the co-existence of apoptosis and necrosis indicates the pathological result of focal cerebral ischemiareperfusion damage. reperfusion-related brain injury and melatonin melatonin is an interesting compound that, among other tissues in mammals, is mainly synthesized in the pineal gland. in response to environmental lightdark cycles, its secretion, primarily at night, is regulated circadically by the suprachiasmatic nucleus, and has been associated with several significant physiological phenomena that have been attributed to the timing of pineal melatonin secretion. [6] in addition to its related physiological functions, it is recognized that melatonin performs direct and indirect antioxidant activities both at physiological and endogenous concentrations and at concentrations exceeding physiological levels by many orders of magnitude. it is understood that overproduction of free radicals during cerebral ischemia and reperfusion leads to functional dysfunction and neuronal death, among other pathophysiologic mechanisms. as a consequence, in view of its antioxidant activities compared to the detrimental cellular actions of free radicals, attention was given to melatonin as a neuroprotective medication against ischemia/reperfusion brain injury. the key causes of permanent brain injury and damage are focal cerebral ischemia induced by thromboembolic occlusion of the major cerebral artery, often the middle cerebral artery, as well as global cerebral ischemia caused by cardiac arrest, extreme hypotension, or significant hemorrhage, leading to temporary or permanent interruption or decrease of blood flow in particular brain structures or the entire brain. [8] as a consequence of its specific biochemical features, the brain is particularly susceptible to oxidative damage. [9] chemical substrates for further increasing cellular changes, neuronal death and neurological deficits can also include reperfusion and reoxygenation of the ischaemic tissue, which must be restored within minutes in an attempt to avoid serious neurological damage and facilitate the survival of individuals. [10] nlrp3 and ros in reperfusion injury of the brain it is well known that the brain damage initially caused by ischemia can be aggravated by reperfusion, causing an i/r injury. [11] inflammation and oxidative stress are involved in the pathogenesis of brain i/r among the different underlying mechanisms of stroke, and adequate inflammatory level control can play a critical role in the prevention and treatment of stroke. [12] the role of inflammasomes, especially nlrp3, in postischemic inflammation after stroke has been recognized in recent years. since inflammation is triggered by the inflammasome, nlrp3 inflammasome modulation can regulate the inflammatory response. however, from a molecular point of view, a number of molecular signalling systems in the i/r brain can activate the nlrp3 inflammasome pathway and several mechanisms have not yet been completely identified. specifically, this cytokine is produced by macrophages or microglial cells during central nervous system disease or after brain injury [14], and molecular mediators such as mitochondrial ros and lysosomal protease cathepsin b are essential for the development of interleukin-1β by microglial cells [14]. reperfusion injury treatments in the post-ischemic environment, many pharmacological agents often protect the brain when given. (s)-emopamil, a novel blocker of the calcium channel and antagonist of serotonin s2, reduces infarct size when administered after permanent and temporary occlusion of mca. blocking of amino-3-hydroxy-5-methyl-4-isoxazole (ampa) receptors by the 2,3-dihydroxy-6-nitro-7sulfamoyl-benzo(f) quinoxaline (nbqx) blocker, a selective antagonist for the excitatory amino acid receptor subtype ampa/kainate, has also been shown to protect both global and focal ischemia histopathologically. most recently, when given after the first provocation, the non-competitive n-methyld-aspartate (nmda) antagonist mk-801 protected the brain from the cumulative effects of repeated brief ischemic episodes. ischemia-induced calcium ion treatment techniques and neurotransmitter disturbances are critical areas for ongoing study. in 477 reperfusion injury in brain stroke the pathogenesis of reperfusion injury, several studies have implicated oxygen radicals. [13] references 1. lyden, p. d., k. p. madden, w. m. clark & k. c. sasse. incidence of cerebral hemorrhage after treatment with tissue plasminogen activator or streptokinase following embolic stroke in rabbits [corrected]. stroke 1990; 21: 1589-1593. 2. ginsberg md. adventures in the pathophysiology of brain ischemia: penumbra, gene expression, neuroprotection: the 2002 thomas willis lecture. stroke 2003; 34 (1): 214–23. 3. weinstein pr, hong sba, sharp fr. molecular identification of the ischemic penumbra. stroke 2004; 35 (11): 2666–70. 4. graham sh, chen j. programmed cell death in cerebral ischemia. j cereb blood flow metab 2001; 21 (2): 99–109. 5. chen l, xue z, jiang h. effect of propofol on pathologic time-course and apoptosis after cerebral ischemiareperfusion injury. acta anaesthesiol scand. 2008;52(3):413-419. 6. pandi-perumal sr, srinivasen v, maestroni gjm, et al. melatonin. nature’s most versatile biological signal? febs j 2006; 273:2813–2838. 7. lim c, alexander mp, lafleche g. the neurological and cognitive sequelae of cardiac arrest. neurology 2004; 63:1774– 1778. 8. hartman re, lee jm, zipfel gj, wosnia df. characterizing learning deficits and hippocampal neuron loss following transient global cerebral ischemia in rats. brain res rev 2005; 1045:48–56. 9. reiter rj, tan dx, leon j et al. when melatonin gets on your nerves: its beneficial actions in experimental models of stroke. exp biol med 2005; 230:104–117. 10. margaill i, plotkine m, lerouet d. antioxidant strategies in the treatment of stroke. free rad biol med 2005; 39:429– 443. 11. d. l. carden and d. n. granger, “pathophysiology of ischaemia-reperfusion injury,”the journal of pathology, vol. 190, no. 3, pp. 255–266, 2000. 12. m. ahmad, n. j. dar, z. s. bhat et al., “inflammation in ischemic stroke: mechanisms, consequences and possible drug targets,” cns and neurological disorders— drug targets, vol. 13, no. 8, pp. 1378–1396, 2014. 13. a. denes, p. thornton, n. j. rothwell, and s. m. allan, “inflammation and brain injury: acute cerebral ischaemia, peripheral, and central inflammation,” brain, behavior, and immunity, vol. 24, no. 5, pp. 708–723, 2010. 14. r. von bernhardi, l. eugen´ın-von bernhardi, and j. eugen´ın, “microglial cell dysregulation in brain aging and neurodegeneration,” frontiers in aging neuroscience, vol. 7, article 124, 2015. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article butterfly vertebra: a case report d. adam, d. iftimie, gina burduşa, cristiana moisescu romania doi: 10.1515/romneu-2017-0012 80 | adam et al butterfly vertebra             doi: 10.1515/romneu-2017-0012 butterfly vertebra: a case report d. adam1,2, d. iftimie1, gina burduşa1, cristiana moisescu1 1department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania abstract: background and importance: butterfly vertebra is an uncommon congenital spinal anomaly, which can be easily mistaken for vertebral fracture, infection or tumor. clinical presentation: we report the case of a 20-year-old male patient with a 3-year history of intermittent mid-thoracic spinal pain. local examination showed a mild thoracic kyphoscoliosis. neurological examination was normal. computer tomography revealed the presence of a t6 butterfly vertebra associated with morphological anomalies in adjacent vertebral bodies and t6-t9 schmorl's nodes. mri scan confirmed the diagnosis and additionally showed a mild spinal stenosis caused by apparent posterior epidural fat hypertrophy. the patient was treated with painkillers and physical therapy. conclusion: butterfly vertebra is a benign condition. once diagnosed, additional diagnostic procedures are not necessary. neurosurgeons must be aware of this congenital anomaly that should not be confused with a vertebral fracture. key words: butterfly vertebra, congenital vertebral anomaly background and importance back pain is a common complaint, mainly caused by degenerative spinal disease. thoracic spine pain is less frequently encountered in comparison with the lumbar or cervical regions. congenital spinal anomaly at this level is a rare cause pain. butterfly vertebra, which consists of a sagittal cleft in the vertebral body, is a congenital malformation that gives vertebrae the particular appearance of butterfly wings on anterior-posterior view of imaging studies. we report the case of a patient diagnosed with this rare spinal anomaly and perform a literature review concerning this condition. clinical presentation a 20-year old male patient was admitted to our neurosurgical department, complaining of intermittent mid-thoracic spinal pain, particularly while maintaining a sitting position for prolonged periods of time. onset of symptoms occurred 3 years before presentation, with progressive worsening and alleviation after bed rest and occasional overthe-counter pain medication. romanian neurosurgery (2017) xxxi 1: 80 – 84 | 81             medical history was unremarkable. the patient mentioned a pulmonary condition at birth and a restrictive pulmonary syndrome diagnosed in his teens, but the he could not supply any medical documents for confirmation. taking into consideration his particularly considerable height (208 cm), he had previously undergone basic endocrinological testing which was normal. he denied any history of trauma and no other probable cause of symptoms could be identified. local examination revealed a mild thoracic kyphoscoliosis. no abnormalities were detected after a thorough neurological examination. chest x-ray and routine blood tests were normal. ct scan of the thoracic spine revealed a congenital anomaly of the t6 vertebral body with a butterfly vertebra appearance (figure 1.a). the vertebra appeared incompletely developed with a hypoplastic aspect, only the posterior third of the vertebral body being visible, which consisted of two unjoined halves (figure 1.b); the posterior vertebral arch was normal. the thoracic kyphosis was augmented at this level. other encountered anomalies included morphological changes of adjacent vertebral bodies with a t5-t7 incomplete vertebral block tendency (figure 1.c) and schmorl nodes at t7-t9 levels. mri of the thoracic spine confirmed the diagnosis of t6 butterfly vertebra (figures 2.a, 2.b, 2.c). additionally, it showed a mild spinal stenosis at this level caused by the apparent hypertrophy of posterior epidural fat tissue with no intramedullary signal changes. no thoracic disc protrusions or herniations were observed (figure 2d). the patient was recommended pain medication and physical therapy with good outcome at follow-up. 82 | adam et al butterfly vertebra             figure 1 ct scan of thoracic spine revealing t6 butterfly vertebra (a) coronal view showing the characteristic twowinged aspect (white arrows) of butterfly vertebra. (b): axial slice at t6 level displaying the two unjoined hemivertebrae (white arrows). (c): sagittal view showing the augmented kyphosis at t6 level and t5t7 incomplete vertebral block aspect (white arrow) figure 2 t2-weighted mri scan of thoracic spine with t6 butterfly vertebra coronal (a), axial (b) and sagittal (c) t6-level centered images, confirming specific butterfly vertebra aspect. (d): sagittal slice revealing mild spinal canal stenosis at t6 level caused by posterior epidural fat hypertrophy (arrow-head); multiple schmorl nodes can be seen (the largest at the superior t7 endplate arrow) romanian neurosurgery (2017) xxxi 1: 80 – 84 | 83             discussion rokitansky first described butterfly vertebra in 1844, located at the 12th thoracic vertebra1. this is a congenital anomaly of the spine, which has received various names: sagittal cleft vertebra, anterior rachischisis, anterior spina bifida and anterior somatoschisis. since its first description, very few cases of this malformation have been reported. butterfly vertebra develops between the 3rd and 6th gestational week, when the two chondrification centers fail to fuse while giving rise to the vertebral body. these centers remain separated by notochordal tissue, which normally regresses from the level of the vertebral body and develops into the nucleus pulposus of the intervertebral disc. thus, the vertebral body is comprised of two hemivertebrae and the notochordal derived tissue between them. this explains the anteroposterior x-ray appearance of two hemivertebrae separated by an empty space or cleft, more or less large. this malformation can be associated with other spinal anomalies, such as lumbosacral transitional vertebrae, spina bifida, diastematomyelia and several congenital syndromes: allagille syndrome, jarcho-levin syndrome, klippel-feil syndrome or with gastrointestinal and genitourinary anomalies (2, 3). the etiology is supposed to be genetic (deletions of chromosome 20) (4) or a congenital deficiency of vascularization (5). butterfly vertebra is usually asymptomatic. patients with this malformation are diagnosed incidentally or may present atypical chronic pain. this condition can be diagnosed prenatally with 3d transabdominal ultrasound images6 or after birth with plain x-ray or bone window computer tomography. on plain radiography, butterfly vertebra appears wedge-shaped in lateral view and can be easily misdiagnosed as a compression fracture. anteroposterior spine x-ray reveals the vertebral body split in two halves. mri shows the particular butterfly vertebra aspect on sagittal, axial and coronal images, other possibly associated congenital anomalies or intervertebral disc prolapses. the butterfly vertebra malformation has been described not only in clinical cases, but also in dry bone specimens from archeological excavations of necropolises (7, 8). the differential diagnosis of butterfly vertebra can be made with a compression fracture of the vertebral body, either osteoporotic or pathologic in nature. this is the reason why a dexa test or laboratory investigations are sometimes necessary in order to rule out osteoporosis, neoplasia or infection. there have been reports of butterfly vertebra cases associated with disc protrusion or herniation of nucleus pulposus at the abnormal vertebral body level (5, 9–11). patients with alagille syndrome present atresia/hypoplasia of the intrahepatic biliary tree, chronic cholestasis, peculiar facies (hypertelorism, sunken eyes, straight nose, pointed chin, abnormal dental implantation), pulmonary stenosis and skeletal abnormalities (butterfly vertebra, phalangeal or ulnar 84 | adam et al butterfly vertebra             shortening, pelvic abnormalities, osteoporosis) (2). clinicopathological spectrum of jarcholevin syndrome is composed of a short neck and trunk, constricted thorax, rib and vertebral anomalies (butterfly vertebrae, hemivertebrae, fused or hypoplastic vertebrae) (3). when a butterfly vertebra is detected prenatally in association with other anomalies, it can usually lead to the termination of pregnancy6.in the case of postnatal diagnosis in children, only follow-up is necessary in order to exclude potentially associated rare syndromes. this condition is a benign spinal anomaly which must be differentiated from other pathological conditions. in adult patients with butterfly vertebra, physical therapy is recommended to achieve unrestricted and pain-free movements. once the diagnosis of butterfly vertebra has been established, patients must be informed that it represents a benign anomaly and further investigation procedures can be avoided. conclusion butterfly vertebra is a rare, benign condition. once diagnosed, additional diagnostic procedures are not necessary. neurosurgeons must be aware of this congenital anomaly, that should not be confused with a vertebral fracture. references 1. müller f, o’rahilly r, benson dr. the early origin of vertebral anomalies, as illustrated by a “butterfly vertebra”. j anat. 1986;149:157-169. http://www.ncbi.nlm.nih.gov/pubmed/3693103. accessed january 30, 2017. 2. berrocal t, gamo e, navalón j, et al. syndrome of alagille: radiological and sonographic findings. a review of 37 cases. eur radiol. 1997;7(1):115-118. http://www.ncbi.nlm.nih.gov/pubmed/9000411. accessed january 31, 2017. 3. vázquez-lópez me, lópez-conde mi, somoza-rubio c, pérez-pacín r, morales-redondo r, gonzález-gay ma. anomalies of vertebrae and ribs: jarcho levin syndrome. description of a case and literature review. jt bone spine. 2005;72(3):275-277. doi:10.1016/j.jbspin.2004.06.007. 4. silverman f, kuhn j. caffey’s pediatric x-ray diagnosis: an integrated imaging approach. 9th ed. st. louis: c.v. mosby company; 1993. 5. sonel b, yalçin p, oztürk ea, bökesoy i. butterfly vertebra: a case report. clin imaging. 25(3):206-208. http://www.ncbi.nlm.nih.gov/pubmed/11679230. accessed january 30, 2017. 6. youssef a, zagonari s, salsi g, et al. prenatal diagnosis of isolated butterfly vertebra. ultrasound obstet gynecol. 2014;44(6):725-726. doi:10.1002/uog.13457. 7. anderson t. a medieval example of a sagittal cleft or ?butterfly? vertebra. int j osteoarchaeol. 2003;13(6):352-357. doi:10.1002/oa.695. 8. keenleyside a. sagittal clefting of the fifth lumbar vertebra of a young adult female from apollonia pontica, bulgaria. int j osteoarchaeol. 2015;25(2):234237. doi:10.1002/oa.2268. 9. delgado a, mokri b, miller gm. butterfly vertebra. j neuroimaging. 1996;6(1):56-58. http://www.ncbi.nlm.nih.gov/pubmed/8555665. accessed january 30, 2017. 10. cho h-l, kim j-s, paeng ss, lee s-h. butterfly vertebra with lumbar intervertebral disc herniation. j neurosurg spine. 2011;15(5):567-570. doi:10.3171/2011.6.spine1178. 11. ozaras n, gumussu k, demir se, rezvani a. differential diagnosis of multiple vertebral compression: butterfly vertebrae. j phys ther sci. 2015;27(11):36013603. doi:10.1589/jpts.27.3601.   flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article long term prognosis of ventriculoatrial shunt for idiopathic normal pressure hydrocephalus in the elderly tsukasa kawase, kyosuke miyatani, riki tanaka, yasuhiro yamada, shamim ul haq siddiqui, yoko kato, kiyoshi takagi, ahmed ansari japan, india doi: 10.1515/romneu-2017-0076 490 | kawase et al long term prognosis of ventriculoatrial shunt doi: 10.1515/romneu-2017-0076 long term prognosis of ventriculoatrial shunt for idiopathic normal pressure hydrocephalus in the elderly tsukasa kawase1, kyosuke miyatani1, riki tanaka1, yasuhiro yamada1, shamim ul haq siddiqui1, yoko kato1, kiyoshi takagi2, ahmed ansari3 1fujita health university banbuntane hotokukai hospital, nagoya, japan 2chiba kashiwa tanaka hospital, japan 3upums, saifai, up, india abstract: objective: a retrospective study was conducted to access the long-term prognosis of inserting the ventriculoatrial (va) shunt in the elderly for the idiopathic normal pressure hydrocephalus (inph). material and methods: retrospective data is collected from april 2004 to august 2015, and 1065 patients were selected. patients who underwent surgical examination or surgery in suspected inph were included. tap test is done in all cases and found to be effective for 968 cases and 656 va shunts for 614 cases. out of 614 cases there are 440 cases in which patient age were over 75 years. of these 440 cases only 141 cases were able to observe 03 years or more after the surgery, 37 deaths and 05 cases with survival and unknown prognosis were found among them. so we analyzed this group mainly in 99 cases that the prognosis after 03 years was known. we access the outcome of va shunt by the modified rankin scale (mrs), inph grading scale (inphgs) and complications in the operative 656 cases and in 03 years follow up of 141 patients. results: of 141, there are 78 males and 63 females. age at the time of va shunt insertion was 81.5±4.1 years and age at final follow-up was 85.2±4.4 years. the proportion of patients who achieved a favorable outcome by complications was 97.9% in 03 years follow-up period and 87.7% in which follow-up is less than 03 years. at the time of va shunt insertion out of 141, 57 patients lies between 75-79 years, 57 between 80-84, 24 between 85 to 89, and only 03 were found to be 90 years or more. at the time of final follow-up at 03 years, 15 patients lies between 75 to 79 years, 56 between 80 to 84 years, 57 between 85 to 89 years and 23 patents were found to be 90 years or greater. 70 cases or almost 50% exceeded 85 years. at the time of va shunt 1, 11, 39, 51, 36, 3, 0 patients were in 0 to 6 modified rankin scale score respectively and at 03 years follow-up 8, 19, 32, 29, 9, 2, 37 were in 0 to 6 mrs romanian neurosurgery (2017) xxxi 4: 490 494 | 491 respectively. comparison of the study is done with siphoni study on vp shunt and lp shunt. conclusion: patients suspected of having idiopathic normal pressure hydrocephalus were treated by va shunt and found no significant difference in serious adverse effects. this study shows that va shunt is an effective choice for inph in the late elderly population, but it needs more randomized control trial to establish its efficacy. key words: idiopathic normal pressure hydrocephalus, ventriculoatrial shunt, hydrocephalus introduction the clinical triad of cognitive decline, gait and balance impairment, and urinary incontinence with normal cerebrospinal fluid (csf) pressure measured through lumbar puncture is called normal pressure hydrocephalus (nph) was described by first described by hakim and adams (1). nph has further subdivided into two, one in which cause is known and the other in which no etiology can be identified or called idiopathic nph. although there has been significant improvement in the field of radiological imaging and despite the development of sensitive imaging modalities the diagnosis of patient having the nph remain problematic and worse which patients would benefit from the surgical intervention is also very challenging. even more difficult is to choose the diversion; either peritoneum through ventricle or lumbar spine or from ventricles to the atrium. because the nph is relatively a disease affecting the old population and also it is not uncommon for the elderly of having the obesity, constipation, and colorectal cancer and other diseases, performing the ventriculoperitoneal (vp) or lumboperitoneal (lp) shunt is not without complications. japan is progressing aging at a remarkably rapid rate compared to other developed countries, especially 2025 when the babyboomer generation reaches the age of 75, it is predicted that the burden of nursing care and medical social security expanses will increase significantly (2). at present, vp shunt and lp shunt is the most commonly used intervention and va shunts are relatively less used. va shunts are not as much of as vp or lp because of technical issues and reporting of the cardiopulmonary complications. there are also a small number of studies which directly comparing the long-term prognosis vp or lp to va shunts in inph. this study is going to evaluate the long-term prognosis of va shunts in inph and explore the effectiveness of its use in the elderly patients. material and methods we conducted a retrospective evaluation of 1065 patients from april 2004 to august 2015 who underwent surgical examination in suspected inph. we done lumbar puncture tap test to check the effectiveness of the procedure. the tap test was effective for 968 cases and 656 ventriculoatrial shunts for 614 cases. among the 614 cases, 440 cases were in 492 | kawase et al long term prognosis of ventriculoatrial shunt which the age at surgery was over 75 years. of these, only 141 patients were able to observe 03 years or more after surgery. out of 141, 37 cases meets death and 05 patients with unknown prognosis was found among them. so, we analyzed this group mainly in 99 cases that the prognosis after 03 years was known. results the effect of the va shunt is done in five stages (table 1), and also mrs (table 2) and inphgs (table 3) are also used. there were 495 cases in evans index (ei) > 0.3 (67.3%), disproportionally enlarged subarachnoid space hydrocephalus (desh) only 212 cases (28.9%), (table 4). the frequency of this desh is almost the same as the results announced from brain surgery facility in london at the international society of hydrophilia. fulfilling the guidelines, that is, ei>0.3, desh was only 177 cases (24.1%), which was less than the overall quarter. complication of va shunts was accessed in 656 cases, in which 76 requires intervention including shunt infection in 4 cases, valve part ulcer in 2, venous thrombosis in 4, shunt revision in 40, cardiopulmonary complication in 08, cervical subcutaneous abscess in 02, chronic subdural hematoma in 16 and 35 cases which doesn’t need intervention including postoperative brain hemorrhage in 05 cases and chronic subdural hematoma in 30. these adverse events were also observed for more than 03 years were only 2.1% and including which requires intervention venous thrombosis in 2 cases, chronic subdural hematoma in 1 case, shunt revision in 13, and cervical subcutaneous abscess in 01, while 01 case of post-operative brain hemorrhage and 10 cases of chronic subdural hematoma doesn’t need any intervention. during the follow-up period of 3 years or more no cases of shunt infection, valve part ulcer, and cardiopulmonary complications observed. discussion in our study of 141 patients, 78 males and 63 females and average age at the time of va shunt was found to be 81.5 ± 4.1 years. age at final follow-up was 85.2 ± 4.4 years. at the time of va shunt insertion and at final follow-up 57 and 15 cases were in 75 to 79 years of age, 57 and 56 cases were in 80 to 84 years, 24 and 57 cases were in 85 to 89 years and 03 and 22 cases were in 90 or above age respectively (figure 1). during the follow-up period of 3 years or more there are out of 141 patients there are 37 deaths within 03 years. out of 104 patients 33 patents had been observed for 3 to 4 years, 36 for 4 to 5 years, 20 for 5 to 6 years, 11 for 6 to 7 years and only 4 patients for up to 7 years. this study is trying to compare the effects of shunt in cases under 75 or over 75 years of age. 174 cases were under the age of 75 and 440 cases were over 75 years old. under 75 years of age patients out of 174, there were 120, 19, 26, 5, 0, and 5 cases which were excellent, good, fair, poor, dead, and undetermined. over 75 years of age patients out of 440, there were 287, 72, 51, 11, 03, and 16 cases which were excellent, good, fair, poor, dead, and undetermined. if good and more are shunt responder, 79.9% (139 out of 174) at the age of 75 years and 81.6% (359 out romanian neurosurgery (2017) xxxi 4: 490 494 | 493 of 440) at the age of 75 and older, were able to judge that the effect of shunt was effective. the shunt effect is the best prognostic judgment during the postoperative course. about shunt effect, there were 106 cases were excellent, 13 were good, 15 were fair, 4 were poor, and 03 cases of death. one year later follow-up shows prognosis of excellent, good, fair, poor, death and unknown in 97, 14, 8, 2, 19, 1 cases respectively. three years later follow-up shows prognosis of excellent, good, fair, poor, death and unknown in 63, 10, 7, 19, 37, and 5 cases respectively (figure 2). regarding the functional status of the patients after va shunt we use modified rankin scale score. it is considered that mrs 2 or more is independent. in the preoperative cases, 51 cases (36.3%) were independent. one year later, 86 out of 121 surviving (71.1%) were independent. three years later, 59 out of 99 surviving (59.6%) were independent (figure 3). we compare our study with previous multicenter, prospective cohort study; study of idiopathic normal pressure hydrocephalus on neurological improvement (sinphoni). in sinphoni for vp shunt (3); the number of cases were 100 and in 15% severe adverse effects develop. in sinphoni 2 for lp shunt (4) 93 cases were enrolled; out of this 22% develop adverse effects. out study comprises 656 cases and out of this 12.3% develop adverse effects. conclusion in our study of va shunt for inph serious complications were few even in patients who were 75 years old or older at the time of surgery and 03 years or more after surgery. the prognosis of 3 years after va shunt even in elderly is better than before surgery at 74% in mrs. approximately 25% of the cases meet the diagnostic criteria of guidelines. although our study shows va shunt surgery is an effective choice for inph, there is need for other randomized control trials. table 1 determining effect of va shunt excellent mrs improvement, mmse 3 or better, or incontinence good although mrs has not improved, it reduces the burden on care-givers, increased patient activity fair only slight improvements are observed, no effect (facial expression improved, walking was slightly improved) poor worsening dead death table 2 modified rankin scale score 0 no symptoms at all 1 no significant disability despite symptoms; able to carry out all usual duties and activities 2 slight disability; unable to carry out all previous activities, but able to look after own affairs without assistance 3 moderate disability; requiring some help, but able to walk without assistance 4 moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance 5 severe disability; bedridden, incontinent and requiring constant nursing care and attention 6 dead 494 | kawase et al long term prognosis of ventriculoatrial shunt table 3 grading scale score for nph gait disturbance 0=normal 1=unstable, but independent gait 2=walking w/ one cane 3=walking w/ two canes or a walker frame 4=walking not possible dementia 0=w/in normal range 1= no apparent dementia but apathetic 2 -socially dependent but independent at home 3 =partially dependent at home 4 =totally dependent urinary incontinence 0=absent 1= absent but w/ pollakisuria or urinary urgency 2 =sometimes only at night 3 =sometimes even during the day 4 =frequent table 4 non-desh desh total ei ≤ 0.3 304 35 239 ei > 0.3 318 177 (24.1%) 495 (67％) total 522 212 (28.9%) 734 figure 1 figure 2 figure 3 correspondence tsukasa kawase, associate professor, fujita health university banbuntane hotokukai hospital, nagoya, japan references 1. hakim s, adams rd: the special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure. observations on cerebrospinal fluid hydrodynamics. j neurol sci 2: 307–327, 1965. 2. japan: super-aging society preparing for the future naoko muramatsu, phd hiroko akiyama, phd. the gerontologist, volume 51, issue 4, 1 august 2011, pages 425–432, https://doi.org/10.1093/geront/gnr067. 3. hashimoto m, ishikawa m, mori e, kuwana n: diagnosis of idiopathic normal pressure hydrocephalus is supported by mri-based scheme: a prospective cohort study. cerebrospinal fluid res 7:18, 2010. 4. kazui h, miyajima m, mori e, ishikawa m: lumboperitoneal shunt surgery for idiopathic normal pressure hydrocephalus (sinphoni-2): an open-label randomised controlled trial. lancet neurol 14:585–594, 2015. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 405 409 | 405 chronic subdural hematoma associated with idiopathic thrombocytopenic purpura in an elderly female: a rare case report sachin chhabra, ashok gupta department of neurosurgery, sms medical college, jaipur, rajasthan, india abstract: intracranial hemorrhage is the most fatal complication of idiopathic thrombocytopenic purpura(itp) and is very rare(<1%) mostly in young females and intraparenchymal or subarachnoid in most of the cases. we report a case of 63 years of female presented with acute sdh with petechiae in both lower limbs and headache. after ruling out all causes patient was diagnosed as having idiopathic thrombocytopenic purpura(itp).considering her haematological and neurological profile patient was kept conservatively. platelets and steroids were given to the patient following which platelet counts improved but patient deteriorated clinically. hence patient was operated and surgical evacuation of sdh was done through burr hole. although some studies have shown disappearance of chronic sdh with medical management, but it failed in our case and so surgical evacuation was done. key words: subdural hematoma (sdh), idiopathic thrombocytopenic purpura (itp) introduction intracranial hemorrhage is the most fatal complication of idiopathic thrombocytopenic purpura (itp) and is very rare (<1%). in most of the cases it is either intraparenchymal or in subarachnoid space or at multiple sites (1, 2). only a few cases of isolated subdural haematoma (sdh) with itp have been reported in literature (1-7). itp associated chronic sdh more often occurs in females and younger age was considered as a significant risk factor in its occurrence (7). in this report we describe the rare occurrence of itp associated sdh in an elderly patient and its management. case report a female patient, 63 years of age working as housewife, presented in outpatient department with chief complaints of generalized headache since 1 day associated with nausea with history of loss of consciousness 1 day back. she was not having any chronic illness and was not taking any medications. she did not give any history of trauma. on examination, she was afebrile and was not having any neck stiffness. patient had no neurological deficit. patient pulse rate was 64/minute and blood pressure was 138/80 mm hg. she was having multiple small painless petechiae present on both upper limbs. on 406 | chhabra, gupta chronic subdural hematoma associated with idiopathic thrombocytopenic purpura admission, patient was having hb 11.5, tlc 8,000, platelet count 70,000. patient random blood sugar and other biochemical investigations were in normal limit. on next day patient platelet count came down to 14000 which further reduced to 9000 on subsequent day. patient prothrombin time (pt) was in normal limits (13.9 sec with inr 1.07). ncct head at the time of admission revealed hyperdensity in right frontotemporoparietal region with compressed ventricle on right side with midline shift towards left suggestive of subdural hematoma (figure 1). in view of patient condition and platelet count, patient was kept conservatively and platelets were transfused. patient was further investigated for low platelet count and peripheral blood film of patient showed marked thrombocytopenia with few large platelets. rbc were normocytic normochromic and normal in count. no immature cells or atypical cells or parasite seen. bone marrow aspiration cytology revealed marked thrombocytopenia, mild rouleaux formation with adequate megakaryocytes on aspirate smears and normal myeloid and erythroid series suggestive of megakaryocytic thrombocytopenia. patient coagulation profile, total leucocyte count and differential leucocyte counts were in normal limits. viral infection was ruled out. dengue igg and igm antibodies were negative. anti nuclear antibodies were negative. hepatic viral markers and liver function tests were normal eliminating the hepatic cause. considering patient history and clinical examination and ruling out all possible case of low platelet count, a diagnosis of itp was made. as patient was having low platelet count, initially conservative treatment was done by transfusing 11 units of random donor platelets and steroids (prednisolone) were started under strict glucose monitoring and in tapering dose. after 9 days of conservative treatment patient platelet count improved but general condition deteriorated. patient became drowsy and her gcs dropped from 15 to 12.repeat ct scan showed right frontotemporoparietal chronic sdh with mass effect and midline shift towards left (figure 2). patient hb was 11.2 and platelet count came out to be 1.37 lacs. right frontal and parietal burr hole was made and drainage of haematoma done on urgent basis. postoperatively patient was conscious and was obeying commands and was relieved of headache. she was discharged on fourth post operative day. romanian neurosurgery (2016) xxx 3: 405 409 | 407 figure 1 showing acute frontotemporoparietal sdh at the time of admission 408 | chhabra, gupta chronic subdural hematoma associated with idiopathic thrombocytopenic purpura figure 2 showing repeat scan of the patient having chronic sdh with mass effect discussion itp is a disorder characterized by antibody mediated destruction of platelets resulting in isolated low platelet count. although it may cause bleeding but intracranial hemorrhage is very rare and most serious complication of itp. subdural hematoma is extremely rare in these patients of itp developing intracranial hemorrhage. chronic sdh is usually due to trauma but seckin h et al in their review found that it may occur spontaneously in cases of. sdh associated with itp (3). itp most commonly occurs in females and h takase et al showed that younger age was a significant risk factor for itp associated sdh(7).in our case it occurred in 63 year old female with no past history of bleeding and trauma. romanian neurosurgery (2016) xxx 3: 405 409 | 409 as it is a rare condition, no definite guidelines are given regarding management and management remains controversial. previously surgery with evacuation of hematoma used to be the primary treatment. but in 1997, gupta et al used medical management to treat an asymptomatic case successfully (4). lee and kim in their meta analysis of seven patients found that five patients improved non surgically (6). later on sreedharan et all in 1999 (2) and h seckin et all 2006 (3) treated such patients conservatively. conservative treatment involves intravenous administration of steroids or immunoglobulins or a combination of these two along with platelet transfusion. however any deterioration in patient clinical status demands an urgent repeat neuroimaging to decide about surgical evacuation. considering our patient’s neurological and haematological profile, patient was given medical management. various studies have shown spontaneous resolution of sdh with transfusion of platelets and steroids. but in our case patient’s platelet count improved but worsened neurologically after 9 days of conservative treatment. therefore, surgical drainage of chronic sdh through burr hole was done. thus, by our case report we emphasize that in such patients although a trial of conservative treatment can be given but it has to be weighed against patient haematological and neurological status. correspondence dr. sachin chhabra resident, department of neurosurgery, sms medical college, jaipur rajasthan (india) mobile: 7877377683 e-mail: drsachinchhabra@gmail.com references 1. miyamoto t, sasaki k, ohshima t, matsumoto k, itoh j. a case of chronic subdural hematoma associated with idiopathicthrombocytopenic purpura (itp). no shinkei geka 1997;25:157-61. 2. sreedharan ps, rakesh s, sajeev s, pavithran k, thomasm. subdural haematoma with spontaneous resolution-rare manifestation of idiopathic thrombocytopenic purpura. j assoc physicians india 2000;48:432-4 3. seckin h, kazanci a, yigitkanli k, simsek s, kars hz. chronic subdural hematoma in patients with idiopathic thrombocytopenic purpura:a case report and review of the literature. surg neurol 2006;66:411-4 4. gupta sk, khosla vk, verma sc. spontaneous resolution of chronic subdural haematoma secondary to chronic idiopathic thrombocytopenic purpura. neurol india 1997;45:95-7. 5. shinmyozu k, okadome t, maruyama y, maruyama i, osame m, tara m. occurrence of subdural hematoma closely associated with danazol administration in a patient with refractory itp. rinsho ketsueki 1990;31:674-5 6. lee ms, kim wc. intracranial hemorrhage associated with idiopathic thrombocytopenic purpura: report of seven patients and a meta-analysis. neurology 1998;50:1160-3. 7. hajime t, junya t, naoki i, daisuka y, mizuki h, makoto t. therapeutic suggestions for chronic subdural haematoma associated with idiopathic thrombocytopenic purpura: a case report and literature review, nmc case report journal 2015:3:118-122 microsoft word 5adamd_filum romanian neurosurgery (2018) xxxii 2: 217 223 | 217             doi: 10.2478/romneu-2018-0028 filum terminale paraganglioma with associated cyst: a case report danil adam1,2, cristiana moisescu2, dragos iftimie2, gina burdusa2 1„carol davila” university of medicine and pharmacy, bucharest, romania 2department of neurosurgery, „saint pantelimon” clinical emergency hospital, bucharest, romania abstract: background and importance: paragangliomas are neuroendocrine tumors that occur most often within the adrenal glands. the most frequent extra-adrenal locations include the carotid body and the jugular bulb. filum terminale paragangliomas are extremely rare, with just 33 cases reported to date. imagistic appearance is similar with other types of intradural extramedullary tumors such as ependymomas and schwannomas. histopathological examination is the only method of establishing a definitive diagnosis. they are classified as grade i who tumors with favorable prognosis in the case of total resection. clinical presentation: a 46-year-old woman without any relevant medical history was admitted to our neurosurgical department, complaining of low back pain with bilateral sciatica. she presented no neurological deficits and routine blood tests, as well as heart rate and blood pressure, were within normal ranges. lumbar spine mri with gadolinium enhancement revealed an intradural tumor with irregular, well defined margins and intense homogeneous enhancement, located at the level of the l3 vertebra. it presented an unenhancing intradural cystic lesion that extended cranially up to the level of the l1 vertebra. the tumor and associated cyst were completely resected through l2-l4 laminectomy. the tumor-cyst complex was attached, yet nonadherent to the conus medullaris and nerve roots, which allowed safe total removal. histopathological examination was suggestive for paraganglioma, a diagnosis confirmed by immunohistochemistry that classified it as moderately differentiated, non-secreting type. serum metanephrines subsequently determined were within normal ranges. also, additional imagistic tests consisting of cervical and abdominal ultrasound and contrast enhanced ct scans did not detect any additional tumors. postoperatively, the patient was neurologically intact, with complete remission of presenting symptoms at 3 months follow-up. conclusion: filum terminale paraganglioma is a rare diagnosis which is frequently overlooked. however, gross total resection, a common goal for all spinal tumors, can be curative in these particular cases. key words: paraganglioma, filum terminale, imagistic differential diagnosis 218 | adam et al filum terminale paraganglioma with associated cyst             background and importance paragangliomas are neuroendocrine system tumours which regularly occur within the adrenal medulla. most frequent extraadrenal locations are represented by carotid body, glomus jugulare, mediastinum and retroperitoneum. (1) in extremely rare situations, paragangliomas can develop within the spinal canal, usually confined to the cauda equina, with approximately 200 such cases described in the literature. (2) originally described in 1970 as a “secretory ependymoma” (3) and two years later defined as a distinctive tumour by lerman et al (4), paragangliomas present a key histological characteristic, namely the presence of cytoplasmic granules which contain catecholamines. considering spinal paragangliomas, like most other extra-adrenal lesions, the majority are non-functional neoplasms. (5) spinal paragangliomas usually present with radicular pain and neurological deficits and, since cauda equina is often involved, they may cause cauda equina syndrome. magnetic resonance imaging (mri) represents the investigation of choice in evaluating lesions of the cauda equina. due to their similarities in imagistic appearance, paragangliomas can be easily mistaken for ependymomas or schwannomas. (6) spinal paragangliomas are benign lesions and they need to be distinguished from more aggressive tumour pathology, considering that their prognosis is excellent after total surgical resection, which currently represents the gold standard in treatment. (7) we present the case of a patient with filum terminale paraganglioma, addressing the clinical and imagistic characteristics, as well as histopathological aspects. clinical presentation a 46-year-old woman was admitted to our department with a one year history of low back pain and bilateral sciatica, symptoms which have aggravated over the past two months. her general physical examination was normal. the neurological examination revealed an anteflexion of 70° and a bilateral straight leg raise test of 80°. motor and sensory examination, deep tendon reflexes, peri-anal sensitivity and anal tone were within normal range. also, the patient had no history of bowel or bladder dysfunction. routine blood tests, as well as heart rate and blood pressure, were within normal ranges. due to persistent symptoms, an enhancing magnetic resonance imaging examination of the lumbar spine was performed. the study revealed an intradural mass (isointense in t1 sequence and hypointense in t2, respectively) located at the level of the inferior half of l3 vertebra, developed within the cauda equina as a uniformly enhancing nodule with irregular, polylobular contour. the described lesion measured 15.5 mm in antero-posterior diameter and occupied approximately 85% of the spinal canal. it also associated a cystic lesion that extended cranially up to the level of l1 intervertebral disc, at the top of the conus medullaris, providing an overall distended aspect of the spinal canal (figure 1, figure 2). romanian neurosurgery (2018) xxxii 2: 217 223 | 219             figure 1 ovoidal intradural mass developed at the level of cauda equina, isointense in t1-weighted mri images (a), hypointense in t2-weighted mri images, in sagittal (b) and coronal (c) sections, presenting an overlying cystic lesion extended up to the level of l1 vertebra figure 2 the tumour showed homogenous enhancement after injection of gadolinium in sagittal (a) and axial (b) t1 contrast weighted mri sequences the patient was brought in for surgery and a l2–l4 laminectomy was performed. after opening the dura mater, an oval shaped, redcoloured, with firm consistency, vascular, well-circumscribed mass was identified (figure 3). 220 | adam et al filum terminale paraganglioma with associated cyst             figure 3 intraoperative image: after opening the dura mater, a red-coloured, firm, well-circumscribed mass contiguous with the filum terminale nerve roots was identified although contiguous with filum terminale nerve roots at its inferior aspect, the tumour was non-adherent to the dura mater, nor to the spinal roots. these characteristics allowed a total en bloc removal of the tumour and its cystic component (figure 4). figure 4 intraoperative image showing complete removal of cauda equina tumour and its cystic component the patient presented an uneventful postoperative course. the radicular pain subsided completely and the neurological examination was normal at discharge, as well as at 3 months follow-up. the histopathological examination of the tumour revealed small nests of chromaffin cells (chief cells) with pale eosinophilic staining separated into groups by segmenting bands of fibrovascular stroma, surrounded by supporting sustentacular cells, aspect known as zellballen pattern (figure 5). immunohistochemical testing showed a positive reaction for chromogranin and a negative reaction for glial fibrillary acidic protein (gfap) in the chief cells. all these findings supported the diagnosis of paraganglioma. it was further classified as moderately differentiated, non-secreting type. figure 5 histopathological examination of the tumour showing typical zellballen architecture h&e (x 10) taking into consideration the diagnosis, further investigations were conducted, in order to identify secondary paragangliomas, if present. abdominal ultrasonography, cervical spine and abdominal contrast enhanced ct scan and cervical doppler were performed, that did not find any other tumors. serum metanefrines were also within normal ranges. romanian neurosurgery (2018) xxxii 2: 217 223 | 221             discussion the majority of paragangliomas over 90% of cases develop in the adrenal gland whereas approximately 90% of extra–adrenal paragangliomas occur in the carotid body and jugular gland. (8) the development of paragangliomas in the central nervous system is extremely rare. intracranially, they have been described in the sellar, pineal and petrous ridge region. (9) regarding the spinal canal, around 200 paragangliomas with this location have been described so far, mostly intradural. in particular, only 33 cases of filum terminale paraganglioma have been reported in the literature. (10) they can also develop extradurally but most extradural spinal paragangliomas are metastatic tumours, appearing more frequently at the level of the thoracic spine. (11, 12) the case that we reported was a spinal paraganglioma located at the level of the filum terminale, representing a solitary case among the spinal tumours diagnosed in our department over the last two years. the clinical presentation usually depends on the location and size of the tumour, radicular pain and neurological deficits being most frequently encountered. however, paragangliomas can occasionally cause uncommon manifestations such as accelerated heart rate and arterial hypertension due to overproduction of catecholamines (2), manifestations which we did not encounter in our case. the gold standard imagistic investigation for spinal pathology is mri, however filum terminale paragangliomas do not present specific mri characteristics. herman et al. described in an article published in 1998 the mri characteristics of spinal paragangliomas and reported that mri fails in differentiating paragangliomas from other tumours. (13) paragangliomas present as hypoor isointense masses in t1 – weighted images, hypointense in t2 – weighted images, with diffuse contrast enhancement. nevertheless, other spinal tumours, such as ependymomas, have similar imagistic appearance which makes the preoperative radiological diagnosis of paraganglioma extremely difficult. in our case, the tumour had no particular mri features: it presented as an ovoidal intradural mass developed at the level of cauda equina, isointense in t1-weighted images, hypointense in t2-weighted images, with homogenously contrast enhancement. the mass presented an associated cystic lesion extending cranially to the level of l1 vertebra with complex signal intensity (figure 1, figure 2). the pathogenesis of the cyst formation is not completely understood but it is not an unusual occurrence in association with paragangliomas. in 1997, faro et al reported a case of paraganglioma of the cauda equina with an associated overlying intramedullary cyst. the author offered two possible hypothesis for cyst development: firstly, the normal flow of csf could have been obstructed inferiorly by the tumour thus creating a differential pressure, forcing fluid into the spinal cord; secondly, the cysts could have been created by the fluid from abnormal tumour vessels extravasated into the interstitial space in the spinal cord. (9) nevertheless, the presence of overlying cystic 222 | adam et al filum terminale paraganglioma with associated cyst             lesions is not characteristic for paragangliomas, as they occur in association with a considerable number of spinal tumours, including ependymomas. microscopically, paragangliomas show typical nuclear monomorphism and display “zellballen” pattern (large chief cells arranged in nests). immunohistochemistry studies show reactivity for markers of neural differentiation, including chromogranin and synaptophysin and lack of reactivity for glial fibrillary acidic protein (gfap). this particular immunoprofile, which we encountered in our case as well, is helpful in order to exclude ependymoma from the differential diagnosis, considering that ependymomas are immunoreactive for gfap and s-100 protein. (14) the recommended treatment for spinal paragangliomas is total resection. in such cases, the postoperative prognosis is very good, associating a recurrence rate of only 4% at 12 years after surgery. (15) in case of subtotal resection, radiotherapy may be used, although resistance to this type of treatment has been noted. chemotherapy has no therapeutic role. (16) few cases of metastatic paraganglioma have been reported in the published literature. (11, 12) the patient that we presented was further investigated in order to identify the potential presence of other tumors. however, there was no evidence of secondary paragangliomas. conclusion filum terminale paragangliomas are benign tumours which, in the majority of cases, can be successfully treated by total resection. although extremely rare, they should be included in the differential diagnosis of spinal intradural tumours as they need to be distinguished from more aggressive tumours, given the excellent prognosis that they associate. references 1. lack ee. paragangliomas. in: mills se, ed. sternberg’s diagnostic surgical pathology. lippincott williams & wilkins; 2004:669-696. 2. gelabert-gonzález m. paragangliomas of the lumbar region. j neurosurg spine. 2005;2(3):354-365. doi:10.3171/spi.2005.2.3.0354 3. miller ca, torack rm. secretory ependymoma of the filum terminale. acta neuropathol. 1970;15(3):240-250. http://www.ncbi.nlm.nih.gov/pubmed/4193811. accessed may 29, 2018. 4. lerman ri, kaplan es, daman l. ganglioneuromaparaganglioma of the intradural filum terminale. j neurosurg. 1972;36(5):652-658. doi:10.3171/jns.1972.36.5.0652 5. glenner gg, grimley pm, (u.s.) afi of p. tumors of the extra-adrenal paraganglion system (including chemoreceptors). 1974:90 pages. file://catalog.hathitrust.org/record/007401029. 6. aghakhani n, george b, parker f. paraganglioma of the cauda equina region--report of two cases and review of the literature. acta neurochir (wien). 1999;141(1):8187. http://www.ncbi.nlm.nih.gov/pubmed/10071690. accessed may 29, 2018. 7. soni t v, gupta a. spinal paraganglioma : a rare tumour. http://medind.nic.in/gaa/t14/i1/gaat14i1p110.pdf. accessed may 29, 2018. 8. pacak k, linehan wm, eisenhofer g, walther mm, goldstein ds. recent advances in genetics, diagnosis, localization, and treatment of pheochromocytoma. ann intern med. 2001;134(4):315-329. http://www.ncbi.nlm.nih.gov/pubmed/11182843. accessed may 29, 2018. 9. faro sh, turtz ar, koenigsberg ra, mohamed fb, chen cy, stein h. paraganglioma of the cauda equina with associated intramedullary cyst: mr findings. ajnr romanian neurosurgery (2018) xxxii 2: 217 223 | 223             am j neuroradiol. 1997;18(8):1588-1590. http://www.ncbi.nlm.nih.gov/pubmed/9296205. accessed may 29, 2018. 10. landi a, tarantino r, marotta n, et al. paraganglioma of the filum terminale: case report. world j surg oncol. 2009;7:95. doi:10.1186/1477-7819-7-95 11. lau d, la marca f, camelo-piragua s, park p. metastatic paraganglioma of the spine: case report and review of the literature. clin neurol neurosurg. 2013;115(9):1571-1574. doi:10.1016/j.clineuro.2013.01.006 12. lázaro b, klemz m, flores ms, landeiro ja. malignant paraganglioma with vertebral metastasis: case report. arq neuropsiquiatr. 2003;61(2b):463-467. doi:10.1590/s0004-282x2003000300026 13. herman m, pozzi-mucelli rs, skrap m. paraganglioma of the cauda equina: case report and review of the mri features. acta univ palacki olomuc fac med. 1998;141:27-30. http://www.ncbi.nlm.nih.gov/pubmed/9684477. accessed may 29, 2018. 14. suri vs, tatke m, singh d, sharma a. histological spectrum of ependymomas and correlation of p53 and ki67 expression with ependymoma grade and subtype. indian j cancer. 41(2):66-71. http://www.ncbi.nlm.nih.gov/pubmed/15318011. accessed may 29, 2018. 15. makhdoomi r, nayil k, santosh v. primary spinal paragangliomas: a review. neurosurg q. 2009;19(3):196-199. doi:10.1097/wnq.0b013e3181a45c15 16. say cc, hori j, spratt j. chemodectoma with distant metastasis: case report and review of the literature. am surg. 1973;39(6):333-341. http://www.ncbi.nlm.nih.gov/pubmed/4350420. accessed may 29, 2018. doi: 10.33962/roneuro-2021-032 lateral orbitotomy in the management of an intra-orbital lipoma. a case report mandour cherkaoui, ait lhaj el houssaine, khouya ali adil, gazzaz miloudi, e.l. mostarchid brahim romanian neurosurgery (2021) xxxv (2): pp. 204-206 doi: 10.33962/roneuro-2021-032 www.journals.lapub.co.uk/index.php/roneurosurgery lateral orbitotomy in the management of an intra-orbital lipoma. a case report mandour cherkaoui1, ait lhaj el houssaine2, khouya ali adil2, gazzaz miloudi3, e.l. mostarchid brahim3 1 department of neurosurgery, 5th military hospital, guelmim, morocco 2 department of ophthalmology, 5th military hospital, guelmim, morocco 3 department of neurosurgery, military hospital mohammed v, rabat, morocco abstract introduction: lipomas are benign subcutaneous mass, but the intra-orbital location is rarely reported in the literature and it can resemble a variety of other orbital lesions. case report: we describe a 15-year-old girl who presented with left exophthalmia. orbital magnetic resonance imaging showed an encapsulated intra-conal mass displacing the optic nerve medially, the external right muscle laterally and the globe anteriorly. excisional biopsy of the mass by lateral orbitotomy approach resolved the exophthalmia, and histology revealed a primary orbital lipoma. conclusion: the diagnosis of an intra-orbital lipoma is not easy and the surgical approach represents a challenge to achieve a total excision while avoiding complications. introduction lipoma is a benign mesenchymal neoplasm composed of mature adipose tissue surrounded by a fibrous tissue capsule1. the majority is developed in the subcutaneous soft tissue in the neck, shoulder and back, but it is uncommon in the orbital region2. we describe a case of exophthalmia caused by an intra-orbital lipoma and review of the literature. case report a 15-year-old moroccan girl, admitted to our department for treatment of a progressive left exophthalmia for 06 months. there was no history of trauma, visual disturbances, and significant ocular or medical histories. on ocular examination, she had visual acuity of 20/20 in both eyes with a left axile, reducible and non-pulsatile exophthalmia. orbital magnetic resonance imaging (mri) revealed an encapsulated intraconal mass (2.5 x 1,7 x 0,5 cm) in the posterolateral compartment of the left orbit. the mass was displacing the optic nerve medially, the external keywords exophthalmia, lateral orbitotomy, lipoma, orbital corresponding author: mandour cherkaoui department of neurosurgery, 5th military hospital, guelmim, morocco mandour1978@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 205 lateral orbitotomy in the management of an intra-orbital lipoma right muscle laterally and the globe anteriorly with resultant exophthalmia. hypointense at t1 and hyperintense at t2 taking the contrast (figure 1-2). a left lateral orbitotomy approach was utilized with an excisional biopsy (figure 3-4). histopathological evaluation revealed well-encapsulated, mature adipose tissue consistent with a primary orbital lipoma. after surgery, exophthalmia had subsided with a normal ocular motility. figure 1. post contrast axial t1-weighted mri showing hyper intense lesion (arrow). figure 2. axial t2-weighted mri showing hyper intense lesion (arrow). figure 3. preoperative photograph showing the incision for a left lateral orbitotomy. figure 4. intra-operative photograph showing tumor excision. discussion lipoma is a benign lobulated tumor composed of mature adipose tissue surrounded by a fibrous tissue capsule. frequently it is localized subcutaneously around the torso, neck, and proximal limbs3, but in the orbital region is uncommon with the reported incidence of 0.6% in adults and 2.8% in children4. the exact etiology of lipoma formation is unknown, but there are instances following trauma4,5. also some hypotheses have been mentioned as hypertrophy theory (the growth of the tumor is caused by obesity) and metaplasia theory (the growth of lipoma occurs due to differentiation of mesenchymal cells into lipoblast) 6. generally, orbital lipoma slow growing and often asymptomatic until large enough to be palpable, visible or cause mass effect. rarely grows and compresses the optic nerve causing disturbance in visual function7. the radiological appearance of orbital lipoma, on computed tomography the tumor has a distinctive low attenuation with a finely defined border. on mri it is generally hyperintense on t1-weighted imaging and indistinct to orbital blood on t2-weighted images, hypointense after fat suppression. however, it is not enhanced after contrast images8, but in our case the lesion was hyperintense. due to the various presentations of lipoma, the diagnosis is not always easy and other orbital masses should be considered in the clinical differential diagnosis, such as dermoid cyst, fibrous histiocytoma, schwannoma and cavernous hemangioma9. the recommended treatment is the surgical excision and it is a challenge because of the complex anatomy of the orbital structures10, 11. in our case, the patient was operated by a lateral orbitotomy with removal of the tumor. the long-term outcome after surgery is seen to be excellent however, recurrence of the tumor may occur due to incomplete excision12. conclusion we present a case of a rare intra-orbital tumor whose surgical approach such as lateral orbitotomy is a real challenge for neurosurgeons. consent written informed consent was obtained from the patient for publication of this case report and accompanying images. abbreviations mri: magnetic resonance imaging 206 mandour cherkaoui, ait lhaj el houssaine, khouya ali adil et al. author’s contributions: c m: manuscript writing; a l and a k: manuscript preparation; b e and m g: manuscript analysis. all authors read and approved the final manuscript. acknowledgements this study received no funding conflicts of interest the authors declare no potential conflict of interest references 1. pranav shrestha; gulshan bahadur shrestha. orbital lipoma as an uncommon cause of unilateral proptosis: a case report. international medical case reports journal. 2020:13 415–418. 2. rodiah rahmawaty lubis. giant preseptal upper eyelid lipomai. a case report. euromediterranean biomedical journal. 2020: 15 (13) ; 58–60. 3. weiss s. lipomatous tumours. monogr pathol 1996; 38: 207–239. 4. cpt matthew; chorost mc ; ltc vladimir yakopson, and al. posttraumatic encapsulated orbital lipoma. military medicine. 2020:185, 9/10:e1876. 5. aust mc, spies m, kall s, joukuszies a, gohritz a, vogt p. lipomas after blunt soft tissue trauma: are they real? analysis of 31 cases. br j dermatol 2007; 157(1): 92–9. 6. kumaraswamy s, madan n, keerthi r, shakti s. lipomas of oral cavity: case reports with review of literature. j maxillofac oral surg. 2009. 8(4):394–397. 7. chi mj, roh jh, lee jh and al. a case of orbital lipoma with exophthalmos and visual disturbance. jpn j ophthalmol. 2009;53(4):442–444. 8. shah nb, chang wy, white va and al. orbital lipoma: 2 cases and review of literature. ophthal plast reconstr surg. 2007;23(3):202–205. 9. ali sf, farber m, meyer dr: fibrolipoma of the orbit. ophthalmic plast reconstr surg 2013; 29(3): 79–81. 10. r. malarvizhi, k. vasumathi, a. anuradha and al. a clinical study on evaluation, indications, surgical techniques and complications of various orbitotomies done in a tertiary care centre. delhi j ophthalmol 2020; 30; 22-26. 11. zeynel a. karcioglu. surgical techniques for orbital tumors. surgical ophthalmic oncology. 2019-october: pp 117-127. 12. vasconcelos js, gharaibeh f, nittinger hc. trauma as pathogenesis of a plantar forefoot fibrolipoma: first case and review of the literature. case rep surg. 2013:691276. doi: 10.33962/roneuro-2021-049 possible predictive markers in surgical decision making in patients with degenerative or isthmic lumbar spondylolisthesis ulas yuksel, mustafa ogden, mustafa ilker karagedik, turgut kultur, bulent bakar romanian neurosurgery (2021) xxxv (3): pp. 294-303 doi: 10.33962/roneuro-2021-049 www.journals.lapub.co.uk/index.php/roneurosurgery possible predictive markers in surgical decision making in patients with degenerative or isthmic lumbar spondylolisthesis ulas yuksel1, mustafa ogden1, mustafa ilker karagedik1, turgut kultur2, bulent bakar1 1 kirikkale university, faculty of medicine, department of neurosurgery, kirikkale, turkey 2 kirikkale university, faculty of medicine, department of physical medicine and rehabilitation, kirikkale, turkey abstract background: although age, comorbidity, duration and severity of symptoms, slippage degree, and flexion-extension slipping stability during x-ray imaging are effective in making a surgical decision in patients with spondylolisthesis, these factors are rarely based on definitive evidence. the aim of this study was to determine the efficacy of clinical, radiological and biochemical findings in surgical decision making in these patients. materials and methods: patients’ data including age, gender, degree and type (i.e. degenerative or isthmic) of the spondylolisthesis, urinary incontinence, neurogenic claudication were recorded. radiological imaging studies (lumbar dynamic x-ray, computed tomography, magnetic resonance imaging), serum glucose, c-reactive protein and erythrocyte sedimentation rate values of the patients obtained during hospital admissions were evaluated. results: forty patients were followed conservatively and 12 patients were treated surgically. degenerative spondylolisthesis was seen in 22 patients. nine patients had neurogenic urinary incontinence and 19 patients had neurogenic claudication. when the patients were divided into two groups with and without surgical treatment, the presence of the pars defect, slipping distance in a neutral position and slipping distance in flexion position was significantly different between groups. a positive correlation was found between pars defect and surgical treatment. likelihood ratio test results revealed that the presence of pars defect, neurogenic claudication and neurogenic urinary incontinence could be the best parameters in decision making the surgical treatment. conclusion: the presence of pars defect, neurogenic claudication and urinary incontinence could be the best parameters that may help the surgeon to make the surgical treatment decision. introduction lumbar spondylolisthesis which described as slipping of a vertebral body over the adjacent vertebral body may be caused by a combination keywords degenerative spondylolisthesis, isthmic spondylolisthesis, surgery corresponding author: ulas yuksel kirikkale university, faculty of medicine, department of neurosurgery, kirikkale, turkey ulasyksl@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 295 possible predictive markers in surgical decision in patients with degenerative or isthmic lumbar spondylolisthesis of osteoarthritis and degenerative changes in the disc and facet joints. this slipping may lead to varying degrees of spinal stenosis, resulting in mechanical low back pain associated with hip and leg pain clinically (1). in literature, it is advocated that these patients should be treated with conservative treatment as the first choice, but surgical treatment should be applied when this treatment fails (2-5). today, surgical treatment options include decompression and fusion to slipping vertebrae with instrumentation (611). however, other clinical studies have demonstrated that there will be no difference in spine fusion between instrument use and non-use (12), some of the systematic reviews have reported that the use of instrumentation can increase the likelihood of obtaining spinal fusion (1). in clinical practice, it is generally reported that the patient's age, comorbidity, duration and severity of the symptoms, degree of slippage, and flexionextension slipping stability during x-ray imaging are effective on making of the surgical decision, but these factors are rarely based on definitive evidence. it is generally believed that patients with symptoms of neural compression due to spondylolisthesis can be useful for simple decompression and less extensive fusion surgery, and extensive fusion surgery is generally recommended when serious "instability" is detected (12). this study aimed to determine the efficacy of clinical, radiological and biochemical findings in surgical decision making in patients with degenerative or isthmic lumbar spondylolisthesis. materials and methods patient groups this single-center retrospective study was conducted after approval by the local ethics committee for clinical trial. in this study, the information of patients who were treated with conservatively and surgically was included between january 2015 and december 2018. icd-10 (international statistical classification of diseases and related health problems) coding was used to scan hospital records. patients were divided into groups according to gender, whether there was a pars defect, according to the degree of spondylolisthesis, and whether surgical treatment was performed. patients with missing data, patients coded with the wrong icd-10 code, patients with pathological spondylolisthesis due to a tumor, rheumatic disease, and infection, and patients in the pediatric age group (<16 years) were excluded from the study. furthermore, patients with cauda equine syndrome which is considered as an emergency procedure, patients who underwent spinal surgery including unilateral or bilateral fenestration, hemilaminectomy, laminectomy, laminarthrectomy, laminotomy, foraminotomy, discectomy, flavectomy, sequestrectomy including anterior interbody fusion between adjacent vertebrae, instrumented fusion (with/without decompression) including intervertebral stabilization such as transforaminal interbody fusion (tlif), anterior lumbar interbody fusion (alif) or posterior lumbar interbody fusion (plif), extreme lateral lumbar interbody fusion (xlif) were ruled out from the study. moreover, vascular claudication and other conditions/ joint problems limiting walking capacity have been ruled out materials the patients' parameters including the age, gender, degree of spondylolisthesis according to meyerding grade, type of the spondylolisthesis (degenerative or isthmic spondylolisthesis according to the evidence of the pars defect), presence of the radiculopathy pain, urinary incontinence and neurogenic claudication were recorded. radiological images (lumbar dynamic x-ray, computed tomography (ct), magnetic resonance imaging (mri), serum glucose, c-reactive protein (crp) and erythrocyte sedimentation rate (esr) values of the patients obtained during hospital admissions were evaluated. the approach for measurements acquisition was adopted after review of available literature (13,14). surgical method after general anesthesia applied to the patients who were considered surgery, paravertebral muscles were dissected by midline incision while the stabilization level was determined by scopy while in prone position and stabilization was applied to the vertebrae using transpedicular screws. a standard laminectomy was performed to remove spinal cord compression. following hemostasis, surgical layers were closed according to anatomy and the operation was terminated. the patients walked on the first postoperative day after wearing a lumbosacral corset. 296 ulas yuksel, mustafa ogden, mustafa ilker karagedik et al. biochemical analysis study results were obtained from the venous blood samples of the patients taken at their initial admission to the hospital. esr (reference range <20 mm / h) was measured using an analyzer (esr 40, cystate diagnostics). serum glucose (reference range 74-109 mg/dl) and crp (reference range 0.155 mg/dl) levels were obtained by the immunoturbidimetric method using an analyzer (roche diagnostic cobas c501). table 1. table shows the patients’ data according to the gender. chi-square test, mann whitney u test, p<0.05 gender variable male female x2 / z p pars defect degenerative 4 (18.2%) 18 (81.8%) 0.229* 0.632 isthmic 4 (13.3%) 26 86.7%) meyerding grade 1 3 (27.3%) 8 (72.7%) 3.453* 0.178 2 5 (17.2%) 24 (82.8%) 3 0 (0.0%) 12 (100.0% treatment modality conservative 7 (17.5%) 33 (82.5%) 0.596* 0.440 surgery 1 (8.3%) 11 (91.7%) number of screws 0 7 (17.5%) 33 (82.5%) 0.916* 0.633 4 0 (0.0%) 4 (100.0%) 6 1 (12.5%) 7 (87.5%) incontinence no 6 (14.0%) 37 (86.0%) 0.391* 0.532 yes 2 (22.2%) 7 (77.8%) radiculopathy pain no 7 (26.9%) 19 (73.1%) 5.318* 0.021 yes 1 (3.8%) 25 (96.2%) claudication no 5 (15.2%) 28 (84.8%) 0.004* 0.951 yes 3 (15.8%) 16 (84.2%) glucose 93.50 (81-206 ) 95.00 (79-140) -0.038 0.970 c-reactive protein 2.61 (0-28) 4.36 (1-54) -0.311 0.755 esr 10 (9-46) 19 (5-71) -0.210 0.834 (*) chi-square test number of patients (%) or median (minimum-maximum) value x2: chi-square score, z: z score, esr: erythrocyte sedimentation rate statistical analysis the power analysis for the results of this study was performed using the "gpower 3.1” package program and it was concluded that the patients included in the study were sufficient to form the study. chi-square test, kruskal wallis test, and mannwhitney u test was used to compare the nonparametric data between the groups (p <0.05). parametric data were analyzed using independent samples t-test (p<0.05). spearman's rho correlation test was used to determine the relationship between the parameters (p <0.05). roc-curve test and logistic regression test were used to determine the predictive markers in the decision of surgical treatment. the likelihood ratio test was used to estimate the “best” variable in decision-making in patients undergoing surgery (p <0.05). results fifty-two patients (male = 8, female = 44) were included in the study. nine patients (17.31%) had neurogenic urinary incontinence and 19 patients (36.54%) had neurogenic claudication. twenty six patients (50%) suffered from radiculopathy pain. serum glucose median values were 94.5 (79-205) mg / dl, crp median values were 4.29 (0-54) mg / dl, and esr median values were 19 (5-71) mm / hour. when the patients were divided into two groups according to their gender, no statistically significant difference was found in terms of study parameters except radiculopathy pain (x2 = 5.318, p = 0.021) (table 1). forty of the patients were followed conservatively and 12 patients were treated surgically. when the patients were divided into two groups with and without surgical treatment, there was found a statistically significant difference in terms of pars 297 possible predictive markers in surgical decision in patients with degenerative or isthmic lumbar spondylolisthesis defect (x2 = 4.202, p = 0.040) (table 2). on the other hand, there was a statistically different between the two groups in terms of the slipping distance in the neutral position of the patient (t = 3.113, p = 0.006) and slipping distance in flexion position of the patient (t = 3.380, p = 0.003). however, changing the degree of the slippage angle was not different between the groups. in non-operated patients, the median slipping distance position was 0.22 ± 0.18 mm and the slippage angle was 7.03 ± 9.1 degrees in the neutral position while the mean slipping level was 0.24 ± 0.22 mm and the slippage angle was 7.26 ± 0.31 degrees in the flexion position (figure 1 and figure 2). in operated patients, the median slipping distance was 15.52 ± 13.78 mm and the slippage angle was 6.78 ± 5.49 degrees in the neutral position while the mean slipping distance was 17.26 ± 14.11 mm and the slippage angle was 4.93 ± 5.61 degrees in the flexion position (figure 3 and figure 4). figure 1. lumbar dynamic x-ray images which were obtained in the neutral position and in flexion position showing the slipping distance of patient who was not operated. table 2. table shows the data of patients who were treated surgically and conservatively. chi-square test and mann whitney u test, p<0.05 treatment modality variable conservative surgery x2 / z p gender male 7 (87.5%) 1 (12.5%) 0.596* 0.440 female 33 (75.0%) 11 (25.0%) pars defect degenerative 20 (90.9%) 2 (9.1%) 4.202* 0.040 isthmic 20 (66.7%) 10 (33.3%) meyerding grade 1 9 (81.8%) 2 (18.2%) 0.953* 0.621 2 23 (79.3%) 6 (20.7%) 3 8 (66.7%) 4 (33.3%) number of screw s 0 40 (100.0%) 0 (0.0%) 52.000* <0.001 4 0 (0.0%) 4 (100.0%) 6 0 (0.0%) 8 (100.0%) incontinence no 33 (76.7%) 10 (23.3%) 0.004* 0.947 yes 7 (77.8%) 2 (22.2%) 298 ulas yuksel, mustafa ogden, mustafa ilker karagedik et al. radiculopathy pain no 22 (84.6%) 4 (15.4%) 1.733* 0.188 yes 18 (69.2%) 8 (30.8%) claudication no 27 (81.8%) 6 (18.2%) 1.219* 0.270 yes 13 (68.4%) 6 (31.6%) glucose 94 (79-206) 98 (83-139) -1.055 0.292 c-reactive protein 4.33 (0-28) 4.03 (1-54) -0.421 0.673 esr 19 (5-71) 10 (6-51) -0.941 0.347 (*) chi-square test number of patients (%) or median (minimum-maximum) value x2: chi-square score, z: z score, esr: erythrocyte sedimentation rate figure 2. lumbar dynamic x-ray images which were obtained in the neutral position and in flexion position showing the slippage degrees of patient who was not operated table 3. table shows the patients’ data according to the type (i.e. degenerative and isthmic type) of spondylolisthesis. chi-square test and mann whitney u test, p<0.05 type of spondylolisthesis variable degenerative isthmic x2 / z p gender male 4 (50.0%) 4 (50.0%) -0.229* 0.632 female 18 (40.9%) 26 (59.1%) meyerding grade 1 10 (90.9%) 1 (9.1%) 14.605* <0.001 2 10 (34.5%) 19 (65.5%) 3 2 (16.7%) 10 (83.3%) treatment modality conservative 20 (50.0%) 20 (50.0%) 4.202* 0.040 surgery 2 (16.7%) 10 (83.3%) number of screw s 0 20 (50.0%) 20 (50.0%) 4.885* 0.087 4 0 (0.0%) 4 (100.0%) 6 2 (25.0%) 6 (75.0%) 299 possible predictive markers in surgical decision in patients with degenerative or isthmic lumbar spondylolisthesis incontinence no 22 (51.2%) 21 (48.8%) 7.981* 0.005 yes 0 (0.0%) 9 (100.0%) radiculopathy pain no 13 (50.0%) 13 (50.0%) 1.261* 0.262 yes 9 (34.6%) 17 (65.4%) claudication no 12 (36.4%) 21 (63.6%) 1.307* 0.253 yes 10 (52.6%) 9 (47.4%) glucose 93.00 (79-139)* 96.5 (83-206)* -1.076 0.282 c-reactive protein 3.96 (1-17)* 4.58 (0-54)* -0.771 0.441 esr 19 (5-71)* 14 (6-68)* -0.600 0.548 (*) chi-square test number of patients (%) or median (minimum-maximum) value x2: chi-square score, z: z score, esr: erythrocyte sedimentation rate figure 3. lumbar dynamic xray images which were obtained in the neutral position and in flexion position showing the slipping distance of patient who was operated. table 4. table shows the data of patients according to the grade (i.e. meyerding grade) of spondylolisthesis. chi-square test and kruskal wallis test, p<0.05 grade of the spondylolisthesis variable 1 2 3 x2 / z p gender male 3 (37.5%) 5 (62.5%) 0 (0.0%) 3.453* 0.178 female 8 (18.2%) 24 (54.5%) 12 (27.3%) pars defect degenerative 10 (45.5%) 10 (45.5%) 2 (9.1%) 14.605* 0.001 isthmic 1 (3.3%) 19 (63.3%) 10 (33.3%) treatment modality conservative 9 (22.5%) 23 (57.5%) 8 (20.0%) 0.953* 0.621 300 ulas yuksel, mustafa ogden, mustafa ilker karagedik et al. surgery 2 (16.7%) 6 (50.0%) 4 (33.3%) screw s number 0 9 (22.5%) 23 (57.5%) 8 (20.0%) 7.319* 0.120 4 0 (0.0%) 4 (100.0%) 0 (0.0%) 6 2 (25.0%) 2 (25.0%) 4 (50.0%) incontinence no 11 (25.6%) 23 (53.5%) 9 (20.9%) 3.030* 0.220 yes 0 (0.0%) 6 (66.7%) 3 (33.3%) radiculopathy pain no 8 (30.8%) 13 (50.0%) 5 (19.2%) 2.916* 0.233 yes 3 (11.5%) 16 (61.5%) 7 (26.9%) claudication no 4 (12.1%) 21 (63.6%) 8 (24.2%) 4.539* 0.103 yes 7 (36.8%) 8 (42.1%) 4(21.1%) glucose 92 (81-139) 94 (79-206) 97 (80-125) 0.375 0.829 c-reactive protein 4 (1-17) 2.61 (0-54) 5 (1-28) 0.539 0.764 esr 20.50 (9-59) 19 (5-71) 10 (5-68) 0.978 0.613 (*) chi-square test number of patients (%) or median (minimum-maximum) value x2: chi-square score, z: z score, esr: erythrocyte sedimentation rate figure 4. lumbar dynamic x-ray images which were obtained in the neutral position and in flexion position showing the slippage degrees of patient who was operated degenerative spondylolisthesis was seen in 22 patients (male=4, female=18) and isthmic spondylolisthesis was found in 30 patients (male=4, female=26). when the patients were divided into two groups according to their pars defect (degenerative spondylosisthesisvs isthmic spondylolisthesis), the grade of spondylolisthesis (x2= 14.605, p <0.001), surgical treatment (x2= 4.202, p = 0.040) and urinary incontinence (x2= 7.981, p = 0.005) was found to be different between the groups (table 3). eleven patients (21.15%) had grade 1, 29 patients (55.77%) had grade 2 and 12 patients (23.08%) had grade 3 spondylolisthesis. when the patients were divided into three groups according to the degree of spondylolisthesis, only the pars defect was found to be different between the groups (x2= 14.605, p = 0.001) (table 4). at the end of the correlation analysis applied to the data of all patients, a positive correlation was found between the gender and radiculopathy pain (r 301 possible predictive markers in surgical decision in patients with degenerative or isthmic lumbar spondylolisthesis = 0.320, p = 0.021), between pars defect and the grade of spondylolisthesis(r = 0.491, p <0.001), between the pars defect and receiving the surgical treatment (r = 0.284, p = 0.041), between the pars defect and urinary incontinence (r=0.392, p=0.004), between the urinary incontinence and radiculopathy pain (r=0.356, p=0.010) and between urinary incontinence and neurogenic claudication (r = 0.392, p = 0.004). however, a negative correlation was seen between the age and pars defect (r = -0.390, p = 0.004). at the end of the roc-curve test and logistic regression tests, it was determined that no parameter could be a sensitive and specific predictive marker in the decision of surgical treatment. however, the likelihood ratio test results revealed that the presence of pars defect (x2 = 10.576, p = 0.001), the presence of neurogenic urinary incontinence (x2 = 8.203, p = 0.004) and the presence of neurogenic claudication (x2 = 8.003, p = 0.005) could be auxiliary parameters in decision making the surgical treatment (table 5). besides, it was considered that the angulation change or slipping distance in the slipping spine segment detected on dynamic x-ray images was not sensitive or specific or an auxiliary parameter in decision making the surgical treatment. table 5. table shows the best possible markers to make a decision of the surgery in patients with spondylolisthesis. roccurve test and likelihood ratio test, p<0.05 roc-curve test likelihood ratio test variable area p x2 p pars defect 0.667 0.082 10.576 0.001 meyerding grade 0.575 0.434 0.001 0.973 incontinence 0.496 0.965 8.203 0.004 radiculopathy pain 0.608 0.259 1.468 0.226 claudication 0.588 0.362 8.003 0.005 discussion it has been shown in the literature that loss of height in the disc space, facet joint hypertrophy, hypertrophic ligamentumflavum, subchondral sclerosis, the presence of osteophyte, multifudis atrophy and presence of the “pars interarticularis” fracture may cause either severe canal stenosis and foraminal stenosis and anterior and / or lateral slipping in the vertebrae (3-5). isthmic spondylolisthesis may result from a stress fracture, acute fracture or elongation defect. it is typically seen in children aged 5-7 years, but the defect can reach and be seen in adulthood. lesions often occur in l5 s1 but in trauma cases above the l5 level. it may be asymptomatic or may cause low back pain, hamstrings stiffness, knee contractures, and bladder and bowel incontinence (15). in a study, degenerative changes in the lumbar spine were examined in 3 groups and group 1 patients had transient dysfunction; group 2 patients had an unstable spine and group 3 patients had restabilization. it was reported that group 1 patients benefited more from conservative treatment, conservative approaches were applied to those in the early stage of group 2 patients, while conservative treatments were inadequate and fusion surgery was performed in late group 2 patients. group 3 patients had severe stenosis and these patients underwent spinal decompression with or without instrumentation (16). in another study, it was suggested that the micro-instability period could be unnoticed. therefore, a classification was formed by scoring the changes in x-ray, ct, and mri for a decision on which the treatment would be done in these patients. according to the classification, it was aimed to provide early diagnosis and treatment to the patient in the period of micro-instability (17,18). in our study, it was thought that the complaint of radiculopathy pain occurred mostly in women, but gender did not affect other study parameters. on the other hand, it was found that most of the patients (n = 30) had pars defect and 10 of them had surgical treatment. most of the patients had grade 2 spondylolisthesis (n = 19) and most of them (n = 40) were treated conservatively, whereas surgical treatment was preferred in patients with pars defects (n = 10), and most patients (n = 43) did not have urinary incontinence. most of the patients (n = 30) had pars defect and 19 patients had grade 2 and 10 patients had grade 3 spondylolisthesis. surgical treatment was applied to 2 patients without pars defect and 10 patients with pars defect; 6 of these patients had grade 2 and 4 had grade 3 spondylolisthesis. although it was seen that most of the patients with grade 2-3 isthmic spondylolisthesis underwent surgery, it was thought that type or grade of spondylolisthesis could not be a criterion for deciding on the surgical treatment because of a small number of patients. 302 ulas yuksel, mustafa ogden, mustafa ilker karagedik et al. correlation analysis showed that pars defect may be an important factor in the formation of spondylolisthesis and neurogenic urinary incontinence. it was also thought that urinary incontinence may also occur if the patient had symptoms and signs of radiculopathy pain or neurogenic claudication. however, it was argued that there was no statistical relationship between the degree of spondylolisthesis and the findings of radiculopathy pain, neurogenic claudication or urinary incontinence. esr or crp values, which are known as acute and / or chronic inflammation markers, could not be correlated with any parameters. with this result, it was argued that pars defect and / or spondylolisthesis detected in patients could not be the result of an inflammatory process. on the other hand, at the end of the roc-curve analysis, it was concluded that none of the parameters evaluated in this study could be a predictive marker in deciding on surgical treatment. however, likelihood ratio test results demonstrated that the presence of pars defect in the patient, the presence of neurogenic claudication and urinary incontinence findings could be the parameters that may help the surgeon to decide on surgical treatment. however, it was thought that the degree of spondylolisthesis could be ineffective in deciding for surgical treatment. some limitations of this study are as follows: first, the retrospective character of this study limited the discussion of the mid-term or long-term follow up results of the patients. second, the number of the study population was very small. nevertheless, it can be easily said that the results of this study were very impressive and novel to discuss the predictive markers in deciding on surgical treatment. third, in some cases, determining the correct level to identify spondylolisthesis was a challenge due to the difficulty in counting spinal levels with the possibility of lumbar-sacral segments or sacralized lumbar segments or a variable total number of spine levels. fourth, because some mr and / or ct images were from external institutions, they could not be evaluated retrospectively. therefore, the relationship between the x-ray images and ct / mr images which could support more relevant data was not investigated. finally, the present study included computerized abstracted information that required personal measurements that could be prone to random error. conclusion at the end of this study, it was seen that the presence of pars defect (isthmic spondylolisthesis) in the patient, the presence of neurogenic claudication and urinary incontinence findings could be the parameters that may help the surgeon to make the surgical treatment decision. however, it was considered that the presence of the radiculopathy suffering of the patient or the grade of spondylolisthesis could be ineffective in the decision of surgical treatment. references 1. martin cr, gruszczynski at, braunsfurth ha, fallatah sm, o'neil j, wai ek. the surgical management of degenerative lumbar spondylolisthesis: a systematic review. spine (phila pa 1976) 2007;32(16):1791-8. 2. weinstein jn, lurie jd, tosteson td, zhao w, blood ea, tosteson an, et al. surgical compared with nonoperative treatment for lumbar degenerative spondylolisthesis. four-year results in the spine patient outcomes research trial (sport) randomized and observational cohorts. j bone joint surg am 2009;91:1295-1304. 3. miao j, wang s, park wm, xia q, fang x, torriani mp, et al. segmental spinal canal volume in patients with degenerative spondylolisthesis. spine j 2013;13:706-12. 4. wang g, karki sb, xu s, hu z, chen j, zhou z, et al. quantitative mri and x-ray analysis of disc degeneration and paraspinal muscle changes in degenerative spondylolisthesis. j back musculoskelet rehabil 2015;28:277-85. 5. akgul t. degenerative lomber spondylolisthesis: diagnosis and treatment. totbi̇d dergisi 2015;14:290–7. 6. katz jn, lipson sj, lew ra, grobler lj, weinstein jn, brick gw, et al. lumbar laminectomy alone or with instrumented or noninstrumented arthrodesis in degenerative lumbar spinal stenosis. patient selection, costs, and surgical outcomes. spine (phila pa 1976) 1997;22:1123-31. 7. watters wc 3rd, bono cm, gilbert tj, kreiner ds, mazanec dj, shaffer wo, et al. an evidence-based clinical guideline for the diagnosis and treatment of degenerative lumbar spondylolisthesis. spine j 2009;9:609-14. 8. kornblum mb, fischgrund js, herkowitz hn, abraham da, berkower dl, ditkoff js. degenerative lumbar spondylolisthesis with spinal stenosis: a prospective long-term study comparing fusion and pseudarthrosis. spine (phila pa 1976) 2004;29:726-34. 9. ghogawala z, benzel ec, amin-hanjani s, barker fg 2nd, harrington jf, magge sn, et al. prospective outcomes evaluation after decompression with or without instrumented fusion for lumbar stenosis and degenerative grade i spondylolisthesis. j neurosurg 303 possible predictive markers in surgical decision in patients with degenerative or isthmic lumbar spondylolisthesis spine 2004 oct;1(3):267-72. 10. okuda s, oda t, miyauchi a, haku t, yamamoto t, iwasaki m. surgical outcomes of posterior lumbar interbody fusion in elderly patients. surgical technique. j bone joint surg am 2007;89(suppl 2):310-20. 11. fischgrund js, mackay m, herkowitz hn, brower r, montgomery dm, kurz lt. 1997 volvo award winner in clinical studies. degenerative lumbar spondylolisthesis with spinal stenosis: a prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. spine (phila pa 1976) 1997;22:2807-12. 12. abdu wa, lurie jd, spratt kf, tosteson an, zhao w, tosteson td, et al. degenerative spondylolisthesis: does fusion method influence outcome? four-year results of the spine patient outcomes research trial. spine (phila pa 1976) 2009;34:2351-60. 13. meyerding hw. spondylolisthesis; surgical fusion of lumbosacral portion of spinal column and interarticular facets; use of autogenous bone grafts for relief of disabling backache. j int coll surg 1956;26(5 part 1):56691. 14. wiltse ll, winter rb. terminology and measurement of spondylolisthesis. j bone joint surg am 1983;65(6):768772. 15. alhammoud a, schroeder g, aldahamsheh o, alkhalili k, lendner m, moghamis is, et al. functional and radiological outcomes of combined anterior-posterior approach versus posterior alone in management of isthmic spondylolisthesis. a systematic review and meta-analysis. int j spine surg 2019;13:230-8. 16. kirkaldy-willis wh, farfan hf. instability of the lumbar spine. clin orthop relat res 1982;165:110-23. 17. landi a, gregori f, mancarella c, maiola v, maccari e, marotta n, et al. lumbar spinal degenerative "microinstability": hype or hope? proposal of a new classification to detect it and to assess surgical treatment. eur spine j 2015;24(suppl 7):872-8. 18. pearson am, lurie jd, blood ea, frymoyer jw, braeutigam h, an h, et al. spine patient outcomes research trial: radiographic predictors of clinical outcomes after operative or nonoperative treatment of degenerative spondylolisthesis. spine (phila pa 1976) 2008;33(25):2759-66. microsoft word 16hedaooketan_gcsscore 314 | hedaoo et al diffuse axonal injury             doi: 10.2478/romneu-2018-0039 gcs score and mri grading does not predicts the outcome in dai patients a prospective study ketan hedaoo1, vikas rajpurohit2, sunil garg1, sharad thanvi1, vallabh b nagocha1 1neurosurgery department; 2anesthesia department s.n. medical college, rajasthan university of health science, jodhpur, rajasthan, india abstract: diffuse axonal injury (dai) is a type of brain injury due to extensive lesions in white matter tract occurring over a wide area. it is one of the most common and devastating types of traumatic brain injury and major cause of unconsciousness and persistent vegetative state after head trauma. dai occurs in about half of all cases of severe head trauma. the study was undertaken to correlate the gcs at time of admission and grade of dai with the outcome. aim: to correlate gcs score and mri grading with the outcome in dai patients. setting and design: a 3 months prospective study was conducted in department of neurosurgery. material and method: sources of data: patients admitted with clinical diagnosis of diffuse axonal injury under department of neurosurgery. sample size: 50 cases of diffuse axonal injury. inclusion criteria: all traumatic dai patients requiring icu care. exclusion criteria: head injury patients requiring surgery. patients other findings on imaging as contusion, edh, sdh, ivh.patients with sepsis. patients with other co morbid illness as dm, hypertension. patients who were haemodynamically unstable at the time of admission. patients with other systemic injuries. statistical analysis. data so collected was analysed using ibm spss statistics windows, version 20.0 (armonk, ny: ibm corp) for the generation of descriptive and inferential statistics. the statistical significant difference among age groups was determined by chi square test and one way analyses of variance. the level of significance was set at p˂0.05. results: distribution of patients according to gender and mri grading shown in table 1. total 50 patients were evaluated out of which 38 (76%) were male and 12 (24%) were female. number of patients according to grading [table 2 and fig. 1] out of 50 patients admitted 10% (5) constitutes grade 1 dai, 28% (14) grade ii, and 62% (31) grade iii. grades of dai according to age of patients [table 3]. mean age in grade i patients was romanian neurosurgery (2018) xxxii 2: 314 321 | 315             20.83±3.63, grade ii 23.36±7.089 and in grade iii 22.32±11.38. comparisons of mean icu stay mean hospital stay and mortality in different gcs groups [table 4]. in patients with gcs 3-8 the mean icu stay was 18.48±14.53, mean hospital stay was 37.24±12.31 and mortality was 15.21%, in patients with gcs 9-12, mean icu stay was 10.5±4.12, hospital stay 19.4±5.79 and mortality was 25%. comparison of mean icu stay, and ventilator stay in different mri grade [table 5]. in patients with grade i dai mean icu stay was 17.13±14.65 and mean ventilator stay was 6.24±2.57, in grade ii dai mean icu stay was 20.57±15.45 and ventilator stay was 12.01±3.82 and in grade iii mean icu stay was 23.4±15.41 and mean ventilator stay was 10.89±2.58. mortality of patients in different grades and gcs groups [table 6 and fig 2] in patients with gcs 9-12 and grade iii only 1 patient died, while in patients with gcs 38 total 7 died, 2 in grade i, 2 in grade ii and 3 in grade iii. complications [table 7] out of 5 patients in grade i, electrolyte imbalance was seen in 1 patient in the form of hypernatraemia, 1 patient developed seizure, and septicaemia was seen in 1 and 1 patient developed shock. in patients with grade ii dai out of 14 patients 1 had ventilator associated pneumonia, hypernatraemia was seen in 1, 1patient developed bed sore, seizures seen in 3, 2 had septicaemia & shock was seen in 2, and in 1drug reaction occurred. out of 31 patients with grade iii dai 2 developed ventilator associated pneumonia, hypernatraemia and hyponatraemia was seen in 2 & 1 patient respectively, 2 developed bedsore, seizure in 1 and septicaemia and shock was seen in 3-3 patients. conclusion:-diffuse axonal injury is a very common finding in traumatic head injury patients. magnetic resonance imaging and gcs scoring does not have appropriate prognostic value in pure dai patients and a better survival rate can be achieved with dedicated neurocritical care and neurosurgical management key words: dai, icu stay, gcs, mri. introduction head injury includes injury to brain and other parts of head as scalp, skull and can be of open or closed types. closed head injuries causes two major types of traumatic brain injury – focal brain injury and diffuse axonal injury. in focal brain injury, orbitofrontal cortex, ventromedial prefrontal cortex and temporal pole are frequently damage because of shape of skull base. [1] dai is one of the most common pathology of traumatic brain injury, occurring in both mild and severe cases and is one of the major causes of traumatic brain injury leading to coma. [2] it occurs most often in rta, fall or assaults in which strong inertial force causes axons to loose their normal elasticity and become brittle. [3] dai occurs in 40-50% of traumatic brain injury. [4] 316 | hedaoo et al diffuse axonal injury             in dai, subcortical neuronal damage results from stretching and shearing of axons as brain moves inside skull. histopathologically dai is characterized by wallerian type axonal degeneration in parasagittal white matter, corpus callosum and dorsal upper brainstem due to shearing forces by acceleration, deceleration or rotation of brain. [5] in dai brain damage was thought to occur diffusely in white matter [6] while the effect on grey matter or whole brain is poorly understood. diffuse degeneration of cerebral white matter was first defined by strich in a study of patients with severe posttraumatic dementia in 1956. [7] the time course of pathological changes were established by adams et al. [8] diffuse axonal injury can be diagnosed using clinical signs and radiological evidence. brain magnetic resonance imaging (mri) is the most sensitive method to diagnose diffuse axonal injury, especially in gradient echo image. [9, 10, 11] method of collection of data after taking detailed history all patients were examined and investigated. severity of head injury was assessed via modified glasgow coma score and mri brain. according to gcs head injury is classified as mild having gcs 14-15, moderate 9-13, and severe with gcs less than 8. we divided patients into three groups according to grade of mri finding according to classification proposed by adams. grade 1. involves grey-white matter interface, most commonly parasagittal regions of frontal lobes, periventricular temporal lobes, less commonly: parietal and occipital lobes, internal and external capsules and cerebellum. grade 2. involves corpus callosum in addition to stage 1 locations, most commonly: posterior body and splenium but does advance anteriorly with increasing severity of injury grade 3. involves brainstem in addition to stage 1 and 2 locations most commonly: rostral midbrain, superior cerebellar peduncles, medial lemniscus, and corticospinal tracts. table 1 mri grading male female chi square p-value grade 1 5(10%) grade 2 11(22%) 3(6%) 0.57 0.751 grade 3 22(44%) 9(18%) table 2 grade i 10% (5 patients) grade ii 28% (14 patients) grade iii 62% (31 patients) table 3 mri grading age group (mean +sd) anova test p-value grade i 20.83±3.63 grade ii 23.36±7.089 0.1317 0.8769 grade iii 22.32±11.38 romanian neurosurgery (2018) xxxii 2: 314 321 | 317             table 4 gcs groups icu stay hospital stay mortality 3-8 18.48±14.53 37.24±12.31 7(15.21%) 9-12 10.5±4.12 19.4±5.79 1(25%) anova, p-value 1.17,0.283 8.12,0.006 table 5 mri grading icu stay(mean±sd) ventilator stay(mean ±sd) grade i 17.13±14.65 6.24±2.57 grade ii 20.57±15.45 12.01±3.82 grade iii 23.4±15.41 10.89±2.58 anova test,pvalue 0.4408,0.6461 <0.01 table 6 mri grading gcs mortality gcs mortality grade i 9-12 3-8(5) 2 grade ii 9-12(2) 3-8(12) 2 grade iii 9-12(2) 1 3-8(29) 3 table 7 m r i g ra di ng v a p h yp er na tr em ia h yp on at re m ia be ds or e se iz ur e se pt ic em ia sh oc k d ru g r ea ct io n i 1 1 1 1 1 ii 1 1 1 3 2 2 1 iii 2 2 1 2 1 3 3 figure 1 figure 2   318 | hedaoo et al diffuse axonal injury             romanian neurosurgery (2018) xxxii 2: 314 321 | 319             discussion diffuse axonal injury (i.e., widespread damage to axons in white matter of brain) is well recognized severe posttraumatic head injury. [12] it is defined as prolonged post traumatic coma following injury without demonstrable intracranial mass lesion. [13, 14, 15] in 1956, strich [7] defined the “diffuse degeneration of cerebral white matter” in a series of patients with severe post-traumatic dementia diffuse axonal injury is caused by acceleration-deceleration effects of mechanical input to head on shaking of brain within skull.[14,15] this results in shearing or stretching of nerve fibres with consequential axonal damage. mostly, this injury mechanism is caused by traffic accidents producing comparatively prolonged acceleration and is dependent on direction, magnitude and speed of head motion during injury. diffuse axonal injury readily occurs in coronal acceleration of head and occasionally in sagittal or oblique direction. [16] in mild head injury lesions are localized to frontotemporal cerebral white matter and stronger rotatory acceleration causes additional lesions in corpus callosum and brain stem. gannarelli et al [16] reported severe head injury has a tendency to cause deeper lesions. adam et al established pathological changes in due time course [8].in humans, instantaneous injury occurs to numerous axons in white matter of brain manifested by axonal retraction balls visible on microscopic examination. gross lesion associated with severe diffuse axonal injury in humans consist of haemorrhagic tears in corpus callosum and dorsolateral quadrant or rostral brain stem. several days later, microglial clusters appear and axonal retraction balls start to disappear. months later bulk of white matter is reduced and and long tract degeneration is seen. [16] diffuse axonal injury can be diagnosed clinically (level of consciousness and neurological deficits) and radiological findings. zimmerman[17] reported first study 320 | hedaoo et al diffuse axonal injury             of radiological diagnosis of diffuse axonal injury that includes small hemorrhagic lesion on corpus callosum, upper brainstem, corticomedullary junction, parasagittal area and basal ganglia .brain computed tomography findings lack accuracy in prediction of patients outcome and do not correspond well to patient’s gcs score or neurological state[10,18]. brain mri gradient echo imaging is far more sensitive than spin echo imaging on paramagnetic lesion such as hemorrhage or calcification for a long time , and is considered most sensitive for conforming presence of small hemorrhagic lesion in white matter, corpus callosum, and brain stem in diffuse axonal injury.[9,10,11] as the studies done by gannarelli.t.a et al, r.kalff et al, and levati et al shows that patients presenting with low gcs have poorer outcome but in our study in patients with gcs less than 8 the mortality was only 15% (7 out of 46) and in patients with gcs more than 8 the mortality was 25% (1 out of 4). oh.et.al and kim et al reported worse outcome in patients with grade ii and iii dai, but in our study in patients with grade i dai mortality was 40% (2 out of 5) in grade ii dai mortality was 14.21% (2 out of 14) and in patients with grade iii dai mortality was 12.9% (4 out of 31) better outcome seen our study can be due to early referral of patients, better neurocritical care, early tracheostomy, early recognition of complications and its management. correspondence ketan hedaoo postal address of corresponding author: room no 110, pg hostel; mathuradas mathur hospital, department of neurosurgery, dr. s.n. medical college, jodhpur – 342001, rajasthan, india references 1. adams jh, graham di, scott g.et al .brain damage in fatal non missile head injury. journal of clinical pathology 1980; 33: 1132-1145. 2. smith d., meaney d., & shull w. diffuse axonal injury in head trauma .j head trauma rehabil.2003;18:4. 3. wang h., ma y. experimental models of traumatic axonal injury. journal of clinical neuroscience.2010; 172. 4. thomas m. & dufour l. challenges of diffuse axonal injury diagnosis. rehabil nurs.2009; 34(5): 179-80. 5. meythaler jm, peduzzi jd, eleftheriou e, et al. current concepts: diffuse axonal injury-associated traumatic brain injury. archives of physical medicine and rehabilitation 2001; 82: 1461-1471. 6. gentry lr, godersky jc, thompson b et al.prospective comparative study of intermediate-field mr and ct in evaluation of closed head trauma .american journal or roentgenology: 1988; 150, 673-682. 7. strich sj. diffuse degeneration of the cerebral white matter in severe dementia following head injury . j neurol neurosurg psychiatry.1956;19:163-185. 8. adams h, mitchell de, graham di, doyle d. diffuse brain damage of immediate impact type. its relationship to “primary brain stem damage” in head injury. brain.1977; 100:489-502. 9. kim ch, lee hk, koh yc, hwang dy .clinical analysis of diffuse axonal injury (dai) diagnosed with magnetic resonance image (mri) j korean neurosurg soc. 1997;26:241-248. 10. kim hj, park is, kim jh, kim kj, hwang sh, kim es, et al. clinical analysis of the prognosis of the patients with cerebral diffuse axonal injuries, based on gradientecho mr imaging. j korean neurosurg soc.2001;30:168172. 11. oh ks ,ha si ,suh bs, lee hs, lee js. the correlation of mri findings to outcome in diffuse axonal romanian neurosurgery (2018) xxxii 2: 314 321 | 321             injury patients. j korean neurosurg soc. 2001; 30(suppli): s20-s24. 12. adams jh, graham di, murray ls, scott g. diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. ann neurol. 1982; 12:557-563. 13. alberico am, ward jd, choi sc, marmarou a, young hf.outcome after severe head injury: relationship to mass lesion, diffuse injury, and icp course in paediatric and adult patients. j neurosurg.1987; 67:648-656. 14. eisenberg hm, gary he, jr, aldrich ef, saydjari c, turner b, foulkes ma, et al .initial ct findings in 753 patients with severe head injury .a report from nih traumatic coma data bank. j neurosurg.1990;73:688698. 15. eum sw, lim dj, kim br , cho th, park jy, suh jk, et al .prognostic factors in patients with diffuse axonal injury. j korean neurosurg soc. 1998; 27:16681674. 16. gannarelli t., thibault l., adams j., graham d., thompson c., & marcincin r., diffuse axonal injury and traumatic coma in the primate .ann neurol.1982;12:564-574. 17. zimmerman ra, bilaniuk lt, ganneralli t. computed tomography of shearing injuries of cerebral white matter .radiology. 1978; 127:393-396. 18. zimmerman ra, bilanuik lt , hackney db. goldberg hi , grossman ri. head injury: early results of comparing ct and high field mr . ajr am j roentgenol. 1986; 147:1215-1222. 19. ganneralli ta, spielman gm, langfitt tw, gildenberg pl, harrington t, jane ja, et al influence of the type of intracranial lesion on outcome from severe head injury. j neurosurg. 1982;56:26-32. 20. kalff r, kocks w, pospiech j, grote w. clinical outcome after head injury in children. childs nerv syst. 1989; 5:156-159. 21. laveti a, farina ml, vecchi g, rossanda m, marrubini mb. prognosis of severe head injuries. j neurosurg . 1982;57:779-783. microsoft word _2.formatata_neacsu.doc romanian neurosurgery vol. xvi nr. 2 8 cerebral cavernomas in the adult. review of the literature and analysis of 61 surgically treated patients angela neacsu md, prof. radu mircea gorgan md phd, narcisa bucur md phd, mihai viorel pruna md first neurosurgical clinic, fourth neurosurgical department clinic emergency hospital “bagdasar-arseni”, bucharest background and purpose. authors review the latest data regarding modern, multimodal management of single and multiple intracranial cavernomas, based on their experience, on a consecutive series of 61 cases. methods. during 2001 to 2009, 61 patients (33 men, 28 women) with intracerebral cavernous angiomas underwent surgical treatment in our center, and they were included into the present uncontrolled clinical study. the average age of the patients at the time of operation was 41.4 years. all patients underwent preoperative magnetic resonance imaging, and pre and postoperative clinical examination. the clinical course was documented using the karnofski performance scale. a simplified version of engel’s classification of the outcome of the patients with chronic seizures was applied. results. the most common clinical presentation of cavernous angiomas was seizures, significant part of which was chronic. in the group of patients presenting with headache, sporadic seizures, or intracerebral hemorrhage, good postoperative outcome was achieved in 86,84% of the patients. of the patients who underwent operation for seizure control, significant seizure reduction or elimination after surgery was observed in 80,95% of the patients. conclusions. cavernomas are benign lesions, surgically resectable; the excision must be complete, any rests causing rebleeding. microsurgical removal of cavernous angiomas and surrounding hemosiderin plate tends to significant reduction or elimination of epileptic seizures and improved postoperative neurological status. keywords: cavernous angioma, cavernomas, epilepsy, hemorrhage, surgery introduction cavernous angiomas (cas) or cavernomas are benign vascular malformations, which can be found at any region within the brain as well as in other organs (22, 33). cas affecting the central nervous system represent approximately 5 to 10% of the central nervous system malformations (23, 24) and are present in about 0.4 to 0.8% of the population, according to the findings of autopsy series (26) and large magnetic resonance imaging (mri)-based studies (13, 29). most commonly, cavernomas are found at the supratentorial region (75%) and rarely in the brainstem, accounting for approximately 20% of all intracerebral cavernous angiomas(23, 24, 31). despite numerous case reports, retrospective or prospective studies and reviews, cerebral cavernous angiomas remain as one of the most negotiable and controversial topics in neurological and neurosurgical practice. in the present study, we present a statistical evaluation of initial presentation, preoperative neurological findings, surgical and outcome of 61 consecutive surgically treated patients with intracerebral cavernous angiomas. material and methods patients. during 2001 to 2009, 61 patients (33 men, 28 women) with intracerebral cas underwent surgical treatment in fourth neurosurgical department, clinic emergency hospital “bagdasar-arseni”, bucharest, and these were included into the present uncontrolled clinical study. the average age of the patients at the cerebral cavernomas in the adult romanian neurosurgery vol. xvi nr. 2 9 time of operation was 41.4 years (age range, 18–72 years). all patients underwent preoperative mri included standard t1and t2weighted sequences. a board-certified neuroradiologist reviewed all images. in each patient, lesions were identified based on typical characteristics and were classified according to number, location, size, and presence or absence of extralesional hemorrhage. extralesional hemorrhage was defined as blood signal intensity extending beyond the low-signal-intensity rim of the lesion. the definition of hemorrhage was taken to be the presence of extralesional hemorrhage accompanied by a change in clinical status. 21 patients had a history of chronic seizures, and 11 patients presented with sporadic seizures. the data on age at the onset of seizures and the response to antiepileptic drugs were recorded retrospectively. all patients underwent preand postoperative clinical examination. the clinical course was documented using the karnofski performance scale (kps). a simplified version of engel’s classification of the outcome of the patients with chronic seizures was applied in the categories seizurefree, improved, no change, and worse (34). surgery. operative removal of cavernous angioma was performed under standard microsurgical conditions.the surgical strategy was lesionectomy, limiting the removal to the ca and surrounding hemosiderin plate. in some patients, extralesional hematoma was also removed if it was present. clinical follow-up data for the patients with chronic seizures were obtained at clinic visits. results there were 71 cavernous angiomas in 61 patients. lesions were solitary in 55 patients (90,16%) and multiple in 6 patients (9,83%). of the patients with multiple lesions, 3 had two lesions, 2 had three lesions and 1 had four lesions. the locations of 71 cavernous angiomas in 61 patients are presented in table 1. table 1 location of 71 cavernous angiomas in 61 patients supratentorial 59 (83.09%) subtentorial 12 (16.90%) frontal 24 (33.80%) cerebellar 5 (7.04%) temporal 21 (29.57%) brainstem 7 (9.85%) parietal 11 (15.49%) occipital 2 (2.81%) deep supratentorial (thalamus) 1 (1.40%) ct and mri of cavernomas of different location are presented in fig. 1-3. fig. 1a fig. 1b angela neacsu romanian neurosurgery vol. xvi nr. 2 10 fig. 1a,1b,1c ct cavernous angioma in the frontal lobe, sagital section, native and contrast, revealing a isodense lesion with contrast ring enhancement, in a phase of subacute bleeding, with regional mass effect (male, 65 yo, frontal syndrome and sporadic seizures) fig. 1d,1e,1f,1g preoperative mri, axial, sagital, and coronar sections,t1 and t2, to the same patient, revealing subacute bleeding with hemosiderin products, and regional mass effect fig. 1h,1i ct scan, axial sections, to the same patient, postoperative, without contrast, revealing a hipodense zone, in the area of the removed lesion fig. 2a, 2b axial ct with contrast, of cavernous angioma, revealing pseudotumoral mass contrast enhancing, with perilesional edema, in the posterior temporal lobe, due to repeated bleeding and healing (female, 33 yo, chronic seizures) fig. 2c cerebral cavernomas in the adult romanian neurosurgery vol. xvi nr. 2 11 fig. 2d fig. 2e fig. 2c, 2d, 2e preoperative mri, sagital, coronar and axial sections, t2 with contrast, revealing gliotic peri-lesional area with different age hemosiderin products, in the same patient fig. 2f, 2g postoperative axial ct without contrast, revealing the hypodense area of the resected lesion fig. 3a, 3b ct scan of cavernous angioma in brain stem, revealed with trauma occasion in a patient of 37 yo, who suffered a car crash. in the image appears a small hematoma within the left cerebellar peduncule fig. 3c, 3d, 3e, 3f angela neacsu romanian neurosurgery vol. xvi nr. 2 12 fig. 3g fig. 3c, 3d, 3e, 3f, 3g magnetic resonance imaging in the same patient, coronar sections t1, axial sections t2, and sagital sections t1, without contrast, in the subacute phase, revealing the tumoral nodule and perilesional hemosiderin ring, corresponding to hematoma resorbtion at initial presentation, headache was reported in 19 patients, seizure in 32, and focal neurological deficit in 27 (table 2). twenty-one (34.42%) patients presented with symptomatic extralesional hemorrhage. there were no statistically significant differences between males and females in regard to initial clinical presentation. table 2 clinical presentation of 61 patients with cavernous angioma* headache no(%) seizure no(%) focal deficit no(%) hemorrhage no(%) 19 (31.14) 32 (52.45) 27 (44.26) 21 (34.42) *some patients presented with more than one symptom. the size of cavernomas ranged from 0.3 cm to 5.0 cm (median, 2.0 cm) in their largest diameter. 21 patients with seizures had a history of chronic epilepsy and a longer mean duration of illness; 11 patients had only single or sporadic seizures and a fast diagnosis of cavernous angioma and surgical treatment. four patients with seizures had multiple lesions. this accounted for 66.66% (4/6) of all patients with multiple lesions in a group. the results of the preoperative neurological examination were normal in 23 patients. the other 9 had focal neurological signs. five patients had intracerebral bleeding, which in 3 of these 5 was subsequent to the onset of epilepsy. after exclusion of patients with multiple lesions, temporal location of cavernous angioma was more frequent in both the patients with chronic seizures and those with sporadic seizures. according to the kps, out of 38 patients presenting with headache, sporadic seizures, or intracerebral hemorrhage, preoperative neurological status was inferior or equal to 70 in 12 patients and superior or equal to 80 in 26. in 33 (86.84%) patients of this group, the kps score at discharge was 80 to 90 (good outcome). table 3 clinical presentation by lesion location in 55 patients with single lesion lesion location patients no headache no(%) seizure no(%) focal deficit no(%) hemorrhage no(%) supratentorial frontal temporal parietal occipital 47 19 20 7 1 15(31.91) 4(21.05) 7(35) 4(57.14) 28(59.57) 10(52.63) 14(70) 3(42.85) 1 17(36.17) 8(42.10) 5(25) 4(57.14) 16(34.04) 7(36.84) 6(30) 3(42.85) subtentorial cerebellar brainstem 8 3 5 3(37.5) 2(25) 1(12.5) 8(100) 3(100) 5(100) 3(37.5) 1(12.5) 2(25) cerebral cavernomas in the adult romanian neurosurgery vol. xvi nr. 2 13 poor outcome was defined by death in 1 patient (2.63%) or a postoperative kps inferior or equal to 70 in 4 patients (10.52%). postoperative focal neurological signs (sensorimotor defects) were present in 3 patients (7.89%). of the 21 patients who underwent operation for seizure control, 17 (80.95%) reported significant seizure reduction or elimination after surgery. three patients reported the same frequency and type of seizures as before operation. worsening of epileptic seizures was observed in one patient (4.76%) of the group. discussion and literature review cavernous angiomas are considered congenital vascular hamartomas composed of closely approximated endothelial-lined sinusoidal collections without significant amounts of interspersed neural tissue. cavernous angiomas are not encapsulated, but well separable from brain parenchyma. however, the surrounding brain usually exhibits evidence of prior microhemorrhage, hemosiderin, discoloration, and hemosiderin-filled macrophages. this indicates recurrent microbleedings or leakage of red blood cells. thrombi of varying age are characteristic and are present within many of the vessels. calcification and surrounding gliosis typify the margins of the lesion. although cas have been generally regarded as congenital lesions that arise as a result of disordered mesodermal differentiation during the early stages of embryogenesis, recent studies have documented the growth and “de novo” appearance of sporadic or familial cas (15). repeated intralesional microhemorrhages and their breakdown products can also initiate a series of responses such as cellular proliferation and fibrosis that promote new vessel formation and hemorrhagic angiogenic proliferation. however, the molecular mechanisms underlying the genesis and maintenance of these abnormal vascular phenotypes are not well known. despite many detailed radiologic and pathologic studies on the subject, controversy still exists regarding their classification as true vascular malformations or as capillary vessels slow-growing tumors, due to their occurrence and growing pattern, which is still incomplete elucidated (35). cavernomas may occur sporadically (18), after radiation therapy (3) and hereditarily following an autosomal dominant trait(19). cavernous angiomas can be found in any part of the brain because they can occur at any location along the vascular bed. frontal and temporal lobes are the most common sites of occurrence (8), and 80-90% of the lesions are supratentorial (11, 13, 22). cavernomas are preferentially located cortically or in the subcortical white matter. a deep location in the basal ganglia, hypothalamus, or ventricular system is infrequent. in our series, just one patient had a cavernous angioma located in the right thalamus. cerebral cavernomas are dynamic lesions that are prone to vary in number and size over time (2, 27). the size of cavernomas reported in the literature ranges from 0.1 cm to 9 cm in their largest diameter (21). usually cavernomas reach a larger size in children (6.7 cm on average) than in adults, in whom it tends to be 2–3 cm (25). we have not observed such a tendency, as two largest cavernomas were observed in 24and 32-year-old female patients. well in accord with the results of other studies, we have also found no associations between size of cavernoma and the initial presentation of cavernoma (25, 30). many authors have reported imaging and/or surgical evidence of an association between cavernoma and local developmental venous anomalies (1, 20). in our series, just one patient had venous angioma in addition to cavernous angioma what is much lower compared to other reports. most studies support equal male/female prevalence for cas (13,16, 29), and our results confirm these findings. according to the literature, the prevalence of multiple cavernoma varies between 3% and 50% (22, 23, 24, 28). in our series, nearly 10% of the patients had multiple cavernomas. patients with cavernous angioma present with a variety of symptoms. seizures are reported as the most common symptom, accounting for 38%–55% of patient’s complaint. angela neacsu romanian neurosurgery vol. xvi nr. 2 14 other symptoms include focal neurologic deficits in 12%–45% of patients, recurrent hemorrhage in 4%– 32%, and chronic headaches in 5%–52% (11, 13, 22, 30). intracranial hypertension syndrome and/or focal neurological deficits are usually related to acute hemorrhage, which is recognized as the first clinical presentation in nearly 40% of cases (13, 22, 33). any hemorrhage found on ct scans in a relatively young patient should be characterized further, and cavernous angioma must be considered a possible etiology. in the workup of a patient with a seizure disorder, cavernous angioma must be considered the underlying etiology, especially if the patient is aged 20-40 years. brainstem cavernomas nearly never cause seizures. most of these patients do have typical brainstem symptoms like diplopia, face or body sensory disturbances, or ataxia.without imaging, this subgroup of patients with infratentorially located cavernomas can closely mimic the clinical picture of multiple sclerosis. the majority of patients become symptomatic between the third and fifth decade, and there is no definite association between symptoms and gender. the frequency of asymptomatic cavernomas is not precisely known, but according to the reports of zabramski et al. (36) and brunereau et al. (4, 5) it seems to be as high as 40%. thus, our series is not different and fits well within the reported ranges. most common clinical presentation of cas was seizures (52,45%), significant part of which was chronic. 34.42% patients presented with symptomatic extralesional hemorrhage. no significant differences in the likelihood of presenting with hemorrhage between supratentorial and subtentorial lesions were detected. 31,14% patients prezented with headache and 44,26% with focal deficit. mri is the method of choice for the long-term follow-up of patients with cavernous angiomas and for the assessment of family members in whom similar lesions are suspected. in addition, mri is extremely helpful in presurgical planning to assess the extent of the lesion, define borders, and plan the surgical approach and exposure. most cavernous malformations are angiographically occult, and when they are evident on angiograms, the findings are nonspecific. when the lesions occur in combination with other vascular malformations, as they do in as many as 30% of patients with venous malformations, mri characteristics become more complicated and less specific. in these patients, angiography can be helpful in further defining the lesions. treatment indication in cavernous angioma depends mainly on the natural course of the lesion, as well as its location and surgical accessibility. the latter depends on the skill of the surgeon and the position of the lesion relative to eloquent areas of the brain. in general, therapeutic strategies include: observation of patients with asymptomatic or inaccessible lesions; surgical excision of symptomatic and accessible lesions; radiosurgery for progressively symptomatic but surgically inaccessible lesions (questionable). the recommendations for the management of patients with cavernous angioma have varied throughout the years and are still not homogeneous. treatment of intracranial cavernomas must be individualized in each patient. a multidisciplinary medical team, formed by specialists in cerebrovascular pathology (neurologist, neurosurgeon, neuroradiologist), together with the patient and his family, decide whether treatment is mandatory and which is the best therapeutical option. difficulties and controversies in decision making are especially in asymptomatic, incidental or deep lesions, without hemorrhage. in the group of patients presenting with headache, sporadic seizures, or intracerebral hemorrhage, good postoperative outcome was achieved in 86.84% of the patients. of the patients who underwent operation for seizure control, significant seizure reduction or elimination after surgery was observed in 80.95% of the patients. our results indicate that the excision of cas leads to a favorable epilepsy outcome as it was pointed out by other studies (14,22). a proportion of those seizure free or with a marked reduction in seizure frequency was somewhat higher than that reported by churchyard et al. (9) or by moran et al. (22) yet lower compared to the overall positive effect of surgery in which up to 94% of the patients became seizure-free, or at least experienced a marked reduction in seizure frequency (6,11,32,33). the unfavorable epilepsy outcome cerebral cavernomas in the adult romanian neurosurgery vol. xvi nr. 2 15 observed in one patient of our series was presumably caused by the presence of multiple cas. in order to cure epilepsy, according to some authors it is necessary to remove the hemosiderin capsule surrounding the malformation (11,12) and possibly representing an irritating element (17,33). other authors do not judge this to be necessary because it is in many cases difficult to discern it from the surrounding compressed or atrophied brain (25) or because they failed to find any substantial evidence that the additional excision of the hemosiderin-stained tissue around the cavernoma provided better results than merely resection of the cavernoma (7,37). we prefer to remove the hemosiderin plate surrounding the cavernoma as we support the hypothesis that breakdown products of blood could facilitate the initiation of seizures (17,33). conclusion cavernomas are benign lesions, surgically resectable; the excision must be complete, any rests causing re-bleeding. asymptomatic patients are encouraged to live a normal life, without any solicitant physical activity. removal of cavernous angiomas together with surrounding hemosiderin plate or/and intracerebral hemorrhage using microsurgical techniques was relatively safe procedure that significantly reduced the frequency or even eliminated epileptic seizures as well as improved postoperative neurological status in the majority of our patients with chronic seizures, and with headache, sporadic seizures or intracerebral hemorrhage, respectively. references 1.abe t, singer rj, marks mp, norbash am, crowley rs, steinberg gk. coexistence of occult vascular malformations and developmental venous anomalies in the central nervous system: mr evaluation. am j neuroradiol 1998;19:51-7. 2.aiba t, tanaka r, koike t, kameyama s, takeda n, komata t. natural history of intracranial cavernous malformations. j neurosurg 1995;83:56-9. 3.amirjamshidi a, abbassioun k (2000) radiation-induced tumors of the central nervous system occurring in childhood and adolescence. four unusual lesions in three patients and a review of the literature. childs nerv syst 16:390–397 4.brunereau l, labauge p, tournier lasserve e, laberge s, levy c, houtteville jp (2000a) familial form of intracranial cavernous angioma: mr imaging findings in 51 families. french society of neurosurgery. radiology 214:209–216 5.brunereau l, levy c, laberge s, houtteville j, labauge p (2000b) de novo lesions in familial form of cerebral cavernous malformations: clinical and mr features in 29 non-hispanic families. surg neurol 53(5):475–482; discussion 482–483 6.cappabianca p, alfieri a, maiuri f, mariniello g, cirillo s, de divitiis e. supratentorial cavernous malformations and epilepsy: seizure outcome after lesionectomy on a series of 35 patients. clin neurol neurosurg 1997;99:179-83. 7.casazza m, broggi g, franzini a, avanzini g, spreafico r, bracchi m, et al. supratentorial cavernous angiomas and epileptic seizures: preoperative course and postoperative outcome. neurosurgery 1996;39:26-32. 8.cavalheiro s, braga fm. cavernous angiomas. in: choux m, di rocco c, hockley ad, walker ml, editors. pediatric neurosurgery.london: churchill livingstone; 1999. p. 691-701. 9.churchyard a, khangure m, grainger k. cerebral cavernous angioma: a potentially benign condition? successful treatment in 16 cases. j neurol neurosurg psychiatry 1992;55:1040-5. 10.ciricillo sf, cogen ph, edwards msb (1993) cryptic vascular malformations in children: presentation, radiology, treatment and outcome in 36 consecutive patients. j neurosurg 78:354 11.cohen ds, zubay gp, goodman rr. seizure outcome after lesionectomy for cavernous angiomas. j neurosurg 1995;83: 23742. 12.cosgrove gr. occult vascular malformations and seizures. neurosurg clin n am 1999;10:527-35. 13.del curling o jr, kelly dl jr, elster ad, craven te. an analysis of the natural history of cavernous angiomas. j neurosurg 1991;75:702-8. 14.hennessy mj, elwes rdc, rabe-hesketh s, binnie cd, polkey ce. predictors of outcome and pathological considerations in the surgical treatment of intractable epilepsy associated with temporal lobe lesions. j neurol neurosurg psychiatry 2001;70:450-8. 15.keun-hwa jung md et al.: cerebral cavernous malformations with dynamic and progressive course, arch neurol. 2003;60:16131618 16.kondziolka d, lunsford ld, kestle jrw. the natural history of cerebral cavernous malformations. j neurosurg 1995;83: 820-4. 17.kraemer dl, awad ia. vascular malformations and epilepsy: clinical considerations and basic mechanisms. epilepsia 1994; 35(suppl 6):s30-43. 18.kupersmith mj, kalish h, epstein f, yu g, berenstein a, woo h, jafar j, mandel g, de lara f (2001) natural history of brainstem cavernous malformations. neurosurgery 48:47–53 19.labauge p, laberge s, brunerau l, levy c, tournier lasserve e (1998) hereditary cerebral cavernous angiomas: clinical and genetic features in 57 french families. societe fran-caise de neurochirurgie. lancet 352:1892–1897 20.latchaw re, truwit cl, heros rc. venous angioma, cavernous angioma, and haemorrhage. am j neuroradiol 1994;15: 1255-7. angela neacsu romanian neurosurgery vol. xvi nr. 2 16 21.maraire jn, awad ia. intracranial cavernous malformations: lesion behavior and management strategies. neurosurgery 1995;37:591-605. 22.moran nf, fish dr, kitchen n, shorvon s, kendall be, stevens jm. supratentorial cavernous haemangiomas and epilepsy: a review of the literature and case series. j neurol neurosurg psychiatry 1999;66:561-8. 23.moriarity jl, clatterbuck re, rigamonti d. the natural history of cavernous malformations. neurosurg clin n am 1999;10:411-7. 24.moriarity jl, wetzel bs, clatterbuck re, javedan s, sheppard j-m, hoenig-rigamonti k, et al. the natural history of cavernous malformations: a prospective study of 68 patients. neurosurgery 1999;44:1166-71. 25.mottolese c, hermier m, stan h, jouvet a, saint-pierre g, froment jc, et al. central nervous system cavernomas in the pediatric age group. neurosurg rev 2001;24:55-71. 26.otten p, pizzolato gp, rilliet b, berney j. a propos de 131 cas d’angiomes caverneux (cavernomes) du s.n.c., repérés par l’analyse rétrospective de 24 535 autopsies. (131 cases of cavernous angioma (cavernomas) of the cns, discovered by retrospective analysis of 24,535 autopsies.) neurochirurgie 1989;35:82-3. 27.pozzati e, acciari n, tognetti f, marliani f, giangaspero f. growth, subsequent bleeding, and de novo appearance of cerebral cavernous angiomas. neurosurgery 1996;38:662-70. 28.rigamonti d, drayer bp, johnson pc, hadley mn, zabramski j, spetzler pf. the mri appearance of cavernous malformations (angiomas). j neurosurg 1987;67:518-24. 29.robinson jr, awad ia, little jr. natural history of the cavernous angioma. j neurosurg 1991;75:709-14. 30.robinson jr, awad ia, magdinec m, paranadi l. factors predisposing to clinical disability in patients with cavernous malformations of the brain. neurosurgery 1993;32:730-5. 31.sandalcioglu ie, wiedemayer h, secer s, asgari s, stolke d. surgical removal of brain stem cavernous malformations: surgical indications, technical considerations, and results. j neurol neurosurg psychiatry 2002;72:351-5. 32.schroeder hw, gaab mr, runge u. supratentorial cavernous angiomas and epileptic seizures: preoperative course and postoperative outcome. neurosurgery 1997;40:885. 33.stefan h, hammen t. cavernous hemangiomas, epilepsy and treatment strategies. acta neurol scand 2004;110:393-7. 34.vickrey bg, hays rd, engel j jr, spitzer k, rogers wh, rausch r, et al. outcome assessment for epilepsy surgery: the impact of measuring health-related quality of life. ann neurol 1995;37:158-66. 35.william p. dillon, university of california, san francisco: cryptic vascular malformations: controversies in terminology, diagnosis, pathophysiology, and treatment, ajnr 18:1839–1846, nov 1997 36.zabramski jm, wascher tm, spetzler rf, johnson b, golfinos j, drayer bp, brown b, rigamonti d, brown g (1994) the natural history of familial cavernous malformation: results of an ongoing study. j neurosurg 80:422–432 37.zevgaridis d, van velthoven v, ebeling u, reulen hj. seizure control following surgery in supratentorial cavernous malformations: a retrospective study of 77 patients. acta neurochir wien 1996;138:672-7 7zakariawael_hyperostotic romanian neurosurgery | volume xxx | number 4 | 2016 | october december article hyperostotic sphenoid wing meningioma en plaque: proptosis management wael k. zakaria, ahmed n. taha egypt doi: 10.1515/romneu-2016-0079 498 | zakaria, taha hyperostotic sphenoid wing meningioma en plaque doi: 10.1515/romneu-2016-0079 hyperostotic sphenoid wing meningioma en plaque: proptosis management wael k. zakaria, ahmed n. taha neurosurgery department, mansoura university, egypt abstract: background: en plaque sphenoid wing meningioma is morphological unique in comparison with other intracranial meningiomas, characterized by a carpet-like usually small soft tissue component which invade the dura and extensively involve the bone specially the sphenoid wing and orbit causing significant hyperostosis. patients & methods: a retrospective analysis of the clinical data, neuro-radiological features, and operative techniques of eighteen patients underwent transcranio-orbital approach sphenoid wing meningioma presented with proptosis during the period from september 2011 to april 2014 in the neurosurgery department, mansoura university. patients age ranged from 38 years to 54 years and there was sex males and twelve females. chief complaints were progressive proptosis and visual acuity deficits. all patients were operated up on using a fronto-temporal approach with orbital decompression. the extent of tumor resection and postoperative complications were investigated. results: total removal was achieved in fourteen cases (77.8%) over a mean follow-up period of 36 months. pathological examination showed that twelve patients (66.67%) were meningothelial meningiomas. after surgery, proptosis improved in all patients, visual acuity improved in fifteen patients (83.3%). cerebrospinal fluid leakage was found in one patient. there were no operation-related deaths or other significant complications. four patients had residual tumor (22.2%); two of them underwent surgical re-attack of the tumor and the other two cases were sent for gamma knife radio-surgery. conclusions: sphenoid wing meningioma en plaque, mainly meningothelial meningiomas, are characterized by the associated bony hyperostosis that gives them a distinct radiological appearance. the bony hyperostosis is of neoplastic nature and is responsible for many of the clinical manifestation of such tumors and hence should be totally drilled to achieve cure and avoid recurrence. extensive tumor removal is crucial for correction of proptosis and adequate visual decompression to achieve satisfactory cosmetic and functional outcome. romanian neurosurgery (2016) xxx 4: 498 – 506 | 499 introduction intracranial meningiomas can be classified into two morphological types; global and flat. the terms “meningioma en masse” and “meningioma en plaque” was initially described by cushing and eisenhardt (1938) to differentiate between them. (15) the most frequent type encountered is meningioma en masse while meningioma en plaque is a rarer subgroup characterized morphologically by a thin, widespread, carpet like mass infiltrating the dura with variable degrees of bone invasion causing progressive hyperostosis which may involve the bone orbit causing proptosis. meningioma en plaque almost always involve the sphenoid wing. (2, 4, 17) sphenoorbital or en plaque meningiomas is considered as a distinct entity which is different from sphenoid wing meningiomas. such morphological characteristic of these tumors put them in differential diagnosis with others osseous skull lesions as fibrous dysplasia, osteoma and some metastatic lesions. (2, 3, 4, 15) hyperostosis is a common phenomenon occuring in different meningiomas with incidence ranging from 25 to 49% of meningiomas.it is most commonly seen in sphenoid wing and convexity meningioma. the biological behavior and growth pattern of spheno-orbital meningiomas is variable and unpredictable. in some patients; the tumor is slowly growing and symptoms are minimal while in others; the disease progression is rapid with marked affection of vision, significant proptosis, and disfiguring. (2-7, 11-19) spheno-orbital meningiomas usually involve important areas including the orbit, superior orbital fissure, optic canal, the cavernous sinus. tumor commonly compress the optic nerve and the cranial nerves withen the cavernous sinus. (1, 2, 6, 9, 10) extensive dural, bone, and orbital involvement makes total resection of such tumors not achievable and hazardous hence some authors in previous report reccomended conservate approach in dealing with these tumors and surgery should be restricted to rapidly progressive lesions. total resection of these tumors necessiate extensive bone drilling to the sphenoid and orbital bone with may cause significant cranial deformity and cosmotic difigurement and hence adequate orbital and skull reconstruction is essential for good functional and cosmotic outcome. early and aggressive surgical resection is considered by many authors the only to cure the patient and to achieve sound cosmotic outcome and to correct proptosis as longstanding proptosis is not surgically correctable. (1-4, 6-8, 11-19) radiation therapy either conventional or radio-surgey has been described as an alternative or adjuvant to non radical surgery to achieve tumor control but the proximity to optic pathway increase the risk for progressive visual deterioration. (2, 13, 15) clinical material and methods patients characteristics: between 2011 and 2014, eighteen patients with hyperostotic sphenoid wing meningiomas underwent surgery at the neurosurgery department, mansoura university. patients with extensive 500 | zakaria, taha hyperostotic sphenoid wing meningioma en plaque hyperostosis, en plaque dural invasion, minimal intracranial tumor were included in the study. we did not include patients with nonhyperostotic sphenoid wing meningiomas, hyperostotic sphenoid wing meningiomas with a moderate or large intracranial tumor portion, or clinoid or primary optic nerve sheath meningiomas. the most common presentation (table i) was proptosis. other symptoms and signs included deficits of visual acuity (twelve patients (66.67%)), headache (eight patients) and seizure (one patient). radiographic studies all patients received pre-operative computed tomography (ct) and magnetic resonance imaging (mri) scans. axial and coronal ct bone window scans were excellent for visualization of the hyperostosis. on ct scans, the typical features were significant hyperostosis of the great wing of sphenoid bone and involving adjacent bone, including the middle cranial fossa bone, the lateral orbital wall and the orbital roof, the walls of the sphenoid sinus and ethmoidal cells. the edges of hyperostosis were rough and brushlike. on ct scans, the soft-tissue component of meningioma was carpet-like, isodense and homogeneously enhanced after contrasted. mri showed t1 intensity was isointensity or hypointensity, t2 intensity was hyperintense. gadolinium enhancement showed typical features for meningioma. the dura in the soft-tissue component was homogeneously enhanced, but the hyperostotic bone was not enhanced. postcontrast fat suppression t1-weighted mri was useful to evaluate the extension of dural enhancement and soft-tissue involvement of the orbital content in those patients with tumor extending into the orbit. post-operative follow up imaging studies (both computed tomography (ct) and magnetic resonance imaging (mri) scans) were performed to assess the extent of tumor resection and to plan for any subsequent management. surgical technique sixteen patients were operated up on via the classic pterional approach and in two patient the orbito-zygomatic approach was performed. ipsilateral fronto-temporal craniotomy under general anesthesia was used for all patients. patients were placed in a supine position with the head tilted 20 degrees to the contralateral side. the scalp incision began 1cm superior to the anterior aspect of the auricle and curved anteriorly, ending at the hairline, 1 cm from the midline. care was given to avoid injury to the temporal branch of the facial nerve. initially we removed the extracranial soft tissue part of the tumor which was fequently encountered then we did extensive drilling of the all invaded bones of the lesser and greater sphenoid wings. in most cases; it was necessary to remove the anterior clinoid process and optic canal was opened when it was involved by the hyperosteosis. the infilterated dura was removed totally in all cases and we removed the small intradural soft tissue component. the component of the tumor in the cavernous sinus and the superior orbital fissure were left not to endanger the important structures to avoid significant postoperative morbidies. dural graft and abdominal fat was used to achieve watertight dural closure. orbital reconstruction was done using muscle and split calvaric bone. romanian neurosurgery (2016) xxx 4: 498 – 506 | 501 results our series included 12 women and 6 men, ranging in age between 36 and 54 years. the clinical manifestations present at the onset of disease in these cases are summarized in table 1. the most common presenting symptom was proptosis, which was observed in 15 patients (83.3%), followed by progressive visual loss in 12 patients (66.67%), and headache in 8 patients (44.4%). preoperative neuroradiological evaluations demonstrated hyperostosis in all 18 patients. the sphenoid ridge was a constant location for hyperostosis (observed in all cases), followed by the lateral and superior walls of the orbit, in 77.78 and 33.3% of patients, respectively (table 2). table 1 presenting symptoms in 17 cases of sphenoid wing meningioma symptoms number of cases (%) proptosis progressive vision loss 15 (83.3%) 12 (66.67%) headache 8 (44.4%) diplopia 2 (11.1%) eye swelling 1 (5.56%) seizures ptosis 1 (5.56%) 2 (11.1%) table 2 correlation of neuro-imaging and histological findings of hyperostosis case no. sex areas of hyperostosis on neuroimages histological confirmation 1 f sphenoid ridge, lat & sup walls of orbit yes 2 m sphenoid wing, lat wall of orbit yes 3 f sphenoid ridge, optic canal yes 4 m sphenoid ridge, lat & sup walls of orbit yes 5 f sphenoid wing, lat wall of orbit yes 6 m sphenoid ridge yes 7 f sphenoid ridge, lat & sup walls of orbit yes 8 f sphenoid wing, lat wall of orbit yes 9 f sphenoid wing, lat wall of orbit yes 10 m sphenoid ridge yes 11 f sphenoid wing, lat wall of orbit yes 12 f sphenoid ridge, lat & sup walls of orbit yes 13 f sphenoid wing, lat & sup walls of orbit, ant wall of middle fossa yes 14 f sphenoid wing, lat wall of orbit yes 15 m sphenoid ridge, lat & sup walls of orbit yes 16 m sphenoid ridge yes 17 f sphenoid wing, lat wall of orbit yes 18 f sphenoid wing, lat wall of orbit yes 502 | zakaria, taha hyperostotic sphenoid wing meningioma en plaque table 3 histological tumor growth patterns and pathological bone invasion case no. tumor histology who grading bone invasion 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 meningotheliomatous i yes meningotheliomatous i yes meningotheliomatous i yes transitional i no meningotheliomatous i yes chordoid ii yes meningotheliomatous i yes chordoid ii yes meningotheliomatous i yes meningotheliomatous i yes meningotheliomatous i yes transitional i yes mixoid i yes meningotheliomatous i yes meningotheliomatous i yes meningotheliomatous i yes meningotheliomatous transitional i i yes yes surgical results there were no deaths related to the surgical procedures in this series of cases. cerebrospinal fluid rhinorrhea happened in one patient and was improved after insertion of lumbar drain for three days. preoperative proptosis improved in all patients (figure 1), and 83.3% of patients had improved vision after surgery. one patient showed worsening of vision after surgery and hadn't improved on subsequent follow up. total tumor removal was achieved in 14 patients (77.8%). in four patient; we found residual tumor (22.2%) on follow up imaging. in two patient the residual tumor involved no drilled bone hyperosteosis and the tumor progressed on subsequent imaging and 2nd surgery was performed for both of them. the other two patient were refered for gamma knife radiosurgery as the residual tumor was left in the cavernous sinus. preoperative mri showed extensive bone invasion with small intracranial soft tissue component romanian neurosurgery (2016) xxx 4: 498 – 506 | 503 postoperative ct and mri showed tumor excision and proptosis subsidence on patient figure 1 48 female patient with excised large sphenoid ridge meningioma presented with progressive proptosis histological results the results of histopathological evaluation are summarized in table 3. bone invasion was confirmed histologically, but most of the hyperostotic bone was removed by drilling. in 16 of the 18 cases, the tumors were histologically benign (who grade i); the other two tumors showed some chordoid features and were thus classified as who grade ii. meningotheliomatous growth patterns predominated in most of the tumors (12 of 18). bone invasion by the tumor was confirmed histologically in 17 of 18 patients. histological examination did not show tumor invasion into the bone in one case, but this finding can be attributed to a loss of involved bone through aggressive drilling and the consequent evaluation of an inappropriate specimen because of the drilling. discussion the cure for hyperosteotic sphenoid ridge meningiomas was difficult to be achieved as shown in different case series and this was attributed to their extensive bone, orbital, and neural involvement. they tumors usually grow following the contour of the inner table of the skull base with involvement of a large surface area. the characteristic hyperostosis is often disproportionate to the relatively small tumor. the cause for hyperosteosis is debatable in the literature but the widely accepted theory in most recent publications is that it’s tumor invasion rather than bone irritation or just new osteoblastic bone formation. hence, cure would not be possible without extensive bone drilling to remove all the involved bone. these tumors also insinuate themselves into the surrounding structures by way of natural openings. extension into the orbit, superior orbital fissure or optic canal adds challenge to such tumors making the overall prognosis less favorable. (1, 2, 9, 10, 16, 18, 19) 504 | zakaria, taha hyperostotic sphenoid wing meningioma en plaque the clinical presentation of such challenging tumors is mostly due to associated hyperostosis and the most common presentation in different series is unilateral slowly progressing proptosis. other manifestations include headache, visual impairment, seizures and affection of ocular motility. in our series the clinical presentations of those lesions matches with what have reported in other case series. (2, 6, 7, 11, 15, 17) the development of proptosis is reported to occur in up to 100% of cases according to different series and it is explained either due to direct tumor invasion into the orbit, hyperosteosis of the bony orbit and / or cavernous sinus and superior orbital fissure invasion causing impairment of the venous drainage of the orbit. for correction of proptosis; it is necessary to do extensive excision of the invaded bone which should also remove the involved bone of the optic canal and superior orbital fissure to improve symptoms caused by cranial nerves compression especially visual impairment and ocular motility affection. both magnetic resonance and ct images are essential to allow precise determination of anatomical relationships of these tumors and pattern of their extensions enabling planning of the surgical treatment. (2-6, 14, 15, 17-19) the goal of surgery is to achieve total resection of the entire tumor both the soft and bony component. hyperostotic bone should be extensively removed to prevent tumor recurrence. (2-6, 14, 15, 17-19) most of the cases in our study were operated up on via the classic pterional approach while in 2 cases the orbito-zygomatic approach was performed. drilling of the hyperosteotic bone improved the visualization making removing the zygomatic arch not necessary in most of the cases. despite aggressive bone drilling to achieve to resection of such tumors is usually attempted however total resection was not always feasible and there is still a potentiality for tumor recurrence. tumor extension into the cavernous sinus and the superior orbital fissure hinders the attempt for total tumor resection. meningiomas in the cavernous sinus encircle the cranial nerves and vascular structures within sinus and manipulation of such tumors inside sinus increase the possibility of permanent ophthalmoplegia and even vascular injuries. (1, 2, 4, 6, 11, 15, 16, 19) we have four cases in our study in whom there was residual tumor on subsequent imaging; two of them due to missed invaded bone on the initial surgery and were followed up and 2nd surgery was performed for tumor progression. the other two cases the tumor was left in the cavernous sinus and was sent for gamma knife radio-surgery. furthermore; extensive drilling of sphenoid bone and orbit had a significant risk for postoperative cranial deformities and cranial and orbital reconstruction should be considered with surgical planning. on the other hand; aggressive bone drilling was not able to correct long standing tumor related proptosis. (2, 3, 7, 12, 15, 19) the resection of the involved hyperostotic bone from the sphenoid and the orbit disrupts the structural integrity that the sphenoid wing provides to the orbit and the anterior and romanian neurosurgery (2016) xxx 4: 498 – 506 | 505 middle cranial fossa. lack or improper orbital reconstruction have its potential risk for aditional postoperative morbidities ranging from meningoceles, postoperative infection up to complete ophthalmoplegia and a nonfunctional globe. hence, proper surgical reconstruction is as important as adequate tumor resection for achievement of a successful outcome. (2, 8, 12, 14, 18, 19) as in all the cases in our study, it was essential to remove all in invaded dura of the base, we considered thefirest step to achieve sound reconstruction and prevent the potential morbidities is to perform water tight dural closure. we prefer to use autologus dural graft either pericranium or fascia lata as needed in adition to autologus fat graft. skeletal calvarial and orbital reconstruction is another crucial step that we performed in all our cases. although many authors described various techniques and variable reconstructive materials, we prefered to do autologus skeletal reconstruction in all of our cases presented in this study. the result was acceptable without any significant functional or cosmotic sequalae and avoidance the potential risk of using synthetic materials to achieve such reconstruction. although in other studies, many authors utilized different synthetic materials that proved to be safe and effective in achievement of cosmotically sound orbital reconstruction and their results are more favorable than we do but all must be individually fashioned pre-operatively to have the symetrical shape for the orbit that have to be reconstructed. unfortunately, such technology wasnot feasible for us apart from the potential problem with management of potentially possible recurrence and the need for subsequent imaging studies. (2, 8, 12, 14, 15, 18, 19) conclusions early and radical surgery for hyperosteotic sphenoid ridge meningiomas is essential for both achievement of good cosmetic and functional outcome and prevention of tumor recurrence. however extensive bone involvement and tumor extension into cavernous sinus and superior orbital fissure hinder the capability for total resection and increase the potential risks for aggressive surgical interference. radio-surgery is a useful alternative for residual tumor in the cavernous sinus. adequate dural repair and orbital reconstruction is important to achieve good cosmetic and functional outcome. references 1.abdel-aziz km, froelich sc, dagnew e, jean w, breneman jc, zuccarello m, et al.: large sphenoid wing meningiomas involving the cavernous sinus: conservative surgical strategies for better functional outcomes. neurosurgery 54:1375–1384, 2004 2.bikmaz, k, mrak r, al-mefty o: management of boneinvasive, hyperostotic sphenoid wing meningiomas. j neurosurg 107: pp. 905-912, 2007 3.boari n, gagliardi f, spina a, bailo m, franzin a, mortini p.: management of spheno-orbital en plaque meningiomas: clinical outcome in a consecutive series of 40 patients. br j neurosurg; 27(1):84–90, 2013 4. de jesús o, toledo mm: surgical management of meningioma en plaque of the sphenoid wing. surg neurol 55:265–269, 2001. 5.elder, jb, atkinson r, zee cs, chen tc: primary intraosseous meningioma. neurosurg focus 23: pp. e13, 2007 6.honig s, trantakis c, frerich b, sterker i, kortmann rd, meixensberger j.: meningiomas involving the 506 | zakaria, taha hyperostotic sphenoid wing meningioma en plaque sphenoid wing outcome after microsurgical treatment–a clinical review of 73 cases. cent eur neurosurg;71(4):189–98, 2010 7.honeybul s, neil-dwyer g, lang da, evans bt, ellison dw: sphenoid wing meningioma en plaque: a clinical review. acta neurochir (wien) 143:749–758, 2001 8.leake d, gunnlaugsson c, urban j, marentette l: reconstruction after resection of sphenoid wing meningiomas. arch facial plast surg 7:99–103, 2005 9.lee jh, sade b, park bj: a surgical technique for the removal of clinoidal meningiomas.neurosurgery 59:ons108 ons114, 2006 10.margalit ns, lesser jb, moche j, sen c: meningiomas involving the optic nerve: technical aspects and outcomes for a series of 50 patients. neurosurgery 53:523–533, 2003 11.marcus h, schwindack c, santarius t, mannion r, kirollos r. image-guided resection of spheno-orbital skull-base meningiomas with predominant intraosseous component. acta neurochir (wien);155(6):981–8, 2013 12.mirone g, chibbaro s, schiabello l, tola s, george b: en plaque sphenoid wing meningiomas: recurrence factors and surgical strategy in a series of 71 patients. neurosurgery 65:6 suppl 100–109, 2009 13.oya s, sade b, lee jh: sphenoorbital meningioma: surgical technique and outcome. j neurosurg 114(5):1241–9. 2011. 14.pieper, dr, al-mefty, o, hanada, y, buechner, d: hyperostosis associated with meningioma of the cranial base: secondary changes or tumor invasion. neurosurgery 44: pp. 742-746, 1999. 15.ringel f, cedzich c, schramm j.: microsurgical technique and results of a series of 63 spheno-orbital meningiomas. neurosurgery;60 (4 suppl 2):214–221; discussion 221–12, 2007. 16.roser f, nakamura m, jacobs c, vorkapic p, samii m: sphenoid wing meningiomas with osseous involvement. surg neurol 64:37–43, 2005. 17.scarone p, leclerq d, heran f, robert g. long-term results with exophthalmos in a surgical series of 30 sphenoorbital meningiomas. clinical article. j neurosurg; 111(5):1069–77, 2009. 18.schick u, bleyen j, bani a, hassler w: management of meningiomas en plaque of the sphenoid wing. j neurosurg 104:208–214, 2006. 19.shrivastava rk, sen c, costantino pd, della-rocca r: sphenoorbital meningiomas: surgical limitations and lessons learned in their long term management. j or neurosurgery 103 (3): 491-497, 2005. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article rapid recurrence of a malignant meningioma: case report oguz baran, sima sayyahmeli, taner tanriverdi, pamir erdincler turkey doi: 10.1515/romneu-2017-0027 178 | baran et al rapid recurrence of a malignant meningioma doi: 10.1515/romneu-2017-0027 rapid recurrence of a malignant meningioma: case report oguz baran1, sima sayyahmeli2, taner tanriverdi2, pamir erdincler2 1istanbul research and training hospital, neurosurgery clinic, istanbul, turkey 2istanbul university cerrahpasa medical faculty, department of neurosurgery, istanbul, turkey abstract: this short report presents a case that developed rapid recurrence of a malignant meningioma. the meningioma was located on the right temporal lobe and total removal (simpson grade-ii) was performed. radiotherapy was not given and the lesion recurred within four months. the mib-1 (ki-67) index was 30 % and the tumor fulfilled all the criteria of anaplasia. after the second surgery, patient was transferred to the radiation oncology for radiotherapy. should we questioned the extent of surgery? neurosurgeons should be careful and close follow-up the patients with malignant meningioma. key words: anaplasia, malignant meningioma, recurrence, surgery, radiotherapy introduction meningiomas are among the most common extra-axial central nervous system (cns) tumors, ac-counting almost 30 % of all cns tumors (5). the majority are histologically benign which were graded as grade-i by world health organization (who). in 2007, who introduced some criteria and grade-ii (atypical) and grade-iii (anaplastic or malignant) variants have been introduced into the current literature (3). among the three groups, malignant meningiomas are very rare, accounting 1-3 % and show aggres-sive behavior and high recurrence rate (5). in this short report, we want to present a case of a malignant meningioma which had rapid recurrence. case report this 69-year-old female was admitted to a local hospital with severe headache. magnetic resonance imaging (mri) of the head revealed a mass with hypointense on t1and iso hyperintense on t2-weighted images on the right temporal lobe. the lesion measures 33 mm diameter and showed massive edema. on the contrasted images, the lesion showed heterogeneous enhancement with irregular margins (figure 1). then the patient was consulted to us and our neurological examination was normal. the patient underwent surgery in which the lesion was totally removed and the dura of origin was coagulated (simpson grade-ii). early postoperative mri confirmed total removal (figure 2) and histopathological romanian neurosurgery (2017) xxxi 2: 178 181 | 179 diagnosis was malignant meningioma (who grade-iii). on the histopathological report, the lesion fulfilled the criteria for anaplasia with high mitotic activity and necrosis. immunostaining showed strong positive staining for vimentin and partially positive staining for epithelial membrane antigen (ema). proliferation index for ki-67 was found to be 30 % and no rhabdoid or papillary features was re-ported. the postoperative period of the patient was uneventful and discharged from the hospital without any neurological deficit. although the radiotherapy was advised, the patient refused to have it because of its side effects. thus we decided to close follow-up either with clinically or radiologically. four months after the surgery, the patient again complained of severe headache accompanying with nausea and vomiting. ct scan of the head in the local hospital revealed a mass on the right temporal lobe with 7 mm midline shift causing midbrain compression (figure 3). then the patient was transferred to our clinic. the neurological examination was normal and mri showed a recurrence which had increased in size on the right temporal lobe. reoperation was performed in which total removal again was achieved (figure 4). the postoperative period was uneventful and the patient was sent to the radiation oncology for radiotherapy. second histological study including immunohistochemical staining revealed that ki-67 has increased to 70 % and malignant characteristics of sarcoma. figure 1 a contrasted image shows heterogeneously with irregular margin on the right temporal lobe figure 2 early postoperative contrasted image showed total removal and no contrast enhancement 180 | baran et al rapid recurrence of a malignant meningioma figure 3 four months after surgery, t1-weighted image revealed a heterogeneously con-trasted with irregular border recurrence which had increased in size compared to the previ-ous mass figure 4 early ct scan of the head confirmed the total removal discussion malignant meningiomas are very rare clinical entity and satisfactory results from the treatment including surgery and radiotherapy in general are not possible. despite total surgical removal (simpson grade-i) and following radiotherapy, recurrence at 5 years has been reported to be very high, accounting for almost 80 % (1). the median time to recurrence is 1 to 3 years and survival is less than 2 years (1, 5). in the current literature, reports with respect to rapid recurrence in malignant meningiomas are very scarce and only two case reports have been encountered. petridis, et al. (4) reported a case of a 71-year-old man who operated on a malignant meningioma. the tumor was removed totally (simpson grade-i) and radiotherapy was given. the proliferating index (mib-1) was found as 60%. however; eight months after surgery, the authors found recurrence with multiple meningiomas which were spread all over the brain. the authors tried to make a connection between the rapid recurrence and the radiation therapy although they underlined that whether the occurrence of the new tumors was due to radiation cannot be proved. another case was reported by kawahara, et al. (2) who operated on a 62-year-old patient with malignant meningioma. they performed simpson grade-iii surgery due to the attachment of the tumor to the middle cerebral artery. forty-three days following the first surgery, follow-up revealed a tumor recurrence which was bigger than that of primary tumor size. the mib-1 index was romanian neurosurgery (2017) xxxi 2: 178 181 | 181 found to be 70 % and after second surgery the patient was treated with radiotherapy. the very short time to recurrence was according to the authors due to the high mib-1 index which was found to be correlated with the rapid tumor growth. in their case sub-total removal might be the cause of recurrence but the authors underlined that the extent of surgery is not correlated with the onset of recurrence. our case fulfilled the anaplastic criteria determined by who but mib-1(ki-67) was not high. ex-tent of surgery (simpson gradeii) is appropriate in our case in which the tumor was removed to-tally and the dura was coagulated. radiotherapy was not given in our case so that radiotherapy cannot be blamed for the rapid recurrence. radiotherapy is generally given for the recurrent or residual tumors but we agree that it surgery should aim to remove in toto (simpson grade-i) which should be followed by radiotherapy which can increase the recurrence interval. conclusion conclusion from our short report and the two reports mentioned above should be that whatever the extent of surgery, radiotherapy should be considered immediately and the patients with malignant meningiomas should be followed-up closely because of very malignant nature or behavior. correspondence oguz baran. istanbul research and training hospital, neurosurgery clinic, istanbul; turkey. e-mail: oguzbaran@gmail.com telephone number: +905325990034 fax number: +902124596230 mailing address: istanbul egitim ve arastirma hastanesi, beyin ve sinir cerrahisi klinigi. kasap ilyas mah. org. nafiz gurman cad. 34098 samatya/istanbul references 1.jaaskelainen j, haltia m, servo a. atypical and anaplastic meningiomas: radiology, surgery, radiotherapy, and outcome. surg neurol 1986; 25: 23342.
 2.kawahara y, nakada m, hayashi y, watanabe t, tamase a, hayashi y, uchiyama n, nitta h, hamada j. anaplastic meningioma with extremely rapid recurrence: a case report. neu-rol med chir (tokyo) 2011; 51: 3868. 3.perry a, louis dn, scheithauer bw, budka h, von deimling a. meningiomas. in: louis dn, ohgaki h, wiestler od, cavenee wk, editors. who classification of tumours of the central nervous system. 4th ed. lyon: iarc press; 2007.p.164-74. 4.petridis ak, doukas a, mahvash m, dörner l, hugo hh, mehdorn hm. a case of rap-id-growing anaplastic meningiomas. bmj case rep 2009; doi:10.1136/bcr.05.2009.1862 5.riemenschneider mj, perry a, reifenberger g. histological classification and molecular genetics of meningioma. lancet neurol 2006; 5: 1045-54. microsoft word _4.formatata_balan.doc romanian neurosurgery vol. xvi nr. 2 20 decompressive craniectomy – from option to standard part i corneliu balan1, bernard alliez2 1clinical hospital “prof. dr. n. oblu”, iasi, romania 2hopital nord, chu marseille, france authors intend an update to the theoretical and practical data on a seldom utilized technique but often considered as last therapeutically option, so the necessity to realize it correctly. the authors present the history, the physiopathology of the technique, the surgical steps and options, together with details on the complications, surgical indications. keywords: decompressive craniectomy, indications introduction the decompressive craniectomy is a surgical technique known for more than a century, but its utility variated from none to everything according to neurosurgeons. actually, it reappears after the papers of guerra [1] from 1998 and is utilised for a wide range of pathologies, from traumatic to vascular and tumoral, but all realising an refractory intracranial pressure. unfortunately there is a lack of consensus upon when to realize a decompressive craniectomy among authors, which leads to the fact that most neurosurgeons seldom see a correct deompressive craniectomy and even less performs one. history the first decompressive craniectomies were presented by kocher in 1901, cushing in 1903 and horsley in 1906, in a period when most surgery was realized through a large „exploratory”bone flap – when no lesion was found, some authors suggested removing the bone flap to decompress the brain from the lesion. unfortunately, the aesthetical results were disastrous and led to limiting the technique. in traumatic pathology the method knew supporters and detractors [2]: erlich (1940) suggested a decompressive craniectomy for all head injuries with persistant coma for more than 24-48 hours – without a specific diagnosis most cases woul have died anyway. rowbotham (1942) recommanded decompressive craniectomy for all traumatic comas which improved at first and when medical treatment was ineffective for 12 hours. munro (1952) suggested that if intraop the brain was contused and swollen to realize a large craniectomy and opening the dura mater. among adversaries are mayfield, lewin, moody, whose papers during 1960-1970 note a high mortality rate for the technique and discourage its utilisation. after the introduction of ct scan, in 1975 , ramshoff, morantz and others present series of comatose patients wiht acute subdural hematomas, operated during the first 6-12 hours, with decompressive craniectomies realized by necessity. despite technical and esthetical problems, they report a survival rate of 40% with 27 % return back to a previous life – however the method doesn’t meet a genereal approval. the desert of redescovering the decompressive craniectomy belongs to guerra in 1999 who presents in journal of neurosurgery his personal results of 20 years of decompressive craniectomy using ct scan and icp monitoring. his good results lead to the acceptance of the technique as second-tier therapy for decompressive craniectomy romanian neurosurgery vol. xvi nr. 2 21 refractory intracranial pressure. the following 5 years know more than 50 papers[4] dedicated to decompressive craniectomy leading to sections of neurosurgical meeting dedicated to the technique and at least 2 prospective double blind multicentric studies in going on its indication in traumatic pathology physiology the purpose of decompressive craniectomy is to diminish the intracranial pressure, no matter its the lesion, when icp raises to alarming values. the threshold of icp variates from children, which tolerate larger values when sutures are still open, to adults and according to pathology. the limits of well tolerated icp, together with lowering of cpp, variate from 18-20 mm hg in subarachnoid hemorrhage, 20-22 mm hg for malignant sylvian stroke, 25 mm hg for trauma and 3040 mm hg for slow growing tumors and hydrocephalus [5]. some of these values are among what is considered a normal icp but with an ailing brain. when medical treatment becomes ineffective, the decompression realizes an „enlargement” of the intracranial space, preventing a further raise of icp and cerebral herniations. moreover, doppler and perfusion mri studies showed an increase of blood flow in leptomeningeal vessels, an increase of backward flow in the sylvian artery togther with the perfusion of the ischemic penumbra area. in order to realize a real decompression, we need to evaluate the volume gained on surgery – considering a circular craniectomy and a bulging of just 10% of the surface to prevent ischemia on the bone flap’s edge, aschoff calculated the following [fig. 1]: volum suplimentar considerind craniectomia circulara 0 0 1 9 23 47 86 152 0 20 40 60 80 100 120 140 160 0 2 4 6 8 10 12 14 16 diametrul craniectomiei (cm) vo lu m s ul pi m en ta r (m l) fig. 1 fig. 2 fig. 3 apparently a craniectomy of 8 cm large would appear large enough but in fact it gives just 23 ml additional volum so 1.5% of total cerebral volume. to obtain a real decompression, most authors recommend a minimum corneliu balan romanian neurosurgery vol. xvi nr. 2 22 diameter of 12 cm or more (86 ml additional volume) fig. 2, 3. the additional volume obtained by a decompressive craniectomy is consequently superior to the one realized by hyperventilation (2 ml / mm of lowering pco2); superior to a ventricular tap of 20-30 ml and without the risk of rebound of loop diuretics. surgical procedure mainly there are two types of decompressive craniectomies – the hemicraniectomies, most frequent, when bone resection involves just one hemisphere; bilateral craniectomies, seldom used. 1. hemicraniectomy – ideally would imply bone resection over one whole hemisphere, including the temporal fossa till the zygomatic bone, going posterior to a line which connects the tragus with asterion and respecting the horizontal segments of the skull in the superior parietal area. practical, more often we realize just a wide craniectomy, more than 12 cm diameter, which descends in the temporal fossa and goes posterior according to a vertical line through the asterion. if available, the head of the patient shoyld be fixed in a mayfield head holder, with two screws in the occipital area and one in the frontal, maintaining thus the anteroposterior axe of the head parallel to the ground. in absence of the mayfield, any lateral supine position is convenient, providing a fixation of the head to the operatory table with no reduction of the operatory field.. the incision should provide wide access to the whole hemicranium, with two common technical options. fig. 4 fig. 5 the first option [fig. 4] is analogous to the classical “question mark” flap, utilized in traumatic pathologies but extended more posterior. the incision starts at temporal level then goes superior, in order to preserve the blood supply of the fla p from the superficial temporal artery. the temporal muscle is dissected in one plane, attached to the flap (some prefer to harvest the temporal fascia for later duroplasty). the advantage of this incision resides in the fact that most neurosurgeons are accustomed to anatomical structures – but in the posterior segment of the flap the blood supply is low and leads to several complications, especially dehiscent wound or skin necrosis. if when starting the incision the supperficial temporal artery is accidentally cut, it is mandatory to use the second incision [fig. 5], less classic and time consuming but withut ischemic complications at the operatory wound due to preserving the occipital artery and thus a better blood supply. bone resection is realized with available craniotomes or gigli saw [fig. 6, 7]. dura mater is incised radial or with pedicle on the middle meningeal artery and the duroplasty with periost, muscle fascia or quicker with dural substitutes. we do not advise to let the dura mater intact because it is not elastic, compromising the purpose of the operation; again we do not advise to let the dura mater free because it will be more difficult to realize the dissection on cranioplasty. the bone flap is preserved, (in theory), by introduction in the abdominal fat – practical the manoeuvre extends the operation for at least one hour and that’s why most prefer the organ bank (where available) or simple freezing. decompressive craniectomy romanian neurosurgery vol. xvi nr. 2 23 fig. 6 fig. 7 2. bilateral craniectomies involve the bone resection described previously on both sides while preserving a bone ridge of 3-4 cm over the superior longitudinal sinus. the intraop positioning is difficult, due to the impossibility of using the mayfield holder. additional problems arise later, being difficult to avoid the bone resection in a supine position and maintaining the patient head directed to the zenith. far more common used is the bifrontal decompressive craniectomy [fig. 8, 9], especially on diffuse cerebral edema or contusive bifrontal lesions [6]. the dural incision is bilateral, directed towards the sagital sinus, with duroplasty at the inferior (temporal) segment, while respecting the technical indications from unilateral craniectomy. a variant of the bifrontal craniectomy implies preserving a frontal median bone ridge over the sagital sinus. fig. 8 fig. 9 complications no surgical technique is exempt of complications and decompressive craniectomy is no exception. moreover, lack of experience of surgeons who realize it once per year or unknowing the correct technique can lead to additional complications to those inherent to a very large craniectomy. acute complications: • hemorrhagic contusions at the level of the decompressed brain – classical complications, corneliu balan romanian neurosurgery vol. xvi nr. 2 24 characteristic to traumatic pathology, is due to lowering the intracranial pressure to normal values, but allowing hemorrhage from anterior compressed capillaries (initial high pressure realized hemostasis through compression). it does not represent a complication but a normal evolution of the lesion and there is no way to prevent it. fig. 10 a fig. 10 b fig. 10 c the images present the case of a 21 y old patient, with severe head injury due to a politrauma – initial gcs at 11 (fig. 10a), aggravated during transport to gcs = 5 (fig. 10b) who was decompressed even before installing a monitoring of icp. ct scan realized on d2 reveals large areas of hemorrhagic contusions at the level of the decompressed hemisphere. • fongus cerebri, the herniation of the brain (“mushroom”), at the level of the bone flap is most frequent the result of a bone flap not enough large, when cerebral decompression is not sufficient and high intracranial pressure displaces the already contused brain through a small breech in the skull – aspect wide known to neurosurgeons, especially for acute subdural hematomas to the initial raised intracranial pressure is superposed the compression of cortical veins on the bone’s edge, realizing thus venous stasis and later venous infarction. the difference between these later lesions and cortical contusions resides in the moment of onset, later than for brain contusions and the more homogenous aspect of hemorrhage adjacent to the bone’s edge (fig. 11). such compression can be avoided by realizing the “vascular tunnel” described by csokay [9]. decompressive craniectomy romanian neurosurgery vol. xvi nr. 2 25 • the development of controlateral hematomas especially acute subdural or epidural was already described, its mechanism being similar to hemorrhagic contusions, through bleeding from a bridge vein or a bone fracture. these hematomas are characteristic to traumatic pathology decompressed in the first 24h. fig. 11 fig. 12 less frequent is the apparition of compressive higromas (fig. 12) on the same side as decompression, with a more unclear mechanism. • wound dehiscence is frequent due to the high pressure from interior which maintains sutures in tensions and concomitant ischemic / necrotic phenomena due to a low blood supply for the flap’s dimensions. it occurs more frequent when accidentally coagulating the superficial temporal artery when realizing the skin flap. late complications • posttraumatic hydrocephalus – frequent, due to obstruction of resorbtion of csf by traumatic sah and to modifications of csf pressure and circuit by decompression. among the factors contributing to posttraumatic hydrocephalus, mazzini [10] calculated a p=0.01 significance fro decompressive craniectomy so high statistic. many problems occur on treating this hydrocephalus which is different from the classic one due to the large bone flap. it is mandatory to use an adjustable valve, initially fixed on medium pressure then progressively raising to high pressure, to avoid the overdrainage with sinking of cutaneous flap (fig 13). after realizing a cranioplasty, the pressure in the valve should be returned to nomal. • problems connected to cranioplasty occur due to resorbtion of autologuos bone – the devitalized bone is considered as foreign body. • infections are the most frequent and most dangerous among the complications of decompressive craniectomy, especially for traumatic pathology. despite a correct bone flap and even more without a correct technique, due to a long bed rest in the icu department, with one position of the head, wound dehiscence appear, sometimes even after a month postop, with csf fistula, bacterial colonization. some can be treated by resuturing the wound, but most of them realize an infection with icu germs, multiresistant, leading to subdural empyema or brain abscess (fig 14). another germ source is ventilated associated pneumonia, quite common after several days of intubation, on a patient with clean operatory wound. • the «trephined patient» syndrome unites symptoms difficult explicated by othe pathologies which disappear after cranioplasty. most frequent manifestation is as focal neurological signs, developed after 3-6 months after initial surgery and absolutely without lesions on ct/mri. fig. 13 decompressive craniectomy, drained from the frontal horn with overdrainage and “sinking flap” corneliu balan romanian neurosurgery vol. xvi nr. 2 26 fig. 14 subdural empyema under the decompressed area and frontal brain parafalx indications there is actually just one class i indication for decompressive craniectomy malignant sylvian stroke in people less than 60 old [8], and still there are controversies. most studies involving decompressive craniectomy are retrospective and the few prospective ones were realized on patients with refractory raised intracranial pressure as salvage therapy. there are at least 2 prospective studies ongoing – rescue icp – european multicentric study initiated by cambridge (uk) and another one in australia, initiated by teams of sidney and canberra, both on traumatic cases, but till summer 2008 less than 120 cases were included. there are also several proposals of using profilactic decompressive craniectomies whenever exists a high risk of evolution towards a refractory raised intracranial pressure [7] or when the neurosurgeon’s experience suggests this – like acute subdurals hematomas associated with large contusion, subarachnoid hemorrhage or severe meningitis [11, 12]. these indications will be discussed in part 2 of the article. references 1. guerra wk, gaab mr, dietz h, et al: surgical decompression for traumatic brain swelling: indications and results. j neurosurg 90: 187-196, 1999 2. m. holland, p. nakaji craniectomy: surgical indications and technique, operative techniques in neurosurgery, vol 7, no 1 (march), 2004: pp 10-15 3. kontopoulos v, foroglou n, patsalas j, et al: decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered? acta neurochir (wien) 144:791-796, 2002 4. albanese j, leone m, alliez jr, et al: decompressive craniectomy for severe traumatic brain injury: evaluation of the effects at one year. crit care med 31:2535-2538, 2003 5.aschoff a.,schwab s., spranger m, et al the value of intracranial pressure monitoring in acute hemispheric stroke, neurology 47 (1996): 393-398 6. polin rs, shaffrey me, bogaev ca, et al: decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. neurosurgery 41:84-92, 1997 7. coplin wm, cullen nk, policherla pn, et al: safety and feasibility of craniectomy with duraplasty as the initial surgical intervention for severe traumatic brain injury. j trauma 50:1050-1059, 2001 8. vahedi k, hofmeijer j, juettler e, et al (2007). "early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials". lancet neurology 6 (3): 215-22 9. csokay a, nagy a et al avoidance of vascular compression in decompressive surgery for brain edema caused by trauma and tumor ablation, neurosurgical review, vol 4-6, 2001 10. mazzini l, campini r, angelino e posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. arch phys med rehabil. 2003, nov;84(11):1637-41. 11. skoglund, ts; eriksson-ritzen c, jensen c, rydenhag b (2006). "aspects on decompressive craniectomy in patients with traumatic head injuries". journal of neurotrauma 23 (10): 15021059. 12. schneider, gh; bardt t, lanksch wr, unterberg a (2002). "decompressive craniectomy following traumatic brain injury: icp, cpp and neurological outcome". acta neurochirurica (supplement) 81: 77-79 microsoft word 25sivakumarr_descriptive 384 | sivakumar et al descriptive study of cranio-cerebral injuries             doi: 10.2478/romneu-2018-0048 a descriptive study of cranio-cerebral injuries admitted in tertiary care center of coastal andhra pradesh r. sivakumar1, b.v. subrahmanyam1, s.v. phanindra1, ashok munivenkatappa2, s. satish kumar3, amit agrawal4 1forensic medicine, department of forensic medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 2national institute of epidemiology, icmr, chennai – 77, tamil nadu, india 3emergency medicine, department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 4department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: introduction: demographic and clinical profile of traumatic brain injury (tbi) of a particular place is very crucial for strengthening the guidelines. the details of same are scant from a tertiary institute, nellore district. the present study aims to explore the demographic, injury and clinical aspects of cerebro-cranial injury patients from an institute setup. methods: the study consists of two years retrospective data and one year prospective data. the study was approved by institute ethical committee. the patient data was entered on pre designed proforma that includes the desired variables. the data analysis was done using statsdirect software. both prospective and retrospective data was merged for analysis. percentages for categorical data and mean values for continuous data were calculated. results: there were total of 336 patients. patients in age group of 21 to 50 years constituted 67% and males were four times higher than females. nearly one fourth of patients were influenced by alcohol. three fourth of accidents were due to road traffic accidents (rtas) followed by falls (17%) and assault (6%). about one tenth of patients were pedestrians. one fourth of patients had associated injuries other than head and brain. on ct findings majority of patients had cerebral contusion (46%) followed by skull fracture (40%), sdh (28%) and edh (23%). twenty two patients died in the study period. conclusion: knowledge of injury and its later consequences to public is very important. strict rules to consider safety precautions and compulsory family insurances should be encouraged. rules to prevent paediatric drive. key words: age, gender, tbi, institute, ct findings, urban, rta, guidelines romanian neurosurgery (2018) xxxii 2: 384 390 | 385             introduction traumatic brain injury (tbi) has long been recognized as a leading cause of mortality and permanent neurological disability worldwide and has been described as a silent and causing a significant social and financial burden for them, their families and the public health system. [1] in year 2014 the national crime report bureau reported that there were a total of 4,81,805 traffic accidents and out of these 4,50,898 were road accidents which were responsible for 1,41,526 deaths. [2] in india, road traffic injuries projected to become the second leading cause of death by the year 2020. [3] there are few studies from india that have described the epidemiology of tbi and discussed related issues, including the need for public awareness campaigns and enforcement of legislation to reduce the number of injuries. [4-8] most of these studies have been conducted in different parts of country at institute level and the present study is aimed to describe epidemiological characteristics, pattern of injuries and related clinical parameters of tbi from a tertiary care setup located in the coastal area of southern india. materials and methods narayana medical college and general hospital is a multi and super specialty hospital located in costal andhra district, nellore. it is a three years study that included data from 2011 to 2014. the study was approved by institute ethical board. the data was collected on a standard proforma. the proforma includes details of age, sex, causes of head injury, pattern of head injuries, computer tomography (ct) findings like skull fractures, parenchymal injuries, intracranial hemorrhages, and discharge outcome (alive or death). statistical analysis the data analysis was done using statsdirect version 3.0.150 (statsdirect statistical software. http://www.statsdirect.com. england: 2015). for analysis both retrospective and prospective data was combined together. percentages were calculated for categorical data, and mean, standard deviation was calculated for continuous data. results during study period there were 336 cases, of them 116 were prospective and 220 were retrospective cases. the mean age was 35.05 ± 16.36 years. sixty seven percent of patients were in 3rd, 4th and 5th decade of age group (figure 1). males were four times more than females. about 50% of patients were from urban setup. sixty six percent of injuries occurred on road. about 75 patients (22.3%) were influenced by alcohol (table-1).   386 | sivakumar et al descriptive study of cranio-cerebral injuries             table 1 demographic variable of cranio cerebral injury patients variables n (%) age (years) 35.05 ± 16.36 gender male 269 (80) female 67 (20) location of injury urban 169 (50.3) rural 167 (49.7) place of injury road 224 (66.7) home 47 (14) streets 25 (7.4) fields 11 (3.3) others 29 (8.6) alcohol influence yes 75 (22.3) figure 1 decade wise distribution of tbi patients road traffic accidents (rtas) was major cause of injury accounting for 75.6%, followed by falls (17.9%) and assault (6%). among rtas the motorcycle victim was affected in higher number (42.3%) followed by motor vehicle driver (15.2%) and pedestrian (12.2%). none of two wheelers worn helmet while riding vehicle. two wheeler was most common victim vehicle (54.8%) followed by four wheeler (4.8%) and three wheeler (4.5%). associated injuries were present among 23.3% of patients (table-2). table 2 details of mode and associated injuries among traumatic brain injury variables n (%) cause of injury road traffic accident (rta) 254 (75.6) fall 60 (17.9) assault 20 (6) object fall 2 (0.6) accident victim among rta motorcycle rider 142 (42.3) motor vehicle driver 51 (15.2) pedestrian 41 (12.2) passenger 20 (6) associated injuries present extremities fracture 45 (13.4) lung and pleura 11 (3.2) cervical spine 21 (6.3) dorsal spine 1 (0.3) external injuries of head scalp 278 (82.7) face 213 (63.4) on ct findings; 40% of patient had skull fractures. among intra cranial brain lesion, brain contusion (45.8%) was present among majority of patients, followed by sdh (28.5%) and edh (23%). midline shift was present among 13% of patients (table-3). during the study period 22 (6.5%) patients died.   romanian neurosurgery (2018) xxxii 2: 384 390 | 387             table 3 ct scan findings among traumatic brain injuries variables n (%) skull fracture 135 (40.1) right 62 (46) left 53 (39.2) bilateral 16 (11.8) midline 4 (3) extra dural hematoma (edh) 77 (23) right 38 (49.3) left 33 (42.8) bilateral 3 (3.8) sub dural hematoma (sdh) 96 (28.5) right 52 (54.1) left 36 (37.5) bilateral 4 (4.1) brain contusion 154 (45.8) right 60 (39) left 50 (32.4) bilateral 35 (22.7) midline 9 (5.8) coup brain injuries 77 (23) contre-coup injuries 35 (10.4) midline shift 44 (13.1) discussion the current study is conducted in a tertiary care hospital that provides medical service to main city and surrounding villages and districts. in present study about two third of patients were in 3rd-5th decades of life and out of these two thirds were males belonging to the financially productive age group and reflect the vulnerability of this age group and gender for accidents.[9,4,6,7,10-13] there was equal number of patients from urban and rural areas reflecting the proximity of the hospital to both city and surrounding villages. [14] the alcohol consumption was more prevalent male patients and there were more of assault patients (30%) followed by rta patients (26.5%).as previously reported [15, 16] the same scenario is reflected from our study regarding the time of the day and injury incidence which is commonly reported between 5-9 pm probably these are the peak traffic hours in cities. [3,7,12,17]. in the present study road traffic accidents were the commonest cause of injuries followed by falls and assault and in literature the incidence of injuries from rtas ranges from 55 to 72%, followed by falls ranging from 20 to 30% and assaults ranging from 1 to 10% respectively. [5,18-22] most of the incident victims were motorcycle riders (skid and fall) followed by motor vehicle drivers and pedestrian injuries these findigns were similar to the fidnigns reopprted in a a prospective case-study from eastern china where the authors observed that 61% of traumatic brain injuries were related to road traffic injuries, of these approximately one-third were motorcyclists, 31% pedestrians, and motor-vehicle passengers accounted for only 14%. [5] in another study from maharashtra the studied pattern of fatal vehicular accidents involving head injuries during 2010-2012 and observed that most of the victims were drivers (52.5%), followed by pedestrian (29.7%) and passengers (17.8%). [3] another interesting finding in our study was the pattern of fall from height related injuries which involved mainly farmers where the victims were fallen down from coconut tree and the the other common reason was fall from height at construction sites. 388 | sivakumar et al descriptive study of cranio-cerebral injuries             old people are commonly affected in ground level fall because of age related disabilities they spend most of the time in home where accidental falls are common in home. fall from tree was next common due to inexperience or weather changes cause alteration in tree texture. a study form us during 2001-2008 and observed a large majority of fall injuries occurred at home (72.8%), while 15.2% occurred at locations outside the home. 23 a study found falls from heights were responsible in 48.9%, slipping in bathrooms in 31.9% and from staircase or ladders in 19.2%. these findings are consistent with our study. in the present study ct findings reports that skull fractures were present in 135(40.1%) cases and 97 (28.8%) had base of skull fracture. studies have reported 34 to 35% of skull fractures among tbi patients. [13,24] abnormal intracranial findings were; brain contusion was present in 154(45.8), sdh in 98(28.5%) and edh in 77(23%). studies have reported cerebral contusion ranging from 21 to 53% [6,19,25,26], high percentage of sdh ranging from 50 to 90% [19,27,28] and about 10 to 20% edh. [19,27,28] in the present study nearly one fourth of tbi patients had associated injuries. extremities was most common to involve (13.4%) followed by spine (6.6%) and chest (3.2%). pedestrian injuries from a tertiary institute reported 90% of associated injuries (new). the current study reported less percentage of associated injuries the reason for the same is not clear. possibly only tbi patients were referred to the trauma centre. limitations of the study are; the sample population is limited and sample size is small. simple statistics is used. conclusions the three year study from a tertiary centre on tbis highlights that 3rd, 4th and 5th decade of age group is commonly affected with male predominant. one fourth of injured patients are influenced by alcohol. rta is a major cause of tbi accounting for 75%, followed by falls and assault. the incidence of head injuries is almost equal in rural and urban areas. twelve percent of patients are pedestrians. two wheelers were the commonest vehicle involved in road traffic accidents and the most common mechanism of accident was skid and fall from bike and the commonest victims were motorcycle riders. home was the commonest place of incidence of fall from height and ground level falls. on ct findings cerebral contusion was most common, followed by skull fracture, sdh and edh. death was reported among 6.5% of patients. public awareness about tbi consequences and possible preventable measures that can benefit general population is detailed from the demographic and clinical details. correspondence dr. amit agrawal, professor of neurosurgery department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore524003 andhra pradesh (india) emaildramitagrawal@gmail.com mobile+91-8096410032 romanian neurosurgery (2018) xxxii 2: 384 390 | 389             references 1. agrawal a, kakani a, baisakhiya n, galwankar s, dwivedi s, pal r. developing traumatic brain injury data bank: prospective study to understand the pattern of documentation and presentation. the indian journal of neurotrauma 2012;9:87-92. 2. ncrb. traffic accidents [online]. available at: http://ncrb.nic.in/statpublications/adsi/adsi2014/cha pter-1a%20traffic%20accidents.pdf. accessed 2016-1215 15:17:12. 3. akhade sp, rohi kr, dode cr. pattern of fatal vehicular accidents involving head injuries in southern marathwada region of maharashtra. medicolegal update 2014;14:206-210. 4. kumar s, singh rkp. pattern of craniocerebral injuries in fatal vehicular accidents in patna (bihar). journal of indian academy of forensic medicine 2014;36:125-129. 5. puvanachandra p, hyder aa. the burden of traumatic brain injury in asia: a call for research. pak j neurol sci 2009;4:27-32. 6. modi ad. demographic profile of head injury cases in bhavnagar region, gujarat amit d. modi, amit p. parmar 2, vanraj n. parmar 3, dharmesh s. patel 4, rajanibhai v. bhagora 5, jashwant a. darji 6. int j res med 2014;3:154-157. 7. dinesh k. descriptive study of head injury and its associated factors at tertiary hospital, northern india. journal of community medicine & health education 2012. 8. reddy sp, kumar hn. retrospective study of road traffic accident cases at harsha hospital nelamangala, bangalore rural. indian journal of forensic medicine & toxicology 2013;7:193. 9. pruthi n, ashok m, kumar vs, jhavar k, sampath s, devi bi. magnitude of pedestrian head injuries & fatalities in bangalore, south india: a retrospective study from an apex neurotrauma center. the indian journal of medical research 2012;136:1039-1043. 10. mishra pk, singh s. fatal head injury in homicidal deaths in bhopal region of central india. international journal of pharma and bio sciences 2012;3:1103 1108. 11. patil am, vaz wf. pattern of fatal blunt head injury: a two year retrospective/prospective medico legal autopsy study. 2010. 12. gudadinni mr, nuchhi uc, angadi mm. a study of road traffic accident cases admitted in bldeu's shri bm patil medical college hospital and research centre, bijapur. indian journal of forensic medicine & toxicology 2013;7:254-287. 13. punia rk, verma lc, pathak d. pattern of fatal head injuries in road traffic accidents at sms hospital, jaipur-an autopsy based study. medico-legal update 2014;14:30-34. 14. prajapati t, tandon rn. patterns of fatal head injuries cases brought to civil hospital mourtuary, ahmedabad. indian journal of forensic medicine & toxicology 2013;7:209. 15. kakeri sr, bagali ma, goudar es, qadri sy. pattern of injuries and death sustained by the occupants of the two-wheeler during road traffic accidents. 2014. 16. swarnkar m, singh pk, dwivedi s. pattern of trauma in central india: an epidemiological study with special reference to mode of injury. the internet journal of epidemiology 2010;9. 17. plunkett j. fatal pediatric head injuries caused by short-distance falls. the american journal of forensic medicine and pathology 2001;22:1-12. 18. ahmed a, mustahsan sm, tariq f, abidi sma, aslam mo. a cross-sectional study: head injury in children of karachi. 2015. 19. borkar sa, sinha s, agrawal d, satyarthee gd, gupta d, mahapatra ak. severe head injury in the elderly: risk factor assessment and outcome analysis in a series of 100 consecutive patients at a level 1 trauma centre. the indian journal of neurotrauma 2011;8:7782. 20. nath pc, mishra ss, deo rc, jena sp. spectrum of pediatric head injury with management and outcome–a single tertiary care centre study. the indian journal of neurotrauma 2015. 21. parchani a, maull ki, sheikh n, sebastian m. injury prevention implications in an ethnically mixedpopulation: a study of 764 patients with traumaticbrain injury. panamerican journal of trauma, critical care & emergency surgery 2012;1:27-32. 22. saxena mk, saddichha s, pandey v, rahman a. prehospital determinants of outcome in traumatic brain injury: experiences from first comprehensive integrated pre-hospital care providers in india: gvk—emri experience. the indian journal of neurotrauma 2010;7:129-133. 390 | sivakumar et al descriptive study of cranio-cerebral injuries             23. rosen t, mack ka, noonan rk. slipping and tripping: fall injuries in adults associated with rugs and carpets. journal of injury and violence research 2013;5:61. 24. khan mk, hanif sa, husain m, huda mf, sabri i. pattern of non-fatal head injury in adult cases reported at jnmc hospital, am u, aligarh. journal of indian academy of forensic medicine 2011;33:21-23. 25. ahmad z, karmakar rn. an epidemiological study of acute head injury and it's evaluation by ct scan. journal of indian academy of forensic medicine 2014;36:173-175. 26. yadav a, kohli a, aggarwal nk. study of correlation between intracranial hemorrhages and skull fractures. journal of forensic medicine and toxicology 2008;25:42-46. 27. kumar a, lalwani s, agrawal d, rautji r, dogra td. fatal road traffic accidents and their relationship with head injuries: an epidemiological survey of five years. the indian journal of neurotrauma 2008;5:63-67. 28. pathak a, desania nl, verma r. profile of road traffic accidents & head injury in jaipur (rajasthan). 2008. 17satyartheeguru_wasting romanian neurosurgery | volume xxx | number 4 | 2016 | october december article wasting of calf muscle and spastic foot drop caused by falcine meningioma in 22 -year adult male: revisit of uncommon but important localizing sign guru dutta satyarthee1, luis rafael moscote-salazar2, anil kothiwala1, a.k. mahapatra1 1india, 2colombia doi: 10.1515/romneu-2016-0089 552 | satyarthee et al parietal lobe lesion causing calf muscle wasting doi: 10.1515/romneu-2016-0089 wasting of calf muscle and spastic foot drop caused by falcine meningioma in 22 -year adult male: revisit of uncommon but important localizing sign guru dutta satyarthee1, luis rafael moscote-salazar2, anil kothiwala3, a.k. mahapatra4 1associate professor, department of neurosurgery, neurosciences centre, aiims new delhi, india 2neurosurgeon-critical care, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia senior resident 3department of neurosurgery, neurosciences centre, aiims new delhi, india 4professor, department of neurosurgery and director, aiims bhuwneshwar, orrissa, india abstract: wasting of muscle is usually a feature of lower motor neuron pathology, astonishingly parasagittal intracranial lesion affecting parietal lobe of cerebral hemisphere may be associated with wasting of contralateral calf muscle. it can be associated with spastic foot drop. foot drop is a common neurological state presenting with weakness involving anterior tibialis muscle causing inability of foot extension. foot drop is commonly caused lower motor neuron disease pathology and a common cause includes l4-l5 radiculopathy or peroneal peripheral neuropathy. however, extremely rarely can be caused by intracranial pathology e.g. falcine meningioma and represents an important localization sign. authors report an interesting case of calf muscle wasting caused by falcine meningioma, which may escape detection to remind rare but extremely important neurological localizing sign and ask for through and further neurological evaluation prior to concluding a final neurological diagnosis. key words: foot drop, parasagittal meningioma, spasticity, upper motor neuron introduction foot drop is a neurological condition characterized by weakness of anterior tibialis muscle causing inability to carry out foot extension leading to difficulty in walking and climbing stair with repeated injury to foot and ulceration. foot drop, is commonly associated with weakness of extensor digitorum longus and extensor hallusis longus muscles. common causes of are lower motor neuron romanian neurosurgery (2016) xxx 4: 552 – 556 | 553 pathology includes herniation of nucleus pulposus or stenosis of neural foramina causing l4-l5 radiculopathy or peroneal peripheral neuropathy [1], [2], [3]. however, pathology in the central nervous system can very rarely cause foot drop. foot drop has been reported to occur in 52% to 67% of patients with spinal upper motor neuron pathology along the umn tracts: interhemispheric motor cortex homunculus mass lesion, anterior cerebral artery stroke, corona radiata, internal capsule, cerebral peduncle, medulla, and spinal cord pyramidal tract (myelopathy). physician evaluating a case of foot drop generally consider the peripheral nerve lesions. although this is true in most cases, it would be sometime very erroneous as delay in the diagnosis and may have worse or extreme rarely fatal neurological outcome. foot drop may be rarely caused due to intracranial pathology involving parietal lobe. lesion in the parasagittal region near the motor strip for the leg area may produce foot drop. this type has been called spastic foot drop [4] [5]. case illustration a 22-yearmale admitted with complains of headache associated with left foot drop along with wasting of calf muscle for last three months. neurological examination revealed, steppage of gait with left foot drop, wasting of left calf muscle (diameter of left calf-27cm, right-36cm). (figure 1) fundi showed papilloedema and weakness of left tibialis anterior and dorsiflexor of left foot. left ankle jerk was brisk with plantar extensor response. straight leg raising test was negative and rest of neurological examination were within normal limit. there were no sign of occult spinal dysraphism, cutaneous markers including sinus, tufts of hairs or dimple along spine and occipital region. cranial mri showed extra-axial mass lesion with epicenter over falx based measuring 6.1x4.7x3.7cm (figure 2 ) located in the high frontal region (figure 3) in midline compressing adjacent high frontal parenchyma on both sides. (figure 4) it was showing homogenous enhancement on contrast enhanced mri imaging (figure 5). mr veinography revealed a mass lesion, which is causing completely encasement and attenuating superior sagittal sinus in the mid 1/3 suggestive of invasion over a length of 3.2 cm and associated few collateral are seen along anterior part of sinus and draining into superficial middle cerebral vein and further into sphenoparietal sinus. (figure 6) a presumptive diagnosis of meningioma was considered. he underwent bifrontal scalp flap and biparietotemporal craniotomy with simpson grade two excision of bifalcine meningioma with excision of invaded middle 1/3 sagittal sinus. during postoperative period no fresh neurological deficit was observed. he was discharged on fourth post-operative day. histopathology was suggestive of transitional meningioma. at last follow-up after nine months following surgery there was no improvement in foot drop was observed. 554 | satyarthee et al parietal lobe lesion causing calf muscle wasting figure 1 clinical photograph showing foot drop associated with wasting of calf muscle of left lower limb figure 2 mri brain, t2w image, sagittal section, showing falcine meningioma figure 3 mri brain t2wi, axial section showing falcine meningioma causing mass effect figure 4 gadolinium contrast enhanced mri brain axial section, showing heterogeneously enhancing falcine meningioma figure 5 gadolinium contrast enhanced mri brain sagittal section, showing heterogeneously enhancing meningioma figure 6 mr venography of brain showing complete attenuation of middle third of superior saggital sinus. falcine meningioma discussion foot drop is usually considered as lower motor neuron or peripheral nerve lesion by physician [6], [7]. although this situation may stand true in most cases, however upper motor neuron causes also needs consideration [4] [8]. brain localization studies of motor cortex have precisely determined the somatotopic localization of ankle and toe in the parasagittal region [2]. however, there remains a group of foot drop patients with central pathology. these patients have a clinical presentation resembling peripheral causes of foot drop but an upper motor neuron lesion may be differentiated if the babinski sign or hyperactive ankle jerk is present [7]. the classical presentation of lumbar disk herniation is with clinical findings such as leg pain, sensory deficits, atrophy, impaired motor function, positive straight leg raising test, and hyporeflexia. motor evoked potential and tibial somatosensory evoked potential recordings are abnormal with cranial lesions while electromyography (emg) and neuropsychological tests give normal results [6].these electrophysiological study can be utilized to differentiate central lesions from peripheral causes of foot drop. in our case, the spastic foot drop was caused by parasagittal meningioma. this case reminds us about importance of the foot drop caused by intracranial cerebral lesions; the clinicians may lack such experience. accordingly, to the best of our opinion, lack of publication of such cases in the literature is another factor leading to romanian neurosurgery (2016) xxx 4: 552 – 556 | 555 inappropriate clinical decisions. this case emphasizes foot drop may also occur with brain lesions, especially located in the parasagittal region, near the motor strip area representing for the leg area in the human homnoculus [5], [9], [10]. a cerebral lesion should be suspected in patients, who have either a babinski sign or brisk deep tendon reflexes. headache is another important clue of a central cause, if also associated with projectile vomiting occurring in the early morning and being relieved by vomiting correctly suggestive of raised intracranial pressure [1], [4], [11], [12]. in conclusion, clinicians should always also keep in mind about possibility of existence of central cause while evaluating the case of foot drop. failure to consider this possibility may result in unnecessary investigations, cost and precious time loss and delay in diagnosis and initiating early treatment with consequent worsening of the neurological morbidity [6], [7], [13]. summary the muscle wasting is usual presentation of lower motor neuron pathology, but occasionally intracranial lesion situated in the parasagittal region in the parietal lobe may also cause wasting of contralateral calf muscle and spastic foot drop. these findings can be especially helpful in the establishment of proper diagnosis and avoiding unnecessary investigation and sparing valuable time and early initiation of therapeutic intervention. the evaluating clinicians should always also keep in mind about possibility of existence of central cause while evaluating the each and every case of foot drop to avoid last minute surprise. correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: duttaguru2002@yahoo.com references 1. baysefer a, erdogan e, sali a, sirin s, seber n. foot drop following brain tumours: case report. minim invas neorusurg 1998; 41:97-98. 2. eberhard ef. motor function of cerebral cortex: in: patton hd, ed. textbook of physiology. 1989; vol 1 : pp 608-631 3. eskandary h, hamzei a, yasamy mt. foot drop following brain lesion. surg neurol 1995;43: 89-90. 4. guthrie bl, ebersold mj, scheithauer bw. neoplasms of the intracranial meninges. in: youmans jr, (ed.) neurological surgery. philadelphia: w.b. saunders, 1990, pp 3250-3315 5. ozdemir n, citak g, acar ud. spastic foot drop caused by a brain tumour: a case report. br j neurosurg 2004; 18: 314-315. 6. pozzessere g, valle e, tomaselli m, d'alessio m, bianco f, pierelli f, morocutti c. crural amyotrophy associated with a parietal lesion: a case report. acta neurol (belg.) 1995; 95:96-100. 7. talbert or. general methods of clinical examination. in:youmans er, ed. neurological surgery. 3rd ed. vol 1. philadephia: w.b. saunders 1990, pp 3-36. 8. van lange hove m, pollefliet a, vanderstraeten g. a retrospective electro diagnostic evaluation of foot drops in 303 patients. electromyography clin neurophysiology 1989; 29: 145-152. 9. agrawal d, saini r, singh pk, sinha s, gupta dk, satyarthee gd, misra mc. bedside computed tomography in traumatic brain injury: experience of 556 | satyarthee et al parietal lobe lesion causing calf muscle wasting 10,000 consecutive cases in neurosurgery at a level 1 trauma center in india. neurol india 2016;64:62-5 10. satyarthee gd, mahapatra ak. giant pediatric glioblastoma multiforme causing primary calvarial erosion and sutural diastasis presenting with enlarge head in 13-year old boy: rare entity. j ped neurosciences 2015;10:290-293 11. satyarthee gd, suri a, mahapatra ak giant sphenoethmoidal osteoma in a 14-year boy presenting with visual impairment and facial deformity: short review j pediatr neurosci 2015;10(1):48-50 12. dawar p, satyarthee gd, sharma bs. total resolution of large scalp welling due to calvarial tuberculosis with medical management only: case report and review of literature. turkish neurosurg, 2015; 25(2):313-6. 13. raheja a, satyarthee gd, mahapatra ak chronic subdural hematoma development in accelerated phase of chronic myeloid leukemia presenting wit seizure and rapid progression course with fatal outcome. roman neurosurgery. 2015; 29(2):199-202; romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article efficacy of carotid thrombus penetration with a balloon guiding catheter to fast recanalization of acute extraand intra-cranial carotid artery tandem occlusion a preliminary report ahmed ansari, tomotaka ohshima, shunsaku goto, taiki yamamoto, kojiro ishikawa, yoko kato india, japan doi: 10.2478/romneu-2018-0008 romanian neurosurgery (2018) xxxii 1: 65 – 72 | 65 doi: 10.2478/romneu-2018-0008 efficacy of carotid thrombus penetration with a balloon guiding catheter to fast recanalization of acute extraand intra-cranial carotid artery tandem occlusion a preliminary report ahmed ansari1, tomotaka ohshima2, shunsaku goto2, taiki yamamoto2, kojiro ishikawa2, yoko kato3 1assistant professor neurosurgery, upums, saifai, up, india 2kariya toyota general hospital, nagoya, japan 3professor and head, department of neurosurgery, fujita health university bantanne hotokukai hospital, nagoya, japan abstract: acute ischemic stroke with ipsilateral internal carotid artery (ica) stenosis presents a great management dilemma. we present our preliminary report of retrograde retrieval of clot from middle cerebral artery (mca) followed by delayed carotid artery stenting (cas) with dual anti platelet therapy (dapt). key words: carotid artery stenosis, ischemic stroke, carotid artery stenosis introduction ten-to-twenty percent of patients with acute ischemic stroke have a high-grade ipsilateral extracranial ica stenosis, which usually causes major stroke if an additional intracranial large artery occlusion of the anterior circulation is present. (1,2) iv thrombolysis alone has a very limited rate of successful recanalization in such patients.(3) an option in such cases is endovascular therapy with stent implantation at the level of ica stenosis along with mechanical thrombectomy. a major concern in these patients is the risk of post interventional symptomatic intracranial hemorrhage (sich), which may be influenced by the mandatory antiplatelet medication of the stent-placement procedure, which has been reported to vary from 0% to 20%. (4-6) the limited time duration for intervention in these patients along with delayed arrival of these cases to the neruointerventionists makes the task all the more difficult. we describe our experience of retrograde retrieval of clot from middle cerebral artery (mca) followed by delayed carotid artery stenting (cas) with dual anti platelet therapy (dapt). 66 | ansari et al efficacy of carotid thrombus penetration with a balloon guiding catheter materials and methods we included four cases in the present study. patients presenting with sudden onset hemiparesis within four hours were included. these patients had an embolic intracranial vessel occlusion of the anterior circulation and at the same time presented with atherosclerosis-related high-grade cervical ica stenosis or ica occlusion. patients with arterial dissections were excluded from this analysis. on admission, ct/cta or mr imaging/mra, including diffusion and perfusion imaging, was performed to evaluate the extension of the ischemic lesion and the potential tissue at risk (penumbra). patients were selected for endovascular stroke treatment if they had cta-proved vessel occlusion of the distal ica or m1/2 segment and absence of early signs of an extensive and advanced infarction (more than one-third of the mca territory) on ctor mra-proved vessel occlusion of the distal ica or m1/2 segment, a dwi lesion less than one-third of the mca territory. interventional procedure all procedures were performed with the patient under local anesthesia. as vascular access, a 9f sheath was placed in the right common femoral artery. then, a 9f guiding catheter was placed in the ipsilateral common carotid artery, and the cervical ica stenosis was passed with a 0.035-inch microwire and 5f jb2 coaxially. the balloon guide microcatheter was advanced through the thrombus in the mca, and the tip was placed distal to the thrombus. for thrombectomy, the stenting device and microcatheter were simultaneously pulled back under continuous aspiration through the catheter. in case of incomplete recanalization, thrombectomy was repeated. this process clears the thrombus and paves way for the blood to flow with the stipulated time (figure 1). the patient is then placed on heparin for three days and dual anti platelet therapy (dapt) and two weeks later, cas is performed using a 9f sheath in the right common femoral artery, followed by 9f guiding catheter in the common carotid artery till ica stenosis is passed. a self-expanding stent was advanced to cover the stenosis. after stent implantation, balloon dilatation was performed. if necessary, the stenosis was predilated with a percutaneous transarterial angioplasty balloon to allow fast access to the intracranial vasculature (figure 2). angiographic images were analyzed regarding the following data: time to flow restoration (time interval between the first diagnostic angiographic image and the first image with evidence of re-established perfusion within the occluded mca vessel segment), and time to complete revascularization (time interval between the first diagnostic image and the completion angiogram). the breakage of primary thrombus and its emboli in the mca leading to hemiparesis is dealt with in the emergency setting. later, after heparin for three days and dapt is given for 2 weeks, cas is performed (figure 3). we avoided emergency simultaneous cas due to high risk of in-stent thrombosis, as no anti platelets were used. romanian neurosurgery (2018) xxxii 1: 65 – 72 | 67 figure 1 figure 2 figure 3 illustrated case 1 a 62 years nondiabetic male presented with sudden onset left hemiparesis within three hours of onset. he had no previous history of medications. mri dwi images suggested hyperintense signals in right mca distribution (figure 4). a 9f balloon guide catheter was inserted in ica and its stenosis seen along with thrombus in right mca. emergent clot retrieval from right mca was performed, and blood flow restored (figure 5,6). unstable plaque was noted in right ica in the neck on mr imaging (figure 7). heparin was given for three days and dapt for two weeks, following which cas was performed (figure 8). 68 | ansari et al efficacy of carotid thrombus penetration with a balloon guiding catheter figure 4 figure 5 figure 6 figure 7 figure 8 illustrated case 2 a 73 years male presented with sudden onset right hemiplegia two hours after onset. mr imaging showed small left capsular infarct (figure 9). immediate dsa was performed which showed left ica stenosis and thrombus in left mca (figures 10, 11). emergent retrieval of the blood clot was done from the mca and blood flow restored (figure 12). mri neck showed unstable plaque in left ica (figure 13). heparin was given for three days and dapt for two weeks. cas was done after two weeks (figure 14) in order to prevent in stent thrombosis. romanian neurosurgery (2018) xxxii 1: 65 – 72 | 69 figure 9 figure 10 figure 11 figure 12 figure 13 figure 14 70 | ansari et al efficacy of carotid thrombus penetration with a balloon guiding catheter discussion in acute ischemic stroke, fast recanalization of the occluded vessel is probably the most important precondition for favorable clinical outcome.(7,8) however,< 20% of patients (9) with intracranial vessel occlusion have additional high-grade cervical ica stenosis or even total occlusion. interventional procedures are a promising treatment option using combination of ica stent placement and intraarterial thrombolysis which seems to improve the outcome.(10) the primary cause of symptoms and clinical outcome are mainly because of thrombus in the mca rather than occlusion of the cervical ica.(11) the lenticulostriate arteries (lsas) are functional end-arteries without collateral. thrombus in the proximal segment of the mca may lead to occlusion of the orifices of these arteries and cause cerebral infarction.(12) the final status of lsas and time for restoration of blood flow determines the outcome. in the absence of sufficient leptomeningeal collaterals, expansion of the infarct core into surrounding hypoperfused tissue occurs earlier. several published studies of intra-arterial thrombolytic therapy indicate that treatment initiated within 3 to 4 hours of symptom onset is associated with higher rates of recanalization and better outcome.(13,14) moreover, successful recanalization of ica and mca vessels may not reflect clinical outcome because of evolving cerebral infarction. prompt reperfusion of initially still viable tissue and prevention of subsequent expansion of cerebral infarction are the critical factors to achieve a favorable neurologic outcome. usually micro guidewires and catheters can easily traverse the freshly occluded vessels, blind probing may result in vessel perforation or dissection or entering into the false lumen. moreover, possibility of dislodgement of thrombus into the distal segment is always present. emergent angioplasty of ica carries an increased risk of hyperperfusion syndrome, although there are chances of higher recanalization rate but at the risk of expanding brain infarction. the final status of lsas and time for restoration of blood flow determines the outcome. previously, antegrade approach was performed in which firstly, cas or carotid pta was done followed by mca clot retrieval. this may lead to valuable loss of time and ultimately, irreversible neurological deficit. we followed retrograde approach and mca clot retrieval was done emergently. this was followed by dapt for two weeks and heparin for three days. a 2mm lumen of ica is kept for two weeks. two weeks later, cas was performed. an additional benefit apart from saving immediate valuable time in blood restoration was prevention of in stent thrombosis, as usage of dapt for two weeks reduced it significantly. matsubara et al (15) published a report on 16 patients with acute cervical carotid occlusions caused by atherosclerosis, atrial fibrillation, or dissection. ten of their patients had additional intracranial tandem occlusions. the patients were treated with various recanalization techniques. no stent retrievers were used. recanalization was successful in a high number of patients with cervical romanian neurosurgery (2018) xxxii 1: 65 – 72 | 71 occlusion (81.3%). in 43.8% of their patients, successful extracranial and intracranial flow was reached. although one-third of their whole patient cohort presented with a favorable clinical outcome, only 20% of their patients with cervical and intracranial occlusion reached an mrs score of 0–2. malik et al (16) reported their experience with recanalization procedures of 77 patients with tandem occlusion. they used various recanalization devices and techniques and achieved a high recanalization rate (75.3%). not surprising, ica stent implantation leads to a prolonged procedure time until recanalization. in one of our patients, the time taken for retrieval of clot from mca was just under 11 minutes. in carotid artery stent placement, antithrombotic medication is administered to prevent acute stent thrombosis. however, it bears a potential risk of intracranial hemorrhage. the antithrombotic treatment concept differs in the literature. in the study of matsubara et al, (15) patients received a loading dose of aspirin and another antiplatelet drug, depending on the clinical conditions, if the postprocedural imaging showed no hemorrhage. the hemorrhage rate (6.3%) was low. the hemorrhage rate (10.4%) reported by malik et al(16) was slightly higher. in their study, glycoprotein iib/iiia inhibitor was administered before stent placement, and an oral load of clopidogrel and aspirin was initiated if postprocedure imaging showed no hemorrhage. we have further reduced the risk of thrombosis by using dapt two weeks prior to cas. none of our patients suffered post procedure hemorrhage and all had an improved outcome. the data published by heck and brown(17) and stampfl et al(18)was 21% and 17% respectively for spontaneous ich. the high rate of sich in the heck and brown cohort might be associated with the use of abciximab and a high mean age of their patients. several limitations have to be considered when interpreting the current data, most important a small study design, and the missing control groups which might have biased. the usage of the retrograde technique was at the sole discretion of the endovascular neurosurgeon. conclusion emergent clot retrieval from the mca followed by two weeks of dapt and then finally cas appears an effective way to reduce the valuable time in these ischemic patients along with faster restoration of blood flow. the authors clearly understand that more patients are needed to validate the results. correspondence ahmed ansari, assitant professor neurosurgery, upums, saifai, up, india references 1. grau aj, weimar c, buggle f, et al. risk factors, outcome, and treatment in subtypes of ischemic stroke: the german stroke data bank. stroke 2001;32:2559–66 2. rubiera m, ribo m, delgado-mederos r, et al. tandem internal carotid artery/middle cerebral artery occlusion: an independent predictor of poor outcome after systemic thrombolysis. stroke 2006;37:2301–05 3. kim ys, garami z, mikulik r, et al; clotbust collaborators. early recanalization rates and clinical outcomes in patients with tandem internal carotid 72 | ansari et al efficacy of carotid thrombus penetration with a balloon guiding catheter artery/middle cerebral artery occlusion and isolated middle cerebral artery occlusion. stroke 2005;36:869–71 4. lockau h, liebig t, henning t, et al. mechanical thrombectomy in tandem occlusion: procedural considerations and clinical results. neuroradiology 2015;57:589–98 5. heck dv, brown md. carotid stenting and intracranial thrombectomy for treatment of acute stroke due to tandem occlusions with aggressive antiplatelet therapy may be associated with a high incidence of intracranial hemorrhage. j neurointerv surg 2015;7:170– 75 6. maurer cj, joachimski f, berlis a. two in one: endovascular treatment of acute tandem occlusions in the anterior circulation. clin neuroradiol 2014 jul 3. 7. khatri p, abruzzo t, yeatts sd, et al. good clinical outcome after ischemic stroke with successful revascularization is time-dependent. neurology 2009;73:1066–72 8. rha jh, saver jl. the impact of recanalization on ischemic stroke outcome: a meta-analysis. stroke 2007;38:967–73 9. grau aj, weimar c, buggle f, et al. risk factors, outcome, and treatment in subtypes of ischemic stroke: the german stroke data bank. stroke 2001;32:2559–66 10. kwak hs, hwang sb, jin gy, et al. predictors of functional outcome after emergency carotid artery stenting and intra-arterial thrombolysis for treatment of acute stroke associated with obstruction of the proximal internal carotid artery and tandem downstream occlusion. ajnr am j neuroradiol 2013;34:841–46 11. adams hp, bendixen bh, leira e, et al. antithrombotic treatment of ischemic strokeamongpatients with occlusion or severe stenosis of the internal carotid artery: a report of the trial of org 10172 in acute stroke treatment (toast). neurology 1999;53:122–25 12. donnan g, norrving b, bamford j, et al. striocapsular infarcts. oxford, uk: oxford university press; 2002:195– 208 13. suarez ji, sunshine jl, tarr r, et al. predictors of clinical improvement, angiographic recanalization, and intracranial hemorrhage after intra-arterial thrombolysis for acute ischemic stroke. stroke 1999; 30: 2094–100 14. zaidat oo, suarez ji, santillan c, et al. response to intra-arterial and combined intravenous and intraarterial thrombolytic therapy in patients with distal internal carotid artery occlusion. stroke 2002 ;33 :1821– 27 15. matsubara n, miyachi s, tsukamoto n, et al. endovascular intervention for acute cervical carotid artery occlusion. acta neurochir (wien) 2013;155:1115– 23 16. malik am, vora na, lin r, et al. endovascular treatment of tandem extracranial/intracranial anterior circulation occlusions: preliminary single-center experience. stroke 2011;42:1653–57 17. heck dv, brown md. carotid stenting and intracranial thrombectomy for treatment of acute stroke due to tandem occlusions with aggressive antiplatelet therapy may be associated with a high incidence of intracranial hemorrhage. j neurointerv surg 2015;7:170–75 18. stampfl s, ringleb pa, mo¨hlenbruch m, et al. emergency cervical internal carotid artery stenting in combination with intracranial thrombectomy in acute stroke. ajnr am j neuroradiol 2014;35: 741–46 08 08ansariahmed_efficacy flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article quadrigeminal cistern lipoma amit agrawal india doi: 10.1515/romneu-2017-0037 226 | agrawal quadrigeminal cistern lipoma doi: 10.1515/romneu-2017-0037 quadrigeminal cistern lipoma amit agrawal department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh, india introduction intracranial lipomas are rare slow growing benign lesions, commonly involve the corpus callosum, quadrigeminal/superior cerebellar cistern, suprasellar/interpeduncular cistern, cerebellopontine angle cistern and sylvian cistern and account for 0.1-0.5% of all primary brain tumors. (1-5) a 30 year female presented with headache of one and half year duration. there was no history of fever, vomiting, loss of consciousness or focal deficits. she was not a known diabetic or hypertensive. here general and systemic examination was normal. higher mental functions and cranial nerves were normal. fundus examination was normal. there were no motor or sensory deficits. in view of persistent headache a ct scan of the brain was performed 6 months back. it showed a hypodense non-enhancing lesion in the region of right quadrigeminal cistern without any mass effect (figure 1). to further confirm the diagnosis and growth of the lesion an mri of the brain was performed. it showed a welldefined lesion in the region of right quadrigeminal cistern brightly hyperintnse lesion of t1w images, mildly hyperintense on t2w images, hyperintense on flair images and hypointense on fat suppression sequences (figures 1 and 2). there was no evidence of mass effect on surrounding structures. all these findings were suggestive of quadrigeminal cistern lipoma. the patient responded well to counseling and mild analgesics. figure 1 (a) ct scan of the brain showing a hypodense non-enhancing lesion in the region of right quadrigeminal cistern without any mass effect, (b) mri brain showing a well-defined lesion in the region of right quadrigeminal cistern brightly hyperintnse lesion of t1w images and (c) mildly hyperintense on t2w images figure 2 (a) on mri sagittal t2w image the lesion is mildly hyperintense, (b) hyperintense on flair coronal image and (c) hypointense on fat suppression sequences romanian neurosurgery (2017) xxxi 2: 226 228 | 227 lipoma in the quadrigeminal region has been addressed with many names including lipoma in the quadrigeminal cistern, the quadrigeminal plate, the ambient cistern, the superior vermis, or the superior medullary velum. (6, 7) these lesions are rare and have been described in children and young adults. 8 most of the time quadrigeminal cistern lipoma are asymptomatic (3, 4, 6, 9) but it has been reported that in about 20% of patients, lipomas of the quadrigeminal plate/ambient cistern produce symptoms. (2) because of the mass effect, some patients may present with pressure symptoms (obstructive hydrocephalus or raised intracranial pressure) and neurological deficits. (1, 10) as was seen in present case, it can be an incidental finding in patients who have been investigated for headache (although may not be responsible for the headache). (3) characteristic and definitive radiological findings have been described for quadrigeminal cistern lipoma hence histological confirmation is almost never required. (3, 5, 6, 10) as in present case, on ct scan the quadrigeminal cistern lipoma is characterized by non-enhancing hypodense lesions with attenuation values of fat density (50 to -100 hounsfield units). (5, 11, 12) mri will provide greater details and on mri these lesions has short t1 and t2 and are hyperintense t1-weighted images and a relatively low to moderately hperintense on t2-weighted images. (5, 10) the lesion was moderately hyperintense of flair images and hypointense on fat suppression sequence in the present case confirming the diagnosis of a lipoma. although imaging findings can help to narrow the diagnosis but from a theoretical point of view, there are many pathologies which can present in quadrigeminal cistern region on imaging. (6) these lesions needs to be differentiated with other lesions of quadrigeminal cistern region including arachnoid cysts, tectal plate cyst, tectal gliomas, abscess, dermoid and epidermoid cysts, and rarely pineal region tumors. (3, 10) as in present case, asymptomatic lesions which are identified on neuroimaging may not need any surgical intervention except reassurance and management of the headache. (4-6, 13) however, if there are features of mass effect than the patient may need decompression of the lesion and or csf diversion procedure i.e. ventriculo-peritoneal shunt. (3, 6, 10) correspondence dr amit agrawal professor of neurosurgery department of neurosurgery narayna medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 references 1.yilmazlar s, kocaeli h, aksoy k. quadrigeminal cistern lipoma. journal of clinical neuroscience : official journal of the neurosurgical society of australasia 2005;12:596599. 2.ono j, ikeda t, imai k, et al. intracranial lipoma of the quadrigeminal region associated with complex partial seizures. pediatric radiology 1998;28:729-731. 3.ogbole g, kazaure i, anas i. quadrigeminal plate cistern lipoma. bmj case reports 2009;2009. 228 | agrawal quadrigeminal cistern lipoma 4.khoshnevisan a, mirkoohi m, arjipour m. tectal lipoma: a case report and review of literature. tehran university medical journal 2012;70. 5.panil kumar b, hegde k, agrawal a. lipoma of the quadrigeminal plate. journal of cranio-maxillary diseases 2012;1:51. 6.senoglu m, altun i. lipoma of the quadrigeminal plate cistern. the internet journal of radiology [internet] 2009. 7.yildiz h, hakyemez b, koroglu m, yesildag a, baykal b. intracranial lipomas: importance of localization. neuroradiology 2006;48:1-7. 8.hayashi t, shojima k, yamamoto m, hashimoto t, fukuzumi a, honda e. [intracranial lipomas--report of six cases]. no to shinkei = brain and nerve 1983;35:257268. 9.ambrosetto p, martinelli p, bacci a, daidone r. lipoma of the quadrigeminal plate cistern. ital j neuro sci 1985;6:347-349. 10.nikaido y, imanishi m, monobe t. lipoma in the quadrigeminal cistern--case report. neurologia medicochirurgica 1995;35:175-178. 11.kazner e, stochdorph o, wende s, grumme t. intracranial lipoma. diagnostic and therapeutic considerations. journal of neurosurgery 1980;52:234-245. 12.zimmerman ra, bilaniuk lt, dolinskas c. cranial computed tomography of epidermoid and congenital fatty tumors of maldevelopmental origin. the journal of computed tomography 1979;3:40-50. 13.sala f, talacchi a, scarpa p, bricolo a. surgical treatment of quadrigeminal plate lipoma presenting with seizures and behavioural disorders. journal of neurology, neurosurgery, and psychiatry 1998;64:818-819. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article extradural spinal schwannoma in a 5 year old non nf child: a rare entity maneet gill, vikas maheshwari, amit narang india doi: 10.1515/romneu-2017-0036 222 | gill et al extradural spinal schwannoma in a 5 year old non nf child doi: 10.1515/romneu-2017-0036 extradural spinal schwannoma in a 5 year old non nf child: a rare entity maneet gill, vikas maheshwari, amit narang department of neurosurgery, armed forces medical college, pune, india abstract: pediatric spinal schwannomas constitute 2.5-4% of all pediatric spinal tumors. they often occur in the setting of neurofibromatosis type 2 (nf-2) and are almost always intradural (with/without dumbbell extension). rarely are they confined to extradural space alone. till date only one case of totally extradural lumbosacral schwannoma in a non nf child has been reported. we here report the second case of totally extradural spinal schwannoma in a non nf child. a five year old female child presented with progressively increasing paraperesis and bladder symptoms, with no clinical features of neurofibromatosis type i or ii. imaging revealed a dorsolumbar extradural lesion from dv11 to lv1. patient underwent laminoplasty with total excision of tumour. intraoperatively, the tumor was confined to extradural space alone. histopathology confirmed schwannoma. this case highlights that possibility of schwannomas should be considered as a differential diagnosis for intraspinal extradural tumors even in children without nf. key words: extradural schwannoma, neurofibromatosis – 2, pediatric spinal schwannoma introduction spinal tumors constitute 1-10% of all pediatric central nervous system tumors. (7, 9) schwannomas comprise about 30% of primary intraspinal neoplasms. (5) pediatric spinal schwannomas/neurofibromas constitute 2.54% of all pediatric spinal tumors (6), and only 0.7% of all schwannomas occur in children. pediatric spinal schwannomas often occur in the setting of neurofibromatosis type 2(nf-2). (8) they usually present as intradural mass lesions (with/without dumb-bell shaped extensions) and are rarely confined to the extradural space alone. (3) till date only one case of giant totally extradural lumbosacral schwannoma in a non nf child has been reported. (4) we are reporting a rare case of 5 year old non nf female child of totally extradural schwanomma. this is probably the second such reported case. case history a five year old female child presented to us with subacute onset and progressively increasing weakness in bilateral lower limbs and frequent falls of 3 months duration. she romanian neurosurgery (2017) xxxi 2: 222 – 225 | 223 had developed dribbling of urine for the last 7days. on examination she had spastic paraparesis (mrc grade 4/5) with 50% loss of all modalities of sensation in left l5, s1, s2 dermatomes.deep tendon jerks were brisk in bilateral lower limbs and plantars were extensor bilaterally. there were no clinical features suggestive of neurofibromatosis type i or ii. x-ray dorsolumbar spine showed widened dv12lv1 inter vertebral foramina and scalloping of dv12 vertebral body (figure 1). contrast mri showed an extradural lesion extending from dv11 to lv1; it was isointense to hypointense on t1 weighted images and heterogenously enhancing on post contrast imaging (figures 2a & 2b). the lesion was seen to expand the spinal canal with extension of the tumor through the left dv12-lv1 neural foramen with associated widening of foramen and left paravertebral extension. the spinal cord was severely compressed by the tumor and displaced anteriorly towards right. patient underwent laminoplasty dv10 – lv1 with total excision of tumor. intra operatively the lesion wass totally extradural, soft, moderately vascular, yellowish pink in colour and extending from d11-l1 with left paravertebral extension through dv12-lv1 foramen. the dura was opened and it was confirmed that there was no intradural component (figure 3). histopathological examination showed monomorphic spindle cells arranged in parallel arrays in a variably collagenous stroma with verrocay bodies. final opinion was compatible with schwannoma. post operatively patient improved neurologically with power of mrc 5/5. post op mri showed complete resection of tumor (figure 4). urinary symptoms also improved. patient is on regular follow up for past 3 months and has no neurological symptoms suggestive of recurrence. figure 1 x ray dorsolumbar spine showing widened intervertebral foramen (white arrows) and scalloped vertebral body (black arrow) figure 2 pre op contrast mri. sagittal (a) and axial (b) images showing the extradural tumor with transforaminal extension 224 | gill et al extradural spinal schwannoma in a 5 year old non nf child figure 3 introperative image showing totally extradural tumor (a) and compressed spinal cord (b) figure 4 post op contrast mri showing no residual lesion (asagittal, b axial) discussion schwannomas are more commonly found in the intradural, extramedullary space. extra dural schwannomas have been reported in adults. (1) in pediatric age group, schwanomas are very rare and when they occur they are intradural and generally in the setting of nf-2. common extradural spinal tumors in paediatric population are sarcoma, neuroblastoma, teratoma, ganglioneuroma and lymphoma. (3) there is no significant prevalence difference between males and females. however, some studies indicate a higher incidence of spinal schwannomas in males. (2) extradural schwannomas in pediatric age group have rarely been reported and they are generally see in nf children. to our knowledge, till date only one case of giant extradural lumbosacral schwannoma in a non nf child has been reported by kataria et al. (4) their patient was an eight year male who presented with backache. clinically there was no neurological deficit. radiological evaluation revealed a large extradural mass from l4 to s2 level with paravertebral extension. the patient underwent l3 to s2 laminectomy with complete excision of the spinal part of the lesion and partial excision of the paravertebral part, with good clinical result. our patient is a five year old female child, tumor was extradural only and was not associated with neurofibromatosis. we believe this is the second such reported case. postoperative results are consistent with literature, which suggests that nerve sheath tumors of the spine are often single, benign lesions that are straightforward to remove and are associated with a good postoperative outcome. patients with intra spinal extradural schwannoma require early intervention in order to prevent irreversible neurological deficits especially when they start exhibiting neurological signs and symptoms. (3, 6, 8) romanian neurosurgery (2017) xxxi 2: 222 – 225 | 225 conclusion schwanomas are rare in pediatric age group and when they are there they occur in nf children. even in the nf children they are rarely, totally confined to extradural space. ours is probably the second such reported case. though histologically benign they can produce profound neurological deficits. microsurgical excision for spinal schwannomas usually results in good postoperative functional outcomes. this case highlights that possibility of schwannomas should be considered as a differential diagnosis for extradural intraspinal tumors even in children without nf. correspondence dr. maneet gill (e mailmaneet5@yahoo.com) department of neurosurgery, armed forces medical college pune – india – 411040 phone: +917028050776 references 1.conti p, pansini g, mouchaty h, capuano c, conti r. spinal neurinomas: retrospective analysis and longterm outcome of 179 consecutively operated cases and review of the literature. surg neurol 61: 34-43, 2004 2. dorsi mj, belzberg aj. paraspinal nerve sheath tumors. neurosurg clin n am15:217–222, 2004 3.jeng tc, abdullah jm, george j, tharakan kj j, casilda s, ghazali mm, jaafar h, salmah wm. extradural spinal schwanoma in 12year old child :a case report. malays j med sci 12:60-63, 2005 4.kataria r, kurmi dj, mehta j, sinha vd. giant lumbosacral schwannoma in a child. j pediatr neurosci 7(2):126-128, 2012 5.kim nr, suh yl, shin hj: thoracic pediatric intramedullary schwannoma: report of a case. pediatr neurosurg 45:396–401, 2009 6.kulkarni a, srinivas d, somanna s, indira db, ananthakrishna cb.pediatric spinal schwannoma an institutional study. j pediatr neurosci 7(1):1-3, 2012 7.loh jk, lin ck, hwang yf, hwang sl, kwan al, howng sl. primary spinal tumors in children. j clin neurosci. 12:246–248, 2005 8.vadivelu s, prasad p, adesina am, kim e, luerssen tg, jea a. giant invasive spinal schwannoma in children: a case report and review of the literature. j med case rep 30;7:289, 2013 9. wilson pe, oleszek jl, clayton gh. pediatric spinal cord tumors and masses. j spinal cord med. 30(suppl 1):15–20, 2007 romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article management and outcome of moderate head trauma: our experience mohammed t. alshaimaa, mohammed a. sultan, wael k. zakaria, mohammed e. elshehawi egypt doi: 10.2478/romneu-2018-0016 romanian neurosurgery (2018) xxxii 1: 129 148 | 129 doi: 10.2478/romneu-2018-0016 management and outcome of moderate head trauma: our experience mohammed t. alshaimaa, mohammed a. sultan, wael k. zakaria, mohammed e. elshehawi department of neurosurgery, mansoura university hospital, mansoura, egypt abstract: objective: the aim of this study is to follow up patients with moderate head trauma who were admitted to mansoura university hospital in the period from 1 dec. 2015 to 30 jul. 2016 until discharge and determine the outcome of head trauma. material and methods: this prospective study were conducted on all patients with moderate head trauma admitted to mansoura emergency hospital during the period from 1 dec. 2015 to 30 jul. 2016 with exclude polytrauma, bleeding disorders, severe liver and kidney disease patients. results: in this study, we correlated different risk factors with management and with outcome. management may be surgical or conservative and outcome may be alive or dead. we have 60 patients with 17 cases (28.3%) were treated surgically and 43 cases (71.6%) were treated conservatively. according to outcome 36 cases (60%) were alive and 24 cases (40%) died, all cases managed in icu. according to sex, 10 cases (17%) were female and 50 cases were male (83%) with statistically nonsignificant effect on outcome (p = 0.7) and management (p =0.7). road traffic accidents is most common cause of injury with 33 cases (55%), and cause of injury had statistically significant effect on management (p = 0.02) and statistically non-significant effect on outcome (p = 0.4). gcs on admission had no statistically significant effect on management (p=0.8) and outcome (p=0.1) with mean of 10.1±1.2 and gcs on discharge had no statistically significant effect on management (p=0.6). conclusion: there were significant effect of age of patients, systemic diseases (such as dm, htn, chronic kidney diseases, and chronic liver diseases), type of lesions (especially sdh, sah), and serum electrolytes (especially serum sodium) on outcome which determined by gcs at discharge, length of hospital stay, and the state of the patient at discharge. key words: road traffic accident, glasgow coma scale introduction in all of the world, traumatic brain injury (tbi) considered as a critical public health and socio-economic problem. it is considered a major cause of death, in young adults, and result in lifelong disability in those who recovered³²’³³. tbi looks like a silent epidemic, 130 | alshaimaa et al moderate head trauma because unawareness of the society about the magnitude of this problem²⁸’⁴⁰. in egypt, tbi is a serious public health problem ³⁹. treating patients with tbi in usa cost about more than 9$ billion per year ⁴⁹. tbi has two peaks of high incidence: first among young adult male between 15 to 24 years old, and other among elderly people of both sex older than 75 years ³⁹’⁴⁰⁴¹. incidence in male is about 12–16% which double females incidence (8%). male have high incidence to be hospitalized and are nearly 3 times more to die from this injury ³’¹⁰. most people who survived a head injury presented with a normal or mild deterioration of conscious level (glasgow coma scale more than 12) with the majority of fatal outcomes happened in the moderate or severe head injury groups, which represent only 5% of cases. we defined head injury as any trauma to the head other than any superficial injuries to the face ³⁹’⁴⁰. it can be classified by mechanism of injury to closed injury or penetrating injury, by morphology to fractures, focal intracranial injury, and diffuse injury, or by severity of injury to mild, moderate, and severe. primary brain injury define as immediate brain damage happened upon time of impact. this includes different verities as cerebral contusions, diffuse axonal injuries, and acute subdural or epidural hematomas, subarachnoid hemorrhage and intracerebral hemorrhage. secondary brain injury include other pathology as progressive cerebral oedema, ischemia, and increase size of cerebral contusions and the surrounding focal oedema, which lead to increase in intracranial pressure and can lead to cerebral herniation and death¹⁹’⁴⁰’⁴¹. disabilities of tbi patients change according gcs: we have 47% moderate to severe disabilities at 12 months and a third do not return to work for patients with mild injuries (gcs 13–15),. for patients with moderate brain injuries (gcs 9–12), moderate to severe disabilities are 45% , and while 48% of severely injured patients have moderate to severe disabilities, only 14% have a good outcome at one year after trauma ⁴⁹’⁵⁵. pathophysiology of tbi: we divided traumatic brain injury into the primary neuronal injury which followed by secondary injury. the primary injury define as the initial injury of neuron that occurs immediately at time of impact. ⁴’²². while secondary injury occurred minutes, hours or days after injury impact and lead to worsen the primary lesions ⁵⁷’⁵⁹. secondary injury considered as cellular and molecular processes which started by the primary injury and aggravated by the cerebral damage as result of hypotensive or hypoxic events, hypoglycemia, and elevated intracranial pressure cause cerebral ischemia. andrriesson³’⁴. glutamate excitotoxicity, neuronal depolarization, disturbance of ionic homeostasis, nitric oxide and oxygen free radicals, lipid peroxidation, disruption of blood-brain barrier, cerebral edema and ischemia, mitochondrial dysfunction, axonal disruption and necrotic cell death considered as mechanisms of secondary injury ³⁸’⁴⁵. tbi start a close circle of neurotoxic phenomena which aggravate each other and end finally in cell death either by apoptosis or cell necrosis ⁵⁹. diagnosis of tbi: assessing the gcs and size of pupils and romanian neurosurgery (2018) xxxii 1: 129 148 | 131 reaction to light considered as initial neurologic examination. prove alcohol intoxication lowers initial gcs in tbi patients ¹⁸’²⁴. computed tomography (ct) of the head is used for both confirming tbi and follow up patients over time after impact. ct scan can be used to know the type and severity of the injury; with upper hand for detecting intracranial hematoms ³²’³³. 50% of moderate tbi patients have abnormal finding in ct scan¹⁹. treatment: treatment divided into: pre-hospital, casualty department, and other, which includes both surgical treatment and intensive care unit treatment ⁸’⁹. prognosis and outcome: mortality in moderate tbi is 15 %, and 75 % of these deaths happen in sever injured patients¹⁹’²⁹. more than 50% of the survivors after moderate tbi suffer cognitive problem and whose recover without significant disability only 20 %²¹. death incidence 3.5 years after injury in teenagers and adults affected by moderate or severe tbi who were discharged from hospital after treatment was more than twice compared to persons in the general population of similar age, sex, and race ³’¹⁹. there are many predictors factors of outcome after tbi include gcs after resuscitation, age, pupillary reactivity, ct findings, and the presence of major associated extra-cranial injury ⁴⁵’⁵⁷. material and methods this prospective study, after approval by the local ethical committee of anesthesia & surgical intensive care department mansoura university hospital were conducted on all patients with head trauma admitted to mansoura emergency hospital during the period from 1 dec. 2015 to 30 jul. 2016. inclusion criteria: patients with head trauma only, different age group (pediatrics from 0 to 15 years, adults from 15 to 65 year, geriatrics more than 65 year)., patients with moderate head injury gcs (9-12), patients with intracranial hemorrhage, patients with skull fracture depressed or linear, patients with cerebral contusions, patients treated surgically and treated conservative, drug abuse patients and alcohol drinkers, diabetic patients smokers, controlled hypertensive patient, patient with mild liver disease and mild renal disease controlled with treatment. exclusion criteria: polytrauma patients (abdominal injury, chest injury, fracture spine, bone fractures), patients with bleeding disorders, patients on anticoagulant therapy, severe liver disease patients, severe kidney disease patients, mild head injury gcs (13-15) and severe head injury gcs (8 or less). results in this study, we correlated different risk factors with management and outcome. management may be surgical or conservative and outcome may be alive or dead. we found that total number of cases treated surgically was 17 cases (28.3%) and 43 cases (71.6%) were treated conservatively. according to outcome 36 cases (60%) were alive and 24 cases (40%) 132 | alshaimaa et al moderate head trauma died, all cases managed in icu, figures (1, 2). in this study, total number of cases was divided into 3 groups according to age: 1) children: 16 cases (26.7%) with age ranging from 1 month to 16 years. 2) adult: 38 cases (63.3%) with age ranging from 17 years to 59 years. 3) elderly: 6 cases (10%) with age ≥ 60 years, table (1) and figure (3). according to sex, 10 cases (17%) were female and 50 cases were male (83%), according to p value sex had statistically nonsignificant effect on outcome (p = 0.7) and management (p =0.7), table (2) and figure (4). according to the cause of injury, falls was 19 cases (31.6%), road traffic accidents (rta) 33 cases (55%), struggle 4 cases (6.6%) and direct head trauma (dht) 4 cases (6.6%). cause of injury had statistically significant effect on management (p = 0.02) and statistically non-significant effect on outcome (p = 0.4), as shown in table (3, 4) and figure (5). in this study, patients who had dm 10 cases, 9 cases had htn, only 1 case had history of drug abuse and 6 cases had other medical disorder e.g. cld, ckd, epilepsy, cardiac diseases. these cases might have only one disease or might have more than one systemic diseases, as shown in table (5). gcs on admission had no statistically significant effect on management (p value =0.8) and outcome (p=0.1) with mean of 10.1±1.2 and gcs on discharge had no statistically significant effect on management (p=0.6), as shown in table (6). in our study, we depended on ct diagnosis to illustrate type of tbi and its relation to management and outcome. patients who had edh were13 cases, 20 cases had sdh, 8 cases had sah, 18 cases had contusions, 2 cases had ich, 4 cases had dai, 12 cases had brain edema, 19 cases had fissure fracture, 2 cases had depressed fracture, 1 case had fracture base of skull, 5cases had pneumocephalus, tables (7, 8,9) and figure (6). according to measured data we observed that blood pressure had statistically significant effect on outcome (p value = 0.006 for systolic bp and p value = 0.002 for diastolic bp) and non-significant effect on management (p value=0.2 for systolic bp & p=0.1 for diastolic bp). arterial blood gases (abg) had statistically significant effect (p = 0.04) on management and no statistically significance on outcome (p=0.7). serum sodium (na.) value had statistically significant effect in outcome (p=0.004) while it had no statistically significant effect on management (p=0.5). serum potassium (k.) had neither statistically significant effect on management (p=0.3) nor on outcome (p=0.2). inr in most cases was within normal range with mean 1.2±0.2 which had neither statistically significant effect on management (p=0.9) nor on outcome (p=0.4). liver enzymes (alt) had no statistically significant effect on management (p=0.08) while it had statistically significant effect on outcome (p=0.03). all cases had leukocytosis (normal wbcs 4000-11000) which had neither statistically significant effect on outcome (p=0.9) nor management (p=0.07). hemoglobin (hg.) had neither statistically significant effect on management (p=0.7) nor outcome (p=0.1). platelets had neither statistically significant effect on management (p=0.6) nor outcome (p=0.3). serum creatinine had statistically non-significant effect on management (p=0.6) while it had statistically significant effect on outcome romanian neurosurgery (2018) xxxii 1: 129 148 | 133 (p≤0.001). random blood sugar (rbs) had no statistically significant effect on management (p=0.4) while it had statistically significant effect on outcome (p≤0.001), as shown in table (10). according to the duration of hospital stay, survived patients had longer duration of hospital stay than dead patients with mean duration of hospital stay for survived 8(4-45) and for dead 7(1-27), which had statistically non-significant effect on outcome (p =1). patients treated surgically had longer duration of hospital stay than treated conservatively with mean of duration of hospital stay for surgical treatment 8 (2-45) and for conservative treatment 7.5(1-30) day which had no statistically significant effect on management (p =1), as shown in figures (7, 8). figure 1 illustrates percentage of dead to alive figure 2 illustrates percentage of surgical to conservative treatment figure 3 illustrates age groups figure 4 illustrates percentage of male to female figure 5 illustrates cause of injury figure 6 illustrates relation between hospital stay and outcome figure 7 illustrates relation of hospital stay to management 134 | alshaimaa et al moderate head trauma table i correlates age groups to management and outcome management outcome surgical n=17 no (%) conservative n=43 no (%) significance test alive n=36 no (%) dead n=24 no (%) significance test child 3(17.6) 13 (30.2) p = 0.5 mct p=0.5 15 (41.7) 1 (4.2) p = 0.003* mct p=0.001* adult 13(76.5) 25 (58.1) p = 0.3 20 (55.6) 18 (75) p = 0.1 elderly 1(5.9) 5 (11.6) p = 0.8 1 (2.8) 5 (20.8) p = 0.07 table ii correlates sex to management and outcome management outcome surgical n=17 no (%) conservative n=43 no (%) significance test alive n=36 no (%) dead n=24 no (%) significance test age:median (min-max) 25 (2 74) 20 (0.5 74) z =0.3, p = 0.7 18.5 (0.5 71) 49.5 (5 -74) z = 4.1, p ≤ 0.001* female 2 (11.8) 8 (18.6) fet p= 0.7 7(19.4) 3(12.5) fet p= 0.7 male 15 (88.2) 35 (81.4) 29(80.6) 21(87.5) z of mann-whitney test sd: standard deviation fet: fisher’s exact test mct: monte carlo test p: probability p value is significant if ≤ 0.05, highly significant if ≤ 0.0001 romanian neurosurgery (2018) xxxii 1: 129 148 | 135 table iii correlates cause of injury to management and outcome management outcome surgical n=17 no (%) conservative n=43 no (%) significance test alive n=36 no (%) dead n=24 no (%) significance test falls 2(11.8) 17 (39.5) p = 0.08 mct p = 0.02* 14(38.9) 5(20.8) p = 0.2 mct p = 0.4 rta 12(70.6) 21 (48.8) p = 0.2 17(47.2) 16(66.7) p = 0.2 struggle 3 (17.6) 1 (2.3) p = 0.1 2(5.6) 2(8.3) p = 1 dht 0 (0) 4 (9.3) p = 0.5 3(8.3) 1(4.2) p = 0.9 *there is significant correlation between cause of injury and management (p=0.02) table iv correlates cause of injury to age groups cause of injury significance test falls n = 19 rta n =33 struggle n =4 dht n =4 age group child 10 (52.6) 4 (12.1) 0 (0) 2 (50) mct p = 0.001* adult 4 (21.1) 28 (84.8) 4 (100) 2 (50) elderly 5 (26.3) 1 (3) 0 (0) 0 (0) *there is statistically significant correlation between age of patient and the cause of injury (p=0.001) 136 | alshaimaa et al moderate head trauma table v correlates systemic diseases to management and outcome management outcome surgical n=17 no (%) conservative n=43 no (%) significance test alive n=36 no (%) dead n=24 no (%) significance test dm 3 (17.6) 7 (16.3) fet p = 1 1(2.8) 9(37.5) fet p = 0.001* hypertension 1 (5.9) 8 (18.6) fet p= 0.4 1(2.8) 8(33.3) fet p= 0.002* drug abuse 1 (5.9) 0 (0) fet p= 0.3 1(2.8) 0(0) fet p= 1 other systemic diseases….. 1 (5.9) 5 (11.6) fet p= 0.7 2(5.6) 4(16.7) fet p= 0.2 *there is significant correlation between dm, htn and outcome (p=0.001), (p=0.002) respectively table vi correlates gcs to management and outcome management outcome surgical n=17 no (%) conservative n=43 no (%) significance test alive n=36 no (%) dead n=24 no (%) significance test initial gcs 10.1±1.2 10.3 ± 1.2 p = 0.6 10.2778 ±1.1 10.1 ± 1.3 p = 0.6 9.00 8 (47.1) 14 (32.6) p=0.9 mct p = 0.8 10 (27.8) 12 (50) p = 0.08 mct p = 0.1 10.00 3 (17.6) 12 (27.9) p =0.6 12(33.3) 3 (12.5) p = 0.1 11.00 3 (17.6) 8 (18.6) p=1 8 (22.2) 3 (12.5) p = 0.5 12.00 3 (17.6) 9 (20.9) p =1 6 (16.7) 6 (25) p = 0.4 gcs on discharge 14.00 2 (4.3) 7 (28.6) fet p = 0.6 15.00 7 (35.7) 20 (71.4) romanian neurosurgery (2018) xxxii 1: 129 148 | 137 table vii correlates type of lesion to management and outcome according to ct on admission management outcome surgical n=17 no (%) conservative n=43 no (%) significance test alive n=36 no (%) dead n=24 no (%) significance test edh: only other lesion 4(44.4) 5(55.6) 1(33.3) 3(66.7) fet p = 1 5 (50) 5 (50) 0 (0) 3 (100) fet p = 0.2 sdh: only and other lesion 3(33.3) 6 (66.7) 5(45.5) 6(54.5) fet, p = 0.7 4 (57.1) 3 (42.9) 4(30.8) 9 (69.2) fet p= 0.4 sah: only and other lesion 0(0) 0 (0) 2(12.5) 6 (87.5) fet p = 1 0 (0) 1 (100) 2 (28.6) 5 (71.4) fet p= 1 contusion: only and other lesion 0 2 (100) 2(100) 14 (87.5) fet p = 1 2 (25) 6 (75) 0 (0) 10 (100) fet p = 0.2 ich: only and other lesion 0(0) 0 (0) 1(50) 1 (50) fet p = 1 0 (0) 1 (100) 1 (100) 0 (0) fet p = 1 fissure fracture: only and other lesion 0 7 (100) 2(16.7) 10 (83.3) fet p = 0.5 2 (18.2) 9(81.8) 0 (0) 8 (100) fet p = 0.5 depressed fracture: only and other lesion 0 1 (100) 0 (0) 1(100) fet p= 1 0 (0) 1 (100) 0 (0) 1(100) fet p=1 fracture base skull: only and other lesion 0 0 0 (0) 1 (100) fet p =1 0 (0) 1 (100) 0 (0) 0 (0) fet p=1 brain edema: only and other lesion 0 0 4(33.3) 8(66.7) fet p = 1 3 (33.3) 6 (66.7) 1 (33.3) 2 (66.7) fet p=0.4 dai: only dai dai and other lesion 0 (0) 0(0) 4 (100) 0 fet p = 1 4 (100) 0 (0) 0 (0) 0 (0) fet p = 0.1 pneumocephalus: only and other lesion 0 (0) 2 (100) 0 (0) 3 (100) fet p = 1 0 (0) 5 (100) 0 (0) 0 (0) fet p = 0.07 138 | alshaimaa et al moderate head trauma table viii correlates type of lesion to outcome outcome significance test alive n = 36 dead n = 24 no (%) no (%) edh 10 (27.8) 3 (12.5) 1.9=2א p = 0.2 sdh 7 (19.4) 13 (54.2) 7.8 = 2א p = 0.005* sah 1 (2.8) 7 (29.2) fet p = 0.005* contusion 8 (22.2) 10 (41.7) 2.6 = 2א p = 0.1 ich 1 (2.8) 1 (4.2) fet p = 1 fissure fracture 11 (30.6) 8 (33.3) 0.05= 2א p = 0.8 fracture depressed 1 (2.8) 1 (4.2) fet p = 1 fracture base of the skull 1 (2.8) 0 (0) fet p = 1 brain edema 9 (25) 3 (12.5) fet p = 0.3 dai 4 (11.1) 0 (0) fet p = 0.1 pneumocephalus 5 (13.9) 0 (0) fet p = 0.08 *there is significant correlation between sdh, sah and outcome (p=0.005), (p=0.005) respectively. romanian neurosurgery (2018) xxxii 1: 129 148 | 139 table ix correlates age with type of lesion child n=16 no (%) adult n=38 no (%) elderly n=6 no (%) significance test edh 3(18.8) 9(25) 1(12.5) mct p = 0.7 sdh 1(6.3) 15(41.7)* 4(50) mct p= 0.03* sah 1(6.3) 5(13.9) 2(25) mct p = 0.5 contusion 5(31.3) 10(27.8) 3(37.5) mct p = 0.9 ich 0(0) 1(2.8) 1(12.5) mct p = 0.3 fracture: fissure 9(56.3) 10(27.8)* 0(0) mct p = 0.02* fracture: depressed 0(0) 2(5.6) 0(0) mct p= 0.7 fracture base skull 1(6.3) 0(0) 0(0) mct p= 0.4 brain edema 5(31.3) 7(19.4) 0(0) mct p= 0.2 dai 1(6.3) 3(8.3) 0(0) mct p= 0.8 pneumocephalus 2(12.5) 3(8.3) 0(0) mct p= 0.7 *there is significant correlation between age of patients and type of lesion sdh, fissure fracture (p=0.03), (p=0.02) respectively. 140 | alshaimaa et al moderate head trauma table x correlates lab. data to management and outcome *there is significant correlation between ph and management (p=0.04), sr. na and outcome (p=0.004), alt and outcome (p=0.03), sr. creatinine and outcome (p≤0.001). discussion we discussed in this study different risk factors which affect management and outcome of tbi patients. these risk factors include age, sex, cause of injury, systemic diseases, drug abuse, gcs on admission, and type of lesion. in the present study we found that children and adults had better outcome than elderly who had poor outcome. there is significant correlation between age and outcome (p=0.001), especially child group and outcome (p= 0.003). some studies found that increasing age is a strong independent factor in prognosis of tbi, with a significant increase in fair outcome in patients older than 60 years of age, parameter management outcome surgical n= 17 mean ± sd conservative n=43 mean ± sd significance test alive n=36 mean ± sd dead n=24 mean ± sd significance test systolic bl.\p 118.3 ±18.6 127.1 ± 25.8 p = 0.2 116.9 ± 17.5 135.8 ± 28.1 p = 0.006* diastolic bl.\p 73.9 ± 6.9 78.1 ±14.2 p = 0.1 72.8 ±10.03 82.9±13.7 p = 0.002* inr 1.2 ± 0.1 1.2405± 0.2 p = 0.9 1.2 ± 0.2 1.3 ± 0.2 p = 0.4 abgph 7.29 ± 0.1 7.34 ± 0.07 p = 0.04* 7.3 ± 0.1 7.3 ± 0.07 p = 0.7 abg.pco2 37.7 ± 11.1 35.5 ± 8.8 p = 0.4 36.4± 9.1 35.7± 10.3 p = 0.8 abg.hco3 20.7 ± 3.2 20.1 ± 4.2 p = 0.6 20.5 ± 3.8 20.01 ± 4.2 p = 0.7 abg: na 147.1 ± 8.3 148.8 ± 8.1 p = 0.5 145.9 ± 7.3 151.9 ± 8.04 p = 0.004* abg.k 3.4 ± 0.5 3.3 ± 0.5 p = 0.3 3.4 ± 0.5 3.2 ± 0.6 p = 0.2 alt: median(min-max) 20 (13 50) 25 (13 196) z = 1.7, p = 0.08 22 (13 196) 26 (16 92) z = 2.1, p = 0.03* wbcs 19370.6 ± 3954.1 16786.1±5172.9 t= 1.9,p = 0.07 17530.6 ± 5464.99612 17500 ± 4222.50698 t= 0.02,p = 0.9 hb 11.3±1.6 11.5±2.2 t= 0.3,p= 0.7 11.1 ±2.3 11.9 ±1.5 t= 1.7,p= 0.1 platelets 248823.5 ±72919.7 233253.5 ±101687.2 t=0.6,p = 0.6 249083.3 ± 100879.7 220537.5 ± 81934.09 t=1.2,p = 0.3 rbs 171.9 ±63.9 157.1 ±55.1 t=0.9,p = 0.4 135.7 ±34.4 199.8 ±64.2 t=4.5,p≤0.001* sr. creatinine 0.9 ±0 .2 0.8 ±0.3 t=0.5,p= 0.6 0.7 ± 0.3 1.02 ± 0.3 t=3.7,p≤0.001* duration of hospital stay: median(min-max) 8 (2 45) 7.5 (1 30) z = 0, p = 1 8 (4 45) 7 (1 27) z = 0.9, p= 1 romanian neurosurgery (2018) xxxii 1: 129 148 | 141 that's due to a higher rate of co-medication and anticoagulants administration which increase the extent of intracerebral bleeding⁸’⁹. xueyan et al. ⁵⁷, illustrated in his study, several factors were found to contribute to the poor outcome in elderly patients, including lower glasgow coma scale scores, existing systemic diseases as hypertension, systemic complications, midline shift, and inefficient intensive care unit. in the present study, we found that incidence of tbi in male was higher than female with a ratio of (5:1) respectively which indicates that male gender was a risk factor for tbi due to the higher incidence of rta which affects mainly males who are the main workers and drivers in egypt although sex did not affect outcome of tbi. this finding was in agreement with taha᾽s (2015) results of his study which was about closed severe traumatic brain injury and was done in egypt. he found that out of 80 cases, 71 male (88.8%), and the rest are female (11.2%) with mean age of 27.45± 16.46 year. brock᾽s et al. ¹⁰ also reported that the incidence of tbi in male was 12–16% and 8% in females so men were more likely to be admitted in hospital and are nearly three times more likely to die after tbi. albrecht et al. ² found that same mortality following isolated tbi among older adults in both sex. in the present study, we found that the most frequent causes of tbi were road traffic accident, falling from height, struggle and direct head trauma (dht) respectively. there is statistically significant correlation between age of patient and the cause of injury (p value =0.001). falls represented the most common cause of traumatic brain injury in extremes of age group while rta and struggle were the most common causes in adult group. this finding was in agreement with taha᾽s (2015) results of his study which was done in egypt, as he reported that rta was the most important cause of head injury in 52 (65%) of patients with severe tbi followed by falls in 12 (15%) of those patients. tagliaferri and his collagues ⁵²and raja et al. ⁴⁷considered road traffic accidents is the commonest causes of head injury in adults (40%) and falls (37%). the commonest cause of injury was pedestrian (36%), and falls (24%) in children. maas et.al. ³² illustrated in his study that the incidence of tbi was increasing due to the increased use of motor vehicles especially in middle and low income countries but in high income countries which have traffic safety regulations result in decline in traffic-related tbi. vulnerable road users (pedestrians, cyclists, etc.) were particularly at risk. according to systemic diseases and substance abuse we found that patients with systemic diseases had poor prognosis and worse outcome than other patients who did not have systemic diseases. there is significant correlation between dm, htn and outcome (p=0.001), (p=0.002) respectively. lustenberger et. al. ³¹ found that tbi associated with diabetes mellitus have an almost 1.5 fold increased mortality when compared to patients with isolated tbi. they reported significantly increased in-hospital mortality in patients with vs without dm (22.6% vs. 16.8%. p=0.002). 142 | alshaimaa et al moderate head trauma timur et. al. ⁵⁴ reported in his result that patients with tbi and pre-hospital htn showed significantly higher mortality than tbi patients with normotensive blood pressure (13.5% vs. 25.3%, p<0.001). changes in blood pressure during the pre-hospital period, also resulted in higher hospital mortality. rixen et.al. ⁴⁸ illustrated the mechanism by which htn increase morbidity and mortality through elevating cerebral perfusion pressure, which leads to enforced dilatation of cerebral arterioles and rise in cerebral blood volume with elevating intra-cerebral pressure. this in turn leads to deterioration of the blood brain barrier with inversion of the hydrostatic gradients and finally to the formation of cerebral edema and/or hemorrhage. in our study, we found that there is significant correlation between alt and outcome (p = 0.03). lustenberger et.al. ³⁰, illustrated that tbi with liver disease was associated with two-fold increased mortality. in our study, we found a significant effect of chronic kidney diseases on outcome (p ≤ 0.001) and this finding was in agreement with liao et. al. ²⁹results as they found a significant difference between tbi with end stage renal disease patients and patients without renal disease on mortality (p ≤ 0.0001). this is due to a greater number of comorbidities, such as diabetes mellitus, stroke, systemic hypertension, and heart disease in those patients than non-esrd patients admitted to the icu. in the present study, we found that only one case of drug abuse which had good outcome, may be other cases of drug abuse were missed, this was due to lack of screening tests for substance abuse to patients with tbi in our hospital. o᾽phelan et.al. ⁴³unexpectedly found that alcohol intake to be associated with decreased mortality. mathias and osborn (2016) found that alcohol had either deleterious or protective effects on the brain after a tbi and pre-injury alcohol abuse only had a very limited impact on the cognitive outcomes of their intoxicated mild tbi sample. alternatively, dinh et. al. (2014) found that alcohol consumption may lead to more serious injuries which, in turn, may contribute to poorer cognitive outcomes. intoxicated patients affecting gcs through decreasing it by 2–3 points are challenging to classify and should be treated with higher attention (harry et.al. 2007). according to gcs at time of admission as a risk factor that affect outcome we found that cases with gcs 9 had worse outcome than cases with gcs 12. so the lower gcs, the more chance for surgical treatment and the worst outcome. perel et al. (2008) and agrawal et al. (2012) considered that gcs after full resuscitation was one of the most important predictor factor of outcome after tbi. baum j. et.al. (2016) illustrated that every 1-point decline in initial gcs at hospital presentation was associated with a 14% increased risk for fair outcome. osler et.al. (2016) considered that gcs was an important predictor of mortality in both tbi and non-tbi patients but gcs is a more stronger predictor of death in tbi patients and patients with lower gcs have poor outcome than others. romanian neurosurgery (2018) xxxii 1: 129 148 | 143 in the present study, most patients who survived had gcs 15 on discharge and good outcome and mostly managed conservatively. we determined outcome of patients at hospital discharge. we did not evaluate long term outcomes because difficulty in follow-up of many patients after discharge. maas et.al. (2008) suggested that outcome after head injury is better to be assessed at 6 months after injury, as experience showed that about 85% of recovery happened within this time period, but further improvement could occur later. according to type of lesion, baum et. al. (2016) found that tbi outcome is more dependent on the severity of the brain injury and less so on extra cranial injuries. in the present study, we found that most common type of hemorrhage was sdh, its incidence was 33% of cases of the study which was in agreement with mackenzie (2000) result who found that acute sdh was the commonest type of traumatic intracranial hematoma. in the present study, acute edh incidence was 22% of cases of moderate head trauma and was common in adult group 9 cases versus 3 children and 1 elderly. bullock et. al. (2006) illustrated that edh is rare in the elderly group, due to dura adherent to the skull. edh generally had good outcome 27% of patients were alive but if associated with intracranial lesions outcome become poor (12% died). grandhi et al. (2014) showed that asdh compared with edh had worst outcome due to severity of underlying brain damage associated with asdh, and the rate of mortality are greater especially in elderly patients group with poor initial gcs, and other systemic injuries in the present study, sah was a common intra-cerebral lesion, its incidence was 13% of moderate head trauma. it had worst outcome especially if associated with other lesion and mostly treated conservatively if not associated with other intra-cerebral lesions. borczuk et. al. (2013) found that patients with isolated traumatic sah were at lower risk of deterioration in comparison with patients having other intracranial injuries. gaetani et al. (1995) considered that sah was a negative prognostic factor in traumatic head injuries especially if there was an associated intracerebral hematoma. quigley et al. (2013) illustrated that management of traumatic sah was usually conservative in isolated traumatic sah without other intracranial lesions. in the present study, cerebral contusions were a common lesion, its incidence was 30% of moderate head trauma patients and its management was mainly conservative. generally cc had poor outcome especially if associated with other intra-cerebral lesions. this was in agreement with houseman et. al. (2012), soustiel et. al. (2008) and maas (2016) results who found cerebral contusions were one of the most common traumatic findings and it presented in more than 50% of patients of moderate and severe tbi. saeed et al. (2014) result reported not all patients with cc require surgical intervention, 56% of patients can manage conservative and the remaining 44% need surgical evacuation, surgery was done for other intracranial lesions. chieragato et al. (2005) study showed intracranial lesions which increase the chances of a bad neurological outcome were (cerebral 144 | alshaimaa et al moderate head trauma contusions, subdural hematoma and subarachnoid hemorrhage). in the present study, we found that fissure fracture was the most common type of fracture, it had good outcome and was treated conservatively especially if not associated with other lesions. raja et. al. (2013) had confirmed this findings in his study as the dominant type of skull fracture was linear (fissured) fracture in 50% of cases followed by depressed fracture in 30%, comminuted fracture in 20%. in the present study, we found only one case of fracture base of the skull that documented on ct scan of the head. actually there were 15 cases of tbi presented with periorbital hematoma, csf rhinorrhea and\or csf otorrhea, bleeding per nose and\or per ear. this finding was explained in chawla et.al. (2105) study, as to detect a fracture on a ct scan there must be discontinuity of the skull. a linear fracture that comes in the same plane of a ct slice may not be visualised. linear fractures in the base of the skull were difficult to be identified by ct scan unless depressed or separated. in the present study, we found 4 cases of dai and their ct scan was normal presented by disturbed conscious level only and not associated with other injuries and all were treated conservative and had good outcome. yuh el (2013) suggested that up to one third of patients presented with mild traumatic brain injury (gcs 13-15) and a normal ct scan upon presentation will demonstrate structural abnormalities on later mr imaging. joshue et. al. (2013) unexpectedly found that diffuse axonal injury was rarely fatal but was associated with increased possibilities of a poor functional recovery, prognosis was generally considered poor. in the present study, we found that brain edema was considered a secondary lesion which mostly occurred associated with other lesions and it was present in 20% of all moderate tbi patients. adults were more susceptible to brain edema than children. it was mostly treated conservatively and generally had good outcome. makarenko et. al. (2016) found that secondary brain injury cause a significant morbidity and mortality partly due to brain edema which reduces intracranial compliance and may cause a dangerous rise in intracranial pressure which leads to reduced cerebral blood flow and cerebral perfusion. in the present study, the incidence of pneumocephalus was 8.3% of moderate head trauma, occurring in adult more than in children. it always occurred associated with other lesions, treated conservatively and had good outcome. in the present study, we found that incidence of moderate traumatic brain injury in children was 26.6%, the most common hemorrhages in this group were contusion (31%), edh (19%), sdh (6.3%), and sah (6.3%) respectively. fissure fracture was common in child group (56%). we found that adult group were more prone to injury than any age group due to increased incidence of rta in our country, common hemorrhages in these group were asdh (41.7%), contusion (27.8), edh (25%), sah (13.9%) respectively. the common fracture in this group was fissure (27.8%), depressed (5.6%). romanian neurosurgery (2018) xxxii 1: 129 148 | 145 bullock et. al. (2006) found that elderly population is more liable to hge due to increased fragility of blood vessel walls and increasing antithrombotic and anticoagulant drugs usage. also we found that the most common hemorrhages in elderly were sdh (50%) contusion (37.5%), sah (25%), edh (12.5%), and ich (12.5%) respectively. in the present study, we found that serum na had significant effect on outcome (p=0.004). hypernatremia may be attributed to the use of normal saline (0.9%) for the first 24 hours, the use of hyperosmolar diuretics (mannitol) and loop diuretics (furosemides) and its allowed to have high serum na till 160 -170 mmol\l in such patients. this cause hyperosmolarity of blood which withdraws water from brain cells and decreasing brain edema. our results was in agreement with maggiore and picetti (2009) results, they reported the incidence of hypernatremia was significantly related with increased patients mortality (p = 0.003). this is due to the coexistence of precipitating factors such as impaired sensorium, altered thirst, central diabetes insipidus, and increased insensible losses. also, these patients often receive dehydrating measures to reduce cerebral edema and controlling intracranial pressure. bradshaw and smith (2008) and xing et.al. (2015) illustrated that electrolyte disorder was a common problem in tbi patients who are at a high risk for the development of hypokalemia, hypernatremia. hypernatremia occurs in tbi patients less commonly than hyponatremia. hypernatremia is often an indicator of the severity of the underlying disease. hypokalemia is a common electrolyte disorder in hospitalized patients, with a prevalence of 21% and according the severity of post-traumatic hypokalemia, the severity of head injury can be assisted. conclusion the most common cause of injury is road traffic accidents with cause of injury had statistically significant effect on management and statistically non-significant effect on outcome. patient gender had no effect on management and outcome. we found significant effect of age of patients, systemic diseases (such as dm, htn, chronic kidney diseases, and chronic liver diseases), type of lesions (especially sdh, sah), and serum electrolytes (especially serum sodium) on outcome which determined by gcs at discharge, length of hospital stay, and the state of the patient at discharge. references 1-agrawal d, joshua sp, gupta d, sinha s, satyarthee gd. (2012). can glasgow coma score at discharge represent final outcome in severe head injury? j emerg trauma shock 5(3):217–9. 2-albrecht js, mc-cunn m, stein dm, simoni-wastila l, smith gs. (2016). sex differences in mortality following isolated traumatic brain injury among older adults. the journal of trauma and acute care surgery. 81(3):486492. 3-andriessen tm, horn j, franschman g, van der naalt j, haitsma i, jacobs b, et al. (2011). epidemiology, severity classification, and outcome of moderate and severe traumatic brain injury: a prospective multicenter study. j neurotrauma. 28:2019–31. 4-andriessen tm, jacobs b, vos pe. (2010). clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury. j cell mol med. 14(10):2381–2392. 146 | alshaimaa et al moderate head trauma 5-baum j, entezami p, shah k, medhkour a. (2016). predictors of outcomes in traumatic brain injury. world neurosurg. 6borczuk p, penn j, peak d, chang y. (2013). patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention. j trauma acute care surg 74:1504-1509. 7-bradshaw k and smith m. (2008). disorders of sodium balance after brain injury critical care & pain | volume 8 number 4. 8-brain trauma foundation (btf), american association of neurological surgeons, congress of neurological surgeons, joint section on neurotrauma and critical care. (2007). guidelines for the management of severe traumatic brain injury. journal of neurotrauma. 24 supplement 1:s1-s95. 9-brain trauma foundation (btf). (2000). early indicators of prognosis in severe traumatic brain injury. j neurotrauma 17:535–627. 10-brock f.r. thomas j. farrer, mark primosch, dawson w. hedges. (2013). prevalence of traumatic brain injury in the general adult population: a meta-analysis. neuroepidemiology, 40:154–159. 11bullock m.r., chesnut r., ghajar j., gordon d., hartl r., newell d.w. et al. (2006). surgical management of acute epidural haematomas. neurosurgery vol. 58 :( supplement) 52-7. 12-bullock m.r., chesnut r, ghajar j, gordon d, hartl r, newell dw, servadei f, walters bc, wilberger je. (2006). surgical management of acute subdural hematomas. neurosurgery 58:s2-16-s2-24. 13-bullock mr, chesnut r, ghajar j, et al. (2006). surgical management of depressed cranial fractures. neurosurgery, 58:s56. 14bullock rm, chesnut r, ghajar j, gordon d, hartl r, newell dw, et al. (2006). surgical management of traumatic parenchymal lesions. neurosurgery. 58:s2-25– 46. 15-chavli k. h., sharma b. r., harish d., anup sharma. (2006) head injury: the principal killer in road traffic accidents. jiafm, 28(4) issn: 0971-0973. 16-chawla h., yadav kr, griwan sm, malhotra r, and paliwal kp. (2015). sensitivity and specificity of ct scan in revealing skull fracture in medico-legal head injury victims. australas med j. 8(7): 235–238. 17-chieragato a, fainardi e, morselli-labate am, antonelli v, compagnone c, targa l, kraus j, servadei f. (2005). factors associated with neurological outcome and lesion progression in traumatic subarachnoid hemorrhage patients. neurosurgery. 56:671–680. 18-christopher wood g. and bradley a. boucher. (2011). management of acute traumatic brain injury. psapvii. neurology and psychiatry. 19-compagnone c., d’avella d., servadei f., angileri f.f., brambilla g., conti c., et al. (2009). patients with moderate head injury: a prospective multicenter study of 315 patients. neurosurgery, 64:690–697. 20-daniel agustın godoy, andre´s rubiano, alejandro a. rabinstein, ross bullock. juan sahuquillo. (2016). moderate traumatic brain injury: the grey zone of neurotrauma. neurocrit care, page 4. 21-fabbri a, servadei f, marchesini g, stein sc, vandelli a. (2008). early predictors of unfavourable outcome in subjects with moderate head injury in the emergency department. j neurol neurosurg psychiatry, 79:567–73 22-frattalone ar, ling gsf. (2013). moderate and severe traumatic brain injury: pathophysiology and management. neurosurg clin n am. 24(3):309-319. 23gaetani p, tancioni f, tartara f, carnevale l, brambilla g, mille t, et al. (1995). prognostic value of the amount of posttraumatic subarachnoid haemorrhage in a six month follow up period. j neurol neurosurg psychiatry; 59:635—7. 24-grandhi r, bonfield cm, newman wc, okonkwo do. (2014). surgical management of traumatic brain injury: a review of guidelines, pathophysiology, neurophysiology, outcomes, and controversies. j neurosurg sci. 58:249–59. 25-harry mcnaughton, michael ardagh, andrew beattie. (2007). traumatic brain injury: diagnosis, acute management and rehabilitation acc2404. new zealand guidelines group for acc.p.4. 26-houseman c, belverud s, narayan r. closed head injury. in: ellenbogen r, abdulrauf s, editors. (2012). principels of neurological surgery, philadelphia: saunders elsevier; pp. 325–47. 27joshua m. levine and monisha a. kumar. (2013). traumatic brain injury. neurocritical care society practice update.p6. 28-langlios j.a. & sattin, r.w. (2005). traumatic brain injury in united states: emergency department visits, hospitalizations, and deaths research and programs of the centers for disease control and prevention (cdc). j.head trauma rehabil. 20,187-188. romanian neurosurgery (2018) xxxii 1: 129 148 | 147 29-liao jc, ho ch, liang fw, wang jj, lin kc, chio cc, kuo jr. (2014). one-year mortality associations in hemodialysis patients after traumatic brain injury. an eight-year population-based study. plos one 9(4). 30-lustenberger t, talving p, lam l, inaba k, branco bc, plurad d, demetriades d. (2011). liver cirrhosis and traumatic brain injury: a fatal combination based on national trauma databank analysis. am surg. mar; 77(3):311-4. 31-lustenberger t1, talving p, lam l, inaba k, bass m, plurad d, demetriades d. (2013). effect of diabetes mellitus on outcome in patients with traumatic brain injury: a national trauma databank analysis. brain inj. 27(3):281-5. 32-maas a. (2016). traumatic brain injury: changing concepts and approaches, chinese journal of traumatology xxx 1-4. 33-maas a., stocchetti n., bullock r. (2008). moderate and severe traumatic brain injury in adults. lancet neurol. 7: 728–41. 34-maas al, hukkelhoven cw, marshall lf, steyerberg ew. (2005). prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. neurosurgery j. 57:1173. 35-mackenzie ej. (2000). epidemiology of injuries: current trends and future challenges. epidemiol rev. 22:112-119. 36 maggiore u., picetti e., antonucci e., parenti e., regolisti g., mergoni m., vezzani a., cabassi a. and fiaccadori e. (2009). the relation between the incidence of hypernatremia and mortality in patients with severe traumatic brain injury. critical care,13:r110. 37-makarenko s, griesdale e. d., gooderham p., sekhon m.s. (2016). multimodal neuromonitoring for traumatic brain injury: a shift towards individualized therapy. journal of clinical neuroscience 26, 8–13. 38-mathias j. l. and osborn a. j. (2016). impact of dayof-injury alcohol consumption on outcomes after traumatic brain injury: a meta-analysis. neuropsychological rehabilitation. 39-mchugh gs, engel dc, butcher i, et al. (2007). prognostic value of secondary insults in traumatic brain injury: results from the impact study. j neurotrauma; 24:287. 40montaser, ahmed hassan, ahmed ibrahim. (2013). epidemiology of moderate and severe traumatic brain injury in cairo university hospital in 2010.scandinavian journal of trauma, resuscitation and emergency medicine.21, suppl 2. 41-national institute for health and clinical excellence (nice). (2014). head injury triage, assessment, investigation and early management of head injury in children, young people and adults. clinical guideline published: 22 january. 42national institute of neurological disorders and stroke. (2002). traumatic brain injury: hope through research. 43-national institute of neurological disorders and stroke. ninds. (2015). common data elements: traumatic brain injury. august 12. 44-o'phelan, kristine, mcarthur, david l. chang, cherylee w. j. green, deborah, hovda, david a. (2008). the impact of substance abuse on mortality in patients with severe traumatic brain injury. journal of traumainjury infection & critical care: september volume 65 issue 3 pp 674-677. 45-osler t., cook a., glance l.g., lecky f., bouamra o., garrett m., buzas j. s., hosmer w. d. (2016). the differential mortality of glasgow coma score in patients with and without head injury. injury, int. j. care injured 47, 1879–1885. 46-perel p, arango m, clayton t, et al. (2008). mrc crash trial collaborators. predicting outcome after traumatic brain injury: practical prognostic models based on large cohort of international patients. bmj. 336(7641):425–429. 47-quigley mr, chew bg, swartz ce, wilberger je. (2013). the clinical significance of isolated traumatic subarachnoid hemorrhage. j trauma acute care surg 74:581-584. 48-raja r, verma a, rathore s. (2013). pattern of skull fractures in cases of head injury by blunt force. j indian acad forensic med. october-december, vol. 35, no. 4 (0971-0973) 49-rixen d, steinhausen e, dahmen j, bouillon b, german society of trauma surgery (dgu). (2012). [s3 guideline on treatment of polytrauma/severe injuries. initial surgical phase: significance--possibilities-difficulties?]. unfallchirurg. jan; 115(1):22-9. 148 | alshaimaa et al moderate head trauma 50-rutland b.w., langlois ja, thomas ke, xi yl. (2006). incidence of traumatic brain injury in the united states, 2003. j head trauma rehabil. 21:544-548 51-saeed m., ahmed s., ali a. (2014). current consideration regarding operative versus nonoperative outcome of brain contusion patients. pakistan journal of medicine and dentistry. vol.3 (01). 52-soustiel jf, mahamid e, goldsher d, zaaroor m. (2008). perfusion-ct for early assessment of traumatic cerebral contusions. neuroradiology.50:189–96. 53tagliaferri f, compagnone c, korsic m, servadei, kraus j. (2006). asystematic review of brain injury epidemiology in europe. acta neurochir (wien) 148:255–68. 54-timmons sd. (2008). extra-axial hematomas. in: loftus cm, editor. neurosurgical emergencies. 2nd ed: thieme medical publishers. p. 53-67. 55timur s., miersch d., kienbaum p., flohé s., johannes s., lefering r., and trauma registry dgu. (2012). the impact of arterial hypertension on polytrauma and traumatic brain injury. dtsch arztebl int. dec; 109(49): 849–856. 56-tsang kkt, whitfield pc. (2012). traumatic brain injury: review of current management strategies. british journal of oral and maxillofacial surgery 50; 298–308. 57-xing w., xin l., xiangqiong l., jian y., sun y., zhuoying d., xuehai w., ying m., liangfu z., sirong w., jin h. (2015). prevalence of severe hypokalaemia in patients with traumatic brain injury. injury, int. j. care injured 46, 35–41. 58-xueyan w., shengwen l., wang s., zhang s., yang h., ou y., min z., james l., shu k., chen j., lei t. (2016). elderly patients with severe traumatic brain injury could benefit from surgical treatment. world neurosurg. 89:147-152. 59yuh el, mukherjee p, lingsma hf, et al. 2013. magnetic resonance imaging improves 3-month outcome prediction in mild traumatic brain injury. ann neurol. 73: 224-235. 60-zammit c, knight wa. (2013). severe traumatic brain injury in adults. emerg med pract.15:1–28. 16 16alshaimaamohammed_management flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 446 | moscote-salazar et al traumatic dural venous sinus thrombosis traumatic dural venous sinus thrombosis: a mini review luis rafael moscote-salazar1, willem guillermo calderónmiranda2, nidia escobar-hernandez3, marticela cabeza-morales4, andrés m. rubiano5, hernando raphael alvis-miranda6, nasly zabaleta-churio7, amit agrawal8 1neurosurgery, red latino, latin american trauma & intensive neuro-care organization, bogotá, colombia; 2radiology, hospital gea gonzalez, universidad nacional autonoma de mexico, mexico; 3radiology, hospital gea gonzalez, mexico; 4faculty of medicine, universidad de cartagena, cartagena de indias, colombia; 5neurosurgery, universidad el bosque, bogotá, red latino, latin american trauma & intensive neuro-care organization, bogotá, colombia; 6neurosurgery, universidad de cartagena, cartagena de indias, colombia; 7red latino, latin american trauma & intensive neuro-care organization, bogotá, colombia; 8neurosurgery, mm institute of medical sciences & research, maharishi markandeshwar university, mullana-ambala, haryana, india abstract: the dural venous sinus thrombosis is a benign disease, representing about 1% of cerebral vascular events. in some cases the development of the disease increased intracranial pressure or symptomatic epilepsy. the development towards a dural venous sinus thrombosis is rare, but is a condition to be considered before the development of ischemic vascular events and a history of recent head trauma. intracranial hematomas or skull fractures can lead to the establishment of obstructive pathology of the dural venous sinuses. the knowledge of this entity is necessary for the critical care staff and neurosurgery staff. key word: craniocerebral trauma, neurosurgery, cranial sinuses, thrombosis introduction the dural sinus thrombosis (tsd) is a rare (1) event, which occurs most often in young adults and children, with an estimated adult 34 incidence for 1,000,000 inhabitants, and 7 per 1,000. 000 for children (2). approximately 75% of patients are women (3), with dominant 3: 1 compared to men. the incidence when produced as a result of traumatic brain injury (tbi) is unknown; although some believe it is underdiagnosed because usually when the presence of tce omitted this diagnosis is evaluated. symptoms to establish a dural venous sinus thrombosis may be nonspecific, from mild headache to the development of severe neurological deficits including coma due to increased intracranial pressure associated with ischemic events and / or bleeding (4). romanian neurosurgery (2016) xxx 3: 446 451 | 447 risk factors once submitted tbi there are factors that act as promoters of the tsd, in fact in 85% of patients with cerebral sinus thrombosis are prothrombotic risk factors or direct causes (5). in the international study of thrombosis of the dural sinuses and cerebral veins (iscvt), where 624 adults from 89 centers in 21 countries were included, it was found that genetic or acquired thrombophilia, and the use of oral contraceptives were common risk factors (5), which may explain the female predominance of this entity (3). other conditions considered tsd promoters are neoplasms, cns disorders (and dural arteriovenous fistulas), hematologic, nephrotic syndrome, systemic vasculitis, central nervous system infections (bacterial meningitis, cerebral malaria) (6, 7), disease intestinal (5) inflammatory drugs (cisplatin (8), methotrexate, steroids), neurological surgery, lumbar puncture, pregnancy and postpartum period (7). despite the long list of risk factors for approximately 20% of cases are considered idiopathic (3-5, 9). pathogenesis when a tbi occurs with head injury, skull fractures or intracranial hematomas can generate thrombosis either by direct compression of the breast or endothelial damage in this, generating the activation of the coagulation system resulting in occlusion breast. it is unusual for the tsd occurs in the absence of diastasis of cranial sutures (10), when it occurs in these cases, it means that the associated mechanism is endothelial damage within the venous sinus. the brain also contains an abundance of thromboplastin that is released after injury cause abnormal hypercoagulable state leading to destruction of platelets and erythrocytes followed by thrombus formation (10). cerebrospinal fluid normally drains into the superior sagittal sinus, through the arachnoid villi. thrombosis of these sinuses leads to increased venous pressure, which changes the mechanism of absorption of cerebrospinal fluid (csf), and consequently increases the intracranial pressure (2), added to this can generate cytotoxic and interstitial edema (11 ) and venous infarction located. this produces dilated and enlarged veins, edema and ischemic neuronal damage, with petechial hemorrhages, which can bind and bruising (2). the most affected areas are in order: transverse sinus, sagittal sinus, sigmoid sinus and straight sinus (11, 12). often the coexistence of several affected breast (2). clinical manifestations headache is the main symptom in these patients, the intensity is still not considered pathognomonic of tsd, described intensity from mild to severe (3, 5). other nonspecific manifestations described are: nausea, vomiting and papilledema (5, 10). the frequency of the appearance of symptoms including headache (70%), followed by convulsions (39.3%), paresis (37.2%), papilledema (28.3%), altered mental status (22%), aphasia (19.1%) , stupor or coma (13.9%), diplopia (13.5%) and visual deficit (13.2%) (3). 448 | moscote-salazar et al traumatic dural venous sinus thrombosis clinical evaluation conducting a thorough neurological examination is vital to ascertain the presence or absence of signs and symptoms, just as should look for the presence of fractures (4), to better approach and early treatment improves the patient's condition (5). patients with increased intracranial pressure isolated, usually only have severe headache and diplopia if intracranial pressure is very high, the sixth cranial nerve compression. in the fundus papilledema is observed, with temporary visual impairment, which may be permanent (2). diagnosis the diagnosis of this entity is by imaging studies. the first study used is computed tomography (ct) without contrast (12), which reveals: edema, indicating areas hyperdensity hemorrhagic infarction (40% of cases), accompanied by string sign, which is a hyperdense area with cortical vein thrombosed transverse sinus area (13, 14); and the sign of the empty delta (10) which is a triangular area of enhancement with a relatively attenuated in the region of the superior sagittal sinus, considered pathognomonic of this sinus thrombosis occurs in about 28.6% of center these patients and has been found associated with poor prognosis. the appearance of this sign is probably due to the increased flow of the abundant collateral dural venous circulation, the breast surrounding the thrombosed producing central low attenuation (15). however, the absence of these findings does not exclude the diagnosis (5). in more than 25% of cases this study reported no abnormalities (5). magnetic resonance imaging (mri) is considered one of the best methods for diagnosis of this entity, because it allows the visualization of the intracranial vasculature, and can better determine the location and time of the thrombus within the dural sinus (5). on mri, the thrombus is easily recognizable in the subacute phase (10), primarily to exploration on t1, around the 15th thrombus signal it appears strongly hyperintense on t1 and t2 weighted images, perhaps this is the period of greatest important because it is where most diagnoses (16) are made. in the acute phase, the thrombus is isodense with brain on t1weighted images and low signal on t2weighted images. this aspect can be mistaken for blood flow; but by using magnetic resonance venography (mrv) no flow (11, 12) demonstrated. t2 has been proven more sensitive than single t1 or t2 .however, mri and mrv are likely to flow artifacts techniques and in doubtful cases, particularly if deep venous infarction or cortical venous thrombosis, an endoluminal technique is suspected high resolution as conventional venography or ct is recommended (11). gold standard diagnosis is digital subtraction angiography, but because it is invasive and difficult to access, only used in cases where there is doubt about the diagnosis has not been determined by other methods (10-12) or when it is suspected a longstanding tsd with rm images unclear (16). it has been proposed the use of d-dimer to assess the risk of tsd, in patients in the emergency room, it has reported a sensitivity romanian neurosurgery (2016) xxx 3: 446 451 | 449 of 97.1% and a negative predictive value of 99.6% and specificity of 91.2% with a positive predictive value of 55.7% (5), despite this, this test is not considered routine, and can be performed in all patients, and can be altered in the presence of coexisting conditions (5). treatment the three pillars of treatment are: management of intracranial pressure, convulsions and antithrombotic prevention treatment (1). the goal of this therapy is to stop the underlying thrombotic process and prevent venous thrombosis of other sites that may potentially aggravate the clinical picture. in antithrombotic therapy, anticoagulation with heparin has long been the traditional treatment, even sometimes is used regardless of the presence of hemorrhage (17, 18). it has further been reported using long-term warfarin (4, 11, 12), of monitored so as to avoid overdose (11). care should be taken in patients who undergo surgery immediately in the presence of a tce, because in them is generally contraindicated postoperative anticoagulation, which can lead to progress tsd therefore requires the suspect initial of this entity in the presence of tce and even more if there are risk factors (4). the use of thrombolytic agents which lyse the clot has quickly emerged as a therapeutic modality, supported interventional neuroradiology techniques to release the agent locally at the site of thrombosis. no randomized, double-blind, placebo-controlled cases, that support thrombolysis as the firstline therapy in patients with thrombosis of the cerebral venous sinuses, compared with unfractionated heparin. numerous case reports and nonrandomized single study has shown that it is comparatively safe and can rescue patients rapidly deteriorate despite treatment with unfractionated heparin. this practice should be restricted to centers with experience in this therapy (19). it is indicated in patients with progressive deterioration and do not respond to anticoagulant therapy for rapid recanalization of the obstructed sinus (9, 12). when thrombolytic therapy is administered within 72 hours of diagnosis, it has been demonstrated that complete recanalization is obtained in 56.5% and 43.5% partial recanalization in (9). among the most commonly used thrombolytic agents include: urokinase (73.7%) followed by recombinant plasminogen tissue activator (tpa) (21.5%), and thrombectomy or angioplasty (12.2%) (9). in a retrospective study of 25 patients with dural sinus thrombosis the role played by cerebral venous congestion and the management of these patients patients were administered anticoagulation showed a steady course, those who were given thrombolytic therapy had analyzed more outcome of adverse effects, and who underwent thrombectomy presented initial clinical worsening; demonstrating the benefits of antithrombotic therapy as the main management and the role they may have to thrombectomy and thrombolytic therapy in the development of central venous congestion. apparently the only anticoagulant therapy is not appropriate in these patients when they develop cerebral venous congestion, perhaps due to the loss of collateral flow (20). 450 | moscote-salazar et al traumatic dural venous sinus thrombosis consideration of local or systemic thrombolysis in patients clinically deteriorate despite adequate anticoagulation recommended. there is no consensus to determine the optimal medication, dose, route and method of administration (5). it is considered a serious event of great associated mortality, that causes a progressive deterioration of the patient or improving the clinical condition, which can lead to serious neurological complications or death if not treated in a timely manner (4, 11). it has reported a lower specific mortality of 10%, but neurologic deficits are present at follow-up 17% of the survivors, and the consequences may require long-term rehabilitation (11). for best results, follow with neuroimaging at least 1 year after the event. due to increased intracranial pressure, which occurs in some cases, there may be compression of the optic nerve and visual impairments therefore monitoring is recommended together with ophthalmology (11). conclusions head trauma constitutes a risk factor for developing thrombosis of dural (21) venous sinuses. a correct clinical history and imaging studies allow us to make an accurate diagnosis and timely managing this complication. especially in young patients with recent head trauma who develop symptoms of intracranial hypertension and which they should discard neurosurgical pathology or intracranial hematomas adjacent to venous structures (2224). prognosis depends on the treatment and the other structures involved with head trauma. correspondence dr. luis rafael moscote-salazar e-mail: mineurocirujano@aol.com references 1.harrahill, m., an unusual case of cerebral venous sinus thrombosis in a trauma patient. j emerg nurs, 2011. 37(2): p. 203-4. 2.stam, j., thrombosis of the cerebral veins and sinuses. n engl j med, 2005. 352(17): p. 1791-8. 3.ferro, j.m., et al., prognosis of cerebral vein and dural sinus thrombosis: results of the international study on cerebral vein and dural sinus thrombosis (iscvt). stroke, 2004. 35(3): p. 664-70. 4.dobbs, t.d., et al., cerebral venous sinus thrombosis complicating traumatic head injury. j clin neurosci, 2012. 19(7): p. 1058-9. 5.fischer, c., j. goldstein, and j. edlow, cerebral venous sinus thrombosis in the emergency department: retrospective analysis of 17 cases and review of the literature. j emerg med, 2010. 38(2): p. 140-7. 6.krishnan, a., et al., cerebral venous and dural sinus thrombosis in severe falciparum malaria. j infect, 2004. 48(1): p. 86-90. 7.filippidis, a., et al., cerebral venous sinus thrombosis: review of the demographics, pathophysiology, current diagnosis, and treatment. neurosurg focus, 2009. 27(5): p. e3. 8.karam, c. and s. koussa, cerebral dural sinus thrombosis following cisplatin chemotherapy. j clin neurosci, 2008. 15(11): p. 1274-5. 9.hocker, s.e., r.m. dafer, and l. hacein-bey, successful delayed thrombolysis for cerebral venous and dural sinus thrombosis: a case report and review of the literature. j stroke cerebrovasc dis, 2008. 17(6): p. 429-32. 10.lakhkar, b., b.r. singh, and a. agrawal, traumatic dural sinus thrombosis causing persistent headache in a child. j emerg trauma shock, 2010. 3(1): p. 73-5. 11.dlamini, n., l. billinghurst, and f.j. kirkham, cerebral venous sinus (sinovenous) thrombosis in children. neurosurg clin n am, 2010. 21(3): p. 511-27. 12.kubiak, b.d., et al., transverse sinus thrombosis after internal jugular vein ligation. j emerg med, 2012. 43(1): p. e5-9. 13.teasdale, e., cerebral venous thrombosis: making the most of imaging. j r soc med, 2000. 93(5): p. 234-7. romanian neurosurgery (2016) xxx 3: 446 451 | 451 14.vijay, r.k., the cord sign. radiology, 2006. 240(1): p. 299-300. 15.lee, e.j., the empty delta sign. radiology, 2002. 224(3): p. 788-9. 16.ayanzen, r.h., et al., cerebral mr venography: normal anatomy and potential diagnostic pitfalls. ajnr am j neuroradiol, 2000. 21(1): p. 74-8. 17.shafqat, s., a.k. kamal, and m. wasay, heparin in the treatment of cerebral venous thrombosis. j pak med assoc, 2006. 56(11): p. 541-3. 18.de bruijn, s.f. and j. stam, randomized, placebocontrolled trial of anticoagulant treatment with lowmolecular-weight heparin for cerebral sinus thrombosis. stroke, 1999. 30(3): p. 484-8. 19.kamal, a.k., thrombolytic therapy in cerebral venous sinus thrombosis. j pak med assoc, 2006. 56(11): p. 538-40. 20.tsai, f.y., et al., cerebral venous congestion as indication for thrombolytic treatment. cardiovasc intervent radiol, 2007. 30(4): p. 675-87. 21.matsushige, t., et al., cerebral sinovenous thrombosis after closed head injury. j trauma, 2009. 66(6): p. 1599604. 22.barbati, g., et al., post-traumatic superior sagittal sinus thrombosis. case report and analysis of the international literature. minerva anestesiol, 2003. 69(12): p. 919-25. 23.kumar, g.s., a.g. chacko, and m. chacko, superior sagittal sinus and torcula thrombosis in minor head injury. neurol india, 2004. 52(1): p. 123-4. 24.alvis-miranda, h.r., et al., cerebral sinus venous thrombosis. j neurosci rural pract, 2013. 4(4): p. 427-38. microsoft word _1.formatata_tataranu.doc romanian neurosurgery vol. xv nr. 1 3 neuroprotection against surgically induced brain injury ligia tataranu, md, phd, m. r. gorgan, md, phd, b.o. ene, md, v. ciubotaru, md, phd, aurelia sandu, md, adriana dediu, md department of neurosurgery, „bagdasar-arseni” emergency hospital, bucharest, romania neurosurgical procedures are carried out routinely in hospitals across the world. every neurosurgical procedure, regardless the purpose, involves a certain degree of brain injury that results from the procedure itself because of the unique nature of the nervous system. brain tissue is at risk of injury by various means, including incisions and direct trauma, electrocautery, hemorrhage, and retractor stretch. fortunately there are various substances with neuroprotective effect on human brain, with different molecular pathways, which can be used, together with surgical protective measures, as therapeutically drugs preventing brain damage during surgery. among them steroids, some anesthetic agents intraoperative hypothermia are suggested to provide cerebral neuroprotection, but also new established therapeutic agents, such as erythropoietin and statins, src tyrosine kinase inhibitor, used clinically in patients for different nonneurological disorders, which have also shown promise as neuroprotectants in experimental studies. any form of pretreatment that proved effective when used before brain injury may have a significant impact on patient recovery and outcome of procedures. this review is intended to raise the question about neuroprotection methods and agents against surgically induced brain injury available today in neuroscience scientific community and stimulate discussions about future approaches and therapies. keywords: surgery, brain injury, neuroprotection introduction although many innovations in the clinical practice have been implemented, especially with the advent of microscopy and endoscopy, neurosurgical procedures remain invasive regardless of whether they are performed in elective or emergency settings. some of the neurosurgical interventions such as surgeries for brain stem and spinal cord pathologies are intrinsically linked to postoperative neurological deficits and may lead to serious neurological injuries regardless of how carefully the operation is carried out. a key issue during most neurosurgical procedures is that there is always an element of inevitable injury inflicted on the functional and normal brain while dissecting or eliminating the pathological tissues. this unavoidable injury may exist in many forms, including predetermined cortical incisions to access any deeper pathological tissue [1], retraction of brain lobes or hemispheres [2, 3], intraoperative bleeding [4], and thermal injury due to electrocoagulation. endoscopic surgeries and stereotaxic guided procedures are designed to minimize the invasiveness of neurosurgical procedures. however, these procedures are also associated with inevitable brain injuries and complications [4-7]. to reduce the postoperative effects of these brain injuries and decrease the subsequent neurological deficits, osmotic agents, diuretics, and steroids are routinely used [8]. steroids, although well established in ameliorating brain tumor–associated edema, have not shown a definite therapeutic effect in clinical trials for traumatic brain injury. some anesthetic agents themselves [9, 10] and therapeutic modalities, such as intraoperative hypothermia [11, 12], are suggested to provide cerebral neuroprotection. even with adjunct treatments, the standard neurosurgical maneuvers, can cause damage to the surrounding brain tissue and may contribute to or result in critical early postoperative ligia tataranu romanian neurosurgery vol. xv nr. 1 4 complications such as brain edema and ischemia or delayed healing [13, 14]. even if there are no life-threatening or serious complications in most cases, neurosurgical patients have to be monitored closely, especially in the intensive care unit. this translates into longer hospital stay with significant implications for the patient, the healthcare system, and the society. the neurological and neurobehavioral functional deficits can additionally be a source of long-term emotional, social, physical, and financial duress. moreover, the concerns of causing injury to the surrounding normal and functional brain, especially in vulnerable areas such as brain stem [15], may hamper the approach of the neurosurgeons. classically, inevitable brain injury resulting from neurosurgical interventions is not treated separately or prevented by neuroprotective regimen but rather is left to be healed on its own. presently, new therapeutic agents, such as erythropoietin and statins, used clinically in patients for different cerebrovascular disorders, which have shown neuroprotective effects in experimental studies [16]. we want to take advantage of such therapeutic modalities for use as pretreatment against surgically induced brain injury, as well as any other new procedure. incidence of postoperative complications in literature in a study of consecutive patients [2] undergoing craniotomy from 1976 to 1984, with ct scans obtained within 7 days of surgery, intracerebral hematomas were detected in 80 of 275 craniotomies for brain tumors (29%) and 15 of 184 craniotomies for intracranial aneurysms (8%). in 31 of the brain tumor procedures (11%) and 7 of the aneurysm procedures (4%), the hematoma measured 3 cm or more in diameter. only clinically significant hematomas were reported, and routine postoperative scans were not considered. intracerebral hematomas, most likely to be related to retraction constituted 60% of all hematomas. the highest incidence of hematomas was in surgery for anterior circulation aneurysms (2.1%), where brain retraction is almost certain to have occurred. it is not possible from such studies to separate entirely retraction-induced injury from bleeding into the tumor resection bed or hemorrhagic infarction secondary to vasospasm. more recent reports on cranial base surgery report an incidence of approximately 10% of complications that are likely related to brain retraction or maneuvers intended to decrease retraction-induced injury. these complications included intracerebral hematomas, aphasia, hemiparesis, and numbness. in a report on surgery for unruptured aneurysms of the posterior circulation (1971 through 1988), the authors thought that 6 of 167 patients suffered retraction-induced brain injuries (4%). with regard to pineal region tumors, 2 of 12 surgical patients (17%) suffered permanent visual field defects, which the authors attributed to occipital lobe retraction. several groups investigating brain retraction pressure have reported on probable retraction-induced injuries during either brain tumor or intracranial aneurysm surgery. clinically significant postoperative deficits appeared in 3 to 9% of cases. however, one study reported a 22% incidence of ct-evident infarction beneath the tip of the retractor blade; most of the infarctions were not clinically obvious. infarctions in the region of the retractor blade were particularly common when a relatively high retraction pressure was employed. it is likely that brain injury secondary to retraction occurs in approximately 10% of major cranial base tumor procedures, and 5% of intracranial aneurysms or cranial tumor (other than the base) procedures. a highresolution ct or magnetic resonance imaging scan obtained several days postoperatively is necessary to detect lesions not readily apparent at the bedside clinical examination. undoubtedly, there is considerable variation in the incidence of retraction-induced injury, depending on the difficulty of the procedure, resources available, skill of the operating team, and the criteria used to define brain injury. research of surgically induced brain injury various animal models have been proposed and used for simulating the classical surgical approaches neuroprotection against surgically induced brain injury romanian neurosurgery vol. xv nr. 1 5 and their associated complications. among them dog, cat, rat or swine models have been chosen and demonstrated the lesional mechanism. brain edema jadhav and al. [17] created a in vivo model to study brain injury caused exclusively by neurosurgical procedures. the frontal lobe surgical injury rat model simulates the surgically induced brain injury by causing cortical and parenchymal damage and the postoperative complications that follow neurosurgical procedures. in addition, it allows the study of molecular mechanisms and signaling pathways involved in surgically induced brain injury and the testing of different pretreatment modalities for neuroprotection. this model is not intended to mimic any specific neurosurgery operations. instead, the goal is to produce a standard and reproducible model with certain amount of brain tissue loss and injury that will produce neuronal death, as well as bbb dysfunction leading to brain edema that occurs during routine neurosurgical operations in clinical practice. secondly, there is intraoperative bleeding that is controlled by packing and saline irrigation. electrocoagulation is also used to control bleeding and to make incisions to gain access to deeper structures. there are variations in its usage in voltage, frequency, and duration of application. preliminary studies revealed that there is presence of localized edema around the operative site, in fact, surgically induced brain injury. this edema, indicated by brain water content calculated using standard methods, was present only in the ipsilateral frontal area, the area contiguous to the surgically induced brain injury. time course performed experiments further revealed that this localized edema peaked at 24 hours, started declining after 3 days, and almost entirely resolved by 1 to 2 weeks after the procedure, thus mimicking a clinical situation appropriately. further studies also revealed that there was a disruption of the bbb as indicated by standard methods such as igg staining and evans blue dye extravasation. in addition, using nissl staining, we identified neuronal death in the area bordering the surgically induced brain injury. moreover, a clear transition zone, that is, gradual change from dead cells to viable cells, could be identified, thus enabling the extent of injury. brain injuries caused by lobe retraction were not considered because of variability in usage of retractors. moreover, miniature instruments producing consistent pressure and stretch injuries seen with retractor usage are required for this particular brain injury component. brain retraction, a necessary trauma in neurosurgery because effective surgical treatment for deep brain lesions, intracranial aneurysms, arteriovenous malformations, and cranial base tumors requires exposure that frequently can be obtained only by direct brain retraction, numerous animal models were proposed to measure this feature and to discover protective methods to be translated into intraoperative interventions that minimize the risk of brain retraction injury. brain retraction injury is caused by focal pressure (the retractor blade) on the brain, producing a local deformation of brain tissue for a finite period of time. such a deformation causes a reduction or cessation of local perfusion (focal ischemia). it may also cause direct injury to brain tissue (neurons, their processes, and/or glia). both the ischemia and the direct injury are probably dependent on the shape and number of the retractors as well as on the pressure and duration of the retraction. andrews and al. [2] review the published articles on brain retraction, principally during either brain tumor or intracranial aneurysm surgery and concluded retraction pressures used in clinical practice by neurosurgeons are usually in the range of 20 to 40 mm hg. it has been suggested that the use of two small retractor blades may provide exposure equivalent to one large blade with a lower retraction pressure. he also used a swine animal model to mimic a major neurosurgical intervention, and to evaluate all the possibilities for neuroprotection, such as various therapeutical agents, hypothermia, hypotension or hyperventilation. he concluded his experiments proposing a protocol for any major brain intervention, combining judicious retraction, appropriate anesthetic and pharmacological ligia tataranu romanian neurosurgery vol. xv nr. 1 6 management, and aggressive intraoperative monitoring. optimal brain retraction protection will most likely be afforded by a protocol that has several complementary beneficial effects: augmented blood flow, minimized calcium fluxes and excitotoxic injury, free radical scavenging, and decreased acidosis operative exposures preventing surgically induced brain injury positioning the patient to minimize retraction and using intraoperative csf drainage are practical and cost-effective ways to increase exposure. extensive cranial base removal or craniofacial osteotomy may be essential to expose certain lesions. positioning the patient so that gravity aids the exposure may reduce the need for direct brain retraction. examples include the use of the sitting/semi sitting position to expose the supracerebellar/pineal region and the lateral decubitus position to approach ipsilateral midline and paramedian lesions. the use of cerebrospinal fluid (csf) drainage, combined with the opening of the csf cysternas, either by lumbar puncture or ventricular puncture, requires caution. although csf drainage has been reported to facilitate exposure while decreasing the brain retraction pressure required, significant neurological complications have been attributed to excessive csf drainage. hyperventilation has serious drawbacks in the form of decreased cbf and increased alkalosis. if hyperventilation is used in conjunction with significant brain retraction, nimodipine perioperatively should be considered. brain resection is an inelegant means of gaining exposure and should be resorted to only after the techniques above have been exhausted. however, in a very few situations, it may be the safest way to accomplish the surgical goal. brain retraction should be limited to 15 minutes maximum at a pressure of less than 40 mm hg, with a 5-minute recovery period between retractions. the use of multiple, narrow blades may be less injurious than a single, wide blade. the advent of stereotactic craniotomy has reduced the amount of retraction required to approach many lesions. a micromanipulator for the brain spatula represents an intraoperative equivalent of the stereotactic tower holder of the strain gauge retractor, and the results obtained in the laboratory suggest its effectiveness during the surgery. because experience has clearly demonstrated the deleterious effect of excessive brain retraction, resection of brain tissue is frequently employed in certain neurosurgical procedures (e.g., the gyrus rectus approach to the anterior communicating artery region and lateral cerebellar resection for large masses in the cerebellopontine angle). other invasive, if not destructive, techniques have been developed to facilitate exposure of the cranial base region: petrous bone resection (possibly together with the division of the sigmoid sinus or the sacrifice of hearing) and orbitofrontal osteotomy. to maximize the clinical efficacy of operative management for many tumors, aneurysms, and arteriovenous malformations, it is important to employ all possible techniques to minimize the brain injury that may result from the need for adequate exposure. electrophysiological monitoring should be a part of procedures involving significant brain retraction unless the region of brain undergoing retraction is not amenable to the available monitoring techniques. brain electrical activity monitoring it has been well established that brain electrical activity, both spontaneous (eeg) and evoked potentials (ep), is altered and then lost at a cbf level above the of permanent brain injury. an approximately linear relationship between ssep amplitude and cbf has been observed in primates. monitoring the eeg has the advantage of being a measure of the depression of cerebral metabolism by agents such as barbiturates and etomidate, but may not be as effective as ep at detecting deep, white-matter ischemia. brain stem auditory ep (baep) and ssep (including brain mapping with arrays placed on the cortical surface) have been used for cerebroprotective monitoring under general anesthesia, particularly during complex surgery for intracranial aneurysms and arteriovenous malformations and surgery for tumors near the sensorimotor cortex. for extensive cranial base procedures, all three monitoring techniques (eeg, baep, and ssep) have been used concurrently. with neuroprotection against surgically induced brain injury romanian neurosurgery vol. xv nr. 1 7 an experienced team, intraoperative baep or ssep mapping or monitoring can be performed with little operative or perioperative delay. stimulating earphones or electrodes are applied while the anesthesia is being induced and the lines are placed; ep acquisition requires only a minute or so during which electrocautery and other sources of interference must not be used. monitoring brain electrical activity can be a very useful aid to cerebral protection. blood flow monitoring although there are many methods of focal cbf measurement that can be used in the laboratory, intraoperative cbf measurement that is feasible for monitoring brain retraction ischemia has been elusive. only laser-doppler and thermal diffusion measurements of cbf have become accepted techniques for neurosurgical operating room use. there are a number of technical difficulties with laser-doppler flowmetry that make it difficult for routine intraoperative use: the probe must not be placed over a superficial vessel, which yields falsely elevated cbf readings, the probe must not move during the procedure, and the effects of changes in hematocrit (e.g., with bleeding, hemodilution, or with mannitol, ambient lighting, temperature, etc., are uncertain. thermal diffusion flowmetry is also subject to limitations, particularly the uncertain effects of changes in temperature. transcranial doppler blood velocity monitoring has also been used intraoperatively during craniotomy. not only is it physically challenging to perform transcranial doppler monitoring on hemispheric vessels during surgery, as opposed to monitoring velocities in the contralateral hemisphere, with current technology, the spatial resolution of transcranial doppler is insufficient to be a reliable monitor of the focal ischemia resulting from brain retraction. although focal cbf monitoring could be very useful to protect against brain retraction ischemia, at the present time, the available techniques are probably neither sufficiently accurate nor practical for routine intraoperative use. retractor blade pressure monitoring two basic types of retractor blade pressure monitoring have been used in brain retraction research, both in the laboratory and intraoperatively. the first is n air-tight plastic sleeve fits over the tip of a retractor blade, with opposing electrodes on the retractor tip and the sleeve between the tip and the brain surface. a pump causes the air pressure within the sleeve to cycle with the contact and the release of the electrodes. other studies have used a strain gauge attached to the brain retractor spatula. the strain gauge is reliable and inexpensive. if strain gauges are attached to both sides of the retractor blade, the effects of temperature changes on the calibration are obviated. anesthesiology protection anesthetic agents isoflurane, often in combination with nitrous oxide and a narcotic such as fentanyl, is probably the most widely used anesthetic agent for intracranial procedures. it has been well studied in ischemia, hypotension, and hypocapnia. isoflurane has been tried recently as a cerebroprotective agent in neurosurgical procedures. propofol is an intravenous anesthetic used for intracranial procedures. one advantage of propofol may be more reliable intraoperative ssep recordings (better signal-to-noise ratio) than with isoflurane/nitrous oxide/fentanyl. propofol was found to be more cerebroprotective than nitrous oxide/fentanyl in a rat model of incomplete cerebral ischemia. propofol also decreased brain retraction pressure during clinical neurosurgical procedures in comparison with a control anesthesia of isoflurane/nitrous oxide/fentanyl. however, it also caused a larger decrease in blood pressure, thus resulting in a reduction in cerebral perfusion pressure in the region of retraction. barbiturates have been used for intraoperative cerebral protection. knowledge of the effects of barbiturates on intraoperative electrophysiological monitoring is essential. it has been shown that intraoperative pentobarbital increases latencies in both baep and ssep. the latency increase is particularly important in interpreting the central conduction time. etomidate, an intravenous imidazole anesthetic, is a potential cerebral protection agent that has been used intraoperatively. its advantages over barbiturates include a relative lack of cardiodepression and a rapid ligia tataranu romanian neurosurgery vol. xv nr. 1 8 recovery from anesthesia, but direct comparison of the cerebroprotective effect of etomidate versus barbiturates has yet to be performed. hyperventilation, induced hypotension, and induced hypertension hyperventilation is frequently used to decrease brain volume and thus to improve exposure with minimal retraction. however, cbf decreases as well, and the net result on local cerebral perfusion pressure may be detrimental. hyperventilation causes alkalosis, which has recently been shown to be detrimental to cultured cortical neurons undergoing hypoxic or excitotoxic injury. several groups have investigated hypotension and/or hypocapnia in large animal models while monitoring various combinations of the following: brain electrical activity (eeg and/or ssep), cbf, and measures of cerebral metabolism. because many neurosurgeons have had the impression that induced hypotension is particularly detrimental in conjunction with brain retraction or temporary vessel occlusion, intraoperative-induced hypotension is probably less commonly used now than previously. induced hypertension as a cerebroprotective measure during temporary vessel occlusion in aneurysm surgery has recently been advocated. hypothermia the cerebroprotective effects of hypothermia have been utilized in two ways: deep hypothermia for cardiopulmonary bypass and circulatory standstill (20°c), and mild hypothermia (32°c). deep hypothermia requires cannulation of the femoral vessels and extracorporeal circulation and runs a significant risk of coagulopathy. for certain extremely difficult aneurysms, however, it may represent the only feasible way of obtaining sufficient exposure. mild hypothermia represents a compromise that may prove to be of considerable benefit in many cases. although the cooling and warming protocols place a burden on operating room personnel, and recovery and extubation may be delayed an hour or two, mild hypothermia has fewer complications than deep hypothermia. the magnitude of the cerebroprotective benefit of mild hypothermia is probably substantial, but its role in relationship to other intraoperative cerebroprotective interventions remains to be established (105). corticosteroids although corticosteroids are commonly used perioperatively in neurosurgical procedures involving brain retraction, particularly in patients with preoperative cerebral edema, there is no conclusive evidence that corticosteroids are cerebroprotective against focal brain ischemia. mannitol mannitol has many potentially beneficial effects during brain retraction: improved blood flow in the microcirculation; 2) free radical scavenging; and 3) decreased brain water content or edema. mannitol has been shown to improve cbf and ph in regions of moderate ischemia, as well as regulating viscosity. however, mannitol leads to significant, acute changes when administered in high doses, including hyponatremia, decreased hematocrit, and increased osmolality. other detrimental effects include hypotension, acidosis, and hyperkalemia. thus, mannitol may be more cerebroprotective during brain surgery if it is administered in frequent, small doses (0.5 g/kg/h) or by a low-dose continuous infusion, rather than a bolus administration every 4 to 6 hours. nimodipine the dihydropyridine calcium channel blocker, nimodipine, has been tried as a prophylaxis for cerebral ischemia caused by cerebral vasospasm after a subarachnoid hemorrhage and as a treatment for acute stroke. nimodipine has undergone numerous trials in cerebral ischemia models; one frequent (but not universal) finding being that it usually elicits an increase in cbf during both the ischemic phase and the delayed hypoperfusion phase. nimodipine has multiple, potentially beneficial effects for brain retraction ischemia: cerebral vasodilatation, amelioration of k+induced vasoconstriction, antagonism of calcium entry into neurons via the l-channel, anticonvulsant properties, and reduction of acidosis. although the data on nimodipine's effect on cbf with changes in pco2 (hyperventilation) are inconclusive, there are data to support the use of nimodipine for its cerebroprotective effect in the alkalosis induced by hyperventilation. neuroprotection against surgically induced brain injury romanian neurosurgery vol. xv nr. 1 9 the effects were investigated on animal models of mannitol plus nimodipine on cerebral blood flow (cbf) and evoked potentials (ep) ipsilateral and contralateral to brain retraction, in comparison with either agent alone, during both normoventilation and hyperventilation. intravenous mannitol (2 g/kg over 15 min) and/or nimodipine (1 microgram/kg/min constant infusion) was administrate. mannitol plus nimodipine was superior both to controls and to either mannitol alone or nimodipine alone in preserving ep amplitude ipsilateral to retraction during both normoventilation and hyperventilation. mannitol alone was effective in normoventilation at preserving ep, while nimodipine alone was effective in hyperventilation. no significant asymmetries in cbf or ep were seen with mannitol plus nimodipine in either normoventilation or hyperventilation. by five minutes post retraction cbf had returned to pre retraction values for all groups, and ep amplitude had returned also except for hyperventilated controls. dextromethorphan, a noncompetitive n-methyl-daspartate receptor antagonist, has been shown to be effective in small animal models of cerebral ischemia. like nimodipine, dextromethorphan appears to be particularly effective in focal ischemia and may result in improved cbf in ischemic regions. because of its efficacy in excitotoxic injury, dextromethorphan is currently under investigation in acute stroke patients and may offer intraoperative cerebral protection in addition to that offered by nimodipine. dextromethorphan is an n-methyl-d-aspartate receptor antagonist with the advantages of safety and easy administration in humans. tromethamine, a weak base buffering agent, has been shown to be efficacious during prolonged hyperventilation, such as in the treatment of severe head injury. in experimental brain injury, it improves brain energy status (phosphocreatine to inorganic phosphate ratio), brain edema, and acidosis (in blood and probably brain as well). tromethamine has been shown recently to ameliorate lactate acidosis after focal brain injury (128). tromethamine may prove to be efficacious in conjunction with hyperventilation during neurosurgical procedures requiring lengthy brain retraction. tirilazad mesylate is a 21-aminosteroid antioxidant that appears to reduce tissue necrosis in ischemia with reperfusion, probably by decreasing free radical production. it is not clear whether tirilazad mesylate improves cbf in ischemia. tirilazad mesylate is undergoing trials in acute ischemic stroke and in subarachnoid hemorrhage and may prove advantageous for intraoperative use. molecular pathways provide future protective measures besides proving a good anatomical base for sham surgeries, animal models also allow studying the cellular signaling mechanisms by performing molecular techniques on the affected brain tissue. delineating the signaling pathways will elucidate the key molecular targets for potential neuroprotection against surgically induced brain injury. inhibition of src tyrosine kinase preliminary experiments using inhibitors of key molecular targets, such as src tyrosine kinase, have yielded very promising results. src acts as a common signaling mediator involved in a broad spectrum of physiological responses, including gene transcription, adhesion regulation, and cell differentiation and survival [17]. recent studies have shown that src is activated by signals that increase intracellular ca2+ concentration and that src serves as a signaling protein for pathological mechanisms of neuronal degenerative disease, including ischemia and seizure. in vitro kinase assays have shown the ischemia/reperfusion-induced activation of src [17], and it have been shown by immunoblotting with antibody against tyr416 phosphorylated src, that tyr416 phosphorylation of src is increased in the rat hippocampus following transient forebrain ischemia. these results, confirmed by the in vivo models, suggest that src signaling is involved in microglial activation in response to ischemic injury. pp1 is a selective inhibitor for src tyrosine kinase [18], which is an upstream regulator of mapks. src tyrosine kinase and the ubiquitous mapks are well implicated in brain injury resulting from different causes such as cerebral ischemia, trauma, and hemorrhage [19, 20] and have an important role in cerebral edema ligia tataranu romanian neurosurgery vol. xv nr. 1 10 [19, 21]. inhibition of src tyrosine kinase with pp1 reduces the expression of vegf, protects the bbb, and reduces brain edema immediately after subarachnoid hemorrhage [22]; it also offers cerebral protection against stroke by influencing the vegfmediated vascular permeability and cerebral edema [18]. treatment with pp1 was associated with decreased edema, decreased breakdown of the bbb, decreased expression of both vascular endothelial growth factor and phosphorylated extracellular signalregulated kinase 1 and 2, and preservation of zo-1 expression. erythropoietin erythropoietin was administered (5000 u/kg) intraperitoneally to a rat animal model on the day before surgery, the day of surgery, and for two postoperative days. epo did not improve histological, immunohistochemical, or magnetic resonance imaging outcomes. the absence of epo-related neuroprotection in this study was somewhat surprising, given the multitude of other models in which epo functions as a neuroprotectant. it is possible that alternate administration methods, such as direct, intracavity epo treatment, may result in improved antiapoptotic outcomes. we conclude that tissue injury in surgery brain injuries involves bbb breakdown, edema, and apoptosis. pretreatment with erythropoietin does not improve outcomes in this model, and may increase brain edema early after surgery. 17β-estradiol pretreatment with 17β-estradiol reduces the size of acute (after 4 h) glutamate-mediated lesion by almost 47%. the pre-treatment with high doses of estradiol activates the production of lactate that has been shown to occur after cortical application of glutamate [23], suggesting that lactate may be an important effector of 17β-estradiol. although for many years lactate has been considered as a major detrimental factor in ischemic brain damage, many studies now suggest that lactate, produced by glycolysis mainly in glial cells during an anaerobic period, becomes the obligatory substrate for aerobic energy metab-olism, in particular upon reoxygenation [24]. glutamate uptake into astrocytes is conducted by specific glutamate transporters [25] and has been shown to stimulate aerobic glycolysis inducing glucose utilisation and lactate production in vitro [26] and in vivo. lactate is an efficient energy substrate for neurons and can fully substitute for glucose for oxidative metabolism [24]. lactate produced in astrocytes and released in the ecf does not readily diffuse through membranes and therefore must be transported across them by monocarboxylate transporters, mct1 and mct2. the blockage of neuronal mtcs with 4-cin abolished the neuroprotective effect of 17β-estradiol by preventing lactate uptake into neurons. lactate accumulates in extracellular space and can not be used as an energy supply therefore a large lesion is obtained that reflects the lack of energy for neurons in the penumbra. higher concentration of lactate observed after 17βestradiol pre-treatment provides neurons with enough energy to survive after glutamate overstimulation. this increase in glutamate-stimulated lactate production may lead to neuroprotection as illustrated by the reduction of the volume of the lesion. the abolition of lactate production observed after 120 min in the presence of the anti-estrogen tamoxifen suggests that the enhancement of glutamate-driven production of lactate by 17β-estradiol is dependent on the estrogen receptors matrix metalloproteinase inhibition this study describes the neuroprotective effects of mmp inhibitor-1 by preservation of bbb and attenuation of brain edema after sbi. on a rodent model of sbi, localized edema was observed in the brain tissue bordering the surgical injury after a disruption of bbb. the increase in bbb permeability, evaluated by igg staining and mri studies, was localized to the brain tissue surrounding the sbi, which compared well with the localized brain edema (ipsilateral frontal lobe). increased mmp-9 and mmp-2 enzyme activities were seen in the brain tissue surrounding the sbi at time points corresponding to maximal brain edema. mmp-2 enzyme activity, although significant, was only mildly increased after surgical injury. immunohistochemical evidence further suggested that the mmp-9, but not mmp-2 expression, increases in neurons and the recruited neutrophils in the brain tissue adjoining the sbi. neutrophils have been implicated as a major cellular source of mmp-9 neuroprotection against surgically induced brain injury romanian neurosurgery vol. xv nr. 1 11 after brain injury [27]. mmp-9 promotes bbb breakdown secondary to micro vascular lamina proteolysis leading to edema formation after brain injuries [1, 28]. thus, increased mmp activity, especially that of mmp-9, could produce bbb disruption and lead to brain edema after sbi. inhibition of mmp-9 and mmp-2 enzymatic activity in the affected brain resulted in reduced brain edema and preservation of bbb. mri studies further supported a neuroprotective role for mmp inhibitors as early as 3 hours after sbi. although t2-weighted imaging showed accelerated edema formation at 3 hours after treatment, the contrast-enhanced t1-weighted imaging showed beneficial effects of mmp inhibitor-1 on bbb permeability, which translated into attenuation of brain edema at later stages. previously, it was thought that vascular engorgement or cerebral blood volume contributes to brain swelling after brain injury. however, recent clinical studies have shown that brain edema contributes to the brain swelling [29]. brain water content is a good indicator of brain swelling resulting from the edema. a 1% increase in brain water content is equivalent to a 4.3% increase in tissue volume, which can cause raised intracranial pressure. present findings show significant early neurological deficits over days 1 to 3, which resolve over 1 to 2 weeks, paralleling the natural resolution of brain edema. in the untreated animals, mmp-9 activity persisted through day 3 after sbi even though the neurological deficits seemed to improve with natural resolution of brain edema. this persistent mmp9 activity may likely be due to inflammatory changes after sbi. the mmp-9 levels, however, were reduced in mmp inhibitor-1-treated animals, suggesting that mmp9 inhibition can decrease brain edema. mmp inhibitor treatment regimens decreased brain edema and bbb permeability. however, they did not show a significant difference in neurological scores between different groups. mmp inhibitor-1 has promise as a neuroprotectant by preserving the bbb and attenuating brain edema. this effect of mmp inhibitor-1 is mechanistically distinct from agents in current clinical practice, including osmotic agents, diuretics, and steroids. drugs that are neuroprotective in this model such as mmp inhibitor-1 may enable more aggressive surgical approaches, aid with surgery in anatomically confined regions of the cranial vault, and ultimately provide a greater margin of safety for patients. conclusion brain surgery is associated inevitable with a degree a brain injury, due to retraction, focal ischemia, hemorrhage or electrocoagulation. all these contribute to postoperatively complications or prolonged hospitalization periods. therefore it is recommended for new complete protocols, combining surgical technical procedures, anesthesiology agents and modalities, and lately, involvement with molecular pathways associated to brain injury. references 1.solaroglu i, b.e., kaptanoglu e, okutan o, ak f, taskin y. , transcortical-transventricular approach in colloid cysts of the third ventricle: surgical experience with 26 cases. neurosurg rev, 2004. 27: p. 89-92. 2.andrews rj, m.r., retraction brain ischaemia: cerebral blood flow, evoked potentials, hypotension and hyperventilation in a new animal model. neurol res, 1992. 14: p. 12-28. 3.hernesniemi j, l.s., management outcome in third ventricular colloid cysts in a defined population: a series of 40 patients treated mainly by transcallosal microsurgery. . surg neurol 1996. 45: p. 2 14. 4.hellwig d, b.h., bauer bl, tirakotai w. , pontine hemorrhage. j neurosurg, 2003. 99: p. 796-7. 5.decq p, l.g.c., brugieres p, djindjian m, silva d, keravel y, melon e, nguyen jp. , endoscopic management of colloid cysts. neurosurgery 1998. 42 p. 128894. 6.freudenstein d, w.a., ernemann u, duffner f. , subdural hygroma as a complication of endoscopic neurosurgery—two case reports. neurol med chir, 2002. 42: p. 5549. 7.schroeder hw, n.w., gaab mr. , complications of endoscopic third ventriculostomy. j neurosurg, 2002. 96: p. 103240. 8.menon d, critical care medicine: management of raised intracranial pressure. 4th ed. oxford textbook of medicine, ed. c.t. warrell da, firth jd. vol. 2. 2000, newyork: oxford university press. 9.kawaguchi m, f.h., patel pm. , neuroprotective effects of anesthetic agents. j anesth, 2005. 19: p. 1506. 10.sanders rd, m.d., maze m. , anaesthesia induced neuroprotection. best pract res clin anaesthesiol, 2005. 19: p. 461 74. 11.baughman vl, brain protection during neurosurgery. anesthesiol clin north america, 2002. 20: p. 315-27. ligia tataranu romanian neurosurgery vol. xv nr. 1 12 12.wagner kr, z.m., local brain hypothermia for neuroprotection in stroke treatment and aneurysm repair. neurol res, 2005. 27: p. 23845. 13.fasano va, p.g., postoperative complications in neurosurgery. minerva anestesiol 1992. 58: p. 1521. 14.manninen ph, r.s., boyle k, el beheiry h. , early postoperative complications following neurosurgical procedures. can j anaesth, 1999. 46: p. 7 14. 15.deletis v, s.f., the role of intraoperative neurophysiology in the protection or documentation of surgically induced injury to the spinal cord. ann ny acad sci 2001. 939: p. 13744. 16.dawson tm., preconditioning-mediated neuroprotection through erythropoietin? lancet 2002. 359: p. 96-7. 17.jadhav v, m.g., hsu fp, zhang jh., inhibition of src tyrosine kinase and effect on outcomes in a new in vivo model of surgically induced brain injury. j neurosurg, 2007 106: p. 680-6. 18.paul r, z.z., eliceiri bp, jiang q, boccia ad, zhang rl, chopp m, cheresh da., src deficiency or blockade of src activity in mice provides cerebral protection following stroke. nat med, 2001. 7: p. 222 7. 19.kitagawa h, w.h., sasaki c, zhang wr, sakai k, shiro y, mitsumoto y, mori t, abe k., immunoreactive akt, pi3-k and erk protein kinase expression in ischemic rat brain. neurosci lett, 1999. 274: p. 458. 20.nozaki k, n.m., hashimoto n., mitogen-activated protein kinases and cerebral ischemia. mol neurobiol, 2001. 23: p. 1 19. 21.mori t, w.x., aoki t, lo eh. , downregulation of matrix metalloproteinase-9 and attenuation of edema via inhibition of erk mitogen activated protein kinase in traumatic brain injury. j neurotrauma, 2002. 19: p. 1411 9. 22.kusaka g, k.h., kusaka i, perkins e, nanda a, zhang jh. , contribution of src tyrosine kinase to cerebral vasospasm after subarachnoid hemorrhage. j neurosurg, 2003. 99: p. 38390. 23.alessandri b., h.l., h. langemann, j. gregorin, j. hall, o. gratzl, application of glutamate in the cortex of rats: a microdialysis study. acta neurochir. suppl. (wien), 1996. 67: p. 6–12. 24.schurr a, r.s.p., j.j. miller, b.m. rigor,, brain lactate is an obligatory aerobic energy substrate for functional recovery after hypoxia: further in vitro validation. j. neurochem, 1997. 69 p. 423– 426. 25.debernardi r., p.j.m., l. pellerin, , trans-inhibition of glutamate transport prevents excitatory amino acidinduced gly colysis in astrocytes. brain res. , 1999. 850 p. 39–46. 26.pellerin l., p.j.m., excitatory amino acids stimulate aerobic glycolysis in astrocytes via an activation of the na1/k1 atpase. dev. neurosci 1996. 18: p. 336–342. 27.justicia c, p.j., sole s, cervera a, deulofeu r, chamorro a, planas am: , neutrophil infiltration increases matrix metalloproteinase-9 in the ischemic brain after occlusion/reperfusion of the middle cerebral artery in rats. j cereb blood flow metab, 2003. 23: p. 1430–1440. 28.abilleira s, m.j., molina ca, monasterio j, castillo j, alvarezsabin j, matrix metalloproteinase-9 concentration after spontaneous intracerebral hemorrhage. j neurosurg, 2003. 99. 29.matchett g, h.j., obenaus a, zhang j., surgically induced brain injury in rats: the effect of erythropoietin. j neurosci methods, 2006 158: p. 234-41. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0055 article a comparative study of endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery at tertiary care centre in india anurag sahu, sharad pandey, kulwant singh, vivek sharma india      romanian neurosurgery (2018) xxxii 3: 443 457 | 443             doi: 10.2478/romneu-2018-0055 a comparative study of endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery at tertiary care centre in india anurag sahu1, sharad pandey2, kulwant singh1, vivek sharma1 1department of neurosurgery, sir sunder lal hospital, ims, bhu, varanasi, india 2department of neurosurgery, p.g.i.m.e.r. dr. ram manohar lohia hospital, new delhi, india abstract: introduction: the transsphenoidal route for pituitary surgery is considered the standard treatment for pituitary adenomas. the disadvantage of the smaller exposure of this route is partially compensated for by the introduction of the microscope with its coaxial illumination, stereoscopic view, adequate magnification, and microsurgical instruments. however, there are only few reports about the outcome of endonasal endoscopic transphenoidal technique. aims & objectives: current study has been conducted to compare the efficacy, advantages and dis advantages of endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery. material and methods: a controlled study was done in the department of neurosurgery, at tertiary care hospital in india, from the period of august 2012 to december 2017 prospectively. in group a 30 patients in whom endoscopic transnasal trans sphenoidal pituitary surgery and in group b 30 patients, intraoperative neuronavigation was used. observations and results: both the groups were similar in demographic variables. the most common age group of pituitary tumor patients was 30-40 years. fourteen (46.6 %) patients in group a and fifteen (50 %) of the patients in group b had tumor volume less than 5 ml. in group a, thirteen (43%) patients had intrasellar tumors with no suprasellar extension, while in group b, fifteen (50%) patients had intrasellar tumors with no extension. operative time was noted from incision to closure and average time taken in both the groups was compared. twenty five (83%) cases of group a took between 2-3 hours and only four cases (13%) took more than 3 hours. while in group b, twenty (66%) cases took between 4-5 hours. this shows a significant difference by fisher extact test (p<0.001) in the operative time required in both the groups. eighteen (60%) patients in group b had a residual volume between 1-1.5 ml while only two patients in group a had so. this difference is also significant fischer exact test (p<0.001). four (13.3%) patients in group a had diabites insipidus while only half of this, i.e. two (6.6%) had so in group b. however 444 | sahu et al endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery             this difference in postoperative complication rate is not statistically significant between two groups. conclusion: the results of our study correlate with many previous studies to compare endoscopic and microscopic transsphenoidal surgery. these two approaches are equally efficacious in oncological outcomes and the complication rates are comparable. key words: endoscopic transphenoidal, navigation guided, pituitary surgery introduction the transsphenoidal route for pituitary surgery, via either sublabial or septal incisions, is now considered the standard treatment for pituitary adenomas [13]. its main advantage lies in its safety. the midline access avoids injury to the internal carotid artery and optic nerves. in contrast to the transfrontal approach, the use of the transsphenoidal technique minimizes the risk of brain trauma, with the resultant short and uncomplicated postoperative course. the disadvantage of the smaller exposure of this route is partially compensated for by the introduction of the microscope with its coaxial illumination, stereoscopic view, adequate magnification, and microsurgical instruments. except for the use of the operating microscope, the transsphenoidal approach advocated and popularized by hardy [13], has changed little over the years. resection of the pituitary tumor is then performed under microscopic magnification and intraoperative fluoroscopic imaging [5]. the visualization provided by the operating microscope is also limited by the optical properties of the lens and light source. the success of endoscopic paranasal sinus surgery has aroused the interest in the use of endoscopes during pituitary surgery [5]. other investigators used the direct endonasal endoscopic transphenoidal technique [5, 4, 3, 29]. however, there are only few reports about the outcome of this technique. aims & objectives current study has been conducted to compare the efficacy, advantages and dis advantages of endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery. material & methods a controlled study was done in the department of neurosurgery, at tertiary care hospital in india, from the period of august 2012 to december 2017 prospectively. during this period a total number of 60 patients were enrolled in the study. radiological support was provided by department of radio diagnosis at the institute. the inclusion criteria for the study were as follows: 1. mri/ct proven pituitary macroadenoma cases 2. cases of pituitary microadenoma in which medical treatment has failed and have been planned for surgery. all the patients were admitted in the neurosurgery wards. appropriate consent was taken from all the patients. the patients were randomly divided in two groups: 1. group a 30 patients in whom endoscopic transnasal trans sphenoidal pituitary surgery was done. romanian neurosurgery (2018) xxxii 3: 443 457 | 445             2. group b 30 patients, in whom intraoperative neuronavigation was used for localization of sphenoid sinus and sella turcica during transsphenoidal surgery for removal of pituitary tumor. pre-operative ct/mri was done to assess tumor size, different anatomical variations of sinus (degree of pneumatization, sellar configuration and substation pattern) and intercarotid distance. in group a, pre-operative endoscopic and imaging evaluation of paranasal sinuses and position of nasal septum were noted. in group b, contrast enhanced ct scan of the patients was taken in neuronavigation protocol one day prior to surgery. the data was stored in nr cd/dvd in dicom format and was loaded on treon plus stealth station medtronic. postoperatively, all the patients were shifted to neurosurgical icu for elective ventilation. they were extubated in the next morning. a postoperative ct scan (plain and contrast enhanced) of head was done for assessment of residual tumor volume / hematoma in all patients. endonasal packing was removed after 48 hours and patients were allowed orally. patients were followed up in the postoperative period for any complication. patients were discharged after removal of abdominal stitches on seventh post-operative day. patients were called for follow-up after 2 weeks. results and discussion the present study was done in the department of neurosurgery, from the period of august 2012 to december 2017 prospectively. demographic characteristics of all patients like age, gender, tumor volume and suprasellar extension of tumor were noted as on table 1. both the groups were similar in demographic variables as shown in the table. the most common age group of pituitary tumor patients was 30-40 years. there is no significant sex predilection in patients of pituitary tumors. fourteen (46.6 %) patients in group a and fifteen (50 %) of the patients in group b had tumor volume less than 5 ml. in group a, thirteen (43%) patients had intrasellar tumors with no suprasellar extension, while in group b, fifteen (50%) patients had intrasellar tumors with no extension. none of the patient in both the groups had intradural or extradural extension into cavernous sinus. clinical presentation and operative and postoperative findings of patients were noted as in table 2. eleven (36 %) patients in group a and fourteen (46 %) patients in group b presented to the opd with endocrine syndromes due to hypersecretory tumors. most common were prolactinomas followed by growth hormone related symptoms. operative time was noted from incision to closure and average time taken in both the groups was compared. twenty five (83%) cases of group a took between 2-3 hours and only four cases (13%) took more than 3 hours. while in group b, twenty (66%) cases took between 4-5 hours. only two (7 %) cases could be completed in less than 4 hours and eight (26%) cases even took beyond 5 hours. this shows a significant difference by fisher extact test (p<0.001) in the operative time required in both the groups. 446 | sahu et al endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery             table 1 demographic characteristics of patients group a (n=30) group b (n=30) sex male 13 15 female 17 15 age group 10-20 yrs 1 1 20-30 yrs 5 6 30-40 yrs 21 20 40-50 yrs 3 3 tumor volume (ml) <5 14 15 5-10 11 10 10-15 4 3 15-20 1 2 suprasellar extension absent 13 15 suprasellar extension present 17 15 a. expanding into suprasellar cistern 11 9 b. obliteration of anterior recess of third ventricle 5 4 c. gross displacement of floor of third ventricle 1 2 d. intradural/ intracranial extension 0 0 extradural extension(into or beneath cavernous sinus) 0 0   romanian neurosurgery (2018) xxxii 3: 443 457 | 447             table 2 clinical presentation and operative and post-operative findings of patients clinical presentation group a group b endocrine syndromes 11 14 prolactin 6 5 growth hormone 4 8 acth 1 1 mass effect 17 15 pituitary apoplexy 2 1 operative time group a group b p<0.001 up to 2 hours 1 0 2-3 hours 25 0 3-4 hours 4 2 4-5 hours 0 20 >5 hours 0 8 intra operative complication group a group b p<0.001 hemorrhage <100ml 25 5 >100ml 5 25 csf leak 6 4 p<0.217 residual tumor volume (ml) group a group b p<0.001 0-0.5 20 3 0.5-1.0 8 4 1.0-1.5 2 18 1.5-2.0 0 3 >2.0 0 2 post-operative complications group a group b p=0.176 diabitis insipidus (transient) 4 2 csf rhinorrhea 3 3 meningitis 0 3 vision loss 0 2 sinusitis 1 3 448 | sahu et al endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery             figure 1 imaging studies. a: coronal computer tomography (ct) image showing the sphenoid sinus. b: coronal magnetic resonance imaging (mri) showing the relationship between the pituitary tumor, the internal carotid arteries and the sphenoid sinus. c: axial mri to evaluate the lateral extension of the tumor and any involvement of the cavernous sinus. d: sagittal mri romanian neurosurgery (2018) xxxii 3: 443 457 | 449             figure 2 patient’s head fixed on sugita head clamp with reference frame attached on supporting arm figure 3 photograph showing navigation probe in midline at the floor of sphenoid sinus 450 | sahu et al endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery             endonasal endoscopic view with 00 endoscope right nostril with choana and turbinate tumor removal & examination of sella repair of the sellar floor with abdominal fat & fibrin glue pre-operative mri images coronal & sagittal sections showing pituitary macroadenoma romanian neurosurgery (2018) xxxii 3: 443 457 | 451             post-operative ct scan images coronal & sagittal sections showing complete tumor resection with enhancing normal pituitary 1 2 452 | sahu et al endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery             1 2 pre (1) & post (2) operative mri images (sagittal & coronal sections) of endoscopically operated pituitary macroadenoma intraoperative blood loss amounting to <100 ml was noted in twenty five (83%) patients of group a while blood loss of >100 ml was seen in twenty five (83%) patients of group b. the p value comes out to be less than 0.001. the major reason behind this difference could be attributed to the prolonged surgery in group b patients. another major complication, i.e. csf leak was seen in six (20%) case in group a while in four (13.3%) cases in group b. maximum patients in group a, i.e. twenty (66.67%) had residual tumor volume of less than 0.5 ml while only three (10%) patients in group b had so. eighteen (60%) patients in group b had a residual volume between 1-1.5 ml while only two patients in group a had so. this difference is also significant fischer exact test (p<0.001). as we can see from this table, four (13.3%) patients in group a had diabites insipidus while only half of this, i.e. two (6.6%) had so in group b. postoperative csf rhinorrhea was seen in an equal number of patients (10%). sinusitis was more common in group b (10% vs 3%).vision loss was present in two (6.67%) cases in group b while none in group a. however this difference in postoperative complication rate is not statistically significant between two groups. pituitary tumors are most commonly approached through the transsphenoidal corridor, and tumor resection is most often performed using the operating microscope. more recently the endoscope has been introduced for use either as an adjunct to or in lieu of the microscope. almost from the outset, the transsphenoidal approach has been minimally invasive. the earliest transsphenoidal surgeries (1907-1909) by schloffer, van elsberg [26], required external rhinotomy incisions. endonasal and sublabial approaches were introduced in 1910 by hirsch and halstead [14], respectively. image guidance in pituitary surgery began with the use of intraoperative air encephalography and c-arm video fluoroscopy, and continues to expand with the romanian neurosurgery (2018) xxxii 3: 443 457 | 453             addition of newer techniques such as intraoperative ultrasound, computer-based neuronavigation, intraoperative mri, and endoscopic assisted surgery [16-20]. jankowski et al. [15] were the first to bring their application to access of the pituitary in 1992. endoscopic transsphenoidal approach was popularized in the late 1990s by jho and carrau [16] from the university of pittsburgh medical center. advances in endoscopic endonasal neurosurgical techniques at pittsburgh continue in the work of kassam, et al. [21], and carrau [17], who have expanded the scope of complex skull base tumors accessible by the endoscope. in europe the neurosurgical groups of cappabianca and de divitiis [8] and frank, et al. [11], have also made important contributions in heralding a new era in contemporary endoscopic pituitary surgery. several authors have discussed the potential outcome of the endoscopic technique. deklotz et al.[9] used a metaanalysis to reveal the superior rate of gtr (79% versus 65%, p < 0.0001) as well as the lower rates of csf leak (5% versus 7%, p < 0.01), septal perforation (0% versus 5%) and post-operative epistaxis (1% versus 4%, p < 0.0001) for the endoscopic approach compared with the sublabial approach. rotenberg et al. [25] concluded that the two approaches had similar outcomes (gtr, hormonal abnormality resolution) but that the endoscopic approach was associated with fewer complications as well as a shorter hospital stay and length of operation. goudakos et al. [12] demonstrated that the rates of gtr/csf leakage were similar between the two techniques. however, the study also revealed a lower incidence of postoperative di and a shorter hospital stay in the studied endoscopic groups. other systematic reviews also support the safety and short-term efficacy of endoscopic pituitary surgery [4,16]. interestingly, ammirati et al. [2] recently reported a meta-analysis concluding that endoscopic removal of pituitary adenoma, in the short term, does not seem to confer any advantage over the microscopic technique and the incidence of vascular complication was higher with endoscopic than with microscopic removal of pituitary adenomas. the current study compared the endonasal endoscopic and neuronavigation guided microscopic transsphenoidal pituitary surgery for pituitary tumors. in this study we compared tumor remission, intraoperative and immediate postoperative complications among the most widely used methods of endoscopic and neuronavigation assisted microscopic transsphenoidal pituitary surgery. all patients in both groups underwent transsphenoidal removal of pituitary adenomas, using identical surgical techniques with an operating microscope. in our study, we had 30 patients in group a (endoscopic) and 30 patients in group b (navigation guided microscopic). both these groups had a similar distribution of patients according to age, sex, tumor volume, tumor spread and their clinical presentation. so all these above mentioned criteria presented no confounding factors in our study. outcomes of transsphenoidal pituitary surgery were measured along several parameters, first and foremost of which were complications related to surgery. mortality rates of transsphenoidal 454 | sahu et al endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery             surgeries are low, generally occurring at a rate of less than 1% [22,23,6,7]. there was no mortality in our study. the first significant difference noted in our study was the average duration of surgery from incision to closure in both the techniques. the total operating room time includes the time required for the initial set up of the navigation machine and tracer registration along with the actual surgical time (incision to closure). the average time required for surgery was 3-4 hrs in the neuronavigation group. the total operating time in endoscopic group was initially about 4-5 hours, later it was 2–3 hours as the endoscopic expertise increased. the complications heralded by the prolonged surgery are thus obvious. it leads to increased morbidity due to prolonged exposure to anesthesia, & more blood loss. the shortened duration of procedure in group a is due to the easy and accurate localization of the sella turcica and sphenoid sinus which facilitates tumor removal. the surgical time for only four patients in group a was more than 3 hours. the initial three cases in which initial lack of endoscopic skill and intra operative bleeding increased surgical time. in group b intra operative ct registration and neuronavigation, and use of microscope increased the operative time significantly. the time-effectiveness of intraoperative ct registration and electromagnetic neuronavigation in transsphenoidal pituitary surgery was also assessed by eboly, shafa et al. they concluded that the use of ict/mr imaging-guided neuronavigation for microscopic transsphenoidal surgery is a time-effective, cost-efficient, safe, and technically beneficial technique [10]. in our study increased incidence of csf leak seen in group a could be the result of overenthusiastic resection for tumor removal because of better visualization. this should be discouraged. with an incidence of postoperative csf leak of 20% our endoscopic series shows slightly higher csf leak as most of which occurred during initial few endoscopic procedures. other systematic review by rotenberg [1] found a mean incidence of 14.3% and the meta-analysis of ammirati [2], evaluated it to be 7.0% (4.84 to 9.52%). in our study there was a significant difference noted in the amount of intraoperative blood loss as estimated by the amount collected in suction bottle. in our study there was a significant difference noted in the amount of intraoperative blood loss as estimated by the amount collected in suction bottle. this significant difference however was not due to any major hemorrhage which took place during surgery rather it was seen due to the continuous oozing of blood from the mucous membrane during the procedure which is more with the endoscopic surgery. patel, youssef et al concluded that computer guided endonasal transsphenoidal surgery provides a three-dimensional image to the surgeon, allowing for greater visual accuracy and surgical precision and a faster procedure without radiation exposure or the need for additional personnel [24,28]. we determined the presence and volume of residual tumor by a ct scan postoperatively. the residual tumor volume in romanian neurosurgery (2018) xxxii 3: 443 457 | 455             66.6% patients of group a was 0-0.5 ml while it was 1-1.5 ml in 60% of patients in group b. none of the group a cases had residual tumor volume more than 1.5 ml while five patients in group b had so we believe these improved outcomes are the result of superior illumination, visualization and angled view provided by the endoscope. we followed the patients in our study during their postoperative hospital stay and further on follow-up after two weeks. the significant difference in the postoperative complication rate further stresses upon the need of increased accuracy of tumor removal and minimal damage to the nearby structures during surgery. the accuracy of a surgeon's localization of sellar margins during transsphenoidal surgery for pituitary adenomas using a neuronavigational system was also studied by wang and thiryayi et al in 2011 and they established that the margin of error increases for giant adenomas, with greater invasiveness and parasellar spread, and the use of neuronavigation can be especially useful in such cases [27]. clinical application of a neuronavigation system in transsphenoidal surgery of pituitary macroadenoma was also studied by zhao, yu et al in 2006 [30,31] and found that the neuronavigation system is quite helpful for transsphenoidal surgery of pituitary macroadenoma. its accuracy of location is very useful and important in determining anatomical structure and protecting normal tissues and vessels. conclusion the results of our study correlate with many previous studies to compare endoscopic and microscopic transsphenoidal surgery. we have focused solely on transsphenoidal pituitary surgery though some previous researchers have advocated the use of ct/mri based neuronavigation in variety of other neurosurgical procedures also as also the use of endoscope in skull base surgery. the panoramic view afforded by the endoscope is unparalleled as compared with the traditional conical view of the microscope. this technique has been shown to have a statistically significant reduction in operative time, length of hospital stay. there is also a trend toward improved endocrine outcomes and rate of return of visual defects. these two approaches are equally efficacious in oncological outcomes and the complication rates are comparable. with longer follow-up of this developing field it may be shown that complication rates are decreased, surgical reconstruction is less time consuming, and tumor resection is more complete due to improved visualization in the sellar and parasellar areas. in addition, the use of endoscopes facilitates extended approaches, reaching a myriad of skull base lesions that are suprasellar, retrosellar, and parasellar, which permits visualization beyond the abilities of the microscope. correspondence sharad pandey department of neurosurgery, p.g.i.m.e.r. dr ram manohar lohia hospital, new delhi 110001, india drsharad23@yahoo.com mobile no: 9454939067   456 | sahu et al endoscopic versus navigation guided microscopic transsphenoidal pituitary surgery             references 1. ahmadi h, larsson em, jinkins jr: normal pituitary gland: coronal mr imaging of infundibular tilt. radiology 177:389-392, 1990. 2. ammirati m, wei l, ciric i: short-term outcome of endoscopic versus microscopic pituitary adenoma surgery: a systematic review and meta-analysis. j neurol neurosurg psychiatry 2013, 84:843-849. 3. black pm, zervas nt, candia gl. incidence and management of complications of transsphenoidal operation for pituitary adenomas. neurosurgery. 1987 jun;20(6):920-4 4. cappabianca p, cavallo lm, de divitiis e. endoscopic endonasal transsphenoidal surgery. neurosurgery 2004; 55:933–941. 5. carrau rl, jho hd, ko y. transnasal-transsphenoidal endoscopic surgery of the pituitary gland. laryngoscope 1996;106:914–918. 6. ciric i, ragin a, baumgartner c, pierce d. complications of transsphenoidal sur¬gery: results of a national survey, review of the literature, and personal experience. neurosurgery. 1997 feb;40(2):225–36. 7. cooke rs, jones rac. experience with the direct transnasal transsphenoidal approach to the pituitary fossa. br j neurosurg 1994;8:193–196. 8. de divitiis e, cavallo lm, cappabianca p, esposito f. extended endoscopic endonasal transsphenoidal approach for the removal of suprasellar tumors: part 2. neurosurgery 2007; 60:46–58. 9. de klotz tr, chia sh, lu w, makambi kh, aulisi e, deeb z: meta-analysis of endoscopic versus sublabial pituitary surgery. laryngoscope 2012, 122:511-518. 10. eboli p, shafa b, mayberg m. intraoperative computed tomography registration and electromagnetic neuronavigation for transsphenoidal pituitary surgery: accuracy and time effectiveness. j neurosurg. feb;114(2):329-35, 2011. 11. frank g, pasquini e, doglietto f, et al. the endoscopic extended transsphenoidal approach for craniopharyngiomas. neurosurgery 2006; 59:ons75o– ns83. 12. goudakos jk, markou kd, georgalas c: endoscopic versus microscopic transsphenoidal pituitary surgery: a systematic review and meta-analysis. clin otolaryngol 2011, 36:212-220. 13. hardy j. transphenoidal microsurgery of the normal and pathological pituitary. clin neurosurg. 1969;16:185– 217. 14. hirsch o: pituitary tumors. a borderland between cranial and trans-sphenoidal surgery. n engl j med 254: 937-939, 1956. 15. jankowski r, auque j. simon c, et al: endoscopic pituitary tumor surgery. laryngoscope 102:198-202, 1992. 16. jho hd, carrau rl endoscopic endonasal transsphenoidal surgery: experience with 50 patients. j neurosurg 87:44-51, 1997. 17. jho hd, carrau rl ko y: endoscopic pituitary surgery. in rengachary ss, wilkins rh (eds): neurosurgical operative atlas, vol 5. baltimore, williams & wilkins, 1996, pp 1-12. 18. jho hd, carrau rl, ko y, daly m. endoscopic pituitary surgery: an early experience. surg neurol 1997;47:213–223. 19. jho hd, carrau rl, mclaughlin ml, somaza sc. endoscopic transsphenoidal resection of a large chordoma in the posterior fossa. acta neurochir (wien) 1997;139: 343–348. 20. jho hd, carrau rl. endoscopic endonasal transsphenoidal surgery: experience with 50 patients. j neurosurg 1997;87: 44–51. 21. kassam a, horowitz m, welch w, et al. the role of endoscopic assisted microneurosurgery (image fusion technology) in the performance of neurosurgical procedures. minim invasive neurosurg 2005; 48:191– 196. 22. laws er jr, sheehan jp (eds): pituitary surgery – a modern approach. front horm res. basel, karger, , vol 34, pp 46–63, 2006. 23. laws er jr. pituitary surgery. endocrinol metab clin north am 16:647-665, 1987. 24. patel sn, youssef as, vale fl, padhya ta. reevaluation of the role of image guidance in minimally invasive pituitary surgery: benefits and outcomes. comput aided surg.; 16 (2):47-53, 2011. 25. rotenberg b, tam s, ryu wh, duggal n: microscopic versus endoscopic pituitary surgery: a systematic review. laryngoscope 2010, 120:1292-1297. 26. schloffer h. erfulgrieche operation hypophys ent tumors on nasal wege. wien klin wochenschr 1907; 20:621–624. romanian neurosurgery (2018) xxxii 3: 443 457 | 457             27. wang yy, thiryayi wa, ramaswamy r, gnanalingham kk. accuracy of surgeon's estimation of sella margins during endoscopic surgery for pituitary adenomas: verification using neuronavigation. skull base. may; 21(3):193-200, 2011. 28. winder mj, spooler a, mayberg mr. the evolution of intraoperative imaging and neuro-navigation in transsphenoidal surgery. j surg radiol. jan 1;2(1), 2011. 29. wurster cf, smith de: the endoscopic approach to the pituitary gland. arch otolaryngol head neck surg 120:674, 1994. 30. zhang y, wang z, liu y, et al. endoscopic transsphenoidal treatment of pituitary adenomas. neurol res 2008; 30:581–586. 31. zhao b, wei yk, li gl, et al. extended ranssphenoidal approach for pituitary adenomas invading the anterior cranial base, cavernous sinus, and clivus: a single-center experience with 126 consecutive cases. j neurosurg 2010; 112(1):108-117. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article anterior communicating artery aneurysm clipping versus coiling: a comparative study of 50 cases pradeep kumar, shashi k. jain, virendra d. sinha, trilochan srivastava india doi: 10.1515/romneu-2017-0060 368 | kumar et al anterior communicating artery aneurysm clipping versus coiling doi: 10.1515/romneu-2017-0060 anterior communicating artery aneurysm clipping versus coiling: a comparative study of 50 cases pradeep kumar, shashi k. jain, virendra d. sinha, trilochan srivastava sawai man singh medical college, jaipur, india abstract: introduction: aneurysmal subarachnoid hemorrhage (asah) remains a devastating and often fatal form of stroke. the aneurysm is targeted for obliteration to prevent re-bleeding and to manage the possible complications from the event. endovascular coiling has emerged as a less invasive alternative to conventional surgical clipping to treat aneurysms. patients and methods: this study was done in 50 cases of anterior communicating (acommm) aneurysm presented in the department of neurosurgery, sms medical college, jaipur from november 2015 to august 2016 to evaluate the outcome of both modalities used in the treatment of ruptured acommm aneurysm. 50 patients with hunt and hess (h&h) grade i, ii or iii were classified into two groups of microsurgical clipping and endovascular coiling. results: mortality rate was comparable in both groups that were 21. 21% in the clipping group and 23. 52% in the coiling group. good glasgow outcome score (gos) were found in 60. 60% of clipping and 58. 58% of coiling group. all the complications found to be more in clipping group but that were not statistically significant except for hyponatremia which was significantly higher in clipping group(p=0. 007). conclusion: there was no statistically significant difference in gos at 6 month of follow up between the two groups. we recommend further interventional studies with larger sample sizes and longer follow up for better evaluation of the modalities. key words: acommm aneurysm, clipping, coiling, gos introduction aneurysmal subarachnoid hemorrhage (asah) is a very disastrous and fatal emergency requiring immediate intervention as approximately 12% of patients die before receiving medical supports, 33% within 48 hours and 50% within 30 days of asah and 50% of survivors suffer from permanent disability and dependency. [1] the acommm aneurysm is the most common location of cerebral aneurysms and it accounts for about 36% of aneurysms. [2] among patients admitted to hospital in good clinical status for the treatment of ruptured acommm aneurysm, about 80% have achieved favourable outcome. [3] about 46% of romanian neurosurgery (2017) xxxi 3: 368 377 | 369 survivors after sah may have cognitive impairment. [2, 4] endovascular coiling has increasingly become an alternative procedure for surgical clipping in both ruptured and unruptured aneurysms in last few decades. [5, 6] however, there are some risks and complications such as thromboembolism, aneurysm rupture, patent artery occlusion, coil migration and vasospasm in endovascular therapy. [7] both modalities have their own advantages and disadvantages which make them as complementary rather than competitive. [6] the most prominent advantage of surgical clipping is long term durability which is controversial in endovascular coiling. long-term follow up performed by intracranial subarachnoid aneurysm trial (isat) showed that coiling had higher risk of rebleeding than clipping. [7, 8, 9] the disadvantage of surgical clipping is that it requires open surgery which is accompanied with more morbidity in elderly patients. [10] so, durability of endovascular coiling is not a major concern in the old age group of patients. [9] the advantages of endovascular coiling are less invasiveness, easy access to vertebrobasilar system and multiple aneurysms in different areas. [6] however, coiling is not useful in all aneurysms as it cannot remove intracerebral hemorrhage or mass effect of giant aneurysms. [11] this paper will evaluate the outcome of microsurgical clipping versus endovascular coiling in the treatment of 50 patients with ruptured acommm artery aneurysm performed in the department of neurosurgery, sms medical college, jaipur, india to provide the best protocol of management for this condition. patients and methods this study was done in 50 cases of acommm aneurysm presented in the department of neurosurgery, sms medical college, jaipur from november 2015 to august 2016 and an ethical clearance taken from the ethical committee of the institute(reference number 2187 mc/ec/2016). all patients were divided into two groups depending upon the therapeutic intervention performed (a) microsurgical clipping (33) (b) endovascular coiling (17) all patients included must fulfil the following inclusion criteria 1. diagnosed cases of acommm aneurysm by ct angiography or digital substraction angiography (dsa) 2. hunt and hess grade i, ii & iii exclusion criterias: 1. h &h grade iv&v 2. other than acommm aneurysm 3. multiple aneurysms all the patients were examined first by neurologist or neurosurgeon. the benefits and complication associated with both procedures were thoroughly explained to the patients and their relatives and they had a choice to choose one of the procedure. there was a proforma which was filled for all patients at the time of admission including demography, risk factors, h & h grade, characteristics of aneurysm, the procedure performed including complications and glasgow outcome scale(gos) recorded during at least 6 months of follow up after intervention. extracted data were analysed with spss 370 | kumar et al anterior communicating artery aneurysm clipping versus coiling (version22, spss inc., chicago, il, usa). chisquare, fisher exact, independent-t, paired-t and mann–whitney u tests were used and considered as statistically significant at p < 0. 050. results seventeen patients underwent endovascular coiling and thirty three patients underwent surgical clipping. there were 22 females (44%) and 28 males (56%) as shown in table 1. mean age of patients allocated to surgical treatment was 49. 75 years and mean age of patients allocated to endovascular therapy was 52. 17years (p = 0. 5080). the risk factors associated were featured in table 2. the above table 2 revealed that there was no significant difference between the two groups with regards to associated risk factors as p-values were >0. 05 although hypertension (78%), smoking(34%) and hyperlipedemia (30%) were present in asah. there were 2 (4%) patients who had no any known risk factors. the main presenting complaints of the patients were severe headache 48 (96%), focal neurological deficits 23 (46%), vertigo 12 (24%) and asymptomatic or mild headache in 2 (4%). the difference in mean h & h grade of clipping and coiling group were not statistically significant as the independent sample t test revealed that t (48) =1. 115, p=0. 271 as shown in table 3. but, mann-whitney u test reveals that there is no statistically significant difference between these two groups as p-value=0. 265 as in table 4. there were 27(54%) aneurysm present at right acommm-anterior cerebral artery (aca) complex with dome size of 3mm14mm and mean neck size of 3. 05mm in clipping and 2. 69mm in coiling group. the difference in mean neck size of clipping and coiling group was not statistically significant as the independent sample t test revealed that t (48) =0. 596, p=0. 554. therefore, there was no difference in these two groups. hypoplastic a1 branch of aca was found in 7(14%) with one bilateral p1 hypoplastic artery. only two (4%) had bilobed aneurysm. the direction of projection of fundus of aneurysm based on ct angiography or dsa coronal and saggital images was as shown in table 5. the mean duration of operation for surgical clipping was 2. 9697 hours and for endovascular coiling was 2. 1971 hours. at t (48) =6. 555, p=0. 0001, reveals that mean duration of operation was significantly higher in clipping than coiling. the mean duration of hospital stay was 10. 0741 days and 8. 2308 days in clipping and coiling group respectively. the difference in mean days of hospital stay of live patients was not statistically significant as t (38) = . 831, p=0. 411. the following complications were found in the follow up of 6 months durations as shown in table 6. as far the gos was concerned there was no significant difference between the two groups at 6 months of follow up. the patients were categorized as good outcome (grade 4 & grade 5) and poor outcome (grade 2 & grade 3) as shown in table 7. romanian neurosurgery (2017) xxxi 3: 368 377 | 371 table 1 showing sex distribution between the two groups cases total type of operation male female clip 17(51.5%) 16(48.5%) 33(100%) coil 11(64.7%) 6(35.3%) 17(100%) 28(56%) 22(44%) 50(100%) table 2 risk factors associated with acommm aneurysm risk factor clipping n(%) coiling n (%) pvalue hypertension 24 (72.7%) 10 (58.8%) 0.318 smoking 10 (30.3%) 7 (41.2%) 0.442 hyperlipedemia 9 (27.3%) 6 (35.3%) 0.558 alcohol 1 (3%) 3 (17.6%) 1.04 diabetes 1 (3%) 1 (5.9%) 1.00 cocaine 0% 1 (5.9%) 0.34 table 3 distribution of patients according to h & h grade h & h grade clip coil i 1 (2%) 1 (2%) ii 15 (30%) 9 (18%) iii 17 (34%) 7 (14%) 33 (66%) 17 (34%) table 4 group statistics according to h & h grade type of operation n mean std. deviation std. error mean h&h grade clip 33 2.4848 .56575 .09848 coil 17 2.2941 .58787 .14258 table 5 projections of acommm aneurysm fundus clip coil total(%) superior 13 5 18 (36%) anterior 8 4 12 (24%) posterior 3 6 9 (18%) inferior 5 2 7 (14%) complex 4 0 4 (8%) 33 17 50 (100%) table 6 complications associated with clipping and coiling groups complications clip coil p-value(chisquare) intraoperative rupture 1 2 0.218 vasospasm 11 3 0.242 infarct 9 4 0.775 ich/ivh 4 1 0.486 hydrocephalos 1 0 0.468 hyponatremia 11 2 0.007 cognitive impairment 10 2 0.146 death 7 4 0.520 table 7 gos at 6 months of follow up group poor gos n (%) [gos2 & 3] good gos n (%) [gos-4 & 5] clip 6 (18.18%) 20 (60.60%) coil 3 (17.64%) 10 (58.58%) 372 | kumar et al anterior communicating artery aneurysm clipping versus coiling figure 1 ct angiography shows acomm aneurysm projecting anteroinferiorly figure 2 intraoperative image showing sac of aneurysm figure 3 post operative ct angiography shows patent bilateral aca with clip in situ figure 4 dsa shows coils insitu with complete obliteration of sac with patent bilateral aca discussion this study had been done to compare the surgical clipping with endovascular coiling in treatment of asah due to ruptured acommm aneurysms in terms of risk factors, preprocedural clinical findings of the patients, the aneurysmal characteristics, procedural complications and 6 months follow up disability status based on gos. the endovascular coiling had been introduced as the brain aneurysm treatment since 1990s and approved as a relatively minimal invasive method. [7] few studies have focused on the comparison of the coiling and clipping in the treatment of disease. it is thought that about 6% of the international population harbor intracranial aneurysms with a greater prevalence in the asian and finnish populations (4–9%). [12] risk factors associated with the presence and rupture of intracranial aneurysms have included high blood pressure, smoking, hyperlipidemia, genetic and ethnic related factors. however, the prevalence of lesions is still thought to be approximately 2% in those without any known romanian neurosurgery (2017) xxxi 3: 368 377 | 373 risk factors [12]. the annual risk of rupture is being reported to be between 0. 1% and 8%, depending on variable lesion characteristics [12]. the international study of unruptured intracranial aneurysms (isuia) reported in two recent publications that the risk of aneurysm rupture was substantially lower than previously thought, that is, approximately 2% in anterior circulation aneurysms in those less than 7 mm. [13,14] the patients who experience subarachnoid hemorrhage (sah) after aneurysmal rupture, approximately one third return to a functional life, one third have a significant morbidity, and one third do not survive. [12,14,15] the greatest risk after the initial aneurysmal rupture is re-rupture. after securing the aneurysm either operatively or by endovascular treatment, the risks are of cerebral vasospasm leading to ischemic complications and of developing hydrocephalus from such an event, thereby underlying the importance of early intervention and close monitoring in the postrupture period. [16] in 1996, moret et al. reported the results of endovascular treatment in 36 acommm aneurysms. the treatment was failed in seven of these cases (20%). the reason of failure can be explained because the technical armamentarium in the mid-1990s was not as advanced and sophisticated as it is today. of the 29 treated aneurysms, a complete occlusion was possible in 23 cases (79%) and partial occlusion with neck remnant in the remaining 6 cases (21%). these investigators found a post-procedural temporary neurological deficit in two cases, and the procedure-related permanent morbidity was 3. 5% (1case). there was no procedure-related death. [17] in 2002 kazekawa et al. published the clinical and angiographic evaluation in nineteen patients with acommm aneurysms who were treated with coils. complete obliteration was obtained in 68% of cases, with a neck remnant was seen in 32% of cases. regarding the clinical outcome, 3 patients (15%) who were originally categorized in h & h grades iv and v died, 1 (5%) was moderately disabled, and 15(80%) had a good recovery. [18] with recent technical advancements, such as rotational angiography, new microcatheters and microguidewires, small and super-soft coils, and compliant balloons for the balloon assisted technique, the failure rate of coiling of acommm aneurysms is diminishing. in 2009 guglielmi et al. in their large endovascular series on 306 ruptured acommm aneurysms treated by coiling reported a complete occlusion achieved in 139 cases (45. 5%). a neck remnant was detected in 145 aneurysms (47. 5%), and in 22 cases (7%) a residual filling of the aneurysm was observed. regarding the overall clinical neurological outcome, 280 patients (91. 5%) remained neurologically intact, improved, or unchanged from their initial clinical status. two large, wide-necked, subtotally occluded aneurysms ruptured 3–7 months after the procedure, with subsequent death of the patients. the procedure-related morbidity and mortality rates were 3. 5% (11 cases) and 1 % (3 cases), respectively. [19] guglielmi et al. observed a 16% rate of recanalization of the 374 | kumar et al anterior communicating artery aneurysm clipping versus coiling aneurysms on the follow-up angiograms. the important factors related to the aneurysm recanalization were the use of soft and smaller coils, large size of the aneurysm, large size of the neck of the aneurysm and packing density. another factor that predisposes to recanalization is the spatial direction of the acomm aneurysm. the lesions that point upward and posteriorly are more difficult to treat. in this type of aneurysm there is difficulty of safe catheterization. it is important to steam-shape the microcatheter properly to improve its positioning and anchoring. a second session of embolization was performed in the majority of recanalized aneurysms, with a very low rate of iatrogenic complications. in our study, 2 out of 17 cases (11. 76%) had recanalization in the follow up angiogram done after 6 months, recanalization occurred in the two cases were due to a small neck remnant with no filling of sac, hence left as such. in the study of a. z ahmed and his colleagues in the year 2010-2011, 15 cases underwent endovascular coiling with hunt and hess grade i–iii total occlusion was achieved in 13 cases (86. 6%) with neck remnant left in 1 case (6. 7%) and failure in one case(6. 7%) due to a thrombotic event which was overcome by antiplatelets. the patient was coiled in a second session. the outcome measured on gos was good in 12(80%), poor in 2 cases (13. 3%) and mortality in 1case (6. 7%). [20] in the study of mp cherian et al. in 2011, 103 patients undergone endovascular coiling. total occlusion achieved in 94% with neck remanants seen in 5. 8%. there were 14 (13. 59%) mortality with 85(82. 44%) had good outcome. [21]in our study, 17 cases underwent endovascular coiling with hunt and hess grade i–iii. total occlusion was achieved in 14 cases (82. 35%) with neck remnant left in 2 cases (11. 76%) and 2 cases with intaoperative rupture of the aneurysm sac (11. 76%). the outcome measured on gos was good in 10 cases (58. 82%), poor in 3 cases (17. 64%) and mortality in 4 (23. 52%). the initial results of the international subarachnoid aneurysm trial (isat): of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms were originally published in 2002, and were conducted to establish comparative outcomes in a prospective randomized fashion in patients equally suitable for either endovascular or surgical treatment. [22] for such patients, the absolute reduction in death and morbidity was 6. 9% and the relative risk reduction was 23%. [23] a complete analysis at 1 year revealed that the absolute and relative risk reductions had increased to 7. 4 and 24%, respectively[22]. the presence of symptomatic moderate or severe vasospasm is not a contraindication of the coiling of acomm aneurysms. it is possible to perform pharmacological manipulation of the spasm before coiling. the immediate occlusion of the aneurysm allows intense medical or endovascular therapy for the arterial vasospasm. a significant advantage over surgery is that there is no need for any kind of manipulation or resection of an ‘‘angry swollen’’ brain to reach the aneurysm. [19] in our study, all the patients received triple h therapy (hypertension, hypervolaemia and romanian neurosurgery (2017) xxxi 3: 368 377 | 375 hemodiluton) after securing the ruptured aneurysm either surgically or by coiling to counter vasospasm, despite this protocol, 28% of the total number of cases included in the study suffered from vasospasm either clinically or radiologically. however, we could not relate the vasospasm to the line of management used either in surgery or endovascularly, but as sequelae of sah as reported in the literature. rupture alone or surgical repair of acommm aneurysm may result in cognitive deficits such as memory impairment and personality changes, which are referred to as ‘‘acommm syndrome’’. [24,25] even patients with a postoperative glasgow outcome scale score of 4 or 5 may have significant cognitive deficits. [25] the only study that compares the cognitive outcome between surgically and endovascular treated patients was published by chan et al. on 18 patients with ruptured acommm aneurysm. [26] half of them had undergone surgical clipping and the other half had endovascular embolization. endovascular treatment showed significantly fewer severe cognitive deficits than those with surgical clipping. [24] in our study 10 (30. 30%) patients of clipping and 2 (11. 76%) of coiling developed cognitive impairment which showed that surgical clipping had more chance to injury of perforators supplying the hypothalamus and thalamus leading to more chance of cognitive impairment. suzuki et al. reported on the post-surgical overall clinical outcome in 603 patients with acommm aneurysm. of these patients, 367 (61%) had an excellent outcome, 107 (18%) had a good outcome, 99 (16%) had poor outcome, and 30(5%) died. of the 264 patients who presented in h & h grades i–iii, 86% had an excellent or good outcome. [27] fukushima et al. reported on the overall clinical outcome post-surgery in 138 patients with acommm aneurysm. in 119 cases (86%) the outcome was excellent or good, and 8 (6%) died. of the 83 patients presenting in hunt and hess grades i–iii, 92% had an excellent or good outcome. [28] in the study of a. z ahmed and his collegues in the year 2010-2011, 15 cases underwent surgical clipping with hunt and hess grade i–iii the outcome measured on gos was 5 in 8 cases (53. 3%), 4 in 1 case (6. 7%), 3 in 2 cases (13. 3%) and 1 in 4 cases (26. 7%)(20). in our study of 33 cases undergone for surgical clipping the gos were excellent or good in 20(60. 60%) and poor in 6(18. 18%) and grade 1 in 7(21. 21%). as far as different complications associated with surgical clipping and coiling were concerned there were no statistically significant difference between the two groups except for electrolyte imbalance especially hyponatremia which was significantly(p=0. 007) more in clipping group as shown in table number 7. in our surgical limb we did not have any method for intraoperative assessment of residual aneurysm or a follow up angiogram schedule. one important point in large scale comparison of two procedures is the cost analysis. of course, the total final cost also depends to the initial situation of the patients regarding the aneurysm rupture. the patients could be discharged to home, short term facilities, long term facilities or could be dead. these situations are associated with different costs. there is no any comprehensive cost 376 | kumar et al anterior communicating artery aneurysm clipping versus coiling analysis study in our country comparing the clipping versus coiling, but it seems regardless of physician payment, the most part of cost in clipping treatment relates to hospital stay while in coiling, it relates to the coil preparation. surgical clipping seems to be more economical than coiling in the goverment institutions like our institute where most of facilities are provided on free of cost. the scenario would be completly different in private hospitals which need further study and analysis to reach any conclusion regarding cost of treatment between the two groups. hoh et al in a study of nis in 2002-2006 found that the clipping patients experienced significantly higher hospital stay and total hospital costs than coiling among patients with ruptured aneurysms. [29] in our surgical limb we did not have any method for intra-operative assessment of residual aneurysm or a follow up angiogram schedule. however, a further study of a larger number of cases and introduction of intraoperative indocyanine green (icg) angiography are mandatory to exclude residual aneurysm after microsurgical clipping. conclusion at the centre where well experienced neurosurgeons and neurointerventionist are available, there is no overall difference in the clinical outcomes, complications and mortalities in both the groups. however, the selection of the patient should be done based on clinical status and radiological characteristic of aneurysm because there are some groups of patients having severe brain oedema or large hematoma in which surgical clipping would be preferable which give opportunity to not only secure the aneurysm but also to deal with the mass effect. otherwise both modalities have their own advantages and disadvantages which make them as complementary rather than competitive. correspondence dr. pradeep kumar department of neurosurgery, sms medical college, jaipur, india email: dr. pradeepk28@gmail. com phone number: +91 9828929366 references 1. sehba fa, hou j, pluta rm, zhang jh. the importance of early brain injury after subarachnoid hemorrhage. prog neurobiol2012; 97(1): 14-37. 2. brisman jl, song jk, newell dw. cerebral aneurysms. n engl j med 2006;355:928–39, 10. 1056/nejmra052760 3. proust f, debono b, hannequin d, gerardin e, clavier e,langlois o, et al. treatment of anterior communicating artery aneurysms: complementary aspects of microsurgical and endovascular procedures. j neurosurg 2003;99:3–14. 4. suarez ji, tarr rw, selman wr. aneurysmal subarachnoid hemorrhage. n engl j med 2006;354:387– 96, 10. 1056/nejmra052732 5. ryttlefors m, enblad p, kerr rs,molyneux aj. international subarachnoid aneurysm trial of neurosurgical clipping versus endovascular coiling: subgroup analysis of 278 elderly patients. stroke 2008; 39(10): 2720-6. 6. hwang js, hyun mk, lee hj, choi je,kim jh, lee nr, et al. endovascular coiling versus neurosurgical clipping in patients with unruptured intracranial aneurysm: a systematic review. bmc neurol 2012; 12: 99. 7. seibert b, tummala rp, chow r, faridar a, mousavi sa, divani aa. intracranial aneurysms: review of current treatment options and outcomes. front neurol 2011; 2: 45. 8. molyneux a, kerr r, stratton i, sandercock p, clarke m, shrimpton j, et al. international subarachnoid aneurysm trial (isat) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured romanian neurosurgery (2017) xxxi 3: 368 377 | 377 intracranial aneurysms: a randomised trial. lancet 2002; 360(9342): 1267-74. 9. campi a, ramzi n, molyneux aj, summers pe, kerr rs, sneade m, et al. retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the international subarachnoid aneurysm trial (isat). stroke 2007; 38(5): 1538-44. 10. zhang qr, zhang x, wu q, shi jx, wanghd, hang ch, et al. the impact of microsurgical clipping and endovascular coiling on the outcome of cerebral aneurysms in patients over 60 years of age. j clin neurosci 2012; 19(8): 1115-8. 11. mason am, cawley cm, barrow dl. surgical management of intracranial aneurysms in the endovascular era : review article. j korean neurosurg soc 2009;45(3): 133-42. 12. weir b. unruptured intracranial aneurysms: a review. j neurosurg 2002;96:3–42, 10. 3171/jns. 2002. 96. 1. 0003 13. unruptured intracranial aneurysms–risk of rupture and risks of surgical intervention, international study of unruptured intracranial aneurysms investigators. n engl j med 339:1725–1733,1998, 10. 1056/nejm199812103392401. 14. wiebers do, whisnant jp, huston 3rd j, meissner i, brown jrrd, piepgras dg, et al. unruptured intracranial aneurysms:natural history, clinical outcome, and risks of surgical and endovascular treatment. lancet 2003;362:103–10. 15. woo d, khoury j, haverbusch mm, sekar p, flaherty ml,kleindorfer do, et al. smoking and family history and risk of aneurysmal subarachnoid hemorrhage. neurology 2009;72:69–72,10. 1212/01. wnl. 0000338567. 90260. 46. 16. diringer mn. management of aneurysmal subarachnoid hemorrhage. crit care med 2009;37:432– 40, 10. 1097/ccm. 0b013e318195865a 17. moret j, pierot l, boulin a, castaings l, rey a. endovascular treatment of anterior communicating artery aneurysms using guglielmi detachable coils. neuroradiology 1996;38:800–5. 18. kazekawa k, tsutsumi m, aikawa h, iko m, tanaka a, go y,et al. endovascular treatment of anterior cerebral artery aneurysms using guglielmi detachable coils: midterm clinical evaluation. radiat med 2002;20:291–7. 19. guglielmi g, vin˜ uela f, duckwiler g, jahan r, cotroneo e,gigli r. endovascular treatment of 306 anterior communicating artery aneurysms: overall, perioperative results. j neurosurg2009;110:874–9. 20. ahmed a. z, zohdi ahmed m, zaghloul mohamed s, elsamman amar k. endovascular coiling versus surgical clipping in the treatment of ruptured anterior communicating artery aneurysm in cairo university hospitals. the egyptian journal of radiology and nuclear medicine (2013) 44, 523–530. 21. cherian mp,praneh m b,mehta p,vijayan k,bhaskar p,kalyanpur tm,narsinghpura ks. outcomes of endovascular coiling of anterior communicating artery aneurysms in the early postrupture period:a prospective analysis. neurol india2011;59:218-23 22. molyneux a, kerr r, stratton i, sandercock p, clarke m,shrimpton j, et al. international subarachnoid aneurysm trial(isat) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. lancet 2002;360:1267–74. 23. raymond j, guilbert f, weill a, georganos sa, juravsky l, lambert a, et al. long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils. stroke 2003;34:1398– 403, 10. 1161/01. str. 0000073841. 88563. e9. 24. alexander mp, freedman m. amnesia after anterior communicating artery aneurysm rupture. neurology 1984;34, 752–752. 25. mavaddat n, sahakian bj, hutchinson pj, kirkpatrick pj. cognition following subarachnoid hemorrhage from anterior communicating artery aneurysm: relation to timing of surgery. j neurosurg 1999;91:402–7, 10. 3171/jns. 1999. 91. 3. 0402 26. chan a, ho s, poon ws. neuropsychological sequelae of patients treated with microsurgical clipping or endovascular embolization for anterior communicating artery aneurysm. eurneurol 2002;47:37–44. 27. suzuki j, mizoi k, yoshimoto t. bifrontal interhemispheric approach to aneurysms of the anterior communicating artery. j neurosurg 1986;64:183–90, 10. 3171/jns. 1986. 64. 2. 0183. 28. fukushima t, miyazaki s, takusagawa y, reichman m. unilateral interhemispheric keyhole approach for anterior cerebral artery aneurysms. acta neurochir suppl (wien) 1991;53:42–7. 29. hoh bl, chi yy, dermott ma, lipori pj, lewis sb. the effect of coiling versus clipping of ruptured and unruptured cerebral aneurysms on length of stay, hospital cost, hospital reimbursement, and surgeon reimbursement at the university of florida. neurosurgery 2009; 64(4):614-9. doi: 10.33962/roneuro-2021-011 primary multiple cerebral hydatid disease in a young patient with surgically-treated intracerebral haemorrhage. a case report anwar n. hafedh, awfa a. aktham, zahraa f. alsharshahi, ahmed ibrahim al-jorani, sama albairamani, zahraa a. alsubaihawi, aktham o. al-khafaji, samer s. hoz romanian neurosurgery (2021) xxxv (1): pp. 71-74 doi: 10.33962/roneuro-2021-011 www.journals.lapub.co.uk/index.php/roneurosurgery primary multiple cerebral hydatid disease in a young patient with surgically-treated intracerebral haemorrhage. a case report anwar n. hafedh1, awfa a. aktham1, zahraa f. al-sharshahi1, ahmed ibrahim al-jorani2, sama albairamani3, zahraa a. alsubaihawi4, aktham o. al-khafaji4, samer s. hoz1 1 department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 medical student, alkindy college of medicine, university of baghdad, iraq 3 medical student, college of medicine, al-iraqia university, iraq 4 medical student, college of medicine, university of baghdad, iraq abstract introduction: cerebral hydatid disease (chd) is rare and the multiple-cystic variety is even rarer. in this paper, we report a case of multiple chd and explore a possible link with a preceding spontaneous intracerebral haemorrhage (ich). case presentation: a 27-year old gentleman with a history of surgically-evacuated, spontaneous ich presented with severe headache, left-sided weakness medical research council (mrc) grade ii and recurrent tonic-clonic seizures, while on a full dose of anti-epileptic medication. brain magnetic resonance imaging (mri) scans showed multiple intra-axial cystic lesions in the right hemisphere. the cysts were removed intact using dowling’s technique through a large temporoparietal craniotomy. the surgery went uneventful and the patient recovered as expected. post-operatively, a prophylactic course of albendazole (200 mg) was prescribed. on his one-year follow-up visit, the patient was symptom-free and his weakness had improved (left upper limb: mrc grade iv and full power of the left lower limb). the computed tomography (ct) scan showed no new findings. conclusion: primary cerebral hydatid disease is rare and the multiple-cyst variety is even rare. in this case, a peculiar association with a surgically-treated ich was explored with possible theories to suggest future research directions. introduction hydatid disease is a parasitic infection caused by an endemic parasite, echinococcus granulosis, mostly present in sheep-raising countries (1, 2). tapeworm larvae develop in the intestinal tract then pass through the bloodstream to reach the liver, lungs, kidney, and brain (3). cerebral hydatid disease (chd) comprises only 2% of all hydatid-cyst cases and is classified as “primary” or “secondary” (4). “primary” chd keywords cerebral hydatid disease, multiple, primary, intracerebral hemorrhage corresponding author: zahraa f. al-sharshahi neurosurgery teaching hospital, baghdad, iraq zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 72 anwar n. hafedh, awfa a. aktham, zahraa f. alsharshahi et al. presents is rare and presents as a solitary single cyst surrounded by a broad capsule while the “secondary” type is characterized by multiple cerebral cysts that result from the rupture of a single cyst (1,5). preoperative diagnosis is necessary to avoid intra-operative cyst rupture. cerebral hydatid cysts typically present with signs and symptoms related to raised intracranial pressure with or without focal neurological deficits depending on cyst size and location (5,6). the authors report a case of a young patient with primary multiple cerebral hydatid disease and question its theoretical link with a prior, surgicallytreated spontaneous ich presenting at the age of 24. case report a 27-years-old male presented with a single incidence of a generalized tonic-clonic seizure, headache, and vomiting. the patient had no history of head trauma. on examination, he had a left-sided weakness (mrc grade iii) of both upper and lower limbs. initial cranial ct scan (figure 1a) revealed an acute intracerebral hemorrhage (ich) in the right parietal lobe. the hematoma was evacuated through the right parietal parasagittal approach. the postoperative ct scan revealed complete evacuation of the hematoma (figure 1b) and the post-operative course went uneventful. one month later, the patient’s symptoms had resolved and the ct scan revealed no new findings (figure 1c). figure 1. (a) pre-operative ct scan (axial section), showing a well-defined, intracerebral hyperdensity representing intracerebral hemorrhage (ich). (b) post-operative cerebral ct scan (axial section) (c) follow-up cerebral ct scan axial section shows no intracranial abnormalities. (d) flair mri coronal section showing a cystic lesion with a thin, hypointense marginal membrane with a marked mass effect causing contralateral displacement of midline structures. three years later, the patient presented with severe headache, left-sided weakness (mrc grade ii), and recurrent tonic-clonic seizures, not responding to a full dose of anti-epileptic medication (carbamazepine 400mg bid). cerebral ct and mri scans (figure 1d) showed multiple intra-axial cystic lesions in the right hemisphere (figure 1). the cysts were removed intact using dowling’s technique through a large temporoparietal craniotomy. the surgery went uneventful. post-operatively, the patient was started on a prophylactic course of albendazole (200 mg). his left-sided weakness remained the same (mrc grade 2). during his one-year follow-up visit, the patient was symptom-free and his weakness had improved (left upper limb: mrc grade iv and full power of the left lower limb). the ct scan showed no new intracranial pathology. discussion echinococcosis is an endemic infection in mediterranean countries and middle eastern including iraq. chd is rare in comparison to other organ involvement, particularly the liver and lungs (7). cerebral hydatid disease accounts for 0.05% of all cerebral mass lesions and is 2-3 times more common in children (3,8,9). chd can be primary or secondary. primary chd is the product of direct larval infestation in the brain without evidence of extracerebral disease. secondary chd occurs when the larvae exit the capillary beds of the lungs or liver to systemic circulation until they settle in the brain (10, 11). primary chd is uncommon, accounting for 1-2 percent of all echinococcus granulosus infections, and multiple primary chds are even rarer (11-13). cerebral hydatid cysts are benign, slowly growing lesions with an annual growth rate of 1.5 to 10 cm and they can reach a considerable size before manifesting clinically. headache, vomiting, symptoms of elevated intracranial pressure (icp) are 73 primary multiple cerebral hydatid disease some of the common presentations of cerebral hydatidosis (14). other presentations are dictated by cyst size and location and may include hemiparesis, seizures, visual field disturbances, and gait disorders. symptoms of raised icp tend to predominate in the pediatric populations, while adults are more likely to present with focal neurological deficits and seizures (15,16). cerebral hydatid cysts are most frequently located in the territory of the middle cerebral artery, commonly in the parietal lobe. the cysts are often found in the supratentorial regions and only rarely in the posterior cranial fossa, ventricles, or orbit (17). surgical excision of cysts without disruption of the capsule remains the standard management of chd. a variety of surgical techniques have been developed to prevent cystic rupture. the most widely accepted method is dowling’s technique, in which the cyst is removed intact by injecting saline between the cyst wall-brain interface. this is made possible by the minimal adhesions that surround the cyst wall (18). other techniques include cyst puncture and aspiration before removal or using cortical incision over the cyst, and ejection of the cyst by air insufflation of the contralateral ventricle (19). possible postoperative complications include subdural effusions, obstructive hydrocephalus, and cortical collapse. in our case, the large spaces left behind after removing the three cysts were filled with isotonic saline prior to dural closure, in an attempt to reduce the risk of cortical collapse which carries a mortality of 7% (1,15). the follow-up ct scan showed a decrease in cavity size and an increase in brain tissue. medical treatment of hydatid cyst is required in cases of cyst rupture, recurrence, or systemic hydatid disease. it may also be used pre or postoperatively to shrink the cysts and prevent a recurrence, respectively (19-22). our patient presented with three large cysts of different sizes and thus albendazole was prescribed postoperatively. whether this patient's past history of surgically evacuated ich is related to chd deserves further analysis. although the sequence of events may be coincidental, the presence of spontaneous ich in an otherwise healthy gentleman hints to a potential underlying connection. one theory is that surgical leukomalacia encouraged cystic development, particularly that the two pathologies are located in the same hemisphere. one other hypothesis is that the ich provided an earlier manifestation of an occult chd. hemorrhagic chd is, however, an uncommon occurrence. another explanation is that this patient is a case of iatrogenic hydatidosis, which warrants institutional inquiry. in either case, we felt that documenting this case and discussing the possibility of association could direct further research efforts to better understand the etiology and presentation spectrum of chd. conclusion primary cerebral hydatid disease is rare and the multiple-cyst variety is even rare. in this case, a peculiar association with a surgically-treated ich was explored with possible theories to suggest future research directions. abbreviations chd: cerebral hydatid disease; ich; intracerebral hemorrhage; mrc: medical research council; mri: magnetic resonance imaging; ct: computed tomography; icp: intracranial pressure. references 1. çataltepe o, tahta k, çolak a, erbengi a. primary multiple cerebral hydatid cysts. neurosurgical review. 1991 sep 1;14(3):231-4. 2. chatzidakis e, zogopoulos p, paleologos ts, papageorgiou n. surgical planning for the treatment of a patient with multiple, secondary, intracranial echinococcal cysts. the surgery journal. 2016 mar;2(1):e7. 3. braunsdorf ew, schmidt d, rautenberg m. cerebral manifestation of hydatid disease in a child. child's nervous system. 1988 aug 1;4(4):249-51. 4. abbassioun k, rahmat h, ameli no, tafazoli m. computerized tomography in hydatid cyst of the brain. journal of neurosurgery. 1978 sep 1;49(3):408-11. 5. yüceer n, güven mb, yilmaz h. multiple hydatid cysts of the brain: a case report and review of the literature. neurosurgical review. 1998 jun 1;21(2-3):181-4. 6. tuncer c, ahmet ö, aydın y. multiple intracranial hydatid cysts in a boy. turkish neurosurgery. 2009;19:203-7. 7. ramosaço e, kolovani e, ranxha e, vyshka g. primary multiple cerebral hydatid cysts in an immunocompetent, low-risk patient. idcases. 2020 jan 1;21:e00882. 8. lunardi p, missori p, di lorenzo n, fortuna a. cerebral hydatidosis in childhood: a retrospective survey with emphasis on long-term follow-up. neurosurgery. 1991 oct 1;29(4):515-8. 74 anwar n. hafedh, awfa a. aktham, zahraa f. alsharshahi et al. 9. mahdi nk, benyan ak. hydatidosis among iraqi children. annals of tropical medicine & parasitology. 1990 jan 1;84(3):289-92. 10. karadağ ö, gürelik m, özüm ü, göksel hm. primary multiple cerebral hydatid cysts with unusual features. acta neurochirurgica. 2004 jan 1;146(1):73-7. 11. yurt a, avcı m, selçuki m, özer f, çamlar m, uçar k, taşlı f, altınörs n. multiple cerebral hydatid cysts: report of a case with 24 pieces. clinical neurology and neurosurgery. 2007 nov 1;109(9):821-6. 12. baysefer a, erdoǧan e, gönül e, kayali h, timurkaynak e, seber n. primary multiple cerebral hydatid cysts: case report with ct and mri study. min-minimally invasive neurosurgery. 1998 mar;41(01):35-7. 13. al zain tj, al-witry sh, khalili hm, aboud sh, al zain jr ft. multiple intracranial hydatidosis. acta neurochirurgica. 2002 nov 1;144(11):1179-85. 14. el-shamam o, amer t, el-atta ma. magnetic resonance imaging of simple and infected hydatid cysts of the brain. magnetic resonance imaging. 2001 sep 1;19(7):965-74. 15. ciurea av, fountas kn, coman tc, machinis tg, kapsalaki ez, fezoulidis ni, robinson js. long-term surgical outcome in patients with intracranial hydatid cyst. acta neurochirurgica. 2006 apr 1;148(4):421-6. 16. onal c, unal f, barlas o, izgi n, hepgul k, turantan mi, canbolat a, turker k, bayindir c, gokay hk, kaya u. longterm follow-up and results of thirty pediatric intracranial hydatid cysts: half a century of experience in the department of neurosurgery of the school of medicine at the university of istanbul (1952–2001). pediatric neurosurgery. 2001;35(2):72-81. 17. gupta s, desai k, goel a. intracranial hydatid cyst: a report of five cases and review of literature. neurology india. 1999 jul 1;47(3):214. 18. alok r, mahmoud j. successful surgical treatment of a brain stem hydatid cyst in a child. case reports in surgery. 2020 jan 23;2020. 19. chen s, li n, yang f, wu j, hu y, yu s, chen q, wang x, wang x, liu y, zheng j. medical treatment of an unusual cerebral hydatid disease. bmc infectious diseases. 2018 dec;18(1):1-4. 20. todorov t, vutova k, petkov d : albendazole treatment of multiple cerebral hydatid cysts : a case report. trans r soc trop med hyg 1988; 82 : 150-152. 21. singounas eg, laventis as, sakas ds et al : successful treatment of intracerebral hydatid cysts with albendazole : case report and review of literature. neurosurgery 1992; 31 : 571-574. 22. hidatik pm, kist po. primary multiple cerebral hydatid disease: still symptomatic despite pathologically confirmed death of the cyst. turkish neurosurgery. 2013;23(4):505-8. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article cirsoid aneurysm of the scalp: a case report faran ahmad, deepak kumar singh, hanuman prasad prajapati, anuj chhabra india doi: 10.1515/romneu-2017-0069 426 | ahmad et al cirsoid aneurysm of the scalp doi: 10.1515/romneu-2017-0069 cirsoid aneurysm of the scalp: a case report faran ahmad, deepak kumar singh, hanuman prasad prajapati, anuj chhabra department of neurosurgery, dr rml ims lucknow uttar pradesh, india abstract: cirsoid aneurysms (arteriovenous malformations [avms]) are anomalous fistulous arteriovenous communications of scalp with ill-defined natural course that are rarely encountered in neurosurgery. patients with avm of the scalp present clinically with headache and either a small innocuous-looking subcutaneous scalp lump or a large, pulsatile mass with or without bruit, which has a propensity to massive hemorrhage. complex vascular anatomy and interconnections and high shunt flow make their management difficult. we report a rare case of a 40-year-old man who presented with a swelling over his occipital region that progressively enlarged over the course of 6 years. being high flow shunt surgical excision was attempted. key words: avmarteriovenous malformation, scalp, high flow shunt, occipital, cirsoid, arterio venous fistula introduction aberrant persistence of primitive arteriovenous interconnections due to defective differentiation of the primary vascular complex leads to formation of arteriovenous malformations (avm).avm of scalp are rare occurrences among vascular lesions. various names being used to describe the vascular malformations of the scalp include aneurysm cirsoid, aneurysma serpentinum, aneurysm racemosum, plexiform angioma, arteriovenous fistula and arteriovenous malformation [1]. arteriovenous fistula was first described by hunter in 1757. [2] the term cirsoid aneurysm was applied to vascular malformations of the scalp in 1833 by brecht [2] and is used to describe a fistulous connection between the arterial feeding vessels of the scalp and the draining veins without an intervening capillary bed. avm are composed of complex tangle of feeding arteries and draining veins, without an intervening capillary bed forming a ‘nidus’located within the subcutaneous layer. the draining veins often are dilated owing to the high velocity of blood flow through the fistulae. the location of scalp arteriovenous fistulas is roughly evenly distributed among the frontal, temporal and parietal regions [1]. the incidence of cirsoid aneurysms of scalp is rare and infrequently encountered by the romanian neurosurgery (2017) xxxi 3: 426 430 | 427 neurosurgeon. [3] they are usually congenital in etiology however traumatic fistulas have also been described.. whatever the cause,clinically patient presents usually with an innocuous looking subcutaneous scalp lump or a visible large, pulsatile scalp mass associated with headache, tinnitus and hemorrhage. [4] a clear understanding of the diagnostic and treatment algorithms involved with avm management is imperative, because avms are a cause of haemorrhage in young adults. surgical treatment is primarily indicated in order to prevent bleeding and haemorrhagic complication along with resolution of cosmetic problems [1]. however the treatment of these lesions is difficult because of their complex vascular anatomy, high shunt flow, and cosmetic disfigurement. the treatment options of these lesions include endovascular treatment, direct intralesional injection of sclerosing agents, ligation of feeders, and surgical excision. [5–10] in this case report we describe the clinical features and discuss the results of the surgical management of scalp vascular malformations. case report a 40 year male complained of slowly progressive swelling localized over right occipital region of the scalp since around 5-7 years duration. it was associated with occasional headache and tinnitus. the swelling had been gradually increasing in size since 6 yrs. and was now pulsatile. there was no previous history of trauma or head injury. no history of recurrent massive bleeding, any visual disturbances or paresis. neurological examination was normal. there was no other systemic abnormality detected. local examination showed large swelling around 6cm-7cm in diameter, in midline extending over the right occipital region (figure 1). the swelling was densely adherent to scalp. local temperature was not raised. the swelling was pulsatile, nontender and soft in consistency. a bruit was also demonstrated over the swelling. multiple tortuous & prominent, intensely enhancing vessels along occipital surface of the scalp was evident on computerised tomography scan. mri scan revealed a vascular lesion under the scalp in the occipital region containing tortuous dilated high contrast filled vessels. digital subtraction angiography showed large occipital complex vascular network with simultaneous early filling of venous circulation in the scalp confirming the presence of an arteriovenous fistula (avm) (figure 2). the avm had feeding arteries from bilateral occipital branches of external carotid arteries. right occipital artery is more hypertrophied, dilated, and tortuous. venous drainage appears from the communicating emissary veins to the internal jugular veins, and few tributaries to the external jugular veins. it appeared fairly high flow arterio-venous communication. there was no evidence of communication with intracranial circulation showed normal intracerebral circulation. surgical procedure en block surgical excision of the lesion was planned. the patient was positioned with head elevated 30 degrees above the heart level. a question mark scalp flap was planned. after infiltrating 2% lignocaine with adrenaline, scalp incision was made in short 428 | ahmad et al cirsoid aneurysm of the scalp segments, ligating the feeding vessels and draining veins as they were encountered. once the scalp flap was raised, the bleeding from the bone was controlled with bone wax and monopolar diathermy. after complete devascularization, the lesion along with pericranium, galea was excised circumferentially from the subcutaneous tissue with the use of bipolar diathermy and sharp dissection without breaching the skin (figure 3 a,b). intra-op, it was very difficult to get plane of dissection due to very large tortuous venous varix. there was no significant blood loss during surgery. on microscopic examinations, the histopathological specimen contained various well-developed arteries and dilated veins in the connecting tissue. repeat computed tomography (ct) angiogram showed complete disappearance of avm without any remnant. the patient was advised to continue follow-up. on microscopic examinations, the histopathological specimen contained various well-developed arteries and dilated veins in the connecting tissue. endothelial cells and perivascular cells in arteries were positive with immunohistological staining for vascular endothelial growth factor (vegf); the major feeding arteries and draining vein were vegf-negative. there was no recurrence of fistula at the 3-month follow-up examination (figure 3c). figure 1 rear view pre-op photograph of the patient figure 2 pre-op digital subtraction angiography image a romanian neurosurgery (2017) xxxi 3: 426 430 | 429 b c figure 3 intra-op photograph before ligation of feeding arteries (a) and en block excision of the lesion (b). post-op photograph of the patient after surgery (c) discussion aberrant persistence of primitive arteriovenous interconnections is known as avm. scalp avm are rare despite the intense vascularity of scalp and relatively high frequency of trauma to this region. [3,10] the etiology of cirsoid aneurysm is still controversial. it is accepted that it may be either congenital or traumatic. congenital was more common in large series published in the literature. [11,12]. in our case, traumatic etiology was the probable initiating factor. due to the large size and complexity of the lesion, en block excision was planned. ligation of feeding vessels followed by resection of the lesion has occasionally met with success. multiple treatment schemes have been described and, as yet, no standard form of therapy exists. some of the reported treatments include radiation therapy, electrothrombosis, scalp tourniquet, scalp compression with pads and springs, direct injection with alcohol, and embolization. [11,13]. surgical resection of the fistula is usually successful, as was for this patient. direct surgical excision risks severe intraoperative blood loss. the abnormal vascular channel dilatation over the scalp often results in deformity of the scalp that is usually not lifethreatening unless it causes hemorrhage but can lead to substantial cosmetic and social disturbances. [8,13] scalp arteriovenous fistulas are roughly evenly distributed among the frontal, temporal, and parietal regions. occipital region scalp avms have been remotely reported, which is found in our present case report. the avm feeder vessels mainly arise from the subcutaneous tissue layer of the scalp. the source of feeder arteries most frequently includes the external carotid, occipital, and supraorbital arteries. clinical manifestations relate to the size of fistula, and patient may present with loud bruit, hemorrhage, headache, and, in severe cases, scalp necrosis. [8]. the lesion usually begins as small subcutaneous lump, which, over a period of time, evolves into grotesque, 430 | ahmad et al cirsoid aneurysm of the scalp deforming mass. digital subtraction angiography is the gold standard investigation for these lesions, which provides a road map of arterial supply and venous drainage. [3] although the lesion lies in the subcutaneous layer of scalp, the pericranial component of the lesion is of surgical importance [2]. an important part of surgery is the excision of pericranial component with control of bone bleeding using bone wax. endovascular and percutaneous occlusions of the fistulas have been described. the results of endovascular occlusion are dependent on the angioarchitecture of the fistula, the supplying arteries, and draining venous structures. arterial approaches may not often be successful in occluding the entire fistula due to the problem of multiple feeding arteries. in our case, complex multiple feeding arteries were present, so endovascular approach was not considered. recurrence has been reported as late as 18 years after complete surgical excision [14]. hence, regular follow-up is recommended. correspondence dr. faran ahmad department of neurosurgery, dr rml ims lucknow, uttar pradesh (india) email-faran2312@gmail.com references 1.pukar mm, patel is, mewada sg. cirsoid aneurysm of scalp occipital regiona case report. int j res health sci [internet]. 2014 apr 30;2(2):698-702. 2.elkin dc. cirsoid aneurysm of the scalp with the report of an advanced case. ann surg. 1924; 80 :332–40. [ pmc free article ] [ pubmed ] 3.muthukumar n, rajagopal v, manoharan av, durairaj n. surgical management of cirsoid aneurysms. actaneurochir. 2002; 144 :349–56. [ pubmed ] 4.baysefer a, gönül e, erdoģan e, akay k m, bedük a, sehe n. cirsoid aneurysms of the scalp.eur j plastsurg. 1998; 21 :48–50. 5.heilman cb, kwan es, klucznik rp, cohen ar. elimination of a cirsoid aneurysm of the scalp by direct percutaneous embolization with thrombogenic coils. j neurosurg. 1990; 73 :296–300. [ pubmed ] 6.hendrix le, meyer ga, erickson sj. cirsoid aneurysm treatment by percuataneous injection of sodium tetradecyl sulfate. surgneurol. 1996; 46 :557–61. [ pubmed ] 7.mourao gs, hodes je, gobibn yp, casasco a, aymard a, merland jj. curative treatment of scalp arteriovenous fistula by direct puncture and embolization with absolute alcohol. j neurosurg. 1991; 75 :634–7. [ pubmed ] 8.barnwell sl, halbach vv, dowd cf, higshida rt, hieshima gb. endovascular treatment of scalp arteriovenous fistulas associated with a large varix. radiology. 1989; 173 :533–9. [ pubmed ] 9.fisher-jeffes nd, domingo z, madden m, de villiers jc. arteriovenous malformations of the scalp. neurosurgery. 1995; 36 :656–60. [ pubmed ] 10.nagasaka s, fukushima t, goto k, ohjimi h, iwabuchi s, maehara f. treatment of scalp arteriovenous malformations. neurosurgery. 1996; 38 :671–7. [ pubmed ] 11.gurkanlar d, gonul m, solmaz i, gonul e. cirsoid aneurysms of the scalp. neurosurg rev. 2006; 29 :208– 12. [ pubmed ] 12.khodadad g. familial cirsoid aneurysm of the scalp. j neurol neurosurg psychiatry 1971;34(6):664–667 13.chatterji p, purohit gn, soni nk. cirsoid aneurysm of the auricle and adjoining scalp. j laryngol otol 1977;91(11):997–1002 14.wilkinson ha. recurrence of vascular malformation of the scalp 18 years following excision. case report. j neurosurg 1971;34(3):435–437 romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article use of high performance technologies in the treatment of chronic neuropathic pain ion streltov, marcela nour, madalina radu, mihai malcoci, oana bisoc, ecaterina olaru, iulia aldea romania doi: 10.2478/romneu-2018-0001 romanian neurosurgery (2018) xxxii 1: 3 15 | 3 doi: 10.2478/romneu-2018-0001 use of high performance technologies in the treatment of chronic neuropathic pain ion streltov1, marcela nour2, madalina radu3, mihai malcoci4, oana bisoc5, ecaterina olaru6, iulia aldea7 1primary neurosurgeon, clinical hospital emergency "prof. dr. n. oblu" iasi, romania 2neurosurgeon, clinical hospital emergency "prof. dr. n. oblu" iasi, romania 3resident plastic surgery, “sf. spiridon” hospital iasi, romania 4resident neurosurgery, clinical hospital emergency "prof. dr. n. oblu" iasi, romania 5primary neurologist, clinical hospital emergency "prof. dr. n. oblu" iasi, romania 6primary anesthesia-intensive care, clinical hospital emergency "prof. dr. n. oblu” iasi, romania 7principal psychologist, clinical hospital emergency "prof. dr. n. oblu "iasi, romania abstract: spinal cord neurostimulation is a minimally invasive treatment method for chronic neuropathic pain that is refractory to treatment, and is part of top technology in field. relatively recent introduction of this method in the neurosurgery clinic "prof. dr. n. oblu "of iasi has aligned the clinic's therapeutic arsenal to world standards. this has made it possible to treat in romania a category of patients who would be treated abroad until now. our clinic has entered the "national program for diagnostic and treatment using high performance equipment "subprogram of treatment of neuropathic pain by implant of a spinal cord neurostimulator and is currently the only one in romania where this treatment can be done. this represents a new step in the transformation process of the clinical hospital emergency "prof. dr. n. oblu" iasi in a real center of excellence in the field neurosurgery. the team dealing with the implant consists of 3 neurosurgeons, a neurologist, pa sychologist and an anesthetist, trained in a specialized foreign center. key words: spinal cord stimulation, back pain, central nervous system stimulation, complex regional pain syndrome, failed back surgery syndrome history electrotherapy of pain by neurostimulation began shortly after in 1965 r.melzack and p. wall proposed gate control theory (theoretical basis) spinal cord neurostimulation, wherefore they received the nobel prize [1]. according to this theory, nerves that carry painful peripheral stimuli, touch sensations and vibration end in the dorrsal horn (the gate) of the spinal cord. thus, it has been hypothesized that this entry may be manipulated to "close the gate", thus 4 | streltov et al high performance technologies in chronic neuropathic pain blocking the spread of the painful impulse. on this theory, in 1971, shealy et al. [2] performed the first implant of the spinal cord neurostimulator in the treatment of chronic pain. shimogi et al [3] published the analgesic effect of neurostimulation. later spinal cord neurostimulation developed very rapidly over the last two decades by introducing implantable neuropeacemakers using guided surgical systems. [4]. every year, over 50,000 neurostimulation implants are performed worldwide. [5]. chronic neuropathic pain pain is “an unpleasant experience that we primarily associate with tissue damage or describe in terms of tissue damage.” (international association for the pain study (iasp, 1986)). according to statistics, in europe 1 out of 5 patients (70 millions of adults) suffer from chronic pain [6]. if in most patients the pain is the symptom of a disease, this is not always true. in 7 8% of the patients the pain persists even after removing the trigger factor. this pain ceases to be one symptom, becoming itself a disease. in recent years, medicine has begun to recognize that chronic pain is a self-esteem disease, after a long time it was considered a psychological and overlooked problem. this type of pain is refractory to common medication (nonsteroidal analgesics, anti-inflammatory drugs, opioids), physiotherapy and infiltration local. therefore, it requires a totally different approach to traditional treatment strategies. the difficulty of treating neuropathic pain is also explained by the lack of knowledge the mechanisms that trigger it. up to now, at least 20 such pathophysiological mechanisms have been known. neuropathic pain is caused by a decrease in the excitability threshold of a receptors, poor processing of nociceptive stimuli (neurons become over-excited, continuing to emit electrical impulses long after the trigger factor has been removed), disruption of the neuronal control mechanism (ineffective cells with inhibitor effect on it), etc. the pain process goes through 4 stages: transduction, transmission, perception, and modulation. factors stimulants (atp, gaba, glutamate, nitric oxide, prostaglandin and substance p mediators) irritate the free nervous terminations that respond to pain, and transformation into the electrical signal by transduction appears. this signal enters the spinal cord through the posterior horns and propagates ascending to the brainstem, and from there to the limbic system and thalamus. here the signals of pain are processed and contextualized in the perception process. through modulation, the brain can alter the transmission of subsequent nerve impulses by amplifying or reducing the release of neurotransmitters. symptomatology of chronic neuropathic pain due to the long-term nervous disorders, the symptoms are more important in the distal extremities (soles, palms) than in thighs or arms. no visible damage dysaesthesia an alteration of sensitivity leading to spontaneous unpleasant sensations such as those tingling, sting and burning; allodynia pain caused by stimuli that are normally painless. this stimulus can be touch romanian neurosurgery (2018) xxxii 1: 3 15 | 5 (for example, touching a feather) or heat (when the pain is caused by a temperature that would not normally be disturbing); a paradoxical combination of loss of sensitivity and hyperalgesia of painful area, the presence of paroxysms autonomic hyperactivity abnormal blood flow, hyperthermia and skin sweating accompany the painful sensation and contribute to its persistence (for example, in complex regional pain syndromes). chronic neuropathic pain is refractory to treatment with analgesics or opioids, but it improves with antidepressants, antiepileptic and vasodilators, as well as application to the painful place of hot-cold compresses. spinal cord neurostimulation a) indications: fbss failed back surgery syndrome (fbss); regional complex pain syndrome (cprs) type i (also called sympathetic dystrophic reflex) and type ii (also called causal); diabetic neuropathy; neuralgia postherpetica. amyloidosis neuropathy; neuropathy from fabry disease; polyradiculoneurita guillain-barré; neuropathy from peripheral vascular disease; lyme disease (borreliosis, 1000-sided illness); toxic (ethanolic) neuropathy; neuropathy from vitamin deficiencies in group b; ghost pain in vertebral-medullary trauma; pain in oncology pathology; and so on b) contraindications: the presence of other electrical devices in the body (cardiac pacemaker, cochlear implant), because the electrical impulses of the neurostimulator can interfere with the electrical impulses of these devices; serious heart disease (class iii-iv n.y.h.a., valvular stenosis, angina pectoris); blood clotting disorders patients with chronic anticoagulant therapy present an increased risk of developing peridural hematomas at the implant site and spinal cord compression, sometimes with motor deficits; psychiatric disorders, drug abuse and / or addiction; trophic or gangrene ulcers; local infections; immune system deficiencies; patient incapacity to use implanted device and inability to present at control visits; age under 18. female candidates with fertile potential should have a urine pregnancy test and use contraceptive methods recommended by the investigator. c) the neurostimulation system it includes several components: electrode, extension, impulse generator (trial and permanent), patient remote control, physician programmer. stimulation electrode. there are several types of electrodes that differ in number of contacts, stimulation contact length, contact distance etc. we used electrodes with lengths between 50 and 75 cm and diameter of 1.5 mm, with 8 contacts and resistance up to 250ω. 6 | streltov et al high performance technologies in chronic neuropathic pain figure 1 different types of stimulation electrodes figure 2 stimulation electrode – schema the extension connects the stimulating electrode to the impulse generator. figure 3 – extension figure 4 external generator (trial) the pulse generator is a device designed to provide electrical impulses to the stimulating electrode. includes a battery with at least 2.5 ah, which generates pulses with maximum voltage up to 10.5 volts, frequency between 50 and 120 hz and duration between 100 and 500 msec. the generator stores the stimulus program set up by the physician only from the amplitude, frequency, duration of the impulse, and the order of the stimulation contacts on electrode. it also memorizes the start and stop times of the generator, as well as the changes of the amplitude performed by the patient via the remote control. figure 5 compatible irm impulse pump generator romanian neurosurgery (2018) xxxii 1: 3 15 | 7 the life span of the power supply is 3 to 5 years and can be replaced after consumption. new generators are irm compatible, rechargeable and automatically adjusts their pulse voltage depending on the position of the body. remote. it is used by the patient to transmit and receive wirelessly data to the spinal cord neurostimulator. through this, the patient can optimize settings, can completely reset or shut down the spinal cord neurostimulator in case of fluctuations feeding or accidental exposure to a powerful electromagnetic field, adjusts the amplitude of the pulse based on the limits prescribed by the physician. using the remote control the patient can check the status of the spinal cord neurostimulator battery located in the generator pulses, patient remote control battery and confirmation that the neurostimulator has received the information from the remote control. figure 6 patient remote control n-vision is a small portable computer specializing in the programming of generators pulses. the data transmission between nvision and the generator is 2.4 ghz. through the programmer, the physician sets up a stimulus program adapted to each patient by modifying the parameters of these impulses to the maximum therapeutic efficiency and order electrode stimulation contact. figure 7 the n'vision programmer the mechanism of action of the spinal cord neurostimulator consists in blocking the transmission painful impulses in the upward spinal tracts to the thalamus and limbic system, where integration, analysis and awareness of suffering is taking place. the effect of neuromodular, which consists of suppressing the release of inhibitory chemical neuromodulators suppress the transmission of pain. this mechanism of functioning also derives from the fact that the pain is suppressed minutes, hours to even days after stopping the pacemaker. this could is due to the fact that the spinal cord neurostimulation increases the synthesis of the gaba 8 | streltov et al high performance technologies in chronic neuropathic pain neurotransmitter, which has an effect of removing amino acid excitators. until the introduction of spinal cord neurostimulation, the only way to resolve pain was surgery to discontinue the paths carrying the pain signals. but the key success was the finding of carrier tracts, often the intervention being a failure. objectives this study presents the preliminary results of the stimulation of the posterior tracts of spinal cord via neurostimulatory implant in chronic neuropathic pain, performed in the clinic of neurosurgery iasi. selection of patients from 2015 until now in our clinic we have performed 36 implant procedures at 22 patients: 14 women and 8 men between 40 and 76 years of age with an average disease progression of 2.8 years and an average of 2 to 3 neurosurgical interventions per patient. 20 cases were with failed back surgery syndrome (fbss) after repeated neurosurgical interventions for both herniated lumbar discs, as well as after decompression in foraminal and / or spinal stenosis, degenerative spondylolistezis, peridural and radicular fibrosis, 1 case with ghost pain after dorsal inferior vertebromedular trauma, 1 complex complex regional posttraumatic pain syndrome (crps) type i (sympathetic dystrophic reflex) and a case of persistent pain after repeated interventions for trigeminal neuralgia. the implant was done in 2 steps test stimulation and permanent implant. figure 8 vas scale neurological consult. the vast majority of cases selected for the implant were patients with the failed back surgery syndrome, with outstanding pain, irradiated in the inferior limb neuropathy-like (spontaneous, noneffortless, with paroxysmal exacerbations), with an intensity of over 7 in the analog-visual scale (vas), measured 3 times a day within 3 days. all the patients did medical treatment, physiotherapy and spinal infiltration up to 6 months. there were followed the beginning, character, duration, intensity, territory and evolution of pain. the essential features of this type of pain was allodynia, hyperalgesia and hyperpathia. the neurological examination showed that these clinical signs coexisted frequently in our cases and were very difficult to differentiate. psychological consultation has been done in all patients, primarily to exclude any psychological problem that could affect the outcome. the most common effects secondary romanian neurosurgery (2018) xxxii 1: 3 15 | 9 to the neuropathic pain were depression, anxiety, somatization, sleep, family and / or marital problems. cases with obvious signs of somatization of pain and those with a history of suicidal ideas were sent to psychiatric examination and excluded from the batch. it was important to establish realistic expectations by the patient: the efficiency of stimulation between 40% and 60% of the cases, and the efficiency criterion the reduction by at least 50% of the intensity pain and decreased analgesic drug intake. it is also important to grant support and encourage pain patients. the roland-morris questionnaire (2004) the patient draws on the dermatomus distribution charts in different colors the location of the pain, a numbness or burning feeling. figure 9 these charts are very useful intraoperatively for covering painful areas patients with inflammatory and purulent skin rashes, as well as those with local irritation secondary to various physiotherapeutic procedures located even at a distance from the placement of the electrode impose the delay of the surgery until these are resolved. preparing the patient for the implant. the selected cases for the implant benefited from spinal mri exam, primarily to exclude injuries that would require reintervention, the level of the conus medullaris. sometimes we use ct to evaluate the anatomical area of the implant (highlighting the possible spinal abnormalities, narrow spaces, etc.) that could pose technical problems in performing the implant safely. figure 10 ct reconstruction for the anatomical evaluation of the implant area 10 | streltov et al high performance technologies in chronic neuropathic pain provisional implant technique the patient's position on the operative table is ventral decubitus. anesthesia is intravenous, the patient being conscious throughout the intervention. radiological survey a projection of laryngeal apophyses l3-l4. figure 10 set up the implant room after local anesthesia with xilina 1%, vertical cutaneous incision is performed on a length of 3-4 cm, on the median line. touhy needle (hypodermic needle, slightly curved at the end, also used in implantation of epidural catheters) is inserted at 45° from the spinal axis, obliquely to the median line, on left or right to spinous apophyses (depending on lateral pain) until cessation resistance after passing the yellow ligament. typically the channel is entered through the l2-l3 lamina below the level of the conus medullaris (to avoid direct lesion). after extraction the stylet through the needle lumen, one inserts the electrode into the posterior epidural space. the electrode must cross at least 4 vertebrae from the place of introduction to the stimulation area. the electrode is driven under c-arm control to the desired location, depending on the location of the pain area in the lower limbs (usually up to the back of the d9-d10 vertebral body). figure 11 insertion of the electrode to the posterior epidural space figure 12 radiological control of correct positioning of the electrode the electrode is connected via extension to n'vision programmer and the unscrubbed physician produces the first electrostimulation of the posterior cords. the patient indicates the area the painful condition is covered by paresthesia ("tingling") and decreased intensity of pain. figure 13 intraoperative medullary stimulation romanian neurosurgery (2018) xxxii 1: 3 15 | 11 after radiological confirmation of correct electrode position and good stimulation intraoperatively, the extension is transcutaneously exteriorized on the lateral side of the trunk and sutured to the tegument. the wounds are sutured, and the distal end of the extension connects to the temporary impulse generator. the whole system is attached to the skin with adherent drape. figure 14 externalization of the extension and connection to the external generator suture suppression is done after 6-7 days postoperatively. for 2 to 3 weeks the patient is in the neurostimulation test period. the patient is called for visits repeatedly to adjust the electrical parameters of impulse by intensity, voltage, amplitude and its duration. depending on the position of the body (bent, sitting or orthostatism) the electrode can move farther or closer to the back of the spinal cord requiring manual adjustment to the patient's power of impulse for an effective stimulation of the spinal cord. the patient is taught to control his own pain by using his personal remote depending on his daily activities. security measures. patients have forbidden activities involving sudden shocks, twists or excessive trunk flexion, as it may cause disconnection or breakage of the components system. this can lead to intermittent stimulation or even loss of stimulation. special warnings and increased attention are required when a defibrillation is required, electrocauterizations, mri exams, radiofrequency ablation and endoscopy for therapeutical purpose, as powerful sources of electromagnetic interference can cause overheating the components of the neurostimulation system with tissue damage. there can occur instantaneous increases in stimulation intensity or intermittent stimulation, and the patients may feel vibrations or shocks, return to initial symptoms or even need reprogramming the neurostimulator. although it can create discomfort, all of this does not lead to device malfunction or serious injury to the patient. the permanent implant technique if during the test stimulation the pain intensity decreased by at least 4 to 5 points on pain scale or more than half of its intensity with gradual decrease in medication doses, is decided to perform the permanent implant. it involves the replacement the external provisional generator with a sterile one. the place where the generator will be implanted must either be easily accessible to the patient for easy synchronization with personal remote control. the exact location of the implant is established preoperatively in agreement with 12 | streltov et al high performance technologies in chronic neuropathic pain the patient to avoid it overlaps with the level at which he usually wears his belts / trousers. internalisation of the sterile generator is done subcutaneously, usually on the anterior face of the abdomen, paraumbilical left. the permanent implant is done under general anesthesia via oro-tracheal intubation. the position of the patient on the operating table is in lateral decubitus, with the painful side up. preparation the operator field is similar to the provisional implantation technique with the reference that apart from the lumbar region it will disinfect the anterior face of the abdomen, where the sterile impulse generator is to be implanted. figure 15 prepare the operator field for the permanent implant figure 16 subcutaneous tunneling of the extension the wound is reopened where the connection between the electrode and the extension was made. one disconnects and suppress the extension with the non-sterile external generator. another extension is added, sterile, that is connected to the electrode implanted in the previous intervention. extension cable is tunned subcutaneously to the anterior face of the abdomen, where it connects to the sterile generator and itself inserted into the subcutaneous paraumbilical pocket. the generator is fixed with non-resorbable sutures to the abdominal muscle. the wound will be sutured with vicryl 3.0 (skin ethilon 3.0). figure 17 connect the extension to the generator figure 18 internalizing the generator in the paraumbilical pocket romanian neurosurgery (2018) xxxii 1: 3 15 | 13 surgical electrodes in chronic pain management. another type of electrodes we used are the specify ™ surgical electrode. it has the shape of a 16-palletized blade programmable independently and assigned in 3 rows 5-6-5. figure 19 specify ™ surgical electrodes this type of electrode offers several options and configurations for customized therapy individually to each patient. first, it is more effective in cases of associated irradiated pain with vertebral syndrome. the specify ™ electrode is implanted after a good stimulation with percutaneous electrode during the test period. the surgical implant is made with general anesthesia after bilateral traction of muscle masses and lower partial lamina resection at level d11. figure 20 radiological control specify ™ electrode positioned at d9 insert the electrode into the d9 d10 retrodural space. otherwise connections to the generator are performed via the extension – similar to the tehnique of implant of the percutaneous electrode. the surgical electrode has the advantage of a larger coating and the minimal risk of slipping from the percutaneous space, but has the greater risk of septic complications. from the point of view of battery consumption, the surgical electrode has one much higher than the percutaneous yield, being the electromagnetic field at the surgical one is oriented in one direction, while the percutaneous electrode is directed at 360°. intraoperative incidents: of the 30 procedures performed in 2 cases we found the presence of csf in the penetration of the yellow ligament with the touhy needle. both cases required 2 3 days of bed rest, the period of postpunctional cephalalgia. 2 cases with the migration of the electrode required repositioning, 3 cases of remediation with the 14 | streltov et al high performance technologies in chronic neuropathic pain replacement of the damaged elements of the circuit and a case of infection with the staphylococcus aureus required system suppression. results the effectiveness of spinal cord neurostimulation was based on average comparison results of pain intensity before and after implant, performed 3 times a day. we have noted a reduction in pain intensity on average by 4.7 p. on the vas scale and improvement in functional capacity and quality of life in 67% of cases. the best results were obtained in patients aged 20-60 years with a disease progression up to 2 years, with a maximum of 2 to 3 neurosurgical interventions on the spine, prevalence of radicular syndrome on the vertebral syndrome and with minimal psychological changes. perspectives: we intend to extend the procedure's indications to neuropathies of various etiologies, stimulation of sacral nerve in sphincter disorders, gastric and colon stimulation for gastrointestinal disorders, vagal nerve stimulation in epilepsy, carotid stimulation for hypertension, etc conclusions the spinal cord neurostimulator is a medical standard that benefits tens of thousands of people worldwide every year; neurostimulation reduces the need for drugs and their side effects. neuroaugmentation is a minimally invasive, nonablative and reversible procedure a relatively low incidence of complications and a wide range of benefits. the level of spinal cord stimulation can be adjusted and programmed hourly, day and night; it does not produce irreversible changes in the spinal cord or nerves, and the system implanted can be disabled or removed without consequences; does not cause habit or addiction; absence of complications or sequelae characteristic of destructive methods within surgical treatment; neurostimulation radically improves the quality of life and enables social and economics reintegration of patients. correspondence streltovion@gmail.com references 1. melzack, r., and wall, p.d. (1965). pain mechanisms: a new theory. science, vol. 150, 971-979. 2. shealy, c.n., mortimer, j.t., and resnick, j. electrical inhibition of pain by stimulation of the dorsal columns: preliminary reports. j. int. anesth. res. soc., 46: 489-491, 1967. 3. shimoji k, higashi h, kano t, asai s, morioka t. electrical management of intractable pain. (1971) masui (the japanese journal of anesthesiology), 20: 444-447. 4. dilorenzo, d. j.; and bronzino, j.d. (2008). neuroengineering.crc press.chapter 7. 5. nagy a. mekhail md, phd, jianguo cheng md, phd, samer narouze md, leonardo kapural md, phd, mark n. mekhail bsc, timothy deer md. practical pain. clinical applications of neurostimulation: forty years later. volume 10, issue 2 march/april 2010 pages 103– 112. 6. breivik h., et. al european journal of pain, 2008. 7. timothy deer md, jason pope md, salim hayek md, samer narouze md, parag patil romanian neurosurgery (2018) xxxii 1: 3 15 | 15 md, phd, robert foreman phd, ashwini sharan md, robert levy md, phd. neurostimulation for the treatment of axial back pain: a review of mechanisms, techniques, outcomes, and future advances. neuromodulation: technology at the neural interface volume 17, issue s2 october 2014 pages 52–68 8. sweet w.h., wepsic j.g. control of pain by focal electrical stimulation for suppression. ariz med. 1969. vol. 83. p. 1042-1045. 5. sweet w.h., wepsic j.g. stimulation of the posterior columns of the spinal cord for pain control: indications, technique and results. clin. neurosurg. 1974. vol. 21. p. 278-310. 9. barolat g., sharan a.d. future trends in spinal cord stimulation. neurol. res. 2000. vol. 22. p. 279-284. 10. masnyk t., brown f. spinal cord stimulation in the treatment of failed back surgery syndrome. curr. rev. pain. 1998. vol. 2. p. 77-84. 11. dostrovsky j., lozano a. mechanisms of electrostimulation. mov. disord. 2002. vol. 17, suppl. 3. p. 63-69. 12. cioni b., meglio m., pentimalli l. et al. spinal cord stimulation in the treatment of paraplegic pain. j. neurosurg. 1995. vol. 82. p. 35-39. 13. taylor r.s. spinal cord stimulation in complex regional pain, syndrome and refractory neuropathic back and leg pain failed back surgery syndrome: results of a systematic review and meta-analysis. j. pain symptom manage. 2006. vol. 31, n 4. p. 13-19. 14. grahn p.j., mallory g.w., berry b.m. et al. restoration of motor function following spinal cord injury via optimal control of intraspinal microstimulation: toward a next generation closed-loop neural prosthesis. front. neurosci. 2014 sept 17. doi: 10.3389/fnins.2014.00296. 15.taylor rs, van buyten j-p, buchser e. complex regional pain syndrome. eur j pain 2006; 10: 91–101. 16.thomson sj, cruglov d, duarte rv. a spinal cord stimulation service. neuromodulation, 2017; e-pub ahead of print. doi: 10.1111/ner. 12587. 01 01streltovi_useof flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 410 | ansari lobster claw sign in cervical cord injury lobster claw sign: a new sign depicting central cervical cord injury at or below that level. case report ahmed ansari department of neurosurgery, hamdard institute, jamia hamdard, new delhi, india abstract: traumatic cervical central cord spinal injuries (css) are now more readily recognized both clinically and on radiolgical scans. in this article, we introduce a lobster claw sign due to a particular positioning of spinous process of c2 and c3 with cord contusion from c3-c5 following injury. key words: traumatic central cervical cord, lobster claw sign introduction mckinley found that 9.2% of all spinal cord injuries were attributed to central spinal cord syndrome.1 when presenting to emergency rooms, typically with greater upper vs. lower extremity neurological deficits, css patients first undergo x ray or computed tomography (ct) studies to rule out fracture/dislocation, and secondarily have mr examinations looking for classical central cord contusion /edema / hematomas. we present a typical sign of lobster claw on plain x ray cervical spine with underlying cord contusion on mr. case report a 56 year old man with fall of heavy object overhead presented to us five days after injury with quadriparesis. there was no bowel and bladder involvement. power in his right upper limb was 1/5 and 2/5 in left upper limb. bilateral lower limb power was 3/5. ct head suggested linear fracture in occipital bone on right side reaching till foramen magnum. x ray cervical spine lateral view (figure 1) showed a typical appearance of spinous process of c2 and c3, resembling a lobster claw along with degenerative changes. mri cervical spine (figures 2, 3, 4) was performed which showed cord contusion from c3-c5. figure 1 xray cervical spine lateral view showing the typical lobster claw sign owing to spinous process of c2 and c3 romanian neurosurgery (2016) xxx 3: 410 412 | 411 figure 2 sagittal mri showing cord contusion from c3c5 level figure 3 axial mri at c3-c4 level with cord contusion figure 4 axial mri at c4-c5 level with cord contusion discussion nowak et al. considered css to be the most common type of incomplete spinal cord injury that typically occurs following traumatic hyperextension events in older patients with underlying cervical spondylosis/stenosis. (2) deficits may vary from weakness in the hands/forearms with relative sensory preservation, to severe quadriparesis (with sacral sparing consistent with an incomplete injury). li and dai assessed the stress distribution to the cervical cord under different injury conditions to better understand the etiology of acute ccss. (3) histopathologic studies typically revealed that css occurs due to predominant white matter injury. in their feline model, cervical cord injuries were simulated in hyperextension (pinch force anterior (a) or posterior (b); flexion injuries (c)), and vertical compression (pinch force anterior (d) or posterior (e)). results were analyzed utilizing a representative crosssection analysis. they attributed upper extremity weakness to damage involving the corticospinal tracts and motor neurons in the anterior horn. schneideret al. originally defined this syndrome in 1954, citing the predominant hyperextension mechanism in the absence of fracture/dislocation following various traumatic events (e.g. motor vehicle accidents, falls, and diving injuries). his definition included the greater upper vs. lower extremity motor deficits, the presence of bladder dysfunction, and variable sensory below the locus of the trauma. his study included a 412 | ansari lobster claw sign in cervical cord injury review of 15 patients who presented with minor or major cervical injuries, in patients ranging in age from 18 to 85. most injuries were attributed to acute mechanical compression attributed to hyperextension, resulting in the “pincer compression” of the cord between the spondylotic osteophytes anteriorly and acute inward buckling of the yellow ligament posteriorly. aarabi et al. evaluated traumatic central cord syndromes (tccss) characterized by incomplete spinal cord injuries. (4) in up to 50% of patients, they are due to hyperextension events in those with underlying congenital/degenerative spinal stenosis. song et al. assessed the clinical/prognostic value of dynamic x-rays and mr studies in 23 patients with ccs without fracture/dislocation.5 they evaluated multiple x-rays and mr factors including; prevertebral hyperintensity (hi), cord compression, intramedullary high-signal intensity (imhsi), with/without instability. in our patient, we were able to find this new sign on plain x-ray, namely “lobster claw”, which we think should raise the suspicion of central cervical cord injury. this, all the more signifies the importance of plain radiology at small centres which are not equipped enough with advanced scanners. although, "lobster-claw” is a classic sign in uroradiology, (6, 7) it is a sign of papillary necrosis and it is due to complete sloughing of the central papilla with distortion of a residual “claw-shaped” calyx. we clearly understand more cases are needed to validate this sign “lobster claw” in neuro radiology. correspondence dr. ahmed ansari ahmed.ansari2@gmail.com +91-9997456045 references 1.mckinley w, santos k, meade m, brooke k. incidence and outcomes of spinal cord injury clinical syndromes. j spinal cord med. 2007;30:215–24. 2.nowak dd, lee jk, gelb de, poelstra ka, ludwig sc. central cord syndrome. j am acad orthop surg. 2009;17:756–65. 3.li xf, dai ly. acute central cord syndrome: injury mechanisms and stress features.spine (phila pa 1976) 2010;35:e955–64. 4.aarabi b, koltz m, ibrahimi d. hyperextension cervical spine injuries and traumatic central cord syndrome. neurosurg focus. 2008;25:e9. 5.song j, mizuno j, inoue t, nakagawa h. clinical evaluation of traumatic central cord syndrome: emphasis on clinical significance of prevertebral hyperintensity, cord compression, and intramedullary high-signal intensity on magnetic resonance imaging.surg neurol. 2006;65:117–23. 6.dunnick nr, sandler cm, newhouse jh, amis es, jr. textbook of uroradiology 3rd ed. baltimore, md: williams & wilkins,2001; 300. 7.hartman gw, torres ve, leago gf, williamson b, hattery rr. analgesic-associated nephropathy. jama 1984; 251:1734-1738 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article unusual cranial trauma caused by pencil in teenager: case report amer saeed rashid, saif saood abdelrazaq, samer s. hoz, huber padilla, ramos-villegas yancarlos, daniela lópez-cepeda, mohammed al-dhahir, luis rafael moscote-salazar iraq, colombia, yemen doi: 10.1515/romneu-2017-0085 romanian neurosurgery (2017) xxxi 4: 545 550 | 545 doi: 10.1515/romneu-2017-0085 unusual cranial trauma caused by pencil in teenager: case report amer saeed rashid1, saif saood abdelrazaq2, samer s. hoz3, huber padilla4, ramos-villegas yancarlos4, daniela lópezcepeda4, mohammed al-dhahir5, luis rafael moscote-salazar6 1neurosurgeon, al sadar teaching hospital, najaf, lecturer in medical college, kufa university, najaf, iraq 2resident of neurosurgery, neurosurgerical teaching hospital baghdad, iraq 3neurosurgeon, neurosurgerical teaching hospital baghdad, iraq 4university of cartagena, cartagena de indias, colombia 5al thawra modern general hospital sana'a, yemen 6neurosurgeon, department of neurological research, health sciences and neurosciences (cisneuro) research group; department of neurosurgery, cartagena de indias, colombia abstract: introduction: penetrating lesions by pencil in the temporal lobe in children and adolescents are uncommon. we present the case of a teenager with penetrating injury by strange object in the temporal lobe. case: twelve years old male patient, with history of trauma while he was playing with his friends, presents alteration of the consciousness state, weakness in right hemibody and dysphasia. urgent surgery is practiced employing an incision in "c" form with improvement of the consciousness state during post-operative. discussion: penetrating lesions in the skull and brain are classified as missiles and non-missiles depending of their impact velocity. the wood is a porous organic material that provide a natural deposit of microbian agents, making it potentially lethal. pre-operative radiological evaluation allows check the trajectory of the penetrating object and secondary lesions present guiding de neurosurgical approach. the prognostic depends on penetration site, timely handling and complications associated. conclusion: penetrating lesions by pencil are uncommon, an appropriate imaging evaluation is fundamental to determine the neurosurgical approach that allows prevent and/or decrease secondary damage. key words: penetrating injuries, neurotrauma, head injury, trauma 546 | rashid et al unusual cranial trauma caused by pencil in teenager introduction cranioencephalic trauma caused by penetrating pencil lesions in children and adolescents are relatively rare and generally presented in the skull based, orbital cavity and temporal bone, being this one the less frequent. we present the case of 12 years old child with penetrating lesion by pencil in the temporal lobe. case report a 12-years-old male patient, with an imprecise history of trauma while he was playing with his friends, who presented altered state of consciusness with a glasgow scale score of 8/15, associated to grade 2 weakness in right hemibody and dysphasia. a small wound is observed on bleeding left temporal side, initially sutured in the emergency room, where a computed tomography (ct) scan of the brain was performed, and empiric antibiotic treatment and prophylactic antiepileptic drugs were started (fig. 1). five hours post trauma was performed an urgent surgery using an incision in “c” form centered around the wound, with bottom flap base. (fig. 2, 3 a and b). intraoperative it was observed a circular orifice followed by a circumferential craniotomy. the intracranial fragment of the pencil was extracted with minimal bleeding and the fragment of the pencil located intracerebrally measured 7.7cms. (fig.4). the source of the bleeding was from the tract that ceased with the irrigation disposed of the extraction of the pencil with debridation of the bone. postoperative tomography showed small residual intracerebral bleeding. after the intervention, the patient shows improvement of the state of consciousness in the respiratory care unit (rcu) followed by 5 days in the neurosurgery room. to be discharged completely conscious and with minimal weakness and improvement in speech. figure 1 ct scan penetrating object associated with bleeding figure 2 preoperative image showing site and size of the wound romanian neurosurgery (2017) xxxi 4: 545 550 | 547 a b figure 3 a and b a small craniotomy near the entrance hole is done in order to facilitate removal of the pencil. we removed the fragment of the pencil by pulling gently figure 4 a picture of the pencil after extraction figure 5 immediate postoperative brain ct-scan discusion penetrating head injuries are among the most severe traumatic injuries and with the higher incidence of morbidity and mortality, representing approximately 0.4% of all injuries (1). bursick et al., carried out a review of 21 cases of intracranial injuries by pencil, in which 82% of the cases were children and approximately 53% of those children were boys. in addition, they found that one of the less frequent areas is the squamous portion of the temporal bone (2). only 4 cases of penetrating lesions in the temporal bone have been found in the literature (3–5). penetrating lesions in skull and brain are classified as missiles and non missiles, wich differ in the impact velocity. in non missiles lesions the impact velocity is >100m/s, causing lesions due to laceration and maceration; on the other hand, missile lesions cause injuries due to kinetic and thermal energy. besides, the object penetration can be of two types: those that cross a natural orifice and the objects that cross the skull causing fracture, giving rise an artificial orifice(6). penetrate areas by low velocity are the foramen of the skull base, orbital cavityand 548 | rashid et al unusual cranial trauma caused by pencil in teenager squamous portion of temporal bone, being this one the less common. this cause a direct damage on brain tissue with possible laceration or vascular occlusion(7). penetrating lesions non missiles, unlike missiles, they not present concentric zone of coagulative necrosis caused by dissipated energy, and this allows a better management that contributes to get better the patient prognosis (1). these injuries are usually the results of both intentional and unintentional events, caused by cloves, screwdrivers, chopsticks, keys, electric drills, knifes and pens (8). the wounds by pencil are infrequent, and are considered dangerous by nature inherent of the wood due to it is an organic porous material that provides a natural deposit of microbian agents, also is soft, can be fragmented easily and usually it is not detected in routine radiological exams. this make that it is considered potentially letal (9). the involvement of the cerebral parenchyma by penetrating wounds through the temporal bone is facilitated by the thin thickness of this structure, short distance to the brain and vascular structures. in addition, it is more likely to present major neurological deficits and infectious complications including scalp cellulitis, subdural abscess formation, osteomyelitis, subdural and epidural empyema, meningitis, ventriculitis, cerebritis, and brain abscesses (2,10). the radiological evaluation allows to verify the trajectory of the penetrating object and the secondary lesions present guiding the neurosurgical approach. the simple radiograph offers information about the penetrating object but does not allow to analyze the cerebral parenchyma in search of damages of the intracranial structures (1,6,7,10). computed tomography (ct scan) adequately identifies the extent of the lesion, facilitating the detection of associated contusions, hematomas, major vascular lesions or brainstem lesions (1,6,10). moreover, it allows a better evaluation of the bony structures and informs about the relation of the penetrating object with the adjacent structures. ct scan is also useful in the monitoring of postoperative complications (7). many foreign bodies, especially organic materials, have densities very close to those of the soft intracranial and orbital tissues, which is why they are lost in ct scan, so a magnetic resonance imaging (mri) should be performed when we suspect them, being more sensitive t1 sequence than t2(1,2,6,9,11,12). if a major vascular lesion is suspected in the venous sinus and in cases of late subarachnoid hemorrhage or intracerebral hemorrhage, angiography by digital brain subtraction may be indicated after intervention for surgical planning (6,7,9,10,13). if the first scan is negative, it is best to repeat the examination 2 to 3 weeks later (14). penetrating lesions by non-sterile foreign bodies tend to become infected and lead to brain abscesses and meningitis, so prophylactic treatment with broad-spectrum antibiotics is necessary to cross the bloodbrain barrier in order to minimize romanian neurosurgery (2017) xxxi 4: 545 550 | 549 complications (1,6,7). the most frequent germ is staphylococcus aureus followed by other gram-negative bacteria and occasionally anaerobic bacteria (2,6,15). about 30% to 50% of patients with direct traumatic injury to the cerebral cortex develop seizures due to subsequent scarring (7,16). the use of antiepileptic medication prevents the onset of attacks early, but not late. for this reason, prophylaxis is recommended for the first 7 days after injury (1,7). among the cerebrovascular injuries reported in the literature are post-traumatic aneurysms, arteriovenous fistulas, occlusion of large vessels, venous thrombosis and vasospasm (1). outcome of csf is a rare complication with incidence of 0.5% and 3% (1,17). pituitary, immediate or late dysfunctions can occur (1). however, pituitary dysfunction as a direct result of trauma has been rarely reported (18). regardless of the type of cranial lesion, surgical management is recommended taking into account the point of entry (natural or not), object size, number of fragments, and secondary cerebral or vascular lesions. its objectives include local debridement of damage to the scalp, skull, dura and cerebral parenchyma, followed by dural closure, cranioplasty and cutaneous suture to prevent csf leakage and infection (1,6). surgical treatment is usually determined by factors such as location of the foreign body, path traveled, mechanism and extent of brain injury. it is for this reason, that the treatment seeks to prevent or reduce the risk of complications or secondary damages. craniotomy is the most commonly used surgical intervention because it allows the protection of critical neurovascular structures, debridement of the necrotic tissue of the brain, evacuation of the hematoma and repair of dural defects after extraction(1). however, surgical intervention is complicated if there is a lesion in a large vessel or venous sinuses, because they can lead to massive intraoperative blood loss, in these cases the treatment should have an endovascular approach (1,7). the prognosis of patients with this type of lesion depends on the site of penetration, timely management, associated complications, among other factors. penetrating lesions in the frontal, temporal and occipital lobe present a better prognosis (1). conclusions penetrating lesions by pencil are rare, this object may enter through a natural hole or not. adequate preoperative imaging is essential to determine the appropriate neurosurgical approach to prevent and / or reduce secondary damage (6). in the postoperative phase, antibiotic prophylaxis and anticonvulsive administration are recommended to reduce the presence of infectious and epileptic complications (1). correspondence dr. luis rafael moscote-salazar. universidad de cartagena, cartagena de indias, colombia e-mail: mineurocirujano@aol.com 550 | rashid et al unusual cranial trauma caused by pencil in teenager references 1. li x-s, yan j, liu c, luo y, liao x-s, yu l, et al. nonmissile penetrating head injuries: surgical management and review of the literature. world neurosurg. 2017;98:873.e9-873.e25. 2. erkutlu i, alptekin m, dokur m, geyik m, gök a. unusual penetration of a construction nail through the orbit to the cranium: a case report. ulus travma acil cerrahi derg. 2011;17(1):79–82. 3. foy p, hospital w, lane r. cerebral abscesses in children after pencil-tip injuries. lancet. 1980;662–3. 4. gupta a, chacko a, anil ms, karanth ss, shetty a. pencil in the brain: a case of temporal lobe abscess following an intracranial penetrating pencil injury. pediatr neurosurg. 2012;47(4):307–8. 5. bursick dm, selker rg. intracranial pencil injuries. surg neurol. 1981;16(6):427–31. 6. de holanda lf, pereira bja, holanda rr, neto jt, de holanda cvm, giudicissi filho m, et al. neurosurgical management of nonmissile penetrating cranial lesions. world neurosurg. 2016;90:420–9. 7. zyck s, toshkezi g, krishnamurthy s, carter da, siddiqui a, hazama a, et al. treatment of penetrating nonmissile traumatic brain injury. case series and review of the literature. world neurosurg. 2016;91:297–307. 8. srivastava c, singh sk, ojha bk, chandra a. intracranial penetrating glass injury: a case report. neurotrauma soc india. 2012;9(1):64–6. 9. hansen je, gudeman sk, holgate rc, saunders ra. penetrating intracranial wood wounds: clinical tomography. j neurosurg. 1988;68(5):752–6. 10. chowdhury fh, haque mr, hossain z, chowdhury nk, alam sm, sarker mh. nonmissile penetrating injury to the head: experience with 17 cases. world neurosurg. 2016;94:529–43. 11. turbin re, maxwell dn, langer pd, frohman lp, hubbi b, wolansky l, et al. patterns of transorbital intracranial injury: a review and comparison of occult and non-occult cases. surv ophthalmol. 2006;51(5):449–60. 12. smely c, orszagh m. intracranial transorbital injury by a wooden of ct and mri findings. br j neurosurg. 1999;13(2):206–11. 13. herring cj, lumsden ab, tindall sc. transcranial stab wounds: a report of three cases and suggestions for management. neurosurgery. 1988;23(5):658–62. 14. gutiérrez-gonzález r, boto gr, rivero-garvía m, pérez-zamarrón á, gómez g. penetrating brain injury by drill bit. clin neurol neurosurg. 2008;110(2):207–10. 15. kazim s, shamim m, tahir m, enam s, waheed s. management of penetrating brain injury. j emerg trauma shock. 2011;4(3):395–402. 16. kazim sf, bhatti a-a, godil ss. craniocerebral injury by penetration of a t-shaped metallic spanner: a rare presentation. surg neurol int. 2013;4:2. 17. pease m, marquez y, tuchman a, markarian a, zada g. diagnosis and surgical management of traumatic cerebrospinal fluid oculorrhea: case report and systematic review of the literature. j neurol surg reports. 2013;74(1):57–66. 18. kusanagi h, kogure k, teramoto a. pituitary insufficiency after penetrating injury to the sella turcica. j nippon med sch. 2000 apr;67(2):130–3. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article a rare case of cervical epidural extramedullary plasmacytoma presenting with monoparesis okan turk, ibrahim burak atci, hakan yilmaz, nuriye guzin ozdemir, salim katar, veysel antar, oguz baran, buket bambul sigirci turkey doi: 10.1515/romneu-2017-0013 romanian neurosurgery (2017) xxxi 1: 85 – 89 | 85             doi: 10.1515/romneu-2017-0013 a rare case of cervical epidural extramedullary plasmacytoma presenting with monoparesis okan turk1, ibrahim burak atci1, hakan yilmaz2, nuriye guzin ozdemir1, salim katar1, veysel antar1, oguz baran1, buket bambul sigirci3 1istanbul education and research hospital, department of neurosugery, istanbul, turkey 2usak university education and research hospital, department of neurosugery, usak, turkey 3istanbul education and research hospital, department of pathology, istanbul, turkey abstract: multiple myeloma and other plasma cell disorders are characterized by production of a large number of plasma cells in the bone marrow. on the other hand, plasmacytoma results from proliferation of abnormal plasma cells in the soft tissue or skeletal system. neurological complications are frequently observed in these diseases. the most commonly known complications among those complications are spine fractures, spinal cord compressions, and peripheral neuropathies. although neurological involvements are common in plasmacytomas, extramedullary spinal epidural localizations have been reported very rarely. in this case report, we aimed to present a plasmacytoma case that presented with acute onset of upper extremity monoparesis. a 40-year-old woman was admitted to our clinic with complaints of sudden weakness and numbness in her left arm following neck and left arm pain. emergency cervical magnetic resonance imaging (mri) revealed an epidural mass and the patient underwent emergency surgery. the patient showed improvement postoperatively and the pathology was reported as plasmacytoma. following hematology consultation, systemic chemotherapy was initiated and radiotherapy was planned after wound healing. key words: cervical epidural, extramedullary, plasmacytoma introduction plasmacytoma, a member of plasma cell dyscrasias and a rare disease among monoclonal gammopathies, describes situations in which multiple myeloma disease is seen outside the bone marrow. multiple myeloma is malignant and uncontrolled proliferation of plasma cells. the incidence of multiple myeloma is approximately 48/100,000 (1). plasmacytoma is frequently observed in solitary bone tissue and 86 | turk et al cervical epidural extramedullary plasmacytoma             extramedullary tissue. while the incidence of solitary plasmacytoma in all plasma dyscrasias is 5%, the incidence of extramedullary plasmacytoma is 3% (1, 2, 4). the extramedullary spinal epidural localization of plasmacytomas is very rare and only 6 cases have been reported in the literature. in this case report, we aimed to present a rare case of plasmacytoma who was evaluated in the emergency room with diagnosis of spinal epidural mass and paresis and underwent emergency surgery. case report a 40-year-old female patient was admitted to our emergency department with complaints of neck pain, weakness and numbness of the left upper extremity that last for 10 days. from the patient’s history, it was learned that her complaints were present for the last 3 months and that the numbness in the left hand worsened and weakness developed during the last 5 days. the patient's neurological examination revealed painful neck movements in all directions, limited flexion and extension and 3/5 muscle strength in the distal and proximal of right upper extremity. deep tendon reflexes were found to be increased in left upper extremity. hoffman test was positive on the left side. sensory examination revealed hypoesthesia conforming to the c3-c4-c5 dermatomes in the left upper extremity. both non-contrast and contrast enhanced emergency cervical mri scans were performed with the preliminary diagnoses of cervical disc herniation or spinal mass. cervical mri revealed a 5x4x5 cm, multilobulated, multicompartmental, well-demarcated soft tissue mass that fills the central spinal canal with expanding anterior epidural space at c3c4-c5 levels, extends into prevertebral and parapharyngeal space through left neural foramina and rests against the posterior border of sternocleidomastoid muscle (scm). the mass was hypointense on t1 and hyperintense on t2-weighted images and homogeneously enhanced on post-contrast examinations and it was evaluated as a tumor of peripheral nerve origin (figure 1 a, b, c, d). the patient underwent emergency surgery with the diagnosis of schwannoma. preoperative blood count blood test, sedimentation rate and c-reactive protein levels were normal. in the prone position, c3c4-c5 laminectomy was performed with posterior approach. following laminectomy, an off-white mass consistent with tumor that was compressing the dura posteriorly and laterally was seen. laminectomy boundaries were expanded laterally with moving the operating microscope laterally. the soft tumoral mass was dissected from the dura and biopsies were taken. the tumoral mass was found to extend laterally and to anterior part of the dura. the surgery was completed after deciding achieving enough decompression with partial excision. the patient did not have any additional neurological deficit post-operatively and improvement was observed in the neurological deficit in the distal left arm. pathology was reported as plasma cell tumor (figure 2). the patient was referred to hematology, systemic chemotherapy was initiated and radiotherapy was planned after wound healing. romanian neurosurgery (2017) xxxi 1: 85 – 89 | 87             figure 1 a, b,c,d mass lesion, compressing the spinal cord by filling the posterior c3-c4-c5 epidural space, that is hyperintense on sagittal t2-weighted mri, hypointense on sagittal t1-weighted mri figure 2 histopathological examination of the specimen showing plasma tumor cells with atypical nuclei (400x, h & e) discussion uncontrolled proliferation of blymphocytes and plasma cells, which are involved in antibody production, may result in development of plasma cell dyscrasias and plasmacytoma. diseases observed in plasma cell dyscrasias are divided into three groups. these are multiple myeloma, solitary plasmacytoma and extramedullary plasmacytoma, in descending order. there are proliferating malignant plasma cells in the bone marrow and diffuse lytic bone lesions in multiple myeloma. the incidence of plasmacytoma, one of the plasma cell dyscrasias, is 3%. the prognosis of plasmacytoma, in which solitary bone and extramedullary tissue involvement is also seen, is better than multiple myeloma. multiple myeloma usually accompanies extramedullary plasmacytoma and close follow-up is necessary for cases without accompanying multiple myeloma. a transformation rate of 32-70% to multiple myeloma in the following years has been reported in the literature (1,2,4). diagnosing plasmacytoma patients with preoperative mri scans and clinical findings is extremely difficult. mri reveals spinal epidural metastasis or spinal mass image. patients can be admitted with cord compression and myelopathy due to multiple myeloma. spinal cord compression can occur due to vertebral body compression fractures, spinal epidural tumor extension or extension of multiple myeloma in another tissue to epidural space (3,6,7). compression fractures can be seen in 55-70% of patients with 88 | turk et al cervical epidural extramedullary plasmacytoma             multiple myeloma with or without spinal cord compression. the incidence of paresis related to plasma cell dyscrasias is 5-10%. spinal column is one of the regions that involvement is seen in plasmacytomas. extramedullary plasmacytomas usually involve submucosal areas and necks of various organs. extramedullary plasmacytoma localized only in the epidural space is very rare (8). review of the literature revealed only 14 cases of cervicothoracic localization (cervical localization with 6 case and thoracic localization with 8 case). all these cases were observed to have myelopathy due to compression. the first case was reported by sod and wiener in 1957. it was a patient with metastatic spinal epidural tumor at thoracic 5 level and who presented with paraparesis (10). the first case of cervical region localized plasmacytoma was presented by kim et al. a 69 year-old female patient presented with paraparesis and was operated for a detected lesion extending from c6 to t10. in 1992, another 52 years old patient, who was presented with paraparesis and was found to have a lesion extending from c7 to t4, was reported (5,9). the last patient with cervical epidural plasmacytoma was reported in 2011. the 45-year-old patient was admitted with progressive paresis and an epidural mass extending from c4 to c7 was determined on mri (8). while the youngest patient was 40 years old, the oldest patient was 85 years old. however, all the patients except one were accompanied by multiple myeloma. patients with plasmacytoma should be consulted to hematology department and multiple myeloma screening should be performed. it should be kept in mind that multiple myeloma develops in 70% of such cases during follow-up (8). the optimal treatment of extramedullary plasmacytoma cases is not clear. radiation therapy should be added to treatment, as they are highly radiosensitive tumors. there are some tumor cases in which local control was achieved with only radiotherapy. besides, chemotherapy may also extend survival and recurrence time, thus preventing the transformation to multiple myeloma. the treatment is surgical excision and postoperative radiotheraphy chemotheraphy in patients with cord compression (8). conclusion we presented a 40-year-old patient who was admitted with neck pain and left upper limb paresis and who was diagnosed having a very rare case of plasmacytoma with epidural metastases. extramedullary plasmacytomas must be kept in mind in differential diagnosis of masses with spinal epidural metastasis and especially extension to neck. correspondence op. dr. hakan yılmaz address: usak university education and research hospital, department of neurosugery, usak, turkey tel: +90 506 621 18 29 e-mail: dr_hakanyilmaz@hotmail.com romanian neurosurgery (2017) xxxi 1: 85 – 89 | 89             references 1. alexanian r, weber d, liu f. differential diagnosis of monoclonal gammopathies. arch pathol lab med 1999; 123: 108-13. 2. durr hr, wegener b, krodel a, muller pe, jansson v, refior hj. multiple myeloma: surgery of the spine: retrospective analysis of 27 patients. spine 2002; 27: 3204. 3. galieni p, cavo m, pulsoni a, et al. clinical outcome of extramedullary plasmacytoma. haematologica 2000; 85: 47-51. 4. kelly jj jr, kyle ra, miles jm, o'brien pc, dyck pj. the spectrum of peripheral neuropathy in myeloma. neurology 1981; 3124-31. 5. kim fm, rosenblum j. extramedullary plasmacytoma manifested as an epidural mass. ajr am j roentgenol 1992; 159(4): 904-5. 6. latov n. pathogenesis and therapy of neuropathies associated with monoclonal gammopathies. ann neurol 1995; 37: 32-42. 7. lecouvet fe, malghem j, michaux l, et al. vertebral compression fractures in multiple myeloma. part ii. assessment of fracture risk with mr imaging of spinal bone marrow. radiology 1997; 204: 201-5. 8. lourbopoulos a, ioannidis p, balogiannis i, stavrinou p, koletsa t, karacostas d. cervical epidural plasmacytoma presenting as ascending paraparesis. spine j 2011; 11(5): 1-4. 9. matsui h, fujie h, tsuji h. extraosseous epidural tumor of immunoglobulin d myeloma. j spinal disord 1992; 5: 366–9. 10. sod lm, wiener lm. intradural extramedullary plasmacytoma: case report. j neurosurg 1959; 16: 107109. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article surgical treatment of rare metastatic tumor in meckel’s cave: a case report mugurel radoi, florin stefanescu, ram vakilnejad, fugaciu rodica romania doi: 10.1515/romneu-2017-0045 272 | radoi et al surgical treatment of rare metastatic tumor in meckel’s cave doi: 10.1515/romneu-2017-0045 surgical treatment of rare metastatic tumor in meckel’s cave: a case report mugurel radoi1, florin stefanescu1, ram vakilnejad2, fugaciu rodica2 1umf “carol davila” bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases – bucharest, romania 2neurosurgical department of the national institute of neurology and neurovascular diseases – bucharest, romania abstract: objectives: metastases in meckel’s cave are a rare tumor entity, but they should be considered in patients with a known primary malignancy and who complain of trigeminal neuralgia. methods: the case of a patient with a left trigeminal neuralgia caused by a metastatic tumor involving the meckel’s cave and gasserian ganglion is reported. preoperative symptoms included headache, trigeminal hyperesthesia and facial pain. results: the patient underwent microsurgical resection of the tumor, obtaining a histological diagnosis and a resolution of the pain. trigeminal motor function was preserved. conclusion: the best treatment for tumors of meckel’s cave, including metastases, is complete microsurgical removal. although good results have been reported with radiosurgery, this treatment should be reserved only for nonresectable and residual tumors. key words: metastases; meckel’s cave; trigeminal neuralgia; microsurgery introduction tumors of meckel’s cave involving the gasserian ganglion are usually benign and are either meningioma or trigeminal neurinomas (1,8). they represent less than 0.5% of all intracranial tumors (4). patients can complain of a variety of symptoms, but most of them present with dysfunction of the fifth cranial nerve (14). metastases in meckel’s cave are a rare tumor entity and should be considered as important differential diagnosis, especially if the patient suffers from a known primary malignancy. we report the case of a patient with left atypical trigeminal neuralgia caused by a metastatic tumor that involved the meckel’s cave. he was previously diagnosed with a pulmonary neoplasm. romanian neurosurgery (2017) xxxi 3: 272 280 | 273 case report a 50 years old man presented with a six months history of burning and stabbing pain around the left infraorbital ridge and cheek. the pain was limited in the territory of the distribution of the trigeminal nerve. during the last month, the frequency and severity of episodes increased, without occasional spontaneous remissions as before. all the symptoms were unilateral. the patient had undergone several therapeutic attempts to control his pain. previous treatment included dental extractions, diphenylhydantoin and carbamazepine administration. he had normal findings on physical examination, presenting no objective trigeminal motor loss, but a mild hyperesthesia in the left side of his face. cerebral computerized tomography (figure 1) showed a 3x2,5 cm. contrast enhancing lesion in meckel’s cave on the left, without erosion of the apex of the petrous bone, but with little extension in the posterior fossa through the tentorial incisure. axial t1weighted mri with gadolinium enhancement (figure 2) revealed a relatively well-defined mass in meckel’s cave, with less peritumoral edema. the tumor uniformly enhanced gadolinium and extended to the left cavernous sinus without infiltrated it, and down to the cerebello-pontine angle. during his hospitalization, the patient was diagnosed, due to a preoperative chest radiography with a right lung lesion. we performed a contrast chest computed tomography which revealed a large right lung and a hilar mass, with smooth, lobulated margins, having around 10 cm. in the largest diameter (figure 3). the patient underwent a left temporal craniotomy and a subtemporal intradural approach to the tumor. the craniotomy was enlarged to the base of the temporal fossa to obtain a flat viewing angle across the floor of the middle fossa. we performed a microsurgical complete resection of the supratentorial portion of the tumor, except for the portion that adhered to the inferior margin of the tentorial incisures (figure 4). the tumoral mass intimately adhered to the dura mater that overlying the meckel’s cave and gasserian ganglion. it was debulked and its capsule was dissected from the dura (figure 5). the dura mater was incised, but no extradural extension was noted. without drilling the petrous apex we did not properly exposed the posterior fossa portion. the histological diagnosis was metastatic carcinoma with neuroendocrine differentiation (figure 6). postoperatively, the patient did well, but continued to have a partial fifth nerve dysfunction involving the second division. he presented episodic double vision, for the next two month, due to a mild sixth nerve paresis. 274 | radoi et al surgical treatment of rare metastatic tumor in meckel’s cave figure 1 (a, b) preoperative axial contrast ct scan showed a relatively not well circumscribed tumor, with little peritumoral edema, which enhanced the contrast and extended down in the left cerebellopontine angle figure 2 (a, b) – axial t1-weighted images with gadolinium enhancement showed a 2,5x3 cm diameter tumor, with relatively uniform enhancement of gadolinium contrast, located in the left meckel’s cave, extending to the left cavernous sinus without infiltrated it, and down to the cerebello-pontine angle romanian neurosurgery (2017) xxxi 3: 272 280 | 275 figure 3 (a, b) nonenhanced ct scan of the chest showed a large right lung and a hilar mass, with smooth, lobulated margins, having around 10 cm. in the largest diameter, and extending right near the pleura figure 4 (a, b) – control native ct scan performed 6 days after surgery. the rest of the tumor attached to the inferior margin of the tentorial incisura was noticed 276 | radoi et al surgical treatment of rare metastatic tumor in meckel’s cave figure 5 (a, b) intraoperative images obtained under microscope during a subtemporal intradural approach. (a) – black arrows: tentorium; white arrowmicroscopic aspect of the tumor overlying meckel’s cave; (b) – black arrows: tentorium after removing the tumor over the gasserian ganglion; white arrow – the rest of the tumor extending inferiorly into the cpa discussion the most common tumors in meckel’cave are neurinomas and meningiomas (3, 4). besides this two entities, other types of pathological lesions have been reported in the region of the gasserian ganglion: metastatic carcinomas, sarcomas, arteriovenous malformations and amyloidomas (2, 4). we presented the case of a patient harboring a metastatic tumor in the meckel’s cave, who had been previously diagnosed with a lung primary malignancy. figure 6 hystopathology of the tumour (hematoxylin-eosin): metastatic carcinoma with neuroendocrine differentiation; typical histopathology includes nests of small primitive appearing cells with hyperchromatic nuclei, high nuclear to cytoplasmic ratio, mitotic figures and necrosis the incidence of brain metastases is difficult to determine with precision. in earlier neurosurgical series the overall incidence of cerebral metastases was 20%30% for all patients with systemic cancer (16). estimates based on more recent series and autopsy studies show a much higher incidence of brain metastases, with incidences varying between 8.3 and 11.1 per 100.000 individuals (11). approximately 40% of intracranial neoplasms are metastatic (7). these estimates place brain metastases first in frequency among all intracranial tumors, before intracranial glioma and meningioma (26). the histological type of the primary tumor appears to be the major factor of the frequency and pattern of intracranial spread. multiple, large autopsies series suggest that, in order of romanian neurosurgery (2017) xxxi 3: 272 280 | 277 decreasing frequency, lung, breast, melanoma, renal and colon cancer are the most common primary tumors that metastasize to brain (7, 11, 26). primary lung tumors account for 30% to 60% of all brain metastasis cases (8). breast cancer ranks second, contributing 10% to 30% (12) of all brain metastases among women (19), and renal cancer has a frequency of 11% (24). when the ability of a primary tumor to spread to the brain is considered, melanoma ranks first followed by lung and breast cancers (7, 15). the first sign of a tumor of meckel’s cave is usually that of trigeminal nerve dysfunction. facial hypalgesia along the distribution of the trigeminal nerve is the most common symptom. this is usually constant and burning in nature. a diminish corneal reflex and motor involvement of the fifth cranial nerve usually follows. not all tumors of the gasserian ganglion presented with pain. according to jefferson (10), those tumors located in the posterior fossa, compressing the sensory root, are thought to be typically painless, with posterior fossa and pyramidal signs. in our case, the tumor had little extension down in the cerebello-pontine angle, most of it compressing the gasserian ganglion in the meckel’s cave. that’s why our patient presented with stubbing facial pain and numbness, especially involving the second division of the trigeminal nerve, and no pyramidal signs were noticed. computerized tomography (ct) and magnetic resonance imaging (mri) permit the detection of small tumors in the region of meckel’s cave. mri study gives the best information concerning the localization and extent of the tumor in addition to revealing the displacement of neighboring structures and involvement of the cavernous sinus and vessels (20). sometimes, the limits of the tumor were very indistinct on ct scan, and only the presence of bone erosion suggests a mass lesion (2). in low-density tumors, such as lipoma, epidermoid cyst or chordoma, magnetic resonance imaging was especially useful. in our case, axial mri t1-weighted images with gadolinium enhancement showed a tumor, which enhances the contrast relatively uniform, located in the left meckel’s cave, extending to the left cavernous sinus without infiltrated it, and down to the cerebello-pontine angle. differential diagnosis must include meningiomas, neurinomas, epidermoid cysts, metastasis, chordomas, chondrosarcomas and maxillary sinus tumors (23). the surgical approach usually depends on the extent of the tumor. the main part of the tumor is located in the middle fossa but it may have extracranial extension or posterior fossa extension. these modifications are important to assure the best surgical approach for each type of lesion. these tumors can be resected via an extradural approach or an intradural approach. most of them are extirpated via a middle fossa approach, either intradurally (for large lesions) or extradurally (for small lesions). the degree of difficulty in radical surgical removal depends on the particularities of each case, but, mainly, it depends on anatomical extension of the tumor. in order of their frequencies, the most used approaches are: middle fossa approach, retrosigmoid approach and presigmoid approach (20). the 278 | radoi et al surgical treatment of rare metastatic tumor in meckel’s cave last two approaches are especially used in the resection of tumors with important extension in the posterior fossa. in cases of small extranevraxial lesions, such as meningiomas and neurinomas, a safe surgery could be performed only by using an extradural approach (20, 23). the majority of tumors in meckel’s cave location are amenable to be resected via the subtemporal intradural approach. hyperventilation and intraoperative spinal drainage reduced brain bulk, and temporal bone retraction was minimal. the tumor could extend from meckel’s cave to the superior orbital fissure and down to the cerebellopontine angle. the mass is usually well circumscribed and total removal can be achieved, leaving only remnants of capsule adherent to the fifth cranial nerve. under microscope magnification, a dural opening must be made parallel to the tentorial edge in order to avoid cutting across fibers of the trigeminal nerve that lie directly beneath. most of the tumors in this location are benign and can be totally resected. when flecks of capsule from the tumor is adherent to nerve fibers and brain stem, or is important extension in the cpa, attempts to remove the entire tumor would significantly increase the neurological deficits (5). for the rest of the tumor, fractioned radiation therapy is used. using microsurgical techniques, the outcome of tumors involving meckel’s cave and gasserian ganglion is usually favorable. the most frequent symptom after surgery is trigeminal hypesthesia, which is transient in most cases. facial pain may persist after surgery, but most patients report improvement or total relief during follow-up. patients who had experienced preoperative atypical trigeminal pain reported a resolution of their symptoms after surgery. diplopia, csf leak or even meningitis have been also described as possible complications (20, 21). most new cranial nerve deficits present resolution within 4-6 months (22). several contemporary series have demonstrated no deaths or major surgical complications with radical removal of tumors in the meckel’s cave and gasserian ganglion (6, 21). for small, nonresectable and residual tumors, good results have been reported with radiosurgery (17, 18). long-term follow-up of patients treated with this method is still needed to evaluate the exact role of the radiosurgery in the late control of these lesions (17, 18). lesions in meckel’s cave can have a varied and unusual presentation, as well as an assortment of pathology. beside neurinomas and meningiomas, metastatic tumors have been reported occupying meckel’cave and compressing gasserian ganglion. metastatic involvement of the meckel’s cave occurs either via hematogenous dissemination from distant metastatic or perineural spread from tumors of the head and neck. very few cases of metastatic involvement of the meckel’s region have been published. on a meta-analysis (2010) of malignant tumors involving this region, soni rc et al. (23) found 20 cases, including theirs, of malignant involvement of meckel’s cave described in the literature. most primary neoplasm involved were: small cell lung cancer (2 cases), breast cancer (4 cases), adenocarcinoma of colon (2 cases), lymphoma romanian neurosurgery (2017) xxxi 3: 272 280 | 279 (4 cases), renal cell cancer (1 case) and folicullar thyroid cancer (1 case) (9, 13, 25). conclusion malignant lesions involving the structures of meckel’s cave are uncommon and may present later in life compared to meningioma and schwannoma. we underline the importance to thoroughly investigate the patients early for a possible primary as well as metastases, in those patients found to present a lesion in meckel’s cave. moreover, it is difficult to distinguish metastatic tumors from benign tumors solely based on clinical or radiographic characteristics. we believe that the best treatment is microsurgical removal of the metastases, followed, when necessary, by fractioned radiation therapy for any rest of the tumor. correspondence dr. mugurel radoi umf “carol davila” bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases bucharest email: muguradoi@yahoo.com references 1.baker hl jr. cerebellopontine angle myelography. j neurosurg 36:614-624, 1972. 2.beck dw, menzes ah. lesions in meckel’s cave: variable presentation and pathology. j neurosurg 67:684689, 1987. 3.butti c, gaetani p, giorgdana mt, et al. meningiomas of meckel’s cave. surg neurol 20:305-309, 1983. 4.de benedittis g, bernasconi v, ettore g. tumors of the fifth cranial nerve. acta neurochir 38:37-64, 1977. 5.delfini r, innocenzi g, ciappetta p, domenicucci m, cantore g. meningiomas of meckel’s cave. neurosurgery 1992;31 (december):1000-6, discussion 6-7. 6.goel a, muzumdar d, raman c. trigeminal neuroma: analysis of surgical experience with 73 cases. neurosurgery 52:783-790, 2003. 7.gorgan m., bucur n, neacsu a, pruna vm, craciunas s, et al. deontological issues – possible misdiagnosis of cerebral metastases. romanian neurosurgery 2011; 13:240-254. 8.hedeman ls, lewinsky bs, lochridge kg, trevor r. primary malignant schwannoma of the gasserian ganglion. report of two cases. j neurosurg 48:279-283, 1978. 9.hirota n, fujimoto t, takahashi m, fukushimay. isolated trigeminal nerve metastasis from breast cancer: an unusual causeof trigeminal mononeuropathy. surg neurol 1998; 49(may):558-61. 10.jefferson g. the trigeminal neurinomas with some remarks on malignant invasion of the gasserian ganglion. clin neurosurg 1:11-54, 1951. 11.kehrli p. epidemiologie des metastases cerebrales. neurochirurgie, 1999, 45, nr.5, 357-363. 12.markesbery wr, brooks wh, gupta gd, et al: treatment for patients with cerebral metastases. arch neuro135:754-756,1978. 13.mastronardi l, lunardi p, osman farah j, puzilli f. metastatic involvement of the meckel’s cave and trigeminal nerve. a case report. j neurooncol 1997; 32(march): 87-90. 14.nager gt. neurinomas of the trigeminal nerve. am j otolaryngol 5:301-333, 1984. 15.nussbaum es, djalilian hr, cho kh, hall wa. brain metastasis. histology, multiplicity, surgery and survival. cancer 1996; 78: 1781-1788. 16.percy ak, elveback lr, okazaki h, et al: neoplasms of the central nervous system: epidemilogic considerations. neurology 22:40-48, 1972. 17.peter s, bayrakli f, kilic t, pamir mn. gamma-knife radiosurgery in the treatment of schwannomas. acta neurochir (wien) 149:1133-1137,2007. 18.phi jh, paek sh, chung ht, jeong ss, park ck, jung hw et al. gamma knife surgery and trigeminal schwannoma: is it possible to preserve cranial nerve function? j neurosurg 107:727-732, 2007. 19.posner jb: neurologic complications of cancer. philadelphia, f. a. davis, 1995, pp. 3¬14; 77-110. 20.ramina r, mattei ta, soria mg, da silva eb, leal ag, neto mc, fernandes yb. surgical management of 280 | radoi et al surgical treatment of rare metastatic tumor in meckel’s cave trigeminal schwannomas. neurosurg focus 25(6): e6, 2008 21.samii m, migliori mm, tatagiba m, babu r. surgical treatment of trigeminal schwannomas. j neurosurg 82: 711-718, 1995 22.shrivastava rk, sem c, post kd. trigeminal schwannomas, in winn hr (ed): youmans neurological surgery. philadelphia: wb saunders company, 2004 pp1343-1350. 23.soni r, kumar g, sahota p, miller dc, litofsky ns.metastases to meckel’s cave: report of two cases and comparative analysis of malignant tumors with meningioma and schwannoma of meckel’s cave. clinical neurology and neurosurgery 112 (2010) 927-932. 24.steinfeld ad, zelefsky m: brain metastases from carcinoma of bladder. urology 29:375-376, 1987 25.theuer se. metastasis in meckel’s cave. clin neuroradiol 2007; 17:41-7. 26.wingo pa, tong t, bolden s: cancer statistcs, 1995. ca cancer j olin 45:8-30, 1995. microsoft word 6marciucemilia_unusual 224 | marciuc et al unusual posttraumatic vascular and cerebral injuries in young patients             doi: 10.2478/romneu-2018-0029 unusual posttraumatic vascular and cerebral injuries in young patients emilia marciuc1,2, m. barcan1, b. dobrovăţ1,2, roxana popescu1,2, cornelia tudorache2, danisia haba1,2 1department of radiology and medical imaging of emergency hospital „prof. dr. n. oblu”, iasi, romania 2”grigore t. popa” university of medicine and pharmacy, iasi, romania abstract: blunt carotid artery injury is a relatively rare but potentially lethal injury that predominantly occurs in high-impact mechanisms such as motor-vehicle collision. any simptoms or neurological deficits following a multiple trauma patient mandates a thorough evaluation and consideration of bci. this is a case report on two young patients with neurologic simptoms developed after blunt trauma in the cervical region. both patients had left internal carotid artery dissection diagnosed on a ctangiography, followed by middle cerebral artery territory infarction. although it can be a delayed onset with no signs of vascular demage, we believe that, by implementing a protocol with additional imaging for early detection, we can prevent a devastating outcome. key words: cerebral infarction, internal carotid artery dissection, trauma introduction blunt carotid artery injury is a rare condition first described by yamada et al. in 1967(yamada s 1967)that predominantly occurs in high-impact mechanisms such as motor-vehicle accidents. it is observed in 1%2.6% of blunt trauma cases and it’s associated with high rates of ischemic stroke (up to 60%) and mortality (19-43%)(thomas s. lee 2014). because it’s a life-threatening condition, early detection is mandatory and requires a good understanding of injury mechanism and thorough evaluation which can be a key point in offering the patient a favorable outcome. case report case 1 a 27 years old female patient, motorvehicle collision victim (driver) was brought to the emergency room presenting headache, dizziness and multiple contusions including a cervical region blunt trauma. an initial non contrast head ct was performed that showed no posttraumatic lesions. after 24 hours, the romanian neurosurgery (2018) xxxii 2: 224 229 | 225             patient’s condition worsened and a head mri revealed a t2wi, flair, t2*ge high-signal and t1wi low-signal in the cortical and deep white matter cerebral area of the left frontal, temporal and parietal lobes. the axial diffusion-weighted image demonstrates high signal in the same area with corresponding low signal on the apparent diffusion coefficient (adc) maps, consistentwith true restricted diffusion and an acute/subacute infarction in the middle cerebral artery territory (figure 1). figure 1 acute/subacute infarction in the middle cerebral artery territory (a. axial t2wi, b. axial flair, c. dwi, d. adc map) another area with same aspects, with a diameter of 13 mm in the right cerebellar hemisphere is shown, consistent with a recent lacunar infarction or a diffuse axonal lesion (figure 2). figure 2 recent lacunar infarction or a diffuse axonal lesion (a. axial t2wi, b.axial t2*) also, in the se sequences, no signal-void in the cervical, petrous, lacerum, cavernous and supraclinoidiansegments of left internal carotid artery is visualized, aspect which indicates for a slow flow or occlusion of left aci (figure 3 a,b). same absence of signalvoid for v3 and v4 segments of right vertebral artery (figure 3 c). figure 3 – spin echo sequences (a,b. axial t2wi, c. coronal t1wi) 226 | marciuc et al unusual posttraumatic vascular and cerebral injuries in young patients             a head and neck ct angiography was recommended that showed complete occlusion of left aci right above bifurcation and partially occlusion of right vertebral artery in v3 and v4 segments (figure 4). figure 4 complete occlusion of leftaci right above bifurcation (a,b) and partially occlusion of right vertebral artery in v3 and v4segments (c,d). on non-contrast head ct scan was observed a midline shift of 9 mm which was an indication for a decompressive craniectomy (figure 5 a,b). the following ct scans showed the ischemic area throughout all stages. after 4 month the patient came back for follow-up (figure 5 c) and presented with improvements in motor control and regained the capacity to carry out activities of daily living. figure 5 – pre-op (a), post-op (b) and after 4 months(c) radiological aspects case 2 a 17-year old male patient suffered a cervical trauma after getting his neck caught between the doors of an elevator with no immediate symptoms. after approximatively 2 hours, the patient presented neurologic symptoms (aphasia, motor impairment) and a left cervical hematoma. after another 3 hours is brought to the emergency room where a non-contrast head ct scan is performed, which reveals a loss of grey-white matter differentiation,hypoattenuation of deep nuclei, cortical hypodensity with associated parenchymal swelling and resultant gyral effacement in the left frontal, temporal and parietal lobes. also the hyperdense middle cerebral artery sign (figure 6 a)andmiddle cerebral artery dot sign are present (figure 6 b), all aspects are consistent with an acute stroke in the left middle cerebral artery territory. carotid ultrasound was performed and detected a free-floating thrombus of the romanian neurosurgery (2018) xxxii 2: 224 229 | 227             left carotid artery (figure 7 a,b). the vascular neurosurgical team was consulted and an endovascular treatment with stenting of the carotid artery was immediatly performed (figure 8), but the evolution of the patient was variable. the post-surgery head ct scan showed a massive edema with a midline shift of 10 mm (figure 9a), so a decompressive craniectomy (figure 9b) was indicated, but the outcome of the patient was unfortunate with exitus in the next 72 hours. figure 6 – acute stroke in left middle cerebral artery territory hyperdense middle cerebral artery sign (a) and middle cerebral artery dot sign (b). figure 7 – us free-floating thrombus of the left carotid artery (a. sagital view, b. transversal view) figure 8 endovascular treatment with stenting of the left carotid artery figure 9 – pre-op (a) and post-op (b) radiological aspects. discussions blunt carotid artery injuries are uncommon and considered life-threatening because of the delayed onset of neurologic deficits which can lead to a poor outcome for patients. therefore, knowledge regarding the injury mechanism may be of aid in making an earlier diagnosis and treatment. mechanisms of injury include a direct blow to anterolateral aspect of the cervical region, hyperextension, flexion or rotation of the neck, even the vasocompression of the internal carotid artery between the cervical spine and mandible (george galyfos 2016). these forces are present in the setting of motor-vehicle collisions, cervical spine or 228 | marciuc et al unusual posttraumatic vascular and cerebral injuries in young patients             mandible fractures, chiropractic manipulation (thomas s. lee 2014) and can lead to small lesions of the vessel wall which may result in intimal tears, creating the potential for vessel dissection (separation of vesselwalltissuelayers) or intramural thrombus formation, leading to vessels stenosis or complete occlusion (thomas s. lee 2014). these events lead to failure of brain perfusion and ischemic stroke which can have different outcomes even in young patients with no other comorbidities. these patients were both diagnosed with carotid artery dissection but the timing of diagnosis was different. in the first case, a high index of suspicion given by the traumatic mark in the cervical region and the mechanism of injury should be an important determinant in ordering a ct angiography despite the poor clinical signs. most likely, the internal carotid artery dissection was caused by the hyperextension of the neck in the moment of impact combined with the seatbelt injury in the lateral aspect of the neck. although the patient wasn’t a good candidate for endovascular treatment, the outcome was satisfying considering the reduction in the extent of neurologic impairment. another particularity of the case was the dissection of right vertebral artery induced also by shearing forces in hyperextension/flexion during collision but with no consequences for the posterior cerebral artery territory of the brain. traumatic blunt vertebral artery injury is a rare condition, the reported incidence is variable in the literature (0.5-2% of all trauma patients)(fassett dr 2008). motor vehicle accidents are the first cause of this type of injury but the v2 segment is most commonly affected while in v3 and v4 segments the artery has a greater mobility and is more resistant to blunt trauma(r. m. desouza 2011). most commonly, these dissections are sub-intimal and cause stenosis (48%) or occlusion (35%) (karthikeyan y.r. 2017). in the second case, there was an earlier onset of neurologic deficits which established the diagnosis of carotid artery dissection and an endovascular stenting was possible within a few hours after presenting to the emergency room. however, the outcome was unfortunate. carotid artery dissection is a rare but lifethreatening condition that should be considered in patients with a mechanism of injury that places these major vessels at risk. knowledge regarding the mechanism of injury may facilate an early diagnosis with major impact in the patients’ prognosis. a study conducted by miller pr has identified specific findings that may suggest a blunt carotid artery injury including c-spine fracture, le fort ii/iii facial fracture, horner’s syndrome, skull base fracture involving the foramen lacerum and soft tissue injury in the cervical region. (miller pr 2002). although, digital substraction angiography (dsa) is the gold standard for the diagnose of a possible dissection(thomas s. lee 2014), computed tomography angiography (cta) is more accessible, can be easily performed in cases of severe trauma and can be a useful diagnosis tool. romanian neurosurgery (2018) xxxii 2: 224 229 | 229             conclusions patients with traumatic blunt carotid artery dissection are a subgroup of cases which demand special management in an interdisciplinary setting and additional imaging in order to provide a good outcome, especially in young patients. despite the subtle clinical picture at the beginning, the morbidity and mortality rates are high, so the early detection is a key factor for an optimal result. correspondence dr. bogdan dobrovăț, university of medicine and pharmacy "gr. t.popa" iasi email: bogdan.dobrovat@yahoo.com references 1. fassett dr, dailey at, vaccaro ar. "vertebral artery injuries associated with cervical spine injuries: a review of the literature." j spinal disord tech, 21(4) : 252–258, 2008. 2. george galyfos, konstantinos filis, fragiska sigala, argiri sianou. "traumatic carotid artery dissection: a different entity without specific guidelines." vascular specialist international, 32(1): 1-5, 2016. 3. karthikeyan y.r., sanjeev chopra, somnath sharma, devendra purohit. "post traumatic vertebro basilar dissection: case report and review of literature." romanian neurosurgery, 31(3): 310-315, 2017. 4. lee ts, ducic y, gordin e, stroman d. "management of carotid artery trauma." craniomaxillofac trauma reconstruction: 175-189, 2014. 5. miller pr, fabian tc, croce ma, cagiannos c, williams js,vang m, qaisi wg, felker re, timmons sd. "prospective screening for blunt cerebrovascular injuries. analysis of diagnostic modalities and outcomes." ann surg, 236(3): 386–395, 2002. 6. r. m. desouza, m. j. crocker, n. haliasos, a. rennie, a. saxena. "blunt traumatic vertebral artery injury: a clinical review." eur spine j, 20(9): 1405–1416, 2011. 7. thomas s. lee, yadranko ducic, eli gordin, david stroman. "management of carotid artery trauma." craniomaxillofac trauma reconstruction, 7(3): 175– 189, 2014. 8. yamada s, kindt gw, youmans jr. "carotid artery occlusion due to nonpenetrating injury." j trauma, 192(1): 333–342, 1967. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article clinical outcome and prognostic factors for central neurocytoma, a study of 14 cases mohamed abdel bari mattar, ashraf el badry egypt doi: 10.2478/romneu-2018-0009 romanian neurosurgery (2018) xxxii 1: 73 84 | 73 doi: 10.2478/romneu-2018-0009 clinical outcome and prognostic factors for central neurocytoma, a study of 14 cases mohamed abdel bari mattar, ashraf el badry department of neurosurgery, mansoura university, egypt abstract: background: since they’re rare, the intraventricular neoplasms “central neurocytoma” best management got diverse, and mystifying. aim of the work: to assess outcome for patients with central neurocytoma and value of specific factors like tumor size, surgical resection extent, atypia, and concomitant other modality of treatments by radiotherapy in their survival. patients & methods: 14 patients (8 males, 6 females) were managed surgically between 2012 and 2016. they were assessed clinically, radiologically and their outcome in relation to selected factors. results: median age at diagnosis was 28.3 years in average (range 16–58). median follow-up was 32.2 months.we lost 2 cases to follow-up in post-operative period. six patients had recurrent of neurocytoma tumours.five patients (35.7 %) obtained gross total resections (gtr) while 9 patients (64.2 %) had subtotal resections (str). two str patients (14.2 %) received dose of radiation post operatively that significantly enhanced overall pfs (p =0.047). our series data propose that radiation therapy following (str) usually increase (pfs). two patients proved to have atypical neurocytoma by pathological reports died at 2.3 and 10.2 months after the microsurgical procedures. mib-1 tagging index higher than 4 % is an indicator for poor outcome. we used kaplan–meier beside cox proportional hazards methods in determining the progression-free survival (pfs) in our study. conclusion: the extent of surgical resection may improve the neurological condition but not the survival, atypia was the most important factor determine the recurrence & survival while radiotherapy improve the survival quietly. key words: atypical central neurocytomas, benign central nervous system tumor, central neurocytomas, mib-1 tagging index, progression free survival introduction central neurocytoma (cn) is an uncommon central nervous system tumor which encompass only 0.1–0.5 % of all primary brain tumors. it was firstly described by hassoun and colleagues in 1982 and, by the early 1990s; it had become a well-defined clinical and pathological entity [8]. it was classified by the world health organization in 74 | bari mattar et al clinical outcome and prognostic factors for central neurocytoma the year of 2000 a.d. as grade ii but malignant variant have been reported [13]. however only not more than one thousand patients with cn have been stated worldwide [10]. earlier studies showed that cn derived from ectodermal/nervous system tissue and mainly located in deep mid-line structures near the foramen of monro (so it can arise from the walls of the lateral ventricles, fornix, the septum pellucidum), it is typically situated supratentorially filling the lateral ventricle(s) and/or the third ventricle with evolving of neurological symptoms related to intracranial hypertension (headaches beside plus or minus visual disturbances. the clinical symptoms period usually not more than 6 months [25]. neurocytomas may be found away from the ventricles and have been defined by who as an extraventricular neurocytomas (evns). this extraventricular neurocytomas (evns) beside its different places, it have a broader scope in morphology compared with intraventricular neurocytomas. [13] cn frequently arose in youth period, 70% of cn patients present in the third and fourth decade of life. tumor incidence shows no significant gender preponderance [3, 15, 24]. in spite of most cn were benign and most of the patients with cn survived for long time after a gross total removal but atypical pathological variation have been described and even residual tumors parts after surgery may transformed to have possibility of more malignant features [11, 23]. surgery is the basic traditional treatment for these cases and the degree of surgical excision is the major element affecting the clinical outcome. furthermore, radiotherapy (rt) can efficiently control remaining tumor following partial microsurgical removal or in recurrent cases [12, 17]. the standard guidelines as a stepladder treatment for this neoplasm has not so far been recognized, particularly that the role of radiation therapy after the surgery stays debatable [7, 19, 22]. central neurocytomas that possess atypical pathologic characteristics act more violently and might be associated with high recurrence rate. the usage of mib-1 with specific threshold as an objective marker to signifying atypia is debatable [4, 9, 21]. mib-1 marker have been used in many studies for grading of astrocytoma cases. these studies postulate that e3 ubiquitin-protein ligase mib1 act as an enzyme which encoded by the human mib1 gene in regulating apoptosis. [16] the clinical management of neurocytoma remain unclear, in this paper, we discussed the management of these cases and investigated whether initial tumor size, degree of tumor excision, mib-1 tagging index and postoperative dose of radiotherapy have impact on clinical outcomes or not. patients and methods all cn patients were treated at mansoura university hospitals (muh) between 2011 and 2016. the patients of our study have the following inclusion criteria: (1) primary surgery was achieved at muh, (2) original management documents was available, and (3) the tumor pathology results were obtainable in the patient’s records. all existing cases were included in our study regardless the follow-up period because of the rarity of this tumor, the medical reports were reviewed and the demographic, treatment options used and outcome data were collected. tumor size was romanian neurosurgery (2018) xxxii 1: 73 84 | 75 calculated by using t1 imagines post-contrast and t2-weighted brain mri films in the 3 orthogonal directions, for the tumor volume determination. degree of tumours excision was clarified according to the operative notes reviewing and post-operative radiology. gross total resection (gtr) was defined by images as complete tumor surgical removal and neartotal excision while all other surgical techniques as well as partial resection, biopsy with or without cyst aspiration, took in account as subtotal resection (str). patients were followed in post-operative period clinically and radiologically (mri and/or ct) during the post-surgical follow-up period. tumor evolution was expressed as ≥25 % expansion of the above mentioned radiologic tumor volume estimation. outcomes of interest included progression free survival (pfs) from the date of primary surgery besides overall survival (os) of the same period. statistical analysis the evaluation of (pfs) and (os) was done by using the kaplan–meier method. while the log-rank test and univariate cox proportional hazards methods were applied to validate the following items as prognostic factors, for instance: degree of tumor removal, tumor volume, mib-1 tagging index, and concomitant postoperative radiotherapy through its affection on pfs and os. we used p ≤ 0.05 as statistical significance threshold in our research. results demographic data: a sum of 14 cn patients (it showed histological and immunohistochemical classical features) were treated in our department but only 12 patients were alive at time of study (table 1). two patients were lost to follow-up afterward primary surgery but were still incorporated in the study. the proportion of male to female was 1.3:1. the median age at tumor diagnosis was 28.3 years (range 16.2– 58.4 years). all patient suffered from manifestation of high icp and three cases had seizures. radiological results: ct brain of these cases showed a well demarcated, isoor faintly hyper dense in the supra tentorial intraventricular space. calcifications have been seen in eight cases. images obtained after administration iodide contrast substances displayed moderately homogeneous enhancement lesions in the images of all cases. while cystic changes appeared in 6 cases. mri images of the cases revealed: large heterogeneously enhancing intraventricular mass which has a “soap bubble” appearance on t2. in all cases and broad attachment to the septum pellucidum. most patients (12 cases) had their tumors in the cavity of the lateral ventricle, and (2 cases represent 14%) experienced midline ventricular lesions. the median biggest tumor dimension was 6.7 cm (vary between 3.8–9.6 cm) on preoperative mri examination. anterior trans callosal approach (tca) was selected in six cases, and anterior transcortical approach (tco) was selected in eight cases. five of the fourteen cases had gtr, on other hand 64 % of cn patients (9/14) had str. massive intraoperative bleeding is crucial point of resectability. all tumors were considered as who grade ii on histopathologic examination. three of the 14 tumors (21 %) were distinguished as atypical on neuropathological study. 76 | bari mattar et al clinical outcome and prognostic factors for central neurocytoma almost 65 % (9/14) of patients had hydrocephalus that mandated the application of a ventriculoperitoneal shunt at different perioperative durations. one patient who had a gtr was given a dose of external beam radiotherapy (ebrt) while only two cases with str (14.2%) were given radiation therapy after primary surgical excision. the remaining 7 cases did not receive any radiation. outcomes follow-up of the study ranged 10.6–43.8 months (median duration was 32.2 months).it was found that along the study time period, six patients (42 %) developed recurrent or progressive disease while the residual cases of the study did not. two cases of mortality in the study (14.2 %) were reported. the 2-year pfs was 71 % in our research beside predictable 5years pfs was 52 % (table 2). the age and gender notably did not influence pfs. as regard tumor size, p value was 0.79 which statistically significant: pfs for 2-years was 72 % when tumors size lower or equal to 6.1 while it was 76% for tumors size higher than 6.1 cm concerning tumor atypia in pathological examination & immunohistochemical staining, 2-year pfs was 89% for mib tagging higher or equal to 4 versus 49 % for mib tagging below 4% (p = 0.0025). the use of radiotherapy following surgery for patients with subtotal resection str showed that the overall pfs progress was significant with p= 0.047. as regard the two mortality cases, one happened 2.3 months after surgery due to intracranial hemorrhage. while the second occurred 10.2 months due to disease progression. notably both patients had high tumor atypia in their pathological reports, where mib-1 labeling were 5.9 in the first case and 6.7 % in the second case. table 1 demographic and treatment data romanian neurosurgery (2018) xxxii 1: 73 84 | 77 table 2 progression free survival rates (pfs) in relation to clinical factors management of cases with progressive course quite a few executive approaches were applied for the 6 patients who had cn with progressive course or recurrence. two patients (30%) administrated course of chemotherapy. first case who was a course of ccnu had good radiographic images and stable disease for 2 years later. the other one was treated with temozolomide, and had almost three years of stable tumor course before restrained progress. two other cases (30 %) had radiosurgery courses. both showed radiographic images proved the effectiveness of radiation in control of the tumours development on follow ups. the last two patients (33 %) had repeat surgery. one of them was transferred to urgent surgery as a sequelae of intracerebral hemorrhages. the surgery did not improve the neurological condition of the patient and the patient died few days after. case illustration first case 29 years old lady complained from manifestation of intracranial hypertension in the form of sever persistent headache not responding to medical treatment with blurring of vision frequent vomiting, tinnitus and urination disorder. imaging studies of the brain:  c.t. (figure 1) that show a large lesion measuring 9x7x5cm in both lateral ventricle & centered on septum pellucidum. there are numerous high density foci concomitant with tumor calcification  mri (figure 2, figure 3) revealed large minimal enhancing intraventricular mass which has a “soap bubble” appearance on 78 | bari mattar et al clinical outcome and prognostic factors for central neurocytoma t2. it has also broad attachment to the septum pellucidum  digital subtraction angiography “dsa” (figure 4) show tumor feeder from anterior & posterior choroidal arteries  2-deoxy-2[f-18] fluoro-d-glucose positron emission tomography “fdgpet” (figure 5) show slight accumulation in the left side part of the mass (60%) figure 1 a preoperative axial ct images demonstrating a large lesion measuring 9x7x5cm in both lateral ventricle & centered on septum pellucidum figure 2 mri of the same tumor: a a:t1wi, b:dwi (axi), c:t1wi+ce(cor), d:t2wi (axi), e:t1wi+ce(axi), f:t1wi+ce(sag) figure 3 mri of the same tumor coronal cuts with contrast show the wide connection to septum pellucidum figure 4 digital subtraction angiography dsa show feeder from anterior & posterior choroidal arteries figure 5 2-deoxy-2[f-18] fluoro-d-glucose positron emission tomography fdg-pet show slight accumulation in the left side part of the mass (60%) romanian neurosurgery (2018) xxxii 1: 73 84 | 79 first step was forming extra ventricular drainage “evd” through frontal burr whole as the patient showed deterioration in conscious level gcs was 11/15. the opening pressure was 40 cm h2o (figures 6, 7). figure 6 a diagram for the site of frontal burr hole for evd figure 7 a.ct brain (axi): show proximal intraventricular catheter of evd. opening pressure 40cmh20. b. ct brain (axi): after 2 days of evd insertion surgical procedure detail • transcortical trans ventricular approach through middle frontal gyrous. (figure 8b) • the tumor outside is a dark purple soft tumor, the inside is a grayish hard tumor with calcification. tumor removed piece meal identification of anterior septal vein & thalamostriate vein of right lateral ventricle (figure 8c) • identification of the vascular structures in the field: anterior septal vein, thalamostriate vein & internal cerebral vein of right lateral ventricle at the end stage of tumor resection (figure 8d,e). • open foramen of monro figure 8 a-e show diagrams of surgical steps in resection of cn mass of 29 years old female diagram for the site of frontal burr hole for evd figure 9 a-e show microscopic pictures of surgical steps in resection of cn mass of 29 years old female till complete removal 80 | bari mattar et al clinical outcome and prognostic factors for central neurocytoma a. he stain (×100) b. he stain (×400) c. gfap (+) d. olig2 (-) e. synaptophysin f. nf (-) g. mib 1 (+) 3 % figures 10 a-g a microscopic histopathological examination pictures showed: a&b revealed neurocytic tumor composed of cells with round to oval nuclei [he stain (×100), 8 he stain (×400)]. c. showed positive result for gfap. d. showed negative result for oligo2. e. revealed diffuse immunolabeling for synaptophysin. f. showed negative presence of nf. g the mib-1 labelling index was about 3% overall figure 11 ct brain (axi) one day post-operative showed complete removal of cn tumor & some pneomocephalous figure 12 ct brain (axi) five day post-operative showed complete removal of cn tumor & pneomocephalous cessation romanian neurosurgery (2018) xxxii 1: 73 84 | 81 figure 13 mri brain t1wi (axi) five day postoperative showed complete removal of cn tumor figure 14 mri brain t1wi+ce (axi) five day postoperative showed complete removal of cn tumor discussion it has been thoughtlong time ago -that the worldwide guidelines for management of cn has not been recognized and remain indistinct, particularly that the effectiveness of rt after tumor surgical removal stays debatable,and this idea has been augmented because of limited cases.in our study, likewise most institutions, we recommend surgical excision as first line therapy [19]. although the majority of patients will have good prognosis; apparent hazard factors that responsible for fair outcome are growing. gtr had better results than str, atypical pathological cn have worse local control os in comparison to the tumours with classical pathological features, and this has been demonstrated in a collective data of more than 400 patients from international researches [19]. it is currently well recognized that more aggressive behavior is coupled with a higher mib-1 labeling index [4, 21]. in our study, only twelve cases had pathological smears for mib-1 immunohistochemical stain (range = 0.65–7, 7 %).the recurrent cases possessed a higher mean mib-1 index. future treatment guidelines might integrate mib-1 results as one of other factors that will determine further need of adjuvant treatment subsequent to str [14].nevertheless, broadly ‘‘atypical neurocytoma’’ as a pathological classification term with high mib-1 values as a sign for more worse prognosis stay in doubt. many researches failed to proof any association between high mib-1 value and possibility of recurrence. although in this series, even mib1index value of more than 2 % was not linked to worse prognosis [1]. one of the early studies to identify the relationship between mib-1 tagging index and recurrent possibility assumed higher than 2 % as an indicator of more aggressive disease course [14, 21]. a higher threshold has been anticipated based on a meta-analysis achieved on some scientific papers about a decade ago, signifying that >3 % is interrelated with superior recurrence rates and lower os [18]. in the current study, notably elevated risk of progression were found in tumors with preliminary mib-1 indices higher than 4 %. this finding make parallel with other studies that suggest higher thresholds for definition of 82 | bari mattar et al clinical outcome and prognostic factors for central neurocytoma atypical pathological features with subsequent more aggressive disease course [9]. on the other hand many researches failed to proof any association between high mib-1 value and possibility of recurrence. although in this series, even mib-1index value of more than 2 % was not linked to worse prognosis [1]. in spite of the threshold, agreement is present that multimodality treatment must be chosen for managing those tumors with elevated mib-1 values. the tumours with large volumes that expanded aggressively in lateral ventricle alone or/and the third ventricle, possibly will call for more than single operation using anterior or/and posterior approaches, as in most scientific papers, the neurosurgeons could not accomplish gtr for cn patients.this fact denoting the technical difficulties in surgical removing of the intraventricular tumors like cn. however, in this study, the degrees of primary surgical excision and lesser primary tumor volume did not look to illustrate a relationship with better local control. whereas most previous case series [7, 19, 22] stress that partial resection of cn tumours linked to high rate of recurrence, but this fact is still debatable. a modern series of 45 central neurocytoma patients data was collected retrospectively, found that a favorable patients outcome beside tumor control was in patients with lesser mitotic values. meanwhile it did not proof any noteworthy distinction in tumor local control or patient’s outcome between gtr and str [12]. in a new methodical review, resection degree was not associated with better local control [5]. it should be mentioned here that assessment of patients’ survival & quality of life variances between str and gtr is not feasible, owing to the relatively limited patient’s number in this study. the role of post-operative radiation dose in improving tumor local control & os was mentioned progressively in many current studies [2]. considering the intrinsic restriction of limited cases, our figures advocate more favorable tumor local control for patient who had been exposed to post-operative poster dose of radiotherapy in comparison to those patients who did not. the suitable and effective management for patients who had recurrent cn tumours still uncertain, with many alternatives which may be only single line of treatment or combined to be more than one. this include re-surgery, single or multiple sessions of ebrt, gamma knife (srs) beside single or multiple cycles of chemotherapy [3]. similarly, on looking to the current study, the management multimodalities highlights the diversity of these tumours treatment guidelines. genc et al. have examined employment of srs for patients with remaining or relapsed cn tumours in one of the largest series and after median period of follow up approximately 37 months, they reported reduction in tumours volume for 15/22 patients while the cn tumours size remain stable in 6/22 and only a case showed disease progression [6]. for lesions with lower mib-1, they described a tendency towards a better response; nevertheless, these findings remain trivial beside its inherited defect of short follow up periods. it was recently found that for recurrent or residual tumors fractionated ebrt and srs both represent a romanian neurosurgery (2018) xxxii 1: 73 84 | 83 sound option and this was based on a systematic review that also discovered a trivial statistical effect of srs on enhancement of cn residual tumor local control and improvement of patients’ outcomes beside inferior complications rates [5]. the researchers warn that the current evidence is typically low-level. this may advocate that the cons and pros of both treatment lines maintain to be weighed for every patient individually, consequently prospective data would be so helpful. we are in agreement that the maximal harmless cn tumours microsurgical excision still the golden standard treatment option. the presence of tumor atypia features and high mib-1 label in pathological examination & immunohistochemical staining films should guide us to give these patient post-operative dose of radiation. in more detail, the usage of a mib-1 label value of 4 % as a landmark for tumours atypia and disease aggressiveness is supported by our study findings and we advise co-specialties of concern consultations for those patients. on reviewing our study we can conclude that the post-operative ebrt could diminish the chances of growth for partly surgical removed cn tumours. lastly, srs as a modern treatment modality can be a valuable option, especially in recurrent cases. conclusion the extent of surgical resection may improve the neurological condition but not the survival, atypia was the most important factor determine the recurrence & survival while radiotherapy improve the survival quietly. references 1. bertalanffy a, roessler k, koperek o, gelpi e, prayer d, knosp e (2005) recurrent central neurocytomas. cancer 104:135–142 2. chen y-d, li w-b, feng j, qiu x-g (2014) long-term outcomes of adjuvant radiotherapy after surgical resection of central neurocytoma. radiat oncol lond engl 9:242 3. choudhari ka, kaliaperumal c, jain a, sarkar c, soo mys, rades d, singh j (2009) central neurocytoma: a multi-disciplinary review. br j neurosurg 23:585–595 4. christov c, adle-biassette h, le guerinel c (1999) recurrent central neurocytoma with marked increase in mib-1 labelling index. br j neurosurg 13:496–499, 5. garcia rm, ivan me, oh t, barani i, parsa at (2014) intraventricular neurocytomas: a systematic review of stereotactic radiosurgery and fractionated conventional radiotherapy for residual or recurrent tumors. clin neurol neurosurg 117:55–64 6. genc a, bozkurt su, karabagli p, seker a, bayri y, konya d, kilic t (2011) gamma knife radiosurgery for cranial neurocytomas. j neurooncol 105:647–657 7. hallock a, hamilton b, ang lc, tay ky, meygesi jf, fisher bj, watling cj, macdonald dr, bauman gs (2011) neurocytomas: long-term experience of a single institution. neuro-oncol 13:943–949 8. hassoun j, gambarelli d, grisoli f, pellet w, salamon g, pellissier jf, toga m. (1982): central neurocytoma. an electron-microscopic study of two cases. acta neuropathol (berl). 56: 151–6. 9. kaur g, kane aj, sughrue me, oh m, safaee m, sun m, tihan t, mcdermott mw, berger ms, parsa at (2013) mib-1 labeling index predicts recurrence in intraventricular central neurocytomas. j clin neurosci off j neurosurg soc australas 20:89–93 10. kim c-y, kim dg, joo j-d, kim yh.( 2015):clinical outcome and quality of life after treatment of patients with central neurocytoma. neurosurg clin n am.; 26: 83–90. doi: 10.1016/j.nec.2014.09.007 11. kim jw, kim dg, kim ik, kim yh, choi sh, han jh, park c-k, chung h-t, park s-h, paek sh, jung hw. (2013): central neurocytoma: long-term outcomes of multimodal treatments and management strategies based on 30 years’ experience in a single institute. neurosurgery. 72: 407-413-414. doi: 10.1227/neu.0b013e3182804662 84 | bari mattar et al clinical outcome and prognostic factors for central neurocytoma 12. leenstra jl, rodriguez fj, frechette cm et al (2007) central neurocytoma: management recommendations based on a 35-year experience. int j radiat oncol biol phys 67:1145–1154 13. louis dn, ohgaki h, wiestler od, et al. (2007),the 2007 who classification of tumours of the central nervous system. acta neuropathol. 114:97–109. 14. mackenzie ir (1999) central neurocytoma: histologic atypia, proliferation potential, and clinical outcome. cancer 85:1606–1610, 15. maiuri f, spaziante r, de caro ml, cappabianca p, giamundo a, iaconetta g. (1995) central neurocytoma: clinico-pathological study of 5 cases and review of the literature. clin neurol neurosurg.; 97: 219–28 16. mib1. omim.url: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=6 08677. accessed on: april 3, 2015 17. paek sh, han jh, kim jw, park ck, jung hw, park sh, kim ih, kim dg (2008): long-term outcome of conventional radiation therapy for central neurocytoma. j neurooncol, 90(1):25–30 18. rades d, fehlauer f, schild se (2004) treatment of atypical neurocytomas. cancer 100:814–817 19. rades d, schild se (2006) treatment recommendations for the various subgroups of neurocytomas. j neurooncol 77:305–309 20. rades d, schild se, fehlauer f (2004) prognostic value of the mib-1 labeling index for central neurocytomas. neurology 62:987–989 21. so¨ylemezoglu f, scheithauer bw, esteve j, kleihues p (1997) atypical central neurocytoma. j neuropathol exp neurol 56:551–556 22. vasiljevic a, franc¸ois p, loundou a, fe`vremontange m, jouvet a, roche p-h, figarella-branger d (2012) prognostic factors in central neurocytomas: a multicenter study of 71 cases. am j surg pathol 36:220– 227 23. yang i, ung n, chung lk, nagasawa dt, thill k, park j, and tenn s. (2015) clinical manifestations of central neurocytoma. neurosurg clin n am.; 26: 5–10. doi: 10.1016/j. nec.2014.09.011 24. yasargil mg, von ammon k, von deimling a, valavanis a, wichmann w, wiestler od. (1992) central neurocytoma: histopathological variants and therapeutic approaches. j neurosurg. 76: 32–7. doi: 10.3171/ jns.1992.76.1.0032 25. zhang b, luo b, zhang z, sun g, wen j.( 2004) central neurocytoma: a clinicopathological and neuroradiological study. neuroradiology. 46: 888–95. doi: 10.1007/ s00234-004-1289-9 09 09barimattarmohamedabdel_clinicaloutcome_bun doi: 10.33962/roneuro-2021-079 ferrans and powers quality of life index for spinal cord injury: to adapt in local language t.v.s. divyalasya, a. kiran kumar, n.r. sahana bhat, m. jahnavi, ranjan kumar jena, ram lakhan, b.v. subrahmanyam, amit agrawal romanian neurosurgery (2021) xxxv (4): pp. 472-474 doi: 10.33962/roneuro-2021-079 www.journals.lapub.co.uk/index.php/roneurosurgery ferrans and powers quality of life index for spinal cord injury: to adapt in local language t.v.s divyalasya1, a. kiran kumar2, n.r. sahana bhat3, m. jahnavi4, ranjan kumar jena5, ram lakhan6, b. v. subrahmanyam7, amit agrawal8 narayana medical college hospital, chinthareddypalem, nellore, ap, india 1 md, assistant professor, department of pharmacology 2 mpt, professor of neuro-rehabilitation, department of physical medicine and rehabilitation 3 md, resident, department of hospital administration 4 mbbs: intern, department of neurosurgery 5 md: assistant professor, department of neurosurgery 6 drph, bmr, department of epidemiology, school of public health, jackson state university, usa 7 md, professor, department of neurosurgery 8 mch, professor, department of neurosurgery abstract objective: to translate and culturally adapt the telugu version of quality-of-life tool among spinal cord injury patients. method: it’s a prospective cross-sectional study conducted at a tertiary neuro centre care hospital. the english version was translated into telugu by two expert medical professionals and cross-checked by three experts in telugu vocabulary. nursing students who had good proficiency in reading and writing in english and telugu languages were chosen for checking tool reliability. initially english language was administered on the satisfaction domain followed by the importance domain one month apart. after two months telugu version was administered in the same way as the english version. the reliability analysis was done. results: the tool was administered to 50 nursing students. the cronbach’s alpha for the satisfaction domain was 0.97 and the importance domain was 0.91, indicating excellent reliability. conclusion: the telugu version of the qol tool had excellent reliability. therefore it can be administered in the telugu language for evaluating the quality of life of people with spinal cord injury. introduction spinal cord injury (sci) is a major public health issue. in india, due to rapid advancement in motorization and industrialization the sci are keywords spinal cord injury, quality of life, telugu language, satisfaction corresponding author: amit agrawal narayana medical college hospital, chinthareddypalem, nellore, ap, india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published october 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 473 ferrans and powers quality of life index for spinal cord injury increasing every year. sci results in motor and sensory impairment which may be temporary for short time or permanent throughout lifetime depending on the severity of injury and individual factors. 1, 2 majority of sci survivors will have permanent non-repairabledamage to spinal cord thus they will suffer from secondary complications which will have major effect on their daily activities. quality of life (qol) is an important parament of disabled patient, especially among scis. the parameter in qol includes subjective and objective aspects of injured patient. 3 therefore; evaluating qol among sci patients is a challenging issue. the tool has been widely adapted and translated in major languages across the world. as per the census of 2001, the telugu is a first language of over 74 million people in india. at present, telugu is a third major language that is spoken in the country. hence it is very important to have qli in telugu language. thus, there is lack of reliable studies addressing qli tool in telugu language. the objective of the present study is to translate and culturally adapt the ferrans and powers quality of life (qli), spinal cord injury-iii in telugu language. methods it’s a prospective cross-sectional study conducted at the department of neurosurgery, narayana medical college, nellore. permission through email was sought from farren to translate and validate this tool in telugu language. the study was approved by institute ethical committee. the tool was translated by two medical professionals who were proficient in reading, writing, and speaking of telugu and english languages. all 37 items of both parts of health quality; satisfaction and importance were translated4,5. the translated items were read by three independent professionals. independent readers have ensured that the translation in telugu is accurate and flawless by giving their suggestions. the final draft of telugu version was finalized after incorporation of suggestions and corrections of readers. fifty nursing students, well proficient in english and telugu languages were chosen for the study. the informed written consent was obtained from all the participant. participants did not receive any incentives for their participation in the study. two interviewers (not know to each other) administered the tool in english language on all the participants. all standard procedures for administering the tool were followed. the questions of satisfaction and importance domains were administered with one month apart. the telugu translated questionnaire was administered after 2 months of administering english language. a gap of one month was maintained between administration of satisfaction and importance domain. statistical analysis the data was analyzed with the help of statistical package for the social science, version 18. the cronbach’s alpha and correlation were calculated for difference between interviewee responses on english and telugu questionnaire. results the cronbach’s alpha coefficient was calculated for qli in telugu language among telugu speaking population. the domains of satisfaction and importance had a cronbach’s alpha coefficient of ≥ 0.9, indicating excellent reliability. table 1 revels result of the reliability analysis. ferrans and powers quality of life no. of items alpha satisfaction domain 37 0.97 importance domain 37 0.91 table 1. reliability table for the quality-of-life tool discussion there are many tools available but none are without limitations. the most accepted and commonly used tools are from developed countries and have been adapted in developing countries in their native languages. among such tools the ferrans and powers quality of life (qli) is very reliable and a valid tool that has been found very comprehensive and applicable in assessing the quality of life in sci patients3,6. the qli spinal cord injury version iii, is a specific version which was specifically designed for spinal cord injury7. the study result reports that satisfaction and importance domains of qli in telugu language had excellent internal consistency as reflected by cronbach’s alpha value (α≥0.9). the intercorrelation between satisfaction and importance domains of qli in english and translated telugu language is very high. the result of all the telugu translated items of tool are all most same as english language, because intercorrelation between the translation and english 474 t.v.s. divyalasya, a. kiran kumar, n.r. sahana bhat et al. language is excellent. hence both the satisfaction and importance domains of qli in telugu language have excellent reliability. a study from brazil translated qli for sci into portuguese cultural vocabulary and reported that the kappa coefficient was statistically stable of all the items of the tool. 8 a study translated qli in norwegian version and reported excellent reliability with alpha value of 0.93. 9 various studies have reported internal consistency reliability ranging from 0.73 to 0.93 for health and functioning domains of qli. 10, 11 in order to adapt qli for sci in the telugu speaking population their cultured vocabulary was used. exact translation and substitution of english sentence with same meaning in telugu was done by expert person. the present study results report that telugu translated qli have excellent reliability and can be used among telugu population. conclusion the telugu translated quality of life index spinal cord injury version iii showed that the tool is suitable from satisfaction and importance domain point of view and provides way for easy application to evaluate the qol among sci people. references 1. chiu wt, lin hc, lam c, chu sf, chiang yh, tsai sh. review paper: epidemiology of traumatic spinal cord injury: comparisons between developed and developing countries. asia-pacific journal of public health 2010;22:918. 2. rajasekaran s, kanna rm, shetty ap. diffusion tensor imaging of the spinal cord and its clinical applications. the journal of bone and joint surgery british volume 2012;94:1024-1031. 3. may la, warren s. measuring quality of life of persons with spinal cord injury: external and structural validity. spinal cord 2002;40:341-350. 4. ferrans ce, marjorie jp. quality of life index [online]. available at: https://qli.org.uic.edu/. 5. ferrans ce, marjorie jp. ferrans and powers quality of life index© generic version iii [online]. available at: https://qli.org.uic.edu/questionaires/pdf/genericversioni ii/generic.pdf. 6. ferrans ce, powers mj. [quality of life index: development and psychometric properties]. recherche en soins infirmiers 2007:32-37. 7. tulsky ds, kisala pa, victorson d, et al. overview of the spinal cord injury – quality of life (sci-qol) measurement system. j spinal cord med 2015;38:257269. 8. reis pam, carvalho zmdf, darder t, et al. cross-cultural adaptation of the quality of life index spinal cord injury version iii. revista da escola de enfermagem da usp 2015;49:401-408. 9. rustøen t, wiklund i, hanestad br, burckhardt cs. validity and reliability of the norwegian version of the ferrans and powers quality of life index. scand j caring sci 1999;13:96-101. 10. derick mussen h. ferrans and powers quality of life index [online]. available at: https://www.mussen health.us/quality-life/ferrans-and-powers-quality-of-lifeindex.html. 11. kimura m, silva jvd. ferrans and powers quality of life index. revista da escola de enfermagem da usp 2009;43:1098-1104. microsoft word 26onciulrazvan_anunforgettable romanian neurosurgery (2018) xxxii 2: 391 393 | 391             doi: 10.2478/romneu-2018-0049 an unforgettable congress the 12th international conference of the asian congress of neurological surgeons (acns) onciul razvan1, a.v.ciurea2 1stud. 6th year, “carol davila„ university of medicine and pharmacy, bucharest, romania 2neurosurgery department sanador hospital, bucharest; “carol davila” u.m.ph., bucharest, romania all congresses organized in dubai as a preferential location have an exceptional quality standing, due to the exotic location conditions with all the possible facilities at this time. for many years dubai has been concentrating many medical activities symposiums, conferences, congresses due to the organizational standard, and why not, the extraordinarily pleasant climate in the winter months in europe. 392 | onciul et al an unforgettable congress             the acns congress started with an initiative by professor tetsuo kanno, who in 1993 made toyota the first such congress as a congress of neurological surgeons surgeons (cns) that takes place annually in the us. the extraordinary idea of japanese teacher tetsuo kanno was immediately adopted by almost all states with neurosurgical activities in asia. thus, after the first congress implementation in recognized neurosurgical locations like osaka and nagoya, acns conquered other locations in jakarta, mumbai, kula lumpur, with the 12th congress being held in dubai. the organizer and president of the xiith congress appointed by acns was professor imad n. kanaan who works in saudi arabia and opened an exceptional gateway to the gulf countries. the topics were neuroanatomy, neuro-oncology, cerebrovascular, skull-base & pituitary, neuroendoscopy, spine & peripheral nerves, pediatric neurosurgery, stereotactic & functional neurosurgery, neuro-trauma & cristical care, neurosurgeons, research, education and innovation, ethics and socioeonomics covering the whole neurosurgical pathology and the significant number of invited speakers (143) have raised the scientific quality of this outstanding manifestation. a number of works in the areas of intracranial anaevrisms: yoko kato and jacques morcos, endoscopy: h. schroeder and f. gentili, brain tumors: isabelle germano and natale fracaviglia, craniofaringiomas: j. steno and c. deopujari, brain tumors in children: mourice chux, spine surgery: r. delfini, skull base surgery: sebastien froehlich, m. ammirati, anil nanda and traumatology: f. servadei, i. cerian have been highlighted. accomodation was made at the grand hayat hotel in extraordinary conditions and had over 500 participants from different countries, all under the aegis of the world's neurosurgery federation. (w.f.n.s.) according to the president's presentation, the motto of the congress was "inspiration and innovation". the inspiration was due to the numerous presentations made by recognized personalities and the innovation was brought about by the major elements of technology in neuroimage and neurochirurgical interventions. the romanian delegation had three participants prof. dr. stefan florian, prof. dr. a.v. ciurea, dr. alex florian. in terms of presentations prof. dr. stefan florian had two speeches: "brainstem tumors how to approach" and "complications of avm surgery" and prof. dr. a.v. ciurea also had two presentations: "new trends in aneurysm management in romania" and "new gains in medulloblastoma in children (1992-2017) can it be cured?". all these four papers raised the general interest, being appreciated in plenary. dr. alexandru florian presented an extremely interesting work on "brainstem cavernomas in infancy case reports", an extremely rare pathology at this age. the preconference workshop consisted of the neuroendoscopy module, the spine module and the neuroanatomy module and the skull base, which also had an romanian neurosurgery (2018) xxxii 2: 391 393 | 393             extraordinary audience on the part of the neurosurgery residents in the arab countries. overall, we believe that this congress has fully achieved its goal of, on the one hand, an international opening of neurosurgical activity with the combination of procedures in this field, of asia teams, especially with those in europe, on the other hand, a model of elegance and attitude in addressing the various topics discussed and debated lately, especially from vascular pathology (coils vs clipps) and oncological skull base pathology. in the end, any national participation in such a congress is mandatory in order to reveal the neurochirurgical centers in romania and to know the experience in this field of other acknowledged world neurosurgery centers. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article intradural spinal, extramedullary, t4-t5 cavernous hemangioma case report g. iacob, b. rotund, a. iancu, a. madalan, andreea marinescu, g. simion romania doi: 10.1515/romneu-2017-0005 32 | iacob et al intradural spinal, extramedullary, t4-t5 cavernous hemangioma             doi: 10.1515/romneu-2017-0005 intradural spinal, extramedullary, t4-t5 cavernous hemangioma case report g. iacob1, b. rotund1, a. iancu1, a. madalan1, andreea marinescu2, g. simion3 university hospital bucharest, romania 1neurosurgery department, 2neuroradiology department, 3pathology department abstract: a very rare, purely intradural, spinal, extramedullary cavernous hemangioma was fortunately discovered in a 56 years old woman, presenting with bilateral brachial paresthesia. using conventional spin‐echo t1 proton density,t2‐weighted magnetic resonance and gadolinium images an intradural spinal t4-t5, an extramedullary cavernous hemangioma was discovered. the patient underwent surgery, with laminectomy and microsurgical resection followed by an uneventful postoperative clinical course. similar as in cerebral locations a mixed signal intensity in all sequences on magnetic resonance images might be indicative of cavernous hemangioma, rendering a presumptive preoperative diagnosis of the lesion and surgical planning for a good microsurgical resection. key word: intradural spinal, extramedullary, cavernous haemangioma introduction cavernous hemangioma, also known as: cavernous angioma, cavernoma, cavernous malformation or hemangioma is a developmental vascular anomaly of dilated blood vessels collection; represent about 7% of all vascular malformations, it can occur anywhere in the central nervous system, with approximately 5% of the cases located in the spine (1-7). either capillary or cavernous, intradural, spinal, extramedullary hemangiomas can be solitary or multiple; they are well-defined lesions composed of blood-filled endothelial spaces lined by thickened, hyalinised walls without elastic fibers or smooth muscle; they are also very rare (8-16). we report an intra dural spinal extramedullary, t4-t5 cavernoma in a 56years-old woman, who underwent microsurgical resection. case report this 56-years-old woman complained of bilateral brahial paresthesia, without neurologic deficits or sphincterian disturbances. the patient underwent cranial and spinal mr examinations and romanian neurosurgery (2017) xxxi 1: 32 – 40 | 33             postoperative mr imaging in a 1,5-tesla mr imager (general electric). sagittal t1 and t2 weighted images and axial t2 – weighted mr images of the cervico-thoracal spine revealed cervical c4-c6 disc protrusions. incidentally it was also discovered an intradural, extramedullary lesion at t4-t5, of 6/4 mm – a well-defined postero-lateral lesion, with discreet compression on the spinal cord, which is displaced to anterior and lateral on the right, with heterogeneous signal abnormality in both t1 and t2 – weighted images, representing blood products of various ages, without bone involvement. the lesion was surrounded by a low signal intensity, representing iron storage products and medullary perilesional oedema, occupying most of the thoracic spinal cord. the lesion suggests the diagnosis of an extramedullary thoracal cavernoma (figures 1-3). a b c d e figure 1 sagital t2 mri: a cervical spine examination for bilateral brahial paresthesia incidental discovery of a lesion in the thoracal spinal canal – an extramedular, intradural lesion, t7 vertebral hemangioma, b & c sagital t2, d sagital t1 after gadolinium injection – with heterogenous signal in t2w and e sagital t1 w (calcifications possible) + poor enhancement of the lesion figure 2 axial t2 mri emphasize intradural lesion, in postero-lateral left position, with discreet compression over the spinal cord, displaced anteriorly and laterally and to the right 34 | iacob et al intradural spinal, extramedullary, t4-t5 cavernous hemangioma             figure 3 axial 3d t1 fatsat postgd – poor enhancement of the lesion the patient underwent laminectomy from t4 to t5 using a microsurgical approach. when the dura and arachnoid were opened, an extradural polilobulated, violet-dark red mass, of 6/4/3 mm, located dorsally, was identified. the tumor exerted discreet compression over the spinal cord, displacing it anteriorly and laterally to the right. clearly demarcated from the adjacent spinal cord tissue, with a good cleavage from the dura, the tumor was completely excised and gently extracted from the the hemosiderin-stained bed of the spinal cord (figure 4). after the lesion has been completely resected, no extraspinal extension or bony involvement was found. the histological aspect was characteristic of a cavernous hemangioma: multiple, closely spaced lined by a single layer of benign endothelial cells, dilated vascular channels containing blood, without nuclear pleomorphism and mitotic figures (figures 5-7). a romanian neurosurgery (2017) xxxi 1: 32 – 40 | 35             b figure 4 preand postoperatory view a b c d figure 5 histologic cavernous hemangioma features col he 10×10 a-d: dilated vascular channels filled with red blood cells, lined of endothelial cells; without intervening neural tissue and vascular wall muscle fibers figure 6 cavernous hemangioma, he coloration 10×40, detail image: dilated and narrowed vascular channels with red blood cells figure 7 cavernous hemangioma, van gieson coloration 10×40, detail images, dilated vascular channels with red blood cells 36 | iacob et al intradural spinal, extramedullary, t4-t5 cavernous hemangioma             postoperatively evolution of the patient was uneventful. no adjuvant therapy was given. six months after surgery, a follow-up mri scan was performed, showing no evidence of secondary lesion or recurrence. discussion spinal cavernous and capillary hemangiomas can be found in two forms: sporadic 90% and familial 10% (17); they can be solitary or multiple, and they may be associated with similar lesions in other organs of the body in up to 18.7% of cases (18). spinal cavernous hemangioma (1-22) can be found in several topographic locations: confined to the vertebrae, extended epidurally from the vertebral lesions, entirely extradural lesions with no bone involvement, and also purely intradural, extramedullary from the inner surface of the dura or the pial surface of the spinal cord; very rarely, intramedullary in about 3% of cases (21)(24), adherent to the blood vessels of the nerve roots in the cauda equina (16). intradural spinal, extramedullary, cavernous hemangiomas are most frequently found in the adult population (only 4 pediatric cases cited in literature), mostly in women (23), in the thoracic spine 80% of cases (9)(12) or lower thoraco-lumbar region (13)(20), with posterior location within the spinal canal in 93% of cases; also with possible lateral recesses extensions; less common in cervical location (7)(8) and mostly adherent to the nerve root or spinal cord (8)(24). capillary hemangiomas are found in the skin and soft tissues in younger people, and rarely occur in the central nervous system; more frequent they are located around or attached to nerve roots of cauda equina and conus medullaris (25), extremely rarely intradurally (16). intradural extramedullary capillary hemangiomas tend to present in the fourth or fifth decade of life (mean age: 49 years), with male predominance, especially in the thoracic spine (between t4 and t11 vertebrae) and in the lumbar or conus medullaris region. (1, 2, 4, 5, 9, 13, 16, 25) clinical symptomatology at presentation is variable, depending on the size and topography, with the more frequent symptoms beeing: acute spinal pain, radiculopathy and/or myelopathy, progressive gait disturbance, slowly progressive paraparesis, or even asymptomatic – very rare, as in our case (5, 18, 26-28). cavernous hemangiomas may present in four major clinical patterns: acute episodes of step wise deterioration, slow progression, acute onset with rapid deterioration, and acute onset with gradual decline (10, 12, 14, 15, 18). acute clinical deterioration is present in cavernous hemangiomas associated with subarachnoid hemorrhage induced by intralesional hemorrhage, lesion growth, thrombotic venous occlusion; bleedind can occur due to the thin-walled vessels, stasis of blood flow in the lesion, estrogen mediated neoangiogenesis in the lesion or drainer compression by a gravid uterus (22)(23)(29). intradural extramedullary lower thoracic spinal cord capillary hemangiomas can have a variable onset of presentation: low back pain, radiculopathy or cauda equine syndrome (13)(25) romanian neurosurgery (2017) xxxi 1: 32 – 40 | 37             cavernous hemangioma are diagnosed by mri the investigation of choice; these lesions have no communication with the spinal arterial circulation and are angiographically occult (30-32). computed tomography scan may show hyperdense or calcified lesions on plain studies. there may be minimal or no enhancement with contrast (18)(32). the mri signal intensity and character of the spinal epidural cavernous hemangioma reflects its histopathology: both t1and t2-weighted images lack of a low-signal hemosiderin ring relate to the more rapid removal of blood degradation products outside the blood-brain barrier (3132) low or intermediate signal intensity on t1‐weighted, and high‐signal intensity on proton density and t2‐weighted images, with strong homogeneous enhancement after contrast medium injection (14) marked hyperintense t2 ‐ weighted signal reflects the high water content and the intense flow enhancement into the numerous vascular channels of the lesion sinusoidal vascular structure (36). heterogenous signal on all pulse sequences, with ring enhancement on postcontrast images – rare, due to intralesional hemorrhage and related degeneration (37) hyperintense signal has been reported on both t1 and t2 weighted images, related to the presence of hemorrhage in the subacute phase (14)(38) profoundly hypointense signal areas in the t2 and gradient echo sequences due to acute hemorrhage containing deoxyhemoglobin or as a result of hemosiderin deposition related to recurrent hemorrhages (39). complete lack of enhancement in case of sclero-hyaline degeneration features of capillary hemangioma on mr images are: isointense lesion on t1-weighted images, hyperintense relative to the spinal cord on t2-weighted images, and homogenous, strong enhancement on contrast-enhanced t1-weighted images (9, 25, 40, 41), and also the presence of enlarged draining perimedullary veins (9). capillary and cavernous hemangiomas arise from the same cell type, showing distinct demarcation from the surrounding parenchyma. they can be differentiated on histopathology by vessel size: capillary hemangioma, uncommon in the spinal canal, is composed of small, capillary networks surrounded by collagenous stroma (2), without hemosiderin deposition, while the cavernous hemangioma is composed of irregular, dilated sinusoidal vascular channels lined by a monolayer of benign endothelium, with the large sinusoidal lumina almost adjacent to one another, without intervening mother tissue (6)(8)(11)(12). moderate stromal chronic inflammation is often present. these are well-circumscribed lesions, with discrete borders, dark to purple in color, and can be multilobulated. associated calcification and thrombosis may occur. the blood flow in these lesions is slow and, therefore, it is not visualized in standard angiography. hemorrhages are common in the intra-axial lesions, but less frequent in extra-axial ones. 38 | iacob et al intradural spinal, extramedullary, t4-t5 cavernous hemangioma             the usual differential diagnosis of intradural, extramedullary, epidural cavernous hemangioma (8)(11)(14) occurring at the thoracic level is made with other spinal epidural tissue masses: schwannoma: frequently seen in the middle age, with equal sex predilection; the signal intensity usually is hypo-intense, less frequently iso-intense, on t1-weighted images, hyper-intense on t2-weighted images, with cystic changes or necrosis on mri meningioma: it is seen the 50–70 years age group, with m:f=1:5; the mass usually shows iso-intensity or slight hypo-intensity on t1-weighted images, and iso-intensity or slight hyper-intensity on t2-weighted images; it has a characteristic broad-based dural attachment, with dural tail sign on the contrast-enhanced study. sometimes it is difficult to differentiate the intradural extramedullary capillary hemangioma from the other common intradural tumors by mri. nerve sheath tumors are linear, ovoid or characteristically dumbbell-shaped in configuration, of uniform hyper-intense signal in t2 disk prolapse ruled out for its lack of anatomic connection with the neighboring intervertebral disk or the exiting nerve root, after gadolinium injection – with heterogeneous signal in t2 (20) paraganglioma rarely occurs epidurally, with heterogeneous salt and pepper appearance due to vascular signal voids on mr imaging mimicking capillary hemangioma (6)(42) epidural lymphoma shows characteristic low t2 signal drop metastasis usually appears as multiple small nodular and/or linear enhancing lesions within the thecal sac (10) filum terminale ependymoma may present intratumoral cystic changes and a less strong degree of contrast enhancement round cell tumor eosinophilic granuloma, ruled out for the absence of any bony changes sarcoidosis (43), lymphoma with a discrete solitary mass, with a multifocal patchy or linear enhancing lesion histiocytosis, angiolipoma representing less than 6% of all spinal neoplasms tuberculosis is uncommon, mostly epidural, associated with other systemic signs and symptoms as well as with mediastinal lymphadenopathy, with craniocaudal extension along to more than one vertebral body. complete surgical resection is the treatment of choice for intradural extramedullary hemangioma, with no recurrence (3)(6-9)(12)(14)(15)(24)(25)(37). microsurgical excision of such lesions, in accessible locations, especially for lesions located posteriorly, is the treatment of choice. because of sudden intralesional hemorrhage, which can lead to spinal cord compression and subsequent severe disability, cavernous hemangioma should be included in the differential diagnosis of purely extradural soft tissue lesions of the spine. romanian neurosurgery (2017) xxxi 1: 32 – 40 | 39             conclusion intradural spinal, extramedullary, cavernous hemangioma are very rare; early recognition by accurate diagnosis using mri, followed by complete excision of the lesion is important, because of the risk of enlargement or hemorrhage, which may produce sudden neurologic deterioration. because resection is in general possible without causing morbidity, and because the outcome depends on the severity of preoperative neurological dysfunction, precise diagnosis and timely treatment are mandatory. references 1. roncaroli f, et al. capillary hemangioma of the spinal cord report of four cases. j neurosurg 2000, 93, 148-151 2. nowak d.a., widenka d.c. “spinal intradural capillary haemangioma: a review,” european spine journal, 2001,10, 6, 464–472 3. mastronardi l, et al. intradural extramedullary cavernous angiomas: case report. neurosurgery 1991, 29, 924-926 4. shin jh, et al. spinal intradural capillary hemangioma: mr findings. ajnr am j neuroradiol 2000, 21, 954-956 5. choi b.y. et al. spinal intradural extramedullary capillary hemangioma: mr imaging findings, ajnr 2001, 22, 799–802 6. goyal a. et. al. spinal epidural cavernous haemangioma: a case report and review of literature, spinal cord 2002, 40, 4, 200-202 7. aoyagi n et al. review of spinal epidural cavernous hemangioma, neurol med chir (tokyo) 2003, 43, 471475 8. kazuhiko n. et al. spinal intradural extramedullary cavernous angioma, case report, journal of neurosurgery: spine, 2003, 99, 3, 316-319 9. abdullah d.c. et al.thoracic intradural extramedullary capillary hemangioma, ajnr am j neuroradiol 2004, 25, 1294–1296 10. hatiboglu ma, et al. epidural spinal cavernous angioma. neurol med chir (tokyo) 2006, 46, 455-458 11. er u, yigitkanli k., et al spinal intradural extramedullary cavernous angioma: case report and review of the literature. spinal cord 2007, 45, 9, 632-636 12. antunes a. et al hemangioma cavernoso extradural da coluna torácica, arq. neuro-psiquiatr. 2011, 69, 4 13. sonawane d.v. et al. intradural extramedullary capillary hemangioma of lower thoracic spinal cord, indian j orthop. 2012, 46, 4, 475–478 14. khalatbari mr et al. solitary spinal epidural cavernous angioma: report of nine surgically treated cases and review of the literature, eur spine j. 2013, 22(3), 542-547 15. luca d et al. spinal epidural cavernous angiomas: a clinical series of four cases, acta neurochir 2014, 156, 283–284 16. takata y. et al. intradural extramedullary capillary hemangioma in the upper thoracic spine: a review of the literature, case reports in orthopedics, 18 june 2014 17. labauge p. familial forms of central nervous system cavernomas: from recognition to gene therapy neurochirurgie 2007, 53, 152-155 18. satpathy d.k. et al. spinal epidural cavernous hemangioma with myelopathy: a rare lesion, neurology india, 2009, 57, 1, 88-90 19. richardson rr, cerullo lj. spinal epidural cavernous hemangioma. surg neurol. 1979;12:266–8; 20. rovira a, rovira a, et al. lumbar extradural hemangiomas: report of three cases. ajnr 1999;20:27– 31. 21. iacob g, olarescu angela spinal intramedullary cavernomas. personal experience reffering to six cases, romanian neurosurgery 2014, 21, 4, 407–415 22. jellinger k. pathology of spinal vascular malformations and vascular tumors. in: pia hw, djindjian r, editors. spinal angiomas: advance in diagnosis and therapy. new york: springer; 1978. pp. 9–20; 23. sarikaya-seiwert s, gierga k, et al. solitary spinal epidural cavernous angiomas in children presenting with acute neurological symptoms caused by hemorrhage, j neurosurg pediatr. 2010, 5, 89–93 24. ogilvy cs, louis dn, ojemann rg. intramedullary cavernous angiomas of the spinal cord: clinical presentation, pathological features and surgical 40 | iacob et al intradural spinal, extramedullary, t4-t5 cavernous hemangioma             management. neurosurgery 1992, 31, 219–229; discussion 229–230 25. sonawane d.v. et al. intradural extramedullary capillary hemangioma of lower thoracic spinal cord, indian j orthop. 2012, 46(4), 475–478 26. minh nh. cervicothoracic spinal epidural cavernous hemangioma: case report and review of the literature. surg neurol. 2005, 64, 83–85 27. zevgaridis d, büttner a, et al. spinal epidural cavernous hemangiomas. report of three cases and review of the literature. j neurosurg. 1998, 88, 903–908 28. kivelev j., et al.cervical intradural extramedullary cavernoma presenting with isolated intramedullary hemorrhage. journal of neurosurgery 2008, spine 8, 1, 88-91 29. jellinger k. vascular malformations of the central nervous system: a morphological overview. neurosurg rev. 1986, 9, 177–216 30. crispino m., vecchioni s., et al spinal intradural extramedullary haemangioma: mri and neurosurgical findings, acta neurochirurgica 2005, 147, 11, 1195-1198 31. zander dr et al . magnetic resonance imaging features of a nerve root capillary hemangioma of the spinal cord: case report, can assoc radiol j 1998, 49, 398-400 32. nagi s, et al. imaging features of spinal epidural cavernous malformations, j neuroradiol 2004, 31, 208213 33. carlier r, engerand s, et al. foraminal epidural extra osseous cavernous hemangioma of the cervical spine: a case report. spine (phila pa 1976) 2000, 25, 629– 631 34. clatterbuck re, cohen b, et al. vertebral hemangiomas associated with familial cerebral cavernous malformation: segmental disease expression.case report. j neurosurg.2002, 97, 227–230 35. fontaine s, melanson d, et al. cavernous hemangiomas of the spinal cord: mr imaging. radiology 1988,166, 839–841 36. shen w, chou g, et al. magentic resonance imaging of spinal extradural cavernous hemangioma. acta neurol sing. 1994, 3, 223–226 37. feider hk, yuille dl. an epidural cavernous hemangioma of the spine. ajnr am j neuroradiol. 1991, 12, 243–244 38. graziani n, bouillot p, et al. cavernous angiomas and arteriovenous malformations of the spinal epidural space: report of 11 cases, neurosurgery.1994, 35, 856– 864 39. jo bj, lee sh, chung se, et al. pure epidural cavernous hemangioma of the cervical spine that presented with an acute sensory deficit caused by hemorrhage, yonsei med j. 2006, 47, 877–880 40. kim kj, lee jy, lee sh. spinal intradural capillary hemangioma. surg neurol. 2006, 66, 212–214 41. abe m, tabuchi k, et al. capillary hemangioma of the central nervous system. j neurosurg. 2004, 101, 73– 81 42. faro sh, turtz ar, et al. paraganglioma of the cauda equina with associated intramedullary cyst: mr imagings, ajnr 1997,8,1588-1590 43. nesbit gm, miller gm, et al. spinal cord sarcoidosis: a new finding at mr imaging with gddtpa enhancement, .radiology 1989, 173, 839-843 doi: 10.33962/roneuro-2021-020 subarachnoid haemorrhage. a critical neurosurgical emergency alexandra bibiriță, daniel teleanu, alexandru vlad ciurea romanian neurosurgery (2021) xxxv (2): pp. 129-134 doi: 10.33962/roneuro-2021-020 www.journals.lapub.co.uk/index.php/roneurosurgery subarachnoid haemorrhage. a critical neurosurgical emergency alexandra bibiriță1, daniel teleanu2,3, alexandru vlad ciurea4,5 1 resident of neurosurgery at bucharest university emergency hospital, romania 2 chief of neurosurgery department at bucharest university emergency hospital, romania 3 assoc. professor of neurosurgery at “carol davila” university of medicine and pharmacy, bucharest, romania 4 chief of neurosurgery department and scientific director of sanador clinical hospital, bucharest, romania 5 professor of neurosurgery at “carol davila” university of medicine and pharmacy, bucharest, romania abstract subarachnoid haemorrhage (sah) accounts for 3% of all strokes and is the cause of 5% of stroke mortality. sah by rupture of cerebral aneurysm or arterial-venous malformation (avm) remains the most devastating cerebrovascular disease. during admission for sah, about 30-70% of patients suffer a rebleed, and from all rebleeds, about 90% lead to death no matter the treatment. available current scales help predict the prognosis and guide the therapy. considering that the lifestyle risk factors for sah are of increasing prevalence, it is expected that it will affect even more people in the future. sah should not be regarded as a disease but rather a set of events with devastating complications requiring adequate management from debut extending long after patient discharge. epidemiology subarachnoid haemorrhage stands for 3% of all cerebral vascular strokes and is responsible for the 5% mortality coming from cvas. incidence peak for sah is 55-60 age group. during hospital admission for this pathology 30-70% of patients suffer a rebleed and approximately 90% of all rebleeds will end in death whatever the treatment. physiopathology and aetiology subarachnoid haemorrhage occurs as a consequence of a blood vessel rupture in the subarachnoid space or near it. following this rupture, blood will invade the space between the pia mater and the arachnoid, keywords risk factors, neurosurgical emergency, ct, angiography, subarachnoid haemorrhage scales, cerebral vasospasm corresponding author: alexandra bibirita bucharest university emergency hospital, romania alexandra.bibirita@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 130 alexandra bibiriță, daniel teleanu, alexandru vlad ciurea the subarachnoid space, which normally contains just cerebrospinal fluid. etiologically, which is considering the reason that led to the event, following types of sah stand out – traumatic sah or spontaneous. the spontaneous form of sah occurs in cases of high arterial blood pressure (hypertensive sah) or is the direct consequence of an aneurysmal rupture, a cerebral or spinal arterial-venous malformation rupture or secondary to cervical-cerebral arteries dissection. [3,12] actually about 85% of all sah forms are due to the rupture of a cerebral aneurysm. brain aneurysm typically occurs during spring and autumn and is considered directly linked to temperature changes, similar to cvas. [2,12] a rare form of spontaneous sah is the idiopathic subarachnoid hemorrhage, in the presence of risk factors considered non-traditional and modifiable – alcoholism, smoking, cocaine or amphetamine abuse. besides these forms, literature provides a series of traditional risk factors, which are not subject to medical or lifestyle intervention and thus called non-modifiable, frequently linked to sah occurrence: family history of sah, soft tissue disease (polycystic kidney disease, neurofibromatosis type i, ehlersdanlos syndrome mainly type iv and other collagen abnormalities), female sex (1.5 times the risk), african descent (2 times the risk), japanese or finnish descent, vasculitis, even more rare factors – parasitosis, moya-moya disease, eclampsia, blood disorders, coagulation disorders. [1,2,11,12] it is important to point out that as prevalence of the nonmodifiable risk factors gets higher, it is expected that sah incidence will increase in the following decades. clinic of subarachnoid haemorrhage clinically the first symptom and nonetheless the most constant is severe headache with sudden onset – approximately 97% of cases, describes as a thunderclap headache and acknowledged by the patient as “the most intense headache i ever had”. [12] a more particular situation is the sentinel headache – a sudden and severe pain that goes away, allowing for a symptom-free period with neglection of said episode, followed shortly by severe mental status alteration, paroxysmal phenomena known by neurosurgeons as “walk, talk and die patients.” [1,3] photophobia as an accompanying symptom is frequent, together with ocular symptoms such as subhialoid hemorrhage, retinal or vitreous hemorrhage. in medical literature vitreous hemorrhage associated with sah is known as terson’s syndrome. [8] eye fundus examination may reveal papillary edema secondary to increased intracranial hypertension secondary to bleeding into the subarachnoid space. vegetative phenomena such as emesis or syncope are common. sometimes, although not rarely the patient seeks medical attention after a loss of consciousness episode or for altered mental status, as neurological status on admission might vary from slight confusion to deep coma. epileptic seizures occur frequently as about 20% of patients develop such symptoms in the first 24 hours since debut. they are considered to be a straight effect of increased intracranial pressure, associated hyponatremia or aneurysm site, especially when it involves sylvian arteries territory. [3,9] neurological examination reveals early meningeal signs: neck stiffness, headache, photophobia, ocular pain, emesis. neck stiffness usually develops within 6 to 24 h from the debut of sah. within a few hours from debut signs such as kernig, brudzinki or bilateral lassegue can appear or focal neurological signs. psychiatric acute onset is more common and sometimes even specific among elderly patients. some other accompanying signs or symptoms are acute urinary retention, diminished or abolished osteo-tendinous reflexes (usually after 4 to 6 h from the debut of the hemorrhage) and eventually focal neurological signs. elderly patients, most commonly after 70 years old very often present with a far worse neurological status on admission. [9,12] diagnosis the elective diagnostic tool in sah is the plain cerebral ct examination on arrival in the emergency room, which shows blood in the subarachnoid space. the fisher grade is thus immediately established. this diagnostic imaging tool is nonetheless the actual gold standard in diagnosing the subarachnoid hemorrhage, its limitation being that when not enough time since the debut of the hemorrhage has passed, the first examination might turn out negative 131 subarachnoid haemorrhage. a critical neurosurgical emergency and will become positive a few tens of minutes later. the fisher grading system is based upon the results of the plain cerebral ct examination and it appreciates the risk of developing cerebral vasospasm. it is summarized in the table below. [14] fischer grade presence of blood in the sa space other aspects vasospasm risk grade 1 no blood in the cisterns no clots 21% grade 2 blood <1 mm thickness no clots 25% grade 3 blood >1 mm thickness +/clots 37% grade 4 rare blood, diffusely in the basal cisterns intraventricular hemorrhage or parenchymal 21-37% table 1. fisher scale (1982). figure 1. cranio-cerebral ct axial sequences showing the 4 fisher grades (1 – grade 1, 2 – grade 2, 3 – grade 3, 4 – grade 4). source future neurol @ 2013 future medicine ltd. if the ct examination is negative but the clinical suspicion of sah is still high, a lumbar puncture may be helpful for diagnostic purpose, but it is to be performed with every precaution and only after eye fundus examination excludes intracranial hypertension, in order to avoid cerebral herniation. this procedure can induce a rebleed if intracranial pressure is too abruptly decreased, which is why a minimal amount of a csf sample is to be drawn. [3,5] lumbar puncture is according to available date the most sensitive diagnostic tool for sah. a positive result consists of increased csf pressure, xanthochromic csf, more than 100 000 thousand erythrocytes per mm3, increased proteinorrhachia (>50 mg/dl) and normal or slightly decreased glycorrhachia (<50-70 mg/dl) [3,4,5]. cerebral mri imaging with flair sequencing, ct angiography or mri angiography do not add very much relevance to the sah diagnosis in the first 2448 hours following debut, but they prove to be excellent between day 3 and 7, with good premises for identifying a cerebral aneurysm and its anatomical features. [7] figure 2. axial enhancement cerebral ct sequence – red arrow points to an anterior communicating artery aneurysm – collection of neurosurgery i clinic, emergency university hospital of bucharest. digital subtraction angiography (dsa) now a tool of capital importance in the management of subarachnoid hemorrhage – consists of selectively injecting contrast material using a catheter inserted into a large artery under radiologic screen. it is an extremely useful resource in the evaluation of cerebral aneurysms and it can also come in as a both diagnostic and therapeutic tool, providing the possibility of simultaneously embolizing the incriminated aneurysm or avm. 132 alexandra bibiriță, daniel teleanu, alexandru vlad ciurea figure 3. right sylvian artery giant dissecting aneurysm near m1 and m2 segments junction. right internal carotid angiography clichee. collection of neurosurgery i clinic, emergency university hospital of bucharest. aneurysm with sacs smaller than 5 mm are ideal for endovascular coiling, while for the rest of them the risk of recanalization or incomplete occlusion are considered too high, thus needing stent or balloon assisted coiling. figure 4. digital subtraction angiography sequence – black arrows points to a anterior communication artery aneurysm – open source image. management once the diagnosis has been confirmed therapeutic measures are immediately started based on patient’s clinical and neurological status and in closed connections with sah etiology. diagnosis is further completed with other needed tests. the patient should be admitted into a neurosurgical service with dedicated intensive care unit in case of need of advanced vital function support. drug treatment consists of maintaining an optimal blood pressure of systolic bp < 160 mmhg, considering that high blood pressure values are associated with worsening sah and rebleed risk. vasospasm prevention is to be addressed by administering nimodipine. cerebral edema prevention, maintaining normal volemia and preventing hyponatremia are the next medical considerations, as even with maximal therapy they are extremely difficult to correct if they occur. antiseizure prophylaxis is mandatory because of the irritation of cerebral cortex by blood in the subarachnoid space. [6,9] the neurological status of the patient suffering from sah is to be appreciated with the help of hunt & hess scale and wnfs scale (world neurosurgical federation society scale 1988) and it is extremely important in the surgical indication. classification into a hunt & hess (1968) grade is determined after clinical and neurological assessment as follows: [15] grade i: absent or mild headache, absent or minimal neck stiffness grade ii: severe headache, franc neck stiffness, possible cranial nerves paresis grade iii: confusion or lethargy, mild focal deficits grade iv: stuporous, hemiparesis forte, decerebrate grade v: comatose, decerebrate. wfns scale is based upon glasgow comma scale and the presence or absence of neurological deficits as such: grade i: gcs 15 points, no neurological deficits grade ii: gcs 13-14 points, no neurological deficits grade iii: gcs 13-14 points, present neurological deficits grade iv: gcs 7-12 points, whatever the neurological deficits grade v: gcs 3-6 points, whatever the neurological deficits. another scale of great clinical and therapeutical significance is the fisher scale previously presented, with four degrees of severity, based upon computedtomography aspects such as the presence of blood 133 subarachnoid haemorrhage. a critical neurosurgical emergency in the ventricular system or parenchymal hematoma and thickness of subarachnoid blood. the right moment to perform surgery in aneurysmal sah is nowadays considered to be at 2472 hours from debut in patients with hunt & hess grades 1 or 2 and consists of aneurysm securement through classical surgical clipping or endovascular coiling. patients with a higher hunt & hess grade (altered mental status or neurological deficits) are to be admitted and monitored in the intensive care unit for vital functions support with the goal of obtaining a better neurological status in order for the aneurysm securement to be achievable with a more favorable risk/benefit balance. exception to this rule occurs when sah of any etiology is accompanied by large parenchymal hematoma (fisher grade iv) that come with vital risk to the patient and it requires emergency intervention whatever the hunt & hess grade. a similar situation occurs when patient’s life is endangered on the sortterm due to intracranial hypertension (secondary to acute obstructive hydrocephalus following sah) a external ventricular drainage is placed together with an intracranial pressure monitoring device – in order to obtain clinical and neurological amelioration until definitive treatment of the cause that led to sah is possible. [9, 10] following surgery, after securing the aneurysm whose rupture produced the subarachnoid hemorrhage, together with general medical measures and complications prevention, a transcranial doppler ultrasound is needed in order to appreciate the blood flow through the main cerebral arteries and possible vasospasm, as well as control cerebral ct examination for the verifying of occlusion devices used and for the visualizing the aspect of the ongoing sah. in cases of drug resistant vasospasm intraarterial endovascular vasodilator therapy may be used – vasodilator agents are selectively injected directly into the cerebral arteries under angiographical control. complications in the postoperative period medical treatment measures must be continued. considering the risk of rebleed, which stand at 30-70% despite adequate treatment and knowing that 90% of rebleed lead to death, postsurgical patients must be monitored in the intensive care unit. despite these therapeutic resources, the major risk of devastating complications particularly difficult to treat persists – cerebral vasospasm and late cerebral ischemia, vegetative phenomena of central origin, parenchymal hematoma, rebleed, electrolytes imbalance, normal pressure hydrocephalus. [10] the risk of developing cerebral vasospasm stands present since the debut of sah but is considered to be at its highest between days 3-7 and extending up to 3 weeks. it is very accurately appreciated with the help of the fisher grading system, risk correlation being proportionate with a higher grade. figure 5. résumé of sah complications and their mechanism. personal illustration. neurological rehabilitation the treatment of subarachnoid hemorrhage is a multidisciplinary one, step-by-step and one which address simultaneously the etiological factor, the worsening factor and at the same time the prevention of complications. [2,12] for a favorable outcome and prognosis, and also for survivors’ rehabilitation a quick and adequate diagnosis is required. it should happen in a primary neurosurgery center with radiology and intensive care optimal facilities available at all times. the prognosis of these patients and their neurological rehabilitation require the right cooperation between the medical team consisting of emergency room physician – radiologist – interventionist – neurosurgeon – intensivist – neurologist and rehabilitation physician. conclusions a curative treatment of subarachnoid hemorrhage is out of the question at the moment, with it being not actually a disease but rather a course of pathological events that develop in a chain like manner and that 134 alexandra bibiriță, daniel teleanu, alexandru vlad ciurea imply a series of serious consequences over cerebral structures, both short term and long term. methods of treatment of sah complications are currently under development, and even though they are based on hypotheses decades old, some of them are highly debatable according to some authors, such as subarachnoid space washout-out with drugs designed to prevent vasospasm. [13] considering that about 15-20% of patients that suffer from sah decease before getting to medical attention of any kind according to who data, and that 40% of survivors from sah of any kind will have permanent neurological deficits, two things stand out: early identification of high suspicion sah cases is critical and referral to an emergency neurosurgical service is of paramount need. abbreviations avm – arterial-venous malformation; bp – blood pressure; csf – cerebrospinal fluid; cva – cerebrovascular accident; icp – increased intracranial pressure; who – world health organization. conflicts of interest the authors have no conflicts of interest to declare. references 1. kameda-smith m, aref m, jung y, ghayur h, farrokhyar f, determining the diagnostic utility of lumbar punctures in ct negative suspected subarachnoid hemorrhage: a systematic review and meta-analysis, world neurosurg. 2020; 148: e27-e34. 2. kellermann i, kleindienst a, hore n, buchfelder m, brandner s., early csf and serum s100b, concentrations for outcome prediction in traumatic brain injury and subarachnoid hemorrhage, clin neurol neurosurg. 2016; 145:79-83. 3. nadkarni na, maas mb, batra a, kim m, manno em, sorond fa, prabhakaran s, naidech am, liotta em, elevated cerebrospinal fluid protein is associated with unfavorable functional outcome in spontaneous subarachnoid hemorrhage, j stroke cerebrovasc dis. 2020 29(4):10460. 4. lenhart m, bretschneider t, gmeinwieser j, ullrich ow, schlaier j, feuerbach s, cerebral ct angiography in the diagnosis of acute subarachnoid hemorrhage, acta radiol., 2013, 38(5):791-6. 5. raevis j, elmalem vi, pseudotumor cerebri syndrome causing a terson like syndrome, am j ophthalmol case rep. 2020; 20: 100993. 6. vivancos j, gilo f, clinical management guidelines for subarachnoid haemorrhage. diagnosis and treatment, neurologia, 2014;29(6):353-70. 7. wu l, chen g, signaling pathway in cerebral vasospasm after subarachnoid hemorrhage: news update, acta neurochir suppl. 2016; 121:161-5. 8. veldeman m, albanna w, weiss m, conzen c, schmidt tp, schulze steinen h, wiesmann m, clusmann h, schubert ga, invasive neuromonitoring with an extended definition of delayed cerebral ischemia is associated with improved outcome after poor-grade subarachnoid hemorrhage, j neurosurg. 2020; 15:1-8. 9. veldeman m, albanna w, weiss m, conzen c, schmidt tp, clusmann h, schulze-steinen h, nikoubashman o, temel y, schubert ga, treatment of delayed cerebral ischemia in good-grade subarachnoid hemorrhage: any role for invasive neuromonitoring?, neurocrit care. 2020. 10. probst ma, hoffman jr, md, computed tomography angiography of the head is a reasonable next test following a negative non-contrast head computed tomography in the emergency department work up of subarachnoid hemorrhage, ann emerg med. 2016 june; 67(6): 773–774. 11. hughes jd, bond km, mekary ra, dewan mc, rattani a, baticulon r, kato y, azevedo-filho h, morcos jj, park kb, estimating the global incidence of aneurysmal subarachnoid hemorrhage: a systematic review for central nervous system vascular lesions and metaanalysis of ruptured aneurysms, world neurosurg. 2018;115:430-447. 12. flemming kd, lanzino g, management of unruptured intracranial aneurysms and cerebrovascular malformations, continuum (minneap minn). 2017 feb;23(1, cerebrovascular disease):181-210. 13. kodama, namio & sasaki, tatsuya & kawakami, masahisa & sato, masahiro & asari, jun. (2000). cisternal irrigation therapy with urokinase and ascorbic acid for prevention of vasospasm after aneurysmal subarachnoid hemorrhage. outcome in 217 patients. surgical neurology. 53. 110-7; 53(2):110-7. 14. lindvall p, runnerstam m, birgander r, koskinen lo. the fisher grading correlated to outcome in patients with subarachnoid haemorrhage. br j neurosurg. 2009 apr;23(2):188-92. 15. rosen ds, macdonald rl. subarachnoid hemorrhage grading scales: a systematic review. neurocrit care. 2005;2(2):110-8. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article association of abnormal metopic suture causing hypertelorism, interfrontal encephalocele with craniofacial cosmetic deformity associated with myelomeningocele: management literature review willem guillermo calderon-miranda, guru dutta satyarthee, huber padilla-zambrano, yancarlos ramosvillegas, hernando raphael alvis-miranda, joulen mo-carrascal, johana maraby, luis rafael moscote-salazar mexico, india, colombia doi: 10.1515/romneu-2017-0028 182 | calderon-miranda et al – encephalocele associated with myelomeningocele doi: 10.1515/romneu-2017-0028 association of abnormal metopic suture causing hypertelorism, interfrontal encephalocele with craniofacial cosmetic deformity associated with myelomeningocele: management literature review willem guillermo calderon-miranda1, guru dutta satyarthee2, huber padilla-zambrano3, yancarlos ramos-villegas3, hernando raphael alvis-miranda4, joulen mo-carrascal5, johana maraby5, luis rafael moscote-salazar6 1resident of radiology, universidad nacional autonoma de mexico, ciudad de mexico, mexico 2neurosurgeon, department of neurosurgery, neurosciences cengtre, aiims new delhi, india 3university of cartagena, cartagena de indias, colombia 4resident of neurosurgery, university of cartagena, cartagena de indias, colombia 5physician, university of cartagena, cartagena de indias, colombia 6neurosurgeon, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia abstract: myelomeningocele may be associated with other neural and extraneural anomalies. authors present association of metopic suture abnormality, an interfrontal encephalocele with widening of metopic suture and abnormal shape frontal bones in the forehead in those associated with hydrocephalus. authors describes two neonates with interfrontal encephalocele, representing first series reporting in neonate. management and pertinent literature is briefly discussed. key words: metopic sututre abnormality, hypertelorism, meningomyelocele, hydrocephalus, neonate introduction the meningomyelocele may be associated with chiari malformation, hydrocephalus, and corpus callosal agenesis. the hydrocephalus may produce large bulging forehead with sunset sign. (1-5) however, abnormal persistence of widely spaced unfused metopic suture is extremely uncommon. the widely opened metopic suture extends superiorly to the anterior fontanelle and inferiorly also extends to the roots of nose causing romanian neurosurgery (2017) xxxi 2: 182 185 | 183 hypertelorism and moulding of frontal bones. (4-8) through the metopic suture defect, the brain parenchyma may herniates and herniated brain may remain vulnerable to external injury and associated consequences. the hydrocephalus is postulated to potentially aggravate further herniation of brain. these calvarial and brain parenchymal abnormity cases may not require surgery, and the repair of meningocele with ventriculoperitoneal shunt surgery may be sufficient. such cases were reported in late childhood. (8) however, both of our current cases were in the neonatal age, representing first of it’s in the western literature. author reports two interesting cases. here, we present series of five mmc children with interfrontal encephalocele and unfused wide metopic suture and describe the typical feature of this rare abnormality, the probable differences with other mmc patients, associated problems, and management. case illustration case #1 newborn male with evidence of myelomeningocele in sacral region. born at 32.8 gestation weeks with a weight of 2900 grams and a cephalic perimeter of 53 centimeters, from a 26 years old mother, g6 p3 a3 c3, the six pregnancies with differents fathers, prenatal controls since the first month of pregnancy, attending 8 consultation in all, she performed 4 prenatal ecographies, of which none of them made the diagnosis of myelomeningocele, ambiguous genitals, bilateral varus equine foot and/o metopic suture defect in u form. serologic evaluation for hiv, syphilis, toxoplasma and hbv were non-reactive. to physical examination feels a distracted metopic suture, observes ambiguous genitals (scrotum bifidus, hypospadia and micropenis), bilateral varus equine foot, bilateral simian fold and myelomeningocele with fistula, which was operated immediately. simple skull tc with 3d reconstruction evidences metopic suture defect in u form. (fig. 1). cerebral and total spine mri shows inconspicuous asymmetric cerebellar atrophy predominating on the left side, in the right occipital lobe the rotations are disorganized, there is hypoplasia of the corpus callosum, syringomyelia, low tonsils, supratentorial hydrocephalus and sacral meningocele. correction is performed through resection of ruptured myelomeningocele, dural graft and fasciocutaneous flap, hemodynamically stable evolution after 16 days of prophylactic scheme for neuroinfection is ordered the discharge. figure 1 ct scan showing an abnormal metopic suture 184 | calderon-miranda et al – encephalocele associated with myelomeningocele case # 2 full term newborn male, product of a fifth pregnancy, from a 41 years old mother, apparently healthy. pregnancy evolved with adequate prenatal care. born by caesarea, punctuation apgar was 9/10 with appropriate weight to the age, (3850 grams). physical examination was found to be defective in the lumbar region, suggestive of myelomeningocele. in the cephalic region is evidenced dolichocephalic skull shape, with protrusion on the forehead. brain ct scan was performed which showed partial agenesis of the frontal bone. (figure 2 a and b). it neurosurgery performed to correction of neural tube defect. the patient presented communicating hydrocephalus a week later which required development ventriculoperitoneal shunt placement, with satisfactory postoperative evolution. discussion the metopic suture is also called median frontal suture, often associated with frontal sinus hypoplasia or agenesis. metopic suture extends through the nasion to the bregma, in the midline across the frontal bone and often remain incomplete and usually fuses by around nine months after birth. (1,2) rarely, the metopic suture can persist as an anatomical variant, which can be mistaken for fracture of the frontal bone, which is differentiated radiologically the metopic sutures lies in the midline and sutural interdigitations. (3) a premature fusion of the suture is termed metopic synostosis which characterically result into trigonocephaly. (2) figure 2 a and b ct scan showing an abnormal metopic suture myelomeningocele develops during the neurulation phase of embryonic life due to failure in posterior neuropore closure. lacunar skull caused by membranous bone dysplasia typically have well-defined lucent parts and other are frontal dysplasia cranium bifida, [4, 5, 6]. nejat et al postulated the persistent of lacuna in frontal bones in the region of metopic suture may cause scalloping of the frontal bone with predisposition to persist romanian neurosurgery (2017) xxxi 2: 182 185 | 185 widely opened metopic suture, pulsation of herniated neural tissue causes abnormality in the metopic suture region also causing cosmetic deformity. (7) the metopic suture abnormality progression is usually halted with ventriculoperitoneal shunt surgery and usually separate surgery for metopic suture is not advocated, however, rarely cases with severe hypertelorism and cosmetic deformity may be advised. (7) nejat et al. analyzed five children with mean age of six month and all were male. meningomyelocele was located in the lumbar and lumbosacral areas. neurological deficits included a spectrum of presentation from sphincter disturbance to paraplegia. all had associated hydrocephalus and required csf shunt surgery. cranial neuroimaging showed intracranial, interfrontal encephalocele, asymptomatic chiari malformation, and corpus callosum agenesis in five, five, and three patients, respectively. these cases had anterior fontanel anomalies called as interfrontal encephalocele, associated with open metopic suture extending widely to the nasal radix producing hypertelorism accompanied by interfrontal herniation of frontal lobes. the associated hydrocephalus exaggerates the interfrontal encephalocele and shunt surgery ameliorates interfrontal encephalocele. however, some patient may have surgical correction of metopic suture for cosmetic (7). conclusion authors reports two cases of forehead interfrontal encephalocele in two neonate, who had associated myelomeningocele. patients had widened metopic suture and association with herniation of frontal lobe through the midline calvarial defect interfrontal encephalocele causing hypertelorism. correspondence luis rafael moscote-salazar, red latino latin american trauma & intensive neuro-care organization, bogota, colombia email: mineurocirujano@gmail.com references 1. vu hl, panchal j, parker ee et-al. the timing of physiologic closure of the metopic suture: a review of 159 patients using reconstructed 3d ct scans of the craniofacial region. j craniofac surg. 2001;12 (6): 527-32. 2. weinzweig j, kirschner re, farley a et-al. metopic synostosis: defining the temporal sequence of normal suture fusion and differentiating it from synostosis on the basis of computed tomography images. plast. reconstr. surg. 2003;112 (5): 1211-8. 3. glass rb, fernbach sk, norton ki et-al. the infant skull: a vault of information. radiographics. 2004;24 (2): 507-22. 4. anegawa s, hayash t, torigoe r, hashimoto t (1993) myelomeningocele associated with cranium bifidum: rare coexistence of two major malformations. child nerv sys 9:278–281 5. gilbert jn, jones kl, rorke lb, chernoff gf, james he (1986) central nervous system anomalies associated with meningomyelocele, hydrocephalus, and the arnold– chiari malformation: reappraisal of theories regarding the pathogenesis of posterior neural tube closure defects. neurosurgery 18:559–564 6. nayak pk, mahapatra ak (2006) frontal bone agenesis in a patient of spinal dysraphism. pediatr neurosurg 42:171–173 7. nejat f, kamali s, el khashab m. interfrontal encephalocele: a rare feature of forehead in hydrocephalic myelomeningocele patients. clinical feature, probable mechanisms, and management. childs nerv syst. 2013 aug;29(8):1349-52. 8. nicolaides kh, campbell s, gabbe sg, guidetti r ultrasound screening for spina bifida: cranial and cerebellar signs. lancet 1986; 2:72–74 8kocamanumit_sciatica romanian neurosurgery | volume xxx | number 4 | 2016 | october december article sciatica due to pelvic hematoma: case report umit kocaman, muhammet bahadir yilmaz, hakan yilmaz turkey doi: 10.1515/romneu-2016-0080 romanian neurosurgery (2016) xxx 4: 507 – 511 | 507 doi: 10.1515/romneu-2016-0080 sciatica due to pelvic hematoma: case report umit kocaman1, muhammet bahadir yilmaz1, hakan yilmaz2 1university of izmir of medicine, department of neurosurgery, izmir, turkey 2usak state hospital, department of neurosurgery, usak, turkey abstract: sciatica is defined as pain in the sciatic nerve distribution. the most common reason of sciatica is radiculopathy due to lumbar disc hernia. other causes can be congenital, acquired, infectious, neoplastic, or inflammatory. the piriformis syndrome is another cause. the pain starts in an insidious manner when the cause of sciatica is an extraspinal tumor. it is intermittent at first but a constant and progressive pain that does not decrease with position or rest gradually develops in all patients. the possibility of an intraabdominal or pelvic mass should always be considered and the relevant tests requested when the cause of the sciatica cannot be explained. we present an 83-year-old male who presented with non-traumatic and non-vascular lumbosacral plexopathy due to a large hematoma in the left adductor muscle following the use of warfarin sodium. key words: lumbosacral plexopathy, pelvic hematoma, sciatica introduction sciatica is defined as pain in the distribution of the sciatic nerve. the sciatic nerve consists of components from the l4-s3 nerve roots. the nerve exits the pelvis from the greater sciatic foramen along the posterior part of the thigh. it divides into the tibial and main peroneal nerves in the lower third of the thigh (7). the most common cause of sciatica is radiculopathy due to lumbar disc hernia. other causes can be congenital, acquired, infectious, neoplastic, and inflammatory. the pyriformis syndrome is another cause. pain of vascular origin, reflected pain not of spinal origin, and peripheral neuropathies can mimic sciatica (1,7). the pain increases slowly when the cause of the sciatica is an extraspinal tumor. it is intermittent at first but a constant and progressive pain that does not decrease with position or rest gradually develops in all patients. the possibility of an intraabdominal or pelvic mass should always be considered and the relevant tests requested when the cause of the sciatica cannot be explained (1,7). we present an 83-year-old male who presented with non-traumatic and nonvascular lumbosacral plexopathy in the left adductor muscle due to a large hematoma following the use of warfarin sodium. 508 | kocaman et al sciatica due to pelvic hematoma lumbosacral plexopathy due to a hematoma in the left adductor muscle caused by warfarin use is rare in the literature. our colleagues should be as careful when injecting substances in the canal as they are when injecting them outside the canal during magnetic resonance imaging (mri) investigations. we presented this case to emphasize the importance of this precaution. case report an 83-year-old man presented with back pain, left leg pain and loss of strength in the left leg. the patient said that the pain had been continuing for the last 10 days while the loss of strength had appeared in the last 3 days. the pain was resistant to medical treatment and did not resolve with rest. the patient stated that the pain was gradually becoming more severe. the patient was on warfarin sodium due to a heart valve disease but did not have his inr measured regularly. the left lasegue test was positive at 40 degrees on neurological examination. the left femoral strain test was positive. the left knee extension strength was 4/5 and left ankle dorsiflexion 3/5. the left patella was hypoactive and there was hypoesthesia of the left l3, l4, l5 dermatomes. left wallex sensitivity was interpreted as positive. back movements were painful and limited. the patient could only be mobilized with a wheelchair due to the pain. lumbar mr revealed lumbar degenerative changes and moderate-sized central protrusions at l4-5 and l5-s1. the sections also revealed marked atrophy of the left psoas muscle and low t2 signals in the iliacus muscle (figure 1). pelvic computerized tomography (ct) was therefore requested and the images were consistent with hematoma in the left iliacus muscle (figure 2). the usg revealed a solid mass. the patient was on irregular warfarin and prothrombin time was 34 sec. the patient was referred to the general surgery department for the intraabdominal hematoma. surgery was not planned due to the additional systemic problems. the patient was hospitalized for pain control. the pain decreased and became tolerable with tramadol and the hematoma was therefore left to resorb spontaneously. the necessary recommendations for ptz followup were obtained from the hematology department and applied. the patient was later discharged and called back for follow-up to the neurosurgery outpatients a week later. figure 1 low t2 signals in the iliacus muscle in mri figure 2 hematoma in the left iliacus muscle in pelvic ct romanian neurosurgery (2016) xxx 4: 507 – 511 | 509 discussion sciatica is defined as pain in the sciatic nerve distribution. the sciatic nerve consists of components from the l4-s3 nerve roots. the nerve exits the pelvis from the greater sciatic foramen along the posterior part of the thigh. it divides into the tibial and main peroneal nerves in the lower third of the thigh (7). the most common cause of sciatica is radiculopathy due to lumbar disc hernia. other causes can be congenital, acquired, infectious, neoplastic, and inflammatory. the pyriformis syndrome is another cause. pain of vascular origin, reflected pain not of spinal origin, and peripheral neuropathies can mimic sciatica (1,7). the pain starts in an insidious manner when the cause of sciatica is an extraspinal tumor. it is intermittent at first but a constant and progressive pain that does not decrease with position or rest gradually develops in all patients (7). the possibility of an intraabdominal or pelvic mass should always be considered and the relevant tests requested when the cause of the sciatica cannot be explained. bushby et al have reported lumbosacral plexopathy and sciatica due to a ruptured main iliac artery aneurysm. their patient presented with back pain and sciatica, loss of sensation, loss of strength and numbness that included the l4-s1 roots. ct imaging revealed a large hematoma in the left side of the pelvis due to an 8 cm main iliac artery aneurysm. one must be careful about pelvic and intraabdominal space-occupying lesions while searching for sciatica etiology, especially when atypical neurological symptoms are present (1). melikoğlu et al reported a 50-year-old woman with trauma to the thorax, abdomen and left hip. severe left sciatica and left foot drop developed approximately three weeks after the trauma. magnetic resonance imaging showed a large hematoma area next to the lumbosacral plexus and ct angiography revealed a left internal iliac artery aneurysm. the pain resolved immediately with surgical treatment while the foot drop only recovered partially (6). this case emphasizes the importance of considering pseudoaneurysm in cases with sciatica or neurological deficits that develop following incidental trauma or in an iatrogenic manner. there are many causes of sciatica. intraabdominal masses may cause sciatica through their effect on the lumbosacral plaxus following local invasion or distant metastases. lumbosacral plexopathy usually develops due to a compressive effect of the tumor. invasion is a less frequent mechanism (5). lin et al have reported a 67-year-old female who presented with neurogenic claudication, back pain and left foot drop that had been increasing for the last three months. this was accompanied by increasing abdominal distension. imaging studies revealed a large pelvic mass compressing the left lumbosacral plexus. direct plexus invasion was not found on imaging or with observation during surgery. bilateral ovarian borderline mucinous cystic tumor accompanied by pseudomyxomaperitonei was found and surgically removed, leading to a dramatic recovery in the sciatica (5). 510 | kocaman et al sciatica due to pelvic hematoma ladha et al mention a different spread mechanism for the lumbosacral plexopathy caused by prostate cancer. they report two lumbosacral plexopathy and sciatica cases that developed without any pelvic of extraprostatic spread. they state that the possible mechanism here is direct perineural spread from the prostatic nerves to the lumbosacral plexus. this could be a rare potential spread mechanism of cancer (4). dyck et al have divided lumbosacral plexopathy into two groups as diabetic and non-diabetic using a different approach. they state that the cause is ischemic injury due to microvascular damage in many cases thought to be idiopathic. they also emphasize the importance of immunotherapy although the evidence is currently inadequate (2). ko et al have described some features of lumbosacral plexopathies. they state that nontraumatic lumbosacral plexopathies are due to a neoplasm in 59.3%, radiotherapy in 22.2%, neurological amyotrophy in 7.4%, and a psoas abscess in 3.7%. the idiopathic cases make up 7.4%. pain is the presenting symptom in 82.2 of the neoplastic cases (3). lumbosacral plexopathy with nontraumatic, non-vascular spontaneous retroperitoneal hematoma due only to warfarin use has been reported very rarely. this hematoma was also present in the lumbar mr images of our patient. a careful history should be obtained when evaluating sciatica. resistance to medical treatment, progressive increase of the pain, no recovery with position or rest could indicate lumbosacral plexopathy. atypical neurological deficits and atypical distribution of the pain on neurological examination can again suggest lumbosacral plexopathy. the most important signs indicating lumbar plexopathy are sciatica unexplained by the spinal column pathology on lumbar mr together with the examination findings. it is important to thoroughly evaluate the adjacent spinal canal in addition to the spinal column on mr images. radiologists should be consulted regarding this matter and the images should be evaluated together with the radiology report. abdominal tomography can be used as an additional test if necessary. conclusion the history, physical examination and radiology play a very important role in the evaluation of the patient with sciatica. the most important signs indicating lumbar plexopathy are sciatica unexplained by the spinal column pathology on lumbar mr together with the examination findings. it is important to thoroughly evaluate the adjacent spinal canal in addition to the spinal column on mr images. radiologists should be consulted regarding this matter and the images should be evaluated together with the radiology report. written informed consent of the patient was obtained. correspondence hakan yilmaz, usak state hospital, department of neurosurgery, usak, turkey. e-mail: dr_hakanyilmaz@hotmail.com tel: +90 5066211829 romanian neurosurgery (2016) xxx 4: 507 – 511 | 511 references 1. bushby n, wickramasinghe sy, wickramasinghe dn: lumbosacral plexopathy due to a rupture of a common iliac artery aneurysm. emerg med australas 2010; 22(4): 351-3 2. dyck pj, thaisetthawatkul p: lumbosacral plexopathy. continuum (minneap minn) 2014; 20(5): 1343-58 3. ko k, sung dh, kang mj, ko mj, do jg, sunwoo h, kwon tg, hwang jm, park y. clinical, electrophysiological findings in adult patient with nontraumatic plexopathies. ann rehabil med 2011; 35(6): 807-15 4. ladha ss, spinner rj, suarez ga, amrami kk, dyck pj: neoplastic lumbosacral radiculoplexopathy in prostate cancer by direct perineural spread: an unusual entity. muscle nerve 2006; 34(5): 659-65 5. lin hl, chen jt, liu yf, cho dy: sciatica caused by pseudomyxoma peritonei. j chin med assoc 2009; 72(1): 39-41 6. melikoglu ma, kocabas h, sezer i, akdag a, gilgil e, butun b: internal iliac artery pseudoaneurysm: an unusual cause of sciatica and lumbosacral plexopathy. am j phys med rehabil 2008; 87(8): 681-3 7. oruckaptan h: translation of ’handbook of neurosurgery’ (mark s. greenberg 6. ed. thieme, new york, 2006). ankara: gunes medical bookstore, 2012 18regesv_adult romanian neurosurgery | volume xxx | number 4 | 2016 | october december article adult medulloblastoma s.v. rege, harshad patil, sharadendu narayan, harshad patil india doi: 10.1515/romneu-2016-0090 romanian neurosurgery (2016) xxx 4: 557 – 561 | 557 doi: 10.1515/romneu-2016-0090 adult medulloblastoma s.v. rege, harshad patil, sharadendu narayan, harshad patil department of neurosurgery, sri aurobindo medical college and pg institute, indore, madhya pradesh, india abstract: medulloblastoma is a highly malignant central nervous system (cns) tumor that arises from the cerebellum. it is the most common primary malignant intracranial childhood neoplasm. in adults, medulloblastoma are much less common, accounting for < 1% of all adult brain tumors. herein, author has described a rare case of cerebellar medulloblastoma in adult. key words: adult, medulloblastoma, posterior fossa introduction medulloblastoma is the most common cns tumor of childhood, accounting for 15% to 30% of all childhood brain tumors, and 30% to 40% of all posterior fossa tumors. (1) in adults, the tumor is much less common, accounting for approximately 1% of adult primary brain tumors, 80% of which occur before the end of the fourth decade. (2) the adult tumor is said to occur more often in the cerebellar hemispheres than the vermis and is more often desmoplastic in histology. the exact etiology of medulloblastomas is not known. herein, author has described a rare case of cerebellar medulloblastoma in adult. case report a 45 years old male presented in neurosurgery department with headache and gait disturbance for last three months. neurological examination revealed cerebellar signs with ataxic gait. magnetic resonance imaging (mri) of brain showed heterogeneous intensity mass lesion in posterior fossa mainly involving midline (figures 1 and 2). in view of symptoms patient was taken up for surgery. gross total excision of the tumour was done via midline suboccipital craniectomy. intraoperatively tumour was greyish white, mainly present in midline involving vermis and extending into the right cerebellum (figure 3). tumour was sent for histopathological examination which revealed medulloblastoma desmoplastic variety. after the surgery, the patient was alert, his neurological examination showed only mild truncal ataxia. no obvious mass lesion was present in postoperative imaging of brain (figure 4). to rule out drop metastasis, mri whole spine was done which was essentially normal (figure 5). after suture removal patient was sent for radiotherapy and no recurrence was found in 6 months of follow up. 558 | rege et al adult medulloblastoma figure 1 post contrast mri brain axial section showing heterogeneous intensity mass lesion in posterior fossa mainly involving midline figure 2 post contrast mri brain sagittal section showing midline cerebellar mass romanian neurosurgery (2016) xxx 4: 557 – 561 | 559 figure 3 intra operative image showing greyish white mass, mainly present in midline involving vermis and extending into the right cerebellum figure 4 postoperative image showing no obvious mass lesion 560 | rege et al adult medulloblastoma figure 5 mri whole spine showing no drop metastasis discussion medulloblastoma is a highly malignant cns tumor that arises from the cerebellum. it is the most common primary malignant intracranial childhood neoplasm, accounting for 25% of all childhood tumors. (1) more than 80% of medulloblastomas are diagnosed in children during the first 15 years of life, the median age at diagnosis being 5 years. in adults (patients ≥ 16 years of age), medulloblastomas are much less common, accounting for < 1% of all adult brain tumors. the incidence of adult medulloblastomas is approximately 0.5 per million per year, and decreases with increasing age. the exact etiology of medulloblastomas is not known. (2) medulloblastoma is thought to arise from a primitive cell in the external granular layer of the cerebellum, but the specific cell of origin has not been identified. pathologically medulloblastomas consist of small round blue cells. it has two variants classical and desmoplastic. the latter variant has large amounts of reticulin and collagen.3 medulloblastoma is located in posterior fossa thus it often produces hydrocephalus and symptoms of increased icp, as well as cerebellar signs (eg, truncal and limb ataxia, nystagmus) (4) which was present in our case. disease may exist as nodular lesions outside the primary site anywhere within the neuraxis, including the spine and supratentorial cerebrum, and may involve the csf.4 in our case there was no drop metastasis in spine. magnetic resonance imaging (mri) brain is the investigation of choice. lesions are usually iso to hypointense on t1wi, have variable signal on t2wi, and frequently demonstrate contrast enhancement. these tumors tend to be homogenous in appearance, with occasional cystic or necrotic areas. (5) surgery is the treatment of choice. the goal of surgery is to remove all visible tumour. survival of adult medulloblastoma patients may be influenced by the extent of residual disease following surgery, particularly for patients without evidence of dissemination. treatment of associated hydrocephalus can be managed by external drainage with tumor decompression, tumor decompression alone, or by the use of various shunting procedures. (6) in our case gross total excision of tumour was done. craniospinal axis radiation therapy is the standard of care for the treatment of adult medulloblastoma patients, as medulloblastomas are quite radiosensitive. standard radiation doses to the craniospinal romanian neurosurgery (2016) xxx 4: 557 – 561 | 561 axis involve delivering 35 to 45 gy to the brain and 30 to 40 gy to the spine, with a dose of 54 gy to the primary tumor site. (6) in contrast to childhood medulloblastoma, the role of chemotherapy in adult medulloblastoma patients is undetermined. prados and colleagues found that those patients who received adjuvant chemotherapy (mostly nitrosourea-based regimens) had a statistically significantly longer survival as compared to those who did not receive adjuvant chemotherapy. (7) in our case, patient was received craniospinal irradiation. the recurrence rate for medulloblastomas in adults is approximately 50% to 60%. the median survival after recurrence has been reported to be approximately 1.3 years. the most common site of recurrence is the posterior fossa. other sites of recurrence include the spine, csf, supratentorial cerebrum, bone, and other extraneural sites. (8) in our case recurrence was not found after 6 month of follow up. conclusion adult variety of medulloblastomas have notable differences as compared to the pediatric type. there is higher frequency of lateral cerebellar location, desmoplastic histology, and late recurrences in the adult variety. the 5-year overall survival rates are comparable between the adult and pediatric population.the management of adult medulloblastoma patients involves a thorough staging work-up (including brain and wholespine mri and csf cytology analysis), as complete a resection as possible, and postoperative craniospinal axia (csa) irradiation. nitrosourea-based chemotherapy is reserved for recurrent disease, as adjuvant chemotherapy has not shown significant benefit in adult medulloblastoma patients. prospective studies are needed to accurately define significant prognostic factors and treatment regimens for adult patients with medulloblastomas. correspondence dr. harshad patil address: department of neurosurgery, sri aurobindo medical college and pg institute, indore, madhya pradesh, india email: dr.harshadpatil@gmail.com phone: +919893894242 references 1. rutka jt. medulloblastoma. clin neurosurg. 1997;44:571-85. review. 2. bloom hj, bessell em. medulloblastoma in adults: a review of 47 patients treated between 1952 and 1981. int j radiat oncol biol phys. 1990;18:763–72. 3. rorke lb, trojanowski jq, lee vm. et al. primitive neuroectodermal tumors of the central nervous system. brain pathol. 1997;7:765–84. 4. tomlinson fh, scheithauer bw, meyer fb, smithson wa, shaw eg, miller gm, groover rv. medulloblastoma: i. clinical, diagnostic, and therapeutic overview. j child neurol. 1992 apr;7(2):142-55. review. 5. raybaud c, ramaswamy v, taylor md, laughlin s. posterior fossa tumors in children: developmental anatomy and diagnostic imaging. childs nerv syst. 2015 oct;31(10):1661-76. doi: 10.1007/s00381-015-2834-z. epub 2015 sep 9. 6.paulino ac. current multimodality management of medulloblastoma. curr probl cancer. 2002 novdec;26(6):317-56. review. 7. prados md, warnick re, wara wm. et al. medulloblastoma in adults. int j radiat oncol biol phys. 1995;32:1145–52. 8. carrie c, lasset c, alapetite c. et al. multivariate analysis of prognostic factors in adult patients with medulloblastoma. retrospective study of 156 patients. cancer. 1994;74:2352–60. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article large intraventricular epidermoid with bobble head doll syndrome in an adult amit agrawal india doi: 10.1515/romneu-2017-0038 romanian neurosurgery (2017) xxxi 2: 229 232 | 229 doi: 10.1515/romneu-2017-0038 large intraventricular epidermoid with bobble head doll syndrome in an adult amit agrawal department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: intracranial epidermoid tumors are rare (0.2–1.8%), histologically benign, slow-growing, congenital neoplasms of the central nervous system arising from the retained ectodermal implants. we report an unusual case of intra third ventricular epidermoid in an adult presenting with the bobble-head doll syndrome and review the relevant literature. key words: epidermoid tumor, third ventricle, bobble head doll syndrome introduction intracranial epidermoid tumors are rare (0.2–1.8%), histologically benign, slow-growing, congenital neoplasms of the central nervous system arising from the retained ectodermal implants. (1-4) these lesions tend to spread along normal cleavage planes, and slowly fill any available subarachnoid space, including the sulci, cisterns, fissures, and ventricles. (4, 5) because of this unique behavior the expanding tumor conforms to the shape of the cavities, however the tumor does adhere to and surround the vital structures. (6, 7) case reports a 55 year gentleman presented with headache of 6 months duration with vomiting off and on for last 15 days. he also had bobbing movements of the head. there was no history of focal motor or sensory weakness. his general and systemic examination was unremarkable. higher mental functions were normal. cranial nerves were normal except bilateral papilloedema. extraocular movements were and there was no nystagmus. his voice was of low volume and without slurring. motor power was normal and sensory functions were also normal. he was able to walk with support. he had fine trmors in both the hands. on examination he had bobbing movements of the head (movie). computed tomography scan (ct scan) of the brain showed a large discrete area of radiolucency in the third ventricle and there was ventriculomegaly without any evidence of periventnicular edema. (figure 1). magnetic resonance (mr) imaging of the brain was showed a large, mass lesion in the third ventricle also insinuating in the basal cisterns; 230 | agrawal large intraventricular epidermoid with bobble head doll syndrome however there was no extension of the lesion into the fourth ventricle (figure 2). the mass was slightly hyperintense relative to csf on t1-weighted images, hyperintense t2weighted with heterogeneous appearance and heterogeneous nature was better appreciated on flair images. on diffusion-weighted (dw) images, there was overall restricted diffusion with areas of free diffusion. there was no significant enhancement of the tumor after intravenous administration of gadolinium contrast material. based on these imaging findings a diagnosis of intraventricular epidermoids was made. (8-11) the patient underwent right parietal parasagittal craniotomy, interhemispheric transcallosal approach and near total decompression of the tumor. after opening the spleinum of the corpus callosum a pearly structure with an appearance characteristic of an epidermoid tumor was seen filling the ventricle completely, that was near totally decompressed. histopathological evaluation showed typical features consistent with epidermoid. the patient had unremarkable postoperative course and improved in his abnormal movements and gait. figure 1 ct scan showing large third ventricular epidermoid figure 2 mri showing extension of the lesion discussion the commonest sites of intracranial epidermoids include cerebellopontine angle and the chiasmal region, however these lesions can also appear in the cerebral hemisphere and the intraventricular cavities. (2, 8, 12) intraventricular location of the particulary third and lateral ventricle is extremely uncommon with only few cases in the literature. (13-16) their can be a direct occurrence of the epidermoids in the ventricular or the ventrcles can be secondarily involved as in present case, (16-18) however it is often extremely difficult to say exactly where an epidermoid has originated. (17-19) the bobble-head doll syndrome is a rare and unique movement disorder characterized by continuous or episodic involuntary forward and backward and side to side movement of the head that mainly encountered in children. (20-22) the etiology of this syndrome include third ventricular tumors, suprasellar arachnoid cysts, aqueductal stenosis and other lesions in the region of the third ventricle along with communicating hydrocephalus. (20, 22) usually the decompression of the romanian neurosurgery (2017) xxxi 2: 229 232 | 231 third ventricle results in the abolition of the abnormal movements. (20, 22) as in present case these movements can be abolished after the removal of the ventricular lesion. (8) although total removal is ideal, but close proximity of tumours to cranial nerves and the brain stem pose technical difficulties in total removal. (9, 10) endoscopic removal is another option for the removal of these tumors. (23) long-term prognosis for patients with intraventricular epidermoids and wellpreserved neurological conditions is good, even in the case of subtotal excision. (9, 13) correspondence dr amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.baxter jw, netsky mg: epidermoid and dermoid tumors: pathology, in wilkins rh, rengachary ss (eds): neurosurgery, vol 1. new york, mcgraw-hill, 1985, pp 655–661 2.osborn ag, preece mt. intracranial cysts: radiologicpathologic correlation and imaging approach. radiology 2006;239:650–664. 3.osborn ag. diagnostic imaging: brain. salt lake city, utah: amirsys, 2004. 4.greenberg ms: handbook of neurosurgery, vol 1. lakeland, fla, greenberg graphics inc, 1997, pp 304–306, p 314 5.carmel pw: brain tumors of disordered embryogenesis, in youmans jr (ed): neurological surgery, ed 3. philadelphia, wb saunders, 1990, pp 3223– 3249 6.guidetti v, gagliardi fm: epidermoid and dermoid cysts: clinical evaluation and late surgical results. j neurosurg 47: 12–18, 1977 7.sabin hi, bordi lt, symon l: epidermoid cysts and cholesterol granulomas centered on the posterior fossa: twenty years of diagnosis and management. neurosurgery 21: 798–805, 1987 8.gelabert-gonzález m, garcía-allut a, gonzález-garcía j, martínez-rumbo r. [epidermoid cyst of the third ventricle][article in spanish] neurocirugia (astur). 2002;13(5):389-92. 9.meng l, yuguang l, shugan z, xingang l, chengyuan w. intraventricular epidermoids. j clin neurosci. 2006;13(4):428-30. 10.bougeard r, mahla k, roche ph, hallacq p, vallée b, fischer g. [epidermoid cyst of the lateral ventricles] [article in french] neurochirurgie. 1999;45(4):316-20. 11.koot rw, jagtap ap, akkerman em, den heeten gj, majoie cb. epidermoid of the lateral ventricle: evaluation with diffusion-weighted and diffusion tensor imaging. clin neurol neurosurg. 2003;105(4):270-3. 12.issaragrisil r, nimmannitya j, bhoopat w, suthipongchai s, varojpiputhn s. computed tomography of intraventricular masses. j med assoc thai. 1990;73(10):556-64. 13.bhatoe hs, mukherji jd, dutta v. epidermoid tumour of the lateral ventricle. acta neurochir (wien). 2006;148(3):339-42. 14.kendall b, reider-grosswasser i, valentine a. diagnosis of masses presenting within the ventricles on computed tomography. neuroradiology. 1983;25(1):1122. 15.lepoire j, pertuiset, b. (1957). les kystes tpidermoides crdnioence'phaliques. masson: paris. 16.pennybacker j, tytus js. pearly tumours in relation to the central nervous system. j neurol neurosurg psychiatry. 1956;19(4):241-59. 17.jefferson g, jackson h. tumours of the lateral and of the 3rd ventricles sectional proceedtngs of the royal society of medicine vol. xxxii page 59 1105 18.eekhof jl, thomeer rt, bots gt. epidermoid tumor in the lateral ventricle. surg neurol. 1985;23(2):189-92. 19.higashi k, wakuta y. epidermoid tumor of the lateral ventricle. surg neurol. 1976;5(6):363-5. 232 | agrawal large intraventricular epidermoid with bobble head doll syndrome 20.bhattacharyya kb, senapati a, basu s, bhattacharya s, ghosh s. bobble-head doll syndrome: some atypical features with a new lesion and review of the literature. acta neurol scand. 2003;108(3):216-20. 21.necker r. head-bobbing of walking birds. j comp physiol a neuroethol sens neural behav physiol. 2007;193(12):1177-83. 22.zamponi n, rychlicki f, trignani r, polonara g, ruggiero m, cesaroni e. bobble head doll syndrome in a child with a third ventricular cyst and hydrocephalus. childs nerv syst. 2005;21(5):350-4. 23.gaab mr, schroeder hw. neuroendoscopic approach to intraventricular lesions. j neurosurg. 1998;88(3):496505. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article severe brain trauma injury: when no intracranial pressure monitoring is available luis rafael moscote-salazar, guru dutta satyarthee, alexis rafael narvaez-rojas colombia, india doi: 10.2478/romneu-2018-0017 romanian neurosurgery (2018) xxxii 1: 149 150 | 149 doi: 10.2478/romneu-2018-0017 severe brain trauma injury: when no intracranial pressure monitoring is available luis rafael moscote-salazar1, guru dutta satyarthee2, alexis rafael narvaez-rojas1 1department of neurosurgery, researcher, latin america foundation of neurotrauma & neuro critical care, red latino, colombia 2department of neurosurgery, neurosciences centre, aiims, new delhi, india brain trauma injury is a major issue in latin american countries, which has the highest incidence worldwide (1, 2) and the lack of economic resources for the treatment of this condition was the ideal setting to prompt discussion on developing cost-effective approaches that may be of benefit not only for the region but around the world, since as the authors pointed out, even in high-income countries (hics), intracranial pressure monitors are not always available due to cost issues as described in previous articles. (3–6) by the other hand, the ongoing research on the imaging and clinical exam (ice) approach may be crucial for the design of future evidence-based guidelines around the world, although in many countries is considered almost illegal not using intracranial pressure monitoring (icp), the reality is, where are the evidence-based guidelines to manage patients when no icp monitoring is readily available at the point-of-care? or when transferring from certain areas may be difficult or take a lot of time and may worsen patients’ outcomes, especially during a disaster or war times and second, the research methods that can be used even overseas may cause a great impact in the pool of knowledge by gathering experience from many regions at a very cost-effective approach. intracranial pressure monitoring, considered to be the standard of care as analyzed in the 4th edition of the guidelines for the management of severe traumatic brain injury (gmstbi) developed in 2016 (7) in reference to the quality of information on icp monitoring, one class 1 study, four class 2 and five class 3 along with four class three studies from the third edition, where in the only class 1 study, icp showed lower mortality especially in patients <65 years of age, (8) found 9.9% of the variation in mortality across center due to the use of icp. the studies evaluated in the gmstbi were observational, the authors suggested that the selection of patients for monitoring could influence importantly the observed outcomes. (7) chesnut et al. on the benchmark evidence from south american trials: treatment of intracranial pressure (best:trip) trial, 150 | moscote-salazar et al severe brain trauma injury developed a multicenter, parallel-group trial, with randomized assignment to intracranialpressure monitoring (icp group) or imaging and clinical examination (ice group) in bolivia and ecuador with 324 participants, where the monitoring-based interventional algorithm tested did not show the superiority of icp use over ice approach.9 this trial is the most important body of knowledge in this specific subject and a good reason to develop consensus guidelines to manage severe tbi in places where icp monitoring is unavailable (war/terrorism/disaster/lic). in the 21st century, we have multiple software available across-platforms enabling communication via the internet, with almost universal access, by expanding the use of this methods to achieve consensus, we will empower multidisciplinary discussion and eventually improve patient care. finally we believe, it can be of important benefit to be evaluated by hic to provide health-care personnel tools for an emergency where settings may change from what they are used to. correspondence luis rafael moscote-salazar, md, neurosurgeon. mineurocirujano@aol.com +1 612 254 5285 address: facultad de medicina, campus de zaragocilla, universidad de cartagena, cartagena de indias, colombia references hyder aa, wunderlich ca, puvanachandra p, gururaj g, kobusingye oc. the impact of traumatic brain injuries: a global perspective. neurorehabilitation. 2007;22(5):341-353. http://www.ncbi.nlm.nih.gov/pubmed/18162698. accessed december 10, 2017. 2. roozenbeek b, maas air, menon dk. changing patterns in the epidemiology of traumatic brain injury. nat rev neurol. 2013;9(4):231-236. doi:10.1038/nrneurol.2013.22. 3. stocchetti n, penny ki, dearden m, et al. intensive care management of head-injured patients in europe: a survey from the european brain injury consortium. intensive care med. 2001;27(2):400-406. http://www.ncbi.nlm.nih.gov/pubmed/11396285. accessed december 11, 2017. 4. sahjpaul r, girotti m. intracranial pressure monitoring in severe traumatic brain injury--results of a canadian survey. can j neurol sci. 2000;27(2):143-147. http://www.ncbi.nlm.nih.gov/pubmed/10830348. accessed december 11, 2017. 5. myburgh ja, cooper dj, finfer sr, et al. epidemiology and 12-month outcomes from traumatic brain injury in australia and new zealand. j trauma inj infect crit care. 2008;64(4):854-862. doi:10.1097/ta.0b013e3180340e77. 6. hesdorffer dc, ghajar j. marked improvement in adherence to traumatic brain injury guidelines in united states trauma centers. j trauma inj infect crit care. 2007;63(4):841-848. doi:10.1097/ta.0b013e318123fc21. 7. carney n, totten am, hawryluk gwj, et al. guidelines for the management of severe traumatic brain injury 4th edition. 2016. https://braintrauma.org/uploads/03/12/guidelines_for_ management_of_severe_tbi_4th_edition.pdf. accessed december 11, 2017. 8. alali as, fowler ra, mainprize tg, et al. intracranial pressure monitoring in severe traumatic brain injury: results from the american college of surgeons trauma quality improvement program. j neurotrauma. 2013;30(20):1737-1746. doi:10.1089/neu.2012.2802. 9. chesnut rm, temkin n, carney n, et al. a trial of intracranial-pressure monitoring in traumatic brain injury. n engl j med. 2012;367(26):2471-2481. doi:10.1056/nejmoa1207363. 17 17moscote-salazarluis rafael_severe brain microsoft word _5.formatata_popescu.doc romanian neurosurgery vol. xvi nr. 2 27 1-year experience with solis peek cages in cervical discectomy and fusion c.e. popescu1, jan-uwe muller2, b. costachescu1 1clinical hospital “prof. dr. n. oblu”, neurosurgical department 2department of neurosurgery, ernst-moritz-arndt university, greifswald, germany objective:this study evaluates the efficacy of peek cages in interbody fusion in 32 consecutive patients treated for cervical disc herniation. methods: during one-year period, 32 patients were treated in our department for cervical disc disease using interbody fusion with peek cages there were 19 men and 13 women, aged between 33 and 68 years (mean 44 years). we used autologus cancelous bone for cage packing and no plate fixation. the mean follow-up was 12 months. results: we judged the success of surgery using the following criteria: recovery of neurological function/radiculopathy, positioning of the cage, extent of fusion at 1year follow-up, and return to work. conclusion: the use of peek cages in interbody fusion for the treatment of cervical disc disease seems to be a good alternative to classic acdf using tricortical bone graft. keywords: interbody fusion, cervical disc, peek cage introduction age-related degeneration of the cervical spine is a common condition in general population. symptomatic degenerative cervical disc disease may produce neck pain, referred pain, radicular arm pain, or clinical myelopathy. radicular arm pain is the most common indication for surgical intervention (3). treatment of cervical radiculopathy has been a subject of controversy for the past decades (2). the operative approaches are as numerous as it’s clinical presentations and the choice of surgical approach is a major consideration. it seems that the best approach is the most direct operative option that provides the best exposure of the offending pathology and that is associated with minimal patient morbidity and a high rate of success (8). although each patient is considered individually, most cervical disc herniations are located ventrally. anterior cervical discectomy has proven to be a safe and effective procedure for the treatment of degenerative disc disease (11). the purpose of this study was to evaluate the safety and efficacy of solis peek cage in the treatment of cervical disc disease. material and methods patients over a 1-year period, between january 2007 and january 2008, a total of 32 singleor double-level cervical discectomies were performed in our department. twenty-five patients suffering from cervical degenerative disc disease underwent single-level acd and seven patients two-level acd and intervertebral fusion using solis peek cages (stryker spine sas, france); no plate stabilization was used. there were 19 men and 13 women, aged between 33 and 68 years (mean 44 years) (fig. 1). c.e. popescu romanian neurosurgery vol. xvi nr. 2 28 0 5 10 15 20 c4-c5 c5-c6 c6-c7 men women total fig.1 distribution of treated levels all patients were clinically and neurologically evaluated and underwent mri examination. patient inclusion criteria were: clinical evidence of disc degeneration (neck pain, rediculopathy or myelopathy), clinic-imaging correlation, and failure of conservative treatment. poly-ether-ether-ketone (peek) is a semicrystalline aromatic polymer with a modulus of elasticity resembling bone that has been used to create structural spinal implants (2, 13). peek implants combine superior strength and impact resistance with radiolucency and don’t produce artifacts on plain films, ct scans or mri. four titanium pins are inserted on both surfaces of the spacer for better bone fixation and for x-ray localization (fig. 2). peek implants elicit minimal inflammatory response or cytotoxic response in in vivo and in vitro models (13). they have excellent resistance to corrosion, are nonresorbable, are insoluble in most solvents, and have long-term biocompatibility (4). surgical procedure patient positioning, localization and surgical approach are identical as those from the standard anterior cervical approach for the midcervical region. placement of peek spacer: after complete removal of disc material and adequate lateral decompression, the end-plates are smoothed flat and lightly decorticated with a high-speed drill. it is essential that the surfaces be flat to maximize graft contact and equal load distribution (5) (fig. 3). fig. 2 solis peek cage fig. 3 endplate decortication 1-year experience with solis peek cages romanian neurosurgery vol. xvi nr. 2 29 following removal of the pll and complete decompression of the neural elements the dimensions of the disc space are determined and an appropriately sized peek implant is selected for placement. the use of the solis system facilitates implant selection and placement. starting with the smallest template or trial, sequentially larger trials are tamped completely into the disc space (fig. 4). the center of the spacer should be filled with cancellous bone harvested with minimal invasive procedure from the iliac crest. autograft harvest is done with minimal exposure to avoid complications (fig. 5). the solis peek cage that corresponds to the final trial is chosen and gently placed into the disc space using the graft holder. the implant is tapped into the disc space using the tamp and mallet (fig. 6). fig. 4 implant tapping fig. 5 cage filled with cancelous bone fig. 6a c.e. popescu romanian neurosurgery vol. xvi nr. 2 30 fig. 6b fig. 6c fig. 6 a,b,c c5-c6 acdf using solis peek cage all the patients in this series were a cervical collar for 1 month after surgery. results the follow-up period was 12 months. we judged the success of surgery using the following criteria: recovery of neurological function/radiculopathy, positioning of the cage, extent of fusion at 1-year follow-up, and return to work. neuroimaging assessment. all patients sustained mr imaging before surgery. postoperative lateral radiography was performed in all patients immediately postoperative, at 2, 6, and 12 months. fusion was assessed on dynamic lateral radiography obtained 1 year after surgery. fusion was considered successful if radiography demonstrated on flexion-extension views no movement between vertebral bodies or spinous processes, and trabecular bone bridging the vertebral bodies. the height of the disc space was measured on the neutral lateral cervical radiograph. clinical results. all 29 patients suffering from radiculopathy improved after surgery. one of the three patients with myelopathy had an improvement of the myelopathic signs. radiographic results. after cage implantation, the height of the disc space was restored in all patients (fig. 7). there was one case of asymptomatic cage subsidence at 1-year follow-up. each segment was deemed fused if no more than 2° of segmental motion was observed on lateral dynamic radiographs (fig. 8). solid fusion was achieved in 31 patients (fig. 9). return to work. all patients presented with radiculopathy improved after surgery and returned to their previous jobs. the two patients with myelopatic signs and no improvement after surgery had no return to work at the time of 1 year follow-up. surgery-related complications. one patient suffered from mild disphagia in the first 3 weeks after surgery. one patient developed a superficial wound seroma at the place of iliac crest bone harvest. 1-year experience with solis peek cages romanian neurosurgery vol. xvi nr. 2 31 fig. 7 disc height restoration fig. 8 fusion assessed on flexion-extension radiography c.e. popescu romanian neurosurgery vol. xvi nr. 2 32 fig. 9 solid fusion at 1 year follow-up discussion anterior cervical surgery has become an accepted route for treatment of the cervical disc herniation. whether interbody fusion is necessary after acd remains controversial and no single technique has been show to be better or to produce superior results (12, 14). some surgeons believe that there is no need for cervical fusion after acd. wilson and campbell reported excellent results after acd alone in 85% of their series patients (15). martins reported good results after acd and acdf, but a higher rate of cervical kyphosis in patients who underwent simple discectomy (6). sontag have advocated acd alone; fusion should be performed when instability occurs. in his series, acd was associated with longer periods of neck and interscapular pain (11). we believe that acdf improves the outcome in these patients. the role of the intervertebral disc in providing stability was demonstrated by munro; in an experimental study he demonstrated that the intervertebral disc together with anterior and posterior ligaments provide significant stability (9). by removing two of these three components, acd impairs the stability. it has been accepted that the loss of disc height and increase motion are involved in the pathophysiology of spondylosis. there is no universally accepted acdf method; the ideal implant has not yet been found. in the last years there has been a growing trend in the implantation of cage devices for cervical interbody fusion (7, 10). the peek cage is a polyetheretherketone, which provides strength and stiffness in the intervertebral space. the fusion rate seems to be superior to the autologus bone graft application. in our study we didn’t observe cage migration or breakage, and only one case of subsidence. since we did not used plate fixation, we suggest that bottom pins are enough to keep the cage in the disc space and do not lead cage migration. another advantage of the peek cage is it’s radiotransparency and mri compatibility, that provides excellent spinal cord and root visualization, without implant artifact. in our study the peek cages biocompatibility was excellent. conclusion this paper summarizes our short-term experience with peek cages in cervical interbody fusion after acd. we believe that this is a safe, easy to use, and effective device, as an alternative to bone autografting after acd. based on these results, larger prospective, randomized studies, focused on long-term results, comparison with other cervical cages or substitutes, are needed. abbreviations used in this paper: acdf = anterior cervical discectomy and fusion; acd = anterior cervical discectomy; mri = magnetic resonance imaging; pll = posterior longitudinal ligament. the authors state no conflict of interest. references 1.boakye m, mummaneni pv, garrett m, et al. anterior cervical discectomy and fusion involving a polyetheretherketone spacer and bone morphogenetic protein. j neurosurg spine. 2005;2:521–525. 2.caspar w, geisler fh, pitsen t: anterior cervical plate stabilization in oneand two-level degenerative disease: overtreatment or benefit? j spinal disodr 11: 1-11,1998 3.cho dy, lee wy, sheu pc. treatment of multilevel cervical fusion with cages. surg neurol. 2004;62:378–386. 1-year experience with solis peek cages romanian neurosurgery vol. xvi nr. 2 33 4.kandziora f, pflugmacher r, schaefer j, scholz m, ludwig k, schleicher p, haas np (2003) biomechanical comparison of expandable cages for vertebral body replacement in the cervical spine. j neurosurg spine 99(1):91-97 5.malone q, lynn j, lunn j (2003) surgical outcome for anterior cervical discectomy and fusion using the signus rabea peek cage. proceedings of the nass 18th annual meeting / the spine journal 3:129s-130s 6.martins an: anterior cervical discectomy with and without interbody bone graft. j neurosurg 44:290-295, 1976 7.matge g (2002) cervical cage fusion with 5 different implants: 250 cases. acta neurochir (wien) 144(6):539-50 8.mcaffee pc: interbody fusion cages in reconstructive operations on the spine. j bone joint surg am 81: 859-880, 1999 9.munro d: the factors that govern the stability of the spine. paraplegia 3:219-228, 1966 10.murphy ma, trimble mb, piedmonte mr, et al. changes in the cervical foraminal area after anterior discectomy with and without a graft. neurosurgery. 1994;34:93–96. 11.sonntag vkh, klara p: controversy in spine care. is fusion necessary after anterior cervical discectomy? spine 21:1111-1113, 1996 12.thorell w, cooper j, hellbusch l: the long-term clinical outcome of patients undergoing anterior cervical discectomy with and without intervertebral bone graft placement. neurosurgery 43:268-274, 1998 13.toth jm, wang m, estes bt, et al. polyetheretherketone as a biomaterial for spinal applications. biomaterials. 2006;27:324–334. 14.watters wc iii, levinthal r. anterior cervical discectomy with and without fusion: results complications, and long-term follow-up. spine. 1994;19:2343–2347. 15.wilson dh, campbel dd: anterior cervical discectomy without bone graft. report of 71 cases. j neurosurg 47:551-555, 1977 doi: 10.33962/roneuro-2021-026 long term clinical outcome following decompressive surgery for cauda equina syndrome. a single centre experience from india lohar vishnu kumar, jaiswal gaurav, gupta tarun kumar, jain sachin kumar, lodha krishna govind, yadav kaushal romanian neurosurgery (2021) xxxv (2): pp. 162-173 doi: 10.33962/roneuro-2021-026 www.journals.lapub.co.uk/index.php/roneurosurgery long term clinical outcome following decompressive surgery for cauda equina syndrome. a single centre experience from india lohar vishnu kumar, jaiswal gaurav, gupta tarun kumar, jain sachin kumar, lodha krishna govind, yadav kaushal department of neurosurgery, maharana bhupal government hospital & ravindra nath tagore (rnt) medical college, udaipur, rajasthan university of health sciences, jaipur, india abstract study design: retrospective study with prospective long-term clinical follow-up. background: cauda equina syndrome (ces) is a neurosurgical emergency, mostly caused by herniated lumbar disc for which urgent surgical decompression is indicated. data on long-term clinical outcome of bladder, bowel & sexual function following decompression are elusive. aim: to evaluate the effectiveness of surgical decompression on recovery of ces symptoms at long-term follow-up & role of timing of surgery on the outcome. methods: records of 35 ces patients who underwent surgical decompression for herniated lumbar disc during a five years period retrospectively analysed & patients called for follow-up visits. outcome measures comprised of history & clinical examination pertinent to bladder, bowel & sexual function. results: twenty-four patients (68.5%) were included for final evaluation who attended follow-up visits, with a minimum follow-up period of one year. most common complaint at presentation was bladder dysfunction (100%) with urinary retention in 16 patients (66.6%), faecal incontinence in 11 (45.8%), saddle anaesthesia in 22 (91.6%) & erectile dysfunction in 6 patients (out of 15 males). only four patients underwent surgery within 48 hours of ces symptom onset, rest cases after 48 hours duration. at follow-up, bladder dysfunction present in 33.3% with urinary retention in 16.6%. faecal incontinence persisted in 4 patients (16.6%) & saddle anaesthesia in 7 (29.1%). sexual dysfunction was the most persistent complaint. conclusion: long-term follow-up shows significant recovery of sphincteric function in ces patients after surgical decompression. urinary & bowel dysfunction improve significantly. timing to surgery didn’t affect the long-term outcome. introduction cauda equina syndrome (ces) is clinically characterized by varying degree of loss of bladder, bowel & sexual function & is often associated with one or more of features like low back pain, unilateral or bilateral keywords cauda equina syndrome, long term follow-up, surgical decompression, time to surgery corresponding author: jaiswal gaurav department of neurosurgery, rnt medical college, udaipur, india drvishnulohar@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 163 long term outcomes following ces surgery sciatica, leg weakness & is caused by compression of lumbar and sacral nerve roots in cauda equina [1, 2, 25, 33, 35]. it is considered a neurosurgical emergency & prompt surgical decompression represents the therapeutic gold standard [1, 18, 28]. the most common cause of ces is herniated lumbar disc (hld) & ces is considered the only primary absolute indication for surgery in hld patients [1, 8, 18, 28]. there are differing reports in the literature regarding the optimum time to surgery but because of the rare occurrence of this syndrome, there is a lack of unified criteria for deciding the best timing for surgery and determining factors that positively influence the clinical outcome. hence, the influence of timing of surgery on outcome has been a topic of debate in literature and most studies show that decompression within 48 hours yield better outcome [1, 3, 18]. but many others disagree & indicate that timing of surgery does not appear to significantly improve the outcome [4, 14, 25, 26, 28]. regardless of the disease onset, it is logical to conclude that operating sooner rather than later is better. long term follow-up of ces patients is required for evaluation of bladder, bowel & sexual function recovery following surgical decompression and several studies do include individual population with follow-up of several years, however, those patient numbers are small and evaluation of outcome seldom includes defecation and sexual function [20]. aim of this study was to present our experience at this institute and assess the effectiveness of surgical decompression on functional recovery of ces symptoms after long term follow-up with regards to bladder, bowel as well as sexual dysfunction & evaluate the factors affecting the longterm outcome after surgery following development of ces symptoms, together with a thorough review of literature. materials & methods study design medical records & clinical data of consecutive patients operated for lumbar herniated disc at this tertiary care regional government hospital during a five years period from july 2014 to june 2019 with coded admission diagnosis & clinical presentation of ces were retrospectively reviewed for their baseline characteristics, presenting complaints, pre-operative neurological status, surgical complications, clinical parameters at the time of discharge from the hospital. then selected patients included in the study were called upon telephonically for follow-up visits arranged in outpatient care clinic. all patients had pre-operative mri of lumbosacral spine for definitive diagnosis of herniated disc causing clinical cauda equina syndrome. the minimum follow-up period was set to one year with mean follow-up of 28 months and maximum of 5 years. patients were evaluated for clinical improvement & outcome of micturition, defecation, and sexual function and possible predictors of outcome. the study was approved by institutional review board. inclusion criteria patients with newly diagnosed ces operated within the study period. pre-operative mri suggestive of herniated lumbar disc causing cauda equina nerve root compression (figure 3 & 4). follow-up of at least one year. exclusion criteria cause of ces other than hld, like tumors or degenerative lumbar stenosis. patients with re-operation for persistent symptoms with post-operative mri suggestive of residual/recurrent disc herniation. didn’t attend the follow up clinic. a total of 35 patients were identified by screening the records of all patients operated by the two experienced senior neurosurgeons for lumbar herniated disc at this institution & out of these, 24 patients were included for the final evaluation. rest eleven patients didn’t meet the inclusion criteria due to various reasons & were excluded. operative procedure all patients underwent standard laminectomy & removal of herniated lumbar disc causing compression of lumbosacral nerve roots. no patient in this study had spinal fusion or any instrumentation for instability. demographic & clinical data baseline parameters like age, sex, level of disc, associated comorbidities, smoking status, presenting symptoms, duration of symptoms of ces 164 lohar vishnu kumar, jaiswal gaurav, gupta tarun kumar et al. & time to surgery were analyzed (table-1). limb weakness was graded according to mrc (medical research council) scale. symptoms of bladder, bowel & sexual dysfunction were separately measured. patients who were catheterized at the time of presentation were considered having urinary retention. incontinence of faeces due to sphincteric dysfunction & saddle anesthesia were included as symptoms of bowel dysfunction relevant to ces & were evaluated. sexual dysfunction was present in male patients as erectile dysfunction. post-operative complications were also noted & patient-related clinical data at the time of discharge from the hospital were analyzed. characteristics (n=24) median age (in years) 40.0 years (range 30-65) sex – male female 15 09 level of hld l2-3 1 (4.1%) l3-4 5 (20.8%) l4-5 11 (45.8%) l5-s1 9 (37.5%) two level hld 2 (8.3%) comorbidities dm-2 3 htn 4 smoking status smoker 8 non-smoker 16 (hld herniated lumbar disc; dm-2 diabetes mellitus type-2; htn hypertension) table 1. pre-operative patient related parameters. outcome measures a follow-up visit was arranged during a period between july to august 2020 for all screened patients of ces as per their convenience to attend the outpatient care & relevant clinical history was taken regarding present status of pain, limb weakness & improvement in bladder, bowel & sexual function. thorough neurological examination was performed in all patients including presence of motor deficit, anal tone & perineal sensation. improvement in limb weakness was considered significant if it upgraded at least two mrc (medical research council scale) grades from the pre-operative record. outcome of individual parameters was assessed & compared between two intergroups of chronological order 1) pre-operative v/s at discharge & 2) at discharge v/s long term follow-up. this comparison was done to evaluate the importance of a long-term follow-up & long recovery time required to see the results of surgical decompression. statistical analysis the recorded data were analyzed using ibm-spss software version 24.0 for windows os 10 (spss inc. chicago). comparing independent groups with categorical variables was done with chi square test. for comparisons between paired groups of categorical variables, mcnemar's test was done with yates correction for continuity and validated with a binomial exact test. binary logistic regression models were used to evaluate predictors for bladder, bowel and sexual dysfunction at long term follow-up, with inclusion of the following variables: age, sex, level of herniated disc at presentation, duration of complaints of ces at presentation & time to decompression. statistical significance determined by a p value < 0.05. results a total of 594 patients underwent laminectomy with discectomy surgery for herniated lumbar disc during the five years study period at this institution, out of which thirty-five (35) patients were diagnosed having ces. so, the incidence of ces among patients operated for lumbar herniated disc was 5.9% at our center. out of these 35 patients, eight didn’t attend the follow-up visit due to various reasons (three of them couldn’t be contacted, five didn’t came for follow-up even after several requests made telephonically & so couldn’t be examined at followup). three patients demonstrated significant residual or recurrent disc herniation in the follow-up mri scans and were re-operated, so excluded from the final evaluation. hence, twenty-four patients (68.5%) with ces were included in our study for evaluation. demographic parameters of the patients who were included are summarized in table-1. the median age was 40 years with 15 males & 9 females. the most common level of disc herniation was l4-5 (in 45.8%) followed by l5-s1 (37.5%) & two-level disc herniation in two cases (8.3%), one with l2-3 & l3-4 levels & other one with l3-4 & l4-5 levels, & these 165 long term outcomes following ces surgery two patients underwent laminectomy & discectomy at both levels simultaneously. pre-operative clinical parameters the common presenting clinical features are listed in table-2. the most common presenting symptoms were radicular leg pain (87.5%), urinary dysfunction (100%) & saddle anesthesia (91.6%). other common complaints were weakness of either or both legs (54.1%) & bowel dysfunction in form of faecal incontinence of varying severity (45.8%). two patients had partial foot drop at presentation which improved at long term follow-up. the least common complaint reported was sexual dysfunction (25% in whole sample) as 6 male patients having erectile dysfunction (40%). none of the females reported any sexual dysfunction. sixteen patients (66.6%) were catheterized either at the time of admission or before surgery for urinary retention. per-rectal examination revealed perineal hypoesthesia in thirteen (54.1%) & decreased anal tone in nineteen (79.2%) patients. three patients who reported absence of radicular pain, also had bilateral lower limb weakness, complete saddle anesthesia with urinary retention. symptoms/signs overall (n=24) low back pain 22 (91.6%) radicular leg pain unilateral bilateral 21 (87.5%) 16 (66.6%) 5 (20.8%) motor deficit u/l leg weakness b/l leg weakness foot drop (u/l & partial) 13 (54.1%) 8 (33.3%) 3 (12.5%) 2 (8.3%) bladder dysfunction urgency/dysuria overflow incontinence retention 24 (100%) 3 (12.5%) 5 (20.8%) 16 (66.6%) bowel dysfunction fecal incontinence 11 (45.8%) sexual dysfunction (male) erectile dysfunction 6/15 (40.0%) perineal hypoesthesia 13 (54.1%) saddle anesthesia complete partial 22 (91.6%) 15 (62.5%) 7 (29.1%) anal tone normal decreased 5 (20.8%) 19 (79.2%) table 2. pre-operative clinical parameters. disease duration and time to surgery the duration of complaints related to herniated lumbar disc disease with low backache &/or radicular leg pain are summarized in table-3. the most important parameter to be measured was the mean duration of onset of cauda equina syndrome symptoms (bladder &/or bowel dysfunction with or without leg weakness) to surgical decompression. for this, the duration of symptoms at admission was added to the duration from admission to surgery. the mean duration was 117 hours (approximately 5 days) with only four patients (16.6%) undergoing surgery within 48 hours from symptom onset. we do not have emergency spine surgery unit at this institution; hence all cases were posted for surgery on urgent priority basis in the elective theatre on the same day or within 48 hours of admission. the time to surgical decompression from onset of ces symptoms of all included patients is shown in figure1 & the time to surgery from admission to the hospital in figure-2. the average duration of hospital stay was 6.5 days. mean follow-up period was 28 months with range from 12-60 months. the duration of symptoms relevant to herniated disc like low backache and radicular pain with or without limb weakness were also noted from patient’s history sheets. many of these were on conservative approach of management with analgesics alone. those cases first presented to us with acute involvement of bladder & bowel function. some cases developed ces without prior symptoms of hld. the longest duration of ces symptoms recorded was 15 days in two cases (figure-1). duration (range) mean duration from onset of symptoms of hld to presentation (in days) 152.3 (10-730) mean duration of onset of ces complaints to surgery (in hours) 117.0 (36-360) mean duration from admission to surgery (in hours) 33.5 (12-48) average duration of hospital stays (in days) 6.5 (3-13) table 3. duration of symptoms & time to surgical decompression. surgical complications all patients underwent standard laminectomy & discectomy surgery to decompress the cauda equina 166 lohar vishnu kumar, jaiswal gaurav, gupta tarun kumar et al. nerve roots, intraoperatively dural tear was encountered in two cases but they were recognized & managed intraoperatively without closure of dura required & they had no post-operative csf leak. post-operatively no major complications were reported before discharge except one patient having diabetes developed superficial wound infection on post-operative day-4 which was managed conservatively with antibiotics alone. no worsening of neurological status reported in the post-operative period & at discharge from hospital. all patients were shifted to elective icu care at least for 24 hours postoperatively, no patient required ventilatory support or prolonged icu stay. injectable antibiotics were given routinely to all patients for a minimum of three days post-operatively, no steroid use documented for any patient. figure 1. duration from ces symptom onset to surgery of all patients. clinical outcome at long-term follow up at a minimum follow-up period of one year, most of the patients had significant improvement in their pre-operative deficits (table-4). age at onset of ces, sex, comorbidities, smoking status & level of disc were not found to influence the outcome (not statistically significant). the assessment of pain relief was subjective & patient reported & this was not quantified on pain scale. our study shows that a significant number of patients (37.5%) still complain of radicular leg pain at follow up. patients who had limb weakness show significant improvement when compared to preoperative & discharge records, & only 4 patients (16.6%) had reported residual deficits. figure 2. time to surgery after admission of all patients. pre-operative at discharge (average 6.5 days) at long-term follow up p-value** radicular leg pain unilateral bilateral 21 (87.5%) 16 (66.6%) 5 (20.8%) 15 (62.5%) 11 (20.8%) 4 (8.3%) 9 (37.5%) 6 (25.0%) 3 (12.5%) mny 0.003 be <0.001 motor deficit* -u/l leg weakness -b/l leg weakness -foot drop 13 (54.1%) 8 (33.3%) 3 (12.5%) 2 (8.3%) 12 (50.0%) 8 (33.3%) 3 (12.5%) 1 (4.1%) 4 (16.6%) 3 (12.5%) 1 (4.1%) 0 (0.0%) mny 0.016 be <0.001 * if no improvement in motor power by at least 2 mrc grades; **outcome at long-term; mny – mcnemar’s test with yates correction; be – binomial exact test table 4. long-term outcome of leg pain & motor deficits. 167 long term outcomes following ces surgery pre-operative at discharge (average 6.5 days) at long-term follow up p-value# urgency/dysuria 3 (12.5%) 3 (12.5%) 2 (8.3%) overflow incontinence 5 (20.8%) 4 (16.6%) 2 (8.3%) retention 16 (66.6%) 14 (58.3%) 4 (16.6%) total 24 (100%) 21 (87.5%) 8 (33.3%) mny <0.001 be <0.001 # outcome at long-term; mny – mcnemar’s test with yates correction; be – binomial exact test table 5. long-term outcome of bladder dysfunction. long-term outcome of bladder dysfunction at follow-up, 33.3% of patients complained of bladder involvement at follow-up & this improvement, when compared with either preoperative or at discharge data using mcnemar’s test with yates correction for continuity, was statistically significant (table-5). binomial exact test was used to check the validity of this calculation. out of 16 patients with retention initially, 12 were free from catheter at long-term & only 16.6% were still dependent on it despite proper bladder training in post-operative period. two of the cases who had retention before surgery, however, reported complaints of dysuria or urgency at follow-up but were not catheter-dependent. out of the four patients operated within 48 hours after ces symptom onset, three had retention & one had incontinence pre-operatively, out of which one patient still had retention at the follow-up visit. when compared with the group of rest of the 20 patients operated >48 hours after ces onset, no statistically significant difference was observed in outcome of bladder function between the two groups. table 6. long-term outcome of bowel & sexual dysfunction. bowel & sexual dysfunction bowel dysfunction was measured with four different parameters (table-6). two subjective parameters including saddle anaesthesia & faecal incontinence as reported by the patients. saddle anesthesia present pre-operatively in 22 cases (91.6%) including 15 complete & 7 partial loss of sensation in saddle region. it improved at follow-up visit to seven (29.1%), four (16.6%) & three (12.5%) respectively. faecal incontinence with partial or complete loss of control over defecation including either intermittent incontinence or soiling was reported by 11 patients pre-operative at discharge (average 6.5 days) at long-term follow up p-value## saddle anaesthesia complete partial 22 (91.6%) 15 (62.5%) 7 (29.1%) 19 (79.1%) 13 (54.1%) 6 (25.0%) 7 (29.1%) 4 (16.6%) 3 (12.5%) mny <0.001 be <0.001 faecal incontinence 11 (45.8%) 11 (45.8%) 4 (16.6%) mny 0.046 be 0.004 perineal hypoaesthesia 13 (54.1%) 11 (45.8%) 8 (33.3%) mny 0.131 be 0.016 anal tone -decreased 19 (79.2%) 15 (62.5%) 7 (29.1%) mny 0.005 be <0.001 sexual dysfunction in males (ed), n=15 6 (40.0%) 6 (40.0%) 4 (26.6%) mny 0.479 be 0.50 ## outcome at long-term; mny – mcnemar’s test with yates correction; be – binomial exact test 168 lohar vishnu kumar, jaiswal gaurav, gupta tarun kumar et al. (45.8%) before surgery which improved significantly at follow-up & prevalent in only 4 cases (16.6%) at follow-up. objective parameters of bowel dysfunction included presence or absence of perineal hypoaesthesia & demonstration of anal tone. at presentation, hypoaesthesia was present in 13 patients & decreased anal tone i.e. lax anal sphincter in 19 patients, which improved at follow-up. the association of saddle anaesthesia & decreased anal tone with presence of urinary retention at presentation & follow-up was statistically significant (p-value < 0.05) & all 4 patients with retention at follow-up had saddle anaesthesia, perineal hypoaesthesia & decreased anal tone. hence, presence of saddle anaesthesia with perineal hypoaesthesia and a lax anal tone was a predictor of urinary dysfunction. sexual dysfunction which was prevalent in 25% of the study cohort & reported by 6 male patients (40%) having erectile dysfunction at presentation was still present in 4 of them at follow-up. the lower initial incidence of this complaint as compared to other sphincteric disturbances may be due to response bias, as none of the females complained any form of sexual dysfunction, possibly reflecting some form of barrier on both patient’s side as well as on doctor’s side regarding the discussion of sexual health. discussion this study is one rare of its kind to prospectively assess the long-term outcome following surgery for ces secondary to herniated lumbar disc by directly obtaining patient history & performing clinical examination in the outpatient care clinic after a minimum of one year. the primary aim of this study was to evaluate clinical outcome after a long period following surgery, specifically the outcome of sphincteric function. this long term follow-up is required for neurological recovery which tends to occur many years after decompression [5, 25]. some previous studies by korse et al. & hazelwood et al. have evaluated outcomes at relatively longer duration [13, 20]. together with highlighting the importance of a long term follow up, we also reviewed the literature to describe other features relevant to the context of cauda equina syndrome and their possible association with the outcome. the sample size (n=24) in our study was relatively small but considering the rare occurrence of this syndrome [9, 15, 23], number of patients in this study were considerable. we achieved a response rate of 68.5% due to unwillingness of many patients (31.5%) to participate for the follow-up evaluation for various reasons, personal or social. this shows a significant number of patients were lost to follow-up & indicates towards an attrition bias, but it could well be because of dissatisfaction from the delivered care also & must have been a major factor affecting the overall outcome assessment. the incidence of ces in patients undergoing surgery for lumbar disc herniation in this study was 5.9%, which is slightly higher than previous literature that quotes approximate incidence of 1-3% [8, 9, 14, 16, 19, 23, 25]. recently korse et al. quoted a higher incidence of 10.8% in their study on 75 patients [19]. the most common cause of ces is lumbar disc herniation [18, 34]. others include tumors, spinal stenosis, hematomas, trauma, and iatrogenic causes [21]. the most common level of cauda equina nerve root compression is l4-5 or l5-s1 level [6, 8, 16] and our study population also reflects the same with almost 83.3% (20/24) of cases demonstrating disc at these two levels. we couldn’t demonstrate a correlation between the level of disc and long-term outcome. the exact definition of cauda equina syndrome is not available. it is described by various authors in different terms and there is no agreed definition [32]. there have been attempt to quantify the clinical aspects of cauda equina syndrome by n. v. todd based on bladder and bowel dysfunction but has not been validated for clinical practice [2, 35]. the five characteristic features of ces are bilateral neurogenic sciatica, reduced perineal sensation, altered bladder function ultimately to painless urinary retention, loss of anal tone and sexual dysfunction. not all will be present in any individual patient [8, 32]. results demonstrated that bladder dysfunction, radicular leg pain, saddle anaesthesia with decreased or loss of anal tone are the most prevalent complaints within this population, while leg weakness & bowel dysfunction being comparatively less common and sexual dysfunction reported least frequently. bilateral sciatica also, was a less common feature (in 20.8%). unilateral foot drop is also described as a feature of ces & two patients in this study had partial unilateral foot drop 169 long term outcomes following ces surgery along with sphincter dysfunction with evidence of disc herniation at l3-4 & l4-5 levels respectively. these two patients recovered at follow-up. bilateral foot drop can also occur but is an extremely rare condition as described by mahapatra et al. in a case of ces due to l3-4 prolapsed disc [24]. low-backache being non-specific, was not assessed as an independent outcome measure, though many cases still had this complaint in post-operative and followup period. there has also been an attempt to classify ces by ‘the british association of spinal surgery’ into three subgroups as cess (suspected ces with absence of sphincter dysfunction), cesi (cess plus dysuria, urgency or altered urinary sensation) and cesr (painless retention with faecal or urinary overflow incontinence) [10, 14]. however, classification into two broad groups of incomplete (cesi) and complete (cesr) cauda equina syndrome seems more realistic for the true evaluation of the clinical outcome, as these two groups represent the definite involvement of sphincter function, specifically the bladder function. we followed the same criteria to describe ces clinically. all the 24 patients in our study cohort had some form of bladder dysfunction and 21 of them fall into cesr subgroup (16 with retention & 5 with overflow incontinence). thereby, a comparison couldn’t be made with the rest of the three patients falling into cesi subgroup due to such skewed distribution of variables. the long-term outcomes related to bladder, bowel & sexual dysfunction in this study broadly agree with previous literature. however, similar to previous studies, the proportions of patients with residual symptoms differ in individual categories. our study noted a lower rate of bladder dysfunction (33.3%) at long term follow up than previous studies, with hazelwood et al. finding 76%, korse et al finding 36.1% & mccarthy et al finding 43% of patients to have bladder dysfunction at long term follow-up [13, 20, 25]. the higher incidence of bladder dysfunction by hazelwood et al. may be due to use of the objective usp score (urinary symptoms profile score) which have a high sensitivity to a range of urological symptoms and patients would often report a symptom-free bladder, only to show dysfunction on the usp [5, 36]. this is likely due to the neural damage sustained in ces that would preferentially affect detrusor innervation and function over pelvic floor strength or urethral patency [10]. olivero et al. have described an improvement of bladder function in more than 90% of their cases with a sample size of 31 patients [26]. kaiser et al. noted good outcomes in 70% of their patients with cesr [16]. similar to these, patients in the retention group also had good recovery patterns in our study with a prevalence of 66.6% reducing to 16.6% at follow-up. this improvement is significant considering the generally described poor outcome in previous studies [18, 20]. konig et al. found no improvement in bladder dysfunction in any case of a grade-4 ces (based on shi classification) regardless of the timing of surgery [18, 31]. we did not classify our patients into these grades as described by shi et al. but the classification seems promising and further prospective studies on its application in prognostication of ces patients are recommended [31]. two important aspects of bladder dysfunction not sufficiently mentioned in the previous literature are the pre & post-operative urodynamic study (uds) and electromyography of bladder musculature. uroflowmetry and post-void residual urine (pvr) are simple objective tests to establish the neurovesical involvement in ces [17]. these can be further confirmed with invasive multichannel uds to exclude other possible causes responsible for persistent bladder dysfunction in the post-operative period. yamanishi et al. in their study on urodynamic evaluation of surgical outcome of ces stated that most of the patients could empty their bladder only by straining or changing their voiding postures postoperatively [37]. this adaptation by the ces patients in post-operative period could well be a reason for the subjective improvement of bladder dysfunction in the present study and their catheterfree status at follow-up, despite the presence of a residual bladder dysfunction on objective assessment. lee et al. have evaluated the role of electromyography as a tool for evaluating the integrity of sacral spinal segments 2 to 4 to predict the outcome of bladder dysfunction in ces & found that results of electrically induced bulbocavernosus reflex (e-bcr) examination seemed to give excellent positive and negative predictive values for the recovery of bladder function in patients with ces [22]. these two factors should be considered relevant predictors of bladder dysfunction and should be evaluated in the follow-up. bowel dysfunction is a complex domain of cauda equina syndrome and includes two subjective and 170 lohar vishnu kumar, jaiswal gaurav, gupta tarun kumar et al. two objective parameters as previously mentioned. we describe a high prevalence of 91.6% saddle anaesthesia and 45.8% faecal incontinence. this incontinence of varying degree was strongly related to the presence of two objective parameters of perineal sensory loss and decreased anal tone. all patients having some form of faecal incontinence also had both these findings present. most of the previous studies report poor outcome of bowel disturbances with korse et al. finding a prevalence of 43% at long term follow-up from 47% at initial followup and mccarthy et al. finding 60% bowel disturbance at follow-up & one-third of these having intermittent faecal incontinence or soiling [20, 25]. our findings correlate with the previous studies but since there is no unified criteria of defining bowel dysfunction or disturbance in different studies [4, 13, 20] we could not compare individual parameters, however, the overall recovery is significant for all these 4 parameters. the role of rectal examination testing the anal tone is described in previous studies. sphincter disturbance and saddle anaesthesia appear to be the most reliable predictors of outcome after surgery [7, 12, 21, 25]. there are few studies suggesting that early surgery increases the likelihood of an improvement in bowel dysfunction [8, 18, 25]. however, we could not verify this association. sexual dysfunction was reported less commonly and complained only by the male population with erectile dysfunction. there was no patient showing any functional recovery at the time of discharge but 33.3% (2 of 6) patients had reported improvement in erection at long term follow-up though it was not statistically significant (p value 0.479). none of the females reported any form of sexual dysfunction, however this doesn’t rule out its prevalence in this population considering the under-reported complaints related to sexual dysfunction. mccarthy et al. reported 50% of patients had some degree of sexual dysfunction, and korse et al. reported dysfunction prevalence of 56% at 2 months, marginally improving to 53% at 13 years [20, 25]. in our study, patients operated before 48 hours fared no better than those operated after 48 hours, specifically the sphincter function. however, since only four cases were operated before 48 hours, this conclusion didn’t reach a statistical significance. but, considering the significantly good recovery in those operated after 48 hours, it can be concluded that a more important factor predicting the outcome is ‘time factor’ post-surgery, thus emphasizing the role of a long-term follow-up of these cases. four cases presented more than 10 days after the onset of their ces symptoms (figure-1), but had no statistically significant difference between the outcome when compared with those operated early upon. what are the factors then, governing the neurological recovery in such patients remains unanswered. figure 3. pre-operative t1-weighted sagittal mri image of a 36 years old male patient showing a large herniated disc at l5-s1 level (yellow-coloured arrow mark). recently, bydon et al. in their study on 45 patients of ces have stated that determinants of outcome in ces are elusive, similar to the state of the literature on surgical management of acute spinal cord injury, in which the timing of surgery has not been conclusively correlated with outcome [4]. studies in the porcine model have shown that cauda equina compression can cause injury after as little as 2 hours [4, 27, 29]. they have further postulated that timedependent cellular and physiologic effects of cauda equina impingement are irreversible well before patients reach surgery, leaving outcome dependent on other factors. this together with the delayed presentation of patients to seek medical help, unavailability of adequate medical facilities in the developing countries and delayed diagnosis by primary care physician leads to a significant delay in time to surgery. heyes et al. in their recent series of 136 patients, demonstrated that regardless of type of ces and independent of timing of surgical intervention, most patients see a significant improvement in bowel and bladder function following surgical decompression [14]. the majority 171 long term outcomes following ces surgery of patients in their series also presented with symptom duration of greater than 48 hours. we consider this related to the long time required for natural recovery of damaged nerve fibers after decompression. nerve injury is not necessarily a direct result of injury to the nerve at the level of the cauda equina but more a mechanical injury to the bladder wall musculature. schoenfeld aj & bono cm stated in their systematic review of timing on postoperative recovery in lumbar discectomy, functional outcome was only adversely affected if decompression was carried out 6 months post onset of symptoms [30]. considering all these facts, outcome in our study were fairly good irrespective of duration of ces symptoms & time to surgery. figure 4. pre-operative axial mri image of the same patient as in figure-3, showing large postero-central disc herniation at l5s1 level causing compression over ventral thecal sac (yellowcoloured arrow mark). we also reviewed the pre & post-operative mri scans wherever available to evaluate the possible role of mri findings in clinical outcome (figure-3 to 6). three of the cases not included in our study cohort but were first operated during the study period, had evidence of significant residual or recurrent disc herniation on post-operative mri, were re-operated for their persistent sphincteric dysfunction. this role, of ineffective decompression or recurrence of disc herniation, has not been considered in most of the previous studies. residual disc or recurrent disc herniation can be a cause of long term sphincteric dysfunction in these population of patients and should not be overlooked. another factor which can influence the outcome is disc herniation size and degree of compression of cauda equina nerve roots. a previous study by kaiser et al. however, found no significant correlation between the size of disc herniation relative to size of spinal canal and postoperative urinary function in patients with ces [16]. further research is recommended to evaluate this probable association. figure 5. post-operative sagittal mri image of same patient as in figure-3. figure 6. post-operative axial mri image of same patient as in figure-4. we also reviewed the literature for comparison of different surgical techniques and found that most of the previous studies recommend a wider decompression [11]. there is no significant difference with either bilateral laminectomy or 172 lohar vishnu kumar, jaiswal gaurav, gupta tarun kumar et al. hemilaminectomy or interlaminar fenestration with discectomy, with fusion or without fusion. dave et al. found patients operated with trans-foraminal lumbar interbody fusion (tlif) have decreased incidence of surgical complications but similar neurological outcome compared with non-fusion group [6]. all the patients included in current study underwent standard unilateral or bilateral laminectomy with discectomy and without fusion. overall, the outcome predictors of ces surgery are difficult to prognosticate. timing of surgery is the most extensively studied parameter in ces patients but till now no consensus exists for the optimum time window of surgery. however, we still recommend urgent surgical decompression once the patient presents with ces symptoms. we also recommend a strict follow-up schedule for all operated patients of ces till recovery of sphincteric dysfunction achieved so as to further evaluate the other causes responsible for delayed long-term outcomes. limitations all pre-operative data were obtained retrospectively from the history files of the patients from hospital’s medical record section. this implicates an observer’s bias & limitation of the data quality. most of the recorded parameters were patient reported & subject to individual variation. conclusion this study assesses most of the issues relevant to ces & demonstrated that regardless of timing of surgical intervention, most of the patients see a significant improvement in pain, limb weakness, bowel and bladder function following surgical decompression & this requires a long-term followup. recovery is not complete in all patients but urinary & bowel dysfunction improve significantly. sexual dysfunction, however, have poor recovery. this long-term outcome after surgery has highlighted the importance of a strict schedule of follow-up of all ces patients. timing of surgery was not shown to influence the clinical outcome in this study. this doesn’t mean surgery should be deferred, but better outcomes are not guaranteed even after earlier surgical decompression. since it is not always practical for most of the patients of ces to operate within the first 48 hours after symptom onset, especially in the developing countries, we should focus further research on other relevant outcome parameters to prognosticate this rare neurosurgical disease entity. references 1. ahn um, ahn nu, buchowski jm, garrett es, sieber an, kostuik jp. cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. spine 2000;25:1515-22. 2. angus m, berg a, carrasco r, horner d, leach j, siddique i. the cauda scale validation for clinical practice. br j neurosurg 2020;34:453-6. 3. arrigo rt, kalanithi p, boakye m. is cauda equina syndrome being treated within the recommended time frame. neurosurgery 2011;68:1520-6. 4. bydon m, lin ja, garza-ramos rdl, macki m, kosztowski t, sciubba dm, et al. time to surgery and outcomes in cauda equina syndrome: an analysis of 45 cases. world neurosurg 2016;87:110-5. 5. chang hs, nakagawa h, mizuno j. lumbar herniated disc presenting with cauda equina syndrome long term follow-up of four cases. surg neurol 2000;53:100–5. 6. dave br, samal p, sangvi r, degulmadi d, patel d, krishnan a. does the surgical timing and decompression alone or fusion surgery in lumbar stenosis influence outcome in cauda equina syndrome? asian spine j 2019;13:198-209. 7. domen pm, hofman pa, santbrink hv, weber wej. predictive value of clinical characteristics in patients with suspected cauda equina syndrome. eur j neurol 2009;16:416-9. 8. fraser s, roberts l, murphy e. cauda equina syndrome: a literature review of its definition and clinical presentation. arch phys med rehabil 2009;90:1964-8. 9. gardner a, gardner e, morley t. cauda equina syndrome: a review of the current clinical and medico-legal position. eur spine j 2011;20:690-7. 10. germon t, ahuja s, casey ath, todd nv, rai a. british association of spine surgeons standards of care for cauda equina syndrome. spine j 2015;15:2-4. 11. gitelman a, hishmeh s, morelli bn, joseph jr sa, casden a, kuflik p, et al. cauda equina syndrome: a comprehensive review. am j orthop (belle mead nj) 2008;37:556-62. 12. gooding bwt, higgins ma, calthorpe dad. does rectal examination have any value in the clinical diagnosis of cauda equina syndrome? br j neurosurg 2013;27:156-9. 13. hazelwood je, hoeritzauer i, pronin s, demetriades ak. an assessment of patient-reported long-term outcomes following surgery for cauda equina syndrome. acta neurochir (wien) 2019;161:1887-94. 14. heyes g, jones m, verzin e, mclorinan g, darwish n, eames n. influence of timing of surgery on cauda equina syndrome: outcomes at a national spinal centre. j orthop 2018;15:210-5. 173 long term outcomes following ces surgery 15. hoeritzauer i, wood m, copley pc, demetriades ak, woodfield j. what is the incidence of cauda equina syndrome? a systematic review. j neurosurg spine 2020;32:832–41. 16. kaiser r, nasto la, venkatesan m, waldauf p, perez b, stokes om, et al. time factor and disc herniation size: are they really predictive for outcome of urinary dysfunction in patients with cauda equina syndrome? neurosurgery 2018;83:1193-200. 17. kalidindi kkv, chhabra hs, suman d, mannem a, bhat mr. cauda equina syndrome: false‑positive diagnosis of neurogenic bladder can be reduced by multichannel urodynamic study. eur spine j 2020;29:1236-47. 18. konig a, amelung l, danne m, meier u, lemcke j. do we know the outcome predictors for cauda equine syndrome (ces)? a retrospective, single-center analysis of 60 patients with ces with a suggestion for a new score to measure severity of symptoms. eur spine j 2017;26:256572. 19. korse ns, pijpers ja, zwet ev, elzevier hw, vleggeertlankamp cla. cauda equina syndrome: presentation, outcome, and predictors with focus on micturition, defecation, and sexual dysfunction. eur spine j 2017;26:894-904. 20. korse ns, veldman ab, peul wc, vleggeert-lankamp cla. the long term outcome of micturition, defecation and sexual function after spinal surgery for cauda equina syndrome. plos one 2017;12. 21. lavy c, james a, wilson-macdonald j, fairbank j. cauda equina syndrome. bmj 2009;338:b936. 22. lee dg, kwak sg, chang mc. prediction of the outcome of bladder dysfunction based on electrically induced reflex findings in patients with cauda equina syndrome. medicine (baltimore) 2017;96:e7014. 23. long b, koyfman a, gottlieb m. evaluation and management of cauda equina syndrome in the emergency department. am j emerg med 2020;38:143-8. 24. mahapatra ak, gupta pk, pawar sj, sharma rr. sudden bilateral foot drop: an unusual presentation of lumbar disc prolapse. neurol india 2003;51:71-2. 25. mccarthy mjh, aylott cew, grevitt mp, hegarty j. cauda equina syndrome: factors affecting long-term functional and sphincteric outcome. spine 2007;32:20716. 26. olivero wc, wang h, hanigan wc, henderson jp, tracy pt, elwood pw, et al. cauda equina syndrome (ces) from lumbar disc herniations. j spinal disord tech 2009;22:202-6. 27. pedowitz ra, garfin sa, massie jb, hargens ar, swenson mr, myers rr, et al. effects of magnitude and duration of compression on spinal nerve root conduction. spine 1992;17:194-9. 28. qureshi a, sell p. cauda equina syndrome treated by surgical decompression: the influence of timing on surgical outcome. eur spine j 2007;16:2143-51. 29. rydevik bl, pedowitz ra, hargens ar, swenson mr, myers rr, garfin sr. effects of acute, graded compression on spinal nerve root function and structure. spine. 1991;16:487-93. 30. schoenfeld aj, bono cm. does surgical timing influence functional recovery after lumbar discectomy? a systematic review. clin orthop relat res 2015;473:196370. 31. shi j, jia l, yuan w, shi g, ma b, wang b, et al. clinical classification of cauda equina syndrome for proper treatment. acta orthop 2010;81:391-5. 32. todd nv, dickson ra. standards of care in cauda equina syndrome. br j neurosurg 2016;30:518-22. 33. todd nv. guidelines for cauda equina syndrome: red flags and white flags, systematic review and implications for triage. br j neurosurg 2017;31:336-9. 34. todd nv. letter to the editor concerning ‘‘cauda equina syndrome treated by surgical decompression: the influence of timing on surgical outcome’’ by qureshi a, sell p (2007). eur spine j 2009;18:1391-3. 35. todd nv. quantifying the clinical aspects of the cauda equina syndrome the cauda scale (tcs). br j neurosurg 2018;32:260-3. 36. wakrim b, kaboré fa, sebbani m, sarf i, amine m, lakhmichi a, et al. sensitivity to change of the usp score (urinary symptoms profile) after surgical treatment of benign prostatic hyperplasia (bph). prog urol 2014;24:229–33. 37. yamanishi t, yasuda k, yuki t, sakakibara r, uchiyama t, kamai t, et al. urodynamic evaluation of surgical outcome in patients with urinary retention due to central lumbar disc prolapse. neurourol urodyn 2003;22:670-5. microsoft word _6.formatata_balasa.doc romanian neurosurgery vol. xvi nr. 2 34 subperiosteal and intraconal haematoma associated with frontal and subfrontal extradural haematoma. case report d. balasa1, a. tunas1, m. bardas2, g. butoi2, s. daniela3 1department of neurosurgery, 2department of radiology, 3department of neurology clinical emergency hospital constanta adress reprint request to: daniel balasa, department of neurosurgery, academical emergency hospital constanta, boulevard tomis 145. email:daniel_balasa@hotmail.com intraorbital subperiostal haematoma is a rare entity described in the radiology, ophthalmology and neurosurgical literature produced in most of the cases by head traumas. the authors present the case of a woman suffered a car accident who caused deep coma, bilateral exophtalmia with dominance in the right eye, left hemiparesis. ct scan of the head showed dai, huge extradural right frontotemporal haematoma, subperiostal and intraorbital haematoma in the right orbit, intraventricular hemorrhage, falx cerebelli hemorrhage, fracture of the etmoidal bone with etmoid haemosinus. it was done emergent succesfull surgical removal of the epidural haematoma, and partial removal of the subperiostal and intraorbital haematoma. by trepanation of the orbit on the fracture site. postoperative evolution was eventless and control ct scann showed healed radiologically. keywords: subperiostal hematoma, head trauma, extradural haematoma intraorbital subperiostal haematoma is a rare with pathology reported in the literature the etiology of subperiostal haematoma of the orbit is in most of the cases of traumatic origin (4, 6, 17) and may be associated with an adjacent orbital fracture a much more rare entity appears to be the sickle cell and kidney disease.the haemorhage admits a vascular, bony or mixt etiology. the suggested mechanism of subperiosteal orbital hematomas is bleeding from subgaleal vessels, that enlarges and dissects the subgaleal space, extending to the orbita. a fracture of the orbital roof can dissect the periorbita and create room for blood to collect. differential diagnosis includes subperiosteal abscess, rhabdomyosarcoma, orbital pseudotumour, lymphangioma, carotid cavernous fistula, arteriovenous malformation, orbital haematoma, or frontal sinus mucocele. case report female, 36 years old, admitted as an emergency at the department of neurosurgery, ceh constanta, for multiple trauma with head and face injury due to a car accident, 2 hours after the accident. clinical examination revealed: deep comatose pacient, intense alcoholic halena, bilateral exophthalmia, non axial, with dominance in the right eye, left hemiparesis. ct scan of the head showed: huge extradural right frontotemporal haematoma, multiple hemorrhagic concussions (right posterior thalamus, left frontal-dai), intraventricular hemorrhage (right frontal and left occipital horn of the lateral ventricles), falx cerebelli hemorrhage, multiple frontal pneumocephalus. fracture of the etmoidal bone with etmoid haemosinus, haemorhage in the left maxilar sinus, fracture of the medial wall of the right orbit, subperiostal and intraorbital haematoma in the right orbit especially in the superior part. (fig. 1, 2, 3, 4, 5, 6) subperiosteal and intraconal haematoma romanian neurosurgery vol. xvi nr. 2 35 fig. 1, 2 falx cerebelli hemorrhage (white arow), left intraventricular haemorhage, occipital horn (black arrow), left etmoid sinus haemorhage, left maxilar sinus haemorhage, medial right orbital wall fractures fig. 3, 4 huge extradural right frontotemporal haematoma, subperiostal haematoma in the right orbit especially in the superior part (double white arrows), intraconal haematoma especially in the lateral right orbit (triple white arrows) dai (right frontal basal haemorhage, right posterior thalamus haemorhage (double black arrows), left frontal concussion), left intraventricular haemorhage (occipital horn) d. balasa romanian neurosurgery vol. xvi nr. 2 36 fig. 5 fig. 6 huge extradural right frontotemporal haematoma (double headed white arrow), multiple frontal pneumocephalus (special white arrow) surgical therapy i found a frontal fracture which crossed the roof of the right orbita and the lateral frontal bone bleeding in the extraconal space of the right orbita and in the extradural space. frontotemporal craniotomy was performed on the right side (for the extradural right frontotemporal haematoma) and the opening of the roof of the orbit was done by a small craniectomy in the roof of the orbita followed by removal of few mililiters of fresh blood, two small clots under pressure and lavage with warm serum. a frontal extradural and upper intraobital extraconal drain was left for 24 hours. postoperative ct scann: healed surgically (fig 7, 8, 9). fig. 7 cerebrum window fig. 8 fig. 9 bone window the fracture line lateral fronto-orbital trepanated is figured with duble duble headed white arrow. the ophtalmologic control done in the 4th day postoperative was normal. the patient was transferred to other hospital at the 20th day with gos 5. discussion orbital hematomas are classified by landa5 either as intraorbital or subperiostal. subperiosteal haematomas of the orbit are rare lesions, reported in early literature as “blood cyst”. almost all cases are associated with trauma. proptosis, downward globe displacement, ophtalmoplegia,chemosis, lid hematoma, subgaleal hematoma and visual dysfunction are the most commonly related to clinical manifestations, that occur most often acutely or within days of the traumatic event. the differencial diagnosis should include carotidcavernous fistulae, orbital subperiostal abcess, orbital roof fractures, frontal mucocele, sinusites,complication of orbital and sinus surgery, tumors subperiosteal and intraconal haematoma romanian neurosurgery vol. xvi nr. 2 37 (rhabdomyosarcoma, leukemia, lymphangioma) andcoagulopathies. the suggested mechanism of subperiosteal orbital hematomas is bleeding from subgaleal vessels, that enlarges and dissects the subgaleal space, extending to the orbita. a fracture of the orbital roof can dissect the periorbita and make room for blood to colect.. treatment options include observation, needle aspiration, and surgical evacuation. neddle aspiration is less technically demanding, but has the disadvantages of possible rebleedingand of not allowing removal of clotted blood. with orbital exploration, the surgeon can stop any active bleeding, reduce possible orbital roof fractures, remove coagulated blood and to leave a drain, if necessary. extradural hematoma (edh) is a frequent lesion, with an incidence varying from 0.2 to 6% in patients admitted to hospital due to traumatic head injury. the association of edh with subperiosteal intraorbital hematomas is rarely reported. we founded in the literatute only 5 cases reported. (7, 8, 13, 16, 17) in our case, the etiology was a linear lateral frontal fracture prolonged in the lateral orbital roof who bled in 3 compartments: anterior cranial fossae, middle cranial fossae (with dominance in the anterior cranial fossae) and the orbit. (fig. 10) with dominance in the periorbital space. fig. 10 the fracture line is figured in red colour we choose to approach the hematomas with craniotomies instead of using any of other approachs, because it was the only option to treat properly the extradural haematoma and intraorbital haematoma (with dominance in the subperiosteal space). we propose the protocol used by the most of the authors (7, 8, 18): in comatose patients or those with important impairement of the level of consciouness, a subperiostal haematoma must be operated as soon as possible. for the conscious patient surgical solution becomes necessary if the blurred vission and/or paralisis of the eye movements develops. in case of an association between extradural haematoma and subperiostal haematoma, emergency surgical intervention for both haematomas is mandatory. conclusion all the patients with craniofacial injuries with clinical signs or symptoms of eye lesions (proptosis, downward globe displacement, ophtalmoplegia, chemosis, lid hematoma, subgaleal hematoma and visual dysfunction) must be suspected of having a subperiosteal or intraorbital haematoma. the surgical decompression of the orbit is an emergency and is mandatory for saving the patient eyes function. early diagnosis is mandatory to the potential for severe neurological sequela, including transient or permanent blindness. in case of an association between extradural haematoma and subperiostal haematoma, emergency surgical intervention for both haematomas is mandatory for saving patients life and eyes function. references 1.amit a1, sankalp d1, rajnish j2 et all subperiosteal hematoma of the orbit associated with subfrontal hematoma presenting as proptosis neurology india 2007, 55, 4, 423-424 2. atalla m.l.,mc nab a. a., sullivan t.j et all non traumatic subperiosteal orbital hemorrhage. ophtalmology. 2001 jan;108(1): 183 –189. 3. carrion lt. edwards w.c., perry ld. spontaneous subperiostal orbital hematoma. ann. ophtalmol., 1979; 11: 1754 – 1777. 4. jones tw:protrusion of the eyeball,with blindness:disease of the kiddneys, with haemorrhagic diathesis.br med j 1:453,1 d. balasa romanian neurosurgery vol. xvi nr. 2 38 5. landa m.s., landa e. h. levine m. r. subperiosteal hematoma of the orbit: case presentation. ophtal. plast. reconstr. surg. 1998 may; 14(3): 189 – 192. 6.law f.w:spontaneous orbital haemorrhage. br j ophthalmol 55:556,1971 7. le bourdon g, riffaud l., godey b., morandi x.hématome subpériosté de l’orbite associé à un hématome extra-dural frontal. ophtalmo, 1999; 22, 6, 659 – 661 8.o’neill o.r., delashaw j.b., phillips j.p. subpériosteal hematoma of the orbit associated with subfrontal extra-dural hematoma case report. surg. neurol., 1994; 42: 308 – 311 9. privat c., bellamy j., courthaliac c., kinn t., ravel a., mondie j., bacin f., boyer l.chronic hematic cyst. of the orbit ( orbital subperiosteal hematoma ). j. radiol. 2000.; 81 (7): 811814 . 10. robert c., kersten m.d., charles d., rice m.d. subperiosteal orbital hematoma: visual recovery following delayed drainage. exophtalmic surgery, 1987, vol. 18, n° 6, 11-13 11.rojas,1 m c, j a eliason,2 and d r fredrick3 needle aspiration of a traumatic subperiosteal haematoma of the orbit br j ophthalmol. 2002; 86(5): 593–594 12.sabet s.j., tarbet k.j., lemke b.n.,smith m.e., albert d. m. subperiostal hematoma of the orbit with osteoneogenesis. arch. of ophtalmol.2001.; 19(2): 301 – 303. 13.sharma ak, diyora bd, shah sg et al. orbital subperiosteal hematoma associated with subfrontal extradural hematoma. j trauma 2007;62:523-5. 14.shannon d. crawford and mahesh r. patel bilateral supraorbital masses after prolonged headlock injury: an unusual manifestation of orbital subperiosteal hematomas department of radiology, santa clara valley medical center, 751 s. bascom ave., san jose, ca 95128. 16, 2004 15.smith p. a case of intra-orbital haemorrhage and other eye complications in connection with haemophilia. roy lond ophthal hosp rep 12: 70, 1888 16. stewart cr., salmon jf., domingo z et all. proptosis as a presentating of extradural haematoma. br. j. ophtalmol, 1993; 77: 179 – 180 17.umansky f., pomenanz sh. epidural haematoma and unilateral exophtalmos. a review acta neurochir. (wien), 1989; 99: 145 – 147 18. william m., gillun m.d., richard l et all. irreversible visual loss in subpériostal hematoma. ophtal. surg. march 1981 vol. 12, n° 3. 19. wolter j.r.: subperiosteal hematomas of the orbit in young males a serious complication of trauma or surgery in the eye region. trans am ophtalmol soc. 1979; 77: 104 – 120. doi: 10.33962/roneuro-2021-031 paediatric brain abscesses in tribal region of india. a single centre experience sachin kumar jain, gaurav jaiswal, tarun kumar gupta, krishna govind lodha, vishnu kumar lohar, kaushal yadav romanian neurosurgery (2021) xxxv (2): pp. 199-203 doi: 10.33962/roneuro-2021-031 www.journals.lapub.co.uk/index.php/roneurosurgery paediatric brain abscesses in tribal region of india. a single centre experience sachin kumar jain, gaurav jaiswal, tarun kumar gupta, krishna govind lodha, vishnu kumar lohar, kaushal yadav department of neurosurgery, r.n.t. medical college, udaipur, india abstract introduction: brain parenchymal abscesses are relatively infrequent but potentially serious infections in the paediatric population. surgical intervention in addition to a prolonged administration of antibiotics is generally appropriate management. aims and objective: we performed this study to assess the clinical profile, aetiology and outcome of paediatric brain abscess which are treated surgically only by aspiration in the tribal region of rajasthan. material and method: a single-centre retrospective study was conducted over a 5 year period (2014–2019) in the department of neurosurgery in rnt medical college, udaipur, rajasthan. we treated approx. 60 patients of which 25 patients treated conservatively and 5 patient treated by craniotomy and abscess excision. so only 30 patient included in our study in which abscess treated by aspiration only. patients<18 years of age with a confirmed intra-parenchymal abscess were included. patient records were reviewed for abscess location, microbiology results, clinical features, surgical intervention, and outcome using the glasgow outcome score at 3 months. result: 11 patients had an abscess in the temporal lobe and streptococcus was the most common causative micro-organism (n¼15). 25 patients (80%) had an identifiable source which included: ent infections, congenital cardiac malformations, recent dental surgery and meningitis. the most common symptom is fever f/b headache, seizure and vomiting. but despite previous studies seizure (10/30) presentation is comparatively more. all 30 patients underwent aspiration. conclusion: in tribal regions of india ent infections are a more common source of brain abscess because of poor hygiene and illiteracy and their ignorance of ent infections and also not taking seriously to fever, headache and other health issues. but at present, there are also decreasing trends of brain abscess by ent infections and rising trends by congenital heart disease which is a good sign that the health and educational infrastructure is strengthening in the tribal region also. introduction a brain abscess is an intra-parenchymal collection of pus in the brain. the incidence of brain abscess among intracranial masses varies from 1-2% in western countries, to about 8% in developing countries1. it is still a life threatening and fatal entity and often leads to serious disability and even death if misdiagnosed or treated improperly2. brain abscesses are relatively less common in the paediatric population compared to adults; however, they remain a serious, life-threatening infection3. keywords abscess, aspiration, paediatrics, ent corresponding author: gaurav jaiswal department of neurosurgery, r.n.t. medical college, udaipur, india drsachinj6184@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 200 sachin kumar jain, gaurav jaiswal, tarun kumar gupta et al. the causes of brain abscesses are highly variable in children. the major predisposing conditions in children are: an adjacent focus of infection, trauma, haematogenous seeding, neurosurgical procedures, cyanotic heart disease and immunocompromised states4,5,6. associated sites of infection commonly include sinusitis, mastoiditis, dental infections and chronic otitis media where aerobic bacterial infections such as streptococci and staphylococci predominate4,7 the gold standard treatment of brain abscesses continues to be aspiration or excision combined with antibiotic therapy.5 however the outcome has improved dramatically in recent decades due to improvements in diagnostic techniques and broadspectrum antibiotics8. magnetic resonance imaging is more sensitive at diagnosing early cerebritis9 and has increased the prognosis of brain abscess by improving the speed of diagnosis. despite all of these advances abscesses are still a significant cause of morbidity and mortality10. in addition, abscess growth can result in rupture of the abscess into the ventricular system. this lifethreatening event will result in an acute decompensation and symptoms of a purulent meningitis11. we performed this study to assess the clinical profile, aetiology, and outcome of paediatric brain abscess in the tribal region of rajasthan. material and method a single-centre retrospective study was conducted over a 5-year period (2014–2019) in department of neurosurgery in rnt medical college, udaipur, rajasthan. we treated approx. 60 patients in which 25 patients treated conservatively and 5 patients treated by craniotomy and abscess excision. so only 30 patients included in our study in which abscess treated by aspiration only. the final cohort of 30 patients comprised 20 male patients (45.8%) and 10 female patient and had a mean age of 6.5 ± 4 years patients < 18 years of age with radiological confirmed intra-parenchymal abscess were included. patient records were reviewed for abscess aetiology, location, size, microbiology results, surgical intervention, and outcome using the glasgow outcome score at 3 months. we include the patients in which abscess treated only by aspiration and then antibiotics. aspiration of abscess may be single or multiple times. size of abscess is more than 2.5 cm. the total antibiotic duration was discernible from the medical notes for all patients and the mean time was 5.8 ± 2.0weeks. this comprised a mean of 2.9 ± 1.5 weeks intravenous and3.0 ± 1.8 weeks oral antibiotics. white cell count >11109/l and/or c-reactive protein >5mg/l was classed as raised inflammatory markers. functional outcome was measured using the glasgow outcome score (gos) at 3 months from discharge. those with isolated subdural empyema, extradural abscess, or an unknown abscess location were excluded from the study. result most common symptom is fever followed by headache, seizure and vomitting. (table-3). the classic triad of headache, fever and focal neurological deficit was seen in two patients (8.6%). drowsiness or reduced level of consciousness on presentation was recorded in 6 patients (34.8%). age of patients are mostly 5-10 years. (table-1) the temporal lobe was the most common abscess location (11). the remainder of the abscesses were in the parietal lobe (8), frontal lobe (7), cerebellum (2), thalamus (1), pons (1) (table 4) .22 patients had a solitary lesion at presentation and rest 8 has more than one lesion. the patient with aspergilloma had two lesions in the same location. figure 1. pre-operative scan of 10-month male child left temporo-parietal brain abcess (original pics). s. n. age number percentage 1 2 3 <5 year 5-10 yr 10-18 yr 6 15 9 20% 50% 30% table 1. 25 patients (80 %) had an identifiable source which include post meningitic (4), congenital cardiac malformations (7), otogenic and mastoditis (11), post 201 paediatric brain abscesses in tribal region of india traumatic (3). rest 5 has other non-identifiable sources (table-2). streptococcus was the most common organism cultured from the abscesses (18). other microorganisms include staphylococcus aureus (5), coliforms (1), propriobacterium (1), mycobacterium tuberculosis (2), gram negative rods (1) and mixed anaerobes (2). all 30 patients underwent surgery. all 30 patients had burr hole aspirations (figure 1 and 2) (17 patients had single aspiration). more than 2.5 cm size of abscess aspirated or treated surgically, rest were treated conservatively. pre-operative imaging was available for all 30 patients and volumetric analysis showed an average pre-operative volume of 16.3ml. figure 2. post-operative scan of this 10-month male child after single burr hole aspiration (original pics). s. n. predisposing factor no. percentage 1 2 3 4 5 otitis media and mastoditis congenital heart disease meningitis posttraumatic others 11 7 4 3 5 36.66% 23.33% 13.33% 10% 16.66% table 2. according to size 2.53.5 cm total 16 cases in which 4 cases require single re aspiration (28.57%) , but in 3.5-4.5 cm size total 10 cases in which we require 6 re aspiration (60%) , in which 4 cases require single reaspiration and 2 require two reaspiration. more than 4.5 cm total 4 cases in which 3 patients requires re aspiration. (75%), in which 1 case require two re aspiration and rest 2 cases required three reaspiration (figure-3). but the good thing is that all treated with aspiration and antibiotics. location dose not significantly co-relate with re –aspiration. figure 3. huge abscess in left temporoparietal region in 2.5month old child (original pics). gos score at 3-month -22 patient has 5, 3 patients has score 4 and 3 patient had score 3 or less. 2 patients expired – 1 due to some cardiac problem in congenital heart disease, second is due to severe sepsis in otitis media patient. rest 28 patients survived. according to symptoms fever resolved in all patients. seizure resolved in 6/8 patients in 3 months follow up. motor deficit corrected in 6/8 patients in 3 months follow up. s.n. symptoms and signs number percentage 1 2 3 4 5 6 7 8 fever headache seizure altered sensorium vomitting meningism motor deficit sensory deficit 14 11 10 6 5 5 8 4 46.66% 36.66% 33.33% 20% 16.66% 16.66% 26.66% 13.33% table 3. s.n. site of abscess number percentage 1 2 3 4 5 temporal frontal parietal cerebellum others(pons,thalamus) 11 7 8 2 2 36.66% 23.33% 26.66% 6.66% 6.66% table 4. 202 sachin kumar jain, gaurav jaiswal, tarun kumar gupta et al. discussion the change in practice towards early prescription of antibiotics for oto-sinogenic infections has resulted in a change in the infective etiologies associated with brain abscess12. in studies from the pre-ct era ent infections were the cause in 38-76% of brain abscesses in children; however this has fallen to 836% .in the modern era with congenital heart disease and immunosuppression becoming a more commonly recognized causative factor11,12,13,14.but in the present study, temporal lobe abscess following middle ear infection and mastoiditis was the commonest finding15,16. temporal lobe abscess following otogenic infection has been found in previous studies22. in tribal area due to poor hygine and others late responding to fever and ignorance of ear infection or maltreatment of ear infection develop a simple meningitis and ear infection into a brain abscess15,16. in our study, males are more affected than females. males are more exposed to outdoor activities with greater chance of ear infection and predisposing to brain abscess 17. regardless of the changes in etiology, streptococcus remains the most commonly reported causative microbe both in this series and those published in the literature17,18. the presentation of brain abscesses is non-specific but most commonly includes, headache, fever, altered mental status, meningism and seizures5,.according to samull et al nowadays suggest that headache and fever is the most common symptoms and seizures is not so common in abscess but in this study seizure is also common complain (10/30-30%) because involvement of temporal lobe is more . those who present with altered mental status and rapid neurological deterioration are more likely to have an increased mortality rate19. 2 patient expired in this study had low gcs and altered mental status. so preoperative gcs is important for prognosis. multiple aspirations were associated with a larger initial abscess volume. these will leave a larger cavity that is slower to involute and thus leave a nidus of infection that can re-accumulate. half of the patients in this series required more than one aspiration and thus patients should be counselled accordingly.12 modern series report lower mortality rates than the pre-ct era ranging from 8 to 25%20 and the large series by tekkok and erbengi21 even managed 0% mortality at the end of their study period. neuroimaging was done in all cases. ct scan was done in 25 cases and mri was done 5 cases. the only added advantages of mri over ct scan are: better differentiation of edema from necrosis, more sensitivity in detection of early cerebritis, greater sensitivity for early satellite lesion23. most common neuroimaging finding was ring enhancing lesion. this has been reported in previous studies from india and abroad24,25. one reason for a low mortality rate may be an aggressive approach towards abscess drainage and also sepsis source control. poor glasgow coma scale (gcs) at time presentation has been associated with poor outcome. previous studies in india, nepal and pakistan have also reported poor gcs as negative prognostic factor in their studies24,25 conclusion this study demonstrates that in the modern era with ready access to ct imaging and broad-spectrum antibiotics, low rates of morbidity and mortality can be achieved. drainage of paediatric abscesses remain the mainstay of treatment both to relieve mass effect and provide a microbiological diagnosis. patients and their families should be counselled to expect multiple procedures. but in this study most common predisposing factor for abscess is otitis media than congenital heart disease. because in tribal region exposed to outdoor activities with greater chance of ear infection and predisposing to brain abscess. also, illiteracy and poor hygiene leads to more chances of chronic ear discharge and brain abscess formation in future. so we need to educate the people of tribal region for proper hygine and also early consult to doctor for any ear infection. we have to educate them about their proper health checkup and consult if child had fever, seizure, headache and vomitting. if infant and less than 3 yr age child had excessive irritability then also take consultation. we can also promote pneumococcal vaccination. but at present there are also decreasing trends of brain abscess by ent infections (11/30 -36.66%) and rising trends by congenital heart disease (7/3023.33%) which is a good sign that the health and educational infrastructure is strengthening in tribal region also. 203 paediatric brain abscesses in tribal region of india conflict of interest there is no conflict of interest to disclose. informed consent informed consent was obtained from all individual participants included in this study. references 1. sharma bs, gupta sk, khosla vk. current concepts in the management of pyogenic brain abscess. neurol india. 2000;48:105–11. 2. kao pt, tseng hk, liu cp, su sc, lee cm. brain abscess: clinical analysis of 53 cases. j microbiol immunol infect. 2003;36:129–36. 3. frazier jl, ahn es, jallo gi. management of brain abscesses in children.neurosurg focus2008;24:e8. 4. brook i. brain abscess in children: microbiology and management.j childneurol1995;10:283–8. 5. hakan t, ceran n, erdem i, berkman mz, goktas p. bacterial brain abscesses: an evaluation of 96 cases.j infect2006;52:359–66. 6. tandon s, beasley n, swift ac. changing trends in intracranial abscesses secondary to ear and sinus disease. jlo2009;123:283. 7. shachor-meyouhas y, bar-joseph g, guilburd jn, lorber a, hadash a,kassis i. brain abscess in children epidemiology, predisposing factors and management in the modern medicine era.acta paediatr2010;99:1163–7. 8. saez-llorens x. brain abscess in children.semin pediatr infect dis2003;14:108–14. 9. mathisen ge, johnson jp. brain abscess.clin infect dis1997; 25:763–79.quiz 80-1. 10. felsenstein s, williams b, shingadia d,et al.clinical and microbiologic features guiding treatment recommendations for brain abscesses in children.pediatr infect dis j2013;32:129–35. 11. jasonp. sheehan,johna. janejr etal. brain abscess in children:journal of neurosurgery 2008/24/6/e6. 12. goodkin hp, harper mb, pomeroy sl. intracerebral abscess in children:historical trends at children’s hospital boston.pediatrics2004;113:1765–70. 13. samuel halla, shirley yadub, benjamin gaastraa, nijaguna mathada, owen sparrowa, ryan watersa, aabir chakrabortya and vassilios tsitouras et al. paediatric brain abscesses: a single centre experience,british journal of neurosurgery:may 2019:33(550-554). 14. canpolat m, ceylan o, per h,et al.brain abscesses in children: results of24 children from a reference center in central anatolia, turkey.j childneurol2015;30:458–67. 15. kafle p, sharma mr, shilpakar sk, sedain g, pradhanang a, shrestha rk, et al. pediatric brain abscess clinical profile, management and outcome at tertiary care centre in nepal. jcms nepal. 2018;14:102–6. 16. clinical profile and outcome of brain abscess in children from a tertiary care hospital in eastern uttar pradesh , rajniti prasad, john biswas, kulwant singh,1 om p. mishra, and ankur singh,ann indian acad neurol. 2020 may-jun; 23(3): 303–307. 17. sharma r, mohandas k, cooke rp. intracranial abscesses: changes in epi-demiology and management over five decades in merseyside.infection2009;37:39–43. 18. nathoo n, nadvi ss, narotam pk, van dellen jr. brain abscess: manage-ment and outcome analysis of a computed tomography era experiencewith 973 patients.world neurosurg2011;75:716–26. discussion 612-7. 19. seydoux c, francioli p. bacterial brain abscesses: factors influencing mor-tality and sequelae.clin infect dis1992;15:394–401. 20. auvichayapat n, auvichayapat p, aungwarawong s. brain abscess in infants and children: a retrospective study of 107 patients in northeast thailand.j med assoc thai2007;90:1601–7 21. tekk€ok ih, erbengi a. management of brain abscess in children: review of 130 cases over a period of 21 years.childs nerv syst1992;8:411–6. 22. malik s, joshi sm, kandoth pw, vengsarkar us. experiences with brain abscess. indian pediatr. 1994;31:661–6. 23. schmidek hh. suppurative intracranial infections. in: schmidek hh, roberts dw, editors. schmidek & sweet operative neurosurgical techniques. indications, methods, and results. 5th ed. philadelphia: elsevier, inc; 2006. pp. 1591–9. 24. atiq m, ahmed us, allana ss, chishti kn. brain abscess in children. indian j pediatr. 2006;73:401–4. 25. singh d, gupta v, singh ak, sinha s. evolution of otogenic brain abscess and management protocol. indian pediatr. 2001;38:169–73. microsoft word _6.formatate_selected_abstracts.doc romanian neurosurgery vol. xv nr. 2 30 selected abstracts from the 7th national conference of the romanian society of neurosurgery 2008, iasi, românia contemporary management of trigeminal neuralgias prof. m. sindou department of neurosurgery, hopital neurologique, university of lyon, lyon, france overview based on literature review and personal experience (2478 patients referred for trigeminal neuralgia) first step is to recognize, with appropriate investigations, symptomatic neuralgias. as an example, they accounted for 3.6 % in our series of 2478 patients referred over the 28 past years for appearently a primary trigeminal neuralgia (tn). symptomatic neuralgias are generally treated with success by attempting at the radical cure of the causative lesion. when multiple sclerosis (ms) is suspected, mr imaging is completed with electrophysiological and csf biological investigations.thermorhyzotomy is the treatment most often used for ms patients. in our series of 72 ms patients, results were constantly good, but recurrences were frequent; redoing thermorhyzotomy was generally effective. the key-examination for diagnosis is encephalic mri including cervico-occipital junction.it allows to evidence: chiari-malformation, platybasia, smallcapacity posterior fossa,brain-stem lesions, cerebellopontine angle tumors or vascular malformations,cavernous sinus neoplasias,as well as any type of skull base pathologies in relation with the trigeminal nerve. special mri studies, as for instance spgr mr, may help to identify vascular images at the contact of the trigeminal root.when they are pronounced and the root dislocated, these images constitute arguments for a neuro-vascular conflict (nvc) at the origin of the neuralgia. our experience on hundreds of mri for primary tn leads us to estimate that the absence of an obvious image of nvc frequently coexists with a clearcut nvc at surgery, and that vascular images in the close vicinity of the root are far from to correspond to the real conflicting vessels seen intraoperatively. the second step is the choice of the surgical method. surgery has to be indicated only after having checked that the classical medical treatment with anticonvulsants has been rigorously applied and controlled by a neurologist. the fact that during posterior fossa exploration, a nvc was almost constantly found in patients referred for primary tn that is in 96.7 % of our 579 patients studied (9) leads us to propose the micro-vascular decompression (mvd) procedure (2, 4) as the first surgical treatment. all candidates need a general examination, so that the anesthesiologist controls that the patient ‘s general conditions are compatible with general anesthesia and open surgery. on that basis, we performed 726 mvd procedures over the past 24 years. when the patient is considered too aged (70 – 75 years seems to be a”sensible” limit) and /or having a precarious general status,a percutaneous procedure,under slight neuro-sedation and short lasting general iv anesthesia, is indicated.the thermorhyzotomy procedure according to sweet’s technique (13) has our preference. over the past 28 years, we performed 1752 of such a procedure, mainly for elderly patients. but glycerol injection (3) or balloon compression (6) are chosen by many other teams as the first percutaneous procedure.the recently selected abstracts romanian neurosurgery vol. xv nr. 2 31 developed stereotactic radiosurgical gamma-knife treatment (5) is progressively taking a place in the neurosurgical armamentarium for intractable tn. microvascular decompression (2, 4) is based on the hypothesis that the main responsible factor of the neuralgia is a nvc at the level of the root,especially at the root entry zone (rez). in our series of 579 cases studied (9), an elongated superior cerebellar artery (alone or in association with other conflicting vessel(s) ) was found in 88% of the patients,an anterior-inferior cerebellar a. in 25.1%, a vein embedded in the nerve in 27.6%, the basilar a. in 3.5%.of prime importance,several conflicting vessels were found in association in as much as 37.8% of the patients.missing one of these multiple vessel(s) could lead to failure or recurrence location of the nvc was at the rez in 52.3%, at the midthird of the root -i.e., at its cisternal portionin 54.3%, and at the exit of the root from meckel cave in 9.8%. this means that the entire root has to be explored from brainstem to porus of meckel cave. the degree of severity of the conflict was a simple contact with the nerve in 17.6%, a distorsion of the nerve in 49.2%,and a marked indentation in 33.2%. in addition, alterations of the whole root were frequently observed.in 42% of the patients, the nerve had a significant degree of global atrophy, likely related to a coexisting” neuropathy “ of the trigeminus.in 18.2%,there was a local thickening of arachnoid membranes,adherent to the root.in 12.6%,the root had a marked angulation on crossing over the petrous ridge.finally in 3.9%,the nerve was compressed between pons and petrous bone,due to small size of posterior fossa. in our practice we found it of importance, in addition to transposing away the offending vessel(s), to free the root from all the arachnoidian adhesions and to reroute it as normally as possible. as regard to the procedure, most surgeons agree to consider important the following technical points (7): patient placed on the table in the contralateral lying position, the head moderately elevated,slightly flexed and rotated 15° toward the contralateral side; retromastoid craniectomy, of the key-hole type,made just posterior to the base of the mastoid process,so as to expose the dura in the angle formed by the transverse and the sigmoid sinuses; trigeminal nerve accessed via infratentorialsupracerebellar route, along the superior petrosal sinus, not to retract from lateral-to-medial the cerebellum and consequently stretch the 7th-8th nerve complex as well as the labyrinthine artery; large opening of the arachnoid around the superior petrosal veins,so as avoiding their avulsion and preventing venous infarction of the cerebellum ; care must be taken not to damage the tiny trochlear nerve especially with the sucker.the least opening of the arachnoid in front of the 8th nerve, the less hearing complications. -to prevent damaging the trigeminal root during decompression,release from the vascular compression has to be performed without manipulations of the nerve with the surgical instruments.attempt to dislodge the offending vessel(s) is better made by gently pulling on the vessel(s) with small tapes of teflon fiber felt passed around.the vessel(s) is (are) transposed away and then kept apart,better by means of a prosthesis but without contact to the nerve so as to avoid “neocompression” (12). throughout the vascular manoeuvers, application of drops of papaverine in saline is important to antagonize mechanical vasospastic reactions in the arteries. -to make dura watertight, a piece of subcutaneous fascia taken from the operative wound is affixed extradurally ;and if mastoid cells were largely opened,rather than waxing it is better to pack with fat tissue harvested from as for instance the thigh. long-term follow-up studies, with actuarial curve calculation, show that mvd is able to provide a stable cure of the disease in more than three-quarters of the cases (1, 11).in our series of 579 patients followed for 3 to 20 years,9 y on average,the success rate was 76.1%.mortality was 0.30% and severe neurological selected abstracts romanian neurosurgery vol. xv nr. 2 32 complications (cerebellar ischemic stroke) another 0.30%. percutaneous techniques are lesioning methods, and must be better reserved for elderly patients. rfthermorhyzotomy, as developed by sweet (13), has our preference because more accurate, provided performed precisely.the method is based on the existence of a somatotopia in the trigeminal fibers, not only at the level of the gasserian ganglion but also of the triangular plexus and the adjacent portion of the sensory root,the two later being the ideal target for the thermo-lesion. the ophtalmic fibers (v 1) are situated in a supero-medial,the mandibular(v 3) in an infero-lateral and the maxillary (v 2) in an intermediate location ; the motor (masticatory) root courses independently, more medially, from a superior position in the cpa cistern to an inferior location in the meckel cave trigeminal cistern.the best location of the tip of the electrode to achieve the optimum effect on pain with the minimum side-effects or complications is the immediate retrogasserian part of the root,i.e., the triangular plexus,as demonstrated through our series (10). an accurate control of the appropriate location of the electrode needs intraoperative fluoroscopy and even more an electro-stimulation test, prior performing the thermo-lesion (8). the use of a current with a frequency of 5 hz makes it possible, not only to evoke paresthesias in the trigeminal territory (which necessitates the patient awake),but also to produce clinically observable motor twitches in the face (that can be noticed by the surgeon himself). these twitches may, not only affect the masticatory muscles being direct masticatory responses (dmr) to the direct stimulation the motor root -, but also muscles innervated by the facial nerve -being evoked motor responses (emr), hypothesized to correspond to trigemino-facial reflexes elicited by the stimulation of the sensory rootlets -. so, navigation within the trigeminal system under x-ray and using neurophysiologic guidance does help to locate the uninsulated tip of the electrode in the optimal place, that is in the sensory fibers corresponding to the trigger-zone at the level of the triangular plexus (sindou 1999). the right location is –at the same time the one in which threshold for eliciting dmr is high and threshold for evoking facial emr in the trigger-zone is low.emr in orbicularis oculi is indicative of location in the rootlets corresponding to v 1 territory ; emr in levator labii, of v 2 territory rootlets; emr in orbicularis ori, of v 3.when twitches cannot be clearly seen in the lower face (which is not rare) and pain is in v3 and /or v2, one may rely on the progressive cessation of twitches evoked in the upper part facial muscles while the electrode is slowly withdrawn from a supero-medial to an infero-lateral position in the triangular plexus region. the landmark of the later on lateral x-ray is the crossing between upper ridge of petrous bone and clivus. in our series of 1752 patients operated on since 1975 and up to now (average follow-up: 14 years), the procedure produced relief of pain in all but 3 pts. with a marked degree of hypoesthesia in the trigger zone deliberately searched -,the overall recurrent rate was as low as 7%. 6% of patients complained of dysesthesias and 2% of disabling hypoesthesia ;there was corneal hypoesthesia in 16%,with episodes of (reversible) keratitis in 5%. in conclusion, the surgical management of idiopathic trigeminal neuralgia needs to have recourse to two types of procedures.the first type, the mvd, is directed to the main causative factor, i.e., the nvc; it is conservative and curative ; but it is an open operation with some potential vital risks. the second type is represented by the percutaneous techniques ; they are lesioning and palliative methods ;but being less invasive, they can be useful in aged patients with precarious general conditions. in the future, it might be that the stereotactic radiosurgical gamma-knife technique replaces –at least partly the percutaneous methods. references 1. barker fg, jannetta pj, bissonnette dj, larkins mv, jho hd. the long-term outcome of microvascular selected abstracts romanian neurosurgery vol. xv nr. 2 33 decompression for trigeminal neuralgia. new engl j med 334:17:1077-1083, 1996 2. gardner wj. concerning the mechanism of trigeminal neuralgia and hemifacial spasm. j. neurosurg 19:947-958, 1968 3. hakanson s. trigeminal neuralgia treated by the injection of glycerol into the trigeminal cistern. neurosurgery9:638-646, 1981 4. jannetta pj. arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia. j neurosurg 26:159-162, 1967 5. leksell l. the stereotactic method and radiosurgery of the brain. acta chir scand 102:316-319, 1951 6. mullan s, lichtor t. percutaneous microcompression of the trigeminal ganglion for trigeminal neuralgia. j neurosurg 59:1007-1012, 1983 7. sindou m. microvascular decompression for trigeminal neuralgia. in: kaye ah, black pm (eds). operative neurosurgery, vol.2 churchill-livingstone. london, pp15951614, 2000 8. sindou m, fobe jl, berthier e, vial c. facial motor responses evoked by direct electrical stimulation of the trigeminal root. localizing value for radiofrequency thermorhizotomy. acta neurochir 128:57-67, 1994 9. sindou m, howeidy t, acevedo g. anatomical observations during microvascular decompression for idiopathic trigeminal neuralgia (with correlations between topography of pain and site of the neurovascular conflicts). prospective study in a series of 579 patients. acta neurochir 144:1-13, 2002 10. sindou m, keravel y. thermocoagulation percutanée du trijumeau dans le traitement de la névralgie faciale essentielle. résultats en fonction du siège de la thermocoagulation. neurochirurgie 25:166-172,1979. 11. sindou m, leston j, chapuis f. long-term outcome and prognostic factors in microvascular decompression for trigeminal neuralgia. 2003 (submitted for publication). 12. sindou m, mertens p, amrani f. does microsurgical vascular decompression for trigeminal neuralgia work through a neocompressive mechanism? anatomical-surgical evidence for a decompressive effect. acta neurochi [suppl] 52:124-127, 1991 13. sweet wh, wepsic jg. controlled thermocoagulation of trigeminal ganglion and rootlets for differential destruction of pain fibers. part i. trigeminal neuralgia. j neurosurg 40:143-156, 1974 drug-delivery to the spinal cord tagged with nanowire enhances neuroprotective efficacy and functional recovery following trauma to the rat spinal cord hari shanker sharma1, syed f ali3, w. dong4, z. ryan tian4, r. patnaik5, s. patnaik5, aruna sharma1, arne boman2, per lek2, elisabeth seifert2 torbjörn lundstedt2 1laboratory of cerebrovascular research, department of surgical sciences, anaesthesiology and intensive care medicine, university hospital, uppsala university, 2acurepharma ab, ulleråkersv 38, uppsala, sweden 3neurochemistry laboratory, division of neurotoxicology, national centre for toxicological research/fda, jefferson, ar, usa 4department of chemistry and biochemistry, university of arkansas fayetteville, ar 72701, usa 5department of pharmacy, institute of technology, banaras hindu university, varanasi-221005, india drug delivery to the spinal cord or brain following injury is still a serious problem because of the presence of blood-brain and blood-spinal cord barriers [1, 2]. thus, various methods are used to enhance drug delivery to the cns in normal or in pathological conditions to achieve therapeutic success [2]. recently, drugs attached to innocuous nanowires are considered as a suitable method for enhanced delivery within the central nervous system (cns). there are few reports in the literature that indicates that drugs when delivered in combination with nanowires; their therapeutic efficacy is enhanced [see 1]. however, most of these investigations are carried out in vitro models. thus, these novel aspects of therapeutic enhancement of drugs or compounds tagged with nanoparticles require additional investigation using in vivo models. this investigation was undertaken to examine whether drugs attached with nanowires when applied over the traumatized spinal cord in rats may have better therapeutic efficiency compared to the parent selected abstracts romanian neurosurgery vol. xv nr. 2 34 compound in terms of neurological outcome and/or spinal cord pathology. for this purpose, 3 different compounds named sci1, sci2 and sci5 (acure pharma, sweden) having potential neuroprotective efficacy in cns injury were identified and tagged with tio2-based nanowires using standard procedure. normal compounds were used for comparison. spinal cord injury (sci) was produced by making a longitudinal incision into the right dorsal horn of the t10-11 segments under equithesin anaesthesia [2]. in separate group of rats sci1, sci2 and sci5 alone or tagged with nanowires were applied topically within 5 to 10 min after sci and the rats were allowed to survive 5 h. in these animals, behavioral outcome, blood-spinal cord barrier (bscb) permeability, edema formation and cell injury were examined at 5 h [3]. a focal sci resulted in severe motor paralysis, widespread disruption of the bscb to evans blue albumin (eba), [131] iodine or lanthanum tracers and exhibited profound edema formation [3,4]. cell or tissue destruction was present around the lesion site extending up to t8 and t12 segments [4]. topical application of normal compounds sci1, sci2 or sci5 in high quantity (10 µg in 20 µl) markedly attenuated behavioral dysfunction that are prominent around 2-3 h after sci. bscb disruption, edema formation and nerve cell, glial cell and axonal injuries are less pronounced in drug treated injured animals. these beneficial effects are most marked in animals that received sci2 treatment compared to sci1 or sci5. interestingly, when these compounds were administered tagged with nanowires, their beneficial effects on functional recovery and spinal cord pathology were further enhanced. thus, sci2 tagged with nanowires was able to attenuate functional disturbances up to 5 h after trauma. spinal cord cell and tissue destruction was minimal in nanowire-tagged sci2 treated group compared to sci2 treatment alone. in nanowire-tagged group also the most larked beneficial effects were seen in sci2 treatment compared to other compounds. topical administration of nanowires alone did not influence spinal cord pathology or motor function after sci. taken together, our results probably for the first time indicate that the drug-delivery and their therapeutic efficacy is enhanced when the compounds are administered with nanowires. the possible mechanisms of nanowire-drug combination induced enhanced neuroprotection is not known and currently being investigated in our laboratory. references 1. emerich df, thanos cg. the pinpoint promise of nanoparticle-based drug delivery and molecular diagnosis. biomol eng. 2006 jun 10; [epub ahead of print] pmid: 16843058. 2. sharma hs, skottner a, lundstedt t, flardh m, wiklund l. neuroprotective effects of melanocortins in experimental spinal cord injury. an experimental study in the rat using topical application of compounds with varying affinity to melanocortin receptors. j neural transm. 2006 apr;113(4):463-76. 3. sharma hs. neuroprotective effects of neurotrophins and melanocortins in spinal cord injury: an experimental study in the rat using pharmacological and morphological approaches. ann n y acad sci. 2005 aug;1053:407-21. 4. sharma hs. pathophysiology of blood-spinal cord barrier in traumatic injury and repair. curr pharm des. 2005;11(11):1353-89. review. a new paradigm for neuroprotection and neuroplasticity in tbi – pleiotropic and multimodal drugs dafin f. muresanu professor of neurology, chairman department of neurology, dean of faculty of health sciences; university of medicine and pharmacy “iuliu hatieganu”, cluj-napoca, romania; secretary general of the society for the study of neuroprotection and neuroplasticity every lesion in the nervous system triggers in the first minute an endogenous neuroprotective reaction. an endogenous repair process, known as neuroplasticity follows this as a second answer. these two processes are initiated and regulated by selected abstracts romanian neurosurgery vol. xv nr. 2 35 neurotrophic factors. neurotrophic factors are produced by different players in the brain tissue and are acting in a pleotropic way against pathological cascades. the same molecules, due to a complex genetically regulated process, are able to induce immediately after achieving the endogenous neuroprotective effect, neuroplasticity, so, they have also not only pleotropic activity but also multimodal way. neuroprotection and neuroplasticity, processes that are apparently independent, with different control, represent in fact two sequences of the same process. therefore, they are attractive candidates as therapeutic agents in most important neurological disorders, including tbi and we already have positive clinical data proving this. there is always a crosstalk between neuroprotective mechanisms and brain edema development. the only available drug nowadays containing active fragments of neurotrophic factors is cerebrolysin. central nervous system edema, neurotrophic factors and neuroprotection bogdan o. popescu laboratory of molecular medicine, “victor babeş” national institute of pathology, spl. independenţei 99-101, sector 5, 050096, bucharest, romania. department of neurology, university hospital bucharest, ‘carol davila’ university of medicine and pharmacy bucharest, spl. independenţei 169, sector 5, 050098, bucharest, romania. central nervous system (cns) edema is a deleterious complication of impacting and lifethreatening neurological diseases, such as brain and spinal cord trauma, stroke or tumor. based on pathophysiological criteria, cns edema occurring in neurological diseases is currently classified as cytotoxic, when blood brain barrier (bbb) remains intact and water swell cells, and vasogenic, when fluid accumulates into the extracellular space due to breakdown of bbb. cns edema causes an increase in the volume of affected tissue and results in a supplemental neuronal death if persists long enough. therefore, the treatment of cns edema is of crucial importance and identification of new therapeutic targets for cns edema is in the current focus of neuroscience research. current treatment is based on administration of diuretics and corticosteroids, with uncertain results estimated by evidence based methodology. however, in cns trauma, tumor and stroke numerous studies show a dysregulation of trophic factors transcription. moreover, specific actions of neurotrophic factors on cns edema are already documented, such as an exacerbating effect of vascular endothelial growth factor (vegf) and an alleviating effect of pigment epithelium-derived factor (pedf). this review focuses on mechanisms of signaling by different types of neurotrophines, on changes in gene expression in both acute and subacute phases of brain and spinal cord stroke, trauma and tumor, and on the therapeutic potential of growth factors and growth factor-like peptides. neuroregeneration in spinal cord injury : theory and surgical practice st.m. iencean1, n. ianovici1, a.v. ciurea2 1neurosurgery, emergency clinical hospital “n. oblu”, iasi 21st neurosurgical clinic, clinical hospital ‘bagdasar-arseni’, bucharest the mechanisms of a spinal cord injury must be considered as a multi-step cascade in which the primary lesion [direct mechanical disruption or cotusion of nerve tracts] is progressively extended of the secondary damage. today only the decompression and administration of high doses of steroids are used. a future efficient treatment in spinal cord lesions must combine four main approaches: -replacement of damaged neural tissue of tissue or cell transplantation, selected abstracts romanian neurosurgery vol. xv nr. 2 36 -providing growth-stimulating factors (neurotrophic factors), -blocking factors which inhibit neural regeneration and -modulation of inflammatory response following spinal cord injury. we present our experience of seven patients with spinal cord injuries and the results of the microsurgical resection of the spinal scar and the implant of bonemarrow tissue in the site of the spinal cord lesion. methods seven patients with chronic thoracic spinal cord injury and paraplegia underwent a laminectomy to expose the site of the spinal cord injury and partial resection of the medular scar and implant of bonemarrow tissue with a mixture of drugs in the site of spinal cord injury. ethical approval was obtained from the ethical committee of hospital. results sensory improvements were noticed to all patients, but no significant motor improvements were observed twelve to eighteen months afterwards. at one patient with t10-t11 complete spinal cord injury five years earlier the ressult was at two years: complete sensory recovery, return of sensation of passive legs movements, return of bladder control and return of both patellar reflex. conclusions this surgical procedure consist of microsurgical remove of the spinal cord scar and implanting of the bone-marrow tissue into the spinal cord injury site.the bone-marrow tissue transplantation procedure has no complications. scar reduction make the post – injury scar more permeable to neuronal axons attempting to regrow through the injury site. these results are promising, but much follow-up work is needed to document long-term benefits. new trends and perspectives in neurosurgery peter m. black, md, phd franc d. ingraham professor of neurosurgery, harvard medical school, boston, usa neurosurgery is an evolving field with very exciting frontiers. i will discuss the use of new energy systems for destroying tumors, local application of chemotherapy, image-guided surgery and robotics and new and exciting developments in the field. concerning novel energy systems, laser hyperthermia and focused ultrasound systems may radically change some therapies for tumors especially for focal tumors of low-grade. in malignant tumors we have been able to demonstrate that local application of anti growth factor molecules such as gleevec and antiangiogenic molecules such as endostatin, pex and pf4 can be a potent local therapeutic agents. stem cells can also be important therapeutic agents. imageguided neurosurgery includes intraoperative imaging and robotics. this develops the concept of the neurosurgeon as local oncologist, which is a potentially important idea for future chemotherapy. predictive outcome factors in intracranial aneurysm prof. a.v. ciurea1, m.d, a. tascu1, md, a. iliescu1, md, a. chefneux2, md, n. dima 2, md, d. popiel 2, r. rizea1, md, f. brehar1, md 11st neurosurgical clinic, 2neuroradiology department clinical hospital ‘bagdasar-arseni’, bucharest, neurosurgical department keywords: intracranian aneurysms, neuroprotection, neuroplasticity, neurorehabilitation subarachnoid hemorrhage, hunt & hess scale, 3d ct angiography microsurgery, embolization, rebleeding, vasospasm, nimotop, 3h therapy, fischer scale, guglielmi detachable coils (gdc), glasgow outcome scale (gos) background the intracranial aneurysm (i.a.) represent a prevalence between 0,2-7,9% in the literature data. the variability depends of hospital referral, neuroimaging selected abstracts romanian neurosurgery vol. xv nr. 2 37 findings and autopsy pattern. the pathology of i.a. is a dominant element in neurological and neurosurgical activity, because of multiple preoperatory and management problems. ia affected prepoderently the active age (40 and 60 years old) and the male sex. the cerebral circulation must be evaluated in totality and aneurysms in particular and the accuracy management is necessary for limitation of important lifethreatring complication (rebleeding and ischemic stroke). therapeutical solution: early neurosurgical approach or endovascular aneurysm obliteration. actually the 3n therapies (neuroprotection, neuroplasticity, neuroregeneration) represent an important steps to improve the global outcome in cerebral vascular aneurysm. material & methods the authors present a study about 528 consecutive operated patients with i.a., operated in first neurosurgical department between 1996-2007 – 12 years (34 children and 494 adults). most cases (240 cases-45,5%) were between 41 and 50 years old. the predominant sex is male 359 cases (68%) (2,1: 1). the symptoms were dominated by: headache (98%), stiffneck (94%) and focal neurologic deficit (91%). most patients were hunt and hess 2 (194 cases, 36,7%), hunt and hess 3 (81 cases, 15,3%) at admition. the associated pathology was: systemic arterial hipertension (396 cases, 75%) and obesity/hypercolesterolemia (180 cases, 34,1%), ischemic cardiopathy (85 cases,16,1%), diabetus melitus (85 cases,16,1%), chronic alcoholism (69 cases,13%), ischemic stroke (63 cases,12%), atrial fibrilation (53 cases, 10%), miscellanea (74 cases, 14%, e.g. anticoagulant therapy). the main investigations were: ct scan, ds angiography. actually, the most important and non invasive is 3d ct angiography. the common localization of intracranial aneurysms was the anterior communicating artery 178 cases (33,7 %); the other locations were: medium cerebral artery 157 cases (29,7%), posterior comunicating artery 95 cases (18%), internal carotid artery 70 cases, (13,3%), basilar top 18 cases (3,4%) and vertebral artery 10 cases (1,9%). multiple aneurysm represent in our data 45 cases (8,5%). all cases were operated, as soon as possible after onset of the subarachnoid hemorrhage (sah) and ia angiography diagnosis. “early surgery” eliminates the risk of re-bleeding and facilities the treatment of vasospasm which peak is between 6-8 days post sah. from all complications two are very critical for life and morbidity: aneurysm rebleeding and cerebral ischemia. the therapeutical operative measures for intraoperatory aneurysm rupture prevention are: mild hyperventilation (pac02 30-35 mmhg); elevation of the head; deliberate hypotension; temporary clip. the most important intraoperatory aneurysms surgery is the perfect microsurgical approach which realized the perfect aneurysm dissection with all perforates, collaterals and magistral arteries; the clip application on the aneurysm neck is the surgical procedure to cure the vascular malformation (gold standard aneurysm obliteration). also as intraoperative neuroprotective measures for vasospasm prevention we mention: local papaverine solution administration and abundant saline water washing. during postoperative period we noticed the following complications: vasospasm, obstructive hydrocephalus, seizures, cerebral edema, and general complications, in connection with associated pathology. the following neuroprotective measures for postoperative complications preventions are: 3h therapy (hypertensive therapy, hypervolemic, hemodilution). nimotop therapy could be used in preoperative period also, for cerebral ischemia prevention. (3-7 ml/h depends on arterial systemic pressure), but 3h therapy could be applied with maximum efficiency only in postoperative period (after aneurysm clipping). the glasgow outcome scale (gos) in our data (at 1 months postoperator) shows: good recovery 353 cases (66.8%), moderate disability 125 cases (23.7%), severe disability 26 cases (4.9%), persistent vegetative state 6 cases (1.1%), death 18 cases (3.4%). selected abstracts romanian neurosurgery vol. xv nr. 2 38 actually, an important number of ia will be treated by endovascular embolization. the guglielmi detachable coils (gdc) represent an electrolytically detachable platinum coils placed via endovascular techniques. this gdc is a perfect therapeutic solution for vertebro-basilar aneurysm in which the open microsurgical approach is difficult. our experience in 1st neurosurgical dpt. consist in 33 cases of embolization (1 case, two times embolization). also in this procedure appears many complication: aneurysm rupture, cerebral ischemia, neurological deficit and consciousness status modification. conclusions ia represents an important neurological and neurosurgical challenge. also i.a. by the rupture and complication is the real lifethreatering diseases. complete vascular exclusion is the treatment of choice by open microsurgical approach or endovascular embolization. the important measures to avoid rebleeding and cerebral ischemic stroke in intracranial aneurysms are perfect evaluation and early approach, perfect aneurysm dissection and neuroprotective measures (pre, intra and postoperatory). neuroprotective agents – useful to avoid cerebral ischemic stroke the timing of aneurysm surgery is one of the key of avoidance lifethreatring complication. in our data predictive outcome factors remains patient age, associated pathology, seize and volume of aneurysm, the grade of sah with or without ventricular invasion (fischer scale), time between rupture and hospital icu admition with all neurovascular facilities. 667 cerebral aneurysms: changes of treatment between 1990 and 2004 uwe kehler1, bernd eckert2, martin brunken1 1dept. of neurosurgery, asklepios klinik altona, hamburg, germany 2neuroradiology, asklepios klinik altona, hamburg, germany in the last years coiling of aneurysms gained more importance. however, clipping is still in many cases the treatment of choice. this study shows changes in aneurysm treatment in the last 15 years and compares results of coiling and clipping. methods aneurysm treatments (n= 667) between 1990 and 2004 were analyzed. treatment modalities (clip or coil) were compared in respect of clinical presentation, outcome, aneurysm-localisation, duration of intervention, rebleeding and reperfusion. results in the years from 1990 to 2004 667 aneurysms were treated: 432 were clipped, 235 were coiled. in the first 5 years of this period all aneurysms were operated upon, whereas in the last 5 years only 26% were operated upon. the posterior circulation was the domain of posterior circulation, in the acoa and acm localisation surgery had a light dominance. no difference between clipped or coiled aneurysms was found for initial clinical presentation (hunt and hess) and outcome (gos). however, in the last years clipping for patients with h and h 4/5 was dramatically reduced. in 3480 post-surgical patient-years 6 reruptures and one re-perfusion of clipped aneurysms occurred, respective in 345 patient-years no re-rupture and 22 reperfusions for coiled aneurysms. the duration of intervention was significantly shorter for coiling than of surgery. discussions coiling developed fast in the last 15 years. however, each individual case should be discussed to find the best therapeutic option. depending of the situation coiling or clipping could be advantageous. therefore coiling and clipping should not be regarded as competitive but as complementary. a neurovascular centre should have both therapeutic options available. selected abstracts romanian neurosurgery vol. xv nr. 2 39 surgical management of aneurismal subarachnoid hemorrhage in 308 patients with anterior circulation aneurysms i.st. florian1, z. andrasoni2, c. popa2, c. matei2 1university of medicine and pharmacy iuliu hatieganu clujnapoca, cluj county emergency hospital, neurosurgical department, 2cluj county emergency hospital, neurosurgical department there is still an on-going debate concerning whether neuroradiologic or open-surgery approaches should be used as “best choice” in the treatment of aneurismal subarachnoid hemorrhage. we designed a retrospective study regarding the indications, the results, and the features of our series of 308 patients who underwent open-surgery for ruptured anterior circulation aneurysms between 1997 and 2008. the main objective was to determine the value of the surgical treatment and especially that of early surgery. all cases underwent open surgery, in 96% of the cases definitive clipping was achieved. the results were evaluated using gos at discharge, comparing these with the clinical findings at admission. in our series of patients with hunt & hess grade i and ii, 88,4% had good outcome and 7,2% died. the patients with hunt & hess grade iv and v underwent early surgery in as many cases as possible with the following results: 63% of the patients survived, from which 34% had good results. the outcome depended on preoperative clinic state of the patients, age, the localization and morphology of the aneurysm, unruptured associated aneurysms and associated diseases. all in all open-surgery and especially early opensurgery remains a viable option in the treatment of aneurismal sah. our experience with ruptured aneurysms surgery in difficult for coiling cases ion poeata, ziyad faiyad, m. rotar, m. ivanov, n. dobrin, al. chiriac keywords: intracranian aneurysm, clipping, coiling, endovascular, microsurgical the objective of this study is to analyze the aneurysmal cases difficult for coiling in a consecutive series of 620 ruptured aneurysms clipped. the difficult for coiling cases analyzed were: small aneurysm – preaneurysmal ruptured lesions, ruptured complex aneurysms with arterial branch arising from aneurymal bag, large neck aneurysms. we retrospectively analyze the aneurysms difficult for coiling. preop images: ct, angiography (catheterism, ct, mri), 3-d preoperative planning – virtual surgery, intraoperative recordings, and outcome were analyzed. endovascular is a continuously developing technique and new types of coils, materials, and combination of stent and embolization maybe will improve the possibilities of this technique with the above mentioned lesions. microsurgical technique, new clips, wrapping materials, and anastomotic possibilities on the other hand are expected also to improve the results with difficult aneurysms. in this presentation we emphasize video aspects of aneurysms difficult for coiling and our surgical strategies in these cases. selected abstracts romanian neurosurgery vol. xv nr. 2 40 supraorbital approach in surgical treatment of anterior circulation cerebral aneurysms prof. gr. zapuhlih, v. andronachi, v. chirita department of neurosurgery, institute of neurology and neurosurgery, chişinau, republic of moldova background we report our experience with the minimally invasive supraorbital approach to the aneurysms of ipsilateral anterior cerebral circulation. methods 113 patients were operated in our clinic between 2000 – 2007, with age range from 17 to 74 years, 93 % with acute subarachnoid hemorrhage. supraorbital keyhole approach was used in last 16 patients with 18 aneurysms: ccoa – 9, ica – 8, cma – 1 as well as 9 patients with acute sah, 7 in the “cold” period. positive diagnosis was established using clinical and anamnesis data, cerebral ct scan, cerebral angiography and, recently introduced, ct scan angiography with digital substraction. results in all 16 cases surgery was successful. 5 cases with intraoperative rupture were solved by proximal control. all patients were discharged in relatively good condition. conclusions implementations and use of new methods of diagnosis of cerebral vascular pathology such as ct scan angiography have lead to better planning and more precise surgical approach of cerebral aneurysms. development of microsurgical techniques with tendency of minimalization of surgical trauma allow the use of microsurgical supraorbital anatomy for surgical treatment of supratentorial aneurysms in “cold” period and in noncomplicated hemorrhagic period in patients with relatively good condition with good postoperative and cosmetic results. neuroendovascular steps in iasi medical center n. dobrin1, a. chiriac1, i. poeata1, patrick courtheoux2, m. rotar3 1spitalul clinic "nicolae oblu" iasi, 2chu-caen, france, 3institutul de cardiologie iasi the endovascular treatment for cranial and spinal lesions started in iasi medical center with a team composed of both neurosurgeons and cardiologists from university of medicine and pharmacy “gr. t. popa” iasi, romania working under the coordination of professor patrick courteoux (neuroradiologist from chu-caen, france)wich have realized the first steps in november 2004. they began with implementing a stent for the exclusion of an aneurysm of the basilar trunk, a partial embolisation of a spetzer v parietal left avm and an embolisation of an important parietal left meningioma (en plaque). we propose to present our experience and some intreresting cases solved in our clinic. multiple cerebral aneurysms localized in front division of willis ‘s circle: the surgical treatment of the 103 patients in acute period of subarachnoid hemorrhage v.v. krylov1, r.a. karamyshev1, n.v. hutornoy1, v.g. dashian2 1sklifosovsky emergency care institute, moscow, russia 2medical stomathology university of moscow, chair of neurosurgery and neurocritical care, moscow, russia were analyzed the results of the surgical treatment of the 103 patients with 222 aneurysms and sah from january 1992 till december 2007 in our hospital. 88 patients had two aneurysms, 14 patients 3 and 1 patient 4 aneurysms. the initial clinical condition was: i-8% of patients; ii-54%; iii-33,1%; iv-4% and v-0,9%. selected abstracts romanian neurosurgery vol. xv nr. 2 41 in all cases was used unilateral pterional approach and, if it is possible, single-stage clipping of all ma. for correct location of the ruptured aneurysm and choose the side of the approach was successfully used combined analysis of results of ct, eeg and ca. 97% of aneurysms were clipped, 3% were wrapped or not clipped. results and discussion patients with ma, localized in front division of willis’s circle, were presented in 11% of all patients with intracranial aneurysm. the results of the surgical treatment were: i-ii 71,1% of patients; iii-7%; iv-0,9% and mortality 21%. the severity condition of patients and the intensity of cerebral ischemia before the surgical treatment correlated with poor outcome after the surgical treatment. conclusion the surgical treatment of patients with ma in acute period of sah is the best management, because only the surgical treatment gives the good chance for fully clipping of aneurysms, good possibility to detect and to stop intraoperative aneurysmal bleeding and evacuate clots from basal cisterns for the prophylaxis of vasospasm. before the surgical treatment is very important to detect all factors of risk: severity condition of patients and the intensity of cerebral ischemia surgical treatment of basilar artery apex aneurysms: review of a 26-year experience l. dănăilă, c. toader, fl. ştefănescu, c. tancu neurosurgical department, national institute of neurology and neurovascular diseases, bucharest, românia keywords: basilar aneurysms, subarachnoid hemorrhage, pterional approach, subtemporal approach background the surgical treatment of basilar artery apex aneurysms (baa) represents a technical challenge for the practicing neurosurgeon. many of these aneurysms are currently treated by endovascular techniques, but complex baa frequently fail endovascular treatment. we report our experience and try to provide information regarding the expected clinical outcomes and sources of morbidity in surgical management of basilar apex aneurysms. method we conducted a retrospective study of 119 patients with baa surgically treated in our institution in the last 26 years. the preoperative clinical presentation, computed tomography (ct) and angiographic characteristics of the patients and the surgical approach were analysed in relation with the clinical outcome. clinical grading using the modified glasgow outcome scale (gos) was conducted at the time of hospital discharge and for 85% of the surviving patients at 6 months after surgery. results the patients with baa represented 4,75% of the patients with cerebral aneurysms operated in this period. only 80,5% of cases presented with subarachnoid hemorrhage. in 5 patients (4,20%) the angiography revealed a giant aneurysm and in 17 patients (14,28%) an aneurysm of large size (1,75-2,5 cm). in 73% of the cases we used a pterional transsylvian approach and in 27% a subtemporal approach. the temporary clipping was rarely used. good outcomes (mgos scores of i or ii) were achieved in 78,15% of the patients (93 cases) at the time of discharge and in 88,23% of the patients (105 cases) at 6 months after surgery. seven patients (5,88%) had a poor outcome and 7 patients died (5,88%). there was no incidence of postoperative subarachnoid hemorrhage. residual aneurysm was revealed by postoperative angiography in 3,3% of the cases. factors found to be statistically linked to poor outcome included poor admission status (hunt and hess grades iv and v), symptoms attributable to brain stem compression, patient age older than 65 years, computed tomographic demonstration of thick basal cistern clot and aneurysm size greater than 20 mm. selected abstracts romanian neurosurgery vol. xv nr. 2 42 conclusion the data presented suggest that, in “experienced hands”, surgical clipping should be still considered an important component of a multimodality approach to the treatment of patients with basilar apex aneurysms. endoscopic third ventriculostomy (etv) in communicating hydrocephalus uwe kehler, martin brunken department of neurosurgery, asklepios klinik altona, hamburg, germany etv is safe, restores physiological csf circulation, has fewer complications in the long term run, and is cheaper than ventriculo-peritoneal shunting. therefore hydrocephalus types suitable for etv should be detected to avoid unnecessary shunts. etv is generally accepted for obstructive hydrocephalus especially for aqueductal stenosis, whereas communicating hydrocephalus (commh) is considered as contraindication. however, we describe a subtype of commh with free communication between the ventricles and subarachnoid space but with infratentorial intracisternal obstructions suitable for etv. methods infratentorial intracisternal obstructive hydrocephalus (infinoh) shows in mri a downward bulged floor of the third ventricle and a discrepancy of sizes between the great and prepontine cistern. we have detected 26 hydrocephalic patients with these mri patterns and analyzed clinical outcome after etv as well as shunt independence. patients with follow-up of less than 3 months were excluded; follow-up was terminated, when shunting was necessary. in 3 cases intrathecal gadolineum was administered to demonstrate directly the intracisternal obstruction. results we could analyze 22 patients with medium follow up of 17 months (0-126 months). symptoms were consistent with chronic hydrocephalus. ten cases were classified as idiopathic normal pressure hydrocephalus due to symptoms and history. mris with inthecal gadolineum showed a retarded passage into the supratentorial subarachnoid space. fourteen of 22 patients (64%) showed a clinical improvement after etv and remained shunt-free. discussion the success-rate of 64% supports the theory of infinoh. further mri and pathophysiological studies should help in detecting this hydrocephalus subtype. in consequence patients´ selection for etv should be improved. the need of a programmable gravitational valve for hydrocephalus treatment uwe kehler, niels langer, department of neurosurgery, asklepios klinik altona, hamburg, germany hydrocephalus shunting may be complicated by overor underdrainage. gravitational driven shunt assistants (sa) could reduce but by far not exclude overdrainage. an analysis is done to improve the choice of valve and gravity device settings. methods icp in patients with ventriculo-peritoneal shunts can be calculated with the following equation: icp = valve opening pressure – hydrostatic pressure difference (hpd) + setting of sa + intra-abdominal pressure (iap). for horizontal and vertical position different valve and gravity device settings were calculated to reach physiological icp (in horizontal position around 5-10 cmh2o and in vertical position around 0 to-5 cmh2o). results to reach physiological icp in horizontal and vertical position a differential valve is not necessary, a solely selected abstracts romanian neurosurgery vol. xv nr. 2 43 gravity device is sufficient: example: patient, 180cm height, 80 kg (hdp: 40 cm; est. iap: 5 cmh20): with a solely sa of 30 cmh2o, icp results for vertical position in -5cmh2o and for horizontal position in 5 cmh2o. however, hdp changes in growing (pediatric) patients and iap changes with weight, constipation, gravidity and in different body positions in a manner difficult to predict. these variations might result in unacceptable icps and may cause overor underdrainage. discussion differential valves are not necessary for hydrocephalus shunting if gravity assisted devices like a shunt assistant is present. to cope with the variables and the unpredictable iap, programmable gravity devices are necessary to avoid improper csf drainage. the newly designed programmable shunt assistant “prosa” has to show in clinical trials how realistic these advantages are. late complications of myelomeningocele (mmc) prof j.c. marchal neurochirurgie pédiatrique, département de neurochirurgie, hôpital central, nancy, france “the least afflicted children are the most vulnerable, as they have more function which may be further impaired.” fred epstein nowadays the refinements of appropriate and multidisciplinary management of mmc lead to a longer lasting life expectancy. that is why it is of real interest to focus on the factors affecting both the late functional and vital outcomes and the means to prevent them. we have pointed out 5 groups of factors: hydrocephalus: 25% amongst the newborns are presenting with hydrocephalus. amongst the remaining: 75% will develop a ventricle enlargement and 80-90% will require a shunt placement. there are multiple causes of late neurological deteriorations: acii malformation, hydromyelia, secondary tethering, associated spinal cord abnormalities, lumbar canal stenosis. they are often intermingled and the usual problem is to deal with the pathological conditions consistent with the symptoms. the general outcome is affected by specific complications: epilepsy: 25%, metabolic syndrome: 55% in teenagers, scoliosis: affects many patients amongst them 2.5% require surgery the prevalence of latex sensitisation and allergy in mmc population goes up to 29-72% and clinical allergy to15% (anaphylactic reaction). in the literature the mortality rate depends upon the authors: 2,4% → 24%. the main causes are: shunt malfunction/infection, renal scarring and urinary sepsis, bulbar failure to conclude we emphasize the general conditions affecting the physical function and occupation, the cognitive and psychological function: on the one hand the level of the mmc (below or above l1), on the other hand the number of shunt revisions. supine position for posterior cranial fossa surgery: a feasibility study uwe kehler, senol jadik, dept. of neurosurgery, asklepios klinik altona, hamburg, germany we report our results and experience of posterior fossa surgery performed in supine position as an alternative to semi-sitting or prone position to prevent hemodynamically relevant air embolism. methods sixty patients were operated upon posterior cranial fossa lesions in supine position between 2005 and 2007. the head was rotated 40-60° to the opposite side. surgery was performed for 15 trigeminal neuralgias, 11 acoustic neuromas, 25 diverse cpatumours and 9 cerebellar hematomas. five neurosurgeons skilled with semi-sitting and prone selected abstracts romanian neurosurgery vol. xv nr. 2 44 position performed the surgeries in supine position and reported their experience, pros and cons. results in all cases supine position offered good access to the lesion. no permanent morbidity or mortality happened related to the supine position. there is no need for preoperative transesophageal echocardiography examination (tee) and for intraoperative air embolism monitoring, simplifying the patients preparation for surgery. advantages reported are: less retraction due to gravity promoted cerebellar descent; gravity promoted drainage of blood and cerebrospinal fluid like in semi-sitting position; faster patient’s positioning than in semi-sitting or prone position; no hemo-dynamically relevant arterial blood pressure decrease and heart rate increase related to body/head elevation; less swelling compared to prone position. disadvantages reported: less ergonomically situation of the surgeon compared to prone position; no access to cranio-cervical junction and medially located posterior fossa lesions, and limitations due to rigid necks and high shoulders. conclusions supine position for surgery of posterior cranial fossa lesions is in most cases good feasible. it is fast in patient's positioning and combines the advantages of the semi-sitting and prone position, reducing unanimously the disadvantages, so it is in well indicated cases superior to the semi-sitting or prone position. deep brain micropotential recordings in parkinson disease surgery jean ciurea, a. rasina clinical emerg. hosp. “bagdasar-arseni” bucuresti introduction implantation of subthalamic nucleus (stn) deep brain stimulator (dbs) electrodes is a recognized and effective method for parkinsonian patients. also it has been proved that microelectode brain activities recording and analysis (mer) is beneficial, it remains unclear at what extent it improve the clinical efficacy. method a total of ten patients with parkinson disease were implanted in the last 4 year. all implantations were based on mr images fused in different environments. mer were performed in all, initially by leadpoint and latter by guideline fhs. direct target calculation, framelink coordinates and mer were employed. mer defined the stn boundaries along one or more parallel tracks. micro and macrostimulation were used for final implantation decision. results since the microelectrods inbetween distance is of 1 mm, we encountered a difference of less of 1 mm when all above mentioned methods were used. all patients presented a clinical improvement after surgery. discussions the maximum available number of track is 5. this is an invasive alternative. we used maximum 4 tracks in only one case and 2 or 3 in most cases. based on symmetry, there were used only one track for the opposite side electrode implantation in most cases. the final placement of the stimulation electrode decision is still under debate in literature. there are minor adjustments in electrodes trajectory which are analyzed. conclusion mer is optional, but its use can offer more accuracy for dbs implantation technique. selected abstracts romanian neurosurgery vol. xv nr. 2 45 endoscopical treatment of pineal region tumors prof. dr. grigore zapuhlih, dr. r. safta departemnt of neurosurgery, institute of neurology and neurosurgery of moldova objective tumors of the pineal region represent a diverse collection of tumors with a variety of natural histories. the authors evaluate their results in the management of patients with tumors in the pineal region methods this is a retrospective clinical evaluation of 14 patients with primary tumors of the pineal region treated by microsurgery and endoscopy. there were 5 pineocytoma, 4 pineoblastomas, 3 low-grade gliomas, one germinoma and one teratoma. there were 8 male and 6 female patients. their median age was 15.5 years (range 3-49 years). in 1 case the endoscopic procedure represented the only surgical treatment (with total removal of a pineocytoma). in 13 cases, microsurgical removal of the lesions and/or etv or ventriculo-peritoneal shunts placement were performed for the management of hydrocephalus. results all neoplasms were treated surgically with good results. the etvc was successfully performed without complication in 5 patients and a ventriculoperitoneal shunt was done in four. a total tumor removal was achieved in 9 operations, subtotal in 4 and partial in 1. conclusions early surgical resection combined with etv or diversion of cerebrospinal fluid is effective in the treatment of pineal lesions. the endoscopic management of patients with pineal region tumors affords a minimally invasive way to obtain resolution of obstructive hydrocephalus by endoscopic third ventriculostomy (etv and tissue diagnosis) and sometimes can be an only surgical treatment. when a direct microsurgical approach is indicated, the choice among the surgical approaches depends on the size and the location of the lesion in the pineal area and its relation to the ventricular system. intraoperative thermography in patients with malignant brain tumours first results of an ongoing study wendt u, fässler a, hebecker r, piek j abteilung für neurochirurgie, chirurgische universitätsklinik rostock, germany objective the current study was designed to find out whether differences in brain surface temperature may serve as a useful adjunct to current methods of neuronavigation. methods in 17 patients (age 30 82 years) with various supratentorial malignancies (8 glioblastomas, 8 metastases, 1 lymphoma) surface temperatures of the tumour itself as well as of the surrounding brain were studied by means of intraoperative thermography (thermacam b20, flir systems, frankfurt). results differencies in mean surface temperature (up to 5.1 c) were detected in 16 of the 17 patients studied. in 11 patients tumour temperatures were lower (range 24.2 31.7 c; mean 28,4 c), in 5 patients higher (range 28.9 35.1 c; mean 32.3 c) as compared to healthy surrounding brain tissue. while most metastases had a lower temperature as compared to the surrounding tissue, glioblastomas showed an equal distribution of "hot" and "cold" tumours. temperature within the individual tumour also varied remarkably. the usual pattern observed in "cold" tumours was that of the lowest temperature in the tumour center whereas in "hot" tumours the center had the highest temperature. selected abstracts romanian neurosurgery vol. xv nr. 2 46 conclusions from the first results of our 17 patients in this ongoing study we can conclude that remarkable temperature differences exist when comparing intracranial malignancies with normal brain tissue. further studies may show whether these differencies can be utilized as an intraoperative adjunct to conventional neuronavigation. acknowledgement: parts of this study were supported by the else kröner-fresenius-stiftung. regional distribution of brain surface temperature of healthy brain tissue in patients with brain tumours methods of measurement and first results fässler a, wendt u, hebecker r, piek j abteilung für neurochirurgie, chirurgische universitätsklinik rostock objective the present study was designed to determine brain surface temperature in "normal" brains in order to get reference values when applying intraoperative thermography to various pathologies with the longdistance aim to integrate thermography into cranial navigation. methods in 25 patients with various supratentorial malignancies brain surface temperatures in a distance of at least 2 cm from the tumour was measured by means of intraoperative thermography. a conventional thermograpic camera (thermacam b20, flir systems, frankfurt) with an accuracy of 0.1 k and a resolution of 540 x 480 pixels was used for this purpose. room temperature and body core temperature was parallely determined in this ongoing study. results under general anaesthesia body core temperatures of the patients were remained quite constant (35.7 +/ 0.61 c). surprisingly a very heterogenous interand intraindividual distribution of brain surface temperatures was observed. minimal temperatures were 28.7 +/4.8 c, maximal temperatures 32.5 +/3.7 c. regional differences were as high as 7.8 c in the individual patient. conclusions brain surface temperatures vary extremely in peritumoral brain tissue and show an inhomogenous distribution. the reason for this phenomenon up to now cannot be explained. regional inhomogenities in blood flow may be responsible for this phenomenon. further studies in other pathologies (decompressive craniectomy, aneurysm surgery, basal meningeomas) are on the way to create hypotheses which might explain the results obtained. mayxbe additional parameters (local cbf, local po2) are needed to clarify the points mentioned above. acknowledgement: parts of this study were supported by the else kröner-fresenius-stiftung. functional magnetic resonance imaging (fmri), diffusion tensor imaging (dti) and tractography in neurosurgery d.a verganelakis1, g.m peristeris1, e.d. gotsis1, p.a toulas1, i.z. kapsalakis2, s. giannakodimos2, k. fountas3, h. gogos4 1encephalos – euromedica, rizariou 3, halandri, attiki 152 33, greece, 2general state hospital “g. genimatas”, mesogion, athens, greece, 3university hospital of larissa, greece, 4general hospital iasso, holargos, attiki, greece purpose functional magnetic resonance imaging (fmri) and diffusion tensor imaging (dti) are relatively new tools that can facilitate a successful neurosurgery planning in numerous pathological cns’ cases. fmri can help in: determining the dominant hemisphere for selected abstracts romanian neurosurgery vol. xv nr. 2 47 the surgery of epilepsy; pre-surgical control by determining the spatial correlation of centers responsible for speech, motion, vision etc with respect to the lesion; surgical planning for maximizing the tumor tissue removal, while minimizing the postsurgical functional deficit; the plasticity in ischemics, e.t.c. dti can give a more detailed picture of pathological neural deficiencies by providing qualitatively information, such as fractional anisotropy, as well as quantitatively such as tractography. methods and materials in our prospective study, 24 patients with various types of pathologies, such as epilepsy, gliomas, etc. were examined with fmri and dti. anatomical and functional images were acquired at 1.5 tesla signa hdx system (ge, milwaukee, usa). fmri data was processed off-line with post-acquisition (pa) brainwave (ge) software, while dti was processed with functool (ge). results motor and speech centers were determined and together with mr tractography findings were fused on high resolution 3d images in all patients. multiple paradigms ensured the reproducibility of the fmri results. various cases-examples (shown and discussed here) demonstrate the capabilities of fmri and dti. conclusion the techniques of fmri and dti can picture the functioning of brain as well as its neural fibers, facilitating like this the neurosurgical pre-planning. modern imaging technologies for intracranial lesions horia ples phd, stanca ples, md, constantin costea phd, dan costea md neurosurgical clinic, county hospital timisoara, romania new development in imaging technologies brings for neurosurgeons important preoperative and postoperative prospects for intracranial lesions evaluation.the new mri techniques we currently use in neurosurgical clinic, county hospital timisoara are: dti (diffusion tensor imaging ), cerebral spectroscopy, swi (susceptibility weighted imaging). dti (diffusion tensor imaging)mri techniqueapplication is useful for localising white mater tracts in relation with intracranial lesions, mri spectroscopy – can evaluate intralesional components ( metabolites). offers the opportunity for establishing differential diagnosis (ischemic, inflammatory, tumoral). in tumor pathology it is used to establish tumoral grading. swi (susceptibility weighted imaging)a very new sequence in mri which evaluates magnetic properties of blood, iron and other structures. now it is used for diffuse axonal injuries, micro bleeds, angiogenesis in tumors, venous angiomas ( slow flow vessels). acquisitions are made with 1,5 t mri. we have used in our clinic 16 preoperative spectroscopies, 15 preand postoperative patients having dti, 45 cases using swi: 20 for venous malformation, 10 for trauma – axonal injuries, 10 cases in tumors and arteriovenous malformation pathology. controversis in craniopharingiomas experience of 137 cases children vs adults ( gks included) a.v. ciurea1, a. tascu1, a. iliescu1, virginia rotarascu2, r.e.rizea1, f. brehar1, n.a. gheorghita3, carmen radoslav3 11st clinic of neurosurgery, 2psychology department, 3icu department, neurosugical clinic, “bagdasar arseni” clinical hospital “carol davila” medical school, bucharest, românia keywords: craniopharyngioma (cph), mri, children, adamantinoma, cph scale, recurrences, regrowth, gamma kinfe surgery (gks) objectives craniopharyngiomas (cph) are benign slowgrowing intra-cranial calcified tumors, preponderant in children. cph expand in the pituitary stalk axis, from the sphenoid body to the third ventricle. mri improves the anatomical location, the tumor diagnosis and the selected abstracts romanian neurosurgery vol. xv nr. 2 48 operative strategy. microsurgery represents the main treatment option in spite of major difficulties. the goal of this study is to analyze the outcome of a series of 102 cph cases of pediatric population and 35 cph in adults, treated surgically. methods authors performed a retrospective analysis of 102 consecutive children (0 – 16 year old) and 35 adults with cph diagnosed and operated at the “bagdasararseni” clinical hospital, bucharest, during a period of 17 years (1990 – 2006). in this cohort of children, males were slowly preponderant (54 boys and 48 girls), affecting predominantly the age group 7 – 10 y.o. (41 cases – 40.2%). clinical features consisted of visual impairment (71 cases 69.6%), endocrine dysfunction (83 cases 81.5%) and increased icp syndrome (68 cases 66.6%). visual and endocrine symptoms prevailed. headache, was frequently encountered 88 cases (86.3%). hydrocephalus was present preoperatively in 26 cases (25.5%) and was dealt with vp shunt before definitive tumor therapy in 13 cases (12.7%). the essential neuroimaging findings were ct scan and actually mri. no dsa investigation was carried out routinely. in adults (preponderently 31-40 y.o., 21 cases) main clinical picture was characterized by headache 31 cases (88.5%), visual impairment 28 cases (80%), and endocrine dysfunction 15 cases (42.8%). none of them received radiotherapy and/or stereotactic radiosurgery, before surgical approach. all the cases underwent thorough endocrinological and neurosurgical investigations, preand postoperatively. pathology the adamantinous type was preponderant in children (93 cases-91.3%) and papillary type in adults (31 cases-88.5%). all the cases were followed up during a period going from 6 months to 15 years. in our series, in children, the most frequent location of cph was the suprasellar retrochiasmatic region (75 cases – 73.5%). pathologically, combined forms (cystic forms with calcifications) are prevalent: 55 cases (53.9%). a personal craniopharyngiomas grading scale was presented. in children, surgical approach was adapted to the tumor location: bilateral subfrontal (33 cases–32.4%), unilateral frontal (22 cases-21.6%), and pterional (22 cases–21.6%), followed by midline interhemispheric (17 cases–16.6%), transcallosal (3 cases–2.9%) and combined (5 cases-4.9%). actually, the fronto-lateral and pterional approach were preponderant surgical strategy both in children and adults. in adults, surgical approach was: subfrontal (20 cases-57.1%, subfrontal bilateral 12 cases, 34,3%, unilateral frontal 8 cases, 22,8%), interhemispheric (2 cases-6.3%), pterional (11 cases-31.2%), transcallosal 0 cases, transsphenoidal 2 cases (6.3%), combined approaches 0 cases. results in children: the total removal of the cph was the goal of the surgery, but this was achieved in only 55 cases (54.3%), because of the risk of functional impairment or possible operative mortality. in 9 cases (8.7%) we performed near-total resection, in 34 cases (33.7%) partial resection, and 3 cases (3.3%) were biopsies. we performed biopsy with cyst evacuation only on giant, extremely compressive forms, in which the tumor collapse was accompanied by cardiac bradycardia. hydrocephalus was present in 26 cases (25.5%). no intraoperative death occurred. in the first month, there were 5 deaths (4.9 %), due to hypothalamic injury, in each case total removal having been attempted. the real recurrences occurred in 17 cases from 55 cases of total removal (30%); tumor regrowth was noticed in 35 cases (76.2%) from a total of 46 cases with remnant tumor (near-total, partial and biopsies). in adults series the total removal was achieved in 24 cases (68.5%), near total removal in 4 cases (11.4%), partial in 7 cases (20 %), and no biopsy. no perioperative death in 35 cases cph, operated in adults. recurrences and regrowth occurred in 4 cases (11,4%). selected abstracts romanian neurosurgery vol. xv nr. 2 49 gamma kinfe surgery (gks) was performed in 6 cases in children and 7 cases in adults, all with reccurences, but the results remain disputable because the tumoral chist pression asked a surgical approach. neuropsychological assessments revealed no altered iq at individual level. the intracranial hypertension (icp) and the tumor localization determine attention deficits. extended tumor localization determines the deficient mental control and the apathy. the recidivated tumor determines psychological dysfunction: attention, memory and the orientation. the depression is dependent by age old of the patients and the qol is dependent by the tumor localization. psychosocial reinsertion is affected by memory dysfunction, medium moodiness and the forceless ego. a good rehabilitation recorded in 50%patients who underwent counseling before neurosurgical interventions. conclusions surgical treatment remains the main option, but the important number of complications, regrowths and recurrences prove the necessity of a multidisciplinary approach: microsurgery, radiosurgery and endocrinological treatment. the adamantinomas type was very important in reccurences and regrowths of cph. also, the authors present a cph scale which facilitates the perfect location, surgical approach and outcome in this kind of tumor. invasive pituitary adenoma prof. ibrahim sbeih, mbchb, frcs, frcssn department of neurosurgery, jordan university of science and technology and ibn alhaytham hospital, amman – jordan pituitary adenomas are the third most common intracranial tumor after meningiomas and gliomas. some adenomas are typical but others may be invasive, aggressive, premetastatic or carcinomatous. invasive adenomas can infiltrate bone, dura, nasal sinuses, cranial nerves and venous sinuses. the goal of surgery in the invasive nonsecretory adenomas is gross total resection, followed by radiotherapy, radiosurgery or conservative follow up. in the inasive seretory group, surgery is followed by medical treatment, radiotherapy or radiosurgery. we are presenting our experience with giant invasive pituitary adenoma in the period between 1990 – 2006. 42 patients were encountered: 29 males and 13 females. age of patients ranged from 16 – 68 years with mean age of 36.7 years. main presentation was visual failure and diabetus insipidus. twenty three patients were non secreting adenomas, 12 prolactin secreting, 3 acth and 3 gh secreting. 40 patients needed transcranial and two patients needed trannasal surgical excision. indication of surgery in nonfunctioning adenoma was neurosurgical deterioration. in the secretory group indication was deterioration of neurological condition in spite of medical treatment. transcranial surgery was needed where invasive adenoma extended to posterior, middle or anterior fossa. one preferred surgical approach by us is transbasal subfrontal, among other approaches. the aim of surgery was gross total resection whenever possible. postoperative adjuvant therapy was needed for all patients: radiotherapy in 28 patients, gamma radiosurgery in 6 patients and drug therapy in 6 patients. the dose in gamma knife varying between 14 – 22 gray. follow up in our patients ranged from 20 – 154 months with mean follow up period of 58.2 months. mortality in this series occurred in 2 patients: one patient died of meningitis after major csf leak and one died of pulmonary embolism. no carcinomatous change was seen in any of our patients. we believe that surgical cure is not possible for all invasive secretory and nonsecretory adenomas. invasiveness is an issue decided by radiological, histological, and operative findings. most invasive adenomas are giant ones. selected abstracts romanian neurosurgery vol. xv nr. 2 50 endoscopic and endoscopic assisted transsphenoidal surgery for pituitary adenomas prof. e. knosp vienn, austria endoscopes have been used for transsphenoidal surgery since more than 15 years and become popular meanwhile. because of the confined area and the potential risks for this surgery special training to handle the endoscopes is mandatory. the question arose whether the introduction of endoscopic surgery should be on step wise or not. we followed a 2-step development from microsurgery to endoscopic assisted microsurgery and from endoscopic assisted surgery to pure endoscopic surgery (as step 2) to overcome these problems. we describe the differences of these techniques their goals and compare the results for both techniques. we analysed 127 endoscopic assisted operations and 73 pure endoscopic procedures: in both series we had no mortality, no cerebral complication nor optic nerve lesion. the rate of csf leaks requiring reoperations were more often in the endoscopic assisted series (6 % vs 2,7 % during endoscopic surgery). in 7 % of endoscopic assisted and 8 % in pure endoscopically operated cases we had postoperative diabetes insipitus. the cure rate in the combined series was 70% (no tumor in mri or cure from hypersecretion). in conclusion: endoscopic surgery of the sella and beyond the sella seems to be a promising and challenging future for this technique. the results are comparable and promising, but pure endoscopic surgery, although it seems to be more demanding to begin with, may offer more possibilities. how could we achieve a definitive cure in acromegaly? v. ciubotaru1, irina ogrezeanu1, r. perin1, corin badiu2, c. tanase3, m. coculescu2, a. constantinovici1 13rd neurosurgical department, emergency hospital “prof. dr.bagdasar-arseni”, bucharest 2“c. i. parhon. 3national institute of pathology “victor babes”, bucharest, romania in acromegaly, disease caused by hypersecretion of growth hormone (gh) due to a pituitary adenoma, stringent criterias to define the biochemical remisiion of acromegaly were introduced. transsphenoidal surgery is considered the primary therapeutic option, medical therapy, represented by somatostatin analogs has usually an adjuvant role and because of the high number of side effects, conventional fractioned radiothrapy tends to be replaced by gamma knife radiosurgery. our study presents the two years experience (2006-2008) of the 3rd neurosurgical department, emergency hospital “bagdasar-arseni” on gh-secreting pituitary adenomas with a special aim: to analyse the optimal therapeutic interval to apply medical treatment (somatostatine agonists) as adjuvant therapy to surgery and radiosurgery, based on the conclusions of the most recent analysis of long-term results regarding tumor shrinkage and hormonal effects of gamma knife radiosurgery, that suggested a significant reduction or normalization of hormone secretion obtained only after more than 36 months. suprasellar meningiomas, personal experience in 37 cases prof. ibrahim sbeih, mbchb, frcs, frcssn department of neurosurgery, jordan university of science and technology and ibn alhaytham hospital, amman – jordan introduction suprasellar meningiomas arising from dura mater around tuberculum sellae or diaphragma sellae are rare selected abstracts romanian neurosurgery vol. xv nr. 2 51 tumors constituting 2-6% of all intracranial meningiomas. tumors of these regions can cause insidious visual loss unilaterally or bilaterally. they are challenging lesions because of their close proximity to major neurovascular structures. methods we are presenting our experience with 37 suprasellar meningiomas (30 tuberculum sellae and 7 diaphragma sellae) in the period between 1990 – 2005. there were 27 females with age from 35 – 70 years (mean age of 51 years) and 10 males ranging in age between 29 – 51 years (mean age of 43 years). thirty four patients were operated upon for the first time while 3 patients had previous surgery at other institutions. results the presenting symptoms were mostly visual deterioration (100%). the most common visual fields encountered were unilateral temporal hemianopia in 14/37 patients, and bitemporal hemianopia in 9/37 patients. other presenting symptoms includes bitemporal headache, memory changes, epilepsy and endocrine dysfunction. surgical approaches utilized were interhemispheric transbasal in 32 patients, unilateral subfrontal in 3 patients and unilateral pterional in 2 patients. we achieved gross total resection in 35 patients. subtotal excision was achieved in 2 patients. histopathological studies showed transitional and meningothelial types in most cases. optic canal was involved in 6 patients where deroofing of optic canal was needed. anterior clindectomy was needed in 2 patients only. follow up in our patients ranged from 24-149 months (mean follow up 78 months). three patients only were lost for follow up. results showed improved visual outcome in 20/34, patients unchanged vision in 12/34 and worsening of vision in 2/34 patients. other morbidity included anosmia, csf leak, and temporary diabetus insipidus. there was no mortality encountered in this series. recurrence occurred in one patient 4 years after his initial surgery. conclusion tuberculum sellae and diaphragma sellae meningiomas are rare and challenging lesions. these tumors could and should be totally resected. results of surgical excision depend on microsurgical techniques to preserve blood supply to visual apparatus and minimize surgical insult by delicate handling. this advantage is offered by the interhemispheric transbasal approach which puts the surgeon in total control of neurovascular structures and gives him/her the chance of achieving gross total resection with minimal complications. sellar and parasellar lesions – 30 months retrospective study of a c onsecutive series of 40 cases with microsurgical pterional resection in the era of gamma-knife i. poeata, n. ianovici, ziyad faiyad, m. ivanov, a. chiriac, b. iliescu iasi, românia keywords: sellar, parasellar, pterional, microsurgery objective to analyze the last 30 months series of pterional tumoral resection for sellar and parasellar lesions cases. methods a series of 40 consecutive cases of sellar and parasellar lesions operated during january 1st 2006 – june 31st 2008 is analyzed. we used the following protocol: mri diagnosis, preoperative prednisolone, 25 mg per day, pterional microsurgical approach, prechiasmatic and carotido-optic windows tumoral exposure, supplementary exposure in particular cases, total resection when possible, partial resection with ulterior gamma-knife when preor intraoperative surgical dangers were assessed. microadenomas are not subject of this study being resected trans-sphenoidally. selected abstracts romanian neurosurgery vol. xv nr. 2 52 results the histology consisted of: pituitary adenomas in 24 cases, craniopharyngiomas, 7 cases, meningiomas, 6 cases, metastasis, 2 cases, trigeminal schwannoma, 1 case. sex distribution: 22 males and 18 females with a male to female ratio of 6:1 for craniopharyngiomas, and 6:5 for adenomas. complete surgical removal, mri documented was obtained in 24 cases. in 7 cases small residuals were stable with mri follow-up and no additional treatment was recommended until now. the remaining 9 cases with residual tumor were sent for gamma-knife treatment. the complications documented in this series were: 2 postoperative deaths, one by diencephalic complications and one by trombembolism, 2 meningitis cases cured under antibiotics but with subsequent hydrocephalus requiring dvp in one case, one surgical recurrence, early postoperative diabetes insipidus, in 9 cases, but only 2 remained hormonal substitution dependent. we detail some particular cases in this series: 2 pituitary apoplexy and one case with pituitary adenoma associated with cavernous sinus meningioma. conclusion big or infiltrating parasellar tumors remain difficult surgical cases. the policy of a more conservative microsurgical removal leaving dangerous parts of the tumor for radiotherapy or simply for imagistic follow-up seems to improve the results comparing with previous series. cervical myelopathy – a 5 years retrospective study fl. exergian, m.d., ph.d., n. soare, m.d., m. podea, m.d. spinal surgery department, clinical emergency hospital “bagdasar-arseni”, bucharest surgical treatment of cervical myelopathy is still raising discussions and postoperative results seem not to be constantly positive. the paper analyses all the patients with cervical myelopathy admitted in the spinal surgery department of the emergency hospital “bagdasar-arseni” during the last 5 years. the study is retrospective and refers to 129 patients with symptomatic cervical myelopathy operated on via anterior (diskectomy and/or corpectomy) or/and posterior approaches (laminectomy). the mean age of the patients was 50,1 years with limits between 23 and 79 years. the minimal follow-up was 2 months and the maximal 4 years. the higher incidence was noted at the age group of 40 – 49 years. the cord compression was most frequent at c5-c6 level – 69 patients and c4-c5 level – 47 patients. the study defines the diagnosis criteria for cervical myelopathy, includes considerations on the surgical technique to be adopted and analyses the treatment results. anterior and/or posterior approach for cervical myelopathy st.m. iencean neurosurgery, emergency clinical hospital “n. oblu”, iasi, romania cervical spondylosis affects the vertebral bodies and intervertebral disks of the neck as well as the contents of the spinal canal (nerve roots and/or spinal cord). symptoms of cervical spondylosis may appear in persons as young as 30 years but are found most commonly in individuals aged 40-60 years and radiologic spondylotic changes increase with patient age. cervical spondylotic myelopathy is the most common cause of nontraumatic paraparesis and tetraparesis. 1. indications for surgery include the following: progressive neurologic deficits ; documented compression of the cervical nerve root and/or spinal cord ; intractable pain. 2. the aims of surgery are to relieve pain and selected abstracts romanian neurosurgery vol. xv nr. 2 53 neuronal structured compression, as well as, in select cases, to achieve stabilization. 3. approaches for surgery are anterior or posterior. a. anterior approaches include the following: diskectomy without bone graft; diskectomy with bone graft; cervical instrumentation b. posterior approaches include the following: decompressive laminectomy and foraminotomy; hemilaminectomy ; laminoplasty the results of the surgical treatment of the 70 operated patients for cervical spondylotic myelopathy were analyzed. the posterior approach is accepted as a standard decompression procedure in patients who have more than 3 segments of stenotic changes; fixed local or global kyphosis is a relative contraindication. laminoplasty and its variants preserve the lamina to avoid excessive scar formation and to reduce the incidence of postlaminectomy kyphosis and for the treatment of multilevel csm. laminectomy combined with lateral mass fusion may yield excellent results without progression to spinal instability or kyphosis. the anterior approach is indicated for csm when identifiable anterior compression or kyphotic deformity is present. myelopathy due to osteophytes confined to 1-2 levels is treated using acd and fusion with removal of the osteophytes. in severe cases, extensive decompression is performed using multilevel vertebrectomies (corpectomy) and reconstruction with bone graft and instrumentation. the chances for improvement after surgery for cervical spondylotic myelopathy are approximately 60%. anterior cervical microdiscectomy – 3 years retrospective study of a consecutive series of 68 cases ion poeata, ziyad faiyad, sergiu gaivas, marcel ivanov, bogdan iliescu neurosurgery, emergency clinical hospital “n. oblu”, iasi keywords: cervical, anterior microdiscectomy, fusion, herniation objective to analyze the last 3 years series of anterior microdiscectomy cases without fusion in cervical disk herniation. methods a series of 68 consecutive cases of cervical disk herniation operated by the authors’ surgical team during july 1st 2005 – june 31st 2008 using the above mention technique is analyzed. kerrison and hooks under microsurgical visualization were mostly used to remove soft and hard disk herniations at the canalar and foraminal levels. uncal joints were always preserved. in a few cases a median partial corpectomy was performed to enlarge the visual field and stabilization with a long iliac crest bone graft was performed only in the cases with cervical stenosis at more than 3 levels (2 cases). results in 68 patients 103 herniated cervical disks were resected (8 at c3-c4 level, 14 at c4-c5level, 39 at c5c6 level, 36 c6-c7, and 6 c7-d1). 24 cases presented multiple disk herniations with multiple discectomy (2 disks in 15 cases, 3 disks in 7 cases, and 4 disks in 2 cases). there were 35 males and 33 females, most affected age groups being 50-59 with 27 cases and 4049 with 17 cases, ranging from the youngest at 25 and the oldest patient at 69. some particular cases were observed during this period: a centro-medullary spontaneous hemorrhagic infarction associated with disk herniation (necroptic study in a non-surgical case – early fatal outcome before interventional decision), a traumatic disk herniation, an adjacent cervical level herniation arising 1 year after the first discectomy, and 4 cases of cervical disk herniation in diskopatic patients with history of lumbar disk surgery. as complications we mention transient dysphonia, in 7 cases, and transient brachial paresis in 4 cases, all these deficits completely resolved at 2 months followup. local post-operative hematoma, 3 hours after the closure was rapidly evacuated and the arterial source selected abstracts romanian neurosurgery vol. xv nr. 2 54 coagulated in one case with clinical consequences. the patients were advised to wear cervical orthosis if they feel necessary but that happened in only 7 cases for a period longer than 10 days. at 2 months follow-up no patient presented with signs of cervical instability and none needed the cervical orthesis longer than that. there were no deaths, and no additional permanent deficits in this series. conclusion anterior cervical microdiscectomy without fusion is a safe and relatively quick procedure to solve patients with single or multiple level disk herniation. patients with 4 levels discectomy were fused so we have no experience whether discectomy at more than 3 levels without fusion has any consequences on vertebral stability. however, despite controversies in the literature we didn’t observe signs of persistent cervical vertebral instability in our 66 patients with discectomy at 1 to 3 levels without fusion. microsurgical treatment of lumbosacral radicolopathies substained by lateral recess stenosis trough combined microsurgical root decompression and bacjac interspinous device implant giuseppe gambardella, carmelo pecora, sezione chirurgia vertebro-midollare casa di cura villa salus, emanuele puglisi, sezione microchirurgia vertebrale casa di cura cristo re messina lumbosacral radicolopathies substained by lateral recess stenosis are common pathologies in increment in the latest years for increasing of medium age of the life. the aim of this study is to evaluate the improvement of these radicolopathies trough combined treatment of root's microsurgical decompression and implant of an interspinous spacer device,as the bacjac (pioneer technologies). we enrolled 85 patients in a prospective study, all affected by radicolopathy from lateral recess stenosis. all of theme underwent a microsurgical root decompression and 40 have been treated by combine implant of interspinous device, and 45 decided voluntarily to not concur the implant and have been used as control group. results obtained were valutated trough comparation of specific tests performed preoperatively and 3 6 12 months after surgery, and clearly have shown that the microsurgical decompression is well effectiv on neurological deficits, but quality of life and reintervention requests are better in the group treated also by interspinous device implant. statistical evaluation of the clinical benefits of rehabilitation in patients with spine cord inury undergoing complexe treatment with specific therapeutical factors from techirghiol helth resort olga surdu m.d. ph d, associate professor1, research and development director2, aurora prăjitură2 senior physician, head of children rehabilitation department, traian-virgiliu surdu, assistant, drd1 1ovidius university constanta, 2balneary and rehabilitation sanatorium, techirghiol objectives to evaluate the clinical benefits of rehabilitation using natural factors from techirghiol health resort: climate, sapropelic mud, salty water of the lake. methods retrospective case-control study on 35 patients hospitalised in brs techirghiol from june, 1st 2007 to june, 1st, 2008 (12 month) with spine cord injury, undergoing specific rehabilitation treatment; qol scale, asia/ais score, ashworth scale were selected abstracts romanian neurosurgery vol. xv nr. 2 55 applied before the beginning and at the end of cure according to the standard procedure used in rehabilitation department; cure duration: 18 days; including and exclusion criteria were applied; complex treatment concerning: hydrotherapy and hydrokinetotherapy with salt water, mud bath or plant extract bath, kinetotherapy “à sec” in the gym room, massage and electrotherapy; statistic analysis of the results materials sapropelic mud, mineral water from techirghiol lake, glycerinate extract of medicinal plants; all medical rooms and devices (sswimming pool, tubes, electrotherapy devices, kinetotherapy rooms and devices, massage rooms) batch presentation: total number of patients: 35 24 male and 11 female, with age average 41.3 years old, 17 of them with paraparesis, 11 of them with tetraparesis and 7 with other neurological damages (pain, dizziness, itch, needles), produced by: car accident (14 cases), fall down (13 cases) and other traumatic conditions (8 cases) were assessed using qol and asia/ais scale; time from the injury: mean 3.1 years with the limits between 2.5 month (3 cases) and 26 year (1 case) results increase of asia/ais scores for patients with b, c, d type of spine cord damage; improvement of sphincter control; improvement of sleep quality and duration; increase of ashworth score; improvement of quality of life. complex treatment concerning: hydrotherapy and hydrokinetotherapy with salt water, mud or plant extract, kinetotherapy “à sec” in the gym room, massage and electrotherapy. conclusions correct evaluation of patients status, using specific scales allowed to prescribe a complex treatment with specific natural therapeutical factors; adequate administration of natural factors corroborate with progressive intensity of kinetotherapy and hydrokinetotherapy lead to the improvement of scores of patients; increased duration and quality of sleep is produced by plant extract and/or mud bath; due to the chemical and physical property of mud, muscle activity became better, spasticity decrease, sleep is deeper and concentration of patients during the therapeutical programme is higher; socialisation is easier within a community of peoples with same problemmes and is stimulated further by the clinical benefits obtained during the cure; quality of life of our patients is increase in many fields: self esteem, interest for treatment, encouraging other patients, implication in family life; the sooner balnear rehabilitation starts the better are the results. achievement of an experimental mechatronic orthotic device to assist /rehabilitate orthostatism and walk in patients with complete paraplegia prof. onose g., md,phd1, cardei v., eng., prof. ciurea a.v.,md,phd1, ciurea j.,md,phd1, onose l.,md3, craciunoiu t.st.,eng.,phd2, avramescu v., eng., postgrad2, grajdenescu r., eng.2, paun l., eng2, dogariu c., eng., phd5, racicovschi v., eng., phd6, ursu t., eng., phd6, modreanu m., eng.6, visileanu e., eng.,phd7, prof. carpus e.,eng.,phd7, dorogan a., eng.7, moldovanu a.,eng.,phd8, huian g.,eng.8, epureanu g., eng., postgrad9, assoc. prof. surdu o., md, postgrad.4,assoc. prof. padure l.md, phd, assist univ. chendreanu c, prep. univ. md1, mirea a., md1, ioana andone, md1, haras m., md1, spanu a., md1, popescu c., md1 1the clinical emergency hospital “bagdasar-arseni” bucharest, 2the research institute for machinery building technologies bucharest, 3metrorex bucharest, 4balneary and rehabilitation sanatory techirghiol, 5politechnical university bucharest, 6electrotechnical research and designing institute bucharest, 7rdini for textiles and leather bucharest, 8rdini for fine mechanics bucharest, 9”prof. c. popovici” foundation bucharest introduction this paper synthesizes the progressive development of an original type of mechatronic orthotic device (mod – selected abstracts romanian neurosurgery vol. xv nr. 2 56 which’s integrator concept won the gold medal at the international fair for inventions, geneva, 2008 – fig.1), dedicated to the assistance/ rehabilitation of orthostatism and walk in paralyzed people, disabled “oldest olds” and/or in patients with severe cardiorespiratory conditions. materials and methods from the descriptions analyses of some representative robotic orthotic structures, made by a variety of institutions, it resulted the necessity of improvement both on conceptual and functional plans, for which haven’t yet been found the most adequate constructive solutions (1-5). we consider that a robotic/ mod, in order to be really functional/ useful, must basically satisfy (6): weight & dimensions as reduced as possible; low energetic consumption and production costs; possibility of wearing it under clothes, including easy ways for dressing/ undressing; safe and comfortable position of the assisted person related to the mod; biocompatibility properties, thermophysiologic and sensitive comfort at the skin-orthose interface(assisted person’s skin airing, uniforming & reducing contact pressure -including equipment for improving the venous-lymphatic return in the lower limbs – through an incorporated mobile peristaltic airwaves generator fig. 2); automatic maintaining of the orthostatic position and ability of straightening when disturbing factors occur; achievement of the main lagging functions, through a simple/ user-friendly selection of desired movements, by the assisted person; simple procedure of training, for optimal “manmachine interaction”. results in the first stage on achieving/ testing mod’s main modules: actuators, specific to the working condition, (low weight & dimensions, high power & efficiency, max. 10ºc overheating); equipment and commanding programs of the main locomotors functions in sagittal plan (standing up, sitting down, forward movement, going up/ down on stairs, slopes); testing of functional and constructive aspects, for both mechanical ones and respectively, for those assuring biocompatibility conditions with the assisted person (optimized interaction solutions between mod’s internal face and the skin at contact areas; modulated underclothes system made of micro fiber with enlarged elasticity, bioactive, with increased comfort: seamless, brief trousers, co-chain type socks fig. 3); achievement subsequently, of an assay stand for mod (fig.4). in the second stage, were achieved and studied: the equipment with sensors (fig. 5) for accomplishing automatic control elements of orthostatism and some of its straightening abilities to accidental disturbing factors, in sagittal plan; advanced construing of the main locomotors tasks accomplished by mod. in the third stage (under actual sustained testing and improvement) there are successively optimized: supporting structure (fig. 6), sensor equipment, command & actuating components, in purpose to upgrade mod, in the future, in an under-wearable robotic orthotic suit; subsequently, the main steps are: safe real ground lagging (on plain surfaces); mod’s fitting out with spatial “hip” articulations; miniaturizing of all components; matching actuating with supporting structure/ functions. mod might be improved too, adding to it a non-invasive – our option is not for the invasive way (7) eeg (“wet” or even better “dry”) collector cap (8, 9) of voluntary brain motor bio potentials (and possibly eye-tracking) records, real time decoded and wireless transmitted to mod’s actuating systems. preliminary, in relation with a non-exoskeleton fitted robotic device, there seem to be promising results, even on severe paralyzed (tetraplegic) patients (a cooperation of our clinic with a berliner team of researchers – unpublished yet data). discussion mod’s components have many new elements – part of them under patenting with possibilities to be used, some of them, as separated products, as well. selected abstracts romanian neurosurgery vol. xv nr. 2 57 conclusions the achievement of most of the mentioned requirements of a functional mod/ robotic suit, represents both, a major assistive/ rehabilitative objective and a hard interdisciplinary – in principal medical and engineering – challenge. references 1. lee s, sankai y. the natural frequency based power assist control for lower body with hal-3. proceedings of the ieee international conference on systems, man and cybernetics; 2: 1642-7; 2003 2. www.sanlab.kz.tsukuba.ac.jp 3. www.argomedtec.com 4. www.robosavvy.com 5. www.ferrati.com 6. onose g, cardei v, ciurea av, anghelescu a,, onose l, craciunoiu st et al. robotized orthotic system to assist/rehabilitate standing & walk in paralyzed patients and elderly. poster (p31: p. 291) at the joint event of the international and nordic spinal cord societies 46th iscos annual scientific meeting and 10th noscos congress, 2007; reykjavík, iceland 7. patil pg, carmena jm, nicolelis ma, turner da. ensemble recordings of human subcortical neurons as a source of motor control signals for a brain-machine interface. neurosurgery 2004; 55(1):27-35 8. makeig s, delorme a, westerfield m, jung t, townsend j, courchesne e et al.. electroencephalographic brain dynamics following manually responded visual targets. plos biol 2004; 2(6):e176 9. popescu f, fazli s, badower y, blankertz b, muller kr. single trial classification of motor imagination using 6 dry eeg electrodes. plos one 2007; 2(7):e637. advanced bio – materials/devices & technologies supporting spine and cord repair/regeneration assoc. prof. g. onose, md, phd1, prof. a.v. ciurea, md, phd1, r. rizea, md1, liliana onose, md2, a. anghelescu, md, postgrad1, cristina daia chendreanu, md1, monica haras, md, postgrad1, f. brehar, md, postagrad1 keywords: sci, non-resorbable / resorbable gel-type implants, self-assembling scaffolds, organ 3d printing inside repair/ regeneration, scaffold-like structure rna nanoscale machines introduction although spinal cord injuries (sci) are a major public health problem because of their huge invalidating potential and outcomes little progress has been made yet, to improve neurological status which consist, in many cases, in lifelong disability. this fact put an important burden on the affected individuals, their families and society. its annual social cost is estimated, for instance in the usa at $4-6 billion or even more. background the central nervous system (cns) being the most sophisticated known structure within the universe is perfect example for maximal interdependence between structure and function. the lower part of cns, i.e. the spinal cord, couldn’t make an exception; therefore, to heal lesions at this level implies not only cellular/axonal re-growth or/ replacement but of equal importance – reproducing the cord’s pre-lesion local architecture. so, regeneration/ repair and consequently, functional restoring / rehabilitation after sci, passes inevitably through the cutting-edge process (at present still mainly experimental in the domain) of tissue engineering, in purpose to effectively reconstruct and thus, cure the spinal (injured) cord. basically, tissue engineering means a controlled assembly of (stem) cells, growth factors, ligands, blood vessels/ angiogenesis, etc, in vitro or in vivo (eg. through in situ 3-d “bio-ink” printing or “filling the gap” by injecting into the lesion area elaborated scaffolds – some of the newest: self assembling capable to host and facilitate local bone or neural/ axonal growth, structuring and re-connection). main items and achievements: the advanced biomaterials contributive to spine & cord repair/ regeneration are divided in two main groups: nonresorbable and respectively, resorbable, gel-type implants. within the first group recently, there have been started few human trials. the second category also having a few products in clinical trials comprises: organic, bioactive, resorbable (and/or selfassembling/nano-processed – including recently, selected abstracts romanian neurosurgery vol. xv nr. 2 58 multiple-channel) scaffolding biomaterials. they might serve as a guide for neo-forming tissues, as delivery vehicles for cells and growth factors, as adjuvant in autologous or allogenic bone grafting and/or as an artificial, biodegradable material to stimulate bone or/and neural regeneration. very recently, some of them evolved to different types of neuro gels, containing specific peptides, cell-adhesive region or fibronectin, (a near future “living glue”); a groundbreaking principle: the use of a (micro)-inkjet printer, to “print” a “biological ink” (“bio-ink”), composed of cell aggregates, into a 3-d, biodegradable polymer gel, resulting in building organs from the groundup, by the use of desktop printing technology; a novel laser forward-transfer process to direct write biological materials for matrix assisted pulsed laser evaporation (maple dw), through which stem cells could be individually inseminated at the level of a matrix (tridimensional, biodegradable, scaffold, which imitates the nervous structures), able to induce also embryonic stem cell differentiation with appropriate growth factors, to determine cells to exhibit 3-d organization and thus, resembling primitive neural, cartilage or liver tissue; latest and seeming valuable: engineering nerve jumper cables for spinal cord repair in animal model, holds promise also for humans; a new biodegradable polymer matrix, "spherogel“ is meant to deliver/coax embryonic ensheathing stem cells to grow inside the sci gap; a sort of adavnced and complex biomaterials awaiting to be marketed hopefully soon: the therapeutic system of cordaneurin, respectively cordachron (in combination with e.g. chemokine sdf-1gamma for the neuronal growth promotion and glial scar prevention). very interesting and introducing bio/nano technological remarkable skills: the scaffold-like structure rna nanoscale machines, from biological components. discussion & conclusion the enounced, very new (last five years) and seeming revolutionary biomaterials and connected methods, are happily merging with strong advances in intimate cellular therapeutic manipulation techniques. at present and continuing for the next about three years, some reliable, specific trials, are/will be on going: for the first time it may be possible to expect from their results, consistent may be decisive improvements in sci therapeutic rehabilitative outcomes. the emergency hospital “bagdasar – arseni”/ physical & rehabilitation medicine clinical division’s expertise in the neurotrauma within polytrauma, complex, post-acute approach prof. onose g., md, phd, prof. ciurea a.v., md, phd, anghelescu a., md, postgrad., mardare d.c., spt, anca mihaescu, spt, prof. purghel f., md, phd, assoc. prof. grigorean v., md, phd, assoc. prof. liliana padure, md, phd, psich. virginia rotarescu, postgrad., univ. assist. cristina chendreanu, monica haras, md, postgrad., md, cristina popescu, md keywords: neurotrauma, polytrauma, tbi, sci, rehabilitation background polytrauma means the presence of one or more (violent) traumatic lesions (multifarious and often associated: axial – including skull/ spine – or/and peripheral bone fractures, visceral contusions and/or ruptures) in minimum two anatomic regions, among which, at least one, is actually or potentially life threatening within our clinical emergency hospital, the polytraumatised patient is examined by the emergency medical team, which evaluates and tries to stabilize the patient’s vital signs and biological markers. basic radiological and imaging investigations orientate the interventions of the multidisciplinary team (neurosurgeon, general surgeon, orthopedic surgeon). afterwards, in the early post-acute phase, the stabilized patient is admitted in our prm clinical division. selected abstracts romanian neurosurgery vol. xv nr. 2 59 objective statistically presentation and evaluation of our results in the neurotrauma within polytrauma complex, post-acute approach. material and method retrospective statistical study, on a series of 93 cases (gender 68m, 25f), admitted during 2007, splitted following the principal nevraxial lesion criteria: 38 (40.9%) tbi, 28 (30.1%) sci, and mixed associated tbi plus sci 27 (29%) subjects. the mean hospitalization length was 30 days for each patient; some of them were readmitted. the comprehensive neuro-motor rehabilitation was physical/ kinetically therapy programs based, adapted to the peculiar clinical neurological and general status of each patient, including initially rehabilitative nursing. all the inpatients received aside, a rather equivalent complex, pharmacological therapy, icluding the modern neurotrophics cerebrolysin® or/and actovegin® the assessment of patients was objectived by functional independence measure (fim) at admission/discharge. results etiology was: car accidents (68.8%), falls from height (25.8 %), diving in water (2.1%), same level falls (2.1%), aggression (1.1%) the associated traumas were: orthopedic lesions (39.8 %); visceral contusions or/ and ruptures (48.4%), mixed bone fractures associated with visceral lesions. within the tbi, lot were 16 aphasic patients (12 improved, 4 stationary at discharge – assessed with our specific clinical scale). regarding fim: for the tbi lot (afim= 45,3; dfim=60,9); the sci group (afim= 54,8; dfim=74); for the mixte neuraxial polytrauma (afim= 52,7; dfim=66,6). evolution status at discharge: improvement in 87.1 % cases; stationary at 12.9 % patients. discussion our results are, overall, comparable to those obtained in different good neurotrauma within polytrauma units, worldwide conclusions precocious, comprehensive, multi-/interdisciplinary team approach is the appropriate treatment algorythm, for the polytraumatized, with neurotrauma patient. microsoft word 9ciureaavmicrosurgical.doc a.v. ciurea et al microsurgical approach in a thoracic meningioma 81 microsurgical approach in a thoracic meningioma in elderly. case report a.v. ciurea, al. tascu, c.l. palade university of medicine and pharmacy “carol davila” bucharest 1st neurosurgery clinic “bagdasar-arseni” clinical hospital, 10-12 berceni street, 041915, bucharest correspondence to: claudiu_palade@yahoo.com, rsneurosurgery@gmail.com abstract improved results in the treatment of intraspinal tumors have followed greater sophistication of diagnostic modalities and surgical techniques. whereas originally tumors could be diagnosed radiologically only by bone erosion seen on radiographic films, now mielography, computed tomography (ct) and magnetic resonance imaging (mri) provide precise localization. indeed, mri is a stand-alone diagnostic preoperative study for virtually all intradural tumors. with the advent of the operating microscope, microsurgical instruments, bipolar cautery and intraoperative ultrasonography, combined with ultrasoniccavitation devices and other techniques, surgeons can approach these tumors with greater ease. keywords: intradural spinal tumor, meningioma, neurosurgical results introduction in the literature, spinal meningiomas account for 25-46% of spinal tumors, with 7,5-12,7% of all meningiomas occurring in the spinal canal. the arachnoid cap cells or immature fibroblasts of the dura are considered to be the tumor precursor cells of meningiomas. most meningiomas are found entirely intradurally. however, transdural growth or entirely extradural growth is also possible. invasive growth or hyperostotic reaction of the bone is rare. the tumor attachment is often lateral with a ventral or dorsal extension. meningiomas are observed predominantly in the cervical (28%) and thoracic spine (64%). lumbar meningiomas are rare (8%). they are evenly distributed around the spinal cord an may be located anteriorly (26%), posteriorly (25%), or laterally (48%). in the cervical area, anterior meningiomas are more common than in the thoracic spine (47% and 18%, respectively), whereas most of the thoracic meningiomas are located laterally compared to the cervical area (55% and 38%, respectively). in the lumbar region, 55% were located posteriorly. the ratio of spinal to intracranial meningiomas is about 1:8; the mean age at presentation is 56 years. multiple spinal meningiomas are rare. due to the predilection for the thoracic location and 82 romanian neurosurgery (2010) xvii 1: 81 87 functonal adaptability of the spinal cord, clinical symtoms are very insidious. a complete removal of spinal meningiomas is achieved in the vast majority of cases, with a recurrence rate of less than 10%. case report a 74 year old male noticed gait disturbance of gradual onset with motor weakness of the inferior limbs (frankel score=d) and a sensory impairment below the level of t9, without sphincter disturbances. since 3 months previously, he had suffered from progressive thoracic pain. since 1 month previously the thoracic back pain had worsened associated with paresthesias in both legs, more on the right side. the mri scan presented an intraduralextramedullary tumor on the right side at thoracic level t1-t2, with severe compression of the spinal cord. figure 1 preoperative mri scan (in sagital and axial incidence) showing intradural extramedullary tumor a laminectomy at two levels (t1 and t2) was performed and a meningioma (who grade i) was totally removed. the sensory roots at the level were completely preserved. the operation was performed with general anesthesia. central venous acces and arterial pressure monitoring are helpful. the operation was performed with the patient in the prone position. all presure points were well-paded. a comfortable head rest is essential. for patients with upper thoracic or cervical tumors, three-point skull fixation with the cervical spine in neurtral position is best. priot to preparation and draping, anterior-posterior roentgenograms were obtained in this case, in order to best localize the lesion. alternatively, the patient may be taken to the radiology department prior to surgery, where fluoroscopy can be employed to localize these lesions relative to surface anatomy. although intraoperative evoked potential a.v. ciurea et al microsurgical approach in a thoracic meningioma 83 monitoring may be beneficial in some cases, intradural extramedullary tumors can be resected safely without this additional monitoring. figure 2 a exposure of the posterior medullar surface at t1-t2 level figure 2 b tumor dissection and decompression of the medullar stem figure 2 c reapproximation of the dura mater after gross total removal after preparation and draping, a midline incision was employed and the fascia was incised down to the spinous processes. the muscular attachments were stripped bilaterally in the subperiosteal plane, exposing the laminae out to the facet joints. the spinous processes and laminae of the 1 st and 2 nd thoracic vertebrae were carefully removed using bone rongeurs. enough bone was removed both above and below the tumor to permit an adequate dural opening. at this point, the operating microscope was brought into the field. the dura was opened in the midline, taking care to preserve the arachnoid intact. a microdissector was used to separate the dura and arachnoid. dural tack-up sutures were placed and cottonoid pledgets were laid over the exposed dura. tension on the sutures provides better exposure and relative hemostasis from the epidural space. the tumor was already visible beneath the arachnoid. the arachnoid was carefully opened by sharp dissection. the tumor was dissected within the tumor-cord interface. the plane between the tumor and the spinal cord was well-developed and easy to delineate, allowing circumferential arachnoid dissection and delivery of the tumor capsule. meticulous hemostasis is essential prior to dural closure. a watertight closure followed. muscle, fascia and subcutaneous tissue were closed in anatomic layers. an external drain was used. the skin was finally closed and a sterile gauze was placed above. 84 romanian neurosurgery (2010) xvii 1: 81 87 perioperative antibiotic prophylaxis, careful wound closure, and dexamethasone administration lessen the risks of postoperative infection and cerebrospinal fluid leakage. the drain was discontinued the next day. figure 3 postoperative mri scan ,1 month after surgery the postoperative sagittal mri scan of the thoracic region demonstrated tumor removal and the contour of the spinal cord without any signs of compression. two days after surgery the motor weakness of the lower extremity was improved, and the sensory impairment diminished considerably. discussion the key feature of slowly growing tumors is the long history of signs and symptoms due to the substantial plasticity of the spinal cord. acute onset with a subarachnoid hemorrhage can also be a rare presentation of spinal cord tumors (such as neurinomas and cavernous angiomas). the signs and symtoms differ, depending on: level, location,size of tumor and speed of growth among patients with meningiomas, four groups can be distinguished a.v. ciurea et al microsurgical approach in a thoracic meningioma 85 according to the growth pattern and histology of the tumor: encapsulated, en plaque growing, atypical, and malignant meningiomas. with encpasulated meningiomas, the preoperative history is almost twice as long as compared to the remaining groups. of pacients with encapsulated meningiomas, the vast majority (72%) complain about gait and motor deficits as their major concern at the time of surgery. with en plaque growing tumors, the situation is quite different, as pain and disesthesias become more predominant (45%). with atypical meningiomas, 71% are mainly concerned about pain and disesthesias, while 29% are disabled by gait problems. with malignant meningiomas, 50% are troubled by pain, and the other half by gait ataxia. in general, extramedullary tumors produce radicular and segmental deficits. the above tumors reveal long tract symptoms and signs in their advanced stage. lateralization or assimetry of early signs and simptoms reflects the lateral location of a tumor. hemicord syndrome or brown-sequard’s syndrome is observed commonly at the advanced stage. the cardinal symptoms are: progressive local pain, pain during recumbency (nocturnal pain), radicular or mielopathic pain, non-painful sensory disturbances, motor weakness (gait disturbance) , clumsiness and ataxia, sphincter disturbances (usually urogenital, less commonly anal) the pain might be of the radicular type, with radiation often increasing with valsalva’s maneuver and/or spine movement. segmental or medullary pain (non-radicular, diffuse non-describable pattern) might be present continuously, radiating into the whole leg or onehalf of the body without affection of movement. a thorough neurological examination is key to the assesment of spinal tumors. findings on clinical examination include: sensory deficits , motor weakness, gait disturbance, ataxia, bowel and bladder dysfunction, torticollis and spinal diformity (scoliosis and kyphosis) diagnostic modalities 1. magnetic resonance imaging the golden standard magnetic resonance imaging should be performed as the first diagnostic modality when symptoms and signs indicate a spinal tumor should be suspected. the other imaging modalities are second in line. mri is the diagnostic imaging procedure of choice. t1w – and t2w weighted images as well as gadoliniumenhanced t1w images should be sistematically obtained. the entire spinal cord must be studied. at least two different imaging planes should be used in order to locate the tumor properly and to differentiate intramedullary tumors from extramedullary tumors. coronal sections can demonstrate a tumor in relation to the bony structures in the same view as in the operating room, which can be helpful in planning the extent of laminectomy. meningiomas present as isointense with cord on t1w images and t2w images; moderate contrast enhancement with or without association of dural tail; there is no bone distruction; calcification is occasional. 2. ct and myelo-ct 86 romanian neurosurgery (2010) xvii 1: 81 87 these are the methods of choice in patients in whom mri cannot be performed because of contraindications (e.g., pacemaker). typical findigs are: bony deformation such as destruction, scalloping, widening of the spinal canal and/or the intervertebral foramen, calcification, contrast enhancement, spinal cord compression. surgical treatment the goal of surgery for any benign intradural neoplasm is gross total resection. recent technological developments such as mri, ultrasonography, the cavitron ultrasound aspirator (cusa), and microsurgical technique with intraoperative neurophysiological monitoring have brought about a remarcable improvement in surgical results. the target level should be marked under the fluoroscope prior to surgery. extension of laminectomies should be one more lamina above and below tumor extension. this enables surgical manipulation to be easy and safe and is also appropriate for decompression. if benign extramedullary tumors are found, osteopladtic laminotomy might also be considered to prevent traction damage or kyphosis. care should be taken at lest to maintain the integrity of the facets to preserve spinal stability. intraoperative neurophysiological monitoring with somatosensory evoked potentials (sseps) is recommended. there is no convincing reliable and useful monitoring system which includes motor evoked potentials at the moment. knowledge of standard peri-and intraoperative management such as: edema prevention, respiratory management in cervical tumors, critical interpretation of neurophysiological monitoring , is key to succesful surgery. possible surgical complications include: blader and bowel disfunction, bleeding or hematoma, csf leak, infection, chronic pain, neurological deterioration, sexual disfunction, spinal instability, ventilator dependence, wound dehiscence in terms of outcome, postoperative neurological orbidity in the surgery of extramedullary tumors is usually less then 15%. total recurrence rate of meningiomas is 7-15%. neurological function of a patient after surgical intervention mostly depends on his or her preoperative neurological condition. surgical approach for intradural extramedullary tumors localization of intradural extramedullary tumors can be classified as: posterior, posterolateral, lateral, anterolateral, anterior. although most tumors can be managed by standard laminectomy, the approach can be varied accordingly such as by using: hemilaminectomy and complete laminectomy, costotransversectomy, extracavitary approach, far lateral laminectomy and partial facetectomy, posterolateral approach through the facet joint and pedicle, transthoracic approach, far lateral approach transcondylar approach for tumors at the cervicomedullary junction, ventral corpectomy. almost all meningiomas can be completely removed, with excision or coagulation of the dural attachment. the recurrence rate following complete resection is around 7-15%. there is no a.v. ciurea et al microsurgical approach in a thoracic meningioma 87 clear correlation between the result and the extent of resection of the dural attachment. the surgical approach is usually via a laminectomy for midline dorsal tumors. a hemilaminectomy can sometimes be performed in small tumors more laterally located. for tumors in a lateroventral location, a lateral approach has to be performed. conclusions 1. the use of spinal mr imaging, with extremely accurate details, provides the most useful and dependent diagnostic tool 2.the surgical approach is usually via a laminectomy for midline dorsal tumors. a hemilaminectomy can sometimes be performed in small tumors more laterally located. 3.the modern operating microscope provides an outstanding illumination and magnification of the operating field and allows a very careful and gentle tumor dissection and removal 4. the use of the intraoperative “carm” roentgen equipment is extremely beneficial, allowing a very exact localization of the lesion 5. knowledge of peri-and intraoperative management such as: edema prevention and respiratory management in cervical tumors is key to succesful surgery. references 1. ciapetta p, domenicucci m, raco a (1988) spinal meningiomas: prognosis and recovery factors in 22 cases with severe motor deficits. acta neurol. scand 77:27-30 2.ciurea av, constantinovici a (1998) tumorile spinale. in: ciurea av, constantinovici a ghid practic de neurochirurgie, editura medicala, bucuresti, p 341 3.cohen-gadol aa, zikel om, koch ca, scheitauer bw, krauss we (2003) spinal meningiomas in patients younger than 50 years of age: a 21-year experience. j neurosurg (spine3) 98: 258-263 4.el-mahdy w, kane pj, powell mp, crockard ha (1999) spinal intradural tumours: part i – extramedullary. br j neurosurg 13:550-557 5.feiring eh, barron k (1962) late recurrence of spinal cord meningioma. j neurosurg 19:652-656 6.gamache fw jr, wang jc, deck m, heise c (2001) unusual appearance of an en plaque meningioma of the cervical spinal canal: a case report and literature review. spine 26:e87-e89 7.gambardella g, gervasio o, zaccone c (2003) approaches and surgical results in the treatment of ventral thoracic meningiomas. review of our experience with a postero-lateral combined transpedicular-transarticular approach. acta neurochir (wien) 145:385-392 8.gezen f, kahraman s, canakci z, beduk a (2000) review of 36 cases of spinal cord meningioma. spine 25:727-731 9.goldhahn we, schmidt u (1989) das spinale meningiom. zentralbl neurochir 50:18-23 10.gottfried on, gluf w, quinones-hinojosa a, kan p, schmidt mh (2003) spinal meningiomas: surgical management and outcome. neurosurg focus 14: article 2 11.herkowitz h, garfin s, eismont f, bell g, balderston r (2006).in: rothman-simeone the spine, elsevier 12.klekamp j, sammi m (2007) extramedullary tumors. in: klekamp j, sammi m (eds) surgery of spinal tumors, springer verlag, berlin-heidelberg, pp 248-260 13.mccormick pc, post kd, stein bm (1990) intradural extramedullary tumors in adults. in: stein bm, mccormick pc (eds) neurosurgery clinics in north america. vol.1 no.3. intradural spinal surgery. wb saunders, philadelphia, pp591-608 14.mccormick pc, stein bm (1996) spinal cord tumours in adults. in : youmans jr (ed) neurological surgery, 4th edn. saunders, philadelphia, pp 3102-3122 15.morandi x, haegelen c, riffaud l, amlashi s, adn m, brassier g (2004) results in the operative treatment of elderly patients with spinal meningiomas. spine 29: 2191-2194 16.schick u, marquardt g, lorenz r (2001) recurrence of benign spinal neoplasms. neurosurg rev 24: 20-25 17.solero cl, fornari m, giombini s, lasio g, oliveri g, cimino c, pluchino f (1989) spinal meningiomas: review of 174 operated cases. neurosurgery 25: 153-160 18.souweidane mn, benjamin v (1994) spinal cord meningiomas. neurosurg clin n am 5:283-291 19. yonekawa y, marugg r (2008) intradural tumours. in: boos n, aebi m (ed) spinal disorders – fundamentals of diagnosis and treatment, springer verlag, berlin heidelberg, pp 997-1019 romanian neurosurgery (2019) xxxiii, 1: 59-62 doi: 10.33962/roneuro-2019-011 www.journals.lapub.co.uk/index.php/roneurosurgery isolated fourth ventricle haemorrhage: “think beyond intracranial source’’ unusual presentation of lumbosacral spine arteriovenous malformation presentation naresh panwar1, manish agrawal2, ghanshyam agrawal2, v. d. sinha2 1 department of neurosurgery, fortis escorts heart & research institute, new delhi, india 2 department of neurosurgery, sms medical college, jaipur, rajasthan, india abstract spinal arteriovenous malformations (savms) are rare vascular lesions and account for about 4% of primary intraspinal masses. since savms can involve any location along the spinal column and produce a host of different problems, the symptoms are extremely variable. there are few reports of simultaneous cerebral sah and intraventricular hemorrhage (ivh) following rupture of a spinal avm (savms). herein, we present a rare case of lumbo sacral spine arteriovenous malformation, which clinically manifests as sudden onset of severe headache and vomiting due to isolated fourth ventricle hemorrhage (ivh) without cerebral subarachnoid hemorrhage. introduction being a rare category, spinal vascular malformations (savms) account for about 4 % of primary intraspinal masses (3). rosenblum and coworkers described two major types of spinal avm intradural versus dural on the basis of location of nidus: intradural versus dural. intradual avms were classified as intramedullary and dural avfs (arteriovenous fistula). they usually present with pain, numbness, and weakness, loss of bowel/bladder control, incoordination, and impotence is few of the issues. in majority of cases savms first come to medical attention by bleeding this usually presents as acute, severe back pain, followed by sudden onset weakness, numbness, incontinence; severity ranges from no neurologic dysfunction to complete paralysis, depending on location and extent of bleeding. the natural history of spinal vascular malformations (savms) is unpredictable and varies from acute subarachnoid hemorrhage of spine to venous congestion of cord. as far as cranial manifestation of savms concerns cerebral sub arachnoid hemorrhage (sah) has been reported in english literature, and seems to be caused by rupture of same intra ventricular bleed due keywords spinal arteriovenous malformations (savms), fourth ventricle, intraventricular hemorrhage (ivh), cerebral sah corresponding author: naresh panwar department of neurosurgery, fortis escorts heart & research institute, new delhi, india panwaralice2005@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 60 naresh panwar, manish agrawal, ghanshyam agrawal, v. d. sinha to savms has been reported four times in last decade. we believe this to be the first reported case of a lumbosacral savms presenting as isolated fourth ventricle hemorrhage (ivh.) we also need a kind attention regarding left lower limb swelling; it might be due to raised venous pressure which was resolved spontaneously after definitive surgical management of savms. case report a twenty-year-old adult male experienced sudden onset severe headache associated with episodes of vomiting in a morning during defecation, which was preceded by severe lower back pain. there was no history or signs of trauma, no previous history of back pain, radiculopathy, or myelopathy were reported. on examination it was revealed that patient was conscious, oriented and without any focal neurological sign. he had left lower limb swelling which was misdiagnosed as varicose vein of limb and was operated 6 months back for same, but swelling did not subsidize. non contrast computed tomography (ct) of head was done, which showed fourth ventricle hemorrhage with concomitant sparing of bilateral lateral and third ventricle, all cisterns were seen normally and had no evidence of cisternal bleeding and sub arachnoid hemorrhage (figure 1). magnetic resonance imaging (mri) brain, ct angiography brain and digital subtraction angiography (dsa) brain did not reveal any intra cranial source of bleeding, but mri lumbo sacral region (figure 2) and spine digital subtraction angiography revealed spinal perimedullary avm (savms) at l1 to s1 level (conus medullaris) with feeding artery aneurysm and venous drainage from spinal vein to perimedullary vein and extending cranially(figure-3). the lesion was treated surgically as cauterization and disconnection of the vein. till the writing of this report 12 month follow up has been completed and he is neurologically intact and most importantly lower limb swelling subside within first month of surgery (figure 4). discussion spinal arteriovenous malformation (savm) is a rare, abnormal tangle of blood vessels on, in or near the spinal cord and account approximately 10% of cns vascular malformations in all age groups. these lesions are directly supplied by radicular arteries and drained by spinal cord veins, although dural supply can occur as with dural arteriovenous fistulas. (3, 7) on the basis of location these lesions are divided into either intradural or extradural, and intradural f u r t h e r s u b d i v i d e d i n t o i n t r a m e d u l l a r y o r extramedullary. most are thoracolumbar, posterior, and outside the cord (extramedullary). the rest are cervical or upper thoracic and often inside the cord figure 1. ncct head showed small hyper density in 4th ventricle suggestive of recent intraventricular bleed. figure 2. mri l s spine t2 weighted with gre shows multiple flow void in intradural lumbo-sacral region extending from l1 to s1 levels. subtle enhancement is seen in blood vessel with slow flow. no enhancement is seen with blood vessel with high flow suggestive of spinal dural avf. figure 3. spinal dsa showing lumbo-sacral dural avf with pre nidal aneurysms with feeder from left t 10 rediculomeningeal artery. figure 4. swelling left leg, which reduced drastically after treating primary pathology along with hyper pigmentation on dorsum of foot. (intramedullary). avms may be small and localized or may affect up to half the cord. (3,6) in majority of patients the ultimate fate of spinal avm is progressive neurological deficit in terms of sensory, motor or bladder/ bowel involvement. in 61 isolated fourth ventricle haemorrhage some situation rarely, high cervical avms rupture into the subarachnoid space, causing subarachnoid hemorrhage with sudden and severe headache, nuchal rigidity, and impaired consciousness (4). the natural history of savms is characterized by venous congestion causing progressive neurological deficits in majority of patients. (3,8) in the literature, a thoracolumbar savms presenting with both sah and ivh appears to be a rare occurrence. although there are few reports of concomitant cerebral sah and intraventricular hemorrhage (ivh) following rupture of a spinal savms (2,3,5). there have been three case reports of savms presenting in the adult population and two in pediatric age group with intraventricular hemorrhage (ivh) exist in the literature. in both groups, the clinical, radiographic, and surgical findings suggested that the savm was the source of the hemorrhage. in 1999 p bazro et al reported first case of intraventricular hemorrhage attributed by the rupture of conus medullaris avm in a young patient. (1). es marlin et al reported a case of intraventricular hemorrhage in both lateral, third and fourth ventricle in a 2-year-old female child caused by rupture thoraco lumber savms, who died in next few days probably due to re rupture. (3). recognition of such cases in future may allow earlier diagnosis and treatment before catastrophic re hemorrhage. masanori et al reported another case who presented with intraventricular hemorrhaging (ivh) into the fourth and third ventricles that was caused by a cervical intramedullary arteriovenous malformation. (4) to the best of our knowledge, this is the first case report of an adult patient in whom initial imaging demonstrated isolated fourth ventricle hemorrhage (ivh) without sub arachnoid hemorrhage (sah) secondary to a ruptured low lumbosacral savms. till the date only five cases of intraventricular hemorrhage is reported in literature. table 1. patients presenting with ivh caused by rupture of spinal avms s.no. author(s) year age/sex ventricular hemorrhage location of spinal avm 1 h baharvahdat et al (2) 2016 48 year/male b/l lateral, third & fourth ventricle and sah conus medullaris avm 2 e. s. marlin et al. (3) 2014 2 year/ female child b/l lateral, third & fourth ventricle thoraco lumber spinal avm 3. kenning. t.et al (5) 2009 1 year 2 month /female childe b/l lateral, third & fourth ventricle and sah thoraco lumber spinal perimedullary avm 4 masanori ito et al (4) 2007 33 year /male third & fourth ventricle cervical intramedullary spinal avm 5 p barzó et al (1) 1999 28 year /male b/l lateral, third & fourth ventricle conus medullaris avm 6 present case 2017 20 year/male isolated fourth ventricle lumbo sacral spinal avm although to kept lumbosacral savms as a differential diagnosis for isolated spontaneous fourth ventricle ivh is beyond the imagination particularly in adult patient, where the distance between the bleeding source and presenting site is significant. the present case suggests that mri of 62 naresh panwar, manish agrawal, ghanshyam agrawal, v. d. sinha the entire spine with dedicated blood detected sequence gre & swi should be considered if cranial angiography does not reveal a source. (2,3). there must be some possible hypothesis of raised venous pressure behind the swelling of left leg due to savms being wrongly operated for varicocities. so, such possibilities in these cases should also be considered. conclusions the case reported raises necessity of complete spinal neuraxis evaluation especially in young group of patients presenting with angiographically negative intraventricular hemorrhage. evaluation for thoracolumbar spinal vascular malformations must be included in the initial work up. a whole spinal workup should be considered, when bleeding from intracranial origin is carefully excluded. this is reminder to treating neurosurgeon along with concern medical fraternity as neurointerventionalist for careful consideration this rare differential and it has to be kept in mind that presentation can varied from head to toe. abbreviations ivh intra ventricular hemorrhage sah sub arachnoid hemorrhage savm spinal arterio vascular malformation davf dural arterio venous fistula mri magnetic resonance imaging (mri) dsa digital substraction angiography swi -susceptiblity weighted imaging references 1. barzó p, vörös e, bodosi m: intraventricular hemorrhage as a false localizing sign of a thoracolumbar arteriovenous malformation: case report. surg neurol 51:430–434, 1999. 2. h baharvahdat et al. diffuse subarachnoid and intraventricular hemorrhage as the presenting sign of a conus medullaris arteriovenous malformation: case report neurol neurochir pol. 2016 nov dec; 50(6):487490. 3. es marlin et al thoracolumbar spinal vascular malformation as a rare cause of isolated intraventricular hemorrhage: j neurosurg pediatr 14 (1), 12-15. 2014. 4. masanori ito et al.spinal intramedullary arteiovenous mal formationdraining into petrosal and straight sinusresulting in intraventricular hemorrhage: acase report .spinal surgery 21 (1); 35-41,2007. 5. kenning tj, deshaies em, adamo ma, waldman jb, boulos as: onyx embolization of a thoracolumbar perimedullaryspinal arteriovenous fistula in an infant presenting with subarachnoid and intraventricular hemorrhage. case report. j neurosurg pediatr 3:211–214, 2009. 6. kim lj, spetzler rf: classification and surgical management of spinaarteriovenous lesions: arteriovenous fistulae and arteriovenous malformations. neurosurgery 59 (5 suppl 3): s3-195–s3-201, 2006. 7. niimi y, setton a, berenstein a: spinal dural arteriovenous fistulae draining to the anterior spinal vein: angiographic diagnosis.neurosurgery 44:999–1004, 1999. `8. yaşargil mg, symon l, teddy pj: arteriovenous malformations of the spinal cord. adv tech stand neurosurg 11:61–102, 1984. 1giovania_a giant romanian neurosurgery | volume xxx | number 4 | 2016 | october december article a giant solid cystic inferior fourth ventricle subependymoma – case report and literature review a. giovani, narcisa bucur, ana gheorghiu, lena papadopol, r.m. gorgan romania doi: 10.1515/romneu-2016-0073 romanian neurosurgery (2016) xxx 4: 455 – 460 | 455 doi: 10.1515/romneu-2016-0073 a giant solid cystic inferior fourth ventricle subependymoma – case report and literature review a. giovani, narcisa bucur, ana gheorghiu, lena papadopol, r.m. gorgan “bagdasar-arseni” emergency hospital, bucharest, romania abstract: subependymomas are a rare subtype of ependymomas, slow growing who grade i tumors that develop either intracranial from the subependymal glial precursor cells layer of the ventricles or intramedullary. these tumors originate in the undifferentiated subependymal layer of cells that can become either ependymocytes or astrocytes. most of the subependymomas are located inside the fourth ventricle (5060%). we reviewed the case of a 40 years old woman with a giant solid cystic fourth ventricle ependymoma. the patient underwent total resection of the tumor through a subociipital transvermian approach. we discussed the characteristics of these benign tumors and reviewed the literature on this subject and concluded that total resection is the treatment of choice for symptomatic subependymomas localized in posterior fossa. key words: subependymoma, giant, solid cystic, fourth ventricle introduction subependymomas are a rare subtype of ependymomas, slow growing who grade i tumors that develop either intracranial from the subependymal glial precursor cells layer of the ventricles or intramedullary.[7,13] ependymomas are more frequent in pediatric patients accounting for 6–12% of all intracranial tumours. the intramedullary location is the most frequent, these tumors accounting for 50-60% of all spinal cord lesions. the term of subependymomas was coined in 1945 and since than many authors published only case reports, reflecting the rarity of this tumor, with an incidence between 0,2% and 0,7%. [8] most of the subependymomas are located inside the fourth ventricle (50-60%) and become symptomatic when large enough to compress the cerebellum, the floor of the fourth ventricle or to obstruct the csf flow with progressing secondary hydrocephalus [10]. these tumors originate in the undifferentiated subependymal layer of cells that can become either ependymocytes or astrocytes [3]. a few reports documented the familial occurrence of subependymoma. 456 | giovani et al giant solid cystic inferior fourth ventricle subependymoma case report a 40 years old woman presented with an 8 months history of intense headache nausea and vomiting, signs of increased intracranial pressure, posture and gait ataxia, horizontal nystagmus walking fatigueability and paresthesia in both inferior limbs. her eye exam showed a mild bilateral papilledema. a brain mri revealed a well-delimitated tumor occupying the caudal part of the fourth ventricle with an associated cyst on the superior aspect compressing the vermis and cerebellar hemispheres. the solid portion was inhomogeneous on t1 showing moderate and irregular enhancement, a hypointense core and periphery and a hyperintense ring, sign of intratumoral bleeding in between. (figure 1). the tumor also showed microcalcifications around the hypodense core on ct scan. surgery the patient was placed in prone position with the head slightly elevated and flexed for a better opening of the space between the occiput and c1. using a midline occiput c6 incision, a bilateral suboccipital craniotomy was performed including the posterior c1 arch. opening the arachnoid over the cisterna magna relieved csf under pressure and relaxed the cerebellum. the inferior pole of the tumor became visible in the cerebellomedullary fissure as it enlarged the foramen magendie and displaced the cerebellar hemispheres laterally and the vermis superiorly. figure 1 frontal, axial and sagittal preop mri showing a giant iv ventricular lesion, with solid and cystic component presenting some core hipo/hyperintensities. the lesion compresses the brainstem and the cystic component displaces the vermis reaching the tentorium romanian neurosurgery (2016) xxx 4: 455 – 460 | 457 figure 2 a) the suboccipital approach was performed, and the arachnoid opened showing centrally a large tumor that displaces the cerebellar hemispheres laterally invading most of the cysterna magna. b,c) the tumor is internally debulked until the cystic portion is reached and a dark yellow viscous fluid is aspirated. d) the tumor is circumferentially dissected from the parenchima without traction , and resected piecemeal. e) the floor of the iv ventricle is visible between some tumor portions attached to the inferior vellum. f) final aspect, after gross total resection was achieved with the white floor of the ivth ventricle visible between the tonsils figure 3 the 2nd day postoperative ct scan showng no tumor remnant 458 | giovani et al giant solid cystic inferior fourth ventricle subependymoma a big portion of the tumor was bulging into the cisterna magna and the first step in approaching it was internal debulking and aspiration of the dark yellow cyst fluid, incision of the vermis revealed a firm lobulated tumor that entirely occupied the cavity of the fourth ventricle. step by step, the tumor capsule was detached from the surrounding tissue, with fine movements avoiding traction on the walls of the ivth ventricle. using cotton pledges in the plane between the tumor and parenchima eased the dissection. as the tumor was firm and not attached to the floor of the ventricle it could be removed piecemeal. frozen-section examination of a tumor specimen revealed the typical histological picture of subependymoma. we did not encounter important bleeding from the tumor during resection. immediately postoperative the ataxia, nistagmus and the signs of increased intracranial pressure disappeared but she presented mild transitory dysphagia. her sensibility improved to normal at 2 months follow up. the pathology result confirmed the diagnostic of subependimoma. discussion these benign who grade 1[15], soft tumors are asymptomatic until they reach an important size even when localized in ivth ventricle so many of them are autopsy reports, with an incidence of 0,4% [9] scheithauer et al.[12] reported 21 cases of symptomatic large subependymomas, 8.3% of a large series of ependymomas, 11 of which were located in the fourth ventricle. a 10 years span retrospective study on subependymomas performed at beijing tiantan hospital analyzed 43 patients (0.07% of 60000 surgical), 7 of which were located in the fourth ventricle [2]. most of the tumors in this study 90% were located in the ventricular system, and most of them presented a multicystic pattern on mri. p. clarenbach et al. reported subependymomas of the fourth ventricle in identical twins suggesting that that not only histology and topology but also growth dynamics were prenatally determined. [5] both ct scan and mri are useful in orienting the preoperative diagnosis towards subependymoma by comparison with medulloblastoma and low-grade astrocytoma, the other frequent fourth ventricle neoplasms, sometimes the resemblance of subependymomas with astrocytomas is so big in both t1 and t2 mri sequences that only the presence of microcysts can make the difference. the mri characteristics of subependymomas are nonspecific, but mri spectroscopy showing normal choline/creatinine peaks and decreased naa peak can help in directing the diagnosis. [4, 6] our patient had no cranial nerve deficits given by compression of forth ventricle floor because the tumor enlarged the foramen magendie and was expressed in the cisterna magna displacing the vermis superiorly and the tonsils and cerebellar hemispheres laterally. the tumor was approached using a transvermian approach as we considered this better than telovelar approach, for large tumors that cross into the cisterna magna through the foramen of magendie. there are reports of transitory akinetic romanian neurosurgery (2016) xxx 4: 455 – 460 | 459 mutism associated with the transvermian approach, yet we didn’t encounter such cases in our experience [14]. we consider that in big tumors inside the ivth ventricle especially those attached to the roof, this approach is better than the telovelar approach. for most tumors involving the floor of the ivth ventricle we prefer the telovelar approach. like most cases reviewed in literature, our case had a mixt cystic solid aspect that made the resection easier. once the cyst was punctured, enough space was gained for the circumferential dissection of the tumor from the adiacent parenchima. the tumor did not infiltrate the floor of the fourth ventricle which explained the lack of cranial nerve deficits at presentation. gross total resection is the main treatment, assuring a long-term survival. a study from barrow institute compared gross total resesction (gtr) with gtr followed by radiotherapy found a statistical superiority for the latter in terms of improving the long term local control [11]. our treatment protocol for posterior fossa ependymomas also includes postoperative radiotherapy that is efficient in recurrences control and well tolerated by the patients, but we don’t recommend it for subependymomas. there were previous reports of using 5 ala for a better identification of the tumor margins [1]. this technique was not available in our case but the tumor was well encapsulated and the gross total resection could be documented by simple inspection. conclusions total resection is the treatment of choice for symptomatic subependymomas localized in posterior fossa. a meticulous surgical technique is the mainstay of a favorable outcome for the tumors located in the fourth ventricle. the choice of the approach should balance the extent of access to the tumor with the risk of damaging surrounding eloquent structures. references 1.bernal garcía lm, cabezudo artero jm, marcelo zamorano mb, gilete tejero i. ; fluorescence-guided resection with 5-aminolevulinic acid of subependymomas of the fourth ventricle: report of 2 cases: technical case report. ; neurosurgery. 2015 jun;11 suppl 2:e364-71; discussion e371 2.bi z, ren x, zhang j, jia w.; clinical, radiological, and pathological features in 43 cases of intracranial subependymoma. j neurosurg. 2015 jan;122(1):49-60. doi 10.3171/2014.9.jns14155. 3.brown df, rushing ej: subependymomas: clinicopathologic study of 14 tumors. arch pathol lab med 123:873, 1999. 4.chiechi mv, smirniotopoulos jg, jones rv: intracranial subependymomas: ct and mr imaging features in 24 cases. ajr am j roentgenol 165:1245– 1250, 1995. 5.clarenbach p, kleihues p, metzel e, dichgans j. simultaneous clinical manifestation of subependymoma of the fourth ventricle in identical twins. case report. j neurosurg. 1979 may;50(5):655-9. 6.hoeffel c, boukobza m, polivka m, lot g, guichard jp, lafitte f, reizine d, merland jj: mr manifestations of subependymomas. ajnr am j neuroradiol 16:2121– 2129, 1995 7.jooma r, torrens mj, bradshaw j, brownell b: subependymomas of the fourth ventricle. surgical treatment in 12 cases. j neurosurg 62:508–512, 1985 8.lobato rd, sarabia m, castro s, esparza j, cordobes f, portillo jm, rivas jj: symptomatic subependymoma: report of four new cases studied with computed 460 | giovani et al giant solid cystic inferior fourth ventricle subependymoma tomography and review of the literature. neurosurgery 19:594– 598, 1986. 9.matsumura a, ahyai a, hori a, schaake t.; intracerebral subependymomas. clinical and neuropathological analyses with special reference to the possible existence of a less benign variant. acta neurochir (wien). 1989;96(1-2):15-25. 10.ragel bt, osborn ag, whang k, townsend jj, jensen rl, couldwell wt. ; subependymomas: an analysis of clinical and imaging features. neurosurgery. 2006 may;58(5):881-90; discussion 881-90. 11.rogers l1, pueschel j, spetzler r, shapiro w, coons s, thomas t, speiser b. is gross-total resection sufficient treatment for posterior fossa ependymomas? j neurosurg. 2005 apr;102(4):629-36. 12.scheithauer bw: symptomatic subependymoma. report of 21 cases with review of the literature. j neurosurg 49:689–696, 1978. 13.shuangshoti s, rushing ej, mena h, olsen c, sandberg gd: supratentorial extraventricular ependymal neoplasms: a clinicopathologic study of 32 patients. cancer 103:2598–2605, 2005. 14.tamburrini g, frassanito p, chieffo d, massimi l, caldarelli m, di rocco c. cerebellar mutism. ; childs nerv syst. 2015 oct;31(10):1841-51. doi: 10.1007/s00381015-2803-6. epub 2015 sep 9. review. 15.wiestler od, schiffer d: subependymoma, in kleihues p, cavenee wk (eds): pathology and genetics of tumours of the nervous system. lyon, international agency for research on cancer (iarc) press, 2000, pp 80–81. 17guptaneha_outcome 322 | gupta et al traumatic bilateral basal ganglia hemorrhage doi: 10.2478/romneu-2018-0040 outcome of traumatic bilateral basal ganglia hemorrhage: rarest entity: prospective study of five cases: single institutional experience neha gupta1, vivek kumar kankane2, tarun kumar gupta3 1ananta institute of medical science, udaipur, india 2department of neurosurgery, sms medical college, jaipur (rajasthan) india 3department of neurosurgery, r.n.t. medical college, udaipur (rajasthan) india abstract: traumatic basal ganglia hemorrhage is rare entity but bilateral basal ganglia hematoma after trauma is extremely rare and is limited to case reports. we describe five cases of traumatic bilateral basal ganglia hemorrhage, and its outcome and management. all cases were managed conservatively. the general incidence of tbgh is reported between 2.4-3% of closed head injury. however, the incidence is higher in post mortem studies (9.8%). five consecutive patients of tbgh, shown in initial noncontrast ct (ncct) head, admitted in our institute from august 2013 to august 2016, during this period total patient admitted of head injury is 1061 so incidence of traumatic bilateral basal ganglia hemorrhage in our series is 0.47% which is very less compare to previous literature formed the prospective study group. there were 3 males and 2 females; age ranging from 20 to 45 years (average 30 years).hypertensive patients, drugs abuse history, history of coagulopathy with doubtful history of trauma or unknown mode of injury was excluded from the study. all patients had sustained road traffic accidents. ncct head done of all patients after initial resuscitation. gcs at admission were 9 to 12 (mean 10.4), outcome assessed by glasgow outcome score. all patients outcome was good. average follow up 8.54 months. key words: basal ganglia, trauma, bilateral, memorrhage introduction traumatic basal ganglia hemorrhage (tbgh) is defined as a hemorrhagic lesion located in the basal ganglia or neighboring structures such as internal capsule or thalamus. tbgh is relatively uncommon [1,2, and 3]. an incidence of 3–10% of head injuries has been reported [1,3,4] the incidence is higher in autopsy series when compared with clinical studies [1,3] bilateral basal ganglia hematoma after trauma is extremely rare and is limited to case reports romanian neurosurgery (2018) xxxii 2: 322 331 | 323 [4,5] the mechanism is unclear though it is proposed to arise from shear strain of the lenticulostriate or anterior choroid vessels caused by acceleration/deceleration forces at the time of injury [1,6]. the fact that basal ganglia hematoma can be due to trauma but its takes importance in the medico legal cases where bleeding may be attributed to a non traumatic cause. thus, the recognition of tbgh is of prime relevance. material & method five consecutive patients of tbgh, shown in initial noncontrast ct (ncct) head, admitted from january 2012 to january 2017 in the department of neurosurgery at r.n.t. medical college and m.b. hospital, udaipur, rajasthan, formed the prospective study group. a written informed consent was taken from of all patients, as applicable. the diagnosis of tbgh was made on the basis on ncct and outcome assessed by glasgow outcome score. results during study period total patient admitted of head injury is 1061 so incidence of traumatic bilateral basal ganglia hemorrhage in our series is 0.47% which is very less compare to previous literature formed the prospective study group. there were 3 males and 2 females; age ranging from 20 to 45 years (average 30 years (table1)). hypertensive patients, drugs abuse history, history of coagulopathy with doubtful history of trauma or unknown mode of injury was excluded from the study. all patients had sustained road traffic accidents. ncct head done of all patients after initial resuscitation. gcs at admission were 9 to 12 (mean 10.4), outcome assessed by glasgow outcome score (table 2). all patients outcome was good, outcome were labeled as excellent (gos-5), fair (gos-4) and poor (gos1-3) average follow up 8.54 months. we described all patients detailed in case descriptions (case-1 to case-5). table 1 demography, management and outcome of patient serial no. age sex mode of injury gcs at the time of admission focal neurological deficit management outcome measure by gos 1 20 yr male rta(road traffic accident) 9/15 right side hemiparesis conservative excellent(5) 2 40 yr male rta 9/15 left side hemiparesis conservative excellent(5) 3 35 yr female rta 10/15 no conservative excellent(5) 4 25yr female rta 12/15 no conservative excellent(5) 4 30 yr male rta 12/15 no conservative excellent(5) 324 | gupta et al traumatic bilateral basal ganglia hemorrhage table 2 glasgow outcome score gos score functional status 5 resumption of normal life; there may be minor neurological and or psychological deficit 4 able to work in a shattered environment and travel by public transportation 3 dependent for daily support by reason of mental or physical disability or both 2 unresponsive for weeks or months or until death 1 death case 1 20 year old male admitted in neurosurgery ward with head injury in unconscious state. there was no history of ear bleed, nose bleed, convulsion, csf leak. there was no history of significant illness, substance abuse, or any history suggestive of any bleeding disorder. patient was a non-diabetic non-hypertensive. prior to the accident, he was not on any medication. his glasgow coma scale (gcs) was e1v3m5. pupils were 2 mm bilaterally, reacting to light. right side grade 3 hemiparesis present. a ncct brain showed deep intracerebral bleed [figure 1a] in the basal ganglia involving the corona radiata on the right (approximately 11 mm by 14 mm) and left (approximately 18 mm by 14 mm). sulcal spaces and basal cisterns were normal and no midline shift. all blood parameters and clotting profile were within normal limits. antibiotic & phenytoin sodium was given. 2nd of admission patient became conscious, oriented & gcs was 15/15 but hemiparesis is still present with improvement of grade 3 to grade 4, 3 month of follow up of patient was alright without any hemiparesis , gcs 15/15 and advised repeat ncct head which revealed complete resolution of hemorrhage [figure 1b]. figure 1a deep intracerebral bleed in the basal ganglia involving the corona radiata on the right (approximately 11 mm by 14 mm) and left (approximately 18 mm by 14 mm) figure 1b complete resolution of bilateral basal ganglia hemorrhage case 2 45 year old male, met with a road traffic accident when he was riding a motor cycle and was hit by another motor cycle. history of loss of consciousness and nose bleed was present, there was no history of ear bleed, and convulsion vomiting & csf leak .his gcs was e2v3m5. pupils were 2 mm bilaterally, romanian neurosurgery (2018) xxxii 2: 322 331 | 325 reacting to light. left side hemiparesis grade 3 was present. plain computerized tomogram (ct) showed intracerebral bleed [figure 2a] in the basal ganglia involving the corona radiate & capsuloganglionic region on the right (approximately 22 mm by 17 mm) and left capsuloganglionic region (approximately 3 mm by 2 mm) and multiple hemorrhagic contusions are seen right temporal lobe. basal cisterns were normal no midline shift. all blood parameters and clotting profile were within normal limits. primary suturing of wound and antibiotic & phenytoin sodium was given. 3rd day of admission patient became conscious but hemiparesis was still present which was improved to grade 3 to grade 4 on 8th day of admission, patient was discharge 10th day of admission 3 month of follow up of patient was alright without any hemiparesis and advised repeat ncct head which revealed complete resolution of hemorrhage [figure 2b]. figure 2a intracerebral bleed in the basal ganglia involving the corona radiate & capsuloganglionic region on the right (approximately 22 mm by 17 mm) and left capsuloganglionic region (approximately 3 mm by 2 mm) and multiple hemorrhagic contusions are seen right temporal lobe figure 2b complete resolution of bilateral basal ganglia hemorrhage case 3 35 year old female, was admitted with history of road traffic accident in neurosurgery ward in unconscious state. there was no history of ear bleed, nose bleed, convulsion, csf leak. there was no any history suggestive of any bleeding disorder. patient was a non-diabetic non-hypertensive. his gcs was e2v3m5. pupils were 2 mm bilaterally, reacting to light. bilateral limb movement was equal. a plain computerized tomogram (ct) showed deep intracerebral bleed [figure 3a] in the bilateral basal ganglia which was mirror image to each other, it was also a rarest presentation on imaging. basal cisterns were normal and no midline shift. all blood parameters and clotting profile were within normal limits. phenytoin sodium was given. 2nd of admission patient became conscious, oriented & gcs was 15/15 and no focal neurological deficit, then patient was discharge 5th of admission. 3 month of follow up of patient was alright without any neurological deficit, and advised repeat ncct head which revealed complete resolution of hemorrhage [figure 3b]. 326 | gupta et al traumatic bilateral basal ganglia hemorrhage figure 3a showed deep intracerebral bleed in the bilateral basal ganglia which was mirror image to each other figure 3b complete resolution of bilateral basal ganglia hemorrhage case 4 35 year old female was admitted in neurosurgery ward with head injury in unconscious state. there was no history of ear bleed, nose bleed, convulsion, csf leak. there was no any history suggestive of bleeding disorder. patient was a non-diabetic nonhypertensive. prior to the accident, he was not on any medication. his gcs was e2v3m5. pupils were 2 mm bilaterally, reacting to light. bilateral limb movement was equal. a plain computerized tomogram showed deep intracerebral bleed [figure 4a] in the bilateral basal ganglia which was mirror image to each other. basal cisterns were normal and no midline shift. all blood parameters and clotting profile were within normal limits. phenytoin sodium was given. 2nd of admission patient became conscious, oriented & gcs was 15/15 and no focal neurological deficit, then patient was discharge 5th of admission. 3 month of follow up of patient was alright without any neurological deficit and advised repeat ncct head which revealed complete resolution of hemorrhage [figure 4b]. figure 4a – showed deep intracerebral bleed in the bilateral basal ganglia which was mirror image to each other figure 4b complete resolution of bilateral basal ganglia hemorrhage case 5 30 year old male, came with a road traffic accident. he was admitted in neurosurgery ward in unconscious state. his gcs was e3v3m6. pupils were 2 mm bilaterally, reacting to light. bilateral limb movement was romanian neurosurgery (2018) xxxii 2: 322 331 | 327 equal. a plain computerized tomogram showed small deep intracerebral bleed [figure 5a] in the bilateral basal ganglia basal cisterns were normal and no midline shift. phenytoin sodium was given. 2nd of admission patient became conscious, oriented & gcs was 15/15 and no focal neurological deficit, then patient was discharge 5th of admission. 3 month of follow up of patient was alright without any neurological deficit, and advised repeat ncct head which revealed complete resolution of hemorrhage [figure 5b]. patient still in follow up, he has not any deficit. figure 5a – small deep intracerebral bleed in the bilateral basal ganglia figure 5b complete resolution of bilateral basal ganglia hemorrhage discussion the general incidence of tbgh is reported between 2.4-3% [1,3, and 7] of closed head injury. however, the incidence is higher in post mortem studies (9.8%). [1,3] bilateral traumatic basal ganglia hematoma is extremely rare. descriptions are limited to case reports [1,2,4, and 5], however, kumar et al. found one patient with bilateral basal ganglia bleed amongst 10 cases of tbgh (10%) [8]. it was previously believed that tbgh were small, multiple, sometimes bilateral and located in the zone of lentiform nucleus and external capsule, whereas spontaneous hemorrhages were large solitary, large causing mass effect and in the region of thalamus and internal capsule. a patient suffering from a head injury and having a lesion of the latter type was considered to be due to a spontaneous bleed causing the event [9]. later on, in a patient of fatal severe head injury, mosberg et al. [10] at autopsy confirmed a massive hematoma in the palladium and a ruptured twig of the anterior choroidal artery. after histopathology, the arterial tear was confirmed to be traumatic. maki et al. [11] (1980), reported tbgh, where the mechanism was supposed to be anterior stretch of the lateral branch of the perforator of the middle cerebral artery. kinoshita et al. [12] (2008) have also postulated anterior choroidal artery causing basal ganglia bleed. fujioka et al. [13] have demonstrated that the traumatic dissection of the middle cerebral artery causing 328 | gupta et al traumatic bilateral basal ganglia hemorrhage hemorrhage and infraction in the basal ganglia and thalamus. in both our patients, there was a clear cut history of trauma, and no evidence, historically, clinically, and radiologically to suggest any other cause of this lesion, thereby confirming it to be tbgh. however, in the second case, the age may favor hypertensive bleed, but his blood pressure had been normal during his inpatient stay. it has been postulated that if trauma occurs while the head is in motion, and the impact sufficient to deform the skull is applied to the vertex, forehead or occipital area and directed to the tentorium, it shifts the brain through the tentorial notch, producing shearing forces leading to the damage to the vessels described above. both coup and countercoup injuries can cause this and this may cause bilateral lesions [13] tbgh may be classified as large if more than 2 cm in diameter or small if less than 2 cm in diameter [1,3]. small lesions in the basal ganglia have also been described as a part of diffuse axonal injury. however, the mechanism is shearing strain on the axons and it also involves the cerebral white mater, corpus callosum, and upper brainstem [14, 15]. treatment is based on protocol as for intracranial hematoma taking into account the neurological status, presence of mass effect and response to other means of controlling icp. treatment options for tbgh include conservative, open surgery, ct guided stereotactic or ultrasound guided aspiration [6]. boto et al. [6] recommend surgical evacuation for all lesions having a volume greater than 25 ml. in the series by kumar et al. [8] all the patients were managed conservatively (average volume 13.2 ml). however, all patients had a volume less than 25 ml (maximum 23ml). in the case of bilateral tbgh by jang et al. [4] the patient had a gcs of 15 and hence was conservatively managed. outcome of tbgh has been found to be variable. amongst 37 patients studied by boto et al. [6] 59% died, 5 % were vegetative, 19% experienced severe disabilities, and 16% made a favorable recovery. in contrast, in a study of 10 patients by kumar et al. [8] all patients had a favorable outcome (glasgow outcome score of 4 or 5) and mortality was nil. katz et al. [16] kimura et al, [17] lee et al. [18] jang et al. [4] have also reported good prognosis for tbgh, we mentioned all previous reported case in (table-3). large size, associated coagulation disorders, dai, presence of other bleeds like intraventricular of brain stem hemorrhage, age greater than 60, abnormal pupillary response, abnormal motor response to pain, and severe head injury are reported to be indicators for poor prognosis[3,7,8,18]. kankane et al reported bilateral traumatic basal ganglia bleed and both the patient managed conservatively and outcome was good and no focal neurological deficit[19] zhang yx, et al reported single case of 45 year female of traumatic bilateral traumatic basal ganglia bleed and patient managed conservatively and outcome was good and mild unilateral hemiparesis [20] willem guillermo et al reported a 28-year old man, a victim of caraccident have hyperdense lesion in the basal ganglia romanian neurosurgery (2018) xxxii 2: 322 331 | 329 bilaterally, with the presence of right parietal epidural hematoma. craniotomy and epidural hematoma drainage were considered, associated to conservative management of gangliobasal traumatic contusions. on day 7 the patient had sudden neurologic deterioration, cardiac arrest unresponsive to resuscitation. [21] recently jain and colleagues [22] reported a 38-year old fully conscious male, who presented with bilateral basal ganglia haematoma and extradural hematoma. the patient was also undergone craniotomy and hematoma evacuation pandey et al reported a 37-year-old man with traumatic left frontotemporal acute subdural hematoma, left side traumatic subarachnoid hemorrhage (tsah) and bilateral bgh with punctuate hemorrhages in the corpus callosum. left frontotemporoparietal decompressive craniectomy was done in the emergency. the patient was on ventilatory support postoperatively and remained comatose. he was in the neuro intensive care unit for 2 weeks and also required tracheostomy. at discharge, 4 weeks after injury his gcs was e4vtrm2.outcome was poor. [23] moriya t reported [24] a case of traumatic hematoma in the basal ganglia multiple gliding contusions in the left frontal and parietal lobe in 65 year old male that showed deterioration after arrival at the hospital the patient died on the 13th day of trauma . in our study all five patients had isolated bilateral tbgh without secondary brain injury. all patients managed conservatively and had good outcome. table 3 description of previous reported cases serial no. author year no. of case age of patient sex of patient description of patient management outcome 1 yanaka k et al 1991 2 17 year male tbbgh surgical good 75 year male tbbgh conservative good 2 kimura m et al 1994 2 adult male tbbgh conservative good adult male tbbgh conservative good 3 kumar et al 2009 1 35 female tbbgh conservative fair 4 bhargava et al 2012 2 male tbbgh conservative good male tbbgh conservative good 5 kankane vk et al 2016 2 20 yr male traumatic bilateral basal ganglia bleed (tbbgh), right side hemiparesis, gcs 9/10 conservative good 40 yr male tbbgh ,lt side hemiparesis, gcs 9/10 conservative good 6 zhang yx 2016 1 45yr female tbbgh conservative good 7 willem 2014 1 28 yr male tbbgh with epidural craniotomy death 330 | gupta et al traumatic bilateral basal ganglia hemorrhage guillermo et haematoma 8 jain sk et al 2013 1 38 year male tbbgh with epidural haematoma craniotomy good 9 pandey et al 2014 1 37 year male tbbgh with acute subdural hematoma craniotomy poor 10 moriya t 2013 1 65 year male tbbgh with multipal contusion conservative death 11 present study 2017 5 20yr, 40yr, 35yr, 25yr, 30yr 3 male and 2 female tbbgh conservative excellent conclusions traumatic bgh is rarely reported, and bilateral bgh is very rare entity only few cases reported in world’s literature. we reported consecutive 5 cases in a single institute in first time in world literature. bghs are compatible with a favorable recovery if not associated with damage to other cortical and sub cortical structures and present in isolation. the bghs seem to be hemorrhagic contusions as a result of a shearing injury due to high velocity impact. it can be managed conservatively. prognosis is variable and dependant on many factors. correspondence vivekkankane9@gmail.com (vivek kumar kankane) references 1. bhargava p, grewal ss, gupta b, jain v, sobti h. traumatic bilateral basal ganglia hematoma: a report of two cases. asian j neurosurg. 2012 jul; 7(3):147-50 2. jain sk, sundar iv, sharma v, prasanna kl, kulwal g, tiwari r bilateral large traumatic basal ganglia haemorrhage in a conscious adult: a rare case report. brain inj. 2013; 27(4 3. adams g, doyle d, graham di. deep intracerebral (basal ganglion) hematomas in fatal non-missile injury in man. j neurol neurosurg psychiatry. 1986; 49:1039– 43. 4. jang kj, jwa cs, kim kh, kang jk. bilateral traumatic hemorrhage of the basal ganglia. j korean outcomeneurosurg soc. 2007; 41:272–4 5. yanaka k, egashira t, maki y, takano s, okazaki m, matsumaru y, et al. bilateral traumatic hemorrhage in the basal ganglia: report of two cases. no shinkei geka. 1991;19:369–737. 6. boto gr, lobeto rd, rivas j. basal ganglion hematoma in severely head injured patients: clinicoradiological analysis of 37cases. j neurosurgery. 2001;94:224–25. 7. katz di, alexander mp, seliger gm, bellas dn. traumatic basal ganglia hemorrhage: clinicopathologic features and outcome. neurology. 1989; 39:897–04. 8. kumar s, jha d, abbey p, mishra v, handa a. outcome of traumatic basal ganglia hemorrhage. internet j neurosurg. 2009:61. 9. courville cb, blomquist oa. traumatic intracerebral hemorrhage: with particular reference to its pathogenesis and its relation to “delayed traumatic apoplexy” arch surg. 1940;41:1–28. 10. mosberg wh, lindenberg r. traumatic hemorrhage from the anterior choroidal artery. j neurosurg. 1959; 16:209–21. 11. maki y, akimoto h, enomoto t. injuries of basal ganglia following head trauma in children. childs brain. 1980; 7:113–23. 12. kinoshita y, yasukouchi h, harada a, tsuru e, okudera t. case report of traumatic hemorrhage from the anterior choroidal artery, no shinkei geka. 2008;36:891–4 13. fujioka m, maeda y, okuchi k, kagoshima t, taoka t. secondary change in the substantia niagra induced romanian neurosurgery (2018) xxxii 2: 322 331 | 331 by incomplete infarct and minor hemorrhage in the basal ganglia due totraumatic middle cerebral arterial dissection. stroke. 1999;30:1975–7 14. lindenberg r. trauma of meninges and brain. in: minckler j, editor. pathology of the nervous system. vol. 2. new york: mcgraw-hill; 1971. pp. 1705–65. 15. shimura t, nakazawa s, kobayashi s, yokota h, otsuka t, nakamura t. clinicopathological studies of diffuse axonal injury-five autopsy cases. no shinkei geka. 1988;16(5 suppl):647–53 16. katz di, alexander mp, selinger gm. traumatic basal ganglion hemorrhage: clinicopathologic features and outcome. neurology. 1989;39:897–904 17. kimura m, sobata e, suzuki s. traumatic basal ganglion (caudate) with favorable prognosis: report of two cases. no shinkei geka. 1994;22:155–8. 18. lee jp, wang adj. post-traumatic basal ganglia hemorrhage: analysis of 52 patients with emphasis on the final outcome. j trauma. 1991;31:376–80. 19. kankane vk, gupta tk, jaiswal g. traumatic bilateral basal ganglia bleed: a report of rare two cases and review of the literature. asian j neurosurg 2016;11:457. 20. zhang yx, wei sq, xing yy, liu q, he wj bilateral traumatic hemorrhage of the basal ganglia.chin j traumatol. 2016 aug 1;19(4):247-8 21. willem guillermo calderon-miranda, hernando raphael alvis-miranda, gabriel alcala-cerra, andres m. rubiano, luis rafael moscote-salazar: bilateral traumatic basal ganglia hemorrhage associated with epidural hematoma: case report and literature review. bull emerg trauma. 2014 jul; 2(3): 130–132. 22. jain sk, sundar iv, sharma v, prasanna kl, kulwal g, tiwari rn. bilateral large traumatic basal ganglia haemorrhage in a conscious adult: a rare case report. brain inj. 2013;27(4):500-3 23. nityanand pandey, ashok mahapatra, and pankaj kumar singh: bilateral large traumatic hemorrhage of the basal ganglion. asian j neurosurg. 2014 oct-dec; 9(4): 240. 24. moriya t, tagami r, furukawa m, sakurai a, kinoshita k, tanjoh k. a case of traumatic hematoma in the basal ganglia that showed deterioration after arrivalat the hospital. acta neurochir suppl. 2013;118:147-9. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article mirror image extradural hematoma in elderly population: management strategy with surgical bilateral or unilateral evacuation or conservative treatment modality with literature review guru dutta satyarthee, rajpur yada, luis rafael moscote-salazar, amit agrawal india, colombia doi: 10.1515/romneu-2017-0087 romanian neurosurgery (2017) xxxi 4: 555 559 | 555 doi: 10.1515/romneu-2017-0087 mirror image extradural hematoma in elderly population: management strategy with surgical bilateral or unilateral evacuation or conservative treatment modality with literature review guru dutta satyarthee1, rajpur yada1, luis rafael moscotesalazar2, amit agrawal3 1department of neurosurgery, neurosciences centre, aiims new delhi, india 2neurosurgeon-critical care, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia 3department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: extradural hematomas (edh) represent one of common imaging findings in cases sustaining traumatic brain injury. bilateral extradural haematoma is considered rare and even rarer in elder people male. bilateral extradural hematoma is usually acute, and generally associated with severe traumatic head injury. mirror-image extradural hematomas (medh) constitute a special type of bilateral extradural hamatomas, which is placed anatomically symmetrically on both the sides of the intracranial compartment, requires prompt diagnosis and emergent surgical intervention as it carry high mortality if evacuation of hematoma is not carried out expeditely. the mortality rate still remains higher in comparison to unilateral single extradural hematomas. the postoperative outcome depends on preoperative neurological status, total volume of blood, accurate diagnosis and prompt shifting to neurosurgical facility, expatiation of surgical procedure, prehospital care. authors report a case of a 65-year-old man who presented with acute simultaneous bilateral extradural haematomas following road traffic accident, underwent bilateral trephine craniotomy and simultaneous evacuation on both side led to good recovery. key words: mirror image extradural hematoma, simultaneous evacuation, bilateral trephine craniotomy introduction mirror-image extradural hematomas (medh) are usually placed anatomically symmetrically on both side of the intracranial compartment. it occurrence is extremely unusual and carries associated high mortality 556 | satyarthee et al mirror image extradural hematoma in elderly population and morbidity due to rapid rise in the intracranial pressure which lead to transtentorial herniation so need to be managed by surgical evacuation on emergency basis. the incidence is about 1.8 %. (1) further acute extradural hematomas are infrequent among elderly patients. a greater adhesion between calvarial bone and endosteal layers of dura is responsible for very low incidence elderly persons and lucid interval is less common. (2) the most frequent mechanisms in elderly for extradural hematomas include falls and assaults. (2) case illustration a-65year male presented with loss of consciousness following motor vehicular accident, while he was riding bicycle hit by speeding car with right sided hemiparesis associated with repeated episodes vomiting and earnose bleed with one episode of generalized tonic clonic seizure. he was immediately intubated in emergency services nad put on ventilatory support. examination at arrival, vitals were stable with gcs was 8/15(e3m4vet). on neurological examination revealed, his right pupil was dilated not reacting to light with left sided paucity of movement. non-contrast ct scan head revealed presence of bilateral extradural hematoma located over frontoparietal region on both side of intracranial compartment, more on left side with right temporal contusion with presence of mass effect producing mass effect, as chinked ventricle on right side with subfalcine herniation. (figure 1) he was rushed to operation theatre from ct room, bilateral trephine craniotomy (figure 2) was made with about 25 ml hematoma on right side and 100 ml on left sided was evacuated (figures 3, 4a&b, 5, 6) the source of bleed was identified and coagulated, hemostasis secured. at the end of surgery the brain was lax, multiple hitch sutures was taken. the bone flap was replaced and central hitch taken subgaleal extradural drain placed and wound were closed in layers. following surgery, he was extubated on third postoperative day with slow recovery of hemiparesis. figure 1 ncct head showing mirror image extradural hematoma causing mass effect with subfalcine herniation figure 2 ncct head showing mirror image extradural hematoma causing mass effect with subfalcine herniation romanian neurosurgery (2017) xxxi 4: 555 559 | 557 figure 3 intra-operative view of bilateral trephine craniotomy figure 4a intra-operative photograph showing left side extradural hematoma figure 4b intra-operative photograph showing right side extradural hematoma figure 5 clinical photograph of evacuated hematoma of mirror image extradural hematoma figure 6 clinical photograph of trephine bone flap raised for evacuation of mirror image extradural hematoma 558 | satyarthee et al mirror image extradural hematoma in elderly population discussion usually, bilateral extradural hematoma tends to occur more commonly in the young adult patients. the reported incidence range varies 2 to 10%. [6-8] male to female ratio is 5:1; as male are more affected as outdoor activity, can be found across the midline in about 50-70% of cases. ([8-10) there is associated skull fracture observed in about 95-100% of patients in their imaging study. [7, 8, 9, 11] in that case of bilateral edh with fractures across the midline, the source of bleeding may result from the superior sagittal sinus. [12] edhs are contact injuries resulting from blunt trauma to the skull; it was thought that the initial impact with cranial fracture detaches the dura and injures blood vessels once bleeding begins, the extradural space fills with blood. (2-60) depending on the source of bleed in extradural hematoma, the bilateral extradural hematoma can be classified into venous and arterial origin. the venous bleeding source type is much commoner, as blood accumulate slowly, so presents with delay following accident but may present quite rapidly and patient can show neurological deterioration very quickly. further venous bleeding is slower, so tends to be smaller in size and less severe due to the ease of spontaneous arrest. arterial bleeding produces hydrostatic water pressure effects progressively stripping away the dura from the skull and widening the perimeter of the hematoma. the elderly are less likely to manifest signs or symptoms of increased intracranial pressure due to cerebral atrophy, and almost all haematomas commonly used to occur in the parietal area (3). medh usually follows sustaining significant head trauma resulting in rapid, occasionally late deterioration in sensorium, even in patients with initial no neurological deficits; this indicates rapid expansion with imminent tentorial herniation of the brain with rapid rise of intracranial pressure. [12] rarely, medh may develop sequentially rather than simultaneously and may escape imaging evaluation on initial cranial ct scan further serial cranial ct scanning is also important for diagnosis when a patient deteriorates in the postoperative period following removal of the unilateral haematoma . [7, 12] verma et al. advocated rapid evacuation for such lesions, which is the key for good neurological outcome. (1) majority of cases with medh require surgical evacuation, sometimes bilateral simultaneous craniotomies as our case was managed by bilateral trephine craniotomy with evacuation of extradural hematoma. [10, 11] however, few surgeons in past tried conservative measure of management [10] but need vigilant clinical observation in icu setup with no neurological deficit, very small amount of intracranial blood, serial cranial computed tomography imaging, and arrangement for bed side burrhole or trephine facility should be available. we strongly feel bilateral evacuation is usually required as patient presents with delay, having poor gcs, imaging showing sizeable blood collection wit associated mass effect. romanian neurosurgery (2017) xxxi 4: 555 559 | 559 post-operative results were satisfactory. hamlat et al. analyzed 14 elderly male with unilateral extradural hematoma, which was managed with surgical evacuation with 7.2 % mortality, highlighting early diagnosis and urgent surgical treatment is highly advocated. (3) authors concluded extradural hematoma in elderly following a fall, carries better prognosis. (3) huda et al. analyzed 46 patients with double extradural hematoma, 39 cases with bilateral edh underwent bilaterally surgical evacuation. (5) conclusion mirror image extradural hematoma (medh) are anatomically and symmetrically placed extradural hematoma on both side of the intracranial compartment needs prompt diagnosis, early referral to neurosurgical centre and emergent bilateral surgical evacuation in poor neurological grade patients can improve the neurological outcome as our had good neurological outcome. correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: drguruduttaaiims@gmail.com references 1. verma, s k, borkar s a, sharma b s mirror-image epidural hematoma. indian j neurotrauma 2015: 12: 164-167 2. teixeira, saulo araujo; becco-neto, eliseu; ramosjunior, francisco; rolim-neto, modesto leite. acute extradural hematoma in elderly case report. health med; 2012; 6: 32163219 3. hamlat a , mazzon a , adn m, morandi x, riffaud l, guegan y, brassier g intracranial epidural haematomas in elderly patients: observations in 14 patients. acta neurochir (wien) (2005) 147: 1055-1060 4. amit a. bilateral symmetrical parietal extradural hematoma j surg tech case rep. 2011 ; 3(1): 34–36. 5. huda mf, mohanty s, sharma v, tiwari y, choudhary a, singh v p double extradural hematoma: an analysis of 46 cases. neurology india. 2004, 52: 450452 6. udoh d o. bilateral post-traumatic acute extradural hematomas: a report of four cases and review of literature. niger j clin pract 2012;15:104-7 7.reale f, biancotti r. acute bilateral epidural hematoma. surg neurol 1985;24:260-2. 8.gelabert-gonzález m, iglesias-país m, serramitogarcía r, fernández-villa j, garcía-allut a, martínezrumbo r. simultaneous bilateral epidural haematomas. neurocirugia (astur) 2005;16:256-60. 9. dharker sr, bhargava n. bilateral epidural haematoma. acta neurochir (wien) 1991;110:29-32. 10. gorgulu a, cobanoglu s, armagan s, karabagli h, tervuz m. bilateral epidural hematoma. neurosurg rev 2000;23:30-3. 11. idei m, shima t, nishida m, yamane k, mihara c, hatayama t, et al. symmetrical bilateral extradural haematoma after head injury in the mid-parietal region: case report. no shinkei geka 2004;32:379-82. 12. bret p, gavin c, massini b, bascoulergue y, huppert j. bilateral extradural haematomas. report of two cases. neurochirurgia (stuttg) 1987;30:193-6. microsoft word 10musawael_surgery 272 | musa et al surgery for recurrent high-grade gliomas             doi: 10.2478/romneu-2018-0033 surgery for recurrent high-grade gliomas: the dilemma of debate wael musa, ahmed n. taha department of neurosurgery, mansoura medical school, egypt abstract: background: treating recurrent gliomas is a big dilemma in the literature and no uniform protocol is approved to treat such disappointing problem. although improvement in the rt techniques, new ctx techniques and new techniques including targeted therapy and gene therapy; all fail to dramatically improve the outcome and solve the problem of significant mass effect when the recurrent tumor is big so resurgery play a role in treating such challenging problem. the aim of the study: to assess the goal and outcome of surgery in treatment of recurrent malignant glioma. methods: we retrospectively analyzed the data of 56 patients who were operated upon for recurrent or progressed high grade gliomas in the mansoura neurosurgery department allover 2007 to 2016. we have excluded patients with recurrent thalamic gliomas and patients with kps score less than 70. results: 12 patient underwent sterotactic biopsy for their tumor and were sent for adjuvant radiotherapy, 29 patients underwent partial tumor resection and gross total resection was done in 15 patients. the median time to progression was 5 months. all patients were sent after surgery for poster radiotherapy and chemotherapy. the median overall survival was 4 months. conclusion: recurrent high grade glioma is one of unsolved problem and optimal management is no longer available. redo surgery is quiet challenging with higher minorities and no add to overall survival. surgery is indicated to relieve significant mass effect. outcome of surgery is better for those who did aggressive surgical resection at initial surgery than those who did only partial resection. key words: rt radiotherapy, ctx chemotherapeutic, kps karnofsky performance status introduction high grade gliomas are the most common primary brain tumor and the most challenging regarding the treatment opportunities.¹⁻²⁻³ safe gross total resection followed by adjuvant treatment including radiotherapy and chemotherapy (temozolomide) is the standard treatment that could be offered to such dismal tumors.4 despite advancement in the treatment modalities; the outcome is improved mostly in the functional status but romanian neurosurgery (2018) xxxii 2: 272 282 | 273             the potential survival has not significantly improved and recurrence is mostly inevitable. treating recurrent gliomas is a big dilemma and no uniform protocol is approved to treat such disappointing problem. although improvement in the radiotherapeutic techniques making re-irradiation for recurrent gliomas is potentially safe and new chemotherapeutic techniques and the development of new techniques including targeted therapy and gene therapy; all fail to dramatically improve the outcome and solve the problem of significant mass effect when the recurrent tumor is big making redo surgery play a role in treating such challenging problem. 5⁻6 surgery for recurrent high-grade glioma should be tailored and individualized based on the patient’s age, clinical status, karnofsky performance status score. the extent of resection and numbers of redo surgeries played an important role regarding the quality of life and expected survival for recurrent grade iii or iv gliomas.6 the aim of this retrospective study is to assess the goal and outcome of surgery in treatment of recurrent malignant glioma. patients and methods we retrospectively analyzed the data of 56 patients who were operated up on for recurrent or progressed high grade gliomas in the neurosurgery department, mansoura university during the period from 2007 to 2016. previous treatment for those cases was surgery followed by adjuvant treatment in the form of radiotherapy with or without chemotherapy. we have excluded patients with recurrent thalamic gliomas and patients with karnofsky performance status score less than 70. results patient characteristics are shown in table 1. median age was 47.79 years. thirty-three patients were male, and 23 were female. histology was who grade 4 in 44 patients and grade 3 in 12 patients. at last follow-up, 32 of 56 patients had died. median follow-up from the date of reoperation was 7 months (range, 0–94 months) for all patients and 11 months (range, 0–94 months) for surviving patients. predictors of survival we chose certain factors to predict the survival of our patient from diagnosis and from reoperation to be included in this study, and these factors are; age, size of 2ry tumor, interval between operation, pathology of 2ry tumor and treatment offered after reoperation. as regard age of patients, median survival rate from diagnosis for patients less than 50 years was 11.00 and 9.00 for patients more than 50 years( p value 0.034) figure 1-a; median survival rate from reoperation for patients less than 50 years was 5.00 and 4.00 for patients more than 50 years( p value 0.060) figure 1-b   274 | musa et al surgery for recurrent high-grade gliomas             table 1 patient characteristics age mean ± sd 47.79 9.81 size of 1ry_tumor (cm) median min – max 5.00 3-7 time to recurrence (m) median min – max 5.00 2-15 size of recurrence (cm) median min – max 4.00 2.5-7 survival time (m) median min – max 5.00 1-13 sex male 33 58.9% female 23 41.1% tumor location rt frontal 8 14.3% rt t/p 4 7.1% lf f/t/p 3 5.4% lf f/t 5 8.9% lf temporal 4 7.1% rt temporal 4 7.1% rt p/o 2 3.6% lf f/p 2 3.6% rt f/t/p 5 8.9% corpus callosum 9 16.1% lf p/o 2 3.6% lf p 3 5.4% lf t/p 2 3.6% lf f 1 1.8% rt f/p 1 1.8% rt p 1 1.8% pathology of 1ry tumor gbm 39 69.6%% g3 8 14.3% primary ttt gtr rt 19 33.9% ptr rt ch 7 12.5% gtr rt ch 10 17.9% ptr rt 9 16.1% stb rt ch 3 5.4% stb rt 8 14.3% pathology of 2dry t gbm 44 78.6% g3 12 21.4% surgery complication no 22 39.3% lt hemiparesis 7 12.5% coma 6 10.7% aphasia 2 3.6% rt hemiparesis 9 16.1% seizures 9 16.1% csf leakage 1 1.8% romanian neurosurgery (2018) xxxii 2: 272 282 | 275             figure 1-a median survival rate from diagnosis according patients age figure 1-b median survival rate from reoperation according patients age survival from diagnosis and from reoperation acording to size of 2ry tumor is shown in figure 2-a,b. median survival rate from diagnosis for 2ry tumor less than 5cm in size was 11.00 and for more than 5 cm was 7.00 with p value 0.004,while it was from reoperation for tumor less than 5cm 5.00 and 3.00 for larger tumor size with p value < 0.001. figure 2-a survival from diagnosis according to size of 2ry tumor figure 2-b survival from reoperation according to size of 2ry tumor on the other hand, if we are looking for survival from diagnosis and from reoperation according to interval between operation as shown in figure 3-a, b. we found that the median survival rate from diagnosis for patients whom underwent another surgery for the tumors in less than 6 months from the primary surgery was 8.00 and its increase to 18.00 for patients did 2nd surgery in period more than 6 months from first tumor attacking with p value 0.001. while median survival rate from reoperation for patients whom underwent 276 | musa et al surgery for recurrent high-grade gliomas             another surgery for the tumors in less than 6 months from the primary surgery was 4.00 and its increase to 7.00 for patients did 2nd surgery in period more than 6 months from first tumor attacking with p value < 0.001. figure 3-a survival from diagnosis according to interval between operation figure 3-b survival from reoperation according to interval between operation according to pathology of 2ry tumor, survival from diagnosis and from reoperation shown figure 4-a, b. we found that the median survival rate from diagnosis for patients whom 2ry tumor pathology was gbm was 9.00 and its 15.00 for patients whom 2ry tumor pathology was grade 3 with p value 0.003.while median survival rate from reoperation for patients whom 2ry tumor pathology was gbm was 4.00 and its 7.00 for patients whom 2ry tumor pathology was grade 3 with p value 0.011. figure 4-a survival from diagnosis according to pathology of 2ry tumor figure 4-b survival from reoperation according to pathology of 2ry tumor romanian neurosurgery (2018) xxxii 2: 272 282 | 277             finally, according to treatment offered after reoperation, survival from diagnosis (table 2, figure 5-a) and from reoperation (table 3, figure 5-b). table 2 survival from diagnosis according to treatment offered after reoperation ttt_offered total n n of events censored median survival time p n percent gtr_rt_cht 6 6 0 0.0% 12.000 ˂0.001 ptr 2 2 0 0.0% 6.000 gtr_cht 15 15 0 0.0% 18.000 ptr_rt 1 1 0 0.0% 11.000 ptr_cht 18 18 0 0.0% 9.000 ptr_rt_cht 8 8 0 0.0% 9.000 ptr_dc 6 6 0 0.0% 4.000 overall 56 56 0 0.0% 9.000 figure 5-a survival from diagnosis according to treatment offered after reoperation 278 | musa et al surgery for recurrent high-grade gliomas             table 3 survival from reoperation according to treatment offered after reoperation ttt_offered total n n of events censored median survival time p n percent gtr_rt_cht 6 6 0 0.0% 7.000 ˂0.001 ptr 2 2 0 0.0% 1.000 gtr_cht 15 15 0 0.0% 8.000 ptr_rt 1 1 0 0.0% 6.000 ptr_cht 18 18 0 0.0% 4.000 ptr_rt_cht 8 8 0 0.0% 3.000 ptr_dc 6 6 0 0.0% 1.000 overall 56 56 0 0.0% 5.000 figure 5-b survival from reoperation according to treatment offered after reoperation romanian neurosurgery (2018) xxxii 2: 272 282 | 279             in our current study we have different patient complications varied from hemiparesis, coma, csf leakage, and aphasia (table 4) table 4 patient complications sex male female surgery complication no count 14 8 % 63.6% 36.4% lt hemiparesis count 6 1 % 85.7% 14.3% coma count 4 2 % 66.7% 33.3% aphasia count 1 1 % 50.0% 50.0% rt hemiparesis count 5 4 % 55.6% 44.4% seizures count 3 6 % 33.3% 66.7% csf leakage count 0 1 % 0.0% 100.0% treating recurrent high-grade gliomas is a big dilemma and debate still exist in the literature about the value of redo surgery in improving the overall prognosis of such dismal tumors. patient age and karnofsky performance status (kps) are very important detectors for the quality and duration of survival after reoperation. patients with recurrent high-grade glioma with kps more than 70 have better outcome than those less than 70. age and preoperative kps score had a significant effect on duration of high-quality survival after reoperation.8⁻¹²⁻¹³⁻¹4⁻¹5⁻¹6⁻¹7⁻¹9⁻²º⁻²¹ some studies compared the quality of survival and duration of survival for patients with recurrent high-grade gliomas who offered re-operation to those who not operated up on. one study found a 9-month survival (operated group) compared with 5.75 months (non-operated group). 9⁻²²⁻²5⁻²6⁻²7 many published data showed 5-50% 280 | musa et al surgery for recurrent high-grade gliomas             improvement in kps after re-operation for recurrent high-grade gliomas. improvement in the adjuvant treatment protocols with the use of conformal fractionated radiotherapy with the use of temozolomide chemotherapy helped to improve the clinical outcome and overall survival for high-grade glioma. despite such improvement; the chance of tumor progression or recurrence still exist and still there is a big debate if adjuvant treatment alone is enough for recurrence or there is a role for re-operation.4 in a one retrospective study done by on 65 patients who underwent reoperation for progressing high grade gliomas. median time to second surgery was 7.1 months. the indications to reoperation were increase in the tumor size on magnetic resonance imaging, new neurological deficit, manifestation of increased intracranial pressure and epilepsy. the authors found better overall survival for those who did reoperation the those who did not.9 many other reports addressed such controversial problem and they found that outcome of re-operation for recurring high-grade gliomas is multifactorial and more favorable outcome was found for those patients with age 50 years or less, time interval more than 9 months between operations, achieving gross total resection (gtr), and kps scores 70 at reoperation.9⁻²²⁻²5 some studies addressed the role of either radiotherapy plus temozolimide or temozolimide alone for treating progressing high-grade gliomas and despite initial good results; the found less capabilities of achieving good tumor control and overall survival compared to re-operation with adjuvant treatment. however; there was no difference in outcome of the patient functional status.¹¹ improvement in neurosurgical techniques, neuro-anesthesia, and post-operative icu care minimized procedure related morbidities and mortalities. however, proper patient selection is very important to choose the case who might get benefit from re-operation. beside the patient age, kps, the time to recurrence; other factors may play an important role be considering the outcome. 5⁻7⁻8⁻¹º⁻¹²⁻¹³⁻¹5⁻¹8⁻²¹⁻²³⁻²8 the tumor size and the degree of central necrosis play an important role regarding the outcome and it was found in some studies that the prognosis was favorable with patients having tumor necrosis rather than tumor recurrence. smaller tumor volume had a more favorable outcome compared with bigger tumor volume at time of re-operation. the extent of tumor removal is another prognostic indicator for the outcome which is also dependent on the tumor size and location with more favorable outcome occur with achieving adequate gross total resection at both the time of primary and re-operations. it was found the re-operation for recurrent tumor after initial gross total resection has a better outcome than after partial resection or just biopsy.²4 gross total resection (gtr) is recognized by many studies as an independent predictor of improved survival in patients with recurrent high-grade glioma. it was found that the residual tumor volume has its impact on outcome of temozolomide chemotherapy after re-operation.² one study on recurrent highgrade gliomas reported a median survival of romanian neurosurgery (2018) xxxii 2: 272 282 | 281             11months after gtr compared to 5 months after only partial resection disregarding patient age and performance status.²³ in another study; authors analyzed a series of 107 patients with re-operation for recurring highgrade glioma. they addressed the value of the extent of tumor resection at the initial and subsequent surgery. the found the best survival outcome with subtotal resection at the initial surgery and gtr at re-operation with median overall survival of 16.7-month and the worst outcome with partial resection at both surgery with 7.4 median overall survival.5 patients age play an important role in overall prognosis for recurrent high-grade gliomas and the younger the age the better the prognosis. although some centers did not offer surgery for elderly with recurrent highgrade gliomas; some studies concluded that surgery should be considered for all patients with favorable kps disregarding the age of the patient.²9 the goal of surgery for recurrent highgrade gliomas is to do safe adequate resection with limited morbidities. the potential morbidities for re-operation was studied in many case series. some studies showed no difference in the incidence of morbidities while others showed higher chance of surgery related morbidities. in one study; 18% patients had neurological deterioration for surgery of recurrent cases compared to 8% neurological deterioration after the initial surgery. 7 conclusion: although advancement in neurosurgical techniques; recurrent high grade glioma is one of unsolved problem for neurosurgical practice and optimal management is no longer available. redo surgery is quiet challenging with higher minorities and no add to overall survival. surgery is indicated to relieve significant mass effect. outcome of surgery is better for those who did aggressive surgical resection at initial surgery than those who did only partial resection. but if resurgery is indicated due to mass effect of the tumor may help to improve survival and should be considered in patients with a favorable kps score at time resugery. references 1. deangelis lm. brain tumors.n engl j med.2001;344(2):114-123. 2. deorah s, lynch cf, sibenaller za, ryken tc. trends in brain cancer incidence and survival in the united states: surveillance, epidemiology, and end results program, 1973 to 2001.neurosurg focus.2006;20(4):e1. 3. surawicz ts, davis f, freels s, laws er jr, menck hr. brain tumor survival: results from the national cancer data base. j neurooncol. 1998;40(2):151-160. 4. stupp r, dietrich py, ostermann kraljevic s, et al. promising survival for patients with newly diagnosed glioblastoma multiforme treated with concomitant radiation plus temozolomide followed by adjuvant temozolomide.j clin oncol.2002;20(5): 1375-1382. 5. bloch o, han sj, cha s, et al. impact of extent of resection for recurrent glioblastoma on overall survival: clinical article. j neurosurg. 2012;117 (6):1032-1038. 6. chaichana kl, zadnik p, weingart jd, et al. multiple resections for patients with glioblastoma: prolonging survival.j neurosurg. 2013;118(4):812-820. 7. chang sm, parney if, mcdermott m, et al. perioperative complications and neurological outcomes of first and second craniotomies among patients enrolled in the glioma outcome project. j neurosurg. 2003;98(6):1175-1181. 8. harsh gr, levin va, gutin ph, seager m, silver p, wilson cb. reoperation for recurrent glioblastoma and anaplastic astrocytoma. neurosurgery. 1987;21(5): 615621. 9. helseth r, helseth e, johannesen tb, et al. overall survival, prognostic factors, and repeated surgery in a 282 | musa et al surgery for recurrent high-grade gliomas             consecutive series of 516 patients with glioblastoma multiforme.acta neurol scand.2010;122(3):159-167. 10. rusthoven ke, olsen c, franklin w, et al. favorable prognosis in patients with high-grade glioma with radiation necrosis: the university of colorado reoperation series. int j radiat oncol biol phys.2011;81(1):211-217. 11. terasaki m, ogo e, fukushima s, et al. impact of combination therapy with repeat surgery and temozolomide for recurrent or progressive glioblastoma multiforme: a prospective trial.surg neurol.2007;68(3):250-254. 12. young b, oldfield eh, markesbery wr, et al. reoperation for glioblastoma. j neurosurg. 1981;55(6):917-921. 13. ammirati m, galicich jh, arbit e, liao y. reoperation in the treatment of recurrent intracranial malignant gliomas. neurosurgery. 1987;21(5):607-614. 14. azizi a, black p, miyamoto c, croul se. treatment of malignant astrocytomas with repetitive resections: a longitudinal study.isr med assoc j. 2001;3(4):254-257. 15. barker fg ii, chang sm, gutin ph, et al. survival and functional status after resection of recurrent glioblastoma multiforme.neurosurgery. 1998;42(4):709-720. 16. clark aj, butowski na, chang sm, et al. impact of bevacizumab chemotherapy on craniotomy wound healing.j neurosurg. 2011;114(6):1609-1616. 17. clark aj, lamborn kr, butowski na, et al. neurosurgical management and prognosis of patients with glioblastoma that progresses during bevacizumab treatment. neurosurgery. 2012;70(2):361-370. 18. dirks p, bernstein m, muller pj, tucker ws. the value of reoperation for recurrent glioblastoma. can j surg.1993;36(3):271-275. 19. durmaz r, erken s, arslantas a, atasoy ma, bal c, tel e. management of glioblastoma multiforme: with special reference to recurrence. clin neurol neurosurg.1997;99(2):117-123. 20. keles ge, lamborn kr, chang sm, prados md, berger ms. volume of residual disease as a predictor of outcome in adult patients with recurrent supratentorial glioblastomas multiforme who are undergoing chemotherapy.j neurosurg.2004; 100(1):41-46. 21. landy hj, feun l, schwade jg, snodgrass s, lu y, gutman f. retreatment of intracranial gliomas. south med j.1994;87(2):211-214. 22. mandl es, dirven cm, buis dr, postma tj, vandertop wp. repeated surgery for glioblastoma multiforme: only in combination with other salvage therapy.surg neurol.2008;69(5):506-509. 23. mcgirt mj, chaichana kl, gathinji m, et al. independent association of extent of resection with survival in patients with malignant brain astrocytoma.j neurosurg. 2009;110(1):156-162. 24. park jk, hodges t, arko l, et al. scale to predict survival after surgery for recurrent glioblastoma multiforme. j clin oncol.2010;28(24):3838-3843. 25. pinsker m, lumenta c. experiences with reoperation on recurrent glioblastoma multiforme. zentralbl neurochir.2001;62(2):43-47. 26. rostomily rc, spence am, duong d, mccormick k, bland m, berger ms. multimodality management of recurrent adult malignant gliomas: results of a phase ii multiagent chemotherapy study and analysis of cytoreductive surgery. neurosurgery. 1994;35(3):378388. 27. salcman m, kaplan rs, ducker tb, abdo h, montgomery e. effect of age and reoperation on survival in the combined modality treatment of malignant astrocytoma.neurosurgery. 1982;10(4):454-463. 28. sipos l, afra d. re-operations of supratentorial anaplastic astrocytomas.acta neurochir (wien).1997;139(2):99-104. 29. stark am, hedderich j, held-feindt j, mehdorn hm. glioblastoma: the consequences of advanced patient age on treatment and survival.neurosurg rev. 2007;30(1):5661.   microsoft word _2.formatata_iencean.doc romanian neurosurgery vol. xv nr. 1 13 progressive parenchymatous intracranial hypertension – review st.m. iencean1, a.v. ciurea2, n. ianovici3, i. poeata3 1neurosurgery, “prof. dr. nicolae oblu” hospital, iasi, romania 2clinical emergency hospital “bagdasar arseni” bucharest, the university of medicine and pharmacy “carol davila”, bucharest, romania 3clinical emergency hospital “prof dr nicolae oblu” iasi, the university of medicine and pharmacy “gr.t. popa”, iasi, romania the parenchymatous intracranial hypertension is the intracranial pressure increase caused by the intracranial volume modifications due to an intrinsic parenchymatous lesion (expansive intra-parenchymatous lesion, brain edema, etc.) or an extrinsic lesion (tumor, traumatic, infectious extra-parenchymatous compression, etc.). depending on the location and the development manner, intracranial expansive processes cause the progressive increase in the intracranial pressure and then the occurrence of the ich syndrome by the development of a supplementary volume. benign intracranial tumors have a slow volume increasing rate and the neurological syndrome is installed progressively, while the ich syndrome may occur late. malign tumors have a rapid development rate and the neurological syndrome occurs precociously. the clinical decompensation represents the aggravation of the symptomatology by the tumor extension or by exceeding the compensating capacities of the intracranial pressure increase. keywords: brain gliomas, brain metastases, chronic subdural hematoma, intracranial hypertension, intracranial pressure, decompensation of intracranial hypertension introduction the parenchymatous intracranial hypertension is the intracranial pressure increase caused by the intracranial volume modifications due to an intrinsic parenchymatous lesion (expansive intraparenchymatous lesion, brain edema, etc.) or an extrinsic lesion (tumor, traumatic, infectious extraparenchymatous compression, etc.). the primary cerebral lesion and the secondary endocranial volume changes (expansive or compressive new volume, hypoxic or traumatic brain edema, etc.) cause disorders of the intracranial pressure equilibrium mechanisms. the infraclinical stage includes the compensating mechanisms of the intracranial pressure increase and, if these mechanisms are exceeded by the pressure increase, the characteristic clinical and paraclinical charts of the intracranial hypertension syndrome are shown. [6, 20, 21] the parenchymatous intracranial hypertension develops depending on the existing etiology, on how rapidly the parenchymatous lesion extends, on the compensating mechanisms of the pressure increases, and on the efficiency of the medical and/or neurosurgical treatment. the development of the parenchymatous intracranial hypertension includes: • an incipient ich syndrome, • a compensated ich syndrome, or • a complete development till decompensation – the acute form with brainstem ischemia or with cerebral hernia. st.m. iencean romanian neurosurgery vol. xv nr. 1 14 the parenchymatous intracranial hypertension can occur in: • the intracranial space-replacing lesions: cerebra tumors, hematomas, cerebral tumors, intracranial hematomas, cerebral abscesses, intracranial cystic lesions, etc., • the traumatic brain edema, • the hypoxic brain edema through posttraumatic secondary cerebral ischemia or in sub-arachnoid hemorrhage, • general intoxications with neurotoxins: endogenous or exogenous. the parenchymatous intracranial hypertension varies in its starting manner, intensity of symptoms and development, which depend on: • the nature of the lesion, which determines the development speed and the effect of the lesion on the neighbouring cerebral parenchyma (brain edema), • the location of the lesion, which can involve the sector or integral cerebral parenchyma (encephalitis, generalized brain edema), depending on the involvement of the cerebral vessels or of the anatomic paths of circulation of the cerebrospinal fluid. the vascular compression causes ischemic disorders and the blockage of the cerebrospinal fluid circulation can lead to an obstructive hydrocephalus. depending on these characteristics, intracranial disorders may present a specific, focal symptomatology, (epileptic crises, motor and sensorial deficits, etc.) or general symptoms (asthenia, cephalea, psychic disorders, endocrine disorders, etc.) or they may start as an intracranial hypertension syndrome. there are significant differences from the point of view of evolution, prognosis and therapy between intracranial disorders that start as an intracranial hypertension syndrome and those starting as a focal or non-characteristic symptomatology, and which subsequently present an ich syndrome. [20, 21, 22] a distinction is made between: • the parenchymatous intracranial hypertension with an acute start, and • the parenchymatous intracranial hypertension with an progressive start. pathogenesis of progressive parenchymatous intracranial hypertension intracranial expansive processes with a progressive development can have the initial clinical manifestation of a neurological focus syndrome or by a non-specific symptomatology, to which the symptomatology of the intracranial hypertension is gradually added afterwards. depending on the location and the development manner, intracranial expansive processes cause the progressive increase in the intracranial pressure and then the occurrence of the ich syndrome by the development of a supplementary volume. [18, 20, 21, 35, 38] the new endocranial volume may be represented by: the lesion that replaces the intracranial space (endocranial tumor, intra-parenchymatous hematoma, subdural chronic hematoma, cerebral abscess, etc.), whose volume has increased progressively; the secondary brain edema of a primary lesion having a relatively reduced volume; extended brain edema with a compressive (mass) effect on the fluid spaces and on adjacent parenchymatous structures. benign intracranial tumors have a slow volume increasing rate and the neurological syndrome is installed progressively, while the ich syndrome may occur late. malign tumors have a rapid development rate and the neurological syndrome occurs precociously. the clinical decompensation represents the aggravation of the symptomatology by the tumor extension or by exceeding the compensating capacities of the intracranial pressure increase, and it manifests itself by: increase in the frequency of comitial crises, occurrence or accentuation of neurological deficits, occurrence of symptoms and installation of the ich syndrome, occurrence of consciousness disorders: confusion syndrome, apathy, etc. installation of coma. progressive parenchymatous intracranial hypertension romanian neurosurgery vol. xv nr. 1 15 the occurrence of the intracranial hypertension syndrome depends on the characteristics of the endocranial lesions. these lesion characteristics refer to: the speed of the increase in the supplementary endocranial volume, which depends on the nature of the lesion (benign or malign tumor, intra-cerebral hematoma, subdural chronic hematoma, etc.): benign tumor lesions have a slow increase, with moderate cerebral suffering, the sudden occurrence of the intracranial hypertension may suggest a rapid expansion at the level of the tumor by producing an intratumor hemorrhage or the accelerated development of a tumor cyst the biological effect on the adjacent cerebral tissue (direct, compressive edematous effect, etc.): malign gliomas lead to the occurrence of the brain edema, they produce neoformation vessels, etc. cerebral metastases are accompanied by an important brain edema and the intracranial hypertension is frequently present. the location of the supplementary volume (direct compression on the vital structures, blockage of the cerebrospinal fluid circulation): subtentorial tumors evolve more frequently with ich compared to supratentorial tumors, because the circulation of the cerebrospinal fluid may be blocked by the peritumoral edema and by the location of the tumor, tumors, even the malign ones localized at the frontal, occipital pole, can develop for long periods of time with no ich syndrome. the period that includes the changes in the intracranial pressure, reaching and then exceeding the normal pressure limit values is long, with a slow increasing speed of the intracranial pressure, and decompensation can take place rapidly or after a longer period of time. during the infraclinical period, there is a compensation of the pressure increases caused by the newly added volume, but the limit pressure is reached. once the compensating capacities are exceeded, the intracranial pressure increase is rapid, and the duration of these pathological pressure values is short due to the rapid decompensation. fig. 1 subtentorial tumor with blocked fourth ventricle fig. 2 acute icp increase, with a prolonged infraclinical period and a rapid decompensation; the interval to-t1 is prolonged, weeks or even months, and the decompensation may last for a few days there is also the possibility of a slow increase in intracranial pressure: with a prolonged infraclinical period and a long period of pathologic icp increase. the intracranial pressure increases slowly and progressively up to the normal limit value, and it continues its slow increase depending on the ich etiology. the ability to compensate the pressure increase allows a prolonged maintenance of the cerebral sanguine flux, and there is a long period of the pathological pressure values. the ich syndrome is prolonged and its aggravation is rapidly produced, st.m. iencean romanian neurosurgery vol. xv nr. 1 16 surpassing all the compensating methods of pressure increases. etiology of progressive parenchymatous intracranial hypertension 1. brain gliomas with a reduced degree of malignity they are cerebral tumors with a slow increasing rate, most frequently they have a supratentorial location, especially frontal and temporal, or they may be developed in the brainstem, and they are more frequent in young adults. the dominating symptoms are motor deficient, epileptic crises, cephalea and psychic disorders. the ich syndrome with a papillary edema occurs more rarely because the location does not affect the circulation of the cerebrospinal fluid and because the dominating symptoms bring the patient to the physician before the increase in the tumor volume, which produces signs of intracranial hypertension. 2. brain gliomas with an increased degree of malignity they are malign cerebral tumors, usually located deep into the white matter, but sometimes they may also have an intra-ventricular development or, from the deep cerebral hemispheric white matter, they may have a cortical extension. the mechanisms that lead to the occurrence of the symptomatology are: local parenchymatous effects; compression on the neighbouring structures: nervous parenchyma, cerebral vessels or the circulation paths of the cerebrospinal fluid, the tumor invasion on the neighbouring structures: nervous parenchyma and/or cerebral vessels, local tissue destruction with the formation of the cellular degrading products, hypoxia of the neighbouring nervous tissue by the direct compression of the sanguine vessels too, metabolic and electrolytic disorders release of cytokines, of free radicals, etc. diffuse intracranial effects caused by: the increase in the intracranial pressure by the tumor volume the secondary effects of the volume increase on the cerebral parenchyma, on the blood circulation and on the dynamics of the cerebrospinal fluid. the clinics is represented by: focal neurological syndromes: irritation syndrome: psychic disorders, epileptic crises syndrome in a deficit: sensitive or motor. syndrome of progressive intracranial hypertension: psychic disorders, cephalea, vomiting, papillary edema, etc. 3. brain metastases cerebral metastases are accompanied by an important brain edema, and intracranial hypertension is frequently present. the single cerebral metastasis may be focalized anywhere in the cerebral parenchyma and it practically has the characteristics of a malign cerebral tumor; multiple metastases usually exceed the direct surgical therapeutic possibilities. the symptomatology depends on the location of the lesion/lesions and on the occurrence of the intracranial hypertension through well-known mechanisms. 4. intra-cerebral hematoma in the primary intra-cerebral hematomas, the occurrence and development of the intracranial hypertension depends on preexistent factors (elements of hypertensive encephalopathy), on the volume of the hematoma and on the superficial or deep lumbar location, in the oval center, on the communication with the ventricular system, and perhaps on the circulating blockage of the cerebrospinal fluid. 5. chronic subdural hematoma the chronic subdural hematoma is a well-known neurosurgical entity; it occurs after a usually minor cranial traumatism, and it is characterized by the slow evolution of the “pre-clinical” period. usually, the focal neurological symptomatology is of a first ground interest, but, sometimes, the ich syndrome may be marked, especially in the case of a cranial-cerebral traumatism, which subsequently produces clinical decompensation. 6. benign intracranial tumors progressive parenchymatous intracranial hypertension romanian neurosurgery vol. xv nr. 1 17 benign intracranial tumors are represented by meningiomas, neurinomas, hypophysial tumors, etc. the benign intracranial tumors present a slow increasing rate, and the symptomatology is represented by the focal neurological syndromes, and, usually at a delayed stage, by the intracranial hypertension syndrome. they most frequently cause the occurrence of the ich syndrome by blocking the circulation of the cerebrospinal fluid, producing an intracranial hypertension by disorders of the cerebrospinal fluid dynamics. secondly, the benign intracranial tumor induces a peritumoral brain edema, which brings about the occurrence of a parenchymatous intracranial hypertension with a progressive evolution. 7. other endocranial lesions other types of expansive intracranial lesions – cerebral abscesses, dural empyemas, parasitoses (hydatid cyst), etc., present variable evolutions of the intracranial hypertension syndrome based on the same characteristics: location of the lesion, the expansion speed and the edematous character of lesions. the relationship between lesion location and ich occurrence in the case of a parenchymatous ich with a gradual start, the relation between the location of the lesion and the occurrence of the intracranial hypertension syndrome seems less significant because the blocking mechanism of the cerebrospinal fluid circulation with the ich occurrence by the compressive lesion of the ventricular system, belongs to the intracranial hypertension by disorders of the cerebrospinal fluid dynamics. the multiple concomitant regional monitoring of the intracranial pressure has revealed the existence of significant pressure differences between the values of the sector intracranial pressure, especially in the case of temporal lesions, which may evolve towards decompensation by cerebral hernia before the icp equalization in all the endocranial compartments. usually, the occurrence and rapid decompensation of the intracranial hypertension, which is explained by the location of the lesion, frames this type in the ich by blocking the circulation of the cerebrospinal fluid and by the occurrence of the acute obstructive hydrocephalus. references 1. adamides aa, winter cd, lewis pm, cooper dj, kossmann t, rosenfeld jv. current controversies in the management of patients with severe traumatic brain injury. anz j surg. 2006 ;76(3):163-74. 2. albanese j, leone m, alliez jr, kaya jm, antonini f, alliez b, martin c. decompressive craniectomy for severe traumatic brain injury: evaluation of the effects at one year. crit care med. 2003.;31(10): 2535-8. 3. allan r, chaseling r. subtemporal decompression for slitventricle syndrome: successful outcome after dramatic change in intracranial pressure wave morphology. report of two cases. j neurosurg. 2004; 101( suppl):214-7. 4. ayr lk, yeates ko, taylor hg, browne m. dimensions of postconcussive symptoms in children with mild traumatic brain injuries. j int neuropsychol soc. 2009 ;15(1):19-30. 5. balestreri m, steiner la, czosnyka m. sex-related differences and traumatic brain injury. j neurosurg. 2003 99(3):616 . 6. bedford rf, morris l, jane ja. intracranial hypertension during surgery for supratentorial tumor: correlation with preoperative computed tomography scans. anesth analg. 1982 ; 61(5):430-3. 7. bell mj, kochanek pm. traumatic brain injury in children: recent advances in management. indian j pediatr. 2008 nov;75(11):1159-65. 8. berger s, schwarz m, huth r. hypertonic saline solution and decompressive craniectomy for treatment of intracranial hypertension in pediatric severe traumatic brain injury. j trauma. 2002 ; 53(3):558-63. 9. caricato a, conti g, della corte f, mancino a,et al effects of peep on the intracranial system of patients with head injury and subarachnoid hemorrhage: the role of respiratory system compliance. j trauma. 2005; 58(3):571-6. 10. ciurea av, nuteanu l, simionescu n, georgescu s. posterior fossa extradural hematomas in children: report of nine cases. childs nerv syst. 1993 ;9(4):224-8. 11. cruz j, minoja g, okuchi k. major clinical and physiological benefits of early high doses of mannitol for intraparenchymal temporal lobe hemorrhages with abnormal pupillary widening: a randomized trial. neurosurgery. 2002 ;51(3):628-37. 12. dziedzic t, szczudlik a, klimkowicz a, rog tm, slowik a. is mannitol safe for patients with intracerebral hemorrhages? renal considerations.clin neur neurosurg. 2003 ;105(2):87-9. 13. figaji aa, fieggen ag, peter jc. early decompressive craniotomy in children with severe traumatic brain injury.childs nerv syst. 2003; 19(9):666-73. 14. flierl ma, smith wr, morgan sj, stahel pf. molecular mechanisms and management of traumatic brain injury missing the link? world j emerg surg. 2009 4;4:10. 15. fritsch mj, doerner l, kienke s, mehdorn hm. hydrocephalus in children with posterior fossa tumors: role of st.m. iencean romanian neurosurgery vol. xv nr. 1 18 endoscopic third ventriculostomy. j neurosurg. 2005 ;103(1 suppl):40-2 16. grande po, naredi s. clinical studies in severe traumatic brain injury: a controversial issue. intensive care med. 2002 ;28(5):529-31 17. he xs, zhang x. giant calcified chronic subdural haematoma: a long term complication of shunted hydrocephalus.j neurol neurosurg psychiatry. 2005 ;76(3):367. 18. hlatky r, valadka ab, robertson cs. intracranial hypertension and cerebral ischemia after severe traumatic brain injury. neurosurg focus. 2003 ,15;14(4):e2. 19. huang wd, pan j, xu m, su w et al changes and effects of plasma arginine vasopressin in traumatic brain injury. j endocrinol invest. 2008; 31(11):996-1000. 20. iencean st m a new classification and a synergetical pattern in intracranial hypertension. medical hypotheses , 2002; 58(2):159-63. 21. iencean st m pattern of increased intracranial pressure and classification of intracranial hypertension. journal of medical sciences, 2004, vol.4,nr.1 :5258 22. iencean st m classification and essential conditions of decompensation in intracranial hypertension rom j neurosurgery 2004, 1;1,. 3-13 23. inenaga c, tanaka t, sakai n, et al: diagnostic and surgical strategies for intractable spontaneous intracranial hypotension. case report. j neurosurg 94:642–645, 2001 24. kamat p, vats a, gross m, checchia pa. use of hypertonic saline for the treatment of altered mental status associated with diabetic ketoacidosis. pediatr crit care med. 2003 ;4(2):239-42. 25. kontopoulos v, foroglou n et al decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered? acta neurochir (wien). 2002 ; 144 (8):791-6. 26. marcoux kk. management of increased intracranial pressure in the critically ill child with an acute neurological injury. aacn clin issues. 2005 ;16(2):212-31. 27. mathew p, teasdale g, bannan a, oluoch-olunya d. neurosurgical management of cerebellar haematoma and infarct. j neurol neurosurg psychiatry. 1995; 59: 287–292. 28. mori k, ishimaru s, maeda m. unco-parahippocampectomy for direct surgical treatment of downward transtentorial herniation. acta neurochir. 1998; 140: 1239–1244. 29. mowery nt, gunter ol, guillamondegui o et al stress insulin resistance is a marker for mortality in traumatic brain injury. j trauma. 2009 ;66(1):145-51; 30. mussack t, huber sm, ladurner r, hummel t, mutschler w. bilateral decompressive craniectomy due to intracranial hypertension during acute posttraumatic liver dysfunction. j trauma. 2005; 58(5):1061-5. 31. owler bk, besser m. extradural hematoma causing venous sinus obstruction and pseudotumor cerebri syndrome. childs nerv syst. 2005; 21(3):262-4. 32. psarros tg, coimbra c. endoscopic third ventriculostomy for patients with hydrocephalus and fourth ventricular cysticercosis: a review of five cases. minim invasive neurosurg. 2004 ; 47(6):3469. 33. roberts i, schierhout g, wakai a. mannitol for acute traumatic brain injury. cochrane database syst rev. 2003;(2):cd001049. review. 34. salim a, hadjizacharia p, dubose j et al persistent hyperglycemia in severe traumatic brain injury: an independent predictor of outcome.am surg. 2009 ;75(1):25-9. 35. scarone p, losa m, mortini p, giovanelli m. obstructive hydrocephalus and intracranial hypertension caused by a giant macroprolactinoma. prompt response to medical treatment. j neurooncol. 2006; 76(1):51-4. 36. schneider gh, bardt t, lanksch wr, unterberg a. decompressive craniectomy following traumatic brain injury: icp, cpp and neurological outcome. acta neurochir suppl. 2002;81:77 37. shiozaki t, nakajima y, taneda m, etc all. efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia. j neurosurg. 2003; 99(1):47-51. 38. soffietti r, ruda r, mutani r. management of brain metastases.j neurol 2002; 249(10):1357 39. steiner la, balestreri m, johnston aj et al predicting the response of intracranial pressure to moderate hyperventilation. acta neurochir (wien). 2005 ;147(5):477-83. 40. vincent jl, berre j. primer on medical management of severe brain injury. crit care med. 2005 ;33(6):1392-9. 41. watling cj, cairncross jg. acetazolamide therapy for symptomatic plateau waves in patients with brain tumors. report of three cases. j neurosurg. 2002 ;97(1):224-6. 42. winter cd, adamides aa, lewis pm, rosenfeld jv. a review of the current management of severe traumatic brain injury.surgeon. 2005; 3(5):329-37. 43. winter cd, adamides a, rosenfeld jv.the role of decompressive craniectomy in the management of traumatic brain injury: a critical review.j clin neurosci. 2005 ;12(6):619-23. doi: 10.33962/roneuro-2021-012 radiological features of the intracranial extra-skeletal mesenchymal chondrosarcoma.a report of two cases insight in the literature review anas abdallah, i̇rfan çınar romanian neurosurgery (2021) xxxv (1): pp. 75-79 doi: 10.33962/roneuro-2021-012 www.journals.lapub.co.uk/index.php/roneurosurgery radiological features of the intracranial extra-skeletal mesenchymal chondrosarcoma. a report of two cases insight in the literature review anas abdallah, i̇rfan çınar1 department of neurosurgery, private aile hospital, istanbul, turkey abstract background: mesenchymal chondrosarcomas are the most malignant form of chondrosarcomas. they have mostly affected bones. rarely, these tumors can be intracranial extraskeletal (iemc) that originates from the meninges or parenchyma. methods and materials: we presented two iemc patients who were treated at our institutions and followed up for the long-term. to understand the radiological features of iemc, we conducted a systematic literature review for previously reported series and cases of iemcs. results: we surgically treated two young males with iemc initially diagnosed at their age of 18 and 20 years. the patients initially treated with gross total resection (gtr) and gtr followed by radiotherapy, and followed-up for 218 and 73 months, respectively. with both patients, we obtained 83 reported iemc patients from the literature. among them, only 30 cases were reported with their radiological mri details. the mean age of the reported cases was 24.5±16.0 years (2 months–71 years). female predominance was 54.2%. the mean progression-free and overall survivals were 27.9 and 39.0 months, respectively. most iemcs showed a partially calcified mass on roentgenography and a highly vascular mass on angiography. on t1wis, iemcs almost show hypoto isointensity and intense heterogeneous enhancement after administering a contrast substance. on t2wis, iemcs show isoto hyperintensity. conclusions: iemcs usually show dural attachment without a net dural tail sign and a well-identified brimmed vascular nodule on tof-mra. this nodule appears as a prominent blooming on swi. tof-mra and swi images can help in the radiological diagnosis of iemcs. 1. background intracranial extraskeletal mesenchymal chondrosarcomas (iemcs) are rare malignant neoplasms. they almost occurred among pediatric and young people. primary intracranial chondrosarcomas constitute about 0.15% of all brain tumors.1 after including our two patients and an exhaustive literature review, we find only 83 reported patients with iemcs. microscopically, iemc characterizes by two distinct components with a frequently abrupt transition between these two components. keywords intracranial extraskeletal mesenchymal chondrosarcoma, tof-mra, swi, vasogenic edema, diagnosis corresponding author: anas abdallah department of neurosurgery, private aile hospital, istanbul, turkey dr.anasabdallah@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 76 anas abdallah, i̇rfan çınar the first component is comprised of highly cellular and undifferentiated mesenchymal cells. the second component is comprised of islands of welldifferentiated and benign-appearing cartilage.1,2 the recommended appropriate management is gross total resection (gtr) followed by radiotherapy; however, iemcs have a high propensity for neural axis dissemination.1-4 iemcs are reported to be aggressive, quick-growing tumors with high mitotic index properties.1,2 therefore, preoperative radiological distinguishing the subtype of chondrosarcoma is essential in managing these patients. in this study, we discuss the diagnostic radiological features that can help in distinguishing these rare malignant lesions by evaluation of the data from our two patients and followed with a brief review. 2. methods and materials we presented two iemc patients who were treated at our institutions and followed up for the long-term. both patients gave written consent to applied surgeries and for publications. to understand the radiological features of iemc, we conducted a systematic literature review for previously reported series and cases of iemcs. to understand the radiological features of iemcs, we identified the publications reported series or cases of iemc. the selection criteria were; full-text published in english and accessed by medline, google scholar, and pubmed databases irrespective of the setting, study design, or details. then, we analyzed the pooled sample after adding our two patients (n = 83). the search in the mentioned databases was up to oct 1, 2020. we excluded the cases reported bone destructions, epidural location, tumors originate from skull bones, or reports did not identify non-skeletal situations. statistical analysis since the cases reported with sufficient data were less than 50 (cases with mri and ct details 30 and 25 cases, respectively), most reported cases were case reports, and the early reported iemc cases miss the important details regarding radiological examinations, we could not achieve meta-analysis. 3. results our illustrative cases case 1: an 18-year-old boy presented to our outpatient clinic with a one-month history of headaches. a contrast-enhanced mri revealed a well-capsulated heterogeneously enhanced tumoral mass measuring 4.9x4.5x4.2 cm. it was located in the right temporoparietal region. the intense contrast well-enhanced tumor was iso-hyperintense on t2wis and iso-hypointense on t1wis (fig. 1). presumptive diagnosis indicated that it is an atypical meningioma. at the time of surgery, we observed that the tumor had attached to the dura. gtr was applied to the mass. histopathologically, the tumor was confirmed to be an mc. we discharged him on pod3 with no neurological deficits. no adjuvant treatment was applied. the postoperative metastatic work-up (petct) demonstrated no extracranial involvement. up to the pom22, his postoperative course was uneventful. at his yearly control visit, he had no symptoms. a contrast-enhanced mri revealed a lobulated heterogeneously enhanced tumoral mass measuring 5.2x3.8x3.2 cm. it was located in the same first operation field. the tumor was resected completely. the tumor was confirmed histopathologically to be a recurrence of the first tumor. the patient received rt. on his pom72, he had been free of tumor recurrence or extracranial metastatic lesions. the patient had done his attended school. he works as an accountant for more than two years. figure 1. an 18-year-old boy presented to our outpatient clinic with a one-month history of headaches. his neurological examination was intact except for increases in dtrs. a contrast-enhanced mri revealed a well-capsulated heterogeneously enhancing tumor measuring 4.9x4.5x4.2 cm. the mass was located in the right temporoparietal region and surrounded by diffuse edema. the lesion made a 7-8 mm shift to the left side and extending into the underlying brain 77 radiological features of iemcs parenchyma. [a]: t1wis demonstrated the lesion with two compartments. the lateral (small) one was hypointense and surrounded by the larger medial compartment. the medial compartment showed slight hypointensity compared to grey matter. [b]: t2wi-axial images demonstrated the lesion with separate two components. a small hypointense one was surrounded by the larger one that was hyperintense. [c]: t2wicoronal images showed diffuse edema. [d]: tof-mra images showed a lateral hypointense nodule resembles the same as those that are seen in high vascularized lesions. the medial component was a slight inhomogeneous iso-hypointense. [e]: contrast-enhanced t1wis showed intense heterogeneously enhanced mas with two compartments. [f]: brimmed prominent blooming nodule surrounded by the larger mild hyperintense component. case 2: a 38-year-old man referred to us with three days' duration of difficulties in speech, changes in consciousness, and severe headaches. a contrastenhanced mri revealed a multilobulated and wellcapsulated mass. it was a heterogeneously enhanced tumor and measuring 8.2x6.2x5.6 cm. the tumor was located in the left frontotemporal region and surrounded by diffuse vasogenic edema. it was hyperintense on t2wis and hypointense on t1wis (fig. 2). the tumor was diagnosed as intra-axial metastasis of mc. the patient received gross total resection followed by rt for right parietal iemc 18 years ago. over 18 years, he had received multiple mandibular and maxilla surgeries and twice adjuvant rt for several metastases. in his last presentation, he was lethargic and had not full responses to alters. ntr was achieved. after the surgical intervention, the patient required icu care and died of disease on pod93. figure 2. a 38-year-old man referred to us with three days' duration of difficulties in speech, changes in consciousness, and severe headaches. a contrast-enhanced mri revealed a multilobulated heterogeneously intense enhanced tumor measuring 8.2x6.2x5.6 cm. the mass was located in the left frontotemporal region and surrounded by diffuse edema. the patient received gross total resection followed by rt for right parietal iemc 18 years ago. over 18 years, he had received multiple mandibular and maxilla surgeries and twice adjuvant rt for several metastases. [a]: contrast-enhanced t1wis revealed a multilobulated, heterogeneous, and intense enhanced tumor with distributed hypointense areas. [b]: t1wis showed a mild hypointense lesion with a brimmed hypointense nodule. [c]: tof-mra images showed a hypointense lateral compartment. it resembles the nodule is seen in a high vascularized lesion. the medial component was a slight inhomogeneous iso-hypointense. [d]: t2wi showed heterogeneous hyperintense surrounded by diffuse vasogenic edema while the medial nodule was hyperintense. literature review we surgically treated two young males with iemc initially diagnosed at their age of 18 and 20 years. the patients initially treated with gross total resection (gtr) and gtr followed by radiotherapy, and followed-up for 218 and 73 months, respectively. with both patients, we obtained 83 reported iemc patients from the literature. among them, only 30 cases were reported with their radiological mri details. thirty-three patients were reported without any radiological details. the mean age of the reported cases was 24.5±16.0 years (2 months–71 years). female predominance was 54.2%. the mean progression-free and overall survivals were 27.9 and 39.0 months, respectively. the most commonly affected intracranial region was frontal that was seen in 22 patients (26.5%). the mean preoperative maximal diameter of 31 reported tumors was 6.0±2.3 cm (1.8–11.0 cm). the parenchymal origin was reported in 13 cases while falcine and tentorial originate were reported in 15 and 8 cases, respectively. the early reported cases were reported with details regarding roentgenography and angiography. early reports mentioned that iemcs demonstrate several intracerebral flecks of calcification, destructive lesions, mottled calcification, or dense flocculent calcification on roentgenography. some iemcs showed a highly vascular mass on angiography. twenty-five cases were reported with ct details. most iemcs showed a lesion with two compartments; one compartment had density higher than calcium and the other had 78 anas abdallah, i̇rfan çınar density lower than calcium on ct scan. sometimes they show bone destructions. on t1wis, iemcs almost show hypoto isointensity and intense heterogeneous enhancement after administering a contrast substance. on t2wis, iemcs show isoto hyperintensity. 4. discussion histopathologically, iemc is a biomorphic tumor that comprises of undifferentiated cell mesenchymal mixed with differentiated cartilaginous tissue. therefore, the tumor in most cases showed heterogeneous intensity in most sequences. contrast-enhanced mri remains the gold standard to demonstrate these lesions. however, the radiological findings are not pathognomonic for iemcs. calcifications that may appear incidentally on ct could be aware of the radiologist regarding iemc. icmes almost are extra-axial, well-capsulated, and lobulated in shape. however, 13 cases were reported to be intra-axial (parenchymal in origin) lesions.5 tof-mra and swi techniques help in the radiological diagnosis of iemcs. the apparent dural tail is one of the most characteristic radiological features of meningioma. in our two cases, the dural tail sign wasn't net while we identified the brimmed vascular nodule without vessel dilatations on tofmra. this nodule appears as a prominent blooming on swi. this nodule is the same as those seen in vascular lesions. although it is not pathognomonic, vasogenic peritumoral edema on flair and t2wis usually is prominent. the same features are seen in angiomatous meningiomas too. however, calcification can be distinguishable features for iemcs. additionally, we can recognize vascular lesions such as avm and aneurysms by tof-mra. up-to-date, no study could differentiate iemc from meningioma by radiological scanning studies. iemcs are misdiagnosed as atypical meningioma,1,2 hemangiopericytoma,3 schwannomas,4 dural-based metastasis,5 gliomas, or oligodendroglioma.6 iemcs vary from hypoto isointense on t1-wis with intense heterogeneous enhancement after administering a contrast substance. on t2wis, iemcs demonstrate isoto hyperintensity. these lesions show an isoto hyperintensity on mra images that mimic arteriovenous malformations. sometimes iemcs demonstrate extremely hypervascular on angiographic images.3,4 included in our two cases, the radiological features were mentioned in 30 patients. six among them were reported to have cystic components, four were highly vascular, and three were hemorrhagic. tof-mra can guide the surgeon in understanding the vascularity of the tumor, as tofmra demonstrates the main vessels that passing through the tumors and is useful to identify tumor involvement with the cavernous sinus and main vascular structures. swi technique is beneficial for detecting smaller vascular lesions that otherwise are missed by other sequences. the craniospinal meninges are the most commonly seen location of iemcs in cns.1,3-6 we can divide iemcs into dural or parenchymal. the most commonly affected region was the frontal with a dural attachment that was seen in 23 patients. most of the reported lesions with a dural or meningeal attachment are usually supratentorial (71 patients); 49 were reported to be lateral lesions while 22 were midline lesions. parenchymal origin was reported in 13 tumors. one of the most challenging in diagnosis the lesion is taken small biopsy or specimens from one component without pieces from the second one when obtained pieces without the cartilaginous elements.1,3-6 the lesion is generally demonstrated well-circumscribed, the rubbery firm solid, multilobulated, gray or reddish-brown colored, and almost invasive. prominent vascularity and focal calcification are the main features of the lesion's cut surface. the present study suffered from a few limitations, most of the early reported iemc cases miss the important details needed to define the natural history and applied treatment, the recently reported cases miss sufficient data regarding the radiological examinations, and the pooled data were not sufficient to achieve meta-analysis review. 5. conclusions in our patients, we utilized tof-mra and swi images to distinguish these malignant lesions from other benign lesions. most reported iemcs show hypoto isointense and isoto hyperintensity on t1-wis and t2-wis, respectively. they showed intense heterogeneous enhancement with contrast. on t2wis, iemcs show isoto hyperintensity. although we can't emphasize this due to their rarity, a brimmed vascular nodule on tof-mra and a prominent blooming (nodule) sign on swi may distinguish these highly vascularized solid firm 79 radiological features of iemcs lesions. they uncommonly have cystic, highly vascular, or hemorrhagic components. declarations consent for publication: informed written consent was obtained from both patients and their relatives for publication. competing interests: none funding: none authors’ contributions: aa: conceptualization, methodology, software, supervision, formal analysis, statistical analysis, literature review, visualization, investigation, writing – original draft, writing – review, and validation. i̇ç: validation, writing, reviewing, literature review, and supervision. both authors deserve the first name. acknowledgements: none. authors’ information: both authors work at the department of neurosurgery, private aile hospital, 34590 istanbul, turkey. abbreviations cns = central nervous system, dtrs = deep tendon reflexes, er = emergency department, gtr = gross-total resection, iemc = intracranial extraskeletal mesenchymal chondrosarcoma, mc = mesenchymal chondrosarcoma, ntr = near-total resection, pod = postoperative day, pom = postoperative month, rt = radiotherapy, t1wis = t1-weighted mr images, t2wis = t2-weighted mr images, tof-mra = time-of-flight magnetic resonance angiography. references 1. tanvir i, riaz s, khan ha, et al. mesenchymal chondrosarcoma arising in the central nervous system: a diagnostic pitfall. int j head neck surg 4(3):2013;152–5. 2. dahlin dc, henderson ed. mesenchymal chondrosarcoma: further observations on a new entity. cancer 1962;15:410–7. 3. vergeer ra, vink r, avenarius jk, et al. a 71-year-old woman with an intracranial duralbased mesenchymal chondrosarcoma. j clin neurosci 2012;19:1170–1. 4. lin l, varikart w, dexter m, et al. diagnostic pitfall in the diagnosis of mesenchymal chondroma arising in central nervous system. neuropathology 2012;32:82–90. 5. yassa m, bahary jp, bourguoin p, et al. intra-parenchymal mesenchymal chondrosarcoma of the cerebellum: case report and review of the literature. j neurooncol. 2005;74:329–31. 6. nokes sr, dauito r, murtagh fr, et al. intracranial mesenchymal chondrosarcoma. ajnr am j neuroradiol. 1987;8:1137–8. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article safety and e ectiveness of microvascular decompression for treatment of hemifacial spasm through mini craniotomy ashraf elbadry, nabil mansour ali, ahmed abdelkhalek egypt doi: 10.1515/romneu-2017-0077 romanian neurosurgery (2017) xxxi 4: 495 – 509 | 495 doi: 10.1515/romneu-2017-0077 safety and effectiveness of microvascular decompression for treatment of hemifacial spasm through mini craniotomy ashraf elbadry, nabil mansour ali, ahmed abdelkhalek skull base unit, neurosurgery department and diagnostic radiology department, faculty of medicine, mansoura university, egypt abstract: background: the hemifacial spasm (hfs) defined as involuntary intermittent twitching of the muscles of the face (usually unilateral). the spasms characteristically begin around the eye and then extend to affect other muscles of the ipsilateral face. it is caused by vascular element compressing the facial nerve that may be either the anterior or the posterior inferior cerebellar arteries in most cases. objective of our work: to describe the operative technique (pearls and common mistakes), the efficacy and morbidity of microvascular decompression technique for hemifacial spasm through mini craniotomy, determine the prognostic factors affecting success rate of the surgery. material & method: a retrospective study of 23 cases of hemifacial spasm treated by mini craniotomy retro sigmoid approach and microvascular decompression at neurosurgery dept., mansoura university hospital in last 10 years was investigated. this include epidemiological, clinical and imaging details, selected treatment options and patients’ outcome. results: complete resolving of symptoms was conducted in 19 cases 82.6% while reoperated in 2 cases with improvement in one case. facial palsy appeared postoperative in 6 cases 4 of them improved in 3 months, transient hearing loss in 4 cases17.4% which improved later, cerebrospinal fluid leak appeared in 3 cases 13% which managed conservatively. conclusions: mvd relieves symptoms of hfs in about 80% of patients while recurrence still in low percentage. the study reported low permanent complications and generally transient. key words: hemifacial spasm, vascular decompression, microvascular, face muscle twitches, micro vascular surgery introduction hemifacial spasm (hfs) usually defined as an involuntary, unilateral in most cases, paroxysmal, tonic-clonic facial musculature contraction that is innervated by ipsilateral facial nerve “the seventh cranial nerve”. in 496 | elbadry et al microvascular decompression for treatment of hemifacial spasm majority of the cases these twitches begin around the eyes “orbicularis oculi muscle “then spread progressively to the cheek, mouth, and neck “platysma “inferiorly & frontalis (i.e., muscles of the forehead) superiorly muscles in severe cases. [1] the incidence of hfs is around 0.8 per 100,000 persons. [2] while others reported higher prevalence of hfs as i9.8 per 100,000 persons [3] or even higher in worldwide as 14.5 per 100,000 women and 7.4 per 100,000 men [2, 4]. maybe this due to underdiagnoses lead to reduction of the cases discovered [5] the aetiology of the primary hfs is vascular element compressing the facial nerve at root (exit or entry) zone. this vascular element may be the anterior inferior cerebellar artery (aica), posterior inferior cerebellar artery (pica), vertebral artery (va), veins ,perforators or even un-named vessels ,especially if there was lateral deviation of one or both vertebral arteries that play as major risk factor [6,7].usually the compression occurred as a result of the vessel loop indenting the facial nerve or arachnoid thickening between the brainstem and the offending vessels stretching the nerve during pulsations[8] .some cases showed more than one offending vessel and may be this one of causes of microvascular decompression [9].in some case unfortunately did not have any recognisable cause [10]. the pathophysiology of hfs hypothesis speculate demyelination of the facial nerve at ( entry -exit ) nerve zone that is termed as the alteration site between central zone myelination by (oligo-dendrocytes) and peripheral zone myelination by (schwann) cell myelination which is enclosed by arachnoid membrane without any interfascicular connective tissue or epineurium isolating the fibres leading to more susceptibility to injury by compression [11] the second hypothesis of hfs stated the ectopic excitation and ephaptic transmission along the facial nerve due to demyelination lead to emerging an abnormal impulses at lower threshold level that spread through the facial nerve making short circuit at the site of the lesion[12] . the last but not the least of hfs theory conducted that central demyelination with subsequent connection reorganization of the affected facial nucleus making it hyper excitable because of dendritic spike formation [13] sympathetic hypothesis suggested the sympathetic endings in adventitia of the offending vessels induce abnormal action potential at neuromuscular junction inducing hemifacial spasm [14] the diagnosis of primary hfs by presence of “brow-lift sign” that consist of eyebrow lifting with the same side eye closure, triggering the activity of the frontalis in addition to orbicularis oculi muscles in the exact time during hfs. [15] radiological investigation especially t2-weighed mri imaging and ultra-resolution thin sections are most frequently used to demonstration possible vascular compressive elements [11]. other new techniques in mri like combination between steady-state mr images and three-dimensional time-of-flight mr angiography may show the approximate actual anatomy of the facial nerve at root exit zone (figure 1). [16] emg can assist in diagnosis of hfs by appearance of high-frequency synchronized ignition [12] romanian neurosurgery (2017) xxxi 4: 495 – 509 | 497 figure 1mri brain t2we thin axial cuts showed aica compressing the facial nerve in one of hfs cases figure 2 a, branches of the facial nerve (cn vii); without cervical branch. b, monitoring for the abnormal lateral spread response (lsr). the facial nerve zygomatic branch is excited by electricity and the produced emg response in the orbicularis oculi muscle could be recorded. in hfs patients, an abnormal induced response appeared as what is called lsr in the mentalis muscle, temporal; zygomatic; buccal; marginal mandibular. [22] the traditional medical treatment to hfs botulinum neurotoxin injections that can relief the manifestation of hfs in approximate 85% of cases [17] but it must be repeated every 3-6 months and other drawback is tolerance beside atrophy of the injected muscles in long run [18] while medical treatment by anticonvulsive drugs show failure in most case except early and very mild hfs case who may show infrequent improvement. the alternative curative treatment is surgical micro vascular decompression (mvd) that give a long duration relief of manifestation of hfs .this management offering a solution for those patents who did not give response or had tolerance to botulinum toxin injections or could not withstand lifetime frequent facial nerve injections [18].the procedure principle depend on separation of the offending vessel from the facial nerve exit zoon by isolator material after sharp dissection of the neurovascular arachnoid. the corner stone depend on identification of the vessel that compressing the nerve intraoperative by neurophysiological monitoring [19]. this intraoperative neurophysiological monitoring includes monitoring of brainstem auditory evoked (brai) responses is usually applied to discover eighth nerve dysfunction [20]. it also includes monitoring and recording of lateral spread response (lsr) which can intraoperatively give the surgeon a proof of adequate neurovascular decompression. lsr provoked by electrical stimulation of facial nerves branches that led to electrophysiological specific waves denoting hfs which disappear after adequate neurovascular decompression. the value of lsr as predictor of surgical outcome still controversial [20-22] objective of our work to describe the operative technique (pearls and common mistakes), the efficacy and morbidity of microvascular decompression for hfs through mini craniotomy, determine the prognostic factors affecting success rate of the surgery. 498 | elbadry et al microvascular decompression for treatment of hemifacial spasm material & method a retrospective study of 23 cases of hfs treated by mini craniotomy retro sigmoid approach and microvascular decompression at neurosurgery dept., mansoura university hospital in last 10 years was investigated. this include epidemiological, clinical and imaging details, selected treatment options and patient’s outcome. all patient in our study suffering from primary hfs. the patients had secondary hfs due to tumors, vascular aneurysms besides arteriovenous malformations avm in the cerebello-pontine angle site as discovered by standard head ct or mri investigation were excluded. also, patients with severe systemic sickness and patients with hfs due trauma viral infections have been disregarded. the surgical technique of lateral suboccipital approach: • general anaesthesia • the lateral position. “military position” with the affected side up • the neck is slightly in flexed position with turning the head a few degrees to the ipsilateral side of the proposed craniotomy • linear or curved skin incision. (figure 3: showed intraoperative picture anatomical landmark of the mastoid process and the position of planned mini craniotomy) • burr hole at the junction of the transverse and sigmoid junction • quarter coin craniectomy or craniotomy (figure 3) figure 3 showed intraoperative picture anatomical landmark of the mastoid process and the position of planned mini craniotomy a b figure 4 a showed the planned curved skin incision & mini craniotomy of hfs case to do mvd. b: showed ct 3d of operated mvd of hfs case revealed the retro mastoid quarter coin craniectomy romanian neurosurgery (2017) xxxi 4: 495 – 509 | 499 • the medial edge of the sigmoid sinus is exposed by drilling the mastoid bone • the opened mastoid air cells during craniotomy were closed by bone wax • inferolateral cerebellar approach using the microscope • slowly release of csf in the cerebellopontine cistern superior petrosal and supra cerebellar veins injury • opening the basolateral cisterns by elevating the flocculuscerebelli carefully • in some cases, we adopt jannetta technique who has suggested a method for protecting the cerebellar cortex during the advancement of the cottonoid around the cerebellum by lining it with a piece of glove (called rubber dam) • we used fukushima teardrop suction tube and a micro scissors for dissecting the arachnoid • the arachnoid membranes just inferior to superior petrosal and supracerebellar veins is sharply fenestrated and an additional amount of csf released. the arachnoid that surround both vii/vii cranial nerves is usually left intact. the retractor blade is placed barely below the superior petrosal vein • special attention was given to labyrinthine artery which enters the internal auditory canal beside the vii/viii cranial nerves complex • retraction is parallel to the glossopharyngeal course. the retractor blade is then placed on the cerebellum just superficial to the visible part of cranial nerve ix • aggressive manipulation of the nerve should be avoided • the root exit zone of the facial nerve appears grayish, anterior and slightly inferior to eighth cranial nerve that have whit color appearance and may be directly visualized upon gentle elevation of nerve viii using a fine dissector • adequate exposure of the root entry zone of the facial nerve to see the offending vessels that compressing the facial nerve. • the technique of decompression was by interposition of teflon sponges between the nerve and the offending blood vessel (ball-shaped). overzealous use of the teflon implant should be avoided. • not only using teflon as interposition but also making loop with teflon & fibrin glue to pull the vessel away from the facial nerve “sling retraction method” • filling the surgical cavity by saline to release air bubbles • tight closure of the dura the continue closure in anatomical layers results average patient age was 51.5 ± 11.3 years (range, 23 – 64 years), with ratio female to male was 1.55:1. the mean follow-up period was 38.4 ± 14.3 months (range: 7 – 76.2 months) 500 | elbadry et al microvascular decompression for treatment of hemifacial spasm table 1 smarmy of demographic data and clinical features of 23 hfs cases variable number of patients 23 gender female male 14 9 side left right 19 14 botox usage 12 h-b classification of facial weakness grade ii 16 grade iii 5 grade iv 2 preoperative symptom diminished corneal reflex 2 tinnitus 3 reduced hearing 5 tonus 14 platysmal involvement 11 specific triggers 8 compressing vessel aica 10 pica 8 va 3 multiple or veins 2 aica, anterior inferior cerebellar artery; pica, posterior inferior cerebellar artery; va, vertebral artery. complete resolving of symptoms was conducted in 19 cases 82.6% while reoperated in 2 cases with improvement in one case. facial palsy appeared post-operative in 6 cases 4 of them improved in 3 months, transient hearing loss in 4 cases17.4% which improved later, cerebrospinal fluid leak appeared in 3 cases 13% which managed conservatively. table 2 shows the success rate in relation to the time following surgery. the complications of these surgery presented in the following diagram (figure 5). table 2 the success rate of mvd surgeries in relation to post-operative periods no spasm spasm immediate postoperative 13 10 on discharge 15 8 on follow up 19 4 figure 5 showed mvd complications of our 23 hfs cases cases of presentations case 1: 62 years female complain of mild persistent left facial spasm not responding to medication and she had been injected with botox. (figure 6: mri brain axial cuts showed no significant secondary pathology in left cerebellopontine angle). on the other hand (figure 7 which is mri brain t2we topography thin axial cuts revealed compression of the left facial nerve at (root exit zone) by left pica &vertebral artery). the plan of surgery steps as described earlier in our paper (figure 8 a-h). the actual operation steps demonstrated in figure 10 (a-q). romanian neurosurgery (2017) xxxi 4: 495 – 509 | 501 a b figure 6 a &b mri brain axial cuts showed no significant secondary pathology in left cerebellopontine angle figure 7 mri brain t2we topography thin axial cuts revealed compression of the left facial nerve in root exit zone by left pica artery figure 9 the root exit zone of nerve vii (grayish in color) is anterior and slightly inferior to nerve viii (more whitish in color) and may be directly visualized upon gentle elevation of nerve viii using a fine dissector. adequate exposure of the root entry zone of the facial nerve to see the offending vessels that compressing the facial nerve which is left paica & vertebral artery 502 | elbadry et al microvascular decompression for treatment of hemifacial spasm a b c d e f g h figure 8 a linear or curved skin incision. b dissection of the first muscles layer .c dissection of the second muscles layer. d mini craniotomy flap in retro mastoid area e removal of the mini craniotomy free bone flap and exposure of the dura. f the medial edge of the sigmoid sinus is exposed by drilling the mastoid bone. the opened mastoid air cells during craniotomy were closed by bone wax. g inferolateral cerebellar approach using the microscope. h opening the basolateral cisterns by elevating the flocculuscerebelli carefully a b c romanian neurosurgery (2017) xxxi 4: 495 – 509 | 503 d e f g h i j k l m n o p q figure 10 a linear skin incision retro mastoid. b dissection of the muscles layers. c making retro mastoid burr hole. d mini craniotomy flap in retro mastoid area. e the medial edge of the sigmoid sinus is exposed by removing some bone of the mastoid & surrounding bone. the opened mastoid air cells during craniotomy were closed by bone wax. f opening the dura & making fixing stitches to keep it opened. g inferolateral cerebellar 504 | elbadry et al microvascular decompression for treatment of hemifacial spasm approach using the microscope. h opening the basolateral cisterns by elevating the flocculuscerebelli carefully. i the root exit zone of nerve vii (grayish in color) is anterior and slightly inferior to nerve viii (more whitish in color. adequate exposure of the root entry zone of the facial nerve to see the offending vessels that compressing the facial nerve which is left paica & vertebral artery in this case. j microscopic picture show the offending vessel that compress the left facial nerve which is paica in this case and dissecting all the arachnoid surrounding it. k microscopic picture revealed retracting left paica away from the left facial nerve without injuring any branches. l interposition of teflon sponges between the nerve and the offending blood vessel (ball-shaped). m making loop with teflon & fibrin glue to pull the vessel away from the facial nerve “sling retraction method”. n tight dural closure after filling the cavity with saline. o fixing the mini craniotomy flap by bur hole plate. p muscles layer closure by stitches anatomically. q skin closure in two layers the patient improved on discharge. case 2: 50 years male had left facial spasm 13 years ago. he had history of botox injection with some weakness in orbicularis oculi 5 years ago. mri brain t2we topography thin cuts showed compression of the left facial nerve by aica “anterior inferior cerebellar artery “(figure 11). figure 11 mri brain t2we topography thin axial cuts revealed compression of the left facial nerve in root exit zone by left aica artery the plan of surgery steps as described earlier to relief the aica artery pressure on left facial nerve (figure 12 a-c: an operative patient position. b retro mastoid surgical skin incision & mini craniotomy target. c interposition of teflon sponges between the nerve and the offending aica artery (ballshaped) & making loop with teflon & fibrin glue to pull the vessel away from the facial nerve “sling retraction method”). operative steps present in (figure 13 a-i). a b c figure 12 a-c a operative patient position. b retro mastoid surgical skin incision & mini craniotomy target. c interposition of teflon sponges between the nerve and the offending aica artery (ball-shaped) & making loop with teflon & fibrin glue to pull the vessel away from the facial nerve “sling retraction method” romanian neurosurgery (2017) xxxi 4: 495 – 509 | 505 a b c d e f g h i figure 13 a linear skin incision retro mastoid. b dissection of the muscles layers .c making mini craniotomy flap in retro mastoid area. d exposure of the dura e inferolateral cerebellar approach using the microscope. & opening the basolateral cisterns by elevating the flocculuscerebelli carefully. exposure of the root entry zone of the facial nerve to see the offending vessels that compressing the facial nerve which is left aica in this case. f microscopic picture revealed retracting left aica away from the left facial nerve without injuring any branches. g making loop with teflon & fibrin glue to pull the vessel away from the facial nerve “sling retraction method” h complete relieving the compression on the left facial nerve i interposition of teflon sponges between the nerve and the offending blood vessel (ball-shaped). j tight dural closure after filling the cavity with saline. j the patient hfs diminished immediate post-operative & follow up mri brain t2we topography thin axial cuts revealed relief all the compression of the left facial nerve at (root exit zone) caused by left aica artery. 506 | elbadry et al microvascular decompression for treatment of hemifacial spasm figure 14 follow up mri brain t2we topography thin axial cuts revealed relief all the compression of the left facial nerve in root exit zone by left aica artery discussion in our research hfs female patients represented about 60.9% of all cases and represent three of four failed mvd cases. the offending vessels in our cases was aica 10 cases, pica 8 cases, va 3 cases and multiple vessels & veins 2 cases which like what conducted by many previous researches [7, 23, 24]. mvd surgery has become more popular as definitive treatment for symptomatic primary with increasing its safety and effectiveness. despite its postulation by j. gardner in 1962 in limited number & result, and its modification by jannetta and others but the following forty years made it with better reputation by improved outcomes, less complications and preservation of facial & auditory nerve structure & function. [25] our success rate of mvd of facial nerve to relief hfs on follow up was 82.6%. in reviewing the previous papers about the effectiveness of mvd for hfs as definitive management we found its cure rates results extending roughly from 70.00% to 94.70%. maybe we did not reach the optimum as over 90% in the cases or more due to small number of cases that make the statistics not accurate, absence of endoscopic usage to see the area before of the facial nerve rez (2-3 mm) which cannot be visualised by microscope due to limited craniotomy bone window and condensed anatomical strictures in posterior fossa. many literatures stated that the angled lens endoscope can assists the surgeons in finding the compressing vessels, checking the teflon material position and appropriate volume in 100% of the cases. [26] the cases in our series showed success rate rise in follow up period. this may be due to period needed for remyelination of the impaired portions of facial nerve, in addition to the reappearance of normal facial moto nucleus excitability [21] the previous application of botox injection in 12 cases did not influence mvd operations success rate in 23 hfs cases statistically which conducted by several papers. [22] we can suggest the cause of that, absence of sever muscle atrophy in territory of affected facial nerve beside reversible of its damage. the corner stone in this operation type is identification of the offending vessel that have many features indicate its involvement like presence of its loop compressing the facial nerve at rez, presence of brown atherosclerotic plaque at this area, presence of depression of facial nerve opposite this offending vessel especially due to operative positioning and brain shift after opening of the dura may making the offending vessel away from the facial nerve. [26, 27] the mvd success rate did not show any statistically romanian neurosurgery (2017) xxxi 4: 495 – 509 | 507 significant between young and elderly patients that goes with statement of sekula et al. [25] the failed 4 cases had many characteristics: one of them was reoperated upon and hfs was improved post 2nd mvd operation. the reason of failure can be explained by in adequate facial nerve decompression, missed another offending vessel or not shredded teflon sponge migration against the involved facial nerve as conducted by many studies. [24] in the light of the previous causes, in our case who improved after 2nd mvd, the cause was in adequate facial nerve decompression as a sequela of teflon implant migration while the other three cases despite adequate mvd decompression they did not show any hfs improvement including the other case who had 2nd mvd exploration. many reasons can clarify this result. one of it: all 3 cases had platysmal involvement that indicate sever hfs [22]. this also strength the theory conducted that central demyelination with subsequent connection reorganization of the affected facial nucleus making it hyper excitable because of dendritic spike formation [13] so the cause may be related to monotonous active facial nerve nucleus. 2 patients from the three cases have facial palsy grade 4 and the last one was grade 3 that also indicate severe facial nerve impairment that might be not reversible despite adequate mvd. the permanent facial nerve palsy appeared in two cases post mvd operation. the aetiology may be facial nerve stretching in the step of cerebellar retraction or dissection in cerebellopontine angle area. heat may produce damage to nearby vessels and nerves after bipolar coagulation was applied in cerebellopontine angle critical area. inappropriate stimulation of nerves during dissection in addition to stripping in surgery can cause internal auditory artery spasm or rupture. [26] the rest of complications in our series had limited patients’ numbers (table 3) which comparable with the complications in 5700 cases who have been treated by mvd presented in 22 studies summarized in the following diagram (figure 15). [28] table 3 complications of mvd in 23 hfs cases complications number of cases transient facial palsy 4 transient hearing loss 4 recurrent hfs 2 csf leak 3 repeated mvd 2 permanent facial palsy 2 figure 15 the complications in 5700 cases who have been treated by mvd presented in 22 studies [28] other complications were transient and managed conservatively i.e. transient facial palsy and transient hearing loss that improved in 6 weeks as a result of resolving the edema of facial& auditory nerve while csf leak cases 508 | elbadry et al microvascular decompression for treatment of hemifacial spasm improved in two weeks by medical treatment & lumbar drain. no cases in our series showed hearing deficit postoperative in spite its presence in other papers [28]. thus, could be as a result of little patients’ number and absence of audiometry for all cases pre& post mvd surgeries. we depended on the complaint of the patients about their hearing postoperative. conclusions mvd relieves symptoms of hfs in about 80% of patients while recurrence still in low percentage. the study reported low permanent complications and generally transient. correspondence ashraf el badry m.d., ifaans, faculty of medicine, mansoura, university hospital egypt, mansoura, elgomhorya st., mansoura university hospital, neurosurgery department. tel. 0502267011-12 fax. 050 2267015-16 email: ashrafbadry@hotmail.com mobile: 0201111300033 references 1. g. abbruzzese, a. berardelli, and g. defazio, “hemifacial spasm,” handbook of clinical neurology, vol.100, pp.675–680. 2011. 2. auger rg, whisnant jp. hemifacial spasm in rochester and olmsted county, minnesota, 1960 to 1984. arch neurol, vol. 47, pp. 1233-1237, 1990 3. b. nilsen, k.-d. le, and e. dietrichs, “prevalence of hemifacial spasm in oslo, norway,” neurology, vol.63, no.8, pp.1532–1533, 2004. 4. l. w. kemp and s. g. reich, “hemifacial spasm,” current treatment options in neurology, vol.6, no. 3, pp.175–179,2004. 5. n. c. tan, e.-k. tan, and l. w. khin, “diagnosis and misdiagnosis of hemifacial spasm: a clinical and video study,” journal of clinical neuroscience, vol. 11, no. 2, pp. 142–144, 2004. 6. c. carlo, b. matteo, l. simona et al., “a comparative study of primary and secondary hemifacial spasm,” archives of neurology, vol.63, no.3, pp. 441–444,2006. 7. m. p. sindou, “microvascular decompression for primary hemifacial spasm. importance of intraoperative neurophysiological monitoring,” acta neurochirurgica, vol.147, no.10, pp. 1019–1026, 2005. 8. j. s. park, d.s. kong, j.a. lee, and k. park, “hemifacial neurovascular compressive patterns and surgical significance,” acta neurochirurgica, vol.150, no. 3, pp.235–241,2008. 9. m. campos-benitez and a. m. kaufmann, “neurovascular compression findings in hemifacial spasm,” journal of neuro-surgery, vol.109, no. 3, pp.416– 420,2008. 10. c. yaltho and j. jankovic, “the many faces of hemifacial spasm: differential diagnosis of unilateral facial spasms,” movement disorders, vol. 26, no. 9, pp. 1582–1592, 2011. 11. c. rosenstengel, m. matthes, j. baldauf, s. fleck, and schroeder, “hemifacial spasm: conservative and surgical treatment options,” deutsches ¨arzteblatt international, vol.109, no. 41, pp. 667–673, 2012. 12. s. i. choi, m.w. kim, d. y. park, r. huh and d jang, “electrophysiologic investigation during facial motor neuron suppression in patients with hemifacial spasm: possible pathophysiology of hemifacial spasm: a pilot study,” annals of rehabilitation medicine, vol.37, no.6, pp.839–847, 2013. 13. v. k. nielsen, “electrophysiology of the facial nerve in hemifacial spasm: ectopic/ephaptic excitation,” muscle & nerve, vol.8, no.7, pp.545–555,1985. 14. n. n. dou, j. zhong, and q. m. zhou, “the mechanism of hemifacial spasm: a new understanding of the offending artery,” journal of neurology research, vol.37, no 2, pp.184-188, 2015 15. j.-l. devoize, “hemifacial spasm in antique sculpture: interesting the “other babinski sign”,” journal of neurology, neurosurgery and psychiatry, vol.82, no.1, article 26,2011. 16. k. iijima, k. horiguchi, and y. yoshimoto, “microvascular compression of the root emerging zone for hemifacial spasm: evaluation by fusion magnetic romanian neurosurgery (2017) xxxi 4: 495 – 509 | 509 resonance imaging and technical considerations,” acta neurochirurgica, vol.155, no. 5, pp.855–862, 2013. 17. t. peeraully, s. f. tan, s. m. fook-chong, k. m. prakash, and e. k. k. tan, “headache in hemifacial spasm patients,” acta neurologica scandinavica, vol.127, no.5, pp. e24–e27, 2013. 18. gardner wj, sava ga. hemifacial spasm-a reversible pathophysiologic state. neurosurg, vol.19. pp.240 – 247, 1962 19. e. c. lim and r. c. seet, “use of botulinum toxin in the neurology clinic,” nature reviews neurology, vol.6, no.11, pp. 624–636, 2010. 20. j. zhong, j. zhu, h. sun et al., “microvascular decompression surgery: surgical principles and technical nuances based on 4000 cases,” neurological research, vol. 36, no. 10, pp. 882–893,2014 21. s yamashita, t kawaguchi, m fukuda, et al. lateral spread response elicited by double stimulation in patients with hemifacial spasm. muscle nerve., vol. 25, pp.845849, 2002. 22. d parthasarathy. thirumala, c aalap. shah, n tara, et al. microvascular decompression for hemifacial spasm: evaluating outcome prognosticators including the value of intraoperative lateral spread response monitoring and clinical characteristics in 293 patients. clinical neurophysiology. 28, number 1, pp,56-66, february 2011 23. hj choi, sk choi, ba rhee. microvascular decompression for hemifacial spasm due to four offending vessels: a case report. turk neurosurg. vol. 23, pp.241-244,2013 24. y yuan, y wang, sx zhang, l zhang, r li, j guo. microvascular decompression in patients with hemifacial spasm: re-port of 1200 cases. chin med j (engl). vol. 118, pp. 833–836, 2005 25. dh perlmutter, al petraglia, r barbano, et al. microvascular decompression in patient with atypical features of hemifacial spasm secondary to compression by a tortuous vertebra basilar system: case report. neurosurgery vol. 66, e1212 ,2010 26. qi hongwu, weining zhang, xudong zhang, et al. microvascular decompression surgery for hemifacial spasm. the journal of craniofacial surgery vol. 27, number 1, january 2016 27. r.f. sekula, a.m. frederickson, g. d. arnone, m.r. quigley, and m. hallett, “microvascular decompression for hemifacial spasm in patients >65years of age: an analysis of outcomes and complications,” muscle and nerve, vol. 48, no. 5, pp. 770–776, 2013. 28. larry e. miller & valerie m. miller. safety and effectiveness of microvascular decompression for treatment of hemifacial spasm: a systematic review. brit. j. neurosurg., vol. 26, issue 4, pp.438–444, august 2012. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article antioxidant therapies in traumatic brain injury: a review hector rolando romero-rivera, marticela cabeza-morales, enrique soto-zarate, guru dutta satyarthee, huber padilla-zambrano, andrei f. joaquim, andres m. rubiano, alfonso pacheco hernandez, amit agrawal, luis rafael moscote-salazar colombia, india, brazil doi: 10.1515/romneu-2017-0053 romanian neurosurgery (2017) xxxi 3: 319 334 | 319 doi: 10.1515/romneu-2017-0053 antioxidant therapies in traumatic brain injury: a review hector rolando romero-rivera1, marticela cabeza-morales1, enrique soto-zarate1, guru dutta satyarthee2, huber padillazambrano1, andrei f. joaquim3, andres m. rubiano4, alfonso pacheco hernandez5, amit agrawal6, luis rafael moscote-salazar7 1universidad de cartagena, cartagena de indias, colombia; 2neurosurgery, all india institute of medical sciences, new delhi, india; 3neurosurgery, department of neurology, state university of campinas, campinas, sao paulo, brazil; 4neurosurgery, el bosque university, bogota, colombia; 5neurosurgery, cartagena university, cartagena de indias, colombia; 6neurosurgery department, mm institute of medical sciences & research, maharishi markandeshwar university, mullana ambala, haryana, india; 7neurosurgery, critical care unit, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia abstract: oxidative stress constitute one of the commonest mechanism of the secondary injury contributing to neuronal death in traumatic brain injury cases. the oxidative stress induced secondary injury blockade may be considered as to be a good alternative to improve the outcome of traumatic brain injury (tbi) treatment. due to absence of definitive therapy of traumatic brain injury has forced researcher to utilize unconventional therapies and its roles investigated in the improvement of management and outcome in recent year. antioxidant therapies are proven effective in many preclinical studies and encouraging results and the role of antioxidant mediaction may act as further advancement in the traumatic brain injury management it may represent aonr of newer moadlaity in neurosurgical aramamentorium, this kind of therapy could be a good alternative or adjuct to the previously established neuroprotection agents in tbi. key words: traumatic brain injury, oxidative stress, antioxidants introduction traumatic brain injury (tbi) still remains one of the leading causes of death and disability, worldwide (1–6). tbi constitutes a major global health and socio-economic problem with neurobehavioral sequelae contributing to long-term disability (7). the incidence of tbi progressively continues to rapid rising trends and according to predictions, the neurotrauma will continue to 320 | romero-rivera et al antioxidant therapies in traumatic brain injury representing a growing number of deaths worlwide by 2020 (8, 9). moderate and severe tbi produces in the greatest disability andresponsible for consumes the most resources per individual, yet magnitude of mild tbi and societal ramifications are often underestimated. despite the label “mild”, many of these injuries result in immense long-term morbidities10. regarding the mechanisms responsible to produce secondary damage of brain tissue following tbi, a distinction is made between primary and secondary injury mechanisms. primary injury includes the direct effects of the mechanical energy on the brain tissue (1, 11). the secondary brain injury, which sets in at the time of injury and could continue for several weeks, is a complex neurodegenerative process, involving multiple cellular and molecular pathways, including inflammation andoxidative stress (3). free radical formation and oxidative damage are extensively investigated and validated as important contributors to the pathophysiology of acute central nervous system injury. the generation of reactive oxygen species (ros) and reactive nitrogen species (rns) is an early event following injury occurring within minutes of mechanical impact (12). various mechanisms are postulated to promote free radical production, including glutamate release, intracelular calcium overload, increase in arachidonic acid and its metabolites, hemoglobin denaturation, and iron ion release (1). the production of free radicals evoked by brain injury plays a crucial role in the initiating and propagating the pathogenesis of post-traumatic secondary injury, through oxidation and nitration of the cellular membrane, proteins, and dna (3, 13– 16). the blockade of oxidative damage seems to be a rational intervention to reduce secondary brain injury after tbi, and establishing the time course of oxidative damage provides information on a possible therapeutic window for protection against secondary brain injury (1, 17, 18). therefore, to find pharmacological agents specifically aiming to inhibit oxidative stress and modifying the expression of inflammatory cytokines might be a critical strategy; thus, antioxidants have been a major point for consideration (19). related to the above, the need for news therapies for traumatic brain injury is more than evident. therefore, this article aims to do a review about the pathophysiology of secondary injury, mainly the oxidative stress and new proposal of therapies antioxidants proposed as a treatment of traumatic brain injury. secondary injury mechanisms tbi is understood to be the result of 2 phases: initial primary neuronal injury followed by secondary insults (20). during primary injury to the head, it causes rapid deformation of brain tissue with destruction of brain parenchyma and blood vessels causing damage to cell membranes with the immediate release of intracellular contents. the initial injury event cannot be treated, only prevented (21). these effects induce secondary mechanisms which are potentially amenable to post-injury therapeutic intervention because of delayed onset and progression course over hours to days and months after the initial trauma (22). romanian neurosurgery (2017) xxxi 3: 319 334 | 321 secondary brain injury mechanism involves a host of cellular and molecular cascades that promote cell death include: neuronal depolarization, disturbance of ionic homeostasis, glutamate excitotoxicity, generation of nitric oxide and oxygen free radicals, lipid peroxidation (lp), blood-brain barrier disruption, ischemia, cerebral edema, mitochondrial dysfunction, axonal disruption, inflammation, and apoptotic and necrotic cell death (23) (figure 1). in addition to initiating ischemic and apoptotic cell injury cascades, primary brain injuries make injured, but salvageable, brain tissue vulnerable to secondary brain insults (sbis). these insults are usually well-tolerated but, when occurring in an injured brain, can lead to further cell death and worsened patient outcome. hypotension, hypoxia and hypoglycemia are all examples of sbis in which decreased substrate delivery to an injured brain further worsens injury. on the other hand, fever, seizures and hyperglycemia are examples of sbis in which increased metabolic demand may outstrip compensatory mechanisms and result in further injury (24). the brain is particularly vulnerable to oxidative stress because of its high rate of oxygen consumption, intensive production of ros, low antioxidant capacity, high level of transition metal, and polyunsaturated fatty acids (1, 4, 17, 25, 26). oxidative stress is currently thought to be a major contributor to the secondary injury cascade following tbi by ros/rns-induced damage to cellular membranes and organelles by lipid peroxidation, protein oxidation and nucleotide breakdown (21). figure 1 basic concept of primary and secondary injury in traumatic brain injury. from: marklund niklas/british journal of pharmacology. simplistic illustration of major preclinical ‘molecular’ secondary injury factors as well as clinical secondary injury factors (named ‘avoidable factors’ in the neurocritical care setting). early post-injury, glutamate releaseand ionic disturbances (na+, ca2+ and k+) cause an energy metabolic disturbance complicated by an early decrease in cerebral blood flow. at this time, mitochondrial disturbance is marked and a large increase in reactive oxygen/nitrogen species (ros/rns) is observed. hyper or hypocoagulation may also be present either causing microthrombosis or increased haemorrhages respectively. neuroinflammation and axonal injury is emerging in the immediate post-injury phase. clinically, an increased icp and/or decreased cpp must urgently be treated and both too low and too high blood glucose levels corrected. it is also crucial that hypoxaemia and hypotension, seizures and fever is detected and treated. chronically, marked hormone disturbance may be observed. these factors have been shown to contribute to the progression of the primary injury (indicated by the enlarging circles) and may be suitable targets for pharmacological intervention to reduce the extent of final injury. ca2+, calcium ions; cpp, cerebral perfusion pressure; glc, glucose; icp, intracranial pressure; k+, potassium; na+, sodium; rcbf, regional cerebral blood flow 322 | romero-rivera et al antioxidant therapies in traumatic brain injury reactive oxygen species reactive oxygen species (ros) are a group of chemically reactive molecules derived from oxygen (o2) (27). ros are formed as necessary intermediates of metal catalyzed oxidation reactions. atomic oxygen has two unpaired electrons in separate orbits in its outer electron shell. this electron structure makes oxygen susceptible to radical formation. the sequential reduction of oxygen through the addition of electrons leads to the formation of a number of ros including superoxide, hydrogen peroxide, hydroxyl radical, hydroxyl ion, and nitric oxide (28). at physiological low concentration levels, ros function as redox messengers in intracellular signaling and regulation, whereas excess of ros induce oxidative modification of cellular macromolecules ie. lipids, proteins, nucleic acids and carbohydrates, inhibit protein function, and promote cell death. the initial reaction generates a second radical, which in turn can react with a second macromolecule to continue the chain reaction. among the more susceptible targets are polyunsaturated fatty acids. abstraction of a hydrogen atom from a polyunsaturated fatty acid initiates the process of lipid peroxidation (29). there are also some mechanisms to detoxify radicals. the key metabolic steps are superoxide dismutasa (sod) catalysis of the dismutation of superoxide to hydrogen peroxide and oxygen and the conversion of h2o2 to 2h2o by glutathione peroxidase or to o2 + h2o by catalase (30). oxidative stress in traumatic brain injury various mechanisms are proposed, which have been described to promote free radical production, including glutamate release, intracellular calcium overload, increase in arachidonic acid and its metabolites, hemoglobin denaturation, and ionic iron release (1). damaging reactive oxygen species (ros) and reactive nitrogen species (rns) are formed as unavoidable by-products of metabolism but their damaging effects are normally counteracted by endogenous antioxidant enzymes (e.g. catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase) and substances e.g. glutathione, metallothionein, vitamin a, vitamin c, and vitamin e) (31). stressors arising from traumatic brain injury generate an imbalance between free radical production and the cells' antioxidant capacity, resulting in a state of oxidative stress (32). accumulation of ros/rns can result in a number of detrimental effects such as lipid peroxidation, protein oxidation, and dna damage. lipid peroxidation disrupts normal structure and function of lipid bilayers of the cell membrane increasing the permeability. lipid peroxidation may ultimately result in the production of multiple aldehyde species (e.g. acrolein, malondialdehyde (mda)) that further contribute to toxicity. protein modifications by accumulated ros/rns include protein fragmentation, protein misfolding, protein–protein cross-linkages, production of protein carbonyls, and priming of oxidized proteins for proteasomal degradation (31). alteration of different dna structural changes including direct romanian neurosurgery (2017) xxxi 3: 319 334 | 323 modification of nucleotide bases, formation of apurinic/apyrimidinic sites, dna single strand breaks and double strand breaks. guanine is the most susceptible to oxidative modifications due to the fact that it has the lowest reduction potential. hydroxyl radicals have been shown to interact with the c4, c5, and c8 positions in the imidazole ring of guanine forming of 8-hydroxyguanosine (8oxog). peroxynitrite is also capable of reacting with guanine to form 8-nitroguanine. it is known that preferential target of oxidative damage are telomeres. for example, trf2 may prevent atm-mediated initiation of oxidative dna damage signaling, pot1, which maintains stability of telomeric ends, is also known to inhibit another dna damage kinase atr. both atm and atr are known to initiate apoptotic neuronal death in the context of dna damage through activation of p53 (31). neuroprotection and emerging roles of nrf2 not all mediators induced in the perilesional zones necessarily contribute to celllular death. as is the case for damageinducing pathways, protective pathways also appear to be similar if not identical in ischemic and traumatic injury. these mediators possess damage-reducing properties and represent endogenous efforts to counteract ischemic or traumatic damage and improve neuronal repair. some of the protective mechanisms include: 1) heat shock proteins (hsps). they are induced early after ischemic onset and their induction prior to ischemia may confer ischemic tolerance. 2) anti-inflammatory cytokines. certain cytokines have antiinflammatory capabilities such as il-10 may be protective against ischemic damage, mainly by inhibiting production of the inflammatory cytokines. 3) growth factors. nerve growth factor (ngf), brain derived neurotrophic factor (bdnf), glial derived growth factor (gdnf), basic and acidic fibroblastic growth factors (fgf) and members of the transforming growth factor super family (tgf). these growth factors are thought to confer protection mainly by interfering with apoptotic pathways and preventing apoptotic death. 4) erythropoietin. this kidney-derived cytokine acts as a growth factor and inhibits apoptotic cell death. 5) sex hormone. estrogen was shown to protect the brain from experimental cerebral ischemia, likely through both vascular and neuronal cellular mechanisms. 6) endogenous antioxidant mechanisms. antioxidant enzymes and lowmolecular-weight antioxidants are all induced in the early hours following ischemia and trauma. such antioxidants include mn-sod (superoxide dismutase), extracelular sod and cu-zn-sod and also gluthatione (33). there are few current researches showing excessive generation of oxygen free radicals after is the core pathological link leading to the nerve cell injury and apoptosis. nf-erythroid 2-related factor 2 (nrf2) is a recently discovered nuclear factor. in physiological state, it is mainly located in the cytoplasm and forms a complex combining with cytoplasmic protein keapl. when oxidative stress stimulus occurs, it is decoupled with keapl through phosphorylation, transfers into nucleus, combines with antioxidant response element 324 | romero-rivera et al antioxidant therapies in traumatic brain injury (are) sequence, forms nrf2/are pathway and then starts the gene expression of phase ii detoxifying enzymes and antioxidases (h0-1, nqo1, etc) regulated by are. nrf2/are pathway plays an important role in endogenous anti-oxidation process in vivo and can be induced by external factors (14). yan wei at el. demonstrated the activation of nrf2–are pathway occurs after tbi. moreover, emerging evidence suggests that nrf2, in addition to its antioxidant functions, may also play an important role in regulating inflammation in the brain. these findings connect nrf2 not only to an elevated antioxidant capacity but also to expression of other types of protective proteins i.e. brain derived neurotrophic factor, the antiapoptotic b-cell lymphoma 2, the antiinflammatory interleukin (il)-10, the mitochondrial transcription (co)-factors nrf1 and peroxisome proliferator-activated receptor gamma coactivator1-alpha (pgc-1a), the iron exporter ferroportin 1, and the autophagic protein p62 (36, 34). nrf2 activation also protects the blood brain barrier during tbi. tbi causes a biphasic opening of the bbb. the first opening used happens within hours (acute phase) after tbi and the other secondary phase peaks 1–3 days after injury. the latter opening is associated with a loss of endothelial cells and tight junction proteins. enhanced nrf2 staining can be detected in the blood brain barrier following tbi (35). it was demonstrated that the patientsdeficient (nrf2-/-) mice exhibited poorer outcomes than the wild-type mice, while administration of tbhq or histone deacetylase inhibitors could protect against tbi by activation of nrf2. these evidences demonstrate that activation of the nrf2–are pathway is beneficial for tbi. (16) it is now accepted that the nrf2–are pathway can be regulated in many different ways (14, 16, 36). antioxidant therapeutic strategies the gradual processes of secondary injury may provide doctors with so-called ‘‘golden hour’’ wibndowfor pharmacological based intervention, and a lot of agents and compounds targeting secondary brain injury factors are shown to be protective in experimental tbi models3. however, clinical trials for neuroprotective therapies of tbi still continue to have a high failure rate (37). several researches have described the antioxidant mechanism of some agents, but most of them have unfortunately failed in their efforts to provide neuroprotection in moderately to severely injured tbi patients. some of these therapies have demonstrated inadequacies include polyethyleneglycolconjugated-sod (peg-sod) and tirilazad. the non-glucocorticoid lp inhibitor tirilazad, which inhibits lp propagation reactions by membrane stabilization and scavenging loo• was tested as a tbi therapeutic in the early 1990s. factors contributing to the failure of the tirilazad study were the apparent inability of the agent to cross the blood–brain barrier in high enough concentrations in severely injured patients as well as gender differences in treatment outcomes and drug metabolism. on the other hand, peg-sod was limited in its therapeutic value based on its large size and romanian neurosurgery (2017) xxxi 3: 319 334 | 325 rather narrow therapeutic window to scavenge the short-lived primordial o2•− radical (12). edaravone (3-methyl-1-phenyl-2pyrazolin-5-one) is a derivative of antipyrin and was approved as free radical scavenger. edaravone was first reported to strongly scavenge hydroxyl radicals (oh−) produced by the fenton reaction in vitro and to decrease lipid and l-tyrosine oxidation. edaravone was used in other neural injury models such as spinal cord injury, tbi, and brain hemorrhage38. however, in a study conducted by pratyush chaudhuri, no significant difference was observed in the outcome scales between the group administered edaravon and the group not administered edaravon. on the other hand, the mortality rate was also higher in the edaravon group. the possible etiology from this investigation was the drug induced hepatic dysfunction resulting in persistently reduced serum albumin levels and thereby causing a decrease in the circulating volume (39). numerous experimental studies in recent years have suggested that erythropoietin (epo) is an endogenous mediator of neuroprotection in various central nervous system disorders, including tbi (18). erythropoietin is a glycoprotein and cytokine of 34kda which is produced mainly by the fetal liver and the adult kidney in response to hypoxia. erythropoietin (epo) and the epo receptor (epor), are also expressed in the brain. while epo and epor are only weakly expressed in normal adult brain, expression of epo and epor is greatly increased in response to different types of brain injury. inhibition of epo activity by the administration of soluble epors worsens the severity of neuronal injury, suggesting that endogenous epo is directly involved in an intrinsic neuronal repair pathway (40). because of the potential thromboembolic complications caused by epo, it may be difficult to achieve neuroprotection with epo in tbi patients without further increasing potentially life-threatening complications. however, development of derivatives of epo that do not bind to the classical epor (carbamylatederythropoietin or cepo) or that have such a short half-life in the circulation that erythropoiesis is not significantly stimulated (asialoerythropoietin or neuroerythropoietin) have clearly demonstrated that the neuroprotective effects of epo can be separated from the hematopoietic effects18. specifically, the receptor complex mediating the neuroprotective effects of epo has been reported to be associated with the common receptor (cr) subunit, also known as cd131, which is the signal-transducing component used by the granulocyte macrophage colony stimulating factor (gm-csf), il-3, and il5receptors (41). current promising antioxidant therapies currently, there is no neuroprotective agent, which demonstrated improved neurological outcomes in a large phase iii clinical trial. efforts should focus on developing novel strategies, with thorough preclinical studies and clinical trials that consider the translational barriers of a heterogeneous pathology such as tbi. the 326 | romero-rivera et al antioxidant therapies in traumatic brain injury potential use of unconventional treatments, such as antioxidant defense system reinforcement, could play a key role in the management. this reinforcement appears as a safe, low-cost and multifunctional novel therapeutic approach in tbi patients. antioxidant therapies are effective over a long period of time, allowing for suitable use in clinical settings. due to the encouraging preclinical results and the antioxidant drug profiles, acute antioxidant reinforcement is emerging as a highly cost-effective alternative for neuroprotection in tbi patients (42). u-83836e the 21-aminosteroids (lazaroids) are a new family of steroid compounds, which inhibit lipid peroxidation reactions. they are novel antioxidant agents, which have been shown to prevent free radical-mediated blood-brain barrier damage (43). u-83836e is a second-generation lazaroid with a non-steroidal structure characterized by a ring portion of alpha-tocopherol bonded to various amine groups. its structure enables the dual functionality of lp inhibition and scavenging loo•, thereby making it much more effective than the endogenous scavenger vitamin e44. u-83836e treatment can attenuate post-traumatic lp in cerebral cortical tissue or mithochondria together with a preservation of aerobic respiratory function and ca++-buffering capacity (45). more recently u-83836e has also been shown to inhibit calpain-mediated cytoskeletal degradation signifying the intricate relationship between post-traumatic lp, disruptions in neuronal ca2+ homeostasis and calpain-mediated cytoskeletal damage (12). if u-83836e given prophylactically, enhances na+/k+ and mg2+/ca2+-atpase activities and attenuates edema in cerebral trauma in rats (46). u-83836e also has been shown to inhibit protein nitration (3-nt) in injured cortical tissue and mitochondria even though it does not interact directly with the reactive nitrogen species peroxynitrite. further studies to determine the pharmacokinetics of u-83836e in humans are strongly recommended, as the compound appears to inhibit a crucial step of the secondary brain injury cascade of events (42). resveratrol resveratrol (3, 4’, 5-trihydroxystilbene) is a phytoalexin polyphenolic structurally related to stilbenes. it is found in two isomers, cis(z) and trans(e) resveratrol47. resveratrol is present in relatively large amounts in grapes and red wine and, to a much lesser extent, in white wines (47–50). many studies have demonstrated resveratrol has a wide range of pharmacological properties, including antioxidant, cardioprotective and anticancer effects. in addition to these beneficial actions, resveratrol also noted for its antiinflammatory, immunomodulatory, chemopreventive and neuroprotective activities. in this respect it has been shown that resveratrol readily crosses the intact blood– brain barrier (48). recently, resveratrol was found to be a potent neuroprotective agent against excitotoxicity, ischemia, and hypoxia, in both in vitro and in vivo models (51). resveratrol has demonstrated efficacious in reducing neuropathological and behavioral sequelae. some studies have also found that romanian neurosurgery (2017) xxxi 3: 319 334 | 327 traumatic brain injury (tbi) in both adult and immature animals is amenable to treatment with resveratrol (52, 55). in rat traumatic brain injury, a single high dose of resveratrol (100 mg/kg) administerd immediately after trauma reduced brain edema and oxidative stress, and attenuated brain pathology 14 days later (49). many different pathways determining the possible actions of resveratrol have been proposed including anti-inflammatory properties, inhibition of no toxicity, induction of neuroprotective enzymes such as heme oxygenase-1 (ho1), free radical scavenging, nf-kb mediated suppression of proinflammatory genes, upregulation of enos and vegf, inhibition of mmp-9, and by mimicking ischemic preconditioning via the sirtuin pathway (53). a relationship exists between ho1 and nos. the nuclear factorerythroid-2-related factor 2 (nrf2) regulates ho1 transcription, which acts as a scavenger of no and an inhibitor of inos. it has been reported that resveratrol modulates ho1 and inos expression in glial cells, so ho1 can also be critical to signaling the antioxidant response of resveratrol (54). allicin allicin (which formed by the interaction of the enzyme alliinase with its substrate alliin) is responsible for most of active ingradient of garlic. allicin treatment has showed decrease the expression of tnf-α. some studies have reported a significant reduction of brain water content when allicin administrated 2 or 4 h after injury, but not when the administration is delayed by 8 h. treatment with allicin can reduce brain edema, attenuate neurological deficit and inhibit tbi-induced apoptotic neuronal death (3). edaravone edaravone, a free radical scavenger, suppresses axonal injury and oxidative stress in the cortex, corpus callosum, and hippocampus 24h after injury. the neuroprotective effects of edaravone were observed in mice receiving 1.0, 3.0, or 10 mg/kg immediately after impact. with treatment 1 h after impact, axonal injury was also significantly suppressed and this therapeutic effect persisted up to 6 h after impact. edaravone therapy protects against memory deficits following tbi mediated by suppression of traumatic axonal injury and oxidative stress (13). tempol tempol (4-hydroxy-2, 2, 6, 6tetramethylpiperidine-n-oxyl) is a watersoluble stable and paramagnetic nitroxyl radical or nitroxide. tempol is a sod mimetic, and hence an efficient scavenger of free radicals. endogenous sod is a much more efficient antioxidant than vitamins, since the rate constant for interaction of sod with o2− is about 1.6–2.4x109mol l−1 s−1, whereas that of vitamin e with o2− approximates 0.59 mol l−1 s−1. tempol is therefore not as powerful as endogenous sod, but it is much more powerful than vitamins (55). the neuroprotective effects of tempol is reported in both models of tbi and spinal cord injury. in the mouse controlled cortical impact (cci) tbi model, tempol reduced post-traumatic lp and protein nitrationinduced oxidative damage, which resulted in 328 | romero-rivera et al antioxidant therapies in traumatic brain injury preserved mitochondrial bioenergetics, reduced calpain-mediated cytoskeletal damage and reduced neurodegeneration (12). tempol showed cerebroprotective effects in terms of limiting edema formation, ameliorating blood–brain barrier disruption, and improving functional recovery. it has been concluded that the beneficial effects of tempol were because of its catalytic scavenging of superoxide radicals. more recent experiments have suggested that an important antioxidant property that may contribute significantly to the inhibition of posttraumatic oxidative damage in brain tissue involving catalytic scavenging of the pn-derived radicals ●no2 and ●co3 (56). tempol can shuttle between the nitroxide radical, the reduced hydroxylamine and the oxidized oxoammonium cation form with 1 and 2 electron transfer reactions. these are facilitated by “boat and chair” conformational changes that underlie the rapidity and catalytic nature of the reactions. the reaction of tempol with superoxide anion (o2•−) to form hydrogen peroxide (h2o2) accounts for its “superoxide dismutase (sod) mimetic” action. tempol is effective as a catalase-like agent in preventing the generation of•oh from h2o2 in the presence of transition metals in the fenton reaction and it has high capacity to permeate cell membranes, the gastrointestinal tract (git) or the blood-brain barrier which accounts for its effectiveness after oral administration and central nervous system actions57. previous studies have shown that tempol can decrease brain 3-nt after controlled cortical impact-induced tbi (ccitbi), but only if administered during the first hour. thus, attempting to block pn formation by either inhibiting •no synthesis or scavenging pn radicals does not appear to be a practical therapeutic approach to reducing early pn-mediated oxidative damage from a therapeutic window point of view58. however, effects of tempol remains promising and requires further investigation. in addition, tempol may be an ideal candidate for combination therapy with other neuroprotective approaches (12). melatonin melatonin (n-acetyl-5methoxytryptamine), a hormone secreted from pineal gland and synthesized from tryptophan or formed as the metabolic end product of serotonin, is a non-enzymatic antioxidant and neuroprotective agent. melatonin has been shown to exert neuroprotection in several central nervous system disease models, including brain and spinal cord trauma, cerebral ischemia, subarachnoid hemorrhage, and intracerebral hemorrhage (59). melatonin is a major molecule in protecting membrane constituents from oxidative agents. this molecule also optimizes the physiology of membrane receptors and channels as well as maintaining the shape of the cell. the effects of melatonin as a potent protective substance in post-tbi injuries have been shown in both in vivo and in vitro studies. it has been recognized that melatonin administration in both low and high doses can significantly decrease brain edema and blood-brain barrier permeability at 72 h after tbi. moreover, this inhibitory effect is associated with improvement of neurologic scores (60). romanian neurosurgery (2017) xxxi 3: 319 334 | 329 melatonin is also well tolerated even at supraphysiological doses (61). melatonin is a significant free radical scavenger and antioxidant at both physiological and pharmacological concentrations in vivo. like other secondary metabolites, melatonin exerts antioxidant properties as a direct free radical scavenger and by stimulating antioxidant enzymes. indeed, melatonin is able to scavenge h2o2 in a dose-dependent manner. moreover, the biological activities of melatonin metabolites n(1)-acetyl-n(2)-formyl-5methoxykynuramine (afmk) and n1-acetyl5-methoxykynuramine (amk) have been described. afmk is a potent antioxidant providing protection to dna and lipids viaseveral mechanisms. amk is also a potent antioxidant and inhibits prostagladin biosynthesis. melatonin can scavenge other reactive oxygen species such as onoo, no and h2o2. additionally, due to its amphiphilic structure, melatonin has no barriers of distribution and may have the advantages of having a lower side effect profile and producing fewer pharmacokinetic or phamacodynamic interactions compared to xenobiotic antioxidants (62–64). mammalian target of rapamycin (mtor) pathway is an essential cellular signaling pathway involved in a number of important physiological functions like cell growth, proliferation, metabolism, protein synthesis and autophagy. activation of microglia following tbi might results-frodue to m cell proliferation or size enlargement induced by phosphorylation and activation of mtor pathway. in previous studies in rodents, pmtor, p-p70s6k and p-s6rp were markedly increased in ipsilateral cortex 24 h post-tbi in mice, suggesting activation of mtor pathway following tbi. it has also showed that injection of melatonin repressed phosphorylation of mtor and its downstream substrates. furthermore, melatonin restrained the activation of microglia and decreased protein expression of il-1b and tnf-α, thereby increasing the number of neurons in peri-contusive cortex at 24 h after tbi (65). melatonin has been shown to promote nrf2 protein translocation from the cytoplasm to the nucleus and to prevent antioxidant enzyme activities decline, including superoxide dismutase and glutathione peroxidase66. some studies have proved combination therapy with melatonin and other therapies. the therapy with melatonin (10 mg/kg) and dexamethasone (0.025 mg/kg) is signigficantly able to reduce edema and brain infartions (67). sulforaphane recently, the nrf2 signaling pathway, which is been considered an endogenous antioxidant mechanism in the cellular defense against oxidative or electrophilic stress, has generated increasing interest. the ability to induce phase 2 detoxifying genes and antioxidant enzymes at the transcriptional level could have significant advantages over more conventional approaches. previous studies have shown that the nrf2-are pathway was activated in the brain and played an important role in limiting inflammation and apoptosis after tbi (68). 330 | romero-rivera et al antioxidant therapies in traumatic brain injury sulforaphane, a naturally occurring compound generated from cruciferous vegetables such as broccoli, is a potent inducer of antioxidant and detoxifying enzymes. as such, this compound has been suggested to provide broad protection against a variety of cellular threatseg. example, application of sulforaphane to neuron-astrocyte co-cultures protects neurons against nonexcitotoxic glutamate and hydrogen peroxide toxicity. these beneficial effects of sulforaphane have been shown to involve induction of nrf2driven genes (69–71). activation of the transcription factor nfe2-related factor-2 (nrf2) by sulforaphane, increase the expression of endogenous cytoprotective genes in brain tissue and microvessels. post-injury administration of sulforaphane reduce the loss of endothelial cell markers and tight junction proteins and preserve blood–brain barrier function. these protective effects are dependent on the activity of nrf2 (72). in vitro studies, sulforaphane is demonstrated to disrupt the nrf2/keap1 interaction, leading to nrf2 stabilization and nuclear localization and the expression of are-containing phase ii genes, which play a major role in the detoxification of ros produced by xenobiotics (42, 73). some of the effects related to the use of sulforaphane are only observed when the treatment is initiated within the first hr, but not 6 hr, post-injury (69). several studies support the use of sulforaphane in the treatment of tbi, and the fact that nrf2 activation may be a prime candidate for the attenuation of oxidative stress and subsequent neurotoxicity. nevertheless, considering the narrow time window of sulforaphane use observed in preclinical studies, the success of sulforaphane in clinical settings is uncertain42. vitamin c and vitamin e vitamin c (ascorbic acid, ascorbate) is a potent watersoluble antioxidant in humans. it also behaves as an enzyme modulator, causing the up-regulation of endothelial nos (enos) and down-regulation of nadph oxidase. antioxidant and pharmacodynamic properties allow ascorbate to protect neurons from nmda-induced excitotoxicity and to prevent lipid peroxidation induced by various oxidizing agents, especially in combination with a-tocopherol, in cell cultures. interestingly, there is one clinical trial of vitamin c involving in patients with severe tbi and the radiologic diagnosis of diffuse axonal injury. patients received a total dose of 32 g of intravenous vitamin c during the first 7 days after tbi, with a maximum single dose of 10 g on the first day, resulting in a significant earlier stabilization of the perilesional edema compared with the placebo group. although the absence of many parameters of clinical importance and monitoring techniques may make the interpretation of these results challenging, although encouraging results regarding the use of vitamin c in humans (42). on the other hand, vitamin e, mainly alpha-tocopherol, is the major peroxyl radical scavenger in biological lipid phases such as cell membranes, and its antioxidant mechanism is related to the inhibition of lipid peroxidation and nadph oxidase. one clinical trial of vitamin e has been performed in patients with romanian neurosurgery (2017) xxxi 3: 319 334 | 331 severe tbi and the radiologic diagnosis of diffuse axonal injury. for 7 days, patients received vitamin e at 400 iu/day intramuscularly, which resulted in improved clinical outcome and reduced mortality at discharge. despite promising results, clinical trials using vitamins c and e, isolated or in combination, are needed to change current therapeutic measures in patients suffering tbi (42). correspondence dr. luis rafael moscote-salazar e-mail: mineurocirujano@aol.com references 1. petronilho f, feier g, de souza b, et al. oxidative stress in brain according to traumatic brain injury intensity. j surg res. 2010;164(2):316-320. doi:10.1016/j.jss.2009.04.031. 2. kumar a, loane dj. neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. brain behav immun. 2012;26(8):1191-1201. doi:10.1016/j.bbi.2012.06.008. 3. chen w, qi j, feng f, et al. neuroprotective effect of allicin against traumatic brain injury via akt/endothelial nitric oxide synthase pathway-mediated antiinflammatory and anti-oxidative activities. neurochem int. 2014;68(1):28-37. doi:10.1016/j.neuint.2014.01.015. 4. hohl a, gullo jda s, silva cc, et al. plasma levels of oxidative stress biomarkers and hospital mortality in severe head injury: a multivariate analysis. j crit care. 2012;27(5):523 e11-e19. doi:10.1016/j.jcrc.2011.06.007. 5. ahmad a, crupi r, impellizzeri d, et al. administration of palmitoylethanolamide (pea) protects the neurovascular unit and reduces secondary injury after traumatic brain injury in mice. brain behav immun. 2012;26(8):1310-1321. doi:10.1016/j.bbi.2012.07.021. 6. otani n, nawashiro h, shima k. pathophysiological findings of selective vulnerability in the hippocampus after traumatic brain injury. j exp clin med. 2011;3(1):22-26. doi:10.1016/j.jecm.2010.12.003. 7. sivanandam tm, thakur mk. traumatic brain injury: a risk factor for alzheimer’s disease. neurosci biobehav rev. 2012;36(5):1376-1381. doi:10.1016/j.neubiorev.2012.02.013. 8. luo p, fei f, zhang l, qu y, fei z. the role of glutamate receptors in traumatic brain injury: implications for postsynaptic density in pathophysiology. brain res bull. 2011;85(6):313-320. doi:10.1016/j.brainresbull.2011.05.004. 9. alvis-miranda hr, alcala-cerra g, rubiano m, ramirez o, moscote-salazar lr. therapeutic hypothermia in brain trauma injury : controversies. 2014;2. 10. feigin vl, barker-collo s, krishnamurthi r, theadom a, starkey n. epidemiology of ischaemic stroke and traumatic brain injury. best pract res clin anaesthesiol. 2010;24(4):485-494. doi:10.1016/j.bpa.2010.10.006. 11. kunz a, dirnagl u, mergenthaler p. acute pathophysiological processes after ischaemic and traumatic brain injury. best pract res clin anaesthesiol. 2010;24(4):495-509. doi:10.1016/j.bpa.2010.10.001. 12. bains m, hall ed. antioxidant therapies in traumatic brain and spinal cord injury. biochim biophys acta. 2012;1822(5):675-684. doi:10.1016/j.bbadis.2011.10.017. 13. ohta m, higashi y, yawata t, et al. attenuation of axonal injury and oxidative stress by edaravone protects against cognitive impairments after traumatic brain injury. brain res. 2013;1490:184-192. doi:10.1016/j.brainres.2012.09.011. 14. cheng zg, zhang gd, shi pq, du bs. expression and antioxidation of nrf2/are pathway in traumatic brain injury. asian pac j trop med. 2013;6(4):305-310. doi:10.1016/s1995-7645(13)60061-9. 15. li r, liang t, xu l, zheng n, zhang k, duan x. puerarin attenuates neuronal degeneration in the substantia nigra of 6-ohda-lesioned rats through regulating bdnf expression and activating the nrf2/are signaling pathway. brain res. 2013;1523:1-9. doi:10.1016/j.brainres.2013.05.046. 16. xu j, wang h, ding k, et al. luteolin provides neuroprotection in models of traumatic brain injury via the nrf2-are pathway. free radic biol med. 2014;71c:186-195. doi:10.1016/j.freeradbiomed.2014.03.009. 17. ansari m a., roberts kn, scheff sw. oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury. free radic biol med. 332 | romero-rivera et al antioxidant therapies in traumatic brain injury 2008;45(4):443-452. doi:10.1016/j.freeradbiomed.2008.04.038. 18. ponce ll, navarro jc, ahmed o, robertson cs. erythropoietin neuroprotection with traumatic brain injury. pathophysiology. 2013;20(1):31-38. doi:10.1016/j.pathophys.2012.02.005. 19. samuel elg, duong mt, bitner br, marcano dc, tour jm, kent t a. hydrophilic carbon clusters as therapeutic, high-capacity antioxidants. trends biotechnol. 2014:1-5. doi:10.1016/j.tibtech.2014.08.005. 20. frattalone ar, ling gsf. moderate and severe traumatic brain injury: pathophysiology and management. neurosurg clin n am. 2013;24(3):309-319. doi:10.1016/j.nec.2013.03.006. 21. marklund n, hillered l. animal modelling of traumatic brain injury in preclinical drug development: where do we go from here? br j pharmacol. 2011;164(4):1207-1229. doi:10.1111/j.14765381.2010.01163.x. 22. morales dm, marklund n, lebold d, et al. experimental models of traumatic brain injury: do we really need to build a better mousetrap? neuroscience. 2005;136(4):971-989. doi:10.1016/j.neuroscience.2005.08.030. 23. levine jm. traumatic brain injury. 2013. doi:10.1038/nrneurol.2011.101. 24. hemphill jc, andrews p, de georgia m. multimodal monitoring and neurocritical care bioinformatics. nat rev neurol. 2011;7:451-460. doi:10.1038/nrneurol.2011.101. 25. rocamonde b, paradells s, barcia jm, et al. neuroprotection of lipoic acid treatment promotes angiogenesis and reduces the glial scar formation after brain injury. neuroscience. 2012;224:102-115. doi:10.1016/j.neuroscience.2012.08.028. 26. alfieri a, srivastava s, siow rcm, modo m, fraser p a, mann ge. targeting the nrf2-keap1 antioxidant defence pathway for neurovascular protection in stroke. j physiol. 2011;589(pt 17):4125-4136. doi:10.1113/jphysiol.2011.210294. 27. topic af, glasgow s, edited j, bagshaw c, cambridge gb. proteins : structure and function. 2006;(july):953956. 28. held p. an introduction to reactive oxygen species measurement of ros in cells. biotek instruments. 2012:1-14. http://www.biotek.com/resources/articles/reactiveoxygen-species.html. 29. wang xl, rainwater dl, vandeberg jf, mitchell bd, mahaney mc. genetic contributions to plasma total antioxidant activity. arterioscler thromb vasc biol. 2001;21:1190-1195. doi:10.1161/hq0701.092146. 30. spranger m, krempien s, schwab s, donneberg s, hacke w. superoxide dismutase activity in serum of patients with acute cerebral ischemic injury : correlation with clinical course and infarct size. stroke. 1997;28:2425-2428. doi:10.1161/01.str.28.12.2425. 31. smith j a., park s, krause js, banik nl. oxidative stress, dna damage, and the telomeric complex as therapeutic targets in acute neurodegeneration. neurochem int. 2013;62(5):764-775. doi:10.1016/j.neuint.2013.02.013. 32. semple bd. early preservation of mitochondrial bioenergetics supports both structural and functional recovery after neurotrauma. exp neurol. 2014;261:291297. doi:10.1016/j.expneurol.2014.07.013. 33. leker rr, shohami e. cerebral ischemia and trauma different etiologies yet similar mechanisms: neuroprotective opportunities. brain res rev. 2002;39(1):55-73. 34. sandberg m, patil j, d’angelo b, weber sg, mallard c. nrf2-regulation in brain health and disease: implication of cerebral inflammation. neuropharmacology. 2014;79:298-306. doi:10.1016/j.neuropharm.2013.11.004. 35. zhang m, an c, gao y, leak rk, chen j, zhang f. emerging roles of nrf2 and phase ii antioxidant enzymes in neuroprotection. prog neurobiol. 2013;100(1):30-47. doi:10.1016/j.pneurobio.2012.09.003. 36. yan w, wang hd, hu zg, wang qf, yin hx. activation of nrf2-are pathway in brain after traumatic brain injury. neurosci lett. 2008;431(2):150-154. doi:10.1016/j.neulet.2007.11.060. 37. jain kk. neuroprotection in traumatic brain injury. drug discov today. 2008;13(23-24):1082-1089. doi:10.1016/j.drudis.2008.09.006. 38. miyamoto k, ohtaki h, dohi k, et al. therapeutic time window for edaravone treatment of traumatic brain injury in mice. biomed res int. 2013;2013:379206. doi:10.1155/2013/379206. 39. chaudhuri p. edaravon: caution for use in traumatic brain injury. experience in 127 patients. indian j romanian neurosurgery (2017) xxxi 3: 319 334 | 333 neurotrauma. 2013;10(1):19-23. doi:10.1016/j.ijnt.2013.04.008. 40. zhang y, xiong y, mahmood a, et al. therapeutic effects of erythropoietin on histological and functional outcomes following traumatic brain injury in rats are independent of hematocrit. brain res. 2009;1294:153164. doi:10.1016/j.brainres.2009.07.077. 41. grasso g, sfacteria a, meli f, fodale v, buemi m, iacopino dg. neuroprotection by erythropoietin administration after experimental traumatic brain injury. brain res. 2007;1182(1):99-105. doi:10.1016/j.brainres.2007.08.078. 42. fernández-gajardo r, matamala jm, carrasco r, gutiérrez r, melo r, rodrigo r. novel therapeutic strategies for traumatic brain injury: acute antioxidant reinforcement. cns drugs. 2014;28:229-248. doi:10.1007/s40263-013-0138-y. 43. durmaz r, deliorman s, isiksoy s, uyar r, erol k, tel e. antiproliferative properties of the lazaroids u-83836e and u-74389g on glioma cells in vitro. pathol oncol res. 1999;5:223-228. doi:10.1053/paor.1999.0202. 44. campo gm, squadrito f, campo s, et al. antioxidant activity of u-83836e, a second generation lazaroid, during myocardial ischemia/reperfusion injury. free radic res. 1997;27:577-590. doi:10.3109/10715769709097861. 45. mustafa ag, wang ja, carrico km, hall ed. pharmacological inhibition of lipid peroxidation attenuates calpain-mediated cytoskeletal degradation after traumatic brain injury. j neurochem. 2011;117:579588. doi:10.1111/j.1471-4159.2011.07228.x. 46. durmaz r, kanbak g, akyüz f, et al. lazaroid attenuates edema by stabilizing atpase in the traumatized rat brain. can j neurol sci. 2003;30:143-149. 47. rocha-gonzález hi, ambriz-tututi m, granadossoto v. resveratrol: a natural compound with pharmacological potential in neurodegenerative diseases. cns neurosci ther. 2008;14:234-247. doi:10.1111/j.1755-5949.2008.00045.x. 48. dragone t, cianciulli a, calvello r, porro c, trotta t, panaro ma. resveratrol counteracts lipopolysaccharide-mediated microglial inflammation by modulating a socs-1 dependent signaling pathway. toxicol vitr. 2014;28:1126-1135. doi:10.1016/j.tiv.2014.05.005. 49. zhang f, liu j, shi js. anti-inflammatory activities of resveratrol in the brain: role of resveratrol in microglial activation. eur j pharmacol. 2010;636:1-7. doi:10.1016/j.ejphar.2010.03.043. 50. a. ma, l.f.d. s, r. w, a.l. d. perspectives on molecular biomarkers of oxidative stress and antioxidant strategies in traumatic brain injury. biomed res int. 2014;2014. http://www.hindawi.com/journals/biomed/\nhttp://ovid sp.ovid.com/ovidweb.cgi?t=js&page=reference&d=e med11&news=n&an=2014186606. 51. sönmez u, sönmez a, erbil g, tekmen i, baykara b. neuroprotective effects of resveratrol against traumatic brain injury in immature rats. neurosci lett. 2007;420:133-137. doi:10.1016/j.neulet.2007.04.070. 52. singleton rh, yan hq, fellows-mayle w, dixon ce. resveratrol attenuates behavioral impairments and reduces cortical and hippocampal loss in a rat controlled cortical impact model of traumatic brain injury. j neurotrauma. 2010;27:1091-1099. doi:10.1089/neu.2010.1291. 53. karalis f, soubasi v, georgiou t, et al. resveratrol ameliorates hypoxia/ischemia-induced behavioral deficits and brain injury in the neonatal rat brain. brain res. 2011;1425:98-110. doi:10.1016/j.brainres.2011.09.044. 54. quincozes-santos a, bobermin ld, tramontina ac, et al. oxidative stress mediated by nmda, ampa/ka channels in acute hippocampal slices: neuroprotective effect of resveratrol. toxicol vitr. 2014;28:544-551. doi:10.1016/j.tiv.2013.12.021. 55. simonsen u, christensen fh, buus nh. the effect of tempol on endothelium-dependent vasodilatation and blood pressure. pharmacol ther. 2009;122:109-124. doi:10.1016/j.pharmthera.2009.02.002. 56. deng-bryant y, singh in, carrico km, hall ed. neuroprotective effects of tempol, a catalytic scavenger of peroxynitrite-derived free radicals, in a mouse traumatic brain injury model. j cereb blood flow metab. 2008;28:1114-1126. doi:10.1038/jcbfm.2008.10. 57. wilcox cs. effects of tempol and redox-cycling nitroxides in models of oxidative stress. pharmacol ther. 2010;126:119-145. doi:10.1016/j.pharmthera.2010.01.003. 58. hall ed, wang j a., miller dm. relationship of nitric oxide synthase induction to peroxynitrite-mediated oxidative damage during the first week after experimental traumatic brain injury. exp neurol. 2012;238(2):176-182. doi:10.1016/j.expneurol.2012.08.024. 334 | romero-rivera et al antioxidant therapies in traumatic brain injury 59. ding k, wang h, xu j, et al. melatonin stimulates antioxidant enzymes and reduces oxidative stress in experimental traumatic brain injury: the nrf2-are signaling pathway as a potential mechanism. free radic biol med. 2014;73:1-11. doi:10.1016/j.freeradbiomed.2014.04.031. 60. dehghan f, khaksari hadad m, asadikram g, najafipour h, shahrokhi n. effect of melatonin on intracranial pressure and brain edema following traumatic brain injury: role of oxidative stresses. arch med res. 2013;44(4):251-258. doi:10.1016/j.arcmed.2013.04.002. 61. barlow km, brooks bl, macmaster fp, et al. a double-blind, placebo-controlled intervention trial of 3 and 10 mg sublingual melatonin for post-concussion syndrome in youths (playgame): study protocol for a randomized controlled trial. trials. 2014;15:271. doi:10.1186/1745-6215-15-271. 62. fernández-mar mi, mateos r, garcía-parrilla mc, puertas b, cantos-villar e. bioactive compounds in wine: resveratrol, hydroxytyrosol and melatonin: a review. food chem. 2012;130:797-813. doi:10.1016/j.foodchem.2011.08.023. 63. ates o, cayli s, gurses i, et al. effect of pinealectomy and melatonin replacement on morphological and biochemical recovery after traumatic brain injury. int j dev neurosci. 2006;24(6):357-363. doi:10.1016/j.ijdevneu.2006.08.003. 64. kelso ml, scheff nn, scheff sw, pauly jr. melatonin and minocycline for combinatorial therapy to improve functional and histopathological deficits following traumatic brain injury. neurosci lett. 2011;488(1):60-64. doi:10.1016/j.neulet.2010.11.003. 65. ding k, wang h, xu j, lu x, zhang l, zhu l. melatonin reduced microglial activation and alleviated neuroinflammation induced neuron degeneration in experimental traumatic brain injury: possible involvement of mtor pathway. neurochem int. 2014;76:23-31. doi:10.1016/j.neuint.2014.06.015. 66. ding k, wang h, xu j, et al. melatonin stimulated antioxidant enzymes and reduced oxidative stress in experimental traumatic brain injury: the nrf2-are signaling pathway as a potential mechanism. free radic biol med. 2014;73:1-11. doi:10.1016/j.freeradbiomed.2014.04.031. 67. campolo m, ahmad a, crupi r, et al. combination therapy with melatonin and dexamethasone in a mouse model of traumatic brain injury. j endocrinol. 2013;217:291-301. doi:10.1530/joe-13-0022. 68. hong y, yan w, chen s, sun c, zhang j. the role of nrf2 signaling in the regulation of antioxidants and detoxifying enzymes after traumatic brain injury in rats and mice. acta pharmacol sin. 2010;31:1421-1430. doi:10.1038/aps.2010.101. 69. dash pk, zhao j, orsi s a., zhang m, moore an. sulforaphane improves cognitive function administered following traumatic brain injury. neurosci lett. 2009;460(2):103-107. doi:10.1016/j.neulet.2009.04.028. 70. darvekar sr, elvenes j, brenne hb, johansen t, sjøttem e. spbp is a sulforaphane induced transcriptional coactivator of nrf2 regulating expression of the autophagy receptor p62/sqstm1. plos one. 2014;9. doi:10.1371/journal.pone.0085262. 71. tarozzi a, angeloni c, malaguti m, morroni f, hrelia s, hrelia p. sulforaphane as a potential protective phytochemical against neurodegenerative diseases. oxid med cell longev. 2013. doi:10.1155/2013/415078. 72. zhao j, moore an, redell jb, dash pk. enhancing expression of nrf2-driven genes protects the blood brain barrier after brain injury. j neurosci. 2007;27:1024010248. doi:10.1523/jneurosci.1683-07.2007. 73. jo c, kim s, cho sj, et al. sulforaphane induces autophagy through erk activation in neuronal cells. febs lett. 2014;588(17):3081-3088. doi:10.1016/j.febslet.2014.06.036. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0050 article anton-babinski syndrome as a rare complication of chronic bilateral subdural hematomas d. adam, d. iftimie, cristiana moisescu, gina burduşa romania      romanian neurosurgery (2018) xxxii 3: 399 403 | 399             doi: 10.2478/romneu-2018-0050 anton-babinski syndrome as a rare complication of chronic bilateral subdural hematomas d. adam1,2, d. iftimie1, cristiana moisescu1, gina burduşa1 1department of neurosurgery, „saint pantelimon” clinical emergency hospital, bucharest 2“carol davila” university of medicine and pharmacy, bucharest, romania abstract: clinical presentation: we report the case of a 68-year-old patient that presented at our department 6 weeks after a mild traumatic brain injury with confusion and drowsiness. emergency head ct scan revealed chronic bilateral subdural hematomas with no midline shift. his neurological status quickly deteriorated after admission (gcs of 9 points) and he was operated immediately. although surgery was uneventful and his neurological status markedly improved, in the first postoperative day he developed blindness with visual anosognosia and visual confabulations, suggestive for anton-babinski syndrome. emergency head mri performed on the same day was normal but a repeat head mri in the seventh postoperative day revealed bilateral occipital ischemia, thus explaining his symptoms. the patient became aware of his deficit two weeks after surgery, but was surprisingly ambivalent regarding it. conclusion: cortical blindness (sometimes presenting in the context of anton-babinski syndrome) is a rare complication of chronic bilateral subdural hematomas, a rather common neurosurgical pathology. although it can be overlooked on the initial neurological examination, it should be taken into account, prompting emergency surgical treatment in order to prevent permanent visual deficits. key words: chronic bilateral subdural hematoma, visual anosognosia, visual confabulations clinical presentation a 68-year-old patient, without significant medical history, suffered a mild traumatic brain injury secondary to a car accident, presenting no immediate symptoms at the time, nor for more than a month posttraumatic. also, a ct scan was performed on the day of the accident, which was interpreted as normal. his family denied any other subsequent significant head trauma. he was admitted in our department 6 weeks after trauma, presenting confusion and drowsiness, symptoms that began six days prior to admission with progressive worsening. he was uncooperative, thus making a thorough neurological examination 400 | adam et al anton-babinski syndrome in chronic bilateral subdural hematomas             difficult and seemed to present no motor or cranial nerve deficits at the time. his gcs score at admission was noted as 13 by the attending physician. emergency head ct scan revealed chronic bilateral subdural hematomas (separated type according to the nakaguchi classification1) with a maximal thickness of 1,6 cm on the left side and 1,3 cm on the right with no midline shift (figure 1). figure 1 preoperative emergency head ct revealing bilateral chronic subdural hematomas with no midline shift his neurological status rapidly deteriorated, with a gcs score of 9 several hours after admission. emergency evacuation of bilateral hematomas was performed with fronto-parietal craniotomies. the operation was uneventful. in the first postoperative day, his neurological status markedly improved, (gcs score of 14 points) but presented signs of visual disturbances which were not obvious at admission. blindness with visual anosognosia and visual confabulations were noted, features suggestive for anton-babinski syndrome. ophthalmological examination revealed no abnormalities and raised the suspicion of cortical blindness. emergency mri performed on the first postoperative day revealed no ischemic lesions (figure 2). figure 2 postoperative day 1 emergency head mri with a normal postoperative appearance (left: t2 weighted image, right: dwi) romanian neurosurgery (2018) xxxii 3: 399 403 | 401             over the next few days, the patient presented no improvement, and remained blind. however, about two weeks after surgery he became permanently aware of his visual loss and his visual confabulations disappeared. the patient did not appear to be emotionally affected by this deficit and surprisingly remained in good spirits throughout his admission in our department. in the seventh postoperative day, an angiomri with contrast was performed in an attempt to objectify the cause of the patient’s blindness, that revealed bilateral occipital ischemia (figure 3). figure 3 postoperative day 7 head mri revealing bilateral occipital ischemic lesions (left: t2, right: dwi) he was transferred to a rehabilitation department, his visual deficit remaining complete at a later follow-up. discussion montaigne (1533-1592) was probably the first to describe in one of his books a case of anton-babinski syndrome, describing a nobleman who did not believe he was blind despite obvious signs. gabriel anton (18581933) was the first to describe patients with blindness and deafness which were not aware of their deficit. babinski was the one that later named this sign anosognosia. (2) blindness secondary to bilateral chronic subdural hematoma is a rare complication thus very few cases have been discussed in the literature. (3,4) the majority of these cases presented progressive visual loss as a result of posterior cerebral artery infarction secondary to tentorial herniation. according to keane’s report, despite surgical evacuation, these patients were either left blind or with almost complete visual loss. in 2008, kabir reported a case of sudden blindness as a clinical manifestation of a chronic subdural hematoma. (5) in his case, following prompt surgical decompression, the patient’s visual acuity returned to almost normal. however, in this case, the sudden blindness was proved to be caused by severe acute papilloedema, with no evidence of posterior cerebral artery territory ischemia, representing the only reported case of reversible blindness after chronic subdural hematoma evacuation. in 2017, balasubramanian et al (6) reported the case of a male patient who, after evacuation 402 | adam et al anton-babinski syndrome in chronic bilateral subdural hematomas             of a chronic bilateral subdural hematoma, developed bilateral posterior cerebral artery infarction and blindness. based on a literature review, only four cases of blindness following chronic bilateral subdural hematoma evacuation are reported and all patients suffered permanent visual loss. the exact etiopathogenesis and mechanism of this rare complication are not completely understood. we presented the case of a male patient with chronic bilateral subdural hematomas and postoperative permanent blindness as a result of bilateral occipital lobe ischemia. however, the case that we reported had a particularity: in addition to the cortical blindness, the patient also presented anosognosia with visual confabulation (characteristic for anton babinski syndrome), symptoms which were relevant only in the postoperative period. the anton babinski syndrome could have been present hours before the operation but it was not objectified as the patient was uncooperative at the time of admission, making a proper neurological examination difficult. imaging evidence of bilateral occipital lobe ischemia was obtained in the seventh postoperative day. based on a review of the literature, it is difficult to establish awareness of blindness in patients with anton-babinski syndrome. nevertheless, in one report, a patient with antonbabinski syndrome was aware of blindness within 2 weeks, without presenting any vision improvement. (7) in our case, the patient began to be aware of his visual loss approximately two weeks from the onset. however, he remained oddly optimistic given the circumstance. when asked every morning how he was feeling, he used to answer nonchalantly: „i cannot see but other than that, i am very well”. as far as we know, it would seem that this is the first case of chronic bilateral subdural hematomas associated with postoperative anton-babinski syndrome reported in the literature. conclusion cortical blindness (sometimes presenting in the context of anton-babinski syndrome) is a rare complication of chronic bilateral subdural hematomas, a rather common neurosurgical pathology. although it can be overlooked on the initial neurological examination, it should be taken into account, prompting emergency surgical treatment in order to prevent permanent visual deficits. references 1. nakaguchi h, tanishima t, yoshimasu n. factors in the natural history of chronic subdural hematomas that influence their postoperative recurrence. j neurosurg. 2001;95(2):256-262. doi:10.3171/jns.2001.95.2.0256 2. maddula m, lutton s, keegan b. anton’s syndrome due to cerebrovascular disease: a case report. j med case rep. 2009;3:9028. doi:10.1186/1752-1947-00030000009028 3. keane jr. blindness following tentorial herniation. ann neurol. 1980;8(2):186-190. doi:10.1002/ana.410080209 4. soza m, tagle p, kirkham t, court j. bilateral homonymous hemianopia with sparing of central vision after subdural hematoma. can j neurol sci. 1987;14(2):153-155. http://www.ncbi.nlm.nih.gov/pubmed/3607617. accessed august 22, 2018. 5. kabir s, kamat a, carroll t. sudden onset blindness as a presenting feature of chronic subdural haematoma: case report. vol 6.; 2008. romanian neurosurgery (2018) xxxii 3: 399 403 | 403             https://print.ispub.com/api/0/ispub-article/13546. accessed august 22, 2018. 6. chitra balasubramanian s, adimoolam s, shunmugam s. bilateral chronic subdural hematoma and blindness: bilateral infarction to the posterior cerebral artery following evacuation of bilateral chronic subdural hematoma — a rare case report and review of literature. indian j neurotrauma. 2017;14. 7. chen j-j, chang h-f, hsu y-c, chen d-l. antonbabinski syndrome in an old patient: a case report and literature review. psychogeriatrics. 2015;15(1):58-61. doi:10.1111/psyg.12064 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article brain hydatidosis: review of the literature johana maraby-salgado, joulen mo-carrascal, jorge aquino-matus, willem guillermo calderon-miranda, amit agrawal, andrei f. joaquin, mohammed al-dhahir, samer hoz, maria teresa pacheco-hernandez, huber padilla, luis rafael moscote-salazar colombia, mexico, india, brazil, yemen, irak doi: 10.1515/romneu-2017-0061 378 | maraby-salgado et al brain hydatidosis doi: 10.1515/romneu-2017-0061 brain hydatidosis: review of the literature johana maraby-salgado1, joulen mo-carrascal1, jorge aquino-matus2, willem guillermo calderon-miranda3, amit agrawal4, andrei f. joaquin5, mohammed al-dhahir6, samer hoz7, maria teresa pachecohernandez1, huber padilla1, luis rafael moscote-salazar8 1universidad de cartagena, colombia; 2department of internal medicine, universidad nacional autonoma de mexico, ciudad de mexico, mexico; 3department of radiology, universidad nacional autonoma de mexico, ciudad de mexico, mexico; 4department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh, india; 5department of neurology, neurosurgery division, state university of campinas, campinas-são paulo, brazil; 6neurosurgery, al-thawra modren general hospitakl, yemen; 7neurosurgery, neurosurgery teaching hospital, bagdad, irak; 8neurosurgery, red latino, organización latinoamericana de trauma y cuidado neurointensivo, bogota, colombia abstract: hydatidosis is a common disease worldwide. the causal agent may compromise any organ of the body, the cerebral location is infrequent. the infection is caused by the larval form of cestodo echinococcus granulosus. the man is an accidental intermediary host for food consumption or water contaminated with eggs present in animal feces. we present a review of the literature. at the imaging level, the disease has a classic characteristic consisting of single, usually unilocular and less frequent multilocular, intra-axial and more frequently hemispheric cerebral lesions, compromising the vascular territory of the middle cerebral artery by the hematogenous dissemination of the parasite. key words: echinococcosis, brain neoplasms, cysts, neurosurgery introduction hydatidosis (echinococcosis) is a global zoonotic parasitic disease produced by the larval phase of tenia echinococcus (1, 2, 3). there are two types of echinococcus infections: echinococcus granulosus is the most common type, whereas echinococcus multilocularis is less common but more invasive, generally with malignant behavior (1, 2, 3, 4, 5, 6, 7, 8). most cases of cystic echinococcosis are found in endemic areas such as australia, new zealand, the mediterranean, the middle east, and south america, and cases of alveolar echinococcosis are found in north america, central europe, russia, china, and turkey (6). romanian neurosurgery (2017) xxxi 3: 378 384 | 379 the overall incidence of organ infestation is highest in the liver reaching 50% to 77%, followed by lungs with 8.5% to 43%, and 10% found in other organs such as brain, muscles, pericardium, kidneys, ocular orbit, tibia, and bone marrow (4, 6, 7, 8). what is neurohidatidosis? central nervous system (cns) involvement is rare and occurs in approximately 2to 3% of all cases, and accounting for only 2% of all lesions occupying the intracranial space (1, 3, 4). neurohidatidosis is more frequent in children and young adults (approximately 50 to this affects more men than women (62%) from 21to 40 years -old in the general population (3, 4, 8). the cyst affects the cns in 1% of cases and is usually diagnosed in childhood. it has been reported a prevalence of 60-93% in children with a male predominance (5, 8). cycle the life cycle of the parasite requires two hosts: a definitive host and an intermediate host. the main definitive hosts are mainly dogs for e. granulosus and foxes, jackals and coyotes for e. multilocularis, which generally maintain the wild cycle. the main intermediate hosts are sheep for e. granulosus and wild rodents for e. multilocularis (6, 7). the adult worm lives in the intestine of the definitive host, which expels eggs in feces (infective form) that are ingested by the intermediate host. after the ingestion of eggs, the enzymes in the intestinal tract digest the outer lining of the eggs and the embryo is released. the embryos have small hooks and pacifiers with which they attach to the mucosa of the intestine, perforate the wall and disseminate through the circulatory and lymphatic system (1, 4, 5, 7, 8), and then to the liver, lungs, brain and other tissues. the embryo develops into a cyst within which protoscolices are produced. the cycle is completed when the final host ingests the larval form (5, 6, 7, 8). humans may be infected incidentally as intermediary hosts after ingesting the eggs of the parasite directly by contact with a final host or indirectly with contaminated food or water (6, 7). histopathology histopathologically the e. granulosus cyst wall consists of a germinal inner layer (endochisis) and a laminated outer layer (exocyst). the host reacts to the cyst by forming a capsule of connective tissue (pericyst), vascularized that provides nutrients for the parasite. in the brain, the pericystic layer is thin because and exhibits minimal inflammatory reaction. e. granulosus cysts are usually solitary and commonly supratentorial, located in the distribution of the terminal branches of the middle cerebral artery, usually temporo-parieto-occipital (1, 8) e. granulosus cysts are usually unique and spherical, well demarcated from the surrounding tissue (which does not present major inflammatory changes), and have smooth and thin walls; they can reach a large size as a result of slow but continuous growth (7, 8). the cystic lesions are homogeneous 380 | maraby-salgado et al brain hydatidosis with liquid content like that of cerebrospinal fluid, glycolipoproteins, carbohydrates, amino acids and metacestode metabolism salts. some of its components, such as albumin and immunoglobulins are derived from the host. in the cns, cysts can grow mainly from the direct implantation of oncospheres or from the metastatic dissemination of a visceral cyst (1, 6, 8). in contrast to the cyst of e. granulosus, the cyst of e. multilocularis grows by external budding of the germinal membrane with progressive infiltration of the surrounding tissue. cysts are small, tend to aggregate in clusters resembling a bunch of grapes and proliferate rapidly eroding brain tissues; they have little fluid within a semi-solid structure and many small vesicles embedded in a calcified stroma. they are commonly surrounded with connective tissue edema, and cause a severe immune reaction in the host. they usually do local and distant metastases, especially in the liver, lung, marrow, and brain. the extent of injury to brain tissue is characterized as "crab claws", which is extremely dangerous for the human body (4, 9, 10). multiple brain hydatid cysts are rare. most of the cases are due to surgical, spontaneous or traumatic rupture of a viable primary lesion with implantation of the scythe within the cerebral parenchyma. these lesions are called secondary and are infertile as they lack breeding and scolex capsules. it is believed that multiple cysts can also grow after rupture of a cyst located in a left heart cavity or large arterial vessels (4, 8, 9). in the literature, there are 81 patients reported with multiple cerebral hydatid cysts: 77 by al zain et al., 5 by tu'zu`n et al., and 2 by buktea et al. (3) multiple primary cyst without any clinical or radiological evidence of hydatidosis in other parts of the body are rare and are usually result from arterial embolism secondary to the ingestion of multiple larvae (6, 7, 8). in both species, the larva of the parasite can be found within the cysts (7, 8, 9). spinal hydatidosis is rarely seen and occurs in less than 1% of all cases of hydatid disease. thoracic disease is more common with mainly vertebral and paravertebral involvement (1). clinical manifestations the clinical manifestations of neurohydatidosis are closely related to their location. the lesions may remain asymptomatic until they become quite large (10). the main symptoms are headache, vomiting, nausea, and other nonspecific symptoms such as hemiparesis, seizures, altered visual field and gait disorders; all of them varying with the intracranial location of the lesions. neurological signs may also manifest as result of increased intracranial pressure (8, 11). the most common clinical manifestations of spinal hydatidosis include paraparesis (62%), paraplegia (26%), back pain and radicular pain (55%), hypoesthesia (36%), and loss of sphincter control (3%) (8, 9, 10, 11). diagnosis the diagnosis of the disease hydatidosis is based on serological tests and imaging techniques. immunological data are irrelevant for diagnosis, and the most reliable methods romanian neurosurgery (2017) xxxi 3: 378 384 | 381 are neuroradiological imaging and histopathological examination (6, 7, 8, 10, 12). image techniques diagnostic methods useful for human hydatidosis include ultrasonography (us), computed tomography (ct) and magnetic resonance imaging (mri) (13, 14, 15, 16). (figure 1). ct (as well as mri) is essential to the diagnosis of cerebral hydatid cyst. ct sensitivity ranges from 90% to 97%. mri adequately shows the main characteristics of the hydatid cyst (6, 8, 12, 13). although neurohydatidosis can locate in any part of the brain, there are most often found in both hemispheres, particularly in the territory of the middle cerebral artery. in younger patients, skull x-rays may demonstrate suture separation, unilateral and widening of the vault, or erosion of posterior clinoid processes (1, 6, 7, 8, 9, 10). the evaluations of hydatid cysts by cranial ct and mri reveal a solitary parenchyma with homogeneous, most commonly supratentorial, spherical and large cysts with well-defined borders, and peripheral edema. the density of cyst fluid is the same as that of cerebrospinal fluid (8, 12). although the lesion may cause extrinsic compression of the ventricle system with posterior hydrocephalus, there is associated edema as seen typically in abscesses and cystic tumors. the lesion does not improve after the intravenous administration of contrast material, and calcification is extremely rare (6, 7, 8). on non-contrast ct, the cyst wall is isodense or hyperdense to the brain tissue (7, 8). in mri the cyst wall usually shows a low intensity border in both t1 and t2-weighted images. in t2-weighted mri, the presence of a hypointense border has been described as a characteristic of hydatidosis (6, 8). mri is the preferred imaging modality when spinal hydatidosis is suspected. the walls of the cyst are thin and regular, with no septa. the presence of a markedly hypointense cyst wall in t1-weighted and t2-weighted images, and the absence of enhancement of the wall with gadolinium, are characteristic of hydatid disease (6, 8, 13, 14). it is believed that mri should be considered as the imaging aid of choice in planning for surgical approach because of the ability to obtain coronal and sagittal images; and also, because it reveals the anatomical relationships of the lesions to the grooves and ventricles (7, 8, 10, 15). figure 1 cerebral ct scan showing cysts of hydatidosis 382 | maraby-salgado et al brain hydatidosis in imaging tests, cerebral alveolar hydatidosis are shown as solid, calcified lesions with surrounding edema, in the form of cauliflower. this pattern has also been reported in other studies and may help distinguish cerebral alveolar hydatidosis from other brain masses, particularly in cysticercosis, coenuresis, toxoplasmosis, fungal infections, brain abscesses and oligodendrogliomas (10, 12, 13, 16). experimentally it has been shown that a cyst takes from 3 to 16 months to grow to 1 cm in diameter (12). serological analysis is in most cases negative. the advantage of histopathological examination is that reveals the degree of infestation of the parenchyma around the cyst that contributes to the enlargement of the process. although radiological characteristics are characteristic, the definitive diagnosis of hydatidosis is based on the histopathological examination of the surgical specimen (6, 11, 12, 13, 15). serology the test of choice for the serological diagnosis of hydatidosis is based on the detection of igg antibodies against cyst fluid derived from native or recombinant b antigen subunits, either by enzyme-linked immunosorbent assay (elisa) or in immunoblots. antibodies are found up to 92.2% against a new 32 kda epc1 antigen of the germ layer of the hydatid cyst of e. granulosus, compared to 84.5% against the b antigen (11, 12, 13, 14, 15, 16). e. granulosus has been shown to induce both cellular and humoral immune response, therefore increasing the number of cd8 in peripheral blood (10, 14, 15, 17). in other laboratory tests, the globular sedimentation rate is always high and peripheral eosinophilia could not be a significant feature. lumbar puncture i usually avoided since changes in cerebrospinal fluid are not specific and the risk of complications due to increased intracranial pressure is high (14, 15, 18). evidence for the fixation of the complement (weinberg) and the reaction of casoni (immediate hypersensitivity skin test) is limited; weinberg is positive in 40 to 70% of patients, and false positives are frequently obtained with the casoni reaction. (14, 15) measurement of specific immunoglobulin e circulation is not a diagnostic test but may be used to monitor the response to medical treatment (14, 15, 17) the release of histamine from basophils and particularly the degranulation tests used to detect ige binding to basophils, are more sensitive than common tests and may be used to confirm diagnosis in endemic regions (13, 14, 15). differential diagnosis the differential diagnosis of cerebral cystic echinococcosis includes brain abscess, cystic tumor, arachnoid cyst, and encephalic cyst. hydatid lesions can be differentiated from brain abscess and cystic tumor by the absence of edema around the lesion and mural nodules. other cystic lesions such as arachnoid cysts and brain cysts are not spherical and are not surrounded by brain matter (7, 8, 15, 16). romanian neurosurgery (2017) xxxi 3: 378 384 | 383 the differential diagnosis of cerebral alveolar echinococcosis includes gliomas, metastases, tuberculomas and fungal infections. the diagnosis should be suggested by evidence of a primary hepatic foci, clinical history, patient clinical manifestations, geographic location with high prevalence of infection in the host, and laboratory data (include information about csf, western blot, or pcr before surgery (10, 11, 14, 15) lack of transparency or sclerosis within adjacent bone in the absence of disc disease in vertebral hydatid disease may help to differentiate from tuberculous spondylitis. (1) treatment the treatment of this infection consists of surgical intervention, medical treatment, and chemotherapy (19, 20, 21, 22). medical treatment with mebendazole, albendazole and praziquantel have shown good results in the hydatid cyst of liver and abdomen. few data have been published in the medical treatment of intracranial hydatidosis with respect to drug penetration through the blood-brain barrier and the intracranial hydatid cyst membrane, however reports of isolated cases showed complete disappearance of multiple intracranial hydatid cysts with albendazole therapy at a daily dose of 10 mg/kg three times daily for 4 months (7, 14, 15, 20, 21, 22). nonetheless, surgical removal of the cerebral hydatid cyst remains the treatment of choice. the rate of intact removal of an intracranial hydatid cyst is about 60 to 70%. intraoperative rupture of the cyst produces a high risk of recurrence and can be fatal due to the dissemination of scolex, which can lead to replantation, anaphylaxis, and chemical meningitis (14, 15, 21, 22, 23). medical treatment with albendazole is beneficial in cases of recurrence, rupture of an intraoperative cyst, giant or multiple hydatid cysts, or both before and after surgery. longterm follow-up of patients with intracranial hydatidosis in whom rupture of the cyst occurred intraoperatively confirm the excellent prognosis reported previously (8, 12). currently the dowling-orlando technique is the technique most used in the surgical treatment of hydatid cysts. when the dowling technique is combined with microsurgery, large cerebral hydatid cyst can be successfully removed without rupture (14, 15, 21, 22, 24). the correct treatment of spinal hydatidosis and neurological compromise is laminectomy with removal of the cyst to achieve local decompression. however, cysts that compromise the spine may not be safely cleared, therefore the risk of recurrence is up to 40%, even after extensive surgery (4, 21, 22, 23, 24). currently, surgery is the accepted method for the treatment of cases of cerebral alveolar hydatidosis, but chemotherapy is mandatory after the surgical intervention (10) (figure 2). figure 2 appearance of a typical cyst at removal 384 | maraby-salgado et al brain hydatidosis correspondence dr. luis rafael moscote e-mail: mineurocirujano@aol.com references 1.akgoz a, mukundan s, lee tc. imaging of rickettsial, spirochetal, and parasiticinfections.neuroimagingclin n am. 2012;22(4):633-57. 2.sadjjadi sm1, mikaeili f, karamian m, maraghi s, sadjjadi fs, shariat-torbaghan s, kiaeb.evidencethattheechinococcusgranulosus g6 genotype has anaffinityforthebrain in humans.int j parasitol. 2013;43(11):875-7. 3.gana r ,skhissi m, maaqili r, bellakhdarf.multipleinfected cerebral hydatidcysts.journal of clinicalneuroscience. 2007;15:591–593. 4. altas m, serarslan y, davran r, evirgen o, aras m, yilmazn.the dowling-orlando technique in a giantprimary cerebral hydatidcyst: a case report.neurologia i neurochirurgiapolska 2010; 44, 3: 304–307. 5.pedrosa i,saíz a, arrazola j,ferreirós j, pedrosa cs.hydatiddisease:radiologic and pathologicfeatures and complications.radiographics. 2000; 20:795–817. 6.tuzun m, altınor n, arda is, hekimoglub..cerebralhydatiddisease: ct and mr imagingfindings.journal of clinical imaging.2002;26: 353– 357. 7.yurt a, avci m, selçuki m, ozer f, camlar m, uçar k, taşli f, altinörs n. multiple cerebral hydatidcysts. report of a case with 24 pieces.clinneurolneurosurg. 2007;109(9):821-6. 8.limaiem f, bellil s, bellil k, chelly i, mekni a, khaldi m, haouet s, zitouna m, kchirn.primaryhydatidosis of the central nervoussystem: a retrospectivestudy of 39 tunisiancases.clinneurolneurosurg. 2010;112(1):23-8. 9.juan ma, sailikeduishanbai , chun-hui jiang, jun lu , wen-ya liu , jianwang.quantitativeanalysis of cerebral alveolar echinococcosis and braintuberculomaby mr diffusionweightedimaging.radiology of infectious diseases.2016;xx: 1-5 10.ma zl1, ma lg, ni y.cerebral alveolar echinococcosis: a report of twocases.clinneurolneurosurg. 2012;114(6):717-20. 11.talan-hranilovic j, sajko t, negovetic l, lupret v, kalousekm.cerebralcysticercosis and echinococcosis: a preoperativediagnosticdilemma.archmed res. 2002 ;33(6):590-4. 12.müfit k, nejat i, mercan s, ibrahim k, mete uy, yükselk.growth of multiplehydatidcystsevaluatedbycomputedtomography.j clinneurosci. 1998;5(2):215-7. 13.bükte y, kemaloglu s, nazaroglu h, ozkan u, ceviz a, simsekm.cerebralhydatiddisease: ct and mr imagingfindings.swissmedwkly. 2004;134(31-32):45967. 14.shuklas,trivedia,sharma v. craniospinalhydatidosis: report of three cases. jpediatrneurosci .2008;3: 146-9 15.senapati sb, parida dk, pattajoshi as, gouda ak, patnaika.primaryhydatidcyst of brain: two cases report. asian j neurosurg. 2015 ;10(2): 175–176. 16.khan mb, riaz m, bari me.multiple cerebral hydatidcysts in 8 yearoldboy: a case report and literaturereview of a rarepresentationsurgneurolint. 2015; 6: 125. 17.wang j, cai b, youc.surgicaltreatmentoptionsfor cerebral alveolar echinococcosis: experience in sixpatients.neurol india. 2009 ;57(2):157-61. 18.alvarez rojas ca, romig t, lightowlersmw.echinococcusgranulosus sensu lato genotypesinfectinghumans--review of currentknowledge.int j parasitol. 2014;44(1):9-18. 19.sadjjadi sm1, mikaeili f, karamian m, maraghi s, sadjjadi fs, shariat-torbaghan s, kiaeb. evidencethatthe echinococcusgranulosus g6 genotype has anaffinityforthebrain in humans.int j parasitol. 2013;43(11):875-7. 20.singounas eg, leventis as, sakas de, hadley dm, lampadarios da, karvounis pc. successfultreatment of intracerebral hydatidcysts 21.alvarez rojas ca, romig t, lightowlers mw..echinococcusgranulosus sensu lato genotypesinfectinghumans--review of currentknowledge.int j parasitol. 2014;44(1):9-18. 22.todorov t, vutova k, petkov d, balkanski g. albendazoletreatment of multiple cerebral hydatidcysts: case report. trans r soc trop med hyg. 1988;82:150–2. 23.topsakal c, aydin y, aydin f, sahin y, bilge t, kasaroglu d, delibalta n.cerebral alveolar hydatidosis: case report. surg neurol.1996;45:575-81 24.h del brutto o.taenia (includingcysticercosis) and hydatid disease. medicine.2005;33(8): 70-73. microsoft word 8balancdecompressive.doc c. balan, b. alliez decompressive craniectomy 73 decompressive craniectomy – from option to standard – part ii c. balan1, b. alliez2 1neurosurgery, emergency hospital “prof. dr. n. oblu” iasi, romania 2hopital nord, chu marseille, france abstract the paper intends an update to the theoretical and practical data on a seldom utilized technique but often considered as last therapeutically option, so the necessity to realize it correctly. in this second part are presented the indications of the technique for each type of pathology, together with the results and latest guideline indications. keywords: decompressive craniectomy, indications indications there is actually just one class i indication for decompressive craniectomy malignant sylvian stroke in people less than 60 old [1], and still there are controversies. most studies involving decompressive craniectomy are retrospective and the few prospective ones were realized on patients with refractory raised intracranial pressure as salvage therapy – last option available. there are also several suggestions of using profilactic decompressive craniectomies whenever exists a high risk of evolution towards a refractory raised intracranial pressure or when the neurosurgeon’s experience suggests this – like acute subdurals hematomas associated with large contusion, subarachnoid hemorrhage or severe meningitis[2,3]. the purpose of this paper is not to argue in favor or not the extending of decompressive craniectomy in different pathologies but to present the authors experience together with a review of the literature, as the second author was one of the first who pleaded for the importance of knowing the technique and its limitations [4] after 1999, when guerra re-introduced decompressive craniectomy after several decades of oblivion. traumatic pathology decompressive craniectomy has been applied in patients with traumatic brain injury for several years but only within the past 10 years, the modern era of neurointensive care, there have been observational studies. the primary indication for decompressive craniectomy is persistent raised intracranial pressure, which cannot be controlled by other therapeutic measures (hyperventilation, deep sedation, diuretics or csf withdrawal). after several minutes (and sometimes hours) of raised icp over 22-25 mm hg, especially on a contused brain and when medical therapy proved ineffective, a decompressive craniectomy can be tempted. from wurzburg [5] who reported a favorable outcome rate of 56% and a mortality rate of 11%, with later de 74 romanian neurosurgery (2010) xvii 1: 73 80 compressions averaging 68 hours postinjury in 28 patients and have been guerra [6] who reported a favorable outcome rate of 58% and mortality rate of 19% to noawadays there are over 100 papers on decompressive craniectomy in traumatic refractory raised intracranial pressure. we distinguish two types of decompressive craniectomies realized for traumatic brain injuries : early decompression, realized when operating in emergency an acute subdural hematoma, with subjacent contusions and when the brain swelling prevents the reposition of the bone flap; late decompression, in patients without surgical masses, usually at 3-7 days after trauma, when icp raises and becomes refractory to other medical treatments. on a serie presented by the first author[10], during 5 years, among 937 patients with severe brain injury (gcs < 7), 44 decompressive craniectomies were realized, among which: •27 early decompressive craniectomies for acute subdural hematomas or contusions when ct scan suggested a possible consecutive aggravation •17 late decompressive craniectomies, for refractory icp, higher than 30 mm hg for 30 minutes the results in term of gos at one year are presented in tabel 1. the high level of deaths among early decompressive craniectomies is explained by the important concomitant brain lesions. the main complications on the whole lot were wound dehiscence or infection (19 cases), ventilated associated pneumonia (18 cases), brain abscesses or empyema (6 cases). the high level of good outcomes (gos 4-5) for patients operated late is due to the fact that these late decompressive craniectomies were realized in already stabilized patients, who presented a top in their icp, refractory to medication – this raised icp treated, no more problems were encountered and early cranioplasty was realized. below are the images of one of our cases : figure 1a in day 1, gcs=9; figure 1b in day 2, secondary aggravation, gcs= 5, icp over 50 mm hg; figure 1c in day 17, gcs=12; figure 1d in day 104, after cranioplasty with autologous bone. tabel 1 early decompression late decompression gos 1 – death 14 (51%) 5 (29%) gos 2-3 8 (30%) 5 (29%) gos 4-5 5 (18%) 7 (41%) total 27 17 c. balan, b. alliez decompressive craniectomy 75 figure 1 a figure 1 b figure 1 c figure 1 d guidelines and data from the literature: •guidelines for management of brain injury – 2006 [7] – there is no statistically significant difference between acute subdural hematomas operated with craniotomy with reposition of the bone flap or decompressive craniectomy, reason why further studies are recommended. however, the authors admit that in several papers, patients operated with simple craniotomy were in better neurological status than those operated with decompressive craniectomy. •guidelines for management of brain injury of the american brain trauma foundation (2007)[8] – for intraparenchymal traumatic lesions, the decompressive techniques (decompressive craniectomy, temporal lobectomy) are considered as option whenever exists refractory raised intracranial pressure and radiological signs (ct scan) of cerebral herniation. bifrontal decompressive craniectomy is an option whenever exists diffuse lesions and refractory raised intracranial pressure but no herniation on ct scan if surgery is performed in the first 48 hours. the conclusion is that literature data suggest but not prove that decompressive procedures represent the best available option. •guidelines for management of brain injury of the american brain trauma foundation (2007) for pediatric patients[8] – there are evident data that decompressive craniectomy in children with refractory intracranial pressure leads to better neurological outcome, shorter hospitalization in icu, better icp control. the results were obtained from randomized studies, however due to small cohorts of patients the data are not statistically significant. •in europe, the cochrane database of systematic reviews in 2006 [9] has concluded that there is no evidence to support the routine use of decompressive craniectomy to reduce unfavorable outcomes in adults with severe traumatic brain injury and medically refractory elevated icp. the literature demonstrates a wide range of clinical outcomes, with no clear consensus regarding the indications for surgery. some of the indications mentioned are icp above 25-30 mm hg in adults and 24 mm hg in children for more than 30 minutes, refractory to medical treatment; cerebral perfusion pressure below 60 mm hg, age below 50 , midline shift over 1 cm whenever there is 76 romanian neurosurgery (2010) xvii 1: 73 80 no intracranial mass and even the opinion of the neurosurgeon on call. are excluded patients with gcs 3 or bilateral mydriasis. there are actually two independent multicenter double blind randomized studies in going on the utilizing of decompressive craniectomy for tbi : •the rescueicp is a multicenter european randomized trial in which decompressive craniectomy is compared with medical management coordinated by the university of cambridge, uk, and the european brain injury consortium. patients (600 cases for the main study) with tbi and elevated icp (. 25 mm hg) refractory to initial treatment measures are eligible for the study. patients are randomized to one of two arms: continuation of optimal medical management (including barbiturates) and surgery (decompressive craniectomy). outcome is assessed using the extended gos and 36-item short form health survey at 6 months posttreatment, with additional surrogate end points (icp control and duration of stay in the intensive therapy unit). the pilot phase of the study (50 cases) has been completed in 2007 and has demonstrated that randomizing patients with tbi to decompressive craniectomy as opposed to optimal medical management is feasible. whether this operation is effective and safe remains to be seen. •the decra study, coordinated by the university of melbourne, has enrolled 153 patients from australia and new zealand till october 2009. refractory icp in this study was defined as the spontaneous persistent increase in icp despite optimal conventional icu therapies (including intermittent evd venting) of >20mm hg for more than 15 mins (continuously or cumulative over one hour). patients were randomised to one of two groups: the first group will receive best current management together with an early decompressive craniectomy operation. the second group will receive best conventional therapy alone (which does not include the early dc operation). the study was expected to end at 165 patients in december 2009, patients being evaluated by gose at 6 months. ischemic stroke – according to european stroke organization (2008) and accepted by the romanian society of neurology in 2009, decompressive craniectomy is considered as guideline class i a in the treatment of malignant sylvian stroke. the main paper in literature to support this opinion was published by vahedi [1] and resumes the results of three european independent multicenter trials from france, germany and the netherlands. because of their similar design and outcome measures, the steering committees planned a pooled analysis of the data from these trials while they were still ongoing to increase the chances of obtaining sufficient data and to minimize the number of patients involved in individual trials. this pooled analysis included 93 patients younger than 55 to 60 years who underwent decompressive craniectomy within 48 hours from the onset of stroke. the primary outcome measure for the pooled analysis was the proportion of patients with an mrs score of 4 or lower in the surgical and medical c. balan, b. alliez decompressive craniectomy 77 treatment groups at 1 year posttherapy. survival and an mrs score of 3 or lower were secondary end points. the results have suggested that significantly more patients in the surgical group than in the control group had an mrs score of 4 or lower (75% compared with 24%; pooled absolute risk reduction 51%, 95% ci 3469), an mrs score ≤ 3 (43% compared with 21%; pooled absolute risk reduction 23%, 95% ci 5-41), and survived (78% compared with 29%; pooled absolute risk reduction 50%, 95% ci 33-67). this effect was highly consistent across the three trials and did not change on adjustment for baseline differences. this study represents the best evidence available to date (and possibly ever) on the role of surgical decompression in malignant brain swelling associated with extensive cerebral infarction. however, despite the good results, the data cannot be translated automatically into the widespread use of decompressive surgery in all eligible patients: first, because the findings of an improved outcome cannot be extrapolated to older patients and those who undergo surgery within the first 48 hours after the onset of stroke; and second, although surgery doubles the number of patients who require minor support (mrs score ≤ 3), it increases 10-fold the number of patients with a moderately severe disability (mrs score ≤ 4) that requires almost continuous assistance. this fact must be carefully considered and discussed with the next of kin in each individual case before proceeding to surgery. moreover, the number of ischemic sylvian strokes in patients under 60 years old represents only 3.5-5 % of all ischemic strokes. as criteria to decompress, the study considered patients under 60 years old, with clinical signs of mca stroke , radiological signs of malignant stroke (ct scan >50% acm territory or/and mri territory > 145 cm3) in the first 48 hours from the onset of the stroke. patients having any of: mca stroke before with mrs 2 or worse, contralateral infarction, hemorrhagic transition of stroke, comorbidity influencing outcome, disturbances of blood coagulation were excluded. from personal cases: figure 2a with a mca stroke and midline shift over 1.5 cm., gcs = 6; figure 2b, the same patient after decompressive craniectomy, no more shift, gcs = 9, still hemiplegic. figure 2 a 78 romanian neurosurgery (2010) xvii 1: 73 80 figure 2 b subarachnoid hemorrhage in contrast to traumatic brain injuries, there are substantially fewer published studies on the experience of decompressive craniectomy as a treatment for brain edema following sah. it is already known for more than 15 years that a brain with sah tolerates lower icp level than a normal one and that a pressure of 18-20 mm hg is considered raised after an episode of sah [13]. smith et al. [14] proved that even a limited craniectomy, realized by removal of the bone flap, considering that the bone flap for pterional craniectomy is far smaller than the decompressive one for trauma, can lower significant the icp after clipping an aneurysm. several other studies were realized, among the newest: schirmer [15] described the results of decompressive craniectomy in the treatment of refractory elevated icp in 16 patients with aneurysmal sah, half treated with endovascular coil embolization and the other half with surgical clip application. sixty-nine percent of patients survived, and at the follow-up (median 450 days) 64% of them had an mrs score of 0 to 3 and 36% a score of 4 to 5. early craniectomy performed within 48 hours after sah was associated with a better outcome. buschmann and colleagues [16] have reported the results of 38 patients following decompressive hemicraniectomy after early aneurysm clipping. the pooled data from all 38 patients showed a favorable outcome (gos scores 4 and 5) in 53% of patients, severe disability in 26% (gos score 3), and death in 21%. after 12 months, a good functional outcome was seen in 52% of the cases in group 1, in 60% in group 2, in 83% in group 3, and in 17% in group 4. these authors concluded that decompressive craniectomy is a useful adjunctive modality in the management of refractory intracranial hypertension in patients with poor-grade aneurysmal sah, even in the absence of extensive intraparenchymal hemorrhage. in more than half of the patients with intractable intracranial hypertension after aneurysmal sah, a good functional outcome could be achieved after decompressive craniectomy. patients with progressive brain edema but no radiological signs of infarction and those with hematoma may benefit the most; and that the indication for decompressive craniectomy should be set restrictively if secondary infarction is present. c. balan, b. alliez decompressive craniectomy 79 figure 3 a figure 3 b other indications decompressive craniectomy has also been applied occasionally in the treatment of brain hemorrhage or predominantly in single cases or small case series of meningitis, acute encephalitis, subdural empyema and cerebral venous and dural sinus thrombosis [17]. figure 3 c figure 3 d figure 3 a sah with sylvian hematoma, mca aneurysm in day 1. figure 3 b after surgery, day 2, removal of the bone flap due to edema figuri 3 c midline shift, brain herniation in day 6 when a real decompression was realized figure 3 d day 17 after sah, important brain herniation but without midline shift 80 romanian neurosurgery (2010) xvii 1: 73 80 conclusions decompressive craniectomy as a surgical treatment for brain edema has been performed for many years and for several different pathophysiologies, including tbi, sah, and ischemic stroke. the medical literature contains a wealth of information on decompressive craniectomy, especially observational series from individual centers. the role of this procedure remains unclear, however and randomized studies are expected to provide class i evidence in treating patients with refractory intracranial hypertension and brain edema. references 1. vahedi k, hofmeijer j, juettler e, et al (2007) early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. lancet neurology 6 (3): 215-22 2.skoglund, ts; eriksson-ritzen c, jensen c, rydenhag b (2006) aspects on decompressive craniectomy in patients with traumatic head injuries. journal of neurotrauma 23 (10): 1502-1059. 3.schneider, gh; bardt t, lanksch wr, unterberg a (2002). decompressive craniectomy following traumatic brain injury: icp, cpp and neurological outcome. acta neurochirurica (supplement) 81: 77-79 4.albanese j, leone m, alliez jr, alliez b, et al(2003): decompressive craniectomy for severe traumatic brain injury: evaluation of the effects at one year. crit care med 31: 2535-2538 5.kunze e, meixensberger j, janka m. et al (1998): decompressive craniectomy in patients with uncontrollable in tracranial hypertension. acta neurochir suppl 71:16-18, 1998 6.guerra wk, gaab mr, dietz h. et al: surgical decompression for traumatic brain swelling: indications and results. j neurosurg 90:187-196, 1999 7.bullock, ross.; chesnut, randall.; ghajar, jamshid et al – surgical management of acute subdural hematomas – neurosurgery suppl, vol 58, issue 3, march 2006 8.www.braintrauma.org 9.sahuquillo j, arikan f decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. cochrane database syst rev: cd003983, 2006 10.balan c, alliez jr, albanese j et al – decompressive cranientomy for severe traumatic brain lesions – results at one year in proceedings of the 13th world congress of neurological surgery, medimond, 2005 11.www.rescueicp.com 12.www.decra.org.au/ 13.fisher cm, ojemann rg. bilateral decompressive craniectomy for worsening coma in acute subarachnoid hemorrhage: observations in support of the procedure. surg neurol. 1994;41:65–74 14.smith e, carter b proposed use of dc in poor grade sah patients with large sylvian hematomas, neurosurgery july 2002 15.schirmer cm, hoit da, malek am decompressive hemicraniectomy for the treatment of intractable intracranial hypertension after aneurysmal subarachnoid hemorrhage. stroke 38: 987-992, 2007 16.buschmann u, yonekawa y, fortunati m, decompressive hemicraniectomy in patients with subarachnoid hemorrhage and intractable intracranial hypertension. acta neurochir (wien) 149:59-65, 2007 17.hutchinson p, timofeev i., kirkpatrick p.surgery for brain edema, neurosurg. focus, vol. 22, may 2007 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article orbitocranial penetrating injury by a metallic foreign body. case report and anatomical considerations dana mihaela turliuc, a.i. cucu, r.arbore-sorete, gabriela florenta dumitrescu, anca sava, claudia florida costea romania doi: 10.1515/romneu-2017-0070 romanian neurosurgery (2017) xxxi 4: 437 – 443 | 437 doi: 10.1515/romneu-2017-0070 orbitocranial penetrating injury by a metallic foreign body. case report and anatomical considerations dana mihaela turliuc1,2, a.i. cucu2, r.arbore-sorete2, gabriela florenta dumitrescu2, anca sava1,2, claudia florida costea1,2 1“grigore t. popa” university of medicine and pharmacy iasi, romania 2“prof. dr. n. oblu” emergency clinical hospital iasi, romania abstract: orbitocranial penetrating injuries (opi) represent a rare type of head injuries encountered in clinical practice. these appear after falls or motor vehicle accidents and are more frequent among children. we present the case of a male patient with opi, associated with large frontal hemorrhagic contusion, with minimal periorbital trauma findings related to brain injury. knowing and understanding the clinical anatomy of the orbit and the patterns of injuries in opi are mandatory, since failure in detecting intracranial complications may lead to the increase of the neurological morbidity, visual loss and death. key words: orbitocranial penetrating injury, orbital roof fractures, transorbital penetrating brain injury, visual acuity loss introduction orbitocranial penetrating injuries (opi) represent about 24% of penetrating head injuries in adults and 45% in children (36), and they represent a significant threat for the intracranial and ocular structures. opi occur relatively rare among adults and more frequent in children and teenagers, because they are prone to injuries while they play games in inappropriate ways (29, 37). short case report we present the case of a 38 year old male patient hospitalized at the 2nd neurosurgery clinic of “prof. dr. n. oblu” emergency clinical hospital iasi with an opi by a metallic foreign body within the context of a work accident. on admission, the patient’s gcs was 15, with headache and bradypsychia, and the local ophthalmologic exam revealed a hematoma of the upper right eyelid (figure 1. a), a wound in the upper angle and a right eyelid ptosis (figure 1. b.), with absence of the foreign metallic body because the patient has pulled it out by himself immediately after the accident. the ophthalmologic exam also concluded that the visual acuity of the right eye was no light perception. the slit lamp 438 | turliuc et al orbitocranial penetrating injury by a metallic foreign body examination of the anterior segment of the right eye showed a subconjunctival hemorrhage and corneal oedema. dilated fundus exam of the right eye revealed the absence of the red reflex and hemorrhage in the vitreous. the visual acuity of the left eye was 6/6. the slit lamp examination of the anterior and posterior segment of the left eye revealed a normal anterior and posterior segment. the head ct scan showed an orbitocranial penetrating injury (figure 2, 3) with a complex fracture in the right orbital roof and intracranial migration of the bone fragments (figure 2, 3) and right frontal contusion associated with a frontal intracerebral hemorrhage (figure 2.c-f). the ocular ultrasound (b-scan ocular ultrasound) of the right eye showed retinal detachment, vitreous hemorrhage and choroidal hematoma (figure 3. f). prognosis related to brain lesions was favorable, but with loss of the visual function in the right eye. discussion the orbit is a osseous structure shaped as a horizontal pyramid, with a quadrangular base formed by the orbital rim, and with triangular orbital walls that converge to the apex, where the superior orbital fissure (sof), inferior orbital fissure (iof) and optic canal (oc) are found (12, 36) (figure 4. b). two important anatomical characteristics make the orbit vulnerable to opi: 1. the pyramid shape which makes that penetrating objects to be directed towards the apex, and sof, iof (posterior portion) and oc (35) allowing the passage to the middle cranial fossa and 2. thin walls, which make the orbit the most vulnerable structure of the skull (3). depending on the kinetic energy, opi can be classified into two main categories, and also the kinetic energy directs the damage pattern: opi with low-velocity and opi with highvelocity. the opi severity does not depend only on this kinetic energy, but also on the size and the shape of the foreign body, its entry point, its force and trajectory (24, 29). opi with low-velocity makes the penetrating foreign bodies to be directed by the orbit’s configuration towards the apex and to cross to the cranial cavity through sof, iof or oc, injuring nerve and vascular structures, such as: cranial nerves iii, iv, v, vi, cavernous sinus, carotid artery and arteries of the willis circle (16), suprasellar cistern, brainstem or temporal lobe (1, 2, 26, 27, 33, 34, 39). for opi with low-velocity, the most frequent injury pattern encountered in 68% of cases is represented by the damage of temporal lobe, brainstem and cavernous sinus (36). in opi with low-velocity, foreign bodies usually penetrate the orbit through the medial chantus (10), and due to its shape characteristics, it offers direct access towards the cranial cavity through sof, iof and oc, even in absence of globe injury or of a significant bone fracture (4). so that in case of opi with low-velocity, intracranial brain injury may occur in presence of minimal periorbital trauma, without bone fractures. the explanation would be represented by toughness of the sclera coat and the motility of the eyeball within the surrounding bed of intraorbital fat (11, 26) that protects eyeball romanian neurosurgery (2017) xxxi 4: 437 – 443 | 439 from penetration during opi with lowvelocity (36). opi with higher-velocity usually cause fractures of the orbital walls, and their penetration in cranial cavity is directed by the trajectory of the penetrating bodies (17, 23, 30, 32). so that the foreign bodies, which are vertically directed (upward), would perforate the roof of the orbit, causing frontal lobe injury (7, 14, 18, 21), and those horizontally directed would perforate lamina papyracea of ethmoid bone or the posterior orbital wall (3, 6, 15, 23). if the high velocity is high enough, along the 45 grade angle of the lateral wall, foreign bodies can cross midline and destroy the collateral structures (11). out of all opi with higher-velocity, the most frequent are those that perforate the orbital roof and they usually appear when the patient falls into objects that are directed in an upward direction (29). in these situations, the thin superior orbital plate of the frontal bone in the anterior cranial fossa floor is fractured, causing frontal lobe injury. according to some authors, the great incidence of those opi with roof fractures is due to the instinctive tendency of humans to extend the neck backwards in a defensive position at the moment of orbital trauma (28, 32). because at the time of trauma humans avoid turning their heads, this may guide horizontally approaching objects into the medial canthus region and along the medial orbital wall (22). in our patient’s case, the foreign body penetrated the orbit at the medial canthus and followed a posterior, medial and superior trajectory through the orbital roof (figure 3. a, b, d, e) with a foreign body penetrating the frontal lobe and causing a contusion and frontal hemorrhage (figure 2). if in opi with low-velocity the ocular complications are minimal or even absent, this is not the case for opi with high-velocity, such as pellet and nail gun injuries or work accidents, in which despite the small diameter of penetrating foreign body, there is important damage done to the eye globe (2, 32, 36). the most frequent ocular complications encountered are: ocular laceration, retrobulbar hematoma, proptosis and optic nerve damage with severe loss of vision (19, 31), and in our patient’s case, despite the minor damage done to the eyelid (figure 1), the damage done to the globe was severe: eyelid ptosis, vitreous hemorrhage, retinal detachment (figure 1, figure 3. c, f), with loss of the visual function in the right eye. based on the anatomic patterns of injuries, turbin et al. (2006) has classified the ocular surface in four zones: zone 1 includes central, lateral, upper eyelid or superior conjunctival entry points; zone 2 includes central, lateral, lower eyelid, or conjunctival entry points; zone 3 includes all medial and canthal cutaneous zones of entry points, subclassified in zone a, b and c (upper, middle, lower) and zone 4, which inclu des lateral upper and lower eyelid and conjunctival lacerations (zone 1 + zone 2) (36) (figure 4). in regards to brain injury, the pathophysiology of opi with high-velocity is similar to closed head injuries, such as intracranial hemorrhage or cerebral contusion, but on the other hand, opi are prone to infections (13). in the brain, the initial event in opi with high-velocity is 440 | turliuc et al orbitocranial penetrating injury by a metallic foreign body represented by direct crushing and laceration along the tract of penetrating injury. brain swelling or bleeding due to cerebral contusion, which leads to increase of intracranial pressure, occur secondarily. most deaths by opi are due to hemorrhage or ischemia secondary to damage of blood vessels (5). immediate complications of opi are intracerebral hematoma, brain contusion, intraventricular hemorrhage, pneumocephalus, cranial nerve damage, brainstem injury and cerebrovascular injury (25, 38), while delayed complications are orbital cellulitis, endophthalmitis and retinal detachment (8, 9, 20), cerebrospinal fluid fistula, carotid-cavernous fistula, meningitis and cerebral abscesses, traumatic aneurysm and delayed intracranial hemorrhage (20). fortunately for our patient, there were no delayed complications, the neurologic prognosis being a good one, except for the visual function. the literature also considers that in absence of direct injury of brainstem and laceration of major cerebral vessels, the prognosis is overall good in opi (20). figure 1 – periorbital ecchymosis with sutured wound on the medial canthus of the right eyelid (blue arrows) (a); subconjunctival hemorrhage in the right eye and the entry point of foreign metallic body on the right medial canthus (blue arrows) (b) romanian neurosurgery (2017) xxxi 4: 437 – 443 | 441 figure 2 head ct-scan with: right orbital roof fractures (a, b); right frontal contusion and intracerebral hemorrhage (c-f) that respects the trajectory of the foreign body in intracranial cavity figure 3 – complex fracture in the right orbital roof (a, b, d, e). 3. c. vitreous hemorrhage and choroidal hematoma of the right eyeball; ocular ultrasound (b-scan) that shows retinal detachment, vitreous hemorrhage, and choroidal hematoma (f) 442 | turliuc et al orbitocranial penetrating injury by a metallic foreign body figure 4 turbin’s diagram of ocular surface applied to our patient (36) (a). to observe zone 3 for entry of foreign body; schematic diagram of ocular surface, adapted after turbin 2006 (36) (b) (dr. mihaela turliuc’s personal collection) conclusion knowing and understanding the clinical anatomy of the orbit and the patterns of injuries in opi are mandatory for an early diagnosis, as well as developing a surgical plan if needed. in this regard, modern imaging techniques, such as ct, mri and angiography, are helpful. accidents or falls, which involve foreign bodies, should raise suspicions of brain injury, even in the absence or in case of minimal ocular or neurological findings, because failure in detecting intracranial complications may lead to increase of neurological morbidity, visual loss and death. correspondence a.i. cucu “prof. dr. n. oblu” emergency clinical hospital iasi, romania e-mail: andreiucucu@yahoo.com references 1.albert d, burns w, scheie h. severe orbitocranial foreignbody injury. am j ophthalmol. 1965; 60:11091111. 2.alexandrakis g, davis jl. intracranial penetrating orbital injury. ophthalmic surg lasers. 2000; 31:61-63. 3.arslan m, eseoğlu m, güdü bo, demir i. transorbital orbitocranial penetrating injury caused by a metal bar. j neurosci rural pract. 2012; 3: 178-181. 4.bard l, jarrett w. intracranial complications of penetrating orbital injuries. arch ophthalmol. 1964; 71:332-342. 5.behera sk, panigrahi s, mishra ss et al. transorbital penetrating brain injury by a wooden stick: a neuroophthalmologic emergency. asian j neurosurg. 2016; 11:321–322. 6.bowen di. self-inflicted orbitocranial injury with a plastic ballpoint pen. br j ophthalmol. 1971; 55:427-430. 7.carver g, durham n, patterson w. transorbitocranial foreign body. surgery. 1954; 35:475-481. 8.costea cf, cucu ai, dimitriu g et al. understanding the psychological impact in a clinical case of eye globe rupture with forensic implications. romanian journal of oral rehabilitation. 2016; 8:61-65. 9.costea cf, sava a, dumitrescu gf et al. forensic aspects of ocular trauma. aperito journal of ophthalmology. 2015; 1:1-5. romanian neurosurgery (2017) xxxi 4: 437 – 443 | 443 10.davis ga, holmes ad, kulg gl. delayed presentation of transorbital intracranial pen. j clin neurosci. 2000; 7:545‑548. 11.devilliers j, sevel d. intracranial complications of transorbital stab wounds. br j ophthalmol. 1975; 59:5256. 12.dobrovat b, popescu r, nemtoi a et al. orbital trauma: from anatomy to imaging patterns a pictorial review. romanian neurosurgery. 2011; 18:525-532. 13.domenicucci m, qasho r, ciappetta p et al.surgical treatment of penetrating orbito‑cranial injuries. case report. j neurosurg sci. 1999; 43:229-234. 14.duffy gp, bhandari ys. intracranial complications following transorbital penetrating injuries. br j surg. 1969; 56:685-688. 15.dujovny m, osgood cp, maroon jc, et al. penetrating intracranial foreign bodies in children. j trauma. 1975; 15:981-986. 16.dunya im, rubin p, shore jw. penetrating orbital trauma. int ophthalmol clin. 1995; 35:25-36. 17.fanning wl, willett lr, phillips cf, et al. puncture wound of the eyelid causing brain abscess. j trauma. 1976; 16:919-920. 18.guthkelch an. apparently trivial wounds of the eyelids with intracranial damage. br med j. 1960; 5202:842-844. 19.kane n, jamjoom a, teimory a. penetrating orbitocranial injury. injury. 1991; 22:326-337. 20.kitakami a, kirikae m, kuroda k, ogawa a. transorbital-transpetrosal penetrating cerebellar injury: case report. neurol med chir (tokyo). 1999; 39:150-152. 21.kjer p. orbital and transorbital stab wounds. arch ophthalmol. 1954; 51:811-821. 22.lasky jb, epleykd,karesh jw. household objects as a cause of self-inflicted orbital apex syndrome. j trauma. 1997; 42:555-558. 23.lee j, lee j, oum b, et al. orbitocranial injury caused by wood. korean j ophthalmol. 1999; 13:128-132. 24.mackerle z, gal p. unusual penetrating head injury in children: personal experience and review of the literature. child's nerv syst. 2009; 25:909-913. 25.matsuyama t, okuchi k, nogami k, et al. transorbital penetrating injury by a chopstick: case report. neurol med chir (tokyo). 2001; 41:345-348. 26.mcclure c, gardner j. transorbital intracranial stab wounds. cleveland clin q. 1949; 16:118-125. 27.merritt rd, chisholm l, fleming af, et al. foreignbody penetration through the superior orbital fissure. arch ophthalmol. 1973; 90:67-68. 28.miller cf, brodkey js, colombi bj. the danger of intracranial wood. surg neurol. 1977; 7:95-103. 29.mzimbiri jm, li j, bajawi ma, et al. orbitocranial low-velocity penetrating injury: a personal experience, case series, review of the literature, and proposed management plan.world neurosurg. 2016; 87:26-34. 30.o’neill or, gilliland g, delashaw jb, et al. transorbital penetrating head injury with a hunting arrow: case report. surg neurol. 1994; 42:494-497 31.potapov aa, eropkin sv, kornienko vn, et al. late diagnosis and removal of a large wooden foreign body in the cranio-orbital region. j craniofac surg. 1996; 7:311314. 32.scarfo gb, mariottini a, palma l. oculocerebral perforating trauma by foreign objects: diagnosis and surgery. j neurosurg sci. 1990; 34:111-116. 33.schneider r, henderson j. registry of interesting casespenetrating orbital wound with intracranial complications. arch ophthalmol. 1952; 47:81-85. 34.siegel eb, bastek jv, mehringer cm, et al. fatal intracranial extension of an orbital umbrella stab injury. ann ophthalmol. 1983; 15:99-102. 35.smely c, orszagh m. intracranial transorbital injury by a wooden foreign body: re-evaluation of ct and mri findings. br j neurosurg. 1999; 13:206-211. 36.turbin re, maxwell dn, langer pd, et al. patterns of transorbital intracranial injury: a review and comparison of occult and non-occult cases. surv ophthalmol. 2006; 51:449-460. 37.turliuc dm, costan vv, cucu ai, costea cf. intraorbital foreign body. rev med chir soc med nat iasi. 2015; 119:179-184. 38.yamashita t, mikami t, baba t, et al.transorbital intracranial penetrating injury from impaling on an earpick. j neuro-ophthalmol. 2007; 27:48-49. 39.zentner j, hassler w, petersen d. a wooden foreign body penetrating the superior orbital fissure. neurochirurgia (stuttg). 1991; 34:188-190. romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article epidemiological study of insular glioma – an institutional experience kumar praveen, aggrawal manish, sinha virendra deo, bhandari anu india doi: 10.1515/romneu-2017-0014 90 | praveen et al epidemiological study of insular glioma             doi: 10.1515/romneu-2017-0014 epidemiological study of insular glioma – an institutional experience kumar praveen1, aggrawal manish2, sinha virendra deo3, bhandari anu4 1resident in neurosurgery, sms medical college and hospitals jaipur, india 2professor in neurosurgery, sms medical college and hospitals jaipur, india 3professor and head of department, department of neurosurgery, sms medical college and hospitals jaipur, india 4professor department of radiology j. k. lone hospital jaipur, india abstract: object: insular gliomas are difficult and challenging tumors to operate and manage due to the inherent complexity and the adjacent vital structures around them. our aim is to define the morbidity profile and the mortality associated with the maximum possible safe resection of these less common tumors. methods: the study was conducted on patients who were diagnosed as insular gliomas on mri. all grades of patients treated by microsurgical techniques at our center from 2010 to 2016 were included in the study. results: median age at diagnosis was 39.52 years, mean kps score was 92.male patients constituted 23 of all patients.68% patients had right sided tumors.who grade 2 was most common grade and constituted 64% of all cases.one patient developed expressive aphasia and five patients developed hemiparesis .there was one mortality due to unrelated causes. conclusion: with the use of meticulous microneurosurgical technique, safe yet aggressive resection of the insular gliomas can be accomplished with comparable morbidity and mortality rates even when the modern neurosurgical tool such as intraoperative neuromonitoring and neuronavigation systems are unavailable. key words: insular glioma, microneurosurgery, intraoperative neuronavigation introduction insular gliomas are difficult and challenging tumors to operate and manage due to the inherent complexity of the insular region and the adjacent vital structures around them. although it constitutes a small region of cerebral cortex i.e. less than 2% but it is very important functionally and anatomically. it is involved in various important functions like speech production, pain perception, processing of social emotions like anger, fear, disgust, joy and romanian neurosurgery (2017) xxxi 1: 90 – 96 | 91             sadness. its most anterior part considered as part of the limbic system. the clinical presentation of insular gliomas is somewhat associated with the grade. epilepsy was the presenting symptom in 58% of cases without neurological deficit in low grade insular gliomas [duffau et al., 2005] (3). on the other hand, high grade gliomas (hggs) frequently cause surrounding vasogenic edema with adjacent tissue infiltration, resulting in local and hemispheric mass effect and sensorimotor and/or language deficits.insular region gliomas have long been considered as difficult and challenging cases to be operated upon.this was due to the reason that these tumor arises in the region which has eloquent areas and microvasculature which supplies the important language and motor areas. with all these concerning issues it is difficult to decide the most appropriate treatment for lgg and hgg arising in the insular region. insular gliomas are not rare and importantly most of these are low grade gliomas as reported in the previous epidemiological study by duffau and capelle, (3) these lesions accounted for 25% of all lgg and 10% of all hgg. as insular gliomas have an inherent tendency to be low grade because of which most of the patients having these tumors have a prolonged and slowly progressive clinical course. based upon these observations we will study the various epidemiological factors associated with these tumors and to define the morbidity profile associated with the aggressive resection of these neoplasms. in this study we will assess the morbidity and mortality associated with the insular gliomas surgery without using the modern neuronavigation and intraoperative neuromonitoring system which is not available at all neurosurgical centres in the devolping countries. methods the study was conducted in the department of neurosurgery s.m.s. medical college&hospital, jaipur, india. all the insular glioma cases (age >18 years) operated and managed from january 2010 to february 2016 were included in the study. histopathological tumor grading was done according to the who guidelines.patient with multifocal lesions were excluded from study. the clinical data was collected from the patient records. ethical committee of s.m.s. medical college, jaipur approved the study. technique patient was positioned with a rest pad under the ipsilateral shoulder with the head turned 60 degree contralaterally, which allows the frontal and temporal lobes to separate so that the sylvian fissure can be exposed easily without applying the retraction. this position provides a better orientation and exposure of the posterior insular lobule, which is hidden by both the preand postcentral gyri [hentschel & lang, 2005] (16). all cases were operated by standard microsurgical technique under general anaesthesia. awake craniotomy (for speech centre localization) was not done in any of the patients. intraoperative neuromonitoring or the neuronavigation system was not used. frontotemporal craniotomy was planned in standard fashion to include the whole perisylvian area from the pars orbitalis of the inferior frontal gyrus to the postcentral sulcus which is the widest sulcus opening in to the sylvian fissure and 92 | praveen et al epidemiological study of insular glioma             which limits the posterosuperior corner of the insula followed by the meticulous microsurgical dissection taking care of the vascular anatomy as avulsion of the short branches of the mca may injure the parent vessel with serious consequences. the long perforators, supplying the corona radiata, must be saved during surgery to avoid ischemic injury of the white matter (lang et al., 2001) (4). in the area of the limen insulae, the lenticulostriate arteries originates commonly from the medial or superior aspect of the mca, five mm or less around its bifurcation, their injury could lead to ischemic damage of the internal capsule and hence needs to be protected during the tumor dissection. gross total removal of the tumor was done and tumor tissue was sent for histopathological examination. patient outcome measurement patient was assessed and neurological examination was done in peri-operative period. later, the patient was assessed at 1 week and at 4 week interval for any residual neurological deficit or improvement in any postoperative neurological deficit. results patients’ demographics the study population included a total of 25 patients, in which 23 were men and 2 were women, with mean age of 39.5 years (range 2164 years) as illustrated in (table 1). out of 25 patients 23 patients (92%) were male and 2 patients (8%) were females. most common presentation was headache in 18 (68%) patients followed by seizure of recent onset in 64% patients. none of our patient has any sensory and language deficit. right sided insular gliomas were seen in 17 (68%) patients whereas 8 (32%) patients had left sided tumors. the most common histologic grade of the tumor was who grade 2 in 16 patients (64%) followed by who grade 3 in 8cases (32 %) while who grade 4 was found only in 4 cases (4%). there was no who grade 1 tumor patients in our series. kps score of the patients ranged from 30 to 100 with a mean score of 92. table 1 summary of patient, disease and treatment characteristics parameters number(%) age at diagnosis (yrs) median 39.52 range 21-64 sex male 23(92%) female 2(8%) kps score (at diagnosis) median 92 range 30-100 symptoms at presentation seizure 16(64%) sensory 0 headache 18(68%) language deficit 0 incidental 0 side of tumor rt 17(68%) lt 8(32%) who tumor grade grade ii 16(64%) grade iii 8(32%) grade iv 1(4%) romanian neurosurgery (2017) xxxi 1: 90 – 96 | 93             piechart: sex distribution of insular glioma bar diagram: showing symptoms of insular glioma pie chart: showing location of gliomas histogram: showing grades of insular glioma chart: showing outcome of patients with insular glioma morbidity profile we assessed the patients at four weeks and found that one patient (4%) developed expressive aphasia (table 2) which did not improve after four weeks. none of the patients developed motor aphasia. five of our patients (20%) developed hemiparesis. out of these two patients had total functional recovery, one patient had partial recovery while two patients had no recovery in a four week follow up. there was no incidence of facial hemiparesis, hand weakness or new sensory deficits in the postoperative follow up in any patients. mean kps score at presentation was 92 and the postoperative mean kps score was also 92. there was one mortality and patient died on 18 postop day due to unrelated causes. there is no intraoperative death in our series. discussion insular gliomas are the brain tumors which arise from the glial cells in the insular region. the island of reel (insula) is composed of anterior and posterior lobule divided by a central sulcus. it is a hidden lobe situated in the depth of sylvian fissure. it is 94 | praveen et al epidemiological study of insular glioma             pyramid shaped and its perimeter is defined by anterior, inferior and superior peri insular sulci. the limen insulae represents the medial limit of insula .it is a white matter structure which lies between the anterior perforated substance and the insular pole along the sylvian stem, and lies parallel to the lateral olfactory striae (true et al. ,1999) (12). deep to the central portion of the insula, in a lateralto-medial direction, lies the external capsule, claustrum, external capsule and putamen with its subjacent globus pallidus. insular gliomas are heterogenous in nature because of the variations in the histological grading, involved genetic factors and tumor locations (sanai et al) (1). surgical treatment of glial tumours arising in the insula is specially challenging due to its proximity to the internal capsule. (v. vanaclocha et al) (17, 18). surgical management of these tumors is recommended to improve the patient survival and increase the recurrence-free period [duffau et al., 2009; sanai et al., 2010] (1, 2). since the first report by (yasargil et al., 1992) (12), few authors have dealt with the surgical treatment of tumours infiltrating the insula [duffau et al., 2005; hentschel & lang, 2005; lang et al., 2001; sanai et al., 2010; zentner et al., 1996] (1, 3, 13, 16, 17). the blood supply of the insula is derived from the second (m2) segment of the middle cerebral artery (mca) through its short and medium sized perforating branches. long perforators overlying the posterior lobule are larger in diameter and may supply the corona radiata, particularly, the corticospinal tract fibres and thalamocortical fibers [hentschel&lang, 2005] (16). in the present study the incidences of insular gliomas in males were 92% and in females it was 8% whereas in previous study by sanai et al (1) male and female incidence was 42% and 62% respectively. most common symptoms of presentation in the previous study by sanai et al1 was seizure in 72.1%, sensory deficit in12.5%, headache in 6.7%, language deficit in 4.8% and incidental in3.8%. duffau et al (2) had seizure as most common presentation in 98% patients but in our series most common symptom was headache in (68%) followed by seizure (64%), none of our patient had language deficit, sensory disturbance or incidental presentation. left side of tumor was more common (55.7%) as compared to rt. side tumors (44.3%) in the study by sanai et al (1), whereas in our study right side tumor was more common and involved 17 patients (68%) and left side tumor was seen in 8 patients (32%). in our study 23 patients (92%) were male and 2 patients (8%) were females whereas in the previous study by sanai et al (1) female patients constituted 59.6% and male patients constituted 40.4%. in our study who grade 2 was most common and constituted 64% grade 3 32% and grade 4 4% patients whereas in series published by sanai et al (1) also, who grade 2 tumor was most common and constituted 60.1%, grade 3 30.4% and grade 4 8.7% patients. karnofsky performance scale score of the patients ranged from 30 to 100 and mean kps score was 92 whereas in sanai et al (1) study the mean kps score was 84. in the postop period one patient (4%) developed motor aphasia and five patients (20%) developed romanian neurosurgery (2017) xxxi 1: 90 – 96 | 95             hemiparesis. none of the patient developed new sensory deficit, hand weakness or facial droop. mean kps score at presentation was 92 and in the postoperative follow up also it was 92 at four weeks. there was one postoperative death in our series which was unrelated to the primary disease. important predictors of outcome in insular glioma surgery were who grade of the tumor, age of the patient and karnofsky performance scale score at the time of surgery. inspite of the fact that we have operated all our cases under ga and we have not used awake craniotomy (for speech centre localization), intraoperative neuromonotoring, neuronavigation system our morbidity profiles are comparable to the previous published series. although it is true that we can significantly increase the safe extent of resection with the use of above mentioned diagnostic tools and these should be used whenever these are available. but our small volume yet significant study has provided us encouraging results that similar results in terms of morbidity and mortality are achievable with the use of meticulous microneurosurgical technique. conclusion insular glioma surgery is challenging surgery due to its peculiar anatomical characteristics and carries substantial morbidity and complications. better knowledge and understanding of locoregional anatomy and insular pathophysiology has helped us a lot in decreasing the morbidity and mortality associated with these tumors. although our series is a small series of 25 cases but inspite of not using the neuromonitoring and neuronavigation system the postoperative morbidity profiles are comparable to the previous publications. however this does not negate the fact that better results and outcome is achievable with modern neuro-navigation and neuromonitoring support and their use should be encouraged to promote better patient care. correspondence dr. praveen kumar sms medical college and hospitals jaipur, india +917727834376 praveenthkr30 @gmail.com references 1.insular glioma resection: assessment of patient morbidity, survival, and tumor progression nader sanai, m.d., mei-yin polley, ph.d mitchel s. berger, m.d j neurosurg 112:1–9, 2010. 2. duffau h: a personal consecutive series of surgically treated 51 casesof insular who grade ii glioma: advances and limitations j neurosurg 110:696-708,2009 3. duffau, h.; taillandier, l.; gatignol, p. & capelle, l. (2005). the insular lobe and brain plasticity: lessons from tumor surgery. clinical neurology and neurosurgery,vol.108, no.6, (september 2005), pp.543548 4.lang ff, olansen ne, demonte f, gokaslan zl, holland ec,kalhorn c, et al: surgical resection of intrinsic insular tumors: complication avoidance. j neurosurg 95:638–650, 2001 5.mehrkens jh, kreth fw, muacevic a, ostertag cb: long term course of who grade ii astrocytomas of the insula of reil after i-125 interstitial irradiation. j neurol 251:1455– 1464, 2004 7.moshel ya, marcus jds, parker ec, kelly pj: resection of insular gliomas: the importance of lenticulostriate artery position.j neurosurg 109:825–834, 2008 8.sanai n, berger ms: glioma extent of resection and its impact on patient outcome. neurosurgery 62:753–756, 2008 96 | praveen et al epidemiological study of insular glioma             9.schramm j, aliashkevich af: surgery for temporal mediobasal tumors: experience based on a series of 235 patients. neurosurgery 60:285–295, 2007 10. simon m, neuloh g, von lehe m, meyer b, schramm j: insular gliomas: the case for surgical management. j neurosurg 110:685–695, 2009 11.tanriover n, rhoton al jr, kawashima m, ulm aj, yasuda a: microsurgical anatomy of the insula and the sylvian fissure. j neurosurg 100:891–922, 2004 12.türe u, yaşargil dc, al-mefty o, yaşargil mg: topographic anatomy of the insular region. j neurosurg 90:720–733, 1999 13. zentner, j.; meyer, b.; stangl, a. & schramm, j. (1996). intrinsic tumors of the insula: a prospective surgical study of 30 patients. journal of neurosurgery, vol.85, no.2,(august 1996), pp.263-271 14.yasargil, mg.; von ammon, k.; cavazos, e.; doczi, t.; reeves, jd. & roth, p. (1992). tumors of the limbic and paralimbic systems. acta neurochirurgica, vol.116, no.2-4, (march1992), pp.147-149 15.signorelli, f.; guyotat, j; elisevich, k. & barbagallo, gm. (2009). review of current microsurgical management of insular gliomas. acta neurochirurgica, vol.152, no.1,(january 2010), pp.19-26, 16.hentschel, sj. & lang, ff. (2005). surgical resection of intrinsic insular tumors. neurosurgery, vol.57, no.1, (july 2005), pp.176-183 17. surgical treatment of insular gliomas.vanaclocha v1, sáiz-sapena n, garcía-casasola c. acta neurochir (wien). 1997;139(12):1126-34 18. technical nuances for surgery of insular gliomas: lessons learned. rey-dios r1, cohen-gadol aa. neurosurg focus. 2013 feb;34(2):e6 romanian neurosurgery | volume xxxi | number 1 | 2017 | january march article unusual aggressive and rapidly growing glioblastoma multiforme – case presentation m. dabija, l. eva, i. poeata, alina paiu, v. dorobat, raluca munteanu romania doi: 10.1515/romneu-2017-0006 romanian neurosurgery (2017) xxxi 1: 41 – 46 | 41             doi: 10.1515/romneu-2017-0006 unusual aggressive and rapidly growing glioblastoma multiforme – case presentation m. dabija1,2, l. eva2,3, i. poeata1,2, alina paiu4, v. dorobat4, raluca munteanu2 1“grigore.t.popa ‘’ university of medicine and pharmacy iasi, romania 2neurosurgery, emergency clinical hospital ‘’prof. dr. n. oblu’’ hospital, iasi, romania 3“apollonia’’ university, iasi, romania 4resident of neurosurgery, emergency clinical hospital, “prof. dr. n. oblu”, iasi, romania abstract: glioblastoma multiform is one of the most rapidly progressing cerebral tumors and the most aggressive one in our neurosurgical experience. we present the case of a 45 year old patient with very aggressive type of tumor who had come to our service for the following: intense headache, confusion, right hemiparesis installed approximately one month before. irm scan shows up the presence of a large tumoral mass without a precise border in the left temporal-parietal region which had extended all the way down to the thalamus. the planned intervention used 5-aminolevulinic acid (5-ala) for the precise removal of the tumor mass, suboptimal because of the risk of lesioning the motor tracts – indicated by the intraoperative electrophysiological monitoring. after surgery the outcome was good with the partial regression of the motor deficit, but only after 3 weeks due to the unexpected tumor growth the neurological status started to decay and even worsened. the patient underwent surgery again with the partial remission of the symptoms although following imagistic controls showed up fast tumor growth once more. he was recommended to oncology service for the beginning of radiotherapy. we consider the evolution and invasion of this tumor in only a 3 weeks period being impressive. key words: glioblastoma multiform, 5-aminolevulinic acid (5-ala), recurrent disease, re-operation background glioblastoma multiforme is one of the most rapidly growing cerebral tumors and the most aggressive one in our neurosurgical experience. it is a glial cell tumor, a glioma and it originates in the support cells of the brain – glial cells or in their precursors. unfortunately, it is the most common primary brain tumor occurring during adulthood (20%), and the most frequent glial cell tumor – 51% of all gliomas (1). the confirmation of a glioblastoma by histological diagnosis is a 42 | dabija et al aggressive and rapidly growing glioblastoma multiforme             devastating condition, and it certainly represents a turn point in our patients’ journey. american brain association indicates an average survival rate of 14 months, less than 10% of all the patients managing to survive more than 5 years with all the current available therapeutic methods (2). we can tell without a doubt, it’s quite aggressive, for example, one of the worst and well known tumors for their high malignancy rate –the small cell lung carcinoma – has a median survival rate of 20 months and 20% of the patients are still alive after 5 years (3). the term of multiforme suggests that gbm are complex tumors with various aspects in grossly, microscopy and in various types of imaging methods, with complex clinical manifestations, complex genetic patterns, and, of course, various growing behavior. the current standard treatment include a radical surgical resection followed by radio and chemotherapy. the important thing for us as surgeons and what matters above all else is what we can surgically do to improve the patient’s survival rate and his quality of life. there are many studies that emphasized the importance of the gross total resection (gtr) in the treatment of these aggressive tumors. gtr may be considered as a valuable independent prognostic factor for our patients survival, and a gtr of 98% or more of the tumor volume, as it can be appreciated on mri enhanced images, is considered mandatory for a better evolution and prognosis (4, 5, 6). other important prognostic factors are patient age and performance status (7). despite improved surgical techniques, therapies and radiotherapies, prognosis for this type of pathology remains very poor: most patients die within 12–18 months from diagnosis (8). in order to improve the extent of the resection we use 5-aminolevulinic acid (5ala)-induced fluorescence to guide our procedure and, of course, the intraoperative neuromonitoring for the safety of our resection. case presentation we present a 45 year-old man which was admitted in december 2016 to the emergency clinical hospital “prof. dr. n oblu’’, iasi; for about a month he had been suffering from intense headache, confusion, and loss of strength of the right arm and leg. a ct and mri scan showed the presence of a tumor in the temporal-parietal region of the left hemisphere with thalamic extension (figure 1) we performed a tumor excision using 5aminolevulinic acid (5-ala), and electrophysiological monitoring of the motor cortex and tracts with favorable outcome after surgery and progressive remission of the previously installed motor deficit. he attended neuromotor rehabilitation treatment. the resection was less than desired -subtotal because of the mep-s which indicates the vicinity of the motor tracts. after 3 weeks from the procedure, before attending any oncological complementary treatment, he came to the emergency department of our hospital with motor aphasia, right hemiplegia and sleepiness which had occurred 3 days before. ct scan with contrast shows up unexpected large tumor growth and invasion and hydrocephalus due to the monro and sylvius aqueduct compression (figure 3). the patient was reoperated on the next day. postoperative evolution was favorable with partial remission of the motor deficit and aphasia, and the patient was addressed to the oncological department in 2 weeks for radiotherapy and temozolomide treatment. romanian neurosurgery (2017) xxxi 1: 41 – 46 | 43             figure 1 a) ct scanaxial section b) mri scan axial and coronal sectionsimage preoperative – glioblastoma involving the left thalamus figure 2 enhanced ct scan first day after surgery – small tumoral remnant in thalamus [1] 44 | dabija et al aggressive and rapidly growing glioblastoma multiforme             figure 3 ct with ivc showing the large, precocious, invasive tumor evolution figure 4 mri post-op [2] romanian neurosurgery (2017) xxxi 1: 41 – 46 | 45             figure 5 ct post radiotherapy simulation discussion the aggressively character of glioblastomas was described for the first time since 1926, when bailey and cushing described some unusual rapidly growing forms of astrocytic tumors (9). there are many studies now which emphasize the importance of molecular and genetic abnormalities in the behavior of a particular type of glioblastoma. even some gbm may be histologically identical, they are molecularly distinct, and this individuality influence their evolution, but, of course, may require a specific tailored treatment (10). we believe that our patient had one of this very aggressive type of tumor, the evolution and invasion in only a 3 weeks period being impressive. the use of substances like 5aminolevulinic acid hydrochloride (11), which mark and thus make tumoral tissue easier to identify during an operation, have improved surgery for cerebral gliomas; in fact they allow for a more thorough excision (12), but increased the risk for postoperative complications like neurological deficit, so the using of intraoperative neuromonitoring is mandatory in order to decrease this potential risk. we experienced that in our case, finally we were not able to resect all the amount of tumor revealed by 5-ala intraoperative visualization because of the electric imperative risk signs for motor deficit. in fact the initial motor deficit increased after the surgery but with good recovery, that may indicate the value of the electrophysiology in stopping us in time, but also it indicates that the use of the 5ala may be risky in the absence of experience and carefully monitoring. repeat surgery may play a role in debulking the tumor, providing symptom relief, and differentiating tumor recurrence from pseudo-progression or radiation necrosis (grade of recommendation: b). however, before surgical intervention, it is essential to clearly define treatment goals and the effect on prognosis and quality of life for the patient (13). studies have shown that gbm recurrence most often occurs in the form of a local continuous growth within 2 to 3 cm from the border of the original lesion. choucair, et al. reported that more than 90% of patients with glioma showed recurrence at the original tumor location and that multiple lesions 46 | dabija et al aggressive and rapidly growing glioblastoma multiforme             developed in 5% after treatment (14). we emphasize the importance of performing oncology treatment. an important part of a high-grade glioma treatment is radiotherapy. in typical situations, patients begin radiation treatments within 2 to 4 weeks after tumor resection (15). our patient has not started radiotherapy after the first intervention, which probably caused tumor growth. conclusion unfortunately, despite all intensive studies, surgical and oncological advances, gbm remains the cerebral tumors with the worst prognosis. between these bad tumors, there are some cases with even quicker evolution and extensive invasion. what make them behave like is a subject for many molecular and genetic studies. the use of 5-ala and intraoperative neuromonitoring may help the extension of a safety resection. the precocity of radio-chemotherapy treatment is mandatory, especially in aggressive cases. correspondence dabija marius e-mail: mariusdabija.md@gmail.com references 1.adamson, c., kanu, o. o., mehta, a. i., di, c., lin, n., mattox, a. k., et al. (2009). glioblastoma multiforme: a review of where we have been and where we are going. expert opinion on investigational drugs, 18(8), 10611083 2.american brain tumor association. retrieved from www.abta.org 3.comprehensive cancer information-national cancer institute. retrieved from www.cancer.gov 4.eljamel, m.s. brain photodiagnosis (pd), fluorescence guided resection (fgr) and photodynamic therapy (pdt): past, present and future. photodiagn. photodyn. ther. 2008, 5, 29–35. 5.eljamel, s. photodynamic applications in brain tumors: a comprehensive review of the literature. photodiagn. photodyn. ther. 2010, 7, 76–85. 6.della puppa, a.; ciccarino, p.; lombardi, g.; rolma, g.; cecchin, d.; rossetto, m. 5-aminolevulinic acid fluorescence in high grade glioma surgery: surgical outcome, intraoperative findings, and fluorescence patterns. biomed. res. int. 2014, 2014, 232561. 7.felicity v, connon, mark a., rosentha, katherine drummond.,2015, glioblastoma multiforme in the very elderly, neurosurgery rev 8.a.m. stark, j. van de bergh, j. hedderich, h.m. mehdorn, nabavi a. glioblastoma clinical characteristics, prognostic factors and survival in 492 patients 9.bailey p, cushing h, a classification of the tumors of the glioma group on a histo-genetic basis with a correlated study of prognosis, philadelphia: j b lippincott co. (1926). 10.louis d n, holland e c, cairncross j g et al.,”glioma classification: a molecular reappraisal”, am. j. pathol. (2001);159 (3): pp. 779-786. 11.w. stummer, u. pichlmeier, t. meinel, o.d. wiestler, f. zanella, h.j. reulen, fluorescence-guided surgery with 5-aminolevulinic acid for resection of malignant glioma: a randomised controlled multicentre phase iii trial, lancet oncology, 7 (5) (2006), pp. 392–401 12. riccardo caruso, alessandro pesce, venceslao wierzbicki, a very rare case report of long-term survival: a patient operated on in 1994 of glioblastoma multiforme and currently in perfect health, international journal of surgery case reports, available online 20 february 2017 13. j.c. easaw md phd, w.p. mason md, j. perry md, n. laperrière md, d.d. eisenstat md ma, r. del maestro md phd, k. bélanger md, d. fulton md, and d. macdonald md, canadian recommendations for the treatment of recurrent or progressive glioblastoma, multiforme, 2011, current oncology—volume 18, number 3. 14.lewis c. hou, m.d., anand veeravagu, b.s., andrew r. hsu, b.s., and victor c. k. tse, m.d., ph.d., recurrent glioblastoma multiforme: a review of natural history and management options, journal of neurosurgery, apr, 2006 15.john w. henson, m.d, glioblastoma multiforme and anaplastic gliomas: a patient guide, mgh brain tumor center, from: https://brain.mgh.harvard.edu/patientguide.html   9regesv_isolated romanian neurosurgery | volume xxx | number 4 | 2016 | october december article isolated traumatic intraventricular hemorrhage in adult with good prognosis s.v. rege, harshad patil india doi: 10.1515/romneu-2016-0081 512 | rege, patil isolated traumatic intraventricular hemorrhage in adult with good prognosis doi: 10.1515/romneu-2016-0081 isolated traumatic intraventricular hemorrhage in adult with good prognosis s.v. rege1, harshad patil2 department of neurosurgery, sri aurobindo medical college and pg institute, indore, madhya pradesh, india 1professor& head of department; 2senior resident abstract: isolated intraventricular hemorrhage of traumatic origin (tivh) is a rare finding. mostly found in paediatric age group and rarely reported in adults. intraventricular hemorrhage is associated with poor outcome. despite of this, our patient recovered well. we have herein presented a rare case of isolated tivh in an adult. key words: traumatic intraventricular hemorrhage, severe head injury, adult introduction traumatic intraventricular hemorrhage (tivh) is usually associated with other lesions such as intracerebral contusion or hemorrhage, subarachnoid hemorrhage, and diffuse brain edema. the presence of ivh indicates that a severe force has been applied to the head and generally is a sign of severe head injury and has a poor prognosis. the incidence of ivh in nonpenetrating head injury is 1.5 to 3% and 10 to 25% of patients with severe head injury (gcs less than 8). (1) isolated traumatic intraventricular hemorrhage (tivh) is a rare finding. it commonly found in paediatric population but rarely reported in adults. herein author reported a rare case of isolated tivh in adult. case report a 60 years old male admitted in neurosurgery department after road traffic accident. he had history of loss of consciousness for 30 minutes with vomiting 2 episodes. at the time of admission his glasgow coma score (gcs) was e2 m4 v2 and his pupis were miotic and sluggishly reacting to light. there was no neurological deficit. on the day of admission patient developed seizure. patient was intubated, antiedema and anticonvulsant drugs were started. computed tomography (ct) on admission showed an isolated hemorrhage in the lateral ventricles and third ventricle without hydrocephalus (figure 1). ct angiography was performed in order to rule out any vascular pathology. there were no vascular or tumoral lesion was found (figure 2). romanian neurosurgery (2016) xxx 4: 512 – 516 | 513 the follow-up ct scans showed a progressive improvement of the tivh (figure 3) and ten days after his admission, patient was extubated and returned to the ward. the patient was discharged from the hospital three weeks after his admission with gcs of 15. figure 1 ct brain showing an isolated hemorrhage in the lateral ventricles and third ventricle without hydrocephalus 514 | rege, patil isolated traumatic intraventricular hemorrhage in adult with good prognosis figure 2 normal ct angiogram romanian neurosurgery (2016) xxx 4: 512 – 516 | 515 figure 3 follow up ct scan showing resolution of bleed discussion isolated tivh is extremely rare, and its outcome is unclear. the prevalence of tivh ranges from 0.4 to 4% in all head trauma patients who undergo ct scanning. (1) the presence of ivh indicates that a severe force has been applied to the head and generally is a sign of severe head injury. in evaluating intraventricular hemorrhage other causes such as hypertensive intracerebral hemorrhage extending to the ventricles, rupture of the intracranial aneurysms, and vascular malformation, systemic bleeding tendencies and neonatal germinal matrix hemorrhage should be considered and differentiated from pure traumatic ivh. in the absence of intraparenchymal hemorrhage ivh is most often caused by tearing of the subependymal veins in the fornix, septum pellucidum or choroid plexus found in autopsy studies. (2, 3) in our patient there were no co-morbid conditions presents so the probable cause of isolated tivh may be due to tearing of the subependymal veins. due to deficient fibrinolysis and hemolysis of csf the spontaneous resolution of ivh is very slow. current treatment modalities include external ventricular drainage and more recently the controversial administration of fibrinolytics such as tissue plasminogen activators. although both treatments can expedite the clearance of ivh but no conclusion can be drawn from the effect on clinical outcome. (4) seizures are well known complications of any kind of intracranial lesions including tivh. antiepileptic medications should be started because an epileptic fit might cause the deterioration of the patient. prophylaxis is also used in trauma patients who have hemorrhagic lesions because of the irritating effect of the blood. (5) atzema et al. reviewed 8,374 patients with blunt head trauma and the prevalence of tivh was 1.41% among all trauma patients. in this study among tivh patients, 70% had a "poor outcome" and 76% had a "combined outcome." the authors concluded that the prognosis of tivh was determined by associated brain injuries, rather than by the tivh itself. (1) lee jp et al studied 25 patients of acute post-traumatic intraventricular hemorrhage (ivh) after closed head injury. in this series 6 patients were of isolated tivh and auther found good outcome in isolated tivh. (6) is m. et al reported isolated tivh in paediatric patient with good prognosis. (7) we reported isolated tivh in adult with good outcome. the exact cause of poor prognosis in these patients is not known. it can be due to the presence of blood in the ventricle, due to 516 | rege, patil isolated traumatic intraventricular hemorrhage in adult with good prognosis induced hydrocephalus or increased intracranial pressure. (8) in our patient antiepileptic and antiedema drugs were given and our patient recovered well. conclusion isolated tivh is extremely rare and its outcome is unclear. although our patient was admitted with a low gcs, he had a good clinical outcome without requiring any surgical intervention. therefore the motto of treatment in such patients is “one should treat the patient not the radiological investigations”. correspondence dr. harshad patil address: department of neurosurgery, sri aurobindo medical college and pg institute, indore, madhya pradesh, india email: dr.harshadpatil@gmail.com phone: +919893894242 references 1.atzema c, mower wr, hoffman jr, holmes jf, killian aj, wolfson ab: national emergency x-radiography utilization study (nexus) ii group: prevalence and prognosis of traumatic intraventricular hemorrhage in patients with blunt head trauma. j trauma 60: 1010-1017, 2006 2.karavelis a, sirmos c: primary post-traumatic intraventricular hemorrhage. j neurosurg sci 39: 253256, 1995. 3.hashimoto t, nakamura n, ke r, ra f. [traumatic intraventricular hemorrhage in severe head injury]. no shinkei geka. 1992 mar;20(3):209-15. 4.machdonald, r louch md. phd: thrombolysis for intraventricular hemorrhage. neurosurgery quarterly 15 (4): 211-222, dec 2005. 5.brain trauma foundation: guidelines for the management of severe traumatic brain injury 3rd edn. journal of neurotrauma 24 (suppl 1):s1-s106, 2007 6.lee jp, lui tn, chang cn. acute post-traumatic intraventricular hemorrhage analysis of 25 patients with emphasis on final outcome. acta neurol scand. 1991 aug;84(2):85-90. 7.is m, gezen f, akgul m, dosoglu m. traumatic intraventricular hemorrhage with a good prognosis. turk neurosurg. 2011 jan;21(1):107-9. 8.leroux pd, haglund mm, newell dw, grady ms, winn hr: intraventricular hemorrhage in blunt head trauma: an analysis of 43 cases. neurosurgery 31(4): 67884; discussion 684-5, oct 1992. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article preoperative mapping of the eloquent cortical areas using navigated transcranial magnetic stimulation combined with intraoperative neuronavigation for intracerebral lesions g. petrescu, cristina gorgan, a. giovani, f.m. brehar, r.m. gorgan romania doi: 10.2478/romneu-2018-0002 16 | petrescu et al mapping the cortical areas using navigated transcranial magnetic stimulation doi: 10.2478/romneu-2018-0002 preoperative mapping of the eloquent cortical areas using navigated transcranial magnetic stimulation combined with intraoperative neuronavigation for intracerebral lesions g. petrescu1,2, cristina gorgan3, a. giovani1, f.m. brehar1,4, r.m. gorgan1,4 1neurosurgery department, “bagdasar-arseni” emergency hospital, bucharest, romania 2phd student, “carol davila” university of medicine and pharmacy, romania 3neurology department, “bagdasar-arseni” emergency hospital, bucharest, romania 4neurosurgery department, “carol davila” university of medicine and pharmacy, romania abstract: introduction: maximal surgical resection with the preservation of cortical functions is the treatment of choice for brain tumors. achieving these objectives is especially difficult when the tumor is located in an eloquent area. navigated transcranial magnetic stimulation (ntms) is a modern non-invasive, preoperative method for defining motor and speech eloquent areas. material and methods: patients with tumors located in motor and speech eloquent areas who presented at our institution between march 2017 and december 2017 were prospectively included. exclusion criteria were frequent generalized epileptic seizures and cranial implants. for lesions involving motor eloquent areas we performed a ntms motor mapping and for lesions involving speech eloquent areas we supplemented the motor mapping with speech and language mapping. mr images were exported from the ntms system in a dicom format and then loaded in the intraoperative neuronavigation system. based on these findings, the optimal entry point and trajectory were determined, in order to achieve a maximum surgical resection of the lesion, while avoiding new postoperative neurological deficits. results: nineteen patients underwent an ntms brain mapping procedure between march 2017 and december 2017. in all cases a motor mapping procedure was done, but only in eight cases a speech mapping was also performed. three patients presented new minor postoperatory deficits that consecutively remitted. the rest of the patients presented no added neurological deficits after surgery. in five cases the preexistent deficit was ameliorated after surgery and in three cases the deficit remitted. in one patient there was no improvement in the neurologic deficit after surgery. conclusion: ntms is a reliable romanian neurosurgery (2018) xxxii 1: 16 24 | 17 tool for the preoperative planning of eloquent area lesions. it must be taken into account that functional areas have a high individual variability. therefore, knowing preoperatively the extent of the eloquent area helps the neurosurgeon adapt the surgical approach in order to obtain a better functional outcome. key words: navigated transcranial magnetic stimulation, preoperative mapping, neuronavigation, eloquent areas, intracerebral lesions introduction maximal surgical resection with the preservation of cortical functions is the treatment of choice for brain tumors (1–3). achieving these objectives is especially difficult when the tumor is located in an eloquent area (i.e. precentral gyrus, postcentral gyrus, broca’s area, wernicke’s area). numerous methods have been used in order to determine preoperative and/or intraoperative the eloquent areas. navigated transcranial magnetic stimulation (ntms) is a modern non-invasive, preoperative method for defining motor and speech eloquent areas (4,5). this method integrates a frameless neuronavigation system and a tms coil that delivers a precise focal electrical field at the level of the cortex. this article describes our experience with ntms brain mapping and reviews the advantages and common pitfalls of this method. material and methods patients patients with tumors located in motor and speech eloquent areas who presented at our institution between march 2017 and december 2017 were prospectively included. exclusion criteria were frequent generalized epileptic seizures and cranial implants. a thorough neurologic examination was performed preand post-operatory for each patient. brain mapping procedure the brain mapping procedure was performed using a nexstim navigated brain stimulation system 5 (nexstim, helsinki, finland). a high-quality head mri with 1-mm thick slices, that included the vertex, nasion and ears was performed for all patients and then was loaded in the ntms system. these anatomical landmarks are used for registering the patient into the frameless stereotactic navigation. consecutively, surface electromyography (emg) recording electrodes (neuroline 720, ambu, ballerup, denmark) are placed at the level of abductor pollicis brevis (apb), abductor digiti minimi (abm), flexor carpi radialis (fcr) and when needed also at the level of the tibilias anterior (ta), abductor hallucis (ah) and extensor hallucis longus (ehl). a figure-of-eight stimulation coil is used to deliver precise stimulation pulses based on the neuronavigation guidance. after the initial determination of the motor threshold, the actual mapping is performed. tms pulses were delivered in a systematic way at 110% of the resting motor threshold, in the areas of interest. motor-evoked potentials (meps) were recorded by the emg and their exact location was noted on the mri. additionally, for lesions involving speech eloquent areas we 18 | petrescu et al mapping the cortical areas using navigated transcranial magnetic stimulation supplemented the motor mapping with speech and language mapping. using the nexspeech software (nexstim, helsinki, finland) the patients were subjected to an object-naming task by displaying illustrations of common objects or numbers on a monitor and their performance was recorded by a video camera (fig. 1). in order to determine the baseline, the initial task was performed without tms. the picture display time (pdt) and the interpicture interval (ipi) were usually 700 ms and 2500 ms respectively, with variations based on the patients’ grade of neurologic deficit. pictures that were not recognized by the patients were excluded. this procedure was typically repeated two or three times. then, navigated repetitive tms (nrtms) pulses were delivered as a train of 5 pulses with a frequency of 5 hz, at 100% of the resting motor threshold and at a picture-to-trigger (ptt) interval of 0 ms. the results were then analyzed and compared to the baseline. naming errors were defined as follows: no response, semantic error, performance error, error due to muscle stimulation and other. afterwards, the results were recorded on the brain mri. neuronavigation system integration and surgical planning mr images were exported from the ntms system in a digital imaging and communications in medicine (dicom) format and then loaded in the intraoperative neuronavigation system sonowand invite (sonowand as, trondheim, norway). based on these findings, the optimal entry point and trajectory were determined, in order to achieve a maximum surgical resection of the lesion, while avoiding new postoperative neurological deficits. in cases of infiltrative tumors, an intraoperative 3d ultrasound probe was used to determine the extent of resection. results nineteen patients underwent an ntms brain mapping procedure between march 2017 and december 2017. there were 13 male patients and 6 female patients. the median (range) age of the patients was 53 (18-73) years. in all cases a motor mapping procedure was done, but only in eight cases a speech mapping was also performed. in seventeen cases a surgical resection of the lesion was performed, while one patient underwent only a stereotactic biopsy procedure. in one case the surgery was contraindicated because of the late-stage of primary cancer and other serious comorbidities. the pathology report revealed eight cases of glioblastoma, one case of a grade ii astrocytoma, three cases of cavernoma, one of meningioma, one case of non-hodgkin lymphoma and one cerebral abscess. other three cases were cerebral metastasis of various primary origin. the patient that did not undergo surgery had a history of pulmonary carcinoma that relapsed, so the cerebral lesion probably had a pulmonary origin. three patients presented new minor post-operatory deficits that consecutively remitted. the rest of the patients presented no added neurological deficits after surgery. in five cases the preexistent deficit was ameliorated after surgery and in three cases the deficit remitted. in one patient there was no improvement in the neurologic deficit after surgery. no seizures occurred during the procedures and no other adverse effects were noted. the characteristics of each case are described in table 1. romanian neurosurgery (2018) xxxii 1: 16 24 | 19 tabel 1 depicts the characteristics of each case. m male, f – female, gbmglioblastoma, nhl – nonhodgkin lymphoma, f frontal, p parietal, t – temporal, lv – lateral ventricle, ththalamus, l left, r – right, ? – not verified no. sex age lesion location mapping procedure preop. deficits postop. deficits 1 m 61 gbm ftp/r motor surgery none none 2 m 37 abscess f/l motor surgery r. hemiparesis remitting 3 m 73 gbm ftp/l motor surgery none none 4 m 53 metastasis fp/l motor surgery r. hemiparesis remitting; facial palsy remitted 5 f 23 cavernoma fp/l motor surgery r. brachial paresis remitted 6 m 21 cavernoma p/r motor surgery none r. crural deficit – remitting 7 m 18 cavernoma f/l motor/language surgery none none 8 f 70 metastasis fp/l motor/language surgery none none 9 m 65 gbm tp/l motor/language surgery aphasia, r. hypoesthesia remitting 10 m 62 gbm t/l motor/language surgery r. hemiparesis dysphasia remitting remitted 11 m 73 metastasis? f/r motor none l. hemiparesis 12 m 41 nhl lv/l motor surgery aphasia r. hemiparesis aphasia r. hemiparesis 13 m 46 gbm fp/l motor/language surgery r. facial palsy r. hemiparesis remitting 14 f 49 meningioma fp/l motor surgery none r. crural hemiparesis – remitting 15 f 31 astrocytoma gr. ii th/l motor biopsy r. hemiparesis r. hemiparesis 16 m 54 gbm f/l motor/language surgery aphasia r. hemiparesis remitted 17 f 64 metastasis fp/r motor/language surgery l. hemiparesis remitting 18 f 61 gbm t/l motor/language surgery aphasia confusion remitted 19 m 42 gbm tp/l motor surgery none none figure 2 a patient with a squamous cell carcinoma metastasis located at the level of the left central sulcus. a – red dots represent low-intensity meps and the yellow dots medium-intensity meps in relation to the cortical surface. b – red dots represent low-intensity meps and the yellow dots medium-intensity meps in relation to the tumour. c – intraoperative image after the tumor was completely resected; the small corticomy and the numerous drainage veins at the level of the cortex and their structural integrity following surgery must be noted. figure available in color online only 20 | petrescu et al mapping the cortical areas using navigated transcranial magnetic stimulation figure 1 snapshot from the video recorded during the ntms language mapping. in the upper right corner is the representation of a lock that was displayed on the monitor during the object-naming task. figure available in color online only figure 3 left temporoparietal glioblastoma in a 65year-old patient that presented with aphasia and right-sided hypoesthesia. a – motor mapping, red dots represent low-intensity meps, yellow dots medium-intensity meps and white dots highintensity meps; blanguage mapping, white dots – no response error, green dots – performance error, blue dots – semantic error, red dots – unclear interpretation. figure available in color online only figure 4 intraoperative view from the neuronavigation system. a – ntms-positive points appear as white dots. b – the 3d ultrasound probe is used to determine in real-time the extent of resection. figure available in color online only discussion the theory that the brain is structured in multiple static centers, each responsible for a certain cortical function is more and more challenged by recent advances in imaging and mapping techniques and as well by the clinical experience that proves that patients with lesions in presumed eloquent areas can still recover function (4). a hodotopic model is proposed that defines the brain as a set of large dynamic networks that cooperate in order to preserve or recover the cortical functions (6,7). brain tumors tend to disrupt the normal anatomy and can even determine plastic restructuring (8,9). taking these into account, romanian neurosurgery (2018) xxxii 1: 16 24 | 21 when facing an eloquent area lesion, neurosurgeons cannot rely only on good anatomical knowledge. the surgical planning must also include brain mapping methods that can help determine precise location of the eloquent area and its relation to the lesion. many methods have been used for mapping of cortical eloquent areas, preoperatively, as well as intraoperatively, including: functional mri (fmri), diffusion tensor imaging (dti), magnetoencephalography (meg), positron emission tomography (pet), single-photon emission computed tomography (spect) and direct cortical stimulation (dcs) (10–12). fmri has been regarded as one of the most frequently used and reliable methods for preoperative mapping (13–15), but more recent studies question its’ precision and role, particularly in tumors that affect the normal vascularization and consequently alter the metabolic mapping (16,17). regarding motor mapping dcs remains the “gold-standard” method for assessing the precise location of the motor function (5). ntms motor mapping has been proved to have comparable results to dcs (17,18). also, ntms has a better accuracy than fmri (19), while also having the advantage of not being limited by the usage of voluntary motor tasks that do not necessarily trigger only the primary motor areas and can also be used in patients that are less compliant (20). another usage of ntms is that the precise location of meps can be used as seed-points when performing dti, thus achieving a better and more accurate image of the corticospinal tract (21–23). knowledge of such information is critical for obtaining a good surgical outcome, since damage to the subcortical structures can probably produce more severe and permanent neurological deficits than an injury localized at the cortical surface (4). in our series, a 53-year old male presented with a left frontoparietal lesions, located at the level of the central sulcus. the preoperative neurologic exam revealed right-sided hemiparesis. during the ntms mapping procedure, only low-intensity and a couple medium-intensity meps were recorded (fig. 2a). this could be explained by the preexistence of a motor deficit. a few meps were recorded above the tumor (fig. 2b). given the numerous drainage veins located at the cortical surface, in the vicinity of the tumor, only one entry-point could be chosen, in order to preserve the integrity of the veins, hence avoiding a poor outcome. following the resection of the tumor through an area with ntms-positive motor points, the patient had a transient worsening of the neurologic deficit. this situation is not uncommon. moser et al. published a study in which of the thirteen patients that underwent the resection of ntms-positive motor points, eight had new permanent neurologic deficits and two only transient ones (24). similarly, to the motor mapping, the dcs with an awake patient is considered the “goldstandard” for language mapping (25). in order to obtain the best results it is necessary to achieve a state of optimal conscious sedation (10). besides the technical difficulty, not all patients are comfortable enough to undergo an awake surgery. in this context, ntms offers the extraordinary advantage of doing the 22 | petrescu et al mapping the cortical areas using navigated transcranial magnetic stimulation procedure preoperatory, offering a comfortable solution for both the patient and the surgeon. the only question that remains is how reliable is ntms for language mapping. language mapping using ntms was proven more sensitive, but less specific than fmri, when compared with dcs, but similar results to dcs can be achieved by combining ntms and fmri (26,27). picht et al. reported that even though, ntms was less specific than dcs, particularly in the supramarginal, angular and posterior superior temporal gyri, the negative responses were similar to those recorded by dcs (28). because of the repetitive nature of the pulses used for language mapping, side effects including seizures and headaches might be encountered. in our series no such events were record, this being consistent with data reported from other study (14). in our series, a 65-year-old male, that presented with aphasia and right-sided hypoesthesia was admitted. the brain mri revealed a left temporoparietal mass (fig 3). the optimal entry point was chosen accordingly to the location of the languagepositive points and post-operatory the patient’s neurologic function improved. in some cases, it is very difficult to perform and interpret a language mapping because of the preexistent neurological deficits. two patients had difficulties in recognizing the objects that were illustrated in the pictures, the problem being especially in the initiation of the command, because after the examiner aided them with the first syllabus of the word, their performance improved. in these two cases, the patients did very well when they were asked to recognize numbers, so this baseline was used instead. schwarzer et al. also noted that in patients with aphasia it is more difficult to rely on the ntms language mapping (29). when combined with intraoperative neuronavigation, ntms offers a major benefit when, as it highlights the eloquent areas which are sometimes much more extended than expected and helps the neurosurgeon choose the safest entry points. also, the 3d ultrasound probe adds more value, the surgical team being able to determine in real-time the extent of resection (fig.4). combined, these tools facilitate the achievement of a maximum resection while avoiding new postoperative neurological deficits. conclusions navigated transcranial magnetic stimulation is a reliable tool for the preoperative planning of eloquent area lesions. its results are similar to dcs for motor mapping and it does not have the disadvantages of awake surgery regarding language mapping. it must be taken into account that functional areas have a high individual variability. therefore, knowing preoperatively the extent of the eloquent area helps the neurosurgeon adapt the surgical approach in order to obtain a better functional outcome. correspondence petrescu george emil dragoș gedpetrescu@gmail.com romanian neurosurgery (2018) xxxii 1: 16 24 | 23 references 1. lee c-h, kim dg, kim jw, han jh, kim yh, park ck, et al. the role of surgical resection in the management of brain metastasis: a 17-year longitudinal study. acta neurochir (wien). 2013;155(3):389–97. 2. sanai n, berger ms. g lioma e xtent of r esection and and methods. neurosurgery. 2008;62(4):753–66. 3. li ym, suki d, hess k, sawaya r. the influence of maximum safe resection of glioblastoma on survival in 1229 patients: can we do better than gross-total resection? j neurosurg. 2016;124(4):977–88. 4. picht t. current and potential utility of transcranial magnetic stimulation in the diagnostics before brain tumor surgery. cns oncol. 2014;3(4):299–310. 5. lefaucheur jp, picht t. the value of preoperative functional cortical mapping using navigated tms. neurophysiol clin. 2016;46(2):125–33. 6. de benedictis a, duffau h. brain hodotopy: from esoteric concept to practical surgical applications. neurosurgery. 2011;68(6):1709–23. 7. duffau h. hodotopy, neuroplasticity and diffuse gliomas. neurochirurgie. 2017;63(3):259–65. 8. takahashi s, jussen d, vajkoczy p, picht t. plastic relocation of motor cortex in a patient with lgg (low grade glioma) confirmed by nbs (navigated brain stimulation). acta neurochir (wien). 2012 nov;154(11):2003–8; discussion 2008. 9. conway n, wildschuetz n, moser t, bulubas l, sollmann n, tanigawa n, et al. cortical plasticity of motor-eloquent areas measured by navigated transcranial magnetic stimulation in patients with glioma. j neurosurg. 2017;127(november):1–11. 10. darder jmg, lopez pg. management of brain tumors in eloquent areas. in: diagnostic techniques and surgical management of brain tumors. intech; 2011. p. 15–22. 11. mazziotta jc. imaging: window on the brain. arch neurol. 2000 oct;57(10):1413–21. 12. desmond je, sum jm, wagner ad, demb jb, shear pk, glover gh, et al. functional mri measurement of language lateralization in wada-tested patients. brain. 1995;118(6):1411–9. 13. lehéricy s, duffau h, cornu p, capelle l, pidoux b, carpentier a, et al. correspondence between functional magnetic resonance imaging somatotopy and individual brain anatomy of the central region: comparison with intraoperative stimulation in patients with brain tumors. j neurosurg. 14. picht t, schmidt s, woitzik j, suess o. navigated brain stimulation for preoperative cortical mapping in paretic patients: case report of a hemiplegic patient. neurosurgery. 2011;68(5):1475–80. 15. tieleman a, deblaere k, van roost d, van damme o, achten e. preoperative fmri in tumour surgery. eur radiol. 2009;19(10):2523–34. 16. holodny ai, schulder m, liu wc, wolko j, maldjian ja, kalnin aj. the effect of brain tumors on bold functional mr imaging activation in the adjacent motor cortex: implications for image-guided neurosurgery. am j neuroradiol. 2000;21(8):1415–22. 17. krieg sm, shiban e, buchmann n, gempt j, foerschler a, meyer b, et al. utility of presurgical navigated transcranial magnetic brain stimulation for the resection of tumors in eloquent motor areas. j neurosurg. 2012;116(5):994–1001. 18. picht t, schmidt s, brandt s, frey d, hannula h, neuvonen t, et al. preoperative functional mapping for rolandic brain tumor surgery: comparison of navigated transcranial magnetic stimulation to direct cortical stimulation. neurosurgery. 2011;69(3):581–8. 19. coburger j, musahl c, henkes h, horvath-rizea d, bittl m, weissbach c, et al. comparison of navigated transcranial magnetic stimulation and functional magnetic resonance imaging for preoperative mapping in rolandic tumor surgery. neurosurg rev. 2013 jan;36(1):65–6. 20. frey d, schilt s, strack v, zdunczyk a, sler jr, niraula b, et al. navigated transcranial magnetic stimulation improves the treatment outcome in patients with brain tumors in motor eloquent locations. neuro oncol. 2014;16(10):1365–72. 21. frey d, strack v, wiener e, jussen d, vajkoczy p, picht t. a new approach for corticospinal tract reconstruction based on navigated transcranial stimulation and standardized fractional anisotropy values. neuroimage. 2012;62(3):1600–9. 22. krieg sm, buchmann nh, gempt j, shiban e, meyer b, ringel f. diffusion tensor imaging fiber tracking using navigated brain stimulation—a feasibility study. acta neurochir (wien). 2012;154(3):555–63. 23. weiss lucas c, tursunova i, neuschmelting v, nettekoven c, oros-peusquens am, stoffels g, et al. functional mri vs. navigated tms to optimize m1 seed 24 | petrescu et al mapping the cortical areas using navigated transcranial magnetic stimulation volume delineation for dti tractography. a prospective study in patients with brain tumours adjacent to the corticospinal tract. neuroimage clin. 2017;13:297–309. 24. moser t, bulubas l, sabih j, conway n, wildschutz n, sollmann n, et al. resection of navigated transcranial magnetic stimulation-positive prerolandic motor areas causes permanent impairment of motor function. neurosurgery. 2017;81(1):99–110. 25. duffau h, lopes m, arthuis f, bitar a, sichez j-p, van effenterre r, et al. contribution of intraoperative electrical stimulations in surgery of low grade gliomas: a comparative study between two series without (1985–96) and with (1996–2003) functional mapping in the same institution. j neurol neurosurg &amp;amp; psychiatry. 2005 jun 1;76(6):845 lp-851. 26. ille s, sollmann n, hauck t, maurer s, tanigawa n, obermueller t, et al. impairment of preoperative language mapping by lesion location: a functional magnetic resonance imaging, navigated transcranial magnetic stimulation, and direct cortical stimulation study. j neurosurg. 2015 aug;123(2):314–24. 27. ille s, sollmann n, hauck t, maurer s, tanigawa n, obermueller t, et al. combined noninvasive language mapping by navigated transcranial magnetic stimulation and functional mri and its comparison with direct cortical stimulation. j neurosurg. 2015 jul;123(1):212–25. 28. picht t, krieg sm, sollmann n, rösler j, niraula b, neuvonen t, et al. a comparison of language mapping by preoperative navigated transcranial magnetic stimulation and direct cortical stimulation during awake surgery. neurosurgery. 2013;72(5):808–19. 29. schwarzer v. aphasia and cognitive impairment decrease the reliability of rntms language mapping. 2017; 02 02petrescug_preoperative flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 2 | 2017 | april-june article sinking skin flap syndrome in a patient with giant thrombosed posterior cerebral artery aneurysm: a case report ona lapteva, ugnius ksanas, jelena scerbak lithuania doi: 10.1515/romneu-2017-0029 186 | lapteva et al sinking skin flap syndrome doi: 10.1515/romneu-2017-0029 sinking skin flap syndrome in a patient with giant thrombosed posterior cerebral artery aneurysm: a case report ona lapteva, ugnius ksanas, jelena scerbak centre of neurosurgery, vilnius university hospital santariskiu klinikos, vilnius, lithuania abstract: sinking skin flap syndrome is a rare complication following decompressive craniectomy. the pathogenesis is based on disturbed cerebral autoregulation and as a consequence dicreased cbf and cerebral metabolism. this results in neurologic disturbances, i. e. mental changes and focal deficits. the authors present the patient who developed the motor trephine syndrome after decompressive craniectomy following complicated giant posterior cerebral artery aneurysm clipping. key words: sinking skin flap, motor trephine syndrome, syndrome of the trephined, decompressive craniectomy, cranioplasty introduction the sinking skin flap syndrome, or motor trephine syndrome, is a rare complication following decompressive craniectomy [2]. this pathologic entity may be explained by athmospheric pressure gradient that is even more exaggerated by csf hypovolemia as a result of ventriculoperitoneal shunting, excessive dehydration or position change [2]. thus athmospheric pressure gradient exceeds intracranial pressure and as far as cerebral autoregulation is disturbed, paradoxical herniation leading to neurologic deterioration, coma and death may result [3]. urgent cranioplasty is required to reverse the neurologic deterioration [1]. case report 58-year old male presented with right upper limb weakness and clumsiness, resulting in inability to hold a spoon and write. brain magnetic resonance imaging (mri) revealed partially thrombosed giant posterior cerebral artery (pca) aneurysm with brain stem and thalamus compression and perifocal edema (figures 1, 2). the patient was referred to neurosurgeon for the operative treatment. the frontotemporal transcavernous approach with extradural clinoidectomy and partial orbitotomy was performed. at the time of manipulating temporary clips intraoperative rupture of the neck of the aneurysm occured. the pca was sacrificed after making sure that distal pca as well as romanian neurosurgery (2017) xxxi 2: 186 190 | 187 posterior communicans artery and visible perforant arteries are flow-patent. three hours postoperatively computed tomography (ct) perfusion showed no perfusion restriction and symmetrical cerebral blood flow (cbf) and volume (cbv). nevertheless, the patient woke up in the intensive care unit (icu) having severe right side hemiparesis and sensorimotor aphasia. subsequent ct and mri revealed ischemia in the left pca territory. one week later the patient's level of consciousness deteriorated, and ct scan showed cerebral edema and midline shift to the right. the patient underwent left decompressive craniectomy. his neurologic condition improved postoperatively. he was transferred from the icu to the department of neurosurgery. rehabilitative treatment was initiated and the patient gradually recovered. at the end of the treatment the patient was fully oriented with slight partial sensorimotor aphasia and moderate right side hemiparesis: upper extremity (ue) 4/5, lower extremity (le) 3/5. after 7 weeks of rehabilitation and physiotherapy program the patient started progressively deteriorating: he became drowsy and disorientated, and right side hemiparesis increased in severity: ue 3/5, le 2/5. head ct scan revealed concave depression of the scalp flap with underlying cerebral hemisphere and lateral ventrical compression, midline shift of 6 mm to the contralateral side and effacement of the cortical sulci (figure 3). the postdecompressive skin flap was deeply sunken and kept being immobilised when the patient was laid down on his left side (figure 4). the patient underwent cranioplasty with autologous bone flap on urgent basis. postoperative ct scan showed the reexpansion of the brain to fulfill the intracranial cavity, normal sulcal patterns and restoration of the midline (figure 5). the postoperative period was uneventful and the patient recovered to his preoperative state. figure 1 brain mri, t2-weighted image. partially thrombosed giant posterior cerebral artery (pca) aneurysm with brain stem and thalamus compression and perifocal edema 188 | lapteva et al sinking skin flap syndrome figure 2 brain ct angiography. giant posterior cerebral artery (pca) aneurysm figure 3 ct scan. concave depression of the scalp with underlying cerebral hemisphere and lateral ventrical compression, midline shift of 6 mm to the contralateral side and effacement of cortical sulci romanian neurosurgery (2017) xxxi 2: 186 190 | 189 figure 4 sunken skin flap figure 5 post-cranioplasty ct scan. the brain re-expanded and fully occluded epidural dead-space. normal sulcal patterns and restoration of the midline. chronic ischemic cerebral malacia in the left pca territory discussion neurologic symptoms such as headaches, mental changes, language and motor disorders has been in reported in sinking skin flap syndrome, or the syndrome of the trephined [3, 4]. motor trephine syndrome has been used by some authors to highlight delayed motor dysfunction following craniectomy [2]. often the symptoms arise in upright position and diminishes in supine position [2, 4]. the 190 | lapteva et al sinking skin flap syndrome causative factors are local cortical compression along with the local ischemia and csf circulation disturbances [2]. a variety of issues arrise following decompressive craniectomy. cerebrospinal fluid dynamics alterations may result in hydrocephalus, subdural or subgaleal fluid collections [1]. cerebral perfusion pressuse and blood flow is reduced. the impaired venous return and obliteration of the subarachnoidal space due to the direct atmospheric pressure on the brain may be the cause of it [1]. the atmospheric pressure is resisted by two mechanisms: the elastance of the brain that resists deformation and ventricular csf that keeps the brain expanded. the parenchymal injury with tissue loss is a predictive factor for the development of the sinking skin flap syndrome [2]. prolonged dehydration and upright position often precipitates this condition [4]. paradoxical herniation is a potentially devastating event. the effect of atmospheric pressure along with gravitational forces lead to herniation syndrome [1]. patients are more susceptible to this syndrome after the csf drainage procedures, i. e. external ventriculostomy, ventriculoperitoneal (vp) shunting and lumbar drainage [1]. the csf hypovolemia along with atmospheric pressure potentiate the brain being pushed down through the incisural notch [1]. the traditional treament for brain herniation such as mannitol, csf drainage, and hyperventilation reduce intracranial contents and exacerbate paradoxical herniation due to increasing pressure gradient across the craniectomy defect [1]. paradoxic measures are applied to counteract the atmospheric pressure, i.e. trendelenburg position, excessive hydration, closing the csf drainage (clamping or re-programming the vp shunt) and discontinuation of the hyperosmolar treatment [1]. the definitive treatment is performing cranioplasty on urgent basis [1]. if clinical and neurologic deterioration occurs after initial improvement, the skin flap over the craniectomy defect is concave and ct scans is characteristic of the syndrome of the trephined [2], early cranioplasty must be considered once other causes are excluded. correspondence ona lapteva, centre of neurosurgery, vilnius university hospital santariskiu klinikos, santariskiu 2, 08661, vilnius, lithuania email: ona.lapteva@msn.com references 1.akins pt, guppy kh. sinking skin flaps, paradoxical herniation, and external brain tamponade: a review of decompressive craniectomy management. neurocrit care 2008; 9(2): 269-276. 2.krishnan p, chowdhury sr. posture-dependent aphasia: focal cortical dysfunction in the sinking scalp flap syndrome. j neurosci rural pract 2015; 6(2): 225227. 3.kwon sm, cheong jh, kim jm, kim ch. reperfusion injury after autologous cranioplasty in a patient with sinking skin flap syndrome. j korean neurosurg soc 2012; 51(2): 117-119. 4.romero fr, zanini ma, ducati lg, gabarra rc. sinking skin flap syndrome with delayed dysautonomic syndrome – an atypical presentation. int j surg case rep 2013; 4(11): 1007-1009. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article ozone therapy – a rare and avoidable source of infectious pathology of the spine corneliu balan, mihai schiopu, daniel balasa, corina balan romania doi: 10.1515/romneu-2017-0046 romanian neurosurgery (2017) xxxi 3: 281 288 | 281 doi: 10.1515/romneu-2017-0046 ozone therapy – a rare and avoidable source of infectious pathology of the spine corneliu balan1, mihai schiopu1, daniel balasa1, corina balan2 1neurosurgery department, clinical emergency hospital, constanta, romania 2icu department, clinical emergency hospital constanta, romania abstract: ozone therapy is considered by many as an effective therapy for spinal degenerative pathologies. despite its possible favorable results, we present a series of serious infectious complications, clearly related to ozone therapy and their treatment. the authors discuss their results compared with the literature and advocate for prudence when recommending ozone therapy. injection therapy for low back pain is a technique dating from the 1970’ for relieving pain from spinal stenosis and spinal disc herniation. using a needle, corticosteroids and a local anesthetic are injected in: • trigger points, intramuscular and ligamentous regions of the lower spine, considering that they perpetuate the pain • facet joints, considering the facet joint syndrome, aggravated by straining and heavy bending • epidural space in the proximity of the nerve roots. imaging guidance (fluoroscopy and later ct scan) ensures the correct placement of the needle with low risk of damaging nerve structures and maximizes the physician's ability administer therapy. without imaging, the risk increases for the injection to be incorrectly placed. all these techniques using medication are heavy disputed among experts as they are invasive, doubly of clinical benefit in acute phase and no certified studies have adequately investigated their efficacy at 3 months. some of them proved same efficacy as normal saline [1] and in practice guidelines are considered level iii therapeutic recommendations. despite being practiced in many countries of europe, the fda has not approved the use of corticosteroids for epidural injection due to the short time relief and non impact on the need for surgical intervention [2]. while the administration of classical medication is disputed, in the last 15 years there is a new trend consisting of administering ozone infiltrations, as solution, either local or intradiscal. this technique raises an even larger number of controversies given the unclear mechanism of action and high risk of complications. 282 | balan et al ozone therapy in the following paper we will present such serious complications hospitalized in the neurosurgery dept. of the emergency clinical hospital of constanta during the last 2 years, with the arguments of discontinuation of further ozone therapy. as summary, we dealt with 4 cases of serious spinal infections in 2 years time, in patients with no serious previous pathology, all connected with ozone therapy. three of them were operated in our department, the fourth transferred at the patient’s request then came back. all 4 required long-term antibiotics and two of them remained paraplegic, despite best medical and surgical treatment. 1. p.i., male, 58 yo, accused diffuse back pain located in the thoracic area for several years. after a course of balnear treatment, he was proposed by his gp, ozone therapy injected in trigger points. 12 days after the injections he started developing rapid paraparesis and was admitted in neurology. after excluding ms with lumbar puncture and guillan barre syndrome, he had an mri, almost a week since onset. on mri several infectious lesions were discovered, as discitis, spinal epidural abscess and infection on the traject of injection. one remark is that during anamnesis he told nothing about ozone therapy. the patient was transferred to neurosurgery, operated – evacuation of the spinal epidural abscess by a laminectomy on 2 levels. the germ responsive was s. aureus, sensible to multiple antibiotics. despite adequate medical treatment, 2 months after he still presented paraparesis, with force deficit at 2/5 in lower limbs and urinary catheter. romanian neurosurgery (2017) xxxi 3: 281 288 | 283 2. c.s, female, 46 yo, known with rheumatoid arthritis for several years. she accused low back pain for several months and received injections with ozone in lumbar muscles, while being on corticoids. almost 3 weeks after the injections, she was admitted for intense back pain, meningism, fever 38’8 c and monoparesis of the right lower limb. she received a lumbar puncture which revealed less than 50 elements/mmc but was directed to infectious diseases. an mri noted an abscess in the lumbar paravertebral muscles, extended in the epidural space and spondilodiscitis at c5-c6 space with small epidural and retropharyngeal abscesses. she was then transferred to neurosurgery for surgical treatment – evacuation of the collections from the lumbar area, continued with ceftriaxone and ciprofloxacine for two months (s. aureus with multiple sensibilities). she had a good motor recovery despite the initial extension of the lesions. 284 | balan et al ozone therapy 3. u.v, female, 65 yo, was admitted in rheumatology complaining about hyperalgic lumbago, with muscle stiffness and sciatica with paresis on the right foot. the symptoms developed soon after ozone therapy realized in private practice for low back pain. after several days of treatment including opioids, she had an mri which revealed spondilodiscitis situated at l5-s1 level, epidural and intramuscular abscess. she was transferred to neurosurgery and operated – evacuation of the intramuscular and epidural abscess. the germ involved was s. aureus, sensible to vancomicin. clinical evolution after 2 months of antibiotherapy was favorable but one must consider she had never had any motor deficit, just pain. 4. c.l. female, 64 yo, nurse (!), with a history of 3 years of low back pain. eleven days after an infiltration with ozone in the lumbar area she is admitted in neurology paraplegic with acute onset in the last 2 days. mri revealed spondylodiscitis, extended anterior and in the spinal canal as well an infection in the paravertebral muscles, left side. her family asked for her to be transferred to another hospital in bucharest. operated, she had just a slight motor improvement at 4 months. case 3 romanian neurosurgery (2017) xxxi 3: 281 288 | 285 case 4 facts ozone therapy is a non conventional technique similar to classic spinal infiltrations, consisting of injecting ozone (o3) in small doses intradiscal to realize a dehydration of the disc and diminishing intradiscal pressure and nerve compression. another possibility is the administration intraarticular or periganglionic / periradicular areas, all under ct scan control. there are also reports of ozone injected in lytic areas of spondylolisis / spondylolisthesis. however, due to its high diffusion coefficient, in many cases where ct scan is not available, ozone is simply administered intramuscular or even subcutaneous in the vicinity of the painful area, up to 20-30 ml of gas. some ozone therapy enthusiasts promote even ozone rectal insufflation the introduction about a certain amount of humidified gaseous ozone that enters the bloodstream through the intestinal walls and would represent alternative therapy for hepatitis b and c, crohn’s disease, ulcers, ischemic disease, fistulas, gastritis, chronic colitis, liver cirrhosis, detoxification and premature aging. the medical use of ozone is not licensed either by fda or emea as there are yet no meta-analysis or multicentric studies to prove its efficacy. however, it is realized in some countries in europe (france, italy, spain) or south america (brazil), with local license by their national health services, mostly in private practice as high rewarding for those who realize it. in italy, for instance, there is even “rivista italiana di ossigeno-ozonoterapia” founded in 2002, with papers mainly from italy, spain, cuba and brazil [3] which evolved in 2008 as the”international journal of ozone therapy” , together with a world federation for oxygen-ozone therapy [4] production: medical ozone is obtained from pure medical oxygen to avoid the presence of toxic byproducts and other gases. conversion is achieved with ozone generators, 286 | balan et al ozone therapy close to the moment of use, due to gas lability. most generators are still based on the corona system created by werner siemens, founder of the industrial conglomerate named after him till today. the most important is to use an ozone generator suitable for a clean product, pure and uncontaminated. this is possible only when ozone reaches glass electrodes (never metal or ceramic) as still in the generator. if triatomic oxygen comes in contact with metal, plastic, rubber or other oxidizable materials, the decomposition of these materials will contaminate ozone. ozone is in fact, a mixture of ozone and oxygen (o3/ o2) where ozone is no more than 5% of total mixture. richer ozone concentrations are used for intradiscal injections and accelerate disc dehydration and degenerative disc changes, decreasing compression caused by hernias. poorer concentrations are used for regenerative responses. the oxygen/ozone mixture is highly safe with regard to toxicity, even in relatively high concentrations such as 20 to 30 μ per ml, and may be applied even when disc hernia is non contained. some authors classify ozone therapy as the safest type of chemonucleolysis as compared to papain physiopathology (according to those who use it) ozone is approximately 10 times more soluble than oxygen, the same being true for its tissue diffusion and penetration. when in contact with biologically active tissue, ozone immediately reacts with several biomolecules which, together, make up real antioxidant buffering systems. most of these biomolecules play important anti-inflammatory and analgesic roles, simultaneously to antioxidant actions. ozone therapy acts on red blood cells with the formation of peroxides and metabolism activation by the glutathione system with improved oxygen release and increased tissue energy and atp. o3 increases 2,3dpg concentration with decreased affinity of oxyhemoglobin for o2 and a shift to the left in the hbo2/hb curve with consequent better peripheral oxygenation. antioxidant response which follows oxidizing stimulation supplied by medical ozone is represented by the increase of substances classically known as natural anti-inflammatory, while most analgesic effects come from this response. most pains mediated by increased muscle activity are relieved by ozone therapy as increased oxygen supply and energetic build up, translated by increased atp concentration, give tissues metabolic protection against the anaerobic option and lower chemical stimulation to pain receptors. when combined with steroid injection, ozone therapy would have anti-inflammatory synergism which occurs in different chronologic times. trials and published papers – there are many reports of using medical ozone in spinal pathology in fact most of them refer to treatment of lumbar disc hernias and spinal stenosis. we are going to present a few of them in order to offer an unaltered opinion on ozone therapy. trial registered as nct00566007 [5] on the effect of ozone therapy for lumbarherniated disc: ozone is being evaluated for its efficacy infiltration and its effectiveness in comparison with microdiscectomy in the romanian neurosurgery (2017) xxxi 3: 281 288 | 287 treatment of lumbar-herniated disc with criteria for surgery. the study is currently in its phase 2 studies, which is sponsored by kovacs foundation. the study also evaluates the efficacy of infiltration in presence of corticoids, anesthetics, which is being compared by replacing o3 by oxygen. the study ended in 2014 after 7 years ans no results were published till now. bonetti and his team from brescia, italy have many papers published on ozone therapy. they administered ozone intraforaminally with ct guidance followed by 4 paralumbar injections weekly, on a serie of 129 elderly people with degenerative spine disease. the amelioration at 3-6 months made them conclude that ozone therapy is a safe, repeatable and innocuous treatment [3]. in another serie of 306 patients, bonetti reported that 57.5% of 80 patients in the disc disease group treated with steroid deemed the clinical outcome to be excellent, whereas in the ozone therapy group, 74.4% of 86 patients with disc disease reported complete remission of pain [6]. in this study, differences in favor of o3 treatment were statistically significant in patients with disc disease. in another randomized study, gallucci et al [7] observed a satisfactory success rate with ozone-therapy combined with intraforaminal and intradiscal steroid and anesthetic injection compared to steroid alone. zambello et al randomized 351 patients with low back pain for treatment with either ozone or steroid (epidural) and planned a crossover during the follow-up to the other group in case of failure to respondto treatment after 4 weeks of therapy. the long-term outcome remained excellent or good in 47.3% of 171 patients treated by epidural steroid injections and in 77.1% of 180 patients treated with o2-o3 [8]. many other authors also present favorable results on all kind of spinal degenerative pathologies when administering ozone, some in journals with important impact factor [9, 10, 11]. however, despite publishing the papers, reviewers have presented some discrepancies in the papers like those from acta neurochirurgica in 2016 [12,13] two systematic reviews of the literature, published in 2013 (spain)[14] and 2014 (brazil)[15], after analyzing several hundred cases conclude that the indicated level of evidence is ii-3 (evidence obtained from diagnostic studies of uncertainty) according to u.s. preventive services task force for ozone therapy applied intradiscally and ii-1 ( evidence obtained from at least one properly conducted diagnostic accuracy study of adequate size) for ozone therapy applied paravertebrally on long-term relief in low back pain secondary to disc herniation. according to same studies, the grading the strength of recommendations and quality of evidence in clinical guidelines is 1c for ozone therapy applied intradiscally and 1b for ozone applied at the paravertebral muscles or periforaminally (strong recommendation, moderate to low quality evidence). conclusion the data given above try to offer an impartial (if possible, as we are surgeons) view on ozone therapy, without approving or negating the results from other papers 288 | balan et al ozone therapy published. as neurosurgeons, we were confronted with a large number of complications from ozone therapy, realized by several doctors, in a short period of time ( 4 cases of severe spine infections in less than 2 years). we don’t know exactly how many patients received ozone therapy during the last 2 years nor their state of health now, as this is realized in private practice mostly. we cannot and will not evaluate the indications of other colleagues’ practice, nor the quality of asepsia on injections or their competence.. however, given the already known dispute on classic infiltrations with lack of studies on efficacy of corticoids and the complications we have already seen on infiltration with ozone, we suggest, if not abstention for this new method, at least a well considered evaluation of the risks and benefits before realizing it. references 1 frost fa, jessen b et al – double blind comparison of mepivacaine injections versus saline injections for myofascial pain, lancet, , 1980, 1, 499-501 2. pdr fda datasheets depomedrol / kenalog | 2010 3. m.bonetti, a fontana, d mardighian – ozone therapy for degenerative spine disease in elderly, rivista italiana di ossigeno-ozonoterapia, 5: 25-32, 2006 4. www.wfoot.org/wp-content/uploads/.../ijot_7_1_ id62.pdf 5. https://clinicaltrials.gov/ct2/show/nct00566007 6. bonetti m, fontana a, cotticelli b, volta gd -. intraforaminal o2-o3 versus periradicular steroidal infiltrations in lower back pain: randomized controlled study. ajnr am j neuroradiol 2005; 26:996-1000. 7. gallucci m, limbucci n, zugaro l sciatica: treatment with intradiscal and intraforaminal injections of steroid and oxygen-ozone versus steroid only. radiology 2007; 242:907-913 8. zambello a, fara b, tabaracci g, bianchi m. epidural steroid injection vs paravertebral o2-o3 infiltration for symptomatic herniated disc refractory to conventional treatment: a prospective randomized study, rivista di neuroradiologia 2009; 5:123-127. 9. andreula cf , simonetti l, de santis f minimally invasive oxygen-ozone therapy for lumbar disk herniation. ajnr am j neuroradiol. 2003 may;24(5):996-1000. 10. muto m, ambrosanio g, guarnieri g,.low back pain and sciatica: treatment with intradiscalintraforaminal o(2)-o (3) injection. our experience, radiol med. 2008 aug;113(5):695-706 11. muto m, andreula c, leonardi m. treatment of herniated lumbar disc by intradiscal and intraforaminal oxygen-ozone (o2-o3) injection. j neuroradiol. 2004 jun;31(3):183-9. 12. manuel c.,. gonçalves v.m. – intraforaminal ozone therapy, acta neurochir 2016 158:489–490 13. baeza-noci j comments on "intraforaminal ozone therapy and particular side effects: preliminary results and early warning"., acta neurochir 2016 may;158(5):989-90. doi: 10.1007/s00701-016-2754-z. epub 2016 mar 1. 14. f. j. hidalgo-tallón y l. m. torre ozonoterapia en medicina del dolor. revisión, rev. soc. esp. dolor vol.20 no.6 nov./dic. 2013 15. francisco n. de oliveira magalhaes, md, luciana dotta, md, andre sasse, ozone therapy as a treatment for low back pain secondary to herniated disc: a systematic review and meta-analysis of randomized controlled trials, pain physician 2014; 15:e115-e129 microsoft word _editorpage.doc romanian neurosurgery editor’s page november 2010 st.m. iencean, editor clinical emergency hospital “prof. dr. nicolae oblu” iasi, romania e-mail: mirceasteffan@yahoo.com romanian neurosurgery 2010 this is the final issue of romanian neurosurgery for 2010 and this is a good time for some reflections. we have had a good year: together we managed to provide quarterly publication of romanian neurosurgery with important neurosurgical subjects of romanian and foreign authors and this year our journal was classified first time in the b + category by national council for scientific research in higher education (cncsis). between 28 september – 2 october, the 7th national congress of the romanian society of neurosurgery with international participation in cluj was very successful and enjoyable. in this issue several important manuscripts are included on different topics. first, this issue presents a historical paper on assoc. professor stefan tristan iacob who was the founder of neurosurgery in cluj and who published with professor constantin arseni one of the first romanian neurosurgical book , the volume entitled vertebral sciatica, 1948. particularly special is the study of ketter et al. on prognostic genetic markers in malignant gliomas showing that p15 methylation can act as an additional prognostic factor for survival in glioblastomas. iamandei et al. showed that increased amounts of polyunsaturated fatty acids in the membranes of nerve cells can justify the positive evolution of animals in assessing the performance of concomitant behavioral tests. an original contribution of rotariu et al. deals with aspects of malignant transformation of low grade gliomas into glioblastoma and iliescu, negru and poeata evaluated the efficacy of mr tractography for preoperative planning in patients with cerebral tumors in eloquent areas. the need of protocols for a comprehensive management of mild and moderate head injuries in adults is presented by turliuc et al. and also very interesting is the article by costachescu and popescu, which focuses on the modern management in vertebral metastases. there are also more very interesting case reports: a retrospective study on five cases of craniocerebral gunshot wounds (majer and iacob), a case with severe spinal lumbar and thoracic stenosis in an adult patient with achondroplasia (iliescu et al) and others, and we hope you enjoy reading all these articles. this issue ends with selected abstracts from our national congress during september october at cluj and with the report of general assembly of the romanian society of neurosurgery. from the editorial office, we wish you all a very nice end of 2010, a happy new year and we look forward to further cooperation in 2011. romanian neurosurgery (2010), xvii, 4, 381 romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article scalp arteriovenous malformation: a case report with review asheesh kumar gupta, s.n. iyengar, anand sharma india doi: 10.2478/romneu-2018-0018 romanian neurosurgery (2018) xxxii 1: 151 155 | 151 doi: 10.2478/romneu-2018-0018 scalp arteriovenous malformation: a case report with review asheesh kumar gupta, s.n. iyengar, anand sharma department of neurosurgery, g.r. medical college gwalior, india abstract: arteriovenous malformation (avm) of the scalp is a rare lesion whose natural history remains to be elucidated. clinical symptoms, usually, range from an asymptomatic lesion, local discomfort, headaches to necrosis and massive hemorrhage. selective angiography remains the cornerstone for investigation. complete surgical excision, embolization or an approach combining the modalities is curative. it can also cause massive hemorrhages due to dryness of the overlying skin and injuries. in this report we describe the clinical and radiological features of a patient with a scalp arteriovenous malformation. key words: avm, sta, nidus introduction arteriovenous malformation (avm) of the scalp is a rare vascular lesion that is characterised by abnormal fistulous connections between supplying arteries and draining veins without an intervening capillary network in the subcutaneous plane of the scalp. (1) the scalp avm comprises of 8.1% of total avm and more common in young adults. a well-known fact states their origin attributable to anomalous primitive fistulous connection between feeding arteries and draining veins, with the absence of intervening capillary bed. this state of high shunt flow between the two distinct vessel types and the complex vascular anatomy makes their treatment a challenging undertaking. we present one case of scalp avm with review of literature. case report a 20 year female presented to neurosurgery opd with painless swelling over left fronto-parietal region of scalp since birth increasing in size for the past 1-2 years. initially, it was small reddish swelling till adolescent and become larger in size and causing esthetic problem to her. on examination, there was a soft, bluish and nontender lesion in the left fronts-parietal region of scalp. the overlying skin is coarse and dry; however there was neither ulceration nor active haemorrhage present (figure 1). there was no previous history of trauma or head injury. bruit was heard on auscultation of 152 | kumar et al scalp arteriovenous malformation the lesion. the vital signs were stable and all other systems were normal. ultrasound showed mixed echoic lesions in scalp soft tissue planes which are supplied by dilated, tortuous (serpigenous) vessels. color doppler revealed high velocity low resistance arterial flow is seen. non contrast ct head revealed soft tissue component with mild tortuously in the extracranial soft tissue scalp anteriorly on left side. underlying bones are normal. no intracranial communication seen (figure 2). mr angiography showed high flow vascular malformation comprises multiple tortuous and dilated extra cranial arcade in the scalp particularly at the high frontal and vertex region with feeders coming from the branches of bilateral superficial temporal, occipital arteries, branches of external carotid arteries and supraorbital arteries, branches of facial arteries forming small nidus and vinous drainage in to scalp veins (figure 3). after discussion of risk and benefits patient underwent gross total excision of scalp avp. the pathological diagnosis of the patient was consistent with avm. the histopathological specimen contained various well-developed arteries and dilated veins in the connecting tissue. the patient was discharged with no postoperative problems. discussion avm of the scalp is an uncommon entity. (9, 10) the vascular malformation of the scalp is an abnormal arteriovenous communication situated within the subcutaneous fatty layer of the scalp with the feeding arteries derived from the vessels supplying the scalp. various names are used to describe the vascular malformations of the scalp, including aneurysm cirsoides, aneurysm serpentinum, plexiform angioma, arteriovenous fistula, and avm. the most frequent sites of involvement are frontal, temporal, and parietal regions. (11, 12, 13, 14) the origin of the main feeder is in the subcutaneous tissue of the scalp. the origin of these main feeders, most frequently, arises from the external carotid, occipital, and supraorbital arteries. the superficial temporal artery is frequently involved in traumatic cirsoid aneurysm due to its long unprotected course. (4) figure 1 lesion over scalp romanian neurosurgery (2018) xxxii 1: 151 155 | 153 figure 2 mri brain with axial, saggital and coronal cuts with no intracranial pathology figure 3 mr angiography showed high flow vascular malformation comprises multiple tortuous and dilated extra cranial arcade in the scalp particularly at the high frontal and vertex region with feeders coming from the branches of bilateral superficial temporal, occipital arteries, branches of external carotid arteries and supraorbital arteries, branches of facial arteries forming small nidus and vinous drainage in to scalp veins 154 | kumar et al scalp arteriovenous malformation spontaneous avm of the scalp may present at birth, but in most patients, it is asymptomatic until adulthood. traumatic avm of the scalp develops months or years after the scalp trauma. about 10 to 20% of scalp avms develop following penetrating or non-penetrating trauma to the scalp. clinical signs are associated with the size of the avm. the patients may present with headache, numbness, and/or hemorrhage. others may present with severe symptoms such as scalp lesions. hemorrhage is generally uncommon and may develop in the event of large vascular malformations. recurrent hemorrhage, which rapidly deteriorates the neurological table, may be seen in some of the patients. (15) most of the patients reported in the literature had a history of progressive increase in the size of the lesion and had become symptomatic in the third decade of life.(10,16) angiography is the gold standard investigation to delineate the lesion and to exclude an intracranial component.(17) management of scalp arteriovenous malformation is difficult because of its high shunt flow, complex vascular anatomy and cosmetic problems. the indication of treatment includes cosmetic relief of the pulsatile mass, prevention of hemorrhage and other symptoms such as headache and tinnitus. the treatment options include surgical excision, (2) ligation of feeding vessels, transarterial and transvenous embolization, (3 4) injection of sclerosant into the nidus (5 6) and electro thrombosis. (7 8) surgical excision is the most common and successful method of dealing with scalp arteriovenous malformation. (10, 16)various techniques have been used to control the hemorrhage during surgery including percutaneous sutures of the feeding vessels, interlocking suture along the line of incision, and use of tourniquet and intestinal clamp over the base of the flap. (18) a step-wise incision as suggested by other authors with careful pressure control is a useful method to control the scalp bleeding. we reflected the pericranium along with the scalp flap to prevent inadvertent rupture of the nidus. contrary to some reports, we did not find any significant pericranial component of the malformation. as scalp avm has a potential to evolve, the anomalous arteriovenous communication must be completely eliminated because recurrence or enlargement is reported after an incomplete treatment. incomplete treatment can also cause scalp necrosis and bleeding. we have used a wide based scalp flap including uninvolved scalp arteries and ligation of the feeding artery near the nidus to prevent scalp necrosis. kumar et al series of 31 patient concluded preoperative embolisation with cyanoacrylate or sclerosent agent followed by surgical excision gives better results compare to direct excision. preoperative embolisationn reduses vascularity, and helps in easy identification of avm during surgery thus achieving complete excision. despite these treatments, recurrence due to feeding collaterals may develop. the most important step is total surgical excision without causing scalp necrosis and excessive blood loss. furthermore, a better cosmetic result may be obtained. romanian neurosurgery (2018) xxxii 1: 151 155 | 155 conclusion the ultimate aim of scalp avm treatment is to give the patient′s comfort by eliminating the sypmtoms. treatment options include surgery, endovascular/percutaneous embolization, electrothrombosis, and combined approaches. definitive treatment may be provided with embolization in those patients with appropriate angiographic characteristics. in the event of scalp necrosis and excessive blood loss, total excision is the treatment of choice. correspondence dr. asheesh kumar gupta m.ch. resident department of neurosurgery g.r. medical college gwalior. adressroom no. 39 senior boys hostel g.r. medical college gwalior mobile no.7828832632 emailasheesh_gsvm@yahoo.com references 1. hasturk ae, erten f, ayata t; giant nontraumatic arteriovenous malformation of the scalp. asian journal of neurosurgery. 2012; 7(1): 39-41. 2. domingo z, fisher-jeffes nd, devilliers jc. surgical management of arteriovenous malformations of the scalp. in schmidek hn, editor. operative neurosurgical techniques: indications, methods and results. 4th ed. philadelphia: saunders company; 2000. p. 1331-8. 3. nagasaka s, fukushima t, goto k, ohjimi h, iwabuchi s, maehara f. treatment of scalp arteriovenous malformation. neurosurgery 1996;38:671-7. 4. barnwell sl, halbach vv, dowd cf, higashida rt, hieshima gb. endovascular treatment of scalp arteriovenous fistulas associated with a large varix. radiology 1989;173:533-9. 5. mourao gs, hodes je, gobin yp, casasco a, aymard a, merland jj. curative treatment of scalp arteriovenous fistulas by direct puncture and embolization with absolute alcohol. report of three cases. j neurosurg 1991;75:634-7. 6. hendrix le, meyer ga, erickson sj. cirsoid aneurysm treatment by percutaneous injection of sodium tetradecyl sulfate. surg neurol 1996;46:557-60. 7. gardner amn, stewart ia. treatment of arteriovenous malformation by endarterial electrocoagulation. br j surg 1972;59:146-8. 8. heilman cb, kwan es, klucznik rp, cohen ar. elimination of a cirsoid aneurysm of the scalp by direct percutaneous embolization with thrombogenic coils. case report. j neurosurg 1990;73:296-300. 9. senoglu m, yasim a, gokce m, senoglu n. nontraumatic scalp arteriovenous fistula in an adult: technical report on an illustrative case. surg neurol. 2008;70:194–7. 10. muthukumar n, rajagopal v, manoharan av, durairaj n. surgical management of cirsoid aneurysms. acta neurochir (wien) 2002;144:349–56. 11. shenoy sn, raja a. scalp arteriovenous malformations. neurol india. 2004;52:478–81. 12. massimi l, de bonis p, esposito g, novegno f, pettorini b, tamburrini g, et al. vertex scalp mass as presenting sign of a complex intracranial vascular malformation. j neurosurg pediatr. 2009;3:307–10. 13. heilman cb, kwan es, klucznik rp, cohen ar. elimination of a cirsoid aneurysm of the scalp by direct percutaneous embolization with thrombogenic coils.case report. j neurosurg. 1990;73:296–300. 14. burrus tm, miller gm, flynn lp, fulgham jr, lanzino g. neuroimages. symptomatic left temporal arteriovenous traumatic fistula. neurology. 2009;73:570. 15. fisher-jeffes nd, domingo z, madden m, de villiers jc. arteriovenous malformations of the scalp. neurosurgery. 1995;36:656–60. 16. khodadad g. arteriovenous malformation of the scalp. ann surg 1973;177:79-85. 17. wilkinson ha. recurrence of vascular malformation of the scalp 18 years following excision. case report. j neurosurg 1971;34:435-7. 18. hochberg j, ardenghy m, pait tg. scalp tourniquet. br j plast sur 1994;47:194-8. 18 18kumarguptaasheesh_scalparteriovenous romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article surgical treatment of preschool childhood spinal thoracic tuberculosis: two case reports and technical note mehmet nuri erdem, anas abdallah, sinan karaca, mehmet aydoğan turkey doi: 10.2478/romneu-2018-0010 romanian neurosurgery (2018) xxxii 1: 85 93 | 85 doi: 10.2478/romneu-2018-0010 surgical treatment of preschool childhood spinal thoracic tuberculosis: two case reports and technical note mehmet nuri erdem1, anas abdallah2, sinan karaca3, mehmet aydoğan4 1department of orthopaedic surgery, hisar intercontinental hospital, umraniye/istanbul, turkey 2department of neurosurgery, bezmialem vakif university, istanbul, turkey 3department of orthopaedic surgery, fatih sultan mehmet training and research hospital atasehir, istanbul, turkey 4orthopaedist, fulya orthopaedic and spine institute, istanbul, turkey abstract: background: the development of paraplegia and kyphosis are two important problems related to spinal tuberculosis (pott’s disease) in children. the current study aims to present two pediatric pott’s disease, point out the progression of this disease in children, surgical options and surgical outcomes. materials and methods: two cases of childhood pott’s disease were referred to our department with progressive neurological deficits (both of children were experienced bilateral weakness in lower extremities; grade c according to frankel scale) during short periods (less than one month per each). both cases’ mris are demonstrated abscesses in thoracic spine. both patients are treated surgically. we discussed in this study the technical notes in both cases, especially in 2year-old child. results: both cases were treated surgically after decompressing nerve roots and thecal sac posterior instrumentation was applied. microbiological examination of both samples revealed on m.tuberculosis. orthoses are applied three months after operations. antituberculosis medication protocol was applied. preoperative paraparesis had recovered completely and muscle strengths all returned to normal in both children. there is no loss of correction during the follow-up periods. conclusion: spinal tuberculosis is a dynamic disease that may lead to severe deformities in childhood. especially in cases where two or more vertebrae are affected, early surgical treatment is essential to prevent severe kyphosis. surgical intervention accompanied with antituberculosis medications protocol is essential to cure treatment in pediatric population. in children aged ≤6 years and more than one vertebrae were affected, fıbula can be used to allow growth of the child vertebral column. key words: childhood pott’s disease, corpectomy, instrumentation, spinal tuberculosis, fibula as autograft 86 | erdem et al surgery of preschool childhood pott's disease introduction spinal tuberculosis (pott’s disease), is the most common form of extrapulmonary tuberculosis. the incidence of this condition has shown a rapid increase recently in especially undeveloped or developing countries [1]. unfortunately, spinal tuberculosis in children is different from their adult counterpartners. in the treatment of the child spinal tuberculosis, we have to find answers to two major questions; first, what is the clinical presentation of child patient who was involved with pott's disease? second, does medical treatment sufficient to treat child patient? recent technological advancements in diagnosis of spinal tuberculosis in adults have not been validated in children. for example, mri scanning in preschool children needs general anesthesia. similarly, trials of new medications and development of pediatric formulations of standard firstand second-line medications are lagging behind [2]. although the condition can be successfully treated with antituberculosis medications, the development of paraplegia, kyphosis and even sharp angular kyphosis (gibbous) deformity are significant problems. especially childhood spinal tuberculosis with destruction of two or more thoracic vertebrae may result in severe spinal tuberculosis and a progressive kyphosis deformity that exceeds 100 degrees may occur. these deformities are often associated with neurologic deficits and respiratory problems [3]. in such cases, medical treatment will not be sufficinet to correct such deficits and deformities without surgery. in the present two reports, the authors aim to present the surgical techniques and outcomes of pott’s diseases in preschool pediatric population. pott’s disease acts progressively in preschool children, however, surgical intervention combined with antituberculosis medications gives good results. case reports first case report a 4-year-old boy was referred to our department with back pain and failure to walk that began one month ago and progressed thereafter. he had severe spastic paraparesis and his neurologic condition was assessed as grade c according to the frankel scoring system. mri showed destruction at t 4-5-6 levels, proximal thoracic gibbous deformity, and that the local kyphosis angle between t3t7 had increased to 71 degrees (figure 1 a, b, c). a paraspinal abscess that caused severe anterior compression at t4-5-6 levels and compression of the spinal cord due to destruction in the vertebrae were detected. destruction of discs and bones was notably. therefore, presumptive diagnosis was that of pott’s disease. surgical procedure under general anesthesia and using intraoperative neurophysiological monitoring (ionm) the patient is positioned prone using supporting roll on each side to preserve the current kyphosis. a midline skin incision is performed between spinous processes of t1 and t9. after dissecting the paraspinal muscles which are retracted laterally. the laminae and transverse processes between t2t8 are exposed. bilateral pedicle screws were inserted at t2-3 proximally, and t7-8 distally, then an appropriately shaped temporary rod was placed to the right and locked (stryker romanian neurosurgery (2018) xxxii 1: 85 93 | 87 xia pediatrics). total posterior laminectomies are performed at levels t4-t5t6. the abscess drainage is done upon opening of the posterior lamina. the dissection is advanced bilaterally at levels t4t5-t6, exposing the costotransverse joints and the proximal aspects of the ribs. after the pleura is carefully stripped off the vertebrae, the heads of the 4th, 5th, and 6th ribs are bilaterally excised together with costotransverse joints paraspinal dissection is completed by bilateral ligation of t4-5-6 nerve roots. the dissection is advanced retropleurally, between the vertebra and pleura. first the t3-t4 disc, followed by the t6-t7 disc, are evacuated and the disc spaces are cleaned with osteotomes and curettes. the vertebral bodies of t4-5-6 are removed together with sequestered bone fragments. the surgical field is irrigated with copious saline. dura decompression is performed fully, thus spinal cord compression is removed. the closing-opening wedge osteotomy, described by rajasekaran et al. [3], is performed and correction is achieved without traction or folding of the spinal cord. rods contoured according to physiologic kyphosis are implanted. then a mesh cage, filled with allogenous graft, is placed between corpuses of t3 and t7. this followed by the posterior compression (figure 2a, 2b). the correction is evaluated using fluoroscopy, then the system is locked over the rods. especially during the correction stage, the neurologic condition is controlled using ionm through the operation. no neurologic complications were recorded during or after the operation. figure 1 1.case’s preoperative mri demonstrated a large paraspinal abscess and kyphosis. [a]: sagittal t2weighted image; [b]: coronal t2-weighted image: abscess formalation was indicated by (*); [c]: preoperative ct scan images 88 | erdem et al surgery of preschool childhood pott's disease figure 2 1.case’s early postoperative radiographic images. [a]: lateral plain; [b]: ap plain second case report a 2-year-old boy presented with severe back pain and paraparesis of one-month duration. neurological examination revealed a paraparesis, which was evaluated as grade c according to frankel scoring system. thoracic mri demonstrated destruction with a large paraspinal abscess involving t5-t6-t7 levels, compressing the spinal cord (figure 3) [4]. destruction of discs and bones at the same time was notably. therefore, presumptive diagnosis was that of pott’s disease. x-rays of chest and thoracic spine showed destruction at the t5-t6-t7 levels and the local kyphosis angle was 37° at this level (figure 4b). there was no other infection focus in physical examination, radiological, hematological and biochemical tests. emerge surgical procedure was performed after preoperative evaluation was completed. romanian neurosurgery (2018) xxxii 1: 85 93 | 89 surgical procedure under general anesthesia using transthoracic approach after removing the fifth rib in right side and ionm the patient is positioned lateral decubit position. after exposure, the paraspinal abscess drained spontaneously. t5, 6 and t7 corpectomies are performed. decompression was carried out until duramater was visible through anterior approach, so all affected vertebrae are extracted. anterior fusion is performed with structural one autogenous fibula and one autogenous rib graft. periost of the fibula is prevented and closed anatomically after resection. anterior instrumentation using one screw to each vertebra at t4 and t8 is performed. the system is locked, thorax drainage system is applied and thoracotomy is closed. the patient is positioned prone. bilateral polyaxial pedicle screws are inserted at t4 and t8 levels and rods are placed for permanent fixation. pediatric spinal screw systems are preferred for the immature pedicles (figure 4a, 4c, 4d). figure 3 2. case’s preoperative mri; sagittal, axial and coronal t2-weighted images 90 | erdem et al surgery of preschool childhood pott's disease figure 4 2. case’s intraoperative and radiographic images. [a]: intraoperative photo shows anterior instrumentation with structural autogenous fibula and autogenous rib grafts; [b]: preoperative ap plain x-ray; [c]: postoperative sixth week ap plain x-ray; [d]: postoperative sixth week lateral x-ray postoperative period microbiological examination of both samples which were obtained from the abscesses and soft tissues revealed on mycobacterium tuberculosis. a minerva orthosis in first case and thoracolumbosacral orthoses in second case are applied three months after operations. antituberculosis treatment protocol was applied for nine months (inh-rifampicin-pyrazinamidestreoptomycin for 3 months, followed by inhrifampicin-pyrazinamide). the patients were discharged five and eight days after the operations, respectively. 1. case could walk inside the room with the help of an orthosis. 2. case could sit on the bed or walk around one week after surgery. on their 6th week, preoperative paraparesis had recovered completely, muscle strengths all returned to normal and the neurologic condition was evaluated as frankel e in both children. on their 6th, 12th, 24th and 36th (for second case) month follow-up visits, local kyphosis angle between both of t3 and t7 measures 31 and 32 degrees, respectively. there is no loss of correction during the follow-up period. romanian neurosurgery (2018) xxxii 1: 85 93 | 91 discussion vertebral tuberculosis is an instable lesion that progresses until bone fusion, and the best proof that it has healed is formation of fusion [5]. in general, kyphosis is detected in more than 80% of the patients at the time of referral [6]. the disease is cured with antituberculosis drugs, however the deformity persists. in cases with severe bone destruction, the healthy vertebra moves forward and makes contact with the distal healthy vertebra. these patients (3-5%) end up with greater than 60 degrees deformity [7]. the final outcome of the deformity depends on the initial vertebral destruction, patient’s age and the level of the lesion [8]. the pott's disease is relatively rare diagnosed in preschool children. recently published study reported 43 cases of pott's disease which were diagnosed in patients aged between 10-69 years [9]. despite the fact that the study was carried out in younde which is considered as one of the endemic regions of pott's disease, the study did not report any preschool pott's patient. the pediatric spine is more flexible and prone to destruction. unfortunately, if the deformity at the time of diagnosis is greater, it has a greater tendency for collapse during recovery [8]. additionally, the progression of the deformity continues once the disease has healed, because of continued skeletal growth [3]. in preschool pediatric patients (< 6 years), the correction surgery still a challenge for spine surgeons. in case 1, we could have avoided cutting nerve roots on one side as we need to more space on the side from where we want to insert the cage, while on the other side, only debridement is needed that can be done without cutting the nerve roots. we could have used fibula in this case too as fibula has the tendency to increase its diameter with growth. case 2 is only 2 years old, without much kyphotic deformity. we could have just done costotransversectomy, draining the abscess and posterior fusion at that level to avoid crankshaft phenomenon in future, followed by chemotherapy. to understand those spinal tuberculosis cases under a risk of progressive deformity, rajasekaran et al. tried to determine some of the factors during the early phase of the disease. according to their study, facet joint separation; posterior retropulsion of the affected vertebral segment; lateral translation of the vertebral column; and anterior contact of the upper and lower healthy vertebra due to anterior movement of the upper healthy vertebra are defined as risk factors, and the authors emphasized the signficance of achieving bone fusion during the early phase by treatment [10]. numerous options have been defined for the surgical treatment of spinal tuberculosis, including anterior debridement and arthrodesis [11], plates and screws [12, 13], titanium cages [14], and posterior instrumentation combined with single or two staged anterior decompression [15, 16]. fusion with anterior debridement and autogenous bone grafts are accepted as the classical method. it provides effective debridement, a rapid bone union occurs with grafts, also the kyphosis and progressive collapse are prevented [17]. however in cases where two or more levels are affected, it is 92 | erdem et al surgery of preschool childhood pott's disease more difficult to obtain successful results with this method because of graft failure and progressive kyphosis deformity [1, 12, 18]. anterior radical debridement and/or posterior instrumentation are necessary to preserve the achieved correction [18, 19]. according to our experience, in spinal tuberculosis cases with severe kyphosis where 2 or more areas are affected, titanium cage and 360° with posterior instrumentation method provides effective stabilization, early mobilization, effective correction of the kyphosis and maintaning the correction after the operation [15]. despite that the fact appropriate antituberculosis therapy is still the basis of treatment of tuberculosis in general and of pott’s disease in particular, surgerical intervention still plays a diagnostic and therapeutic role especially in cases which patients referred at a late stage after complications have developed (spinal compression, deformity and instability). presence with severe neurological deficit at surgery is an important prognostic factor. surgical decompression should be early as soon as possible before a total neurological deficit is developed, which signifies the presence of irreversible, ischemic lesions (frankel a) [9]. in patients with sharp angle gibbosity having also severe bone destruction, corpectomy with the posterior approach to avoid the morbidity of decompression through the anterior route, evacuation of the area anterior to the spinal cord, and gradual correction of local kyphosis with closingopening wedge osteotomy is an effective and reliable method [2]. in order to increase the stability of the cage placed into the corpectomy area and maintain the correction achieved, a posterior instrumentation was also performed. in a study which discussed the safety of transpedicular instrumentation was the best method for achieving a stable fixation in children [20]. the major limitation of this study was presence of two preschool pediatric pott's disease which were analyzed retrospectively. randomized prospective controlled studies with larger series and a longer follow-up period are required in the future. conclusion in cases of thoracic vertebral osteomyelitis with severe anterior column destruction in the toddlerhood (preschool period) age, the use of anterior structural grafts and instrumentation in combination with posterior instrumentation is safe and effective in maintenance of the correction achieved and allows efficient stabilization and early mobilization. however, thoracic spinal tuberculosis cases cause severe anterior column destruction in preschool children, posterior instrumentation, corpectomy and closing-opening wedge osteotomy approach is enough. correspondence anas abdallah, md department of neurosurgery, bezmialem vakif university, adnan menderes bulvari, vatan street, 34093 fatih, istanbul, turkey e-mail: abdallahanas@hotmail.com; aabdallah@bezmialem.edu.tr phone: +90 212 5232288-2175 cell-phone: +905532233535fax: +90212 453 18 69 romanian neurosurgery (2018) xxxii 1: 85 93 | 93 references 1.moon ms: spine update: tuberculosis of the spine. spine 1997; 22: 1791–1797. 2.swaminathan s, rekha b: pediatric tuberculosis: global overview and challenges. clinical infectious disease 2010; 50(53): s184–s194. 3.rajasekaran s, kanna prm, shetty ap: closing – opening wedge osteotomy for severe, rigid, thoracolumbar post – tubercular kyphosis. eur spine j 2011; 20: 343–348. 4.erdem mn, sever c, korkmaz mf, karaca s, kirac f, tezer m: pott’s disease in 2-year-old child treated by decompression and anterior-posterior instrimented fusion (case report): case report in orthopedics 2014; 2014: article id 252973. 5.boachie-adjei o, squillante rg: tuberculosis of the spine. orthop clin north am 1996; 27: 95–103. 6.moon ms, lee mk: the changes of the kyphosis of the tuberculous spine in children following ambulant treatment. korean orthop assoc 1971; 6: 203–208. 7.yilmaz c, selek hy, gurkan i, erdemli b, korkusuz z: anterior instrumentation for the treatment of spinal tuberculosis. j bone joint surg (am) 1997; 81: 1261–1267. 8.rajasekaran s: the problem of deformity in spinal tuberculosis. clin orthop 2002; 398: 85–92. 9.djientcheu vp, mouafo tambo ff, ndougsa is, eloundou nj, kouna tsala in, ngowe ngowe m, andze og, sosso ma: the role of surgery in the management of pott's disease in younde. a review of 43 cases. orthopaedics and traumatology: surgery et research 2013; 99? 419–423. 10.rajasekaran s: the natural history of childhood spinal tuberculosis: a 15-year prospective study. j bone joint surg br 2001; 83: 954–962. 11.medical research council working party on tuberculosis of the spine: a 10-year assessments of controlled trials comparing debridement and anterior spinal fusion in the management of tuberculosis of the spine in patients on standard chemotherapy in hongkong. j bone jt surg (br) 1982; 64: 393–398. 12.benli it, acaroğlu e, akalın s, kis m, duman e, un a: anterior radical debritment and anterior instrumentation in tuberculosis spondylitis. eur spine j 2003; 12: 224–234. 13.ruf m, harms j: pedicle screws in 1and 2-year-old children: technique, complications, and effect on further growth. spine 2002; 27: 460–466. 14.hee h, majd m, holt r, pienkowski d: better treatment of vertebral osteomyelitis using posterior stabilisation and titanium mesh cages. j spinal disord 2002; 15: 149–156. 15.erturer e, tezer m, aydogan m, mirzanli c, ozturk i: the results of simultaneous posterior–anterior–posterior surgery in multilevel tuberculosis spondylitis associated with severe kyphosis. eur spine j 2010; 19: 2209–2215. 16.moon ms, woo yk, lee ks, kim ss, sun dh: posterior instrumentation and anterior interbody fusion for tuberculous kyphosis of dorsal and lumbar spine. spine 1995; 20: 1910–1916. 17.hodgson ar, stock fe: anterior spinal fusion: preliminary communication on radical treatment of pott’s disease and pott’s paraplegia. clin orthop relat res 1994; 300: 16–23. 18.kim dj, yun yh, moon sh, riew kd: posterior instrumentation using compressive laminar hooks and anterior interbody arthrodesis for the treatment of tuberculosis of the lower lumbar spine. spine 2004; 29: 275–279. 19.fukuta s, miyamoto k, masuda t, hosoe h, kodama h, nishimoto h, sakaeda h, shimizu k: two-stage (posterior and anterior) surgical treatment using posterior spinal instrumentation for pyogenic and tuberculotic spondylitis. spine 2003; 28: 302–308. 20.tuli sm: severe kyphotic deformity in tuberculosis of the spine. int orthop 1995; 19: 327–333. 10 10erdemmehmet nuri_surgical treatment doi: 10.33962/roneuro-2021-050 surgical site infections in neurosurgery. case series in a single centre alberic fabrice bocco, lievin panu, abdelmajid chellaoui, abdelhakim lakhdar, abdessamad naja romanian neurosurgery (2021) xxxv (3): pp. 304-308 doi: 10.33962/roneuro-2021-050 www.journals.lapub.co.uk/index.php/roneurosurgery surgical site infections in neurosurgery. case series in a single centre alberic fabrice bocco, lievin panu, abdelmajid chellaoui, abdelhakim lakhdar, abdessamad naja department of neurosurgery, ibn rochd university hospital centre, casablanca, morocco abstract background: surgical site infections in neurosurgery are serious due to their proximity to the central nervous system and their management is a challenge. the aim of our work is to report surgical site infections (ssi) in patients who underwent brain or spinal surgery and to describe their characteristics. materials and method: we conducted a retrospective study involving patients who underwent surgery in our facility's neurosurgical emergency department over 5 years from january 2015 to december 2019. the data were collected from medical hospital and follow-up records. results: fifty-eight cases of ssi were identified out of 2889 operations in total, for a frequency of 2%. the series consisted of 36 men (62.07%) and 22 women (37.93%). the average age was 43.9 years (19-72 years). 46 patients (79.31%) had undergone urgent surgery and 12 patients (20.69%) for delayed surgery. 40 patients (68.97%) had undergone cranial intervention and 18 patients (31.03%) underwent spinal surgery. the identified germ was staphylococcus aureus in 13 cases (76.48%). mortality was 13.8% (8 out of 58 cases). conclusion: the majority of microorganisms that cause the infections contaminate the surgical site intraoperatively. preventive measures can reduce the rate of surgical site infections. introduction the incision of the skin barrier to perform the surgical procedure connects the inner environment with the external environment. postoperative infections are the result of exogenous or endogenous contamination not controlled by the body's local and general defenses. this iatrogenic risk rises due to increased accessibility of surgical procedures and the development of surgical services activity. surgical site infections (ssi) are a challenge for all surgical services. neurosurgical site infections are severe because of their proximity to the central nervous system and their potential complications. ssi support also has a significant financial impact [1]. understand the risk factors and identify the pathogens germs are essential to the management. keywords infections, neurosurgery, surgical site corresponding author: alberic fabrice bocco department of neurosurgery, ibn rochd university hospital centre, casablanca, morocco fabricebocco@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 305 surgical site infections in neurosurgery the purpose of our work is to report surgical site infections in patients who have had cranial and spinal surgery in a neurosurgical emergency unit and to describe their characteristics. materials and method this is a retrospective study that focused on patients operated in a neurosurgical emergency department of our institution over a period of 5 years from january 2015 to december 2019. patients who underwent neurosurgical procedures and follow-up postoperatively were included. the data were collected from medical hospital and follow-up records. the variables studied were: age, sex, patient origin, type of intervention, antibiotic prophylaxis, surgical indication and site of intervention, duration of surgery, type of germs identified, evolution. quantitative variables were presented as an average. the qualitative variables in the form of a percentage. urgent surgery was defined as a surgical procedure that was performed within the first 48 hours of admission, and delayed surgery was a procedure that took after 48 hours. the classification of narotam [2] was used to classify the type of intervention into categories to determine the potential to develop sepsis: clean, clean with foreign body, clean-contaminated, contaminated, dirty. results fifty-eight cases of surgical site infections were identified out of 2889 operations in total, for a frequency of 2%. the average age was 43.9 years (1972 years). the series consisted of 36 men (62.07%) and 22 women (37.93%). 34 patients (58.62%) lived in urban areas and 24 patients (41.37%) in rural areas. 46 patients (79.31%) had undergone urgent surgery and 12 patients (20.69%) for delayed surgery. 40 patients (68.97%) had undergone cranial intervention and 18 patients (31.03%) underwent spinal surgery. according to narotam's classification, surgical procedures were clean in 4 cases (6.3%), cleancontaminated in 6 cases (9.4%), contaminated in 16 cases (25%), and dirty in 32 cases (59.4%). the average duration of the intervention was 260 minutes with extremes ranging from 45 minutes to 540 minutes. the average length of hospitalization was 13 days with extremes of 6 days to 45 days. all patients had benefited from prophylactic antibiotics. table 1 summarizes the characteristics of patients who developed a surgical site infection. table 1. general characteristics of patients with ssi variables number of patients percentage (%) sex female 22 37.93 male 36 62.07 origin rural 24 41.37 urban 34 58.62 type of surgery urgent 46 76.31 delayed 12 20.69 wound classification clean 04 06.30 clean-contamined 06 09.40 contamined 16 25.00 dirty 32 59.40 table 2. initial procedure performed to patients and diagnosis of the ssi variables number of patients percentage (%) craniotomy procedures traumatic 36 90.00 tumoral 02 05.00 infectious 02 05.00 spine surgery procedures traumatic 08 44.44 degenerative 07 38.89 tumoral 03 16.67 diagnosis of ssi in cranial location superficial wound infection 07 17.50 osteitis 02 5.00 meningitis 24 60.00 abcess or empyema 07 17.50 diagnosis of ssi in spinal location superficial wound infection 06 33.33 meningitis 02 11.11 deep infection 10 55.56 initial surgical indications in cases of surgical site infection at the cranial level were traumatic in 36 cases (90.00%), tumor, and infectious each in 2 cases (5.00%). the supratentorial location was reached in 306 alberic fabrice bocco, lievin panu, abdelmajid chellaoui et al. 34 cases (85%), and infratentorial in 6 cases (15%). the distribution of the type of cranial infection was: superficial wound infections in 7 cases (17.50%), osteitis in 2 cases (5.00%), meningitis in 24 cases (60.00%), abscess or empyema in 7 cases (17.50%). in the cases of surgical site infection at the spinal level, the surgical indications were traumatic pathologies in 8 cases (44.44%), degenerative in 7 cases (38.89%) and tumors in 3 cases (16.67%). the location of the infection was cervical in 1 case (5.55%), dorsal in 10 cases (55.56%), dorsolumbar in 4 cases (22.22%), and lumbar in 3 cases (16.67%). the type of infection at the operative site after spinal surgery was: superficial wall infection in 6 cases (33.33%), meningitis in 2 cases (11.11%), and deep infection on osteosynthesis material in 10 cases (55.56 %). table 2 summarizes the indications for the initial procedure and the type of infections presented by patients. hyperleukocytosis was found in 24 patients (41.37%) and an increase in the c-reactive protein in 26 patients (44.82%). the culture was positive in 29.31%of cases (17 patients). the most frequently identified germs were: staphylococcus aureus in 13 cases (76.48%), pseudomonas aeruginosa 1 case (5.88%), escherichia coli 1 case (5.88%), proteus mirabilis 1 case (5.88%), enterobacter cloacae 1 case (5.88%). full recovery without significant neurological sequelae was in 75.9% of cases. six patients had epilepsy (10.3%). in all mortality was 13.8% (8 cases) in the series. discussion prevalence and risk factors in our series, the prevalence of postoperative neurosurgery infections was 2%. the rate varies between 0.5% and 8% in studies [1,3–5]. the effect of prophylactic antibiotics helps to control the infection rate of less than 5% [6]. in our study, the low rate could be explained by routinely prophylactic antibiotics in all patients. antibiotic prophylaxis alters the morbidity of surgical operations. the rate of postoperative meningitis is decreased by antibiotic prophylaxis [7]. several risk factors for surgical site infections have been reported [5,8–11]. a long operation duration has been reported by several studies [8,9,11,12]. an intervention time of more than 4 hours increases the risk of developing a ssi [8,13]. in our series, the average duration was 4 hours and 20 minutes which was relatively high. males were considered as a risk factor [13]. however, another study [14] showed that male sex, age, alcohol consumption, and steroid use were not associated with increased incidence of spinal ssi. an urgent surgery remains an important risk factor for ssi [8]. in our work, 79.3% of postoperative infections were admitted through emergencies. patients admitted as an emergency, especially in the traumatic setting, carry scalp injuries contaminated by foreign debris. in our study, the initial procedure of the ssi was considered clean in only 6.3% of cases. the presence of foreign bodies was significantly associated with a risk of developing postoperative infection [5,8]. other risk factors for ssi were: a high american society of anesthesiologists score (asa) [12,13], sinus opening [8], an intervention considered contaminated [10,12], a csf leak [13,14]. closure of surgical wounds by staples and use of dural substitute was also reported as risk factors in a study [11]. in the same study, craniotomy was identified as a risk factor and a complicated surgical procedure as a predictor in the development of ssi [11]. tumor surgery was the most difficult type of intervention for deep infections [4]. in our study, traumatic surgery was the most performed intervention because our unit was dedicated to the management of neurosurgical emergencies. the surgeon's experience plays a role in the risk of infection [12]. an experienced surgeon contributes to the reduction in the duration of the operative procedure and therefore to the reduction of postoperative infectious complications. postoperative drainage would increase the risk of infection [12]. several general factors have been reported as purveyors of post-operative infections. these factors associated with postoperative infection were: diabetes [5], intraoperative blood transfusion [12], use of immunosuppressors [15], urinary tract infection, and smoking in spinal surgery [14]. in our series, diabetes was found in 10 patients and no patients had immunosuppressors medication. pathological entities of ssi the superficial wound infection and flap osteitis are not grouped into the same category of infections. although the pathophysiology is similar, their consequences and their management are very different. in the case of superficial wound infection, 307 surgical site infections in neurosurgery antibiotics alone or debridement can be achieved. in the case of osteitis, aggressive surgery associated with re-reconstruction can be required. in our series, superficial wound infections were 26% of all ssi. deep infections that affect the central nervous system are serious and can be accompanied by significant morbidity with a high risk of neurological damage. meningitis was commonly found and can have lethal complications. in our series, meningitis is the most common infection after cranial procedures but its frequency was lower in the spinal procedures. ventriculitis is an evolutionary complication of meningitis that affects the cranial ventricular cavities and often causes severe damages. in our series, no cases of ventriculitis were observed. intracranial suppurations most often develop by contiguousness with a local outbreak, but also by the hematogenic path of parenchyma. in our series, intracranial suppurations were diagnosed in 7 out of 40 patients or 17.50%. the most common complication in our series at the spinal level is an infection on osteosynthesis material. the use of foreign materials is a predictor in the development of ssi. pathogen germs before starting antibiotic treatment, bacteriological documentation is imperative to guide antibiotic therapy for these postoperative bacterial infections depending on the germ in question and its sensitivity. the bacteriological examination of the csf and the samples from the surgical site is essential and culture was performed to identify pathogens germs. the germs implicated in postoperative infections are different from those identified in community-acquired infections. in our series, the most frequently identified pathogenic germ was staphylococcus aureus in 76.48% of cases. the most common pathogens in the literature are staphylococcus aureus [3–5] and gram-negative bacilli [4,5,16] namely acinetobacter baumanii [5,17] and pseudomonas aeruginosa [16,17], and escherichia coli [16,17]. other germs such as propionibacterium acnes can also be found [3,10]. the majority of microorganisms that cause the infections contaminate the surgical site intraoperatively. the ecosystem of the unit must be known to allow the prescription of a good probabilistic antibiotic therapy taking into account the bacterial resistance specific to each institution. the management of ssi requires a multidisciplinary approach. the urgency of starting antibiotic therapy varies from situation to situation, but delays in some cases, such as meningitis and intracranial suppurations, can be lethal. the choice of antibiotic is based on bacteriological data and the antibiotic. the front door must be treated urgently if it exists. corticosteroids could decrease the penetration of antibiotics and the use of mannitol may be preferable during the first 48 hours. prevention efforts in operating theatres to improve the quality of care, the determination of clean and dirty circuits can significantly reduce the rate of post-operative infections. recommendations for ssi prevention are surgical handwashing and the use of antibiotic prophylaxis [10]. decolonization oriented towards staphylococcus aureus reduces the frequency of ssi [18]. postoperatively, other recommendations are the observance of rigorous asepsis when handling drains and dressings, as well as strictly enclosed maintenance of the drainage system. surgical drainage of the surgical site should not exceed 48 hours. conclusion this study presents the profile of surgical site infections, and the germs involved in our neurosurgical emergency unit. the most common germs are staphylococcus aureus and less commonly gram-negative bacilli. the majority of microorganisms that cause the infections contaminate the surgical site intraoperatively. preventive measures can reduce the rate of surgical site infections. abbreviations ssi: surgical site infections csf: cerebrospinal fluid references 1. o’keeffe ab, lawrence t, bojanic s. oxford craniotomy infections database: a cost analysis of craniotomy infection. br j neurosurg. 2012;26(2):265-269. doi:10.3109/02688697.2011.626878 2. narotam pk, van dellen jr, du trevou md, gouws e. operative sepsis in neurosurgery: a method of classifying 308 alberic fabrice bocco, lievin panu, abdelmajid chellaoui et al. surgical cases. neurosurgery. 1994;34(3):409-415; discussion 415-416. doi:10.1227/00006123-19940300000004 3. mcclelland s, hall wa. postoperative central nervous system infection: incidence and associated factors in 2111 neurosurgical procedures. clin infect dis off publ infect dis soc am. 2007;45(1):55-59. doi:10.1086/518580 4. dashti sr, baharvahdat h, spetzler rf, et al. operative intracranial infection following craniotomy. neurosurg focus. 2008;24(6):e10. doi:10.3171/foc/2008/24/6/e10 5. erman t, demirhindi h, göçer ai, tuna m, ildan f, boyar b. risk factors for surgical site infections in neurosurgery patients with antibiotic prophylaxis. surg neurol. 2005;63(2):107-112; discussion 112-113. doi:10.1016/j. surneu.2004.04.024 6. haines sj, walters bc. antibiotic prophylaxis for cerebrospinal fluid shunts: a metanalysis. neurosurgery. 1994;34(1):87-92. 7. barker fg. efficacy of prophylactic antibiotics against meningitis after craniotomy: a meta-analysis. neurosurgery. 2007;60(5):887-894; discussion 887-894. doi:10.1227/01.neu.0000255425.31797.23 8. raggueneau jl, cophignon j, kind a, et al. [analysis of infectious sequelae of 1000 neurosurgical operations. effects of prophylactic antibiotherapy]. neurochirurgie. 1983;29(4):229-233. 9. valentini lg, casali c, chatenoud l, chiaffarino f, ubertifoppa c, broggi g. surgical site infections after elective neurosurgery: a survey of 1747 patients. neurosurgery. 2008;62(1):88-95. doi:10.1227/01.neu.0000311065.95496.c5 10. lópez pereira p, díaz-agero pérez c, lópez fresneña n, et al. ‘epidemiology of surgical site infection in a neurosurgery department’. br j neurosurg. 2017;31(1): 10-15. doi:10.1080/02688697.2016.1260687 11. abu hamdeh s, lytsy b, ronne-engström e. surgical site infections in standard neurosurgery proceduresa study of incidence, impact and potential risk factors. br j neurosurg. 2014;28(2):270-275. doi:10.3109/026886 97.2013.835376 12. isik o, kaya e, dundar hz, sarkut p. surgical site infection: re-assessment of the risk factors. chir buchar rom 1990. 2015;110(5):457-461. 13. fang c, zhu t, zhang p, xia l, sun c. risk factors of neurosurgical site infection after craniotomy: a systematic review and meta-analysis. am j infect control. 2017;45(11):e123-e134. doi:10.1016/j.ajic.2017.06.009 14. meng f, cao j, meng x. risk factors for surgical site infections following spinal surgery. j clin neurosci off j neurosurg soc australas. 2015;22(12):1862-1866. doi:10.1016/j.jocn.2015.03.065 15. eton v, sinyavskaya l, langlois y, morin jf, suissa s, brassard p. effect of pre-operative use of medications on the risk of surgical site infections in patients undergoing cardiac surgery. surg infect. 2016;17(5):557-562. doi:10.1089/sur.2016.007 16. chidambaram s, nair mn, krishnan ss, cai l, gu w, vasudevan mc. postoperative central nervous system infection after neurosurgery in a modernized, resourcelimited tertiary neurosurgical center in south asia. world neurosurg. 2015;84(6):1668-1673. doi:10.1016/j.wneu.2015.07.006 17. wang k-w, chang w-n, huang c-r, et al. postneurosurgical nosocomial bacterial meningitis in adults: microbiology, clinical features, and outcomes. j clin neurosci off j neurosurg soc australas. 2005;12(6):647650. doi:10.1016/j.jocn.2004.09.017 18. nusair ar, el nekidy ws, reynolds l, evans d, el-lababidi r, alatoom a. comprehensive approach to reduce surgical site infections in patients undergoing neurosurgical procedures. surg infect. 2021;22(2):217221. doi:10.1089/sur.2020.020 doi: 10.33962/roneuro-2021-036 burr-hole craniostomy versus minicraniotomy in the treatment of chronic subdural hematomas. analysis of clinical results andré tokpa, moussa diallo, louis kéabléon derou, yves soress dongo, bernard fionko, adéréhime haïdara romanian neurosurgery (2021) xxxv (2): pp. 219-224 doi: 10.33962/roneuro-2021-036 www.journals.lapub.co.uk/index.php/roneurosurgery burr-hole craniostomy versus minicraniotomy in the treatment of chronic subdural hematomas. analysis of clinical results andré tokpa1, moussa diallo2, louis kéabléon derou1, yves soress dongo1, bernard fionko1, adéréhime haïdara1 1 neurosurgery department of the teaching hospital of bouaké, côte d’ivoire 2 neurosurgery department of the teaching hospital grabriel touré, bamako, mali abstract although cases of spontaneous recovery or under medical treatment have been reported, the treatment of chronic subdural hematoma is mainly surgical. the optimal surgical technique for the treatment of chronic subdural hematomas is still open to debate. the purpose of this study was to compare the clinical outcomes between burr-hole craniostomy and craniotomy in patients with chronic subdural hematoma. materials and methods: we have performed a retrospective study in patients operated for chronic subdural hematoma in the neurosurgery department of the teaching hospital of bouaké between july 1, 2016, and june 30, 2020. we compared the data of patients operated by a single burr-hole craniostomy (group a) and those operated by minicraniotomy (group b). demographic parameters, clinical signs, complications and neurological findings were analyzed. fisher’s exact test, chisquared, and student’s t-test were performed. results: group a included 46 patients and group b 55 patients. there was no significant difference between the two groups about age (59.5 years vs 59.8 years p = 0.89), sex (man: 74% vs 78.2%, p = 0.645), comorbidities, clinical signs on admission and location of the hematoma. there was also no significant difference between recurrence rates (4.3% vs 3.6% p = 0.55), postoperative complications (15.21% vs 7.27% p = 0.172) and neurological findings between the two groups. conclusion: patient outcomes are similar in the treatment of chronic subdural hematomas by craniostomy and minicraniotomy. introduction chronic subdural hematoma (csdh) is a collection of aged blood that lies between the dura mater and the arachnoid. in many patients, it develops slowly after a mild head trauma often overlooked by them [9], but the number of patients without a history of trauma is increasing, probably due to anticoagulant or antiaggregant treatment [8]. although keywords burr hole, chronic subdural hematoma, craniotomy corresponding author: andré tokpa neurosurgery department of the teaching hospital of bouaké, côte d’ivoire valentin_tokpa@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 220 andré tokpa, moussa diallo, louis kéabléon derou et al. cases of spontaneous recovery [1,10] and recovery with medical treatment (corticosteroid or atorvastatin-based) [6] have been reported, the treatment of csdh is mainly surgical. surgery for chronic subdural hematoma itself is based on several techniques, including evacuation through a small bone flap associated or not with a drainage system or through one or more burr-holes also associated or not with a system of continuous drainage or percutaneous twist drill craniostomy. the optimal surgical procedure is still subject to debate. the purpose of this study was to compare the clinical outcome of patients who had chronic subdural hematoma evacuation and drainage through a single burr hole craniostomy and those who had chronic subdural hematoma evacuation and drainage through a minicraniotomy. materials and method we carried out a retrospective study on 101 patients who were hospitalized in the neurosurgery department of the teaching hospital of bouaké between july 1, 2016 and june 30, 2020 for the management of a chronic subdural hematoma. due to the retrospective nature of this study, no consent was given and all records have been anonymised. the diagnosis of chronic subdural hematoma was made by ct scan without injection of contrast medium. we compared the data of the patients who had been operated by a burr hole craniostomy (group a) and those of those who had been operated by a minicraniotomy (group b). patient data was collected from records available in the neurosurgery department. the following parameters were analyzed: age, sex, history, clinical and paraclinical signs, the etiology retained, the surgical technique used, the complications and the clinical course. during the postoperative period, regression of signs and symptoms of csdh was expected as clinical improvement. data were entered and statistically analyzed using ibm spss 22.0. fisher’s exact test, chisquared and student’s t-test were performed to compare the 2 groups. all the tests were bilateral. the p-value (p) <0.05 was considered statistically significant. surgical technique in group a a single burr-hole was made while in group b it was a minicraniotomy. the technique used was the choice of the surgeon. all patients (regardless of the technique) were operated under general anesthesia with endotracheal intubation. a skin incision of 4 to 5 centimeter was made across the maximum thickness of csdh. a burr hole craniostomy of 1 centimeter diameter was performed in group a, followed by a cruciform opening of the dura mater and outer membrane of csdh after thermo coagulation. in group b, instead of the burr hole craniostomy, a bone flap of 3 centimeter diameter was cut with the trephine. subsequently, like group a, the dura mater and the outer membrane of the hematoma were incised crosswise after their thermo coagulation. whatever the group, rinsing of the subdural space was performed with isotonic saline (0.9%) until the rinsing liquid returned clear followed by drainage of the subdural space with a closed system. by siphoning (depending on gravity without continuous suction). in group b, the dura is sutured around the drain followed by placement of the bone flap. in group a, the same closed siphoning subdural drainage system is put in place but the dura is left open. in bilateral subdural hematoma, surgery was done bilaterally. regardless of the technique used, the inner membrane of the hematoma as well as the arachnoid were not open. the rest of the care is identical in both groups. it consisted of suturing the surgical wound followed by the dressing. patients were strictly bedridden for 48 hours and, the drainage bag is placed on the patient's bed. the drains were removed in all the patients after 48 hours. results during our study period 102 patients were treated for a chronic subdural hematoma, including 1 patient treated medically (corticosteroid therapy) and 101 others treated surgically, i.e. 99%. a total of 101 patients were included in this study, 46 in group a (patients who had burr hole craniostomy) and 55 in group b (patients who had mini-craniotomy). our study population had a mean age of 59.7 +/13.35 years with extremes of 24 and 100 years. patients under the age of 65 years accounted for 69.3% and those aged 65 years and over represented 30.7%. there were 24 women (23.8%) and 77 men (76.2%). the demographic, clinical and paraclinical characteristics of patients before their surgical 221 burr-hole craniostomy versus mini-craniotomy in the treatment of chronic subdural hematomas treatment are summarized in table 1. the clinical evolutionary aspects of the patients are presented in table 2. clinical examination at 3 months and 1 year postoperatively showed full recovery in the 97 patients who survived. table 1. characteristics of patients before their surgical treatment. variables group a(burr hole craniostomy), n = 46 (45.5%) group b (minicraniotomy), n = 55 (54.5%) total (n = 101) test p value age (years) 59.5 +/-14.56 (min = 24 and maxi = 100) 59.8 +/-12.396 (min = 26 and maxi = 84) 59.7 +/13.35 (min 24 and maxi = 100) t-student = 0.139 p = 0.89 gender x2 = 0.252 p = 0.645 male 34 (74) 43 (78.2) 77(76.2) female 12 (26) 12 (21.8) 24(23.8) aetiology fisher = 2.134 p = 0.372 head trauma 31 (67.4) 40 (72.7) 71(70.3) hemostatic disorder 0 2 (3.63) 2(1.98) no cause identified 15 (32.6) 13(23.6) 28(27.72) delay (trauma and diagnosis (days) 31 30.7 symptoms headache 35(76%) 42(76.3%) 77(76.2%) vomiting 9(19.5%) 11(20%) 20(19.8%) behavior disorder 7(15.2%) 8(14.5%) 15(14.8%) epileptic seizure 1(2.1%) 1(1.8%) 2(1.9%) mean glasgow score on admission 13.22 +/-2.511 min = 6 et max = 15 13.4 +/2.257 min = 7 et max = 15 13.32+/-2.366 min = 6 max = 15 mode = 15 t-student = 0.385 p = 0.701 motor deficit on admission 34 (74%) 46 (83%) 80(79.2%) x2=1.438 p = 0.23 co-morbidities fisher = 12.51 0.27 chronic arterial hypertension 6(13%) 8(14.5%) 14(13.8%) chronic alcoholism 8(17.4%) 5(9%) 13(12.8%) parkinson disease 0 1(1.8%) 1(0.9%) hepatocellular insufficiency 0 1(1.8%) 1(0.9%) hiv infection 0 2(3.6%) 2(1.9%) tuberculous meningitis 1(2.1%) 0 1(0.9%) heart disease under diuretics 0 1(1.8%) 1(0.9%) stroke and chronic hypertension 1(2.1%) 1(1.8%) 2(1.9%) blindness 0 2(3.6%) 2(1.9%) prostatic adenocarcinoma 1(2.1%) 0 1(0.9%) no comorbidity 27(58.7%) 34(61.8%) 61(60.4%) location fisher = 1.787 p = 0.455 right 16 (15.8%) 22 (21.8%) 38(37.6%) left 24(23.8%) 30(29.7%) 54(53.4%) bilateral 6 (5.9%) 3 (3%) 9(8.9%) 222 andré tokpa, moussa diallo, louis kéabléon derou et al. table 2. evolution of patients according to the surgical technique used. variable group a (burr hole craniostomy), n = 46 (45.5%) group b (minicraniotomy), n = 55 (54.5%) total (n= 101) test p value evolution of consciousness 48 hours postoperatively 14.58 +/1.59 14.65+/-1.30 p = 0.81 improvement in motor skills 48 postoperatively 31(67.39%) 44(80%) 75(74.25%) x2= 4.03 p = 0.133 immediate post-operative complications 7(15.21%) 4(7.27%) 11(10.89%) fisher = 6.223 p = 0.172 clinically manifested pneumencephaly 3(6.5%) 2(3.6%) 5(4.9%) acute bleeding 0 2(3.6%) 2(1.9%) brain contusion 1(2.1%) 0 1(0.9%) brainstem haemorrhage 2(4.3%) 0 2(1.9%) post-operative epilepsy 1(2.1%) 0 1(0.9) recurrence during the first year 2(4.3%) 2(3.6%) 4(3.96%) fisher = 1.57 p = 0.55 3 months outcome x2 = 0.483 p = 0.328 mortality rate 3(6.5%) 1(1.8%) 4(3.9%) full recovery 43(93.4%) 54(98.1%) 97(96%) discussion chronic subdural hematoma (csdh) is one of the most common neurosurgical conditions. its incidence increases considerably with age and ranges from approximately 3.4 per 100,000 in patients younger than 65 years old to 8 to 58 per 100,000 among those over 65 years [2,16]. contrary to observations made in developed countries, our study population consists mainly of patients under the age of 65 (approximately 70% of our patients). this is partly explained by the characteristics of the ivorian population, which is made up mainly of young people. indeed 97.15% of the ivorian population is under 65 years old with a life expectancy of 61.8 years [17]. karibe h et al like rauhala m et al. in their various studies carried out in japan and finland respectively, showed that the incidence of chronic subdural hematoma increased with age [7,13]. some authors have also found an average age of occurrence of chronic subdural hematomas less than 65 years, such as mwanyombet et al in gabon [9] who observed that 80% of their patients were between 60 and 65 years old; jaiswal et al in india reported in their series an average age of 53 years [5]. we also observed a male predominance. the sex ratio in our study was 3.2: 1. the higher incidence in men may be due to higher rates of head trauma in them. head trauma has been identified as the most common factor associated with 25% to 75% of cases of csdh in most studies. in our study, a head trauma was reported in 70% of patients. this proportion varied according to the studies: in that of goyal rk, it was 75% [3], in that of santarius et al. it was 61% [15], in that of zumofen et al. it was 79.6% [20] and in that of ramachandran and hegde it was 56% [12]. although spontaneous resolutions [10] or under medical treatment of chronic subdural hematomas [4] have been reported, the treatment of chronic subdural hematomas is resolutely surgical. the treatment decision is based on clinical manifestations and radiological signs including the volume of the hematoma and its mass effect on the parenchyma [18]. several surgical techniques have been described, however, no study can formally conclude the superiority of a technique in terms of efficiency and safety. in our study, we concluded that the two evacuation and drainage procedures that are burr hole craniostomy and minicraniotomy gave similar results in terms of complications, recurrence rate and neurologic course. 223 burr-hole craniostomy versus mini-craniotomy in the treatment of chronic subdural hematomas no statistically significant difference was observed in the clinical course of patients either in the immediate postoperative period or in the medium and long term. in fact, there was no statistically significant difference in the evolution of the consciousness and motor deficit in the two groups. the occurrence of postoperative complications were also statistically superimposable in the two groups as were the recurrence rates. therefore, the two techniques had identical efficiencies. regan m. et al, after a comparative study of these 2 surgical techniques, concluded that evacuation by craniotomy was associated with a higher re-operative rate (24.1%) than evacuation by burr hole craniostomy with p = 0.0156 [14]. they argued that the re-operation was mainly due to a residual chronic subdural hematoma or secondary to one or more acute haemorrhages. their result was related to the lack of drainage in their patients who had had craniotomies. weigal and. al. had shown in a study that the use of a closed drainage system reduced the risk of recurrence of hematoma [19] and therefore of the need for reoperation. santarius et al. in a randomized study comparing two groups of patients treated for csdh by burr holes craniostomy, one group having had drainage and the other not. those with drain were found to have a lower reoperation rate due to a decrease in hematoma recurrence [15]. however, raghavan a et al. for their part found that burr hole craniostomy was associated with a higher reoperative rate [11]. the recurrence rate was relatively low in our series compared to that reported in the literature, especially the series from developed countries. the low rate of recurrence in our series could be explained by the characteristics of our population which was essentially made up of young adults with very little cerebral atrophy on the one hand and on the other hand by a low rate of comorbidity requiring the taking antiaggregant or anticoagulant. indeed, it is accepted that cerebral atrophy and increased subdural space observed in elderly patients make them vulnerable to the development of chronic subdural hematomas [5]. also according to regan m. et al. in their series, there was a higher incidence of postoperative complications in the craniotomy group than in the burr hole craniostomy group. moreover, it clearly appears that the duration of the procedures was significantly longer in craniotomies than burr holes craniostomies [14]. we were unable to compare the duration of different surgeries in our study due to unavailability of data. conclusion evacuation and drainage of chronic subdural hematoma by burr hole craniostomy or minicraniotomy are comparable in terms of clinical outcome. however, other factors not analyzed in our study, such as surgical procedure duration and the type of anesthesia, could help surgeons to choose the appropriate surgical technique on a case-by-case basis. future prospective, randomized, multicenter studies taking into account several factors that may influence surgery for chronic subdural hematoma and the vital and functional prognosis of patients are needed. references 1. baehr m, frotscher m. duus topical diagnosis in neurology. 5th ed. rio de janeiro, rj: guanabara koogan; 2014. 2. ellis h. clinical anatomy: a revision and applied anatomy for clinical students. 8th ed. london: blackwell scientific publications; 1992: 209. 3. moore kl, dalley af. clinically oriented anatomy. 5th ed. baltimore: lippincott williams & wilkins; 2006: 777. 4. romanes gj. cunningham’s textbook of anatomy. 12th ed. new york, ny: oxford university press; 1981: 328329. 5. standring s. gray’s anatomy. 39th ed. edinburgh: elsevier churchill livingston; 2005: 847-877. 6. hur ms, woo js, kim hj, lee ks. frequency and quantity of the c7 contribution to the ulnar nerve. korean j phys anthropol. 2013;26(3):101-104. 7. fuss fk. die radix lateralis des nervus ulnaris [the lateral root of the ulnar nerve]. acta anat (basel). 1989;134(3):199-205. 8. pyun sb, kang s, kwon hk. anatomical and electrophysiological myotome corresponding to the flexor carpi ulnar is muscle. j korean med sci. 2010; 25:454-57. 9. kumar sv, ranganath p. morphology of the ulnar nerve in axilla and arm and its variations. int j anat res. 2014;2(4):677-680. 10. guru a, kumar n, ravindra shanthakumar s, et al. anatomical study of the ulnar nerve variations at high humeral level and their possible clinical and diagnostic implications [published online july 12, 2015]. anat res int. doi:10.1155/2015/378063 11. emamhadi m, chabok sy, samini f, et al. anatomical variations of brachial plexus in adult cadavers; a descriptive study. arch bone jt surg. 2016;4(3):253-258. 12. koo jh, lee ks. anatomic variations of the spinal origins of the main terminal branches of the brachial plexus. korean j phys anthropol. 2007;20(1):11-19. 224 andré tokpa, moussa diallo, louis kéabléon derou et al. 13. harris w. the true form of the brachial plexus, and its motor distribution. j anat physiol. 1904;38(pt 4):399-422. 14. linell ea. the distribution of nerves in the upper limb, with reference to variabilities and their clinical significance. j anat. 1921;55(pt 2-3):79-112. 15. ramachandran k, kanakasabapathy i, holla sj. multiple variations involving all the terminal branches of the brachial plexus and the axillary artery – a case report. eur j anat. 2006;10(3):61-66. microsoft word 10catanamtraumatic.doc 88 romanian neurosurgery (2010) xvii 1: 88 92 traumatic lumbar spondylolisthesis. case report m. catana, v. pruna, anca buliman, m.r. gorgan first neurosurgical clinic, fourth neurosurgical department clinic emergency hospital “bagdasar-arseni” bucharest abstract only few cases of traumatic spondylolisthesis (from the cranial to lumbosacral joint) have been reported to date. recovery of neurological function is dependent on the time of decompression and stabilization. we highlight the paramount importance that the time past between injury and surgical decompression have on neurological recovery and implant durability. authors present the case of a 26 years old patient who suffered a motor crash 10 days ago before admission in our institution for cauda equina syndrome (l5 level). he also presented abdominal trauma with left kidney contusion, spleen contusion, thoracic contusion and left fibular fracture. x-ray and mri examinations of the lumbosacral spine revealed grade 3 of spondylolistesis (60% anterior dislocation l5 s1, intervertebral disc and posterior ligaments laceration, severe compression of the dural sac and dural laceration with csf leakage through the posterior muscular mass). surgery performed 14 days after the injury consisted in a posterior approach with l5 laminectomy, dural decompression and duroplasty with fascia lata, segmental reduction and stabilization with transpedicular screws, l5-s1 discectomy and anterior intervertebral grafting with two tricortical iliac crest grafts. posterior lumbar interbody fusion was carried out using titanium screws (solas system). decompression, reduction with l5, s1 pedicular screw fixation, l5 – s1 disc excision and anterior intervertebral grafting with two tricortical iliac crest grafts is an appropriate surgical technique wich offer a good stabilization and fine functional recovering. keywords: spondylolisthesis, spinal trauma, cauda equina syndrome, dilacerated dural sac spondylolisthesis describes the anterior displacement of a vertebra or the vertebral column in relation to the vertebrae below. it was first described in 1782 by belgian obstetrician, dr. herbinaux (6), who reported a bony prominence anterior to the sacrum that obstructed the vagina of a small number of patients. the term “spondylolisthesis” was coined in 1854, from the greek “spondyl” for vertebrae and “olisthesis” for slip. the variant "listhesis" is sometimes applied in conjunction with scoliosis. these "slips" occur most commonly in the lumbar spine. spondylolisthesis is officially categorized into five different types (10) by the wiltse classification system: i. dysplastic, ii. isthmic, iii. degenerative, iv. traumatic, and v. pathologic. the most common grading system for spondylolisthesis is the meyerding grading system for severity of slip. the system categorizes severity based upon measurements on lateral x-ray of the distance from the posterior edge of the superior vertebral body to the posterior m. catana et al traumatic lumbar spondylolisthesis 89 edge of the adjacent inferior vertebral body. this distance is then reported as a percentage of the total superior vertebral body length: •grade 1 is 0–25% •grade 2 is 25–50% •grade 3 is 50–75% •grade 4 is 75–100% •over 100% is spondyloptosis, when the vertebra completely falls off the supporting vertebra. traumatic lumbosacral spondylolisthesis is a very uncommon lesion. watson-jones described the first case in 1940 (9). only 8 cases of traumatic spondylolisthesis (from the cranial to lumbosacral joint) have been reported to date (1, 2, 4, 8). the specific features of the lesion, as well as the different possible radiographic and clinical findings that characterize it, have encouraged many researchers to attempt to propose possible interpretations of the kinematics of the lesion. case report the case of a 26 years old patient is presented, who suffered a motor crash 10 days ago before admission in our institution for cauda equina syndrome (l5 level). he also presented abdominal trauma with left kidney contusion, spleen contusion, thoracic contusion and left fibular fracture. x-ray showed anterolisthesis of l5 on s1 (figure1). mri examinations of the lumbosacral spine revealed grade 3 of spondylolistesis (60% anterior dislocation l5 s1), intervertebral disc and posterior ligaments laceration, severe compression of the dural sac and dural laceration with csf leakage amoung the posterior muscular mass (figure 2). figure 1 preoperative x-ray showing 60% anterior dislocation l5-s1; a, lateral. b, anteroposterior 90 romanian neurosurgery (2010) xvii 1: 88 92 figure 2 mri scan. a, t1 weighted image; b, t2 weighted image; c, d. axial – t2 weighted image surgery performed 14 days after the injury consisted in a posterior approach with l5 laminectomy, dural decompression and duroplasty with fascia lata, segmental reduction and stabilization with transpedicular screws, l5-s1 discectomy and anterior intervertebral grafting with two tricortical iliac crest grafts (fig. 3). posterior lumbar interbody fusion was carried out using titanium screws (solas system) (fig. 4). control radiograph was performed at 24 hours postoperative. the patient healed without complications, with neurological status improved. he was able to walk five days after surgery without spinal instability signs. follow-up at two months found the patient in a good status. figure 3 postoperative x-ray. a, anteroposterior; b, lateral figure 4 a m. catana et al traumatic lumbar spondylolisthesis 91 figure 4 solas spine system. a, instrument case with 3 inner trays; b, solas lateral view; c, poly screws ø 6 mm: gold color, d, poly screws ø 7 mm: blue color discussion traumatic spondylolisthesis is a fracture of the posterior elements, rather than the pars interarticularis, leading to instability and listhesis. only a few cases of traumatic spondylolisthesis of the lumbosacral joint have been reported. early decompression promotes recovery of neurological function. the timing of decompression and the degree of spinal canal narrowing are the main factors affecting neurological recovery. different treatment modalities are proposed to treat the dislocation. although there are some reports of successful conservative treatment, open decompression and to a certain site reduction with internal segmental fixation and fusion are the most accepted treatment modalities (7). there is no any neurological worsened case after the operation; they remained same or improved clinically at the reported cases. in the event of a traumatic disruption of the disc material, it should be excised for decompression, preferably with interbody fusion. interbody fusion allows higher degree of stability and fusion rate. the anterior support reduces the risk of implant failure (5). it may be performed anteriorly, especially if the disc height is needed to be restored, otherwise it may be done posteriorly. in grade 2 or more, listhesis reduction should be achieved before interbody placements. autologous bone substitute is the gold standard with or without a cage insertion. if the disc material is intact, especially with ligamentous structures, at grade 1 or 2 spondylolisthesis, the necessity of the interbody fusion may be controversial, but it is mandatory to search neural canal and bilateral foraminal compression due to a disc protrusion especially after reduction. the facet joints do not support axial loads unless the spine is in an extension posture. also at the lumbosacral junction, the angle of the sacrum in relation to the l5 vertebral body may substantially affect pathological processes (3). the coronal facet orientation of l5–s1 and lumbosacral joint angle explains the 92 romanian neurosurgery (2010) xvii 1: 88 92 reason why traumatic spondylolisthesis occurs mostly on l5–s1 level. it may be speculated that the weakness of the tip of this patient’s inferior articular process is the reason of l4–l5 traumatic spondylolisthesis. we believe that traumatic spondylolisthesis with laminar fracture may probably be caused by an extension and axial load combination type injury. however, in traumatic spondylolisthesis without laminar fracture, hyperflexion type injury is the most likely cause. asymmetric lesions includes rotational component. but the occurrence mechanism in each particular case will be challenging to be exactly defined, because both type of injury patterns with their subtypes may cause to similar radiological findings. biomechanical studies may help to understand the pathogenic mechanisms. conclusion decompression, reduction with l5, s1 pedicular screw fixation, l5 – s1 disc excision and anterior intervertebral grafting with two tricortical iliac crest grafts is an appropriate surgical technique wich offer a good stabilization and fine functional recovering. time delay has a paramount importance in functional recovery, it means the shorter the time between injury and surgery, the greater neurological outcome. a good understanding of the complex regional biomechanics is needed for adequate surgical approach. references 1. abdel-fattah h, rizk ah: complete fracturedislocation of the lower lumbar spine with spontaneous neurologic decompression. clin orthop:140-143, 1990. 2.ahmed a, mahesh bh, shamshery pk, jayaswal a: traumatic retrolisthesis of the l4 vertebra. j trauma 58:393-394, 2005. 3.benzel ec, kayanja m, fleischman a, roy s: spine biomechanics: fundamentals and future. clin neurosurg 53:98-105, 2006. 4.chatani k, yoshioka m, hase h, hirasawa y: complete anterior fracture-dislocation of the fourth lumbar vertebra. spine 19:726-729, 1994. 5.lamm m, henriksen se, eiskjaer s: acute traumatic l5-s1 spondylolisthesis. j spinal disord tech 16:524527, 2003. 6.newman ph: spondylolisthesis, its cause and effect. ann r coll surg engl 16:305-323, 1955. 7.reinhold m, knop c, blauth m: acute traumatic l5s1 spondylolisthesis: a case report. arch orthop trauma surg 126:624-630, 2006. 8.suomalainen o, paakkonen m: fracture dislocation of the lumbar spine without paraplegia. a case report. acta orthop scand 55:466-468, 1984. 9.watson-jones r: the classic: "fractures and joint injuries" by sir reginald watson-jones, taken from "fractures and joint injuries," by r. watson-jones, vol. ii, 4th ed., baltimore, williams and wilkins company, 1955. clin orthop:4-10, 1974. 10.wiltse ll, newman ph, macnab i: classification of spondylolisis and spondylolisthesis. clin orthop:23-29, 1976. microsoft word 15tudorachecorneliatheposttraumatic.doc 238 conelia tudorache et al posttraumatic occlusion of the vertebral artery the posttraumatic occlusion of the vertebral artery case presentation cornelia tudorache1, adriana moldovanu1,2,3, anda esanu1, e. moldovanu1,2,3, carmen gherman1,3, c. ichim1, c. popescu4, m. dabija4, danisia haba1,2 1department of radiology, emergency hospital “prof. dr. n. oblu”, iasi 2“gr.t. popa” university of medicine and pharmacy, faculty of dentistry, general and dental radiology discipline 3mri departament “supermeditest” iasi 4neurosurgery, emergency hospital “prof. dr. n. oblu”, iasi abstract we investigate radiographic features of vertebral artery injury/occlusion associated with nonpenetrating cervical spine trauma and to demonstrate the importance of the cta in high-risk cases. with the popularization of cta (computed tomography angiography) and mra (magnetic resonance angiography), vertebral artery injury has been a common complication of cervical spine trauma. the occlusion of the vertebral artery secondary to non-penetrating trauma of the cervical spine (fractures and/dislocations) can be found in approximately 20% of the cases. vertebral artery occlusion was rarely symptomatic because of sufficient collateral blood supply through not only contralateral vertebral artery but also the circle of willis. keywords: occlusion of the vertebral artery, computed tomography angiography. case presentation we are presenting the case of a 61-yearold patient, who has suffered multiple trauma as result of a fall from a great height. the patient was tetraplegic. he had radio-imagistic investigations done: x-ray, irm exam for the cervical spine and cervical angio-ct scan (cervical angio-ct scan, with sections of 1 mm, pitch 1,5 mm, reconstructions 0,8 mm, followed by mpr and mip processing). the cervical spine x-ray has shown posterior fracture dislocations c3-c4, with segmental kyphosis at the same level. in addition to this, the irm exam revealed haemorragic and edematous medullary contussion c2-c5, in the stage of extracellular methemoglobin: low signal intensity on t1-weighted image with a small area of high signal, and high signal intensity on t2-weighted image (figures 1 a, b), traumatic disc injury at c3-c4: areas of high signal intensity on stir t2 image (figure 1b), occlusion of the right vertebral artery: absence signal void t2, with vertebral artery dissection (figure 2). the intra-surgery diagnosis was traumatic lesion c3-c4 with hyperextension. during surgery, a hematic collection could be found laterocervical on the right, in the vicinity of the dislocation centre; hemostasis was performed with gelaspon strips, and also the ablation of the broken disc c3-c4. romanian neurosurgery (2010) xvii 2: 238 – 245 239 1a 1b figure 1 mri exam – sagital sections: a stir t2-weighted axial image, b t1-weighted axial image: posterior fracture dislocations c3-c4, with anterior angulation at the same level edematous and hemorrhagic medullary contussion c2-c5, in the stage of extracellular methemoglobin (low signal intensity on t1-weighted image with a small area of high signal, and high signal intensity on t2-weighted image) traumaic disc injury at c3-c4 (areas of high signal intensity on stir t2 image) 2a 2b figure 2 mri of the cervical spine t2-weighted image axial and sagital sections: high signal intensity of the right vertebral artery, occlusion of the lumen with vertebral artery dissection postoperative, an angio-ct cervical exam was performed, which highlighted the absence of the contrast of the right vertebral artery, having the inferior limit at the level of a section plan, which passes through the superior end-plate of the vertebral body c5, and the superior one – at the level of a 240 conelia tudorache et al posttraumatic occlusion of the vertebral artery section plan, which passes through the inferior end-plate c2 (figures 3, 5), with the presence of a reduced contrast at the level of the base of the cranium and a good intra-cranial contrast (figure 4). cta also showed a hemorrhagic collection with fine airy bubbles lateral-vertebral on the right, with dimensions of 14/29 mm in an axial plane, between the vertebral body c2 and the intervertebral space c5-c6. the diagnosis was cervical trauma, fracture-dislocations c3-c4, cervical medullary contussion c4, right vertebral artery occlusion (thrombosis of right vertebral artery segment v2). in the case of these types of trauma lesions, the prognosis is extremely poor, the patient dying in ten days after checking in. 3a 3b figure 3 cta of the cervical spine axial sections: no signal flow along the vertebral artery – v2 segment 4a 4b figure 4 cta of the cervical spine axial sections: a low signal flow along the vertebral artery – v3 segment; b normal blood flow in v4 segment discussion although vertebral artery injuries caused by penetrating injuries to the neck, chiropractic manipulation, yoga, and sustained physiologic movement have been well described, those associated with nonpenetrating cervical spine injuries were thought to be infrequent because most of them were asymptomatic.[1-5] in the past, this lesion was thought to be infrequent because it was rarely symptomatic, and conventional angiographic screening has rarely been performed because of its inherent risks. thereafter, with the popularization of noninvasive mra, several prospective studies using mra were conducted to romanian neurosurgery (2010) xvii 2: 238 – 245 241 determine the incidence of this lesion. [4,68,12] the incidence derived from these clinical series was within a narrow range between 18.9% and 25.5%.[4,6,7,12] vertebral artery occlusion can be considered a common complication in approximately 20% of cervical spine fractures and/or dislocations. 5a 5b figure 5 cta of the cervical spine a sagital and b coronal reconstructions: absence of the contrast of the right vertebral artery, – v2 segment 6a 6b figure 6 angiorgaphy of the vertebral arteries: a lateral view: 1,2 vertebral arteries, 3 posterior inferior cerebellar artery, 4 basilar artery, 5 anterior superior cerebellar artery, 6,7 posterior cerebellar arteries, 8 posterior communicating artery b frontal view: v2, v3 and v4 segments v4 v3 v2 242 conelia tudorache et al posttraumatic occlusion of the vertebral artery anatomically, the vertebral artery is divided into 4 segments: first, subclavian to entrance to the foramen transversarium (c6 or c7); second, c6-c1, in which the vertebral arteries pass through the foramen transversariumthird, c1 to entrance into the dura; and fourth, entrance to its termination in the basilar artery. [3,34] (figure 6). the most common site of vertebral artery injury associated with cervical spine trauma was the second segment.[13] vertebral artery injury generally occurs either through excessive distraction and stretching of the vessels between 2 adjacent foramina transversia (as observed in facet dislocation) [1,3,5,7,8] or through direct trauma to the vessel wall (as observed in fractures involving the articulating facet or the foramen transversarium).[5,14] previously, hyperextension injuries had been accepted as the most common mechanism of vertebral artery injury. [15,16] however, recent reports have identified distractive flexion injury as the main cause of this lesion. [4,5,7,8,17] facet dislocation, especially the unilateral one, was closely related to this lesion. [4,7,8,17] patients with vertebral artery occlusion had traumatic spinal cord lesion. however, vertebral artery occlusion without spinal cord injury was reported in the literature. [4,7,8] there was no significant correlation between vertebral artery occlusion and severity of spinal cord injury. vertebral artery injury secondary to cervical spine trauma includes a wide spectrum of vessel damages, such as intimal dissection, aneurysm, intramural or subintimal hematomas, and occlusion. the most common lesion shown in previous studies using varying imaging methods was occlusion.[5,6] a pathomechanism of traumatic vertebral artery occlusion is: intimal disruption initially occurs, then secondary events such as thrombus formation may lead to clot occlusion of vessel lumen. [4,5] the natural history of vad (vertebral artery dissection is unknown). it can heal spontaneously, it can develop occlusion or it can form a pseudoaneurysm. the clinical significance of vad lies in its potential to form intra-luminal thrombosis and this has potential for embolization. the mechanism of occlusion in a compressive injury is likely to be vasospasm or minor artery dissection, which may cause reversible occlusion, [18,19] because, comparatively, vessels are subjected to less severe stretching in compressive injuries than in distractive injuries. flow disturbance caused by vasospasm can be restored within a short period. [4] furthermore, occlusion secondary to vertebral artery dissection can be recanalized up to 85% within 3 months by spontaneous mechanism, which could have depended on the intrinsic condition of the vessels. [18] therefore, the potential for restoration of blood flow may be higher in compression injuries than in distraction injuries. treatment for vad is controversial; it not clear whether patients must be heparinized, be treated with antiplatelets (aspirin) or treated at all. once thrombosis occurs, it is also controversial whether anticoagulation or antiplatelet therapy should be the treatment of choice. vadim beletsky et al[32] showed that the recurrence rate for embolization is decreased significantly (by 8.3%) in patients on anticoagulation compared to those on aspirin (12.4%). this difference in outcome at one year was not statistically significant. it is prudent to seriously romanian neurosurgery (2010) xvii 2: 238 – 245 243 consider prophylactic treatment (unless contra-indications exist) because the prognosis for brainstem ischaemia is very poor. one of the most controversial issues in traumatic cerebro-vascular trauma is what is the best modality for investigating blunt cerebro-vascular injury. the gold standard is digital subtraction angiography (dsa). the problem with dsa is that it is an invasive procedure. other modalities available are multi-detector ctangiography (cta), mri, and mriangiography . mra is quite accurate in the detection of near or total occlusion of the extracranial neck vessels. [6, 20, 21] on the other hand, slow blood flow in the small vessels on mra can be confused with occlusion as a result of insufficient resolution. [5,22] although conventional angiography is a much more invasive modality, it is superior to mra in the detection of nonoccluded intimal disruption, which occasionally causes distal embolization. however, because occlusion is the most common vertebral artery injury, the majority can be successfully detected by noninvasive mra. [5,6] . alexander l. eastman et al. [33] in a large series of 162 patients demonstrated that cta is a very good screening tool for blunt cervical injury. they demonstrated that the overall sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of cta for the diagnosis of blunt cerebro-vascular injury were 97.7%, 100%, 100%, 99.3%, and 99.37, respectively. symptoms of vertebrobasilar ischemia include headaches, dizziness, vertigo, tinnitus, unsteady gait, dysarthrias, diplopia, visual field defect, blurry vision, ptosis, drowsiness, syncope, altered consciousness, nystagmus, and dysphagia.[4-8,17] a low frequency of vertebrobasilar ischemia in patients with cervical spine trauma has been shown in many published reports. however, it is also apparent that vertebrobasilar ischemia can have devastating consequences (mortality rate 75% to 86%).[23] unilateral occlusion of the vertebral artery rarely results in a neurologic deficit because of sufficient collateral blood supply through the contralateral vertebral artery. [4-6, 13, 17] whereas, approximately 15% of patients have hypoplasia of one vertebral artery, which emphasizes the fact that there may not always be sufficient collateral arterial supply in a patient with unilateral occlusion. [14,17] there are other potential sources of collateral circulation to the vertebrobasilar territory, such as the posterior communicating arteries, which are the important elements of the circle of willis, [28] the posterior inferior cerebellar arteries, [29] distal branches of the thyrocervical and costocervical trunks, the occipital artery, interspinal branches, and muscular branches. [13, 30, 31] the circle of willis plays an important role in the collateral pathway between the anterior and posterior circulation of the brain.[28] in patients with a complete circle of willis, sufficient collateral circulation is present even when bilateral vertebral artery occlusion occurs.[10,28] a possible explanation for this phenomenon is the existence of sufficient collateral blood flow from anterior circulation via the posterior communicating artery and/or early restoration of blood flow in the occluded artery. 244 conelia tudorache et al posttraumatic occlusion of the vertebral artery conclusion based on the literature and on this case report, we make the following recommendation: cta (computed tomography angiography) has the advantage of minimally invasive speed of acquisition that is vital in the acute setting; cta is a very good screening tool for blunt cervical injury; -vertebral artery injury must be excluded in high-risk cases, cta or mra are increasingly used to help make the diagnosis; -the practical disadvantage of cta is the confounding effect of vessel wall calcifications on image interpretation; -prophylactic treatment must be seriously considered unless there are contra-indications: aspirin 650 mg orally twice a day for three months. references 1.deen hg, mcgirr sj. vertebral artery injury associated with cervical spine fracture. spine 1992;17:230–4. 2.miyachi s, okamura k, watanabe m, et al. cerebellar stroke due to vertebral artery occlusion after cervical spine trauma. two case reports. spine 1994;19:83–8. 3.parent ad, harkey hl, touchstone da, et al. lateral cervical spine dislocation and vertebral artery injury. neurosurgery 1992; 31:501–9. 4.vaccaro ar, klein gr, flanders ae, et al. long-term evaluation of vertebral artery injuries following cervical spine trauma using magnetic resonance angiography. spine 1998;23:789–94. 5.willis bk, greiner f, orrison ww, et al. the incidence of vertebral artery injury after midcervical spine fracture or subluxation. neurosurgery 1994; 34:435–42. 6.friedman d, flanders a, thomas c, et al. vertebral artery injury after acute cervical spine trauma: rate of occurrence as detected by mr angiography and assessment of clinical consequences. ajr am j roentgenol 1995; 164: 443–7. 7.giacobetti fb, vaccaro ar, bos-giacobetti ma, et al. vertebral artery occlusion associated with cervical spine trauma. a prospective analysis. spine 1997; 22:188–92. 8.veras lm, pedraza-gutierrez s, castellanos j, et al. vertebral artery occlusion after acute cervical spine trauma. spine 2000; 25:1171–7. 9.allen bl, ferguson rl, lehmann tr. a mechanistic classification of closed, indirect fractures and dislocations of the lower cervical spine. spine 1982; 7: 1–27. 10.hartkamp mj, grond jvd, everdingen kjv, et al. circle of willis collateral flow investigated by magnetic resonance angiography. stroke 1999; 30: 2671–8. 11.hoksbergen awj, legemate da, csiba l, et al. absent collateral function of the circle of willis as risk factor for ischemic stroke. cerebrovasc dis 2003; 16:191–8. 12.parbhoo ah, govender s, corr p. vertebral artery injury in cervical spine trauma. injury 2001; 32:565–8. 13.prabhu v, kizer j, patil a, et al. vertebrobasilar thrombosis associated with nonpenetrating cervical spine trauma. j trauma 1996; 40:130–7. 14.weller sj, rossitch e, malek am. detection of vertebral artery injury after cervical spine trauma using magnetic resonance angiography. j trauma 1999; 46:660–6. 15.simeone fa, goldberg hi. thrombosis of the vertebral artery from hyperextension injury to the neck. j neurosurg 1968; 29:540–4. 16.six eg, stringer wl, cowley ar, et al. posttraumatic bilateral vertebral artery occlusion: case report. j neurosurg 1981; 54:814–7. 17.louw ja, mafoyane na, small b, et al. occlusion of the vertebral artery in cervical spine dislocation. j bone joint surg 1990; 72-b: 679–81. 18.caso v, paciaroni m, corea f, et al. recanalization of cervical artery dissection: influencing factors and role in neurological outcome. cerebrovasc dis 2004; 17:93–7. 19.pelkonen o, tikkakoski t, leinonen s, et al. extracranial internal carotid and vertebral artery dissections: angiographic spectrum, course and prognosis. neuroradiology 2003; 45:71–7. 20.bowen bc, quencer rm, margosian p, et al. mr angiography of occlusive disease of the arteries in the head and neck: current concepts. ajr am j roentgenol 1994; 162:9–18. 21.heiserman je, drayer bp, fram ek, et al. carotid artery stenosis: clinical efficacy of two-dimensional time-of-flight mr angiography. radiology 1992; 182:761–8. 22.rodriguez m, tyberghien a, matge g. asymptomatic vertebral artery injury after acute cervical spine trauma. acta neurochir (wien) 2001; 143:939–45. romanian neurosurgery (2010) xvii 2: 238 – 245 245 23.becker kj, monsein lh, ulatowski j, et al. intraarterial thrombolysis in vertebrobasilar occlusion. ajnr am j neuroradiol 1996; 17:255–62. 24.brandt t, kummer rv, mueller-kueppers m, et al. thrombolytic therapy of acute basilar artery occlusion. stroke 1996; 27:875–81. 25.cross iii dt, moran cj, akins pt, et al. relationship between clot location and outcome after basilar artery thrombolysis. ajnr am j neuroradiol 1997; 18:1221–8. 26.schellinger pd, schwab s, krieger d, et al. masking vertebral artery dissection by severe trauma of the cervical spine. spine 2001; 26:314–9. 27.wirbel r, pistorius g, braun c, et al. bilateral vertebral artery lesion after dislocating cervical spine trauma. a case report. spine 1996; 21:1375–80. 28.wentz ku, roether j, schwartz a, et al. intracranial vertebrobasilar system: mr angiography. radiology 1994; 190:105–10. 29.golueke p, sclafani s, phillips t. vertebral artery injury–diagnosis and management. j trauma 1987; 27:856–65. 30.faillace wj, okawara sh. pontomedullary infarction from sustained cervical spine hyperflexion. surg neurol 1986; 26:282–6. 31.jabre a. subintimal dissection of the vertebral artery in subluxation of the cervical spine. neurosurgery 1991; 29:912–5. 32.beletsky vadim, nadareishvili zurab, lynch john, shuaib ashfaq, woolfenden andrew, norris johnw. cervical arterial dissection: time for a therapeutic trial? stroke. 2003; 34:2856–2860. doi: 10.1161/01.str.0000098649.39767.bc. 33.eastman alexander l, chason david p, perez carlos l, mcanulty amy l, minei joseph p. computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready forprimetime? j trauma. 2006; 60:925–929. 34.aldescu c., neuroradiodiagnostic, 1982, 98, 99. microsoft word _1.formatata_kato.doc romanian neurosurgery vol. xvi nr. 1 3 neurorehabilitation in neurotrauma yoko kato1, anil sangli, sachiko yamaguchi, isao morita, tetsuo kanno, hirotoshi sano 1department of neurosurgery, fujita health university, japan since time immemorial, neurotrauma has been recorded in various continents. the advancement in neurotraumatology ever since denny brown and trussell’s landmark experimental study of concussion, has come a long way with major contributions from neuropathology, neurophysiology, neurochemistry, biomedical sciences, public policies, intensive care medicine and last but not the least, genetics. a simple introduction of lap and shoulder belt have reduced majority of serious accidents. continuous recording of intracranial pressures, recognition of acute brain swelling with characteristics of cerebral blood flow in brain damage and development of glasgow coma and outcome scales by a well-designed multi-centered multi-national outcome study in head injuries brought in major changes in squealae and outcome by preventing and reducing the secondary insults. computed tomography (ct) and improvement in morbidity and mortality of acute extra axial hematomas by immediate surgery, has influenced and guided several organizations in developing research and formulating guidelines for treatment of acute neurotrauma. the recognition of the spectrum in head injury, aids in prevention of injury and measures to improve outcome by ever developing neuro-rehabilitative measures, apart from advancements in the genetic aspects of understanding the brain’s response to injury along with attention to modern principles of neuro-intensive and critical care, has manipulated neurotrauma towards achieving innovative newer frontiers. assessment of the extent of injury and the deficits in neurotrauma is as challenging as the management itself. several criteria including the japanese coma scale and the proposition for the international coma scale have been attempted. once the baseline characters and the psychology1 of the patient is understood along with the extent and nature of the severity of the injury, a defined patterned timescale with a schedule can be created & tailor made to every patient and all out efforts instituted to rehabilitate not only the individual but also the whole family and the society at large. keywords: traumatic brain injury, neurorehabilitation, coma scales, minimally conscious state, vegetative state, outcome scales, neurorehabilitatory interventions introduction and historical review multiple casualties in the world war i brought innumerable casualties along with challenges to treat them. most of the neurorehabilitation developed by the end of the first world war slowly dwindled after the war. onset of world war ii brought in renewed interest to neurorehabilitation with specialized hospital based programs. it was with the advances of harvey cushing, in neurosurgery techniques and dr. howard a. rusk in active rehabilitatory measures which revolutionized the concept of neurorehabilitation. newer challenges crept up with the advent of motor vehicle and sport injuries. rancho los amigo hospital is one of the first institutes established solely for the purposes of neurorehabilitation and still has one of the best methods of established cognitive 2 and physical rehabilitation schedules. one of the most frightening aspects in neurotrauma is that permanent disability or death often is the rule in many including asian and oceanic countries3. the concept of neurorehabilitation is still at its infancy and requires a cohered effort of all involved to prevent neurotrauma and improve rehabilitatory measures (4). evaluation criteria in rehabilitation for neurotrauma yoko kato romanian neurosurgery vol. xvi nr. 1 4 among the several definitions of disability, impairments etc., who definition is more acceptable which terms ‘impairment’ as any loss or abnormality of the physical, functional and psychological aspects. if the activity or the range of activity considered to be normal for a human is unable to be performed, then, it may be termed as disability40. the result of the disability or impairment causing prevention of fulfillment of the role, normal for the individual is termed handicap. several assessment modalities to find out the extent of impairment, resulting disability or handicap are recognized (5, 6, 7, 8). they have their own advantages and dis-advantages and not one in isolation shall fulfill all criteria. the most popular among these are in table 1. response to close monitoring and documentation of the response is difficult in gos; (table 2). functional improvement can be evaluated with barthel index but the neurocognitive recovery is not evaluated by it. the functional independence measure (fim) evaluates functional states and can be applied easily on admission at timely intervals and during discharge. the disability rating scale (drs) is further, a simpler version of the fim developed for head trauma. individuals with a scale between 0-30 are ideal in patients who have entered the chronic phase of recovery. the rlas (rancho’s los amigo scale) though has restrictions of being able to be applied individually in evaluation of the functional criteria, can never-the-less be applied to redirect individuals to assign specific protocols in rehabilitation. the orientation and post-traumatic amnesic disorder accompanying trauma can be assessed to the goat (galveston orientation and amnesia test) (37-39). sequelae in neurotrauma neurotrauma taxes the individual, family and the society in almost all the areas by bestowing the ugly and most affronting squealae. to mention a few among the many, the anatomical integrity, functional measures and the psychological factors take a toll on the individual impeding his return to the society as it requires after neurotrauma (11, 12, 13). multiple medical problems associated with neurotrauma includes ulceration, skin breakdown, infections, seizures, contractures, hypertension, gi complication, hepato-biliary complication, dvt, endocrine abnormalities in the acute or chronic phase, spasticity, heterotopic ossification, contractures all are long term problems causing serious deterioration in rehabilitation (14, 15, 16). table 1 sl. no. assessment scale 1 gos – glasgow outcome scale 2 bi – barthel index 3 fim – functional independence measure 4 drs – disability rating scale 5 rlas – rancho los angio scale for cognitive function table 2 glasgow outcome scale (from jennett b, bond mr: assessment of outcome in severe brain damage: a practical scale, lance 1:480-484, 1975) outcome description good recovery resumption of normal daily activities independently moderate disability impairments or disabilities persist, but with adaptive or assistive equipment, worksite modifications, or other compensatory strategies ; the neurorehabilitation in neurotrauma romanian neurosurgery vol. xvi nr. 1 5 individual remains functionally independent outcome description severe disability impairments of disabilities persist and assistance of others is required to perform daily activities persistent vegetative state patient does not survive death table 3 injuries can cause sensory, motor, cognitive, emotional or psychosocial impairments sensory impairment blindness deafness anosmia sound, light, head intolerance motor impairment hemiparesis, quadriparesis gait disturbances inco-ordination seuzures cognitive impairment deficits in alteration deficits in memory language and communication disorder visuo-spatial disorder problem solving disorder emotional impairment irritability restlessness frustration anger depression mood alteration elation denial loss of energy fatigability psychological impairment dependency change of states lack of respect loss of family, economic resources sexual maladjustment drug and alcohol abuse language, non-verbal and neuropsychological sequelae most elusive and difficult to understand and treat is perhaps the language function; whether it be motor or sensory aphasia. recovery depends on several factors like the extent of injury and the neurological dysfunction. controlled oral word association test (cowat) is the most frequently used verbal fluency yoko kato romanian neurosurgery vol. xvi nr. 1 6 test (17, 18). constructional apraxia, word finding difficulty, disordered geometric organization, facial recognition, attention and concentrate deficits, speed of processing information, selective attention, hyper or hypo-arousal disorders, memory disturbances, modulation of cognition to achieve goal directed behaviors are the most challenging among neurotrauma rehabilitation. pitfalls in neuropsychological assessment intelligent quotient (iq) has been a predictor for the evaluation of cerebral function. iq measures and summarizes all the quotients as a single score. this depends on the emotional and motivating factors and not necessarily on sole cerebral function. nevertheless, wais-iii [wechester adult intelligent scale-iii] measures the verbal iq and performance iq. language disturbance, tasks requiring adaptable abilities are all affected in neurotrauma and may alter the scores (2731). if the iq after neurotrauma drops, it does not necessarily mean that the individual is has an infant brain. in fact, it is still not fully surmised regarding the confusional and functional cognitive balance that is due to an uneven compromise in neural function. low or high iq does not mean anything since it may not cover the full scale of the cerebral function or cater to that aspect of the deficit in the cognitive behavior which is at stake. other factors affecting neurorehabilitation the mentality of the individual, psychological background, the social and emotional conditioning at childhood, the strengths and weakness, pre-injurypsychological problems, medical problems, alcohol, tobacco or drug abuse, economic background, depression, antisocial traits, marital harmony, family background and support, psychological conditioning at the time of trauma may all compound idealistic assessment methods and confuse management (32, 33, 34). running a battery of neuropsychological test helps to assess multiple domains to analyze the strengths/weakness apart from going through the academic records and records at pre-injury work area. even, poor scholastic records may not directly relate to cognitive skills, since they may defer due to multiple factors and practicality issues. adjustment to the postinjury lifestyle may take a longer time and hence the emotional and other abilities come into play causing altered results thus giving a wrong picture (19, 20). capacity to think in a normal way, going back to preinjury passions like music, hobbies, language, somatization of emotions, self-care, law abiding nature etc., cannot be individually or in total be evaluated by any single test and requires usually a battery of tests. motivating an individual to get better, to relearn all that he has lost requires a great deal of immense dedication and commitment on the part of the family or caretakers. cognitive awareness of the deficiency with the acquired will and motivation gives a great boost to achieve. by and large premorbid perfectionists, attention seeking, grandiose, histrionic, somatoform disordered patients require proper expert guidance (21, 22). remembrance of the near death experience is more problematic especially in rape or assault etc. several medical, social, psychological, sensory and motor modalities of rehabilitation are in vogue (9, 10). sensory modality by dorsal column stimulation, deep brain stimulation, medial nerve stimulation, touch, speech, music, visual stimuli etc., has given varying benefits26. thus, an overall intensive management in acute trauma for medical complications and in the later stages for psychosocial and functional complications helps in a better assessment and functioning (35, 36). conclusion the neuropsychological testing and testing for various cognitive functions must include proper reliability, validity and standardization wherein presently the main domains such as sensory, motor, intellectual and attention deficits along with language and memory disorders become the major part. the same test must be examined by different clinicians using various parameters in the same way and note down the observations stereotypically, thus making any result, examiner-independent (25). neurorehabilitation in neurotrauma romanian neurosurgery vol. xvi nr. 1 7 the degree to which a positive co-relation exists by applying the same examination in the same individual at different points of time, indicates the reliability which for which the co-relation co-efficient should be at least >/=0.8 it is important to know what a particular test measures, it’s aim is and how well the aim is achieved. it is mandatory to transcend our own disciplines and make a conscious, reliable, affordable and practical decision to make a traumatic brain injury patient live inside and outside and face day-to-day problems. a holistic approach is thus required, since patients may have anatomical, physiological and psycho-emotional or cognitive problems (23, 24). it is a multi-disciplinary attitude with the neurosurgeon, neuropsychologist and other health care professionals who can perpetuate to this extremely difficult, noble task of bringing a patient back to reality. references 1.anastasi a: psychological testing, 6th ed. new york, macmailllan, 1988 2.bigler e, steinman d, newton j: clinical assessment of cognitive deficit in neurological disorder. ii. cerebral trauma clin neuropsychol 3:13-18, 1981 3.boring e: a history of experimental psychology, 2nd ed. new york, appleton-century-crofts, 1957 4.campbell d: evolutionary epistemiology. in schlipp p (ed): the philosophy of karl popper, vol. 14 [i and ii]. la salle, ill, open court, 1974, pp. 416-463 5.crawford j: current and premorbid intelligence measures in neuropsychological assessment. in: crawford jr, parker dm, mckinlay ww (eds): a handbook of neuropsychological assessment. hove, uk: lawrence erlbaum, 1992 6.cullum c, steinman d, bigler e: relationship between fluid and crystallized cognitive functions using category test and wais scores. int j clin neuropsychol 6:172-174, 1984 7.delisa ja, gans bm: rehabilitation medicine. philadelphia, lippincott-ravem. 1998 8.france e, clves wm: do women fare worse: a meta-analysis of gender differences in outcome after traumatic brain injury. j neurosurg 93:539-545, 2001 9.funabashi t, komai n, ogura m, kuwata t, nakai m and tsuji n: effects of and indications for apidural stimulation of the cervical spinal cord in prolonged consciousness disturbance. neurological surgery 17 (10):917-923, 1993 10.greenberg rp, becker dp, miller jd, mayer dj: evaluation of brain function in severe human head trauma with multimodality evoked potentials. j neurosurg 47:163-177, 1977 11.hagen c, malkmus d, durham p: levels of cognitive functions. in rehabilitaitn of head-injured adult: comprehensive physical management. jdjownesy; ca, professional staff association, rancho los amigos hospital, 1979 12.heiskanen h, sipponen p: prognosis of severe brain injury. acta neurol scand 46:343, 1970 13.herneasniemi j: outcome following head injuries in the aged. acta neurochir (wien) 49:67, 1979 14.jacobs he: behavior analysis guidelines and brain injury rehabilitation: people, principles and programs. new york, aspen, 1993 15.jennett b, bond mr: assessment of outcome in severe brain damage. a practical scale. lancet 1: 480-484, 1975 16.jennett b, teasdale g: management of head injuries. philadelphia, fa davis, 1981, pp 1191-1239 17.katz m, lyerly s: methods for measuring adjustment and social behavior in the community. i. rationale, description, discriminative validity and scale development. psychol rep 13:503-535, 1963 18.klonoff p, snow w, costa l: quality of life in patients two to four years after closed head injury. neurosurgery 19: 735-743, 1986 19.konno t, kamei y, yokoyama t and konno k: relationships between neurosurgical patients and prolonged consciousness disturbance. neurosurgeons 10:339-345. 1991 20.kuwata t: basic and clinical studies of spidural electrical stimulation of the cervical spinal cord for prolonged consciousness disturbance. neurological surgery 21(4) 325-331, 1993 21.lezak m: subtle sequelae of brain damage: perpexity, distractability and fatigue. am j phys med 57:9-15, 1978 22.national institutes of health: rehabilitation of persons with traumatic brain injury. nih consensus statement 16:1-41, 1998 23.ohta t, takeuchi e: pilot study: scale for impaired consciousness in the chronic stage. the society for treatment of coma 2, pp 209-224, neuron publ. co., tokyo, 1993 24.pittenger de: heterotpic ossification. orthop rev 20:33-39, 1991 25.rehabilitation of persons with traumatic brain injury: nih consensus conference: jama 282: 974-983, 1999 26.rey a: l’examen psychologique dan les cas dencephalopathie traumatique. arch psychol 28:286-340, 1941 27.ruff r, evans r, marshall l: impairment of verbal and figural fluency following traumatic head injury. arch clin neuropsychol 1:87-101, 1986 28.rutherford w, merret j, mcdonald j: symptoms at one year following concussion from minor head injuries. injury 10:226-230, 1979 29.sano k, manaka s, kitamura k, kagawa m, takeuchi k, ogashiwa m, kameyama m, tohgi h, yamada h: statistical studies on evaluation of mild disturbance of consciousness j neurosurg 58: 223-230, 1983. 30.sarno m: verbal impairment after closed head injury. j nerv ment dis 172:475-479, 1984 yoko kato romanian neurosurgery vol. xvi nr. 1 8 31.silver jm, yudofsky sc, hales re: neuropsychiatry of traumatic brain injury. in kraus jf, sorenson sb (eds): epidemiology. washington dc, americal psychiatric press, 1994, pp 3-41 32.skinner j, yingling c: central gating mechanisms that regulate event-related potentials and behavior: a neural model for attention. in desmedt j (ed): attention, voluntary contraction and eventrelated cerebral potentials: progress in clinical neurophysiology, vol. 1, karger, basel, 1977, pp 30-69 33.squire l: memory and brain. new york, oxford university press, 1987 34.takeuchi k: prolonged consciousness disturbance. standard neurosurgery. igaku shoin (tokyo) 1884 pp 133 35.thompsen i: late outcome of very severe blunt head trauma: a 10-15 year second follow-up. j neurol neurosurg psychiatry 47:260-268, 1984 36.tsukahara t, keyaki a, ishikawa m, yamashita s, mori k and handa h: dorsal column stimulation for persistent pain. nippon geka hokan 49(2): 209-211, 1980 37.varney n, roberts r: the evaluation and treatment of mild traumatic brain injury. london, lawrence erlbaum, 1999. 38.warrington ek: recognition memory test. windsor, england, national foundation for educational research, 1984 39.wechsler d, wechsler memory scale – revised manual. new york, psychological corporation, 1987 40.world health organization: international classification of impairments. disabilities and handicaps: a manual of classification relating to the consequences of disease. genva, world health organization, 1980. microsoft word _2.formatata_ciurea.doc romanian neurosurgery vol. xv nr. 2 8 olfactory ensheathing cells in the treatment of the tethered cord syndrome: case report prof. dr. a.v. ciurea1, dr. st.m. iencean2, prof. dr. n. ianovici2, dr. f.m. brehar1 1first neurosurgical clinic, emergency clinic hospital “bagdasar-arseni”, bucharest 2neurosurgery ii, emergency hospital “prof dr n oblu ”iasi correspondence address emergency clinical hospital “bagdasar-arseni” berceni street 10-12, bucharest, romania tel/fax: +40213343025/+40213347350, e-mail: rsn@bagdasar-arseni.ro there are several data and commentaries regarding the role of the stem cells as effective therapies in the treatment of the central nervous system’s lesions. even if at the experimental level there have been reported very promising results, when these methods have been applied in clinical field the results were not very successful. in this context, the numerous reports about patients with significant improvement of the neurological status after stem cells inoculation or olfactory ensheathing cells (oecs) inoculation performed by the researchers from beijing xishan hospital, beijing, china, adds a discordant note in this general pessimist background. therefore, we will present the original discharge letter from the beijing xishan hospital, beijing, china then we will make some commentaries and will draw the final conclusions. keywords: olfactory ensheating cells, tethered cord, myelo-meningocelle case report patient presentation: a 5-year-5-month-old girl from romania, was admitted to beijing xishan hospital, beijing, china on november 7, 2007 with 5 years history of paraplegia, urinary and bowel movement incontinence due to a meningomyelocele accompany with hydrocephalus. he underwent neoplasty of meningomyelocele and ventriculo-peritoneal shunt on right side three months after her born. after operation, she was not able to move her legs and the feeling in her legs almost disappeared. svere scoliosis was noticed. urinary and bowel movement was incontinence. she was able to sit and crawl by herself. her intelligence development was normal. she went to school followed with study well. admission diagnosis: tethered cord syndrome physical examination: motor: upper extremities were 5/5 bilaterally; lower extremities: hip flexors was 2/5 on the right, 3/5 on the left; knee extensors, ankle dorsflexors, ankle plantar flexors and long toe extensors were 0/5 bilaterally. sensation: light touch decreased at l1-2 on the right, at l1-l3 on the left and disappeared from l3 on the right, from l4 on the left. muscular tension in her legs was mildly decreased. moderate atrophy was noticed and hypropreflexia could be found in her legs. pathologic reflex were negative bilaterally. severe scoliosis was noticed. she was not able to perform heel-to-shin examination. preoperator score: asia motor score was 27 points on the right, left 28 points asia light touch score was 40 points on the right, left 41 points asia pin prick score was 38 points on the right, olfactory ensheathing cells romanian neurosurgery vol. xv nr. 2 9 left 42 points score of xishan hospital spinal cord injury functional rating scale was 24 points operation procedure: following the procedure of cell hla-matching between the donor and recipient, under general anesthesia, the surgical transplantation of olfactory ensheating cells was done on november 12,2007. 100 microl containing about 1 million cells were injected into the spinal cord conus of the patient. at the same time the surgical lysis of tethered cord was done at the segments at l4 post-operative course she was treated by the adjunct regimens including the massage, physical therapy and acupuncture therapy during the whole admission. when the patient discharged, neurological functional improvement was found. she felt that the sensation low down and the muscular power of her legs increase. also the sweating on her legs were found, while before not. motor: upper extremities were 5/5 bilaterally; lower extremities: hip dorsflexors, ankle plantar flexors and long toe extensors were 0/5 bilaterally. sensation: light touch decreased at l2-3 on the right, at l2-l4 on the left and disappeared from l4 on the right, from l5 on the left. pin prick decreased at l2 on the right, at l2-l3 on the left and disapperead from l3 on the right, from l4 on the left. as her incision has not healed completely due to its edges located in the skin part were not well. so she needed to keep lying on the bed, if possible lying on the stomach is the best. she should let the incision be pressed with bandage which was aseptic all the time, till it cured well. but don’t press the incision hardly in order not to pierce it in case of infection. postoperative score: asia motor score was 28 points on the right, left 29 point asia light touch score was 41 points on the right, left 42 points. asia pin prick score was 41 points on the right, left 42 points. score of xishan hospital spinal cord injury functional rating scale was 25 points, which increased by 1 point than before including the aspect of sweating. discharge order 1. please require the local surgeon check the incision carefully every three days. if they have some questions about the incision, please let them inform us. 2. the patient should get plenty of suitable and soft standardized exercise. 3. she should let the incision be pressed with bandage all the time, till it cured well. but don’t press it too much in order to keep it blocking. if the cut can not cure and open, she had better to take the skin flap transplantation. 4. don’t get up and sit and keep lying on the bed, if possible lying on the stomach is the best. 5. don’t pierce the incision blocking. 6. after returning home, the patient was required to be followed up by her primary care physician and her family. she will undergo checkups at interval of 1 month, 2 months, 3 monthss, 6 months, 1 year, 2 year, and 5 years. these checkups must include the evaluation completed by the physician or patient’s family. discussions objective of this paper is to compare findings of a patient with clinical complete tethered cord syndrome before and after receiving olfactory ensheating cellular implants. no improvement in sensory function, motor function, and other functional amelioration could be observed after the injection of olfactory ensheathing cells (oecs). the neurosurgical procedure lead postoperatively to unhealed incision and it will need aseptic bandages all the time, till it will cure well. we can consider that the period after surgery is too short for a correct assessment. also in this case, the neurosurgeon will obtain his follow up about the injection of olfactory ensheathing cells (oecs) into the spinal cord for tethered cord by email: „the patient will be followed up by her primary care physician and she will undergo checkups at interval of 1 month, 2 months, 3 monthss, 6 months, 1 year, 2 year, and 5 years. these checkups must include the evaluation completed by the physician or a.v. ciurea romanian neurosurgery vol. xv nr. 2 10 patient’s family”. we consider that the neurological examinations must be associated with mri examination; mri will be used as a spinal cord lesion assessment tool before and after the surgical procedure. (3) the risk of foetal olfactory ensheathing cells transplant is an immune rejection and it could compromise the effectiveness of the transplanted cells. there are enough studies about autologous transplantation of olfactory ensheathing cells into the spinal cord, after nasal biopsy and olfactory ensheathing cell culture. (5) there are a lot of data about the cells therapies in the treatment of the central nervous system’s lesions. stem cells are feasible candidates for cell therapy of spinal cord’s lesions. different therapeutic strategies based on stem cells have been developed and studied. several strategies support cell replacement of the damaged tissue while others rely on therapeutic effects induced by cell transplantation. there are no fully restorative treatments for spinal cord lesions, but various rehabilitative therapies have been tested in animal models. several researcher groups have tryed to transplante stem cells or other types of cells into human with chronic spinal cord lesions. the preliminary reports showed modest improvements but the peerreviewed results have not yet been reported. (6) the olfactory nerve is the only part of the central nervous system that is known to regenerate continuously throughout adult life. it is thought that the ability of the olfactory nerve to regenerate continuously is assigned to the presence of olfactory ensheathing cells (oecs). olfactory ensheathing cells are specialised glial cells that surround the olfactory sensory axons in the nose. they have properties of schwann cells in promoting and assisting growth of axons. they are unique among the glia in residing both inside and outside the central nervous system, in the olfactory bulb and olfactory nerve, respectively (5). the olfactory ensheathing cell (oec) has attracted much interest recently because of its potential for transplantation-based therapy of cns disease. rat oecs are able to remyelinate demyelinated axons and support regeneration of damaged axons. (1) these properties have led to an increasing use of olfactory ensheathing cells in preclinical models of transplantation for spinal cord repair including complete transection, hemisection, tract lesion, and contusion with over 50 studies published in the last years. olfactory ensheathing cells and stem cells are different. there is a difference of the pathophysiology between the tethered cord syndrome with paraplegia, urinary and bowel movement incontinence and the traumatic spinal cord injury. during the spinal cord injury there is a complete or an incomplete section; therefore there is a disrupted spinal cord or some types of contusion, compression, penetration or laceration of the spinal cord. spinal cord injury leads to the death of cells, including neurons, oligodendrocytes, astrocytes and precursor cells, and any resulting cavities and cysts may interrupt descending and ascending axonal tracts, although circumferential white matter is often spared. after the initial insult to the spinal cord, additional structure and function are lost through active secondary processes (ongoing apoptosis of oligodendrocytes and loss of myelin). demyelinated axons are observed up to a decade after human spinal cord injury, and the extent to which these axons survive unmyelinated or become remyelinated by central or peripheral myelin is very important for spinal cord. fig. 1a ct image of a left acute extradural hematoma [male patient , 43 years old , gcs = 6] olfactory ensheathing cells romanian neurosurgery vol. xv nr. 2 11 fig. 1b the same case: icp monitoring after surgery fig. 1c post – traumatic hydrocephalus occurs four months after traumatic brain injury when the spinal cord is tethered, this abnormal stretching puts tension on the cord and there are a maldevelopment of the nerves that control the legs, feet, bowel and bladder. therefore there are a ageneses of the conus medullaris and of the cauda equina, also of the lumbar and sacral nerves. several clinical trials worldwide have been initiated that use transplantation of olfactory tissue containing oecs into the damaged spinal cord of humans. the olfactory ensheathing cells (oecs) inoculation in the scar of the traumatic spinal cord injury has the purpose to induce remyelination at this level, as well as to allow for regeneration in specific circumstances and transplanted schwann cells (scs) share these repair properties too. (7) specifically, oecs promote axon regeneration and functional recovery indirectly by augmenting the endogenous capacity of host schwann cells to invade the damaged spinal cord. together with schwann cells, oecs create a 3-dimensional matrix that provides a permissive microenvironment for successful axon regeneration in the adult mammalian central nervous system. (2) theoretically the olfactory ensheathing cells (oecs) inoculation in tethered cord can not regenerate the neurons of the agenesed conus medullaris; olfactory ensheathing cells (oecs) inoculation will permit only an axon regeneration if prior to this there were functional neurons and functional axons. therefore the use of olfactory ensheathing cells is used for regrowth of lesioned axon projections and restoration of neuronal connectivity. (8) the chinese neurosurgeons have performed olfactory ensheathing cellular transplants from aborted fetuses in more than 400 patients with sci and 100 patients with amyotrophic lateral sclerosis (als) at xishan hospital, beijing. they extract oecs from fetal olfactory bulb tissue. after cultivation and purification of the cells (a 10 to 14 days process), they obtain a “clinical standard oecs” that can be used for the surgery. they have treated patients with different cns diseases, such as amyotrophic lateral sclerosis, spinal cord injury, multiple sclerosis, freidriech's ataxia, cerebral palsy, brain trauma, spinal muscular atrophy, a.v. ciurea romanian neurosurgery vol. xv nr. 2 12 persistent vegetable status, sequela of stroke, dementia, hereditary spastic paraparesis, myelitis etc. therefore the olfactory ensheathing cellular transplants were used in a various cns diseases, with different pathophysiology and without clear inclusion criteria into clinical trials. the search for new therapies must be based on scientific methods. patients must meet a specified criteria for entry in a scientific trial, are randomly assigned to one of two treatments, are carefully examined for the duration of the likely benefit of the experimental and other intervention, and are examined at the end of the trial by physicians who do not know which treatment was given (4). conclusions 1. based on the observation of this case and on other series of presented operated subjects, the efficacy of olfactory ensheathing cells implantation procedure are unclear. 2. in this case the period after surgery is too short for a correct assessment. 3. there are numerous articles that show the transplanted olfactory ensheathing cells are able to remyelinate demyelinated axons into the traumatic spinal cord injury. there is a difference of the pathophysiology between the tethered cord syndrome and the traumatic spinal cord injury 4. most of researchers prefer autologous transplantation of olfactory ensheathing cells into the spinal cord, after nasal biopsy and olfactory ensheathing cell culture. 5. in china the olfactory ensheathing cellular transplants were performed in various cns diseases, with different pathophysiological mechanisms and without clear inclusion criteria into clinical trials. references 1. barnett sc, alexander cl, iwashita y,. gilson jm et al. identification of a human olfactory ensheathing cell that can effect transplant-mediated remyelination of demyelinated cns axons. brain, 2000, 123; 8, 1581-1588 2. boyd jg, doucette r, kawaja md defining the role of olfactory ensheathing cells in facilitating axon remyelination following damage to the spinal cord the faseb journal. 2005;19:694-703. 3. dobkin bh, curt a, guest j cellular transplants in china: observational study from the largest human experiment in chronic spinal cord injury. neurorehabilitation and neural repair 2006, 20 (1); 5 -13 4. enserink m. stem cell research. a season of generosity and jeremiads. science. 2006 8;314(5805):1525. 5. feron f, perry c, cochrane j et al. autologous olfactory ensheathing cell transplantation in human spinal cord injury. brain, 2005, 128: 2951–2960. 6. iencean st.m., ciurea a.v., ianovici n., onose g. chronic traumatic spinal cord injury; perspective of autologous bone marrow tissue implant. international conference on recent advances in neurotraumatology (icran), tianjin, china, 19 22 sept 2007. 7. lakatos a, franklin rj, barnett sc. olfactory ensheathing cells and schwann cells differ in their in vitro interactions with astrocytes. glia. 2000;32(3):214-25 8. ruitenberg mj, vukovic j, sarich j, busfield sj, plant gw. olfactory ensheathing cells: characteristics, genetic engineering, and therapeutic potential, journal of neurotrauma., 2006, 23(3-4): 468-478. romanian neurosurgery (2019) xxxiii, 1: 67-70 doi: 10.33962/roneuro-2019-013 www.journals.lapub.co.uk/index.php/roneurosurgery cystotoperitoneal shunt surgery during infancy in porencepahalic cyst located in frontal region led to regaining of developmental milestone guru dutta satyarthee1, luis rafael moscote-salazar2, amit agrawal3 1 department of neurosurgery, neurosciences centre, aiims new delhi, india 2 neurosurgeon-critical care red latino, latin american trauma & intensive neuro-care organization, bogota, colombia 3 neurosurgery department, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract porencepahalic cyst is considered as an extremely uncommon developmental disorder of the central nervous system, being characterized by the presence of a fluidfilled cysts or cavities located within the cerebral hemispheres. it can be associated with varied aetiology and can present with a spectrum of clinical presentation varying from asymptomatic to grossly spastic limbs, mental retardation, cognitive impairment and intractable seizure. extensive pubmed and medline search did not yield any result when searched for term “infancy, porencepahalic cyst, cystoperitonreal shunt.” however, clear guideline for management is still lacking. authors report an interesting case of giant porencepahalic cyst located in the right frontal region in infancy and underwent cystoperitonreal shunt surgery, which lead to good outcome with remarkable recovery of delayed milestones with adequate scholastic performances along with marked diminution in the size of porencepahalic cyst. introduction porencepahalic cyst is considered as an extremely rarer encephalaomalatic disorder of the central nervous system characterized by the presence of a fluid-filled cavities or cysts. [1] it usually represents the end result of various types of the cerebral parenchymal injury, but can also be congenital developmental disorder, or consequences of intracerebral hemorrhage. [2,3] author reports an interesting case of porencepahalic cyst located in the right frontal region, who underwent cystotoperitoneal shunt surgery, led to recovery of regressive milestones and currently child is extremely well scholastically at four years following csf diversion surgery. keywords porencephaly, raised intracranial pressure, cystoperitoneal shunt surgery. corresponding author: guru dutta satyarthee department of neurosurgery, neurosciences centre, aiims new delhi, india duttaguru2002@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 68 guru dutta satyarthee, luis rafael moscote-salazar, amit agrawal case ilustration a oneyearold male infant was brought to our neuroscience emergency services with complaint of failure to thrive, delayed developmental milestones with repeated episodes of vomiting and progressive head enlargement for the last six months. on general physical examination at admission, vitals were stable, with bulging anterior frontanelle and head circumference was 54 cm. on neurological examination, he was alert, crying. evaluation of milestones, he was unable to can sit up without support and not able to crawl and could not use the pincer grasp. he was not able to begin to make recognizable syllables like "ma” and also had regression of language development. fundi showed bilateral papilloedema. he had bilateral up gaze paresis with presence of sunset sign. the routine hematological and biochemical parameters were normal limit. the computerized cranial tomography which was carried out after admission (fig. 1) revealed presence of a giant porencepahalic cyst in the right frontal region crossing across the midline and causing mass effect obstruction along the csf pathway leading to dilated lateral ventricles, the third ventricle and. the periventricular ooze was present. (fig. 2) he underwent cysto-peritoneal shunt surgery under general anaesthesia. csf study revealed normal biochemical parameters with normal cell count and further, csf culture did not show growth of microorganism. after surgery he regained milestones like crawling, pincer grip and started telling monosyllabic words over two months after the surgery. (fig. 3) the computerized tomography carried out at follow-up at four years after shunt surgery revealed well decompressed ventricles (fig4) with ventricular catheter well placed, (fig. 5) and marked reduction in the size of porencepahalic cyst with well-functioning shunt. follow-up at three year, he was doing extremely well with developmental milestone appropriate to age and the body weight also appropriate to the age. figure 1. noncontract cranial computed scan showing large porencepahalic cyst figure 2. tomogram showing shut in situ figure 3. noncontract cranial computed scan showing significant diminution in size of porencepahalic cyst figure 4. noncontract cranial computed scan showing signicant diminution in size of porencepahalic cyst with shunt tip in situ 69 cystotoperitoneal shunt surgery during infancy in porencepahalic cyst located in frontal region discussion in 1859, heschl coined the term “porencephaly” to describe presence of a cavity within the human brain. [2] the porencepahalic cavities can result from focal cerebral degeneration secondary to haemorrhages. [8] further de novo or inherited heterozygous mutations in col4a1 coding the type iv α1 collagen chain, which is essential for vascular basement membranes structural integrity is observed in individuals with porencephaly by yonder et al. [8] yoneda et al postulated abnormalities of the α1α1α2 heterotrimers of type iv collagen causes porencephaly. [4] during embryonic life. the large craters develop on the brain surface and gets lined with smooth tissue, filled –up with fluid and causes local mass effect and focal neurological deficit and regression of milestones. [5,6] usually caused by antennal or perinatal insult prior to development of the cerebral gyri due to various pathology i.e. infective, infarction ischemic or intracerebral haemorrhage. depending on the location, size and approximate to the vital region and severity of the defects, symptoms are highly variable and may cause only minor neurological deficit to severe mental retardation and paralysis in extreme cases. the patients with a porencepahalic cyst also frequently suffer with seizure disorder. [4,7] the diagnosis can be also made even during antenatal period with ultrasound and considered as preferred imaging modality during fetal life. in infant, trans-illumination of the skull can also aid in the diagnosis of the porencepahalic cyst. cranial computed tomography reveals location, size; volume, degree of mass effect, associated hydrocephalus and associated developmental pathology and effect of previous treatment and very useful in serial follow-up in assessing the size and evaluating the effect of cystoperitoneal shunt and recurrence of porencepahalic cyst. [6] currently. the magnetic resonance imaging is considered as modalities of choice as it clearly depicts the pathology and associated obstruction along the csf pathway and associated congenital hydrocephalus, agenesis of corpus callosum or other developmental pathology. porencepahalic cyst diagnosis requires detailed clinical and neurological evaluation, families history, clinical observations, or based on neuroimaging findings. neuroimaging establishes the diagnosis and further assessment of intelligence, memory and speech evaluation can further aid in the planning of the holistic management and rehabilitation measures. [4] currently, there is no curative therapy for porencepahalic cyst and various treatments currently offered included physiotherapy for spastic limbs, rehabilitation, providing antiepileptic medication for those suffering with seizures. surgical procedure may include cerebrospinal fluid diversion surgery like cystoperitonreal shunt, vp shunt surgery and surgery for epilepsy with intractable epilepsy. [1] according to the location of porencepahalic cyst, extent of the mass effect, size of cavities, and severity of the disorder, combinations of treatment modalities of treatment are usually made tailor made to suit the case. prognosis of porencephaly depending on various factors i.e. the location of the cyst and extent of the damage of the brain. cases with mild neurological deficit can lead normal lives and self-care is possible, however more seriously disabled cases require lifelong support in the nursing care and rehabilitator measures. [5] early diagnosis, medication, participation in rehabilitation activity related to fine-motor control, and communication skill can significantly improve the symptoms and ability to cope up with the severe disability and prompt to lead to normal life. infants, with proper treatment, can develop good locomotors control as our case, as he was offered surgical treatment at infancy continued antiepileptic medication, led to good recovery of milestones and improvement in cognitive and scholastic performance. conclusion early diagnosis and management of symptomatic raised intracranial pressure in case of porencepahalic cyst, appropriate surgical intervention at early age and antiepileptic medication and rehabilitation measure and regular follow-up cases may aid in not only good neurological recovery and acquiring good motor and cognitive skill and can lead independent life as our cases underwent cystoperitonreal shunt at one-year age. references 1. gul a, gungorduk k, yildirim g, gedikbasi a, ceylan y prenatal diagnosis of porencephaly secondary to maternal 70 guru dutta satyarthee, luis rafael moscote-salazar, amit agrawal carbon monoxide poisoning. arch gynecol obstet. 2009; 279(5):697-700. 2. hirowatari c, kodama r, sasaki y, tanigawa y, fujishima j, yoshikawa t, yabuuchi k, kuwamura y, hirakawa k, kamimura y, maeda h porencephaly in a cynomolgus monkey (macaca fascicularis). j toxicol pathol. 2012; 25(1):45-9. 3. debus om, kosch a, sträter r, rossi r, nowak-göttl u the factor v g1691a mutation is a risk for porencephaly: a casecontrol study. ann neurol. 2004; 56(2):287-90. 4 yoneda y, haginoya k, arai h, yamaoka s, tsurusaki y, doi h, miyake n, yokochi k, osaka h, kato m, matsumoto n, saitsu h. de novo and inherited mutations in col4a2, encoding the type iv collagen α2 chain cause porencephaly. am j hum genet. 2012; 13; 90(1):86-90. 5 shimizu m, maeda t, izumi t the differences in epileptic characteristics in patients with porencephaly and schizencephaly. brain dev. 2012; 34(7):546-52. 6. ho ss, kuzniecky ri, gilliam f, faught e, bebin m, morawetz r congenital porencephaly and hippocampal sclerosis. clinical features and epileptic spectrum. neurology. 1997; 49(5):1382-8. 7. burneo jg, faught e, knowlton rc, martin rc, bebin m, morawetz r, kuzniecky r temporal lobectomy in congenital porencephaly associated with hippocampal sclerosis. arch neurol. 2003; 60(6):830-4. 8. yoneda y, haginoya k, arai h, yamaoka s, tsurusaki y, doi h, miyake n, yokochi k, osaka h, kato m, matsumoto n, saitsu h de novo and inherited mutations in col4a2, encoding the type iv collagen α2 chain cause porencephaly. am j hum genet. 2012 13; 90(1):86-90. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article chondroblastoma of thoracic vertebra in young adult causing paraparesis pramod j. giri, vaibhav s. chavan india doi: 10.1515/romneu-2017-0054 romanian neurosurgery (2017) xxxi 3: 335 338 | 335 doi: 10.1515/romneu-2017-0054 chondroblastoma of thoracic vertebra in young adult causing paraparesis pramod j. giri, vaibhav s. chavan neurosurgery department, super specialty hospital & g.m.c., nagpur, india abstract: chondroblastoma of spine is very rare condition. to best of our knowledge, fewer than 30 cases have been reported in the world literature. almost all of them involved both anterior & posterior component of vertebra. there are only few reports with isolated posterior element involvement. clinical presentation of paraparesis because of vertebral chondroblastoma is very rare. this case report presents 17 yr old male with chondroblastoma involving posterior thoracic vertebra presenting with quadriparesis which improved after successful treatment. early diagnosis and complete excision with periodic follow up is necessary for treatment of this disease. key words: bone tumors, chondroblastoma, thoracic spine. introduction chondroblastoma is benign bone tumor arising most often in the epiphyses of long bones. the most common sites are the proximal tibia, proximal & distal femur, and proximal humerus (9). it was first described by ewing (8) and codman (6), but it was not until 1942 that jaffe and lichtenstein (12) were first to confirm its chondromatous nature and rightfully named it chondroblastoma. the occurance of chondroblastoma in vertebral column is rare with approximately 30 cases reported in whole spine (2). herein we report 17 year old male with chondroblastoma arising from d6/d7 vertebra compressing spinal cord and causing paraparesis. case report history & clinical examination 17 year old male presented with 4 to 5 month history of back pain which was intermittent and aggravated during last month. his pain increased on walking and was relieved with rest. he started having weakness in both lower limbs since last 2 months. he had gait disturbance and eventually needed support while walking. he started feeling numbness below waist since last 2 months, however he had no bowel/bladder complaints. on physical examination he had tenderness over back in thoracic region and there was no deformity. a neurological examination revealed mrc grade 3 power in lower limbs both proximally and distally. there was 336 | giri et al chondroblastoma of thoracic vertebra causing paraparesis decreased sensation for pain, temperature, vibration & proprioception below 8th thoracic vertebra. the deep tendon reflexes of the lower limbs was exaggerated and babinski sign was present bilaterally. radiological examination plain x-ray shows osteolytic lesion involving right side of d6/d7 vertebrae & posterior part of 6th/7th rib. m.r.i. thoracic spine revealed space occupying lesion involving right transverse process, spinous process and right posterior body of d6/d7 thoracic vertebrae causing compression of spinal cord and signal change in the cord (figures 1 & 2). figures 1 & 2 white arrows show tumor compressing on spinal cord at d6 & d7 level surgery he underwent d6 & d7 laminectomy with complete decompression of spinal cord. laminectomy was performed at level of d6 & d7. the spinal cord appeared to be pushed to left side and it did not pulsate. the tumor was greyish yellow and vascular. it was located in epidural space and there was no breach in dura. after tumor debulking spinal cord returned to normal position and began to pulsate. near total excision of tumor was achieved. (figure 3) figure 3 postoperative image showing complete decompression of spinal cord with space around post-operative course postoperatively patient was given thoracolumbar brace and gradually mobilized. there was gradual improvement in lower limb power and patient regained his normal power. there was no postoperative complication. histopathology on histological examination specimen shown multiple polygonal cells arranged in romanian neurosurgery (2017) xxxi 3: 335 338 | 337 loosely cohesive sheets with centrally placed nucleus & scanty cytoplasm. osteoclastic giant cells were also visible along with areas of eosinophilic chondroid matrix. these histopathological findings are consistent with chondroblastoma. (figure 4) figure 4 histological image showing multinucleated giant cells (white arrow), eosinophilic chondroid matrix (black arrow) with loosely cohesive sheets of polygonal cells suggestive of chondroblastoma discussion chondroblastoma is benign cartilaginous neoplasm that generally affects the appendicular skeleton and occurs in the second decade of life (1). it is much more common in men than in women with male to female ratio of 2:1(3, 5). it accounts for for about 1% of primary bone tumors and is considered to be benign with good prognosis in majority of cases (7). although chondroblastoma occur most often in the epiphysis of the major bones this tumor can appear in secondary ossification center which is present in vertebra. occurrence of vertebral chondroblastoma causing neurodeficit is very rare. according to vialle et al, who recently reviewed 26 cases of spinal chondroblastoma reported in the past 50 years, 9 were found in cervical vertebrae, 9 in the thoracic vertebrae, 6 in the lumbar vertebrae and 2 in the sacrum (15). the clinical findings are nonspecific and differ depending on tumor extent and involved level. local pain is most common presenting complaint in extradural spinal tumors (13). in most instances the radiological appearances may be quite characteristic allowing an early diagnosis of chondroblastoma. it manifests as a well circumscribed oval translucent area with a sclerotic rim which rarely causes bone expansion. x ray shows presence of spot like calcification which helps to differentiate this lesion from giant cell tumor of the bone (14). bloem and mulder (1) reported that radiological diagnosis had a sensitivity of 75% and specificity of 99%. the diagnosis is usually confirmed by the histological feature of rounded or polygonal chondroblast like cells, cartilaginous intercellular matrix, multinucleated giant cells and the focal calcification. chondroblastoma is benign tumor hence it is usually treated by local curettage with or without bone grafting or cryosurgery. local recurrence is common problem. huvos and marcone (11) reported that the 3 years recurrence rates were 24% for chondroblastoma and 100% for chondroblastoma associated with aneurysmal bone cyst. resection is advocated with a 338 | giri et al chondroblastoma of thoracic vertebra causing paraparesis margin of surrounding normal tissue when this can be accomplished without great loss of function (4). irradiation is usually reserved for complicated cases because of risk of radiation induced malignant transformation (10). conclusion although rare neoplasm, vertebral chondroblastoma should be included in the differential diagnosis when encountered with destructive lesion of spine. complete surgical excision as for as possible should be achieved but neurodeficit should be avoided. patient needs close long term follow up & may need repeated surgeries. correspondence dr. vaibhav s. chavan neurosurgery department, superspeciality hospital & g.m.c., nagpur. mailing address:dept of neurosurgery, superspeciality hospital and government medical college, nagpur, india. pin code 440008 email address: vschavan86@gmail.com contact number:91 9923377667 references 1)bloem jl, mulder jd. chondroblastoma: a clinical and radiological study of 104 cases. skeletal radiol. 1985; 14(1):1-9. 2)brasse f, schmitt m, hoeffel jc, montaut j, bey p, bretagne mc. [a case of vertebral chondroblastoma]. rev chir orthop reparatrice appar mot.1985; 71(6):389-92. 3)buraczewski j, lysakowska j, rudowski w. chondroblastoma (codman's tumour) of the thoracic spine. j bone joint surg br. 1957 nov; 39-b (4):705-10. 4)carnesale pg. benign (occasionally malignant) tumors of bone. in: canale st (ed). campbell’s operative orthopaedics. vol 1, 9th edn. mosby-year book: st louis, 1998, pp 703–713. 5)chung om, yip sf, ngan kc, ng wf. chondroblastoma of the lumbar spine with cauda equina syndrome. spinal cord. 2003 jun; 41(6):359-64. 6)codman ea. the classic: epiphyseal chondromatous giant cell tumors of the upper end of the humerus. surg gynecol obstet.1931; 52:543. clin orthop relat res.2006 sep; 450:12-6. 7)dahlin dc, ivins jc. benign chondroblastoma. a study of 125 cases. cancer. 1972 aug; 30(2):401-13. 8)ewing j: neoplastic diseases: a treatise on tumours, ed 3. philadelphia, saunders, 1928, p 293. 9)ewing, j., (1928) the classification and treatment of bone sarcoma. report of international conference on cancer (bristol), j write, 1928, 265-267. 10)hatcher ch. the development of sarcoma in bone subjected to roentgen or radium irradiation. j bone joint surg am 1945; 27-a: 179. 11)huvos ag, marcove rc. chondroblastoma of bone. a critical review. clin orthop relat res. 1973 sep ;( 95):300-12. review. 12)jaffe hl, lichtenstein l. benign chondroblastoma of bone: a reinterpretation of the so-called calcifying or chondromatous giant cell tumor. am j pathol. 1942 nov; 18(6):969-91. 13)kumar r, giri pj. pediatric extradural spinal tumors. pediatr neurosurg.2008; 44(3):181-9. 14)lee yh, shin da, kim kn, yoon dh. a case of thoracic vertebral chondroblastoma treated with 3-d image guided resection and reconstruction. j korean neurosurg soc 2005; 37:154-6. 15)vialle r, feydy a, rillardon l, tohme-noun c, anract p, colombat m, de pinieux g, drapé jl, guigui p. chondroblastoma of the lumbar spine. report of two cases and review of the literature. j neurosurg spine. 2005 may; 2(5):596-600. 02_paper romanian neurosurgery | volume xxx | number 4 | 2016 | october december article intra-arterial nimodipine for the treatment of vasospasm due to aneurysmal subarachnoid hemorrhage a. chiriac, georgiana ion, n. dobrin, z. faiyad, i. poeată romania doi: 10.1515/romneu-2016-0074 romanian neurosurgery (2016) xxx 4: 461 – 466 | 461 doi: 10.1515/romneu-2016-0074 intra-arterial nimodipine for the treatment of vasospasm due to aneurysmal subarachnoid hemorrhage a. chiriac, georgiana ion*, n. dobrin*, z. faiyad*, i. poeată “gr. t. popa” university of medicine and pharmacy, iasi, romania “prof. dr. n. oblu” clinic emergency hospital, iasi*, romania abstract: the cerebral vasospasm is still considered the most devastating complication for the patients with aneurysmal subarachnoid haemorrhage. the aim of this study was to evaluate the efficiency of intra-arterial nimodipine administration in cerebral vasospasm diminutions and outcome of the patients. key words: cerebral vasospasm, aneurysmal sah, intra-arterial nimodipine introduction cerebral ischemia due to severe vasospasm is the major factor of secondary morbidity and mortality for the patient with aneurysmal subarachnoid hemorrhage. the medical management of this clinical situation has been improved over the last decades and the current strategies for preventing vasospasm comprise both medical and interventional measures. thus, the use of intraoperative intracisternal thrombolysis or intracisternal application of nicardipine-prolonged implants followed by oral nimodipine administration and hemodynamic therapy demonstrates effectiveness in preventing cerebral vasospasm. even with these therapeutic methods, the level of permanent disabilities due to cerebral vasospasm is still significant (10% 20%) [1, 3, 4]. this situation led to development of alternative endovascular strategies such as balloon angioplasty and intra-arterial spasmolysis with nimodipine or papaverine. the objective of our study was to investigate the effect of intra-arterial nimodipine administration to the patient with aneurysmal subarachnoid hemorrhage treated in our clinic. material and methods 51 patients with aneurysmal subarachnoid hemorrhage were endovascular treated for 54 aneurysm at our institution between september 2015 and september 2016. from this group of patients 10 cases underwent intra-arterial injection of nimodipine for the treatment of subarachnoid hemorrhage induced vasospasm. 7 patients received intra 462 | chiriac et al intra-arterial nimodipine for the treatment of aneurysmal vasospasm arterial nimodipine injection immediately before and after the procedure of aneurysm occlusion with coils. these were due to the delayed addressing to our clinic (day 5 to day 9 after rupture) in which the cerebral vasospasm was imaging and clinical manifested. the other 3 patients benefit of intra-arterial nimodipine injection a few days after the procedure of aneurysm coils occlusion for cerebral vasospasm highlighted on echo doppler monitoring and clinically manifested. the following protocol is discussed to be used at our institution for the management of sever cerebral vasospasm after aneurysmal subarachnoid hemorrhage. after the procedure of aneurysm occlusion, continuous monitoring of intracranial flow velocities detected by transcarnial doppler (tcd) is started daily in at least two arterial segments on both parts. for asymptomatic patients with tcd flow acceleration above 120 cm/s, a moderate hypertensive and hypervolemic therapy is applied along with continuing to use the oral administration of 60 mg of nimodipine doses every 4 hours. when vasospasm is suspected clinically (conscious patient with transient neurological deficits or confused patient), a brain computer tomography is performed to confirm the presence or absence of ischemia. the patient is then transferred to the intensive care unit and a maximal triple h therapy is administrated. if the patient's clinical status continues to worsen and the intracranial flow velocities as detected by tcd exceeds 150 cm/s, a endovascular intra-arterial nimodipine injection is taken in to discussion to be initiated. a catheter it will be placed within internal carotid artery (segment c3-c2) and a bolus of 1mg (5ml nimodipine and 15ml saline) will be administrated in a time of 5 minutes. the follow-up angiography will be performed after 10 minutes. if only minor angiographic effects are visualized a second bolus injection is performed. for the next 7 days a treatment with 1 mg of nimodipine, i.e. 5 ml nimotop solution, (about 15 μg/kg bw/h), should be infused each hour via a central catheter. patients of body weight less than 70 kg or with unstable blood pressure should be started on a dose of 0.5 mg nimodipine per hour (2.5 ml of nimotop solution), or less if necessary. if the neurological status it will stabilize in this period of time a change to nimotop tablets could be initiated and the total duration of treatment should not exceed 21 days. we retrospectively reviewed clinical dates and imaging reports (angiography and ct) of these 10 patients who received intra-arterial nimodipine administration. the endovascular angiography and procedure were performed using a 5f or 4f diagnostic catheter placed in the internal carotid artery. nimodipine was administrated in a solution of nacl 9% (5ml nimodipine and 15ml nac 9%). the dose varied from 1mg to 3 mg per vessel. blood pressure and heart rate were continuously romanian neurosurgery (2016) xxx 4: 461 – 466 | 463 monitored as parameters for systemic sideeffect. repeat angiography control exposures were performed at 10 minutes after each session of nimodipine administration. the frontal angiography projections on arterial phase were compared with focalization on a1 and m1 segments. the post endovascular procedure clinical examinations were determined as improved, stable or worse. cerebral ct scan acquisitions before and after treatment were confronted to identify same particular signs as edema, infarction, hydrocephalus or a new hemorrhage. results of the 51 patients with ruptured aneurysm treated by endovascular coil occlusion 10 patient received intra-arterial nimodipine administration. the mean age of patients was 53.4 (interval range, 36 to 74 years). the sex (male and female) ratio was equal. 5 patients had hunt&hess grade iii, 2 had grade ii, one had grade iv and 2 had grade i. the average dose of nimodipine per patient was 2 + 0.5mg. only two patients received two separate treatments. nine injection procedures were performed under general anesthesia and three only with local one. notable angiographic vascular dilatation was identified in 9 of the 12 procedures and in 8 patients. the comparative analysis of brain ct scans pre and postprocedural showed ischemic changes in 2 patients. administration of intra-arterial nimodipine had insignificant systemic effects. in two patients the systolic blood pressure dropped with 30 mmhg. there was no severe bradycardia or significant elevation of intracranial pressure (table 1). clinical evolution after the endovascular chemical treatment was improved in 6 patients (gos 5), stable in two (gos 3) and worse in one (gos 4). one patient died at 3 days after second session of intra-arterial nimodipine administration (gos 1) due to an uncontrollably severe vasospasm that caused extensive hemispheric ischemia. illustrative cases a 48 year-old female presented to our clinic with confusion and severe headache syndrome. the family declared the onset of symptoms after seven days. brain ct at admission revealed a slight subarachnoid haemorrhage in left sylvian fissure. a 464 | chiriac et al intra-arterial nimodipine for the treatment of aneurysmal vasospasm figure 1 a diagnostic brain ct revealing a slight subarachnoid haemorrhage in left sylvian fissure; b cta showing a voluminous left internal carotid artery aneurysm (ophthalmic segment); c dsa showing sever diffuse cerebral vasospasm; d – dsa after ian showing good diminishes of vasospasm; e – dsa control after aneurysm embolization and second ian administration; f brain ct postembolization b c d e f romanian neurosurgery (2016) xxx 4: 461 – 466 | 465 table i patients’ characteristics discussion the clinical effects of the endovascular methods used to treat symptomatic vasospasm after aneurysmal subarachnoid haemorrhage were investigated by many studies. intraarterial nimodipine injection and balloon angioplasty are widely accepted as rescue therapies in most of neurosurgical units when maximized medical therapy fails. the balloon angioplasty is well known as the most effective endovascular procedure due to nearly permanent reversal of vasospasm. this procedure is limited to proximal vessel segments and may be accompanied by a series of complications. the most serious complications are vessel occlusion or rupture and coils or clip displacement. because this procedure can be accompanied by several technical difficulties it should be performed in centers with experienced endovascular surgeons [1, 2, 4]. intra-arterial administration of vasodilatators has been demonstrated a good alternative to mechanical angioplasty with optimal results in reversing angiographic vasospasm and in reducing flow velocities detected by tcd. the literature studies have reported using nimodipine, nicardipine or verapamil as calcium channel blockers for intra-arterial treatment of cerebral vasospasm. biondi et al reported a 76% of clinical improvement, 63% notable angiographic vessel dilation after intra-arterial nimodipine administration and 72% of patients with favourable outcome. hanggi and all reported also 63% patients with significant vascular dilatation with a 93% clinical improvement after the procedure [2, 5, 6]. the clear efficiency of ian is still questionable. most of the investigations showed that nimodipine is effective in diminishing vasospasm in case where intensive medical therapy fails, the therapy could be done in the same session with aneurysm coil occlusion, the procedure is temporary and may need repeated sessions, and the administration is more efficient in dilating small branches than large one [4, 7, 8]. patient no age / sex h&h grade fisher grade aneurysm location day of surgery day of ian administration dose of ian/ session gos 1 54/f ii 2 acoa 0 9 1 5 2 42/m iii 3 acoa 8 8 2 3 3 62/f iv 4 mca 6 6, 8 4 1 4 48/f iii 2 aci oft 7 7 1.5 5 5 53/m iii 4 acoa 3 5 1.5 5 6 49/f i 1 mca 5 5 1 5 7 74/m iii 3 pcoa 1 12, 13 4 4 8 55/m i 2 acoa 2 10 2 5 9 36/m ii 2 mca 4 8 2 5 10 61/f iii 4 pcoa 9 9 1 3 466 | chiriac et al intra-arterial nimodipine for the treatment of aneurysmal vasospasm conclusion our study is by some factors like number of cases and additional monitoring investigations (perfusion parameters: mtt – mean transit time, tmax – selective time to peak of the brain parenchyma, rcbv – regional cerebral blood volume, rcbf – regional cerebral blood flow) [3]. the results of our retrospective analysis suggest that ian is effective and safe in selected cases of vasospasm following aneurysmal sah. we consider that a prospective and mare large randomized study is needed to confirm these results. references 1. bashir, a., andresen, m., bartek, j., cortsen, m., eskesen, v., & wagner, a. (2016). intra-arterial nimodipine for cerebral vasospasm after subarachnoid haemorrhage: influence on clinical course and predictors of clinical outcome. the neuroradiology journal, 1971400915626429. 2. biondi, a., ricciardi, g. k., puybasset, l., abdennour, l., longo, m., chiras, j., & van effenterre, r. (2004). intra-arterial nimodipine for the treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results. american journal of neuroradiology, 25(6), 1067-1076. 3. dehdashti, a. r., binaghi, s., uske, a., & regli, l. (2011). intraarterial nimodipine for the treatment of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage: a preliminary study. neurology india, 59(6), 810. 4. hänggi, d., turowski, b., beseoglu, k., yong, m., & steiger, h. j. (2008). intra-arterial nimodipine for severe cerebral vasospasm after aneurysmal subarachnoid hemorrhage: influence on clinical course and cerebral perfusion.american journal of neuroradiology, 29(6), 1053-1060. 5. hockel, k., diedler, j., steiner, j., birkenhauer, u., danz, s., ernemann, u., & schuhmann, m. u. (2016). long-term, continuous intra-arterial nimodipine treatment of severe vasospasm after aneurysmal subarachnoid hemorrhage. world neurosurgery, 88, 104-112. 6. hui, c., & lau, k. p. (2005). efficacy of intra-arterial nimodipine in the treatment of cerebral vasospasm complicating subarachnoid haemorrhage. clinical radiology, 60(9), 1030-1036. 7. kim, j. h., park, i. s., park, k. b., kang, d. h., & hwang, s. h. (2009). intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. journal of korean neurosurgical society, 46(3), 239-244. 8. logallo, n., bøthun, m. l., guttormsen, a. b., holmaas, g., kråkenes, j., thomassen, l., ... & helland, c. a. (2015). continuous local intra-arterial nimodipine for the treatment of cerebral vasospasm. journal of neurological surgery reports, 76(01),e75-e78. microsoft word 18program.doc 128 romanian neurosurgery (2010) xvii 1: 128 130 the national congress of the romanian society of neurosurgery with international participation this national congress of the romanian society of neurosurgery with international participation, 2010, will be held in cluj – napoca between september 28th and october 2nd. main topics: • third ventricle and pineal region tumors • state of art in supratentorial malignant glioma • spinal metastasis • ssnn session • young neurosurgeons session • varia preliminary program wednesday, september 29th, 2010 10:00 18:00 le 15-ème cours francophone de neurochirurgie en roumanie wednesday, september 29th, 2010 19:00 official opening ceremony 20:00 welcome reception thursday, september 30th, 2010 08:30 18:30 scientific sessions (with coffee-breaks and lunch-breaks ) 20:00 folkloric dinner friday, october 1st, 2010 08:30 16:30 scientific sessions (with coffee-breaks and lunch-breaks ) 16:30 18:30 general assembly of romanian society of neurosurgery 20.00 gala dinner saturday, october 2nd, 2010 08:30 12:30 scientific sessions (with coffee-breaks and lunch-breaks ) 12:30 13:00 closing ceremony the national congress of the rsn with international participation 129 registration online • directly on the conference website: http://neurosurgery2010.econgres.ro • by e-mail at contact@neurosurgery 2010.econgres.ro offline please fill-in the registration form and return it to the conference organizer as follows: • by mail, to the conference organizer’s address: econgres medical events, str. a. panu nr. 40, bl. 1a, et. 3, ap. 7, iaşi, 700020, romania • by fax to: +40-232-41.00.60 abstract submission the deadline for submitting the abstracts is july 15th, 2010. the abstracts must be submitted using one of the methods described at registration, excluding the fax possibility. the most recommended way of submitting the abstracts is directly on the conference website (“send abstract” button). in case of submission by mail, you will send a printed version of the paper, together with a cd or a dvd marked with the author’s name and the title of the paper. • only unpublished work will be accepted. authors have full responsibility for the content of their abstracts. • notification of the abstract acceptance will be e-mailed after the 1st of september 2010. • accepted abstracts will be published in the abstract book only on receipt of registration payment in full. • upon submission, indicate one of the topics presented in “preliminary program” section that best describes the abstract. • it is the author's responsibility to submit a correct abstract; any errors in spelling, grammar, or scientific fact will be reproduced as such. • abstracts must be written in english. presentation: oral or poster. the scientific committee reserves its right to accept or reject the submitted abstracts and to select abstracts for oral presentation or poster. 130 romanian neurosurgery (2010) xvii 1: 128 130 registration fees until may 15th, 2010 until august 1st, 2010 after august 1st and on site senior 150 euro senior 200 euro senior 250 euro resident * 100 euro resident * 150 euro resident * 200 euro accompanying persons 125 euro accompanying persons 175 euro accompanying persons 225 euro french course 100 euro french course 150 euro french course 200 euro *for residents, registration forms must be accompanied by a letter from the head of the department, confirming their status. the letter should be printed on a department letterhead and addressed to the registration department of the conference. prof. a.v. ciurea, m.d. vice-president of wfns (at large) honorary president of rsn prof. n. ianovici, m.d. president of rsn prof. st.i. florian, m.d. president of the congress vice-president of rsn microsoft word 7aldeamihaela_metformin 230 | aldea et al metformin delivery using chitosan-capped gold nanoparticles in glioblastoma cell lines             doi: 10.2478/romneu-2018-0030 metformin delivery using chitosan-capped gold nanoparticles in glioblastoma cell lines mihaela aldea1, ioan stefan florian2, monica potara3, olga soritau4, timea nagy-simon3, gabriel kacso1,5 1department of medical oncology and radiotherapy, iuliu hatieganu university of medicine and pharmacy, cluj-napoca, romania 2department of neurosurgery, iuliu hatieganu university of medicine and pharmacy, clujnapoca, romania 3nanobiophotonics and laser microscopy center, interdisciplinary research in bio-nanosciences, and faculty of physics, babes-bolyai university, cluj-napoca, romania 4department of tumor biology, ion chiricuta cancer institute, cluj-napoca, romania 5amethyst radiotherapy center, cluj, romania abstract: introduction: metformin (met), an old anti-diabetic drug, has proven unexpected anti-glioblastoma effects, by impacting cell proliferation, migration and invasion. however, its remarkable anti-cancer efficacy is mainly limited to the use of high millimolar concentrations in in vitro studies, which are hard to be attained in the clinical setting. aim: the aim of this paper was to synthetize gold nanoparticles loaded with met and to test if an enhanced drug delivery via nanotechnology could overcome the limitations of small drug concentrations. materials and methods: gold nanoparticles were functionalized with chitosan (gnpc) and loaded with 80 μm of met. their size, zeta potential and stability were characterized and their internalization within tumor cells was assayed through dark field microscopy. three primary glioblastoma stem cell lines were treated with 5, 10 and 20 μg/ml concentrations of nanoparticles and irradiated. the anti-tumoral effect was evaluated through the mtt cell viability assay. results: met-gnpc are easily synthetized and have a positive zeta potential, spherical shape and a median size of 26 nm. met-gnpc have an increased cell internalization and affect the viability of all three glioblastoma cell lines used compared to control and free met. however, their anti-cancer effect is not statistically different when compared to gnpc, although a slight tendency to a better response may be observed. conclusion:despite an increased cell internalization, the small micromolar concentrations of metformin does not bring an additional benefit to chitosan-based gnps. novel delivery methods being able to carry a higher drug concentration of metformin should be tested. romanian neurosurgery (2018) xxxii 2: 230 239 | 231             introduction metformin (met), a well-known oral antidiabetic, has been regarded as an extremely promising anticancer agent in many cancer types. in vitro and in vivo experiments proved a myriad of mechanisms of action, including decreased cell proliferation, cell cycle arrest, autophagy, apoptosis and cell death in vitro with a concomitant activation of ampk and inhibition of the mtor pathway, while also sensitizing cells to radiotherapy (m. aldea et al., 2014; m. d. aldea et al., 2014; carmignani et al., 2014; nenu et al., 2014; sesen et al., 2015; soritau et al., 2011). our team investigated met in glioblastoma cell lines and proved a surprising reduction of glioblastoma stem-like cells proliferation (m. d. aldea et al., 2014; carmignani et al., 2014; soritau et al., 2011). however, this benefits were observed mainly at supra-clinical doses of 1-10 mm, which are easily obtained in vitro or in vivo experiments, but are unlikely to be obtained in the clinical setting (m. aldea et al., 2014). clinical cancer trials that have tested met with the same doses used in anti-diabetic therapy failed to translate into a relevant tumor response, possibly due to lack of met adequate high concentrations for cancer cell killing (kordes et al., 2015; reni et al., 2016; sayed, saad, el wakeel, elkholy, & badary, 2015). we hypothesize that met tumor targeted delivery by nanotechnology might overcome the ineffectiveness of small drug concentrations. therefore, in this study, we synthetized gold nanoparticles loaded with micromolar concentrations of met in order to test if such low dose compounds reach the anticancer effects observed with high free drug met therapy. materials and methods nanoparticles preparation and metformin loading citrate-capped gold nanoparticles (gnpc) were synthetized following the turkevich−frens method and by slightly modifying the method used in our previous experiments (aldea m, 2018; potara, maniu, & astilean, 2009; turkevich j, 1951). briefly, 100 ml of hydrogen tetrachloroaurate(iii) trihydrate haucl4·3h2o (10-3 m) were heated to a boiling temperature and then mixed to trisodium citrate (10 ml, 38.8 × 10−3 m) (merck) under vigorous stirring. after the formation of a deep-red burgundy colloid, the stirring and boiling processed were continued for 10-15 min. subsequently, the heating was stopped and the stirring process was continued for another 15 min. then, 3 ml of 10-3 m haucl4 were mixed with 18 ml of 2 mg/ml chitosan solution (medium molecular weight), and then heated to 50 ºc. the colloidal solutions were centrifugated and resuspended in ultrapure water. loading of metformin hydrochloride (met) (sigma aldrich) onto the surface of gnpc was performed by incubating the colloidal gnpc with met at ph 3.5. the ph of the mixture was then adjusted to 8 with 1m naoh. the obtained metformin gold nanoconjugates 232 | aldea et al metformin delivery using chitosan-capped gold nanoparticles in glioblastoma cell lines             (met-gnpc) were subsequently washed to remove the free drug. all materials were purchased from sigma aldrich, unless otherwise specified. structural characterization of nps – zeta potential, gold concentration, size optical extinction spectra of nps were collected in a 2 mm quartz cell using a jasco v670 spectrophotometer with 1 nm spectral resolution. the zeta potential was recorded at 25 °c using a malvern zetasizer nano zs-90 instrument. the concentration of gold in the colloidal suspension (μg/ml) was determined by atomic absorption spectroscopy (avanta pm, gbc-australia). transmission electron microscopy (tem) was used in our previous study to determine the median size of gnpc (aldea m, 2018). cell cultures our in vitro experiment used three glioblastoma cell lines and a normal endothelial cell line. gm1 is a primary glioblastoma cell line isolated from freshly resected glioblastoma specimens that has been shown to express both stem cell markers and neural markers, as previously described by our team (12). after isolation and expansion in a serum-free medium enriched with growth factors, gm1 cells were subsequently cultured in ham’s f-12 and dmem media used in 1:1 ratio, supplemented with 15% fetal calf serum (fcs), 100 u/ml penicillin and 100 μg/ ml streptomycin, 2mm l-glutamine, 1% nonessential amino acids (nea), 55 μm betamercaptoethanol and 1 mm sodium pyruvate. also, two commercial glioblastoma cell lines (a172 and u251, purchased from sigmaaldrich) were cultured in dmem medium supplemented with 2mm l-glutamine, 100 u/ml penicillin and 100 μg/ ml streptomycin, 1% nea, 1 mm sodium pyruvate and 10% fcs. human endothelial cells (huvec), purchased from the european collection of cell cultures (ecacc, porton down, salisbury, uk) served as “normal cell model” and were cultured in rpmi medium, supplemented with 10% fetal calf serum (fcs), gentamicin 50 μg/ml, and amphotericin 100 μg/ml (biochrom ag, berlin, germany). cultures were maintained at 37 ºc in a humidified atmosphere of 95 % air and 5% co2. all cell culture reagents were purchased from sigma-aldrich corporation (st louis, mo, usa), unless otherwise specified. np administration and cell internalization for each of the cell lines used, uncapped gnp, gnpc and met-gnpc were administered at dose concentrations of 5, 10 and 20 μg/ml. their internalization within cells was analyzed through dark field microscopy. cells were cultured in ibidi 30 μdish of 50 mm and treated for 24 h at a concentration of 10 μg/ml of each nanoparticle. an inverted zeiss axio observer z1 microscope with a halogen lamp (hal100, 100 w, zeiss) focused on the sample at a constant intensity through a high numerical immersion dark field condenser (na = 1.4) and the scattered light was collected by a ld plan-neofluar ×20 objective (na = 0.4, zeiss). imaging acquisition was made with an axiocam icc digital camera and processed with the zen software. romanian neurosurgery (2018) xxxii 2: 230 239 | 233             cell lines irradiation in order to test if met-gnpc could be used as a radiosensitizer, cell lines were irradiated at megavoltage energies of 1.25 mv with 2, 4 and 6 gy, by using a cobalt theratron100r. control experiments were performed following exactly the same treatment protocol, but without irradiation. cell viability after np administration with or without irradiation after reaching a sub-confluence of 60-80%, cells were incubated with 5, 10 and 20 μg/ml of each nanoparticle and free drug. after 24 h, cell viability was assessed via the mtt proliferation test, which measured the mitochondrial activity of living cells. after removing the medium and washing three times with pbs, the yellow mtt solution [3(4,5-dimethylthiazolyl2)-2,5diphenyltetrazolium bromide] was added and the plate was left at 37 ºc for 1 h to allow mtt to be metabolized. the resulting purple formazan was then re-suspended in 150 μl dmso and placed on a shaking table. the reduction of mtt to formazan takes place only when mitochondrial enzymes are active; therefore, the conversion rate can directly estimate the number of living cells. the concentration was determined by optical density at 492 nm by using a fluorescence microplate reader (synergy 2, biotek, winooski, vt, usa). statistical analysis all experiments were repeated three times and expressed as mean ± sem of three independent biological replicates. the comparison between groups was assessed by the one-way anova followed by bonfferoni’s multiple comparison post-test. the statistical significance was set at p < 0.05 (graphpad version 5.0 san diego ca, usa). results physico-chemical characteristics of metgnpc and gnpc the formation of the met-gnpc nanoparticle was validated through spectroscopic measurements. by analysing the extinction spectra of met-gnpc and gnpc, it may be observed that the coloidal solution maintaines its stability in the presence of met as the form of the spectra does not change. the optical spectra of colloidal solutions in figure 1 exhibit a dominant extinction band located at 525 nm for gnpc, which shows the dipolar plasmon resonance of spherical nps. for the met-gnpc the plasmonic band has smaller wavelengths compared with gnpc. this difference is caused by the change of the refraction index of nanoparticles as a result of met disposal near the gold surface after its incorporation within the polymeric matrix. in the extinction spectrum of the metgnpc, a supplementary extinction band may be observed in the ultraviolet field at 230 nm, characteristic to met, which proves the successful loading of gnpc with met. met loading efficiency and its quantity were assessed through uv-vis measurements of the initial met used for incubation, of the supernatant collected after conjugation, of the mixture of met-gnpc before and after centrifugation. as a supplementary control measurement, the concentration of loaded met was measured by inducing an acid 234 | aldea et al metformin delivery using chitosan-capped gold nanoparticles in glioblastoma cell lines             medium (ph 2.5), which immediately led to the release of the entire met quantity from the gnpc, followed by a 20 min centrifugation at 12.000 rotations per minute. met concentration was determined by measurements of atomic absorption. in optimal incubation conditions, we observed that met loads on gnpc at a concentration of 80 μm. also, the complex stability was monitored in time through uv-vis-nir spectroscopy. it has been observed that in normal 4 degrees refrigerator conditions, the colloidal metgnpc maintains its stability for a minimum of 2 months. in our previous work, we have already demonstrated a positive zeta potential and a medium size of nearly 26 nm of gnpc (aldea m, 2018). the positive zeta potential appears as a result of the protonated amino groups from the chitosan chain which characterizes both gnpc and met-gnpc. figure 1 uv-vis-nir extinction spectra of gnpc (a) and met-gnpc (b) cellular uptake of gnps analyzed by dark field imaging gnps are easily visualized through dark field microscopy because of their surface plasmon resonances which make them able to strongly scatter the visible light. cells were incubated at the same concentration of gnpc and met-gnpc for 24h. the orange-red spots correspond to the light-scattering nanoparticles. as observed in figure 2, both gnpc and met-gnpc are highly internalized within the analyzed cell lines and they are located mostly throughout all the cytoplasm. figure 2 dark field microscopy images of gm1 cells incubated with gnpc and met-gnpc for 24 h. (a), (a) gnpc; (b), (b) met-gnpc gnpc and met-gnpc impacts the viability of glioblastoma cell lines the tested cell lines included both glioblastoma stem-like cells (gm1) and commercial non-stem glioblastoma cells (a172 and u251) in order to investigate if the stem cell character confers any resistance or sensitivity to met-gnpc. also, an endothelial cell lines was used as a normal cell line. romanian neurosurgery (2018) xxxii 2: 230 239 | 235             the mtt viability test showed that the most sensitive cell lines were gm1 and u251, which were impacted by the 10 and 20 μg/ml concentrations of both gnpc and met-gnpc (p<0.001) (figure 3). although met-gnpc significantly affects cell proliferation when compared to control and uncapped gnpc, there is no difference when compared to the chitosan-capped gnpc (p>0.05). therefore, it seems that the tumor cell viability is affected mainly by the chitosan component of the nanoparticles and that the benefit of met loading is only minor and does not lead to an additional benefit in terms of cell viability. met-gnpc and gnpc slightly affect the endothelial cell line, especially when used at the 20 μg/ml concentration (p<0.05). a172 ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t 0.0 0.2 0.4 0.6 20 µg/ml 10 µg/ml 5 µg/ml o d u251 ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t 0.0 0.1 0.2 0.3 0.4 0.5 20 µg/ml 10 µg/ml 5 µg/ml o d huvec ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t 0.0 0.2 0.4 0.6 20 µg/ml 10 µg/ml 5 µg/ml o d gm1 ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t ct rl gn p gn pc me tgn pc me t 0.0 0.2 0.4 0.6 0.8 20 µg/ml 10 µg/ml 5 µg/ml o d figure 3 mtt viability assay after 24h incubation with treatments (control, gnp, gnpc, met-gnpc, met). increasing doses of each treatment (5 μg/ml, 10 μg/ml and 20 μg/ml) showed that cell viability was affected in a dose dependent manner (non-significant for the 5 μg/ml dose). cell viability is mostly affected by the gnpc and met-gnpc used at the 20 μg/ml concentration for each glioblastoma cell line (p<0.001). huvec cells were also affected by np treatments, but only when treated with the 20 μg/ml concentration (p<0.05) 236 | aldea et al metformin delivery using chitosan-capped gold nanoparticles in glioblastoma cell lines             a172 ct rl g n p g np c m et -g np c m et ct rl g n p g np c m et -g np c m et ct rl g n p g np c m et -g np c m et ct rl g n p g np c m et -g np c m et 0.0 0.2 0.4 0.6 ctrl 2 gy 4 gy 6 gy o d u251 ct rl g np g np c m et -g n pc m et ct rl g np g np c m et -g n pc m et ct rl g np g np c m et -g n pc m et ct rl g np g np c m et -g n pc m et 0.0 0.1 0.2 0.3 0.4 0.5 ctrl 2 gy 4 gy 6 gy o d huvec ct rl g n p g n pc m et -g n pc m et ct rl g n p g n pc m et -g n pc m et ct rl g n p g n pc m et -g n pc m et ct rl g n p g n pc m et -g n pc m et 0.0 0.2 0.4 0.6 ctrl 2 gy 4 gy 6 gy o d gm1 c trl g np g n pc m et -g n pc m et c trl g np g n pc m et -g n pc m et c trl g np g n pc m et -g n pc m et c trl g np g n pc m et -g n pc m et 0.0 0.2 0.4 0.6 0.8 ctrl 2 gy 4 gy 6 gy o d figure 4 irradiated versus non-irradiated cells. glioblastoma cell lines are affected by irradiation with a slight tendency of an enhanced response when combined to gnpc and met-gnpc treatment (p<0.05). the addition of nanoparticles does not increase the toxicity of irradiation upon huvec, which are resistant to radiotherapy (p>0.05) radiotherapy shows no additional benefit when combined with gnpc or met-gnpc we investigated if such gnpc with or without met could sensitize cells to irradiation. all tested nps were used at a 10 μg/ml concentration and irradiated with increasing doses of 2, 4 and 6 gy. huvec normal cell lines proved the highest resistance to irradiation and the combination between irradiation and nanoparticles did not impact their viability (p>0.05). the response of the tumoral cell lines was different mainly depending on their proliferation index, but also on their intrinsic radioresistance. the a172 cell line was impacted by the 2 gy and 4 gy irradiation fractions, with a slight benefit when gnpc was combined with 4 gy irradiation, but intriguingly, the 6 gy dose was no different than the unirradiated control. the u251 cell line, which has a lower proliferation index, proved to be resistant at small doses of irradiation, but the combination of 4 gy romanian neurosurgery (2018) xxxii 2: 230 239 | 237             irradiation and gnpc with/without met was more toxic and decreased cell viability compared to each treatment alone (p<0.05). however, this additional benefit was not observed when the 6 gy dose was used, despite the fact that this dose impacted cell proliferation. the stem-like cell gm1 proved the best response when radiotherapy at higher doses was combined with nanoparticles as shown by their decreased viability when 4 and 6 gy doses of irradiation were combined with metgnpc or gnpc (figure 4). discussions met has shown an excellent antiglioblastoma activity in numerous in vitro studies, by inhibiting the self-renewal capacity of glioblastoma stem cells, expression of stem cell markers, as well as their invasion and migration properties. however, the antiproliferative effects of met were proven mainly when used at high drug concentrations, as many in vitro experiments used millimolar metformin concentrations (song et al., 2018). from a translational point of view, such concentrations are not attained in the clinics by the maximal anti-diabetic dose normally used. therefore, in this study, our aim was to test if an enhanced delivery and internalization of met via nanoparticles, could overcome the limitation of small drug concentrations. nanotechnology holds an excellent potential of providing a preferential drug administration within the tumor, with an enhanced internalization and efficient drug delivery at the targeted site (suri, fenniri, & singh, 2007). our team previously synthetized chitosan-capped gnp and proved that such nanoparticles are highly internalized by glioblastoma-stem like cells and by normal osteoblasts cells. intriguingly, gnpc proved a selective anti-proliferative effect for glioblastoma cells, as compared with uncapped gnp which had no anti-tumor effect. despite an important intracellular accumulation within osteoblasts, gnpc showed no toxicity on the normal cell line. the increased intratumoral internalization of gnpc and their selective cytotoxicity on cancer cells have suggested that such nps could be a promising vector for anti-cancer drugs (aldea m, 2018). therefore, our team further synthetized gnpc and managed to functionalize them with small micromolar concentration of met, in order to test if their enhanced delivery would lead to a therapeutic drug efficiency within the tumor cells. the synthesis of met nanoparticles was an easy, reproducible method and resulted in the development of a stable compound, with physico-chemical characteristics similar to gnpc. however, although both gnpc and met-gnpc had an important intracellular accumulation and proved to impact the survival of glioblastoma cells, there were no statistically significant differences between gnpc and met-gnpc, suggesting that met does not bring an additional benefit when used in small micromolar drug concentrations. considering the important anti-cancer effects proved by met used in millimolar concentrations, further research must be made in order to find a suitable delivery method. 238 | aldea et al metformin delivery using chitosan-capped gold nanoparticles in glioblastoma cell lines             kumar et al. synthetized a similar gold nanoparticle for the targeted delivery of metformin by capping gnps with hyaluronic acid. the enhanced met delivery was able to improve the anti-cancer activity of the metgnp complex compared to free met in the treatment of liver cancer cells (kumar, raja, sundar, gover antoniraj, & ruckmani, 2015). an alternative way would be the development of nps that would permit higher met binding, by paying attention also to the fact that the increasing concentration of nps would increase the quantity of excipients within the brain. possible biodegradable nps are more desirable for this purpose. also, another strategy to increase drug concentrations would be the intratumoral administration of met or within the tumoral cavity after surgical resection (aldea et al., 2016). conclusion herein, we have developed a novel gnp loaded with met, by using a biocompatible and biodegradable polymer, chitosan, as a reducing agent. this formulation exhibited high cell internalization due to the use of gnpc and had an increased anti-glioblastoma activity compared to free met used in small micromolar concentrations. however, metgnpc does not add a significant benefit when compared to gnpc possible due to the small met concentrations used for binding. therefore, an increased internalization of met-gnpc loaded with micromolar concentrations of met does not prove the same anti-cancer effectiveness of millimolar concentrations of free met. improved delivery methods with an increased met loading should be tested. acknowledgements this research was financially supported by an eufiscdi national grant pnii-ru-te2014-4-0225 (energy), competition for young teams, program for human resources. m.a. was also financed by a research grant for phd fellows (contract number 7690/2/15.04.2016) offered by the university of medicine and pharmacy (clujnapoca). correspondence prof. ioan stefan florian, md phd victor babes str, no 43, 400012, cluj-napoca, romania e-mail: stefanfloriannch@gmail.com mihaela aldea, md republicii str, no 34-36, 400012, cluj-napoca, romania tel: +40741007967 e-mail: mihaela.aldea1@gmail.com references 1.aldea, m., craciun, l., tomuleasa, c., berindanneagoe, i., kacso, g., florian, i. s., & crivii, c. repositioning metformin in cancer: genetics, drug targets, and new ways of delivery. tumour biology, 35(6), 5101-5110, 2014 2.aldea, m., florian, i. a., kacso, g., craciun, l., boca, s., soritau, o., & florian, i. s. nanoparticles for targeting intratumoral hypoxia: exploiting a potential weakness of glioblastoma. pharm res, 33(9), 2059-2077, 2016 3.aldea m, p. m., soritau o, florian is, florea a, nagysimon t, pileczki v, brie i, maniu d, kacso g. chitosancapped gold nanoparticles impair radioresistant glioblastoma stem-like cells. j buon, 23(3), 800-813, 2018 4.aldea, m. d., petrushev, b., soritau, o., tomuleasa, c. i., berindan-neagoe, i., filip, a. g., kacso, g. metformin romanian neurosurgery (2018) xxxii 2: 230 239 | 239             plus sorafenib highly impacts temozolomide resistant glioblastoma stem-like cells. j buon, 19(2), 502-511, 2014 5.carmignani, m., volpe, a. r., aldea, m., soritau, o., irimie, a., florian, i. s., valle, g. glioblastoma stem cells: a new target for metformin and arsenic trioxide. journal of biological regulators and homeostatic agents, 28(1), 1-15, 2014 6.kordes, s., pollak, m. n., zwinderman, a. h., mathot, r. a., weterman, m. j., beeker, a., wilmink, j. w. metformin in patients with advanced pancreatic cancer: a double-blind, randomised, placebo-controlled phase 2 trial. lancet oncol, 16(7), 839-847, 2015 7.kumar, c. s., raja, m. d., sundar, d. s., gover antoniraj, m., & ruckmani, k. hyaluronic acid cofunctionalized gold nanoparticle complex for the targeted delivery of metformin in the treatment of liver cancer (hepg2 cells). carbohydr polym, 128, 63-74, 2015 8.nenu, i., popescu, t., aldea, m. d., craciun, l., olteanu, d., tatomir, c., filip, a. g. metformin associated with photodynamic therapy--a novel oncological direction. journal of photochemistry and photobiology. b: biology, 138, 80-91, 2014 9.potara, m., maniu, d., & astilean, s. the synthesis of biocompatible and sers-active gold nanoparticles using chitosan. nanotechnology, 20(31), 315602, 2009 10.reni, m., dugnani, e., cereda, s., belli, c., balzano, g., nicoletti, r., . . . piemonti, l. (ir)relevance of metformin treatment in patients with metastatic pancreatic cancer: an open-label, randomized phase ii trial. clinical cancer research, 22(5), 1076-1085. 2016 11.sayed, r., saad, a. s., el wakeel, l., elkholy, e., & badary, o. metformin addition to chemotherapy in stage iv non-small cell lung cancer: an open label randomized controlled study. asian pacific journal of cancer prevention, 16(15), 6621-6626, 2015 12.sesen, j., dahan, p., scotland, s. j., saland, e., dang, v. t., lemarie, a., skuli, n. metformin inhibits growth of human glioblastoma cells and enhances therapeutic response. plos one, 10(4), e0123721, 2015 13.song, y., chen, y., li, y., lyu, x., cui, j., cheng, y., zhao, g. (2018). metformin inhibits tgf-beta1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in gbm via akt/mtor/zeb1 pathway. oncotarget, 9(6), 7023-7035, 2018 14.soritau, o., tomuleasa, c., aldea, m., petrushev, b., susman, s., gheban, d., florian, i. s. metformin plus temozolomide-based chemotherapy as adjuvant treatment for who grade iii and iv malignant gliomas. j buon, 16(2), 282-289, 2011 15.suri, s. s., fenniri, h., & singh, b. nanotechnologybased drug delivery systems. journal of occupational medicine and toxicology, 2, 16, 2007 16.turkevich j, c. s. p., hillier j. a study of the nucleation and growth processes in the synthesis of colloidal gold. discuss. faraday soc., 11, 55-75, 1951 microsoft word 8dorobatgh_controlling.doc romanian neurosurgery (2010) xvii 3: 313 – 319 313 controlling the increased intracranial pressure – a neurointensivist’s point of view gh. dorobăţ anesthesiology and intensive care, umf iasi, dental medicine faculty anesthesia and intensive care unit, iasi neurosurgery hospital p abstract the management of severe traumatic brain injury still represents a challenge for the neurosurgeons and neurointensivist specialists. the central aim of the therapy is lowering the intracranial pressure. there are many ways of accomplishing this goal, by means of medical or surgical treatment. this article is a review of the papers and guidelines in the literature regarding the control of the elevated intracranial pressure. keywords: severe traumatic brain injury, intracranial pressure monitoring, neurointensive care introduction the intracranial pressure (icp) refers to the compartment inside the skull since the brain is almost completely incompressible and the skull is a rigid structure with only one outlet (the formaen magnum), expansion of the volume in any component within the skull causes an increase in the pressure of the cranial compartment. the principles of increased intracranial pressure are defined by the modified monro-kellie doctrine: the normal components within the intracranial space are the brain, blood, and cerebrospinal fluid (csf). to these three sometimes is added a mass lesion such as a hematoma or a tumor which can also contribute to the volume of the intracranial space. an increase in the volume of one of the components contained within the intracranial space can occur only at the expense of the other components. as the volume of edema in the brain or an expanding mass lesion increases, initially the csf volume decreases, then the blood volume decreases. continued expansion of intracranial volume after these compensatory mechanisms are exhausted causes a rapid increase in icp and herniation of the brain. monitoring the intracranial pressure due to specific technical problems, sometimes arise the question – when, how and which patients need monitoring of the icp, not mentioning the costs of the procedure? generally admittance is that patients having suffered mild / moderate head injuries (glasgow coma scale (gcs) 9 to 15) do not undergo icp monitoring. however, patients with severe head injuries (gcs 8 to 3) have a significant chance of developing intracranial hypertension which varies from 5 % to 67% with the descent of gcs [1]. intracranial volume = (constant) cerebral parenchymatous + volume blood volume + volume of cerebrospinal + fluid pathological supplementary volume 314 gh. dorobăţ controlling the increased intracranial pressure according to data from brain trauma foundation, published in 2007 [2]: there are insufficient data for recommending level i indications (based on good quality randomized control trials (rct’s)) level ii (moderate quality rct’s) – icp should be monitored in all salvageable patients with a severe tbi in terms of gcs and an abnormal ct scan (considering hematomas, contusions, swelling, herniations or compressed basal cisterns) -level iii (poor quality rct’s, moderate or poor quality cohorts) – icp monitoring is indicated in patients with severe tbi, normal ct scan but two or more of the followings noted on admission : age over 40, unilateral or bilateral posturing, systolic blood pressure < 90 mm hg to these are added some of the neurointensivists recommendations, whenever possible in comatose patients with intracranial lesions : malignant sylvian infarction, acute hydrocephalus after aneurismal sah, due to the direct data on icp offered. the gold standard for monitoring icp is a ventriculostomy catheter inserted through a burr hole into one of the lateral ventricles. the ventriculostomy catheter is connected to a drainage system and can be used to monitor the icp through a fluid-coupled external pressure transducer. this system provides the most accurate measurement of icp and is stable over time. a ventriculostomy catheter will also allow drainage of csf for control of icp. problems associated with ventriculostomy catheters include blockage of the catheter, displacement of the catheter from the ventricle, and infection. antibioticimpregnated ventriculostomy catheters reduce the risk of infection from 9.4% to 1.3% [3]. other invasive monitors for icp include intraparenchymal, subdural, and epidural monitors. these probes use either a strain gauge or a fiberoptic probe. these probes require zeroing prior to insertion and are subject to drift over time. of these probes, intraparenchymal probes are the most accurate with the least amount of drift. the advantage of these probes is that they do not have to be inserted into the ventricle, which may be difficult to locate if it is collapsed or if there is significant midline shift. a problem in icp monitoring arises from the fact that icp is not identical throughout all the intracranial space. from patients with bilateral symmetric transducers but lesion in one hemisphere, the difference between the 2 sensors can be up to 25 mm hg, especially for acute sdh or contusions[4] the intracranial pressure as a function of increasing volume in the intracranial space is a nonlinear function (figure 1) . early increases in volume of a mass lesion result in displacement of csf from the cranial compartment into the spinal compartment and cause little increase in icp. once the maximal amount of csf has been displaced from the intracranial compartment, the icp increases rapidly. cerebral perfusion cerebral perfusion pressure (cpp) is defined as the mean arterial pressure (map) minus the icp and is the driving pressure for cerebral blood flow (cbf). romanian neurosurgery (2010) xvii 3: 313 – 319 315 figure 1 the relationship between intracranial pressure and volume pressure autoregulation is the intrinsic ability of the cerebral vasculature to maintain flow constant over a wide range of cpp values. normally, the brain is able to autoregulate and to maintain an adequate cbf at cpp values ranging from 50 to 140 mm hg. however, dynamic pressure autoregulation is commonly dysfunctional in the injured brain . when pressure autoregulation is impaired, the lower limit of autoregulation can be shifted upward from 50 to 60 to 90 mm hg [5]. when pressure auto regulation is entirely absent, perfusion passively follows cpp. this loss of normal autoregulation requires careful maintenance of a sufficient map and adequate control of icp to avoid hypoperfusion of the brain. extremely elevated map should also be avoided as it can cause increased icp. the influence of cpp relies in its influence on patients outcome: in traumatic comatose patients with icp over 20 mm hg, the maximizing of cpp over 70 mm hg leaded to a mortality of only 29% with over 80% of the survivors with no or minimal neurological deficits [6]. to maintain such perfusion, aggressive csf drainage was used, together with an association of vasopressors : phenylephrine max. 4ug/kg/min, norepinephrine max. 0.20.4 ug/kg/min and dopamine at renal protection dose. the authors suggest that there is no tendency for high cpp to potentate elevated intracranial pressure. to this maximal cpp theory is opposed “the lund concept”[7] from sweden considering that maintaining cpp at high values may result in vasogenic edema by transudation of fluid through the altered vasculature of the brain. this transcapillary leakage together with inotropic stimulation results in vasodilatation and interstitial edema which contributes in raising the icp. according to them, reduction of icp must be realized with a combination of low dose thiopental (1-3 mg/kg/h) , fentanyl (25 ug/kg/h) and dihydroergotamine (0.1-0.9 ug/kg/h infusion) which acts like a precapillary and large vein vasoconstrictor. metoprolol as β1 antagonist and α2 agonist clonindine may be added to reduce medium arterial pressure to normal ageindexed values. fluid balance is maintained slight negative. while the lund therapy achieved excellent survival ( 49/53 comatose patients, 92%) and recovery (85% had gos 4 and 5), there are no actually randomized studies to compare the two strategies[8]. brain metabolism indirectly connected to the perfusion of the brain is the way the cerebral tissue utilizes glucose and oxygen provided. the insertion of a brain tissue po2 probe allows continuous monitoring of oxygenation in a local region of the brain. the location of the probe is critical and determines the nature of the po2 information that will be obtained. if the probe is inserted near a focal lesion, 316 gh. dorobăţ controlling the increased intracranial pressure oxygenation can be monitored in the tissue at greatest risk should the injury expand. insertion of the probe in uninjured brain allows monitoring of a local area that should be representative of the overall lessinjured oxygenation status of the brain. normal values and critical threshold values for pbo2 are somewhat less accepted. in normal anesthetized subjects, pbo2 in normal brain ranges from 20 to 40 mm hg. recent studies comparing pbo2 values to pet measurements of oxygen extraction fraction (oef) found that the pbo2 value associated with an oef of 40% (the mean value for oef in normal subjects) was 14 mm hg [9]. values of pbo2 that indicate tissue hypoxia / ischemia are probably considerably less than 14 mm hg. prospective studies have demonstrated that pbo2 less than 15 mm hg is associated with poor outcome. some studies have suggested that a treatment protocol aimed at keeping brain po2 higher than 25 mm hg may reduce mortality when compared to patients treated similarly with no brain po2 probe[10]. jugular venous oxygen saturation (sjvo2) can be measured by inserting a catheter into the internal jugular vein and advancing it to the skull base. this allows measurement of the oxygen saturation of the blood exiting the brain, which provides information on the adequacy of cerebral blood flow and oxygen delivery to the brain. fiberoptic continous oxygen saturation monitoring or frequent jugular blood sampling are used to compute the cerebral oxygen consumption: cmr o2 = cbf x difference [conc art. o2 – conc.jug.vein o2] use of sjvo2 and of the cerebral metabolic rate allow an assessment of both brain hemodynamic reserve and its metabolic resolution, limiting potentially deleterious side effects of therapeutic interventions aimed at icp control. sjvo2 is normally between 55-75% and a value less than 50% suggest the use of a therapy aimed at increasing oxygen delivery (raising cbf, ventilation). as long as sjvo2 remains at normal values, it allows the decrease of cpp to lower levels and consecutive icp, by increasing the ventilation level and diminishing paco2. episodes of jugular venous oxygen desaturation are associated with worse neurologic outcome. increased sjvo2 may indicate decreased oxygen uptake in the brain. the major limitation of sjo2 monitoring is that it cannot detect local ischemia within the brain. serial measurements of both sjvo2 and pbo2 suggest that a pbo2 of 8.5 mm hg indicates a similar level of oxygenation as a sjvo2 of 50% [11]. treatment thresholds as it has become possible to measure additional brain-specific physiologic parameters in the icu, different management strategies have evolved that place special emphasis on parameters other than icp.. however, all of these physiologic parameters are related to outcome, and there is no clear evidence that one parameter is more important than the others. the best circumstance occurs when icp, cpp, and brain oxygenation are all maintained in normal ranges, and this should probably be the goal of management. when this is not possible, it is important to understand the limitations of each of the monitors when making therapeutic decisions. additionally, clinical studies are needed to demonstrate what management strategies may best improve neurologic outcome. romanian neurosurgery (2010) xvii 3: 313 – 319 317 table 1 normal values and treatment thresholds for physiologic parameters [12] normal treatment threshold icp 0-10 mm hg 20-25 mmhg cpp 50 mm hg 60 mm hg sjvo2 55-75% 50% pbo2 20-40 mm hg 8-10 mm hg principles of therapy of elevated intracranial pressure a thorough examination by a neurointensivist is mandatory, despite the fact that the patient has been already examined by the neurologist / neurosurgeon. particular attention must be given to the abc of resuscitation: stability and validity of endotracheal tube, ventilation status, arterial blood samples, cardiac rhythm and hemodynamic adequacy. also should be considered the possibly iatrogeniccaly worsened cerebral edema by intravenous fluid at high rate or inappropriate, other injuries that may have escaped at the first examination in the emergency dept. or neurological status aggravated since the first examination. general measures specific factors that may aggravate intracranial hypertension include obstruction of venous return (head position, agitation), respiratory problems (airway obstruction, hypoxia, hypercapnia), fever, severe hypertension, hyponatremia, anemia, and seizures. routine critical care management of the patient at risk for intracranial hypertension should include measures to prevent these factors. •positioning while elevation of the head in order to lower the icp is a well known principle, only later was found that while icp does not significantly decrease when raising from 10 to 45 degrees, cpp, cvp and blood systolic pressure did diminish[13]. among other studies, the best option appear to maintain only a slight elevation, 15-30 degrees, which has little or no effect on cbf and cpp, with the head in neutral position to minimize the decrease in jugular venous outflow •sedation and neuroparalysis sedation with propofol (10-100 ug/kg/min) is preferred to neuromuscular block because it can be quick and completely reversed in minutes. other sedatives can be used as well as short acting benzodiazepine midazolam or longer acting lorazepam, but propofol is preferred due to its fast-off properties, that allow a patient to be sedated and awakened when necessary, not to mention its possible neuroprotective action. if sedatives alone are not capable of controlling an agitated patient, a neuromuscular blocking agent can be added (atracurium or pancuronium). •maintain normoglycemia in any cerebral lesion, hyperglycemia (>150 mg/dl) has been noted to worsen outcome, through decreased oxidative metabolism in local ischemic areas, increase lactate production and cellular disfunctions. ischemic strokes need an even tighter control [14] •hyperventilation therapy is based on the idea that a decrease in paco2 , from 30 to 35 mm hg, can reduce intracranial pressure by constricting cerebral blood vessels and reducing cerebral blood volume, effects mediated by the change in ph induced in the extracellular fluid. the effects of hyperventilation on icp are immediate, but the duration of the effect is brief because the ph of the brain, at least in normal individuals, soon equilibrates to the lower pco2 level. after several studies[15,16], despite good initial results, no significant improve in outcome was 318 gh. dorobăţ controlling the increased intracranial pressure found at 6-12 months ( even with tham to resolve csf acidosis or clinical introduction of sjvo2 to evaluate exaggerate hyperventilation to paco2 of 25-30 mm hg) with long-term hyperventilation, even worse outcomes after traumatic brain injury, possibly secondary to reduction in cbf. the concomitant adverse effect of progressive decreasing pbo2 in the first 5 days[17] make hyperventilation to be used only as a short-term therapeutic intervention, only to control acute increase of the icp after the first 24 hours after injury [18] •osmotic therapy one of the mainstays of treatment of elevated icp is osmotic therapy with either mannitol or hypertonic saline. this treatment can be initiated prior to insertion of an icp monitor if signs and symptoms of herniation are present. the effects of mannitol are correlated to its hyperosmolality, creating an osmolar gradient between the vascular space and the normal brain tissue space, whilst in lesional areas the membrane pump failure prevents partially the movement of water. the initial bolus is 0.25-0.5 g/kg in the first 10 minutes there is an improvement of cbf due to the plasma expansion and improved blood fluidity, then at 30-60 minutes a decrease in icp and cerebral brain volume. the use of small bolus dosages decreases the daily total dose when compared to continuous administration. care should be taken to maintain serum osmolality below 320 mosm, by checking serum sodium levels every 8 hours (max of 150 meq/l) and avoid hypovolemia in order to prevent renal failure. the prolonged use of mannitol over 3 days or in severe lesions with blood-brain barrier destroyed may lead to aggravation of cerebral edema by penetration of mannitol in the interstitial space [19]. although mannitol has been more widely studied, there are studies suggesting that hypertonic saline is more effective at lowering intracranial pressure. these studies have been small and have not demonstrated a statistically significant difference in outcome. the usual dose form is boluses of 7.5% hypertonic saline [20]. other agents that are under investigation include hypertonic saline hetastarch, with studies to compare bolus doses of 7.2% hypertonic saline hetastarch 200/0.5 with 15% mannitol or 7.5% hypertonic saline/6% dextran solution to bolus dosing of 20% mannitol. both studies showed improved reduction of icp over mannitol but no difference in outcome [12,21]. •steroids several randomized, controlled studies have demonstrated no benefit in treating patients with traumatic brain injury with steroids. the recently completed corticosteroid randomization after significant head injury (crash) trial observed an increased risk of death in patients receiving methylprednisolone for 48 hours after injury [22]. steroids are also not recommended for treatment of the cellular edema accompanying stroke. steroids can be useful in treating vasogenic edema associated with brain tumors or selected parasitic infections. •last theoretic options hypothermia and barbiturates. while hypothermia is seldom used due to its uncertain effects besides lowering icp (increased coagulability, increased rate of infections), barbiturates are used sometimes in order to decrease cmro2 and inhibition of free radicals. to achieve a barbituric coma and burst suppression on eeg the loading dose of 10 mg/kg intravenously (iv) over 30 minutes is followed by 5 mg/kg per hour for three doses and maintenance dose of 1 mg/kg per hour, with continuous eeg monitoring if available. however pentobarbital coma is associated with significant morbidity, mainly hypotension which require concomitant administration of vasopressors, high risk of pneumonia, pressure ulcers, and paralytic ileus. •non icu options are those provided romanian neurosurgery (2010) xvii 3: 313 – 319 319 by neurosurgeons removal of csf by ventricular drainage or decompressive craniectomy. conclusions high icp can be caused by several lesions, including stroke, subarachnoid hemorrhage, mass lesion, hydrocephalus, and trauma. initial management is focused on maintaining oxygenation and perfusion using the abcs of resuscitation. if signs of herniation are present, an initial bolus of mannitol should be given. a ventriculostomy catheter should be inserted to allow monitoring of icp. treatment should be initiated with the goal of maintaining icp below 20 to 25 mm hg and the cpp at 60 mm hg. initial treatments of elevated icp include sedation and paralysis, drainage of csf, mild hyperventilation, and bolus administration of osmotic agents such as mannitol. if icp is not controlled with these measures, additional treatments including pentobarbital coma, hypothermia, or decompressive craniectomy can be considered. last problem is that high icp for a stroke or traumatic brain injury may be a normal icp in brain tumors or chronic hydrocephalus. references 1. www.braintrauma.org/coma-guidelines 2009 2. guidelines for the management of severe brain injury. a joint project of the brain trauma foundation. journal of neurotrauma, vol. 24, suppl. 1, 2007 3. chambers ir, kane ij, signorini pf et al – bilateral icp monitoringits importance in detecting the severity of secondary lesions, acta neurochir, 1998, suppl, 71 : 42-43 4. hlatky r, furuya y, valadka ab, et al. dynamic autoregulatory response after severe head injury. j neurosurg. 2002;97:1054 5. rosner mj, rosner sd, johnson ah – cerebral perfusion pressure – management protocol and clinical results, j.neurosurg, 1995, 83:949-962 6. eker c., asgeirsson, b., grande po et al improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation, critical care medicine. 26(11):1881-1886, november 1998. 7. schneck, michael j. treating elevated intracranial pressure: do we raise or lower the blood pressure? critical care medicine. 26(11):1787-1788, november 1998. 8. johnston aj, steiner la, coles jp, et al. effect of cerebral perfusion pressure augmentation on regional oxygenation and metabolism after head injury. crit care med. 2005;33:189 9. stiefel mf, spiotta a, gracias vh, et al. reduced mortality rate in patients with severe traumatic brain injury treated with brain tissue oxygen monitoring. j neurosurg. 2005;103:805 10. kiening kl, unterberg aw, bardt tf, et al. monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue po2 versus jugular vein oxygen saturation. j neurosurg. 1996;85:751 11. elevated intracranial pressure in civetta, taylor and kirby’s critical care, lipincott 2008, chapter 146 12. feldman z., kanter m effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients, j.neurosurg, 1992 vol. 76, 2: 176-183 13. bruno a, biller b, adams hp – acute blood glucose level and outcome in ischemic stroke, neurology, 2004, 57: 280-284 14. muizelaar jp, marmarou a, ward jd, et al. adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. j neurosurg. 1991;75:731 15. cruz j, the first decade of continuous monitoring of jugular bulb oxyhemoglobin saturation. management strategies and clinical outcome, crit. care med, 1998, 26: 344-351 16. suazo, j., antonio c., maas a, et al co2 reactivity and brain oxygen pressure monitoring in severe head injury, crit care med. 28(9):3268-3274, sept 2000 17. layon aj, gabrielli a elevated intracranial pressure in neurointensive carespecific problems in textbook of neurointensive care, saunders, 2004 18. brain trauma foundation.hyperosmolar therapy. j neurotrauma. 2008; 24:s14-s20 19. vialet r, albanese j, thomachot l, et al. isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 ml/kg 7.5% saline is more effective than 2 ml/kg 20% mannitol. crit care med. 2003;31:1683 20. battison c, andrews pj, graham c, et al. randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. crit care med. 2005;33:196 21. edwards p, arango m, balica l, et al. final results of mrc crash, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injuryoutcomes at 6 months. lancet. 2005;365:1957 doi: 10.33962/roneuro-2021-021 meningioma in shape. can the appearance of tumour margins be considered as a prognostic factor? a.i. cucu, mihaela cosman, b. dobrovat, cristina dascalu, ioana jitaru, r.b. sandu, a. tudor, claudia costea, mihaela turliuc, gabriela dumitrescu, anca sava, i. poeata romanian neurosurgery (2021) xxxv (2): pp. 135-142 doi: 10.33962/roneuro-2021-021 www.journals.lapub.co.uk/index.php/roneurosurgery meningioma in shape. can the appearance of tumour margins be considered as a prognostic factor? a.i. cucu1, mihaela cosman2, b. dobrovat3,4, cristina dascalu4, ioana jitaru1, r.b. sandu1, a. tudor1, claudia costea4, mihaela turliuc1,4, gabriela dumitrescu5, anca sava4,5, i. poeata4 1 department of neurosurgery, "prof. n. oblu" emergency clinical hospital, iasi, romania 2 department of neurosurgery, emergency county hospital, braila, romania 3 department of radiology, "prof. n. oblu" emergency clinical hospital, iasi, romania 4 "grigore t. popa" university of medicine and pharmacy, iasi, romania 5 department of pathology, "prof. n. oblu" emergency clinical hospital, iasi, romania abstract objective: the aim of this study was to evaluate the possible relationship between the appearance of tumour margins of atypical meningiomas and the risk of tumour recurrence, as well as progression-free survival. we also evaluated the correlations between the tumour margins and the neuroimaging characteristics (e.g. brain oedema and contrast enhancement) along with pathological features (e.g. brain invasion and mean value of ki-67 li). material and methods: in our study, we included 81 patients diagnosed with atypical meningioma (grade ii meningioma), who have undergone surgery at the "prof. dr n. oblu" emergency clinical hospital iasi, between january 1, 2010, and december 31, 2019. we followed the mri imaging characteristics (e.g. tumour margins patterns, contrast enhancement, oedema grading and tumour volume), but also the pathological characteristics such as brain invasion and the mean value of the ki-67 labelling index. the assessment of tumour recurrence was made using mri imaging (t1+ contrast), over a follow-up period of 5 years after the surgery. results: in our study, we observed that 59.3% (n=48) of meningiomas had an irregular appearance. the irregular margins predominated in the male population (65.1%) and were statistically significantly correlated with brain oedema (p<0.001), contrast enhancement (p<0.01), anatomical location (p<0.014) and the mean value of the ki-67 labelling index (p<0.01). the tumour margins were not correlated with brain invasion or volume of meningiomas. conclusion: in our series of patients we found that the irregular margin was not a prognostic factor for tumour recurrence over a period of 5 years or for progressionfree survival. keywords atypical meningioma, tumour shape, tumour margins, recurrence, prognostic factors corresponding author: mihaela cosman department of neurosurgery, emergency county hospital, braila, romania mihaelacosman@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 136 a.i. cucu, mihaela cosman, b. dobrovat et al. introduction meningiomas are the most frequent primary tumors of the central nervous system and represent about one third of all primary brain tumors (1). a preliminary study of ours has shown that in our region, the incidence of these tumors has increased in recent years (2, 3). the world health organization (who) classification of central nervous system tumors, divides meningiomas into three major groups: who grade i meningiomas are typical or benign (88-94%), grade ii meningiomas are atypical (5-7%), and grade iii meningiomas that are anaplastic or malignant (12%) (4, 5). although the vast majority of meningiomas are benign, these tumors are still a challenge for neurosurgeons and radiologists, especially in terms of neuroimaging features and the orientation of preoperative diagnosis. regading this, various authors have reported certain "malignant" neuroimaging characteristics, such as: bony destruction, hyperostosis of the adjacent skull, extracranial tumor extension through the skull base, marked peritumoral brain edema, arterial encasement, absence of calcifications, presence of irregular margins or "mushrooming" (6–8). however, many of these studies have limitations, and no one can specify a clear predictive value for these characteristics. moreover, there is no mri or ct feature that can clearly distinguish between a benign and a malignant meningioma (9). concerning the prognostic value of the appearance of tumor margins, previous studies have reported that the irregular margins of meningiomas and their lobulated appearance are associated with brain invasion and denote malignant behavior of the tumor (10–14). the development of imaging techniques in recent years, especially mri, allowed to perform a predictive analysis of malignancy degree. this was posible corroborated with clinical data, tumor morphology and also with imaging characteristics (study of perfusion, diffusion coefficient, spectroscopy in mri imaging) (15). it seems that these preoperative imaging studies can improve both the management strategy and the prognosis of these patients (16,17). the aim of our article is to identify in a group of atypical meningiomas (ams), the prognostic value of margins for recurrence and progression-free survival (pfs), but also to analyze the correlations between the tumor margins and other neuroimaging features (brain edema and contrast enhancement) and pathological characteristics such as brain invasion and the mean value of ki-67 labeling index (li). materials and methods in this study we evaluated the imaging characteristics in 81 patients with ams, who had undergone surgery in the department of neurosurgery, from prof. dr. n. oblu emergency clinical hospital, and the patients were followed between january 1, 2010 december 31, 2019. the preoperative mri factors assesed were: (1) tumor margins (regular vs. irregular), (2) the grade of peritumoral brain edema (absent, mild, moderate or severe), (3) contrast enhancement (homogeneous vs. heterogeneous), (4) anatomical location, (5) tumor volume and (6) recurrence. we also evaluated pathological characteristics such as brain invasion and the mean value of the ki-67 li. the tumor margins were delineated on preoperative mri (contrast-enhanced t1wi) and were classified as regular or irregular. brain edema was evaluated in the t2wi sequence, as hyperintense extension adjacent to the tumor and for grading, we used hale scale: (0) no cerebral edema absence of high t2wi signal around the meningioma, (1) mild edema ring of high t2wi signal surrounding the meningioma, but without mass effect, (2) moderate edema more extensive edema, but without mass effect, (3) severe edema mass effect on neighboring structures or deep digitiform edema in the white matter (16,18). regarding the anatomical classification, meningiomas were classified as follows: (1) skull base meningiomas, (2) convexity meningiomas, (3) parasagittal-falcine meningiomas, (4) posterior fossa meningiomas and (5) intraventricular meningiomas. tumor volume was calculated according to the formula = π/6 x length x width x height (18–21), and mean tumor volume was 26.4 cm3. patients underwent mri imaging annually, for a period of 5 years, and tumor recurrence/progression was defined as any contrast-enhancement at the level of the remaining tumor bed, or the increase in volume of the remnant tumor (18). the statistical data processing was made in spss 24.0 (spss inc., chicago, il). the data were characterized through descriptive statistics and frequency distributions. we used the following tests: kolmogorov-smironov test, t-student, anova tests, mann-whitney and kruskal-wallis tests and chisquared test. a p value of 0.05 was considered 137 meningioma in shape significant. the actuarial data were represented with kaplan-meier plots, and the cumulative incidence curves were compared using the log-rank test. the study was approved by the reasearch ethics committee of the "grigore t. popa" university of medicine and pharmacy. results the study group included 81 patients of which 53.1% (n=43) were male. the mean age was 61 years (range 37-87 years). in the study group we observed that 59.3% (n=48) of meningiomas had irregular margins. this appearance of irregular margins was mainly in the male population, in a percentage of 65.1% (28 patients out of a total of 43 men male). results concerning preoperative imaging features the appearance of the tumor margins were found to have a significant statistical influence on brain edema (p<0.001). in the study group, 73.3% (n=22) of patients with severe brain edema had irregular margins and 72.2% (n=13) of patients with moderate edema had irregular margins. beside this, 86.7% of patients without brain edema had regular margins (table 1). between the appearance of tumor margins and contrast enhancement we identified a statistically significant correlation (p<0.01). also, 72.7% of tumors with regular margins were homogeneous. between the tumor margins and the anatomical location of meningiomas, we observed a statistically significant difference (p<0.014). thus, in the cases of parasagical-falcine meningiomas, 90.5% (n=9) had irregular margins, as well as 52.9% (n=9) of the skull base meningiomas. 50% (n=7) of all convexy meningiomas had irregular margins. there were no statistically significant differences between the tumor margins and tumor volume (p<0.221). we noticed instead that 65.9% (n=27) of patients with tumor volume ˃ 26.4 cm3 had irregular margins (table 1). results concerning pathological aspects of the 12 patients with brain invasion, 9 of them had irregular margins. however, we did not identify a statistically significant correlation between the tumor margins and brain invasion. between the mean value of ki-67 li and the appearance of tumor margins we found a statistically significant correlation (p<0.01). 78.9% of patients with regular margins had ki-67 li <7% of the (table 1). on the other hand, 15 patients with irregular marginis, out of 19, had ki-67 li > 8%. recurrence and progression-free survival the tumor margins did not statistically significantly influenced the recurrence rate (p<0.111). however, of patients with irregular margins, 60.4% (n=29) relapsed in the 5-year follow-up period, in contrast to patients with regular margins, who relapsed less (42.4%; n=14). although we did not identify statistically significant differences between the tumor margins and pfs (p<0.067), we observed that patients with regular margins had a better mean pfs (52 months), in contrast to patients with irregular margins, who had had a lower mean pfs (43.7 months). all the results are presented in table 1. characteristics tumor margins p -value irregular n (%) regular n (%) brain edema p<0.001 absent mild moderate severe 2 (13.3%) 13 (86.7%) 11 (61.1%) 7 (38.9%) 13 (72.2%) 5 (27.8%) 22 (73.3%) 8 (26.7%) enhancement p<0.01 homogeneous heterogeneous 27 (56.3%) 9 (27.3%) 21 (43.8%) 24 (72.7%) tumor location p<0.0014 parasagital-falcine skull base convexity posterior fossa 9 (90.5%) 9 (52.9%) 17 (50%) 2 4 volume ˃ 26.4 cm3 < 26.4 cm3 27 (65.9%) 21 (52.5%) 19 (47.5%) pathological aspects brain invasion present (n=12) ki-67 li >8% (n=45) 9 of 12 (75%) 3 15 4 p<0.01 recurrence (5 years) 29 (60.4%) 14 (42.4%) progression-free survival (months) 43.7 52 table 1. imaging and pathological characteristics in relation to tumor margins. discussions in this retrospective study from a single-institution case series of ams, we analyzed the usefulness of evaluating the appearance of tumor margins for tumor recurrence and pfs, but also the correlations between the tumor margins and other radiological 138 a.i. cucu, mihaela cosman, b. dobrovat et al. features (brain edema and contrast enhancement) and pathological findings (brain invasion and the mean value of ki-67 li). correlations between the tumor margins and brain edema analyzing the correlation between tumor margins and the degree of peritumoral cerebral edema, we observed statistically significant differences (p<0.001). thus, almost half of the patients with irregular margins (45.8%) had severe brain edema, while 39.4% of patients with regular margins have no cerebral edema, or it was minimal (21.2%). thus, we can consider that the irregular margins of a meningioma may be a predictor of the occurrence of brain edema (figure 1). figure 1. illustrative examples of the analysed mri variables: (a) axial t1-weighted mri shows an irregular tumor shape with mushroom-like growth and peritumoral edema (white asterisk). (b) t2-weighted mri shows the same tumor, with severe peritumoral edema which compresses the lateral ventricles (hale 3 grade) (black asterisk). consistent with our results, lobato et al. reported a statistically significant difference between the tumor margins and brain edema. he found that patients who had meningiomas with an irregular margins, had a 2.9 times higher risk for brain edema (10). although cerebral edema can also occur as a result of brain invasion, there are additional biological mechanisms involved in the occurrence of this phenomenon, such as ischaemia from tumor mass effect or venous congestion (5, 22). also, nakano observed with his collaborators a statistically significant correlation between brain edema and meningioma margins, both in univariate analysis and in multivariate analysis (23). the conclusion of his study was that the incidence of brain edema was significantly higher in the group of tumors with irregular margins (23). correlations between the tumor margins and contrast enhancement in our study, we identified a statistically significant correlation (p<0.010) between the tumor margins and contrast enhancement. thus, 72.7% of tumors with regular margins was homogeneous (figure 2). the heterogeneous aspect of meningiomas can also be given by the presence of intratumoral necrosis (24), and this can also indicate a malignant histology of the tumor (10, 25). the most common mechanism of necrosis in meningiomas is due to hypoxia (26), and in turn, this occurs due to high metabolic demands, and may be related to a more aggressive tumor progression (27). 139 meningioma in shape figure 2. illustrative examples of the analyzed mri variables: (a) axial and coronal contrast enhanced t1weighted mri showing a sphenoid wing meningioma with irregular margins and heterogeneous enhancement. (b) axial and coronal contrast enhanced t1 weighted mri showing another sphenoid wing meningioma with regular margins and homogeneous enhancement. correlations between the tumor margins and brain invasion analyzing the correlation between the margins and brain invasion, although there was no statistically significant difference between the two variables, we found that of the 12 patients with brain invasion, 9 of them had irregular margins (figure 3, figure 4.b.). figure 3. (a) illustrative examples of the analyzed mri variables: axial t1-weighted mri shows an irregular tumor shape with mushroom-like growth. (b) brain invasion revealed as small ”islands” of tumor cells (black arrow) into adjacent nervous tissue, which also shows astrocytic gliosis (he, x200). (c) brain invasion as irregular projections of the tumor into adjacent nervous tissue without an intervening layer of leptomeninges at the tumor to brain interphase (black arrows). the adjacent brain parenchyma also exhibited astrocytic gliosis (he, x100). some authors consider that the presence of irregular margins, as well as their lobulated appearance with fringed extensions to the brain parenchyma is associated with brain infiltration and denotes malignant tumor behavior (10–14,28). among these authors, adeli et al. observed a statistically significant correlation between irregular margins and brain invasion in 4% of 617 grade i, ii and iii meningiomas (28). in relation to brain invasion, in the evaluation of imaging factors, some authors observed that the absence of a cerebrospinal fluid rim separating the meningioma from brain, would suggest a higher histological degree of the tumor, due to the possibility of invasion of the adjacent brain tissue. correlations between the tumor margins and the mean value of the ki-67 li correlating the tumor margins with the value of the marker ki-67 li, we identified a statistically significant difference (p<0.01). thus, 78.9% of patients with regular margins had ki-67 li <7% on the other hand, out of 19 patients with ki 67 li> 8%, 15 of them had meningiomas with irregular margins. statistical significant differences were also reported by beculic et al. between the two variables, noting that irregular margins were associated with higher ki-67 li values (30). moreover, immunohistochemical detection of ki-67 li remins an important tool in addition to routine histopathological evaluation that can be used to predict tumor behavior of am (31,32) (figure 4). figure 4. (a) meningothelial tumor with sheet-like growth, increased cellularity and two mitotic figures/ high power field (black 140 a.i. cucu, mihaela cosman, b. dobrovat et al. arrows) (he, x400). (b) leptomeningeal tumoral invasion with a thin intervening layer of pia mater at the tumor (black arrow) to brain interphase (white arrow) (ihc, anti-ki67 antibody, x200). (c) nuclear immunoreactivity (8%) for ki-67 li in atypical meningioma, grade ii of malignancy (ihc, anti ki-67antibody, x200) the influence of tumormarginson recurrence until now, several authors have shown that grade of lobulation of a meningioma increases with the malignancy (33,34), so implicitly the irregular appearance of the tumor margins. irregular margins of meningiomas have been attributed to different growth rates in certain regions of the tumor (35) and are associated with increased cell proliferation (33) and an increased risk of tumor recurrence (7). in this regard, zhang et al. demonstrated in a study of 33 ams that tumors with irregular margins are more prone to malignant progression compared with ams with regular margins (36). also, gobran et al. observed in its series of 138 intracranial meningiomas (all grades), that lobed-looking meningiomas had a recurrence rate of 23.5%, and mushroom meningiomas had a recurrence rate of 62.5% over a five-year period, observing a statistically significant correlation (37). when we evaluated the relationship between the tumor margins and the recurrence, although we did not find any statistical corellation between tumor margins and recurrence, according to other studies (6, 38). however, we observed that the majority of meningiomas that recurred had irregular margins (60.4%). moreover, 57.6% of regular-margin tumors did not recur over a 5-year follow-up period. in the literature, the existence of irregular margins or "mushrooming" is considered to be an important prognostic factors for recurrence, as it could reflect the high proliferative potential of the tumor (7). also, nakasu et al. noted that tumors "mushrooming" tumors had the highest recurrence rate, followed by lobulated tumors and then tumors with smooth and irregular margins (7). also ildan et al. observed in 137 patients with grade i-iii meningiomas, that mushroom shaped meningiomas was associated with a significantly higher risk of recurrence than those with smooth margins (39). however, this atypical imaging feature of irregular margins cannot be considered as an indicator of a higher-grade behavior, and cannot be reliable and specific in differentiating benign and malignant meningiomas (40). the influence of tumor margins on the progression-free survival in our study, we observed that patients who had meningiomas with irregular margins had a lower rate of survival than those with regular margins (43.75 months vs. 52 months) (figure 5). as we did not identify a statistically significant difference between the two variables in agreement with other authors (6), we can consider that the irregular appearance of meningiomas did not influence the pfs. however, other authors such as nakasu et al. observed that irregular margins correlates with pfs (7, 41). figure 5. progression-free survival depending on the appearance of meningioma margins. it is notable that patients with regular margins (blue line) had a better progression-free survival (52 months vs. 43.75 months). conclusions we found that in our series of patients, that irregular margins has no prognostic value for tumor recurrence over a period of 5 years follow up and also for pfs, but instead correlates statistically with grade of brain edema, contrast enhancement and the mean value of ki-67 li. even so, the appearance of tumor margins must be a factor to consider when evaluating neuroimaging of meningiomas and such studies should be extended to other types of intracranial tumors. 141 meningioma in shape references 1. budohoski kp, clerkin j, millward cp, et al. predictors of early progression of surgically treated atypical meningiomas. acta neurochir (wien) 2018; 160:1813-22. 2. cucu ai, costea cf, carauleanu a, dumitrescu gf, sava a, sadiye scripcariu i, et al. meningiomas related to the chernobyl irradiation disaster in north-eastern romania between 1990 and 2015. rev chim 2018; 69(6):1562-65. 3. cucu ai, costea cf, turliuc md, ghiciuc cm, costachescu b, popescu r, et al. anatomical localization of intracranial grade ii meningiomas in north-eastern romania: our 25years experience. romanian neurosurg 2019; 33:232-38. 4. louis dn, perry a, reifenberger g, et al. the 2016 world health organization classification of tumours of the central nervous system: a summary. acta neuropathol 2016; 131(6):803e20. 5. salah f, tabbarah a, alarab y n, asmar k, tamim h, makki m, et al. can ct and mri features differentiate benign from malignant meningiomas? clin radiol 2019; 74(11): 898.e15-898.e23. 6. nowak a, dziedzic t, krych p et al. benign versus atypical meningiomas: risk factors predicting recurrence. neurol neurochir pol 2015; 49(1):1-10. 7. nakasu s, nakasu y, nakajima m et al. preoperative identification of meningiomas that are highly likely to recur. j neurosurg 1999; 90(3):455-62. 8. hanft s, canoll p, bruce jn. a review of malignant meningiomas: diagnosis, characteristics, and treatment. j neurooncol 2010; 99(3):433-43. 9. champeaux c, dunn l. world health organization grade ii meningioma: a 10-year retrospective study for recurrence and prognostic factor assessment. world neurosurg 2016; 89: 180-86. 10. lobato rd, alday r, gómez pa et al. brain oedema in patients with intracranial meningioma. correlation between clinical, radiological, and histological factors and the presence and intensity of oedema. acta neurochir (wien) 1996; 138(5):485-93; discussion 493-94. 11. vassilouthis j, ambrose j. computerized tomography scanning appearances of intracranial meningiomas. j neurosurg 1979; 50:320-27. 12. dietemann jl, heldt n, burguet jl et al. ct findings in malignant meningiomas. neuroradiology 1982; 23:207209. 13. new pfj, hesselink jr, o’carroll cp, kleinman gm. malignant meningioma: ct and histological criteria including a new ct sign. ajnr 1982;3:267-76. 14. new pfj, aronow s, hesselink jr. national cancer institute study: evaluation of computed tomography in the diagnosis of intracranial neoplasms. iv. meningiomas. radiology 1980; 136:665-75. 15. ros-sanjuan a, iglesias-moroño s, carrasco-brenes a et al. atypical meningiomas: histologic and clinical factors associated with recurrence. world neurosurg 2019; 125:e248-e256. 16. hale at, wang l, strother mk, chambless lb. differentiating meningioma grade by imaging features on magnetic resonance imaging. j clin neurosci 2018; 8:71-5. 17. lu y, liu l, luan s, xiong j, geng d, yin b. the diagnostic value of texture analysis in predicting who grades of meningiomas based on adc maps: an attempt using decision tree and decision forest. eur radiol 2019; 29(3):1318‐28. 18. cucu ai, costea cf, turliuc md, dascalu cg, jitaru i, dinu r, et al. the tumour volume influence on tumour recurrence and progression-free survival in the case of atypical meningiomas: our experience on a series of 81 cases. romanian neurosurg 2020;52-7. 19. char dh, kroll s, phillips tl. uveal melanoma. growth rate and prognosis. arch ophthalmol 1997; 115:1014-18. 20. gass jd. comparison of uveal melanoma growth rates with mitotic index and mortality. arch ophthalmol 1985; 103:924-31. 21. richtig e, langmann g, müllner k, richtig g, smolle j. calculated tumour volume as a prognostic parameter for survival in choroidal melanomas. eye (lond) 2004; 18(6):619-23. 22. cucu ai, turliuc md, carauleanu a, poeata i, costea cf, dumitrescu gf, et al. chemical aspects of peritumoral cerebral edema in atypical meningiomas. rev chim 2018; 69(10):2804-07. 23. nakano t, asano k, miura h, itoh s, suzuki s. meningiomas with brain edema: radiological characteristics on mri and review of the literature. clin imaging 2002; 26:243-49. 24. osawa t, tosaka m, nagaishi m, yoshimoto y. factors affecting peritumoral brain edema in meningioma: special histological subtypes with prominently extensive edema. j neurooncol 2013; 111(1): 49-57. 25. elster ad, challa vr, gilbert th et al. meningiomas: mr and histopathologic features. radiology 1989; 170: 85762. 26. kano t, kobayashi m, yoshida k, et al. central tumour necrosis of a large meningioma following acute anemia caused by hysterectomy. neurol med chir (tokyo) 2009 ;49(9):424e6. 27. perry a, stafford sl, scheithauer bw, et al. meningioma grading: an analysis of histologic parameters. am j surg pathol 1997; 21(12):1455e65. 28. adeli a, hess k, mawrin c, streckert ems, stummer w, paulus w, et al. prediction of brain invasion in patients with meningiomas using preoperative magnetic resonance imaging. oncotarget 2018; 9(89):35974-82. 29. sheporaitis la, osborn ag, smirniotopoulos jg, et al. intracranial meningioma. ajnr am j neuroradiol 1992; 13(1):29e37. 30. bečulić h. correlation of peritumoral brain edema with morphological characteristics and ki67 proliferative index in resected intracranial meningiomas. acta clin croat 2019; 58:42-9. 31. cucu ai, costea cf, turliuc md, fg, dumitrescu a, sava a, et al. are there any correlations between demographic characteristics, tumor location, and ki-67 labeling index 142 a.i. cucu, mihaela cosman, b. dobrovat et al. in intracranial atypical meningiomas (who grade ii)? rom j morphol embryol 2019; 60:567-572. 32. cucu ai, costea cf, poeată i, turliuc dm. prognostic factors in atypical meningioma. romanian neurosurg 2017; 31(2):165-71. 33. hashiba t, hashimoto n, maruno m, et al. scoring radiologic characteristics to predict proliferative potential in meningiomas. brain tumor pathol 2006; 23:49-54. 34. liu h, zhou j, li w, liu g. comparative analysis of the magnetic resonance imaging features between anaplastic meningioma and atypical meningioma. j craniofac surg 2016; 27:e229-e233. 35. zhou jl, liu jl, zhang j, zhang m. thirty-nine cases of intracranial hemangiopericytoma and anaplastic hemangiopericytoma: a retrospective review of mri features and pathological findings. eur j radiol 2012; 81:3504-10. 36. zhang q, jia gj, zhang gb et al. a logistic regression model for detecting the presence of malignant progression in atypical meningiomas. world neurosurg 2019; 126:e392-e401. 37. gobran a, li fc, xu xk, zhang sy. factors associated with recurrence of postoperative meningioma: a clinical study of 138 patients. romanian neurosurg 2013; 20(4):379-87. 38. streckert ems, hess k, sporns pb et al. clinical, radiological, and histopathological predictors for longterm prognosis after surgery for atypical meningiomas. acta neurochir (wien) 2019; 161(8):1647-56. 39. ildan f, erman t, göçer ai et al. predicting the probability of meningioma recurrence in the preoperative and early postoperative period: a multivariate analysis in the midterm follow-up. skull base 2007; 17(3):157-71. 40. bozdağ m, er a, ekmekçi s. association of apparent diffusion coefficient with ki-67 proliferation index, progesterone-receptor status and various histopathological parameters, and its utility in predicting the high grade in meningiomas. acta radiol 2021;62(3):401-13. 41. spille dc, heß k, sauerland c et al. brain invasion in meningiomas: incidence and correlations with clinical variables and prognosis. world neurosurg 2016; 93:34654. microsoft word 3adamdanildumitrubagdasar romanian neurosurgery (2011) xviii 1: 7 – 10 7 dumitru bagdasar – rediscovered after 70 years d. adam, ioana hornea emergency “st. pantelimon” hospital bucharest abstract the authors present the case of a female patient with sturge-weber disease, who was operated in her childhood by dr. bagdasar and who is hospitalized in the neurosurgery department after 72 years from operation, because of a craniocerebral trauma. the patient presents dr. bagdasar’s hand written documents which reveal the complex medical personality of the one who was the pioneer of modern neurosurgery in romania. keywords: dumitru bagdasar, sturgeweber disease. case presentation the 84 years old patient was hospitalized for a minor craniocerebral trauma, manifested by headache, dizziness and a vertex plague, which occurred after a fall from the same level. following the personal pathologic history, we find that at the age of 13, the patient had attacks of loss of consciousness for which she was admitted to the neurosurgery department, which was led by dr. dumitru bagdasar who performed a surgery for a brain tumor. postoperatively, the crises disappeared for a year; they reappeared and continued over the next 18 years, under treatment with luminal and hydantoin. on the general examination it is discovered the presence of a left frontal cutaneous hemangioma (figure 1). skull radiography shows multiple clips in the left parietal-occipital region underlying a cranial flap attached to the skull with wire and fully welded (figure 2). brain mri examination reveals a left parieto-occipital region with t1 weighted hyposignal and t2 weighted hypersignal, with a disabling stroke aspect; on the t2* sequence there are seen the arc shape haemostatic clips and also infracentimetric injuries of no signal with microcalcification aspect, leukoaraiosis aspect in the periventricular white matter, endocranial arteries without flow abnormalities (figure 3). the patient also gives us two original documents signed by dr. bagdasar. the first shows that she was operated on 1.iv.1938 for a brain tumor (figure 4) and the second one contains detailed recommendations on diet (figure 5). figure 1 photograph of the s.o. patient shows a skin hemangioma located in the left frontal region, marker of sturge-weber disease 8 d. adam, ioana hornea dumitru bagdasar – rediscovered after 70 years a b figure 2 anterior (a) and lateral (b) radiographs of the cranium show multiple vascular clips a b c figure 3 coronal t1 weighted (a) and sagital t1 weighted (b) mr imagines show hypointensity area in p.o. region. axial t2* mr image (c) shows haemostatic clips and microcalcifications romanian neurosurgery (2011) xviii 1: 7 – 10 9 figure 4 figure 5 dr. d. bagdasar bucharest vi 30 dr. e. juvara street (former erbariei) tel: 362-04 dr. d. bagdasar, the undersigned, senior specialist at the central hospital of bucharest, certify that i performed a surgery for a brain tumor, on april 1, 1938, on stefaniu oltea student, daughter of mr. michael stefaniu, official at c.f.r. since the patient is still suffering, she needs to be hospitalized in a specialized department to be monitored and treated. she was admitted to the neurosurgery department today october 6, 1938. dr. d. bagdasar doctor d. bagdasar diseases of nerves and neurosurgery, bucharest, 30 juvara ernest street, tel: 362-04. diet without salt, few carbohydrates (bread and sugar), many fats, not to exceed 400gr in 24 hours. breakfast: 200 g coffee with milk, 40 g butter with a small slice of bread or 1 egg fried in a lot of fat. lunch: 100 g fatty meat, a vegetable sauté with a lot of butter, 150gr cream, 1 cake with hazelnuts or walnuts, 1 fruit, not too cold. dinner: 50 g of fresh fish, 20 g butter with a little bread, a cake with hazelnuts or walnuts. june 4, 1940 dr.d.bagdasar 10 d. adam, ioana hornea dumitru bagdasar – rediscovered after 70 years discussions if the history of the neurosurgery began with the invention of the trepanation of the cranium, modern neurosurgery was recognized as a distinct science in 1921 (1). after graduating medical studies, dr. dumitru bagdasar followed a postgraduate training in the field of neurology and surgery. dr. bagdasar having serious medical knowledge acquired from the romanian medical education, faced the challenge to study a new science in the united states. in the 1928-1929s he followed an internship in the u.s., in the clinic of prof. cushing, where there were formed over 30 neurosurgeons, pioneers of neurosurgery in europe and america. (2) returning in his country, dr. bagdasar worked in hospitals in jimbolia and cernăuţi. in 1935, in bucharest was created the first neurosurgery department, with 10 beds at the hospital for mental diseases, the future hospital 9, today bagdasararseni hospital (3). our case shows that after a limited internship of only two years in america, he successfully treated rather unusual neurosurgical pathology, such as sturgeweber disease. dr. bagdasar was not only a good operator. he was concerned with the complex care for patients, including prescribing a diet, which is quite unusual for today’s neurosurgeons. along with dr. arseni, his collaborator, dr bagdasar founded the modern, scientific romanian neurosurgery. the neurosurgery department at the hospital 9 in bucharest was the main training center of the romanian neurosurgeons for the following 50 years. the followers of this illustrious neurosurgeon and also the patients who still survive, pay him homage. references 1. laws er jr: neurosurgery’s man of the century: harvey cushing. neurosurgery 45: 977-982, 1999. 2. shillito, john; black, peter m.: the harvard neurosurgical service at the children's hospital boston and brigham & women's hospital, 1912-2007. neurosurgery. 63(3):579-593, september 2008. 3. adam, danil: neurochirurgie. curs universitar. editura didactică şi pedagogică, bucureşti, 2005. microsoft word 18matmusaevmaruf_computational 332 | matmusaev et al unusual posttraumatic vascular and cerebral injuries in young patients             doi: 10.2478/romneu-2018-0041 computational fluid dynamics in unruptured intracranial aneurysms maruf matmusaev1, yasuhiro yamada2, tsukasa kawase2, riki tanaka2, miyatani kyosuke2, yoko kato2, ahmed ansari2 1republican specialized scientific and practical medical center of neurosurgery, tashkent, uzbekistan 2department of neurosurgery, banbuntane hotokukai hospital, fujita health university, nagoya, japan abstract: introduction and objective: intracranial aneurysm, also known as brain aneurysm, is a cerebrovascular disorder in which weakness in the wall of a cerebral artery causes a localized dilation or ballooning of the blood vessel. there is no objective way, device or tools, of predicting rupture of aneurysm so far. computational fluid dynamics (cfds) was proposed as a tool to identify the rupture risk. purpose of study: to reveal the correlation of cfd findings with intraoperative microscopic findings and prove the relevance of cfdin the prediction of rupture risk and in the management of unruptured intracranial aneurysms. subjects and methods: a prospective cohort study was conducted inneurosurgery department of fujita health university banbuntane hotokukai hospital, nagoya, japanduring a 3‑month period in 2018,from january to march, ten patientswere diagnosed unruptured intracranial aneurysms (uia). in diagnosis computed tomography (ct) angiogram, cfd and digital subtraction angiogram were included. intraoperatively microscopic examination of the aneurysm wall was carried out and images recorded. the correlation between microscopic dome morphology and cfd information was performed. results: nine cases were found intraoperatively to have a higher risk of rupture based on the thinning of the wall. one cases had an atherosclerotic wall. all cases had low wall shear stress (wss). in 90 % of cases low wss was able to predict the potency rupture risk in the near future. conclusions: this study of cfd and its correlation with intraoperativefindings of the aneurysm suggested that low wss of the aneurysm wall is associated with thin wall aneurysm and hence increased risk of aneurysm rupture. thus cfd can be used to predict the risk of rupture of unruptured aneurysm and for planning of its treatment. key words: computational flow dynamics, intraoperative microscopic findings, unruptured intracranial aneurysms romanian neurosurgery (2018) xxxii 2: 332 339 | 333             introduction intracranial aneurysm, also known as brain aneurysm, is a cerebrovascular disorder in which weakness in the wall of a cerebral artery causes a localized dilation or ballooning of the blood vessel. nowadays about 1%5 % of adult population around the globe suffer from an aneurysm and itcomplications [1,2], varying between <1% in young adults to 4% in the elderly.[4] the fatal outcomefrom a ruptured aneurysm is quite high and in patients surviving it, the morbidity is high.[1,3] it is difficult to determine which aneurysm will rupture in the future.[6] the management of unruptured aneurysms did not prevented from complications. the morbidity and mortality can be as high as 10% and 2.5%, respectively.[7] understanding aneurysm pathogenesis and the patient-specific risk factors associated with rupture would, therefore, be useful in clinical decision-making. several approaches have been considered, including the identification of morphological, histological, and hemodynamic features associated with aneurysm growth and subsequent rupture, with an increasing trend toward the use of cfd in evaluating the role of hemodynamic shear forces on the arterial endothelium.[5,18,19,20,14]. these days, some researches regarding using cfd to predict the rupture chances of an unruptured aneurysm were conducted. cfd, a branch of fluid mechanics in mechanical engineering, has been in use in industry in aerodynamics, hydrodynamics of vehicles and a lot of other fields.[8,9,10].it uses numerical analysis and algorithms to analyze and solve problems that involve fluid flows. itsuse in biomedical engineering has progressed only in the lastdecade. many simulations have been used to study carotid andintra‑cranial cerebrovascular diseases. we were interested inits utilization in cerebral aneurysms in specific. cfd is a device used to study the hemodynamics of an aneurysm and predict the risk of rupture of an aneurysm. there are many opinions and controversies about the interpretation of cfd. while some advocate that lower wall shear stress (wss) increases rupture risk others propose that higher wss increase the rupture risk. our researches based on comparison of the preoperative cfd images and the intraoperative microscopic images of the aneurysm and reveal whether there is correlation and any predictive value for cfd. materials and methods a prospective cohort study was conducted during a 3‑month period in 2018, from january to march, in ten patients with unruptured intracranial aneurysms using computed tomography (ct) angiogram, cfd and digital subtraction angiogram. patient consent was taken for the study. the cases selected for surgery were the ones which had increased rupture risk as per cfd findings. the cfd software used was hemoscope 2 (ziosoft corporation, minato ward, tokyo, japan). cfd codes contain three main components (1) a preprocessor, (2) a solver, and (3) a postprocessor. 334 | matmusaev et al unusual posttraumatic vascular and cerebral injuries in young patients             preprocessor preprocessing consists of inputting a fluid flow problem into a cfd program. most of the time spent is devoted to this process. solver numerical solution techniques are available such as finite difference, finite element, finite volume, and spectral methods. postprocessor cfd analysis requires knowledge of the volumetric region traversed by the fluid (i.e., aneurysm including connected surrounding vasculature) plus information about velocity and pressure of the fluid at the boundaries of the chosen region of interest (boundary conditions). the object of this process is to visualize the computational results. the changes in blood flow profiles, pressure distribution, wss, oscillating shear index, and shear rate can be visualized using color rendering techniques. the wss and pressure at various places in the aneurysm sac can be calculated. focal higher pressure with the translucent thinner regions of the aneurysm wall suggest potentially elevated wall tension, which is approximately inversely proportional to wall thickness and proportional to transmural pressure. on cfd areas with thin wall – low wss, high pressure, parallel vectors, spiral flow signifies a growing aneurysm with a possible rupture. wss is the frictional force applied by flowing blood tangentially on the vessel wall. time-averaged wall shear stress (tawss) taken for one cardiac cycle as wss can change with cardiac systole and diastole. the wss mentioned below is the tawss. we use generic inflow and outflow boundary conditions because patient-specific flow waveforms are generally unavailable. model geometries are produced by using available imaging data and hence are limited by the resolution of the medical scanners. we reveal that in five out of ten cases were internal carotid artery, four cases were middle cerebral artery aneurysm and another one anterior communicating artery (acom) aneurysm [table 1]. the patients were operated, and the aneurysm wall was observed with a microscope. intraoperatively decreased vessel wall thinness was determined by the transparency of the vessel wall and the presence of a bleb on the aneurysm wall using microscope or icg-va visualization of brain vessels anterior circulation. yellowish color of the vessel wall indicates atherosclerosis. ability to see blood flow in the aneurysm or thinning of the vessel wall, i.e., translucency, and bleb on aneurysm wall were predictors for future rupture. intraoperatively, indocyanine video angiography (icg‑va) was also used. the areas of thinning had higher fluorescence and flow of blood could also be noted with icg‑va.   romanian neurosurgery (2018) xxxii 2: 332 339 | 335             table 1 aneurysm data sex age type of aneurysm pressure (mmhg) wss vessel wall character intraoperatively bleb‑present/absent female 66 mca 99.78 low thinning of the aneurysmwall bleb on dome male 54 ic-pc 99.57 low thick wall of the aneurysm female 62 ic-pc 99.64 low thin wall of the dome and thick wall of the neck female 75 mca 99.93 low thin wall of the aneurysm female 48 ica 100.01 low thin wall of the aneurysm female 71 mca 100.15 low thin wall of the aneurysm female 87 ic-pc 99.6 low thin of the wall dome and thick wall of the neck female 77 acom 99.8 low thin and thick wall of the aneurysm female 67 ica 100.1 low thin wall of the aneurysm male 67 mca 99.7 low thin wall of the aneurysm wss – wall shear stress; acom – anterior communicating artery; ic‑pc – internal carotid‑posterior communicating artery; mca – middle cerebral artery; ica – internal carotid artery results cfd studies was done in all the 10 cases which revealed low wss in all the cases suggesting thin walled aneurysm. however intraoperativly only 9 cases were thin walled. thus cfd predicted correctly 90% of the cases. intraoperativly one case had an atherosclerotic plaque involving the dome of the aneurysm. in all cases, the pressure in the aneurysm was increased whereas the wss was low. 336 | matmusaev et al unusual posttraumatic vascular and cerebral injuries in young patients             figure 1-a,bcomputational fluid dynamics image of a middle cerebral artery aneurysm with high pressure in aneurysm dome and low wall shear stress, cintraoperative image of the same aneurysm with thinned wall.arrow:there are parallel vectors which indicate area with thin walled aneurysm. figure 2 a,bcomputational fluid dynamics image of a acom aneurysm with middle pressure in aneurysm dome and low wall shear stress. c, dintraoperative image of the same aneurysm having thin wall with an atherosclerotic bleb. filling of icg is not seen well in the region of thick atherosclerotic wall. arrow: divergent vectors indicatethick walled aneurysm. a b c d c ba romanian neurosurgery (2018) xxxii 2: 332 339 | 337             discussion improvement in the imaging and screening modalities has contributed to the increase in detection of unruptured aneurysms. in some countries, the incidence of intracranial aneurysms is more than the average mentioned in the studies. there is a need to quantify objectively the risk of rupture in the cohort of people with incidentally found aneurysms. cfd which was earlier a purely engineering tool has comeinto vogue in biomedical engineering with its usefulness inknowing the flow dynamics in an aneurysm noninvasively.cfd helps in calculating the velocity of blood flowing in theaneurysm sac, the pressure in the aneurysm sac and the wss. there are many laboratory studies of cfd but they have alimitation that the wall in their studies is rigid and therebychange the outcome of studies. in vivo studies have been few. however, there were no studies which could directly see if the results shown in cfd analysis could be correlated intraoperatively. kadasi l.m et al observed the thinning of the aneurysmal wall in seven cases out of nine which is a predictor for future rupture.[11] increased pressure in the aneurysm sac in all cases shows that hemodynamic factors have been responsible for the initiation and growth of the aneurysm.[12‑15] there is still no consensus regarding whether low wss or high wss contributes to aneurysm formation. meng et al. proposed that high wss correlates with type 1aneurysm formation, i.e., small and transparent aneurysms, whereas low wss contributed to type 2 aneurysm formation, i.e., thick walled atherosclerotic type.[12] cebral et al. reported that ruptured aneurysms have higher wss compared with unruptured aneurysms.[13] xiang et al. have proposed in their study that lower wss contributes to rupture of aneurysm.[14] yoichi et al. in their study proposed that lower shear stress is associated with increased risk of rupture.[15] this controversy has mainly been due the low sample sizes in the studies and a small number of studies so far. in our study, 9 out of 10 cases with low wss had thinning of the vessel wall. one aneurysm had a bleb. cebral jr et al have shown that thinning of vessel wall identified bythe transparency of vessel wall or bleb formation increases the risk of rupture.[16] results shown in cfd analysis highly correlated with intraoperative findings. in 90% of cases, we revealed thinning of the aneurysmal wall during operation which is a predictor for future rupture. hence, using the cfd adjunct the microsurgery assist on choosing adequate microsurgical tactic taking into account predicted risk of aneurysm rupture. this is in contrast to what meng et al. have proposed. they proposed that higher wss leads to thin wall and lower wss leads to thick wall aneurysms.[12] so this shows that the mechanisms proposed so far in aneurysm initiation, growth, and rupture are far from accurate. however in all the cases, it has shown that the pressure in the aneurysm sac is high, which denotes increased risk. 338 | matmusaev et al unusual posttraumatic vascular and cerebral injuries in young patients             there has been no controversy as far the pressure parameter in cfd is considered. the wss component is controversial with regard to the interpretation. laith met al suggest a possible unifying mechanism for aneurysm progression to rupture, whereby low wss is associated with thinning of the wall leading to a theoretical increased wall tension in these thin regions of the aneurysm wall.[17] we accept the limitations of our study due to the small number of patients. while the controversies regarding wss are not resolved, cfd does hold promise as an innovative tool in the management of aneurysm patients. until recently, the lack of reliable imaging techniques to quantify intraaneurysm blood flow in the human body, and the difficulty in measuring the hemodynamic parameters in vivo, have prevented researchers from investigating aneurysmal hemodynamics and its relation to growth and rupture mechanism in depth. recent development in computational fluid dynamics (cfd), however, has given researchers a powerful tool in the investigation of intracranial aneurysms. there are many advantages when considering cfd. cfd provides a means of simulating blood flow, in cerebral vasculature noninvasively. it provides detailed visual and comprehensive information colorfully. it provides the ability to know the pressure, wss, streamlines and vector at various points in the aneurysm and helps us to know the character of blood flow in the aneurysm. besides low wss correlate with the thickness of aneurism walls and assist in defining microsurgical management strategy however, it has some disadvantages. there is difficulty in interpreting the results, software is available only at a few centers, insufficient resolution when using low resolution magnetic resonance imaging or ct, numerical errors can occur during the test leading to incorrect conclusions and wrong management. cooperation between the surgeon and the biomedical engineer is also difficult at times. conclusions this study of cfd and it is correlation with intraoperative findings of the aneurysm suggested that low wss of the aneurysm wall is associated with thin wall aneurysm and hence increased risk of aneurysm rupture. thus cfd can be used to predict the risk of rupture of unruptured aneurysm and for planning of its treatment. references 1. brisman jl, song jk, newell dw. cerebral aneurysms. n engl j med 2006;355:928–39 2. vlak mh, algra a, brandenburg r, et al. prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis. lancet neurol 2011;10:626–36 3. nieuwkamp dj, setz le, algra a, et al. changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex, and region: a metaanalysis. lancet neurol 2009;8:635– 42 4. komotar rj, mocco j, solomon ra. guidelines for the surgicaltreatment of unruptured intracranial aneurysms: the first annual j. lawrence pool memorial research symposium – controversies in the management of cerebral aneurysms. neurosurgery 2008;62:183‑93. romanian neurosurgery (2018) xxxii 2: 332 339 | 339             5. baharoglu mi, schirmer cm, hoit da, gao bl, malek am: aneurysm inflow-angle as a discriminant for rupture in sidewall cerebral aneurysms: morphometric and computational fluid dynamic analysis. stroke 41:1423–1430, 2010 6. unruptured intracranial aneurysms – risk of rupture and risks of surgical intervention. international study of unruptured intracranial aneurysms investigators. n engl j med 1998;339:1725‑33. 7. king jt jr., berlin ja, flamm es. morbidity and mortality from elective surgery for asymptomatic, unruptured, intracranial aneurysms: a meta‑analysis. j neurosurg 1994;81:837‑42. 8. tu j, yeoh gh, liu c. introduction. in: yeoh gh, editor. computational fluid dynamics: a practical approach. 2nd ed. oxford: elesevier; 2013. p. 1‑29. 9. anderson jd, wendt j. computational fluid dynamics. heidelberg: springer; 1995 10. frank m. white., fluid mechanics, potential flow and computational fluid dynamics. university of rhode island, p 590; 2011 11. kadasi lm, dent wc, malek am. cerebral aneurysm wall thickness analysis using intraoperative microscopy: effect of size and gender on thin translucent regions. j neurointerv surg 2013;5:201‑6. 12. meng h, tutino vm, xiang j, siddiqui a. high wss or low wss? complex interactions of hemodynamics with intracranial aneurysm initiation, growth, and rupture: toward a unifying hypothesis. ajnr am j neuroradiol 2014;35:1254‑62. 13. cebral jr, mut f, weir j, putman c. quantitative characterization of the hemodynamic environment in ruptured and unruptured brain aneurysms. ajnr am j neuroradiol 2011;32:145‑51. 14. xiang j, natarajan sk, tremmel m, ma d, mocco j, hopkins ln, et al. hemodynamic‑morphologic discriminants for intracranial aneurysm rupture. stroke 2011;42:144‑52. 15. miura y, ishida f, umeda y, tanemura h, suzuki h, matsushima s, et al. low wall shear stress is independently associated with the rupture status of middle cerebral artery aneurysms. stroke 2013;44:519‑ 21. 16. cebral jr, sheridan m, putman cm. hemodynamics and bleb formation in intracranial aneurysms. ajnr am j neuroradiol 2010;31:304‑10. 17. laith m. kadasi., walter c. dent., and adel m. malek,. colocalization of thin-walled dome regions with low hemodynamic wall shear stress in unruptured cerebral aneurysms. j neurosurg 119:172–179, 2013 18. boussel l, rayz v, mcculloch c, martin a, acevedo-bolton g, lawton m, et al: aneurysm growth occurs at region of low wall shear stress: patient-specific correlation of hemodynamics and growth in a longitudinal study. stroke 39:2997–3002, 2008 19. frösen j, piippo a, paetau a, kangasniemi m, niemelä m, hernesniemi j, et al: remodeling of saccular cerebral artery aneurysm wall is associated with rupture: histological analysis of 24 unruptured and 42 ruptured cases. stroke 35:2287–2293, 2004 20. shojima m, oshima m, takagi k, torii r, hayakawa m, katada k, et al: magnitude and role of wall shear stress on cerebral aneurysm: computational fluid dynamic study of 20 middle cerebral artery aneurysms. stroke 35:2500–2505, 2004 10saurabhjain_superior blow romanian neurosurgery | volume xxx | number 4 | 2016 | october december article superior blow out fracture of orbital roof causing dural tear and frontal contusion saurabh jain, swati jain india doi: 10.1515/romneu-2016-0082 romanian neurosurgery (2016) xxx 4: 517 – 519 | 517 doi: 10.1515/romneu-2016-0082 superior blow out fracture of orbital roof causing dural tear and frontal contusion saurabh jain1, swati jain2 1consultant, neurosurgery, gbh american hospital, udaipur, rajasthan, india 2consultant ophalmology, rajas eye hospital, indore, mp, india abstract: superior orbital blow out fracture causing brain parenchymal injury is rare. we are describing here, a case of facial injury with superior blow out of orbit causing frontal contusion requiring surgical intervention. introduction orbit is almost closed compartment with few small openings. any direct impact causes deformation of its content with increment in pressure which may decompress after bony disruption in any direction known as blow out6. micheal et al described a case of superior blow out fracture with computed tomography scan study without intradural involvement4. we are presenting the case with superior blow out fracture with dural tear and frontal contusion. superior orbital roof blowout causing dural tear and brain contusion is a rarity. on multiple searches in pubmed using different key words we could not find even a single case of this type. though we found few relevant cases (2, 4). this is probably the first case of this type reported till date. case presentation our patient a 34 year old gentleman brought to the emergency department with the history of fall from bike over road, after an accident with head struck to the floor in a tilted manner with right eye facing floor and parallel to it. patient had transient loss of consciousness with recovery within 30 minutes followed by multiple episodes of vomiting. when he came to emergency department he was conscious, oriented, obeying commands. vitals stable. there is small abrasion over right upper eyelid on its lateral half. vision and extraocular movements are unaffected. on imaging he was found to have right frontal contusion with hypodensity along with a free bone piece seen inside the contused brain. on detailed analysis of imaging it was evident that the free bone piece is nothing else than a fractured segment of orbital roof plate. the hypodensity was presumed to be a part of orbital fat. patient was subjected to surgery. bicoronal scalp incision with rught frontal craniotomy was done. intraoperatively there was a 518 | jain et al superior blow out fracture of orbital roof basifrontal dural tear due to free bone piece from superior orbital roof causing brain parenchymal damage along with orbital fat seen. removal of frontal contusion as well as free bone piece with repair of anterior skull base dura enhanced with pedicled pericranial patch done. post-operative period was uneventful. patient discharged on fifth post-operative day. figure 1 axial ct scan bone window shows fractured part of superior orbital wall and migrated inside cranial cavity. frontal bone is intact figure 2 similar to figure 1 more rostral section figure 3 axial ct scan brain window showing frontal contusion figure 4 similar to figure 3, more rostral section figure 5 romanian neurosurgery (2016) xxx 4: 517 – 519 | 519 discussion the orbit is made up of four walls contributed by seven bones. lateral by greater wing of the sphenoid apically and the frontal and zygomatic bones facially. floor by sphenoid, the orbital process of the palatine bone, and the orbital process of the maxillary bone. medial wall by lesser wing of the sphenoid, the ethmoid bone, the lacrimal bone, and the frontal process of the maxilla (7). the fourth wall or orbital roof plate is a quadrilateral flat structure with convexity upward, made up of two parts. anterior segment is made up of frontal bone and posterior segment is made up of sphenoid bone7. the anterior extent is covered up by supra orbital ridge, giving it extra strength. the impact required to cause this type of fracture is usually so severe that it also breaks or cracks other thin facial bones too. another important factor is angle at which orbital roof plate lies. the almost horizontal orientation makes it less amenable to become a victim of direct trauma. various types of blowout fractures depending on the location of disruption have been described. the inferior being the most common and superior the least (1, 3, 5 and 8). curtin et al reported two cases of superior orbital blow out fracture with conventional tomography (2). if the injury occurred directly over the orbit in medial and upward direction then the transient deformation of its content will cause upward movement of orbital roof plate, explaining its fracture and casing dural tear and frontal contusion. michael et al described a case of superior blow out but no intradural pathology was described in that case. the most important factor for diagnosing a superior blow out fracture is high suspicion, as it is easily missed out in acute trauma case with limited study. author recommends thin coronal cuts with three dimensional reconstruction is required for better detection and delineation. the operative approach may be combined with ophthalmic or plastic surgical specialist if required. correspondence dr. saurabh jain opd room no 8, gbh american hospital, udaipur, rajasthan, india pin 313001 references 1. chirico pa, mirvis se, kelman se, karesh jw. orbital “blow-in” fractures: clinical and ct features. j comput assist tomogr 1989; 13:1017–1022 2. curtin hd, wolfe p, schramm v. orbital roof blowout fractures. ajnr am j neuroradiol 1982;3:531–534 3. linz am. blow-in fracture of the lateral wall of the orbit. trans int conf oral surg 1973;4:306–307 4. michael i. rothman, erin m. simon, gregg h. zoarski, and michael t. zagardo superior blowout fracture of the orbit: the blowup fracture, ajnr am rjsugeon neuroradiol 19:1448–1449, september 1998 5. sato o, kamitani h, kokunai t. blow-in fracture of both orbital roofs caused by shear strain to the skull. j neurosurg 1978;49:734– 738 6. smith b, regan wf. blowout fracture of the orbit: mechanism and correction of internal orbital fracture. am j ophthalmol 1957;44: 733–739 7. turvey ta, golden ba. orbital anatomy for the oral and maxillofacial surgery clinics of north america. 2012;24(4):525-536. doi:10.1016/j.coms.2012.08.003. 8. zizmor j, noyek am. orbital trauma. in: newton th, potts dg, eds. radiology of the skull and brain. book 2. st louis: mosby; 1971;1:541–558. microsoft word 7chiriacalembolic.doc romanian neurosurgery (2010) xvii 2: 171 – 181 171 embolic materials for cerebral endovascular theraphy al. chiriac1, jorg baldof2, n. dobrin3, i. poeata1 1“gr.t. popa” university of medicine and pharmacy iasi, romania 2ernst-moritz-arndt-university of greifswald, germany 3“prof. dr. nicolaie oblu” clinical hospital iasi, romania abstract cerebral embolization is one of the most important procedures in neuroendovasculare intervention. fast developments of new microcatheters that can be maneuvered endovascularly into the brain have permitted the treatment of lesions without conventional neurosurgery. also, the progress in biomaterial science has contributed significantly to the development of this new therapeutic modality. various embolic materials in clinical use are reviewed, such as cyanoacrylates, ethylene-vinyl alcohol copolymer mixtures, ethibloc, ethanol, estrogen, poly(vinyl acetate), cellulose acetate polymer, poly(vinyl alcohol), gelatin sponges, microfibrillar collagen, surgical silk sutures, detachable balloons, and coils. these materials are reviewed in the context of treatment application for various brain lesions, such as arteriovenous malformations, cerebral aneurysms, and head and neck tumors. further developments in biomaterial polymer science can bring about progress against brain diseases. keywords: aneurysm, arteriovenous malformation, cerebral embolization, coils, embolic materials introduction cerebral embolization is defined as the "therapeutic introduction of various medical substances or devices into the brain circulation to occlude vessels or other vascular anomalies (aneurysms), either to arrest or prevent hemorrhaging; to devitalize a structure such as tumors, or to occlude its blood supply; to reduce blood flow to an arteriovenous malformation; to remodel a vascular wall or for a blood flow redirectionation. the procedure can be used as a single clinical therapy or in combination with other neurosurgical therapies (microsurgical resection or radiotherapy). embolization, or embolotherapy, is performed in a special dedicated laboratory by neurosurgeons or neuroradiologists who have completed advanced postresidency training (fellowship) in neuroendovasculare intervention. after inserting a catheter into the target vessel, it is carried out by injecting or placing embolization materials via the catheter. indications for arterial embolization include devascularization of tumors, control of hemorrhage, occlusion of arteriovenous malformation or aneurysms, ablation of an epileptic region, and redistribution of blood flow. various embolization materials have been developed 172 al. chiriac et al cerebral endovascular theraphy and used in accordance with these purposes. embolization materials clinically used are; metallic-coils, micro-coils, gelatin sponges, starch microspheres, autoagglutinated blood, dehydrated ethanol, nbca, ibca, lipiodol, embospheres, sapms, pva, pluronic and gelatin particles. the choice of embolization material usually depends on the diameter of the vessel to be embolized and the expected duration of the embolic effect. embolization of large, central vessels usually requires mechanical devices such as metallic coils or detachable balloons and particulate or liquid materials are required for small vessels close to the capillaries. in this exhibit, we will classify these materials into four types; mechanical devices, particulate, liquid agents and sclerosant agents and review these proper indications, uses and mechanisms of action. some experimental results of newly developed embolization materials will be also shown. the materials are categorized as particulate, liquid, and mechanical in form, and as temporary and permanent in durability. the choice of embolization material depends on the size of the artery to be occluded and the duration of occlusion desired. the physical properties of embolization materials also should be considered. embolization may have 3 therapeutic goals: 1. an adjunctive goal (eg, preoperative, adjunct to chemotherapy or radiation therapy) 2. a curative goal (eg, definitive treatment such as that performed in cases of aneurysms, arteriovenous fistulae [avfs], arteriovenous malformations [avms], and traumatic bleeding) 3. a palliative goal (eg, relieving symptoms, such as those of a large avm, which cannot be cured by using embolotherapy alone) medical conditions treated by using embolotherapy can be grouped as follows: 1. vascular anomalies (eg, avm, avf, venous malformation [vm], lymphatic malformation [lm], and hemangioma) 2. hemorrhage (eg, pseudoaneurysms and gi tract, pelvic, posttraumatic, epistaxis, and hemoptysis bleeding) 3. other conditions (eg, tumors, varicoceles, and organ ablation) embolic agents mechanical devices coils endovascular coiling was introduced by italian interventional neuroradiologist dr. guido guglielmi at ucla in 1991. it consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. once the catheter is in the aneurysm, platinum coils are pushed into the aneurysm and released.na guglielmi detachable coil, or gdc, is a platinum coil commonly used in intracranial non-invasive surgery for the occlusion of brain aneurysms. guglielmi in 1990, and was gradually introduced in the later 1990s as an alternative to surgical clipping, which requires invasive surgery. the gdc system consists of a soft platinum coil soldered to a stainless steel delivery wire. when the coil is properly positioned within the fundus a 1 ma current is applied to the delivery wire. the current dissolves the stainless steel delivery wire proximal to the platinum coil by means of electrolysis. at the same time, the positively charged platinum theoretically romanian neurosurgery (2010) xvii 2: 171 – 181 173 attracts the negatively charged blood elements such as white and red blood cells, platelets, and fibrinogen thus inducing intra-aneurysmal thrombosis. once electrolysis occurs the delivery wire can be removed leaving the coil in place. mechanically and electronically detachable coils are currently available. the ball coils initiate a clotting or thrombotic reaction within the aneurysm that, if successful, will block the blood flow into the aneurysm and preventing rupture. in the case of broad-based aneurysms, a stent is passed first into the parent artery to serve as a scaffold for the coils ("stentassisted coiling"). coils are made from stainless steel, platinum, or titanium wire to be visible via x-ray and be flexible enough to conform to the aneurysm shape. most are coated with dacron fibers to elicit greater thrombogenic reactions. coils are made of soft platinum wire smaller than a strand of hair and are available in different diameters and lengths. all detachable coils are scientifically proven to be safe and effective. there are four types of coils (figure 1): bare platinum coils coated platinum coils biologically active coils. radioactive coils the peculiarities of bare platinum coils lie in its physical as well as its electrolytical properties: the material has a high memory effect, allowing it to easily bend and regain its original coil shape. it is also highly sensitive to low currents, which allow the detach from the catheter that carries it, thus receiving the name of "detachable coil". coils can be grouped into microcoils and macrocoils. microcoils (platinum coils) can be delivered through microcatheters (2.2-3.5f). they can be particularly useful when superselective coil embolization is required. microcoils are highly thrombogenic, radiopaque, and biocompatible. collateralization is a potential disadvantage of coil embolization, and it can result in the persistence of flow into the vascular territory of the vessel that was embolized with the coil. additionally, when proximal occlusion occurs with coil embolization, repeat intervention via the same artery becomes difficult, if not impossible. the most used bare platinum coils system used today are gdc coils from boston scientific, micrus coils and trufill dcs orbit detachable coil system from codman neurovascular. macrocoils, also called, were first introduced in 1975. coils have the advantage of being precisely positioned under fluoroscopic control. to increase the thrombogenic effect, dacron wool tails are attached to coils. the coils are available in many sizes and may be delivered through commonly used angiographic catheters (45f). again, the thrombogenic effect primarily results from the addition of silk or synthetic fibers, not from the coil. hydrogel-coated coil (hydrocoil embolic system, microvention, aliso viejo, calif) is one of the biologically active detachable coils that were developed to achieve more durable aneurysm occlusion by improved volumetric percentage occlusion of the aneurysmal cavity. the hydrocoil embolic system (microvention) is a recently developed coil technology designed to improve packing density. hydrogel-coated coils (hydrocoils) consist of platinum coils covered with a hydrophilic polymer that swells in blood. 174 al. chiriac et al cerebral endovascular theraphy figure 1 a, b, c gdc coils system; d: coils de gianturco; e: flipper detachable coil; f: nit-occlud; g: amplatzer duct occlud figure 2 a hydrocoil embolic system; bmatrix coils coil swelling in vivo should theoretically result in greater aneurysm filling compared with inert platinum coils and may translate into more durable therapy (figure 2a). matrix coils are platinum coils covered with an absorbable copolymer. they employ a proprietary outer copolymer coil over an inner platinum main coil. the copolymer runs the entire length of the main coil and constitutes approximately 70% of total coil volume. the absorbable copolymer is typically absorbed by the body within 90 days. matrix coils employ a wellcharacterized polyglycolic-polylactic acid (pgla) copolymer that has been used in many biocompatible devices, such as surgical staples, orthopedic implants, sutures, and drug delivery vehicles. matrix coils utilize electrolytic detachment for coil delivery. because the electrolytic process does not rely on mechanical movement to deliver the coil, it provides precise, motionfree detachment. matrix coils (figure 2b). stents an endovascular stent graft is a tube composed of fabric supported by a metal mesh called a stent. it can be used for a variety of conditions involving the blood vessels, but in neurosurgery most romanian neurosurgery (2010) xvii 2: 171 – 181 175 commonly is used to reinforce a weak spot in an artery (an aneurysm) or to re-establish the blood flow throw a stenosed vessel (figure 3). the stent graft is designed to seal tightly with your artery above and below the aneurysm. the graft is stronger than the weakened artery and it allows your blood to pass through it without pushing on the bulge. brain aneurysm stenting is performed when wide-necked brain aneurysms are treated with endovascular coils. widenecked aneurysms are characterized by a large opening to the blood vessel on which they formed. the large opening makes these aneurysms prone to coil herniation, or displacement of coils from the aneurysm into the parent blood vessel. coil herniation may cause serious complications. stents are small, flexible, tube-like devices. a stent is placed across the aneurysm neck to keep coils inside the wide-necked brain aneurysm during treatment. in this procedure, the stent is intended to help hold the coils within the aneurysm to prevent coil herniation. so, after stent placement another catheter is then navigated through the deployed stent the aneurysm. tiny platinum coils are threaded through the catheter and deployed into the aneurysm, blocking blood flow into the aneurysm and preventing rupture (figure 4 a, b). the severe clinical vasospasm due to aneurysmal subarachnoid haemorrhage or endovacular catheter and coil manipulation remains a great chaleange for neurointerventionist specialists. however, transluminal balloon angioplasty and the intraarterial stent placement represent successful tools in treating severe refractory cerebral vasospasm. figure 3 image of a stent with rx markers (big arrow) and connection points (small arrow) a b figure 4 angiografic image of an pcoma aneurysm embolized by stent and coil technique (a-with and b-with out contrast enhancement) several clinical studies report also, the successful treatment of acute sinus thrombosis by sinus angioplasty with stent deployment. 176 al. chiriac et al cerebral endovascular theraphy the neuroform stent is the first microcatheter-delivered stent designed specifically for the neuroendovascular treatment. the stent functions primarily to provide durable parent vessel protection during the embolization of broad-necked cerebral aneurysms. neuroform3 stents employ a highly flexible, hybrid cell design for better tracking during access and greater conformability within a variety of vessel morphologies. the neuroform3 hybrid cell design is engineered to provide greater scaffolding for coil mass support and sufficient radial force to generate stability within the vessel. baloon occlusion the concept of a catheter-delivered detachable balloon as a therapeutic cerebrovascular device is credited to serbinenko. in north america, the technique (in various permutations) has been popularized by debrun et al and heishima et al for the treatment of direct carotid cavernous fistulas (ccfs) and by others for hunterian occlusion (after successful test occlusion) of giant, intracranial aneurysms(figure 5). figure 5 detachable balloon inflated and deflated the detachable balloon catheter is comprised of latex detachable balloons having a hollow cylinder securely fastened at the neck or entrance to the balloon. a catheter tube is held inside the cylinder by a releasable retainer which permits atraumatic detachment of the catheter tube after placement of the balloon in a lesion. a seal means is installed inside the balloon for sealing the balloon after its placement and inflation. the releasable retainer permits atraumatic detachment by complete separation of the catheter tube from the balloon and its withdrawal after placement of the balloon without any force being applied to the arterial lesion. detachable balloon occlusion may provide an alternative therapy for selected cases of direct arteriovenouse fistulas or difficult aneurysms. under fluoroscopic visualization, a silicone balloon is flowdirected through the intracranial circulation and guided directly into the aneurysm or region of aberrant connection between artery and vein. using real-time subtraction or "road mapping" techniques, the balloon is inflated with a enhancement solution, hydrophilic polymer, hydroxyethyl methacrylate, which solidifies to create a permanent embolic agent. the balloon is then detached within the fistula or aneurysm, and angiography is done to confirm occlusion of the aneurysm with preservation of the parent artery (figure 6a). ectatic aneurysms without a neck may be treated by occluding the aneurysm or the parent artery (or both). the procedures are done from a transfemoral approach using local anesthesia to permit continuous neurologic monitoring of the patient's condition. romanian neurosurgery (2010) xvii 2: 171 – 181 177 a b figure 6 a grafic of a ccf balloon embolization, b angiografy of ica aneurysm treated by ballon embolization the technique has been used to treat aneurysms of the proximal, mid, and distal basilar, posterior cerebral, lateral posterior choroidal, cavernous internal carotid, posterior communicating, carotid ophthalmic, carotid bifurcation, and middle cerebral arteries(figure 6b). although generally accepted as the method of choice for the treatment of direct ccfs, detachable balloon embolization in the cns is a procedure of some complexity, with a potential for significant complications. many factors influencing outcome bear on the critical timing of balloon detachment. previous reports have emphasized detachment of these devices by means of a second, coaxial (4f over 2f) sleeve, which pushes the balloon off the delivery catheter, or by means of simple inflation and gentle traction on the delivery catheter (3). poor tracking of the sleeve and inability to push the balloon into place may hamper the former method. the second technique is fraught with the risk of balloon migration (particularly into the carotid artery) at the time of detachment. particulate polyvinyl alcohol pva is obtained by the reticulation of pva (ivalon) with formaldehyde. pva is available as particles with a large range of sizes. for sizes as large as 710 μ m, a microcatheter can be used as a delivery catheter (figure 7). successful pva-particle embolization depends on the formation of a thrombus in which a large proportion of the embolized vessel is filled with thrombus rather than pva particles. histologically, this agent causes intraluminal thrombosis associated with an inflammatory reaction, with subsequent organization of the thrombus. pva is considered a permanent embolic agent because of the low frequency of recanalization of the embolized vessels. pva is not absorbable, and it likely produces permanent occlusion. 178 al. chiriac et al cerebral endovascular theraphy figure 7 contour microparticle for cerebral embolization pva is usually administered in a mixture of contrast medium and isotonic sodium chloride solution under fluoroscopic guidance. aggregation of pva particles can be minimized by using dilute contrast medium in a matched-density suspension; for example, omnipaque and sodium chloride solution can be used in a ratio of 1:0.4 for contour particle suspension. pva particles have a tendency to aggregate within the vessel once administered, potentially leading to an occlusion that is more proximal than intended. diluted mixtures advance more distally, whereas concentrated mixtures cause more proximal occlusions. tris-acryl gelatin microspheres microspheres (embosphere; biosphere medical, rockland, mass) are biocompatible, hydrophilic, nonresorbable, and precisely calibrated particles produced from an acrylic polymer and impregnated with porcine gelatin. microspheres are available in sizes of 40-1200 μm, and they are supplied in apyrogenic sterile sodium chloride solution. to provide the desired clinical outcome, appropriately sized microspheres and delivery catheters must be chosen to best match the size of the target vessel. for example, when avms are being embolized, choose a particle size that occludes the nidus without passing into the systemic circulation. these particles typically do not aggregate, and this is a distinct advantage of microspheres compared with pva particles. microspheres can tolerate temporary compression of 20-30% to facilitate their passage through the delivery catheter. when a coaxial technique is used, a 2.53.0f microcatheter allows the passage of microspheres as large as 700 μm for embolization. because microspheres are not radiopaque, contrast enhancement must be used to monitor embolization under fluoroscopic guidance. microspheres are considered permanent embolic particles. gelfoam gelfoam is a sterile gelatin sponge intended for application to bleeding surfaces for hemostasis or for use as a temporary intravascular embolic material. it is a water-insoluble, off-white, nonelastic, porous, and pliable material. gelfoam may be cut without fraying, and it can absorb and hold many times its weight in blood and other fluids. gelfoam is usually absorbed completely (depending on the amount used, degree of saturation with blood, and site at which it is used), with little tissue reaction. when used as an embolic material, the vessel recanalizes within a few weeks. gelfoam is supplied in a sterile envelope enclosed in an outer peelable envelope. it is available in sizes from 12 mm to 6 cm. liquid agents cyanoacrylate cyanoacrylate, or n-butyl-2cyanoacrylate (nbca) is a rapidly hardening liquid adhesive often referred to romanian neurosurgery (2010) xvii 2: 171 – 181 179 as glue. the substance hardens (polymerizes) immediately on contact with blood or other ionic fluid. polymerization results in an exothermic reaction that destroys the vessel wall (figure 8). penetration of the capillary bed causes severe tissue injury. because of the rapid polymerization, coaxial catheterization, precise positioning of the delivery catheter and considerable skill are required for nbca embolization. when a suitable location is reached by using a microcatheter, the catheter is flushed with 5% dextrose to clear it of any blood or contrast medium. under real-time fluoroscopic control, a mixture of nbca and oily contrast medium is delivered. as soon as a cast of the vascular tree is seen fluoroscopically, the delivery microcatheter is quickly removed so that the catheter tip does not adhere to the vessel. again, the catheter is flushed quickly with 50% dextrose so that it can be reused during the same procedure. onyx onyx ((evoh) is a bio-compatible liquid polymer that precipitates and solidifies in contact with blood, thus forming a soft and spongy embolus. the application of the ethylene-vinyl alcohol copolymer (evoh) in the endovascular treatment of intracranial avms was first described by taki et al7 and terada et al8 in the early 1990s. a mixture of 60 parts of the solvent dimethyl-sulfoxide (dmso), 5 parts of evoh, and 35 parts of the contrast agent metrizamide was used. evoh is now commercially available as the nonadhesive liquid embolic system under the names onyx 18, onyx 20, and onyx 34 (ev3, irvine, calif) and is ce-marked for the treatment of intracranial avms in europe. figure 8 glubran2 the second generation of cyanoacrylate liquid agent figure 9 angiography anterior and lateral view of an occipital avm embolized with onyx 180 al. chiriac et al cerebral endovascular theraphy since july 2005, onyx 18 and onyx 34 have been approved in the united states by the food and drug administration. the numbers 18, 20, and 34 quantify the viscosity of onyx in centipoises (cp). onyx 18 contains 6% evoh and 94% dmso, onyx 20 6.5% evoh and 93.5% dmso, and onyx 34 8% evoh and 92% dmso. tantal powder is added to the mixture for radiopacity. onyx must therefore be shaken for at least 20 minutes before injection to achieve homogeneous radiopacity of the mixture. dmso is potentially angiotoxic, but this effect is negligible if used with the recommended infusion rates. if the mixture comes into contact with aqueous solutions, precipitation of the polymer is initiated by diffusion of dmso. this process begins on the surface while the core is still liquid, resulting in a soft, nonadherent mass. therefore, onyx has a lavalike flow pattern within blood vessels without any fragmentation during the injection (figure9). due to these properties and because onyx is not absorbable, it is capable of producing permanent vascular occlusion.11 once the microcatheter is wedged into the onyx cast around the tip of catheter, several compartments12 of the nidus can be embolized from a single catheter position. the embolized part of the nidus appears larger than the opacified part during selective contrast agent injections from the microcatheter. because of the nonadhesive properties of onyx, the injection can be interrupted to assess the progress of the embolization and can then be continued. sclerosant agents ethanol ethanol (absolute alcohol) is the most commonly used liquid agent. embolization with absolute alcohol has a direct toxic effect on the endothelium that activates the coagulation system and causes the microaggregation of red blood cells. in the treatment of vascular malformations, ethanol has demonstrated its curative potential compared with the palliative effect seen with other embolic agents. occlusion of the lumen occurs within minutes or days. ethanol can be damaging if it reaches the capillary bed of any given tissue (eg, skin), and it usually causes significant soft-tissue swelling, which may subsequently cause compartment syndrome (nerve compression). when absolute alcohol is mixed with a contrast medium and when small catheters are used, superselective vascular embolization can be safely performed under fluoroscopic guidance. ethiodized oil (ethiodol), an oily contrast medium, is used most commonly. if large amounts of absolute alcohol enter the systemic circulation, toxic effects can occur. these include central nervous system (cns) depression, hemolysis, and cardiac arrest. slow, careful injections by using balloon occlusion arterial catheters for delivery and by applying manual compression on the draining veins (or tourniquet control) or balloon occlusion of the draining system may decrease alcohol washout from the lesion and reduce acute systemic toxicity. ethanol 1 mg/kg is the maximum amount that can be injected during a single session. sodium tetradecyl sulfate sodium tetradecyl sulfate (sotradecol) is another sclerosant. this contains 2% benzyl alcohol and is commonly used for vms and varices. use of this agent is less painful for the patient, and it is considered to be less toxic then absolute alcohol. therefore, some lesions can be treated without general romanian neurosurgery (2010) xvii 2: 171 – 181 181 anesthesia. sodium tetradecyl sulfate can be used as a sclerosant in various concentrations (13%); however, manufacture of this agent has been discontinued in the united states. this author has begun using ethanolamine oleate (ethamolin; questcor pharmaceuticals, hayward, calif) instead of sodium tetradecyl, with the same indications. other materials other less commonly or previously used materials include balloons, microfibrillar collagen (avitene), autologous materials, ethylene vinyl alcohol, alginates, phosphoryl choline, sodium morrhuate, hot contrast material, and 50% dextrose. references 1. amr abdel kerim, fabrice bonneville, betty jean, philippe cornu, lise lejean, and jacques chiras (2010) balloon-assisted embolization of skull base meningioma with liquid embolic agent: technical note 70, journal of neurosurgery, vol. 112, 1:70-72. 2. andrew j. molyneux, saruhan cekirge, isil saatci, gyula gál (2004) cerebral aneurysm multicenter european onyx (cameo) trial: results of a prospective observational study in 20 european centers, american journal of neuroradiology 25:39-51. 3. dong joon kim, sang hyun suh, jae whan lee, byung moon kim, jae wook lee, seung kon huh, dong ik kim (2010) influences of stents on the outcome of coil embolized intracranial aneurysms: comparison between a stent-remodeled and nonremodeled treatment, acta neurochirurgica, vol. 152, n.3 4. kotake hiroshi, furui shigeru (2003) arterial embolization materials, japanisch-deutsche medizinische berichte, vol 48,4:487-492. 5. loffroy romaric, guiu boris, cercueil jean-pierre, krause denis (2009) endovascular therapeutic embolisation: an overview of occluding agents and their effects on embolised tissues, current vascular pharmacology, vol. 7, 2:250-263. 6. matsumaru yuji, hyodo akio, nose tadao, hirano takashi, ohashi, shinichi (1997) embolic materials for endovascular treatment of cerebral lesions, journal of biomaterials science, polymer edition, vol. 8, 7:555569. 7. maimon s, strauss i, frolov v, margalit n, ram z. (2010) brain arteriovenous malformation treatment using a combination of onyx and a new detachable tip microcatheter, sonic: short-term results., am j neuroradiol 25. 8. murayama y., vinuela f., tateshima s. (2002) matrix: new bio-absorbable polymeric coils for the treatment of intracranial aneurysms, international congress series, vol.1247, 119-126. 9. oowaki h., matsuda s., sakai n., ohta t., iwata h., sadato a., taki w., hashimoto n., yoshito ikada (2000) non-adhesive cyanoacrylate as an embolic material for endovascular neurosurgery, biomaterials, vol. 21, 10:1039-1046. 10. raffi l., simonetti l., cenni p., leonardi m. (2007) use of glubran 2 acrylic glue in interventional neuroradiology, neuroradiology, vol. 49, 10:829-836. 11. ruth e. bristol, felipe c. albuquerque, cameron g. mcdougall (2006) the evolution of endovascular treatment for intracranial arteriovenous malformations, neurosurgical focus, vol. 20, 6:1-5. 12. sedat j., chau y., popolo m., gindre s., rami l., orban, j. (2009) restenosis after balloon angioplasty for cerebral vasospasm, cardiovascular and interventional radiology, vol. 32, 2:337-340. 13. taschner christian, leclerc xavier, gauvrit jeanyves, kerkeni anis, el-mahdy mohamed, lejeune jeanpaul, pruvo jean-pierre (2007) safety of endovascular treatment of intracranial aneurysms with a new, complex shaped guglielmi detachable coil, neuroradiology, vol. 49, 9:761-766. 14. young-jun lee, dong joon kim, sang hyun suh, seung-koo lee, jinna kim, dong ik kim (2005) stentassisted coil embolization of intracranial wide-necked aneurysms, neuroradiology, volume 47, n.9 . microsoft word _4.formatata_gorgan.doc romanian neurosurgery vol. xv nr. 1 27 sciatic nerve schwannoma – case report prof m. gorgan md phd, a.m. sandu, md, n. bucur md phd, a. neacsu md, v. pruna md, a. voina md, a. giovani md, d. martin md, a. dediu md emergency clinical hospital “bagdasar-arseni”, fourth department of neurosurgery, bucharest background. schwannomas are common, benign tumors of the sheath of peripheral nerves. sciatic schwannomas are rare. purpose: we report a case of a large sciatic schwannoma, emphasizing the role of nerve preservation. material & methods. a 54 years old female was admitted in our clinic for persistent right sciatalgia, and right l5 and s1 motor loss, symptoms lasting for almost 2 years. patient underwent surgery in a different department, but the operation was stopped, because of excessive bleeding. results neurological examination revealed right sciatalgia, right l5 and s1 motor loss and diminished ankle jerk reflex, but failed to reveal relevant symptoms for disc herniation clinical diagnostic. thigh ct-scan and mri showed a large (70/80/75 mm) encapsulated, contrast-enhancing tumor, located in the middle third of the posterior thigh, in intimated relation with the sciatic nerve. associated chronic myeloproliferative syndrome required oncological treatment and surgery postponement. we performed a subtotal resection of a large, solid tumor, infiltrating the sciatic nerve on 4 cm length, with anatomic integrity of sciatic preservation. histopathological examination found cellular schwannoma. outcome was favorable, and on follow-up examination the patients presents no additional deficits and thigh ct-scan showed no evidence of tumor regrowing. discussions & conclusions. diagnostic is challenging, in many symptoms are attributed to degenerative spinal pathology. any persistent sciatlagia, with irrelevant lumbar mri must raise the suspicion of a peripheral sheath tumor, and must be further investigated. surgery is very demanding and associated co-morbidities must be treated prior surgery. preserving the integrity of the sciatic nerve, assure favorable outcome, with no additional neurological deficits. keywords: sciatic schwannoma, peripheral nerve surgery introduction peripheral nerve tumors are benign or malignant, and neural or non-neural in origin.[1] most common benign neural peripheral nerve sheath tumors are schwannoma (neurilemoma) and neurofibroma.[2-4] schwannomas are common, slow growing benign tumors of the sheath of peripheral nerves, arising from the schwann cells. involvement of the sciatic nerve is rare.[2] diagnosis can be delayed for a long period of time, usually symptoms being attributed to lumbosacral degenerative pathology.[3;5;6] case report a 54 years old female, was admitted into the 4th department of neurosurgery, emergency clinical hospital “bagdasar-arseni”, for persistent right sciatalgia, and right l5 and s1 motor loss. symptoms last for almost 2 years. during this period of time the patient sought medical advice several times, but symptoms were mistakenly attributed to lumbosacral discal radiculopathy. finally, the patient was diagnosed with right sciatic nerve tumor, and underwent surgery twice in a different department, 2 and 3 months before admission in our clinic. both times the operation was stopped, because of the excessive bleeding. on admission, clinical examination revealed an over-height patient, having gross thighs. palpatory examination was difficult because of the gross adipose tissue. m. gorgan romanian neurosurgery vol. xv nr. 1 28 neurological examination revealed right sciatalgia, right l5 and s1 motor loss and diminished ankle jerk reflex. lasègue’s test was negative, the pain was not exacerbated by back movements or coughing, and there was no pain relief under conservative therapy or rest. thigh ct-scan and mri showed a large tumor, 70/80/75 mm in diameter, well-defined, encapsulated, having a thin fibrous capsule, contrast-enhancing mass, located in the middle third of the posterior thigh. the tumor had intimated relation with the sciatic nerve. the tumor displaced, but did not infiltrate surrounding muscles. (fig. 1a, 1b, 1c) inferior limb angiography also confirmed the existence of a thigh tumor. (fig. 2a, 2b) laboratory tests revealed thrombocytosis. the patient was further investigated, and she was diagnosed with chronic myeloproliferative syndrome. surgery was postponed and the patient underwent oncologic therapy. after proper treatment and normalization of blood test, the patient underwent surgery. patient received general anesthesia. patient’s positioning was supine position. we performed a linear midline skin incision on the posterior surface of the thigh. muscles were divided, and we found a well-circumscribed, encapsulated, tumor, originating from the sciatic nerve, growing along the sciatic nerve fascicles. the tumor was solid, greywhite, measuring 70/80/75 mm in diameter. the sciatic nerve was infiltrated by the tumor on 4 cm length. we exposed the sciatic nerve proximal and distal and isolated the tumor. the tumor had no propensity for surrounding tissue infiltration. we opened the sciatic sheath in a longitudinal manner, and carefully dissected the tumors along the nerve fascicles, which were incorporated within the tumor capsule and displaced circumferentially by the tumor. we preserved the anatomic integrity of the sciatic nerve. we achieved a subtotal resection (aproximatively 90%) in order to avoid supplementary nervous fascicles sacrifice, dislocated by the tumor and to reserve the radical solution for regrow or malignization. histopahological examination found cellular schwannoma, associated with muscular, fibrous and adipose tissue; surrounding muscular tissue presented chronic inflammation (chronic miositis) and peritumoral vascular changes. outcome was slowly favorable. right l5 and s1 motor deficits persisted postoperative. on follow-up examination in 1 year, the patient presented no residual pain, no sensory loss, no trophic disturbances, and with residual motor loss (presented preoperative). the patient was able to walk by means of orthosis. fig. 1a fig. 1b sciatic nerve schwannoma romanian neurosurgery vol. xv nr. 1 29 fig. 1c fig. 1a, 1b, 1c preoperative contrast ct-scan of the tight, revealing anatomical position and tumor size fig. 2a fig. 2b fig. 2a, 2b preoperative femoral angiography, revealing tumor blush and arterial pedicles control thigh mri at six and twelve moths showed no evidence of tumor regrowing. (fig. 3a, 3b) discussion clinical presentation schwannomas have a long subclinical course and their clinical presentation is usually misleading. radicular pain or sensory or motor loss are often misdiagnosed for radicular pain secondary to degenerative spine pathology.[7;8] fig. 3a m. gorgan romanian neurosurgery vol. xv nr. 1 30 fig. 3b fig. 3a, 3b postoperative mri with contrast one year after surgery, revealing the absence of the tumor mass and the sciatic nerve in continuity detailed history, with long lasting radicular pain, unresponsive to anti-inflammatory therapy and rest, and physical examination absence of lumbar contracture, a negative lasègue’s test, and lumbar spine irm showing no signs of disc herniation, raise suspicion of non-discogenic sciatica and peripheral nerve pathology.[5;7;9] in such cases mri imaging of the entire limb confirm the diagnosis of a peripheral nerve tumour.[2] unresponsive pain and an irrelevant spinal mri exam must conduct investigations in searching other nerve pathology. emg and ultrasound may, also be useful in establishing the diagnostic of sciatic schawannoma.[10] tumor characteristics the real tumor incidence is unknown, being approximated by some studies at 0.6 cases per 100,000 people. from all benign sciatic tumors 60% are represented by neurofibromas and 38% schwannomas, the rest having other histological types. cellular schwannomas are slow growing tumors, and can achieved large size in time. the patients had a long history of radicular pain and motor loss prior diagnostic.[6] associated pathology patient was operated twice in a different department, and both times the operation was stopped due to excessive bleeding. after this unfortunate event, the patient is found on routine preoperative laboratory examination with elevated thrombocytes level and was further investigated and diagnosed with chronic myeloproliferative syndrome. this association is very unfortunate, carrying surgical pitfall. in spite of high thrombocytes level, coagulation was improper and did not allow surgery. in this situation, surgery must be postponed, and stabilizing the patient should be the treatment of choice. after stabilizing the patient surgery can be performed safely and effective. this association is casual, but it highlights the fact that patients carry a multitude of diseases, many having surgical consequences. preoperative careful clinical and paraclinical examination is mandatory. the operation is extremely demanding and any comorbidity can compromise the result. differential between schwannoma and neurofibroma usually, schwannomas are solitary, wellcircumscribed, encapsulated tumors, eccentrically located on nerve roots, originating from proximal nerves or spinal nerve roots. neurofibromas are multiple, they lack tumor capsule, originate from distal nerves, causing fusiform enlargement of distal nerves.[2] schwannomas arise from a single fascicle, and grow displacing circumferentially the other fascicles within the nerve sheath. neurofibromas arise from perineural fibrocytes, cells having many histological similarities to schwann cells.[1] schwannomas usually originate from the sensory fascicles in mixed nerves, while neurofibromas arise from motor parts. plus, in neurofibromas fascicular bundles are more intimately involved, unlike schwannomas.[1] outcome malignant transformation in schwannomas is rare, the risk of malignization being approximated at 18% in neurofibromatosis type 1, and 5% in schwannomas.[11] sciatic nerve schwannoma romanian neurosurgery vol. xv nr. 1 31 patients with von recklinghausen disease carry a worse outcome. von recklinghausen disease, neurofibromatosis associates multiple nerve sheath tumors. patients may have simultaneous different histological types of nerve tumors, like schwannomas, neurofibromas, and malignant nerve sheath tumors.[1] surgery surgery is the treatment of choice in peripheral nerve schwannomas. during surgery, after finding the tumor, adequate exposure of the nerve, proximal and distal to the tumor, and tumor poles are mandatory. nerve and tumor must be careful isolated and dissected from all adjacent neurovascular and soft tissue structures. only after this wide exposure, the nerve sheath is opened and nerve fascicles are divided and tumor is resected. nerve fascicles stretch over the tumor capsule. the surgeon must identify all intact fascicles over the capsule. longitudinal dissection of the nerve sheath is prohibited because it cuts off vascular supply. in small tumors, extracapsular resection, (under magnification) with gentle dissection of nervous fibers from the tumor capsule is the treatment of choice. in large tumors extracapsular excision cannot be achieved due to tumor size and an intracapsular debulking is needed first. in cases in which functional fascicles cannot be dissected from the capsule is wiser to leave a residual tumor than produce postoperative deficits. we prefer performing a subtotal resection with neurologic function preservation and reserve the radical surgery for tumor regrowth or malignant evolution. surgery in peripheral nerve sheath tumors, tend to be extremely satisfactory, when strict surgical principles are applied.[12] in the great majority of peripheral nerve schwannomas, total tumor resection without residual significant neurologic deficits can be achieved.[1;6;12] conclusions diagnostic is challenging, in many cases late, often symptoms are attributed to degenerative spinal pathology. any persistent sciatalgia, with irrelevant lumbar mri must raise the suspicion of a peripheral sheath tumor, and must be further investigated. surgery is very demanding and any associated comorbidities must be treated prior surgery. preserving the integrity of the sciatic nerve, together with fascicles which are not infiltrated by the tumor, assure favorable outcome, without any additional neurological deficits. references 1. lamond rc, fox b. management of peripheral nerve tumors. limb preservation 11. 2004. 2. maraziotis t, panagiotopoulos t, panagiotopoulos e, panagiotopoulos k. neurilemoma of the popliteal fossa: report of two cases with long subclinical course and misleading presentation. acta orthop belg 71, 496-499. 2005. 3. ghaly rf. a posterior tibial nerve neurilemoma unrecognised for 10 years: case report. neurosurgery 48, 668-672. 2001. 4. gabhane sk, kotwal mn, bobhate sk. morphological spectrum of peripheral nerve sheath tumors: a series of 126 cases. indian j pathol microbiol 52, 29-33. 2009. 5. blanchard c, dam-hieu p, zagnoli f, bellard s. chronic sciatic pain caused by sciatic nerve schwannoma. rev med interne 29, 748-750. 2008. 6. nawabi dh, sinisi m. schwannoma of the posterior tibial nerve: the problem of delay in diagnosis. j bone joint surg br 89, 814816. 2007. 7. kralick f, koenigsberg r. sciatica in a patient with unusual peripheral nerve sheath tumors. surg neurol 66, 634-637. 2006. 8. rafai ma, el otmani h, rafai m, bouhaajaj fz, largab a, trafeh m, adil a, kadiri r, slassi i. peroneal nerve schwannoma presenting with a peroneal palsy. rev neurol 9. kulcu dg, naderi s. differential diagnosis of intraspinal and extraspinal non-discogenic sciatica. j clin neurosci 15, 1246-1252. 2008. 10. padua l, commodari i, zappia m, pazzaglia c, tonali pa. misdiagnosis of lumbar-sacral radiculopathy: usefulness of combination of emg and ultrasound. neurol sci 28, 154-155. 2007. 11. weiss sw, glodblum jr. benign tumors of peripheral nerves and malignant tumors of peripheral nerves. in enzinger and weiss soft tissue tumors. mosby: st. louis; 12. oberle j, kahamba j, richter hp. peripheral nerve schwannomas an analysis of 16 patients. acta neurochirurgica 139, 949-953. 2005. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 4 | 2017 | october-december article incidence, hospital costs and in-hospital mortality rates of surgically treated patients with traumatic cranial epidural hematoma ibrahim burak atci, hakan yilmaz, mehmet yaman, oguz baran, okan türk, bilgehan solmaz, ümit kocaman, nuriye guzin ozdemir, nail demirel, ayhan kocak turkey doi: 10.1515/romneu-2017-0078 510 | atci et al incidence, hospital costs and in-hospital mortality rates doi: 10.1515/romneu-2017-0078 incidence, hospital costs and in-hospital mortality rates of surgically treated patients with traumatic cranial epidural hematoma ibrahim burak atci1, hakan yilmaz2, mehmet yaman1, oguz baran1, okan türk1, bilgehan solmaz1, ümit kocaman3, nuriye guzin ozdemir1, nail demirel1, ayhan kocak1 1istanbul research and training hospital, department of neurosurgery, istanbul, turkey 2usak university hospital, department of neurosurgery, usak, turkey 3izmir cigli research and training hospital, department of neurosurgery, izmir, turkey abstract: background: in this study, the patients who were operated in two clinics due to traumatic cranial epidural hematoma (edh) were assessed retrospectively and the factors that increase the costs were tried to be revealed through conducting cost analyses. methods: the patients who were operated between 2010 and 2016 with the diagnosis of edh were assessed in terms of age, sex, trauma etiology, glasgow coma scale (gcs) at admission, the period from trauma to hospital arrival, trauma-related injury in other organs, the localization of hematoma, the size of hematoma, length of stay in the intensive care unit (icu), length of antibiotherapy administration, number of consultations conducted, total cost of in-hospital treatments of the patients and prognosis. results: distribution of gcs were, between 13-15 in 18 (36%) patients, 9-13 in 23 (46%) patients and 3-8 in 9 (18%) patients. the reasons for emergency department admissions were fall from high in 29 (58%) patients, assault in 11 (22%) patients and motor vehicle accident in 10 (20%) patients. the average cost per icu stay was 2838 $ (range=343-20571 $). the average cost per surgical treatment was 314 $. icu care was approximately 9 times more expensive than surgical treatment costs. the mortality rate of the study cohort was 14% (7 patients). conclusion: the prolonged period of stay in the icu, antibiotherapy and repeat head cts increase the costs for patients who are surgically treated for edh. key words: antibiotherapy, cost analysis, epidural hematoma, traumatic. romanian neurosurgery (2017) xxxi 4: 510 516 | 511 introduction epidural hematoma (edh), which was defined for the first time by hutchinson in 1867, is a common type of traumatic brain injury (tbi) in which blood accumulation occurs between the dura mater and the cranium due to trauma. it is 4 times more common in men than in women. although middle meningeal artery is responsible in 85% of the analyzed case series, life-threatening hemorrhages can also be observed as a result of venous hemorrhages. the mass effect of the blood results in pupillary anomalies, neurological deficits, loss of consciousness and high mortality. the mortality rates vary between %5-45 and immediate surgical intervention is of the utmost importance in required cases [1-3]. in this study, the medical records of 50 patients with edh who were surgically treated in 2 clinics were assessed retrospectively and the factors for increased patient costs were analyzed. methods the patients who were surgically treated for traumatic edh in two clinics between january 2010 and january 2016 were included in this retrospective study. the assessed data were as follows: age, gender, trauma etiology, glasgow coma scale at admission, the period from trauma to hospital arrival, traumarelated injury in other organs, the localization of hematoma, the size of hematoma, length of stay in the intensive care unit (icu), length of antibiotherapy administration, number of consultations conducted, total cost of inhospital treatments of the patients and prognosis. all statistical analyses were performed using statistical package for the social sciences version 15 (spss inc., chicago, usa). the results were expressed as mean±standard deviation or frequency (%). the student’s t-test was used to determine the significance of the differences among groups. a p value of<0.05 was considered statistically significant. results of all patients, 46 (92%) were men and 4 (8%) were women.the mean age of the patients was 35.4±5.6 years (range=7 months68 years). regarding admission gcs, the scores ranged between 13-15 in 18 (36%) patients, 9-13 in 23 (46%) patients and 3-8 in 9 (18%) patients. the most common reason for emergency department admissions was fall from high (58%), followed by assault (22%) and motor vehicle accident (mva) (20%)(table 1). forty-two (84%) patients were admitted to the emergency department within 4 hours of trauma. the concomitant systematic injuries were as follows: extremity fractures in 10 patients, lung contusion in 4 patients, liver laceration in 3 patients, retroperitoneal hemorrhage in 2 patients and non-significant spinal fractures in 8 patients. besides concomitant systematic injuries, 35 patients had concomitant cranial pathologies. there were linear skull fracturesin 44 patients, depression fractures in 5 patients, subdural hematoma in 4 patients, and intracerebral hematoma in 2 patients. all patients were diagnosed with computed tomography (ct) 512 | atci et al incidence, hospital costs and in-hospital mortality rates scans. the intraoperative evaluation revealed that the most common localization of edh was temporal (36%), followed by temporoparietal (24%) and frontal (14%) (table 2). the thickness of epidural hematoma was between 10-15 mm in 10 (20%) patients, 15-30 mm in 32 (64%) patients and >30 mm in 8 (16%) patients. thirty-eight (76%) patients were taken to icu post-operatively, and 12 (24%) patients were taken to neurosurgery clinic beds. the average length of stay in the icu was 8.6 days (range=1-60 days). the daily average cost of icu was 343 $ and the average cost per icu stay was 2838 $ (range=343-20571 $) (table 3, figure 1). the average cost per surgical treatment was 314 $. icu care was approximately 9 times more expensive than surgical treatment costs. during icu followup, an average of 3.8 (range= 2-13) neurosurgery consultations was performed per patient. seven patients died in the icu and the mortality rate of the study cohort was 14%. the admission gcs values of these 7 patients were below 6. besides, all these 7 patients had other concomitant intracranial pathologies and they were operated within 4 hours following the trauma. thirty-one patients were taken to service beds following icu follow-up. the average length of service bed stay was 5.7 days (range=1-28 days) for the remaining 43 patients. the average cost per service bed stay was 2057 $ (range=1285–3428 $). during service stay, patients had undergone an average of 3.7 (range=2-10) repeat head cts. except for the post-operative early control ct, none of the other control cts demonstrated a surgical pathology and affected the treatment. all patients in this study received prophylactic ceftriaxone treatment. during icu follow-up, following pathologic agents were cultivated in serum, urine, feces and tracheal samples: methicillin-resistant staphylococcus aureus (mrsa) in 4 samples, acinetobacter baumannii in 2 samples, enterococcus faecalis in 3 samples, and klebsiella pneumonia in 2 samples. double or triple antibiotherapy was administered to these cases for an average of 10 days. double antibiotherapy was applied and continued for 7 days in another group of 10 patients due to fever although no pathologic agent could be cultivated and their white blood cells (wbc) were within normal ranges. to sum up, double or triple antibiotherapy was administered to 21 patients and these treatments continued for 7-10 days. the total cost of antibiotics constituted 15% of total cost of stay. the total cost of patients who stayed in the icu for ≥10 days and who had double antibiotherapy were significantly higher than the total cost of other patients (p<0.05) (table 4). regarding glasgow outcome scale (gos), thirty-five patients were discharged with low disability (gos 5), four patients with moderate disability (gos 4), three patients with severe disability (gos 3), and one patient with persistent vegetative state (gos 2) (morbidity rate=16%) (table 5). all the patients who were discharged with gos 3 and 2 were ≥50 years of age. when gcs is correlated with cost analysis, a gcs value of ≤8 was statistically significantly correlated with cost (p<0.05). romanian neurosurgery (2017) xxxi 4: 510 516 | 513 table 1 trauma etiology etiology patient number and percentage falling from high 29 (%58) assault 11 (%22) traffic accident 10 (%20) table 2 the localization of epidural hematoma localization patient number and percentage temporal 18 (%36) temporoparietal 12 (%24) frontal 7 (%14) parietal 6 (%12) occipital 5 (%10) posterior fossa 2 (%4) table 3 the daily average cost of icu department icu icu mean charge % of total blood processing 21.26 $ 6.2% central supply 45.27 $ 13.2 pharmacy without antibiotics 35.32 $ 10.3 antibiotherapy (average) 51.45 $ 15 icu physician 6.86 $ 2 labaratory 116.96 $ 34.1 radiology 33.95 $ 9.9 inhalation theraphy 31.89 $ 9.3 total 343 $ 100 table 4 antibiotic use, total financial effects and ct application rates of these patients antibiotic use double or triple antibiotherapy double antibiotherapy single antibiotherapy period of antibiotic use (average) 10 days 7 days 5 days reproduction status 4 mrsa, 3 enterecoccus, 2 acinetobacter, 2 klebsiella no reproduction (high wbc, fever) no reproduction total 11 patients (%22) 10 patients (%20) 29 patients (%58) total cost (%) %40 %28 %32 ct application (average:3.7) 6 4.6 2.5 table 5 distribution of patients according to gos results at discharge gos number % 1 7 14 2 1 2 3 3 6 4 4 8 5 35 70 discussion acute edh constitutes 2.7-11% of tbis. it is frequently seen in men and young adults. regarding analyzed cases, it was seen on lateral surfaces of hemispheres having 70% frequency for central pterion. the most commonly reported causes in the literature are falls, mvas, and assaults. the incidence is lower in children and elderly, as there is close 514 | atci et al incidence, hospital costs and in-hospital mortality rates relationship between the dura and the osseous skull [2, 3]. there were linear fractures in 60% of the skull x-rays in our study group and standard diagnostic procedure was cranial ct. compared to x-rays, linear fractures or complicated compression fractures are more frequently observed at the level of hemorrhage in cranial cts. there is not a consensus to decide which patients will be a candidate for surgical procedure, but a close neurologic and radiologic follow-up is required for foreseeing hematoma growth. generally, symptomatic edhs should be correlated with gcs, and surgery should be planned in cases when the thickness of hematoma exceeds 15 mm [4-7]. in the literature, the most important determinant for prognosis and outcome is gcs. although the general mortality rate is 20-55%, it is 510% in early diagnosed and intervened cases [4, 7]. in our study, it was observed that mortality rate decreased and prognosis was better in younger patients and patients with higher gcs values. since brain injuries frequently include multiple trauma and multiple organ injuries, they require icu follow-up and treatment. many patients are also followed up by anesthesia physicians in icus during the postoperative period. immobile patients become susceptible to infections in the icus. it was found that the cost increased incrementally with prolonged stay in the icu. the reasons for increased costs were analyzed in our study. daily price for icu standard bed is determined by the ministry of health. however, this standard price can be surpassed quite often with costs of examination, treatment and imaging studies, and the institution can experience financial losses. the main reasons for high costs are infection prophylaxis, and broad spectrum combined antibiotics administered to infected cases. the period before an infectious disease clinic consultation and antibiotherapy application is 3 days at maximum particularly in patients who are brought to icu intubated during the postoperative period because of low gcs. the reason for this is pulmonary infections, which occurs following air passage to bronchi after ventilation and passing through physiological ways. central nervous system (cns) infection is not frequent in edhs as they are usually in the form of closed fractures. nevertheless, cns infection rates increase in patients with skull base involvement, and pneumocephalus, rhinorrhea or otorrhea. in these situations, short-term prophylactic antibiotherapy can be applied in selected cases. besides, the risk for atelectasis increases in postoperatively immobile patients andcombined antibiotherapy is applied rapidly due to increased body temperature and leukocytosis. usually prophylactic administration is performed before the results of cultures. the most important factors that can reduce costs, and mortality and morbidity rates in these patients are shortening icu stay, weaning from mechanical ventilation within the shortest time possible, and mobilization. furthermore, another factor that increases the costs is the prophylactic antibiotherapy with the prediagnosis of cns infection or pulmonary infection. in our study, the costs romanian neurosurgery (2017) xxxi 4: 510 516 | 515 of antibiotherapy constituted 15% of the total costs. the antibiotherapy costs of patients who stayed in the icu for 10 or more days and who had double or triple antibiotherapy were significantly higher than other patients. another postoperative cost increasing factor is frequently performed neuroimaging studies. cranial ct is the most frequently used imaging modality during the preand post-operative periods in edh. the followup is made with frequent cranial cts in unoperated patients [8, 9]. in our study, the mean number of ct scans for the follow-up of edh was 3.7. however, ct scans in icu follow-up of patients with longer stays can range between 7-8. yet, the data analysis revealed that ct scans, except for postoperative control brain cts, did not affect our treatment choice. frequent cranial cts in the post-operative period increase the cost and also expose the patient to radiation. close follow-up with neurological examination following ct scan in the postoperative early period can decrease both the costs and the risk of radiation-induced comorbidities. conclusion in conclusion, the length of stay in the icu, double or triple antibiotherapy, and frequent head cts increase the costs for patients undergoing surgery for edh. though human life is a sacred phenomenon over all kinds of cost calculation, we believe institutions and patients will benefit from reduction of unnecessary antibiotherapy and limitation of frequent head cts. what is known about this topic •epidural hematoma, which was defined for the first time by hutchinson in 1867, is a common type of traumatic brain injury (tbi) in which blood accumulation occurs between the dura mater and the cranium due to trauma. •patients with epidural hematoma requires icu follow-up and treatment. what this study adds •the prolonged period of stay in the icu, antibiotherapy and repeat head cts increase the costs for patients who are surgically treated for edh. correspondence ibrahim burak atci. istanbul research and training hospital, department of neurosurgery; istanbul, turkey. telephone: +90 212 459 60 88 cellphone: +90 505 773 31 55 fax: +90 212 459 62 30 e-mail: drburakatci@hotmail.com references 1. sahuquillo-barris j, lamarca-ciuro j, vilalta-castan j, rubio-garciae, rodriguez-pazos m. epidural hematoma and diffuse axonal injury. neurosurgery. 1985;17(2):378379 2. rivas jj, lobato rd, sarabia r, cordobés f, cabrera a, gomez p. extradural hematoma: analysis of factors influencing the courses of 161 patients. neurosurgery. 1988;23(1):44-51 3. cheung ps, lam jm, yeung jh, graham ca, rainer th. outcome of traumatic extradural haematoma in hong kong. injury. 2007;38(1):76-80 4. deniz fe, türk cc, ismailoğlu o, bozkurt g, ozcan oe. rapid spontaneous resolution of epidural hematoma: a case report. ulus travma acil cerrahi derg. 201;16(3):280-282 5. chen ty, wong cw, chang cn, lui tn, cheng wc, tsai md, lin tk. the expectant treatment of 516 | atci et al incidence, hospital costs and in-hospital mortality rates "asymptomatic" supratentorial epidural hematomas. neurosurgery. 1993;32(2): 176-179 6. bejjani gk, donahue dj, rusin j, broemeling ld. radiological and clinical criteria for the management of epidural hematomas in children. pediatr neurosurg. 1996;25(6):302-308 7. bezircioğlu h, erşahin y, demirçivi f, yurt i, dönertaş k, tektaş s. nonoperative treatment of acute extradural hematomas: analysis of 80 cases. j trauma. 1996;41(4):696-698 8. ding j, yuan f, guo y, chen sw, gao ww, wang g, cao hl, ju sm, chen h, zhang pq, tian hl. a prospective clinical study of routine repeat computed tomography (ct) after traumatic brain injury (tbi). brain inj. 2012;26(10):1211-1216 9. shin ds, hwang sc, kim bt, jeong jh, im sb, shin wh. serial brain ct scans in severe head injury without intracranial pressure monitoring. korean j neurotrauma. 2014; 10(1):26-30 microsoft word iordache_severehead_f a. iordache et al severe head injury severe head injury – the place for regional centers a. iordache1, c. caldare2, n. ianovici1 1university of medicine and pharmacy “gr.t. popa” iaşi 2hospital no. 3 iaşi abstract we are discussing the administrative aspect of solving the severe head trauma and the new modern aspects for pre and post operatory survey, using as a point of departure the case of a patient explored and sent to our department. the aim is not always to improve patient prognosis but to be more precise in depicting patient future evolution especially with patient with isolated, severe head injury who are most prone to be subjects for organ transplantation. keywords: administrative management, severe head injury, transcranial doppler introduction severe head injury remains an important problem of public health despite the evolution of the intensive care treatment and the radical improvement in neurosurgical care availability. the severe head injury represents a major source of mortality and posttraumatic disability. nowadays we have a neurosurgical unit in most of the emergency hospital in every county. nevertheless the access to emergency imagery (computer tomography – c.t.) is more difficult especially at night. another problem are the centers where there is a neurosurgical unit but without enough specialists in order to cover the all the on calls for emergencies. most of the severe head injuries sent from tertiary centers to our hospital are already exceeded cases. we present one of this cases that have been diagnosed to late and maybe operated on too late, but who can also provide valuable information about the actual state of the medical system. case presentation adult patient, 47 years old, received in emergency unit in focsani, with glasgow coma scale score 4, intermediate nonreactive pupils, and epicranial hematoma located in parietal area. the patient was found nearby the road. he was known to have epilepsy and being a heavy drunker. he was examined by a emergency doctor, by general surgeon and by neurologist. shortly after admittance he was examined at c.t. the radiologist described a subdural hematoma located on the right side covering the frontal and the parietal lobe, with a width of around 24 mm and midline shift 25 mm; multiple lacerations located superficially in the parietal lobe, traumatic subarachnoid hemorrhage, intraventricular hemorrhage(lateral ventricles, 3-rd ventricle, 4-th ventricle). the patient was operated for the subdural hematoma but intra operatively we asses firstly a parietal fracture with an acute extradural hematoma and opening the dura we found also the acute subdural hematoma with multiple cerebral concussion. romanian neurosurgery (2011) xviii 2 figure 1 acute subdural haematoma a b figure 2 a trauma flap type incision with b linear parietal fracture a b figure 3 a extradural haematoma; b acute subdural heamatoma with temporo-parietal lacerations figure 4 posttraumatic hemispheric ischemia a. iordache et al severe head injury figure 5 transcranial doppler (transtemporal window) of the left sylvian artery, the right sylvian artery was not visible evolution of the case was unfavorable with exitus 48 hours after the intervention. during the evolution we evolution we assessed the cerebral circulation with transcranial doppler. we have noticed the absence of the flow in the sylvian artery on the right side and diminished flow on the left side. the assessment of the blood flow was made preoperatively and postoperatively after 24 hours and the aspects were the same, fact confirmed by the hemispheric ischemia at ct scan. discussion we are discussing the case of a severe head injury with gcs of 4 at presentation. the main question in this case is if earlier intervention would improve the prognosis of the patient. statistics are showing a mortality of more than 80% such severe head injury (gcs 3 and 4). of course we have performed a decompressive craniectomy, expecting for vigorous brain edema, trying to give all the chances to the patient. the decompressive craniectomy was made according to the criteria proposed by the brain trauma foundation and we have performed autologous dural graft with pericranium. transcranial doppler was a valuable tool in assessing earlier the diagnosis of cerebral ischemia. we can predict the usefulness of the transcranial doppler in diagnosis of cerebral death especially for the patient candidate for transplantation. in the case reviewed because of the medico-legal problems the patient was not a candidate for transplantation. this method will be useful in cases with coma grade 4 but who still keeps electrical activity on the eeg. the problem of the early intervention is supposed to be already solved with the many neurosurgical departments opened in the latest years. the original aim for opening those regional centers is to solve swiftly and with better results mostly the neurotraumatic cases. the absence of neurotrauma centers can lead to such unfortunate endings. also a problem is the lack of means of explorations in smaller centers so many cases are referred may be too late or are not at all diagnosed. this kind of cases can be prevented in our opinion with better organization of the resources. every county hospital should have an computer tomography imagery available all the time with a radiologist eventually available on call in order to diagnose the lesion. another aspect is the transportation. people involved in emergency medical transportation should know that the degree of importance of swift transfer for an extradural hematoma is the same as for myocardial infarction and so on. in the same direction we should propose and adopt protocols in order to avoid such cases of surgical intervention in order to avoid medico-legal problems. romanian neurosurgery (2011) xviii 2 conclusion in our opinion transcranial doppler a in severe head injury should be performed preoperatively and postoperatively in order to assess the functional and vital prognosis especially for the patients with gcs 3 or 4. the existence of the neurotrauma centers in each county hospital has been a subject well discussed but unsolved until yet. theoretically most of the county hospitals +have this kind of centers but in many cases they don’t have enough personnel and there is actually no possibility to explore the patient in emergency. creation and implementation of standard protocols for diagnosing the patient and for emergency transfer would create a more efficient medical system. references 1. a.v.ciurea, h.b.davidescu – traumatologie craniocerebrală, editura universitară « carol davila », 2006 2. albanese j, leone m, alliez jr, kaya jm, antonini f, alliez b, et al: decompressive craniectomy for severe traumatic brain injury: evaluation of the effects at one year. crit care med 31: 2535-2538, 2003 3. becker dp, gade gf, miller jd: prognosis after head injury, in youmans jr (ed): neurological surgery, ed 3. philadelphia: wb saunders, 1990, vol 3, pp 2194-2229 4. boishardy n, granry jc, jacob jp, et al: [value of transcranial doppler ultrasonography in the management of severe head injuries.] ann fr anesth reanim 13:172-176,1994 (fr). 5. brain trauma foundation guidelines for the severe traumatic brain injury – 3-rd edition, editura marry ann liebert, 2007. 6. bullock mr, chesnut rm, clifton g, ghajar j, marion dw, na rayan rk, et al: management and prognosis of severe traumatic brain injury. new york: brain trauma foun dation, 2000; 7. ciurea v.a. – tratat de neurochirurgie vol.1 – editura medicală – 2010 8. de luca gp, volpin l, fornezza u, cervellini p, zanusso m, casentini l, et al: the role of decompressive craniectomy in the treatment of uncontrollable post-traumatic intracranial hypertension. acta neurochir suppl 76:401-404, 2000 9. gorgan m. ghid în patologia neurochirurgicală, editura didactică şi pedagogică 2008. 10.munch, elke m.d.; horn, peter m.d.; schurer, ludwig m.d., ph.d.; piepgras, axel m.d., ph.d.; paul, torsten; schmiedek, peter m.d., ph.d management of severe traumatic brain injury by decompressive craniectomy.neurosurgery. 47(2):315-323, august 2000. microsoft word 11petraruddirectcarotid 82 d. petraru et al direct carotid-cavernous fistula and glaucoma direct carotid-cavernous fistula and glaucoma: case reports d. petraru1, d. costin2, g. mihalache3 12nd ophthalmological clinic, university of medicine and pharmacy “gr.t. popa” iasi, phd candidate 2university of medicine and pharmacy “gr.t. popa” iasi, 2nd ophthalmological clinic, clinical emergency neurosurgical hospital 3university of medicine and pharmacy “gr.t. popa” iasi, romania abstract a carotid-cavernous fistula is an abnormal communication between carotid artery system and the cavernous system. the causes that determines the onset of the fistula are trauma or spontaneous. the fistula receives venous blood from the eye and the brain, from the ophthalmic veins and the superficial middle cerebral vein. the abnormal shunt determines raised venous pressure on the cavernous sinus, determining ophthalmic veins stasis. it appear ocular congestion, raised intraocular pressure, exophthalmia, diplopia, decreased visual acuity or cranial nerves paralysis. glaucoma is a potential complication that appear in carotid-cavernous fistula from increased pressure in the episcleral veins. carotid-cavernous fistula diagnosis can be determined clinically and imagistically. this pathology is treated successfully in 90% of all cases, the mortality and morbidity rates are very low. this study presents two case reports, diagnosed with direct carotid-cavernous fistula and glaucoma. keywords: direct carotid-cavernous fistula, glaucoma direct carotid-cavernous fistula appears in 70-90% of all cases with carotidcavernous fistulae cited by keltner et al. in 1987, debrun et al. in 1988. (1) direct fistula can be localized in any intracavernous portion of internal carotid artery. iatrogenic fistulae are reported in transsphenoidal surgery of the pituitary gland or internal carotid artery lesion in endarterectomy or ethmoidal sinus surgery. some direct fistulae can be caused by rupture of an intracavernous aneurysm. ehlers-danlos syndrome, arterial hypertension or artheriosclerosis were associated with carotid-cavernous fistula.(2) cerebral trauma causes 75% of carotidcavernous fistulae at young patients, with pulsatile exophthalmia. 25% of carotidcavernous fistulae are spontaneous, specially middle aged women with atherosclerosis. (3) glaucoma is a potential complication of the direct untreated carotid-cavernous fistula, mentioned by sugar and meyer in 1940, and by madsen in 1970, that appears in 30-50% of all cases.(3) case i a 63 year old female patient, b.i., presented with ocular congestion that appears two weeks ago, retro-orbital mild pain and left eye diplopia. clinical exam revealed the 6th left nerve palsy, 3 mm exophthalmia, discreet orbital bruit and dilated conjunctival vessels. on goldmann tonometry the intraocular romanian neurosurgery (2011) xviii 1: 82 – 87 83 pressure was 22-25 mm hg. during hospitalization were administered topical ocular hipotensors and the diurnal pressure curve was assessed, the pressure normalized between 16 and 18 mm hg. the mriangiography revealed a left carotidcavernous fistula; the patient was transferred in a neurosurgical clinic. all ocular symptoms and signs resolved in four weeks after intravascular closure of the fistula with a detachable balloon ( figure 1a, 1b). the patient continued the ocular hipotensors treatment during neurosurgical hospitalization. at eight weeks, the patient presents in the ophthalmological clinic for re-assessment, the intraocular pressure was between 14-17 mm hg, without antiglaucomatous medication. the ophthalmoscopic exam didn’t revealed pathological findings of the cup-disc ratio, that was 0.2-0.3, the visual field was normal as well, regarding to her age. case ii a 25 year old male pacient, d.m., diagnosed with traumatic carotid-cavernous fistula, presented in the ophthalmological clinic with right eye chronic glaucoma. clinical exam revealed a discreet right eye exophthalmia, dilated conjunctival vessels and the left anterior pole didn’t present any pathological finding. on goldmann tonometry, the intraocular pressure was between 32 and 38 mm hg. the ophthalmoscopic exam on the right eye revealed a mild glaucomatous cupping, cup-disc ratio 0.6 and in the left eyes a normal aspect, without pathological cupping. the mri-angiography revealed the presence of a carotid-cavernous fistula (figure 2); the patient refused the neurosurgical treatment. figure 1a cerebral angiography of the carotidcavernous fistula figure 1b intravascular closure of the fistula with a detachable balloon during hospitalization we administered antiglaucomatous topical medication, intraocular pressure was above normal level (32-34 mm hg); we performed filtering surgery (trabeculectomy) for intraocular pressure decrease; after surgery the intraocular pressure level normalize, between 16 and 18 mm hg. at six weeks after the surgery, the patient had under antiglaucomatous topical treatment values of intraocular pressure between 14 and 16 mm hg. the ophthalmoscopic exam revealed on the right eye a glaucomatous cupping, the left eye was normal. we prescribed antiglaucomatous topical therapy to continue on right eye and periodical ophthalmological assessment. 84 d. petraru et al direct carotid-cavernous fistula and glaucoma figure 2 cerebral angiography of the carotidcavernous fistula in case 2 discussions direct carotid-cavernous fistula has a frequency up to 90% of all carotidcavernous fistulae and glaucoma is a potential complication of untreated direct carotid-cavernous fistula. in 1970, madsen mention untreated carotid-cavernous fistula and glaucoma association. (1) henderson and schneider find that glaucoma was diagnosed on 3050% of all cases with untreated fistula. (1) the most common form is determined by the raise of pressure in episcleral veins. in 1973,spencer et al. mention cases of patients diagnosed with direct carotidcavernous fistula and neovascular glaucoma, always associated with retinal chronic hypoxia and retinal neovascularization, after central retinal vein occlusion. (1) ocular findings of the first patient are related with blood redistribution from the orbital veins, determining decreased arterial blood flow at the cranial nerves level, venous stasis in anterior and posterior circulation in the eye and the orbit, raised pressure in episcleral veins. ocular findings are localized unilateral, same path with the fistula, may be bilateral or in rare cases contralateral. ocular finding path depends of venous blood drainage thru cavernous sinus, especially the intercavernous system and the basilar system, with thrombosis at the sinus level or the superior ophthalmic vein. trauma can determine bilateral cavernous sinus fistula. carotid-cavernous fistulae (direct communications between internal carotid artery and the cavernous sinus) (4), determine a high blood flow, accompanied by unilateral or bilateral pulsatile exophthalmia, orbital bruit, ocular chemosis and diplopia. (5) fistula associates with moderate or severe eyelid inflammation, cyanoses and palpebral derma thickening appear in chronic disease. (6) ocular pulsation is caused by a pulsatile wave from the internal carotid artery level or the ophthalmic artery thru dilated ophthalmic veins. orbital veins become tortuous and secondary congestion of the orbital soft tissue appears, increase of the venous pressure and decrease of the arterial perfusion, local hypoxia, that determines tissue edema and a certain degree of ophthalmoplegia, resulting in anterior segment ischemia. conjunctival chemosis appears in almost all patients diagnosed with direct carotidcavernous fistula, preceeding the exophthalmia in most cases. (7) dilation of the conjunctival vessels is the most obvious sign of this disease. keratopathy is diagnosed frequently, associated with the exophthalmia. (8) cornea can present an edematous aspect, due to secondary glaucoma or anterior segment ischemia. diplopia is caused by common oculomotor nerves damage, ocular movement is limited, complete ophthalmoplegia can occur. ophthalmoplegia cand be caused by the damage of one or multiple oculomotor romanian neurosurgery (2011) xviii 1: 82 – 87 85 nerves due to compression or ischemia; the most affected oculomotor nerve is the abducens nerve, but also the trochlear nerve can be affected, which is situated in the profound layer of the lateral wall of the cavernous sinus. the decrease in the visual acuity produces immediately, being caused by optic nerve damage or it can appear late due to vitreous hemorrhage, retinal dysfunction, anterior ischemic optic neuropathy or corneal ulcer. visual acuity decrease pathology is explained by retinal dysfunction, decreased perfusion pressure in ophthalmic artery and increased venous pressure. the result is chronic hypoxia of the retinal cells. the eye fundus exam reveals dilated veins with spontaneous pulsation, optic disc swelling, retinal hemorrhage, venous stasis retinopathy or venous occlusion. sever pain and local inflammation can suggest ophthalmic vein thrombosis, which can be diagnosed by magnetic resonance imaging or ocular echography. ocular and orbital pain, facial hyperesthesia can be caused by compression of the maxillary and the ophthalmic trunks of trigeminal nerve at the cavernous sinus level. glaucoma is a potential complication which can appear in direct carotidcavernous fistula. (1) the most common form of glaucoma is caused by increased pressure in the episcleral veins as we presented in the two cases. (8) intraocular pressure is moderately raised (24 mm hg), but cases cited have intraocular pressure up to 50-60 mm hg, the normal level being 10-21 mm hg, the fistula often associates with central retinal artery occlusion. orbital congestion is associated with glaucoma, intraocular pressure in these cases being severely raised and the medical treatment is difficult. neovascular glaucoma can appear in patients with carotid-cavernous fistula, following chronic retinal hypoxia, retinal neovascularization or after central retinal vein occlusion. in rare cases, some patients develop angle closure glaucoma by raised pressure in the orbital veins which determines choroidal and iris congestion with forward pulling of the iridolenticular diaphragm, determining angle closure. the diagnosis is based on the clinical findings: rapidly developed conjunctival chemosis, exophthalmia and ocular congestion. patient can present a trauma in the past, am intracavernous aneurysm rupture or diplopia. the paraclinical exams used to establish the diagnosis are: tonometry, ct scan, mri-angiography, ocular echography, cerebral angiography (which helps identifying the presence of the fistula). the optimal treatment of direct fistula is the closure of the abnormal communication with preserving of the internal carotid artery. there are many surgical options for closure: direct surgical closure of the affected intracavernous portion of the internal carotid artery, isobutyl-2cyanoacrilate embolization, particles of polyvinyl alcohol or a detachable balloon placed in the cavernous sinus, in the arterial or venous path, thru inferior petrous sinus or superior ophthalmic vein, directly in cavernous sinus. (9) once the balloon has reached the cavernous sinus it is inflated and detached determining fistula closure. the complications of this therapeutically method include transitory or permanent cranial nerve palsies, visual field loss or pseudo-aneurysm development. (10) it was mentioned in the literature spontaneous closure of fistula in 3 days up to 18 months in 10-60% of all patients. (1) 86 d. petraru et al direct carotid-cavernous fistula and glaucoma after the successfully closure of the fistula, almost all symptoms and ocular signs disappear or improve. (11) ocular pulsation, eyelid edema, conjunctival chemosis, conjunctival vessels dilation, stasis retinopathy, optic disc swelling and raised intraocular pressure disappear immediately. exophthalmia decreases but it may not disappear entirely. similarly, the patients with ophthalmoplegia can have a normal motility and diplopia can disappear. the only symptom of the direct carotidcavernous fistula that don’t improve is the visual acuity loss due to optic neuropathy, that’s why the treatment must be commenced as urgent as possible that the irreversible optic nerve lesions don’t appear. glaucoma necessitated rapid treatment; ocular hypotensors were administered in the first case or the surgical treatment (trabeculectomy) in the second case. the therapy target was to normalize the intraocular pressure and to reduce ischemia and ocular necrosis. beta adrenergic antagonists, carbonic anhydrase inhibitors and alpha 2 agonists have reduced the intraocular pressure in the first case. pilocarpine and prostaglandin analogues are not efficient in this case. prostaglandin analogues treatment can be associated with episcleral venous dilation. filtering surgery was efficient in the second case and made a stable, uniform decrease of the intraocular pressure, when the medical treatment cannot be administered, the patient refused it. in the second case, the trabeculectomy was the surgical method we choose: a scleral flap was created, two-thirds thickening, a rectangular shape (six by four mm), 1,5 mm advance in clear cornea, the profound scleral flap was excised, approximately 2 by 2 mm at the limboscleral junction (the gray zone), tissue that contain the trabecular meshwork. (12) when the trabeculectomy doesn’t provide an efficiently result, we recommend the artificial drainage systems or the trabeculectomy augmented with antimetabolites (5-fluorouracile or mytomicin c). conclussions direct carotid-cavernous fistula doesn’t necessitates rapid treatment, it can be delayed; the untreated fistula lead to progressive ocular symptoms. in months or years, this disease evolves to exophthalmia, chemosis and total visual acuity loss due to glaucoma, ischemic optic neuropathy. in the first case, ocular symptoms necessitate paraclinical exams which showed the carotid-cavernous fistula, surgically treated, the ocular symptomatology disappear after the surgical treatment. the other case with carotid-cavernous fistula necessitates filtering surgery for ocular pressure balance and visual parameters normalize because the patient refused the neurosurgical treatment and doesn’t accept the anti-glaucomatous therapy. even if the direct carotid-cavernous fistula doesn’t present vital risk, it can produce intracerebral hemorrhage, ischemic optic neuropathy, secondary glaucoma and primary open angle glaucoma, diseases that without treatment determine irreversible visual loss. references 1. neil r., miller, m.d. – walsh and hoyt’s, clinical neuro-ophthalmology, 4th edition volume four, 1982. romanian neurosurgery (2011) xviii 1: 82 – 87 87 2. niamtu j 3rd, campbell rl, „carotid cavernous fistula”, journal of oral maxillofacial surgery 1982 jan;40(1):52-6. 3. joel s. glaser – neuro-ophthalmology, third edition, lippincott williams & wilkins,1999. 4. masaki komiyama, hideki nakajima, misao nishikawa, and masanori kan, „traumatic carotid cavernous sinus fistula:serial angiographic studies from the day of trauma”, ajnr am j neuroradiol 19:1641–1644, october 1998. 5. american academy of ophthalmology – basic and clinic science course, san francisco, 2004/vol. 6,7,8,9,11,12. 6. keltner jl, satterfield d, dublin ab, lee bcp. dural and carotid cavernous sinus fistulas.ophthalmology 1987; 94 : 1585–1600. 7. anthony e. harris, md; patrick g. mcmenamin, „carotid artery—cavernous sinus fistula”, archives of otolaryngologyhead and neck surgery. 1984;110(9):618-623. 8. john c.morrison, irvin p.pollack – glaucoma, science and practice, thieme,2003. 9. yang zj, li hw, wu lg, zheng jn, zhang jd, shi xw, chu gr., „prognostic analysis and complications of traumatic carotid cavernous fistulas after treatment with detachable balloon and/or coil embolization”; chin j.traumatology 2004 oct; 7(5):286-8. 10.stanley l barnwell, oisin r o’neill, „endovascular therapy of carotid cavernous fistulas”, endovascular approach to central nervous system disease, vol.5, nr.3, p.485, july, 1994. 11.philippe hantsona benoît espeela, jean-michel guéritb, pierre goffettec, „bilateral carotid-cavernous fistula following head trauma: possible worsening of brain injury following balloon catheter occlusion?” clinical neurology and neurosurgery ,volume 108, issue 6, pages 576-579 (september 2006). 12.kanski j., jack, clinical ophthalmology a systematic approach, 136-137, elsevier science limited, 2003. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery | volume xxxi | number 3 | 2017 | july-september article the many faces of primary cauda equina myxopapillary ependymoma: clinicoradiological manifestations of two cases and review of the literature mohammad zare mehrjardi, samira mirzaei, hamid reza haghighatkhah iran doi: 10.1515/romneu-2017-0062 romanian neurosurgery (2017) xxxi 3: 385 390 | 385 doi: 10.1515/romneu-2017-0062 the many faces of primary cauda equina myxopapillary ependymoma: clinicoradiological manifestations of two cases and review of the literature mohammad zare mehrjardi1,2, samira mirzaei3, hamid reza haghighatkhah1 1department of radiology, shohada tajrish hospital, school of medicine, shahid beheshti university of medical sciences, tehran, iran 2section of neuroimaging, division of clinical research, climax radiology education foundation, tehran, iran 3department of radiology, imam khomeini hospital, school of medicine, tehran university of medical sciences, tehran, iran abstract: introduction: myxopapillary ependymoma (mpe) is a benign and slow growing tumor that originates exclusively from the conus medullaris and cauda equina nervous tissue. it occurs more commonly in young patients. in addition, clinical presentations are non-specific and may mimic benign conditions. magnetic resonance imaging (mri) is the imaging modality of choice for evaluating this tumor. we hereby report on two young patients with long-lasting non-specific symptoms, which were clinically attributed to benign conditions. however, cauda equina tumor was revealed on mri in both patients. case report: two cases of cauda equina mpe, a 19-year-old female and a 38-year-old male, with different clinical manifestations are reported. the first patient presented with paresis and paresthesia of the lower limbs, and the second patient’s complaint was chronic low-back pain and urinary incontinence. in both cases, mri detected a tumor originated from the cauda equina, and histopathologic examination was compatible with mpe. conclusion: cauda equina tumors should be considered as a differential diagnosis in the young patients presented with neurologic deficits in the lower limbs, sphincter or erectile dysfunction, and even a simple low-back pain (particularly when symptoms are long-lasting and/or progressive). key words: cauda equina, ependymoma, magnetic resonance imaging, myxopapillary ependymoma, radiology 386 | mehrjardi et al clinicoradiological manifestations of primary cauda equina mpe introduction ependymoma is the most common spinal cord tumor in adults, which is more commonly presented during the fourth and fifth decades of life [1, 2]. however, it comprises about 30% of pediatric intramedullary tumors as well [3]. in one study, the mean age of patients with spinal ependymoma was 34.6±16 years-old, and it was slightly more common in males (male-tofemale ratio, 4:3) [4]. ependymomas originate from ependymal cells of the central spinal canal. world health organization (who) has classified spinal ependymomas into three discrete types, including myxopapillary type or subependymoma (grade-i), classic type (grade-ii), and anaplastic type (grade-iii) [5]. although primary tumors of lumbosacral spinal nervous tissue (i.e., conus medullaris, and cauda equina nerve roots) are not common, myxopapillary ependymomas (mpe) originate almost exclusively from this region and comprise about 90% of all tumoral lesions in the lumbosacral canal [6, 7]. clinical presentations of cauda equina tumors (including mpe) are not specific, and they may mimic benign conditions such as spondylosis or a prolapsed intervertebral disk [8]. mpe often has a peripheral capsule and a lobulated margin on gross examination. histopathologically, mpe is a heterogeneous tumor due to its mucinous background, and presence of cellular and papillary areas [9, 10]. on immunohistochemical study, tumor cells usually show positive immunoreactivity for glial fibrillary acidic protein (gfap), cytokeratin ae1/ae3, s100 protein, and d240; but they are negative for epithelial membrane antigen (ema), and brachyury [11, 12]. the mainstay treatment of mpe is complete resection of the lesion, because partial removal may lead to tumor recurrence. adjuvant chemotherapy and/or radiation therapy are recommended on occasions [4, 8]. early diagnosis and surgical resection of mpe significantly ameliorates the prognosis of this tumor, because there is the chance of tumor cell dissemination in the cerebrospinal fluid (csf) leading to multiple disseminated lesions [5]. magnetic resonance imaging (mri) is the imaging modality of choice for the diagnosis and evaluation of the cauda equina tumors. however, it is still difficult to determine exact nature and type of the tumor based on the imaging findings [1, 9]. we, hereby, present two cases of cauda equina mpe, and discuss the clinical and neuroimaging findings of mpe. it is important for the clinicians and radiologists to have a detailed knowledge of the clinical and radiological presentations of the cauda equina tumors for making a correct diagnosis, and managing the patient properly. case report informed written consent was obtained from both patients for reporting and disclosing their clinical data with respect to ethical issues. romanian neurosurgery (2017) xxxi 3: 385 390 | 387 case 1: a 19-year-old female presented with a five month history of gradually progressive paresis and paresthesia of the lower limbs. she did not have any sphincter dysfunction. on physical examination, both lower extremities muscle strength and patellar tendon reflex had been reduced to the grade 3/5 and 1+, respectively. muscle tone of both legs was slightly reduced. achilles and plantar reflexes as well as proprioceptive sensation were normal. biochemical examinations revealed no abnormality. based on the clinical data, the first impression was a prolapsed intervertebral disk, and the patient was referred for lumbosacral spine mri. on mri (figure 1), there was an intradural extramedullary mass in the lumbar spinal canal at the level of l2−l3 intervertebral disk, which was originated from the cauda equina. it was isointense compared to the normal cord and slightly hyperintense compared to the csf on t1-weighted, and markedly hyperintense on t2-weighted images. the tumor revealed significant homogeneous post-contrast enhancement following gadolinium-based contrast agent injection. based on mri findings, differential diagnoses were nerve sheath tumors, mpe, and less likely meningioma. histopathological examination following complete surgical tumor removal demonstrated benign ependymal cells with pseudopapillae formation and redundant mucin production in a myxoid stroma, suggestive of mpe. figure 1 lumbosacral spine mri of a 19-year-old female. on coronal (a to c) and sagittal (e to g) sections, a well-defined oval mass is noted within the lumbar spinal canal on the cauda equina nerve roots, at the level of l2−l3 intervertebral disk. it is seen as a filling defect on heavily t2-weighted myelograms (arrows in a and e), and has slightly high signal intensity compared to the surrounding cerebrospinal fluid, and iso-signal intensity compared to the normal cord on t1-weighted images (arrows in b and f). the lesion is homogeneously enhanced on postcontrast t1-weighted with fat saturation images (arrows in c and g). post-contrast enhancement is also evident comparing axial pre(asterisk in d), and post(asterisk in h) contrast injection fat saturated t1-weighted images case 2: a 38-year-old male presented with a 2 year history of low-back pain and mild paresthesia of the lower limbs, as well as a recent urinary incontinence. on physical examination, lower limb muscle strength and tone, as well as deep tendon reflexes were normal on either sides. the initial clinical impressions were congenital spinal canal stenosis, intervertebral disk herniation, and spondylolisthesis. the patient was referred for additional evaluation by lumbosacral spine mri. mri study (figure 2) demonstrated an intradural extramedullary mass in the sacral canal, which had slightly expanded the canal at 388 | mehrjardi et al clinicoradiological manifestations of primary cauda equina mpe s1−s3, and remodeled posterior aspects of the corresponding vertebral bodies. it was hypointense compared to the normal cord and isointense compared to the csf on t1weighted, and markedly hyperintense with internal foci of low signal intensity representing previous episodes of hemorrhage on t2-weighted images. the tumor showed extensive post-contrast enhancement following gadolinium-based contrast agent injection. according to these imaging findings, differential considerations were mpe, paraganglioma, and astrocytoma. histopathological examination after surgical resection was compatible with mpe. figure 2 lumbosacral spine mri of a 38-year-old male. on coronal (a), and sagittal (b) myelograms, a filling defect (arrow) with obstruction of the cerebrospinal fluid flow, and mild canal expansion, is noted at the sacral level (s1−s3). the mass is hypointense on sagittal t1-weighted image (arrow in c), and shows heterogeneous post-contrast enhancement on sagittal fat saturated t1-weighted image (arrow in d). the lesion is hyperintense with internal foci of hypointensity (due to previous hemorrhage) on sagittal t2-weightd (arrow in e), and turbo inversion recovery magnitude (arrow in f) images. heterogeneous post-contrast enhancement with mild canal expansion is also noted on axial contrast-enhanced t1-weighted with fat saturation image (asterisk in g) discussion mpe is a benign and slow growing tumor that exclusively originates from cauda equina nerve roots and/or conus medullaris. it affects young adults and males more common than children and females [1, 10]. common clinical manifestations of this tumor include chronic low-back pain, paresthesia and flaccid paralysis of the lower limbs, and dysfunction of the rectal and urinary sphincters in both genders, as well as erectile dysfunction in males. because the clinical presentations are non-specific and the patients are commonly young, there is usually delay in the diagnosis and treatment [7, 8]. although low back pain etiologies are usually benign in nature and neoplastic conditions comprise less than 1% of all etiologies, neoplasms should be considered as a differential diagnosis because they are associated with significant morbidity and mortality [13]. ngo et al. [13] reported a 19-year-old male with a 3 year history of low back pain, which was attributed to a soft tissue injury and he was prescribed anti-inflammatory drugs. two years later, he developed intermittent erectile dysfunction and difficulty in defecation. finally, a large lumbosacral spinal tumor was diagnosed on mri four years after his first presentation at the age of 23 years. surgical excision was performed and histopathologic examination was compatible with mpe. similarly, demir et al. [14] reported mpe as the cause of chronic low back pain in a 28year-old female. mri is the imaging modality of choice for precise evaluation of these patients. mpe is romanian neurosurgery (2017) xxxi 3: 385 390 | 389 commonly iso to hypointense on t1-weighted, and hyperintense on t2-weighted images [9, 15]. in a study on 20 cases with mpe, mri features of the tumor were not specific. tumors were isointense (75%), hypointense (19%), or hyperintense (6%) compared to the normal cord on t1-weightd images, while they were hyperintense (80%) or isointense (20%) on proton-density, and hyperintense (100%) on t2-weighted images [7]. although this tumor is almost always hyperintense on t2weighted images (due to the mucinous content), areas of low signal intensity secondary to previous hemorrhage may be evident within the tumor. almost all mpes enhance avidly following contrast agent injection. post-contrast enhancement is usually homogenous, but heterogeneous enhancement due to previous hemorrhage and cystic changes is not uncommon [9, 15]. although mri can accurately demonstrate presence of a mass in the spinal canal, it has currently limitations in determining the exact type of the tumor. other benign as well as malignant tumors that may occur in this region include nerve sheath tumors such as schwannoma and neurofibroma, paraganglioma, hemangioblastoma, astrocytoma, primitive neuroectodermal tumor (pnet), ganglioglioma, meningioma, metastasis, lipoma, dermoid, and epidermoid. bavbek et al. [16] reported a 46-year-old man with a 2 year history of progressive paresthesia and paresis of the right leg. lumbar spinal mri showed an intradural extramedullary mass with homogenous postcontrast enhancement at l1−l2. initial radiological differential considerations were schwannoma, neurofibroma, and meningioma. however, postsurgical histopathological examination identified the tumor as a mpe. in another report by kim et al. [17], a 30-year-old male with a 1 year history of low back pain and leg pain was evaluated by mr imaging. mri revealed a well-defined intradural extramedullary tumor with significant homogenous post-contrast enhancement and cystic changes at l3−l4 level, which was initially diagnosed as a nerve sheath tumor based on imaging findings. histopathological examination after resection was, however, compatible with mpe. on the other hand, thoriya et al. [18] reported a case of primary pnet of lumbosacral spine in a 31year-old female with a 4 week history of progressive low back pain and weakness of lower limbs, which was primarily diagnosed as mpe based on mri findings. conclusion although mpe is a rare tumor, it consists the most common neoplasm of the cauda equina nerve roots. it occurs more commonly in the young patients and causes non-specific clinical manifestations; therefore, it should be considered as a differential diagnosis in any young patient with a history of chronic lowback pain, paresis or paresthesia of the lower limbs and sphincter or erectile dysfunction, particularly when the symptoms are progressive and do not respond to the conservative management. mri is the imaging modality of choice for further evaluation of these patients. it may be of help to make differentiation between benign and malignant conditions, but there is currently a significant 390 | mehrjardi et al clinicoradiological manifestations of primary cauda equina mpe overlap between the imaging findings of cauda equina tumors. mri is also helpful to determine boundaries and extensions of the tumor for preoperative planning. correspondence mohammad zare mehrjardi contact no.: +989133530656 e-mail: zare@sbmu.ac.ir mailing address: department of radiology, shohada tajrish hospital, tajrish sq., tehran 1989934148, iran references 1.abul-kasim k, thurnher mm, mckeever p, et al. intradural spinal tumors: current classification and mri features. neuroradiology. 2008;50:301−14. 2.akyurek s, chang el, yu tk, et al. spinal myxopapillary ependymoma outcomes in patients treated with surgery and radiotherapy at m.d. anderson cancer center. j neurooncol. 2006;80:177−83. 3.yuh el, barkovich aj, gupta n. imaging of ependymomas: mri and ct. childs nerv syst. 2009; 25:1203−13. 4.wager m, lapierre f, blanc jl, et al. cauda equina tumors: a french multicenter retrospective review of 231 adult cases and review of the literature. neurosurg rev. 2000;23:119−29. 5.güzin k, bozdağ h, aydın a, et al. uterine cervix metastasis of myxopapillary ependymoma originated from the spinal cord. balkan med j. 2016;33:235−8. 6.duong lm, mccarthy bj, mclendon re, et al. descriptive epidemiology of malignant and nonmalignant primary spinal cord, spinal meninges, and cauda equina tumors, united states, 2004-2007. cancer. 2012;118:4220−7. 7.wippold fj 2nd, smirniotopoulos jg, moran cj, et al. mr imaging of myxopapillary ependymoma: findings and value to determine extent of tumor and its relation to intraspinal structures. ajr am j roentgenol. 1995;165:1263−7. 8.fearnside mr, adams cb. tumours of the cauda equina. j neurol neurosurg psychiatry. 1978;41:24−31. 9.smith jk, lury k, castillo m. imaging of spinal and spinal cord tumors. semin roentgenol. 2006;41:274−93. 10.rege sv, narayan s, patil h, et al. spinal myxopapillary ependymoma with interval drop metastasis presenting as cauda equina syndrome: case report and review of literature. j spine surg. 2016;2:216−21. 11.hayashi t, haba r, kushida y, et al. cytopathologic characteristics and differential diagnostic considerations of osteolytic myxopapillary ependymoma. diagn cytopathol. 2014;42:778−83. 12.cho hy, lee m, takei h, et al. immunohistochemical comparison of chordoma with chondrosarcoma, myxopapillary ependymoma, and chordoid meningioma. appl immunohistochem mol morphol. 2009;17:131−8. 13.ngo tp, dufton j, stern pj, islam o. myxopapillary ependymoma as a cause of back pain in a young male a case report. j can chiropr assoc. 2013;57:150−5. 14.demir mk, yılmaz b, toktaş zo, et al. an unusual cause of low back pain in a young adult: myxopapillary ependymoma of the filum terminale. spine j. 2016;16:e321−2. 15.wein s, gaillard f. intradural spinal tumours and their mimics: a review of radiographic features. postgrad med j. 2013;89:457−69. 16.bavbek m, altinörs mn, caner hh, et al. lumbar myxopapillary ependymoma mimicking neurofibroma. spinal cord. 2001;39:449−52. 17.kim js, choi kc, jung b, lee sh. myxopapillary ependymoma of filum terminale mimicking nerve sheath tumor. kor j spine. 2008;5:95−8. 18.thoriya pj, watal p, bahri nu, rathod k. primary spinal primitive neuroectodermal tumor on mr imaging. indian j radiol imaging. 2015;25:459−63. microsoft word 8.majerc_craniocerebral 438 c. majer, g. iacob cranio-cerebral gunshot wounds cranio-cerebral gunshot wounds c. majer1, g. iacob2 1neurospinal hospital dubai, eau 2neurosurgery clinic, universitary hospital bucharest, romania abstract cranio-cerebral gunshots wounds (ccgw) are the most devastating injuries to the central nervous system, especially made by high velocity bullets, the most devastating, severe and usually fatal type of missile injury to the head. objective: to investigate and compare, using a retrospective study on five cases the clinical outcomes of ccgw. predictors of poor outcome were: older age, delayed mode of transportation, low admission cgs score with haemodynamic instability, ct visualization of diffuse brain damage, bihemispheric, multilobar injuries with lateral and midline sagittal planes trajectories made by penetrating high velocity bullets fired from a very close range, brain stem and ventricular injury with intraventricular and/or subarachnoid hemorrhage, mass effect and midline shift, evidence of herniation and/or hematomas, high icp and/or hypotension, abnormal coagulation states on admission or disseminated intravascular coagulation. less harmful effects were generated by retained missiles, bone fragments with cns infection, dai lesions and neuronal damages associated to cavitation, seizures. material and methods: 5 patients (4 male and 1 female), age ranged 22-65 years, with ccgw, during the period 2004-2009, caused by military conflict and accidental firing. after initial resuscitation all patients were assessed on admission by the glasgow coma scale (gcs). after investigations: xray skull, brain ct, angio-ct, cerebral mri, spect; baseline investigations, neurological, haemodynamic and coagulability status all patients underwent surgical treatment following emergency intervention. the survival, mortality and functional outcome were evaluated by glasgow outcome scale (gos) score. results: referring on five cases we evaluate on a retrospective study the clinical outcome, imagistics, microscopic studies on neuronal and axonal damage generated by temporary cavitation along the cerebral bullet’s track, therapeutics, as the review of the literature. two patients with an admission cgs 9 and 10 survived and three patients with admission cgs score of 3, with severe ventricular, brain stem injuries and lateral plane of high velocity bullets trajectories died despite treatment. conclusion: ccgw is the most devastating type of missile injury to the head. aggressive intensive care management in combination with early management with less aggressive meticulous neurosurgical technique, has significantly reduced the mortality and morbidity associated with these injuries, but they still remain unacceptably high. primary prevention of these injuries remains important, the patient must be monitored closely for possible romanian neurosurgery (2010) xvii 4: 438 – 444 439 complications. keywords: cranio-cerebral gunshot wounds (ccgw), high velocity bullets, neuronal damage, cavitation, dai lesions cranio-cerebral gunshot wounds (ccgw) produce devastating injuries to the central nervous system structures, such as tangential, perforating and penetrating (1) (2) (3), especially by high velocity bullets crossing in the lateral, midline, sagittal (2-6), which are the most severe and usually fatal type of missile injury to the head. material and methods five patients (4 male and 1 female), age ranged 22-65 years, with ccgw, during the period 2004-2009, caused by military conflict and accidental firing, underwent emergency intervention in dubai – 4 cases and romania – 1 case. transportation was initial made by ambulances with low equipment; after resuscitation, assessed by the glasgow coma scale (gcs) all patients were evacuated by plane. assessed on admission by the glasgow coma scale (gcs) two patients has a cgs of 9, respectively 10 and three patients has a cgs score of 3. x-ray skull and ct in bone window demonstrated in all patients bone defects, different fractures types, intact or fragmented missiles, pneumocephalus (fig. 1). cerebral ct scan revealed multilobar injuries made by penetrating high velocity bullets, mass effect and midline shift, evidence of herniation and/or hematomas. brain stem and ventricular injury with intraventricular and subarachnoid hemorrhage were described in two cases, also retained missiles, bone fragments. the lethal wounds were bitemporal, temporooccipital; less aggressive in frontal, parietal wounds without dural venous sinus tears. in two cases were the missile trajectory traverses through the middle cerebral artery, cerebral angiography was performed, to exclude developement of a possible pseudoaneurysm or dural sinus tear. also cerebral mri, spect (figure 1) was performed three weeks after shooting in two survived cases with neuronal damages associated to cavitation, seizures, ischemia, dai lesions. baseline investigations, neurological, haemodynamic and coagulability status were performed in all cases. compatible blood transfusion, treatment of coagulopathy and shock, antibiotics and anticonvulsivant were used; intracranial pressure monitoring was performed in 4 patients placed intraparenchymal cavities created after blood clots evacuation. results all patients underwent surgical treatment including primary closure of the wounds, debridement of skin, hairs, necrotic tissues, removal of hematomas, accessible and visible missiles and bone fragments, haemostasis, duraplasty. no attempts were made to chase any indriven inaccessible bone and missile fragments, in order to avoid additional insult to injured brain. in two cases bullets were intact (20 and 30 mm lenghth, 10 and 14 mm in diameter, 10 and 16 g in weight), but three others deformed, mushroomed and fragmented. therapy with broad spectrum antibiotics, anticonvulsivants, mannitol was started to all patients. three patients with bitemporal, temporo-occipital injury died in the first 48 hours postoperatively despite emergency intervention and surgical treatment by early respiratory arrest. in this 440 c. majer, g. iacob cranio-cerebral gunshot wounds cases brain swelling with midline shift were seen resistent to therapy. for two patients with moderate hemiparesis a rehabilitation program was started. one year after, their medical condition improved, but unable to gain initial activities; continuing anticonvulsivant therapy with depakine for seizures, without another postoperative complications. a forensic neuropathologist reconstruction of brain injuries was made for the three patients who died based on: macroscopic findings reffering on entrance and exit wounds, the missile track and secondary changes corelated to ct reconstruction. microscopic evaluation of the zones of cellular and axonal destruction around the permanent track corresponding to the temporary cavity were performed on three cases. we found that the most dangerous trajectories of high velocity bullets were bitemporal and temporooccipital; also areas of hemorrhagic extravasations surrounding the permanent track, extended about 24-28 mm radially, nerve cells and astrocyte destructions, broken axons into fragments. illustrative case: p.c. aged 25 years old was cranio-cerebral gun shot with high velocity bullets fired by a sniper, in afganistan, on 18.07.2007. the patient developped immediate deep coma and dilated pupils, he was intubated and mechanical ventilated. transferred to dubai on 19.07.2007 at admission he presented: gcs 3, bilateral mydriasis, no reflexes, intubated, mechanical ventilated, with dopamine and cephalosporines infusion. the patient was explored: cerebral ct, cerebral angio ct, spect.; an icp monitoring and a radical debridement of entry point was performed. despite all medical aids he died on 19.07.2007. a postmortem detaliate reconstruction of his brain injuries was performed. a b c d e f g h i romanian neurosurgery (2010) xvii 4: 438 – 444 441 k l m figure 1 a-b cerebral ct scan showing missile in right temporal area; c cerebral ct scan with missile in parieto-occipital area; d ct scan shows the skull fracture underlying cerebral contusion and an intrusive parietal bone fragment, e-g axial cerebral ct scan showing haemorrhagic missile tracks with adiacent small cerebral contusions; h-i temporo-parietal peritentorial bullet on axial and coronal reconstruction cerebral ct scan k-l angio-ct scan 3d shows metallic bullets in both hemispheres, no pseudoaneurysm or dural sinus tear, m spect with severe cerebral ischemia discussions cranio-cerebral gunshot wounds (ccgw) are the most devastating injuries in humans, afecting central nervous system structures, representing a real concern to the community as a whole (1) (2) (6). ccgw could be: penetrating in which a projectile breaches the cranium but does not exit it, made by low-velocity bullets as air rifle, projectiles, nail guns used in construction devices, stun guns used for animal slaughter, shrapnel produced during explosions, but also perforating in which the projectile passes entirely though the head, leaving both entrance and exit wounds, by high-mass and velocity metaljacket bullets fired from military weapons, or guns fired from a very close range as in agression or suicide attempts (2) (3) (6-12) (14). approximately 2 million traumatic brain injuries occur each year and an approximate 50% of all trauma deaths are secondary to traumatic brain injury and gunshot wounds to the head caused 35% of these mortalities (1) (4). the magnitude of this problem in the united states (4) (6-8): 230 milion fire arms in circulation, generating > 700000 injured cases each year, in peaceful time, by firearm-related violence, 24000 deaths, representing the fourth leading cause of death in the united states and the leading cause of death in persons aged 1-44 years. this magnitude is similar with all american losses during vietnam conflict (4); a injury from firearms made the victim of a gunshot wound to the head 35 times more likely to die than is a patient with a comparable nonpenetrating brain injury. cranio-cerebral head injuries (1) (4) (7) are known since 1700 bc in egyptian papyrus reffering to 4 cases of depressed skull fractures treated by anointing the scalp wound with grease, leaving the wound unbandaged, providing free drainage of the intracranial cavity. hippocrates (460-357 bc) performed trephination for contusions, fissure fractures, and skull indentations. galen's experience in 130-210 ad treating wounded gladiators led to recognition of a correlation between the side of injury and the side of motor loss. thought for the centuries incurable, cranio-cerebral head injuries had a high mortality rate: about 76% in homer’s era around 700 bc, 73,9% in the crimean war 442 c. majer, g. iacob cranio-cerebral gunshot wounds and 71,7% in the american civil war (4). in the 17th century, richard wiseman asses that deep wounds had a much worse prognosis than superficial ones, recommended the evacuation of subdural hematomas and the extraction of bone fragments – cited by (4). important advances in the management of craniocerebral injuries in the mid-19th century who dramatically reduced the incidence of local and systemic infections, as well as mortality were related to the work of: louis pasteur (1867), robert koch (1876) in bacteriology and joseph lister (1867) in asepsis (3) (4) (6). using harvey cushing’s measures (1-3) (9-13) since the first world war as: aggressive and meticulously initial debridement all devitalized tissue, removing metal and bone fragments of missile track, exploring the intradural space, watertight closure of dural lacerations was advocated to reduced the rate of infections, abscess formation and the mortality rate dropped from 56% to 28% (9) (13). during world war ii despite ccgw made by high muzzle velocity missiles with very high mass, low-velocity shrapnel wounds, extensive destruction of tissues, the mortality rate was lower: 14% with the advent of antibiotics and 9,7% in vietnam war (1-3) (7-10). ccgw has been changed from one uniquely military to broadly civilian concern in several countries firearms (see irak, yemen a.s.o) considered part of the personality of men, present in hands of most of population and used for many purposes as parties, social conflicts, protecting farms and for entertainments (9). however a higher mortality rate are in military ccgw(1-3) (8) (11) (12) justified especially by differences in wound ballistics. the new military medecine history has noticed a higher mortality rate: 26% iraq-iran war and lebanon war – despite ct scanning, respectively 32% with bullets and 10,6% with shrapnells in the last yugoslav civil war, generated by improvements in weapons technology, especially by the use of snipers (2) (8). after the bullet penetrates the outer and inner tables of the skull, it crosses whole brain structures crushing tissues and a percussion wave is transmitted throughout the brain, causing temporary cavitation, radial tissue displacement, shearing, compression and stretching of cerebral tissue (15). the intracranial effect varies from isolated soft tissue to an "explosive" type of injury with comminuted fractures of the skull or bullet fragments generating laceration of the brain (1) (3) (11), also widespread destruction of neuronal cell membranes, which depends on the physical properties of the projectile, but also by its ballistics (12) (15-18). the enhanced effects of temporary cavitation is generating an enlarged zone of disintegrated tissue, high intracranial pressures expressed morphological by cortical contusion zones, indirect skull fractures and perivascular haemorrhages remote from the tract. varying degrees of cavitation in the brain occur along the bullet’s path, usually several times larger than the diameter of the bullet (1) (3) (5) (17) (18). in addition to the primary destruction of brain tissue readily visible at autopsy (permanent track), gunshot wounding to the brain creates a pulsating temporary cavity due to radial expansion along the bullet's track. surrounding the permanent track, extended about 20 mm radially, a mantle-like zone of astrocyte destruction was found within an area of hemorrhagic extravasation. (18); nerve cells are shrunken; axons had been broken into tiny fragments (19), exhibiting romanian neurosurgery (2010) xvii 4: 438 – 444 443 varicose changes and clumping. the extent of traumatic bleeding could be remarked along the track from entry point to exit point by the temporary cavitation a destruction zone of ca. 3.6 cm around the permanent track, loss of glial fibrillary acid protein expression by astrocytes in the white matter. (17) (18) after ccgw frequently seen effects are: neurodeficits, brain swelling with icp rise, csf leaks with severe infections, caroticocavernous fistulas, pseudoaneurysms correlated with morbidity and mortality (3)(9-12). many ccgw are incompatible with life, but moderately injured patients more frequently are resuscitated and benefit from aggressive treatment of secondary mechanisms of injury. there is considerable variability among neurosurgeons currently as to what constitutes appropriate treatment of ccgw (3) (4) (10): raimondi and samuelson (1970) noted the difference in wound ballistics and offered a classification scheme based on initial neurologic assessment. arendall and meirowsky 1983 found that high mortality associated with penetrating wound of air sinuses can be reduced by prompt and radical debridment, kaufman (14) appreciate the surgical debridement performed, the use of icp monitoring and various medical therapies, helling et all 1992 found that early surgical intervention seemed to result in better survival, gonul 1997, singh 2003 acute or delayed csf leak highly correlated with intracranial infection (9) (12) antibiotics are no substitute for early surgical debridment, a lower mortality rate reflects early triage and survivability decisions as much as treatment effectiveness (3) (13) ccgw treatment comprised of four stages: immediate saving of life by the use of various medical therapies, icp monitoring, prevention of infection, preservation of the nervous tissue, restoration of anatomical structures, with radical debridement (4) (9). duration of antiepileptics and antibiotics remains controversial, as does the use of hyperventilation, hypothermia, and steroids (9) (12). use of jugular bulb catheters and transcranial doppler is institutiondependent (9). there are several predictors of poor outcome in ccgw, correlating with morbidity and mortality (1-6) (8-15): advanced age, high velocity missiles or handguns fired from a very close range as in suicide attempts, admission cgs score 3 and 4 (with mortality rates near 90% and rare satisfactory outcome), bilateral fixed dilated pupils with opac cornea, delayed and poor mode of transportation, apnea at admission, associated injuries to chest, abdomen and great vessels generating massive bleeding, haemodynamic instability (hypotension), postoperative rise in icp, abnormal coagulation states on admission or even dic, ct visualization of diffuse brain damage, bihemispheric, bitentorial, multilobar missile track with lateral > midline sagittal planes trajectories made by high velocity bullets fired from a very close range, brain stem and ventricular injury, ventricular and subarahnoid haemorrhage, vasospasm, mass effect and midline shift, evidence of herniation and/or hematomas greater than 15 ml. less harmful effects are generated by retained missiles, bone and hair intraparenchymal fragments with cns infection, dai lesions, pneumocephalus, and neuronal damages associated to cavitation, seizures (3) (9) (10) (13). 444 c. majer, g. iacob cranio-cerebral gunshot wounds conclusions aggressive intensive care management in combination with early management with less aggressive, meticulous, neurosurgical technique, when appropriate, already has significantly reduced the mortality and morbidity associated with these injuries, but they still remain unacceptably high . primary prevention of cranio-cerebral gunshot wounds remains important, the patient must be monitored closely for possible complications. with the increasing numbers of firearms and firearm-related violence in our society, discussing the issues of violence with patients and offering appropriate intervention becomes the duty of all health care providers. references 1. federico c vinas penetrating head trauma: multimedia, may 27, 2009 2. antic b., spaic m. – penetrating craniocerebral injuries from the former yugoslavia battlefields, ind. j. neurotrauma (ijnt), 2006, 3, 27-30 3. iacob m., iacob g. – plagi craniocerebrale prin arma de foc, simpozionul de neurochirurgie cluj napoca 1987 4. shaffrey m.e. et al. classification of civilian craniocerebral gunshot wounds: a multivariate analysis predictive of mortality, j neurotrauma. 1992 mar; 9, suppl 1:s279-85. 5. izci y., kayali h.,daneyemez m., koksel t. – comparison of clinical outcomes between anteroposterior and lateral penetrating craniocerebral gunshot wounds, emerg. med. j. 2005, 22, 409-410 6. rosenfeld j.v. – gunshot injury to the head and spine, j. clin. neurosci 2002, 9, 9-16 7. marshall l.f., marshall s.b., sean g.m. – modern neurotraumatology: a brief historical review, in youmans neurological surgery, editor: winn h.r., 5th edition saunders, 2004, 5019-5024 8. spaic m., branislav a. – the lost race, indian journal of neurotrauma 2009, 6, 1, 1-4 9. rashid b.a et al. – analysis of 3794 civilian craniocerebral missile injuries – results from 20 years of kashmir conflict, pan arab journal of neurosurgery, 2010, 14,1, 24-32. 10. meirowsky a.m. – secondary removal of retained bone fragments in missile wounds of the brain, j.neurosurg. 1982, 57, 617-621 11. bakir a. et al. – high velocity gunshot wounds to the head: analysis of 135 patients, neurol. med. chir (tokyo) 2005, 45, 281-287 12. erdogan e., gonul e., seber n. – craniocerebral gunshot wounds, neurosurg q. 2002, 12, 1-18 13. gonul e., baysefer a., kahraman s. et al. – causes of infections and management results in penetrating craniocerebral injuries, neurosurg. rev. 1997, 20, 177181 14. kaufman h.h. – civilian gunshot wounds to the head, neurosurg. 1993, 32, 962-964 15. karger b. – penetrating gunshots to the head and lack of immediate incapacitation, wound ballistics and mechanisms of incapacitation, int. j. legal med. 1995, 108,(2), 53-61 16. kim k.a., wang m.y., mcnatt s.a. et al. vector analysis correlating bullet trajectory to outcome after civilian through-and-through gunshot wound to the head: using imaging cues to predict fatal outcome, neurosurgery, 2005: 737-747 17. oehmichen m., meissner c., konig h.g., gehl h. r. – gunshot injuries to the head and brain caused by low velocity handguns and rifles; a. review, forensic science international, congrès european congress of neuropathology no7, helsinki, finlande, 2004, vol. 146, nr.2-3, 111-120. 18. oehmichen m., meissner c., konig h.g. – brain injury after gunshot wounding: morphometric analysis of cell destruction caused by temporary cavitation, journal of neurotrauma. 2000, 17(2): 155162. 19. francisc a., majer c., iacob g. – diffuse axonal injuries: clinical, neuroimaging and microscopic featuresliterature review, romanian journal of legal medicine, 2008, xvi, 3, 172-180 doi: 10.33962/roneuro-2021-064 letter to the editor. face-off between glioma and meningioma dinesh chouksey, nitisha goyal, rishu garg, ajoy sodani romanian neurosurgery (2021) xxxv (3): pp. 376-377 doi: 10.33962/roneuro-2021-064 www.journals.lapub.co.uk/index.php/roneurosurgery letter to the editor. face-off between glioma and meningioma dinesh chouksey, nitisha goyal, rishu garg, ajoy sodani department of neurology, samc and pgi, indore, india abstract gliomas are malignant, and intrinsic cerebral tumours may cause tumour-infiltrative oedema. meningiomas are mostly benign, extrinsic cerebral tumours that do not infiltrate the surrounding parenchyma. meningiomas may give rise to vasogenic oedema in the peritumoral tissue.[1] the radiological diagnosis of cerebral tumours may be non-conclusive on conventional mri in few cases, and diagnosis must rely on histopathological analysis. [2] we report a case that has an atypical clinical presentation with nonconclusive mri brain, and finally, histopathology confirmed the diagnosis. case a 56-year-old male patient presented with a nine months history of progressively increasing urinary frequency and urgency. the patient was seen by a urologist, and he operated for benign prostate hypertrophy, but his symptoms were not relieved. then, he referred to a neurologist for further evaluation. after being admitted to the hospital, a detailed history and clinical examination were made. higher mental function examination showed decreased attentiveness, vigilance, problem-solving and defect in motor programming with usual insight, judgment, language functions, and memory. neurological examination showed bilateral grade iii papilledema, right spastic hemiparesis (mrc grade 4/5), and the right plantar response was extensor. mri brain was suggestive of a large sol with the solid cystic component is noted in the left frontal lobe, size 6.6x4.8x5.6 cm with flow voids of vessels within the lesion. there is significant surrounding oedema with a midline shift of 1.8 cm towards the right side with uncal herniation. post-contrast sequences show moderate enhancement of solid component and wall enhancement in the cystic part. thin enhancement is noted along the overlying dura in the left frontal lobe. spectroscopic sequences show increased choline-creatine ratios in solid component of the lesion ranging from 2 to 4, suggestive of the neoplastic lesion. radiological features that raise the possibility of glioma are significant perilesional oedema, hypervascularity of the tumour, difficulty to localise (intra versus extra-axial), multilobulated keywords angiomatous meningioma, meningioma mimicking glioma, meningioma versus glioma, glioblastoma mri, meningioma mri corresponding author: dinesh chouksey department of neurology, samc and pgi, indore, india dineshmd09@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 377 glioma versus meningioma looks aggressive in nature, heterogeneous enhancement and spectroscopy findings. the patient was operated on, doing well and histopathology report suggestive of angiomatous meningioma. figure 1. 1(a) t2 shows a hyperintense lesion with flow void signals of vessels inside the solid component (white arrow); 1(b) t1shows iso to hypointense lesion; 1(c) flair shows csf cleft sign (black arrowhead) and significant perilesional oedema; 1(d) t1 contrast shows homogenous solid component enhancement with dural tail sign (black arrow); 1(e) t1 contrast shows cystic peripheral enhancement; 1(f) diffusion shows mild restriction. discussion meningiomas are the commonest and around 2030% of the primary tumour of the brain. however, angiomatous meningioma (am) are very rare tumours.[3] the mri characteristics features of am are t1 iso to hypointense and t2 hyperintense with solid cystic components with significant perilesional oedema and flow void signals of vessels with homogenous enhancement commonly and dural tail sign. the higher brain oedema thought to be due to increased capillary permeability due to hypervascularity and vascular endothelial growth factor (vegf) secretion.[4] the most typical site is cerebral convexity, and it is relatively more common in males and has a good prognosis.[4,5] there are few cases reported where glioblastoma can mimic meningioma on mri with the dural tail sign (thickening and enhancement of the adjacent dura), csf cleft sign (a perimeter of csf between the tumour and brain parenchyma), and broad dural contact. moreover, cerebral angiography can reveal tumour feeders commonly associated with meningioma.[6] am is a highly vascular more than 50% vascular component, rare benign tumour with distinct radiological features.[7] to conclude, good clinical history and examination is the gold standard to localise the lesion and to avoid unnecessary iatrogenic burden to a patient and focused radiological examination will give a near accurate diagnosis. references 1. ide m, jimbo m, kubo o, yamamoto m, imanaga h. peritumoral brain edema associated with meningioma-histological study of the tumor margin and surrounding brain. neurol med chir (tokyo). 1992; 32:65–71. [pubmed: 1376862] 2. kondziolka d, lunsford l, martinez a. unreliability of contemporary neurodiagnostic imaging in evaluating suspected adult supratentorial (low-grade) astrocytoma. j neurosurg. 1993; 79:533–6. [pubmed: 8410222] 3. riemenschneider mj, perry a, reifenberger g. histological classifica¬tion and molecular genetics of meningiomas. lancet neurol 2006;5: 1045-54. 4. liu z, wang c, wang h, wang y, li jy, liu y. clinical characteristics and treatment of angiomatous meningiomas: a report of 27 cases. int j clin exp pathol 2013;6:695-702. 5. hwang j, kong ds, seol hj, nam dh, lee ji, choi jw. clinical and radiological characteristics of angiomatous meningiomas. brain tumor res treat. 2016;4(2):94‐99. doi:10.14791/btrt.2016.4.2.94 6. patel m, nguyen hs, doan n, gelsomino m, shabani s, mueller w. glioblastoma mimicking meningioma: report of 2 cases. world neurosurg. 2016;95:624.e9‐624.e13. doi:10.1016/j.wneu.2016.08.048 7. hua l, luan s, li h, et al. angiomatous meningiomas have a very benign outcome despite frequent peritumoral edema at onset. world neurosurg. 2017;108:465‐473. doi:10.1016/j.wneu.2017.08.096. microsoft word _editorpage romanian neurosurgery editor’s page august 2010 st.m. iencean, editor clinical emergency hospital “prof. dr. nicolae oblu” iasi, romania e-mail: mirceasteffan@yahoo.com dear romanian neurosurgery reader, i would like to announce that our national scientific journal, romanian neurosurgery is classified by national council for scientific research in higher education (cncsis) in the b+ category for 2010. like previous issues of our journal, this issue begins with a historical paper, this time on professor nicolae oblu who was the creator of the neurosurgical school in iasi: in 1946 he became resident physician and in 1951 he became the head of the neurosurgical department in iasi. he managed to form a team of neurosurgeons in iasi and thanks to his perseverance and results, the neurosurgical school in iasi is renowned and appreciated in the national and european context. there are three articles about aubarachnoid hemorrhage, cerebral vasospasm and treatment of intracranial aneurysm (subarachnoid hemorrhage of yoko kato and hirotoshi sano; cerebral vasospasm theoretical remarks of p. courtheoux and beatrice sillard; multimodal treatment of intracranial aneurysm of a.chiriac, i. poeata et al) in which the authors present the basic data and the latest news about these subjects. cerebral vasospasm theoretical remarks / vasospasme remarques théorétiques, article of professors p. courtheoux and beatrice sillard is written and published in french with an english abstract, which shows the opening of our journal to the widest possible international cooperation. in the next four articles the authors presents some important subjects: medulloblastoma – an overview of a.v. ciurea and cl. palade; large and giant vestibular schwannomas of g. iacob and m. craciun; controlling the increased intracranial pressure – a neurointensivist’s point of view of gh. dorobăţ and prophylactic antibiotherapy in neurosurgery of g. iacob and simona iacob. three original articles and three case presentations complete this issue. article about posterior fossa meningiomas of dumitrescu, indrei et al. shows the correlation between the site of of tumor origin and pathological characteristics of each subgroup of the posterior fossa meningiomas. the authors identified significant associations: the cerebellar convexity meningiomas presented a female to male ratios of 4:1 and the cerebellopontine angle meningiomas presented a strong preponderance of female patients (5:1). a modern technique that can help the surgical results in lumbar disc herniation is demonstrated in a paper by tacu, ianovici et al., who show the normalization of gait temporospatial parameters after lumbar disc surgery: the normalization of gait is observed in patients with intraforaminal herniation, followed by patients with paracentral disc herniation and the gait is difficult to normalize in patients with extensive lumbar disc herniation. interesting data related to anesthesia by electro acupuncture in neurosurgery are given by gheorghita et al on a group of 12 patients (10 brain surgery and 2 herniated disc surgery). there are three very interesting case reports: use of intraoperative ultrasonography in lowgrade gliomas (pasca, florian and magyoros), a giant asymptomatic intracranial hydatid cyst in a 3 years old child (tascu, ciurea et al) and a case of combined mechanism glaucoma asociated with grave's ophtalmopathy (costin et al). editorial office hope you enjoy reading these articles. romanian neurosurgery (2010), xvii, 3, 253 romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article non-communicating extradural arachnoid cyst: a rare case report with review of literature asheesh kumar gupta, anand sharma, avdhesh shukla, s.n. iyengar india doi: 10.2478/romneu-2018-0019 156 | kumar et al extradural arachnoid cyst doi: 10.2478/romneu-2018-0019 non-communicating extradural arachnoid cyst: a rare case report with review of literature asheesh kumar gupta, anand sharma, avdhesh shukla, s.n. iyengar department of neurosurgery, g.r. medical college gwalior, india abstract: extradural arachnoid cysts in the spine are uncommon causes of spinal cord compression in the paediatric population that are thought to arise from congenital defects in the duramater. in most literatures it is describe that such cysts communicating with the intrathecal subarachnoid space through a small defect in the dura. in this case report we describe a case of a child who presented with spinal cord compression caused by a large spinal extradural arachnoid cyst that did not communicate with the intradural subarachnoid space. an 9 year-old girl presented with progressive lower-extremity weakness, myelopathy, and severe gait ataxia. magnetic resonance imaging of the spine demonstrated a large extradural arachnoid cyst extending from t4 to t9. the patient underwent a thoracic laminectomy for en bloc resection of the spinal extradural arachnoid cyst. intra-operatively, the dura was intact and there was no evidence of communication into the intradural subarachnoid space. postoperatively, the patient’s motor strength and ambulation improved immediately, and no subsequent cerebrospinal fluid leak occurred. key words: eac (extradural arachnoid cysts), csf (cerebro spinal fluid) introduction extradural arachnoid cyst is a rare entity accounting for 1% of all spinal tumors (1). pathogenesis remains unclear and thought to be congenital or develop secondary to infection or trauma. in nearly all cases of eac, communication of csf between the cyst and the intrathecal subarachnoid space through a dural defect has been reported. in this report we present the case of a 9 year-old female with a symptomatic extradural spinal arachnoid cyst of dorsal spine treated successfully by surgery. this case is unique because there was no dural defect or fistulous communication into the intradural subarachnoid space. case report a 9 year old female presented with history of back pain followed by difficulties in walking. neurological examination revealed spasmodic paraparesis. on neurological examination, she had 4/5 strength in all muscle groups of lower limb. proprioception and romanian neurosurgery (2018) xxxii 1: 156 159 | 157 vibratory sensation were diminished in both legs. her reflexes were hyperactive and her gait was severely ataxic. she had no cutaneous stigmata of neurological disease. muscle tone at the lower extremities was increased. mri spine showed a large extradural cyst located posterior to the cord from t4 to t9 with dorsal compression and flattening of thecal sac. the mass was hypointense on t1-weight imaging, was hyperintense on t2 weight weighted imaging, and suppressed signal intensity on fluid-attenuated inversion recovery imaging. the signaling patterns were consistent with csf suggestive of a spinal extradural arachnoid cyst. no obvious communications between the cyst and the intrathecal subarachnoid space were detected on neuroimaging. management after discussion of risks and benefits, patient underwent t4 to t9 laminectomy; lamina overlying the cyst was thinned. a large extradural cyst resembling an arachnoid cyst was identified, with a thick but translucent wall. the cyst was easily dissected from the exterior surface of the thecal sac. the dura mater was inspected and there was no evidence of a dural defect, arachnoid pedicle, or fistulous communication into intradural sub arachnoid space. histopathological finding were consistent with arachnoid cyst. the patient's motor function improved to full strength and she was ambulating well. csf leak did not develop, and he was discharged on the 10th postoperative day. figure 1mri spine saggital and axial view with t1 and t2 sequences showing extradural arachnoid cyst compressing dural tube 158 | kumar et al extradural arachnoid cyst figure 2 showing excised extradural arachnid cyst discussion nabors et al. (2) described a classification system of spinal arachnoid cysts divided into three major categories: extradural cysts without spinal nerve root fibers (type i); extradural cysts with spinal nerve root fibers (type ii); and intradural cysts (type iii). type i is further divided into extradural arachnoid cysts (type ia) and sacral meningoceles (type ib). in nearly all cases of type ia cysts, communication of csf between the cyst and the intrathecal subarachnoid space through a dural defect has been reported. our case represents the type ia variant. the exact origin and pathogenesis of type ia spinal extradural arachnoid cysts remain unknown. it is an out-pouching herniation of arachnoid membrane through a dural defect that may communicate to intradural subarachnoid space (3). the etiology of this herniation is still unclear and can be either congenital or acquired. (4) in 1934, elsberg, et al.(5), attributed the origin of these cysts to either congenital diverticula of the dura or herniation of arachnoid membrane through a congenital dural defect. congenital dural defects appear most commonly at the dural sleeve of the nerve root or at the junction of the sleeve and the thecal sac; they derive less commonly from the dorsal midline of the thecal sac. although less common, spinal arachnoid cysts have been associated with arachnoiditis, surgery, and trauma, leading others to suggest that these cysts arise from acquired dural defects (6). spiegelmann, et al.(7), reported a case in which hemosiderin-containing macrophages found in the cyst wall in a patient with a spinal extradural arachnoid cyst caused spastic paraparesis 10 years after craniospinal injury suggesting acquired etiology for seac. mechanisms of growth for these cysts are not well known. it may be pulsatile csf dynamics, ball-flap mechanism or osmotic gradient (8). according to the theory of mccrum and williams, (9) intermittent surges of pressure in the subarachnoid space are communicated to the cyst and flow occurs into the pouch. when pressure falls again, egress of fluid is impeded by compression of the cyst pedicle. according to the laplace law, the body of the cyst exerts a force on the neck sufficient to close the communication, because its radius and wall tension are greater. this mechanism then allows further enlargement, with persistent csf pulsations. bone erosion of the spinal canal may imply the presence of a valve mechanism that is responsible for producing forces of csf pressure within the romanian neurosurgery (2018) xxxii 1: 156 159 | 159 cyst that are greater than normal hydrostatic forces (10). our case is unusual in that there was no detectable dural defect or communication with the intradural subarachnoid space. we postulate that the noncommunicating cyst evolved from a preexisting communicating cyst that initially formed as a result of a small dural defect secondary to spinal trauma. over time, the cyst enlarged and eventually obliterated the communicating channel to the subarachnoid space because of the laplace law (1). the closure of the dural defect may be due to the proliferation of arachnoid cells. computerised tomography myelography is the diagnostic study of choice to demonstrate the communication of the cyst with the subarachnoid space (1) however, this study was not performed in our case. correspondence dr. asheesh kumar gupta m.ch. resident department of neurosurgery g.r. medical college gwalior. addressroom no. 39 senior boys hostel g.r. medical college gwalior mobile no.7828832632 emailasheesh_gsvm@yahoo.com references 1. liu jk, cole cd, sherr gt, kestle jr, walker ml. noncommunicating spinal extradural arachnoid cyst causing spinal cord compression in a child. j neurosurg. 2005 sep; 103:266-9. 2. naborsmw, paittg, byrdeb, karimno, davisdo, kobrine ai, et al: updated assessment and current classification of spinal meningeal cysts. j neurosurg 68:366–377, 1988. 3. kim k, chun sw, chung sg : a case of symptomatic cervical perineural (tarlov) cyst: clinical manifestation and management. skeletal radiol 41 : 97-101, 2012. 4. lee ch, hyun sj, kim kj, jahng ta, kim hj : what is a reasonable surgical procedure for spinal extradural arachnoid cysts : is cyst removal mandatory? eight consecutive cases and a review of the literature. acta neurochir (wien) 154 : 1219-1227, 2012. 5. elsberg ca, dyke cg, brewer ed: the symptoms and diagnosis of extradural cysts. bull neurol inst ny 3:395– 417, 1934. 6. rohrer dc, burchiel kj, gruber dp: intraspinal extradural meningeal cyst demonstrating ball-valve mechanism of formation. case report. j neurosurg 78:122–125, 1993. 7. spiegelmann r, rappaport zh, sahar a: spinal arachnoid cyst with unusual presentation. case report. j neurosurg 60:613–616, 1984. 8. cilluffojm, gomezmr, reesedf, onofriobm, millerrh:idiopathic (“congenital”) spinal arachnoid diverticula. clinical diagnosis and surgical results. mayo clin proc 56:93–101, 1981. 9. mccrum c, williams b: spinal extradural arachnoid pouches. report of two cases. j neurosurg 57:849–852, 1982. 10.naborsmw, paittg, byrdeb, karimno, davisdo, kobrine ai, et al: updated assessment and current classification of spinal meningeal cysts. j neurosurg 68:366–377, 1988. 19 19kumarguptaasheesh_non-communicating doi: 10.33962/roneuro-2021-013 outcomes of surgical treatment for pituitary metastasis dmytro s. teslenko, mykola o. guk, olga yu. chuvashova romanian neurosurgery (2021) xxxv (1): pp. 80-84 doi: 10.33962/roneuro-2021-013 www.journals.lapub.co.uk/index.php/roneurosurgery outcomes of surgical treatment for pituitary metastasis dmytro s. teslenko1, mykola o. guk2, olga yu. chuvashova3 1 department of neuroendoscopy and craniofacial surgery, si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine 2 department of transsphenoidal neurosurgery, si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine 3 department of neuroradiology and radioneurosurgery, si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine abstract we analyzed the outcomes of surgical treatment for pituitary metastasis (pm) based on 35 observations. we registered the best estimates of resection radicalism in patients with minor pm, its inconsiderable spread ascending and descending from the diaphragm of the sella turcica, slightly bleeding metastasis, and no invading to the cavernous sinus. positive changes in the pm patients’ quality of life are chiefly associated with regressed visual impairment, local pain syndrome, and, to a lesser degree, oculomotor disorders. no post-operative regress or intensifying of hormonal impairments, such as diabetes insipidus and hypopituitarism, were seen. the age of patients, the time interval between the cancer diagnosis and the pm occurrence, control of the underlying disease, size of the tumour are the factors determining the life expectancy in pm patients. introduction metastatic pituitary lesion (hereinafter as pm pituitary metastasis) is a very rare condition of the central nervous system (cns), with its frequency reported by various authors ranging from 0.14 to 20% among all metastatic invasions to the brain. [1-3; 5;8-14]. no way all pm cases require surgical intervention, as the majority of pm diagnosed at autopsy [2;4;6-8;] this evidence is associated with the commonly asymptomatic course: symptomatic pm incidence reaches only 7%. the largest actual studies concerning pm demonstrate heterogeneous and ambiguous treatment outcomes for the patients with this disease. [13;6; 8-14] authors, though, state impossible to prolong the overall survival due to surgical intervention, concluding this based on the results of treatment of a significant number of patients having undergone surgery for pm. the number of observed patients operated on in these series ranges from 36 to 88 cases. [1;5;8] in this study, we attempted to clarify what post-operative outcomes are expected for pm surgery. keywords pituitary metastasis, pituitary carcinoma, surgical treatment, outcomes, survival, skull base, surgery corresponding author: dmytro s. teslenko , si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine tesldim@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 81 outcomes of surgical treatment for pituitary metastasis the purpose of the study is to improve the surgical tactics in pm via analyzing surgical treatment outcomes for the patients with this condition. material and method the work is based on the analysis of surgical outcomes of 35 pm patients treated and monitored at the si «romodanov neurosurgery institute» nams of ukraine, kyiv, ukraine from 2005 to 2015. the pm diagnosis was confirmed histologically in all 35 patients. the study included 17 males (47.9%) and 18 females (52.1%). the mean age of the enrolled individuals was 56.4 ± 10.4 years: 60.8 ± 2.4 years for men, 52.2 ± 2.1 years for women. all 35 patients evidenced the symptomatic course of the disease. among these 35 patients, the most common primary tumor was lung cancer (34.3%), then in descending order, breast cancer (22.9%), renal (8.6%), rectal, prostate (all of 5.7%). diagnostic patterns for pm included clinical and laboratory, neuroimaging evaluations, and examinations of the related specialists (oncologist, ophthalmologist, endocrinologist, therapist). 27 of 35 patients (77.2%) underwent microscopic pm removal. the observations were classified by type of approach, specifically, 7 (20.0%) patients were performed pm transcranial removal, and 20 (57.2%) transsphenoidal surgery. all cases of pm transcranial removal were performed from the subfrontal approach. in 8 patients (22.8%) the removal was carried out by the endoscopic technique. while the statistical analysis of the obtained material, the mann-whitney u test was applied to independent samples, and the wilcoxon signed-rank test to dependent samples to evaluate the probability of differences. statistical correlation of parameters was estimated by the spearman rank correlation test. the kaplan–meier method was applied to patient survival estimation. the cox proportional hazard regression analysis was used to assess the prognosis. results and discussion according to intraoperative findings and the results of post-operative tomographic control, total removal of pm took place in 7 patients (20.0%), subtotal in 17 (48.6%), partial in 9 (25.7%), a biopsy was done in 2 patients (5.7%). the most surgical radicalism was achieved in the patients who were operated on by transnasal endoscopic approach (4 cases). the lowest rates of total resection were registered in the group of patients who underwent microscopic transsphenoidal removal (2 observations). the distribution of pm patients by type and radicalism of the performed surgery is presented in figure 1. figure 1. observations distributed by the intervention radicalism and resection technique. the pairwise correlation method used for assessment of correlation between different factors and radicalism of operative intervention for pm showed an impact of the size of the metastasis, its spread, bleeding of tumor tissue, cavernous sinus lesions (all correlations significant at p <0.05). the best levels of radicalism were seen in smaller sizes, inconsiderable ascending and descending spread from the diaphragm of the sella turcica, slightly bleeding metastasis, and no invading to the cavernous sinus. the significance of these factors impact model in the ordinal regression analysis was p = 0.001 (χ2= 82.9). visual disorders of varying severity were registered in 29 of 35 patients (82.9%). in most patients, visual disorders were the main, and often the only, manifestation of the disease. the request to improve vision or at least stabilize current visual impairments was the main goal of surgical treatment for a considerable number of patients. among 6 (17.1%) of our patients with normal visual acuity and field of vision, no negative post-operative changes of visual functions were detected in any case. if the visual disorders were present primarily, the vision improvement was achieved in 79.3% cases (23 patients). deterioration of vision was registered in 2 patients (6.9%), no changes were observed in 33 patients (13.8%). the paired t-test performed for comparison of two dependent samples (preand post-operative patients) showed the statistical significance of improvement of the visual disorders 1 2 43 12 23 6 0 2 0 5 10 15 transcranial intervention transsphenoidal endoscopic total subtotal partial biopsy 82 dmytro s. teslenko, mykola o. guk, olga yu. chuvashova in our patients undergone operation t = 5.2 at p = 0.000. among 18 patients with initial oculomotor disorders, post-operative improvement occurred in 9 cases (50.0%); no dynamics was seen in 6 patients (33.3%), deterioration occurred in 3 cases (16.7%). in 4 (23.5%) of 17 patients with no pre-operative oculomotor problems, post-operative oculomotor disorders appeared. among 7 patients who developed or augmented oculomotor disorders after surgery, 2 cases of an isolated failure of sixth cranial nerves, 4 cases of third cranial nerves failure, and 1 case of combined lesions of third and sixth cranial nerves were observed. occurrence/deterioration of oculomotor functions in the study group after the endoscopic approach was equal to 14.7% of the total number of patients, and after microsurgical transsphenoidal and transcranial removal, these complications were registered more commonly, in 57.1% and 28.6% of cases, respectively. the obtained results are statistically significant (p = 0.041). among those 4 patients who evidenced pre-operative dysfunction of trigeminal nerve branch, 2 individuals showed improvement (50%) due to decreased numbness in the area of the nerve innervation, 2 patients (50%) demonstrated no changes after surgery. in the postoperative period, trigeminal nerve failure appeared in 2 patients on the side of the tumor invasion into the cavernous sinus cavity. postoperatively, 14 patients with pre-operative hypopituitary disorders demonstrated no change in the severity of the pituitary failure. deterioration of endocrine status, which was associated with the appeared hypothyroidism and hypocorticism, was observed in 3 patients. in the post-operative period, diabetes insipidus occurred in 4 patients who were not affected previously. in 20 patients with preoperative evidence of diabetes insipidus, no changes of this symptom were seen. the results which we obtained prove that endoscopic pm removal leads to a statistically significantly lower rate of endocrine disorders, including the development of diabetes insipidus, compared to microsurgical techniques (p <0.05). onset or increase of hypopituitary disorders was also statistically significantly more common at microsurgical removal of pm (p <0.05). among 6 patients operated on for pm, with the karnofsky performance scale index of the quality of life > 80 in the early post-operative period, no worsening was registered in 5 patients, and in 1 individual the quality of life deteriorated. among 19 patients with the karnofsky performance scale index of the quality of life equal to 70-80 in the early post-operative period, the condition did not worsen in 12 patients, in 7 the quality of life improved. among the 10 patients with the karnofsky performance scale index of the quality of life <70 in the early post-operative period, the condition did not change in 7 patients, in 3 the quality of life improved. the paired t-test comparison of two dependent samples (preand post-operative patients) showed the statistical significance of improving the quality of life of our operated patients (t = -3.01 at p = 0.005). figure 2. overall survival of the patients operated on for pm (kaplan-meier). all 35 observations were assessed with the cox proportional hazards model regression analysis considering the available information on age, sex, the interval between diagnosis of the primary tumor and pm occurrence, the status of the primary lesion, pm maximum diameter, presence of other intracranial lesions, chemotherapy and/or radiation therapy. our mathematical model was significant, p = 0.003 (χ2 = 15.9). the following independent factors were associated with a better prognosis in pm patients (relative risk <1, p <0.05): younger age; female sex; late-onset pituitary metastasis; the smaller size of pm; radiation therapy underwent; control of the primary site condition. sex of patients and the clinical group of medical examination 83 outcomes of surgical treatment for pituitary metastasis considered as the factors with the most pronounced predictive properties in our patients. the average survival time in females was much longer than in males (31.6 ± 3.4 months compared to 15.8 ± 3.0 months, respectively). the average survival time in the patients of the cancer clinical group iv was statistically significantly shorter than in patients of groups ii and iii (7.3 ± 0.5 months compared to 27.3 ± 3.8 and 32.3 ± 4.3 months, respectively) (figure 3b). a. b. figure 3. survival curves of patients with pm (kaplan-meier): a. general survival curves obtained for different gender (male – blue line/female – green line) groups of patients; b. general survival curves obtained for patients of different clinical groups (1st clinical group blue line, 2d clinical group green line, 3rd clinical group – yellow line). thus, the analyzed treatment results of pm patients showed that the attempt to achieve an increased overall survival in pm patients compared to the available literature data failed. [ ] this result of the study indicates that the life expectancy in cancer patients with pm is primarily determined by the control of the underlying disease. in general, the life expectancy of pm patients was determined by the age of patients, the interval between the time of diagnosis of cancer and the occurrence of pm, control of the underlying disease, size of the tumor. the individual tailoring principle should be followed when determining the indications to the surgical intervention for pm. if the tactics, technique of the surgical intervention, and the volume of removal are relevant, the quality of life in pm patients can be improved significantly. the dynamics of clinical manifestations in pm patients is more demonstrative in the long-term post-operative observations, that is associated either with a protracted recovery of neural structures of the sellar area after surgery, or the results of rehabilitation measures, as well. positive dynamics of the quality of life in pm patients is first and foremost associated with the regression of visual disturbances, local pain, and to a lesser extent oculomotor disorders. there is no postoperative regress or intensification of hormonal disorders, such as diabetes insipidus and hypopituitarism. the prognosis for pm patients is poor, but it not attributable to the location, but due to the developing subsequent stages of primary cancer. we know that only 4 patients died of progressing pituitary lesions. the short but definite survival time of pm cancer patients requires a change in the management strategy for these patients at all stages: from diagnosing to terminal care to ensure the long-term quality of life. in this context, we justify rationally in certain situations surgery and pituitary dysfunction treatment, including administration of gonadotropin, cortisol, thyroxine, which is rarely carried out in the complex management of patients with this condition. conclusions 1. the main indications for surgery for pm are present visual disorders, oculomotor impairments, pain syndrome caused by affected optic nerves and 84 dmytro s. teslenko, mykola o. guk, olga yu. chuvashova cavernous sinus, and no verified cancer diagnosis in the presence of clinical manifestations of the disease. these factors influence the choice of approach and methods of pm removal. 2. the radicalism of pm removal is determined by the size of the tumor, bleeding tumor tissue, metastatic invasion to the cavernous sinus, use of endoscopic technologies. 3. the best results of surgical treatment for pm can be achieved in younger patients, individuals with the controlled underlying oncological condition, with good pre-operative neurological status and quality of life, in those undergone radical removals of the tumor. references 1. carey rm, kuan ec, workman ad, patel nn, kohanski ma, tong ccl, chen j, palmer jn, adappa nd, brant ja. a population-level analysis of pituitary carcinoma from the national cancer database. j neurol surg b skull base. 2020 apr;81(2):180-186. doi: 10.1055/s-0039-1683435. epub 2019 mar 15. pmid: 32206537; pmcid: pmc7082172. 2. kaltsas ga, nomikos p, kontogeorgos g, buchfelder m, grossman ab. clinical review: diagnosis and management of pituitary carcinomas. j clin endocrinol metab. 2005 may;90(5):3089-99. doi: 10.1210/jc.20042231. epub 2005 mar 1. pmid: 15741248. 3. raverot g, burman p, mccormack a, heaney a, petersenn s, popovic v, trouillas j, dekkers om; european society of endocrinology. european society of endocrinology clinical practice guidelines for the management of aggressive pituitary tumours and carcinomas. eur j endocrinol. 2018 jan;178(1):g1-g24. doi: 10.1530/eje-17-0796. epub 2017 oct 18. pmid: 29046323. 4. ragel bt, couldwell wt. pituitary carcinoma: a review of the literature. neurosurg focus. 2004 apr 15;16(4):e7. doi: 10.3171/foc.2004.16.4.8. pmid: 15191336. 5. hansen tm, batra s, lim m, gallia gl, burger pc, salvatori r, wand g, quinones-hinojosa a, kleinberg l, redmond kj. invasive adenoma and pituitary carcinoma: a seer database analysis. neurosurg rev. 2014 apr;37(2):27985; discussion 285-6. doi: 10.1007/s10143-014-0525-y. epub 2014 feb 14. pmid: 24526366; pmcid: pmc4322934. 6. heaney ap. clinical review: pituitary carcinoma: difficult diagnosis and treatment [published correction appears in j clin endocrinol metab. 2012 mar;97(3):1064]. j clin endocrinol metab. 2011;96(12):3649-3660. doi:10.1210/jc.2011-2031 7. bengtsson d, schrøder hd, andersen m, maiter d, berinder k, feldt rasmussen u, rasmussen åk, johannsson g, hoybye c, van der lely aj, petersson m, ragnarsson o, burman p. long-term outcome and mgmt as a predictive marker in 24 patients with atypical pituitary adenomas and pituitary carcinomas given treatment with temozolomide. j clin endocrinol metab. 2015 apr;100(4):1689-98. doi: 10.1210/jc.2014-4350. epub 2015 feb 3. pmid: 25646794. 8. in h, bilimoria ky, stewart ak, wroblewski ke, posner mc, talamonti ms, winchester dp. cancer recurrence: an important but missing variable in national cancer registries. ann surg oncol. 2014 may;21(5):1520-9. doi: 10.1245/s10434-014-3516-x. epub 2014 feb 7. pmid: 24504926. 9. fassett dr, couldwell wt. metastases to the pituitary gland. neurosurg focus. 2004 apr 15;16(4):e8. pmid: 15191337. 10. goulart cr, upadhyay s, ditzel filho lfs, beer-furlan a, carrau rl, prevedello lm, prevedello dm. newly diagnosed sellar tumors in patients with cancer: a diagnostic challenge and management dilemma. world neurosurg. 2017 oct;106:254-265. doi: 10.1016/j.wneu.2017.06.139. epub 2017 jun 30. pmid: 28673886. 11. zoli m, mazzatenta d, faustini-fustini m, pasquini e, frank g. pituitary metastases: role of surgery. world neurosurg. 2013 feb;79(2):327-30. doi: 10.1016/j.wneu.2012.03.018. epub 2012 apr 2. pmid: 22480977. 12. post kd. pituitary metastases: what is the role of surgery? world neurosurg. 2013 feb;79(2):251-2. doi: 10.1016/j.wneu.2012.05.006. epub 2012 may 24. pmid: 22634465. 13. ariel d, sung h, coghlan n, dodd r, gibbs ic, katznelson l. clinical characteristics and pituitary dysfunction in patients with metastatic cancer to the sella. endocr pract. 2013 nov-dec;19(6):914-9. doi: 10.4158/ep12407.or. pmid: 23757610. 14. popławska-kita a, wielogórska m, poplawski ł, siewko k, adamska a, szumowski p, myśliwiec p, myśliwiec j, reszeć j, kamiński g, dzięcioł j, tobiaszewska d, szelachowska m, krętowski aj. thyroid carcinoma with atypical metastasis to the pituitary gland and unexpected postmortal diagnosis. endocrinol diabetes metab case rep. 2020 mar 13;2020:19-0148. doi: 10.1530/edm-190148. epub ahead of print. pmid: 32168468; pmcid: pmc7077587. romanian neurosurgery (2019) xxxiii (2): pp. 122-126 doi: 10.33962/roneuro-2019-024 www.journals.lapub.co.uk/index.php/roneurosurgery new technologies for low-grade glioma surgery nicolae-ștefan bogaciu1,3, daniel teleanu1,2,3, a.v. ciurea2,3 1 university emergency hospital, bucharest, romania 2 sanador clinical centre hospital, bucharest, romania 3 “carol davila” university of medicine and pharmacy, bucharest, romania abstract brain surgery has come far from the primitive methods used thousands of years ago. in the last hundred years alone, we have come across countless breakthroughs like the invention of bipolar coagulation, the surgical microscope, microsurgical techniques and a large variety of surgical instruments. the latest years have brought us neuro-navigation, intra-operative imaging techniques and brain activity monitoring. low-grade glioma surgery, in particular, has taken advantage a lot from all these new methods, bringing great benefits for the patients: the safe extent of resection has grown progressively and tumours located in eloquent areas that were thought until recently to be inoperable, have started to be removed in safe conditions. the purpose of this paper is to present these new technologies as a recap for neurosurgical professionals. introduction endovascular brain surgery is one of the oldest procedures to ever be performed on a human being. beginning as trephining, it has known a long period of slow development, only to become one of the top-edge sciences of modern time. it developed from somewhat barbaric procedures with little if any supporting scientific knowledge, to lifesaving procedures performed on a macroscopic scale, to microscopic interventions with progressively smaller „collateral damage” and in the future it might turn into something we would call „molecular surgery”. the purpose of this paper is to highlight the technologies we nowadays use in low-grade glioma surgery, presenting their pearls and pitfalls, benefits and uses. materials computer assisted neuro-navigation. the purpose of this tool in brain surgery is to integrate imaging studies obtained preoperatively with intra-op anatomy in order to localize more accurately the lesions subdue to surgery (picture 1). a neuro-navigation system has the following main parts: a computer-station with built-in software, a a receiver and trackers/pointers (picture 2). keywords intraoperative, imaging, neuro-navigation, low-grade glioma, brain monitoring corresponding author: nicolae-ștefan bogaciu university emergency hospital, bucharest, romania bnicolaestefan@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 123 new technologies for low-grade glioma surgery picture 1 picture 2 the initial step is to upload the preoperative images in the computer. patient is positioned and a patienttracker is placed in the proximity of the patient’s head. landmark registration is performed and checked for accuracy and surgery can commence. intra-operatively, the surgeon may navigate with different tools: pointers, microscope, standard neuro-navigated instruments (aspirator, ultrasonic aspirator, retractors etc.). some systems allow injection of images directly into the microscope for compatible devices (picture 3). picture 3 neuro-navigation is not only useful for accurately localizing a lesion, but also for localizing vasculature and other normal anatomical structures that need to be avoided in glioma surgery. image series used for neuro-navigation can be fused for better describing the anatomy and functionality of different brain areas: tractography, pet, mri, ct, contrast-enhanced imagery etc. the advantages of using neuronavigation in lgg (low-grade glioma) surgery consist of, but are not limited to: smaller scalp incisions, cranial flaps, dural incisions and corticotomies, safer dissection and tumour excision, reduced surgery time. all these imply fewer post-operative complications from surgery, faster discharge, lower costs for patient care. the main disadvantage of neuronavigation systems is that the position of the patient 124 nicolae-ștefan bogaciu, daniel teleanu, a.v. ciurea when obtaining images and the position of the patient during surgery are almost never the same so the brain will have a shift during surgery compared to imaging. another thing is that after beginning the excision of tumoral tissue, the landscape changes, but the images stay the same. some solutions were developed for these problems. other imaging studies may be performed intraoperatively to complete the preoperative study and to increase the accuracy of the neuro-navigation system. intraoperative mri is a known tool which performs the task well, but it is highly inconvenient. its more readily available counterpart is intraoperative ultrasound. tips for successfully removing tumours using neuro-navigation include: removing tumour tissue closer to eloquent areas first, when accuracy is better, performing en-bloc excisions as much as possible, avoiding cysts especially when they are large, until good accuracy is no longer an issue, „rebuilding” volume by placing cottonoids in resulting cavities. in spite of all issues, a surgeon will always find this tool useful and he will always have in mind the fact that he can never rely on solely this in performing his tasks.1,2,3,4 (picture 4). intra-operative ultrasound. ultrasonography (us) is a great mean of obtaining fast, cheap real-time images during brain surgery. images are usually obtained by using a probe of 4-8 mhz which is sufficient for acquiring images in a 2-6 cm distance from it. there are a few ways to use this tool: regular gray-scale brightness mode (b-mode), contrast enhanced ultrasound (ceus), elastosonography. us is of aid in all stages of brain tumour surgery, from the opening of the dura up to the resection of peripheral extensions of the tumour. as opposed to cortical lesions, subcortical lesions are more difficult to identify, and the site of the corticotomy may be tricky to choose. by using us, the surgeon can identify the subcortical tumour and choose an entry site as found suitable. during resection, the surgeon may use us to identify the depth and extent of the tumour and adapt the aggressivity of his resection accordingly. in the final stages of the surgery, one may use us for identifying residual tumoral tissue in the periphery of the mass. not only us may be used for identifying the tumour, but also to characterize it. it can deliver information about the consistency of the tumour. for example, the surgeon may use this information to adapt the power of an ultrasonic aspirator, or to differentiate between low-grade glioma (lgg) and high-grade glioma (hgg): lgg are firmer than hgg (as assessed by elastosonography). ceus brings even more information about the vascularization of the tumour, by real-time angiosonography so that the surgeon may adapt his resection strategy and have even more information about the possible histological diagnosis (lgg are poorly vascularized as opposed to hgg). a common use for intraoperative us in brain surgery is enhancing accuracy of neuro-navigation systems by updating the pre-operative acquired images used for registration and navigation, with real-time images provided by intra-operative us. by doing so, the effects of brain shift and selling may be partly counteracted.1,4–8 intraoperative ct. although it is less preferred by neurosurgeons compared to other imagistic tools, intraoperative ct-scans may be found useful in glioma surgery. as the other intraoperative imaging studies (us, mri), it allows a greater extent of surgical resection by providing real-time intra-operative information regarding tumour mass, as well as updating pre-operative neuro-navigation planning. we may consider some advantages regarding the cost (relatively low compared to intraoperative mri), speed of the procedure and general benefits such as improving accuracy and extent of the resection.9,10 125 new technologies for low-grade glioma surgery intraoperative mri (iomri). intraoperative magnetic resonance imaging is the preferred intraoperative imaging method for low-grade glioma surgery. it is also the most laborious, the most expensive, but more importantly the most accurate. iomri comes in two shapes: low field (≤0,5 tesla) and high field (≥1,5 tesla). regardless of the power of the magnet, iomri aids the surgeon in extending tumour resection in both enhancing and non-enhancing lesions, with greater benefit in the latter. the use of intraoperative mri associates with higher extent of resection which implies longer overall survival and free of symptoms survival in patients with gliomas. setting up an operating room with an mri device can get pretty challenging. although there are tools that can be used within the area closest to the device (an area limited by the 5-gauss border, which is a line beyond which ferromagnetic instruments can be used), most instruments used for microsurgical resection, including microscope and ultrasonic aspirator, have to be used further away from the magnet. residual tumour is observed with high fidelity on images acquired from intraoperative mri and can be readily excised if feasible. the whole range of sequences can be studied: functional, connective or pathological areas can be identified. newly acquired images are integrated into navigation systems making surgeon orientation precise.3,11–13 intraoperative brain mapping and awake craniotomy. although neuroimaging techniques have a great contribution to identifying functional cerebral structures and their relationship to tumor masses, intraoperative brain mapping is the gold standard for establishing tumour surgical strategy for each individual case, especially in the case of low grade glioma (lgg) where it is commonly accepted that the extent of resection (eor) is linked to increase in survival. intraoperative electric stimulation is performed by using a bipolar probe with an electric intensity starting from 2ma, with increments of 1ma up to 6 ma in patients operated with local anaesthesia and up to 16 ma in patients operated with general anaesthesia. during the procedure, when a certain area of the brain is stimulated, it will produce a neurological disturbance which returns to normal after stimulation is stopped. thereby the interested function is noted and the neurosurgeon can make a surgical decision of stopping the resection. areas which when stimulated do not generate a disturbance are considered safe for continuing resection. lgg are slow-growing and rarely present with major neurological deficits, so the benefit of intraoperative brain mapping is large in lgg surgery because you need to preserve functionality for the patient. even more, tumour mass resection is considered to be linked to postoperative seizure control so the possibility of safely increasing the eor with this procedure increases the chance of good seizure control. intraoperative brain mapping even offers the opportunity for safe tumour resection in eloquent areas otherwise considered inoperable. an important factor that contributes to this fact is brain plasticity. brain plasticity also offers the opportunity for re-intervention in lgg of eloquent areas where initial total resection could not be performed, but timing of such a re-intervention must be carefully planned in order not to be too late and face anaplastic transformation.10,14–16 conclusions low-grade glioma is a challenging pathology in the field of neurosurgery due to its infiltrative nature, especially when concerning eloquent areas of the brain. safe resection of such lesions can be performed using a variety of instruments and procedures, but better results can be obtained by combining them. the goal is obtaining an increased extent of resection which is beneficial for the patient, improving survival and quality of life. references 1. khoshnevisan a, allahabadi ns. neuronavigation: principles, clinical applications and potential pitfalls. iran j psychiatry. 2012;7(2):97-103. https://www.ncbi.nlm.nih.gov /pubmed/22952553. 2. ricciardi l, della pepa gm, izzo a, et al. use of neuronavigation system for superficial vein identification: safe and quick method to avoid intraoperative bleeding and vein closure: technical note. world neurosurg. 2018;117:92-96. doi:10.1016/j.wneu.2018.06.018 3. lu c-y, chen x-l, chen x-l, fang x-j, zhao y-l. clinical application of 3.0 t intraoperative magnetic resonance combined with multimodal neuronavigation in resection of cerebral eloquent area glioma. medicine (baltimore). 2018;97(34):e11702. doi:10.1097/md.0000000000011702 4. unsgaard g, ommedal s, muller t, gronningsaeter a, nagelhus hernes ta. neuronavigation by intraoperative three-dimensional ultrasound: initial experience during brain tumor resection. neurosurgery. 2002;50(4):804-12; discussion 812. 126 nicolae-ștefan bogaciu, daniel teleanu, a.v. ciurea 5. pino ma, imperato a, musca i, et al. new hope in brain glioma surgery: the role of intraoperative ultrasound. a review. brain sci. 2018;8(11). doi:10.3390/brainsci8110202 6. del bene m, perin a, casali c, et al. advanced ultrasound imaging in glioma surgery: beyond gray-scale b-mode. front oncol. 2018;8:576. doi:10.3389/fonc.2018.00576 7. prada f, del bene m, rampini a, et al. intraoperative strain elastosonography in brain tumor surgery. oper neurosurg (hagerstown, md). november 2018. doi:10.1093/ons /opy323 8. altieri r, melcarne a, di perna g, et al. intra-operative ultrasound: tips and tricks for making the most in neurosurgery. surg technol int. 2018;33:353-360. 9. coburger j, nabavi a, konig r, wirtz cr, pala a. contemporary use of intraoperative imaging in glioma surgery: a survey among eans members. clin neurol neurosurg. 2017;163:133-141. doi:10.1016/j.clineuro.2017. 10.033 10. barbagallo gm v, morrone a, certo f. intraoperative computed tomography and awake craniotomy: a useful and safe combination in brain surgery. world neurosurg. 2018;119:e159-e166. doi:10.1016/j.wneu.2018.07.078 11. arya n, stark am, lutz d, mehdorn hm. surgical navigation with intraoperative imaging: special operating room concepts. in: quiñones-hinojosa a, ed. schmidek & sweet operative neurosurgical techniques: indications, methods, and results. 6th ed. philadelphia pa: elsevier/saunders; 2012:14-20. 12. whiting bb, lee bs, mahadev v, et al. combined use of minimal access craniotomy, intraoperative magnetic resonance imaging, and awake functional mapping for the resection of gliomas in 61 patients. j neurosurg. january 2019:1-9. doi:10.3171/2018.9.jns181802 13. mohammadi am, sullivan tb, barnett gh, et al. use of highfield intraoperative magnetic resonance imaging to enhance the extent of resection of enhancing and nonenhancing gliomas. neurosurgery. 2014;74(4):339-350. doi:10.1227/neu.0000000000000278 14. gravesteijn by, keizer me, vincent ajpe, schouten jw, stolker rj, klimek m. awake craniotomy versus craniotomy under general anesthesia for the surgical treatment of insular glioma: choices and outcomes. neurol res. 2018;40(2):87-96. doi:10.1080/01616412.2017.1402147 15. frati a, pesce a, palmieri m, et al. hypnosis-aided awake surgery for the management of intrinsic brain tumors versus standard awake-asleep-awake protocol: a preliminary, promising experience. world neurosurg. 2019;121:e882-e891. doi:10.1016/j.wneu.2018.10.004 16. duffau h. cortical and subcortical brain mapping. in: quiñones-hinojosa a, ed. schmidek & sweet operative neurosurgical techniques: indications, methods, and results. 6th ed. philadelphia pa: elsevier/saunders; 2012:80-92. microsoft word _editorpage.doc romanian neurosurgery editor’s page may 2010 st.m. iencean, editor clinical emergency hospital “prof. dr. nicolae oblu” iasi, romania e-mail: mirceasteffan@yahoo.com dear romanian neurosurgery reader, for starters i would like to announce that romanian neurosurgery is classified by national council for scientific research in higher education (cncsis), in the c category and the cncsis accreditation automatically ensure acceptance by the romanian college of physicians of our journal. the articles published in our medical journal will receive 25 credits per each article according to criteria and rules for credit forms of continuing medical education of romanian college of physicians. the previous issue of our journal started the presentation of neurosurgical personalities who contributed to the development of romanian neurosurgery. this issue begins with a paper of ciurea and palade who present the professor thoma ionescu and his numerous contributions in the field of surgical arts and his significant contributions to neurosurgery: the surgery of cervical sympathetic chain, his personal approach for decompresive hemicraniectomies; also he was the promotor of spinal anesthesia with his famous cervical and thoracic spinal puncture for spinal anesthesia. the journal continues with a historical overview about the development of military neurosurgery and of the personality of general md phd iacob gr. mircea and his contributions as pioneer of military romanian neurosurgery . in this issue, a very comprehensive review by the team of professor zhengsong huang from sun yat-sen university, china on neuroform stent-assisted coil embolization presents this procedure and their experience to treat 39 cerebral aneurysms. the neuroform microdelivery stent system is designed to prevent the rupture of an intracranial aneurysm. this system is for use with embolic coils for the treatment of wide neck intracranial aneurysms that cannot be treated by surgical clipping. adam, pevzner and gepstein’s review on the nucleoplasty presents this treatment of discogenic leg pain using bipolar radiofrequency device for vaporising a volume of nucleus pulposus. other interesting topics here are: the second part of the endoscopic endonasal transsphenoidal approach for sellar and parasellar lesions by tataranu, gorgan et al.; a presentation of embolic materials for cerebral endovascular therapy by chiriac, poeata et al.; an analysis of the results of neuronavigation-guided percutaneous radiofrequency thermocoagulation in the treatment of trigeminal neuralgia by ivanov et al.; and a therapeutical imagistic correlation regarding intracerebellar hematomas by albert et al. there are several very interesting case reports: a giant hyperostosis secondary to neglected pott’s puffy tumour and its surgical repair (florian et al.), a non-traumatic spontaneous rhinorrhea generated by a giant atypical meningioma of left posterior fossa (iacob et al.), the radiographic features of a posttraumatic occlusion of the vertebral artery (tudorache, haba et al.), surgical management for a giant extracranial liposarcoma (pruna, gorgan et al.) and a presentation of two cases of bone marrow tissue implant into cervical spinal cord injury. we are convinced you will find all of them interesting and we hope you enjoy this issue of romanian neurosurgery, and welcome your continued help to publish four issues this year. romanian neurosurgery (2010), xvii, 2, 135 microsoft word _7.formatate_selected_abstracts.doc romanian neurosurgery vol. xvi nr. 2 39 selected abstracts from annual national conference of the romanian society of neurosurgery with international participation, 2009 september 29th october 3rd, sibiu, romania challenging reconstructive neurosurgery – 2009 declaration beijing of international association of neuroresotratology (ianr) klaus von wild1 on behalf of the international ianr faculty 1professor of neurosurgery at medical faculty university of münster, and professor of neurorehabilitation and reengineering of brain and spinal cord lesions, ini, hannover, germany objectives reconstructive neurosurgery plays an ever more important part in multidisciplinary neurorehabilitation of impaired higher cortical functioning. up to now medical treatment failed to replace damaged central nervous system (cns) plasticity. this is especially true for severe traumatic brain injuries (tbi), stroke, and a number of degenerative and infectious lesions, when cortical and subcortical structures are disturbed and the connecting fibres of the cns network are disrupted that provide the miraculous functional communication which has been called the social system by the great neuroscientist a. luria. methods intensive experimental studies on neuroregeneration, neurorepair, neuroplasticity, neurotrophicity, neuromodulation, neurorehabilitation aim at neuroprotection and neural repair to enable the damaged cells to survive functionally, to regain or to substitute disturbed motor and or mental-cognitive and neurobehavioral functioning. results the human brain is the one we least know how to repair. its injuries have terrible consequences. now a days due to a better insight and understanding of the underlying physiological and pathological mechanism of brain and neuron damage as demonstrated in various animal experiments new strategies appear on the horizon. the beijing declaration of international association of neurorestoratology (ianr) that was adopted by the 2nd ianr annual conference general assembly, beijing, china, april 26, 2009, was proposed by a number of international researcher and clinicians where i took part too. these instructions should serve as a code for future research and clinical application of neurorestoratology and will be explained by the author on behalf of presidium of the international association to the audience. discussion without ethical controls and external scientific audit of the clinical results that were achieved a number of doctors and so called institutions for neural repair offer worldwide human somatic cell therapies and gen therapies for central nervous system diseases and other surgical interventions for neuromodulation in the internet where the evidence has not yet been demonstrated regarding selected abstracts romanian neurosurgery vol. xvi nr. 2 40 effectiveness and efficiency. this is especially true for severe spinal cord injury and tbi. conclusion the mission of the international society for neurorestoratology is to bring together all the different strands of investigation which aim to repair the brain, nerves and spinal cord, to control the quality of research and clinical application, and to provide the platform for collegial discussions and exchange while respecting the world’s multicultural ethics and statements of religious beliefs. neurorestoratology aims to encourage persistence and cooperation in these many tentative and fragile beginnings of experimental and clinical research, as one has to confess that all attempts are still experimental at present time. mental recovery and social reintegration following severe brain damage. the neurosurgeons impact on early neurosurgical rehabilitation outcome klaus von wild1, birgit kemper2 1professor of neurosurgery medical faculty university münster, former head clinic for neurosurgery and department for early rehabilitation, clemenshospital münster, and professor of neurorehabilitation and reengineering of brain and spinal cord lesions, ini, hannover, germany 2head neuropsiologist, department of neurosurgical early rehabilitation (ern), clemenshospital objectives the number of patients with permanent brain damage is growing as the results of the increased survival rate from such common conditions as severe head injury. incomplete recovery of brain functions has far-reaching consequences because it often produces some degree of mental disability; this calls for a different degree of adjustment than does the need to cope with most physical disabilities. “brain damage has become synonymous with loss of skills, while the rehabilitation of brain-damaged individuals has become known as a method to restructure lives within a social context” quotes the great danish neurophysiologist a-l. christensen,1986. method neurorehabilitation has been established in germany as in other european and non european countries over the last two decades. early neurological and neurosurgical rehabilitation (enr) play a major role within the ongoing chain of holistic rehabilitation that aims at the patient’s reintegration into social life after brain damage. neurorehabilitation is a multidisciplinary challenge. results our multidisciplinary aim of enr is to avoid or to minimize long lasting disability (who) by focussing on brain plasticity and brain protection after acute and secondary insults to higher cortical functioning. in following the outcome of our patients after early neurosurgical rehabilitation at the academic clemenshospital special needs for an adequate neuropsychological long-term treatment became obvious to reach the final target of individuals social reintegration as to be demonstrated by selected typical case reports. discussion in following the pioneering work of c.f. goldstein in the beginning and a.r. luria’s epoch-making neuropsychological social concept of the working brain in the fifties and sixties we were able to introduce major parts for restoration of the brain’s complex impaired functioning after brain trauma according to luria’s legacy in the early nineties of the last century( see anne-lise christensen et al,eds, oxford publishers 2009). enr needs a team approach. neuropsychology selected abstracts romanian neurosurgery vol. xvi nr. 2 41 has a leader role in diagnostics and face to face restoration of impaired higher cortical functions. music therapy became another important adjunct. however, practically mental-cognitive and neurobehavioral impairments are not jet taken into consideration as they should be. but, as described by a. r. luria (1902 1977), activity of the central nervous system has to be considered as a social organ with a coordinated and adaptable cooperation between various segments of the nervous system, and as a result of which constant results are always yielded under varying conditions. take home message: next of kin have to become partners of the therapeutic team to understand and to translate the rehabilitative interventions into the patients to help humanizing the victim’s human skills within the culturalsocial context. mood disorders (coping with grief and loss) are common consequences following tbi. mental-cognitive deficits need early consideration and carefully assessment during enr as the might frustrate a holistic approach in neuropsychological early and long-term rehabilitation. psychotherapy might be indicated in some cases. development of theoretically driven clinical research should be open for different kinds of psychotherapeutic interventions regarding cognitive, behavioural, psychodynamic and mindfulness approaches. cell therapy in spinal cord injury st.m. iencean1, prof. n. ianovici2, prof. a.v. ciurea3 1neurosurgery, “prof dr nicolae oblu” hospital, iasi, romania 2clinical emergency hospital “prof dr nicolae oblu” iasi, the university of medicine and pharmacy “gr t popa”, iasi, romania 3clinical emergency hospital “bagdasar – arseni” bucharest, the university of medicine and pharmacy “carol davila”, bucharest, romania spinal cord injury is a major medical problem worldwide. spinal cord injuries can lead to paraplegia or quadriplegia and have devastating consequences for victims and families. during the spinal cord injury there is a complete or an incomplete section; therefore there is a disrupted spinal cord or some types of contusion, compression, penetration or laceration of the spinal cord appear. spinal cord injury culminates in glial scarring, a multifactorial process that involves reactive astrocytes, microglia and macrophages, fibroblasts and schwann cells. after spinal cord injury there has two types of lesions : complete disruption spinal cord or different types of scars. the scar of the spinal cord can be: a complete and impenetrable glial scar on the site of spinal cord injury, an incomplete scar and a post-traumatic syringomyelia or a post-traumatic cysts on the site of spinal cord injury, a filiform connective scar of the two segments of damaged spinal cord. the glial scar, which is rich in growth inhibitors, including chondroitin sulfate proteoglycan (cspg), is a major impediment to axonal regeneration following injury. the inability to repair spinal cord damage is attributed to several factors : • the presence of inhibitory substances in the tissue that surrounds the lesion, • changes inside adult nerve fibres that make them unable to respond well to growth-inducing signals that are effective in embryonic fibres, • the formation of cysts into the injury site and growing fibres cannot cross, • the lack of nerve growth factors in the injury site, • the formation of scar tissue at the injury site with additional inhibitory substances. selected abstracts romanian neurosurgery vol. xvi nr. 2 42 therefore any treatment must solve the above difficult problems. an efficient treatment in spinal cord lesions must combine more main approaches: minimising the initial damage and protecting surviving neurons neuroprotection, removing barriers : after the injury the scar tissue gradually fills the damaged area and it is an impenetrable barrier and it does not allow regenerating nerve fibres to pass through. blocking factors which inhibit neural regeneration, modulation of inflammatory response following spinal cord injury, preventing inhibition of regrowth, tissue engineering : biocompatible materials can form a bridge across the damaged region, stimulating and guiding – neurotrophic factors, replacing damaged cells – stem cells therapy, correctly reconnect the damaged neural circuits inside and outside the spinal cord there are no fully restorative treatments for spinal cord injury, but various rehabilitative therapies have been tested in animal models to improve functional outcomes after spinal cord injury. the stem cells based therapies are tryed to repair or replace tissues or cells damaged by injuries or diseases and to treat serious chronic diseases, such as spinal cord injuries. three therapeutic concepts are currently being envisaged: 1.transplantation of differentiated cells derived from stem cells. the source for the specific differentiated cell types could be embryonic or somatic stem cells including the patient’s own stem cells. 2. direct administration of stem cells directly to the patient; the stem cells will differentiate into the desired cell type. 3. stimulation of endogenous stem cells, induced by stimulating an individual’s own population of stem cells by administrating growth factors. stem cells are feasible candidates for cell therapy of spinal cord injury. bone marrow cells are the subject of extensive interest because of their stem cell like characteristics and pluripotency. there are more data supporting beneficial effects of bone marrow cells in sci : 1. bone marrow contains multipotent adult progenitor cells that produce a variety of cell types, including neuroectodermal, mesodermal and endodermal cell types. 2. bone marrow cell transplants improve function recovery and differentiate into astrocytes, oligodendroglia and neural presursors in animal experiments. 3. bone marrow cell transplants facilitate remyelination of the spinal cord, appear to be neuroprotective and also promote regeneration in injured animal spinal cords. (7, 8, 9, 10) substances that limit secondary injury processes and promote repair and regeneration of the injured spinal cord such as monosialotetrahexosylganglioside (gm-1), 4-aminopyridine (4-ap), [a potassium-channel blocking agent], brain derived neurotrophic factor (bdnf) and glial-derived neurotrophic factor (gdnf), also inhibitors of nogo (neurite outgrowth inhibitor) and mag (myelin-associated glycoprotein), have been studied. also transplanted tissues and cells, such as blood macrophages, bone marrow transplant with gm-csf, olfactory ensheathing cells, fetal tissues, stem or progenitor cells, appear to produce neurological improvements. in pathological conditions eg.spinal cord injury, the neurotrophins promote survival and rescue nerve cells from death and promote neurite extension, neuronal survival and differentiation. in spinal cord injury, the neurotrophins are capable to enhance axonal regeneration and reduce paraplegia. bunge in 2008 showed that the most efficacious strategy for the acute complete transection of spinal cord was a combination selected abstracts romanian neurosurgery vol. xvi nr. 2 43 of implantation of schwann cells, plus neuroprotective agents and growth factors administered in various ways, olfactory ensheathing cell (oec) implantation and chondroitinase administration. ratan and noble in 2009 concluded that combinations of interventions were needed to surmount the multiple barriers to recovery in spinal cord injury recovery, knoller et al ( 2005) and park et al (2005) in small studies noted sensory improvements to sci patients who underwent autologous bone marrow cell transplantation (bmt) in conjunction with granulocyte macrophage-colony stimulating factor (gm-csf). we present a preliminary study of the autologous bone marrow tissue implant into the lesioned spinal cord at seven complete sci patients and the promising results, but much follow-up work is needed to document long-term benefits. microsurgical results in treatment of small avm with a review of alternative treatment modalities (radiosurgery and embolization) johannes schramm, azize boström, carlo schaller university medical center, department of neurosurgery, bonn, germany this paper addresses the question of treatment results for cerebral avm with special regard for smaller sized avms which could theoretically be treated by the three modalities radiosurgery, embolization, or microsurgery. the presentation reviews the own microsurgical series (n=255) and puts own results into perspective with other microsurgical series. it then focuses on own results for small avms (n=130) and the literature. then embolization series are reviewed. key results are that total obliteration is usually described in the range between 5 and 15% with only 2 exceptional series describing obliteration rates over 40%. side effects are bleeding rates between 4 and 13%, associated morbidities between 4 and 17%, and mortality rates between 1 and 12%, usually around 23%. even more recent results for onyx describe total obliteration rates of only 16-20% with re-bleeding rates between 4 and 6%, new deficit rates between 5 and 24%, and mortality rates again around 2-3%. in the next section many radiosurgical series are summarized: obliteration rates vary between 55 and 79%, in some series for special subgroups around 8792%. it has to be noted that the follow-up time has slowly crept up from two years to four or five years for maximum results. due to this long time re-bleeding rates of 4% to 12% are described. mortality rates vary between 0.6 and 13% but usually are around 2-3%. delayed problems after long term follow-up include cyst formation which starts to develop after five years but may develop as late as from the 11th year. it should be noted that the combination of various treatment modalities implies that the risk of each treatment modality is added on top of the other. palliative treatment was not found to be very effective instead leading to higher re-bleeding rates, mortalities, and major deficits. in a number of analyses the cost effectiveness and economic side of radiosurgery use was analyzed and usually microsurgery was found to be more economical and more effective. finally the question of when and how to intervene and which treatment modality to use under which circumstances will be summarized. the conclusions are that all three treatment modalities are needed. for small avms microsurgery has the highest exclusion rate with less mortality and a comparable rate of complications of all three modalities. there is a place for radiosurgery but only in small avms if an experienced vascular neurosurgeon does not want to operate. selected abstracts romanian neurosurgery vol. xvi nr. 2 44 the use of embolization as a routine presurgical adjunct can not be encouraged at the present time for spetzler-martin grade i-iii. the main application of embolization is transformation of a high risk larger avm into a lower risk operable one. multimodal treatment (microsurgical approach, embolization, gamma knife surgery) in intracranial arteriovenous malformation experience of 194 cases prof. av. ciurea1, md, phd, a. tascu2, m. baltsavias5, a. chefneaux3, f. stoica2, r.e. rizea1, c. palade1, carmen radoslav4 1neurosurgical department, 2gamma-knife division, 3neuroradiological department, 4nicu department, clinic hospital “bagdasar-arseni” bucharest, românia, 5interbalcanic centrum, neuroradiology, tesaloniki, greece keywords: arteriovenous malformation (avm), intracerebral hemorrhage, seizures, ctscan, mr, mra, dsa, spetzler-martin grading system, microsurgery, gks, embolization, outcome, gos introduction avm represents 1/10 of cerebral aneurysms in usa, which count 1/100.000/year cases. the overall annual risk of hemorrhage is 2-4%. important risk factors for avm hemorrhage are: history of a prior bleed; deep location; deep venous drainage; increasing patient age; diffuse avm morphology; one draining vein. material and method authors present 194 consecutive cases of avms: 80 operated, 94 treated with gamma-knife surgery (gks) and 20 cases treated by embolisation, in the 1st neurosurgical department of the “bagdasar-arseni” hospital, bucahrest, in the period of time between 2000-2008 (9 years). the including criteria were: avms, admission, investigation, treatment, follow-up, complex multidisciplinary management in the i-st neurosurgical clinic. all this cases receive at first intention: microsurgical approach, gks or embolization. there are a cohort of cases 32, in which the authors done a multiple therapeutical option (eg. embolization or surgery followed by gks, or embolization followed by surgery). the excluded criteria were: avms treated in other services, galen vein malformations and avm grade vi. these represent 194/6258 cases of mass lesions (3.1%) admitted in this period of time. there were 88 females (45.4%) and 106 males (54.6%) aged between 0 55 years with mean age of 21.9 years. the most affected group was 11-20 years: 68 cases (35%). all the cases followed the same protocol for clinical and neuroimagistic diagnosis (ctscan, mr, mra, dsa). three methods of treatment were performed in these 194 cases: microsurgical approach, gks, embolization and 32 cases combined procedures. the localization of avms was: superficial supratentorial 142 cases (73.1%), deep supratentorial 28 cases (14.4%), brainstem 1 case (0.5%) and cerebellum 23 cases (11.8%). the clinical onset by hemorrhage was present in 161 cases (83%), seizures in 29 cases (15.1%), headache/progressive nonhemorrhagic neurological deficit 19 cases (9.8%). the clinical features was dominated by headache in 166 cases (85.7%), followed by motor deficit in 62 cases (32.1%), seizures 64 cases (33%), neck stiffness 45 cases (23.2 %) and vomiting in 28 cases (14.4 %). the distribution in basis of the spetzler-martin grading system (1986) was: grade i 48 cases (24.7%), grade ii 59 cases (30.5%), grade iii 50 cases (25.7%), grade iv 29 cases (14.9%) and grade v 8 cases (4.1%). the multimodal treatment was adapted in connection with avms, sizes and location, patient condition and age. selected abstracts romanian neurosurgery vol. xvi nr. 2 45 results the postoperative complications were: recurrent hemorrhage 9/80 cases (11.2%) and obstructive hydrocephalus in 11/80 cases (13.7%) in which the v-p shunt was inserted. important complications after the gk therapy were related in this series: 2 cerebral ischemic stroke, 1 intranidal avm haemorhage, 1 malignant brain swelling, 1 focal neurological deficit. other usual complication: diffusse headache, seizures, dizziness. in the cohort of avms embolization (20 cases) the important complications were: intraparenchimal haematoma (1 case), new neurological deficit (3 cases), cranial nerves paresis transitor or permanent (6 cases). the neurological evaluation at 6 months for the whole series showed: focal neurological deficit 42/194 cases (21.4%), seizures 50/194 cases (25,8%), cognitive deficits 47/194 cases (24.1%), mental disturbances 29/194 cases (15.1 %), visual disturbances 31/194 cases (16%) and obstructive hydrocephalus 23/194 cases (11.6%). the global outcome assessment by gos at 6 months for 194 avms cases: good recovery 81 cases (41,8%), moderate disability 92 cases (47.4%), severe disability 16 cases (8,2%), persistent vegetative state 2 case (1%) and death 3 cases (1.5%). conclusions generally intracerebral hemorrhage is the initial symptom in avms. for many years the microsurgery represent the best treatment in gr. ii–iii avms. actually, the gks open a new minimal invasive therapeutic perspective (grade i-iii). the large avms (grade iv–v) and avms in functional areas requires a multimodal treatment: stadial embolization, microsurgical excision and gks, if it is necessary. neuroimaging and microsurgical management of brainstem cavernomas prof. m. tatagiba dept. of neurosurgery, university hospital tuebingen, germany objective brainstem cavernomas are benign vascular malformations; however, they can cause severe neurological deficits when bleeding. removal of these lesions has been related with a high surgical morbidity, and there is no general consent on the surgical management of these lesions. it was the goal of this study to review the surgical results of a recent series of brainstem cavernomas. intraoperative navigation made use of mr based brainstem tractography, whereas intraoperative electrophysiological mapping of the brainstem was done to optimize resection. methods a total of 25 consecutive patients with cavernomas in the brainstem were included in this study. all treated patients suffered at least one hemorrhage before they underwent surgical treatment. presenting symptoms included facial palsy, diplopia, dizziness, headaches and gait disturbance. pre-operative neuroradiological examinations included mri with diffusion tensor imaging (dti) to visualize brainstem tracts. results less invasive approaches including the retrosigmoid and the medial suboccipital approach were used. brainstem mapping was used to determine a safe point of entry. microsurgical resection of the cavernomas was performed under continuous intraoperative monitoring. a total tumor removal was achieved in 23 cases and new cranial nerve deficits were observed in only two patients after surgery. selected abstracts romanian neurosurgery vol. xvi nr. 2 46 conclusion our results show that by using a refined microsurgical technique combined with minimally invasive approaches, neurophysiological monitoring and brainstem mapping, a total resection of brainstem cavernomas can be achieved with a very low surgical morbidity. medulloblastoma in children (21 years of experience) prof. ciurea a.v., md, phd1, tascu a., md, phd1, iliescu a., md, phd1, lisievici m., md, phd2, brehar f., md1, rizea r., md1, n.a. gheorghita, md3 clinic hospital “bagdasar-arseni”, 11st neurosurgery clinic pediatric department, 2histopathologic dpt., 3picu dpt. keywords: medulloblastoma, surgery, radiotherapy, chemotherapy, outcome background medulloblastoma (mbl) represent 30%-40% of posterior fossa tumors in children. the mechanism of tumorigenesis is unknown. for mbl, 5-year progression free, and overall survival is 60 and 59%. authors present a series of 196 consecutive operated cases which represent 21 years retrospective study of mbls in the pediatric neurosurgery department 1st neurosurgery clinic of the bagdasar-arseni hospital, bucharest, for 21 years (1988-2008). authors present the classification of these tumors in basis of the chang system score (1969), the localization, neuroimaging, clinical features, multimodal treatment, follow-up, outcome and q.o.l. although the appearance of ct findings in mbl are highly characteristic, but mr is the preferred for imaging diagnosis, for posterior fossa and supra/subtentorial and spinal dissemination. material & method in the 1st department of neurosurgery, in the period of time between 1988-2008 (21 years), 196 consecutive operated cases of mbl. the most affected age was 4-9 years – 102 cases (52%). there were 114 boys (58%) and 82 girls (42%). the preponderant localization was median, vermis and 4th ventricle in 141 cases (71,9%), paramedian in 49 cases (25%) and cerebellopontine angle in 6 cases (3,1%). at admission, the classification by chang et al. staging (1969): t1 64 cases (32.6%); t2 61 cases (31.1%); t3a 39 cases (19.9%); t3b 22 cases (11.2%); t4 10 cases (5.1%); m0 128 cases (65.3); m1 30 cases (15.3%); m2 8 cases (4.1%); m3 24 cases (12.2%) and m4 6 cases (3.1%). all the cases were investigated by ct-scan and mr. obstructive hydrocephalus was observed in 141 cases (71,9%) and the performed treatment: preoperative evd 42 cases (21,4%), neuroendoscopy 28 cases (14,3%) and vp shunt 71 cases (36,2%). all the cases were submitted to the surgical intervention. the total resection was performed in 92 cases (46.9%), near-total resection in 34 cases (17.3%), subtotal resection in 70 cases (35,7%). according to the international classification the patients was with: “low risk”: age > 3yo, m0 stage, or residual tumor <1.5cmc, and “high risk”: age < 3yo, m1m3 stage and residual tumor >1.5cmc. in our data – 29 operated cases 0-3 years old (14,8%). all the operated cases received multimodal postoperative therapy (radiotherapy, chemotherapy). the standard protocol of radiotherapy was completely to cover the whole cerebro-spinal axis (35-40 gy + 1415 gy boost to tumor bed). total contraindication of radiotherapy: 0-3 years old. concerning of chemotherapy, the protocol (8 drugs in 1 day) is: vincristine, carmustine, procarbazine, hydroxyurea, cisplatin, cytarabine, prednisone, cyclophosphamide realized by oncological institute of bucharest. the chemotherapy treatment was done in 4-6 cure. there is selected abstracts romanian neurosurgery vol. xvi nr. 2 47 no standardized chemotherapy regim; ccnu and vincristine are primary used. the gos at 6 months was: good recovery 97 cases (49,5%), moderate disability 65 cases (33.1%), severe disability 25 cases (12.8%), persistent vegetative state 3 cases (1.5%), death6 cases (3.1 %). the median period of follow-up was 12.2 years (12 months-18 years). lost cases 32 cases (16.3%) and monitoring cases 164 cases (83.7%). local recurrences 25 cases (12.8%), spinal dissemination 74 cases (37.8 %) and supratentorial metastasis 31 cases (15.8 %). conclusions mbl are classified in the pnet group. the neuroimagistic investigation is based especially on cerebral and spinal mr, the main findings for diagnosis. the goal of surgery is the total surgical removal and the pathological diagnosis. in some cases, the neuroendoscopy can be useful for preoperative hydrocephalus. in all the cases postoperative radiotherapy and chemotherapy must be performed. the follow-up is based on mr control to detect recurrences or dissemination. the final prognosis of medulloblastoma remain severe. epilepsy and malformations of cortical development prof. bertrand devaux, france malformations of cortical development (mcd) correspond to a broad spectrum of cerebral lesions resulting from cortical development abnormalities during embryogenesis. they are characterized by cytoarchitectural abnormalities caused by abnormalities of neuronal migration and cortical laminar organization, and are frequently associated with a severe, earlyonset, partial epilepsy, and with variable neurological and cognitive deficits. diagnosis of mcd greatly improved with contemporary imaging, and mcd is an increasing identified cause of medically refractory epilepsy. current classifications based on a combination of clinical, imaging, genetic and pathological data allow analysis of homogeneous patient series and optimal therapeutic strategies. mcd include taylor type focal cortical dysplasias (ttfcd), other focal cortical dysplasias, hemimegalencephaly, bourneville’s disease, tumors associated with cortical dysplasias (dysembrypolastic neuroepithelial tumors and gangliogliomas), heterotopias and polymicrogyria. successful surgical treatment can be proposed to patients with focal lesions such as ttfcd or tumors associated with cortical dysplasias, while favourable outcome can also be obtained in some diffuse cases such tuberous sclerosis, periventricular heterotopias and polymicrogyrias. suggestive neuroimaging features may be lacking in 30% to 40% of patients with fcd, rendering their identification difficult and leading to confusion with cryptogenic partial epilepsy. in these patients, as well as in those with a fcd localized in functional areas, invasive seizure monitoring, especially seeg, has been proved to be helpful to identify typical patterns and to plan surgical resections. seeg has also been useful in determining the organization of epileptogenic zone in each mcd type, and remains necessary in cases of image-negative fcd and diffuse mcd. adequate surgical resection strategy in ttfcd may lead to an excellent seizure outcome, with 90% to 95% of seizure-free patients. in our experience, ttfcd represents the most favourable cause of surgically remediable focal epilepsy, even when located in functional areas. further refinements in neuroimaging modalities should improve detection and delineation of focal mcd, while new surgical techniques, such as multiple stereotactic thermocoagulations, that are under evaluation, could extend surgical armamentarium in deeply or functionally located fcd. selected abstracts romanian neurosurgery vol. xvi nr. 2 48 lumbar canal stenosis in a series of 110 surgical cases ion poeata, bogdan iliescu, sergiu gaivas, smaranda predoaica, cosmin apetrei, daniel rotariu iasi romania in our department we admitted 136 cases for lumbar canal stenosis, in a period of 4 years, during 08.01.2005-07.31.2009, and we selected 110 cases for surgery. the main surgery for these cases was laminectomy with adjacent yellow ligaments resection, superior subjacent laminae resection, and internal part of articular processes resection, with recess reconstruction. this basic surgery was performed in one level 67 cases, 2 levels, 24 cases, and 3 or more levels, 19 cases. herniated disk resections were associated procedures in 45 cases. sometimes, unilateral procedures or foraminotomies were used in multiple level surgeries or in cases with recess/foraminal stenosis alone. the diagnosis was based mainly on mri sometimes on ct images or combined ct/mri studies. we used efilm program for complex image processing and measurements. all the time the images were correlated with symptoms in order to focus surgery on medullar claudication alone, or medullar claudication associated with sciatica. some patients couldn’t be operated due to general condition, with associated diseases characteristic to the age group, and others were planned for partial decompression, addressed to main symptoms. following this attitude we had no lifethreatening postoperative complications. we present preand postoperative images together with our algorithm in deciding the type of surgery according to a specific clinical and imagistic condition. compared to our previous series the number and complexity of cases raised progressively, due to this protocol and increased confidence of this category of patients in a successful surgery. selected combination of neurotrophins potentiate neuroprotection and functional recovery following spinal cord injury in the rat hari shanker sharma, aruna sharma uppsala, sweden previous works from our laboratory showed that topical application of bdnf and igf-1 when given alone separately is able to attenuate bscb breakdown, edema formation and cell injury in a rat model of sci. however, these beneficial effects of neurotrophins are limited to short periods ranging from 5 min to 30 min after sci. thus, it would be interesting to find-out whether a combination of neurotrophins will enhance or neutralize the neuroprotective efficacy of the growth factors in trauma models. in this investigation, the potential efficacy of bdnf in combination with gdnf, nt-3 or ngf in was examined in this investigation. the bdnf was applied over the traumatized spinal cord alone or in combination with other neurotrophins and motor dysfunction, blood-spinal cord barrier (bscb) breakdown, edema formation and cell injury was examined in our rat model. the spinal cord injury (sci) was performed by making a unilateral incision into the right dorsal horn of the t10-11 segment. the rats were allowed to survive 5 h after trauma [5]. topical application of bdnf, gdnf or ngf 30 min after (but not 60 or 90 min) sci in high concentration (0.5 µg and 1 µg) significantly improved the motor functions and reduced the bscb breakdown, edema formation and cell injury at 5h. however, combined application of selected abstracts romanian neurosurgery vol. xvi nr. 2 49 bdnf and gdnf (but not with nt-3 or ngf) at 60 min or 90 min after sci induced a significant reduction in motor dysfunction and spinal cord pathology. these observations suggest that a good combination of neurotrophins may have added therapeutic value for the treatment of sci. primary tumors of the cervical spine zileli mehmet, m.d. ege university faculty of medicine, department of neurosurgery, izmir, turkey objectives often impinging on vascular and neural structures, cervical tumors are surgically challenging lesions. since cervical primary tumors are rare, many issues regarding the best surgical strategy remain unanswered yet. this study is a retrospective review of 66 surgeries performed on 35 patients, ranging in age 7 to 70 years, to clarify the surgical options for primary tumors of the cervical spine and to elucidate which factors influence outcome. methods preand postoperative degree of pain and neurological status were quantified using four point and five-point scales, respectively. radiological investigations were used to detect recurrence and evaluate the stability and/or fusion. data collected on patient characteristics, age, gender, symptoms, histopathology of the tumor, type of the surgery, adjuvant therapies, and complications, and results.. follow-up ranged from 3 months to 10 years 6 months to 15 years (mean 59.9 months). results posterior (26), anterolateral (24), retropharyngeal (9), combined (4), lateral (2), and transmandibular approaches (1) were used. chordomas (n=8) and 17 different types of tumors were encountered. one patient died three weeks post-operatively and 5 died of their disease at follow up. 20 patients had no evidence of disease and 7 patients had recurrent tumors. according to weinstein-boriani-biagini classification, tumor extension into both anterior and posterior columns of a vertebra was correlated with a poor outcome. incomplete resections resulted in tumor recurrence which warranted subsequent surgeries (up to 9), especially in chordoma cases. conclusions complete tumor resection is the oncologically best surgical strategy and should be attempted whenever possible. however, this may not be feasible in every case because of complexity of the cervical spine. in these cases, acceptable mortality-morbidity rates and symptom-free years could be achieved by subtotal resections, even for malignant tumors. surgery for kyphosis mehmet zileli, m.d. ege university faculty of medicine, izmir, turkey goal kyphosis as a sagittal spine deformity causes pain and significant disability. the etiology may be ankylosing spondylitis, scheurmann’s disease, pott’s disease, osteoporotic compression fractures. this paper aims to analyse the technique used to correct severe kyphosis by a posterior only surgery. materials and methods between 1998 and 2008 a total of 44 patients with kyphosis were surgically treated. the reason of kyphosis was ankylosing spondylitis (17 cases), scheurmann’s disease (3 cases), congenital spinal anomalies (12 cases), pott’s disease (5 cases), posttraumatic kyphosis (7 cases). selected abstracts romanian neurosurgery vol. xvi nr. 2 50 21 cases with thoracic and lumbar kyphosis were operated with a posterior only approach using wedge osteotomy technique. 3 cases with cervicothoracic kyphosis were operated with an osteotomy in at c7-t1 level, since that level has no problem with vertebral artery. reduction was achieved with traction and head deflexion. results and discussion significant reduction could be achieved in 37 cases. neurological deficits did not worsen in patients with preoperative deficits. hardware failures, loss of correction, csf leakage and infection were most frequent complications. there were no neurological complications. anterior surgery is indicated in thoracic kyphosis more than 70º degrees, and kyphosis with neurologic deficits. a posterior wedge osteotomy is indicated for long curvature thoracic kyphosis, short curvature thoracic kyphosis between 30-70º and lumbar kyphosis more than 20º. conclusions kyphosis can easily and effectively be reduced by a posterior only approach in many types of kyphosis. since they have no nerological deficits, the patients with ankylosisng sponylitis are most suitable for this surgery. in lumbar kyphosis one level wedge osteotomy (especially at l1 or l2 levels) or egg-shell procedure is appropriate. in thoracic kyphosis multilevel wedge osteotomies should be preferred. in cervicothoracic kyphosis an osteotomy at c7-t1 level should be the procedure of choice. lumbar stenosis: laminectomy versus minimal invasive laminotomy. a prospective analysis of 104 patients u. kehler, e. peters department of neurosurgery, asklepios klinik altona, hamburg, germany with increased life expectancy more patients are seen with symptomatic spinal canal stenosis. in the last decade surgery changed to less invasive procedures. however, outcome of more or less invasive decompressions have to prove their advantages to be accepted. to compare laminectomy and minimal invasive laminotomy with bilateral decompression in cross over technique both methods were prospectively analyzed. methods between 2005 and 2007 104 patients with monolevel lumbar stenosis were analyzed. ninety-six patients (48 in each group) could be evaluated up to august 2008. we compared clinical outcome at discharge and 1 year later, blood loss, necessity of drainage, rebleeding, length of surgery, and postop. pain. results: patients of both groups improves substantially after surgery. blood loss, need of wound drainage (6 versus 42), length of hospital stay (7,4 versus 8,7 days), and back pain (vas 1 vs 2,15) were significantly less in laminotomies, painless walking distance improved in the early follow-up. at the one year follow-up no difference was seen regarding back pain and claudicatio. postoperative instability was seen in one case of each group. conclusions minimal invasive laminotomy has early advantages due to less invasiveness. however, long term results are very similar demonstrating that decompression is received sufficiently in both groups. patient benefit from both procedures but in the short term run laminotomy improves by far the patients’ comfort. selected abstracts romanian neurosurgery vol. xvi nr. 2 51 childhood posterior fossa tumors nejat akalan, md, phd department of neurosurgery, hacettepe university school of medicine, ankara, turkey compared to adults, much higher percentage of tumors arises at the infratentorial area in children. medulloblastomas, ependymomas and astrocytomas together in this location comprise almost half of all brain tumors and 90% of the infratentorial tumors in children. they represent far ends of the spectrum in terms of malignancy and natural course, while sharing the common feature variable that the amount of resection being the only significant variable for a favourable prognosis. one exception is diffuse brainstem gliomas are almost exclusively pediatric tumors that make almost 10% of all posterior fossa tumors. they represent one of the very few childhood tumors that surgery has not been to show any role in treatment. they have distinctive radiological appearance in mri enough to initiate adjuvant therapy without biopsy. a very important detail is to differentiate focal pontine astrocytoma from diffuse form, which comprises 10% of brainstem tumors. focal pontine astrocytoma is a typically surgical disease, which total resection provides cure. miscellaneous tumors like hemangioblastomas, gangliogliomas and cavernomas are intra-axial pathologies occasionally found in children as well as extra-axial schwannomas, meningiomas and chordomas. they are cared accordingly as in adults with respect to age related physiological distinctiveness of children. mri findings are of great value not only in planning the most appropriate approach, but estimating the pathology and disease state. utilization of operative microscope and microsurgical techniques prove classical large bone and dural openings unnecessary which save time, minimize blood loss and wound related complications. postoperative early mri within 24 hours is essential for future therapy planning and survival assessment. this presentation will focus on the surgical approach to the various childhood tumors at the posterior fossa based on the experience on more than 600 tumors of different histopathological origin and location. the variety of histological types of tumors has predilections for different compartments of the infratentorial space which makes it more practical to discuss their surgery according to localization rather than the pathology. special attention will given to specific approaches to common locations and key points unique to childen will be emphasized. microsoft word 7roditisspyridon_hemorrhagic_f 294 spyridon roditis, nicolai ianovici hemorrhagic stroke in young people hemorrhagic stroke in young people spyridon roditis1, nicolai ianovici2 1phd student in neurosurgery, “gr.t. popa” university of medicine and pharmacy, iasi, romania laiko hospital of athens, greece 2neurosurgery, “prof. dr. n. oblu” emergency clinical hospital, iasi, romania abstract the paper presents the incidence, causes, locations, and prognosis of intracerebral hemorrhages (ich) in people aged ≤ 35 years. we retrospectively investigated consecutive 191 patients with neuroimaging evidence or pathological confirmation of symptomatic ich and we found 8 cases of intracerebral hemorrhages in young people (≤ 35 years). the most frequent risk factors were hypertension, tobacco use and alcohol use. the locations of ich in young people were basal ganglia/internal capsule and lobar, and the most common causes was high blood pressure, one case of vascular malformation and cryptogenic ich was considered in two cases. hemorrhagic stroke in young people are mainly located in the basal ganglia in high blood pressure and lobar caused of vascular malformation. mortality and morbidity in the acute phase are low and are related to hypertension as the cause of hemorrhagic stroke. keywords: hemorrhagic stroke, high blood pressure, young people introduction spontaneous intracerebral hemorrhage is approximately 10% 20 % of all stroke cases and the incidence of hemorrhagic stroke in young people (aged <35 years) has been estimated to be 0.5/100 000. the absolute proportion of hemorrhagic stroke in young people is strongly linked to the structure of the population. in western european countries, with a high prevalence of old and very old people, less of strokes occur in subject under 35 years but higher incidence rates have been found in the developing countries. the etiology of ich in young people includes high blood pressure, vascular malformations, and drug use (tobacco use and alcohol use). few series of intracerebral hemorrhage in young people have been published and most do not provide a detailed discussion of the primary causes of hemorrhagic stroke. this study describes the frequency of spontaneous intracerebral hemorrhage and to provide an analysis of causes, location, and prognosis of hemorrhagic stroke in young people. material and methods the study included 191 consecutive patients with spontaneous intracerebral hemorrhage during a calendar year aged between 27 and 93 years with a group of 8 patients under 35 years: 5 men and 3 women. the inclusion criteria were age ≤ 35 years at the time of intracerebral hemorrhage and availability of detailed information relating to risk factors, clinical features, hospital course and final outcome. romanian neurosurgery (2011) xviii 3: 294 – 299 295 we retrospectively analyzed the clinical and radiological data from those patients with neuroimaging or neuropathological evidence of spontaneous intracerebral hemorrhage. the patients with primary subarachnoid and traumatic hemorrhages and those with a previously diagnosed vascular malformation, aneurysm or brain tumor were excluded. we analyzed in each patient the risk factors: high blood pressure, use of antihypertensive drugs, previous medical diagnosis of arterial hypertension, tobacco use, alcohol use and oral contraceptive use, regular use during the last year. classification of each hematoma location was based on the location of the center of the hematoma as lobar (frontal, parietal, temporal, occipital), thalamic, basal ganglia/internal capsule established by ct or mri. (figure 1, 2 and 3). the etiology of hemorrhagic stroke was defined in accordance with the following criteria: arterial hypertension and documentation of high blood pressure, as well as exclusion of other potential cause of ich; arteriovenous malformation confirmed by mri or brain angiography; drug use and tobacco use or alcohol use and the hemorrhagic stroke in close temporal relation to use of drugs and exclusion of other potential causes; hematologic disorders, and cryptogenic, patients without risk factors or predisposing conditions in whom structural abnormalities were not found on mri or cerebral angiography to explain hemorrhagic stroke and with follow-up during a year. table 1 distribution of hemorrhagic stroke by age and sex age man women 27 35 years 5 3 36 93 years 108 75 figure 1 ct image of frontal intracerebral lobar hematoma figure 2 ct image of basal ganglia hematoma 296 spyridon roditis, nicolai ianovici hemorrhagic stroke in young people results the most common locations of hemorrhagic stroke were basal ganglia/internal capsule in 4 patients and lobar in 4 patients . the most common causes of ich were hypertension in five patients, the rupture of an arteriovenous malformation in one patient and in two patients we could not demonstrate the cause of intracerebral hemorrhage. all 5 patients from our series with hemorrhagic stroke related to hypertension had persistent increase of blood pressure. surgery was successful in three patients with lobar intracerebral hemorrhage : the case of the arteriovenous malformation and in two patients with cryptogenic hemorrhagic stroke and they were discharged home with no neurological deficits. discussion spontaneous hemorrhagic stroke in young people ( aged <35 years) has been estimated to be 0.5/100 000 and few series of intracerebral hemorrhage in young people have been published. ruíz-sandoval et al, 1999, analyzed 200 patients aged < 40 years, among 1734 consecutive patients diagnosed with hemorrhagic stroke. they found that the most common risk factors included tobacco use in 20%, hypertension in 13% and alcohol use in 10%. also they found that the most common locations of intracerebral hemorrhage were lobar in 55%, basal ganglia/internal capsule in 22%, the brain stem in 26 (13%), cerebellum in 10 (5%), intraventricular in 4%, and multiple in 3 cases. the most common causes of intracerebral hemorrhage were rupture of an arteriovenous malformation in 33 % of patients, cavernous angioma in 16% of patients and hypertension in 11% and in 15 % patients they could not demonstrate the cause of intracerebral hemorrhage. a b figure 3 a, b mri of hemorrhagic stroke in right occipito-temporal area fuh jl et al, 1994, evaluated 170 patients aged 15–45 years who had nontraumatic hemorrhagic stroke and they found that the main causes of spontaneous intracerebral hemorrhage were hypertension, ruptured arteriovenous malformation and blood dyscrasia. a cause was not found in 42 romanian neurosurgery (2011) xviii 3: 294 – 299 297 patients (24.7%). also they found that young adults with nontraumatic intracerebral are a heterogeneous group and hypertension accounts for about one-third of intracerebral hemorrhage and it is an important preventable cause of hemorrhagic stroke in young adults . we evaluated 191 patients diagnosed with hemorrhagic stroke and young adults with nontraumatic intracerebral hemorrhage were only 8 cases and the main cause of hemorrhagic stroke in young people was high blood pressure (for 5 patients). therefore arterial hypertension is an important preventable cause of hemorrhagic stroke in young adults. but in other series with large number of patients hypertension was responsible for a low percentage of intracerebral hemorrhage and compared with other causes, this produced the worst outcome and resulted in high morbidity, mortality, and recurrence. hypertension as a cause of intracerebral hemorrhage was most common in individuals aged >31 years and the intracerebral hemorrhage was often located in the basal ganglia. we found only a case of intracerebral hemorrhage caused of the rupture of an arteriovenous malformation, but in other series the most common cause of intracerebral hemorrhage was rupture of vascular malformations, including both arteriovenous malformation and cavernous angioma. the most common location of intracerebral hemorrhage resulting from arteriovenous malformations was lobar. cavernous angioma was most commonly located supratentorially but was the most common cause of intracerebral hemorrhage located in the brain stem. cryptogenic intracerebral hemorrhage was considered in two patients, compared with other studies that show cryptogenic intracerebral hemorrhage in 15% of their patients, but the number of our cases is small. risk factors for intracerebral hemorrhage are known: age and race; hypertension, cerebral amyloid angiopathy, arteriovenous malformations, alcohol use and tobacco use. age is the greatest risk factor for intracerebral hemorrhage. incidence rates increase dramatically among persons older than 60 years. hypertension is the most important and prevalent modifiable risk factor for ich. untreated hypertension is a greater risk factor than treated hypertension, and hypertensive patients who discontinue their medications have greater risk than those who continue them cerebral amyloid angiopathy is now considered an important cause of lobar hemorrhage in the elderly. aneurysms and vascular malformations are particularly important as a cause of intracerebral hemorrhage among young people, although in our series the rupture of an arteriovenous malformation was found only in one patient. antiplatelet drugs probably increase the risk of intracerebral hemorrhage by a small amount. the absolute risk of intracranial hemorrhage among elderly persons taking aspirin has been estimated at 0.2–0.3% annually (vs. 0.15% in similar persons not taking antiplatelets or anticoagulants). numerous studies have identified a relationship between alcohol use and the risk of hemorrhagic stroke and also several studies suggest that current smoking increases the risk of intracerebral hemorrhage . spontaneous intracerebral hemorrhage causes 10–15% of first ever strokes and is 298 spyridon roditis, nicolai ianovici hemorrhagic stroke in young people associated with the highest mortality of all cerebrovascular events. the initial diagnostic question in a patient with acute onset of focal neurological deficits is whether or not the deficits are caused by intracerebral hemorrhage . the answer is of utmost importance in determining the direction of treatment. non-contrast ct is the first-line imaging modality in this setting. computerized tomography scans are rapid, readily available, and relatively inexpensive. most importantly they have exquisite sensitivity and specificity, approaching 100%, in the detection of acute blood. because hypertension is the most common cause of spontaneous intracerebral hemorrhage, its treatment in this setting is of considerable importance. intracerebral hematoma growth may be accelerated by hypertension in the setting of acute intracerebral hemorrhage. the occurrence of intracerebral hemorrhage is strongly related to premorbid blood pressure; however, the relationship between the growth of hematoma and uncontrolled blood pressure remains to be clarified. jauch et al demonstrated that there was no definitive correlation between hemodynamic parameters,such as blood pressure and hematoma growth. the recent studies emphasize aggressive blood pressure control for a systolic blood pressure >200 mmhg or mean arterial blood pressure (map) >150 mmhg . for an systolic blood pressure >180 mmhg (or map >130 mmhg), with a suspicion of elevated icp, icp monitoring is recommended; on the other hand if icp elevation is not a concern based on the patient’s neurological examination, a goal of systolic blood pressure <160 mmhg or map <110 mmhg is recommended. surgical therapies have been unable to improve the neurological outcome of the patients with intracerebral hematoma and to minimize brain tissue trauma that is induced by surgical manipulation, and in view of the failure of craniotomy/hematoma evacuation to improve survival and neurological outcome after intracerebral hemorrhage, new modalities as minimally invasive surgery (mis = e.g., stereotacticguided aspiration) have emerged as treatment alternatives that are amenable to testing. studies testing the safety and efficacy of minimally invasive surgery techniques in the treatment of intracerebral hematoma have taken advantage of mainly two different procedures: the use of endoscopic aspiration of the hematoma and the stereotactic placement of a flexible catheter in the core of the hematoma followed by the administration of thrombolytic agents. both approaches are viable treatment alternatives of craniotomy in hematoma evacuation . clot evacuation combining the use of fibrinolysis with clot aspiration has emerged as the most promising surgical modality in the acute care of intracerebral hematoma. conclusion arteriovenous malformations are particularly important as a cause of spontaneous intracerebral hemorrhage in young people intracerebral hemorrhage, although in our series the rupture of an arteriovenous malformation was found only in one patient. the use of non-contrast ct in the initial evaluation of patients presenting with suspected intracerebral hemorrhage is well established and universally accepted. because hypertension is the most common cause of spontaneous intracerebral romanian neurosurgery (2011) xviii 3: 294 – 299 299 hemorrhage, an aggressive blood pressure control for a systolic blood pressure >200 mmhg is needed. the surgical treatment of intracerebral hematoma consist of a conventional craniotomy and evacuation of the clot under direct vision, with or without the microscope; a stereotactic aspiration through a burr hole aspiration of a dense clot can be facilitated either by instillation of fibrinolytic agents or by fragmenting it by means of an ultrasonic device and endoscopic surgery. correspondence: dr spyridon roditis laiko hospital of athens ag.thoma 17, τ.κ. 11527, athens, greece sproditis@yahoo.com references 1. buis dr, van den berg r, lagerwaard fj, vandertop wp. brain arteriovenous malformations: from diagnosis to treatment. j neurosurg sci. 2011 mar;55(1):39-56. 2. coutts sb, matysiak-scholze u, kohlhase j, innes am. intracerebral hemorrhage in a young man. cmaj. 2011 jan 11;183(1):e61-4. 3. ellis c. stroke in young adults. disabil health j. 2010;3(3):222-4. 4. fuh jl, liu hc, wang sj, lo yk , lee ls nontraumatic hemorrhagic stroke in young adults in taiwan, journal of stroke and cerebrovascular diseases, 1994, vol 4, 2 ; 101-105 5. gandolfo c, conti m. stroke in young adults: epidemiology. neurol sci. 2003 may;24 suppl 1:s1-3. 6. hopf nj, füllbier l. minimally invasive neurosurgery for vascular lesions. neurosurg clin n am. 2010 oct;21(4):673-89, vii. review. 7. savadi-oskouei d, sadeghi-bazargani h, hashemilar m, deangelis t. symptomatologic versus neuroimaging predictors of in-hospital survival after intracerebral haemorrhage. pak j biol sci. 2010 may 1;13(9):443-7. 8. stein m, luecke m, preuss m, boeker dk, joedicke a, oertel mf. spontaneous intracerebral hemorrhage with ventricular extension and the grading of obstructive hydrocephalus: the prediction of outcome of a special life-threatening entity. neurosurgery. 2010 nov;67(5):1243-51 9. stemer a, ouyang b, lee vh, prabhakaran s. prevalence and risk factors for multiple simultaneous intracerebral hemorrhages. cerebrovasc dis. 2010 aug;30(3):302-7 10.tang sc, jeng js. management of stroke in pregnancy and the puerperium. expert rev neurother. 2010;10(2):205-15. 11.truelsen t, piechowski-jóźwiak b, bonita r, mathers c, bogousslavsky j, boysen g. stroke incidence and prevalence in europe: a review of available data. eur j neurol. 2006;13(6):581-98. 12.virmani t, agarwal a, klawiter ec. clinical reasoning: a young adult presents with focal weakness and hemorrhagic brain lesions. neurology. 2011 may 31;76(22) 13.yu jl, yang s, luo q, wang hl, wang b, qu yy, xu k. endovascular treatment of intracranial ruptured aneurysms associated with arteriovenous malformations: a clinical analysis of 14 hemorrhagic cases. interv neuroradiol. 2011 mar;17(1):78-86. 14.wong gk, siu dy, abrigo jm, poon ws, tsang fc, zhu xl, yu sc, ahuja at. computed tomographic angiography and venography for young or nonhypertensive patients with acute spontaneous intracerebral hemorrhage. stroke. 2011 jan;42(1):211-3. microsoft word 1.muresangh_stefantristaniacob.doc romanian neurosurgery (2010) xvii 4: 383 – 387 383 stefan tristan iacob founder of neurosurgery in cluj gh. mureşan, i.st. florian, izabella kasza a complex an outstanding personality, assoc. prof. stefan tristan iacob was the one who not only founded but more than that he developed and marked the future progress of neurosurgery in the university center of cluj for many decades after his disappearance. stefan tristan iacob was born in sibiu, on the 20th january 1920 where he attended elementary school (1927-1931), after that the military high school in targumures (1931-1939) and the faculty of medicine in bucharest at the medical military institute in the period of 19391945. between 1940-1945 under the supervision of dr. o. arama, head of the bucharest central military hospital he attended training in neurology. during the war he worked as an intern at the bucharest central military hospital and in hospitals from sibiu, cernavoda, and constanta. during his neurology training he gathered clinical material and elaborated together with dr. grigorescu the monography entitled neuropathology of the war, published in 1943. the volume was prefaced by prof. n. ionescu-siseşti and it was rewarded by the romanian academy with the oroveanu prize in 1945. the book was technically edited under exceptional conditions, thus covering especially medical issues, but also social ones. the authors introduced the notion of the disease after being wounded and raised an original conception above history, underlining the major importance of the physic of the nervous disturbances appeared during the war. in 1946 he quit the army and advised by the o arama, dr. iacob dedicated himself to neurosurgery. with the help of prof. dumitru bagdasar he was named as a resident doctor at the neurosurgery clinic in bucharest, administrated by gen. dr. p. costescu. as a resident of neurosurgery in the period of 1946-1949 under the supervision of prof. c. arseni, he published together with him the volume entitled vertebral sciatica, dedicating it to prof. dimitrie bagdasar. in the autumn of 1948 dr. iacob was transferred as resident to the neurosurgery clinic in targu-mures, administrated by prof. dr. dezso miskolczi şi tibor andrasofszky. during this period he translated from spanish the book entitled „reglas y consejos sobre investigacion cientifica” written by ramon santiago cajal. the translation was published in 1967 and was very well received by the superior council of the spanish scientific research and by the institute of cajal. in the fall of 1949 in cluj he completed his resident training and was transferred to cluj. except with a short period between 1941 -1943, when prof. dr. istvan kornyei 1949 from hungary performed some neurosurgical interventions, no deparment existed in cluj for the surgical treatment of the diseases of the nervous system. after arriving in cluj, he started his medical activity having 2 beds at the 1st surgical clinic. the first two surgeries 384 gh. mureşan et al stefan tristan iacob performed on the 3rd of october 1949 were two cases of lumbar disc herniation, dr. iacob being assisted by prof. aurel nana himself, at that time the head of 1st surgical clinic. in november 1949 with the aid of prof. dezideriu duma, the head of the neurology clinics, he obtained two wards of 10 beds each within the neurology clinics. since august 1950 by an order of ministry of health the actual building was dedicated to neurosurgery, which had one operating room, the same place where prof. istvan kornyei performed his neurosurgical procedures between 1941 and 1943. being interested in the progress of specialty, progressively dr. iacob succeeded in endowing the clinic monopolar coagulation, electroencephalograph and a lysholm craniograph. arteriography was applied by dr. iacob and his collaborators in 1952. prone position for posterior fossa tumors was also introduced by dr. iacob together with dr. istvan balint and dr. gheorghe muresan, this novelty being a nationwide exclusivity. it is also to be mentioned that starting with 1965 two of doctors have been working abroad (dr. ladislau steiner, who is the outmost authority in gamma knife). dr. iacob accorded major attention to the cranio-cerebral neurotraumatology, which has generated the appearance in 1971 of the handbook entitled emergencies in neurotraumatologypractical handbook, elaborated exclusively based on the clinical material of the department where more than 3000 cases of the nervous system traumas were assisted. dr. iacob was interested not only in the progress of specialty but also in development of training in the specialty. in the period of 1949-1952 dr. iacob was an assisting professor and then assoc. prof. in the period of 1950-1954. dr. iacob gave around 100 lectures about neuropathology and neurosurgery. in the period of 19511952 dr. iacob held 30 courses for the students of the faculty of medicine, the 6th year, based on his own iconographic and clinic material. he insisted on the paraclinic examinations (ventricuography, arteriography), methods which were not in use until 1949 in cluj. for that period this was certainly and obvious progress. between 1953-1954 dr. iacob held a series of 20 courses addressed to internist doctors referring to the practical problems in neurosurgery important for the general practitioner or for doctors of other specialties. these conferences were presented within the postgraduate institute of perfection for the doctors in cluj (the department of prof. iuliu hatieganu). romanian neurosurgery (2010) xvii 4: 383 – 387 385 in 1968 dr. iacob was hired full time at the institute of medicine and pharmacy cluj and sustained two courses at the postgraduate institute of perfection for the doctors in cluj. in 1969 this course is repeated with a new series. in 1970 dr. iacon was named assoc. prof. with entire rights at the 2nd surgical department, the discipline of neurosurgery. thus the neurosurgical clinic becomes a university clinic and methodological center as well for the issues of neurosurgery in cluj, crisana and maramures counties. during the conferences the following subjects were covered: the modern principles of neuropathology and neurosurgery, the possibilities and horizons of the rahi-medullar surgery, the vertebral sciatica, and especially the isolation of the group of surgical sciatica, the onset of symptoms in neuropathology, the syndrome of surgical emergencies in neuropathology, the value of interrelations among symptom-pathogen-etiology for the early diagnosis of an active surgical therapy, the neuroanatomic value of the approaches of the brain and its vascularization for establishing the neurosurgical approach, the compared value of the clinical and paraclinical diagnosis methods in neuropathology, and neurosurgery as method of scientific research. outstanding personality dr. ştefan tristan iacob had a prolific research activity contributing to the perfection of the therapy and diagnosis in neurosurgery. 386 gh. mureşan et al stefan tristan iacob under his supervision in the period of 1950-1969 more than 280 very valuable theses were elaborated. some of these papers are original in the romanian specialty literature: brain arteriography consideration on 2000 cases accompanied by an album of neuroanatomy and vascular neuroradiology, this study representing the synthesis of the brain arteriography practice in the clinic; the occlusion of the carotid and his branches consideration on 100 cases; brain aneurysms and angiomas consideration on 100 verified cases. a highly appreciated is the atlas of functional neroanantomy (special consideration to the cerebral vascularization). using the approaches in neurosurgery a series of pieces were prepared, which highlight the different cerebral regions, as they can be seen on live demonstrations. later they were taken photos of with a special technique; the assemblies of these constitute an album to orient the doctor in the different regions of the nervous system. these papers on the cerebral arteriograph and neuroanatomy of the cerebral vascularization were highly appreciated by prof. i. t. niculescu at the 18th conference of neurology-psychiatry and neurosurgery in 1955, who recommended these to the president of the romanian academy for publication. in 1964 dr. iacob successfully represented romania with 3 papers, reflecting the electroencephalographic studies performed in the clinic sent to 3 important scientific congresses (the 8th international congress of thoracic diseases, mexico electroencephalographic changes in hypoxia , the 4th congress of eeg, szeged, hungary, eeg correlations and brain metabolism in the neuronal dystrophies, purkinje international congress, prague, czech republic). the paper entitled syndromes d’ insuffisence circulatoire cerebrale par occlusions vasculaires dans les tumeurs cerebrales” a comparative study on 2000 cerebral arterioraphies was presented at the 3rd european congress of neurosurgery in spain and portugal (madrid, lisabona) in the period of the 23rd -26th april 1967. at this event a photo exhibition of 60 original photos also took place and it was entitled „methode correlative neuroanatomique et arteriographique pour la visualisation cerebrale” signed by dr. stefan trsitan iacob, dr. m. ionescu, dr. gheorghe mureşan and reflecting the effectuated studies by these using the method of the brain arteriography. at the neurosurgery clinic, dr. iacob performed an original research studying crystalographically the normal and pathologic crl. the material of this research was presented at the 4th international congress of neurosurgery, new york, in the period of the 22nd -26th september 1969. the presentation was based on 2500 preparations and a photo album. the study was entitled crystalline structures in the crl and their practical meaning. in 1973 at the 5th international congress of neurosurgery held at tokyo, dr. iacob presented the paper entitled vascular traumatic lesions, surgical and non-surgical considerations on 1072 cases. the paper is a synthesis and also the result of a long-term activity in neurotraumatology on 3000 cases admitted in a period of 20 years. between 1949-1969 under the supervision of dr. iacob the following doctors elaborated their phd thesis: prof. dr ladislau steiner (prefrontal romanian neurosurgery (2010) xvii 4: 383 – 387 387 leucotomy – 1950) and prof. dr. asgian berdj (the modern semiologic integration of the grabbing reflex-1950). outstanding personality dr. stefan tristan iacob imposed himself with the lesson of passion dedicated to the idea of neurosurgery, by his professional probity, through his scientific concerns, and by his original conception impregnated to the school of neurosurgery in cluj. the tradition kept alive since then formed the present generation of neurosurgeons. thus the relay was handed over and on it ambroise parre’s aphorism is written, namely labor improbus omnia vincit. selective references 1. arseni, constantin, momente din istoria neurochirurgiei româneşti, bucureşti, ed. academiei rsr, 1988; 2.crişan. virgil, dr. st. t. iacob (1920-1975) creatorul serviciului de neurochirurgie din cluj-napoca, revista clujul medical, 1986, nr. 59, volum 4, p. 356; 3.florea, l. , -liviu, v., bilanţul a două decenii. muncitorul sanitar, anul xxi, nr. 49 (1017), 2 decemvrie 1969; 4. şt. t. iacob, grigorescu, d., neuropatologie de război, sibiu, kraft und drotleff s.a., 1945, 224 pagini, 60 ilustraţii; 5. iacob, şt. t, arseni, c., sciatica vertebrală, sibiu, ed. velter, 1948, 200 pag., 165 figuri; 6. iacob, t&. şt., memoire d’activiteexpose des travaux scientiques, 1965, 35 pagini; 7. iacob, t. şt., urgenţe în neurotraumatologie îndreptar practic, ed. direcţia sanitară jud. cluj, 1971, 300 pagini; 8. kailan, ana maria, neurochirurgia la cluj (lucrare de diplomă), 1992; 9. marian ion, a fost dată în folosinţă noua secţie de neurochirurgie, ziarul făclia, anul xv, nr. 4368 din 11.11.1960; 10. marin, fl., facultatea de medicină, şcoala medicală clujană şi spitalele din cluj (1500-1990), ed. casa cărţii de ştiinţă cluj, 2004, pag. 526-528; 11. mureşan, gheorghe, 45 de ani de neurochirurgie clujană, „adevărul de cluj “ 8-9 novembrie, 1997, pag. 6. microsoft word 10costea_steinertmyotonic romanian neurosurgery (2013) xx 3: 293 – 296 293 steinert myotonic dystrophy – a multisystemic disorder with occular implication claudia f. costea1, d. petraru2 “grigore t. popa” university of medicine and pharmacy of iaşi faculty of dental medicine 1,22nd clinic of ophthalmology “prof. nicolae oblu” emergency hospital of iaşi abstract the steinert myotonic dystrophy is the most common systemic disease in adults with dominant autosomal transmission. we present two patients, who were hospitalized in the 2nd clinic of ophthalmology, at the "prof. nicolae oblu" emergency hospital of iasi, with the diagnosis of pathological cataract and steinert myotonic dystrophy. key words: steinert myotonic dystrophy, pathologic cataract, palpebral ptosis. introduction myotonic dystrophy is the most common dystrophy in adults, it is an autosomal dominant disease with two distinct genetic types: type 1 – the classical form described by steinert and type 2 identified by ricker (1). the steinert disease or type 1 myotonic dystrophy is a multisystem genetic disease that affects muscles (delayed muscle relaxation), nervous system, eyes and heart (2). the main ocular manifestations of the disease are: pathological cataract, myogenic palpebral ptosis (3) and reticular retinopathy. cataract associated with steinert disease have a pathognomonic aspect: the crystalline lens cortex shows polychromatic iridescent crystals formed from lens fiber plasmolemma (3). we present two clinical cases: a.a., aged 51 years, a.e., 58, siblings diagnosed with pathological cataract bilateral, myogenic ptosis grade 2-3 and steinert myotonic dystrophy. case 1 patient a.a., female, 51 years, from iasi, comes for the symptoms: l.e. gradual decrease of visual acuity and palpebral ptosis. medical history: r.e. operated pathological cataract (10 years ago), o.u. myogenic bilateral ptosis, steinert myotonic dystrophy. local ocular examination: o.u. grade 2-3 ptosis (figure 1). biomicroscopy examination highlights: r.e. pseudophakia, l.e. anterior and posterior cortical and nuclear subcapsular opacities; nucleus sclerosis +3; crystalline with a pathognomonic aspect, iridescent crystals in the cortex and nucleus. v.a.r.e. 1/500, v.a.l.e. 3/500, ophthalmoscopic examination: r.e. pale papilla, narrowed vessels with central emergence, macula with pigment dispersion; l.e. cannot be examined, due to lens opacification. p.r.e.=18 mmhg; p.l.e.=17 mmhg. m.r.i. exam shows cerebral atrophy (figure 2). 294 costea, petraru steinert myotonic dystrophy figure 1 patient a.a., 51 years, with steinert myotonic dystrophy figure 2 patient a.a., 51 years, m.r.i. imagines shows cerebral atrophy a b figure 3 a, b patient a.e., 58 years, with steinert myotonic dystrophy neurological examination shows motor disorders with central and peripheral causes. the biomicroscopy of the cataract indicates a favourable diagnosis (presence of iridescent crystals in the lens nucleus and cortex) and pathological neurological and neurosurgical associations. differential diagnosis: is made in relation to other pathological cataracts (diabetic, chronic eye inflammation, cortisone), senile cataract, traumatic cataract, persistent primary vitreous and coats disease. treatment surgery was performed at le: extracapsular lens extraction and implantation of the intraocular lens in the anterior chamber. postoperative evolution with appropriate medical treatment was favourable. the evolution was favourable after surgery: the corneal edema resolved, the inflammatory syndrome healed, v.a.l.e. 1/8 without correction. in the absence of surgical treatment, the prognosis is reserved, the disease progressing to peripheral blindness. romanian neurosurgery (2013) xx 3: 293 – 296 295 case 2 patient a.e. 58 years, male, from iasi, presents the same clinical picture as in the previous case. the medical history shows: r.e. operated pathological cataract (10 years ago), o.u. myogenic bilateral ptosis, steinert myotonic dystrophy. local ocular examination: o.u. palpebral ptosis grade 2-3. the biomicroscopy highlights: r.e. pseudophakia, l.e. full nucleus and cortex opacification, +3 nucleus sclerosis; polychromatic crystals are found in the lens nucleus and cortex (figure 3 a, b). v.a.r.e. 1/500, v.a.l.e. less than 1/500, p.r.e.=17 mmhg; p.l.e.=16 mmhg. ophthalmoscopic examination r.e.: net shape of optic nerve papilla, temporally pale, central emergence of narrow vessels macula with pigment dispersion;l.e. cannot be examined due to lens opacification. the internal medicine examination establishes the following diagnoses: chronic alcoholism, chronic ischemic cardiomyopathy, thrombocytopenia. m.r.i. exam shows cerebral atrophy (figure 4). figure 4 patient a.e., 58 years m.r.i. imagines shows cerebral atrophy the neurological examination shows motor disorders with central and peripheral causes.the favourable diagnosis that emerges is: l.e. pathological cataract, r.e. pseudophakia, o.u. bilateral myogenic ptosis grade 2-3, steinert myotonic dystrophy, chronic alcoholism, chronic ischemic cardiomyopathy, thrombocytopenia. the diagnosis of pathological cataract is supported by the muscle dystrophy and the particular aspect of the crystalline (presence of iridescent crystals in the lens nucleus and cortex). differential diagnosis: is made in relation to other pathological cataracts (diabetic, chronic eye inflammation, cortisone), senile cataract, traumatic cataract, persistent primary vitreous and coats disease. treatment surgery was performed on l.e.: the phacoemulsification of the lens and implantation the intraocular lens in the posterior chamber with no intraoperative complications.the postoperative evolution under medical treatment was favorable. evolution after surgery was favorable: inflammatory syndrome was completely resolved and v.a. at l.e. 1/3 without correction.the prognosis under surgical treatment is favorable. in the absence of surgical treatment, the prognosis is reserved, the disease progressing to peripheral blindness. case particularity in the first case of pathological cataract due to the anterior and posterior capsule adhesion to the lens nucleus and cortex, a 6-mm wide lens sclerocorneal incision was performed, with extracapsular lens extraction and pseudophak implantation in the anterior chamber. 296 costea, petraru steinert myotonic dystrophy the second case was solved by the method of phacoemulsification with clear corneal incision of 2.7 mm and pseudofak implantation in the posterior chamber. in both cases the cortex and nucleus were very dense and could cause posterior capsule rupture during surgery, resulting in the release of the vitreous and developing secondary glaucoma. in both cases the posterior capsule was very fragile presenting numerous cracks, and the intraocular lens was implanted in the anterior chamber. discussions eyes disorders in steinert disease are common and are characterized mainly by pathological cataract. other possible ocular manifestations are: myogenic ptosis, ocular hypotony due to ciliary body detachment (4) and reticular dystrophy of the retinal pigment epithelium, responsible for variable decrease in visual acuity (5). gjertsen et al. report three cases diagnosed with myotonic dystrophy which developed secondary recurrent opacification of the posterior capsule after cataract surgery. these patients undergo an increased risk of posterior capsule opacification and intraocular fibrosis after cataract surgery (6). in the literature, for myogenic ptosis the treatment recommended is blepharoplasty or eyelid levator resection or frontalis muscle suspension. the eye disorder in our cases was pathological cataract and myogenic palpebral ptosis grade 2-3. patients showed no significant ocular hypotony or retinal changes. we only solved surgically the pathological cataract and later remained to operate ptosis by upper eyelid levator resection. after operation there was no posterior capsule opacification. conclusions patients diagnosed with pathological cataract and steinert myotonic dystrophy are advised to undergo cataract surgery, when there is no severe impairment of respiratory and cardiovascular systems and the surgical technique must be adapted to each case to minimize intraoperative and postoperative complications. myogenic palpebral ptosis is recommended to be solved at a later stage. the long-term vision quality will depend on the progression of neurological damage, which adds to the retinal changes and brain damage (cerebral atrophy). references 1.lusakowska a., sulek-piatkowska a., myotonic dystrophy – a new insight into a well-known disease. neurol.neurochir.pol.-2010, 44(3):264-276. 2.debs r., tiberge m., troubles du sommeil et de la vigilance dans la maladie de steinert, sleep disturbancies in myotonic dystrophy type 1, médecine du sommeil2011, 8:141-144. 3.american academy of ophthalmology, the eye m.d. association, lens and cataract, printed in singapore, section 11, 2008-2009, 61. 4.rosa n., lanza m., borrelli m., de bernardo m.,palladino a., di gregorio m.g., pascotto e., politano i., low intraocular pressure resulting fron ciliary body detachment in patients with myotonic dystrophy. ophthalmology – 2011, 118(2):260-264. 5. tnacheri o., birouk n., benharbit m., ibrahimy w., laghmari m., daoudi r., rabat, maroc, 520 dystrophie réticulée de la macula et maladie de steinert. reticular macular dystrophy and steinert disease.journal français d’ophtalmologie-2008,31:165. 6.gjertsen i.k., sandvig k.u., eide n., olsen b.a., recurrence of secondary opacification and development of a dense posterior vitreous membrane in patients with myotonic dystrophy. j.cataract.retract.surg.-2003, 29(1):213-216. microsoft word 7.gaivass_computational_f.docx 434 s. gaivas et al computational hemodynamics in cerebral aneurysms computational hemodynamics in a patient specific cerebral aneurysms models s. gaivas¹, p. cârlescu², ion poeată³ ¹phd student, “gr.t.popa” umph, iaşi, romania ²“ion ionescu de la brad” university of agriculture science and veterinary medicine, iaşi ³“gr.t. popa” umph iasi abstract backgrounds: hemodinamic factors are known to play an important role in initiation, growth and rupture of intracerebral aneurysms. thorough knowledge of hemodynamic parameters in cerebral arteries and aneurysms are very useful in understanding of pathophysiology and clinical evaluation of cerebral aneurysms. we describe a methodology of computational analysis of hemodinamics in a patient specific aneurysms models. aneurysms are segmented from ct angiography images. method: a total of 6 cerebral aneurysms models were developed from ct angiography images. a computational fluid dynamics analyses were accomplished under realistic flow conditions. we selected only patients with multiple intracerebral aneurysms and conducted hemodynamic studies in un-ruptured aneurysms. we tried to evaluate the rupture risks for these aneurysms. in our series were five middle cerebral artery aneurysm and one basilar artery aneurysm. results: we succeed to set up a methodology in patient specific aneurysms models hemodynamic study. computational analyses of hemodynamic factors were performed for each of these 6 aneurysms models. the results were then processed to determine the average pressure on the arterial wall and inside the aneurysm, stream lines and region of greater impact of hemodynamic forces. conclusions: wall shear stress plays an important role in initiation, growth and rupture of cerebral aneurysms. in vivo measurements of wss values had become most popularly in last decade. aneurysm geometry influences the characteristics of flow conditions. keywords: computational fluid dynamics, aneurysm geometry, wall shear stress. introduction hemodynamics is the study of physical forces involved in blood circulation and namely hemodynamics refers to physical factors governing the flow of blood in circulatory system. hemodynamic parameters are considered to be responsible for initiating, growth and rupture of cerebral aneurysms. hemodynamic factors play a vital role in regulating the structure and function of the endothelial layer. endothelial cell capacity to respond to shear forces is responsible for structural remodeling of the entire vessel lumen diameter (3, 11). this morphological romanian neurosurgery (2011) xviii 4: 434 441 435 variation of vascular endothelial cells results in different degrees of vasoactive substances productions, such as nitric oxide (on) (5, 4, 10). a uniform shear force tends to shape and align endothelial cells in the direction of flow, while a low shear force, in a hemodynamically oscillator environment, causes an irregular shape and lack of specific orientation. in addition, a small shear stress changes the phenotype of endothelial cells from atheroprotection to atherogenesis with an increased rate of cell turnover. increased arterial blood flow produce adaptive response of arterial wall histology, leading to an increase in vessel diameter and a reduction of shear forces to basic physiological values. however, if the forces are high in one place they can cause a focal enlargement and a widening of arterial wall, process called destructive modeling, which is induced by an excessive production of molecules, such as nitric oxyde (on). the flow dinamics have been studied in a multitude experimental models to better understand there role in aneurysms behavior. patients specific aneurysms geometry study of hemodynamic forces have been accomplished by several authors in last decade. (2, 7, 8). the aim of all these studies is to find the correlation between the geometry of aneurysms and flow pattern. the purpose of our study were to demonstrate the feasibility of development of computational analyses of wall shear stress in cerebral aneurysms from ct angiography images in our hospital. methods data acquisition on the 3d geometry of an aneurysm was achieved, in the first stage by performing ct angiography. ct angiography exploration was done using a ct scanner device aura 2001 philips medical systems (tube counts: 273.000, gantry counts: 1,030,018; workstation: sun ultra 10, mrc 162, 3.5 mhu, software upgrade in 2006, dicom, options: bone, 3d, cta, rapid view reconstruction). image acquisition protocol was achieved by setting following radiographic parameters: maximum allowed tube power 120 kv, 150ma, 15 cm field of view, 1-2 mm collimators with 1:1 pitch and at 0.7 to 1 mm reconsctruction intercalation of 0.5-1 mm range. a total of 100 ml contrast agent (300 mg iodine / ml) was injected intravenously in a brachial vein with a self-acting injector at a rate of injection of 2.5 ml / sec. image acquisition is triggered with a delay of 14 seconds from the time of injection of the contrast. in this way were obtained a number of 90-120 axial images in dicom format with extension. dcm. assembly of these images (*. dcm) and contour transformation of the 2d plane images in a 3d volume was performed with the software avizo v6.3. figure 1. avizo software is used to extract an area of interest as follows: 1. defining the region of interest (roi) 2. vascular sascular surface extraction (aneurysm sought) of the 3d image obtained from ct angiography 3. surfacing by rendering using a bright field of voxel intensity between 90 and 130. establish the precise amount is achieved by trial and error method according to the obtained image quality and dimensional accuracy of the vessels. 4. using isosurface command applied to surface is obtained triangulation (obtaining a number of interconnected triangles) and save it as surface triangles in stereolithography format (stl). 436 s. gaivas et al computational hemodynamics in cerebral aneurysms figure 1 3d volume of cerbral arteries seen in avizo software programe *.stl file extension obtained in avizo is imported in cad software program (computer aided design) solidworks 2011 where is processed by removing additional basic areas file without aneurysm geometry changes. these processing are designed to check the quality of the obtained geometry and optimization of file size, saved in ascii format with the extension (*.sat). this method of reconstruction is the most precise and operator influence on final geometry is minimal (figure 2). figure 2 meshing generation file obtained in gambit is imported in software program fluent v.6.3.26 (ansys. inc.) and processed by preprocessing, processing and postprocessing. preprocessing workload dimensional calibration. the quality meshing check. introduction of blood parameters blood is considered a newtonian fluid with density ρ = 1050 [kg/m3] and dynamic viscosity η = 0.004 [kg / m • s] (poiseuille) although blood has actually nonnewtonian behavior in the simulation it is considered newtonian because there were no significant differences in the distribution of wss (wall shear stress) (11) physiological conditions of blood flow at the entrance have been imposed using the flow measurements in internal carotid artery of a normal patient. measurements were made with a doppler ultrasound at the heart beat rhythm of 70 beats / min. average blood flow speed in the artery was 0.344 [m / s] and peak systolic drop occurred at t = 0.13 [s]. time dependence of the mean flow velocity was represented by following 10 factors: a=2559,3; b=10450; c=19138; d=20959; e=15174; f=7391,9; g = 2320,6; h = 418,15; i = 30,93; j = 0,693; k = 0,191. ktjtithtgtftetdtctbtav  2345678910max (1) where: t systole-diastole complete cycle (between 0-0.75[s]). given that the artery is approximately circular, velocity distribution is considered parabolic in the artery entry, with a maximum into a center of the vessel and a minimum close to the vessel wall. complete equation of speed input section is:                   2 22 max, 1 r yz vv rt (2) where: r inner radius of the vessel in the input, y and z coordinates in the plane of entry. velocity equation v is introduced as a function udf (user defined function) written in c + + programming language. womersley number is a dimensionless number used in fluid mechanics. romanian neurosurgery (2011) xviii 4: 434 441 437 the womersley number is also important in determining the boundary layer thickness formed at the vessel wall, while noting that the end effect can be ignored. womersley number (α) depends on: flow rate, model geometry and newtonian fluid viscosity and varies with vessel diameter at the entrance to each case. womersley number equation is:      2 r (3) where: r [m]-entry of the vessel radius, υ [1 / s] flow rate, ρ [kg/m3] blood density, η [kg / m • s] blood viscosity. exact solution given by womersley may be used to input, since α (small values) is very close to the solution for velocity function v (t, r). flow regime is given by the dimensionless reynolds number (re). this number varies with the diameter of the vessel for each case.   dv  re (4) where: ρ [kg/m3] blood density, v [m / s] maximum speed of blood flow at the entrance, d [m] diameter at the entrance of the vessel, η [kg/m•s]-blood viscosity. depending on this number blood flow values in the model can be: laminar when re ≤ 2300, transient time 2300 <re <10000, turbulent when re> 10000. the reynolds number and womersley number governs the dynamic similarity. processing governing equations were solved in fluent which use finite volume method for spatial discretization conducted in gambit. equations of momentum and mass conservation for incompressible fluid can be written as: 0 v (5)            pvv t v (6) where: zyx          laplace operator, ρ density of blood, v-velocity field, p pressure, τ pressure tensor. speed and pressure interpolations were based on power law and second order respectively. pressure coupling was obtained using speed simplec algorithm. (semi-default method for pressure-linked equations consistency) (5) if flow is laminar, wall shear stress is defined as the velocity gradient at the wall, through the relation: n v w    (7) where τw [pa] tension tangential to the wall, η [kg / m • s] blood viscosity, v [m / s] the speed of blood flow in the vessel wall considered, n normal direction to the vessel wall. the condition for the default time was conducted marking the second order scheme, with a time step δt = 0.001 [s]. it was also used for calculating the maximum number of iterations for a time step of 5. the total time of calculation was 0.75 [s]. peak systolic flow is obtained at t = 0.13 [s] and time averaged reynolds number is denoted by rem. the systolic peak flow reynolds number is denoted by re = remax in the table (see table 13). this number is lower than 2300, so that input can be considered as laminar flow. postprocessing in postprocessing wss values are in [n/m2] = [pa], 1 n/m2 = 0.0075 mm hg; speed v [m / s]. results computational models of 6 intracranial aneurysms have been constructed from ct angiography images. two of six aneurysm 3d reconstructed images are shown in figure 3. after reconstruction and meshing of corresponding anatomical aneurysms images cfd simulation analysis were performed for each of the six aneurysm. average values of wss are calculated throughout the cardiac cycle, but we present maximum values of wss at 0.13 sec (peak systolic) and at 0.6 sec (peak dyastolic). the results of maximum wall shear stress at peak systolic and dyastolic flow and the site of maximum wall hit are shown in table 4. wall shear stress inside the aneurysm dome are shown in table 5. 438 s. gaivas et al computational hemodynamics in cerebral aneurysms table 1 womersley and reynolds number values for aneurysms aneurysm model womersley α reynolds conditions imposed in the cfd simulation rem re aneurysm 1 2,074 214,987 271 laminar flow; without boundary layer aneurysm 2 3,249 336,813 424 laminar flow; without boundary layer aneurysm 3 2,350 243,652 307 laminar flow; without boundary layer aneurysm 4 1,382 143,325 181 laminar flow; without boundary layer aneurysm 5 2,212 229,320 289 laminar flow; without boundary layer aneurysm 6 1,866 193,488 244 laminar flow; without boundary layer reference at t = 0.13 resulting vmax = 0.344 [m/s], and at t = 0.6 resulting vmin = 0.202 [m/s]. table 2 values used for aneurysms table 3 number of elements and quality used for each aneurysms aneurysm model number of mesh elements mesh quality mesh type aneurysm 1 36623 0,9 tetraedral aneurysm 2 19824 0,83 tetraedral+hexaedral aneurysm3 82489 0,81 tetraedral+ hexaedral aneurysm4 232730 0,91 tetraedral aneurysm5 100892 0,81 tetraedral+ hexaedral aneurysm 6 90350 0,8 tetraedral+ hexaedral table 4 wall shear stress at peak systole and dyastole heart beat time aneurysm models 0,13 [s] 0,6 [s] wss [pa] wss [pa] area of max wss aneurysm 1 9,2 5,13 origin of bifurcation aneurysm 2 17,3 10,5 origin of bifurcation aneurysm 3 21,7 12,8 origin of bifurcation aneurysm 4 22,3 13,5 origin of bifurcation aneurysm 5 9,01 5,24 origin of a branch aneurysm 6 6,16 3,68 origin of bifurcation aneurysm model r[m] d[m] ρ[kg/m3] η[kg/m·s] v[m/s] υ [hz] t=0,13 [s] t=0,6 [s] aneurysm 1 0,0015 0,003 1050 0,004 0,344 0,202 1,16 aneurysm 2 0,00235 0,0047 1050 0,004 0,344 0,202 1,16 aneurysm3 0,0017 0,0034 1050 0,004 0,344 0,202 1,16 aneurysm4 0,001 0,002 1050 0,004 0,344 0,202 1,16 aneurysm 5 0,0016 0,0032 1050 0,004 0,344 0,202 1,16 aneurysm 6 0,00135 0,0027 1050 0,004 0,344 0,202 1,16 romanian neurosurgery (2011) xviii 4: 434 441 439 figure 3 reconstructed 3d anurysms models table 5 maximum wss inside the aneurysms time aneurysm models 0,13 [s] 0,6 [s] wss [pa] max wss [pa] max aneurysm 1 0,46 0,25 aneurysm 2 1,15 0,7 aneurysm 3 0,7 0,42 aneurysm 4 0,74 0,45 aneurysm 5 0,3 0,17 aneurysm 6 0,3 0,18 fluid movement is viewed using the intuitive stream lines. these stream lines are representative of the speed in a given time. intra-aneurysmal flow velocity shows a variety of model flow in aneurysms studied. each aneurysm has its unique hemodynamic profile, but many aneurysms have the same characteristics. the most common jet inflow had maximum collision in the aneurysm neck. after impact on the wall of the aneurysms, the inflow jet disintegrate into one or more “whirlpools”, depending on the aneurysm geometry. figure 4 shows different types of flow, represented by stream lines, and different models of whirlpools depending on the geometry of the aneurysm. vortices inside the aneurysms differ from simple single vortices, double to chaotic vortices. figure 4 different types of stream lines and whirlpools inside the aneurysm figure 5 two examples of aneurysms models wtih maximum wss values shown in figure 5 are shown two exemples of computational simulation of wss in aneuryms. maximum wss at peak systole and dyastole differ in all 6 examples of our aneurysm simulation. the value vary from 440 s. gaivas et al computational hemodynamics in cerebral aneurysms 6,16 n/m² to 22,3 n/m² at peak systole cardiac beat. in dyastole the value are more smaller, varying from 3,68 to 13,5 n/m². in all aneurysm models the maximum of wss were at the origin of bifurcation branch see figure 6. inside the aneurysm the value of wss were found to be much lower than in other parts of the segmented region. figure 6 all 6 models of aneurysm simulation wtih the maximum wss at the origin of bifurcation branch discussion computational fluid dynamics is used in many areas, especially in engineering world. this new domain provides very detailed information about fluid caracteristics such as velocity, temperature, and concetration. medical science lent this new technology to study hemodynamics within the body. in cerebral aneurysm cfd help us to understand their formation, growth, ant ruprure through study of aneurysms properties such as geometry, blood flow caracteristics, density, viscosity and velocity. by studying of wall shear stress inside the aneurysms resulting from blood flow its become more clearly how aneurysm has occured. the wall shear stress (wss), play a major role in the growth and rupture of cerebral aneurysms. shojima et al. (13) presented the results of statistical analysis of the magnitude of wss in and around aneurysms. his study show that the magnitude of the wall shear is greatest along the aneurysmal neck, and not at the top or aneurysmal pouch. aneurysms growth is produced at the neck level, where wss value are higher , while aneuryms rupture occures in the aneurysm body, where the wss are lower. wss acts directly on endothelial layer, and modulates endothelial cell function (11). it was found that vascular endothelium regulates arterial wall properties through a mechanism related to blood shear forces and maintain physiological reference wss within 15 to 20 dyn/cm2. this is achieved by endothelial cells that plays an important role in the regulation of pressure in the wssphysiological limits, by initiating a process of vascular remodeling (5). in our models the higher wss were found around the region of the aneuryms neck. inside the aneurysm body were found very lower wss values, which leads us to believe that low flow theory is involved in aneurysm rupture. conclusions we presented a methodology for simulation of intraanevrismal flow in a patient specific models of aneurysms. flow analysis shows that flow model is not similar for all patients. flow characteristics are highly dependent on the geometry of the vessels and aneurysms. these techniques based on computer flow study are important for understanding the relationship between hemodynamic parameters and risk of rupture, and will be very useful since it can be done by routine clinical environment. we made developed an seegmentation algorithm to work with the ct angiography images to perform cfd simulations. romanian neurosurgery (2011) xviii 4: 434 441 441 references 1. castro m.a., putman c.m., cebral j.r. ( 2005) application of vascular cfd for clinical evaluation of cerebral aneurysms. computational fluid and solid mechanics. 2. cebral, j.r., castro, m.a., soto, o., lohner, r., and alperin, n., (2003), “blood-flow models of the circle of willis from magnetic resonance data”, j. eng. math., 47, 369-386 3. drexler h., hornig b. endothelial dysfunction in human disease. j. mol. cell. cardiol. 1999;31:51–60. [pubmed] 4. ferziger jh, peric m. computational methods for fluid dynamics.berlin: springer-verlag; 1997.). 5. gibbons gh, dzau vj. 1994. the emeging concepts of vascular remodeling. n. engl.j. med. 330:1431–38 6. guzman rj, abe k, zarins ck. flow-induced arterial enlargement is inhibited by suppression of nitric oxide synthase activity in vivo. surgery. 1997 aug;122(2):273–280. [pubmed] 7. hassan t et al (2004) computational replicas: anatomic reconstructions of cerebral vessels as volume numerical grids at three-dimensional angiography. ajnr am j neuroradiol 25 (8):1356–1365 8. hassan t et al (2005) a proposed parent vessel geometry-based categorization of saccular intracranial aneurysms: computational flow dynamics analysis of the risk factors for lesion rupture. j neurosurg 103(4):662– 680 9. lasheras j.c. the biomechanics of arterial aneurysms, annu. rev. fluid mech. 2007. 39:293–319 10. luscher, t. f. & tanner, f. c. (1993). endothelial regulation of vascular tone and growth. american journal of hypertension 6, 283—293s. 11. malek a.m. and izumo s. mechanism of endothelial cell shape change and cytoskeletal remodeling in response to fluid shear stress. journal of cell science 109, 713-726 (1996) 12. valencia a, zarate a, galvez m, non-newtonian badilla l. blood flow dynamics in the internal carotid artery with a right saccular j-mutual aneurysm. int methods fluids 2006, 50:751-64.) 13. shojima m et al (2004) magnitude and role of wall shear stress on cerebral aneurysm: computational fluid dynamic study of 20 middle cerebral artery aneurysms. stroke 35(11):2500–2505 romanian neurosurgery (2019) xxxiii, 1: 71-73 doi: 10.33962/roneuro-2019-014 www.journals.lapub.co.uk/index.php/roneurosurgery tibial nerve schwanoma: short review of surgical management guru dutta satyarthee1, luis rafael moscote-salazar2, amit agrawal3 1 department of neurosurgery, neurosciences centre, aiims new delhi, india 2 critical care red latino, latin american trauma & intensive neuro-care organization, bogota, colombia 3 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india, india abstract schwannoma is a benign, solitary nerve sheath tumour and accounting for about 5% of soft tissue tumours. it can occur along the peripheral nervous system in any part of body. it presents as a painless, swelling. we report an adult male presented with tibial nerve schwanoma underwent successful surgical excision. however, differentiation with neurofibroma is very important as surgical planning and prognosis is quite different. in lower limb usually incidence of neurofibroma is higher in contrast of upper limb. pertinent literature and management are briefly discussed. introduction schwannoma represents a benign peripheral nerve tumour, originating from schwann cells [1], [2]. it usually presents as a solitary, slow growing mass. it accounting for about 5% of all soft tissue tumours. iot can present with pain, paraesthesia or rarely with neurological deficit [3], [4], [5]. case illustration an adult male reported presented with complaints of painless mass with paraesthesia and difficulty in sitting on chair for twoyears. local examination showed presence of mass in rthe popliteal fossa, about size of 4cm x5 cm, no compressible, nonpulsatile being mobile along transverse axis burt no mobility in craniocaudal axis. a magnetic resonance imaging was carried out to ascertain the nature, revealed presence of a mass lesion causing expansion of tibial nerve. (fig-1) a provisional diagnosis of peripheral nerve sheath tumour was made and planned for surgical excision. he underwent micro-surgical total excision, intraoperative expansion of the nerve was observed, and nerve fascicles were carefully separated from mass lesion, with electrophysiological nerve monitoring. he had relief in pain and keywords tibial nerve schwannoma, painless mass, surgery, neuroimaging corresponding author: guru dutta satyarthee department of neurosurgery, neurosciences centre, aiims new delhi, india duttaguru2002@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 72 guru dutta satyarthee, luis rafael moscote-salazar, amit agrawal paraesthesia in post-operative period. histopathology of resected specimen was suggestive of schwannoma. discussion tibia nerve is continuations of larger terminal branch of the sciatic nerve with root values of l4, l5, s1, s2, and s3 [1], [5], [6], [7] tibial nerve usually lies superficial to the popliteal vessels, extending from the superior angle to the inferior angle of the popliteal fossa, crossing the popliteal vessels from lateral to medial side [8]. peripheral nerve sheath schwannoma symptoms are related to alteration in the function of nerve and surrounding muscle and neurovascular bundles, and mostly commonly present with paraesthesia or pain of insidious onset and progresses slowly [2]-[4]. pain is a much more common symptom than focal motor or sensory deficits. physical examination may reveal the presence of a mass along the course of the nerve, tender, usually mobile along the transverse axis but limited along the longitudinal course of the nerve, and positive tinel sign [6], [9]. however, pre-operative confirmatory diagnosis of schwanoma usually not possible in most cases but can help in delineating shape, size, location, extent and relation with parent nerve and adjacent neurovascular structures and muscle. imaging plays a limited role in distinguishing among various types of peripheral nerve sheath tumours. magnetic resonance imaging may show presence of fusiform mass with characteristic tapering cephalad and distal ends, fasciculation sign and split fat signs [3], [8], [9]. the mass is well-circumscribed and eccentrically placed, and showing isointense signal on t1weighted images and t2 weighted images shows hyperintense signal and peripheral rim demonstrate hypo-intensity signal representing capsule [3], [5]. after confirmation of diagnosis management of peripheral nerve schwanoma is usually surgical except when the mass is very small and not causing any physical disfigurement. treatment of epineurium encapsulated tumour is microsurgical excision with careful preservation of the nerve fascicles. histopathological examination of specimen provides definitive diagnosis [4], [5]. kim et al. analysed 397 cases of peripheral nerve sheath tumour, out of which 91% were benign and the rest were malignant. a total of 251 were located in the brachial plexus region or upper limb. the peripheral nerve sheath tumor involving lower-limbs included 53 cases of neurofibroma and 32 cases of schwannomas [5]. typically showing the incidence of schwanoma is less than neurofibroma. recurrence is uncommon following total surgical excision. usually surgical excision provides good outcome in view of its benign biological nature and malignant transformation is extremely rare. conclusion tibial nerve schwanoma is raer entity compared to neurofibroma and prognosis and surgical planning should be discussed and prognosticated to patient as imaging may also may not definitely distinguish between neurofibroma, schwanoma. however electrophysiological monitoring is an important aid in preserving neurological outcome. hence, every surgical team member should be always considering the possibility of neurofibroma, schwanoma. 73 tibial nerve schwanoma: short review of surgical management references 1. maleux g, byrs p, samson i, sciot r, baert al: giant schwannoma of the lower leg. eur radiol 1997; 7:1031– 1034. 2. arnold ca, kastrup jj, rogers vp: neurilemoma about the knee: a case report. am j sports med 1999; 27:668–670. 3. blanchard c, dam-hieu p, zagnoli f, bellard s: [chronic sciatic pain caused by sciatic nerve schwannoma]. rev med interne. 2008; 29 (9): 748-50. 4. munakomi s, shrestha p: case report: sciatic nerve schwannoma a rare cause of sciatica. f1000research. 2017; 6. 5. kim dh, murovic ja, tiel rl, moes g, kline dg: a series of 397 peripheral neural sheath tumors: 30-year experience at louisiana state university health sciences center. j neurosurg. 2005; 102 (2): 246-55. 6. wasa j, nishida y, tsukushi s, shido y, sugiura h, nakashima h, ishiguro n: mri features in the differentiation of malignant peripheral nerve sheath tumors and neurofibromas.ajr am j roentgenol. 2010; 194 (6): 1568-74. 7. schreuder hw, veth rp, pruszczynski m, lemmens ja,van laarhoven ew: intraosseous schwannoma (neurilemoma) of the cervical spine. sarcoma 2001; 5:101–103. 8. kehoe nj, reid rp, semple jc: solitary benign peripheral nerve tumors: review of 32 years’ experience. j bone joint surg br 1995; 77:497–500. 9. byun jh, hong jt, son bc, lee sw: schwannoma of the superficial peroneal nerve presenting as sciatica. j korean neurosurg soc 2005; 38:306–308. romanian neurosurgery | volume xxxii | number 1 | 2018 | january-march article anterior skull base meningiomas: surgery related hypothalamic sequalae. how to avoid? ashraf el badry, ahmed nageeb taha egypt doi: 10.2478/romneu-2018-0011 94 | elbadry, taha anterior skull base meningiomas doi: 10.2478/romneu-2018-0011 anterior skull base meningiomas: surgery related hypothalamic sequalae. how to avoid? ashraf el badry, ahmed nageeb taha neurosurgery department, faculty of medicine, mansoura university, egypt abstract: introduction: surgical: morbidities related to anterior skull base meningiomas are widely addressed in the literature and mostly related to tumor relations to cranial nerves and vascular structures in this challenging area. however; there is infrequent complications related to hypothalamic insult either from direct affection or via manipulation of vascular supply of this area. the aim of this study: is to address hypothalamic complications occurred after surgery for anterior skull base meningiomas, pitfalls in our surgical technique and the way to minimize such morbidities. patients and methods: retrospective study was conducted on all patients who did surgery for anterior skull base meningiomas in the neurosurgery department, mansoura university during the period from 2011 to 2016. all the patients clinical and radiological data before and after surgery were analyzed. all patients who developed transient or permeant hypothalamic manifestation were included in this study and data regarding their tumor morphology, surgical technique and post-operative early and late imaging were assessed. results: among 93 patients who did surgery for anterior skull base meningiomas; 12 patients developed post-operative sequalae related to hypothalamic function. in 7 patients; tumor was recurrent and in 4 patients; conformal radiotherapy was given after the initial surgery. complication was transient in 3 patients and permeant in 9 patients. 8 patients died from their hypothalamic sequalae. early post-operative imaging showed hypothalamic infarction in 8 patients. conclusion: through reviewing these cases we can address the importance of many factors in the tumours especially size, morphology, recurrence who increase hypothalamic insults. factors in surgery include preservation of arachnoid plain, perforators, meticulous dissection for minimize this complication. introduction anterior skull base meningiomas represent a challenge in the neurosurgical practice because of difficult anatomical orientation in addition to a required adequate training in frequent surgeries for long time to develop efficient learning curves for better surgical outcomes in such cases. despite progressive advancement in skull base surgery and better anatomical understanding nowadays; surgery for those meningiomas still carry its potential risks due to very close relation to important romanian neurosurgery (2018) xxxii 1: 94 104 | 95 neurovascular including the optic pathway, internal carotid artery (ica) and its branches, the cavernous sinus, the orbit, the pituitary gland and hypothalamus (1,3,4,5,9,11). moreover; the tumor itself has its own challenge including its size whatever small or large tumours (figures 1, 2), consistency and the vascularity. the concept of surgery varies between two options: optimistic and realistic (it doesn’t matter how the patient’s post-operative images in relation to pre-operative ones (figures 3, 4, 5, 6) but what is his post-operative conditions. figure 1 mri brain t1wi axial cuts with contrast revealed homogenous enhanced small sellar and suprasellar tumor figure 2 mri brain t1wi axial cuts revealed aggressive clinoidal meningioma extend to the left orbit figure 3 preoperative mri brain t1wi sagittal cut with contrast showed dorsum sellae homogenous enhanced meningioma figure 4 preoperative mri brain t1wi axial cut of the same case figure 5 post-operative mri brain t1wi sagittal cut with contrast showed complete surgical removal of the dorsum sellae meningioma 96 | elbadry, taha anterior skull base meningiomas figure 6 post-operative mri brain t1wi axial cut of the same case with no residual tumor the potential surgical risks increase if these tumors recur after prior surgery with or without irradiation. proper pre-operative evaluation of the patient clinical, laboratory and imaging study play an important role for proper surgical planning that is crucial for better outcome. surgical morbidities related to anterior skull base meningiomas are widely addressed in the literature. however; there is infrequent complications related to hypothalamic insult either from direct affection or via manipulation of vascular supply of this area. the aim of this study is to address hypothalamic complications occurred after surgery for anterior skull base meningiomas, pitfalls in our surgical technique and the way to minimize such morbidities (2, 3, 4, 7, 10). patients and methods this retrospective study was conducted in the neurosurgery department, mansoura university hospitals. all cases with anterior skull base tumors who were operated up on all over the period from 2011 to 2016 were included in the study. all the pre-operative and post-operative data of the patients (clinical, laboratory and radiological) were evaluated. all the operative data were carefully analyzed. the extent of tumor resection and the patient outcome (early and late outcome) was evaluated. all cases that showed transient or permeant hypothalamic dysfunction related to the surgical procedure were included in this study. out of 182 cases of anterior skull base meningiomas that was operated up on; 9 patients developed either transient or permeant morbidities related to hypothalamic dysfunction. results nine cases (4.9%) out of 182 patients of anterior skull base meningiomas (table 1) developed approach related hypothalamic morbidities. the complication was transient in 3 cases and permeant in 6 cases (two of them died). headache was manifest in all patients, visual impairment in 6 patients and behavior changes in one patient of olfactory groove meningioma. table 1 patient characteristics, tumor characteristics tumor size in mm preoperative c/p meningioma location sex age case number 35 headache visual impairment tuberculum sellae f 43 1 50 headache visual impairment right clinoidal f 51 2 romanian neurosurgery (2018) xxxii 1: 94 104 | 97 40 headache visual impairment diaphragma sellae m 62 3 40 headache visual impairment planum sphenoidale f 59 4 35 headache visual impairment tuberculum sellae f 39 5 50 headache olfactory groove m 63 6 35 headache visual impairment dorsum sellae f 48 7 45 headache inner sphenoid wing f 60 8 65 headache behavior changes olfactory groove m 59 9 among the nine patients who developed surgery related hypothalamic dysfunction; 5 cases were newly diagnosed meningiomas while four cases were recurrent. two of the recurrent cases recurred after only previous surgery resection while the other cases received radiation (conformal 3d radiotherapy and gamma knife radiosurgery) after initial surgery. regarding the surgical approach (table 2) utilized to approach the tumor; 2 cases was operated up on via bifrontal craniotomy, 3 cases via unilateral subfrontal approach, 3 cases via modified cranio-orbito-zygomatic approach and one patient via cranio-orbital approach. total tumor resection was achieved in 4 cases while intra-capsular debulking was done in 5 cases. in one of the newly diagnosed cases (right clinoidal meningioma); the tumor was engulfing the internal carotid artery and with trial of posterior capsular dissection; bleeding occurred from a perforator of the a1 segment of the anterior cerebral artery that was controlled by bipolar cautery. another newly diagnosed tumor (dorsum sellae meningioma); total tumor excision was not feasible and during posterior capsular dissection; one of the perforator was injured and unfortunately coagulated. the other 4 cases with only debulking; the tumor was recurrent and there was a lot of adhesion between the tumor capsule and the surrounding neurovascular structures and getting a safe arachnoid plane of dissection was not easily feasible. total excision was feasible in only one recurrent case (medial sphenoid ridge meningioma). in all the 9 cases; hypothalamic manifestations developed in the early post-operative period. all cases developed diabetes insipidus (transient in 3 cases). 4 cases developed electrolyte disturbances. impaired heat regulation in occurred 2 cases. hypocortisolemia occurred in one patients. impaired level of conscious occurred in two case who died 3 days and one week after surgery. table 2 approach and surgery related hypothalamic complication surgery related hypothalamic complication extent of resection surgical corridor previous treat ment case no transient di total cranioorbital de novo 1) tsm dielectrolyte disturbances inracapsular debulking modified coz de novo 2) rt cm dielectrolyte disturbances hypocortisolemia inracapsular debulking rt subfrontal surgery 3) dsm transient di total modified coz de novo 4) psm 98 | elbadry, taha anterior skull base meningiomas di inracapsular debulking rt subfrontal surgery 5) tsm di total bifrontal craniotomy de novo 6) ogm dielectrolyte disturbancesimpaired heat regulationdied inracapsular debulking rt subfrontal de novo 7) dsm transient di total modified coz surgeryrt 8) inner swm dielectrolyte disturbancesimpaired heat regulationdied inracapsular debulking bifrontal craniotomy surgeryrt 9) ogm discussion meningiomas in the parasellar region represent a great neurosurgical challenge considering highly critical surrounding structures including the neurovascular structures, the hypothalamus, the pituitary gland and its stalk. important neurovascular structures include the carotid artery and its branches, in some cases the basilar artery and its branches, the optic pathway and cranial nerves within the cavernous sinus. the consistency, vascularity and arachnoid plane of dissection play an important role in the potential feasibility for safe tumor resection. if these tumors are recurrent after surgery with or without additional radiation; the potential surgical risks increase (1, 3, 6, 8, 11, 12). the goal of treatment of such meningiomas should be total tumor resection without endangering the surrounding critical structures. with accumulating surgical experience, learning curve development and improvement in the surgical techniques; resection of meningiomas and other parasellar tumors becomes more safely feasible. the initial step for successful surgery for these lesion is proper patient position and adequate approach selection. appropriate approach selection means not only adequate tumor resection but also help the resection to be safe with minimal morbidities and better deal with any intra-operative complications. approaching basal meningiomas necessitate good tumor visualization, minimal brain retraction and feasibility of tumor dissection from important adjacent structures. in our early cases we used the traditional approaches including the unilateral or bilateral subfrontal approaches and pterional approach. although such approaches are enough for good tumor visualization, but it necessitates more brain retraction and in many cases the angle of microscopic visualization is hindered by orbital ridge adding challenge to the safety of adequate tumor removal. by improving the learning curve and better surgical facilities; we prefer more basal approaches using the cranioorbital and cranio-orbito-zygomatic approach (figures 7, 8, 9) which tremendously improved our visualization by providing unobstructed access to the anterior fossa floor from planum to the sella and hence increased our capabilities for safe tumor resection (figures 10, 11, 12, 13) and better function outcome. in our series; we have found that the hypothalamic morbidities occurred not only more frequent but more severe with the traditional approach rather than with the extended transbasal approach and the two cases of mortalities occurred with unilateral and bilateral subfrontal craniotomy (2, 3, 4, 6, 7, 9, 10, 12). romanian neurosurgery (2018) xxxii 1: 94 104 | 99 figures 7, 8, 9 intra operative pictures of orbitozygomatic approach in one of our cases figure 10 pre-operative mri brain t1wi sagittal cut figure 11 mri brain t1wi coronal cut represent a patient had planum sphenoidal meningioma figure 12 post-operative mri brain post contrast t1wi sagittal cut 100 | elbadry, taha anterior skull base meningiomas figure 13 mri brain t1wi coronal cut represent a complete removal of the planum sphenoidal meningioma without hypothalamic infarcture that goes with post –operative patients good condition there are some surgical principles in basal meningioma surgery that facilitate tumor resection without affecting the surrounding structures. first of all adequate skull base bone removal by high speed drill especially greater wing of sphenoid , anterior clinoid process and zygomatic arch in coz approach, this step gave us more room for manipulation without any brain retraction in addition to get wide visual angle when using the microscope. opening the basal cistern for csf drainage allowing tumor exposure with minimal need to apply brain retraction as a result of reduction of brain volume by subtract large portion of csf volume that surround the tumor freeing it from neighbor structures especially in presence of arachnoid plane (liliequist membrane) integrity as in most cases. generous opening of the sylvian fissure from distal to proximal part then deeper by arachnoid knife & micro scissor also facilitate tumor exposure and delineating its relationship to the carotid artery and its important branches (figures 14, 15, 16). with opening the sylvian fissure; the dome & posterior capsule of the tumor comes to our vision and all the important perforators along it are easily identified which wouldn't be feasible if we are approaching midline meningiomas via the classic sub frontal approach without sylvian fissure dissection. adequate intracapsular tumor debulking is mandatory before attempting capsular dissection and following the arachnoid plane of dissection is crucial for safe surgical removal of those meningiomas. absence of arachnoid plane of dissection specially in recurrent meningiomas after previous surgery with or without radiation add more risk to the surgery and increased the chance for post-operative morbidities. another important point is to minimize the bipolar coagulation especially at the posterior capsule where the important perforators of the anterior cerebral artery especially those supplying the hypothalamus lie. this can minimize the risk for postoperative hypothalamic sequalae. capacious irrigation during basal meningioma surgery is very important. it facilitates tumor capsule dissection, minimize the need for excessive cauterization and prevent thermal trauma to the important vascular perforators specially those along the posterior capsule (1, 2, 4, 5, 7, 8, 11, 12). romanian neurosurgery (2018) xxxii 1: 94 104 | 101 figures 14, 15, 16 intraoperative microscopic picture for sylvian fissure opening (from distal to proximal) to show both optics and carotid in our cases with hypothalamic complication; we have four recurrent meningiomas and two of them received radiation after the initial surgical resection and intra-operatively there was no arachnoid plane of dissection was feasible. total excision was only achieved in one case and one case died related to hypothalamic morbidities after surgery. also, we have another case of mortality in a newly diagnosed dorsum sellae meningioma that was operated via right sub frontal craniotomy. during posterior capsular dissection; injury occurred to one of the perforators in the posterior capsule that was coagulated, and the patient also died from hypothalamic sequalae. (figures 17, 18, 19, 20, 21) one of the critical factors that augment the chance of hypothalamic infarcture was over dehydration because of cessation of microcirculation in end perforators to vital brain structures like hypothalamus as a result of reduction of intravascular volume with subsequence reduce the blood perfusion pressure . we gave this issue our attention in our cases through avoidance of lowering the cvp (central venous pressure) than 4 c.m h2o2 from the level of the sternum. (figures 22, 23, 24, 25) 102 | elbadry, taha anterior skull base meningiomas figures 17, 18, 19, 20 preoperative mri brain t1wi (axial, coronal and sagittal) cuts with contrast demonstrate homogenous enhanced dorsum sellae meningioma while figure 17 mri brain t1wi of the same tumor figure 21 postoperative ct brain axial cut showed right hypothalamic hypodese area represented infarction that was the cause of the patient’s mortality figures 22, 23 preoperative mri brain t1wi (sagittal, coronal and cuts with contrast demonstrate homogenous enhanced olfactory groove meningioma romanian neurosurgery (2018) xxxii 1: 94 104 | 103 figure 24 mri brain t2wi of the same tumor figure 25 post-operative mri brain post contrast t1wi sagittal cut represent a complete removal of the olfactory groove meningioma by coz approach and moderate dehydration (cvp 4 c.m h2o2without hypothalamic infarcture that goes with post – operative patients good condition conclusion through reviewing these cases we can address many critical points: •surgery for anterior skull base meningioma is challenging no matter the size of the tumor •good anatomical orientation, adequate training and progressive learning curve is crucial •careful studying of all the pre-operative imaging is important to get all the useful information regarding tumor characteristic and its extension •the goal of surgery should be safe total tumor excision if feasible •we can address the importance of many factors in the tumours especially size, morphology, recurrence who increase hypothalamic insults. factors in surgery include preservation of arachnoid plain, perforators, meticulous dissection for minimize this complication •adequate reconstruction is important step of surgery that significantly affect the outcome. correspondence ashraf el badry, m.d., ifaans address: department of neurological surgery mansoura university hospital, egypt email address: ashrafbadry@hotmail.com or ashrafbadry@mans.edu.eg phone: +201111300033 or +201223477444 references 1. adachi k, kawase t, yoshida k, yazaki t, onozuka s (2009) abc surgical risk scale for skull base meningioma: a new scoring system for predicting the extent of tumor removal and neurological outcome. clinical article. j neurosurg 111:1053–1061 2. bassiouni h, asgari s, sandalcioglu ie, seifert v, stolke d, marquardt g (2009) anterior clinoidal meningiomas: functional outcome after microsurgical resection in a consecutive series of 106 patients. clinical article. j neurosurg 111:1078–1090 3. bassiouni h, asgari s, stolke d. tuberculum sellae meningioma; functional outcome in a consecutive series 104 | elbadry, taha anterior skull base meningiomas treated microsurgically. surg neurol 2006;66(1):37–44, discussion 44–45 4. c.a. bowers, t. altay, w.t. couldwell surgical decision-making strategies in tuberculum sellae meningioma resection neurosurg focus, 30 (2011), p. e1 5. fahlbusch r, schott w. pterional surgery of meningiomas of the tuberculum sellae and planum sphenoidale: surgical result with special consideration of ophthalmological and endocrinological outcomes. j neurosurg 2002;96(2):235–243 6. fatemi n, dusick jr, de paiva, neto ma malkasian d, kelly df: endonasal versus supraorbital keyhole removal of craniopharyngiomas and tuberculum sellae meningiomas. neurosurgery64:5 suppl 2269 286, 2009 7. leland rogers, md, igor barani, md, marc chamberlain, md, thomasj. kaley, md, michael mcdermott, md, jeffrey raizer, md, david schiff, md, damien c. weber, md, patrick y.wen, md, and michael a. vogelbaum, md, phd. (2015) meningiomas: knowledge base, treatment outcomes, and uncertainties. a rano review. journal of neurosurgery 122:1, 4-23. 8. margalit n, kesler a, ezer h, freedman s, ram z.: tuberculum and diaphragma sella meningioma— surgical technique and visual outcome in a series of 20 cases operated over a 2.5-year period acta neurochir (wien) 2007;149(12):1199–1204 9. nanda a, ambekar s, javalkar v, sharma m. technical nuances in the management of tuberculum sellae and diaphragma sellae meningiomas. neurosurg focus. 2013;35(6):e7 10. shrivastava rk, sen c, costantino pd, della rocca r: sphenoorbital meningiomas: surgical limitations and lessons learned in their long-term management. j neurosurg 103:491–497, 2005 11. song sw, kim yh, kim jw, park ck, kim je, kim dg, koh yc, jung hw: outcomes after transcranial and endoscopic endonasal approach for tuberculum meningiomas-a retrospective comparison. world neurosurg. 2018 jan; 109: e434-e445. 12. van alkemade h, de leau m, dieleman em, kardaun jw, van os r, vandertop wp, van furth wr, stalpers lj (2012) impaired survival and long-term neurological problems in benign meningioma. neuro oncol 14:658–666. 11 11elbadryashraf_anterior skull microsoft word 10ojo_unusual romanian neurosurgery (2013) xx 4: 375 378 375 unusual complication of ventriculoperitoneal shunt omotayo a. ojo1, olumide elebute2, okezie o. kanu1, olusegun adebisi popoola 1neurosurgery unit, department of surgery, lagos university teaching hospital, idi-araba, lagos state. nigeria 2peadiatric surgery unit, department of surgery, lagos university teaching hospital, idi-araba, lagos state. nigeria abstract ventriculoperitoneal shunt (vps) is the conventional method of managing hydrocephalus until recently that endoscopic third ventriculostomy is becoming popular. the major disadvantage of vps is the fact that it constitutes a foreign body and prone to complications such as mechanical blockage, shunt infection, shunt migration and rarely shunt protrusion. shunt extrusion through the vagina and anus are rare but have been documented. we present a rare case of shunt migrating through the external inguinal ring into the scrotal sac in a patient. key words: hydrocephalus, hydroceole, ventriculoperitoneal shunt, shunt complications, processus vaginalis. introduction hydrocephalus is defined as an active distension of the ventricular system of the brain resulting from inadequate passage of cerebrospinal fluid from its point of production within the cerebral ventricles to its point of absorption into the systemic circulation.(rekate, 2008) it has a worldwide occurrence and its incidence in the general population as documented in a swedish study is 0.66 per 1000 life births.(persson, anderson, wiklund, & uvebrant, 2007) this rate may however be higher in the developing country such as nigeria because the hydrocephalus of infective etiology is forms a large percentage of total hydrocephalic children.(warf & east african neurosurgical research, 2010) (warf, 2005) the standard treatment of hydrocephalus to date is ventriculoperitoneal shunt. in recent times, the advent of endoscopic third ventriculostomy is gaining popularity due to the high complication and failure rates of ventriculoperitonel shunt.(de ribaupierre, rilliet, vernet, regli, & villemure, 2007) the success rate of vp shunt is in the range of 60 % and its failure rate in literature is close to 40 %.(piatt & garton, 2008) infection rate in vp shunt is close to 20 % while complication rates is about 25.8 % in developing countries.(komolafe, adeolu, & komolafe, 2008) failure rate of vp shunt is high because of the different complications seen after the shunt. the complications of vp shunt include infections, shunt malfunction, shunt mechanical failures include breakage and migration. shunt migration is rare and it commonly migrates to the peritoneal cavity. the rarer presentations of shunt 376 ojo et al unusual complication of ventriculoperitoneal shunt migration include migration into virginal, anus and scrotal sac. we present a shunt migration into the scrotal sac as a result of pre-existing hydrocele that was not taken into consideration before the shunt procedure. case report we present a 15 month old baby who was referred to neurosurgery clinic on account of a swollen left hemiscrotum. he was a product of full term delivery and at 6 months of life, the parents realized there was an occasional swelling of left hemiscrotum. it was only notice while the baby was crying and resolved spontaneously. at 9 months of age, he had an episode of fever following upper respiratory tract infection. he was treated empirically at the peripheral hospital with oral antibiotics. the fever subsided and baby became well. two weeks after he was noted to have a gradual increase in head circumference. a ct scan done showed a pan ventricular hydrocephalus. he was otherwise well. the parents made an emergency arrangement to take him out of nigeria for a ventriculoperitoneal shunt. six weeks after the vp shunt and now in nigeria, left hemiscrotum was gradually increasing in size. a diagnosis of hydrocele was made with possible patent processus vaginalis. no attempt was made to operate on the hydrocele. two weeks before presentation to the neurosurgeon in nigeria, mother reported she could feel a hard tubular structure in the left hemiscrotum. attempt to return to the center oversea where vp shunt was done was futile. he was then brought to us. at presentation, he was a playful child with significant craniofacial disproportion. there was no symptom of increasing intracranial pressure, anterior fontanel was soft and sunken, no other signs of hydrocephalus like distended scalp veins, sun set appearance of the eyes. scars on the scalp and the abdomen signifying evidence of vp shunting. general examination was essentially normal. the abnormal findings were in the inguinal region. inspection revealed a swollen left hemiscrotum. no differential warmth, no tenderness on palpation. the inguinal ring was comparatively wider on the left than on the right. it could conveniently accommodate the tip of the index finger. a coil of abdominal catheter part of vp shunt was palpable. clinical photograph demonstration the distal catheter part of the vt shunt was taken. the only imaging done was an ultrasound scan of the pelvis and the scrotum. the distal part of the catheter was identified. figure 1 baby with left scrotal hydrocele. note the right sub chondrial incisionthe entry point of the peritoneal component of vp shunt romanian neurosurgery (2013) xx 4: 375 378 377 figure 2 distal peritoneal shunt migrating through the left external inguinal ring into the scrotal sac in a baby with pre-existing hydrocele he was prepared for surgery. while he was under general anesthesia, the distal end of the catheter in the left hemiscrotum was manipulated and repositioned intraperitoneally before cleaning and draping. a simple herniotomy was done without exposing the shunt. patient did well after the surgery and swelling did not recall anymore. discussion the most common complication of vp shunt in our setting is infection. this is not different from what is seen in other settings including the developed countries. the incidence of post shunt infection is a nigerian tertiary center is 25.7 % as documented by komolafe et al.(komolafe et al., 2008) other reported incidence ranges from 10-20 %. though its been rarely seen in different neurosurgical centers, the incidence of rarer complications are not documented. there are less than ten documented cases of scrotal migration of distal vp shunt when a search was conducted on pubmed. a patent processus vaginalis is a potential route for distal migration of vp shunt due to increased intra-abdominal pressure. the intra-abdominal component of ventriculoperitoneal shunt wanders around the large peritoneal cavity and a patent processus vaginalis is a possible escape route for the distal tip of the shunt. distal migration of the shunt into scrotal sac is potentially frightening for the parents / guardians of a baby with vp shunt. most parents are not sure what it might be, as they have probably not seen a shunt before and not expected to feel it in the scrotal sac. a proper education of all and every possible complication of vp shunt should be explained at the point of taking consent. a shunt in the scrotal sac potentially keeps the external inguinal ring opened and there is a likelihood of bowel herniation forming an inguinoscrotal hernia. the consequences could be grief with attending obstruction and strangulation. although shunt migration into the scrotum is usually associated with hydrocele as in this case, its treatment is less frightening. simple taxing of the distal shunt by serial manipulations while under anesthesia will ensure the catheter is in the peritoneum without the possibility of contaminating the sterile shunt system at surgery. it is imperative this is done under anesthesia to ensure relaxation just before a simple herniotomy is performed by the pediatric surgeon. with the closure of the external ring and without the exposure of the shunt system, the problem of shunt 378 ojo et al unusual complication of ventriculoperitoneal shunt migration is sorted at the same time that of hydrocele. conclusion shunt complications are many but ensuring the processus vaginalis is not patent before the shunt procedure is done can prevent some rarer ones like migration into the scrotal sac. by inference, all children should be checked for inguinoscrotal hernia as well as inguinal hydrocele before vp shunt procedure is done. in cases where there is hydrocele or inguinoscrotal hernia concomitant with hydrocephalus, herniotomy should be done at the same time of vp shunt to prevent migration of distal shunt to the scrotal sac. corresponding author: dr. omotayo a ojo neurosurgery unit, department of surgery. lagos university teaching hospital, idi-araba, lagos state. nigeria email : tayoojo111@yahoo.com tel: +2348033922181 references 1. de ribaupierre, s., rilliet, b., vernet, o., regli, l., & villemure, j. g. (2007). third ventriculostomy vs ventriculoperitoneal shunt in pediatric obstructive hydrocephalus: results from a swiss series and literature review. childs nerv syst, 23(5), 527-533. doi: 10.1007/s00381-006-0283-4 2. komolafe, e. o., adeolu, a. a., & komolafe, m. a. (2008). treatment of cerebrospinal fluid shunting complications in a nigerian neurosurgery programme. case illustrations and review. pediatr neurosurg, 44(1), 36-42. doi: 10.1159/000110660 3. persson, e. k., anderson, s., wiklund, l. m., & uvebrant, p. (2007). hydrocephalus in children born in 1999-2002: epidemiology, outcome and ophthalmological findings. childs nerv syst, 23(10), 1111-1118. doi: 10.1007/s00381-007-0324-7 4. piatt, j. h., jr., & garton, h. j. (2008). clinical diagnosis of ventriculoperitoneal shunt failure among children with hydrocephalus. pediatr emerg care, 24(4), 201-210. doi: 10.1097/pec.0b013e31816a8d43 5. rekate, h. l. (2008). the definition and classification of hydrocephalus: a personal recommendation to stimulate debate. cerebrospinal fluid res, 5, 2. doi: 10.1186/1743-8454-5-2 6. warf, b. c. (2005). hydrocephalus in uganda: the predominance of infectious origin and primary management with endoscopic third ventriculostomy. j neurosurg, 102(1 suppl), 1-15. doi: 10.3171/ped.2005.102.1.0001 7. warf, b. c., & east african neurosurgical research, collaboration. (2010). pediatric hydrocephalus in east africa: prevalence, causes, treatments, and strategies for the future. world neurosurg, 73(4), 296-300. doi: 10.1016/j.wneu.2010.02.009 12samaci_syringomyelia 220 samanci, celik syringomyelia associated with cervical spondylosis syringomyelia associated with cervical spondylosis: a case report yavuz samanci1, suat erol celik2 1neurosurgery department, ministry of health istanbul training and research hospital, istanbul, turkey 2neurosurgery department, ministry of health okmeydani training and research hospital, istanbul, turkey abstract although cervical spondylosis is an extremely common condition causing spinal cord compression, it is rarely involved in syringomyelia formation. here we describe a case of syringomyelia associated with cervical spondylosis. key words: cervical spondylosis, surgery, syringomyelia. case history a 57-year-old woman presented to our outpatient clinic complaining of left arm pain and weakness, progressing over 2 months. on neurological examination, there was muscle atrophy and dissociated sensory loss in the right arm and hand, and exaggerated reflexes in the upper limbs. the patient was subsequently referred for magnetic resonance imaging (mri). sagittal and axial t1 and t2 weighted sequences through the cervical and thoracic spine were performed. this demonstrated degenerative changes at c5-6 with a left foraminal disc protrusion compressing thecal sac. (figures 1 and 2) an unexpected cord syrinx was noted extending from c5 inferiorly to t1. (figures 1 and 3) the craniocervical junction was normal, with no evidence of chiari malformation. no cord mass lesion was demonstrated, and no other potential cause of syrinx was identified. detailed questioning revealed no evidence to suggest previous spinal trauma or infection. no symptoms consistent with spinal ischemia or infarct were elicited. figure 1 sagittal t1 and t2 weighted images through the cervical spine demonstrating spondylotic changes at c5/6 and caudal syrinx formation romanian neurosurgery (2014) xxi 2: 220 223 221 anterior decompression with stabilization at c5-6 was carried out using a standard peek cage (6mm-12mm). her left radicular arm pain disappeared immediately after surgery. mri at 1 month after the surgery demonstrated remarkable reduction of the syrinx (figure 4). figure 2 axial t2 weighted image at c5-6 level demonstrating a left foraminal disc protrusion figure 3 axial t2 weighted image at the level of c67 demonstrating the large central cord syrinx figure 4 sagittal t2 weighted post-operative images through the cervical spine demonstrating remarkable reduction of the syrinx discussion syringomyelia, cystic cavitation of the spinal cord, is generally associated with congenital malformations as well as trauma and tumors. [1] spinal spondylosis is an extremely common condition that has only rarely been described as a cause of syringomyelia. [2–5] t. milhorat et al. reported 115 cases with non-neoplastic spinal cord syrinxes and there was only one patient whose syringomyelia was initially caused by cervical spondylosis. [2] 222 samanci, celik syringomyelia associated with cervical spondylosis major theories of formation of the cyst are as follows: (1) hydrodynamic theory of gardner [6]: systolic pulsations are transmitted with each heartbeat from the intracranial cavity to the central canal. (2) williams’ theory [7]: maneuvers that raise cerebrospinal fluid (csf) pressure cause “hydrodissection” through the spinal cord tissue. (3) heiss-oldfield theory [8]: occlusion at the foramen magnum causes csf pulsations during cardiac systole to be transmitted through virchow-robin spaces which increases the extracellular fluid which coalesce to form a syrinx. it was lately proposed that subarachnoid obstruction leads to formation of transient increases in csf pressure above the block, compared with below. transmural hydrostatic effects may result in the collapse of vessels within the subarachnoid space above the block, and their dilatation below it. this may result in a combination of mechanical stress on the cord parenchyma and disruption of the blood–brain barrier, which in concert with raised intravascular pressure results in ultrafiltration of crystalloids and accumulation of fluid. [9] the fluid may dissect along planes of weakness within the cord resulting in the pathological appearance of a syrinx. the etiology of syringomyelia in association with cervical spondylosis is not completely understood. unanswered question is “why do patients with varying degrees of degenerative cervical spinal stenosis generally not get syringomyelia?” it may simply be that the degree and/or duration of csf obstruction are not usually great enough in cases of spondylosis to engender a syrinx. in our case, we excluded craniovertebral joint malformation and tumors by neuroradiological examination. the patient had no past history of trauma, tumor, spinal infarction, or meningitis. the absence of any other predisposing causes and our case demonstrating collapse of the syrinx and improvement of related symptoms after surgery suggest that there is a causative link between spondylosis and syringomyelia, rather than a simple coincidence. conclusion the concurrence of cervical spondylosis and syrinx should warrant a detailed medical history and examination of imaging findings to exclude another cause for syrinx formation. in cases of syrinx associated with cervical spondylosis, treatment should be directed toward relieving the compressive lesion, rather than primary drainage of the syrinx. correspondence: yavuz samanci, m.d. neurosurgery department, ministry of health istanbul training and research hospital kasap ilyas mah. org. abdurrahman nafiz gurman cad. fatih phone: +90 (212) 459 6000 fax: +90 (212) 632 0060 34098, istanbul, turkey e-mail: mysamanci@hotmail.com suatmd@gmail.com references 1. batzdorf u. primary spinal syringomyelia. j neurosurg spine 3: 429-435, 2005. 2. milhorat th, johnson rw, milhorat rh, et al. clinicopathological correlations in syringomyelia using romanian neurosurgery (2014) xxi 2: 220 223 223 axial magnetic resonance imaging. neurosurgery: 37:20613, 1995. 3. kaar gf, n'dow jm, bashir sh. cervical spondylotic myelopathy with syringomyelia. br j neurosurg: 10:4135, 1996. 4. rebai r, boudawara mz, ben yahia m, et sl. syringomyelobulbia associated with cervical spondylosis: pathophysiology and therapeutic implications. neurochirurgie: 48:120-3, 2002. 5. kimura r, park y-s, nakase h, et al. syringomyelia caused by cervical spondylosis. acta neurochir: 146:1758, 2004. 6. gardner wj. hydrodynamic mechanism of syringomyelia: its relationship to myelocele. j neurol neurosurg psychiatry: 28:247-59, 1965 jun. 7. williams b. syringomyelia. br med j: 14;1(5693):434, 1970 feb. 8. heiss jd, patronas n, devroom hl,et al. elucidating the pathophysiology of syringomyelia. j neurosurg: 91(4):553-62. 1999 oct. 9. levine dn. the pathogenesis of syringomyelia associated with lesions at the foramen magnum: a critical review of existing theories and proposal of a new hypothesis. j neurol sci: 220:3-21, 2004. microsoft word _2.formatata_toulas.doc romanian neurosurgery vol. xvi nr. 1 9 the importance of functional mri (fmri) in the neurosurgical strategy in brain tumors panagiotis d. toulas m.d. neuroradiologist, institute euromedica-encephalos, athens, greece functional mri (fmri) is an indirect depiction of the functionality of brain neurons using local changes of circulation. the continuous evolution of mri led to pulse sequences which could display the circulation of the brain at rest, with or without exogenous contrast agents. fmri seems capable of determining the dominant hemisphere and the language centers. this is important for the pre-operational evaluation of patients with lesions in the frontal or temporal lobes (tumors or epilepsy resistive to medication), which might have extended centers in these lobes. keywords: epilepsy ,functional mri, brain tumors introduction functional mri (fmri) is an indirect depiction of the functionality of brain neurons using local changes of circulation. historically, the first observations of brain circulation and its changes upon brain activity were made by many investigators during the last decades of the 19th century. in 1890 roy and sherrington published experimental observations that correlated increase of blood circulation in the brain with metabolism and consequently, established the close relationship between neuronal activity and circulationmetabolism of the brain (1). the functional mapping of the human brain was studied during the last few decades with positron emission tomography (pet), single photon emission tomography (spet), imaging methods that use radioisotopes as markers, and magnetoencephalography (meg), a method which measures small variations of magnetic fields in the brain. pet in particular is considered the reference method (gold standard) and measures small local variations in the circulation of the brain during a known task. the method can utilize radioisotopes of oxygen (15o) or fdg (2). this method is not readily available in most laboratories because of the high cost of the equipment and operation of the method. furthermore, technical complications and the relatively high radiation involved in the process limit the method for children. the evolution of mri the 80’s was especially spectacular in neuroradiology, and the use of multiple sequences, acquisition of images in all planes, easy availability, relatively low cost and the steadily increasing number of mr imagers worldwide made mri the method of choice for examining the central nervous system. the continuous evolution of mri led to pulse sequences which could display the circulation of the brain at rest, with or without exogenous contrast agents. the discovery of the blood oxygenation level dependent (bold) contrast of the brain in the early 90’s gave birth to functional mri, a method which found remarkable applications in the last few years. explanation of functional mri (fmri) as was previously stated, fmri is an indirect depiction of neuronal activity. such neuronal activity causes local increase of brain metabolism, therefore increased oxygen consumption. this in turn requires an panagiotis d. toulas romanian neurosurgery vol. xvi nr. 1 10 automatic increase of microcirculation locally, with fresh arterial blood rich in oxyhemoglobin, which can provide the required oxygen. the removal of oxygen from oxyhemoglobin leads to de-oxyhemoglobin, a molecule with paramagnetic properties. all in all, during the process, the accumulation of deoxyhemoglobin, prior to its removal through the venous pathways, acts as a local contrast agent, enhancing signal intensity locally by paramagnetic relaxation. this way a natural contrast agent is acted upon the area responsible for a task and this can be depicted by fmri. technique variations of the signal intensity in fmri depend on the static magnetic field bo, they are rather low in magnitude and they require a high signal to noise ratio (snr) in order to be “visible”. the bold phenomenon increases with magnetic field strength and the variation in signal intensity are of the order of 2-5% for usual high field clinical mr imagers (1.5 tesla) but they can reach 20% for higher strength magnets (3-4 tesla). practically such high strength magnets (3-8 tesla) are ideal for specific uses in neurosciences, although their availability is very low worldwide. most studies nowadays are conducted in commercial mr imagers of 1.5 and 2 tesla. the ideal acquisition technique is echo planar imaging, which has several advantages over traditional gradient echo methods (flash, spgr, etc.) in regard to temporal resolution. the same method is also used in dwi and perfusion imaging, acquiring slices covering the entire brain in 3-5 sec. the higher the gradient strength (>20 mt/m) the more effective epi can be. typically t2*-weighted epi images with te>60 msec are acquired in fmri. classical sequences such as spin echo, flash, spgr, etc, can also be utilized for known areas of brain activity, such as motor center areas of the limbs, vision etc. fmri in general has limitations because of artifacts due either to the patient (motion artifacts) or to magnetic susceptibility, flow, and natural physiological noise. epi is particularly sensitive to magnetic susceptibility variations amongst tissues and with air, which are more visible in the skull base and in areas with prior surgery (eg., biopsy). examination protocol the data are acquired usually with the conventional brain coil. initially some sagittal images are acquired (se or spgr) which are used for localization. subsequently axial and/or coronal t1-weighted are acquired, although a 3d set of thin slices covering the entire brain is preferable so that 3d reconstruction can be used for the superposition of the fmri data. from this point on the “actual” fmri starts with the acquisition of epi-gre t2*-weighted images at the proper brain level. all paradigms involve the activation of one specific area (e.g., motion of one hand), or other specific paradigm (e.g., verbal), for the determination of word centers. at our center we use 5-stage paradigms in which two activation periods of 30 sec each are alternated with 3 periods of brain rest (rest-activationrest-activation-rest), for a total time of 2 ½ minutes. the images are acquired continuously, under the guidance of the fmri specialist, who gives the instructions to the patient for activation and rest during the entire acquisition.activation is inspected in real time,using<<brain weave>>, before the patient is out of the magnet so that additional acquisitions can be added in case of artifacts or failure of the patient to perform properly. for the determination of each major center (e.g. motor center, language, memory, etc.) at least 3-4 paradigms are used, thus a typical fmri examination is 15-20 minutes. typically 500 or more images are acquired for each paradigm used. extended data analysis takes place at a separate workstation using apropriete soft-weare (functool). paradigms with significant artifacts which cannot be removed with the proper statistical analysis are rejected in the pre-treatment stage. the paradigms that pass the first stage of quality control are then analyzed extensively and the activation maps are being formed. there is no consensus yet for the statistical tests and the sensitivity threshold to be used. there are many methods as well as programs for analyzing the fmri data and removal of motion artifacts. once the statistical analysis is finished the the importance of functional mri romanian neurosurgery vol. xvi nr. 1 11 fmri color data are superimposed on high resolution images acquired prior to the fmri acquisition, or to depict the x,y,z coordinates of each activated area in stereotactic maps or atlases (e.g., talairach), which allow a better depiction of the activation areas. it is also possible superimposition with tractography (fusion) that correlate activation areas with mains neuronal tracts(e.g. corticospinal tract). there are possibilities of graphing signal intensity variations versus time for each voxel. clinical applications for the depiction of the motor center of the upper limbs the most common paradigm involves the motion of each finger against the thumb (finger-tapping). in special cases there are other types of motion that can be used, such as opening-closing of the hand successively, turning the hand in prone and supine positions successively, etc. for the feet, the most commonly used motion is that of extension-bending of the toes, because motion of the entire foot is being accompanied by motion of the entire trunk/head, increasing the motion artifacts. if sensory paradigms are required light “brushing” of the hands with a brush can be used. keeping in mind that sensory centers coincide with motor centers in the brain this method can be an alternative for patients that are not capable to perform specific tasks (muscular paralysis, coma, etc.). practically, for patients with a hemispheric tumor in the proximity of the sulcus of rolando two paradigms of the corresponding limbs are enough for the mapping of the primitive motor-sensory areas in relation to the tumor. this requires less than 10 minutes of examination time and 15-30 minutes at the workstation for statistical analysis. pre-operational fmri provides useful information for surgical planning, helping the neurosurgeon avoid critical areas in the proximity of or in the tumor (in cases of infiltrating tumors with some functionality). with neuro-navigational techniques available nowadays neurosurgical planning is even more precise and functional information in relationship to the tumor is very important. the determination of the dominant hemisphere and the depiction of the language centers are being accomplished with special verbal paradigms during which words with a special relationship are being utilized (for example words that start with the same letter, conjugation of a verb, thinking of opposite words, spelling, etc.). in order to minimize motion artifacts all paradigms are acquired silently, with the eyes closed. prior to acquisition of images the whole procedure is explained to the patient and it is certain that it has been understood. for the determination of the language centers we routinely use three paradigms in succession (verb conjugation, opposite word formation, rhyming) and some times we also use recitation in addition, which also adds some memory centers. two paradigms, word and concept formation are enough to determine language centers. fmri seems capable of determining the dominant hemisphere and the language centers. this is important for the pre-operational evaluation of patients with lesions in the frontal or temporal lobes (tumors or epilepsy resistive to medication), which might have extended centers in these lobes. the reference examination up to date has been the wada test, in which the patient receives intra-arterial amobarbital, successively in the two carotids during an angiographic examination and checking the corresponding hemisphere with the patient awake. fmri is risk-free compared to angiography and the wada test and of course repeatable without any limitations in case of failure and the results are comparable to the wada test in the adults as well as in children. other applications-prospects in addition to the aforementioned “practical” applications in pre-operational evaluation of the patient there are more prospects. one of the more used applications is the evaluation of brain plasticity, i.e., the gradual functional rehabilitation after an ischemic or traumatic lesion. being a painless examination and having a relatively low cost allows frequent examinations to be panagiotis d. toulas romanian neurosurgery vol. xvi nr. 1 12 performed in order to evaluate the effects of therapy or the degree of rehabilitation. the evaluation of an epileptogenic focus can also be made with fmri. there is also promise for patients with basal ganglia lesions, dystonia, myotonia, chorea, athetosis, etc. numerous are the newest applications in the diagnosis of neurological and psychiatric diseases and also in the evaluation of the effects of certain drugs. finally, fmri in children is an excellent way of determining the evolution of brain. functional organization of the cortex in various diseases, dysplasias, tumors, or malfunctions such as dyslexia, etc., can hopefully be studied and understood, with the ultimate goal being to reach the proper therapy. conclusions fmri is a new, revolutionary, non-invasive method to study and map the functions of the brain. pre-operational fmri provides important functional information for neurosurgical planning, helping the neurosurgeon avoid critical areas. its use is not limited to preand/or post operated patients but also to other groups of patients and also of healthy volunteers, including children. fig. 1 left hand finger-tapping of a patient with an infiltrating tumor (low grade glioma) putting aside the initial enthusiasm for the ten-year initial results of the method, the rapid development and the multiplicity of the clinical applications of the method, we must not forget that additional work is still required to make the method more reliable, simpler in standardization and analysis. fig. 2 signal intensity temporal dependence (off-on-off-on-off, in 30 second activation-inactivation intervals) fig. 3 verb conjugation paradigm, of 36 year old female patient with low grade glioma the importance of functional mri romanian neurosurgery vol. xvi nr. 1 13 fig. 4 verb conjugation of a 52 year old dyslexic right-handed patient. notice the right hemisphere dominancy references 1.1.d'elia a, melone ga, brogna c, formichella a, santoro a, salvati m. radio-induced low-grade glioma: report of two cases and review of the literature.neurol sci. 2009 ;30(2):137-41. 2.2.douglas-akinwande ac, payner td, hattab em. medulloblastoma mimicking lhermitte-duclos disease on mri and ct. clin neurol neurosurg. 2009 ;111(6):536-9. 3.3.foroglou n, zamani a, black p. intra-operative mri (iop-mr) for brain tumour surgery. br j neurosurg. 2009 feb;23(1):14-22. 4.4.sharma mc, jain d, gupta a, sarkar c, suri v, garg a, gaikwad sb, chandra ps. dysembryoplastic neuroepithelial tumor: a clinicopathological study of 32 cases. neurosurg rev. 2009;32(2):161-9 5.song j, li c, wu l, liu m, lv y, xie g, li l, blanco sequeiros r. mri-guided brain tumor cryoablation in a rabbit model. j magn reson imaging. 2009 ;29(3):545-51. microsoft word 2iencean_normalpressure 240 iencean et al normal pressure hydrocephalus normal pressure hydrocephalus active and passive pathogenic mechanisms st.m. iencean1, al. tascu2, a.st. iencean3, i. poeata1, m.r. gorgan2 1“grigore t. popa” university of medicine and pharmacy iasi, romania 2“carol davila” university of medicine and pharmacy bucharest, romania 3“n. oblu” emergency hospital iasi, romania abstract normal pressure hydrocephalus (nph) is characterized by normal csf pressure, less than 18 cm h2o, classical clinical triad: gait disturbance, dementia and incontinence in patients with communicating hydrocephalus on ct or mri. we analyzed retrospectively the nph hospitalized patients in three neurosurgical departments between july 2007 and december 2012. only the cases who met all diagnostic criteria were selected for this study. there were 47 selected cases of patients with nph, including 24 patients with secondary nph and 23 patients with idiopathic nph. ventriculo-peritoneal shunt was performed in all 24 patients with secondary nph and at 11 patients with idnph. the short-term and long-term results were good and very good for cases of secondary nph and good in 60% and poor in 40% in cases of idnph. the mr imaging showed the absence of csf passage through the ventricular wall and the ventricular wall in cases of idnph with poor results after shunting: ependyma and glia limitans interna represents a fluid parenchymal barrier between the brain parenchyma and the ventricles as a glialependymal barrier. we can consider that secondary nph and some cases of idiopathic nph with repeated small increases of icp, with transependymal migration of csf and hydrocephalus causing clinical triad because of the open glial-ependymal barrier, as an active normal pressure hydrocephalus and the shunt has good results. other cases of idnph have not increases of intracranial pressure, no transependymal migration of csf and there are periventricular deep lesions, without brain atrophy, causing clinical triad, as a passive hydrocephalus, it is a passive normal pressure hydrocephalus. key words: glial ependymal barrier, normal pressure hydrocephalus. normal pressure hydrocephalus (nph) is characterized by normal csf pressure, less than 18 cm h2o, classical clinical triad: gait disturbance, dementia and incontinence in patients with communicating hydrocephalus on ct or mri. clinical triad has been explained on the basis of mechanical factors and ischemic factors. nph probably represents the final common pathway for a number of different disease processes. normal pressure hydrocephalus can be secondary in 50 70 % and of unknown causes in 30 50 romanian neurosurgery (2013) xx 3: 240 – 246 241 %, named idiopathic nph (idnph. the diagnosis and management of idiopathic nph remains unclear because the pathogenesis is unclear. in cases of secondary nph the progressive ventricular enlargement follows of the decrease resorption of csf with known cause and in idnph the progressive ventricular enlargement follows a transient increase in icp, ventricles remain enlarged while icp normalized. many studies showed deep white matter ischemia and hypoperfusion dominant in the frontal areas and improvement after shunt surgery. materials and methods we analyzed retrospectively the 47 nph hospitalized patients in three neurosurgical departments between july 2007 and december 2011; there were 24 cases of secondary normal pressure hydrocephalus and 23 cases of idiopathic normal pressure hydrocephalus. history, clinics and the studies of mri imaging and measurement of intracranial pressure allowed the diagnosis. only the cases who met all diagnostic criteria were selected for this study. in 24 cases of secondary normal pressure hydrocephalus and in 13 cases of idnph we used ventriculo-peritoneal shunts with low or medium differential pressure valve. ten cases of idiopathic normal pressure hydrocephalus were not treated with ventriculo-peritoneal shunt. postoperative follow-up included a monthly clinical evaluation and a computed tomographic (ct) scan or a mri at 6 and 12 months after surgery. results the csf opening pressure in 24 cases of secondary nph were between 8 to 17 mm hg and the clinical results after the ventriculo-peritoneal shunts were very good in 19 cases and good in 5 cases. in cases of idiopathic normal pressure hydrocephalus the csf opening pressure was between 6 to 15 mm hg. the results were : good in 6 cases with csf-op = 10 15 mm hg; poor results in 7 cases with csf -op = 7 13 mm hg and in 10 cases with csf -op = 6 12 mm hg no shunts. figures 1 and 2 show the selected brain ct or mr images of these situations. figure 1 a ct image of secondary nph 242 iencean et al normal pressure hydrocephalus figure 1 b ct image of secondary nph after shunt with a very good clinical result figure 2 a ct images of idiopathic normal pressure hydrocephalus, csf op = 9 mm hg romanian neurosurgery (2013) xx 3: 240 – 246 243 figure 2 b the same case after shunt, but poor result discussions the diagnosis and management of nph remains unclear because the pathogenesis is unclear. in normal pressure hydrocephalus the progressive ventricular enlargement follows of the decrease resorption or absorbtion of csf with known cause in secondary nph and unknown cause in idnph and the progressive ventricular enlargement follows a transient increase in icp, and the ventricles remain enlarged while icp normalized. relkin n, marmarou a et all. in 2005 established diagnostic criteria for idiopathic nph and these are shown below: 1. clinical history: a. insidious onset (versus acute) b. origin after age 40 yr c. a minimum duration of at least 3 to 6 mo d. no evidence of an antecedent event such as head trauma, intracerebral hemorrhage, meningitis, or other known causes of secondary hydrocephalus e. progression over time f. no other neurological, psychiatric, or general medical conditions that are sufficient to explain the presenting symptoms 2. brain imaging a. ventricular enlargement not entirely attributable to cerebral atrophy or congenital enlargement (evan’s index 0.3 or comparable measure) b. no macroscopic obstruction to csf flow c. at least one of the following supportive features 1. enlargement of the temporal horns of the lateral ventricles not entirely attributable to hippocampus atrophy 2. callosal angle of 40 degrees or more 3. evidence of altered brain water content, including periventricular signal changes on ct and mri not attributable to microvascular ischemic changes or demyelination 4. an aqueductal or fourth ventricular flow void on mri 3. clinical gait/balance disturbance a. decreased step height b. decreased step length c. decreased cadence (speed of walking) d. increased trunk sway during walking 244 iencean et al normal pressure hydrocephalus e. widened standing base f. toes turned outward on walking g. retropulsion (spontaneous or provoked) h. en bloc turning (turning requiring three or more steps for 180 degrees) i. impaired walking balance, as evidenced by two or more corrections out of eight steps on tandem gait testing cognition evidence of at least two of the following a. psychomotor slowing (increased response latency) b. decreased fine motor speed c. decreased fine motor accuracy d. difficulty dividing or maintaining attention e. impaired recall, especially for recent events f. executive dysfunction, such as impairment in multistep procedures, working memory, formulation of abstractions/similarities, insight g. behavioral or personality changes urinary continence a. episodic or persistent urinary incontinence not attributable to primary urological disorders b. persistent urinary incontinence c. urinary and fecal incontinence or any two of the following a. urinary urgency as defined by frequent perception of a pressing need to void b. urinary frequency as defined by more than six voiding episodes in an average 12-hour period despite normal fluid intake c. nocturia as defined by the need to urinate more than two times in an average night 4. physiological csf opening pressure in the range of 5–18 mm hg (or 70–245 mm h2o) all our 47 cases met the criteria for inclusion in the group of normal pressure hydrocephalus. analysis of the cases showed that there were good results after shunt in all secondary normal pressure hydrocephalus with all clinical criteria, with csf op between 9 to 17 mm hg and on brain imaging there was transependymal migration of csf. also there were good results in cases of idiopathic normal pressure hydrocephalus with all clinical criteria, with cerebro-spinal fluid pressure : 10 15 mm hg. but there were poor results in cases of idiopathic normal pressure hydrocephalus with partial criteria, with csf op = 6 13 mm hg and without transependymal migration of csf on brain imaging. also the cases with low csf pressure have not been treated with drainage, with poor results. therefore good results have been after drainage in the cases with csf-op : 9 17 mm hg and transependymal migration of csf, with the ventricular walls permeable. it seems the ventricular wall consists of the glia limitans interna and the ependymal wall, is a glial-ependymal barrier or a fluid glial barrier and in these cases this barrier was open. there were poor results in the cases with csf op: 6 13 mm hg and without transependymal migration of csf, as a closed fluidglial barrier. these are cases of idnph with hydrocephalus, but they have not increase of csf op, no transependymal migration of csf as a closed fluid glial barrier and the drainage is not effective. internal hydrocephalus may occur by decreasing or blocking csf absorption. normal pressure hydrocephalus seems to be a particular situation of the internal hydrocephalus caused by blockage of csf absorbtion and the increase of intracranial pressure ( csf op) is small and repeted, without exceeding the normal limits. secondary nph has a known etiology: romanian neurosurgery (2013) xx 3: 240 – 246 245 subarachnoid hemorrhage, meningitis etc. and id nph has the same mechanism of developing for hydrocephalus, but unknown etiology for the blockage of csf absorbtion. in cases of secondary or idiopathic nph, produced by blocking of the absorption of csf, hydrocephalus occurs by increasing of csf pressure ( intracranial pressure = icp). these increases of intraventricular pressure are small and repeated, without exceeding the normal values of icp and they cause clinical symptoms, therefore the ventricular drainage with low pressure valve is effective. passive developed hydrocephalus consists in diminution of brain parenchyma with passive replacement by csf of such increased ventricular space. situations with a progressive deep decrease of the periventricular cerebral parenchyma with slow and passive growth of the ventricular dimensions may correspond to cases of normal pressure hydrocephalus in which the ventricular drainage is not effective and which are commonly included in idnph. therefore in these cases clinical triad results of periventricular parenchymal lesions and the ventricular drainage is not effective. it seems that normal pressure hydrocephalus is a communicating hydrocephalus with two types: nph with open fluid glial barrier when hydrocephalus causing the clinical triad and the shunt is effective, and nph with closed fluid glial barrier, when the periventricular deep lesions causing the clinical triad, as a passive hydrocephalus and the ventricular drainage is not effective. therefore normal pressure hydrocephalus with known or unknown etiology, secondary or idiopathic nph, may present clinically with an open fluidglial barrier, with repeated small increases of icp and transependymal csf and hydrocephalus causes clinics as an active normal pressure hydrocephalus with effective ventricular drainage. this is a form of the internal hydrocephalus when the increases of intraventricular pressure are small and repeted without exceeding normal values of icp. the second clinical form is a normal pressure hydrocephalus with a closed fluidglial barrier, without increases of icp and no transependymal csf without brain atrophy but the periventricular deep lesions causing clinics as a passive hydrocephalus and the ventricular drainage is not effective. this is a form of passive hydrocephalus without brain atrophy, but with deep periventricular parenchyma lesions. there are two different pathogenic mechanisms for these two different clinical forms of normal pressure hydrocephalus, but historically they have been included in the same group because of similar characteristics; also the different therapeutic efficiency of the same traitment is an argument for this differentiation. conclusions diagnosis criteria are very important in normal pressure hydrocephalus. we propose a differentiation of nph whatever the etiology, known or unknown of the blockage of csf absorbtion, but in relation to the clinical pathogenic mechanisms. an active normal pressure hydrocephalus, secondary or idiopathic form, in which there are repeated small increases of icp with transependymal csf 246 iencean et al normal pressure hydrocephalus and hydrocephalus causes clinics and the ventricular drainage is effective. a passive normal pressure hydrocephalus has hydrocephalus, but not increases of intraventricular pressure and the clinic triad is caused of the deep periventricular lesions, without brain atrophy, and the ventricular drainage is not effective. correspondence: tascu alexandru " carol davila" university of medicine and pharmacy bucharest, romania e-mail: tascu_alexandru@yahoo.com references 1. adams rd, fisher cm, hakim s, et al. symptomatic occult hydrocephalus with ‘‘normal’’ cerebrospinal pressures: a treatable syndrome. n engl j med 1965;273:117; 2. mchugh pr. occult hydrocephalus. q j med 1964;33:297–308; 3. bradley wg normal pressure hydrocepohalus: new concepts on etiology and diagnosis. commentary. ajnr. 21 oct 2000; 4. u. meier gravity valves for idiopathic normalpressure hydrocephalus: a prospective study with 60 patients acta neurochirurgica supplementum, volume 95, 2005, pp 201-205; 5. iencean stm. simultaneous hypersecretion of csf and of brain interstitial fluid causes idiopathic intracranial hypertension. med hypotheses. 2003 ;61(56):529-32; 6. iencean stm. idiopathic intracranial hypertension and idiopathic normal pressure hydrocephalus: diseases with opposite pathogenesis?med hypotheses. 2003;61(5-6):526-8; 7. relkin n, marmarou a, klinge p, bergsneider m, black pm. diagnosing idiopathic normal-pressure hydrocephalus. neurosurgery. 2005 ;57 (3 suppl):s416; 8. iencean stm, ciurea av. intracranial hypertension: classification and patterns of evolution. j med life. 2008;1(2):101-7; 9. kiefer m, unterberg a. the differential diagnosis and treatment of normal-pressure hydrocephalus. dtsch arztebl int. 2012 ;109(1-2):15-25; 10. verny m, berrut g. diagnosis of normal pressure hydrocephalus in elderly patients: a review. geriatr psychol neuropsychiatr vieil. 2012 ;10(4):415-425. doi: 10.33962/roneuro-2021-038 spectrum of non-traumatic craniovertebral junction disorders. diagnosis and demonstration with magnetic resonance imaging and multidetector computed tomography neha singh, deepak kumar singh romanian neurosurgery (2021) xxxv (2): pp. 228-233 doi: 10.33962/roneuro-2021-038 www.journals.lapub.co.uk/index.php/roneurosurgery spectrum of non-traumatic craniovertebral junction disorders. diagnosis and demonstration with magnetic resonance imaging and multidetector computed tomography neha singh1, deepak kumar singh2 1 department of radiodiagnosis and imaging, dr ram manohar lohia institute of medical sciences, lucknow, india 2 department of neurosurgery, dr ram manohar lohia institute of medical sciences, lucknow, india abstract introduction: craniovertebral junction is the “zone of transition” between the skull and cervical spine so its detailed discussion is lacking in so many standard textbooks addressing these regions. these anomalies are especially common in the indian subcontinent. accurate diagnosis, probable aetiology and pre-treatment evaluation considerably affect the prognosis of patients. the aim of this study was to classify various craniovertebral junction disorders according to their aetiology and to correlate the imaging findings with the clinical profile of the patients and histopathology whenever possible. methods: this prospective observational study was done in our department over the period of one year from august 2016 to july 2017. 57 north indian patients from all age groups and both sex, who had imaging features suggesting craniovertebral junction pathology were selected for the study. results: our study group comprised 34 males and 23 females with a male to female ratio of 1.47: 1. the most common age group was 11-20 years and the most common aetiology being developmental followed by infective, autoimmune and inflammatory disorders. conclusions: cvj abnormalities are a group of treatable neurological disorders, and are approached with much caution by clinicians. thus, it is crucial that radiologists should be able to make a precise diagnosis, categorize them into etiological groups, and give precise anatomical information on mdct and/or mri, as this information ultimately helps determine the management of such abnormalities and their prognosis. introduction the term craniovertebral junction (cvj) refers to a cone shaped area, the upper limit of which is a line joining the internal occipital protuberance to the sphenooccipital synchondrosis& the lower limit is inferior margin of the body of axis.[15] it is a transition site between keywords cvj anomalies, mdct, atlanto-axial dislocation, basilar invagination corresponding author: neha singh department of radiodiagnosis and imaging, dr ram manohar lohia institute of medical sciences, lucknow, india neha.singh.dr@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 229 spectrum of non-traumatic craniovertebral junction disorders mobile cranium and relatively rigid spinal column. disorders of the cvj present a dilemmatic problem due to presence of neurologically vital structures in the vicinity, potentially unstable articulation and grave prognosis, if gone untreated and undetected. our study is an attempt to systematically classify different cvj abnormalities according to their etiopathogenesis and to describe the importance of accurate diagnosis and precise anatomical information for pretreatment evaluation with multidetector computed tomography (mdct) and/or magnetic resonance imaging (mri). the main objectives of our study were: 1. to evaluate the patients with non traumaticcraniovertebral junction disorders by multiplanar and dynamic imaging utilizing mri and/ or multidetector ct. 2. to classify various craniovertebral junction disorders according to their etiology. 3. to correlate the imaging findings with clinical profile of the patients. 4. to correlate radiological diagnosis with diagnosis after medication /surgery / biopsy whenever undertaken. methods this prospective study was done in department of radiodiagnosis & imaging, ram manohar lohia institute of medical sciences, lucknow, over the period of one year from august 2018 to july 2019.the permission from ethics committee of our institute was taken. written informed consent for the study was obtained from each patient prior to the examination. north indian patients from all age groups and both sex, who underwent mri and / or ct for clinical suspicion of non-traumaticcranio-vertebral junction disorder were evaluated. out of these, 57 patients who had imaging features suggesting craniovertebral junction pathology were selected for the study. contrast enhanced imaging was restricted only to those with suspicion of infective, inflammatory or neoplastic etiology. dynamic scanning in neutral, active flexion and extension posture was done in all cases except in those with atlanto-axial instability. only exclusion criterion was presence of at least one absolute contraindication for mri. mr imaging was performed with a 1.5 t whole body mr imaging system (signa excite gemsow) and the following sequences were obtained: 1. sagittal -t1-weighted spin echo (t1w se), t2weighted turbo spin echo (t2w tse) and t2weighted fat suppressed. 2. axialt1-weighted spin echo (t1w se) & t2weighted turbo spin echo (t2w tse). 3. coronal t2-weighted turbo spin echo (t2w tse). 4. t2w tse in flexion and extension whenever required. 5. contrast enhanced t1w fat saturated (fs) images in axial, coronal and neutral sagittal planes. scanning parameters used for t1w se sequence were a repetition time (tr) of 600 ms and an echo time (te) of 9.7 ms; for t2w tse sequence tr of 4,000 ms and te of 100 ms; for t2w fat suppressed sequence tr of 3,300 ms, te of 110 ms. these sequences were done with slice thickness of 4 mm and spacing of 0.5 mm. ct examination was done on a multislice spiral ct scanner (brilliance ct, phillips medical system, nederland, b.v.5684 pc best). after acquisition of thin axial images, multiplanar reconstruction into sagittal and coronal planes was obtained. craniometric measurements used for radiologic assessment of cvj abnormalities include chamberlain's line, mcgregor line, mcrae line, wackenheimclivus line, fishgold digastric line, fishgoldbimastoid line, welcher basal angle, and atlantooccipital joint axis angle. detailed history of the patients was taken with respect to age, sex, socio-economic status, clinical profile & correlated with the spectrum of craniovertebral junction finding on mri and multislice ct. these patients were followed up to look for clinical outcome after conservative or surgical treatment. statistical methods: statistical analysis was done using ratio and percentages for age and gender distribution. percentage distribution was calculated for each disease affecting the cvj. pearson’s chi square test was used to establish the association between two different anomalies. results our study group comprised of 34 males and 23 females with a male to female ratio of 1.47: 1. maximum number of patients (21) was in the age group between 11-20 years, which included 8 females (34.78% of all females) and 13 males (38.24% of all males). this was followed by 21-30years age 230 neha singh, deepak kumar singh group (12 patients) comprising of 3 females (13.04% of all females) and 9 males (26.47% of all males). figure 1. a) sagittal t2w mri shows platybasia with flattened clivus, blocked c2c3 complex with atlanto-occipital assimilation, aad and bi causing compression over cervicomedullary junction b) sagittal t2w mr shows osodontoideum with aad causing compressive myelopathy. c) sagittal ncct shows shallow posterior fossa with hyoplasticclivus related to basioccipital hypoplasia. a bony arch is noted at the tip of clivus which is continuous laterally with occipital condyles consistent with prebasioccipital arch. d, e, f) sagittal dynamic ncct shows mobile type atlantoaxial dislocation with ossiculumterminale causing cord compression. developmental cause of atlanto-axial diseases most commonly presented in 11-20 year age group (18 patients-40.91%), followed by 21-30 year age group (12 patients-27.27%). none of the patient of 51-60 years presented with a developmental cause, while one of these (2.27%) presented in 61-70 years age group. patients with acquired causes of atlanto-axial diseases most commonly presented in 41-50 years age group (4 patients-30.77%) followed by 3 patients each (23.08%) in 11-20 and 51-60 years age group and 2 patients (15.38%) in 31-40 year age group [table 1]. figure 2. a) sagittal t2w mri shows small posterior fossa with hypoplasticclivus and cerebellar tonsillar herniation causing crowding at foramen magnum with compression over proximal cervical cord causing syringomyelia in cervico-dorsal cord. b) axial non contrast bone window image shows anterior and posterior rachischisis with atlanto-axial dislocation and hypoplastic posterior arch of atlas. figure 3. a) sagittal t2w mr image shows inflammatory granuloma in cervical cord with marked edema involving cord and brainstem. t1w fat sat contrast enhanced b) sagittal image showing contrast enhancement in atlas and axis vertebra with erosion of dens. enhancing granulation tissue is noted adjacent to atlanto-axial joint with a large abscess in paraspinal soft tissue. c) sagittal image showing erosion of dens with mild heterogenous contrast enhancement in anterior atlas arch and axis vertebra. enhancing soft tissue s/o pannus is noted adjacent to atlanto-axial joint with increased atlantoaxial interval. d)axial image shows a well defineddural based lesion with strong homogenous contrast enhancement at c1c2 level on left side causing right lateral displacement and compression of cord. radiological diagnosis of meningioma was made. most common presenting symptom was neck pain seen in 33 patients (57.89%), followed by weakness of both upper and lower limb in 24 patients (42.11%) and neck stiffness in 23 patients (40.35%). these were followed by fever, hemiparesis, sensory symptoms, paraparesis, headache and upper limb weakness. however, weakness of limbs (motor 231 spectrum of non-traumatic craniovertebral junction disorders symptoms) was overall the most common clinical feature present in 35 patients (61%). figure 4. a) sagittal ct shows thickened and ossified posterior longitudinal ligament causing spinal canal narrowing. b) axial t2 flair shows hyperintense signals in left cerebral hemisphere involving cortex and subcortical white matter. diagnosis of acute disseminated encephalomyelitis was made. age developmental percentage (%) acquired percentage (%) 0-10 4 09.09% 1 07.69% 11-20 18 40.91% 3 23.08% 21-30 12 27.27% 0 00.00% 31-40 4 09.09% 2 15.38% 41-50 5 11.36% 4 30.77% 51-60 0 00.00% 3 23.08% 61-70 1 02.27% 0 00.00% total 44 100.00% 13 100.00% table 1. age wise distribution of developmental and acquired abnormalities of cranio-vertebral junction. abnormality no. of cases percentage (%) clivus segmentation 6 10.53% basilar invagination 31 54.39% condylar hypoplasia 1 01.75% platybasia 1 01.75% occipitalization 21 36.84% hypoplasia/aplasia of atlas arches 3 5.26% atlantoaxial fusion 0 00.00% fixed atlantoaxial instability 31 54.39% mobile atlantoaxial instability 4 7.01% cord compression with myelopathic changes 30 52.63% osodontoideum 8 14.02% osterminale 1 01.75% syrinx 4 07.02% tuberculosis 6 10.53% spondyloarthropathy 1 01.75% neoplasms 1 01.75% chiari malformation 7 12.51% inflammatory granuloma with myelitis 1 01.75% c2/c3 block vertebra 5 08.77% thickened calcified pll 1 01.75% adem 2 03.51% table 2. spectrum of cranio-vertebral junction diseases most common disorder was developmental anomalies (46 patients, 80%) followed by infective (7patients, 12.2%), autoimmune (2 patients, 3.5%), inflammatory (1 patient, 1.7%) and neoplastic (1 patient, 1.7%) etiology [table 2]. the developmental anomalies were co-existing and were found in various combinations. overall, atlanto-axial instability was the most common abnormality found in 35 patients (fixed in 54.39% + mobile in 7.02%= 61.4% total) followed by basilar invagination (31 patients, 54.39%) and atlanto-occipital assimilation (21 patients, 36.84%) whether partial or complete (figure 1a). osodontoideum was noted in 8 patients (14.04%) (figure1b) and chiari malformation in 7 (12.5%) (figure 2a). others being, c2/c3 block vertebra in 5 cases (08.77%) (figure 1a). syrinx was found in 4 patients (07.02%) each (figure 2a) and hypoplasia/aplasia/rachisis of atlas arches in 3(5.26%) (figure 2b,c), clivus hypoplasia (figure 1a, 1c,2a) and tuberculosis found in 6 patients (10.53%) each (figure 3b). adem were found in 2 patients each (03.51%) (figure 4b), while condylar hypoplasia, platybasia (figure 1), os-terminale (figure 1 d, e, f), spondyloarthropathy, neoplasm, inflammatory granuloma (figure 3) and thickened calcified posterior longitudinal ligament were found in only 1 patient each (1.75%) (figure 4 a). cord compression with myelopathic changes were observed in abovementioned abnormalities in 30 patients (52.63%) and were most frequently associated with atlanto-axial instability and basilar invagination (figure 1). out of 21 patients with occipitalization, basilar invagination was seen in 19 patients (90.48%) with a p value of <.001 indicating a significant association between the two. basilar invagination also had an important association with atlantoaxial instability as out of 31 patients presenting with basilar invagination, 26 also had atlantoaxial instability with a p value of <.001. out of 23 patients who were operated, 22 completely recovered, while partial recovery and post operative worsening was noted in one patient. rests of the patients were managed conservatively. 232 neha singh, deepak kumar singh one of the patients expired while one patient who presented with isolated syrinx was kept on monitoring. discussion craniovertebral junction (cvj) is a collective term for occipital bone, clivus, atlas, axis, supporting ligaments and underlying part of neural axis (medulla, spinal cord and lower cranial nerves)2. any process congenital, developmental or acquired, which affects these structures, can give rise to abnormalities of cvj. cvj has intricate relationship with the major neurovascular structures which can lead to compression over cervico-medullary junction, lower cranial or spinal nerve and vertebral artery [10]. due to its complex anatomy and relationships, cvj disorders are difficult to treat, so, their proper classification, accurate diagnosis and precise anatomical information is of utmost importance as shown in our study. our study group of 57 patients, revealed male to female ratio of 1.47:1 which correlated well with the study done by rajshree u. dhadve et al & n.j.m. mwang’ombe et al which also showed male predilection and a ratio of 1.6:1 and 2:1 respectively.[6,13] in our study, the most common age of presentation was 11-20 years followed by 2130 years (21 patients, 37%) as compared to the studies by n.j.m. mwangómbe et al and de barrorswhich had a peak in third decade.[13,5] most common presenting complaint in our study was neck pain followed by limb weakness and neck stiffness which was in accordance with most of the previous studies.[6,14] however. mwang’ombe stated that most common symptom was weakness of limbs followed by sensory disturbances, headache and neck pain.[13] the imaging features of cranio-vertebral junction in first decade are confusing as ossification is completed only after 12 years of age[11]. these composite disorders need accurate diagnosis and precise anatomical information by experienced radiologists so that decision for management can be tailored on individual basis. due to complex anatomy of cvj and overlap of many soft tissue structures, plain radiographs create limitations in diagnosis and anatomical delineation.[3] so, we used cross-sectional imaging (mri and ct) for its evaluation. due to its capability of volume rendering and multiplanar reformations, mdct is “state of the art” imaging technique for evaluation of complex osseous anatomy of cvj. mri, due to its high soft tissue contrast resolution and multi-planar capabilities, has turned into the mainstay in radiological evaluation of this region [18]. quantitative assessment of the cvj uses a series of lines and angles, as discussed in material and method, to describe various anatomic relationships. [14] in our study, developmental anomalies were the most frequent etiological group, followed by infective, autoimmune, inflammatory and neoplastic which correlated well with the studies done by bhagwati et al [1] and kale.[10] in our study, atlantoaxial dislocation was most common etiology seen in 61.4% cases which was comparable with results produced by j.s. chopra et al who stated that congenital aad accounted for 51.5–68% of all cvj anomalies.[3] atlantoaxial instability was followed by basilar invagination and occipitalization which correlated well with study by rajshree u. dhadve.[6] compressive myelopathic changes were seen in 52.63% cases which was in accordance with studies by ramen talukdar.[17] os-odontoideum was found in 14.02% which was in correspondence with previous studies.[4] os-terminale was seen in 1.75% of the cases among acquired disorders, tuberculosis was most common entity seen in 6 patients (10.5%) which may be explained by high prevalence of the disease in indian subcontinent and correlated well with study done by ramen talukdar.[17] out of these 6 cases, 4 patients showed erosions and destruction of dens and 2 of anterior atlas arch. atlanto-axial dislocation was noted in 5 patients and basilar invagination in two. prevertebral and paravertebral granulation tissue was seen in 5 cases and frank abscess formation in 2 cases. 3 patients showed extension of granulation tissue/ abscess in anterior epidural space and compressive myelopathy was seen in 2 patients. 2 cases showed involvement of the skull base in form of marrow edema and post contrast enhancement in clivus. involvement of occipital bone was not seen in any of these patients. these findings were in accordance with study by rajshree u. dhadve.[6] cvj involvement in rheumatoid arthritis was noted in one patient who showed erosions of dens and associated fibrous pannus resulting in atlantoaxial dislocation. 233 spectrum of non-traumatic craniovertebral junction disorders in our series of 59 patients, four had syringomyelia and two had chiari i malformation. the later entity was associated with platybasia, flattened clivus, blocked vertebra and atlantoaxial dislocation in 100 % of the cases. scoliosis and platybasia were seen in two patients each which was in accordance with previous studies.[17] one patient had neoplastic etiology of cvj, an extra-axial dural based meningioma. elderly patients (between 50-70 years), who presented with complains of neck pain, headache and walking difficulty, developmental cause was seen in only one patient and acquired causes in 3 patients. bony and ligamentous degeneration explained the above complaints in one patient as imaging revealed ossified posterior longitudinal ligament. our study showed basilar invagination in 90% of the cases who had atlanto-occipital assimilation indicating strong association between these two entities. this association was first noted by by grawitz[9] and has since been reported frequently. [2,12,16,19,7] many articles have regarded atlantooccipital assimilation as a characteristic feature of basilar invagination. similar association was also noted between atlanto-axial instability and basilar invagination. previous studies state micro-trauma due to instability related repeated cord injuries to be the defining factor in the entire pathophysiology of basilar invagination. [8] references 1. bhagwati sn. congenital atlantoaxial dislocation. a study of 99 cases. neurol india,38:317–24,1990. 2. chamberlain we. basilar impression (platybasia). a bizarre developmental anomaly of the occipital bone and upper cervical spine with striking and misleading neurologic manifestations. yale j biol med, 11:487-96, 1939. 3. chopra js, sawhney im, kak vk, khosla vk. craniovertebral anomalies: a study of 82 cases. br j neurosurg, 2:455–6, 1988. 4. dai l, yuan w, ni b, jia l. os odontoideum: etiology, diagnosis, and management. world neurosurg, 53:106109, 2000. 5. de barros mc, farias w, ataide l, lins s. basilar impression and arnold chiari malformation. a study of 66 cases. j. neurol neurosurg psychiatry, 31:596-605, 1968. 6. dhadve ru, garge ss, vyas pd, thakker nr, shah sh, jaggi st, talwar ia. multidetector computed tomography and magnetic resonance imaging evaluation of craniovertebral junction abnormalities. n am j med sci, 7: 62-367,2015. 7. goel a. basilar invagination, chiari malformation, syringomyelia:a review. neurol india, 57(3):235-46, 2009. 8. goel a. instability and basilar invagination. j craniovertebr junction spine, 3(1):1-2, 2012. 9. grawitz p. beitragzurlehre von der. basilaren impression des schadels. arch path anat physiol, 80:449, 1880. 10. kale ss, ailawadhi p, yerramneni vk, chandra ps, kumar r, sharma bs, et al. pediatric bony craniovertebral junction abnormalities: institutional experience of 10 years. j pediatrneurosci, 6:91–5, 2011. 11. karwacki gm, schneider jf. normal ossification patterns of atlas and axis: a ct study. am j neuroradiol, 33: 18821887, 2012. 12. mcrae dl. bony abnormalities in the region of foramen magnum: correlation of anatomic and neurologic findings. actaradiol, 40:335-54, 1953. 13. mwang’ombe n, kirongo gk. craniovertebral junction anomalies seen at kenyatta national hospital. east african medical journal, 77:162-164, 2000. 14. sankhe ss, kumar sk. neuroimaging in craniovertebral anomalies as seen in the tropics. neuroimaging clin n am, 21:879–95, 2011. 15. smoker wr. craniovertebral junction: normal anatomy, craniometry, and congenital anomalies. radiographics, 14:255-27, 1994. 16. spillane jd, pallis ch, jones am. developmental abnormalities in the region of the foramen magnum. brain, 80:11-47, 1957. 17. talukdar r, yalawar rs, kumar m.imaging in craniovertebral junction (cvj) abnormalities. iosr-jdms, 14: 33-49, 2015. 18. utz m, khan s, o’connor d, meyers s. mdct and mri evaluation of cervical spine trauma. insights imaging. 2014; 5:67–75. 19. virchow r. untersuchungen fiber die entwicklung des schadelgrundes. berlin: reimer; 1857. microsoft word 10iacobg_prophylactic.doc romanian neurosurgery (2010) xvii 3: 321 – 326 321 prophylactic antibiotherapy in neurosurgery g. iacob1, simona iacob2 1clinic of neurosurgery, university hospital bucharest romania 2matei bals infectious diseases insitute, university of medicine and pharmacy “carol davila”, bucharest, romania abstract prophylactic use of antibiotics in neurosurgery which mean to use an antibiotic before infection start, to reduce the incidence of postoperative wound infections, still is a controversial issue for strong arguments against the use of antimicrobials: promotion of antibioticresistant strains of bacteria, superinfection and adverse drug reactions prophylaxis has become the standard of care for contaminated, clean-contaminated surgery, insertion of artificial devices. the antibiotic: first/second generation of cephalosporins or vancomicin in allergic patients should recover only the cutaneous posibily contaminating flora (s. aureus, s. epidermidis) and shoud be administrated 30’ before the surgical incision, intravenously in a single dose. most studies pointed that identification of the risk factors for infections, correct asepsia and minimal prophylactic antibiotic regimen adopted to each case, help neurosurgeons to improve patient care and decrease mortality without selecting resistant germens. in conclusion in neurosurgical operations it’s mandatory to assure: an optimum protection at operation by a careful evaluation of asepsia prophylactic antibiotics should be used for 24 hours, after patient consent, using a minimal schema, adapted to each operation risk factors and the patient status prophylactic use of antibiotics is different of antibiotherapy; wide spectrum antibiotics of high dosis and for long term used as standard to cover technical errors should to be avoided. keywords: prophylactic antibiotics, neurosurgery, risk of infection postoperatory infections are a major source of morbidity and letality to surgical patients. a prophilactic use of antibiotics is indicated in surgical operations with risk of infection, where the infection risk cover the risk of using antibiotics, even for those choosed for the contaminated flora. in neurosurgery is generally a low risk of infection comparative with another surgical specialities, only 2-3% (1, 2), liated with surgical strategy, the quality and technological progress. postoperatory infections in neurosurgical cases may become dramatic, rapid evolutive from meningitis, epidural abscess, subdural empyema, brain abscess, ventriculitis to sepsis; which demand to start in cranial or spinal surgery prophilactic antibiotics which has proven to be benefic (3-5). recent studies has proved that prophylactic use of antibiotics in neurosurgery still are controversial, for 322 g. iacob, simona iacob prophylactic antibiotherapy in neurosurgery efficacy only on local infections, less on those systemic, selecting resistent germs, difficult to be treated compared to usual cutaneous flora (6-8, 9). in practical use still is a „fight” between progress in aseptic procedures and abusive use as a „standard” of wide spectrum antibiotics of high dosis and for long term to cover technical errors. this study intend to synthetise a clare attitude for each neurosurgeon to prevent and to treat nervous system infections, to perform a prophylactic use of antibiotics adopted to each case, taking care of general and specific conditions. different of the antibiotic therapy representing the use of an antibiotic in already proved infected operation, antimicrobian prophylaxy mean to use an antibiotic before infection start, to prevent operatory skin contamination with germs representing skin flora as staphilococcus. aureus, staphilococcus epidermidis, propionibacterium acnes or when a minimal contamination of the surgical wound is anticipated generating a subclinic infection. antimicrobian prophylaxy was used in neurosurgery since 1925, before antibiotherapy era, using first hexamine – an antiseptic, than a wide range of antibiotics from penicilin to vancomicine; generally considered as benefic with all generated disadvantages. it’s mandatory to remember that harvey cushing – a pioneer of mondial neurosurgery using only water and soap has an postoperatory infection rate of 1%. since cushing era, all neurosurgeons appreciate a meticulous aseptic techniques valuable in all kind of operations (10,11). the main prophylactic used antibiotics are (table 1): table 1 the main prophylactic used antibiotics antibiotic standard dose iv time for readministration standard dose (h) cefazolin 1-2 g 2-5 cefuroxim 1,5 g 3-4 cephradine 1 g 3-4 clindamicin 600900mg 3-6 amoxicilin/ clavulanat 1,2 g 2-3 ampicilin/ sulbactam 1,5 g 2-3 metronidazol 500mg 6-8 vancomicin 1g in pev >1 ora 6-12 cotrimoxazol 960 mg 12 advantages of prophylactic antimicrobian therapy are: avoid systemic septic complications: meningitis, sepsis or local: celulitis, cerebral or spinal abcesses, osteomielitis. disadvantages of prophylactic antimicrobian therapy are multiple: hepatorenal failure, fever, arterial hypotension, alergic reactions even letal; microbian resistence inducing „superinfections” after wide range antibiotics used for resistent germs or fungus, hospital nosocomial infections, increase hospital treatment costs. antimicrobian prophylaxy in neurosurgery, similar as the anesthesia techniques, should be accepted by the patient, mentioned in the informed consent of the surgical tehnical procedure, less for the emmergency cases, applied after following rules: 1. prophylactic utility of an antibiotic should be limited only to operation! (12,13) 2. use an antibiotic with high concentration in the surgical field during intervention with a restrained spectrum on the skin flora; intravenous admininstration, 30’ prior to skin incision, during anesthesia romanian neurosurgery (2010) xvii 3: 321 – 326 323 induction and discontinued within 24 hours from the end of surgery. for important blood loss > 1500 ml or if operation time surpass, antibiotic half time dosis should be repeted. 3. used dosis is generally the therapeutic one, adapted to corporeal weight the utility of an antibiotic used prophylactic should be corelated to the tissulary bactericide levels during intervention and for the first 3-4 hours in postoperatory suite. another way to use an antibiotic as several days before and after operation it’s not justified and represent the real modality to spread resistance in the hospital environement. if operation time extend for some antibiotics a new dose should be given (table 1). using antibiotics for prophylactic activity there are “general” specifications: liated to the patient, infection risc, surgical technique; also “specific” concerning the type of surgical intervention. a. general specifications risc factors for postoperatory infections: extreme ages, nutritional status, smoking, another infection at distance, immunodepression induced by corticotherapy, citostatics, neoplasia, diabetus, hiv infection, prior transplanted organs; several foreign materials used: shunts, intrathecal catethers, cerebral and spinal electrodes for stimulation or neuromodulation procedures, materials for osteosinthesis, hemostasis and s.o. sources for postoperatory infections (14,15): 1. microbian flora colonising skin is represented in 90% of cases by staphiloccocus aureus, coagulase-negative staphiloccocus speciaes, difteroides, some gram + bacilli as propionibacterium acnes generating shunt infections or gram – bacilli acinetobacter, coliforms. it’s important to be mentionated the coagulasenegative staphilococcus capacity to generate glicocalix, transforming into a biofilm in the host tissue, protecting the patogeneus agent for fagocitosis, blocking the antibiotic action. 2. microbian flora of paranasal sinuses may generate infections for transsphenoidal and cranial base operations: streptococcus pneumoniae, staphiloccocus aureus resistent to meticiline, enterococcus resistent to vancomicine, gram negative bacilli, fungus frequent candida albicans. 3. defectous operating room and postoperatory asepsia, the number of staff or visiting persons in the operation room, ventilation and clima used, the quality of sterilisation for all instruments, surgical materials and gloves used. the type of neurosurgical technique, operations time over 4 hours, reinterventions less than 30 days csf fistula exceed infection risc for 13 times, another infection outside meningeal space may generate an infection risc up to 6 time. skull base surgery, paranasal sinuses, otic cavities, debridement for cerebral lacerations may generate infections outside any statiostics to prevent postoperatory infections several mesures are mandatory: correct hand washing, using the sterile gloves, fixing the mask over the nose, skin shaving on the incision direction, etc b. specific specifications 1. for operations not demanding cranial sinuses opening and in absence of all implants “clean nonimplant procedures”, local flora is represented by: staphylococcus 324 g. iacob, simona iacob prophylactic antibiotherapy in neurosurgery aureus -50%, coagulase negative staphylococcus 15%, gram negative aerobe bacilli 15%, streptococcus spp. 10%, another species < 10%. prophilactic antibiotics should cover all mentioned spectrum, which could be realised by a cephalosporine first or second generation, efficace on gram positive cocci, especially staphylococcus aureus and gram negative bacilli (16). last 20 years studies revealed the efficacy of prophylactic use of antibiotics in “clean” neurosurgical interventions using as narrow an antibiotic spectrum, one dosis, considered to have an antimicrobian activity against specific patogenes agents to neurosurgical department or hospital, as: cephradine 1g i.v., cefuroxime 1,5 g i.v., cefazolin 1 g iv to patients < 80 kg and 2 g to those > 80 kg. if alergia to betalactamines exist, vancomicine 1 g in perfusion should be administrated, lent, at least 1 h before incision (vancomicine has a 1/2 time of 3-9 hours). despite several combinations used: cefazolin and gentamicine versus monotherapie with cefazolin or another antibiotics: piperacillin, cloxacillin, no medication has proved to be superior. another antibiotics used represent a suboptimal chose: -i̇zoxazolilpeniciline (oxaciline, flucloxaciline) can not always cover all staphiloccus species and are inefficace on gram negative bacilli -metronidazol: anaerobe germs are very rare in such interventions -vancomicine with or without gentamicine: there are few multiresitant germs to justify such a prophylaxy -clindamicine (tobramicine) could be an alternative to cutaneous germs, but doesn’t cover gram negative flora. 2. operations demanding aeric cranial sinuses, complex approaches of cranial base, transsphenoidal approaches, transoral approaches “clean contaminated procedures”. in such operations which means crossing naso and oropharynx the local flora is variated, including anaerobes. prophilactic antibiotics should be done using ß lactamines/ß lactamases inhibitors (clavulanat or sulbactam) or metronidazol associations: -amoxiciline/clavulanat 1,2 g iv. in anesthesia induction -cephradine 1 g iv + metronidazol 500 mg iv. in anesthesia induction -cefuroxime 1,5 g iv + metronidazol 500 mg iv. in anesthesia induction for rare selected cases: cefotaxime 1 g iv. to patients < 80 kg and 2g la those > 80 kg. to peniciline alergic patients it is recomanded: gentamicine and metronidazol. 3. different prosthetics devices, inclusive csf shunt „surgery involving insertion of artificial devices” shunt surgery has an infection rate > 3% and all authors recomanded prophilactic antibiotics. there is not a consensus for such a prohilaxy for the antibiotic administration method. postoperatory infections are generated by coagulase negative staphylococcus -90%, staphylococcus aureus 13-27%, gram negative aerobe bacilli 10-20%. prophilactic antibiotics in shunt operations means to use rifampicine + clindamicină impregnated shunts to prevent microbian colonisation also one dosis of cefradine 1 g iv or cefuroxime 1g iv. for ventriculitis vancomicine + gentamicine administrated romanian neurosurgery (2010) xvii 3: 321 – 326 325 intraventriculary are useful for the largest spectrum (17,18). for external shunts, monitoring intracranial pressure, the accuracy of neurosurgical technique are essential, prophilactic antibiotherapy is not nedded. 4. skull fracture, csf shunt surgery for such neurosurgical operations it’s recommended: cefotaxime 1 g iv. to patients < 80 kg and 2g to those > 80 kg or cotrimoxazol 960 mg. meningitis is a severe complication of skull fracture with csf fistula, in 11%-25% of cases, the microbian speciae most frequent encountred are streptococcus pneumoniae. to patients with csf fistula prophilactic antibiotics are not indicated, there is a risk for adverse effects of antibiotherapy for long term use, also for antibiotic resistence (19). 5. in spinal surgery infection rate is low. insertion of artificial devices in spinal operations: osteosynthesis material, catethers and electrodes for pain therapy, it’s recommended: cefazolin 1 g iv to patients < 80 kg and 2 g to those over 80 kg or vancomicine, in case of alergia to betalactamines (20) . in conclusion in neurosurgical operation it’s mandatory to assure (21): an optimum protection at operation by a careful evaluation of asepsia prophylactic antibiotics should be used after patient consent, using a minimal schema, adapted to each operation risk factors and the patient status, for 24 hours prophylactic use of antibiotics is different of antibiotherapy; wide spectrum antibiotics of high dosis and for long term used as standard to cover technical errors should to be avoided. references 1.geraghty j, freely m. antibiotic prophylaxis in neurosurgery. a randomized controlled trial, journal of neurosurgery 1984; 60:724–6 2.tenney j, vlahov d, salcman m, et al. wide variation in risk of wound infection following clean neurosurgery, journal of neurosurgery 1985; 62:243–7 3.young rf, lawner pm. perioperative antibiotic prophylaxis for prevention of postoperative neurosurgical infections. a randomized clinical trial, journal of neurosurgery 1987; 66:701–5 4.bullock r, van dellen j, ketelbey w, et al. a double-blind placebo-controlled trial of perioperative prophylactic antibiotics for elective neurosurgery, journal of neurosurgery 1988; 69:687–91 5.catherine t. yu., loreto j. codamos, et al. antibiotic prophylaxis in non-shunt, clean cranial surgical procedures: a meta-analysis, phil j microbiol infect dis 2000; 29(2) 33-36 6.korinek, a.m.; baugnon, t., et al. risk factors for adult nosocomial meningitis after craniotomy: role of antibiotic prophylaxis, neurosurgery, july 2006, 59(1):126-133. 7.zeina a. k., ghenwa k. d., et al. surgical site infections following spinal surgery at a tertiary care center in lebanon: incidence, microbiology, and risk factors, scandinavian journal of infectious diseases, volume 38, number 8, august 2006, 589 – 592 8.brandt r.a., feres junior h. prophylactic antibiotics in neurosurgery, arq neuropsiquiatr. 1979 mar;37(1): 42-7 9.bullock r, van dellen j, ketelbey w, et al. a double-blind placebo-controlled trial of perioperative prophylactic antibiotics for elective neurosurgery. journal of neurosurgery 1988, 69, 687–691. 10.ashp therapeutic guidelines on antimicrobial prophylaxis in surgery am j health syst pharm 1999;56:1839-1888 11.whitby m.; johnson b.c.; atkinson r.l.; stuart g. the comparative efficacy of intravenous cefotaxime and trimethoprim/sulfamethoxazole in preventing infection after neurosurgery: a prospective, randomized study, british journal of neurosurgery, 2000, vol. 14, nr. 1, 13-18 (6) 12.burke jf. the effective period of preventive antibiotic action in experimental incisions and dermal lesions, surgery 1961;50:161-168. 13.classen dc, evans rs, et al. the timing of prophylactic administration of antibiotics and the risk of surgical wound infection, n engl j med 1992;326:281286 14.mangram aj, horan tc, pearson ml, silver lc. guidelines for the prevention of surgical site infection, 1999, infect control hosp epidemiol 1999; 20:247-280 326 g. iacob, simona iacob prophylactic antibiotherapy in neurosurgery 15.simmons bp. guideline for prevention of surgical wound infections, infect control 1982;3:185-196 16.mccutcheon t., lapointe m., osenbach r.k., haines s.j. choice of antibiotics in the prophylaxis and treatment of common neurosurgical problems, in: batjer h. and loftus c.textbook of neurological surgery, ed. lippincott-raven, philadelphia, 2002, vol 4, 3098-3107. 17.brown em, delouvois j, bayston r, et al. antimicrobial prophylaxis in neurosurgery and after head injury, lancet 1994, 344: 1547-1551 18.langley jm, leblanc jc, drake j, milner r. efficacy of antimicrobial prophylaxis in placement of csf fluid shunts: meta-analysis. clin infect dis 1993, 17: 98-103 19.friedman ja, ebersold mj. persistent posttraumatic cerebrospinal fluid leakage, neurosurg focus. jul 2000, 15; 9 (1). 20.barker, fred g. ii, m.d. efficacy of prophylactic antibiotic therapy in spinal surgery: a meta-analysis, neurosurgery, aug. 2002, 51(2):391-401 21.sharma m.s., vohra a. et al. – effect of riskstratified, protocol based perioperative chemoprophylaxis on nosocomial infection rates in a series of 31927 consecutive neurosurgical procedures (1994-2006), neurosurgery 2009, jun 64(6): 1123-30; discussion 1130-1 microsoft word vonwildklaus_responsibility klaus r.h. von wild, birgit kemper responsibility of neurosurgeons responsibility of neurosurgeons in cooperation with clinical neuropsychologists to accomplish full social re-entry and good hrqol for patients following acute brain damage klaus r.h. von wild, birgit kemper* professor of neurosurgery, medical faculty westphalia wilhelm’s university, münster, d professor of reconstructive neurosurgery of brain and spinal cord lesions, ini, hannover, d professor h. c. department physical rehabilitation al azhar university, cairo egy *head neuropsychologist, special unit for early neurosurgical rehabilitation, clinic for neurosurgical, director prof. dr. med. uta schick , clemens hospital, academic hospital of the medical faculty w.w.-university, münster, d abstract objectives: physical neurologic and neuropsychological rehabilitation has an old tradition in europe. clinical recovery of physical neurological impairments following acute brain damaged do not guarantee successful social re-entry when overlooking long-lasting mental – cognitive, behavioural deficits after clinical demission. problems in emotional adjustment are long-lasting and hinder social re-entry. patients and methods: transdisciplinary early neurorehabilitation is based on careful physical and mental cognitive diagnostics for an individualized therapeutic intervention, when neuropsychology is essential in patients with brain lesions. the role of individually planned early neuropsychotherapy is underestimated when dealing with patients catastrophic reactions as first described by kurt goldstein. this was exemplarily demonstrated in a patient with severe higher cortical functioning disturbances after acute intracerebral haemorrhage and coma, followed by secondary hydrocephalus and major emotional adjustment behavioural disturbances. results: the 65 years old business man, who suffered from persisting complex mental-cognitive, behavioural, mood and emotional disturbances recovered full social competence due to professional neuropsychological neuropsychiatric treatment. discussion: early catastrophic reactions and fear of loss of self-identity are important key issues in the emotional adjustment after brain damaged. further research is needed to explaining the links between loss of self-esteem, self-identity and the development of depression. attention needs to be focused on a recovery beyond functional outcome. conclusion: neurosurgical-neuropsychological rehabilitation is a method to reconstruct lives within a social context. keywords: intracerebral haemorrhage, mood disorders, neurosurgicalneuropsychological rehabilitation, psychotherapeutic intervention secondary hydrocephalus, stroke depression romanian neurosurgery (2011) xviii 2 introduction “brain damage has become synonymous with loss of skills, while rehabilitation of brain-damaged individuals has become known as a method to restructure life within a social context” quotation a.l. christensen (p. xv, kluwer acad. press 1988) recently there has been growing interest in the topics of mood disorders after traumatic brain injuries and cerebrovascular diseases (jorge, starkstein & robinson, 2010; lökk & delbari, 2010; robinson, 2010; whelangoodinson et al. 2009; whealangoodinson et al. 2010). it is well known that the severity of depression and neurocognitive impairments in brain injured patients have an impact on the response to rehabilitation, functional recovery, long-term community reintegration, mental well-being and life satisfaction (bullinger et al. 2002, carod – artal & egido, 2009; donellan et al. 2010; green & king, 2010, von steinbüchel et al., 2010; west et al. 2010). emotional and behavioural disturbances after cerebrovascular diseases can be summarized as post-stroke depression and mania, poststroke anxiety disorders, post-traumatic stress disorders and personality changes with special emphasize on apathy (dafer et al. 2008; hama et al. 2007). the varied prevalence rates for depression in stroke patients from 20-50%, with an apparent peak within the first six months of the onset of event, depend on the one hand on study design, diagnostic assessment tools, and time elapsed after stroke onset (hackett et al. 2005; whyte et al. 2004). on the other hand, in many cases pseudodepressive mood disorders in the acute stage are also classified simply as „depression“ without taking into account the differential diagnosis of catastrophic reactions in the sense of kurt goldstein (1948), pseudobulbar affect, apathy and anxiety. although some patients show complete or nearly complete physical recovery following cerebrovascular insults, they may have profound and long-lasting residual neuropsychological deficits and even an increasing risk of developing neuropsychiatric disorders. this raises the question of how the interaction of manifold cognitive disturbances, e.g. attention, memory and language impairments, executive dysfunctions, and kind of emotional coping among these populations, influence their subjectively perceived health. although it is well known that depression may interfere with both functional recovery and long-term social outcome, psychotherapeutic outpatient services and the development of psychotherapeutic approaches for brain injured populations are rare. an explanation could be that the effectiveness of psychotherapy in brain injured patients has controversially been discussed for years (christensen & rosenberg, 1991; judd & wilson, 2005). disorders of self-awareness and the severity of neurocognitive impairment were thought to be a complete contraindication for psychotherapeutic interventions. psychotherapy today is often part of a holistic approach, developed with the main aim of integrating issues such as cognitive rehabilitation and return to work with special attention to identity and awareness changes (coetzer, 2008). especially patients with traumatic brain injury and post-stroke may benefit from these programs. research on psychosocial treatments for depression in non-stroke and stroke population has focused on the impact of klaus r.h. von wild, birgit kemper responsibility of neurosurgeons cognitive and behavioural therapy and problem-focused therapy (broomfield et al. 2010; mynors-wallis et al. 1995; mynorswallis et al. 1997). the role of nursing in stroke survivors was considered important, but therapeutically nonspecific (kirkevold, 2010) in our opinion these programs do not offer adequate interventions for patients who are searching for answers to questions such as what makes life meaningful after suffering completely unexpected brain damage while struggling with reduced self-esteem, grief and deep fear of loss of the individual’s historical view of himor herself. the outcome of psychotherapy after traumatic brain injury and other kind of brain damage, e.g. vascular, hydrocephalus compression, should be discussed against the background of complex interactions of the therapeutic bond, the patient's preinjury personality, injury variables, the selection of special psychotherapeutic elements and the dynamic of the therapy process itself. therefore some authors demand a theoretical core model to guide psychotherapeutic practice and research in brain injured patients (coetzer, 2007). the authors stress that one has to be aware of the strengths and limitations of psychotherapy after acute brain lesions, and that careful selection of patients for psychotherapy is an essential part within holistic neurorehabilitation management (prigatano, 1995; klonhoff, 2010). this can exemplarily be demonstrated by the case report below, in which a 65-year old business man developed a catastrophic reaction, moderate clinical depressive symptoms, and neurocognitive deficits especially in attention and memory four months after his cerebrovascular accident. our psychotherapeutic attitude and interdisciplinary thinking in our neuropsychological work are influenced by the pioneering work and humane rehabilitation approach of goldstein and by prigatano' s principles of neuropsychological rehabilitation (goldstein 1948; christensen et al., 2009, prigatano, 1999). the broad theoretical base, models and practical techniques proposed by barbara wilson also influenced our clinical practice (wilson et al 2009). following the diagnostic procedures we resolved to offer the patient early psychotherapy. case report 1. medical history a 65-year-old very successful businessman, h.w., with an energetic kind of personality, suffered a spontaneous hypertonic mass bleeding in the left cerebellar hemisphere; he was immediately transferred from the neurological department to the nearest neurosurgical hospital. after exclusion of an anomaly of cerebral vessels (e.g. a-v malformation) by angio-cct, a right frontal external ventricular drainage was immediately set in place and left for seven days. during the neurosurgical intensive care treatment the patient regained consciousness (gsc 9, then 11 and 12) and a left cerebellar symptomatology was observed. h.w. was able to interact and communicate with his environment, but he was not oriented to person, place and time. he also showed uncertainties in recognizing close relatives. recovered and slightly oriented (gcs 13, 14 ) the patient strictly refused any kind of further diagnostics and early neurologicalneurosurgical rehabilitation during his post-acute recovery on the internal medical ward, where he had been transferred for romanian neurosurgery (2011) xviii 2 treatment of his high blood pressure and diabetes ii. so after four weeks the patient was sent home. thereafter h.w. had an appointment with the author who had seen the patient as a neurosurgical consultant during the acute stage, having been on cordial terms with the family for some years. the neurological examination was without any deficits while the brain damage, as expected, caused obviously remarkable mental-cognitive and behavioural deficits. hence we started the neuropsychological evaluation as usual. depressive mood turned out to be the patient’s leading complaint. despite the warmth, love, and closeness of his wife who took care of him, it was extremely difficult to convince the gentleman to follow a proper non-medical neuropsychological-behavioural assessment at that time. it was not before six weeks later, upon the neurosurgeon's recommendation, that h.w. underwent his first neuropsychological examination. 2. patient's subjective report cognitive impairment the patient complained of memory problems. he forgot names of well-known customers. he reported that he could not remember telephone conversations in detail. he needed more time for routine activities. he complained of a mental slowness, feelings of visual overwhelming in public facilities, and attention problems during longer conversation and when conducting negotiations with customers. emotional and behavioural changes the patient reported about his tendency to observe every bodily change and his fear to suffer again a sudden cerebral haemorrhage. he felt anxious because he did not understand his obviously reduced toughness and failures in managing his every day and job activities. he could not stop pondering about his health and his future, complained of his deep loss of energy, felt very ashamed of his failures, had a tendency to self-blame, and tried to hide his difficulties. although he was a person enjoying social engagement in his respected role as a businessman in his field, he avoided attending social events and meeting former friends. he questioned most of his life achievements, his identity as a businessman and asked himself if life was still meaningful. asking him about thoughts on committing suicide he negotiated suicidal intentions convincingly. 3. objective neuropsychological test findings the patient was oriented to time and place. he had very vague recollections of the events during his medical treatment at the intensive care unit. an aphasia screening (token-test) showed no abnormal results. the patient's speech was fluent, but results of a word fluency task were reduced (benton word fluency). subtests of the german aachener aphasia test battery comprising naming, reading and writing were completely in the normal range. measures of premorbid intellectual functioning by means of a vocabulary test (mwt-b) suggested that his premorbid iq had most likely been 100 to 110. a computerized diagnostic of basic attention function (tap) demonstrated slow reaction times in an alertness task and a go/no-go test. the patient was overtaxed by a complex divided attention task. further tests of memory function revealed normal results on verbal and non verbal digit span forward and backward. on the rey auditory verbal learning test all test parameters (initial production, learning, immediate und delayed recall, recognition) klaus r.h. von wild, birgit kemper responsibility of neurosurgeons demonstrated results in the abnormal range. non-verbal memory tests also revealed considerable impairments in learning and visual retention (dcs, benton-test). 4. behaviour and communication characteristics during the neuropsychological assessment. during the first brief diagnostics of basic cognitive functions the patient realized his cognitive failures and showed a catastrophic reaction as described by goldstein. during assessment he showed a short moment of deep tearfulness and then refused vehemently to go on with the cognitive tests. he became angry with the therapist, affronted her for her choice of tests which she might do with children. he questioned her academic qualification. after supportive therapeutic interventions, mirroring the perceived tension and expressing understanding of his anger, the patient apologized. it was remarkable that the patient was not able to talk about how he experienced his failures on an emotional level. he never used words like sadness or desperation etc. the therapist's impression was that h.w. fought with himself in order not to lose all his emotional control and tried to present himself as an invulnerable human being. in his role as a solicitous, energetic kind of businessman he wanted also to be the manager of the therapeutic situation. when the therapist undertook a more direct part in the communication, the patient showed a moderate flight of ideas. this approach evoked his defensive denial disturbing the therapeutic communication process. in this context the patient talked about affairs of the hospital and about things happening in the world. he inquired for the therapist's private life. flirtatious behaviour changed with a dominant attitude towards the neuropsychologist. asking him about his relationship with his wife after the haemorrhage, he demanded from the therapist not to speak of and involve her. at the end of the assessment the patient rejected vehemently psychotherapeutic support and treatment options in other rehabilitation centres. after consulting the author neurosurgeon again, towards whom he demonstrated deep respect, the patient came back three weeks later and wanted at least to try to participate in psychotherapy. 5. psychotherapeutic procedure a short overview (see table 1) shows relevant aspects of the medical history and neuropsychological assessment according to a scheme to be found in different case reports of prigatano (1999). results of the diagnostics revealed that neurocognitive deficits have an impact on the perceived health, but the subjectively experienced threat and the resulting catastrophic reaction of the patient's self are most relevant for his emotional suffering. the social withdrawal could pose a higher risk for developing permanent neuropsychiatric disorders and eventually increase the risk of committing suicide. in our opinion h.w. was an eligible candidate to benefit from psychotherapy. he exhibited excellent higher order language skills needed for a verbally mediated kind of therapy. he showed good behaviour control and he did not suffer from anosognosia. despite moderate cognitive impairments in attention and memory, he was able to manage his activities of daily life independently. romanian neurosurgery (2011) xviii 2 table 1 clinical summary of the patient who experienced dimension content history a spontaneous hypertonic mass bleeding in the left cerebellar hemisphere with infiltration into the fourth ventricle and consecutive obstructive hydrocephalus (emergency cct, neurological clinic) at the age of 65 years. patient evaluated during an outpatient consultation, neurological diagnostics without any evidence of functional impairments interview highly ambivalent towards neuropsychological assessment, spontaneous mentioning of cognitive failures “projected” information “you can't help me. i am coming because professor von wild has sent me.” phenomenological experience “i don't know why i feel so much without energy and have difficulties in doing simple things. i am just a silly person. behaviour and emotional/ motivational characteristics during testing catastrophic reaction, rejecting further cognitive tests, self-blame, peevishness towards the therapist, very reduced ability in emotional self-perception, irritable, feeling ashamed of his test results conclusions reactionary catastrophic reaction, symptoms of depression and anxiety neuropsychological moderate attention and memory deficits, excellent preserved language functions, defensive denial towards all recommendations of non-medical treatment options characterological personality solicitous energetic kind of patriarchically structured duteous, very emotionally controlled person we considered four kinds of therapeutic steps in our phases of treatment, constituting the process over six months. the steps were used flexibly in a nonhierarchical way during the therapy. in summary, in our procedure we focused on 1. therapeutic alliance, 2. education about kind and nature of the neuropsychological disorders, 3. supportive psychotherapeutic interventions, 4. computerized cognitive training, and 5. development of compensatory techniques for the management of memory problems during the first month the patient came twice a week, then once a week. every therapy session was limited to 60 minutes. as mentioned above, h.w. was found to be difficult to engage in the therapy because of his denial due to his anxiety and his deep shame of needing psychotherapeutic support, which was not compatible with his premorbid self-identity. klaus r.h. von wild, birgit kemper responsibility of neurosurgeons we believe that the interdisciplinary collaboration between the neurosurgeon and the neuropsychologist at the beginning was a first step to engage the patient in the therapy and to promote the development of a therapeutic alliance, which is a first important step. the therapeutic bond helps an anxious patient to feel safe. the anxiety was expressed by the patient's increased observation of every bodily change and his fear to suffer again a haemorrhage. he was upset and developed irrational fears explaining his difficulties. he sometimes believed that his symptoms could be evidence for a devastating development of alzheimer’s disease. therefore the patient was educated several times on the nature of his neuropsychological impairment. after about three months, his irrational explanations and moments of fear came back again and again. h.w. needed repeated confirmation by his neurosurgeon that the risk for a new bleeding was low. the general fear, the defensive coping strategies of the patient, and the characteristics of his premorbid personality endangered his engagement throughout the whole therapy. during the therapeutic dialogue it became obvious that his fear decreased when the therapist proceeded slowly with a supportive approach. numerous psychotherapy sessions were spent on mourning about his situation and talking about the circumstances of the sudden bleeding, impressions and experiences with physicians in the hospital. the bleeding seemed to be a traumatized event that meant to the patient an extraordinary overwhelming emotional experience in his life close to death. only in two psychotherapy sessions after four months did the patient talk extensively about his past as a businessman, his great success and his ethics in economy, which ended with a surprising emotional outburst and an irrational self-perception (selfdegrading of being nothing now). after such kind of emotional outburst, h.w. released energy to become active in the therapy. he participated in a computerized cognitive training of attention functions. this step represented a great success considering that during the initial neuropsychological assessment the patient had demonstrated a catastrophic reaction. the therapist started with simple tasks to impart success to the patient. this approach motivated the patient to talk more openly about problems in his job and encouraged him to describe his everyday difficulties more precisely. he showed less avoidance when talking about his cognitive impairments. he began to accept being educated on the use of simple compensatory memory aids. he tried different memory aids (e.g. computerized time table, memory book, planning a week, more written notes immediately after important talks). it was obvious that his self-respect increased slowly. he developed a silent feeling of pride to be successful in using the memory techniques and enjoyed the therapist's feedback: “you are really a very good learner”. from a psychological perspective it is interesting that he never mentioned that the compensation techniques were helpful in his everyday life. he increased his working hours to four hours per day and commented on this with “now i am a retired person”. the patient started to participate more actively in his company's business and visited social events more often, together with his wife. when preparing himself, the patient needed further emotional support because of repeated feelings of grief and insight that he romanian neurosurgery (2011) xviii 2 still struggled with cognitive deficits. at the end of psychotherapy h.w. was better able to experience his preserved mental resources. clinically relevant, anxious depressive symptoms were decreased. the patient was on the way to engage in social life again. looking at his achievements in his family and his great success as a businessman over more than 30 years allowed him to change his life-style in his sixties. he experienced that he was definitely able to practice other things that make life worth living. he stopped questioning himself about being worthless. reflection of the psychotherapeutic process in our opinion the greatest challenge was to involve the patient in the therapeutic process, to manage his denial and to minimize the risk of abandoning therapy early. one of the key questions was what can explain the patient's emotional and behavioural changes, which seemed to overcome his depressive symptoms? in our context, the computerized cognitive training had more psychotherapeutic value than impact on the restoration of the functions themselves. acquiring the use of memory compensation aids and computerized cognitive training in the course of the therapy improved his ability to sustain the threatening confrontation with his cognitive deficits. during computerized cognitive training, h.w. also experienced preserved mental resources to help stabilize his self-confidence with a positive influence on his getting involved in social activities again. in small steps h.w. increasingly dared to spend more hours working in his company. it is also important to mention that during the course of the therapy our patient did not give up his denial completely. it is well known that it would be easier for such patients to cope with their denial in a holistic rehabilitation setting including special groups with focus on denial problems. we regret that we could not offer such kind of treatment in our outpatient ward. during psychotherapy we accepted that h.w. arose more superficially his essential subjects of identity in the therapeutic dialogue. it was not possible to discuss openly the sense or non-sense of cognitive schemes, values and beliefs, for instance according to cognitive behaviourally oriented psychotherapy. the avoidance to speak about emotional experiences and his values and beliefs should not per se be interpreted as negative. h.w.'s kind of coping should be understood against the background of his efficiency-oriented premorbid personality. his coping reflected a kind of protection the ambivalent patient needed in his overwhelming emotional life situation. it is remarkable that the patient came to all appointments in spite of his severe ambivalence. our interventions mostly included supportive interventions according to a more clientcentred method. the non-directive therapeutic relationship, the active listening by the psychotherapist and mirroring the patient's different emotional states seemed to reduce his extreme, anxious tension in the post acute state and his pressure to appear always as a perfect guy in the eyes of the therapist. furthermore, the non-confronting approach may help to feel less dependent on other expectations and promote feelings of autonomy that are important in the context of his life role to be a tough businessman in an always leading position. we supported h.w. to be the “leader”, klaus r.h. von wild, birgit kemper responsibility of neurosurgeons because to be a leader is one essential component positioned in his pre-injury self-identity. we also have to consider the impact on mourning about his emotional behavioural changes. mourning is a process of reflection on the essence of something that has been lost (e.g. a relationship, abilities etc.,) but still acts in us (olders, 1989). by passing through the phases of grief, the bereaved person can develop an unconscious ability to change mental structures of meanings about the self (horowitz, et al. 1993) and to develop inner emotional resources. implications for clinical practice complete neurological recovery after brain damage does not imply that mental cognitive and psychiatric functional impairments do not exist. it is well known that mental cognitive and behavioural disabilities are more persistent and count more as a handicap than physical ones. every brain injured person should be screened and repeatedly be carefully assessed for neuropsychiatric disorders and cognitive functioning at different time intervals in a close and trustful cooperation with the next of kin, especially the elderly patients. if patients show emotional adjustment problems one should discuss cautiously if the individual might benefit from psychotherapy. different interventions should be applied without dogmatic focus on psychotherapeutic schools. the main aim of psychotherapy should be to teach the patients to behave in their own best self-interest to avoid chronic manifestation of mood disorders and to promote the patient's quality of life. we hope that our transdisciplinary contribution will help increase awareness of the potential role of psychotherapy in brain injured human beings, outlining the links between denial, psychological distress, self-esteem, grief and loss of self-identities following brain injury (coetzer, 2008; haslam et al. 2008; prigatano, 1991). corresponding author: klaus r.h. von wild prof. prof. h.c. dr.med habil. dr. h.c. frauenburgstrasse 32 48153 münster, germany kvw@neurosc.de fon: +49.251.3977750 fax +49.251.3977751 references 1. broomfield, n.m. laidlaw, k. , hickabottom, e., murray, m.f., pendrey, r., whittick, j.e. & gillespie, d.c. (2010). post stroke depression: the case for augmented, individually tailored cognitive behavioural therapy. clinical psychology and psychotherapy. n/a.doi:10.1002/cpp 711. 2. bullinger, m., azouvi, p. brooks, n., basso, a., christensen, a.l., gobiet, w., greenwood, r., hütter, b., jenett, b., maas, a., truelle, j.l., von wild, k.r. & tbi consensus group (2002). quality of life in patients with traumatic brain injury-basic issues, assessment and recommendations. restorative neurology neuroscience 20 (3-4), 111-24. 3. carod-artal,f. j. & egido, j.a. (2009). quality of life after stroke: the importance of a good recovery. cerebrovascular diseases 27 suppl 1, 204-14. 4. christensen, a-l. & rosenberg, n.k. (1991). a critique of the role of psychotherapy in brain injury rehabilitation. journal of head trauma rehabilitation, 6(4), 56-61. 5. christensen, a-l, uzzel, b. (1988 ). neuropsychological rehabilitation, kluwer academic publihsers boston dordrecht london 6. christensen a-l, goldberg, e, bougakov, d (2009). luria’s legacy in the 21st century oxford university press 7. coetzer, r. (2007). psychotherapy following traumatic brain injury: integrating theory and practice. journal of head trauma rehabilitation 22 (1), 39-47. 8. coetzer, r. (2008). holistic neurorehabilitation in the community: is identity a key issue? neuropsychological rehabilitation 18 (5-6), 766-83. 9. dafer, r. m., rao, m. shareef, a. & sharma, a. (2008). poststroke depression. topics in stroke rehabilitation, 15(1), 13-21. 10. donellan, c., hickey, a., hevey, d. & o`neill, d. romanian neurosurgery (2011) xviii 2 (2010). effect of mood symptoms on recovery one year after stroke. international journal of geriatric psychiatry, 25(12), 1288-95 11.goldstein, k. (1948). after effects of brain injuries in war: their evaluation and treatment. new york: grune and stratton. 12.green, t. l. & king, k. m. (2010). functional and psychosocial outcomes 1 year after mild stroke. journal of stroke cerebrovascular diseases, 19 (1), 10–16. 13.hackett, m. l., yapa, c., parag, v. & anderson, c. s. (2005). frequency of depression after stroke: a systematic review of observational studies. stroke, 36, 1330-40. 14. hama, s., yamashita, h., shigenobu, m., watanabe, a., hiramoto, k., kurisu, k. yamawaki, s. & kitaoka, t. (2007). depression or apathy and functional recovery after stroke. international journal of geriatric psychiatry, 22 (10) 1046-51. 15. haslam, c., holme, a., haslam a., iyer, a., jetten, j. & williams, w.h. (2008). maintaining group membership: social identity continuity predicts well being after stroke. neuropsychological rehabilitation, 18 (5/6), 671-91. 16.horowitz, m.j., bonanno, g.a. & holen, a. (1993). pathological grief: diagnosis and explanation. psychosomatic medicine 55, 260-74. 17.jorge, r. e., starkstein, s. e. & robinson, r. g. (2010). apathy following stroke. canadian journal psychiatry, 55(6), 350-54. 18.judd, d. & wilson, s. l. (2005). psychotherapy with brain injury survivors: an investigation of the challenges encountered by clinicians and their modification to therapeutic practice. brain injury, 19(6), 437-49. 19.kirkevold, m. (2010). the role of nursing in the rehabilitation of stroke survivors: an extended theoretical account. advances in nurse science, 33(1), 27-40. 20.klonhoff, p.s. (2010). psychotherapy after brain injury: principles and techniques. new york: the guilford press. 21.lökk, j. & delbari, a. (2010). management of depression in elderly stroke patients. neuropsychiatric disease and treatment, 7(6), 539-49. 22.mynors-wallis, l. m., gath, d.h., lloyd-thomas, a.r. & tomlinson, d. (1995). randomised controlled trial comparing problem solving treatment with amitriptyline and placebo for major depression in primary car. british medical journal, 310, 44145. 23.mynors-wallis, l., davies, i., gray, a., barbour, f. & gath, d. (1997). a randomised controlled trial and cost analysis of problem-solving treatment for emotional disorders given by community nurses in primary care. british journal of psychiatry, 170, 113-19. 24.olders, h. (1989). mourning and grief as healing processes in psychotherapy. canadian journal of psychiatry 34(4), 271-80. 25.prigatano, g. p. (1991). disordered mind, wounded soul: the emerging role of psychotherapy in rehabilitation after brain injury. journal of head trauma rehabilitation, 6(4), 1-10. 26.prigatano, g. p. (1995). strengths and limitations of psychotherapy after brain injury. advances in medical psychotherapy 8, 23-34. 27.prigatano, g.p. (1999). principles of neuropsychological rehabilitation. new york: oxford university press. 28.robinson, r.g. (2010). neuropsychiatric disorders following stroke. canadian journal of psychiatry 55(6), 339-40. 29.von steinbüchel, n., wilson, l., truelle, j.l., gibbons, h., koskinen, s., bakx, w., bullinger, m., formisano, r., hawthorne, g., maas, a. , neugebauer, e., powell, j. , sarajuuri, j., sasse, n., von wild, k., zitnay, g., and the qolibri group (2010). quality of life after brain injury (qolibri) scale validity and correlates of quality of life. journal of neurotrauma, 27 (7):1157-65 . 30.west, r., hill, k., hewison, j., knapp, p. & house, a. (2010). psychological disorders after stroke are an important influence on functional outcomes: a prospective cohort study. stroke, 41(8), 1723-27. 31.whealan-goodinson, r., ponsford, j., johnston, l. & grant, f. (2009). psychiatric disorders following traumatic brain injury: their nature and frequency. journal of head trauma rehabilitation 24,(5), 324-32. 32.whelan-goodinson, r., ponsford j., schönberger, m. & johnston, l. (2010). predictors of psychiatric disorders following traumatic brain injury. journal of head trauma rehabilitation, 25(5), 320-29. 33. whyte, e. m., mulsant, b. h., vanderbilt, j., dodge, h. h. & ganguli, m. (2004). depression after stroke: a prospective epidemiological study. journal of the american geriatric society, 52(5), 774-78. 34.wilson, b., gracey, f. evans, j. j. & bateman, a. (2009). neuropsychological rehabilitation. cambridge: university press. chiriaca_dural 166 chiriac et al dural arteriovenous fistulas of the cavernous sinus dural arteriovenous fistulas of the cavernous sinus clinical case and treatment a. chiriac, n. dobrin*, st.m. iencean, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi “prof. dr. n. oblu” clinic emergency hospital, iasi* abstract the purpose of our article is to present the results of our treatment of dural arteriovenous fistula of the cavernous sinus by glue embolization of the external carotid artery feeders. by this case presentation we try to clarify the clinical course, with the dural carotid cavernous fistula (ccf), characterizing a pallet of symptoms, paying special attention to radiological finding and endovascular treatment. dural arteriovenous fistulas represent 10% to 15% of all intracranial arteriovenous malformations (a. fox, g. duckwiler, “dural arteriovenous fistula,” presented at the annual meeting of the american society of neuroradiology, st louis, mo, june 1992). dural arteriovenous fistulas are rare clinical situation, especially examples involving the cavernous sinus. most dural fistulas are acquired conditions, typically occurring in postmenopausal women, but sometimes in other patients in association with other condition [1,3]. these dural fistulas are most often “spontaneous” cavernous carotid shunts (usually low-flow) [2, 4, 5], usually related to a past trauma or surgery. the classical triad, represented by pulsating exophthalmos, conjunctival chemosis, and pulsatile-tinnitus are well-known clinical symptoms of these lesions but are not necessary present in the majority of the patients as first indicators. the anatomy of these vascular malformations consists of multiple arterial feeders flowing into cavernous sinus. the arterial feeders are usually meningeal branches arising from the internal carotid artery (ica) or the external carotid artery (eca). however, there are few reports of large series [1], and the clinical entity is not widely known. the purpose of this paper is to present a clinical case of a patient with dural cavernous sinus fistulae, clarify the clinical symptoms course and special attention to results of endovascular treatment. case report a 42-year-old man presented with a 3month history of pulsatile headaches, tinnitus and hyperaemia of left eye. he had a one month history of blurred vision and diplopia in all gaze positions. he declares a history of a head trauma with occipital impact three years ago. the patient was otherwise healthy and was a nonsmoker. romanian neurosurgery (2014) xxi 2: 166 171 167 figure 1 patient photo with affected eye ophthalmological examination revealed conjuctival chemosis with proptosis and arterialisation of the conjuctival blood vessels. patient presents exophthalmia but with no anisocoria. retinal blot haemorrhages and bilateral optic nerve cupping were noted at fundal examination. visual acuity was 20/50 in the right eye and 20/30 in the left eye. the complete neurological and physical examination revealed no other aspects. the patient was investigated by craniocerebral magnetic resonance imaging (mri) and magnetic resonance angiography (arterial tof), performed at an outside institution. these images showed an enlarged left superior ophthalmic vein. cerebral angiography demonstrated a barrow type c indirect ccf supplied by an internal maxillary branches of the left eca. drainage from the cavernous sinus was via superior ophthalmic veins, angular vein and anterior facial vein. there was no cortical venous drainage or drainage to the inferior petrosal sinus from the cavernous sinus. figure 2 mri show an enlarged left superior ophthalmic vein figure 3 anatomy of cranio-facial vein [5] 168 chiriac et al dural arteriovenous fistulas of the cavernous sinus figure 4 dsa images face and profile showing the dural cavernous fistulae figure 5 dsa images showing arterial pedicle microcatheterization and glue injection romanian neurosurgery (2014) xxi 2: 166 171 169 transarterial embolisation via the external carotid arterial feeder was used as it was feared that this might promote a complete occlusion of the fistula. a mixture of 2 ml of lipiodol and gluebran 2 was used to complete occlusion of the dural fistula. a complete remission of symptoms was achieved in 48 hours postintervention. figure 6 dsa images showing total dural cavernous fistulae acclusion discussion a correct diagnosis of a dural cavernous sinus fistula is clinically difficult and may take long time. usually, there are low-flow fistulas with no severe symptoms as in traumatic highflow cavernous sinus fistulas. most patients do not have bruit or pulsatile exophthalmos, which indicate a vascular lesion. however, diagnosis should always be considered in patients with a red eye and arterialized episcleral vessels [1]. classical triad clinical symptoms represented by conjunctival chemosis, pulsating exophthalmos and bruit, are well known to be a strong indication of carotid cavernous fistula related to venous drainage routes. total or partial absence of this classical triad, made patients often have been initially misdiagnosed. taniguchi et al. [1,7] showed that absence of a bruit was the principal cause of misdiagnosis, while walker and allegre [1,3] reported the same situation for exophthalmos. akira kurata et al., presented evidence that dural ccf patients usually do not show the classical triad, cranial nerve palsies being the most common initial symptoms in their patient series. usually, multiple venous drainages route may explain the limitation of symptoms to only cranial nerve palsies. this appears due to dispersion of the arterial flow which will conceal disguise the classical triad. also, in only 36% of cases at least one of the classical triad was the initial symptom. unilateral head pain was reported by newton and al.[1] to be the frequently early symptom usually interpreted as an unusual 170 chiriac et al dural arteriovenous fistulas of the cavernous sinus migraine attack. they also described, unilateral headache as mostly transient symptom with duration of less than 1 month. imaging diagnosis can be performed by contrast-enhanced ct and mr imaging, mr angiography, or doppler imaging studies, which will show enlarged draining veins. mr imaging (t1-weighted images) may suggest thrombosis or slow flow in the superior ophthalmic vein when this structure appears hyperintense (instead of the usual flow void) [1,2]. phase-contrast mr angiography and doppler studies permit identification of flow reversal in the enlarged superior ophthalmic vein. the majority of patients with dural arteriovenouse fistulas of the cavernous sinus follow an extremely benign clinical course. serious complications such as intracerebral hemorrhage are very rare. exceptionally, some patients may present decrease of visual acuity including central retinal thrombosis and cortical venous reflux evident on angiography. spontaneous regression in dural ccf is not uncommon phenomenon and was noted in 5 of 11 cases reported by newton and hoyt, 19 of 26 patients by sasaki et al. [10], and three of 18 by vinuela et al [1,2]. the two major endovascular approaches for dural arteriovenouse fistulas of the cavernous sinus treatment are represented by transarterial embolization and transvenouse route embolization. recently, transvenouse embolization has been proposed as a more appropriate curative treatment than transarterial embolization. anyway, this may result in serious difficult outcomes like embolic stroke as reported by halbach et al. [1,2], especially if performed without prior arterial flow reduction by transarterial embolization. yamashita et al. reported complication occurring in 7 of their 16 patients undergoing transvenouse embolization. they described an epidural extravasation due to perforation of the inferior petrosal sinus, and the other 6 transient aggravations of symptoms (chemosis and sixth/third cranial nerve palsy in three each) [1,2]. cortical venous reflux was demonstrated to be an important feature associated with major complications. en extravasation from the uncal vein during a transvenouse embolization for superior ophthalmic vein and inferior ophthalmic vein via the inferior petrosal sinus was reported by araki et al. he show the importance of early obliterating of cortical venous drainage as soon as possible, even when the reflux is small [1,2]. conclusions endovascular embolization of dural arteriovenous fistulas of the cavernous sinus via external carotid artery feeders has a high success rate. in some fistulas, the endovascular occlusion of external carotid artery system is sufficient, whereas it will cause the decrease of symptoms. in bilateral fistulas situation, endovascular embolization of the most symptomatic side may be followed by a spontaneous occlusion of the contralateral fistula. in case of insufficient fistula occlusion by external carotid artery feeders embolization or a predominant fistula supply from internal carotid artery, a venous embolization is indicated. the aim of venous route romanian neurosurgery (2014) xxi 2: 166 171 171 embolization is to occlude the fistula without redirecting venous drainage to cortical structures. correspondence:: stefan mircea iencean mirceasteffan@yahoo.com references 1. d. quinones, g. duckwiler, p. y. gobin, r. a. goldberg, and f. vinuela: embolization of dural cavernous fistulas via superior ophthalmic vein approach, ajnr am j neuroradiol, may 1997, 18:921– 928; 2. akira kurata, sachio suzuki, kazuhisa iwamoto, kuniaki nakahara, makoto sasaki, chihiro kijima, madoka inukai, katsutoshi abe, jun niki, kimitoshi satou, kiyotaka fujii, shinichi kan. dural arteriovenous fistulas in the cavernous sinus: clinical research and treatment. isrn neurology, 2011; 3. pero, guglielmo, et al. onyx embolization of dural arteriovenous fistulas of the cavernous sinus through the superior pharyngeal branch of the ascending pharyngeal artery. journal of neurointerventional surgery, 2014, neurintsurg-2013-011067. rep.; 4. barrow, d. l., spector, r. h., braun, i. f., landman, j. a., tindall, s. c., & tindall, g. t. (1985). classification and treatment of spontaneous carotid-cavernous sinus fistulas. journal of neurosurgery, 62(2), 248-256. 5. nelson, p. k., russell, s. m., woo, h. h., alastra, a. j., & vidovich, d. v. (2003). use of a wedged microcatheter for curative transarterial embolization of complex intracranial dural arteriovenous fistulas: indications, endovascular technique, and outcome in 21 patients. journal of neurosurgery, 98(3), 498-506. 6. vanlandingham, m., fox, b., hoit, d., elijovich, l., & arthur, a. s. (2014). endovascular treatment of intracranial dural arteriovenous fistulas. neurosurgery, 74, s42-s49. 7. macdonald, a., plaha, p., & byrne, j. (2014). an unusual presentation of a dural arteriovenous fistula of the sphenoparietal sinus. journal of neurointerventional surgery, neurintsurg-2014. 12agrawalamit_transverse2014 romanian neurosurgery (2014) xxi 1: 85 89 85 transverse cervical skin incision and vertical platysma splitting approach for anterior cervical vertebral column exposure amit agrawal, g. malleswara rao professors of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract anterior surgical approaches provide direct access to symptomatic areas of the cervical spine, allow management of the vast spectrum of cervical spine pathologies and there are many articles in the literature that discussed these techniques in detail. cosmesis is an important issue for patients who undergone surgeryon neck structures as an improperly placed incision attracting significant morbidity and few publications discuss this issue in details. the purpose of the present article is to describe our experience with transverse cervical skin incision and vertical platysma splitting approach for anterior cervical vertebral column exposure. key words: cervical spine, neck incision, platysma, cosmesis, anterior cervical discectomy, cervical fusion. introduction anterior surgical approaches provide direct access to symptomatic areas of the cervical spine, allow management of the vast spectrum of cervical spine pathologies and there are many articles in the literature that discussed these techniques in detail. (1, 2) cosmesis is an important issue for patients who undergone surgeryon neck structures as an improperly placed incision attracting significant morbidity and few publications discuss this issue in details. (3-7) the purpose of the present article is to describe our experience with transverse cervical skin incision and vertical platysma splitting approach for anterior cervical vertebral column exposure. material and methods a total 56 patients were treated for cervical spine disease through anterior cervical approach. all patients had lesions in the upper neck, and all the lesions were preoperatively diagnosed by mri scans. informed consent was approved by the insti¬tutional review board and obtained from all patients in this study. the patients underwent surgery with diagnostic or curative intents. surgical technique under general anesthesia, the head of patient was rotated to the opposite side, and the neck was extended by placing a pillow under the upper chest. surgery was performed by the same consultant surgeon using standard techniques of neck dissection. the site of lesions informed by 86 agrawal, malleswara rao skin incision for anterior cervical vertebral column exposure preoperative mri scans and physical examination was delineated, and a skin incision was marked on right side of the neck in all patients (figure 1 a). the patient was placed in the supine position with the head in slight extension and turned to left. a transverse skin crease incision was made in all patients; the length of the incision was determined by the extent of vertical exposure.the incision was started from the midline anteriorly and extended laterally just over anterior one third of sternomastoid (figure a-f). the incision was carried down through the subcutaneous fat onto the platysmamuscle, and the flap was elevated by creating a plane between subcutaneous flap and platysma muscle by blunt and sharp dissection (figure 2 a-f). platysma was split vertically along the direction of its fibers (figure 2 c). standard procedure to create an avascular dissection plane was followed to develop between the esophagus/trachea, medially, and the sternocleidomastoid/ carotid sheath, laterally. (8-12) hand held retractors were utilized to provide initial exposure of the anterior vertebral column and the adjacent longuscolli muscles. the other procedures for management of lesions were as per the standard indications.briefly, following apposition of the strap muscles of the neck and closure of platsyma and skin incision was performedwith continuous subcutaneous sutures using 4-0 vicryl (figure 3 a-c). all patients received a standard postoperative protocol and analgesic regimen to achieve tolerance of fluids and diet prior to discharge. figure 1 (a) cervical incision marking, (b) incision through subcutaneous fat, (c) subcutaneous fat plane exposure, (d) dissection through subcutaneous fat, (e) creating plane between skin flap and platysmaand (f) creating plane between skin flap and platysma figure 2 (a) creating plane between skin flap and platysma, (b) platysma split vertically along muscle fibers, (c) creating plane between esophagus/trachea medially and carotid laterally, (d) creating plane between esophagus/trachea medially and carotid laterally, (e) creating plane between esophagus/trachea medially and carotid laterally and (f) approximating platysma edges romanian neurosurgery (2014) xxi 1: 85 89 87 figure 3 (a) approximating platysma edges, (b) closure with subcutaneous sutures and (c) closure with subcutaneous sutures figure 4 (a, b and c) showing follow-up images with good cosmetic outcome results all the patients were followed with careful examinations of the wound and it healed well in all. there were no incidences of wound infection, flap necrosis or wound gaping (figure 4 a-c). figure 5 (a, b and c) cutting the platysma can be associated with puckering of the skin and poor cosmetic results 88 agrawal, malleswara rao skin incision for anterior cervical vertebral column exposure discussion anterior cervical approaches has been described as most appropriate in patients with decompression of the cervical spine and nerve roots as it allows safe and direct decompression of the spinal cord at the site of compression. (8, 13) the surgical technique has been well discussed and has evolved one of the most popular spinal surgery operations over the past century. (8-10) in anterior cervical approach, the vertebral column is approached through a transversal or vertical cervical incision and the cervical spine is reached between the trachea and oesophagus medially, and the carotid-jugular group laterally. (1, 2, 11, 12, 14-16) platysma muscle can be cut (11) or split (17) in line with the skin incision to expose the anterior border of sternomastoid muscle. however cutting the paltysma may be associated with puckering and poor scar formation (figure 5 a, b and c). there is growing enthusiasm for the use of smaller incisions in head and neck region with better cosmetic outcome while following the application of well-known cosmetic principles and achieving optimum and safe exposure of area of interest. (18, 19) there has been increasing concern about cosmesis and invisible postoperative scars of the face and neck (18, 20-23) as the face and neck are considered as the most important parts of human body in terms of beauty. (19) cutting of platysma may result in puckering of skin and cosmetic concern to the patient. also the final cosmetic appearance of a neck wound is also of great importance to patients as the wound is likely to be permanently on view. (23) conclusions skin closure technique is aimed to precisely oppose the skin edges without tension for sufficient time to allow healing to take place. (23) it has been proposed that skin closer in the sagittal plane, more aligned with langer's lines for a 'neck-line' incision results in a more aesthetic outcome. (24) we followed this in present study to achieve cosmetically acceptable scar in the neck. the present surgical incision allowed splitting of platysma (in contrast to cutting in line of skin incision), adequate exposure of the cervical spine and cosmetically acceptable scar in the neck. address for correspondence: dr amit agrawal professor of neurosurgery department of neurosurgery narayna medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 references 1. denaro v, di martino a. cervical spine surgery: an historical perspective. clinical orthopaedics and related research 2011;469:639-648. 2. fransen p. a simplified technique for anterior cervical discectomy and fusion using a screw-plate implanted over the caspar distractor pins. acta orthopaedica belgica 2010;76:546-548. 3. ready ar, barnes ad. complications of romanian neurosurgery (2014) xxi 1: 85 89 89 thyroidectomy. the british journal of surgery 1994;81:1555-1556. 4. bartel m, rupprecht h, schubert h. mediastinoscopy and scar-keloid's in boeck's sarcoid (author's transl)]. zeitschrift für erkrankungen der atmungsorgane 1976;145:388. 5. eldridge pr, wheeler mh. stitch granulomata after thyroid surgery. the british journal of surgery 1987;74:62. 6. jancewicz s, sidhu s, jalaludin b, campbell p. optimal position for a cervical collar incision: a prospective study. anz journal of surgery 2002;72:1517. 7. ridgway dm, mahmood f, moore l, bramley d, moore pj. a blinded, randomised, controlled trial of stapled versus tissue glue closure of neck surgery incisions. annals of the royal college of surgeons of england 2007;89:242-246. 8. moran c, bolger c. operative techniques for cervical radiculopathy and myelopathy. advances in orthopedics 2012;2012:916149. 9. cloward rb. lesions of the intervertebral disks and their treatment by interbody fusion methods. the painful disk. clinical orthopaedics and related research 1963;27:51-77. 10.smith gw, robinson ra. the treatment of certain cervical-spine disorders by anterior removal of the intervertebral disc and interbody fusion. the journal of bone and joint surgery american volume 1958;40-a:607624. 11.patnaik v, singla rajan k, gupta p, bala s. surgical incisions-their anatomical basis part v-approaches to spinal column. j anat soc india 2002;51:76-84. 12.kavanagh rg, butler js, o'byrne jm, poynton ar. operative techniques for cervical radiculopathy and myelopathy. advances in orthopedics 2012;2012:794087. 13.hilibrand as, carlson gd, palumbo ma, jones pk, bohlman hh. radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. the journal of bone and joint surgery american volume 1999;81:519-528. 14.crenshaw a. campbell’s operative orthopaedics, mosby, st. louis, mo 1992:1681-1683. 15.abbott kh. anterior cervical disc removal and interbody fusion. a preliminary review of 101 patients followed for one to three years. bulletin of the los angeles neurological society 1963;28:251259. 16.lied b, roenning pa, sundseth j, helseth e. anterior cervical discectomy with fusion in patients with cervical disc degeneration: a prospective outcome study of 258 patients (181 fused with autologous bone graft and 77 fused with a peek cage). bmc surgery 2010;10:10. 17.mayer hm, siepe c, korge a. [the microsurgical anterior approach for total cervical disc replacement]. operative orthopadie und traumatologie 2010;22:454467. 18.terris dj, seybt mw, elchoufi m, chin e. cosmetic thyroid surgery: defining the essential principles. the laryngoscope 2007;117:1168-1172. 19.maillard gf, clavel pr. aesthetic units in skin grafting of the face. annals of plastic surgery 1991;26:347-352. 20.roh jl. retroauricular hairline incision for removal of upper neck masses. the laryngoscope 2005;115:21612166. 21.ikeda y, takami h, niimi m, kan s, sasaki y, takayama j. endoscopic thyroidectomy by the axillary approach. surgical endoscopy 2001;15:1362-1364. 22.monfared a, saenz y, terris dj. endoscopic resection of the submandibular gland in a porcine model. the laryngoscope 2002;112:1089-1093. 23.selvadurai d, wildin c, treharne g, choksy sa, heywood mm, nicholson ml. randomised trial of subcuticular suture versus metal clips for wound closure after thyroid and parathyroid surgery. annals of the royal college of surgeons of england 1997;79:303-306. 24.cooke m, talbot jc, branfoot t. 'neck-line' incision for open reduction and internal fixation of the clavicle. annals of the royal college of surgeons of england 2009;91:437-438. microsoft word 9.iliescub_severespinal.doc romanian neurosurgery (2010) xvii 4: 445 – 448 445 severe spinal stenosis in an adult achondroplastic dwarf – case report b. iliescu1, s. gaivas1, c. apetrei1, i. poeată1,2 1“prof. dr. n. oblu” emergency clinical hospital, neurosurgery department, iasi 2“gr.t. popa” university of medicine and pharmacy, iasi abstract achondroplasia is the most common form of human short-limbed dwarfism and is one of a spectrum of diseases caused by mutations in the fgfr3 gene. achondroplasia is estimated to occur in 1 in 10,000–30,000 live births4,7. the disease is autosomal dominant, but 80% of patients have new mutations. it is commonly associated with several neurological conditions such as hydrocephalus, cervicomedullary compression, cervical or thoracic cord compression, and lumbar spinal compression due to bone stenosis along the neuraxis. we report a case with severe spinal stenosis at the lumbar and thoracic levels, with minimal involvement of the cervical spine with late neurological onset in an adult patient with achondroplasia. neurological and radiological findings and surgical procedures are discussed. the patient was admitted with profound spastic lower paraparesis and urinary incontinence. in the first operation we performed lumbar decompression and the patient improved and on the fifth day she was able to take a short walk. 3 months after the first surgery we intervened on the thoracic spine with a multi-level decompression which allowed for further neurological improvement, continued in a specialized medical facility. the case stands out as the clinical picture was dominated by the lumbar stenosis (although both lumbar and thoracic stenosis were severe at the time of presentation) with a late onset and sparing of the cervical spine. keywords: achondroplasia; spinal stenosis; surgical decompression introduction achondroplasia is the most common form of congenital bony dysplasia human and is one of a diseases group caused by mutations in the fgfr3 gene (1,8). it is characterized by abnormal formation of enchondral bone that leads to the stenosis of the craniospinal axis (6). the classic features of achondroplasia include a long, narrow trunk and short limbs. the head is generally large, with frontal prominence, and the face is hypoplastic. hypotonia is a common feature in infancy and is a factor in motor developmental delay. thoracolumbar kyphotic deformity is common. the spinal x-rays demonstrate a narrowing of the interpedicular distances in the lumbar spine (8). head and spine mri is recommended in achondroplasia to document the extent of spinal stenosis, cranio-spinal abnormalities (such as stenosis of foramen magnum) and the presence of hydrocephalus). the surgery of choice is currently considered to be the decompression of the spine as early as 446 b. iliescu et al severe spinal stenosis possible to avoid significant damage to the spinal cord (8). it is worth noting that the earliest report of neurological complications associated with achondroplasia was provided by walter dandy in 1921 (2). we present the case of an adult achondroplastic dwarf with thoraco-lumbar spinal stenosis with relative sparing of the cervical spine with a late onset of neurological symptoms and with good response to the decompressive procedures. case report a 40 year old female presented for severe hypotonic paraparesis (4/5), ongoing for two years with worsening in the last two months prior to presentation, urinary incontinence, paresthesias with hypoaesthesia in the lower limbs, and sciato-cruralgia. the upper limbs were spared of neurological deficit, motor or sensory. she presented a typical picture of achondroplasic dwarf, with a large head, short arms and legs. she exhibited hypotonic paraparesis, with babinski sign bilaterally and ankle clonus positive bilaterally. an mri study of the brain and entire spine was performed (figure 1 a c). the brain mri showed no sign of hydrocephalus. spine mri showed instead a severe spinal canal stenosis at the level of lumbar spine (the minimal diameter was 4mm), especially at l2-l5 levels as well as a equally severe stenosis at the level of thoracic spine, maximal at d7-d10 levels (with a minimal diameter of 6 mm). the cervical spine showed signs of stenosis but they were minimal. correlated with clinical status of the patient we decided a two staged decompressive surgery of the spine, starting with the lumbar stenosis. a laminectomy was performed from l2 through l4 with recalibration of the lumbar canal through resection of the interior aspects of the articular processes. bilateral foraminotomies were performed at all levels of the decompression. a romanian neurosurgery (2010) xvii 4: 445 – 448 447 b c figure 1 a. t2 weighted mr images (left – sagittal, right – axial) of the thoracic spine showing the the minimal stenosis at level of d9. b. t2 weighted mr image of the lumbar spine with measurements of the stenosis at all levels. c. t2 weighted mr imageof the cervical spine showing the relative sparing of the cervical and cranio-cervical junction elements. postoperatively, on the 5th day she was able to walk assissted. although initially she was reserved to undergo a surgical operation on the spine, the clinical improvement after the first operation result was so significant that she decided to come back for a second surgery, on the thoracic spine, fearing a future worsening of the paraparesis. the second operation took place four months later when a decompression at d7-d10 levels was performed with further improvement in the clinical status and she entered a recovery program in a specialized facility. no complications related to surgery or anesthesia were documented during any of the interventions. discussion stenosis of the achondroplastic vertebral canal is progressive and is the substrate of neurological deficits such as intermittent claudication, nerve root compression, paraparesis, paraplegia and quadriplegia, depending on the level of stenosis. hydrocephalus is frequently seen in these patients yet it is frequently asymptomatic and stops progressing (5). the achondroplasia presents a difficult management problem in spinal surgery and the preoperative duration of signs and symptoms and the age of the patient may equally determine the outcome of the operative treatment. generalized stenosis is considered to be a poor prognostic factor 448 b. iliescu et al severe spinal stenosis (due mostly to the cervical stenosis and its possible complications) (6). prospective studies will be necessary to document that prophylactic decompression is indicated in those patients before the onset of a neurological deficit. the third and fourth decades of life are the most common age for development of thoracolumbar spinal stenosis syndrome in achondroplasia. the mean age on admission with spinal stenosis is 31 (22–37) years (4). multi-level laminectomy is indicated if the clinical features mainly result from a narrow canal. the indication, timing, and procedure for surgical treatment of spinal canal stenosis with thoracolumbar kyphosis in achondroplasia have not been well established. our case confirms the fact that a decompressive laminectomy even without instrumentation is a useful procedure in treating the severe spinal stenosis at both lumbar and thoracic level with a good functional outcome and an effective relief of neurological symptoms (as long as a critical clinical exam assigns the neurological status to stenosis and not to other neuraxis pathology). conclusions our patient presented in her fifth decade of life with a clinical picture dominated by the lumbar stenosis (although both lumbar and thoracic stenosis were severe at the time of presentation). her cervical spine and cranio-cervical junction were spared from osseous stenosis typically associated with achondroplasia. the initial lumbar decompression through multileveled laminectomy provided significant relief of the neurological function. a second operation, multileveled laminectomy at the thoracic level, was performed due to clear imagistic aspects and patient’s understading of possible future development, with further improvement in neurological outcome. references 1. bellus g.a., hefferon t.w., ortiz de luna r., hecht j.t., horton w.a., et al. achondroplasia is defined by recurrent g380r mutations of fgfr3. am. j. hum. genet. 56:368-373, 1995 2. dandy we. hydrocephalus in achondroplasia. bull johns hopkins hospital 32:5–10,1921 3. fortuna a, ferrante l, acqui m, santoro a, mastronardi l. narrowing of thoraco-lumbar spinal canal in achondroplasia. j neurosurg sci 33:185-96, 1989 4. martinez-frias m.l., herranz i., salvador j., prieto l., ramos-arroyo m.a., rodrigue -pinilla e., et al. prevalence of dominant mutations in spain: effect of changes in maternal age distribution. am j med genet 31:845–852, 1988 5. menezes ah. congenital and acquired abnormalities of the craniovertebral junction. in: youmans jr, editor. neurological surgery. vol. 2. 4th ed. philadelphia: w.b. saunders company, 1035–89, 1996 6. morgan df, young rf. spinal neurological complications of achondroplasia. results of surgical treatment. j neurosurg 52:463–72, 1980 7. orioli i.m., castilla e.e., barbosa-neto j.g. the birth prevalence rates for the skeletal dysplasias. j med genet 23:328–332, 1986 8. tolo v. spinal disorders associated with skeletal dysplasias and metabolic diseases. in: rothman rh, simeone fa, editors. the spine. vol. 1. 3rd ed. philadelphia: w.b. saunders company, 349–64, 1992 9. uematsu s, wang h, kopits se, hurko o. total craniospinal decompression in achondroplastic stenosis. neurosurgery 35:250–8, 1994. microsoft word gaivass_intradiploic_f s. gaivas et al intradiploic epidermoid cyst of the skull intradiploic epidermoid cyst of the skull. case report s. gaivas1*, d. rotariu1*, g. dumitrescu2, b. iliescu1, c. apetrei1, i. poeata1 1department of neurosurgery; 2anatomopathology, “gr.t. popa” university of medicine and pharmacy, iasi, romania *both authors have equally contributed to this paper abstract authors describe a giant intradiploic epidermoid cyst of the cranial vault with massive intraand extracranial extension and analyze the clinicopathological, imaging features and treatment of these lesions in the light of the most important published data. a 38-years old male patient with a history of chronic headache reported a painless subcutaneous swelling 4 months ago on the right frontoparietal scalp. ct and mri evaluation revealed a large welldefined extracerebral mass in the frontoparietal scalp with destruction of both the inner and outer tables of the bone. the patient underwent a total microsurgical resection of the tumor and the cranial defect produced by the resection of the space-occupaying lesion was repaired with titanium wire mesh and methyl methacrylate cranioplasty. the histological examination has shown a cystic structure lined by squamous epithelium and containing laminated keratin material, aspects that are suggesting a epidermoid cyst. the patient post-operative course was uneventful, without any neurological deficit and was discharged after 48 hours of hospitalisation in a good medical condition. the review of the literature shows that the parietal bone location for intradiploic epidermoid tumors in rare. complete surgical resection represent the gold standard of treatment, and no adjuvant therapy is needed. recent advances in diagnostic imaging and treatment of these lesions are reviewed. keywords: dermoid, epidermoid, intracranial tumor, radical removal, skull tumor intracranian epidermoid cyst, although rare, is well documented. also known as epidermoid tumor or ectodermal inclusion cyst, or “pearly tumor”, epidermoid cyst is a benign congenital inclusion cyst that account for 1% of all intracranial tumors (1, 11). it is thought to arise from defects in the separation of the neuroectoderm during the formation of the neural tube, leading to sequestration of ectodermal remnants within the cranial bones (5). intracranial epidermoid cysts are well circumscribed and most often occur within the diploe (1) , in the parasellar region, sylvian fissure, cerebellopontine angle, posterior fossa, and fourth ventricle. intradiploic epidermoid cysts are less common than the intradural varieties (9). in general, epidermoid cysts typically appear on ct scans as low-density, hypodense, nonenhancing lesions, similar to the fat density. on mri this lesion demonstrates high signal intensity in t1weighted and variable t2-weighted signal. sometimes, the cyst contents can be hyperdense, mimicking a haemorrhage. romanian neurosurgery (2011) xviii 2 case report history. a 38-years old man was admitted with a history of chronic headache, mainly in the right parietal region, which had recently increased in severity and frequency. for 4 months he had noticed a small painless bulge under the scalp. examination. neurological exam, didn’t reveal any deficits but physical examination found a right frontoparietal soft, nontender lump, which had no mobility over the underlying bone and the skin covering the lesion could not be retracted. contrast-enhanced computed tomography showed destruction of the right parietal bone by a large extracerebral hypodense intradiploic tumor. in bone windows the ct scan shows erosion of both inner and outer table of the calvarium and compression on the right parietal lobe (figure 1). on the mri examination the mass demonstrated homogenously high signal intensity during both t1and t2 weighted sequences, and no perifocal cerebral edema was detected on the t2weighted sequence (figure 2). operation. the patient underwent a right parietal craniotomy. when the scalp flap was reflected, a white encapsulated, mostly intradiploic large tumor was identified. the 7 cm tumor with irregular calcified borders was herniating through bone defect (figure 3) the tumor was resected within the apparently normal bone followed by the excision of the markedly thickened dura. a duroplasty with a galeal flap and a reconstruction of the skull bone with a titanium mesh were performed (figure 4). postoperative course. after the intervention, the patient’s neurological status remained stable with intact motor strength and sensation. histologically, a diploic epidermoid cyst was established. a b figure 1 a computerized tomography scans demonstrating a well circumscribed extracerebral hypodence area surrounded by a hyperdence rim. b: ct with bone window reveals erosion of both tables of the vault. s. gaivas et al intradiploic epidermoid cyst of the skull a b c bd figure 2 preoperative plain mri images. a: axial t1-weighted section revealing well demarcated tumor. b: tumor did no show enhancement after gd administration. c: coronal section. d: t2-weighted axial section show no perifocal edema. discussion intracranial epidermoid cysts are congenital lesions with benign histological features and very slow growth, via progressive accumulation of normally dividing cells (epidermal cells) (11). this tumor arise from ectodermal cellular remnants, during gestation ( weeks 3-5), as a result of incomplete cleavage of the neural ectoderm from the cutaneous ectoderm (4). the most common presentation is within the third or fourth decade of life with a painless, long-standing lesion, subcutaneous scalp swelling covered with normal skin (10). men are affected more often than women (2). epidermoid cysts have a thin capsule of stratified squamous epithelium filled by keratin, cellular debris and cholesterol, and do not contain hair or other dermal elements which differentiate them from the dermoid tumor (2,7). the epidermoids are having a slow growing rate, romanian neurosurgery (2011) xviii 2 approximating that of normal skin, a condition which allows the intracranial structures, by using its reserve spaces, to adapt and tolerate the presence of mass lesion until all the reserve spaces are used, situation in which further compensation is no longer possible and the lesion becomes symptomatic (according to the localization and the compressed structures) (12, 8). figure 3 intraoperative photograph showing this large tumor, which is located between the inner and outer table of the bone. figure 4 cranioplasty with titanium mesh. figure 5 1: photomicrograph of resected intradiploic epidermoid cyst demonstrates multiple concentric laminated layers of keratin within the lumen. the cyst is lined by a squamous epithelium. in this area there is normal osseous lamella adjacent to squamous epithelium. (hematoxylin-eosin, original magnification x 40). figure 5 2: another low-power photomicrograph of resected intradiploic epidermoid cyst shows normal striated muscle and conjunctive tissue below the epidermoid cyst wall as the bone was distructed and the cyst penetrate beyond it. (hematoxylineosin, original magnification x 40). a possible complication of intradiploic epidermoid tumors is the spontaneous cyst rupture with secondary discharge of the cystic content (keratin, cellular debris and cholesterol) into the subarachnoid space, producing aseptic meningitis which frequently leads to chronic granulomatous arachnoiditis (5). s. gaivas et al intradiploic epidermoid cyst of the skull findings of ct are acknowledged to give correct diagnosis for intradiploic epidermoid cyst preoperatively. on ct, simultaneous erosion of inner and outer table of the skull is reported to occur in up to 72% of cases with intradiploic epidermoids (10). they are soft masses, which may be hypointense or isointense to the brain, and the dural infiltration is reported in 10% of the cases (3). other lesions of the scalp and skull to be considered in differential diagnosis include: calcified cephalhematomas, occult meningocele and eosinophilic granuloma, osteolytic intradiploic metastasis (8, 4).the goal of surgery in the treatment of epidermoid tumors is total surgical removal of the tumor together with its capsule, wich is the only living and growing part of the tumor. conclusions we recommend the prophylactic removal of these tumors through surgery and primary repair when required. adequate exposure of the epidermoid cyst is needed to allow complete excision of the tumor and its capsule, with the goal of preventing recurrences, inflammation and the possibility of malignant transformation. references 1. alberione f, caire f, fischer _lokou d, gueye jj, moreau jj, quiste epidermoide intradiploico infratentorial gigante, neurocirugia, 2007, 18:423-426 2. bach ca, baujat b, baglin a-c, et al. epidermoid cyst of the frontal bone invading the frontal sinus: a case-report. fr orl ;2005,86:38–40 3. constans jp, meder jf, de divitiis e et al, giant intradiploic cysts of the skull. report of two cases, j neurosurg, 1985, 62: 445-448 4. han g-y, won y-s, yang j-y, et al. intradiploic epidermoid cyst of the skull. j korean neurosurg soc; 2005,38:68 –70 5. kalgutkar a, kini s, jambhekar n, et al. intradiploic primary epithelial inclusion cyst of the skull. ann diagn pathol 2006;10:20 –23 6. kerem bikmaz, murat cosar sirzat bek, cem a. gokduman, mahmut arslan, a. celal iplikcioglu, intradiploic epidermoid cysts of the skull: a report of four cases, clinical neurology and neurosurgery, 2005, 107, pp. 262-267 7. liu jk, gottfried on, salzman kl, et al. ruptured intracranial dermoid cysts: clinical, radiographic, and surgical features. neurosurgery, 2008 62:377–384 8. meersschaert j, mermuys k, wilms g. intradiploic epidermoid cyst. jbr-btr 2008;91:18 9. revuelta-gutiérrez r, díaz-romero paz rf, valeshidalgo lo, hinojosa-gonzales r, barges-coll j. cerebellopontine angle epidermoid cysts. experience of 43 cases with long-term follow-up, cir cir; 2009, 77:257-65; 241-8 10. rubin g. pasqualin a. rosta l et al: craniocerebral epidermoids and dermoids. acta neurochurirgica, 1989, 97:1-16 11. servet inci, atilla akbay, vural bertan. intradiploic epidermoid cyst of the temporal bone, turkish neurosurgery 2, 1992, : 155 – 157 12. watanabe k, wakai s, nagai m, et al. epidermoid tumor with unusual ct and mr findings. neurol med chir (tokyo) 1990;30:977–979 doi: 10.33962/roneuro-2021-022 the role of mri-guided focused ultrasound in neurosurgery. a narrative review marius gabriel dabija, ioan sebastian nechifor, vlad andrei dabija, bogdan costachescu, lucian eva romanian neurosurgery (2021) xxxv (2): pp. 143-147 doi: 10.33962/roneuro-2021-022 www.journals.lapub.co.uk/index.php/roneurosurgery the role of mri-guided focused ultrasound in neurosurgery. a narrative review marius gabriel dabija1,2, ioan sebastian nechifor1, vlad andrei dabija3, bogdan costachescu1,2, lucian eva1 1 department of neurosurgery. “nicolae oblu” emergency clinical hospital, iasi. romania 2 department of neurosurgery. “gr. t. popa” university of medicine and pharmacy, iasi. romania 3 “gr. t. popa” university of medicine and pharmacy, iasi, romania abstract introduction. mrgfus is a novel technology, which can have profound implications in the current treatment of neurological disorders. its applications range widely, from the alteration of the blood-brain barrier, ablation of tumours to the treatment of movement disorders. objective. to review, following thorough research of the literature, the principles of its use in the treatment of neurological diseases and the main reported evidence of its clinical implementation. material and method. interrogation of the medline database, using the pubmed search engine, for the following mesh words: “mrgfus”, “fus” “brain”, from 2000 to the current year. conclusion. mrgfus can be safely used today for the treatment of essential tremor. new research is warranted for the evaluation of its safety and effectiveness in other neurological disorders. introduction mri guided focused ultrasound (mrgfus) of the brain is a novel technology which has the potential to be implemented successfuly in our modern neurosurgical practice. because of its capability to alter the blood brain barrier, ablate tumors and proven to be effective as a treatment of different movement disorders, it is worthy for us to gain familiarity with this technique. unfortunately, novelty and the specific technicality of this instrument confuses the clinician. therefore, we aim in this paper, by the means of a narrative review, to provide an insight on the working mechanism and the uses of the technology and to address the benefits and limitations of its applicability in the clinical practice. keywords mrgfus, movement disorders, blood-brain barrier, high focused ultrasound corresponding author: bogdan costachescu department of neurosurgery. “nicolae oblu” emergency clinical hospital, iasi, romania costachescus@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 144 marius gabriel dabija, ioan sebastian nechifor, vlad andrei dabija et al. method research of the medline database, using the pubmed search engine, for the following mesh words: “mrgfus”, “fus” “brain”, from 2000 to the current year. background. first studied by lynn (1) at the start of the 20th century, the ability to focus ultrasound waves in order to produce a biological effect on the intracranial content was a tempting idea. aided by the recent advances in high resolution mri imaging, neuronavigation and the development of hemispheric piezoelectric transducer systems, we are now able to accurately focus the ultrasound waves intracranially, as demonstrated by the commercially available system exablate 4000 (insightec ltd). the result of their application on the tissue can be divided into thermal and mechanical effects. as ultrasounds propagates through the tissue, they raise the local temperature and interact with the gas molecules, producing bubbling, oscillation and finally cavitation with the stretching of the cellular membrane as a result (2) . based on these mechanical and thermal effects they can reversibly or irreversibly alter the brain tissue, depending on their strength and frequency. the role of mrgfus in tumor ablation ultrasound can aid in the treatment of deep brain neoplastic lesions, considered unresectable, or in patients that are unfit for surgery. unfortunately, the data is scarce due to the relative novelty of the technology and the absence of clinical trials (3), (4). in 2014, daniel coluccia published the results regarding the thermoablation of a left thalamic recurrent glioma, using ultrasound. he noticed a 10% reduction in tumoral volume at 5 days post procedure, with improvement in the neurologic status of the patient. at the 21th day check-up no increase in the volume of the tumor was observed (5). preliminary results, published by ernst martin, creates an insight on the thermoablative tumoral effect of the hifus system. although the author reported clinical improvement in only one patient, it opens the pathway to the development of new clinical trials (6). the role of mrgfus on the permeability of the blood-brain barrier the bbb is a complex structure serving the role of an interface between the blood and the cerebral tissue. its cytoarchitecture is mainly represented by a layer of endothelial cells, binded one to another by tight junction proteins, interconnected with neurons, perycites and astrocytes (7). this renders it virtually impermeable to exogeneous molecules and thus limiting the effectiveness of different pharmaceuticeuticals. mrgfus can be used to transiently open the bbb. hynynen et.al, in his in vivo study, demonstrated that the bbb can safely be opened in rabbits, by applying low strength ultrasounds combined with the intravenous administration of preformed microbubbles. after applying the ultrasound field, these microbubbles oscillate, modify their form, thus stimulating the cerebral blood capillaries and opening the bbb. the effects are transient without significant side-effects (8) (fig 1.). combining the microbubbles with contrast agent, enables us to accurately pinpoint the target anatomic structure, with the aid of imaging (9). figure 1. vascular cells being stimulated (red cubes) by the ultrasound induced cavitation of the microbubbles (green spheres). agessandro abrahao et al, in their human trial of 4 participants suffering from als, demonstrated the successful opening of the bbb, after sonification, without side effects (10). mrgfus can be used in conjunction with systemic chemotherapy in the treatment of intracranial neoplasms. liu hl et al, in their rat glioma model study, demonstrates a significant survival improvement in the combined 145 the role of mri-guided focused ultrasound in neurosurgery treatment group versus the single treatment group (53 days versus 29 days) (11). it appears that the opening of the barrier can significantly enhance the effect of immunotherapy on brain metastases, as demonstrated by thiele kobus et al, in their study (12). finally, it has been shown that mrgfus cand aid gene therapy pharmaceuticals in their permeation of the bbb as shown by liu et al in their study (13). the role of mrgfus in the treatment of movement disorders and chronic neuropathic pain lesioning of the brain by stereotactic techniques along with dbs represent the mainstay of neurosurgical treatment in movement disorders. however, despite their effectiveness, they are not without potential side effects and contraindications. mrgfus can be a valuable alternative tool in the treatment of these pathologies. based on the principle of cavitation and thermoablation they can produce discrete lesioning of target anatomical areas, similar with stereotactic radiosurgery, but without harming the surrounding healthy tissue (14). clearly, a positive ratio of reward versus risk associated with the technique has led different authors to implement it into clinical practice. zaaroor et al, in their study investigating the treatment of symptomatic parkinson disease and essential tremor by hifu vim thalamotomy, reported a significant improvement in quality of life and reduction of symptomatology by approximatively 50% in the treated subjects. the effects persisted in all but 6 patients, at the 24th month follow-up. common side effects were transient and represented by gait ataxia, hand paresthesia and asthenia (15). martínez-fernández et al, in their randomised trial investigating the role of hifu sub-thalamotomy for the treatment of parkinson disease numbering 40 subjects, 27 assigned to the procedure group versus 13 to the sham procedure, reported improvement of symptoms at 4 months post procedure by approximatively 50% in the treated subjects vs. the placebo. common reported side effects are represented by slurred speech, dyskinesia and gait disturbance, with long term persistence in 6 treated patients (16). elias et al, in their trial with 76 enrolled participants, investigating the role of hifu vim thalamotomy in the treatment of patients suffering from essential tremor refractory to conservative therapy, reported a 41% improvement of the tremor at 3 months post procedure, respectively a 35% percent improvement in the treated group versus the placebo group. common adverse effects included gait ataxia and paresthesias ,these being present in approximative 36% of the treated subjects (17). jin woo chang et al, which investigated the use of hifu vim thalamotomy in the treatment of refractory essential tremor in 76 patients, reported an overall of 53% improvement of the tremor at one year post procedure. gait disturbances and paresthesias are reported as the most common adverse effects (18). another study investigating the role of hifu thalamotomy in the treatment of essential tremor, with 26 participants, published similar results (19). the evidence offered by the literature, which proves that hifu thalamotomy is safe and efficient has led the fda to approve it, in 2016, for the treatment of essential tremor (20), marking a cornerstone in it’s pathway for clinical implementation. it has been proven that mrgfus can be used in the treatment of chronic neuropathic pain. first described in 2009, fus medial thalamotomy can be a viable therapeutic approach of chronic neuropathic pain (21). marc n gallay et al, reports improvement of trigeminal neuralgia after central lateral fus thalamotomy (22). further clinical trials are needed in order to adequatly asses the possibility of these technique to be safely and successfully used. discussion as previously shown focused ultrasound therapy has the capability to significantly alter the current paradigm of treatment used in neurological diseases. regarding it’s use on opening the bbb, it is possible that the translation of fundamental science into clinical practice, aided by the future realisation of clinical trials, will usher a new era in neurooncology (23), (24) and in the treatment of neurodegenerative disorders. several studies are currently investigating its role in the treatment of brain ischemia (25), (26). it remains to be seen if it will be effective. in the field of movement disorders, unfortunately it is now limited only to the treatment of essential tremor, but probably in the near future, will be extended for parkinson disease (27). 146 marius gabriel dabija, ioan sebastian nechifor, vlad andrei dabija et al. new progress in our understanding of the neurological pathology combined with technical improvements will probably advance this technology as a treatment for chronic pain (28) and other neuropsychiatric disorders, such as obsessivecompulsive disorder and depression (29), (30). conclusion mrgfus is a promising technology in the field of neuroscience. although currently used in the treatment of movement disorders, further studies are needed for clear identification of its role in the treatment of different neurological diseases. references 1. lynn jg, zwemer rl, chick aj, miller ae. a new method for the generation and use of focused ultrasound in experimental biology. j gen physiol. 1942 nov 20;26(2):179–93. 2. al-bataineh o, jenne j, huber p. clinical and future applications of high intensity focused ultrasound in cancer. cancer treat rev. 2012 aug;38(5):346–53. 3. ram z, cohen zr, harnof s, tal s, faibel m, nass d, et al. magnetic resonance imaging-guided, high-intensity focused ultrasound for brain tumor therapy. neurosurgery. 2006 nov;59(5):949–55; discussion 955956. 4. park j-w, jung s, jung t-y, lee m-c. focused ultrasound surgery for the treatment of recurrent anaplastic astrocytoma: a preliminary report. 2006 may 1;829:238– 40. 5. coluccia d, fandino j, schwyzer l, o’gorman r, remonda l, anon j, et al. first noninvasive thermal ablation of a brain tumor with mr-guided focused ultrasound. j ther ultrasound. 2014 oct 16;2:17. 6. martin e, werner b, bauer r, leyen k van, coluccia d, fandino j. clinical neurological hifu applications: the zurich experience. transl cancer res [internet]. 2014 oct [cited 2021 apr 26];3(5). available from: https://tcr.amegroups.com/article/view/3156 7. daneman r, prat a. the blood–brain barrier. cold spring harb perspect biol [internet]. 2015 jan [cited 2021 apr 25];7(1). available from: https://www.ncbi.nlm.nih.gov /pmc/articles/pmc4292164/. 8. hynynen k, mcdannold n, vykhodtseva n, jolesz fa. noninvasive mr imaging-guided focal opening of the blood-brain barrier in rabbits. radiology. 2001 sep;220(3):640–6. 9. treat lh, mcdannold n, vykhodtseva n, zhang y, tam k, hynynen k. targeted delivery of doxorubicin to the rat brain at therapeutic levels using mri-guided focused ultrasound. int j cancer. 2007 aug 15;121(4):901–7. 10. abrahao a, meng y, llinas m, huang y, hamani c, mainprize t, et al. first-in-human trial of blood–brain barrier opening in amyotrophic lateral sclerosis using mr-guided focused ultrasound. nat commun. 2019 dec;10(1):4373. 11. liu h-l, hua m-y, chen p-y, chu p-c, pan c-h, yang h-w, et al. blood-brain barrier disruption with focused ultrasound enhances delivery of chemotherapeutic drugs for glioblastoma treatment. radiology. 2010 may;255(2):415–25. 12. kobus t, zervantonakis ik, zhang y, mcdannold nj. growth inhibition in a brain metastasis model by antibody delivery using focused ultrasound-mediated blood-brain barrier disruption. j controlled release. 2016 sep 28;238:281–8. 13. lin c-y, hsieh h-y, pitt wg, huang c-y, tseng i-c, yeh c-k, et al. focused ultrasound-induced blood-brain barrier opening for non-viral, non-invasive, and targeted gene delivery. j controlled release. 2015 aug 28;212:1–9. 14. fishman ps, frenkel v. treatment of movement disorders with focused ultrasound. j cent nerv syst dis [internet]. 2017 jun 6 [cited 2021 apr 26];9. available from: https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5 462491/. 15. zaaroor m, sinai a, goldsher d, eran a, nassar m, schlesinger i. magnetic resonance–guided focused ultrasound thalamotomy for tremor: a report of 30 parkinson’s disease and essential tremor cases. j neurosurg. 2017 feb 24;128(1):202–10. 16. martínez-fernández r, máñez-miró ju, rodríguez-rojas r, álamo m del, shah bb, hernández-fernández f, et al. randomized trial of focused ultrasound subthalamotomy for parkinson’s disease. n engl j med [internet]. 2020 dec 23 [cited 2021 apr 20]; available from: https://www.nejm.org/doi/10.1056/nejmoa2016 311. 17. elias wj, lipsman n, ondo wg, ghanouni p, kim yg, lee w, et al. a randomized trial of focused ultrasound thalamotomy for essential tremor. n engl j med. 2016 aug 25;375(8):730–9. 18. chang jw, park ck, lipsman n, schwartz ml, ghanouni p, henderson jm, et al. a prospective trial of magnetic resonance–guided focused ultrasound thalamotomy for essential tremor: results at the 2-year follow-up. ann neurol. 2018;83(1):107–14. 19. iacopino dg, gagliardo c, giugno a, giammalva gr, napoli a, maugeri r, et al. preliminary experience with a transcranial magnetic resonance–guided focused ultrasound surgery system integrated with a 1.5-t mri unit in a series of patients with essential tremor and parkinson’s disease. neurosurg focus. 2018 feb 1;44(2):e7. 20. fishman ps. thalamotomy for essential tremor: fda approval brings brain treatment with fus to the clinic. j ther ultrasound. 2017 jul 13;5(1):19. 21. martin e, jeanmonod d, morel a, zadicario e, werner b. high-intensity focused ultrasound for noninvasive functional neurosurgery. ann neurol. 2009 dec 1;66(6):858–61. 147 the role of mri-guided focused ultrasound in neurosurgery 22. gallay mn, moser d, jeanmonod d. mr-guided focused ultrasound central lateral thalamotomy for trigeminal neuralgia. single center experience. front neurol. 2020;11:271. 23. dauba a, delalande a, kamimura has, conti a, larrat b, tsapis n, et al. recent advances on ultrasound contrast agents for blood-brain barrier opening with focused ultrasound. pharmaceutics [internet]. 2020 nov 21 [cited 2021 apr 26];12(11). available from: https://www.ncbi. nlm.nih.gov/pmc/articles/pmc7700476/ 24. zhang dy, dmello c, chen l, arrieta va, gonzalezbuendia e, kane jr, et al. ultrasound-mediated delivery of paclitaxel for glioma: a comparative study of distribution, toxicity and efficacy of albumin-bound versus cremophor formulations. clin cancer res off j am assoc cancer res. 2020 jan 15;26(2):477–86. 25. daffertshofer m, gass a, ringleb p, sitzer m, sliwka u, els t, et al. transcranial low-frequency ultrasound-mediated thrombolysis in brain ischemia: increased risk of hemorrhage with combined ultrasound and tissue plasminogen activator: results of a phase ii clinical trial. stroke. 2005 jul;36(7):1441–6. 26. brown at, flores r, hamilton e, roberson pk, borrelli mj, culp wc. microbubbles improve sonothrombolysis in vitro and decrease hemorrhage in vivo in a rabbit stroke model. invest radiol. 2011 mar;46(3):202–7. 27. a randomized, sham-controlled trial of transcranial magnetic resonance-guided focused ultrasound thalamotomy trial for the treatment of tremor-dominant, idiopathic parkinson disease | cochrane library [internet]. [cited 2021 apr 26]. available from: https://www.cochranelibrary.com/central/doi/10.1002/c entral/cn-01407058/full 28. goellner e, rocha ce. anatomy of trigeminal neuromodulation targets: from periphery to the brain. neuromodulation facial pain. 2020;35:18–34. 29. jung hh, kim sj, roh d, chang jg, chang ws, kweon ej, et al. bilateral thermal capsulotomy with mr-guided focused ultrasound for patients with treatmentrefractory obsessive-compulsive disorder: a proof-ofconcept study. mol psychiatry. 2015 oct;20(10):1205–11. 30. kim m, kim c-h, jung hh, kim sj, chang jw. treatment of major depressive disorder via magnetic resonanceguided focused ultrasound surgery. biol psychiatry. 2018 jan 1;83(1):e17–8. microsoft word gramada_lumbar_f.docx romanian neurosurgery (2012) xix 1 lumbar pseudomeningocele after spinal surgery: case report f.m. gramada1, d. haba2 “n. oblu” hospital iasi 11st neurosurgical department; 2neuroradiological departement abstract among the intraoperative complications of lumbar spinal surgery the most frequently is incidental dural tear, which is encountered in 10% of the primary interventions and a double number of cases in relapses. this paper describes a case followed 10 months with repeated mri imaging demonstrating the effectiveness of percutaneus evacuating puncture of pseudomeningocele followed by lumbar compression and 3 days bed rest in trendelenburg position. the paper presents also other methods of treatment described in the literature: the role of prophylactic antibiotherapy, blood patch, bed rest in trendelenburg, lumbar drainage and surgical revision. keywords: back surgery complications, pseudomeningocele, lumbar cerebrospinal fluid (csf) fistula, incidental durotomy based on a recent operated case complicated with pseudomeningocele we try to analyze the characteristics of this pathology and its treatment. case presentation patient gv, woman, 47 years was operated in august 2009 for left herniated lumbar disc l3/l4 and l4/l5, realized by left l3 and l4 hemilaminectomies and the ablation of l3/l4 and l4/l5 hernias. evolution was favorable until november 2010 when the patient returns with left lombosciatic pain. mri revealed lumbar hernia recurrence at l3/l4. she was operated practicing the ablation of l3/l4 disc hernia by enlarging left l3 hemilaminectomy. during discal content emptying maneuvers there was a breach of the anterior dura face, and we tried to close it with muscle and gelaspon. the patient presented in postoperative evolution a subcutaneous lumbar fluctuant mass at the operative site without csf leak out. in january 2011 an mri examination revealed the existence of a pseudomeningocel with size of 6.3 / 2.7 / 2.3 cm located at the level of left hemilaminectomies (figure 1). under bed rest and intravenous infusion, the symptoms (headache, local lumbar expansion) improved. clinical favorable evolution until march 2011 when she returns for recurrence of symptoms, mri revealing persistent fluid collection at the same dimensions (figure 2). we practiced one percutaneous puncture in the collection and we evacuated 70 ml of cerebrospinal fluid. after that the patient was immobilized 3 days in bed rest in trendelenburg with compressive abdominal corset. in may 2011 lumbar mri shows important reduction of the dimensions of the fluid collection (figure 3). the last lumbar mri was performed at the end of august 2011 which confirmed the disappearance of fluid collection (figure 4). f.m. gramada, d. haba lumbar pseudomeningocele after spinal surgery figure 1 lumbar pseudomeningocele 6,3/2,7/2,3 cm figure 2 persistent of csf collection dimensions figure 3 important diminution of collection dimensions figure 4 absence of csf collection discussion producing a breach in the spinal duramater in the spinal interventions is an unwanted but possible complication, reported in the literature in various percentages. morgan-hough et al., in 2003, on a statistic of 531 operations for lumbar disc herniation reported 46 (8.7%) complications with 29 dural tears (5.5%) with 3 cases of occurrence of pseudomeningocele who needed reintervention (9). jones et al. reveals in the literature an incidence of this complication of 0.3-13%, with 4% on he’s own statistic (6). jankowitz et al. has in 4835 cases of lumbar surgery 547 (11.3%) patients with an intraoperative incidental durotomies with a frequency of 9% at the first surgery and 21% at relapse (5). the occurrence of dural tears during surgery for a herniated lumbar disc may occur in various situations: after a myelography or spinal puncture, after an aggression caused by a bone fragment, maneuvering of an inappropriate tool or excessive traction of the root. romanian neurosurgery (2012) xix 1 if the crack is located on lateral or posterior side of dura-mater a suture it’s possible coupled with a muscle patch. for lesions located above the suture is impossible and the only attitude that can be used is the application intraoperatively of muscle or fibrin patch. these cases are those which may be followed by pseudomeningocele or external lumbar csf fistula. the risk of fistula increases in cases with imperfect suture of aponeurosis or skin (2). because at lumbar level the tension inside dura is higher especially in orthostatic position, the mechanisms permitting the closure doesn’t realize its purpose. this liquid in tension force and realize a new “way” trough exterior and so external fistula appear. there is the possibility that the cerebrospinal fluid fistula close spontaneously if dural defect is not important and the patient is kept at least 3 days in the trendelenburg position to provide fluid pressure loss at the lumbar level. among the factors that influence the producing of dural tears include the existence of a connective tissue of bad quality after irradiation, infection, treatment with cortisone or in case of relapse. clinical signs relevant for the existence of a cerebrospinal fluid leak after lumbar spinal intervention are postural headache and low back pain persisting. at the local level may not be any pathological signs. in same cases there is a palpable fluctuating mass under the surgical scar with increasing dimensions in the moment of cough or vertical standing in pseudomeningocele or there is leakage of fluid through wound in fistula. this last possibility is the most dangerous because the possibility of developing meningitis (1, 3, 7). confirmation of these conditions shall be made by nuclear magnetic resonance which shows a sub/supra-aponeurotic fluid (hypo signal in t1 and hyper signal in t2). sometimes it is useful a simple myelography or (better) combined with computer tomography to specify the location of the dural defect through which cerebrospinal fluid flows (4). in case of exteriorization of leakage the confirmation is made by detection of beta 2-transferrin existing in cerebrospinal fluid (10). in case with metallic instrumentation is helpful an ultrasound examination. conservative treatment consists of bed rest in trendelenburg position and abdominal binders and focal compression. antibiotic prophylaxis has a questionable role (3), instead applying a percutaneous epidural blood patch is confirmed to be effective in 50%. some authors use external drainage to 5 days with the known risks of infection (11). if the above methods are inefficient (jankowitz et al. 11.7%) we hate to use radical treatment: the surgical suture use nonresorbable 4-0 to 7-0 wire with or without patch of fascia, dura mater or other agents such gelfoam or muscle (8). the suture must be not too close, determining a compression on the nerve. in the case presented above a contributing factor to produce the crack is the presence of the dural periduroradicular scars, in which situation the dissection of the adhesions can be difficult. usually a simply application of muscular tissue with/or fibrin at the level of breach is sufficient to avoid the accumulation of csf. in cases with visible defect of dural wall we use suture with non-resorbable material. in our case this wasn’t possible because the defect was sitated anterior. conservative f.m. gramada, d. haba lumbar pseudomeningocele after spinal surgery treatment was not effective, as evidenced the mri images effectuate a few months away. in this case we chose to do before surgery a single transcutaneus evacuation which allowed removal of 70 ml of fluid, followed by bed rest in trendelenburg and the local compression. both mri controls performed immediately and after a few months showed that the fluid collection was almost entirely disappeared and the patient's symptoms had improved. we believe that this gesture of percutaneous evacuation is a method that can be effective in some cases rebel to conservative treatment measures. references 1. aldrete j. a., ghaly r.: postlaminectyomy pseudomeningocele. an unsuspected cause of low back pain. reg. anesth. 1995, 20, 1, 75-79. 2. couture d., branch jr. ch. l.: spinal pseudomeningoceles and cerebrospinal fluid fistulas: pathophysiological features., neurosurg. focus, 2003,15,6,1-5. 3. eljamel m. s.: antibiotic prophylaxis in unrepaired csf fistula. br. j. neurosurg., 1993, 7, 5, 501-505. 4. hawk m. w., kim k. d.: review of spinal pseudomeningoceles and cerebrospinal fluid fistulas. neurosurg focus, 2000, 9, 1, article 5, 1-8. 5. jankowitz b. t., attenberry d. s., gerszen p. c., karausky p., cheng b. c., faught r., welch w. c.: effect of fibrin glue on the prevention of persistent cerebral spinal fluid leakage after incidental durotomy during lumbar spinal surgery. european spinal journal 2009, 18, 8, 1169-1174. 6. jones a. a., stambough j. l., balderston r. a., rothman r. h., booth jr. r. e.: long-term results of lumbar spine surgery complicated by unintended incidental durotomy. spine 1989, 14, 4, 443-446. 7. leis a. a., leis j. m., leis j. r.: pseudomeningoceles: a role of mechanical compression in the treatment of dural tears. neurology 2001, 56, 8, 1116-1117. 8. maycock n. f., van essen j., pfiitzner j.: postlaminectomy cerebrospinal fluid fistula treated with epidural blood patch. spine 1994, 19, 19, 2223-2225. 9. morgan-hough c. v. j., jones p. w., eisenstein s. m.: primary and revision lumbar discectomy. j. bone joint surg. 2003, 85-b, 871-874. 10.reisinger p. w., hochstrasser k.: the diagnosis of csf fistulae on the basis of detection of beta 2transferrin by polyacrylamide gel electrophoresis and immunoblotting. j. clin chem clin biochem. 1989, 27, 3, 167-172. 11.waisman m., schweppe y.: postoperative cerebrospinal fluid leakage after lumbar spine operations. conservative treatment. spine, 1991, 16, 5253. microsoft word 1.iacobb_reflections_f.doc romanian neurosurgery (2012) xix 4: 247 – 250 247 reflections on medical malpractice stress disorders in neurosurgery g. iacob1, c. majer2 1neurosurgery clinic, univeritary hospital bucharest, romania 2neurospinal hospital, dubai, uae murphy's law: “if anything can go wrong, it will!” medicine is a practice based on scientific proofs. neurosurgeons are a high-risk group for allegations of malpractice; also theyare humans and they do make mistakes “errarehumanumestsedperseverarediabolicum” (seneca). the most frequent allegations 56% involved the spinal surgery cases, 39% the head and/or brain and 5% are miscellaneous (1). of particular significance in terms of improved diagnostic methodology were spinal operations at the wrong level as well as failure to diagnose sentinel bleeds, aneurysms, arteriovenous malformation and other cerebral lesions (2). therefore every day a busy neurosurgeon may confront in consultations, operations or even after discussions with resposibles of medical staff the fears of medical malpractice: loss of reputation, loss of of significant supporters, lack of knowledge about the potential process and outcomes, loss of livelihood, loss of control, loss of assets. the magnitude of the problem (3): in 2005 alone,in theusa, for 3,229 active neurosurgeons certified by the american board of neurological surgeons (abns) neurosurgeons paid a total of $28 million in malpractice claims, to provide remediation for negligent medical care;with the highest average payment per specialist surgeon $465,000 and the single highest payment of any claim in any specialty $5.6 million.also an overzealous application of malpractice in the united states can have devastating effects on practicing neurosurgeons as the council of state neurosurgical societies (csns) survey in 2002 proof: nearly half of all respondents were likely to restrict their practice for example, limiting their practice to only spine or not providing emergency or trauma coverage at a local emergency room. nearly one third of respondents at that time stated that they were considering retirement, rather than continue to practice in the face of increasing insurance costs, especially in that states with high malpractice claims and high malpractice insurance premiums (so called "crisis" states) one fifth stated that they were considering moving their practice to a state with "better" malpractice conditions, affecting patients demanding neurosurgical procedures. several facts in my plea concerning medical malpractice in neurosurgery are: no neurosurgeon is immune from medical malpractice; practicing good neurosurgery, in and of itself, is not a guarantee that sombody will avoid being hit with a medical malpractice lawsuit; to 248 iacob, majer reflections on medical malpractice stress disorders in neurosurgery failedto meet the prevailing standard of care,especially negligence allegation the main cause for malpractice incidence of malpractice claims is increasing influenced by the number and selection of patients, the anvergure of the procedure, but also by the social systems: compensation claims increasing the incidence rate bad outcomes may result even with the best of medical care; it’s important to explain that bad results don’t equate with malpractice and good results don’t mean that the patient has had the best of care ! being sued for medical negligence, a predictable hazard of medical practice in our times may lead to frustrated, dissatisfied patients; the neurosurgeon with malpractice is perceived as a “wound to the heart”. as a consequence and risks of excessive encouragement of medical complaints, most neurosurgeons are not well prepared to deal with bad consequences of medical malpractice on themselves, their family and their medical practice neurosurgeons will avoid treating high risk cases, no longer performing high risk neurosurgical procedures such as aneurysm surgery, complex spine surgery, pediatric tumors or not treating neurosurgical emergencies (4); they leave the community/cities or even countries where the risks of being sued easily (because of unhappy patients) patients will not find the appropriate specialist to treat them and they may lose chances to receive the accurate treatment in the needed time; this may even negatively influence any investment from the medical community a neurosurgeon's chances of being sued for malpractice are not necessarily related to the medical complexity of a particular case but rather to the types of cases with which the physician is involved. elective spinal surgery cases constitute the majority of litigation (2). diagnosis of medical malpracticeare based on the following three elements: negligence: deviation from the standard of medical care, which means that you did something outside your area of expertise or did it in a fashion that others in your profession would not have done, affecting the same degree of skill used by other physicians under the same or similar circumstances proximate cause: to prove causal connection, the direct link between the negligence and damage damage: proof of damage, directly resulted from the breach of the alleged standard of medical care once a medical malpractice case appear,the stress of being accused with malpractice make the accused neurosurgeon:extremely stressful and traumatic and may lead to what was recognized as “medical malpractice stress syndrome” which manifest first by psychological symptoms such as anxietysymptoms: irritability, tiredness, restlessness, difficulty in concentration, excessive worry may occupy more than 50% of working hours, tense muscles, insomnia, depression and if this last it leads to physical illness, affecting his life at work and at home.if neurosurgeon has a weak personality, stress of medical malpractice stress syndrome and the resulting dissatisfaction lead to burnout of the medical practice, early retirement or even may generate extreme reaction, deep depression leading to suicide.another aspect of the problem is economic: the costs of defensive medicine generated by the romanian neurosurgery (2012) xix 4: 247 – 250 249 stress physicians to protect themselves from being sued: ordering unnecessary tests, referrals and hospitalizations are tremendous; some estimate $55.6 billion annually, cited by (5). neurosurgeons can take steps to reduce their vulnerability to potential litigation, avoiding or reducing medical malpractice stress: to define risk management “the process of attempting to identify and reduce or manage incipient risk of injury to patients in the clinic, hospital or any medical care setting” to avoid negligence: limit your activity, made a good selection for patient, for surgical skills, thinking before surgery to availability of resources and facilities in your hospital; make sure you are fully prepared; avoid to do something new that you are not adequately trained for, outside of your expertise;avoid to do something in careless way.you should never regret to loose effort ad time for patient and relatives education about any possible complications even about unexpected outcome that can reduce your risk of getting sued, complete carefully the informed consent if you have a complication,an unexpected result be forthcoming with the reason, communicates openly and explain to the patient how and why it occurred; don’t avoid the patients or hide the facts most patients simply want to know what happened and most important knows you care.document complication in your recordwhich should be “concrete” (use neuroinvestigations, explaining when, how and why they occurred, visit the patient more offen!). in such situation noattorney wants to put time and money necessary to pursue litigation into a case involving unavoidable complications; also the lawyer can tell the patient that they are dealing with a complication rather than negligence. accused neurosurgeon should be prepared: your goal is to be successful in demonstrating that what occurred was a complication rather than a deviation from the standard of medical care, to reduce vulnerability to potential litigation and to increase the odds of a successful defense (1): do not hide information, all hidden information it will be found work to help the patient recover, making him a very strong defendant try to keep the patient away from the attorney’s office or discourage the attorney from accepting the case and pursuing the claim against you;allways thinkto an ancient romanian saying: “it’s better to accept a wrong consent, instead of a fair judgment” seek advice from experienced colleagues, malpractice and estates lawyers, counselors, consultants; identify a qualified expert knowledge is power be actively involved in the defense team; discuss your ideas and suggestions with your lawyer but follow their instructions ask questions and acknowledge that this is not the neurosurgeon’s sphere of expertise be careful about possible conflicts of interest between the insurer and the neurosurgeon attend supportive educational meetings, read available materials on litigation stress support seek support, understanding and comfort from family, professional colleagues and organizations, friends, defense counsel 250 iacob, majer reflections on medical malpractice stress disorders in neurosurgery conclusions medical malpractice litigation is one of the most stressful events of the life of any physician, from which the physician can actually become a better doctor; it’s a survivable and surmountable event. everyneurosurgeon may become a stronger and better doctor – “there is only one answer to defeat,the victory” sir w. churchill. best solutions still remain education, training or new techniques at any level & any age and a good communication with the patients, their relatives. adapting techniques to medical experience, hospital resuources and a good chronic disease patients selection are mandatory.in medical malpractice litigation professional support from neurosurgeonscollegues, local medical societies and associations is needed; evensupportive2-nd opinion from international professional organizations (medico-legal committees) will be of great help. references 1. rovit rl, simon as, et al. neurosurgical experience with malpractice litigation: an analysis of closed claims against neurosurgeons in new york state, 1999 through 2003, j neurosurg.2007 106(6):1108-14. 2. fager c.a. malpractice issues in neurological surgery, surgical neurology 2006, 65(4): 416-421. 3. betsy van die study analyzes how the malpractice environment impacts practicing neurosurgeons, aans communications department, 2008 apr 28, (312) 949-3205. 4. berenson ra, kuo s, may jh, medical malpractice liability crisis meets markets: stress in unexpected places, issue brief cent stud health syst change. 2003 sep;(68):1-7. 5. sacopulos m.j. dealing with malpractice litigation stress, comment surgistrategies, apri; 23, 2012. microsoft word 1ianovicin_professornoblu.doc romanian neurosurgery (2010) xvii 3: 255 – 260 255 professor nicolae oblu creator of the neurosurgical school in iasi 1912-1995 n. ianovici president of romanian society of neurosurgery he was born on august 7th 1912 in olteniţa (calarasi county), he graduated from “c. alimăşteanu” high school. in 1932 he applied to the faculty of medicine in iaşi. as a student he worked since 1936 as a post-graduate who wanted to become a scientifical candidate in the laboratory of descriptive anatomy led by professor grigore t. popa. after graduating from the faculty in 1938 he continued his activity as a lecturer and afterwards he worked as an assistant in anatomy while simultaneously being an intern at the emergency surgery department at „sfantul spiridon” hospital. on april 18th 1940 he presented his thesis entitled correlations entre le caliber des vaisseaux nouricieres ou fonctionels et le masse totale des organs qu’ils desservent (brawo typography iasi, 1940) becoming doctor of medicine and surgery (diploma no. 2024/1940). since june 2nd 1940 he obtained the physician’s right to profess medicine (published in m.o. 127/1940). at this time he began working as a resident physician in the surgery hospital of social security house in iasi, and since 1944 he worked also as a resident physician in “charity” hospital in iasi, under the guidance of professor al. moruzi. since early years, the latter kept a close watch on his surgical activity impelling him to choose neurosurgery. it is worth mentioning that professor moruzi had always been preoccupied to separate the field of neurosurgery from the surgical specialities, being considered the founder of this speciality in romania together with d. bagdasar in bucharest. the medical documents of the time show that the first modern neurosurgical interventions were performed under his guidance at socola hospital in iasi in 19321934, and afterwards the department was moved to “charity” hospital in iasi until 1951. in this latter hospital, al. moruzi was in charge of this department in 1934-1948 and in 1948-1951 dr. vsevolov urbanovici was the head of the department. on 22nd of march 1946 he takes the exam and becomes a resident physician (decizia m.s. 138.260/1946) and in 1951 oblu is offered the title of master in surgery and becomes the head of the neurosurgical department; on october 1st 1964 he is transferred to the neurosurgical clinic within the department of medical training and specialization at the institute of medicine and pharmacy. during the period in which the department belonged both to the “charity” hospital, and to the “parhon” hospital within the second department of surgery (headed by professor o. francke) in iasi, dr. oblu also continued his educational activity becoming a lecturer on topographic anatomy and operative surgery (m.s. decision 94249/1944) and lecturer in neurosurgery (m.i. decision 1964). 256 n. ianovici professor nicolae oblu figure 1 phd thesis of prof n oblu after tenure, he was appointed head of neurology, neurosurgery, endocrinology and psychiatry department in the institute of medicine and pharmacy (ordin m.i. 3652/1964). in 1966 he takes the exams and becomes professor of neurosurgery. as a professor, he remained in charge of the neurosurgical department in iasi until his retirement in 1977. his extremely meticulous activity was rewarded with “the victory medal” (1946), “liberation from the fascist yoke” medal (1954), order of the star of the romanian people’s republic (1955), the great prize for his activity in the health network (1962), the medal for the 20th anniversary of the liberation of the homeland (1964), order of the star of the romanian people’s republic (1964), the 25th anniversary of the romanian people’s republic (1969). he was appointed eminent doctor of the rsr and honorary member of the romanian academy. the entire activity of professor nicolae oblu was a path to success: medical assistance, education, research, administration. in terms of medical assistance he approached every modern neurosurgical field, although the technical possibilities left a lot to be desired most of the times. professor oblu improved his knowledge on descriptive and topographic anatomy and operative surgery thanks to his outstanding theoretical preparation, being an ideal surgeon for his collaborators. with great operating skill, professor oblu impressed by the finesse of his gestures and by the instant solutions that solved the most difficult cases. he approached the skull, the spine, the peripheral nerves, the trauma and the tumours, the ablative or functional neurosurgery masterly. due to his rigour, but mostly due to his remarkable presence, he managed year after year to assemble the best students in the faculty for the study of the nervous system (n. oblu: memoir of titles and papers, thesis: tetraru c.: valoarea angiografiei in tumorile cerebrale, 1965, ianovici n.: sciatica paralizanta, urgenta neuro chirurgicala). thanks to his perseverance and results, he also managed to form a team of neurosurgeons in iasi, the only neurosurgeons in the country who had not been trained in professor c. arseni’s clinic in bucharest, but whose results have always been at the highest level. after this “golden team” (m. rusu, a. stanciu, gh. săndulescu), he created the premises of the 2nd (th. obreja, t. cozma) and 3rd generation (r. lăcătuşu, romanian neurosurgery (2010) xvii 3: 255 – 260 257 c. robu, n. ianovici), and consequently the neurosurgical school in iasi is renowned and appreciated even today in the national and european context. he edited numerous courses for students in anatomy and nervous system (course in central nervous system, the anatomy of vegetative nervous system, the anatomy of sense organs). professor oblu organized numerous conferences dealing with problems of neurosurgical emergencies (traumatology, tumours, infections, etc) attended by local neurosurgeons and neurologists and he contributed to the entry of these specialization courses for this type of doctors in neurosurgery clinic in iasi. his scientific activity was prodigious. in 1988 in the monograph entitled momente din istoria neurochirurgiei romanesti, there are mentioned over 101 scientific papers and articles that were published and communicated. let me list several titles so that you can get an idea about his preoccupations and the fields he approached during the years: normele şi variantele părţilor moi (exceptând creierul şi vasele sale) la români gr. t. popa, lucinescu e., frasin i., oblu. n. etc. congresul internaţional de antropologie bucureşti, 1937. tumora cerebrală moruzi a., oblu n. comunicare soc. endocr., neurolog., psihiatrie, martie 1944. un caz particular de tumoră medulară moruzi a., oblu n., urbanovici v. comunicare soc. medici şi naturalişti iaşi, 12 martie 1944. asupra unui caz de lobectomie frontală moruzi a., oblu n., comunicare soc. endocr., neurolog., psihiatrie iaşi, 1954. figure 2 article of cranioplasty published in russian journal, 1964 258 n. ianovici professor nicolae oblu figure 3 article in archives de l’union medicale balkanique and article presented in scientific meeting tratamentul sindroamelor dureroase ireductibile prin intervenţii chirurgicale pe nervii cranieni şi trunchiul cerebral oblu n. raport prezentat sfatului ştiinţific al ministerului sănătăţii în martie, 1951. consideraţii asupra unor paraplegii prin hernie de disc oblu n., rusu m., stanciu a. revista medico-chirurgicală iaşi, nr. 1, 1957. un model de foaie de observaţie clinică neurochirurgicală oblu n., rusu m. soc. neurologie, psihiatrie, neurochirurgie iaşi, 14 martie, 1958. he published together with b. pollingher at esculap publishing house in iasi ateroscleroza cerebrală, with th. obreja hematomul intracerebral primar, with ianovici n.v fistulele lichidiene cranio nazale, with rusu m. patologia sistemului vertebro-bazilar, he was co-author of the international treaty on neurology in vinken. romanian neurosurgery (2010) xvii 3: 255 – 260 259 figure 4 author of chapter in vinken’s treaty of neuroology figure 5 article in neurochirurgie (paris) he published many articles in the journals in the country, especially in neurology, psychiatry, neurosurgery, and abroad: rezultatele operatorii în arahnoidita optochiasmatică oblu n., rusu m. reviewed in arch. d’ophtalmologie et rev. générale d’ophtalmologie, nr. 20, p. 678, 1960. tulburări de schemă corporală în cadrul comiţialităţii oblu n., rusu m. revue neurologique france, 1964, recenzată în ann.psychologique nr. 122, t. nr. 4, aprilie 1964, p. 466. cranioplastiile cu acrilic oblu n., stanciu a., rusu m. voprosi neirochirurghii nr. 3, 1964, moscova. donné cliniques et resultants thérapeutiques sur l’hématome intracranien post traumatiques ; étude sur 308 obs oblu n., săndulescu gh., rusu m., stanciu a., banu t., petrovanu i., ciubotaru p. jounal de chirurgie, febr. 1965, t. 89, nr. 2, p. 221, 230 france. considerations clinico-thérapeutiques sur les fractures fermées de l’arc posterior de la premiére vertebre cervical – oblu n., săndulescu gh. acta orthopedica belgica mai 1965. cercetări experimentale privind patogenia chistului epidermoid oblu n., wasserman l., săndulescu gh., onofrei t. l’opportunité de la fermeture opératoire des fistules liquidiennes frontoetmoido-nasales post traumatiques oblu n., săndulescu gh., cozma n. rev. d’oto-neuro-ophtalmologie. t. xxxvii, nr. 2, 1965 france. he was a member of the society of doctors and naturalists in iaşi in 1947, member of the neurology and neurosurgery society, member of the ent society, member of the morphological society, vice president of the national society of psychiatry and endocrinology. in his administrative activities, professor oblu excelled in being a prestigious organizer, an authentic manager in the current sense of the word. 260 n. ianovici professor nicolae oblu figure 6 surgical team in operating theatre figure 7 opening ceremony of neurosurgical hospital, iasi after establishing a neurosurgical service with 30 beds in socola hospital, he developed it soon by opening a second pavilion with a second operating room as well as intensive care unit (icu) cores with 7 beds (dr. pop), neuroradiology (dr. aldescu), neuropathology (dr. c. tetraru, dr. anghel, dr. costachescu), functional exploration (dr. v. cozma). however, the masterpiece of his life was the inauguration of the neurosurgery hospital in iasi, the biggest hospital with this profile in the country. working with professor oblu at that time, i could observe his exceptional ability to mobilize himself totally in order to achieve his goals; his day was split between responsibilities, surgeries, lectures, visits on building sites, displacements in moldova to obtain building materials (concrete, bricks, plates); he was calling upon the competent organs, interceding with different people and only occasionally going fishing or hunting to relax. he possessed a vast store of knowledge, he spoke french fluently, he was an admirer of paintings, having an impressive collection, and he also was an adoring grandfather for his two grandchildren. for those who met him, he was a role model, although he was temperamental and sometimes he held grudge against some for too long. this may be the reason why it was impossible to establish collaboration between the schools in iasi and bucharest. or maybe it was professor arseni’s infinite pride that did not let him admit that another neurosurgeon could be as good as he. thanks to his entire career, professor nicolae oblu is a milestone in the modern era of romanian neurosurgery, the creator of the school in iasi. microsoft word 12traboulayprogressandpromise 88 e.a. traboulay, jr. progress and promise of regenerative medicine rehabilitative medicine – progress and promise of regenerative medicine: from molecule to society december, 2010 “the 3rd annual conference ortho posturo gnosis – the knowledge to influence and control the disease” took place in iasi during the 4th of december, 2010, addressed to all of the doctors which contributed to this scope for therapy (neurologists cardiologists, rehabilitative in medicine, reumathologists, neurosurgeons, orthopedists etc). the theme of this year was interesting and promising field for the future of the medicine: rehabilitative medicine – progress and promise of regenerative medicine: from molecule to society. we choose from the conference same specials lectures which were selected by the scientific committee. assoc. prof. dr. sorin ioan stratulat chief of the clinic, rehabilitative functional medicine, balneoclimatology cf clinic hospital iasi, umf gr. t. popa iasi president of scientific committee progress and promise of regenerative medicine – molecule to society e.a. traboulay, jr. introduction on this auspicious occasion of celebration i take this opportunity to make a brief presentation on the theme of this conference the knowledge to influence and control diseases – as it applies to my field of biotechnology. an intriguing question that we can ask is how can we use regenerative medicine to increase lifetimes while allowing us to age gracefully? in my presentation i will provide some interventions and try to cover the following topics: 1) the history of tissue and organ regeneration; 2) approaches to regenerative medicine; 3) current clinical trials underway; 4) current research projects in my laboratory and 5) some economic factors influencing our industry. what exactly is regenerative medicine? the origins of regenerative medicine are based in greek mythology and i am sure evidence can be found elsewhere in other civilizations. as the story goes, zeus, who was the supreme ruler of the 12 gods on mount olympus, was upset that prometheus gave the technology of making “fire” to the greeks. to punish prometheus, zeus ordered him tied to a romanian neurosurgery (2011) xviii 1: 88 – 93 89 rock and sent an eagle to eat his liver each day. well prometheus was able to survive the ordeal because his liver was able to regenerate itself daily. fortunately today we still have that regenerative ability to some extent. to begin it is necessary to define regenerative medicine as it has different meanings to different people. this is because the field has become populated with engineers, physicists, biopolymer/biochemists, molecular biologists, mathematicians, nanotechnologists and computer specialists bringing diverse tools such as finite element analysis and computer aided designs to create scaffolds and a host of bio-materials for use in regenerative medicine. so today we can define regenerative medicine as “understanding the body’s healing process and speeding-up that process to a clinically acceptable time scale or outcome.” this involves using stem cell therapy, regenerative factors, specific acellular scaffolds, therapeutic cloning and finally integration in-vivo of the organ or tissue to affect a regenerative outcome in a patient. despite having some 100 trillion cells, the human body is very poor at repair as we seem to be in acute or chronic decline through disease, trauma or aging. the “holy grail” of regenerative medicine would be the duplication in humans the regenerative power of amphibians like the salamander which can regenerate an amputated limb in 70-days1. the history of tissue and organ regeneration as we survey the historical medical landscape we see interesting “tippingpoints” occurring every 100 years or so that have transformed the way doctors treat patients and the resulting improvement in successful outcomes. the giants like pasteur, lister and koch led a revolution in modern medicine. however, it took another 100 years before immunosuppressive drugs became available to doctors and then we saw a flurry of organ transplants between 1954 and 1967 – liver, lung, pancreas and heart. in the 90’s we were fascinated with wilmot’s somatic cell nuclear transfer cloning of “dolly.” biotechniques have been developed to quantitatively decellularize complex organs such as heart, liver, and kidney. these acellular matrices can provide attractive scaffolds for repopulation with the recipient’s own cells for tissue engineering as the extracellular matrix template contains appropriate three-dimensional architecture and regional-specific cues for cellular adhesion. in 2006 this work was pioneered by atala2 whose tissue engineered bladder was successfully transplanted using the patient’s own cells without antigenicity. in 2008 macchiarini3 and his multinational team at the university of barcelona was the first to have successfully transplanted a trachea into a patient, with end-stage airway disease, without antigenicity. the patient presented with dysphonia and cough due to tuberculosis infiltration of the cervical trachea and entire left main bronchus. a ct scan showed a circumferential, near-occlusive 3 cm airway stenosis starting 2 cm subglottically, and a hypoplastic left main bronchus with expiratory collapse. macchiarini removed cells and the major histocompatibility complex (mhc) antigens from a human donor trachea (cadaver), which was then readily colonized by epithelial cells and mesenchymal stem-cell-derived chondrocytes that had been cultured from 90 e.a. traboulay, jr. progress and promise of regenerative medicine cells taken from the recipient bone marrow. this graft was then used to replace the recipient's left main bronchus. the patient is healthy after 4 months and had no antidonor antibodies and is not on immunosuppressive drugs. approaches to regenerative medicine as we step through the frontiers of the 21st century, we are all witnesses to the cinderella story in the form of the induced pluripotent stem cells (ipsc’s). the process developed by yamanaka4 of reprogramming adult somatic cells to derive (ipsc’s) with the wand of transcription factors (oct4, sox2, klf4, and c-myc) and then differentiating them back to adult somatic cells. this is the most fascinating breakthrough in regenerative medicine since the structure of dna was elucidated. rossi5 further improved efficiencies by developing a non-integrating strategy for reprogramming cell fate based on administration of synthetic mrna modified to overcome innate antiviral responses – no teratomas. 3.1 intervention bioengineered tooth unlike other vertebrates, mammals can replace only their deciduous teeth. during mammalian evolution this regenerative capacity was lost6. the deterioration and loss of teeth that comes with old age affects more than smiles. periodontal disease has been associated with increased risk for heart disease and might quicken the pace of aging. poor nutrition after tooth loss could also cause problems. etsuko7 led a tooth regeneration team that devised an ambitious plan that sought to use stem cell biology, engineering, and computational biology to replicate the developmental program for odontogenesis. they proposed a laboratorygrown tooth rudiment that would be capable of executing the complete program for odontogenesis when transplanted into a mouse host, recreating all of the dental tissues, periodontal ligament, cementum, and alveolar bone associated with the canonical tooth. to this end epithelial and mesenchymal stem cells were placed within a collagen gel and cells were expanded (ex-vivo) for 7days to obtain ~200,000 cells which were then transplanted with the correct orientation into a properly-sized bony hole in the upper first molar region of the alveolar bone. the results showed that the cusp tip of the bioengineered tooth was exposed into the oral cavity with full occlusion at 36.7± 5.5 days after transplantation. a more elegant solution would be to design a gene to allow a third set of teeth erupting at the age of 55. this would be an ingenious fix if we ignore the pain some of us experienced with the eruption of our molars. 3.2 regenerating the articular surface of a synovial joint osteoarthritis is a debilitating disease that manifests as structural breakdown of cartilage and bone that affects over 80 million individuals in the usa alone8. to understand the nature of the problem the synovial joint consists of multiple tissues including articular cartilage, subchondral bone, hematopoietic marrow, and synovium making repair somewhat problematic. current therapy requires arthritic joints to be replaced by total joint arthroplasty using metallic and synthetic materials which fail mainly because of aseptic loosening or infection induced by wear debris9. this is an interesting problem that can only be solved by biological regeneration. although stem cell transplantation has been tried, the results romanian neurosurgery (2011) xviii 1: 88 – 93 91 are mixed for a variety of reasons, with some patients finally having joint arthroplasty. to solve this problem, jeremy mao10 and his team regenerated the articular surface of the synovial joint of a rabbit with a biological cue spatially embedded in an anatomically correct bioscaffold. the surface morphology of a rabbit proximal humeral joint (cadaver) was captured with laser scanning and reconstructed by computer-aided design. the team fabricated an anatomically correct bioscaffold using a composite of poly-ecaprolactone and hydroxyapatite. the entire articular surface of humeral condyles of skeletally mature rabbits was surgically excised and replaced with the bioscaffolds spatially infused with transforming growth factor ß3 (tgfß3)-adsorbed or tgfß3free collagen hydrogel. locomotion and weightbearing were observed in the test rabbits 3–4 weeks after surgery. at 4 months the entire articular surface of the synovial joint was regenerated without cell transplantation. regeneration of complex tissues is probably by homing of endogenous cells, as exemplified by stratified avascular cartilage and vascularised bone. clinical trials the first approved u.s. clinical trial to use human embryonic stem cells to treat a disease has enrolled its first patient. geron corp., which is sponsoring the trial using stem cells to treat spinal cord injury, announced that the first patient was treated on october 8th 2010 at a hospital in atlanta. the primary objective of this phase i study is to assess the safety and tolerability of grnopc1 in patients with complete american spinal injury association (asia) impairment scale grade a thoracic spinal cord injuries. participants in the study must be newly injured and receive grnopc1 within 14 days of the injury. geron will be testing oligodendrocyte progenitor cells, precursors to some nervous system cells the company developed from one of the original human embryonic stem cell lines developed by james thomson’s lab at the university of wisconsin, madison. the goal is not to create new nerve fibers but to support those still intact by making the nerve insulator myelin. to prevent rejection, patients will take immunesuppressing drugs for about 60 days. although the primary goal is to assess safety, geron will be looking for hints that the cells had an effect—for example, improving bladder and bowel function, sensation, or mobility. advanced cell technology will conduct the second fda approved clinical trial using embryonic stem cell–derived retinal pigment epithelial cells to treat stargardt’s macular dystrophy, a congenital eye disease. the company is also filing an application to try the treatment in agerelated macular degeneration, a disease with similar characteristics that affects as many as 30 million people in the united states and europe. cell therapy seems promising for the disease for several reasons. first, the eye is an immune-privileged site, so researchers hope that patients won't have to take antirejection drugs after receiving the transplant. second, because the retina can be observed at the single cell level it should be possible to follow the transplanted cells' behavior very precisely. the patients will receive up to 200,000 retinal pigment epithelium (rpe) cells that the company derived from hes cells, transplanted directly into the eye. 92 e.a. traboulay, jr. progress and promise of regenerative medicine our laboratory our laboratory is specialized in the isolation, expansion and cryostorage of stem cells obtained from umbilical cord blood, wharton’s jelly, deciduous teeth and adipose tissue. we are currently in the process of making therapeutic doses for sale. our laboratory (450 m2) has clean rooms and is fully certified having iso 14644-1/1999, iso 14644-2/2000, iso 14644-3/2005, iso 9001:2008, fda/gmp annex1/2003 with fact-netcord pending. although this is a hybrid commercial laboratory, we have embarked on a modest research project to regenerate the retina in patients suffering from trauma, disease and age-related loss of vision using autologous mesenchymal stem cells. this is a joint project with prof. fotiadiou at the university of basel, switzerland and local greek ophthalmologists. hopefully at our next meeting i would be able to report some results. economic considerations in the us it is generally believed that there are approximately 1.400 biotech laboratories with approximately 300 traded on wall street. these companies have produced over 200 approved therapies using stem cells which have been approved in the us, europe and australia. the geographical split of the biotech market in 2004 shows the us accounting for 59.6% of the global market, or $26.4bn, around 2.8 times the total combined sales in the top five european countries – france ($2.4 billion), germany ($2.8 billion), italy ($1.6 billion), spain ($1.3 billion) and the uk ($1.2 billion). the rest of the world estimated at $5.5 billion. this is a significant difference considering that a similar number of products were available in both regions at any given time. the total worth of the global biotech market in 2004 was $44.3 billion11. i have performed a more comprehensive analysis of the global biotech market for 2009 and the results show an impressive gain of 122% in the 5-year period amounting to $98.7 billion – see table 1. table 1 global biotech market global biotech market 2009 technology 2009 (us mill $) stem cell transplant 9.250 cord blood collection and storage 1.800 tissue engineering 25.500 blood transfusion products 36.000 cell-based gene therapy 9.000 encapsulated cell therapy 2.700 cell-based cancer vaccines 2.200 xenotransplantation 2.700 supporting technologies: cell lines, cell culture, delivery devices 9.563 total 98.713 in summary, i believe that in the future is bright for biotechnology companies allowing us to gain the knowledge to influence and control diseases. in 2011 we will see the cost for a personal genome analysis below $1.000 and results taking less than one week. this will open a new field that will allow nanotechnology to design robots to repair our dna before the onset of debilitating diseases. furthermore in the very near future, it will be possible for every person to have their own ips cell lines, romanian neurosurgery (2011) xviii 1: 88 – 93 93 prepared when they were still healthy, for future applications in clinical examination and/or therapy. references 1. brockes jp, kumar a. 2005. appendage regeneration in adult vertebrates and implications for regenerative medicine. science 310(5756), 1919–1923 (2005). 2. atala, et. al. 2006. tissue-engineered autologous bladders for patients needing cystoplasty. the lancet, volume 367, issue 9518, pages 1241 1246, april 2006. 3. macchiarini, p. et al. 2008. clinical transplantation of a tissue-engineered airway. the lancet, vol. 372 no. 9655 pp 2023-2030. 4. keisuke okita, masato nakagawa, hong hyenjong, tomoko ichisaka and shinya yamanaka. 2008. generation of mouse induced pluripotent stem cells without viral vectors. science vol 322 p 949-952. 5. luigi warren et al. 2010. highly efficient reprogramming to pluripotency and directed differentiation of human cells with synthetic modified mrna. cell stem cell 7, 1–13, november 5, 2010. 6. kawasaki, kazuhiko, suzuki, tohru, and weiss, kenneth m. (2005). phenogenetic drift in evolution: the changing genetic basis of vertebrate teeth. pnas vol. 102, no. 50, p18063-18068. 7. etsuko ikedaa et al. 2009. fully functional bioengineered tooth replacement as an organ replacement therapy. pnas vol. 106, no 32 p134713480. 8. lawrence rc, helmick cg, arnett fc, et al. (1998). estimates of the prevalence of arthritis and selected musculoskeletal disorders in the united states. arthritis rheum 1998; 41: 778–99. 9. park dk, della valle cj, quigley l, moric m, rosenberg ag, galante jo. (2009). revision of the acetabular component without cement. a concise follow-up, at 20 to 24 years, of a previous report. j bone joint surg am 2009; 91: 350–55. 10. chang h lee et al. 2010. regeneration of the articular surface of the rabbit synovial joint by cell homing: a proof of concept study. the lancet, doi:10.1016/s0140736(10)60668-x july 2010. 11. global biotech market. http://www.globalbusinessinsights.com a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 443-448 doi: 10.33962/roneuro-2019-070 www.journals.lapub.co.uk/index.php/roneurosurgery paediatric traumatic brain injury. study of analysis of outcome predictors vibhushankar parashar, vivek kumar kankane, gaurav jaiswal, tarun kumar gupta department of neurosurgery, r.n.t. medical college & m.b. groups of hospital udaipur (rajasthan), india abstract introduction. traumatic brain injury is a leading cause of death and disability among children, adolescents. therefore, analysing outcome predictors and initiating preventive policies may contribute to decreased incidence and better prognosis. aim. aim to describe the epidemiologic characteristics, mechanism of injury, radiological findings and also to analyse the determinants of outcome that could help to provide better critical care and also to establish effective preventive policies. material and methods. we conducted a prospective study including patients ≤18 years admitted to our neuro-intensive care unit at r.n.t. medical college ,udaipur, rajasthan, india from september 2016 to june 2018.factors including age, gender ,mode of injury, glasgow coma score(gcs) at admission ,pupillary size-reaction, radiological findings and their relation to outcome was assessed .patients were divided into mild, moderate and severe head injury according to gcs. outcome of patients was assessed by glasgow outcome scale. for statical analysis used chisquare test. statistical analysis was carried out using stata 11.0(college station, texas, usa) results. the study comprised of 84 paediatric patients. 44.4%of patients were within 1–5-year age group. the most common cause for trauma was falls and traffic accidents. patients with mild, moderate and severe head injury were 38.1%, 47.6%and 14.3% respectively. poor outcome predictors included severity of head injury, pupil size and reaction, midline shift on ct. conclusion. this study emphasizes increased burden of paediatric brain injury with assessment of predicting factors for more effective critical care of patients and emerging need for effective fall and traffic accidents prevention strategies. introduction traumatic brain injury(tbi) is a main cause of functional disability and death in children and adolescents worldwide.[1,2,3] falls and road traffic accidents have emerged as the major causes of pediatric head injuries and their prognosis in children differ from adults due to the different mechanisms of head injury and the structures of the skull.[4,5] infants and young children are more vulnerable to abuse because of their dependency on adults.[6] pediatric head injuries are critically important because of the risk of high mortality and potential for lifelong neurological disability which could mean dependence on others for keywords traumatic brain injury, paediatric, outcome predictors. corresponding author: vivek kumar kankane department of neurosurgery, southern tohoku general hospital, koriyama, fukushima, japan vivekkankane9@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 444 vibhushankar parashar, vivek kumar kankane, gaurav jaiswal et al. activities of daily living and years of compromised quality of life. the study aims to describe various factors and determinants of outcome that could help to improve care and make better preventive policies. material and methods this study includes 84 patients of ≤18 years of age who presented with head injury and admitted in neuro-intensive care unit at r.n.t. medical college, udaipur, and rajasthan, india from september 2016 to june 2018. we further analyzed those 84 patients on the basis of various factors including clinical factors(age, gender), mode of injury, glasgow coma score (gcs)at admission and glasgow outcome scale (gos).patients were subjected to detailed general physical examination, systemic examination, and central nervous system(cns) examination including gcs, pupil size and reaction. based on gcs, the patients were divided into mild head injury (gcs 13– 15), moderate head injury (gcs 9–12), and severe head injury (gcs ≤ 8) categories. all the patients were subjected to plain ct scan head, and ct findings were noted. after prior stabilization and workup, the patients were managed conservatively or surgically as and when needed. the outcomes of all these patients were assessed by glasgow outcome scale and divided into good (gos-4,5) and poor (gos-1,2,3) outcome. outcome was assessed in relation to age, sex, gcs, pupil size and reaction, noncontrast computed tomography scan (ncct head) features and other associated bodily injuries. for statical analysis used chisquare test. statistical analysis was carried out using stata 11.0(college station, texas, usa). results mean age was 8.4 years. 44.4% of patients were within 1–5year age group. the male to female ratio was 2.1 to1. it was evident from our series that age and sex had no statistical significance in outcome (p>0.05).for statical analysis used chisquare test. [table 1] number of patients good outcome poor outcome gender male 57(67.9 %) 51 (89.5%) 6 (10.5%) female 27(32.1 %) 24 (88.9%) 3 (11.1%) age (yr) <=5 37(44.1%) 34(91.9%) 3(8.1%) 6-12 19(22.6 %) 17(89.5%) 2(10.5%) 13-18 28(33.3 %) 24(85.7%) 4(14.3%) total 84(100%) 75(89.3%) 9(10.7%) table 1. correlation of age, gender with the outcome analysis the most common cause for trauma were falls(51.1%) followed by road traffic accidents(rtas) (40.5%), assault (2.4%), sports injury (2.4%)and others (3.6%) which include injury by some object on head .rta had a poor outcome in 14.7%while patients with fall had a poor outcome of 7% . [table 2] table 2. correlation of mode of injury, gcs score, pupil size with outcome analysis number of patients good outcome poor outcome mode of injury falls 43(51.1%) 40(93.0%) 3(7.0%) traffic accidents 34(40.5%) 29(85.3%) 5(14.7%) assault 2(2.4%) 2(100%) 0(0%) sports injury 2(2.4%) 2(100%) 0(0%) others (e.g.fall of heavy objects) 3(3.6%) 2(66.7%) 1(33.3%) gcs score 13-15 32(38.1%) 31(96.9%) 1(3.1%) 9-12 40(47.6%) 39(97.5%) 1(2.5%) <=8 12(14.3%) 5(41.7%) 7(58.3%) pupil size normal 74(88.1%) 71(96%) 3(4%) fixed and dilated 3(3.6%) 0(0%) 3(100%) anisocoria 7(8.3%) 4(57.1%) 3(42.9%) total 84(100%) 75(89.3%) 9(10.7%) 445 paediatric traumatic brain injury the percentage of patients with mild head injury (gcs of 13–15), moderate (gcs of 9-12, and severe (gcs <=8) were 38.1%, 47.6%, and 14.3% respectively. poor outcome was seen in the category of gcs ≤8 at 58.3%, followed by patients in group gcs 9–12 at 2.5% and group of patients with gcs 13– 15 at 3.1%, which was statistically significant (p< 0.05) for statical analysis used chisquare test, statistical analysis was carried out using stata 11.0(college station, texas, usa). [table 2] out of the 84 patients, 74(88.1%) patients had normal pupils, 7(8.3%) had anisocoria, and 3(3.6%) patients had fixed dilated pupils. fixed dilated pupil had poor outcome (100%) followed by anisocoria (42.9%) and normal pupils (4%), which was statistically significant (p< 0.05) for statical analysis used chisquare test. [table 2] ct scan findings were noted as normal in 12 patients(14.3%), isolated skull fracture in 20(23.8%), contusion or hematoma in 20(23.8%), extradural hemorrhage(edh) in 13 (15.5%),subdural hemorrhage(sdh)in 7(8.3%), brain edema in 7(8.3%), and subarachnoid hemorrhage in2(2.4%), pneumocephalus in 3(3.6%).among the mode of injury, it is evident that diffuse brain edema had poor outcome in 28.6%, sdh in 28.6%, contusion in 5%, while in edh it was7.7%. [table 3] from our series, we also concluded that poor outcome was most strongly associated with midline shift (mls) >3 mm (66.7%) and it was 20% with mls of<3 mm and it was 7.9% in patients with no mls (p< 0.05) for statical analysis used chisquare test. [table 3] table 3. correlation of radiological findings on ct and assessment of midline shift with outcome analysis number of patients good outcome poor outcome radiologicalct findings fracture 20(23.8%) 19(95%) 1(5%) edh 13(15.5%) 12(92.3%) 1(7.7%) sdh 7(8.3%) 5(71.4%) 2(28.6%) sah 2(2.4%) 2(100%) 0(0) contusion/hem atoma 20(23.8%) 19(95%) 1(5%) edema 7(8.3%) 5(71.4%) 2(28.6%) pneumocephal us 3(3.6%) 2(66.7%) 1(33.3%) normal 12(14.3%) 11(91.7) 1(8.3%) midline shift(mls) no 76(90.5%) 70(92.1%) 6(7.9%) yes<3mm 5(5.9%) 4(80%) 1(20%) yes >3mm 3(3.6%) 1(33.3%) 2(66.7%) total 84(100%) 75(89.3%) 9(10.7%) on analysis for associated injuries, fractures of face were noted in 10(10.7%), limb fractures in 6(7.1%), abdominal trauma in 4(4.8%), spinal trauma in 2(2.4%), chest trauma in 2(2.4%), multiple traumas in 2(2.4%), and isolated head trauma in 59(70.2%). it was noticed that chest, spinal, and multiple injuries were associated with a poor outcome (p< 0.05). [table -4]. outcome of patients was assessed by glasgow outcome scale [table -5]. table 4. correlation of associated other bodily injuries with outcome analysis no of patients good outcome poor outcome associated injury no injury(head trauma only) 59(70.2%) 57(96.6%) 2(3.4%) fracture facial bones 9(10.7%) 7(77.8%) 2(22.2%) abdominal organ injury 4(4.8%) 3(75%) 1(25%) fracture – limbs 6(7.1%) 5(83.3%) 1(16.7%) injury to chest 2(2.4%) 1(50%) 1(50%) spinal injury 2(2.4%) 1(50%) 1(50%) multiple injuries 2(2.4%) 1(50%) 1(50%) total 84(100%) 75(89.3%) 9(10.7%) 446 vibhushankar parashar, vivek kumar kankane, gaurav jaiswal et al. table 5. glasgow outcome scale in the study group glasgow outcome scale functional status no. of patients outcome 5 resumption of normal life, there may be minor neurological and or psychological deficit 5 (6%) poor 4 able to work in a shattered environment and travel by public transportation 2 (2.4%) poor 3 dependent for daily support by reason of mental or physical disability or both 2 (2.4%) poor 2 unresponsive for weeks or months or until death 6 (7.1%) good 1 death 69 (82.1%) good out of the 84 patients, 58(69.1%) were managed conservatively and 26 (30.9%) patients were managed surgically. the various surgical procedures performed in patients include fracture debridement and elevation in 12 (46.2%), hematoma removal with fracture debridement in 3 (11.5%), and hematoma (edh, acute sdh, hematoma removal with decompressive craniotomy in 8 (30.8%)) decompressive craniotomy alone (for cerebral edema with midline shift of more than 5 mm)) in 3 (3.57%), we followed up our patients for a week to maximum of 12 months. discussion pediatric tbi remains an important public health concern worldwide, but with the advent of state of art intensive care unit and incorporation of multidisciplinary approach in developed countries, the outcome of the tbi patients has improved. yet, it still continues to be a major challenge in our part of the world, which further necessitates the adoption and implementation of strict prevention strategies. rivara et al. reported that boys have double the rate of brain injuries when compared with female counterparts. [7] in our study, 67.9% of the patients were boys. although gender differences were important in the rate of injury, they did not appear to adversely affect neurological outcome. in literature, there has been discrepancy regarding outcome in the pediatric age group. in our study, 37 (44.1%) were less than 5 year of age. one group of reports has indicated that outcome tends to be better in children under10 years of age[8,9]while others report that children under five have a higher mortality rate.[10]although in our series there was no difference in poor outcome in children below5 years or above 5 years as was reported by suresh et al.[11] falls and traffic accidents account for the majority of injuries in pediatric head trauma.[11,12]fall from height is the most common cause of injury in our study(51.1%) similar to study by garget al.[12]motor vehicle accidents accounted for nearly 40.5% of cases. in 2.4%of patients, assault was the cause of trauma. as age increased, the incidence of falls decreased but that of traffic accidents increased greatly. this is in contrast to the reports in which high-velocity trauma is the most common mode. [13] many studies show that the initial gcs is an excellent predictor of mortality [12,14] however, we observed that the classification of head injury into mild, moderate, and severe on the basis of initial gcs is a good prognostic factor for predicting chances of mortality.[12,15]suresh et al. reported poor outcome in the group of gcs 3–5 as 58.5%, gcs 6–8 had 35.2%, gcs 9–12 had 11.4%, and gcs 13–15 had1.3%.[11] beca et al. found that the initial gcs score was the single most important factor affecting outcome.[16] in our study, we found abnormal pupillary response being the strongest predictor of outcome. poor outcome in patients with normal pupils was 4%, patients with anisocoric pupils were 42.9%, and with fixed dilated pupils was 100%. astrand et al. reported 100% poor outcome in dilated pupils unresponsive to light. [17] we found isolated skull fracture in 20 (23.8%) patients with good outcome in 95% and poor outcome in 5%. suresh etal.had17% patients with isolated skull fracture with good outcome in 94.1% and poor outcome in 5.9%.[11]astrand et al.reported 48% of patients of edh with good outcome in 98% and poor outcome in 2%.[17]extradural hematoma is significantly less common in children than in adults and is even more rare in infants.[18] the outcome of patients with sdh is significantly 447 paediatric traumatic brain injury worse than that of patients with edh, mainly because of the underlying brain damage accompanying sdh and the resultant increased intracranial pressure. in our series, sdh was seen in 7 (8.3%) patients and out of those poor outcomes was noted in 2(28.6%) patients. in our study, diffuse brain edema was observed in 7(8.3%) with poor outcome in 2 (28.6%) patients. suresh et al. reported the incidence of diffuse brain edema as 30% with poor outcome in 25%. [11] quattrocchi et al. found prognostic significance of the presence or absence of midline shift(mls)on the basis of ct findings.[19] in our study, we found major prognostic significance of midline shift and strong predictor of poor outcome. athiappan et al. found the prognostic value of mls to be more important in patients with single contusions or intracerebral hematoma than for those with multiple lesions and extra axial or subdural hematoma. [20] in our study, we found that 70.2% of patients had only head trauma, 10.7% had facial trauma, 7.1% had limb fractures, 4.8% had abdominal solid organ injury, 2.4% had spinal injuries, 2.4% had chest trauma, and 2.4% had multiple injuries. paret et al. reported chest trauma in 62%, limb fracture in 32%, facial fractures in 29%, abdominal solid organ lesions in 20%, spinal cord injuries in 5% and multiple in 67%.[21]this difference is because we included all patients irrespective of severity of injury. the overall outcome of our series of patients revealed a mortality of 6% and good outcome of 82.1% with 7.1% patients have moderate disability and 4.8% patients being completely dependent for their day-to-day activities. [table5] conclusion rtas are more common in school children and adolescents, and falls are commoner in toddlers and preschool children. poor outcome was seen in the category of gcs ≤8 patients had fixed dilated pupils had poor outcome followed by anisocoria. from our series, we also concluded that poor outcome was most strongly associated with midline shift (mls) >3, there is an emerging need for effective fall and traffic accidents prevention strategies for children which includes educating about traffic rules and enforcement of road safety. prompt and accurate assessment of the severity of injury may lead to early initiation with better critical care which may prevent mortality in these patients. references 1. mazurek a. pediatric injury patterns. int anesthesiol clin1994;32:11–25. 2. jagannathan j,okonkwo do, yeoh hk, dumont as, saulle d, haizlip j, etal.long‑term outcomes and prognostic factors in pediatric patients with severe traumatic brain injury and elevated intracranial pressure. j neurosurgpaediatr 2008;2:237‑9. 3. rodriguez jg. childhood injuries in the united states. a priority issue. am j dis child1990;144:625–6. 4. keenan ht,bratton sl. epidemiology and outcomes of pediatric traumatic brain injury. dev neurosci2006;28:256263. 5. margulies ss, thibault kl. infant skull and suture properties: measurements and implications for mechanisms of pediatric brain injury. j biomecheng2000;122:364-371. 6. kumar r, mahapatra ak. the changing “epidemiology” of pediatric head injury and its impact on the daily clinical practice. childs nerv syst2009;25:813‑23. 7. rivara fp, bergman ab, logerfo jp, weiss ns. epidemiology of childhood injuries. ii. sex differences in injury rates. am j dis child1982;136:502-6. 8. carlsson ca, von essen c, lofgren j. factors affecting the clinical course of patients with severe head injuries. part 1: influence of biological factors. part 2: significance of posttraumatic coma. j neurosurg1968;29:242‑51. 9. comninos sc. early prognosis of severe head injuries in children. acta neurochir suppl1979;28:144‑7. 10. raimondi aj, hirschauer j. head injury in the infant and toddler. coma scoring and outcome scale. childs brain1984;11:12‑35. 11. suresh hs, praharaj ss, indira devi b, shukla d, sastry kolluri vr. prognosis in children with head injury: an analysis of 340 patients. neurol india2003;51:16‑8. 12. garg k, sharma r, gupta d, sinha s, satyarthee gd, agarwal d,kale ss, sharma bs, mahapatra ak.outcome predictors in pediatric head trauma: a study of clinicoradiological factors. j pediatrneurosci2017;12:14953 13. kokoska er, smith gs, pittman t, weber tr. early hypotension worsens neurological outcome in pediatric patients with moderately severe head trauma. j pediatr surg1998;33:333-8. 14. levin hs, aldrich ef, saydjari c, eisenberg hm, foulkes ma, bellefleur m, et al. severe head injury in children: experience of the traumatic coma data bank. neurosurgery1992;31:435-43. 15. chesnut rm, marshall lf, klauber mr, blunt ba, baldwin n, eisenberg hm, et al. the role of secondary brain injury in determining outcome from severe head injury. j trauma1993;34:216-22. 16. beca j, cox pn, taylor mj, bohn d, butt w, logan wj, et al. somatosensory evoked potentials for prediction of outcome in acute severe brain injury. j pediatr1995;126:44‑9. 17. astrand r, undén j, hesselgard k, reinstrup p, romner b. 448 vibhushankar parashar, vivek kumar kankane, gaurav jaiswal et al. clinical factors associated with intracranial complications after pediatric traumatic head injury: an observational study of children submitted to a neurosurgical referral unit.pediatrneurosurg2010;46:101‑9. 18. choux m, grisoli f, peragut jc. extradural hematomas in children 104 cases. childs brain1975;1:337‑47. 19. quattrocchi kb, prasad p, willits nh, wagner fc jr. quantification of midline shift as a predictor of poor outcome following head injury. surg neurol1991;35:183‑8. 20. athiappan s, muthukumar n, srinivasan us. influence of basal cisterns, midline shift and pathology on outcome in head injury. ann acad med singapore1993;22:452‑5. 21. paret g, ben abraham r, berman s, vardi a, harel r, manisterski y, et al. head injuries in children – clinical characteristics as prognostic factors1999;136:677‑81. microsoft word 8tataranuligiaendoscopic.doc 182 ligia tataranu et al endoscopic endonasal transsphenoidal approach endoscopic endonasal transsphenoidal approach in the management of sellar and parasellar lesions: alternative surgical techniques, results, complications (part ii) ligia tataranu1, m. gorgan1, v. ciubotaru1, anica dricu2, adriana dediu1, b. ene1, d. paunescu1, andra albert1, v. pruna1 1neurosurgical clinic, “bagdasar-arseni” clinical emergency hospital, bucharest, romania 2university of medicine and pharmacy, craiova, romania abstract the endoscopic endonasal transsphenoidal approach is a minimally invasive surgical technique for the removal of sellar and parasellar lesions. it allows panoramic vision of the surgical target and surrounding structures, with minimal trauma and a low complication rate. the procedure has been gaining in popularity in recent years. there are now surgical instruments intentionally conceived to respond to the specific characteristics of the neuroendoscopy. the widespread use of the endoscope in transsphenoidal surgery has recently contributed to the extension of the approach superior, inferior or lateral. this expansion carries significant potential for the resection of skull base lesions. for selected patients, the various techniques of the endoscopic endonasal transsphenoidal approach are valid alternatives to transcranial approaches. macroadenomas, suprasellar or even intraventricular craniopharyngiomas, tuberculum sellae or even planum sphenoidale meningiomas and clival tumors become accessible for removal via an endoscopic approach. the authors review the main alternative surgical techniques of the endoscopic endonasal transsphenoidal approach. they also present the results and the complications of the endoscopic transsphenoidal surgery. due to an improvement and refinement of the surgical procedures, the endoscopic endonasal transsphenoidal approach can be considered a good choice for the excision of the sellar and parasellar lesions. keywords: craniopharyngioma, endoscopy, meningioma, minimally invasive surgery, parasellar lesion, pituitary tumor, sellar lesion, transsphenoidal surgery. endoscopic endonasal transsphenoidal surgery was developed in the past decade under minimally invasive strategy. this endoscopic approach of the sellar and parasellar lesions introduces various advantages compared with the transsphenoidal microsurgical approach. the endoscope is used as a unique optical device. a wide view of the surgical field is obtained through angled scopes. the standard procedure is performed through a paraseptal route, via an anterior sphenoidotomy, without the traditional mucosal incision. it does not require the romanian neurosurgery (2010) xvii 2: 182 – 191 183 use of a transsphenoidal retractor or of an intraoperative fluoroscopic c-arm. also, postoperative nasal packing have been proved unnecessary. postoperative discomfort is minimal and the complication rate is low. the reduction in hospital stay significantly reduced the cost of patient’s management. endoscopic endonasal transsphenoidal surgery have been proved to be safe and effective. the operative technique is now standardized. standard endoscopic endonasal transsphenoidal approach uses a paraseptal route (between the middle turbinate and nasal septum) (figure 1). the approach of the sphenoid rostrum is made between nasal septum and lateral luxated middle turbinate. the vomer and the nasal septum are detached from the sphenoid rostrum and moved controlaterally (figure 2). sometimes, the fracture of the vomer bone can be difficult. however, changes in the standard technique are necessary in selected cases to optimize the surgical resection in minimally invasive conditions and to preserve anatomic structures [1]. one could use a minimal approach (hemisphenoidotomy), an extended or a bilateral approach (table 1). in this paper, we present variations of the standard endoscopic procedure designed to customize it for different lesions. 1. alternative surgical techniques of the endoscopic endonasal transsphenoidal approach 1. 1. transseptal approach deep-transseptal approach is an alternative technique. the septal mucosa is incised medial to middle turbinate and the cartilaginous septi is separed from the vomer. the controlateral septal mucosa is dissected from the controlateral surface of the vomer towards the sphenoidal rostrum. the vomer is removed and an anterior sphenoidotomy is performed. the mucosa from the ipsilateral part of the vomer is detached together with the vomer [2] (figure 3). 1.2. minimal approach particularly, in small intrasellar tumors developed in the inferior half of the sella turcica, the endoscopic approach can be minimal. only a hemisphenoidotomy ipsilateral to the lesion is performed, the anterior wall of the sphenoid sinus is removed until the midline is reached, and then a partial opening of the sellar floor is performed [1, 3] (figure 4). this technique is simpler when the interior septa of the sphenoid are absent or deviated, which is true for 75% of the cases [4]. this approach can be performed in ghsecreting or prl-secreting microadenomas with a lateral location, but not in acthsecreting microadenomas, because they are often multifocal [1]. figure 1 standard opening of the sphenoid sinus and the sellar floor for the resection of a pituitary macroadenoma 184 ligia tataranu et al endoscopic endonasal transsphenoidal approach figure 2 schematic drawings of the nasal cavity depict coronal (a) and axial views (b) of a paraseptal approach to the sella. the nasal septum and vomer are detached from the rostrum of the sphenoidal sinus and an anterior sphenoidotomy hole is made (of approximately 1.5 cm in diameter) figure3 schematic drawings of the nasal cavity depict coronal (a) and axial views (b) of a deeptransseptal approach to the sella table 1 alternative surgical techniques of the endoscopic endonasal transsphenoidal approach alternative surgical techniques of the endoscopic endonasal transsphenoidal approach nr. approach type surgical route 1 standard approach endoscopic, unilateral, endonasal transsphenoidal route 2 minimal approach endoscopic, unilateral, endonasal transsphenoidal route with hemisphenoidotomy 3a extended approach endoscopic, unilateral, transnasal transethmoidal transsphenoidal route 3b extended approach endoscopic, endonasal transsphenoidal route with planum sphenoidale opening 3c extended approach endoscopic, unilateral, endonasal transsphenoidal route with clival fenestration 3d extended approach endoscopic, unilateral, transnasal, transethmoidal transsphenoidal route, with superior turbinectomy 4 bilateral approach endoscopic, bilateral, endonasal transsphenoidal route romanian neurosurgery (2010) xvii 2: 182 – 191 185 figure 4 hemisphenoidotomy performed via an endonasal ipsilateral approach for the resection of a laterally located microadenoma figure 5 opening of the superior part of the anterior sellar wall, extending to the posterior part of the planum sphenoidale. the optic chiasm (1) and the anterior communicating artery complex (2) are visible after opening of the dura 1.3. extended approaches the endoscopic endonasal transsphenoidal approach can be extended superior, inferior or lateral. superior extended approach is used for lesions developed in the posterior part of the planum sphenoidale (meningiomas of the tuberculum sellae or small meningiomas of planum sphenoidale) and for lesions with a prechiasmatic extension (craniopharyngiomas and rathke’s cleft cysts) [1, 5]. the patient’s head is slightly hyper extended. the anterior wall of the sellar floor and the posterior part of the planum sphenoidale (1 – 1.5 cm) are removed with a micro drill or micro punches. the dura is incised starting from the anterior sellar wall and extending to the posterior portion of the planum sphenoidale, after coagulation and sectioning of the superior intercavernous sinus. the prechiasmatic region is exposed (figures 5, 6). the main challenge is the difficulty of obtaining a reliable watertight closure of the enlarged base opening. inferior extended approach is indicated in clival tumor (clival chordomas) [1, 6]. the patient’s head is slightly flexed. fenestration of the clivus, in the absence of any pathological lesion arising in or extending into this region, seems to be very difficult, because of rich vascularization from the dorsal meningeal artery and the basilar venous plexus and the presence of the paraclival internal carotid artery. when pathological lesions arising in or extending into the clivus are present, lesion removal is easier because of the displacement of these vascular structures [1] (figure 7). lateral extended approach is performed in sellar lesions with important extension to the cavernous sinus, usually pituitary adenomas. if only the medial aspect of the cavernous sinus compartment is the site of the parasellar development of the lesion, then it is possible to treat the lesion from the controlateral nostril, by using the standard endoscopic procedure [1]. 186 ligia tataranu et al endoscopic endonasal transsphenoidal approach a b c d e f figure 6 cystic suprasellar craniopharyngioma. a, b, c – mri images (in coronal view on observe anterior cerebral artery). d, e, f – endoscopic views (superior extended endoscopic endonasal transsphenoidal approach). d – the capsule of the craniopharyngioma is visualized after opening of the sellar dura. e – the optic chiasm is visible. f the optic chiasm and anterior cerebral artery complex are directly visible figure 7 opening of the lower part of the anterior sellar wall, extending to the upper clivus. fenestration exposes the basilar tip, the posterior cerebral arteries, the superior cerebellar arteries and the iiird cranial nerves if the lateral aspect is also involved, it is necessary to extend the anterior sphenoidotomy, with removal of the superior turbinate, to expose the lateral wall of the sphenoid sinus. the removal of the superior turbinate must be performed with regard for the lateral lamella of the cribriborm plate to avoid csf leak. additional room can be obtained with removal of the posterior ethmoid cell, with a limited maxillectomy and partial removal of the medial aspect of the pterygoid process [1] (figure 8). romanian neurosurgery (2010) xvii 2: 182 – 191 187 figure 8 lateral extended approach, with excision of the superior turbinate and opening of the posterior ethmoid cells, for removal of a lesion extending into the ipsilateral cavernous sinus. the dotted line indicates the commonly used sphenoidotomy by this route figure 9 the bilateral approach can be indicated for the convergent action of instruments, especially to visualize and to reach the controlateral suprasellar region 1.4. bilateral approach bilateral approach is used when the nostril are very narrow (in children), when the combined actions of more then two instruments could facilitate bleeding control or lesion removal, when an opposite working angle of two instruments inside the sella could provide enhanced surgical effectiveness [1]. in these cases, it is necessary to perform an extended anterior sphenoidotomy (figure 9). 2. results of the endoscopic endonasal transsphenoidal approach the endoscopic endonasal transsphenoidal approach has the same efficiency as the microsurgical transsphenoidal approach. this procedure is a safe and effective method, with a low rate of complication and morbidity [7-10]. minimal postoperative discomfort, quick recovery and short hospital stays of the patient have been noted [11-13]. jho (2002) reports 200 patients treated with the endoscopic endonasal transsphenoidal approach [13]. among them 160 had pituitary adenomas, 10 had skull base meningiomas, 8 had clival chordomas, and additional 22 had other skull base pathologies. 55 patients had previously undergone surgical treatment, radiation treatment or both. amongst the 160 patients with pituitary adenomas, 37 (37.5%) patients had microadenomas and 123 (62.5%) patients had macroadenomas. amongst the 90 patients with hormone nonsecreting adenomas, 71 (79%) patients underwent gross total removal. amongst the 38 patients with prolactinomas, prolactin levels normalized after surgery in 25 (68%) patients. of 18 patients with cushing’s disease, 13 (72%) had normal postoperative levels of cortisol. amongst the 13 patients with acromegaly, 11 (84%) had normalized postoperative levels of igf 1. postoperative complications included deterioration of anterior pituitary function in 11%, csf leak in 6%, meningitis in 1.2%, temporary diabetes insipidus in 4%, permanent diabetes insipidus in 3%, and sinusitis in 1.2%. one patient who had a large calcified recurrent fibro sarcoma died 188 ligia tataranu et al endoscopic endonasal transsphenoidal approach after surgery from bilateral occlusion of the internal carotid arteries. the length of the hospital stay was less than one day in 75% of the patients [13]. cappabianca et al. (2002) studied 100 patients who underwent an endoscopic endonasal transsphenoidal approach [7]. amongst the 87 pituitary adenomas, total resection of the tumor was performed in 51 patients, subtotal resection in 20 patients (80%) and a partial resection in 16 patients. 4 craniopharyngiomas was totally resected, one intrasellar arachnoid cyst was evacuated and in two clivus chordomas was performed a biopsy. two patients with sphenoidal sinusitis and three patients with spontaneous csf leak underwent endoscopic treatment successfully [7]. the authors consider the endoscopic endonasal transsphenoidal approach less traumatic then transsphenoidal microsurgery. the hospital stay was reduced to two days in 40% of the cases [7]. traditional transsphenoidal surgery had proved to be a reasonably safe procedure when performed by experienced surgeons. although the mortality rate is low, usually below 1%, morbidity is not negligible and complications still occur [8, 10, 14-16]. in 1997, ciric et al. presented the results of a study on the complications of transsphenoidal microsurgery. the study is based on personal experience and data submitted by 958 neurosurgeons from the united states who responded to a detailed questionnaire. the authors assigned each respondent to one of three groups based on the number of transsphenoidal operations performed (<200, 200-500, >500), and the results show the percentage of operations resulting in complications decreases as experience increases [10]. the results are presented in table 2. 3. complications of the endoscopic endonasal transsphenoidal approach complications of the endoscopic endonasal transsphenoidal approach were divided into groups according to the anatomical structures and the system that may be involved. the following categories are defined: nasofacial, sphenoid sinus, sella turcica, parasellar, suprasellar and endocrine complications [8]. 3. 1. nasofacial complications the most common complication is epistaxis and it is often delayed. the bleeding derives from the small branches of the sphenopalatine artery usually in acromegalic patients with nasal mucosa hypertrophy. the incidence of the epistaxis is reduced in endoscopic transsphenoidal approach (1.3%) as compared to the transsphenoidal surgery (3.4%) [8, 10]. the treatment of delayed postoperative bleeding from the sphenopalatine artery requires an anterior and/or posterior nasal packing for two days [17]. posterior packing provides compression of the posterior aspect of the middle turbinate, which in turn compresses the sphenopalatine and internal maxillary arteries. patients with refractory epistaxis required surgical re-intervention with the identification and coagulation of the sphenopalatine artery. an alternative treatment is the embolization of the internal maxillary artery [17, 18]. the sphenopalatine artery is the terminal branch of the maxillary artery. this artery enters the nasal cavity through the sphenopalatine foramen, topographically located behind the end of the middle turbinate, on the lateral wall of the nasal cavity, which also corresponds to the hidden inferior lateral corner of the sphenoid sinus. romanian neurosurgery (2010) xvii 2: 182 – 191 189 table 2 complications resulting from transsphenoidal pituitary surgery complications resulting from transsphenoidal pituitary surgery. comparative results number of surgical intervention series (ciric) < 200 200-500 >500 average 146 nr. type of complication % % % % % 1 septal perforation 7.6 4.6 3.3 6.7 0 2 epistaxis 4.3 1.7 0.4 3.4 1.36 3 sinusitis 9.6 6.0 3.6 8.5 2.05 4 carotid artery injury 1.4 0.6 0.4 1.1 0.68 5 central nervous system injury 1.6 0.9 0.6 1.3 0.68 6 hemorrhage / swelling of the residual tumor 2,8 4,0 0,8 2,9 0,68 7 visual dysfunction 2.4 0.8 0.5 1.8 0 8 ophthalmoplegia 1.9 0.8 0.4 1.4 0.68 9 csf leak 4.2 2.8 1.5 3.9 2.05 10 meningitis 1.9 0.8 0.5 1.5 0.68 11 anterior pituitary insufficiency 20.6 14.9 7.2 19.4 13.6 12 diabetes insipidus 19.0 7.6 17.8 3.42 13 death 1.2 0.6 0.2 0.9 0.68 inside the nasal cavity, the sphenopalatine artery splits into two branches: the nasopalatine artery (medial) which passes above the choana and leads to the nasal septum, and the posterior nasal artery (lateral) which reaches the lateral wall of the nasal cavity (figure 10). the risk of damaging the artery is potentially higher in the endoscopic endonasal procedure, because the approach to the sphenoid sinus is more lateral than in microscopic transseptal surgery. the sphenopalatine artery can be damaged during anterior sphenoidotomy, especially when the enlargement of the anterior wall of the sphenoid sinus is made in the inferior lateral or downward direction. the best way to avoid injury of the sphenopalatine artery or its nasopalatine branch is to laterally displace the mucosa and to remove the bony structures only. when an intraoperative bleeding occurs, bipolar coagulation of the bleeding vessel is recommended. 3.2. sphenoid sinus complications the postoperative sphenoid sinusitis can be diagnosed clinically or on sellar mri. medical treatment reduces the inflammation of the sinus. its incidence is 2% in the endoscopic approach and 8.5% in the conventional procedure [8, 10]. these results are due to a large opening of the sphenoid sinus, postoperative preserved pneumatization of the sphenoid sinus, not using the transsphenoidal retractor and respecting the osteomeatal landmarks. 190 ligia tataranu et al endoscopic endonasal transsphenoidal approach figure 10 schematic drawing illustrating the course of the branches of the right sphenopalatine artery. 1 – middle turbinate; 2 – nasal septum; 3 – choana; 4 – sphenoid sinus; 5 – sphenopalatine artery; 6 – nasopalatine artery; 7 – posterior nasal artery 3.3. sella turcica complications postoperative, csf leak can occur when the arachnoid is injured. an external lumbar drainage or endoscopic reconstruction of the sella can be used. this complication appears in 2% of patients in endoscopic approach, and 3.9% in microsurgical approach [8, 10]. 3.4. suprasellar complications in large tumors, in which partial removal was performed, ct scan revealed swelling of the residual lesion with compression of the proximal anatomical structures and neurological deficits. an intrasellar / suprasellar hematoma can appear and meningitis can occur as well. 3.5. parasellar complications in case of accidental lesion of the intracavernous carotid artery, major bleeding occurs and can be life-threatening. small lesions are intraoperative controlled with tamponade. once the bleeding has been controlled, a carotid cavernous fistula or a false aneurysm usually develops later on [17]. because massive bleeding can occur, a neuroradiological follow-up is recommended (non-invasive imaging techniques: angio-ct and mri). angiography can be employed as a second line of study. if a pseudo-aneurysm is present the endovascular techniques are preferred because they are more easily performed, are associated with lower mortality and morbidity and permit a complete exclusion of the lesion from the arterial circulation, with preservation of the patent artery [17]. lesions of the intracavernous nerves can also occur. 3.6. endocrine complications an anterior or posterior pituitary insufficiency (diabetes insipidus) can be diagnosed. diabetes insipidus may be transitory or permanent. conclusions neurosurgical treatment of sellar and parasellar lesions has undergone considerable changes in recent years. it has become possible to perform regular noninvasive follow-ups by mri, there are developments in drug therapy, the advent of gamma-knife allows for significant reduction of operative aggressiveness and minimal invasive surgery was extended [19]. nevertheless, despite all technical progress, results is still strongly dependent on how the surgery itself is performed and is determined by the operative approach. in transsphenoidal surgery, the endoscopic endonasal transsphenoidal approach can be considered a very good choice for the removal of different sellar and parasellar lesions. romanian neurosurgery (2010) xvii 2: 182 – 191 191 *correspondence to: ligia tataranu, md, phd, “bagdasar-arseni” clinical emergency hospital, sos. berceni 10-12, 041514 bucharest, romania e-mail: medic@neurochirug.ro phone: +40744-375 000 references 1.de divitiis e, cappabianca p, cavallo lm, endoscopic transsphenoidal approach: adaptability of the procedure to different sellar lesions. neurosurgery, 2002. 51(3): p. 699-707. 2.jho hd, alfieri a, endoscopic transsphenoidal pituitary surgery: various surgical techniques and recommended steps for procedural transition. british journal of neurosurgery, 2000. 14(5): p. 432-440. 3.moreland db, diaz-ordaz e, czajka ga, endoscopic endonasal hemisphenoidotomy for resection of pituitary lesions confined to the sella: report of 3 cases and technical note. minimally invasive neurosurgery, 2000. 43: p. 57-61. 4.rhoton al, harris fs, renn wh, microsurgical anatomy of the sella region and cavernous sinus. clinical neurosurgery, 1977. 24: p. 54-85. 5.jho hd, endoscopic endonasal approach to the optic nerve: a technical note. minimally invasive neurosurgery, 2001. 44: p. 190-193. 6.jho hd, carrau rl, mclaughlin ml, somaya sc, endoscopic transsfenoidal resection of a large chordoma in the posterior fossa. acta neurochirurgica (wien), 1997. 139: p. 343-348. 7.cappabianca p, cavallo lm, colao a, del basso de caro m, esposito f, cirillo s, lombardi g, de divitiis e, endoscopic endonasal transsphenoidal approach: outcome analysis of 100 consecutive procedures. minimally invasive neurosurgery, 2002. 45(4): p. 193200. 8.cappabianca p, c.l., colao am, de divitiis e, surgical complications associated with the endoscopic endonasal transsphenoidal approach for pituitary adenomas. journal of neurosurgery, 2002. 97: p. 293298. 9.cappabianca p, c.l., de divitiis e, endoscopic endonasal transsphenoidal surgery. neurosurgery, 2004. 55(4): p. 933-941. 10.ciric i, ragin a, baumgartner c, pierce d, complications of transsfenoidal surgery. results of a national survey, review of the literature and personal experience. neurosurgery, 1997. 40: p. 225-237. 11.badie b, nguyen p, preston k, endoscopic-guided direct endonasal approach for pituitary surgery. surgical neurology, 2000. 53: p. 168-173. 12.cho dy, liau wr, comparison of endonasal endoscopic surgery and sublabial microsurgery for prolactinomas. surgical neurology, 2002. 58: p. 371376. 13.jho hd, endoscopic transsphenoidal tumor surgery. operative techniques in neurosurgery, 2002. 5(4): p. 218-225. 14.black pmcl, zervas nt, candia gl, incidence and management of complications of transsfenoidal operation for pituitary adenomas. neurosurgery, 1987. 20: p. 920-924. 15.laws er jr, kern eb, complications of transsfenoidal surgery. clin neurosurg, 1976. 23: p. 401-416. 16.semple pl, laws er, complications in a contemporary series of patients who underwent trassfenoidal surgery for cushing's disease. journal of neurosurgery, 1999. 91: p. 175-179. 17.cavallo lm, b.f., cappabianca p, maiuri f, valente v, tortora f, volpe a, messina a, elefante a, de divitiis e, hemorrhagic vascular complications of endoscopic transsphenoidal surgery. minimally invasive neurosurgery, 2004. 47: p. 145-150. 18.cockroft km, carew jf, trost d, fraser ra, delayed epistaxis resulting from external carotid artery injury requiring embolization: a rare complication of transsphenoidal surgery: case report. neurosurgery, 2000. 47: p. 236-239. 19.marquardt g, y.h., hermann e, seifert v, direct transnasal approach for pituitary surgery. neurosurgical review, 2004. 27: p. 83-88. microsoft word 15.ianovicin_treaty_f.docx romanian neurosurgery (2012) xix 1: 81 – 82 81 neurosurgery – second volume nicolai ianovici head of ist neurosurgical department, “prof. n. oblu” clinical hospital iaşi we are happy to announce the publication of the second volume of “national book of neurosurgery”, which deals with approaches to neurosurgical pathology. this volume begins by presenting the outstanding personalities who made possible the accumulated adaptations which were strictly necessary in order to reach a certain level which allowed the implementation of a treaty. the chapters that are concerned with vascular diseases comprise: subarachnoid hemorrhage has clinical, paraclinical and therapeutic presentations. the intracranial aneurysms have a complicated pathology and they usually lead to subarachnoid hemorrhage. the chapter entitled “cerebral arteriovenous malformations” represent a sensitive and disputed element analysis in neurosurgery. the endovascular treatment of cerebral aneurysms and of cerebral arteriovenous malformations joins the effort to solve this extremely difficult pathology. brain cavernomas are a unique vascular category. the chapters that are concerned with functional neurosurgery comprise: the surgical treatment for epilepsy is a chapter in which it is stressed the fact that the interdisciplinary collaboration is strictly necessary. the surgical techniques, the vagal and deep structure stimulation which are specific to epilepsy surgery are presented in a modern way. the neurosurgical procedures used for the treatment of abnormal muscle tone and movement is presented in sub-chapters (parkinson disease, essential tremor, secondary tremor of multiple sclerosis, posttraumatic tremor, dystonia, cervical dystonia, facial hemispasm, spasticity), each sub-chapter having a separate bibliography. the neurosurgical procedures used for the treatment of chronic pain include intrathecal drug administration, neurostimulation, lesion techniques. stereotaxic is used not only in functional neurosurgery, but also in stereotaxic biopsy – a method which is more complex than any other biopsy. neuronavigation is included in the neurosurgical pathology. 82 nicolai ianovici neurosurgery – second volume spinal cord injuries represent, more often than not, a dramatic pathology. the recovery after suffering spinal cord injuries complements the previous chapter. the chapters that are concerned with spinal pathology comprise several chapters: the experimental stem cells treatments for spinal cord injuries is presented pertinently – but as the title suggests, it is experimental, without being able to establish any kind of efficiency. the psychological aspects of spinal cord injuries explains the role the psyche plays in the evolution and recuperation of these patients, in improving the quality of their lives. the chapter entitled “the intramedullary spinal tumors” presents the possibilities of the surgical act (in many cases, the obtained results are good – see the results and the prognostic), the complications, as well as how to avoid them. spinal arteriovenous malformations have reduced incidence, and some of them receive efficient treatments. degenerative pathology of the cervical and thoracic spine is becoming more and more frequent. in addition to this, cervical arthroplasty and other pathologies like ossification of the posterior longitudinal ligament should not be neglected. long time ago, degenerative lumbar spine pathology was regarded as “the neurosurgeon’s bread and butter”. degenerative lumbar spinal stenosis ends with the recommendation that the spinal instability should be corrected. lumbar spondylolisthesis is a current issue and the therapeutic solutions can be different. the chapter entitled “surgical expansive intraorbital processes” presents the expansive intraorbital processes (tumoral, infectious, inflammatory, traumatic, vascular). neurosurgical endocranian suppurations represent a pathology which must be very well known, with all the elements of etiopathogenesis, microbiology, clinical picture, evolutionary forms which allow a prompt and correct treatment (sometimes of emergency) in order to avoid any catastrophic developments. parasitic nervous system infections is a chapter which deals with increasingly rare cases which should not be overviewed. gamma knife stereotactic radiosurgery provides data about cerebral arteriovenous malformations and cerebral meningiomas. brain trauma neuroprotection and neuroplasticity is a chapter which deals with pathological mechanisms under which therapeutic possibilities are established. the management of the department of neurosurgery poses problems to the wellknown neurosurgeons who run this department. it is not a surprise that this volume, as well as the first volume, is realized in exceptional graphic conditions. microsoft word 2ciureaprofessor.doc 6 romanian neurosurgery (2010) xvii 1: 6 11 professor constantin arseni between myth and reality a.v. ciurea, r.e. rizea universitary hospital bagdasar-arseni, bucharest av. berceni, no.10-12, sector 4, bucharest, romania; e-mail: rsn@bagdasar-arseni.ro in romania, neurosurgery developed as a separate specialty starting with 1932. until then neurosurgical activity was sporadically, represented by operations on the nervous system performed by the great surgeons of the time in romania. constantin n. arseni (1912-1994) is born on 3 february 1912 în dolhasca, suceava region. he graduated the faculty of medicine of cluj in 1935, and sustained his doctor's thesis on "juxtaprotuberance neurotomy in the treatment of intermittent neuralgia of the trigeminus" on june 30, 1936 (figure 1). like student he worked in clinic of professor iuliu hatieganu in clujnapoca, but the youngest arseni loved the surgery of the brain after he see an operation of dimitrie bagdasar in emergency hospital from bucharest. at the age of 23, begins the indenture in domain of neurosurgery, below adminstration and direction of prof. d. bagdasar, returned from united states [4]. these first beginnings prove his definite orientation towards neurosurgery, bringing into romanian specialty literature a problem with neurosurgical implications. figure 1 juxta-protuberance neurotomy in the treatment of intermittent neuralgia of the trigeminus after a stage in the surgical department of the emergency hospital, bucharest, under prof. i. iacobovici, dr. c. arseni accepted prof. bagdasar's proposal to work in the neurosurgical unit of the central hospital of mental, nervous and endocrinological diseases, a.v. ciurea, r.e. rizea professor constantin arseni 7 bucharest. [7; 8] during the 1936 1946 period, c. arseni worked directly with prof. bagdasar, but completed his surgical skill during a three years concomitant activity in the emergency hospital. he likewise developed his knowledge of pathologic neurology when appointed university lecturer at the chair of pathologic anatomy under prof. i. t. niculescu (1937 -1944). [2; 3] embracing a career that had not yet been clearly outlined anywhere in the world, he devoted most of his time to the service created by prof. d. bagdasar, working with particular enthusiasm in this direction. he was the only surgeon assisting bagdasar during that period and substantially contributed to the progress of the neurosurgical department and its good management. he was at first responsible for the clinical and surgical treatment of neurosurgical patients, and tried to improve and complete his knowledge and understanding of the newly created specialty. the clinical and laboratory studies carried out during this period were essential for his contribution to the “traite of neuchirurgie" published together with prof. d. bagdasar in 1950 (figure 2). [1;9]. at the age of 34 (in 1946) – after the premature death of prof. d. bagdasar the young doctor c. arseni becomes head of the neurosurgical department in the central hospital for mental, nervous and endocrinological diseases, the only department of this kind in the country. after taking up duty in 1946, in a department with 80 beds after strenuous endeavors, arseni was able to have the present clinic of neurosurgery extending, in bucharest, as it now stands, thus contributing to the development of this specialty in the country. at the university, he was appointed associate professor in 1952 and professor of neurosurgery in 1963. [6]. the clinic of neurosurgery of bucharest developed rapidly, approaching the most various aspects of neurosurgical pathology. the increased number of subjects with which the clinic was concerned necessitated a constant effort of organization, technical development and research work. in 1964, the number of beds had increased to 220, distributed in the various sections strictly according to the specialties: two surgical sections for cerebral expanding processes, one each for vertebromedullary surgery, infantile neurosurgery, cerebrovascular surgery, epilepsy and dyskinesia, head and spinal injuries, with a subsection of general traumatology. there are two operative blocks with 7 operation theaters. in 1960, a special anesthesia and intensive care unit was opened and equipped according to the most modern requirements. paraclinical activity and scientific research was carried out at that time (1964) by a laboratory of electroencephalography with 4 modern apparatus, a laboratory of electromyography, of neuromorphopathology and of biochemistry. the neuroradiology department developed both in the direction of standard investigations and complex research work with contrast media: angiography, ventriculography, iodoventriculography, air and iodine ventriculography. the surgery of epilepsy may be applied owing to a: stereotaxic surgical equipment. 8 romanian neurosurgery (2010) xvii 1: 6 11 figure 2 traite of neuchirurgie figure 3 prof. c. arseni under professor c. arseni (figure 3), the neurosurgical clinic of bucharest is transformed in 1975 into the "prof. dr. d. bagdasar" clinical hospital of neurosurgery, the largest hospital of neurosurgery in europe, with 550 beds and, subsequently, 650 beds. it appears as a crowning and a confirmation of the value of neurosurgery within the framework of medical specialties. conceived and built according to carefully skilled and daring plans, the new clinic of neurosurgery is structured in seven clearly separate clinical departments, including also a pediatric neurosurgical department. in the neurosurgical clinic there is an independent icu department with 26 beds. the operatory activity is carried out within two operating theaters with 13 operating rooms. the simple mention of the services within the neurosurgical clinic founded in 1975 (figure 4), reflects just a little the reality. practically in this clinic is managed the surgical pathology of the expanding intracranial processes, the cerebrovascular surgery, the tumoral surgery, vertebromedullary trauma and degenerative pathology, head injuries, the surgery of epilepsy and dyskinesia, pediatric neurosurgical pathology, peripheral nerves surgery and, as a special element, the neuro-orthopedic pathology. figure 4 clinic of neurosurgery bucharest, 1975 a.v. ciurea, r.e. rizea professor constantin arseni 9 with time, the clinic of neurosurgery, bucharest has gradually acquired a paraclinical equipment corresponding to european requirements for this period (1975-1980). thus, there is a complete neuroradiological department in which all standard and contrast medium neurosurgical investigations, are performed under closed circuit tv screens. air angiography and myelography with iodine substances are likewise carried out. the brain scintiscanner is in a separate laboratory; direct examination with 99mtc and radiocisternography with 168yb are also done in this unit. elctroencephalography and ultrasonoencephalography, with 3 simultaneous operating apparatus, occupies a special unit for this purpose. of importance is the laboratory of morphoneuropathology. a close cooperation exists with the "dr. v. babes" and "dr. i. cantacuzino" institutes in research work on neurologic and neurosurgical diseases carried out in the electron microscope. the investigations within the biochemistry laboratory are adapted to emergency procedures, assuring the complete emergency service. also clinical and paraclinical investigations can be carried out in the ophtalmological and ent departments. in the developing process of the neurosurgical clinic of bucharest, an important element was the use of the ctscan (1982) raising immediately the diagnosis value and assessment possibilities in the neurosurgical pathology. within the clinic of neurosurgery, bucharest, especially under the guidance of prof. c. arseni, took place a persevering scientific activity stimulated by his personality. the articles in the romanian medical literature were designed to inform the medical staff in general concerning neurosurgical diseases and to obtain early, competent diagnosis. among the most interesting publications, some of which have become classical, are: "vertebral sciatica" (1948) by c. arseni and st.t. iacob; "vascular diseases of the brain and spinal cord" (1965) by c. arseni, i. petrovici, f. nash, v. cunescu; "pain" (1967) by c. arseni and i. oprescu; "neuro-ophthalmologic diagnosis" (1967) by c. arseni, m. david, et al.; "spinal neurosurgical pathology" (1968) by c. arseni and m. simionescu; "viscero-autonomic and trophic disturbances in lesions of the brain" (1971) by c. arseni and m. botez; "raised intracranial pressure" (1972) by c. arseni, al. constantinescu; "craniocerebral traumatology" (1972) by c. arseni, i. oprescu; "intracranial space occupying processes" (vol. i, ii) (1973) by c. arseni et al.; "spinal cord and peripheric nerve injuries" (1974) by c. arseni, al. constantinovici, g. panoza; "neurosurgical semeiology" (1977) by c. arseni, al. constantinescu, m. maretsis; "pathologic anatomy of tumors of the nervous system" (1978) by c. arseni and m. carp; "the cerebrospinal fluid" (1979) by c. arseni, d. chimion et al.; "neuroendocrinology" (1988) by c. arseni and m. maretsis; "neurologic semeiology" by c. arseni and l. popoviciu; "cervical vertebromedullary pathology" (1982) by c. arseni and g. panoza. 10 romanian neurosurgery (2010) xvii 1: 6 11 in the fields of pediatric neurosurgery, a self-standing specialty since 1960, the following reference publications were edited: "problems of neurosurgical diagnosis in infantile pathology" (1978), "neurosurgical diseases in infants and young children" (1979), "infantile neurosurgical pathology" (1980) by cooperation of the teams under c. arseni, l. horvath and a.v. ciurea, on the basis of their experience achieved in the department of pediatric neurosurgery. in the modern neuroimaging diagnosis period the team of the clinic of neurosurgery, under the guidance of prof. c. arseni, published different monographs in the most various fields of neurosurgery : "parasitic diseases of the brain" 1981 (c. arseni, a. v. ciurea, a. cristescu, lenke horvath, v. marinescu), "cerebral and medullary vascular pathology" , in three volumes 1982-1983 (c. arseni, l. danaila, l. popoviciu, l. pascu), "intracranial surgical suppurative diseases" 1983 (c. arseni, a.v. ciurea), "cerebral metastasis" 1990 (c. arseni, al. constantinescu). with the contribution of the entire clinic of neurosurgery in the various fields of this specialty 64 monographs and treatises were edited under prof. c. arseni. an editorial board under c. arseni published with the substantial contribution of the medical staff of the clinic, the "treatise of neurology" in 5 volumes, during the 1979 -1982 period. together with well known specialists from bucharest and other centers, this treatise discusses in detail the principal neurologic and neurosurgical diseases. an important role in the neurosurgical training and the new aspects of diagnosis and treatment have had the library of the clinic from the "dr. d. bagdasar" bucharest, with numerous books (about 6000) and journals (12 titles), one of the best library of neurosurgery from europe. the romanian society of neurosurgery (rsn) was founded in 1982, the first president being prof. c. arseni (1982-1991). he was the president of romanian science medical academy (1982-1989) and member of romanian academy (1985). prof. constantin arseni continued with perseverance the activity and he can’t disunite from purpose of his life: the neurosurgery. he past away in 1994. prof. c. arseni represented the element of formation for modern neurosurgery school from romania, after the second war. the personality of prof. c. arseni dominated scientific and organizational the romanian medicine and neurosurgery of second part of xx century. his paper are knowed in entire world being path breaker in neurosurgery: traumatic brain injury, neurosurgical approaches for basals ganglia, pediatric neurosurgery pathology, intracranial parasitosis, etc. from year 2002 the clinic of neurosurgery from bucharest have his name: hospital bagdasar-arseni. references 1.aldea h: neurochirurgi celebri, ed. glasul bucovinei, 1993 2.arseni c: the development of neurosurgery during the last 20 years in neurology psihiatry neurosurgery, 9, 305-308, 1964 a.v. ciurea, r.e. rizea professor constantin arseni 11 3.arseni c: viitorul in neurologie si neurochirurgie, ed. academiei, 1984 4.arseni c, aldea h.: momente din istoria neurochirurgiei romanesti, ad. academiei, 1988 5.arseni c, ciurea a.v.: the history of romanian neurosurgery, ed. medicala, 1981. 6.maretsis m.: aniversarea unei prodigioase activitati neurochirurgicale. neurol. psihiat. neurochir., bucharest, 25, 4, 289-290, 1980 7.mateos j.h., neurosurgery, a triumph of human kind. romanian neurosurgery, 2, 107-118, 1993 8.wertheimer p., david m.: naissance et croissance de la neurochirurgie. neurochirurgie, paris, 25, 5-6, 253263, 1979 9.bagdasar d., arseni c.: traite de neurochirurgie, ed. academiei rsr, bucharest, 1951. microsoft word 1ciureaavprofessorthoma.doc romanian neurosurgery (2010) xvii 2: 137 – 142 137 professor thoma ionescu – founder of modern surgical practice in romania a.v. ciurea, cl. palade 1st neurosurgery clinic, “bagdasar arseni” emergency clinical hospital 10-12 berceni street, 041915, bucharest professor thoma ionescu was born in ploiesti in 1860. he attended primary school at the buholtzer institute in bucharest and high school at st. sava. he graduated in 1878 and went to paris where he enrolled in the faculty of medicine and the faculty of law 1879. he followed the same time studies at both colleges until 1882, when law becomes licensed. that same year the hospital discharged promotes competition in paris. during medical activities, he completed the first year of surgery with prof. nicaise at laënec hospital, second year with professor guyau at beaujon hospital, and the third year with professor tillaux also at beaujon hospital.[1][12] in 1885 is provisionally appointed by national contest of hospitals to serve his residency under professor bourneville in the bicêtre hospital. in 1886 he was installed as resident (interne des hôpitaux de paris), and spends four years of training in the surgical specialty, and is, in turn, resident of professor peyrot (bicêtre), paul berger (tenon), le dentu (st. louis) and verneuil (pitie).[1][12] in 1887 he obtained through competition the title of anatomy assistent (aide d'anatomie) and is ranked first in the series of that year. after the competition for the post of prosector of the faculty of medicine, he will provisionally occupy this position for 3 years (1888, 1889 and 1890) and in 1891 is acknowledged as defined prosector of the faculty of medicine. in 1890, the memorial called "internal retroperitoneal hernias " got the „laborie french academy award for medicine. two years later, in 1892, obtained a phd in medicine with his thesis: "evolution of intrauterine pelvic colon”.[3] 138 a.v. ciurea, cl. palade professor thoma ionescu in 1892, professor thoma ionescu attends the aggregate for anatomy of the faculty of medicine of paris and is allowed after the first theoretical and practical evidence. that same year, france's ministry of public intruction delegates prof. dr. thomas ionescu, at that time prosector of the faculty of medicine, to study and report the anatomical education in universities in germany and austria. in 1894, together with prof. paul poirier, then head of anatomical works (chef des travaux anatomiques) of the faculty of medicine in paris, adrien charpy professor at the faculty of medicine of toulouse and professor nicolas of the faculty of medicine of nancy, dr. thomas ionescu collaborated in drafting the first installment of volume iv of the anatomy of the most important treaty designed in france by that date ("traité d'anatomie humaine, masson et cie ed, paris 1894).[2][4] it is worth mentioning here that professor thomas ionescu was the anatomist who first described in detail in a anatomy treaty the sigmoidian large bowel, called by him "pelvic colon”.[4] also in 1894, a special law created the institute of topographical anatomy and experimental surgery in bucharest, and the jury's decision was that the chair will be occupied by professor thoma ionescu. thus, in february 1895, professor thoma ionescu took the directorate of the institute of topographical anatomy and experimental surgery and of the surgical clinic of the „coltea hospital”. in 1903, the institute was relocated to the premises of the faculty of medicine in bucharest, where it acquired new dimensions by creating a library and a museum of normal and pathological anatomy. in the surgical clinic, professor thoma ionescu introduced rigorous aseptical techniques,removing all antiseptical methods, this being a european pioneer in a time when all major surgery clinics were still practicing the old antiseptic methods. to make known his work and his collaborators, professor thoma ionescu founded in paris in 1896 the journal „archives des sciences médicales”, together with prof. victor babes and prof. nicholas kalinderu,with international collaborators, and in bucharest he established the „surgical review” his contributions have been numerous in the field of surgical arts. we merely present a few of them during this material. thus, he made significant contributions to general surgery, to gynecology, orthopedics and neurosurgery. an important aspect of surgical activity of prof. thoma ionescu was the surgery of cervical sympathetic chain. disregarding the results of experiments carried on animals by claude bernard, brown-sequard, vulpian, etc. which seemed to be create a "noli me tangere" out of the cervical sympathetic chain because of the grim postoperative consequences, especially autonomic, after experimental resection, professor ionescu expanded surgery of the cervical sympathetic chain. convinced at first that the simple section of the sympathetic chain or partial resection of a portion of it could not give satisfactory results in the illnesses for which it was adressed (basedow disease, angina, glaucoma), from the first intervention, he extended the resection from the skull to the lower cervical ganglion. in terms of neurosurgery, professor ionescu successfully practiced maxillary nerve interruption and meckel ganglion resection, in a original surgical procedure, described together with dr. bruckner. surgery consisted of 4 stages: practicing a frontal-temporal-zigomatic skin flap temporal muscle aponeurosis incision and cutting zygomatic apophysis romanian neurosurgery (2010) xvii 2: 137 – 142 139 lateral orbital wall resection, anterior to the superior orbital fissure; then the maxillary nerve is found and traced to the round foramen, at which level it was sectioned zygomatic arch and soft tissues suture [12] a second type of intervention practiced by prof. thoma ionescu followed optic nerve tumor ablation with preservation of the eye, through temporary resection of the external orbital wall, modifying the technique classically described by krönlein.[12] also, professor thoma ionescu imagined a personal approach for decompresive hemicraniectomies, with very favorable results. perhaps the most famous surgical maneuver connected with the name of thoma ionescu is the practice of spinal anesthesia. it is his merit to popularize this method, initiated by august bier in germany and theodore tuffier in france in 1898. until 1908, spinal anesthesia was limited to surgery in the lower abdominal region, and any attempt to perform this technique at higher levels was considered an absolute impossibility (even by initiator of the method tuffier, which in one report held in london at the 17th international congress of medical sciences, concluded that general anesthesia is contraindicated in surgical interventions above the umbilical level). professor thoma ionescu, by his experiences and by long practice has made this concept disappear and showed that, in the hands of a gifted surgeon, puncture of the rachis at any point from the atlanto-occipital membrane and back to sacral vertebral level can be done without significant risk.[5] [6] regarding the instruments utilized, professor thoma ionescu differentiate from the rest of the operators by using a needle with low profile gauge, almost identical to that used at the modern age. anesthetic used was stovaine (a cocaine related substance, with a 3-fold lower toxicity) in combination with strychnine (to overcome the effects of depression), and, later, with caffeine.[7] in his first work, professor ionescu indicated three regions where he had practiced the spinal tap depending on the areas requiring surgery. thus, the first location was mid-neck, between 3rd and 4th cervical vertebra, the second was cervicalthoracic, between the 7th cervical vertebra and first thoracic vertebra or between the first and second thoracic vertebrae, the third thoraco-lumbar, between the 12th thoracic vertebra and first lumbar vertebra. after sustained surgical experience and practice, the author was convinced that the midcervical puncture was unnecessary because the same anesthetic effects could be obtained in the cervico-thoracic junction case. besides the location of thoraco-lumbar, professor ionescu also punctured lower lumbar region, between the 4th and 5th lumbar vertebrae. upper or cervical puncture was performed for surgical interventions aimed at the cephalic extremity, cervical region, brachial, antebrachial and hand region, and also on the upper chest.[8] [9] [10] thoraco-lumbar puncture was used for abdominal-pelvic surgery and pelvic limb. for some interventions, however, aimed at the thoracic and pelvic level, professor thoma ionescu used combined taps. thus, for large interventions in the thoracic region he practiced 2 punctures: a cervical-thoracic and thoraco-lumbar, injecting 1 / 3 of the anesthetic dose at the upper level and 2 / 3 at a lower level. [10] surgery of the pelvic region, and especially in the sphere of gynecologic practice showed professor thoma ionescu that thoracolumbar puncture did not completely anesthetised the lumbar plexus and traction sensitivity persisted. this problem has been overcome by using a double puncturing: first thoraco-lumbar level, and then the lower lumbar level, for each location using one half standard dose of anesthetic. 140 a.v. ciurea, cl. palade professor thoma ionescu figure 1 cervical and thoracic spinal puncture figure 2 thoraco-lumbar spinal puncture romanian neurosurgery (2010) xvii 2: 137 – 142 141 figure 3 combined spinal puncture (cervicalthoracic and thoraco-lumbar) figure 4 combined spinal puncture (thoracolumbar and mid-lower back) regarding benefits of spinal anesthesia method, they were in number three, after the author's experience: conservation of gag reflex and facial muscle movements, the language of the larynx and pharynx, avoiding notable complications of inhaled anesthesia full muscle relaxation of the perineum and pelvic memebrelor cancellation of abdominal visceral reflexes it is worth mentioning that professor thoma has conducted numerous demonstrations and surgical procedures using spinal anesthesia in london, new york at the mount sinai hospital, in philadelphia, at pennsylvania univesity, in chicago and also in the mayo clinic. during these demonstrations, he was watched and praised, among others, by william and charles mayo and by the renowned neurosurgeon charles frazier. as a recognition of his merits in advancing surgical science in 1909, was received at the white house by president william howard taft, who thanked him for his tireless work in his purpose of alleviating human suffering. the famous american newspaper „the new york times” titrated on its first page in november 24-th, december 8-th and 17-th 1909 the following: “thomas jonnesco, head of the medical department of the university of bucharest, who has been demonstrating successfully here the use of stovaine as an anaesthetic, sailed for new york on the krinprinzessin cecilie on wednesday on a brief visit at the invitation of a number of medical friends in america. bucharest scientist demonstrates the value of stovaine as an anaesthetic; 4 operations performed; the patients remain perfectly conscious although entirely 142 a.v. ciurea, cl. palade professor thoma ionescu insensible to pain. dr. thomas jonnesco, the famous scientist, was received by president taft at the white house this morning. dr. jonnesco was introduced by horace knowles, american minister to nicaragua who, when he was minister to roumania, became a close friend of the distiguished surgeon. dr. jonnesco is in washington as mr. knowles’s guest and he has announced that he will hold no clinics while here his visit to the capital will end tomorrow, when he and his party will leave for chicago.”[13] in romania, prof.toma ionescu founded the periodicals “archives medicales des sciences (1896), “review of surgery” (1897) and the romanian society of surgery (1897). he was a member of the academy of medicine in paris, the international society of surgery and honorary member of the romanian academy (1925). professor thoma ionnescu passed away on march the 28-th 1926, leaving behind a huge surgical activity, taken and developed by his disciples, trained in the topographical anatomy and experimental surgery institute at the coltea hospital. correspondence to: claudiu_palade@yahoo.com; rsneurosurgery@gmail.com references 1. faure j.l.: thomas jonnesco (1860-1926), la presse médicale, avril 1926, 475-476. 2. jonnesco th. anatomie de la région duodénale in hernies internes rétro-péritonéales. paris, g. steinheil, 1890, 307 p. 3. jonnesco th. sur l'évolution intra-utérine du côlon pelvien. thèse de doctorat, paris, g. steinheil, 1892. 4. jonnesco th. anatomie du tube digestif. traité d'anatomie humaine par p. poirier, a. charpy, a. nicolas, a. prenant et th. jonnesco, paris, bataille, 1894, 1ère édition. in: t. iv, premier fascicule, 392 p. 5. jonnesco th. l'anesthésie générale par injections intra-rachidiennes. actes, 2ème congrès de la société internationale de chirurgie, bruxelles, 1908 (séance du 23 septembre). 6. jonnesco th. anesthésie générale par injections intrarachidiennes. bull. acad. méd. paris, 1909, ii, 270. 7. jonnesco th. die rachianasthesie zur anasthesierang samitlicher korperregionen. deutsche medizinische wochenschrift, berlin, 1909, no 49. 8. jonnesco th. remarks on general spinal analgesic. british med. journal, london, nov. 1909. 9. jonnesco th. remarks on general spinal analgesic. new york med. journal, jan. 1910, p. 43. 10. jonnesco th. la rachi-anesthésie générale. paris, masson, 1919, 1 vol., 127 p. 11. jonnesco th. la question roumaine. paris, payot, 1919, i, 2 vol., 214 p. 12. livre jubilaire publié à l'occasion de sa trentième année d'enseignement.: thomas jonnesco: sa vie, son oeuvre. bucarest, imprimerie de la cour royale, f. gobl fils, 1926. 13. the new york times online archive (november, december 1909) 6zenteno_clinical2014 50 zenteno et al implications of internal carotid artery tortuosity, kinking and coiling clinical implications of internal carotid artery tortuosity, kinking and coiling: a systematic review m. zenteno1, f. viñuela2, l.r. moscote-salazar3, h. alvis-miranda4, r. zavaleta5, a. flores6, a. rojas7, a. lee8 1md, professor of neurological endovascular therapy, departamento de terapia endovascular neurológica, instituto nacional de neurología y neurocirugía, universidad nacional autónoma de méxico; stroke unit, hospital ángeles del pedregal. 2md, director, interventional neuroradiology, professor, ucla department of radiology, ronald reagan ucla medical center, los angeles, ca. 90095, 3md, facultad de medicina, universidad de cartagena, cartagena de indias, colombia 4md, facultad de medicina, universidad de cartagena, cartagena de indias, colombia 5md, departamento de terapia endovascular neurológica, instituto nacional de neurología y neurocirugía, universidad nacional autónoma de méxico; stroke unit, hospital ángeles del pedregal. 6md, departamento de terapia endovascular neurológica, instituto nacional de neurología y neurocirugía, universidad nacional autónoma de méxico; stroke unit, hospital ángeles del pedregal. 7md, departamento de terapia endovascular neurológica, instituto nacional de neurología y neurocirugía, universidad nacional autónoma de méxico; stroke unit, hospital ángeles del pedregal. 8md, department of neurosurgery, instituto nacional de ciencias médicas y nutrición salvador zubirán; stroke unit, hospital ángeles del pedregal, mexico city, mexico abstract anatomical variations of the internal carotid artery are diverse. abnormalities in their geometry and paths are commonly identified by ultrasonography and angiography. the surgical correction of symptomatic cas is better in preventing stroke compared with best medical therapy, as well as it completely eliminates the symptoms in patients with nonhemispheric symptoms. the ica anomalies may be dangerous and represent a risk factor for massive bleeding. suture ligatures can penetrate and occlude torn vessels, scalpels or biting instruments can lacerate vessels, and indirectly conducted electric cauterization can burn the soft of bony tissues. key words: internal carotid artery, carotid kinking, carotid coiling, anatomical variation, vascular surgery. anatomical variations of the internal carotid arteries and its clinical implications search strategy and selection criteria we identified references for this review from pubmed searches between january, 1960 and 2014, from the reference lists of relevant articles and through searches of the authors' romanian neurosurgery (2014) xxi 1: 50 59 51 own files. search terms included combinations of the following key words: “internal carotid artery”, “kinking”, “tortuosity”, “clinical implications”, “complications”, and “clinical trials”. we reviewed titles and abstracts for content relevant to the topics covered in this review, and basic science articles were included if the authors judged their methods to be of high quality. we excluded articles if they were not published in english. introduction the anatomical variations of the internal carotid artery (ica) are diverse. the cervical segment of ica extends from the bifurcation of the common carotid artery until its entry into the skull base, its origin is located posterior or posterolateral to the external carotid artery (eca), then it ascends posteromedial to this vessel with a path that can be straight, curved or angled. (1,2) according to most of the anatomy references, the cervical portion of the ica runs a straight course to the base of the cranium without branching. the major abnormalities in the cervical segment of the ica occur near of its origin or at the distal portion, at level of the atlas or axis. weibel after performing 1438 angiographies of neck vessels, found that 75% of aci kinks were placed at 2-4 cm of the carotid bifurcation. (3) ica alterations such as coiling, kinking, and tortuosity have been matter of debate because of up to date the natural history of such anomalies is not well known, furthermore, some authors consider these conditions due to a benign angiopathy,4 while others suppose that they are burdened with disabling, even fatal neurological complications. (5) one of the main authors in the field of ica alterations are weibel et al (3), they defined “tortuosity” as any ripple or elongation of the ica in an "s" or "c" fashion, while "coiling" is the elongation or redundancy of ica configuration with a "s" exaggerated or circular configuration, finally “kinking” is the angle of one or more segments associated with stenosis of the vessel segment. considering the confusion and the broad description of terms to describe irregularities (table i) of the course of ica is preferable to divide these alterations only in two categories, namely: the tortuosity and kinking; thus, elongation, redundancy, and "s" configurations are grouped as tortuosity, of which the vast majority have no clinical repercussion, on the other hand, kinking is considered as the acute angulation of the vessel, a condition that is considered to be acquired. (6) the most comprehensive definition is that of metz, who refers to the bend of the ica is due to an elongation of the vessel, and defined as the abrupt angulation of the vessel axis from 90° or less, and in turn classified into three grades: grade 1: bending of 90-60°; grade 2: 60 to 30°; grade 3: <30°. (7,8) we suggest defining the tortuosity of the ica as any degree of abnormality in the dynamics of the vessel in relation to their normal morphology, 52 zenteno et al implications of internal carotid artery tortuosity, kinking and coiling which is underlying structural injury of the carotid vessel. the aim of this review is to highlight the clinical implications of the carotid artery abnormalities such as kinking and tortuosity. epidemiology the occurrence of carotid abnormalities (cas), based on the anatomical, ultrasound and angiography studies, are reported to be seen in a wide range of frequency between 10 and 43% of the population with no history of atherosclerotic disease, diabetes or hypertension. (3,9,10) pioneering studies of carotid kinking showed prevalence of 5% to 25% in patients with cerebrovascular symptoms or asymptomatic carotid stenosis incidentally diagnosed. one of the most representative series of kinkings (1000 angiograms) found a prevalence of 16% in a hospital population that is widely accepted today. (11,12) table i term definition symptoms kinking any sharp bend in the vessel mild: angulation of elongated ica with an angle ≥60 ° medium: angulation of elongated ica with angle between 30 ° – 60 ° ± severe: angulation of elongated ica with angle < 30 ° + tortuosity any ripple or elongation of the ica in an "s" or "c" fashion. subsumes the elongation, redundancy, undulation, and s shaped curves coiling elongation or redundancy of ica configuration with a "s" exaggerated or circular configuration ± kinking occurs mostly in elderly men, and is associated with atherosclerotic pathology, while coiling is more common in younger women. (13) from a series of more than 800 cases of tortuosity and kinking of the ica, there was a predominance in terms of sex, and some of these abnormalities were bilateral. (14) cas are rarely observed in children or in young adults. (15) beigelman et al16 in a series of 885 patients, aged 1 to 90 years, showed no difference in the prevalence of kinking or coiling among age groups, favoring the embryogenic mechanism of the development of cas. kink in the elderly is considered to be an acquired lesion most commonly seen in patients suffering arteriosclerosis and hypertension 9,17,18 while in children and younger patients the kinks and coils are congenital. (15,16,19) acquired form of kinking and coiling is most commonly associated with aging, hypertension and traditional risk factors for atherosclerosis, (20–22) it is characterized by degenerative changes and elastic tissue destruction of the vessel wall, which causes elongation of the vessel and also a bending stress, additionally in each systole there is a momentary elongation may increase the kink. (6) the prevalence of arterial hypertension in patients with kinking appears to be greater than those without this anomaly, pancera et al studied romanian neurosurgery (2014) xxi 1: 50 59 53 590 patients with neurological symptoms by ultrasound (usg) doppler of neck vessels, and found a prevalence of 28.4% in normotensive and 37.8% in hypertensive patients, with significant difference in both groups (p <0.01). (21) currently it is known that arterial blood vessels are prone to deformation when exposed to elevated blood pressure. (13,23–26) however, a clear link between vascular risk factors and kinking and coiling is still not fully understood. as suggested by benes et al (17), there are 2 types of kinks in adults. first, those which may be congenital and only become clinically significant at an older age, it is more common in females, and most frequently in patients in their late fourties and early fifties; the second type which are caused by arteriosclerotic changes, are usually situated at the end of an arteriosclerotic plaque. clinical and histopathologic features it is generally recognized the difficulty to establish a clear relationship between clinical signs and cas, especially because the natural history of these abnormalities. although the incidence of these anomalies can be up to 46%, as previously mentioned, the incidence of cas responsible for symptomatic cerebrovascular insufficiency is 4–16%. (4) clinical presentation of kinks in general is the same as that of the regular carotid stenosis, (17) however there are cases where the two circumstances are present at same time, being difficult to establish whether the symptomatology is caused by ica stenosis (more likely) or concurrent kink. it is generally accepted, that the carotid kinking may be either the source of cerebral emboli or the vessel may be temporarily occluded by head/neck rotation thus causing symptoms of cerebral ischemia. (9,27) in both instances the resulting clinical presentation may be transient ischaemic attacks (tia) and/or completed stroke, usually a minor one, (9,27), probably due to the hemodynamic changes (i.e., the flow within the kinked vessel is not laminar but turbulent) and/or thromboembolic mechanisms including flow changes due to mechanical occlusion associated with changes in head position, microembolization and flow stasis at the kink level. (28,29) in the koskas et al (9) series of 166 adult patients, predominantly strokes and tia were observed. in the anecdotal reports on the haemodynamic significance of congenital kinking of the ica in children, hemiparesis, loss of vision, aphasia and seizures have been described. (30) there are some uncertainties about the pathophysiology of cerebral ischemia caused by the kink. in the case of a kink without a plaque, positional occlusion of the vessel is blamed. (17) the hemodynamic mechanism becomes important the higher the degree of bending, the blood flow can be reduced to less than 40%, with an angle of 60° in the aci and 60% at an angle of 30°. isolated cas can lead to cerebral symptoms, without the presence of 54 zenteno et al implications of internal carotid artery tortuosity, kinking and coiling atherosclerotic changes. the appearance of symptoms of kinking and coiling of the ica is associated with intracranial and extracranial occlusive disease, frequent and sudden and transitory hypotension during sleep or sudden and extreme unfavorable movements of the head and neck. (3,20,27) in the majority of patients, symptomatology generally withdraws with the return of the head in neutral position. ischemic cerebrovascular accident occurs in about 11%–33% of cases with cas. (13) it has been proven that reduction in regional cerebral flow in cases of extracranial elongation of carotid segments appears with 30–35 ml per min (normal range 50–60 ml/min/100g. brain tissue). (13) however the previously mentioned, biegelman et al (31) using doppler echography demonstrated that carotid kinks are not a mechanism of acute cerebral ischemia, and therefore are unlikely to be a cause of neurological events or symptoms. histopathologic findings in the ca segment are primarily non-inflammatory and non ateroesclerotic changes of the media and intima layers. la barbera et al (32) demonstrated that elastic and muscular tissue is substituted by loose connective tissue, configuring a metaplasia of tunica media limited to the ica. they hypothesized that extracranial ica, being a segment of transition between an elastic vessel (common carotid artery) and a muscular vessel (intracranial ica), is particularly subject to metaplastic transformation, as happens in other transition zones in human body. because the histopathological findings are suggestive of a metaplasia, the presumption that some subjects are genetically predisposed to develop ica metaplasia following a stimulus, probably hemodynamic forces (arterial hypertension?) that in other subjects do not cause it can be done. the changes in tunica media are mainly marked for degeneration with fragmentation and disorganization of elastic tissue, hyperplasia, and finally areas of fibromuscular hyperplasia alternating with areas of thinning of the tunica media. (33,34) concerning the origin of the cas it is generally believed that coiling is due to embryological causes while tortuosity and kinking are ascribed to atherosclerosis or fibromuscolar dysplasia (32). complementary studies the use of ultrasound examination in the ongoing clinical practice has enabled rapid, morphological and also functional studies of cas. (13) del corso et al (20) had demonstrated that more than half of the number of patients with cerebrovascular symptoms had some forms of cas diagnosed by ultrasound technique. cerebral angiography has been of great value in these patients, it is the gold standard to characterize anatomically the cas, must be obtained projections of 4 intracranial vessels, it is important to assess the kink in different projections, currently with 3d reconstruction angiography can be accurately measured the degree of the romanian neurosurgery (2014) xxi 1: 50 59 55 kink. dynamic studies such as cineangiography are useful to demonstrate the hemodynamic within the kinked vessel. the delay in opacification of the intracranial vessels is indicative of a major commitment secondary to the kink. usg doppler technique is based on the change in frequency of an echo emitted by a moving sound source, when approaching a receiver it is observed an increase in the perceived frequency and decreasing when move away. thus, it is possible to determine blood flow velocity based on the frequency change reflected by red blood cells moving in relation to a fixed transducer. for the assessment of aci, is a safe, effective, non-invasive and low cost method. for carotid disease it showed a sensitivity of 83 to 86% and a specificity of 89% to 94% for stenosis greater than 70%, for the aci kinking also exist studies that have proved its usefulness, applying the metz classification, systolic velocities greater than 120cm/seg support the diagnosis of hemodynamic compromise secondary to the ica kinking. (35) therapeutical options the most important study in the field that to some extent clarified the dilemma of treat medically o surgically an entity that is not completely recognized as the cause of the symptoms, was performed by ballota et al (36), it was conducted in symptomatic patients with elongation (coiling and kinking) of the ica, the patients were randomized to surgical treatment group (n = 92) or to medical treatment group (n = 90). the purpose was to determine stroke, death at 30 days and late occlusion. the incidence of late hemispheric and retinal tia was significantly lower in the surgical group than medical treatment group, 7,6% vs. 21,1% (p = 0,01) and 3,2% vs. 12,2% (p = 0.03), respectively. they concluded that the surgical correction of symptomatic cas is better in preventing stroke compared with best medical therapy, as well as it completely eliminates the symptoms in patients with non-hemispheric symptoms. there are few other reports suggesting that the clinical course of carotid kinking can be benign. (34) different surgical techniques described for the management of carotid kinking: (3,38) 1) arterial transposition, criticized for not removing arterial elongation. 2) lysis of adhesions. 3) vascular procedures such as segmental resection and end to end anastomosis. 4) endarterectomy technique with eversion, which allows correction of severe elongation and kinking of the ica. the surgical technique of resection of tortuous segment, with dilatation and reimplantation has become the method of choice in treating carotid kinking and coiling. in the same procedure eversion carotide endarterectomy can be done. correction of kinking and coiling is performed with peroperative mortality rate below 1% and low postoperative 56 zenteno et al implications of internal carotid artery tortuosity, kinking and coiling morbidity. (5,13) it is noteworthy that all internal carotid reconstructive procedure is subject to technical difficulties and complications associated with surgery. surgical correction of cas is indicated for patients with tia (focal, hemispheric ischemic simptoms); patients in whom angiography demonstrated hemodinamically significant kinking and/or coiling; if ct and mri examination excludes other significant ischemic brain injury; and in symptomatic and asymptomatic patients with one-sided cas and occlusion of contralateral carotid artery; bilateral kinking and/or coiling, with the correction of one side first, if the symptoms do not disappear, then the other side as well, and patients with simultaneous lesions of vertebral artery. (13) there are reports showing that kink of ica is a potentially hazardous condition and surgical treatment with revascularization offers good results. (11,34) some studies concluded that in patients with cerebrovascular insufficiency associated with stenotic kinking, ruling out any other cause of symptomatology, the kink correction improves symptoms and protects against recurrent ipsilateral cerebral ischemia. (11,34) however, bilateral high kinking with distal dissection of ica is indicated for surgical repair but only in cases with confirmed cerebral symptoms. this type of intervention is associated with frequent peripheral nerve lesions and high mortality rate. (13) recurrences of kinking and coiling are rare and can appear in patients with uncontrolled hypertension. (20,37) the ica anomalies may be dangerous and represent a risk factor for massive bleeding. (3,43) suture ligatures can penetrate and occlude torn vessels, scalpels or biting instruments can lacerate vessels, and indirectly conducted electric cauterization can burn the soft of bony tissues. (44) angioplasty in carotid disease at present there are no studies addressing the kinking treatment by angioplasty with stent, the available information comes from studies performed on carotid angioplasty in atherosclerotic stenotic carotid disease. in recent years, carotid angioplasty with stenting has been an alternative, particularly in patients at high risk for carotid endarterectomy complications. (39) the two aspects that drove the development of carotid angioplasty with stenting were seeking a better therapeutic option in high-risk patients and the tendency to perform minimally invasive surgery. some authors suggest that this procedure is safer, less traumatic and more cost-effective than carotid endarterectomy. several clinical trials have compared stent angioplasty with carotid endarterectomy with similar results in terms of morbidity and mortalidad. (40,41) endovascular procedures have the inherent risk of damage to the intima and the subsequent risk of thrombosis; furthermore, all stents are thrombogenic, therefore, patients undergoing these procedures must receive antiplatelet therapy. clopidogrel in combination with acetylsalicylic acid is currently the standard treatment. (42) conclusions abnormalities in the geometry and paths of the ica are commonly identified in ultrasonography and angiography. romanian neurosurgery (2014) xxi 1: 50 59 57 classification of ca in tortuosity, kinking and coiling was introduced in 1965 by weibel and fields. this classification offers tortuosity as an elongation in the form of “s” or “c”; coiling as the elongation or the redundancy of the artery, resulting in a deformation that resembles an s or a circular configuration. the surgical correction of symptomatic cas is better in preventing stroke compared with best medical therapy, as well as it completely eliminates the symptoms in patients with nonhemispheric symptoms. currently is accepted that transient neurological symptoms produced by rotation of the head is an indication for the treatment of ica kink. the ica anomalies may be dangerous and represent a risk factor for massive bleeding. suture ligatures can penetrate and occlude torn vessels, scalpels or biting instruments can lacerate vessels, and indirectly conducted electric cauterization can burn the soft of bony tissues. contributors a.l, h.a.m y and l.r.m contributed equally to the literature search and review and to the writing of this manuscript. conflicts of interest mc, fv, al, ha and lrm declares that they have no conflicts of interest. corresponding author: luis rafael moscote-salazar, md universidad de cartagena, cartagena de indias, colombia, southamerica e-mail: mineurocirujano@aol.com references 1. akpek s, arat a, morsi h, klucznick rp, strother cm, mawad me. self-expandable stent-assisted coiling of wide-necked intracranial aneurysms: a single-center experience. ajnr am j neuroradiol 2005; 26: 1223–31. 2. bates mc, kyer pd, kavasmaneck c, aburahma a, crotty b. stent-supported angioplasty correction of symptomatic critical carotid angulation. w v med j 2003; 99: 22–4. 3. weibel j, fields ws. tortuosity, coiling, and kinking of the internal carotid artery. ii. relationship of morphological variation to cerebrovascular insufficiency. neurology 1965; 15: 462–8. 4. perdue gd, barreca jp, smith rb, king ow. the significance of elongation and angulation of the carotid artery: a negative view. surgery 1975; 77: 45–52. 5. ballotta e, abbruzzese e, thiene g, et al. the elongation of the internal carotid artery: early and longterm results of patients having surgery compared with unoperated controls. ann vasc surg 1997; 11: 120–8. 6. blanc r, deschamps f, orozco-vasquez j, thomas p, gaston a. a 6f guide sheath for endovascular treatment of intracranial aneurysms. neuroradiology 2007; 49: 563–6. 7. byrne j. interventional neuroradiology: theory and practice, 1st ed. new york, oxford university press, 2002. 8. metz h, murray-leslie rm, bannister rg, bull jw, marshall j. kinking of the internal carotid artery. lancet 1961; 1: 424–6. 9. koskas f, bahnini a, walden r, kieffer e. stenotic coiling and kinking of the internal carotid artery. ann vasc surg 1993; 7: 530–40. 10. togay-işikay c, kim j, betterman k, et al. carotid artery tortuosity, kinking, coiling: stroke risk factor, marker, or curiosity? acta neurol belg 2005; 105: 68– 72. 11. connors ji, wojak j, editors. interventional neuroradiology: strategies and practical techniques. philadelphia, wb saunders, 1999. 12. vannix rs, joergenson ej, carter r. kinking of the internal carotid artery. clinical significance and surgical management. am j surg 1977; 134: 82–9. 13. radak d, babić s, tanasković s, et al. are the carotid kinking and coiling underestimated entities? da 58 zenteno et al implications of internal carotid artery tortuosity, kinking and coiling li su morfološke abnormalnosti karotidne arterije (kinking i coiling) 2012; 69: 616–9. 14. fiorella d, albuquerque fc, deshmukh vr, mcdougall cg. usefulness of the neuroform stent for the treatment of cerebral aneurysms: results at initial (36-mo) follow-up. neurosurgery 2005; 56: 1191–201; discussion 1201–2. 15. fisher rg. strokes in children. their relationship to intrinsic pathology of the carotid artery. am surg 1982; 48: 344–50. 16. beigelman r, izaguirre am, robles m, grana dr, ambrosio g, milei j. are kinking and coiling of carotid artery congenital or acquired? angiology 2010; 61: 107– 12. 17. benes v, mohapl m. alternative surgery for the kinked internal carotid artery. acta neurochirurgica 2001; 143: 1267–71. 18. ozgur z, celik s, govsa f, aktug h, ozgur t. a study of the course of the internal carotid artery in the parapharyngeal space and its clinical importance. european archives of oto-rhino-laryngology: official journal of the european federation of oto-rhinolaryngological societies (eufos): affiliated with the german society for oto-rhino-laryngology head and neck surgery 2007; 264: 1483–9. 19. ovchinnikov na, rao rt, rao sr. unilateral congenital elongation of the cervical part of the internal carotid artery with kinking and looping: two case reports and review of the literature. head & face medicine. 2007; 3: 14–29. 20. del corso l, moruzzo d, conte b, et al. tortuosity, kinking, and coiling of the carotid artery: expression of atherosclerosis or aging? angiology 1998; 49: 361–71. 21pancera p, ribul m, presciuttini b, lechi a. prevalence of carotid artery kinking in 590 consecutive subjects evaluated by echocolordoppler. is there a correlation with arterial hypertension? journal of internal medicine 2000; 248: 7–12. 22. pancera p, ribul m, de marchi s, arosio e, lechi a. prevalence of morphological alterations in cervical vessels: a colour duplex ultrasonographic study in a series of 3300 subjects. int angiol 1998; 17: 22–7. 23. taylor wr. mechanical deformation of the arterial wall in hypertension: a mechanism for vascular pathology. am j med sci 1998; 316: 156–61. 24. weizsäcker hw, lambert h, pascale k. analysis of the passive mechanical properties of rat carotid arteries. j biomech 1983; 16: 703–15. 25. hayashi k, naiki t. adaptation and remodeling of vascular wall; biomechanical response to hypertension. j mech behav biomed mater 2009; 2: 3–19. 26. stoitsis j, golemati s, bastouni e, nikita ks. a mathematical model of the mechanical deformation of the carotid artery wall and its application to clinical data. conf proc ieee eng med biol soc 2007; 2007: 2163–6. 27. rosenthal d, stanton pe, lamis pa, mcclusky d. surgical correction of the kinked carotid artery. am j surg 1981; 141: 295–6. 28. van damme h, gillain d, désiron q, detry o, albert a, limet r. kinking of the internal carotid artery: clinical significance and surgical management. acta chir belg 1996; 96: 15–22. 29. higashida rt, meyers pm, phatouros cc, connors jj, barr jd, sacks d. reporting standards for carotid artery angioplasty and stent placement. stroke 2004; 35: e112–34. 30. huemer m, emminger w, trattnig s, freilinger m, wandl-vergesslich k. kinking and stenosis of the carotid artery associated with homolateral ischaemic brain infarction in a patient treated with cyclosporin a. european journal of pediatrics 1998; 157: 599. 31. beigelman r, izaguirre a, robles m, grana d, ambrosio g, milei j. kinking of carotid arteries is not a mechanism of cerebral ischemia: a functional evaluation by doppler echography. int angiol 2011; 30: 342–8. 32. la barbera g, la marca g, martino a, et al. kinking, coiling, and tortuosity of extracranial internal carotid artery: is it the effect of a metaplasia? surgical and radiologic anatomy: sra 2006; 28: 573–80. 33. howington ju, hanel ra, harrigan mr, levy ei, guterman lr, hopkins ln. the neuroform stent, the first microcatheter-delivered stent for use in the intracranial circulation. neurosurgery 2004; 54: 2–5. 34. hunt we, kosnik ej. timing and perioperative care in intracranial aneurysm surgery. clin neurosurg 1974; 21: 79–89. 35. nishino k, ito y, hasegawa h, kikuchi b, fujii y, tanaka r. modified buddy wire technique for coil embolization of posterior circulation aneurysms. neuroradiology 2007; 49: 49–55. 36. ballotta e, thiene g, baracchini c, et al. surgical vs medical treatment for isolated internal carotid artery elongation with coiling or kinking in symptomatic patients: a prospective randomized clinical study. j vasc surg 2005; 42: 838–46; discussion 846. 37. bowen jc, garcia m, garrard cl, mankin cj, fluke mm. anomalous branch of the internal carotid artery maintains patency distal to a complete occlusion diagnosed by duplex scan. j vasc surg 1997; 26: 164–7. romanian neurosurgery (2014) xxi 1: 50 59 59 38. kis b, weber w, berlit p, kühne d. elective treatment of saccular and broad-necked intracranial aneurysms using a closed-cell nitinol stent (leo). neurosurgery 2006; 58: 443–50; discussion 443–50. 39. white jb, kallmes df. utility of the “buddy” wire in intracranial procedures. neuroradiology 2008; 50: 185–7. 40. yuzawa i, kurata a, suzuki s, et al. efficacy of a direct puncture approach for anterior circulation aneurysms using a newly developed guiding catheter especially for geriatric patients. surg neurol 2007; 67: 30–4; discussion 34. 41. zenteno m, modenesi freitas jm, aburto-murrieta y, koppe g, machado e, lee a. balloon-expandable stenting with and without coiling for wide-neck and complex aneurysms. surg neurol 2006; 66: 603–10; discussion 610. 42. zenteno ma, santos-franco ja, freitas-modenesi jm, et al. use of the sole stenting technique for the management of aneurysms in the posterior circulation in a prospective series of 20 patients. j neurosurg 2008; 108: 1104–18. 43. galletti b, bucolo s, abbate g, et al. internal carotid artery transposition as risk factor in pharyngeal surgery. laryngoscope 2002; 112: 1845–8. 44. sho e, nanjo h, sho m, et al. arterial enlargement, tortuosity, and intimal thickening in response to sequential exposure to high and low wall shear stress. j vasc surg 2004; 39: 601–12. 13pankajgupta_bilateral 224 gupta et al bilateral basal ganglia haemorrhage following motor vehicle accident bilateral basal ganglia haemorrhage following motor vehicle accident: a case report pankaj gupta1, r.s. mittal2, devendra purohit3, jitendra singh shekhawat4, ugan singh meena5 1senior resident, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 2dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 3professor, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 4assist. professor, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 5senior resident, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan abstract bilateral basal ganglia haemorrhage following motor vehicle accident is extremely rare in field of neurosurgery. this is presumed to be secondary to rupture of lenticulostriate or anterior choroidal artery by shearing, as a result of acceleration/deceleration forces. although the exact mechanism is still not known. isolated bilateral basal ganglia haemorrhage carries favourable prognosis. we report a rare case of 50 years old lady having bilateral basal ganglia haemorrhage with diffuse axonal injury following motor vehicle accident. patient was managed conservatively and improved. key words: motor vehicle accident, basal ganglia, diffuse axonal injury. introduction post-traumatic bilateral basal ganglia haemorrhage is extremely rare entity. it consists of haemorrhagic lesions in basal ganglia (caudate nucleus, putamen, globus pallidus), internal capsule or thalamus. (3, 5, 6) incidence of post-traumatic basal ganglia bleed is 3% after motor vehicle accident (mva) in clinical series, while it is 10-12% in autopsy series. (3, 6) traumatic basal ganglia haemorrhage (tbgh) is classified as ‘large’ if it is >2 cm in diameter, and as ‘small’ if <2 cm in diameter. the exact mechanism is still not clear but, it is believed to arise from a shear strain in the ganglionic region. this shear strain is produced by acceleration/ deceleration forces during high velocity injury, which produces rupture of lenticulostriate or anterior choroidal artery, hence bilateral basal ganglia bleed. (1) there is single case report of bilateral basal ganglia haemorrhage following lightning strike, where it is related to preferential conduction pathways through the brain. bilateral tbgh can occur as isolated lesion or in association with diffuse axonal injury (dai), cerebral contusions, subdural hematoma (sdh), extradural hematoma (edh) or, subarachnoid haemorrhge (sah). romanian neurosurgery (2014) xxi 2: 224 226 225 (7) bilateral tbgh carries dismal prognosis. isolated tbgh has good outcome. case report a 50 years old female patient was admitted to our institute with history of mva. at the time of admission, she was unconscious (gcs = 7) and pupils were 4mm size, reacting normally to light. non-contrast ct head showed bilateral (mirror-image) basal ganglia haemorrhage, tentorial bleed, posterior interhemispheric bleed and scalp hematoma over left frontal region. there was no evidence of ventricular compression, effacement of basal cisterns, mass effect or midline shift. cerebral ct angiography was within normal limits and routine blood investigations did not reveal any evidence of coagulation disorder. figure 1 ncct head showing mirror image acute haemorrhage in bilateral basal ganglia region with tentorial bleed and extra-calvarial scalp hematoma patient was intubated immediately to avoid aspiration of secretions as gcs score was 7. later on tracheostomy was done after 24 hours. patient was kept on mannitol, antibiotics and anticonvulsants. on 8th day, patient’s gcs was 10 with left sided hemiparesis. she was discharged on 14th day after decannulation of tracheostomy tube, with residual left hemiparesis. discussion bilateral tbgh is extremely rare but a serious complication of head injury. (1, 2) tbgh is usually small and located in the region of lentiform nucleus or external capsule, while spontaneous hypertensive basal ganglia bleed is principally located in the region of thalamus and internal capsule. to the best of our knowledge, only 2 cases have been reported till date. regarding mechanism of tbgh, mosberg & lindenberg demonstrated traumatic tear of a pallidal branch of anterior choroidal artery as the source of origin of pallidal hematoma in an autopsy case. (1) when there is a strong impact to the vertex, forehead or occiput and directed towards the tentorium, there would be a shift of brain, through the tentorial notch with stretching and tearing of vessels by shearing forces, resulting in basal ganglia haemorrhage. the final prognosis of patients with tbgh is strongly related to existence of associated dai. in our case, dai was considered as patient was unconscious after injury and ct findings were also consistent with dai. 226 gupta et al bilateral basal ganglia haemorrhage following motor vehicle accident in addition, differentiation of traumatic from spontaneous basal ganglia bleed is very important from medicolegal point of view, since the basal ganglia is a frequent site of spontaneous hypertensive bleed. tbgh are dynamic lesions and tend to expand in volume during acute post-traumatic period, hence there is importance of serial ct scanning. surgical options available for these cases are open surgery or, usg/ct guided stereotactic aspiration but, the outcome of most surgically treated patients was poor. (4, 8) the absolute indication of surgery in these cases are, volume of lesion > 25 ml and increasing size of hematoma with deterioration of neurological condition of patient. in aaddition, medical and supportive treatment includes icp monitoring, elective ventilation and close monitoring in icu. (6) the good prognostic factors in tbgh are younger age (<60yrs), small lesions (<2cm), gcs >9 at the time of admission, isolated lesion. the bad prognostic factors are old age (>60yrs), large lesion (>2 cm), gcs <7 at the time of admission, basal ganglia haemorrhage alongwith associated dai, edh, sdh, sah or cerebral contusions and coexisting medical comorbidities like hypertension, diabetes or coagulation disorders. (7) tbgh carries the tendency of delayed (within 48 hours) expansion of hematoma, which is again a bad prognostic indicator. (2, 7) conclusion the tbgh are usually haemorrhagic contusions, as a result of shear forces after mva. the overall mortality is high and morbidity is considerable in survivors. patients with isolated tbgh do well with conservative management. footnotes source of support: nil. conflicts of interest: none declared. correspondence: dr. devendra purohit (mch.) professor (neurosurgery) deptt. of neurosurgery, s.m.s. medical college, jaipur, rajasthan, 302004. email: drpankaj.gupta@yahoo.co.in devendrapurohit@rediffmail.com references mosberg wh jr, lindenberg r. traumatic hemorrhage from the anterior choroidal artery.j neurosurg 1959; 16: 209-21. yanaka k, egashira t, maki y, et al. bilateral traumatic hemorrhage in the basal ganglia: report of two cases.no shinkei geka 1991;19: 369-73. boto gr, lobeto rd, rivas j. basal ganglion hematoma in severely head injured patients: clinicoradiological analysis of 37cases.j neurosurg 2001; 94:224-32. kim sh, song sh, youm jy, kim y: clinical analysis of the traumatic basal ganglia hemorrhage. j korean neurosurg soc 25: 1223-1229, 1996. crooks da. pathogenesis ana biomechenics of traumatic intracranial hemorrhages. virchows arch a pathol anat histopathol 1991;418:479-483. yamakawa n, furuno m, okada m et al. traumatic basal ganglia haemorrhage: report of 7 cases. j clin neurosci 1995; 2:55-58. kimura m, sobata e, suzuki s. traumatic basal ganglion (caudate) with favourable prognosis: report of two cases. no shinkei geka 1994;22:155-158. 8. yanagawa y, kiyozumi t, terai c et al. a case of traumatic hematoma in the basal ganglia: successful drainage with ultra-sound guided aspiration surgery via burr hole. no shinkei geka 1997;25:1105-1108 (jpn). microsoft word 9pintea_fronto_f 80 pintea et al fronto temporal approach in sellar and parasellar tumors fronto temporal approach in sellar and parasellar tumors bianca pintea1, andreea mogyoros2, zorinela andrasoni2, i.st. florian3 1phd student, “iuliu hatiaganu” umph, cluj-napoca 2cluj-napoca emergency hospital 3“iuliu hatiaganu” umph, cluj-napoca abstract introduction: the fronto-temporal approach represent the shortest distance to the ipsilateral optic nerve and carotid artery, and allow the direct verification of the optical nerves, the carotid arteries, the pituitary stalk, the tumor and its relationship with the suprasellar structures. objective: the purpose of this study is to advocate an available cranial base technique for removing these tumors and to delineate the technique’s advantages that aid in achieving an improved extent of tumor resection and enhancing the patients’ overall outcome. materials and methods: we present a retrospective study of a single surgeon experience on 355 consecutive cases with sellar and parasellar tumors admitted and operated by transcranial approaches in our department between january 2000 and december 2012. results: tumors in the sellar region represent 11, 8% of all tumors operated in our department. the most common type of tumor was pituitary adenomas, 165 of cases, followed by sellar and parasellar meningiomas, 128 of cases. craniopharyngioma represent 12% of cases encountered in this region. all our cases underwent surgery by transcranial approach, unilateral frontotemporal in 252 of cases (71%). in pituitary adenomas total and near total resection was achieved in 100% of patients operated by transcranial approaches. for resection of craniopharyngiomas we have frequently chosen the extended fronto-temporal approach. the most common surgical related complications were: postoperative hematomas 9 of cases; wound infections, 6 of cases and csf leakage, 12 of cases; transient visual alteration in 12 cases, transient third cranial nerve palsy in 6 of cases, transient motor deficit in 7 cases, hydrocephalus, 6 cases; transient diabetes insipidus in the large majority of pituitary adenomas and craniopharingiomas. only 4 cases of pituitary adenomas and 6 of craniopharingiomas recurred after subtotal resection, requiring re-intervention. the mortality rate in our study was 2%. conclusions: our experience demonstrated that the management of the large suprasellar tumors via fronto-temporal approach remains the main route for these tumors with significant extrasellar extension, fibrous tumors, cases with unrelated pathology that might complicate a transsphenoidal approach and recurrent tumors after previous transsphenoidal surgery. in our opinion there is no need for larger osteotomies or extensive drilling of romanian neurosurgery (2013) xx 1: 80 91 81 cranial base. “instead of bone, remove the tumor; it's easier even for the patient”. key words: craniotomy, extent of resection, fronto-temporal approach, pituitary adenomas, suprasellar meningiomas introduction sellar and parasellar tumors are challenging lesions to resect completely and safely. in nowadays neurosurgery when endoscopic endonasal techniques have gained more and more indications, the classical intracranial approach seems to decrease in importance. but there are still numerous indications for intracranial approach, especially related to the size, extension and involvement of neurovascular structures in the region. most of the lesions approached intracranial are large tumors, so they are life threatening, they compress optic pathways, engulf carotid arteries and their ramifications, obstruct csf circulation and disturb the functions of pituitary gland and hypothalamus. sometimes do to their dimensions they alter the cognitive functions of frontal lobes. (3, 13, 17) by removing this tumor totally our intension is to preserve or sometimes to restore the normal function and to salvage the life of the patients. selection of the approach is based on the size, configuration, location and extent of the tumor. recent advances in cranial base exposures, microsurgical techniques, neuroimaging, neuronavigation and neuroanesthesia have resulted in an improved extent of resection and patient outcome. (1, 4, 18) the fronto-temporal approach (aka fronto-pterional) has the great advantage to be very familiar to most of neurosurgeons, represent the shortest distance to the ipsilateral optic nerve and carotid artery, and allow the direct verification of the optical nerves, the carotid arteries, the pituitary stalk, the tumor and its relationship with the suprasellar structures. by opening of the entire sylvian fissure this approach offers multiple ways to reach de sellar region: prechiasmatic, suprachiasmatic, trans-lamina terminalis, between on and ica, lateral to ica, above the ica bifurcation, representing the widest used techniques in today’s neurosurgery practice. (4, 6, 11) based on our experience, there is no need for larger opening for multidirectional approach because that means multiple ways for brain injury. the key points are proper positioning, proper opening, brain relaxation and surgical experience. yasargil was credited to the standard and maybe the most important approach, pterional or fronto-temporal approach. many modifications of this approach by new neurosurgeons have been created. (22, 23) objective the purpose of this study is to advocate an available cranial base technique for removing these difficult tumors and to delineate the technique’s advantages that aid in achieving an improved extent of tumor resection and enhancing the patients’ overall outcome. we aim to describe our experience in the last 10 years concerning the surgery of sellar and parasellar tumors using fronto-temporal approach. materials and methods we present a retrospective study of a single surgeon experience on 355 82 pintea et al fronto temporal approach in sellar and parasellar tumors consecutive cases with sellar and parasellar tumors admitted and operated by transcranial approaches in our department between january 2000 and december 2012. we discussed the tumor’s characteristics that could influence the treatment decision and the choice of the most reliable approach. surgical approach frontopterional approach is fashioned according to the tumor dimensions and extensions. the patient positioned supine with the head turned about 15 degrees for subfrontal approach, 30°-pterional approach, to the opposite side along the ala minor of the sphenoid wing and slightly retroflexed about 10°. the scalp incision starts just anterior to the tragus, behind the superficial temporal artery then it continue superiorly behind the hairline towards the midline; interfascial dissection to preserve the frontal branch of the facial nerve. frontal burr hole is performed at maximum 3 cm anterior to “key hole”, with bone removal extending to the skull base anteriorly. before dural opening the lumbar drainage is opened and in few minutes a good brain relaxation is obtained. the dura is opened in a semicircular fashion, centered on the pterion. using only the microsurgical aspirator and a bayoneted forceps we enter subfrontal until the optic nerve, which is the most constant landmark. the arachnoid above the on is sharply opened and than dissection goes medially and laterally in order to gain more space. with the opening of the basal cisterns the brain is relaxing progressively and offers enough space for microsurgical exploration of the entire region. results tumors in the sellar region represent 11, 8% of all tumors (3006 cases) operated between january 2000 and december 2012. there is a significant female predominance (m/f 46% vs. 56%) with a sex ratio of 1, 28. (graphic 2) the peak incidence was in the 5th decade. (graphic 3) in a pathological point of view, the most common type of tumor in our study was pituitary adenomas, 165 of cases (46%), followed by sellar and parasellar meningiomas, 128 of cases (36%). we classified the meningiomas in this region in the median group (tuberculum, diaphragma, planum sphenoidale) 66 of cases and lateral group (clinoidal, sphenoorbital, spheno-cavernous) 62 of cases. craniopharyngioma represent 12% of cases encountered in this region (42 of cases). other tumors were represented by low grade gliomas of the optic pathway and hypothalamus (8 cases -2%), germ-cell tumor 4 cases (1%), metastasis 3 cases (1%), rathke cleft cyst 3 of cases (1%) and 2 cases of immature teratoma (1%). (graphic 1) at the pediatric age approximately half of all suprasellar tumors are craniopharyngiomas, compared with only 10% in adults. regarding the clinical presentation, headache and eye pain were present in 80% of cases. the most common ophthalmic disturbance was blurred vision, in 68% of cases, followed by visual field defect – uni/bilateral hemianopia in 42% of cases and diplopia in 28% of cases. except the cases with pathological hypersecretion from functional pituitary adenomas, a certain grade of pituitary hipofunction was detected 26% cases. romanian neurosurgery (2013) xx 1: 80 91 83 other signs were memory impairment (20%) and seizures in only 5% of the cases. (graphic 4) the mean duration of symptoms was 11, 5 months. (graphic 5) all our cases underwent surgery by transcranial approach, unilateral frontotemporal in 252 of cases (71%), unilateral subfrontal in 64 of cases (18%), bifrontopterional in 14 of cases (4%), bifrontal in 10 of cases (3%), interemispheric transcallosal in 9 of cases (3%) and frontoorbitozigomatic in 3 of cases (1%). (graphic 6) graphic 1. type of tumors graphic 2. sex ratio 84 pintea et al fronto temporal approach in sellar and parasellar tumors graphic 3. age distribution (peak incidence in the 5th decade) graphic 4. clinical features graphic 5. the interval between onset and diagnostic romanian neurosurgery (2013) xx 1: 80 91 85 graphic 6. surgical approaches all the patients of sellar and parasellar meningiomas underwent surgery by transcranial approach; modified frontopterional approach was performed in majority of cases and total resection was achieved with minimal complications. in 118 patients (92%) complete tumor removal was achieved, total resection being confirmed by postoperative mri scans. we must underline that in this region complete removal is in the large majority of cases a grade ii according to simpson’s classification, this being more available in diaphragmal meningiomas. in many cases removal of involved dura along with hiperostotic bone was possible, but there are still regions of dura mater with pathological neovascularisation that could not be removed and it was only coagulated. recurrences have been found in 6 cases of clinoidal and spheno-cavernous meningiomas. three cases died after the surgery, in all cases being reintervention after previous operated spheno-cavernous meningiomas. (figure 1a, b; figure 2a, b; figure 3a, b) in pituitary adenomas total and near total resection (fragment of capsule adherent to the chiasm, residual tumor on the floor of the sella, fragments infiltrating the cavernous sinus discovered at the postoperative mri) was achieved in 100% of patients operated by transcranial approaches. (figure 4a, b) for resection of craniopharyngiomas we have frequently chosen the extended fronto-temporal approach (57%); all other cases have been approached transcallosal interemispheric or subfrontal interemispheric by bifrontal craniotomy; bifrontopterional craniotomy and combined routes were reserved for multidirectional approach of giant tumors. gross total removal was achieved in over half of cases. reasons for incomplete resection were a firm adherence to hypothalamus, large calcifications, and adherence to perforating vessels or greater vessels from the polygon of willis. (figure 5a, b), (figure 6a, b, c, d) surgical related complications were: local (postoperative hematomas, 9 of cases; wound infections, 6 of cases; ica tearing, 3 of cases and csf leakage, 12 of cases) and neurological (transient visual alteration in 12 cases, transient third cranial nerve palsy in 6 of cases, anterior cerebral artery vasospasm in two of cases, transient motor 86 pintea et al fronto temporal approach in sellar and parasellar tumors deficit in 7 cases, cerebral infarction in 3 cases, hydrocephalus, 6 cases; transient diabetes insipidus in the large majority of pituitary adenomas and craniopharingiomas. only 4 cases of pituitary adenomas and 6 of craniopharingiomas recurred after subtotal resection, requiring re-intervention. (table 7) the mortality rate in our study was 2%. a b figure 1 a, b clinoidal meningioma t1 weighted contrast enhanced sagital mri shows a large clinoidal meningioma that invades the lateral wall of the cavernous sinus and incorporates carotid artery at this level; postoperative mri shows complete removal of the tumor a b figure 2 a, b spheno-cavernous meningioma preoperative and postoperative t1 w enhanced sagital mri showing a left sphenocavernous meningioma completely removed by a pterional approach romanian neurosurgery (2013) xx 1: 80 91 87 a b figure 3 a, b suprasellar meningioma t1 weighted contrast enhanced sagital mri demonstrating giant suprasellar meningioma with superior extension in third ventricle and posterior in perimesencephalic cistern, completely removed by a fronto-temporal approach as is demonstrated by third month follow -up mri a b figure 4 a, b pituitary adenoma t1w enhanced mri in a macroprolactinaoma near total removed by a fronto-temporal approach. the intrasellar remnant is stable after six years, without adjuvant radiotherapy 88 pintea et al fronto temporal approach in sellar and parasellar tumors a b figure 5a, b craniopharyngiomas preoperative mri showing a suprasellar solid craniopharyngioma extending from the infudibular area into the third ventricle, removed completely by fronto-temporal approach a b c d figure 6 a, b, c, d diencephalic glioma pre and postoperative mri aspect to a 3 years old child with an opto-diencephalic glioma with malignant transformation. the 24 hour postoperative mri demonstrate a near total removal, performed by a fronto-temporal approach table 7 surgical complications complications no. of cases transient diabetes insipidus 57 csf leak 12 worsen of visual deficits 12 transient motor deficit 7 transient third cranial nerve palsy 6 hydrocephalus 6 infection of surgical wound 6 intracerebral hematoma 9 anterior cerebral artery vesospasm 3 ica tearing 3 cavernous sinus injury 1 romanian neurosurgery (2013) xx 1: 80 91 89 discussion this study presents the favorable surgical outcomes when using a frontotemporal approaches for sellar and parasellar tumors. in particular, their midline location and encasement of neurovascular structures create challenges for access. the delicacy of microsurgical techniques relieves the surgical outcome for patients with parasellar region lesions, leading to improved survival and quality of life. (1, 4, 18) there are many publications of surgical approaches for the tumors of this area since its first report. all of these approaches have their advantages and disadvantages, but in the present time only several approaches are popular among neurosurgeons, those are pterional, unilateral frontal, frontolateral, bifrontal, and their modifications, and transsphenoidal. (3, 12, 15) the first fronto lateral craniotomy was described by dandy in 1933 to expose the optic chiasm and the pituitary region and was later refined by kempe (6, 9, 23). the yasargil’s classical description of pterional craniotomy centered in fronto-temporal fissure was first popularized in 1970 and has been widely used to approach lesions of the sellar or suprasellar region, circle of willis and sylvian fissure. (8, 17, 19) this approach consists of accessing the brain and the anterior skull base through their lateral aspect by removing the frontal and temporal bones and the lateral two thirds of the lesser sphenoid wing, including the microsurgical dissection and opening of the sylvian fissure and cistern. (13, 21, 22) several variants of this technique have been proposed to reduce the bone flap of the pterional craniotomy and to limit functional and aesthetic complications. chehrazi, in his study of 1992, proposed fronto-lateral craniotomy located entirely underneath the temporal muscle that extends about 3.0 cm beyond pterion, which required extensive dissection of muscle temporal with functional and cosmetic implications. (2) in 2006 figueiredo demonstrated that the distal dissection of the sylvian fissure offered no extra benefits for anatomical exposure of the neurovascular structure from this area. (6, 7) regarding the position, there are no debates: supine with head rotate to opposite site 15-30° (15 degrees for subfrontal approach, 30°-pterioanal approach). moderate hyperextension is needed as is the elevation of the head from the heart level. as far as we are concerned, whenever there is an suprasellar extension that adheres intimately to optic nerves, the carotid, or reaches the level of third ventricle, although situated in the direction of possible transphenoidal approach, we prefer a surgical decompression a "at sight ", by intracranial approach. the bone flap position can be modified anteriorly, posteriorly or in length, depending on the localization of the tumor in which to provide an optimal access to the lesions with minimal retraction of the brain. (20) the goals of surgery for suprasellar meningiomas are to perform as complete a removal as possible with preservation of visual function and normalize any hormonal abnormalities. (10, 16, 18) the best approach to use depends on the anatomic location or spread of the tumor, along with a degree of familiarity and confidence that the surgeon has with a given approach. most suprasellar meningiomas can be removed completely and safely. the most used surgical approach is the standard fronto-temporal approach, 90 pintea et al fronto temporal approach in sellar and parasellar tumors with preservation and even improvement of visual function after surgery. this approach has the considerable advantage of facilitating complete resection of dural tails thereby preventing recurrence, and it provides reliable surgical procedures for treatment of anterior skull base meningiomas. (5, 16, 19) when a pituitary adenoma meets the indications for transcranial approach, the approach must still be tailored according to the direction and the extend of extrasellar tumor, the reasonable goals of surgery, the particular experience of the surgical team. in our experience, radical resection of cph represented the first and almost unique treatment modality. although not insignificant, post-operative mortality and morbidity do not seem to represent a major contraindication in attempting a radical tumor resection whenever possible. on the other hand, extensive hypothalamic involvement should suggest a less aggressive attitude. (9, 14, 21) the ultimate goal of total resection consists in no recurrence while avoiding complications, is often difficult because of: involvement of vital neural and/or vascular structures; invasion of the bony tissue; poor delimitation; increased malignancy. (20) conclusions our experience demonstrated that the management of the large suprasellar tumors via transcranial approach remains the main route for these tumors with significant extrasellar extension (in the middle fossa, posterior fossa or suprasellar), fibrous tumors, cases with unrelated pathology that might complicate a transsphenoidal approach (infections of the sphenoid sinus, parasellar aneurysms) and recurrent tumors after previous transsphenoidal surgery. we agree that complete microsurgical removal, when safe, is the treatment of choice that offers the best chance of cure. overall, craniotomies will continue to play a role in the management of patients with sellar/parasellar tumors, although patient selection and careful preoperative evaluation are key elements in choosing the most appropriate approach. in our opinion there is no need for extensive craniotomies in the large majority of the cases. a proper positioning, good brain relaxation, appropriate microsurgical technique and instrumentation and surgical experience are the key elements for a complete removal of the tumor. by progressive debulking we gain more and more space for tumor mobilization and removal. “instead of bone, remove the tumor; it's easier even for the patient” references 1.aydin, i. h.; takçi, e.; kadioğlu, h. h. et all,: pitfalls in the pterional approach to the parasellar area (review)*min minimally invasive neurosurgery; issue 04, 1995 2.chehrazi bb: a temporal transsylvian approach to anterior circulation aneurysms. neurosurgery 30:957– 961, 1992. 3.day jd surgical approaches to suprasellar and parasellar tumors. neurosurgery clinics of north america 14 109–122, 2003 4.de oliveira e, siqueira m, tedeschi h, peace da. technical aspects of the fronto-temporo-sphenoidal approach craniotomy. in: matsushima t (ed). surgical anatomy for microneurosurgery vi: cerebral aneurysm and skull base lesions. fukuoka city: sci med publications: 3-8, 1993 5.fahlbusch r, schott w. pterional surgery of meningiomas of the tuberculum sellae and planum sphenoidale: surgical results with special consideration of ophthalmological and endocrinological outcomes. j neurosurg.96:235–43, 2002 6. figueiredo eg, oliveira am, plese jp, teixeira mj. perspective of the frontolateral craniotomies. arq neuropsiquiatr 68:430-432, 2010 7.figueiredo eg, deshmukh p, zabramski jm, preul mc, crawford nr, spetzler rf. the pterionaltranssylvian approach: an analytical study. romanian neurosurgery (2013) xx 1: 80 91 91 neurosurgery 2006; 59:263-269. 8.heuer gj. the surgical approach and treatment of tumors and other lesions about the optic chiasm. surg gynecol obstet 53: 489–518, 1931 9.hoffmann hj, craniopharyngiomas: the continuing controversy on management. concepts pediatr neurosurg 2: 14-28, 1982 10.jallo g, benjamin v. tuberculum sellae meningioma: microsurgical anatomy and surgical technique. neurosurgery. 51:1432–40, 2002 11. kim e, delashaw jb jr. osteoplastic pterional craniotomy revisited. neurosurgery. 68:s125-s129, 2011 12.knosp e. practical handbook of neurosurgery from leading neurosurgeons. in: sindou m, editor. springer verlag: new york; pp. 79–94, 2009 13.liu jk, weiss mh, couldwell wt: surgical approaches to pituitary tumors. neurosurg clin n am 14:93–107, 2003 14.nakamura m, samii m. berlin, heidelberg: springer verlag; 2008. in: ramina r, aguiar ph, tatagiba m, editors. samii's essentials in neurosurgery. springer verlag: berlin heidelberg; pp. 98–105, 2008. 15.nakamura m, roser f, struck m, vorkapic p, samii m. tuberculum sellae meningiomas: clinical outcome considering different surgical approaches. neurosurgery.59:1019–29, 2006 16.oreste de divitiis, enrico de divitiis. anterior cranial fossa meningiomas: a new surgical perspective. world neurosurgery 77:5-6, 623-624, 2012 17.samandouras g, kerr rs & milford ca minimally invasive biopsy of parasellar lesions: safety and clinical applications of the endoscopic, transnasal approach. british journal of neurosurgery 19 338–344, 2005 18.samii m, gerganov vm. surgery of extra-axial tumors of the cerebral base. neurosurgery. (suppl 3):1153–61, 2008 19.shulev, yuri; akobyan, ovanes pterional approach to management of anterior skull base meningiomasskull base; issue 03, 2009 20.stanila a, florian is et al, ghid de neurooftalmologie, edit. universitatii l.blaga sibiu, 2007; 54-78 21.yaşargil mg, curcic m, kis m, siegenthaler g, teddy pj, roth p: total removal of craniopharyngiomas. approaches and long-term results in 144 patients. j neurosurg 73:3–11, 1990 22..yasargil mg, krisht af, türe u, al-mefty o, yasargil dch. microsurgery of insular gliomas: part i. surgical anatomy of the sylvian cistern. contemporary neurosurgery 2002; 24:1-8. 23.wen ht, oliveira e, tedeschi h, andrade fc, rhoton al. the pterional approach: surgical anatomy, operative technique, and rationale. operat techneurosurgery 2001; 4:60-72. microsoft word 3adamdanil_oerativetreatment_f romanian neurosurgery (2011) xviii 3: 255 – 262 255 operative treatment of lumbar spinal stenosis with interspinous implants. general overview d. adam1, cristina adam2, ioana hornea3 1“carol davila” medicine and pharmacy university, bucharest, romania 2zentral klinikum augsburg, neurologische klinik, germany 3emergency clinic hospital “st. pantelimon”, bucharest, romania abstract interspinous process devices are an alternative treatment of symptomatic lumbar spinal stenosis (lss) to conventional surgery. are presented various kinds of interspinous devices: x-stop, in-space, superion, aperius, ceramic spacers. pathophysiology of lumbar spinal stenosis is presented together with biomechanics of interspinous implants which reduce loads on the facet joints, reduce pressure in the posterior annulus, increase foraminal and spinal canal dimensions. indications, contraindications and precautions related to interspinous device surgery are presented. the results of in vitro studies are confirmed in randomized clinical trials. the improvements are statistically and clinically important, compared to those reported for laminectomy. keywords: lumbar spinal stenosis, interspinous devices. introduction lumbar spinal stenosis is one of the most common diseases in the elderly. spinal stenosis is a narrowing of the spinal canal or neural foramina. some patients are born with this narrowing, but most often spinal stenosis is the result of a degenerative condition with hypertrophy of the ligamentum flavum and facet joints, osteophytes, spondylolisthesis and disc protrusion. symptoms of spinal stenosis constitute neurogenic claudication syndrome first described by verbiest in 1954 [1]. symptoms of pain or numbness in the legs are caused by lumbar spinal stenosis (47,4%) and by other diagnoses: diabetic neurophaty, peripheral artery disease [2]. characteristics associated with lumbar spinal stenosis include age greater than 60, intermitent claudication, exacerbation of symptoms when standing up, improvement upon bending forward, absence of diabetes, good peripheral artery circulation. a positive straight leg raise test and symptoms induced with lumbar flexion are negatively correlated with the diagnosis of lumbar spinal stenosis. the lifetime risk has been estimated to be approximately 10% with a slight predominance of women. some studies have documented that a large proportion of patients have stable symptoms for many years. lumbar spinal stenosis is a progressive disabling condition which compromises an individual`s ability to perform their 256 d. adam et al interspinous implants in lumbar spinal stenosis activities of daily living, reduces quality of life and threatens one`s independence. pathophysiology in 1954 verbiest [1] published a series of 7 case reports of patients with intermitent neurogenic claudication. in each case myelography showed a block in the lumbar region, which was confirmed at operation. in 1978 kirkaldy-willis [3] described the pathophysiology of lumbar spinal stenosis based on cadaveric dissections and patients’ laminectomy. lss begins with repetitive minor trauma over many years. lss is the result of destruction of the posterior joints causing synovial reaction, cartilage destruction, osteophyte formation and intervertebral disc disruption. these changes lead to loss of disc height, facet instability, buckling of the ligamentum flavum, narrowing of the neural foramina and spinal canal and impinging each or all together upon structures within them. this lead to chronic compression of the nerve roots causing decreased blood flow, ischemia and local edema. the load bearing structures in each vertebra are the vertebral body and the two facets. changes of lumbar facet joints are responsive of 15-40% of chronic low back pain. facet specific back pain is exacerbated by hyperextension and lessened in a recumbent position or flexion. during extension, deformation of the joint capsule is the source of pain. the capsule surrounding the facet joint is innervated by afferent nociceptive fibers, which are activated by mechanical stresses. increased facet loading is a consequence of disc degeneration. in the case of facet joint degeneration or removal, the motion segment is unstable, allowing greater sagital displacement and acceleration of disc degeneration. long term lumbar segment instability results in degenerative spondylolisthesis. treatment of lumbar spinal stenosis in the past lumbar spinal stenosis had only a conservative treatment. conservative treatment includes physical therapy, non-steroidal anti-inflammatory drugs, opioid analgesics, epidural steroid injections and lumbar corsets. pain relief from epidural injection may be temporary and patients are usually advised to get no more than 3 injections per 6 month period. physical therapy and / or exercises help stabilize the spine, build endurance and increase flexibility. while some patients obtain relief from symptoms with this "conservative" therapy, others do not. patients often fail conservative therapy because these treatment options do not alter the anatomic pathology that causes symptoms, do not enlarge the spinal canal or foramina. when conservative management fails is indicated surgical intervention in the form of mechanical decompression of the posterior spinal elements. the conventional surgical treatment for spinal stenosis is a lumbar laminectomy. wide decompressive laminectomy has been the standard procedure, though recently less invasive surgical approaches have been tried. gibson [4] in a systematic review of recent studies suggests that laminectomy alone had better results than laminectomy associated with instrumented or noninstrumented fusion. the author concluded that there was no clear evidence regarding romanian neurosurgery (2011) xviii 3: 255 – 262 257 the most effective technique for surgical decompression of spinal stenosis. studies have been unable to identify patient characteristic that predict who is likely to respond best to surgery and who will respond to conservative management [5]. the study of weinstein et all [6] suggests that surgical management of degenerative lumbar spinal stenosis achieves better than nonsurgical care. however, major surgery, an invasive surgical treatment, especially can lead to complications, therapy, miminimally invasive surgery is an important option for elderly patients who tend to present with comorbidities and other health risks. as a result, interspinous process distraction with different spacers has been used widely over the past years. devices the first interspinous implant for the lumbar spine was developed in the 1950s by knowles (cited by kondrashov, 2006). owing to flaws in design, material, surgical technique and applied indications its use was abandoned. technological advances, which have contributed to improved safety and efficacy, have rekindled an interest in ipd implantation. now exist various kinds of interspinous devices: 1. the x-stop interspinous process decompression (ipd) (st. francis medical technologies, concord system ca) is the first alternative to conventional spinal stenosis surgery proven to significantly improve symptom severity and physical function. the x-stop device is a titanium metal implant designed to fit between spinous processes of the vertebrae (figure 1). it is designed to remain safely and permanently in place without attaching to the bone or ligaments. it is mri safe but can produce artifacts on mr image. figure 1 x-stop implant 258 d. adam et al interspinous implants in lumbar spinal stenosis x-stop ipd is available in europe since 2002 and received fda approval in 2005. x-stop is currently the only ipd device available in the united states. 2. the in space interspinous spacer (synthes usa, llc) is another percutaneous minimally invasive device which put the stenotic segment in slight flexion, enlarge the spinal canal and foramen (figure 2). senegas [7] found positive long term results with the first iss, which was implanted in 1986. 3. in japan, since 2002 is used a new distraction device (pentax co, tokyo, japan) made of hydroxy-apatite and calcium phosphate. his shape is cylindrical and on the surface of the midportion it harbors grooves (figure 3)[8]. figure 2 in space interspinous spacer figure 3 ceramic spacers 4. the superion interspinous spacer (iss) (vertifeex, ca, usa) (figure 4) is an device composed of titanium alloy, and consists of a single component with deployable superior and inferior projections that engage the spinous processes to secure it is opened, thus providing distraction at the affected spinal segment. superion has been ce marked since 2007 and is currently an investigational device in the u.s. it is the most advanced and least invasive spacer and allows for the procedure to be done local anesthesia on an outpatient basis. 5. aperius perclid system (figure 5) can be used at any level between l1 and l5 [9]. a b figure 4 superion implant: device (a) and intraoperative fluoroscopic image (b) romanian neurosurgery (2011) xviii 3: 255 – 262 259 a b figure 5 aperius perclid system: device (a) and postoperative spine radiographs (b) biomechanics of interspinous spacers biomechanical results reported by panjabi et all [10], anatomic results reported by inufusa et all [11] and clinical results reported by fredericson [12] et all have shown that when individuals shift their spine from an extended position, the cross-sectional foraminal area increases and nerve root compression is relieved. an interspinous spacer is designed to hold the stenotic level in flexion. an interspinous spacer produce an unloading of the stenotic middle column of the spine, which is evident as an increase in foraminal height, related to increased foraminal area and decreased canal stenosis. lazaro et all [13] observed that foraminal height, after the iss was inserted, decreased during extension with 1.4% compared with 4.7% decreased without iss. foraminal area is with 4.2% larger during extension after iss implantation. with iss facet loads were reduced by more than 50% during full extension. richards et all [14] found that foraminal area increased by 25% during extension after x-stop implantation. lee et all [15] reported that the mean dural sac area increased by 23% after xstop placement and intervertebral foraminal area improved by 36%. siddiqui et all [16] found that the spinal cross section examination with mri, the mean canal dimension increased 20% in standing patients, and 27% in extension with x-stop implantation. wiseman et all [17] showed that the mean pressure of the facet joint was reduced by 39% at the x-stop implanted level. chiu [18] reported that x-stop unloads posterior annulus pressure by 63%, posterior nucleus pulposus pressure by 41% and facet force by 68%. these in vitro studies of interspinous spaces have shown increased foraminal and spinal canal dimensions at the implanted level in extension, a reduction of the pressure in the posterior annulus in extension and off-loading of the facet joints without altering the dimensions or pressures in the adjacent non-operated levels. thus, these spaces may prevent the development of disorders at there levels. 260 d. adam et al interspinous implants in lumbar spinal stenosis indications for use of interspinous devices all kind of interspinous implants are indicated for the treatment of patients aged 50 or older, suffering from pain or intermitent neurogenic claudication in the legs secondary to a confirmed diagnosis of central and/or lateral process lumbar spinal stenosis and not responding to at least 6 month of non-operative treatment. these patients have to have lumbar stenotic symptoms of moderate severity with pain relief in flexed lumbar and exacerbation when in an extended position. other indication for interspinous implants are contained hnp, spondylolisthesis up to 35% (grade 1.5/4) with intermitent neurogenic claudication, facet syndrome, degenerative and/or iatrogenic (post-discectomy) disc syndrome, baastrup`s syndrome (kissing spine) and for unloading of disc adjacent to a lumbar fusion procedure. interspinous devices can be implanted at one or two lumbar levels. contraindications of interspinous devices these devices are contraindicated in patients with: •an allergy to titanium or titanium alloy •spinal anatomy or disease that would prevent implantation of the device or cause the device to be unstable in the body: significant instability of the lumbar spine acute fracture of the spinous process or pars interarticularis significant scoliosis (cobb angle greater than 25 degrees) an ankylosed segment at the affected level •cauda equina syndrome •severe osteoporosis in the spine, defined as bone mineral density more than 2,5 sd below the mean of adult normal. •active systemic infection or infection localized to the site of implantation precautions implantation of interspinous devices can be an effective treatment option, but it is not a panacea for all patients with degenerative lumbar spine conditions. the interspinous device does not replace microsurgical decompression in patients with massive stenosis and continuous claudication. to avoid the postoperative complications of x-stop interspinous distractor, not only the clinical indications deserve attention, but also the patient’s lumbar anatomic characteristics. barbagallo et all [19] scrutinized these characteristics and proposed a novel anatomic scoring system to classify the patient’s anatomic features and to make a good patient selection, for this decompression procedure (table 1). table 1 anatomic scoring system according to barbagallo score inferior sp morphology accessible sp length interspinous area shape 1 concave entire sp length parallel 2 straight posterior 2/3 of the sp posterior v shape 3 convex / dysmorphic posterior 1/3 of the sp --- sp spinous process. romanian neurosurgery (2011) xviii 3: 255 – 262 261 there are 17 possible combinations in the scoring system: a score of 3-4, suitable conditions for placement of an interspinous device a score of 5-6, risk conditions a score of 7-8, potential contraindications. a v-shaped posterior interspinous area is a risk factor for device dislocation, and a potential contraindication. a parallel interspace is a more suitable anatomic finding. the issues analyzed by barbagallo et all have to thoroughly considerent among the inclusion / exclusion criteria before surgery, to obtain a high success rate. insertion of an interspinous devices is not without risk. the potential adverse events of interspinous implants are: implant dislodgement / migration, fracture of the spinous process, foreign body reaction, mechanical failure of the device, additional surgery with removal of the implant. the anatomic improvements demonstrated in prior cadaveric studies were confirmed in vivo, in randomized clinical trials [8, 20, 21, 22, 23]. the outcomes were strongly in favor of interspinous devices when compared to those reported for laminectomy. the improvements were statistically and clinically important. references 1. verbiest h. a radicular syndrome from developmental narrowing of the lumbar vertebral canal. j bone joint surg br 1954; 36-b:230-237. 2. konno s, hayashino y, fukuhara s, kikuchi s, kaneda k, seichi a, chiba k, satomi k, nagata k, kawai s. development of a clinical diagnosis support tool to identify patients with lumbar spinal stenosis. eu spine j 2007; 16:1951-1957. 3. kirkaldy-willis wh, wedge jh, yong-hing k, reilly j. pathology and pathogenesis of lumbar spondylosis and stenosis. spine (phila pa) 1978; 3:319-328. 4. gibson jn, waddell g. surgery for degenerative lumbar spondylosis: updated cochrane review. spine. oct 15 2005;30(20):2312-2320. 5. amundsen t, weber h, nordal hj, magnaes b, abdelnoor m, lilleas f. lumbar spinal stenosis: conservative or surgical management?: a prospective 10-year study. spine. jun 1 2000; 25(11):1424-1435; discussion 1435-1426. 6. weinstein jn, tosteson td, lurie jd, et all. surgical versus nonsurgical therapy for lumbar spinal stenosis. n engl j med ,2008; 358: 794-810. 7. senegas j. mechanical supplementation by non-rigid fixation in degenerative intervertebral lumbar segments: the wallis system. eur spine j. 2002;11(suppl 2):s164– s169. epub 2002 jun. 8. yano s, hida k, seki t, aoyama t, akino m, iwasaki y. a new ceramic interspinous process spacer for lumbar spinal canal stenosis. neurosurgery, 2008 jul;63(1 suppl 1): ons108-13; discussion ons114. 9. nardi p, cabezas d, rea g, pettorini bl. aperius perclid stand alone interspinous system for the treatment of degenerative lumbar stenosis: experience on 152 cases. j spin disor tech 2010; 23:203-207. 10. panjabi mm, takata k, goel vk. kinematics of lumbar intervertebral foramen. spine, 1983, 8(4): 348357. 11. inufusa a, an hs, lim th et all. anatomic changes of the spinal canal and intervertebral foramen associated with flexion-extension movement. spine 21: 2412-2420, 1996. 12. fredericson m, lee su, welsh j, et all. changes in posterior disc bulging and intervertebral foraminal size associated with flexion-extension movement: a comparison between l4-5 and l5-s1 levels in normal subjects. spine j, 2001, 1(1): 10-17. 13. lazaro bcr, brasiliense lbc, sawa agu, et all. biomechanics of a novel minimally invasive lumbar interspinous spacer: effects on kinematics, facet loads, and foramen height. neurosurgery, 2010, 66(3 suppl operative):126-32; discussion 132-3. 14. richards jc, majumdar s, lindsey dp, beaupre gs, yerby sa. the treatment mechanism of an interspinous process implant for lumbar neurogenic intermittent claudication. spine. apr 1 2005;30(7):744749. 15. lee j, hida k, seki t, iwasaki y, minoru a. an interspinous process distractor (xstop) for lumbar spinal stenosis in elderly patients: preliminary experiences in 10 consecutive cases. j spine dis tech 2004; 17:72-77; discussion 78. 16. siddiqui m, nicol m, karadimas e, smith f, wardlaw d. the positional magnetic resonance imaging changes in the lumbar spine following insertion of a novel interspinous process distraction device. spine 262 d. adam et al interspinous implants in lumbar spinal stenosis (phila pa) 2005; 30:2677-2682. 17. wiseman cm, lindsey dp, fredrick ad, et al. the effect of an interspinous process implant on facet loading during extension. spine. 2005;30:903–907. 18. chiu jc: interspinous process decompression (ipd) system (x-stop) for the treatment of lumbar spinal stenosis. surg technol int 15: 265-275, 2006. 19. barbagallo g, olindo g, corbino l, et all. analysis of complications in patients treated with x-stop interspinous process decompression system: proposal for a novel anatomic scoring system for patients selections and review of the literature. neurosurgery, vol.65, no.1, 2009, 7: 111-119. 20. zucherman jf, hsu ky, hartjen ca, et al. a prospective randomized multi-center study for the treatment of lumbar spinal stenosis with the x-stop interspinous implant: 1-year results. eur spine j. 2004;13:22–31. 21. zucherman jf, hsu ky, hartjen ca, et al. a multicenter, prospective, randomized trial evaluating the xstop interspinous process decompression system for the treatment of neurogenic intermittent claudication. spine. 2005;30:1351–1358. 22. kondrashov dg, hannibal m, hsu ky, zucherman jf. interspinous process decompression with the xstop device for lumbar spinal stenosis. a 4-year follow-up study. j spinal disord tech, vol 19, no. 5, 2006, 7: 323-327. 23. fokter sk, yerby sa. patient-based outcomes for the operative treatment of degenerative lumbar spinal stenosis. eur spine j. dec 21 2005:1-9. doi: 10.33962/roneuro-2022-034 delayed cerebrospinal fluid ascites following ventriculoperitoneal shunt. a case report with literature review ahtesham khizar, soha zahid romanian neurosurgery (2022) xxxvi (2): pp. 186-195 doi: 10.33962/roneuro-2022-034 www.journals.lapub.co.uk/index.php/roneurosurgery delayed cerebrospinal fluid ascites following ventriculoperitoneal shunt. a case report with literature review ahtesham khizar1, soha zahid2 1 pakistan institute of medical sciences, islamabad, pakistan 2 jinnah medical and dental college, karachi, pakistan abstract background: cerebrospinal fluid (csf) ascites is an abnormal accumulation of csf within the peritoneal cavity caused by the peritoneum's inability to absorb the csf, following a ventriculoperitoneal (vp) shunt surgery. excessive csf production (e.g, choroid plexus papilloma and choroid plexus villous hypertrophy), high csf protein secondary to chronic infection (e.g., tuberculosis), and brain tumours (e.g, optic gliomas and craniopharyngiomas) have all been suggested as contributing factors to the formation of csf ascites. peritoneal inflammation as a result of several shunt revisions or some non-specific inflammatory reaction to shunt material has also been explored. case presentation: a 3-year-old girl with lumbar myelomeningocele and delayed csf ascites following vp shunt is reported. therapeutic paracentesis was employed to relieve abdominal distension, although recurring accumulation was common. the vp shunt was removed and instead of a ventriculo-atrial shunt, she underwent endoscopic third ventriculostomy (etv). csf ascites gradually disappeared after etv over a two-week period. conclusions: abdominal paracentesis to relieve ascites and conversion of a ventriculoperitoneal shunt to a ventriculo-atrial shunt are commonly used to treat csf ascites, however endoscopic third ventriculostomy, where feasible, is another alternative treatment that can be performed to treat this condition. introduction the most frequent procedure for hydrocephalus is a ventriculoperitoneal (vp) shunt. they have been linked to a variety of issues, including dysfunction, infection, blockage, and migration. rarely, the patient may develop increasing abdominal distention as a result of cerebrospinal fluid (csf) accumulation. this is commonly referred to as a pseudocyst. the omentum produces a cyst at the tip of the shunt as a result of inflammation, resulting in a fluid-filled sac. ascites is caused by a production-absorption mismatch or a non-absorbing peritoneum in very uncommon cases.[46] ascites owing to hepatic, renal, or cardiac illness must be distinguished from csf ascites, which is an abnormal buildup of csf within the peritoneal cavity[38]. csf ascites is a distinct condition in which there is an excessive keywords hydrocephalus, cerebrospinal fluid ascites, endoscopic third ventriculostomy corresponding author: ahtesham khizar pakistan institute of medical sciences, islamabad, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 187 delayed cerebrospinal fluid ascites following ventriculoperitoneal shunt accumulation of csf in the peritoneal cavity due to the peritoneum's inability to absorb it. this incapacity could be the result of a large amount of csf being produced.[23] there have been several hypotheses on what factors may lead to the development of csf ascites. excessive csf production (as in choroid plexus papilloma and choroid plexus villous hypertrophy), high csf protein secondary to chronic infection (e.g. tuberculosis), and brain tumours (e.g, optic gliomas and craniopharyngiomas) have all been suggested as contributing factors to the formation of csf ascites. peritoneal inflammation as a result of several shunt revisions or some non-specific inflammatory reaction to shunt material has also been explored.[46] after ensuring that there is no infection, the vp shunt associated csf ascites is treated by converting the shunt to a ventriculoatrial shunt. endoscopic third ventriculostomy (etv) is another treatment option that can be done to treat this condition in selective cases. figure 1. a: csf swelling at reservoir site of vp shunt with distended abdomen and umbilical hernia due to csf ascites, b: abdominal incisional scar for vp shunt, c: lumbar myelomeningocele. figure 2. a & b: x-ray shunt series showing vp shunt tubing marked by yellow arrows 188 ahtesham khizar, soha zahid table 1. detailed literature review of 77 previously reported cases of csf ascites and their treatment. s.no. author's name year reported no. of cases reported gender/age cause/type of hydrocephalus treatment for csf ascites 1 r h ames[1] 1967 1 m/2 years congenital hydrocephalus ventriculo-atrial shunt 2 d f dean[2] 1972 1 m/1 year aqueductal stenosis ventriculo-atrial shunt 3 j d rosenthal[3] 1974 1 f/3 years suprasellar mass (astrocytoma) ventriculo-jugular shunt 4 michael j. weidmann[4] 1975 1 f/3 months aqueductal stenosis multiple paracentesis followed by ventriculoatrial shunt 5 sw parry[5] 1975 1 m/7 months communicating hydrocephalus ventriculo-atrial shunt 6 j cummings[6] 1976 1 unknown 7 r f lees[7] 1978 2 unknown 8 j m noh[8] 1979 1 unknown 9 s c ohaegbulam[9] 1980 1 3rd ventricle compression by recurrent craniopharyngioma spontaneous resolution following paracentesis 10 a b adegbite[10] 1982 1 f/11 years recurrent craniopharyngioma vp shunt removal leading to resolution of ascites followed by new vp shunt 11 fp agha[11] 1983 1 m/7 years suprasellar astrocytoma ventriculo-atrial shunt 12 r a yount[12] 1984 4 1-f/6 years, 2-f/20 years, 3-m/4 years, 4-f/3 years 1-communicating hydrocephalus, 2-unknown, 3-optic nerve glioma, 4-optic nerve glioma 1-ventriculo-cholecystic shunt, 2-paracentesis and multiple taps of shunt reservoir, 3-paracentesis and lowsodium diet, 4-spontaneous resolution with fluidrestricted diet 13 gairi tahull jm[13] 1984 1 f/5 years communicating hydrocephalus ventriculo-atrial shunt 14 ds rush[14] 1985 4 vp shunt revisions 189 delayed cerebrospinal fluid ascites following ventriculoperitoneal shunt 15 d madruga acerete[15] 1988 1 f/12 years dandy-walker malformation 16 g m goodman[16] 1988 1 f/11 years hydrocephalus following lumbar myelomeningocele repair ventriculo-atrial shunt 17 s niikawa[17] 1988 1 f/45 years post-infectious obstructive hydrocephalus 18 f pérez peña[18] 1990 1 m/17 years malformation hydrocephalus 19 a suárez[19] 1993 1 m/22 years craniopharyngioma ventriculo-atrial shunt 20 a west[20] 1994 3 1-m/6 months, 2-m/6 years, 3-m/8 months optic pathway gliomas ventriculo-atrial shunts 21 a shuper[21] 1997 1 f/4 years optic chiasm glioma ventriculo-atrial shunt 22 michiko yukinaka[22] 1998 1 f/23 years congenital hydrocephalus with spina bifida ventriculo-atrial shunt 23 b chidambaram[23] 2000 2 1-f/3 months, 2-m/7 years 1-congenital hydrocephalus, 2-optic chiasm glioma 1-ventriculo-atrial shunt, 2-ventriculo-atrial shunt 24 z gil[24] 2001 4 1-m/9 years, 2-m/0.5 years, 3-m/0.5 years, 4-m/4 years 1-optic pathway glioma, 2-optic pathway glioma, 3-optic pathway glioma, 4-chiasmatic glioma ventriculo-atrial shunts 25 bh lee[25] 2001 1 m/68 years vp shunt removal and antibiotics 26 gf longstreth[26] 2001 1 f/28 years communicating hydrocephalus ventriculo-atrial shunt 27 gy lee[27] 2002 1 f/33 years congenital hydrocephalus ventriculo-atrial shunt 28 nayyar yaqoob[28] 2003 1 m/17 years tuberculous meningitis anti-tuberculous therapy followed by ventriculo-atrial shunt 29 raj kumar[29] 2003 4 1-m/9 years, 2-m/2 years, 1-thalamic glioblastoma, 1-paracentesis revealed peritoneal mets, 190 ahtesham khizar, soha zahid 3-m/4 years, 4-m/8 years 2-choroid plexus papilloma of 3rd ventricle, 3-tuberculous meningitis, 4craniopharyngioma 2-ventriculo-atrial shunt followed by total excision of tumor, 3-intraperitoneal cyst decompression, 4-abdominal exploration and vp shunt revision 30 sj pawar[30] 2003 2 1-m/8 months, 2-m/2 years choroid plexus papilloma of posterior 3rd ventricle 1-vp shunt revision, 2-ventriculo-atrial shunt 31 greg olavarria[31] 2005 4 1-m/8 months, 2-m/8 months, 3-f/12 months, 4-f/12 months optic chiasmal hypothalamic astrocytoma 1-ventricular gallbladder shunt, 2-ventricular gallbladder shunt, 3-ventricular gallbladder shunt, 4-ventricular gallbladder shunt converted to ventriculoatrial shunt 32 michael l diluna[32] 2006 1 m/4 years arachnoid cyst ventriculo-atrial shunt 33 rajeev kariyattil[33] 2007 5 3 males, 2 females mean age: 3.7 years 1 posterior fossa arachnoid cyst, 1 hemorrhage, 1 optic chiasm glioma, 1 craniopharyngioma, 1 meningomyelocele 4 ventriculo-atrial shunts, 1 spontaneous resolution after hypoproteinemia treatment 34 paik i[34] 2010 1 f/21 years myelomeningocele ventriculo-atrial shunt 35 s das[35] 2010 1 m/7 years craniopharyngioma ventriculo-atrial shunt 36 n montano[36] 2010 1 f/51 years obstructive hydrocephalus due to large vestibular schwannoma vp shunt removal, evd placement, iv teicoplanin and multiple ascitic fluid taps 37 wj wilma houtmanvan duinen[37] 2011 1 f/29 years congenital cervical meningocele ventriculo-atrial shunt 38 mwang’ombe nimrod junius[38] 2012 1 m/7 years aqueductal stenosis ascites resolved within two weeks of endoscopic third ventriculostomy 39 yin yee sharon low[39] 2012 1 f/48 years brain mets from breast carcinoma with obstructive hydrocephalus peritoneal drain 191 delayed cerebrospinal fluid ascites following ventriculoperitoneal shunt 40 atakan comba[40] 2013 1 f/6 years myelomeningocele ventriculo-atrial shunt 41 j woodfield[41] 2013 1 f/1 year craniopharyngioma ventricular gallbladder shunt converted to ventriculo-atrial shunt 42 hira jamal[42] 2016 1 f/37 years idiopathic intracranial hypertension vp shunt removal, antibiotics and ventriculo-atrial shunt 43 maheen siddiqi[43] 2017 1 f/16 years congenital hydrocephalus ventriculo-atrial shunt 44 d sachan[44] 2017 1 m/5 years choroid plexus papilloma tumor resection and vp shunt removal 45 h han[45] 2017 1 m/20 years dandy-walker syndrome ventriculo-atrial shunt 46 g. musa[46] 2018 1 f/3 years communicating hydrocephalus ventriculo-atrial shunt 47 aa khan[47] 2018 2 endoscopic third ventriculostomy 48 darrick k li[48] 2019 1 f/26 years loeys-dietz syndrome and congenital hydrocephalus multiple therapeutic paracentesis followed by peritoneovenous (denver) shunt 49 saud e. suleiman[49] 2020 1 f/32 years hydrocephalus due to brain malformation (corpus callosum agenesis) multiple therapeutic paracentesis followed by ventriculo-atrial shunt 50 george a.alexiou[50] 2021 1 f/60 years bilateral frontal meningiomas and obstructive hydrocephalus ventriculo-atrial shunt 51 m mathew[51] 2022 1 f/7 years craniopharyngioma ventriculo-atrial shunt 52 n mehta[52] 2022 1 m/29 years communicating hydrocephalus ventriculo-atrial shunt case presentation a 3-year-old girl appeared to us as an outpatient with complaints of frequent episodes of vomiting and reluctance to feed for three days, as well as abdominal distention for two weeks. she was born with a lumbar myelomeningocele and congenital hydrocephalus after a normal vaginal delivery at term. at the age of one month, she had a ventriculoperitoneal shunt placed, but she never had lumbar myelomeningocele repair surgery. she had been doing well since her ventriculoperitoneal shunt surgery until her current presentation. she was lethargic during the physical examination. there was a csf surge at the vp shunt's reservoir site. her belly was bloated, and she had an umbilical hernia and rectal prolapse, most likely as a result of excessive 192 ahtesham khizar, soha zahid intra-abdominal pressure caused by csf ascites. (figure 1; a,b,c). the vp shunt's reservoir was slow. we performed an x-ray shunt series, a computed tomography (ct) brain plain, and an abdominal ultrasound. shunt tubing was found to be totally undamaged on x-ray (figure 2; a&b). ventriculomegaly was discovered on a ct scan. an abdominal ultrasound revealed complicated ascites. after a diagnostic paracentesis, the ascitic fluid was revealed to be normal. csf ascites were confirmed through biochemical analysis. to reduce abdominal distension, therapeutic paracentesis was employed, although recurrent accumulation was common. instead of a ventriculo-atrial shunt, the vp shunt was removed, and she underwent endoscopic third ventriculostomy. following etv, csf ascites gradually disappeared over a two-week period. discussion following the implantation of vp shunts for the treatment of hydrocephalus, a number of abdominal complications have been described. perforation of the gut, gallbladder, vagina, umbilicus, and volvulus, as well as abdominal csf encystation and csf ascites, have all been documented.[5] infections[12,26], malignancies, particularly choroid plexus papillomas and optico-chiasmatic gliomas[12,20,21,24,31], shuntdisseminated metastasis[39], and foreign body reactivity to the peritoneal catheter have been linked to csf ascites.[23] high protein content of the csf, particularly in optico-chiasmatic gliomas[10,20,31]; increased csf production, as in choroid plexus hyperplasia and papillomas; tumor-secreted vascular permeability factors;[24] and persistent serosal inflammation are among the different causes reported.[26,33] to the best of our knowledge, akdegbite et al. were the first to identify elevated csf proteins as a probable cause of ascites.[10] as little is known about the aetiology of csf ascites[4], various mechanisms have been proposed, including subclinical peritonitis, which obstructs lymphatic drainage[23], elevated csf protein, which causes peritoneal malabsorption[10,24,28], and csf overproduction exceeding absorptive capacity.[38] multiple shunt revisions[2,22], an immunological reaction to vaccination[2], or shunt degradation[26] can all cause peritoneal irritation. chronic illnesses such as tuberculosis[28] and brain tumours (e.g. optic gliomas and craniopharyngiomas)[24] have high csf protein levels. overproduction of the choroid plexus papillomas causes ascites.[30] a diagnosis of csf ascites is strengthened by comparing the biochemistry of csf shunt aspirate and ascitic fluid from paracentesis. csf ascites resolve spontaneously when csf flow is redirected using a ventriculo-atrial shunt or etv.[38] a previous shunt is linked to a higher rate of etv failure.[47] in our situation, etv was used, and symptoms were resolved within two weeks. a detailed literature review of 77 reported cases of csf ascites until march 2022 is given in table 1. congenital hydrocephalus, obstructive hydrocephalus, choroid plexus papilloma, craniopharyngioma, and posterior fossa tumour were all common etiological causes. revision of the vp shunt to a ventricular-atrial shunt is the treatment of choice for csf ascites, although revision in choroid plexus papilloma will only relieve ascites with the risk of congestive heart failure and bacteremia. the definitive cure is surgical excision of the papilloma.[44] ascites developed and csf protein levels increased in a craniopharyngioma instance that underwent vp shunt insertion due to hydrocephalus. csf protein levels were reduced and ascites was alleviated after the recurring tumour was removed.[10] one patient with ascites and elevated protein levels was treated with a fluid-restricted diet by yount et al.[12] according to the literature, the most common treatment overall for csf ascites is abdominal paracentesis and conversion to a ventriculo-atrial shunt. the time between vp shunt surgery and the onset of ascites might range from 1 day to 12 years.[23,38] it appeared in our patient 2.9 years after the vp shunt. in vp shunting, the peritoneal lining is particularly effective for quick absorption from the peritoneal cavity because it is made up of specialized mesothelial cells that promote rapid lymphatic drainage from the peritoneal cavity into the adjacent lymphatic lacunae.[39] in dehydrated children, the peritoneum can absorb up to 500 ml of normal saline per 24 hours, and following the osmotic absorption phase, the average fluid absorption rate is 33 ml/h.[51] csf ascites is defined as an excessive buildup of csf in the peritoneal cavity due to the peritoneum's failure to absorb the csf.[23] according to literature study, this state of disequilibrium could be caused by primary peritoneal failure, increased csf volume, increased csf protein, infections (peritonitis), eosinophilic catheter rejection, immunological response to immunisation, or in 193 delayed cerebrospinal fluid ascites following ventriculoperitoneal shunt certain cases, no clear cause. csf ascites has been linked to tumours such optic gliomas and craniopharyngiomas, possibly due to elevated csf proteins.[12, 23, 41] in addition to the probable unique proteins produced by optic gliomas, a disruption in the blood-brain barrier could allow tumour proteins to escape into the subarachnoid csf, resulting in elevated protein levels and impaired csf absorption through the arachnoid villi.[23] patients with csf ascites have an insidious onset, gradual abdominal distention, and no pain. hepatic, renal, or cardiac dysfunction are not present. the duration between the shunt being placed and the onset of symptoms might range from days to years. to rule out other probable causes of ascites, a thorough study is required. in patients with a history of vp shunt surgery the likelihood of csf ascites must be kept in mind, which can be validated by an ascitic fluid β2 transferrin assay. after making the diagnosis of csf ascites, the treatment includes redirection of csf flow, preferably ventriculo-atrial shunt but endoscopic third ventriculostomy is a viable approach in certain circumstances. conclusions patients with csf ascites have an insidious onset, progressive and painless abdominal distention. the time between the shunt insertion and the onset of symptoms might range from days to years. an extensive workup is required to rule out other probable causes of ascites. after ensuring that there is no infection, the vp shunt linked csf ascites is treated by converting the shunt to a ventriculoatrial shunt. csf ascites can be treated effectively by abdominal paracentesis and conversion of the vp shunt to a ventriculo-atrial shunt, but endoscopic third ventriculostomy is a viable approach in some selected cases. list of abbreviations: csf: cerebrospinal fluid vp: ventriculoperitoneal etv: endoscopic third ventriculostomy ct: computed tomography acknowledgements: not applicable. funding: no funding was required for this work. conflict of interest: the authors have no conflicts of interest. references 1. ames rh. ventriculo-peritoneal shunts in the management of hydrocephalus. j neurosurg. 1967;27(6):525-529. doi:10.3171/jns.1967.27.6.0525 2. dean df, keller ib. cerebrospinal fluid ascites: a complication of a ventriculoperitoneal shunt. journal of neurology, neurosurgery & psychiatry. 1972 aug 1;35(4):474-6. 3. rosenthal jd, golden gt, shaw ca, jane ja. intractable ascites: a complication of ventriculoperitoneal shunting with a silastic catheter. the american journal of surgery. 1974 may 1;127(5):613-4. 4. weidmann mj. ascites from a ventriculoperitoneal shunt: case report. journal of neurosurgery. 1975 aug 1;43(2):233-5. 5. parry sw, schuhmacher jf, llewellyn rc. abdominal pseudocysts and ascites formation after ventriculoperitoneal shunt procedures: report of four cases. journal of neurosurgery. 1975 oct 1;43(4):476-80. 6. cummings j, sonntag kh, scott rm. ascites complicating ventriculo-peritoneal shunting in an adult. surg neurol. 1976;6(2):135-136. 7. lees rf, harrison rb, shaffer jr ha, hamby lp. cerebrospinal fluid ascites. journal of the canadian association of radiologists. 1978 jun;29(2):132-3. 8. noh jm, reddy mg, brodner ra. cerebrospinal fluid ascites following ventriculoperitoneal shunt. report of a case and review of the literature. mt sinai j med. 1979;46(5):475-477. 9. ohaegbulam sc. cerebrospinal fluid ascites complicating a ventriculoperitoneal shunt. international surgery. 1980 sep 1;65(5):455-7. 10. adegbite ab, khan m. role of protein content in csf ascites following ventriculoperitoneal shunting: case report. journal of neurosurgery. 1982 sep 1;57(3):423-5. 11. agha fp, amendola ma, shirazi kk, amendola be, chandler wf. unusual abdominal complications of ventriculo-peritoneal shunts. radiology. 1983 feb;146(2):323-6. 12. yount ra, glazier mc, mealey j, kalsbeck je. cerebrospinal fluid ascites complicating ventriculoperitoneal shunting: report of four cases. journal of neurosurgery. 1984 jul 1;61(1):180-3. 13. jm gt, jm cc. ventriculo-peritoneal shunt, hypovolemic shock and cerebrospinal fluid ascites. anales espanoles de pediatria. 1984 aug 1;21(2):147-52. 14. rush ds, walsh jw, belin rp, pulito ar. ventricular sepsis and abdominally related complications in children with cerebrospinal fluid shunts. surgery. 1985 apr 1;97(4):4207. 15. madruga acerete d, vascónez muñoz f, práxedes alonso m, cincuendez morcuendez r, salazar rojas f, taracena del piñar b. ascitis por líquido cefalorraquídeo como 194 ahtesham khizar, soha zahid complicación en derivación ventriculoperitoneal: aportación de un caso y revisión de la literatura [ascites of the cerebrospinal fluid as a complication of a ventriculoperitoneal shunt: report of a case and a review of the literature]. an esp pediatr. 1988;28(6):565-568. 16. goodman gm, gourley gr. ascites complicating ventriculoperitoneal shunts. journal of pediatric gastroenterology and nutrition. 1988 sep 1;7(5):780-2. 17. niikawa s, hara a, nokura h, uno t, ohkuma a, yamada h. central nervous cryptococcosis giving rise to ascites after ventriculo-peritoneal shunting--a case report. no shinkei geka. neurological surgery. 1988 jun 1;16(7):8815. 18. pérez peña f, aparicio campillo g, lópez asenjo ja, et al. ascitis por acúmulo de líquido cefalorraquídeo [ascites due to cerebrospinal fluid accumulation]. rev clin esp. 1990;187(3):128-130. 19. suarez a, riestra s, navascues ca, sotorrio ng, rodríguez m, alonso jl, pérez r, rodrigo l. a ventriculoperitoneal shunt as a rare cause of ascites. revista espanola de enfermedades digestivas: organo oficial de la sociedad espanola de patologia digestiva. 1993 apr 1;83(4):285-7. 20. west a, berger ms, geyer r. childhood optic pathway tumors associated with ascites following ventriculoperitoneal shunt placement. pediatric neurosurgery. 1994;21(4):254-9. 21. shuper a, horev g, michovitz s, korenreich l, zaizov r, cohen ij. optic chiasm glioma, electrolyte abnormalities, nonobstructive hydrocephalus and ascites. medical and pediatric oncology: the official journal of siop— international society of pediatric oncology (societé internationale d'oncologie pédiatrique. 1997 jul;29(1):335. 22. yukinaka m, nomura m, mitani t, kondo y, tabata t, nakaya y, ito s. cerebrospinal ascites developed 3 years after ventriculoperitoneal shunting in a hydrocephalic patient. internal medicine. 1998;37(7):63841. 23. chidambaram b, balasubramaniam v. csf ascites: a rare complication of ventriculoperitoneal shunt surgery. neurol india. 2000;48(4):378-380. 24. gil z, beni-adani l, siomin v, nagar h, dvir r, constantini s. ascites following ventriculoperitoneal shunting in children with chiasmatic-hypothalamic glioma. child's nervous system. 2001 jun;17(7):395-8. 25. lee bh, kang sd, kim jm. csf ascites complicating ventriculoperitoneal shunting-a case report. journal of korean neurosurgical society. 2001;30(11):1345-7. 26. longstreth gf, buckwalter nr. sterile cerebrospinal fluid ascites and chronic peritonitis. n engl j med. 2001;345(4):297-298. doi:10.1056/nejm200107263450417 27. lee gy, daniel rt, jones nr. ventriculoperitoneal shunt failure as a secondary complication of ovarian hyperstimulation syndrome. case report. j neurosurg. 2002;97(4):992-994. doi:10.3171/jns.2002.97.4.0992 28. yaqoob n, abbasi sm, hussain l. cerebrospinal fluid ascites. journal of the college of physicians and surgeons--pakistan: jcpsp. 2003 may 1;13(5):289-90. 29. kumar r, sahay s, gaur b, singh v. ascites in ventriculoperitoneal shunt. the indian journal of pediatrics. 2003 nov;70(11):859-64. 30. pawar sj, sharma rr, mahapatra ak, lad sd, musa mm. choroid plexus papilloma of the posterior third ventricle during infancy & childhood: report of two cases with management morbidities. neurology india. 2003 jul 1;51(3):379. 31. olavarria g, reitman aj, goldman s, tomita t. post-shunt ascites in infants with optic chiasmal hypothalamic astrocytoma: role of ventricular gallbladder shunt. child's nervous system. 2005 may;21(5):382-4. 32. diluna ml, johnson mh, bi wl, chiang vl, duncan cc. sterile ascites from a ventriculoperitoneal shunt: a case report and review of the literature. child's nervous system. 2006 sep;22(9):1187-93. 33. kariyattil r, steinbok p, singhal a, cochrane dd. ascites and abdominal pseudocysts following ventriculoperitoneal shunt surgery: variations of the same theme. journal of neurosurgery: pediatrics. 2007 may 1;106(5):350-3. 34. paik i, kotler d, ganjhu l. cerebrospinal fluid ascites as a rare complication of ventriculo-peritoneal shunt: a case report: 714. official journal of the american college of gastroenterology| acg. 2010 oct 1;105:s258. 35. das s, bhansali a, upreti v, dutta p, gupta sk, ananthraman r, walia r. a child with suprasellar mass and ascites. case reports. 2010 jan 1;2010:bcr0620092030. 36. montano n, sturiale c, paternoster g, lauretti l, fernandez e, pallini r. massive ascites as unique sign of shunt infection by propionibacterium acnes. british journal of neurosurgery. 2010 apr 1;24(2):221-3. 37. houtman-van duinen wj, ende-verhaar ym, de ruiter gc, van der torren-conze am. cerebrospinal fluid ascites from a ventriculoperitoneal shunt. nederlands tijdschrift voor geneeskunde. 2011 jan 1;155(50):a4035-. 38. mwang’ombe nj, thiong’o gm, boore jk. cerebrospinal fluid ascites. a case report and literature review. african journal of neurological sciences. 2012;31(1):55-7. 39. low yy, thomas j, wan wk, ng wh. brain metastases as a cause of malignant cerebrospinal fluid ascites: case report and review of the literature. cns oncol. 2012;1(1):29-37. doi:10.2217/cns.12.2 40. comba a, gülenç n, çaltepe g, dagçinar a, yüce ö, kalayci ag, ulus a. ascites and abdominal pseudocyst: two uncommon ventriculoperitoneal shunt complications in two cases. the turkish journal of pediatrics. 2013 nov 1;55(6):655. 41. woodfield j, magdum s. failure of peritoneal and gallbladder shunts in a child with craniopharyngioma. journal of pediatric neurosciences. 2013 sep;8(3):221. 195 delayed cerebrospinal fluid ascites following ventriculoperitoneal shunt 42. jamal h, abrams g. a corny cause of cerebrospinal fluid ascites: a case report and review of literature. sage open medical case reports. 2016 jul 26;4:2050313x16661961. 43. siddiqi m, kesavan a, siddiqi m. cerebrospinal fluid ascites as a late complication of ventriculoperitoneal shunt placement. consultant. 2017;57(11):677-8. 44. sachan d. choroid plexus papilloma causing csf shunt ascites: a rare presentation. ann clin case rep. 2017; 2. 2017;1376. 45. han h, critelli k, davis aw, squires je, fox md. case 6: ascites in a 20-year-old man with dandy-walker syndrome, hydrocephalus, and ventriculoperitoneal shunt. pediatr rev. 2017;38(10):494-495. doi:10.1542/pir.2016-0140 46. musa g, gots a, lungu mc, mutumwa m. cerebrospinal fluid ascites: a patient case report and literature review. medical journal of zambia. 2018;45(4):230-3. 47. khan aa, gondal ss, sharif mm, yousaf m, akhtar n. outcome of endoscopic third ventriculostomy. journal of rawalpindi medical college. 2018 mar 30;22(1):4-7. 48. li dk, platt jm, shay je, yarze jc. sterile cerebrospinal fluid ascites presenting as high saag ascites: a case report. bmc gastroenterology. 2019 dec;19(1):1-4. 49. suleiman se, tambovtseva a, mejery e, suleiman z, alaidy z. ventriculoperitoneal shunt-associated ascites: a case report. cureus. 2020 jun 15;12(6). 50. alexiou ga, gavra mm, ydreos j, papadopoulos e, boviatsis ej. ascites with elevated csf protein levels after ventriculoperitoneal shunt surgery in an adult. case report and systematic literature review. clinical neurology and neurosurgery. 2021 jan 27;202:106519-. 51. mathew m, chikani mc, okpara se, uzoanya mu, ezemba n, mezue wc. challenges in the management of cerebrospinal fluid ascites: a case report. child's nervous system. 2022 feb 17:1-3. 52. mehta n, somani v, shah s, siddiqui a, chauhan p. csf ascites post vp shunt after 17 years: csf ascites-a rare occurence. bombay hospital journal. 2022 feb 23;64(1). microsoft word 13florian_rezumate the 1st regional congress of neurosurgery in the danubecarpathian region neurosurgical controversies in the danube-carpathian region the romanian society of neurosurgery in collaboration with the university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, and the society for the study of neuroprotection and neuroplasticity successfully closed the 1st regional congress of neurosurgery in the danube-carpathian region, held at cluj-napoca, romania, between the 24th of may and the 27th of may 2011, congress which gathered for this short period 24 representatives of the countries located in this region, and also 150 participants both at the course and at the congress. the 1st regional congress of neurosurgery in the danube carpathian region neurosurgical controversies in the danube-carpathians region was a congress organized with the aim of identifying the common points in the field of diagnosis, treatment and research, but especially to identify together the weakness, the existing controversies and maybe to find keys for the future collaboration in the field of neurosurgery in the danube-carpathians region. with over a 10 years’ tradition the german-romanian course preceded the congress; the course was organized for the third time consecutively at cluj-napoca in collaboration with prof. dr. jurgen piek from germany. invited speakers form hamburg, heidelberg, rostock, bucharest, iasi and cluj-napoca guaranteed the high scientific level of this event. the congress was opened in the presence of the representatives of cluj county, in the person of prof. dr. florin stamatian, prefect of cluj county, dr. sorin apostu, the mayor of clujnapoca, prof. dr. constantin ciuce, the rector of the university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, prof. dr. a.v. ciurea, honorary president of the romanian society of neurosurgery, prof. dr. dafin fior muresanu, vice-dean of the faculty of medicine, university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, dr. robert offner (germany) and prof. dr. ioan stefan florian vice-dean of the faculty of medicine, university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, president of the romanian society of neurosurgery. distinguished guests from germany, hungary, czech republic, bulgaria, slovakia, austria, republic of moldova, greece, and romania shared their experience with the audience. the discussion and debates on different topics such as controversies in the treatment of gliomas, severe brain injury, intracranial lesion, cerebro-vascular pathology, degenerative spine surgery, neuroreabilitation and decision making were designed to improve the daily neurosurgical practice. the scientific program evidenced different experiences and field of interest in order to create a high level communication platform, providing the opportunity to build a european knowledge. it was a great achievement for all the participants, who witnessed the exchange of experience and expertise of leading neurosurgeon over this great field. along with the various social programs, the joy of discovering cluj-napoca, one of the most beautiful cities of romania, enriched the experience of this congress. we hope this congress to become a source of education, scientific exchange, innovation and collaboration among countries in the danube-carpathian region. considering in this respect the neurosurgical controversies in the danube carpathians region a commencement, and also the beginning of a fruitful, long-term collaboration in this region, we warmly welcome you all at the second regional congress of neurosurgery in the danube-carpathian region at cluj-napoca in 2012. prof. dr. ioan stefan florian president of the romanian society of neurosurgery microsoft word 9.gaivassergiu_multiple_f.docx 450 sergiu gaivas et al multiple intracranial aneurysms multiple intracranial aneurysms: incidence and outcome in a series of 357 patients sergiu gaivas1, daniel rotariu1, bogdan iliescu2, faiyad ziyad2, cosmin apetrei2, ion poeată3 1phd student “gr.t. popa” university of medicine and pharmacy iasi 23rd department of neurosurgery “prof. dr. n. oblu” clinical emergency hospital, iasi 3“gr.t. popa” university of medicine and pharmacy iasi abstract patients with multiple intracranial aneurysms carry an additional risk of poor outcome due to presence of other aneurysms and the complexity of treatment. patient’s age is crucial in decision making because of its major effect on outcome and mortality. objectives: the purpose of this study was to assess incidence and outcome in multiple aneurysmal sah in a series of 357 consecutive patients. material and method: we retrospectively analyzed a series of 366 patients with ruptured aneurysms treated between jan 2006 and dec 2009 in our department. we study the incidence, localization, surgical outcome and treatment method for individualized patients. we analyzed shortterm outcome of multiple aneurysm in comparison to the single in accordance to glasgow outcome scale at discharge. data of all patients with aneurysmal sah treated between 2006 an 2009 in our department were collected from their chart; operative notes and used to evaluate the incidence and outcome for three patient’s age category. results: for both single and multiple aneurysms the incidence was significantly higher in women than in men. outcome differ statistically between patients with multiple and single aneurysms in age groups 40-69 and 70-89 years. conclusions: the incidence of multiple intracranial aneurysms is higher in women than in men, the site of rupture are different between the two groups in male the site of rupture is dominated by the anterior communicating artery aneurysms while in women it is represented by the internal carotid artery aneurysms. patients with multiple intracranial aneurysms had a higher mortality than patients harboring single intracranial aneurysms. keywords: aneurysm, multiple aneurysms, subarachnoid hemorrhage introduction the prognosis for aneurysmal sah has remained unaffected despite improvement in neurosurgical treatment and 10% to 20% of patients will remain severely disabled, and only approximately 40% will recover to an independent state after sah (3, 16, 17, 20). romanian neurosurgery (2011) xviii 4: 450 455 451 intracranial multiple aneurysms are found in 15 to 35% patients with sah (5, 13). patients harboring multiple intracranial aneurysms are at higher risk of poor outcome because of the complex treatment management and complications from hemorrhage. region moldova, located in the east part of romania, has a population of ≈ 4, 7 million in an area of 45000 km², that is served by 6 neurosurgical centers. with only few exceptions, patients with sah are committed to our institution for investigation and treatment. the purpose of this study was to review our patients’ population to determine the incidence of multiple aneurysms and to find the prognosis of patient with multiple aneurysms among sah patients treated in our department between 2006 and 2009. subjects and methods our series comprised 366 patients with sah secondary to aneurysm rupture admitted at “prof. dr. n. oblu” clinical emergency hospital, in iasi between 2006 and 2009. our center serves as a care center for patients with sah in moldova region. the patients neurological status on admission was graded according to hunt and hess scale. in order to assess neurological outcome at discharge we used the glasgow outcome scale. on admission all patients was investigated with ct scan, as first imagistic tool. the presence of sah on ct was confirmed in all patients and was graded according to fisher scale. of 366 patients, 47 (12.5%) had grade 1 sah, 82 (27.2%) grade 2, 108 patients (28.7%) grade 3 and 111 patients (29.5%) grade 4. in our institution as a second imagistic tool we use angio-ct with reconstruction of vascular architecture to identify the source of sah. of 376 patients, 292 (77.6%) patients was investigated using only angio-ct, and 59 (15.7%) was investigated supplementary with angiography because of poor quality images on angio-ct or unidentifiable source of sah. 24 patients (6.4%) were investigated with angiography from the beginning because of suspicion on ct of sah from aneurysms rupture in posterior circulation or aneurysm location in contact with bone structures (12). a number of 33 (8, 77%) patients wasn’t explored with angio-ct or angiography because of poor condition on admission or because of necessity of emergency operation, due to presence on ct scan of intracerebral hematomas. multiple aneurysms were identified in 64 (17.02%) patients of whom 52 (81.2%) had 2 aneurysms, 9 (14.1%) had 3 (4.7%) aneurysms and 3 patients had 4 aneurysms. overall incidence of multiple aneurysms in women was 19.38% and in men was 14.2%. direct surgical treatment was conducted in 223 of the 312 patients (71, 47%) with single aneurysms and in 54 of 64 patients (84.36%) with multiple aneurysms. in patients with multiple aneurysms the site of rupture was determined by the size and shape of the aneurysms on the angiogram and by the thickness of the sah on the ct scan. the outcome of patients with multiple aneurysms was compared with the outcome of patients with single aneurysm. for this comparison the patients were classified according to three age categories: 20-39, 4069 and 70-89. (table 1) 452 sergiu gaivas et al multiple intracranial aneurysms table 1 number of patients with sah secondary to aneurysm rupture: age and sex distribution age category, years no. of patients with ruptured aneurysms frequency of multiple aneurysms, % men women men women 20-39 22 17 5,12 7,69 40-69 106 171 5,05 12,99 70-89 13 36 7,14 9,52 results from patients with sah and multiple aneurysms, 52 patients were operated with a total number of 67 surgically secured aneurysms at the first surgical intervention. the percent of patients with single ruptured aneurysms and with low-grade sah (h&h 1,2) was 28.8%, grade 3 sah was found in 48.3% of patients and highgrade sah ( h&h 4,5) in 22.8% of patients. in comparison, lowgrade sah in patients with multiple aneurysms was found in 25%, fischer grade 3 sah in 53.1% and high-grade sah in 21.8%. for patients in age category 20-39 the incidence of multiple aneurysms was 12.8% which increase to 17.9% in age category 40-69 and to 18% in age category 70-89. between patients with multiple aneurysms, in age category 20-39, 60 % were women, in age category 40-69, 68% were women but decrease to 55.5% women in 70-89 age group. in our series the incidence of ruptured aneurysms in accordance with age groups and grade of sah did not differ statistically. (table 2) table 2 incidence of ruptured aneurysms in different age groups and sah grade grad e of sah age distribution of patients with single ruptured aneurysms age distribution of patients with multiple ruptured aneurysms 20-39 40-69 70-89 20-39 40-69 70-89 1,2 14 (4,6 %) 65 (21,4 %) 7 (2,3 %) 1 (1,6 %) 14 (21,9 %) 2 (3,1 %) 3 12 (3,9 %) 111 (36,5 %) 19 (6,25 %) 4 (6,25 %) 26 (40,6 %) 4 (6,25 %) 4-5 8 (2,6 %) 51 (16,7 %) 9 (2,9 %) 0 11 (17,2 %) 1 (1,6 %) the most common site of aneurysms location in male patients with single aneurysms was represented by the anterior communicating artery (61.2%) while in women it was represented by the internal carotid artery (34.4%). in female patients with multiple aneurysms the most common site of aneurysms which ruptured was the ica 17 (38.6%) with net preponderance of posterior communicating artery aneurysms (14), but in male patients the most frequent site of ruptured aneurysms was the anterior communicating artery 10 (50%). figure 1 the site of ruptured aneurysm was confirmed during the surgery in all surgical treated patients. in patients treated conservatively the site of rupture was found by evaluation of distribution of the sah on ct scan (19). the overall mortality in our series was 14.1% (52 patients), 37 (10%) patients remained severely disabled after sah and 58.5% good and excellent outcome on discharge. 17 out of 52 died patients wasn’t operated because of very poor condition on admission, 23 patients had underwent romanian neurosurgery (2011) xviii 4: 450 455 453 aneurysms clipping and 8 patients was operated for intracerebral hematomas. among 52 patients who died, 11 patients had multiple aneurysms. the mortality rate between patients with multiple aneurysms was 17.2% but in patients with single aneurysms the mortality rate was 13.5%. in the age group 20-39, 3 (7.7%) patients had unfavorable outcome (gos 1) and died, and 31 patients (76.9%) had good outcome (gos 4 to 5). in 40-69 age category, 13.3% patients had gos grade 1, and 69.4% had good outcome. among patients in 70-89 age groups poor outcome was significantly higher (31.6%) and good outcome was achieved in 36.8%. (figure 2) in patients with multiple aneurysms favorable outcome wasn’t significantly different from that of patients with single aneurysms in 20-39 category age but in the category 40-69 the difference between outcome of multiple and single aneurysms started to increase, with a less number of patients with favorable outcome in patients with multiple aneurysms. (figure 2) figure 1 the most frequent sites of rupture in men and women with multiple aneurysms figure 2 number of ruptured aneurysms in each age category and outcome at discharge. 0 2 4 6 8 10 12 14 16 18 mca acoa ica post circ site of rupture n o. o f a ne ur ys m s women men 3 37 12 5 48 12 31 193 26 0 20 40 60 80 100 120 140 160 180 200 gos 1 gos 2-3 gos 4-5 age groups outcome 20-39 40-69 70-89 454 sergiu gaivas et al multiple intracranial aneurysms figure 3 frequencies of favorable outcome by age category. the presence, on admission of intracerebral hematomas in patients with multiple aneurysms was associated with poor outcome. twelve of 25 patients (48%) with intracerebral hematomas had unfavorable outcome (gos 1 and 2) in comparison with only 5 of the 35 (14.3%) patients with ich had favorable outcome. discussions the frequency of multiple aneurysms varies considerably, ranging from 5 to 33.3 %. kaminogo et al. reported an overall frequency of multiple aneurysms of 20% in women and 12.4% in men in a series of 2425 patients with sah (5). nehls et al found 33.5% incidence of multiple aneurysms in a series of 206 patients. (2) ellamuschi et al reported a total number of 108 (27.5%) patients with multiple aneurysms from a total number of 392 patients with aneurysm included in their study. (4) in our report the overall incidence of multiple aneurysms was 17.4%. the incidence of multiple aneurysms in women was 19.38% and 14.2% in male patients. comparing with incidences reported in other studies our reported incidence of multiple aneurysms is lower than data from the literature (10, 11). we think that this is due to a small number of patients explored with 3or 4-vessel angiography (9, 14). the incidence of multiple aneurysms increases with age in all categories. as reported in previous studies, our study also showed that in every age category the frequency of multiple aneurysms was higher in women than in men (8, 22). the most common site of aneurysm rupture in male was represented by the acoa aneurysms, both for patients with single and multiple aneurysms (15). in women patients the most frequent site of aneurysm rupture was the ica (6). czepko et al. reported that 64 (75.3%) out of 85 patients with multiple aneurysm presented very good and good condition on discharge, 5.9% were severe disabled, and 16 (18, 8%) died. (1) lynch et al. reported on a series of 337 patients with aneurysms and found the 0 10 20 30 40 50 60 70 80 90 20-39 40-69 70-89 age category fa vo ra bl e ou tc om e % multiple single romanian neurosurgery (2011) xviii 4: 450 455 455 overall mortality of 6.9% and successful results were obtained in 88.8% patients. (7) yasargil found excellent and good results in 94.7% of his series of 1012 aneurysms patients operated. (21) in our series the overall mortality was lower between patients with single aneurysm (13.5 %.) than in patients with multiple aneurysms (17.2%). surgical mortality in our patients was 11.7% conclusion the incidence of multiple aneurysms in our series was higher in women, in all age categories. in cases with multiple aneurysms the most common localization of ruptured aneurysms was the ica in women and acoa in male patients. the mortality rate in our series was lower in patients with single aneurysms comparing with that of patients with multiple aneurysms. references 1. czepko r, rybak m, potoczny p, kwinta b, ossowski p. surgical strategy and outcome in multiple cerebral aneurysms. przegl lek.;61(5):477-81, 2004 2. daniel g. nehls, richard a. flom, l. philip carter,and robert f.spetzler. multiple intracranial aneurysms: determining the site of rupture. j neurosurg.; 63:342-348, 1985 3. dănăilă l., ştefănescu f., anevrismele cerebrale. editura academiei române, 2007 4. ellamushi he, grieve jp, jager hr, kitchen nd.risk factors for the formation of multiple intracranial aneurysms. j neurosurg; 94: 728 –732, 2001 5. makio kaminogo, masahiro yonekura, shobu shibata. incidence and outcome of multiple intracranial aneurysms in a defined population. stroke;34;16-21,2003 6. kongable gl, lanzino g, germanson tp, truskowski ll, alves wm, torner jc, kassell nf. gender-related differences in aneurismal subarachnoid hemorrhage. j neurosurg ;84:43– 48, 1996 7. josé carlos lynch, ricardo andrade, celestino pereira, milton souza neto, roque dominguez. outcome of 337 intracranial aneurysms patients operated in a public hospital. arq neuropsiquiatr ;56(3b):528-532, 1998 8. lanzino g, kassell nf, germanson tp, kongable gl, truskowski ll, torner jc, jane ja. age and outcome after aneurysmal subarachnoid hemorrhage: why do older patients fare worse? j neurosurg ;85:410 – 418, 1996 9. mizoi k, suzuki j, yoshimoto t. surgical treatment of multiple aneurysms: review of experience with 372 cases. acta neurochir (wien);96:8 –14, 1989 10. østergaard jr, høg e. incidence of multiple intracranial aneurysms: influence of arterial hypertension and gender. j neurosurg.;63: 49–55, 1985 11. qureshi ai, suarez ji, parekh dp: risk factors for multiple intracranial aneurysms. neurosurgery 43:22– 27, 1998 12. rice bj, peerless sj, drake cg. surgical treatment of unruptured aneurysms of the posterior circulation. j neurosurg;73:165-173, 1990 13. rinne j, hernesniemi j, niskanen m, et al: management outcome for multiple intracranial aneurysms. neurosurgery 36: 31–38, 1995 14. rinne j, hernesniemi j, puranen m, saari t. multiple intracranial aneurysms in a defined population: prospective angiographic and clinical study. neurosurgery;35: 803– 808, 1994 15. rosørn j, eskesen v, schmidt k. clinical features and outcome in females and males with ruptured intracranial saccular aneurysms. br j neurosurg ;7:287– 290, 1993 16. sacco rl, wolf pa, bharucha ne, meeks sl, kannel wb, charette lj, mcnamara pm, palmer ep, d’agostino r. subarachnoid and intracerebral hemorrhage: natural history, prognosis, and precursive factors in the framingham study. neurology;34: 847– 854, 1984 17. saveland h, sonesson b, ljundggren b, brandt l, uski t, zygmunt s. outcome evaluation following subarachnoid hemorrhage. j neurosurg.;64:191–196, 1986 18. vajda j: multiple intracranial aneurysms: a high risk condition. acta neurochir 118:59–75, 1992 19. weir b. unruptured intracranial aneurysms: a review. j neurosurg.;96:3-42, 2002. 20. wiebers do, whisnant jp, huston j iii, et al, international study of unruptured intracranial aneurysms investigators. unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. lancet; 362: 103-110, 2003 21. yasargil mg. microneurosurgery; vol 11. stuttgart: georg thieme verlag: 331-339, 1984 22. yoshimoto y, kwak s. age-related multifactorial causes of neurological deterioration after early surgery for aneurysmal subarachnoid hemorrhage. j neurosurg.; 83: 984 –988, 1995 microsoft word 16enes_zoophilic_f romanian neurosurgery (2011) xviii 3: 349 – 355 349 zoophilic behavior in a patient with posterior cerebral arterial aneurysm s. ene1, a. săsăran2 1consultation-liaison psychiatry department, emergency clinical hospital bagdasar-arseni, bucharest 2neurosurgery department iv, bagdasar-arseni hospital, bucharest abstract this paper presents a clinical comorbidity between a cerebral arterial aneurysm and a zoophilic behavior. this association has not been previously described before in the literature cited by pubmed. a 42-years old patient, without previous medical history, presented at the hospital with quite sudden onset of zoophilic behavior, disorientation and altered consciousness, was investigated and diagnosed with an aneurysm in the posterior cerebral artery. the case is unique due to the uncommon psychiatric presentation (zoophilic behavior), and its organic substrate: the presence of posterior cerebral arterial aneurysm with interpeduncular location. keywords: cerebral aneurysm, zoophilic behavior, comorbidities. introduction cerebral aneurysms are pathologic focal dilatations of the cerebrovasculature that are prone to rupture. 90% of all cerebral aneurysms and are located at the major branch points of large arteries. cerebral aneurysms frequently break into the subarachnoid space, accounting for 70-80% of spontaneous subarachnoid hemorrhages (28). aneurysmal rupture also may result in intraparenchymal, intraventricular, or subdural hemorrhage. giant saccular aneurysms, defined as greater than 25 mm in diameter, represent 3-5% of all intracranial aneurysms. although giant aneurysms may cause sah, these lesions frequently produce mass effects and result in distal thromboembolism (1). symptoms associated with cerebral aneurysms producing sah are related to the location of the aneurysm, most frequent: headache, altered consciousness, seizures, meningeal irritation signs, autonomic disturbances (fever, nausea or vomiting, sweating, chills, and cardiac arrhythmias), focal neurological complaints (weakness, hemisensory loss, language disturbances, neglect, memory loss, or olfactory disturbances), visual symptoms (blurring of vision, diplopia, or visual field defects), respiratory dysfunction or cardiovascular instability, hormonal dysfunctions. cerebral aneurysms (either treated or not) account for a wide range of neurological, psychiatric and cognitive disorders: long-term cognitive deficits (31), temporal seizures as memory flashbacks (27), cognitive disturbances and low expectancies regarding the quality of life 350 s. ene, a. săsăran zoophilic behavior in a patient with aneurysm (21), sudden headache, vomiting and blackout of consciousness, neck stiffness (11), delusional disorder (5), dysphasia (26), personality changes (33), amnesic syndrome, disorientation, alterations of verbal fluency and abstraction (36), confabulation (13), neuroendocrine disturbances contributing to disturbed quality of life, depression and sleeping disturbances (24), migraine with aura (10), anxiety, depression and lower functional status (20), deficits in decision-making (28), impairment of memory, executive functions, or attention (7). there is also a reported case where the rupture of the aneurysm and the subsequent sah produced long-term resolution of bipolar ii disorder and panic disorder (12). zoophilia is a disturbance in the sexual behavior, consisting in sexual interest and sexual arousal related to animals(2). zoophilic behavior is, sometimes and in certain environments and cultures, quite a socially acceptable behavior. usually, zoophilia is a pervasive pattern of sexual behavior, with no identyfiable external reason or trigger. there are several medical conditions accounting for zoophilic behavior, such as cerebral tumors located in the frontal lobe or in the lymbic system or hypothalamus. case report a 42 years-old male was admitted in the neurosurgery department for headache, dizziness and psychiatric symptoms (cognitive impairment, memory loss, iritability alternating with somnolence). at the admission the patient was aware (glasgow coma scale score of 15), cooperative, but with temporal and spatial disorientation. neurologic exam revealed a right peripheric facial palsy, with no other motor deficits, no ataxia, no nistagmus, negative romberg sign. he had no signs of meningism, no speech disturbances, normal visual field and sharpness.. the blood preasure was 135/85 mm hg, heart rate was 68/min, regular rithm . the rest of physical examination revealed no other abnormalities. lab results were in normal range, as well as paraclinical investigations (ecg, pulmonar radiography). on the ophthalmologic examination: normal fundus, right eye lagophthalmos, and hypermetropic astigmatism were found. the ear, nose, mouth and throat examination diagnosed, beside the right peripheral facial palsy, deafness of the right ear. neuroimaging studies were performed. on cranio-cerebral computer-tomography was described suprachiasmatic expansive process, 35/21 mm, with calcifications, and intense iodofilia on a peripherical zone of 2 cm raising the suspicion of partial thrombosed aneurysm. further exams (mri and angio mri (figure 1) described a well defined mass, 32/26/21 mm, with heterogeneous signal (degradation products of hemoglobin to hemosiderin stage) and with central enhance contrast, localized interpeduncular (compression on the left peduncle), retroselar, posterior optochiasmatic region, leading to compression on right thalamic and subthalamic region (partial thrombosed aneurysm). four-vessels angiography (figure 2) revealed a normal bilateral carotid system and a sacular aneurysm with maximum diameter 22 mm and at the right p1 segment of the posterior cerebral artery located at about 3 mm from the basilar trunk origin, with the highest axis oriented superiorly; the aneurysm compresses both pca origin (especially the left one). romanian neurosurgery (2011) xviii 3: 349 – 355 351 a b c d e figure 1 mri examination described an partial trombosed aneurysm: well defined mass of 32/26/21 mm, with heterogeneous signal and with central enhance contrast (figure a and b – axial t1 section). the location is interpeduncular retroselar posterior to optochiasmatic region, and compress the left peduncle, leading to compression on right thalamic and subthalamic region (as shown in figure c, d on midline sagittal sections and e on pons coronal section) 352 s. ene, a. săsăran zoophilic behavior in a patient with aneurysm a b c figure 2 four-vessel angiography: the sacular aneurysm with maximum diameter 22 mm at the right p1 segment of the posterior cerebral artery located, at aproximativelly 3 mm from the basilar trunk origin, with the highest axis oriented superiorly; the aneurysm compresses both pca origin especially left (figures a and b). also the 3d reconstruction (figure c) was available. on psychiatric exam: the patient had temporal and spatial disorientation, with marked slowed ideative rythm, marked memory deficits for late and recent events, answers with long latencies, mostly irrelevant, inadequate behavior. the history of the actual episod provided by the family show the actual syptoms (disorientation, confusion, iritability) started suddenly several days ago, with increasing intensity thereafter. an extremely important aspect was the change in patient’s sexual behavior, as he started to behave with zoophilic tendencies. therefore, the patient’s wife said the first intriguing sign in patient’s behavior (that appeared few weeks ago) was the sexual interest towards the hens in his own yard, as she found him several times in explicit postures. at those moments the patients was not able to coherently explain what he was doing. the family members did nothing but to closely watch the patient and they brought him to the hospital only when his behavior became grossly disorganized. considering the major risks of surgical intervention, based on the deep location of the aneurysm, a conservative approach was decided, and the the patient was referred to a neurologic department. diagnosis at discharge (according to icd-10): 1. giant partial thrombosed unruptured aneurysm of right posterior cerebral artery. 2. right peripheral facial palsy. romanian neurosurgery (2011) xviii 3: 349 – 355 353 3. other sexual preferences. the patient died several weeks after due to the rupture of the aneurysm. discussion data from english-literature available on pub-med do not present any case of a patient with neurosurgical condition in comorbidity, namely the aneurysm, with a paraphilic behavior. the presented case represents, according to the authors knowledge, the only case reported until now presenting a cerebral aneurysm as the cause of a zoophilic behavior. even more, the psychiatric nosographies (icd-10, dsm-iv-tr) do not include a valid code for a paraphilic disorder due to a general medical condition. this disorder will probably receive more attention in the dsm-v (16,25) this cause-effect association is due to the aneurysm’s location in a region which accounts for the instinctive life (compression on sub-thalamic region and on lymbic system). the rapid development of the symptoms, in several weeks from the onset of the inadequate behavior, might indicate an aneurysm’s growing in dimensions, with increasing compression on these cerebral structures. should the patient’s family have brought him earlier at the hospital, the neurosurgical condition would have been totally different. delaying presentation at the hospital presumably resulted in an enlargement of the aneurysm and in cerebral compression to the point when the operatory risk became inacceptabile. nonetheless, the patient died several weeks after the discharge, the cause of death being the aneurysm’s rupture. several case reports described various clinical symptoms in patients with interpeduncular aneurysms. choreic movements represented the clinical presentation of an giant unruptured aneurysm impinging upon the left thalamus, putamen, globus pallidus, cerebral peduncle, midbrain, and subthalamic nucleus (4). other movement disorders like hemibalism (34)(30) or paroxysmal dyskinesia (14) were associated with subthalamic lesions. interpeduncular basilar aneurysm was found as cause of progressive locked-in syndrome (19). depresive symptoms were the clinical equivalent of the aneurysm due to subthalamic lesions (22). zoophylia, as paraphylic behaviour, has different approaches: an ethical/moral and legal approach (15), that led to the need of a clasification and nosological unification as terms of zoophilism, bestiality, zooerasty and zoorasty have been used (2). several studies, mentioned that the prevalence of zoophylia seems to be overlooked and therefore stress the need of questions exploring this topic that should be included in the psychiatric interview. (3,6). in a study performed in 1991, psychiatric patients were found to have a statistically significant higher prevalence rate (55%) of bestiality than the control groups (10% medical in-patients and 15% psychiatric staff) (3). the only link we could found related to the organic pathway of the lesion in subthalamic area with our case, is another case report on a patient with parkinson disease who developed zoophilia as a possible complication of dopaminergic therapy (17). the 74-year old man started the treatment with controlled-release levodopa and increased dose of bromocriptine for marked disability during the off periods and severe peak-of-dose dyskinesias. he developed hypersexuality 354 s. ene, a. săsăran zoophilic behavior in a patient with aneurysm with zoophilia 5 days after the initiation of treatment. this abnormal behavior ceased 2 days after the doses were reduced. the pedunculopontine nucleus was described as playing a role in the pathophysiology of parkinson's disease (8, 37). there are several case reports were hypersexuality is linked to dopaminergic drug treatment in parkinsonian patients (38) (39) (29, 32) (9, 35). on the other hand, selective serotonine reuptake inhibitors have been used in the treatment of paraphilias (23). as regard to the neurobiology of paraphilia and the known endocrinological, pathophysiological and genetic aspects of this disorders, in an elegant review, jordan et al (18), discussed about the role of changes in hypothalamic-pituitary function, prolactine levels, and dopaminergic or serotonergic functions. as the pedunculopontine nucleus has a role in the pathophysiology of parkinson's disease (8, 37) as mentioned above, we can speculate that lesions in this zone can be linked to zoophilia. conclusion we present a patient with zoophilic behavior as result to an aneurysm of the posterior cerebral artery in the interpeduncular region with compression in subthalamic areas. this peculiar condition was produced probably by organic disrupture of serotoninergicdopaminergic pathways. as zoophilia can occur in relation with several psychiatric and neurological conditions like treated parkinson diseases, investigation of such behavior in the patient’s interview should be useful. references 1. http://www.mayoclinic.com/health/brainaneurysm/ds00582. accessed 10-july-2011. 2. aggrawal a. a new classification of zoophilia. j forensic leg med 18(2):73-78, 2011. 3. alvarez w.a. and freinhar j.p. a prevalence study of bestiality (zoophilia) in psychiatric in-patients, medical in-patients, and psychiatric staff. int j psychosom 38(14):45-47, 1991. 4. barreiro de madariaga l.m., sian j.e., parera i.c. and micheli f. arm chorea secondary to an unruptured giant aneurysm. mov disord 18(11):1397-1399, 2003. 5. begovac b., begovac i. and paladino j. [delusional disorder of the paranoid type and unruptured intracerebral aneurysm--is there an association?]. acta med croatica 62(1):61-64, 2008. 6. bhatia m.s., srivastava s. and sharma s. 1. an uncommon case of zoophilia: a case report. med sci law 45(2):174-175, 2005. 7. bottger s., prosiegel m., steiger h.j. and yassouridis a. neurobehavioural disturbances, rehabilitation outcome, and lesion site in patients after rupture and repair of anterior communicating artery aneurysm. j neurol neurosurg psychiatry 65(1):93-102, 1998. 8. breit s., lessmann l., benazzouz a. and schulz j.b. unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat. eur j neurosci 22(9):22832294, 2005. 9. cannas a., solla p., floris g., tacconi p., loi d., marcia e. and marrosu m.g. hypersexual behaviour, frotteurism and delusional jealousy in a young parkinsonian patient during dopaminergic therapy with pergolide: a rare case of iatrogenic paraphilia. prog neuropsychopharmacol biol psychiatry 30(8):15391541, 2006. 10.de filippis s., salvatori e., bozzao a., fantozzi l.m. and martelletti p. migraine with aura, bipolar depression, acm aneurysm. a case report. j headache pain 6(2):93-96, 2005. 11.demirgil b., gunaldi o., tugcu b., postalci l., colluoglu b., tanriverdi o. and asilturk m. multiple aneurysms of the distal posterior inferior cerebellar artery: two case reports. minim invasive neurosurg 51(5):249-252, 2008. 12.etches s.m., schmidt m., alda m., hajek t. and kahn d.a. resolution of bipolar ii and panic disorders following subarachnoid hemorrhage. j psychiatr pract 15(2):145-149, 2009. 13.fotopoulou a., conway m., griffiths p., birchall d. and tyrer s. self-enhancing confabulation: revisiting the motivational hypothesis. neurocase 13(1):6-15, 2007. 14.garcia-ruiz p.j., villanueva v., gutierrez-delicado e., echeverria a., perez-higueras a. and serratosa j.m. romanian neurosurgery (2011) xviii 3: 349 – 355 355 subthalamic lesion and paroxysmal tonic spasms. mov disord 18(11):1401-1403, 2003. 15.hensley c., tallichet s.e. and dutkiewicz e.l. childhood bestiality: a potential precursor to adult interpersonal violence. j interpers violence 25(3):557567, 2010. 16.hinderliter a.c. defining paraphilia in dsm-5: do not disregard grammar. j sex marital ther 37(1):17-31, 2011. 17.jimenez-jimenez f.j., sayed y., garcia-soldevilla m.a. and barcenilla b. possible zoophilia associated with dopaminergic therapy in parkinson disease. ann pharmacother 36(7-8):1178-1179, 2002. 18.jordan k., fromberger p., stolpman g. and muller j.l. the role of testosterone in sexuality and paraphilia-a neurobiological approach. part ii: testosterone and paraphilia. j sex med, 2011. 19.khan s.i., beaujon w. and ross e.d. interpeduncular basilar aneurysm causing progressive locked-in syndrome: to coil or not to coil. eur neurol 60(3):159-161, 2008. 20.king j.t., jr., kassam a.b., yonas h., horowitz m.b. and roberts m.s. mental health, anxiety, and depression in patients with cerebral aneurysms. j neurosurg 103(4):636-641, 2005. 21.king j.t., jr., tsevat j. and roberts m.s. cognitive impairment and preferences for current health. health qual life outcomes 7:1, 2009. 22.klein j., winter c., coquery n., heinz a., morgenstern r., kupsch a. and juckel g. lesion of the medial prefrontal cortex and the subthalamic nucleus selectively affect depression-like behavior in rats. behav brain res 213(1):73-81, 2010. 23.kraus c., strohm k., hill a., habermann n., berner w. and briken p. [selective serotonine reuptake inhibitors (ssri) in the treatment of paraphilia]. fortschr neurol psychiatr 75(6):351-356, 2007. 24.kreitschmann-andermahr i., poll e., hutter b.o., reineke a., kristes s., gilsbach j.m. and saller b. quality of life and psychiatric sequelae following aneurysmal subarachnoid haemorrhage: does neuroendocrine dysfunction play a role? clin endocrinol (oxf) 66(6):833-837, 2007. 25.krueger r.b. critical appraisals of the proposed dsm-5 paraphilia diagnoses. j am acad psychiatry law 39(2):237, 2011. 26.liechty j.a. and heinzekehr j.b. caring for those without words: a perspective on aphasia. j neurosci nurs 39(5):316-318, 2007. 27.locurto m. and peera m.a. temporal lobe seizures from a posterior cerebral artery aneurysm presenting as memory flashbacks. cjem 11(4):389-392, 2009. 28.mavaddat n., kirkpatrick p.j., rogers r.d. and sahakian b.j. deficits in decision-making in patients with aneurysms of the anterior communicating artery. brain 123 ( pt 10):2109-2117, 2000. 29.nielssen o.b., cook r.j., joffe r., meagher l.j. and silberstein p. paraphilia and other disturbed behavior associated with dopamimetic treatment for parkinson's disease. mov disord 24(7):1091-1092, 2009. 30.nishioka h., taguchi t., nanri k. and ikeda y. transient hemiballism caused by a small lesion of the subthalamic nucleus. j clin neurosci 15(12):14161418, 2008. 31.perea bartolome m.v., ladera fernandez v. and maillo sanchez a. [long-term cognitive deficits in patients operated on for cerebral aneurysm by craniotomy and clipping]. neurologia 24(6):379-385, 2009. 32.pineau f., schupbach m., corvol j.c., flamandrouviere c., vidailhet m. and roze e. long-standing paraphilia induced by dopamine agonists in parkinson's disease. mov disord 25(7):963-965, 2010. 33.preiss m., koblihova j., netuka d., klose j., charvat f. and benes v. ruptured cerebral aneurysm patients treated by clipping or coiling: comparison of long-term neuropsychological and personality outcomes. zentralbl neurochir 68(4):169-175, 2007. 34.renard d., le floch a., castelnovo g., collombier l., kotzki p.o. and labauge p. hemiballism due to an ipsilateral subthalamic nucleus lesion. j neurol 258(3):507-509, 2011. 35.shapiro m.a., chang y.l., munson s.k., okun m.s. and fernandez h.h. hypersexuality and paraphilia induced by selegiline in parkinson's disease: report of 2 cases. parkinsonism relat disord 12(6):392-395, 2006. 36.szakacs r., kalman j., barzo p., sas k. and janka z. [amnesic syndrome following lesion of the fornix or does reversible korsakow's syndrome exist?]. neuropsychopharmacol hung 9(1):39-43, 2007. 37.touchon j.c., moore c., frederickson j. and meshul c.k. lesion of subthalamic or motor thalamic nucleus in 6-hydroxydopamine-treated rats: effects on striatal glutamate and apomorphine-induced contralateral rotations. synapse 51(4):287-298, 2004. 38.van deelen r.a., rommers m.k., eerenberg j.g. and egberts a.c. [hypersexuality during use of levodopa]. ned tijdschr geneeskd 146(44):2095-2098, 2002. 39.vogel h.p. and schiffter r. hypersexuality--a complication of dopaminergic therapy in parkinson's disease. pharmacopsychiatria 16(4):107-110, 1983. microsoft word _3.formatata_poeata.doc romanian neurosurgery vol. xvi nr. 1 14 cerebral cavernoma i. poeata1, st.m. iencean2 1clinical emergency hospital “prof dr nicolae oblu” iasi, university of medicine and pharmacy “gr.t. popa”, iasi, romania 2neurosurgery, clinical emergency hospital “prof dr nicolae oblu” iasi, romania cerebral cavernoma can be located in any brain region, be of varying size and present with different clinical disorders. some cases are found incidentally. conservative treatment is recommended if the patient has an asymptomatic lesion or the malformation is located in a critical brain region but the patient has only minimal symptoms and no history of symptomatic bleeding or the patient has multiple cavernous malformations and the actual symptomatic lesion could not be determined. the main indications for surgery are based on reductions or control of seizures, reversal of symptoms or deficits related to mass effect, and prevention of hemorrhage or recurrent hemorrhage. generally surgical results are very good. keywords: cerebral cavernoma, gamma knife, hemorrhage, surgery introduction cerebral cavernoma or cavernous angiomas are cerebral cavernous malformations and they are relatively rare lesions, comprising 5 to 13% of the central nervous system vascular anomalies. after thrombosed arteriovenous malformations, cavernomas are the second most common histological subgroups of angiographically occult cerebrovascular malformations. with the advent of magnetic resonance imaging (mri) there has been a substantial increase in the number of patients diagnosed with these lesions. pathological studies have demonstrated that multiple lesions may represent more than 25% of the cases. there is no sex prevalence , although a familial form has been confirmed by several investigators. cavernous angiomas can be located in any brain region, be of varying size and present with different clinical disorders. histopathology cerebral cavernoma resembles a honeycomb of irregular blood-filled vascular spaces (caverns). the vascular walls are thin and consist of a single layer of flattened endothelial cells. recent analysis by transmission electron microscopy show that the thin walls of cerebral cavernoma lack significant subendothelial support and contain very few intact tight junctions between the endothelial cells. these findings help explain the recurrence of microhemorrhage in cerebral cavernoma. the vascular spaces of cerebral cavernomas are separated by a collagenous matrix devoid of elastic lamina or smooth muscle. deposits of calcium are often found in cavernomas, especially within vascular walls. the lesion is well demarcated from the surrounding normal tissue by a zone of gliosis. the absence of intervening neural tissue previously was recognized as a criterion for diagnosis and a cardinal feature distinguishing cavernous angioma from telangiectasia. several pathological variations of cerebral cavernomas can be distinguished and mixed lesions containing an arteriovenous component or combined with capillary telangiectases have been reported. most cavernomas show evidence of hemorrhage, microscopic or gross, and many show evidence of cerebral cavernoma romanian neurosurgery vol. xvi nr. 1 15 repeated hemorrhage. small hemorrhages followed by organization, fibrosis and calcification probably account for slow progressive growth of cerebral cavernomas in patients with long clinical histories. clinical presentation patients with a cavernous malformations may present with seizures, hemorrhage or mass lesions. some cases are found incidentally. there might be a correlation between the clinical and radiological manifestation and the histological type, but there are not enough data to support this concept. the propensity of cerebral cavernomas to bleed is well established. most of the hemorrhages consist of intralesional or perilesional “slow ooze” or “cluster of bleeding sites” and result in subacute or stepwise worsening of the neurological signs. these bleeding patterns have been attributed to the low blood pressure found in this type of malformation. there are no factors that predict the degree or rapidity of hemorrhage in individual patients. in many patients multiple microscopic hemorrhages occur, but are often not clinically detected. the data regarding the incidence of bleeding and rebleeding of cavernous malformations have the most clinical relevance because they affect the decision regarding surgery. the incidence of symptomatic hemorrhage of cavernous angiomas in general is low. the most important risk factor for subsequent hemorrhage is the occurrence of a prior hemorrhage. an annual hemorrhage rate of 4.5% was described for the patients whose first clinical presentation was hemorrhage. several authors proposed that female hormones are implicated in the pathogenesis of hemorrhage from an intracranial cavernous angiomas. higher bleeding rates from cavernous malformations was found during pregnancy, particularly in the first trimester, which is characterized by vascular proliferation of the endometrium associated with secretion of human chorionic gonadotropin, progesterone, end estrogens. the size of cavernous malformations is known to increase during pregnancy and to decrease after delivery. the increase in the blood volume occurring during pregnancy might be an important factor in angioma rupture as well. cavernous malformations of the brain stem account for between 18 and 22% of all intracranial cavernous malformations (yasargil). clinical malignancy of brain stem and basal ganglia cavernomas could be related to the high sensitivity of these areas even to a small amount of bleeding. the rebleeding rate after a first hemorrhage in this group was found to be as high as 21% per year per lesion. the natural history of familial cavernous malformations is less benign than that of the sporadic form. the rate of symptomatic hemorrhage was found to be higher in this group 6.5% per patient per year and recently labauge showed a hemorrhage risk of 2.5% per lesion-year in a study of 40 patients familial cavernous malformations. eleven patients (27.5%) developed new lesions during a mean follow-up of 3.2 years. development of de novo lesions in familial form of cerebral cavernous malformations is known and the clinical features have been described. radiographic evaluation size, location, pathological architecture, degree and rapidity of hemorrhage within the lesion presumably determine the neuroradiological appearance and the clinical course. cerebral angiography cerebral angiography is relatively insensitive and is diagnostic in only 10%. delayed imaging during the venous phase and careful subtraction may present the cavernoma as an avascular region in the capillary phase or as an avascular mass with displacement of adjacent vessels. a dense venous pooling pattern and a localized area of capillary staining that persists into the late venous phase have both been described as diagnostic feature of cavernous malformations. computerized tomography computerized tomography studies often detect lesions consistent with cavernous malformations, but i. poeata romanian neurosurgery vol. xvi nr. 1 16 the ct findings are not specific for this entity. the lesion commonly appears hyperdense, or mixed hyperdense and isodense. mass effect is frequently present. faint contrast enhancement has been described. by ct criteria alone it is often difficult to differentiate glioma or infarction from a cavernous angioma. computerized tomography may occasionally miss even relatively large lesions. mri the sensitivity of mri increases the probability of detecting a cavernous malformation. t2 weighted studies are more sensitive than t1 weighted images. mri is also particularly valuable in terms of specificity. on t2 weighted images cavernomas appear as areas of mixed signal intensity with “reticulated” appearance and a prominent surrounding rim of decreased signal intensity, thought to represent hemosiderin. presence of multiple lesions, a reticulated core of increased and decreased signal intensity, a prominent surrounding rim of decreased signal intensity strongly support the diagnosis of cavernous malformation. management management strategy are based on a combination of factors including the natural history, age of the patient, location of the lesion, and risk of operative removal. when dealing with a patient harboring several lesions or a family affected by the hereditary form of this condition, an aggressive approach is not always advisable. conservative treatment conservative treatment is recommended if: the patient has an asymptomatic lesion; the malformation is associated with a medically controlled seizure disorder; the malformation is located in a critical brain region but the patient has only minimal; symptoms and no history of symptomatic bleeding; the patient is elderly or the patient has multiple cavernous malformations and the actual symptomatic lesion could not be determined. surgery the main indications for surgery are based on reductions or control of seizures, reversal of symptoms or deficits related to mass effect, and prevention of hemorrhage or recurrent hemorrhage. generally surgical results are very good. the location of the cavernous malformation is the most significant factor in determining prognoses. worse surgical outcome was associated with lesions located in the thalamus, basal ganglia, pineal region, brain stem, and spinal cord and with subtotal resections. although the definitive risk is not known, it appears that thalamic cavernous angiomas have a significant surgical complication rate and nonoperative approaches have to be seriously considered in stable patients. surgical excision for a symptomatic brain stem cavernous angioma is recommended because of the poor ability of the brain stem to withstand mass expansion from hemorrhage. for those women with known cavernous malformations who are considering having children, surgical intervention may be entertained prior to conception if the cavernous angioma is accessible. for those patients diagnosed during pregnancy conservative management may be appropriate if the mother is neurologically stable. cerebral cavernoma romanian neurosurgery vol. xvi nr. 1 17 fig. 1 axial and sagittal mri scan showing cavernous malformation in the pons fig. 2 right occipital cavernoma radiotherapy the role of conventional radiotherapy and stereotactic radiosurgery for deep cerebral cavernomas is limited because of the possibility of incomplete exclusion and the inherent risk of bleeding during the latency period before definitive vascular obliteration. additionally, the risk of hemorrhage and of radiation induced complications following stereotactic radiosurgery for cavernous malformations are high. although radiosurgery has limited impact on the control of hemorrhage, gamma knife radiosurgical treatment is showing promise for the control of seizures due to cerebral cavernoma. in 49 patients with drugresistant epilepsy, presumably caused by cm, that were treated with gk, 26 patients (53%) were seizurefree and another 10 patients had a significant decrease in seizure frequency at follow-up (regis). the authors recommend that gk surgery be considered in the treatment of refractory epilepsy when the cerebral cavernoma is located in a highly functional area. references 1. brunereau l, levy c, laberge s, houtteville j, labauge p. de novo lesions in familial form of cerebral cavernous malformations: clinical and mr features in 29 non-hispanic families. surg neurol. 2000;53(5):475-82. 2. dammers r, delwel ej, krisht af. cavernous hemangioma of the mesencephalon: tonsillouveal transaqueductal approach. neurosurgery. 2009;64(5 suppl 2):296-9. 3. fritschi ja, reulen hj, spetzler rf, zabramski jm. cavernous malformations of the brain stem. a review of 139 cases. acta neurochir (wien). 1994;130(1-4):35-46. 4. kivelev j, niemelä m, kivisaari r, dashti r, laakso a, hernesniemi j. long-term outcome of patients with multiple cerebral cavernous malformations. neurosurg. 2009; 65(3):450-5. 5. labauge p, brunereau l, lévy c, laberge s, houtteville jp. the natural history of familial cerebral cavernomas: a retrospective mri study of 40 patients. neuroradiology. 2000; 42(5):327-32. 6. li h, ju y, cai bw, chen j, you c, hui xh. experience of microsurgical treatment of brainstem cavernomas: report of 37 cases. neurol india. 2009;57(3):269-73 7. massa-micon b, luparello v, bergui m, pagni ca. de novo cavernoma case report and review of literature. surg neurol. 2000;53(5):484-7. 8. mitchell p, hodgson tj, seaman s et al. stereotactic radiosurgery and the risk of haemorrhage from cavernous malformations.br j neurosurg. 2000;14(2):96-100. 9. régis j, bartolomei f, kida y, kobayashi t et al. radiosurgery for epilepsy associated with cavernous malformation: retrospective study in 49 patients.neurosurg. 2000; 47(5):1091-7. 10. tripathy ln, singh sn. multiple giant cavernous angiomas of the brain. neurol india. 2009;57(3):350-1. 11.tu j, stoodley ma, morgan mk, storer kp, smee r. different responses of cavernous malformations and arteriovenous malformations to radiosurgery. j clin neurosci. 2009;16(7):945-9. microsoft word 2adam_mild romanian neurosurgery (2013) xx 4: 309 317 309 mild traumatic brain injury: epidemiology, management, outcome d. adam1,2, a. enache2, cristina moisescu2 1department of neurosurgery, “carol davila” university of medicine and pharmacy, bucharest 2“sf. pantelimon” emergency hospital, bucharest abstract introduction: mild traumatic brain injuries represent 80% of the total traumatic brain injuries. their management is conducted as recommended by ebic (european brain injury consortium) or wfns (world federation of neurosurgical societies). the aim of the study is to analyze the management of patients with mild traumatic brain injuries who present at the emergency department (ed), of the admitted ones, the paraclinical investigations used and the cerebral lesions which these identify. material and methods: during a 3 months period, 533 patients with mild traumatic brain injuries presented at the ed. we have followed these patients regarding the demographic data, the causes that led to the mild traumatic brain injuries and the paraclinical investigations used. regarding the admitted patients, we have taken into consideration risk factors, neurological symptoms, the need to repeat a paraclinical investigation, their management and outcome. results: out of the 533 patients who presented at the ed, 248 (65%) were adults and 158 (29.64%) were third age patients. the remaining 27 (5%) were aged between 0-18 years old. male patients (359; 67%) were more frequently affected than female patients (174; 32.6%). the top three causes were aggressions (57%), car accidents (27%) and same level falls (6.3%). the patients were investigated by skull x-rays (47.8%) and cerebral ct (computed tomography) scans (52.35%). out of the total number of patients, 198 were admitted; these had the following risk factors: age > 65 years old (31%), alcohol use (18.6%), seizures (7.57%) and the following clinical symptoms: headaches (71%), vomiting (9.6%), dizziness (36.8%), loss of consciousness (31.8%). out of the admitted patients, only 12 presented cerebral lesions: hemorrhagic brain contusions (n=5), small subdural blood collections (n=3), traumatic subarachnoid hemorrhages (n=2), acute subdural hematoma (n=1) and intraventricular hemorrhage (n=1). the patient with acute subdural hematoma was operated on and had a favorable outcome. the patient with intraventricular hemorrhage, who was 90 years old and presented with coagulopathy, has deceased. all the other patients were discharged after a mean hospitalization period of 3 days. 310 adam et al mild traumatic brain injury conclusions: out of the patients with mild traumatic brain injuries, only a small number present cerebral lesions. for their diagnosis, expensive paraclinical investigations are used in both the ed and the neurosurgical department. careful monitoring of the evolution of the neurological status and performing a cerebral ct scan only in case of neurological deterioration would save resources that could be targeted for the therapeutic stage. abbreviations: ed = emergency department, ebic = european brain injury consortium, wfns = world federation of neurosurgical societies, gcs = glasgow coma scale, ct = computed tomography. introduction a mild traumatic brain injury is defined as a maximum 20 minutes consciousness loss or as a short period of retrograde amnesia, gcs (glasgow coma scale) score of 13-15, without focal neurological deficits, without seizures and with normal ct scan. mild traumatic brain injuries represent 80% of the total traumatic brain injuries. their management is conducted according to ebic or wfns regulations, between which there are minor approach differences. through their multitude, mild traumatic brain injuries consume an important part of the budget allocated to ed or neurosurgical departments from the emergency hospitals. the aim of this study is to analyse the evolution of patients with mild traumatic brain injuries and their management in ed as well as in the neurosurgical department. material and methods we identified patients with mild traumatic brain injuries between april and june of 2013, taking into consideration some epidemiological data (age, sex, living environment – urban/rural), causes and investigation methods in the ed (cerebral ct scan, skull x-ray). for patients hospitalized in the neurosurgical departments we noted: risk factors, reasons of hospitalization, signs of neurological worsening, necessity of paraclinical investigations, treatment and outcome. results during the three months period of study, 533 patients presented at the ed with mild traumatic brain injuries. two thirds were men and one third were women; 72.8% were from an urban environment and 27.2% were from a rural environment. middle aged patients were twice as many as elderly ones (patients over 65 years). these represent a third of the total of patients admitted with mild traumatic brain injuries. causes of traumatic brain injuries are presented in table 1; the top three causes are aggressions (57.03%), followed by car accidents (27.01%) and same level falls (6.38%). patient’s investigations in the ed were carried out by skull x-rays and ct scans in approximately equal proportions, with a slightly higher incidence of ct scans. these investigations pointed out extracranial, facial and intracranial lesions (table 1). following the paraclinical investigations we established that 12 patients had intracranial lesions, 5 of which were hemorrhagic brain contusions, 3 small subdural blood collections, 2 cases of traumatic subarachnoid hemorrhages, 1 acute subdural hematoma and 1 intraventricular hemorrhage. among the 533 patients who presented romanian neurosurgery (2013) xx 4: 309 317 311 at the ed, 198 were admitted in the neurosurgical department, out of which 195 (98.48%) performed cerebral ct scan in the ed and 3 had skull x-rays. 252 patients were sent home and 83 refused admission. out of the 252 patients who were sent home, 82 (32.54%) had normal cerebral ct scans and the rest presented with normal skull x-rays. out of the 83 patients who refused admission, 2 (2.4%) presented diffuse cerebral edema (marshall type ii lesion) on the ct scans and the rest had normal skull x-rays. admission was motivated by the presence of the risk factors, clinical symptoms, as well as the presence of traumatic intracranial lesions revealed by the cerebral ct scan (table 2). the characteristics of admitted patients are presented in table 2. out of the admitted patients, 194 presented with gcs score of 15 points, 3 with gcs score of 14 points and one patient with gcs score of 13 points. the gcs score of patients who presented at the ed and of adimtted patients is presented in table 3. all patients with gcs score of 14 and 13 points were investigated by cerebral ct scan. they were admitted and the ct scan was repeated on the neurosurgical department. among the patients with gcs score of 15 points at admission, 275 (51.98%) out of 529 were investigated by cerebral ct scan. 191 patients (69.45%) were admitted with ct scan and 3 with skull x-rays. out of the 279 patients who were investigated by cerebral ct scan in the ed, 195 (69.89%) were admitted and one patient (0.51%) was operated on for an acute subdural hematoma. table 1 characteristics of patients who presented at the ed no. % age 0-18 years old 19-64 years old >65 years old total 27 248 158 533 5.07 65.29 29.64 100 sex m w 359 174 67.35 32.65 cause aggressions car accidents same level fall unspecified conditions bike fall other level fall accident at work sports accident 304 144 34 20 13 10 6 2 57.03 27.01 6.38 3.75 2.44 1.88 1.13 0.38 investigations skull x-ray cerebral ct scan 255 279 47.84 52.35 revealed lesions skull fractures intracranial lesions scalp abrasions scalp plagues epicranian hematoma facial lesions 5 12 75 127 36 287 0.94 2.25 14.07 23.83 6.75 53.84 312 adam et al mild traumatic brain injury table 2 characteristics of admitted patients no. % age 0-18 years old 19-64 years old >65 years old total 0 136 62 198 0 68.69 31.31 100 risk factors age >65 years alcoholism epilepsy previous neurosurgical interventions coagulopathy 62 37 15 1 6 31.31 18.68 7.57 0.5 3.03 clinical symptoms headache vomiting dizziness loss of consciousness retrograde amnesia scalp plagues 142 19 73 63 4 71 71.72 9.6 36.87 31.82 2.02 35.86 neurological signs motor deficit 1 0.5 skull lesions revealed by x-ray or ct scan cranial fissures skull fractures withoutclogging 0 5 0 2.52 cerebral lesions revealed by the ct scan hemorrhagic contusions traumatic subarachnoid hemorrhage acute subdural hematoma small subdural blood collections intraventricular hemorrhage 5 2 1 3 1 2.52 1.01 0.5 1.51 0.5 hospitalization period <24 hours 24-48 hours 48-72 hours >72 hours mean hospitalization period 9 80 60 49 4.55 40.4 30.3 24.75 3.03 days table 3 the relationship between the gcs score and the ct scan investigation gcs patients ct no. % no. % patients in ed 15 529 99.25 275 51.98 14 3 0.56 3 100 13 1 0.19 1 100 admitted patients 15 194 97.97 191 98.45 14 3 1.52 3 100 13 1 0.51 1 100 romanian neurosurgery (2013) xx 4: 309 317 313 table 4 the results of the cerebral ct scan performed in the ed number of patients observations positive results intracranial lesions 12 admitted cerebral edema 2 refused admission total 14 negative results normal ct scan 82 sent home normal ct scan 183 admitted total 265 in the neurosurgical department, 3 patients (1.51%) presented neurological deterioration, one of each group of patients with gcs score of 15, 14 and 13 points. one patient was operated on for an acute subdural hematoma. the rest of the patients with intracranial lesions were clinically monitored and also, the cerebral ct scan was repeated when needed, the patients being discharged in an improved condition. discussions over 10 million traumatic brain injuries are produced annually worldwide (1). following the statement of hippocrates, no trauma „is too trivial to ignore”. the patients with mild traumatic brain injuries, who are the majority, represent 80% of the admitted patients with traumatic brain injuries (2). both ebic and wfns developed classifications of traumatic brain injury, as well as recommendations for management (table 5, table 6). epidemiological data of our study is consistent with the literature. mild traumatic brain injuries prevail among male patients. since we only refer to mild traumatic brain injuries, their main cause is represented by aggressions (57%), followed by car accidents (27%). in other studies, car accidents represent the main cause both regarding the mild traumatic brain injuries as well as brain traumas overall (3, 4, 5). figures show a tendency to aggression among our poor educated population. older patients represent almost a third of the patients with mild traumatic brain injuries. these patients with multiple comorbidities requiring investigations and prolonged hospital admission are resource consumers. our survey data on patients with craniocerebral traumas reveal that ct scan examination was widely used in the ed, on 52% of the patients who were examined. 48% of the patients were examined using the skull x-ray. skull lesions were identified among 5 patients (0.94%) and intracranial lesions were identified among 12 patients (2.25%). ct scan examination identified 5 cases of hemorrhagic brain contusions, 2 cases of traumatic subarachnoid hemorrhages, 3 cases of small subdural blood collections and one case of acute subdural hematoma which was operated. 314 adam et al mild traumatic brain injury table 5 ebic classification of mild traumatic brain injuries degree gcs score observations 13-15 does not include cases with: -focal neurological deficits -fractures with clogging -csf fistula 0 -without loss of consciousness -without amnesia -sent home 0 with risk of late deterioration alcoholism -drugs -age (both limits) -epilepsy -history of neurosurgical interventions -cerebral ct scan -24 hours hospitalization 1 -loss of consciousness < 5 minutes -retrograde amnesia -headache, vomiting -large scalp plagues -cerebral ct scan in the first 6 hours -24 hours hospitalization 2 -sleepy patients -gcs score of 14-13 points for 30 minutes after the trauma -cerebral ct scan -hospitalization until improvement table 6 neurotrauma committee of the wfns model for mild head injury low risk medium risk high risk gcs score 15 15 with clinical findings 14 or 15 with: -neurological deficits or -skull fracture or -risk factors with/ without clinical findings clinical findings no amnesia diffuse headache vomiting loss of consciousness amnesia diffuse headache vomiting loss of consciousness neurological deficits no no yes cranial fracture no no yes risk factors no no yes: coagulopathy, age > 60 years, previous neurosurgical interventions, epilepsy, misuse of alcohol, drugs imaging no ct scan/ skull x-ray ct scan disposition sent home hospitalization: -3-6 h after the ct scan examination -24 h after skull x-ray followed by home observation hospitalization (24-48h) fallowed by home observation romanian neurosurgery (2013) xx 4: 309 317 315 one patient with thrombocytopenia, diabetes and chronic renal failure presented intraventricular hemorrhage. this patient, aged 90 years old, with gcs 13 points at admission died after 9 days. except for 3 patients, all the other patients who were hospitalized benefited from ct scan examination in the ed. out of the 533 patients who presented at the ed, 279 benefited from ct scan examination, but only 195 were hospitalized. 84 patients were not admitted. out of these patients, 82 presented a normal cerebral ct scan and were sent home and 2 refused admission even though the ct scan showed diffuse cerebral edema. the remaining 81 patients who refused admission were investigated by skull x-ray. among the patients who presented at the ed and were investigated by ct scan, 275 presented with gcs score of 15 points. according to the wfns classification, 118 patients (42.9%) presented medium risk and 157 (57.1%) presented high risk of neurological deterioration. although the wfns classification regarding patients with mild traumatic brain injuries provides their investigation via ct scan or skull x-ray and hospitalization for 3-6 hours or 24 hours if those are negative, the patients included in this study were investigated using the ct scan in 52.34% of the cases and the admitted ones were hospitalized for a longer period, of 3 days in average. considering the same group of patients, the ebic classification recommends ct scan examination during the first 6 hours and 24 hours hospitalization. regarding these classifications which are not a hundred percent concordant, having different recommendations for management, ed doctors and neurosurgeons chose overinvestigation and longer hospitalization period in order to avoid accusations of malpractice. this was achieved by increasing the costs of medical services. among the admitted patients, 3 presented neurological deterioration from the moment of admission, one case out of each group of patients with gcs score of 15, 14 and 13 points. they represent 1.51% of the total number of admissions. our study provides contradicting evidence. on one hand, even patients with mild traumatic brain injuries may have intracranial lesions, supporting the need for paraclinical investigations via ct scan and hospital admission. on the other hand, the number of patients with neurological deterioration who require surgery is small. regarding the patients with medium risk based on wfns classification, it is preferred a consuming fund exploration and a longer period of hospital observation. the media attack on the health system determines the doctors to inefficiently spend public money and, regarding the alternative – skull x-ray and 24 hours hospitalization – they prefer examination via ct scan and 48 hours hospitalization. regarding the small number of patients with mild traumatic brain injuries with a positive cerebral ct scan, the national institute of clinical excellence of england and wales (nice) established in 2009 the following criteria for requesting a ct scan examination for this group of patients:gcs score < 13 points at any moment after the trauma, gcs score > 13-14 points 2 hours after the trauma, suspecting open or clogged skull fracture, signs of skull base fracture, at least one vomiting episode, retrograde amnesia > 30 minutes; 316 adam et al mild traumatic brain injury regarding the patients with loss of consciousness or posttraumatic amnesia, the ct scan will be done immediately even if the patient: is aged ≥ 65 years, presents coagulopathy or presents dangerous lesion mechanism (car accident, more than 1 meter fall). miller and jeret stated that ct scan examination in case of mild traumatic brain injuries is indicated in patients with gcs score < 15 points, when there are skull fractures, clinical signs for skull base fracture, seizures, focal neurological signs or persistent headache (6, 7). in the usa, annually, 800000 patients with mild traumatic brain injuries are examined in various medical facilities and 1200000 are examined in the ed. in the ed, the evaluation of patients with concussions is often done through the ct scan. currently in the usa there is a consensus to reserve cerebral ct scan and mri when there are suspicions of intracerebral structural lesions: prolonged loss of consciousness (> 1 minute), focal neurological deficit, worsening of clinical symptoms. unlike usa, in romania, all patients with mild traumatic brain injuries are examined in the ed and, even though the vast majority presents with gcs score of 15 points, 52% of them were investigated using the ct scan. in moore’s study only 1% of patients with mild traumatic brain injury underwent surgical intervention (8). we only operated on one patient with acute subdural hematoma out of the 195 patients hospitalized with ct scan performed in the ed (0.51%). because of patients’ high expectations of having top imagistic procedures, of financial incentives for doctors (in case the ct scan was requested) and of practicing a defensive medicine style, this imagistic method is highly used. however, some consider that 20-50% of top imagistic procedures are not necessary and don’t bring useful clinical information (9). information received from the patient’s history and from the neurological examination is neglected and there is a high emphasis on cerebral ct scan examination. because the health system is confronting with budgetary restrictions, a rational and efficient use of resources with an aim to sustain not only the diagnostic stage but the therapeutic one is needed. minimizing resources on investigation and treatment of patients with mild traumatic brain injuries can be performed thorough methods of preventing the occurrence of traumatic brain injuries by reducing aggressions and car accidents and also by reducing the prevalence of risk factors. conclusions mild traumatic brain injuries affect people of all ages and, among the traumatic brain injuries in general, they are the most frequent. their management is conducted according to the recommendations of ebic or wfns, among which there are certain differences. the paraclinical investigations, skull xray and cerebral ct scan, are used in similar proportions. the imagistic investigations, which are used in an increasingly large percentage because of the fear of malpractice, detect cerebral lesions in a small number of cases. a thorough neurological monitoring can avoid expensive imagistic overinvestigation. romanian neurosurgery (2013) xx 4: 309 317 317 references 1. schouten jw, mass air: epidemiology of traumatic brain injury. in: winn hr, el. youmans neurological surgery. philadelphia elsevier saunders 2011: 32703277. 2. kraus jv, mac arthur dl: epidemiologic aspect of brain injury. neural clinics 14:435-450, 1996. 3. kalsbeek w, mc laurin r, harris b, et al.: the national head and spinal cord injury. survey: major findings. j neurosurg (suppl) 63, s19-s31, 1980. 4. ring i, berry g, dan n: epidemilogy and clincal outcomes of neurotrauma in nsw. nz j surg 56:557566, 1986. 5. kraus j, nourjah p: the epidemiology of mild, uncomplicated brain injury. j trauma 28:1637-1643, 1998. 6. miller jd: assesing patients with head injury. br j surg 77, 241-242, 1990. 7. jeret js, mandell m, anziska b et al: clinical predictors of abnormality disclosed by computed tomography after mild head trauma. neurosurgery 32, 9-16, 1993. 8. moore mm, pasquale md, badelino m: impact of age and anticoagulation: need for neurosurgical intervention in trauma patients with mild traumatic brain injury. j trauma 2012, 73:126-130. 9. brenner dj, hall ej: computed tomography – an increasing source of radiation exposure. n engl j med 2007; 357 (22): 2277-2284. microsoft word 11gobran_factors romanian neurosurgery (2013) xx 4: 379 387 379 factors associated with recurrence of postoperative meningioma: a clinical study of 138 patients alfotih gobran, fang cheng li, xin ke xu, shang yi zhang sun yat sen memorial hospital, neurosurgery department, sun yat sen medical university, guang zhou, guang dong province, people’s republic of china abstract background and purpose: as the postoperative recurrence of meningioma can have devastating effects, it is important to identify factors that can be used to predict this type of tumor recurrence. material and methods: we have performed a retrospective study involving 138 patients who were surgically treated for intracranial meningioma between 2005 and 2010. the patient population consisted of 80 females and 58 males, with an age range of 23 to 77 years old (mean age = 52 years). we measured associations between meningioma recurrence and clinical features (age, sex, extent of resection, histological type), or radiological features (tumor size, location, shape, calcification, bone changes, brain tumor interface, tumor necrosis, and mri enhancement). results: we found statistically higher levels of postoperative meningioma recurrence in patients with high simpson grade resections, high histological types, tumor diameters > 5 cm, tumors located in the base of the skull or the parasagittal sinus, tumors with unclear border, irregular enhancements on mri, edema around the tumor, bleeding and necrosis within the tumor, and irregularly shaped tumors (e.g., lobulated or mushroom-shaped). in addition, calcification, age, sex, bone change, and dural tail sign provided no predictive value. conclusions: we have shown that histological type, degree of resection, bleeding, necrosis, edema, irregular enhancement, location, shape, size, and margin serve as strong predictors for the postoperative recurrence of meningioma tumors. key words: factors, meningioma, neurosurgery, recurrence. introduction meningiomas can remain asymptomatic throughout a person’s life and are typically non-life-threatening because they exhibit little (less than 1 cm²) or no growth over many years. in a small number of cases, however, these kinds of tumors pose a real danger. this is particularly true during postoperative regrowth of a meningioma, which can cause devastating outcomes for the patient. our study highlights factors that can be used to predict the recurrence of postoperative meningioma. material and methods we collected data associated with patients who underwent meningioma resection at the sun yat sen memorial hospital between 2005 and 2010. there were 138 patients, of which 58 (42%) were 380 gobran et al factors associated with recurrence of postoperative meningioma male and 80 (58%) were female. ages ranged from 23 to 77 years old, with a mean age of 52.13 years. we excluded patients with multiple intracranial tumors, severe organ failure, patients who underwent postoperative radiation therapy, and patients whose tumor-resection procedure received a simpson grade of iv or v. the criteria we used to diagnose the recurrence of postoperative meningioma were radiological measurements (e.g., computed tomography (ct) scan, and magnetic resonance imaging (mri)) and the recurrence of clinical symptoms after the remission period. to determine the relative risks of meningioma recurrence associated with fifteen independent variables we used the chi square test (χ2 ) to perform binary logistic regression analysis. see tables 1 and 2. table 1 radiological predictors predictor cases percentage (%) margin clear unclear 128 10 92.8 7.2 bone changes (+) (–) 35 103 25.4 74.6 calcification (+) (–) 25 113 18.1 81.9 shape circular lobulated mushroom 113 17 8 81.9 12.3 5.8 dura tail sign (+) (–) 61 77 44.2 55.8 t1 enhancement regular irregular 119 19 86.2 13.8 necrosis (+) (–) 9 129 6.5 93.5 bleeding (+) (–) 7 131 5.1 94.9 edema (+) (–) 34 95 31.2 68.8 location parasagittal skull base other 34 47 57 24.6 34.1 41.3 size ≤ 5 cm > 5 cm 104 34 75.4 24.6 romanian neurosurgery (2013) xx 4: 379 387 381 table 2 clinical predictors predictor cases percentage (%) sex male female 58 80 42.03 57.97 age > 50 ≤ 50 60 78 43.00 57.00 resection degree (simpson) i ii iii 77 36 25 47.1 31.2 21.7 histological type benign atypical malignant 115 13 10 87.0 9.4 3.6 table 3 results of comparing radiological factors predictor patients with recurrence patients without recurrence recurrence rate (%) χ2 p value margin clear unclear 12 5 116 5 9.4 50.0 14.172 0.000 bone change (+) (–) 9 8 26 95 25.7 7.8 7.790 0.05 calcification (+) (–) 3 14 22 99 12.0 12.4 0.03 0.957 shape circular lobulated mushroom 8 4 5 105 13 3 7.1 23.5 62.5 23.500 0.000 dura tail sign (+) (–) 6 11 55 66 9.8 14.3 0.624 0.430 t1 enhancement regular irregular 7 10 112 9 5.9 52.6 33.151 0.000 necrosis (+) (–) 7 10 2 119 77.8 7.8 38.149 0.000 bleeding (+) (–) 5 12 2 119 71.4 9.2 23.835 0.000 382 gobran et al factors associated with recurrence of postoperative meningioma edema (+) (–) 13 4 30 91 30.2 4.2 18.557 0.000 location skull base parasagittal other 12 5 0 35 29 57 25.5 14.7 0.0 15.784 0.000 size > 5 cm ≤ 5 cm 10 7 24 97 29.4 6.7 12.203 0.000 table 4 result of comparing clinical factors predictor patients with recurrence patients without recurrence recurrence rate (%) χ2 p value sex male female 11 6 47 74 19.0 7.5 4.092 0.043 age > 50 ≤ 50 5 12 55 66 8.3 15.4 1.561 0.212 resection degree (simpson) i ii iii 1 6 10 76 30 15 1.3 16.7 40.0 27.023 0.000 histological type benign atypical malignant 5 4 8 110 9 2 4.3 30.8 80.8 53.271 0.000 table 5 binary logistic regression analysis variable influence score p value sex 4.092 0.043 age 0.849 0.381 calcification 0.003 0.957 bone change 7.790 0.005 location 23.500 0.000 irregular enhancement 33.151 0.000 edema 18.557 0.000 dural tail sign 0.624 0.430 shape 22.228 0.000 margin 14.172 0.000 necrosis 38.194 0.000 bleeding 23.853 0.000 size 12.203 0.000 resection degree 27.023 0.000 histological type 52.114 0.000 romanian neurosurgery (2013) xx 4: 379 387 383 results seventeen patients had a recurrence of meningioma, resulting in a recurrence rate of 12.32%. ten factors were significant predictors of recurrence, namely the degree of tumor resection, histological type, location, necrosis, bleeding, edema, shape, margin, irregular enhancement, and size (p < 0.05). for the factors sex and bone change, the significance of their predictive value was unclear (p = 0.043, and p = 0.05, respectively). histological type, the extent of tumor resection, necrosis, bleeding, location, and irregular enhancement had strong effects on the postoperative recurrence of meningioma. see tables 3, 4, and 5. to illustrate one case, a 36-year-old male patient presented with a headache that had lasted 6 months and 3 days of vomiting. after being admitted to our department, head mri revealed a 57 × 60 mm compressive cystic solid mass in the right temporal region with surrounding edema. magnetic resonance spectroscopy results included a reduced n-acetyl aspartate (naa) peak, an elevated choline (cho) peak elevated, and a cho/naa ratio of 3.18, which suggested a malignant tumor in the right temporal lobe (figure 1 a, b). the patient was subjected to a right temporal lobe lesionectomy. results of the postoperative tumor biopsy were: anaplastic (malignant) meningioma, who grade iii (figure 2 c, d). three months later the patient started to have a mild headache. a follow up head mri t2, t1 + c indicated tumor recurrence (figure 3 a, b). figure 1 (a) mri revealed a 57 × 60 mm compressive cystic solid mass in the right temporal region with surrounding edema. (b) magnetic resonance spectroscopy results included a reduced n-acetyl aspartate (naa) peak, an elevated choline (cho) peak, and a cho/naa ratio of 3.18, which suggested a malignant tumor in the right temporal lobe figure 2 postoperative tumor biopsy revealed an anaplastic (malignant) meningioma, who grade iii. loss of meningiomatous tissue and numerous typical and atypical mitoses 384 gobran et al factors associated with recurrence of postoperative meningioma figure 3 follow up head mri t2, t1 + c indicated tumor recurrence discussion meningiomas are generally benign tumors that originate from the meninges, in particular cells of the arachnoid villi. these types of tumors represent ~15–20% of all intracranial tumors, with an annual incidence of ~2 per 100,000 within the general population. likelihood of developing meningioma increases with age, as they commonly occur in the fourth to sixth decades of life. females are twice as likely to be diagnosed with meningioma than males, which may result from the expression of female hormone receptors by meningioma tumors cells [4]. however this sex distribution does not characterize the pediatric population [6]. as mentioned above, meningioma tumors are generally benign, but can recur after surgical resection. our study shows that meningioma recurrence was significantly associated with a number of predictive factors, namely histological type, the degree of resection, location, edema, necrosis, bleeding, shape, size, enhancement pattern, and margin. whether patient sex contributes to the recurrence of meningioma remains controversial, as some studies have shown that male patients tend to recur [9], whereas other studies have detected no relationship between sex and recurrence [11]. in our patient sample, the association between sex and recurrence yielded an ambiguous level of significance (p = 0.043). we conclude that sex may not influence the recurrence of meningioma. patients in their fourth decade have a higher rate of recurrence than other age groups [18,20]. however, our study did not find that age was a significant factor in the recurrence of meningioma (p > 0.05). concerning the radiological features of meningioma, we found that location plays the primary role in the recurrence of meningioma. meningioma can be found in the base of the skull, the parasinuses, the intraventricule system, or on the convexity of the brain far from the sinuses. meningiomas at the base of the skull and the parasagittal sinus are difficult to treat because these tumors adhere to neurovascular structures. this makes it difficult to perform zero or grade i simpson resection, providing a chance for these tumors to recur after surgery. we have recommended, therefore, postoperative radiotherapy for residual tumor tissue within these areas [10]. romanian neurosurgery (2013) xx 4: 379 387 385 the skull bone often reacts to neighboring meningioma, and is sometimes invaded by tumor cells. meningioma can cause hyperostosis or osteolysis to the nearby skull, and patients with osteolysis show higher recurrence rates than those with hyperostosis [19]. here we divided our 138 patients into two groups, those with and without bone changes. we found no significant difference between these two groups (p = 0.05). dural tail sign can be visualized using mri with contrast agents like gadoliniumdiethylenetriaminepentacetate (gd-dtpa), and can distinguish between meningiomas that are attached to the dura and other types of tumors. in 1990 goldsher et al. [5] described dural tail sign as: (1) the presence of at least two consecutive sections through the tumor at the same site in more than one imaging plane, (2) greatest dural thickness adjacent to the tumor and tapering away from it, and (3) more intense enhancement of dural tissue than of the tumor itself. furthermore, goldsher et al. suggested that the presence of dural tail sign adjacent to a peripherally located mass is a highly specific sign of meningioma [5]. tumor cells have been shown to invade the dural tail [15], although this is not always the case [23]. previous studies have detected no correlations between dural tail sign and meningioma recurrence [13], which agrees with our current result (p = 0.430). in some rapidly growing forms of meningioma, like anaplastic meningioma, the insufficient supply of oxygen can cause necrosis. areas of breakdown or bleeding inside a tumor that result from necrosis are characterized by irregular enhancement on mri t1 gd-dtpa. these irregular meningioma enhancements, as visualized by ct scans or mri, have been associated with high rates of recurrence [2, 24]. others have suggested that hypointense areas or irregular enhancements on ct scans or mris indicate malignant types of meningioma [3, 21]. dietemann et al. found that for 4 of 5 patients with malignant meningioma, their ct/mri scans revealed irregular enhancement [3]. patients in our study that had necrosis, bleeding, or irregular mri enhancements exhibited higher rates of recurrence than others groups (p < 0.05). we divided patients into three groups based on the shape of the meningioma: spherical, lobulated, and mushroom. there was a significant difference between these three groups (p < 0.05), as spherical, lobulated, and mushroom shapes had recurrence rates of 7.1%, 23.5%, and 62.5%, respectively. previous studies have also shown that mushroom-shaped meningiomas exhibit very malignant behavior [1, 7, 16]. most studies have shown that the presence of intratumoral calcification indicates a low rate of tumor recurrence. in fact, levels of calcification and the histological type of the tumor are closely correlated [14]. we have noticed that benign meningioma tumors are generally calcified compared with malignant ones. in addition, calcified meningiomas have low rates of recurrence [14]. our data show that calcification was not able to predict meningioma recurrence (p > 0.05), but it can be use to differentiate between benign and malignant tumors. we also divided patients into two groups based on meningioma size: ≤ 5 cm or > 5 cm. although some studies have suggested that large-diameter tumors are more likely to recur [13], we found no significant 386 gobran et al factors associated with recurrence of postoperative meningioma difference between these two groups (p � 0.05). the incidence of edema around meningioma is ~60% [17]. peritumoral edema promotes tumor-cell invasion of brain parenchyma, making it more difficult to surgically remove all the tumor cells and increasing the likelihood of recurrence [12]. for patients in our study group the presence of moderate or severe edema resulted in higher rates of recurrence (p < 0.05). clinical care providers are fully aware that meningioma recurrence is related to the extent of resection. as such, the simpson grading system is used around the world [22]. we have found it difficult to perform grade zero or i resections for tumors: 1) located at the base of the skull, 2) that were invading sinuses, or 3) with unclear margins (particularly tumors with irregular shapes). our study indicated that higher simpson grades are associated with higher rates of recurrence. finally, we divided meningioma patients into three groups according to world health organization (who) histological classifications: benign (i), atypical (ii), and malignant (iii). recurrence rates associated with groups i, ii, and iii were 4.3%, 30.8%, 80.0%, respectively, which represented significant differences (p < 0.05). this agrees with a previous report that measured five-years recurrence rates after meningioma resection of 3%, 38%, and 78% for grades i, ii, and iii, respectively [8]. conclusions we have shown that degree of tumor resection, histological type, pattern of enhancement, necrosis and bleeding within the tumor, peritumoral edema, tumor size, margin characteristics, shape, and location are important factors for predicting the postoperative recurrence of meningioma tumors. correspondence address: alfotih gobran, sun yat sen memorial hospital, neurosurgery department, sun yat sen medical university, p.o. box 510120, guangzhou, guangdong province, people’s republic of china, tel: 008613066381670, email: gta_alfotih@yahoo.com references 1. alvarez f., roda j.m., perez r.m, et al. malignant and atypical meningioma: a reappraisal of clincal, histological and computed tomographic features. neurosurgery 1987; 20: 688-694. 2. chen t.c., zee c.s., miller c.a., et al. magnetic resonance imaging and pathological correlates of meningioma. neurosurgery 1992; 31: 1015-1022. 3. dietemann j.l., heldt n., burquet j.l., et al. ct findings in malignant meningioma. neuroradiology 1982; 23(4): 207-209. 4. donnell m.s., meyer g.a., donegan w.i. estrogenreceptor protein in intracranial meningiomas. j neurosurg 1979; 50: 499-502. 5. goldsher d., litt a., pinto r., et al. dural “tail” associated with meningiomas on gd-dtpa enhanced mr images: characteristics, differential diagnostic value, and possible implication for treatment. j radiology 1999; 176: 447. 6. haddad g., al-mefty o., abdulrauf s. meningiomas. in: winn h.r. [ed.]. youmans neurologicalsurgery, vol. 1, ed. 5. saunders, philadelphia 2003, pp. 10991131. 7. jääskeläinen j., haltia m., servo a. atypical and anaplastic meningioma: radiology, surgery, radiotherapy, and outcome. j surg neurol 1989; 3: 101108. 8. jääskeläinen j. seemingly complete removal of histologicaly benign intracranial meningioma:late recurrence rate and factors predicting recurrence in 657 patients: a multivariate analysis. j surg neurol 1986; 26(5): 461. 9. kajiwara k., fudaba h., tsuha m. et al. analysis of recurrence of meningiomas following neurosurgical resection. no shinkei geka 1989; 12: 1125-1131. 10. kamitani h., masuzawa h., kanazawa i., et al. recurrence of convexity meningiomas: tumor cells in the arachnoid membrane. j surg neurol 2001; 56(4): 228. romanian neurosurgery (2013) xx 4: 379 387 387 11. mahmood a., qureshi n.h., malik g.m. intracranial meningiomas: analysis of recurrence after surgical treatment. acta neuroehir 1994; 126(2-4): 5358. 12. mantle r.e., lach b., deigado m.r., et al. predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning. j neurosurg 1999; 91(9): 375-383. 13. nakasu s., nakasu y., nakajima m., et al. preoperative identification of meningioma that are highly to recur. j neurosurg 1999; 90: 455-462. 14. nakasu s., nakajima m., matsumura k., et al.meningioma: proliferating potential and clinicoradiological features. neurosurgery 1995; 37: 1049-1055. 15. nakau h., miyazawa t., tamai s., et al. pathological significance of meningeal enhancement "flair tail" of meningioma on mri. j surg neurol 1997; 48: 584-591. 16. new p.f.j., hesselink j.r., o’carroll c.p., et al. malignant meningioma: ct and histologic criteria, including a new ct sign. anjr 1982; 3: 26. 17. park k.j., kang s.h., chae y.s., et al. influence of interleukin6 on the development of peritumoral brain edema in meningiomas. j neurosurg 2010;112(1): 7380. 18. perry a., stafford s.l., scheithauer b.w., et al. an analysis of histologic parameters. am j surg pathol 1997; 21(12): 1455-1465. 19. rohringer s., yoshioka h., hama s., et al. recurrence of meningiomas. cancer 2001; 89(5): 11021104. 20. stafford s.l., perry a., suman v.j., et al. primarily resected maningioma: outcome and prognostic factors in patients, 1978 through 1988. mayo clinic pro 1998; 73(10): 936-942. 21. servo a., porras m., jääskeläinen j., et al. computed tomography and angiography do not reliably discriminate malignant tumor from benign one's. neuroradiol 1990; 32: 94-97. 22. simpson d. the recurrence of intraeranial meningiomas after surgical treatment. j neurosurg psychiatry 1957; 20: 22-39. 23. tokumaru a., o'uchi t., eguchi t., et al. prominent meningeal enhancement adjacent to meningioma on gd-tpa enhanced mri images: histopathological correlation. radiology 1990; 175: 431433. 24. zee c.s., chin t., segall h.d., et al. magnetic resonance imaging of meningioma. semin ulrasound ct mr 1992; 13: 154-169. microsoft word rajendrash_arachnoidcyst_f.docx romanian neurosurgery (2012) xix 1 arachnoid cyst complicated by spontaneous chronic subdural hematoma in the infant shrestha rajendra1, pradhan reeka2, jianguo xu1, chao you1 1department of neurosurgery, west china hospital, sichuan university, china 2international medical school, tianjin medical university, china abstract arachnoid cyst is collections of fluid that develop within the arachnoid membrane because of splitting or duplication of this structure. arachnoid cyst can present at any age with or without symptoms. chronic subdural hematoma most common in elderly patients several weeks after a head injury prior to onset of symptoms. but here we report 1 year-old-boy presented with epileptic seizures for one month. computed tomography and magnetic resonance imaging of brain disclosed that left parietal an arachnoid cyst and frontotemporo-pareital chronic subdural hematoma. after admission, cyst was excised and hematoma was evacuated through fronto-parietal craniotomy approach. the patient had a good recovery postoperatively. arachnoid cyst with chronic subdural hematoma in the infant is a serious condition with a high mortality rate. however, surgical resection seems to be very favorable. keywords: arachnoid cyst, infant, spontaneous chronic subdural hematoma introduction arachnoid cysts are benign, congenital, intra-arachnoidal space occupying lesions that are filled with clear cerebral spinal fluid (csf) like fluid (11). however, they are most often found in the middle cranial fossa (2, 4). cysts of the middle fossa occur nearly three times as often in males as in females and nearly twice as often on the left side than on the right. trauma has been recognized as an important factor in the development of csdh (1). arachnoid cyst is a risk factor for chronic subdural hematoma after head injury (9). but our case report involves a one-year-old male having arachnoidal cyst with spontaneous chronic subdural hematoma. case report this one-year-old male presented with epileptic seizures on and off for one month. the seizures lasted about ten second with stiffness but not associated with fever, turning of eye, foaming around the mouth, or incontinence. there was no history of trauma. his medical and family histories were unremarkable. the neurological and physical examinations were normal. at the local hospital, computerized cranial tomography (ct) scan revealed a left parietal hypodense lesion “arachnoid cyst” (figure 1 a) and left fronto-temporoparietal iso-hypodense lesion “chronic subdural hematoma” (figure 1 b). magnetic resonance imaging demonstrated hyper-intense on t2-weighted images “left parietal arachnoid cyst and left frontotemporo-parietal chronic subdural hematoma” (figure 2 a, b). shrestha rajendra et al arachnoid cyst a b figure 1 ct scan of brain showing left parietal arachnoid cyst and fronto-temporoparietal chronic subdural hematoma workup for coagulopathy was negative. a left fronto-parietal craniotomy was performed. dura was intact with tension. it was separated carefully from cyst wall and removed dark red blood about 50ml by drainage and irrigation. arachnoid cyst was in yellow, tough envelop having maximum blood vessels adhesion and also compression of brain tissue. the arachnoid membrane was also excised under microscope and sent for pathological examination. a b figure 2 magnetic resonance examination of brain also showing left parietal arachnoid cyst and frontotemporo-parietal chronic subdural hematoma the operative course was uneventful. a postoperative the computerized cranial tomography (ct) showed obliteration of arachnoid cyst and subdural hematoma (figure 3). the pathological examination and culture showed negative for infection. romanian neurosurgery (2012) xix 1 figure 3 a postoperative ct scan shows the absence of subdural hematoma and an arachnoid cyst discussion arachnoid cysts represent 1% of all nontraumatic intracranial masses. the most common site is sylvian fissure (49%) followed by cerebellopontine angle (11%), supracollicular (10%), vermian (9%), sellar, suprasellar (9%), interhemispheric (5%), cerebral convexity (4%) , and clival (3%) (8). most arachnoid cysts are asympotomatic. however, they may become symptomatic as they progressively enlarge and interfere with adjacent neural structures or with cerebrospinal fluid circulation. symptoms and signs include cranial enlargement, localized cranial bulging, clinical manifestations of increased intracranial pressure, epileptic seizures, psychomotor retardation, and focal neurological deficits (2, 3). the most important diagnostic tools are ct and mri. these tools have increased the detection of incidental asymptomatic arachnoid cysts as well (2, 10). chronic subdural hematoma (csdh) tends to occur more commonly in elderly patients with a history of mild head injury (9). occurrence of csdh in infant is rare. it is also extremely rare without trauma. our case is interesting in how the two distinct clinical entities sporadically occurred in the same patient. in our knowledge, firstly the arachnoid cyst may enlarge over time as a result of the production of fluid from the cyst walls and leads to increased pressure inside cyst. an arachnoid cyst can even rupture spontaneously. secondly, tearing of the outer wall of the arachnoid cyst is associated with subdural hemorrhage caused by rupture of bridging veins, unsupported blood vessels around the cyst wall, and leptomeningeal vessels in the base of the cyst (5). j chan et al. said an association between arachnoid cysts and subdural hematomas was first noted in 1971 (7). since then, there have only been about twenty cases reported in medical literature6. to our knowledge, we couldn’t find any case of two distinct clinical entities sporadically occurring in an infant in literature. so our case report will be the first reported case. the treatment of csdh associated with arachnoid cyst is still controversial. a conservative approach should be chosen if a child with a cyst has no symptoms, is neurologically intact, and undergoes close clinical and radiological observation. in sdh cases, the conventional therapy has been drainage and irrigation through a burr-hole. in arachnoid cases, membranectomy and cyst communication to the basal cisterns must be performed (5, 10). page et al. recommended craniotomy, membranectomy, and hematoma drainage for middle fossa acs complicated by csdh (10). in our case, we performed fronto-parietal craniotomy and confirmed shrestha rajendra et al arachnoid cyst the presence of the chronic sdh and evacuated it. when the arachnoid cyst membrane was revealed, we fenestrated the cyst wall and widely resected the membrane under microscope to prevent recurrence. we performed operation successfully with low operative risk and an excellent outcome. conclusion spontaneous chronic subdural hematoma with arachnoid cyst is extremely rare in infant which could not find in the literature. the operation is helpful and successful treatment for the symptomatic patients with an arachnoid cyst combined with chronic subdural hematoma. correspondence to: prof. you chao, department of neurosurgery, west china hospital, sichuan university, 37 guo xue xiang, wuhou district, chengdu 610041, china e-mail: youchaowch@gmail.com references 1. adhiyaman v, asghar m, ganeshram kn, bhowmick bk. chronic subdural haematoma in the elderly. postgrad med j. 2002 feb;78(916):71-5. 2. clavel, m., taborga, f. g., and onzain, i.: arachnoid cysts as a cause of dementia in the elderly. acta neurochir, 1985;78:28–32. 3. di rocco, c., caldarelli, m., and di trapani, g.: infratentorial arachnoid cysts in children. child's brain, 1981;8:119–133. 4. galassi e, tognetti f, gaist g ，fagioli l, frank f, frank g : ct scan and metrizamide ct cisternography in arachnoid cyst of middle cranial fossa: classification and pathophysiological aspect. surg neurol: 1982;17:363 – 369. 5. galassi e, piazza g, gaist g, frank f: arachnoid cysts of the middle cranial fossa: a clinical and radiological study of 25 cases treated surgically. surg neurol 1980;14 : 211-219. 6. hideo hamada, nakamasa hayashi, kimiko umemura, kunikazu kurosaki, shunro endo: middle cranial fossa arachnoid cyst presenting with subdural effusion and endoscopic detection of tear of the cyst; neurol med chir (tokyo) 2010;50:512-514. 7. j chan, c huang, y liu, c lin, j huang: chronic subdural hematoma associated with arachnoid cyst in young adults: a case report; kaohsiung j med sci, 2008; 24: 41-44. 8. mark s. greenberg (1990/2010):handbook of neurosurgery seventh edition .new york: thieme, page 222. 9. mori k, yamamoto t, horinaka n, maeda m: arachnoid cyst is a risk factor for chronic subdural hematoma in juveniles: twelve cases of chronic subdural hematoma associated with arachnoid cyst. j neurotrauma 2002; 19 : 1017-1027. 10.page a, paxton rm, mohan d: a reappraisal of the relationship between arachnoid cyst of the middle fossa and chronic subdural hematoma. j neurol neurosurg psychiatry: 1987;50: 1001 – 1007. 11.van burken mm, sarioglu ac, o'donnell hd. supratentorial arachnoidal cyst with intracystic and subdural haematoma. neurochirurgia (stuttg). 1992; 35(6):199-203. microsoft word 2.ketterralf_prognosticgenetic.doc 388 ralf ketter et al prognostic genetic markers in malignant gliomas prognostic genetic markers in malignant gliomas ralf ketter1, silke wemmert2, stefan linsler1, wolf-ingo steudel1, steffi urbschat1 1department of neurosurgery, saarland university, 66421 homburg/saar, germany 2department of otolaryngology, saarland university, homburg/ saar, germany abstract glioblastomas are the most frequent and malignant brain tumors in adults. surgical cure is virtually impossible and despite of radiation and chemotherapy the clinical course is very poor. epigenetic silencing of mgmt has been associated with a better response to temozolomide-chemotherapy. we previously showed that temozolomide increases the median survival time of patients with tumors harbouring deletions on 9p within the region for p15(ink4b), p16(ink4a), and 10q (mgmt). the aim of this study was to investigate the methylation status of p15, p16, 14arf and mgmt in glioblastomas and to correlate the results with the clinical data. only patients with kps > 70, radical tumor resection, radiation and temozolomide-chemotherapy after recurrence were included. we observed promoter methylation of mgmt in 56% (15/27) and of p15 in 37% (10/27) of the tumors, whereas methylation of p16 and p14arf were rare. interestingly, methylation of p15 emerged as a significant predictor of shorter overall survival (16.9 vs. 23.8 months, p=0.025), whereas mgmt promoter methylation had no significant effect on median overall survival under this treatment regimen (22.5 vs. 22.1 months, p=0.49). in the presence of other clinically relevant factors, p15 methylation remains the only significant predictor (p=0.021; cox regression). although these results need to be confirmed in larger series and under different treatment conditions, our retrospective study shows clear evidence that p15 methylation can act as an additional prognostic factor for survival and underlines that this tumor suppressor, involved in cell cycle control, can act as an attractive candidate for therapeutic approaches in glioblastomas. keywords: glioblastoma, o(6)methylguanine-dna methyltransferase (mgmt), methylated mgmt, temozolomide introduction glioblastomas [world health organization (who) grade iv] are the most frequent and the most malignant brain tumors in adults. they arise either de novo without recognizable precursor lesions or develop from lower grade astrocytomas (secondary gbm). despite of multimodal therapy approaches, the prognosis is generally poor but varies markedly between the malignancy grades and even between individuals with the same malignancy grade. less than half of the romanian neurosurgery (2010) xvii 4: 388 – 395 389 patients survive more than a year. (1) besides radical surgery, a higher preoperative karnofsky performance score (kps) and younger age are predictors of a more favourable clinical course. (2-5) over the past decades, genetic abnormalities involved in pathogenesis and progression of these tumors were identified. several alterations were also shown to be correlated with prognosis. in novel studies progression-associated genetic markers in differing tumor entities as well as in gliomas are increasingly observed. because of the mostly focal appearance of the changes to start with, the molecular-cytogenetic methods with their high dissolving ability are on this occasion essential. in a study which has just been finished, we compared the genetic aberration profile of the diffuse gliomas with the response rate of temozolomide chemotherapy. because of the observation, we assume that there is minority of patients who survive for longer than 5 years after the recognition of a glioblastoma, surgery and a combined radioand chemotherapy. we could show an until now unknown correlation of the patterns of genetic changes with the varying response rate of patients on this chemotherapy. using cgh and loh we could prove that gliomas patients with a tumor which shows a loss of 9p or 10q significantly benefit from temozolomide treatment. the gene for the o (6) methylguanine-methyltransferase (mgmt) is localised on chromosome 10 (10q26) and encoded as the dna repairenzyme o(6) -alkylguanine-dnaalkyltransferase (ogat). the function of ogat is the protection of the cells from alkylating substances by the removal of damaging dna-methylisations i.e. for the demethylisation of methylguanine. the effect of the alkylating cytostaticum temozolomide is based exactly on these damaging dna methylisations. the effect of the chemotherapeuticum is therefore impeded by mgmt and a loss of this would because of this be of advantage for the treated patients. interesting for secondary studies is the question if the appropriate chromosomal regions on the apparently intact second chromosome 10 are mutated, methylated or still active. therefore the expression status and the methylisation pattern of mgmt in the post-characterised gliomas be analysed on a dna-level. for that reason it should be clarified if the mgmt gene on the apparently intact chromosome 10 is still active of if it has been made inactive by the promotor-hypermethylisation and if a reduced dose of the gene will already be sufficient for therapeutic success. current studies on anaplastic astrocytomas and glioblastomas have shown that patients with a promotor hypermethylisation of the mgmt gene benefit significantly from a nitrosoharn substance and temozolomide chemotherapy in comparison to patients whose tumors do not show any methylisation in the mgmt gene (27, 28). deletion or mutation of the p16(ink4a)/arf/p15(ink4b) locus on chromosome 9p21 is among the most common alterations seen in human cancer and in human gliomas. (6-9) the ink4a locus encodes two gene products that are involved in cell cycle regulation through inhibition of cdk4-mediated rb phosphorylation (p16) and binding to mdm2 leading to p53 stabilization (p14arf). the tumor suppressor gene products p16 and p15 are both capable of binding to cdk4 and cdk6, these kinases associate with d-type cyclines and these 390 ralf ketter et al prognostic genetic markers in malignant gliomas binary complexes are responsible for phosphorylation of rb-protein at mid g1 of the cell cycle. the phosphorylation of rb is assumed to be critical for progression through g1 and entry into s-phase of the cell cycle. binding of ink4 to cdk4/6 inhibits its kinase activity and thereby arrests progression through the cell cycle in mid-late g1. (10) over half of the high grade gliomas lack a functional ink4a/arf locus. gliomas with intact ink4a/arf carry mutations in other components of the rb and p53 pathways implicating these two pathways as being absolutely critical in cell growth and death control. (11-14) previous studies showed that deletion of 9p including the ink4a/b locus is a significant unfavorable prognostic factor for survival of glioblastoma patients. (15, 16) further on, this alteration has been reported to be inversely correlated with the chemosensitivity of malignant gliomas. (17) over the past years aberrant dna methylation was shown to be a common molecular lesion in human tumors as well, which had also impact on patient prognosis and treatment response. epigenetic silencing of p16 and p15 was shown in a variety of human neoplasms, in glioma patients hypermethylation is reported in about 30% of the cases. (18-21) whereas in other tumors inactivation of both tumor suppressor genes was associated with prognosis and response to chemotherapy, a prognostic and predictive role in gliomas is not shown. (22-25) on the other hand, epigenetic silencing of the dna repair gene o6methylguanine-dna methyltransferase (mgmt) on chromosome 10q26 by hypermethylation has been linked to a better prognosis for glioblastoma patients treated with alkylating agents like temozolomide. (26-29) a benefit was not observed for patients with mgmt promoter methylation and bcnuchemotherapy. (30) another study comparing different treatment regimens showed that the prognostic effect was only significant when patients were treated simultaneously with radio and chemotherapy. (31) these results suggest that the reported impact of mgmt methylation is strongly dependent on therapeutic modalities and schedules. in our previous study we identified the negative prognostic impact for deletions on 9p and 10q, which can be compensated by temozolomide treatment. (16) in the current setting, our aim was to investigate the methylation status of p15, p16, p14arf and mgmt, and correlate the results with the clinical data of the glioblastoma patients. materials and methods patients and tumor samples the retrospective study included 27 glioblastoma patients (23 primary and 4 secondary gbm) who underwent surgery at the department of neurosurgery of the saarland university, homburg, germany. after radical tumor surgery, all patients received standard radiation therapy (rt) (1.8-2 gy, total dose of 60 gy) and adjuvant temozolomide chemotherapy in case of recurrence. the doses were 150 mg/m² for 5 days in 4 week cycles. specimens of resected tumor were immediately shock frozen in liquid nitrogen and stored at – 80°c or fixed in formalin and embedded in paraffin. all patients gave written informed consent for the use of the tumor samples for genetic analysis. romanian neurosurgery (2010) xvii 4: 388 – 395 391 methylation-specific polymerase chain reaction (ms-pcr) dna of the tumor samples was isolated following standard protocols with chloroforme followed by sodium bisulfite modification. promoter hypermethylation of the mgmt, p15, p16 and p14arf genes were determined by ms-pcr as described previously. (18, 26, 32) the amplified products were electrophoresed on 3.5% agarose gels and visualized with ethidium bromide. methylated blood dna was included in each pcr set as methylated and unmethylated controls, respectively. statistical analyses comparison of survival times between groups defined by methylation status was performed by kaplan-meier curves and with two-sided log rank tests. multivariate cox regression analysis was performed to identify significant predictors for survival. effects in these models were quantified by hazard ratio estimates with 95% confidence intervals. median survival rates were calculated using the kaplan-meier method. results clinical data median age at surgery was 49 years (range 26-70), the sex ratio was 2.375 (19 men / 8 women) (table 1) and median post operative kps was 100 (range 80-100, 18 patients with kps 100). case histologic age/ st mgmtp15p16p14arf type sex [months] status status status status t4789 gbm 38/m 55,3 m u u u 596/98 gbm 32/m 21,1 u u u u 1099/98 gbm 49/m 23,8 u u u u 1782/98 sgbm 26/m 24,2 m u u u 896/99 gbm 51/m 13 u m u u 1326/99 gbm 56/m 19,2 u u u u 1349/99 gbm 54/m 72,6 m u u u 1460/99 gbm 31/f 11,9 m m u u 1795/99 sgbm 31/m 6,9 m u u u 265/00 gbm 46/f 23,1 u m n.a. u 497/00 gbm 58/f 16,9 m m u u 1106/00 gbm 70/m 19,8 m m u u 1691/00 sgbm 39/f 80,2 m u u u 1707/00 gbm 47/m 29,4 u u u u 643/01 gbm 54/f 26,6 u u u u 662/01 gbm 70/m 13,4 u m u u 1405/01 gbm 53/m 7,4 u m m u 6/02 gbm 41/m 26,2 m u u u 369/02 sgbm 37/m 20,2 m u u u 947/02 gbm 46/m 17,7 m m u u 1536/02 gbm 53/m 15,1 u u u u 1940/02 gbm 54/f 14,3 m m u u xxl/02 gbm 45/m 8,6 m u u u 392 ralf ketter et al prognostic genetic markers in malignant gliomas 316/03 gbm 63/f 23,7 u u n.a. u 784/03 gbm 52/m 22,5 m u u u 831/03 gbm 58/m 53 u u n.a. u 1457/03 gbm 37/m 49,1 m m n.a. u methylation analyses the mgmt promoter was methylated in 15/27 cases (55.6%), the p15 promoter was methylated in 10/27 (37%) glioblastomas. all secondary gbm (4/4) showed a methylated mgmt promoter and an unmethylated p15 promoter. methylation of p14arf was absent in all (27/27) investigated gbm. methylation status of p16 was available for 23/27 glioblastomas. hypermethylation of p16 was detected in only 1/23 cases (4.3%) (table 1). clinical outcome overall median survival was 22.5 months with a two-year survival rate of 35.0%. in univariate analyses, mgmt methylation had no impact on overall survival (22.5 vs. 22.1 months, p=0.49, logrank test, fig. 1a), whereas p15 methylation was associated significantly with a shorter overall survival (16.9 vs. 23.8 months; p=0.0252, log-rank test, figure 1b). table 2 contains estimated hazard ratios and pvalues for univariate analyses for all examined variables. we also performed a multivariate analysis including parameters previously identified as significant. as shown in table 3, only p15 methylation emerged as a significant prognostic factor after adjusting for kps, sex, age and mgmt. in the first analysis, the predictors kps and age enter as numerical variables in the model, in the second analysis kps and age are dichotomized with cutoffs 90 and 50 in order to reduce model complexity. the gender variable sex is set to 1 for females and 0 for males. both analyses yield very similar results, identifying p15 methylation as only significant predictor. discussion a better understanding of the genetic alterations predicting disease outcome and therapy response in patients with high grade gliomas will help to optimize both treatment and overall outcome. in our study setting, mgmt promoter methylation had no significant impact on survival, in contrast with other studies that observed a strong effect on patient response and on survival in larger cohorts treated with radioand temozolomidechemotherapy. (26, 28) this discrepancy might result, besides our smaller patient cohort, from the different treatment schedules. actually, comparing various treatment modalities in glioblastomas, the prognostic effect of mgmt methylation was observed only when simultaneous chemoirradiation was administered. (26, 31) further on, our pcr-results showed besides the methylated band also unmethylated bands in a large number of tumors. taking into account this heterogeneity and that we are dealing with diffusely growing gliomas, (33, 34) this observation arises most likely from a different tumor cell population and from normal cells contaminating the tumor sample. nevertheless, this heterogeneous methylation pattern may also result in different amounts of mgmt and therefore affect chemotherapy response. romanian neurosurgery (2010) xvii 4: 388 – 395 393 all evidence collected to date implicates that the ink4a/arf gene products are critically important in control of growth arrest and senescence. loss of p16 and arf expression is associated with many human cancers, particularly gliomas. (20) a number of studies have shown that reconstitution of ink4a/arf expression in glioma cells altered growth characteristics, reduced tumorigenicity and decreased invasive potential. these studies demonstrate the importance of the ink4a/arf pathway in suppression of the neoplastic phenotype and suggest that restoration of a functional ink4a/arf locus will be an important means of controlling the growth of gliomas. (36, 37) a striking observation of our study is the significant correlation of p15 methylation with a poorer clinical course. loss of p15 had not been widely investigated previously as a potential determinant of chemoand radiosensitivity or as a prognostic factor. to our knowledge, this is the first study showing inactivation of p15 by promoter hypermethylation to be a predictor for an unfavorable clinical course. cyclin dependent kinase inhibitors (p16, p21, p27) were shown to exhibit an antitumor effect in malignant gliomas inducing growth arrest and apoptosis in cell culture. (36, 37) further on, retrovirus mediated transfer of ink4a halts glioma formation in a rat model. (38) this corroborates the idea that retrovirus mediated gene transfer of ink4a/b may also be an effective means to arrest human gliomas. therefore, restoring the normal function of p15 by gene therapy is an attractive goal in the treatment of human gliomas. furthermore, our finding that glioblastomas have not simultaneously hypermethylated the investigated tumor suppressor genes on 9p implicates that these tumors carry no general defect in their pattern of cpg island methylation. interestingly, all secondary gbm (4/4) showed a methylated mgmt promoter and an unmethylated p15 promoter which indicates that distinct molecular pathways constitute for primary and for secondary glioblastomas and let them differ both in biological behavior and in clinical outcome. this corresponds to the finding that methylation of p14arf is associated with a shorter patient survival and is mutually exclusive of mgmt promoter methylation except of one case in low grade astrocytoma who underwent progression or recurrence. (35) in our patient cohort that mainly consists of primary glioblastoma, p14arf was not observed, supporting that this alteration is mainly restricted to secondary glioblastoma and therefore in the pathway of astrocytoma progression. although these results need to be confirmed in larger series, our retrospective study suggests that p15 hypermethylation can act as an additional important prognostic factor for survival in glioblastomas. further investigations have to clarify if p15 methylation is a predictive factor for temozolomide treatment response and can act as a prognostic parameter for survival, independent of therapy. references 1. louis dn, ohgaki h, wiestler od, cavenee wk. who classification of tumours of the central nervous system. 4thed. lyon: international agency for research on cancer, 2007 2. burger pc, green sb. patient age, histologic features, and length of survival in patients with glioblastoma multiforme. cancer 1987;59:1617-25 3. kreth fw, warnke pc, scheremet r, ostertag cb. surgical resection and radiation therapy versus biopsy and radiation therapy in the treatment of glioblastoma multiforme. j neurosurg 1993;78:762-6 394 ralf ketter et al prognostic genetic markers in malignant gliomas 4. lacroix m, abi-said d, fourney dr, gokaslan zl, shi w, demonte f, lang ff, mccutcheon ie, hassenbusch sj, holland e, hess k, michael c, et al. a multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. j neurosurg 2001;95:190-8 5. stummer w, reulen hj, meinel t, pichlmeier u, schumacker w, tonn jc, rohde v, oppel f, turowski b, woiciechowsky c, franz k, pietsch t. extent of resection and survival in glioblastoma multiforme: identification of and adjustment for bias. neurosurgery 2008;62:564-76 6. jen j, harper jw, bigner sh, bigner dd, papadopoulos n, markowitz s, willson jk, kinzler kw, vogelstein b. deletion of p16 and p15 genes in brain tumors. cancer res 1994;54:6353-8 7. schmidt ee, ichimura k, reifenberger g, collins vp. cdkn2 (p16/mts1) gene deletion or cdk4 amplification occurs in the majority of glioblastomas. cancer res 1994;54:6321-4 8. simon m, köster g, menon ag, schramm j. functional evidence for a role of combined cdkn2a(p16/p14(arf))/cdkn2b (p15) gene inactivation in malignant gliomas. acta neuropathol 1999;98:444-52 9. rasheed a, herndon je, stenzel tt, raetz jg, kendelhardt j, friedman hs, friedman ah, bigner dd, bigner sh, mclendon re. molecular markers of prognosis in astrocytic tumors. cancer 2002;94:2688-97 10. gil j, peters g. regulation of the ink4b-arfink4a tumour suppressor locus: all for one or one for all. nat rev mol cell biol 2006;7:667-77 11. he j; olson jj, james cd. lack of p16ink4 or retinoblastoma protein (prb), or amplificationassociated overexpression of cdk4 is observed in distinct subsets of malignant glial tumors and cell lines. cancer res 1995;55:4833-6 12. ichimura k, schmidt ee, goike hm, collins vp. human glioblastomas with no alterations of the cdkn2a (p16ink4a, mts1) and cdk4 genes have frequent mutations of the retinoblastoma gene. oncogene 1996;13:1065-72 13. ichimura k, bolin mb, goike hm, schmidt ee, moshref a, collins vp. deregulation of the p14arf/mdm2/p53 pathway is a prerequisite for human astrocytic gliomas with g1-s transition control gene abnormalities. cancer res 2000;60:417-24 14. fulci g, labuhn m, maier d, lachat y, hausmann o, hegi me, janzer rc, merlo a, van meir eg. p53 gene mutation and ink4a-arf deletion appear to be two mutually exclusive events in human glioblastoma. oncogene 2000;19:3816-22 15. kamiryo t, tada k, shiraishi s, shinojima n, nakamura h, kochi m, kuratsu j, saya h, ushio y. analysis of homozygous deletion of the p16 gene and correlation with survival in patients with glioblastoma multiforme. j neurosurg 2002;96:815-22 16. wemmert s, ketter r, rahnenführer j, beerenwinkel n, strowitzki m, feiden w, hartmann c, lengauer t, stockhammer f, zang kd, meese e, steudel wi, et al. patients with high-grade gliomas harboring deletions of chromosomes 9p and 10q benefit from temozolomide treatment. neoplasia 2005;7:88393 17. simon m, voss d, park-simon tw, mahlberg r, köster g. role of p16 and p14arf in radio-and chemosensitivity of malignant gliomas. oncol rep 2006;16:127-32 18. herman jg, graff jr, myöhänen s, nelkin bd, baylin sb. methylation-specific pcr: a novel pcr assay for methylation status of cpg islands. proc natl acad sci u s a 1996;93:9821-6 19. herman jg, jen j, merlo a, baylin sb. hypermethylation-associated inactivation indicates a tumor suppressor role for p15ink4b1. cancer res 1996;56:722-7 20. esteller m, corn pg, baylin sb, herman jg. a gene hypermethylation profile of human cancer. cancer res 2001;61:3225-9 21. uhlmann k, rohde k, zeller c, szymas j, vogel s, marczinek k, thiel g, nürnberg p, laird pw. distinct methylation profiles of glioma subtypes. int j cancer2003;106(1):52-9 22. uchida t, kinoshita t, nagai h, nakahara y, saito h, hotta t, murate t. hypermethylation of the p15ink4b gene in myelodysplastic syndromes. blood 1997;90:1403-9 23. kudoh k, ichikawa y, yoshida s, hirai m, kikuchi y, nagata i, miwa m, uchida k. inactivation of p16/cdkn2 and p15/mts2 is associated with prognosis and response to chemotherapy in ovarian cancer. int j cancer 2002;99:579-82 24. lee m, sup han w, kyoung kim o, hee sung s, sun cho m, lee sn, koo h. prognostic value of p16ink4a and p14arf gene hypermethylation in human colon cancer. pathol res pract 2006;202:415-24 25. rasheed a, herndon je, stenzel tt, raetz jg, kendelhardt j, friedman hs, friedman ah, bigner dd, bigner sh, mclendon re. molecular markers of prognosis in astrocytic tumors. cancer 2002;94:2688-97 26. paz mf, yaya-tur r, rojas-marcos i, reynes g, pollan m, aguirre-cruz l, garcía-lopez jl, piquer j, safont mj, balaña c, sanchez-cespedes m, garcíavillanueva m, et al. cpg island hypermethylation of the dna repair enzyme methyltransferase predicts response to temozolomide in primary gliomas. clin cancer res 2004;10:4933-8 27. stupp r, mason wp, van den bent mj, weller m, fisher b, taphoorn mj, belanger k, brandes aa, marosi c, bogdahn u, curschmann j, janzer rc, et al. romanian neurosurgery (2010) xvii 4: 388 – 395 395 european organisation for research and treatment of cancer brain tumor and radiotherapy groups; national cancer institute of canada clinical trials group. radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. n engl j med 2005;352:987-96 28. hegi me, diserens ac, gorlia t, hamou mf, de tribolet n, weller m, kros jm, hainfellner ja, mason w, mariani l, bromberg je, hau p, et al. mgmt gene silencing and benefit from temozolomide in glioblastoma. n engl j med 2005;352:997-1003 29. watanabe t, katayama y, komine c, yoshino a, ogino a, ohta t, fukushima t. o6-methylguaninedna methyltransferase methylation and tp53 mutation in malignant astrocytomas and their relationships with clinical course. int j cancer. 2005 feb 10;113:581-7 30. blanc jl, wager m, guilhot j, kusy s, bataille b, chantereau t, lapierre f, larsen cj, karayan-tapon l. correlation of clinical features and methylation status of mgmt gene promoter in glioblastomas. j neurooncol 2004;68:275-83 31. crinière e, kaloshi g, laigle-donadey f, lejeune j, auger n, benouaich-amiel a, everhard s, mokhtari k, polivka m, delattre jy, hoang-xuan k, thillet j, et al. mgmt prognostic impact on glioblastoma is dependent on therapeutic modalities. j neurooncol 2007;83:173-9 32. sato f, harpaz n, shibata d, xu y, yin j, mori y, zou tt, wang s, desai k, leytin a, selaru fm, abraham jm, et al. hypermethylation of the p14(arf) gene in ulcerative colitis-associated colorectal carcinogenesis. cancer res 2002;62:1148-51 33. loeper s, romeike bf, heckmann n, jung v, henn w, feiden w, zang kd, urbschat s. frequent mitotic errors in tumor cells of genetically microheterogeneous glioblastomas. cytogenet cell genet 2001;94:1-8 34. jung v, romeike bf, henn w, feiden w, moringlane jr, zang kd, urbschat s. evidence of focal genetic microheterogeneity in glioblastoma multiforme by area-specific cgh on microdissected tumor cells. j neuropathol exp neurol 1999;58:993-9 35. watanabe t, katayama y, yoshino a, yachi k, ohta t, ogino a, komine c, fukushima t. aberrant hypermethylation of p14arf and o6-methylguaninedna methyltransferase genes in astrocytoma progression. brain pathol 2007;17:5-10 36. komata t, kanzawa t, takeuchi h, germano im, schreiber m, kondo y, kondo s. antitumor effect of cyclin-dependent kinase inhibitors (p16(ink4a),p18(ink4c), p19(ink4d). p21 (waf1(cip1) and p27 (kip1)) on malignant glioma cells. br j cancer 2003;88:1277-80 37. inoue r, moghaddam ka, ranasinghe m, saeki y, chiocca ea, wade-martins r. infectious delivery of the 132 kb cdkn2a/cdkn2b genomic dna region results in correctly spiced gene expression and growth suppression in glioma cells. gene ther 2004;11:1195204 38. strauss be, fontes rb, lotfi cf, skorupa a, bartol i, cipolla-neto j, costanzi-strauss e. retroviral transfer of the p16ink4a cdna inhibits c6 glioma formation in wistar rats. cancer cell int 2002;2:1-9 microsoft word 13cotrutzactivemolecules 94 carmen elena cotrutz et al active molecules in regenerative medicine active molecules in regenerative medicine carmen elena cotrutz1, t.petreuş1, cristina dascălu2 1department of cell and molecular biology 2department of medical informatics and biostatistics university of medicine and pharmacy “gr.t. popa”, iasi, romania background biomaterials play central roles in modern strategies in regenerative medicine and tissue engineering as designable biophysical and biochemical environments that direct cellular behavior and function. new generations of synthetic biomaterials are being developed at a rapid pace for use as three-dimensional extracellular microenvironments to mimic the regulatory characteristics of natural extracellular matrices (ecms) and ecmbound growth factors, both for therapeutic applications and basic biological studies. the ultimate decision of a cell to differentiate, proliferate, migrate, apoptosis or perform other specific functions is a coordinated response to the molecular interactions with these ecm effectors. the flow of information between cells and their ecm is highly bidirectional, as, for example, observed in processes involving ecm degradation and remodeling. matrix metalloproteinases (mmp) are zn and ca dependent enzymes and represent a class of structural and functional kindred enzymes that are involved in altering the natural compounds of the extracellular matrix [1,2]. mmp are synthesized as zymogens that can be inhibited by 4 classes of natural inhibitors called timps (tissue inhibitor for matrix metalloproteinases) [3]. mmp plays important roles in physiological processes, but their overexpression plays also crucial roles in pathological processes as multiple sclerosis, arthritis, alzheimer disease and especially in cancer and metastasis [4-8]. among these biological molecules we have investigated expression of metalloproteinase 8 (mmp-8) and metalloproteinase 9 (mmp-9) in the periimplantar tissues remodelling. methodology we have performed an indirect immunohistochemical technique using hematoxilin/eosin (he) staining by peroxidase induced conversion of dab (3,3-diaminobenzidine), an enzyme conjugate, which reveals the localisation of antibody-bound antigenic sites by means of a coloured reaction. dab, a chromogenic substrate for peroxidase, stains the antigenantibody sites in brown, indicating the presence of the metalloproteinases-8 (mmp-8) in the cells surrounding the implant. mmp-8 are usually present in the neutrophils infiltrating the connective tissue or bone in an accute phase of inflamatory process. data analysis was done using an olympus bx40 optical microscope with a color ccd camera mounted on. we have also performed molecular docking and molecular dynamics investigations regarding simulations of the catalytic romanian neurosurgery (2011) xviii 1: 94 – 95 95 domain of a known matrix metalloproteinase (mmp), in the absence of the substrate or a known inhibitor, starting from proteindatabank published data (id-1qib). this study emphasizes the role of the atomic position in this site regarding to further simulations for conceiving a rather modulating inhibitor for these enzymes. results and conclusions immunolabelling with mmp-8 is reduced and limited to the perivascular area. mmp-9 has a more diffuse presence, without precise localization and therefore shows no remodeling processes (1st and 2ndtype). after 2 months mmp-8 immunolabelling was more pronounced outside blood vessel walls as a proof of chronic inflammation. mmp-9 was found perivascular (in the wall of small capillaries) more diffuse but also more intense. this suggests a lot of active remodeling here (3rd and 4th type). for 2nd type mmp-9 is present in a diffuse but more intense way suggesting accelerated tissue remodeling. these preliminary phenomenon modulated by the presented molecules are crucial for newly grown bone tissue formation and healing, even allowing implant primary fixation. molecular modelind and dynamic studies on mmp2 catalytic site showed that root mean square fluctuation (rmsf) was performed, compared with the nmr starting structure and the hydrophobic solvent accessible surface area (hsas) of the mmp2 catalytic site. we have observed small fluctuations for the catalytic zn area (high stability); however we have noticed some fluctuations, especially in some loop regions near the catalytic site of the mmp, in 192-250 region of the mmp2 pdb file. this study emphasizes the role of the atomic position in the catalytic site for mmps, regarding to further simulations for conceiving a rather modulating inhibitor for these enzymes. references 1. shapiro sd. “a concise yet informative stroll through matrix metalloproteinases and timps.” j.cell.sci., no. 113, vol.19, 2000, pp.3355-3356. 2. woessner jf jr. “matrix metalloproteinase inhibition. from the jurassic to the third millennium”. ann n y acad sci. vol.30, no.878, 1999, pp.388-403. 3. brew k, dinakarpandian d, nagase h, “tissue inhibitors of metalloproteinases: evolution, structure and function.” biochim biophys acta, vol.1477, 2000, pp.1-2. 4. fang l, huber-abel f, teuchert m, hendrich c, dorst j, schattauer d, zettlmeissel h, wlaschek m, scharffetter-kochanek k, tumani h, ludolph ac, brettschneider j. “linking neuron and skin: matrix metalloproteinases in amyotrophic lateral sclerosis (als)”. j neurol sci. 2009, epub. 5. ribeiro bf, iglesias dp, nascimento gj, galvão hc, medeiros am, freitas ra. “immunoexpression of mmps-1, -2, and -9 in ameloblastoma and odontogenic adenomatoid tumor.” oral dis. 2009, epub. 6. korpos e, wu c, sorokin l. “multiple roles of the extracellular matrix in inflammation.” curr pharm des. vol.15 no.12, 2009, pp. 1349-57. 7. ando a, hagiwara y, tsuchiya m, onoda y, suda h, chimoto e, itoi e. “increased expression of metalloproteinase-8 and -13 on articular cartilage in a rat immobilized knee model”. tohoku j exp med. no.217, vol 4, 2009, pp.27127-8 8. gentner b, wein a, croner rs, zeittraeger i, wirtz rm, roedel f, dimmler a, dorlaque l, hohenberger w, hahn eg, brueckl wm. “differences in the gene expression profile of matrix metalloproteinases (mmps) and their inhibitors (timps) in primary colorectal tumors and their synchronous liver metastases. anticancer res. no.29, vol.1, 2009, pp.67-74. doi: 10.33962/roneuro-2021-088 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours. speech disorders orest i. palamar, andriy p. huk, dmytro s. teslenko, ruslan v. aksyonov, dmytro i. okonskyi, nazarii v. lazko romanian neurosurgery (2021) xxxv (4): pp. 511-517 doi: 10.33962/roneuro-2021-088 www.journals.lapub.co.uk/index.php/roneurosurgery postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours. speech disorders orest i. palamar1, andriy p. huk1, dmytro s. teslenko1, ruslan v. aksyonov1, dmytro i. okonskyi1, nazarii v. lazko2 1 si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine 2 municipal non-commercial enterprise “kyiv city clinical hospital no. 1”, kyiv, ukraine abstract neurosurgical approaches to lesions of the lateral and the third ventricles are divided into two fundamentally different groups: transcortical neurosurgical approaches, including endoscopic and interhemispheric transcallosal microneurosurgical approaches. complications in surgery of lateral and third ventricle tumours are often associated with the specific approach technique and could be transient. we analyzed postoperative neurological complications and the approach criteria on mri or ct scans in postoperative period such as localization of corticotomy, distance from corticotomy to coronal suture, “angle of attack” after the frontal transcortical approach to the lateral and third ventricle based on 54 cases and presume transient nature of specific to approach complications and approaches’ factors that have role in postoperative mutism. introduction neurosurgical approaches to the tumors of the lateral and the third ventricles are divided into two fundamentally different groups: transcortical neurosurgical approaches, including endoscopic and interhemispheric transcallosal microneurosurgical approaches. two different approaches to the ventricular system cause distinct brain injuries: tightly compressed commissural fibers of the corpus callosum are injured by the interhemispheric transcallosal approach, while the transcortical approach damages gray and white matter of the brain on its way [1,2]. complications in surgery of lateral and third ventricle lesions are often associated with the specific approach technique and today is a widely discussed problem [3,4]. when applying the abovementioned approaches, the most common complications are aphasia, mutism, hemiparesis, seizure, memory impairment, apatheia/abulia, endocrinopathy, subdural hygroma, etc. [1,16]. keywords endoscopic, lateral ventricle, mutism. third ventricle, transcortical approach corresponding author: nazarii v. lazko si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine naztar02@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 512 orest i. palamar, andriy p. huk, dmytro s. teslenko et al. manifestations of mutism, which are currently little studied in the context of the use of these neurosurgical approaches, constitute a field of particular scientific interest. mutism is a clinical state, in which a conscious patient is unwilling to or unable to speak, resulting in the absence or marked paucity of verbal output. the patients can be mute while their ability to write or comprehend spoken language is intact [1,11]. mutism can occur as a result of damage to the broca area, premotor cortex, and supplementary motor area of the dominant hemisphere, association fibers of white matter, the anterior part of the cingulate gyrus, commissural fibers of the corpus callosum, damage of the corticalbulbar fibers bilaterally, bilateral thalamotomy and damage of reticular formation of the midbrain [ 7,5]. materials and methods a retrospective analysis of 54 patients with neoplasms and lesions of lateral (anterior horn, body, atrium) and third ventricles who underwent surgery in the period from october 2015 to may 2021. male – 26 patients, the mean age was 44.5 years (range: 20-71 years), female – 28 patients, the mean age was 42.4 years. (range: 15-74 years). mean preoperative karnofsky performance statuse score (kps) was 76.37. localization of neoplasm: the third ventricle 41 (75.9 %) patients; lateral ventricular tumors 13 (24.1 %) patients. histological distribution depending on the location is given in table. no. 1. histopathological evaluation of these 54 neoplasms and lesions indicated 15 distinct diagnostic entities including brain tumors of glial origin with invasion in the ventricular system (diffuse and anaplastic astrocytoma, glioblastoma, oligodendroglioma, and anaplastic oligoastrocytomas) accounted for 35,2% (fig. 1), subependymoma and ependymomas varying degrees of malignancy – 14,8%, colloid cysts 13%, central neurocytomas 11.1%, craniopharyngiomas 11.1%, germinomas 7.4%, others 7.4% histopathology lateral ventricles (n-13) third ventricle (n41) pilocytic astrocytoma, who gr i 1 diffuse astrocytoma, who gr ii 2 3 anaplastic astrocytoma, who gr iii 3 glioblastoma, who gr iv 1 5 oligodendroglioma, who gr ii 1 2 anaplastic oligoastrocytomas who gr iii 1 subependymoma, who gr i 1 1 typical and atypical meningiomas, who gr i та ii 2 central neurocytomas, who gr ii 4 2 pineoblastoma, who gr iv 1 ependymoma, who gr ii, anaplastic ependymoma who gr iii 1 5 craniopharyngioma, who gr i 6 colloid cysts 7 germinomas 4 mature teratoma 1 table 1. histopathology of intraventricular neoplasms. a. b. figure 1. a-b. tumor in the posterior part of the third ventricle (glioblastoma), preoperative contrast-enhanced, t1w images. preoperative symptoms include: cephalalgia 49 (90.7 %) patients, sings of elevated icp 32 (59.25 %) patients, neurocognitive disorders and psychoorganic syndrome 10 (18.5%) patients, oculomotor dysfunction 10 (18.5%) patients, motor deficits 9 (16.6%) patients, short term memory loss 8 (14.8%) paients, decreased visual acuity and loss of peripheral vision 7 (12.9%) patients, 513 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours endocrinopathy 4 (7.4%) patients, seizures 2 (3.7%) patients. a. b. figure 2. a-b. tumor in the posterior part of the third ventricle (ependymoma), preoperative contrast-enhanced t1w images and t2w images. preoperative contrast-enhanced magnetic resonance imaging (mri) (fig.2) of the brain and computer tomography (ct) were also used for the preoperative planning of the approach side, optimal for the resection of the neoplasm and minimization of postoperative complications. we analyzed the localization of the neoplasms in the ventricular system, the side with greater distribution, signs of occlusive hydrocephalus, the side with the wider interventricular foramen of monro, localization of estimated corticotomy ("entry point"), and the best "angle of attack ". in surgery of neoplasms of the lateral (anterior horn, body, atrium) and third ventricle, we use endoscopic frontal (craniotomy over the frontal lobe) transcortical (corticotomy through the upper or middle frontal gyrus) approache. we perform an endoscopic frontal transcortical approach via parasagittal craniotomy over the non-dominant hemisphere of the brain (or over the priority hemisphere for approach) with the centration at the kocher’s point. corticotomy up to 2.2 cm. is carried out through the top of the middle or upper frontal gyrus. the next stage is white matter fibers dissection to the front horn of the lateral ventricle and the subsequent introduction of intracerebral retractors. depending on the location of the tumor or lesion in the third ventricle, its size, and available hydrocephalus we used transventricular (through the cavity of the lateral ventricles) approach and further transforaminal (approach to the third ventricle through the interventricular foramen of monro) or extended transforaminal transchoroidal approach (approach to the third ventricle through the interventricular foramen of monro with the anterior choroidal dissection). surgery was performed using an endoscopic stand based on the hdendoscope “image-1hd” (karl storz, germany). rigid endoscopes "karl storz" 4 mm in diameter with viewing angles of 0 and 35 degrees were used as the main tool for visualization of the operating field. approach through the right hemisphere has been performed in 38 (70.4 %) cases and through the left one in 16 (29, 6 %) cases. endoscopic frontal transcortical approach to the lateral ventricles was used in 13 (24.1 %) cases; endoscopic frontal transcortical transentricular transforaminal approach to the third ventricle 13 (24.1 %) cases, extended transforaminal transchoroidal approach 28 (52%) cases. in all cases, a 100% endoscopic technique ("fully endoscopic resection") was performed. in case of clinical and mr signs of occlusive hydrocephalus and with the purpose of preventing the progression of hydrocephalus in 22 (40.7%) cases with simultaneous resection of tumor we performed endoscopic third ventriculostomy. in the early postoperative period, all patients underwent contrast-enhanced ct or mri in order to detect residual component of the tumor, potential postoperative ischemia and bleeding, and evaluations of the ventricular system. the follow-up ranged from 3 to 42 months, at average 12.5 months. during the follow-up examination of patients, which was performed approximately 2-4 months after the surgery, we assessed the overall health status, neurological status, contrast-enhanced mri of the brain (fig. 3). on mri we evaluated the presence of residual component of the tumor or tumor growth, ventricular system (presence of hydrocephalus), expansion/narrowing of the transcortical channel in the matter of the frontal lobe. results and discussion extent of resection in our series: gross total resection/near total resection 34 (63 %) patients, subtotal/partial resection 15 (27.7 %) cases, biopsy 5 (9.2 %) cases. 39 (72.2 %) patients had no postoperative complications, 15 (27.7 %) patients had at least one postoperative complication. postoperative complications included: 514 orest i. palamar, andriy p. huk, dmytro s. teslenko et al. a. b. c. d. figure 3. a-b. tumor in the right lateral ventricle (ependymoma), preoperative t1w images. c-d. 5-month postoperative contrast-enhanced t1w images depicted gross total resection of the tumor. speech disorders such as mutism 6 (11.1 %) patients and apathia/abulia 5 (9.2%) patients . we observed that 4 patients with postoperative manifestations of apathia/abulia also had concomitant mutism. in the postoperative period, at the follow-up examination 2-4 months after the surgery, a complete or partial regression of both mutism and apathia/abulia was observed in all 6 patients; short term, "fixation" memory loss 5 (9.2 %) patients. in all 5 cases the endoscopic transcortical transventricular transforaminal or extended transforaminal transchoroidal approach to the third ventricle was applied. in the postoperative period, at the follow-up examinations during the next 2-6 months after the surgery, a complete or partial regression was observed in 3 patients; oculomotor dysfunction 5 (9.2%) patients. oculomotor dysfunction included paresis of n. oculomotorius and/or parinaud syndrome and in all 5 cases have been associated with tumor resection of the posterior part of the third ventricle. in the postoperative period, complete or partial regression was observed in 1 patient; motor deficits 4 (7, 4%) patients. in our series, we associate the occurrence of this complication either with resection of the glial tumor (originated in close proximity to corticospinal tracts) with the invasion in the third ventricle or with the premotor cortex and supplementary motor area injury. we observed the complete regression in 2 patients during the next 4 months after the surgery; neurocognitive disorders 4 (7.4%) patients which regressed in 1 patient 4 months after the surgery; endocrinopathy 3 (5.5%) patients. we associate this complication with the resection of tumors that have been tightly fused to the hypothalamic area of the bottom of the third ventricle. regression was observed in 1 patient after 3 months. postoperative hemorrhage – 2 (3,7%) patients; postoperative wound infection occurred in 1 (1.85%) patient; postoperative meningitis 1 (1.85%) patient. in our series, seizures, as a postoperative complication, did not occur. postoperative mortality 1 (1.9%) patients due to hypothalamic dysfunction, leading to acute electrolyte shifts, after the resection of craniopharyngioma with the significant spread in the third ventricle. compared with the series brian d. milligan at al in the group transcortical approach, short-term memory loss in the postoperative period was recorded in 6 (12 %) patients, that is 2.8% higher than in our series. motor deficits were recorded in 18 (35%) patients, that is 27.6 % higher than in our series. neurocognitive disorders were 4.6% higher than in our series, and the percentage of patients with endocrinopathy was the same as in the series brian d. milligan at al. [16] the average kps on the day of discharge was 83,35%. in the early postoperative period, all patients underwent contrast-enhanced ct or mri of the brain and, among other things, we evaluated the following approach criteria (table. 2) using radiant dicom viewer software: 1) localization of corticotomy, "entry point" (upper/middle frontal gyrus (upper parts); 515 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours 2) the distance from the coronal suture to the corticotomy in front; 3) "angle of attack " (the angle between the sagittal plane and plain "entry point" the point of entry into the frontal horn of the lateral ventricle). (fig. 4). localization of corticotomy right hemisphere n-38 (70,4%) left hemisphere n -16 (29,6%) upper frontal gyrus 12 (31,5 %) 7 (43,7%) middle frontal gyrus, upper part 26 (68,5 %) 9 (56,3%) distance from the coronal suture to the corticotomy (mean, min-, max). 2,8 cm, min1,2, max3,6 2,8 cm, min0,5, max2,9 "angle of attack" (mean, min-, max). 27,4○, min-17○, max35○ 26,7○, min-21○, max34○ table 2. approach criteria a. b. figure 4. a. tumor of the third ventricle (craniopharyngioma), preoperative, contrast-enhanced t1w image. b. 4-month postoperative contrast-enhanced t1w images, “angle of attack” calculation using using radiant dicom viewer software. in our series, mutism, as a manifestation of specific speech disorders caused by the frontal transcortical approach to the lateral and third ventricles, was observed in the postoperative period in 6 (11.1 %) patients (approach on the left 6 patients). this clinical condition was transient and regressed within 4 months after the surgery. we indicate that corticotomy in patients who had postoperative mutism was performed in the upper frontal gyrus – 4 patients, in the middle frontal gyrus – 2 patients. we presume that postoperative mutism is related to the following features of the approach: 1) the approach side dominant hemisphere. 2) corticotomy in the upper frontal gyrus and at a distance of less than 2 cm. from the coronal suture. 3) "angle of attack" less than 26.7○. in their series, s. asgari et al reported that when applying the transcortical approach, transient mutism occurred in 11% of patients, while via interhemispheric/transcallosal approach in 18% of patients, that equals and is 8.2% higher compared to our series respectively [7]. r. g. ellenborg concluded that speech disorders are a fairly common complication when applying a transcortical approach through the dominant hemisphere and occur in 1030% of patients [13]. in the article by brian d. milligan et, when comparing transcortical and interhemispheric approaches, mutism is not distinguished as a complication, instead this clinical condition is classified as a separate group of complications aphasia/abulia, which occurs in 31% and 25% of cases, respectively, when applying transcortical and transcallosal approaches [16]. in our series of cases, aphatia/abulia manifested in the postoperative period in 5 (9.2%) patients, in all cases together with mutism. it is uncertain whether there is a direct link between apathy, abulia and mutism. however, there is some evidence that the medial part of the frontal lobes, especially the cortex and fibers of the anterior cingulate gyrus, may play a role in manifestations of aphatia/abulia along with signs of mutism, as well as akinetic mutism [12]. the anterior part of the cingulate gyrus has a complex relationship with the limbic structures, other parts of the frontal cortex and periaqueductal gray matter of the midbrain. it is involved in interaction between the decision-making process and the "emotional" world of the limbic system, which is considered crucial for the start of speech and vocalization [6,19]. functionally, the corpus callosum is closely related to speech function [9,20]. mutism often occurs in the postoperative period after the interhemispheric approach with callosotomy [8,18]. jin hong et al suggested that damage to the corpus callosum can lead to speech disorders [15]. ishizaki et al describe that transcallosal diaschisis is a possible mechanism of aphasia [14]. in our opinion, the commissural fibers of the corpus callosum and forceps minor fibers injury while applying the transcortical approach to the ventricular system, may play a role in the development of transient mutism. 516 orest i. palamar, andriy p. huk, dmytro s. teslenko et al. utilizing magnetic resonance diffusion-tensor tractography and comparing two different localizations of corticotomy (through the middle frontal gyrus and through the upper frontal gyrus) applying transfrontal transcortical access, t. szmuda et al concluded that the application of access through the upper and middle frontal gyrus one way or another leads to trauma, including the upper longitudinal fascicles ii, which is partially responsible for the relationship between the fields of brock and wernicke [21]. although most of the fibers involved in the speech network and connecting the middle and lower frontal gyrus and posterior part of superior temporal gyrus are a part of the so-called upper longitudinal fasciculus iii (anterior fibers of arcuate), they are located more caudally to the potential injury of the white matter via frontal transcortical approach in our cases [17]. injury to the supplementary motor area and the premotor cortex, especially of the dominant hemisphere of the brain, can also cause mutism. penfield and welch used cortical stimulation to identify the boundaries and functions of this area. the connections of this cortex are quite branched and include the upper temporal gyrus, the intraparietal sulcus, the caudate nucleus, the thalamus, and other. [10] conclusion the endoscopic frontal transcortical approach in surgery of neoplasm and lesions of the lateral and third ventricle is effective and minimally invasive approach. the transient nature of postoperative complications is due to the gentle manipulations of anatomical structures when applying this approach. specific surgical approach complications such as mutism, apathia/abulia, motor deficits (due to the injury of the premotor cortex and supplementary motor area) were mostly transient and had a tendency to regress immediately in the postoperative period and most of them completely regressed from 2 to 4 months after the surgery. the nature of mutism as a manifestation of speech complications when applying endoscopic frontal transcortical approach is multifactorial. the development of postoperative speech complications, namely of transient mutism when applying the endoscopic frontal transcortical approach is not a frequent complication and according to our observations regresses within 4 months. in our opinion, in order to reduce the risk of mutism in the postoperative period, endoscopic frontal transcortical approach should be performed via the non-dominant hemisphere (unless otherwise specified during preoperative planning) and in the upper part of the middle frontal gyrus at a distance more than 2 cm from the coronal suture. corticotomy should be gentle and based on our series no more than 2.2 cm in length, "angle of attack" should be no less than 26.7○ which reduces cerebral cortex and white matter injury and the risk of postoperative complications associated with the application of this approach, including manifestations of mutism. references 1. altshuler ll, cummings jl, mills mj (1986) mutism: review, differential diagnosis, and report of 22 cases. amer j psychiatry 143:1409 1414. 2. anderson rc, ghatan s, feldstein na. surgical approaches to tumors of the lateral ventricle. neurosurg clin n am. 2003;14(4):509-525. 3. apuzzo ml, chikovani ok, gott ps, et al. transcallosal, interfornicial approaches for lesions affecting the third ventricle: surgical considerations and consequences. neurosurgery. 1982;10(5):547-554. 4. apuzzo mlj (1987) surgery of the third ventricle. williams & wilkins, baltimore. 5. apuzzo mlj, litofsky ns. surgery in and around the anterior third ventricle. in: apuzzo mlj, ed. brain surgery: complication avoidance and management. new york: churchill-livingstone; 1993:541-579. 6. arnts h, van erp ws, lavrijsen jcm, van gaal s, groenewegen hj, van den munckhof p. on the pathophysiology and treatment of akinetic mutism. neurosci biobehav rev. 2020 may;112:270-278. 7. asgari s, engelhorn t, brondics a, sandalcioglu ie, stolke d. transcortical or transcallosal approach to ventricleassociated lesions: a clinical study on the prognostic role of surgical approach. neurosurg rev. 2003 jul;26(3):1927. 8. bogen je (1987) physiologicai consequences of complete or partial commissural section. in: apuzzo mlj (ed) surgery of the third ventricle. williams & wilkins, baltimore london los angeles sydney, pp 175-194. 9. catani m, jones dk, ffytche dh, et al. perisylvian language networks of the human brain. ann neurol 2005;57:8–16. 10. crutchfield js, sawaya r, meyers ca, moore bd 3rd. postoperative mutism in neurosurgery. report of two cases. j neurosurg. 1994 jul;81(1):115-21. 11. cummings jl, benson df, houlihan jp, etal (1983) mutism: loss of neocortical and iimbic vocalization. j nerv ment dis 171:255-259. 12. darby rr, joutsa j, burke mj, fox md. lesion network 517 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours localization of free will. proc natl acad sci u s a. 2018 oct 16;115(42):10792-10797. 13. ellenbogen rg. transcortical surgery for lateral ventricular tumors. neurosurg focus. 2001 jun 15;10(6):e2. 14. ishizaki m, ueyama h, nishida y, et al. crossed aphasia following an infarction in the right corpus callosum. clin neurol neurosurg 2012;114:161–5. 15. jin hong , song xiaojing , song , et al. clinical analysis of 14 cases of corpus callosum infarction. chin j clin res 2010;23:1016–1016. 16. milligan bd, meyer fb. morbidit y of transcallosal and transcor tical approaches to lesions in and around the lateral and third ventricles: a single-institution experience. neurosurgery. 2010 dec;67(6):1483-96; discussion 1496. 17. nakajima r, kinoshita m, shinohara h, nakada m. the superior longitudinal fascicle: reconsidering the frontoparietal neural network based on anatomy and function. brain imaging behav. 2020 dec;14(6):2817-2830. 18. sass kj, novelly ra, spencer dd, spencer ss. postcallosotomy language impairments in patients with crossed cerebral dominance. j neurosurg. 1990 jan;72(1):85-90. 19. shenhav a, botvinick mm, cohen jd. the expected value of control: an integrative theory of anterior cingulate cortex function. neuron. 2013 jul 24;79(2):217-40. 20. sussman nm, gur rc, gur re, o'connor mj. mutism as a consequence of callosotomy. j neurosurg. 1983 sep;59(3):514-9. doi: 10.3171/jns.1983.59.3.0514. 21. szmuda t, słoniewski p, szmuda m, waszak pm, starzyńska a. quantification of white matter fibre pathways disruption in frontal transcortical approach to the lateral ventricle or the interventricular foramen in diffusion tensor tractography. folia morphol (warsz). 2014 may;73(2):129-38. vegamontesinoss_flat2014 90 vega-montesinos et al flat panel detector-ct for cerebral arteries imaging flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note susana vega-montesinos1, marco zenteno1, carlos andres ferreira-prada1, jorge a. santos-franco2, angel lee3, luis rafael moscote salazar4 1instituto nacional de neurologia y neurocirugia “manuel velasco suarez”, mexico 2imss “la raza”, mexico 3hospital angeles del pedregal, mexico 4universidad de cartagena, colombia introduction the diagnosis and management of cerebral vascular disease has improved due to the constant development of imaging techniques. digital subtraction angiography (dsa) is the gold standard, but still involves high cost and risk (1). the certainty of the images obtained by noninvasive methods currently has facilitated the identification of therapeutic surgical or endovascular decisions in many centers of the world regardless of the asd. at other times, the ct angiography is useful as a tool for control and monitoring in patients already treated (2–6), however it is still ineffective for proper evaluation of intra-stent stenosis (7–9). the flat-panel detector ct (fpdct) is a relatively new technology that provides extremely useful images in cerebral vascular disease, especially for its ability to show relationships between soft tissue and bone, detect complications during the procedure, display of intra and extracranial coils and stents, however it require the intraarterial injection of contrast material (10–12). there are few articles that show the intravenous injection technique for fpdct. n this paper we show a novel technique developed at the national institute of neurology and neurosurgery for imaging with intravenous injection. equipment: we used a biplane system c-arm with flat detector angiography, axiom artis dba (siemens, erlangen, germany) with a system of dynamic imaging plane detector with high spatial resolution and contrast resolution of 14 bits, detector input plane 30 x 40 (48 cm diagonal) with a pixel size of 154 um and input level detector 20 x 20 (25 cm diagonal) with a pixel size of 184 um, with acquisition of dsa images in real time with up to 7.5 imag./s, 10, 15, january 30 imag. / s in biplane in 1024 x 1024 matrix romanian neurosurgery (2014) xxi 1: 90 – 95 91 with a depth of up to 14-bit digitization (7.5 imag./s at 2,480 x 1,920 matrix) dr dynavision rotational angiography and dsa dynavision up 60 imag./s. the specifications for the processing of the images were: standardized platform with syngo user interface, simultaneous display of subtraction fluoroscopy/digital subtraction fluoroscopy and original images by roadmap plus (digital subtraction fluoroscopy plus); dicom print (services printing), dicom send/storage commitment (commitment storage/ shipping) and dicom query/retrieve (search and retrieval); full dicom functionality in both, patient data acquisition and in documentation and archiving; and dyna ct program (siemens) intravenous fd-cta imaging was performed after removal of the diagnostic catheter and introducer sheath about 25 to 30 min after the last dsa series. the patient was asked to close the eyes and to breathe calmly. a dedicated fd-ct program (dynact, siemens ag, healthcare sector, forchheim, germany) with a mask run (native) and a second fill run (contrast-enhanced) rotation as described before [11] with an optimised contrast medium application method was used. data acquisition per run was carried out using the following parameters: acquisition time 10 s per run, 70 kv, 512 × 512matrix, projection on30 × 40cm flatpanel size, 200° total angle, 0.8°/frame, 250 frames total. to control contrast medium influx we used the bolus watching method [11] to visualise a proper time point to start the fill run acquisition as follows (fig. 1): contrast medium injection is started 5 s after the start of the mask run. the mask run acquisition is completed within 10 s. the c-arm returns to the start position, this requires an interval of 5 s. it can be assumed that within 10 s contrast material injected into a peripheral cubital vein will not reach the cerebral arteries. after the c-arm returns to the start position (10 s after contrast medium injection) then standard 2d-dsa acquisitions are initiated at a rate of two images per second. when contrast opacification of the large arteries is visible the second rotation (fill run) is initiated manually. acquisition method fpd-ct: iopamidol 300 (0.612 g) (iopamiron, bayer schering, germany) was injected via, preferably left cubital vein. the injection volume was 60 cc at a rate of 4cc/seg, injection pressure 150 psi with a power injector (mark v provis angiographic injection system, medrad). for adquisition we used the program dynact (siemens) with the following parameters: 20 seconds of rotation, 60 frames per second (1200 images) with a projection angle of 219° ctdiw about 35mgy, which allows the reconstruction of a not truncated volume of approximately 25cm (on a diagonal plane) with a pixel size of 184um. the patient is positioned supine on the angiography table, as usual, upon proper 92 vega-montesinos et al flat panel detector-ct for cerebral arteries imaging head position confirmation by fluoroscopy, is activated the head dynact 20s program to immediately start injecting intravenous contrast material. with a delay of 10 seconds starts acquisition of the mask (mask run) that surely leads to the acquisition fill run, without using the display method of the contrast bolus described in elsewhere article (7). the images were sent to the workstation leonardo (siemens). the images obtained by the described technique in this article were compared with dsa images, volumetric reconstructions and of mip angiotomography. dsa images were obtained in two teams, one axiom artis angiography (siemens) and sygo angiography (siemens) and those of angiography by 64-slice ct scanner (siemens). the images were compared by two independent observers and results were collated later. the image comparison was made in order to assess specific aspects: 1) subjective, such as vascular image quality, image quality of intra-aterial devices such as stents and coils, image quality within stents, quality of close vascular images or embedded within bone structures, and 2) objectives, such as vascular diameter measurement, measurement of intracranial aneurysms, measuring of intra-stent stenosis, relation with bony structures. ilustrative case case: female, 40 years old patient, who after indirect cervical trauma developed severe neck pain radiating to the occipital region. it was suspected arterial dissection. the ct angiography confirmed the suspicion, showing extensive dissection of the left vertebral artery that compromised their v2 and v3 segments. sda was performed and the same procedure was treated by placing three self-expanding stents of 5mm x 30mm (wallstent, boston scientific) in v2 segment and balloonexpandable stent (taxus, boston scientific) in v3 segment. control at 6 months was obtained with ct angiography and intravenous dynact. (figure 1 a, b, c, d, e). discussion the diagnosis and management of cerebral vascular disease has greatly improved thanks to the constant development of imaging techniques. certainly, cerebral angiography since its inception became the gold standard technique that has been enriched progressively from the digital subtraction images in 3d to arterial injection. however despite this spectacular development remains a high cost procedure that involves economic and risk problems (1). complications may include cerebral ischemia, dissection, intra or extracranial hematomas typically range from 0.6 to 1% even in well-equipped centers and in experienced hands. romanian neurosurgery (2014) xxi 1: 90 – 95 93 a b c d e figure 1 in addition and in parallel, the development of noninvasive methods such as ct and mri angiography, has led that, on many occasions and in various institutions around the world, the mip and volumetric reconstructions been taken as the only parameter to therapeutical surgical or endovascular decisions regardless of cerebral angiography. in other circumstances, the ct angiography is useful as a tool for control and 94 vega-montesinos et al flat panel detector-ct for cerebral arteries imaging monitoring in patients already treated (2), as has happened in our experience in the management of intracranial aneurysms (3– 6). in contrast, the mri angiography is not useful in patients already treated by artifacts that modify endovascular materials (coils and / or stents) (7), and that the image quality is often overcome by angioct. however, in regard to the evaluation of intrastent stenosis should be noted that the multislice ct scanners have a limited spatial resolution that makes them useless for this purpose (7–9). the dynact is a new technology consisting in the use of a c-arm equipped with flat panel detectors to produce images of ct cone-bean volume, all while the patient is in the angiography table. it has been shown that the images obtained by dynact with arterial contrast injection are useful for understanding and analyzing of cerebral vascular diseases, especially for its ability to show relationships between soft tissue and bone, detect complications during the procedure, display of intra and extracranial coils and stents, however it require the intraarterial injection of contrast material (10–13). these data are not always obtained with digital subtraction angiography, and image quality can be superior in the 3d angiography, and may be similar to the advantage of ct angiography obtained without moving the patient from the hemodynamics room. however dynact technique persist with the inconveniences of all endovascular invasive procedures, as mentioned above (1), while intravenous contrast application avoids the risks associated with intra-arterial catheterization. in our study the parameters were sufficient to be compatible with the intravenous injection with imaging that we consider to be superior to ct angiography regardless of intraaterial injection of intraraterial dynact. this advantage has been extremely useful in our patients, especially those attending outpatient aftercare control. it should be mentioned that technique used at our institution differs in some respects to that used in other centers. (13). the volume of contrast used is smaller (60cc vs 100cc), not diluted contrast and lower osmolarity 300uo vs. 370 uo. while there seems not to be a remarkable difference, however it is important when is tried the possibility of reducing kidney damage in susceptible patient, e.g., diabetes mellitus, arterial hypertension, etc. it should be noted that this aspect closely resembles the contrast volume used in ct angiography. regarding the duration of the procedure, in our technique, we obviate the preview contrast injection, which is always imaged in 20 seconds, whereas the previously described technique requires approximately 30 seconds. as mentioned for the contrast, this appears to be a minor daub, however, we believe it is a possible gain to reduce at maximum, the emission and radiation exposure to both, the patient and the personal occupationally exposed, without sacrificing image quality. romanian neurosurgery (2014) xxi 1: 90 – 95 95 conclusions with the technique of intravenous dynact, described in this article, we can obtain good quality images, with less contrast quantity and osmolarity, and less exposure time. this technique is also safe without the complications of intra-arterial injection and without the need to mobilize the patient from the angiography suite. it can also be a valuable tool for both outpatient, initial diagnosis and follow-up. the assessment of intrastent images appear to be more accurate than angiotomography; it is required a larger comparative study that aims to prove statistically this aspect, and also would be avoided the risk inherent in intra-arterial catheterization. references 1. willinsky ra, taylor sm, terbrugge k, farb ri, tomlinson g, montanera w. neurologic complications of cerebral angiography: prospective analysis of 2,899 procedures and review of the literature. radiology 2003;227:522–8. 2. buhk j-h, kallenberg k, mohr a, dechent p, knauth m. evaluation of angiographic computed tomography in the follow-up after endovascular treatment of cerebral aneurysms--a comparative study with dsa and tofmra. eur radiol 2009;19:430–6. 3. zenteno m, modenesi freitas jm, aburto-murrieta y, koppe g, machado e, lee a. balloon-expandable stenting with and without coiling for wide-neck and complex aneurysms. surg neurol 2006;66:603–10; discussion 610. 4. zenteno ma, santos-franco ja, freitas-modenesi jm, gómez c, murillo-bonilla l, aburto-murrieta y, díazromero r, nathal e, gómez-llata s, lee a. use of the sole stenting technique for the management of aneurysms in the posterior circulation in a prospective series of 20 patients. j neurosurg 2008;108:1104–18. 5. zenteno m, gómez cr, santos-franco j, vinuela f, aburto-murrieta y, lee a. ten-year follow-up of giant basilar aneurysm treated by sole stenting technique: a case report. j med case rep 2010;4:64. 6. santos-franco ja, zenteno m, lee a. dissecting aneurysms of the vertebrobasilar system. a comprehensive review on natural history and treatment options. neurosurg rev 2008;31:131–40; discussion 140. 7. struffert t, kloska s, engelhorn t, deuerling-zheng y, ott s, doelken m, saake m, köhrmann m, doerfler a. optimized intravenous flat detector ct for noninvasive visualization of intracranial stents: first results. eur radiol 2011;21:411–8. 8. turk as, rowley ha, niemann db, fiorella d, aagaard-kienitz b, pulfer k, strother cm. ct angiographic appearance of in-stent restenosis of intracranial arteries treated with the wingspan stent. ajnr am j neuroradiol 2007;28:1752–4. 9. trossbach m, hartmann m, braun c, sartor k, hähnel s. small vessel stents for intracranial angioplasty: in vitro evaluation of in-stent stenoses using ct angiography. neuroradiology 2004;46:459–63. 10.namba k, niimi y, song jk, berenstein a. use of dyna-ct angiography in neuroendovascular decisionmaking. a case report. interv neuroradiol 2009;15:67– 72. 11.benndorf g, claus b, strother cm, chang l, klucznik rp. increased cell opening and prolapse of struts of a neuroform stent in curved vasculature: value of angiographic computed tomography: technical case report. neurosurgery 2006;58:ons–e380; discussion ons–e380. 12.benndorf g, strother cm, claus b, naeini r, morsi h, klucznik r, mawad me. angiographic ct in cerebrovascular stenting. ajnr am j neuroradiol 2005;26:1813–8. 13. heran ns, song jk, namba k, smith w, niimi y, berenstein a. the utility of dynact in neuroendovascular procedures. ajnr am j neuroradiol 2006;27:330–2. microsoft word 1editorpage.doc editor’s page dear romanian neurosurgery reader, i am pleased to introduce the first editor’s notes of the romanian neurosurgery journal. we will try to publish four issues of our journal this year; we have received an increasing number of excellent submissions and to support our aim to publish as many high –quality articles, we will therefore revise the instructions to authors and we will publishe these in next issue, but as soon as on the site of the journal. the articles are published in advance online before being assigned to a print issue, ensuring that the final version of your paper is published in the next issue; our site is http://www.roneurosurgery.eu. the february issue starts with historical paper on professor constantin arseni who in the 20th century spent most of his professional life studying neurosurgery in romania and published the first comprehensive neurosurgical works in our country. this is followed by an extensive article on brain monitoring in severe traumatic brain injury; the brainit group worked collaboratively on developing standards for collection and analyses of data from brain injured patients. in this study they have shown that it is feasible to collect the brainit dataset from multiple centres in an international setting with it based methods and that the accuracy of the data collected is greater than or equal to 94%. there are several original studies dealing with different aspects of unruptured arteriovenous malformations of the brain, meningioma association with different cell types, the first part of a study on endoscopic endonasal transsphenoidal approach in the management of sellar and parasellar lesions, the second part of a study on decompressive craniectomy and its indications and a histological study of the diagnostic value of silver nitrate staining in cerebral astrocytic tumors. more clinical studies, case reports and technical notes of interest are also included, on subjects such as: microsurgical approach in a thoracic meningioma in eldery and complete tumour resection using the operating microscope, a case of a medial temporal arterio-venous malformation and its surgery, atlanto-axial distraction with complete spinal cord injury, multiple small meningiomas with transitory stroke like symptoms and others. the management of a polytrauma patient with severe traumatic brain injury in a multidisciplinary approach based on trauma protocols is presented, also a case of traumatic lumbar spondylolisthesis and a case of a giant frontal and cerebellopontine angle epidermoid cyst are presented. the editorial office hope you enjoy reading this issue; i remenber you we need your help to publish four issues this year. romanian neurosurgery (2010), volume xvii, february st.m. iencean editor-in-chief e-mail: mirceasteffan@yahoo.com doi: 10.33962/roneuro-2021-039 possibilities of endoscopic endonasal transsphenoidal surgery in treatment of growth-hormone pituitary adenomas ruslan v. aksyonov, orest i. palamar, andriy p. huk, dmytro s. teslenko, dmytro i. okonskyi romanian neurosurgery (2021) xxxv (2): pp. 234-238 doi: 10.33962/roneuro-2021-039 www.journals.lapub.co.uk/index.php/roneurosurgery possibilities of endoscopic endonasal transsphenoidal surgery in treatment of growth-hormone pituitary adenomas ruslan v. aksyonov, orest i. palamar, andriy p. huk, dmytro s. teslenko, dmytro i. okonskyi si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine abstract pituitary adenomas are one of the most common primary central nervous system tumours and have an estimated prevalence of 17%. management of hormonesecreting pituitary adenomas involves a multidisciplinary approach that can incorporate surgical, medical, and/or radiation therapies. acromegaly is a rare, chronic disorder that mostly results from growth hormone (gh)-secreting pituitary adenoma. we analyzed the outcomes of surgical treatment for growth hormone (gh) pituitary adenomas based on 28 cases and determine factors that lead to biochemical remission. introduction growth-hormone (gh) pituitary adenomas occur in 13-20% of all hormonally active pituitary adenomas [1, 21]. increased levels of gh can cause the progression of cardiovascular and cerebrovascular diseases, which leads to increased mortality [4, 5] these pituitary adenomas are invasive to the surrounding structures around the sellar area, which reduces the radicality and makes hormonal remission unattainable. [6, 15]. ghpituitary adenomas treatment includes surgery, radiotherapy and medical therapy. surgery allows to reduce the gh level insulin-like growth factor 1 (igf-1) rapidly and is the primary method in gh pituitary adenomas [10, 11]. currently, almost all pituitary adenomas are removed by endoscopic endonasal route which is highly effective and allows to achieve a high remission rate with a low number of complications [6, 12]. material and methods a retrospective analysis of 28 patients with gh pituitary adenomas in the period from 2013 to 2019. all patients underwent surgical treatment by endoscopic endonasal route. information about patients, tumor characteristics, clinical symptoms and biochemical remission is shown in table 1. patients were divided by age and gender: men – 12 keywords endoscopic, endonasal, transsphenoidal, pituitary adenomas corresponding author: ruslan v. aksyonov si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine aksyonovrv@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 235 endoscopic endonasal transsphenoidal surgery in treatment of growth-hormone pituitary adenomas (42.9%), women 16 (57.1%), the average age was 40.67 years. gh pituitary adenomas were classified by size: microadenoma (up to 10 mm) 5 (17.9%) patients, macroadenoma (10-39 mm) 21 (75%) patients, giant pituitary adenoma (> 40 mm) 2 (7,1%) patients. сavernous sinus extension was classified according knosp scale [18]: grade 0, 1 and 2 are defined as noninvasive tumors, grade 3 and 4 are defined as invasive tumors. age (mean, range) 40,67 (18-64) male 12 (42,9%) female 16 (57,1%) tumor size micro macro giant 5 (17,9%) 21 (75%) 2 (7,1%) cavernous sinus invasion no invasion invasion 18 (64,3%) 10 (35,7%) pre-gh level (mean, range) 39, (5,7 – 252) ng/ml symptoms and signs acromegaly visual field defect 6 nerve palsy headache 28 (100%) 9 (32,1%) 1 (3,6%) 11 (39,3%) long term follow-up results remission persistence recurrence 23 (82,1%) 3 (10,7%) 2 (7,1%) table 1. patients, tumor characteristics, clinical symptoms and biochemical remission for 28 patients. there were 18 (64,3%) cases with noninvasive cavernous sinus extension and 10 (35,7%) cases with invasive tumors. all patients were tested for gh and igf-1 level before surgery, 3 months after surgery, and annually. acromegaly was diagnosed on the basis of relevant clinical features: mean gh level >5 μg /l, plasma igf-1 level greater than normal appropriate to age and gender. the serum gh level ranged from 5.7 to 252 ng / ml (at average 39), igf-1 level ranged from 592 to 1506 ng / ml (at average 960.9). preoperative clinical manifestations were observed in all 28 cases. all patients had clinical signs of acromegaly, visual impairment were found in 9 (32.1%) patients, oculomotor disorders in one patient (3.6%), headache was observed in 11 (39.3%) cases. all patients underwent magnetic resonance imaging (mri) with intravenous contrast enhancement. the endoscopic endonasal transsphenoidal (eet) approach was used in all cases. surgery was performed using an endoscopic stand based on the hd-endoscope “image-1hd” (karl storz, germany). rigid endoscopes "karl storz" 4 mm in diameter with viewing angles of 0 and 35 degrees were used as the main tool for visualization of the operating field. the follow-up ranged from 12 to 60 months, at average 25.4 (2.1 years) months. the serum level of gh and igf-1 was determined in 3 months after surgery and annually. the criteria for endocrine remission or treatment were the lowest serum gh level of <0.4 ng/ml after oral glucose challenge, and subsequent normal igf-1 levels appropriate to age and gender. results radical removal: complete resection of somatotroph pituitary adenomas (pa) was achieved in 22 (78.6%) cases, of which in 19 (86.4%) patients without invasive extension to the cavernous sinus, and in 3 (13.6%) patients with invasive extension of knosp 3. subtotal resection was in 5 (17.8%) cases, of which non-invasive extension was found in 2 patients, in one of which the growth of pa was prolonged. the size of these tumors was from 30 to 40 mm. invasive extension with subtotal resection of somatotroph pa knosp 3 and knosp 4 was revealed in 3 cases. partial removal in 1 (3.6%) case, where there was extension to the cavernous sinus during knosp 3. figure 1. range of gh and igf-1 serum level after surgery. postoperative radiation therapy was performed in 4 cases, in 3 of them subtotal resection was performed, in one case due to partial removal. growth recurrence after radiation therapy was observed in 2 (7.1%) cases, resulting in repeated 236 ruslan v. aksyonov, orest i. palamar, andriy p. huk et al. surgery. clinical laboratory remission (clr) was achieved in 23 (82.1%) patients. igf-1 serum level ranged from 1 to 649 (mean 378,) gh level ranged from 0,4 to 5,7 (mean 2,9) (fig. 1). in patients who underwent only radiation therapy after surgery, clr was achieved in 2 patients. in patients who underwent radiation therapy and repeated surgery for a prolonged growth of pa, clr was achieved in 1 case (out of 2 patients), which is associated with radical removal of pa. postoperative nasal cerebrospinal fluid was observed in 3 (10.7%) cases, for which lumbar drainage was inserted in all 3 cases. diabetes insipidus was detected in 1 (3.6%) case, which required the assignment of replacement therapy. there is no postoperative mortality. discussion currently, in the treatment of tumors sellar region transsphenoidal approach is generally accepted and widely used in surgical practice [1,9,10,17]. pituitary adenomas of various sizes and hormonal activity can be completely removed using eet approach [6, 22]. eet approach is currently the main method of surgical treatment of somatotroph pituitary adenomas [2]. the use of eet approach allows to achieve rapid decompression of the optic nerves and chiasm, affect the regression of acromegalic changes, reduce the risk of cardiovascular diseases and decrease mortality due to the rapid release of gh excess [22]. compared to the microsurgical transsphenoidal approach, the eet approach is effective and allows one to achieve a larger number of totally removed pituitary adenomas and achieve biochemical remission surgically [6]. in our study, radical resection was achieved in 22 (78.6%) cases, of which 19 (86.4%) patients without invasive extension to the cavernous sinus, 3 (13.6%) patients with invasive extension knosp3, subtotal resection 5 (17.8%) cases, of which non-invasive extension was found in 2 patients. the size of these tumors was from 30 to 40 mm. invasive extension with subtotal resection of these tumors was found in 3 cases. partial removal in 1 (3.6%) case, where there was a spread to the cavernous sinus during knosp3. biochemical remission in endoscopic endonasal transsphenoidal removal of somatotroph pituitary adenomas was achieved in 23 (82.1%) patients. according to the literature, biochemical remission in surgical series can be achieved in 60% -86% of cases [13, 16, 22]. it is noted in studies that biochemical remission is influenced by the invasiveness of somatotroph pituitary adenomas, the level of preoperative gh [20]. in our series of observations, the radical removal of somatotroph pituitary adenomas depended on the invasive extension of these tumors to the cavernous sinus. at the same time the achievement of hormonal remission depended on the degree of removal of pituitary adenomas and their extension to the cavernous sinus. it was noted that hormonal remission was different depending on the size of somatotroph pituitary adenomas (p <0.05). in pituitary microadenomas, hormonal remission was achieved in all patients (5 cases), in macroadenomas 18 (85.7%), in giant pituitary adenomas in one (out of two cases). a b c d figure 2. a-b preoperative mri scans with gadolinium. macroadenoma 27х25х38 mm in size with knosp 3b extension into the cavernous sinus. c-d mri scans with gadolinium after surgery, follow-up 5 years. gh level – 4,6 ng\ml. among invasive gh pituitary adenomas, biochemical remission was achieved in 8 (72.7%) patients, among noninvasive tumors, biochemical remission was achieved in 16 (94.1%) patients. as a clinical case we illustrate outcome of surgical treatment patient with large gh pituitary adenoma (fig. 2). patient with clinical manifestation of acromegaly, visual 237 endoscopic endonasal transsphenoidal surgery in treatment of growth-hormone pituitary adenomas disturbances, high level of gh -233 ng\ml and increased igf-1 1288 ng\ml. preoperative mri scans with gadolinium shown large pituitary adenoma 27х25х38 mm in size with knosp 3b extension into the cavernous sinus. endoscopic endonasal approach was used to remove the tumor. visual disturbances regressed after surgery. clr was achieved after surgery in a few months and stay stable during all follow-up period (5 yeas). mri scans with gadolinium after surgery and 5 years after shown gross-total tumor resection and no recurrence. serum gh level – 4,6 ng\ml, igf-284 ng\ml. recurrence and low level of hormonal remission are associated with the volume of tumor removal, its extension to the cavernous sinus. thus, in 6 patients there was incomplete resection of gh pituitary adenoma. the size of these tumors was more than 3 cm in diameter. in 4 cases there was an invasive extension to the cavernous sinus. in two cases, there was a prolonged growth of tumors which were operated on at another center. adjuvant therapy, which includes drugs that reduce gh, repeated surgery or radiation therapy, plays an important role in the long-term treatment of patients who have not achieved hormonal remission after surgery [8, 9]. postoperative radiotherapy was performed in 4 cases. recurrence of growth after radiation therapy was observed in 2 (7.1%) cases, resulting in repeated surgery. thus, hormonal remission in the group of patients with incomplete resection of gh-pituitary adenoma was achieved in 4 (66.7%) patients. according to the literature, complications during pituitary adenoma surgery occur on average in 10% of cases, hypopituitary syndrome is manifested in less than 10% of cases, nasal cerebrospinal fluid 13.9%, oculomotor nerve injuryin 6% [3, 17, 19]. postoperative nasal cerebrospinal fluid was observed in 3 (10.7%) cases. diabetes insipidus 1 (3.6%) case, for which was prescribed the replacement therapy. there is no postoperative mortality. conclusions 1. endoscopic endonasal transsphenoidal approach in the treatment of gh pituitary adenomas is effective, allowing to achieve hormonal remission in 82.1%, and is safe method reducing the number of postoperative complications. 2. cavernous sinus extension of gh pituitary adenomas reduces the possibility of radical removal of these tumors, clinical and laboratory remission can be achieved in 85.7% of patients. 3. radiotherapy can reduce the number of recurrences, while clinical laboratory remission was achieved in 66.7% of patients. references 1. agustsson tt, baldvinsdottir t, jonasson jg, olafsdottir e, steinthorsdottir v, sigurdsson g, thorsson av, carroll pv, korbonits m, benediktsson r. the epidemiology of pituitary adenomas in iceland, 1955-2012: a nationwide population-based study. eur j endocrinol. 2015 nov;173(5):655-64. doi: 10.1530/eje-15-0189. pmid: 26423473. 2. bourdelot a, coste j, hazebroucq v, gaillard s, cazabat l, bertagna x, bertherat j. clinical, hormonal and magnetic resonance imaging (mri) predictors of transsphenoidal surgery outcome in acromegaly. eur j endocrinol. 2004 jun;150(6):763-71. doi: 10.1530/eje.0.1500763. pmid: 151 91345. 3. briceno v, zaidi ha, doucette ja, onomichi kb, alreshidi a, mekary ra, smith tr. efficacy of transsphenoidal surgery in achieving biochemical cure of growth hormone-secreting pituitary adenomas among patients with cavernous sinus invasion: a systematic review and meta-analysis. neurol res. 2017 may;39(5):387-398. doi: 10.1080/01616412.2017.1296653. pmid: 28301972. 4. buliman a, tataranu lg, ciubotaru v, cazac tl, dumitrache c. the multimodal management of ghsecreting pituitary adenomas: predictive factors, strategies and outcomes. j med life. 2016;9(2):187-92. 5. campbell pg, kenning e, andrews dw, yadla s, rosen m, evans jj. outcomes after a purely endoscopic transsphenoidal resection of growth hormone-secreting pituitary adenomas. neurosurg focus. 2010;29(4):e5. https://doi.org/10.3171/2010.7.focus10153. 6. chen cj, ironside n, pomeraniec ij, chivukula s, buell tj, ding d, taylor dg, dallapiazza rf, lee cc, bergsneider m. microsurgical versus endoscopic transsphenoidal resection for acromegaly: a systematic review of outcomes and complications. acta neurochir (wien). 2017 nov;159(11):2193-2207. doi: 10.1007/s00701-0173318-6. epub 2017 sep 14. pmid: 28913667; pmcid: pmc6558977. 7. de los reyes km, gross ba, frerichs ku, dunn if, lin n, rincon-torroella j, annino dj, laws er (2015) incidence, risk factors and management of severe posttranssphenoidal epistaxis. j clin neurosci 22:116–122. 8. ding d, starke rm, sheehan jp. treatment paradigms for pituitary adenomas: defining the roles of radiosurgery and radiation therapy. j neurooncol. 2014 may;117(3):445-57. doi: 10.1007/s11060-013-1262-8. pmid: 24122025. 238 ruslan v. aksyonov, orest i. palamar, andriy p. huk et al. 9. ding d, yen cp, starke rm, lee cc, sheehan jp. unyielding progress: recent advances in the treatment of central nervous system neoplasms with radiosurgery and radiation therapy. j neurooncol. 2014 sep;119(3):513-29. doi: 10.1007/s11060-014-1501-7. epub 2014 aug 14. pmid: 25119001. 10. gondim ja, ferraz t, mota i, studart d, almeida jp, gomes e et al. outcome of surgical intrasellar growth hormone tumor performed by a pituitary specialist surgeon in a developing country. surg neurol; 2009;72(1):15-9. https://doi.org/10.1016/j.surneu.2008.02.012. 11. gondim ja, schops m, almeida jp, albuquerque la, gomes e, ferraz t et al. endoscopic endonasal transsphenoidal surgery: surgical results of 228 pituitary adenomas treated in a pituitary center. pituitary. 2010;13(1):68-77. https://doi.org/10.1007/s11102-009-01 95-x . 12. guinto g, abdo m, zepeda e, arechiga n, mercado m (2012) acromegaly: role of surgery in the therapeutic armamentarium. int j endocrinol 2012:306094 j clin endocrinol metab. 2011 sep; 96(9):2732-40. 13. jane ja jr, starke rm, elzoghby ma, reames dl, payne sc, thorner mo, marshall jc, laws er jr, vance ml. endoscopic transsphenoidal surgery for acromegaly: remission using modern criteria, complications, and predictors of outcome. j clin endocrinol metab. 2011 sep; 96(9):2732-40. 14. krieger md, couldwell wt, weiss mh. assessment of long-term remission of acromegaly following surgery. j neurosurg. 2003 apr;98(4):719-24. doi: 10.3171/jns.2003.98.4.0719. pmid: 12691394. 15. mehta gu, lonser rr. management of hormonesecreting pituitary adenomas. neuro oncol. 2017 jun 1;19(6):762-773. doi: 10.1093/neuonc/now130. pmid: 27543627; pmcid: pmc5464431. 16. nishioka h, fukuhara n, horiguchi k, yamada s. aggressive transsphenoidal resection of tumors invading the cavernous sinus in patients with acromegaly: predictive factors, strategies, and outcomes. j neurosurg. 2014 sep;121(3):505-10. doi: 10.3171/2014.3.jns132214. epub 2014 jul 11. pmid: 25014437. 17. paluzzi a, fernandez-miranda jc, tonya stefko s, challinor s, snyderman ch, gardner pa. endoscopic endonasal approach for pituitary adenomas: a series of 555 patients. pituitary. 2014 aug;17(4):307-19. doi: 10.1007/s11102-013-0502-4. pmid: 23907570. 18. pituitary adenomas with invasion of the cavernous sinus space: a magnetic resonance imaging classification compared with surgical findings. knosp e, steiner e, kitz k, matula c. neurosurgery. 1993 oct; 33(4):610-7; discussion 617-8. 19. rutkowski m, zada g. management of pituitary adenomas invading the cavernous sinus. neurosurg clin n am. 2019 oct;30(4):445-455. doi: 10.1016/j.n ec.2019.05.005. pmid: 31471051. 20. takahashi ja, shimatsu a, nakao k, hashimoto n. early postoperative indicators of late outcome in acromegalic patients. clin endocrinol (oxf). 2004 mar;60(3):366-74. doi: 10.1046/j.1365-2265.2003.01900.x. pmid: 15009003. 21. tjörnstrand a, gunnarsson k, evert m, holmberg e, ragnarsson o, rosén t, filipsson nyström h. the incidence rate of pituitary adenomas in western sweden for the period 2001-2011. eur j endocrinol. 2014 oct;171(4):519-26. doi: 10.1530/eje-14-0144. epub 2014 aug 1. pmid: 25084775. 22. zheng y, chen dm, wang y, mai rk, zhu zf. surgical management of growth hormone-secreting pituitary adenomas: a retrospective analysis of 33 patients. medicine (baltimore). 2020 may;99(19):e19855. doi: 10.1097/md.0000000000019855. pmid: 32384430; pmcid: pmc7220440. microsoft word 10.nicada_multiplecerebral.doc romanian neurosurgery (2010) xvii 4: 449 – 455 449 multiple cerebral aneurysms of middle cerebral artery. case report d.a. nica1, tatiana rosca1, a. dinca2, m. stroi3, mirela renta4, a.v. ciurea5 1neurosurgery clinic, 2icu department, clinic emergency hospital “sf. pantelimon”, 3institute of vascular diseases and microsurgery 4emergency hospital “floreasca”, bucharest 5clinic emergency hospital “bagdasar-arseni” bucharest abstract multiple cerebral aneurysms present a wide variation in incidence with averages of 13% at angiographic studies and 22.7% at autopsy. high blood pressue, cigarette smoking, stress and possible also age and female sex seem to be risk factors for multiple intracranial aneurysms (mian) in patients of working age who have suffered a subarachnoid hemorrhage (sah). aneurysms were situated on the same side in one-third of the patients with two aneurysms and the most common site was the middle cerebral artery (mca). to manage these challenging lesions neurosurgeons must use all available innovations and advances, including diagnostic, technical and perioperative adjuncts. the author presents a case of middle age female, with two saccular aneurysms situated on the same side (right mca), who was operated in our clinic, 20 days after first sah episode, i grade on hunt/hess scale. the angio mri was performed before, and control ds angiography after operation. after pterional approach, the author used the magnification, microsurgical technics, temporal clip, and two permanent yasargil curved clips. a postoperative good recovery enable the patient go to work and drive one month later. keywords: angio-mri, multiple intracranial aneurysms, middle cerebral artery, subarachnoid haemorrhage, substraction angiography introduction arterial aneurysms (aa) are local outpouching of a blood vessel wall. the most frequent sites for the aneurysms are the sites of bifurcation, anastomosis of the basal arteries of the circle of willis, where the hemodynamic forces are higher, and in rare cases, the aneurysm can form directly from the sidewall of the non-branching artery. the aneurysmal sack may have a narrow neck or wide base (or detach from an artery on a wide stalk). in time, because it is supposed to chronic hypertension the vessel wall thickens and the aneurism enlarges and eventually ruptures, usually associated to an acute rising in blood pressure. the incidence of multiple aneurysms varies from 14 to 45% presenting with sah (3, 7, 15). there are a few variables that need to be taken into account in making the diagnosis of multiple aneurisms, including the experience of the radiologist, the number of vessels injected at angiography, 450 d.a. nica et al multiple cerebral aneurysms of middle cerebral artery and the quality of the angiography equipment. multiple aneurysms are observed in a fifth to a third of all cases at intracranial locations of aneurysm (13, 14). about 75% of patients have two aneurysms, 15% have three and in 10%, more than three aneurysms. in cases with multiple aneurysms, an association with gender (more frequently in women) has been observed. multiple aneurysms are often observed in patients with diseases such as vasculopathy, fibromuscular dysplasia and polycystic renal disease factors that lead to aneurism development: •traumatic brain injury such as a blow to the head (less than 1% of all cases) •an infection (termed a mycotic aneurysm, (2% of all known cases) •a hereditary predisposition (they can run in families; this accounts for 20% of all aneurysms) •cigarette smoking and hypertension or high blood pressure •use of drugs such as cocaine and amphetamines •certain blood disorders: fibromuscular dysplasia, cerebral arteritis, arterial dissection. the risk factors for an aneurysm rupture are: •medical family history •hypertension •tobacco use •female sex (3:2 female to male ratio for aneurismal rupture) •between the ages of 35 and 60. the cause of aneurysm bleeding remains unknown in most cases. studies have shown, however, that the following increase the risk of a rupture: •hypertension •strong emotions such as anger can raise blood pressure and cause a rupture (9). in outlining symptoms of ruptured cerebral aneurysm, it is useful to make use of the hunt and hess scale of subarachnoid hemorrhage severity: clinical status grade asymptomatic, mild headache, slight nuchal rigidity 1 moderate to severe headache, nuchal rigidity , no neurologic deficit other than cranial nerve palsy 2 drowsiness / confusion, mild focal neurologic deficit 3 stupor, moderate-severe hemiparesis 4 coma, decerebrate posturing 5 case report the patient is a 49-year-old female, smoker, presenting with sudden onset of severe excruciating headache followed by vomiting episodes. she was a known hypertensive and often disrupted her treatment, heavy smoker of about 20-30 cigarettes/day, one liter light coffee/day and occasionally alcohol consumer. 25 years ago, the patient was operated for persistent ductus arteriosus. she was admitted 18 days after the simptomatology onset. her clinical exam revealed an alert and oriented individual, slight neck stiffness, and no visual disturbances. no other deficits were recorded. a clinical diagnosis of subarachnoid hemorrhage, hunt and hess grade-i was made. mriangiography revealed a small sah in the right sylvian fissure, moderate ventriculo-megaly and on right middle cerebral artery, two saccular and bilobated aneurysms. first aneurism located at the junction of m1 with m2, 6 mm in diameter, with an inferior and lateral orientation was ruptured. the second, unruptured aneurism rested at the bifurcatiom of the right m2, with a diameter of 7 mm, was oriented superiorly. romanian neurosurgery (2010) xvii 4: 449 – 455 451 figure 1, 2 angio-mri show two saccular and bilobated aneurysm: first to the junction m1 with m2 (ruptured) and the second between the two branches of m2 split (unruptured) preoperatory preparation: nimotop (60 mg in each 4 hours per os), algocalmin (500 mg three times a day), glycerin suppository was the preoperative medication. after standard investigations (blood, ecg, x-ray lung), we operated the patient two day after admission. the general anesthesia permitted the oro-traheal intubations, lumbar catheter for lcs evacuation and patient positioning: supine position, the head fixation in 45◦ left rotated and up to the cord line, with zygoma in top. the right pterional approach (yasargil) was performed. after we performed the craniotomy, the dura was exposed and the rim of sphenoid wing was drilled off. dura was opened in a curved fashion and temporary suspended. from that moment we were used the magnification, the microsurgical instruments and leyla self-retractors. using the lateral trans-sylvian approach, we dissected the m1 segment of right acm and we found a large (12mm), saccular, bilobated aneurysm on the m1m2 junction. the dissection was difficult in that moment because of adherences 452 d.a. nica et al multiple cerebral aneurysms of middle cerebral artery secondary to sah. the wall of first aneurism was impregnated with calcium plates. during the sharp dissection of aneurysm’s neck, hypotension was induced. when we dissected the aneurysm dome, it started to bleed and the temporary clip on m1 before the junction was necessary. the sharp dissection continued and the dimension of the aneurysm was diminished by bipolar coagulation. finally we clipped the aneurysm’s neck with a permanent curved yasargil clip, it was verified by puncture of aneurysm’s sac, and we suspended the temporary clip. it was easier to dissect the m2 segment of acm, because no adherences occurred and the second aneurysm was more easily found between the two branches of m2 segment. the neck of the distal aneurysm was clipped safety. no other supplementary branches occurred, except that two. the puncture of the aneurismal sac was negative. no complications appeared when the anesthetist increased the ta tilt 140/80 mm hg occurred. after 80 mg papaverinum in situ, we sutured the dura watertight (3.0 silk), and suspended it, the bone was fixed in four points, left a subgaleal drenage and finally, the muscular and subcutaneous and then the skin were close with interrupted sutures. 24 hours later the patient was in good condition with a glasgow coma scale of 15 and begun mobilization with kinetotherapist. discussion the modern era of aneurysm surgery emerged in 1933, when egas monitz demonstrated, an aneurysm with the technique of cerebral angiography, which he discovered (11). figure 3 a, b control angiography one month after the operation, shown the efficient position on the clips and the absence of both aneurysms. she was return to work and drive immediately after angiography the first malleable hemostatic clips in neurosurgery were introduced by cushing in 1911, but they are not appropriate to the standards of aneurysms clipping. (19) the first planned intracranial operation for a saccular aneurysm was performed by dott in 1933 by wrapping technique (9). in 1937 dandy clipped the neck of an aneurysm with a thiny metal clip and shriveled the sac with electrocautery. aided by technical advances and general progress in radiology, anesthesia, and intensive care, many neurosurgeons achieved progressively lower postoperative mortality rates after operations for romanian neurosurgery (2010) xvii 4: 449 – 455 453 intracranial aneurysms like yasargil and drake in the 1960s-1970s (5). it is generally agreed that multiple aneurysms should be treated medically unless there is evidence of rupture, or persistence or enlargement during or after treatment. if surgery is considered, all aneurysms easily approached ad the time of surgery should be clipped. in suzuki’s personal series of 1080 cases, single aneurysms constituted 85% of the series, and multiple aneurysms 15 %. he reviewed seven other clinical series, totaling 10,795 cases, in witch the incidence of multiple aneurysms was 14.1% overall, with the range of 7.7 to 29,8%. he similarly reviewed six autopsy series in which 1404 cases were studied to reveal multiple aneurysms cases in 23.5% (range 18.9 to 50%) (22). in two cooperative studies involving 6842 patients, 19 % of patients had more than one aneurysm ( 8,20). at autopsy, 22% of patients in the study had multiple aneurysms (20). the lower rate of clinical detection probably reflects the fact that four-vessels angiography was not routinely carried out in 1969. in the multiple aneurysms cases of the conservatively managed patients in the cooperative study and in suzuki’s personal series, patients having two aneurysms constituted 71 and 77%; three aneurysms, 23 and 15%; and four or more aneurysms, 7 and 6% of multiple aneurysms cases, respectively. multiple aneurysms are relatively more common in females (74%) than males (20). the same study showed that 47 % of multiple aneurysms are on opposite sides. 21% are on the some side. 29% have one in the midline and one on the side, and 3% have both in the midline. when two internal carotid aneurysms coexist, the chance of their being “mirror” aneurysms is three times greater than that of their both being on the same side. similarly, with two middle cerebral aneurysms the chance is four times greater. when an aneurysm of anterior circulation is found, the chance of second aneurysm existing on the posterior circulation is between 3 and 5%. with internal carotid and middle cerebral aneurysms, there is a tendency toward either symmetric aneurysms or a second aneurysm on the same vessel. how it is possible to tell which aneurysm has ruptured? no clinical method predicts with 100% accuracy which aneurysm has bled. traditionally, the largest of the aneurysm has ruptured (11). other angiographic signs of rupture are a local mass or vasospasm, irregular aneurysm shape, or intra-aneurysmal clot. when two aneurysms are on the same vessel, unless the proximal aneurysm is thrombosed, the proximal aneurysm has ruptured (2). clinical signs and usually not helpful, although a third nerve palsy or unilateral retro-orbital pain, for example, would suggest that an aneurysm had ruptured at the origin of the posterior communicating artery. localized collections of subarachnoid blood on the ct-scan may point to the offending lesion. an algorithm for identifying the ruptured aneurysm (12), was as follows: exclude extradural aneurysms, look for focal blood on the ctscan, check for focal mass or vasospasm on angiogram, observe size and shape(the larger aneurysms is more likely to bleed; if they are of similar size, look for irregularity of the sac or daughter loculus), use clinical signs, repeat the angiogram later and look for changes in the aneurysms, and finally 454 d.a. nica et al multiple cerebral aneurysms of middle cerebral artery choose the aneurysms site with the highest probability of rupture (11, 25). subtle local changes may appear on mri and angio-mri (figure 1, 2 ) a new study in usa reveled the trends in the treatment of cerebral aneurysms (1). the unruptured aneurysms are treated by endovascular therapy and the ruptured aneurysms are treated with clip placement. surgical clipping procedures remained stable while the number of aneurysms treated by means of endovascular therapy procedures doubled (1). in our case, the patient had two aneurysms of mca from the same side: first was ruptured and the second was unruptured. because in our clinic we don’t use the endovascular procedures yet, we clipped both aneurysms in the same session. conclusion the risk factors of multiple aneurysms, in order of importance are: cigarette smoking, high blood pressue, family history of cerebrovascular disease and stress, especially on the female in work age (1560 years). the prognosis for subarachnoid hemorrhage remains reserved frequently despite the very good improvement of medical and neurosurgical treatment. multiple intracranial aneurysms are discovered in 15% to 35% of patients with aneurysm who present with subarachnoid hemorrhage. these aneurisms have the tendency to appear bilaterally at bifurcations but the author presents a case with multiple aneurisms situated unilaterally. the second particularity of the case is that the aneurisms were clipped in the same intervention. whether the prognosis for subarachnoid hemorrhage patients with multiple aneurysms is less favorable than that for subarachnoid hemorrhage patients with a single aneurysm is also not well established. it also remains controversial whether surgical outcome in subarachnoid hemorrhage in patients with multiple intracranial aneurysms is actually worse than that in subarachnoid hemorrhage to patients with a single aneurysm. references 1. andaluz, n., zuccarello m. recent trends in the treatment of cerebral aneurysms: analyses of a nation wide in patients database. j. neurosurgery 2008; 108:1163-1169 2. cromptom mr. mechanism of growth and rupture in cerebral berry aneurysms. br.med j 1966,1:11381142. 3. ellamushi he, grieve jp, jager hr, kitchen nd. risk factors for the formation of multiple intracranial aneurysms. j neurosurg. 2001; 94: 728–732. 4. j.a. friedman , dg. piepgras. middle cerebral artery aneurysms, youmans. 2004, 115: 1959-1970. 5. o. heiskanen. surgical management of unrupted cerebral aneurysms, schmideck. 1995, 90:1155-1161. 6. inagawa t. surgical treatment of multiple intracranial aneurysms. acta neurochir (wien). 1991; 108: 22–29. 7. inagawa t. multiple intracranial aneurysms in elderly patients. acta neurochir (wien). 1990; 106: 119–126. 8. kassell nf,torner jc, haley ec jr,et al. the international cooperative study on the timing of aneurysm surgery. part i: overall management result. j neurosurg 1990, 73:18-36. 9. makio kaminogo, md; masahiro yonekura, md shobu shibata, md incidence and outcome of multiple intracranial aneurysms in a defined population stroke. 2003,34:16. 10. mizoi k, suzuki j, yoshimoto t. surgical treatment of multiple aneurysms: review of experience with 372 cases. acta neurochir (wien). 1989; 96: 8–14. 11. moniz e. anevrysms intra-cranien de la carotid interne droite rendu visible par l”arteriographie cerebrale.rev otoneuroophthalmol 1933, 11:746-748. 12. nehls rj, flom ra, carter lp, spetzler rf. multiple intracranial aneurysms: determining the site of rupture. j neurosurg 1985,63:342-348. 13. orrison ww (ed) (2000) neuroimaging, vol 1. saunders, philadelphia, p 943 14. osborn a (1999) diagnostic cerebral angiography, 2nd edn. lippincott williams & wilkins, philadelphia, p 462 romanian neurosurgery (2010) xvii 4: 449 – 455 455 15. ostergaard jr, hog e. incidence of multiple intracranial aneurysms: influence of arterial hypertension and gender. j neurosurg. 1985; 63: 49–55. 16. qureshi ai, suarez ji, parekh pd, sung g, geocadin r, bhardwaj a, tamargo rj, ulatowski ja. risk factors for multiple intracranial aneurysms. neurosurgery. 1998; 43: 22–27. 17. b.e .pollock , jj. schindler, d.a. nichols, f.b. meyer. multimodality management of complex cerebrovascular lesions, youmans. 2004, 124:2121-2122. 18. rinne j, hernesniemi j, puranen m, saari t. multiple intracranial aneurysms in a defined population: prospective angiographic and clinical study. neurosurgery. 1994; 35: 803–808. 19. rinne j, hernesniemi j, niskanen m, vapalahiti m. management outcome for multiple intracranial aneurysms. neurosurgery. 1995; 36: 31–38. 20. sahs al,perret ge, locksley hb, nishioka h (eds). intracranial aneurysms and subarachnoid hemorrhage: a cooperative study, philadelphia: lippincott,1969. 21. seppo juvela, risk factors for multiple intracranial aneurysms. stroke. 2000, 31:392-397. 22. suzuki j .multiple aneurysms: treatment. in pia hw, langmaid c, zierski j (eds): cerebral aneurysms: advances in diagnosis and therapy, berlin: springer.1979,352-363. 23. vajda j. multiple intracranial aneurysms: a high risk condition. acta neurochir (wien). 1992; 118: 59–75. 24. b. weir, rl mcdonald. intracranial aneurysms and subarachnoid hemorrhage: an overview.1995,214:21942195. 25. wood eh. angiographic identification of the ruptured lesion in patients with multiple cerebral aneurysms. j. neurosurgery 1964, 21:182-198. 14amitagrawal_asymptomatic romanian neurosurgery (2014) xxi 2: 227 229 227 asymptomatic spina bifida occulta involving sacrum in an elderly female amit agrawal, g. malleswara rao professors of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) it has been estimated that 20% of all myelomeningoceles involve the sacral level and majority of these patients with sacral level lesions have fewer complications than with high level lesions. (1-5) figure 1 posterior view of the sacrum shows a dry bone specimen of sacral spina bifida occulta, where there is failure of closure of the sacral canal at all sacral levels a 60 year female presented with low back pain of two year duration, non-radiating in nature but increased by bending forward. there was no history of bowel or bladder disturbances. she had swelling over low back region since childhood not associated with pain. her general and systemic examination was normal. there was diffuse, non-tender, non-pulsatile swelling over sacral region. skin over the swelling was healthy. plain lumbosacral x-ray demonstrated a sacral bone defect. pelvic computed tomography (ct) showed a defect at the dorsal aspect of the sacrum with diffuse soft tissue swelling (figure 1). patient responded to conservative management and physiotherapy. there are many reports on the incidence of sacral spina bifida occulta and it has been suggested that 90-100% of patients with a sacral level lesion are ambulant. (1, 6-10) the reported clinical significance of sacral spina bifida occulta ranges from an anatomical variant of little or no importance on its own to a very important cause of meningomyelocele or neurological deficits. (1, 6, 10-17) in absence of external manifestations occult spina bifida of the sacrum can be associated with a number of 228 agrawal, rao asymptomatic spina bifida occulta conditions including backache, posterior disc herniation, enuresis and functional disorders of the lower urinary tract, and neurological abnormalities of the feet. (10, 18-20) it has been hypothesized that the absence of the first sacral spinous process and the ligaments that normally run between it and the spinous process of the fifth lumbar vertebra spina bifida occulta may be associated with low back pain. (21) awareness and knowledge of the congenital defect of sacrum must be considered before undertaking any procedure on the sacrum (i.e. caudal epidural block, internal fixation via transpedicular and lateral mass screws) as if the anomaly is overlooked it can lead to serious complications. (2, 5, 22) correspondence: dr amit agrawal professor of neurosurgery department of neurosurgery narayna medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.brinker mr, rosenfeld sr, feiwell e, granger sp, mitchell dc, rice jc. myelomeningocele at the sacral level. long-term outcomes in adults. the journal of bone and joint surgery american volume 1994;76:12931300. 2.senoglu n, senoglu m, gumusalan y. total spina bifida occulta of the sacrum. international journal of anatomical variations 2008;1:27-28. 3.romanes g. cunningham's textbook of anatomy (ed. 11) oxford university press. new york 1972:295. 4.williams pl. gray&s anatomy: churchill livingstone new york, 1995. 5.srijit d, shipra p. spina bifida with higher position of sacral hiatus: a case report with clinical implications. bratislavske lekarske listy 2007;108:467-469. 6.schoenmakers m, gulmans v, gooskens r, helders p. spina bifida at the sacral level: more than minor gait disturbances. clinical rehabilitation 2004;18:178-185. 7.asher ef, garrison rn, ratcliffe dj, fry de. endotoxin, cellular function, and nutrient blood flow. archives of surgery (chicago, ill : 1960) 1983;118:441445. 8.findley tw, agre jc, habeck rv, schmalz r, birkebak rr, mcnally mc. ambulation in the adolescent with myelomeningocele. i: early childhood predictors. archives of physical medicine and rehabilitation 1987;68:518-522. 9.hoffer mm, feiwell e, perry r, perry j, bonnett c. functional ambulation in patients with myelomeningocele. the journal of bone and joint surgery american volume 1973;55:137-148. 10.albrecht tl, scutter sd, henneberg m. radiographic method to assess the prevalence of sacral spina bifida occulta. clinical anatomy (new york, ny) 2007;20:170174. 11.barazi sa, cudlip s, johnston f. high and low pressure states associated with posterior sacral meningocele. british journal of neurosurgery 2003;17:184-187. 12.wolf ls, mclaughlin jf. early motor development in infants with meningomyelocele. pediatric physical therapy 1992;4:12-17. 13.ong lc, lim yn, sofiah a. malaysian children with spina bifida: relationship between functional outcome and level of lesion. singapore medical journal 2002;43:12-17. 14.pierre-kahn a, zerah m, renier d, et al. congenital lumbosacral lipomas. child's nervous system: chns: official journal of the international society for pediatric neurosurgery 1997;13:298-334; discussion 335. 15.holmbeck gn, faier-routman j. spinal lesion level, shunt status, family relationships, and psychosocial adjustment in children and adolescents with spina bifida myelomeningocele. journal of pediatric psychology 1995;20:817-832. 16.mcdonald cm, jaffe km, mosca vs, shurtleff db. ambulatory outcome of children with romanian neurosurgery (2014) xxi 2: 227 229 229 myelomeningocele: effect of lower-extremity muscle strength. developmental medicine and child neurology 1991;33:482-490. 17.schwartz s, cohen me, herbison gj, shah a. relationship between two measures of upper extremity strength: manual muscle test compared to hand-held myometry. archives of physical medicine and rehabilitation 1992;73:1063-1063. 18.avrahami e, frishman e, fridman z, azor m. spina bifida occulta of s1 is not an innocent finding. spine 1994;19:12-15. 19.fidas a, macdonald hl, elton ra, mcinnes a, wild sr, chisholm gd. prevalence of spina bifida occulta in patients with functional disorders of the lower urinary tract and its relation to urodynamic and neurophysiological measurements. bmj (clinical research ed) 1989;298:357-359. 20.galloway nt, tainsh j. minor defects of the sacrum and neurogenic bladder dysfunction. british journal of urology 1985;57:154-155. 21.de anquin ce. spina bifida occulta with engagement of the fifth lumbar spinous process a cause of low back pain and sciatica. journal of bone & joint surgery, british volume 1959;41:486-490. 22.sekiguchi m, yabuki s, satoh k, kikuchi s. an anatomic study of the sacral hiatus: a basis for successful caudal epidural block. the clinical journal of pain 2004;20:51-54. microsoft word 2ciureaavgeneral.doc romanian neurosurgery (2010) xvii 2: 143 – 146 143 general mircea iacob promotor of military neurosurgery activity in romania a.v. ciurea1, g. iacob2 1clinical emergency hospital “bagdasar arseni” bucharest, university of medicine and pharmacy “carol davila”, bucharest, romania 2clinic of neurosurgery, university hospital bucharest romania general md. mircea iacob, distinguished personality of romanian military medicine and a pioneer of military romanian neurosurgery, was born on june 7, 1922 in craiova, dolj county, romania. he attended the university of medicine and pharmacy from bucharest (1941-1947) as well as the sanitary military institute, were he was promoted lieutenant in november 1945 and captain medical doctor in december 1947. after graduation he served as an intern for the 2nd surgery department of the central military hospital under the guidance of colonel m.d. petre costescu. on april 21, 1948 he defended his ph.d thesis entitled: “lombar sympatectomy indications”. thereafter he was a resident (1948-1950) and a specialist surgeon (1950-1952) at the military hospital from oradea. he completed his residency in neurosurgery at the neurosurgery clinic of bucharest directed at that time by ass. prof. arseni constantin. in december 1952 he was promoted major. the first neurosurgery military nucleus (hospital) with 10 beds, was inaugurated on december 15th, 1952 at to the bucharest central military hospital under the supervision of col. md. eugen mareş. here dr.iacob started neurosurgical activity with cranio-cerebral and vertebromedular traumatology cases, lumbar disc hernia, cranioplasty; his first results were published and presented at conferences, advocating the importance of military neurosurgery even during peace times. in august 1955 he was promoted lieutenant-colonel md. since 1957 the neurosurgery nucleus was augmented to 15 beds at the second surgery department, directed by general md. gheorghe petrulian. in september 1959 he earned the first prize at a national neurosurgery contest. 144 a.v. ciurea, g. iacob general mircea iacob in august 1961 he was promoted colonel md. the neurosurgery nucleus reached 25 beds at the trauma and neurosurgery department directed by col md. niculescu gheorghe. between november 14th 1964 and november 14th 1965, he was granted a one-year scholarship by the world health organisation in functional neurosurgery and worked at the neurosurgery clinic of prof. jean talairach at sainte anne hospital, in paris france. he was nominated “assistent étranger” at the medical faculty in paris – france january 13, 1966 after submitting the thesis “mouvements anormaux nonparkinsoniens”. january 11, 1966 – a 30 beds neurosurgery department is founded at the bucharest central military hospital. in 1970 this department extended to 50 beds, directed by colonel md. mircea iacob until june 1, 1990. his co-workers (in a chronological order) were: m.d. nicolae dobosciuc specialist neurosurgeon, md. bezu aleman and m.d. cramer emil. he is the first to have introduced stereotactic neurosurgery in a neurosurgery clinic in bucharest. as from 1969 he also started using radioactive isotopes for lesions in different functional neurosurgery pathologies. dr. iacob surgical activity was presented in romanian medical revues such as: “revista sanitara militara”, “revista neurologia, neurochirurgia, psihiatria”, “revista oftalmologia” as well as in various publications from england, france and bulgaria. at the international medical military congress held in 1973, bucharest romania he presented a lecture entitled: “delayed emergency and evacuation after destination principles for cranio-cerebral and vertebromedullary trauma during big calamities”. starting february 2, 1974 he was appointed first degree senior neurosurgeon by the health ministry. as a reward for his neurosurgical activity a new neurosurgical department was opened on december 10th, 1979 at the central military hospital consisting of 65 beds, two modern surgery units – one of them prepared for stereotactic procedures with new radiological equipment able to perform teleradiographies, a neuroradiology compartment, functional investigations laboratory, post-operatory rooms protected with pb. here he started a wide surgical activity including functional stereotactic procedures using instruments made after french technology, cerebral biopsies, micro-surgical procedures. in 1981 he also founded a curie-therapy laboratory at the central military hospital for radioisotopes used in stereotactic procedures (such as 198au, 192ir). in december 1982 he was promoted general md. he was also assigned member in the romanian science people association – neural section in 1987. he retired at june 1, 1990. however, he continued to offer advice for patients with various neurosurgical problems. 7 years later he passed away suddenly on april 11th, 1997 after a cerebral stroke induced by an atrial fibrillation treated for 30 years. he was buried at his wish in craiova. general md. phd mircea iacob had a career marked by enthusiasm for developing new methods and applying cutting-edge technology to neurosurgery. he is the author of 9 medical books, 77 papers for romanian or foreign revues, 82 other unpublished papers; a record to be nominated docent doctor – professor. he also devised an autostatic spraeder for lumbar paravertebral musculature; with romanian neurosurgery (2010) xvii 2: 143 – 146 145 assiduous efforts he made the talairach stereotactic frames with local resources. throughout his scientific activity he advanced the following problems: craniocerebral and vertebro-medullary traumatology during peace and war, concerning emergency principles; disc hernia, functional neurosurgery, the use of radioisotopes in stereotactic procedures.he was also interesed: decreasing the usage of radioisotopes on anterior pituitary in order to reduce malignant oedematous exoftalmia, evolutive acromegalia; controlling the outcome diabetic patients who also developed retinopaty, handling the evolution of malign malanoma cerebral metastasis, breast and prostate metastasis. other approached subjects include the treatment for extrapiramidal illnesses, epilepsy, psychosurgery, pain surgery especially in trigeminal neuralgia, thalamic hyperpatia, malignant pains; but also for interstitial radiotherapy for small, deep brain tumors. he addresed neurosurgery problems in both editions of “surgery in war” of 1956 and 1965 and was a coworker for the “atlas d’anatomie stéréotaxique du télencéphale” under prof. jean talairach supervision, published in masson publishing house in 1967. other contributions were brought to the books of prof. c. arseni: “tratat de neurologie” 1979, “cancerul sistemului nervos” 1982, “durerea în cancer” 1983, “metode de neurofiziologie clinica 1984”, “momente din istoria neurochirurgiei româneşti” 1988. general md, phd iacob is the first to have introduced electrocorticography, stereoelectroencephalograpy, stereotactic cerebral biopsies and the use of stereotactic procedures to precise metallic foreign bodies inside brain in romania. he also took an interest in other therapeutic approaches regarding pineal tumors, tumors in elderly the use of subarachnoidian methotrexate for meduloblastoma and ependimoma spinal spreads. his remarkably rich didactic and social activity can be summarized as follows: 1946-1947 anatomy assistant at carol davila university of medicine and pharmacy 1948-1952 secretary of the military medical society union 1950 professor for military md 1949 he grounded the targu mures military hospital 1959 war surgery professor for civilian surgeons 1961-1974 member of the editorial board for “revista sanitara militara” figure 1 atlas d’anatomie stéréotaxique du télencéphale, under prof. jean talairach supervision, with coworker mircea gr. iacob, published in masson publishing house in 1967 146 a.v. ciurea, g. iacob general mircea iacob 1964-1966 member of neurosurgery commissions promoting neurosurgeons 1973-1990 member of the leading committee from the neurology and neurosurgery society consultant neurosurgeon for the highest political members of the romanian parliament he successfully fulfilled several medical missions in korea, egypt, france, morocco, spain and was accordingly rewarded with romanian and foreign medals and orders. for his activity in the 2nd world war as sub-lieutenant md he was granted the title “war veteran”. distinguished pupil of prof. c. arseni and prof. jean talairach, general iacob grigore mircea has become one of the most famous and appreciated romanian neurosurgeon and the neurosurgery department of bucharest central military hospital. despite his cardiac illness he imposed himself a severe working discipline, tenacity, respect for all patients regardless of military or social position. he was modest and impartial in his relation with patients, coworkers, determined and confident in different medical or social situations. he was also able to pass on his life-long passion to his son, prof. dr. iacob gabriel – head of the neurosurgery department at the universitary hospital. pioneer of military romanian neurosurgery general md phd iacob gr. mircea was a model of professional integrity, exceptional medical personality, with teaching and research capabilities, but most important dedicated to patients for whom he sacrificed his entire life. microsoft word 2.chiriaca_technique_f.doc 96 chiriac et al volumetric assessment of intracranial aneurysms technique possibilities for volumetric assessment of intracranial aneurysms a. chiriac, b. iliescu, n. dobrin, i. poeată clinic of neurosurgery, “gr.t. popa” university of medicine and pharmacy iasi “prof. dr. n. oblu” clinical emergency hospital, iaşi, romania abstract volume measurement techniques of intracranial aneurysms from 3d rotational angiography vary on different factor settings and, therefore, are operator-dependent. the purpose of this study was to evaluate the application and the precision of ellipsoidal approximation (mathematics and computer technique) and software methods to measure intracranial aneurysms volume starting from planar (dr and sd) and 3dimensional (3d) angiographic images. the reliability of the methods was statistically compared in a clinical setting of 42 angiograms and 100 measurements performed by the same users. this study suggests that both techniques could be used for clinical applications with similar efficiency results. the 3d rotational angiography is an increasingly used method for cerebral aneurysms treatment planning. this complex imagistic method permits a better evaluation of cerebral aneurysms anatomy by an improved delimitation of vessels and aneurysms contours. moreover, the 3d dataset can be used to calculate aneurysm volume. it is known the important role of aneurysm volume calculation in coil embolization treatment. to assess an optimal degree of coils aneurysm packing, it has become imperative to determine preoperatively the volume of the aneurysm to be embolized. methods retrospective assessment of aneurysm volume was achieved with two measurement methods by using twodimensional copies or 3d reconstruction images (digital or printed form in sagittal and coronal angiography section) obtained with a siemens artis angiograph with rotational digital subtraction possibilities for 42 intracranial aneurysms. ellipsoid approximation method this method of volume measuring is based on the assumption that the aneurysms shape could be geometrical approximated with an ellipse. an ideal ellipsoid volume can be calculated using the mathematical relationship between the length (l) large diameter (d) and small diameter (d). for these measurement techniques we have gone on the premise that exposure of an aneurysm with a two-dimensional angiography is performed with the vascular lesion located exactly or very close to isocenter of mobile c-arm. the distance between x-ray source and image amplifier was maximum (117 cm and 130 cm for exposures ap [anterior-posterior] that romanian neurosurgery (2012) xix 2: 96 – 102 97 exposures profile) to ensure that there is plenty of room to manoeuvre both the patient and the mobile c-arm during the procedure. diameter of the image intensifier entrance was known for all angiography. two-dimensional images obtained by contrast injection and fluoroscopic exposures were printed on transparent film or paper. also the digital images in dicom format obtained through angiography dr and sd regime were processed using e-film medical software in multiplanar reconstruction (mpr). mathematical technique by this technique the printed image of aneurysm was measured with a ruler directly on film, while digital images were measured using e-film medical software that allow a direct measurement of aneurysm size (figure 1). aneurysm volume was estimated by using mathematical equation corresponding to the formula of volume of a perfect ellipse: figure 1 aneurysm measuring on e-film multiplanar reconstruction computerized technique by the second technique the surface reconstruction of a volume can be achieved by establishing correspondence between points on two images. the relationship between the two images defined by the connection points is used to reproduce the epipolar geometry and create the epipolar images used for volume generation. materialization of connection points can be automatically or interactively achieved. automatic generation of connection points envi algorithm can automatically generate the contact points, based on figure characteristics from the image. choosing the option of interactive definition of connection points requires a manually definition of them between the two stereo images. automatic generation control contains specific parameters that correctly defined can lead to a right-left correlation of the two images as real as possible and finally to extract a volume close to reality. epipolar geometry constrains the epipolar points that lie on an epipolar line in the left image to be projected on the epipolar line corresponding in the image on the right. fundamental matrix is collinearity that offer a correlation between the epipolar lines and allows us to establish the epipolar line equation of the right image corresponding to a given point in left image and vice versa. fundamental matrix is calculated from one or more pairs of images with the same characteristics of magnification and focusing. figure 2 aneurysm measuring by epipolar geometry 98 chiriac et al volumetric assessment of intracranial aneurysms thus, the aneurysm image on film or print paper is scanned using an epson perfection v700 photo scanner at around 1000 x 1000 pixels. these digitized images were calibrated for the magnification and angle of entry of x-ray flux and then exposed to the same three-dimensional coordinate system. adjust brightness / contrast and demarcation contours were used for manual segmentation of the aneurysm. after segmentation of the aneurysm in two projections, a computer program (autocad) was used to reconstruct three-dimensional aneurysm as a superposition of several ellipses. each ellipse is reconstructed based on four points corresponding to intersection of the epipolar plan with the outline aneurysm in both projections. numerical integration of the multiple overlapping ellipses provides the estimated volume of aneurysm (figure 2). aneurysm is reconstructed by the superposition of at least 60 ellipses. 3d-generation softwear methods the images acquisition for 3d reconstruction of vessels is done by using an 3d inspace acquisition program option. this is a basic technique for 3d reconstructing data set form acquired 2d imaging in dynavision rotational angiography mode. by this protocol images acquisition a series of 150 to 200 axial images are acquired in a period of 5-8 seconds. dynavision is a system-integrated solution for 3d imaging reconstruction in rotational angiography. dynavision acquisition for the softwaer inspace 3d benefits by predefined setup parameters. 3d dsa radiological parameters are preset as: the tube voltage 90kv, tube current in 173m, pulsed 3.9 ms, focusing 0, frame rate 10p / s. dynavision generates exposure under extremely precise radiation emission angles, providing optimal overlap of mask and contrast images, even at their low frame rates and high speed rotation. also ensure minimize radiation dose to the patient, reduced examination time and improve image quality and patient comfort. the imaging projections obtained on the basic computer system are transferred automatically to the post-processing computer unit (syngo workplace-syngo fastview) by selection of send to 3d command. thus, the 3d images are automatically reconstructed and displayedon the monitor unit syngo workplace. for the aneurysm volume measurement the volume analysis command is selected (figure 3). a new window it will open requesting a manual contrast / brightness adjustment that will allow a clear highlight of the vascular tree. then, there will be a manually demarcation of the volume of interest to be measured (aneurysmal neck and sac) by selecting inspace you command. finally, to get automatic calculation of anuerysm volume the compute volume command will be selected. the volume of demarcated vascular area is quantified by integration of all pixels enrolled in 2d vascular contour. the result is visualised in four windows on the workplace syngo monitor (figure 3). imaging technique validation for the beginning, we had to establish if the angiographic image acquisition system has a similar precision for 2d images (face, profile) and 3d images and if it’s sufficiently precise to allow accurate volumetric measurement. thus, our angiographic system (siemens axiom artis dfa, germany) was tested by using four steel balls with different diameters (shall appear 1). romanian neurosurgery (2012) xix 2: 96 – 102 99 figure 3 aneurysm measuring by software methods their diameters were chosen in order to cover most of the dimensional limits of intracranial aneurysms. thus, in a first phase metal balls were accurately measured with a micrometer with an accuracy of 0.01mm (figure 4 a, b, c, d). the values obtained were considered the actual dimensional values. figure 4 aneurysm measuring by micrometer, and on dr, sd and 3d images tabel 1 nr. test diametru prin masurare cu micrometru (ømm) diametru prin masurare pe achiziţie imagistica plană (ømm) diametru prin masurare pe achiziţie imagistica 3d (ømm) dr sd bila 1 6,45 6,1 6,0 6.27 bila 2 10,25 10,4 10,1 10,4 bila 3 15,05 15,3 15.0 15.4 bila 4 20,45 19,8 20.1 20,4 after that, balls were investigated by planar angiographic imaging acquisition 2d (face and profile) and 3d, using the same acquisition parameters as for routine clinical investigations. 2d angiographic imaging acquisition was made in dr (direct) and sd (digital subtraction) modes (figure 3). four ball diameter values obtained by direct measurement in 2d (dr and sd) and 3d are presented in table 1. discrepancy (measurement error) between the real volume and that obtained by angiographic imaging acquisition varied upward or downward from 0.2% for ball 100 chiriac et al volumetric assessment of intracranial aneurysms test of 20.45 mm to 2.9% for ball test of 6.45 mm. these small discrepancies obtained were considered statistically nonsignificant. the method of percutaneous angiographic acquisition and image processing unit allows us to obtain angiographic images with near-realdimensional features. statistic analysis in this study we statistically compared each of the two methods of analysis in each measurement techniques by nonparametric tests because the scores of subjects with measurements is not a normal distribution (gaussian). statistical test applied to verify differences in overall was non-parametric friedman test for more than two sample pairs (with repeated measurements, because each subject was measured by all three analysis techniques: ellipsoidal approximation mathematical / computer technique and software) and when there were found global significant differeces between the three measurments techniques, nonparametric wilcoxon test of was applied for two paired samples (two repeated measurements) to compare two by two analysis techniques applied in each measurmet methods used. results mean of patient’s age from the study group was 51.19 years (aged between 22 and 69 years). gender distribution showed a dominance of females at a ratio of 2:1. distribution depending on location of aneurysms show a dominance of lesions from the anterior circulation (13 antcoa, 10 mca, 4 icabif, 3 ophthalmic, pericalosala 2) to those of the posterior circulation (7 postcoa, 2 basilar tip, one pica). average values of measured aneurismal volume were 398.1mm3 for ellipsoidal approximation method by mathematical technique, 320.4mm3 for ellipsoidal approximation method by computer technique of and 320.1 mm3 for software measurement method. statistical correlation between means aneurysm volumes depending on the method of measurement related to their location showed that the best correlation was for the location of the basilar tip a and the weakest for the location of ophthalmic a (table 2, chart). based on statistical analysis obtained from the friedman test we found statistically significant differences at p £ 0,05 threshold between the three techniques of analysis [χ2 (2) = 8.714, p = 0.013] (annex 6). test statistics a 42 8.714 2 .013 n chi-square df asymp. sig. friedman testa. tabel 2 localization ellipsoidal approximation – mathematical technique ellipsoidal approximation –computer technique software methods acm 341,7726 314,7585 314,4954 acoant 116,0076 127,9095 128,0657 a.copost 724,6029 533,1759 532,3124 bif.aci 199,7813 186,2480 185,7411 a.oft 1407,4156 1008,4773 1006,7750 a.perical 296,3897 237,2902 236,3053 a vf.bazil 107,0950 108,1665 108,5917 pica 195,0467 152,3627 150,7513 romanian neurosurgery (2012) xix 2: 96 – 102 101 to check significant differences between the three techniques of analysis we applied the wilcoxon test. the results were as follows: there were significant differences at p £ 0,05 threshold between ellipsoid approximation method by mathematical technique and software method [z = 2.107, p = 0.035], meaning that measurements by ellipsoid approximation by mathematical technique are significantly higher compared with measurements obtained by software; there are significant differences at p £ 0,05 threshold between ellipsoid approximation method by mathematical technique and ellipsoid approximation method by computer technique [z = 2.169, p = 0.030], meaning that measurements by ellipsoid approximation method by mathematical technique are significantly higher compared with measurements obtained ellipsoid approximation method by computer technique; there were no statistically significant differences at p £ 0,05 threshold between method software and ellipsoid approximation method by computer technique [z = 1.532, p = 0.126]. discussions these discrepancies have been highlighted statistics on the difference "imaging behaviour" between different types of aneurysms after injection of the contrast in interventional procedures. also, precision of planar angiographic imaging acquisition and of the 3d is usually estimated by manual injections of contrast, known that speed of injection is a relative variable factor. in addition, it is important to note that the measurement volume purchases based on angiographic imaging may vary depending on how the display was chosen by the operator. for standardization of angiographic images of aneurysms, window settings should be adjusted for the purposes of background suppression artefacts and quality of aneurysm contour edges. 3d reconstructions based on rotational angiographic images are influenced by technical and physiological limitations of the method of acquisition. possible distortion of system acquisition due to equipment vibration, dilution of contrast medium due to blood flow dynamics and data degradation due to pulsation, amplified respiratory movements and heterogeneity of surrounding tissue can reduce image quality. these degradations generally cause unclear imaging data, resulting in increased difficulty in segmentation of structures of interest, such as aneurysmal contours. to maximize the aneurysmal sac filling with contrast agent throughout the rotational cycle, it has been shown that the quality of the contrast bolus injection (volume, flow rate) improves visualization of aneurysms on 3d reconstruction compared with continuous flow technique. visualisation of saccular aneurysms by 3d reconstruction of angiographic imaging acquisition dates is directly related to intraaneurysmal hemodynamic, which in turn is 102 chiriac et al volumetric assessment of intracranial aneurysms closely related to the geometric relationship between the aneurysm and parent vessel. in case of the bifurcation or terminal aneurysms hemodynamic experiments described a rapidly intra-aneurysmal circulation without the formation of vortices and stasis, while for lateral aneurysms were described a regular flow model with inflow to the distal extremity of the neck, vortex flow in the centre and reflux along the aneurysm wall. while the bifurcation aneurysms (such as those described often in the middle cerebral artery, communicating artery pericallosal, carotid bifurcation and basilar tip) can be identified with a highly accurate imaging, lateral aneurysms viewing (internal carotid artery in cavernous segment, ophthalmic and other supraclinoid aneurysms) with small neck can sometimes be affected by incomplete filling with contrast. conclusions restrictions mentioned above may be sources of measurement errors of aneurysmal volume. however, discrepancies identified between the real volume and that obtained by angiographic imaging for small and medium size aneurysms were lower, the methods and techniques measurement are considered valid for clinical use. references 1. bland jm, altman dg. comparing methods of measurement: why plotting difference against standard method is misleading. lancet 1995;346:1085–1087; 2. javier oliva´n besco´s, marjan j. slob, cornelis h. slump, menno sluzewski, and willem jan van rooi (2005) volume measurement of intracranial aneurysms from 3d rotational angiography: improvement of accuracy by gradient edge detection, am j neuroradiol 26:2569–2572; 3. tamatani s, ito y, abe h, koike t, takeuchi s, tanaka r. evaluation of the stability of aneurysms using detachable coils: correlation between stability of aneurysms and embolized volume of aneurysms. ajnr am j neuroradiol 2002; 23:762-767; 4. vincent costalat, igor lima maldonado, olivier strauss, alain bonafé (2011) toward accurate volumetry of brain aneurysms: combination of an algorithm for automatic thresholding with a 3d eraser tool, j neurosci methods 7. microsoft word 9ciureaav_tascua_intraventricular_f 306 a.v. ciurea et al intraventricular meningioma in 4 years old child intraventricular meningioma in 4 years old child: case presentation a.v. ciurea, iulia vapor, a. taşcu “bagdasar-arseni”clinical emergency hospital, bucharest, romania abstract meningiomas represent a rare entity in pediatric population. also, in small children, intracranial tumors can reach giant dimensions with minimal neurological findings due to some special features of the brain and cranial vault at this age. the main diagnosis tool is the mri. we choose to present the case of a 4 years old child with a giant intraventricular meningioma. keywords: child, meningioma, intraventricular tumour, mri introduction although meningiomas represent the most common benign tumor in adult population, it accounts for less than 3% of primary intracranial tumors in children. in pediatric population, the features of this histological entity are very different from the adults. in children, meningiomas have unusual localizations more frequently than in adults. for example intraventricular meningiomas have an incidence of approximately 17% in the first two decades of life, compared with adults in which the incidence is approximately 5%. other localizations more frequent seen in children are posterior fossa and primary intracerebral without any obvious dural attachment. another feature frequently seen in children is lack of dural attachment (28.5%), whereas it is extremely rare in adults. this fact is probably due to the origin of the meningioma in the leptomeningeal elements located within the parenchyma or near the ventricles rather than the dura mater. case presentation a four years old girl was admitted in the hospital for partial right brachial motor seizures, with progressive evolution in the last 3 months, and headache. the neurological exam revealed a right hemiparesis, right central facial palsy and gait disturbance. the development was normal and she had no history of trauma or medical problems. the brain mri revealed a well-enhanced tumor with maximal dimensions 71x78x74 cm, noninfiltrative (figure 1) located in the left lateral ventricle with secondary left ventriculomegaly and midline shift of approximately 1, 5 cm (figure 2). laboratory analyses were normal and the ophthalmological exam revealed papillary edema. a left frontal transcortical transventricular approach was performed to remove the tumor. we found a well defined mass, noninfiltrative, with high consistency, very well vascularized. gross total resection was accomplished with no significant intraoperative incidents. after the operation the patient was conscious, with right hemiparesis, right central facial palsy. romanian neurosurgery (2011) xviii 3: 306 – 309 307 a b c figure 1 (a, b, c): preoperative mri: t1 with contrast enhancement images shows a well defined, noninfiltrative tumor, located in the left lateral ventricle with secondary left ventriculomegaly and midline shift , with dimensions of 71x78x74 cm. figure 2 preoperative mrit2 weighted image reveales the secondary ventriculomegaly with signs of transependimal absorbtion od csf, but no surrounding tumoral edema. the ct-scan performed 24 hours after the operation confirmed the gross total resection. the patient was discharged 7 days postoperative with the neurological deficits partial recovered. the histopathological result was atypical meningioma with small areas of necrosis, patternless aspect, with small cells with high nucleocytoplasmic ratio. the immunohistochemical tests showed ema positive, pgr positive in 30% and ki 67 positive in 15%, those data confirming the histopathological aspect. the child was referred to the oncology department to establish the opportunity of radiotherapy or chemotherapy at this moment. 308 a.v. ciurea et al intraventricular meningioma in 4 years old child a b c figure 3 (a, b, c): one month postoperative mri confirms the gross total removal, but also shows a compresive subdural hydroma. at the one month follow-up control the patient presented with the neurological deficits improved from the discharge moment. the brain mri showed no signs of residual tumor, but revealed a subdural hydroma, with compressive effect on the brain (figure 3) so we decided to operate again the patient and evacuate the hydroma. after the operation the motor deficit improved. in case of unfavorable evolution of the hydroma at the next follow-up control we will insert a subduroperitoneal shunt. discussions meningiomas can affect any age group, but usually their incidence increases with advancing age, in pediatric population representing less than 3% of all primary brain tumors. congenital or infantile cases are extremely uncommon and are encountered in the literature as case presentations. there are two well known predisposing factors for appearance of meningiomas in children: neurofibromatosis 2 and prior exposure to ionizing radiation. approximately 20-40% of children with meningiomas have nf-2, especially those with multiple tumors. the localizations of meningiomas in children are different from their adult counterparts: convexity (50%), temporal (17%), lateral ventricles (17%) and falxtentorial junction (17%). in adults the localizations are: parasagital (30.8%), convexity (15.2%), tuberculum sellae (12.8%), sphenoidal ridge (11,9%), olfactory groove (9,8%), falx (8%), lateral ventricle (4,2%), tentorial (3,6%) and others (3,7%). the symptomatology depends on the age of and the localization of the tumor. in small children the tumors can reach giant romanian neurosurgery (2011) xviii 3: 306 – 309 309 dimensions due to the ability of the skull to compensate the volume changes, the increased volume of csf in the subarachnoid spaces and the cisterns and a higher volume of water in the extracellular space. later, the symptomatology depends on the localization of the tumor and is represented by focal neurological deficits, the signs of increased intracranial pressure and seizures. the lack of symptoms in small children can lead to giant tumor dimensions at the moment of diagnosis with many intra and postoperative complications. also in children the incidence of highgrade meningiomas is higher than in adults, have a tendency to grow more rapidly and undergo malignant changes. due to this features the rate of reccurence is much higher. the most important prognostic factor is the total resection.the radiotherapy is prohibite at ages smaller than 3 years old. conclusions we presented a case of giant intraventricular atypical meningioma in a small child (4 years old). this tumor is very rare at this age and in the literature this pathology is reported usually as case presentations or small series due to the rarity of this affection at this age. the simptomatology is poor, the dimensions at the time of diagnose are usually giant and the outcome depends on the grade of tumor resection. abbreviations used in this paper: ema=epithelial membrane antigen; pgr=progesterone receptor; csf= cerebrospinal fluid; mri=magnetic resonance imaging; nf-2=neurofibromatosis type 2; ctcomputed tomography. correspondent author: dr. al. tascu “bagdasar-arseni” clinical emergency hospital, bucharest, romania tascu_alexandru@yahoo.com references 1. albright al, pollack if, adelson fp: principles and practice of pediatric neurosurgery: 1191-1192, 2009. 2. ciurea av, arseni c, lenke horvath: neurosurgical diseases of infant and young child (0-3 years). medical publishing house. bucharest, 1979 3. ciurea av, arseni c, lenke horvath: paediatric neurosurgical pathology. academy publishing house. bucharest, 1980. 4. elisabeth j. rushing, cara olsen, mena h, mariaeugenia rueda, youn-soo lee, keating rf, packer rj, mariarita santi: central nervous system meningiomas in the first two decades of life: a clinicopathological analysis of 87 patients. j neurosurg pediatrics 6: 489495, 2005 5. kyung sun song, sung-hye park, byung-kyu cho, kyu-chang wang, ji hoon phi, seung-ki kim: third ventricular chordoid meningioma in a child. case report. j neurosurg pediatrics 2: 269-272, 2008. 6. lakhdar f, arkha y, el ouahabi a, melhaoui a, rifi l, derraz s, el khamlichi a: intracranial meningioma in children: different from adult forms? a series of 21 cases. neurochirurgie. 56(4):309-14, 2010. 7. mark s greenberg. hanbook of neurosurgery: 238239, 2006 8. morina a, kelmendi f, morina o, pazanin l, dragusha s, ahmeti f, morina d: rhabdoid meningioma in an eight-year-old child. med arh. 64(2):123-4, 2010 9. rohringer m, southerland gr, louw df, sima aa: incidence and clinicopathological features of meningioma. j neurosurg 71: 665-672, 1989. 10. sheikh by, siqueira e, dayel f: meningioma in children: a report of nine cases and a review of the literature. surg neurol. 1996; 45(4):328-35 11. vachhrajani s, jea a, rutka ja, susan blaser, cusimano m, rutka jt: meningioma with dural venous sinus invasion and jugular vein extension. case report. j neurosurg pediatrics 2: 391-396, 2008. doi: 10.33962/roneuro-2021-062 hyperbaric oxygen therapy. application in traumatic brain injury ivan david lozada-martínez, oscar javier diaz-castillo, michael gregorio ortega-sierra, jhon jairo gonzález -monterroza, teddy javier padilla-durán, h. sebastián castillo-pastuzan, jhoan sebastián robledo-arias, maria paz bolaño-romero, alfonso pacheco-hernández, luis rafael moscote-salazar romanian neurosurgery (2021) xxxv (3): pp. 365-369 doi: 10.33962/roneuro-2021-062 www.journals.lapub.co.uk/index.php/roneurosurgery hyperbaric oxygen therapy. application in traumatic brain injury ivan david lozada-martínez1,2,3,4, oscar javier diaz-castillo5, michael gregorio ortega-sierra6, jhon jairo gonzálezmonterroza7, teddy javier padilla-durán7, harold sebastián castillo-pastuzan8, jhoan sebastián robledo-arias9, maria paz bolaño-romero1, alfonso pacheco-hernández1,2,3, luis rafael moscote-salazar1,2,3 1 medical and surgical research centre, cartagena, colombia 2 colombian clinical research group in neurocritical care, university of cartagena, cartagena, colombia 3 latin american council of neurocritical care, cartagena, colombia 4 globan neurosurgery committee, world federation of neurosurgical societies 5 medical and surgical research centre, universidad del sinú, cartagena, colombia 6 school of medicine, corporación universitaria rafael nuñez, cartagena, colombia 7 school of medicine, universidad del magdalena, santa marta, colombia 8 school of medicine, universidad de nariño, pasto, colombia 9 school of medicine, universidad del quindío, armenia, colombia abstract the extent and progression of neurological impairment in traumatic brain injury depend significantly on the area of perilesional gloom, where neuronal apoptosis occurs. inhibition of apoptosis becomes a therapeutic strategy to preserve brain tissue and promote functional recovery. hyperbaric oxygen therapy is a treatment by which 100% oxygen is administered, with the aim of achieving a higher pressure than atmospheric pressure at sea level, to decrease ischemia and intensity of inflammatory processes triggered, compromising the viability of the tissues. for mild traumatic brain injury, studies indicate that hyperbaric oxygen therapy is no better than sham treatment. for acute treatment of moderate to severe traumatic brain injury, although the methodology is questionable in certain studies due to the complexity of the brain injury, hyperbaric oxygen therapy has been shown to be beneficial as a relatively safe adjunctive therapy. the objective of this review is to discuss aspects related to the pathophysiology of traumatic brain injury, the mechanism of action of hyperbaric oxygen therapy, and correlate these results with the use of this therapy in the prevention of neuronal injury, supported by original studies reported in the scientific literature keywords hyperbaric oxygenation, traumatic brain injuries, brain hypoxia-ischemia, inflammation, neuroprotection corresponding author: ivan david lozada-martínez medical and surgical research centre, cartagena, colombia ilozadam@unicartagena.edu.co copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 366 ivan david lozada-martínez, oscar javier diaz-castillo, michael gregorio ortega-sierra et al. introduction traumatic brain injury (tbi) is generated when there is a sudden acceleration-deceleration process inside the skull caused by all kinds of external forces, among which traffic accident is one of the most common causes [1]. it is considered a major global health problem, being one of the main causes of death and disability, entailing functional, social and economic consequences [2,3] brain injury in cranial trauma is triggered in two stages, the first occurs immediately after the initial mechanical impact, and in most patients is terminated before admission to the medical institution, representing a permanent neuronal loss [1,4]. subsequently, within hours, days, and sometimes even weeks, given the insufficient oxygen supply of the surrounding regions, biochemical and metabolic processes are generated that culminate in the apoptosis of neuronal cells [4]. considering the fact that energy metabolism in the brain is based on aerobic processes, hyperbaric oxygen therapy (hbot) has been proposed in recent years as a neuroprotective strategy directed towards the containment of secondary processes, in addition to the preservation and reactivation of the penumbra area [5,6]. the objective of this review is to discuss aspects related to the pathophysiology of traumatic brain injury, the mechanism of action of hyperbaric oxygen therapy, and correlate these results with the use of this therapy in the prevention of neuronal injury, supported by original studies reported in the scientific literature. how hyperbaric oxygen therapy works? hbot targets tbi-induced ischemia by exposing patients to an environment that exponentially increases the amount of o2 inspiration, producing hyperoxia in the plasma, and consequently, an accentuation of o2 supply for diffusion to brain tissue, where hypoxia can be decreased, and thus, prevent neuronal death [7,8]. for mild tbi, studies indicate that hbot is no better than sham treatment [9]. for acute treatment of moderate to severe tbi, although the methodology is questionable in certain studies due to the complexity of the brain injury, hbot has been shown to be beneficial as a relatively safe adjunctive therapy [7,9]. the therapeutic effects in moderate tbi, are attributed to several pathophysiological mechanisms, including: increased arterial oxygen pressure and oxygen levels in brain tissue, increased diffusion velocity and effective oxygen diffusion distance, reduction of brain tissue edema and intracranial pressure, neuronal protection from ischemic death by acceleration of collateral circulation, stimulation of angiogenesis and neurogenesis accompanied by repair of injured microcirculation, and prevention of microthrombus formation [7,8,10]. other studies have shown that repetitive application of hbot after moderate tbi attenuates reactive astrogliosis and glial scarring, in addition to decreasing the expression of inflammatory mediators [11]. additionally, research in murine models with moderate tbi induced and treated with hbot showed improvement in spatial learning and memory [7,12]. during the acute phase of severe tbi, the metabolic demands of the brain increase, but o2 delivery to the brain is limited due to a reduction in cerebral blood flow, as well as diffusion barriers caused by capillary endothelial edema [7,8,13]. this o2 deficiency causes failures in cellular respiration and other aerobic biochemical events, activating the anaerobic machinery, with consequent depletion of cellular energy (atp), and finally, cell death [8]. the crisis resulting from inadequate o2 supply produces electrolyte imbalance, secondary to the lack of energy for the normal function of the na+/k+ atpase pump within the cells of the nervous system [8,14,15]. this imbalance leads to increased calcium influx, resulting in considerable release of excitatory neurotransmitters, and further disruption of mitochondrial metabolism, resulting in excessive accumulation of free radicals and as the neuroinflammatory response continues, apoptosismediated proteins initiate the process of cell death [8,16]. mechanism of neuroprotection most of the damage following tbi occurs due to a secondary process. this includes cell death, oxidative stress, neuroinflammation and glutamate excitotoxicity [14,15,17]. baratz-goldstein et al [7]. showed how immediate and delayed hbot, can ameliorate the elevation of reactive astrocytes seen after moderate tbi, successfully preventing the demyelination process [7]. in addition, it has been reported that following tbi, there is a decrease in previously elevated inflammatory processes, such as inhibition of caspase 3, tnf-α expression, nf-κb, 367 hyperbaric oxygen therapy upregulated microglia, and elevation of il-10 [13,18,19]. based on the above, it can be said that hbot exhibits multiple mechanisms of neuroprotection (table 1). considering the above, when additional o2 is available for diffusion through the capillary endothelium, anaerobic metabolism is converted back to aerobic metabolism, allowing mitochondria to restore depleted cellular energy [8,16]. the upregulation of nrf2 was suggested as one of the mechanisms that help protect neuronal loss [18]. yang et al [19]. evaluated hbot treatment following intracerebral hemorrhage in murine models, finding that this intervention upregulated microglia characteristics, potentially decreasing diminished neuronal loss [19]. another explanation for the neuroprotective qualities of hbot in moderate tbi is related to changes in cerebral blood flow [7,8]. hbot stimulates vasoconstriction, leading to a decrease in cerebral blood flow. this mechanism promotes neuroprotection as it reduces trauma-induced intracranial pressure and cerebral edema, thus improving cognitive functions [8,16]. this effect on cerebral blood flow after the use of hbot is mainly attributed to a decrease in the concentration of nitric oxide in the brain, as well as to an inclination in the production of reactive oxygen species [20]. following this treatment, dependent improvements in general motor function, cognitive and behavioral tests, neurological function and locomotor coordination have been observed [8]. proteomic studies, have observed that in acute tbi there is a decrease in the levels of pakt/akt, pgsk3β/gsk3β, and β-catenin, which facilitates neuronal apoptosis. he et al [13]. demonstrated increase in these proteins after instituting hbot [13]. table 1. neuroprotective effects of hyperbaric oxygen therapy reduces inflammation induces bcl-2 and bcl-xl, reduces cas-3 inhibits neutrophil adhesion to endothelial cells inhibits permeability of mptp decreases il-8, tnf-α and mmp-9; increases il-10 decreases endothelin levels and regulates blood flow inhibits tlr4 and nf-κb expression reduces intracranial pressure inhibits apoptosis promotes neurogenesis and angiogenesis. increases pao2 of brain tissue. enhances nrf2 and ho-1 preserves tissue metabolism importance neuroinflammation is well established as a key secondary injury mechanism after tbi, and has long been considered to contribute to sustained damage after brain injury [5,21]. with hbot, the effect of high pressure, increased solubility and o2 diffusion characters are expected to improve oxygenation, modulation of inflammation and immune function, as well as promote angiogenesis [1]. comprehensive management of traumatic brain injury generally aims at maintaining oxygenation and perfusion, so hyperbaric oxygen has been proposed as a complementary therapy for tbi, both for the preservation of the functional capacity of the affected person, as well as for the increase in survival rate [2,6,9]. efficacy the prognosis of traumatic brain injury clearly depends on the cell death and survival processes occurring within the injured tissues, so neuroprotective therapies aim to improve function within the remaining viable perilesional brain tissue [16]. increased oxygen supply under hyperbaric conditions facilitates oxygen diffusion into the injured tissue, improving cellular energy metabolism, which attenuates cell signaling and cytosolic ischemic cascades, thereby reducing programmed cell death and subsequent necrosis [22]. many studies have consistently corroborated that hbot compared with standard care significantly improves markers of oxidative metabolism in the relatively uninjured brain [22]. hbot may also counteract vasodilation of capillaries within hypoxic tissues, thus minimizing extravascular fluid accumulation, reducing cerebral vasogenic edema and intracranial pressure [16]. this is why it has been postulated that hbot stimulates the restoration of antioxidant, angiogenic, neurogenic and anti-inflammatory gene expression. this translates into greater neurological recovery, as evidenced by the improvement of the glasgow score [5,13,23]. to obtain the benefits described above, this therapy should be started within the first hours, and several sessions should be established [5]. 368 ivan david lozada-martínez, oscar javier diaz-castillo, michael gregorio ortega-sierra et al. generalities hbot is a therapeutic option that consists in the inhalation of 100% oxygen, in a sealed hermetic chamber that increases the pressure to more than one absolute atmosphere (ata); (ata=101.3kpa) [1,3,4,5,16,24]. generally, a pressurization of 1.5-3.0 ata is used for one or more times a day, for one or two hours [25]. this ensures the administration of a higher partial pressure of oxygen in the blood, improving mitochondrial metabolism and tissue oxygenation [5,6,16]. the benefits found in this therapy have allowed recommending its use in a large number of pathological conditions (table 2), which is increasing over the years. hbot allows hemoglobin to be saturated to 100% and the volume of oxygen fraction bound to plasma to be elevated [4,16]. the latter can be used more easily than that bound to hemoglobin, so that oxygen is supplied even in conditions with erythrocyte deficit; therefore, hbot causes an increase in oxygen transport in the blood, increasing the force of oxygen diffusion in the tissues [16]. table 2. indications for hyperbaric oxygen therapy traumatic brain injury [6] cerebral palsy stroke [6] decompression sickness [6,16] anoxic brain injury [6] carbon monoxide poisoning cerebral edema*[7] minimization of tissue damage induced by radiotherapy [4,16] ictus [7] enhancing skin grafts [4,16] spinal cord injury*[7] autism* [16] acute central retinal artery insufficiency*[7] multiple sclerosis* [16] traumatic ischemia [7] air or gas embolism [4] gas gangrene [4] compartment syndrome [4] intracranial abscess [4] osteomyelitis [4] burns [4] wounds [4] non-approved use hbot has been in use for more than 50 years, but its application in the treatment of traumatic brain injury has been performed since the early 1960s [7]. in 1966, the first study reporting the neuroprotective effect of this therapy in rats was published by coe & hayes [26]. almost immediately, dunn & lawson [27]. demonstrated reduced mortality in a canine model with cerebral contusion, and since then, studies on the effect of hbot on blood flow, cerebral edema and intracranial pressure have been carried out. conclusion traumatic brain injury is a common health problem that causes permanent sequelae and considerably decreases the functional capacity of the sufferer. unfortunately, to date there is no treatment or intervention that fully ensures neurological functionality. hyperbaric oxygen therapy is a therapeutic option with the potential to decrease neuronal death by improving oxygen supply to the injured brain, thus controlling inflammation and apoptotic processes. the effectiveness of the intervention, however, depends on prompt medical attention and constant monitoring of hemodynamic and neurological variables. references 1. xing p, ma k, li l, wang d, hu g, long w. the protection effect and mechanism of hyperbaric oxygen therapy in rat brain with traumatic injury. acta cirúrgica bras. 2018; 33(4):341–53. 2. klugar m, kelnarová z, marečková j. the effectiveness of hyperbaric oxygen therapy on mortality in adults with craniotrauma: a systematic review protocol. jbi database syst rev implement reports. 2014; 12(12):54–66. 3. deng z, chen w, jin j, zhao j, xu h. the neuroprotection effect of oxygen therapy: a systematic review and meta‑analysis. niger j clin pract. 2018; 21(4):401–16. 4. brkić p, sanja p, danijela k, jovanović t. hyperbaric oxygenation as an adjuvant therapy for traumatic brain injury: a review of literature. period biol. 2014; 116(1):29– 36. 5. hu q, manaenko a, xu t, guo z, tang j, zhang jh. hyperbaric oxygen therapy for traumatic brain injury: bench-to-bedside. med gas res. 2016; 6(2):102–10. 6. yadav a, pawar m, garg r, banerjee n. to compare the effects of multiple sessions of hyperbaric oxygen therapy in neurological improvement in head injury patients: a prospective randomized trial. j neuroanaesth crit care. 2015; 2(2):110–3. 7. baratz-goldstein r, toussia-cohen s, elpaz a, rubovitch v, pick cg. immediate and delayed hyperbaric oxygen therapy as a neuroprotective treatment for traumatic brain injury in mice. mol cell neurosci. 2017; 83:74–82. 8. thorpe m, hubbard m, daly s, bergman t, samadani u, rockswold s, et al. hyperbaric oxygen therapy in the treatment of acute severe traumatic brain injury: a systematic review. j neurotrauma. 2017; 35(4):623–9. 9. crawford c, teo l, yang em, isbister c, berry k. is hyperbaric oxygen therapy effective for traumatic brain injury? a rapid evidence assessment of the literature 369 hyperbaric oxygen therapy and recommendations for the field. j head trauma rehabil. 2017; 32(3):e27–37. 10. vallée n, blatteau j-e, besnard s, abraini j, risso j-j, chazalviel l. effects of normobaric versus hyperbaric oxygen on cell injury induced by oxygen and glucose deprivation in acute brain slices. med gas res. 2016; 6(3):169. 11. jovanovic t, pekovic s, stojiljkovic m, savic d, dacic s, brkic p, et al. repetitive hyperbaric oxygenation attenuates reactive astrogliosis and suppresses expression of inflammatory mediators in the rat model of brain injury. mediators inflamm. 2015; 2015:1–17. 12. liu s, shen gy, deng sk, wang x, wu q, guo as. hyperbaric oxygen therapy improves cognitive functioning after brain injury. neural regen res. 2013; 8(35):3334–43. 13. he h, li x, he y. hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via akt/gsk3β/β-catenin pathway. neuropsychiatr dis treat. 2019; 15:369–74. 14. faden ai, loane dj. chronic neurodegeneration after traumatic brain injury: alzheimer disease, chronic traumatic encephalopathy, or persistent neuroinflammation? neurotherapeutics. 2015; 12(1):143–50. 15. kabadi sv, faden ai. neuroprotective strategies for traumatic brain injury: improving clinical translation. int j mol sci. 2014; 15(1):1216–36. 16. huang l, obenaus a. hyperbaric oxygen therapy for traumatic brain injury. med gas res. 2011; 1:21. 17. lozano d, gonzales-portillo gs, acosta s, de la pena i, tajiri n, kaneko y, et al. neuroinflammatory responses to traumatic brain injury: etiology, clinical consequences, and therapeutic opportunities. neuropsychiatr dis treat. 2015; 11:97-106. 18. meng xe, zhang y, li n, fan df, yang c, li h, et al. effects of hyperbaric oxygen on the nrf2 signaling pathway in secondary injury following traumatic brain injury. genet mol res. 2016; 15(1):1–7. 19. chen q, zhang b, li l, zhu g, tao y, tang j, et al. hyperbaric oxygen preconditioning attenuates neuroinflammation after intracerebral hemorrhage in rats by regulating microglia characteristics. brain res. 2015; 1627:21–30. 20. sánchez ec. mechanisms of action of hyperbaric oxygenation in stroke: a review. crit care nurs q. 2013; 36(3):290–8. 21. chen x, duan x-s, xu l-j, zhao j-j, she z-f, chen w-w, et al. interleukin-10 mediates the neuroprotection of hyperbaric oxygen therapy against traumatic brain injury in mice. neuroscience. 2014; 266(1):235–43. 22. gajewski bj, berry sm, barsan wg, silbergleit r, meurer wj, martin r, et al. hyperbaric oxygen brain injury treatment (hobit) trial: a multifactor design with response adaptive randomization and longitudinal modeling. pharm stat. 2016; 15(5):396–404. 23. liu w-c, wen l, wang h, gong j-b, zhan t-x, meng y-y, et al. neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats. j neurorestoratology. 2017; 5(1):85–91. 24. huang l, obenaus a, hamer m, zhang jh. neuroprotective effect of hyperbaric oxygen therapy in a juvenile rat model of repetitive mild traumatic brain injury. med gas res. 2016; 6(4):187-193. 25. bennett mh, trytko b, jonker b. hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury. cochrane database syst rev. 2012; 12:cd004609. 26. coe je, hayes tm. treatment of experimental brain injury by hyperbaric oxygenation. preliminary report. am surg. 1966; 32:493-495. 27. dunn je, lawson dd. effects of hypobaric and hyperbaric oxygen on experimental brain injury. in origins of hyperbaric medicine. national research council. 1966; 447-454. microsoft word 5.balasa.docx romanian neurosurgery (2012) xix 4: 279 – 288 279 our experience in surgical treatment of chiari type 1 malformations adrian bălaşa1, dorin nicolae gherasim2 1head of neurosurgery departement, targu mures clinical emergency hospital 2resident, neurosurgery departement, targu mures clinical emergency hospital abstract introduction: there are four types of chiari malformations described in the literature. due to the fact that it is a common finding in the general population (true chiari being present in 0,75% of the population), chiari 1 malformation was also called chiari anomaly. material and methods: in the last 5 years 17 patients with chiari i malformation have been treated in our clinic. there were 12 women and 5 men. the mean age was 43 years (between 21 and 60 years). the symptoms were grouped in 6 syndromes: brain stem and bulbar palsy syndrome, cerebellar syndrome, central cord syndrome, paroxysmal intracranial hypertension, scoliosis, pyramidal syndrome. surgical treatment: according to recent literature patients respond best when operated within 2 years from the onset of symptoms. we recommend early surgery for symptomatic patients. surgical treatment of chiari i malformation should accomplish several golds. first of all, there is the obvious need to decompress the lower part of the cerebellum. chiari i malformation being related to a small posterior fossa, the surgical treatment should realise enlargement of the total volume of the posterior fossa(7, 12). in the author’s opinion the key point in surgical treatment of chiari 1 malformation should be to reestablish the csf flow at the level of the foramen of magendie and foramen magnum. various approaches were used in the last five years in our clinic for the treatment of symptomatic patients: only osseous decompression in 2 patients; osseus decompression with dural grafting and intradural dissection of adhesions in 4 patients; osseous decompression with dural grafting, intradural dissection, and tonsillar coagulation in 11 patients results: the long-term (6 months postoperative) surgery-related result was considered excellent if symptoms resolved (7 patients). the result was considered good if the patient experienced significant improvement but also residual symptoms (8 patients). a poor result indicated no change in symptoms (2 patients). as for the surgical technique used, the vast majority of patients with good or excellent outcome at 6 months underwent osseous decompression with dural grafting, intradural dissection, and tonsillar coagulation conclusions: regarding chiari i malformations, the author considers that a proper patient selection is critical to prevent unnecessary procedures and maximize the outcome. in light of this study results and recent literature, the author considers that the surgical gold standard consists in three 280 bălaşa et al surgical treatment of chiari type 1 malformations key steps: posterior fossa craniectomy followed by durotomy and subarachnoid decompression of csf flow and last duroplasty. key words: small posterior fossa, osseous decompression, dural graft, syringomyelia introduction chiari malformations are perhaps one of the most controversial topics in neurosurgery today. there is a lack of agreement as to what defines these malformations, their symptoms and their natural history. if treatment is necessary, a wide variety of techniques have been proposed (9, 12). there are four types of chiari malformations described in the literature. due to the fact that it is a common finding in the general population (true chiari being present in 0.75% of the population), chiari 1 malformation was also called chiari anomaly while chiari 2 malformation is usually associated with myelomeningocele and is found only in this population (23, 29). chiari 3 and 4 malformations are extremely rare pathologies and are usually fatal until the age of two. epidemiology in a large series of patients, the mean age of onset of chiari i malformation is reported to be 25 years, and women account for 75% of patients. average duration of symptoms clearly related to chiari i is 3.1 years (range 1 month – 20 years)(9). material and methods in the last 5 years 17 patients with chiari i malformation have been treated in our clinic. there were 12 women and 5 men. the mean age was 43 years (between 21 and 60 years). the symptoms were grouped in 6 syndromes: 1. brain stem and bulbar palsy syndrome: caused by brainstem compression or syringobulbia ,including variable involvement of the cranial nerves, lower brain stem. symptoms include “down-beating” nystagmus (1 patient), sleep apnea (2 patients), vocal cord dismotility (2 patients), extraoccular eye movement abnormality (2 patients), hearing loss (2 patients), tinnitus (2 patients), dysphagia (5 patients) , headache (9 patients), neck pain (6 patients). 2. cerebellar syndrome: ataxia of the limbs or trunk (3 patients), nystagmus (2 patients), dizziness (6 patients) and dysarthria (3 patients) 3. central cord syndrome: caused by canal compression or syringomyelia, including pain (frequently “ burning” ) (7 patients), dissociated and posterior column sensory loss (12 patients). 4. paroxysmal intracranial hypertension: exertional headache and nausea, vomiting, and dizziness associated with a headache episode (in 2 patients) 5. pyramidal syndrome: stiffness and/or spasticity and hyperreflexia (10 patients), motor weakness and variable long tract signs (8 patients), atrophy (3 patients). 6. scoliosis (3 patients). mri evaluation magnetic resonance imaging of the cranio-spinal junction represents the gold standard diagnostic tool. a descend of tonsils of 5 mm or more below the foramen magnum is considered a pathological romanian neurosurgery (2012) xix 4: 279 – 288 281 tonsilar ectopia (18, 20), but this is still under debate (figure 1). in our study we classified the tonsils ectopia into two major groups: tonsils descended to c-1 (12 patients) and tonsils descended to c-2 or lower (5 patients). we also realised head ct scans which revealed osseous anomalies such as small posterior fossa in 3 patients and platybasia in one patient. we have also stoduied the presence of syrinx associated with chiari type 1 malformation (figure 2). a b figure 1 a: sagittal t1-weighted mr image of the brain showing herniation of cerebellar tonsils and a low-lying obex characteristic of chiari malformation type i. b: sagittal mr images of the cervicothoracicspine revealing syringomyelia figure 2 t2-weighted mr images of the spinal cord showing a holocord syrinx indications for surgery according to recent literature patients respond best when operated within 2 years from the onset of symptoms. we recommend early surgery for symptomatic patients. asymptomatic patients may be followed and operated upon if and when they become symptomatic (6, 8, 13). for patients who have been symptomatic and stable for years, we consider that observation is the correct management, surgery being indicated only if signs of deterioration appear. there are several strong indications for posterior fossa decompression such as drop attacks, dysphagia with aspiration, apnea and the presence of syrinx (1, 2). headache represents a controversial indication for surgery when it is the only symptom. we recommend using imagistic studies such as cine mri to establish csf flow impairment at the foramen magnum. if positive, surgery should be considered (4). objectives of surgery in the author’s opinion, surgical treatment of chiari i malformation should accomplish several golds. first of all, there is the obvious need to decompress the lower part of the cerebellum. chiari i malformation being related to a small posterior fossa, the surgical treatment should realise enlargement of the total volume of the posterior fossa (7, 12). in the author’s opinion the key point in surgery treatment of chiari 1 malformation should be to reestablish the csf flow at the level of the foramen of magendie and foramen magnum. although numerous techniques of surgery have been proposed since chiari first described the patology, all of them have been reported with advantages and 282 bălaşa et al surgical treatment of chiari type 1 malformations disadvantages, and none of them managed to fully accomplish the desired golds of surgery. techniques of surgery various approaches have been used for the treatment of symptomatic patients in our clinic in the last five years: only osseous decompression in 2 patients; osseus decompression with dural grafting and intradural dissection of adhesions in 4 patients; osseous decompression with dural grafting, intradural dissection, and tonsillar coagulation in 11 patients. we perform a more aggressive decompression and intradural dissection when a syrinx is present. i. osseus decompression (cranio-vertebral decompression/ laminectomy) first of all, the craniectomy should not be larger than 3x3 cm in order to avoid cerebellar sag (11, 16, 24). the author recommends c1 laminectomy in most cases, but extension to c2 laminectomy is also possible this being directly related to caudal displacement of the cerebellar tonsils (figure 3). figure 3 suboccipital craniectomy and c1 laminectomy ii. opening of the dura + intra-arachnoid dissection opening of the dura and intraarachnoid dissection of the scarring are, in the author’s opinion, the essential steps in chiari i surgery. the author strongly recommends them because osseus decompression only, does not achieve one of the main objectives of surgery, increasing the global volume of the posterior fossa. the dura is opened through a y shaped incision (figure 4 a). the next step is represented by intraarachnoid dissection of the arachnoid scarring, reestablishing the normal csf flow. visualization of the choroid plexus of the 4th ventricle and free flow of csf into the subarachnoid space consist in our opinion the proof of adequate decompression (figure 4 b). the author prefers not to aggressively resect the herniated tonsils; instead he realises a controlled and intended tonsillar ischaemia with bipolar coagulation of pica tonsillar branches. the author also tries to maintain the flow of the csf through the foramen of magendie, by lateral suspension of the medial part of the tonsills (figure 4 c). the author prefers to reserve syringomyelic drainage for patients who fail to respond (clinically, not radiologically) to initial posterior fossa decompression. avoiding the risks and complications associated with shunting procedures is desirable. a romanian neurosurgery (2012) xix 4: 279 – 288 283 b c figure 4 a y shaped durotomy; b internal debulking and coagulation of tonsils; c lateral suspension of the medial part of the tonsils iii. dural graft dura mater being inextensible, the author considers that in order to achieve one of the goals of treatment (enlargement of the posterior fossa), it needs to realise a dural graft. the author uses autologous graft – pericranium – in order to achieve a tight closure of the dura without csf leak (figure 5). tight closure of the dura is mandatory in our opinion because it prevents blood leakage from the extradural to the intradural space thus preventing subdural/intraarachnoid scarring. also, it prevents csf leakage and pseudomeningocele (30, 33). typical postoperative care involved the patient staying overnight in an intensive care unit. patients were discharged from the hospital between 4 and 10 days postoperatively. figure 5 duroplasty with pericranium results postoperatively, the condition of the patients was reassessed at the follow-up visits (1 month, 3 months, 6 months, 1 year) according to: symptoms resolution; signs and symptoms improvement; no change; signs and symptoms worsening. those associated with poor outcome include, signs or symptoms suggestive of syringohydromyelia; atrophy suggest a 284 bălaşa et al surgical treatment of chiari type 1 malformations similarly poor prognosis, whereas weakness in the presence of atrophy is bad response to surgery, as might be expected with the loss of alpha motor neurons. sensory loss has been widely recognized as largely unresponsive to surgery (figure 6). headache specifically, sleep apnea, and cervical pain in general appear to respond best. weakness in the absence of atrophy tends to respond well, while mild scoliosis, seems to respond reasonably well to surgery (figure 7). patients with signs of cerebellar syndrome and paroxysmal intracranial hypertension respond best to surgical management, followed by patients with pyramidal and brain stem syndromes. postoperative mr imaging assessment of the operative site in all patients demonstrates that the level of cerebellar tonsils was normal, the cisternal space at the level of the foramen magnum was indeed enlarged, and the width of csf column around the spinal cord was enlarged. postoperative spinal mr images obtained to assess the syringomyelia revealed the disappearance of the syrinx in 5 cases, and a significant decrease in syrinx size in 7 patients (figure 8). the long-term (6 months postoperative) surgery-related result was considered excellent if symptoms resolved (7 patients). figure 6 poor outcome symptoms and signs figure 7 good outcome signs and symptoms figure 8 preoperative/postoperative mri showing the reduction of syrinx the result was considered good if the patient experienced significant improvement but also residual symptoms (8 patients). a poor result indicated no change in symptoms (2 patients). romanian neurosurgery (2012) xix 4: 279 – 288 285 as for the surgery technique used, the vast majority of patients with good or excellent outcome at 6 months underwent osseous decompression with dural grafting, intradural dissection, and tonsillar coagulation (figure 9). figure 9 long-term outcome in relation to the surgery technique used complications there are several types of complications. we distinguish between complications related to conservative surgery (inadequate surgery) and actual postoperative complications (9, 11). in our study the complications were mostly postoperative complications and included csf leakage (1 patient), aseptic meningitis (2 patients), intraoperative changes in cardiovascular parameters (1 patient), and pseudomeningocele (1 patient). postsurgical moderate headaches, neck pain and fever represent the so-called "aseptic" meningitis and were regarded as adverse events rather than outright complications. analysis of a csf sample did not reveal evidence of infection and were successfully treated with steroid and analgesic medications. the symptoms resolved within a postoperative period no longer than 3 weeks and had no influence on the final treatment result. the csf leak required wound revision and lumbar drainage. at later follow up, a pseudomeningocele was clinically and radiologically demonstrated in one patient. no treatment was required. we had one recurrence due to conservative surgery (incomplete decompression). in this case only an extradural decompression was realised, so we performed dural grafting, intradural dissection, and tonsillar manipulation and coagulation on the second surgery. discussion in our clinic’s series, surgical treatment of chiari i malformation consisted of suboccipital craniectomy only (2 cases), arachnoid dissection of scarring (4 patients), reestablishing the csf flow at the foramen of magendie by shrinkage of the tonsils and duraplasty with autologous material (pericranium) (11 patients). the most important question that remains to be answered is whether good results could be achieved by leaving the arachnoid or dura intact. according to some authors, leaving the dura and the arachnoid intact can result in lower complication rates, but this data is counterbalanced by high rates of recurrence of symptoms and the need for revision surgeries. also, leaving the dura and the arachnoid intact results in 0 1 2 3 4 5 6 7 simple osseus decompression osseus decompresion +intraarachnoid dissection +dural graft osseus decompresion +intraarachnoid dissection and tonsilar coagulation+dural graft poor outcome good outcome excelent outcome 286 bălaşa et al surgical treatment of chiari type 1 malformations lower rates of syrinx reduction (7, 14, 22). the outcome data resulted from mcgirt et al study (21) (which used a simple decompressive craniectomy in 116 cases or craniectomy+duraplasty without arachnoid dissection in 140 cases) was significantly worse than the data provided by kleklamp et al (14) in their study (craniectomy, opening the arachnoid, opening the foramen of magendie and duraplasty in 371 cases). in our clinic’s series one of the two patients who underwent a simple suboccipital craniectomy experienced reccurence of symptoms, and needed a second surgery for intraarachnoid dissection and tonsils coagulation with duraplasty. given the low morbidity rates of these studies and the much better long term results in the literature for surgery techniques that involve at least duraplasty, the autor does not support decompression without duraplasty (2, 14, 22, 24). as for arachnoid opening and dissection there is also no unanimous protocol. the lower morbidity and complication rates reported by some authors are in favor of leaving the arachnoid intact (21). in his study, kleklamp revealed a correlation between arachnoid scarring and preoperative clinical symptoms and neurological outcome, and recommended opening the arachnoid in every decompression in order to restore csf pathways (27). in light of these studies, the author also recommends opening the arachnoid and dissection of scarring in order reestablish the csf flow at the level of foramen of magendie. because of high rates of morbidity related to syrinx drainage, the author does not recommend this maneuver as first choice (2, 8, 27). conclusions regarding chiari i malformations, the author considers that a proper patient selection is critical to prevent unnecessary procedures and maximize outcomes. the author belives that preoperatory longtime neurological deficit is a predictor of poorer outcome, making early surgery, mandatory. the key point of surgery in chiari i malformation is to allow a csf flow at the level of foramen of magendie. in light of this study results and recent literature, the author considers that the surgical gold standard consists of three key steps: posterior fossa craniectomy followed by durotomy and subarachnoid decompression of csf flow and last, duroplasty. corespondence: dr. adrian florian balasa phone: +40 265 212111 int. 297 +40 740 651053 fax:+40 265 210621 email: adrian.balasa@yahoo.fr address: spitalul clinic universitar de urgenta targu mures clinica de neurochirurgie str. gheorghe marinescu, nr. 50, et. 3 code 540136 references 1. abe t, okuda y, nagashima h, isojima a, tani s. surgical treatment of syringomyelia [in japanese]. rinsho shinkeigaku. 1995;35(12):1406-1408. 2. aghakhani n, parker f, david p, et al. long-term follow-up of chiari-related syringomyelia in adults: analysis of 157 surgically treated cases. neurosurgery. 2009; 64(2):308-315; discussion 315 3. alden, tord d. m.d., jeffrey g. ojemann, m.d., and t. s. park, m.d., surgical treatment of chiari i malformation: indications and approaches, neurosurg focus 11 (1):article 2, 2001. 4. aliaga l, hekman ke, yassari r, straus d, luther g, chen j, sampat a, frim d., a novel scoring system for assessing chiari malformation type i treatment outcomes., neurosurgery 70:656-665, 2012 romanian neurosurgery (2012) xix 4: 279 – 288 287 5. alzate, juan c. m.d., karl f. kothbauer, m.d., george i. jallo, m.d., and fred j. epstein, m.d., treatment of chiari type i malformation in patients with and without syringomyelia: a consecutive series of 66 cases, neurosurg focus 11 (1): article 3, 2001 6. bejjani, ghassan k. m.d., definition of the adult chiari malformation: a brief historical overview, neurosurg focus 11 (1):article 1, 2001 7. durham sr, fjeld-olenec k. comparison of posterior fossa decompression with and without duraplasty for the surgical treatment of chiari malformation type i in pediatric patients: a metaanalysis. j neurosurg pediatr. 2008;2(1):42-49. 8. ellenbogen, richard g. m.d., rocco a. armonda, m.d., dennis w. w. shaw, m.d., and h. richard winn, m.d., toward a rational treatment of chiari i malformation and syringomyelia, neurosurg focus 8 (3):article 6, 2000 9. galarza m, sood s, ham s. relevance of surgical strategies for the management of pediatric chiari type i malformation. childs nerv syst. 2007;23(6):691-696. 10. greenberg, sm, md, handbook of neurosurgery, 7th edition 2010, thieme 11. haroun ri, guarnieri m, meadow jj, kraut m, carson bs. current opinions for the treatment of syringomyelia and chiari malformations: survey of the pediatric section of the american association of neurological surgeons. pediatr neurosurg. 2000;33(6):311-317. 12. holly lt, batzdorf u. management of cerebellar ptosis following craniovertebral decompression for chiari i malformation. j neurosurg. 2001;94(1):21-26. 13. kaye, ah, md, phd, black, p., phd operative neurosurgery, 1st edition, 1999 14. klekamp, jorg md, surgical treatment of chiari i malformation—analysis of intraoperative findings, complications, and outcome for 371 foramen magnum decompressions, neurosurgery 71:365–380, 2012 15. klekamp j, samii m. introduction of a score system for the clinical evaluation of patients with spinal processes. acta neurochir (wien). 1993;123(3-4):221223. 16. klekamp j, samii m. syringomyelia—diagnosis and treatment. heidelberg, germany: springer verlag; 2001 17. kumar r, kalra sk, vaid vk, mahapatra ak. chiari i malformation: surgical experience over a decade of management. br j neurosurg. 2008;22(3):409-414. 18. loukas, marios m.d., ph.d.,1 brian j. shayota, b.s.,1 kim oelhafen, b.s.,1 joseph h. mill er, m.d.,2,3 joshua j. chern, m.d., ph.d.,2 r. shane tubb s, m.s., p.a.-c., ph.d.,2 and w. jerry oakes, m.d., associated disorders of chiari type i malformations: a review , neurosurg focus 31 (3):e3, 2011 19. mauer, uwe max m.d.,1 andreas gottschalk, m.d.,2 carolin mueller, m.d., linda weselek, m.d.,1 ulrich kunz, prof., m.d.,1 and chris schulz, m.d. resonance imaging in the clinical course of patients with chiari malformation type i, neurosurg focus 31 (3):e5, 2011 20. mazzola, catherine a. m.d., and arno h. fried, m.d, revision surgery for chiari malformation decompression, neurosurg focus 15 (3):article 3, 2003 21. mcgirt mj, attenello fj, datoo g, et al. intraoperative ultrasonography as a guide to patient selection for duraplasty after suboccipital decompression in children with chiari malformation type i. j neurosurg pediatr. 2008;2(1):52-57. 22. milhorat th, chou mw, trinidad em, et al. chiari i malformation redefined: clinical and radiographic findings for 364 symptomatic patients. neurosurgery. 1999;44(5):1005-1017. 23. mueller, diane n.d., r.n., c-f.n.p., and john j. oro’, m.d., prospective analysis of self-perceived quality of life before and after posterior fossa decompression in 112 patients with chiari malformation with or without syringomyelia, neurosurg focus 18 (2):ecp2, 2005 24. mutchnick is, janjua rm, moeller k, moriarty tm. decompression of chiari malformation with and without duraplasty: morbidity versus recurrence. j neurosurg pediatr. 2010;5(5):474-478. 25. novegno, federica m.d., massimo caldarelli, m.d., antonio massa, m.d., daniela chieffo, ph.d., luca massimi, m.d., benedetta pettorini, m.d., gianpiero tamburrini, m.d., and concezio di rocco, m.d., the natural history of the chiari type i anomaly, j neurosurg pediatrics 2:179–187, 2008 26.payner td, prenger e, berger ts, crone kr. acquired chiari malformations: incidence, diagnosis, and management. neurosurgery. 1994;34(3):429-434; discussion 434. 27. proctor, mark r. m.d.,1 r. michael scott, m.d.,w. jerry oakes, m.d., and karin m. muraszko, m.d., chiari malformation, neurosurg focus 31 (3):introduction, 2011 28. sakamoto h, nishikawa m, hakuba a, et al. expansive suboccipital cranioplasty for the treatment of syringomyelia associated with chiari malformation. acta neurochir (wien). 1999;141(9):949-960; discussion 960-961. 29. sindou m, chávez-machuca j, hashish h. craniocervical decompression for chiari type i-malformation, adding extreme lateral foramen magnum opening and expansile duraplasty with arachnoid preservation. technique and long-term functional results in 44 consecutive adult cases—comparison with literature data. acta neurochir (wien). 2002;144(10):1005-1019. 288 bălaşa et al surgical treatment of chiari type 1 malformations 30. stevenson, kevin l. m.d., chiari type ii malformation: past, present, and future neurosurg focus 16 (2):article 5, 2004 31. tubbs rs, lyerly mj, loukas m, shoja mm, oakes wj. the pediatric chiari i malformation: a review. childs nerv syst. 2007;23(11):1239-1250. 32. tubbs rs, beckman j, naftel rp, et al. institutional experience with 500 cases of surgically treated pediatric chiari malformation type i. j neurosurg pediatr. 2011; 7(3):248-256. 33. wetjen nm, heiss jd, oldfield eh. time course of syringomyelia resolution following decompression of chiari malformation type i. j neurosurg pediatr. 2008;1(2):118-123 34. winn r., md, youmans neurological surgery 6th edition, 2011, elsevier 35. won dj, nambiar u, muszynski ca, epstein fj. coagulation of herniated cerebellar tonsils for cerebrospinal fluid pathway restoration. pediatr neurosurg. 1997;27(5):272-275. 36. yanni ds, mammis a, ebersole k, roonprapunt c, sen c, perin ni. revision of chiari decompression for patients with recurrent syrinx. j clin neurosci. 2010;17 (8):1076-1079. 37. yarbrough ck, powers ak, park ts, leonard jr, limbrick dd, smyth md. patients with chiari malformation type i presenting with acute neurological deficits: case series. j neurosurg pediatr. 2011;7(3):244247. 38. yilmaz a, kanat a, musluman am, et al. when is duraplasty required in the surgical treatment of chiari malformation type i based on tonsillar descending grading scale? world neurosurg. 2011;75(2):307-313. 39. zhang zq, chen yq, chen ya, wu x, wang yb, li xg. chiari i malformation associated with syringomyelia: a retrospective study of 316 surgically treated patients. spinal cord. 2008;46(5):358-363 40. zhang y, zhang n, qiu h, et al. an efficacy analysis of posterior fossa decompression techniques in the treatment of chiari malformation with associated syringomyelia. j clin neurosci. 2011;18(10):1346-1349. microsoft word 8iacobgabriel_techniques 240 | iacob et al techniques of surgery for lumbar spinal stenosis             doi: 10.2478/romneu-2018-0031 techniques of surgery for lumbar spinal stenosis: a comparative study gabriel iacob, abdul salam, abdul rahman hawis “carol davila” university of medicine and pharmacy, bucharest, romania abstract: aim: to compare between classic open surgeries and minimally invasive surgeries in lumbar spinal stenosis. methods: a comparative descriptive study, involved 117 patients suffering from lumbar canal stenosis, aged between 40-70 years; admitted to department of neurosurgery from march 2011 till august 2016 in king fahad hospital in saudi arabia. study groups are consisted of group a as patients managed with classical laminectomy, group b as patients managed with endoscopic spinal procedures and group c as patients managed with microscopic decompression facilitated by the metrex tubular system. spss was used in data entry and analysis, and ethical considerations taken into consideration and participants filled the required inform consents. results: age of particaoncet ranged from 45 63 year, mean +/50. the degenerative canal stenosis with acute disc single level (cauda equina syndrome) was the most common type of lumbar canal stenosis encountered in group a, the unilateral foraminal and lateral recess stenosis without disc prolapse was the most common type of lumbar canal stenosis encountered in group b, while the unilateral foraminal and lateral recess stenosis without disc prolapse was the most common type of lumbar canal stenosis encountered in group c. classic laminectomy and disectomy used mostly in group a, endoscopic unilateral decompression lamino-foraminotomy without discectomy used mostly in group b and bilateral microscopic laminectomy without discectomy followed by unilateral microscopic lamino-foraminotomy without discectomy used mostly in group c. mean of operation duration was the highest in both gender of group a, followed by group b, then group c. unintended durotomy was the most common intra operative complications occurred in the whole study especially in group a. mean of blood lost was the highest in both gender of group a, followed by group b, then group c. postop complications in the patients of study groups was the highest in group a (33.3 %) ,followed by group b (8.5 %) and then group c (2 %). conclusion: microscopic decompression facilitated by the metrex tubular system is the most effective techniques of surgery for lumbar spinal stenosis and the least intraoperative and post-operative complications. key words: minimally invasive microscopic technique is the golden standard in lumbar canal stenosis. romanian neurosurgery (2018) xxxii 2: 240 261 | 241             introduction lumbar spinal stenosis (lss) is a common and often disabling, well-recognized spinal disorder that generally occurs in the sixth or seventh decade of life, although it can uncommonly occur in younger individuals. degenerative lss including intervertebral disc bulge, ligamentum flavum hypertrophy/calcification, facet joint hypertrophy, cause neural compression in the vertebral canal, lateral recess, or intervertebral foramen, resulting in pain, impaired function, and decreased quality life [6,39]. lumbar spinal stenosis or “loss of epidural reserve “could affect the central lumbar spinal canal± lateral recess ± the neuro-foramen or any combination of these, causing nervous impingement and vascular structures compression [36,75]. lumbar canal stenosis is the disease of elderly patients which interfere with the quality of the life of those patients which cannot tolerate the pain and it is impaired their function. recently there were increasing in the diagnosis of lss due the revolution in the radiological machines and increasing our experience in this disease as it is become the most common spinal surgery nowadays. surgical treatment of lss is recommended after failure of conservative medical therapy; however, the optimal procedure is still debated [45,73,74]. the treatment choice in lss should consider the following: a medical treatment should precede the surgical one. there is no recommendation referring to the timing of surgery, except motor deficit, cauda equina syndrome with bladder/bowel dysfunction. it is important to inform the patient about the difference between lumbar pain and the diagnosis of radicular syndrome and that surgery is not effective in lumbar pain. the number of nerve roots requiring decompression is often smaller than what appears in radiological studies. therefore, surgical procedures should not be based on x-ray studies alone. our surgical strategy according to the therapeutic objectives, constraints and physiological analysis of imbalances was clearly precised in the informed consent, corresponding with patients expectations: never preventive, minimally invasive decompressive technique for the lumbar canal and the roots, to minimize tissue damage, avoiding destabilization, minimizing time of surgery, postoperative morbidity, length of hospital stay and avoiding complications to achieve a good quality of life using a minimally invasive techniques for “maximum effect with minimum trauma”, thinking to an unique surgical procedure. material and methods a descriptive study involved 100 patients suffering from lumbar canal stenosis, aged between 40-75 years; admitted to department of neurosurgery from march 2011 till august 2016. spss was used in data entry and analysis, and ethical considerations taken into consideration and participants filled the required inform consents. 242 | iacob et al techniques of surgery for lumbar spinal stenosis             study groups group a: classical laminectomy. group b: endoscopic spinal procedures group c: microscopic decompression facilitated by the tubular lumbar system. all patients of this study were enrolled and surveyed 3, 6 12 and 24 months post operatory, for symptomatic lumbar spine stenosis at one/several levels or lumbar stenosis with aggravating factors. as a precondition for inclusion in the study, (unsuccessful) conservative treatment was first tried to all patients with radiculalgia, for at least 3 months, in an effort to reduce pain, augmenting walking distance, maintaining a better posterior pelvic tilt, improving muscles strength, endurance and flexibility. inclusion criteria included: co-existing multiple or single level disc prolapse with a multistage lumbar spinal stenosis without scoliosis, degenerative listhesis and posterior arthrosis at one or several levels, scoliosis with a small and a big radius of curvature and facet joint cyst. the conservative treatment methods that were used based on observation and clinical judgments included: activity restrictions like avoiding hyperextension and side bending, lumbo-sacral orthoses for a limited number of hours per day, to avoid atrophy of paraspinal muscles, physical therapy as active exercises in the form of stretching to increase lumbo-pelvic muscular stabilization, distraction, manipulation and neural mobilization, encouraging lumbar flexion and flattening of the lumbar lordotic curve, also exercises performed during lumbar flexion, such as bicycling, in aditiuon to massage, acupuncture, biofeedback, hot or cold packs and ultrasounds, analgesics such as antiinflammatory medications, vasodilators, anxiolytic and antidepressive medication, and epidural injections with corticoid products made blindly or under fluoroscopic control that used when pain relievers were ineffective and conservative treatment has failed to give adequate results in 3 months, surgical alternative was applied in all patients. characteristics of the study groups demographic characteristics of group a – classic open laminectomy group a included 21 patients who underwent classic open laminectomy under several procedure variations. age distribution of laminectomy patients the age distribution per gender within group a was balanced between sexes, with a smooth distribution between the extreme ages. the extreme ages, -both minimal (45 in both sexes) and maximal ages (66 vs. 68) in both sexes were well matched as were the age distributions in both sexes, despite the different number of patients per gender in this group, with slightly older (68 vs. 66) male patient. the patients in group b had ages between 45 and 63 years, with an average age of a 49.2381years for females and 49.80769 for males. the median value for the group was 48 for the female patients and 49 for the male patients, just a bit lower than the average age for the group, with a standard deviation of 4.369265years for the female patients and 3.370688 for the male patients, suggesting a well-balanced study group with a distribution romanian neurosurgery (2018) xxxii 2: 240 261 | 243             only approximating a normal distribution as shown in table 1. the extreme ages, -both minimal and maximal ages in both sexes were well matched as were the age distributions in both sexes, despite a slightly older (63 vs. 58) female patient and the different number of patients per gender in this group. the overall mean age in group b was 49.55319, with a standard deviation of 3.815349 for the entire group b, and a general median of 49. the patients in group c had ages between 45 and 62 and 58 years respectively in females and in males, with an average age of 49.284years for females and 49.5 for males. the median value for group c was 47 for the female patients and 48.5 for the male patients, just a bit lower than the average age for the group, with a standard deviation of 5.161395 for the female patients and 3.451528 for the male patients, suggesting a well-balanced study group with a distribution only approximating a normal distribution as shown in table 1. the overall mean age in group c was 49.77083, with a standard deviation of 4.357628for the entire group c, and a general median of 49. the age distribution by gender –the so called “age pyramid” of the sample – the study group-, is very well-shaped for such a small sample size, with a minimal skew due to the difference of 1 case in the age group 4550 years. table 1 age distribution of study groups parameter group a group b group c minimal age of the whole group 45 45 45 maximal age of the whole group 63 63 62 mean average age of patient of the whole group 52.76 49.23 49.77 standard deviation of the mean for the whole group 7.09 4.36 4.35 female minimal age 45 45 47 female maximal age 66 63 62 mean average age of female patient 53.62 49.23 49.84 standard deviation of the mean 7.90 4.36 5.16 median age of the female 51.5 48 49 males minimal age 45 45 45 males maximal age 68 58 58 mean average age of male patient 52.23 49.80 49.5 standard deviation of the mean in the males 6.83 3.37 3.45 median age of the males 51 49 48.5 type of pathologies the type of pathology exhibited by the patients included in each of the study groups it was surgically distinct for the 3 study groups as shown in table 2. in this regard, group a exhibited 8 types of pathologies. 244 | iacob et al techniques of surgery for lumbar spinal stenosis             the degenerative canal stenosis with acute disc single level was the most common type of lumbar canal stenosis encountered in group a, with 5 cases more than the central lumbar canal stenosis, which came in second with 4 cases. the least number of cases were encountered for the degenerative canal stenosis with facet cyst single level and the unstable canal stenosis with degenerative scoliosis from l2-l5 (large curve) which presented only 1 case each. the patients from group b exhibited 4 types of pathology, as summarized in table 2. the unilateral foraminal and lateral recess stenosis without disc prolapse was the most common type of lumbar canal stenosis encountered in group b, with 7 cases more than the bilateral foraminal and lateral recess stenosis without disc prolapse, which came in second with 13 cases. the least number of cases were encountered for the bilateral foraminal and lateral recess stenosis with disc prolapse which presented only 4 cases. from this we can conclude that the most common type of lumbar canal stenosis encountered in our study is the peripheral one. the patients from group c exhibited 3 types of pathology. the unilateral foraminal and lateral recess stenosis without disc prolapse was the most common type of lumbar canal stenosis encountered in group c, with 7 cases more than the bilateral foraminal and lateral recess stenosis withoutdisc prolapse, which came in second with 13 cases. the least number of cases were encountered for the bilateral foraminal and lateral recess stenosis withdisc prolapse which presented only 4 cases. table 2 type of pathologies group a n. group b n. group c n. central lumbar canal stenosis 4 unilateral foraminal and lateral recess stenosis without disc prolapse 20 unilateral foraminal and lateral recess stenosis without disc prolapse 30 mixed(lateral and central)lss 2 unilateral foraminal and lateral recess stenosis with posterolateral disc prolapse 10 unilateral foraminal and lateral recess stenosis with posterolateral disc prolapse 6 degenerative lss with facet cyst single level 1 bilateral foraminal and lateral recess stenosis without disc prolapse 13 bilateral foraminal and lateral recess stenosis without disc prolapse 13 degenerative lss with acute disc prolapse single level 5 bilateral foraminal and lateral recess stenosis with disc prolapse 4 unstable lss with two levels disc prolapse 3 romanian neurosurgery (2018) xxxii 2: 240 261 | 245             unstable lss with one level disc prolapse 2 unstable lss with degenerative scoliosis small curve from l2 to l5 3 unstable lss with degenerative scoliosis big curve from l2 to l5 1 type of procedure used in the study for the surgical management of the patients in the study group a several types of the classical open surgical procedures were used. in this regard, the patients in the study group a had undergone the most numerous variations of surgical procedures, as 9 types of procedures were used in this group for only 21 patients in total, as shown in table 3. the most common procedure used in group a is the classic laminectomy and disectomy with 5 patients. it was followed by fusion and correction of deformity after bilateral facectomy and decompression from l2-l5 with 4 cases treated this way. three types were the least common procedures each used for 1 patient; these being: i decompression and facectomy and fusion ii weiner technique iii hinge osteotomy for the surgical management of the patients in the study group b several types of the minimally invasive surgical procedures with endoscopic approach were used. in this regard, the patients in the study group b had undergone less numerous variations of surgical procedures than group a, as only 4 types of procedures were used in this group for a total of 47 patients in this group, as shown in table 3. the most common procedure used in group b is the endoscopic unilateral decompression without discectomy which was performed on 20 of the patients in group b. it was followed by bilateral endoscopic decompression without discectomy. with 13 cases treated this way, almost the same as the endoscopic unilateral decompression with discectomy which was performed on 10 patients. the least common procedure was the bilateral endoscopic lamino foraminectomy with discectomy used for 4 patients. for the surgical management of the patients in the study group c several types of microscopic decompresion surgical procedures were used. in this regard, the patients in the study group c had undergone less numerous variations of surgical procedures than groups a, as 5 types of procedures were used for a total of 49 patients in this group, as shown in table 3. the most common procedure used in group c (on 13 patients) is the bilateral microscopic laminectomy without discectomy followed by microscopic lamino-foraminotomy without discectomy which was performed on 11 of the 246 | iacob et al techniques of surgery for lumbar spinal stenosis             patients out of 49 in group c, almost the same as the unilateral microscopic laminectomy. with 10 cases treated this way. the least common procedure was the unilateral microscopic lamino-foraminotomy with discectomy used for 1 patient. table 3 types of procedure used in the study groups group a n. group b n. group c bilateral decompression laminectomy, facetectomy from l2 to l5 and correction of degenerative scoliosis by fusion 4 bilateral endoscopic lamioforaminectomy with discectomy 4 unilateral microscopic lamino-foraminotomy and discectomy one level laminectomy and medial facetectomy, discectomy, cage with tlif fusion 2 bilateral endoscopic lamioforaminectomy without discectomy 13 unilateral microscopic lamino-foraminotomy two levels laminectomy and medial facetectomy, discectomy with pli fusion 3 endoscopic unilateral decompression with discectomy 10 bilateral microscopic lamino-foraminotomy without discectomy classic laminectomy and discectomy 5 endoscopic unilateral decompression without discectomy 20 unilateral microscopic laminectomy with discectomy two levels decompression laminectomy, facetectomy and fusion 1 unilateral microscopic lamino-foraminotomy one level laminectomy and artherectmy 2 unilateral microscopic laminectomy weiner technique 1 hinge osteotomy 1 classic laminectomy and bilateral foraminectomy 2 duration of surgical interventions for the patients included in the study group a, a total number of 2540 hours of intervention time was spent, split 1370/2140 respectively between females and males. the times for the males had a larger variance and standard deviation than for females as shown in table 4. in study group, the total time required for the surgical procedures was higher in male patients than in the female patients (2140/1370), also the maximal absolute values (300 min in males vs. 240 min in females) and the average times of surgical procedures (166.92307±64.50253424min in males vs. 171.25 ±56.10895min in females) but not the minimal absolute times which had higher romanian neurosurgery (2018) xxxii 2: 240 261 | 247             values in female patients than in male patients(90 min in males vs. 95 min in females), as shown in table 4. the median time required for a surgical intervention in group a was also lower in male patients than in female patients (145 min in males vs. 180min in females). for the patients included in the study group b a total number of 2434 hours of intervention time was spent, split 1034/1400 respectively between female patients and male patients in study group, the total time required for the surgical procedures was higher in male patients than in the female patients, also the maximal absolute values (75 min in males vs. 70 min in females) and the average times which had higher values in male patients than in female patients (53.84615 ± 11.51588min in males vs. 52.85714 ± 9.561829min in females), as shown in table 4. the median time required for a surgical intervention in group b was equal in both sexes (55min). for the patients included in the study group c a total number of 2090 hours of intervention time was spent, split 1040/1050 respectively between female patients and male patients. in study group c, the total time required for the surgical procedures was higher in females than in males, also the maximal absolute values (90 min in males vs. 60 min in females) but not the average times which had higher values in male patients than in female patients (43.75 ± 8.628819 min in males vs. 42.8 ± 12.75408 min in females), as shown in table 4. the median time in group c was also higher in males than in females (45 min in males vs. 40 min in females). table 4 duration of surgical interventions among study groups parameter group a group b group c maximal time duration in the female / minute group minimal time 95 40 30 minimal time duration in the female group time 240 70 90 mean duration in the female group 171 52.8 42.8 standard deviation of the mean in the female group 565 9.5 12.7 median duration in the female group 180 55 40 minimal time duration in the in the male group 90 40 30 maximal time duration in the in the male group 300 75 60 mean duration in the male the group 166 53.8 43.7 standard deviation of the mean in the male group 64.5 11.5 8.6 median duration in the male the group 145 55 45   248 | iacob et al techniques of surgery for lumbar spinal stenosis             intraoperative complications in the study group a one type of intraoperative complications occurred, represented by unintended durotomy in 3 cases out of 21, which makes for 14.3% of the total number of surgical interventions performed in this study group as shown in table 5. the patients in group b exhibited only one case of nerve root injury, making for a percentage of complications of 2.1% in a total number of 47cases in group b, as shown in table 5. from the above table we can conclude that patients who had undergone minimally invasive surgeries like endoscopic and microscopic procedures had the least intraoperative complications. of the 3 intra operative complications occurred in the whole study, the patients in group c exhibited only one case of failure to access target, making for a percentage of complications of 2% in a total number of 49cases in group c, as shown in table 5. table 5 intra operative complications of study groups complication type group a group b group c unintended durotomy 3 0 0 failure to access target 0 0 1 nerve root injury 0 1 0 percentage of complications 14.3% 2.1% 2% intra-operative blood loss for the patients included in the study group a a total amount of 3150 ml of blood was lost during surgical procedures, split 1215/1935ml respectively between female patients and male patients. in study group a, the total amount blood lost during surgical procedures was higher in male patients than in the female patients, both in the maximal absolute individual values (240 ml in males vs. 200 ml in females) and in the average amounts which had higher values in male patients than in female patients (148.85 ± 32.414ml in males vs. 141.88 ± 31.275 ml in females), as shown in table 4. the median amount of blood lost during surgical procedures was lower though in male patients than in the female patients in group a (140ml vs. 152.5ml) the very large value of the standard deviation in the male group was due to the one outlier case which lost 240ml of blood during the surgical procedure, apparently making the distribution in this segment of group a non-normal distribution. besides the statistical argument, such a large amount of blood lost in this type of surgical procedure is totally uncharacteristic for such procedure; therefore exclusion of that case from the sample also makes a clinical sense. the unusually high amount of blood lost during the surgical procedure was correlated with a longer procedure and also with the longer time spent in hospital by that patient. eliminating the outlier from the sample and excluding the outlier value of 240ml brings the maximal amount of blood loss in the male group to 185ml, a value still higher than the corrected one in the female group (180ml), the mean in the male group to 141ml, the standard deviation to 18.106, and the median in males to 140ml, brings the romanian neurosurgery (2018) xxxii 2: 240 261 | 249             statistics closer to the ones for the female segment of group a, as shown in table 6. deviation in group a to 31.225, and the median in group a to 140ml, as shown in table 4. this makes this group relatively well balanced also with regard to the amount of blood loss during surgical procedures, confirming the validity of the sample group. eliminating the outliers from the sample and excluding the outlier values of 200ml and 240ml brings the overall maximal amount of blood loss in group a to 185ml, the overall mean amountof blood loss in group a to 145.588ml, the standard. for the patients included in the study group b a total amount of 2400 ml of blood was lost during surgical procedures, split 1075/11325 respectively between female patients and male patients in study group b, the total amount blood lost during surgical procedures was higher in malepatients than in the female patients, also the maximal absolute values (80 ml in males vs. 75 ml in females) but not in the average amounts which had higher values in female patients than inmale patients (51.19048± 16.9488ml in females vs. 50.96154± 17.49395ml in males), as shown in table 6. the median amount of blood lost during surgical procedures was higher in males than in females in group b (52.5 vs. 50) as shown in table 6. table 6 intra-operative blood loss in surgical interventions of study groups parameter group a grou p b grou p c minimal amount of blood loss in the male group / ml 120 30 15 maximal amount of blood loss in the male group 240 80 60 mean amount of blood loss in the male group 148.85 50.96 32.70 standard deviation of the mean in the male group 32.41 17.49 9.77 median amount of blood loss in the male group 140 52.5 30 minimal amount of blood loss in the female group 120 30 15 maximal amount of blood loss in the female group 200 75 120 mean amount of blood loss in the female group 151.88 51.19 30.8 standard deviation of the mean in the female group 31.27 16.94 20.34 median amount of blood loss in the female group 152.5 50 25 post-operative complications the patients in group a exhibited relatively many post-operative complications, of 5 types comprising with a total of 7 cases, this making for a percentage of complications of 33.3% in a total number of 21cases in group a, as shown in table 7. the patients in group b exhibited few post-operative complications, comprising 3 types (2 cases of persistent radiculopathy, and one case each of wound infection and discitis, 250 | iacob et al techniques of surgery for lumbar spinal stenosis             representing 8.5% of complications in a total number of 47cases in group b, as shown in table 7. the patients in group c exhibited even fewer post-operative complications than the other 2 study groups, comprising 1 type (1 cases of persistent radiculopathy), this making for a percentage of complications of 2% in a total number of 47cases in group c, as shown in table 7 for the patients included in the study group c a total amount of 1555 ml of blood was lost during surgical procedures, split 770/785 respectively between female patients and male patients in study group c, the total amount blood lost during surgical procedures was higher in female patients than in the male patients, also the maximal absolute values (120 ml in females vs. 60 ml in males) but not in the average amounts which had higher values in male patients than in female patients (32.70833ml ± 9.777877ml in males vs. 30.8ml ± 20.34494in females), as shown in table 7. the median amount of blood lost during surgical procedures was higher in male patients than in the female patients in group c (30ml vs. 25ml) the very large value of the standard deviation in the female group was due to the one outlier case which lost 120ml of blood during the surgical procedure, apparently making the distribution in this segment of group c a non-normal distribution. besides the statistical argument, such a large amount of blood lost in this type of surgical procedure is totally uncharacteristic for such procedure; therefore, exclusion of that case from the sample also makes a clinical sense. the unusually high amount of blood lost during the surgical procedure was correlated with a longer procedure as the patient was converted to open classic laminectomy because she was marked obese and we fail to access our target and also with the longer time spent in hospital by that patient. eliminating the outlier from the sample and excluding the outlier value of 120ml brings the maximal amount of blood loss in the female group to 50ml, a value lower than the one in the male group (60ml), the mean in the female group to 27.08333ml, the standard deviation to 8.459194, while the median remains 25ml, bringing the statistics very close to the ones for the male segment of group c as shown in table 7. this makes this group very well balanced also with regard to the amount of blood loss during surgical procedures, confirming the validity of the sample group. table 7 postop complications in the patients of study groups type of complication group a group b group c csf leak 3 0 0 persistent weakness 1 0 0 persistent bladder dysfunction 1 0 0 wound infection 1 1 0 persistent lbp 1 0 0 persistent radiculopathy 0 2 1 discitis 0 1 0 total no. of cases 21 47 49 percentage of complications 33.3% 8.5% 2% romanian neurosurgery (2018) xxxii 2: 240 261 | 251             hospital time spent by patients for the patients included in the study group a, the total amount of 158 days was spent in hospital associated with the surgical procedures, split 73/85 between female patients and male patients. in study group a, although the total time spent in hospital associated with the surgical procedures was longer in male patients than in the female patients, the maximal absolute individual values was not (14 in males vs. 21 days in females) but not in the average amounts which had higher values in female patients than in male patients (9.125 ± 6.356942212 days in females vs. 6.538461538 ± 2.78733399 days in males), as shown in table 8. though, the median hospital time spent by laminectomy patients was equal in male patients and in the female patients in group a (5 days) the very large value of the standard deviation compared to the value of the mean in the female group was due to the one outlier case which spent 21 days in hospital care but also 2 other patients that spent 14 days each in hospital care, apparently making the distribution in this segment of group a a non-normal distribution. besides the statistical argument, such a long period of time being totally uncharacteristic for such procedure, therefore exclusion of that case from the sample also makes a clinical sense. eliminating the outlier from the sample and excluding the outlier value of 21 days brings the overall time spent by the females in hospital care to 52 days, the mean to 7.428571429, the standard deviation to 4.503966506, while the median remains 5, bringing the statistics closer to the ones for the male segment of group a. for the patients included in the study group b a total amount of 67days was spent in hospital associated with the surgical procedures, split 27/40 between female patients and male patients in study group b, the total time spent in hospital associated with the surgical procedures was longer in male patients than in the female patients, also the maximal absolute values (14 in males vs. 5 days in females) and also the average hospital times which had higher values in female patients than in male patients (1.538462± 2.549208 days in males vs. 1.285714± 0.956183 days in females), as shown in table 8. though, the median hospital time spent by mip endoscopy patients was equal in male patients and in the female patients in group b (1 day). the standard deviation much greater than the mean in the male group was due to the one outlier case which spent 14 days in hospital care, apparently making the distribution in this segment of group b a nonnormal distribution. besides the statistical argument, such a long period of time being totally uncharacteristic for such procedure, therefore exclusion of that case from the sample also makes a clinical sense. eliminating the outlier from the sample and excluding the outlier value of 14 days brings the overall time spent in hospital care to 26 days, the mean to 1.04, the standard deviation to 0.2, while the median remains 1, bringing the statistics very close to the ones for the female segment of group b, as shown in table 8. 252 | iacob et al techniques of surgery for lumbar spinal stenosis             for the patients included in the study group c a total amount of 52 days was spent in hospital associated with the surgical procedures, split 28/24 between female patients and male patients in study group c, although the total time spent in hospital associated with the surgical procedures was longer in male patients than in the female patients, also the maximal absolute values (14 in males vs. 5 days in females) but not in the average amounts which had higher values in female patients than in male patients (1.538462± 2.549208 days in males vs. 1.285714± 0.956183 days in females), as shown in table 8. though, the median hospital time spent by microscopic decompression patients was equal in male patients and in the female patients in group c (1 day). the very large value of the standard deviation compared to the value of the mean in the male group was due to the one outlier case which spent 3 days in hospital care, apparently making the distribution in this segment of group c a non-normal distribution. besides the statistical argument, such a long period of time being totally uncharacteristic for such procedure, therefore exclusion of that case from the sample also makes a clinical sense. eliminating the outlier from the sample and excluding the outlier value of 3 days brings the overall time spent in hospital care to 25 days, the mean to 1.04167, the standard deviation to0.204124, while the median remains 1, bringing the statistics very close to the ones for the female segment of group c as shown in table 8. table 8 in-hospital time of study groups parameter group a group b group c minimal hospital time in the in the male group 4 1 1 maximal hospital time in the in the male group 14 5 1 mean time of hospital time in the male group 6.53 1.28 0 standard deviation of the mean in the male group 2.78 0.95 2.54 median time of hospital time in the male group 5 1 1 minimal hospital time in the female group 4 1 1 maximal hospital time in the female group 21 14 3 mean time of hospital time in the female group 9.12 1.53 1.12 standard deviation of the mean in the female group 6.35 2.54 0.43 median time of hospital time in the female group 5 1 1 discussions lumbar spinal stenosis is a spinal disorder, congenital or acquired, focal or diffuse (multilevel), defining a osteoligamentous narrowing (congenital) or shrink (secondary – acquired) of the lumbar spinal canal, a conflict between the lumbar spinal canal with vertebral body osteophytes, romanian neurosurgery (2018) xxxii 2: 240 261 | 253             hypertrophy of the ligamentum flavum, zygapophyseal joint, lumbar disc hernia or a combination of these and the content represented by the cauda quina roots, lumbar spinal roots and ganglia, generating a complex set of symptoms of which the hallmark is neurogenic claudication, physical findings and radiological abnormalities [1,2,6,20,27]. lumbar stenosis (lss) could appear also with aggravating factors presented in chapter 5, which should have special considerations and treatment [2,6,9,20,21,27,31,36,42-44,46,47]:  co-existing multiple disk prolapses or single level disk prolapsed with a multistage lumbar spinal stenosis, without scoliosis  combined lss with degenerative listhesis and posterior arthrosis at one or several levels  combined lss with scoliosis: with a small radius of curvature scoliosis and a big radius of curvature installed in adolescence a big radius of curvature, with rapid evolution 5-100 in one year generating both radiculalgia and instability  scoliosis with rotation and rapid evolution to 30-500 affecting several levels  combined stenosis and facet joint cyst  lss with severe polineuropaty, with or without uni/bilateral paresis the pathophysiology of spinal stenosis causing neurologic symptoms is likely from a combination of anatomic compression of nerve roots as well as impaired blood flow primarily to the nerve roots [1,2,5,6,10-13]. to solve such condition, the surgical treatment is not only a solution for resistant symptoms in patients with lss, but really makes sense: in cases of consistent clinical and radiological findings after adequate conservative therapeutic measures have failed for a time at least three months span of control, to patients with realistic expectations; certified although by few evidence-based insights into the treatment options [13,6,7,10-14,20,21] there are several points to consider into the preoperative planning: medical status & physiologic age of the patient, clinical and morphologic aspects, comorbidities, if lss is symptomatic. it’s also art of surgery – adequacy for enlarged lumbar spinal canal it’s a balance between doing too much and not doing enough: suppressing the conflict between the lumbar spinal canal with disco-ligamentary structures and the content represented by the dural sac and radicular nerves, decompressing the neural foramina, eliminating pressure on the spinal nerve roots, without generating spinal instability, never prophylactic. it means also a functional surgery – never operate pictures with the aim to alleviate symptoms; surgical treatment should be applied to each patient, with a perfect correspondence between neuro-radiologic and clinical findings, to normalize daily life activities, improving functional capacity, achieving a good quality of life the timing for surgery has not been clearly decided. data comparing the outcomes of patients who underwent surgery earlier versus 254 | iacob et al techniques of surgery for lumbar spinal stenosis             later in the disease suggest no difference in outcome is there deformity/instability too ?, the suggested decompression technique alone may lead to segmental instability ? a fusion technique should be performed to all cases ? – see loss of mobility of the operated segment, possible adjacent segment decompensation or unless instability is present pre-op; for older patients ability to fuse may be compromised, also fixation may not be adequate it's mandatory to inform patient that lss surgery has no action on: focal or diffuse low back pain and/or stiffness, “degenerative” illness, no patient will be completely free of complaints, no patient will have a new lumbar spine after the operation it's a difficult surgery – most aged patients, fragile, with chronic illness; thinking to an unique surgical procedure, but there are still 20% unsatisfactory results the proposed surgical procedure should achieve a good quality of life using a technique for “maximum effect with minimum trauma”: continue with current best practice surgical expertise relating especially to modern techniques and experience for patient selection & for surgical skills, inform patients of surgical choices and availability of resources and facilities in institution, using local or regional anesthesia combined with conscious sedation informed consent, with the aim to minimize tissue disruption, decompress the lumbar channel and the roots, avoid reintervention, never preventive, avoid to destabilize, no stabilization, no instrumentation, minimal blood loss, minimize time of surgery and length of hospital stay, minimize post operative morbidity, avoiding complications, with earlier return to activities and work; easier operative approach in obese patients. while this debilitating condition has been treated successfully in the past with open laminectomies, miss approaches are rapidly becoming the “standard” technique used by spine surgeons. the development of minimally invasive surgical techniques is driven by the quest for better patient outcomes. there is some evidence for the use of minimally invasive surgery for degenerative lumbar spine stenosis (lss), but there are currently no studies comparing outcomes with matched controls [20-24,2729,32-34,37,38,40,48,49,5-59,62-65]. the object of this study was to compare outcomes following minimally invasive spinal decompression procedures to a standard “open” laminectomy for lss. the first therapeutic approach should always be the conservative treatment and our study included only patients that had undergone conservative treatment, but failed to show adequate response. this is however consistent with other recent randomized controlled studies have shown greater improvements in patients after surgery than after conservative treatment [12,14]. a recent systematic review comparing surgery to conservative treatment in lss suggested that for patients with radicular pain caused by lss, in whom a trial of 3-6 months of conservative treatment had failed, surgery did not improve walking ability but improved pain, function than continuing conservative treatment [10]. small improvements are romanian neurosurgery (2018) xxxii 2: 240 261 | 255             generally reported by patients treated conservatively and serious complications or deterioration are rare with conservative treatment [1-12,14]. a study done by parikh [48] included among the possible disadvantages of minimally surgery techniques the increased operation time due to the steep learning curve. this disadvantage was minimal in our study as all the surgical procedures were performed by the same highly skilled surgeon, with extensive experience using both minimally invasive and open techniques, thus eliminating the potential bias due to the steep learning curve. taking into account the relative sample sizes with a slight larger sample size for males than females, the procedure time distribution over gender of laminectomy patients was well balanced in both sexes, the surgical time required for the various versions of laminectomy performed on the patients in with classic laminectomy being uniformly split between sexes for every time interval (30-60 minutes and 60-120 minutes and > 240 minutes) per surgical intervention, but with a slight bias towards shorter times, in comparison to mis approaches. the median time required for a surgical intervention in endoscopy group was equal in both sexes (55 min) and (30-60 minutes and 60-120 minutes) per surgical intervention with equal frequency in females and a slight bias towards lower times in males mis microscopy group. the intra-operative complication rates may be one of the very few possible disadvantages of mis techniques, due to difficulty manipulating instruments through a small portal, especially in cases requiring contralateral access [25,27,42-44,60,61,65]: symptomatic csf leaks, wound infections and post operative spinal spondylolisthesis. in my experience unintentional durotomies have decreased with the use of a protective sleeve drill bit and preservation of the underlying ligamentum flavum during bony decompression. the use of a retractable, single sided guard on the pneumatic drill bit protects the dura from inadvertent injury on one side while allowing visualization of the drill bit tip from the other slide. the ligamentum flavum is kept intact until the bony decompression with the drill and kerrison is completed. the senior author recently showed a 4.5 incidence of durotomies in obese patients undergoing minimally invasive procedures for lumbar stenosis comparing to our study [57]. regarding the intra-operative complications, we conclude that patients who had undergone minimally invasive surgeries have the least intra-operative complication as follows: 1 patient we failed to access the target in group c due to patient obesity with a percentage of complications 2%. 1 patient with nerve root injury in group b with a total percentage of complication 2.1%. on the other hand the rate of complications were higher in group a in the form of 3 patients had unintended durotomy with a total percentage of 14.3% regarding the post-operative complications it was higher in group a as follows: 3 patients with persistent csf leak 256 | iacob et al techniques of surgery for lumbar spinal stenosis             1 patient with persistent limb and bladder weakness (patient with preoperatory cauda equina) 1 patient with wound infection. 1 patient with persistent lbp with a total percentage of complications 33.3%. in the other hand the post-operative complications were less in group b as follows: 2 patients with persistent radiculopathy 1 patient with post-operative discitis with a total percentage of 8.5%. the least complications were happened in group c with only 1 patient with persistent radiculopathy and total percentage of complications 2% as in a series of studies done by armin [40], khoo lt [59], jayarao m [62]. in a study done by madjetko [44], sengupta d.k. [46,47] post-operative, long term spinal instability is a real concern in patients undergoing laminectomy for lumbar canal stenosis, especially if the patients have pre-operative spondylolisthesis. review of literature shows that patients with preoperative spondylolisthesis have a higher rate (40-100%) of post operative progression of instability on dynamic x-ray at a long term follow-up [44]. comparatively, in our study, among the patients with unstable canal stenosis that had been operated by decompression, instrumentation and fusion, progression of instability had occurred in 2 patients = 22.2%. in another study [6] it showed no significant difference in complication and re-operation rates between minimal invasive surgery treated and conventionally treated patients. this could be accounted by our study’s short duration of follow-up, as reoperation rates increase in the long term when bony regrowth occurs in an inadequate decompression. however, our study showed no significant difference in complication and reoperation rates between ulbd (unilateral laminectomy bilateral decompression) treated and conventionally treated patients. other studies have shown that the difficulty manipulating instruments through a small portal mis has intrinsic potential disadvantage of literally leaving “little room for mistakes”, resulting in more postoperative complications including more significant dural sac retraction and a higher possibility of dural tears [23,24,28,29], higher recurrence and reoperation rates due to minimal exposure leading to inadequate decompression [29,30,32-41]. despite these previous findings in the literature, our study failed to find these short-comes of the mis approach. this could be accounted for by our study’s short duration of follow-up, as reoperation rates increase in the long term [34,35] when bony re-growth occurs in an inadequate decompression; additionally, the procedures in this study were performed by a single senior surgeon with extensive experience using both minimally invasive and open techniques, thus reducing the impact of the learning curve for mis patients. our study demonstrates several benefits of mis microscopic the post operative course. as most patients with lss are elderly and have numerous preoperative comorbidities, decreasing postoperative hospital stay, time to mobilization, post operative pain and disability can significantly decrease patient romanian neurosurgery (2018) xxxii 2: 240 261 | 257             morbidity. longer hospital stays and delayed recovery are associated with more post operative complications, such as deep vein thrombosis, urinary tract infections, cardiopulmonary problems, pulmonary embolism, ileus and prolonged narcotic use as well as with and increased cost of care [6,20,21]. therefore, in our study, the significantly shorter average time to mobilization (1.6 vs 33.3 hours) and average duration of post operative hospital stay (55.1 vs 100.8 hours) for patients in the mis group compared with those in the conventionally treated group were advantages. mean post operative hospital stay is ranging from 42 to 80 hours [23,24,40] and from 45 to 172 hours [21,25,26,29] for ulbd treated and conventionally treated patients, respectively. in another study, [23] which conclude the significantly shorter average time of mobilization (15.6 vs 33.3 hours) and average duration of post operative hospital stay 55.1 vs 100.8 hours for patients in the minimally invasive procedures group compared with those in the conventionally treated group more advantageous. by comparison, in our study the duration of hospital stay was higher in group a with mean hospital stay 7.5 days and shorter b with a mean hospital stay 1.4 days and the shortest period was in group c with 1.06 days. opioids have unwanted side effects that may require additional medications and unnecessarily prolong hospital stay [20], therefore decreasing opioid requirements avoids these complications and allows for less complicated recovery, increased patient comfort and faster return to normal activities of daily living. in our study, the mean value of total iv morphine equivalent units consumed was significantly smaller in mis – treated patients (9.3 vs 42.8 morphine equivalent units). while this could be due to the significantly longer mean post operative stay in the conventionally treated group, a significantly larger proportion of patients in the mis group did not use any opioids at all (52% vs 15%). this is supported by khoo and fessler’s 2002 study [59] in which opensurgery patients required almost 3 times the amount of narcotics as patients treated with micro-endoscopic decompression laminotomy (73.7 vs 31.8 morphine equivalent units, respectively) after adjusting for length of stay. while we cannot definitely state that patients treated with mis consume fewer morphine equivalents units, we can conclude they are more likely to not use any opioids, suggesting that mis is associated with less post-operative pain and discomfort. in the literature, the minimally invasive surgery achieved a significantly greater improvement in post operative pain than did the open approach. however, neither approach was superior in improving function or quality of life. furthermore, neither approach or satisfaction rate, while greater percentage of patients in the minimally invasive approaches 85% felt they had a good outcome than the open group 62%, the difference was not statistically significant [49]. our study showed that there was a significant improvement in patient status in the study group that underwent minimally invasive surgery, it was significant 258 | iacob et al techniques of surgery for lumbar spinal stenosis             improvement in patient function of both endoscopic 97.8% and microscopic groups 100% and significant improvement of the patient self assisting score in the endoscopic group 14% in the last 3 months to 2.5 over 2 years of annual follow-up and in the microscopic group from 12% to 2.5% over the same period. conclusion the initial management of lss should be non-surgical, surgical intervention is considered only in patients with intractable back or radicular pain that interfere with the patient life style or in occurrence of neurological deficit. pre-operative detailed assessment of age and other investigations including mri, dynamic x-rays, and emg should be reviewed carefully to determine preoperative instability or presence of associated neurological deficit and also to define which level are we going to decompress. we established an extrusive relation between the radiological degree of canal stenosis and the severity of symptoms and its association of neurological deficit. it was noticed that the predominance of back pain over the radicular symptoms has carried less favorable outcome. also, operating patients after full trials of conservative treatment for at least 3 to 6 months carry a better outcome and it enhances the result of surgery with net improvement of 60 to 30%. abbreviations css central spinal stenosis ct computed tomography d decompression df decompression and fusion dos duration of symptoms ds degenerative spondylolisthesis fs foraminal stenosis lrs lateral recess stenosis lss lumbar spinal stenosis odi oswestry disability index plif postero-lateral interbody fusion rct randomized controlled trial sd standard deviation sf-36 medical outcomes study short form survey, 36 items sport spine outcomes research trial vas visual analog scale ge general electric srfs self reported functional status sswbs symptoms specific well-being score gwbs general well-being score anacova data analysis ft fisher test anova analysis of data mis minimal invasive surgery csf cerebrospinal fluid cs canal stenosis ulbd unilateral laminectomy bilateral decompression emg electromyogram dvt deep venus thrombosis mip minimal invasive procedure tlif transforaminal lumbar interbody fusion references 1. albert p.wong, zachary a. smith, rohan r. lall,lacy e. bresnahan and rishcahrd g. fessler. department of neurological surgery, northwestern university, 676 n. st. clair street, suite 2210, chicago il 60611, usa. revised 16 march, 2012; accepted 7 june 2012 2. armin ss, holly lt, khoo lt: minimally invasive decompression for lumbar stenosis and disc herniation. neurosurg focus 25(2): e11, 2008. 3. atlas sj, deyo ra, keller rb, chapin am, patrick dl, long jm, et al. the maine lumbar spine study part ii 1 year outcomes of surgical and non-surgical management lumbar spinal stenosis, spine 1996: 21(15):1787-95. 4. c.r. martin, a.t. gruszczynski, h.a. braunsfurth, s.m. fallatah, j. o'neil, and e.k. wai, "the surgical management of degenerative lumbar spondylolisthesis: a systematic review", spine, vol. 32, no. 16, pp. 1791-1798, 2007. view at publisher. view at google scholar. view at scopus. romanian neurosurgery (2018) xxxii 2: 240 261 | 259             5. costa f. sassi m, cardia a, ortolina a, de santis a, luccarrel g, et al: degenerative lumbar spinal stenosis: analysis of results in a series of 374 patients treated with unilateral laminotomy for bilateral microdecomposition. j. neurosurg. spine 7:579-586, 2007. 6. d.k. sengupta and h.n. herkowitz, "degenerative spondylolithesis: review of current trends and controversies", spine, vol. 30, supplement 6, pp.s71s81,2005. 7. d.k. sengupta, "point of view: dynamic stabilization, in addition to decompression for lumbar spinal stenosis with degenerative spondylolisthesis", spine, vol. 31, no. 4, p. 450, 2006. view at publisher. view at google scholar. view at scopus. 8. h. bassewitz and h. herkowitz, "lumbar stenosis with spondylolisthesis: current concepts of surgical treatment", clinical orthopedics and related research, no. 384, pp. 5460, 2001, view at google scholar. view at scopus. 9. ikuta k, arima j, tanaka t, oga m, nakano s, sasaki k, et al: short-term results of microendoscopic posterior decompression for lumbar spinal stenosis. technical note. j. neurosurg spine 2:624-633, 2005. 10. j.e. o'toole, k.m. eichholz, and r.g. fessler, "surgical site infection rates after minimally invasive spinal surgery: clinical article", journal of neurosurgery: spine, vol. 11, no. 4, pp. 471-476, 2009. view at publisher. view at google scholar. view at scopus. 11. j.j. shin, s.u. kuh, and y.e. cho, "surgical management of spontaneous spinal epidural hematoma", european spine journal, vol. 15, no. 6, pp. 998-1004, 2006. view at publish. view at google scholar. view at scopus. 12. jayarao m, chin ls: results after lumbar decompression with and without discectomy: comparison of the transspinous and conventional approaches. neurosurgery 66 (3 suppl operative): 152160, 2010. 13. khoo lt, fessler rg: microendoscopic decompressive laminotomy for the treatment of lumbar stenosis. neurosurgery 51 (5 suppl): s146-s154, 2002. 14. kovacs fm, urrutia g, alarcon jd. surgery versus conservative treatment for symptomatic lumbar spinal stenosis: a systematic review of randomized controlled trials. spine 2011:36:e1335-1351. 15. likert, r. (1932). a technique for the measurement of attitudes. archives of psychology, 140, 1–55. 16. malmivaara a, slatis p, heliovaara m, sainio p., kinnunen h, kankare j, et. al. surgical or non-operative treatment for lumbar spinal stenosis. a randomized controlled trial. spine 2007: 32(1):1-8. 17. mariconda m, zanforlino g, celestino ga, brancaleone s, fava r, milano c. factors influencing the outcome of degenerative lumbar spinal stenosis. j spinal disord 2000:13(2):131-7. 18. mariconda m, fava r, gatto a. longo c. milano c: unilateral laminectomy for bilateral decompression of lumbar spinal stenosis: a prospective comparative study with conservatively treated patients. j. spinal disord tech 15:39-46, 2002. 19. oertel mf, ryang ym, korinth mc. gilsbach jm, rohde v: long-term results of microsurgical treatment of lumbar spinal stenosis by laminotomy for bilateral decompression. neurosurgery 59-:1264-1270, 2006. 20. p. shin, a.p. wong, t.r. smith, a.i. lee, and r.g. fessler, "complications of open compared to minimally invasive lumbar spine decompression", journal of clinical neuroscience, vol. 18, no. 10, pp. 1360-1364, 2011. view at publisher. view at google scholar. view at scopus. 21. parikh k, tomasino a, knopman j, boockvar j, hartl r: operative results and learning curve: microscope-assisted tubular microsurgery for 1 and 2 level discectomies and laminectomies. neurosurg focus 25(2): e14, 2008. 22. ralph jasper, praveenan sivabalan , and prashanth j. rao :comparison between minimally invasive decompression laminectomy and open open laminectomy . 23. s.m. madjetko, p.j. connolly, and s. shott, "degenerative lumbar spondylotisthesis: a meta-analysis of literatue 1970-1993", spine vol. 19, supplement 20, pp. 2256s, 1994. view at google scholar. view at scopus. 24. v. surin, e. hedelin, and l. smith, "degenerative lumbar spinal stenosis. results of operative treatment", acta orthopedica scandinavica, vol. 53, no. 1, pp. 79-85, 1982. view at google scholar. view at scopus. 25. weinstein jn, lurie jd, tosteson td, hanscom b, tosteson ana, blood ea, et al. surgical versus nonsurgical treatment for lumbar degenerative spondylolisthesis. n. engl j med 2007:356(22):2257-70. 26. weinsterin jn, tosteson td, lurie jd, teteson ana, blood e, hanscome b, et al. surgical versus non 260 | iacob et al techniques of surgery for lumbar spinal stenosis             surgical theraphy for lumbar spinal stenosis. n. engl j med 2008: 794-810. 27. z.a. smith, "obesity and patient outcomes following lumbar microendoscopic decompression of stenosisoutcomes and complications in 111 conservatively treated patients", northwestern university, chicago ill, usa, p. 19, 2012. 28. atlas s.j. et al. long-term outcomes of surgical and non surgical management of lumbar spinal stenosis : 8 to 10 year results form maine lumbar spine study, spine 2005, 30, 936-943 . 29. johnsson k.e. lumbar spinal stenosis, a retrospective study of 163 cases in southern sweden, acta orthop scand 1995, 66, 403–405 . 30. mazanek d.j. et al. lumbar canal stenosis: start with nonsurgical therapy,cleveland clinic journal of medecine, 2002, 69, 11, 909-917. 31. fritz jm, et al. lumbar spinal stenosis: a review of current concepts in evaluation, management and outcome measurements, arch phys med rehabil 1998, 79(6), 700-708 . 32. kovacs f.m., et al. – surgery versus conservative treatment for symptomatic lumbar spinal stenosis, spine 2011, 9. 33. herno a et al. lumbar spinal stenosis: a matched pair study of operated and nonoperated patients, br j neurosurg 1996, 10, 461–465. 34. treatment of degenerative lumbarspinal stenosis summary. evidence report/technology assessment number 32.rockville, md: agency for healthcare research and quality, 2001, ahrqpublication no.01 e047,accessed january28, 2008 athttp: /www.ahrq.gov/ clinic/epcsums/stenosum.htm. 35. iacob g. craciun m personal experience in lumbar spinal stenosis (lss), romanian neurosurgery 2011, xviii, 4, 400-411 . 36. iacob g. neurochirurgia in managementul coloanei dureroase, congresul asociatiei romane pentru studiul durerii, “managementul durerii acute pentru medicii dinambulator” howard-johnson grand plaza, bucuresti, 1415. 10. 2011. 37. iqbal j. surgery for lumbar canal stenosis: micro or macro?, dubai spinal course 2008. 38. jakola et al. clinical outcomes and safety assessment in elderly patients undergoing decompressive laminectomy for lumbar spinal stenosis: a prospective study, bmc surgery 2010, 10:34 . 39. rosen d.s. et al. – minimally invasive lumbar spinal decompression in the elderly: outcomes of 50 patients aged75 years and older, neurosurgery 2007, 60, 3, 503 . 40. assaker r. lumbar stenosis, minimal invasive decompression, spinal congress dubai 2012. 41. wiltse l.l., kirkaldy-willis wh, mcivor gw. the treatment of spinal stenosis, clin orthop relat res 1976, 83. 42. court c. rationale for wiltse approach for l5-s1 mini-invasive arthrodesis, dubai spinal congress 2008. 43. nellensteijn j. et al. – transforaminal endoscopic surgery for lumbar stenosis: a systematic review, eur. spine j. 2010, 19(6), 879-886. 44. guiot bh, khoo lt, fessler rg. a minimally invasive technique for decompression of the lumbar spine. spine 2002, 27, 432–438 . 45. papavero l et al. – lumbar spinal stenosis: prognostic factors for bilateral microsurgical decompression using a unilateral approach, neurosurgery 2009, 65[ons suppl 1], ons182–ons187 73. 46. rosen d.s., o’toole j.e., eichholz k.m.,et al. minimally invasive lumbar spinal decompression in the elderly: outcomes of 50 patients aged 75 years and older, neurosurgery2007, 60, 503-510. 47. colak a. et al. a less invasive surgical approach in the lumbar lateral recess stenosis: direct approach to the medial wall of the pedicle, eur spine j 2008, 17, 1745– 1751. 48. tuite g.f., et al. outcome after laminectomy for lumbar spinal stenosis. part ii: radiographicchanges and clinical correlations, j. neurosurg. 1994; 81, 707–715. 49. tuite g.f., et al. diagnosis and treatment of surgery for lumbar spinal stenosis, burr ridge (il): north american spine society (nass), 2007, 262, 394 references. 50. iacob g. craciun m, hawis a.a. – general considerations in lumbar spinal stenosis (lss), romanian neurosurgery 2015, xxix (xxii), 1, 77-84. 51. iacob g. craciun m, hawis a.a. – treatment of lumbar spinal stenosis (lss) and outcome, romanian neurosurgery 2015, xxix , 2, 200-229. 52. djurasovic m, et al. contemporary management of symptomatic lumbar spinal stenosis, orthop. clin. north am. 2010, 41 (2), 183–191 romanian neurosurgery (2018) xxxii 2: 240 261 | 261             53. amundsen t, et al. lumbar spinal stenosis: conservative or surgical management? a prospective 10year study, spine 2000, 25, 1424–1436 54. mazanek d.j. et al. lumbar canal stenosis: start with nonsurgical therapy,cleveland clinic journal of medecine, 2002, 69, 11, 909-917 55. kovacs f.m., et al. – surgery versus conservative treatment for symptomatic lumbar spinal stenosis, spine 2011, 9 56. verbeek j. et al. patient expectation of treatment for back pain. a systmatic review of qualitative and quantitative studies, spine 2004, 29, 2309-2318 57. cooper g, lutz ge, et al. effectiveness of transforaminal epidural steroid injections in patients with degenerative lumbar scoliotic stenosis and radiculopathy, pain physician 2004, 7, 311-317 58. fukusaki m, kobayashi i, et al. – symptoms of spinal stenosis do not improve after epidural steroid injection, clin j pain 1998, 14, 148-151 59. armon c, argoff ce, et al. assessment: use of epidural steroid injections to treat radicular lumbosacral pain: report of the therapeutics and technology assessment subcommitteeof the american academy of neurology, neurology 2007, 68, 723-729 60. simotas c.a. et al.-nonoperative treatment for lumbar spinal stenosis. clinical and outcome results and a 3-year survivorship analysis, spine 2000, 25, 197–203 61. costandi s., chopko b. et al. – lumbar spinal stenosis: therapeutic options review, pain practice 2015, 15, 1, 68-81 62. porter rw, miller cg neurogenic claudication and root claudication treated with calcitonin. a double-blind trial spine 1998, 13, 1061–1064 63. podichetty vk, et al. effectiveness of salmon calcitonin nasal spray in the treatment of lumbar canal stenosis: a double-blind, randomized, placebocontrolled, parallel grouptrial, spine 2004; 29, 2343– 2349 64. yoshihara h. – prostaglandin e, treatment for lumbar spinal canal stenosis, review of the literature, pain practice 2015 65. toyonne et al. – patients expectations in lumbar spine surgery, spine 2005 66. k. iwatsuki et al. bilateral interlaminar fenestration and unroofing for the decompression of nerve roots by using a unilateral approach in lumbar canal stenosis, surgical neurology 2007, 68, 487–492 67. assaker r. lumbar stenosis, minimal invasive decompression, spinal congress dubai 2012 68. court c. rationale for wiltse approach for l5-s1 mini-invasive arthrodesis, dubai spinal congress 2008 69. nellensteijn j. et al. – transforaminal endoscopic surgery for lumbar stenosis: a systematic review, eur. spine j. 2010, 19(6), 879-886 70. endoscopy guidelines from ismiss, feb. 2008 71. yoshida m. et al.surgical procedures and clinical results of endoscopic decompression for lumbar canal stenosis, in dezawa a., chen p.q., chung j.y. state of the art for minimally invasive spine surgery, springerverlag tokyo 2005, 18-25 72. foley kt, smith mm microendoscopic discectomy, techniques neurosurg 1997, 3, 301–307 73. ji yc, kim yb, hwang sn, park sw, kown jt, min bk: efficacy of unilateral laminectomy for bilateral decompression in elderly lumbar spinal stenosis. j korean neurosurgery s 37: 410-415,2005. 74. turner ja, ersek m, herron l, deyo r: surgery for lumbar spinal stenosis, attempt meta-analysis of the literature. spine (phila pa1976) 17: 1-8,1992. 75. awmf-leitlinie: leitlinien der deutschen gesellschaft für neurochirurgie„lumbale spinal kanal stenose“ 2005,http://www.uni-duesseldorf.de/awmf/llna/008-022.htm. microsoft word 3zenteno_endovascular romanian neurosurgery (2013) xx 3: 247 – 257 247 endovascular remodeling of tortuous cervical segments of the internal carotid artery that hinder the management of complex intracranial aneurysms marco antonio zenteno1, jorge arturo santos-franco2, luis rafael moscote-salazar3, ángel lee4 1chairman of the department of neurological endovascular therapy of the instituto nacional de neurología y neurocirugía “manuel velasco suárez”. profesor of neurological endovascular therapy at the universidad nacional autónoma de méxico. comprehensive stroke unit, hospital ángeles del pedregal; 2department of neurosurgery at the centro médico nacional “la raza”. assistant professor in neurosurgery at the universidad nacional autónoma de méxico. mexico d.f.; 3md, universidad de cartagena, cartagena de indias, colombia; 4comprehensive stroke unit, hospital ángeles del pedregal. department of neurosurgery, instituto nacional de ciencias médicas y nutrición, salvador zubirán, mexico city, mexico. abstract introduction: severe tortuosity of the cervical segment of the internal carotid artery (ica) may hamper the navigation of intravascular devices for the management of complex intracranial aneurysms and even conventional techniques of ica access can fail. in a group of selected cases, we analyzed the efficacy and safety of carotid stenting to straighten the severe tortuosity for direct navigation of the devices. methods: a case series of 16 patients harboring 18 intracranial aneurysms with a difficult endovascular approach because of a cervical ica with severe tortuosity were prospectively recruited at our institution from january 2005 to december 2007. when traditional means of correction could not surmount this obstacle, an overlap stenting with a distal-to-proximal technique was used to overcome the severe tortuosity. the efficacy of the procedure was defined as the ability to reach and be able to treat the target lesion with a smooth navigation of the endovascular devices. safety was documented by procedure-related complications. results: the straightening of the vessel by the stent helped to overcome pitfalls, making possible an obstacle-free navigation of the endovascular devices to the target lesion in all cases. in 5 cases with severe or double kinking, a distal transfer of the curve beyond the stent was observed, without impact on the efficacy of the procedure. one case of periprocedural related technical complication occurred with a permanent stroke. during the follow-up period (22.7 ± 8.4 months) no case of stent-related stroke or severe hyperplasia was observed. conclusions: carotid stenting is an available option when a cervical ica with severe tortuosity hampers a smooth 248 zenteno et al endovascular remodeling of tortuous cervical carotid artery catheterization of the intracranial circulation, in carefully selected cases. it allows a relatively safe and free navigation and/or deployment of additional endovascular devices needed for the treatment of complex intracranial aneurysms. key words: carotid stenting, carotid kinking, guiding catheter stability, intracranial aneurysm, carotid tortuosity, overlapping stenting. introduction endovascular treatment is an accepted worldwide method for the management of intracranial aneurysms, most of the lesions are now amenable to this kind of treatment (1, 2). a subgroup of complex lesions require the use of special techniques as balloon-remodelling (3), stent-assisted coiling (2, 4, 5) or sole stenting (6–9), thus enlarging the application of endovascular therapy to those challenging lesions. successful navigation with use of the aforementioned techniques is usually possible; however, in some patients, the navigability, trackability and deliverability of these devices can be hindered by excessive vascular intracranial tortuosity (5, 10–13). in fact, failed attempts for coiling the targeted lesions can be up to 16%, mainly because of the inability to catheterize the aneurysm. (32) the issue of the extracranial tortuosity is not less important (14). guiding catheters have progressively improved their flexibility while maintaining sufficient stability at their distal end, with sufficient back-up support (14, 15); however, this advantage is difficult to accomplish in cases of kinked or very tortuous extracranial ica. some newer guiding catheters have been introduced, but still have some limitations especially when an assisted coiling is required. the recent technical improvements of intracranial stents have not completely resolved the problem of navigability in cases of hostile extracranial anatomy. (52, 53) transitory endovascular strategies to straighten this kink have been devised (double-wire and coaxial double– guiding catheter technique) (15, 16), but are sometimes not sufficient to allow easy navigation or delivering the devices at the intended position, representing additional manipulations, carrying the risks of cause dissection and occlusion/subocclusion of the artery (17, 18). other strategies have been described, as the direct puncture of the ica (10, 19) or cut-down techniques with surgical exposure of the artery (17, 20). these maneuvers are not devoid of complications and seem not easy in distal kinkings. carotid stenting is now widely used in the management of atherosclerotic cerebrovascular disease with safety (21–24), however, the use of this technique to provide straightforward access to the intracranial aneurysms and avoid potential complications has never been described. the goal of this paper is to present the results of a case series of selected complex intracranial aneurysms with a failed access using traditional strategies, and requiring the correction of extracranial k-t for successful treatment. material and methods study design and patient selection this is a prospective case series of patients harboring intracranial aneurysms of the anterior circulation who underwent endovascular straightening of the k-t of the cervical ica to enable safe embolization of the target lesion. the patients were consecutively recruited in a period romanian neurosurgery (2013) xx 3: 247 – 257 249 encompassing from january 2005 to december 2007. the study was conducted following the guidelines for reporting observational studies. (50) demographic features and previous medical history were recorded. the aneurysms were classified according to their clinical presentation into: ruptured (acute or previous hemorrhage) and non-ruptured (either incidental or symptomatic). the patients with subarachnoid hemorrhage (sah) were assessed using the hunt and kosnik scale (25), while the rest were evaluated using the modified rankin scale (mrs) (26). preprocedural imaging assessment prior to their enrollment, all the patients were assessed by digital subtraction angiography (dsa) using a 3d axiom artis dba (siemens medical systems, erlangen, germany) and morphologic evaluation and measurements of the parent vessel were done on a separate workstation by using reconstructed 3d-dsa images (leonardo workstation). for the evaluation of the tortuosity, the angiographic projection with the best visualization was chosen and was measured by drawing a midaxis line of the involved vessel in the segments proximal and distal to the tortuous segment (27). the intersection of both lines allowed measuring the angle. the elongation of the internal carotid artery (ica) was defined according to preestablished criteria (28, 29, 46, 47, 48, 49, 50, 51, 52). aneurysms. intracranial aneurysms were classified according to their size, location, shape, and site of origin. regarding size, the universal criteria for small, large and giant were kept. neck size and dome-neck ratio were also noted. technical obstacles leading to the indication of stenting. they were categorized as follows: 1) inability to cross the kinked segment 2) partially obstructing guiding catheter 3) instability/excessive mobility of the guiding catheter, 4) unstable or difficult navigation/delivering/deploying an intracranial of intracranial devices (e.g., coils). the difficulty to straighten the kinked vessel was foreseen according to the supplementary maneuvers that were required. either a hydrophilic 0.038” or 0.035” guidewire was capable of correcting the vessel, or in some cases, a single supportive guidewire or a double supportive “buddy” guidewire was needed. endovascular procedure carotid stenting. the morphologic evaluation and measurements of the parent vessel allowed the planning of the strategy and the choice of tailored devices. an 8 f guiding catheter (guider, boston scientific, fremont, ca) was placed in the common carotid artery via the femoral route. in all cases, a transitory correction of the kinking was attempted by using a 0.035” or 0.038” hydrophilic guidewire, stiff 0.014” guidewires (30) or a double supportive “buddy” guidewire. once the vessel has been transitorily “straightened” with these methods, a selfexpanding stent (wallstent, boston scientific, natick, ma.) is navigated to the desired position. no protection devices were employed. the planned technique was to deploy the first stent as distally as possible in the ica (transition to petrous segment) and to place a second stent proximally with an overlapping technique. in certain cases, 250 zenteno et al endovascular remodeling of tortuous cervical carotid artery additional stents were necessary until the kinking resolved completely. once the stent was deployed, tirofiban (aggrastat™) was prescribed in all cases at a conventional dosage of 0.4 μg/kg/min for half an hour and 0.1 μg/kg/min for the next 24 hours. later on, the treatment was switched to a double oral regime with clopidogrel 75mg qd and aspirin 100mg qd for the next 6 months (7, 8, 31). management of the aneurysms. they were treated with the required strategy for the corresponding parent vessel-aneurysm complex pattern: simple coiling, stentassisted coiling or sole stenting. the navigability of the devices and the percentage of occlusion were noted. efficacy and safety of the procedure. the procedure was considered technically successful whenever the guiding catheter permitted independent coaxial mobility of the device contained therein and a successful navigation/delivery/deployment of the intended devices and inadequate when the ancillary procedure did not allow a better result when treating of the target lesion. the procedure-related complications were categorized as follows: access site– related complications, hemodynamic effects (hypotension, bradycardia), and neurological impairment (classified as transient, reversible or permanent) (14). clinical and imaging follow-up every single patient was clinically assessed at discharge and at 3rd, 6th and 12th months using the mrs (26). the aneurysm and the stents were assessed by dsa at 3, 6 and 12 months. statistical analysis we employed descriptive statistics with measures of the central tendency and dispersion (± standard deviation) in case of continuous variables and proportions and percentages in nominal variables. non parametric inferential statistic for nominal or ordinal variable was applied (χ2 or exact fisher test), using spss statistical package (spss, chicago, il), the level of significance was set at a probability value of less than 0.05. ethical considerations the decision was jointly taken with the department of neurosurgery. all the patients either did not qualify or refused neurosurgical treatment. a written informed consent form was obtained from all the patients and/or their relatives, in accordance with established protocols by our institutional committee of ethics and with the declaration of helsinki.(54) results clinical and imaging features over a period of 3 years a total of 286 patients with cerebral aneurysms were treated, we found 40 (14%) patients with kinking and 32 (9%) with tortuosity of the cervical ica, from these subgroups, 16 patients (5.6% of the total) underwent endovascular stenting of the ica tortuosity carotid with 18 corrected arteries. the sex ratio was of 7:1 for a female predominance, with a mean age of 62 ± 7.8 years. the only relevant fact in their past medical history was systemic hypertension in 6 cases (43%). aneurysms. they were all saccular and only one case of recent acute rupture was included (hunt and kosnik grade 3). in the group of non-ruptured cases, 7 (38%) were incidental, 7 (38%) presented with cranial nerve compression and 3 (16%) were seen because of a previous rupture of another aneurysm. they were located in the supraclinoid ica in 16 (88%) of the cases romanian neurosurgery (2013) xx 3: 247 – 257 251 and two (11%) on the anterior communicating artery. concerning size, 8 (44%) were large and 3 (16%) were giant. the average neck size was of 6, 4 mm (± 3, 4) and dome-neck ratio was below 2 in 15 (83%) cases. five patients harbored multiple aneurysms. kinking features. the kinking was mild in 8 (44%), moderate in 5 (27%), and severe in 3 (16%) cases. tortuosity was present in only 2 (11%) cases. tandem or double kinkings were found in 5 (27%) of the cases. technical obstacles leading to the indication of stenting. some of them may coexist in the same vessel, and according to the aforementioned categories, their relative frequency was as follows: 1) inability to cross the kinked segment was observed in 3 (16%) 2) a partially obstructing guiding catheter was present in 4 (22%) cases, 3) the instability/excessive mobility of the guiding catheter existed in 3 (16%) arteries, 4) the instability/difficult navigation of intracranial devices (e.g., coils) was encountered in 3 (16%) cases, and 5) difficulties in delivering/deploying/stabilizing an intracranial stent 10 (55%) of the total. procedure carotid stenting. a carotid wallstent (boston scientific, fremont, ca) was used in all patients and a single 0.014” microguide wire (choice® pt extra support guide wire, boston scientific, fremont, ca) in most cases (10/18) 55%. in three patients an additional “buddy” microguide wire was necessary to provide an extra support, when a marked or a double kinking was present. in two cases a single stent was used, but the kinking was transferred beyond the stent. from then on, the aforementioned distal-to-proximal stenting technique was employed. two stents were used in 11 (61%) cases, and three (16%) stents in 5 arteries. according to the aforementioned convention, all the arteries were satisfactorily corrected providing sufficient stability allowing a successful treatment of the target lesion, specifically facilitating the navigation of the microcatheter into the sac, sufficient packing of the aneurysm and the deployment of the intracranial stent in all cases. when considering the angiographic result, a complete correction was seen in 13 (72%) cases and a distal transfer of a curve in 5 (27%) of the cases, especially when a severe or double kinking was present. (fisher's exact test, 2-sided, p = 0, 047). complications. no hemodynamical effects were seen. there was one case of postoperative groin hematoma. in another case, the stent was misdeployed producing an ica dissection. the aneurysm was coiled and subsequent intraarterial and mechanical vascular rescue were attempted, with partial recanalization. the patient presented a left opercular stroke with residual aphasia, which was rehabilitated thereafter. aneurysm management. stent-assisted coiling was the commonest strategy of treatment, either with a self-expandable stent (ses) in 10 cases (55%) or with a balloon-expandable stent (bes) in 5 cases (27%). ses were neuroform3 stents (boston scientific, fremont, ca) and bes were pharos stents (micrus endovascular, sunnyvale, ca). three patients underwent a single coiling procedure and another two a sole stenting procedure. there was only one case of an acutely ruptured aneurysm which was partially coiled first, with a further stent-assisted coiling which required a stenting of the cervical carotid artery. 252 zenteno et al endovascular remodeling of tortuous cervical carotid artery complications. one patient presented angiographic occlusion of a distal branch due to the treatment of the aneurysm. the clot resolved after intravenous glycoprotein iib/iiia receptor antagonist therapy. no clinical or imaging evidence of stroke could be shown. follow-up the mean clinical follow-up period was of 22.7 ± 8.4 months (range: 8-40 months). at 6 months follow-up, the mrs was of 0 to 2 in 16(88%) patients, and mrs 3 in two patients, one stroke due to cerebral vasospasm, and other case of procedurerelated stroke (stent placement). an asymptomatic intimal hyperplasia occurred in two cases. discussion cervical tortuosity can limit endovascular approach (32). cai et al treated 63 patients for ruptured and unruptured aneurysms, 10 patients required direct carotid puncture, and in other 3 cases, selective embolization of the aneurysm failed as the result of vessel tortuosity (32). technical limitations because of the anatomy of the cervical ica and the anterior bend of its cavernous segment also affected 2 in another series of 36 patients scheduled for endovascular management of an intracranial stenosis (33). severe tortuosity, kinkings and intracranial aneurysms. in angiographic series, a kinking of the cervical ica is present in 15 to 25% of the subjects (28, 34). to our knowledge, there is no report specifying how the coexistence of intracranial aneurysms and ica severe tortuosity is frequent. however, in our multicenter/institutional series of intracranial aneurysms (n = 286) this association yielded an overall frequency of 14%. the principal technical obstacles due to severe tortuosity of the ica were categorized in five groups: 1) inability to cross the kinked segment is the first obstacle. ideally, the guiding catheter should be positioned as close of the skull base as possible to maintain a good support to navigate any endovascular device to the intracranial circulation (12). however, in certain cases, a standard guiding catheter cannot be pushed across a kinked segment with the normally used guidewire. the attempts to overcome these resistance, may lead to complications as vascular dissection or rupture. 2) partially obstructing and instability guiding catheter placement of a guiding catheter through a tortuous vessel may result in reduction or occlusion of blood flow (35), increasing the risk of local and distal thromboembolism (36). fusionar 3) instability/excessive mobility of the guiding catheter. besides, even if the kinking is crossed and the guiding catheter is deep-seated in the right position, the catheter partially retains the curvature formed following the vasculature pathway. this is familiar to every interventionalist: the guiding catheter unavoidably drops down and goes back into the aorta. when a catheter inserted in a tortuous vasculature and is either obstructive or mobile beyond suitable limits, additional complications can arise, like dissection or ischemic events. neuron delivery catheter (penumbra, inc., san leandro, ca) was developed to enable distal catheterization of the intracranial vasculature with added stability and support of the microcatheter, but there are some limitations; the inner diameter of the romanian neurosurgery (2013) xx 3: 247 – 257 253 catheter limits the ability to simultaneously advance a second microcatheter in cases such as balloon remodeling during aneurysm treatment. as reported by these authors, there was little success in using this system as initially designed: in general, the 0.018-inch wire was not robust enough to select the supra-aortic vessels easily. 4) instability/difficult navigation of intracranial devices was another important cause of technical failure. the ability to advance and maintain the stability of additional treatment devices is often a product of guide catheter steadiness (37, 38). even if the aneurysm is catheterized, the intrasaccular delivery of the coils needs some backup support. for instance, a soft coil can nearly always be passed through the microcatheter into the aneurysm, but sometimes the last loops cannot be deployed because the relatively stiff delivery wire will not negotiate very tortuous arteries (10). 5) difficulties in delivering, deploying and stabilizing an intracranial stent was the last, but not the least important obstacle to overcome. the major benefit of ses is their higher flexibility that allows endovascular access to distal and tortuous arteries (39). early published experience with the neuroform demonstrated higher rates of failure, but newer neuroform iterations have resulted in some improvement in navigability, but a 4% inaccurate deployment rate was reported more recently (4, 40). early published experience with enterprise showed a 2% inaccurate deployment rate and a 3% inability-todeploy rate because patients’ anatomy (41). on the other side, when a ses is required, its navigation and deployment require more complex maneuvers, as the stabilizer must be kept in place, while unsheathing stent for deployment. (1) in our previous experience with elongated vessels, the most frequently encountered obstacle was a difficult navigation when using bes. however, the use of newer devices, as the bes pharos® (micrus endovascular, sunnyvale, ca) allows a smoother navigation in tortuous vessels (6, 42). transitory straightening of the severe tortuosity the straightening of the curved segments would abate these five aforementioned difficulties and enable a navigation involving minimal effort. most of the anomalies were corrected by the placement of an extra support guidewire alone. the use of a second “buddy guidewire” has recently been introduced to neurointerventional procedures (15, 30, 37, 38) for the purpose of providing more steadiness to the guiding catheter in hostile anatomy. in some cases, this maneuver produces a mechanical distortion of tortuous arteries mimicking spasm or dissection and has been termed as “accordion effect” (43). in our experience this transitory correction is by no means guarantee of a sufficient stability of the whole system. correction of the ica with a stent the technique of carotid stenting in this series has progressively evolved. there are two points of fixation of the cervical ica, a proximal at the bifurcation and a distal at the entry into the pyramid bone (44): a straightening of the kinked segment only can in some cases produce another stentinduced kinking (45) beyond the stented segment (27). in the distal-to-proximal technique, a first stent must be placed and deployed as close as possible to the base of the skull and the following must be deployed with an overlapping technique 254 zenteno et al endovascular remodeling of tortuous cervical carotid artery (46) until the full length of the ica is straight. to achieve an adequate straightening, we consider that two stents are usually sufficient; in cases of severe kinking three stents may be required . the straightening effects on vascular curves due to a lack of longitudinal flexibility of the wallstent (45) are desirable in these particular cases. in cases of severe or of double kinking, a distal transfer of a slight curve occurred, but this little “step” did not prevent a farther comfortable navigation (figure 1). our target is not the cosmetical result, but the functional result. efficacy and complications the straightening of the ica allowed our final end point: a safe navigation of the devices and the treatment of the target lesion in all cases (complex aneurysm). the technique is not devoid of complications and a stroke occurred in one case. a more rigorous technique of this particular procedure can allow a minimization of the complications. symptomatic intimal hyperplasia is exceptional, as a less intense inflammatory reaction is expected than in atherosclerotic vessels. we stress on the fact that is an ultimate resource, required only in cases where other maneuvers are more risky or impossible and was not used in a liberal fashion, as only 5,6% of the total aneurysm have been treated with previous stenting of the cervical ica. figure 1 step by step of zenteno technique of correction of carotid tortuosity romanian neurosurgery (2013) xx 3: 247 – 257 255 other options in case of carotid for the management of severe tortuosity (19, 20, 46, 47, 48) the surgical cut-down techniques (20) have been used for direct access to the vertebral artery, bypassing the aortic arch and proximal brachiocephalic vessels. it also has been recently applied in severe ica tortuosity (17). however, as it requires surgical dissection and exposure of the carotid artery, it is not bereft of complications. on the other hand, current regimes of anticoagulant/antiplatelet agents, coupled with demands for large guiding catheters for certain interventions, make direct carotid puncture risky both in terms of arterial injury and control of access site bleeding at the end of the intervention (19). limitations of the technique all our cases were highly challenging lesions requiring complex procedures and other available resources had failed. the use of an additional device (the carotid stent) can be adduced, but in complex cases, the use of multiple guidewires, the exchange of guiding catheters, the damage of intracranial stents navigated forcefully through this hostile anatomy also represent additional risks and costs, often ending up in an unsuccessful procedure. antiplatelet treatment is not an issue as most of these patients have an indication for these drugs because of an intracranial stent. the use of newer technologies may render this procedure unnecessary in the near future. those devices are not always effective and may be unavailable in some centers. in the meantime, this procedure remains an option which can be used if necessary. conclusions tortuous of cervical carotid artery can increase the technical difficulties for a safe navigation of devices when treating aneurysms, especially in cases of assisted techniques. in selected cases, carotid stenting is an effective and relatively safe ancillary tool providing sufficient support guiding catheter. this stability facilitates an eventful and successful procedure, especially when intracranial stent placement is required. technical refinements include the distal-to-proximal overlapping technique which affords a complete correction and avoids the transferal of the severe tortuosity beyond the stented segment. references 1. koebbe cj, veznedaroglu e, jabbour p, rosenwasser rh. endovascular management of intracranial aneurysms: current experience and future advances. neurosurgery 2006;59:s93–102; discussion s3–13. 2. lanzino g, kanaan y, perrini p, dayoub h, fraser k. emerging concepts in the treatment of intracranial aneurysms: stents, coated coils, and liquid embolic agents. neurosurgery 2005;57:449–59; discussion 449– 59. 3. moret j, cognard c, weill a, castaings l, rey a. the “remodelling technique” in the treatment of wide neck intracranial aneurysms. angiographic results and clinical follow-up in 56 cases. interv neuroradiol 1997;3:21–35. 4. fiorella d, albuquerque fc, deshmukh vr, mcdougall cg. usefulness of the neuroform stent for the treatment of cerebral aneurysms: results at initial (36-mo) follow-up. neurosurgery 2005;56:1191–201; discussion 1201–2. 5. howington ju, hanel ra, harrigan mr, levy ei, guterman lr, hopkins ln. the neuroform stent, the first microcatheter-delivered stent for use in the intracranial circulation. neurosurgery 2004;54:2–5. 6. zenteno m, modenesi freitas jm, aburto-murrieta y, koppe g, machado e, lee a. balloon-expandable stenting with and without coiling for wide-neck and complex aneurysms. surg neurol 2006;66:603–10; discussion 610. 7. zenteno ma, santos-franco ja, freitas-modenesi 256 zenteno et al endovascular remodeling of tortuous cervical carotid artery jm, gómez c, murillo-bonilla l, aburto-murrieta y, díaz-romero r, nathal e, gómez-llata s, lee a. use of the sole stenting technique for the management of aneurysms in the posterior circulation in a prospective series of 20 patients. j neurosurg 2008;108:1104–18. 8. zenteno m, santos-franco j, aburto-murrieta y, modenesi-freitas j-m, ramírez-guzmán g, gómezllata s, lee a. superior cerebellar artery aneurysms treated using the sole stenting approach. technical note. j neurosurg 2007;107:860–4. 9. zenteno ma, murillo-bonilla lm, guinto g, gomez cr, martinez sr, higuera-calleja j, lee a, gomez-llata s. sole stenting bypass for the treatment of vertebral artery aneurysms: technical case report. neurosurgery 2005;57:e208; discussion e208. 10. byrne j. interventional neuroradiology: theory and practice. 1st ed. new york: oxford university press; 2002. 11. murayama y, nien yl, duckwiler g, gobin yp, jahan r, frazee j, martin n, viñuela f. guglielmi detachable coil embolization of cerebral aneurysms: 11 years’ experience. j neurosurg 2003;98:959–66. 12. nakahara t, sakamoto s, hamasaki o, sakoda k. double wire technique for intracranial stent navigation. j vasc interv radiol 2003;14:667–8. 13. pierot l, boulin a, castaings l, rey a, moret j. endovascular treatment of pericallosal artery aneurysms. neurol res 1996;18:49–53. 14. blanc r, deschamps f, orozco-vasquez j, thomas p, gaston a. a 6f guide sheath for endovascular treatment of intracranial aneurysms. neuroradiology 2007;49:563–6. 15. lee th, choi ch, park k-p, sung sm, lee sw, lee b-h, kim dh, kim hj, kim cw, kim s. techniques for intracranial stent navigation in patients with tortuous vessels. ajnr am j neuroradiol 2005;26:1375–80. 16. kwon bj, han mh, kang h-s, jung c. protection filter-related events in extracranial carotid artery stenting: a single-center experience. j endovasc ther 2006;13:711–22. 17. wehman jc, hanel ra, levy ei, hopkins ln. giant cerebral aneurysms: endovascular challenges. neurosurgery 2006;59:s125–38; discussion s3–13. 18. connors ji, wojak j, editors. interventional neuroradiology: strategies and practical techniques. philadelphia: wb saunders; 1999. 19. yuzawa i, kurata a, suzuki s, ozawa h, hagiwara h, niki j, yamada m, fujii k, kan s, kitahara t. efficacy of a direct puncture approach for anterior circulation aneurysms using a newly developed guiding catheter especially for geriatric patients. surg neurol 2007;67:30–4; discussion 34. 20. ross ib, luzardo gd. direct access to the carotid circulation by cut down for endovascular neurointerventions. surg neurol 2006;65:207–11; discussion 211. 21. samuelson rm, yamamoto j, levy ei, siddiqui ah, hopkins ln. the argument to support broader application of extracranial carotid artery stent technology. circulation 2007;116:1602–10; discussion 1610. 22. roubin gs, iyer s, halkin a, vitek j, brennan c. realizing the potential of carotid artery stenting: proposed paradigms for patient selection and procedural technique. circulation 2006;113:2021–30. 23. ringleb pa, allenberg j, brückmann h, eckstein h-h, fraedrich g, hartmann m, hennerici m, jansen o, klein g, kunze a, marx p, niederkorn k, schmiedt w, solymosi l, stingele r, zeumer h, hacke w. 30 day results from the space trial of stent-protected angioplasty versus carotid endarterectomy in symptomatic patients: a randomised non-inferiority trial. lancet 2006;368:1239–47. 24. higashida rt, meyers pm, phatouros cc, connors jj, barr jd, sacks d. reporting standards for carotid artery angioplasty and stent placement. stroke 2004;35:e112–34. 25. hunt we, kosnik ej. timing and perioperative care in intracranial aneurysm surgery. clin neurosurg 1974;21:79–89. 26. rankin j. cerebral vascular accidents in patients over the age of 60. ii. prognosis. scott med j 1957;2:200–15. 27. berkefeld j, martin jb, théron jg, zanella fe, guimaraens l, treggiari-venzi mm, rosendahl h, rüfenacht da. stent impact on the geometry of the carotid bifurcation and the course of the internal carotid artery. neuroradiology 2002;44:67–76. 28. metz h, murray-leslie rm, bannister rg, bull jw, marshall j. kinking of the internal carotid artery. lancet 1961;1:424–6. 29. togay-işikay c, kim j, betterman k, andrews c, meads d, tesh p, tegeler c, oztuna d. carotid artery tortuosity, kinking, coiling: stroke risk factor, marker, or curiosity? acta neurol belg 2005;105:68–72. 30. surmely j-f, cook s. variation on the anchor balloon technique for difficult stent delivery. kardiovaskuläre medizin 2007;10:397–9. 31. santos-franco ja, zenteno m, lee a. dissecting aneurysms of the vertebrobasilar system. a comprehensive review on natural history and treatment options. neurosurg rev 2008;31:131–40; discussion 140. 32. cai y, spelle l, wang h, piotin m, mounayer c, vanzin jr, moret j. endovascular treatment of intracranial aneurysms in the elderly: single-center experience in 63 consecutive patients. neurosurgery 2005;57:1096–102; discussion 1096–102. 33. lylyk p, cohen je, ceratto r, ferrario a, miranda romanian neurosurgery (2013) xx 3: 247 – 257 257 c. angioplasty and stent placement in intracranial atherosclerotic stenoses and dissections. ajnr am j neuroradiol 2002;23:430–6. 34. illuminati g, ricco j-b, caliò fg, d’urso a, ceccanei g, vietri f. results in a consecutive series of 83 surgical corrections of symptomatic stenotic kinking of the internal carotid artery. surgery 2008;143:134–9. 35. mathis jm, zoarski g. use of a guide catheter as a temporary stent during microcatheter intervention. ajnr am j neuroradiol 1998;19:932–3. 36. tanemura h, hatazaki s, asakura f, kawaguchi k, kuraishi k, toma n, sakaida h, maeda m, taki w. angioscopic observation during carotid angioplasty with stent placement. ajnr am j neuroradiol 2005;26:1943–8. 37. nishino k, ito y, hasegawa h, kikuchi b, fujii y, tanaka r. modified buddy wire technique for coil embolization of posterior circulation aneurysms. neuroradiology 2007;49:49–55. 38. white jb, kallmes df. utility of the “buddy” wire in intracranial procedures. neuroradiology 2008;50:185–7. 39. kis b, weber w, berlit p, kühne d. elective treatment of saccular and broad-necked intracranial aneurysms using a closed-cell nitinol stent (leo). neurosurgery 2006;58:443–50; discussion 443–50. 40. biondi a, janardhan v, katz jm, salvaggio k, riina ha, gobin yp. neuroform stent-assisted coil embolization of wide-neck intracranial aneurysms: strategies in stent deployment and midterm follow-up. neurosurgery 2007;61:460–8; discussion 468–9. 41. mocco j, snyder k v, albuquerque fc, bendok br, alan s b, carpenter js, fiorella dj, hoh bl, howington ju, jankowitz bt, liebman km, rai at, rodriguez-mercado r, siddiqui ah, veznedaroglu e, hopkins ln, levy ei. treatment of intracranial aneurysms with the enterprise stent: a multicenter registry. j neurosurg 2009;110:35–9. 42. freitas jmm, zenteno m, aburto-murrieta y, koppe g, abath c, nunes ja, raupp e, hidalgo r, pieruccetti ma, lee a. intracranial arterial stenting for symptomatic stenoses: a latin american experience. surg neurol 2007;68:378–86. 43. tsutsumi m, kazekawa k, onizuka m, aikawa h, iko m, kodama t, nii k, matsubara s, etou h, tanaka a. accordion effect during carotid artery stenting: report of two cases and review of the literature. neuroradiology 2007;49:567–70. 44. székely g, csécsei gi. anteposition of the internal carotid artery for surgical treatment of kinking. surg neurol 2001;56:124–6. 45. tanaka n, martin j-b, tokunaga k, abe t, uchiyama y, hayabuchi n, berkefeld j, rüfenacht da. conformity of carotid stents with vascular anatomy: evaluation in carotid models. ajnr am j neuroradiol 2004;25:604–7. 46. lesley ws, weigele jb, chaloupka jc. outcomes for overlapping stents in the extracranial carotid artery. catheter cardiovasc interv 2004;62:375–9. 47. gavrilenko av, abramian av, kuklin av. comparative analysis of the outcomes of surgical and conservative treatment of patients with pathological kinking of carotid arteries. angiol sosud khir. 2012;18(4):93-9 48. cong tc, duan x, gao wh, zhao em, yang xd, wang h, xiao sf, qin y.tortuosity and kinking of cervical segment of internal carotid artery: an analysis of 7 cases. zhonghua er bi yan hou tou jing wai ke za zhi. 2012 nov;47(11):913-7. 49. pokrovskiĭ av, beloiartsev df, adyrkhaev za, timina ie, losik ia. remote results of reconstructive operations in pathological deformity of the internal carotid artery. angiol sosud khir. 2012;18(1):92-104. 50. cohen je, gomori jm, leker rr, itshayek e.a reappraisal of the common carotid artery as an access site in interventional procedures for acute stroke therapies. j clin neurosci. 2012 feb;19(2):323-6 51. pokrovskiĭ av, beloiartsev df, timina ie, adyrkhaev za. clinical manifestations and diagnosis of pathological deformity of the internal carotid artery. angiol sosud khir. 2011;17(3):7-18. 52. derubertis bg, hynecek rl, kent kc, faries pl. carotid tortuosity in patients with prior cervical radiation: increased technical challenge during carotid stenting. vasc endovascular surg. 2011 oct;45(7):61926. 53. hosokawa s, mineta h. tortuous internal carotid artery presenting as a pharyngeal mass. j laryngol otol. 2010 sep;124(9):1033-6. 54. robert v carlson, kenneth m boyd,1 and david j webb. the revision of the declaration of helsinki: past, present and future br j clin pharmacol. 2004 june; 57(6): 695–713. microsoft word 11dumitrescugabriela_posteriorfossa.doc romanian neurosurgery (2010) xvii 3: 327 – 338 327 posterior fossa meningiomas: correlation between site of origin and pathology gabriela-florenţa dumitrescu1, anca indrei2, m.el husseini3, danisia haba4, n. ianovici3, i. poeată3, dana turliuc3 1department of pathology, emergency clinical hospital “prof. dr. n. oblu” iaşi 2department of human anatomy, faculty of medicine, university of medicine and pharmacy “gr. t. popa” iaşi 3department of neurosurgery, faculty of medicine, university of medicine and pharmacy “gr. t. popa” iaşi 4department of general and dental radiology, faculty of medicine, university of medicine and pharmacy “gr. t. popa” iaşi abstract aim: to identify the possible correlation between demographic data of the patients, site of tumor origin, and pathological characteristics of each subgroup of the posterior fossa meningiomas as the anatomical location of these tumors is a critical determinant of the operative approach that will be chosen. materials and methods: we analyzed medical records of 35 patients with posterior fossa meningiomas who underwent surgery between january 2005 and december 2009 at neurosurgery department, iaşi. the analysis included: age and gender of the patients, tumor location, and pathologic findings. according to the anatomical relationship with posterior fossa structures, these 35 meningiomas were classified into 5 types: cerebellar convexity, cerebellopontine angle, petroclival, foramen magnum, and unclassified tumors. according to the classification scheme of who 2007 (19), all cases were classified into three histopathological groups: benign, atypical, and malignant meningiomas, and every histopathological subtype was noted. results: posterior fossa meningiomas have a 3.33:1 female-to-male ratio with a mean age of 51.6 years. 29 patients had anatomically distinct attachment to the dura of the 4 chosen compartments of the posterior fossa (cerebellar convexity – 14.28%, cerebellopontine angle – 48.57%, petroclival – 11.42%, and foramen magnum – 8.57%) and 6 patients (17.14%) had giant tumors with broad attachment in multiple areas of the posterior fossa. grade i meningiomas encountered in majority of cases (82.85%), whereas grade ii meningiomas were diagnosed in 11.42% of the operated case, and anaplastic meningiomas (grade iii) accounted only 5.71%. the most common benign histological subtypes among posterior fossa meningiomas were fibrous (37.79%) and psamomatous (24.13%). petroclival meningiomas accounted a higher incidence then that presented in other studies (11.42% of all posterior fossa meningiomas). the mean age for female patients was older (55 years) then in other 328 gabriela-florenţa dumitrescu et al posterior fossa meningiomas studies. there were various benign histological subtypes (psammomatous, meningothelial, and secretory) and even an atypical one that was diagnosed in a male patient. foramen magnum meningiomas affected only females with a mean age of 52.66 years. all tumors were benign (grade i) with psammomatous subtype being the most common histological subtype (66.66%). cerebellar convexity meningiomas presented a female to male ratios of 4:1. female patients were older (64.25 years) then the mean age of patients with posterior fossa meningiomas. in cerebellar convexity location, all meningiomas presented only benign histology (fibrous subtype, 100%) that made us thinking to a different tumorigenesis for this tumors comparative with other locations. cerebellopontine angle meningiomas presented a strong preponderance of female patients (5:1). though majority of cerebellopontine angle meningiomas had grade i of malignancy, they exhibited a large variety of histological subtypes. conclusion: in our series, posterior fossa meningiomas are clearly various tumors in their histology and demographic data. we identified a significant association between age and gender of the patients, histology of posterior fossa meningiomas, and their site of origin. keywords: posterior fossa, meningioma, histopathological subtypes, age, gender, anatomical location meningiomas account for approximately 20-30% of all intracranial tumors, depending of the series (3). in clinical practice, meningiomas are most commonly classified according to site of origin. cushing and eisenhardt established in 1938 the modern classification of meningiomas by site of origin. cushing's cumulative experience of 313 cases published in 1938 very closely resembles our contemporary understanding of the frequency of meningiomas by location (23). there are many different classification schemes for meningiomas. since the work of cushing and eisenhardt, there have been some other classifications of meningiomas according to their site of origin on the dura. these classification systems offer no insight into the biology of the tumors, but neurosurgeon can get important information about the challenges of surgical treatment (13). the posterior fossa, deeply concave, is formed by the occipital, the petrous and mastoid portions of the temporal. it is separated from the middle fossa in the median line by the basilar suture and on each side by the superior border of the petrous portion of the temporal bone. this serves for the attachment of the tentorium cerebelli, is grooved externally for the superior petrosal sinus, and at its inner extremity presents a notch, upon which rests the fifth nerve. its circumference is bounded posteriorly by the grooves for the lateral sinuses. in the centre of this fossa is the foramen magnum, bounded on either side by a rough tubercle, which gives attachment to the odontoid ligaments; and a little above these are seen the internal openings of the anterior condyloid foramina. in front of the foramen magnum is the basilar process, grooved for the support of the medulla oblongata and pons varolii, and articulating on each side with the petrous portion of the temporal bone, forming the petro-occipital suture, the anterior half of which is grooved for the inferior petrosal sinus, the posterior half romanian neurosurgery (2010) xvii 3: 327 – 338 329 being encroached upon by the foramen lacerum posterius or jugular foramen. above the jugular foramen is the internal auditory foramen. behind the foramen magnum are the inferior occipital fossae, which lodge the lateral lobes of the cerebellum, separated from one another by the internal occipital crest, which serves for the attachment of the falx cerebelli, and lodges the occipital sinuses. these fossae are surmounted, above, by the deep transverse grooves for the lodgment of the lateral sinuses (15). posterior fossa meningiomas have been usefully classified by sekhar et al into six groups: type i: cerebellar convexity lateral tentorial (tentorium, transverse sigmoid sinuses); type ii: cerebellopontine angle (petrous ridge, internal acoustic conduct); type iii: jugular foramen (cerebellomedullary angle, internal jugular vein, extracranial); type iv: petroclival (upper 2/3 clivus, cavernous sinus, meckel's cave, petrous ridge); type v: foramen magnum (lower 1/3 clivus, c12 area); type vi: unclassified (entire clivus, mid and lower clivus, other types) (16). subsequently, different nomenclatures have been proposed by several authors. bradac et al (7) subdivided posterior fossa meningiomas into four groups: 1. tentorial meningiomas are those located under the surface of the tentorium cerebelli; 2. clival meningiomas proceed from upper third of the clivus bone in the direction of the middle cranial fossa or the direction of the brainstem; 3. cerebellopontine angle meningioma arise from the medial portion of the petrous bone; 4. foramen magna meningiomas arise at or near the anterior rim of the foramen. the present study analysed the posterior fossa meningiomas initially classified on their site of origin by ct, irm and surgical observation, in order to identify the possible correlation between demographic data of the posterior fossa meningiomas patients, site of tumor origin, and pathological characteristics of each subgroup as the anatomical location of the meningioma is a critical determinant of the operative approach that will be chosen. materials and methods emergency clinical hospital “prof. dr. n. oblu” iaşi admits neurosurgical patients from moldova region that has a population of almost 5 million people. taking into account this large addressability, we analyzed medical records of 35 patients with posterior fossa meningiomas who underwent surgery between january 2005 and december 2009 at neurosurgery department. the analysis included: age and gender of the patients, tumor location, and pathologic findings. according to the anatomical relationship with posterior fossa structures, these 35 meningiomas were classified into 5 types: cerebellar convexity (tentorium cerebelli, transverse sigmoid sinuses), cerebellopontine angle (petrous ridge, internal acoustic conduct), petroclival (upper 2/3 clivus, foramen jugular), foramen magnum (lower 1/3 clivus, c1-2 area), and unclassified (broad dural attachment in multiple areas of the posterior fossa) tumors (figure 1). according to the classification scheme of who 2007 (19), all cases were classified into three histopathological groups: benign, atypical, and malignant meningiomas, and every histopathological subtype was noted. 330 gabriela-florenţa dumitrescu et al posterior fossa meningiomas results there was no great variation in the annual number of pf meningiomas, excepted 2008, when we observed a maximum of the operated cases (10 patients) (figure 2). in our series, meningiomas have a 3.33:1 female-to-male ratio. of the 35 cases of posterior fossa meningiomas, 27 cases (77.14%) were females with an age ranging between 36-73 years, and a mean age of 52.8 years, and 8 cases (22.86%) were males with an age ranging between 35 – 57 years, and mean age of 47.1 years. figure 1 anatomical location of posterior fossa meningiomas: cerebellar convexity (1); cerebellopontine angle (2); petroclival (3); and foramen magnum (4) mean age for all posterior fossa meningiomas was 51.6 years. giant meningiomas affecting a great part of posterior fossa encountered in male patients younger then mean age (43.33 years). female patients were older then mean age when meningiomas were located in cerebellar convexity location (64.25 years) (table 1). grade i meningiomas encountered in majority of cases (82.85%), whereas grade ii meningiomas were diagnosed in 11.42% of the operated case (figure 6), and anaplastic meningiomas (grade iii) accounted only 5.71%. the atypical meningiomas (grade ii) were diagnosed in cerebellopontine angle and in the petroclival location. the malignant meningiomas couldn't be located in one specific compartment of the posterior fossa as they were of great dimensions at the moment of diagnosis (table 2). 0 1 2 3 4 5 6 7 8 2005 2006 2007 2008 2009 female male figure 2 the annual distribution of pf meningiomas correlated with gender of the patients romanian neurosurgery (2010) xvii 3: 327 – 338 331 tabel 1 posterior fossa meningiomas: sites of origin, gender, and mean age of the patients tumor location unclassified cerebellar convexity cerebellopontine angle petroclival foramen magnum pacient gender f m f m f m f m f m pacient mean age (years) 52 43.33 64.25 49 50.93 49.33 55 50 52.66 tabel 2 posterior fossa meningiomas: sites of origin, gender and histological degree of malignity histological degree of malignity unclassified cerebellar convexity cerebello pontine angle petroclival foramen magnum no. cases (%) f m f m f m f m f m grade i grade ii grade iii 1 1 1 2 1 4 1 13 2 3 3 1 3 29 (82.85%) 4 (11.42%) 2 (5.71%) tabel 3 posterior fossa meningiomas: sites of origin and histological subtypes histological type un classified cerebellar convexity cerebello pontine angle petro clival foramen magnum no. cases (%) fibrous 1 5 5 11 (37.79%) psammomatous 2 2 1 2 7 (24.13%) meningothelial 3 1 4 (13.79%) secretory 2 1 1 4 (13.79%) angiomatous 3 3 (10.34%) atypical 1 2 1 4 (11.42%) anaplastic 2 2 (5.71%) total 6 (17.14%) 5 (14.28%) 17 (48.57%) 4 (11.42%) 3 (8.57%) 35 (100%) twenty nine patients had anatomically distinct attachment to the dura of the 4 chosen compartments of the posterior fossa (cerebellar convexity – 14.28%, cerebellopontine angle – 48.57%, petroclival – 11.42%, and foramen magnum – 8.57%) and 6 patients (17.14%) had giant tumors with broad attachment in multiple areas of the posterior fossa (table 3). the most common benign histological subtypes were fibrous (37.79%) and psamomatous (24.13%). there were only few cases (10.34%) of angiomatous subtype meningiomas. atypical and anaplastic meningiomas represented 17.13% of all pf meningiomas. taking into consideration the histological subtype, cerebellar convexity location was associated only with fibrous meningioma (figure 3). the unique location of angiomatous subtype was cerebellopontine angle. psamomatous subtype prevailed in the foramen magnum location (figure 4). cerebellopontine angle exhibited all the histological subtypes of meningiomas, inclusive the secretory meningioma (table 3, figure 5). 332 gabriela-florenţa dumitrescu et al posterior fossa meningiomas figure 3 female pacient, 73 years: fibrous meningioma of the cerebellar convexity (hematoxylin-eoyin, original magnification x100) figure 4 female pacient, 44 years – old: meningothelial meningioma of the cerebellopontine angle (hematoxylin-eoyin, original magnification x100) figure 5 female pacient, 53 years-old: secretory meningioma of cerebellopontine angle (hematoxylin-eoyin, original magnification x100) figure 6 male patient, 50 years-old: atypical meningioma of the petroclival area (hematoxylineoyin, original magnification x100) disscusion harvey cushing was the first to use the term “meningioma” in 1922, although this tumor was known under various names since the 17th century (16). in 1614, felix plater, professor of medicine from the university of basel, made the first report to a lesion that is most comparable with a meningioma. he descried the symptoms as well as the autopsy findings of a “noble knight” intracranial tumor which he described as: “a round fleshy tumor, like an acorn. it was hard and full of holes and was as large as a medium –sized apple. it was covered with its own membrane and was entwined with veins. however, it was free of all connections with the matter of the brain, so much so that when it was remove by hand, it left behind a remarkable cavity” (23). the first documented report of a tumor resembling a meningioma was published in 1774 by french surgeon antoine louis, who called it fungus durae matris. various description and terms followed: in 1834 cruveilhier depicted them in a pathology atlas; in 1847, they were named romanian neurosurgery (2010) xvii 3: 327 – 338 333 psammomas (sandlike) by virchow, who was the first to note the presence of granules; in 1864, bouchard named them epitheliomas; and in 1869, golgi named them endotheliomas (4). although the first pictures of a meningioma were published in 1730, the earlier work that dealt with these tumors was written in 1774 by antoine louis in mémoires de l'academie royale de chirurgie. he called them tumeurs fongueuses de la dure-mere. virchow, who noted the presence of small hard granulations in meningiomas, called them psammomas (tumors like sand) in 1859 and considered that they are related to the sarcomas. golgi, on the other hand, called them endotheliomas in 1869, indicating a benign histology (4). meningiomas are now known to arise from arachnoidal cap cells of the leptomeninges. arachnoidal granulations were first described by antonio pacchioni in rome in 1705, believing them to be nervous system counterpart to lymph glands. in 1846, rainey suggested that arachnoidal or pacchionian granulations arose from the meninges. this association was confirmed by luschka in 1852 and later by meyer in 1859. it was nor until john cleland in 1864, however, that the association between pacchionian granulations and meningeal tumors was drawn. working in glasgow, cleland descriebed two leptomeningeal tumors at autopsy and deemed them “villous tumors of arachnoid”, as he was able to separate the growths from the dura. he hypothesized their origin as from the pacchionian granulations. in 1915 harvey sided with cleland and considered that meningeal tumors arose from arachnoidal cap cells. seven years later, harvey cushing proposed the term “meningioma” for these tumors and the term achieved global acceptance. working together with his student, percival bailey, at the peter bent brigham hospital, he adopted a histopathological classification system that listed four variants: meningothelial, fibroblastic, angioblastic and osteoblastic. later, bailey and bucy expanded the initial histopathological classification scheme of meningiomas in such a manner as the new who histological classification 2007 is almost the same despite new discoveries made by molecular biology, biochemistry and technology from the last years (23). posterior fossa meningiomas have presented a formidable challenge throughout the history of neurosurgery and many, especially those arising from petroclival region, were considered “inoperable” up until the 1970s. however, with the advent of the operating microscope, ct and mr imaging, microsurgical techniques and the development of various skull base approaches, it became possible to safely resect the majority of posterior fossa meningiomas. tumor location is the single most important feature regarding therapy since it practically defines the terms of surgical interventions. they occur most commonly along the tentorium, cerebellar hemispheres, and cerebellopontine angle, but they can also be found along the clivus and the anterior margin of the foramen magnum (17). considering the location frequency, it is conceivable that true meningiomas tend to occur where meningothelial cells and arachnoid cap cells are most numerous. the arachnoid granulations or villi have large number of cap cells and therefore are common sites of origin for meningiomas, especially along the dural venous sinuses 334 gabriela-florenţa dumitrescu et al posterior fossa meningiomas where the villi are mostly concentrated, or along the cranial sutures where arachnoid granulations or rests of arachnoid cells are often present (12). the frequency of meningiomas at various intracranial sites varies from study to study. according to some studies, posterior fossa meningiomas represent 615% cerebellar convexity meningiomas account for approximately 5%, cerebellopontine angle meningiomas for 24%, clivus less than 1% from all intracranial meningiomas (12). meningiomas of the cerebellopontine angle are the most common posterior fossa meningiomas. foramen magnum meningiomas are uncommon. clival meningiomas are less common (19). bernstein reported the same percentages: 50% of posterior fossa meningiomas are located in the cerebellopontine angle, 40% occur around the tentorium or cerebellar convexity, 9% are at the clivus, and 6% occur in the vicinity of the foramen magnum (9). roberti et al. found some other different percents for posterior fossa meningiomas. in their report there were 68.32% petroclival meningiomas, 13.04% foramen magnum meningiomas, 8.69% cerebellar convexity meningiomas, 5.59% cerebellopontine angle meningiomas, and 4.34% jugular foramen meningiomas (25). in our study, the most common site of posterior cranial fossa meningiomas was cerebellopontine angle as 48.57% of them were found to have dural attachment in this area. only 8.57% of posterior fossa meningiomas were situated at the foramen magnum. intracranial meningiomas predominantly affect patients in the 5th to 7th decades of life with various female-to-male ratios that range from 1.4:1 to 2.7:1 (16, 23), but posterior fossa meningiomas presented even a greater preponderance of female patients. garcía-navarrete and sola presented 26 successive patients with posterior fossa meningiomas treated at servicio de neurocirurgia in hospital universitario de la princesa from madrin, spain. there were 24 women and two men (14). roberti et al. reported 161 consecutive cases of pf meningiomas operated on between 1993 and 1999 at the george washington university medical centre. the ratio f:m were 3.9:1 (mean age 47 years, range 10-81 years) (25), almost similar values with the ratio found in our study as the mean age was 51.6 years (range 35-73 years) with a female:male ratios of 3.3:1. the vast majority of intracranial meningiomas (92%) have a benign histology, whereas 8% show atypical or malignant features. for all meningiomas, the most common histopathological subtype is the meningotheliomatous type (63%), followed by transitional (19%), fibrous (13%), and psamomatous (2%) meningiomas (23). fewer then 10% of meningiomas are malignant (24). in the present study, the most common benign histological subtypes among posterior fossa meningiomas were fibrous (37.79%) and psamomatous (24.13%). atypical and anaplastic meningiomas represented 17.13% of all posterior fossa meningiomas, but this series contained too small number of cases to draw a pertinent conclusion. petroclival meningioma accounts for approximately 3%-10% of all pf meningiomas (13, 32, 29). these rare, slowly growing tumors arise from the area of the synchondrosis of the sphenoid and romanian neurosurgery (2010) xvii 3: 327 – 338 335 occipital bones on the clivus. originating in the clivus and petrous apex region, the tumor may involve the medial part of the tentorium, meckle's cave, cavernous sinus and parasellar region and, as a consequence, poses a great technical challenge to neurosurgeons because of its location (32). petroclival meningiomas present a slight female preponderance, and reported female:male ratios range from 1.4:1 to 2.8:1 (13). the mean age at presentation in patients with petroclival meningiomas is the mid-40s with a very wide range (29). in 5 years, zhu et al. operated 25 patients with petroclival meningiomas. of the 25 patients there were 4 men and 21 women, aged 28-67 years (average 47.2 years) (32). 109 consecutive patients operated during a 12-years period by couldwell included 40 men and 69 women ranging in age from 25 to 75 years (mean 51 years). four recurrent cases demonstrated histological compatibility with malignant meningioma (10). in our study, petroclival meningiomas accounted a higher incidence then that presented in other studies (11.42% of all posterior fossa meningiomas). the mean age for female patients was older (55 years) then in cited studies and for male patients it was 50 years. petroclival meningiomas included various benign histological subtypes (psammomatous, meningothelial, and secretory) and even an atypical one that was diagnosed in a male pacient. among the meningiomas of the posterior fossa, foramen magnum (fm) meningiomas deserve special consideration as they have the worst outcome in terms of surgical results and operative morbidity (29). due to their unique characteristics and challenges, foramen magnum meningiomas were separated from other posterior fossa meningiomas and recently have received more attention, due to great improvement in the surgical approach during the last decade (21). foramen magnum meningiomas are rare and account for only 0.3% to 3.2% of all meningiomas, and between 4.2% and 20% of all posterior fossa meningiomas (1, 9, 5). the first case description of a meningioma arising at the foramen magnum was provided by hallopeau at lariboisiere hospital in 1872 (21). in their monograph on meningiomas, cushing and eisenhard divided foramen magnum meningiomas into two groups: craniospinal and spinocranial tumors. the craniospinal type arose above the foramen magnum ventral to the neuraxis and projected downward, displacing the medulla and cervical spinal cord. the spinocranial type was found dorsal or dorsolateral to the spinal cord and projected upward into the posterior fossa cisterns (5, 30). welling et al (30) reported a definite female predominance for meningiomas of foramen magnum, with ratios from 2:1 to 3.6:1. they become symptomatic in the fourth through decades of life. marin sanabria et al. reviewed 492 intracranial and spinal meningiomas treated at kobe university hospital between 1972 and 2001. seven patients of 492 were identified as foramen magnum meningioma. the seven patients were five women and two men aged 39 to 66 years (mean 53.3 years). they found a female preponderance (2.5:1) (21). over a 5-year period, borba et al. operated 15 patients presenting with meningiomas of the foramen magnum. fourteen patients were females, and one was male, ranging in age from 42 to 74 years (mean 55.9 years) (6). in recent 336 gabriela-florenţa dumitrescu et al posterior fossa meningiomas literature there are a number of cases which appeared to children. mahx bracho et al. reported a 3-year-6-month-old boy with chordoid meningiom of foramen magnum (20). due to the rarity of the published cases, there is only limited information about the histology of these meningiomas. tsao et al. presented the histopathology of a foramen magnum meningioma as meningothelial type (28). on the other hand, avninder et al. presented a case of a lymphoplasmacyte-rich meningioma arising at the foramen magnum (2). in the present study, foramen magnum meningiomas affected only females being in the fourth through sixth decades of life (mean age = 52.66 years). all foramen magnum meningiomas were benign (grade i) with psammomatous subtype being the most common histological subtype. this presentation is similar to spinal meningiomas which are mainly psammomatous in appearance (66%) (26) probably because both tumoral location are in close vicinity. cerebellar convexity meningiomas are rare. a small number of series reported in the literature are often included in the wider coverage of posterior fossa meningiomas, and therefore, an accurate metanalysis is not possible. nevertheless, it may be assumed that they account 6%–18% of the posterior fossa meningiomas and represent about 1.5% of all meningiomas (11, 9). in their surgical series of meningiomas from 1938, cushing and eisenhard encountered only three cases of pure cerebellar convexity meningiomas (about 1% of their entire series) (11). in the present study, 14.28% of all 35 cases of posterior fossa meningiomas were located on cerebellar convexity. female to male ratios was 4:1. female patients with cerebellar convexity meningiomas were older (64.25 years) then mean age of patients with posterior fossa meningiomas. in cerebellar convexity location, all meningiomas presented only benign histology (fibrous subtype, 100%) that made us thinking to a different tumorigenesis for this tumors comparative with other locations. although less than 20% of all meningiomas occur in the posterior fossa, half of these are located in the cerebellopontine angle (22). in our study, cerebellopontine angle meningiomas represented 48.57% of all 35 cases. there was a strong preponderance of female patients (5:1). the mean age, irrespectively of gender, was close to mean age for all posterior fossa meningiomas. 11.74% of cerebellopontine angle meningiomas had grade ii of malignancy, and the remaining 88.23% exhibited benign histology. though majority of cerebellopontine angle meningiomas had grade i of malignancy, they exhibited a large variety of histological subtypes (fibrous, meningothelial, secretory subtypes). only in this location could be find the angiomatous subtype as the posterior petrous surface of temporal bone is relatively unique in its relationship to the venous sinuses because the sigmoid, superior petrosal, inferior petrosal, and cavernous sinuses form a ring surrounding the posterior face of the petrous bone and the meningiomas located in this region have a very close relationship with the four aforementioned sinuses (31). on the other hand, chung et al. gave another explication for histopathological variations of meningiomas as he considered that meningiomas arise from polyblastic and functionally multipotent arachnoid cells (8). romanian neurosurgery (2010) xvii 3: 327 – 338 337 taking into account the histology of normal leptomeninges, lee et al. explained the existence of so many subtypes of meningiomas. the outer layer of the arachnoid membrane is formed by the arachnoid cap cells, whereas the trabecular cells form the inner layers, which are separated by basal lamina. histologically, fibrous and transitional meningioma subtypes have features similar to the fibroblast found in the deeper layers of the arachnoid close to the subarachnoid space, whereas meningothelial subtype resemble the arachnoid cap cells of the outer layers. so, lee considered that differential leptomeningeal embryogenesis may result in the predominance of one cell type (cap cells of the outer layer of the arachnoid membrane as opposed to trabecular fibroblast of the inner layer) in certain location (18). conclusion in our series, posterior fossa meningiomas are clearly various tumors in their histology and demographic data. we identified a significant association between age and gender of the patients, histology of posterior fossa meningiomas, and their site of origin. there was a predominance of female patients with a mean age situated in the sixth decade of life. benign meningioma was the unique histological category for cerebellar convexity and foramen magnum, but there were different subtypes (i.e. fibrous versus angiomatous) characteristic for every location. this study establishes a foundation for future basic, clinical, and public health research to examine specific histologies (i.e. meningiomas) in specific location (i.e. posterior fossa) and incidence over times. references 1.arnautović kl, al-mefty, husain m. ventral foramen magnum meningiomas. j neurosurg. 2000; 92(1 suppl):71-80. 2.avninder s, gupta v, sharma kc. lymphoplasmacyte-rich meningioma at the foramen magnum. br j neurosurg. 2008 ; 22(5) :702-4. 3.black p. mcl., loeffler js (eds), cancer of nervous system, cambridge: blackwell science, 1997, p. 329. 4.bondy m, lee ligon b. epidemiology and etiology of intracaranial meningiomas. j neuro-oncol. 1996; 29:197-205. 5.borba la and colli bo : foramen magnum meningiomas, in meningiomas. diagnosis, treatment, and outcome, ed. joung h. lee, springer-verlag, london, 2009, p. 449. 6.borba la, de oliveira jg, giudicisi-filho m, colli bo, surgical management of foramen magnum meningiomas, neurosurg rev. 2009; 32(1):49-58. 7.bradac gb, ferszt r, kendall be, cranial meningiomas. diagnosis, biology, therapy. springerverlag, berlin, 1990, p. 125. 8.chung s-b, kim c-y, park c-k, kim dg, jung hw. falx meningiomas: surgical results and lessons learned from 68 cases. j korean neurosurg soc. 2007; 42:276-280. 9.cohen-gadol aa, al-mefty o. skull base tumors, in neuro-oncology. the essentials, eds. mark bernstein and mitchel s. berger, 2nd edition, thieme, 2008, usa, p. 323. 10.couldwell wt, fukushima t, giannota sl, weiss mh. petroclival meningiomas surgical experience in 109 cases. j neurosurg. 1996; 84(1):20-8. 11. delfini r, santoro a, pichierri a. cerebellar convexity meningiomas, in meningiomas. diagnosis, treatment, and outcome, ed. joung h. lee, springerverlag, london, 2009, 457. 12.drevelegas a, karkavelas g, chourmouzi d, boulogianni g, petridis a, dimitriadis a. meningeal tumors, in imaging of brain tumors with histological correlations, ed. antonios drevelegas, springer-verlag, berlin, 2002, p. 178. 13.erkmen k, al-mefty o. nonschwannomatous lesions of the cerebellopontine angle. petroclival tumors, in surgery of the cerebellopontine angle, eds. bambakidis nc, megerian ca, spetzler rf, peoplés medical publishing house, usa, 2009, p. 227. 14.garcía-navarrete e, sola rg, clinical and surgical aspects of the meningiomas of the base of the skull. iii. meningiomas of the posterior fossa, rev neurol. 2002; 34(8):714-23. 15.gray h, carter hv. anatomy, descriptive and surgical, philadelphia, henry c. lea, 1867, p. 101. 16.kaye h. posterior fossa meningiomas, in practical handbook of neurosurgery: from leading 338 gabriela-florenţa dumitrescu et al posterior fossa meningiomas neurosurgeons, ed. marc sindou, vol. 2, 2009, springer-verlag, germany, p. 181. 17.kraemer dl, bullard de. clinical oresentation of the brain tumor patient, in brain tumors: a comprehensive text, eds. robert a. morantz and j. w. walsh, 1994, marcel dekker, usa, p. 204. 18.lee jh, sade b, chol e et al. meningothelioma as the predominant histological subtype of midline skull base and spinal meningioma. j neurosurg. 2006; 105:60-64. 19.louis dn, ohgaki h, wiestler od, cavenee wk, burger pc, jouvet a, et al. the 2007 who classification of tumors of the central nervous system, acta neuropathol. 2007; 114:97-109. 20.marhx-bracho a, rueda-franco f, ibarra-de la torre a, garcíagonzalez o. et al. chordoid meningioma of the foramen magnum in a child : a case report and review of the literature. childs nerv syst. 2008 ; 24(5):623-7. 21.marin sanabria ea, ehara k, tamaki n, surgical experience with skull base approaches for foramen magnum meningioma, neurol med chir (tokyo). 2002; 42; 472-480. 22.neil r. miller, nancy j. newman, valérie biousse, john b. kerrison (eds.). walsh and hoyt's clinical neuro-ophthalmology: volume two, 6th edition, p. 1508. 23.okonkwo do, laws er. meningiomas: historical perspective, in meningiomas: diagnosis, treatment, and outcome, ed. joung h. lee, springer-verlag, london, 2009, pp. 3-11. 24.park bj, kim hk, sade b, lee jh. epidemiology, in meningiomas: diagnosis, treatment, and outcome, ed. joung h. lee, springer-verlag, london, 2009, p. 11. 25.roberti f, sekhar ln, kalavakonda c, wright dc. posterior fossa meningiomas: surgical experience in 161 cases. surg neurol. 2001; 56(1):8-20. 26 26.schaller b. spinal meningioma: relationship between histological subtypes and surgical outcome? j neurooncol. 2005; 75(2):157-161. 27.singh a. and selesnick sh. meningiomas of the posterior fossa and skull base references and further reading may be available for this article. to view references and further reading you must purchase this article., in neurotology, 2th edition, eds. robert k. jackler and derald e. brackmann, mosby, 2005, p. 792. 28.tsao gj, tsang mw, mobley bc, cheng ww. foramen magnum meningioma: dysphagia of atypical etiology, j gen intern med. 2008; 23(2):206-209. 29.ware ml, pravdenkova s, erkmen k, al-mefty o. petroclival and upper clival meningiomas i: an overview of surgical approaches, in meningiomas. diagnosis, treatment, and outcome, ed. joung h. lee, springer-verlag, london, 2009, p. 403. 30.welling b, park y-k, al-mefty o. primary extramedullary tumors of the craniovertebral junction, in surgery of the craniovertebral junction, eds. curtis a. dickman, robert friedrich spetzler, volker k. h. sonntag, thieme, usa, 1998, p. 240. 31.zhe bao wu, chun jiang, shu sen guan. posterior petrous meningiomas: 82 cases, j neurosurg., 2005; 102:284-289. 32.zhu w, mao y, zhou l, yhang r, chen l. keyhole approach surgery for petroclival meningioma, chinese medical journal, 2006, 119: 1339-1342. 4xalvis-miranda_what 172 alvis-miranda et al cerebral venous anomalies what the neurosurgeon needs to know about cerebral developmental venous anomalies hernando raphael alvis-miranda1, nancy duarte-valdivieso2, gabriel alcala-cerra3, willem calderon-miranda4, marco zenteno5, angel lee6, luis rafael moscote-salazar1 1universidad de cartagena, colombia 2chang gung memorial hospital, linkou, taiwan 3neurosurgeon, universidad de cartagena, colombia 4neurosurgeon, universidad del magdalena, colombia 5instituto nacional de neurologia y neurocirugia “manuel velasco suarez”, mexico d.f, mexico 6hospital angeles del pedregal, mexico, mexico d.f abstract venous angiomas or developmental venous anomalies (dva) are extreme variations of normal transmedullary veins that are necessary for the drainage of white and gray matter, also are one type of cerebrovascular malformation (cvm), sharing category with capillary telangiectesias, cavernous malformations (cm), and arteriovenous malformations (avm), each of which may also be associated with a dva. dva are the most commonly encountered cvm, accounting for up to 60% of all cvm. we present a review of the literatura key words: developmental venous anomalies, venous angiomas, neurointervention introduction developmental venous anomalies (dva) are extreme variations of normal transmedullary veins that are necessary for the drainage of white and gray matter, also are one type of cerebrovascular malformation (cvm), (1) sharing category with capillary telangiectesias, cavernous malformations (cm), and arteriovenous malformations (avm), each of which may also be associated with a dva. (2) dva are the most commonly encountered cvm, accounting for up to 60% of all cvm. their prevalence is around 2.5– 9%, and they are usually solitary. (3) huang et al., in 1984 (4) analyzed the angiographic findings of dva and proposed terming them “medullary venous malformations,” and russel and rubinstein (5) defined cerebrovascular malformations as “cerebral vascular hamartomas” as intention to embrace malformations with a pathological process, however, the most accurate term, dva, was first suggested by lasjaunias and burrows in 1986, (6), because venous romanian neurosurgery (2014) xxi 2: 172 182 173 malformations originate from persisting embryologic medullary veins related to alterations in the embryonic period; thus it has been used to describe what is also known as venous angioma, cerebral venous malformation, and cerebral venous medullary malformation. abandonment of the other designations reflects the nature of the dva, although the exact etiology remains unknown, does not involve endothelial proliferation, has no proliferative potential, no direct arteriovenous shunts, and generally normal brain parenchyma between the dilated veins. (6, 7) the use of current neuroimaging techniques has led to great advances in the diagnosis of cvm, and particularly the dva diagnosis (1), the aim of this work is to review relevant issues regard dva, which can help a better understanding of the natural course of this type of cerebrovascular malformation. dva architechture an appropriate knowledge of the cerebral venous anatomy is necessary to understand how dva is constituted and which can be the meaning of its architecture, thus next will be discussed briefly the cerebral venous anatomy. cerebral venous anatomy the superficial venous system: this system drains the outer 2 centimeters of white matter and cortex in centrifugal direction through subcortical and intracortical veins toward pial veins, cortical veins and then dural sinuses. subcortical veins are composed of three segments: medullary, arcuate and intracortical, in their traveling to the brain surfaces. white matter have also a superficial drainage provided by superficial medullary veins. the cortex’s superficial drainage is predominatly from intracortical veins, which travel to join either pial or superficial cortical veins. pial veins, which lays in the brain surface, deep to the pia matter, collect blood drained from intracortical, subcortical and superficial medullary veins. pial veins coalesce into cortical veins and then toward a dural venous sinus. the deep venous system also known as galenic venous system, drains blood in centripetal fashion from the more central white matter and paraventricular nuclei through tributaries of the great cerebral vein to the straight sinus. the deep medullary veins perform the deep drainage of white matter, they connect with subependimal vein, and as they traverse in their travel converge into 4 zones: include (1) a superficial zone within the white matter just below the corticomedullary junction; (2) a candelabra zone formed by horizontal connections between deep medullary veins; (3) a palmate zone consisting of connections between very small deep medullary veins just superficial to the lateral ventricles; and (4) a subependymal zone that represents the convergence of the venous trunks that drain from the palmate zone. the internal cerebral veins (icv) or the vein of galen are the major collectors of the subependymal zone. the bilateral icv converge at or near the midline along with the bilateral basal veins of rosenthal and medial and lateral atrial veins to form a singular midline vein: the great vein of galen. 174 alvis-miranda et al cerebral venous anomalies the drained blood runs into the major dural sinuses: superior sagittal sinus (sss), inferior sagittal sinus (iss), lateral sinus (ls), cavernous sinus and straight sinus, and then to the internal jugular vein (ijv). superficial venous system predominantly drains the sss and the ls. deep white matter and basal ganglia are drained by the deep venous system toward the vein of galen. between these two cerebral vein system can be found many anastomoses. dva constitution dva consist of radially oriented and converging dilated medullary veins, which drain centripetally into a transcerebral collector (enlarged transcortical or subependymal draining vein) that opens either into the superficial subcortical or deep pial veins. they are composed of angiogenically mature elements; indeed they are widely accepted to represent anatomic variants of normal venous drainage. (3) histologically the veins are enlarged and sometimes hyalinized, but otherwise normal. (3) because of the absence of normal or subependimal veins draining outer zone of the white matter and the cortex to the pial veins, it is generated an abnormal venous arrange or disposition, in which is produced a reversing of the drainage pattern, i.e., instead of superficial venous drainage, the blood is drainage toward the deep subependimal veins, in a centripetally fashion. the deep venous territory, instead of draining blood centripetally from the more central white matter and paraventricular nuclei, drains blood in a centrifugal fashion toward either the pial veins or directly into a dural venous sinus. (2) figure 1 – angio ct – venous angiomas on right side depending on their location, they may feed into the superficial (dural) or the deep venous systems. posterior fossa dva tend to direct venous blood to the veins of the lateral recess of the fourth ventricle, the precentral veins, a transpontine vein, or the longitudinal intrategmental vein, as detected by venous phase angiography. (8) hypothesis their etiology and mechanism of development are unknown, but it is currently accepted that they act like a compensatory system of cerebral parenchyma venous drainage due to early failure, abnormal development, or an intrauterine occlusion of normal capillaries or small transcerebral veins and thrombosis of normal parenchymal veins. (7) these drainage pathways may have developed as a method for maintaining the hemodynamic equilibrium of the transcortical venous drainage. according to saito and kobayashi (9), during embryogenesis, some accident occurs during the formation of the romanian neurosurgery (2014) xxi 2: 172 182 175 medullary veins or their tributaries, such as occlusion or maldevelopment, and as compensation results cva, thus, the main suggested etiology for the formation of cva is an embryologic accident that results in either arrested formation or thrombosis of the developing venous drainage of the specific region (10–12), that is followed by a secondary compensatory mechanism in which embryologic medullary venules persist and cluster locally in a large draining vein (6, 9, 10, 13). thus, they may be better described as being the result of a fetal pathological event rather than true anatomic variations. associated parenchymal abnormalities although the parenchyma drained by a cva is generally reported as normal brain tissue, there have been reports of parenchymal abnormalities in the vicinity, and they are more common than previously thought (2). the essential role of cva in normal cerebral venous drainage is shown when cases of catastrophic venous ischemic and haemorrhagic complications arise as consequence from their surgical removal (14). brain abnormalities found within the drainage territory of a cva are (15): locoregional brain atrophy, which is observed in close to 30% of patients, followed by white matter, lesions (28.3% on mri, 19.3% on ct), cm (13.3% of mri investigations) and dystrophic calcification (9.6% of ct investigations). to take into account, parenchymal abnormalities are equally observed in small-, medium-, and large-sized cva, indicating that size is not a determining parameter for their development. regard to the number of cva, in the san millán et al series, was observed that only 1.2% of patients harboured two coexisting cva, a lower incidence than the 12% reported by uchino et al (16). the coexistence of two or more cvm within the same location has been documented (17–19). the prevalence of this specific subtype of mixed vascular malformations has a wide range, 2.1-25.9% (20–22). amongst these, the co-occurrence of cm and cva has been reported most commonly (15, 21, 23, 24), almost up to 40% of cva (15, 25, 26), this fact generally explains presenting neurological symptoms if there is concordance with the location of a cva and the cm (13, 20, 27). other parenchymal abnormalities, including signal modifications of white matter on magnetic resonance imaging (mri) scans, dystrophic calcification and locoregional brain atrophy (13,25,28), however with no clear information regard the significance of these findings. dva may also be present adjacent to brain tumors, infarcts, demyelinating areas, and moyamoya malformations; also associated congenital anomalies of the cerebral arterial system such as primitive trigeminal artery, fetal origin of the posterior cerebral arterial system, as well as fetal venous anomalies such as retention of the primitive falcial, occipital, and marginal tentorial sinuses, (29) lending credence to the theory that embryonic origin of cvs. the neuropathologic changes underlying the radiographic changes associated with dva or dva-associated clinically significant syndromes are very poorly understood. vaitkevicius et al (8) reported histopathologic evidence of vascular remodeling related to altered hemodynamics in the region of a dva, including microvascular wall hyalinization and calcification, which are consistent with 176 alvis-miranda et al cerebral venous anomalies chronic regional blood flow alternation and venous hypertension. clinical presentation cva are usually asymptomatic, and are frequently discovered incidentally during medical imaging studies of the brain. (3, 15), probably because cva generally provide sufficient venous drainage of the involved territory (2). sometimes dva may present with headache, seizure, focal neurological deficit, dizziness, and ataxia. (23, 30, 31) symptoms can be produced either by venous congestion related to flow obstruction or mechanical compression (e.g., hydrocephalus or nerve compression). (32) the clinical sequelae of a cva are likely related to the regional changes that occur near it. as previously mentioned, cva can be associated with cavernous venous malformations in up to 40% cases, and are considered now to be responsible for the vast majority of symptoms attributed to cva in the pre-ct/mri era (33, 34). cva have been linked with ischemic or haemorrhagic infarctions, or with focal neurological symptoms (28, 35), probably due to stenosis or thrombosis of the collecting vein. several authors have documented impaired brain perfusion attributed to venous congestion in areas drained both by small and large cva (36, 37). garner et al. (31) retrospectively evaluated the risk of hemorrhage associated with dva to be of 0.22% per year, while mclaughlin et al (33) prospectively found that risk to be of 0.68% per year, though only half of their patients were symptomatic. it was initially proposed that cva located in the posterior cranial fossa had a higher propensity to bleed than supratentorial dva, but that is not currently considered as truth. only in about 25% of cases are cva diagnosed because of the occurrence of epileptic seizures (38). moreover, these lesions are often difficult to relate causally or topographically to the epileptogenic zone (19). more often they are occasionally observed during the diagnostic evaluation of different clinical pictures. pereira et al. (7) reviewed the pathomechanisms of symptomatic dva. based on imaging findings and clinical symptoms, two major pathomechanisms can be identified: mechanical and flow-related. although mechanical complications lead either to hydrocephalus or to vessel–nerve conflicts, flow-related mechanisms can be further subdivided into those that are related to an increase in inflow into the dva or to an obstruction of the outflow. see tabel 1. imaging the cva is a large transparenchymal venous structure with many abnormal tributaries that converge into a larger vein, which in turn drains into a venous sinus (39, 40). the morphological hallmark of a cva is a cluster of venous radicles that converge into a larger collecting vein, giving the cva typical “caput medusae” appearance, demonstrable through both, ct and mri, allowing confident diagnosis of cva without the need to obtain digital subtracted angiography (dsa). (12) romanian neurosurgery (2014) xxi 2: 172 182 177 tabel i pathomechanisms of symptomatic dva s y m p to m a ti c d v a m e c h a n ic a l hydrocephalus interventricular foramen aqueduct neurovascular compression cn v, vii, viii f lo w -r e la te d increased inflow microshunt into dva avm draining into dva dreased outflow anatomical obstruction of the venous collector obstruction of the draining sinus functional distant high flow shunt cn: cranial nerve; dva: developmental venous anomaly as mentioned previously, the collecting vein crosses the brain parenchyma to either join the superficial or deep venous system. (41) noncontrast ct may show a collecting vein as isodense or slightly hyperdense to cortex (11). contrast-enhanced ct readily detects the draining vein of a cva as a linear or curvilinear focus of enhancement that courses from the deep white matter to a cortical vein or to a dural sinus. (35) however, because of its higher temporal resolution, dsa remains the best imaging modality to study the hemodynamic behavior of cva. for this reason, dsa is performed in patients presenting with ischemic or hemorrhagic complications within the drainage territory of a cva, or whenever an associated vascular malformation is suspected on ct or mri (2, 12). dva have begun to be studied by resonance magnetic techniques, appearing as a hypointense signal globular or linear phase and hypo or hyperintense tl t2 in the same way hyperintensity found surrounding parenchymal injury in 50% of cases. t1and t2-weighted images demonstrate a characteristic parenchymal flow void corresponding to cva. the enhancement of both the draining vein and the caput medusae may be seen also on gadolinium-enhanced t1weighted sequences. mri is particularly useful and far superior to ct for the evaluation of related parenchymal abnormalities as well as for the detection of highly associated cavernous malformations (15). overall, developmental venous anomalies are low-flow vascular malformations, which are usually less conspicuous in conventional non-contrast mr images (42). susceptibility weighted imaging is ideal for screening patients with a high clinical suspicion of lowflow vascular malformations (43) and limits the use of contrast studies and digital subtraction angiograms in their 178 alvis-miranda et al cerebral venous anomalies demonstration. state-of-the-art 320multidetector row ct (320-mdct) is available in a few institutions and can perform dynamic subtracted ct angiography, allowing for morphologic as well as hemodynamic analyses of dva. arterialized dav (venous predominant parenchymal avms or arterialized venous malformations) these are atypical dva which are characterized by early angiographic opacification during the mid or later arterial phases, are also known as. (44) although the pathogenesis of this subtype of dva remains uncertain, they may represent a spectrum evolving from a simple dva to a “classic” avm, (2, 12) in which the dva may serve as a foundation for future avm development. management conservative management is strongly suggested (45). their management requires a thorough understanding of the nature of cva, including their frequent coexistence with other types of vascular malformation, and the existence of more complex but rare forms of presentation, such as the arterialized dvas. indications for surgical removal are reserved for patients with large or recurrent hemorrhage, poorly controlled seizures, secondary trigeminal neuralgia or refractory to medical treatment, hemifacial spasm or hydrocephalus for aqueduct compression. (46) despite being the most frequent cvm, its treatment principles have not been established. a number of case series have reported a favorable outcome in dva thrombosis after anticoagulation. (30, 47–53) prevailing this benefit despite hemorrhage. (48, 51) because most patients do well, no aggressive therapy, surgical or radiologic, needs to be performed. failure to recognize this may cause needless anxiety and will result in potentially injurious treatment. it is certainly important to provide careful followup monitoring because aging can cause hemodynamic stress to dva, causing possible occlusion and venous infarction. correspondence luis rafael moscote-salazar, universidad de cartagena, cartagena de indias, colombia. e-mail: mineurocirujano@aol.com references 1. striano s, nocerino c, striano p, boccella p, meo r, bilo l, et al. venous angiomas and epilepsy. neurol. sci. off. j. ital. neurol. soc. ital. soc. clin. neurophysiol. [internet]. department of neurological sciences, epilepsy center, federico ii university, naples, italy.: springer-verlag italia; 2000 jun;21(3):151–5. available from: http://search.ebscohost.com/login.aspx?direct=true&db =mnh&an=11076003&lang=es&site=ehost-live 2. pearl m, gregg l, gandhi d. cerebral venous development in relation to developmental venous anomalies and vein of galen aneurysmal malformations. semin. ultrasound, ct mri [internet]. 2011 jun;32(3):252–63. available from: http://www.sciencedirect.com/science/article/pii/s08872 1711100028x 3. cakirer s. de novo formation of a cavernous malformation of the brain in the presence of a developmental venous anomaly. clin. radiol. [internet]. 2003 mar;58(3):251–6. available from: romanian neurosurgery (2014) xxi 2: 172 182 179 http://www.sciencedirect.com/science/article/pii/s00099 26002004701 4. huang y, robbins a, patel s, chaudhary m. cerebral venous malformations and a new classification of cerebral vascular malformations. cereb. venous syst. its disord. orlando: grune & stratton; 1984. 5. russell ds, rubinstein lj. pathology of tumours of the nervous system. arnold e, editor. london; 1989. 6. lasjaunias p, burrows p, planet c. developmental venous anomalies (dva): the so-called venous angioma. neurosurg rev [internet]. 1986 jan [cited 2013 apr 20];9(3):233–42. available from: http://www.ncbi.nlm.nih.gov/pubmed/3550523 7. pereira vm, geibprasert s, krings t, aurboonyawat t, ozanne a, toulgoat f, et al. pathomechanisms of symptomatic developmental venous anomalies. stroke [internet]. 2008 dec [cited 2013 oct 11];39(12):3201–15. available from: http://www.ncbi.nlm.nih.gov/pubmed/18988912 8. vaitkevicius h, erdemli he, anderson ws, zamani aa, friedlander rm, folkerth rd. biopsy neuropathology of cerebral ischemia associated with a developmental venous anomaly. clin neurol neurosurg [internet]. 2013 may [cited 2013 oct 13];115(5):621–3. available from: http://www.ncbi.nlm.nih.gov/pubmed/22771305 9. saito y, kobayashi n. cerebral venous angiomas: clinical evaluation and possible etiology. radiology [internet]. 1981 apr [cited 2013 apr 20];139(1):87–94. available from: http://www.ncbi.nlm.nih.gov/pubmed/7208947 10. hong y, chung t-s, suh s, park c, tomar g, seo k, et al. the angioarchitectural factors of the cerebral developmental venous anomaly; can they be the causes of concurrent sporadic cavernous malformation? neuroradiology [internet]. 2010 oct;52(10):883–91. available from: 10.1007/s00234-009-0640-6 11. ruíz dsm, yilmaz h, gailloud p. cerebral developmental venous anomalies: current concepts. ann neurol [internet]. 2009 sep [cited 2013 apr 21];66(3):271–83. available from: http://www.ncbi.nlm.nih.gov/pubmed/19798638 12. san millán ruíz d, gailloud p. cerebral developmental venous anomalies. child’s nerv. syst. chns off. j. int. soc. pediatr. neurosurg. [internet]. neuroradiology unit, department of diagnostic and interventional radiology, hospital of sion, avenue du grand-champsec 80, 1951, sion, valais, switzerland. diego.san-millan-ruiz@rsv-gnw.ch: springer verlag; 2010 oct;26(10):1395–406. available from: http://search.ebscohost.com/login.aspx?direct=true&db =mnh&an=20703485&lang=es&site=ehost-live 13. wilson cb. cryptic vascular malformations. clin neurosurg [internet]. 1992 jan [cited 2013 apr 20];38:49–84. available from: http://www.ncbi.nlm.nih.gov/pubmed/1537199 14. senegor m, dohrmann gj, wollmann rl. venous angiomas of the posterior fossa should be considered as anomalous venous drainage. surg neurol [internet]. 1983 jan [cited 2013 apr 20];19(1):26–32. available from: http://www.ncbi.nlm.nih.gov/pubmed/6828991 15. san millán ruíz d, delavelle j, yilmaz h, gailloud p, piovan e, bertramello a, et al. parenchymal abnormalities associated with developmental venous anomalies. neuroradiology [internet]. division of interventional neuroradiology, johns hopkins hospital, 600 n. wolfe street, baltimore, md 21287, usa. dsanmil1@jhmi.edu: springer-verlag; 2007 dec;49(12):987–95. available from: http://search.ebscohost.com/login.aspx?direct=true&db =mnh&an=17703296&lang=es&site=ehost-live 16. uchino a, hasuo k, matsumoto s, masuda k. double cerebral venous angiomas: mri. neuroradiology [internet]. 1995 jan [cited 2013 apr 20];37(1):25–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/7708183 17. hammoud d, beauchamp n, wityk r, yousem d. ischemic complication of a cerebral developmental venous anomaly: case report and review of the literature. j comput assist tomogr [internet]. 2002 [cited 2013 apr 20];26(4):633–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/12218833 18. dillon wp. cryptic vascular malformations: controversies in terminology, diagnosis, pathophysiology, and treatment. ajnr am j 180 alvis-miranda et al cerebral venous anomalies neuroradiol. [internet]. 1997 [cited 2013 apr 20];18(10):1839–46. available from: http://www.ncbi.nlm.nih.gov/pubmed/9403438 19. awad ia, robinson jr, mohanty s, estes ml. mixed vascular malformations of the brain: clinical and pathogenetic considerations. neurosurgery [internet]. 1993 aug [cited 2013 apr 20];33(2):179–88; discussion 188. available from: http://www.ncbi.nlm.nih.gov/pubmed/8367039 20. wilms g, bleus e, demaerel p, marchal g, plets c, goffin j, et al. simultaneous occurrence of developmental venous anomalies and cavernous angiomas. ajnr am j neuroradiol [internet]. 1994 aug [cited 2013 apr 20];15(7):1247–54; discussion 1255–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/7976933 21. perrini p, lanzino g. the association of venous developmental anomalies and cavernous malformations: pathophysiological, diagnostic, and surgical considerations. neurosurg focus [internet]. 2006 jan [cited 2013 apr 20];21(1):e5. available from: http://www.ncbi.nlm.nih.gov/pubmed/16859258 22. abdulrauf si, kaynar my, awad ia. a comparison of the clinical profile of cavernous malformations with and without associated venous malformations. neurosurgery [internet]. 1999 jan [cited 2013 apr 20];44(1):41–6; discussion 46–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/9894962 23. töpper r, jürgens e, reul j, thron a. clinical significance of intracranial developmental venous anomalies. j neurol neurosurg psychiatry [internet]. 1999 aug [cited 2013 apr 20];67(2):234–8. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=1736473&tool=pmcentrez&rendertype=abstract 24. zhang p, liu l, cao y, wang s, zhao j. cerebellar cavernous malformations with and without associated developmental venous anomalies. bmc neurol [internet]. 2013 oct 3 [cited 2013 oct 13];13(1):134. available from: http://www.ncbi.nlm.nih.gov/pubmed/24088363 25. huber g, henkes h, hermes m, felber s, terstegge k, piepgras u. regional association of developmental venous anomalies with angiographically occult vascular malformations. eur radiol [internet]. 1996 jan [cited 2013 apr 20];6(1):30–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/8797947 26. crecco m, floris r, vidiri a, squillaci e, sergiacomi gl, mattioli m, et al. venous angiomas: plain and contrast-enhanced mri and mr angiography. neuroradiology [internet]. 1995 jan [cited 2013 apr 20];37(1):20–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/7708182 27. rigamonti d, spetzler rf, medina m, rigamonti k, geckle ds, pappas c. cerebral venous malformations. j neurosurg [internet]. 1990 oct [cited 2013 apr 20];73(4):560–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/2398388 28. uchino a, sawada a, takase y, abe m, kudo s. cerebral hemiatrophy caused by multiple developmental venous anomalies involving nearly the entire cerebral hemisphere. clin imaging [internet]. 2001 [cited 2013 apr 20];25(2):82–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/11483414 29. pryor j, setton a, berenstein a. venous anomalies and associated lesions. neurosurg clin n am [internet]. 1999 jul [cited 2013 oct 13];10(3):519–25. available from: http://www.ncbi.nlm.nih.gov/pubmed/10419576 30. lo s, cheung y, tang k, chan c, siu c, kwok k, et al. non-haemorrhagic pontine venous infarct due to thrombosed cerebellar venous angioma. j hk coll radiol. 2009;12:79–84. 31. garner tb, del curling o, kelly dl, laster dw. the natural history of intracranial venous angiomas. j neurosurg [internet]. 1991 nov [cited 2013 apr 20];75(5):715–22. available from: http://www.ncbi.nlm.nih.gov/pubmed/1919693 32. griffiths d, newey a, faulder k, steinfort b, krause m. thrombosis of a developmental venous anomaly causing venous infarction and pontine hemorrhage. j. stroke cerebrovasc. dis. [internet]. (0). available from: http://www.sciencedirect.com/science/article/pii/s10523 05713001614 33. mclaughlin mr, kondziolka d, flickinger jc, lunsford s, lunsford ld. the prospective natural history of cerebral venous malformations. neurosurgery romanian neurosurgery (2014) xxi 2: 172 182 181 [internet]. 1998 aug [cited 2013 apr 20];43(2):195–200; discussion 200–1. available from: http://www.ncbi.nlm.nih.gov/pubmed/9696070 34. rigamonti d, spetzler rf. the association of venous and cavernous malformations. report of four cases and discussion of the pathophysiological, diagnostic, and therapeutic implications. acta neurochir [internet]. 1988 jan [cited 2013 apr 20];92(1-4):100–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/3407463 35. truwit cl. venous angioma of the brain: history, significance, and imaging findings. ajr am j roentgenol [internet]. 1992 dec [cited 2013 apr 20];159(6):1299– 307. available from: http://www.ncbi.nlm.nih.gov/pubmed/1442406 36. tomura n, inugami a, uemura k, hadeishi h, yasui n. multiple medullary venous malformations decreasing cerebral blood flow: case report. surg neurol [internet]. 1991 feb [cited 2013 apr 20];35(2):131–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/1990481 37. matsuda h, terada t, katoh m, ishida s, onuma t, nakano h, et al. brain perfusion spect in a patient with a subtle venous angioma. clin nucl med [internet]. 1994 sep [cited 2013 apr 20];19(9):785–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/7982312 38. tannier c, pons m, treil j. [cerebral venous angiomas. 12 personal cases and review of the literature]. rev neurol [internet]. 1991 jan [cited 2013 apr 20];147(5):356–63. available from: http://www.ncbi.nlm.nih.gov/pubmed/1853033 39. kraemer dl, awad ia. vascular malformations and epilepsy: clinical considerations and basic mechanisms. epilepsia [internet]. 1994 jan [cited 2013 mar 19];35 suppl 6:s30–43. available from: http://www.ncbi.nlm.nih.gov/pubmed/8206013 40. lasjaunias p. vascular diseases in neonates, infants and children. berlin heidelberg new york: springerverlag; 1997. p. 445–71. 41. ruíz dsm, gandhi d, levrier o. venous anomaly. j neurosurg [internet]. 2010 jan [cited 2013 apr 20];112(1):213–4; author reply 214. available from: http://www.ncbi.nlm.nih.gov/pubmed/20043726 42. somasundaram s, kesavadas c, thomas b. susceptibility weighted imaging in holohemispheric venous angioma with cerebral hemiatrophy. neurol. india [internet]. medknow publications & media pvt. ltd.; 2008 jan;56(1):104–5. available from: http://search.ebscohost.com/login.aspx?direct=true&db =a9h&an=31208816&lang=es&site=ehost-live 43. reichenbach jr, jonetz-mentzel l, fitzek c, haacke em, kido dk, lee bc, et al. high-resolution blood oxygen-level dependent mr venography (hrbv): a new technique. neuroradiology [internet]. 2001 may [cited 2013 apr 20];43(5):364–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/11396739 44. im s-h, han mh, kwon bj, ahn jy, jung c, park sh, et al. venous-predominant parenchymal arteriovenous malformation: a rare subtype with a venous drainage pattern mimicking developmental venous anomaly. j neurosurg [internet]. 2008 jun [cited 2013 oct 13];108(6):1142–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/18518718 45. kondziolka d, dempsey pk, lunsford ld. the case for conservative management of venous angiomas. can j neurol sci [internet]. 1991 aug [cited 2013 apr 21];18(3):295–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/1913363 46. abarca-olivas j, botella-asunción c, concepciónaramendía la, cortés-vela jj, gallego-león ji, ballenilla-marco f. [two cases of brain haemorrhage secondary to developmental venous anomaly thrombosis. bibliographic review]. neurocir. [internet]. 2009 jun [cited 2013 oct 13];20(3):265–71. available from: http://www.ncbi.nlm.nih.gov/pubmed/19575131 47. masson c, godefroy o, leclerc x, colombani jm, leys d. cerebral venous infarction following thrombosis of the draining vein of a venous angioma (developmental abnormality). cerebrovasc dis [internet]. 2000 [cited 2013 oct 13];10(3):235–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/10773651 48. merten cl, knitelius ho, hedde jp, assheuer j, bewermeyer h. intracerebral haemorrhage from a venous angioma following thrombosis of a draining vein. neuroradiology [internet]. 1998 jan [cited 2013 oct 13];40(1):15–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/9493181 182 alvis-miranda et al cerebral venous anomalies 49. thobois s, nighoghossian n, mazoyer jf, honnorat j, derex l, froment jc, et al. [cortical thrombophlebitis and developmental venous anomalies]. rev neurol [internet]. 1999 jan [cited 2013 oct 13];155(1):48–50. available from: http://www.ncbi.nlm.nih.gov/pubmed/10093849 50. walsh m, parmar h, mukherji sk, mamourian a. developmental venous anomaly with symptomatic thrombosis of the draining vein. j neurosurg [internet]. 2008 dec [cited 2013 oct 13];109(6):1119–22. available from: http://www.ncbi.nlm.nih.gov/pubmed/19035729 51. gama rl, nakayama m, távora dgf, alvim tc de l, nogueira cd, portugal d. [neuronal ceroid lipofuscinosis: clinical and neuroradiological findings]. arq neuropsiquiatr [internet]. 2007 jun [cited 2013 oct 13];65(2a):320–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/17607436 52. prasad s, hurst rw, kasner se. postpartum thrombosis of a developmental venous anomaly. neurology [internet]. 2009 jan 6 [cited 2013 oct 13];72(1):92–3. available from: http://www.ncbi.nlm.nih.gov/pubmed/19122037 53. brasse g, stammel o, siemens p, töpper r. [thrombosis of developmental venous anomaly and consecutive venous infarction]. nervenarzt [internet]. 2008 jun [cited 2013 oct 13];79(6):703–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/18389202 microsoft word 11chiriaca_first 100 chiriac et al intracranial aneurysm occlusion by balloon assisted coiling technique first experience in intracranial aneurysm occlusion by balloon assisted coiling technique a. chiriac, b. iliescu1, n. dobrin1, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract particular anatomical situation like wideneck aneurysms or a large neck/fundus ratio, located on an arterial bifurcation or a small artery, are still a challenge for endovascular coil occlusion. these are due to the risk of coil migration or coil protrusion into the parent vessels. in our study we describe the balloon assisted coiling technique regarding the efficacy and safety of its practice and the problems that could appear. key words: aneurysms, balloon remodeling technique, aneurysm coiling introduction endovascular treatment of intracranial aneurysms has evolved rapidly and become an remarkable alternative to conventional neurosurgical treatment especially due to the development and use of various detachable coils and the appropriate techniques. even with spectacular advancement in endovascular materials and coil configuration, aneurysms with wide neck or with a large neck/fundus ratio still remain a technically challenging problem in terms of uniformly complete coil packing of the aneurysm neck. because of standard coil embolization technique inability to occlude wide-neck aneurysms due to the risk of coil migration or coil protrusion into the parent vessel with embolic complication, or a parent artery thrombosis, several imbunatatiri, including stent-supported coiling or balloon remodeling techniques have been incorporated into the treatment. in 1997, moret et al1 described a new endovascular approach of this cohort, known as balloon remodeling or balloonassisted coiling technique. the balloonassisted technique consists of temporary inflation of a nondetachable balloon across the aneurysm neck to facilitate optimal coil placement and to avoid inadvertent coil protrusion into the parent artery. the technique has been reportedly as an optimal choice in safety placement of the initial coils within wide-necked aneurysms, as a “rescue” method in cases of coil prolepses and to allow for more optimal “packing” of the aneurysm fundus and neck region (4). in this article, we describe our first experience with selective embolization of wide-necked intracranial aneurysms, located on a small artery bifurcation, using the remodeling technique with a hyperform balloon microcatheter. technical procedure the procedure is performed with the patient under general anesthesia. the femoral access could be unilateral or bilateral. if the vascular approach is unilateral a 6f vascular sheath provides access and femoral catheterization will be romanian neurosurgery (2013) xx 1: 100 105 101 done with a 6f guiding catheter equipped with a triple push-pull valve. the valve system will provide gateway for both continuous irrigation and injection of contrast (via a 2-way tap) and access for the coiling system and hyperform balloon system. in case of bilateral femoral access, we use a 6f sheath with a 6f guiding catheter for introduction of coiling and hyperform balloon systems via a double push-pull valve, and a 5f sheath with 5f diagnostic catheter for angiography control. 6f guiding catheter is introduced into the proximal parent artery (internal carotid artery or vertebral artery). at first cerebral angiography is performed to evaluate morphologic features of the aneurysm and parent vessel, and to establish the optimal visual working projection for aneurysm coil occlusion. the collateral supply to the vascular territory with risk due to proposed balloon occlusion is also angiographic analysed. a 6f guiding catheter is introduced into the proximal parent artery at which the target aneurysmal lesion is located. trough this guiding catheter a two-marker gdc microcatheter of 1.7f to 2.5f distal outer diameter is used to selectively microcatheterize the aneurysm. after the decision of a balloon-assisted endovascular neck bypass technique to be used, a nondetachable balloon microcatheter supported by an indwelling 0.010or 0.014inch microguidewire is introduced and the balloon is gently inflated within the parent artery over the neck of the aneurysm. sometimes in a very large neck aneurysm microcatheterisation of neck aneurysm with a hyperform balloon can be extremely difficult. in this situation, the balloon is delivered with a microguidewire of 0.010 or 0.012. most commonly the microguidewire will enter inside aneurysm and not distaly into the patern artery. thus, microguidewire is advanced into the aneurysm and easily pushed to the front along the inside wall of the aneurysm until it makes a loop inside the aneurysm following the flow direction and to go then into parent artery distal to the aneurysm. the hyperform balloon is then advanced over the wire and placed distal to the aneurysm. figure 1 a – e. steps of balloon assisted coiling technique (1) 102 chiriac et al intracranial aneurysm occlusion by balloon assisted coiling technique the balloon is gently inflated to stabilize it in this position. this will help to flatten the looped balloon catheter to position it bridging the neck of the aneurysm without losing the access. then, the balloon microcatheter is pulled very slowly to remove the slackened part within the aneurysm sac. because the balloon is inflated distally, it does not move while its loop inside the aneurysm gets straightened by gently pulling the balloon catheter. the balloon is then deflated (5). after aneurysm neck balloon securization the initial framing coil is deployed through the intraaneurysmal microcatheter into the aneurismal sac. the balloon is immediately deflated when a stable coil configuration is considered to be reached. after balloon deflation, an interval time of 1 to 2 minutes of waiting is indicated before coil detachment to ensure that stability of coil placement could be ascertained. if no coil movement is noted, the coil is detached. the balloon is then reinflated before deployment of the next coil. the cycle is repeated until a densely packed configuration into the aneurysm is obtained. also, the treatment is considered completed when a further balloon inflation is considered insufficient for a secure deployment of an additional coil. the patient will received an intravenous bolus of 5000 to 7000 u of heparin just after first coil deployment and next balloon inflation. this will be followed by intravenous infusion of 500 to 1000 u/h for the entire duration of the procedure to ensure maintenances of two times baseline of the activated coagulation time. treatment is followed by 2 to 3 days of systemic anticoagulation with 0.3 u fraxiparine two times per day. case report a 53-year-old man known with upper gastrointestinal bleeding operated two years ago, gastroduodenal ulcers medical treated and chronic alcohol abuse was admitted to the department of neurosurgery in the “n. oblu” clinical emergency hospital as an emergency due to sudden headache, vertigo accompanied by by impaired balance and disturbed vision. the neurological examination revealed horizontal nystagmus and left-sided hemiparesis. the patient was referred to an urgent non-contrast brain ct that showed a left pontine hemorrhage. because of suspicion of a vascular pontine malformation the patient was referred also to an non-contrast brain magnetic resonance imaging examination that revealed a thin traces of subarachnoid haemorrhage filling the anterior interhemispheric and sylvian fissures and a suspicion of a left pontine cavernous malformation. in this situation a cerebral angio-ct was performed additionally. a middle cerebral artery bifurcation aneurysm (m1 segment) and an infundibular dilatation of the left posterior communicating artery were found. diagnostic procedures were complemented by a conventional cerebral angiography 12 days later. the symptom completely release at two weeks. after vascular neurosurgeon and neuroanaesthesia team consultation, the patient was proposed to an endovascular occlusion of the aneurysm due to comorbidities risks. the aneurysm was endovascular completely occluded 19 days later by a balloon assisted coiling technique. the patient’s postinterventional course was uneventful. he was discharged one week after the intervention and returned to usual daily activity. romanian neurosurgery (2013) xx 1: 100 105 103 figure 2. mri imaging in sequences t1, t2 and t2* showing a left pons hemorrhage due to a cavernoma figure 3. mri imaging in sequences t1showing a a thin traces of interhemispheric hemorrhage 104 chiriac et al intracranial aneurysm occlusion by balloon assisted coiling technique figure 4. dsa showing a mca aneurysm occluded by a balloon assited coiling technique discussion recently published results from the cerebral aneurysm treatment study1 suggest that balloon assisted or stent assisted coiling techniques strongly supporting efforts to achieve as complete aneurysm exclusion as possible. the balloon-assist method has brought same additional benefits. the balloon microcatheter could serves as a reference point in the two-dimensional space of the angiographic plane due to its capability to outlines the three-dimensional course of the parent vessel during angiography. this will enable the practitioner to clearly show the aneurysm neck by an optimal orthogonal projection achievement. also, placing a microcatheter balloon in its uninflated or partially inflated state may be sufficient to allow optimal arrangement of coils loops that would otherwise herniated into the parent artery. the complex bifurcation aneurysm are difficult to approached by “classic” remodelling technique with a single lowcompliance balloon due to its limitation for protection of both the neck and arterial branches. this is limited to sidewall aneurysms. these difficulties have been overcome with the introduction of a compliant latex balloon (b1; balt, montmorency, france) glued to the tip of a flow-dependent microcatheter (eg, spinnaker; target/boston scientific). the round shape and high compliance of such a latex balloon conforms easily to the arterial bifurcation and the flow-dependent characteristics of the microcatheter make stabilization of the balloon in the correct position sometimes difficult (6). some concern, however, must be tacked into consideration concerning adjunctive use of balloons. the potential problems are represented by an increased incidence of thromboembolism, even under optimized anticoagulation and aneurysmal perforation during the procedure due to balloon manipulation. the risk factors involved are the presence of a balloon in the parent vessel as promoter of stasis, thrombus formation or platelet aggregation, reaction to foreign material in the vascular system and repeated inflations and deflations of the balloon, which may lead to intimal injury. romanian neurosurgery (2013) xx 1: 100 105 105 the incidence of thromboembolic complications during balloon-assisted embolization were reported at 8.1% in literature (7). another technique problem is the aneurysm perforation by microcatheter during balloon inflation or coil delivery. this may occurs due to actively deflection or pushing of microcatheter against the wall by balloon inflation, or due to advancement of the coil that may result in wall perforation because the catheter is pinned and has decreased freedom(6, 7). conclusion the balloon assisted coiling technique was demonstrated to be a successful tool for the treatment of wide-necked or unfavorable neck/fundus ratio intracranial aneurysms, located on an arterial bifurcation or for the so-called sidewall aneurysms. the technique has improved the safety and efficacy for these patients. however, the standard balloon remodelling technique is still a challenging for some complex aneurysms located at arterial bifurcations with a small artery. references 1. b. ross, gurmeet s. dhillon : balloon assistance as a routine adjunct to the endovascular treatment of cerebral aneurysms, surgical neurology 2006, 6: 593601; 2. mu shi-qing, yang xin-jian, li you-xiang, zhang you-ping, lü ming and wu zhong-xue : endovascular treatment of wide-necked intracranial aneurysms using of “remodeling technique” with the hyperform balloon, chinese medical journal 2008; 121(8):725-729. 3. sang o youn, jae il lee, jun kyung ko, tae hong lee, chang hwa choi : endovascular treatment of wide-necked intracranial aneurysms using balloonassisted techniquewith hyperform balloon, korean neurosurg soc 2010; 48 : 207-212; 4. m. shapiro, j. babb, t. becske, p.k. nelson: safety and efficacy of adjunctive balloon remodeling during endovascular treatment of intracranial aneurysms: a literature review, ajnr am j neuroradiol 2008; 29:1777– 81; 5. m. essiga, n. anzaloneb, s.e. combsc, a. dörflerd, s.-k. leee, p. picozzib, à. roviraf, m. wellerg and m. lawh: mr imaging of neoplastic central nervous system lesions: review and recommendations for current practice, ajnr 2012, 33: 803-817; 6. s. baldi, c. mounayer, m. piotin, l. spelle, j. moret: balloon-assisted coil placement in wide-neck bifurcation aneurysms by use of a new, compliant balloon microcatheter, ajnr am j neuroradiol 2003; 24:1222–1225. 7. sang o youn, jae il lee, jun kyung ko, tae hong lee, chang hwa choi : endovascular treatment of wide-necked intracranial aneurysms using balloonassisted technique with hyperform balloon, j korean neurosurg soc 2010; 48 : 207-212. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 449-454 doi: 10.33962/roneuro-2019-071 www.journals.lapub.co.uk/index.php/roneurosurgery burden of traumatic brain injury in refugee population: unmet need of care and gaps in knowledge harsh deora1, amit agrawal2, ranabir pal3, luis rafael moscotesalazar4, muhammad hussam alothman5, guru dutta satyarthee6 1 assistant professor of neurosurgery, national institute of mental health and neurosciences (nimhans), bengaluru, karnataka, india orcid id: https://orcid.org/0000-0003-3247-1117 2 professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, ap, india orcid id: https://orcid.org/0000-0002-3287-5448 3 department of community medicine, mgm medical college & lsk hospital, kishanganj, bihar, india orcid id: https://orcid.org/0000-0002-8602-0162 4 neurosurgery-critical care, red latino, organización latinoamericana de trauma y cuidado neurointensivo, bogota, colombia orcid id: https://orcid.org/0000-0002-4180-6962 5 university of hama, faculty of medicine, syria orcid id: https://orcid.org/0000-0001-9479-497x 6 associate professor, department of neurosurgery, all india institute of medical sciences, new delhi orcid id: https://orcid.org/0000-0002-5454-6477romania abstract background and objectives. due to marked increase in violence, the world is facing problem of refugee population either as a source of refugee population or shelter provider. these refugee population is exposed to prolonged physical and emotional distress over years, may result into spectrum of neuropsychiatric disease conditions including traumatic brain injury (tbi). although trauma is one of the major events faced by refugee population, the exact details of the injuries still not documented and there is paucity of published literature; further these injuries may be recorded as unspecified. methods. the present article is intended to provide a theoretical overview of existing knowledge and gaps on trauma and injuries in refugee population. authors analysed all relevant articles available on pubmed and medline using the key words: “refugee”, “traumatic brian injury”, “head injury”. results. there is a gap in knowledge for this particular demographic population. they suffer a wide range of physical and emotional to social traumatic events. the most common cause of head injury was assault; however, motor vehicle accidents were less prevalent, and there is an ongoing struggle for resources to fulfil basic needs keywords traumatic brain injury, refugee population, prevalence, management options, asylum seekers corresponding author: amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem, india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 450 harsh deora, amit agrawal, ranabir pal et al. leading to health care taking a backseat. there is high prevalence of post-traumatic stress disorder. many of the refugees are settled in relative economically poorer countries which further add to the burden of a nation already besotted with internal requirements. there is a need for an international collaboration to tackle unique problem. conclusion. authors recommends urgent need to handle the root causes responsible for the generation of refugee population and at the same time it is necessary to identify the epidemiology, patterns, management challenges and consequences of injuries and barriers to seek and provide care in refugee population. introduction increased prevalence of violence across the globe, forced a large population to leave their homes which started since the world war ii. 1 according to an estimate approximately 60 million people are displaced globally and of which about 22 million have crossed an international border (i.e. refugees). 1 authors observed most of the world is facing problem of refugee population either as a source or as a shelter provider to refugee population. 2-10 these refugee population is exposed to prolonged physical and emotional distress 11 which can result in spectrum of neuropsychiatric disease conditions 12 including traumatic brain injury (tbi). 13 it is being reported that approximately 2.1 million or 8.8% of refugees and asylum seekers has been given shelter in five wealthiest nations 10 still they do struggle to access health care. 14 in spite of the importance of these issues there is not much literature address many of the disease condition in refugee (or displaced) population13, 15-17 which include injuries and tbi as well. 18, 19 the present is intended to provide a theoretical overview of existing knowledge and gaps on trauma and injuries in refugee population. injury distribution although trauma constitute one of the major events faced by refugee population, however the less number of published studies and inadequate data collection largely restricts the detail information regarding injury patterns. 20, 21 the trauma can range from physical and emotional to social traumatic events resulting in impairment in physical or emotional functions. 22-24 the exact details of the injuries may not be available and additionally the injuries may be recorded as unspecified. 21in one study the patients presented with the complaint suggestive of head injury, fractures, skin injuries and burn injuries. 20, 25 the common cause of head injury was assault however, the motor vehicle accidents were less prevalent (probably due to limited access in refugee camps). 20 although studies have tried to identify the causes of traumatic brain injury and recognized tbi as a significant cause of morbidity but the details are restricted by paucity of published data and further most of these studies are restricted to single center studies. 26 many studies have highlighted that tbi is related to longterm neuropsychiatric sequel 27-30 however exact burden and spectrum is lacking and also the need of the patients in refugee population is not assessed. studies have further highlighted, refugee patients population usually prefer to use emergency services instead of regular outpatient’s services, as these are easily available, affordable and accessible. 20,25 challenges in providing health care identifying the injured and injuries and providing care to them in refugee camps and refugee population is a big challenge as there is ongoing struggle for resources to fulfill basic needs (adequate food, clean water, shelter, and security) and at the same time no extra support the finances. 31 this can be easily understood by taking the example of refugee population who is settled in united states for years but still barriers to access healthcare. 32 this is not because of the limited resources alone; this may be due to the non-awareness the people to adequately utilize the services as well. 32-34 how to approach? approach to the patients who seek care shall need a good understanding and trust between the victim and health care provider, safe environment, several interviews and overcoming the barriers (language and cultural). 35,36, 37 it has been shown that in the presence of culturally competent people 36-38 and professional interpreter 39-41 the chance of getting details information are more than when there is no interpreter or there was a non-professional interpreter 42 the current situation amnesty international defines a refugee “as a person who has fled their country and is unable or unwilling to return because of a well-founded fear of being persecuted due to their race, religion, nationality, membership of a particular social group, or political 451 burden of traumatic brain injury in refugee population opinion”. an asylum seeker is defined as an individual who is seeking international protection and whose claim has not been decided by the country to which they have submitted it. ultimately, not all asylum seekers will be recognized as refugees. traumatic brain injury is an injury resulting in abnormal brain function arising from the application of an external force to the cranium. it carries immense significance in this population as can be deciphered from our discussion. this significance can be viewed in terms of the difficulty in adapting to a new system and the spectrum of injuries experienced by this population. spectrum of injuries [1] in a retrospective study of refugees of the ongoing civil war in syria a major portion of the referrals were due to trauma cases when compared to the local population. the most common types of trauma were (in order of prevalence) head injury, fracture, skin injuries, and burns. compared to the local population motor vehicle accidents were not the common cause of head injuries rather assaults was the most common cause. this was especially prevalent in young males and as expected included larger number of contusions and extra-dural hematoma. still the amount of reported cases of assaults was less as compared to local population as access to the police department was limited. the lower prevalence of motor vehicle accidents likely reflects the limited presence of motor vehicles in camps and the greater number of people with a driving license and cars in the local population. another critical aspect of the refugee population is the prevalence of post-traumatic stress disorder among these cases. these problems of syrian refugees arise due to further cofounding problems such as low living standards lack of adequate child care and hygiene, somatization of psychological disorders, and also the possible underlying relationship between posttraumatic stress disorder and physical violence which needs further evaluation. trauma can be a direct cause of this as contusion or injury to the prefrontal cortex may lead to loss of executive function and cause difficulty in adjustment and adaptation. depression can affect the cognitive functions and delay the return to daily activities. prefrontal cortex damage leads to higher rates of substance abuse but most studies on psychiatric evaluation of these cases place current use of alcohol or any banned substance as an exclusion criterion and hence this aspect may be missed totally. any discussion on the status of refuge and asylum seekers is incomplete without discussing of the aspect of pediatric head injuries. minors are a substantial portion of the refugee population around the world and trauma, in general, was more common among refugee children than in the locally residing population. interestingly, minor closed head injury was much more common in local children as compared to refugee children who were more prone to open head injuries. this may be due to the fact that while local population children with concussions and emesis after closed head injury are primarily admitted and observed in a population to avoid a computed tomography of the head and the associated radiation exposure, refugee children are often given step-motherly treatment and discharged. also, minor head trauma may not be perceived as a compelling reason to come to the hospital for evaluation by refugee families to the same extent as it is for resident parents, explaining the discrepancy observed. burden on state health resources and adoption by refugees [2] one of the most critical aspects of treating a refugee population is the burden it places on the local health care system. while trauma admissions are actually a relatively small fraction of overall emergency admissions (a little over 2% for both refugees and local population), but their possible outcomes such as surgical procedures, extensive operations, longer hospital stays, repeated radiological and laboratory studies, control examinations as outpatients can cripple the existing health care system which may not be adequately geared up for the same. there is a risk of leaving permanent physical and more importantly mental damage in patients, which will increase health costs and thus emphasizes their importance to look at them more than just numerical values among other admissions. refugees usually tend to admit to emergency clinic for various reasons such as relatively easier accessibility of the emergency clinic and abuse of health system to leave the camps more easily. this can potentially harm the local population emergency and thus lead to unintentional consequences. then there is the difficult aspect of adoption of 452 harsh deora, amit agrawal, ranabir pal et al. the local health care system. entering and navigating a largely westernized healthcare system can be intimidating to someone with no knowledge of the procedures and mental trauma to boot. these individuals may place their own medical needs behind more dominant concerns of safety, securing food and clothing for their family, housing, utilities, or finding legal representation if seeking asylum. again, opening to their past trauma is a painful aspect which many may not be willing to undergo. two-thirds of refugees and asylum-seeking patients report not initiating discussion related to war injuries with their physicians. reasons reported by refugees for withholding this information about a history of injury or trauma included feeling like they should be asked first before bringing anything up and “not wanting to think about it again”. even when medical encounters are successful, adherence to necessary care can prove inconsistent in refugees and asylum seekers. this problem is further magnified when they are finally granted asylum and the follow up has to be at a different hospital. eighty-six percent of the world’s refugees and asylum seekers populations are resettled in poorer developing nations that may already be struggling to provide adequate resources for their own citizens. even if some of these refugees make it to a developed nation healthcare costs become the prohibitive factor. almost all the cases are uninsured and thus may have difficulty affording necessary care. in a focus group, one individual expressed frustration stating, “doctors always tell us, ‘don’t worry about money, your health is more important.’ but they do not understand our situation”. even after years of struggle and work health care costs at these places prevent from seeking treatment even for their progeny. table 1: prospective problems and solutions for refugee head injury and health care20, 43 problems possible solutions larger patient load and burden to local resources possible health centres near refugee camps set exclusively for the same mobilization of international funds and international health agencies possible incentives to health care personnel higher rates of open head injuries and emergency admissions better availability of minimum barebones setup emergency services and imaging to be the focus of health care poor follow up and adherence improved local touch points and integrated health records mental health issues possible digital solutions to psychiatric care and assessment increase training of health care personnel for psychiatric counselling paediatric head injuries specialized resources and specialists for the same resuscitation fluids, medicines catered for the same. health care costs subsidized health care, universal funding conclusions there is an urgent need to have a strong will to handle the root causes responsible for the generation of refugee population and at the same time it is necessary to identify the epidemiology, patterns, management challenges and consequences of injuries and barriers to seek and provide care in refugee population. the future not only focuses on the physical nature and its consequences but it should also address neuropsychological, financial and social sequel of the injuries. while taking care of the refugee population that we should be compromising care to local or hosting population as it may result in social imbalance and can create insecurity in the local population. there is a need to further confirm these findings and ascertain that these should be able to access regular services rather than emergency department visits and thus reducing the burden on emergency care services. references 1. refugees ootunhcf. global trends: forced displacement in 2016: united nations high commissioner for refugees, 2017. 2. unhcr. syria regional. response plan. strategic overview [online]. available at: http://www.unhcr.org/syriarrp6/ midyear/docs/syria-rrp6-midyear-full-report.pdf. 3. naufal h. syrian refugees in lebanon: the humanitarian approach under political divisions2012. 4. association ap. online assessment measures [online]. available at: https://www.psychiatry.org/psychiatrists/pra ctice/dsm/educational-resources/assessment-measures. 5. crosby a. the boundaries of belonging: reflections on migration policies into the 21st century: inter pares, 2006. 453 burden of traumatic brain injury in refugee population 6. pell sk. adjudication of gender prosecution cases under the canada guidelines: the united states has no reason to fear an onslaught of asylum claims. ncj int'l l & com reg 1995;20:655. 7. castles s, de haas h, miller mj. the age of migration: international population movements in the modern world: macmillan international higher education, 2009. 8. unhcr. unhcr statistical yearbook 2011, 11th edition [online]. available at: http://www.unhcr.org/statistics/coun try/516282cf5/unhcr-statistical-yearbook-2011-11th-editio n.html. 9. castles s, de haas h, miller mj. the age of migration: international population movements in the modern world: macmillan international higher education, 2013. 10. international o. a poor welcome from the world’s wealthy | oxfam international [online]. available at: https://www. oxfam.org/en/research/poor-welcome-worlds-wealthy. 11. refugees unhcf. introduction [online]. available at: http://www.unhcr.org/introduction.html. 12. murthy rs, lakshminarayana r. mental health consequences of war: a brief review of research findings. world psychiatry 2006;5:25-30. 13. kelly g, winkler d. long-term accommodation and support for people with higher levels of challenging behaviour. brain impairment 2012;8:262-275. 14. rhtac. affordable care act | refugee health ta [online]. available at: https://refugeehealthta.org/access-tocare/affordable-care-act/. 15. kozaric-kovacic d, ljubin t, grappe m. comorbidity of posttraumatic stress disorder and alcohol dependence in displaced persons. croatian medical journal 2000;41:173178. 16. hwang sw, colantonio a, chiu s, et al. traumatic brain injury in the homeless population: a toronto study. finding, 2009. 17. steel z, silove d, brooks r, momartin s, alzuhairi b, susljik i. impact of immigration detention and temporary protection on the mental health of refugees. the british journal of psychiatry : the journal of mental science 2006;188:58-64. 18. staudenmayer kl, diaz-arrastia r, de oliveira a, gentilello lm, shafi s. ethnic disparities in long-term functional outcomes after traumatic brain injury. journal of trauma and acute care surgery 2007;63:1364-1369. 19. george m. a theoretical understanding of refugee trauma. clinical social work journal 2010;38:379-387. 20. duzkoylu y, basceken si, kesilmez ec. physical trauma among refugees: comparison between refugees and local population who were admitted to emergency department&#x2014;experience of a state hospital in syrian border district. journal of environmental and public health 2017;2017:5. 21. goodman lf, jensen gw, galante jm, farmer dl, taché s. a cross-sectional investigation of the health needs of asylum seekers in a refugee clinic in germany. bmc family practice 2018;19:64. 22. bogic m, njoku a, priebe s. long-term mental health of warrefugees: a systematic literature review. bmc international health and human rights 2015;15:29. 23. mcelrath k. drug use and drug markets in the context of political conflict: the case of northern ireland. addiction research & theory 2004;12:577-590. 24. adams km, gardiner ld, assefi n. healthcare challenges from the developing world: post-immigration refugee medicine. bmj: british medical journal 2004;328:1548. 25. saunders nr, macpherson a, guan j, guttmann a. unintentional injuries among refugee and immigrant children and youth in ontario, canada: a population-based cross-sectional study. injury prevention 2018;24:337-343. 26. goh ky, poon ws. children's head injuries in the vietnamese refugee population in hong kong. injury 1995;26:533-536. 27. keatley e, d'alfonso a, abeare c, keller a, bertelsen ns. health outcomes of traumatic brain injury among refugee survivors of torture. journal of head trauma rehabilitation 2015;30:e1-e8. 28. calvani s. medical aspects of torture. the lancet 1990;336:1448. 29. mcpherson ji. traumatic brain injury among refugees and asylum seekers. disability and rehabilitation 2017:1-5. 30. perry dc, sturm ve, peterson mj, et al. association of traumatic brain injury with subsequent neurological and psychiatric disease: a meta-analysis. journal of neurosurgery 2016;124:511-526. 31. asgary r, segar n. barriers to health care access among refugee asylum seekers. journal of health care for the poor and underserved 2011;22:506-522. 32. wagner j, burke g, kuoch t, scully m, armeli s, rajan tv. trauma, healthcare access, and health outcomes among southeast asian refugees in connecticut. journal of immigrant and minority health 2013;15:1065-1072. 33. kane wg, wright da, fu r, carlson kf. racial/ethnic and insurance status disparities in discharge to posthospitalization care for patients with traumatic brain injury. the journal of head trauma rehabilitation 2014;29:e10-e17. 34. mcfarlane ac, de girolamo g. the nature of traumatic stressors and the epidemiology of posttraumatic reactions. 1996. 35. dubus n. interpreters' subjective experiences of interpreting for refugees in person and via telephone in health and behavioural health settings in the united states. health & social care in the community 2016;24:649-656. 36. miklavcic a, leblanc mn. culture brokers, clinically applied ethnography, and cultural mediation. cultural consultation: springer, 2014: 115-137. 37. lehti v, antas b, kärnä t, tuisku k. the assessment of traumatized refugees: clinical practices at the cultural psychiatry outpatient clinic. psychiatria fennica 2016. 38. alizadeh s, chavan m. cultural competence dimensions and outcomes: a systematic review of the literature. health & social care in the community 2016;24:e117-e130. 39. bauer am, alegria m. impact of patient language proficiency and interpreter service use on the quality of 454 harsh deora, amit agrawal, ranabir pal et al. psychiatric care: a systematic review. psychiatric services (washington, dc) 2010;61:765-773. 40. karliner ls, jacobs ea, chen ah, mutha s. do professional interpreters improve clinical care for patients with limited english proficiency? a systematic review of the literature. health services research 2007;42:727-754. 41. casas r, guzman-velez e, cardona-rodriguez j, et al. interpreter-mediated neuropsychological testing of monolingual spanish speakers. the clinical neuropsychologist 2012;26:88-101. 42. eytan a, bischoff a, rrustemi i, et al. screening of mental disorders in asylum-seekers from kosovo. the australian and new zealand journal of psychiatry 2002;36:499-503. 43. mcpherson ji. traumatic brain injury among refugees and asylum seekers. disability and rehabilitation 2019;41:12381242. microsoft word 9ciureachoroid.doc 192 a.v. ciurea et al choroid plexus papilloma of the fourth ventricle choroid plexus papilloma of the fourth ventricle – case report and review of the literature a.v. ciurea, d. talianu, c.l. palade university of medicine and pharmacy “carol davila” bucharest 1-st neurosurgery clinic introduction choroid plexus tumors (cpt) are defined as papillary neoplasms originating from the epithelium of the choroid plexus within the ventricles. they are classified into mainly two types: -benign choroid plexus papillomas (cpp) (world health organization who grade i) and -choroid plexus carcinomas (who grade iii). [1,3] an intermediate group lies between the two groups and is referred to as atypical choroid plexus tumors. however, it is very rare for benign papillomas to convert to carcinomas.[1] anatomically, the choroid plexus is the junction between the brain pia and the ventricular ependymal layer in all four ventricles [12,13]. embryologically, it is derived from the specialization of ventricular neuroepithelium along certain neural tube segments. interestingly, there is a common ontogeny between choroid epithelium and cells of glial origin. on occasion this may create a source of diagnostic confusion. physiologically, the choroid plexus is specialized in cerebrospinal fluid production [9,10] choroid plexus tumors are seen in all age groups, with an overall incidence of 0.5% to 0.6% of all brain tumors (10% to 20% in infants). however, they are primarily tumors of childhood with higher incidence rates ranging from 1.8% to 2.9% in the pediatric population. haddad [16] et al and galassi [17] et al have reported that choroid plexus tumors constitute 12.8% to 14% of all tumors in infants. laurence reported that 45% of choroid plexus tumors occur in the first year of life and 74% in the first decade of life. he also concluded that 50% were in the lateral ventricles, 37% in fourth ventricle, 9% in the third ventricle, and the remainder in other locations. there has been no sex predilection shown in many of these studies. they are always solitary tumors. however, rare case reports have been published documenting multiple cpps. overall, choroid plexus carcinomas constitute 29% to 39% of all choroid neoplasms. choroid plexus papilomas are more commonly found in the fourth ventricle in adults. keywords: choroid plexus papillomas, microsurgical techniques case presentation a 34 year old female noticed gait disturbance of gradul onset associated with progressive intracranial hypertension syndrome. since 6 months previously, she had suffered from slowly progressive headache, nausea, irritability and malaise. on non-contrast ct, the tumor was noted to be similar in density to brain romanian neurosurgery (2010) xvii 2: 192 – 201 193 tissue, but there was dramatic enhancement with intravenous injection of a contrast agent (figure 1). on mri, the tumor had a signal similar to that of the surrounding brain, and following gadolinium infusion, a strong increase in the signal was noted (figure 2, figure 3, figure 4). figure 1 preoperative ct-scan figure 2 preoperative mri –scan (axial incidence) 194 a.v. ciurea et al choroid plexus papilloma of the fourth ventricle figure 3 preoperative mri-scan (sagittal incidence) figure 4 preoperative mri-scan (coronal incidence) romanian neurosurgery (2010) xvii 2: 192 – 201 195 after completion of ancillarry diagnostic tests and complete medical evaluation, the surgical indication was established and a full consent was documented. of the three possibilities for positioning (prone, lateral oblique and sitting) we chose the prone position [9,10].there are many advantages to this position: the anatomy is clearly visualized, it is easy for two operators to work togheter and the multiple complications of the sitting position do not occur. the main disadvantage of the prone position is venous congestion that can lead to more significant blood loss, pooling of blood in the operative field and soft-tissue swelling of the face. the neck of the patient was placed in moderate flexion of the upper cervical spine 9to open up the space between the foramen magnum and the arch of the c1) and less flexion of the lower cervical spine (to bring the occiput parallel with the patient’s back). the chin and chest were at least two fingers apart. the table was positioned so that the neck was parallel to the floor and the head was above the level of the heart. a linear midline incision was outlined 1 to 2 cm above the external occipital protuberance down to the level of c4. the skin was then eleveted with toothed forceps and a plane of dissection developed with monopolar coagulation, sparing the occipital artery and nerve. retractors were then placed to maintain exposure. next, the fascia was incised in a linear direction, allowing the use of avascular plane between the splenius capitis and semispinalis capitis muscles. muscle flaps werw then developed with monopolar cautery and periosteal elevators, stripping the muscle from the bone as far as the mastoid emissary vein. the muscle insertions are stripped off the spinous process and laminae of c2. finally, the junction between the pericranium and dura at the foramen magnum was sharply dissected from the inner table of the occipital bone using a curet. the suboccipital craniotomy was begun with burr holes on either side of midline just below the transverse sinuses, aproximately 3 cm from midline. the dura near the burr hole was then stripped using a dissector and the bone was cut using the aesculap craniotome. inferiorly, the craniotomy included the posterior edge of the foramen magnum, to prevent laceration of the brain against the closed bony rim when cerebellar elements are retracted downward and minimize damage from herniation if hematoma or swelling should occur postoperatively. to expose the posterior arch of c1, the soft tissues overlying it were reflected laterally using a small periosteal elevator, stripping the inferior arch first. the posterior arch of c1 was the removed, using a small angled curet to strip the deep surface of the bone and then using a kerisson punch. the wound was the irrigated and the microscope prepared. the dura was then incised in a ,,y’’ shaped manner. the arachnoid was then opened next to the cisterna magna to allow drainage of the csf. gentle separation of the cerebellar tonsils exposed the cerebellomedullary fissure through the opened vallecula, givin an unimpeded view of the inferior roof of the fourth ventricle. narrow maleable autostatic retractors were then positioned to maintain separation of the tonsils. the 196 a.v. ciurea et al choroid plexus papilloma of the fourth ventricle operating microscope was brought into the field. the tumor was then removed in a „piece-meal” fashion. the real challenge in the surgical management of cpp was related to its „attachment” to the floor of the fourth ventricle. in this case, this attachment was broad and had the appearance of a „veil” covering much of the ependymal surface. in other cases is a more focal point of origin. in this situation it was critical from a surgical perspective not to violate the posterior surface of the floor of the fourth ventricle. this is because these tumors are not extending anteriorly into the substance of the brainstem, but posteriorly into the ventricle. as a result of this, the neural structures of the fourth ventricle are in their anatomic position and any effort to remove the tumor, which is essentially „en plaque”, will disrupt functioning cranial nerve nuclei and pathways. because disruption may involve a wide area, the optimal end-point of removal is to leave a very thin veil of tumor, making no effort to remove all of it. it is critical to recognize that this is impossible and that the operation must be terminated at this point. after the completion of the tumor resection, the retractors were removed and the cerebellar hemispheres were allowed to fall back into place. the dura was closed using interrupted 3.0 polypropylene sutures. the suture line was covered with surgicel. the bone flap was secured with sutures. the fascia was closed with interrupted sutures to approximate the muscle and fascia. the scalp was then closed in layers, ending with subcutaneous reapproximation using interrupted sutures with inverted knots. perioperative antibiotic prophylaxis and dexamethasone administration were used to lessen the risk of postoperative infection and cerebrospinal fluid leakage [9,10] the postoperative enhanced ct-scan (second day after the intervention) disclosed no tumoral remnants (figure 5). figure 5 postoperative enhannced ct-scan (second day after the intervention) romanian neurosurgery (2010) xvii 2: 192 – 201 197 figure 6 postoperative aspects of the patient discussion clinical findings the clinical features depend on the age of the patient and location of the tumor. in infants, an enlarging head related to associated hydrocephalus may be the only sign. in children, symptoms of increased intracranial pressure, such as nausea, vomiting, irritability, and headache, secondary to hydrocephalus may be seen[14,21]. other findings include papilledema, hemiparesis, hyperreflexia, abducens nerve palsy, stupor, and coma. those with posterior fossa lesions are more likely to have brainstem and cerebellar findings, including cranial nerve abnormalities, pyramidal tract signs, and ataxia. the duration of symptoms before diagnosis varies from 1 day to 4 years (median 4 weeks), with earlier symptom onset in younger patients and patients with cpc. hydrocephalus is a near ubiquitous finding in those with cpts, and several reasons for its development have been suggested, including obstruction of csf pathways by the tumor, hypersecretion of csf by the tumor, and blockage of csf absorption from repeated tumor microhemorrhage or elevated csf protein concentrations [29]. of these, csf overproduction is considered the principle mechanism with one series identifyinga patient with csf production almost doubling the norm. diagnostic studies the diagnosis of cpts relies on modern imaging modalities such as computed tomography (ct), magnetic resonance imaging (mri), and magnetic resonance angiography (mra)[27,31] laboratory studies have limited sensitivity and specificity in detecting or predicting this type of tumor. studies 198 a.v. ciurea et al choroid plexus papilloma of the fourth ventricle examining csf are of low diagnostic yield. on radiological modalities, their unilaterality and peripheral lobulations can help distinguish cpts from other tumors, including meningiomas, ependymomas, and metastasis.cpp and cpc are generally isodense or hyperdense intraventricular masses on unenhanced ct scans. they show intense enhancement on contrastenhanced ct images. ct is superior to mri in detecting associated intratumoral calcifications. however, mri is the imaging modality of choice because of its inherent superb anatomic detail, tissue contrast, ability to directly image in multiple planes, and increased sensitivity in determining tumor extent [30,31,33]. the uncalcified portions of cpps appear isointense or hypointense to normal brain parenchyma on t1-weighted images and hyperintense on t2-weighted images. if doubt remains about the imaging diagnosis with mri, a simple noncontrast ct may improve diagnostic because, in general, adult fourth ventricular cpps will appear markedly calcified, whereas ependymomas will not. contrast enhancement on mri tends to be uniform and intense, and flow voids are common. mra or conventional angiograph are not routinely necessary but may demonstrate enlarged choroidal arteries supplying the tumor [27]. the distinction between cpp and cpc is not always possible on imaging studies. differentiation of the two is based on histology, not radiology. cpts with a benign imaging appearance may be carcinomas histologically, and those with an aggressive imaging appearance may turn out to be papillomas. nonetheless, proper imaging characterization of cpts preoperatively may affect surgical approach to the tumor. cpcs tend to have more heterogeneous t1and t2-weighted imaging and enhancement characteristics. this reflects the presence of more tumor necrosis due to the tumor’s rapid growth rate. extraventricular extension into brain parenchyma and presence of associated vasogenic edema favor cpc over cpp [22]. csf dissemination can occur with cpp or cpc but is much more common with the latter. the degree of hydrocephalus in cpc has been noted to be less than that seen with cpps. functional imaging with positron-emission tomography (pet) may demonstrate increased metabolic activity in cpc. seeding of the cerebrospinal fluid has been reported in both cpps and cpcs. however, clinically significant seeding is much more common in patients with a cpc. therefore imaging of the spinal neural axis may be helpful in detecting csf dissemination [20,22]. histopathology in the current world health organization (who) classification, cpp is a who grade i neoplasm, whereas cpc corresponds to a who grade iii neoplasm. macroscopic features cpts are often soft to rubbery, having a cauliflower-like form, and may have a gritty texture due to calcifications. the tumors are often orange-brown, and an attachment to the normal choroid plexus or the ventricular wall may be present. some cpcs, and rare cpps, bleed profusely [1,3,11,18] surgical treatment surgery is the mainstay of treatment for cpps and a necessary first step in diagnosis and treatment of cpcs. as noted romanian neurosurgery (2010) xvii 2: 192 – 201 199 previously, the younger the patient, the more likely it is that cpps are found within the lateral or third ventricle, and as the patient approaches adulthood tumors in the fourth ventricle or cerebellopontine angle are more common. also, the younger the patient, the more likely it is that the tumor will be associated with hydrocephalus. therefore the goals in the management of these patients are relieving hydrocephalus, establishing a tissue diagnosis, and complete tumor removal. complete tumor removal is the goal with cpps and can be achieved in most cases even if this requires more than one operation. however, with cpcs subtotal resection is more common. the treatment of associated hydrocephalus and the surgical approaches to each of the ventricular sites are unique and beyond the scope of this text, but some general comments can be made [6,9,10]. hydrocephalus associated with these tumors can usually be managed with an external ventricular drain as necessary before or at the time of definitive tumor removal. we avoid a permanent shunt system before tumor removal, because in many patients tumor removal can solve the problem, and intraventricular surgery is associated with postoperative blood products that need to be cleared from the ventricle over several days and may obstruct permanent systems. ellenbogen et al found that after tumor removal in children, 63% did not require a permanent shunt. in some patients, despite tumor removal, ventriculoperitoneal shunting may be necessary for communicating hydrocephalus, and some will require subdural to peritoneal shunting for subdural fluid collections that persist after transcortical approaches to tumors of the lateral ventricles [10,13,14]. intra-axial tumors surgery for these tumors is complicated by their extreme vascularity and an inability to preoperatively embolize the arteries supplying the tumor. the tumors are quite friable, and blood loss can be a limiting factor in achieving gross-total tumor removal in neonates and infants.48 staged surgery for cpps is always an option. the blood supply to these tumors comes from the named choroidal arteries that normally supply the plexus, and these small vessels (anterior choroidal, posterior medial choroidal, posterior lateral choroidal, choroidal branch of the posterior inferior cerebellar artery) cannot be cannulated or embolized by interventional neuroradiologists for technical reasons (small caliber, distal arterial tree location) of risks of interference with blood supply to normal brain by the same artery (anterior choroidal, posterior inferior cerebellar) [9,13]. ideally, once the tumor is exposed, interruption of the feeding artery before tumor resection is begun is recommended. some authors have described en bloc removal of smaller tumors after doing just that. in adults, fourth ventricular tumors may be heavily calcified at diagnosis and may be relatively avascular. tumors of the lateral ventricles (frontal horn, temporal horn, body) are approached either by an interhemispheric transcallosal approach (anterior to midbody of lateral ventricle; third ventricle) or a transcorticaltransventricular route (temporal horn, posterior body to atrium). transcortical incisions may be associated with ventriculosubdural connections that account for the fluid collections requiring subdural to peritoneal shunting postoperatively. most surgeons will attempt a sulcal splitting 200 a.v. ciurea et al choroid plexus papilloma of the fourth ventricle approach to limit the amount of subcortical white matter cut and to reduce the chance of fluid collections developing. for tumors of the fourth ventricle a midline suboccipital craniotomy is used, and planes of dissection between the cerebellum and brainstem can be developed that allow for adequate exposure without the need for splitting of cerebellar tissue. tumors of the cerebellopontine angle are approached by a retrosigmoid (more lateral) suboccipital craniotomy. in both cases, because of proximity to cranial nerves within the subarachnoid space, neurophysiologic monitoring of these nerves is routine to reduce the chance of nerve injury with exophytic or large tumors. in general, complete removal of cpps is possible in the majority of cases even if more than one operation is required. complete removal holds the best chance for long-term tumor control or cure. for cpcs, which are often disseminated at diagnosis and more often invading brain, subtotal removal is the norm [10,14]. conclusions the optimum treatment of patients with cpts requires logical decision making and surgical skills of the neurosurgeon who plays a pivotal role in caring for these patients. recent developments in neurosurgical technology have reduced the morbidity and mortality of patients undergoing cpt surgery. the use of the operating microscope allows the surgeon to observe in detail the operative field and perform an almost totally safe tumor resection. correspondence to: claudiu_palade@yahoo.com, rsneurosurgery@gmail.com references 1. aguzzi a, brandner s, paulus w: choroid plexus tumours. in kleihues p, cavanee w(eds): pathology and genetics of tumours of the nervous system. lyon, france, iarc, 2000. 2. allen j, wisoff j, helson l, et al: choroid plexus carcinoma— responses to chemotherapy alone in newly diagnosed young children. j neurooncol 12:69–74, 1992. 3. ang lc, taylor ar, bergin d, kaufmann jc: an immunohistochemical study of papillary tumors in the central nervous system. cancer 65:2712–2719, 1990. 4. berger c, thiesse p, lellouch-tubiana a, et al: choroid plexus carcinomas in childhood: clinical features and prognostic factors. neurosurgery 42:470– 475, 1998. 5. bielschowsky m, unger e: kenntinis der primaren epithelgeschwultse der adergeflechte des gehirns. arch klin chir 81:61–82, 1906. 6. boyd mc, steinbok p: choroid plexus tumors: problems in diagnosis and management. j neurosurg 66:800–805, 1987. 7. cardozo j, cepeda f, quintero m, et al: choroid plexus papilloma containing bone. acta neuropathol (berl) 68:83–85, 1985 8. chow e, jenkins jj, burger pc, et al: malignant evolution of choroid plexus papilloma. pediatr neurosurg 31:127–130, 1999. 9. ciurea av (2007) tumorile intracraniene. in: ciurea av tratat de chirurgie, editura academiei, bucuresti, p 172 10. ciurea av, constantinovici a (1998) papilomul de plex coroid. in: ciurea av, constantinovici a ghid practic de neurochirurgie, editura medicala, bucuresti, p 341 11. coates tl, hinshaw db, jr., peckman n, et al: pediatric choroid plexus neoplasms: mr, ct, and pathologic correlation. radiology 173:81–88, 1989. 12. cushing h: intracranial tumors, springfield, charles c. thomas,1932. 13. dandy w: diagnosis, localization and removal of tumours of the third ventricle. bull johns hopkins hosp 33:188, 1922. 14. ellenbogen rg, winston kr, kupsky wj: tumors of the choroid plexus in children. neurosurgery 25:327–335, 1989. 15. enomoto h, mizuno m, katsumata t, doi t: intracranial metastasis of a choroid plexus papilloma originating in the cerebellopontine angle region: a case report. surg neurol 36:54–58, 1991. 16. galassi e, godano u, cavallo m, et al: intracranial tumors during the 1st year of life. childs nerv syst 5:288, 1989. 17. haddad sf, menezes ah, bell wf, et al: brain tumors occurring before 1 year of age: a retrospective romanian neurosurgery (2010) xvii 2: 192 – 201 201 review of 22 cases in an 11year period (1977–1987). neurosurgery 29:8, 1991. 18. itoh y, kowada m, mineura k: choroid plexus carcinoma. report of a case with positron emission tomographic study. neuroradiology 28:374, 1986. 19. kato t, fujita m, sawamura y, et al: clinicopathological study of choroid plexus tumors: immunohistochemical features and evaluation of proliferative potential by pcna and ki-67 immunostaining. noshuyo byori 13:99–105, 1996. 20. ken jg, sobel df, copeland bf, et al: choroid plexus papillomas of the formane of luschka. mr appearance. ajnr amjneuroradiol 12:1201-1203,1991 21. kepes jj: “xanthomatous” changes in a papilloma of the choroid plexus. acta neuropathol (berl) 16:367– 369, 1970. 22. koeller kk, sandberg gd: from the archives of the afip. cerebral intraventricular neoplasms: radiologicpathologic correlation. radiographics 22:1473–1505, 2002. 23. levy ml, goldfarb a, hyder dj, et al: choroid plexus tumors in children: significance of stromal invasion. neurosurgery 48:303– 309, 2001. 24. mcevoy aw, harding bn, phipps kp, et al: managent of choroid plexus tumors in children20 years experience at a single neurosurgical centre. pediatr neurosurg 32:192-199, 2000 25. mcgirr sj, ebersold mj, scheithauer bw, et al: choroid plexus papillomas: long-term follow-up results in a surgically treated series. j neurosurg 69:843849,1988 26. niikawa s, ito t, murakawa t, et al: recurrence of choroid plexus papilloma with malignant transformation—case report and lectin histochemistry study. neurol med chir (tokyo) 33:32– 35, 1993. 27. packer rj, perilongo g, johnson d, et al: choroid plexus carcinoma of childhood. cancer 69:580–585, 1992. 28. paulus w, janisch w: clinicopathologic correlations in epithelial choroid plexus neoplasms: a study of 52 cases. acta neuropathol (berl) 80:635–641, 1990. 29. pencalet p, sainte-rose c, lellouch-tubiana a, et al: papillomas and carcinomas of the choroid plexus in children. j neurosurg 88:521–528, 1998. 30. shin jh, lee hk, jeong ak, et al: choroid plexus papilloma in the posterior cranial fossa mr, ct, and angiographic findings. clin imaging 25:154-162,2001 31. vazquez e, ball ws, jr, prenger ec, et al: magnetic resonance imaging of fourth ventricular choroid plexus neoplasms in childhood. a report of two cases. pediatr neurosurg 17:48–52, 1991. 32. wolff je, sajedi m, brant r, et al: choroid plexus tumours. br j cancer 87:1086–1091, 2002. 33. yap wm, chuah kl, tan ph: choroid plexus papilloma with chondroid metaplasia. histopathology 31:386–387, 1997. microsoft word _4.formatata_iencean.doc romanian neurosurgery vol. xvi nr. 1 18 intracranial hypertension due to disorders in the cerebospinal fluid dynamics review st.m. iencean1, a.v. ciurea2, i. poeata3 1neurosurgery, “prof dr nicolae oblu” hospital, iasi, romania 2clinical emergency hospital “bagdasar arseni” bucharest, the university of medicine and pharmacy “carol davila”, bucharest, romania 3clinical emergency hospital “prof dr nicolae oblu” iasi, university of medicine and pharmacy “gr.t. popa”, iasi, romania the intracranial hypertension due to disorders in the cerebrospinal fluid dynamics is the intracranial pressure increase caused by disorders of the cerebrospinal fluid circulation from at the moment of its formation at the level of the choroid plexuses and until its passage in the venous circulation. the dynamic disorders of the cerebrospinal fluid are: circulation disorders of the cerebrospinal fluid from formation to the resorption place and disorders of the cerebrospinal fluid passage in the venous drainage system (resorption). the obstructive hydrocephalus is caused by a partial or complete obstruction of the ventricular system or by a blockage of the csf flow. intracranial hypertension due to resorption disorders or of a meningeal cause is the intracranial pressure increase caused by the reduction in the cerebrospinal fluid resorption due to various causes, which directly affect the resorption mechanisms. keywords: cerebrospinal fluid dynamics introduction the intracranial hypertension due to disorders in the cerebrospinal fluid dynamics is the intracranial pressure increase caused by disorders of the cerebrospinal fluid circulation from at the moment of its formation at the level of the choroid plexuses and until its passage in the venous circulation. [1, 3, 11, 17, 18] the dynamic disorders of the cerebrospinal fluid are: circulation disorders of the cerebrospinal fluid from formation to the resorption place and disorders of the cerebrospinal fluid passage in the venous drainage system (resorption). the circulation disorders of the cerebrospinal fluid are caused by an obstacle along the fluid route (ventricular system, magna cistern, basal cisterns) due to an obstruction by a ventricular or paraventricular tumor, an intra-ventricular hemorrhage or an obstruction due to various causes of the sylvian aqueduct. the segments of the ventricular systems, which are superjacent to the obstruction, increase their volume, creating an obstructive internal hydrocephalus. the resorption disorders of the cerebrospinal fluid occur due to the injury of the anatomic structures or due to disorders of the physiological mechanisms that assure the cerebrospinal fluid passage in the drainage venous system. these phenomena occur in acute meningitis, in sub-arachnoid hemorrhage, in meningeal carcinomatosis, in chronic sarcoidosis meningitis, etc. most frequently there is a thickening of the leptomeninges blocking the pachioni arachnoid corpuscles and decreasing the cerebrospinal fluid absorption. the cerebrospinal fluid accumulates in the ventricular system and a communicating hydrocephalus occurs, with a periventricular hydrocephalic brain intracranial hypertension romanian neurosurgery vol. xvi nr. 1 19 edema and with a generally sub-acute intracranial hypertension syndrome, designated as meningeal intracranial hypertension. the clinical presentationand the type of intracranial pressure increase resemble the intracranial hypertension syndrome met in the obstruction cases of cerebrospinal fluid circulation. [17,18] disorders in cerebrospinal fluid flow and obstructive hydrocephalus the obstructive hydrocephalus is caused by a partial or complete obstruction of the ventricular system or by a blockage of the csf flow. [1, 2, 4, 5, 8] the ventricular blockage is achieved by: stenosis of sylvian aqueduct – malformation, tumor, by intra-ventricular hemorrhage or inflammatory secondary stenosis. expansive intra-ventricular processes of 3rd ventricle or 4th ventricle that block the circulation of the cerebrospinal fluid. extrinsic blockage of the ventricular system due to paraventricular lesions. these may be expansive intracranial processes of cranium base, of posterior cerebral fosse, of median line (sellar, parasellar, etc.), which, through local compression and cerebral movement, cause the ventricular obstruction (the 3rd ventricle, sylvian aqueduct or the 4th ventricle). the obstruction of the communications with the sub-arachnoid cisterns – magendie foramen, luschka foramens; or the blockage of the basal sub-arachnoid space secondary to the sub-arachnoid hemorrhage or of an inflammatory origin. [9, 10, 12, 13] therefore, there is a rapid increase in the intracranial pressure, which exceeds the normal limit values of 20 mm hg. the increased intracranial pressure reduces the auto-regulation of the cerebral circulation. there are significant icp differences between the cerebrospinal compartments, which leads to the occurrence of cerebral herniation phenomena. clinical presentation the symptoms of hydrocephalus vary according to the illness age, the hydrocephalus progression type and the individual characteristics. the evolution of the ich syndrome is rapid, and, if the appropriate therapy is not applied, the decompensated intracranial hypertension may occur the usual signs in infants and young children are as follows: increase in the cranium dimensions, swelling of the anterior fontanelle, somnolence, vomiting, irritability, “sunset” glance. comparison between the two forms of ich by disorders of the cerebrospinal fluid dynamics: ich by dynamics disorders of the cerebrospinal fluid obstruction of the cerebrospinal fluid flow disorders of resorbtion csf ( meningeal ich) known etiology: obstruction of the cerebrospinal fluid circulation known etiology: meningeal inflammation, etc. obstructive hydrocephalus with periventricular or generalized edema communicating hydrocephalus with periventricular or generalized edema rapid icp increase moderate icp increase critical icp value ≈ 20 mm hg critical icp value ≈ 20 mm hg icp differences between the cerebrospinal compartments no icp differences between the cerebrospinal compartments the increased icp decreases the auto-regulation of the cerebral circulation the inflammatory vasculitis may affect the auto-regulation of the cerebral circulation short action duration of the increased icp varied duration of the pressure – time fluctuation complete evolution towards decompensated ich etiology dependent evolution, usually towards a complete or incomplete ich syndrome neurosurgical treatment: etiologic or ventricular drainage symptomatic and/or etiologic treatment; sometimes a ventricular drainage in acute hydrocephalus st.m. iencean romanian neurosurgery vol. xvi nr. 1 20 in older children and adults, the symptomatology includes: cephalea preceded by vomiting, diplopia, “sunset” glance, development delay, disorders of walking, coordination, sphincter disorders, psychic disorders: of personality, of memory, irritability, etc. in the case of the acute hydrocephalus, there is an escalation of the previous symptoms, or they are rapidly installed from the beginning: cephalea, vomiting, walking and equilibrium disorders, visual disorders. hydrocephalus diagnosis it is based on the clinical data and the paraclinical explorations: echography in infants and young children, cerebral computer tomography, nuclear magnetic resonance and intracranial pressure monitoring. [14, 15, 16, 17] treatment the purpose of the treatment is to reestablish the balance between the production and the absorption of the cerebrospinal fluid and the removal or avoidance of the causes that lead to a blockage of the cerebrospinal fluid circulation. [21, 22, 25, 28, 30, 31] depending on the etiology and pathogenic mechanism, the following treatment is applied: the medical treatment that may diminish the production of the cerebrospinal fluid – acetazolamide, the etiologic neurosurgical treatment of the compressive lesion, the neurosurgical treatment of the cerebrospinal fluid drainage: a ventricular-peritoneal shunt is set up, the endoscopic ventriculostomy is applied for the 3rd ventricle, repeated, lumbar draining punctures are used. [21, 22, 24, 25] intracranial hypertension due to resorption disorders intracranial hypertension due to resorption disorders or of a meningeal cause is the intracranial pressure increase caused by the reduction in the cerebrospinal fluid resorption due to various causes, which directly affect the resorption mechanisms. [2, 6, 10, 17] the diminished resorption of the cerebrospinal fluid can be caused by disorders of the cerebrospinal fluid resorption due to disorders of the membrane transfer mechanisms in the venous drainage system or to lesions of the anatomic structures that secure this transfer. the pressure gradient changes from the drainage venous system by the venous sanguine pressure increase in the malformations of the galien’s vein (in children) or the longitudinal sinus thrombosis or the syndrome of the superior cavus vein, etc., reduce the cerebrospinal fluid resorption with the occurrence of the ich syndrome, but the responsible pathogenic mechanism includes this form in the intracranial hypertension of vascular etiology. the anatomic structures that ensure the drainage of the cerebrospinal fluid in the venous sinuses may be interested in acute meningitis, in sub-arachnoid hemorrhage of traumatisms, aneurisms, etc, in meningeal carcinomatosis, in chronic sarcoidosis meningitis, etc. most frequently, there is a thickening of the leptomeninges by blocking pachioni arachnoid corpuscles and by decreasing the absorption of the cerebrospinal fluid. the cerebrospinal fluid is accumulated in the ventricular system and a communicating hydrocephalus is produced, with a periventricular hydrocephalic brain edema and with a generally sub-acute intracranial hypertension syndrome, which is designated as the meningeal intracranial hypertension. [19, 20, 26, 27, 32] the intracranial pressure increase is moderate and there are differences between the cerebrospinal compartments. due to the meningeal inflammation, there may be an inflammatory vasculitis, which affects the superficial cerebral circulation in various degrees. the clinical presentationand the type of intracranial pressure increase are similar to the intracranial hypertension syndrome in cases of obstructed circulation of the cerebrospinal fluid. the evolution depends on etiology, and it is usually headed towards a complete or incomplete ich syndrome, usually with no occurrence of decompensation phenomena. intracranial hypertension romanian neurosurgery vol. xvi nr. 1 21 the treatment is symptomatic and/or etiologic depending on identifying etiology and of the pathogenic mechanisms; a ventricular drainage is rarely needed in order to prevent an acute hydrocephalus. [21, 23, 26, 29]. references 1.adamson dc, dimitrov df, bronec pr. upward transtentorial herniation, hydrocephalus, and cerebellar edema in hypertensive encephalopathy. neurologist. 2005;11(3):171-5. 2. agrawal d, chaturvedi dk. shunt dependent hydrocephalus.br j neurosurg. 2004; 18(4):403 3. akbar m, stippich c, aschoff a. magnetic resonance imaging and cerebrospinal fluid shunt valves. n engl j med. 2005 29;353(13):1413-4 4. barbagallo gm, platania n, schonauer c. long-term resolution of acute, obstructive, triventricular hydrocephalus by endoscopic removal of a third ventricular hematoma without third ventriculostomy. case report and review of the literature. j neurosurg. 2005;102(5):930 5. bejjani gk. association of the adult chiari malformation and idiopathic intracranial hypertension: more than a coincidence.med hypotheses. 2003;60(6):859-63. 6. castano a, volcy m, garcia fa, uribe cs,et al headache in symptomatic intracranial hypertension secondary to leptospirosis: a case report. cephalalgia. 2005;25(4):309-11. 7. cestari dm, rizzo jf intracranial hypertension following epidural blood patch. neurology. 2003. 11;61(9):1303. 8. czosnyka m, czosnyka zh, richards hk, pickard jd. hydrodynamic properties of extraventricular drainage systems. neurosurgery. 2003;52(3):619-23. 9. czosnyka zh, cieslicki k, czosnyka m, pickard jd. hydrocephalus shunts and waves of intracranial pressure. med biol eng comput. 2005;43(1):71-7. 10.eide pk. the relationship between intracranial pressure and size of cerebral ventricles assessed by computed tomography.acta neurochir (wien). 2003;145(3):171-9; 11.forsyth r, baxter p, elliott t. routine intracranial pressure monitoring in acute coma.cochrane database syst rev. 2001;(3):cd002043. 12.fritsch mj, doerner l, kienke s, mehdorn hm. hydrocephalus in children with posterior fossa tumors: role of endoscopic third ventriculostomy. j neurosurg. 2005;103(1 suppl):40-2 13.hamlat a, heckly a, doumbouya n, et al epidural hematoma as a complication of endoscopic biopsy and shunt placement in a patient harboring a third ventricle tumor. pediatr neurosurg. 2004 sep-oct; 40(5):245 14.he xs, zhang x. giant calcified chronic subdural haematoma: a long term complication of shunted hydrocephalus.j neurol neurosurg psychiatry. 2005;76(3):367. 15.iannelli a, rea g, di rocco c. csf shunt removal in children with hydrocephalus.acta neurochir (wien). 2005;147(5):503-7. 16.iencean st m idiopathic intracranial hypertension and idiopathic normal pressure hydrocephalus: diseases with opposite pathogenesis? medical hypotheses. 2003;61(5-6):526-8. 17.iencean st m pattern of increased intracranial pressure and classification of intracranial hypertension. journal of medical sciences, 2004,.4,1 :5258 18.iencean st m simultaneous hypersecretion of csf and of brain interstitial fluid causes idiopathic intracranial hypertension. medical hypotheses. 2003;61(5-6):529-32. 19.joffe ar. prognostic factors in adults with bacterial meningitis. n engl j med. 2005, 3;352(5):512-5. 20.johnston m. the importance of lymphatics in cerebrospinal fluid transport.lymphat res biol. 2003;1(1):41-4. 21.kurtcuoglu v, poulikakos d, ventikos y. computational modeling of the mechanical behavior of the cerebrospinal fluid system. j biomech eng. 2005;127(2):264-9. 22.mathew p, teasdale g, bannan a, oluoch-olunya d. neurosurgical management of cerebellar haematoma and infarct. j neurol neurosurg psychiatry. 1995; 59: 287–292. 23.olson s. the problematic slit ventricle syndrome. a review of the literature and proposed algorithm for treatment. pediatr neurosurg. 2004;40(6):264-9. 24.perrin rg, bernstein m. tension pneumoventricle after placement of a ventriculoperitoneal shunt: a novel treatment strategy. case report. j neurosurg. 2005;102(2):386-8. 25.psarros tg, coimbra c. endoscopic third ventriculostomy for patients with hydrocephalus and fourth ventricular cysticercosis: a review of five cases. minim invasive neurosurg. 2004; 47(6):346-9. 26.ramadan nm. meningeal enhancement and low csf pressure headache. an mri study. cephalalgia. 2005;25(7):558 27.riva m, bacigaluppi s, galli c, citterio a, collice m. primary leptomeningeal gliomatosis: case report and review of the literature. neurol sci. 2005;26(2):129-34. 28.rogg jm, ahn sh, tung ga, et al prevalence of hydrocephalus in 157 patients with vestibular schwannoma. neuroradiology. 2005;47(5):344-51. 29.singh d, sachdev v, singh ak, sinha s. endoscopic third ventriculostomy in post-tubercular meningitic hydrocephalus: a preliminary report.minim invasive neurosurg. 2005;48(1):47-52. 30.sotelo j, arriada n, lopez ma. ventriculoperitoneal shunt of continuous flow vs valvular shunt for treatment of hydrocephalus in adults.surg neurol. 2005;63(3):197-203. 31.van toorn r, georgallis p, schoeman j. acute cerebellitis complicated by hydrocephalus and impending cerebral herniation. j child neurol. 2004;19(11):911-3. 32.wang kw, chang wn, chang hw, wang hc, lu ch. clinical relevance of hydrocephalus in bacterial meningitis in adults.surg neurol. 2005;64(1):61-5 33.woodworth gf, mcgirt mj, williams ma, rigamonti d. the use of ventriculoperitoneal shunts for uncontrollable intracranial hypertension without ventriculomegally secondary to hivassociated cryptococcal meningitis. surg neurol. 2005;63(6):529-31 microsoft word 17ciuchilanelena_epidemiology_f 356 elena ciuchilan et al epidemiology in trafic accidents epidemiology in trafic accidents elena ciuchilan1, tatiana iov2, liviu pendefunda3 1phd student umph ”gr.t.popa”iaşi, forensic pathologist, the forensic service of neamţ romania 2forensic pathologist, phd, the institute of forensic medicine of iaşi, romania 32nd neurology department, the emergency clinical hospital “prof. dr. n. oblu” iaşi, umph “gr.t. popa” iaşi, romania abstract the industrialization and the technological advance we can affort more and more, allowed the car numbers increasing and the car accident as well. the paper presents the victim number status of neamţ area for the period of 2005-2008, split on sex and type of participant in accident. the aim is to help out the local authorities with information, more precisely the police, in order to improve the car trafic safety by getting specific measures. keywords: car accidents, epidemiology, forensic issues introduction the heavy industrialization in the last decades, as well as the technological progress to which mankind has access on a daily basis, have made it an absolute necessity to consider the prophylaxis of traffic accidents as a research topic in epidemiology studies. currently, at a global level, traffic accidents are the first in top worldwide on the list of causes of violent death. up to 75% of the number of traffic accidents are reported in developing or transition countries, although only around 30% of the total percentages of vehicles are owned by them. in industrialized countries, the problem of traffic accidents has spread in the first decades of the 20th century, when, in the usa, for instance, the number of motor vehicles has suddenly climaxed. after the second world war, they gained importance in many european countries, as well as in japan. after the 1970s, the developing countries become strongly dependent on motor vehicle transport, and at the same time the number of traffic accidents raised. a context of epidemic proportions is thus created. as a result, accidents become a public health issue through the impact they have in public health systems from the perspective of the money cost and human resources necessary for their management. statistics have shown that most accidents occur on sundays and the fewest on wednesdays. we are concerned with the issue of traffic accidents from a forensic perspective because of the consistent number of deaths and injuries that occur in vehicle crashes (1), (2), (6). for 2004, a number of 1.2 million deaths caused by traffic accidents and approximately 50 million injured persons was estimated worldwide (oms, 2004) (8). these numbers are however rather imprecise, since they concern mortality on the spot. most deaths occur at the location of the accident and because of the improvement of the safety systems romanian neurosurgery (2011) xviii 3: 356 – 361 357 installed on the motor vehicles, the causes of death in the case of traffic accidents have evolved, including even the safety systems designed for protection (the safety belt, the airbag) (4), (5). post-accident deaths are not considered in the statistics. the traffic accident is a dynamic process that usually involves two main actors, namely the one who causes the accident and the one who suffers from it. but there are also many situations when the one who causes the accident is also the one who suffers, without necessarily injuring another person. the information gathered for the developing countries for the 1970s show that pedestrians, cyclists, and motorcycles account for up to 74% of the number of deceased persons, compared to the developed countries, where they represent up to 20% (8). these differences actually come from the structure of the vehicle park, irrespective of whether we consider motor vehicles (cars), two-wheel motor vehicles (motor bikes, scooters) or vehicles with no motor (bicycles). this makes the balance differ from one region of the globe to another. for example, in asia, motorcycles are responsible for most accidents because of the high number of the owners of such vehicles, while in latin america, pedestrians and bicyclists represent this majority (8). men have been identified as representing most victims of traffic accidents. before including them in any statistics, we have to consider the role played in a traffic accident. statistically, women cause fewer traffic accidents as drivers, but this is because women have started to own licenses in significant numbers only during the last two decades. what is certain is that irrespective of the position of men or women, the former are on the first position among the victims of traffic accidents. work also contributes to this situation, through the number of work trips, etc. at the end, the percentage would be approximately 75% of the deaths as pedestrians and 86% as vehicle passengers(8). method several factors lie at the basis of the occurrence of the various traffic accidents. obviously, they start from the human one, represented either by the motor vehicle driver, who breaks the legal speed limit, drives the vehicle under the influence of alcohol, has no experience, is tired, uses tranquilizers or ataraxics, suffers from a pathological condition, or by the pedestrian, who can be in a state of ethyl intoxication, is distracted, does not observe the traffic rules, etc. the technical factor refers to the technical state of the motor vehicle, to the condition of the safety systems, of the braking, direction, or light system, to the state of the tires, etc. the final factor is chance. it can be often avoided by driving preventively, especially in conditions of road humps, descents, instable roads, rain, glaze or snow, or mud. given the important forensic implications of the car accidents, we focused on the forensic aspects and epidemiological data for neamt area in terms of such events. we analyzed the accidents produced in the period 20052008. we were interested on the number of health care days in car accidents victims. we counted and split up the cases in ranges framed by law. the sex of the victims was an item considered as well. the task of the medical examiner in case of traffic accidents is to draw a forensic report that presents the forensic 358 elena ciuchilan et al epidemiology in trafic accidents conclusions that will objectify the legal end of the legal report between the parties involved in the accident (3), (7), where applicable (if the parties conciliate and the law allows it). of the information included in the examination report, we can mention the evaluation of the duration of medical care, based on which the event (deed) will be classified in a specific article of the penal code, a differentiation of the lesions that have been produced in a traffic accident from those that exclude or question this possibility, an evaluation of the general mechanisms of lesion occurrence (less important than in deadly accidents), a mention of all the consequences of the traumatic injuries – loss of an organ, loss of the function of an organ, permanent physical or psychological invalidity, abortion, the presentation of the victim’s condition – driver, passenger, pedestrian, when the injuries may heal faster (especially in the case of children, youngsters), initial conclusions should not be definitive. a reexamination of the injured person should be requested around this “limit” interval, in order to allow making definite evaluations. results in order to support the forensic importance that should be given to traffic accidents, in what follows we present some epidemiologic information from 20052010. we intended to stress the incidence of these types of events in the region of neamţ. in figure 1 we can see, for the period 2005-2008, a much higher incidence of men as victims of traffic accidents, than that of women. the number of days of medical care is concentrated around the segment under 10 days, followed by the period 2060 days. 0 10 20 30 40 50 60 70 80 m f m f m f m f 2005 2006 2007 2008 0 <10 10-20 20-60 >60 figure 1 victims of traffic accidents, with the number of days of medical care, according to gender, for the period 2005-2008 romanian neurosurgery (2011) xviii 3: 356 – 361 359 figure 2 victims of traffic accidents for the period 2005-2008 figure 3 victims of traffic accidents, according to the number of days of medical care, per type of accident participant the total number of victims for the period 2005-2008 is graphically described in figure 2. the average evolves around the value of 290 victims in traffic accidents in the region of neamţ, per year. most incidents occur with pedestrians, but they do not necessarily require over 10 days of medical care, as we can see in figure 3. the tendency to group the majority of cases for which medical care has been granted according to gender is in the area of the group under 10 days. from a forensic perspective, the number of days of medical care is very important for the classification in a specific article of the penal code. discussions as the studies and our data showed, the car accidents number has the tendency to increase year by year. from the romanian law system point of view, a car accident, in case human casualties occur, special procedures must be done. the measures include among them the forensic certificate the pathologist should provide to the court. in order to force drivers to reduce the number of traffic accidents and to help the forensic pathologists for better framing of any particular case, the penal code includes a series of articles referring to the latter. these are: art. 178 cp – murder in default. “when a person is killed by a mechanical drive vehicle driver, whose alcohol impregnation in blood breaks the legal limit or who is inebriated, the punishment is 5 to 15 years in prison”. art. 180 – impact or other violence. “impact or violence that caused an injury that requires medical care for at least 20 days in order to heal is punished with 3 months to 2 years in prison, or with a fine. the deeds mentioned in paragraph 2 that affect family members are punished with one to 2 years in prison or with a fine. the penal action starts upon the initial complaint of the injured person. in the case of the deeds mentioned in paragraphs 11 and 21, the penal action can also start ex officio. the conciliation of the parties eliminates penal accountability, even in case the penal action has started ex officio”. art. 181 – bodily injury. the deed that causes a damage to the physical integrity or to health, which requires medical care for at most 60 days in order to heal, is punished with 6 months to 5 years in prison. the deed mentioned in paragraph 1, if it affects family members, is punished with one to 5 years in prison. the penal action starts upon the initial complaint of the injured person. in the case of the deeds mentioned in paragraph 1, the penal action can also start ex officio. the conciliation of the parties eliminates penal accountability, even in case the penal action has started ex officio. art. 182 – serious bodily injury. the deed that causes a damage to the physical integrity or to health, which requires medical care for over 60 days in order to heal. 360 elena ciuchilan et al epidemiology in trafic accidents art. 184 – bodily injury in default. the deed mentioned in paragraph 180 that has caused a damage that requires medical care for over 10 days in order to heal, as well as that mentioned in paragraph 181, performed in default. the conciliation of the parties eliminates penal accountability. the number of traffic accidents has increased in the last few years, together with their seriousness. the blame consistently belongs to the drivers. in order to increase traffic safety and to reduce the number of accidents, the patterns that favor their occurrence should be identified. patterns are defined by causes, by the behavior of the traffic participants, and by their attitudes. annually, a significant number of people lose their lives in traffic, and many others remain affected following traffic accidents (physical disabilities). the development of modern technologies and their implementation on motor vehicles make the topic of traffic accidents be always present. the interest increases as the standard injuries tend to move their center of gravity from injuries caused by impacts against objects inside the vehicle or with the vehicle itself to lesions caused by the safety systems mounted on the vehicles. the mechanical causes of the lesions, deadly or not, are completed by thermal or chemical causes generated by airbags or safety belts. among the most frequent causes of mortality in traffic accidents, skull traumas account for approximately 70% of the total mortality rate in the persons under 45 years of age (the population for which traffic accidents are the main cause of death). the date we obtained from our study shows that most of the victims were pedestrians and, fortunately, most of the cases asked for less than 20 days of medical assistance. the victim should be examined shortly after the occurrence of the accident and necessarily after a larger interval, when the evolution and prognosis of the lesion are stated. it is compulsory to analyze all the medical documents. the observation sheet sent by the medical doctor from the hospital where the person injured in the traffic accident was sent is very important. re-examination is indicated after the clinical healing and the exhaustion of all the therapeutic means of recovery in case invalidity sequel are indicated. the objective of the examination in case of non-deadly injuries is establishing the truth and date when the injury occurred, the conditions and manner in which they occurred, the seriousness of the trauma from the perspective of medical care, the occurrence of permanent invalidity or the loss of a sense/organ, their functional stop, etc. as well as the belated consequences of the injury on the injured person from a material perspective. the studies showed that the countries with most number of car accidents are those with a pour road infrastructure, with weak traffic control systems, such are ethiopia, tanzania, lesotho, nekya, bangladesh, pery, etc. at the other hand, the countries with fewer accidents would be uk, japan, usa, new zeeland. from the data of our study, we anticipate our position somewhere in between. the data from the study showed an important cut of the whole statistics on the pedestrian side as victims. there could be two points here. one is that the pedestrians were the accident initiators as paying less attention to the walking near the roads rules. the other is that the driver initiated the accident by crossing the speed limit or loosing car control on wet or icy roads. at romanian neurosurgery (2011) xviii 3: 356 – 361 361 the end the statistic is the same, pedestrian victims. anyway, an interesting result is that the drivers are not the most important part of the victim statistic. they are placed between pedestrians and passengers. interesting is the fact that the passengers as victims exceed the drivers. this would be based on the fact the belt is not always used by others than the driver. conclusions the statistics collected for the region of neamţ, presented in this paper, include a number of 1143 cases, divided over a period of 4 years (2005-2008). because of the forensic implications, we are interested in the allocation of medical resources to the victims of traffic accients, especially in the number of days of medical care necessary for the recovery. we have identified the fact that the number of cases that required days of medical care mainly focuses in the segment under 10 days of medical care, followed by the segment from 20 to 60 days of medical care. another important fact we want to emphasize is that the passengers group is quite important in the car accidents victim statistic. this is a warning flag that in spite the fact this is requested by law for both the driver and the front passenger, and for the children under 12 years old on the back seat, we assume this is not happening all the time. given the first and second authors field of expertise, we can confirm many such cases. from the forensic perspective, most of the cases were not subject of law prosecution as the mentioned articles from the penal code would frame. the final impact of the car accidents is on the public system that must support the biggest part of the expenses like local authorities investigations, victim medical investigations, court procedures and so on. the solution to save such resources would be a better drivers informing system, road infrastructure development and correct maintenance and public education in general using all available ways. correspondence author: tatiana iov e-mail: tatianaguritencu@yahoo.com references 1. beliş v., dragomirescu v., naneş c., gacea e., panaitescu v., drugescu n., medicina legală, ed. teora, bucureşti, pg. 93-94, 1992 2. beliş v., tratat de medicină legală, ed. medicală, bucureşti, vol. 1, pg. 739-742, 1995 3. ciurea a.v., davidescu h.b., traumatologie craniocerebrală, editura universitară „carol davila”, bucureşti, 2007 4. har ntsb/ss-86-03, ntsb safety study: “performance of lap belts in 26 frontal crashes”, 225230, 2003 5. lupaşcu c., lupaşcu c., grămadă s., grigoriu c., scripcaru c., airbag-ul: consideraţii tehnice, clinicochirurgicale şi medico-legale, revista română de medicină legală, vol. xi, nr. 3, bucureşti, 208-215, 2003 6. ommaya a.k., biomechanics of head injury: experimental aspects, in nahum a.m., melvin j., eds., the biomechanics of trauma, norwalk ct., appleton-century-crofts, 245-269, 1985 7. plăhteanu m., baciu gh., pădure a., aspecte medicolegale lezionale în traumatologia mecanică, ed. performantica, iaşi, pg. 224-236, 2004 8. vasconcellos e.a., traffic accident risks in developing countries: superseding biased approaches, ictct extra workshop, campo grande, pg. 1-11, 2005 microsoft word 4onosegtraumaticbrain romanian neurosurgery (2011) xviii 1: 11 – 30 11 traumatic brain injury: current endeavours and trends for neuroprotection and related recovery g. onose, cristina daia-chendreanu, monica haras, a.v. ciurea, a. anghelescu the teaching emergency hospital “bagdasar-arseni” (tehba), bucharest abstract this paper aims to give a brief overview on traumatic brain injuries’ (tbis) main pathophysiological mechanisms, to summarize the current available therapeutic strategies and offer a glimpse at possible future advancements in the field. the impact of tbi on health care systems and society is tremedous. while the surgical and intensive care management are relatively well standardized for acute tbi, subsequent, therapeutic interventions remain at the physician’s choice/ professional skills, and their clinical utility is still questionable. previous experience and numerous trials have failed to demonstrate a consistent benefit from therapies like corticosteroids, lazaroids, nsaids vasodilators, glutamate blockers, immune modulators, or general hypothermia. novel achievements in neuroprotection are now expected from developing antiapoptotic agents (such as caspase and/or calpain inhibitors), from more potent antioxidants, cholinergic agents, alpha blockers from researching various physiologic substances, like melatonin, protirelin, inosine, progesterone, and including from regenerative medicine and physiatric, assisstive technology/ bioengineering advancements. keywords: neuroprotection, primary brain damage, secondary brain injury, traumatic brain injury introduction in head traumas, the primary brain damage occurs at the time of initial impact, and is refractory to most prophylactic/ therapeutic actual strategies. the secondary injuries’ ”cascade” is the result of complex (quite similar in traumatic injuries of the central nervous system (cns), i.e. both, the brain and the spinal cord; they have been detailed, in some of our previous articles, so we shall not further develp them here) pathophysiological events that unreel over a longer period of time and are, at least in theory and partially, preventable and treatable. the main physical mechanisms of the primary brain injuries are: • direct impact/ physical contact with the under-skull tissue: penetrating head injuries the dura is pierced (bullet or knife wounds to the head are such examples). • indirect impact/ physical contact with the under-skull tissue: closed head injuries. closed or blunt head injuries represent the majority of cases in civilians; many of these injuries are produced by motion without impact and/ or external evidence of injury to the head. the most common causes are 12 g. onose et al traumatic brain injury sudden acceleration or deceleration. the dura remains intact. the physical factors influencing – mainly through inertial and/ or contact forces – the type and severity of a closed injury to the brain, include energy load per unit area, duration, velocity and direction of the force, configuration of various parts of skull, rate of acceleration or deceleration, and diffusion of forces resulting in agitation of the entire cerebrum. more precisely, three principal physical mechanisms are described: impact loading (percussion of the head with a solid object, at a significant speed may involve coup and contrecoup injuries, if the moving head hits a fixed object), impulsive loading (abrupt motion/ cessation of motion of the head, without significant contact with other objects) and static or quasistatic loading (external forces applied gradually – therefore the importance of the impact velocity is not always determinant – with a crushing effect; it is a rare occurrence). (21, 37) as a bottom line it is stated that the amount of brain damage is proportional to the rotational acceleration achieved and the mass of the brain, because contact and/or inertial forces may strain the brain tissue – i.e. the amount of its deformation beyond its structural tolerance, thus leading to injury. there are described three basic types of tissue deformation: by compression (compressive), by tissue stretching (tensile) and by tissue distortion, when sliding over other tissue/s (shearing) (21, 37). considering the aspects described above, primary brain injuries can be classified as focal injuries (penetrating wounds with skull fractures -, intracranial hemorrhages, lacerations, contusions, multiple possible trauma at auditory-vestibular level – in striking of the temporal region) or diffuse ones (diffuse axonal injuries – dai, including a form considerate mild: concussions)(21, 37) the major lesional / pathophysiological conditions involved in the secondary brain damages are currently considered to be (94): • brain tissue swelling • hemorrhage (extradural, subdural, subarachnoid, intracerebral, intraventricular) • loss of the local/ regional blood flow – generating ischemia • (and possibly/ added) infection they correspond, at cellular and subcellular level, to (what modern research has identified as a cascade of intimate events leading, in vicious circles, to the secondary injury): failure of cellular energy metabolism, local intense generation of reactive oxygen species/ oxidative stress (folowed by biological membranes’ lipid peroxidation, dna and proteins damage/ misfolding), immune shifts/ inflammatory processes/ acidosis, global and/or focal multifactorial ischaemia, ischemic penumbra and alteration of regional microcirculation, ionic disturbances (leading to cells swelling including massive edema – followed, because of suddenly installed osmolysis – by cell induced necrosis/ passively dying off), excitotoxicity (excess of neurotransmitters – especially glutamate – and also enhanced intracellular influx of calcium ions) and related activation of apoptotic genes and thus of different pathways of “delayed mechanisms of cell death”: apoptosis and apoptosis-like processes (60, 94). hence, the secondary events’ ”cascade” entails an extremely complex and extended romanian neurosurgery (2011) xviii 1: 11 – 30 13 reaction, practically of the entire body: from its gene level to the ”macroscopic”/ clinical, one. therefore, the concept of secondary brain injuries has become the basis – many of them being inmtimate targets – for developing an array of neuroprotective modern therapies. neuroprotective therapies below we give an extensive list of potential neuroprotective therapies, classified by mechanism of action and clinical use. this classification paradigm also appeared in one of our previous papers, dedicated to neuroprotection in spinal cord injury (sci), published in 2009, the october issue of spinal cord journal. we will further discuss some of these therapeutic drugs and procedures. our color code serves to achieve a balanced, selective approach; the present paper refers to the drugs effective/ researched in tbi and to some equally effective/ researched in both tbi and scis; considering both conciseness and a selective review of recent and/or less discussed matters, not all items will be elaborated: colour code: • mainly used/researched for brain injuries • rather equal efficiency in sci and tbi • mainly used/researched for spinal cord injuries “classical” drugs, with a long history of clinical use • peptide mixtures with neurotrophic actions (cerebrolysin®, actovegin®) • musculotropic vasodilators • nootropic agents • anesthetic agents (including xenon gas, with anti-excitotoxic properties) • (other) hormones • sex hormones (progesterone) • trh (thyrotropin-releasing hormone) and analogues • anti-inflammatory drugs and immune modulators: • saids (methylprednisolne) • lazaroids (21-aminosteroids) • nsaids (cox2 inhibitors) • il 10 (interleukin 10) • glatiramer acetate (copaxone®) • anti-excitotoxic agents (glutamate blockers) • xenon gas • nmda blockers • ampa blockers • kdi tripeptide • iron kelators (deferoxamine, 2,2’bipyridine, quercetin) • vitamins and other nutritional supplements (b vitamins, tioctic acid, selenium, zinc, magnesium, etc.) • ca2+ channel antagonists (nimodipine) • lithium • statins (simvastatin) – acting as antagonists of growth inhibitory signals in central nervous system • dopamine agonists: • bromocriptine • lisurid • cholinergic agents • citicoline • rivastigmine (exelon) new / experimental drugs • kdi tripeptide • monosialoganglioside gm 1 14 g. onose et al traumatic brain injury • igf-1(insulin-like growth factor) • neurotrophins – characterized by pleiotropic effects • gdnf (glial derived neurotrophic factor) • bdnf (brain derived neurotrophic factor) • ngf (nerve growth factor) • nt-3 (neurotrophin-3) • cntf (cliary neurotrophic factor) • apoptosis inhibitors • protease inhibitors (caspase inhibitors, calpain inhibitors) • parp (poly(adp-ribose) polymerase) inhibitors • dmso (dimethyl sulfoxide) • antioxidants • glutamate transporters (eaac1 protein) • free radical scavangers: ascorbate, vitamin e, beta-carotene, alphatocopherol, penicillamine, superoxide dismutase, q10 coenzime • l-cysteine • selenium, zinc, magnesium • cell adhesion molecules (l1-cam) • erythropoietin • melatonin • inosine (axosine™) • ait-082 (leteprinim potassium, neotrofin) • 4-aminopyridine (fampridine) • riluzole • antogonists of the growth inhibitory signals in cns • monoclonal antibodies to nogo • phosphodiesterase inhibitors (rolipram) • dibuthyril cyclic amp (db camp) • inhibitors of rho signaling (cethrin) • scar preventing substances (chondroitinase, cordaneurin, epha4 antagonists) new / experimental procedures • local hypotermia • combinatory (‘combo’) strategies • hyperbaric oxygen therapy • fusion technology (polyethylene glycol) • physical therapy • low-level laser therapy • oscillating field stimulator (ofs) • functional electrical stimulation • immunetherapy with activated macrophages or lymfocytes pharmacological and physiatric stimulation of the spinal central pattern generator (cpg) neurotrophic peptide mixtures cerebrolysin cerebrolysin is a mixture containing 85% free amino acids and 15% biologically active low-molecular weight petides, prepared by enzymatic lysis of lipid-free pig brain products. its exact mechanisms of action are not known, but the drug has been proven useful in a large number of conditions, including neurological trauma of any type (3, 108), stroke (48), alzheimer’s and other degenerative disorders of the brain. the most numerous clinical studies with cerebrolysin® were conducted in patients with dementia (alzheimer’s and vascular) and they yelded good results, with significant improvement of cognition in the treated subjects (35). to date, there are no reported significant adverse reactions to cerebrolysin®, except romanian neurosurgery (2011) xviii 1: 11 – 30 15 for allergies and seldom cns excitability enhancements. the small molecules contained by the mixture readily cross the blood-brain barrier. they exert neuroprotective, neuroptrophic, nootropic and neuromodulating – i.e. multimodal – effects on the cns, similar to those of the naturally occuring growth factors, especially the nerve growth factor. many experimental studies (67, 74, 82) and clinical trials (3, 48, 108) suggested a variety of mechanisms for these beneficial effects: • an increase in the efficiency of the aerobic neuronal metabolism • stimulation of protein synthesis in the cns • stimulation of neuronal differentiation • inhibition of reactive oxygen species formation • inhibiton of lipid peroxidation (67) • anti-excitotoxic actions (74) • anti-apoptotic effects (32) • immunoactive properties (84) figure 1 correspondence between cerebrolysin’s main effects and pathways of the secondary injuries cascade it targets/ counteracts: pleiotropic, but by stimulating neuro-/ synaptogenesis and respectively, neuroplasticty, it results in a multimodal way of action, too (g. onose et al. neuroprotective and consequent neurorehabilitative clinical outcomes, in patients treated with the pleiotropic drug cerebrolysin, journal of medicine and life, 2(4): 350-61, 2009) actovegin actovegin is a deproteinized hemoderivative of calf blood, obtained by ultrafiltration. it contains electrolytes, essential trace elements and 30% organic components: amino acids, oligopeptides, nucleosides, inositol phosphooligosaccharides (ipos), intermediary products of the carbohydrate and of the lipid metabolism, and components of the cellular membranes, such as glycosphingolipids. the molecular weight 16 g. onose et al traumatic brain injury of the organic components is below 6000 da. the main effect of actovegin® is to increase the cellular energy metabolism, by increasing the respiratory capacity of mitochondria, the oxygen and the glucose uptake. also, the ipo fraction of actovegin® demonstrated a positive effect on glucose carrier activity (glut1): it stimulates glucose uptake by the cerebral tissues, as well as other tissues and activated glucose oxidation. the ipo fraction acts indirectly on the citric acid cycle, by increasing acetyl coenzyme a synthesis(12). several small clinical studies found benefits of actovegin® administration in elderly patients with organic brain syndrome(45), in dyscirculatory encephalopathy(55, 100) and in tbis, where the investigators found some positive effects of the drug on the eeg changes(92). actovegin® is very well tolerated, and few adverse reactions have been described; allergies are the most frequent side effects and severe anaphylaxis has been reported in one case(56). musculotropic asodilators papaverine cerebral vasospasm is a severe complication that can develop in 5% to 50% of patients with tbi(97), especially in relation to subarachnoid hemorrhage (sah) or other intracranial hemorrhages. the posttraumatic cerebral vasospasm can lead to massive stroke, increasing the morbidity and the mortality after head injuries, which is why treating it is one of the main neuroprotective measures in these patients. papaverine (an opium alkaloid) is a potent smooth muscle relaxant, but hypotension limits its systemic application. it has been used in topical (with a syringe, gelfoam, cotton pledgets, or controlledrelease drug pellets) application on arteries during surgery(85). local application in a controlled-release matrix has been clinically tested in a study involving 117 patients. the results showed that the procedure effectively prevented the development of symptomatic vasospasm and improved neurological outcome in treated patients, with no adverse effects(17). it has also been administered as intraarterial injections, but the effectiveness of this method in reversing vasospasmassociated cerebral hypoperfusion is controversial. some authors found it useful(52), but some found no beneficial effect of intra-arterial papaverine(96). also, there is one case report of transient severe brain stem depression during intra-arterial papaverine(6). vinpocetine (cavinton) vinpocetine is a synthetic derivative of vincamine, an alkaloid derived from vinca minor. it was discovered during the late 1960s and has been used in the treatment of cerebrovascular and cognitive disorders for decades. its primary mechanism of action is direct vasodilation of cerebral vessels, enhancing the cerebral blood flow, but hypotension is a rare side effect. it also reduces platelet aggregation (by inhibiting its capacity to take in adenosine), increases platelet plasticity and decreases blood viscosity. more recent studies suggested that vinpocetine and vincamine may decrease the mitochondrial disfunction induced by glutamate excitotoxicity (63, 22, 93). in vitro and in vivo experiments demonstrated the the compound inhibits phosphodiesterase 1, blocks voltageoperated calcium channels and voltagedependent natrium channels (13), and has romanian neurosurgery (2011) xviii 1: 11 – 30 17 antioxidative action(68). a clinical trial with vinpocetine in newborns with intracranial birth trauma demonstrated that the compound inhibits posttraumatic epileptic activity (25). a small hungarian clinical study showed that intravenous administration vinpocetine in stroke patients increases the cerebral blood flow and the glucose metabolism, especially in the thalamus and caudate nucleus(90). all this accumulating data suggests that intraveous vinpocetine might a useful therapeutic tool for head injury treatment, but further evidence is needed. vincamine (ceredia, oxybral, oxicebral, cetal, devincan, pervincamin) appears to have the same pharmacological characteristics, except the risk of hypotension and cardiac arrhythmias is higher with intravenous administration. clinical trials found orally administered vincamine beneficial in primary degenerative and vascular dementia, but there are no studies vincamine for cns tauma. ginkgo biloba extract (tanakan) ginkgo biloba is the best-selling phytomedicine on the european market. it has been widely used to treat a variety of conditions, including peripheral vascular disease, vertigo, ischemic heart diseases, eye diseases, depression, ischemic stroke, demetia and tbi. the extract contains flavone glycosides, ginkgolides, bilobalides and other constituents. pharmacological effects include peripheral arterial dilation, free radical scavanging, inhibition of reactive oxygen species formation, inhibition of lipid peroxidation, activation of energy metabolism, decreasing platelet aggregation. in therapeutic doses, the side effects are mild: gastro-intestinal irritation, headache, allergic skin reations. very large doses have been reported to cause diarrhea, nausea, vomiting and restlessness. a few case reports described spontaneous bleedings related to ginkgo biloba. experiments with ginkgo biloba on rat models of tbi showed that the extract improved the behavioural outcome in the injured animals, and histology demonstrated that the treated rats developed less cerebral edema in response to injury (4). nootropics nootropic drugs form a large group of substances known to enhance cognitive abilities in cerebrovascular, involutive and post-traumatic disorders. currently, they are successfuly used as part of the rehabilitation therapy for the patients with chronic tbis. no significant adverse reactions have been reported. pyritinol (encephabol, enerbol) the compound is chemically affined to pyridoxine and penicillamine. it facilitates the passing of glucose across the bloodbrain barrier and increases its metabolism in neuronal tissue; also has antioxidant properties (44). pyritinol is successfuly used as an immune-enhancer in rheumatoid arthritis (50). it has been tested in small clinical studies for comatose patients (after head traumas). the results showed slightly improved neurological outcome and a significant decrease in mortality (18, 102). the drug is generally well tolerated; adverse reactions are more frequent with prolonged administration and high doses: agitation, insomnia, gastrointestinal symptoms, nausea, headache, and rarely allergies. a survey of six cases suggested a link between 18 g. onose et al traumatic brain injury pyritinol and severe cholestatic hepatitis (58); another rare side effect is acute pancreatitis (89). racetams piracetam (pyracebral, nootropil, pyramen, gabacet) is a cyclic derivative of gaba (gamma-aminobutyric acid). its proposed mechanisms of action are: improvement of cross-hemispheric information transfer, stimulation of the cholinergic system (via muscarinic receptors), decrease of neuronal oxygen consumption, increase of glucose oxidation, with subsequent atp formation. clinical studies indicate a weak protective effect against hypoxia. piracetam has been extensively studied for its beneficial effects in dyslexia (probably due to the enhancement of crosshemispheric communication). yet, a recent clinical study found no significant improvements on speech disorders after ischemic stroke with prolonged (6 months), high doses of piracetam (36). a polish clinical trial, which included 100 patients, concluded that high doses of piracetam improved clinical outcome in head injury patients, if started immediately after the trauma (33). still, a recent paper classifies piracetam among the drugs detrimental for neuroprotection (40). pramiracetam (pramistar®) is a liposoluble racetam derivative. recent clinical trials indicate that it might be the most potent nootropic substance. it accelerates the acethylcholine turnover by activating the hacu (high affinity choline uptake) system and the nitric oxide-synthase, it inhibits the cerebral neuropetidase, it has antidepressant actions. reports suggested that the drug improved cognition in tbi patients (57). anaesthetic agents anaesthetic agents are used during brain surgery or in head traumas refractory to conventional therapy. some authors used them prophylactically, in an attempt to improve outcome in tbi patients. anaesthetics make the object of another of our articles, and are only briefly discussed in the present paper. we will mention that of all the clinically available anaesthetics, the barbiturates seem to have the greatest neuroprotective potential (26). they reduce the functional activity of the brain, the cerebral metabolic rate of oxygen (cmro2), therefore lowering the cerebral metabolic demands (94), the cerebral blood flow and the intracranial pressure (icp). this results in an increase of global cerebral perfusion and oxygenation. there have been many published clinical trials with barbiturates in head injury patients, but none of them demonstrated that this therapy has significant benefits. moreover, barbiturates were associated important complications, like hypotension, infection, hypothermia( 81) and severe hypokalaemia with rebound hyperkalaemia (62). in conclusion, analysis of currently available data on the use of barbiturates shows that they might be beneficial in selected, hemodynamically stable, patients with important, intractable elevations of icp. sex hormones the observation that female laboratory animals recover better than males after traumatic and ischemic brain injuries (5, 51, 78) led to the hypothesis that progesterone and estrogens might have neuroprotective properties. subsequent studies showed that romanian neurosurgery (2011) xviii 1: 11 – 30 19 both estrogen and progesterone reduce the effects of tbi when administered to males or ovariectomized females (64). while estrogens were also shown to exacerbate the brain damage, especially in animal models of ischemic stroke (16, 38), progesterone had no significant side effects in preclinical studies. it could be given to both males and females, without affecting gender differentiation and sexual functions (88). intensive research during the last decade demostrated that sex steroid hormones are up-regulated in the cns following traumatic injuries (31) and exert an important neuroprotective and neuroregenerative effect. the mechanisms for these beneficial effects are complex, diverse and not completely understood. it has been demonstrated on animal models that progesterone markedly reduces edema after brain injury (16), modulates glial cell activity (31), decreases lipid peroxidation, reduces the expression of proinflammatory genes, attenuates mitochondrial dysfunction (87), decreases pro-apoptotic and increases anti-apoptotic enzymes (24), enhances remyelination, synaptogenesis and dendritic arborization (75). a phase ii randomized, double-blind, placebo-controlled clinical trial (called ‘protect’) was conducted at the emory university, atlanta, to test the effects and assess the safety of intravenous progesterone in acute tbi. the study enrolled 100 adults with blunt head injury. the progesterone administration was started within the first 11 hours of initial trauma and patients were re-assessed at 30 days. the results of the study showed that no significant adverse effects were found, and progesterone reduced the 30-day mortality to less than half of the controls. in the treated group, the patients with moderate tbi had better functional scores, but those with severe head injury had longer duration of coma (109). other small clinical studies gave encouraging results with the use of this hormone in both, male and female patients (86) and several phase ii and iii clinical studies are currently ongoing or recruiting, to study the effects of intravenously administered progesterone in acute tbi (42). trh and analogs the tripeptide thyrorotropin-releasing hormone (trh, protirelin) and some of its analogues have long been recognized as neuroprotective factors. studies showed that trh administration improves neurological outcome in animal models of cns trauma (29, 99). protirelin and its analogues seem to antagonize a variety of mechanisms that lead to the secondary damage in tbi: the opiate receptor activation by injury-induced endorphin release, the glutamate toxicity (99), the lipid peroxidation, the inflammatory cytokines. a major drawback for the clinical use of these compounds as neuroprotectives are their undesired endocrine, autonomic and analeptic effects. also, trh has a poor blood-brain barrier penetration and this raises the problem of the route of administration. a small clinical trial was conducted in california with intravenous trh in patients with acute spinal cord injuries. they found no significant side effects; the treated group showed a better neurological outcome, but these results are difficult to interpret, given the small number of patients included in the study (72). there have been no clinical trials to test trh in tbi. 20 g. onose et al traumatic brain injury several analogues with better brain penetration and lesser endocrine effects have been synthesized, and some of them are currently under evaluation for possible entry into future trials (27, 28). xenon gas xenon is a naturally occuring gas that may prevent or ameliorate acute neuronal injury, as it seems to inhibit the activity of glutamate receptors (106). brain damage, with neurocognitive deficit, is for instance, a potential postoperative-complication following coronary artery by-pass grafting (cabg). one study showed that xenon administration before cabg, while on hypothermic cardiopulmonary bypass, using both a standard anesthetic breathing circuit and the oxygenator had no harmful effects (53). anti-excitocitotoxic agents the recognition of the role of excessive amounts of glutamate in the intracellular calcium accumulation in cns lesions has opened an entirely new research field. the role of excitatory neurotransmitters in the progression of various neurologic disorders, including trauma, stroke, dementia, multiple sclerosis, epilepsy, glaucoma is attracting more and more attention (65). currently, the glutamate-receptor antagonists are probably the most important issue in neuroprotection research. figure 2 schematic synthesis of the main effects of glutamate and, consequently, of its blockers. legend: ca2+ – calcium ions; nos – nitric oxyde synthase; no – nitric oxyde; pla2 – phospholipase a2; ros – reactive oxygen species; aa – arachidonic acid; lts – leucotriens; pgf2α – prostaglandin f2α; txa2 – tromboxane a2 (g. onose et al. integrative emphases on intimate, intrinsic propensity/ pathological processes – causes of self recovery limits and also, subtle related targets for neuroprotection/ pleiotropicity/ multimodal actions, by accessible therapeutic approaches in spinal cord injuries. journal of medicine and life, 3(3): 262-74, 2010) romanian neurosurgery (2011) xviii 1: 11 – 30 21 glutamate has 4 types of receptors: nmda (n-methyl-d-aspartic acid), ampa (alpha-amino-3-hydroxy-5methylisoxazole-4-propionic acid), kainic acid and the metabotropic receptors, linked to the g protein. a large number of glutamate receptors has been identified, and as a consequence, a huge variety of glutamate antagonists were developed and studied. unfortunately, several clinical trials of glutamate antagonists failed to confirm the encouraging data from in vitro and in vivo studies. selfotel (cgs19755), a competitive nmda blocker, was the first glutamate antagonist that underwent phase iii clinical trial in tbi, but the research project had to be shut down due to an increased mortality report from the simultaneously running stroke trials (7, 65). dexanabinol (hu-211) is a cannabinoid and a non-competitive nmda antagonist. it also acts as a free radical scavanger inflammatory cytokine inhibitor. in phase ii trials, results showed if administered within 6 hours of injury, it reduced mortality, it lowered icp and had no significant side effects. but the recently published results of o phase iii multicentric clinical trial, involving 861 patients with severe tbi demonstrated that though it is safe, dexanabinol has no therapeutic benefits in head injuries (54). traxoprodil (cp-101,606) is a noncompetitive nmda antagonist, highly selective for the nr2b subunit. phase ii clinical trials found it to be safe, but with no consistent therapeutic benefits. a phase iii randomized, double-blind, placebocontrolled trial tested the efficacy of a 72hour infusion of traxoprodil, started within 8 hours of the initial brain injury. it provided no substantial evidence of the drug’s efficacy in tbi (115). eliprodil also failed to show any therapeutic efficacy. aptiganel (cerestat) another noncompetitive nmda antagonist, entered a clinical trial, but the study was stopped following negative reports from the concurrently running ischemic stroke trial (65). d-cpp-ene (sdz eaa-494) a competitive nmda antagonist, failed to demonstrate any benefit in a phase iii clinical trial. xenon, an anaesthetic gas, has also been identified as a non-competitive nmda receptor antagonist. studies on neuronal cultures and lab animals demonstrated that it provides protection against hypoxiainduced excitotoxicity (41, 69, 70). the advantage of xenon is its long history of clinical use (as an anaesthetic) which has proven it safe in humans. nutritional supplements magnesium is a non-competitive nmda antagonist and it may exert neuroprotective actions through several other mechanisms: increased cerebral blood flow to ischemic areas, competitive antagonist at all voltage-sensitive calcium channels, amendament of cellular energy metabolism, enhanced mitochondrial calcium buffering. studies on animal models of brain trauma showed that magnesium sulfate infusion, administered immediately after injury, significantly reduces the tissue loss and improves neurological outcome (14, 39). a pilot clinical trial was conducted to test the safety and efficacy of field administration of intravenous magnesium sulfate in acute stroke patients (the fast 22 g. onose et al traumatic brain injury mag trial). the results were encouraging: magnesium significantly ameliorated recovery with no severe side effects (one patient with skin flushing) (80). currently, the fast-mag trial is recruiting patients for phase iii (42). magnesium appears to be a promising neuroprotective tool in tbi, but further evaluation is needed. ca2+ channel antagonists the proposed mechanisms of action for calcium-channel blockers in tbi are the reduction of the calcium cellular influx and the prophylaxis/ lysis of the cerebral vasospasm that may accompany acute traumas, especially when subarachnoid hemorrhage (sah) is associated (7). nimodipine (nimotop) is dihydropyridine calcium channel blocker. since it has greater lipid solubility than the other similar compounds and consequently some selectivity for the cerebral vasculature, the drug is already established for the prevention and treatment of cerebral vasospasms. it is approved by fda, in oral administration, for the therapy of cerebral ischemia following sah (2, 23). the use of nimodipine in unselected tbis is however questionable, given the known side effects of calcium-channel blockers: systemic hypotension, cerebral vasodilation, decreased cerebrovascular reactivity. large clinical studies, led by the head injury trial group (hit i, ii and iii) were carried on in unselected tbi patients in europe and they and they found some outcome improvements in injuries associated with traumatic sah (61, 95). a review of six randomised controlled trials with nimodipine in unselected patients with acute tbi concluded that the drug may only have some beneficial effects in selected subjects, with sah, while being potentially harmful in other brain injuries (49). another review, of four randomised controlled trials with nimodipine for traumatic sah, found no beneficial effects (98). dopamine agonists dopamine agonists are used as cortical stimulants, to treat a variety of neurological symptoms: aphasia, akinetic mutism, amotivational syndrome/ apathy/ abulia/ anergia, attention disorders, neglect, depression (34). recent studies suggested that these compounds may also provide neuroprotection by inhibiting glutamate neurotoxicity (83). bromocriptine, an ergot alkaloid is a potent agonist for d2 dopamine receptors and some serotonine receptors, currently used in the treatment of pituitary tumors (with hyperprolactinaemia or acromegaly), parkinson's disease, neuroleptic malignant syndrome, and type 2 diabetes. it has been shown to interfere with the activity of astroglial glutamate transporter glt-1 (eaat2) (83). bromocriptine has been used with good clinical results in the paroxysmal autonomic instability with dystonia (paid)/ “diencephalic seizures” – a syndrome consisting in tachicardia, tachipneea, hyperthermia, diaphoresis and decerebrate posturing, following severe tbis (10, 15). also, the administration of bromocriptine to posttraumatic vegetative state and minimally conscious state patients led to improvements of the motor and cognitive outcomes (66). the most common side reactions of bromocriptine are: orthostatic hypotension, nausea, headaches and vomiting, liver toxicity (107). romanian neurosurgery (2011) xviii 1: 11 – 30 23 cholinergic agents cholinergic agents (rivastigmine – exelon) are currently used in the treatment of mild to moderate dementia in alzheimer’s and parkinson's diseases, with some beneficial results in cognitive functions. their use is based on the hypothesis that the cholinergic system stimulates brain areas related to learning and memory. citicoline – cytidine diphosphatecholine (cdp-choline) is an intermediate product in the generation of phosphatidylcholine from choline. it is sold in many countries as a psychostimulant/ nootropic dietary supplement. the presumed mechanisms for it’s neuroprotective effects include: counteracting excitotoxicity, maintaining cellular adenosine 5'-triphosphate levels, stimulating neuronal plasticity (43). it has been used for many types of cognitive impairment, especially of vascular and degenerative ethiology (30). a few small clinical studies reported significant improvements with the use of this compound (20), but larger trials are needed to establish the efficacy of citicoline. apoptosis inhibitors traditionally, neuroprotective therapies have been mainly focused on reducing necrotic cell death, by antagonizing various factors that eventually lead to the failure of cellular metabolism. but after cns trauma, necrosis is an early event, and the therapeutic window for these strategies is short. recent experimental work substantiated the important role of apoptosis as a secondary injury mechanism. in contrast to necrosis, apoptosis is a more delayed process, that enreels for days, even weeks after the initial trauma, which is why modulating it is likely to be a more effective approach. apoptotic inhibitors are currently in the experimental phase, but they are a dynamic and very promising research field. calpain inhibitors calpains are constitutively expressed intracellular, non-lysosomal cysteine proteases. they are classified as ubiquitous and tissue-specific. the ubiquitous isoforms, μ-calpains (or calpains i) and mcalpains (or calpains ii), are abundantly expressed in the central nervous system (cns). their activation requires the presence of ca2+ (in micromolar concentrations for calpains i and in millimolar concentrations for calpains ii) (73). figure 3 activation of calpains within the calpains pathway of apoptosis (g. onose et al. integrative emphases on intimate, intrinsic propensity/ pathological processes – causes of self recovery limits and also, subtle related targets for neuroprotection/ pleiotropicity/ multimodal actions, by accessible therapeutic approaches in spinal cord injuries. journal of medicine and life,3(3): 262-74, 2010) although various calpain substrates have been identified (cytoskeletal proteins, growth factor receptors, adhesion molecules, transcription-related proteins), the precise function of these enzymes in vivo is still poorly understood (111). the massive cellular ca2+ influx associated with cns injury inevitably activates calpains, which, in conjunction with caspases, promote irreversible damages to 24 g. onose et al traumatic brain injury key cellular structures that finally lead to apoptosis. the endogenous specific inhibitor of calpains is calpastatin (cast), but overactivation of calpain may degrade calpastatin. a number of cell-permeable calpain inhibitors (e.g. epoxysuccinate derivatives, aldehydes, and alpha-keto carbonyl compounds) (71) have been synthesized and tested on animal models of tbi and other cns injuries, and some of them showed important neuroprotective effects (47, 73). caspase (cysteinyl aspartic acid-protease) inhibitors based on their substrate specificity, there have been identified 14 mammalian caspases (110). these enzymes are translated as zymogen proforms and upon activation, caspases may cleave their own precursors or other procaspases, resulting in a caspase activation cascade (112). caspases are involved in several interrelated apoptotic pathays, which are not yet completely understood. caspase-3 has received most of attention, since it appears to be the major effector in neuronal apoptosis. initial strong evidence supporting the specific role for this protease came from studies on caspase-3 knock-out mice, in which brain development was severely altered (110). later, in vivo and in vitro experiments with semispecific peptide caspase inhibitors (z-devd-fmk, zietd-fmk, z-lehdfmk) (8) established the role of this protease in injury-induced neuronal loss (47). cathepsin inhibitors like calpains, cathepsins also belong to the papain superfamily of cystein proteases. cathepsins are found predominantly in the lysosomes, but also in the cell nuclei and cytosol. these enzymes have also been implicated in neuronal injury, and inhibitors such as ca-074 and e-64c have been proven to significantly decrease neuronal death(113). parp-1 [poly(adp-ribose) polymerase -1] inhibitors recent research shows that while mild damages to dna activate the repair mechanisms, severe insults induce parp-1 overactivation and cell death (11). parp-1 is an abundant nuclear protein, functioning as a dna damage-sensor and signaling molecule. upon binding to dna breaks, activated parp-1 cleaves nad+ into nicotinamide and adp-ribose and polymerizes the latter into branched nucleic acid-like polymers, covalently attached to nuclear acceptor proteins. the negative charge of these covalently attached adpribose polymers severely alter the function of target proteins (such as histones, topoisomerases, dna polymerases, dna ligases, transcription factors and parp-1 itself) (11). researchers tested a large number of parp-1 inhibitors (nicotinamide, 3aminobenzamide, monoaryl amides, bi-, tri-, or tetracyclic lactams), most of them acting as competitive inhibitors that block the binding of nad+ to the catalytic domain of the enzyme. some benzamides have also been shown to inhibit the binding of parp to dna(104). many of these compounds have been shown to protect neuronal tissue against various insults, in vitro and in vivo (91, 101). a recent study demonstrated that minocycline and other tetracycline derivatives, previously researched for their neuroprotective properties, also inhibit parp-1 activity and reduce neuronal death (1). romanian neurosurgery (2011) xviii 1: 11 – 30 25 antioxidants oxidative stress in one of the key mechanisms of secondary injury in cns traumas and an attractive target for neuroprotection. the oxygen free radicals cause peroxidation of membrane phospholipids and oxidation of cellular proteins and nucleic acids, damaging both neurons and cerebral vasculature. superoxide dismutase (sod) sod is a physiological antioxidant, an enzyme that reduces the superoxide anion concentration by dismutation to hydrogen peroxide, which is then converted to water. sod has a very short half-life (of about 5 minutes), which limits its clinical utility, but conjugation with polyethylene glycol (peg) extends its half-life to approximately 5 days (105). the polyethylene glycol-conjugated sod (peg-sod, pegorgotein) proved to be safe in phase ii clinical trials and seemed to improve the outcome of head-injured pacients (59). as a consequence, it underwent a phase iii, multicentric, randomized, placebo-controlled trial. the study enrolled 463 patients with severe, closed head injury. the treated groups received a single intravenous dose of eithr 10 000 u/kg, or 20 000 u/kg of pegorgotein. no significant difference in neurologic outcome or mortality was found at 3 or 6 months between the treated groups and the placebo group (114). new / experimental procedures local hypothermia hypothermia (the intentional reduction of core temperature below 36°c) is thought to protect the blood-brain barrier and prevent inflammation, the development of vasogenic edema and intracranial hypertension, while decreasing cerebral metabolic rate for oxygen and energy requirements (94, 106). whole body hypothermia has been intensively studied as a neuroprotective intervention, especially in newborn. a number of clinical trials studied the effects of general hypothermia in ischemic stroke, neonatal hypoxicischemic encephalopathy and ischemic stroke (42). though experimental and clinical results showed that this procedure exerts some neuroprotective effects, the use of whole body cooling is hindered by serious complications (e.g. sedation, arrhythmia, coagulopathies, increased risk of infection, tremor, hypotension, hyperkalaemia) (79, 94). local hypothermia is a newer and apparently safer intervention. experiments showed that even profound local hypothermia does not damage cortical neurons (106). a phase iii clinical trial is currently on going, to assess the feasibility and efficacy of discrete cerebral hypotermia in tbi (42). hyperbaric oxygen therapy oxygen is largely used as a therapeutic agent. hyperbaric oxygen therapy consists in administering 100% oxigen at pressures higher than 1 atmosphere (0,1mpa) using a small hyperbaric chamber or a mask (9). this procedures achieves hyperoxia, leading to an increase of the physically disolved blood oxygen, wich is proportional to the partial pressure of the oxygen in the ambient. hyperoxia exerts a variety of beneficial effects: improvement of tissue oxygenation, decrease of inflammation, stimulation of tissue repair mechanisms, antibacterial effects and consequently it has a broad range of clinical applications, for conditions that involve ischemia, impairment of tissue repair, inflammation, infection. hyperbaric 26 g. onose et al traumatic brain injury oxygen is an an established therapy, approved in many countries for many indicatons such as: monoxide poisoning, decompression sickness, gas embolism, necrotizing soft tissue infections, diabetic wounds, osteoradionecrosis. (9). the main concern with the use of hyperbaric oxygen therapy is systemic vasoconstriction (9), but the extensive clinical experience with this procedure proved it’s safety if application parameters are rigourously controlled (duration, pressure). a consistent body of research exists for the use of this intervention in tbi and it has been suggested that, despite the cerebral vasoconstriction it produces, hyperoxia has many beneficial actions that may sum up to better rehabilitative outcomes: increasing the partial pressure of oxygen in brain tissue, restoring the mitochondrial redox potential (enhancing damaged mitochondrial recovery) (19, 76), decreasing intracranial pressure (9,77). a prospective, randomized clinical trial compared the effect of hyperbaric to normobaric hyperoxia when aplied to severe tbi patients within 24 hours of injury; while both procedures increased brain oxygenation and improved indices of oxidative metabolism (in comparison to the control group), only hyperbaric oxygen lowered intracranial pressure. however, these effects were transient, lasting only a few days after the intervention. no significant adverse reactions were recorded (77). a phase ii clinical trial is presently on going to assess the feasibility of hyperbaric oxygen therapy in patients with chronic sequelae following brain injury (42). conclusions in experimental conditions, various pharmachological agents lead to impressive reductions in the extent of brain damage and consequent significant neurological recovery after tbi, inciting high expectations of a clinical benefit. but to date, all the clinical trials failed to demonstrate a radical improvement with any of these agents. furthermore, many of these substances (like many glutamate receptor antagonists) were found to have serious side effects. yet, on one hand, compound products such as cerebrolysin (more and more largely used and tested in standardized, multicentric clinical trials – including our involvement for one of them) and on the other, citicoline (which, as previously emphasized, is considered in in many countries a supplement – and therefore is easily accesible and very widely) seem to be in a recent prestigious review (40) the most efficient substances used in connection with neurorehabilitation practice. novel achievements in neuroprotection are now expected from developing anti-apoptotic agents (such as caspase and/or calpain inhibitors), from more potent antioxidants, cholinergic agents, alpha blockers, from researching various physiologic substances, like protirelin, inosine, progesterone, and including from regenerative medicine and physiatric, assisstive technology/ bioengineering advancements, all within multidisciplinary and intricate endeavours – on a still long and windy road. romanian neurosurgery (2011) xviii 1: 11 – 30 27 references 1. alano cc, kauppinen tm, valls av, swanson ra. minocycline inhibits poly(adp-ribose) polymerase-1 at nanomolar concentrations. proc natl acad u s a. 2006, 103(25): 9685-90 2. al-tamimi yz, orsi nm, quinn ac, homervanniasinkam s, ross sa. a review of delayed ischemic neurologic deficit following aneurysmal subarachnoid hemorrhage: historical overview, current treatment, and pathophysiology. world neurosurg. 2010, 73(6): 65467 3. alvarez xa, sampedro c, perez p et al. positive effects of cerebrolysin on electroencephalogram slowing, cognition and clinical outcome in patients with post-acute traumatic brain injury: an exploratory study. int clin psychopharmacol. 2003, 18(5): 271-78 4. attella mj, hoffman sw, stasio mj, stein dg. ginkgo biloba extract facilitates recovery from penetrating brain injury in adult male rats. exp neurol. 1989, 105(1): 62-71 5. attella mj, nattinville a et al. hormonal state affects recovery from frontal cortex lesions in adult female rats. behav neural biol. 1987, 48(3): 352-67 6. barr jd, mathis jm, horton ja. transient severe brain stem depression during intraarterial papaverine infusion for cerebral vasospasm. am j neuroradiol. 1994, 15(4): 719-23 7. beauchamp k, mutlak h, smith wr, shohami e, stahel pf. pharmacology of traumatic brain injury: where is the "golden bullet"? mol med. 2008, 14(1112):731-40 8. berger ab, sexton kb, bogyo m. commonly used caspase inhibitors designed based on substrate specificity profiles lack selectivity. cell res. 2006, 16(12): 961-3 9. bitterman h. bench-to-bedside review: oxygen as a drug. critical care 2009, 13:205-12 10.blackman ja, patrick pd, buck ml, rust rs. paroxysmal autonomic instability with dystonia after brain injury. arch neurol. 2004, 61: 321-8 11.blackman s. a matter of life and cell death: solidifying parp's role in dna repair and apoptosis. the scientist. 2005, 19(4): 22-3 12.boiarinov ga, penkovich aa, mukhina iv. the metabolic effects of the neurotropic action of actovegin during hypoxia. eksp klin farmacol. 1999, 62(2): 61-3 13.bonocz p, gulyas b, adam-vizi v, et al. role of sodium channel inhibition in neuroprotection: effect of vinpocetine. brain res bull. 2000, 53: 245-54 14.browne kd, leoni mj, iwata a, chen xh, smith dh. acute treatment with mgso4 attenuates longterm hippocampal tissue loss after brain trauma in the rat. j neurosci res. 2004, 77(6): 878-83 15.bullard de. diencephalic seizures: responsiveness to bromocriptine and morphine. ann neurol. 1987, 21: 609-11 16.carswell hv, bingham d, wallace k, nilsen m, graham di, dominiczak af, macrae im. differential effects of 17β-estradiol upon stroke damage in stroke prone and normotensive rats. cerebr blood flow metab. 2004, 24(3): 298-304 17.dalbasti t, karabiyikoglu m, ozdamar n, oktar n, cagli s. efficacy of controlled-release papaverine pellets in preventing symptomatic cerebral vasospasm. j neurosurg. 2001, 95(1): 44-50 18.dalle ore g, bricolo a, alexandre a. the influence of the administration of pyritinol on the clinical course of traumatic coma. j neuroserg sci. 1980, 24(1): 1-8 19.daugherty wp, levasseur je, sun d, rockswold gl, bullock r: effect of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid percussion injury in rat. j neurosurg. 2004, 101: 499-504 20.dávalos a, secades j. citicoline preclinical and clinical update 2009-2010. stroke. 2011, 42(1 suppl): s36-9 21.dawodu st. traumatic brain injury (tbi) – definition, epidemiology, pathophysiology. http://emedicine.medscape.com/article/326510overview 22.deszi l, kis-varga i, nagy i, komlodi z, karpati e. neuroprotective effects of vinpocetine in vivo and in vitro. apovincaminic acid derivatives as potential therapeutic tools in ischemic stroke. acta pharm hung. 2002, 72(2): 84-91 23.dipalma jr. nimodipine in subarachnoid hemorrhage. am fam physician. 1989, 40: 143-5 24.djebaili m, guo q, pettus eh, hoffman sw, stein dg. the neurosteroids progesterone and allopregnanolone reduce cell death, gliosis, and functional deficits after traumatic brain injury in rats. j neurotrauma. 2005, 22(1): 106-18 25.dutov aa, gal’tvanitsa ga, volkova va, sukhanova on, lavrishcheva tg, petrov ap. cavinton in the prevention of the convulsive syndrome in children after birth injury. zh nevropatol psikhiatr im s s korsakova. 1991, 91(8): 21-2 26.eisenberg hm, frankowski rf, contant cf, marshall lf, walker md. high-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. j neurosurg. 1988 69(1): 15-23 27.faden ai, knoblach sm, cernak i. novel diketopiperazine enhances motor and cognitive recovery after traumatic brain injury in rats and shows neuroprotection in vitro and in vivo. j cereb blood flow metab. 2003, 23(3): 342-54 28.faden ai, knoblach sm, movsesyan va, cernak i. novel small peptides with neuroprotective and nootropic properties. j alzheimers dis. 2004, 6[suppl]: 593-7 29.faden ai. trh analog ym-14673 improves outcome following traumatic brain and spinal cord injury in rats: dose-response studies. brain res. 1989, 486: 228-35 28 g. onose et al traumatic brain injury 30.garcía-cobos r, frank-garcía a, gutiérrezfernández m, díez-tejedor e. citicoline, use in cognitive decline: vascular and degenerative. j neurol sci. 2010, 299(1-2): 188-92 31.garcia-ovejero d, azcoitia i, doncarlos ll, melcangi rc, garcia-segura lm. glia-neuron crosstalk in the neuroprotective mechanisms of sex steroid hormones. brain res. 2005, 48(2): 273-86 32.gomazkov oa. apoptosis in neuronal structures and the role of neurotrophic growth factors. biochemical mechanisms of brain derived peptide preparations. zh nevrol psikhiatr im s s korsakova. 2002, [suppl7]: 17-21 33.goscinski i, moskaia m, cichonski j et al. clinical observations concerning piracetam treatment of patients after craniocerebral injury. przegl lek. 1999, 56(2): 119-20 34.gualtieri t. brain injury and mental retardation: psychopharmacology and neuropsychiatry. lippincott williams & wilkins, philadelphia, 2002 35.guekht ab, moessler h, novak ph, gusev ei; on behalf of the cerebrolysin investigators. cerebrolysin in vascular dementia: improvement of clinical outcome in a randomized, double-blind, placebo-controlled multicenter trial. j stroke cerebrovasc dis, 2010 jul 23. [epub ahead of print] 36.güngör l, terzi m, onar mk. does long term use of piracetam improve speech disturbances due to ischemic cerebrovascular diseases? brain lang. 2011 jan 10. [epub ahead of print] 37.halliday al. pathophysiology. in: marion dw, editor. traumatic brain injury. ny: thieme medical publishers. 1999, p. 29-38 38.harukuni i, hurn pd, crain bj. deleterious effect of beta-estradiol in a rat model of transient forebrain ischemia. brain res. 2001, 900(1): 137-42 39.heath dl, vink r. improved motor outcome in response to magnesium therapy received up to 24 hours after traumatic diffuse axonal brain injury in rats. j neurosurg. 1999, 90(3): 504-9 40.hoemberg v. pharmacology in neurorehabilitation. invited lecture at the 6th world congress for neurorehabilitation, viena, 2010 41.homi hm, yokoo n, ma d et al. the neuroprotective effect of xenon administration during transient middle cerebral artery occlusion in mice. anesthesiology. 2003, 99(4): 876-81 42.http://clinicaltrials.gov 43.hurtado o, lizasoain i, moro má. neuroprotection and recovery: recent data at the bench on citicoline. stroke. 2011, 42(1 suppl): s33-5 44.jiménez-andrade gy, reyes-garcía g, sereno g, ceballos-reyes g, vidal-cantú gc, granados-soto v. pyritinol reduces nociception and oxidative stress in diabetic rats. eur j pharmacol. 2008, 590(1-3): 170-6 45.kanowski s, kinzler e, lehmann e, schweizer a, kuntz g. confirmed clinical efficacy of actovegin in elderly patients with organic brain syndrome. pharmacopsychiatry. 1995, 28(4): 125-33 46.knoblach sm, alroy da, nikolaeva m, cernak i, stoica ba, faden ai. caspase inhibitor z-devd-fmk attenuates calpain and necrotic cell death in vitro and after traumatic brain injury. j cereb blood flow metab. 2004, 24(10): 1119-32 47.kuida k, zheng ts, na s et al. decreased apotosis in the brain and premature lethality in cpp32-deficient mice. nature. 1996, 384: 368-72 48.ladurner g, kalvach p, moessler h; cerebrolysin study group. neuroprotective treatment with cerebrolysin® in patients with acute stroke: a randomised controlled trial. j neural transm. 2005, 112(3): 415-28 49.langham j, goldfrad c, teasdale g, shaw d, rowan k. calcium channel blockers for acute traumatic brain injury. cochrane database syst rev. 2003;(4): cd000565 50.lemmel em. comparison of pyritinol and auranofin in the treatment of rheumatoid arthritis. the european multicentre study group. br j rheumatol. 1993, 32(5): 375-82 51.liao s, chen w, kuo j, chen c. association of serum estrogen level and ischemic neuroprotection in female rats. neurosci lett. 2001, 297: 159-62 52.liu jk, tenner ms, gottfried on, et al. efficacy of multiple intraarterial papaverine infusions for improvement in cerebral circulation time in patients with recurrent cerebral vasospasm. j neurosurg. 2004, 100(3): 414-21 53.lockwood gg, franks np, downie na, taylor km, maze m. feasibility and safety of delivering xenon to patients undergoing coronary artery bypass graft surgery while on cardiopulmonary bypass: phase i study. anesthesiology. 2006, 104(3): 458-65 54.maas ai, murray g, henney h 3rd et al. efficacy and safety of dexanabinol in severe traumatic brain injury: results of a phase iii randomised, placebocontrolled, clinical trial. lancet neurol. 2006, 5(1): 38-45 55.macheret il, khanenko nv. drug therapy of patients with dyscirculatory encephalopathy. lik sprava. 2002, 3-4: 84-7 56.maillo l. anaphylactic shock with multiorgan failure in a cyclist after intravenous administration of actovegin. ann intern med. 2008, 148(5) :407 57.malykh ag, sadaie mr. piracetam and piracetamlike drugs: from basic science to novel clinical applications to cns disorders. drugs. 2010, 70(3): 287-312 58.maria v, albuquerque a, loureiro a, sousa a, victorino r. severe cholestatic hepatitis induced by pyritinol. bmj. 2004, 328(7439): 572-4 59.muizelaar jp, marmarou a, young hf. improving the outcome of severe head injury with the oxygen radical scavenger polyethylene glycol-conjugated romanian neurosurgery (2011) xviii 1: 11 – 30 29 superoxide dismutase: a phase ii trial. j neurosurg. 1993, 78(3): 375-82 60.mureşanu d. neuroprotection and neuroplasticity in traumatic brain injury and spinal cord trauma. communication at the 5th congress of the romanian society of neurosurgery, with international participation, tg. mureş, romania, oct., 2005 61.murray gd, teasdale gm, schmitz h. nimodipine in traumatic subarachnoid haemorrhage:a re-analysis of the hit i and hit ii trials. acta neurochir. 1996, 138: 1163-7 62.neil mj, dale mc. hypokalaemia with severe rebound hyperkalaemia after therapeutic barbiturate coma. anesth analg. 2009, 108(6): 1867-8 63.nyakas c, felszeghy k, szabó r, keijser jn, luiten pg, szombathelyi z, tihanyi k. neuroprotective effects of vinpocetine and its major metabolite cisapovincaminic acid on nmda-induced neurotoxicity in a rat entorhinal cortex lesion model. cns neurosci ther. 2009, 15(2): 89-99 64.o’connor ca, cernak i, vink r. both estrogen and progesterone attenuate edema formation following diffuse traumatic brain injury. brain res. 2005, 1062(12): 171-4 65.palmer gc. neuroprotection by nmda receptor antagonists in a variety of neuropathologies. curr drug targets, 2001, 2: 241-71 66.passler ma, riggs rv. positive outcomes in traumatic brain injury-vegetative state: patients treated with bromocriptine. arch phys med rehabil. 2001, 82(3):311-5 67.patockova j, krsiak m, marhol p, tumova e. cerebrolysin inhibits lipid peroxidation induced by insulin hypoglycemia in the brain and heart of mice. physiol res. 2003, 52(4): 455-60 68.pereira c, agostinho p, moreira pi, duarte ai, santos ms, oliveira cr. neuroprotection strategies: effect of vinpocetine in vitro oxidative stress models. acta med port. 2003, 16(6): 401-6 69.petzelt c, blom p, schmehl w, muller j, kox wj. prevention of neurotoxicity in hypoxic cortical neurons by the noble gas xenon. life sci. 2003, 72(17): 1909-18 70.petzelt c, blom p, schmehl w, muller j, kox wj. xenon prevents cellular damage in differentiated pc-12 cells exposed to hypoxia. bmc neurosci. 2004, 5: 55-63 71.pietsch m, chua kc, abell ad. calpains: attractive targets for the development of synthetic inhibitors. curr top med chem. 2010, 10(3): 270-93 72.pitts lh, ross a, chase ga, faden ai. treatment with thyrotropin-releasing hormone (trh) in patients with traumatic spinal cord injuries. j neurotrauma, 1995, 12(3): 235-43 73.ray sk, banik nl. calpain and its involvement in the pathophysiology of cns injuries and diseases: therapeutic potential of calpain inhibitors for prevention of neurodegeneration. curr drug targets cns neurol disord. 2003, 2(3): 173-89 74.riley c, hutter-paier b, windisch m, doppler e, moessler h, wronski r. a peptide preparation protects cells in organotypic brain slices against cell death after glutamate intoxication. j neural transm. 2006, 113(1): 103-10 75.robertson cl, puskar a, hoffman ge, murphy az, saraswati m, fiskum g. physiologic progesterone reduces mitochondrial dysfunction and hippocampal cell loss after traumatic brain injury in female rats. exp neurol. 2006, 197(1): 235-43 76.rockswold sb, rockswold gl, defillo a: hyperbaric oxygen in traumatic brain injury. neurosurg res. 2007, 29: 162-72 77.rockswold sb, rockswold gl, zaun da, et.al. a prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury. j neurosurg. 2010, 112(5): 1080-94 78.roof rl, hall ed. estrogen-related gender difference in survival rate and cortical blood flow after impact-acceleration head injury in rats. j neurotrauma. 2000, 17(12): 1155-69 79.sarkar s, barks jd. systemic complications and hypothermia. semin fetal neonatal med. 2010, 15(5): 270-5 80.saver jl, kidwell c, eckstein m, starkman s, for the fast-mag pilot trial investigators. prehospital neuroprotective therapy for acute stroke. results of the field administration of stroke therapy – magnesium (fast-mag pilot trial). stroke. 2004, 35: 106-8 81.schalen w, messeter k, nordstrom ch. complications and side effects during thiopental therapy in patients with severe head injury. acta anaesthesiol scand 1992, 36: 369-77 82.schauer e, wronski r, patockova j et al. neuroprotection of cerebrolysin® in tissue culture models of brain ischemia: post-lesion application indicates a wide therapeutic window. j neural transm. 2006, 113(7): 855-68 83.shirasaki y, sugimura m, sato t. bromocriptine, an ergot alkaloid, inhibits excitatory amino acid release mediated by glutamate transporter reversal. eur j pharmacol. 2010, 643(1): 48-57 84.sotnikova ny, gromova oa, novikova ea, burtsev em. immunoactive properties of cerebrolysin. russ j immunol. 2000, 5(1): 63-70 85.sreedhar r, gadhinglajkar sv. pharmacological neuroprotection. indian j anaesth. 2003, 47(1): 8-22 86.stein dg, wright dw. progesterone in the clinical treatment of acute traumatic brain injury. expert opin investig drugs. 2010, 19(7): 847-57 87.stein dg. brain damage, sex hormones and recovery: a new role for progesterone and estrogen? trends neurosci. 2001, 24(7): 386-91 88.stein dg. progesterone in the treatment of traumatic brain injury. acnr. 2005, 5(4): 18-9 30 g. onose et al traumatic brain injury 89.straumann a, bauer m, pichler wj, pirovino m. acute pancreatitis due to pyritinol: an immunemediated phenomenon. gastroenterology. 1998, 115(2): 452-4 90.szilagyi g, nagy z, balkay l, et al. effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a pet study. j neurol sci. 2005, 229-30: 275-84 91.takahashi k, pieper aa, croul se, zhang j, snyder sh, greenberg jh. post-treatment with an inhibitor of poly(adp-ribose) polymerase attenuates cerebral damage in focal ischemia. brain res. 1999, 829: 46-54 92.talypov ae, ioffe ius, miatchin miu, kuksova ns. actovegin in the treatment of brain injuries of mild and moderate severity. zh nevrol psikhiatr im s s korsakova. 2008, 108(8): 20-3 93.tárnok k, kiss e, luiten pg, nyakas c, tihanyi k, schlett k, eisel ul. effects of vinpocetine on mitochondrial function and neuroprotection in primary cortical neurons. neurochem int. 2008, 53(6-8): 289-95 94.teasdale gm, bannan pe. neuroprotection in head injury. in: reilly p and bullock r, editors. head injury. london: chapman & hall; 1997, p. 423-38 95.the european study group on nimodipine in severe head injury. amulticenter trial of the efficacy of nimodipine on outcome after severe head injury. j. neurosurg. 1994, 80: 797-804 96.vajkoczy p, horn p, bauhuf c, et al. effect of intraarterial papaverine on regional blood flow in hemodinamically relevant cerebral vasospasm. stroke. 2001, 32(2): 498-505 97.vardiman ab, kopitnik ta, purdy pd, batjer hh, samson ds. treatment of traumatic arterial vasospasm with intraarterial papaverine infusion. am j neuroradiol. 1995, 16: 319-21 98.vergouwen md, vermeulen m, roos yb. effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: a systematic review. lancet neurol. 2006, 5(12): 1029-32 99.veronesi mc, aldouby y, domb aj, kubek mj. thyrotropin-releasing hormone d,l polylactide nanoparticles (trh-nps) protect against glutamate toxicity in vitro and kindling development in vivo. brain res. 2009, 1303: 151-60 100.vesel’skii ish, sanik av. the korinfar and actovegin treatment of patients with a chronic ischemic disorder of the cerebral circulation. lik sprava. 1992, 6: 116-9 101.virag l, szabo c. the therapeutic potential of poly(adp-ribose) polymease inhibitors. pharmacol rev. 2003, 54: 375-429 102.von wild k, simons p, schoeppner h. effect of pyritinol on eeg and ssep in comatose patients in the acute phase of intensive care therapy. pharmacopsychiatry. 1992, 25(3): 157-65 103.wagner kr, zuccarello m. local brain hypothermia for neuroprotection in stroke treatment and aneurysm repair. neurol res. 2005, 27(3): 238-45 104.wallis ra, panizzon kl, girard jm. traumatic neuroprotection with inhibitors of nitric oxide and adp-ribosylation. brain res. 1996, 710: 169-77 105.warner ds, sheng h, batinic-haberle i. oxidants, antioxidants, and the ischemic brain. j exp biol. 2004, 207: 3221-31 106.weigt hu, fohr kj, georgieff m, georgieff em, senftleben u, adolph o. xenon blocks ampa and nmda receptor channels by different mechanisms. acta neurobiol exp (wars). 2009, 69(4): 429-40 107.weil c. the safety of bromocriptine in long-term use: a review of the literature. curr med res opin. 1986, 10(1): 25-51 108.wong gk, zhu hl, poon ws. beneficial effects of cerebrolysin® on moderate and severe head injury patients: result of a cohort study. acta neurochir suppl. 2005, 95: 59-60 109.wright dw. progesterone for acute traumatic brain injury. acad emerg med. 2006, 13(5): 10 110.yakovlev ag, faden ai. caspase-dependent apoptotic pathways in cns injury. mol neurobiol. 2001, 24: 131-44 111.yakovlev ag, faden ai. mechanisms of neural cell death: implications for development of neuroprotective treatment strategies. neurorx. 2004, 1(1): 5-16 112.yamashima t. implications of cystein proteases calpain, cathepsin and caspase in ischemic neuronal death of primates. prog neurobiol. 2000, 62: 273-95 113.yoshida m, yamashima t, zhao l et al. primate neurons show different vulnerability to transient ischemia and response to cathepsin inhibition. acta neuropathol (berl). 2001, 104: 267-72 114.young b, runge jw, waxman ks et al. effects of pegorgotein on neurologic outcome of patients with severe head injury. a multicenter, randomized, controlled trial. jama. 1996, 276(7): 569-70 115.yurkewicz l, weaver j, bullock mr, marshall lf. the effect of the selective nmda receptor antagonist taxoprodil in the treatment of traumatic brain injury. j neurotrauma. 2005, 22(12): 1428-43 microsoft word okezieobasi_armoured_f.docx romanian neurosurgery (2012) xix 1 armoured brain: a case of bilateral calcified chronic subdural haematoma complicating infantile hydrocephalus okezie obasi kanu1, adaeze i. igwilo1, olugbenga daini2, efosam ukponmwan1, olufemi bankole1, sarajudeen oladele arigbabu1 1neurosurgery division, department of surgery lagos university teaching hospital, idi-araba, lagos state, nigeria 2radiology department, lagoon specialist hospital, apapa, lagos state, nigeria abstract chronic subdural haematoma is one of the late complications of shunting procedures. calcified chronic subdural haematoma (ccsdh) which is very rare, follows untreated or asymptomatic chronic subdural haematomas. when it occurs bilaterally it gives the typical appearance of an “armoured brain” also known as “matrioska head”. the authors present a case of bilateral ccsdh found on follow-up ct brain scan 15 years after the shunt procedure. the parents had objected to surgical drainage at the time the initial diagnosis was made. the patient is neurologically stable with functional ventriculoperitoneal shunt. the discussion includes a review of relevant literature and treatment options. keywords: armoured brain, calcified chronic subdural haematoma, infantile hydrocephalus, complications of shunts introduction chronic subdural haematomas (csdh) is one of the late complications of shunting procedures for infantile hydrocephalus (5, 9, 15, 17). calcified chronic subdural hematoma (ccsdh) is a rare condition and when it occurs bilaterally, may give the appearance of “armoured brain” (5, 12, 20) or “matrioska head” (18). the authors present a case of bilateral ccsdh in a 16 yr old male with epilepsy following a shunt procedure for infantile hydrocephalus. case report aa is a 16 yr old male (dob 24/7/1993) who was first seen at 3 months of age and treated for severe post-meningitic hydrocephalus by a ventriculoperitoneal (vp) shunt. there was also an associated seizure disorder which was controlled with antiepileptic drugs. he had a shunt revision surgery in june 1999. he had features of delayed milestone. a follow-up computerized tomography (ct) brain scan done in september 2006 showed a bilateral chronic subdural haematoma. the ventricles were normal in size and the ventricular catheter was in place. patient was essentially asymptomatic with good control of seizures. an evacuation of the csdh was planned but the parents absconded and patient was temporarily lost to follow-up. patient returned to the hospital in march 2010 and a repeat ct brain scan was performed which revealed a bilateral calcified chronic subdural haematoma; the ventricular size appeared normal with no evidence of active okezie obasi kanu et al armoured brain hydrocephalus. the ventricular catheter was in the ventricle but shows evidence of inward migration (figure 1). we elected to continue observation of this patient as there was no acute neurological deterioration. discussion chronic subdural hematoma is one of the late complications of shunting for infantile hydrocephalus. the risk of postshunting subdural hematomas in children ranges from 2.8 to 5.4% (17). calcified csdh is rare and when it occurs bilaterally may give the typical appearance of an “armoured brain” so-called because the calcified subdural collection appears as “bone under bone” or “double skull” on computerized tomographic (ct) scan (figure 2), as if a shell or carapace is encasing the brain (2, 12). sgaramella et al had used the term “matrioska head” to describe the same condition (18). ccsdh is seen more in children but has been reported in adults also (2, 6, 8, 16, 22). the reported frequency of radiologically demonstrable ccsdh ranges from 0.3 to 2.7% (11, 14, 22). the degree of calcification varies from thin rim of calcified membrane to dense calcification of the hematoma (8), and rarely ossification of the hematoma (1, 4, 11, 21). subdural hematomas occur possibly due to over-drainage of the ventricles especially in patients whose cranial sutures have fused but the pathogenesis and mechanisms of calcification are still debatable. there has been no record of this complication in patients who were treated with endoscopic third ventriculostomy. etiological factors considered include poor circulation, delayed haematoma absorption and stagnation, leading ultimately to calcification (14). figure 1 a non-contrast ct brain scan of the patient showing bilateral calcified subdural haematoma. the ventricles appear normal in size. the ventricular catheter appears insitu with evidence of minimal migration figure 2 the bone window of the same ct scan shows “bone in bone” or “double skull” appearance as a result of the calcified haematoma romanian neurosurgery (2012) xix 1 others have suggested that metabolic anomalies may also play a role (1, 19). central to these factors is time: a subdural haematoma that is not diagnosed or not drained in time and not completely resorbed will ultimately undergo calcification. this was the case in this patient whose parents objected to surgical evacuation and absconded, now returning with ccsdh. many cases of ccsdh are asymptomatic (7, 10, 11, 14), presenting as a radiological surprise in otherwise normal patients undergoing routine follow-up investigation. clinical presentations vary and include chronic headaches, new-onset or worsening seizures, dysphasia, mental retardation, deteriorating visions paresis, gait disturbance and altered sensorium (1-3, 6, 19, 24). it has been suggested that the presence of brain atrophy may have been the reason why some cases are asymptomatic (13, 14). a ct brain scan is adequate for diagnosis and is preferred (12), though magnetic resonance imaging (mri) has been used to describe the features (16, 23). our patient was managed as postinfective hydrocephalus with seizures over 15 years ago and is presently on antiepileptic drugs with good control, the shunt is functional and appears within normal sized ventricles with no evidence of active hydrocephalus (figure 1). we have chosen to follow him up closely. surgical excision though feasible could be very tasking and is considered in symptomatic patients with acute or progressive neurological deficits and seizures not adequately controlled with antiepileptic drug (2, 6, 16, 24), but some authors have surgically removed asymptomatic ccsdh (14). there is also a risk of damage to underlying brain tissue (6, 16). when shunt revision becomes necessary, a new access point may have to be used and the previous ventricular catheter which may be encased in the calcified hematoma, is left insitu (15). conclusion calcified chronic subdural hematomas are rare complications of shunting, whose management is based on the clinical status of the individual patient. interval ct scans during the long-term follow-up of these patients will detect asymptomatic chronic subdural hematomas that can be treated early to forestall calcification. surgical excision is feasible but should be limited to symptomatic cases. acknowledgements the authors are grateful to dr njideka okubadejo for her critical review of this manuscript and her useful comments. dr allan friedman provided technical support through dr kanu. correspondence okezie obasi kanu, fwacs neurosurgery secretariat room 219, department of surgery, lagos university teaching hospital pmb 12003, surulere, lagos state, nigeria e-mail: drkanu@gmail.com tel:+234 806 891 8462 (mobile) references 1. afra d, ossification of subdural hematoma. report of two cases. j neurosurg 18:393-397, 1961. 2. al wohaibi m, russell n, al ferayan a, a baby with an armoured brain. cmaj 169:46-47, 2003. 3. amr r, maraqa l, choudry q, 'armoured brain'. a case report of a calcified chronic subdural haematoma. pediatr neurosurg 44:88-89, 2008. 4. bahadir ar, marx p, on a case report of calcified and ossified subdural hematomas. neurochirurgia (stuttg) okezie obasi kanu et al armoured brain 10:224-228, 1967. 5. barmeir ep, stern d, harel s, holtzman m, krije tj, calcified subdural haematomas associated with arrested hydrocephalus--late sequelae of shunt operation in infancy. eur j radiol 5:186-189, 1985. 6. dammers r, ter laak-poort mp, maas ai, neurological picture. armoured brain: case report of a symptomatic calcified chronic subdural haematoma. j neurol neurosurg psychiatry 78:542-543, 2007. 7. debois v, lombaert a,: calcified chronic subdural hematoma. surg neurol 14:455-458, 1980. 8. galldiks n, dohmen c, neveling m, fink gr, haupt wf, a giant bilateral calcified chronic subdural hematoma. neurocrit care 12:272-273, 2010. 9. he xs, zhang x, giant calcified chronic subdural haematoma: a long term complication of shunted hydrocephalus. j neurol neurosurg psychiatry 76:367, 2005. 10. ide m, jimbo m, yamamoto m, umebara y, hagiwara s, asymptomatic calcified chronic subdural hematoma--report of three cases. neurol med chir (tokyo) 33:559-563, 1993. 11.iplikcioglu ac, akkas o, sungur r, ossified chronic subdural hematoma: case report. j trauma 31:272-275, 1991. 12.ludwig b, nix w, lanksch w, computed tomography of the “armored brain”. neuroradiology 25:39-43, 1983. 13. mclaurin rl, mclaurin ks, calcified subdural hematomas in childhood. j neurosurg 24:648-655, 1966. 14. niwa j, nakamura t, fujishige m, hashi k, removal of a large asymptomatic calcified chronic subdural hematoma. surg neurol 30:135-139, 1988. 15. papanikolaou pg, paleologos ts, triantafyllou tm, chatzidakis em, shunt revision after 33 years in a patient with bilateral calcified chronic subdural hematomas. case illustration. j neurosurg 108:401, 2008. 16. per h, gumus h, tucer b, akgun h, kurtsoy a, kumandas s, calcified chronic subdural hematoma mimicking calvarial mass: a case report. brain dev 28:607-609, 2006. 17. puca a, fernandez e, colosimo c, lauretti l, pallini r, tamburrini g, hydrocephalus and macrocrania: surgical or non-surgical treatment of postshunting subdural hematoma? surg neurol 45:376382, 1996. 18. sgaramella e, sotgiu s, miragliotta g, fotios kalfas crotti fm, “matrioska head”. case report of calcified chronic subdural hematoma. j neurosurg sci 46:28-31; discussion 31, 2002. 19. sharma rr, mahapatra a, pawar sj, sousa j, athale sd, symptomatic calcified subdural hematomas. pediatr neurosurg 31:150-154, 1999. 20. spadaro a, rotondo m, di celmo d, simpatico s, parlato c, zotta dc, albanese v, bilateral calcified chronic subdural hematoma. further pathogenetic and clinical consideration on the so-called “armored brain”. j neurosurg sci 31:49-52, 1987. 21. tacoma j, subdural ossification. folia psychiatr neurol jpn 62:465-471, 1959. 22. waga s, sakakura m, fujimoto k, calcified subdural hematoma in the elderly. surg neurol 11:5152, 1979. 23. yamada k, ohta t, takatsuka h, yamaguchi k, high-field magnetic resonance image of a huge calcified chronic subdural haematoma, so-called “armoured brain”. acta neurochir (wien) 114:151-153, 1992. 24. yan hj, lin ke, lee st, tzaan wc, calcified chronic subdural hematoma: case report. changgeng yi xue za zhi 21:521-525, 1998. microsoft word 12agrawal_intracranial 388 agrawal et al intracranial-extracranial meningioma intracranial-extracranial meningioma mimicking an aggressive skull bone tumor amit agrawal1, k.v. murali mohan2, vissa shanthi3, umamaheshwar reddy4 narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 1professor of neurosurgery, department of neurosurgery 2professor of pathology, department of pathology 3associate professor of pathology, department of pathology 4assistant professor of radiology, department of radiology abstract intracranial meningiomas with extracranial extension are rare lesions with only few reported cases in literature. in present article we report a case of 62 year male patient presented with progressive swelling over right side frontal region of 2 year duration. in our case the tumor was in close proximity to right fronto-parietal suture and there was a possibility that suture line could have paved the way for its extracranial spread and also there was evidence of transdiploic extension on histopatholgical examination. key words: meningioma, head injury, extracranial meningioma, intracranialextracranial. introduction meningioma account for 24-30% of primary intracranial tumors and typically arises in proximity to the meninges (1, 2, 3). intracranial meningiomas with extracranial extension are rare lesions with only few reported cases in literature (3-8). in present article we report a case of intracranial and extra-cranial menigioma. case report a 62 year male patient presented with progressive swelling over right side frontal region of 2 year duration. weakness of left upper and lower limbs of one month duration. there was history of headache and vomiting for last 3-4 days. local examination revealed a non-tender, hard swelling over right fronto-parietal region, non-pulsatile, with bruit. skin over the swelling was healthy and there were no prominent vessels. there was history of trauma at the same site about 15 year back. his general and systemic examination was unremarkable. there was mild upper motor neuron type of weakness of left facial nerve. other cranial nerves including fundus were normal. he was conscious, alert and oriented to time, place and person. there was grade 4/5 weakness of left upper and lower limbs. deep tendon reflexes were exaggerated on left side and were normal on right side. planter was extensor on left side and was flexor on right side. ct scan brain plain with bone window revealed a large tumor consisting of intracranial and extracranial parts with erosion of the calvaria involving right frontal and parietal and crossing the coronal suture on right romanian neurosurgery (2013) xx 4: 388 392 389 side (figure 1 a-f). the tumor was invading the parenchyma and there was significant peri-lesional edema. based on the imaging findings a high grade malignant lesion was considered. the patient underwent right fronto-parietal craniotomy and total excision of the tumor including excision of the involved bone. the tumor was attached to the dural and infiltrating the bone. it could be easily separated from the underlying brain parenchyma. histopathological examination of the tumor confirmed the diagnosis of meningioma (figure 2 and 3). the patient recovered well and the postoperative course was uneventful. discussion the reported incidence of intracranial meningiomas with extracranial extension is up to 20% of cases (9, 10). there is strong evidence there is an elevated risk brain tumor after head trauma particularly for meningiomas in males (1, 11-16). many explanations have been put forward to explain extracranial spread of tumor and the extracranial extension in meningiomas may occur by direct extension of an intracranial meningioma through a natural, traumatic, or iatrogenic skull defect (17, 18). this may occur through skull foramina, through the supraorbital fissure (into the orbit), through the cribriform plate (into the nasal cavities and nasopharynx), through floor of middle cranial fossa (into paranasal sinuses and pterygoid region) and extracranial extension through the suture line of the skull (4, 9, 10, 19-23). in a case report the transdiploic extension was suggested as the underlying mechanism for the extracranial spread of the meningioma (8). figure 1 (a-f) ct scan brain showing extensive osteolytic lesion in right fronto-parietal region with intra-extracranial components and adjacent hyperostosis of frontal and parietal bones 390 agrawal et al intracranial-extracranial meningioma figure 2 (a) spindle shaped tumor cells forming whorling pattern (h&e,x100)., (b) spindle shaped tumor cells with areas of hyalinization (h&e,x100), (c) tumor cells infiltrating the skeletal muscle bundles and congested blood vessels (h&e,x100) and (d) spindle shaped tumor cells with psammoma body (h&e,x100) figure 3 showing the bony trabeculae with interstitial tissue showing infiltrating tumor cells and psammoma bodies (h&e,x100) in our case the tumor was in close proximity to right fronto-parietal suture and there was also a possibility that suture line could have paved the way for its extracranial spread and also there was evidence of transdiploic extension on histopatholgical examination. clinical symptoms are usually non-specific and can be according to the site of involvement (20). if the extracranial component is large enough and there is extensive hyperostosis the lesion can be palpable through the scalp (18). both mri and ct will help to suggest the extent of the lesion and this can be romanian neurosurgery (2013) xx 4: 388 392 391 confirmed by fnac prior to surgical intervention (4, 7, 24). whenever possible the complete excision of the tumor is the treatment of choice as this has been shown to be associated with best long-term outcome compared with subtotal excision (19, 23, 25, 26 27 28, 29). the recurrence rate ranges from 7% to 84% (30, 31) and the recurrences usually develop at the primary site of lesion and probably represent the residual disease rather than true recurrence (27, 30, 31). address for correspondence: dr. amit agrawal professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 references 1.longstreth wt, dennis lk, mcguire vm, drangsholt mt, koepsell td. epidemiology of intracranial meningioma. cancer 1993;72:639-648. 2.louis d, ohgaki h, wiestler o, cavenee w, fuller c. world health organization classification of tumours of the central nervous system. journal of neuropathology and experimental neurology 2008;67:260. 3.russell d, rubinstein l. pathology of tumors of the central nervous system. london: butleeer & tanner 1989:421-428. 4.neeff m, baysal e, homer j, gillespie j, ramsden r. intracranial/extracranial meningioma arising in the hypoglossal canal: case report. skull base : official journal of north american skull base society [et al] 2007;17:325-330. 5.cech da, leavens me, larson dl. giant intracranial and extracranial meningioma: case report and review of the literature. neurosurgery 1982;11:694-697. 6.djindjian m, raulo y. [giant intra-extracranial meningioma of the calvaria]. neuro-chirurgie 1984;30:341-345. 7.nakagawa h, lusins jo. biplane computed tomography of intracranial meningiomas with extracranial extension. journal of computer assisted tomography 1980;4:478-483. 8.akif m. intra-extracranial meningioma. turkish neurosurgery 1993;4:170-172. 9.farr hw, gray gf, vrana m, panio m. extracranial meningioma. journal of surgical oncology 1973;5:411420. 10.friedman cd, costantino pd, teitelbaum b, berktold re, sisson ga. primary extracranial meningiomas of the head and neck. the laryngoscope 1990;100:41-48. 11.preston-martin s, pogoda jm, schlehofer b, et al. an international case-control study of adult glioma and meningioma: the role of head trauma. international journal of epidemiology 1998;27:579-586. 12.barnett gh, chou sm, bay jw. posttraumatic intracranial meningioma: a case report and review of the literature. neurosurgery 1986;18:75-78. 13.carpenter av, flanders wd, frome el, cole p, fry sa. brain cancer and nonoccupational risk factors: a case-control study among workers at two nuclear facilities. american journal of public health 1987;77:1180-1182. 14.inskip pd, mellemkjaer l, gridley g, olsen jh. incidence of intracranial tumors following hospitalization for head injuries (denmark). cancer causes & control : ccc 1998;9:109-116. 15.claus eb, bondy ml, schildkraut jm, wiemels jl, wrensch m, black pm. epidemiology of intracranial meningioma. neurosurgery 2005;57:1088-1095; discussion 1088. 16.wiemels j, wrensch m, claus eb. epidemiology and etiology of meningioma. journal of neuro-oncology 2010;99:307-314. 17.teague sd, conces dj. metastatic meningioma to the lungs. journal of thoracic imaging 2005;20:58-60. 18.younis g, sawaya r. intracranial osteolytic malignant meningiomas appearing as extracranial softtissue masses. neurosurgery 1992;30:932-935. 19.thompson ld, gyure ka. extracranial sinonasal tract meningiomas: a clinicopathologic study of 30 cases with a review of the literature. the american journal of surgical pathology 2000;24:640-650. 20.thompson ldr, bouffard j-p, sandberg gd, mena h. primary ear and temporal bone meningiomas: a clinicopathologic study of 36 cases with a review of the literature. modern pathology : an official journal of the united states and canadian academy of pathology, inc 2003;16:236-245. 21.chang cy, cheung sw, jackler rk. meningiomas presenting in the temporal bone: the pathways of spread from an intracranial site of origin. otolaryngology-head and neck surgery : official journal of american academy of otolaryngology-head and neck surgery 392 agrawal et al intracranial-extracranial meningioma 1998;119:658-664. 22.batsakis jg. invasion of the microcirculation in head and neck cancer. the annals of otology, rhinology, and laryngology 1984;93:646-647. 23.panjvani si, gandhi mb, sarvaiya an, chaudhari br, gupta gs. an extracranial invasive meningioma mimicking malignant bone tumor–“carpet meningioma”. 2013. 24.saloner d, uzelac a, hetts s, martin a, dillon w. modern meningioma imaging techniques. journal of neuro-oncology 2010;99:333-340. 25.naguib sm, shalaby amr. differentiation of meningiomas from histologic mimics via the use of claudin-1. pan arab journal of neurosurgery:10. 26.condra ks, buatti jm, mendenhall wm, friedman wa, marcus jr rb, rhoton al. benign meningiomas: primary treatment selection affects survival. international journal of radiation oncology* biology* physics 1997;39:427-436. 27.possanzini p, pipolo c, romagnoli s, et al. primary extra-cranial meningioma of head and neck: clinical, histopathological and immunohistochemical study of three cases. acta otorhinolaryngologica italica : organo ufficiale della societa italiana di otorinolaringologia e chirurgia cervico-facciale 2012;32:336-338. 28.crawford ts, kleinschmidt-demasters bk, lillehei ko. primary intraosseous meningioma. case report. journal of neurosurgery 1995;83:912-915. 29.inagaki k, otsuka f, matsui t, ogura t, makino h. effect of etidronate on intraosseous meningioma. endocrine journal 2004;51:389-390. 30.mirimanoff ro, dosoretz de, linggood rm, ojemann rg, martuza rl. meningioma: analysis of recurrence and progression following neurosurgical resection. journal of neurosurgery 1985;62:18-24. 31.stafford sl, perry a, suman vj, et al. primarily resected meningiomas: outcome and prognostic factors in 581 mayo clinic patients, 1978 through 1988. mayo clinic proceedings mayo clinic 1998;73:936-942. microsoft word 14onoseendeavours 96 g. onose, monica haras endeavours and trends in spinal cord injury repair endeavours and trends in spinal cord injury repair (syllabus) g. onose, monica haras “carol davila” university of medicine and pharmacy, bucharest background sci current data and statistics • prevalence and incidence worldwide • prevalence and incidence in romania • average age at injury, male: female ratio medical and social consequences of scis • clinical classifications of scis • medical complications/ co-morbidities current therapeutic means and their limitations in scis current context of regenerative medicine integrative emphases regarding limits, detrimental pathways and related targets for neuroprotection/ recovery, in sci morpho-functional, inner restrictions of the cns/ spinal cord’s post injury selfrepair primary injuries in sci secondary injuries pathophysiological events’ cascade targets for neuroprotection final (irreversible) consequences of scis current trends in sci (experimental) therapies integrative emphases – clinical/ therapeutic connections “classical” drugs, with a long history of clinical use new/ experimental drugs/ procedures stem cells & tissue engineering background medical and social potential brief history of stem cell research spontaneous regeneration phenomena in lower vertebrates definition of regenerative medicine definition and clinical use of tissue engineering stem cells: • definition • classifications • main characteristics & properties • embryonic stem cells • adult stem cells regenerative medicine in sci repair main issues/ problems • ethical concerns • the availability of suitable stem cells • the inhibitory environment of the lesioned sc, especially in chronic sci (glial scar, cyst formation) → grafts fail to survive • immune reactions to allografts/ xenografts • regeneration with aberrant reconnections → neuropathic pain, spasticity • contamination of the stem cell lines with feeder cells, bacteria and/or transfection with feeder cells genic material • high proliferative capacity of esc → cancer risc the role of glial scar prevention therapy (regeneration promoting therapy) •cordaneurin romanian neurosurgery (2011) xviii 1: 96 – 98 97 •cordachron •chondroitinase abc current status of preclinical and clinical research of stem cells in sci repair •clinical studies currently underway human embryonic stem cells (hescs) fetal stem cells: •fetal oeg (olfactory ensheathing glia) •fetal schwann cells •umbilical cord blood cells adult stem cells: •mesenchymal stem cells/ marrow stromal cells (msc) •olfactory ensheathing glia (oeg) including of differentiated ones transplants •schwann cells including of differentiated ones transplants •adult-derived neural progenitor cells npcs stem cell research at the teaching emergency hospital “bagdasar-arseni”, bucharest, romania tissue engineering in sci repair •polymeric scaffolds used for spinal cord regeneration properties •“smart” biomaterials characterized by stereospecificity and self-assembling nano-scale self-assembling bio-scaffolds •recent conceptual & technological breaktroughs: implants built by 3dprinting •rp (rapid printing) machine (for replacement organs and whole bodies) •“direct writing” printing implants by maple-dw conclusions considering the complexity of sci pathobiology, it is important to adopt multifactorial (combinatory) strategies, that may include: (stem) cell replacement long distance guidance of neural regrowth and re-connection advanced scaffolding/ encapsulation (for cells replacement)/ tissue reconstruction local delivery of neuroprotective/ neurotrophic substances (e.g. scar formation inhibitors, growth factors, neurotrophins) surgical removal of glial scars, posttraumatic cysts integrated physical therapy acknowledgements for their endeavors within our team to: a. anghelescu*/**, r. mihai**, a. mirea*, c. giuglea**, v. grigorean*/**, c. daia chendreanu*/**, l. onose***, a. spânu**, c. popescu, i. andone**, a. mihăescu**, d.c. mardare** *the university of medicine and pharmacy ”carol davila”, bucharest, romania **the emergency hospital “bagdasararseni”, bucharest, romania ***metrorex medical service, bucharest, romania references 1. address no. 602/ 17.03.2010 of the national school for public health, management and perfecting in the sanitary domain, bucharest 2. barakat dj, gaglani sm, neravetla sr, et al. survival, integration, and axon growth support of glia transplanted into the chronically contused spinal cord. cell transplant, 14: 225–40, 2005 3. bradbury ej, carter lm. manipulating the glial scar: chondroitinase abc as a therapy for spinal cord injury. brain res bull. [epub ahead of print] jul 8, 2010 4. brower v. us bioethics commission promises policy action. nature 462: 553, 2009 5. bruce jh, norenberg md, kraydieh s, puckett w, marcillo a, dietrich d. schwannosis: role of gliosis and proteoglycan in human spinal cord injury. j neurotrauma, 17: 781-8, 2000 98 g. onose, monica haras endeavours and trends in spinal cord injury repair 6. bryant sv, endot., and gardiner, dm. vertebrate limb regeneration and the origin of limb stem cells . int j dev biol, 46:887-96, 2002 7. cedar ch, cooke ja, luo z, patel mj, minger sl. from embryos to embryonic stem cells – biopolitics and therapeutic potential reprod biomed online, 13(5): 725-31, 2006 8. chen bk, knight am, de ruiter gc, et al. axon regeneration through scaffold into distal spinal cord after transection. j neurotrauma 26(10):1759-7, 2009 9. chen s, hilcove s, ding s. small molecules control stem cells. mol biosyst 2, 2006 10.chrisey db, doraiswam a, narayan rj. direct writing of biomaterials; a paradigm shift in tissue engineering. biomaterials forum, 27(3): 10-11, 2005 11.claydon ve, steeves jd, krassioukov a. orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology. spinal cord, 44: 341-51, 2005 12.constans a. machining the body. rapid prototyping techniques promise better design and fabrication of tissue-engineering scaffolds, the scientist, 19(9): 1-7, 2005 13.dahlberg a, perttila i, wuokko e et al. bladder management in persons with spinal cord lesion. spinal cord 42:694-8, 2004 14.dasari vr, spomar dg, gondi cs, et al: axonal remyelination by cord blood stem cells after spinal cord injury. j neurotrauma 24: 391–410, 2007 15.dobkin bh, curt a, guest j: cellular transplants in china:observational study from the largest human experiment inchronic spinal cord injury. neurorehabil neural repair 20: 5–13, 2006 16.eftekharpour e, karimi-abdolrezaee s, fehlings mg. current status of experimental cell replacement approaches to spinal cord injury. neurosurg focus 24(3, 4): e18, 2008 17.fehlings mg, baptiste dc. current status of clinical trials for acute spinal cord injury. injury, 36[suppl 2]: b113-22, 2005 18.grudeva popova jg. cellular therapy – the possible future of regenerative medicine. folia med, 47(3-4): 510, 2005 19.hall ed, springer je. neuroprotection and acute spinal cord injury: a reappraisal. neurorx, 1: 80-100, 2004 20.harris ml, doraiswamy a, narayan nj, patz tm, chrissey db. recent progress in cad/cam laser direct-writing of biomaterials. mater sci eng, 28(3): 59365, 2008 21.harris ng, mironova ya, hovda da, sutton rl. chondroitinase abc enhances pericontusion axonal sprouting but does not confer robust improvements in behavioral recovery. j neurotrauma. 27(11): 1971-82, 2010 22.hochedlinger k, yamada y, beard c, jaenisch r. ectopic expression of oct4 blocks progenitor cell differentiation and causes dysplazia in epithelial tissues. cell , 121: 465-77, may, 2005 23.hovatta o, jaconi m, töhönen v, et al. a teratocarcinoma-like human embryonic stem cell (hesc) line and four hesc lines reveal potentially oncogenic genomic changes. plos one. 23;5(4):e10263, 2010 24.http://assembly.coe.int/documents/adoptedtext/ta0 2/erec1560.htm 25.http://clinicaltrials.gov 26.http://neu.neuraxo.de/cordaneurin/?l=1 27.http://www.sci-info-pages.com/facts.html 28.http://www.travisroyfoundation.org/pages/resourcesstats.htm 29.https://www.nscisc.uab.edu/public_content/facts_fig ures_2009.aspx 30.iencean sm, ianovici n, ciurea av, onose g. repair of spinal cord injury. poster at the european association of neurosurgical societies, antalya, turkey, february, 2007 31.izrael m, zhang p, kaufman r, et al. human oligodendrocytes derived from embryonic stem cells: effect of noggin on phenotypic differentiation in vitro and on myelinationin vivo. mol cell neurosci 34:310– 23, 2007 32.jones la, lammertse dp, charlifue sb, et al. a phase 2 autologous cellular therapy trial in patients with acute, complete spinal cord injury: pragmatics, recruitment, and demographics. spinal cord, 48(11): 798-807, 2010 33.kachramanoglou c, li d, andrews p, east c, carlstedt t, raisman g, choi d. novel strategies in brachial plexus repair after traumatic avulsion. br j neurosurg, 2010 [epub ahead of print] 34.klimanskaya i, chung y, becker s, lu sj, lanza r: human embryonic stem cell lines derived from single blastomeres. nature, 444: 48-5, 2006 35.lin vernon w, cardenas diana d, et al. spinal cord medicine: principle and practice demos medical publishing, inc., new york, 2003 36.mackay-sim a. olfactory ensheathing cells and spinal cord repair. keio j med, 54(1): 8–14, 2005 37.maynard fm, jr, bracken mb, creasey g, ditunno jf jr, donovan wh, et al. international standards for neurological and functional classifcation of spinal cord injury. spinal cord, 35: 266-74, 1997 38.mc donald jw. repairing the damaged spinal cord. sci ame, 281(3): 64-73, 1999 39.mironov v, boland t, trush t, forgacs g, markwald rr. organ printing: computer-aided jet based 3d tissue engineering. trends biotechnol. 21(4); 157-61, 2003 14agrawalamit_largecerebello2014 96 agrawal et al large cerebello-pontine epidermoid tumor in a child large cerebello-pontine epidermoid tumor in a child amit agrawal1, nitish baisakhiya2, p.t. deshmukh3, s.r. joharapurkar4, prasenjit mukherjee5 1associate professor in neurosurgery, department of surgery, datta meghe institute of medical sciences, sawangi (meghe), wardha (india) 2assistant professor in ent, department of ent, datta meghe institute of medical sciences, sawangi (meghe), wardha (india) 3professor in ent, department of ent, datta meghe institute of medical sciences, sawangi (meghe), wardha (india) 4professor and director, dmdpgme & r, datta meghe institute of medical sciences, sawangi (meghe), wardha (india) 5registrar in surgery, department of surgery, datta meghe institute of medical sciences, sawangi (meghe), wardha (india) abstract cerebellopontine angle lesions are more commonly found in adults; however, they are uncommon in children. 13 year female child presented with progressive cerebellar signs and decreased hearing in left ear. magnetic resonance imaging was suggestive of left cerebello-pontine angle epidermoid tumor that was treated surgically. in this rare case we discuss the imaging findings and review the relevant literature. key words: cerebellopontine angle, brain tumors, children, epidermoid introduction cerebellopontine angle (cpa) lesions are more commonly found in adults; however, they are uncommon in children. (1) we report a rare occurrence of epidermoid tumor in a child, discuss the imaging findings and review the relevant literature. case report this 13 year female child presented with history of difficulty in walking for last one and half year, pain both lower limbs since last 1 year and swaying to either side more on left side of last 6 months duration. she also noticed decreased hearing in left ear for last three months. there was no history of focal weakness, seizures, headache, vomiting or bowel and bladder disturbances. here general and systemic examination was unremarkable. higher mental functions were normal. fundus and vision was normal. cranial examination revealed left 6th, 7th and 8th cranial nerve paresis and bilateral bilateral 5th nerve weakness. there were bilateral cerebellar signs more on left side. all deep romanian neurosurgery (2014) xxi 1: 96 99 97 tendons exaggerated and planters were extensor. motor and sensory examination was normal. blood investigations were normal and audiometry showed sensorineural deafness in left ear. magnetic resonance imaging (mri) of the brain showed left sided cerebello-pontine angle which was hypo-and hyperintense on t1 and t2 weighted images, respectively. on diffusion weighted (dw) mri, the lesion was hyperintense, which suggested that they were a cerebello-pontine angle epidermoid tumour (figures 1 and 2). figure 1 mri brain, the lesion in hypointense on t1 image (a), hyperintense on t2 image (b), hypointense on flair image with honeycomb appearance (c) and hyperintense on diffusion-weighted images (d) figure 2 mri t1 saggital image (left) and t2 coronal image (right) the patient underwent a left suboccipital retrosigmoid craniotomy, which showed a classical pearly tumour encasing the branches of the basilar artery and anterior inferior cerebellar artery. a subtotal removal of the cyst contents was achieved because some of the areas of the lesion were inaccessible. similarly, some of the capsule was excised, but capsule that was densely adherent to the brain stem was left in place. postoperatively the patient had new left-sided seventh nerve palsy despite anatomical continuity of the nerve. she otherwise made an unremarkable recovery except minimal would leak that was managed conservatively. discussion epidermoid cyst, or pearly tumor, is congenital in origin and accounts for about 1% of intracranial tumors. (2) though the cpa is the most common intracranial location for an epidermoid inclusion cyst, (3) these lesions are rare in children. (1, 4) an epidermoid tumor is a congenital lesion that arises from inclusion of ectodermal epithelial elements. (5) the 98 agrawal et al large cerebello-pontine epidermoid tumor in a child natural history of epidermoid cysts is well described. they are benign tumors of embryonal origin, usually occur in isolation, and constitute 1% of all intracranial tumors. (6, 7) epidermoid cysts arise from normal epithelial cells included during neural tube closure and their growth is due to accumulation of keratin and cholesterol produced by desquamation of the squamous epithelium lining the mass. these slow-growing tumors encase and surround nerves and arteries in the cisterns rather than displacing them. (5) grossly, epidermoid tumors are typically well defined lesions with an irregular nodular outer surface and a shiny “mother of pearl” appearance. (8, 9) epidermoid tumours have a thin capsule consisted of stratified keratinised squamous epithelium without vascularity. (5, 10) this thin capsule may rupture spontaneously and can cause bouts of chemical meningitis. (10) patients with an epidermoid usually present in the 4th and 5th decades of life. (11) the cerebellopontine angle epidermoids cause symptoms and signs of a slowly expanding mass lesion and may present with symptoms of cranial nerve, cerebellar, and brain stem compression as well as with obstructive hydrocephalus and meningeal irritation. (12, 13) intracranial epidermoid cysts can closely mimic cerebrospinal fluid on magnetic resonance imaging and computed tomography. (14) epidermoid cysts typically show undulating margins and model their shape to conform to the cerebropontine angle. the cyst has a tendency to insinuate itself around the nerves and blood vessels in the cerebropontine angle. (14) on ct scans, epidermoid cysts appear hypoattenuating, almost isoattenuating to csf, and have characteristic irregular, lobulated margins. (15) on mr imaging, epidermoid tumors typically have low signal intensity on t1weighted images, high signal intensity on t2-weighted images, and no enhancement on gadolinium-enhanced images. (5, 15, 16) on diffusion-weighted imaging epidermoid cysts have high signal intensity unlike arachnoid cysts, those have very low signal intensity. (16) differentiation of epidermoid tumors particularly from arachnoid cysts is important for appropriate patient care because the treatment is different for each lesion. (16) the differential diagnosis of the cerebellopontine angle includes acoustic neurilemoma, meningioma, epidermoid tumor, and other rare neoplasms involving this region. (17) the treatment of choice or cp angle epidermoid is surgical resection, however complete excision of the tumor capsule is often not possible due to the high risk of damaging adherent neural or vascular structures. (12) as a consequence, there are a number of these lesions that recur, usually many years after the original surgery. (6) in our case mri facilitated the diagnosis of cp angle epidermoid and accordingly surgical approach could be planned. also preoperative knowledge is important to avoid chemical meningitis. (15) romanian neurosurgery (2014) xxi 1: 96 99 99 address for correspondence: dr amit agrawal associate professor (neurosurgery) clinical and administrative head division of neurosurgery datta meghe institute of medical sciences sawangi (meghe) wardha442005, maharashtra, india. phone: +91-7152-3956552 fax: +91-7152-2245318 email: dramitagrawal@gmail.com references 1. zuccaro g, sosa f. cerebellopontine angle lesions in children. childs nerv syst. 2007; 23(2):177-83. 2. hsieh ch, huang km, kao mc, peng s, wang cc. hemorrhage in intracranial epidermoid cyst. j formos med assoc. 1996; 95(2):173-5. 3. salazar j, vaquero j, saucedo g, bravo g. posterior fossa epidermoid cysts. acta neurochir (wien). 1987; 85(1-2):34-9. 4. resnick dk, levy ei, jannetta pj. microvascular decompression for pediatric onset trigeminal neuralgia. neurosurgery. 1998; 43(4):804-7. 5. gao py, osborn a, smirniotopoulos j, harris cp. epidermoid tumor of the cerebellopontine angle. ajnr am j neuroradiol 1992; 13:863-872. 6. berger ms, wilson cb. epidermoid cysts of the posterior fossa. j neurosurg 1985;62:214-219 7. yamakawa k, shitara n, genka s, manaka s, takakura k. clinical course and surgical prognosis of 33 cases of intracranial epidermoid tumors. neurosurgery 1989;24: 568-573 8. desouza ce, desouza r, da costa s, sperling n, yoon th, abdelhamid mm, sharma rr, goel a. cerebellopontine angle epidermoid cysts: a report on 30 cases. j neurol neurosurg psychiatry. 1989; 52(8):98690. 9. ochi m, hayashi k, hayashi t, morikawa m, ogino a, hashmi r, iwanaga m, yasunaga a, shibata s. unusual ct and mr appearance of an epidermoid tumor of the cerebellopontine angle. ajnr am j neuroradiol. 1998; 19(6):1113-5. 10.yilmazlar s, kocaeli h, cordan t. brain stem stroke associated with epidermoid tumours: report of two cases. j. neurol. neurosurg. psychiatry 2004; 75; 13401342. 11.rubinstein u. tumors ofthe central ncrvous system. in: atlas of tumor pathology, fasc 6, ser 2. washington, dc: armed forces institute of pathology, 1972; 288292. 12.samii m, tatagiba m, piquer j, carvalho ga. surgical treatment of epidermoid cysts of the cerebellopontine angle. j neurosurg 1996;84:14-19 13.russel ds, rubinstein lj. tumors and tumor like lesions of maldevelopmental origin. in: russel ds, rubinstein lj, eds. pathology of tumors of the nervous system, 5th ed. london: edward arnold, 1989:693-5. 14.atalar mh, sener rn, icagasioglu d. epidermoid cyst in a girl: constructive interference in steady-state and diffusion-weighted imaging findings. journal of pediatric neurology 2006; 4 (3):211-214. 15.chen cy, wong js, hsieh sc, chu js, chan wp. intracranial epidermoid cyst with hemorrhage: mr imaging findings. ajnr am j neuroradiol. 2006; 27(2):427-9. 16.nguyen jb, ahktar n, delgado pn, lowe lh. magnetic resonance imaging and proton magnetic resonance spectroscopy of intracranial epidermoid tumors. crit rev comput tomogr. 2004; 45(5-6):389427. 17.bonneville f, sarrazin jl, marsot-dupuch k, iffenecker c, cordoliani ys, doyon d, bonneville jf. unusual lesions of the cerebellopontine angle: a segmental approach. radiographics. 2001; 21(2):419-38. microsoft word 3iencean_classification 318 iencean, adam characteristics of the intracranial hypertension classification of the intracranial hypertension and characteristics of intracranial pressure increase. review st.m. iencean1, d. adam2 1neurosurgery, “grigore t. popa” university of medicine and pharmacy iasi 2neurosurgery, “carol davila” university of medicine and pharmacy, bucharest intracranial hypertension represents the increase in the intracranial pressure (icp) due to disorders of the regulating mechanisms for intracranial pressure. it is caused by the intrinsic changes in the volumes of the intracranial compartments: brain parenchyma, cerebrospinal fluid and blood content, and/or by adding a pathological volume (extrinsic – tumor, haematoma, cerebral abscess, etc.). at first, the increase in the intracranial pressure is caused by the modification of the volume-pressure relations in correlation with time (the speed of occurrence and the duration of changes), which is induced by various etiologies; afterwards, the intracranial hypertension generates physiopathological disorders which cause specific modifications to the endocranial structures, and, therefore, the subsequent icp increase is accompanied by its own symptomatology. in relation to its causal mechanism, the intracranial hypertension is and it may remain a symptom (increased intracranial pressure), or it evolves as a syndrome (increased intracranial pressure associated with other signs and symptoms). there are intracranial pressure values that are considered to be at the normal limit or moderately increased values, which do not induce evolutionary physio-pathological mechanisms by themselves. the subsequent evolution of the intracranial hypertension as a syndrome results from the very transformation of the initial icp increase into a pathogenic mechanism and from the progression of the characteristic symptoms, whose intensity may exceed even the symptomatology of the initial illness. depending on the etiology and on the pathogenic mechanism that generates the disorder in the volume-intracranial pressure relation, and based on the variation of the intracranial pressure in time, there is now an etiopathogenic classification of the intracranial hypertension, which includes both the etiopathogenic mechanisms and the clinical data (iencean 2001, revised in 2003). many of the previous observations and findings of other authors have foreseen this systematization. 1. parenchymatous intracranial hypertension it occurs in the expanding intracranial processes (cerebral tumors, intracranial haematoma, cerebral abscesses, etc.), in the traumatic cerebral edema, in the cerebral ischemia with hypotoxic cerebral edema, in general intoxications with neurotoxins (endogenous or exogenous), etc. the primary cerebral etiology is known and it generates modifications of the intracranial volume; the cerebral edema occurs afterwards, and it evolves in parallel to the increase in the icp. the parenchymatous lesion initially occurs as a result of the romanian neurosurgery (2013) xx 4: 318 325 319 intrinsic cerebral etiology and of the primary modifications in the intracranial volume (expansive, compressive, hypotoxic or traumatic cerebral edema). the parenchymatous intracranial hypertension may have a complete evolution to its acute form with a brain stem ischemia or cerebral hernia. 2. intracranial hypertension due to disorders of the cerebrospinal fluid dynamics the dynamics of the cerebrospinal fluid includes the circulation of the cerebrospinal fluid at the time of its creation at the level of the choroid plexuses, and until its passage into the venous circulation. the dynamic disorders of the cerebrospinal fluid may be: circulation disorders of the cerebrospinal fluid from its creation until resorption, and disorders in the passage of the cerebrospinal fluid in the venous drainage system (resorption). the circulation disorders of the cerebrospinal fluid are produced when there is an obstacle in the fluid itinerary (ventricular system, magna cistern, basal cisterns) due to the existence of a ventricular or para-ventricular tumor, intraventricular hemorrhage, or obstruction of various causes of the sylvian aqueduct. a dilatation of the segments of the ventricular system occurs, those that are supra-adjacent to the obstruction, while the clinical chart and the evolution are related to the obstructive internal hydrocephaly. the resorption disorders of the cerebrospinal fluid occur on account of the lesions of the anatomic structures that provide the passage of the cerebrospinal fluid from the sub-arachnoid spaces into the venous drainage system in acute meningitis, in sub-arachnoid hemorrhage, in meningitis carcinomatosis, in sarcoidosis chronic meningitis, etc. a thickening of the leptomeninx occurs, blocking the pachioni arachnoid corpuscles, and decreasing the absorption of the cerebrospinal fluid. the cerebrospinal fluid accumulates in the subarachnoid spaces and in the ventricular system, leading to a communicating hydrocephaly, with a peri-ventricular hydrocephalic cerebral edema and with an intracranial hypertension syndrome, which is usually a sub-acute one (called the meninx intracranial hypertension). the clinical chart and the increase in the intracranial pressure resemble the intracranial hypertension syndrome in cases of cerebrospinal fluid circulation obstruction. 3. vascular intracranial hypertension the icp increase is caused by disorders of the sanguine, cerebral or extra-cerebral circulation. the increased volume of the cerebral parenchyma in vascular ich is produced by a cerebral edema or by an increase in the cerebral sanguine volume (“congestive brain”). the cerebral edema and/or the congestive cerebral parenchyma will lead to an increased intracranial pressure. the increase in the cerebral sanguine volume occurs when there is an increased intracranial arterial sanguine supply or a decreased blockage of the venous drainage. when the venous drainage is reduced, there is also a decrease in the resorption of the cerebrospinal fluid. the “congestive brain” aspect is caused by the increase in the intra-cerebral sanguine volume, and the volume-intracranial pressure conflict occurs. at the level of the structure represented by the nervous parenchyma – vascular capillary, two types of modifications are produced, which may be separate or have an evolutionary 320 iencean, adam characteristics of the intracranial hypertension connection between them: the stage of a cerebral edema, due to water accumulation in the parenchyma, and the stage of congestive cerebral edematization (congestive brain), with an increase in the volume of the cerebral parenchyma due to vascular dilatation. the vascular intracranial hypertension occurs in: cerebral illnesses: by affecting the venous return and blocking the cerebrospinal fluid absorption in cerebral venous thromboses, thrombosis of superior sagittal sinus, cerebral thrombophlebites, mastoiditis (“otitic hydrocephalus”, described by symonds – thrombosis of venous sinuses, secondary to otomastoiditis), etc., by slowing down or decreasing the venous flow in the superior longitudinal sinus in the arterio-venous shunt in certain types of intra-cerebral vascular malformations, especially galien vein aneurysms, or by decreasing the sanguine feeding in cerebral ischemias with secondary ischemic cerebral edema, as in the ischemic stroke caused by the occlusion or stenosis of the big cerebral vessels, with a serious form of malign ischemic infarct within the territory of the middle cerebral artery (massive sylvian infarct). extra-cerebral illnesses: hypertensive encephalopathy with congestive cerebral edematization and with extra-cellular hydrostatic cerebral edema (by ultrafiltration); in the cervical or thoracic venous blockage. the vascular intracranial hypertension usually develops only until the occurrence of a complete ich syndrome; but, sometimes, it may develop until the occurrence of the acute form of ich due to the secondary disorders of the cerebral sanguine circulation. in the case of the massive ischemic infarct within the territory of the middle cerebral artery, the cerebral edema occurs quickly, it is extensive and the intracranial hypertension has an acute evolution, with a mortality of up to 80% of the cases. 4. idiopathic intracranial hypertension this form of ich has also been designated as pseudotumor cerebri, essential or cryptogenic ich, a terminology that is outdated. the etiology could not be established. it occurs in endocrine illnesses, metabolic disorders or various hematological illnesses, etc. not long ago, physio-pathological mechanisms were thought to include various disorders of the cerebrospinal fluid secretion and absorption, so that the increase in the icp is secondary to the decrease in the cerebrospinal fluid absorption without the occurrence of hydrocephaly (this theory is also sustained by the efficiency of the lumbar-peritoneal shunt). moreover, the cerebral edema could be generated by the so-called non-specific “associated factors”, which lead to the icp increase, without the possibility of establishing an etiological relation. the most probable current pathogenic hypothesis about the idiopathic intracranial hypertension is based on the dynamics of the intracranial fluid circuits that allow maintaining the auto-regulation of the cerebral circulation and of the cerebral sanguine flow. in idiopathic ich, there are various pathologic conditions that cause progressive damage to the hematoencephalic barrier with a hyper-production of interstitial fluid and the occurrence of the extra-cellular cerebral edema. the cerebrospinal fluid is normally produced, and the increased pressure from the cerebral parenchyma is equalized by the romanian neurosurgery (2013) xx 4: 318 325 321 pressure of the cerebrospinal fluid by means of increased exchanges from the interstitial fluid towards the cerebrospinal fluid at the pial trans-cerebral and transependyma level. the increase in the fluid pressure is followed by the increase in the resorption of the cerebrospinal fluid and by a rapid venous efflux, so that the increased intracranial pressure does not affect the cerebral circulation, which is maintained within the normal limits. the transependyma and the trans-pial circuit of the interstitial fluid towards the cerebrospinal fluid represents and efficient compensating mechanism when the intracranial pressure increases gradually and allows the cerebral circulatory auto-regulation. therefore, the idiopathic ich occurs due to the impact on the hematoencephalic barrier, by various causes that are not established yet, with a hyperproduction of interstitial fluid and an extracellular cerebral edema, with increased exchanges from the interstitial fluid towards the cerebrospinal fluid at the transependyma and pial trans-cerebral level; an increased resorption of the cerebrospinal fluid occurs, and there is a rapid venous efflux. the idiopathic ich develops into an incomplete ich syndrome, despite the increased icp values and the presence of the papillary edema. the causes established for certain forms of ich, which are considered idiopathic, will probably include them into one of the ich forms with a known etiology: vascular, meningeal or parenchymatous. the ich syndrome may also occur as a form of transition between the four forms of ich, or it may be induced by several concomitant pathogenic mechanisms of the cerebral edema in: bacillary meningoencephalitis, neoplasia, hydroelectrolytic disorders, diabetic keto-acidosis, pres, etc. the comparison between the ich forms underlines the existing differences very clearly the decompensation in parenchymatous intracranial hypertension is more rapid and it is produced at lower values than the ones in idiopathic ich due to the existence of the pressure differences between the cranio-spinal compartments and the occurrence of the cerebral circulation disorders with a decrease in the cerebral perfusion pressure in parenchymatous ich. the increased critical values of the intracranial pressure, the period of icp increase and the duration of the icp action are the main parameters that control the intracranial biomechanical fluid stability, and which cause the pressure and circulatory decompensation. the state of clinical instability is produced by the passage to more increased values of the intracranial pressure, and it occurs when the icp action time is longer than the compensation cerebral capacity. the pressure-time fluctuation defines the pressure increase in relation to the action duration of the increased intracranial pressure, which induces the auto-regulation disorder of the cerebral sanguine circulation. the limit decompensation conditions occur when the duration of the increased icp action is longer than the period corresponding to the same pressure values in the pressure compensation situation, or the icp values are higher than the icp values corresponding to the same duration of action. the evolution of intracranial hypertension has three stages and it overcomes the critical icp moments the moment it passes to the next stage: 322 iencean, adam characteristics of the intracranial hypertension a. at first, the icp increase is an alarm signal; b. afterwards, the icp increase exceeds the critical value for the occurrence of the ich syndrome; the ich syndrome evolves based on the existing etiology and the maintenance of auto-regulation of the cerebral sanguine circulation. the compensating mechanisms may stop the pressure-time fluctuation. c. finally, the acute critical icp values lead to the alteration of the circulatory autoregulation, and the compensating mechanisms may no longer stop the evolution towards the acute stage. the first and the second stages are reversible, and the third stage corresponds to a phase of maximum instability when the decompensation with clinical aggravation occurs via brainstem ischemia or cerebral hernia, which generates irreversible cerebral lesions. the etiological temporal relation classifies the causes of the intracranial hypertension into: acute causes that lead to the acute increase in the intracranial pressure and the rapid installation of the ich syndrome, and which include the cranial-cerebral traumatisms, acute ischemic lesions or intra-cerebral hemorrhage; exogenous or endogenous intoxications with the rapid formation of the cerebral edema, as well as infections such as encephalitis or meningitis may lead to ich, too; chronic causes, which produce the progressive increase in the intracranial pressure and the belated decompensation of the ich; they include many of the intracranial tumors with slow evolution, progressive blockage of the cerebrospinal fluid circulation, the chronic subdural haematoma, the idiopathic intracranial hypertension, etc. characteristics of intracranial pressure increase intracranial pressure increase is specific for every pathogenic mechanism of cerebral illnesses, and the icp monitoring reveals characteristic features that establish the clinical evolution of the intracranial hypertension: • the intracranial pressure increasing speed to the normal limit values of 20 mm hg and above this value: therefore, there are two segments of the icp increase: 1. pressure increase segment up to the normal limit 2. pathological pressure increase segment, up to the maximum value • the maximum pathological value reached by the intracranial pressure, • duration of the pathological intracranial pressure maintenance, • the period of recovery to normal pressure values • the frequency of pressure increase reoccurrence or the frequency of remissions. several types of pressure increases may be described based on the above-mentioned characteristics and on the clinical evolution: figure 1 supra-acute intracranial pressure increase; intervals to-t1 and t2-t1 are short, of a few hours romanian neurosurgery (2013) xx 4: 318 325 323 1. the supra-acute intracranial pressure increase with rapid decompensation. the intracranial pressure increase is very rapid up to the value of 20 mm hg, and afterwards to a maximum pressure value. this pressure increase occurs in supraacute cases of intracranial hematoma, of traumatic cerebral edema, or in the extending edema of the sylvian artery malign stroke, when a supplementary volume is rapidly developed at the intracranial level. the infraclinical period is very short and the intracranial hypertension decompensation is accelerated due to the high increasing speed of the supplementary intracranial volume and to the exceeding of the compensating capacities. pressure increases very rapidly and the pathological values of the intracranial pressure are of up to 30 40 mm hg. these pathological values are maintained for a short while due to the rapid decompensation. figure 2 acute icp increase, with a prolonged infraclinical period and a rapid decompensation; the interval to-t1 is prolonged, it may last for weeks or even months, and the decompensation lasts for a few days 2. acute intracranial pressure increase, preceded by a prolonged infraclinical period. in these cases, the period when the intracranial pressure reaches and exceeds the normal pressure values is long, with a slow speed of intracranial pressure increase. this is the type of intracranial pressure increase that occurs in cerebral tumors, cerebral abscesses, chronic subdural hematomas, etc., usually when the occurrence and development of the supplementary intracranial volume is slowly progressive. during the infraclinical period, there is the compensation of the pressure increases caused by the newly added volume, reaching the limit value. once the compensating capacities have been exceeded, the intracranial pressure increase is rapid up to the maximum values, which are of approximately 30 40 mm hg. the period of these pathologic pressure values is short due to the rapid decompensation. figure 3 acute icp increase, with a short infraclinical period, and a prolonged period of the decompensation risk; the interval to-t1 is short, of a few hours; the interval t1-t2 is prolonged 3. the acute increase, with an infraclinical period of short duration and a longer period of pathological pressure increase. the intracranial pressure increase to the normal limit of 20 mm hg is rapid but slower than the supra-acute pressure increase. once the normal pressure values have been exceeded, the icp increase is gradual, but at a slower speed compared to the previous period. it reaches pathological pressure values of approximately 30 mm hg. this occurs in hypertensive encephalopathy, which includes a self-limiting mechanism: the intracranial pressure increase caused by the arterial tension increase and the occurrence 324 iencean, adam characteristics of the intracranial hypertension of the cerebral vasodilatation eventually lead to the collabation of the intracranial sanguine vessel walls, with the decrease to a certain degree in the cerebral sanguine volume. it is clinically manifested as an incomplete or complete intracranial hypertension syndrome, which may be decompensated unless appropriately treated. the period when the pathological icp values are maintained depends on the efficiency of the etio-pathogenic therapy of the arterial hypertension and on the pathogenic therapy of the ich syndrome. figure 4 slow icp increase, with a long infraclinical period and a prolonged period of pathological pressure values 4. the slow intracranial pressure increase with a prolonged infraclinical period and a long period of pathological icp increase. this type of pressure increase occurs in cases of diminished resorption of the cerebrospinal fluid in acute meningitis, subarachnoid hemorrhage, cerebral venous thromboses and thrombosis of dural sinuses, cerebral thrombophlebites, etc. intracranial pressure increases slowly and gradually until it reaches the normal limit value of 20 mm hg, and it continues its slow increase with periods when it returns to normal pressure values, according to the etiology of the ich syndrome. the compensating capacity of the pressure increase allows a prolonged maintenance of the cerebral sanguine flux, and the period of the pathological pressure values is rather long. there is a development towards a prolonged, complete or incomplete ich syndrome, without leading to clinical decompensation. figure 5 chronic icp increase, with prolonged infraclinical period and an extremely long period of pathologic pressure values 5. the “chronic”, extremely slow increase in intracranial pressure. this occurs in cases of idiopathic intracranial hypertension and in certain cases of thromboses of intracranial venous sinuses. a very slow intracranial pressure increase occurs, which allows good pressure compensation and the maintenance of the cerebral sanguine flux to almost normal values. the pathogeny of the idiopathic intracranial hypertension syndrome is complex, but the intracranial pressure increase has a “chronic” aspect. the pathogenic icp values are very high, reaching to 60 80 mm hg; these are valued that may be maintained in a plate for long periods of time. there is a clinical evolution towards an incomplete ich clinical syndrome, with no decompensation. corresponding author: d. adam neurosurgery, “carol davila” university of medicine and pharmacy, bucharest adamdanil950@gmail.com romanian neurosurgery (2013) xx 4: 318 325 325 references 1. lee s, cho bk, kim h.hypertensive encephalopathy with reversible brainstem edema. j korean neurosurg soc. 2013 aug;54(2):139-41. 2. suetterlin k, borg n, joy h, lovett jk, ghosh bc. when is 'idiopathic intracranial hypertension' no longer idiopathic? pract neurol. 2013 oct 29. doi: 10.1136/practneurol-2013-000680. 3. lindvall p, koskinen lo. intracranial hypertension due to cerebral venous sinus thrombosis following head trauma: a report of two cases. case rep neurol. 2013 sep 25;5(3):168-74 4. suh sy, kim sj. iih with normal csf pressures? indian j ophthalmol. 2013 oct 22. 5. değerliyurt a, teber s, karakaya g, güven a, seker ed, arhan ep, sayli tr. pseudotumor cerebri/idiopathic intracranial hypertension in children: an experience of a tertiary care hospital. brain dev. 2013 oct 16. doi:pii: s0387-7604(13)00288-x. 10.1016/j.braindev.2013.09.007. 6. barnett m, sinha md, morrison d, lim m intracranial hypertension presenting with severe visual failure, without concurrent headache, in a child with nephrotic syndrome. bmc pediatr. 2013 oct 10;13:167. doi: 10.1186/1471-2431-13-167. 7. batra r, sinclair a. idiopathic intracranial hypertension; research progress and emerging themes. j neurol. 2013 oct 2. 8. aylward sc. pediatric idiopathic intracranial hypertension: a need for clarification. pediatr neurol. 2013 nov;49(5):303-4. doi: 10.1016/j.pediatrneurol.2013.05.019. 9. schwartz r, kliper e, stern n, dotan g, berliner s, kesler a. the obesity pattern of idiopathic intracranial hypertension in men. graefes arch clin exp ophthalmol. 2013 nov;251(11):2643-6. doi: 10.1007/s00417-013-2420-6. 7radoi_surgery2014 60 radoi et al surgery in tumors of the lateral ventricles surgery in tumors of the lateral ventricles – last 8 years experience mugurel radoi, leon danaila, florin stefanescu, daniel petrescu, ram vakilnejad neurosurgery clinic of the national institute of neurology and neurovascular diseases, bucharest abstract introduction: tumors of the lateral ventricle are rare lesions including a large variety of benign or malignant tumors. these tumors could originate in the ventricular wall or arising and expanding within the lateral ventricle from the surrounding neural structures. the purpose of this study is to discuss postoperative results and factors that affected the preference for transcallosal or transcortical approach. material and methods: we performed a retrospective study, lasted between 20052013, that comprised 26 consecutive patients who underwent operation for lateral ventricle tumors. the main clinical symptoms and signs were associated with the localization and size of the tumors. cerebral computed tomography and magnetic resonance imaging were used to determine the location and expansion of each tumor. the transcortical approach was used in 17 patients and the transcallosal approach was used in 9 patients. results: total tumor resection was achieved in 73% of cases (19 patients). most frequent histological tumor’s type was glioblastoma, choroid plexus papilloma, ependymoma and meningioma. signs of increased intracranial pressure were most dominant. one patient died because of postoperative intraventricular hemorrhage. additional neurological deficits were seen in 3 patients and postoperative seizure occurred in three patients. one patient with preoperative hydrocephalus required ventriculoperitoneal shunting after tumor’s resection. two patients developed postoperative epidural hematoma and one required reoperation. 15 of 26 patients received postoperative radiotherapy and 6 of them received adjuvant chemotherapy. the mean duration of postoperative evaluation was 24,32 (range 5-92). excepting the cases with subtotal resection, two patients were reoperated for recurrences. conclusions: the nature, size, location and vascularization of intraventricular tumors are the most important elements influencing the choice of surgical approach. surgeons must evaluate all these factors and prefer the short and safe way to remove the tumor. romanian neurosurgery (2014) xxi 1: 60 72 61 introduction tumors of the lateral ventricle are rare lesions including a large variety of benign or malignant tumors. intraventricular tumors are more common in children than in adults, accounting for approximately 13% of adult brain tumors (4,5,9), and till 16% of childhood and adolescent brain tumors (9). of intraventricular brain tumors, 49% in adults are found in the lateral ventricle (9). tumors of the lateral ventricle originate from the ependyma and subependyma that line the ventricles, from the choroid plexus arachnoid and epithelium, or from ectopic tissue rests that have become trapped within the ventricle or its lining (2). tumors expanding within the ventricular cavity cause symptoms and signs of obstruction of the normal cerebrospinal fluid (csf) pathways, compression of the adjacent neural structures, or hydrocephalusinduced by overproduction of csf (13,14,25). the most frequently encountered pathologic diagnosis in tumors of the lateral ventricle, in adults, is astrocytoma, meningioma, ependymoma and choroid plexus papilloma (5,9,13). other rare intraventricular lesions are: subependymoma, subependymal giant cell astrocytoma, neurocytoma, teratoma,epidermoid tumors and metastatic carcinoma (5,11,13,20). magnetic resonance imaging (mri) has become the preferred modality for preoperative evaluation because it provides the best three-dimensional images of these intraventricular tumors and their relationship to surrounding structures. microsurgical resection is the treatment of choice for lateral ventricle tumors. the optimal approach depends on the location and size of the lesion, the size of the lateral ventricles, and the relationship of the tumor to the third ventricle. the transcortical or transcallosal routes afford the surgeon the possibility to completely remove most of these tumors. the location of the lateral ventricles makes passing through cortical structures mandatory in all approaches to these tumors (25). the transcallosal approach may decrease the risk of postoperative seizures and functional deficits (2,6,26). anterior or posterior transcallosal approaches can be safely used to excise tumors located in the ventricular body or atrium. the transcortical approach has the advantage of simplicity, and became an attractive alternative to the transcallosal approach for many tumors located in the frontal, temporal and occipital horn and atrium (19). the presence or absence of preoperative neurologic deficits also influences the surgeon’s decision in selecting a particular approach (4,6,8). we presented our clinical and surgical data for a consecutive series of 26 patients with lateral ventricle tumors. material and methods between january 2005 and august 2013 in our neurosurgical department of the national institute of neurology and neurovascular diseases, there were 26 62 radoi et al surgery in tumors of the lateral ventricles consecutive patients who underwent surgery for tumors of the lateral ventricles. we performed a retrospective study that included clinical, radiological, surgical and pathological data from our recordings. we included in our series neoplasms that originate in the lateral ventricle wall (primary ventricular tumors) and neoplasms arising in the adjacent brain structures but with exophytic grow within the ventricles. two main surgical approaches were used in tumor resection: transcortical approach (17 patients) and transcallosal approach (9 patients). we analyzed the factors that influenced the choice of surgical approach: location of the tumor within the third ventricle, expansion and size of the tumor, approaching from dominant/non-dominant hemisphere, size of ventricles, postoperative residue tumor size and postoperative complications. the 26 patients included 14 males and 12 females. the mean age at admission was 38 years (range 17 to 69 years). there was no pediatric population in our study. the number of males and females was approximately equal in all tumor categories, excepting glioblastoma (male dominancy 3m:1f) and meningioma (female dominancy 1m:4f). the distribution of patients according to the age and sex groups is shown in table i. clinical signs and symptoms depended on the location of the tumor (table ii). the symptoms and signs for tumors located in the ventricular body were high intracranial pressure syndromes, mental disturbances, motor and sensorial deficits. for tumors located in the frontal horn neurological signs were headache, seizures, mental disturbances and high intracranial pressure syndromes. patients with tumors located in the temporal horn or occipital horn developed mainly headache, motor and sensorial deficits, visual deficits and aphasia for the dominant hemisphere. clinical symptoms and signs for tumors located in the atrium included high intracranial pressure signs, mental disturbances, motor and sensorial deficits. preoperative computed tomography (ct) and magnetic resonance imaging (mri) images, both contrast-enhanced and unenhanced, were examined to determine the location and expansion of each tumor, appearance and specific tissue signs characteristics. the arterial supplies of the tumor, arterial and venous anatomy of the region, were studied with cerebral angiography in 7 patients. preoperative hydrocephalus was noted in 4 patients. tabel i the distribution of the patients according to the age groups and gender age (years) no of patients male female 0-11 0 0 0 11-20 4 2 2 21-30 6 4 2 31-40 3 1 2 41-50 6 2 4 51-60 4 3 1 61-70 3 2 1 >71 0 0 0 total 26 14 12 romanian neurosurgery (2014) xxi 1: 60 72 63 table ii signs and symptoms according to the tumor location tumor location no of patients high ip signs seizures mental disturbances motor deficits sensorial deficits aphasia visual deficits ventricular body 8 7 1 2 4 5 0 0 frontal horn 4 2 2 2 1 0 1 0 temporal horn 5 3 2 0 2 2 2 1 occipital horn 3 3 0 0 1 1 0 1 atrium 5 4 0 1 1 1 1 0 septum 1 1 0 1 1 0 0 0 total 26 20 5 6 10 9 4 2 localization of the lateral ventricle tumors were the ventricular body (8 patients), frontal horn (4 patients), temporal horn (5 patients), occipital horn (3 patients), atrium (5 patients) and septum pellucidum (1 patient). the distribution according to the tumor’s histology is presented in table iii. most of the tumors had transependymal expansion, mainly in the frontal and temporal horn and corpus callosum. only choroid plexus papilloma and arachnoid cysts had no transependymal expansion. in choosing the surgical approach we took into account the location, expansion and the size of the tumor, whether it is in the dominant or non-dominant hemisphere. we used the frontal transcortical approach (5 cases), temporal transcortical approach (8 cases), parietal transcortical approach (4 cases), anterior transcallosal approach (7), and posterior transcallosal approach (2). results surgical results regarding the extent of tumor removal and approach used according to tumor origin are shown in table iv. for tumors located in the frontal horn we used in all 4 patients the transcortical middle frontal gyrus approach (figure 1). total excision was achieved in 2 cases. the temporal horn tumors were accessed through a cortical middle temporal gyrus (figure 2) or occipitotemporal incision. difficulty was encountered in tumors located in dominant hemisphere due to lack of cortical stimulation and mapping. total resection was achieved in 4 cases. for occipital horn tumors transcortical approach was used in all cases (figure 3). a superior parietal cortical incision was made in 2 cases, one of them in dominant hemisphere, and a temporooccipital cortical incision was made for removing a choroid plexus papilloma. total excision of 64 radoi et al surgery in tumors of the lateral ventricles tumors was performed in all 3 cases. for tumors located in the body of the lateral ventricles, anterior transcallosal approach was used in most of the cases (figure 4 and figure 5). only a frontal transcortical approach was used for resection of a glioblastoma. with the exception of glioblastomas, the other tumors did not exhibit transependymal extension. subtotal resection was performed in 2 patients with glioblastoma and total resection in 6 cases. tumors located in the atrium (figure 6) were resected through a temporal or parietal transcortical route in 3 cases, and a posterior transcallosal route was used for the excision of an arachnoid cyst. total resection was achieved in 4 out of 5 patients. for a single patient with a small tumor located in the septum pellucidum, we achieved total resection through a posterior transcallosal approach. table iii distribution of patients depending on tumor’s histology tumor histology no of patients glioblastoma 4 choroid plexus paplilloma 5 meningioma 5 ependymoma 4 oligodendroglioma 2 arachnoid cysts 1 anaplastic astrocytoma 1 fibrilar astrocytoma 1 subependymal giant cell atrocytoma 1 subependymoma 1 metastasis 1 table iv type of approach and grade of resection of the tumors depending on their location frontal horn histologic type extension surgical approach grade of resection oligodendroglioma frontal lobe f transcortical subtotal meningioma frontal lobe f transcortical total glioblastoma frontal lobe f transcortical subtotal metastasis frontal lobe f transcortical total temporal horn histologic type extension surgical approach grade of resection meningioma (2) temporal lobe t transcortical total fibrilar astrocytoma temporal lobe t transcortical total ependimoma temporal lobe t transcortical subtotal choroid plexus papilloma no t transcortical total ventricular body histologic type extension surgical approach grade of resection glioblastoma (2) corpus callosum f transcortical/ant transcallosal subtotal ependymoma (2) no ant transcallosal total romanian neurosurgery (2014) xxi 1: 60 72 65 choroid plexus papilloma (2) no ant transcallosal total oligodendroglioma no ant transcallosal total subependymal giant cell astrocytoma no ant transcallosal total atrium histologic type extension surgical approach grade of resection ependymoma parietal lobe p transcortical subtotal meningioma (2) temporal lobe/occipital lobe t transcortical total choroid plexus papilloma no t transcortical total arachnoid cyst no post transcallosal total occipital horn histologic type extension surgical approach grade of resection glioblastoma parietal lobe p transcortical total choroid plexus papilloma no p transcortical total anaplastic astrocytoma parietal lobe p transcortical total septum pellucidum histologic type extension surgical approach grade of resection subependymoma no post transcallosal total f,t,p transcortical – frontal, temporal, parietal transcortical approach; ant/post transcallosal – anterior or posterior transcallosal approach. total tumor resection was achieved in most of the benign or low-grade tumors, and subtotal resection was performed mainly in patients with malignant tumors. from 26 patients who underwent surgery, total resection was achieved in 73% (19 patients). we performed subtotal resection in 6 patients: 3 with glioblastoma, 2 with ependymoma and one with oligodendroglioma. one patient with ependymoma died 12 days after initial surgery because of intraventricular hemorrhage. the postoperative complications are presented in table v. postoperative intraventricular hemorrhage was noted in 2 patients who needed immediate re-operation. epidural postoperative hematoma needing reoperation was recorded for a patient with choroid plexus papilloma, and ventriculoperitoneal shunt application was performed for a patient with glioblastoma and no preoperative hydrocephalus. a small subdural hematoma occurred in one patient and required no treatment. additional neurological deficits were seen in 3 patients. postoperative seizure occurred in 2 patients with oligodendroglioma and, respectively, meningioma. no additional visual defects 66 radoi et al surgery in tumors of the lateral ventricles were seen. 15 out of 26 patients received postoperative radiotherapy and 6 of them received adjuvant chemotherapy. the mean duration of postoperative evaluation was 24.31 months (range 5 to 92 months). shortest follow-up period was recorded in glioblastoma patients with 5, 8 and, respectively 11 months. long periods of follow-up were encountered in patients with meningioma: 84 and, respectively, 92 months, and choroid plexus papilloma with 72 months of follow-up. at the end of follow-up, there were no recurrences or increased in tumor sizes in meningioma, choroid plexus papilloma, subependymal giant cell astrocytoma, subependymoma and arachnoid cyst. the maximum recurrences and increased tumor size were seen in glioblastoma. excepting the cases with subtotal resection, 2 patients with recurrences were reoperated (ependymoma and anaplastic astrocytoma). table v number of postoperative complications related to the tumor’s histology and initial number of patients tumor type no of patients postoperative complications glioblastoma 4 intraventricular hemorrhage and reoperation (1); ventriculo-peritoneal application (1); additional neurological deficits (2); no complication (2). choroid plexus papilloma 5 epidural hematoma and reoperation (1) ependymoma 4 intraventricular hemorrhage and death (1); no complication (3). meningioma 5 brain edema (1); seizure (1) oligodendroglioma 2 seizure (1) arachnoid cyst 1 no complication anaplastic astrocytoma 1 additional neurological deficits (1) fibrilar astrocytoma 1 no complication subependymal giant cell astrocytoma 1 no complication subependymoma 1 no complication metastasis 1 no complication figure 1 metastasis developed in the frontal horn of the left lateral ventricle and expanding in ipsilateral frontal lobe; preoperative and postoperative contrast ct scan; left transcortical middle frontal gyrus approach; total resection. romanian neurosurgery (2014) xxi 1: 60 72 67 figure 2 fibrilar astrocytoma developed in the temporal horn of the right lateral ventricle; preoperative contrast mri and postoperative contrast ct scan; right cortical middle temporal gyrus approach; total resection. figure 3 anaplastic astrocytoma developed in the occipital horn of the right lateral ventricle; preoperative and 2 months postoperative ct scan; approach through a right parietal transcortical route; total resection. figure 4 subependymal giant cell astrocytoma developed in the ventricular body; preoperative and postoperative mri; anterior transcallosal approach; total resection. 68 radoi et al surgery in tumors of the lateral ventricles figure 5 ependymoma developed in the ventricular body; preoperative and postoperative (14 days after surgery) cerebral ct scan; anterior transcallosal approach; total resection. figure 6 meningioma developed in the atrium of the lateral ventricles; preoperative and postoperative mri; left temporooccipital transcortical approach; total resection. discussions the histopathologic diagnosis of the lateral ventricle tumors varied with the age of the patients (5,12). in children, these tumors were often choroid plexus tumors, whereas in adults they tended to be gliomas (4,7). in our study there were not pediatric patients. the youngest patient was 18 years old at the time of surgery. the number of males and females was approximately equal in all tumor categories, excepting glioblastoma (male dominancy 3m:1f) and meningioma (female dominancy 1m:4f). tumors of the lateral ventricle most often grow very large before they become clinically manifest. in order of decreasing frequency they occur in the frontal horns, ventricular body and atrium (1). in another series, the most common localizations of lateral ventricle tumors were atrium, frontal horn, ventricular body and temporal horn (10). goklap et al (5) reported 112 lateral ventricle tumors in their study, and the most frequent sites of the tumors were the frontal horn, body and the atrium. in our series, the incidence of tumor localization within the lateral ventricles in descending order of frequency was reported as ventricular body (30.76%), atrium (19.23%), temporal horn (19.23%) and frontal horn (15.38%). neoplasms that originate in the ventricular wall and its lining are considered primary ventricular tumors, and, the majority of these are benign or low-grade lesions (meningioma, choroid plexus papilloma, ependymoma) (14,16). tumors that arise in the adjacent brain structures with important exophytic growth within the ventricle are considered secondary ventricle tumors with transependymal development, and they are commonly gliomas (3). in this report, the romanian neurosurgery (2014) xxi 1: 60 72 69 most frequent tumor types were meningioma (19.23%), choroid plexus papilloma (19.23%), glioblastoma (15.38%) and ependymoma (15.38%). the best surgical approach to the tumors of the lateral ventricles is that which offers the shortest distance to the lesion with a perpendicular field of view, requires minimal retraction of the brain, avoids trajectory through functional structures and provides clear visualization of the vascular feeding branches (24). surgical approaches to the lateral ventricles could be summarized as follow: (1) anterior approaches: anterior transcortical and anterior transcallosal, (2) posterior approaches: posterior transcortical and posterior transcallosal, (3) temporal and subtemporal transventricular approaches, inferior posterior frontotemporal (25). due to microsurgical techniques we achieved total resection of the tumor in 73% (19 patients). in this series, transcortical middle frontal gyrus approach was used in 5 patients for resection of tumors in the ipsilateral frontal horn or the anterior ventricular body. most of these tumors were large and cause obstruction of the foramen of monro. in such cases, is important to locate the foramen of monro and avoid the damage of the fornix (25). this approach is facilitated when the lateral ventricles are enlarged. in our series, 3 out of 5 tumors operated with this approach were resected subtotally, two of them being glioblastoma multiformes. the transcortical approach to the temporal horn is the best method to remove lesions in this area. this approach provides a short trajectory to the tumor. in the non-dominant hemisphere, this is a very acceptable route, causing minimal morbidity. we used the middle temporal gyrus approach, on the non-dominant hemisphere, to totally remove 2 tumors located in the temporal horn and 2 in the atrium. in the dominant hemisphere, the presence of the language cortex represents an important issue. in such cases, this approach requires careful dissection and retraction, refinement in techniques and the use of cortical stimulation and mapping (19). on the left hemisphere, we used this approach in 3 cases and achieved total resection with minimal postoperative aphasia. the superior parietal approach is very suitable for reaching tumors located in the posterior part of the ventricular body and atrium, especially for large masses with a superior development (4,5). cortical incision should be performed high enough to avoid visual field, because calcarine gyrus is adjacent to the medial wall of the atrium. because the vascular supply to the tumor is deep, this approach did not provide access to vascular control before tumor removal. we safely performed this approach in the 4 tumors, two of them located in the dominant hemisphere. we achieve total resection of 3 tumors in the occipital horn, and a subtotal resection for an ependymoma located in the atrium. 70 radoi et al surgery in tumors of the lateral ventricles the transcallosal approaches to the lateral ventricle tumors was performed in 9 cases in our series. there are several advantages of these approaches over the transcortical route: reduce the risk of brain injury with appropriate brain relaxation and minimal retraction, reduce the risk of postoperative porencephalic cyst and subdural hygroma formation, low risk of postoperative seizures, low risk of functional deficits, need normal sized ventricles (18,22). in the anterior transcallosal approach, the callosal section must spare the genu of the corpus callosum, especially near the rostrum and the anterior commissure anteriorly, and the posterior part of the sectioned callosum must not go beyond the interparietal commissure (23). as reported in the literature, the large tumors of the occipital horn and atrium were not suitable for posterior transcallosal resection, as the tumor itself prevented the hemispheric retraction that is required to achieve tumor removal, and for proper choroidal vessel control (17). in our series, the anterior transcallosal approach was used in 7 cases of tumors located in the ventricular body. total tumor removal was achieved in all cases, except one patient with a glioblastoma multiforme. all tumors had small or medium size (not larger than 35 mm.). the posterior transcallosal approach was used for resection of an arachnoid cyst from the atrium and a small ependymoma from the septum pellucidum. in 65.5% cases we had no postoperative complications. preoperative hydrocephalus was noted in 4 patients, but we performed shunt application in one patient who had a bifrontal glioblastoma and was operated by the anterior transcallosal approach. the number of patients requiring a shunt vary based on different factors (19). approximately 10% to 50% of patients will ultimately required cerebrospinal fluid diversion (15). the reported incidence of postoperative seizures after transcortical approaches varied widely from 19% to 75% (3,4). in our series, there were 5 patients who experienced postoperative seizures (19.23%), but only two of them required prolonged antiepileptic treatment, operated using a frontal, respectively, temporal transcortical approach. in this series, the authors reported a low mortality rate of 3.84%, meaning that one out of 26 patients died secondary to an important postoperative intraventricular hemorrhage. the deaths in the last decades reported series are lower than 10% and are usually due to severe postoperative hemorrhage or pulmonary emboli (5,6,15). conclusions tumors of the lateral ventricles are rare, deep-seated lesions, relatively slow growing and can became larger before causing symptoms. because of their large size the treatment is surgical resection. the selected approach must take into account the size, location, expansion, vascularization, the critical brain structures nearby the tumor and the consequent neurologic sequelae. our goal was romanian neurosurgery (2014) xxi 1: 60 72 71 complete resection of the tumor using microsurgical techniques, but when the tumor was malignant or attached to eloquent structures, subtotal resection was preffered. there were no significant differences in complications between the transcortical and transcallosal approaches. finally, we can conclude that the surgeon should prefer the shortest, most familiar and the most safe way in removing a lateral ventricle tumor. corresponding author: dr. radoi mugurel e-mail address: muguradoi@yahoo.com tel: 0723527292 references 1.abosch a, mcdermott wm, wilson cb. lateral ventricular tumors. in: kaye ah and black pmcl , eds. operative neurosurgery. london-new york –sydney: churchill livingstone 2000, pp. 799-814 2.apuzzo ml, chikoyani ok, gott ps, teng el, zee cs, giannotta sl, weiss mh. transcallosal, interfornicial approaches for lesions affecting the third ventricle: surgical considerations and consequences. neurosurgery 10:547-554, 1982 3.d’angelo va, galarza m, catapano d, monte v, bisceglia m, carosi e. lateral ventricle tumors: surgical strategies according to tumor origin and development – a series of 72 cases. neurosurgery 56 (suppl 1): 36-45, 2005. 4.ellenbogen rg. transcortical surgery for lateral ventricular tumors. neurosurg, focus 10(6): article 2, 2001. 5.gokalp hz, yuccer n, arasil e, deda h, attar a, erdogan a, egmen n, kanpolat y. tumors of the lateral ventricle. a retrospective review of 112 cases operated upon 1970-1997. neurosurg rev 21:126-137, 1998. 6.jeeves ma, simpson da, gellen g. functional consequences in the transcallosal removal of intraventricular tumors. j neurol neurosurg psychiatry 42:134-142, 1979. 7.jelinek l, simimiotopoulos jg, parisi je, kanzer m. lateral ventricular neoplasms of the brain: differential diagnosis based on clinical, ct, and, mri findings. ajr 155:365-372, 1990. 8.kasowski h, piepmeier jm. transcallosal approach for tumors of the lateral and third ventricles. neurosurg focus 10 (6): article (3), 2001. 9.koos wt, miller mh. tumors of the ventricular system. in: koos wt, miller mh. intracranial tumors of infants and children. stuttgart: verlag, 1970:233-253. 10.lapras c, deruty r, bret ph. tumors of the lateral ventricle. in: symon l, eds. advances and technical standards in neurosurgery. wien-new york: springerverlag, 1984. 11.nishito s, fujiwara s, tashima j, takheshita i, fuji k, fukui m. tumors of the lateral ventricular wall, especially the septum pellucidum: clinical presentation, and variations in pathological features. neurosurgery 27: 224-230, 1990. 12.osborn ag. diagnostic neuroradiology. st louis, mosby; 1994: 401-528. 13.pendl g, ozturk e, haselberger k. surgery of tumors of the lateral ventricle. acta neurochir 116:128136, 1992. 14.piepmeier jm, sass kj. surgical management of lateral ventricular tumors. in: paoletti p, takakura k, walker m, eds. neuro-oncology, dordecht. kluwer academic publishers, 1991: 333-335. 15.piepmeier jm, spencer dd, sass k: lateral ventricular masses. in: apuzzo mlj, eds. brain surgery: complication avoidance and management. new york, churchill livingstone, 1993: 581-599. 16.piempier jm, westerveld m, spencer dd, sass k. surgical management of intraventricular tumors of the lateral ventricle. in: schimdek hh, sweet wh, eds. operative neurosurgical techniques. indications, methods and results. philadelphia: w.b saunders company, 1995: 725-738. 17.rabb ch, apuzzo mlj. options in the management of ventricular masses. in: tindall gt, cooper pr, barrow dl, eds. the practice of neurosurgery. baltimore: williamsαwilkins, 1996, 1229-1242. 18.rhoton al jr. the lateral and third ventricles. neurosurgery 51 (suppl 1): s1-207-s1-271, 2002. 19.secer hi, duz b, izci y, tehli o, solmaz i, gonul e. tumors of the lateral ventricle: the factors that affected the preference of the surgical approach in 46 patients. turkish neurosurgery 2008, vol. 18, no. 4, 345-355. 20.shen ho y, plets c, goffin j, dom r: hemangioblastoma of the lateral ventricle. surg neurol 33: 407-412, 1990. 72 radoi et al surgery in tumors of the lateral ventricles 21.spencer dd, collins wf, sass kj. surgical management of lateral intraventricular tumors. in: shmidek hh, sweet w, eds. operative neurosurgical techniques. orlando: gruneαstratton, 1988:583. 22.suchart w. anterior transcallosal and transcortical approaches. in: apuzzo mlj, eds. surgery of the third ventricle. baltimore: williamsαwilkins, 1987, pp. 303325. 23.takafumi nishizaki. surgical approaches for lateral ventricular trigone meningiomas. in: monleon d, eds. meningiomas – management and surgery. isbn 978953-51-0175-8., 2012. 24.tew jmjr, lewis al, reichert kw. management strategies and surgical techniques for deep-seated supratentorial arteriovenous malformations. neurosurgery 36:1065-1072, 1995. 25.timurkaynak e, rhoton md jr, barry m. microsurgical anatomy and operative approaches to the lateral ventricles. neurosurgery 19: 685-723, 1986. 26.winston kr, cavazzuti v, arkins t: absence of neurological and behavioral abnormalities after anterior transcallosal operation for third ventricular lesions. neurosurgery 4:386-393, 1979. doi: 10.33962/roneuro-2021-046 multiple intracranial aneurysms in subarachnoid haemorrhage. which one has bled? a diagnostic dilemma. zahraa f. al-sharshahi, samer s. hoz, mustafa m. altaweel romanian neurosurgery (2021) xxxv (3): pp. 277-280 doi: 10.33962/roneuro-2021-046 www.journals.lapub.co.uk/index.php/roneurosurgery multiple intracranial aneurysms in subarachnoid haemorrhage. which one has bled? a diagnostic dilemma zahraa f. al-sharshahi, samer s. hoz, mustafa m. altaweel department of neurosurgery. neurosurgery teaching hospital. baghdad. iraq abstract this paper is intended as an illustrative teaching case. it gives a porotype case of a patient with subarachnoid haemorrhage and multiple intracranial aneurysms, where the ct data is non-conclusive as to the source of haemorrhage. the paper then discusses the diagnostic challenges and management pearls, pertaining to such scenarios. the paper concludes with a few “take-home points” that summarise the criteria to be applied in such cases. case description a 39-year-old male patient with autosomal dominant polycystic kidney disease (adpkd) presented to the emergency department with a sudden-onset, severe headache and vomiting followed by an altered level of consciousness (gcs:10-e2m5v3). a computed tomography (ct) scan of the head revealed diffuse subarachnoid hemorrhage (sah) (the typical star-shape sign), but did not give a clue for the source of bleeding (figure 1.a). cerebral ct angiography (cta) revealed two intracranial saccular aneurysms in the anterior communicating artery (acom) and the right middle cerebral artery (mca); of 7 mm each with no vasospasm observed (figure 1.b,c). however, it could not be determined from the cta data which aneurysm has ruptured. cerebral catheter angiography is not available in our country. thus, the team assumed that the ruptured aneurysm was located at the acom, and planned the surgery accordingly. the patient underwent surgery on the day of admission. intraoperatively, it was evident that the anterior communicating artery (acom) was indeed the source of bleeding. the aneurysm was clipped and secured, without complications. early postoperative cranial ct scan showed 2 clips in position with no other significant findings (figure1.d). the patient had an uneventful recovery and he remained well. keywords subarachnoid haemorrhage, multiple intracranial aneurysms corresponding author: zahraa al-sharshahi neurosurgery teaching hospital. baghdad. iraq zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 278 zahraa f. al-sharshahi, samer s. hoz, mustafa m. altaweel a b c d figure. a 39-year-old male patient with autosomal dominant polycystic kidney disease (adpkd) presented to the emergency department with a sudden-onset, severe headache and vomiting followed by an altered level of consciousness (gcs:10-e2m5v3). a: an initial cranial ct scan showing sah in the basal cisterns (the typical star-shape sign) with no clue to the source of bleeding. b and c: a cerebral ct angiography3d reconstructionrevealing multiple intracranial saccular aneurysms in the acom (b inferior view with an arrow pointing to the acom aneurysm) and the right mca (b anterior view with an arrow on the superiorly directed, right mca aneurysm); both aneurysms are regular, rounded-shaped, have no murphy’s teat and, have a size of 7 mm each with no vasospasm noticed. d: an early, post-operative cranial ct scan showing 2 clips in position with no other significant findings discussion the incidence of multiple intracranial aneurysms (mias) amongst all patients with aneurysms is around 15-33.5% [7] [4] [10]. hypertension has been identified as the risk factor most commonly associated with mias [2]. mias are more common in women, with a female to male ratio of 5:1. the ratio is even higher (11:1) in patients with three or more aneurysms [10]. overall, the anterior communicating artery (acom) is the most common location for intracranial aneurysms (35%) [8]. common sites for multiple intracranial aneurysms include the posterior communicating artery (pca) the middle cerebral artery (mca), the anterior communicating artery, and the ophthalmic artery [10]. in patients with sah and mias, verifying the source of bleeding is not always a straightforward task. furthermore, misidentification of the true ruptured aneurysm is a major cause of postoperative re-bleeding and mortality. in one series that examined a cohort of 76 patients with sah and mias, the rate of false localization of the ruptured aneurysm was 9%, resulting in rebreeding and mortality at the rates of 5.3% (n=4/76) and 2.6 (n=2/76), respectively [6]. the rate of rupture site misidentification is even higher in patients with a non-definitive bleeding pattern on initial ct scan, quoted at 16.2% [11] the only absolute evidence for aneurysm rupture is angiographic dye extravasation or the “smoking gun” sign [10]. this is, however, an uncommon sign that indicates a grim prognosis [10]. other highly accurate angiographic findings include focal spasm, aneurysm shape irregularities (murphy’s teat), larger size, focal mass effect and aneurysm shape shifts on repeat imaging [3, 10]. while these signs have a high predictive value of the rupture site, they are fairly rare [10]. clinical signs are less reliable when it comes to identifying the site of hemorrhage. reports on their usefulness vary, with a sensitivity range of 7-33%[10] [1]. sometimes, the ct scan shows a clear hemorrhage pattern that suggests the source of the bleeding [5]. nevertheless, where there is a diffuse, symmetrical pattern of hemorrhage or localized bleeding along with numerous aneurysms in the vicinity, the ct is unable to delineate the site of rupture [5]. one reliable sign is that might give a clue to the site of rupture is the location of the epicenter of hemorrhage (area with most contraction) on ct or mri [3]. in our case, none of the above-mentioned radiological signs were present, and hence prediction of the site of the ruptured aneurysm was responsibility of the treating neurovascular team. in this case, the acom was presumed to be the ruptured site given the frequency of these aneurysms and the fact that they are more prone to rupture than mca aneurysms. in this case, the surgery was directed only at the ruptured acom aneurysm. some surgeons opt for the treatment of all significant aneurysms at the time of surgery to 279 multiple intracranial aneurysms in subarachnoid haemorrhage. which one has bled? reduce the risk of late re-bleeding, while others recommend treating the ruptured aneurysm only [12]. in either case, prompt identification and treatment of the ruptured aneurysm remains a priority, as it has significant implications on patient outcomes. in fact, it has been shown that the most common cause of late re-bleeding is the originally ruptured aneurysm which was not identified at the time of initial surgery [9]. it is not yet determined whether mias are associated with worse surgical outcomes. however, several risk factors have been investigated for their prognostic significance in patients with sah and mias. one population-based study has shown that for patients > 70 years of age, the prognosis is less favorable for those with sah and multiple aneurysms as compared to those with sah and a single aneurysm [7] in summary, the present case has illustrated the potential challenging nature of sah in patients with mias and emphasized on the importance of adopting a systematic, step-wise progression through preoperative planning, and the critical impact this has on surgical outcomes. take-home points: patients with mias and sah present a challenge to the neurovascular surgeon. when the bleeding pattern on the initial ct scan is non-definite, meticulous examination of the cta and/or dsa data becomes very important and should take into consideration the following criteria [3] -ct/mri: where is the area exhibiting the greatest concentration (aka. the epicenter of sah)? -cta/dsa: where is the area with local vasospasm? -morphology: is there a “murphy’s teat” – a daughter cystor an area of irregularityin any of the aneurysms? -size: which aneurysm is larger? if none of the above criteria applies, as in this case, then the judgment of the treating team is critical. the caveat is that, when such a timesensitive decision is required, it is safer to assume that the acom is culprit site, as it is the predilect site of intracranial aneurysms, and is , hence, overall the most common site of rupture. abbreviations adpkd: autosomal dominant polycystic kidney disease gcs: glasgow coma scale emv: eye movement and verbal response ct: computed tomography sah: subarachnoid haemorrhage 3d: three dimensional acom: anterior communicating artery mca: middle cerebral artery cta: computed tomographic angiography mias: multiple intracranial aneurysms mca: middle cerebral artery pca: posterior communicating artery n: number mri: magnetic resonance imaging dsa: digital substraction angiography aka: also known as references 1. almaani ws, richardson ae. multiple intracranial aneurysms: identifying the ruptured lesion. surg neurol 1978;9(5):303-305. 2. ellamushi he, grieve jp, jäger hr, kitchen nd. risk factors for the formation of multiple intracranial aneurysms. j neurosurg 2001;94(5):728-732. 3. greenberg ms. handbook of neurosurgery. 9th ed: thieme medical publishers; 2020. 4. hadjiathanasiou a, schuss p, brandecker s, welchowski t, schmid m, vatter h, et al. multiple aneurysms in subarachnoid hemorrhage identification of the ruptured aneurysm, when the bleeding pattern is not self-explanatory development of a novel prediction score. bmc neurology 2020;20(1):70. 5. hadjiathanasiou a, schuss p, brandecker s, welchowski t, schmid m, vatter h, et al. multiple aneurysms in subarachnoid hemorrhage identification of the ruptured aneurysm, when the bleeding pattern is not self-explanatory development of a novel prediction score. bmc neurology 2020;20(1):70. 6. hino a, fujimoto m, iwamoto y, yamaki t, katsumori t. false localization of rupture site in patients with multiple cerebral aneurysms and subarachnoid hemorrhage. neurosurgery 2000;46(4):825-830. 7. kaminogo m, yonekura m, shibata s. incidence and outcome of multiple intracranial aneurysms in a defined population. stroke 2003;34(1):16-21. 8. keedy a. an overview of intracranial aneurysms. mcgill j med 2006;9(2):141-146. 9. kwak r, niizuma h, ohi t, suzuki j. angiographic study of cerebral vasospasm following rupture of intracranial aneurysms: part i. time of the appearance. surg neurol 1979;11(4):257-262. 10. nehls dg, flom ra, carter lp, spetzler rf. multiple intracranial aneurysms: determining the site of rupture. j neurosurg 1985;63(3):342-348. 11. orning jl, shakur sf, alaraj a, behbahani m, charbel ft, 280 zahraa f. al-sharshahi, samer s. hoz, mustafa m. altaweel aletich va, et al. accuracy in identifying the source of subarachnoid hemorrhage in the setting of multiple intracranial aneurysms. neurosurgery 2018;83(1):62-68. 12. winn hr, almaani ws, berga sl, jane ja, richardson ae. the long-term outcome in patients with multiple aneurysms. incidence of late hemorrhage and implications for treatment of incidental aneurysms. j neurosurg 1983;59(4):642-651. microsoft word 11.elephteriosb_titaniummesh 456 bogris elephterios et al titanium mesh cranioplasty for patients with cranial defects titanium mesh cranioplasty for patients with large cranial defects – technical notes bogris elephterios1, n. dobrin2, a. chiriac2 1“gr.t. popa” university of medicine and pharmacy, iasi 2emergency clinical hospital “prof. dr. n. oblu”, neurosurgery department, iasi abstract we propose to describe some personal points of view concerning the repair of large cranial defects using titanium mesh, and in this sense we present few cases. also we expose the presurgical planning by 3d imaging acquisition with the radiologic digital system which allow a computer aided design for a precise measurement of the shape and the curvature of cranial defect. keywords: cranioplasty, titanium, computer-aided design, skull defects introduction there are a lot of pathological processes with involve the cranium including calvarial and skull base anatomical regions, traumatic defects, congenital, iatrogenic injuries, septic and all this processes leave the cranial defects exposing in this manner the brain with the soft covers, dura mater and the skin layers and also the imperfection of the skull shape induce important variations in intracranial pressure especially in positional movements orto-clinostatism. we insist on the aesthetic aspect because these large defects have also an important cosmetic impact. titanium (ti22) was discovered in 1791 by william gregor in england and is a soft metal, very resistant to corrosion, used in various alloys of iron, vanadium, aluminum, etc. titanium is used especially in aerospace, military and increasingly more in medical prosthetics. characteristic of this metal is the ratio strength / weight, pure titanium (unalloyed) has greater resistance to the same strength as steel and 45% less mass, so it is a soft metal, very resistant to mechanical forces and fully biocompatible and corrosion resistant. these properties make the material of choice today in cranial and spinal prosthesis. clinical cases we simply want to show some cases admitted in our hospital with diverse cranial pathology who had bone defects of varying sizes and lack of bone that was solved by implantation of titanium mesh prosthesis . case 1. m. 25 yrs. admitted after a head trauma with parieto occipital bilateral brain laceration with multiple comminuting fractures. in the first time the acute trauma surgery was needed and in the second time the cranial defects were corrected by titanium implants. we must emphasize that we have developed a preimplantation rotational 3d ct to assess the lack of bone size and curvature radius of the head and then, post implantation we realize a 3d verification to appreciate the correct position of prosthesis and its connection to romanian neurosurgery (2010) xvii 4: 456 – 460 457 the plate bone by titanium screws. this technique was performed with siemens axiom artis system in a acquisition 3d rotational protocol with 60frames /sec on 20 seconds that means about 1000 frames which need reconstruction in special software . figure 1, figure 2 case 2. f 38 yrs. admitted after multiple intervention for septic problems, subdural empiema and osteitis with frontosinusal origin, presented three large cranial postoperative defects. the correction intervention was made after 4 years from the septic episode after controlling the septic problems, imaging revealed that the risk is practically null. underwent anterior eradication of septic foci, 3d exploration highlights accurately whether or not there are septic risk. figures 3, 4, 5, 6, 7. figure 1, 2 3d aspects pre and post implants 458 bogris elephterios et al titanium mesh cranioplasty for patients with cranial defects figures 3, 4, 5, 6, 7 first image present the preoperative aspect the others reveals the correct insertion of titanium prosthesis mesh and screws and also is the inside view to appreciate the endocranium discussions the titanium is considerate the most compatible metal and can be easy integrated in the human body. its biocompatibility make it the election material in joint replacement, dental and craniofacial implants. usual the titanium is alloyed with aluminium or vanadium. an interesting property of titanium is the possibility to osseointegrate in this way there are prosthesis from titanium migrated with osteogenic substances (polyvinyl lactic acid) in plasma spray. another property of titanium is the special radiolucency so the non ferromagnetic capacity permit the safe examination in mri high field, useful for long term follow-up of the patients. it should be added that very important that the properties titanium is compatible with mri exploration (not ferromagnetic) and does not induce any major artifacts exploring the ct or mri, by providing such accurate postoperative imaging (radiolucent). osseous defects of various sizes and forms can be solved by attaching autologous bone fragments fixed with titanium plates and screws. it also shows that titanium plate are also elastic and has resistance well calculated to allow easy intraoperative modeling, establish appropriate curvature of the head. romanian neurosurgery (2010) xvii 4: 456 – 460 459 figure 8 some aspects of the devices used during surgery sites. the fitting skull comes with special drills for every type of screw sizes and can control the insertion depth of bone figure 9 intraoperative aspect figure 10 intraoperative aspect figures 9, 10 titanium dynamic mesh prosthesis covers the whole area and is perfectly connected between bone and the basal region of bifrontal convexity. conclusions in the neurosurgical pathology there are many processes that interested the brain and bone shell, for various reasons (postsurgical, traumatic, post-replacement process), require resection with restoration per primam or a subsequent time for remaining defect. there are several principles: the implant must be stable, resistant to daily activities and possibly minor injuries, to effectively protect the brain, not skid spontaneous, to be perfectly biocompatible, does not interfere with voucher skin vasculature and not least to make a adequate cosmetic correction. now there are a variety of biomaterials that meet these goals. of all the titanium site is best suited for cranioplasty . surgical procedure is relatively simple but requires a well set up infrastructure and obviously a degree of skill. basically so far i have not reported immediate or delayed complications. is it true that high prices are often prohibitive, but the cost-effectiveness, ease of implantation process, significantly reducing operator time and duration of hospital stay makes it preferable. research news after fraunhofer institute for manufacturing and advanced materials ifam, september 2010, a new titanium based material a foam like structure was created to replace injured bones. this new form of titanium presentation in medical practice will open a lot of possibility, in 460 bogris elephterios et al titanium mesh cranioplasty for patients with cranial defects bone pathology including vertebrae replacement. the technology involve open cell polyurethane foam saturated with titanium powder which make a material very close with human bone consistency. interests the authors declare no conflict of interests. references 1. carr jc, fright wr, beatson rk (1997) surface interpolation with radial basis functions for medical imaging. ieee trans med imag 16(1):96–107 2. lee m-y, chang c-c, lin c-c et al. (2002) custom implant design for patients with cranial defects. ieee eng med biol mag 21(2): 38–44 3. mingzhe li, yuhong liu, shizhong su et al. (1999) multi-point forming: a flexible manufacturing method for a 3-d surface sheet. j mater process technol 87:277–280 4. cai zy, li mz (2002) multi-point forming of threedimensional sheet metal and the control of the forming process. int j pressure vessels piping 79:289–296 5. li mz, cai zy, sui z et al. (2002) multi-point forming technology for sheet metal. j mater process technol 129:333–338 6. chen j (2001) the study of multi-point forming cad and sectional multi-point forming process. dissertation, jilin university 7. sanan a, haines sj. repairing holes in the head: a history ofcranioplasty. neurosurgery 1997;40:588 – 603. 8. miyake h, ohta t, tanaka h. a new technique forcranioplasty with l-shaped titanium plates and combinationceramic implants composed of hydroxyapatite and tricalciumphosphate (ceratite). neurosurgery 2000;46:414 – 8. 9. agner c, dujovny m, gaviria m. neurocognitive assessment before and after cranioplasty. acta neurochir (wien) 2002;144:1033 – 40; discussion 1040. 10. segal dh, oppenheim js, murovic ja. neurological recoveryafter cranioplasty.neurosurgery 1994;34:729 – 31; discussion 731. 11. yoshida k, furuse m, izawa a, iizima n, kuchiwaki h, inaos. dynamics of cerebral blood flow and metabolism in patientswith cranioplasty as evaluated by 133xe ct and 31p magneticresonance spectroscopy. j neurol neurosurg psychiat 1996;61:166 – 71. 12. blum ks, schneider sj, rosenthal ad. methyl methacrylatecranioplasty in children: long-term results. pediat neurosurg1997;26:33 – 5. 13. titanium foams replace injured bones research news 09-2010-topic 1 – fraunhofer-gesellschaft. fraunhofer.de. retrieved on 2010-09-27. 14. winter, mark (2006). "chemistry: periodic table: titanium". webelements http://www.webelements.com/webelements/elements/te xt/ti/index.html. retrieved 2006-12-10. microsoft word 2katoyoko_subarachnoid.doc romanian neurosurgery (2010) xvii 3: 261 – 274 261 subarachnoid hemorrhage yoko kato, hirotoshi sano department of neurosurgery, fujita health university, japan abstract intracranial aneurysms represent the most common etiology of nontraumatic subarachnoid hemorrhage. management of intracranial aneurysms must be meticulous and tailor made for each patient. various strategies in the management include main artery ligation, aneurysm neck occlusion, wrapping or coating, clipping or coiling. this article presents an overview on subarachnoid hemorrhage, pathophysiology, investigations, a management guideline and outcome in intracranial aneurysms. keywords: subarachnoid hemorrhage, cerebral blood flow, clinical grades aneurysm introduction modern management of intra-cranial aneurysms must be very meticulous and tailor made for each patient. various strategies in the management include main artery ligation, aneurysm neck occlusion, wrapping or coating, clipping or coiling. indications for treatment include unruptured symptomatic aneurysms, aneurysms with mass effect, cranial nerve deficits, ischemia, small leak, size less than 3mm, family history of aneurysms. contraindications to treatment include elderly patients, medical comorbidity and intra-cavernous aneurysms. guidelines for treatment in japan include young ageless than 6, history of previous rupture, family history of sah, large aneurysms more than 7 mm, symptomatic patient, increasing size of aneurysm on follow-up, location of the aneurysm in a low surgical risk area. epidemiology epidemiological studies have shown that 60% of patients die or are disabled due to aneurismal rupture, with the primary cause of death being an initial bleed or a rebleed with vasospasm. subarachnoid hemorrhage (sah) caused by the rupture of an intracranial aneurysm is one of the most common neurosurgical emergencies with one third of strokes having sah and aneurysms accounting for 70% of these. aneurysms rupture in a rate of 12 per 100,000 population per year, especially in the 5th and 6th decades, with high mortality and morbidity, especially from the first hemorrhage in about 43% of the cases and surgeons can attempt to avoid re-bleed, since surgery and the strategies for management have become very safe with modern technical gadgets. 2.5% of normal population can harbor unruptured aneurysms with a prevalence of 0.65% with a preponderance of aneurysms in the ratio of 2: 1 among women. ica aneurysms are more common in women, where as acorn aneurysms are more common in men, with presence of multiple aneurysms in 15 30% of the patients. with gain of more operative skill and experience, it is safer to deal with these aneurysms regardless of their size or position. 262 yoko kato, hirotoshi sano subarachnoid hemorrhage figure 1 ct scan of the brain showing subarachnoid hemorrhage figure 2 axial ct scan of the brain showing subarachnoid hemorrhage surgical decision making, timing of surgery, prevention of re-bleed, use of endovascular techniques along with grade of the patient, presence or absence of intraparenchymal or intraventricular bleed, with or without vasospasm, affect the outcome. etiopathogenesis and neurogenetics the exact etiopathogenesis of intracranial aneurysms is not clear. implications of risk factors include smoking, hypertension, genetic factors with association of connective tissue disorders like polycystic kidney disease, ehler’s – danolos syndrome type iv, marfan’s syndrome, nf-1, pseudoxanthoma elasticum and alpha-1 antitrypsin deficiency. at least 5% of pacients detected with intracranial aneurysms have heritable connectivity tissue disorder. it can also arise due to new mutations. în pacients with polycystuc kidney disease, one în four pacients have aneurysms and account for 6 to 7% of all pacients. sub-arachnoid hemorrhage and mortality is more în pacients with polycystic kidney disease. the gene is localized on chromosome 16 and chromosome 4. similarly, type iv ehler’s -danolos syndrome have the gene located in pro-alpha 1-3 chain collagen type iii of chromosome 2. patients with alpha-i antitrypsin deficienc suffer with vascular problems like aneurysms, arterial dissections and fmd. with risk of subarachnoid bleed, the gene is located on allele piz and pis marker genes on chromosome 14, which is a polymorphic gene. patients with marfans syndrome have gene mutation encoding fibrillin-1, which is involved in connective tissue structural integrity. in nf-l, gene encoding neurofibromin with gap guanosine romanian neurosurgery (2010) xvii 3: 261 – 274 263 triphospate activating protein is involved. in pseudo xanthoma elasticum, the elastic fibers and basic molecular defect is involved in the vessels and is an autosomal recessive and / or dominant variant, mapped on to chromosome 16p13.1. familial aneurysms are not associated with heritable ctd. the actual inheritance pattern is not known but an inheritance either autosomal dominant or recessive or multifactorial type of transmission may be involved with genetic heterogeneity. they have a tendency to rupture 5 years earlier than sporadic aneurysms and also rupture at a size smaller by 2 mm than the sporadic variants. screening studies for detection of familial intracranial aneurysms has been performed by ct angrography or mr angiography and is indicated even in asymptomatic first degree relatives in families with two or more affected members with a detection rate of 10% and with aneurysms detected in 30% of these patients, being larger than 5mm in diameter. there are no actual guidelines for screening. however, a medical history, family history, physical exammation, genetic counseling, renal sonography, collagen analysis and screening of relatives is warranted. advances in genetics have made linkages to chromosomal locus or an intracranial aneurysm gene. genetic polymorphism of angiotensin 1 converting enzyme and endoglin genes may be implicated in these patients. risk factors there are several confounding factors which determine the rate of rupture like the size of the aneurysm, the location, multiplicity, growth, symptoms, age, sex and a predisposing history of hypertension and/or smoking. the most important variable is the size of the aneurysm. the risk of rupture is very less in aneurysms, less than 10 mm (1.4% 1.8% per year). several investigations by rinkel and colleagues, isuai data give a cumulative rate of rupture between 0.05% per year for less than 10 mm size aneurysms and 1% for those larger than 10 mm and 6% for those larger than 25mm. patients with larget than 25mm have a grave prognosis. the location of the aneurysm is an independent variable with greater risk in posterior circulation aneurysms than in anterior circulation aneurysms (42% v s 7% in sevaral studies). approximately, 15 20% of patients harboring aneurysms: have multiple aneurysms and the finnish data supports a greater likelihood of rupture in such patients. japanese data also supports an increased risk of rupture in multiple aneurysms. the growth of the aneurysm is not a conclusive determinant for rupture. aneurysms with clinical features, unrelated to hemorrhage, are said to be symptomatic and may manifest with mild or recurrent headaches, cranial nerve palsies, brain stem signs in about 20 32% of the cases. risk of rupture also is 8 10 times higher in a symptomatic aneurysm, than in an asymptomatic one. more often, symptomatic aneurysms are found in greater incidence in the posterior circulation than in the antenor circulation. increasing age, causes an increases in the risk of aneurismal rupture, evident in several studies with a rupture rate of 45 50% in patients in more than 60 years and about 25% in younger patients with aneurysms less than 10 mm. hypertension, as an independent risk factor for aneurismal rupture, is not conclusively proved. 264 yoko kato, hirotoshi sano subarachnoid hemorrhage however, data suggests that co-existence of hypertension and sub-arachnoid hemorrhage can be more risky with greater incidence of complications. cigarette smoking increases the risk of rupture by 2.5 times and causes rupture in younger age groups. it is more often seen in women than in men. assessment of the natural history, the availability of investigations and capability for effective management, determines the effective plan and management criteria that should be tailor-made for every patient. the american heart guidelines have published several criteria for management of aneurysms and recommended clipping for aneurysms greater than 5 7 mm în diameter with acceptable risk. management should be tailor-made based on the surgical skill, experience, patient's age, availability of other modalities of treatment etc. pathophysiology sub-arachnoid hemorrhage is the pathological condition with existence of blood in the sub-arachnoid space, which occurs spontaneously without any traumatic etiology. the blood escaping from the aneurysm may vary from a very small warning leak to massive amounts (more than 150 ml) and can lead to death. the consequences depend upon the location of the bleed, the volume of bleed, the volume of csf space, age of the patient, pre-morbid conditions, clinical grade, risk of vasospasm, seizures, hydrocephalus, icp, cerebral blood flow, cerebral metabolism and systemic implications of hyponatremia, hypovolemia, catabolic state and cardiac arrhythmias. high flow rates of aneurysms with tear of the wall produce large volume sah in a short time with rapid rise of icp, whereas, a small continuous leak may gradually increase the sah. there is a progressive increase in the icp with worsening grade, with an average of 10 mm hg, in clinical grade i and ii and 15 mm hg with clinical grade ii and iii and 30 mm hg in clinical grade iii to v. other causes of sub-arachnoid hemorrhage like infections, trauma, drug intoxications avm ruptures, amyloidosis, sle, pan, cvt, pregnancy, hematological disorders like leukemia, lymphoma, myeloma, dic etc., must be ruled out apart from other intracranial space occupying lesions. the cerebral blood flow is globally decreased after sah to about 35 45 ml/100gm/min in patients with grade i to iv without vasospasm and 33 38 ml/100gm/min in patients with grade i to iv with vasospasm. the cmr02 cerebral metabolic rate of oxygen, is markedly reduced. vasospasm caused narrowing of skull base vessels and dilation of distal intracerebral vessels. the cerebral blood flow and metabolism is reduced for weeks together after sah. development of infarction is heralded by cmr02 fall with increased hyperemia. the toxic effect of sub-arachonoid blood by a neural mechanism can cause global ischemia, lactic acidosis, mitochondrial respiration, sodium-potassium atp activity and extracellular calcium and potassium alterations. the blood pressure, the partial pressure of carbon-di-oxide, also get altered with an impaired auto regulation, depending upon the extent of the vasospasm and the reduction in the cerebral blood flow, causing vasomotor paralysis. intra-arterial xenon-133, transcranial doppler's studies have demonstrated impaired co2 reactivity. romanian neurosurgery (2010) xvii 3: 261 – 274 265 figure 3 axial ct scan: subarachnoid hemorrhage of posterior cranial fossa and in the fourth ventricle figure 4 ct angiography reconstruction of posterior inferior cerebellar artery (pica) aneurysm clinical features patients can have a sudden severe headache, never experienced earlier in their life, coming as a bolt from the blue. some individuals can have warning bleeds with severe headaches of sudden onset associated with nausea, vomiting, giddiness ete. the warning hemorrhage is extremely important to prevent a catastrophic sah and must not be misdiagnosed. features like vomiting, onset of headache with exertion, altered level of consciousness, meningism, focal deficits are all sinister and ominous. depending on the site and size of the aneurysm, patients can have hemiparesis, monoparesis, visual field loss, visual loss with or without diplopia and extra-ocular movement impairment. patients can also have dysphasia and dysarthria. loss of consciousness and mucal rigidity is a very important finding. sudden death can occur in up to 15% of the patients with large sah. 3rd nerve palsy and other cranial nerve deficits can occur. the diagnosis must not be confused with viral headaches, systemic infection, migraine, hypertension, cervical spine pathologies, intra-cranial space occupying lesions, sinusitis, aseptic meningitis and intoxications. depending on the site of the aneurysm, patients can have specific symptomatology in the form of bilateral lower limb weakness in aca ruptures, hemiparesis, hemianopia, dysarthria, dysphasia and paresthesia with mca ruptures, seizures with aca or acom ruptures, 3rd nerve lesions with ica or pca lesions, unilateral visual loss with carotid ophthalmic aneurysms etc. focal deficits, vasospasm, seizures and mass lesion due to bleed can confound and complicate signs and symptoms. 25% of patients can have vitreous hemorrhage and hemiparesis. aneurysm ruptures are also associated with specific causative factors like sudden exertion, lifting weights, emotional strain, defecation, coital acts, profound coughing or during parturition. 266 yoko kato, hirotoshi sano subarachnoid hemorrhage investigations non-enhanced ct (nect) remains the first step in diagnosis with majority of cases being detected on the day of ictus. patients may have sah, ivh, ich, sdh or hydrocephalus at the time of first ct itself. with facilities of high resolution scannings, ct-angio can be performed at the same sitting. the volume of blood on ct is a factor for prognostication in relation to vasospasm and outcome, with a system of grading proposed by fisher. in cases of doubt regarding sah, lumbar puncture may be performed in the absence of raised icp, which shows a constant count of rbcs of a few thousands to about 300 cells per cc and the blood having a propensity not to clot. the spectro photometry of the sample shows xanthochromia. microscopy shows a decrease in rbc: wbc count and an increase in the protein and csf pressure. hemosiderin laden macrophages are seen after a few days. a tap at another level also reveals a constant count of rbcs. catheter based 4-vessel angiography is the gold standard and is usually performed in all cases, except in several centers with very good ct-angio facilities. magnification, subtraction and stereoscopy will delineate the cause of the bleed, the site of the lesion, the shape of the lesion, the direction of the aneurysm and the domeneck relationship. risk of angiography and rupture during angiography are complications which are very rare. in multiple aneurysms, the site of the aneurysm which has bled, can be reliably deciphered by following an algorithm exclusion of extra-dural aneurysms, ct with contrast, site of vasospasm or mass effect on angiography, an irregularly shaped aneurysm, focal deficits, highest chance of rupture in accordance with statistics and repeated studies. the most proximal and the largest aneurysm which is irregular in shape, usually ruptures. in among 10 30% of the patients, no actual cause of sah is found. an mri or an mra in such patients or repeated angiograms may delineate a missed lesion, especially in the acom territory and perimesencephalic area. investigations for diagnoses can be performed by a multi-phase 256 row multislice ct scan and 4d ct, which is much better than 64 row multi-slice ct. it gives a very good multi-phasic scan and helps in delineating the artery, vein and the bone very clearly. even very small aneurysms are very clearly depicted. 4d ct and dynamic flow, also called 'ecg gated helical ct, is extremely advantageous in identification of a thin wall region and helps în detecting dangerous, unruptured aneurysms, impending ruptures and help in either clipping or coiling. the hemodynamic stress at the site of bifurcation and analysis of the dynamic flow in large aneurysms, the stress at the bifurcation of aneurysms are very clearly portrayed. apart from this, the jet flow in the parent artery can be made out very clearly. however, in many centers, the gold standard of diagnoses remains 4vessel digital angiography. clinical grading clinical grading is important to document the condition on arrival, prognostication and usefulness of the method of treatment. botterell grade, hunt and hess's grad and the wfns grade of aneurismal bleed is tabulated below. romanian neurosurgery (2010) xvii 3: 261 – 274 267 grade botterell classification hunt and hess wfns i conscious +/symptoms aymptomatic/minimal gcs 15, no motor of sah headache/slight mucal rigidity deficits moderate headache and mucal ii drowsy, no deficits rigidity / no deficits other than cranial nerve palsy gcs 13 14, no deficits iii drowsy, with deficits, with ich drowsy, confused with mild focal deficit gcs 13 14, with deficits stuper, moderate to severe iv major deficit, large clot hemiparesis, early decerebration gcs 7 12, with / without deficits and vegetative state v moribund state with deep coma, decerebration, gcs 3 6, with or extensor rigidity moribund state without deficits. management guidelines a proper history, physical examination and assessment of the airway, breathing, circulation, level of consciousness, cranial nerve, sensory and motor function are all mandatory. emergent placement of an evd may be necessary and life-saving. unconscious patients must be intubated and ventilated. intra-thecal tpa may be required for reducing the risk of re-bleed. treatment is based on the history, findings, age, grade, location, size, site, family history, associated diseases etc. patients must be kept in icu setting in a darkened room, limited visitors and minimal external stimulation and least mobilization, with good analgesia and adequate oxygen apart from measures to prevent dvt. the vital signs, neurological chart, the tcd must be monitored at regular intervals. if facilities are available, cerebral blood flow also can be monitored. a cvp or swan-ganz cathether can be placed for assessing intravascular volume status for fluid replacement. fluid intake must be regulated, depending upon the output and must be approximately around 2 3 liters. the hematocrit should be maintained more than 30% for maintaining good oxygenation. advantages with hhh therapy are controversial. nirnodipine, in a dose of 60 mg, 4th hourly, with sah grade i iii may help and is recommended for three full weeks. hypotension and intestinal obstruction must be watched for. steroid use is controversial. the optimal blood pressure must be maintained so that the cerebral perfusion pressure is adequate. administration of good analgesics, propofol, anti hypertensives like sodium nitroprusside, labetelol and other calcium channel blockers are given. in patients with a grade iv or a grade v sah, the initial management is to resuscitate the patient by intubation and administration of anti edema measures along with ventilation. the basic aim is to stabilize the patient and subsequently perform a head ct to evaluate for the 268 yoko kato, hirotoshi sano subarachnoid hemorrhage presence of subarachanoid hemorrhage and/or intracerebral hemorrhage. a ct angio can be done at the same sitting. if the patient has an intracerebral hemorrhage, 4vessel angiogram can also be done. with the presence of hydrocephalus or intraventricular bleed, a ventriculostomy and a simultaneous introduction of an intracranial pressure monitoring device can be done. an angiogram gives the diagnosis of the site of bleed, size of aneurysm, the direction of the sac, the association of other adjacent structures ete. with the patient's intracranial pressure well controlled and in those patients less than 65 years, without any medical problems, a craniotomy can be performed immediately. in very elderly gentlemen, patients with associated comorbid medical problems, the option of endovascular treatment can be considered. also, in patients whose icp is not controlled, endovascular treatment with coiling can be considered. patients can be re-assessed after stabilization, improvement in intracerebral pressure and then taken up for rehabilitative measures. ich increases the likelihood of mortality. patients in whom the intracerebral hemorrhage is evacuated, younger age group, better clinical grade, smaller ich volume less than 25 ml, are associated with better outcomes, than in patients who are comatose with brain stem compression and larger ich. larger bone flaps are preferable to prevent brain herniation and strangulation, as also, good relaxation with mannitol and proper exposure with drilling of the sphenoid wing and orbital roof. measures should be taken to prevent retraction of the brain and some times before closure, lobectomy or ventriculostomy or dural augmentation without bone replacement may be necessary in severe cerebral swelling and herniation. acute hydrocephalus and intraventricular hemorrhage is associated with poor grade and an evd is necessary in such patients. infusion of urokinase has been tried without good outcome in several series. vasospasm is associated with acute hydrocephalus and ventricular drainage, ventilation and hyperdynamic treatment is necessary. chronic hydrocephalus is seen in 1/4 of the patients with sah and is associated with poor clinical grade, hypertension, alcoholism, female sex, pneumonia and meningitis. it requires a longer duration of evd placement or lumbar puncture or laminaterminalis fenestration or a shunt. within 48 hours after sah the vasospasm is seen in 15% of the patients and is associated with arterial narrowing and poor prognosis. immediate aneurismal obliteration and aggressive management of symptomatic vasospasm is required in patients such conditions to have a reasonable neurological recovery and prevent infarction. intra-operative aneurismal rupture, major vessel occlusion, cerebral contusion due to retraction, evacuation of ich, decompression by lobectomy, inexperienced operator, improper technique and other primary factors not favoring an easy surgery like the aneurismal size, site, morphology, calcified necks etc., are associated with poor prognosis and post-operative complications even în preoperatively good grade patients. they may also have neuro psychological, cognitive deficits after surgery. special situations of patients with advanced age, very young age, traumatic romanian neurosurgery (2010) xvii 3: 261 – 274 269 aneurysms, mycotic aneurysms, pregnant ladies, aneurysms with awms, fuciform or microaneurysms or those associated with co-existing carotid artery disease or giant aneurysms or residual aneurysms, need to be treated with caution. advanced age is associated with poor outcome, as also aneurysms in children. they are usually in a very poor clinical grade and have other confounding factors like hypertension, etherosclerosis, vasospasm and other co-morbid medical complications that alter the operative outcome and post-operative sequelae. pregnant ladies have major physiological alterations in the body, hormonal changes, risk to the foetus, more so in the last trimester and can lead to more risk for both the baby and the mother. care should be taken to avoid hypotension, administration of mannitol, prevention of uterine hypoperfusion, fetal hyperosmolality, hyper ventilation and a stand-by team for a section in case there is a mishap during surgery. as far possible, surgery should be deferred until the end of the second trimester and drugs like anti-convulsants and calcium channel blockers must be avoided. 5 – 6% of the aneurysms are mycotic and are associated with infective endocarditis, immunocompromise with fungal infections, bacterial infections etc., and are located in the distal mca territory. 50% resolve or reduce in size with antibiotic treatment and need to be followed up with serial blood cultures. aneurysms associated with abscess or clots need to be operated with precautions for either excision, by-pass or ligation. less then 1% of aneurysms are traumatic and are usually due to penetrating injuries or stab wounds and manifest within 3 weeks after injury. a neck is usually not found and are prone for intra-operative rupture. they may require encircling clips or trapping or excision, with or without bypass. aneurysms with avms account for up to 15% cases and arise due to hemodynamic stress in avms at the site of branching. they may be of type-i, located at a distance from the avm. in type-ii, they are more proximal to the feeding vessel. type-iii lesions are pedicular varieties in the middle of the feeding pedicle and type-iv lesions are intranidal in the avm. the treatment strategy, the natural history, management protocol for each of these is different. skull-base aneurysms are more often fuciform and are located in the vertibrobasilar territory, characterized by dilatation, elongation, etherosclerosis, dolichoectasia and tortuosity of the vessels, associated with turbulence and thrombos formation causing ischemic symptoms. they usually require wrapping, anti coagulation and sometimes huntarian ligation. aneurysms less than 3mm are microaneurysms and cannot be either coiled or clipped. open surgery with coagulation and wrapping may help. co-existent lesions like carotid artery disease and aneurysms are treated with precedence given to the lesion with the worse natural history. giant aneurysms approximately represent 4% to 6% of intracranial aneurysms and have a high 2-year mortality between 60 100%. the aim is to prevent rupture and treat mass effect. wide exposure, proximal and distal control and clip reconstruction are the basic technical considerations in these aneurysms. cerebral protection with barbiturates, skull base techniques for vascular control and collaboration with other techniques help in giving a better prognosis. 270 yoko kato, hirotoshi sano subarachnoid hemorrhage endovascular techniques can be used for aneurismal occlusion in anticipated surgical difficulty, medical contraindications and failed surgery. the limiting factors include a wide neck more than 4mm with a dometo-neck ratio of less than 2 and inadequate endovascular access or an unstable intraluminal thrombos. aneurysms of the mca are those with a branch arising from the neck, are also difficult candidates. by-pass techniques are not needed in patients who maintain a cerebral perfusion of more than 30 ml/100gm/minute, who are neurologically stable during occlusion and those who remain neurologically intact. the basic techniques in giant aneurysms include the short time-trapping, evacuation of the aneurysm either directly or through interventional radiography and reconstruction of the artery, either by a standard pterional ipsilateral approach and / or removal of anterior clinoid process, to facilitate proper exposure and evacuation of hematomas in ruptured cases. intraoperative use of digital subtraction angiography, endoscopy and in the very recent past, use of infrared indo cyanine green (icg) video angiography has helped a great deal in assessment of intraoperative completeness of clipping. this is a revolutionary technology and helps in intra-operative proper visualization and closes the gap between speculation and reality, supplying vital information, enhancing efficacy since synchronous video recording of infra-red and white light is possible. the mechanism involved is that the blood, being seen as a white flow after icg bolus on a dark background and the microscope switching from white light to infra-red light immediately. no extra instrumentation is required and can be repeated as and when required for conformation of results. it is completely integrated on to the microscope. various difficulties in clipping due to either a narrow operative field, the wall thickness, partial thrombosis of sac, requirement for preservation of perforators, selection of clips and clipping techniques, along with reducing the ischemic time and evaluation of by-pass surgeries, can be overcome with expertise and experience. partially thrombosed mc aneurysms require a thrombectomy and / or an aneurysmecto along with end-to-end anastomosis with a great emphasis for preserving the perforators. the anatomy of the vasculature, the location of the aneurysm, the size, the shape, the direction, the branches of the main vessels, presence of perforators all determined the operative plan and strategy. intentional neck reconstruction in fuciform or multi lobulated aneurysms with parent artery branching or perforators arising from base or dome, creating a smaller neck for complete occlusion by coiling, preserving parent artery patency to alter flow physiologically between inflow and outflow vessels and minimize risk of dissecting tight adherent zone between neck or wall and parent artery or perforators are important strategies in management. the suction decompression of giant aneurysms followed by clip reconstruction of the parent vessel, thrombectomy in partially thrombosed aneurysms where suction was not effective and anerysmectomy in strategically located aneurysms with a hard thrombus at the neck, are strategies in the management of giant aneurysms. preservation of the patency of the parent vessel, perforators requiring dome-side clipping or drilling of the related bone like anterior clinoid, to get romanian neurosurgery (2010) xvii 3: 261 – 274 271 full access and exposure with the use of proper lighting, instrumentation, endoscopy, intra operative angiography, intra operative doppler and near infra-red indo cyanine green angiography and open surgeries are indicated in young patients with small aneurysms with no associated co-morbid medical disorders and those which are easily accessible or in patients with a bleb on the aneurysmal sac. temporary trapping is always safe if less than 5 minutes, usually safe if around 10 minutes, probably safe if around 15 minutes and is of questionable safety if more than 20 minutes. hypo thermia may be required, if it is required for more than 20 minutes. complications complications like re-bleed, increase in the icp, ich, ivh, hydrocephalus, vasospasm, seizures etc, must be adequately looked for and treated aggressively. medical complications like anemia, hypertension, cardiac arrhythmias, fever, respiratory tract infection, urinary tract infection, enzyme abnormalities, electrolyte disturbances, pulmonary edema and atelectasis and pneumonia can cause very serious morbidity and mortality. venous thromboembolism can occur in 2-4% of patients which can progress to pulmonary thrombo embolism and be fatal in up to 50% of these. potential risk factors include lower limb trauma, varicosities, puerperal state, pregnancy, concomitant use of oral contraceptives, patients with prior infection, malignancy or antithrombin-iii, protein c, protein s deficiencies. low dose, low molecular weight, heparin may be started in patients with high risk, with proper monitoring of the coagulation profile. ecg abnormalities can occur in almost all patients with peak p waves, pathological q waves, increased qrs complexes and st depression, with inverted t-waves and a prolonged qtc interval and / or large u waves. they must be differentiated from myocardial infarction. patients can develop tachycardia, extrasystoles, couplets, svt, bradycardia and arrhythmias. electrolyte balance must be adequately maintained, as patients with sah are prone for hypo or hyper natremia and hyopkalemia. they can even have hyopvolemia. patients can develop features of siadh, cerebral salt wasting and diabetes insipidus. the differentiation between them can be made by the volume status. acute change in body weight, change in hematocrit, bun gives idea regarding changing volume status. treatment for salt wasting is adequate water and sodium replacement to keep it at normal levels and prevention of sodium loss by administration of fludrocortisone acetate. fluid restriction is the main treatment for siadh. di can be treated by fluid replacement with hypotonic 5% dextrose or 0.45% saline. desmopresin or ddavp can be administered exogenously, with 1 2 microgram intranasal bolus doses. patients can have weight loss, infection, impaired wound healing and may require gastrostomy or jejunostomy tube insertions apart from tpn. stress ulcerations of the gi tract can occur and must be treated with h2 blockers, proton pump inhibitors or surcalfate. thick clot in the sub-arachnoid space, poor gcs on admission, age less than 35 and more than 65 years, with pre-existing hypertension and cigarette smoking, all predispose patients to severe vasospasm. the blood in the sub-arachnoid space can cause a structural proliferative vasculopathy of immune etiology and vascular 272 yoko kato, hirotoshi sano subarachnoid hemorrhage inflammation causing extra cellular wall contraction. it may be associated with vasoconstriction due to release of free radicals, lipid peroxidases, neurogenic factors, nitric oxide deficits, endothelin excess and deranged production of eicosanoids. the oxy-hemoglobin is converted into free radicals which cause hydrolysis of phosphor lipids causing an increase in the calcium and calpine activation and protein degradation causing sustained vasoconstriction. removal of sub-arachnoid blood during surgery, proper fluid management, maintenance of cpp more than 70 mmhg, hypervolemia, calcium channel blockers and off late, administration of tirilazad mesylate, can prevent vasospasm. 21 aminosteroids, anti-oxidants, lipid peroxidase inhibitors, help in prevention of ischemic damage. intrathecal vasodilators and endothelin inhibitors to prevent vasospasm are in the experimental stage. intra arterial papaverine, per cutaneous, transluminal, balloon angioplasty, intraventricular nitroprusside and hypervolemia hemodilution and hypertension are all tried for tackling vasospasm. an unexplained leucocytosis and fever can appear in almost all patients. prognosis and outcome the natural history of aneurysms is its outcome without medical or surgical intervention. the natural history of ruptured and unruptured anterior circulation aneurysms, are different. unruptured aneurysms with no recent or remote sah or symptoms related to bleed are diagnosed with screening tests, patients with familial origin and their management is very challenging and confronting to all neurosurgeons. rupture in previously undiagnosed aneurysms is a potential complication with 50 80% dying with sah. treatment is aimed at prevention of rupture, prolonging life, expectancy with consideration to the patient's age, sex, medical and family history. treatment may be either surgical or endovascular with its own advantages and disadvantages. persons affected in the population at a specific time divided by the number of persons in the whole population at the given time, will give the prevalence of aneurysms, which are obtained by autopsy and radiological studies. 12% of patients die before coming into medical attention and in the surgical series, 25% of the patients who come to hospital die and about 50 60% recover in several large series. 40% of those patients reaching hospital die. patients can have severe cognitive and higher cortical dysfunction, only due to sah. the timing of admission to hospital, the risk of rebleed, salvage after bleed and other criterion, already alluded, help in achieving a good outcome. the types of patients, clipping of aneurysms before or after rupture, proper identification of the strategy in management determine the outcome. results also depend upon the site, size and grade of the aneurysm, duration of bleed, direction of fundus, operative skill, experience and technical expertise, neurological status, timing of surgery, postoperative vasospasm, mass effect, brain stem compression, strokes, institution of tripleh therapy, brain protection with sendai cocktail, pre-operative deficits, fisher's grade and severity of sah. hunt and hess scale, post-operative glasgow outcome scale, pre-operative gcs and japanese coma scale, requirement for re romanian neurosurgery (2010) xvii 3: 261 – 274 273 operation due to incomplete clipping of the aneurysmal lumen and requirement for additional procedures like clipping after coiling or coiling after clipping in a great way determines the overall outcome and results of the series. complications of endo-vascular treatment include problems with re-canalization in 20%, intra procedural rupture in 2%, compaction of the coil in less than 20%, delayed rupture in 1.6% and arterial thromboembolism. more often, complete coiling is achieved in only 70% of the aneurysms in expert hands and these may also reform and bleed. heros shows a series of re-canalization in 2 to 37% of aneurysms, more often in large aneurysms. clipping after coiling is a decision in residual or recurrent aneurysms, post embolization, decided upon by more than two expert neurosurgeons. defective arterial wall is excluded to ensure anatomical continuity of normal wall. in gdc coils, early vasospasm may make the coil appear compact, but following resolution of spasm, re-canalization can occur and a partial thrombosed may lead to the formation of a rupture point, usually at the neck. further endovascular treatment with recent methods like improved coils, stents, balloon remodeling, must be considered before surgery and surgery must be reserved for patients not amenable for reendovascular management, young patients, accessibility of the aneurysm and the size of the remnant being twice the size of the neck. the north american trial for unruptured and ruptured aneurysms (nature) may clear certain doubts and short comings. the cost constraint in endo vascular treatment is compensated by saving in hospital stay, staff and earlier return to paid employment. the size and location of the aneurysm determines morbidity and mortality which is 0% for aneurysms less than 7mm, 6% for aneurysms between 10 and 25 mrn, 20% for aneurysms greater than 25 mm. posteriorly, superiorly projecting aneurysms, clinoidal segment aneurysms and aneurysms in the cavernous ica have high morbidity and mortality. the location of perforators from the wall of aneurysm, border of the neck or opposite side of the parent artery also determine prognosis. risk of seizures is lower with coiling and re-bleed lower with clipping. recurrence thrombo-embolism, worsening mass effect in endo-vascular and calcified aneurysm, posteriorly projecting dome, high basilar bifurcation, high risk poor grade, have limitations in coiling. small length of acom, acute angle of adjacent vessels are difficult to coil. wide neck, large aneurysms, geometrically complex with incorporated branch artery or perforator, acom aneurysm, inability to navigate delivery system, partially thrombosed fuciform or giant aneurysm, blister aneurysms or dissecting aneurysms are difficult to coil. conclusion team work and multi disciplinary approach is mandatory along with a goal of acquiring the best possible training and delivering the best possible treatment. incompletely coiled aneurysm transforms a simple aneurysm into a lesion substantially more formidable. advances in neuro genetics, intra arterial injection of tgfb one adeno virus, clipping, coiling, new stents, by-pass treatment, combined treatment, fluorescence and / or near infrared video angiography for intra-operative recognition of incomplete clipping, closes 274 yoko kato, hirotoshi sano subarachnoid hemorrhage the gap between speculation and reality and provides vital information, enhancing the efficacy of aneurysmal management. bioactive coils cause progressive thrombosis and require further evaluation before recommendation. deeply situate aneurysms in elderly patients with co-morbid medical complications may require endo-vascular treatment. minimally invasive surgery in big aneurysms is done to preserve the natural flow. artistic combination of endo vascular coiling, combined microsurgical clipping, revascularization for complex surgically incurable aneurysms is required with a favor towards reconstruction of the neck followed by coiling or clipping after an attempted incomplete coiling. other novel strategies and nuances in the advancement of treatment need to be integrated in the near future. this article was published first in “essential practice of neurosurgery” 2009, a neurosurgical text-book accepted by the world federation of neurosurgical societies – wfns, as the official book for teaching neurosurgery. we thank the authors who allowed us to republish the material in this issue of romanian neurosurgery. doi: 10.33962/roneuro-2022-035 a comprehensive review on pituitary hydroscopy and the role of endoscopic diving techniques ahtesham khizar, adnan khaliq, mian iftikhar ul haq, sajjad ahmad romanian neurosurgery (2022) xxxvi (2): pp. 196-202 doi: 10.33962/roneuro-2022-035 www.journals.lapub.co.uk/index.php/roneurosurgery a comprehensive review on pituitary hydroscopy and the role of endoscopic diving techniques ahtesham khizar1,5, adnan khaliq2,5, mian iftikhar ul haq3,5, sajjad ahmad4,5 1 pakistan institute of medical sciences, islamabad, pakistan 2 saidu group of teaching hospitals, swat, pakistan 3 hayatabad medical complex, peshawar, pakistan 4 gajju khan medical college, swabi, pakistan 5 punjab institute of neurosciences, lahore, pakistan abstract pituitary hydroscopy is a new technique in skull base surgery that involves transnasal neuroendoscopy and gentle fluid distention of the sella turcica. hydroscopy allows for a more thorough inspection of the sellar region and may make it easier to remove additional tumour cell foci. endoscopic diving technique, on the other hand, uses a continuous water flow that is driven in front of the endoscope to aid explore the surgical cavity and improve image clarity. after tumour removal, a double-path aspirator is implanted inside the sella turcica and tumour cavity, providing a pressured flow with continuous irrigation in the modified endoscopic diving technique. several groups' recent uses of diving techniques attest to the increased interest in these approaches. the development of dedicated surgical devices will improve the efficacy of diving procedures in the future. more research is needed right now to improve the effectiveness of diving techniques. introduction to understand the current renaissance of endonasal pituitary surgery, it's necessary to look back at the historical and anatomic progression of thought that has led to contemporary technical advancements and better patient care. shorter operative times, decreased blood loss, improved differentiation between normal tissue and tumour, better visualisation of intrasellar and parasellar structures, shorter hospital stays, improved patient satisfaction, and decreased need for nasal packing have all been seen since the endoscope was married to the trans-sphenoidal approach. furthermore, this union has brought the otolaryngologist and the neurosurgeon together as a true surgical team, allowing novel concepts like extracapsular tumour dissection, new approaches to investigate the tumour bed, improved tumour removal with angled views and hydroscopy.6 keywords pituitary surgery, skull base surgery, hydroscopy, endoscopy, diving techniques corresponding author: ahtesham khizar pakistan institute of medical sciences, islamabad, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 197 a comprehensive review on pituitary hydroscopy and the role of endoscopic diving techniques pituitary hydroscopy is a new technique in skull base surgery that involves transnasal neuroendoscopy and gentle fluid distention of the sella turcica. hydroscopy provides for a more thorough inspection of the sellar region during minimally invasive pituitary surgery, as well as the excision of extra tumour cell foci. when compared to typical neuroendoscopic procedures, preliminary data suggests that hydroscopy may result in a lower rate of cerebrospinal fluid (csf) leak and revision surgery. hydroscopy is a safe and effective addition to traditional pituitary techniques, and endoscopic skull base surgeons should include it in their toolkit. endoscopic resection of pituitary neoplasms appears to have the major benefit of a broader, potentially angled field of view, which may be especially advantageous for big tumours with extrasellar extension, according to the data. endoscopic pituitary surgery has been linked to better rates of gross total resection, endocrinological cure, visual prognosis, shorter hospital stays, less postoperative discomfort, septal perforation, csf leak, and a lower rate of diabetes insipidus as a result of its benefits.16 a constant water flow is propelled in front of the endoscope in davide locatelli's9 endoscopic diving technique (edt). edt is a flexible tool for exploring the surgical cavity and enhancing visibility. after tumour removal, a double-path aspirator is implanted inside the sella turcica and the tumour cavity in marco ceraudo's3 modified endoscopic diving technique. this creates a pressured flow with continual irrigation, which aids in the removal of more minor tumour foci. history the creation of the cystoscope by nitze in the 1800s provided the technological foundation for hydroscopy.11 herman schloffer used a lateral rhinotomy to perform the first transsphenoidal approach to the pituitary in 1907. after an open approach via the nasal dorsum, kocher described the first submucosal resection of the bony nasal septum and vomer to get access to the rostrum of the sphenoid in 1909.8 hirsh, a rhinologist, invented and championed the substantial breakthrough of the transnasal, transseptal technique in 1910. hirsch tweaked the techniques he'd learned to access the sphenoid for infection therapy. the submucosal excision of the septum, developed by kilian in 1904, was later added to his basic procedure. in 1914, cushing described his sublabial, transseptal, transsphenoidal method using these techniques as well as those of kanavel and halstead. following that, in the 1960s, the adoption of an operational microscope considerably increased visualisation of the sella.13 for vision of urological structures, early cystoscopes depended on air insufflation; later developments of this technology incorporated fluid distention, which enhanced patient comfort and surgeon visibility. the first attempts to apply endoscopic techniques to neurological pathology focused on the ventricles and other fluid-filled regions, with victor l'espinasse, a french urologist, examining the choroid plexus of two children with hydrocephalus using a cystoscope in 1910.17 jankowski performed the first purely endoscopic, endonasal pituitary excision in 1992, thanks to technological breakthroughs in endoscopes and cameras in the 1970s, and jho and carrau published the first extensive series of endoscopic pituitary surgery in 1997.5 endoscopic transsphenoidal methods to the pituitary have grown quite prominent in the last 25 years. anatomical considerations the pituitary gland is a reddish-grey organ that rests in the sella turcica, a deep depression on the superior portion of the sphenoid bone's body, and measures around 1 cm in diameter. it's hidden behind the tuberculum sellae, which is itself hidden behind the optic chiasm. the dorsum sellae and the posterior clinoid processes define the sella's posterior boundary. the clivus is a bony extension of the dorsum sellae that slopes inferiorly and connects to the occipital bone. the anterior clinoid processes are formed by the tuberculum sellae's lateral expansions. the diaphragm, a dural fold spanned by the pituitary stalk, forms the roof of the fossa. the diaphragm and the pituitary capsule are separated by an arachnoid invagination. the roof of the cavernous sinus is formed by the diaphragm's lateral expansion. the optic chiasm and nerves, the carotid arteries, the third, fourth, fifth, and sixth cranial nerves in the cavernous sinus, as well as the basilar artery and brainstem posteriorly, are all within close proximity to the pituitary gland. as a result, proper anatomy knowledge is required during these approaches.15 the sphenoid sinus is pneumatized into the 198 ahtesham khizar, adnan khaliq, mian iftikhar ul haq et al. sphenoid bone in a variety of ways, and three types of sphenoid pneumatization patterns are classified based on their relationship to the sella. a conchal type is one that has just slightly pneumatized and yet has thick bone across the sella's face. sellar type denotes a sinus that has pneumatized to the sella's face, whereas post-sellar type describes a sinus that has pneumatized beyond the sella's face. the sellar and post-sellar types of sinuses make up the majority of adult sinuses.15 the two sphenoid sinuses are separated by a septum that is off the midline in 60 to 70% of cases, resulting in asymmetry between the two cavities. additionally, numerous septations may be present. the walls of the sphenoid sinuses have many structures running along them. the vidian nerve's canal goes laterally along the floor. at approximately 5 and 7 o'clock, the carotid arteries flow along the lateral walls. at approximately 2 and 11 o'clock, the optic nerves run more superiorly along the lateral walls. between the bulges of these two structures is the optico-carotid recess, which can extend into the anterior clinoid process. the sphenoid ostium runs along the anterior wall's superior aspect.14 principles of endoscopic diving technique the diving technique makes use of hydraulic concepts (flow and pressure) as well as visual approaches (lens effect given by liquid film). the procedure entails not only flushing the surgical cavity, but also the production of a saline solution lens: the first step is to determine the proper distance from the wall to be visualised in order to eliminate any turbulence induced by the liquid flow. the focus, which differs from that utilised in open-air surgery, is changed at this point. the surgeon must generate a field with a stationary flow, which means that the lines of flow must correspond with the lines of current, and the particles must follow trajectories that are not rectilinear but remain constant throughout time. the saline solution within the surgical cavity forms a fluid layer with a stationary flow that works as a concave-convex lens.9 advantages of the technique 1. removal of micro residues with final hydrodissection of the lesion. 2. as a result of the flushing pressure, structures, fistulas, and perforations of the cavernous sinus walls can be seen in the presence of bleeding. 3. exploration of places buried by the cistern's fall as the saline solution flow re-expands the pseudocapsule through pressure and direction adjustments. 4. hematic residues are removed, and bleeding is modest, preventing clear visibility. 5. smaller visual field but greater visualisation due to the lens effect with amplification of vision.9 limitations of the technique 1. a panoramic vision is not possible due to the short focal distance. 2. in a small field, there is no stereoscopic view. 3. bleeding can make you feel disoriented.9 preoperative considerations hydroscopy is recommended for patients undergoing transnasal, endoscopic pituitary and selected parasellar surgery. certain diseases of the sella turcica less often require intraoperative hydroscopy: rathke's cleft cysts can be easily marsupialized without it, while adamantinomatous craniopharyngiomas often have a fibrotic capsule that makes hydroscopy difficult. to continue with surgery, individuals with pituitary pathology must have a thorough preoperative evaluation and be recommended for transnasal, endoscopic surgical therapy. multidisciplinary teamwork across neurosurgery, endocrinology, ophthalmology, and otolaryngology is the best way to make management suggestions. surgical intervention is usually reserved for compressive symptoms, rapid development, or acute apoplexy in hormonally inert tumours. size, type of hormone, and response to medical care are factors that affect surgery for a hormone-secreting tumor. prolactinomas are treated with dopamine agonists at first, with surgical removal reserved for tumours that continue to grow. on the other hand, tumours that produce growth hormone or adrenocorticotropic hormone are frequently treated with surgery up front. unless contraindicated, all patients have thin-cut computed tomography (ct) of the paranasal sinuses and magnetic resonance imaging (mri).2 surgical techniques: on the operating table, the patient is positioned supine with a horseshoe headrest. the head is retained in a neutral position or slightly tilted to the right and elevated 10 to 30 degrees. the image 199 a comprehensive review on pituitary hydroscopy and the role of endoscopic diving techniques guidance and endoscopic monitors, as well as the nurse's table, are all placed at the patient's head, directly in front of the surgeons. the rigid endoscopes 0, 30, 45, and 70 degrees with diameters of 4 and 2.7 mm, 18 cm in length, and an external cover attached to the irrigation system are employed.9 the procedure is performed with a standard 4-mm endoscope with various angulations; for the most part, the straight endoscope gives the best illumination and vision. after the sella is accessed and the tumour is removed, angled scopes are frequently utilised later in the surgery. the use of stereoscopic endoscopes to provide a threedimensional vision has been described.14 the endotracheal tube is attached to the left lower lip to obtain general anaesthesia. the bed is turned 90 degrees counterclockwise, and preoperative ct and mri images are combined before registration with a stereotactic image guidance system using facial surface matching. in the case that a fat graft is necessary for reconstruction, the abdomen is sterilely prepped. the availability of equipment and the strategy for surgical pathology specimens are evaluated, as well as key characteristics of the patient's anatomy.16 pledgets soaked in a solution of 0.05 percent oxymetazoline hydrochloride decongest the nasal canals. greater palatine artery blocks, which are performed by injecting 1.5 ml of a 1 percent lidocaine solution with 1/100,000 epinephrine trans-orally into the greater palatine canal bilaterally, provide further hemostasis. finally, a sphenopalatine artery block is achieved by injecting additional lidocaine with epinephrine endoscopically in the vicinity of the sphenopalatine foramen.1 for better visualisation and subsequent hydroscopy, the endoscopic operation begins with the use of a 0-degree hopkins rod equipped with a suction/irrigation system.16 the sphenoid ostia are recognised and the bilateral middle turbinates are lateralized. a nasoseptal flap may be lifted prior to performing a broad bilateral sphenoidotomy with removal of the rostrum and posterior septectomy, depending on the risk of csf leak. alternatively, the nasoseptal flap pedicle can be shifted inferiorly from the sphenoid face and posterior nasal septum without lifting the flap entirely, protecting the flap pedicle while permitting tissue regeneration if the flap is not required for reconstruction. after visual and imaging guidance, establish the position of the internal carotid arteries and optic nerves, the bony sellar face is removed with a 4-mm diamond drill bit and kerrison rongeur. an inferiorly pedicled, u-shaped incision in the dura is produced, which is then reflected inferiorly and resected, with an otolaryngologist and neurosurgeon working in a twosurgeon, four-handed method. standard microneurosurgical procedures are used to visualise and resect the tumour, taking care not to disturb the normal gland, cavernous sinus, or diaphragm. the 0degree endoscope and irrigating sheath are inserted into the sella after gross total resection, and the sella is irrigated continuously with sterile saline. suction or extra dissection may be used to identify and remove small particles of remaining tumour.16 hydroscopy uses regular saline irrigation with a water pressure of several cm linked to either straight or angled endoscopes. the saline flooding the field expands the sella's soft tissue borders, including the diaphragm, while also increasing visibility by washing away minute amounts of blood and clot. with increased visualisation, this approach allows for a thorough examination of the cavity and the removal of as much tumour tissue as feasible.14 after the surgeon has removed the majority of the lesion and visualised a new cavity, the surgeon can enter the space with the endoscope thanks to continual irrigation from the pump. filling the dead space with saline solution allows the endoscope to be inserted into the tumour, allowing for a great "underwater" view of the remaining tumour, capsule, normal pituitary tissue, and cavernous sinus walls. the tumour is removed using this diving technique, which involves injecting saline solution into the hollow created following tumour resection and testing for residual tumour.9 hemostasis is achieved at the end of the procedure utilising a hemostatic substance such as microfibrillar collagen in thrombin. this is let to sit in the sella for a few minutes before being irrigated out. in the vast majority of cases, sella reconstruction is not required. in present practise, the only rationale for reconstruction is intraoperative suspicion of a csf leak. if a leak is discovered, it is repaired with a little fat plug, sometimes augmented by a small resorbable microplate.14 the endoscopic diving technique was introduced by davide locatelli. the irrigation pump is triggered and the endoscope is put into the surgical cavity according to the surgeon's desire (after full tumour 200 ahtesham khizar, adnan khaliq, mian iftikhar ul haq et al. resection or anytime the amount of resection has to be evaluated). continuous water flow is propelled in front of the endoscope, rapidly filling the cavity and allowing diving to begin. edt is a versatile technique for exploring the surgical cavity and improving image clarity; it varies from senior's "sellar hydroscopy"14 in that it goes beyond simple observation of the surgical field, acting as an operative instrument all around. the irrigation stream's directed force may aid tumour hydro-dissection by washing out residuals. the intra-cavity pressure can contrast bleeding as blood is diluted and washed away inside the cavernous sinus.9 marco ceraudo introduced the modified endoscopic diving technique. the double-path aspirator is put inside the sella turcica and the tumour cavity after tumour removal in this procedure. the surgeon's assistant switches on the tap to flood the tumour cavity with a pressurised flow; if necessary, a nurse can maintain pumping the infusion pressure bag to provide continuous irrigation. the double-path technology lets you halt the suction while also increasing the hydrostatic pressure created by the saline infusion. the endoscope is inserted into the tumour cavity, which is filled with saline solution, allowing a clear view of the diaphragma sellae, cavernous sinus walls, and pituitary gland, as well as the detection of any tumour remnants inside the parapituitary recess that can be washed away from the sella. the optic system and the irrigation supply are divided into two distinct tools in the modified endoscopic diving technique, allowing surgeons to point the flow on a specific structure while the endoscope can be oriented in the same direction or not. furthermore, the irrigation source and the optic system can be located at varying distances.3 there were some changes between locatelli et al's endoscopic diving technique and ceraudo et al's modified endoscopic diving approach. the irrigation system injects saline solution directly onto the endoscope's outer lens in the endoscopic diving technique. second, the distance between the optic and the irrigation system is fixed in the endoscopic diving technique for the same reason. third, a rotary pump produces constant irrigation in the surgical field in the endoscopic diving technique. fourth, despite the fact that the irrigation system utilised during the treatment is included in a comprehensive endoscopic equipment package, it can become an expense in a department's budget. furthermore, many irrigation systems (i.e., irrigation system and optic lens) supplied by different medical corporations are incompatible, which could drive up expenses even more.3 because dedicated instruments are not required, ceraudo's process offers easy reproducibility and lower costs.10 postoperative considerations the patient is admitted to the ward for 48 hours after surgery to allow for routine neurologic monitoring. on the first postoperative day, an mri is conducted to assess the extent of the resection. antibiotics and hormonal replacement, if necessary, are usually given to patients before they are sent home. to avoid mucus being displaced into the open sellar cavity, patients are told not to blow their noses or sneeze through their noses. sinonasal endoscopy is performed at the first postoperative visit, about 3 weeks later, to ensure proper healing; normally, the posterior sphenoidotomy is covered by a healthy mucosal layer.14 complications meningitis, cerebral haemorrhage, ophthalmoplegia, carotid damage, and perioperative death are all rare consequences.9 during the initial postoperative period, diabetes insipidus can be found in up to 60% of patients, but it is usually temporary, with only around 3% of patients requiring long-term care. csf leak is the most prevalent significant consequence.1 results of different studies senior et al13 presented a series of more than 50 cases of pituitary hydroscopy employing the clearess irrigation system in 2005, noting that in about 25% of cases, the use of this approach resulted in an additional tumour diagnosis and removal. senior et al14 described a case series of 176 individuals who underwent a total of 193 minimally invasive pituitary surgery procedures in 2008. the authors found that patients having hydroscopy had a decreased risk of csf leak (24 vs 45 percent, p=0.005). these preliminary findings show that hydroscopy after pituitary surgery may enhance outcomes, but more prospective, controlled trials are needed. davide locatelli9 performed 410 surgical procedures in 2009 to remove lesions in the sellar, cavernous sinus, and clival regions using diving 201 a comprehensive review on pituitary hydroscopy and the role of endoscopic diving techniques surgery. they removed 379 pituitary adenomas (92%), 21 craniopharyngiomas, 5 meningiomas, 4 chordomas, and 1 epidermoid during the procedure. they were able to speed up and improve the surgical excision of numerous lesions in the sellar and parasellar regions using this surgical method. in 2017, china's hai-bin gao7 performed endoscopic diving technique on a total of 37 pituitary adenoma patients. the endoscopic diving approach, he claims, also allows the surgeon to view the undersea environment within the sella turcica. deyan popov12 performed intrasellar hydroscopy on 51 of his endoscopic group's cases in 2018. overall, the endoscopic group had an 81.82 percent remission rate. in 2019, marco ceraudo3 performed 76 endoscopic surgical procedures using the modified endoscopic diving technique. marco ceraudo discovered that by combining the olympus instaclear with a specific irrigation sheath (which is generally used to clean the endoscope lens during surgery), he was able to get a continuous water flow comparable to that generated by locatelli et al9. cleaner and sharper images can be obtained by combining edt with ultra high definition or 4k systems to better understand minute anatomical details (especially in the presence of underwater vision during edt), find tumour residuals or a clear cleavage plane, and differentiate pathological tissues from adherences or scar tissues.3 conclusions pituitary hydroscopy is a safe, new addition to minimally invasive pituitary surgery that allows for a more complete inspection of the sella turcica using moderate saline irrigation. hydroscopy after gross complete tumour excision frequently results in the elimination of extra, undetected tumour, potentially lowering the risk of recurrence and reducing the need for future surgery. several groups' recent uses of diving techniques attest to the increased interest in these approaches. the development of dedicated surgical devices will improve the efficacy of diving procedures in the future. more research is needed right now to improve the effectiveness of diving techniques. list of abbreviations: csf: cerebrospinal fluid edt: endoscopic diving technique ct: computed tomography mri: magnetic resonance imaging acknowledgements: not applicable. conflict of interest: the authors have no conflicts of interest. references 1. bassim mk, senior ba. minimally invasive pituitary surgery. operative techniques in otolaryngology-head and neck surgery. 2006 mar 1;17(1):31-6. 2. bresson d, herman p, polivka m, froelich s. sellar lesions/pathology. otolaryngologic clinics of north america. 2016 feb 1;49(1):63-93. 3. ceraudo m, anania p, prior a, rossi dc, zona g. modified endoscopic diving technique without the traditional irrigation system in endoscopic cranial base surgery. world neurosurgery. 2019 jul 1;127:146-9. 4. ceraudo m, anania p, rossi dc. letter to editor regarding “the endoscopic diving technique in endonasal transsphenoidal surgery: how i do it”. acta neurochirurgica. 2020 sep;162(9):2115-6. 5. doglietto f, prevedello dm, jane ja, han j, laws er. a brief history of endoscopic transsphenoidal surgery—from philipp bozzini to the first world congress of endoscopic skull base surgery. neurosurgical focus. 2005 dec 1;19(6):1-6. 6. ebert c, senior b. a review of minimally invasive pituitary surgery: the evolution from maximally to minimally invasive surgery. otorinolaringologia. 2009;59:97-105. 7. gao hb, wang lq, zhou jy, sun w. investigating the application of diving endoscopic technique in determining the extent of pituitary adenoma resection via the trans-nasal-sphenoidal approach. experimental and therapeutic medicine. 2018 apr 1;15(4):3815-9. 8. landolt am, vance ml, reilly pr. history of pituitary surgery: transsphenoidal approach. pituitary adenomas. new york: churchill livingstone. 1996;307314. 9. locatelli d, canevari fr, acchiardi i, castelnuovo p. the endoscopic diving technique in pituitary and cranial base surgery. neurosurgery. 2010 feb 1;66(2):e400-1. 10. locatelli d, veiceschi p, castelnuovo p. letter to the editor regarding "modified endoscopic diving technique without the traditional irrigation system in endoscopic cranial base surgery: technical note". world neurosurg. 2019;128:634-635. 11. mouton wg, bessell jr, maddern gj. looking back to the advent of modern endoscopy: 150th birthday of maximilian nitze. world journal of surgery. 1998 dec 1;22(12):1256. 12. popov d, hadzhiyanev a, bussarsky a, ferdinandov d. short-term outcome of endoscopic versus microscopic pituitary adenoma surgery in a single center. biomed res (aligarh). 2018;29(14):2971-4. 202 ahtesham khizar, adnan khaliq, mian iftikhar ul haq et al. 13. senior ba, dubin mg, sonnenburg re, melroy ct, ewend mg. increased role of the otolaryngologist in endoscopic pituitary surgery: endoscopic hydroscopy of the sella. american journal of rhinology. 2005 mar;19(2):181-4. 14. senior ba, ebert cs, bednarski kk, bassim mk, younes m, sigounas d, ewend mg. minimally invasive pituitary surgery. the laryngoscope. 2008 oct;118(10):1842-55. 15. sloan ae, black kb, becker dp. lesions of the sella turcica. in: donald pj, ed. surgery of the skull base. philadelphia: lippincott-raven; 1998:555–582. 16. theodore a. schuman, brent a. senior. hydroscopy: application to pituitary surgery. in: aldo c. stamm, joão mangussi-gomes, editors. transnasal endoscopic skull base and brain surgery: surgical anatomy and its applications. 2nd ed. new york: thieme; 2019. p. 362366. 17. walker ml. history of ventriculostomy. neurosurgery clinics of north america. 2001 jan 1;12(1):101-10. microsoft word craciunassc_intramedullarytumors_f s.c. craciunas et al intramedullary tumors intramedullary tumors clinical, radiological and histological correlations s.c. craciunas1, m.r. gorgan, carmen m. cirstea2 , mariana aschie3 1neurosurgery department iv, bagdasar-arseni hospital, bucharest, romania 2hoglund brain imaging center, neurology and physical therapy and rehabilitation science departments, kansas university medical center kansas city, usa 3department of pathology, ovidius university, constanta, romania abstract intramedullary spinal cord (sc) tumors are relatively rare tumors, accounting for only 2% to 4% ofcentral nervous systemtumors.these tumorsaregenerallyslow-growing tumorsthatcouldbenefitfromsurgical removal. a pre-surgery identification of the tumor histology might improve the surgical management of the tumor and also properly predict the functional outcome after surgery. the neuroimaging techniques, provide crucial information about tumors anatomy. by adding the medical history of the present illness and detailed clinical examination, the imaging data might however be extremely helpful in the prediction of tumor histology. this will allow anappropriate surgical managementofthese lesions and provide pertinent predictors of the functional outcome post-surgery. therefore, the surgeon can set the patient’s expectations at a realistic level. the present studyis a prospective study,aiming to use combined clinical and imaging data to predictthe intramedullary sc tumor histology. the primary objectiveis to identify the pathognomonic clinical and imaging pattern for eachtumor type. the study was conducted in the neurosurgery clinic emergency clinic hospital bagdasar-arseni between 2006 and 2009. a total of 36 patients (19 females/17 males) participated. all patients were evaluated for motor, sensory, sphincter, walking and balance functions. mri assessment was used to determine the presence of an intramedullary sc tumor as well as its characteristics. all histological types have a long history of symptoms, which depends of locations in longitudinal plane. all intramedullary tumors presented spinal cord dilatation on mri. we confined the clinico-radiological characteristics of each histological type, strongly correlated with histopathological analysis, extensively presented in the paper. by combining a careful medical history, clinical examination and mri data, we could predict with a reasonable accuracy in preoperative stage the histological type of an intramedullary tumor. keywords: astrocytoma, ependymoma, intramedullary tumor, spinal cord tumor romanian neurosurgery (2011) xviii 2 introduction although the intramedullary spinal cord (sc) tumors are relatively rare tumors, accounting for only 2% to 8.5% of central nervous system tumors, thousands of patients are annually affected (fehlings and craciunas 2010; craciunas 2010). hemangioblastoma and glial tumors represent more than 90% of intramedullary spinal cord tumors, with ependymomas accounting for 35% to 40% of these tumors. these entities are generally slow-growing tumors that could benefit from surgical removal. however, their histology, e.g., benign or malignant, has a particular clinical significance. further, this significance depends on the tumor’s location. for instance, a high cervical area who grade i tumor potentially has a worse prognosis compared to a thoraco-lumbar who grade iii tumor due to high functional and surgical risks associated to the cervical location. therefore, a presurgery identification of the tumor histology might improve the surgical management of the tumor and also properly predict the functional outcome after surgery. the neuroimaging techniques, e.g., magnetic resonance imaging (mri), which have undergone spectacular development in recent years, provide crucial information about tumors anatomy. by adding the medical history of the present illness and detailed clinical examination, the imaging data might however be extremely helpful in the prediction of tumor histology. this will allow an appropriate surgical management of these lesions and provide pertinent predictors of the functional outcome postsurgery. therefore, the surgeon can set the patient’s expectations at a realistic level. the present study is a prospective study, aiming to use combined clinical and imaging data to predict the intramedullary sc tumor histology. the primary objective is to identify the pathognomonic clinical and imaging pattern for each tumor type. specifically, we analyzed: (i) demographic data, e.g., age, gender, (ii) history of the present illness, e.g., the duration of the symptoms until diagnosis, (iii) clinical symptoms, such as the type of neurological dysfunction: motor, sensory, sphincter function, gait, and/or balance; and the degree of functional impairment, as evaluated by mccormick and asia classification, and (iv) imaging data: lesion location, lesion size on the sagittal plan, e.g. number of vertebral segments affected, cyst formation (intratumoral, polar, bulbar), syringomyelia, intensity of t1-, t2-, or t1-gd-weighted signal, filling with contrast, and other imaging features, such as edema, infiltrative appearance. material and methods participants the study was conducted in the neurosurgery clinic emergency clinic hospital bagdasar-arseni between 2006 and 2009. a total of 36 patients (19 females/17 males) participated. patients were included whether (i) they were diagnosed with intramedullary sc tumor, (ii) aged between 18 and 75 years, and (iii) able to perform a mri examination. explicit exclusion criteria were: (i) previous surgery, chemo-, or radio-therapy for an intramedullary tumor, (ii) major cognitive dysfunction, limiting the ability to provide a detailed history, (iii) pre-existing neurological disorders, (iv) history of sc injury, (v) presence of systemic diseases, such as liver s.c. craciunas et al intramedullary tumors failure, metabolic disorders, uremia, transplantation, uncontrolled diabetes, (vi) substance or alcohol abuse, and (vii) treatment with neuroleptics or antiepileptics. medical history was focused on the type of the symptoms onset (acute / subacute / insidious), the duration between symptoms onset and diagnosis, and intensity of the symptoms (as evaluated by a self-reported questionnaires). clinical measurements immediately after the diagnosis of intramedullary sc tumor, all patients completed a neurological examination comprised of motor, sensory, sphincter, walking and balance functions. functional assessment was completed by using mccormick classification (see table 1). table 1 mccormick grades grade description i neurologically normal, mild focal to no functional deficits of the involved limb, mild spasticity or reflex abnormality, normal gait ii mild to moderate limb sensorimotor deficit, mild to moderate gait difficulty, severe pain or dysesthetic syndrome impairing the quality of life. however, the patient function and walk independently iii more severe neurological deficit, with the patient requiring a cane or brace to walk, or with significant bilateral upper extremity impairment; the patient may or may not be able to function independently iv severe deficit, with the patient requiring a wheelchair, cane or brace, with bilateral upper extremity impairment; the patient is usually dependent mri measurements mri assessments were performed for diagnosis. basically, the imaging assessment was used to determine the presence of an intramedullary sc tumor as well as its characteristics, e.g., extent, location, presence or not of cysts and/or fluid cavity, contrast loading, and presence of the cleavage plane between the tumor and the surrounding tissue. histological analysis conventional histological analysis was sufficient to diagnose in most cases. however, for an accurate diagnosis, immunochemistry was added in seven cases and electron microscopy and molecular/genetic tests in one case. statistical analysis statistical analysis was focused on one outcome (tumor histology) and five variables: demographic, neurological and imaging data, type of symptoms onset and symptoms duration. spearman correlations were used to analyze relationships between outcome and variables. significant correlations were considered at p<0.05 (spss 18.0, spss inc. chicago, il). results demographic characteristics in our sample, we found two peaks in age distribution, at 20-29 yrs and 40-59 yrs, with a mean age of diagnosis of 40.5 yrs (range between 18 and 72). we focus the present study on the adult patients (aged more than 18 yrs), although the frequency of intramedullary tumors is almost equal or even higher in pediatric than in adult population (kothbauer 2007; gepp rde et al. 2010; adam et al. 2010; harrop et al. 2009; mcgirt, chaichana, atiba, attenello, romanian neurosurgery (2011) xviii 2 yao, et al. 2008). with regard to the gender, we did not find any gender dominance. 42% of our patients have been diagnosed with ependymoma and 22% with astrocytoma (see table 2). however, the high incidence of ependymoma in our series (42%) is due to the exclusion of pediatric patients from our group, where the astrocytoma is the most frequent intramedullary tumor. the rest of 36% patients presented cavernoma, hamartoma, oligodendroglioma, ganglioglioma, hemangioblastoma, and metastasis (see table 2). table 2 distribution by tumor histology tumor histology # cases ependymoma 15 astrocytoma 8 cavernoma 4 hamartoma 3 ganglioglioma 2 hemangioblastoma 2 oligodendroglioma 1 metastasis 1 in our patients, 86% of tumors were classified who grade i and ii, 11% grade iii, and 3% grade iv. further, the tumors were located particularly at the thoracic level, followed by the cervical level. with regard to tumor length, the majority of tumors extended over one to two vertebral levels. clinical results intramedullary sc tumors produced a clinical picture consistent with their location. local pain (spinal) is a common occurrence. in our patients, the first symptom was paresthesia in 50%, pain in 36%, motor deficit in 11%, and proprioception disturbance in 3% (see figure 1). figure 1 intramedullary tumors – first symptom figure 2 intramedullary tumors – signs and symptoms on admission s.c. craciunas et al intramedullary tumors regarding the interval between symptoms onset and diagnosis, the average time was 20 months, ranging between 0.5 and 240 months. the case with the rapid presentation at the hospital (2 weeks) was due to a progressive cauda equina syndrome generated by a metastatic lung adenocarcinoma. in contrast, the case with the longest interval between symptoms onset and diagnosis (240 months) was a t8t9 thoracic ependymoma. on admission (see figure 2,), the sensitive (both objective and subjective) and motor deficits dominated the clinical features in our patients. however, motor deficits were mostly mild to medium (asia c in 6 cases, d in 23, and e in 7). sphincter disturbances occurred in 53% of cases. in more than half of them were mild disturbances, such as uncontrolled emission of urine in small quantities or mild urinary retention. thirteen patients presented walking impairment (see figure 2). of these, nine patients (70%) were non-ambulatory. as functional impairment, 39% of patients were mccormick i, 39% mccormick ii, and 22% mccormick iii, and no mccormick iv. mri findings spinal cord expansion at tumor’s level was presented in all cases. although the "cap sign" is not pathognomonic, we noticed this feature in 87% of our cases with ependymoma and in 50% of those with hemangioblastoma. however, this feature was absent in our patients with astrocytoma. (see figure 3) small areas of hypointensity on t1and t2-weighted images are reflective for calcifications. we met this feature in only 3% of our cases (dermoid cyst). (see figure 4) intratumoral hypointensities could be interpreted as abnormal vascular flow, corresponding to intratumoral vessels. we noticed these characteristics especially in both cases with hemangioblastoma. the tumor cysts were present in 15 patients (42%). all these patients were diagnosed with glial tumors (astrocytoma, ependymoma, ganglioglioma or oligodendroglioma). polar cysts were present in eight cases (22%), of which five were ependymoma. further, both cases with ganglioglioma also showed polar cysts. in the present study, none of our patients showed bulbar cysts. syringomyelia was present in 39% of cases. three out of the four cases with hamartoma presented syringomyelia. in 20 out of 35 cases, we found peritumoral edema, more notable in patients with hemangioblastoma and ependymoma. in most tumors (33 out of 36 cases), we found varied degrees of contrast enhancement. however, in three cases (pilocytic astrocytoma, subependymoma and cavernous hemangioma), we found no contrast enhancement. discussion clinical results local pain is a common occurrence in intramedulary tumors. this was the most frequent symptom in our series. unlike extramedullary tumors, pain is rarely nerve root type (harrop et al. 2009; garcesambrossi et al. 2009; fehlings and mercier 2009; yang, yang, and hong 2009). romanian neurosurgery (2011) xviii 2 figure 3 ependymoma t9-t10 sagittal t2(a), t1(b), stir(c), t1-gd(d), axial t2(e), t1-gd(f) – to note specific aspects: hyperdense in t2, hypodense in t1, contrast enhancing mass central located in spinal cord figure 4 dermoid cyst t12-l1 – axial ct(a), sagittal ct(b), sagittal t2(c), sagittal t1-gd(d), axial t1(e,f), intraoperative ultrasonography (g,h) inhomogeneous aspect, calcifications present. (thanks to dr. michael fehlings – university of toronto, for allowing us to present the case) since the intramedullary tumors are often developed in the central canal region, there is frequently noticed an early involvement of spino-thalamic tracts, with the sparing of the posterior columns (jallo, freed, and epstein 2003; bowers and weprin 2003; wang and liu 1999; koerbel et al. 2002; maira et al. 2001; clemenceau and lopez 2001). subsequently, these patients develop burning pain involving a f d c b e a b c d e f g h s.c. craciunas et al intramedullary tumors large areas of the body. a typical clinical picture is a segmental, dissociated-type sensibility impairment, affecting the sensitivity for pain and temperature (raco et al. 2005; shrivastava et al. 2005; brotchi 2004; antoniadis et al. 2005). pain is typically funicular-type, and can be triggered by a variety of stimuli, including motion and skin irritation. lhermitte sign is also frequently seen in these patients (yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009; taricco et al. 2008; mcgirt, chaichana, atiba, attenello, yao, et al. 2008; nakamura et al. 2008; mcgirt, chaichana, atiba, attenello, woodworth, et al. 2008). as these tumors grow in size, the pyramidal tracts might be affected. consequently, motor deficits and spasticity may occur in the proximal and then distal affected limb. this is a clinical characteristic of intramedullary tumors (gepp rde et al. 2010; sun et al. 2010; adam et al. 2010; garces-ambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009). intramedullary tumors located in conus and cauda equina often present as early symptom the genital and sphincter dysfunctions (gepp rde et al. 2010; sun et al. 2010; adam et al. 2010; garcesambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009). in addition, these entities can exhibit signs and symptoms of autonomic nervous impairment in conjunction with motor and sensitive deficits. if the lateral horn is involved, horner's syndrome or thermoregulatory and vasomotor dysfunction can occur (gepp rde et al. 2010; sun et al. 2010; adam et al. 2010; garces-ambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009; taricco et al. 2008; mcgirt, chaichana, atiba, attenello, yao, et al. 2008; nakamura et al. 2008; mcgirt, chaichana, atiba, attenello, woodworth, et al. 2008; sala et al. 2007). the clinical course of these tumors is most often an insidious process. in our patients, only one case presented neurological deterioration over 2 weeks, the rest of them having a slow progression of symptoms. patients tend to adapt and compensate the symptoms and as a result they are diagnosed at a relatively advanced stage. however, an acute neurological deterioration can be detected when intratumoral hemorrhage occurs (gepp rde et al. 2010; sun et al. 2010; adam et al. 2010; garces-ambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009; taricco et al. 2008; mcgirt, chaichana, atiba, attenello, yao, et al. 2008; nakamura et al. 2008; mcgirt, chaichana, atiba, attenello, woodworth, et al. 2008; sala et al. 2007). therefore, the typical history of symptoms was a gradual and slow progression, without remission of symptoms. this is an important finding that can be used to differentiate between the intramedullary tumors and inflammatory demyelinating syndromes. the latter rapidly develop significant deficits in days or weeks and then show some variability in terms of intensity and location of symptoms. in contrast, an acute onset of symptoms in intramedullary tumors occurs only in rare cases, usually associated with intratumoral hemorrhage or tumors with high malignancy. (see table 3) romanian neurosurgery (2011) xviii 2 e p e n d y m o m a a s t r o c y t o m a h e m a n g io b l a s t o m a g a n g l io g l io m a o l ig o d e n d r o g l io m a m e t a s t a s is h a m m a r t o m a , e p id e r m o id a n d d e r m o id c y s t s c a v e r n o m a t u m o r t a b l e 3. in t r a m e d u l l a r y t u m o r s d e m o g r a p h ic a n d c l in ic a l c h a r a c t e r is t ic s 40 a du lt: 29 p redom in an ce in 35 19 r are in pediatric age a ged patien ts n o predom in an c e 37 a g e n /a m n /a n /a sligh t m ale predom in an ce n /a n /a f g e n d e r 2-4 4-7 u su ally sm all l on g, can in volve th e w h ole cord n on -specific 2-3 segm en ts u su ally sm all u su ally on e segm en t l e n g t h c , c t m yxopapillary con u s t (67% ), c (49% ) t (50% ) c (40% ) t , c som etim es h olocord t , c t , t l c (45% ) t (35% ) l (8% ) t l t l o n g it u d in a l c -cervical, t -th oracicl lu m bar c en tral e ccen tric su perficial. 50% can h ave extram edu llary com pon en t e ccen tric n on -specific n on -specific n on -specific n on -specific t r a n sv e r sa l 37 5 38 1 m o – 5 y l on g sh ort, u su ally u n der 1 m on th l on g l on g o n s e t p r e s e n t a t io n in t e r v a l r (67% ), s(52% ), m (46% ), p + s(53.6% ) s – predom in an t (especially n on -specific n on -specific m – alm ost all p -70% , s-50% c an associate skin an d su bcu tan eu s featu res p c l in ic p -proprioception , s-sen sitive, r r adicu llar m m otor scoliosis (16% ) scoliosis n on -specific m ore requ en t th an oth er im t scallopin g frequ en tly n on -specific spin a bifida n on -specific b o n e c h a n g e s s.c. craciunas et al intramedullary tumors mri findings there are many radiological techniques available for the diagnosis of spinal pathology such as: standard radiological views, computed tomography (ct), myelography, spinal arteriography and mri. traditional imaging modalities (conventional radiological views and ct) often fail to indicate the true extension of intramedullary neoplasms, being able to detect these entities only when the massive tumor growth occurred. myelography, acquired both by conventional radiology or ct, shows an intramedullary mass blocking (completely or partially) the migration of the contrast agent into the intrathecal space. mri provides a non-invasive method to identify abnormalities associated with these tumors such as cystic formations, syringo/hydromyelia, bleeding and swelling had become a routine in the evaluation of intramedullary spinal masses. in our series, all patients underwent mri for diagnosis and preoperative management. we used other imaging techniques only for confining the anatomy/location of the lesion with supplemental accuracy. currently, mri is the modality of choice for the evaluation of intraspinal masses. mri evaluation should include t1, t2 and t1-gd weighted sequences, in both sagittal and axial planes. contrast agent enhancement is particularly important in determining the solid portion of intramedullary neoplasms and cysts associated with identification and other items that can often change the differential diagnosis (sze et al. 1990; adam et al. 2010; garces-ambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009). although mri is a very powerful diagnostic tool, its ability to predict tumor histology was considered limited in the past. for instance, in a series of 171 patients with intramedullary tumors (brotchi et al. 1991), mri aspects were correlated with the tumor histology in only 70% of cases. in particular, the mri differentiation between astrocytoma and ependymoma was difficult. there are three major mri characteristics for the intramedullary tumors. first, the expansion of the sc (takemoto et al. 1988; adam et al. 2010; garces-ambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009) can be used to differentiate between neoplastic and non-neoplastic entities. specifically, an absence of sc expansion suggests rather a non-neoplastic (e.g., demyelinating disease, sarcoidosis, amyloid angiopatie, pseudotumors, arteriovenous fistulae, spinal cord infarction, cystic myelomalacia) than neoplastic etiology (lee et al. 1996; andrews et al. 1988; dillon et al. 1989; adam et al. 2010; garces-ambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009). obviously, this differentiation is critical for surgical management. explicitly, if there is a high probability for a lesion to be a neoplasm, extensive tumor resection should be recommended. in contrast, if a lesion is likely a non-neoplasm entity, a biopsy rather than a surgical approach would be indicated. subsequently, these patients avoid the risks of aggressive surgery with significantly lower postoperative morbidity (lee et al. 1996; adam et al. 2010; garcesambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009). for example, romanian neurosurgery (2011) xviii 2 in a series of 212 patients with intramedullary masses, nine (4%) had nonneoplastic lesions confirmed on the mri images, e.g., no sc expansion(lee et al. 1996). second, most intramedullary spinal neoplasms show contrast enhancement (parizel et al. 1989; dillon et al. 1989; sze et al. 1988; goy et al. 1986; bydder et al. 1985; froment 1996; adam et al. 2010; garcesambrossi et al. 2009; fehlings and mercier 2009; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009). therefore, in evaluating a patient suspected to have such pathology, it is mandatory to obtain contrast-enhanced images in at least two plans. this is essential for both diagnosis and treatment approaches. however, the absence of contrast enhancement does not exclude a neoplasm (froment 1996) and caution is recommended in the interpretation of this mri characteristic. finally, cystic formations are elements relatively common for the intramedullary tumors. we found cystic entities in almost half of cases, especially in glial tumors. there are two basic types of cysts, tumoral and non-tumoral. cysts located at the poles of solid portion of tumor are usually simple reactive dilations of the central canal (syringomyelia) or they originate in the fluid produced by the neoplasm (epstein and epstein 1982; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009). approximately 60% of all intramedullary tumors show polar cysts. these cystic cavities can be spontaneously decompressed following tumor resection or can be aspirated by the surgeon during resection(epstein, farmer, and schneider 1991; harrop et al. 2009; yang, yang, and hong 2009; sun et al. 2009; manzano et al. 2008; berhouma et al. 2009). these formations are part of the cystic tumor, and therefore will not load contrast (epstein, farmer, and schneider 1991). in contrast, tumor cysts are contained within the tumor and often shows peripheral contrast enhancement (froment 1996; waldron and cha 2006). these entities tend to be observed more frequently in astrocytoma than in ependymoma (epstein, farmer, and schneider 1991; waldron and cha 2006). identifying the contrast-enhancing solid portion of tumor (including the tumor cyst) is vital because current neurosurgical techniques allow laminectomy/laminotomy limited only to these areas, with consequent decreased surgical morbidity. intramedullary tumor mri characteristics topography: the standard radiological views may be useful in precisely determining the level of spinal lesion, especially if vertebral anomalies are present. if this is not possible, imaging studies should include anatomical structures that allow the identification of the level. for instance, using a wide field imaging (e.g. antenna array of 512) allows the location of the two poles of the tumor by counting the vertebrae from the sacral-iliac joint or odontoid process. a central location within the spinal canal favors the diagnosis of ependymoma, while eccentric location suggests a diagnosis of astrocytoma, hemangioblastoma or lipoma (adam et al. 2010; harrop et al. 2009; manzano et al. 2008; waldron and cha 2006; bowers and weprin 2003; hoshimaru 2001). our results were consistent with those reported in the literature. signal characteristics: mri allows differentiating solid and cystic portions of tumors and demonstrates the presence or s.c. craciunas et al intramedullary tumors absence of swelling and signal changes following contrast loading. the solid portions of most intramedullary tumors are hypointense or isointense on t1-weigthed images and isointense or hyperintense on t2-weigthed image. these signal abnormalities are generally well defined and can have either homogeneous or heterogeneous appearance. for example, a clear hyperintensity on t1-weighted image suggests the presence of sub-acute blood (from 3-5 days to a month after bleeding) while a hypointensity on t2-weighted images with margins more or less defined on t1 reflects hemosiderin, characteristic feature of chronic bleeding (months to years after bleeding). another example is the "cap sign", a hypointensity on both poles of the solid tumor that was histologically and intra-operatively correlated with areas of chronic hemorrhage. in our sample, this feature were consistently present in ependymoma cases. cystic formations represent a common feature associated with solid portion of intramedullary tumor and several types of cysts have been reported (adam et al. 2010; harrop et al. 2009; manzano et al. 2008; waldron and cha 2006; bowers and weprin 2003; hoshimaru 2001). the majority of our patients presented cysts. intratumoral cysts usually have a different signal from that of csf due to the highprotein or blood content, e.g., low signal on t1 and high signal on t2-weighed images. they have a well-defined contour and their walls load the contrast substance after injection (adam et al. 2010; harrop et al. 2009; manzano et al. 2008; waldron and cha 2006; bowers and weprin 2003; hoshimaru 2001). polar cysts can be present at both upper and lower poles of the tumor, with a signal similar with that obtained from csf, e.g., low t1 signal and high t2 signal. however, there are some varieties of the signal acquired from these cysts. further, these cysts are characterized by: (i) appearance to be under tension, (ii) often round shape, and (iii) walls that do not load the contrast substance. syringomyelia cavities, associated with intramedullary tumors, have their terminal portions often filiform and satellite cysts may coexist even if the communication with the syringomyelic cavity is not always visible. these cysts also appear to be under tension, but their walls do not have specific characteristics and do not exhibit contrast enhancement. finally, bulbar cysts have a convex appearance and a signal similar to csf. they are usually located under the floor of the fourth ventricle, far from the tumor and communicate with the subjacent syringomyelic cavity. after tumor removal and the subsequent opening of the cyst cavity and drainage of the syringomyelic cavity, these cysts gradually regress and disappear in a several months (adam et al. 2010; harrop et al. 2009; manzano et al. 2008; waldron and cha 2006; bowers and weprin 2003; hoshimaru 2001). (see table 4) peritumoral edema is another feature of the intramedullary tumors that can be identified on mri images, such as a hyperintensity on t2-weigthed images. peritumoral edema can be extensive, especially in hemangioblastoma, and disappears after tumor resection (adam et al. 2010; harrop et al. 2009; manzano et al. 2008; waldron and cha 2006; bowers and weprin 2003; hoshimaru 2001). (see table 4). the capability of these lesions to uptake or not the contrast substance is essential for diagnosis. for instance, contrast romanian neurosurgery (2011) xviii 2 enhancement of the cystic walls suggests a neoplastic nature. for the solid portion of the tumors, the regular appearance is moderately to very intense uptake of the contrast substance (particularly in hemangioblastoma) (waldron and cha 2006). another important feature of the contrast loading is the homogeneity of the uptake, varying from homogeneous loading in epedymoma to heterogeneous in astrocytoma (adam et al. 2010; harrop et al. 2009; manzano et al. 2008; waldron and cha 2006; bowers and weprin 2003; hoshimaru 2001). similar finding was also found in our series. further, the rate of loading and unloading of the contrast sunstance may offer an idea about the tumor histology, e.g., slower load in astrocytoma than ependymoma(adam et al. 2010; harrop et al. 2009; manzano et al. 2008; waldron and cha 2006; bowers and weprin 2003; hoshimaru 2001). (see table 4) although mri examination remains the most valuable investigation in sc pathologies, the clinical and laboratory data may improve its value in the diagnosis of nonspecific pathologies, such as metastatic melanoma, lymphoma and sarcoidosis. however, it is clearly that in some cases, the final diagnosis can be only derived from the histological exam. for instance, in the case of intramedullary sc tumors, mri cannot provide an accurate assessment of the infiltrative nature of these. the sc dilatation or abnormal mri signal within the sc are not pathognomonic for intramedullary tumors. mri signal change in some extramedullary spinal lesions, e.g., enteric cysts, is another example of the mri limitation to distinguished from sc intramedullary masses. one solution for this limitation is the mri acquisition on multiple planes. however, the differential diagnosis between intraand extramedullary tumors can be difficult when intramedullary tumor is partially exofitic. furthermore, sc enlargements are present in other pathologies, such as syringomyelia fluid, multiple sclerosis, vascular malformations and post-irradiation myelopathy. therefore, these pathologies should be excluded. differential diagnosis between hydrosyringomyelia and intramedullary tumors is difficult by using myelography of myelo-ct alone. in contrast, mri diagnosis of intramedullary cavities filled with fluid, on the sagittal and axial images, is relatively a common clinical practice. another mri limitation is in the differential diagnosis between multiple sclerosis (ms) and intramedullary tumor. for example, a ms’ plaque in the acute stage is characterized by a focal intramedullary lesion on t2-weigthed images accompanied by an sc enlargement. clinical context and signs of intracranial demyelination on t2 images (particularly an increased periventricular signal) significantly helps the diagnosis. finally, the lack of the intramedullary contrast several weeks after the baseline mri evaluation confirms the diagnosis of ms. images of vascular structures could be sometimes misleading. although it is relatively easy to diagnose an intramedullary hematoma, this does not exclude the possibility of an intratumoral hemorrhage. a longitudinal mri evaluation will provide required information to avoid the failure of diagnosis. specifically, a structure with a long vascular nidus, visualized on myelography and mri (particularly in t2 s.c. craciunas et al intramedullary tumors weighted images) suggests a spinal medullar angioma. vascular structures may be more visible in hemangioblastoma, but this entity is characterized by a nidus loading intense contrast. perimedular venous drainage of dural fistulas can be associated with extensive hyper-intense areas on t2, but with no significant increasing in spinal cord dimensions. spinal arteriography is used to confirm the diagnosis. in post-radiation myelopathy, the focal loading after contrast administration may raise difficulties in interpretation. history of disease in the area where the radiation has been applied, the clinical course and the characteristic changes in bone matrix are useful diagnostic indices. further, the decisive argument in favor of post-radiation myelopathy is the absence of sc enlargement, although a potential enlargement can occur in the acute phase followed by a regression. furthermore, this regression might continue, and an atrophy of sc can be documented on subsequent mri evaluations. despite all our efforts, we still account a major problem, the distinction between astrocytoma and ependymoma. this distinction is critical for tumor resectability, such as subtotal resection or biopsy for astrocytoma and total resection for ependymoma. astrocytoma, a long tumor with edges poorly demarcated, is frequently located at the thoracic level. these tumors are eccentric, show moderate and partial heterogeneous contrast enhancement, and can present intra-tumoralcysts. in contrast, ependymoma are usually less extensive and well-defined tumors localized particularly at the cervical level. these tumors show intense and homogeneous contrast enhancement, and are often presenting large cysts and cap sign. we need to mention the technical limitations of a mri evaluation. for example, the artifacts related to csf motion are one of the common limitations. using effective techniques for flow compensation however eliminates this. another example is the difficulty to achieve accurate spatial reconstruction in patients with severe spinal deformity. for this, a ge-3d sequences can provide a valuable volumetric image acquisition. finally, the slice thickness must be reduced as much as possible (3mm or less) to avoid partial volume effects and the acquisition in different planes may help to precisely characterize the tumor. conclusions in summary, by combining mri features of intramedullary tumor with medical history and clinical examination the tumor histology could be predicted with a reasonable accuracy. this is important in neurosurgical practice, allowing an appropriate surgical management of these lesions and providing pertinent predictors of the functional outcome post-surgery. romanian neurosurgery (2011) xviii 2 e p e n d y m o m a a s t r o c y t o m a h e m a n g io b l a s t o m a g a n g l io g l io m a o l ig o d e n d r o g l io m a m e t a s t a s is h a m m a r t o m a , e p id e r m o id a n d d e r m o id c y s t s c a v e r n o m a t u m o r t a b l e 4. in t r a m e d u l l a r y t u m o r s – im a g in g f e a t u r e s h ypo iso h ypo iso h yper iso m ixt appearan ce, “salt an d pepper” iso + foci of h yper (m eth b ) c en tral h yposign al area h eterogen eou s h yper t 1 h yper iso h yper h yper + flow artifacts h yper h yper + foci h ypo h em osiderin ) h yper h eterogen eou s h ypoin ten sity rin g t 2 in ten se a lm ost alw ays presen t in ten se en h an cin g n ode in h om ogen eou s, 15 % n on en h an cin g in h om ogen ou s in ten se n on h om ogen ou s n o c o n t r a s t 78-84% f requ en t u su ally presen t m ore frequ en t th an astrocytom a an d n on -specific r are n on -specific n o c y s t s 9-50% f requ en t f requ en t a s oth er im t ’s f requ en t r are n on -specific n on -ch aracteristic s y r in g o m y e l ia > 60% f requ en t m igh t be presen t, bu t n ot r are n on -specific a djacen t lesion in ten se in con stan t n on ch aracteristic e d e m a w ell-con fin ed, cleavage plan , “cap sign ” p oor defin ed borders, in flitrative w ell-con fin ed, localized on dorsal spin al cord su rface c alcification s possible c alcification s possible n on -specific c alcification s possible v ariou s age h em orrh ages o t h e r m r i f e a t u r e s s.c. craciunas et al intramedullary tumors references 1. adam, y., j. benezech, a. blanquet, j. m. fuentes, j. y. bousigue, b. debono, e. duplessis, c. espagno, j. y. plas, j. p. lescure, j. destandau, j. p. hladky, p. grunewald, k. mahla, j. remond, and e. louis. 2010. [intramedullary tumors. results of a national investigation in private neurosurgery]. neurochirurgie 56 (4):344-9. 2. andrews, b. t., p. r. weinstein, m. l. rosenblum, and n. m. barbaro. 1988. intradural arachnoid cysts of the spinal canal associated with intramedullary cysts. j neurosurg 68 (4):544-9. 3. antoniadis, g., m. engelhardt, w. borm, h. p. richter, and s. a. rath. 2005. [spinal intramedullary tumors. when is surgical treatment indicated?]. nervenarzt 76 (2):186-92. 4. berhouma, m., k. bahri, s. houissa, i. zemmel, n. khouja, l. aouidj, h. jemel, and m. khaldi. 2009. [management of intramedullary spinal cord tumors: surgical considerations and results in 45 cases]. neurochirurgie 55 (3):293-302. 5. bowers, d. c., and b. e. weprin. 2003. intramedullary spinal cord tumors. curr treat options neurol 5 (3):207-212. 6. brotchi, j. 2004. [surgical treatment of intramedullary tumors. experience with 316 cases]. bull mem acad r med belg 159 (5-6):335-9; discussion 339-41. 7. brotchi, j., o. dewitte, m. levivier, d. baleriaux, a. vandesteene, c. raftopoulos, j. flament-durand, and j. noterman. 1991. a survey of 65 tumors within the spinal cord: surgical results and the importance of preoperative magnetic resonance imaging. neurosurgery 29 (5):651-6; discussion 656-7. 8. bydder, g. m., j. brown, h. p. niendorf, and i. r. young. 1985. enhancement of cervical intraspinal tumors in mr imaging with intravenous gadoliniumdtpa. j comput assist tomogr 9 (5):847-51. 9. clemenceau, s., and m. lopez. 2001. [intramedullary tumors]. rev prat 51 (11):1206-10. 10.craciunas, s ; aschie, m ; iliesiu, a ; bani-ahmed, a ; cirstea, c. 2010. intramedullary spinal cord tumors: neuroimaging features predict histopathology. society for neuroscience 40th annual meeting, san diego, us, 2010. 11.dillon, w. p., d. norman, t. h. newton, k. bolla, and a. mark. 1989. intradural spinal cord lesions: gddtpa-enhanced mr imaging. radiology 170 (1 pt 1):229-37. 12.epstein, f., and n. epstein. 1982. surgical treatment of spinal cord astrocytomas of childhood. a series of 19 patients. j neurosurg 57 (5):685-9. 13.epstein, f. j., j. p. farmer, and s. j. schneider. 1991. intraoperative ultrasonography: an important surgical adjunct for intramedullary tumors. j neurosurg 74 (5):729-33. 14.fehlings, m. g., and s. c. craciunas. 2010. editorial: high-grade intramedullary astrocytomas: what is the best surgical option? j neurosurg spine 12 (2):141-2; discussion 142-3. 15.fehlings, m. g., and d. mercier. 2009. factors predicting the resectability of intramedullary spinal cord tumors and the progression-free survival following microsurgical treatment. j neurosurg spine 11 (5):5889; discussion 590. 16.froment, a. 1996. [role of patient in the medical decision]. therapie 51 (3):283-6. 17.garces-ambrossi, g. l., m. j. mcgirt, v. a. mehta, d. m. sciubba, t. f. witham, a. bydon, j. p. wolinksy, g. i. jallo, and z. l. gokaslan. 2009. factors associated with progression-free survival and long-term neurological outcome after resection of intramedullary spinal cord tumors: analysis of 101 consecutive cases. j neurosurg spine 11 (5):591-9. 18.gepp rde, a., j. m. couto, m. d. da silva, r. t. da silva, and e. a. neri. 2010. intramedullary tumors in children: analysis of 24 operated cases. arq neuropsiquiatr 68 (3):396-9. 19.goy, a. m., r. s. pinto, b. n. raghavendra, f. j. epstein, and kricheff, ii. 1986. intramedullary spinal cord tumors: mr imaging, with emphasis on associated cysts. radiology 161 (2):381-6. 20.harrop, j. s., a. ganju, m. groff, and m. bilsky. 2009. primary intramedullary tumors of the spinal cord. spine (phila pa 1976) 34 (22 suppl):s69-77. 21.hoshimaru, m. 2001. [diagnosis and microsurgical treatment of intramedullary spinal cord tumors]. no shinkei geka 29 (3):207-14. 22.jallo, g. i., d. freed, and f. epstein. 2003. intramedullary spinal cord tumors in children. childs nerv syst 19 (9):641-9. 23.koerbel, a., c. e. tatsui, d. m. prevedello, r. a. hanel, c. v. grande, l. f. ditzel, j. c. araujo, and a. antoniuk. 2002. [prognostic factors in the treatment of intramedullary spinal cord tumors]. arq neuropsiquiatr 60 (3-b):818-22. 24.kothbauer, k. f. 2007. neurosurgical management of intramedullary spinal cord tumors in children. pediatr neurosurg 43 (3):222-35. 25.lee, m., a. r. rezai, d. freed, and f. j. epstein. 1996. intramedullary spinal cord tumors in neurofibromatosis. neurosurgery 38 (1):32-7. 26.maira, g., p. amante, l. denaro, a. mangiola, and c. colosimo. 2001. surgical treatment of cervical intramedullary spinal cord tumors. neurol res 23 (8):835-42. 27.manzano, g., b. a. green, s. vanni, and a. d. levi. 2008. contemporary management of adult intramedullary spinal tumors-pathology and romanian neurosurgery (2011) xviii 2 neurological outcomes related to surgical resection. spinal cord 46 (8):540-6. 28.mcgirt, m. j., k. l. chaichana, a. atiba, f. attenello, g. f. woodworth, and g. i. jallo. 2008. neurological outcome after resection of intramedullary spinal cord tumors in children. childs nerv syst 24 (1):93-7. 29.mcgirt, m. j., k. l. chaichana, a. atiba, f. attenello, k. c. yao, and g. i. jallo. 2008. resection of intramedullary spinal cord tumors in children: assessment of long-term motor and sensory deficits. j neurosurg pediatr 1 (1):63-7. 30.nakamura, m., k. ishii, k. watanabe, t. tsuji, h. takaishi, m. matsumoto, y. toyama, and k. chiba. 2008. surgical treatment of intramedullary spinal cord tumors: prognosis and complications. spinal cord 46 (4):282-6. 31.parizel, p. m., d. baleriaux, g. rodesch, c. segebarth, b. lalmand, c. christophe, m. lemort, p. haesendonck, h. p. niendorf, j. flament-durand, and et al. 1989. gd-dtpa-enhanced mr imaging of spinal tumors. ajr am j roentgenol 152 (5):1087-96. 32.raco, a., v. esposito, j. lenzi, m. piccirilli, r. delfini, and g. cantore. 2005. long-term follow-up of intramedullary spinal cord tumors: a series of 202 cases. neurosurgery 56 (5):972-81; discussion 972-81. 33.sala, f., a. bricolo, f. faccioli, p. lanteri, and m. gerosa. 2007. surgery for intramedullary spinal cord tumors: the role of intraoperative (neurophysiological) monitoring. eur spine j 16 suppl 2:s130-9. 34.shrivastava, r. k., f. j. epstein, n. i. perin, k. d. post, and g. i. jallo. 2005. intramedullary spinal cord tumors in patients older than 50 years of age: management and outcome analysis. j neurosurg spine 2 (3):249-55. 35.sun, j. j., z. y. wang, j. c. xie, z. d. li, c. c. ma, b. liu, and j. z. zhao. 2010. [comparative analysis between multi-segments intramedullary spinal cord congenital tumors and benign ependymomas]. beijing da xue xue bao 42 (2):183-7. 36.sun, j., z. wang, z. li, and b. liu. 2009. microsurgical treatment and functional outcomes of multi-segment intramedullary spinal cord tumors. j clin neurosci 16 (5):666-71. 37.sze, g., g. krol, r. d. zimmerman, and m. d. deck. 1988. intramedullary disease of the spine: diagnosis using gadolinium-dtpa-enhanced mr imaging. ajr am j roentgenol 151 (6):1193-204. 38.sze, g., g. k. stimac, c. bartlett, w. p. dillon, v. m. haughton, w. orrison, f. kashanian, and h. goldstein. 1990. multicenter study of gadopentetate dimeglumine as an mr contrast agent: evaluation in patients with spinal tumors. ajnr am j neuroradiol 11 (5):967-74. 39.takemoto, k., y. matsumura, h. hashimoto, y. inoue, t. fukuda, m. shakudo, y. nemoto, y. onoyama, t. yasui, a. hakuba, and et al. 1988. mr imaging of intraspinal tumors--capability in histological differentiation and compartmentalization of extramedullary tumors. neuroradiology 30 (4):303-9. 40.taricco, m. a., v. m. guirado, r. b. fontes, and j. p. plese. 2008. surgical treatment of primary intramedullary spinal cord tumors in adult patients. arq neuropsiquiatr 66 (1):59-63. 41.waldron, j. s., and s. cha. 2006. radiographic features of intramedullary spinal cord tumors. neurosurg clin n am 17 (1):13-9. 42.wang, z., and a. liu. 1999. [differential diagnosis and operative timing of intramedullary spinal cord tumors]. zhongguo yi xue ke xue yuan xue bao 21 (2):88-93. 43.yang, s., x. yang, and g. hong. 2009. surgical treatment of one hundred seventy-four intramedullary spinal cord tumors. spine (phila pa 1976) 34 (24):2705-10. microsoft word 3.iamandeig_involvment.doc 396 g. iamandei et al involvement of n6 and n3 polyunsaturated faty acids involvement of n6 and n3 polyunsaturated faty acids on the lipidic profile in central nervous system of the animals of experience g. iamandei1, veronica mocanu1, t. oboroceanu2, veronica luca1 1pathophysiology department, university of medicine and pharmacy “gr.t. popa”, iaşi, romania, 2faculty of biology, university “alexandru ioan cuza”, iaşi, romania abstract introduction: n-3 and n-6 polyunsaturated fatty acids has many involvements in activities within or entering in regulating various physiological processes and in certain pathologies. among systemic physiological effects in which they are involved we mention the central nervous system development and recall of the retina, regulating plasma lipid levels, cardiovascular and immune system functions, regulating the activity of insulin. material and methods: the experiment there were used 60 male wistar rats , weight 180 ± 20 grams, procured from the animal farm of the department of pathophysiology, university of medicine and pharmacy “gr.t. popa”, iaşi. male wistar rats were divided into two study groups: normal control animals (m) and test animals. test group was further divided into three groups each group being composed of 15 animals. administration of the substances was made for 36 weeks (nine months), after which the animals were evaluated and subsequently sacrificed. results: following statistical analysis, we determined the following: • averages of agp n3 were significantly higher in groups 2 (p <0.001) and 3 (p <0.001) compared with group 4 • averages ratio n6: n3 in nerve cell membrane were significantly lower in groups 2 (p <0.001) and 3 (p <0.001) compared with group 4 discussions: our experiment demonstrates that increased amounts of polyunsaturated fatty acids in the membranes of nerve cells which can justify the positive evolution of animals in assessing the performance of concomitant behavioral tests. conclusions: this study brings new light on the importance of the existence of a balance between pufa intake and daily diet. keywords: pufa, central nervous system, lipids profile, mass spectrometry, eicosapentaenoic acid, docosahexaenoic acid n-3 and n-6 polyunsaturated fatty acids (pufas) have many involvements in activities within or entering in regulating various physiological processes and in certain pathologies. among systemic physiological effects in which they are involved we mention the central nervous system development and recall of the retina, regulating plasma lipid levels, romanian neurosurgery (2010) xvii 4: 396 – 402 397 cardiovascular and immune system functions, regulating the activity of insulin (12, 26). at the level of cellular functions, n-3 and n-6 pufas has affects over the cellular membrane composition and function, the synthesis of eicosanoids and thus a role in cell signaling, regulation of gene expression and regulation of cell junctions (12, 24). recent research has shown that the deficit of long chain n-3 pufas is associated with memory loss and decreased cognitive functions. many studies have found a correlation between changes in quantities of long chain n-3 and n-6 pufas, and changes into the profile of these essential fatty acids in neuronal membranes (13, 18). it was suspected that α-linolenic acid (18:3 n-3) controls neuronal membrane composition, theory untested so far. changes into the relative quantities of free fatty acids on neuronal membrane level may be a key element in the physiological role of membranes (6, 25). changes into the composition of long chain pufa diet had effect on function and membrane fluidity because they have a role in reducing serum cholesterol, cholesterol that has a role in controlling membrane fluidity and decrease microviscosity of the nervous tissue (10, 13, 24). identification of predisposing risk factors for both the deficit of the central nervous system development and neurodegenerative pathologies developing increasing incidence in the last period, especially modulation of protective factors through nutritional supplements can make an outstanding attitude in order to find a therapeutic method to prevent, delay or improve the central nervous system diseases and their possible complications (11, 26). material and methods the experiment there were used 60 male wistar rats, weight 180 ± 20 grams, procured from the animal farm of the department of pathophysiology, university of medicine and pharmacy “gr t. popa”, iaşi. male wistar rats were divided into two study groups: normal control animals (m) and test animals (t) (14, 16). test group was further divided into three groups each group being composed of 15 animals, compared with the type of substance administered as follows: group 1 male white wistar rats, aceticysteine (acc) intraperitoneal administration of 35 mg/100 g animal; group 2 male white wistar rats intraperitoneal administration of pufa 50 mg/100 g animal; group 3 male white wistar rats, acc intraperitoneal administration of 35 mg/100 g animal and pufa 50 mg/100 g animal; control group contained one group of 15 animals that received only normal diet without further intervention. -group 4 male white wistar rats, normal diet; (6, 12, 24) administration of the substances was made for 36 weeks (nine months), after which the animals were evaluated and subsequently sacrificed. the animals were evaluated through the morris radial maze and multiple t maze. the morris water maze is a large round tub of opaque water (made white with powdered milk) divided by eight radial arms and a hidden platform located 1-2 cm under the water's surface in one of the arms. the rat was placed on in the center of the maze. the rat has to swim in the maze’s arms until it finds the other platform to stand on. we measured how long it takes 398 g. iamandei et al involvement of n6 and n3 polyunsaturated faty acids for a rat to find hidden platform (12, 16). the multiple t-maze is a complex maze made of many t-junctions. performance in the multiple t-maze is easy to measure because each intersection is identical and has a clear right or wrong answer. multiple t-mazes were used to answer questions of place vs. response learning and cognitive maps. we recorded the time needed for the rat to find the end of the maze (12, 16). in both tests we found significant improvement in learning the mazes for the rats that received n3 pufas via intraperitoneal administration. also we monitored biochemical (glycemic profile, lipids profile and oxidative stress parameters such as malondialdehyde, glutathione peroxidase, and total antioxidant capacity) and zoometrical (weight, length) parameters which showed significant variations for the animals that received pufa n3 treatment. brain lipid profile of wistar rats was carried out using mass spectrophotometry liquid chromatography. results were obtained using agilent 6500 series system accurate-mass quadrupole time-of-flight (q-tof) lc / ms (4, 5, 24). the samples were separated on a reverse phase column zorbax sb-c18 (4.6 x 150 mm, 5 mm). mobile phase consists of h2o with 0.1% formic acid (solvent a) and acetonitrile with 0.1% formic acid (solvent b) filtered and degassed before use (2, 6, 16). the following gradient program was used: 95% to 100% solvent b in 10 minutes, maintaining 100% b up to 25 minutes, then return to 95% b, the total registration was 60 minutes. were injected 10 ml of the sample (dissolved in isopropanol: acetonitrile 1:1) at a rate of 1ml/minut (18, 19 , 26). uv-vis dad detector was monitored between 190-900nm. lc system was directly connected to the electrospray ionization source (esi) of mass spectrometry. terms of the q / tof ms selected were: esi in positive mode, drying gas flow (n2) 7l/min , gas temperature 325 º c, nebuliser pressure 35 psig, capillary voltage 4000 v, 200 v fragmentation voltage, the compounds have been investigated on the m / z 100-1500 (16, 17). results 2x10 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 + scan (7.151 min) m1.d subtract (4) 327.35176 343.33098 305.35397 282.36794 228.31795 272.37584 counts (%) vs. mass-to-charge (m/z) 00 210 220 230 240 250 260 270 280 290 300 310 320 330 340 350 360 370 380 figure 1 mass spectrum of type of formed ions ag in the brain romanian neurosurgery (2010) xvii 4: 396 – 402 399 table i interpretation of mass spectrum for the types of formed ions p1_7,151 min x dad m/z abund charge 228.31795 33198 9-tetradecenoic acid / [m+h+]+ 272.37584 8676 palmitoleic acid sau cis-6-hexadecenoic acid / [m+nh4+]+ 282.36794 91847 1 oleic acid sau elaidic acid / m 283.37284 16569 1 oleic acid sau elaidic acid / [m+h+]+ 287.32845 11087 300.39192 62818 1 linoleic acid /[m+nh4+]+ + (h) ori stearidonic acid / [m+na+]+ + (h) 301.39546 11648 1 gamma-linolenic acid, gla or α-linolenic acid / [m+na+]+ or oleic acid or elaidic acid / [m+nh4+]+ 305.35397 105383 1 arachidonic acid / [[m+h+]+ori oleic acid sau elaidic acid / [m+na+]+ 306.35547 20256 1 dihomo-γ-linolenic acid / m 316.43518 11386 322.39191 11848 eicosapentaenoic acid / eicosapentaenoic acid 327.35176 117434 1 arachidonic acid / [m+na+]+ 328.35426 25140 1 docosahexaenoic acid / m 343.33098 109164 1 344.33403 20977 1 349.35166 13684 403.46611 7813 table ii membrane polyunsaturated fatty acid composition brain % from the total quantity of fat acids group 1 group 2 group 3 group 4 n6 pufas 30.6 37.2 34.1 39.2 linoleic acid 10.1 12.4 10.2 13.8 arahidonic acid 17.2 20.8 20.1 21.2 n3 pufas 8.6 10.9 11.2 9.2 α linoleic acid 2.0 2.2 2.3 2.5 eicosapentaenoic acid 1.8 2.8 2.8 1.8 docosahexaenoi c acid 4.8 5.9 6.1 4.9 n3: n6 report 3.6 3.4 3.0 4.2 following statistical analysis, we determined the following: • averages of agp n3 were significantly higher in groups 2 (p <0.001) and 3 (p <0.001) compared with group 4 (19) • averages ratio n6: n3 in nerve cell membrane were significantly lower in groups 2 (p <0.001) and 3 (p <0.001) compared with group 4 (1, 3). discussions approximately 20% of the dry weight of brain is represented by the long-chain polyunsaturated fatty acids which are incorporated into the phospholipids, substances with a major role for the structural integrity of neuronal membrane, membrane fluidity, and other associated membranes functions, such as receptors, enzymes, ion channels and eicosanoid-type functions (4, 12, 13, 24). the beneficial effects of long-chain polyunsaturated fatty acids are directly related to their action on neuronal membrane composition and fluidity of the central nervous system and the supplementation in elongated and desaturate derivatives with subsequent activation of brain conversion and storage has proven to be effective (23, 24). thus α 400 g. iamandei et al involvement of n6 and n3 polyunsaturated faty acids linolenic acid (18:3 n-3) is a source of acetate for de novo synthesis of palmitic acid and α-linolenic acid (18:3 n-3), essential for membrane integrity (6, 8, 9). from our study we have observed that animal subjects from group 4 (control) had increased levels of n6 pufas in the brain tissue compared to groups 1 (acc), 2 (pufa) and 3 (acc+pufa). the lowest brain tissue levels of n6 pufas were recorded in group (acc), these results may be explained by the anti-inflammatory effect of acetylcysteine (26). the data we have obtained has similar behavior for the linolenic and arachidonic acids in the brain tissue (the most common n6 pufas in the brain) and this is consistent with data obtained by other studies (3, 4, 11). the levels of n6 pufas registered by group 3 (acc+pufa) are higher than in group 2 (pufa), observation that contradict in some matter by findings of other researchers (20, 21) and can be attributed to different absorption of test substances when administrated simultaneous via peritoneum. the highest concentration of n3 pufas (known for their anti-inflammatory, atherosclerosis prevention and membrane fluidity increase effects) in the brain tissue were recorded in group 3 (acc+pufa) as expected. these findings are similar to the data encountered in other studies (11, 14, 21). the most significant increase for a single fatty acid was recorded for the docosahexaenoic acid (dha), in amount of more than 20% and also significant increase levels of eicosapentaenoic acid (epa) were recorded for groups 2 (pufa) and 3 (acc+pufa) but no change in group 1 (acc). the peritoneal administration of salmon oil, rich source of pufas lead to increase neuronal deposits of dha an epa as shown by similar studies (20, 21, 25). the use of new and improved methods of measuring of lipids in tissues and cells created a new, cutting edge, research domain called lipidomics. lipidomics may be defined as the large-scale study of pathways and networks of cellular lipids in biological systems[ the word "lipidome" is used to describe the complete lipid profile within a cell, tissue or organism. lipidomics is a relatively recent research field that has been driven by rapid advances in technologies such as mass spectrometry (ms), nuclear magnetic resonance (nmr) spectroscopy, fluorescence spectroscopy, dual polarisation interferometry and computational methods, coupled with the recognition of the role of lipids in many metabolic diseases such as obesity, atherosclerosis, stroke, hypertension and diabetes (27). lipidomics research involves the identification and quantization of the thousands of cellular lipid molecular species and their interactions with other lipids, proteins, and other metabolites. investigators in lipidomics examine the structures, functions, interactions, and dynamics of cellular lipids and the changes that occur during perturbation of the system. in lipidomic research, a vast amount of information quantitatively describing the spatial and temporal alterations in the content and composition of different lipid molecular species is accrued after perturbation of a cell through changes in its physiological or pathological state. information obtained from these studies facilitates mechanistic insights into changes in cellular function. therefore, lipidomic studies play an essential role in defining the biochemical mechanisms of romanian neurosurgery (2010) xvii 4: 396 – 402 401 lipid-related disease processes through identifying alterations in cellular lipid metabolism, trafficking and homeostasis (27). analysis of brain lipid composition is a new and important subject of study but the number of studies at present time is scarce due to the expensive methods and procedures applied to biological material and reduced availability of specific measuring equipment. mass spectroscopy combined with liquid chromatography aimed at the n3 and n 6 pufas lipid fractions of the brain represent the leading wave in the scientific approach to the understanding the basic foundations and the superior functions of the brain. during our research we have also investigated the learning performance of the animal subjects in two different devices (radial morris maze and the multiple t) and the data we acquired shown that the rats performance improvement was consistent with the increase of brain tissue levels of n3 pufas for groups 2 (pufa) and 3 (acc+pufa). the shortest average time needed for the rats to complete both mazes was recorded by group 3 (acc+pufa) and the longest for group 4 (control). group 2 (pufa) also had average times close to group 3 but the difference was not statistically significant. moderate improvement was recorded also in group 1 rats (acc). our experiment it demonstrates increased amounts of polyunsaturated fatty acids in the membranes of nerve cells which can justify the positive evolution of animals in assessing the performance of concomitant behavioral tests (5, 22). also included in our study were the blood lipid profile and oxidative stress evaluation. cholesterol and triglyceride blood levels were significantly decreased in groups 2 (pufa) and group 3 (acc+pufa) and oxidative stress markers (mda, gpx and tac) also registered significant lower levels for these groups. the zoometric parameters recorded, length and weight had average values higher for groups 1 (acc), 2 (pufa) and 3 (acc+pufa) compared to group 4 (control). conclusions peritoneal administration of salmon oil rich in pufas determined an increase in brain tissue deposits of dha and epa, fact demonstrated trough the mass spectroscopy combine with liquid chromatography. mass spectroscopy combined with liquid chromatography is a valuable and relevant mean to the assess brain lipid concentration, but it is time consuming and expensive. the brain n6 pufa concentration decreased in animals that received only acetylcysteine via peritoneum, which can indicate a hipolipemiant effect; also blood levels of cholesterol and triglycerides were lower. the increased measured levels of n3 pufas in brain tissue overlapped the increased performance measured in the previous behavioral experiment this research makes an important contribution to the study of polyunsaturated fatty acids and the importance of placing them in the daily diet. thus, by improving the diet with polyunsaturated fatty acids we can improve cognitive performance and helps prevent or ameliorate certain neurological diseases such as parkinson or alzheimer disease compared with normal diet, low in these acids. the need for widespread use of 402 g. iamandei et al involvement of n6 and n3 polyunsaturated faty acids polyunsaturated fatty acids is proven by many scientific experiments and the results obtained in experimental animals. this study brings new light on the importance of the existence of a balance between pufa intake and daily diet. references 1. anderson r.e., maude m.b., alvarez r.a., et al plasma lipid abnormalities in the poodle with progressive rod-cone degeneration. exp eye res. 1991;52:349–55. 2. anderson r.e., maude m.b., lewis r.a., et al. abnormal plasma levels of polyunsaturated fatty acid in autosomal dominant retinitis pigmentosa. exp eye res. 1987;44:155–9. 3. astarita g. and piomelli d. lipidomic analysis of endocannabinoid metabolism in biological samples. j. chr. b, epub ahead of print, january 2009. 4. astarita g., ahmed f. and piomelli d. identification of biosynthetic precursors of endocannabinoid anandamide in the rat brain. j. lipid res. 49,48, 2008. 5. baran d., mocanu v., badescu a., iosep i.s., date morfologice privind aterogeneza controlata prin dieta la rozatoare. rev med chir, 2003, 3: 21-25. 6. bazan n.g., scott b.l., reddy t.s., pelias m.z. decreased content of docosahexaenoate and arachidonate in plasma phospholipids in usher’s syndrome. biochem biophys res commun. 1986;141:600 4. 7. berson e.l., rosner b., sandberg m.a. et al further evaluation of docosahexaenoic acid in patients with retinitis pigmentosa receiving vitamin a treatment: subgroup analyses. arch ophthalmol. 2004; 122:1306 14. 8. berson e.l., rosner b., sandberg m.a., et al. clinical trial of docosahexaenoic acid in patients with retinitis pigmentosa receiving vitamin a treatment. arch ophthalmol. 2004;122:1297–305aguirre gd, 9. birch d.g., birch e.e., hoffman d.r., et al. retinal development in very-low-birth-weight infants fed diets differing in omega-3 fatty acids. invest ophthalmol vis sci. 1992;33:2365–76. 10. calvani m., benatti p. polyunsaturated fatty acids (pufa). 2003 sigma-tau s.p.a. scientific department. 11. carmen norris, bertram fong, alastair macgibbon and paul mcjarrow analysis of phospholipids in rat brain using liquid chromatography–mass spectrometry lipids, volume 44, number 11, 10471054, doi: 10.1007/s11745-009-3357-8 12. colev luca veronica, mocanu veronica: dezechilibre metabolice, ed bit, 1999, 111-159. 13. converse c.a., hammer h.m., packard c.j., et al. plasma lipid abnormalities in retinitis pigmentosa and related condition. trans ophthalmol soc uk. 1983;103:508–12. 14. faizv ahmed, giuseppe astarita, hua xiao and daniele piomelli application of hplc-chip/ms to the study of brain lipidomics agilent technologies, inc., university of california irvine, irvine, 92697 usa 15. dhopeshwarkar, g. a. (1983) nutrition and brain development (plenum, new york), pp. 59-69. 16. gong j., rosner b., rees d.g., et al. plasma docosahexaenoic acid levels in various genetic forms of retinitis pigmentosa. invest ophthalmol vis sci. 1992;33:2596 602. 17. haliga r., colev luca v., mocanu v. acizii graşi polinesaturaţi (pufa) n-3 şi factorii de risc cardiovascular: efecte asupra metabolismului lipidic. rev med chir soc med nat iasi, 2003; vol.107, nr.3, supl.2:80-83, issn 0048-7848 18. hoffman d.r., locke k.g., wheaton d.h., et al. a randomized, placebo-controlled clinical trial of docosahexaenoic acid supplementation for x-linked retinitis pigmentosa. am j ophthalmol. 2004;137:704–18. 19. hongjian zhang, jillonne h. hamilton, norman salem jr. and hee-yong kim n 3 fatty acid deficiency in the rat pineal gland: effects on phospholipid molecular species composition and endogenous levels of melatonin and lipoxygenase products july 1998 the journal of lipid research, 39, 1397-1403. 20. marion girod, yunzhou shi, ji-xin cheng and r. graham cooks desorption electrospray ionization imaging mass spectrometry of lipids in rat spinal cord journal of the american society for mass spectrometry volume 21, issue 7, july 2010, pages 1177-1189 21. mocanu v., colev luca v., păduraru i. et al: effects of diets enriched in n-3 fatty acids on oxidative status faseb, 2002, book of abstracts, 22. mocanu veronica, ana maria dăscăliţa, raluca haliga, et al. flaxseed supplementation in hyperlipidemic patients, rev med chir soc med nat iasi, 2005; vol. 109, nr.3:502-506, issn 0048-7848 23. piomelli d., rapaka r. and astarita g. a neuroscientists guide to lipidomics. nature reviews/neuroscience 8, 743, 2007. 24. rikans l.e., hornbrook k.r. lipid peroxidation, antioxidant protection and aging, biochem biophys acta, 1997, 1362: 116-127 25. stephen c. cunnane, chantale r. nadeau and sergei s. likhodii nmr and isotope ratio mass spectrometry studies of in vivo uptake and metabolism of polyunsaturates by the developing rat brain journal of molecular neuroscience volume 16, numbers 2-3, 173-180, doi: 10.1385/jmn:16:2-3:173 26. tirouvanziam r. (2006). "high-dose oral nacetylcysteine, a glutathione prodrug, modulates inflammation in cystic fibrosis". proceedings of the national academy of sciences 103: 4628–33. 27. watson a.d. thematic review series: systems biology approaches to metabolic and cardiovascular disorders. lipidomics: a global approach to lipid analysis in biological systems j. lipid res. 2006 47 (10): 2101–11. 5costachescub_partialvertebrectomy romanian neurosurgery (2014) xxi 2: 183 187 183 partial vertebrectomy with vertebral shortening for thoraco-lumbar fracture-dislocation. case report and technical note bogdan costachescu1,2, cezar e. popescu¹, bogdan iliescu¹, alexandru chiriac¹, ramona filipescu3, liviu pendefunda4 1department of neurosurgery, emergency university hospital “prof. dr. n. oblu”, iasi 2phd student university of medicine and pharmacy “grigore t. popa” iasi 3department of neurosurgery, emergency pediatric university hospital “sfanta maria”, iasi 4department of neurology, emergency university hospital “prof. dr. n. oblu”, iasi abstract thoraco-lumbar fracture-dislocations represent one of the most instable lesions and are frequently associated with neurological deficit. we present a patient with a t11 – t12 fracture-dislocation with complete neurological deficit – asia a, who underwent partial vertebrectomy, shortening of the spine and posterior instrumentation 21 days after a motor vehicle accident. key words: thoraco-lumbar fracturedislocation, spine fracture, partial vertebrectomy, spine shortening. introduction thoraco-lumbar fracture-dislocations represent one of the most instable lesions and are frequently associated with neurological deficit (1). this type of lesion is not very common representing only 16% of thoracolumbar fractures. (2), but are very often associated with other lesions which could delay the timing of spine surgery. the treatment of choice for this lesion, whether anterior, posterior, or combined approaches is still controversial. (3). in this paper we report a case of t11 – t12 fracture-dislocation with complete neurological deficit, and we discuss the surgical treatment, presenting some technical notes. history and examination a 16-years-old boy presented in our emergency department with complete paraplegia and chest pain few hours after a motor vehicle accident (passenger without seat belt). neurological exam showed complete neurological deficit (paraplegia, no voluntary anal contraction, no anal sensation s4, s5 sensory scores ) asia-a. spine exam showed thoraco-lumbar segmental kyphosis with swollen soft tissues. imaging – whole body ct scan depicts t11-t12 fracture-dislocation with fractures of the posterior arch of t11, and t12 (fig. 1, 2), bilateral hemothorax and right pulmonary contusion. 184 costachescu et al partial vertebrectomy with vertebral shortening figure 1 – axial image – t11-t12 dislocation with fractures of posterior arch t11 and t12 figure 2 – sagittal reconstruction – t11-t12 dislocation figure 3 axial image of thorax with bilateral hemothorax and left pulmonary contusion the patient was admitted in the department of pediatric surgery for his respiratory issues. he was subjected to spine surgery 21 days after the accident when the neurological status was unchanged – asia-a. surgical technique we performed partial vertebrectomy with spine shortening in the manner described by reyes –sanchez in 2002 for thoraco-lumbar fractures (4). under general anesthesia the patient was placed in prone position. through a midline incision the muscles are detached in subperiosteal fashion, exposing the laminae from t9 to l2. the dissection was carried out laterally to the tip of the transverse processes; the anterior dislocation was obvious. first there were removed the spinous processes and the laminae t11 and t12. there was a posterior dural tear of 4 mm thorough which instead of csf, there was a “leakage” of spinal cord lacerated tissue. under fluoroscopic romanian neurosurgery (2014) xxi 2: 183 187 185 guidance the screws are inserted bilaterally in the pedicles of t9, t10, l1 and l2. under magnification (loupes x 3) the facet joints t11-t12 were removed. using a highspeed drill the upper part of the t12 pedicles were resected giving access to the superior two thirds of the vertebral body which is emptied. using rongeurs and forceps t11 – t12 disc is taken out. the inferior plateau of t11 is prepared for arthrodesis. the reduction was achieved bending the two rods to restore the anatomy of the sine in sagittal plane and attached first to inferior screws; using the persuader the rods were attached at the end to the superior screws. the screws are tightened in compression in order to build up a firm contact between inferior aspect of t11 vertebral body and the remaining one third of t12 body. cancellous bone was impacted at this level for fusion. finally the dural tear is sutured with 6-0 prolene and packed with gelfoam. the duration of surgery was 190 minutes. postoperative outcome was uneventful. the neurological findings remain unchanged. plain x-rays depict partial reduction of the dislocation and the maintaining of almost normal curvatures of thoraco-lumbar region. figures 4 and 5 – intraoperative images; the suction (inferior left) is spotting the vertebrectomy. note the absence of buckled dura. figure 6 – plain x-rays ap (left), profile (middle) and comparison with preoperative image (right). 186 costachescu et al partial vertebrectomy with vertebral shortening discussion thoraco-lumbar fracture-dislocations are one of the most instable traumatic lesions disrupting all of three columns (5), frequently associated with neurological deficit. in patients with complete neurological deficit the goal of surgery is to reduce the dislocation and to provide a stable spine allowing early rehabilitation. a lesion as we described with dural tear and lacerated spinal cord tissue has less chances to improve even if we achieved partial reduction and performed decompression. the approach for this lesions with disruption of posterior ligament complex due to anterior dislocation associated with complete neurological deficit should be posterior (6). some authors advocate the anterior approach for these lesions but there are many complications worsened by the other posttraumatic lesions such as bilateral hemothorax and left pulmonary contusion in our case (7). partial vertebrectomy with vertebral shortening for thoraco-lumbar burst fracture was described by reyes-sanchez in 2002 (4) in order to treat by posterior approach the lesions which need anterior one. we also used this method for our case because there were 21 days after the accident and we presumed that the reduction without partial vertebrectomy will fail. the surgery for fracturedislocation must be done in less than three weeks in order to obtain an acceptable reduction. (8) in the same time we could consider performing the same shortening by using total vertebrectomy and fusion as described in 2011 by obeid (9). there were some reasons for not using these technique: our case presented only partial dislocation and not complete one as the cases presented in this paper, so we assumed that we can achieve appropriate reduction we could avoid dural buckling removing only two thirds of the vertebral body. in case of complete vertebrectomy we should cut the dural sac and close it separately our instrumentation was shorter 8 screws compared with minimum 12 screws used in total vertebrectomy decreasing the time of surgery, blood loss and the number of vertebral levels blocked. total vertebrectomy is a surgery with important complications rate (10). conclusions partial vertebrectomy with vertebral shortening is a reliable technique for thoracolumbar fracture-dislocation with complete neurological deficit allowing in one step good reduction and fusion for early rehabilitation it should be performed as soon as possible after the injury (before three weeks) for a good reduction of dislocation. references 1. vaccaro ar, kim dh, brodke ds et al. diagnosis and management of thoraco-lumbar spine fractures. instr. course lect. 2004;53: 359-373. 2. gertzbein sd. scoliosis research society. multicenter spine fractures study. spine 1992;17:528-540. 3. smith js, shaffrey ci. thoraco-lumbar injury classification for fracture – dislocations in spine and spinal cord trauma – evidence-based medicine, thieme medical publishers, inc, new york, edited by a. vaccaro, m. f. dvorak, 2010. romanian neurosurgery (2014) xxi 2: 183 187 187 4. reyes-sanchez a, rosales lm, miramontes vp, garin de. treatment of thoraco-lumbar burst fractures. eur. spine j. (2002) 11: 8 – 12. 5. phadnis as, tan cj, raman as, et al. fracture and complete dislocation of the spine with normal motor neurology. injury extra. 2006; 37; 479-483. 6. vaccaroar, lehman ra, hurlbert j, anderson pa, harris m.a new classification of thoracolumbar injuries. the importance of injury morphology, the integrity of the posterior ligamentous complex, and neurologic status. spine volume 30, no. 20, pp 2325–2333, 2005. 7. lubeski d, abdullah kg, steinmetz mp, masters f, benzel ec, mroz te, et al. lateral extracavitary, costotransversectomy, and transthoracic approaches to the thoracic spine: review of techniques and complications. j. spinal disorders tech , vol. 26, no. 4, june 2013. 8. feng wang, ye zhu. treatment of complete fracturedislocation of thoraco-lumbar spine. j. spinal disorders tech. 2013; 26:421-426. 9. obeid i, guérin p, gille o, gangnet n, aurouer n, pointillart v, vital jm. total vertebrectomy and spine shortening in the management of acute thoracic spine fracture dislocation: technical note and report of 3 cases. j spinal disord tech. 2011 jul;24(5):340-5. 10. treatment of subacute thoracic spine fracturedislocation by total vertebrectomy and spine shortening: technical note. barcelos ac, botelho rv. j neurosurg spine. 2013 feb;18(2):194-200. microsoft word 15bis.scutariumonica_paroxysmal_f.docx romanian neurosurgery (2011) xviii 4: 511 516 511 paroxysmal autonomic instability with dystonia after severe traumatic brain injury – a case report monica scutariu¹, c. kakucs², a. oslobanu²,³, şt.i. florian²,³ ¹cluj county emergency hospital, neurosurgical intensive care unit ²cluj county emergency hospital, department of neurosurgery ³“iuliu hatieganu” university of medicine and pharmacy cluj-napoca abstract paroxysmal autonomic instability with dystonia (paid) is a clinical syndrome characterized by episodes of systemic hypertension, tachycardia, tachypnea, hyperthermia, diaphoresis, intermitent agitation and certain forms of dystonia (decerebrate or decorticate posturing, rigidity and spasticity). it is a relatively uncommon complication of distinct cerebral conditions: traumatic brain injury, hydrocephalus, spontaneous subarachnoid or intracerebral hemorrhage, non traumatic brain anoxia. lack of recognising and undertreatment of this syndrome can increase the risk of secondary injury to the brain. the incidence of complete syndrome of paid is low; we present a case of posttraumatic paid displaying the full clinical picture, aggravated by the occurence of sepsis. keywords: paroxysmal autonomic instability, severe traumatic brain injury, sepsis. introduction paroxysmal autonomic instability with dystonia (paid) – formerly known as autonomic dysfunction syndrome (ads) is a clinical syndrome that occurs as an uncommon complication of distinct cerebral conditions: traumatic brain injury, hydrocephalus, spontaneous subarachnoid or intracerebral hemorrhage, non traumatic brain anoxia and suprasellar cysts (13). it consists in episodes of tachycardia, systemic hypertension, tachypnea, hyperthermia, diaphoresis, intermitent agitation and certain types of dystonia (decerebrate or decorticate posturing, rigidity and spasticity). early diagnosis and the appropriate treatment of this complication during the clinical course of patients with severe traumatic brain injury (stbi) can improve their neurological outcome (7); unfortunately, the absence of standardized diagnostic criteria and a confusing nomenclature of this clinical entity still make the systematic clinical research difficult. case report a 16 years old young woman sustained a severe isolated traumatic brain injury after a road accident (pedestrian hit by a car). at the scene her initial glasgow coma scale (gcs) score was 3 and the left pupil was fixed and dilated. an initial computed tomography scan showed: diffuse cerebral edema with no midline shift spots of subarachnoid hemorrhage spread over the supratentorial area multiple microhemorrhages 512 monica scutariu et al paroxysmal autonomic instability in severe traumatic brain injury disseminated within corpus callosum, thalamus, midbrain, corona radiata and a small amount of blood inside the occipital horns of lateral ventricles (figure 1) suggestive for difuse axonal injury (dai). figure 1 initial ct millimetric lessions in the antero-lateral mezencefalic region, right temporal lobe and in the left occipital horn at the arrival to our department she was intubated and sedated with fentanyl and midazolam; the continous sedation was briefly stopped in order to perform an accurate neurological examination: there was no eye opening to verbal or painful stimuli, the left pupil was fixed and dilated and the right pupil intermediate and reactive to light. she was decerebrating on both sides to painful stimuli and spontaneously. the patient was admitted to the neurosurgical intensive care unit for conservative treatment; we decided to induce a barbiturate coma (thiopental 4 mg /kg/h) together with administration of mannitol, furosemide and normocapnic mechanical ventilation. after 24 hours, the neurological condition was slightly improved: decerebrate posturing on the left side and decorticate posturing on the rigt side to pain, unchanged pupillary reaction. a second ct scan performed on the same day revealed a smaller size of the subarachnoid hemorrhage spots, no midline shift and stable intraparenchymal microhemorrhages. the intravenous thiopental was then stopped and a continuous sedation with fentanyl 50 micrograms/ h and midazolam 3 mg/ h was started in order to facilitate ventilatory support, concurrent with anticonvulsant medication (carbamazepine 400mg/ 24 h, enterally). the subsequent clinical evolution was uneventfull; on the fourth posttraumatic day we decided to stop the sedation. after 12 hours the patient developed episodes of synus tachycardia 130-140/min, hypertension sap 160-170 mmhg, fever 38,5 39 °c, profuse sweating associated with flexor rigidity of upper limbs and extensor rigidity of the legs. the episodes were occuring spontaneously, lasting 45 romanian neurosurgery (2011) xviii 4: 511 516 513 minutes on average and were triggered by tracheal suction, current nursing procedures, physical therapy. they abated after repetead boluses of propofol, diazepam and fentanyl. between paroxystic episodes all the vital parameters were comming back to the normal ranges. initially the spells were tought as being vegetative seizures and the daily dose of carbamazepine was increased to 600mg/ day and fenobarbital was also added to the therapeutic scheme (400 mg/24 h) with no result. serial bacteriological work-up was negative until the seventh day and a magnetic resonance imaging (mri) of the brain confirmed the diagnosic of grade iii dai (figure 2). after hading reviewed all the clinical laboratory findings coroborated with the imaging studies we reevaluated the etiology of paroxystic episodes and we regarded them as manifestatons of posttraumatic paroxysmal autonomic instability with dystonia. figure 2 mri sections ( day 7th ) focal lessions within the corpus callosum and the antero-lateral mezencefalic region 514 monica scutariu et al paroxysmal autonomic instability in severe traumatic brain injury the differential diagnosis was made for: malign neuroleptic syndrome (the absence of specific medication) serotonine syndrome (no serotonine agonists or mao inhibitors were previously given and addiction to recreational drugs was not confirmed) delirium tremens (no alcohol addiction) autonomic dysreflexia (lack of cervicothoracic spinal cord injury) sepsis (excluded at the moment of first spells) diencephalic epilepsy (lack of response to anticonvulsant therapy) malignant hyperthermia (no exposure to trigger anesthetics) thyroid storm (no previous thyroid disease, absence of anterior cervical trauma). consequently we added metoprolol – starting with 25mg daily and increasing the dose up to 100 mg/ 24 h with a modest cardiohemodynamic response. adding clonidine (0,45 mg/24 h) led to a notable improvement of blood pressure control. the evolution was aggravated by the occurence of both pulmonary (ventilator associated pneumonia vap on the 7th day) and urinary (day 10th) infectious complications, with positive blood cultures for staphylococcus aureus mrsa. the daily febrile spikes (39,7 -40,5°c) worsened the clinical manifestations of paid: increased spasticity and joint stifness, rabdomyolysis (creatine kinase levels up to 1600 iu/l; normal range: 96 – 140 units/l), tachypnea 45-50 breaths/ min – compelling us to induce deep sedation and paralysis during severe episodes. enteral baclofen (100 mg/24 h) and clonazepam 3 mg / 24 h were added – with slight improvement of dystonia. the evolution of sepsis was favourable under antibiotic therapy; the normal renal function was preserved and no need for vassopressors was noted. on the 20 th daya tracheostomy was performed and the full ventilator weanning was possible on day 35, by t tube. on the 36th posttraumatic day the patient was able to open the eyes spontaneously, to follow simple commands on the right side (ie. grasp the hand); she was exhibiting increased flexor tone in her upper extremity and increased extensor tone in her lower extremity. concomitant with the resolution of the infectious complications the frequence of dystonic episodes diminished; the area of diaphoresis was gradually confined to the chest and cephalic zone, muscle dystonia became asymetrical and maximal values of blood presure and pulse during “crises” decreased. thirthy days later (day 70) the patient was awake, with white blood cells and procalcitonine levels within normal ranges, fed by mouth and decanulated. she was space orientated, with short term memory severely affected, lacunar amnesia, able to speak, with slow ideation; there were also major joint deformity and stifness (ankle, wrist) (figure 3). the paid episodes continued according to a stable pattern (2-3 per day), of reduced intensity, mainly trigerred by emotional stimuli. the young patient was discharged to a rehabilitation facility with a glasgow outcome score of 3p (conscious but requiring others for daily support due to severe disability) under current therapy with metoprolol, clonidine, baclofen, carbamazepine and clonazepam. romanian neurosurgery (2011) xviii 4: 511 516 515 figure 3 major joint deformities (day 70th) discussion paroxysmal autonomic instability with dystonia (paid) is a clinical syndrome characterized by episodes of systemic hypertension, tachycardia ≥ 130/min, tachypnea ≥ 30/min, hyperthermia ≥ 38,5 °c, diaphoresis, intermitent agitation and certain forms of dystonia (decerebrate or decorticate posturing, rigidity and spasticity) that occur at least once per day for at least three days consecutively in a patient with severe traumatic brain injury. (gcs ≤ 8) (9). despite their well defined clinical manifestations, paid episodes are still underdiagnosed. this is the result of a nonunitar nomenclature and a persisting confusion between terms like: autonomic dysfunction, central fever, vegetative storm, acute mesencephalic syndrome, hyperpyrexia with muscle contracture (9). some authors still consider that it is not clear if it is a distinct disorder from diencephalic seizures (13); although the mecanism of paid remains unclear, it is unlikely to have true epileptic basis as seizures have never been confirmed by eeg (10). the pathogeny of paid is partially explained by the “disconnection” theory; according to an excitator/ inhibitor model, following the disconection between cortical and subcortical centers from mesencephalodiencephalic structures, the mesencephalic lesions play a central role in generating paroxysms (5). paid has an estimated incidence of 815% (3) in tbi, more frequent in young people (12) with dai (12). the syndrome has a three stage evolution(8): i – immediately posttraumatic (nonspecific) ii – starts after cessation of current sedation in the intensive care unit and the symptoms occur at maximum intensity, triggered by external stimuli or spontaneously iii – characterized by attenuation of the typical paroxysms it usually overlaps the neurological improvement; the joint stifness with severe motion limitation is 516 monica scutariu et al paroxysmal autonomic instability in severe traumatic brain injury frequent and isolated paid episodes are still possible up to 14 months after initial trauma. (7). paid is a diagnostic of exclusion, based essentially on clinical findings (1,6). the differential diagnosis work-up is made for: malignant hyperthermia, neuroleptic malignant syndrome, serotonine syndrome, thyroid storm (11), sepsis, delirium tremens, autonomic disreflexy, diencephalic epilepsy. the treatment is directed to: blood pressure and heart rate control – by central α agonists (clonidine, dexmedetomidine) and beta blockers (metoprolol, labetalol) fever decrease (antipyretics, external cooling methods) sedation (benzodiazepines: midazolam, clonazepam) reducing contracture and spasticity to prevent permanent joint deformities and rabdomyolysis (baclofen oral or intratechal, dantrolen, orthopedic devices) analgesia (morphine, fentanyl). the use of anticonvulsant is controversial; baguley and all. demonstrated the efficiency of gabapentine in controling paid paroxysms, possibly due to a modulation of spinal transmision of trigger stimuli. (5).bromcriptine (a central dopaminergic agonist) was succesfully used in several case series (2). the case we presented is particular by the presence of all clinical, epidemiological (11) and evolutive features of paid. despite the relative frequent occurence of signs of paid in patients afflicted with severe tbi, the incidence of full syndrome is much lower and the number cases communicated in the literature is scarce. (9). moreover, it suggests that sepsis – a current element of differential diagnosis – can be an aggravating factor for paid evolution. references 1.baguley i.j., nicholls j.l., felmingham k.l., dysautonomia after traumatic brain injury: a forgotten syndrome?. j neurol neurosurg psychiatry. jul 1999;67(1):39-43. 2. baguley i.j. et al, pharmacological management of dysautonomia following traumatic brain injury. brain injury 2004;18(5):409-17 3. baguley i.j. et al, the incidence of dysautonomia and its relationship with autonomic arousal following traumatic brain injury. brain inj 2007;21(11):1175-81. 4. baguley i.j., the excitatory:inhibitory ratio model (eir model): an integrative explanation of acute autonomic overactivity syndromes. med hypotheses 2007. 5. baguley i.j. et al, gabapentin in the management of dysautonomia following severe traumatic brain injury: a case series. j neurol neurosurg psychiatry. 2007 may; 78(5): 539–541 6. baguley i.j., autonomic complications following central nervous system injury. semin neurol 2008;28:716-25. 7. baguley i.j. et al, ie.-diagnosing dysautonomia after acute traumatic brain injury: evidence for overresponsiveness to afferent stimuli. arch phys med rehabil 2009;90:580-6. 8. baguley i.j., perkes i.e., current understanding of dysautonomia after severe acquired brain injury. accesed at http://www.acnr.co.uk/mar_apr_2008/acnrma08_cur rent.pdf, at 20 sept. 2011 9. blackman j.a., patrick p.d., buck m.l., rust r.s., paroxysmal autonomic instability with dystonia after brain injury. arch neurol.2005;61:321-328. 10.buczek m., suarez j.i., chelimsky t.c., treatment of autonomic disorders requiring intensive care management – in critical care neurology and neurosurgery, 2004 edited by jose i suarez, md, humana press inc, totowa, nj. 11. delikoukos s., mantzos f., thyroid storm induced by blunt thyroid gland trauma.the american surgeon 2007,73:11; 1247-1249. 12. 10. hendricks h.t., heerenb a.h., vos p.e., dysautonomia after severe traumatic brain injury. european journal of neurology 2010, 17: 1172–1177 11. li-quan lv et al., risk factors related to dysautonomia after severe traumatic brain injury. j trauma 2011 sep;71(3):538-42. 13. srinivasan s., tchoyoson lim c.c., thirugnanam u., paroxysmal autonomic instability with dystonia. clin auton res (2007) 17: 378-381 microsoft word 15roditisspyridon_spontaneous_f 344 spyridon roditis spontaneous hematoma of the septum pellucidum spontaneous hematoma of the septum pellucidum and corpus callosum: a case report spyridon roditis phd student in neurosurgery, “gr.t. popa” university of medicine and pharmacy, iasi laiko hospital of athens, greece abstract the hemorrhagic lesion in the septum pellucidum and corpus callosum is not common and it can be found in patients with brain trauma (diffuse axonal injury), aneurysms of the pericallosal artery, after ruptured arteriovenous malformations or intracranial tumors. a 59-year-old man, a chronic alcoholic, developed a little hematoma in the septum pellucidum and corpus callosum with subarachnoid haemorrhage on the tentorium and all explorations showed no cause of these. evolution was favorable with conservative treatment. keywords: corpus callosum, septum pellucidum, splenial hematoma, spontaneous hematoma introduction hematoma of the septum pellucidum and corpus callosum have been found in patients with various conditions including brain trauma, aneurysms of the pericallosal artery or after ruptured of arteriovenous malformations, hemorrhage occurring in intracranial tumors or in virus-associated encephalitis with hemorrhagic fever etc. severe head injuries are often associated with rotational forces resulting diffuse axonal injuries. shear injuries commonly occur at gray-white matter junctions, but they are also found in the corpus callosum, centrum semiovale, in the basal ganglionic regions, brain stem and cerebellum. the thalamic and basal ganglia injuries are hemorrhagic in 50% of cases and the shear injuries of the corpus callosum are more often nonhemorrhagic. the hemorrhagic lesion in the corpus callosum is a rare feature in subarachnoid haemorrhage, which may result from aneurysms of the anterior communicating artery or pericallosal artery or after ruptured arteriovenous malformation or arteriovenous fistula. intracranial tumors like pituitary adenoma, glioblastoma multiforme and metastatic tumors are a well recognized but uncommon cause of intracranial hemorrhage. hemorrhage occurring in glioblastoma multiforme are frequently deep into the hemisphere, basal ganglia or corpus callosum. primary cerebral neuroblastoma of the corpus callosum is a cause of hematoma in the corpus callosum and of intraventricular hemorrhage. spontaneous hematoma of the septum pellucidum and corpus callosum is rare and the cause can be a micro arterio-venous malformation in the corpus callosum. romanian neurosurgery (2011) xviii 3: 344 – 348 345 case report a 59-year-old man, a chronic alcoholic, had been admitted to our neurosurgical hospital with episodic generalized tonic-clonic convulsions for the last three days, with intense headache and vomiting, and in a disoriented state in time. patient had normal blood pressure, without history of arterial hypertension and no recent history of head injury. age, the sex and chronic alcoholism are the only detected risk factors. cranial computer tomography demonstrated a hematoma in the septum pellucidum and corpus callosum with subarachnoid haemorrhage on the tentorium. magnetic resonance angiography and cerebral angiography (seldinger technique) did not show any vascular cause of this hematoma into the septum pellucidum and corpus callosum, like aneurysms or ruptured arteriovenous malformation. (figures 1, 2, 3 and 4). the pacient was treated conservatively: after initial antiedematous treatment, antiepileptic therapy and haemostatic therapy, the pacient became conscious and further the patient's condition has improved gradually. figure 1 computer tomography image shows a hematoma in the septum pellucidum and corpus callosum figure 2 computer tomography image shows a subarachnoid haemorrhage on the tentorium. (right side) 346 spyridon roditis spontaneous hematoma of the septum pellucidum figure 3 brain mri without contrast shows the hematoma in the septum pellucidum and corpus callosum figure 4 brain mri with contrast shows the hematoma in the septum pellucidum and corpus callosum and angio mri did not show aneurysms or arteriovenous malformation discussion intracerebral hemorrhage occurs within the brain tissue itself and can occur spontaneously in hemorrhagic stroke or it can be caused by brain trauma. other causes can be ruptured aneurysms or after ruptured of arteriovenous malformations, hemorrhage occurring in intracranial tumors or in virus-associated encephalitis with hemorrhagic fever. intracerebral hemorrhage and can be lobar intracerebral hemorrhage or it may occur in other brain structures, such as the thalamus, basal ganglia, pons, or cerebellum (deep intracerebral hemorrhage). amyloid angiopathy is other cause of intracerebral hemorrhage in old patients and a very small proportion is due to cerebral venous sinus thrombosis. major risk factors for intracerebral hemorrhage include: high blood pressure, diabetes, alcoholic drinks and current cigarette smoking. other factors that raise the risk of intracerebral hemorrhage include: blood and bleeding disorders (decreased levels of blood platelets, hemophilia etc.), liver disease (associated with increased bleeding risk in general) or romanian neurosurgery (2011) xviii 3: 344 – 348 347 use of aspirin or anticoagulant medications. similarly, hematoma of the septum pellucidum and corpus callosum can be caused by abnormalities of the blood vessels (aneurysm or vascular malformation), high blood pressure (hypertensive intracerebral hemorrhage), protein deposits along blood vessels (amyloid angiopathy) or traumatic brain injuries. other causes are hemorrhage occurring in intracranial tumors or in virusassociated encephalitis with hemorrhagic fever. hemorrhage occurring in glioblastoma multiforme are frequently deep into the hemisphere, basal ganglia or corpus callosum also primary cerebral neuroblastoma of the corpus callosum is a cause of hematoma in the corpus callosum and of intraventricular hemorrhage. in some cases, no cause can be found. in literature there are few reported cases of hematoma of the septum pellucidum and corpus callosum. butt et al,1985, reported hemorrhage into the septum pellucidum coexisting with intraventricular hemorrhage in preterm infants and kanpolat and mertol, 1987, reported hematoma of the septum pellucidum in adults secondary to trauma and hypertension. authors showed that mass effect of the haematoma of septum pellucidum may block the foramen of monro, leading to hydrocephalus and increased intracranial pressure. but schulder, hirano and elkin, 1987, ask if the „caval-septal”hematoma exist. ogura et al., 1982 reported two cases of traumatic hematoma in the corpus callosum caused by blunt mechanical head trauma which were accompanied neither by skull fracture nor by scalp injury. the hematomas occupied from the genu to the body of the corpus callosum and they were verified by surgery. shigemori et al., 1986, reported five cases with massive haematoma of the corpus callosum caused by blunt head trauma, the patients presented also concomitant intraventricular and subarachnoid haemorrhages or small haemorrhagic foci in the basal ganglia or thalamus. the authors noted that the sites of the impacts were the frontal and occipital areas which were close to the midline and above the level of the corpus callosum. jackson et al., 1993, analyzed 348 patients with aneurysmal subarachnoid haemorrhage resulted from aneurysms of the anterior communicating artery or pericallosal artery and they found haematomas in the corpus callosum in 8 cases (9 %). authors considered that these haematomas appeared to result from passage of blood up through the cistern of the lamina terminalis into the septum pellucidum and thence into the ventral aspect of the anterior corpus callosum. sorimachi et al. 2010 presented three patients with hemorrhage in the splenium of the corpus callosum at two weeks after the onset of subarachnoid hemorrhage associated with acute hydrocephalus. authors consider that splenial hematoma is a potential cause of neurological deterioration after surgery for subarachnoid hemorrhage, in addition to vasospasm, hydrocephalus, and rebleeding. in 2006 erbaş et al. reported a case of hematoma of the corpus callosum secondary to isolated inferior sagittal sinus thrombosis. authors showed that isolated inferior sagittal sinus thrombosis is an extremely rare condition and it should be considered in the differential diagnosis of non-traumatic corpus callosum hematoma. the presented patient had a limited bleeding of the septum pellucidum and corpus callosum with a small subarachnoid 348 spyridon roditis spontaneous hematoma of the septum pellucidum haemorrhage on the tentorium. ct and mri images show a relatively small volume of the hematoma which is oval-spherical in shape, developed in the splenius of the corpus callosum and extended lower in the septum pellucidum (in the cavum of the septum pellucidum). the simultaneous existence of this hematoma of the septum pellucidum and corpus callosum and of this subarachnoid hemorrhage suggests a common cause for these two hemorrhagic lesions, but history did not reveale head injury and angiographies showed no aneurysms or arteriovenous malformations. also patient had normal blood pressure, without history of arterial hypertension and the only detected risk factors for a hemorrhagic stroke are age, the sex and chronic alcoholism. the evolution was favorable under conservative treatment. conclusion this is one of the few cases of a spontaneous hematoma of the septum pellucidum and corpus callosum and the performed exploration did not reveal a cause of these hemorrhagic lesions. correspondence: dr. spyridon roditis laiko hospital of athens ag.thoma 17, τ.κ. 11527, athens, greece sproditis@yahoo.com references 1. barth p g space-occupying lesions associated with cavum septi pellucidi. http://www.medlink.com/medlinkcontent.asp 2. erbaş g, oner ay, akpek s, tokgoz n. corpus callosum hematoma secondary to isolated inferior sagittal sinus thrombosis. acta radiol. 2006 dec; 47 (10): 1085-8. 3. jackson a, fitzgerald jb, hartley rw, leonard a, yates j. ct appearances of haematomas in the corpus callosum in patients with subarachnoid haemorrhage. neuroradiology. 1993; 35(6):420-3. 4. kanpolat y, mertol t. haematoma of cavum septi pellucidi due to hypertension. acta neurochir (wien). 1987; 89(3-4):135-6. 5. kasahara t, toyokura m, shimoda n, ishida a cerebral hemorrhage restricted to the corpus callosum am j physical medicine & rehabilitation 2005, vol. 84, no5, pp. 386-390 6. komatsu s, sato t, kagawa s, mori t, namiki t. traumatic lesions of the corpus callosum. neurosurgery. 1979 jul; 5(1 pt 1):32-5. 7. lau ls, bannan e, tress b. pseudotumour of the corpus callosum due to subarachnoid haemorrhage from pericallosal aneurysm. neuroradiology. 1984; 26(1):67-9. 8. mochizuki k, ochi h, ogura y, iino m, kuroki h, matoba r. a case of diffuse axonal injury in violent death. leg med (tokyo). 2009 suppl 1:s518-9. 9. ogura k, yamamoto i, hara m, suzuki y, nakane t, watanabe m. computerized tomography of the traumatic hematoma in the corpus callosum. report of 2 cases. no shinkei geka. 1982 dec; 10(12):1299-301. 10. pinto ja, melo jr, pereira jr, veiga-pires ja. haematomas of the septum pellucidum. aetiology and incidence. rofo. 1988 may; 148(5):591-3. 11. schulder m, hirano a, elkin c. "caval-septal" hematoma: does it exist? neurosurgery. 1987 aug; 21(2):239-41. 12. shigemori m, kojyo n, yuge t, tokutomi t, nakashima h, kuramoto s. massive traumatic haematoma of the corpus callosum. acta neurochir (wien). 1986; 81(1-2):36-9. 13. sorimachi t, yajima n, sasaki o, koike t, fujii y. hematoma in the splenium of the corpus callosum in the subacute stage of subarachnoid hemorrhage--three case reports. neurol med chir (tokyo). 2010; 50(3):209-12. 14. takatoshi s, naoki y, osamu s, tetsuo k, yukihiko f hematoma in the splenium of the corpus callosum in the subacute stage of subarachnoid hemorrhage. neurol med chir (tokyo) 50(3):209-12 (2010) 15. yajima y, hayakawa h, mimasaka s, nata m, hashiyada m, funayama m. intracerebral haematoma: traumatic or non-traumatic. j clin forensic med. 2001 sep; 8(3):163-5. doi: 10.33962/roneuro-2022-028 cervicomedullary junction intramedullary hemangioblastoma. a 10 years report of cases and review of literature g. popescu, francesca paslaru, anamaria gheorghiu, a.c. paslaru, m. apostol, m.c. zaharia, m. popescu, r.m. gorgan romanian neurosurgery (2022) xxxvi (2): pp. 155-160 doi: 10.33962/roneuro-2022-028 www.journals.lapub.co.uk/index.php/roneurosurgery cervicomedullary junction intramedullary hemangioblastoma. a 10 years report of cases and review of literature g. popescu1, francesca paslaru1, anamaria gheorghiu1, a.c. paslaru2,3, m. apostol1, m.c. zaharia1, m. popescu4, r.m. gorgan1,2 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 department of genetics, “dr victor gomoiu” children’s clinical hospital, bucharest, romania 4 department of neurosurgery, pitesti emergency hospital, university of pitesti, romania abstract hemangioblastoma is a rare, benign, highly vascularized tumour, that usually presents a muriform nodule. the most frequent localization is the posterior cranial fossa. the frequency of this spinal lesion is very low, representing less than 5% of spinal cord tumours. the presentation of hemangioblastoma can widely vary, from a solid tumour to a lesion with a cystic component. we present the case of a 43 years old patient, admitted to our clinic for left hemiparesis, swallowing disorders, and dysphonia. an mri is performed and it showed a cervicomedullary junction tumour with a solid nodule and an anterior cystic cavity pushing towards the 4th ventricle. the patient underwent surgery for the total removal of the tumour. post-operative ct confirmed the total ablation of the tumour. the patient is discharged with improved symptomatology. in the last 10 years, in our clinic were admitted 23 cases of hemangioblastoma, 14 males (61% of the patients) and 9 females (39%) with an age at presentation varied from 14 to 78 years (mean 48,2 years). only 3 patients (13%) out of the 23 had associated von hippel–lindau syndrome, with hemangioblastomas also present in other locations. the most common location was the posterior fossa, in 13 cases (56,6%). headache (69,5%), ataxia (56%) and balance disorders (52%) were the most common symptoms accused by patients. the followup varied from 6 to 84 months (mean 20 months). only one patient died during hospitalization and one tumour recurrence was noted. most patients improved or remained clinically stable postoperatively. background hemangioblastoma is a rare, histologically benign, highly vascularized tumor, that usually presents an enhancing muriform nodule, having the most frequent localization in the posterior cranial fossa [1]. keywords cervicomedullary, intramedullary, hemangioblastoma corresponding author: g. popescu 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 156 g. popescu, francesca paslaru, anamaria gheorghiu et al. moreover, hemangioblastoma is the most common primary intra-axial posterior fossa tumor in adult population. it is usually identified in the cerebellar hemisphere (including vermis) and brainstem [2], [3], [4]. on the other hand, supratentorial localization is rare, in the literature being described less than 100 cases. furthermore, only 3-13% are reported in the spinal cord [5]. the presentation of hemangioblastoma can widely vary, from a solid tumor to a lesion with a cystic component. usually, sporadic hemangioblastoma is a solid tumor with a pseudocapsule. despite the lack of a proper capsule, the lesion is well circumscribed. the solid nodule is red and very well vascularised, localized close to the pial layer. the cystic cavity usually occurs due to the thinness of the vessel wall that allows water to leak [5], [6]. the walls of the cyst are tapped with nonneoplastic compressed cerebellum cells and the cyst fluid is usually yellow with a high concentration of proteins [6], [7]. both ct (computed tomography) scan and mri (magnetic resonance imaging) can be useful for emphasizing the lesion. on ct scan, the mural nodule is isodense with fluid density surrounding the cyst [8], [20]. on contrast scan, cyst walls usually not enhance and the presence of calcification is rare. the mri scan is superior to the ct scan and it shows vascular signal voids, especially in the periphery of the lesion, as well as, the hemosiderin deposits that can occur due to recurrent hemorrhages [6], [8], [9]. the most common symptoms determined by these tumors are: headaches, hydrocephalus, cerebellar dysfunction and altered mental state. surgical approach is the gold standard for sporadic cases of hemangioblastoma, but not for multiple lesions associated with von hippel lindau syndrome. the outcome of the surgery is good, given that hemangioblastomas are benign lesions [10]. despite that tumoral cells may be spreaded through csf, it still remains a benign tumor. solid lesions are more difficult to excise compared to cystic ones [11]. hemangioblastomas are usually sporadic lesions but around 20% of them are associated with von hippel lindau syndrome [5]. moreover, 6% of cerebellar hemangioblastomas are associated with retinal hemangioblastoma. the retinal hemangioblastoma is usually placed peripherally. it tends to rupture and cause hemorrhage that can lead to retinal detachment. von hipple lindau syndrome is a multysistem neoplastic condition with autosomal inheritance, described by the occurrence of multiple hemangioblastomas in different localisation such as brain, spinal cord and retina [12]. in these cases, individual resection of the central nervous lesions is not the optimal treatment until it became symptomatic, due to the tendency of reccurence and the inconsistent growth pattern of tumor [13], [14]. case presentation we present the case of a 43 years old patient, admitted to our clinic for left hemiparesis, swallowing disorders, and dysphonia. the first symptoms occurred 8 months ago with left intercostal neuralgia. an mri is performed and it shows a cervicomedullary junction tumor with a solid nodule and an anterior cystic cavity pushing towards the 4th ventricle, which lead to our presumptive diagnosis of hemangioblastoma. in order to rule out von hipple lindau syndrome, a whole-body ct scan was performed. no other lesions were identified. the decision was made to perform surgery in order to remove the tumor. the patient was placed in the prone position, and a midline incision was made, with a standard occipital craniectomy and resection of the c-1 posterior arch. after the dura mater was opened, the tumor was identified on the midline, at cervicomedullary junction. under the operating microscope, the hemangioblastoma was dissected, the integrity of the lesion was preserved. the tumor was gently retracted laterally, and the feeding vessels were identified coagulated with bipolar forceps and divided sharply. the main feeder is exposed, clipped, coagulated, and cut. the tumor was sent for pathologic examination and the diagnosis of hemangioblastoma was confirmed. closure of the surgical wound was performed respecting the anatomical planes and leaving an epidural external drain in place. finally, the skin suture was draped in a sterile fashion. after careful hemostasis, the surgical wound is closed layer by layer. no perioperative incidents were reported. the postoperative mri confirmed the total resection of the tumor. 157 cervicomedullary junction intramedullary hemangioblastoma figure 1. cervicomedullary junction tumor with a solid nodule and an anterior cystic cavity pushing towards the 4th ventricle. figure 2. the cervicomedullary junction lesion, after dura mater figure 3. gently dissection of the lesion. the feeders are was opened. coagulated and sharply cut. figure 4. after circumferential dissection, the main feeder is figure 5. the main feeder is clipped and cut. the tumor exposed. is removed “en bloque”. the external drain was removed 24 hours later. symptomatology was improved in the first week postoperative by the patient. mobilization of the patient was allowed 24 hours after the surgery. the skin sutures were suppressed at seven days postop. this is just one out of 23 cases we had in our clinic in the last 10 years. 14 men (representing more than 60% of the study group) and 9 women. their median age was 48, ranging from 14 to 78 years. the average time of hospitalization was 15 days, between 7 to 20 days. 158 g. popescu, francesca paslaru, anamaria gheorghiu et al. headache and ataxia were the most common symptoms accused by patients, accused by more than 70% of the patients. other symptoms were dysphonia, dysphagia, seizures, cecity and hearing loss. table 1. table of the main symptoms accused by patients mri was performed in all cases. it is worth mentioning that in 17 cases hemangioblastoma presented a cystic component. also, in 3 cases were identified multiple lesions. there were 16 cases of intracranial hemangioblastoma, 2 with supratentorial location (frontal and parietal lobe), and in 14 cases, the tumor was located in the posterior fossa, in the cerebellum. just 4 craniospinal junction cases were identified. at the spine level, there were 3 tumors, 2 located in the thoracic spine and 1 in the cervical spine. all of the patients underwent surgery. in 22 out of 23, complete ablation of the tumor was performed. in just one case, total excision was not possible, and a subtotal ablation was performed. the postoperative evolution was good, without complications in 20 cases. 3 patients developed hydrocephalus and in one case a recurrence occurred, a few months after the surgical intervention. postoperative follow-up was between 6 months to 7 years, with a mean follow-up of 20 months. neurological improvement was noted in 18 cases, whereas in 2 cases, the neurological state remained stationary and in 3 cases, the neurological status had worsened. one patient died. as we mentioned before, hemangioblastoma can be associated with von hipple lindau syndrome, a rare genetic disorder with multisystem involvement. it is characterized by visceral cysts and benign tumors with the potential for malignant transformation. 3 patients had associated this syndrome with pancreatic and kidney cysts. discussions one of the greatest complications of hemangioblastomas is the risk of hemorrhage. however, the risk of hemorrhage is lower for the lesions of the spinal cord, where catastrophic neurological impairment is the main risk [6], [15], [16]. in 2007, dr. cornelius et al [17] compared the outcome of perioperative embolization of hemangioblastomas for spinal and cerebellar lesions. the result of embolization was favorable in patients with spinal cord hemangioblastomas, but, for the hemangioblastomas located at the cerebellar level, there were reported acute tumoral bleeding that led to death of the patients. the outcomes following embolization are very different for these two locations possibly because of the different capillary sizes. due to high mortality, the procedure is no longer used. in some cases, due to the clinical state of the patient or the localization of the tumor, surgical intervention cannot be achieved. in 2020, mak et al[18] published the case of an immunocompetent patient that presented with a one-year history of progressive nausea and vomiting. after an mri scan, a homogeneous enhancing intra-axial mass located at cervicomedullary junction was revealed. the surgical removal attempt failed due to multiple bradycardia episodes. however, a biopsy was performed and it confirmed that the lesion was a hemangioblastoma. conservative treatment with bevacizumab, a humanized monoclonal antibody that targets vascular endothelial growth factor (vegf) was initiated and the neurological status of the patient had been improved and the size of the tumor remained stable. moreover, the reduction of the surrounding edema was noticed. hemangiobalstomas are highly vascularized tumors with a rich capillary network. the endothelial cells express the vegf receptor. based on the histopathological characteristics, new treatment approaches are proposed for patients that are not suitable for surgical intervention. in the last couple of decades, stereotactic radiosurgical treatment represented an alternative for the surgically inaccessible locations or for multiple localisations that typically occur in von hippel-lindau disease. moss et al [13] published their almost 20 years experience of radiosurgical treatment for hemangioblastomas. their study comprehends 92 hemangioblastomas from 31 symptom cases percentage headache 18 78,2 ataxia 17 73,9 dysphonia 2 8,69 dysphagia 2 8,69 seizures 2 8,69 loss of visual acuity 1 4,34 hearing loss 1 4,34 159 cervicomedullary junction intramedullary hemangioblastoma patients, 26 of them being diagnosed with von hipple lindau syndrome. the mean age of the patients was 41 years. the radiation dose used to the periphery of the tumor average 23,4 gy with a mean tumor volume of 1,8 cm3. the tumoral response was measured with contrast-enhanced computed tomography scans. in 62% of the cases, the tumor volume remained stable, in 22% the tumor shrank, and 16% of the cases, hemangioblastoma contiuned to grow. these results emphasized that stereotactic radiosurgical treatment is a safe and effective alternative to open surgery. even though there are multiple approaches for the treatment of hemangioblastoma, surgical treatment remains a safe option for patients with a good outcome. in 2020, xiangdong yin et al [19] published a meta-analysis composed of 13 studies that included 473 cases. in this paper, they analyzed the surgical outcomes, including gross total resection, mortality, neurological morbidity, and functional outcome. gross total resection was performed in 98% of the cases. in our study, total resection was achieved in 95,6% of the cases (22 out of 23). neurological improvement was reported in 85% of the cases in their study, compared to our clinic, where 86% of the patients reported an improved neurological state. mortality was also similar between the statistics of metaanalysis and our clinic. in the mentioned study, mortality was 4% (23 out 473) compared to the 4,4% (1 out 23) mortality rate in our clinic. xiangdong yin et al postulated that surgical treatment for hemangioblastomas is still feasible and effective, a statement supported by good statistical outcomes from both their study and from our clinic experience. conclusions hemangioblastoma is a benign, highly vascularized tumor that usually occurs in the posterior fossa but its localization may widely vary. in the most cases, total resection is possible with a significant improvement of the neurological state of the patient. the rate of recurrence is low, even though tumoral cells can be spread by csf. nowadays there are multiple treatment options and every case should be carefully investigated in order to choose the best approach for improving the quality of the patient`s life. references 1. wilkins rh, rengachary ss. neurosurgery. new york 1985. 2. conway je, chou d, clatterbuck re, brem h, long dm, rigamonti d. hemangioblastomas of the central nervous system in von hippel-lindau syndrome and sporadic disease. neurosurgery. 2001 jan 1;48(1):55-63. 3. lindqvist m, steiner l, blomgren h, arndt j, berggren bm. stereotactic radiation therapy of intracranial arteriovenous malformations. acta radiologica. supplementum. 1986 jan 1;369:610-3. 4. neumann hp, lips cj, hsia ye, zbar b. von hippel‐lindau syndrome. brain pathology. 1995 apr;5(2):181-93. 5. lee sr, sanches j, mark as, dillon wp, norman d, newton th. posterior fossa hemangioblastomas: mr imaging. radiology. 1989 may;171(2):463-8. 6. gläsker s, van velthoven v. risk of hemorrhage in hemangioblastomas of the central nervous system. neurosurgery. 2005 jul 1;57(1):71-6. 7. jeffreys r: clinical and surgical aspects of posterior fossa haemangioblastomata. j neurol neurosurg psychiatry 38:105–111, 1975. 8. bonneville f, sarrazin jl, marsot-dupuch k, iffenecker c, cordoliani ys, doyon d, bonneville jf. unusual lesions of the cerebellopontine angle: a segmental approach. radiographics. 2001 mar;21(2):419-38. 9. silver ml, hennigar g. cerebellar hemangioma (hemangioblastoma): a clinicopathological review of 40 cases. journal of neurosurgery. 1952 sep 1;9(5):484-94. 10. wang c, zhang j, liu a, sun b. surgical management of medullary hemangioblastoma: report of 47 cases. surgical neurology. 2001 oct 1;56(4):218-26. 11. resche f, moisan jp, mantoura j, de kersaint-gilly a, andre mj, perrin-resche i, menegalli-boggelli d, lajat y, richard s: haemangioblastoma, haemangioblastomatosis, and von hippel-lindau disease. adv tech stand neurosurg 20:197–304, 1993. 12. takeuchi s, tanaka r, fujii y, abe h, ito y. surgical treatment of hemangioblastomas with presurgical endovascular embolization. neurologia medico chirurgica. 2001;41(5):246-52. 13. moss jm, choi cy, adler jr jr, soltys sg, gibbs ic, chang sd. stereotactic radiosurgical treatment of cranial and spinal hemangioblastomas. neurosurgery. 2009 jul 1;65(1):79-85. 14. jagannathan j, lonser rr, smith r, devroom hl, oldfield eh. surgical management of cerebellar hemangioblastomas in patients with von hippel–lindau disease. journal of neurosurgery. 2008 feb 1;108(2):21022. 15. koda m, mannoji c, itabashi t, kita t, murakami m, yamazaki m, aramomi m, ikeda o, furuya t. intramedullary hemorrhage caused by spinal cord hemangioblastoma: a case report. bmc research notes. 2014 dec;7(1):1-3. 16. kiyofuji s, graffeo cs, yokoyama m, sora s. intramedullary and intratumoral hemorrhage in spinal 160 g. popescu, francesca paslaru, anamaria gheorghiu et al. hemangioblastoma: case report and review of literature. surgical neurology international. 2018;9. 17. cornelius jf, saint-maurice jp, bresson d, george b, houdart e. hemorrhage after particle embolization of hemangioblastomas: comparison of outcomes in spinal and cerebellar lesions. journal of neurosurgery. 2007 jun 1;106(6):994-8. 18. mak g, algird a, greenspoon j, provias j, hirte h. cervicomedullary hemangioblastoma treated with bevacizumab. neuro-oncology advances. 2020 jan;2(1):vdaa076. 19. yin x, li c, li l, duan h. safety and efficacy of surgical treatment for brainstem hemangioblastoma: a metaanalysis. neurosurgical review. 2021 apr;44(2):799-806. 20. ho vb, smirniotopoulos jg, murphy fm, rushing ej. radiologic-pathologic correlation: hemangioblastoma. ajnr: american journal of neuroradiology. 1992 sep;13(5):1343. microsoft word 4adam_caudaequina 258 adam, hornea cauda equina syndrome secondary to lumbar disc herniation cauda equina syndrome secondary to lumbar disc herniation. report of three cases danil adam1,2, ioana hornea2 1associate professor, department of neurosurgery, “carol davila” university of medicine and pharmacy, bucharest, romania 2emergency clinical "st. pantelimon" hospital, șos. pantelimon 240, sect.2, bucharest, romania corresponding author: danil adam, e-mail: adam_danil@yahoo.com abstract cauda equina syndrome produced by the herniated lumbar intervertebral disc is a rare disorder that, if is undiagnosed and untreated in time, can have serious consequences for the patient and medicolegal implications for the surgeon. we report the clinical evolution of 3 patients with lumbar spinal stenosis who still present sphincterian and sexual dysfunctions many years after surgery, even if they were operated on immediately after admission. reviewing the literature on this subject has allowed us to emphasize symptomes, pathophysiological mechanism and management regarding patients with lumbar spinal stenosis. the surgical decompression is indicated as soon as possible. the surgical decompression within 48 hours from onset allows maximum improvement of symptoms and absolves the surgeon of any medico-legal liability. key words: cauda equina syndrome, lumbar herniated disc. introduction cauda equina syndrome (ces) is a rare but devastating neurologic condition resulting from many causes, most commonly secondary to a massive prolapsed intervertebral disc. ces secondary to intervertebral disc herniation was first reported in 1929, by dandy (1). ces may arise also from neoplastic, traumatic, inflammatory causes. the mechanism of injury to the nerves in ces is due to mechanical pressure, ischemia or venous congestion (2). patients complaines are bilateral leg pain and weakness saddle anesthesia and urinary or rectal incontinence. urgent surgery is required to halt or reverse neurological signs and symptoms (3). without surgery ces progresses and became permanent (4, 5). with surgery, recovery occurs over years. it is generally accepted that surgical decompression within 48 hours of the onset of symptoms is necessary for maximum improvement of clinical signs and symptoms (6). we report our 3 cases with ces followed between 1 to 4 years postoperatively and review the literature concerning factors that influence the outcome. romanian neurosurgery (2013) xx 3: 258 – 263 259 clinical presentation case 1 a 39-year-old male was operated for lumbar disc herniation at l3-l4 level, 3 years before. the ct-scan revealed disc protrusions at l4-l5 and l5-s1 level, with 60% lumbar spinal stenosis (figure 1). he continued to do heavy works as unqualified worker and returned with left leg pain, saddle paresthesia which began 5 days prior and urinary incontinence since 1 day. neurologic examination revealed a healthy man in good physical condition. the range of motion of the lumbar spine was painfully reduced in all directions, with anterior flexion limited at 10 degrees. bilateral straight leg raising was painfully limited at 40 degrees. the left achilles tendon reflex was absent. all other deep tendon reflexes were normal. sensation to light touch and pin prick was decreased in l5 and s1 dermatomes. a ct-scan of the lumbar spine revealed a large median disc herniation at the l4-l5 and l5-s1 levels. the patient underwent a discectomy at both levels through bilateral interlamar approach. sexual dysfunction and bowel problems persisted at 1 year follow-up making the patient very unhappy. he tried to commit suicide. at 4 year follow-up sexual dysfunction is still present, with very difficult erection and ejaculation even with entran taken before sexual intercourse. case 2 a 52-years-old man presented in emergency room complaining of back and leg pain on left side since 1 week and paresthesias in left buttock and genitals since 1 day. neurologic examination revealed a limitation of lumbar spine motions with anterior flexion at 45 degrees an left straight leg raising test limited at 45 degrees. patelar and achilles reflexes were present. muscle strength testing demonstrated weak left dorsal extensions of left halux, graded 3/5. sensation to touch and pin prick was decreased along the left l5 dermatome. mri of lumbar spine revealed a large l4-l5 disc herniation, with 12 mm anteroposterior diameter (figure 2). the patient underwent an urgent intervention the next day. during intervention for discectomy, a dural tear appeared without consequences. in the postoperative period saddle anesthesia persisted. at 1 month follow-up he had constipation. a glycerine suppository was inefficient, and enema was necessary for clearing the rectum. figure 1 ct-scan of lumbar spine, sagital section at l4-l5 level shows a huge herniated disc a 260 adam, hornea cauda equina syndrome secondary to lumbar disc herniation b figure 2 preoperative mri: axial section (a) and sagital section (b) reveal a large l4-l5 disc herniation figure 3 t2-weighted mri of lumbar spine, sagital section, demonstrates a large l4-l5 disc herniation case 3 a 41-years-old female, complaining of bilateral sciatica and perigenital and perianal paresthesias since three days, presented at emergency room. neurologic examination revealed a reduced range of motion of the lumbar spine, with anterior flexion limited at 45 degrees and straight leg raising test at 45 degrees. she had achilles tendon reflexes bilateral abolished, spi paresis on the left side, and urinary retention appeared in the day of admission. lumbar ct and mri scans demonstrated a large central disc herniation at l4-l5 level, 11 mm in antero-posterior diameter and a smaller l5-s1 protrusion (figure 3). the patient underwent a l4-l5 discectomy by bilateral interlamar approach, performed in the first 24 hours from presentation. post surgical assessment at discharge, 2 weeks post intervention, failed to demonstrate any improvement in urinary retention. she had urinary infection with klebsiella. she followed motor rehabilitation in a specialized department. five weeks post surgery she was in a wheelchair after that she walked with a gait assessor. sensation of urine pass reappeared after 3 months. at 3 months follow-up she reported stool incontinence and sexual dysfunction with sensation preserved only in left side of vagina but with a complete block in achieving orgasm. at 1 year follow-up she still had difficulties with bladder and bowel function and sexual problem persisted. at eight months postsurgery she start to work part time. romanian neurosurgery (2013) xx 3: 258 – 263 261 discussion the term "cauda equina" was first described by a french anatomist, lazarius in 1600 (7). ces secondary to intervertebral disc herniation was first reported in1929 by dandy (1). the caudal spinal cord is termed the conus medullaris with his most caudal segment situated at the level of the intervertebral disc between l1 and l2 vertebrae. eleven pairs of nerve roots emerging from conus medullaris travels for varying distances before reaching the corresponding neural foramen, exits from spinal canal and arrives to pelvic organs (bowel, bladder), sexual organs, and also to the inferior limbs' muscles. a common cause of cauda equina lesion is prolapse of an intervertebral disc causing nerve roots compression. in the spinal canal, the nerve roots are particularly vulnerable to injury of compressive stress because they have no schwann cells to cover them. nerve root compression, especially in a stenotic canal produce a congestion and dilation of intraradicular and periradicular veins, frequently observed intraoperatively and described as varix. in pathophysiology of ces was incriminated an autoimmune reaction (8) axonal demyelination with wallerian degeneration induced by tnf-α expression (9). ces occurs when the nerve roots within the spinal canal have been damaged. the nerves supplying the muscles of the legs, the bladder, bowel and genitals do not function properly. signs and symptoms of cauda equina root compression include leg pain and leg weakness saddle anesthesia, bladder, bowel and sexual dysfunction. the presence of bladder or bowel dysfunction suggest the diagnosis of ces: urinary retention or overflow incontinence, constipation or faecal incontinence. urological dysfunction and perineal sensory deficit represent the most consistent identifying features of ces. at the beginning they have difficulty in starting or stopping a stream of urine, after wards is present urinary retention or overflow incontinence. sexual problems are rarely reported at presentation. this is very distressing aspects, mostly in young adults, in postoperative period. ces is a rare condition. it is generally accepted that ces occurs in approximately 1-2% of cases of lumbar disc herniations (10, 11, 12, 13). in the management of ces patients there is considerable debate about the expediency with which surgical root decompression is carried out. the early reports have favoured immediate decompression. before the mid 1980s, authors believed that decompression should be carried out within six or eight hours after onset of acute ces. after that, other authors stated that there is no evidence to support the statement that urgent decompression conferred great benefit when bladder dysfunction is present (14, 15, 16). however, the risk for poor outcome increases continuously with increasing time from onset of symptoms to decompression (17) and that patients, operated earlier did statistically better than the patients operated later (16). determining when exactly ces is deemed to be present is difficult. more recent studies questioned previously consensus opinion that delays in 262 adam, hornea cauda equina syndrome secondary to lumbar disc herniation decompression negatively affect outcome (18, 19). the influence of delays in treatment may have historically been overestimated. qureshi and sell (18) consider that the major determinant of outcome may not be the timing, but the severity or density of deficit. if surgical decompression is performed within 48 hours from onset of ces, the outcome cannot be adversely affected. the dogma that decompression must be performed in the first 6 or 8 hours from onset is no more accepted. if the patient with ces is operated as soon as possible after presentation in optimal conditions in the operative theater, the doctor must be absolved from any legal responsibility. if the damage of nerve roots is incomplete, and the nerves are still capable of regrowth, recovery takes time, sometimes even several years. in other cases, the lesion is severe and the damage should be permanent. our three patients had onset of symptoms since several days: back and leg pain, perineal paresthesia. they presented to hospital only when urinary dysfunction appeared. all were operated in the first 24 hours after ct-scan or mri of lumbar spine. however, in the postoperative period, they continue to have dysfunctions and sexual problems. one patient want to commit suicide because of sexual dysfunction. after 1 to 4 years follow-up, with rehabilitation and medication all have a significant improvement of symptoms. conclusion cauda equina syndrome secondary to a massive lumbar disc herniation is a rare but serious condition which must be diagnosed and operated as soon as possible. decompression performed within 48 hours from onset of symptoms absolve the surgeon from any legal responsibility and offers to the patient maximum improvement of symptoms. references 1. dandy we. loose cartilage from intervertebral disk simulating tumor of the spinal cord. arch surg 1929; 9: 660-672. 2. gleave jrw, macfarlane r. prognosis of recovery of bladder function following lumbar central disc prolapse. br j neurosurg 1990; 4: 205-210. 3. arrigo rt, kalanithi p, boakyem: is cauda equina syndrome being treated within the recomended time frame? neurosurgery 2011: 68: 1520-1526. 4. shephard rh. diagnosis and prognosis of cauda equina syndrome produced by protrusion of lumbar disk. br med j 1959; 2: 1434-1439. 5. shapiro s. cauda equina syndrome secondary to lumbar disc herniation. neurosurg 1993; 32: 743-747. 6. ahn um, ahn nu, buchowski jm, et al. cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. spine 2000; 25 (12): 1515-1522. 7. lazarius a. historia anatomica humani corporis. frankfurt germany: becker; 1600: 178. 8. lee sk, wolfe sw. peripheral nerve injury and repair. j am acad orthop surg. 2000; 8(4): 243-252. 9. sekiguchi m, kikuchi s, myers rr. experimental spinal stenosis; relationship between degree of cauda equida compression, neuropathology, and pain. spine 2004; 29 (10): 1105-1111. 10. gitelman a, hishmeh s, morelli bn, et al. cauda equina syndrome. a comprehensive review. am j orthop 2008; 37(11): 556-562. 11. henriques t, olerud c, petre′n-mallmin m, et al. cauda equina syndrome as a postoperative complication in five patients operated for lumbar disc herniation. spine 2001; 26: 293-297. 12. jennett wb. a study of 25 cases of compression of the cauda equina by prolapsed intervertebral discs. j neurol neurosurg psychiat 1956; 19: 109-116. romanian neurosurgery (2013) xx 3: 258 – 263 263 13. o′laoire sa, crockard ha, thomas dg. prognosis for sphincter recovery after operation for cauda equina compression owing to lumbar disc prolapse. br med j. 1981; 282: 1852-1891. 14. kostuik jp, harrington i, alexander d, rand w, evans d. cauda equina syndrome and lumbar disc herniation. jbone joint surg arn 1986; 68: 386-391. 15. gleave jrw, macfarlane r. cauda equina syndrome: what is the relationship between timing of surgery and outcome? br j neurosurg 2002; 16 (4): 325-328. 16. shapiro s. medical realities of cauda equina syndrome secondary to lumbar disc herniation. spine 2000; 25: 348-352. 17. kohles da, karp ap, et al. time-depended surgical outcomes following cauda equina syndrome diagnosis:comments on a meta-analysis. spine. 2004; 29(11): 1281-1287. 18. qureshi a, sell p: cauda equina syndrome treated by surgical decompression: the influence of timing on surgical outcome. eur spine. 2007; 16(12): 2143-2151. 19. hussain sa, gallan rw, chitnavis bp. cauda equina syndrome outcome and implications for management. br j neurosurg. 2003; 17(2): 164-167. microsoft word iacobg_intra_f.docx romanian neurosurgery (2012) xix 1 intra et parasellar chordoma – case report g. iacob1, m. crăciun1, liliana parascan2, maria sajin3 1neurosurgery clinic, universitary hospital, bucharest 2department of pathology cardiovasculary hospital, prof. dr. c.c. iliescu, bucharest 3department of pathology, universitary hospital, bucharest abstract a rare case of giant intra and parasellar chordoma, mimicking a pituitary prolactinoma is presented. the tumor involving pituitary fossa and surrounding structures was removed via a bifrontal approach. the pathology exhibited the typical histological patterns of a chordoma. the authors present a rare case of a giant sellar and parasellar chordoma and review the literature on that. keywords: chordoma, sella turcica, pituitary prolactinoma introduction chordomas represent 1% of all malignant bone tumors and 0.1 to 0.2% of intracranial neoplasms (6, 7). in romania, the pathology department of the bucharest oncologic institute has reported a low frequency for chordoma 0.12%. these embrionary tumors, first described by luschka in 1856 are rare, slow-growing neoplasms with maligne potential, that arise from cell rests, particularly of the proximal and distal extremes of the notochord, characterized by osseous permeation, high local recurrence, local invasiveness (4-14). their metastatic potential cannot be estimated by histological examination, except in cases of sarcomatous transformation (10). the most common site are: 50% in the sacrococcygeal region – mean age 50 years, especially to men, 35% in the base of skull in the midline, especially to childs or young adults; 15% in vertebrae (7). large, intra et parasellar chordomas resembling a pituitary prolactinoma are rare (12). case presentation a 64 year old woman, without pathological antecedents, was admitted in our department for headache, progressive decrease of visual acuity of right eye, double vision instaled over the past 2 months. on general and neurological examination we found decrease of visual acuity of right eye: vod = 2/3 without corection, vos = 1, the external rotation of the right eyeball was not possible, visual field examination disclosed bitemporal hemianopsia; fundus oculi: plane, well contured papila, with tortous and dilated veins, thin arteries, macula without reflex on right eye; the light reflex of both pupils in direct & indirect responses was normal. no endocrinopathy was noted but serum pituitary hormone levels revelead high prolactin levels: 84 ng/ml, reference value 2.5–17, less basal cortisolemia 1,24 μg/dl, reference value 5– 25, betachorionic gonadotropin (hcg), alpha-fetoprotein (fp) and carcinoembryonic antigen (cea) were g. iacob et al intra et parasellar chordoma normal; diabetes insipidus investigation also was normal. radiography of the skull revealed enlargement and distortion of the sella, with osteolysis of its floor and invasion of the sphenoid bone. a high-resolution ct scan revealed a large, partly calcified intrasellar tumor, showing suprasellar extension and erosion of the sphenoid bone. cerebral mri (figure 1) demonstrated a sellar area tumor measured 28/32/34 mm, in its greatest diameter, with hypersignal in t1 and t2-weighted images, omogenous, with slight inside calcifications, polycyclic outlined. this tumor is elevating the pituitary gland and optic chiasm, posterior overpass clivus, is in contact with the basilary artery and on the right side invaded the latero-selar compartment, without affecting the carotid artery. therefore the carotid arteriography was normal. a bifrontal microscopic approach was performed; a yellow encapsulated, soft with necrotic center tumor was discovered, extended intra, supra and right parasellar. the tumor was removed, the latero-selar compartment too, the optic chiasm was decompressed as like as the pituitary stalk, less a small part of the tumor with tight adhesion to the pituitary stalk. microcalcifications in the suprasellar and sellar portions were detected. postoperatory evolution was uneventfull confirmed by cerebral ct (figure 2) and at 6-months follow-up examination after radiotherapy, the patient was asymptomatic, serum pituitary hormone levels revelead normal levels. histologic and immunohistochemistry tests are indicative for a tumoral chordoma. patolology diagnosis was made on macroscopic criteria: lobulated fragments, tan-to-red, of various dimensions, soft consistency, sometimes kistic, diffuse borders, invading adiacent structures. a b c figure 1 cerebral mri studies: axial (a), coronal (b) and sagittal (c) revealing a large mass occupying the pituitary fossa, elevating the pituitary gland and optic chiasm, and invading the right cavernous sinus romanian neurosurgery (2012) xix 1 figure 2 postoperatory ct-scan 1 month after operation on section tumor is gelatinous, translucide with green with red-brune areas. microscopic criteria (figure 3): lobular pattern, more important in central part of the tumor, with different shapes, fibrous septa of variable thickness, more important at the tumor periphery, containing vessels.the arterial supply in the central area were very small, but necrosis was very offen encountred. smaller lobuli, perhaps younger, disposed at the peryphery, contain oval, polygonal or prismatic cells, mimiking a carcinomatous aspect. this cells has important cytoplasma, omogenous, with small vacuolar areas containing glicogen and progressive tendency to coalescence. the nuclei are small, spheric – rarely with reniform shape, disposed central with prominent nucleoli. in the cells with multiple vacuolar areas, nuclei has the tendency to picnosis. in medium or big lobuli the proliferative cells were disposed circumferential and extended to the centrum part of the lobuli with a radial structure. in the central area, intracytoplasmatic vacuoles develop in volume and number; by vacuoles coalescence cells has the tendency to become “physaliphorous cells” with small nuclei disposed central or in the periphery (physaliphorous comes from the greek word physalis = bubble). gigant, multinucleated cells are rare. cytoplasmic vacuoles were smaller than those in the intercellular matrix. another microscopic criteria was represented by an important mucoid stroma with glycogenic component (see the period-acid-schiff method), where cells arranged in lobules are embedded. very rare cells has pseudo-glandular aspects with limphocytes at the periphery, partial limitated by a capsula made by conjunctive tissue. immunocytochemical analysis of the chordoma cells showed focal positivity for vimentin, ema. negative immunoreactivity for cea was noted. ultrastructurally, the tumor was composed of large cells containing irregular nuclei with multiple indentations and prominent nucleoli. analysis of dna revealed a diploid histogram. a b c g. iacob et al intra et parasellar chordoma d e f g h i j figure 3 chordoma: microscopic criteria and details for immunohistochemistry (a) chordoma he ob.10 x: tumoral lobes, different shapes, sepparated by fibrotic septs, (b) detail: chordoma he ob. 20 x: as vacuoles are bigger, the cells limit are estompated, (c) another detail of chordoma he ob. 20 x, (d) vim positive ihc coloration ob.10 x, (e) detail of vim positive ihc coloration ob. 20 x, (f) pas present as a marker of glicogen in mucilaginous substance expelled in extracells space ob. 20 x, (g) detail of mnf (myelinated nerve fibres) 116 positive diffuse – ob. 20 x, (h) detail of ema (epithelial membrane antigen) positive diffuse – ob. 20 x, (i) leu 7 – zonnal positive ob. 20 x, (j) cea (carcinoembryonic antigen) negative ob. 40 x discussion chordomas involving the sellar region are extremely rare, more frequent in younger patients second to fifth decades of life, with a a male/female ratio of 6: 5 (5, 7) most chordomas involving the sellar region depending on anatomical location and clinical features could be devided in three groups (12): parasellar or suprasellar chordomas with optic tract compression and oculomotor nerve palsy; largely or entirely sellar chordomas – are very rare, mimicking pituitary adenoma with chiasm compression and hypopituitarism, clival chordomas with brainstem compression and bilateral sixth cranial nerve paresis. several studies according to thoudou et al. (12) has pointed the misdiagnosed preoperatively as pytuitary adenoma, craniopharingioma based on clinical symptoms (visual deficit as the most common symptom, hyperprolactinemia or hypopituitarism more commonly observed in the sellar and suprasellar chordomas) and radiologic findings (bone distruction involving pituitary fossa, petrous bone, romanian neurosurgery (2012) xix 1 orbit, foramen ovale, jugular foramen and even foramen magnum; calcifications in the tumoral mass or sequestrated bone fragment) the skull base chordomas tend to present osseous permeation, and have a high rate of recurrence (4-7, 10, 14, 15). their metastatic potential cannot be estimated by histological examination, except in cases of sarcomatous transformation (1-3, 6, 8, 10). the imaging method of choice are mri, also ct – scan with contrast and thin slices for reconstructions (7). a sellar chordoma ct scan may reveal a contrast-enhancing intrasellar mass with bony erosions and calcifications well demonstrated in bone window images (11, 15). in general surgery should be complete, the capsular tumoral adhesions to chiasma or another nervous structure made this purpose sometimes impossible and postoperative irradiation are recommended despite inconclusive data (7, 10, 12). the immunohistologic profile of chordoma cells is reactivity to cytokeratins, vimentin, and epithelial membrane (1-3, 7, 9). the only known prognostic study published in 1993 estimated overall survival rates of 51% and 35% at 10 and 20 years, respectively (6). differential diagnosis should be made with other large sellar and suprasellar tumor mass as pituitary adenomas, especially if a calcified intrasellar tumor with bone erosion is diagnosed; chondroid chordoma, chondrosarcoma with mucoid intercellular substance containing calcifications (5, 7, 14). conclusion chordomas are midline slow-growing tumors that arise from proximal and distal extreme remnants of the notochord, are locally invasive, may metastasize and are characterized by local recurrence. these tumor can mimick a pituitary adenomas, especially if a calcified intrasellar tumor with bone erosion is diagnosed. a grosstotal resection followed by radiotherapy, has been the accepted treatment for sellar chordomas. references 1. abenoza p, sibley rk, “chordoma: an immunohistologic study,” human pathology 1986, 17, 7, 744–747 2. bouropoulou v, kontogeorgos g et al, differential diagnosis of chordoma immunohistochemical aspects, archives d’anatomie et de cytologie pathologiques 1987, 35, 1, 35–40 3. coindre jm, rivel j et al, immunohistological study in chordomas, journal of pathology 1986, 150, 1, 61–63 4. cremoux p, turpin u, hamon p, gennes jl, “les chordomes intrasellaires. principaux aspects cliniques, biologiques, radiologiques, évolutifs et histologiques a propos de deux observations,” sem hôp, 1980, 56, 1769–1773 5. elias z, powers sk, “intrasellar chordoma and hyperprolactinemia,” surgical neurology, 1985, 23, 2, 173–176 6. forsyth pa, cascino tl, shaw eg et al, intracranial chordomas: a clinicopathological and prognostic study of 51 cases, journal of neurosurgery 1993, 78, 5, 741– 747 7. hirosawa rm, santos aba, franc mm et al, intrasellar chondroid chordoma: a case report, isrn endocrinology 2011, id 259392, 5, 259392 8. mathews w, wilson cb, “ectopic intrasellar chordoma. case report,” journal of neurosurgery, 1974, 40, 2, 260–263 9. pluot m, bernard mh et al, deux observations de chordome de la selle turcique. etude ultrastructurale et histochimique, archives d’anatomie et de cytologie pathologiques 1980, 28, 230–236 10. raffel c, wright dc, gutin ph, wilson cb, cranial chordomas: clinical presentation and results of operative and radiation therapy in twenty-six patients, neurosurgery 1985, 17, 5, 703–710 11. tan ws, spigos d, khine n, chordoma of the sellar region, journal of computer assisted tomography 1982, 6, 1, 154–158 12. thodou e, kontogeorgos g et al, intrasellar chordomas mimicking pituitary adenoma, journal of neurosurgery 2000, 92, 6, 976–982 13. volpe r, mazabraud a, a clinicopathologic review of 25 cases of chordoma, a pleomorphic and metastasizing neoplasm, american journal of surgical pathology 1983, 7, 2, 161–170 14. watkins ln, khudados es et al, skull base chordomas: a review of 38 patients, 1958-88, british journal of neurosurgery 1993, 7, 3, 241–248 15. zee cs, go jl et al, imaging of the pituitary and parasellar region, neurosurgery clinics of north america 2003, 14, 1, 55–80. microsoft word 6.chiriac.docx romanian neurosurgery (2012) xix 4: 289 – 293 289 our experience in surgical treatment of intraorbital tumors a. chiriac, s. daja1, b. iliescu1, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract orbital tumors are complex lesions representing a great challenge for the neurosurgeons and ophthalmologist. methods: we analyse the database for 57 patients who underwent surgery for the treatment of orbital tumors at our institution between 2001 and 2010. data from clinical notes, surgical reports, and radiological findings were extracted for the statistical analysis. results: predominant symptoms were exophthalmos (68%), visual disturbance (42%) and ocular mobility limitation (37%). the most used surgical approache was superior orbitotomy. orbital tumors histopathological results showed that hemangiomas were the most common tumors type (35%). malignant tumors accounted for 23% of cases. total resection of tumors was achieved in 78% of patients. conclusion: surgical treatment could be considered an optimal treatment option for most of the orbital tumor. a better imaging anatomy analysis of the orbit correlated with good surgical skills is needed to overcome the pitfalls of intraorbital surgery. introduction tumors of the orbit are rare but complex diseases in neurosurgical pathology with a frequency of 3.5 4 % [1, 2]. their direct relation with all anatomic structures of the orbit makes these lesions a great challenge for the neurosurgeons and ophthalmologist. based on the relationship between the tumor and muscle cone the orbital tumors are anatomically divided into three categories: intraconal, extraconal and intracanalicular. the muscle cone is reprezented by the extraocular rectus muscles and their intermuscular septae, and devides the orbital space into: intraconal and extraconal space. patients with orbital tumors commonly present with a variety of signs and symptoms and they are often difficult to diagnose especially in their initial stages. imaging diagnostic methods involves orbital ct and mri either alone or in combination. if the ct scan offers a better evaluation of orbital bones, mri provides a better soft tissue discrimination with superior imaging for the visual pathways. the surgical techniques for orbital lesions involve classic transcranial extradural approaches as subfrontal, frontotemporal or pterional, or directed approaches as transconjunctival, medial or a more extensive lateral orbitotomy. in the present study, we describe our surgical experience on 57 orbital tumors at single institution, with special focus on the clinico-imagistic particularities and treatment results. materials and methods a total number of 57 patients who underwent surgery for the treatment of 290 chiriac et al surgical treatment of intraorbital tumors orbital tumors at our institution between 2001 and 2010 were statistically analyzed. the clinical dates, surgical reports, and imagistic findings were extracted from a database for our analysis. the preoperative radiological investigation by computed tomography (ct) and magnetic resonance (mr) imaging allwowed a detailed study in matters relating to tumor location, size and its relation to neighboring anatomical structures. all surgeries were performed by two neurosurgical teams, lesion being approached as per their anatomical location. morbidity, follow-up and outcome were also analyzed. all the lesions of the present series were histopathological diagnosed after partial or total excision. postsurgical monitoring of these patients in terms of clinical, biological and imaging aspects corelated with applied treatment effectiveness and a clear complications diagnose led us to a prediction parameters for patient with orbit tumor. patients were clinically invetigated at each postinterventional control (at least 6 months, a year, or as needed) and the biological and imagistic balance was made possible quarterly or annually, depending on the rhythm imposed by the surveillance protocol. patients who received active treatment by sterotactic radiation were guided or monitored by a medical letter from our clinic. information resulting from the collection of clinical observations, laboratory and imaging were recorded in a database that was used in statistical processing of the study group in terms of transverse (incidence and prevalence of studied factors and events) and in terms of view of statistical significance of various combinations of factors suspected to have prognostic importance in multimodal treatment of patients with tumors of the orbit. results from a total of 57 patients who underwent surgery for the treatment of orbital tumors 82% presents proptosis at admission. the patients series were separated in to groups based on age categories: 17 children and 40 adults. all the patients were analysed with regard to their sex, age, clinical symptoms, site of involvement, surgical approaches employed for their resection and histological diagnoses. sex and age distribution there were 28 males and 29 females with age ranged from 1 to 72 years (mean age was 38.4 years and median of age was 40.5 years). figures 1 a, b show age distribution of the patients. clinical symptoms the major symptoms recorded at presentation were exophthalmos (68% to adults and 71% to children), visual disturbance (45% to adults and 35% to children) and ocular mobility limitation (35% to adults and 39% to children). the exophthalmos was appreciated as big in 7 cases, mean in 19 cases and small in 13 cases. site of involvement concerning the lateralisation of orbital tumors we detected a 57% of right eye involvement versus 43% of left eye. intraconal tumoral masses were encountered in 18 cases, extraconal tumor masses in 28 cases, intra-extraconal tumor masses in 8 cases and lateral wall in 3 cases. quadrant of involvement was superonasal in 16 patients, superotemporal in 21 patients, inferior quadrant in 11 patients and superior quadrant in 19 patients. among the paraorbital tumors, 1 patients had orbital extension of naspoharyngeal mass and 2 patient had a nasoethmoidal mass extending into orbit. romanian neurosurgery (2012) xix 4: 289 – 293 291 figure 1 patients distribution by age and sex table 1 clinical symptoms symptoms pat.nr. % eye pain 15 26 ptosis 16 28 exophtalmos 39 68 visual disturbance 24 42 ocular mobility limitation 21 37 palpable mass 18 32 table 2 sites of involvement primarily orbital tumor paraorbital tumor with orbit extension nr. % nr. % intraconal mass 16 28 naspoharyngeal mass 1 33 extraconal mass 27 47 nasoethmoidal mass 2 66 intra-extraconal mass 8 14 lateral wall mass 3 5 54 3 table 3 surgical approaches surgical approache pat.nr. % superior orbitotomy 19 33 fronto-pterional approaches 12 21 fronto-orbital 6 10 bicoronal craniotomy 8 14 fronto-orbitotemporal 10 18 trasfacial 1 2 transpalatal and weber orbitotomy 1 2 surgical approaches total, subtotal resection and biopsy were performed for all patients. supraorbitar craniotomy was the most frequent used approach (35%) in this study followed by the fronto-pterional approaches (23%) and fronto-orbito-temporal approaches (19%). in one case of naspoharyngeal angiofibroma with orbital extension a transpalatal and weber orbitotomy approach was used. total or partial orbital exenteration were needed in 3 patients. histology results the anatomo-pathological results is summarized in table 4. overall, hemangiomas were the most common tumors in our study (35%), followed by benign lesions (meningiomas 14%, 0 0.5 1 1.5 2 2.5 3 3.5 4 nu m ar pa ci en ti 1 7 8 15 16 25 26 35 36 45 46 55 56 65 66 75 grupe varsta sex feminin 0 1 2 3 4 5 6 nu m ar pa ci en ti 1 7 8 15 16 25 26 35 36 45 46 55 56 65 66 75 grupe de varsta sex masculin 292 chiriac et al surgical treatment of intraorbital tumors neurofibromas 5%) and inflammatory lesions (15%). malignant tumors accounted for 23% of cases amoung witch carcinoma was the most frequent (9%). table 4 histological results tumor type nr. pat. % carcinoama 5 9 cholesteatoma 1 2 hemangioama 20 35 cystic tumor 2 3 neurofibroma 4 7 glioma 2 3 meningioma 8 14 malignant lymphoma nh 3 5 malignant melanoma 1 2 orbital metastasis 4 7 orbital bone metastasis 1 2 orbital cellulitis 1 2 inflammatory pseudotumor 3 5 miozit 1 2 dacryoadenitis 1 2 complication and monitoring the median follow-up duration was 17 months (range from 7 to 62 months). thus, in the group of patients included in the study, during surveillance, we recorded 11 adverse events: 2 ischemic attacks (one meningioma and an intraconal metastasis with partial resection subsequently to radiotherapy by gammaknife and conformational irradiation and optic nerve ischemic necrosis corresponding to 7-11 months after irradiation), 2 postsurgical bleeding (one intra-orbital in to the bed tumor after resection of a hemangioma and one epidural after a microsurgical approach of an orbital metastasis through a fronto orbito – temporal approach), 2 tumor recurrences (lacrimal gland adenocarcinoma), 1 retinal edema (a giant cavernous hemangioma surgically resected and irradiated gamma-knife with perilesional edema at 7 months after irradiation, probably by early thrombosis of a drainage vein, with favourable evolution under treatment with corticosteroids), 2 damage field and visual acuity (direct traction on on) and 2 cases of ptosis due to intaroperative iii n traumatic injuries (a case of extra-intraconal meningioma and a case of intraconal carcinoma). discussion analysis of symptoms to admission between the two groups of patients with intraorbital tumors showed no significant differences, with one exception. thus, there were more cases of childhood patients with palpable masses at admission compared to adult patients (53% versus 33%). this is explained primarily by smaller dimensions of the orbit in childhood related to tumor growth rate. if in the childhood group the small exophthalmia was dominant, the adult group was dominated by medium and large exophthalmia. this is caused mainly by the difference between the child and adult orbital space and aesthetic deformities tolerance of the adult. based on the benign and malignant tumor pathology criteria we have seen that, the childhood group did not reveal any malignant tumor, while, in adult group 13 cases with neoplasic intraorbitar lesions were diagnosed. thus, about one third of intraorbitar lesions causing proptosis proved to be malignant. synthesis of histological types of intraorbitar tumors had showed that the percentages of different histological types approach those listed in the literature published in recent years. the rate of complications was 8.7% over a period of 3 years, so with an average 2.9% / year, which mean that the risk of late romanian neurosurgery (2012) xix 4: 289 – 293 293 complications of various treatment methods included in our study is similar to the risk and complications described in the literature, assessed at 1.5 3% / year. study of relative risk of complications depending on the lesions size showed a very uneven distribution, with two peaks, one in the range between 0.9 -1.3 lcc being clearly superior to all other dimensions found in the patients studied. from statistical analyses we cane conclude that the dimension of intraorbital lesions represented a significant risk factor on the natural history of patients studied. the p= 0.0088 value recorded by us, was similar with the literature reports, most of them highlighting their size influence on prognosis (parameter included also into prognostic scale). location is generally considered to have a great influence on the prognosis of patients with intraorbital tumors being obvious the neurological disasters that can result from a bleeding / recidive / radionecrosis in on. after a uni-factorial analysis of the statistical significance of the intraorbital tumor location showed that their location in a certain area of the orbit has prognostic importance of the natural evolution of the disease, even if lateralization distribution (left-right) did not influence the prognosis. the predictive value of the method of treatment is insignificant, p = 0.6536, which leads to the conclusion that regardless of the method used, as long as it is effective and correct choose, the natural progression of disease prognosis is the same. since, despite the minimal invasiveness of modern treatment methods and postoperative favorable evolution of all patients included in this study, any microsurgical intervention or irradiation is still encumbered by procedural risks and certain consecutive late complications of surgery. conclussion although the orbit is an extremely difficult anatomical entity approached, so that over the years various specialists were limited to clinical diagnosis, imaging data and recently acquired therapeutic experience make this pathology to be more permissive for specialists with various specializations. frequency of orbital pathology imposed a bigger interest in diagnostic solutions development, but especially for election of miniminvazive surgical solutions with optimal results for the patient. based on an experience that is gained with each patient investigated and observed, together with a close collaboration between different specialists involved, we can say that for this segment of pathology, neurosurgeon is one who must assume the responsibility as receiver and mediator, settlement as decision maker and postoperative observation of these cases. references 1. hassler w., unsöld r., schick uta (2007) orbital tumors: diagnosis and surgical treatment, dtsch arztebl 104(8): a 496–501; 2. hyun joon park, seung-ho yang, il sup kim, jae hoon sung, byung chul son, sang won lee (2008) surgical treatment of orbital tumors at a single institution, j korean neurosurg soc 44.3:146-150; 3. kim h.j, h.-j. kim, y.-d. kim, yim y.j., kim s.t., p. jeon, kim k.h., byun h.s., song h.j. (2008) solitary fibrous tumor of the orbit: ct and mr imaging findings, ajnr am j neuroradiol 29:857– 62; 4. klingenstein a., kufeld m., wowra b., muacevic a., fürweger c., schaller u. c. (2012) cyberknife radiosurgery for the treatment of orbital metastases, technology in cancer research & treatment, 28:1-7; 5. simona dunaritiu, f. birsasteanu, d. onet, magda pascut, d. costea, maria mogoseanu (2008) radioimaging diagnosis of the ocular and orbital tumors, j. of experimental medical & surgical research, xv, 1-2:5-12; 6. parashkevova b., balabanov ch., stateva d. (2007) orbital tumors clinical cases presentation journal of imab annual proceeding, book 1:44-47. 7. somnath saha, vedula padmini saha,sarbani chattopadhyay (2002) orbital and paraorbital tumors clinicopathological profile and surgical management, indian journal of otolaryngology and head and neck surgery 54: 2:117-122; microsoft word 15iliescuadvences romanian neurosurgery (2011) xviii 1: 99 – 100 99 advances in glioblastoma management b. iliescu1, i. poeata2 1“prof. dr. n. oblu” clinical emergency hospital iasi 2“gr.t. popa” university of medicine and pharmacy iasi introduction resection of the maximum amount of tumoral tissue while preserving the function of the brain within or neighboring the tumor region established itself as a fundamental goal of modern oncologic neurosurgery. maximal safe removal of the tumoral tissue has been documented extensively as a major prognostic factor for patients with glioblastoma (8). as such it became imperative for the oncologic neurosurgeon to be able to identify reliably the functional structures, cortical, subcortical, and vascular both preoperatively and in the operating room (5). mapping the eloquent areas of the brain has become a well-established technique using the intraoperative electrophysiology, with reliable methods and results (9,10,11). as well, preoperative mapping of the same areas using functional mri and/or magnetoencephalography (meg) has given clinically useful results in experienced hand (2, 3). however these methods do not provide any information about the white matter tracts that may be affected by invasive, intrinsic brain tumors. the advances in diffusion-tensor (dt) imaging techniques have been used to map white matter tracts in the normal brain (1, 4). methodology the aim of our paper is to demonstrate the role of dt imaging in preoperative mapping of white matter tracts in relation to cerebral neoplasms and the way it can influence the operative decision in our practice. we discuss as well the methods used intraoperatively to identify and recognize functional areas and neighboring white matter tracts in the cases with glioblastoma (6, 7, 8). ten patients suffering from this brain malignancy within or neighboring eloquent cortical areas underwent dt imaging examinations prior to tumor excision. anatomical information about white matter tract location, orientation, and projections was obtained in every patient. depending on the tumor type and location, evidence of white matter tract edema (one patient), infiltration (one patient), displacement (five patients), and disruption (three patients) could be assessed with the aid of dt imaging in each case. diffusion-tensor imaging allowed for visualization of white matter tracts and was found to be beneficial in the surgical planning for patients with intrinsic brain tumors. conclusion our report is both a general and personal. in the first part we analyze the decision making process and protocol in the era of complex preoperative planning, microsurgery, ultrasound aspiration, neuronavigation, awake craniotomy, and 100 b. iliescu, i. poeata advances in glioblastoma management white matter tracts stimulation techniques in the surgical treatment of these cases. we present our experience using these technologies in combination with tractography in the treatment of 10 glioblastoma cases, affecting eloquent areas of the brain. the data strongly suggests that using both pre and intraoperative functional techniques improves significantly the results in terms of postoperative neurological status allowing for a safe maximal tumor removal. references 1. handler t, et. al. delineating gray and white matter involvement in brain lesions: three-dimensional alignment of functional magnetic resonance and diffusion-tensor imaging. j neurosurg 99:1018–1027, 2003. 2. kim p., singh m.s. functional magnetic resonance imaging for brain mapping in neurosurgery. neurosurg. focus, 15(1):1-7, 2003. 3. kober h, nimsky c, möller m, hastreiter p, fahlbusch r, ganslandt o. correlation of sensorimotor activation with functional magnetic resonance imaging and magnetoencephalography in presurgical functional imaging: a spatial analysis. neuroimage, 14(5):1214-28, 2001. 4. krings t, reinges mht, thiex r, gilsbach jm, thron m. functional and diffusion-weighted magnetic resonance images of space-occupying lesions affecting the motor system: imaging the motor cortex and pyramidal tracts. j neurosurg 95:816–824, 2001. 5. lehericy s, duffau h, cornu p, et al: correspondence between functional magnetic resonance imaging somatotopy and individual brain anatomy of the central region: comparison with intraoperative stimulation in patients with brain tumors. j neurosurg 92:589–598, 2000 6. martino, j., taillandier, l., moritz-gasser, s., gatignol, p., duffau, h. re-operation is a safe and effective therapeutic strategy in recurrent who grade ii gliomas within eloquent areas. acta neurochir. 151(5):427-36; discussion 436, 2009. 7. mcdonald jd, chong bw, lewine jd, et al: integration of preoperative and intraoperative functional brain mapping in a frameless stereotactic environment for lesions near eloquent cortex. technical note. j neurosurg 90:591–598, 1999 8. mcgirt m.j., chaichana k.l., gathinji m., attenell f.j., than k., olivi a., weingart j.d., brem h., quiñones-hinojosa a. independent association of extent of resection with survival in patients with malignant brain astrocytoma. j neurosurg 110:156–162, 2009 9. meyer, b. introduction: surgery of limbic and paralimbic gliomas. neurosurg focus 27 (2):e1, 2009. 10. plaza, m., gatignol, p., leroy, m., duffau, h. speaking without broca's area after tumor resection. neurocase, mar 9:1-17, 2009. 11. von lehe, m., schramm, j. gliomas of the cingulate gyrus: surgical management and functional outcome. neurosurg focus 27 (2):e9, 2009. microsoft word 3.radoim_meningioma_f.doc romanian neurosurgery (2012) xix 2: 103 – 109 103 meningioma of the pineal region m. radoi, l. danaila, f. stefanescu, r. vakilnejad, roxana popa neurosurgery clinic of the national institute of neurology and neurovascular diseases, bucharest abstract meningiomas rarely occur in the pineal region, but they can reach huge diameters. we presented the case of a patient with a very large meningioma of the pineal region (6x5x4 cm). the tumor, developed from the falcotentorial junction, was totally removed via an occipital interhemispheric transtentorial approach with minimal postoperative neurological deficits. the postoperative course was complicated with an acute internal hydrocephalus that needed temporary placement of an external ventricular drainage. the supratentorial surgical corridors allow for increased exposure and are best suited for falcotentorial meningiomas. introduction pineal region tumors are very rare comprising about 1% of all intracranial neoplasms (10). neoplasms of the pineal region are of a great hystological variety, which suggest their origin either from the pineal parenchymals cells or from other cell lines (astrocytes, germ cells, arachnoid cells). among this variety of tumors, meningiomas of the third ventricle and pineal gland have been only rarely reported in the literature cushing and eisenhardt (7), in an extensive series of meningiomas, showed no cases of pineal region meningiomas. sachs et al. (21) reported three cases of pineal region meningiomas in 1962 and found only 20 cases in the literature at that time. in a similar review, piatt and campbell (19) revealed in 1983, 37 cases from the literature, including two of their own. in the recent neurosurgical literature, meningiomas of the pineal region are, usually, presented as case reports, included 1-3 cases per report (4, 13, 24). in this report, we presented our surgical experience with one case of a very large pineal meningioma. case report we reported the case of a 67 years old male patient, with a one year history of headache and deficits in memory, symptoms that worsen progressively, being associated in the last month with diplopia and spontaneous tremor in the right hand. on admission in our clinic, the neurological examination revealed irregular balance disorders, without motor deficits, bilateral cutaneous plantar reflex in extension, horizontal nystagmus and vertical paresis of vision (parinaud syndrome). visual acuity decreased in the right eye, but the visual field was normal. fundus examination revealed bilateral papillary oedema. as his psychic was concerned, the patient was alert and oriented (gcs=15 pct.). cerebral ct-scan examination showed a well circumscribed tumor, which measured 6x5x4 cm. in diameters, located 104 radoi et al meningioma of the pineal region periventricular in the pineal region, with uniform and intense contrast enhancement (figure 1 a, b). the tumor presented a small, central, hyperdense area (calcification) and produced moderate supratentorial obstructive hydrocephalus. cerebral angiography showed that the internal cerebral veins and vein of galen were stretched and significantly displaced downwords. a b figures 1 a, b axial contrast cerebral ct-scan showing a well circumscribed, approximately 6 cm. in diameter meningioma, located periventricular in the pineal region, with uniform and intense contrast enhancement the patient was operated using a right occipital interhemispheric transtentorial approach. the tumor was a firm, vascularized tissue mass, whitish-yellowish in colour. under microscope magnification we performed a total resection of the tumor. the histological exam revealed a fibrous meningioma with colagenic proliferation areas. after a good recovery in the first postoperative day, without neurological deficits, the patient became somnolent and soon he lapsed into a superficial coma state. thus, 48 hours after surgery, we performed a cerebral ct scan, which showed an acute internal hydrocephaly. an external ventricular drainage was performed in emergency. in the following days the neurological recovery of the patient was good. the external ventricular drainage was maintained 6 days, and after its removal a cerebral ct-scan was performed, which showed the reduction of the ventricular size. when he had left the hospital, twenty days after the first operation, the patient presented only a moderate left hemiparesis and left homonymus hemianopsia. periodical postoperative follow-ups, at 6, 12 and respectively 24 months demonstrated a good general and neurological condition of the patient with minor neurological deficits. control cerebral ct-scans showed moderate internal hydrocephalus, without signs of periventricular cerebrospinal fluid resorbtion, and absence of any local recurrence (figure 2 a, b). romanian neurosurgery (2012) xix 2: 103 – 109 105 a b figures 2 a, b axial contrast cerebral ct-scan, performed 20 months after the operation, showed reduced hydrocephaly and absence of any intracerebral tumoral mass in the pineal region discussion meningiomas of the pineal region could be divided into two major groups, depending on their origin: 1. meningiomas arising from the free edge of the tentorium, where it is joined by the inferior margin of the falx (falcotentorial jonction); they secondarily invade the pineal and posterior third ventricular region and there were authors who considered that pineal region meningiomas are, in fact, extensions of meningiomas of the posterior falx or midline tentorial meningiomas (6, 17) 2. meningiomas developed from the velum interpositum, the space between the two layers of the tela choroidea. these meningiomas have no dural attachment because tela choroidea is formed only by the pial and arachnoidal layer of the meninges; they are exclusively located in the posterior third ventricle, presenting as a pineal region mass and should be distinguished from those developing in the anterior third ventricle (6). an important difference between the categories that comprise meningiomas of the pineal region, despite their dural attachments, lies in the origin of their blood supply. the velum interpositum meningioma, attached to the tela choroidea, receives its blood supply from the posterior choroidal arteries and, if the tumor extends anteriorly, from the anterior choroidal artery. meningiomas arising from the free edge of the tentorium derive their blood supply from branches of the internal carotid artery supplying the falx and tentorium, of which the bernasconi and cassinari artery is the most important (18). patients with meningioma are usually older than those with other pineal region tumors; there is also a female predominance (14). the most frequent clinical symptoms are related to raise intracranial pressure from insidious hydrocephalus. these most often include headache, gait disturbance, cognitive dysfunction and papilledema. other onset symptoms include signs of 106 radoi et al meningioma of the pineal region ataxia, visual disturbances, hearing loss, hemifacial spasm or vertical paresis of vision (parinaud’s syndrome) (1). in pineal region meningiomas, the cytological examination of the cerebrospinal fluid and the dosage of the malignant germcell markers (-fetoprotein and -human chorionic gonadotropin) in the patients’ blood are negative and provide little diagnostic value in limiting the differential diagnosis. therapeutic considerations the location of the pineal region in the centre of the brain, above the brain stem, presents a surgical challenge to safely expose and resect a pineal region tumor. the goal of surgery for pineal region tumor vary depending on the clinical circumstances of an individual situation. thus, the prognosis for pineal meningiomas became excellent. many are encapsulated, affording a direct microsurgical exposure and disection, and a gross total resection. a minimum goal should be to establish a histologic diagnosis by stereotactic biopsy. it provides direct tumoral tissue sampling for diagnosis and guides further operative or nonoperative therapy (3). al-mefty and al. sustain that if neuroradiologic image is pathognomonic for a meningioma, it is advisable to proceed to direct microsurgical approaches (2). complete resection of pineal region meningiomas depends upon adherence of the tumoral mass to the surrounding vital structures. in general, gross total resection of velum interpositum meningiomas is more likely than of the falcotentorial variety, in which case dural tentorial adherence and venous sinus involvment create the potential for subtotal resection. surgical approaches to the pineal region include the supratentorial and infratentorial approaches. the infratentorial supracerebellar approach is well suited for meningiomas arising from velum interpositum, without dural attachment. the supratentorial approaches are more complicated because of their variable anatomy and are best suited for falcotentorial meningiomas, as they allow intraoperative options for tentorial or falx incisions and permit the deprivations of the tumor’s blood supply at its base. internal hydrocephalus occurs frequently in patients with neoplasm of the pineal region. the choice of optimal surgical attitude varies from case to case. in patients having minimal neurological signs or when a strong suspicion of a potentially benign, excisable tumor exists, direct surgery is the first option, because the removal of the tumor relive hydrocephalus or a temporary ventricular drain can be placed at the time of surgical resection. in patients who have signs of an acute hydrocephalus and in whom a reduction in intracranial pressure is desirable prior to an open resection, a ctguided stereotactic endoscopic third ventriculostomy is the method of choice (11). the choice of optimal approach depends on the anatomical extent of the meningioma, its relation with the surrounding structures, its presumed origin (falcotentorial or velum interpositum) as well as the preference and experience of the operating neurosurgeon (9, 20). in our case we chose a supratentorial occipital linterhemispheric transtentorial approach because we considered that the meningioma developed from the falcotentorial margin. in a brief description we presented some advantages and disadvantages of the main operative approaches. a) the infratentorial supracerebellar approach to the pineal region was first utilized by krause in the 1920s and romanian neurosurgery (2012) xix 2: 103 – 109 107 developed and popularized by stein in the 1970s (26, 27). it is indicated for small meningiomas arising from the velum interpositum. this approach presents the following advantages: (1) – a direct central midline approach to the tumor, (2) – avoidance of injury to the deep venous system since the tumors are ventral to the deep venous system, (3) – has no morbidity related to the parietal or occipital lobe retraction. as disadvantages of this approach could be mentioned: (1) – the narrow space to expose the meningioma, because of the small distance between the coliculi and tentorial hiatus, (2) – the sacrifice of vermian veins, (3) – the difficulty to reach lesions above the tentorial notch. b) the supratentorial approach to the pineal region was first performed by dandy (11) in 1921, then by kunicki (18) and others. dandy utilized a large parietooccipital bone flap and a parasagittal approach to the pineal region. after opening the dura, multiple opperative corridors may be developed depending on the size and location of the tumor in order to allow an optimal intraoperative exposure of the pineal region. these include a tentorial incision, a falcine incision, splenial retraction or incision of the posterior body of the corpus callosum (4, 8, 14, 24): a) the occipital transtentorial approach is indicated for meningiomas arising primarily from the free edge of the tentorium. this approach provides an excellent view both above and below the tentorial notch, a great exposure of the lesion and view of the quadrigeminal region. choosing this approach may damage the occipital lobe and the splenium of the corpus callosum and, also, it may be difficult to reach parts of the meningioma extending to the opposite side. b)the transcallosal interhemispheric approach is the most suitable for large meningiomas, located in the pineal region, in the posterior third ventricle or tumors extending anterior to the level of the adhesio interthalamica. this approach has the advantage of providing an excellent view of meningiomas located in the posterior third ventricle. the main disadvantage is the possible damage of the posterior portion of the corpus callosum or the fornix. the occipital transtentorial approach can be performed with the patient in sitting or the prone position. aussman (4) described a three-quarter prone position for the occipital transtentorial approach to eliminate the risk of embolism. despite the fact the prone position eliminates the need for retraction of the occipital lobe due to gravity and is more comfortable for the surgeon, konvalov (14) prefers the occipital transtentorial approach in sitting position, because the visualization of the controlateral rosenthal vein and surgeon intraoperative orientation are more difficult in prone/three-quarter prone positions. we chose the prone position for our occipital transtentorial approach. sekhar (24) and ziyal et al (29) described transsinus transtentorial approaches to large pineal meningiomas in 1992. after removal of the tumor they resutured the transverse sinus to reestablish the blood circulation. kawashima et al (13) proposed a new approach, but only at the level of anatomical study, called the occipital bitranstentorial falcine approach, which is a modification of occipital transtentorial approach. in the same way, in 1990, van den berg proposed the lateral-paramedian infratentorial approach, which is a modification of the infratentorial supracerebellar approach (28). thus, the 108 radoi et al meningioma of the pineal region unilateral cerebellopontine angle is explored, and from there, the tentorial notch is reached over the ipsilateral cerebellar hemisphere. the meningioma can be dissected between the internal cerebral vein and the basal vein of rosenthal. adjuvant therapy in the treatment of pineal meningiomas has enhanced the possibility of cure or, at least, has improved the postoperative clinical results. for subtotal resected meningiomas radiation therapy should be utilized, either by conventional means or stereotactic radiosurgery. several retrospective studies have supported the use of radiotherapy in the management of pineal meningiomas following subtotal resection (5). this result also applied to subtotal resection following surgery for recurrent meningioma. radiotherapy is indicated for the overall management of aggressive meningiomas (22). taking into account the difficulties of a direct surgical approach to the pineal region, for meningiomas less than 2-3 cm. in size or for the recurrent ones, stereotactic surgery could be a valid solution (5). prognosis the neoplasms of the pineal region have an overall operative mortality in the range of 3%, with morbidity in the range of 4% (27). patients with pineal region tumors have a five-year survival in the range of 55% (1). a favourable outcome occurs over 90% of the time (23). among these, meningiomas, especially total removed meningiomas, have a very good long-term prognosis. in case of pineal region meningiomas, benign and encapsulated tumors, the success rate approaches 100% (4, 13). the long-term prognosis and risk of recurrence was directly related to the extent of surgical resection and the completeness of resection (25). atypical or anaplasic meningiomas have an increased risk of recurrence (12, 27). significant prognostic factors for a pineal region meningioma are: (1) – the extent of removal, (2) – preoperative clinical condition, (3) – postoperative clinical condition and (4) histological type. conclusions pineal region surgery, in which the experience of the neurosurgical team plays a very important role, was continually successful in the last years. total or partial resection of pineal meningioma by direct neurosurgical approaches can be achieved in most cases with low morbidity and depend upon the tumor’s dural attachment at its base and its relationship with the surrounding vital structures. usually, the total removal of the pineal region meningioma reestablish the cerebrospinal circulation at the end of the operation. large pineal region meningioma (> 5cm) should be operated through a unilateral or bilateral occipital interhemispheric transtentorial approach, regardless of the angiographic findings, because this provide a wide operative field and can be followed when necessary, by an infratentorial supracerebellar approach. corresponding author: dr. radoi mugurel e-mail address – muguradoi@yahoo.com references 1. allen jc, bruce jn, kun le, langford la. pineal region tumors. in : levin va, ed. cancer in the nervous system, new york: churchill livingstone, 1996: 171186. 2. al-mefty et al. meningiomas. in: raven press, ltd., new york, 1991: 583-591. 3. apuzzo mlj, chandrasoma pt, breeze re, cohen dm, luxton g, mazumder a. applications of imagedirected stereotactic surgery in the management of intracranial neoplasms. in: heilbrun pm (ed). concepts in neurosurgery: stereotactic neurosurgery, vol 2. baltimore: williams&wilkins, 1988; 73-132. romanian neurosurgery (2012) xix 2: 103 – 109 109 4. ausman ji, malik jm, dujovny m, mann r. pineal region: rare location of a cavernous haemangioma. neurol res 16 (2); 133-136, 1994. 5. bararo nm, gutin ph, wilson cb, sheline je, boldrey eb, wara wm. radiation therapy in the treatment of partially resected meningiomas. neurosurgery 1987; 20: 525-528. 6. camins mb, schlesinger eb. treatment of tumors of the posterior part of the third ventricle and the pineal region: a long-term follow-up. acta neurochir (vienna) 1978; 40: 131-143. 7. cushing h, eisenhardt l. meningiomas: their classification, regional behaviour, life history, and surgical end results. springfield, illinois: charles c. thomas, 1938. 8. danaila l, petrescu da, stefanescu f. our experience in surgery of tumors of the third ventricle. rom neurosurg 1997; new series 1-2: 49-61. 9. dandy we. an operation for the removal of pineal tumors. surg gynecol obstet 1921; 33: 113-119. 10.edwards msb, hudgins rj, wilson cb, levin va, wara wm. pineal region tumors in children. j neurosurg 1988; 68: 689-697. 11.goodman r. magnetic resonance imaging-directed stereotactic endoscopic third ventriculostomy. neurosurgery, 1993; 32: 1043-1047. 12.jaaskelainen j, haltia m, servo a. atypical and anaplastic meningiomas: radiology, surgery, radiotherapy and outcome. surg neurol 1986; 25: 233242. 13.kawashima m, rhoton al jr, matsushima t: comparison of posterior approaches to the posterior incisural space: microsurgical anatomy and proposal of a new method, the occipital bi-transtentorial/falcine approach. neurosurgery 51 (5); 1208-1220, 2002. 14.konovalov an, spallone a, pitzkhelauri di: meningioma of the pineal region:a surgical series of 10 cases. j neurosurg 85;586-590, 1996. 15.kunicki a: operative experience in 8 cases of pineal tumors. j neurosurg 17:815-823, 1960. 16.markwalder tm, markwalder rv, markwalder hm. meningioma of the anterior part of the third ventricle: case report. j neurosurg 1979; 50: 233-235. 17.obrador s, soto m, gutierrez-diaz ja. surgical management of tumours of the pineal region. acta neurochir (vienna) 1976; 34: 159-171. 18.papo i, salvolini u. meningiomas of the free margin of the tentorium developing in the pineal region. neuroradiology 1974; 7: 237-243. 19.piatt jh jr, campbell ga. pineal region meningioma: report of two cases and literature review. neurosurgery 1983; 12: 369-376. 20.rhoton al jr. microsurgical anatomy of the third ventricular region. in: apuzzo mlj (ed). surgery of the third ventricle. baltimore: williams&wilkins, 1987: 92166. 21.sachs e jr, avman n, fischer rg. meningiomas of the pineal region and posterior part of 3rd ventricle. j neurosurg 1962; 19:325-331. 22.salazar om. ensuring local control in meningiomas. int j radiat oncol biol phys 1988; 15: 501-504. 23.schild se, scheithauer bw, schomberg pj, et. al. pineal parenchimal tumors: clinical, pathologic, and therapeutic aspects. cancer 1993; 72: 870-880. 24.sekhar ln, goel a. combined supratentorial and infratentorial approach to large pineal meningioma . surg neurol 37 (3); 197-201, 1992. 25.simpson d. the recurrence of intracranial meningiomas after surgical treatment. j neurol neuropsychiatry 1957; 20: 22-39. 26.stein bm. infratentorial supracerebellar approach. in: apuzzo mlj (ed). surgery of the third ventricle. baltimore: williams&wilkins, 1987; 570-590. 27.stein bm, bruce jn. surgical management of pineal region tumors. in: clinical neurosurgery, vol 39, williams&wilkins, 1992: 509-532. 28.van der bergh r. lateral-paramedian infratentorial approachin lateral decubitus for pineal tumors. clinical neurology and neurosurgery 92 (4); 311-316, 1990. 29.ziyal im, sekhar ln, salas e, olan wj. combined supra/infratentoria-transsinus approach to large pineal region tumors. j neurosurg 88; 1050-1057, 1998. microsoft word 13samanci_extramedullary romanian neurosurgery (2013) xx 4: 393 396 393 extramedullary myxopapillary ependymoma of the filum terminale associated with syringomyelia: a case report yavuz samanci, suat erol celik neurosurgery department, ministry of health okmeydani education and research hospital, istanbul, turkey abstract aim: ependymomas compose the majority of all intradural intramedullary spinal lesions. filum terminale lesions are rarely associated with syringomyelia. here we describe a case of extramedullary myxopapillary ependymoma associated with extensive syringomyelia located in the filum terminale. material and methods: a 34-year-old man admitted to our clinic with complaints of bilateral leg weakness, back pain and urinary dysfunction. the magnetic resonance imaging (mri) of the patient showed us a contrast enhanced intraspinal mass at the level of l2 with a syringomyelia extending from l2 level to th7 level. results: the patient was operated via lumbar laminoplasty and tumor was totally resected. conclusion: the removal of tumor is also sufficient for the resolution of syringomyelia and no additional procedure is essential for the treatment of syringomyelia in such cases. this is the first case of extramedullary tumors of the cauda equine with extensive syringomyelia. key words: ependymoma, filum terminale, syringomyelia. introduction and aim of the paper ependymomas compose the majority of all intradural intramedullary spinal lesions and consist 60% of all glial tumors in spinal cord (1, 2). ependymomas are usually seen in cervical region (44%), followed by thoracic region (26%). intradural intramedullary tumors are commonly related with syringomyelia in the cervicothoracic region and majority of these tumors are glial tumors. filum terminale lesions are rarely associated with syringomyelia. here we describe a case of extramedullary myxopapillary ependymoma associated with extensive syringomyelia located in the filum terminale. material and methods a 34-year-old man was admitted to our hospital with the complaints of bilateral weakness in lower extremities, back pain and urinary dysfunction. the symptoms began three years before the admission and rapidly progressed in the last three months. neurological examination revealed paraparesis (grade 3/5) and diminished sensation below the th 8 level. deep tendon reflexes were reduced at the right lower extremity while they were increased at the right lower extremity. the anal sphincter tone was also decreased. the mri of the patient showed us a contrast enhanced intraspinal mass lesion at the level of l 2 with a syringomyelia extending from l 2 level to th 7 level (figure 1, figure 2). 394 samanci, celik extramedullary myxopapillary ependymoma of the filum terminale a laminoplasty from l1 to l3 was performed. when the dura was opened, a dark brown extramedullary tumor 3 cm in length was encountered. the tumor aroused from the filum terminale and displaced the nerve fibers of cauda equina anteriorly and laterally (figure 3). the tumor was excised by microsurgical techniques. a thin membranous tissue covering syringomyelic cavity was opened during the tumor removal and slightly xanthochromic cystic fluid was drained. figure 1 pre-operative gadolinium-enhanced, t1-weighted sagittal mri of the lumbar spine shows an extramedullary tumor with homogeneous enhancement at the l2 level figure 2 t2-weighted sagittal mri of the thoracic spine demonstrates thoracolumbar syringhydromyelia figure 3 on the left side arrow 1 shows the nerve root, arrow 2 shows the filum and arrow 3shows the extramedullary ependymoma romanian neurosurgery (2013) xx 4: 393 396 395 figure 4 t2-weighted sagittal mri of thoracolumbar spine shows significant improvement of the syringohydromyelic cavity and total removal of the tumor results postoperative course was uneventful and lower extremity weakness of the patient improved (grade 4/5) immediately. histopathological examination was reported as “myxopapillary ependymoma”. three years after the operation, the patient was neurologically intact except an intermittent urinary dysfunction. control mri revealed total removal of the tumor and disappearance of syringomyelia (figure 4). discussion syringomyelia associated with spinal tumors is common. in most cases, tumors are intramedullary glial tumors located in the cervicothoracic region (1, 3). however, the tumors which are located in the distal end of the spinal cord rarely cause syringomyelia (1). barnett and rewcastle reviewed seven cases of cauda equina and filum terminale tumors causing syringomyelia including five autopsy cases and two surgical cases (1). other cases of intramedullary ependymoma of the conus medullaris associated with syringomyelia extending from cervical region were reported by mccormick and sarikaya et al. (4, 5). however, in the case reported by nagahiro et al. the tumor was an extramedullary epandymoma located in the cauda equina (6). in our case the tumor was purely extramedullary and aroused from the filum terminale. this is the first case of extramedullary tumors of the cauda equina with extensive syringomyelia documented in the mri era. the pathogenesis of syringomyelia associated with spinal cord tumors is still not well understood. it is usually believed that the effects of tumor including intramedullary softening due to a disturbed blood supply, stasis of the tissue fluid resulting from occlusion of drainage pathways, spread of edema, and hemorrhage into the cord from the tumor are responsible for the development of syringomyelia (1, 6, 7). however, the reason for the occurrence of syringomyelia associated with the tumors is uncertain. probably the other entity known to be associated with syringomyelia such as chiari i malformation, trauma, arachnoiditis, degenerative diseases of the spine, disturbance of the cerebrospinal fluid flow because of obliteration of the 396 samanci, celik extramedullary myxopapillary ependymoma of the filum terminale subarachnoid space play an important role in the development of the syringomyelia. the subarachnoid space and extracellular space of the central nervous system act as a single fluid compartment without any barrier to prevent the fluid movements between them (7, 8). however, the removal of tumor is also sufficient for the resolution of syringomyelia and no additional procedure is essential for the treatment of syringomyelia in such cases. conclusion a unique patient with extramedullary myxopapillary ependymoma located in the filum terminale associated with extensive syringomyelia has been reported. serial mri demonstrated the total removal of the lesion and spontaneous resolution of the syringomyelia. corresponding author: yavuz samanci, m.d. neurosurgery department, ministry of health okmeydani education and research hospital darulaceze caddesi no: 25, okmeydani-sisli phone: +90 212 2217777 fax: +90 212 2217800, 34384, istanbul, turkey e-mail: mysamanci@hotmail.com suatmd@gmail.com references 1. barnett hjm, rewcastle nb. syringomyelia and tumours of the nervous system. barnett hjm, foster jb, hudgson p, editors. major problems in neurology, vol. 1. london: saunders. 261–300, 1973. 2. ferry dj, hardman jm, earle km. syringomyelia and intramedullary neoplasms. med ann dist columbia. 38:363–5, 1969. 3. sloof jl, kernohan tw, maccarthy cs. primary intramedullary tumor of the spinal cord and filum terminale. philadelphia, saunders. pp 180-189, 1964. 4. mccormick pc, torres r, post kd. et al. intramedullary ependymoma of the spinal cord. j neurosurg. 72:523–32, 1990. 5. sarikaya s, acikgoz b, tekkok ih. et al. conus ependymoma with holocord syringohydromyelia and syringobulbia. journal of clinical neuroscience 14:901– 904, 2007. 6. nagahiro s, matsukado y, kuratsu j. et al. syringomyelia and syringobulbia associated with an ependymoma of the cauda equina involving the conus medullaris: case report. neurosurgery. 18:357–60, 1986. 7. samii m, klekamp j. surgical results of 100 intramedullary tumors in relation to accompanying syringomyelia. neurosurgery. 35:865–73, discussion 73, 1994. 8. pai sb, krishna kn. secondary holocord syringomyelia with spinal hemangioblastoma: a report of two cases. neurol india. 51:67–8, 2003. microsoft word 1_alvis-mirandahernando_traumatic_2 romanian neurosurgery (2013) xx 2: 125 – 137 125 traumatic cerebral contusion: pathobiology and critical aspects hernando alvis-miranda, gabriel alcala-cerra, luis rafael moscote-salazar universidad de cartagena abstract traumatic brain injury is a major cause of mortality in developed countries. cerebral parenchymal injury is evidenced by a significant percentage of patients. the most important structural lesion of the brain is the cerebral contusion, which is a complex and dynamic area, a result of the primary lesion and which is associated with ischemic and inflammatory phenomena that need to be known by the neurosurgeon. we present a review of the most important aspects of brain contusion. key words: brain contusion, focal traumatic brain injuries, traumatic brain injury. introduction traumatic brain injury (tbi) is an important public health problem and is the leading cause of mortality, morbidity, and disabilities in children and young adults, especially in young males (15-35 years old) (1). internationally, tbi accounts for significant socio-economic implications; in the us alone, over 1.7 m individuals suffer a tbi each year (2). one of the main characteristic of tbi is that patients without a severe tbi, can experience subsequent mental and/or medical problems (3, 4). the acute consequences of tbi are just only a half of the complete problem, the longterm repercussions of tbi are substantial especially among adolescents and young adults, whose brains continue to mature and develop (5). focal brain injury, is defined as a localised damage to the brain in form of laceration, contusion and haematoma occurring in the presence or absence of a skull opening from either a pre-trauma trephination or a mechanic fracture caused by the impact itself (6). from the focal brain injuries, cerebral contusions (cc) are one of the most common traumatic findings, being present in up to 31% of initial imaging studies (ct-scans) of patients with tbi (7). it has been reported that contusions occurred in 89% of brains examined postmortem (8). cc is a type of focal tbi, resulting from direct loading and often occurs in the absence of widespread injury (9), representing focal regions of traumainduced subpial hemorrhage and swelling, zones of cellular injury where the microvasculature is also disrupted (10). pure cc are fairly common, found in 8% of all tbi (11, 12) and 13% to 35% of severe injuries (11). the vast majority of contusions occur in the frontal and temporal lobes, although they can occur at almost any site, including the cerebellum and brainstem (13). ratnaike et al (14) founded retrospectively 126 alvis-miranda et al traumatic cerebral contusion that most blows causing cc are to back of the head, being most contusions contrecoup lesions affecting the frontal and temporal lobes. any intracranial contusion, as other focal injuries such as hematoma, or brain laceration falls within the category of severe tbi (15). this work aims to review critical aspects of cc in clinical practice, such as pathophysiology, diagnosis and management. characterization cc are more common in regions that contact bony surfaces in the cranial vault during trauma: frontal and temporal poles, orbitofrontal gyri, perisylvian cortices, and inferolateral temporal lobe surfaces (16). contusions can be characterized by mechanism, anatomic location, or adjacent injuries. table 1 summarizes main characteristics of each one. pathophysiology in tbi, the primary injury to the brain is caused by the initial mechanical impact, resulting in skull fracture, cc, and vascular and parenchymal injury causing intracranial bleed and ich. an inflammatory process, edema formation, and excitotoxicity follow, resulting in further increase in icp and reduced cerebral perfusion pressure (cpp) (17, 18). despite the prevalence of such injury, the injury mechanism leading to cc has long been studied but still remains unclear. as part of tbi, cc is a complex neurological event that results in the disruption of numerous cellular and physiological processes (19). biomechanical forces tbi results from the transfer of energy from the environment to brain tissue that is greater than the amount that can be absorbed without dysfunction. traumatic insults generally occur over short periods of time and are referred to as dynamic loading, and includes both direct or impact loading, as well as impulsive loading whereby no physical contact occurs (9). table 1 characterization of cerebral contusions fracture contusions result from direct contact injuries and occur immediately adjacent to a skull fracture. coup contusions refer to those that occur at the site of impact in the absence of a fracture. contrecoup contusions are those that are diametrically opposite to the point of impact. gliding contusions are focal hemorrhages involving the cortex and adjacent white matter of the superior margins of the cerebral hemispheres; they are due to rotational mechanisms rather than contact forces. intermediary contusions are lesions that affect deep brain structures, such as the corpus callosum, basal ganglia, hypothalamus, and brainstem. herniation contusions can occur in areas where the medial parts of the temporal lobe contact the tentorial edge (i.e., uncal herniation) or where the cerebellar tonsils contact the foramen magnum (i.e., tonsillar herniation). adapted from (16) romanian neurosurgery (2013) xx 2: 125 – 137 127 the loads absorbed by the brain after trauma generally include linear and rotational components called angular loads. the rate and duration of the insult are important because loads applied at high rates tend to result in more damage (9). cc and other focal injuries result from direct loading and often occurs in the absence of widespread injury (9). pericontusional zone (pcz) is recognized as the rim of edematic nonnecrotic tissue surrounding the central necrotic core in the acute phase of traumatic cerebral contusion (20). pcz has the potential to cause prolonged and deteriorated neurological and neuropsychological change (20). there have been arguments regarding whether intracranial pressure (icp) or tissue strain causes cc (21). traditionally, positive (compressive) icp has been believed to induce cc under the impact site (22). cerebral and systemic changes induced by cerebral contusion following tbi, an abundance of biochemical events is directed to the ensuing brain parenchyma destruction. figure 1 schematic cascade of events triggered by tbi adapted from (24) 128 alvis-miranda et al traumatic cerebral contusion focal vascular alterations restrict the delivery of substrates to the brain such as oxygen and glucose, driving to energy depletion, ionic gradients that are necessary to maintaining membrane potential are lost, resulting in neuronal and glial depolarizations (23). the pathogenesis of cc results from interrelated multifactorial phenomena involving anatomical and functional microcirculatory alterations; all are a continuum of deleterious effects that drives brain parenchyma to suffering and death, figure 1, schematizes these effects. tbi is associated with a cerebral inflammatory response characterized by microglial and astrocytic activation, as well as release of inflammatory mediators (25). pro-inflammatory cytokines such as il1β, il-6 and tnf-α have been linked to the early events mediating bbb breakdown and subsequent development of cerebral edema (26). tnf-α directly disturbs bbb integrity, leading to cerebral edema and leukocyte infiltration (27). vascular alteration – cerebral blood flow and perfusion head trauma causes rupture of cerebral small blood vessels at an early period, especially in white matter. spasm of the larger cerebral arteries after head trauma has been postulated in several works to be the main cause of cerebral ischemia; however, measurements of cerebral blood volume are more compatible with compromised microcirculation in the cerebral tissue (28). ischemia and contusion are directly correlated with the severity of the injury (29–31). unfortunately the contusionassociated microvascular alterations have been inadequately studied (32); this is due to the fact that researches focused mainly on alterations in the neural tissue, giving less emphasis to the mechanisms that give rise to ischemic brain damage. however the evidence indicates that three major factors are involved, these are (32): 1. increases in the intercellular cytosolic calcium concentration 2. acidosis 3. free radical production in severe tbi, cpp, which is defined as the difference between mean arterial pressure and icp, at a level lower than 70 mmhg serves as a clinical threshold for adverse outcome (33). in 1957, freytag and lindenberg demonstrated two components of cc: the central core area in which cells undergo necrosis and the peripheral (rim) area in which cellular swelling occurs (34) hacer imágen. in the central core area, the cbf is 4.7 ml/100g/min, and of 16-18 ml/100g/min in the peripheral zone (24). normally, cbf is >50 ml/100g/min, and the ischemic threshold is commonly considered to be 18-20 ml/100g/min (35– 37). the decrease of abp, the development of ich, and decrease in cpp are related to disturbances in blood vessel sensitivity in the hypoperfusional zone (36, 38–40). in the clinical setting, low gcs associated with vasospasm has reported deficiencies in cerebral perfusion (41). the low cerebral perfusion following tbi is accompanied by a parallel decrease in btpo2 (42). katayama et al have reported that blood flow decreases 3 hours after the harmful event, implying the impact of adequate treatment and permanent multimodal monitoring to prevent expansion of this zone into the normal brain (43). romanian neurosurgery (2013) xx 2: 125 – 137 129 this zone can encompass approximately 15% of brain hemisphere, and in patients with poorer outcome can be very extensive, encompassing a large part of brain hemisphere (36, 44–48). however, lebedev et al. reported cases of hypoperfusional zone reduction (49), thus a good clinical management can avoid the increase of this zone and its expansion into the normal brain, preventing an irretrievable brain damage. schröder et al, demonstrated in 1995 the absence of reperfusion in this zone (39). the reduction of cbf may be due to vasoconstriction through the synthesis of endothelin-1 (50) on upregulated endothelin receptors a and b on blood vessels and neurons (51). conversely, a recent finding suggests that arteriolar diameters may increase and that the perceived decrease in vasculature may be due to thrombogenesis which can form within 1 h of injury (52). impairment of cerebral autoregulation bc is likely to cause severe damage in cerebral autoregulation. cerebral or pressure autoregulation is the inherent ability of blood vessels to keep cbf relatively constant over a wide range of arterial blood pressure (abp) or cerebral perfusion pressure levels by the interplay of numerous physiological mechanisms (37,53), mainly active variations of cerebrovascular resistance. once the autoregulatory mechanisms have been abolished, cbf passively follows changes in abp and impaired cerebral pressure. under these conditions, the brain becomes vulnerable to ischemic or hyperemic injuries if perfusion pressure does not remain coupled with metabolic demands (37) abp, icp, and cbf measurements provide important data about cerebral autoregulation (54–56). cerebral vascular autoregulation would recover on the fourth day after severe tbi, and cpp might be increased by recovery of autoregulation. thus, subsequent nonemergent surgery should be performed at least 4 days after severe tbi to prevent secondary brain injury. in addition, it should be kept in mind that the cerebral vulnerability might persist for 4 days after suffering severe tbi (57). excitotoxicity in moderate–severe tbi, the initial trauma from the brain injury can lead to immediate cell death through necrosis where the cell lyses and releases noxious substances such as inflammatory chemokines and cytokines, reactive oxygen species (ros) and proteases. changes in markers of metabolic impairment can occur before the onset of ich, suggesting that biochemical impairment can be present before low cerebral perfusion pressure is detectable (58). in particular, glutamate excitotoxicity is a contributor to cellular damage after injury (59) as it can cause persistent membrane depolarization, resulting in ion dyshomeostasis and consequent cell death (33), also its coagonist aspartate, and structural amino acids (threonine and valine) have been involved in parenchyma microdialysis probes or in cerebrospinal fluid (csf) as associated excitotoxic aminoacids (60,61). these aminoacids have been linked to the causation of both acute and chronic neuronal damage. as has been mentioned, increase of glutamate persistently activates ion channels, particularly n-methyl-d-aspartate channel. the dysregulation will affect the 130 alvis-miranda et al traumatic cerebral contusion physiological processes of the cortex and the hippocampus, because of their dependency regard to this aminoacid (60,62). as consequence of the permanent opening of n-methyl-d-aspartate channels, sodium and calcium penetrate into cells while potassium is extrude to the extracellular space. the consequences of ion dysregulation are velocity dependent, when happens rapid, it can result in massive accumulation of intracellular calcium with rapid neuronal death that can occur during the first day after the trauma, this process is also called “fast excitotoxicity” (24). when calcium entry is retarded neuronal death can be traced within the period of 5-7 days after the injury (63). the extruded potassium into the extracellular space causes a rapid swelling of astrocytes. this can, in turn, lead to “cytotoxic edema,” which is thought to cause ich. the blockage of glutamate by nmethyl-d-aspartate channel antagonists decreases the secondary damage of neuronal cells (64,65). clearly the more severe brain damage, the higher the increase of glutamate (63). heterogeneous mechanisms exist in early edema formation in cc, and cytotoxic edema plays an important role within 48 hours post-trauma; this early cellular swelling in the peripheral area begins within 6 hours following injury, a fact suggesting that the cbf does not decrease to ischemic level immediately following injury (66). brain ischemia cc can be accompanied by altered hemodynamic states, which can aggravate the initial traumatic injury, conducing to ischemia (63), table 2 summarizes some hemodynamic states and its definitions. table 2 altered hemodynamic states related to brain ischemia due to cc state characteristic hypoxemia pao2 < 60 mm hg hypotension < 50 mmhg for > 30 min. prior to resuscitation mean arterial blood pressure (mabp) hemispheric cbf < 20 ml/100g/min herniation fixed dilated pupil cpp < 50 mm hg for > 30 min several authors have suggested that cerebral ischemia or infarction can occur despite adequate control of icp and cpp (67–70). when glutamates increase up to 50-100 mmol/l, neuronal death can be detected within several hours due to their overexcitation (24). cc is crucial for the behavior of glutamate and for the increase of structural amino acids (threonine and valine) resulting from neuronal death. when combining ischemic events with cc the result is a more severe secondary neuronal damage. edema formation brain edema formation is a secondary injury caused by a cascade of mechanisms initiated at the moment of injury (71). in table 3 are listed the phases of brain edema due to cc. ich is a frequent complication of severe tbi (72–74), near to 70% of brain injured patients will present ich (75–78). life threatening episodes of raised icp are usually associated with conditions that afflict wide areas of the brain such as global cerebral swelling after a trauma (79). patients suffering from cc often develop edema and hic with a delayed onset, which causes impairment in neurological function and sometimes herniation although no further bleeding has occurred (80). after the traumatic event, local romanian neurosurgery (2013) xx 2: 125 – 137 131 damage and bbb breakdown lead to neurochemical mediator release and regional changes in cerebral edema (71, 81). the genesis of brain swelling in an area of cc implies multiple, but conventionally considered to result from a combination of vasogenic and cytotoxic edema mechanisms (83): vasogenic edema results from the breakdown of the blood brain barrier and extravasations of fluid into the extracellular space, which sets in only after 12-24 hrs (84) cytotoxic edema is the consequence of a hypoxic insult resulting in membrane pump failure and cellular swelling. it can occur early, but its quantum is insufficient to explain the mass effect that is clinically encountered. as mentioned, the early swelling around a cc which occurs in the first 24 hours and is often life threatening, cannot be explained by either of these factors. it appears that the capacity for edema fluid accumulation increases in the central area and resistance for edema fluid propagation is elevated by cellular swelling in the peripheral area (83). during the initial 2–3 days following tbi brain edema expands from the core, incorporating to the perilesional uninjured tissue (82). imaginological appearance cc appears as heterogeneous areas of brain necrosis, hemorrhage, and infarction and represents mixed-density lesions on brain-ct scan. multiple focal contusions have a “salt and pepper” appearance on ct. however the distinction between contusions and traumatic intracerebral hematomas remains difficult to define. a “salt and pepper” lesion is clearly a cc, but a large hematoma clearly is not. there is a gray zone, and contusions can, over a period of hours or days, evolve into intracerebral hematomas (13). due to the absence of ct-scan cc classification, we propose one, which consider three types (1 – 3) each one with two subtypes (a or b) taking considerations of size, uni/bilaterally location and mass effect, as described in table 4. table 3 brain edema phases in cc phase characteristics frist phase or ultraearly phase occurs within the first 24 hours and is often the cause of clinical deterioration or death. second phase or delayed phase sets in after 24 to 72 hours and progresses for 7-10 days. this swelling rarely contributes to clinically significant ich. third phase sets in with the lysis of rbc in the intracerebral clot. hemoglobin breakdown products activate reactive oxygen species, trigger cytokines (mainly il6 and il10) and activate the complement system (mainly c3d and c9 ) adapted from (10, 82). 132 alvis-miranda et al traumatic cerebral contusion cc are characterized by mixed densities of lesions, which are commonly surrounded by perilesional hypodense areas in close contact with the internal surface of the skull (85). inhomogeneity (a major therapeutic challenge) is often reflected on the initial ct scan by a salt and pepper appearance. although there is little debate that hyperdense regions represent hemorrhagic areas that can be safely evacuated, the significance of surrounding hypodense regions stills controversial (7). table 4 proposal of cerebral contusion imaginological (brain ct-scan) classification type description 1 a lobar microcontusions or cerebral contusions <1 cm b bilateral lobar microcontusions or cerebral contusions 2 a unilateral lobar contusions b bilateral lobar contusions 3 a hemispheric contusions with severe unilateral mass effect b hemispheric contusions with severe bilateral mass effect management because of cc tendency to enlarge over time and become significant space occupying lesions, it could leads rapidly to ich with subsequent clinical deterioration or worsening neurological condition (7, 85, 86), thus cc can become a major therapeutic challenge with critical functional importance whenever surgical removal of the lesion is contemplated in neurologically eloquent areas (7). cc treatment, as in others severe tbi, evolves rapidly with the addition of new technologies. traditionally, therapeutic treatment of tbi relied on strict monitoring and augmentation of icp, map and cpp, but currently the guidelines from the brain trauma foundation have recommended initiating treatment for icp values greater than 20 and maintaining cpp between 50 and 70 mmhg in order to improve outcomes (87). according to the clinical practice guidelines in severe tbi of taiwan (88), one of the indications for icp (grade b) monitors may be used on patients with severe tbi (gcs score 3-8) with abnormal ct scan findings, which include cc, hematomas, brain edema, and compressed basal cisterns, but also in the case of severe tbi with normal ct-scan findings but with at least 2 of the following conditions: (a) ≥40 years old; (b) unilateral or bilateral decerebrate or decorticated posture; (c) systolic blood pressure <90 mm hg; and can be considered individually for mild or moderate tbi. there are high-risk patients for convulsions, which can aggravate its neurological deficit extremely rapidly, which include those with the gcs score ≤10, cortical contusion, depressed skull fractures, subdural hematoma, epidural hematoma, intracerebral hemorrhage, penetrating head injury, and epileptic seizures within 24 hours after injury (88), thus in these patients, anticonvulsants medications should be considered. regard to surgical intervention, there still remain some debate about its value in the evacuation of intraparenchymal lesions, such as cc (89). currently is a readiness to surgically evacuate extraparenchymal hematomas but regard to intraparenchymal lesions have been adopted a conservative approach (89). the rationale include the removal of the edema which is producing osmotic load and also abolishing of necrotic romanian neurosurgery (2013) xx 2: 125 – 137 133 and apoptotic cascades triggered off by the products of blood degradation. cc surgical excision is best done conservatively with minimal or absent trauma to surrounding tissue, and ideally done through a limited and optimally placed cortical incision. in the case of hemorrhagic necrotic brain tissue may be sucked out through an appropriately placed pial-cortical window. however conservative contusectomies are best combined with a decompressive craniectomy. as a tool for the reduction of icp, decompressive craniectomy (dc) is very effective (90–92). the procedure aims at negating the pressure volume relationship of the closed cranial cavity. dc per se does not tackle the pathological brain swelling. however, increasing the size of the container it alleviates the effects of raised intracranial pressure. dc is indicated in a patient with a gcs score ≤13 or less with a midline shift of more than 5mm. bifrontal dc may be used to decrease icp in cases with generalized edema and central herniation. to remember, progression of hemorrhage/contusion (5%–58%) is a potential complications arising from dc (93, 94). conclusions cc is a dynamic and expansive process having pronounced effects not only in the vicinity of the contusion focus but also in more remote areas (hippocampus and the brain stem). cc has the tendency to enlarge over time and become significant space occupying lesions; it could leads rapidly to ich with subsequent clinical deterioration or worsening neurological condition. it can cause severe damage in cerebral autoregulation, leading to suffering parenchymal zones. because had been reported reduction of hypoperfusional zone it is comprehensible that good clinical management can avoid the increase of this zone and its expansion into the sourrounding normal brain. unfortunately the data regard to specifically cc is scarce, it is needed further concepts standardizations to give the best care to tbi patients. correspondence: dr. luis rafael moscote universidad de cartagena, colombia. e-mail: mineurocirujano@aol.com references 1.arabi ym, haddad s, tamim hm, al-dawood a, alqahtani s, ferayan a, al-abdulmughni i, al-oweis j, rugaan a. mortality reduction after implementing a clinical practice guidelines-based management protocol for severe traumatic brain injury. j crit care 2010;25:190–5. 2.faul m, xu l, wald m, coronado v. traumatic brain injury in the united states: emergency department visits, hospitalizations and deaths 2002-2006. atlanta, ga: centers for disease control and prevention 2010. 3.galarneau mr, woodruff si, dye jl, mohrle cr, wade al. traumatic brain injury during operation iraqi freedom: findings from the united states navymarine corps combat trauma registry. j neurosurg 2008;108:950–7. 4.okie s. traumatic brain injury in the war zone. n engl j med 2005;352:2043–7. 5.pujol j, vendrell p, junqué c, martí-vilalta jl, capdevila a. when does human brain development end? evidence of corpus callosum growth up to adulthood. ann neurol 1993;34:71–5. 6.morganti-kossmann mc, yan e, bye n. animal models of traumatic brain injury: is there an optimal model to reproduce human brain injury in the laboratory? injury 2010;41, supple:s10–s13. 7.soustiel jf, mahamid e, goldsher d, zaaroor m. perfusion-ct for early assessment of traumatic cerebral contusions. neuroradiology 2008;50:189–96. 8.cooper p. post-traumatic intracranial mass lesions. in: pr c, editor. head injury, lippincott williams & wilkins; 1982. 9.blyth bj, bazarian jj. traumatic alterations in consciousness: traumatic brain injury. emerg med clin 134 alvis-miranda et al traumatic cerebral contusion n am 2010;28:571–94. 10.mathai ki, sengupta sk, shashivadhanan, sudumbrekar sm. surgery for cerebral contusions: rationale and practice. the indian journal of neurotrauma 2009;6:17–20. 11.mandera m, zralek c, krawczyk i, zyciński a, wencel t, bazowski p. surgery or conservative treatment in children with traumatic intracerebral haematoma. childs nerv syst 1999;15:267–9; discussion 270. 12.bullock mr, chesnut r, ghajar j, gordon d, hartl r, newell dw, servadei f, walters bc, wilberger j. surgical management of traumatic parenchymal lesions. neurosurgery 2006;58:s25–46; discussion si–iv. 13.houseman c, belverud s, narayan r. closed head injury. in: ellenbogen r, abdulrauf s, editors. principels of neurological surgery, philadelphia: saunders elsevier; 2012, pp. 325–47. 14.ratnaike te, hastie h, gregson b, mitchell p. the geometry of brain contusion: relationship between site of contusion and direction of injury. british journal of neurosurgery 2011;25:410–3. 15.heegaard w, biros m. traumatic brain injury. emerg med clin n am 2007;25:655–78, viii. 16.shahlaie k, zwienenberg-lee m, muizelaar jp. clinical pathophysiology of traumatic brain injury. in: bullock mr, hovda da, editors. youmans neurological surgery, saunders elsevier; 2011, pp. 3362–79. 17.greve mw, zink bj. pathophysiology of traumatic brain injury. mt sinai j med 2009;76:97–104. 18.werner c, engelhard k. pathophysiology of traumatic brain injury. br j anaesth 2007;99:4–9. 19.degeorge ml, marlowe d, werner e, soderstrom ke, stock m, mueller a, bohn mc, kozlowski da. combining glial cell line-derived neurotrophic factor gene delivery adgdnf. with l-arginine decreases contusion size but not behavioral deficits after traumatic brain injury. brain research 2011;1403:45–56. 20.bao y-j, li l-z, li x-g, wang y-j. 17beta-estradiol differentially protects cortical pericontusional zone from programmed cell death after traumatic cerebral contusion at distinct stages via non-genomic and genomic pathways. molecular and cellular neurosciences 2011;48:185–94. 21.huang hm, lee mc, lee sy, chiu wt, pan lc, chen ct. finite element analysis of brain contusion: an indirect impact study. med biol eng comput 2000;38:253–9. 22.king ai. fundamentals of impact biomechanics: part i--biomechanics of the head, neck, and thorax. annu rev biomed eng 2000;2:55–81. 23.golding em. sequelae following traumatic brain injury: the cerebrovascular perspective. brain research reviews 2002;38:377–88. 24.ragaisis v. [brain contusion: morphology, pathogenesis and treatment]. medicina kaunas. 2002;38:243–9; quiz 354. 25.alvis-miranda hr, alcala-cerra g, moscote-salazar lr. microglia: roles and rules in brain traumatic injury. romanian neurosurgery 2013;xx:34–45. 26.ramilo o, sáez-llorens x, mertsola j, jafari h, olsen kd, hansen ej, yoshinaga m, ohkawara s, nariuchi h, mccracken gh. tumor necrosis factor alpha/cachectin and interleukin 1 beta initiate meningeal inflammation. j exp med 1990;172:497–507. 27.megyeri p, abrahám cs, temesvári p, kovács j, vas t, speer cp. recombinant human tumor necrosis factor alpha constricts pial arterioles and increases blood-brain barrier permeability in newborn piglets. neurosci lett 1992;148:137–40. 28.rodríguez-baeza a, reina-de la torre f, poca a, martí m, garnacho a. morphological features in human cortical brain microvessels after head injury: a three-dimensional and immunocytochemical study. anat rec a discov mol cell evol biol 2003;273:583– 93. 29.park e, bell jd, siddiq ip, baker aj. an analysis of regional microvascular loss and recovery following two grades of fluid percussion trauma: a role for hypoxiainducible factors in traumatic brain injury. journal of cerebral blood flow and metabolism�: official journal of the international society of cerebral blood flow and metabolism 2009;29:575–84. 30.rafols ja, kreipke cw, petrov t. alterations in cerebral cortex microvessels and the microcirculation in a rat model of traumatic brain injury: a correlative em and laser doppler flowmetry study. neurological research 2007;29:339–47. 31.hekmatpanah j, hekmatpanah cr. microvascular alterations following cerebral contusion in rats. light, scanning, and electron microscope study. journal of neurosurgery 1985;62:888–97. 32.daneyemez m. microangiographic changes following cerebral contusion in rats. neuroscience 1999;92:783–90. 33.kan em, ling e-a, lu j. microenvironment changes in mild traumatic brain injury. brain res bull 2012;87:359–72. 34.freytag e, lindenberg r. morphology of cortical contusions. ama arch pathol 1957;63:23–42. 35.depreitere b, aviv r, symons s, schwartz m, coudyzer w, wilms g, marchal g. study of perfusion in and around cerebral contusions by means of computed tomography. acta neurochir suppl 2008;102:259–62. 36.mclaughlin mr, marion dw. cerebral blood flow and vasoresponsivity within and around cerebral contusions. j neurosurg 1996;85:871–6. romanian neurosurgery (2013) xx 2: 125 – 137 135 37.bor-seng-shu e, kita ws, figueiredo eg, paiva ws, fonoff et, teixeira mj, panerai rb. cerebral hemodynamics: concepts of clinical importance. arq neuropsiquiatr 2012;70:352–6. 38.schalén w, messeter k, nordström ch. cerebral vasoreactivity and the prediction of outcome in severe traumatic brain lesions. acta anaesthesiol scand 1991;35:113–22. 39.schröder ml, muizelaar jp, bullock mr, salvant jb, povlishock jt. focal ischemia due to traumatic contusions documented by stable xenon-ct and ultrastructural studies. j neurosurg 1995;82:966–71. 40.shiina g, onuma t, kameyama m, shimosegawa y, ishii k, shirane r, yoshimoto t. sequential assessment of cerebral blood flow in diffuse brain injury by 123iiodoamphetamine single-photon emission ct. ajnr am j neuroradiol 1998;19:297–302. 41.shahlaie k, boggan je, latchaw re, ji c, muizelaar jp. posttraumatic vasospasm detected by continuous brain tissue oxygen monitoring: treatment with intraarterial verapamil and balloon angioplasty. neurocrit care 2009;10:61–9. 42.jaeger m, dengl m, meixensberger j, schuhmann mu. effects of cerebrovascular pressure reactivityguided optimization of cerebral perfusion pressure on brain tissue oxygenation after traumatic brain injury. crit care med 2010;38:1343–7. 43.katayama y, mori t, maeda t, kawamata t. pathogenesis of the mass effect of cerebral contusions: rapid increase in osmolality within the contusion necrosis. acta neurochir suppl 1998;71:289–92. 44.mcd anderson r, opeskin k. timing of early changes in brain trauma. am j forensic med pathol 1998;19:1–9. 45.adelson pd, whalen mj, kochanek pm, robichaud p, carlos tm. blood brain barrier permeability and acute inflammation in two models of traumatic brain injury in the immature rat: a preliminary report. acta neurochir suppl 1998;71:104–6. 46.baldwin sa, fugaccia i, brown dr, brown l v, scheff sw. blood-brain barrier breach following cortical contusion in the rat. j neurosurg 1996;85:476– 81. 47.lewén a, fredriksson a, li gl, olsson y, hillered l. behavioural and morphological outcome of mild cortical contusion trauma of the rat brain: influence of nmda-receptor blockade. acta neurochir wien. 1999;141:193–202. 48.yamaki t, murakami n, iwamoto y, sakakibara t, kobori n, ueda s, uwahodo y, kikuchi t. cognitive dysfunction and histological findings in rats with chronic-stage contusion and diffuse axonal injury. brain res brain res protoc 1998;3:100–6. 49.lebedev v v, krylov v v. [remarks on the pathogenesis of brain contusions occurring by a counterimpact mechanism in the acute period of their development]. zh vopr neirokhir im n n burdenko 1998:22–6. 50.steiner j, rafols d, park hk, katar ms, rafols ja, petrov t. attenuation of inos mrna exacerbates hypoperfusion and upregulates endothelin-1 expression in hippocampus and cortex after brain trauma. nitric oxide 2004;10:162–9. 51.kallakuri s, kreipke cw, schafer pc, schafer sm, rafols ja. brain cellular localization of endothelin receptors a and b in a rodent model of diffuse traumatic brain injury. neuroscience 2010;168:820–30. 52.schwarzmaier sm, kim s-w, trabold r, plesnila n. temporal profile of thrombogenesis in the cerebral microcirculation after traumatic brain injury in mice. j neurotrauma 2010;27:121–30. 53.lang ew, yip k, griffith j, lagopoulos j, mudaliar y, dorsch nw. hemispheric asymmetry and temporal profiles of cerebral pressure autoregulation in head injury. journal of clinical neuroscience 2003;10:670–3. 54.prat r, markiv v, dujovny m, misra m. failure of cerebral autoregulation in an experimental diffuse brain injury model. acta neurochir suppl 1998;71:123–6. 55.panerai rb. assessment of cerebral pressure autoregulation in humans--a review of measurement methods. physiol meas 1998;19:305–38. 56.[cerebral hemodynamic in acute phase of traumatic brain injury]. anesteziol reanimatol 2012:58–62. 57.yokobori s, watanabe a, matsumoto g, onda h, masuno t, fuse a, kushimoto s, yokota h. time course of recovery from cerebral vulnerability after severe traumatic brain injury: a microdialysis study. j trauma 2011;71:1235–40. 58.belli a, sen j, petzold a, russo s, kitchen n, smith m. metabolic failure precedes intracranial pressure rises in traumatic brain injury: a microdialysis study. acta neurochir wien. 2008;150:461–9; discussion 470. 59.costa t, constantino lc, mendonça bp, pereira jg, herculano b, tasca ci, boeck cr. n-methyl-daspartate preconditioning improves short-term motor deficits outcome after mild traumatic brain injury in mice. j neurosci res 2010;88:1329–37. 60.zlotnik a, sinelnikov i, gruenbaum bf, gruenbaum se, dubilet m, dubilet e, leibowitz a, ohayon s, regev a, boyko m, shapira y, teichberg vi. effect of glutamate and blood glutamate scavengers oxaloacetate and pyruvate on neurological outcome and pathohistology of the hippocampus after traumatic brain injury in rats. anesthesiology 2012;116:73–83. 61.wang y, song j-h, denisova j v, park w-m, fontes jd, belousov ab. neuronal gap junction coupling is regulated by glutamate and plays critical role in cell death during neuronal injury. j neurosci 2012;32:713– 25. 136 alvis-miranda et al traumatic cerebral contusion 62.zlotnik a, gruenbaum se, artru aa, rozet i, dubilet m, tkachov s, brotfain e, klin y, shapira y, teichberg vi. the neuroprotective effects of oxaloacetate in closed head injury in rats is mediated by its blood glutamate scavenging activity: evidence from the use of maleate. j neurosurg anesthesiol 2009;21:235–41. 63.bullock r, zauner a, woodward jj, myseros j, choi sc, ward jd, marmarou a, young hf. factors affecting excitatory amino acid release following severe human head injury. j neurosurg 1998;89:507–18. 64.han r-z, hu j-j, weng y-c, li d-f, huang y. nmda receptor antagonist mk-801 reduces neuronal damage and preserves learning and memory in a rat model of traumatic brain injury. neurosci bull 2009;25:367–75. 65.yoles e, muller s, schwartz m. nmda-receptor antagonist protects neurons from secondary degeneration after partial optic nerve crush. j neurotrauma 1997;14:665–75. 66.maeda t, katayama y, kawamata t, koyama s, sasaki j. ultra-early study of edema formation in cerebral contusion using diffusion mri and adc mapping. acta neurochir suppl 2003;86:329–31. 67.hillered l, vespa pm, hovda da. translational neurochemical research in acute human brain injury: the current status and potential future for cerebral microdialysis. j neurotrauma 2005;22:3–41. 68.le roux pd, newell dw, lam am, grady ms, winn hr. cerebral arteriovenous oxygen difference: a predictor of cerebral infarction and outcome in patients with severe head injury. j neurosurg 1997;87:1–8. 69.valadka ab, gopinath sp, contant cf, uzura m, robertson cs. relationship of brain tissue po2 to outcome after severe head injury. crit care med 1998;26:1576–81. 70.van den brink wa, van santbrink h, steyerberg ew, avezaat cj, suazo ja, hogesteeger c, jansen wj, kloos lm, vermeulen j, maas ai. brain oxygen tension in severe head injury. neurosurgery 2000;46:868–76; discussion 876–8. 71.patro a, mohanty s. pathophysiology and treatment of traumatic brain edema. the indian journal of neurotrauma 2009;6:11–5. 72.barker-collo sl, starkey n, kahan m, theadom a, feigin v. computerised tomography indices of raised intracranial pressure and traumatic brain injury severity in a new zealand sample. n z med j 2012;125:92–4. 73.egea-guerrero jj, gordillo-escobar e, revuelto-rey j, enamorado-enamorado j, vilches-arenas a, pacheco-sánchez m, domínguez-roldán jm, murillocabezas f. clinical variables and neuromonitoring information intracranial pressure and brain tissue oxygenation. as predictors of brain-death development after severe traumatic brain injury. transplant proc 2012;44:2050–2. 74.frutos bernal e, rubio gil fj, martín corral jc, marcos prieto la, gonzález robledo j. prognostic factors in severe traumatic brain injury. med intensiva 2012. 75.abdalla mohamed a, ahmed ibrahim w, fayez safan t. hemodynamic and intracranial pressure changes in children with severe traumatic brain injury. egja 2011;27:273–8. 76.geeraerts t, menon dk. [does intracranial pressure monitoring improve outcome after severe traumatic brain injury?]. ann fr anesth reanim 2010;29:e171–5. 77.armonda ra, tigno ta, hochheimer sm, stephens fl, bell rs, vo ah, severson ma, marshall sa, oppenheimer sm, ecker r, razumovsky a. posttraumatic vasospasm and intracranial hypertension after wartime traumatic brain injury. perspectives in medicine 2012;1:261–4. 78.zeng t, gao l. management of patients with severe traumatic brain injury guided by intraventricular intracranial pressure monitoring: a report of 136 cases. chin j traumatol 2010;13:146–51. 79.mitchell p, gregson ba, vindlacheruvu rr, mendelow ad. surgical options in ich including decompressive craniectomy. j neurol sci 2007;261:89– 98. 80.holmin s, mathiesen t. biphasic edema development after experimental brain contusion in rat. neuroscience letters 1995;194:97–100. 81.harting mt, smith ct, radhakrishnan rs, aroom kr, dash pk, gill b, cox jr. cs. regional differences in cerebral edema after traumatic brain injury identified by impedance analysis. journal of surgical research 2010;159:557–64. 82.unterberg aw, stover j, kress b, kiening kl. edema and brain trauma. neuroscience 2004;129:1021– 9. 83.kawamata t, katayama y, aoyama n, mori t. heterogeneous mechanisms of early edema formation in cerebral contusion: diffusion mri and adc mapping study. acta neurochir suppl 2000;76:9–12. 84.katayama y, kawamata t. edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of cerebral contusion in head trauma patients. acta neurochir suppl 2003;86:323–7. 85.karim aha, jalaluddin wms, ghani ari. computed tomography perfusion imaging on traumatic cerebral contusion: a preliminary report. malaysian journal of medical sciences 2010;17:51–6. 86.katayama y, becker dp, tamura t, hovda da. massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury. j neurosurg 1990;73:889–900. romanian neurosurgery (2013) xx 2: 125 – 137 137 87.eriksson ea, barletta jf, figueroa be, bonnell bw, vanderkolk we, mcallen kj, ott mm. cerebral perfusion pressure and intracranial pressure are not surrogates for brain tissue oxygenation in traumatic brain injury. clinical neurophysiology 2012;123:1255– 60. 88.liao k-h, chang c-k, chang h-c, chang k-c, chen c-f, chen t-y, chou c-w, chung w-y, chiang y-h, hong k-s, hsiao s-h, hsu y-h, huang h-l, huang s-c, hung c-c, kung s-s, kuo kn, li k-h, lin j-w, lin t-g, lin c-m, su c-f, tsai m-t, tsai s-h, wang y-c, yang t-y, yu k-f, chiu w-t. clinical practice guidelines in severe traumatic brain injury in taiwan. surgical neurology 2009;72, supple:s66–s73. 89.li lm, timofeev i, czosnyka m, hutchinson pja. review article: the surgical approach to the management of increased intracranial pressure after traumatic brain injury. anesth analg 2010;111:736–48. 90.stevens rd, huff js, duckworth j, papangelou a, weingart sd, smith ws. emergency neurological life support: intracranial hypertension and herniation. neurocrit care 2012;17 suppl 1:s60–5. 91.wijayatilake ds, shepherd sj, sherren pb. updates in the management of intracranial pressure in traumatic brain injury. curr opin anaesthesiol 2012;25:540–7. 92.bor-seng-shu e, figueiredo eg, amorim rlo, teixeira mj, valbuza js, de oliveira mm, panerai rb. decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury. j neurosurg 2012;117:589–96. 93.kenning tj, gandhi rh, german jw. a comparison of hinge craniotomy and decompressive craniectomy for the treatment of malignant intracranial hypertension: early clinical and radiographic analysis. neurosurg focus 2009;26:e6. 94.stiver si. complications of decompressive craniectomy for traumatic brain injury. neurosurg focus 2009;26:e7. microsoft word 10b.balasad_primary_f.docx romanian neurosurgery (2012) xix 1: 63 – 66 63 primary tuberculomas of the thoracal spinal cord. case report d. balasa1, a. tunas1, a. terzi2, c. serban4, m. aschie3 clinical emergency county hospital, constanta 1neurosurgery, 2anestesiology, 3pathology 4 euromedic private unit, constanta, neuroradiology abstract the authors present an unusual case of intramedullary tuberculoma in a hivnegative patient from the southeast part of romania who demonstrated no other signs of tuberculous infection. clinical exam: extreme spastic paraparesis in triple flexion, dorsal pain and bladder and bowel incontinence. gd enhanced mri revealed ring enhancing lesion with central hypointensity, suggesting granulomatous pathology. surgical excision of the intramedullary lesions was carried out followed by anti-tuberculous chemotherapy and baclofen tablets . !0 days postoperative mri showed total resolution of the lesion. two years follow up showed progressive resolution of spasticity. following surgical excision, the patient improved significantly sensitive and modest the motility and spasticity. the management of this rare lesion is discussed and the literature reviewed. keywords: spinal cord, tuberculosis, primary tuberculomas intramedullary tuberculomas rest a lesion extremelly rare (2 of 100 000 cases of tuberculosis and 2 of 1000 cases of cns tuberculosis). lin and mcdonnell (11, 12) found only 148 cases of intramedullary tuberculomas mentioned in the literature. ratliff (15) present one case of primitive intramedullary tuberculoma. we present the case of un unusual case of intramedullary tuberculoma in a hivnegative patient from the southeast part of romania who demonstrated no other signs of tuberculous infection and presents no sign of involvement of the bony spinal canal. case report presentation: this 20 years old young peasant male was referred to our department for evaluation of his progressivelly (one year and a half) extreme spastic paraparesis in triple flexion, dorsal pain, bladder and bowel incontinence. there was no history of tuberculosis and he was hiv seronegative. examination: on examination the pacient acused un severe spastic paraparesis in triple flexion and the right leg more profoundly affected than the left. patellar and achille relexes was increased. babinsky sign was positive. sensory deficit to p inpick and light touch revealed a t4 level right, t5 level left. chest x-ray films revealed no abnormalities. dorsal mri scan including gd-dtpa mri revealed ring enhancing lesion with central hypointensity, suggesting granulomatous pathology from t4 to t5 levels. 64 d. balasa et al primary tuberculomas of the thoracal spinal cord treatment operation t4-t5 laminectomy, median mielotomy, microsurgical total resection of a well circumscribed yellow-grey mass located cortically and intramedullary. the lesion was very carefully dissected and totally resected along a definable plane by use of the operating microscope. the gross pathological specimen was an encapsulated, yellow-grey firm mass. pathological findings ppathological examination of the lesion revealed multiple epitheloid cell granulomas with langerhan's and foreign body type of giant cells. large areas of caseous necrosis were seen and necrotic material. photomicrograph.: photomicrograph demonstrating epitelioid areas of caseating granulomas with langhans type giant cells. van gieson coloration. postoperative course medical treatment: antituberculous chemotherapy for 52 weeks or more consist of four chemotherapeutic agents to overcome drug resistance: inh 300mg/day, rifampin 600 mg/day, etambuthol 1200 mg/day and pyrazinamide 2000 mg/day and antispastic agents (baclofen tablets). ten days postoperative mri showed total resolution of the lesion. the patients improved significantly sensitivity and modest the motility and spasticity. follow up period: 2 years. figure 1 figure 2 figure 3 romanian neurosurgery (2012) xix 1: 63 – 66 65 figure 4 figure 5 discussion tuberculosis is a chronic bacterial infection produced by mycobacterium tuberculosis tuberculosis of the central nervous system is a rare entity, affecting 0,5-2% of patients with sistemic tuberculosis (14, 3, 15). intramedullary tuberculomas is a lesion extremelly rare seen only 2 of 100 000 cases of tubeculosis and 2 of 1000 cases of tuberculosis of central nervous systems disesase. it is speciffically for the young patients in the developing countries and is associated usually with pulmonay disease, in 69% of cases (11, 12). the first report of intramedullary tuberculoma was by abercrombie in 1828 (1) .the commonest symptoms were progressive lower limbs weakness, paresthesia, and bladder and bowel dysfunction. the major physical findings were paraplegia, either spastic or flaccid. the majority of patients had thoracic sensory level. the mri characteristics have been described by jena et al (10) as low intensity rings with or without central hyperintensity on t2 images and low to isointense rings on t1 images. caseation results in the “target sign” appearance. the choice of treatment is an important consideration. microsurgical total excision and antituberculous agents are widely used in the treatment of intramedullary tuberculoma. macdonnel has reported 65% recovery after surgical treatment. conclusion •intramedullary tuberculoma, is a very rare entity. •microsurgical total excission and antituberculous chemotherapy consisting of three agents was mandatory for the healing this very large intramedullary lesion. •motor recovery of this patient is difficult considering the extreme spastic paraparesis in triple flexion and the evolution of the illness of one and a half year. •will be necessary in time orthopedic procedures for the treatment of spasticity and recovery. corespondence address dr. d. balasa, department neurosurgery, clinical emergency county hospital, boulevard tomis, 145, constanta, romania. e-mail: daniel_balasa@hotmail.com 66 d. balasa et al primary tuberculomas of the thoracal spinal cord references 1. abercrombie j. pathological and practical researches on disease of the brain and the spinal cord. edinburg: waugh and innes, 1828: 371-2 2. alex h.macdonel, robert w.baird, michael s.bronze. intramedullary tuberculomas of the spinal cord:case report and review. review of infectious diseases. vol 12,3:432-436,1990 3. baker rd: postmortem examination. specific methods and procedures. philadelphia, w.b. saunders, 1967, p 175. 4. b. indira devi, s. chandra, s. mongia, chandramouli, k.v.r. sastry, s. k. shankar. spinal intramedullary tuberculoma and abscess: a rare cause of paraparesis. neurology india, vol 50, no 4, dec 2002, 494-496 5. bertrand i, guillaume jm, samson m, gueguen y: tuberculoma intamedullarire dorsal. rev neurol 98:51-54, 1958 6. citow js, ammirati m : intramedullary tuberculoma of the spinal cord. case report. neurosurgery 1994; 35: 3270330 7. dastur hm. diagnosis and neurosurgical treatment of tuberculous disease of the cns. neurosurg review. 1983, 6: 111-117 8. gokalphz, ozkal e: intradural tuberculomas of the spinal cord. j neurosurg 1985, 55:289 9. gupta vk, jena a,sharma a,guha dk, khushu s, gupta ak: magnetic resonance imaging of intracranial tuberculomas. j comput assist tomogr 12:280-285, 1988. 10. jena a, banerji ak,tripathiri, gulati pk, jain rk, khushu s, supra mi. demonstration of intramedullary tuberculosis by mria case report of 2 cases. br j radiol 64:555-557, 1991 11. lin th:i̇ntramedullary tuberculoma of the spinal cord . j neurosurg 17:497-499, 1960 12. macdonell ah, baird rw, bronze ms:intra baird rw, bronze ms: intramedullary tubercullomas of the spinal cord: case report and review. rev infect dis 12:432-439, 1990 13. mohit aa, santiago p, rostomily r. intramedullary tuberculoma mimicking primary cns 14. parmar h, shah j, patkar d, varma r.intramedullary tuberculomas. mr findings in sevens. patients. acta radiol 41:572-7, 2000 15. ratliff jk: intramedullary tuberculoma of spinal cord. j neurosurg(spine) 1999:90:125-128 16. whiteman m, espinosa l, post mdj, bell md, falcon s: central nervous system tuberculosis in hi̇v infection patient. clinical and radiographical finding. ajnr am j neuroradiol 16:1319-1327, 1995 doi: 10.33962/roneuro-2021-089 recent descriptions on physiological concepts of the pineal gland: what's new? d.l. contreras-de la hoz, germán camilo viracacha -lópez, julieth vivian sarmiento -palma, loraine llerena-gutierrez, julio césar mantilla-pardo, g.a. blanco-fernandez, criss madeley millan -puerto, rodrigo alberto caicedo -lozada, a.f. guerrero-ceron, david eduardo espinosa-ortiz, ivan david lozada martinez, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (4): pp. 518-525 doi: 10.33962/roneuro-2021-089 www.journals.lapub.co.uk/index.php/roneurosurgery recent descriptions on physiological concepts of the pineal gland: what's new? dany leonardo contreras-de la hoz1, germán camilo viracachalópez2, julieth vivian sarmiento-palma3, loraine llerenagutierrez4, julio césar mantilla-pardo5, guillermo andre blanco-fernandez6, criss madeley millanpuerto7, rodrigo alberto caicedo-lozada8, anderson fabian guerrero-ceron9, david eduardo espinosa-ortiz10, ivan david lozada martinez11,12, luis rafael moscote-salazar11,12 1 school of medicine, universidad libre, barranquilla, colombia 2 school of medicine, fundación universitaria de ciencias de la salud, bogotá, colombia 3 school of medicine, fundación universitaria juan n. corpas, bogotá, colombia 4 school of medicine, universidad del norte, barranquilla, colombia 5 school of medicine, universidad icesi, cali, colombia 6 school of medicine, universidad ces, medellín, colombia 7 school of medicine, universidad industrial de santander, bucaramanga, colombia 8 school of medicine, universidad libre, cali, colombia 9 school of medicine, universidad del cauca, popayán, colombia 10 school of medicine, universidad de caldas, manizales, colombia. 11 colombian clinical research group in neurocritical care, st mary’s medical group, cartagena, colombia 12 colombian chapter, world federation of neurosurgical societies, cartagena, colombia abstract the pineal gland is an endocrine organ located in the cranial vault. its endocrine function has been extensively studied and has been found to be the cause of important regulatory functions in the physiology of the human body. although the initial approaches to the suggestive action of this organ on the organism were of a philosophical and spiritual nature, in the last century technological advances have made it possible to clearly elucidate its effector function as an endocrine gland. in this order of ideas, the objective of this review is to address basic and recent descriptions of the physiology of the pineal gland. keywords pineal gland, endocrine system, melatonin, central nervous system, physiology corresponding author: ivan david lozada-martinez colombian clinical research group in neurocritical care, st mary’s medical group, cartagena, colombia ivandavidloma@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 519 recent descriptions on physiological concepts of the pineal gland: what's new? introduction the pineal gland (pg) has been described as an organ that is capable of excreting a hormone called melatonin (mlt) that plays an important role in the circadian cycle (1). at the beginning of mankind's interest in anatomy and physiology (renaissance era) this gland was still considered as part of the spiritual component of the body, as science evolved through later discoveries that the pineal gland exerted a regulating and synchronizing effect on the physiology of the organism, it was given physical functions (2). the scope of the hormone it excretes extends to important fields of human physiology such as the circadian cycle, sleep-wake cycle, mood states (its deficit causes depressive states), some topics that we will go into below, but not before addressing what was assumed about this gland throughout history. history the pg has been the subject of debate in philosophical circles. it was ariens-kappers who expressed that the oldest references with physiological-spiritual connotations regarding this gland were made by herophilus, a philosopher who proposed that the pg had control over blood circulation by functioning as a sphincter that regulated the flow of pneuma psychikon, or the breath of life, from the central ventricle to the posterior ventricle in the brain (3). galen proposed that the pg was nothing more than a pseudolymphatic gland that functioned as an anchor site to the intricate network of blood vessels that irrigate the brain mass belonging to the dorsal and posterior diencephalon regions, a somewhat more physical approach, however, still related to spiritual theories (4). in the middle ages, different theories enriched the theoretical corpus regarding the duality between the soul and the body, assigning to the organs some probable spiritual functions, with new thoughts or improvement of the existing ones by important figures such as thomas aquinas, a famous monk influenced by the prevailing christianity of the feudal age (5). in the renaissance there was an explosion in anatomical explorations led by important figures such as leonardo da vinci, who through his detailed drawings of human anatomy deepened the curiosity of the medical eminences of the time about the vital functions of different organs (6). the soul was located in the third ventricle of the brain, while the spinal cord was responsible for distributing the sensations generated in the soul to the body (6). later descartes proposed that the soul should have a physical residence or physical counterpart in the human body, the pg being the abode of the soul. according to him, the cerebral organs were duplicated except for the pg, which was curiously located in the center of the brain (7). descartes' theories were later discredited by figures such as antoine jacques louis jourdan who argued that his ideas were nothing more than chimeras relegated to the realm of fiction (8). descartes' theories were later discredited by figures such as antoine jacques louis jourdan who argued that his ideas were nothing more than chimeras relegated to the realm of fiction (9). in addition, it was also hypothesized that the pineal is an endocrine gland. in 1958, it was determined that the pineal gland secretes melatonin, which regulates the circadian rhythm in the studies of lerner et al (1,10). the history of the pineal gland is long and its functions were only elucidated in the 20th century. in previous centuries the gland's functions were based on superstition and a misunderstanding of its anatomy. however, even with our better understanding of the gland, all of its functions have yet to be determined (11). embryology and histology the pg is formed from the neuroectoderm of the posterior portion of the roof of the diencephalon. it is initially recognized in the caudal portion of the diencephalon as a structure called the pineal body. this pineal body is nothing more than an epithelial thickening in the midline at the level of the diencephalon that from the seventh week begins to undergo a process of invagination that will culminate in the formation of the solid organ (12). histologically the pg is mainly composed of two types of parenchymal cells. pinealocytes and interstitial cells (13). pinealocytes are organized in lobules formed by connective tissue. they are mainly characterized by the production of mlt, a hormone important for metabolic regulation processes, as well as for the control of the sleep-wake cycle (14). interstitial cells constitute approximately 5% of the cell types in this gland, established as supporting cells in the tissue (15). 520 d.l. contreras-de la hoz, germán camilo viracacha-lópez, julieth vivian sarmiento-palma et al. morphological structure the pg has been described as a small, odd, endocrine organ located in the roof of the midbrain, above the superior colliculi and behind the third ventricle (16). it is joined to the habenular and posterior commissures by means of the pineal stalk, whose body is bathed by cerebrospinal fluid and covered by pia mater, the pia mater in turn becomes a capsule that provides the gland with partitions that in turn allow its irrigation (17). the so-called pineal region, however, contains the gland in a wider space, defined by the corpus callosum and the choroid plexus of the third ventricle above, by the lamina quadrigemina and the cerebellum below, and laterally by the thalamus and the cerebral hemispheres (18). the weight of the gland can vary between 100 to 200 mg, and measure between 5 to 8 mm long and 3 to 5 mm wide (12). its innervation is given mainly by the superior cervical ganglion of the paravertebral chain, of sympathetic and parasympathetic type (12,13). on the other hand, its irrigation, unlike others in the body, is considered of a high flow considering that it is a small endocrine organ, in addition to the fact that the blood vessels that integrate it lack a blood-brain barrier (13,16). in addition, a study by macchi & bruce identified that the pg reached a blood flow that equaled the neurohypophysis in rats and was exceeded only by the flow from the kidneys (12,13). cellularly, it has been described that pinealocytes, so called the cells that compose the pg, are equivalent to those found in the retina, more specifically to retinal cones, lower order neurons and glial cells; therefore, it was mainly catalogued as a visual organ (12). neurological pathways and tracts anatomically, the structures that make up the central nervous system comprise a series of complex interconnected pathways for the fulfillment of various functions (15). the pg communicates via the suprachiasmatic nucleus (scn) and the retinohypothalamic tract (rht), such that afferent fibers coming from the rht are mainly located in the ventrolateral region of the cns, while efferents depart to the dorsolateral region (15). the most studied afferent pathway is part of the visual pathway, starting in the ganglion cells of the retina, which are conducted through the optic nerve and optic chiasm until they reach the hypothalamus, however, it is independently of the perception of images (12,15). on the other hand, the efferent fibers that cross the suprachiasmatic nucleus form the so-called multisynaptic pathway of the pg, whose route guides it to the hypothalamus, specifically its paraventricular nucleus, from there its axons depart to preganglionic neurons in the lateral intermediate column of the sympathetic type in the spinal cord between the t1 and t3 segments, and to the superior cervical ganglion where they activate noradrenergic neurons (18). the latter form the nervus conarii, whose fibers reach both sides of the tentorium and unite in the midline to finally enter the pg in its posterior portion, taking the name of pineal nerve (13,18). the parasympathetic innervation is provided by the sphenopalatine nerve and the otic ganglia. and for its part, the trigeminal ganglion through some of its branches also provides innervation to the gland (14). neuroendocrine component the main hormonal molecule secreted by the pg is mlt, which is able to exert many endocrine functions at the cns level and throughout the body physiology, so it is not considered a pure neural hormone (19). mlt is an endogenous indolamine, with circadian regulation given by the suprachiasmatic nucleus; characteristically, it is a lipophilic hormone, which confers it the ability to rapidly cross the blood-brain barrier and target cells of its action (20). mlt is released into the bloodstream, following the endogenous circadian cycle given by the hypothalamus, through the light-dark cycle, i.e. it is produced during the night as long as it is dark, in addition to the sympathetic stimulation given by the adrenergic nerves that make up the hypothalamic retino pathway (18,21). because melanopsin decomposition is stimulated during the day in the retinal ganglion cells, it uses the hypothalamic retinal pathway to carry its signal to the hypothalamus and thus inhibit its synthesis. it is synthesized from an essential amino acid, tryptophan, which is biotransformed by the action of four enzymes (20). initially, tryptophan through the action of the enzyme tryptophan hydroxylase, which adds a hydroxyl group to the 5-position of the indole ring to form 5-hydroxytryptophan (5-htp). subsequently, 5hydroxytryptophan forms serotonin via an aromatic 521 recent descriptions on physiological concepts of the pineal gland: what's new? amino acid decarboxylase. now, before finally being mlt, serotonin is transformed by the enzyme serotonin n-acetyltransferase. and finally, mlt is formed from n-acetyl serotonin as substrate and obligatory step for its synthesis by means of the enzyme hydroxyindole-o-methyltransferase (20-22). after its synthesis, mlt travels through the bloodstream bound to albumin, and upon reaching the liver it is metabolized to 6-hydroxymelatonin by cytochrome p450, mainly in its cyp1a2 isoform, and the latter is conjugated to 6-sulfamethoxymelatonin for its subsequent urinary excretion (21). regulation and functions of the pineal gland it has been difficult to determine all the physiological functions of pg because its main product (mlt) has a complex regulation in vivo, being controlled by various stimuli inside and outside the individual. therefore, experimental studies have not found a way to reproduce the exact pattern of natural mlt production (22-24), but we know that the main regulation comes from the suprachiasmatic nucleus, which is the circadian pacemaker (20,23,24). mlt peaks depend on light exposure and season (due to changes in day length). mlt production increases in the dark phases of the day in almost all animals. light exposure in the retina stimulates the suprachiasmatic nucleus which sends signals that decrease mlt production. this regulation gives the body representation of external environmental conditions (28-31). other factors involved in mlt production are adrenergic stimuli and inflammatory products. another important source of control is known to be the release of noradrenaline (ne) by the sympathetic fibers of the cervical sympathetic ganglia that stimulate its secretion mainly at night (24,30,31,32,33). extra-pineal mlt production is also under the control of several neurotransmitters (glutamate, acetylcholine, vasoactive intestinal peptide, substance p and pituitary adenylate cyclaseactivating peptide), but to a lesser extent than ne (27,30). inflammatory products can increase or decrease mlt production. pathogenand hazardassociated molecular patterns (pamp and damp) modulate nocturnal mlt synthesis during inflammatory processes (27,33). in addition, several cytokines and signaling pathways such as ifn, lps, beta-amyloid peptide, nfκb, jak/stat have been observed to have complex effects on mlt production (33). mlt has a wide range of effects in the body and acts through two g-paired protein receptors (mt1, mt2) and another of the quinone reductase family: mt3 (27). it is involved in important and basic processes in mammalian life, such as the timing of seasonal physiology, reproduction and sleep (table 1). table 1. summary of pineal gland functions (21,24,31). • negative regulation of thyroid activity • hypothermic • sleep inducer • hypotensive by increasing norepinephrine levels, regulating cardiac beta receptors and increasing mesenteric arterial dilation capacity • immunoregulatory through the use of transcription factor nfƙb and binding to ƙb receptors, regulating glucocorticoid and mlt synthesis rates • antioxidant by inducing the nrf2-are signaling pathway and scavenging free radicals • oncostatic • thymic modulator • neuroprotector reproduction pg has several effects on reproduction and sexual maturation due to its effects on the regulation of hormone release at the pituitary level. it determines gametogenesis, sexual maturation, pregnancy and menopause (35). it is considered to have paradoxical effects at the reproductive level as its effect depends on peaks of secretion and the season in which it occurs. however, it is not yet clear how the duration of mlt exposure in the pars tuberalis may affect tsh and gnrh release and its effects on peripheral tissues to regulate reproduction (22,24). sleep park et al investigated the relationship between pineal gland volume (pgv) and symptoms of rem sleep behavior disorder (rbd) in a cohort of previously healthy individuals. they followed the cohort for two years and administered the rem behavioral sleep disorder screening questionnaire (rbdsq) and measured vmp by magnetic resonance imaging (mri). the results showed that individuals with symptoms or at risk for rbd had a smaller pgv (37). this finding is supported by other studies, just 522 d.l. contreras-de la hoz, germán camilo viracacha-lópez, julieth vivian sarmiento-palma et al. as pg calcification and cysts are also known to trigger sleep disturbances (27). mlt deficits due to weight gain and obesity have deleterious effects on sleep, circadian rhythm, and neuroendocrine functions (30,37). in addition, it has been shown in several studies that mlt administration greatly improves sleep disorders (34,37,38). mlt improves sleep through several mechanisms by acting on muscle tone, controlling gabaergic function and improving sleep efficiency (33). circadian rhythm in mammals, pg adjusts organisms to respond to the needs of each season and choose the best time of the year for reproduction, hibernation, etc. as it translates environmental changes depending on changes in light during the day. mlt acts on clock neurons and clock genes to generate a circadian rhythm (33,34). it appears that gestational mlt synchronizes maternal and fetal circadian clocks and also regulates the timing of offspring puberty, as it also determines fetal adrenal development (23,30). nowadays the circadian rhythm can be altered due to exposure to nocturnal light. this alteration may even increase the likelihood of tumor growth as the protective effect of mlt is lost (23). mood pgv is associated with mood disorders (39). there have been reports of abnormal mlt secretion and increased expression of stress hormones at night that alter sleep and, consequently, mood. it has a relationship not only with mood disorders, but also with other mental illnesses such as schizophrenia (26). in depression, mlt has been used as a treatment because its levels decrease during the crisis and increase immediately after recovery (25). pregnancy during pregnancy, mlt is responsible for synchronizing maternal and fetal physiology and guiding fetal development through mlt receptors in the fetal pituitary gland. in addition, the circadian rhythm of maternal control by light exposure and transmitted to the fetus as an mlt signal determines the future behavior of the offspring in terms of growth and sexual maturation (28). on the other hand, mlt levels in lactation show no relationship with offspring behavior and circadian regulation (23). temperature the relationship between mlt and core body temperature is still a matter of debate. some research shows a decrease in mlt during the rise in temperature in the ovulatory phase of the menstrual cycle and a higher peak mlt concentration during the luteal phase than during the follicular phase (35). endocrine control in a case-control study, the pgv was compared with mri techniques. it showed that healthy controls had a larger pgv in contrast to obese people. and that pgv was inversely related to body mass index (bmi). decreased ltm has also been related to insulin resistance and the presence of type ii diabetes mellitus (37). pain mlt has an effect on pain control through its effects on sleep, and control over neurotransmitters such as gaba and dopamine. it can decrease cyclic amp production and activates the opioid receptor directly or indirectly. in addition, in animal models, a decrease in nmda-induced currents in spinal cord gelatinous neurons has been observed (38). oxidative stress mlt protects the cell through its direct and indirect antioxidant and anti-inflammatory effects, as it is a neutralizer of oxygen free radicals, as well as regulating the activation of second messengers that activate pro-inflammatory pathways such as camp and cgmp. it has been shown that it can control transcription factors related to the retinoic acid receptor (ror) (27,30). it has also been shown to have protective effects on x-ray exposure (24). neurogenesis mlt also plays a neuroprotective role in many central nervous system disorders, especially in dementias. mlt is thought to exert antineurodegenerative properties through ror receptors (30) and the disappearance of mlt receptors leads to neuropsychiatric disorders in the elderly (25). in alzheimer's disease (ad) it has been identified that mlt production is impaired and leads to 523 recent descriptions on physiological concepts of the pineal gland: what's new? impaired neurogenesis due to reduced expression of brain-derived neurotrophic factor and glial cellderived neurotrophic factor. mlt stimulates neural stem cell replication in the midbrain and hippocampus, depending on day length (27). other functions the effects of mlt are not only central. in the gastrointestinal tract, mlt has protective effects on the gastric mucosa. in addition, it has regulatory effects on the immune response that controls leukocyte migration, inhibits the activation of inflammatory signaling, and regulates the proliferation and activation of immunocompetent cells (24). it also has regenerative effects on corneal lesions and regulation of intracranial pressure (24). there is evidence that reduced levels of mlt contribute to cognitive impairment in ad patients. this not only affects cognition but also sleep and circadian rhythm (27). in addition, mlt appears to be involved in the pathogenesis of ad, as it is implicated in the inhibition of tau phosphorylation, attenuated levels of beta-amyloid protein precursor production and its deposition in the cns (27). melatonin could be considered a cardioprotective agent, it is associated with a reduction of iatrogenic lipoproteins (40). in a murine model, hypercholesterolemia was induced in rats by a diet rich in lipids and carbohydrates, melatonin was administered orally at a dose of 10 mg/kg/day, presenting in the lipid profiles measured. subsequently, these profiles were characteristically antiatherogenic: total cholesterol, very low-density lipoprotein (vldl) and low density lipoprotein (ldl) concentrations decreased, while high density lipoprotein (hdl) cholesterol concentrations increased (41). another product of pg (and other peripheral tissues), n-dimethyltryptamine, is responsible for perception, consciousness, vision, imagination and dreams, and has potential therapeutic targets for depression, anxiety and psychosis (24). future perspectives include the need to investigate whether there are chronic changes in the physiology of the pineal gland due to the new disease called covid-19, specifically due to the neurotropism of sars-cov-2 and neuroinflammatory mechanisms caused by this virus (42-45). in addition, the development of robotic neurosurgery and other emerging techniques such as neurogenomics and neuroimaging genetics should also be encouraged in order to better understand the pathophysiology of pineal glandassociated diseases (46,47). conclusions the pineal gland is an endocrine organ that fulfills multiple functions in the physiology of the body, so it is very important to understand and study it. its main product is the hormone melatonin, in future research this hormone could play a major role in the therapy of multiple neurodegenerative pathologies, such as alzheimer's disease, schizophrenia and major depressive state, as well as protector of heart and cerebrovascular diseases. references 1. lerner ab, case jd, takahashi y, lee th, mori w. isolation of melatonin, the pineal gland factor that lightens melanocytes 1. j am chem soc. 1958; 80(10):2587–2587. 2. arendt j. melatonin and the pineal gland: influence on mammalian seasonal and circadian physiology. rev reprod. 1998; 3(1):13–22. 3. ariëns-kappers j, pévet p. short history of pineal discovery and research. amsterdam new york: elsevier; 1979. 1–22. 4. zrenner c. early theories of pineal functions. pineal res rev. 1985; 3:1–40. 5. smith cum. descartes’ visit to the town library, or how augustinian is descartes’ neurophysiology? j hist neurosci. 1998; 7(2):93–100. 6. brazier m. a history of neurophysiology in the 17th and 18th centuries: from concept to experiment. by mary. a. b. brazier new york, raven press, 1984. 239. 7. lópez-muñoz f, boya j. the role of the pineal gland in cartesian psychophysiological doctrine. acta physiol pharmacol latinoam. 1992; 42:205–16. 8. jourdan ajl. dictionnaire des sciences médicales. paris; 1820. 9. zrenner c. theories of pineal function from classical antiquity to 1900: a history. pineal res rev. 1985; 3:1–40. 10. lerner ab, lerner mr. congenital and hereditary disturbances of pigmentation. bibl paediatr. 1958; 14:308–313. 11. shoja mm, hoepfner ld, agutter ps, singh r, tubbs rs. history of the pineal gland. child’s nerv syst. 2016; 32(4):583-586. 12. sadler tw, langman j. langman’s medical embyology. 14th ed. philadelphia: lippincott williams & wilkins; 2019. 13. ross mh, pawlina w. histology: a text and atlas: with correlated cell and molecular biology. seventh edition, international edition. philadelphia: wolters kluwer; 2016. 14. sahai a, sahai rk. pineal gland: a structural and 524 d.l. contreras-de la hoz, germán camilo viracacha-lópez, julieth vivian sarmiento-palma et al. functional enigma. j anat soc india. 2013; 62(2):170–7. 15. roa i, del sol m. pineal gland morphology: a literature review. int j morphol. 2014; 32(2):515–21. 16. granados am, ospina c, paredes s. pineal gliosarcoma in a 5-year-old girl. radiol case reports. 2018; 13(1):244–7. 17. yelamanchi sd, kumar m, madugundu ak, gopalakrishnan l, dey g, chavan s, et al. characterization of human pineal gland proteome. mol biosyst. 2016; 12(12):3622–32. 18. guadarrama-ortiz p, ramírez-aguilar r, madrid-sánchez a, castillo-rangel c, carrasco-alcántara d, aguilarroblero r. controladores del tiempo y el envejecimiento: núcleo supraquiasmático y glándula pineal. int j morphol. 2014; 32(2):409–14. 19. hull jt, czeisler ca, lockley sw. suppression of melatonin secretion in totally visually blind people by ocular exposure to white light. ophthalmology. 2018; 125(8):1160–71. 20. chen y, tain y, sheen j, huang l. melatonin utility in neonates and children. j formos med assoc. 2012; 111(2):57–66. 21. amaral fg do, cipolla-neto j. a brief review about melatonin, a pineal hormone. arch endocrinol metab. 2018; 62(4):472–9. 22. abou-easa k, el-magd ma, tousson e, hassanin a, shukry m, salama m. pineal gland plays a role in gonadal development after eyelids separation in puppies. int j morphol. 2015; 33(1):7–18. 23. gorman mr. temporal organization of pineal melatonin signaling in mammals. mol cell endocrinol. 2020; 503:110687. 24. gheban ba, rosca ia, crisan m. the morphological and functional characteristics of the pineal gland. med pharm reports. 2019; 92(3):226–34. 25. zhao w, zhu d, zhang y, zhang c, wang y, yang y, et al. pineal gland abnormality in major depressive disorder. psychiatry res neuroimaging. 2019; 289:13–7. 26. atmaca m, korucu t, caglar kilic m, kazgan a, yildirim h. pineal gland volumes are changed in patients with obsessive-compulsive personality disorder. j clin neurosci. 2019; 70:221–5. 27. song j. pineal gland dysfunction in alzheimer’s disease: relationship with the immune-pineal axis, sleep disturbance, and neurogenesis. mol neurodegener. 2019; 14(1):28. 28. van dalum j, melum vj, wood sh, hazlerigg dg. maternal photoperiodic programming: melatonin and seasonal synchronization before birth. front endocrinol (lausanne). 2020; 10(january):1–7. 29. schwartz wj, klerman eb. circadian neurobiology and the physiologic regulation of sleep and wakefulness. neurol clin. 2019; 37(3):475–86. 30. gunata m, parlakpinar h, acet ha. melatonin: a review of its potential functions and effects on neurological diseases. rev neurol (paris). 2019; 1–18. 31. coon sl, fu c, hartley sw, holtzclaw l, mays jc, kelly mc, et al. single cell sequencing of the pineal gland: the next chapter. front endocrinol (lausanne). 2019; 10:1–11. 32. farias altamirano le, freites cl, vásquez e, muñoz em. signaling within the pineal gland: a parallelism with the central nervous system. semin cell dev biol. 2019; 95:151–9. 33. barbosa lima le, muxel sm, kinker gs, carvalho‐sousa ce, silveira cruz‐machado s, markus rp, et al. stat1‐ nfκb crosstalk triggered by interferon gamma regulates noradrenaline‐induced pineal hormonal production. j pineal res. 2019; 67(3):1–12. 34. maruani a, dumas g, beggiato a, traut n, peyre h, cohen-freoua a, et al. morning plasma melatonin differences in autism: beyond the impact of pineal gland volume. front psychiatry. 2019; 10(11):1–9. 35. oliveira pf, sousa m, monteiro mp, silva b, alves mg. pineal gland and regulatory function. second edition. vol. 1, encyclopedia of reproduction. elsevier; 2018. 472– 477. 36. park j, han jw, suh sw, byun s, han jh, bae j bin, et al. pineal gland volume is associated with prevalent and incident isolated rapid eye movement sleep behavior disorder. aging (albany ny). 2020; 12(1):884–93. 37. grosshans m, vollmert c, vollstaedt-klein s, nolte i, schwarz e, wagner x, et al. the association of pineal gland volume and body mass in obese and normal weight individuals: a pilot study. psychiatr danub. 2016; 28(3):220–4. 38. peres mfp, valença mm, amaral fg, cipolla-neto j. current understanding of pineal gland structure and function in headache. cephalalgia. 2019; 39(13):1700–9. 39. han q, li y, wang j, zhao x. sex difference in the morphology of pineal gland in adults based on brain magnetic resonance imaging. j craniofac surg. 2018; 29(5):e509–13. 40. karolczak k, watala c. the mystery behind the pineal gland: melatonin affects the metabolism of cholesterol. oxid med cell longev. 2019; 2019:4531865. 41. hussain s. a. effect of melatonin on cholesterol absorption in rats. journal of pineal research. 2007; 42(3):267–271. 42. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. 43. camargo-martínez w, lozada-martínez i, escobarcollazos a, navarro-coronado a, moscote-salazar l, pacheco-hernández a, et al. post-covid 19 neurological syndrome: implications for sequelae's treatment. j clin neurosci. 2021; 88:219-225. 44. ortega-sierra mg, durán-daza rm, carrera-patiño sa, rojas-nuñez ax, charry-caicedo ji, lozada-martínez id. neuroeducation and neurorehabilitation in the neurosurgical patient: programs to be developed in latin america and the caribbean. j neurosurg sci. 2021 jun 10. 45. ortega-sierra mg, prado-grajales v, martinez-imbett r, unás-perea k, lozada martinez id. research career in 525 recent descriptions on physiological concepts of the pineal gland: what's new? neurosurgery: a challenge for future neurosurgeons. j neurosurg sci. 2021 aug 3. 46. blanco-teherán c, quintana-pájaro l, narvaez-rojas a, martínez-pérez r, garcía-ballestas e, moscote salazar l, et al. evidence-based medicine in neurosurgery: why and how? j neurosurg sci. 2021 aug 3. 47. lozada-martínez id, díaz-castillo oj, pearson-arrieta ac, galeano-buelvas a, moscote-salazar lr. post-covid 19 neurological syndrome: a new risk factor that modifies the prognosis of patients with dementia. alzheimers dement. 2021 sep 5. doi: 10.33962/roneuro-2021-063 epidemiological, demographic and clinical profile of traumatic brain injury patients. a prospective analysis at a level one trauma centre in northern part of india abhijeet singh sachan, prakrati sachan, sateesh chandra romanian neurosurgery (2021) xxxv (3): pp. 370-375 doi: 10.33962/roneuro-2021-063 www.journals.lapub.co.uk/index.php/roneurosurgery epidemiological, demographic and clinical profile of traumatic brain injury patients. a prospective analysis at a level one trauma centre in northern part of india abhijeet singh sachan1, prakrati sachan2, sateesh chandra3 1 assistant professor of neurosurgery, neurosciences block, gsvm medical college and llr hospital, kanpur, up, india 2 assistant professor of anesthesiology and critical care, department of anaesthesia, rama medical college and research centre, kanpur, up, india 3 associate consultant. neurosurgery, medanta hospital, lucnow, up, india abstract context: traumatic brain injury is a major public health problem worldwide with increasing incidence and severity in developing countries. in india, it becomes a huge burden on society with a lack of proper preventive measures, public awareness, traffic sense and pre-hospital care. therefore, we studied the epidemiological profile and factors predicting outcome. aims: to study the epidemiological, demographic profile of tbi patients to help to improve the healthcare facilities. setting and design: it is an observational prospective study. methods and materials: overall 2134 patients with tbi were enrolled. the data was collected according to the predesigned proforma. the demographic, epidemiological, clinical variables were analysed to determine the current trends and outcomes. result: the male: female ratio was 2.21:1 with most cases from the age group of 2130 years (29.42%). rta was the mode of injury in 64.48% of cases. overall mortality was 10.91%. overall descriptive data was suggestive of poor outcome in old patients, referred cases, acute sdh and brainstem lesions, hypoxic and hypotensive patients, associated injuries, pre-existing disease and with higher rotterdam and iss scores. conclusion: the outcome is dependent on factors like geographical, demographic, pre-hospital, and patient-related. with knowledge about the causes, patterns, and distribution the prognosis of tbi patients can be improved. introduction traumatic head injury is one of the common causes of mortality and morbidity in the world. it has been estimated that, annually around 6070 million people are affected globally. in india around 1.4-2 million keywords epidemiology, head injury, road traffic accident, demography, pre-hospital corresponding author: abhijeet singh sachan gsvm medical college and llr hospital, kanpur, up, india abhijeet1711@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 371 epidemiological, demographic and clinical profile of traumatic brain injury patients persons are affected and 1 million loose their life every year . a study at a tertiary care institute has reported that the occurrence of tbi is approximately 42.5% in rural and 57.5% in urban area .1 the incidence of head injury is increasing mostly due to excessive use of motor vehicles in low and middle income countries (lmic) .2-3 it affects patients of all age groups with young aged persons between 20-40 yr being the majority . males are more commonly affected than females . the most common cause is rta (around 60% ) followed by falls ( 20-30% ), assault ( 10% ) and sports injury( 10% ) .4 india is leading the world in deaths due to road accidents . neurological status at the time of presentation is the most important prognostic factor with others being the age , ct finding , associated injury , vital parameters , mode of injury , and others . the outcome is dependent on severity of primary injury and is a reflection of secondary insult like hypoxia , hypotension , raised icp , cerebral ischemia. so early recognition and prevention of secondary insult results improvement in neurological status . with detailed knowledge of the clinical and demographic profile of tbi , we can provide the appropriate management and thus get the desired favourable outcome. the aim of this study is to determine epidemiology and demography of tbi , clinical status, severity of head injury , associated comorbid conditions and the final outcome . to our knowledge, this is one of the largest data registry in the world and certainly the largest in india. materials and methods this study was done at sms medical college and hospital , jaipur which is a tertiary care level 1 trauma center in northwestern part of india . it was conducted between april 2017 to march 2019 . a total no of 2134 patients were inducted into the study based on the inclusion criteria :1) clinical diagnosis of tbi , 2) clinical indication for ct scan and 3) informed consent obtained according to local and national requirements . the ethical clearance was obtained from the institutes ethical committee. this was a prospective observational study . the data was collected and patients were followed upto final outcome . data obtained was entered into a proforma . data that was collected included demographic parameters , mode of injury ,gcs on admission and discharge ,associated findings , ct findings ,treatment given , duration of hospital and icu stay and outcome including glasgow outcome scale .injury severity and rotterdam score were calculated for every patient. based on gcs ,tbi cases were graded as mild (13-15) , moderate (9-12) and severe (<8) and glasgow outcome scale ( gos) was used to know the final outcome. the data collected was analyzed and compiled with multiple variables showing current trends and demographic profile. results a total no of 2134 patients were inducted into the study . majority of the cases were from rural parts of jaipur . the no of cases from urban and rural areas were 45.82% and 54.17% respectively. age and sex the total no of male and female were 68.89% and 31.11% respectively . most patients affected were in the age group of 21–30 years (29.42% cases) followed by 31–40 years (22.68% cases) (table 1) . the mean age of patients who survived and died was 33.24 + 14.5 and 41.36 + 17.8 years respectively . the outcome was best in patients < 20 years of age and worst in patients >60 years age with 13.61 % of overall deaths. mode of injury figure 1. distribution on basis of mode of injury table 1. distribution of age adjusted mode of injury and outcome age total cases mode of injury deaths in yrs n (%) rta fall assault sports others n (%) n=2134 injury 0-10 191 (8.95) 41(21.47) 130(68.06) nil 12(6.28) 8(4.19) 8(4.18) 372 abhijeet singh sachan, prakrati sachan, sateesh chandra 11-20 233(10.91) 128(54.93) 54(23.17) 15(6.43) 24(10.30) 12(5.15) 12(5.15) 21-30 628(29.42) 511(81.36) 43(6.85) 29(4.61) 5(0.79) 40(6.36) 74(11.78) 31-40 484(22.68) 357(73.76) 69(14.26) 34(7.02) nil 24(4.96) 56(11.57) 41-50 232(10.87) 144(62.06) 54(23.27) 26(11.20) nil 8(3.44) 40(17.24) 51-60 153(7.16) 71(46.41) 35(22.87) 45(29.41) nil 2(1.31) 14 (9.15) >60 213(9.98) 124(58.21) 72(33.80) 13(6.10) nil 4(1.88) 29(13.61) total 2134 1376(64.48) 457(21.41) 162(7.59) 41(1.92) 98(4.59) 233(10.91) severity of injury 49.10% had mild, 31.02% had moderate and 19.86 % severe injury . severe injury was more common with acute sdh, contusions , and brainstem lesions . 39.38% patients having severe injury died. clinical and radiological findings ct finding; the most common ct finding was multiple lesion with 60.82% cases followed by normal ct finding in 36.18% cases and acute sdh in 32.7% cases . other findings were skull bone fracture (34.3%), contusion (30.13%), acute edh (24.5%), sah (17.29%), ich (11.57%), diffuse axonal injury (9.93) ,brainstem injury (8.76%), and chronic sdh (3.56%) cases (table 2). mortality with acute sdh was maximum in 20.99% cases. table 2. description of various ct findings with severity of injury and fatal outcome. ct finding total no of cases severity of injury deaths no(%)n=2134 (gcs on admission) no(%) no(%) mild moderate severe normal ct 772 (36.18) 678(87.82) 86(11.13) 8(1.03) 13(1.68) acute edh 523 (24.50) 381(72.84) 78(14.91) 64(12.23) 41(7.84) acute sdh 698 (32.70) 154(22.06) 299(42.83) 245(35.10) 176(25.21) contusion 643 (30.13) 218(33.90) 223(34.68) 202(31.41) 135(20.99) ich 247 (11.57) 116(46.96) 76(30.76) 55(22.26) 29(11.74) sah 369 (17.29) 265(71.81) 54(14.63) 50(13.55) 43(11.65) brainstem lesion 187 (8.76) 32 (17.11) 94(50.26) 61(32.62) 19(10.16) skull bone fracture 732 (36.18) 465(63.52) 211(28.82) 56(7.65) 29(3.96) multiple lesion 1298(60.82) 708(54.54) 356(27.42) 234(18.03) 167(12.86) loss of consciousness was maximally associated with acute sdh , ich , and brainstem lesions whereas normal ct and contusion mostly presented with history of headache. hypotension and hypoxia was mostly associated with brainstem lesions with 34.75% and 40.55% incidence respectively. pupillary reactivity was absent in patients with mass effect , uncal herniation and brainstem lesions. seizure was seen in association with contusion in most (36.39% ) cases. (table 3) table 3. association of ct finding with clinical spectrum ct finding loc sbp(mmhg) spo2% pupil seizure no yes <90 >90 <90 >90 r nr no yes <5min >5min acute edh 220(42.06) 134(23.70) 169(32.31) 29(5.54) 494(94.45) 34(6.50) 489(93.49) 364(69.59) 159(30.40) 458(87.57) 65(12.42) acute sdh 145(20.77) 114(16.33) 439(62.89) 72(10.31) 626(89.68) 143(20.48) 555(79.51) 510(73.06) 188(26.93) 541(77.50) 157(22.49) ich 78(31.57) 69(27.94) 100(40.48) 34(13.76) 213(86.23) 57(23.07) 190(76.92) 169(68.42) 78(31.57) 202(81.78) 45(18.22) contusion 389(60.49) 90(13.99) 164(25.50) 62(9.64) 581(90.35) 65(10.10) 578(89.89) 501(77.91) 142(22.08) 409(63.60) 234(36.39) sah 102(27.64) 143(38.75) 124(33.60) 32(8.67) 337(91.32) 54(14.63) 315(85.36) 278(75.33) 91(24.66) 338(91.59) 31(8.40) brainstem lesion 21(11.22) 34(18.18) 132(70.58) 65(34.75) 122(65.24) 76(40.55) 111(59.35) 62(33.15) 125(66.84) 175(93.58) 12(6.41) skull fracture 323(44.12) 132(18.03) 277(37.84) 12(1.63) 720(98.36) 76(10.38) 656(89.62) 701(95.76) 31(4.23) 709(96.85) 23(3.14) multiple lesion 780(60.09) 326(25.11) 192(14.79) 102(7.85) 1196(92.14) 231(17.79) 1067(82.20) 976(75.19) 322(24.80) 1154(88.90) 144(11.09) r-reactive,nr-non reactive clinical features loss of consciousness was most the most common presentation in 81.77% cases with vomiting and ent bleed being the next two in 73.94% and 52.62% cases respectively. spinal injury was present in 0.98% 373 epidemiological, demographic and clinical profile of traumatic brain injury patients cases. the overall seizure incidence was 32.28%. (table 4) associated injuries associated injuries were found in 21.23% cases with facial injury being the most common in 61.58% followed by orthopedic injury 56.07 %. among these 453 cases , 77(16.99%) expired . out of the total 77 patients expired with associated injury most common were with orthopedic injury 41.55% followed by chest injury 25.97 %. complications chest infection was seen in 21.39 % patients especially in patients in icu and on ventilator support . post operative wound infection was seen in 3.56 % patients . about 7.87 % patients had csf leak and of which 48.80 % developed meningitis and 8.33% patients died . hydrocephalus was seen in 4.59% cases and csf diversion was performed in 85.71% of these cases . post traumatic epilepsy was diagnosed in 2.10% cases. table 4. distribution of symptoms, frequency of associated injuries and various complications clinical presentation total no of cases no (%) n=2134 associated injury total cases (%) n=453 complications total no of cases no (%)n=2134 loc 1745(81.77) orthopedic injury 254(56.07) chest infection 456(21.39) vomiting 1578(73.94) chest injury 123(27.15) hemiparesis 297(13.91) ent bleed 1123(52.62) facial inury 279 (61.58) cognitive deficit 245(11.48) headache 726(34.30) abdominal injury 65(14.34) meningitis 82(3.84) seizure 689(32.28) spinal injury 21(4.63) csf leak 168(7.87) hypoxia 339(15.88) pressure ulcer 230(10.78) hypotension 249(11.66) hydrocephalus 98(4.59) spinal injury 21(.98) epilepsy 45(2.10) associated injury 453(21.23) wound infection* 23(3.56) facial palsy 356(16.68) loc-loss of consciousness, *percentage of wound infection was calculated from no of operated patients (n=645). management and outcome management 645 cases were operated out of which 16.74% patients died (table 7) . burr hole was done for 11.16% cases, craniotomy in 64.34% , decompressive craniectomy for 20.47% and skull base repair in 4.03% cases .the outcome was poor in patients with decompressive craniectomy and craniotomy with evacuation of sdh (table 5). patients managed in icu were 612(28.67%) with 54.72% operated patients and 42.32% conservatively managed patients . deaths in icu was seen in 209(89.70% of all deaths) of which 136(38.52%) were of operated patients. table 5. description of operative intervention pone total no of cases% associated injury management conservative deaths operated deaths normal ct 772(36.18) 213(27.59) 772(100) 13(1.68) nil nil depressed fracture 279(13.07) 127(45.51) 96(34.40) 6(6.25) 210(75.26) 12(5.71) acute edh 523(24.5) 148(28.29) 296(56.59) 13(4.39) 227(43.40) 28(12.33) acute sdh 698(32.7) 176(25.21) 274(39.25) 45(16.42) 424(60.74) 131(30.89) ich 247(11.57) 54(21.86) 165(66.80) 16(9.69) 82(49.69) 13(15.85) contusion 643(30.13) 45(6.99) 322(50.07) 57(17.70) 321(49.92) 78(24.29) multiple lesion 1298(60.82) 348(26.81) 762(58.70) 124(16.27) 536(41.29) 43(8.02) the numbers here are more than 645 because of multiplicity of the lesions in same patient. table 6. overall outcome of all patients total no of cases % n=2134 discharged total= 1901 (89.08 ) gos 5 1406 (65.89) 4 215 (10.07) 3 184 (8.62) 2 96 (4.49) deaths (gos 1 ) total= 233 (10.91) in icu 209 (89.70)* in ward 24 (10.30)* *percentage of deaths in icu and ward are calculated with respect to total no of deaths n=233 374 abhijeet singh sachan, prakrati sachan, sateesh chandra the overall mortality was 10.91%. the mean iss and rotterdam were 11.3 and 2.1 respectively which were much higher for deceased patients. patients with non reacting pupil, hypotension, hypoxia, history of alcohol/drug intoxication, pre-existing systemic disease and severe head injury performed poorer than others. (table 7) table 7. various parameters showing total survivals and deaths iss-injury severity score,sbp-systolic blood pressure *grading done on the basis of gcs on admission and percentage calculated for each subgroup. discussion traumatic brain injury is a major global public health issue. there is continous rise in incidence in developing countries accounting to increased industrialization and surge in vehicles without improving the infrastructure. it is also associated with huge socioeconomic losses. therefore complete understanding of its epidemiology and characteristics is necessary. there has always been some limitation in catering proper healthcare services to these patients due to lack of detailed good quality data , inadequate policies , proper guidelines, funding and public awareness . in our study , the patients from urban and rural areas were comparable . this was probably due to lack of high quality trauma care in rural india. the mortality among these cases was 25.89%. more than 85% cases were of low or middle income groups . the males outnumbered the females with male:female ratio of 2.21:1. the mean age was 31.65+ 5.1 years reflecting the increase in tbi incidence among young adults in similar view as in other studies . 4-5 rta was the most common mode of injury followed by falls. it was the commonest mode in young adults and males and was responsible for more severe injuries. this was because of less traffic sense, overspeeding , not using helmet or seatbelt and drunk driving . while in pediatric and geriatric population fall was more common. gururaj et al6 also studied about the increasing trend of falls among children. whereas fall remains the most common cause in developed world and with aging indian population it has now emerged as most frequent cause in older individuals.7 mechanism of injury is an significant predictor of outcome in tbi.8-9 acute sdh was the most common single intracranial lesion detected in 32.70% cases and was also associated with poor outcome with mortality of 25.21%. narwade n et al10 reported sdh in 16.83% cases. the severity of tbi was more in patients with cortical lesions and these patients also had more incidence of seizures, loc, pupillary non reactivity. ct findings such as mass effect, midline shift, presence of cerebral edema and sah also effect outcome.11-12 around 30.22% patients were operated, mostly with severe or moderate tbi. according to mchugh et al, hypotension, hypoxia and hypothermia were also an independent risk factors for poor outcome.13prehospital care also determines the favourable outcome with early diagnosis and effective intervention.14 we see a lack of prehospital care in this part of india. in india due to lack of emergency services majority of the patients do not get appropriate management in early periods and major deaths that occur, do so within first 2 hours after injury.15 severe injury is directly related to poor outcome. in our study 39.38% patients with severe injury died. the severity can be graded on the basis of gcs on admission, iss, and rotterdam score. previous studies have also shown them as the major total survived % died % n=2134 age year (mean) 31.65+ 15.1 33.24 + 14.5 41.36 + 17.8 sex male 1470(68.89) 1311(89.18) 159(10.81) female 664(31.11) 590 (88.85) 74(11.14) iss mean 11.3(10.2-12.4) 10.6 (10.0-11.2) 26.5(23.2-29.7) rotterdam score mean 2.1(1.6-2.8) 1.8(1.5-2.1) 3.9(3.5-4.3) gcs on admission mean 13.4(12.1-14.7) 12.0(11.0-13.0) 5.2(4.5-5.9) pupil reactive 1591(74.83) 1534(96.41) 57(3.58) non reactive 543(25.44) 367(67.59) 176(32.41) blood pressure (sbp) <90 mmhg 249(11.69) 156(62.65) 93(37.35) >90 mmhg 1885(88.33) 1745(92.57) 140(7.42) spo2 <90 % 339(15.89) 216(63.71) 123(36.28) >90% 1795(84.11) 1685(93.87) 110(6.12) alcohol/drug intoxication 310(14.52) 243(78.38) 67(21.61) pre-existing systemic disease 163(7.63) 131(80.36) 32(19.63) management conservative 1489(69.78) 1364 (91.60) 125(8.39) operated 645(30.22) 537 (83.26) 108(16.74) severity of injury* mild (13-15) 1048 (49.10) 1036(98.85) 12 ( 1.1 ) moderate(9-12) 662 (31.02) 608(91.84) 54 ( 8.15) severe (<8) 424 (19.86) 257(60.61) 167 (39.38) 375 epidemiological, demographic and clinical profile of traumatic brain injury patients determinant.16,18-19 the overall mortality was 10.91% while other studies by row bothom17 and khursheed et al18 had mortality of 17.55 and 27.8% respectively. mortality was more with severe injuries, operated and patients shifted to icu. the prognosis of these patients is mostly dependent upon the prehospital factors, neurological status (gcs) at the time of admission19 , age , mechanism of injury , iss 18, rotterdam score18 , associated injuries , presence of hypoxia and hypotension13,9 . all patients with severe injury do not have poor outcome. in our study also, 60.61% patients with severe injury survived and thus aggressive and timely management of all patients is necessary. also early and appropriate care is a major factor in avoiding secondary injuries and death .20 with detailed understanding of these factors , we can develop new plans, formulate better policies, increase public awareness. this all will lead to improvement in early diagnosis and management. the data of this study may be used for prognostication, formulation of hypothesis, developing prognostic models21. references 1. pruthi n , ashok m, kumar vs , jhavar k, sampath s, devi bi . magnitude of pedestrian head injuries and fatalities in bangalore , south india : a retrospective study from an apex neurotrauma center . indian j med res 2012;136:1039-43. 2. who . world report on road traffic injury prevention . geneva : world heath organization; 2004. 3. maas ai ,stocchetti n , bullock r. moderate and severe traumatic brain injury in adults . lancet neurol. 2008;7(8):728-41. 4. g. gururaj. an epidemiological approach to prevention prehospital care and rehabilitation in neurotrauma .neurology india 43(3) (1995):95-105. 5. shukla d, devi bi . mild traumatic brain injuries in adults. j neurosci rural pract. 2010;1:82-88. 6. gururaj g, epidemiology of traumatic brain injuries: indian scenario. neurol res. 2002;24:24-28. 7. marmarou a, lu j , butcher i, et al. prognostic value of the glasgow coma scale and pupil reactivity in traumatic brain injury assessed pre-hospital and on enrollment: an impact analysis . j neurotrauma 2007;24:270-280. 8. monsef kasmaei v, asadi p, zohrevandi b, raouf mt. an epidemiologic study of traumatic brain injuries in emergency department.emerg (tehran) 2015;3:141‑5. 9. nortje j, menon dk. traumatic brain injury: physiology, mechanisms, and outcome. curr opin neurol 2004;17:711‑8. 10. narwade n , narwade p, ghosalkar m, shaikh tp, sharma y, khan n et al.clinical profile and management of head injury at tertiary health care center in rural area, india. int j res med sci 2015;3:3137-40. 11. maas ai, hukkelhoven cw, marshall lf, steyerberg ew. prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. neurosurgery. 2005;57:1173-1182. 12. eisenberg hm, gary he jr, aldrich ef, saydjari c , marmarou a, marshall lf et al. initial ct findings in 753 patients with severe head injury . a report from the nih traumatic coma data bank . j neurosurg 1990;73:688698 . 13. mchugh gs , engel dc , butcher i , et al . prognostc value of secondary insults in traumatic brain injury : results from impact study. j neurotrauma 2007;24:287-293. 14. dash hh. prehospital care of head injured patients. neurol india 2008;56:415-419. 15. kamal vk , agrawal d, pandey rm. epidemiology, clinical characteristics and outcomes of traumatic brain injury : evidences from integrated level 1 trauma center in india. j neurosci rural pract. 2016;7:515-525 . 16. leitgeb j, mauritz w, brazinova a, majdan m, wilbacher i. impact of concomitant injuries on outcomes after traumatic brain injury. arch orthop trauma surg. 2013;133:659-668. 17. rowbotham gf , maciver in , dickson j , bousfield me. analysis of 1400 cases of acute injury to the head . br med j. 1954;1(4864):726-30. 18. khursheed et al :predictors of outcome following traumatic brain injuries: experience of a tertiary healthcare institution in northwest india . world neurosurg. 2019 19. teasdale g, jennett b. assessment of coma and impaired consciousness. a practical scale. lancet 1974;2:81-4. 20. murthy tv , bhatia p, sandhu k, prabhakar t, gogna rl. secondary brain injury: prevention and intensive care management . indian j neurotrauma. 2005;2:7-12 . 21. kamal vk , agrawal d, pandey rm. prognostic models for prediction of outcomes after traumatic brain injury based on patients admission characteristics. brain inj. 2016;30:393-406. 16sasikala_kernohan2014 romanian neurosurgery (2014) xxi 1: 109 112 109 kernohan-woltman notch phenomenon and intention tremors in case of chronic subdural hematoma p. sasikala1, bindu menon2, amit agarwal3 narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 1assistant professor of physiology, department of physiology 2professor of neurology, department of neurology 3professor of neurosurgery, department of neurosurgery abstract movement disorders are atypical and rare presentation of chronic subdural hematomas. we report a case of 60 year man who presented with intention tremors and altered sensorium. the patient had kernohan-woltman notch phenomenon on clinical examination. ct scan brain showed a large left fronto-temporo-parietal chronic subdural hematoma with significant mass effect and midline shift. his symptoms relieved completely after surgical evacuation of the hematoma. key words: chronic subdural hematoma, kernohan-woltman notch, tremors, intention tremor. introduction chronic subdural hematomas (csdh) can present with a wide variety of symptoms, however movement disorders (the most common is secondary parkinsonism) in csdh are atypical and rare presentations. (1, 2) kernohanwoltman notch phenomenon appears when any supratentorial mass lesion cause the midline shift and there is compression of the cerebral peduncle against the tentorial edge ipsilateral hemiparesis or hemiplegia and mydriasis. (3-5) the appearance of kernohan-woltman notch phenomenon has rarely been reported in patients with csdh. (4-7) in present article we report an extremely rare presentation as intention tremors and kernohan-woltman notch phenomenon that resolved after surgical evacuation. case report a 60-year-old man presented with progressive stiffness and weakness of all four limbs (left more than right), abnormal movements of right upper limb and altered senosirum of two days duration. there was not history of fall. there was no past history of diabetes or hypertension. he had pulse rate of 50 per minute. other general and systemic examination was unremarkable. on neurological examination he was in altered sensorium. tone was increased in all four limbs. there was weakness of grade 0/5 of left upper 110 sasikala et al kernohan-woltman notch phenomenon in chronic subdural hematoma and lower limbs. he was localizing with right upper limb. all the deep tendon reflexes were brisk and planters were extensor. there was mild papillary asymmetry (left>right) but both were reacting to light. he had irregular low frequency tremor those were becoming grossly uncontrollable with these attempted movements (video-1). routine hematological and biochemical investigations were within normal limits. ct brain plain showed a largely hyperdense collection with layering over left fronto-temporo-parietal region with significant mass effect and midline shift (figure 1). he underwent left frontal and temporal burr hole under local anesthesia and evacuation of chronic subdural hematoma. he made significant improvement over next 24 hours in his sensorium. he regained consciousness, his weakness improved and abnormal movements disappeared over next 48 hours (video-2). figure 1 ct brain plain showing a largely hyperdense collection with layering over left fronto-temporoparietal region with significant mass effect and midline shift discussion sudden onset of movement disorder in the elderly patients requires prompt radiological investigations to rule out treatable causes of these dysfunctions. (2) movement disorders in csdh patients probably caused by a pressure effect on basal ganglia structures (8, 9) or by altering the function of neurotransmitters. (9) compression of midbrain (interfere nigro-striatal dopaminergic transmission) (10) and compression of anterior choroidal artery (11) however in contrast to the resting tremors of the parkinsonism (12, 13) the present patient had intention tremors. intention tremors are mainly occurs in cerebellar disorders, characterized as a kinetic tremor with a prominent intention component and the ipsilateral extremity is involved when a cerebellar hemisphere in involved. (14, 15) also as the cerebellum is connected to contralateral thalamus and cortex, both cerebellar lesions and contralateral thalamocortical lesions can result in cerebellar dysfunction. (15, 16) it has been suggested that the cerebellum, superior cerebellar peduncles, red nucleus, and thalamus can be involved in the generation of intentions tremors and the modulation of cerebello-thalamic projections has been shown to improve the tremors. (17, 18) on imaging studies atrophic structures or changes in signal intensity has been demonstrated in the cerebello-rubral thalamic tract and the etiological significance of the tract has been confirmed as the mechanism of the romanian neurosurgery (2014) xxi 1: 109 112 111 intention tremors. (19) direct pressure on or invasion of deep basal ganglonic structures and brain stem compression due to upward or downward herniations which displaces the midbrain against the tentorial edge (20, 21) could be responsible not only for the tremors but also for the hemiparesis. hemiparesis can be found in up to 58% of cases of csdh and mostly the deficit is contralateral to the lesion (direct pressure on the cerebral hemisphere). (22) in rare circumstances the focal neurological deficit can be ipsilateral to csdh. (5, 22) our patient had ipsilateral weakness, abnormal movements in the upper limb, marginal asymmetry of the pupils, a finding consistent with kernohan-woltman notch phenomenon. (3, 5) apart from that the prompt evacuation leads to complete reversal of kernohan-woltman notch phenomenon and complete recovery of motor functions. (4-6) address for correspondence: dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1. bostantjopoulou s, katsarou z, michael m, petridis a. reversible parkinsonism due to chronic bilateral subdural hematomas. journal of clinical neuroscience: official journal of the neurosurgical society of australasia 2009;16:458-460. 2. gelabert-gonzalez m, serramito-garcia r, aranechabe e. parkinsonism secondary to subdural haematoma. neurosurgical review 2012;35:457-460; discussion 460-451. 3. kernohan jw, woltman hw. incisura of the crus due to contralateral brain tumor. archives of neurology and psychiatry 1929;21:274. 4. moon k-s, lee j-k, joo s-p, et al. kernohan's notch phenomenon in chronic subdural hematoma: mri findings. journal of clinical neuroscience: official journal of the neurosurgical society of australasia 2007;14:989992. 5. albayrak s, ucler n, ayden o, cakin h. kernohanwoltman notch phenomenon related to chronic subdural hematoma: a case report. journal of medical cases 2012;3:20-22. 6. itoyama y, fujioka s, ushio y. kernohan's notch in chronic subdural hematoma: findings on magnetic resonance imaging. journal of neurosurgery 1995;82:645-646. 7. yamasaki f, kodama y, hotta t, yuki k, taniguchi e, hashizume a. [magnetic resonance imaging of kernohan's notch in chronic subdural hematoma]. no to shinkei = brain and nerve 1997;49:563-566. 8. garcía de y'ebenes j, gervas jj, iglesias j, mena ma, martín del rio r, somoza e. biochemical findings in a case of parkinsonism secondary to brain tumor. annals of neurology 1982;11:313-316. 9. sandyk r, kahn i. parkinsonism due to subdural hematoma. case report. journal of neurosurgery 1983;58:298-299. 10. ling mj, aggarwal a, morris jgl. dopa-responsive parkinsonism secondary to right temporal lobe haemorrahage. movement disorders: official journal of the movement disorder society 2002;17:402-404. 11. kotagal s, shuter e, horenstein s. chorea as a manifestation of bilateral subdural hematoma in an elderly man. archives of neurology 1981;38:195. 12. chou sm, gutmann l. deteriorating parkinsonism and subdural hematomas. neurology 2001;57:1295. 13. sandyk r. parkinsonism caused by chronic subdural haematoma. a case report. south african medical journal = suid-afrikaanse tydskrif vir geneeskunde 1982;61:595-596. 14. chou k. diagnosis and management of the patient with tremor. medicine and health, rhode island 2004;87:135. 112 sasikala et al kernohan-woltman notch phenomenon in chronic subdural hematoma 15. crawford p, zimmerman ee. differentiation and diagnosis of tremor. american family physician 2011;83:697. 16. jankovic j, stanley f. physiologic and pathologic tremorsdiagnosis, mechanism, and management. annals of internal medicine 1980;93:460-465. 17. herzog j, hamel w, wenzelburger r, et al. kinematic analysis of thalamic versus subthalamic neurostimulation in postural and intention tremor. brain: a journal of neurology 2007;130:1608-1625. 18. hamel w, herzog j, kopper f, et al. deep brain stimulation in the subthalamic area is more effective than nucleus ventralis intermedius stimulation for bilateral intention tremor. acta neurochirurgica 2007;149:749-758; discussion 758. 19. fukuhara t, gotoh m, asari s, ohmoto t. magnetic resonance imaging of patients with intention tremor. computerized medical imaging and graphics: the official journal of the computerized medical imaging society 1994;18:45-51. 20. oliver l. parkinsonism due to midbrain compression. lancet 1959;2:817. 21. polyzoidis k, mcqueen j, rajput a, macfadyen d. parkinsonism as a manifestation of brain tumor. surgical neurology 1985;23:59-63. 22. luxon lm, harrison mj. chronic subdural haematoma. the quarterly journal of medicine 1979; 48:43-53. doi: 10.33962/roneuro-2022-043 letter to the editor: a new enthusiastic generation of romanian neurosurgery stefan grădinaru, andrei adrian popa, corneliu toader romanian neurosurgery (2022) xxxvi (2): pp. 247-248 doi: 10.33962/roneuro-2022-043 www.journals.lapub.co.uk/index.php/roneurosurgery letter to the editor: a new enthusiastic generation of romanian neurosurgery stefan grădinaru1, andrei adrian popa2, corneliu toader2,3 1 lucian blaga university, faculty of medicine, sibiu, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 national institute of neurology and neurovascular diseases, bucharest, romania abstract at the beginning of every spring, cluj becomes for 3 days the main topic of discussion among students passionate about neurosurgery throughout romania. the ''neurosurgical masterclass'' is the catalyst for young and enthusiastic students to learn the mysteries of the human brain and this year was organized the 10th edition of this interesting congress. the event succeeded in joining together 185 neurosurgery enthusiasts and 36 renowned speakers. image 1. prof. ioan-stefan florian m.d. phd. with attendees of the event. keywords romanian, neurosurgery, new generation corresponding author: corneliu toader national institute of neurology and neurovascular diseases, bucharest, romania corneliutoader@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 248 stefan grădinaru, andrei adrian popa, corneliu toader since neurosurgery is a practical medical specialty, the first day began with unique workshops, from viewing a live operation that familiarized students with some anatomical landmarks, to the dissection of the white substance of the brain. the participants also had a demonstration of correct and complete neurological examination, so that the young students were initiated into the basic neurosurgical terminology. overall, 7 hands-on workshops were organized. in a festive spirit, the guest of honor was the distinguished prof. dr. madjiid samii from the international neuroscience institute (hannover, germany) who opened the proceedings of the congress with the presentation "what i could develop in neurosurgery", offering an auspicious energy and an encouraging word for the students. image 2. stud. dragos font and prof. ioan-stefan florian m.d. phd. presiding over the student session. prof. madjid samii's presentation was followed by the work of our resident colleague at the institute of neurology and neurovascular diseases bucharest, dr. andrei alexandru marinescu, who delighted us with the secrets of cerebral vascularization, presenting in detail the willis' circle. after two sessions of presentations, at the end of the first day, the students had the opportunity to participate in the neuroquiz anatomy competition, having as the prize neurosurgical study materials of the highest quality. the second day of works was very special being marked by renowned european neurosurgeons such as prof. dr. lukas rasulic, prof. dr. stefano ferarresi (italy) or prof. dr. ishan soraloglu (turkey) who offered more gravitas to this event. the founder of the congress, prof. dr. ioan ștefan florian has impressed as always with the novelty of his works, addressing the students in an accessible and friendly speech. at the same time, student dragoș font, copresident of the congress and leader of the student circle of neurosurgery in cluj-napoca, presented ''an operative perspective of the posterior fossa'', in an impeccable manner. the last day was dedicated exclusively to student presentations. the delegation of serbian students, stud. stefan radojevic and stud. aleksa micic (coordinated by prof. lukas rasulic) impressed with detailed presentation of peripheral neuroanatomy. the delegation of students from the "walter e. dandy" neurosurgical club in bucharest distinguished itself through stud. mădalina popescu, stud. max blega (winner of the neuroquiz contest) and stud. firas al-krayem (winner of the contest for presentations of clinical cases). at the end of the 3 days of congress, each participant left with new interesting and “up-to-date” knowledge, and with new memories to share with other neurosurgery enthusiasts. romanian neurosurgery (2019) xxxiii (4): pp. 396-399 doi: 10.33962/roneuro-2019-064 www.journals.lapub.co.uk/index.php/roneurosurgery pitfalls and problems encountered in rat model sciatic nerve surgery marin andrei1, mihai ruxandra ioana1, marin georgiana gabriela2 1 plastic surgery department, “bagdasar arseni” emergency hospital, bucharest, romania 2 cardiology department, “cc iliescu” hospital, bucharest, romania abstract when learning the basics of microsurgery, a trainee must be equipped with patience and perseverance in order to evolve. one must have the ground knowledge when it comes to peripheral nerve injury and nerve regeneration process in order to fully understand that the technique is vital for the outcome and final results. furthermore, a trainee must practice on non-living tissue before performing successful in vivo operations and even in this case, one may be confronted with problems regarding the surgical technique. [1] the following article aims to reveal the main problems/mistakes when performing sciatic nerve surgery in an in vivo experimental model and the solutions for these problems. introduction there are many experimental surgical projects performed on the sciatic nerve of the rat. [2] there are many reasons why researchers choose this model: high similitude in nerve regeneration between the rat and the human; the lab rat (most commonly used the wistar rat) is more available compared to other species and easier to manipulate; the anatomy of the sciatic nerve of the rat offers easy access, without significant comorbidity; the diameter and the length of the nerve permits different types of experiments (direct suture, reconstruction of different gaps with nerve conducts). [3] the sciatic nerve has a length of ~ 2,5-3cm before it divides into 3 terminal branches common peroneal nerve, tibial nerve and sural nerve. although rat’s sciatic nerve is one of the most used models for nerve regeneration it still may cause difficulties for an inexperienced surgeon. the problems one may encounter are related to anesthesia, [4] rat anatomy knowledge or microsurgical technique and each one of these issues may cause an enormous impact on the final outcome. understanding the theoretical aspects of nerve regeneration [5],[6],[7] may help improve the surgical technique, especially when it comes to atraumatic manipulation. keywords sciatic nerve, rat model, experimental surgery, microsurgical technique corresponding author: marin andrei plastic surgery department, “bagdasar arseni” emergency hospital, bucharest, romania marin_dpt@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 397 pitfalls and problems encountered in rat model sciatic nerve surgery material and method for this review there were used wistar rats in different microsurgery training laboratories. the rats varied in age and weight (between 250-350g or 7-9 weeks). the anesthesia protocol consisted of a mixture of ketamine (75mg/kg) and xylazine (10mg/kg) administered intraperitoneally. a precise scale was used to weigh every animal before administrating the anesthesia. there were used proper microsurgical instruments as well as a microscope and appropriate sutures (8-0,9-0,10-0). wistar rat scale microsurgical instruments sciatic nerve exposure after shaving the dorsal aspect of the gluteal and thigh region, the rat is placed in prone position. an oblique-transverse skin incision is made and dissection along the biceps muscle fibers is performed in order to expose the underlying sciatic nerve. mehedintu et al described different types of incisions to access the sciatic nerve. [7],[8] after nerve exposure, the rest of the operation is done under the microscope. this involves nerve dissection, nerve section and subsequent nerve repair. proximal to the its division, the sciatic nerve can be used for various operations (direct suture after section, autografting, using different nerve conducts for iatrogenic nerve defects). results a frequent mistake of the in vivo experiment is the incorrect administration of the anesthesia, which must be very well dosed and not lead to to overdosing and rat death. aside from the anesthetic issues, the most frequent problems when repairing a nerve defect with autograft arise from lack of experience. [9] these are: identifying the sciatic nerve correctly, improper incision site, excessive nerve dissection for a better exposure, choosing an unsuitable location to create the nerve gap, as well as microsurgical technique errors (inappropriate cooptation, high suture tension). inadequate sutures for the nerve size also influence the recovery results. 398 marin andrei, mihai ruxandra ioana, marin georgiana gabriela distal incision beyond the division of the sciatic nerve (marked with arrow) axoplasmatic protrusion (arrow) in the proximal nerve suture due to insufficient proximal dissection identifying the sciatic nerve correctly poses no problem if the skin incision site and the muscle dissection is performed in the right area and in a proper plane. a distal incision (too lateral and caudal), however, may create confusion in case not all branches are visible, thus mistaking the sciatic nerve to one of its branches. a contributing factor to this problem is represented by the placing of the rat in a slight prone-lateral position (instead of the custom prone position). these branches are half or even 1/3 of the sciatic nerve diameter (~1mm). to prevent this situation, the skin incision should be placed more cranial and medial, parallel and 1cm inferior to the femur, with the rat in prone position. when suspecting that the first incision is inappropriate, with exposure of just one branch of the sciatic nerve, extending the incision more proximal can solve the problem by identifying the correct nerve. another technical error is creating the nerve gap 399 pitfalls and problems encountered in rat model sciatic nerve surgery too proximal (or not dissecting enough of the sciatic nerve from the muscle tissue in the proximal part). after nerve sectioning, the elastic fibers in the structure of the nerve determine retraction of the proximal stump in a plane which is hard to access, thus making the nerve suture difficult to perform. in order to prevent this problem, a proper dissection and the selection of the central area of the sciatic nerve to create the gap is recommended. the consequences of suturing a retracted stump are: inappropriate traction of the nerve (which risks injuring the nerve fascicles), unmatched fascicles in the suture (the surgeon is no longer able to observe the epineural vessels to guide a correct cooptation), axoplasmatic protrusion due to excessive traction and uneven suture. in all cases, inappropriate dissection results in prolonged operating times. creating the nerve gap too distal (close to the division of the sciatic nerve) poses a problem for nerve suturing because an epineural suture tends to shred the common sheath of the branches, dividing them into 3 separate nerves (which require individual repair). the ideal distal sectioning site is ~0,7cm proximal to the visible division of the sciatic nerve in order to have enough connective tissue for a strong nerve suture. discussion it is recommended not to operate on rats lighter than 250g and younger than 7 weeks of age. otherwise the nerve diameter might be smaller than 2mm, requiring adequate microsurgery equipment as well as a greater experience in nerve surgery. above 350g or 9 weeks of age, the animals require more substance to induce anesthesia, without any extra benefits. multiple administration of anesthesia might lead to overdose, causing respiratory distress and in the end exitus. for this reason, if the anesthesia doesn’t work accordingly from the beginning with the calculated dose, the operation should be postponed and the anesthetic options should be revised. the iatrogenic nerve gap should be placed centrally, after exposing the sciatic nerve from its origin to its division. conclusions microsurgery requires adequate instruments and special training. calculating the exact quantity of anesthetic reduces the death risk. experience and attention are key factors in avoiding different complications related to nerve surgery. the microsurgical technique involves an atraumatic manipulation of the tissue, correct cooptation without suture tension and right alignment of the nerve fascicles. respecting these rules results in a good nerve regeneration, with positive clinical outcomes. references 1. christensen tj, anding w, shin ay, bishop at, moran sl.the influence of microsurgical training on the practice of hand surgeons. j reconstr microsurg. 2015 jul;31(6):442-9. doi: 10.1055/s-0035-1549443. epub 2015 apr 20. 2. andrei marin, georgiana gabriela marin, anca patea, dan mircea enescu. timing, logistics and bureaucratic process in planning an experimental in vivo nerve regeneration project from a to z. modern medicine | 2019, vol. 26, no. 2 3. marin andrei, marin georgiana gabriela, dobrete nicoleta amalia, enescu dan mircea. learning curve in rat dissection for experimental sciatic nerve repair. romanian neurosurgery (2019) xxxiii (3) september 2019. www.journals.lapub.co.uk/index.php/roneurosurgery 4. costea ruxandra, daniel lastofka, and mihai mehedinţu. "comparison of ketamine–medetomidine-butorphanol and ketamine–dexmedetomidine-butorphanol anesthesia in rats." agriculture and agricultural science procedia 6 (2015): 305-308. 5. lastofka, d., manolescu, n., balint, e., costea, r., & ionescu, m. m. (2017). histopathological modifications in sciatic nerve allograph in wistar rats. journal of biotechnology, 256, s86. 6. scholz t, krichevsky a, sumarto a, et al. peripheral nerve injuries: an international survey of current treatments and future perspectives. j reconstr microsurg 2009;25(6):339– 44 7. andrei, m., ioana, m., & mircea, e. (2019). underlying histopathology of peripheral nerve injury and the classical nerve repair techniques. romanian neurosurgery, 33(1), 17-22. https://doi.org/10.33962/roneuro-2019-003 8. mihai mehedintu-ionescu, ovidiu stefanescu, radu cristian jecan. nervous regeneration allograph type of periferic nerv. modern medicine | 2019, vol. 26, no. 2 9. ionescu, m. m., costea, r., balint, e., & lastofka, d. (2017). surgery technique models of sciatic nerve allograph in wistar rats. abstracts/journal of biotechnology 256s, 44, s116 10. kuffler dp. an assesment of current techniques for inducing axon regeneration and neurological reovery following peripheral nerve trauma. prog neurobiol 2014;116:1-12. microsoft word 12tacucristina_gaittemporospatial.doc romanian neurosurgery (2010) xvii 3: 339 – 347 339 gait temporospatial parameters: assessment tools for postsurgical recovery in patient with different anatomotopographic types of lumbar disc herniation cristina tacu1, n ianovici2, elena rezus3, i.s. stratulat4, silvia nicoleta miu5 1rheumatology, university of medicine and pharmacy “gr.t. popa” iasi, ph d candidate 2neurosurgery, university of medicine and pharmacy “gr.t. popa” iasi 3rheumatology, university of medicine and pharmacy “gr.t. popa” iasi 4functional dental rehabilitation, university of medicine and pharmacy “gr.t. popa” iasi 5precision mechanics department, university of polytechnic, bucharest abstract the development in technology and informatics in the last decades enables integrated analysis of biomechanical and clinical data and facilitates the understanding of relations between human gait characteristic and different medical conditions of a patient. the aim of the study was to demonstrate the importance of gait temporospatial parameters analysis [opposite foot off, opposite foot contact, foot off, cadence, step length, walking speed, step time, step width, stride length, stride time] to quantify the response to surgical treatment for patients with lumbar disc herniation related to the anatomotopographic type of disc herniation. the study was prospective, with consecutive selection of subjects according to eligibility criteria, using a control group. the number of subjects was 64: 41 patients [61% with extensive lumbar disc hernia, 22% with paracentral lumbar disc hernia and 17% with intraforaminal lumbar disc herniation] and 23 healthy subjects. the flowchart had 2 visits: presurgical evaluation and postsurgical evaluation. the patients were evaluated clinically, imagistically and biomechanically. the biomechanical evaluation was performed with vicon mx optical motion capture system. data of interest were temporospatial parameters of gait: opposite foot off, opposite foot contact, foot off, cadence, step length, walking speed, step time, step width, stride length, stride time. specific statistic techniques were used in order to confirm the results. the most consistent response in terms of normalization of gait temprospatial parameters are to be observed in patients with intraforaminal herniation, followed by patients with paracentral disc herniation. the gait temprospatial parameters of patients with extensive lumbar disc herniation responded the least in terms of normalization. keywords: gait, lumbar disc herniation, presurgical, postsurgical 340 cristina tacu et al gait temporospatial parameters introduction the development in technology and informatics in the last decades enables integrated analysis of biomechanical and clinical data and facilitates the understanding of relations between human gait characteristic and different medical conditions of a patient. technological applications in the study of human gait provide medical specialists with accurate data that broaden the spectrum of information, data that they could not achieve through simple clinical observation. there are numerous studies that analyze gait from both kinematical and kinetic points of view and focus on a wide range of neurological pathologies [1, 2, 3, 4] orthopedics pathologies [5, 6], rheumatology pathologies [7, 8], nutritional diseases [9, 10] and thus provided data used in current practice. the study of human gait in relation to spine pathology represents a topic of great interest for medical researchers, given the socio-economic impact that this type of pathology generates [11, 12]. aim of this study is to demonstrate the importance of gait temporospatial parameters analysis [opposite foot off, opposite foot contact, foot off, cadence, step length, walking speed, step time, step width, stride length, stride time] in the assessment of patient recovery after surgical treatment, related to different anatomotopographic types of lumbar disc herniation. material and methods study protocol the study was prospective, with consecutive selection of patients according to eligibility criteria, using a control group. number of subjects was 64: 41 patients and 23 subjects without clinical symptoms who represented the control group. the average (+/standard deviation) age, mass and height of the patients were 41.1 years old (+/-10), 69.8 kg (+/7.3), and 167.5 cm (+/6.8). the average (+/standard deviation) age, mass and height of the subjects from control group were 38,1 years old (+/7.8), 64.2 kg (+/6.5), 168.2 cm (+/8.9). within the group of patients, the anatomotopographic types of lumbar disc herniation cases were divided as follows: 61% extensive herniated disc type, 22% paracentral herniated disc type and 17% intraforaminal type. the study flowchart covered the following steps: patient selection (1-2 days), the preoperative evaluation visit 2 weeks prior to surgery (clinical, biomechanical and imagistic) and the postoperative monitoring visit one month after surgery (clinical and biomechanical evaluation). the procedures during patient selection included: signing the informed consent before the beginning of any study procedure (icf was approved by the ethical commission of the rehabilitation hospital in iaşi) and checking patient eligibility according to inclusion and exclusion criteria. inclusion criteria were: age above 18 when signing the icf, mechanical low back pain unilaterally irradiated on radicular territory of l5/s1 +/neurological signs corresponding to the radicular condition [without motor deficit], slowly resolving clinical phenomena with a duration of at romanian neurosurgery (2010) xvii 3: 339 – 347 341 least 4 weeks, documenting the presence of disc hernia through ct or mri, their independent walking ability. exclusion criteria were: no systemic disease with relevant influence on walking ability, no orthopedic surgeries, conditions which are taken into account during the “red flags” screening and generate low back pain, motor deficit corresponding to radicular pain l5/s1, counter indications in ct or mri exploring, presence of the biological syndrome of inflammation. the biomechanical evaluation was performed inside the biomechanics and motion analysis laboratory belonging to the university of medicine and pharmacy “gr.t. popa” iaşi, using the vicon advanced optical motion capture system the imagistic evaluation was performed using ct or irm in order to demonstrate the existence of lumbar disc herniation and to classify the anatomotopographic type of hernia: paracentral, extensive or intraforaminal. methods material: selected patient group and the control group, lumbar spine images (computed tomography and nuclear magnetic resonance imaging), patients’ clinical exploration data files and vicon optical motion capture system. the biomechanical evaluation included the following steps: preparing the room, preparing the patient (placing the retroreflexive markers on the points of interest according to vicon work protocol), real-time digital translation of retroreflexive markers and reconstruction of their three-dimensional coordinates according to the two-dimensional video images. the study focused on temporospatial parameters: opposite foot off, opposite foot contact, foot off, cadence [step frequency], step length, walking speed, step time, step width, stride length, stride time. statistical processing primary processing, namely the systematization of data by grouping and centralizing, led to the formation of a primary indicators database. data were loaded and processed using statistical functions in excel, epiinfo and spss. the following statistical methods were applied: the anova test, the t-student test and the χ2 test. results and discussion after statistical processing of gait temporospatial parameters monitored one month after surgery for patients with extensive herniated disc the following issues are extensively outlined: 1. average values of opposite foot off, opposite foot contact, foot off, double support time, step time, stride time parameters decreased significantly from a statistical point of view; 2. average values of cadence, step length, speed, step width and stride length parameters increased significantly from a statistical point of view. a significant improvement of gait temporospatial parameters after surgery can be observed in the extensive herniated disc group, but differences from the control group remain highly statistically significant (table 1). 342 cristina tacu et al gait temporospatial parameters table 1 statistical differences of average values of gait temporal-spatial parameters monitored for the patients with extensive herniated disc extensive herniated disc group control group vs. postsurgical extensive herniated disc group parameter presurgically postsurgically t p reference values t p foot strike [%] 0 0 opposite foot off [%] 20.50±4.71 17.00±7.10 2.27 p<0.05 9.69±2.38 6.20 p<0.001 opposite foot contact [%] 49.56±1.33 46.70±5.30 2.30 p<0.05 43.01±4.66 2.93 p<0.05 foot off [%] 68.84±5.28 64.70±8.40 2.34 p<0.05 58.91±1.82 4.38 p<0.001 cadence [step/min] 71.26±16.11 77.30±4.56 2.34 p<0.05 98.23±4.20 18.20 p<0.001 double support time[s] 0.77±0.42 0.60±0.23 2.20 p<0.05 0.42±0.14 3.97 p<0.001 step length [m] 0.39±0.08 0.43±0.07 2.21 p<0.05 0.60±0.04 12.64 p<0.001 walking speed [m/s] 0.47±0.20 0.59±0.13 3.06 p<0.01 1.08±0.12 15.42 p<0.001 step time [s] 0.90±0.29 0.72±0.24 2.83 p<0.01 0.42±0.39 3.37 p<0.002 step width [m] 0.17±0.06 0.20±0.05 2.27 p<0.05 0.24±0.04 3.56 p<0.001 stride length [m] 0.78±0.17 0.90±0.19 2.69 p<0.01 1.33±0.10 12.14 p<0.001 stride time [s] 1.76±0.55 1.41±0.45 2.92 p<0.01 1.23±0.05 2.62 p<0.05 parameter improvement percentage for the group with extensive herniated disc changed as follows (figure 1): opposite foot off, 111.6% higher presurgically and 75.4% higher postsurgically than the value recorded in the control group; the decrease of average values after surgical treatment was 36.1%; opposite foot contact, 15.2% higher presurgically and 8.6% higher postsurgically than the value recorded in the control group; a decrease of 6.6% after surgical treatment; foot off, 16.9% higher presurgically and 9.8% higher postsurgically, with a decrease of 7% after surgical treatment; cadence, 27.5% lower presurgically and 21.3% postsurgically as compared to the control group; the postsurgical increase of cadence was of 6.1%; double support time was presurgically 83.3% higher and postsurgically 42.9% higher than that of the control group; the decrease of the average values after surgical treatment was 40.5%; step length, 35% lower presurgically and 28.3% lower postsurgically as compared to the control group; the postsurgical values increase was 6.7%; walking speed, 56.6% lower presurgically and 45.4% lower postsurgically as compared to the control group; the postsurgical increase compared to presurgical value was 11.1%; step time, 114.3% higher presurgically and 71.4% higher postsurgically as compared to the control group; but the decrease of average values after surgery was 42.9%; step width, 29.2% lower presurgically and 16.7% lower postsurgically as compared to the control group; the postsurgical increase was 12.5%; stride length, 41.4% lower romanian neurosurgery (2010) xvii 3: 339 – 347 343 presurgically and 32.3% lower postsurgically as compared to the control group; it improved postsurgically by 9%; stride time, 44.7% higher presurgically and 14.6% higher postsurgically as compared to the control group; the decrease of average values after surgery was 30.1%. for the paracentral herniated disc patients, the postsurgical evaluation shows significant differences for all parameters, closer to the reference values of the control group: opposite foot contact, step time, step width (table 2). 116.6 15.2 16.9 -27.5 83.3 -35 -56.5 114.3 -29.2 -41.4 44.7 75.4 8.6 9.8 -21.3 42.9 -28.3 -45.4 71.4 -16.7 -32.3 14.6 -80 -60 -40 -20 0 20 40 60 80 100 120 140 op po sit e f oo t o ff op po sit e f oo t c on ta ct fo ot of f ca de nc e do ub le su pp or t st ep le ng th sp ee d st ep tim e st ep w id th st rid e l en gt h st rid e t im e % presurgically postsurgically figure 1 percentage evolution of gait temporospatial parameters for the patients with extensive herniated disc group table 2 statistical differences of average values of parameters monitored for the patients with paracentral herniated disc paracentral herniated disc group control group vs. postsurgical paracentral herniated disc group parameter presurgically postsurgically t p reference values t p foot strike [%] 0 0 opposite foot off [%] 22.78±6.28 13.50±5.99 3.20 p<0.01 9.69±2.38 2.12 p<0.05 opposite foot contact [%] 50.53±2.46 45.20±6.12 2.20 p<0.05 43.01±4.66 1.09 p>0.05 foot off [%] 70.01±3.22 66.10±4.15 2.14 p<0.05 58.91±1.82 5.72 p<0.001 cadence [step/min] 67.48±12.19 87.11±10.15 3.77 p<0.002 98.23±4.20 3.64 p<0.001 double support time [s] 0.81±0.31 0.56±0.13 2.45 p<0.05 0.42±0.14 2.94 p<0.01 step length [m] 0.36±0.08 0.48±0.09 2.92 p<0.01 0.60±0.04 4.40 p<0.001 walking speed [m/s] 0.40±0.16 0.88±0.32 3.71 p<0.002 1.08±0.12 2.09 p<0.05 step time [s] 0.92±0.17 0.62±0.20 3.33 p<0.01 0.42±0.39 2.01 p>0.05 step width [m] 0.17±0.04 0.22±0.05 2.26 p<0.05 0.24±0.04 1.20 p>0.05 stride length [m] 0.69±0.19 0.93±0.22 2.41 p<0.05 1.33±0.10 5.98 p<0.001 stride time [s] 1.85±0.33 1.44±0.32 2.66 p<0.05 1.23±0.05 2.26 p<0.05 344 cristina tacu et al gait temporospatial parameters parameter improvement percentage for the group with paracentral herniated disc changed as follows (figure 2): opposite foot off, 135.1% higher presurgically and 39.3% higher postsurgically as compared to the control group, the decrease of average values after surgery was 95.8%; opposite foot contact, 17.5% higher presurgically and 5.1% higher postsurgically as compared to the control group, with a decrease of 12.4% after surgery; foot off, 18.8% higher presurgically and 12.2% higher postsurgically as compared to the control group, with a decrease of 6.6% after surgery; cadence, 31.3% lower presurgically and 11.3% postsurgically, as compared to the control group; the increase of cadence postsurgically compared to presurgically was 20%; double support time, 92.9% higher presurgically and 33.3% higher postsurgically as compared to the control group, the decrease of the average values was 59.5%; step length, 40% lower presurgically and 20% postsurgically as compared to the control group; the increase was 20%; walking speed, 63% lower presurgically and 18.5% postsurgically as compared to the control group; the increase was 44.4%; step time, 119% higher presurgically and 47.6% postsurgically as compared to the control group; the decrease of the average values postsurgically was 71.4%; step width, 29.2% lower presurgically and 8.3% postsurgically as compared to the control group; the postsurgical increase was 20.8%; stride length, 48.1% lower presurgically and 30.1% postsurgically as compared to the control group; the postsurgical improvement was 18%; stride time, presurgically 50.4% higher and 17.1% postsurgically as compared to the control group; the decrease of average values after surgical treatment was 33.3%. the postsurgical evaluation of intrafornaminal disc hernia patients revealed significant differences of all parameters, close to the reference values of the control group: opposite foot off, foot off, double support, step length, step time, step width, stride length (table 3). 116.6 15.2 16.9 -27.5 83.3 -35 -56.5 114.3 -29.2 -41.4 44.7 75.4 8.6 9.8 -21.3 42.9 -28.3 -45.4 71.4 -16.7 -32.3 14.6 -80 -60 -40 -20 0 20 40 60 80 100 120 140 op po sit e f oo t o ff op po sit e f oo t c on tac t fo ot of f ca de nc e do ub le su pp or t st ep le ng th sp ee d st ep tim e st ep w id th st rid e l en gt h st rid e t im e % presurgically postsurgically figure 2 percentage evolution of gait temporospatial parameters for the patients with paracentral herniated disc group romanian neurosurgery (2010) xvii 3: 339 – 347 345 table 3 statistical differences of average values of parameters monitored for the patients with intraforaminal herniated disc intraforaminal disc hernia group control group vs. postsurgical intraforaminal herniated disc group parameter presugically postsurgically t p reference values t p foot strike [%] 0 0 opposite foot off [%] 18.79±3.65 10.22±2.55 6.55 p<0.001 9.69±2.38 0.67 p>0.05 opposite foot contact [%] 50.08±1.48 46.12±2.58 3.81 p<0.002 43.01±4.66 2.48 p<0.05 foot off [%] 68.72±4.18 59.10±4.22 5.09 p<0.001 58.91±1.82 0.19 p>0.05 cadence [step/min] 74.97±8.42 85.25±6.53 3.21 p<0.01 98.23±4.20 7.63 p<0.001 double support time [s] 0.62±0.21 0.46±0.05 2.95 p<0.01 0.42±0.14 1.13 p>0.05 step length [m] 0.43±0.07 0.58±0.08 4.33 p<0.001 0.60±0.04 1.04 p>0.05 walking speed [m/s] 0.53±0.12 0.88±0.27 3.30 p<0.01 1.08±0.12 3.16 p<0.01 step time [s] 0.81±0.11 0.52±0.17 4.17 p<0.001 0.42±0.39 0.99 p>0.05 step width [m] 0.17±0.05 0.22±0.03 3.01 p<0.01 0.24±0.04 1.73 p>0.05 stride length [m] 0.84±0.13 1.28±0.35 3.24 p<0.01 1.33±0.10 0.65 p>0.05 stride time [s] 1.63±0.21 1.39±0.14 3.27 p<0.01 1.23±0.05 5.06 p<0.001 93.9 16.4 16.7 -23.7 47.6 -28.3 -50.9 92.9 -29.2 -63.9 32.5 5.5 7.2 0.3 -13.2 9.5 -3.3 -18.5 23.8 -8.3 -3.8 13 -80 -60 -40 -20 0 20 40 60 80 100 120 op po sit e f oo t o ff op po sit e f oo t c on tac t fo ot of f ca de nc e do ub le su pp or t st ep le ng th sp ee d st ep ti me st ep w id th st rid e l en gt h st rid e t im e % presurgically postsurgically figure 3 percentage evolution of gait temporospatial parameters for the patients with intraforaminal herniated disc group parameter improvement percentage for the group with intraforaminal herniated disc changed as follows (figure 3): opposite foot off, 93.9% higher presugically and 5.5% higher postsurgically than the values recorded for the control group; the decrease of average values after surgical treatment was 88.4%; opposite foot contact, 16.4% higher presurgically and 7.2% higher postsurgically than the values recorded in the control group; a decrease of 9.2% after surgical 346 cristina tacu et al gait temporospatial parameters treatment as compared to the control group. foot off, 16.7% higher presurgically and 0.3% higher postsurgically, with a decrease of 16.3% after surgical treatment; cadence, 23.7% lower presurgically and 13.2% postsurgically as compared to the control group; the cadence postsurgical increase was 10.5%; double support, 47.6% higher presurgically and 9.5% higher postsurgically than the value recorded in the control group; the decrease of average values postsurgically was 38.1%; step length, 28.3% lower presurgically and 3.3% postsurgically as compared to the control group; the postsurgical increase was 25%; walking speed, 50.9% lower presurgically and 18.5% postsurgically as compared to the control group; the postsurgical increase was of walking speed was 32.4%; step time, 92.8% higher presurgically and 23.8% postsurgically as compared to control group; the average values decrease after surgical treatment was 69%; step width, 29.2% lower presurgically and 8,3% postsurgically as compared to the control group; the postsurgical increase of step width was 20.8%; stride length, 63.9% lower presurgically and 3.8% postsurgically as compared to the control group; the postsurgical improvement was 60.2%; stride time, 32.5% higher presurgically and 13% postsurgically as compared to the control group; the postsurgical decrease of average values was 19.5%. conclusions different types of anatomotopographic lumbar disc hernia are accompanied by different degrees of gait impairment. gait temporospatial parameters can be used in the assessment of postsurgical gait recovery. surgical intervention for lumbar disc hernia is effective, although there is residual gait impairment. the most consistent response in terms of improvement of gait temprospatial parameters are to be observed in patients with intraforaminal lumbar disc hernia, followed by patients with paracentral lumbar disc hernia. the gait temprospatial parameters of patients with extensive lumbar disc hernia responded the least in terms of improvement of gait temprospatial parameters. acknowlegment the present study was possible due to the logistic support of the center for the study and therapy of pain, university of medicine and pharmacy “gr.t. popa” iaşi. references 1.holden mk, gill km, magliozzi mr, gait assessment for neurologically impaired patients. phys ther, 1986. 66: 530-1539. 2.knutsson e, richards c, different types of disturbed motor control in gait of hemiparetic patients. brain, 1979.102: 405-430. 3.wall jc, turnbull gi, gait asymmetries in residual hemiplegia. arch phys med rehabil, 1986. 67: 550-553. 4.brandstater me, de bruin h, gowland c, clark bm, hemiplegic gait: analysis of temporal variables. arch phys med rehabil, 1983. 64: 583-590. 5.lieberman jr, dorey f, shekelle p et al. differences between patients and physicians' evaluations of outcome after total hip arthroplasty. j. bone joint surg am, 1996. 78(6): 835-838. romanian neurosurgery (2010) xvii 3: 339 – 347 347 6.mattsson e., olsson e., & brostörm, l.a., assessment of walking before and after unicompartmental knee arthroplasty. scand j rehabil med., 1990. 22: 45-50. 7.messier sp, loeser rf, & hoover jl, osteoarthritis of the knee: effects on gait, strength and flexibility. arch phys med rehabil., 1992. 57: 571-577. 8.woodburn j, nelson km, lohmann siegel k, kepple tm, gerber lh, multisegment foot motion during gait: proof of concept in rheumatoid arthritis. j rheumatol, 2004. 31: 918-1945. 9.courtemanche r, teasdale n, boucher p, fleury m, lajoie y, bard c, gait problems in diabetic neuropathic patients. arch phys med rehabil, 1996. 77: 849-855. 10.yavuzer g, yetkin i, toruner fb, koca n, bolukbasi n: gait deviations of patients with diabetes mellitus: looking beyond peripheral neuropathy. eura medicophys, 2006. 42: 127-133. 11.morag e, hurwitz de, andriacchi tp, hickey m, andersson gb, abnormalities in muscle function during gait in relation to the level of lumbar disc herniation. spine, 2000. 25 (7): 829-833. 12.russwurm h, bjerkreim i, ronglan e, lumbar intervertebral disc herniation in the young. acta orthopaedica, 1978. 49(2): 158 – 163. doi: 10.33962/roneuro-2021-047 intracranial myopericitoma. a case report of a rare tumour in a rare location in an aids patient branko đurović, danilo radulović, miloš joković, irena cvrkota, marko đurović, nemanja jovanović, vuk aleksić romanian neurosurgery (2021) xxxv (3): pp. 281-284 doi: 10.33962/roneuro-2021-047 www.journals.lapub.co.uk/index.php/roneurosurgery intracranial myopericitoma. a case report of a rare tumour in a rare location in an aids patient branko đurović1, danilo radulović1, miloš joković1, irena cvrkota1, marko đurović1, nemanja jovanović1, vuk aleksić1,2 1 neurosurgery clinic, clinical centre of serbia, belgrade, serbia 2 department of neurosurgery, clinical hospital centre zemun, belgrade, serbia abstract myopericytoma is a benign, soft tissue tumor probably derived from perivascular myoid cells. they are usually found in subcutaneous tissues in the extremities. intracranial localization of myopericitoma is exceedingly uncommon. we report a 43 years old male patient with incidentally found myopericitoma of the posterior fossa. patient was operated and tumor was completely removed. patient was subsequently diagnosed with acquired immunodeficiency syndrome due to human immunodeficiency virus infection. one year after operation tumor showed no signs of recurrence, but patient developed progressive symptoms of aids and started highly active antiretroviral therapy (haart). connection of intracranial myopericitoma appearance and hiv/aids has been reported before, but clear connection is yet to be elucidated. introduction myopericytoma represents a rare benign lesion most frequently found in soft tissue. however, it may arise in any other location. clinical, neurological and radiological features are unspecific with symptoms arising due to compression of surrounding structures. surgical resection is the treatment of choice with excellent prognosis. pathology examination provides the definite diagnosis, but the differential diagnosis is wide. intracranial location is exceedingly uncommon, and we found only several case reports described in the literature2,7. connection of intracranial myopericitoma appearance and human immunodeficiency virus infection has been reported before, but causal connection is yet to be elucidated1. we present a case of a 43 years old male with incidentally found myopericitoma of the posterior fossa. one year after the operation patient was diagnosed with acquired immunodeficiency syndrome due to human immunodeficiency virus infection. keywords aids/hiv, myopericitoma, intracranial tumour corresponding author: vuk aleksić department of neurosurgery, clinical hospital centre zemun, belgrade, serbia aleksicvuk@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 282 branko đurović, danilo radulović, miloš joković et al. case report we present a case of a 43 years old male gynecologist who was first examined 6 years ago because of typical migraine headaches, when brain computed tomography (ct) showed small dural based extra axial hyperdense lesion in the posterior region of foramen magnum without significant compressive effect, which was confirmed with brain magnetic resonance imaging (mri). the patient was motivated for further intermittent follow-up and consecutive mri showed no signs of lesion expansion and patient remain neurologically intact without symptoms and any complains for almost 6 years. however, patient skipped the last two fallowups since he was clinically suspected for covid-19 infectious disease, although three consecutive pcr tests were negative. shortly after resolution of respiratory symptoms patient abruptly developed ataxia and gait disturbance with severe neck pain after which he was admitted in our emergency department and brain ct scan showed significant enlargement of extra axial lesion in the posterior cranial fossa with signs of cerebellar and fourth ventricle compression, but without signs of hemorrhage nor hydrocephalus (figure 1). figure 1. first brain ct after development of signs and symptoms of cerebellar dysfunction, showing tumor in the cerebellum. patient was transferred to neurosurgical clinic of clinical center of serbia. at department admission he presented with cerebellar symptomatology including ataxia, asthenia and astasia-abasia complex without muscle weakness accept of mild bilateral thigh flexors weakness. also, global hyperreflexia with atypical plantar reflex bilaterally was noted. his past medical history was insignificant. brain mri showed large intradural extra-axial ovoid shaped tumor measuring 36 x 31 x 33 mm in diameter (ll x ap x cc) located at the posterior midline aspect of foramen magnum and with signs of cerebellar and fourth ventricle compression (figure 2). patient was prepared for neurosurgical intervention, and mri angiography was performed to visualize v3 and v4 segments of vertebral arteries, and fortunately they were distant from the tumor. figure 2. brain mri showing tumor in the posterior aspect of foramen magnum: (a) axial plane, (b) sagittal plane. on the day of surgery, extremely rare situation occurred. namely, four consecutive transfusion cross-matching blood tests using activated papain showed positive inter-reaction. however, after our blood transfusion institute provided enough units of blood, we proceeded with intervention, and the patient was operated in the sitting position. the skin was incised on the midline from the occipital protuberance down to the upper cervical region. the midline plane was opened between the posterior muscles, up to the occipital protuberance and down to the spinous process of c2. bone opening was performed using a drill and kerrison rongeurs. we decided to perform small right unilateral approach instead of large medial bone opening, since we wanted to avoid occipital sinus injury. posterior margin of foramen magnum has been also removed. the dura was incised in a y-shaped fashion and retracted with stitches. after dura opening and retraction of right cerebellar hemisphere, a tumor with insertion on the midline portion of dura was brought into view. the plan was to be perform tumor debulking with the ultrasound aspirator, however since tumor was highly vascularized, we decided to coagulate and liberate dural insertion, after which the tumor was removed in one piece (figure 3). operation and early postoperative period were uneventful. blood loss during operation was minimal, and there was no need for a blood transfusion. patient recovered well, and preoperative cerebellar symptomatology was less 283 intracranial myopericitoma pronounced. control brain ct showed complete tumor removal. patient was discharged on the 4th postoperative day. the conjugation of morphological, histopathological and immunohistochemical studies allowed the final diagnosis of intracranial myopericytoma. after 6 months patient was without symptoms, and control brain ct showed no signs of tumor recurrence. however, one year from operation patient suffered rapid weight loss, several episodes of recurring fever and profuse night sweats with extreme and unexplained profound fatigue. after investigations patient was diagnosed with acquired immunodeficiency syndrome due to human immunodeficiency virus (hiv) infection. patient recently started highly active antiretroviral therapy (haart). figure 3. (a) intraoperative image showing right unilateral approach during dura opening phase, (b) tumor after removal. discussion myopericytoma is a benign tumor originating from the myoid perivascular cells6. it is often diagnosed in middle-aged patients, and most commonly arises in subcutaneous tissue of distal extremities or sometimes in retroperitoneal space. granter et al. described the first case of myopericitoma and called it perivascular myoma3. according to current nomenclature, these tumors correspond to a continuum morphological spectrum, including myofibroma, myopericitoma and glomangiopericytoma5. first case of intracranial localization of myopericytoma was described by rousseau et al. since then only several cases of intracranial localization have been described8. we present a case of an intracranial myopericitoma with even more rare localization in the posterior cranial fossa. to our knowledge this is the second case of myopericitoma with posterior fossa localization. in the described cases patients had a wide range of age, with slight female predominance7. our patient is a 43 years old male patient. the histological findings were similar in all cases from the literature with tumor composed of large thick walls vessels with myxoid changes, lined by elliptical and oval/spindle endothelial cells7. differential diagnoses included meningioma, solitary fibrous tumor/haemangiopericytoma and angioleiomyoma. however, in all cases, as well as in our patient, immunohistochemical studies confirmed diagnosis of myopericytoma. regarding tumor origin, some studies showed unusual molecular changes such as t(7;12)(p22;q13) and del(6)(q12q15)6. also, some authors postulate a probable relation between epstein-barr infection in aids patients and myopericytoma development1,4. our patient was probably hiv positive many years before operation, and aids symptoms appeared soon after intracranial surgery. although reports on this peculiar association have been described in the literature, more data are needed to clearly show a connection between these entities. intracranial myopericytoma is a low-grade slow growing tumor, with excellent overall survival. in all cases described in the literature only one patient died and it was due to other cause7. one year after the operation, our patient is without neurological symptoms and without signs of tumor recurrence. however, his general condition is worsening due to aids. in conclusion, intracranial myopericytoma is a rare benign neoplasm, successfully treated by surgery and with excellent follow-up. connection of intracranial myopericitoma appearance and hiv/aids is yet to be elucidated. references 1. calderaro j, polivka m, gallien s, bertheau p, thiebault jb, molina jm, gray f. multifocal epstein barr virus (ebv)associated myopericytoma in a patient with aids. neuropathol appl neurobiol 2008;34:115–7. doi: 10.1111/j.1365-2990.2006.00865.x. 2. dray ms, mccarthy sw, palmer aa, bonar sf, stalley pd, marjoniemi v, millar e, scolyer ra. myopericytoma: a unifying term for a spectrum of tumours that show overlapping features with myofibroma. a review of 14 cases. j clin pathol. 2006;59(1):67-73. doi: 10.1136/jcp.2005.028704. 3. granter sr, badizadegan k, fletcher cd. myofibromatosis in adults, glomangiopericytoma, and 284 branko đurović, danilo radulović, miloš joković et al. myopericytoma: a spectrum of tumors showing perivascular myoid differentiation. am j surg pathol. 1998;22(5):513-25. doi: 10.1097/00000478-19980500000001. 4. lau pp, wong ok, lui pc, cheung oy, ho lc, wong wc, to kf, chan jk. myopericytoma in patients with aids: a new class of epstein-barr virus-associated tumor. am j surg pathol. 2009;33(11):1666-72. doi: 10.1097/pas.0b013e3181aec307. 5. lindberg mr. diagnostic pathology of soft tissue tumors. 2nd edn, 2015:344–5. section 8. 6. mentzel t. myopericitoma, including myofibroma: who classification of soft tissue and bone tumors. 4th edn, lyon: iarc, 2013. 7. oliveira rc, velasco r, santos gr, rebelo o. intracranial myopericytoma: a tumour in a rare location. bmj case rep. 2018;2018:bcr2017223111. doi:10.1136/bcr-2017223111 8. rousseau a, kujas m, van effenterre r, boch al, carpentier a, leroy jp, poirier j. primary intracranial myopericytoma: report of three cases and review of the literature. neuropathol appl neurobiol. 2005;31(6):6418. doi: 10.1111/j.1365-2990.2005.00681.x. microsoft word 3aliismailneuroform.doc romanian neurosurgery (2010) xvii 2: 147 – 157 147 neuroform stent – assisted coil embolization new treatment strategy for complex intracranial aneurysms with midterm results ali ismail alhothi, tiewei qi, prof. zhengsong huang, songzhong shi, feng liang, lixuan yang, shaolei guo neurosurgery, first affiliated hospital, sun yat-sen university, guang zhou city, p.r. china abstract objective: to present detailed results of our treatment experience in using neuroform stent-assisted coil embolization to treat complex cerebral aneurysms over 3-year period, emphasizing on the technical difficulties, procedurerelated complications, and to evaluate midterm results. methods: patients underwent neuroform stent-assisted coil embolization were registered in a database. we assessed patients’ history, aneurysm morphology, indications for stenting, and technical details of the procedures, complications and midterm follow-up data. results: this study included twenty-six patients with 39 aneurysms. a total of 32 of 39 aneurysms were treated by neuroform stent-assisted embolization (sac). three anuerysms stented without coiling, 2 aneurysms coiled without stenting and 2 aneuysms surgically clipped. the indications for use included broad-necked aneurysms (n = 28), giant or large aneurysms (n = 6), and fusiform aneurysms (n = 5). of the 32 aneurysms treated by neuroform sac, we achieved complete (100%) and near complete (> 95%) occlusion in 27 aneurysms, and partial (< 95%) occlusion in 5 aneurysms. follow-up angiographic data avialble in 22 of 32 aneurysms treated by neuroform sac (68.7%) (average follow-up, 12 mo; range 4–24 mo) demonstrating recanalization in 3 aneurysms (13.6%), and stable occlusion in 19 aneurysms (86.4%). no delayed progressive embolization or instent stenosis observed. conclusion: neuroform microstent system led to a significant evolution in the endovascular treatment of complex intracranial aneurysms. our results and midterm follow-up showed neuroform stent-assisted coil embolization is safe and effective technique in the treatment of complex cerebral aneurysms. although, the clinically significant complications are uncommon and the evaluation at midterm follow-up is encouraging, further studies needed to assess the long-term stability and durability of the stent. keywords: aneurysm, coil, embolization, midterm follow-up, neuroform, stent introduction the neuroform stent is self-expandable, microcatheter delivered nitinol stent (formed by alloying nickel and titanium (~ 148 ali ismail alhothi et al neuroform stent – assisted coil embolization 50% ni), is a shape memory alloy with superelastic properties) specifically designed for application to intracranial vessels. neuroform stent microdelivery system is divided into three parts: the self-expanding stent itself, a 3f delivery microcatheter, and a (2f stabilizing microcatheter) stabilizer. it has converted some previously ‘untreatable’ aneurysms into endovascular amenable lesions. only few series of patients treated with this stent has been reported in the literature (6, 11, 21 ,22, 23 ,24, and 25). our aim is to report in details our immediate and avialable midterm results in the use of neuroform microstent for the embolization of complex intracranial aneurysms. methods subjects all patients included in this study represents an all-inclusive series of patients underwent neuroform sac embolization in our department during a 36-month period (december 2004 – december 2007). normally, patients were included when the neurointerventionalist advised that the aneurysm could not be treated effectively with traditional endovascular techniques and the risk-to-benefit ratio equal or superior to that of microsurgical clipping based on the aneurysm location and anatomic characteristics combined with the patient clinical status and ability to afford the treatment expenses a total of 26 patients harboring 39 aneurysms were deemed suitable for treatment. there were 11 males and 15 females ranging in age from 25 to 69 years with a mean age of 48.4 years. the patients’ demographics are listed in table 1. twenty-three patients presented with ruptured aneurysms (included two aneurysms in two different patients were presented as recurrence developed after primary coil embolization alone) and three patients had unruptured aneurysms. regarding those aneurysms’ types, there were 28 broad neck aneurysms (dome-toneck ratio < 2 or neck diameter > 4-mm), 6 large aneurysms (dome > 9.5-mm), and 5 fusiform aneurysms. with respect to the broad neck aneurysms, the average dome size 3.6-mm, the average neck size 2.6-mm, and the average dome-to-neck ratio 1.38. pre-procedural arrangements before sac procedure started, routinely, each patient or his/her family provided informed consent for the patient to undergo the procedure. all patients underwent diagnostic cerebral angiography before stent placement. following diagnostic angiography, the neurointerventionalist determines whether the patient is a suitable candidate for the stent-assisted coiling (sac) or not. if a patient had unruptured aneurysm or was not in the acute stage of aneurismal sah and was selected for stent use before the procedure, our anti-coagulation regimen consists of aspirin (enteric coated) 100 mg and clopidogrel 75 mg by mouth for 3 days were administered. if the patient was not selected for stent use before the procedure, it was usually administered a bolus dose of clopidogrel 225 mg with aspirin 100mg through ngt. after the femoral vascular access was obtained, a bolus dose of 2000 to 3000 u heparin was administrated to achieve an activated clotting time (act) of twice to treble of the baseline. romanian neurosurgery (2010) xvii 2: 147 – 157 149 table 1 summary of patients treated with neuroform sac age h&h sizes type immed. f/u f/u pt. /sex aneurysm d/n of stent dsa time dsa no (yrs) status grade location (mm) procedure size results (mth) results 1 38/f r ii (bn)pcoma/l 5.0/3.0 stent/coil 4.5x20 c 9 sta (bn)ica-ophth/l 5.0/3.0 stent/coil 4.5x20 c 9 sta 2 67/m ur 0 (l)acoma 15/12 stent/coil 3.5x20 nc na 3 54/f r iv (bn)basilar 2.0/2.0 stent only 4.5x15 (f)vertebral/l 2.8/2.0 stent/coil 4.5x20 nc na 4 43/f r i (bn)ica-c2/r 3.5/3.5 stent/coil 4.0x20 c 6 sta 5 50/f r iii (bn)ica-c2/r 5.8/5.2 stent/coil 3.5x20 c 11 sta 6 45/f r iv (bn)ica-c4/r 2.4/2.6 stent/coil 3.5x20 c 8 sta 7 47/m r ii (l)ophth/r 10/5.0 stent/coil 4.5x20 c 6 sta (bn)ophth/l 5.0/4.0 stent/coil 4.5x20 nc 6 sta 8 56/f r iii (bn)pcoma/r 2.5/3.0 stent/coil 3.0x20 c na 9 52/f r ii (bn)ica-pcoma/l 5.5/2.8 stent/coil 3.5x15 c 12 sta 10 47/f r i (bn)acoma 4.4/2.3 stent/coil 3.5x20 c 7 rec 11 37/m r ii (bn)ica-c2/r 2.2/1.4 stent/coil 4.0x15 p 17 sta (bn)mca-m2/r 6.5/3.0 clipped 12 62/f r ii (bn)acoma/l 3.8/2.0 coil only (bn)ica-c6/l 2.1/3.3 stent/coil 4.5x20 c 6 sta 13 39/m r iii (bn)acoma/l 4.2/3.8 stent/coil 4.0x20 nc na 14 58/f r iv (bn)mca-m2/r 7.7/3.0 coil only (bn)ica-c3/r 2.0/1.3 stent/coil 4.0x20 c na 15 32/m r ii (bn)ophth/l 4.0/3.0 stent/coil 4.5x20 c 11 sta 16 54/m r ii (bn)acoma 4.7/2.7 stent/coil 4.0x15 p 24 sta (bn)pcoma/l 5.2/3.1 stent/coil 4.0x15 c 24 sta (bn)ophth/l 3.1/3.1 stent/coil 4.0x15 p 24 sta 17 69/m re ii (l)pcoma/r 10.3/4.1 stent/coil 4.5x20 c na 18 25/f r ii (bn)ica-ophth/l 6.4/3.2 stent/coil 3.5x20 c 4 sta 19 26/m re iv (l)achoa/l 9.5/1.6 stent/coil 4.5x20 c na 20 54/f r ii (bn)pcoma/r 6.3/6.0 stent/coil 4.5x15 c na 21 48/f r ii (l)pcoma/r 12/3.0 stent/coil 4.5x20 nc 12 rec 22 69/m ur 0 (f)ica-c3/l 9.7/8.0 stent/coil 4.5x20 p na (f)ica/r 9.0/5.0 stent only 4.5x15 (f)basilar 26/20 stent only 4.5x20 23 51/m r iv (f)mca-m2/r 7.0/10.1 stent/coil 3.0x20 p 14 rec (bn)ica-c2/r 3.7/3.7 stent/coil 4.0x20 nc 14 sta (bn)pcoma/r 3.0/2.1 clipped 24 41/f re 0 (l)ica-opht/l 11/4.2 stent/coil 4.0x20 c 24 sta 25 39/m r ii (bn)mca-m2/r 7.2/5.4 stent/coil 4.5x15 c na 26 56/f r ii (bn)ica-a2/l 4.0/3.0 stent/coil 4.5x20 c 8 sta (bn)ica-a3/r 5.0/4.0 stent/coil 4.5x20 c 8 sta 150 ali ismail alhothi et al neuroform stent – assisted coil embolization after the procedure, heparinization was not reversed. subcutaneously 0.4 ml low molecular weight heparin (lmwh) twice a day, usually administered for three days postoperative. patients were continued on clopidogrel 75 mg for 6 weeks and aspirin 100mg for six months postoperatively. indications the indications for stent placement were categorized as broad neck aneurysm, fusiform/dissecting aneurysm, large/giant aneurysm, residual aneurysms after primary coil embolization and aneurysms with protruded coils (i.e., for patients in whom coils prolapsed or may prolapse into the parent vessel). stent and size estimation stents are sized on the basis of the largest diameter of the parent vessel in which the stent is to be deployed in. however, special attention should be paid to slightly oversized rather than undersized (we usually oversized by 0.5 – 1.0mm) with an overlap of at least 5 mm on each side of the neck of the aneurysm. results a total of 26 patients (11 males and 15 females ranging in age from 25 to 69 years with a mean age of 48.4 years) harboring 39 aneurysms were deemed suitable for neuroform sac treatment. twenty-three patients presented with aneurysmal subarachnoid hemorrhage (sah): whereas, three patients were presented by symptoms not related to the aneurysmal rupture. in regard to the patients presented with aneurysmal sah, 2 patients were hunt and hess grade i, 13 patients were grade ii, 3 patients were grade iii, and 5 ptients were grade iv. in this study group, we used a total of 35 neuroform stents., twenty-three neuroform stents implanted to cover the neck of 23 broad neck aneurysms, 6 neuroform stents implanted to cover the neck of 6 large aneurysms and 3 neuroform stents overlap 3 fusiform aneurysms: meanwhile, we used 3 stents to cover the neck of 1 broad neck aneurysm and to overlap 2 fusiform aneurysms without coiling embolizatiion. the occlusion rates evaluation were ranked in complete occlusion, near complete occlusion and partial occlusion as 100%, > 95%, and <95% respectively. of those 32 aneurysms treated by neuroform sac, complete (100%) occlusion achieved in 21 aneurysms (65.6%), and near complete occlusion (>95%) achieved in 6 aneurysms (18.7%), and partial occlusion (<95%) achieved in 5 aneurysms (15.6%). table 2 complications two clinically evident thromboembolic complications occurred (patient 12 and 23) after stent placement. patient 12 experienced right hemi paresis upon waking after the deployment of stent within the left ica to support the coil embolization of a broad neck aneurysm. however, both of the patients made good functional recovery. those patients were treated in the context of acute sah without pretreatment with antiplatelet medications. no aneurismal rupture was encountered during the prcedure, and no mortality related to the procedure. stent displacement encountered in one patient (patient 22). in this case, the initial plan was to deploy the second stent within the first one to achieve a satisfactory overlap over the aneurysm. unfortunately, the first stent was displaced after the deployment. in this instance, the distal portion of the stent was displaced into the aneurysm sac located in the upper trunk of the basilar artery. the delivery system could not be navigated easily beyond the landing zone from the parent vertebral artery due to the severe romanian neurosurgery (2010) xvii 2: 147 – 157 151 turtuosity between the aneurysm and the distal part of the parent artery which resulted in the displacement of the distal portion of the stent into the aneurysm sac. follow-up angiography follow-up angiographic data are available in only 22 of 32 aneurysms (68.7%) treated by neuroform sac embolization. the high number of followup dropouts (31%) was due to the uncomplying with doctor’s recmmended fullow-up angiography by some patients. the average follow-up time is 12 months (range, 4–24 months). in the available follow-up angiographies, no cases found to develop in-stent stenosis in this study group. no change was observed in 19 aneurysms:however, the size of the residual aneurysm increased in 3 patients (patient 10, 21, and 23) table 2. with respect to the anuerysms treated with stent alone, followup angiographies were are not available in all anuerysms. illustrative cases patient 24 a 41-year-old woman presented with headache. cerebral arteriogram demonstrated a large aneurysm in the left ica-ophth junction (figure 1 a). initially, the aneurysm was coiled only with complete occlusion achieved (figure 1 b). a two-year follow-up arteriogram revealed recurrence. this recurred aneurysm had a poor fundus-to-neck ratio, so she was deemed a good candidate for stent-assisted coiling (figure 1 c & d). a neuroform (4x20) stent was successfully deployed in the optimal segment across the aneurysm neck. subsequent gdc coil sat safely in the aneurysm sac (figure 1 e & f). table 2 summary of patients treated with neuroform sac 2.1. 39 aneurysms treatment stent/coil stent coil clip 32 3 2 2 2.2. occlusion achieved in 32 aneurysms treated by neuroform sac partial(<95%) near complete(>95%) complete (100%) 5 6 21 2.3. follow-ud data of 22 aneurysms treated by neuroform sac progressive recanalization stable in-stent stenosis 0 3 19 0 a b c 152 ali ismail alhothi et al neuroform stent – assisted coil embolization d e f g h figure 1 arteriogram of a 41-year-old woman presented with headache. a. left ica arteriogram demonstrating large aneurysm involving the left ica-ophth. artery take-off. b, control arteriogram showing complete occlusion after coil embolization. c&d, tow-year follow-up arteriogram revealed residual filling. e, poststenting control arteriogram showing successful stent deployment and coiling with complete occlusion. f, unsubtracted film showed the stent and the coils are still in the optimal position. g, control arteriogram after nf (4x20) stenting demonstrating complete (100%) occlusion of the aneurysm. h, two-year follow-up arteriogram demonstrating stable embolization of the recurrent aneurysm. immediate arteriogram showed complete occlusion (figure 1 g) two-year follow-up arteriogram revealed stable occlusion (figure 1 h). patient 10 a 47-year-old woman presented with sah hunt & hiss grade i. diagnostic cerebral angiography revealed a broad neck aneurysm in the right ica at the pcoma take-off (figure 2 a & b). this aneurysm demonstrated a poor dome-to-neck ratio that made her a good candidate for sac embolization. a neuroform (3.5x20) stent was successfully deployed in the optimal segment across the aneurysm neck. subsequent cordis helical fill coil sat safely in the aneurysm sac (figure 2 c & d). postprocedural situation was uneventful. sevenmonth follow-up arteriogram revealed residual filling of recurrence. romanian neurosurgery (2010) xvii 2: 147 – 157 153 a b c d e f figure 2 imaging study of a 47-year-old woman presented with sah hunt & hiss grade i. a, b, cerebral arteriogram demonstrated a wide-neck aneurysm in the right ica at the posterior communicating artery takeoff. c, post nf (3.5x20) stent-assisted coil embolization subtracted arteriogram showed complete occlusion(100%). d,unsubstracted anteroposterior image showed the stent and coil in the optimal position. e, follow up anteroposterior cerebral arteriogram revealed residual filling of recurrence. f, anteroposterior unsubtracted film showed the stent and the coils are still in the optimal position. discussion the goal of endovascular aneurysm treatment is to eliminate the aneurysm from the blood circulation and to prevent the flow of blood into the aneurysm by filling the aneurysm sac with embolization material. (1) the introduction of threedimensional coils, which retain a complex shape after detachment, provided some 154 ali ismail alhothi et al neuroform stent – assisted coil embolization additional flexibility with respect to the ability to treat patients with complex aneurysms (2). however, it is not feasible to perform a coiling procedure for some aneurysms (5% to 14.5 % of cases), (3, and 4) because unusual tortuosity of the vessels renders access difficultly or because the contours of the aneurysm do not permit the coils to sit safely inside. therefore, larger aneurysms and aneurysms with wider necks typically had lower rates of successful occlusion. (5, 6, 7) to overcome the problem of complex morphology aneurysms coiling, moret et al. (8) pioneered the balloon remodeling technique that enables temporary remodeling of the aneurysm neck during coil delivery. we used this technique in seven patients of our study series (e.g. patient 9 figure 1). after the first report of endovascular stent-supported coil embolization for the treatment of experimental carotid sidewall aneurysms in animals in 1994 (9, 10), higashida reported the first use of stent in the human intracranial circulation to prevent backward protrusion of electrodetachable coils in 1997. (11) since then, series of patients treated with self-expandable stents devoted to intracranial aneurysms such as the neuroform stent (9-11, 12, 13) the cordis enterprise stent (14) (cordis endovascular, miami lakes, fl) or the balt leo stent (15) (balt, montmorency, france) have been reported. as reported in other series (9, 12, 13, and 16) we observed in our practice that the navigation of the stent delivery system to and beyond the landing zone was not problematic; the actual deployment of the stent is frequently difficult because of binding of the microwire, the stabilizer, and the stent delivery catheter. lylyk et al. (16) reported difficulties in placing the neuroform stent in 31% of patients, mostly at the beginning of their experience. a second generation of devices resolved this limitation. fiorella et al. (12) confirmed that using the second-generation (neuroform 2) delivery system alleviated the technical problems with stent delivery and deployment encountered in their initial results (17).however, the technical advances in the newer generation of this stent (neuroform 3), which is mounted in a more suitable delivery system, significantly facilitated this stent deployment. several case reports an initial practice with aneurysm stenting have been published, including the use of stents in fusiform and dissecting aneurysms (18, 19, and 20). these reports showed satisfying immediate anatomical exclusion of the aneurysm and safety since the procedurerelated morbidity and mortality rates were low. our series corroborates that the neuroform stent was effective in providing a level of parent vessel protection adequate to allow satisfying packing in the complex aneurysms that were not amenable to conventional endovascular treatment. liang et al reported their clinical experience and 5 year follow-up results using neuroform stent-assisted coiling of intracranial aneurysms for 107 patients, they achieved complete occlusion in 57.2%, neck remnant in 27.3% and incomplete occlusion in 15.5%. (23) biondi et al angiographic results showed 14 (35%) aneurysm occlusions, 18 (45%) neck remnants, and eight (20%) residual aneurysms in 40 aneurysms treated with stent-assisted coiling (24). eduardo wajnberg et al reported their experience romanian neurosurgery (2010) xvii 2: 147 – 157 155 with the neuroform stent for the treatment of 24 wide-necked intracranial aneurysms, their immediate angiography demonstrated complete occlusion in 70.8%, neck reminant in 16.6% and incomplete occlusion 12.5%. (25) in our study group, immediate angiographic occlusion rates of those 32 aneurysms treated with neuroform sac demonstrated complete (100%) occlusion in 21 aneurysms (65.6%), near complete occlusion (>95%) in 6 aneurysms (18.7%), and partial occlusion (<95%) in 5 aneurysms (15.6%). however, in our practice small aneurysms were among the most difficult aneurysms to achieve complete occlusion faced in our study group. the small wide-neck aneurysm did not provide enough space to hold coils and microcatheter tip during coil delivery which pushes the microcatheter out of the sac before coil detachment. in other series, morbidity ranged from 5.8 to 20% and mortality from 2.1 to 8.9% (9, 11, 17, and 16). in our series, we observed a relatively low rate of complications (7.6% morbidity and 0% mortality), which appeared unrelated to the stenting procedures. obviously, the comparison of angiographic outcomes across reported series is difficult. a standard definition of what constitutes complete occlusion and residual aneurysm filling is lacking and quantification and analysis of the results is subjective (26). in addition, few papers report angiographic follow-up in stenting procedures for aneurysms. however, we believe that the high success rate of the combined stenting/coiling treatment in our study group is appreciated to the small number of analyzed patients with their relatively short follow-up time that may produce a positive bias in this study. further more, the high number of followup dropouts (31%) due to uncomplying with doctor’s recmmended fullow-up angiography by some patients could also dramatically change the mortality/morbidity rates that had been presented. our follow-up angiography demonstrated that in no case progressive occlusion or in-stent stenosis found in aneurysms treated with neuroform sac. whereas murayama et al (6), reported rates of 30 and 22% in large and small, widenecked aneurysms, respectively. murayama et al relatively high rate of progressive thrombosis may have contributed to the bioactive coils (matrix coil). fiorella et al. (12) reported delayed and severe in-stent stenosis in three of 64 (4.7%) patients. in our series, asymptomatic stenosis of the parent artery at the proximal end of the stent was not observed. however, our available follow-up data revealed three cases with growth residual that is highly attributed to coil compaction process. the thrombogenicity of the neurofrom stents represents an important limitation with respect to the treatment of aneurysm, particularly those treated in the context of acute sah (27). dual anti-platelet regimens have been established to be superior to aspirin therapy alone (28). clopidogrel is generally used because of its more potent platelet-anti-platelet effect, faster onset of action, and lower incidence of significant adverse effects (29). in our practice, if a patient had unruptured aneurysm or was not in the acute stage of aneurismal sah and was selected for stent use before the procedure, aspirin 100 mg and clopidogrel 75 mg by mouth for 3 days were administered. if the patient was not selected for stent use before 156 ali ismail alhothi et al neuroform stent – assisted coil embolization the procedure or in the acute stage of sah, it was usually administer a bolus dose of clopidogrel 225 mg with aspirin 100mg through the ngt. after the femoral vascular access was obtained, a bolus dose of 2000 to 3000 u heparin was administrated to achieve an activated clotting time (act) of twice to treble of the baseline. low molecular weight heparins (lmwh) have been shown in recent years to be more effective and safer than heparin in the prevention of thromboembolic events after coronary angioplasty and stent placement. (30, 31) n our practice, upon completion of the intervention, heparin was discontinued and anticoagulation was preserved for 3 days with low molecular weight heparins (lmwh). patients were continued on clopidogrel 75 mg for 6 weeks and aspirin 100mg for six months postoperatively. conclusion neuroform microstent system led to a significant evolution in the endovascular treatment of complex intracranial aneurysms. our results and midterm follow-up showed that neuroform stentassisted coil embolization is a safe and effective technique in the treatment of the complex cerebral aneurysms. although ,the clinically significant complications are uncommon and the evaluation at midterm follow-up are encouraging, further studies are needed to assess the long-term stability and the durability of the stent. references 1. richling b, md history of endovascular surgery: personal accounts of the evolution. neurosurgery 59:s3-30-s3-38, 2006 2. malek am, higashida rt, phatouros cc, dowd cf, and halbach vv: treatment of an intracranial aneurysm using a new three-dimensional-shape guglielmi detachable coil: technical case report. neurosurgery44:1142– 1145, 1999. 3. henkes h, fischer s, weber w, et al. endovascular coil occlusion of 1811 intracranial aneurysms: early angiographic and clinical results. neurosurgery 2004; 54: 268-80. 4. brilstra eh, rinkel gj, van der graaf y, van rooij wj, algra a. treatment of intracranial aneurysms by embolization with coils: a systematic review. stroke 1999;30:470-6. 5. shanno gb, armonda ra, benitez rp, rosenwasser rh.assessment of acutely unsuccessful attempts at detachable coiling in intracranial aneurysms. neurosurgery 2001; 48:1066-72. 6. murayama y, nien yl, duckwiler g,et al. guglielmi detachable coil embolization of cerebral aneurysms: 11 years’ experience. j neurosurg 2003; 98:959-66. 7. thornton j, debrun gm, aletich va,bashir q, charbel ft, ausman j. follow-up angiography of intracranial aneurysms treated with endovascular placement of guglielmi detachable coils. neurosurgery 2002; 50:239-49. 8. moret j, pierot l, boulin a, et al.: remodeling of the arterial wall of the parent vessel in the endovascular treatment of intracranial aneurysms. neuroradiology 1994;36:suppl 1:s83. 9. akpek s, arat a, morsi h, klucznick rp, strother cm, mawad me: self-expandable stent-assisted coiling of wide-necked intracranial aneurysms: a single-center experience. ajnr am j neuroradiol 26:1223-1231, 2005. 10. alfke k, straube t, dorner l, mehdorn hm, jansen o: treatment of intracranial broad-neck aneurysms with a new self-expanding stent and coil embolization. ajnr am j neuroradiol 25:584-591, 2004 11. benitez rp, silva mt, klem j, veznedaroglu e, rosenwasser rh: endovascular occlusion of widenecked aneurysms with a new intracranial microstent (neuroform) and detachable coils. neurosurgery 54:1359-1368, 2004. 12. fiorella d, albuquerque fc, deshmukh vr, mcdougall cg: usefulness of the neuroform stent for the treatment of cerebral aneurysms: results at initial (3-6-mo) follow-up. neurosurgery 56:1191-1202, 2005. 13. howington ju, hanel ra, harrigan mr, levy ei, guterman lr, hopkins ln: the neuroform stent, the first microcatheter-delivered stent for use in the intracranial circulation. neurosurgery 54:2-5, 2004. 14. higashida rt, halbach vv, dowd cf, juravsky l, meagher s: initial clinical experience with a new selfexpanding nitinol stent for the treatment of intracranial cerebral aneurysms: the cordis enterprise stent. ajnr am j neuroradiol 26:1751-1756, 2005. 15. pumar jm, blanco m, vazquez f, castineira ja, guimaraens l, garcia-allut a: preliminary experience with leo self-expanding stent for the treatment of romanian neurosurgery (2010) xvii 2: 147 – 157 157 intracranial aneurysms. ajnr am j neuroradiol 26:2573-2577, 2005. 16. lylyk p, ferrario a, pasbon b, miranda c, doroszuk g: buenos aires experience with the neuroform self-expanding stent for the treatment of intracranial aneurysms. j neurosurg 102:235-241, 2005. 17. fiorella d, albuquerque fc, han p, mcdougall cg: preliminary experience using the neuroform stent for the treatment of cerebral aneurysms. neurosurgery 54:6-17, 2004. 18. benndorf g, campi a, schneider gh, wellnhofer e, unterberg a: overlapping stents for treatment of a dissecting carotid artery aneurysm. j endovasc ther 8:566-570, 2001. 19. higashida rt, smith w, gress d, urwin r, dowd cf, balousek pa, halbach vv: intravascular stent and endovascular coil placement for a ruptured fusiform aneurysm of the basilar artery. case report and review of the literature. j neurosurg 87:944-949, 1997. 20. wakhloo ak, lanzino g, lieber bb, hopkins ln: stents for intracranial aneurysms: the beginning of a new endovascular era? neurosurgery 43:377-379, 1998. 21. sekhar ln, stimac d, bakir a, rak r. reconstruction options for complex middle cerebral artery aneurysms. neurosurgery 2005;56(1suppl):66-74 [discussion 66-74]. 22. wanke i, doerfler a, schoch b, stolke d, forsting m. treatment of wide necked intracranial aneurysms with a self-expanding stent system: initial clinical experience. ajnr am j neuroradiol 2003;24:1192-9. 23. liang g, gao x, li z, wei x, xue h. neuroform stent-assisted coiling of intracranial aneurysms: a 5 year single-center experience and follow-up. neurol res. 2009 aug 5. [epub ahead of print] 24. biondi a, janardhan v, katz jm, salvaggio k, riina ha, gobin yp. neuroform stent-assisted coil embolization of wide-neck intracranial aneurysms: strategies in stent deployment and midterm follow-up. neurosurgery 2007;61(3):460-8 [discussion 8-9]. 25. eduardo wajnberg, jorge marcondes de souza, edson marchiori, emerson l. gasparetto. single-center experience with the neuroform stent for endovascular treatment of wide-necked intracranial aneurysms. surgical neurology, volume 72, issue 6, december 2009, pages 612-619 26. katz jm, tsiouris aj, biondi a, salvaggio ka, ougorets i, stieg pe, riina ha, gobin yp: advances in endovascular aneurysm treatment: are we making a difference? neuroradiology 47:695–701, 2005. 27. yahia am, latorre j, gordon v, et al. thromboembolic events associated with. neuroform stent in endovascular treatment of intracranial aneurysms. j neuroimaging. epub ahead of print 26 june 2009 28. leon mb, baim ds, popma jj, gordon pc, cutlip de, ho kk, giambartolomei a, diver dj, lasorda dm, williams do, pocock sj, kuntz re; stent anticoagulation restenosis study investigators: a clinical trial comparing three antithrombotic-drug regimens after coronary-artery stenting. n engl j med 339:1665–1671, 1998. 29. caprie steering committee: a randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (caprie). lancet 348:1329–1339, 1996. 30. daoulah a, segev a, leblanc k, et al. post procedural low molecular weight heparin in patients at high risk of sub acute stent thrombosis. cardiovasc radiat med 2003 oct-dec; 4:182–85 31. yan at, goodman sg. low-molecular-weight heparins in ischemic heart disease. curr opin cardiol 2004; 19:309–16. microsoft word 5pendefundatranscranial romanian neurosurgery (2011) xviii 1: 31 – 37 31 transcranial doppler and vasodilators therapy as predictors of early outcome in acute ischemic stroke l. pendefunda 2nd neurological clinic, “gr.t. popa” university of medicine and pharmacy of iasi, romania abstract the clinical impact of risk factors and vasodilator therapy in prevention of acute ischemic stroke remains uncertain. ischemic stroke was considered severe in the romanian stroke prevention society. poor outcome are at 10 days after onset of a minor ischaemic stroke or a transient ischaemic attack. the association between predictors and outcome was assessed using unconditional multivariable logistic regression. covariates used included age, stroke severity, diabetes mellitus, coronary artery disease, atrial fibrillation, premorbid hypertension and hyper-lipidemia and the results pursuited by transcranial doppler, analyzing the pendefunda’s index. three hundred and twenty-eight patients were included. compared to patients predicted as normal who were found to have an increased stroke risk, our patients decreasd the clinical aspects after the vasodilators administration, while the reactivity in the first week after stroke onset was found to result in a decreased risk. however, neither of these findings remained significant after adjustment for the described covariates if we haven’t test the best reactivity to the drugs. keywords: acute ischemic stroke, brain infarction, clinical management of stroke, prediction of outcome, stroke prognosis, transient ischaemic attack, minor ischaemic stroke introduction transcranial doppler sonography (tcd) is used to assess cerebral blood flow velocity in basal cerebral arteries and is a common tool for the diagnosis and followup of cerebrovascular disease. with more than hundred clinical studies using tcd published annually, indications for its use are expanding. the clinical applications for tcd including delayed vasospasm after subarachnoid hemorrhage, sickle cell disease, atherosclerosis of cranial vessels, ischemic stroke, brain trauma, brain death, carotid artery disease, cerebral venous thrombosis, intraoperative tcd monitoring, arteriovenous malformations, cardiac shunts and preeclampsia, the reactivity after vasodilators of the cerebral arteries. the relevance of acute changes in blood pressure and the impact of vasodilator therapy administered in the acute period are also uncertain. there is currently little data from randomized controlled trials to inform physicians about the management of blood pressure and its relation to patient outcome in acute ischemic stroke. most studies assessing the impact of the risk factors in the acute period have focused on functional outcomes after a minor ischaemic stroke or a transient ischaemic attack. recent clinical studies have suggested that more than 75% of acute ischemic stroke patients present have 32 l. pendefunda transcranial doppler and vasodilators therapy hypertension. however, despite this high prevalence, our understanding of the potential impact of the level of blood pressure in acute stroke remains incomplete. several authors argue that elevated post-stroke blood pressure leads to poor outcome, related to increased cerebral edema and risk of hemorrhagic transformation. alternatively, other reports emphasize a relationship between low blood pressure and poor outcome, citing threats to the ischemic penumbra. prevention of a severe ischaemic stroke is our goal of this present study. methods we reviewed the records of all patients presenting with transient ischemic attack or a minor ichaemic stroke more two days after symptom onset and in-hospital stroke secondary to a surgical or major medical event(s). tcd was first used in 1981 when aaslid and coworkers assessed middle cerebral artery cerebral blood flow velocity in patients with aneurysmal subarachnoid hemorrhage indicating vasospasm. the main difference between aaslid’s “urdoppler” and other, conventional doppler ultrasound devices at the time was that the bidirectional probe was pulsed with a lower frequency of 2 mhz in order to sufficiently penetrate the temporal bone window. its main advantages compared to most other neuroimaging methods are convenience, mobility, low cost, non-invasiveness, and lack of side-effects. the tcd technique is noninvasive and can easily be repeated bedside without any risk for the patient. the agility of the tcd equipment has also raised hopes for ultra early assessment of intracranial dynamics following head injury. however, the results of a tcd examination depend on the experience and diligence of the examiner. clinicians need to follow these developments but should also beware of their often somewhat limited practical value. to assess the usefulness of tcd, it is impracticable or simply not applicable to perform blinded, randomized or placebo-controlled studies. yet, guidance for using tcd should be obtained from prospective studies with sufficiently large patient samples and with a reasonably simple and reproducible technique. our studies fulfilling the criteria of broad study population, validation of tcd by comparison to the other researches, blinded evaluation of the data and statistically dependable diagnostic or prognostic value. the value of tcd recordings in patients with head injury is, however, controversial even though changes in flow velocities may enable early detection of potentially treatable cerebral blood flow disturbances. we introduced new methods in our clinic in 1987 and than developed them in freiburg between the years 1988-89, introducing new indices for the evaluation of the cerebral blood flow. one investigator conducted all tcd examinations. the daily tcd measurements were conducted transtemporally using a traditional 2-mhz transducer (eme tc-64 eden medical records, uberlingen, germany). the tcd measurements were routinely performed bilaterally on the middle cerebral artery and verebro basilar arteries. recordings were pursuited analyzing the gosling’s pulsatility index (pi) calculated according to the method of gosling derived from the difference in the systolic and diastolic flow velocity. than the pi data were correlated to the results after vasodilators administration related to the pendefunda’s reactivity index (ri) romanian neurosurgery (2011) xviii 1: 31 – 37 33 described in 1988. there are more than twenty years that this index, which i described, was used, because i considered necessary an easyar evaluation of the vascular replay to a drug administration. technique in addition to the medical indication to perform tcd, subjects need a sufficiently thin temporal bone window to enable penetration of the 2 mhz waves. the temporal window is suitable for insonation in more than 90% of patients, but may become more difficult to penetrate in older patients, which prompted the development of a 1 mhz probe. tcd permits evaluation of the mca, anterior cerebral artery (aca), posterior cerebral artery (pca) and terminal internal carotid artery (ica). the suboccipital (transforaminal) insonation can be performed on a supine or sitting patient and yields good accessibility of the basilar artery (ba) and possibly the vertebral arteries (va). a transorbital approach can be used to insonate the ica in the carotid siphon and the ophthalmic artery. unless stated otherwise, cerebral blood flow indicates mean flow velocity. ample reference values for it, proper angle and depth of insonation are provided for healthy subjects, including stratifications for age and sex. cerebral blood flow obtained by tcd devices is a result of a spectrum of waves reflected by erythrocytes, and thus depends particularly on hematorheological conditions. in patients with very low hematocrit (under 30%), the velocity is increased due to a decrease in viscosity. thus, tcd interpretation in patients with abnormal blood viscosity requires caution. an insonation of all accessible arteries can help distinguish between a systemic cause of increased velocity (fever, hematocrit) or a focal increase suggesting a local abnormality. moreover, sufficient time to perform a thorough examination and experience are key factors contributing to its accuracy. patients were categorized into those who continued to receive antihypertensives for more than five days out after the transient ischaemic attack or minor ischaemic stroke onset versus those who did not. patients received aht as per the clinical judgment of the treating neurology team. antihypertensive medications included: aadrenergic receptor blockers, angiotensinconverting enzyme inhibitors, angiotensin receptor blockers, (3-adrenergic receptor blockers, calcium antagonists, diuretics, centrally acting agents (including amethyldopa and clonidine), nitric oxide donors, cerebrolysin or actovegin. comorbidities, including history of coronary artery disease, atrial fibrillation, substantial carotid stenosis, chronic hypertension, diabetes mellitus, and hyperlipidemia were recorded using patient histories as documented by the neurology team. in the case of hypertension, diabetes mellitus and hyperlipidemia, premorbid and hospital discharge use of diseasemodifying therapy was also used in defining these conditions. atrial fibrillation was defined as any evidence of atrial fibrillation on history or by electrocardiography. substantial carotid stenosis was defined as more than 50% narrowing of one or more extracranial vessels as docu-mented by carotid doppler. results with repeated carotid doppler sonograms, steiger investigated pi in patients with severe head injury as compared to healthy volunteers. this 34 l. pendefunda transcranial doppler and vasodilators therapy extracranial utilization of pi revealed values between 1.5 to 2.0 in control subjects with a gradual increase in cases with posttraumatic brain edema. pi values were associated with severe intracranial hypertension, and in cases of angiographically demonstrated cerebral circulatory arrest, pi values in the range of 6 to 8 were found. ri was present in a significant correlation between pi and the risk factors we found. the correlation are stronger as compared to previous studies. homburg investigated 10 head injured patients and demonstrated a positive exponential correlation between pi and the blood pressure. mcquire and colleagues performed tcd measurements within 3 hours after injury on 22 head injured patients. moreno correlated tcd measurements and found that an elevated pi predicts poor outcome, and furthermore, we sow a good reactivity in the larger arteries but different between the same in wright or left side, different for the same drug to each patient, more after a minor stroke or a transient ischaemic attack. these findings strongly suggest the presence of high distal vascular resistance in the early phase after head injury. the authors also showed that one-third of patients with severe head injuries have vasospasm, and that vasospasm will significantly change both pi and ri. in our study we found that ri reflectes the best drug we may administrate to a patient, different from one to another and the poor reactivity in the case of a reduced volume flow in the insonated artery, and can hence be helpful to indicate compromised cerebral perfusion. this aspect should guide the choice of a medication able to prevent a new attack. the differences between the drugs we presented in a lot studies in these twenty four years. our results demonstrate that ri may be influenced by different factors, like hemodynamic, respiratory, and hematologic parameters, and, in the case of brain vessels, tissue compliance. for this reason, the absolute value of this index is, in general, not considered sufficient to characterize overall intracranial hemodynamic conditions if no other information is simultaneously provided. the main advantage of ri is that, being a ratio, it is not affected by the pressure created by the heart, but in the arterioles the normal mean pressure drops. during elevated intracranial pressure, the arterioles are easily compressed creating a high peripheral vascular resistance reducing the flow, and thereby, the denominator of the pi after and before the administration of the drug. the numerator of the pi derives from the difference between systolic and diastolic flow velocities. the elasticity of the normal vascular system dampens the flow and flow velocity fluctuations because of blood pressure changes, which is in contrast to a rigid tube where the pressure is directly proportional to the flow velocity. a clinical setting where this is apparent is the elevation of pi in diabetic patients with cerebral microangiopathy and hence depressed vessel compliance. an increased intracranial pressure always results in reduced compliance of the entire brain tissue including increased rigidity of the brain arteries augmenting the velocity variations, which in turn increases the pi. consequently, the great difference between two tcd measurements (a major ri) reflects the changes in the perpheric resistence and the benefices of the vasodilator used. the flow velocity pattern in cerebral arteries is affected both by romanian neurosurgery (2011) xviii 1: 31 – 37 35 cerebrospinal fluid pulsatility and the reactivity of cerebrovascular control mechanisms. the different risk factors pursuited by us showed that atherosclerosis was the worst for the prognostic because the reactivity of a such an artery is practically zero. discussion in the present study, we observed a relationship between initial pi and early functional outcome and survival as determined at two weeks after ischemic stroke onset. poorest outcome was among those with a low ri. this finding remained valid when analyzed in a continuous quadratic model. in addition, these results remained significant after adjustment for multiple covariates including age, initial stroke severity, premorbid history of hypertension, hyperlipidemia, diabetes mellitus, coronary artery disease, atrial fibrillation and substantial carotid stenosis. other previous studies have demonstrated similar relationships. some authors have suggested that levels of blood pressure in the acute post-stroke period increase with initial stroke severity in a compensatory fashion to ensure perfusion of the ischemic territory and that pendefunda’s index suggest a better medication. these authors conclude that the relationship between elevated blood pressure and poor outcome is not a causal one. this would suggest that the initial level does have an effect on short-term outcome that appears to be independent of the initial stroke severity. the our study the elevations of ri more than 15% in the first 24 h may assure good results. on the other hand, some authors have reported that substantial decreases in early blood preasure levels can also be strong predictors of poor outcome. these findings, at first contradictory, would be consistent with the rationale that, while moderate decreases in levels of blood pressure are protective against hemorrhagic transformation and cerebral edema, excessive acute decreases may threaten the ischemic penumbra. this interpretation is consistent and we emphasize a limited and gradual increase in the ri in the acute period. however, our findings may suggest that equally important recommendations should be made to search the best vasodilator after the attack in order to have good results in careing and preventing a major stroke. conclusion our datas show a highly significant correlation between the increased rate of risk factors for the early outcome of an ischaemic head injury and the pursuit of the ri to prevent a major stroke. compared to patients predicted as normal who were found to have an increased stroke risk, our patients decreasd the clinical aspects after the vasodilators administration, while the reactivity in the first week after stroke onset was found to result in a decreased risk. however, neither of these findings remained significant after adjustment for the described covariates if we haven’t test the best reactivity to the drugs. references 1. aaslid r, markwalder t-m, nornes h. noninvasive transcranial doppler ultrasound recording of flow velocity in basal cerebral arteries. j neurosurg 1982;57: 769–74. 2. aaslid r, huber p, nornes h. evaluation of cerebrovascular spasm with transcranial doppler ultrasound. j neurosurg 1984;60:37–41. 3. aaslid r. transcranial doppler software (http://www.transcranial.com), last access: 09/20/2006 36 l. pendefunda transcranial doppler and vasodilators therapy 4. aaslid r. cerebral autoregulation and vasomotor reactivity. in: baumgartner rw, editor. handbook on neurovascular ultrasound front neurol neurosci basel 2006; 216-28. 5. ackerstaff rg, keunen rw, van pelt w, montauban van swijndregt ad, stijnen t. influence of biological factors on changes in mean cerebral blood flow velocity in normal ageing: a transcranial doppler study. neurol res 1990; 12: 187-91. 6. babikian vl, wechsler lr. transcranial doppler ultrasonography. 2 ed. boston, butterworthheinemann. 1999. 7. bland jm, altman dg. statistical methods for assessing agreement between two methods of clinical measurement. lancet 1986;1:307–10. 8. bor-seng-shu e, hirsch r, teixeira mj, de andrade af, marino r, jr. cerebral hemodynamic changes gauged by transcranial doppler ultrasonography in patients with posttraumatic brain swelling treated by surgical decompression. j neurosurg 2006; 104: 93-100. 9. chung e, fan l, degg c, evans dh. detection of doppler embolic signals: psychoacoustic considerations. ultrasound med biol 2005; 31: 1177-84. 10.chung em, fan l, naylor ar, evans dh. characteristics of doppler embolic signals observed following carotid endarterectomy. ultrasound med biol 2006; 32: 1011-23. 11.crutchfield ke, razumovsky ay, tegeler ch, mozayeni br. differentiating vascular pathophysiological states by objective analysis of flow dynamics. j neuroimaging 2004; 14: 97 12.dewitt ld, wechsler lr. transcranial doppler. stroke 1988; 19:915-21. 13.dahl a, russell d, nyberg-hansen r, rootwelt k. a comparison of regional cerebral blood flow and middle cerebral artery blood flow velocities: simultaneous measurements in healthy subjects. j cereb blood flow metab 1992; 12: 1049-54. 14.dreier jp, sakowitz ow, harder a, et al. focal laminar cortical mr signal abnormalities after subarachnoid hemorrhage. ann neurol 2002; 52: 825-9. 15.frontera ja, rundek t, schmidt jm, et al. cerebrovascular reactivity and vasospasm after subarachnoid hemorrhage: a pilot study. neurology 2006; 66: 727-9giller ca, hatab mr, giller am. estimation of vessel flow and diameter during cerebral vasospasm using transcranial doppler indices. neurosurgery 1998; 42: 1076-81 discussion 81-2. 16.gosling rg, king dh. arterial assessment by dopplershift ultrasound. proc r soc med 1974;67:447–9. 17.hoffman wh, pluta rm, fisher aq, wagner mb, yanovski ja. transcranial doppler ultrasound assessment of intracranial hemodynamics in children with diabetic ketoacidosis. j clin ultrasound 1995; 23: 517-23. 18.homburg am, jakobsen m, enevoldsen e. transcranial doppler recordings in raised intracranial pressure. acta neurol scand 1993;87:488–93. 19.jahromi as, cina cs, liu y, clase cm. sensitivity and specificity of color duplex ultrasound measurement in the estimation of internal carotid artery stenosis: a systematic review and metaanalysis.j vasc surg 2005; 41: 962-72. 20.jarus-dziedzic k, juniewicz h, wronski j, et al. the relation between cerebral blood flow velocities as measured by tcd and the incidence of delayed ischemic deficits. a prospective study after subarachnoid hemorrhage. neurol res 2002; 24: 58292.jorgensen lg. transcranial doppler ultrasound for cerebral perfusion. acta physiol scand suppl 1995; 625: 1-44. 21.kirkham fj, padayachee ts, parsons s, seargeant ls, house fr, gosling rg. transcranial measurement of blood velocities in the basal cerebral arteries using pulsed doppler ultrasound: velocity as an index of flow. ultrasound med biol 1986; 12: 15-21. 22.larsen fs, olsen ks, hansen ba, paulson ob, knudsen gm. transcranial doppler is valid for determination of the lower limit of cerebral blood flow autoregulation. stroke 1994; 25: 1985-8. 23.lee ky, sohn yh, baik js, kim gw, kim js. arterial pulsatility as an index of cerebral microangiopathy in diabetes. stroke 2000; 31: 1111-5. 24.lee jh, martin na, alsina g, et al. hemodynamically significant cerebral vasospasm and outcome after head injury: a prospective study. j neurosurg 1997; 87: 221-33. 25.lindegaard kf, nornes h, bakke sj, sorteberg w, nakstad p. cerebral vasospasm after subarachnoid haemorrhage investigated by means of transcranial doppler ultrasound. acta neurochir suppl (wien) 1988; 42: 81-4. 26.marinoni m, ginanneschi a, forleo p, amaducci l. technical limits in transcranial doppler recording: inadequate acoustic windows. ultrasound med biol 1997; 23: 1275-7. 27.markus hs, harrison mj. microembolic signal detection usingultrasound. stroke 1995; 26: 1517-9. 28.markus h, cullinane m, reid g. improved automated detection of embolic signals using a novel frequency filtering approach. stroke 1999; 30: 1610-5. 29.mcquire jc, sutcliffe jc, coats tj. early changes in middle cerebral artery blood flow velocity after head injury. j neurosurg 1998;89:526–32. 30.moreno, ja, mesalles, e, gener, j, et al. evaluating the outcome of severe head injury with transcranial doppler ultrasonography. neurosurg focus 2000; 8(1):article 8. http://www.neurosurgery.org/focus/jan00/8-1-8.html. romanian neurosurgery (2011) xviii 1: 31 – 37 37 31.muller m, voges m, piepgras u, schimrigk k. assessment of cerebral vasomotor reactivity by transcranial doppler ultrasound and breath-holding. a comparison with acetazolamide as vasodilatory stimulus. stroke 1995; 26: 96-100. 32.nadvi ss, du trevou md, van dellen jr, gouws e. the use of transcranial doppler ultrasonography as a method of assessing intracranial pressure in hydrocephalic children. br j neurosurg 1994;8:573–7. 33.pendefunda l.transcranial doppler and the ethiopathogeny of stroke, contact int’l, 1991 34.pendefunda l.the cerebral reactivity, contact int’l, 1995 35.pendefunda l. compendiu de semiologie neurologica, junimea 2007 36.pendefunda l. managementul maladiilor neurologice, vol i-iii, junimea 2010 37.pendefunda l. compendiu de patologie neurologica, junimea 2011 38.rabinstein aa, friedman ja, weigand sd, et al. predictors of cerebral infarction in aneurysmal subarachnoid hemorrhage. stroke 2004; 35: 1862-6. 39.romner b, bellner j, kongstad p, sjo¨holm h. elevated transcranial doppler flow velocities after severe head injury: cerebral vasospasm or hyperemia? j neurosurg 1996;85:90–7. 40.rothberg cs, weir b, overton tr. treatment of subarachnoid hemorrhage with sodium nitroprusside and phenylephrine: an experimental study. neurosurgery 1979;5:588–95. 41.schreiber sj, gottschalk s, weih m, villringer a, valdueza jm. assessment of blood flow velocity and diameter of the middle cerebral artery during the acetazolamide provocation test by use of transcranial doppler sonography and mr imaging. ajnr am j neuroradiol 2000; 21: 1207-11. 42.sloan ma, alexandrov av, tegeler ch, et al. assessment: transcranial doppler ultrasonography: report of the therapeutics and technology assessment subcommittee of the american academy of neurology. neurology 2004; 62: 1468-81 43.soehle m, czosnyka m, pickard jd, kirkpatrick pj. continuous assessment of cerebral autoregulation in subarachnoid hemorrhage. 44.anesth analg 2004; 98: 1133-9, table of contents sorteberg w, lindegaard kf, rootwelt k, et al. blood velocity and regional blood flow in defined cerebral artery systems. acta neurochir (wien) 1989; 97: 47-52. 45.sorteberg w. cerebral artery blood velocity and regional cerebral clood flow in normal subjects. in: newell d, aaslid r, editors. transcranial doppler. new york, raven press. 1992; 57-66. 46.soustiel jf, shik v, shreiber r, tavor y, goldsher d. basilar vasospasm diagnosis: investigation of a modified "lindegaard index" based on imaging studies and blood velocity measurements of the basilar artery. stroke 2002; 33: 72-7. 47.steinmeier r, laumer r, bonda´r i, priem r, fahlbusch r. cerebral heomdynamics in subarachnoid hemorrhage evaluated by transcranial doppler sonography. part 2. pulsatility indicies: normal reference values and characteristics in subarachnoid hemorrhage. neurosurgery 1993;33:10–9. 48.voldby b, enevoldsen em, jensen ft. cerebrovascular reactivity in patients with ruptured intracranial aneurysms. j neurosurg 1985; 62: 59-67. microsoft word 10albertmdtherapeutical.doc 202 m.d. albert et al intracerebellar hematomas therapeutical imagistic correlation regarding intracerebellar hematomas m.d. albert1, n. albert2, i. poeata3, danisia haba2 1radiodiagnostic ward – s.c. “explorarx” s.r.l. iasi / postgraduand neurosurgery ward – clinic and emergency hospital “prof. dr. n. oblu” iasi 2radiology clinic – clinic and emergency hospital “prof. dr. n. oblu” iasi 3neurosurgery , clinic and emergency hospital “prof. dr. n. oblu” iasi abstract intracerebellar hematomas are single or multiple hematic collections localized on the cerebellar parenchyma, with an evolution similar to an intracranial expansive process. if clinical examination opens the way to diagnose, the imagistics not only that can lead to an accurate diagnose in almost every case, but it also dictates the therapeutic strategy.thus, our study is focused on establishing a link between imagistics and clinical presentation at the moment of patient's admission to hospital, patients with intracerebellar hematomas. our study comprised a number of 57 patients, with an age ranging from 32 to 82 years, all of them admitted either to neurology or neurosurgery sections of clinic emergency hospital, “n. oblu”, iasi, over a perioad of 7 years, it was retrospective, descriptive and longitudinal based on a selection of medical data taken from the medical history of the patients diagnosed with intracerebral hematoma. during our study the following aspects were taken into consideration: computed tomograph imagistic aspects hematoma's dimension, localization and associated complication -, cerebellar hematoma's treatment and progress, as well as patient's clinical presentation at the moment of admission, age, gender. keywords: intracerebellar hematoma, cerebellum stroke, posterior fossa syndrome, intraventricular hemorrhage, computed tomography, magnetic resonance imaging. introduction intracerebellar hematomas are single or multiple hematic collections localized on the cerebellar parenchyma, with an evolution similar to an intracranial expansive process. figure 1 intracerebellar hematoma – ct screening romanian neurosurgery (2010) xvii 2: 202 – 213 203 figure 2 intracerebellar hematoma – mri screening if clinical examination opens the way to diagnose, the imagistics not only that can lead to an accurate diagnose in almost every case, but it also dictates the therapeutic strategy. thus, our study is focused on establishing a link between imagistics and therapeutical behavior, within the context of clinical presentation at the moment of patient's admission to hospital, for patients with intracerebellar hematomas. therapeutic indication represents a crucial moment in-between pain and healing, which in most of the cases will be a curative one, either through medical (the conservator approach), or surgical methods. experience, along with results brought together in time, can lead to the expected results, in the absence of contingent complications. there are also anticipating factors that can adjust the therapeutic attitude towards one of those two treatment methods: medical or surgical. nowadays, we can't talk about achievements in intracerebellar hematomas field without efficient imagistic exploration methods (ct and mri). the following methods are used for intracerebellar hematomas imagistic diagnosis: a) computed tomography; b) magnetic resonance imaging; c) angiography (only for certain cases). a – computed tomography (ct) axial computed tomography represents the elected diagnosis method for cerebellar hemorrhages, providing the possibility to discover them during the very first hours after admission. the possibility to diagnose cerebellar hemorrhages in such a short time from the onset, has also changed the therapeutic attitude. most authors agreed that a cerebellar hemorrhage promptly diagnosed can be cured using neurosurgical methods, especially because the results of surgical methods are far superior to those based on medical treatment. ct screening highlightens: 1. the presence of a hyperdense mass on posterior fossa; 2. hematoma's localization on posterior cerebral fossa (medial lateral hemispheric line); 3. signs of cerebral stem, forth ventricle and quadrigeminal cistern compression; 4. obstructive hydrocephaly. using ct screening, without any contrast substance, makes possible for the cerebellar hematomas diagnose to be established from the very beginning, even if their size is smaller than 2.5 cm. the presence of bloody effusion on cerebellar parenchyma can be explained by the presence of a spontaneous hyperdense mass (8090 h.u.), which becomes visible right after the hemorrhagic accident occurrence. this is due to a high attenuation coefficient of protein (globulin) contained by the the hemoglobulin molecule, while the quantity of iron contributes to the total attenuation only in a 7-8%, calcium adding no contribution to the obtained density value. there is a linear relation between the attenuation and patient's hemocrit at the moment of vascular accident occurrence. in the first 24 hours, hemorrhage gets to a maximum attenuation level, while the clot formation and retraction takes place. in this stage the examination of the injury after injecting the intravenous contrast substance is unnecessary. hematoma revile itself as a well-defined, rounded or oval shaped, on the axial section, in very rare cases with an undetermined line, which shows us that in those situations the intraparenchymatous hematomas have a disected shape. 204 m.d. albert et al intracerebellar hematomas during the next hours after hematoma's onset, independently of the hemorrhage's causes at cerebellar tissue level a vasogenic edema will edge the injury area, complicating the mass effect on cerebellar and nearby structures, with a climax in the forth or fifth days, which will impose a surgical operation. sometimes, when the hemorrhagic injury occur near ventricular cavity, mostly the forth ventricle, the images taken show a intraventricular bloody mass, with a variable volume. ventricular flood can complicate the medical prognosis, as well as a mass effect characterized by a violent onset can lead to severe neurological complications. during the subacute phase, lasting from the end of the first week up until the end of a first month since hemorrhagic accident onset, repeated ct screening shows a continuous clot dissemination; density value, due to a progressive lysis, with a centripetal appearance, influencing clot's dissemination in size and density, along with an intensive drop of vasogenic edema, but in a lesser net limits. introducing contrast substance will determine the presence of an annular contrast mesh, secondary to hematoencephalic barrier bursting. during schelar stage or chronic phase an atrofic process bearing a cavitary – cavity encephalomalacia character can be observed – with a density similar to cephalorachidian liquid, which leads to abutting cortical channel enlargement and adjacent ventricular cavity dilatation. using intravenous contrast is necessary when a neoplasm, artherovenous malformation, aneurism is suspected to be responsible for hemorrhage occurrence. the following criterion highlighted through ct screening are aimed for hydrocephaly diagnose: temporal horns (t.h.) are larger than 2 mm, so that sylvian fissure along with interhemispheric fissure and cerebral channels are not visible anymore; temporal horns size is equal to or larger than 2 mm, and f.h./i.d. account is higher than 0.5, where f.h. stands for the range of lateral ventricular frontal horn, and i.d. stands for the internal diameter from one panel to another, and at the same level. more features: lateral ventricular ballooning; transependymal resorption (periventricular hypodensity); when the f.h./i.d. x 100% situates: a) under 40% normal; b) between 40-50% at the edge; c) over 50% hydrocephaly. figure 3 ct native screening – posterior fossa hyperdense blood accumulation with compressive effect on the forth ventricle romanian neurosurgery (2010) xvii 2: 202 – 213 205 figure 4 ct native screening (axial/sagittal) – hydrocephaly aspect b – magnetic resonance (m.r.i.) the well-known sensitivity of a m.r.i along with paramagnetic effect of hemoglobin degradation products are the perfect tool for establishing the hemorrhagic accident's age and etiology. in physiologic conditions most of blood cells which form the hematoma have an initial content of oxygenated hemoglobin, coming from artery circulation. iron is characterized by ferrous state (+2), while two oxygen molecules occupy these electrons, and so oxyhemoglobina becomes slightly hypointense compared to the white substance. t1 and t2 signals depend on serum water concentration from the collected blood. during the next hours after vascular accident occurred the process of deoxyhemoglobinization takes place due to hemoglobin desaturation. this process is facilitated by accumulation of some metabolic products in the bloody collection, as follows: lactic acid; carbon dioxide; hydrogen ions. 4 electrons become unsaturated due to oxygen dissociation, which transforms the compound into a paramagnetic one. deoxyhemoglin becomes isointense with a tendency towards hypointense compared to parenchyma at t1, and obviously balanced at t2. deoxyhemoglobin oxidation process starts with day 3-5 after hemorrhagic accident occurrence. the iron atom becomes converted from ferrous state (four unpaired electrons) to ferric state (five unpaired electrons). other changes occur in hemoglobin, which allows water protons to get close enough to unpaired electrons significantly reducing the relaxation time in t1 and t2. the methemoglobin formation process is ireversible, and s1 occurs within 3 weeks time. in practice, there can be seen a hyperintense signal in t1, while balanced images show a hypointense signal in t2. while degradation process follows its way, ferric ions are released, encouraging the process of hemosiderin and feritin formation. hemosiderin is an unsolvable protein contained by lysozyme and reactive macrophage. feritin is a solvable protein, more visible in glial or macrophage cells, which is why t2 registers a significantly drop in signal intensity. vasogenic edema surrounding the hemorrhage reaches its maximum size and intensity during the fourth or the fifth day, with a progressive dropping over the next 3-4 weeks. balanced images show a hypersignal in t2, while in t1 there can be evidentiated a hypointermediate signal. c-angiography vertebral angiography is recommended when there is a suspicion of arteriovenous malformation or a torn aneurysm. treatment principles in intracerebellar hematomas the neuroimagistics development allowed for the reevaluation of intracerebellar hematomas, due to diagnosis possibilities and monitoring of patients with large hematomas but minimal simptomatology. the initial therapeutic behavior aims at maintaining the vital signs as well as establishing the cerebral suffering degree through the estimation of consciousness and focal neurological signs, followed by providing the necessary cerebral oxygenation with the indication of orotracheal 206 m.d. albert et al intracerebellar hematomas intubation and assisted ventilation in patients presenting the absence of consciousness and signs of cerebral trunck lesion. a – medical treatment b surgical treatment a – medical treatment establishing a certain treatment option is based on 4 randomized studies focused on the efficiency of steroids, hemodilution and gligerol versus placebo treatment in intracerebral hemorrhages. none of these 4 studies revealed any efficiency regarding medical treatment in intracerebral hemorrhages. increased blood pressure treatment studies have shown that the average blood pressure must be maintained at 130 mmhg in patients known to be hypertensive. figure 5 mri exam – intracerebellar hematoma evolution from subacute to chronic stage. hematoma has a subacute consituent (medial) and a chronic constituent (pointer/lateral), with the chronic constituent both hypo-intense t1, and t2 figure 6 mri exam – hydrocephaly appearance figure 7 vertebral angiography. aneurysm of the right posterior cerebellar artery (pointer) romanian neurosurgery (2010) xvii 2: 202 – 213 207 if blood pressure continues to be above 130 mmhg, it is recommended to administer betablockers. if the average blood pressure drops under 90 mmhg pressor agents are needed. in hypotension and bradycardia cases the administration of 0.5-1 mg atropine is recommended. intracranial hypertension treatment the main goal in intracranial hypertension treatment is to maintain values under 20 mmhg and the cerebral perfusion pressure above 70 mmhg. these parameters are obtained through: -keeping the head above the cord; -osmotherapy through administration of 1g/kgc manitol; -hyperventilation through keeping the pco2 values between 30-35 mmhg, when intracranial pressure measurement is possible; -invasive intracranial pressure motorization in patients with consciousness modification (glasgow scale <9). intracranial pressure can be obtained through insertion of intraventricular or intraparenchymal devices. -if normal intracranial pressure cannot be maintained by using the methods mentioned above, hypnotic coma (propofol, benzodiazepines) and finally barbiturate coma will be induced. maintaining normovolemia administration of isotonic saline solutions for hydric balance correction. comitial crisis prevention administration of sodium valproate (depakine) 10 30 mg/kgc. maintaining normothermia administration of antithermic medication (acetaminofen), wrapping or administration of neuroleptic medication. this medical treatment is used for all patients with intracerebellar hemorrhage, and as a unique therapeutic option for the next group of patients: a. patients with 14 on the glasgow scale. some authors take into consideration>9 on the glasgow scale, with 30 40 mm hematomas, where no hydrocephaly is present. if the neurological state is getting worse, those patients will be reevaluated for surgical treatment options. b. comatose patients with large intracerebellar hematomas and central localization. b. surgical treatment surgical treatment options are: 1. suboccipital craniectomy – in patients with hematomas > 3, but not >4 cm; 2. ventriculostomy – in patients with hemorrhage and hydrocephaly; 3. stereotactic fibrinolysis of hematomas. surgical indications are given by: a. patients with hemorrhage >3, characterized by neurological deterioration; b. patients with cerebellar hemorrhages and signs of cerebral trunk compression. external ventricular drainage indications are given by patients with hydrocephaly caused by intraventricular hemorrhage. evolution and therapeutic reevaluation in patients with cerebellar hematomas consciousness and vital function monitoring is necessary in patients diagnosed with intracerebellar hematomas. when these deteriorate emergency surgical intervention should be taken into consideration. medical prognosis in patients with intracerebellar hematomas depends on the size, location and clinical presentation of each patient at the moment of admission. 1. patients with hematomas >4 cm localized on vermis and with absent cerebral trunk reflexes receive a negative prognosis and have no surgical indication. 2. the medical evolution in patients with favorable clinical presentation must be monitored depending on clinical parameters and ct, the following criteria, which could lead to a possible deterioration, must be taken into consideration: blood pressure above 200 mmhg when the patient was admitted; punctiform eyeball and corneal and oculocephalic reflex modification; hematoma extention to cerebellar vermis; hematomas larger than 3 cm; cerebral trunk compression; intraventricular hemorrhage; vermis herniadue to tentorial incisura; acute hydrocephaly. 208 m.d. albert et al intracerebellar hematomas material and methods our studies were conducted in the neurosurgery wards of clinical emergency hospital ”prof dr nicolae oblu”, iasi, romania, during a seven year period, between 2002 and 2009. our study was retrospective, descriptive and longitudinal, based on a selection of medical data taken from the medical history of patients diagnosed with intracerebellar hematoma. this study was conducted on 57 patients, 26 males (45.61%) and 31 females (54.39%), their age ranging from 32 to 82, admitted to the neurosurgery ward for a period of over 7 years, diagnosed with bleeding in the posterior fossa. the women’s average age was significantly larger than the men’s (66.84 ± 7.19 compared to 62.31 ± 11.04, p=0.03), with the case frequency of patients under 50 year of age being significantly larger in men (4 cases 15.39% compared to 0% for women, p= 0.01). the most frequent cases involved men 60 years old and older. the following aspects were taken into consideration: ct screening regarding the hematoma’s dimension, localization and associated complications; angiography (only for certain cases); cerebellar hematoma's treatment: medical, surgical, external ventricular drainage; post-treatment evolution (cured, better, no improvement, worse, deceased). the study also tracked the influence of the patient’s clinical presentation at the moment of admission (coma, posterior fossa syndrome, intracranial hypertension syndrome), age and gender in relation with the efficiency of the treatment and how the patient’s condition evolved. ct screening based on the ct screening, the following items were tracked: 1. the size of the hematoma: the cerebellar hematomas were split into 2 categories, mainly hematomas with a diameter larger than 3 cm (figure 8) and hematomas with a diameter smaller than 3 cm (figure 9). 44 patients presented cerebellar hematomas with a diameter larger than 3 cm, while the remaining 13 patients presented a cerebellar hematoma with a diameter smaller than 3 cm. 2. localization: vermian cerebellar hematomas (figure 9) and hemispheric intracerebellar hematomas (figure 10); 3. complications: mass effect on the fourth ventricle was encountered in 17 cases (figure 10), ventricular flood was encountered in 15 cases (figure 11), and hydrocephaly was encountered in 10 cases and subarachnoid hemorrhage (figure 12). figure 8 native ct scan. cerebellar hematoma with a diameter larger than 3 cm localized on the left hemisphere romanian neurosurgery (2010) xvii 2: 202 – 213 209 figure 9 native ct scan. vermian cerebellar hematoma with a diameter smaller than 3 cm (vermis localized intracerebellar hematoma) figure 10 native ct scan. cerebellar hematoma with a diameter larger than 3 cm, with mass effect on the fourth ventricle, localized on the right hemisphere figure 11 native ct scan. cerebellar hematoma with a diameter smaller than 3 cm and ventricular flood on the fourth ventricle, localized on the fourth ventricle figure 12 native ct scan. ventricular flood and hydrocephaly figure 13 cerebellar hematoma. a. ct representation on the day of onset. b. cerebellar hematoma resorption after medical treatment figure 14 cerebellar hematoma. a. pre-surgery image. b. post-surgery image cerebellar hematoma’s treatment and progress: methods of treatment: a) surgical – 27 cases; b) medical – 25 cases; c) external ventricular drainage – 5 cases. the favorite surgical method was suboccipital craniectomy with the evacuation of the cerebellar hematoma. post-surgery progress was evaluated according to the admission clinical presentation and the complications diagnosed through ct screening. 210 m.d. albert et al intracerebellar hematomas results and discussions in 8 cases (14.03%) the localization (of the cerebellar hematoma) was on the middle, vermian line, with a higher frequency in men 23.08% compared to 6.45% for female patients), and on one side of the cerebellar hemisphere, in 49 cases, with a higher frequency in women (93.55% compared to 76.92% for male patients). in 44 cases (77.19%) the size of the hematoma was smaller than 3 cm, while in 13 cases (22.81%) the size of the hematoma was larger than 3 cm, with no significant difference according to the sex of the patient. regarding medical complications, 15 cases (26.32%) presented no medical complications, while 42 cases (73.6%) presented the following medical complications: 10 cases (17.54%) presented intracranial hypertension, 15 cases (26.32%) presented ventricular flood and 17 (29.82%) cases presented mass effect. the type and the frequency of the complications were not significantly differentiated according to age. 27 cases (47.37%) benefited from medical treatment, 25 (43.86%) cases benefited from surgical evacuation, and 5 (8.77%) cases needed external drainage, with no significant differences based on the sex of the patient. after receiving treatment positive progress was noticed in 56.14% of cases (2 cases were cured – 3.51% and 30 cases got better – 52.63%), no progress was noticed in 2 cases (3.51%) while no positive progress was noticed in 23 cases (11 cases got worse – 19.3% and 12 cases deceased – 21.05%). the post-treatment progress showed no significant differences based on the sex of the patient. throughout our study we also noticed that patients diagnosed with intracranial hypertension and coma at the time of the admission developed hematomas with a diameter larger than 3 cm, while those patients with posterior fossa syndrome presented a greater frequency of cerebellar hematomas with a diameter smaller than 3 cm. these facts also bear little or no statistical relevance. regarding patients with posterior fossa syndrome at the time of admission, a decreased frequency of medical complications was noticed (38.89%), compared to patients with intracranial hypertension at the time of admission (14.29%). regarding comatose admitted patients, we noticed a greater frequency of ventricular flood (38.89%), compared to patients with posterior fossa syndrome (11.11%). the frequency of mass effect was significantly greater with patients with intracranial hypertension at the time of admission (42.86%), compared to patients diagnosed with coma at the time of admission (11.11%). mass effect occurrences were noticed significantly less often in the case of patients with posterior fossa syndrome (33.33%). hydrocephaly was more frequent in men’s case than in women’s case (26.92% compared to 9.68%), while female patients presented a greater frequency of ventricular flood (35.48% compared to 15.38% in men’s case). medical treatment was mainly given to patients with intracranial hypertension (71.43%) and posterior fossa syndrome (55.56%) compared to patients diagnosed with coma (11.11%). surgical evacuation was used generally for patients with coma at the time of admission, compared to those with posterior fossa syndrome (33.33%) and intracranial hypertension (28.57%). at the romanian neurosurgery (2010) xvii 2: 202 – 213 211 same time, external drainage was usually needed for patients with coma (16.67%) compared to patients with intracranial hypertension (0%) and posterior fossa syndrome (11.11%). both cured cases were noticed for patients diagnosed with intracranial hypertension at the time of admission, while the frequency of patients who got better was significantly greater for diagnoses of posterior fossa syndrome (77.78%), compared to diagnoses of coma (38.89%) and intracranial hypertension (42.86%). the frequency of cases that worsened after receiving medical treatment was greater with coma patients (22.22%), and even greater with those diagnosed with intracranial hypertension (28.57%) at the moment of admission compared to posterior fossa syndrome (5.56%). death occurred mainly in patients with coma at the time of admission (38.89%), compared to those who presented posterior fossa syndrome (11.11%) and intracranial hypertension (14.29%). the incidence of cases that got better was notably greater with patients who received medical treatment (66.67%), compared to those who received surgical evacuation (40%). at the same time, death occurred more frequently amongst patients with surgical evacuation (40%), compared to those who received medical treatment (3.7%). positive post-treatment progress was noticed in female patients’ cases, with a greater incidence of cured cases or cases that got better compared to that of men’s (64.51% in comparison to 46.15% with men), while the number of deceased was significantly larger with male patients (34.62% in comparison to 9.68% with women). the patients’ progress was not considerably differentiated according to the localization of the hematoma. greater chances of improvement were noticed with patients with a hematomas smaller than 3 cm in diameter, while with hematomas larger than 3 cm in diameter the risk of getting worse or death was significantly increased. death occurrence frequency was larger with intracranial hypertension patients (50%) in comparison to those with no medical complications (6.67%), or mass effect (5.88%). also, death occurrence frequency was greater with patients diagnosed with ventricular flood (33.33%), compared to patients with no medical complications (6.67%) or mass effect (5.88%). taking into account the following elements: a larger number of male patients presented posterior fossa syndrome at the moment of admission, rather than female patients; with male patients the frequency of intracranial hypertension was greater than with female patients; the post-treatment progress was more responsive in women’s case, with a frequency of cured or improved patients larger than with male patients, while de incidence of deceased patients was significant greater among men, we can assert that with male patients we noticed an increased risk of delayed diagnose, the development of medical complications along with decreased treatment efficiency. the clinical presentation at the time of admission (particularly for comatose patients) has an important influence on the progress of the patient, due to the following aspects: the frequency of hematomas with a diameter larger than 3 cm was greater 212 m.d. albert et al intracerebellar hematomas among patients with intracranial hypertension and coma; the frequency of ventricular flood was significantly larger among patients diagnosed with coma at the moment of admission; the mass effect occurrence was significantly greater among patients with intracranial hypertension at the moment of admission; no improvement was noticed among comatose patients; the frequency of cases that got worse was greater among patients with coma and intracranial hypertension at the moment of admission. hematomas with a diameter larger than 3 cm led to an increased occurrence of ingravescence and death, while the chances of a positive progress were noticed with patients with hematomas smaller than 3 cm. associated medical complications (mainly intracranial hypertension and ventricular flood) can influence the patients’ progress and at the same time, contributes to a significant death occurrence increase. the method of treatment we opted for showed us that the frequency of improved medical conditions was greater among patients who received medical treatment, while death occurred more commonly among patients who needed surgery. conclusions 1.taking into account the fact that coma and posterior fossa syndrome had a higher frequency in male patients, we can assess that males present medical prognostic factor; 2.the factors that could lead to a negative medical outcome are the patient’s neurologic condition at the moment of admission, respectively coma, a hematoma with a diameter larger than 3 cm, ventricular flood and mass effect on the fourth ventricle; 3.imagistic examination's importance is indisputable for diagnose and deciding on medical/surgical therapeutic attitude, the establishment of precise medical indications being imposible without performant imagistic explorations. performant imagistic explorations are used both to eliminate some additional symptomatology responsible for a resambling symptomatology and for accurate injury localization. as far as our study is concerned, the most important imagistic method is by far computed-tomographic screening, due to its complet and precise provided information. 4.therapeutic behavior is characterized by a traditional treatment prescribed for conscious patients with posterior fossa syndrome or intracranial hypertension syndrome and for comatose patients; 5.radical surgical treatment, surgical evacuation of the hematoma through suboccipital craniectomy, will be applied to patients with cerebellar hematomas larger than 3 cm whose clinic condition gets worse; 6.palliative surgical treatment, external ventricular drainage, is recommended for patients initially diagnosed with hydrocephaly, but whose medical condition gets worse. references 1. aldescu, c. et al. computer-tomografia în afecţiuni endocraniene, ed. canova, iaşi, 1995, pp. l62-164/171175; 2. broderich, j.p. et al. guidelines for the management of spontaneus intracerebral hemorrhage, stroke 30, 1999, 905-915; romanian neurosurgery (2010) xvii 2: 202 – 213 213 3. buruian mirceatratat de tomografie computerizată, vol. 1 cap, coloană vertebrală, editura university press, târgu-mureş, 2006, cap. explorarea computertomografică în bolile vasculare cerebrale, pp. 401-457; 4. fisher c.m., picard e.h., polak a. acute hypertensive cerebellar hemorrhage: diagnosis and surgical management. j nerv and ment dis 1965, 140: 38-57; 5. greenberg, m.s. handbook of neurosurgery, 6th edition. 2006, greenberg graphics inc. , pp. 762-773. 6. grumme, t. et al. cerebral and spinal computed tomography, ed. blackwell-science, 1998, pp. l03-117; 7. holpin, s.f.s. et al. prospective evaluation of cerebral angiography and computed tomography in cerebral hematoma, j. of neurol. neurosurg. psychiatr. 57, 1994, ll80-1186; 8. hufschmidt, a. et al. neurologie integrală de la simptom la tratament, ed. polirom, pp. 53-58/61-65; 9. ianovici, n. et al. neurochirurgie. note de curs, casa ed demiurg, iaşi, 1996; 10. ionel, c. compendiu de neurologie, ed. medicala bucureşti, 1982, pp. l62-168; 11. kaye, a.h. essential neurosurgery, 3rd ed. blackwell publishing 2005.pp 45-47; 12. mohsenipour, i. aproaches in neurosurgery central and peripheral nervous system, george thieme med.publisher inc., 1994, pp. l08-125; 13. orrison, w.w.jr. et al. neuroimaging, vol. i, ed. w.b. saunders company, 2000, pp. 742-761/863-864; 14. pollak l., rabey j.m., gur r, schiffer j indication to surgical management of cerebellar hemorrhage. clin neurol neurosurg 1998, 100 (2): 99-103; 15. pendefunda, gh. et al. semiologie neurologica, ediţia a-vii-a, ed. contact international, 1992, pp. 170176/252-265; 16. rusu, m.neurochirurgie, ed. contact international, 1993, pp. 226-233/248-253; 17. selby, f. et al.radiographic anatomy, ed. harwall publishing,1990, pp. l65-197; 18. van der hoop rg, vermeulen m, van gijn j: cerebellar hemorrhage: diagnosis and treatment. surg neurol 1988, 29: 6-10; 19. woodruff, w.w. et al. fundamentals of neuroimaging, ed. w.b. saunders company, 1993, pp. l21-185; 20. wijdicks ef, st louis ek, atkinson jd, li h. clinician's bases toward surgery in cerebellar hematomas: an analysis of decision-making in 94 patients. cerebrovasc dis 2000 mar-apr, 10(2): 93-6; microsoft word 4balderrama_intraarterial 326 balderrama et al intra-arterial chemotherapy for retinoblastoma intra-arterial chemotherapy for retinoblastoma: a practical review jorge balderrama1, carlos a. leal-leal2, hernando alvis-miranda3, angel lee4, marco zenteno1, luis rafael moscote-salazar1 1instituto nacional de neurología y neurocirugía 2instituto nacional de pediatria hospital, idi-araba, lagos state. nigeria 3hospital angeles del pedregal abstract the use of chemotherapy for retinoblastoma constitutes a promising treatment strategy. retinoblastoma is the most common eye cancer in the childhood.. treatment depends on the laterality, intraocular location and tumor extension. radiation therapy became an important element in the management of this type of injury risk of extraocular secondary tumor development. eye salvage is mandatory when vision preserved. the current neuroendovascular techniques constitute a therapeutic tool for these tumors. we present a practical review of current concepts in the management of these tumors. key words: chemosurgery, retinoblastoma, neurointerventional introduction retinoblastoma (rtb) is a tumor that surge from the retinal neuroepithelium, and can differentiate into almost any type of outer or inner retinal cell, including photoreceptors (1). rtb is brought about by biallelic inactivation of the human retinoblastoma susceptibility gene, rb1 (genbank accession number l11910), located on chromosome 13q14 that codes for the rb protein (2). rtb protein (rb) regulates cell cycle progression and suppresses tumorigenesis through the control of e2f transcription factor function, which in turn represents the link between the rb pathway and the induction of p53dependent apoptosis (3–5). rtb arises due to two genetic events involving both the alleles of rb1 and occurs in two forms, the hereditary and non-hereditary. mutation of both the alleles of rb1 is required for tumor initiation (2). rtb can be unilateral or bilateral with sporadic or familial hereditary patterns. patients with unilateral retinoblastoma generally carry a somatic mutation in the rb that is present only in the tumor without a similar mutation in other cells (6). however, almost 10% to 15% of these patients manifest a germinal mutation in all cells of the body, despite the fact that they have unilateral rtb (6). tables 1 and 2, show two classification systems for rtb. the aim of this work is to briefly review the data regard chemosurgery for rtb treatment. romanian neurosurgery (2013) xx 4: 326 332 327 table 1 reese-ellsworth classification for conservative treatment of retinoblastoma group consideration characteristics i very favorable solitary tumor, <4 disk diameters in size, at or behind the equator multiple tumors, none 4 disk diameters in size, all at or behind the equator ii favorable solitary tumor, 4–10 disk diameters in size, at or behind the equator multiple tumors, 4–10 disk diameters in size, behind the equator iii doubtful any lesion anterior to the equator solitary tumors >10 disk diameters behind the equator iv unfavorable multiple tumors, some >10 disk diameters any lesion extending anteriorly to the ora serrata v very unfavorable massive tumors involving over half the retina vitreous seeding table 2 international retinoblastoma staging system stage characteristics 0 patients treated conservatively i eye enucleated, tumor completely resected on histopathology examination ii eye enucleated, microscopic residual tumor present in the form of: •tumor invasion into extrascleral tissue •tumor invasion into cut end of optic nerve iii regional extension: •overt orbital disease •preauricular or cervical lymph node extension iv metastatic •hematogenous metastasis (without cns extension) •single lesion •multiple lesions central nervous system extension (with or without any other site of regional or metastatic disease) •prechiasmatic lesion •central nervous sustem mass •leptomeningeal and cerebrospinal fluid (csf) disease 328 balderrama et al intra-arterial chemotherapy for retinoblastoma rtb general behaviour rtb is the most common malignant intraocular tumor of childhood (1,6,7), with a reported incidence ranging from 1 in 15,000 to 1 in 18,000 live births, independent of race and sex (8,9); kivela (10) has stated that the estimated number of patients per year with rtb worldwide was between 7202 and 8102. approximately 250–300 children are newly diagnosed with retinoblastoma each year in the united states, and unfortunately, substantially higher rates occur in developing countries (11). almost 80% of the cases occur before 4 years of age, while 40% of cases occur during infancy (1). it is a curable cancer if detected at a stage in which it is still contained within the retina, subretinal space or vitreous (12). the most common external features include leukokoria and strabismus (6). approximately 80%-90% of rb1 gene carriers develop ocular tumors. this gene encodes the cell cycle regulatory retinoblastoma gene protein (prb), controls cellular differentiation during both embryogenesis and in adult tissues, regulates apoptotic cell death, maintains cell cycle arrest and preserves chromosome estability [2]. retinoblastoma occurs in two forms: hereditary (30-40%) and nonhereditary (60-70%). despite the classic appearance of rtb, nearly 50% of patients diagnosed initially with possible retinoblastoma prove, on referral to ocular oncologists, to have simulating conditions and not retinoblastoma (13). the most common pseudoretinoblastomas include persistent hyperplastic primary vitreous, coats disease, and ocular toxocariasis (13). management evolution rtb management is complex and depends on many issues including tumor laterality, macular involvement, tumor size, vitreous or subretinal seeding, relationship of the tumor to surrounding tissues including the optic disc, choroid, iris, sclera, and orbit, general patient age and health, and the family desires (12). the treatment of rtb has evolved substantially over the last few decades (12,14,15). conservative treatment of retinoblastoma has improved in the last years. in the past, enucleation and external beam radiation therapy (ebrt) were the only treatments available for these patients (7). systemic chemotherapy for intraocular retinoblastoma was introduced >50 years ago (16). the driving force behind using systemic chemotherapy has been to avoid the radiation-related second cancers that developed in radiated retinoblastoma children (16). as had been mentioned, patients with rtb are young children and although systemic chemotherapy causes dramatic reductions in the size of the tumors (averaging >50% decrease in volume after 3 sessions) clinicians are increasingly reporting worrisome adverse systemic findings in children treated with systemic chemotherapy (16). this therapy in the pediatric population has potential shortand long-term complications, such as neutropenia, fever, port infections, sepsis, anemia, transfusions, and associated hospitalizations have all been reported (17). since 1997 was previsualized newer treatment strategies directed to target cancer cell treatment, such as the delivering of a photosensitizing agent to cancer cells by a carrier molecule such as low-density lipoprotein (6,18), posteriorly, a light source, e.g., laser, is then used to irradiate romanian neurosurgery (2013) xx 4: 326 332 329 the sensitized tumor; allowing for targeted treatment with a particularly intense reaction in the tumor, sparing the normal tissue (6). all management have evolved, and currently, the most commonly employed approach for treating retinoblastoma in developed countries is chemoreduction, a strategy involving neoadjuvant systemic chemotherapy, followed by treatment with focal modalities, such as cryotherapy, laser treatment, or brachytherapy (19). laser photocoagulation, cryotherapy, thermotherapy, and plaque radiotherapy remain vitally important in the management of selective rtb (12). enucleation, intravenous chemoreduction, intra-arterial chemotherapy, and ebrt are used for more advanced retinoblastoma (12). ebrt is usually reserved for last alternative treatment because of its numerous side effects and risks for late onset cancers in germline mutation children (12). chemosurgery ophthalmic artery chemosurgery (oac) for rtb was first performed a lustrum ago by abramson et al (20,21) with the aim of preserv eyes with extensive intraocular rtb scheduled for enucleation. the first attempt to deliver high doses to the eye, while minimizing systemic exposure was performed by reese et al (22) more than 50 years ago, but with a different rationale; they delivered intra-arterial triethylene melanamine (tem) (a nitrogen mustard derivative) via direct carotid artery puncture on the side to be treated attempting to lower the dose of therapeutic radiation used to treat rtb. japanese researchers have been investigated intracarotid administration of chemotherapy. intra-arterial chemotherapy was used in 187 patients in japan between 1988 and 2001 (23,24). initially, they described only technical success, without efficacy or toxicity data. some follow-up data were reported in october, 2011 (25). ophthalmic arterial infusion of melphalan is technically feasible and can result in striking regression of tumour (16,21,26).79–81 these optimistic reports do not specify eligibility criteria, control of retinoblastoma, vision achieved, or survival rates of the eye or patient. however, in their studies, many patients received external beam radiotherapy (ebrt) and intravitreal melphalan, making it difficult to determine how effective the intraarterial injections would be if used alone (11). abramson et al in 2010 (16) introduced the technique of “super selective infusion” by advancing a micro-catheter into the orifice of the ophthalmic artery on the side to be treated (or both sides in the same session in cases of bilateral retinoblastoma ‘‘tandem therapy’’) after introduction of the catheter via the femoral artery in cases of newly diagnosed retinoblastomas. because of their limited systemic toxicity in treating children with advanced intraocular retinoblastoma (most frequently asymptomatic grade 3 neutropenia), they began treating less advanced retinoblastoma and in 2012 they report the success and adverse events in these patients (20); they found that ophthalmic artery chemosurgery for retinoblastoma that was reeseellsworth i, ii and iii (or international classification b or c) was associated with high success (100% of treatable eyes were retained) and limited toxicity with results that equal or exceed conventional therapy with less toxicity. thus, this technique, rapidly become an accepted modality that 330 balderrama et al intra-arterial chemotherapy for retinoblastoma saves eyes with advanced rtb that would otherwise have been enucleated. the evidence showed that many of the eyes initially managed with systemic chemotherapy require additional treatment(s) (radiation or enucleation) to control the cancer (16), making chemosurgery an option of particular interest, because it could be performed repeatedly in young children without significant systemic or local side effects (16); furthermore, in some cases, eyes clearly can have potential useful vision (16). because the most newly diagnosed rtb eyes in the united states are in reeseellsworth group v at presentation (16), the majority of these are treated with primary enucleation; however in the abramson (16) series, 25 of 28 were classified as reeseellsworth group v. they would likely have been primarily enucleated, but the intraarterial approach allowed them to save 27 of these eyes. abramson et al (16) 3-year experience with the use of super selective intra-arterial chemotherapy for rtb suggests that the technique is minimally toxic to the eye in previously untreated cases, has minimal systemic toxicity, can restore vision in some eyes, can be done repeatedly on an outpatient basis, and will replace the use of systemic chemotherapy, ebrt, and enucleation for the majority of retinoblastoma cases. other reports also support those findings (27) the technique chemosurgery is a method of intraarterial chemotherapy is basically a procedure in which a neuro-interventional radiologist or neurosurgeon will thread a catheter into femoral approach, reaching ophthalmic artery and releasing the medications (14). for the super selective technique described by abramson et al (16), under general anesthesia and anticoagulation (intravenous heparin, 75i u/kg), is introduced into the femoral artery a 4-french arterial sheath. microcatheters are then passed into the ophthalmic artery on the affected side using fluoroscopy and roadmapping (16). both flow-directed catheters (such as the magic-balt therapeutics, montmorency, france) with outer diameters of 400 or 500 microns and guidewire-directed catheters (such as the excelsior sl 10 stryker, freemont ca) with an outer diameter of 570 microns have been used. the chemotherapy drugs are then diluted with saline in a 30cc solution, injected in a pulsatile fashion over 30 minutes. at the end of the procedure the catheter is withdrawn, the femoral puncture site is compressed for hemostasis and the child discharged the same day (16). despite its remarkable control for retinoblastoma, some authors consider that intraarterial chemotherapy should be used with caution (14). have been demonstrated some toxic effects of irradiation from fluoroscopy during intraarterial chemotherapy for retinoblastoma, cautioning that accumulated irradiation toxic effects following multiple sessions of intraarterial chemotherapy could be cataractogenic and possibly carcinogenic (28). survival and outcomes survival rates for intraocular rtb have improved dramatically in the past century. a disease that was 95% lethal 100 years ago is now curable in more than 95% of cases (19); its management relies on an experienced team, conformed by the ocular oncologists, pediatric oncologists, radiation oncologists, pediatricians, pediatric romanian neurosurgery (2013) xx 4: 326 332 331 ophthalmologists, geneticists, and occasionally interventional neuroradiologists or neurosurgeons working together for the single goal of saving the child’s life (12). in america, the 5-year survival was 96% between 1995 and 2004 based on surveillance, epidemiology, and end results (seer) data (29). in england, the 5-year survival between 1998 and 2002 was 97% for unilateral retinoblastoma and 100% for bilateral retinoblastoma (30). despite these impressive results, retinoblastoma continues to pose a serious life-threatening problem for children in developing nations, mostly due to late detection and massive tumor. the mortality rate varied tremendously by location with 3–5% mortality in japan, europe, and north america to 20% in latin america/caribbean, 39% in asia (without japan), and up to 70% in africa. he estimated that approximately 3001–3376 children die of retinoblastoma annually worldwide (10). conclusions early detection to minimize visual morbidity remains the focus of research in countries with universal access to healthcare. late presentation with life threatening disease is a major challenge in economically underprivileged countries, and strategies must focus on raising awareness and acceptance of modern treatment methods such as chemosurgery. fortunately the strategies for treating rtb continue evolving, some successfully, and others no. despite advances in treatment options, clinicians continue to face challenges in improving globe salvage rates and mitigating the long-term side effects of therapy. correspondence dr. luis rafael moscote-salazar, universidad de cartagena, cartagena de indias, colombia, mineurocirujano@aol.com references 1. bakhshi s, bakhshi r. genetics and management of retinoblastoma. journal of indian association of pediatric surgeons 2007;12:109–15. 2. ali mj, parsam vl, honavar sg, kannabiran c, vemuganti gk, reddy vap. rb1 gene mutations in retinoblastoma and its clinical correlation. saudi journal of ophthalmology 2010;24:119–23. 3. fortunato p, pillozzi s, tamburini a, pollazzi l, franchi a, la torre a, arcangeli a. irresponsiveness of two retinoblastoma cases to conservative therapy correlates with upregulation of herg1 channels and of the vegf-a pathway. bmc cancer 2010;10:504–10. 4. lamber ep, beuron f, morris ep, svergun di, mittnacht s. structural insights into the mechanism of phosphoregulation of the retinoblastoma protein. plos one 2013;8:e58463. 5. viallard jf, lacombe f, belloc f, pellegrin jl, reiffers j. [molecular mechanisms controlling the cell cycle: fundamental aspects and implications for oncology]. cancer radiother 2001;5:109–29. 6. shields cl, meadows at, leahey am, shields ja. continuing challenges in the management of retinoblastoma with chemotherapy. retina 2004;24:849–62. 7. antoneli cbg, ribeiro kcb, steinhorst f, novaes pers, chojniak mm, malogolowkin m. treatment of retinoblastoma patients with chemoreduction plus local therapy: experience of the ac camargo hospital, brazil. j pediatr hematol oncol 2006;28:342–5. 8. bishop jo, madson ec. retinoblastoma. review of the current status. surv ophthalmol 1975;19:342–66. 9. abramson dh. retinoblastoma incidence in the united states. arch ophthalmol 1990;108:1514. 10.kivelä t. the epidemiological challenge of the most frequent eye cancer: retinoblastoma, an issue of birth and death. br j ophthalmol 2009;93:1129–31. 11.meel r, radhakrishnan v, bakhshi s. current therapy and recent advances in the management of retinoblastoma. indian journal of medical & paediatric oncology 2012;33:80–8. 12.shields cl, shields ja. retinoblastoma management: advances in enucleation, intravenous chemoreduction, and intra-arterial chemotherapy. curr opin ophthalmol 2010;21:203–12. 13.shields cl, shields ja. recent developments in the management of retinoblastoma. j pediatr ophthalmol strabismus 1999;36:8–18; quiz 35–6. 332 balderrama et al intra-arterial chemotherapy for retinoblastoma 14.shields cl, shields ja. intra-arterial chemotherapy for retinoblastoma: the beginning of a long journey. clin experiment ophthalmol 2010;38:638–43. 15.schefler ac, abramson dh. retinoblastoma: what is new in 2007-2008. curr opin ophthalmol 2008;19:526–34. 16.abramson dh, dunkel ij, brodie se, marr b, gobin yp. superselective ophthalmic artery chemotherapy as primary treatment for retinoblastoma (chemosurgery). ophthalmology 2010;117:1623–9. 17.benz ms, scott iu, murray tg, kramer d, toledano s. complications of systemic chemotherapy as treatment of retinoblastoma. arch ophthalmol 2000;118:577–8. 18.schmidt-erfurth u, diddens h, birngruber r, hasan t. photodynamic targeting of human retinoblastoma cells using covalent low-density lipoprotein conjugates. br j cancer 1997;75:54–61. 19.martin ne, kim jw, abramson dh. fibrin sealant for retinoblastoma: where are we? journal of ocular pharmacology & therapeutics 2008;24:433–8. 20.abramson dh, marr bp, brodie se, dunkel i, palioura s, gobin yp. ophthalmic artery chemosurgery for less advanced intraocular retinoblastoma: five year review. plos one 2012;7:e34120. 21.abramson dh, dunkel ij, brodie se, kim jw, gobin yp. a phase i/ii study of direct intraarterial (ophthalmic artery) chemotherapy with melphalan for intraocular retinoblastoma: initial results. ophthalmology 2008;115:1398–1404.e1. 22.reese ab, hyman ga, tapley nd, forrest aw. the treatment of retinoblastoma by x-ray and triethylene melamine. ama arch ophthalmol 1958;60:897–906. 23.suzuki s, kaneko a. management of intraocular retinoblastoma and ocular prognosis. int j clin oncol 2004;9:1–6. 24.yamane t, kaneko a, mohri m. the technique of ophthalmic arterial infusion therapy for patients with intraocular retinoblastoma. int j clin oncol 2004;9:69– 73. 25.suzuki s, yamane t, mohri m, kaneko a. selective ophthalmic arterial injection therapy for intraocular retinoblastoma: the long-term prognosis. ophthalmology 2011;118:2081–7. 26.abramson dh, dunkel ij, brodie se, marr b, gobin yp. superselective ophthalmic artery chemotherapy as primary treatment for retinoblastoma (chemosurgery). ophthalmology 2010;117:1623–9. 27.suzuki s, yamane t, mohri m, kaneko a. selective ophthalmic arterial injection therapy for intraocular retinoblastoma: the long-term prognosis. ophthalmology 2011;118:2081–7. 28.vijayakrishnan r, shields cl, ramasubramanian a, emrich j, rosenwasser r, shields ja. irradiation toxic effects during intra-arterial chemotherapy for retinoblastoma: should we be concerned? arch ophthalmol 2010;128:1427–31. 29.broaddus e, topham a, singh ad. survival with retinoblastoma in the usa: 1975-2004. br j ophthalmol 2009;93:24–7. 30.maccarthy a, birch jm, draper gj, hungerford jl, kingston je, kroll me, stiller ca, vincent tj, murphy mfg. retinoblastoma: treatment and survival in great britain 1963 to 2002. br j ophthalmol 2009;93:38–9. microsoft word 3courtheouxp_vasospasme.doc romanian neurosurgery (2010) xvii 3: 275 – 280 275 cerebral vasospasm theoretical remarks/ vasospasme remarques théorétiques patrick courtheoux, beatrice sillard chu – caen, france abstract vasospasm is a serious complication of subarachnoid hemorrhage and it can cause ischemic brain injury (referred to as “delayed ischemia”) and permanent brain damage due to lack of oxygen in parts of the brain. delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. about one third of all people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those suffer permanent damage as a result. it is possible to screen for the development of vasospasm with transcranial doppler every 24–48 hours. a blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm. a protocol referred to as “triple h” is often used as a measure to treat vasospasm when it causes symptoms; this is the use of intravenous fluids to achieve a state of hypertension (high blood pressure), hypervolemia (excess fluid in the circulation) and hemodilution (mild dilution of the blood). nimodipine is routinely used as prophylaxis against delayed ischemic neurological deficits associated with vasospasm. if the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of vasospasms and administer vasodilator medication: endovascular infusion of vasodilatory substances such as papaverine, or of calcium channel blockers such as verapamil; angioplasty may also be performed. keywords: angioplasty, delayed ischemia, transcranial doppler, vasospasm introduction le pronostic de l’hémorragie sous arachnoïdienne (hsa) post anévrismale reste sévère , en particulier en terme de morbidité, malgré une prise en charge qui s’est considérablement améliorée ces quinze dernières années, en raison essentiellement du vasospasme et de ses conséquences. c’est en effet l’une des complications les plus graves, elle est responsable d’ischémie cérébrale, néanmoins toutes les ischémies cérébrales ne sont pas secondaires à un vasospasme. les patients les plus exposés sont ceux qui ont une hsa importante et un état neurologique initial critique. il suscite de nombreux travaux de recherche pour identifier les mécanismes et les médiateurs responsables. definition le vasospasme (vsp) est une réduction de la lumière artérielle associée à des troubles de la microcirculation, et à des anomalies structurales des vaisseaux. il est lié à la présence de sang dans les 276 patrick courtheoux, beatrice sillard cerebral vasospasm theoretical remarks espaces sous arachnoïdiens. il s’agit d’abord d’une contraction de la fibre musculaire lisse liée à la présence d’oxyhémoglobine puis évolue vers une lésion hyperplasique de la paroi vasculaire. il contribue avec l’altération de la barrière hématoencéphalique à la constitution d’un déficit ischémique différé (did ) il est fréquent, présent angiographiquement chez 60% des patients et symptomatique dans la moitié des cas . chez 10 à 15% des patients il laissera des séquelles définitives. physiopathologie il est lié à la présence de sang dans les espaces sous arachnoïdiens, il fait intervenir de multiples facteurs, mais les mécanismes précis doivent encore être élucidés. la lyse des érythrocytes libère de l’oxyhémoglobine qui joue un rôle indispensable mais pas suffisant. l’oxyhémoglobine est cytotoxique au niveau des cellules endothéliales, musculaires lisses et des terminaisons nerveuses périvasculaires. l’oxyhémoglobine produit une contraction prolongée du muscle lisse, soit par action directe sur les fibres musculaires, soit par des mécanismes indirects, tels que la libération de substances vasoactives par la paroi artérielle ou la production de radicaux libres superoxydes. l’oxyhémoglobine peut activer le gène de l’endothéline 1 (et-1), contrecarrer l’effet vasodilatateur puissant de l’oxyde nitrique (no) au niveau de la paroi vasculaire. ce déséquilibre entre et-1 et no pourrait largement contribuer à la formation du vasospasme. les radicaux superoxydes inhibent le no et stimulent la peroxydation lipidique. d’autres médiateurs ont été incriminés: l’hémoglobine à l’état ferreux, la protéine kinase c. la conséquence est une atteinte morphologique de la paroi artérielle avec une hyperplasie de l’intima et une fibrose sous endothéliale, et une atteinte fonctionnelle avec une altération de la vasodilatation endothélium dépendant et contrôlée par l’innervation extrinsèque. l’oxyhémoglobine contribue à constituer le vasospasme et à le pérenniser. les lésions morphologiques peuvent persister plusieurs semaines après un spasme, bien que les signes cliniques aient régressé. l’une des raisons qui conduit à l’ischémie cérébrale pourrait être une perte de l’autorégulation. diagnostic clinique il peut survenir dès le troisième jour, est maximal au cours de la deuxième semaine et peut durer quatre semaines. il n’est pas toujours symptomatique cliniquement. il est suspecté sur l’apparition de signes cliniques nouveaux tels que confusion, somnolence, troubles de la conscience, déficit neurologique moteur, aphasie. il faut exclure les autres causes de détérioration neurologique, à savoir hydrocéphalie, œdème cérébral, hémorragie intracérébrale, crises convulsives infracliniques, troubles hydroélectrolytiques, hypoxie, hypercapnie, méningite nosocomiale. il s’accompagne d’hyperthermie, d’hta, de leucocytose. le diagnostic paraclinique se fait par le doppler transcrânien (dtc) et l’artériographie. romanian neurosurgery (2010) xvii 3: 275 – 280 277 le dtc est un examen simple, facile non invasif et reproductible. il peut être réalisé quotidiennement au lit du malade, permettant de déceler ou de suspecter un vasospasme et de poser l’indication d’une artériographie cérébrale , qui est l’examen de référence pour confirmer le diagnostic. les artères cérébrales présentent un pic systolique aigu suivi d’une décroissance lente des vitesses laissant persister un flux important en fin de diastole. les paramètres étudiés sont les vitesses circulatoires, moyennes, systoliques et diastoliques, la direction du flux, la résistance vasculaire (ir) qui reflète les résistances du territoire d’aval. le vsp réduisant la section du vaisseau, et comme v= q/s( où v est la vitesse, q le débit et s la section du vaisseau), on comprend aisément que plus le spasme est serré, plus la vitesse est élevée, à condition que le débit soit stable. le vsp est qualifié de discret pour des vitesses moyennes (vm) entre 80 et 130 cm/s, de modéré entre 130 et 200 cm/s et de sévère au-delà de 200 cm/s. une augmentation de la vm en 24 h de plus de 50 cm/s est fortement évocatrice de vsp. il n’est validé en pratique clinique que sur l’artère cérébrale moyenne (acm) accessible au niveau de la fenêtre temporale. sa valeur prédictive positive est bonne, néanmoins la vm peut être accélérée par une augmentation du débit et le diagnostic différentiel avec une hyperhémie n’est pas toujours aisé. on peut s’aider de l’index de lindegaard pour les différencier. l’index de lindegaard est le rapport de la vm de l’acm à celle de la carotide interne cervicale. sa valeur normale et de 1,7. supérieur à 3 il est hautement évocateur de vsp, supérieur à 6 le vsp est sévère. 1 a 1 b figure 1 a, 1 b lateral right ica angiogram with cerebral vasospasm figure 1 c ct image with cerebral ischaemia 278 patrick courtheoux, beatrice sillard cerebral vasospasm theoretical remarks pour distinguer hyperhémie et spasme on peut aussi s’aider de la saturation en o2 du sang veineux à la sortie du cerveau c'est-à-dire au niveau de la jugulaire interne (svjo2). une svjo2 basse (< 55%) correspondant à une grande extraction de l’o2 est en faveur d’un débit bas et donc d’un spasme. les résultats asymétriques au dtc sont également un argument en faveur d’un spasme, mais il existe des spasmes bilatéraux. mais il y a des faux négatifs, les principaux étant le vsp périphérique et le vsp du siphon carotidien avec chute du débit d’aval. l’arteriographi cerebrale c’est l’examen de référence qui confirme le diagnostic, elle visualise le rétrécissement du calibre artériel qui est concentrique, à contour régulier. il peut être focal, segmentaire ou diffus. il existe un délai de remplissage vasculaire accru pouvant imposer une augmentation du temps d’acquisition angiographique avec retard d’apparition des temps parenchymateux et veineux. traitement le traitement préventif est basé sur l’utilisation de la nimodipine, inhibiteur calcique, vasodilatateur, agissant préférentiellement au niveau des artérioles cérébrales. son mode d’action est de minorer les conséquences du vasospasme; ses effets sont liés à une diminution de la calcitoxicité intracellulaire neuronale, à une amélioration de la circulation collatérale leptoméningée et à des effets rhéologiques. elle s’utilise habituellement par voie intraveineuse la première semaine, à la dose de 2mg/h, puis per-os à la dose de 360mg/jour, soit 2 cp toutes les 4h. la durée totale du traitement est de 3 semaines. en fait il n’y a pas d’arguments pour utiliser la voie intraveineuse en dehors d’une intolérance digestive. chez les patients grade 4-5 de la wfns elle doit s’utiliser sous contrôle de la pic. la correction de toute hypotension, de toute hypovolémie participe également à la prévention du vasospasme. d’autres traitements pharmacologiques ont été proposés dans la prévention du vasospasme: la nicardipine, le tirilazad, le magnésium,mais qui actuellement ne peuvent être recommandés dans la prévention et le traitement du vasospasme . le nitroprussiate intrathécal, donneur d’oxyde nitrique, serait intéressant pour la prévention et le traitement du vsp, mais nous n’avons pas l’expérience. l’enoxaparine, héparine de bas poids moléculaire, semble prometteuse, mais elle n’a pas été testée contre la nimodipine qui est actuellement le traitement de référence. le traitement hémodynamique a pour but d’augmenter le débit sanguin cérébral des territoires d’aval. la triple h thérapie associant hypervolémie, hémodilution, hypertension artérielle aurait montré une éfficacité dans la prévention du vsp mais n’améliore pas les déficits ischémiques installés, et donc la survie. elle n’est pas dépourvue d’effets secondaires qu’ils soient neurologiques ou systémiques. (œdème cérébral, htic, infarctus hémorragique) la complication systémique la plus fréquente est l’œdème pulmonaire, surtout après expansion volémique. de ces trois «h» il ne reste en pratique clinique que l’hta associée à une normovolémie, pam souhaitable 120 mmhg, limitée à 100 mmhg quand il existe un infarctus cérébral (avis d’expert). romanian neurosurgery (2010) xvii 3: 275 – 280 279 ce traitement s’effectue en unités de soins intensifs, sous contrôle de la mesure continue de pa sanglante et d’un abord veineux profond. l’hta nécessite souvent le recours à des amines vasopressives, l’amine de choix étant la noradrénaline. il importe de contrôler les paramètres biologiques et cliniques dont la température. le traitement endovasculaire il comporte l’injection intra-artérielle de vasodilatateurs ou la réalisation d’une angioplastie. les vasodilatateurs utilisés sont la papavérine et la nimodipine (1 mg, soit 5ml ramené à 10 ml en 10 à 20 mn). leur demi-vie courte explique que leur action soit transitoire, rendant compte des bons résultats angiographiques et des moins bons résultats cliniques. ils doivent être renouvelés. l’angioplastie n’est réalisée qu’au niveau du siphon carotidien et de la partie proximale de l’acm. elle doit être la plus précoce possible après l’apparition de signes cliniques de déficit ischémique. elle donne de bons résultats mais sa complication majeure est la rupture artérielle. perspectives d’avenir une anti-endothéline est en cours d’évaluation pour le traitement préventif et curatif du vsp. elle serait efficace dans un modèle expérimental, chez l’animal. l’endothéline-1 est un peptide, vasoconstricteur puissant dont l’activité résulte de l’augmentation de la concentration intracellulaire de calcium. son implication dans la physiopathologie du vsp a été prouvée. l’oxyhémoglobine et la thrombine présente dans le lcr après une hsa peuvent augmenter la libération d’endothéline les antagonistes de l’endothéline préviennent et traitent le vsp dans les modèles expérimentaux d’hsa, la molécule en cours d’étude est le clozasentan. les premiers résultats sont encourageants mais doivent être confirmés par une nouvelle étude actuellement en cours (l’étude conscious-1 ) cette perspective encourageante termine cet exposé. conclusion le vsp est en grande partie responsable de la lourde morbidité qui persiste après une hsa post anévrismale. sa prévention, sa détection doivent rester une préoccupation majeure lors de la prise en charge de l’hsa. l’avénement d’un traitement préventif ou curatif constituera un progrès indéniable pour les malades victimes d’hsa. comments in this article courteoux and sillard present more theoretical remarks on cerebral vasospasm following aneurysmal subarachnoid hemorrhage (sah). cerebral vasospasm is a common complication following aneurysmal sah, which can take place in up to half of patients after bleeding occurs. the most common cause of death and disability in patients with sah in a subacute setting is 280 patrick courtheoux, beatrice sillard cerebral vasospasm theoretical remarks delayed cerebral ischemia caused by cerebral vasospasm. the patient with acute subarachnoid hemorrhage needs to be managed in an intensive care unit (icu). low reactivity, drowsiness or lethargy with or without focal neurological deficit means cerebral vasospasm, until proven otherwise and emergency ct must be performed. a prompt diagnosis of cerebral vasospasm is the first step in the management of sah patients. the gold standard in detection cerebral vasospasm is angiography , but it is relevant only 50 % in the diagnosis of hemodynamically relevant vasospasm. there are some diagnosis techniques to assess regional cerebral blood flow (rcbf): positron emission tomography (pet), single photon emission computed tomography (spect), xe-ct, mri.the most prominent technique for a noninvasive assessment of rcbf is transcranial doppler sonography. as treatment hypertensive hypervolemic hemodilution ( triple h) is indicated and the goal is to maximize cerebral blood flow (cbf) to areas of vasospasm to prevent or reverse neurological symptoms. on statin therapy and cerebral ischemia: there are recent studies contradict each other concerning the benefits of statin therapy to prevent vasospasm and delayed cerebral ischemia. also endovascular infusion of vasodilatory substances and angioplasty may be performed. we hope new methods of detection and treatment of vasospasm will lead to a future in which cerebral vasospasm will be a concern of the past and will reduce the incidence of delayed neurological deficits. şt.m. iencean, md, phd editor romanian neurosurgery references 1. aaslid r: hemodynamics of cerebrovascular spasm. acta neu ro chir suppl 72:47–57, 1999 2. adams hp jr: prevention of brain ischemia after aneurysmal sub arachnoid hemorrhage. neurol clin 10:251–268, 1992 3. borel co, mckee a, parra a, haglund mm, solan a, prabha kar v, et al: possible role for vascular cell proliferation in cerebral vasospasm after subarachnoid hemorrhage. stroke 34: 427–433, 2003 4. lu d, mahmood a, goussev a, schallert t, qu c, zhang zg, et al: atorvastatin reduction of intravascular thrombosis, in crease in cerebral microvascular patency and integrity, and en hancement of spatial learning in rats subjected to traumatic brain injury. j neurosurg 101:813–821, 2004 5. sillberg va, wells ga, perry jj. do statins improve outcomes and reduce the incidence of vasospasm after aneurysmal subarachnoid hemorrhage: a meta-analysis. stroke. 2008;39(9):2622-6 6. vergouwen md, de haan rj, vermeulen m, roos yb. effect of statin treatment on vasospasm, delayed cerebral ischemia, and functional outcome in patients with aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis update. stroke. 2010;41(1):e47-52. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 455-463 doi: 10.33962/roneuro-2019-072 www.journals.lapub.co.uk/index.php/roneurosurgery improved pain and quality of life outcomes after percutaneous vertebroplasty for thoraco-lumbar non-osteoprotic compression fractures mostafa m. nabeeh, hanee a. awad, nabil m. ali neurosurgery department, mansoura university, egypt abstract introduction: vertebroplasty is a minimally invasive technique in which percutaneous injection of bone cement under fluoroscopic guidance percutaneous vertebroplasty (pvp) has been widely and successfully accepted in the treatment of osteoporotic and neoplastic vertebral compression fractures to control pain refractory to medical treatment. however, using of vertebroplasty as primary line treatment for traumatic, non-osteoporotic compression fractures still not widely accepted and considered a debatable issue. patients and methods: this prospective comparative study was conducted at neurosurgery department, mansoura university hospital and mansoura emergency hospital through the period between january 2015 and march 2016. 20 patients complaining of back pain due to single level thoracolumbar vertebral compression non-osteoprotic fractures were admitted to the study. patients were divided into two groups 10 patients each, pvp group and conservative group. outcome were assessed as regard pain improvement using visual analogue scale vas and quality of life using short form 36 scale (sf36). results: ten patients in the pvp group received vertebroplasty, eight males (80%) and two females (20%) the age ranged from 29 to 62 years with mean age of 44.2+8.3 (mean+sd) years. the conservative group included ten patients seven males (70%) and three females (30%) the age ranged from 31 to 64 years with mean age of 45.1+9.2 (mean+sd) years. the level of injury ranged from d6 to l4. vas and sf36 results showed significant improvement in post injection results compared to preinjection and to the conservative group conclusion: percutaneous vertebroplasty is safe and effective procedure to improve pain and quality of life in non osteoprotic patients complaining of traumatic compression fractures of thoraco-lumar region it decreases pain, and provide early ambulation of patients which improve their quality of life without significant morbidity. introduction vertebral compression fractures (vcfs) represent a significant health care problem due to high incidence and their direct and indirect negative impact on quality of life, physical function, mental health and missed work hours as well as the burden on health care system keywords vertebroplasty, vertebral compression fractures, quality of life, non-osteoporotic corresponding author: mostafa m. nabeeh neurosurgery department, mansoura university, egypt sasamah2001@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 456 mostafa m. nabeeh, hanee a. awad, nabil m. ali [114,21,25]. vertebroplasty is a minimally invasive technique in which percutaneous injection of bone cement under fluoroscopic guidance into the cancellous bone of a vertebral body with the objective of bone augmentation [19]. galibert et al. in 1987 were the first to describe and introduced vertebroplasty, they used the technique for management of vertebral angiomas in seven patients [10]. percutaneous vertebroplasty is a relatively safe, simple and commonly performed interventional procedure for the management of vertebral compression fractures [11]. percutaneous vertebroplasty (pvp) has been widely and successfully accepted in the treatment of osteoporotic and neoplastic vertebral compression fractures to control pain refractory to medical treatment [2,12, 15 18, 20,24, 25]. taylor et al 2007 published a systematic review and found that there is level iii evidence to support balloon kyphoplasty and vertebroplasty as effective therapies in the management of patients with symptomatic osteoporotic vertebral compression fractures refractory to conventional medical therapy.[23]. however, using of vertebroplasty as primary line treatment for traumatic, nonosteoporotic compression fractures still not widely accepted and considered a debatable issue. decrease fracture healing, risk of infection and effectiveness of alternative conservative and surgical options are raised as rejection points, while minimally invasiveness than surgery and improvement of pain and quality of life than medical treatment are assumed as advantages of the technique [5,6,7,8, 22]. in this study, we compare the percutaneous vertebroplasty pvp and conservative medical treatment in the treatment of traumatic single level non-osteoprotic compression fractures. the 2 groups were compared with respect to baseline pain, quality of life, hospital stay and follow up at 1 and 3 months. patients and methods this prospective comparative study was conducted at neurosurgery department, mansoura university hospital and mansoura emergency hospital through the period between january 2015 and march 2016. 20 patients complaining of back pain due to single level thoracolumbar vertebral compression fractures were admitted to the study. patients were divided into two groups 10 patients each, pvp group and conservative group. the choice between the 2 options was based primarily on patient’s preferences and, to some extent, on counseling by the neurosurgeon on charge, the first and second authors who did the pvp procedure were called for performing the procedure by the neurosurgeons on duty and didn’t involve in the process of decision making. pre-operative evaluation patients were assessed clinically by neurological and local examination. this aimed to exclude neurological deficit and identification of painful vertebra by local tenderness at the fracture site and detection of associated medical or surgical comorbidities. it aimed also at defining the degree of pain by visual analogue scale (vas) for pain assessment with 0 as no pain and 10 as the worst pain ever experienced. short form 36 test (sf 36) for quality of life assessment [4]. imaging studies included plain x-ray radiography to detect the level, type and number of fractures, degree of collapse (relative vertebral body height) and the degree of kyphosis (vertebral wedge or local kyphotic angle). the relative vertebral height (rvh) was measured as the sum of the distance along the vertebral borders at the anterior, middle, and posterior locations of the fractured vertebral body in relation to the adjacent intact vertebral body as a reference. the kyphotic angle was determined by using the cobb method as the angle between the superior and inferior endplates of the collapsed vertebral body. the relative heights of the fractured vertebrae and angle were assessed before and after vertebroplasty on a standard lateral radiograph, and assessed in the conservative group on admission then on discharge and during 1and 3 months follow up. ct scan with sagittal reconstruction was done for all patients to assess the type of fracture and the integrity of posterior wall of the vertebral body. patients included to this study had traumatic fracture with intolerable pain who had a normal bmd t-score (-1 or higher) and their age above 18 years old, compression fracture less than 50% of vertebral height, intact motor power, no or very small retropulsed segment. while pediatric patients, those having neurological deficit, fracture more than 50% , 457 improved pain and quality of life outcomes after percutaneous vertebroplasty unstable fracture with posterior or middle column disruption and compromise the canal, potential infection, bleeding tendency, oral anticoagulant, had previous spine surgery at same level, those have another painful disease of spine or pathological fractures either osteoporotic or neoplastic were excluded from our study. procedure patient was placed in prone position with translucent padding of the regions caudally and cranially from the fractured vertebra(e). oxygen mask was applied oxygen saturation, blood pressure and heart rate are continuously monitored. sterile drapes were put after adequate sterilization of patient's back. procedure is performed under local anaesthesia. identification of the fractured level with the aid of fluoroscopy. (figure 1). figure 1: vertebroplasty procedure: atwo injection needles at place bduring injection cthe needle and injector dc-arm device at neurosurgery department operative room, mansoura university hospital. figure 2: graph of median pain based on vas score, on admission, on discharge 1 month and 3 months following vertebroplasty. vas, visual analogue scale. figure 3: graph of mean quality of life based on sf36 scores on admission, 1 month and 3 months of both groups. figure 4: preand post-operative x-ray ap & lat view the fluoryscopy was manipulated till the fracture level centralized and both pedicle arches were identified on the antero-posterior (ap) image. local anaesthesia was achieved by injection of lidocaine 1% solution using thin spinal needle by which we infiltrated the whole pathway from facet joint till 0 2 4 6 8 v a s conservativ e pvp 0 20 40 60 80 100 s f 3 6 conservativ e pvp 458 mostafa m. nabeeh, hanee a. awad, nabil m. ali subcutaneous tissue. the position of the thin needle used for lidocaine injection determines the direction of the vertebroplasty needle tract during fluoroscopy. under fluoroscopic guidance one (preferred) or two needles were introduced to pedicle then under guidance of lateral fluoroscopy image the needle was advanced till half of vertebra near midline which confirmed again by ap image. during insertion of the needle, the bevelled tip was pointed laterally to gain easy access to the pedicle. after pedicle penetration, the bevelled side was rotated medially to avoid breaching of the medial pedicle wall. the pmma cement (exolent spine, ® italy) was prepared and transferred to an injector. the air was eliminated from the system. after 2-4 minutes of cement mixing (depending on the viscosity of the cement and on the room temperature), the cement reached its proper viscosity (toothpaste-like), and is ready to be injected. the cement was then injected slowly and carefully under constant fluoroscopic imaging in order to achieve good filling of the intertrabecular space of the vertebral body. the injector is disconnected from the needle. the needle(s) was (were) removed with twist to separate the tip from the cement. post procedure care: a post-procedural ct scan was performed to all cases to assess extent of bone cement and detection of any cement leak. then the patient was placed in bed for transport to the ward figure (5). figure 5: pre and post operative ct a preoperative sagittal view b postoperative axial view showed filling of the fractured vertebra with bone cement with no leakage cpost operative sagittal view show restoration of vertebral height and angles. figure 6: unipedicular injection, cement cross the midline and small part of cement start to leak on the left side of vertebra. follow up it was carried out at regular intervals; 2 weeks, 1months and 3 months. in each time the patient were evaluated clinically for neurological examination, pain by visual analogue scale, evaluation of quality of life by short form 36 test [3]. and radiographically by plain x-ray. statistical analysis: data were analysed using the statistical package of social science (spss) program for windows (standard version 21). the normality of data was first tested with one-sample kolmogorov-smirnov test. continuous variables were presented as mean ± sd (standard deviation) for parametric data and median for non-parametric data. the two groups were compared with student t test (parametric data) and mann–whitney test (non parametric data). level of significance for all above mentioned statistical tests done, the threshold of significance is fixed at 5% level (p-value). the results were considered: • non-significant when the probability of error is more than 5% (p > 0.05). • significant when the probability of error is less than 5% (p ≤ 0.05). 459 improved pain and quality of life outcomes after percutaneous vertebroplasty the smaller the p-value obtained, the more significant are the result. results twenty patients complaining of intractable back pain due to thoracolumbar vertebral compression fractures, and not responding to initial conservative measures and not associated with neurological affection. ten patients in the pvp group received vertebroplasty, eight males (80%) and two females (20%) the age ranged from 29 to 62 years with mean age of 44.2+8.3 (mean+sd) years. six patients injured during fall from height while four sustained road traffic accidents. unipedicular injection was performed for six vertebrae (60%), while bipedicular injection performed for four vertebrae (40%). the level of injected vertebra ranged from d8 to l4. the interval between trauma and injection ranged 3 to 12 days mean was 4.6+1.8 the mean post injection hospital stay was 1.7 days ranged from 6 hours to 3 days. the relative kyphotic angle was 10.42+3.8. the relative vertebral height was 77+7mm the conservative group included ten patients seven males (70%) and three females (30%) the age ranged from 31 to 64 years with mean age of 45.1+9.2 (mean+sd) years. 5 patients injured during fall from height while 5 sustained road traffic accidents. the level of fractured vertebra ranged from d6 to l3. the relative kyphotic angle was 10.17+3.5. the relative vertebral height was 78+2mm. table 1: comparison between both group regarding data on admission. vertebral height kyphotic angle age gender pvalue m f conservative 78+2.7 10.17+3.5 45.1+9.2 7 3 >0.05 pvp 78+2.7 10.42+3.8 44.2+8.3 8 2 table 2: comparison between conservative and pvp groups regarding vas preoperative and at different follow up periods. vas conservative (n=10) pvp (n=10) mann whitney test pvalue admission median (min-max) 7 (4-9) 7 (4-9) 0.194 0.846 vas at discharge median (min-max) 5 (4-7) 3 (1-6) 2.778 0.005* vas after 1m median (min-max) 4 (2-5) 2 (0-4) 2.625 0.009* vas after 3m median (min-max) 2 (0-2) 1 (0-1) 2.109 0.035* *significant p <0.05 table 2 showed the results of vas on admission the differences between both group was statistically insignificant (p=0.846) the pain showed statically significant improvement in pvp group patients from preoperative vas and compared to conservative group the level of significance was highest on time of discharge(p=0.005) and gradually decreased till 3 months (p=0.035). in the pvp group preoperative vas ranged from 4 to 9(0% no pain, 0% mild, 10% uncomfortable, 40% distressing, 45% horrible & 5%worst). on discharge vas ranged between 1 to 6(0% no pain, 40% mild, 45% uncomfortable, 10% distressing, 5% horrible & 0% worst). table 1 comparing unipedicular versus bipedicular techniques results, it is found that no significant difference between improvement of vas between both techniques table 3. showed results of vas in unipedicular and bipedicular techniques. 460 mostafa m. nabeeh, hanee a. awad, nabil m. ali table 3: comparison between unipedicular and bipedicular pvp regarding vas preoperative and at different follow up periods. vas unilateral pvp (n=6) bilateral pvp (n=4) mann whitney test pvalue pre-injection median (min-max) 7 (5-8) 7 (4-9) 0.441 0.659 vas at discharge median (min-max) 3 (1-3) 4 (2-6) 1.453 0.146 vas after 1m median (min-max) 2 (0-3) 2 (1-4) 0.775 0.438 vas after 3m median (min-max) 1 (0-1) 1 (0-1) 0.267 0.789 the mean preoperative sf 36 test score was 55.10±12.57 pointsin conservative group versus 59.80±12.16 in pvp group (p=0.407). while the 1 month after discharge mean sf 36 test score was 65.1±10.37 points for conservative group while was 80.70±4.13 (p<0.001). on three months follow up sf36 score was 79.10 ± 6.84 and 86.00 ± 6.16 respectively. the improvement outcome of postoperative values compared with preoperative sf 36 test score was found to be statistically significant (p<0.001). table 4. as the results of vas the difference between unipedicular and bipedicular injection in improving quality of on s36 score were insignificant table 5 comparing unipedicular versus bipedicular techniques results, the difference was found to be statistically insignificant. table 5. there was no mortality in both groups. we had only two cases of cement leakages one case of asymptomatic vascular extravasation of cement and another patient in whom cement leaked into upper disc space. table 4: comparison between conservative and pvp groups regarding sf36 pre injection and at different follow up periods. sf36 conservative (n=10) pvp (n=10) student t-test pvalue pre-injection mean ± sd 55.10±12.57 59.80±12.16 0.850 0.407 sf36 after 1m mean ± sd 65.1±10.37 80.70±4.13 4.29 <0.001* sf 36 after 3m mean ± sd 79.10±6.84 86.00±6.16 2.370 0.029* table 5: comparison between unilateral and bilateral pvp regarding sf36 preoperative and at different follow up periods. sf36 unilateral pvp (n=6) bilateral pvp (n=4) student t-test pvalue pre-injection mean ± sd 55.67±11.39 66.00±11.91 1.381 0.205 sf36 after 1m mean ± sd 80.00±4.09 81.75±4.57 0.633 0.544 sf 36 after 3m mean ± sd 83.50±5.36 89.75±5.91 1.738 0.120 table 5 studies addressed non ostoprotic traumatic fractures 461 improved pain and quality of life outcomes after percutaneous vertebroplasty author study design type of fracture number of patients year chen and lee case report burst 1 2004 chen and lee case series burst 6 patients 2004 amoretti et al case series burst 5 patients 2005 huet et al case series burst 12 2005 szekely et al case report burst 1 2009 knavel et al retrospective review compression 15 patients 2009 szekely gy case series compression 15 patients 2012 elnoamany case series compression 23 patients 2015 discussion conservative management, surgical fixation and vertebroplasty are available treatments options for traumatic vcfs. medical treatment includes rest, thoraco-lumar orthosis and analgesic is indicated in case no neurological deficit, no any signs of instability and kyphotic angle less than 20 degrees and less than 50% vertebral height loss, which are the same indications for percutenous vertebroplasty. for vertebroplasty there is another relative indication which is the integrity of posterior wall of vertebral body [14,17]. surgical intervention is not usually the first line of therapy and mostly is necessary if the kyphosis is above 20 degrees to prevent corporeal collapse and prevent subsequent neurological disorders or low back pain. the signs of instability like involvement of the posterior wall, disruption of the spinal arch or interpedicular olisthesis are indication for surgical intervention [1]. nowadays vertebroplasty become a popular procedure for management of refractory pain in osteoprotic compression fractures and pathological fractures. however, there is a debat about its efficacy in pain relief, quality of life improvement, using it in traumatic cases and its complications. few reports in litreture were addressed the implication of vertebroplasty in management of the nonosteoprotic traumatic vcfs [3, 6, 7, 9, 14, 21, 22], two of them are case reports and the others are limited sample cohort studies. table (5) up to our knowlage, no published comparative study compared the outcome of vertebroplasty to that of conservative management in patients suffering traumatic non osteoprotic thoraco-lumbar vcfs. this study is unique in comparing both treatment modalities in control of pain early mobilization and improving quality of life. our results showed that vertebroplasty was effective in reducing pain in all of the vertebroplasty group's patients within a very short period of time. vas scores obtained on time of patient discharge, 1 month and 3 months after vertebroplasty from our 10 patients of the pvp group showed significant pain relief. and when compared to the vas scores of the conservative group patients, there were statistically significant superiority to the vertebroplasty group. pain relief was rapid and marked. this improvement was maintained and continued to improve through the whole follow up period and didn’t decline by time. our results of pain improvement are supporting the result of szekely et al in their 15 patients' report; all of them showed more than 5 points improvement of vas [22]. el noamany reported injection of 29 vertebrae in 23 patients of non-osteoporotic vcfs, all of them showed improved pain scores both on rest and movement, the improvement started 2 hours post injection and continue during follow up, he advocated pvp as first line treatment of vcfs[9]. chen and lee performed pvp for management of traumatic thoracolumbar spine bursting fractures with statistically significant improvement of pain their six patients[6]. amoretti et al reported 5 patients of stable burst fracture percutaneous vertebroplasty was done under both fluoroscopy and ct guidance, pain improved in 4 out of their 5 patients [3]. the difference between both groups was statistically significant in the time of discharge and one month follow up visit and decline in the 3 months follow up visit. there were no significant differences in these improvements due to the etiology of the fracture or due to the approach used wither unipedicular or bipedicular or the amount of cement used. kallmes et al and buchbinder et al [5,16] published two randomized trials in 2009, they 462 mostafa m. nabeeh, hanee a. awad, nabil m. ali reported that there is no beneficial effect of vertebroplasty compared with a sham procedure ( placebo surgery) in patients with painful osteoporotic vertebral fractures, at 1 week or 1 or 3 months after treatment. no significant differences between groups were seen in the primary outcome of overall pain at 3 months. despite their population were osteoprotic, we have many concerns about this results, as in our study pain improvement was significant which match with most of studies talking about pain improvement following pvp with a variable degree of pain improvement but in this study noting that there is no difference between pvp and sham procedure is questionable. despite small sample size, we found no statistical significance between the six patients received unipedicular injection and the 4 patients received bipedicular injection as regard improving vas scores and quality of life on sf36. the same conclusion was announced by two studies, knavel et al. [17] concluded from their retrospective study that, hemivertebroplasty in which cement is instilled in only one half of the vertebral body was as efficacious as bilateral cement infusion [17]. the results of elnoamany study on non-osteoprotic vcfs confirmed knavel’s study results, since it showed no statistically significant differences in pain or quality of life scores, between hemivertebroplasty and bilateral vertebral filling [9,l7] which may be partially explained by increase the hardness of non osteoprotic bone. in our opinion, this piece of information is significant because it support the minimally invasive nature of the procedure which could be performed optimally through on side injection, and it facilitate performing vertebroplasty by local anesthetic infiltration rather than sedative anesthesia and this will encourage patients for taking their decisions and lastly it will decrease cost especially in poor countries. pain relief was obviously reflected on the quality of life of the patient and his/her resumption of social activities which were obvious in short form 36 test score improvements. as the short form 36 test sf36 take a survey for last month we found it difficult to be applied on time of discharge and that is why we applied it in one and three months follow up visit. the significant improve in sf36 score results in the vertebroplasty group between pre injection and follow up and between the vertebroplasty group and conservative group support the results accumulated from many previous studies that concluded improvement of quality of life after cement injection for compression fractures either in osteoporotic patients[4, 12,13,18] or in traumatic non osteoprotic vcfs[ 3,6,9, 14, 22] but may be our results is the first to compare the conservative treatment to vertebroplasty in head to head prospective randomized study that showed statistical significant improvement in quality of life in the vertebroplasy group. a comparison of the pre and post vertebroplasty scores in the various sf-36 domains has shown a significant and clinically relevant increase in summary scores, thereby indicating a significant overall increase in the quality of life. during the two weeks after vertebroplasty significant improvement was seen only in the domains of physical function, which is known to have the highest correlation with physical faculties and pain, reflecting the results of the numerical pain score. the role physical and role emotional domains showed an obvious, nonsignificant decrease in the first month, probably due to general post-treatment role-inhibiting behavior. there was a significant improvement in summary scores of sf-36 domains at follow-up at one and three months in our series. it has great potential to avoid various problems associated with prolonged bed-rest, including high medical expense used for analgesics and other medications, deterioration in bone density and function of the musculoskeletal system and progression of dementia in elderly patients. persistent back pain may also cause psychological and sleep disorders. conclusion percutenous vertebroplasty is safe and effective procedure to improve pain and quality of life in non osteoprotic patients complaining of traumatic compression fractures of thoraco-lumar region it decreases pain, and provide early ambulation of patients which improve their quality of life without significant morbidity. disclosures all the authors have no personal financial or institutional interest in any of the drugs, materials, or devices described in this article authors contributions this work was carried out in collaboration between all authors. 463 improved pain and quality of life outcomes after percutaneous vertebroplasty author mostafa m. nabeeh, designed the study, author hanee a. awad wrote the protocol and collect clinical data, author nabil m. ali managed the literature research, author mostafa m. nabeeh performed the statistical analysis and revised the final manuscript. all vertebroplasty procedures were carried out by the first two authors. all authors read and approved the final manuscript. abbreviations bmd: bone mineral density. ct: computerized tomography. pvp: percutaneous vertebroplasty pmma: poly methyl methacrylate . rvh: relative vertebral height sf 36: short form 36 vas: visual analog scale vcf1: vertebral compression fracture. references 1. allegretti l, mavilio n, fiaschi p, bragazzi r, pacetti m, castelletti l, barzaggli r. intra-operative vertebroplasty combined with posterior cord decompression. a report of twelve cases. interv neuroradiol. 2014 oct31, 20(5):583-90 2. alvarez l, alcaraz m, perez-higueras a, et al. percutaneous vertebroplasty: functional improvement in patients with osteoporotic compression fractures. spine 2006;31:1113– 8.american college of radiology: john d. barr, michelles s. mathias, jacques e. dion. active guideline for the performance of vertebroplasty. revised 2009. 3. amoretti n, hovorka e, marcy py, et al. burst fracture of the spine involving vertebrae presenting no other lesions: the role of vertebroplasty. clin imaging 2005,29:379-82. 4. brazier j, roberts j, deverill m. the estimation of a preference-based measure of health from the sf-36. j health econ 2002,21:271-92. 5. buchbinder r, osborne rh, ebeling pr, et al. a randomized trial of vertebroplasty for painful osteoporotic vertebral fractures. new engl j med 2009,361:557–68. 6. chen j-f, lee s-t. percutaneous vertebroplasty for treatment of thoracolumbar spine bursting fracture. surg neurol 2004,62: 494–500. 7. chen jf, wu ct, lee st. percutaneous vertebroplasty for the treatment of burst fractures. case report. j neurosurg spine 2004,1:228-31. 8. christodoulou a, ploumis a, terzidis i, pournaras i. vertebral body reconstruction with injectable hydroxyapatite cement for the management of unstable thoracolumbar burst fractures: a preliminary report. acta orthop belg. 2005,71(5):597-603. 9. elnoamany h:percutaneous vertebroplasty: a first line treatment in traumatic non-osteoporotic vertebral compression fractures asian spine j 2015,9(2):178-184 10. galibert p, deramond h, rosat p, et al. preliminary note on the treatment of vertebral angioma by percutaneous acrylic vertebroplasty. neurochirurgie. 1987,33:166–8. 11. galibert p, deramond h, rosat p, le gars d. [preliminary note on the treatment of vertebral angioma by percutaneous acrylic vertebroplasty, revised]. neurosurgery. 2006; 33(17):166-8. 12. garnier l,tonettia j, bodina a, vouaillat h, merloza p, assakerb r et al: kyphoplasty versus vertebroplasty in osteoporotic thoracolumbar spine fractures. j. orthopaedics & traumatology: surgery & research. 2012, 98: 112-119. 13. heini pf, walchli b, berlemann u: percutaneous transpedicular vertebroplasty with pmma: operative technique and early results: a prospective study for the treatment of osteoporotic compression fractures. eur spine j 2000, 9 (5):445—450. 14. huet h, cabal p, gadan r, borha a,: emery e. burstfractures and cementoplasty. j neuroradiol. 2005,32(1):3341. 15. kaemmerlen p, thiesse p, jonas p, et al.: percutaneous injection of orthopedic cement in metastatic vertebral lesions. n engl j med. 1989;321:121. 16. kallmes df, comstock ba, heagerty pj, et al.: a randomized trial of vertebroplasty for osteoporotic spinal fractures. new engl j med 2009,361:569–79. 17. knavel em, rad ae, thielen kr, kallmes df.: clinical outcomes with hemivertebral filling during percutaneous vertebroplasty. ajnr am j neuroradiol 2009,30:496-9. 18. kobayashi k, shimoyama k, nakamura k, murata k: percutaneous vertebroplasty immediately relieves pain of osteoporotic vertebral compression fractures and prevents prolonged immobilization of patients. j eur radiol 2005, 15: 360-367. 19. mccall t, cole c, dailey a.: vertebroplasty and kyphoplasty: a comparative review of efficacy and adverse events. curr rev musculoskelet med. 2008,1(1):17–23. 20. neto pp, kihara en, fontoura ea, andrioli ms, junior aa, romaldiai h et al: percutaneous vertebroplasty with polymethylmethacrylate analysis and results in 57 treated patients. j einstein 2004, 2(4):278-281 21. szekely gy, jósvai a, erbszt a, et al: the use of vertebroplasty in traumatic fractures of the thoracolumbal spine. aarms 2009, vol. 8, no. (1) 133–139 22. szekely gy: the role of percutaneous vertebroplasty in traumatic fractures of the thoracolumbar spine. acta medica marisiensis 2012,58(6):470-473 23. taylor rs, taylor rj, fritzell p.: balloon kyphoplasty and vertebroplasty for vertebral compression fractures: a comparative systematic review of efficacy and safety. spine 2006,31:2747–55. 24. tschirhart ce, finkelstein ja, whyne cm. optimization of tumor volume reduction and cement augmentation in percutaneous vertebroplasty for prophylactic treatment of spinal metastases. j spinal disord tech. 2006,19:584–90. 25. yehya a and el-nekady a: percutaneous vertebroplasty for osteoporotic fracture of dorsolumbar and lumbar vertebra: surgical technique and early outcome. pan arab journal of neurosurgery 2010, 14:2: 63-68. microsoft word 16sirbuminimallyinvasive romanian neurosurgery (2011) xviii 1: 101 – 102 101 minimally invasive plate osteosynthesis using systems with angular stability in complex fractures of the distal femur. fashion or real advantages? regenerative medicine as an option for bone regeneration p.d. sîrbu1, t. petreuș1, r. asaftei1, c.e. cotrutz1, e. carata2, p. botez1, s. stratulat1 1“gr.t. popa” university of medicine and pharmacy, iasi, romania 2“gh. asachi” technical university, iasi, romania keywords: liss, lcp, combi-holes, polyaxial stability, internal fixators introduction complex distal femoral fractures represent a challenge for orthopaedic surgeons. the disadvantages of classic surgery led to the development of new surgical techniques (minimally invasive plate osteosynthesis mipo and transarticular approach and retrograde plate osteosynthesis tarpo) and new implants with angular stability (internal fixators). aims the purpose of this study is to present the preliminary results in treating the distal femoral fractures with plates with angular stability and to exhibit the advantages and differences between these efficient systems. material and methods the study included 22 fractures (4 type a2, 7 type a3, 6 type c2, and 5 type c3 ao). there were 2 periprosthetic knee fractures. the study included 4 open fractures: 2 grade i, 1 grade ii, and 1 grade iiia (gustilo). the authors used a less invasive stabilization system (liss) in 10 cases, locked compression plate (lcp) with combi-holes in 6 cases, and plates with polyaxial stability in 6 cases. for extraarticular fractures, the plates were inserted through a minimally antero-lateral incision beneath the vastus lateralis (by means of an aiming device), after indirect, closed fracture reduction of the metaphysis and shaft area (mipo technique). for articular fractures we have first performed a lateral parapatellar arthrotomy and reconstruction of the articular block (tarpo technique). newer polyaxial locked plates were used in difficult type c3 distal femoral fractures due to some freedom in angulation of screws, prior to final screw plate sitting. results and discussions all fractures less one (with bone loss which required bone grafting after three months) healed within a mean time of 13 weeks (with no infections, implant breakage or secondary displacement), these plates with angular stability represent the ideal treatment in difficult fractures with short distal fragment, osteoporotic fractures, fractures above knee 102 p.d. sîrbu et al minimally invasive plate osteosynthesis arthroplasties and some open fractures. the key to success for internal fixators are: correct/incorrect indications, the usage of the appropriate plates, proper fracture reduction before plate insertion and screw drilling, avoidance of the eccentric plates placement, full-weight bearing allowed when callus is seen in serial postoperative radiographs. the authors prefer the lcp system and a newer polyaxial locked plate due to their advantages of screw pathway adjustment. conclusions close cooperation between orthopaedic surgeon, biomechanics specialist and the departments of cell biology and pathology, will contribute to the development of the ideal internal fixator and will sustain the future experimental investigations in order to elucidate the dynamic and coherent process of callus formation with these biological plates and techniques. references 1. frigg r., appenzeller a, christensen r., frenk a, gilbert s., schavan r. “the development of the distal femur. less invasive stabilization system (liss)”, injury, int. j. care injured, 2001, 32, pp. 24-31. 2. wagner m, frigg r (eds) ao manual of fracture management – internal fixators. thieme stuttgart (2006) 3. richter m, droste p, goesling t, zech s, krettek c. polyaxially-locked plate screws increase stability of fracture fixation in an experimental model of calcaneal fracture. j bone joint surg br. 2006 sep;88(9):1257-63. 4. sirbu p.d., schwarz n., belangero v.d., livani b., list m., botez p., mihaila r.i. minimally invasive plate ostheosynthesis in long bone fractures, casa de editura venus, iasi, romania 2008. 5. sirbu p.d., friedl w., botez p., stratan l., hopulele s., asaftei r. osteosinteza minim invaziva cu placi fixatoare interne, casa de editura venus, iasi, romania 2008 6. ip david, orthopedic traumatology – a resident’s guide; springer berlin-heidelberg 2006 microsoft word 12rajendrash_intrasellarabcess_f 326 shrestha rajendra et al intrasellar abscess after transsphenoidal pituitary surgery intrasellar abscess after transsphenoidal pituitary surgery shrestha rajendra, ji zhang, jin li, shu jiang, chao you department of neurosurgery, west china hospital, sichuan university, 37 guo xue xiang, wuhou district, chengdu 610041, china abstract sellar abscess is extremely rare complication that could occur after a transphenoidal surgery (tss). here we report 45-year-old female patient with left cheek numbness for one month. the magnetic resonance imaging (mri) report suggested a pituitary adenoma. therefore, transphenoidal surgery was performed. during follow up, the patient complained of headache for few days. subsequent mri revealed recurrent or residual pituitary tumor. we attempted to excise the lesion using a transfrontal approach. however, pus in the sellar region was found at operation, and no tumor tissue was identified. after the surgery, the patient received antibiotic therapy and fully recovered. sellar abscess is a serious condition with a high mortality rate. however, a combination of surgical resection and specific antibiotic therapy seems to be very promising. keywords: pituitary adenoma, pituitary surgery, sellar abscess, transphenoidal surgery introduction sellar abscess is a rare clinical entity but one with potentially high mortality and morbidity. preoperative diagnosis of a sellar abscess is difficult, partly because patients with this condition do not commonly show systemic signs of inflammation and also clinical manifestations of sellar abscesses are nonspecific (11). so it may be misdiagnosed as pituitary adenoma. sellar abscess after tss operation of pituitary adenoma has high mortality. early diagnosis and treatment with surgical management and antibiotics are important. our case report involves a 45-year-old female patient with intrasellar abscess formation after transsphenoidal pituitary surgery. case report the patient, a 45-year-old woman, had a numb left cheek for one month. there was no blurring of vision, however. moreover, the patient did not have any complaints of headache, polydipsia, polyphagia, polyuria. on examination, no neurological deficit was detected. on the magnetic resonance imaging (mri) examination of sellar region demonstrated 2.05x1.84x2.2 cm sellar mass with mixed signal, tearing the diaphragma sellae, had waist-like symptoms, little push bilateral optic nerve (figure 1). the computed tomography (ct) of the skull base shows: sellar lesions, mostly the pituitary tumor. patient underwent transsphenoidal surgery (tss) during which we did not find any significant adhesions in surrounding structures and saddle compartment. soft, gray tissue was removed without any complication and hemostasis was maintained on the tumor bed. romanian neurosurgery (2011) xviii 3: 326 – 330 327 a b c figure 1 mri brain showing a sellar suprasellar mass lesion hypo-hyperintense with enlargement of sella suggestive of a pituitary macroadenoma bone chips fixed to surrounding tissues with acrylic glue were used to pack the sella. the tumor bed and sphenoid sinus were loosely packed with adipose or muscle tissue, mucosa, nasal turbinate bone and collagen sponge to prevent cerebrospinal fluid (csf) leakage. histopathological examination revealed pituitary adenoma. the patient had a good recovery postoperatively (figure 4 a).the patient presented with headache for couple of weeks in the four months of follow up. no abnormality was found on examination, however. observe the recurrent or residual pituitary tumor in the mri scan of the head (figure 2). thereafter, craniotomy was done and showed that sellar tension was high, filled with milky white turbid pus, no tumor tissue. the purulence remaining in 328 shrestha rajendra et al intrasellar abscess after transsphenoidal pituitary surgery the sinus and sella was evacuated by irrigation and aspiration. postoperatively patient was managed in the intensive care unit with specific antibiotics, hormonal and fluid therapy. patient was monitored with csf study to know the control of infection. histopathological examination confirmed abscess (figure 4b). patient was discharged following a full recovery. no pituitary mass was observed on the follow-up mri (figure 3). a b c figure 2 after 4 months of follow up, mri brain showing a sellar suprasellar mass lesion hypoisointense with enlargement of sella suggestive of recurrent pituitary macroadenoma or abscess a romanian neurosurgery (2011) xviii 3: 326 – 330 329 b figure 3 mri brain showing no sellar suprasellar mass after second operation discussion the first case of pituitary abscess report was by heslop in 1848 (3). more than 200 cases of pituitary abscess have subsequently been reported in the literature. to our knowledge, there are only three published reports of intrasellar abscess as a complication of tss (4, 9, 10). our case is the fourth case reported in the literature. a sellar abscess is a potentially life threatening disease that is usually misdiagnosed because its presentation is similar to that of a pituitary adenoma. despite recent improvements in radiological evaluation, making a definite preoperative diagnosis of sellar abscess is difficult. mri is the best technique for the radiological evaluation. generally, sellar abscess can be divided into primary and secondary types (2). a primary abscess can spread haematogeneously or by direct extension from meningitis, sphenoid sinusitis, cavernous sinus thrombophlebitis, osteomyelitis or a contaminated csf fistula (8, 12). and one-third of sellar abscesses are secondary, arising within pre-existing lesions, such as adenomas, craniopharngiomas and rathke’s cleft cysts (5, 6). a b figure 4 photomicrograph of the surgical specimen (a) pituitary adenoma (b)necrotic foci and abscess formation with neutrophil infiltration (h&e staining; original magnification x20) 330 shrestha rajendra et al intrasellar abscess after transsphenoidal pituitary surgery in our knowledge, factors leading to abscess development in our case include impaired circulation, areas of necrosis, local immunological impairment or using adipose or muscle tissue during tss. surgery can be performed via the transsphenoidal or transcranial approach. the tss approach is considered to be a better choice to prevent contaminating the csf and causing meningitis or meningoencephalitis (1, 7). in our case, we preferred craniotomy as we suspected remnants of tumor too. our patients treated with tss approach showed favourable outcomes without recurrence. conclusion sellar abscess is extremely rare complication after tss with a high mortality rate. an early diagnosis to prompt surgery and initiation of long term use antibiotics is the single best method for treating a sellar abscess. correspondence to: prof. chao you, department of neurosurgery, west china hospital, sichuan university, 37 guo xue xiang, wuhou district, chengdu 610041, china e-mail: youchaowch@gmail.com references 1. domingue jn, wilson cb. pituitary abscesses. report of seven cases and review of the literature. j neurosurg 1977; 46:601–8. 2. grosskopf d, chamouard jm, bosquet f, et al. pituitary abscess: study of a case and review of the literature. neurochirurgie 1987; 33:228–31. 3. heslop tp. a case of hypertrophy with abscess of the pituitary body. dublin quart j m 1848; 6: 466. 4. henegar mm, koby mb, silbergeld dl, rich km, moran cj. intrasellar abscess following transsphenoidal surgery. surg neurol 1996; 45:183-8. 5. jadhav rn, dahiwadkar hv, palande da. abscess formation in invasive pituitary adenoma: case report. neurosurgery 1998; 43: 616–8. 6. metellus p, levrier o, grisoli f. abscess like formation concomitant with pituitary adenoma in cushing’s disease: case report and pathological considerations. br j neurosurg 2002; 16: 373–5. 7. nelson pb, haverkos h, martinez aj, et al. abscess formation within pituitary tumors. neurosurgery 1983; 12: 331–3. 8. post kd, mccormick pc, bello ja. differential diagnosis of pituitary tumors. endocrinol metab clin north am 1987; 16: 609–45. 9. romanowski b, tyrrell dlj, weir bka, goidsand g.meningitis complicating transsphenoidal hypophysectomy. cma journal 1981;124:1172-5. 10. robinson b. intrasellar abscess after transsphenoidal pituitary adenectomy. neurosurgery 1983; 12:684-6. 11. takahashi t, shibata s, ito k, et al. neuroimaging appearance ofpituitary abscess complicated with close inflammatory lesions: case report. neurol med chir (tokyo) 1998; 38:51–4 12. vates ge, berger ms, wilson cb. diagnosis and management of pituitary abscess: a review of twentyfour cases. j neurosurg 1995; 95: 233–41. doi: 10.33962/roneuro-2022-029 lumbar disc herniation presenting with contralateral neuropathy. case report d. balasa, c. popescu romanian neurosurgery (2022) xxxvi (2): pp. 161-163 doi: 10.33962/roneuro-2022-029 www.journals.lapub.co.uk/index.php/roneurosurgery lumbar disc herniation presenting with contralateral neuropathy. case report d. balasa1, c. popescu2 1 department of neurosurgery, clinical county hospital constanta, romania 2 department of orthopaedics, clinical county hospital constanta, romania abstract we admitted a unique case of right lumbar disc herniation at l4l5 who presented with contralateral symptoms and was successfully treated with a right large l4/l5 fenestration and microdiscectomy. when the operation is considered, intervention only from the herniation side is sufficient. in the case presented, it is probable that kernohan notch‑like phenomenon, venous engorgement and congestion at the contralateral side of the herniated lumbar disc and the contralateral migrated epidural fat are responsible for the emergence of contralateral symptoms. introduction lumbar disc herniation usually presents with varying degrees of pain, numbness and weakness in the distribution of the affected nerve root. case presentation a 46 year-old gentleman who performed intense physical work presented a 6 months old history of low back pain radiating down to his left buttock , posterior thigh, lateral and posterior leg (l5 and s1 dermatomas). examination revealed intense algoparesthesias on the left l5 and s1 dermatomas (vas 8/10), are refractory to conservative management and acupuncture, rotulian and achilian reflexes were absent bilaterally. straight leg raise was positive at 30 degrees on the left side and 40 degrees on the right side. anamnesis revealed l4-l5 disc hernia operated on the right side in 2020 with very good postoperative evolution. mri of his lumbar spine showed a central and right-sided paracentral disc herniation at l4/l5 causing cauda equina compression ( blue arrow) rupture of fibrous ring and posterior longitudinal ligament in the midline (red arrow) figures 1,2) . keywords herniated disc, intervertebral disc displacement, contralateral symptoms corresponding author: d. balasa department of neurosurgery, clinical county hospital constanta, romania balasadaniel100@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 162 d. balasa, c. popescu figure 1. sagittal cut of lumbar spine (t2) l4-l5 disc hernia, ruptured, huge, compressive on the cauda equina figure 1. axial cut at l4/l5 disc level, the right side (t2). central and right-sided paracentral disc herniation at l4/l5 causing cauda equina compression (blue arrow), rupture of fibrous ring and posterior longitudinal ligament in the midline (red arrow), operated (2020) l4-l5 fenestration (yellow arrow). the patient was emergently operated on (enlargment of fenestation l4-l5 on the right side, microsurgical discectomy). postoperative results were very good with dissapearance of the pain and paresthesis. postoperative follow-up period: 6 months. discussion there is no consensus about surgical approac; side or sides and the pathophysiology. some authors like choudhury et al1, kornberg2 , mirovsky and halperin3 performed bilateral explorations not to miss a lesion. however, sucu and gelal4, akdeniz et al5, and karabekir et al6 performed the operative approach only on the lumbar disc herniated side and reported that exploration of the ldh side was enough for the recovery of the contralateral symptoms. radiculopathy from lumbar disc herniation can be a result of mechanical compression7 , ischaemia7 or inflammatory irritation8 of the nerve root. the mechanism for lumbar disc herniation presenting with contralateral leg symptoms is poorly understood. kornberg et al2 proposed that inconsistent dural attachments to the posterior longitudinal ligaments holds the lumbar nerve roots at certain levels resulting in a more symptomatic traction of the contralateral nerve root a radicular pain contralateral to the herniated side is an unusual finding rarely reported in the literature(safdarian9). safdarian hypothesized that the reason for patients’ symptoms contralateral to the apparent compression on imaging studies involves a kernohan notch-like phenomenon. sucu and gelal4 presented five patients with lumbar disk herniations and contralateral. the authors observed that the shape of disk herniations in imaging studies was quite similar in these patients. almost all of them had a broad posterior central-paracentral herniated disk with the apex deviated away from the side of the symptoms. kalemci et al10 reported a case of painless contralateral neurological deficit due to venous engorgement and congestion at the contralateral side of the herniated lumbar disc . karabekir et al6. concluded that a hypertrophied ligamentum flavum was the likely etiology of contralateral sciatica comparing five patients with only contralateral symptoms, with 200 disc herniated patients with ipsilateral symptoms according to jun-song yang11 the migrated epidural fat plays a significant role in the pain mechanism of ldh with contralateral radiculopathy. only via a surgical approach ipsilateral to the herniated side, could clinical improvement be obtained postoperatively. 163 lumbar disc herniation presenting with contralateral neuropathy conclusions patients with lumbar disc herniation may present with radicular symptoms involving the contralateral leg. in the case presented, the mechanism of contralateral symptoms was kernohan notch-like phenomenon, venous engorgement and congestion at the contralateral side of the herniated lumbar disc and the contralateral migrated epidural fat. the operative approach (enlarged fenestration, operative approach of the contralateral disc hernia ) was mandatory for a very good postoperative evolution. references 1. choudhury ar, taylor jc, worthington bs, whitaker r. lumbar radiculopathy contralateral to upper lumbar disc herniation: report of 3 cases. br j surg. 1978;65:842-4. 2. kornberg m. sciatica contralateral to lumbar disk herniation. orthopedics 1994;17:362-4. [pubmed] 3. mirovsky y, halperin n. eccentric compression of the spinal canal causing dominantly contralateral-side symptoms. j spinal disord. 2000;13(2):174-7 4. sucu hk, gelal f. lumbar disk herniation with contralateral symptoms. eur spine j 2006;15:570-4. [crossref] [pubmed 5. akdeniz t, kaner t, tutkan i,ozer af. unilateral surgical approach for lumbar disc herniation with contraletaral symptoms. j neurosurg spine. 2012;17:124-7 6. .karabekir h. s. , izhan a y ,atar e k ,yaycioglu s, gocmenmas n, yazici c. effect of ligamenta flava hypertrophy on lumbar disc herniation with contralateral symptoms and signs: a clinical and morphometric study 7. garfin sr, rydevik b, lind b, et al. spinal nerve root compression. spine (phila pa 1976) 1995;20:1810-20. [crossref] [pubmed] 8. takahashi h, wada a, iida y, et al. antimicrobial prophylaxis for spinal surgery. j orthop sci 2009;14:40-4. [crossref] [pubmed] 9. safdarian m, farzaneh f, rahimi-movaghar v. contralateral radiculopathy: a kernohan–woltman notch-like phenomenon. asian j neurosurg 2018;13:1657. 10. kalemci o, kizmazoglu c, ozer e, arda mn. lumbar disc herniation associated with contralateral neurological deficit: can venous congestion be the cause? asian spine j 2013;7:60-2. [pubmed] 11. jun-song yang, md, dong-jie zhang, ms, and ding-jun hao. lumbar disc herniation with contralateral radiculopathy: do we neglect the epidural fat? 6apetreicosmin_intracranialpressure 188 apetrei et al intracranial pressure monitoring in severe traumatic brain injury intracranial pressure monitoring in severe traumatic brain injury al. cosmin apetrei1,2, a.şt. iencean2, a iordache1,2, b iliescu1,2, ion poeata1,2 1phd student “grigore t. popa” university of medicine and pharmacy iasi 2department of neurosurgery, emergency hospital “prof. dr. n. oblu iasi” abstract intracranial pressure monitoring seems to be an indispensable stage in management of severe traumatic brain injured patient. since 2009, this technique completes our trauma protocol. the study has been carried out from 2011 to 2013 in prof. dr. n. oblu hospital in iasi. there have been included in the study patients with severe craniocerebral trauma, who had traumatic brain lesions ct detected and glasgow score between 3 and 8. the age ranged from 16 to 60, an average of 35.5 years old. 50% of the studied cases had a favorable outcome. diagrams associated to this category of patients showed increases in intracranial pressure above normal values but without repeated values above 50 mm hg. most of those patients had a good evolution under medical treatment. monitoring intracranial pressure is an extremely useful stage in treating intracranial high pressure in traumatology and it should be included in the equipment of any intensive therapy section caring traumatic patients. key words: brain edema, intracranial pressure, severe traumatic brain injury. introduction despite modern medicine advances in brain traumatology, a problem with important socio-economic and family consequences still remains. it is the main death cause with people under 45 in the united states and europe. [1] in the united states about 1,7 million cases of craniocerebral injuries are reported every year [2] among which almost 25% are patients needing hospitalization. the estimated costs required for caring them amounts to 60 billions dollars a year in the united states. [3] monitoring intracranial pressure with patients suffering from severe traumatic brain injury is recommended by brain trauma foundation guides. since the 60s intracranial high pressure has been intensely studied as a predictive factor in the evolution of those with severe craniocerabral injury. at the same time knowing intracranial pressure helps precocious detection of intracranial high pressure as well as finding appropriate treatment for it. romanian neurosurgery (2014) xxi 2: 188 194 189 monitoring intracranial pressure is recommended with all patients suffering from serious brain injury and having glasgow score between 3 and 8 and ct pathological investigation (hematoma, edema, contusion, compression of basal cisterns). patients with severe brain injury and normal ct, if two or more than the following situations are recorded at admission: more than 40 years old, unilateral or bilateral motor deficiency, systolic blood pressure under 90mm, are also recommended monitoring. analysis of studies carried out since the 70s have revealed that patients having benefitted from monitoring their intracranial pressure recorded 12% lower mortality. [4] intracranial pressure can be measures through invasive or noninvasive methods. measuring systems with intracranial pressing transducer are: intraventricular, intraparenchimatous, subdural, epidural.[5] all these devices have been used in our study. material and methods a group of 16 patients with severe brain injury (cgs 3-8) have been studied. their intracranial pressure has been permanently been monitored through invasive method. the study has been carried out from 2011 to 2013 in prof. dr. n. oblu hospital in iasi. there have been included in the study patients with severe craniocerebral trauma, who had traumatic brain lesions ct detected and glasgow score between 3 and 8. the age ranged from 16 to 60, an average of 35.5 years old. intracranial pressure captor was set between 0 and 48 hours since presentation according to ct examination and clinic condition. intraventricular, intraperenchimatos or subdural captors were used, as the case required. in some cases all models compatible with camino mpm l sdc system produced by integra had to be used (figure l). patients suffering from other serious life threatening lesions, needing emergency treatment in other clinics, with severe coagulation troubles, dying people were not included in the program. data have been collected and worked out with the help of mpm l rs 232 interface software program. figure 1 intracranial pressure monitor and intraventricular bolt 190 apetrei et al intracranial pressure monitoring in severe traumatic brain injury results between 2011 and 2013 16 patients with serous traumatic brain injury were invasively monitored. all were ct examined when hospitalized and after setting the implant none developed neither hemorrhagic complications nor malpositionnment. the present study is not meant to present individual cases from the viewpoint of the treatment methods effectiveness but it establishes correlations between certain types of increasement of intracranial pressure and the patient’s evolution. 8 out of 16 monitored patients died despite upmost therapy, four of them benefitted from decompressive craniectomy. the cases were divided into 2 lots according to the evolution and namely those who deceased and those who were discharged. in the first lot it was recorded that the age average was higher (37.5) than in the second (33.5), the age limits being 16 to 60. we could note that the only complication occurred was pneumonia in 3 cases, 18.75%, and that with patients with long hospitalization. the graphic representation given by the monitor soft produced by integra allowed us to identify two pressure variation patterns: diagrams containing repeated spikes of above 50mm hg (the utmost value the soft can represent) (figure 2), were associated to the patient’s unfavorable evolution in all monitored cases. the second pattern where even pathologic pressure were not accompanied by sudden high increases were associated to patients having favorable evolution. (figure 3) figure 2 values more than 50mmhg associated with poor prognosis figure 3 rare spikes, normal values, good prognosis romanian neurosurgery (2014) xxi 2: 188 194 191 discussions monitoring intracranial pressure with patients having serious traumatic brain injury is not a new method of managing treatment and it is continually progressing due to technological advances. alexander monro and his student george kellie proposed the concept of intracranial pressure in the 18th century. the doctrine bearing their names (monro-kellie) states the cranial compartment is not an extendable container, so the volume is constant. the content made of brain tissue, blood, cefalorahidian liquid has a volume balance so that any increase in a component’s volume must be compensated by another component’s volume decrease. 1891 – quinke published the first studies on lumbar puncture. he added a dropper at the end of the needle which measures pressure. [6]. 1965 – lundberg revolutionized monitoring intracranial pressure using manometers for continuous registering by ventriculostomy. at present there are several guides for cranio-cerebral traumatology. in the case of severe traumatic brain injuries the most popular guide is that of brain trauma poundation, “guidelines for the management of severe traumatic brain injury 3rd edition”, accepted by the hospital where this research has been done. as compared to the second edition, the recommendation levels were modified and namely, from standard, guideline and option to level i, level ii and level ii. these levels derive from evidence classes i, ii, iii. according to this guide, intracranial pressure should be monitored with all patients suffering from severe traumatic brain injury (cgs 3-8 after resuscitation), having abnormal ct examination. abnormal craniocerebral ct means hematoma, contusions, swelling, herniations and basal tank compression. intracranial pressure monitoring is indicate with patients suffering from severe brain trauma with normal ct examination if at presentation at hospital they have two or several of the following: more than 40 years old, uni or bilateral motor deficiency, systolic blood pressure lower than 90mm hg. we had noticed that 50% of the studied cases had a favorable outcome. diagrams associated to this category of patients showed increases in intracranial pressure above normal values but without repeated values above 50 mm hg. most of those patients had a good evolution under medical treatment. decompressive cranietomy was required in only 2 out of 8 cases. the diagram pattern of those evolving to multiple spikes above 50mm hg values of intracranial pressure which persisted after aggressive antidedematous treatment. four out of the eight deceased had undergone decompressive cranietomy. two of them were subject to important postoperative intracranial pressure with multiple values above 50 mm hg refractory to any available therapeutic attitude. this study demonstrates that a certain type of raised intracranial pressure represents a factor for the patient’s prognosis. repeated increases of values above 50 mm hg 192 apetrei et al intracranial pressure monitoring in severe traumatic brain injury irresponsive to aggressive treatment for intracranial high pressure correlates to poor outcome 100% of the cases. taking into account this aspect a question arises: should aggressive treatment continue with patients whose diagram suggests an unfavorable prognosis or a supportive therapy is more adequate? the patients being comatose, therapeutic decision shall be taken in agreement with the family, according to the legislation in force, a first degree relative. illustrative case a 25 year old patient comes to hospital in pre comatose condition, cgs 9, after having been aggressed and suffered a brain trauma subsequent to fall. 30 hours after admission his condition worsens to cgs 7, therefore the ct examination is repeated and an intracranial pressure captor is set. figure 4 ct examination of presented case: (left) at admission and (right) 30 hours later after neurological deterioration figure 5 diagram of intracranian pressure showing significant pressure decrease o after manitol and continuous sedation romanian neurosurgery (2014) xxi 2: 188 194 193 measures are taken in order to treat the diffuse brain edema with manitol and sedation with propofol – good evolution (figure 5) 12 hours later he becomes reactive to drug treatment and an unilateral left decompressive cranietomy is carried out. (figure 6) figure 6 intraoperative aspect of left decompressive craniectomy at presented patient figure 7 doppler echography for evaluating the vasospasm, pressure curve with normal values and ct examination conforming hydrocephalus conclusions it is well-known that monitoring intracranial pressure is indispensable in modern neurotraumatology. diagram patterns seem to have predictive value but further studies are needed on a larger lot of patients. nowadays, there are not studies which compare groups of patients treated by means of continuous monitoring intracranial 194 apetrei et al intracranial pressure monitoring in severe traumatic brain injury pressure, to groups of patients who didn’t benefit from it. this study completed on a small group of patients confirm the present data. decompressive craniectomy decreases intracranial pressure. monitoring intracranial pressure is an extremely useful stage in treating intracranial high pressure in traumatology and it should be included in the equipment of any intensive therapy section caring traumatic patients. references 1. hyder aa, wunderlich ca, puvanachandra p, gururaj g, kobusingye oc: the impact of traumatic brain injuries: a global perspective. neurorehabilitation 22:341-353, 2007) 2. jns iunie 2013 pag 1306 3. finkelstein ea, corso ps, miller tr, the incidence and economic burden of injuries in the united states, new york: oxford university press, 2006) 4. stein et all. relationship of aggressive monitoring and treatment to improved outcomes in severe traumatic brain injury. clinical article. j. neurosurg 112: 1105-1112, 2010. 5. iencean st. m. hipertensiunea intracranaiana. institutul european 2006 6. quincke h. ueber hydrocephalus. congresses für innere medizin, zehnter congress. 1891;10:321–331. 7. c. werner* and k. engelhard, pathophysiology of traumatic brain injury british journal of anaesthesia 99 (1): 4–9 (2007) doi:10.1093/bja/aem131 8.lobato rd, cordobes f, rivas jj, et al. outcome from severe head injury related to the type of intracranial lesion. a computerized tomography study. j neurosurg. 1983;59:762. 9. spencer wh. on the changes produced in the circulation and respiration by increase of the intracranial pressure or tension. proceedings of the royal society of london. proceedings of the royal society of london. 1890;48:273-275. 10. (winn, h. richard (2011-06-10). youmans neurological surgery e-book (kindle location 284640). elsevier health. kindle edition.) 11. cerebral vasospasm in traumatic brain injury daniel r. kramer, jesse l. winer, b. a. matthew pease, arun p. amar, and william j. mack department of neurosurgery, university of southern california, 1200 north state street, suite 3300, los angeles, ca 90033, usa received 29 october 2012; accepted 4 june 2013 12. czosnyka m, hutchinson pj, balestreri m, hiler m, smielewski p, pickard jd. monitoring and interpretation of intracranial pressure after head injury. acta neurochir suppl. 2006;96:114-8. 13. crippen d. head trauma. medscape reference. available at http://emedicine.medscape.com/article/433855overview. 14. friedman di, jacobson dm. diagnostic criteria for idiopathic intracranial hypertension. neurology. nov 26 2002;59(10):1492-5 15. spencer wh. on the changes produced in the circulation and respiration by increase of the intracranial pressure or tension. proceedings of the royal society of london. proceedings of the royal society of london. 1890;48:273-275 microsoft word 3piperianthebrainmonitoring.doc 12 romanian neurosurgery (2010) xvii 1: 12 33 the brain monitoring with information technology (brainit) collaborative network: past, present and future direction ian piper1, iain chambers2, giuseppe citerio3, per enblad4, barbara gregson2, tim howells4, karl kiening5, julia mattern5, pelle nilsson4, arminas ragauskas6, juan sahuquillo7, st.m. iencean8, r. donald9, r. sinnott10, a. stell10, on behalf of the brainit group 1clinical physics, southern general hospital, glasgow uk; 2regional medical physics department, newcastle general hospital, newcastle, uk; 3neurorianimazione, hospital san gerardo, monza, italy; 4neurosurgery, uppsala university hospital, uppsala, sweden; 5neurosurgery, ruprecht-karls-universitat hospital heidelberg, germany; 6kaunas university hospital, kaunas, lithuania; 7neurosurgery, vall d’hebron hospital, barcelona, spain 8neurosurgery, emergency hospital “prof dr n oblu ”iasi, romania; 9c3 global ltd, dingwall, scotland; 10national escience centre, university of glasgow, scotland on-behalf of the brain-it group (www.brainit.org). abstract the brainit group works collaboratively on developing standards for collection and analyses of data from brain injured patients and to facilitate a more efficient infrastructure for assessing new health care technology with the primary objective of improving patient care. european community funding supported meetings over a year to discuss and define a core dataset to be collected from patients with traumatic brain injury using it based methods. in this paper, we give an overview of the aims and future directions of the group as well as present the results of an ec funded study with the aim of testing the feasibility of collecting this core dataset across a number of european sites and discuss the future direction of this research network. over a three year period, data collection client and web-server based tools were developed and core data (grouped into 9 categories) were collected from 200 head-injured patients by local nursing staff in 22 european neuro-intensive care centres. data were uploaded through the brainit web site and random samples of received data were selected automatically by computer for validation by data validation (dv) staff against primary sources held in each local centre. validated data were compared with originally transmitted data and percentage error rates calculated by data category. feasibility was assessed in terms of the proportion of missing data, accuracy of data collected and limitations reported by users of the it methods. thirteen percent of data files required cleaning. thirty “one-off” demographic and clinical data elements had significant amounts of missing data (> 15%). validation staff conducted 19,461 comparisons between uploaded database data with local data sources and error rates were commonly less than or equal to 6%, the exception being the surgery data class where an unacceptably high error rate of 34% was found. nearly 10,000 therapies were successfully recorded with start-times but approximately a third had inaccurate or missing end times which limits the analysis of duration of therapy. over 40,000 events and procedures were recorded but events with long durations (such as transfers) were more likely to have “end-times” missed. the brainit core dataset is a rich dataset for hypothesis generation and post-hoc analyses provided studies avoid known limitations in the dataset. limitations in the ian piper et al brain monitoring (brainit) 13 current it based data collection tools have been identified and have been addressed. in order for multi-centre data collection projects to be viable the resource intensive validation procedures will require a more automated process and this may include direct electronic access to hospital based clinical data sources for both validation purposes and for minimising the duplication of data entry. this type of infrastructure may foster and facilitate the remote monitoring of patient management and protocol adherence in future trials of patient management and monitoring. keywords: clinical network, traumatic brain injury, grid, internet background severe traumatic brain injury is a leading cause of death and survivors have serious and long term morbidity [1]. there are significant social and economic effects including loss of employment and an increased burden of care to the victim their families and society as a whole. the aetiology of the disease is complex often implicating multiple organ systems causing a high variation in the presentation of injury and, as a result, a large number of patients are required when assessing new health care technology. recruiting patients from multiple centres will significantly reduce the time to assess new therapies and monitoring devices. however, despite the existence of guidelines for the management of severely head injured patients [2, 3] this group of patients is subject to considerable variability in care across centres [4-9]. to improve the monitoring and management standards in this population, the inter and intra-centre variability in the intensive care management, physiological monitoring and treatment of these patients needs to be assessed on a multi-national basis. to do so requires a standardised, it based, higher resolution methodology for acquiring multi-centre patient management and physiological monitoring information. one consequence of the variability in the clinical management across centres that take care of patients with tbi (traumatic brain injury) is the confounding influence that this may have in multi-centre trials of therapy. despite promising pre-clinical results of several potential neuroprotective drugs most have failed to show efficacy in the head-injured population. a number of reasons have been proposed for these failures which include: poor study design, insufficient dose of drug penetrating the blood brain barrier and inter-species differences in brain injury mechanisms. another factor, not as yet systematically examined, may be the occurrence of secondary insults which are missed through use of inappropriate monitoring methods. recent estimates put the proportion of adverse events missed by using only end-hour recording compared with minute by minute computer based monitored to be in the region of 30% [13]. even in large scale randomised trials an accurate sample size analysis cannot be made without a knowledge of the incidence of the true variability of relevant confounding factors. inaccurate sample size estimates 14 romanian neurosurgery (2010) xvii 1: 12 33 will lead to trials that are not correctly powered. improving the standards and resolution for multi-centre data collection will also effect assessment of new medical technology which is of relevance to the medical device industry. the majority of companies that develop or support devices used to monitor brain injured patients in intensive care are small to medium size enterprises (sme). unlike the pharmaceutical industry smes lack the resources to independently assess their devices in multi-centre clinical trials and this severely limits the ability to provide an evidence base demonstrating the clinical utility of their products. in order to address these issues it is essential to develop an open, collaborative network of centres interested in the realisation of higher resolution and standardised methods for the collection of neuro-intensive care monitoring and management data from patients with traumatic brain injury. such an infrastructure will provide a more efficient means for assessing new and developing health care technology which may be new pharmaceutical compounds, management approaches or monitoring devices. to address these issues, the brain monitoring with information technology (brainit) group was formed (www.brainit.org) . the group has 3 main aims: 1) to develop and disseminate standards for the collection, analysis and reporting of intensive care monitoring and management data collected from brain injured patients. 2) to develop and use a standardised database as a tool for hypothesis generation and the development, testing and validation of new data analysis methodologies. 3) to provide an efficient multi-centre infrastructure for generating evidence on the utility of new invasive and noninvasive intensive care monitoring and management methods. the brainit group have first defined a core dataset collected using pc based tools as part of a european community (ec) funded study (qlgt-2000-00454). a series of meetings spread over one year enabled key stake holders to meet and the group to define a minimum set of data that should be collected from all patients with traumatic brain injury (tbi). the outcome of the study was to define a core dataset which would be useful in most research projects conducted in this population of patients [10]. this paper reports on the results of a subsequent three year ec funded study (qlgc-2002-00160) that enabled the group to develop it methods to collect the core dataset and to assess the feasibility and accuracy for collection of this core-dataset from 22 neuro-intensive care centres across europe. feasibility was assessed in terms of amount of missing data, accuracy of data collected and limitations reported by users of the it data collection methods. to assess accuracy, data validation staff (usually research nurses) were hired on a regional basis (normally country by country) to check samples of the collected data against the local primary clinical record in order to quantify the accuracy of the it based ian piper et al brain monitoring (brainit) 15 data collection methods. this paper describes an analysis of the comparison of the data from 200 patients with that obtained independently by data validation staff . the error rates classed by data category are described and the known limitations of current it data collection methods are considered along with some proposed solutions . methods core dataset definition through european community (ec) funding (qlri-2000-00454), a series of meetings over a one year period brought together neurosurgeons, intensivists, scientists and representatives from the medical device and pharmaceutical industries to define and discuss a “coredataset definition” for data that should be collected from all patients with traumatic brain injury (tbi), irrespective of the underlying project aim. a core dataset was defined and published [10] that consisted of the following nine data categories: i) demographic and “one-off” clinical data (pre-neurosurgical hospital data, neurosurgical hospital admission data and the first and worst ct scan data). this data is collected only once per patient. ii) daily management data (eg: use of sedatives, analgesics, vasopressors, fluid input/output balance etc). this data is collected as an overview of the day to day intensive care management of the patient and is collected only once per day. iii) laboratory data (eg: blood gas, haematology, biochemistry data etc). this is “episodic” data which is data collected more than once but at unpredictable times. iv) event data (eg: nursing manoeuvres, physiotherapy, medical procedures (line insertion), calibrations etc also episodic data). v) surgical procedures. vi) monitoring data summary (eg: type and placement location of icp sensor, bp lines, etc). typically this data is only collected once per patient and is an overview of the monitoring configuration for a patient. vii) neuro event data (eg: glasgow coma score, pupil size and reactivity also episodic data). viii) targeted therapies a set of therapy categories have been defined with some associated therapy type detail. for every therapy given an intended target must also be given (eg: mannitol for raised icp). ix) vital monitoring data. this is bedside monitoring data which is collected at regular intervals with a minimum sampling rate of once per minute. network structure the brainit group network structure consists of a central coordinating and data centre (glasgow) with individual centres clustered into language based regions where each language region contains a sub-coordinating centre. each subcoordinating centre is responsible for coordinating the training and validation activities across centres within their region and to meet this requirement hire a “data validation” nurse responsible for providing training on the data collection tools and web-services to all centres within their own language region. the data validation nurses also provide a data 16 romanian neurosurgery (2010) xvii 1: 12 33 checking and validation service coordinated from glasgow. data collection tools clinical data is entered by local bedside nursing staff either on hand held pda’s or on in-house designed java based software running on a pc. in collaboration with kelvin connect ltd [11] the brainit core dataset definition was implemented in a flexible and easy to use hand-held pda based device. a training course was held for the data validation nursing staff in glasgow on the optimal use of the data collection instruments which also provides data entry in six european languages. an anonymisation routine removed patient identification elements from the collected data and labelled the patient data file with a unique brainit study code generated from the brainit web-site. a local database held in each centre linked the anonymised data to local centre patient id information which was needed during the data checking stage of the study. anonymised data was uploaded via the brainit website. a server side data converter tool converted data from centre specific format into a standardised brainit data format generating nine data category files which are imported into the brainit microsoft sql2005 database. data validation process figure 1 graphically represents the data validation process. centre staff enter data using client side tools such as the hand held pda. data is uploaded via the brainit web-services and a server-side converter formats data into the series of common data format files which are input into the brainit sql database. a validation request tool residing on the database server randomly samples 20% of the data uploaded for each data category and generates a validation request file for each local data validation nurse listing the timestamps and data items to be checked against local data sources. data validators move between their designated centres and enter into a data validation tool the requested data items from source documentation held in each local centre. the resulting validation data file is uploaded to the brainit data coordinating centre via the website and using data validation checking software tools, the validated data is checked against the data items originally sent from which percentage accuracy data was calculated. as part of this validation process, and in addition to the categorical and numeric clinical data being checked for accuracy, we also assessed the minute by minute monitoring data. random samples of monitoring data channels uploaded (eg: icp, sao2) were selected and validation staff asked to manually enter the hourly recorded values from the nurses chart (or local gold standard data source) for the first and last 24 hour periods of bedside monitoring for a given patient for a given channel. these “validation” values could then be compared with a range of summary measures (eg: mean, median) from the computer based monitoring data acquired from the patient. assessing feasibility to assess feasibility, we sought answers to specific questions including: a) what data cleaning was necessary prior to analysis? ian piper et al brain monitoring (brainit) 17 b) what proportion of missing data was found in each data category? c) how accurate is the data that was collected? d) what are the known limitations of the existing it methods for collection of the data? results data description over a two year period, core dataset data (grouped by nine categories) were collected from 200 head-injured patients by local nursing staff. one patient’s data was discarded from the cohort as there was less than 4 hours of monitoring data which fell outside our inclusion criteria leaving 199 patients in the feasibility study dataset. table 1 summarises the key demographic and clinical features of the study cohort. mean age was 36 years with the usual predominance of male patients in such series. using the tcdb classification on worst ct, 100 patients were coded with diffuse injury and 60 with mass lesions. using the extended glasgow outcome scale (gose) there were 33 deaths (20%) with 47% good and 53 % poor outcome respectively. table 2 summarises the quantity of data collected per patient classed by data category. there were 109 “one-off” demographic and clinical data items collected which included pre-neurosurgical (phsh) and neurosurgical hospital (nsh) data. the majority of the data were “episodic” in nature in that they were collected more than once per patient but at unpredictable times. these data types included “icu monitoring” categories describing, for example, the location and type of medical monitoring device placed (eg: right frontal icp bolt), neurological status (icu gcs scores/pupil size and reactivity) , therapies delivered, surgeries performed etc. the largest number of data items collected fell within the “other clinical events” category which included annotations of blood samples, lab results, and other nursing and medical procedures. in this category there was on average greater than 230 recordings per patient. the next most common category of data collected were those of annotations of target driven therapies. in this category there were on average greater than 60 targeted therapies delivered per patient. by far the largest category of data collected was the “periodic” minute by minute physiological monitoring data with over 2 million records in the patient cohort. table 3 lists the number of patients with specific types of monitoring. figure 2 is a histogram plot showing the quantity and spread of time-series data for the main monitored channels: icp, bp, cpp, cvp, sao2, core temperature, etco2 and ptio2. the number of data points sampled per channel ranges from 89,524 for ptio2 to 1.98 million samples for bpm. (bpm = 1,979,284, icpm = 1,748,423, cpp= 1,719,166 , cvpm= 541,524, sao2 = 1,656,614 , tc = 1,372,641, etco2 = 502,524, ptio2 = 89,524. 18 romanian neurosurgery (2010) xvii 1: 12 33 data cleaning on average three raw data files were uploaded per patient giving 600 patient data files uploaded to the central database using the brainit web-services. all data files were validated prior to inclusion into the study dataset and in a proportion of these errors were found with data values needing to be re-checked and corrected by local nursing staff. seven raw data patient files required resolving mismatches between physiological data patient identifiers and other clinical data files (1.2 % of files uploaded). ten raw data files required trimming of physiological data outside the range of clinical data (2% of files uploaded). nineteen patient files required correction of one or more admission, surgery or discharge time stamps (3% of files uploaded). missing data one-off measurements there was missing data across certain data fields. figure 3 is a graph listing those “one-off” demographic and clinical data fields with greater than 15% of missing data. common patterns in the types of fields yielding the highest missing data rates could be identified: a) one third of the fields with significant amounts of missing data were “one off” laboratory data values (eg: glucose, haematocrit, paco2) which should have been obtained from admission notes from either the pre-neurosurgical hospital (pnsh) or the receiving neurosurgical hospital (nsh). b) one third of the missing fields were explanatory variables associated with either the first or worst ct scan classification. these explanatory variables included “yes/no” categories as to whether or not specific pathologies were seen on ct such as sah, pneumoencaphalopathy, hydrocephalus etc. c) fifteen percent of the missing data fields were explanatory variables associated with the 6 month glasgow outcome scale data. these included fields such as “who was the main respondent” to the questionnaire and what was deemed to be the “main cause of disability” (head injury or systemic injury). episodic measurements these data types include therapies, laboratory values and nursing and medical procedures that were entered more than once at un-predictable times. for each episodic data measurement both a “starttime” and “end-time” should have been recorded for each measurement by local nursing staff. nearly 10,000 therapies were successfully recorded with starttimes but approximately a third had missing end times. table 4 is a breakdown of the therapies delivered classed by type listing the proportion with missing “end-times”. clearly the quantity of missing end-times in this part of the dataset severely limits analyses assessing duration of therapy. over 40,000 events and procedures were also recorded but events with long durations (such as transfers outside of the itu for theatre or ct scan) were more than twice as likely to have “end-times” missed. these shortcomings in the acquired episodic data have implications for the design of future data collection/validation tools as well as project training procedures. ian piper et al brain monitoring (brainit) 19 data accuracy in total, 19,461 comparisons were made between collected data elements and source documentation data by data validation research nurses. the number of comparisons made per data category were in proportion to the size of the data received for that category with the largest number checked in laboratory data (5,667) and the least in the surgery data (567) (figure 4). table 5 summarises error rates by data class. error rates were generally less than or equal to 6%, the exception being the surgery data class where an unacceptably high error rate of 34% was found. in the surgery data category, nursing staff had to choose surgical procedures from a fixed list of procedure types: i) icp placement, ii) evacuation of mass lesion, iii) elevation of depressed skull fracture, iv) removal of foreign body, v) anterior fossa repair for csf leak, vi) placement of extra ventricular drain, vii) active external decompression (with bone removal and duroplastia), viii) other. this classification system was used in an attempt to simplify and reduce the burden of data entry. however, through discussions with local nursing and data validation staff it was found that there was particular confusion over when to record icp sensor placement and the presence of skull fractures as the primary surgical procedure. typically, these procedures occur during the same operative procedure as for example during “evacuation of a mass lesion”. confusion over coding these two procedures between the original data entry nurse and the validation nurse accounted for the majority of errors in this data category. the detection rate of acute events was also examined (eg: nursing management, physiotherapy, blood samples etc). it was found that short duration events were rarely missed but longer duration events such as transfer to ct or theatre were more likely to be not recorded. through discussions with local nursing and data validation staff it is believed that the intense nursing activity just prior to and following a transfer is more likely to lead to omissions in recording these events on research systems. finally, we tested the accuracy of the minute by minute monitoring data that was collected. table 6 shows the monitoring data validation results for the 6 data types with the most recorded nursing chart values. data is expressed in terms of bias (+95% cl) between the nurses chart recorded values against the computer collected end hour averages. it can be seen from this data that the computer collected end hour data is an accurate reflection of the nurse’s chart recorded data. as an example, figure 5 shows a scatter plot of computer monitored minute by minute icp data averaged over 60 minutes (icpavg) plotted against nurses chart end hour values (icpvalid) collected by the data validation nurses. there is a good correlation between the two sets of data with a linear regression best fit r2 value of 0.9773. figure 6 is an altman and bland plot showing the average bias (-0.15 mmhg) and 95% confidence limits (0.12, -0.45) for the computer monitored end hour averaged 20 romanian neurosurgery (2010) xvii 1: 12 33 data vs the nurses chart end hourly recorded values collected by the validation nurses. it tool limitations the pda data entry tool and the website-upload tools did not incorporate sufficient validation mechanisms. many fields with the pda tool allowed export and upload of empty data fields. although most it technology nowadays can be configured to explicitly specify required fields and prevent upload of data with specific missing data, at the time this study was designed, such validation facilities were not available off the shelf. also, the pda tool was designed to allow acceptance of new items not part of the drop down selection menu, which could generate multiple terms for the same data element. this caused added burden on the cleaning process to consolidate multiple text terms for the same data element. the most challenging limitation found with the it technology used in this study was an inability to automatically track “continuous” (non-bolus) therapies which were started to ensure that a matching “end-time” was entered. this resulted in approximately 1/3rd of the therapies annotated to have missing end times. discussion this project has studied the feasibility for collection of the brainit core dataset using our first generation it based tools. feasibility has been assessed in terms of amount of missing data, data accuracy for data that was collected and also in terms of identifying limitations in the it technology used to collect the data. good laboratory practice dictates that as part of clinical trial design, acquired data must be checked for accuracy against the primary data sources. this is often implemented through either employing a contract research organisation or independent research nurse staff to perform this duty. in large multi-centre clinical trials, costs to hire research nurse data validation staff can become prohibitively expensive and feasible only if significant industry or research council funding support is provided. now with the adoption of the new medical device standard iso-14155, even small medical device studies are expected to provide some form of check on the accuracy of data collected even as part of a nonregulatory post-marketing study. to our knowledge, this study conducted by the brainit group is one of only a few multi-centre projects to attempt to prospectively assess the data capture error rate within an academic investigator led environment [12]. monitoring data validation we have shown that computer collected minute by minute vital signs data, summarised as end hour averages, correlated well with nursing chart end hour recordings. this allows for the end hour averaged computer records to be used in database analyses that aim to assess nurses chart recorded detection of events with computer based sampling. although, end-hour average data correlates well with the nurses hourly recorded value, this does not indicate that important features of the data are not being missed by employing only hourly recording. for example, zanier and ian piper et al brain monitoring (brainit) 21 colleagues [13] conducted a study showing that although computermonitored end-hour data is accurately reflected by the nurses’ chart value, more complex summary measures (such as the detection of an intracranial pressure (icp) of more than 20 mmhg) are less accurate. their finding that at least one-third of secondary insults for raised icp are not identified from the nursing chart is similar to that reported by corrie and colleagues [14], who also found a similar detection error rate for other signals such as blood pressure, particularly the events of shorter duration. importantly, zanier’s paper has further shown that when data are categorised in terms of percentage of time spent with raised icp, the patients exhibiting instability in icp were most prone to under estimation of icp insults. the data sampling rate may be pertinent here: zanier’s study sampled at 600 samples per minute, whereas other studies used 1 sample per minute [14] or as few as 4 samples per hour [15]. our results here confirm those of other investigations showing that the end hour averaged computer values can be used as estimates of nurse’s paper based end hour recordings and opens up the possibility for further studies assessing the clinical influence of missed short term adverse physiological events without requiring tedious recording of nursing chart values. however, the key question remains unanswered as to whether missed adverse events using higher resolution sampling significantly influences clinical outcome. work conducted by chambers and colleagues may be relevant in this regard [16]. they found that in studies of children with tbi, the choice of summary measure is also important. they used an index termed the “pressure time index (pti)”, which is a composite index taking into account both the duration of the adverse event and the degree of physiological impairment below a given threshold. they found, using roc analysis of the influence of cerebral perfusion pressure adverse events upon clinical outcome (calculated using an age related pti index in children), that models that included the pti measure of cpp burden significantly improved the fit to clinical outcome compared with models that did not include measures of physiological instability. these results are in contrast to those published by signorini et al who they found very little improvement in outcome prediction when “insults” are added to the usual clinical features in prognostic models of patient outcome [17]. the approach developed by chambers and colleagues needs to be repeated in the adult tbi population and is one of the planned analyses on the brainit dataset. validation costs these validation results calculated on a subset of patients provides an estimate of the data quality on a larger patient cohort of 350 patients collected using the same methodology but collected outside of the validation study. however, future data collection projects will generate datasets under differing data collection conditions and will require a separate validation stage if we wish to maintain our confidence in the level of data collection accuracy. the approach used by the brainit group to validate data (using 20% sampling of 22 romanian neurosurgery (2010) xvii 1: 12 33 uploaded data with some automation of generating data lists for validation) still requires significant research nurse time to track down and enter data for validation purposes. to maintain a full time data validation nurse across all participating countries costs in excess of 1 million euro’s per year. such large overheads for an academic network is prohibitively expensive and not sustainable and a more cost-effective solution for data validation must be found. one promising approach now being assessed by the brainit group is developing collaborative research with experts in grid based middleware technology. grid technology comes in a variety of forms and covers more than just access to networks of high end servers in order to solve computationally intensive problems. there is a considerable amount of expertise and open source middleware software solutions now available that provide secure access to distributed medical datasets so that the right people see the correct data in the appropriate context [23]. such an approach, provided local it policy staff are satisfied with the system security, will enable remote data validation systems to directly query hospital based primary data sources for the purpose of checking the quality of previously uploaded data. most research datasets contain large portions of data elements that are collected for routine patient management purposes and the difficulty of accessing hospital based data sources often means that research nurses are employed to re-enter data extracted from local hospital sources into research data entry systems. this results in a high proportion of double data entry which is an inefficient use of nursing resources. using grid technology to interface directly with local hospital data sources will reduce the burden of double data entry. clearly some data validation staff will still be required to support system queries but increased use of automatic data validation procedures and access to hospital based datasets should significantly reduce the cost burden to conduct multi-centre clinical trials. towards this end, the brainit group as part of an ec funded framework vii project are now assessing such an approach in a group of neuro-intensive care centres equipped with the latest grid technology. this project – the avert-it project [18] has installed grid services behind hospital firewalls in six brainit neuro-intensive care units. grid services will interface to local hospital systems, extract data which maps to the brainit core dataset and integrate data from both hospital sources and local avert-it data collection tools (for those elements not collected as part of routine management) into a local database. once every 20 minutes, data is stripped of patient identifiers, encrypted and “pushed” out of local hospital networks to an external secure server cluster hosted at the university of glasgow national escience centre [19]. local databases will be maintained which link local patient identifiers with an anonymous patient identifier. systems running at the brainit coordinating centre in glasgow allow remote monitoring of the data acquired from all six participating brainit centres. such a remote monitoring service in ian piper et al brain monitoring (brainit) 23 quasi real-time (updates every 20 minutes) will allow more efficient collection and validation of hospital based data collected for research purposes while the patient (and their notes) are still within the itu environment. this infrastructure will also support monitoring of patient management for adverse events (such as treatments given for arterial hypotension) and will enable testing and tracking adherence to study protocols. lessons learned a number of lessons have been learned during this feasibility study. first, our surgery classification definition is ambiguous. specifically our definition document did not make it clear how to decide which surgery is the “primary reason for surgery”. for example if a patient undergoes surgery for removal of a mass lesion and repair of depressed skull fracture, some approach must be used to provide a consistent classification response. we are proposing a modified surgery classification to include a “major surgery choice matrix” where individual surgery types are weighted and specific combinations that do occur can be resolved to a single surgical priority. secondly not all staff favoured use of a pda type data tool. by the end of the feasibility study, approximately half the centres collecting data preferred to use pc based systems rather than the hand-held pda’s. increasingly, nursing and medical staff have good it and data entry skills and as a result we have developed new pc based data collection tools. also, our data tools (although state of the art at the time), did not provide sufficient local validation features such as preventing export and upload of empty data fields. most it technology nowadays can be configured to explicitly specify required fields and prevent upload of missing or incorrect data. our current generation of data tools now almost entirely allow only specific choices to be made from drop-down “combo boxes” where the default choice is set to a text value of “not set”. this makes it explicitly clear that a given field has not been entered. our data schema will not allow mandatory fields to be left “not-set” before a patient is discharged from the system. for the entry of treatment information, every treatment must be assigned a specific target and again, the data schema will not accept treatments that have not been assigned a target. furthermore, our next generation data collection tools, as implemented in the avert-it project, allows annotation of any treatment or procedure with only two mouse clicks providing more rapid and efficient data entry for the bed side nurse. the web-client software now includes data validation routines which will prevent upload of missing data in any required fields. patients cannot be fully discharged from the system until all required data is entered. patients with missing data can be partially discharged from the system (when they are discharged from the itu) but they remain in a visible list “patients with missing data”. a single web page displays all missing fields in red and must be completed before the patient can be fully discharged. 24 romanian neurosurgery (2010) xvii 1: 12 33 current status and future direction the aims of the brainit group and their implementation is a staged process. we have successfully defined a core dataset standard, developed some standardised it tools to collect the core dataset and tested the feasibility for collection of the dataset from 22 centres across europe. limitations in our methods have been found and attempts have been made to address those issues prior to starting future studies. inevitably, with each new project, problems will arise and solutions will be found in a cyclical process. our second aim “to develop and use a standardised database as a tool for hypothesis generation and the development, testing and validation of new data analysis methodologies.” has been achieved and a number of publications are now arising from access to this shared resource [20]. we are currently using the 2nd database release with a third release planned, and what is encouraging is that the existence of the database resource was directly responsible for generating and testing the hypothesis about application of bayesian neural network methods for prediction of arterial hypotension adverse events which lead to a project now funded under the viith ec information and communications technology framework [18]. one of the papers arising from the work of the brainit group was a report on its own internal survey of patient management which indicated that international management guidelines are for the most part adhered with [9]. however, there is a risk with surveys that there may be differences in results between what users believe to be the management applied in their centre and studies which measure it directly. in this regard, a recent paper published by one of our collaborators on analyses of the brainit dataset was to assess, subsequent to the brainit survey, whether the use of hyperventilation therapy for the management of raised icp was indeed conducted according to international guidelines. interestingly they found that despite what was suggested by the earlier survey results, and in conflict with current management guidelines, there was significant over use of early prophylactic hyperventilation [22]. this result highlights the importance of directly monitoring the applied management, and if it can be achieved in near real-time, will enable future management trials to monitor protocol adherence and better select when patients data can be recruited to a study. the third and most challenging aim of the brainit group is to use its improved infrastructure to generate new evidence on the utility of monitoring and management methods for patients with tbi. the avert-it project, now underway, will put in place in six brainit centres, grid middleware systems enabling direct access to hospital data and remote monitoring of patient management. we believe that this type of remote monitoring facility is a prerequisite for the conduct of a future multi-centre management trial by the brainit group. discussions of a management trial design have been started at the recent brainit group meeting (vilnius, september 2009) and ian piper et al brain monitoring (brainit) 25 the current avert-it project will pilot the feasibility of the remote monitoring infrastructure required for the conduct of such a trial. conclusions in this study we have shown that it is feasible to collect the brainit dataset from multiple centres in an international setting with our it based methods and the accuracy of the data collected is greater than or equal to 94%, with the exception of the surgery data definition which is being revised. lessons learned about weaknesses with our data collection methods have been met with advances in client/server tools providing improved validation support. we anticipate that the second generation of brainit data collection tools (now being used as part of the current avert-it project) will improve missing data and validation accuracy rates. a future brainit management trial will rely on a grid based infrastructure capable of remotely monitoring patient management and protocol conformance now being piloted in six brainit centres. academic led multi-centre data collection projects must decrease validation costs and to do so will require more direct electronic access to hospital based clinical data sources for both data validation purposes and for reducing the research nurse time needed for double data entry of data currently not accessible from hospital based systems. references 1. olesen j, l. m. the burden of brain disease in europe. european journal of neurology, 2003, 10, 471477. 2. bullock r, chesnut rm, clifton c, et al. (1996) guidelines for the management of severe head injury. j neurotrauma 13:643-734. 3. maas ai, dearden m, teasdale gm, braakman r, cohadon f, iannotti f, karimi a, lapierre f, murray g, ohman j, persson l, servadei f, stocchetti n, unterberg a (1997) ebic-guidelines for management of severe head injury in adults. acta neurochir 139:286294. 4. ghajar j, hariri rj, narayan rk, iacono la, firlik k, patterson rh (1995) survey of critical care management of comatose, head-injured patients in the united states. crit care med 23:560-567. 5. jeevaratnam dr, menon dk (1996) survey of intensive care of severely head injured patients in the united kingdom. bmj 312:944-947. 6. matta b, menon d (1996) severe head injury in the united kingdom and ireland: a survey of practice and implications for management. crit care med 24:17431748. 7. murray gd, teasdale gm, braakman r, cohadon f, dearden m, iannotti f, karimi a, lapierre f, maas a, ohman j, persson l, servadei f, stocchetti n, trojanowski t, unterberg a (1999) the european brain injury consortium survey of head injuries. acta neurochir 141:223-236. 8. stochetti n, penny ki, dearden m, braakman r, cohadon f, iannotti f, lapierre f, karimi a, maas a, murray gd, ohman j, persson l, servadei f, teasdale gm, trojanowski t, unterberg a, on behalf of the european brain injury consortium (2001) intensive care management of head-injured patients in europe: a survey from the european brain injury consortium. intensive care med 27:400-406. 9. enblad p, nilsson p, chambers i, citerio g, fiddes h, howells t, kiening k, ragauskas a, sahuquillo j, yau yh, contant c and piper i. survey of traumatic brain injury management in european brain it centres year 2001, intensive care med (2004) 30:1058 –1065. 10. piper i, citerio c, chambers i, enblad p , nilsson p, chambers i, citerio g, fiddes h, howells t, kiening k, ragauskas a, sahuquillo j, yau yh, contant c. the brainit group: concept and core dataset definition. acta neurochir 145:615-629 2003. 11. http://www.kelvinconnect.com/ 12. citerio g, stocchetti n, cormio m, beretta l. neuro-link, a computer assisted database for head injury in intensive care. acta neurochir (wien)142(7):769-76. 2000 13. zanier e, ortolano f, ghisoni l, colombo a, losappio s, stochetti n. intracranial pressure monitoring in intensive care: clinical advantages of computerised monitoring over manual recording. crit. care med. 11:r7. 2007 26 romanian neurosurgery (2010) xvii 1: 12 33 14. corrie j, piper i, housely a, tocher j, anderson s, midgley s, slattery j, dearden n, miller j. microcomputer based data recording improves identification of secondary insults in head injured patients. british journal of intensive care, june 1993. 226-233. 15. venkatesh b, garrett p, fraenkel dj and purdie d. indices to quantify changes in intracranial and cerebral perfusion pressure by assessing agreement between hourly and semi-continuous recordings. intensive care med 2004; 30: 510-513. 16. chambers ir, jones pa, lo twm, forsyth rj, fulton b, andrews pjd, mendelow ad and minns ra. critical thresholds of intracranial pressure andcerebral perfusion pressure related to age in paediatric head injury. j. neurol. neurosurg. psychiatry 2006;77;234240. 17.[17] signorini df, andrews pjd, jones pa, wardlaw jm and miller jd. adding insult to injury: the prognostic value of early secondary insults for survival after traumatic brain injury. j. neurol. neurosurg. psychiatry 1999;66;26-31 18.[18] http://www.avert-it.org 19.[19] http://www.nesc.ac.uk 20.[20] http://www.brainit.org/bit2web/faces/papers.jsp 21.[21] http://www.brainit.org/bit2web/faces/meetings.jsp 22.[22] neuman j, chambers i, citerio g, enblad p, gregson b, howells t, mattern j, nilsson p, piper i, ragauskas a, sahuquillo j, yau h, kiening k on behalf of the brainit group. the use of hyperventilation therapy after brain injury in europe: an analysis of the brainit database. intensive care medicine 2008; s00134-008-1123-7. 23.[23] http://www.nesc.ac.uk/hub/projects/votes/ acknowledgements we wish to acknowledge the contribution of all data contributing members of the brainit group (www.brainit.org) who supported the eec project: qlgc-2002-01160. investigators and participating centres barcelona spain, prof j sahuquillo; cambridge uk., prof jd pickard; edinburgh uk, prof r mins, prof i whittle; glasgow uk, mr l dunn; gothenburg sweden, dr b rydenhag; heidelberg, germany, dr k kiening; iasi romania, dr st.m. iencean; kaunas lithuania, prof d pavalkis; leipzig germany, prof j meixensberger; leuven belgium, prof j goffin; mannheim germany, prof p vajkoczy; milano italy, prof n stocchetti; monza italy, dr g citerio; newcastle upon tyne uk, dr ir chambers; novara italy, prof f della corte; southampton uk, dr j hell; uppsala sweden, prof p enblad; torino italy, dr l mascia; vilnius lithuania, prof e jarzemaskas; zurich switzerland, prof r stocker corresponding author: ian piper brain-it group coordinator intensive care monitoring dept. clinical physics, 5th floor institute of neurological sciences southern general hospital 1345 govan road, glasgow, uk, g514tf tel:+44(0)141-201-2595 fax: +44(0)141-201-2592 email: ipiper@clinmed.gla.ac.uk ian piper et al brain monitoring (brainit) 27 table 1 demographic and clinical features of feasibility study data set (n = 199) sex tcdb (worst) male 162 diffuse1 9 female 37 diffuse2 51 age diffuse3 34 mean 36.1 diffuse4 12 range 4-83 mass 60 <14yo 7 missing 33 trauma type gose rta 84 1 (dead) 31 pedestrian 16 2 3 fall 55 3 35 assault 18 4 8 sport 6 5 30 work 5 6 17 missing 14 7 30 8 24 missing 21 table 2 summary of data collected data type no. of fields avg no. of rows per patient demographic (eg: pnsh/nsh) 109 1 icu_monitoring (eg: types of device/location…) 12 15.0 neurological status (eg: gcs/pupils) 10 42.3 other_clinical_events (eg: blood samples, suction…) 20 230.9 surgery 11 1.4 target_therapies 59 69.6 daily_observations (eg: daily summaries of management) 11 8.4 total 232 28 romanian neurosurgery (2010) xvii 1: 12 33 table 3 monitoring data distribution channel number of patients bp (blood pressure: mmhg;systolic, diastolic, mean) 199 icp (intracranial pressure: mmhg;mean) 195 cpp (cerebral perfusion pressure: mmhg;mean) 195 hrt (heart rate: bpm) 165 sao2 (arterial oxygen saturation: %;pulse oximetry) 164 tc (core temperature: degrees c) 149 cvp (central venous pressure: mmhg; mean) 105 etco2 (end tidal co2: mmhg) 79 nibp (blood pressure: mmhg;systolic, diastolic, mean) 50 tp (peripheral temperature: degrees c) 17 ptio2 (brain tissue oxygen partial pressure: mmhg) 11 sjo2 (jugular venous oxygen saturation: %) 10 co (cardiac output: ml/hour) 7 brtemp (brain temperature: degrees c) 3 prx (bp-icp reactivity:dimensionless) 1 ian piper et al brain monitoring (brainit) 29 table 4 therapy type vs missing “end times” therapy start entries end entries missing end entries sedation 1108 499 55% analgesia 1032 574 44% paralysis 741 460 38% volume expansion 1674 1308 12% inotropes 614 199 68% anti-hypertensives 63 22 65% anti-pyretics 788 505 36% hypothermia 22 10 55% steroids 51 6 88% cerebral vasoconstr. 0 0 -- osmotics (mannitol) 807 538 33% barbiturates 90 45 50% other 2576 2026 21% totals 9566 6192 35% table 5 percentage error rate by data type class with description of common error types. data class error rate (%) common fields with errors laboratory 2 pco2, fio2 value wrong demographic 4 monitoring time on arrival at neurosurgery, intubation present on arrival at neurosurgery wrong neuro observations 5 pupil size, gcsv (code 1 vs unknown code error) monitoring summary 5 icp type, icp location wrong daily management summary 5 infusion type (bolus vs infusion or both), drug number (1 or > 1) targeted therapy 6 non-standard target, no target specified surgeries 34 icp placement, skull #, mass lesion wrong 30 romanian neurosurgery (2010) xvii 1: 12 33 table 6 monitoring data validation results – bias (+95% cl) between nurses chart recorded values vs computer collected end hour averages data type value icp (mmhg) bp (mmhg) cpp (mmhg) sao2 (%) tc (c) bias -0.15 0.16 0.46 0.46 -0.29 +95% 0.32 1.57 1.81 1.23 0.09 -95% -0.62 -1.25 -0.88 -0.31 -0.67 n 749 558 457 499 223 figure 1 graphical representation of the data validation process. centre staff enter data using client side tools such as the hand held pda. data is uploaded via the brainit web-services and a server-side convertor converts data into the series of common data format files which are input into the brainit sql database. a validation request tool residing on the database server randomly samples 20% of the data uploaded for each data category and generates a validation request file listing the timestamps and data items to be checked by local data validators. data validators move between their designated centres and enter into a data validation tool the requested data items from source documentation held in each local centre. the resulting validation data file is uploaded to the brainit data coordinating centre via the website and using data validation checking software tools, the validated data is checked against the data items originally sent from which percentage accuracy data is calculated ian piper et al brain monitoring (brainit) 31 figure 2 is a histogram plot showing the quantity and spread of time-series data for the main monitored channels: icp, bp, cpp, cvp, sao2, core temperature, etco2 and ptio2. the number of data points sampled per channel ranges from 89,524 for ptio2 to 1.98 million samples for bpm. (bpm = 1,979,284, icpm = 1,748,423, cpp= 1,719,166 , cvpm= 541,524, sao2 = 1,656,614 , tc = 1,372,641, etco2 = 502,524, ptio2 = 89,524 32 romanian neurosurgery (2010) xvii 1: 12 33 0 1 0 2 0 3 0 4 0 5 0 6 0 7 0 8 0 ns h g os e_ m on th s po st in ju ry ns h t im e_ of _d is ch ar ge ns h p o2 ns h f irs t_ ct _ m ain le sio n_ vo lu m e pn sh s ao 2 ns h f irs t_ c t _ s a h ns h f irs t_ c t _ p n e ns h f irs t_ ct _ i ve ns h f irs t_ ct _ h yd ns h f irs t_ c t _i sc ns h d is ch ar ge d_ to ns h p co 2 ns h p h ns h w or st _c t_ is c ns h w or st _c t_ sa h ns h w or st _c t_ pn e ns h w or st _c t_ iv e ns h w or st _c t_ h y d ns h h ct ns h g lu c ns h w or st _c t_ m ai nl es io n_ vo lu m e ns h g os e_ m et ho d ns h g os e_ r e sp on de nt ns h g os e_ ou tc om e _ fa ct or ns h b ps ns h b pd ns h m on ito re d_ ic p pn sh b ps pn sh b pd ns h c au s e o f d ea th d a ta f i e ld t y p e % m is si n g figure 3 graph showing “one-off” demographic and clinical data fields with greater than 15% of missing data figure 4 pie chart showing the distribution of the 19,461 data validation comparisons which were made in proportion to the size of the data received with the largest number checked in laboratory data (5,667) and the least in the surgery data (567) ian piper et al brain monitoring (brainit) 33 figure 5 scatter plot of computer monitored minute by minute icp data from an example patient showing the data averaged over 60 minutes (icpavg) plotted against nurses chart end hour values (icpvalid). linear regression best fit r2 value = 0.9773 figure 6 altman and bland plot from an example patient showing the average bias (-0.15 mmhg) and 95% confidence limits (0.12, -0.45) for the computer monitored end hour averaged data vs the nurses chart end hourly recorded values collected by the validation nurses microsoft word 12alvishernando_latex_ff 106 alvis-miranda et al latex and silicon allergy related to cerebrospinal shunt hardware latex and silicon allergy related to cerebrospinal shunt hardware: a review hernando alvis-miranda1, gabriel alcala-cerra2, sandra milena castellar-leones1, hector farid escorcia3, luis rafael moscote-salazar1 1university of cartagena, 2resident of neurosurgery, 3hospital cari barranquilla abstract a less frequent complications of shunt systems ventriculoperitoneal used for the management of hydrocephalus is the allergy materials which usually are built, silicone and latex. patients undergoing multiple changes device may be at risk of developing high rejection to materials. differential diagnosis should be done with infections and obstructions, usual causes of dysfunction. we present a review updated literature focused neurosurgeon. key words: silicone allergy, shunt malfuncion, hydrocephalus introduction the biomaterials used in the central nervous system include silicone, lipids, natural polymers and synthetic polymers in various forms based on their applications (1). biocompatibility of implants in humans has been classified as “inert”, “tolerated”, and “bioactive” (2). today is well known that silicone and latex are not inert materials, so the body can react in different ways respect to them. the cerebrospinal fluid (csf) shunts typically consist of a proximal catheter, which runs from the cerebral ventricles’ subarachnoid spaces to a valve that connects to a distal catheter and regulates the drainage of csf (1). the distal catheter is a long thin silicone tube that is placed subcutaneously and terminates in a distal body cavity where the csf can be reabsorbed into the body (3-5). in shunttreated patients, catheter-induced complications account for up to 70% of all hardware failures (2), the remainder are due to conditions like allergy or hypersensitivity to latex, and more rarely to silicone, this has now become a worrying health concern, that not only affects patients with multiple surgical interventions, but health care workers too (6).the aim of this review is to remember the clinical relevance of csf shunt related hypersensitivity and allergy, and management repercussions in these circumstances. epidemiology silicon: the incidence of silicone ventricular shunt allergies is rare. evidence of silicone allergy may have been origin for certain complications in breast and joint implants is present since 1984, when gower et al. (7) using electron microscopy, postulated that a small subset of shunt malfunctions could be attributed to silicone allergy. in 1989, snow and kossovsky (8), studied the clinical and pathological findings in 29 patients who underwent surgical procedures to revise malfunctioning ventriculoperitoneal romanian neurosurgery (2013) xx 1: 106 115 107 shunts. a pathologist independently examined the shunt hardware removed, and was observed that three patients had evidence of some hypersensitivity reaction due to the shunt hardware (multiple eosinophils and giant cells in tissue enveloping shunt hardware). in 1992, goldblum, et al. (9) reported two patients who showed severe reactions to ventriculoperitoneal (vp) shunts, using elisa they demonstrated that patients had increased quantities of serum igg, indicating an immunemediated reaction. in 1994, jimenez et al. (10) reported three hydrocephalic patients who developed a clinically heterogeneous entity with an allergic rejection of their silicone ventriculoperitoneal shunts. clinically, the presentation was indicative of shunt infection, but in all three patients there was a sterile csf. patients had recurrent skin breakdowns over the shunt tract, subsequent infections and development of fungating granulomas. the treatment included the replacement in one patient the silicone shunt material to polyurethane plus inmunossupression and in the other patients, the original shunt system was removed without a replacement. in 1999 a single case of bowel perforation caused by silicone shunt allergy was reported (11). latex: when allergies to medical biomaterial do occur, the causative agent is often latex (12, 13). case reports of allergic reactions to latex proteins have been described with various products from 1927 (14, 15), but since 1979 (16), ige-mediated allergy to latex has drawn much attention. latex sensitization remains the second most common cause of anaphylaxis (16.9%), during anesthesia in the general population (17, 18). children with myelomeningocele or spina bifida (sb) and urogenital abnormalities have high incidence of ige-mediated allergic reactions, probably due to a high degree of exposure to latex products through repeated surgical procedures, catheterization, and implant of latex-containing material (19, 20). particularly, patients with sb have more severe and unexpected allergic reactions, linked with surgical procedures (21, 22). patients with sensitization have a 500 times greater risk of serious reactions related to latex intraoperatively than that of the general population (23). nieto et al (24), in their 100 patient series with spina bifida, found a 29% prevalence of sensitization to latex; among patients with a v-p shunt, sensitization to latex was present in 36%, but there was not a single case of sensitization among those patients without it. they tried to identify those factors that may have a causal or predisposing role in the process of sensitization, the analysis disclosed many significant variables, but closely linked. as age increases, so does the rate of sensitization, but also an increase in the number of surgical procedures and, in the number of all diagnostic and therapeutic procedures, as well as in the absolute levels of serum total ige. logistic regression analysis selected the variable “number of operations” as the one that most contributed to the process of sensitization. three other variables (serum total ige levels, presence of a v-p shunt, and personal antecedents of atopic disease in this order) were synergistic and included to build the most parsimonious model. v-p shunt devices are made of silicone and do not contain latex, but has been suggested its co-adjuvant role as a foreign body in the process of sensitization. 108 alvis-miranda et al latex and silicon allergy related to cerebrospinal shunt hardware kattan et al. (25) reported the results of fifty-nine patients, aged 1-20 years, with sb that were evaluated by a questionnaire on type of latex reactions; family and personal history of other allergic disorders, such as asthma, rhinitis, and urticaria; type and number of surgical procedures; and frequency of bladder catheterization and manipulation with latex materials. confirmation of latex sensitivity was measured by skin prick test (spt), cap test, and latex skin challenge. they found allergy to latex in 25% of the study group. there was a significant variation in allergic reaction by sex (males 42%, females 12%) (p<0.01), use of catheters (yes 38%, no 13%) (p<0.05), and urologic surgery (yes 60%, no 18%) (p<0.01). the number of surgical procedures, age of patient, and v-p shunt were not significantly related to allergic reactions, they have no explanation for the difference in their patients, other than the possibility of genetic differences and, perhaps, extra precautions taken by surgeons in minimizing the use of latex articles in such patients. tangsinmankong et al. (26) reported a case of a patient with congenital hydrocephalus and a v-p shunt, who developed csf eosinophilia associated with latex allergy and shunt malfunction. latex allergy latex is an emulsion product from hevea brasiliensis trees (27). today nearly all commercial natural rubber comes from latex of those trees, commercially grown in a number of tropical countries. another source of latex is the guayule bush (parthenium argentatum) (28). interestingly the latex from the guayule bush does not appear to contain proteins cross-reactive with the allergens of hevea latex (29). other closely related materials that have been reported to be potentially cross-reactive with hevea latex are guttapercha and gutta-balata from sapotaceae trees (30). natural latex is widely used in the medical field (e.g., gloves, catheters, tubing, syringes, tourniquets), but also in everyday life (pacifiers, balloons, children's toys, hats and slippers pools, mattresses, shoes, clothes, condoms). latex allergy is a type i allergy, i.e., ige mediated. patients are often associated with food allergy focusing on the fruit (31), especially banana (15). crossed latex and food allergy constitutes a phenomenon of particular concern because the list of food allergens probably involved is steadily increasing. the prevalence of latex allergy is well known in certain risk groups such as those patients with multiple surgical interventions and among health care professionals (31, 32). latex proteins are numerous, and allergy to latex is related to a complex mixture of proteins (33-35).the risk of anaphylaxis is suggested by history of atopic diseases, such as asthma, allergic rhinitis, food allergy, and urticaria, or previous allergic symptoms on exposure to latex-containing materials (25). a series of distinct proteins occurring at either high (heb b 6) or very low concentration (hev b 1–5, hev b 7–13) in the hevea brasiliensis latex, have been identified as the ige-binding allergens responsible for sensitization (36, 37). children at risk for developing latex allergy, are those with allergy to bananas, kiwifruits, avocado, stone fruits, papaya, carrot, raw potato, tomato, chestnuts or peanuts, and those with history of a latex gloveassociated contact dermatitis (38). silicon allergy silicone rubber is a polymer biomaterial of the first generation (39), silicone is a group of synthetic polymers called romanian neurosurgery (2013) xx 1: 106 115 109 organopolysiloxanes, with a molecular structure consisting of alternating silicon and oxygen atoms (40). silicones can be fluids, gels, or solids (elastomers), depending on the length of the polymeric chain and the degree of crosslinking (10). csf shunt devices are manufactured almost solely from medical grade silicone, owing to its chemical stability, minimal biological reactivity, low toxicity and noncarcinogenicity (41-43). currently, silicone is used to make the following shunt components: catheters, access chambers, valve mechanisms, suture clamps and external valve housings (1). silicones are used as encapsulants, adhesives, or coatings in medical devices. they are commonly used in cerebrospinal fluid shunts, intravenous tubing, drug delivery systems, cardiac valves, arthroplasty prostheses, and intraocular lens implants (10). allergy to shunting tube is rare (44), probably because of its high biocompatibility and low biological reactivity (45). silicone has been considered safe and chemically inert, but immune mechanisms related to silicone materials have been proposed for some cases of obstruction of v-p shunts, because of inflammatory cells detected in the tubing lumen (46, 47), and for the evidence derived from patients and from animal experimental data to suggest that silicone can act as an antigen of a hapten complexed to self-proteins (7-9, 48-53) and could elicit inflammatory reactions, confirming that silicone is not inert biologically. furthermore, has been demonstrated that silicone gel is a potent humoral or antibody adjuvant (54), and solid silicone implant can produce a similar type of hypersensitivity (55). implanted silicone prostheses and medical devices are associated with various local (mild fibrosis (56)) and systemic host inflammatory reactions, they have been associated with a form of autoimmune disease (51, 57). heggers et al. (53) investigated the possibility of a cellular immune response to implanted silicone in an animal model. they observed histologically that the cellular response to polydimethylsiloxane in sensitized guinea pigs is consistent with a cellular immune reaction. electron microscopy and x-ray energy spectroscopy have demonstrated intracellular silicon in the intracellular machinery (golgi apparatus, rough endoplasmic reticulum, and at both ends of cytoplasmic bridges) in macrophages and lymphocytes. suggesting that those cells are processing a silicon-containing complex as an antigen (53). according to this theory, macrophages recruited to a foreign body reaction could release oxidizing free radicals capable of attacking the silicone present to liberate the irritating silica, but, this cannot be the sole mechanism responsible since fluid or gel silicone do not contain silica fillings and have also been shown to be irritants (53). kossovsky et al. (48), also tested the hypothesis that silicones may evoke an immunologically mediated inflammatory reaction in a guinea pigs model, they found that animals stimulated with silicone-serum and those passively sensitized had four times greater palpable lesions at approximately 24 h compared to controls (saline solution)when challenged to different intradermal antigens (siliconehomologous serum, pure silicone, salinehomologous serum, and purified protein derivative), biopsies revealed a moderate to marked lymphocytic infiltrate. control sites and naive animals showed only edema at the challenge sites, also suggesting that 110 alvis-miranda et al latex and silicon allergy related to cerebrospinal shunt hardware silicone-protein complexes are potentially immunogenic. first cases of silicone allergy were encountered with the use of silicon stents (58, 59), the histological examination of the material embracing and occluding the tube, was founded abundance of eosinophils and giant cells, meaning an allergic reaction to the silicone material (44). unfortunately, the nature of the silicone antigen that elicits the immune response is not well known (9), another hypothesis to explain or justify the inflammatory reactions associated with silicone shunts is the electrostatic active internal surface of the silicone hardware, that gives the potential to increase the adherence of airborne particles to the shunt and facilitate a foreign tissue reaction by the body leading to a hypersensitivity condition (7, 60, 61). apparently, the most frequent silicone allergy seems to be a type iv or delayedtype hypersensitivity reaction (9). this reaction is mediated by t cells and starts 2 to 7 days after the exposure. interestingly, hashimoto et al. (62) reported the case of a patient with an abdominal csf pseudocyst that resulted from an allergic reaction to silicone. the patient underwent repair surgery of the meningomyelocele associated with the chiari ii malformation, and the vp shunt was instituted at 6 months of age. a formation of the abdominal csf pseudocyst and the consequent shunt malfunction were observed 40 days after the v-p shunt. an increase in the number of the peripheral eosinophils and serum immunoglobulin e (ige), and an infiltration of eosinophils in the specimen harvested from the pseudocyst wall suggested an allergic reaction as the cause of the pseudocyst. a sixth operation to revise the v-p shunt was performed using the shunt system made of “extracted silicone”, which was produced extracting the allergic substances. the serum ige was normalized after surgery and the abdominal csf pseudocyst has not recurred for 22 months. clinical presentation in the case of silicon shunt allergy: the allergic reactions typically occur through local reaction, silicone migration, or human autoimmune disease. the patient may present to the emergency room with symptoms of either indolent shunt infection due to irritability and low grade fever or shunt obstruction due to aggregation of the fenestrated catheter tip with eosinophils and giant cells (44). can be present csf eosinophilia (44, 63). in the case of latex shunt allergy: overall, children at high risk for serious reactions, are those with history of anaphylaxis to latex, history of allergy to latex or rubber (urticaria, dermatitis, eye swelling, bronchospasm), history of atopy, history of multiple (>5) surgical procedures: spina bifida, genitourinary anomalies (38). symptoms of latex allergy can range from mild urticarial to life-threatening events and death. exposure to latex can cause type i immunoglobulin (ig) e mediated hypersensitivity reactions or more commonly an allergic contact dermatitis (type iv) (38). clinical allergy to latex is indicated by repeated immediate reaction on latex exposure, including itching, hives, rhinoconjunctivitis, bronchospasm, angioedema, hypotension, and contact urticaria (64, 65). also can be present csf eosinophilia (66). diagnosis and management silicone: in cases of recurrent malfunctions in romanian neurosurgery (2013) xx 1: 106 115 111 which the origin remains unclear despite extensive routine investigations, it would be appropriate to consider diagnosis of silicone shunt allergy (44). diagnosis of silicone allergy requires first ruling out other forms of shunt complications, such as infection and obstruction (44). potential triggers other than silicone, such as intravenous or topical antibiotics like bacitracin, must also be examined (44). spt and immuno-cap are sensitive and reliable diagnostic tools in detection of sb patients who are at high risk of developing allergic reactions to latex and should be used routinely to exclude the use of latex products in sensitized patients (25). jimenez et al. (10) recommended a battery of resources for evaluating silicone allergy such as assays for erythrocyte sedimentations rate, complement and immunoglobulin levels, fluorescent nuclear antibodies, ribonucleic proteins, extractable nuclear antibodies, and rheumatoid factor, tissues biopsy and human leukocyte antigen typing. they also recommended performing elisas for antisilicone igg antibodies when available. furthermore is recommended the pathological examination of the failed hardware. the elisa for antisilicone igg antibodies was first described by goldblum, et al (9). they demonstrated that elisa is specific to symptomatically allergic patients and not just individuals exposed to silicone (44). because of the multifaceted nature of the reaction to silicone in the rare instance that it does occur, treatment must involve complete removal of the silicone hardware: shunt system can be removed without replacement if the patient can tolerate it (10). shunt removal can be accompanied by a third ventriculostomy (this could be difficult in patients with complicated anatomy due to multiple surgeries) (44) shunt-dependent patients can have the silicone-based hardware removed and replaced with non-silicone based hardware (e.g., polyurethane vp system, if this is selected, is recommended to consider long-term immunosuppression (10)). in the case reported by tangsinmankong et al. (26), they used a daily treatment with 2 mg/kg of methylprednisolone, and observed a reduction of the peripheral eosinophilia and slightly reduced csf eosinophil counts. pulse methylprednisolone, 15 mg/kg, was associated with complete reduction of csf eosinophils and prolonged vp shunt survival. latex: a sensitive, specific, and safe skin test for latex sensitivity appears superior to in vitro testing for latex allergy. age, number of surgical procedures, and the presence of positive allergen skin test responses are significantly correlated with latex sensitization. age alone is significantly correlated with clinical allergy to latex (65). testing for type i natural rubber latex allergy is through serum testing, such as rast (radioallergosorbent test), which identifies what types of ige proteins trigger allergic reactions. currently the only effective preventative strategy is latex avoidance (38). some recommendations in the operating room are: patient should be first on the list, latexfree theatre for at least 2 hours (ideally overnight) prior to case; all staff involved in patient care must be made aware of latex allergy status and warning signs should be posted outside the operating theatre; a 112 alvis-miranda et al latex and silicon allergy related to cerebrospinal shunt hardware latex-free trolley/box should be present with every case, which follows the patient from pre-assessment to postoperative care, and develop completely latex-free surgical areas (38). conclusions hydrocephalus shunt catheters cannot be termed “inert” or “biotolerated”. rather, they must be regarded as “bio-active” implants. the extensive reaction on silicated catheters can act as reference to estimate the biocompatibility of surface modifications (2). sb patients with a history of repeated urologic procedures and a history of urticaria, especially male patients with such history, are most likely to develop allergy to latex products. we conclude that pathological examination of shunt hardware is helpful in understanding noninfectious causes of shunt malfunction. we have identified a subgroup of patients who developed a hypersensitivity-like reaction around the shunt that in certain instances lead to shunt malfunction. correspondence: dr. luis rafael moscote-salazar university of cartagena, cartagena de indias, colombia e-mail: mineurocirujano@aol.com, mineurocirujano@gmail.com references 1.zhong y, bellamkonda rv. biomaterials for the central nervous system. journal of the royal society interface. 2008 september 6, 2008; 5 (26): 957-75. 2.eymann r, kim yj, bohle rm, antes s, schmitt m, menger md, et al. microstructural alterations of silicone catheters in an animal experiment: histopathology and sem findings. acta neurochirurgica supplement. 2012; 113: 87-90. pubmed pmid: 22116430. epub 2011/11/26. eng. 3.garton hj, piatt jh, jr. hydrocephalus. pediatric clinics of north america. 2004 apr; 51 (2): 305-25. pubmed pmid: 15062673. epub 2004/04/06. eng. 4.browd sr, ragel bt, gottfried on, kestle jr. failure of cerebrospinal fluid shunts: part i: obstruction and mechanical failure. pediatric neurology. 2006 feb; 34 (2): 83-92. pubmed pmid: 16458818. epub 2006/02/07. eng. 5.de aquino hb, carelli ef, borges neto ag, pereira cu. nonfunctional abdominal complications of the distal catheter on the treatment of hydrocephalus: an inflammatory hypothesis? experience with six cases. child's nervous system: chns: official journal of the international society for pediatric neurosurgery. 2006 oct; 22 (10): 1225-30. pubmed pmid: 16525849. epub 2006/03/10. eng. 6.bousquet j, flahault a, vandenplas o, ameille j, duron jj, pecquet c, et al. natural rubber latex allergy among health care workers: a systematic review of the evidence. the journal of allergy and clinical immunology. 2006 aug; 118 (2): 447-54. pubmed pmid: 16890771. epub 2006/08/08. eng. 7.gower dj, lewis jc, kelly dl, jr. sterile shunt malfunction. a scanning electron microscopic perspective. j neurosurg. 1984 dec; 61 (6): 1079-84. pubmed pmid: 6502236. epub 1984/12/01. eng. 8.snow rb, kossovsky n. hypersensitivity reaction associated with sterile ventriculoperitoneal shunt malfunction. surgical neurology. 1989 mar; 31 (3): 20914. pubmed pmid: 2922665. epub 1989/03/01. eng. 9.goldblum rm, pelley rp, o'donell aa, pyron d, heggers jp. antibodies to silicone elastomers and reactions to ventriculoperitoneal shunts. lancet. 1992 aug 29; 340 (8818): 510-3. pubmed pmid: 1354277. epub 1992/08/29. eng. 10.jimenez df, keating r, goodrich jt. silicone allergy in ventriculoperitoneal shunts. child's nervous system: chns: official journal of the international society for pediatric neurosurgery. 1994 jan; 10 (1): 59-63. pubmed pmid: 8194064. epub 1994/01/01. eng. 11.brownlee jd, brodkey js, schaefer ik. colonic perforation by ventriculoperitoneal shunt tubing: a case of suspected silicone allergy. surgical neurology. 1998 jan; 49 (1): 21-4. pubmed pmid: 9428890. epub 1998/01/16. eng. 12.kashima ml, tunkel de, cummings cw. latex allergy: an update for the otolaryngologist. archives of otolaryngology--head & neck surgery. 2001 apr; 127 (4): 442-6. pubmed pmid: 11296056. epub 2001/05/05. eng. 13.carver ed, braude bm, atkinson ar, gold m. anaphylaxis during insertion of a ventriculoperitoneal shunt. anesthesiology. 2000 aug; 93 (2): 578-9. pubmed pmid: 10910512. epub 2000/07/26. eng. 14.stern g. uberempfindlichkeit gegen kautschuk als ursache von urticaria und quinckeschem ödem. klin romanian neurosurgery (2013) xx 1: 106 115 113 wochenschr. 1927; 6: 1096-7. 15.lavaud f, prevost a, cossart c, guerin l, bernard j, kochman s. allergy to latex, avocado pear, and banana: evidence for a 30 kd antigen in immunoblotting. journal of allergy and clinical immunology. 1995 2//; 95 (2): 557-64. 16.nutter af. contact urticaria to rubber. the british journal of dermatology. 1979 nov; 101 (5): 597-8. pubmed pmid: 518831. epub 1979/11/01. eng. 17.mertes pm, laxenaire mc. allergy and anaphylaxis in anaesthesia. minerva anestesiologica. 2004 may; 70 (5): 285-91. pubmed pmid: 15181405. epub 2004/06/08. eng. 18.mertes pm, tajima k, regnier-kimmoun ma, lambert m, iohom g, gueant-rodriguez rm, et al. perioperative anaphylaxis. the medical clinics of north america. 2010 jul; 94 (4): 761-89, xi. pubmed pmid: 20609862. epub 2010/07/09. eng. 19.ellsworth pi, merguerian pa, klein rb, rozycki aa. evaluation and risk factors of latex allergy in spina bifida patients: is it preventable? j urol. 1993 aug; 150 (2 pt 2): 691-3. pubmed pmid: 8326624. epub 1993/08/01. eng. 20.konz kr, chia jk, kurup vp, resnick a, kelly kj, fink jn. comparison of latex hypersensitivity among patients with neurologic defects. the journal of allergy and clinical immunology. 1995 may; 95 (5 pt 1): 950-4. pubmed pmid: 7751515. epub 1995/05/01. eng. 21.kelly kj, pearson ml, kurup vp, havens pl, byrd rs, setlock ma, et al. a cluster of anaphylactic reactions in children with spina bifida during general anesthesia: epidemiologic features, risk factors, and latex hypersensitivity. the journal of allergy and clinical immunology. 1994 jul; 94 (1): 53-61. pubmed pmid: 8027499. epub 1994/07/01. eng. 22.schneck fx, bellinger mf. the "innocent" cough or sneeze: a harbinger of serious latex allergy in children during bladder stimulation and urodynamic testing. j urol. 1993 aug; 150 (2 pt 2): 687-90. pubmed pmid: 8326623. epub 1993/08/01. eng. 23.anaphylactic reactions during general anesthesia among pediatric patients--united states, january 1990january 1991. mmwr morbidity and mortality weekly report. 1991 jul 5; 40 (26): 437, 43. pubmed pmid: 2051973. epub 1991/07/05. eng. 24.nieto a, estornell f, mazón a, reig c, nieto a, garcía-ibarra f. allergy to latex in spina bifida: a multivariate study of associated factors in 100 consecutive patients. journal of allergy and clinical immunology. 1996 9//; 98 (3): 501-7. 25.kattan h, harfi h, tipirneni p. latex allergy in saudi children with spina bifida. allergy. 1999; 54 (1): 70-3. pubmed pmid: 5304452. 26.tangsinmankong n, nelson rp, jr., good ra. glucocorticosteroid treatment for cerebrospinal fluid eosinophilia in a patient with ventriculoperitonial shunt. annals of allergy, asthma & immunology: official publication of the american college of allergy, asthma, & immunology. 1999 oct; 83 (4): 341-2. pubmed pmid: 10541427. epub 1999/10/29. eng. 27.aichane a, mahmal a, bouayad z. allergie au latex chez le personnel de santé. revue française d'allergologie et d'immunologie clinique. 1998 //; 38 (7, supplement 1): s141-s4. 28.ownby dr. a history of latex allergy. journal of allergy and clinical immunology. 2002 8//; 110 (2, supplement): s27-s32. 29.siler dj, cornish k, hamilton rg. absence of cross-reactivity of ige antibodies from subjects allergic to hevea brasiliensis latex with a new source of natural rubber latex from guayule (parthenium argentatum). the journal of allergy and clinical immunology. 1996 nov; 98 (5 pt 1): 895-902. pubmed pmid: 8939152. epub 1996/11/01. eng. 30.boxer mb, grammer lc, orfan n. gutta-percha allergy in a health care worker with latex allergy. the journal of allergy and clinical immunology. 1994 may; 93 (5): 943-4. pubmed pmid: 8182237. epub 1994/05/01. eng. 31.mavale-manuel s, paty e, scheinmann p, de blic j. allergie au latex chez l’enfant. archives de pédiatrie. 2003 8//; 10 (8): 700-6. 32.turjanmaa k. natural rubber latex allergy: clinical manifestations (including contact dermatitis) and diagnosis. revue française d'allergologie et d'immunologie clinique. 1997 //; 37 (8): 1177-9. 33.morales c, basomba a, carreira j, sastre a. anaphylaxis produced by rubber glove contact. case reports and immunological identification of the antigens involved. clinical and experimental allergy: journal of the british society for allergy and clinical immunology. 1989 jul; 19 (4): 425-30. pubmed pmid: 2758356. epub 1989/07/01. eng. 34.levy da, charpin d, pecquet c, leynadier f, vervloet d. allergy to latex. allergy. 1992 dec; 47 (6): 579-87. pubmed pmid: 1285566. epub 1992/12/01. eng. 35.tomazic vj, withrow tj, fisher br, dillard sf. latex-associated allergies and anaphylactic reactions. clinical immunology and immunopathology. 1992 aug; 64 (2): 89-97. pubmed pmid: 1643748. epub 1992/08/01. eng. 36.yeang hy, hamilton rg, bernstein di, arif sa, chow ks, loke yh, et al. allergen concentration in natural rubber latex. clinical and experimental allergy: journal of the british society for allergy and clinical immunology. 2006 aug; 36 (8): 1078-86. pubmed pmid: 16911364. epub 2006/08/17. eng. 37.rougé p, culerrier r, campistron m, granier c, bienvenu f, bienvenu j, et al. allergenicity of hev b 13, 114 alvis-miranda et al latex and silicon allergy related to cerebrospinal shunt hardware a major esterase allergen in natural rubber latex (hevea brasiliensis) allergy, does not only depend on its carbohydrate moiety. molecular immunology. 2010 1//; 47 (4): 871-7. 38.ng k, fernandez e. associated medical conditions in children. anaesthesia & intensive care medicine. 2012 9//; 13 (9): 438-47. 39.navarro m, michiardi a, castaño o, planell ja. biomaterials in orthopaedics. journal of the royal society interface. 2008 october 6, 2008; 5 (27): 113758. 40.kunda ld, stidham kr, inserra mm, roland ps, franklin d, roberson jb, jr. silicone allergy: a new cause for cochlear implant extrusion and its management. otology & neurotology: official publication of the american otological society, american neurotology society [and] european academy of otology and neurotology. 2006 dec; 27 (8): 1078-82. pubmed pmid: 17130797. epub 2006/11/30. eng. 41.agnew wf, todd em, richmond h, chronister ws. biological evaluation of silicone rubber for surgical prosthesis. the journal of surgical research. 1962 nov; 2: 357-63. pubmed pmid: 14011239. epub 1962/11/01. eng. 42.del bigio mr, fedoroff s. short-term response of brain tissue to cerebrospinal fluid shunts in vivo and in vitro. journal of biomedical materials research. 1992 aug; 26 (8): 979-87. pubmed pmid: 1429759. epub 1992/08/01. eng. 43.kalousdian s, karlan ms, williams ma. silicone elastomer cerebrospinal fluid shunt systems. council on scientific affairs, american medical association. neurosurgery. 1998 apr; 42 (4): 887-92. pubmed pmid: 9574653. epub 1998/05/09. eng. 44.hussain ns, wang pp, james c, carson bs, avellino am. distal ventriculoperitoneal shunt failure caused by silicone allergy. journal of neurosurgery. 2005; 102 (3): 536-9. pubmed pmid: 15796391. 45.kirwan l. two cases of apparent silicone allergy. plastic and reconstructive surgery. 1995 jul; 96 (1): 2367. pubmed pmid: 7604119. epub 1995/07/01. eng. 46.peimer ca, medige j, eckert bs, wright jr, howard cs. reactive synovitis after silicone arthroplasty. the journal of hand surgery. 1986 sep; 11 (5): 624-38. pubmed pmid: 3531304. epub 1986/09/01. eng. 47.kircher t. silicone lymphadenopathy: a complication of silicone elastomer finger joint prostheses. human pathology. 1980 may; 11 (3): 240-4. pubmed pmid: 6995270. epub 1980/05/01. eng. 48.kossovsky n, heggers jp, robson mc. experimental demonstration of the immunogenicity of silicone-protein complexes. journal of biomedical materials research. 1987 sep; 21 (9): 1125-33. pubmed pmid: 3667638. epub 1987/09/01. eng. 49.bowman bh, schneider l, barnett dr, kurosky a, goldblum rm. novel urinary fragments from human basement membrane collagen. the journal of biological chemistry. 1980 oct 10; 255 (19): 9484-9. pubmed pmid: 7410437. epub 1980/10/10. eng. 50.varga j, schumacher hr, jimenez sa. systemic sclerosis after augmentation mammoplasty with silicone implants. annals of internal medicine. 1989 sep 1; 111 (5): 377-83. pubmed pmid: 2669593. epub 1989/09/01. eng. 51.baldwin cm, jr., kaplan en. silicone-induced human adjuvant disease? annals of plastic surgery. 1983 apr; 10 (4): 270-3. pubmed pmid: 6847084. epub 1983/04/01. eng. 52.irving im, castilla p, hall eg, rickham pp. tissue reaction to pure and impregnated silastic. journal of pediatric surgery. 1971 dec; 6 (6): 724-9. pubmed pmid: 5130591. epub 1971/12/01. eng. 53.heggers jp, kossovsky n, parsons rw, robson mc, pelley rp, raine tj. biocompatibility of silicone implants. annals of plastic surgery. 1983 jul; 11 (1): 3845. pubmed pmid: 6614755. epub 1983/07/01. eng. 54.naim jo, lanzafame rj, van oss cj. the effect of silicone-gel on the immune response. journal of biomaterials science polymer edition. 1995; 7 (2): 12332. pubmed pmid: 7654627. epub 1995/01/01. eng. 55.hunsaker dh, martin pj. allergic reaction to solid silicone implant in medial thyroplasty. otolaryngology-head and neck surgery: official journal of american academy of otolaryngology-head and neck surgery. 1995 dec; 113 (6): 782-4. pubmed pmid: 7501393. epub 1995/12/01. eng. 56.frisch e. technology of silicones in biomedical applications. lr r, editor. new york: cv mosby; 1983. 57.muramatsu y, sugino k, kikuchi n, sano g, isobe k, takai y, et al. [human adjuvant disease which developed after silicone augumentation mammoplasty]. nihon kokyuki gakkai zasshi = the journal of the japanese respiratory society. 2009 mar; 47 (3): 237-41. pubmed pmid: 19348273. epub 2009/04/08. jpn. 58.carroll rp. acute inflammatory reaction to silicone stents. ophthalmic plastic and reconstructive surgery. 1989; 5 (1): 71. pubmed pmid: 2487201. epub 1989/01/01. eng. 59.jordan dr, nerad ja. an acute inflammatory reaction to silicone stents. ophthalmic plastic and reconstructive surgery. 1987; 3 (3): 147-50. pubmed pmid: 3154594. epub 1987/01/01. eng. 60.adegbite ab, paine kw, rozdilsky b. the role of neomembranes in formation of hematoma around silastic dura substitute. case report. j neurosurg. 1983 feb; 58 (2): 295-7. pubmed pmid: 6848694. epub 1983/02/01. eng. 61.sekhar ln, moossy j, guthkelch an. romanian neurosurgery (2013) xx 1: 106 115 115 malfunctioning ventriculoperitoneal shunts. clinical and pathological features. j neurosurg. 1982 mar; 56 (3): 411-6. pubmed pmid: 7057239. epub 1982/03/01. eng. 62.hashimoto m, yokota a, urasaki e, tsujigami s, shimono m. a case of abdominal csf pseudocyst associated with silicone allergy. child's nervous system: chns: official journal of the international society for pediatric neurosurgery. 2004 oct; 20 (10): 761-4. pubmed pmid: 14999512. epub 2004/03/05. eng. 63.kessler la, cheek wr. eosinophilia of the cerebrospinal fluid of noninfectious origin: report of 2 cases. neurology. 1959 may; 9 (5): 371-4. pubmed pmid: 13657297. epub 1959/05/01. eng. 64.niggemann b, breiteneder h. latex allergy in children. international archives of allergy and immunology. 2000 feb; 121 (2): 98-107. pubmed pmid: 10705219. epub 2000/03/08. eng. 65.shah s, cawley m, gleeson r, o'connor j, mcgeady s. latex allergy and latex sensitization in children and adolescents with meningomyelocele. the journal of allergy and clinical immunology. 1998 jun; 101 (6 pt 1): 741-6. pubmed pmid: 9648700. epub 1998/07/02. eng. 66.niggemann b, bauer a, jendroska k, wahn u. latex allergy as a cause of eosinophilia in cerebrospinal fluid in a child with aventricular shunt. journal of allergy and clinical immunology. 1997 12//; 100 (6): 849-50. microsoft word 2.baritchiiadriana_evaluation_f.docx 390 adriana baritchii et al methylprednisolone and cerebrolysin in traumatic spinal cord injury evaluation of the combined therapeutic effect of methylprednisolone and cerebrolysin in traumatic medullar lesion adriana baritchii1, lăcrămioara perju-dumbravă2, anca buzoianu3, aurel oşlobanu4, horaţiu ioani1, dragoş tusnea1, s. cadar5, e. levei5, ioan groza6, aurel muşte6, cristiana ciortea7, ioan ştefan florian4 1cluj county emergency hospital, department of neurosurgery; 2“iuliu hatieganu” umph cluj-napoca, department of neurology, cluj county emergency hospital, department of neurology; 3“iuliu hatieganu” umph clujnapoca; 4“iuliu hatieganu” umph cluj-napoca, department of neurosurgery cluj county emergency hospital, department of neurosurgery; 5icia the research institute for analytical instrumentation; 6university of agricultural science and veterinary medicine cluj-napoca; 7cluj county emergency hospital abstract objectives: the pharmacological effects of methylprednisolone and cerebrolysin have been extensively debated, but from our knowledge there are no studies to evaluate the association of these two drugs in spinal cord injury (sci). methods: twenty-four wistar rats underwent traumatic spinal cord injury by using clip-compression model. the animals were divided into four groups: group i received methylprednisolone (mp); group ii was injected with cerebrolysin (c); group iii received methylprednisolone together with cerebrolysin (mp+c); in the control group we have performed only decompression. the motor recovery of the animals was evaluated using the ferguson et al. modification of the bbb scale. after ten days the rats were sacrificed. results: the study demonstrated that the mp + c group presented the most notable recovery of the motor function, but no statistically significant (p>0,05). the first and the second group also presented better results than the fourth group, but the enhanced recovery of those group relative to control group was not statistically significant (p>0,05) conclusion: the combination of mp and cerebrolysin in experimental conditions seems to have promising results, but more experimental and clinical studies are necessary to evaluate the real benefit for sci patients. keywords: cerebrolysin, methylprednisolone, motor recovery, spinal cord injury. introduction spinal cord injury (sci) is a devastating disease with a high morbi-mortality even in specialized centers. the personal, familial and social implications of an injured patient are hardly quantifiable. there is a lack of evidence regarding this pathology in romania, but according to literature data the incidence fluctuates between 10.4 and romanian neurosurgery (2011) xviii 4: 390 399 391 83.0 per million inhabitants per year, from this one-third of the patients are reported to have tetraplegia and 50% have complete lesions at the mean age of 33. in the department of neurosurgery of the cluj county emergency the incidence of sci operated cases have increased from 45 cases/year in 2000 to 159 in 2009 due to the dramatically growth of the number of traffic accidents, thus increasing the addressability of our department in respect to the nationwide programme for preventing spinal deformity after spine injury. contrary to his important impact, the therapeutic armamentarium is very limited and there is no effective treatment to diminish the damage or to promote functional recovery. if the rationale of early surgery is decompression, in order to theoretically limit the secondary injury by diminishing the local ischemia, and stabilization in order to prevent subsequent lesion by an unstable spine, for secondary injury there are no available clinical proven therapies, in spite of numerous tested drugs in vitro and in vivo conditions. in theory it is possible that at the time of the surgery to add some factors that could block the secondary injury’s cascade or could promote neuronal or axonal recovery at the site of lesion. the great problem is to find the proper factors and the proper way of releasing at the site of the injury. for that reason we designed an experimental study in order to find some substances and the proper way of administration to improve the neurological evolution of this disabling disease. material and method twenty-four albino wistar rats (weight approximately 180-250g) were used during the study. the rats were anesthetized with ketamine 75-100 mg/kg, xylazine 10mg/kg, intraperitoneally. a longitudinal incision was made on the midline of the back, and the paravertebral muscles were dissected to expose vertebrae t8 to t10. a three level (t8-t10) laminectomy was performed to expose the spinal cord with the intact dura matter. in the absence of a standard impactor, the spinal cord injury was produced by applying a yasargil temporary clip 50 grams pressure force for 1 minute, the produced lesions mimicking compressionluxation injury. the layers were closed with 3/0 silk. study groups immediately after sci the rats were randomly grouped in 4 study groups of 6 rats each either : group mp – single dose intrathecal administration of 30mg/kg metilprednisolon 10 minutes after spinal cord injury; group cdaily intraperitoneal administration of 2,5ml/kg of cerebrolysine for 10 days; group mp+c single dose intratecal administration of 30mg/kg at 10 minutes after spinal cord injury and 2,5ml/kg daily, for ten days, i.p.; control group – decompression only ( t8-t10 laminectomy has a decompressive role in condition of spinal cord injury). ten days after the injury the rats were anesthetized (60 mg/kg intraperitoneally) and then decapitated. the spinal cords were rapidly removed and preserved in 10% neutral formaldehyde solution. histopathologic examination serial sections were taken from 2 mm caudal and rostral to and from the epicenter, tissue sections being stained with hematoxylin-eosin before light microscope examination. 392 adriana baritchii et al methylprednisolone and cerebrolysin in traumatic spinal cord injury group mp group c group mp+c control group figure 1 there are no clear differences between the four groups concerning the pathological aspects in h –e staining below 40 x magnifications. in all cases it can be observed a large vacuolization, disorganization of white mater; the nuclei are hipercromatic with nucleollyses. at the level of a dorsal root there are large demielinisations neurological evaluation for the motor evaluation of the wistar rats we used the bbb locomotor rating scale modified by ferguson et al. romanian neurosurgery (2011) xviii 4: 390 399 393 table 1 ferguson et al. modification of the bbb locomotor rating scale 0 no observable hind limb (hl) movement 1 slight movement of one or two joints, usually the hip and/or knee 2 extensive movement of one or two joints or extensive movement of one joint and slight movement of one other joint or slight movement of all three joints 3 slight movement of two joints and extensive movement of the third 4 extensive movement of two joints and slight movement of the third 5 extensive movement of all three joints of the hl 6 sweeping with no weight support or plantar placement of the paw with no weight support 7 plantar placement of the paw with weight support in stance only (i.e., when stationary) or occasional, frequent, or consistent weight supported dorsal stepping and no plantar stepping 8 occasional weight supported plantar steps, no forelimb (fl)-hl coordination 9 frequent to consistent weight supported plantar steps and no fl-hl coordination 10 frequent to consistent weight supported plantar steps and occasional fl-hl coordination 11 frequent to consistent weight supported plantar steps and frequent fl-hl coordination 12 consistent weight supported plantar steps, consistent fl-hl coordination or frequent plantar stepping, consistent fl-hl coordination, and occasional dorsal stepping definitions: slight: partial joint movement through less than half the range of joint motion. extensive: movement through more than half of the range of joint motion. sweeping: rhythmic movement of hl in which all three joints are extended, then fully flex and extend again; animal is usually side lying, the plantar surface of paw may or may not contact the ground; no weight support across the hl is evident. no weight support: no contraction of the extensor muscles of the hl during plantar placement of the paw; or no elevation of the hindquarter. weight support: contraction of the extensor muscles of the hl during plantar placement of the paw; or elevation of the hindquarter. plantar stepping: the paw is in plantar contact with weight support then the hl is advanced forward and plantar contact with weight support is reestablished. dorsal stepping: weight is supported thorough the dorsal surface of the paw at some point in the step cycle. fl-hl coordination: for every fl step an hl step is taken and the hls alternate. occasional: less than or equal to half; frequent: more than half but not always: 51–94% consistent: nearly always or always; 95–100% the data were statistically analyzed with t test and one way anova methods. for the quantitative variables this analysis was done by observing the minimum and maximum values and calculating their means, standard deviations and medians. absolute and percentage frequencies were also calculated. results there were no statistically significant differences between control group and the 394 adriana baritchii et al methylprednisolone and cerebrolysin in traumatic spinal cord injury one who received methylprednisolone (mp) regarding motor recovery. (p=0,89) (figure 2). the same lack of significance was observed between control group and the group that received cerebrolysin (c) (p= 0,79) (figure 3). co nt ro l g ro up m et hy lp re dn is ol on e gr ou p 0 5 10 15 20 25 unpaired t test p value p value summary are means signif. different? (p < 0.05) oneor two-tailed p value? t, df 0.8951 ns no two-tailed t=0.1339 df=16 figure 2 motor recovery in the control group compared to the group that received methylpredinisolone (mp) 0 10 20 30 control group cerebrolysin group unpaired t test p value p value summary are means signif. different? (p < 0.05) oneor two-tailed p value? t, df 0.7918 ns no two-tailed t=0.2679 df=18 figure 3 motor recovery in the control group compared to the group that received cerebrolysin (c) 0 10 20 30 control group mp+ c group unpaired t test p value p value summary are means signif. different? (p < 0.05) oneor two-tailed p value? t, df 0.6844 ns no two-tailed t=0.4108 df=27 figure 4 motor recovery in the control group compared to the group that received methylprednisolone and cerebrolysin average values of scores obtained by rats in the control group are not significantly higher than that the values obtained by the rats which received the combination of methylprednisolone (mp) and cerebrolysin (c) (figure 4). one way anova methods showed no statistically significant differences between different groups in terms of motor recovery in rats. (figure 4). the mp and c group presented functional results that were better than those of the control group but no statistically significant (p> 0,05). discussion several experimental models have been described for producing a spinal cord injury. experimental evaluations of the effectiveness of a drug for animals with a spinal cord injury require the production of a standardized injury that has a motor function response as similar as possible among many animals. we choose to use the clip-compression model because it allows a precise monitoring of the force (50g) and duration of compression (1 minute). it is also a more subtle technique. romanian neurosurgery (2011) xviii 4: 390 399 395 0 10 20 30 control group methylprednisolone group cerebrolysin group mp+ c group bartlett's test for equal variances bartlett's statistic (corrected) p value p value summary do the variances differ signif. (p < 0.05) anova table treatment (between columns) residual (within columns) total bonferroni's multiple comparison test control group vs methylprednisolone group control group vs cerebrolysin group control group vs mp+ c group methylprednisolone group vs cerebrolysin group methylprednisolone group vs mp+ c group cerebrolysin group vs mp+ c group 0.3263 0.9550 ns no ss 12.60 1921 1934 mean diff. -0.4000 -0.9000 -1.500 -0.5000 -1.100 -0.6000 df 3 36 39 t 0.1224 0.2755 0.4591 0.1530 0.3367 0.1836 ms 4.200 53.37 significant? p < 0.05? no no no no no no summary ns ns ns ns ns ns 95% ci of diff -9.522 to 8.722 -10.02 to 8.222 -10.62 to 7.622 -9.622 to 8.622 -10.22 to 8.022 -9.722 to 8.522 figure 5 comparative analysis of the results obtained from the four groups the ideal tool for evaluation of motor function should be sensitive, easy to use, and able of showing small changes. today, the evaluation method that comes closest to those purposes is the bbb scale. because the discontinuous nature of the lower portion of the scale presents a problem for both parametric and nonparametric statistical [1] we used a modification of the scale after ferguson et al. in our study we sacrificed animals ten days after the spinal cord trauma as the purpose was to analyze the functional recovery during the acute phase. we choose to use methylprednisolone because it provides clinical benefits and also improvement in neurological function as demonstrated in several studies [4,12]. 396 adriana baritchii et al methylprednisolone and cerebrolysin in traumatic spinal cord injury cerebrolysin contains a mixture of neurotrophic peptide and it was proven to be a useful treatment for enhancing neurological recovery after stroke [13]. the rationale for our experimental study was to add neuroprotective factors with multiple mechanisms of action on both local and general modes in order to augment the neuroprotective effect methylprednisolone is a glucocorticoid with potent anti-inflammatory properties. this group of drugs induced synthesis and release of many anti-inflammatory peptides. among them, lipocortins inhibit calcium activated phospholipase activity by binding to membrane phospholipid substrates. methylprednisolone is not only an antiinflammatory drug but also a potent immunosuppressive. this drug inhibits phospholipase a2 activity, alters neuronal excitability and improves post-traumatic spinal cord blood flow. yoon et all showed that methylprednisolone has a very short therapeutic window and the best results are obtained with a dose of 30 mg/kg applied within the first 30 minutes after contusion [7]. based on that study, we administrated 30 mg/kg methylprednisolone 10 minutes after the injury. high dose of methylprednisolone causes adverse side effects including pneumonia, wound infections and acute corticosteroid myopathy accompanied by only modest improvements in neurological recovery [8, 17]. there is a need for localized delivery of mp to the lesion site to minimize the systemic delivery related side effects. to achieve this local delivery, we injected the drug into the spinal cord, at the site of injury. the glucocorticoid steroids were widely used in the clinical treatment of spinal cord trauma by the middle of the 60’s and throughout the 1970. the rationale mechanism for their use was centered on the expectation that they would reduce the spinal cord edema. this was based upon the remarkable reduction of peritumoral brain edema the first national acute spinal cord study (nascis 1) that began in 1979 wanted to compare high and low dose of methylprednisolone in spinal cord injury. the trial did not involve a placebo group. the study was published in 1985 and found no significant difference between high and low dose of methylprednisolone started within 48 hours after spinal cord injury. there also was a suggestion that the 10days high-dose regimen increased the risk of infections. the study raised question at that time about the efficiency of glucocorticoids and brought to the forefront the teory of free radicals. in 1990 the second national spinal cord injury study (nascis 2) showed a significant improvement in motor and sensory recover in patients treated with high dose of methylprednisolone within 8 hours after spinal cord injury. however, when started more than 8 hours after the injury the drug was proven not only ineffective but deleterious. this study suggests that a therapeutic time window exists in spinal cord injury. weaver et all demonstrated that the nonselective and enduring effects of immunosuppressive therapy with methylprednisolone not only fail to improve neurological outcomes in rats with spinal cord injury, but also can block the beneficial actions of selective therapies (anti-cd11d mab) [25]. cerebrolysin is a neurotrophic peptidergic mixture with antioxidant romanian neurosurgery (2011) xviii 4: 390 399 397 properties. the drug has been studied since the early 1970’s. in stroke and neurodegenerative diseases, double-blind placebo controlled trials have reported sustained improvements and slowing down of progressive memory loss, cognition impairment, mood changes, and motor and sensory symptoms several studies have suggested that cerebrolysin has neurotrophic and neuroprotective effect in vitro and in vivo. in animals, following cerebral ischemia, cerebrolysin has been shown to ameliorate the effect of oxidative cell stress [9]. the inhibitory effect of the drug on calpain has been demonstrated on a molecular level [26]. cerebrolysin reduces apoptosis triggered by growth factor withdraw and induces neuritis outgrowth in cultivated neurons [20]. tatebayashi et all demonstrated that cerebrolysin enhanced neurogenesis in the dentate gyrus of adult animals, which correlates with improved spatial memory performance in these animals [24]. after bilateral artery occlusion in rats, cerebrolysin reduces mortality of the animals with about 50 %, and also reduces the infarct size as well as the loss of map-2 immunoreactivity in a middle cerebral artery occlusion model [22, 23]. in humans the drug was safely used for the treatment of several conditions [3, 16, 18]. haninec, et al. reported that insulin-like growth factor i (igf-i) and cerebrolysin enhances survival of motoneurons after ventral root avulsion [18]. the drugs were effective when given intrathecally to the spinal cord. in 2005, bul’on, et al published a study that compared the effects of cytoflavin and cerebrolysin in rats after spinal cord compression injury [5]. the neuroprotective effects of cytoflavin were greater than of cerebrolysin’s. in 1999, lombardi, et al [14] demonstrated that applying cerebrolysin to astrocytes and microglia cultures of rats, prevented microglial activation after lps activation and reduced interleukin-1b expression. mallory, et al. [15] reported that when the peptide mixture was applied to the human teratocarcinoma cell line (nt2) cerebrolysin markedly increased expression of synaptic-associated proteins, suggesting that it has synaptotrophic effects mediated through regulation of app expression. alvarez, et al. showed that this drug reduced microglial activation both in vitro and in vivo [2]. in 2002 guttmann et al. demonstrated that cerebrolysin protects cortical neurons cultures of the chickens from cell death caused by a wide variety of factors, including glutamate, iodoacetate, and ionomycin; they proposed that cerebrolysin stabilizes calcium ionic homeostasis [10]. safarova, et al. [19] showed that cerebrolysin improved survival of pc12 cells in serum-free medium. they obtained a decrease of apoptosis from 32% to 10%. in 2005, schauer, et al. found that a single addition of cerebrolysin to culture medium resulted in significant protection of tissue cultures against ischemia and hypoxia for up to 2 weeks. the treatment has the same beneficial effects even if it is delayed for as long as 96 hours [21]. our study has some weakness that could affect the results. firstly the traumatic model is not largely accepted, the produced lesions being possibly too severe, and as a consequence, irreversible. secondly the local administration of methyprednisolone could be harmful per se, adding possible new lesions, in the absence of a special 398 adriana baritchii et al methylprednisolone and cerebrolysin in traumatic spinal cord injury device for microinjection. more than that it is uncertain if the injectable form we used is compatible with a local administration. on the other hand it is known that cerebrolysin is a dose dependent drug. in spite of these criticisms, from our knowledge this is the first experimental study of a combination between mp and cerebrolysin in sci. their mechanism of action is not completely understood, but there are experimental data demonstrating an apoptotic inhibition on the line of calpains. at least for mp there are experimental data proving the favourable action on topic application [6] more experimental data are necessary in order to demonstrate the synergic action of mp and cerebrolysin, the optimal interval for drug administration and the optimal dose of the drugs taking into account that at a dose of 30mg/kg mp have many deleterious effects. cerebrolysin is a dose dependent drug and until now there are no studies regarding the local application of this drug. finally, taking in consideration that in control group, the simple laminectomy group, the results were no significantly different that in those medically treated, the role of urgent decompressive laminectomy cannot be underestimated. conclusion we found that methylprednisolone and cerebrolysin didn’t significantly enhanced neurological recovery in rats with severe clip-compression models of spinal cord injury, administrated alone or in combination from a statistic point of view. methylprednisolone is the first drug shown to improve recovery in human spinal cord injury and remains the only form of treatment shown in a phase 3 trial to have efficiency in managing this injury. therefore, it remains the standard therapy to which all further treatments should be compared. some clinical evidence suggest that cerebrolysin may be beneficial for many neurological conditions, including extrapyramidal hyperkinesis associated to narcoleptic therapy, acute and chronic stroke, brain trauma, organic mental disorders, ischemic encephalopathy, diabetic neuropathy, rett syndrome, vascular dementia, multiple sclerosis, antiaging and other neurodegenerative disorders. little data is available concerning the effect of cerebrolysin on spinal cord injury. more studies are needed to ascertain the benefits of the drug for both acute and chronic spinal cord injuries. acknowledgements this work was financially supported through a grant of the romanian ministry of research and education, project of exploratory research, contract medprot42109. the author responsible for correcting: prof. dr. ioan ştefan florian “iuliu hatiegnau” umph, cluj-napoca; department of neurosurgery cluj county emergency hospital department of neurosurgery 43 victor babes street 40012 cluj-napoca tel/fax number: +40-264-450023 e-mail address: florian_stefan@yahoo.com references 1. adam ferguson, michelle a. hook, guadalupe garcia, jacqueline c. bresnahan, michael s. beattie, james w grau, a simple post hoc transformation that improves the metric properties of the bbb scale for rats with moderate to severe spinal cord injury, journal of neurotrauma, vol 21, no 11, 2004, 16011613 romanian neurosurgery (2011) xviii 4: 390 399 399 2. alvarez xa, lombardi vr, fernandez-novoa l, garcia m, sampedro c, cagiao a, cacabelos r and windisch m (2000). cerebrolysin reduces microglial activation in vivo and in vitro: a potential mechanism of neuroprotection. j neural transm suppl. 59:281-92. 3. bae, c. -y., cho, c. -y., cho, k., oh, b. h., choi, g. k., lee, h. s., et al., (2000). a double-blind, placebo-controlled, multicenter study of cerebrolysin for alzheimer’s disease, j am ger soc 48, 1566-1571. 4. bracken mb. pharmacological interventions for acute spinal cord injury. cochrane database syst rev 2: cd001046, 2000. 5. bul’on vv, kuznetsova nn, selina en, kovalenko al, alekseeva le and sapronov ns (2005). neuroprotective effect of cytoflavin during compression injury of the spinal cord. bull exp biol med. 139:3946. 6. chen-guang yu, aashish joshi, james w. geddes : intraspinal mdl28170 microinjection improves functional and pathological outcome following spinal cord injury ;journal of neurotrauma 25:833–840 (july 2008) 7. do heum yoon, young soo kim, wise young, yonsei therapeutic time window for methylprednisolone in spinal cord injured rats, medical journal, vol 40, no 4, pp 313-6. 8. gerndt sj, rodriguez jl, pawlik jw, taheri pa, wahl wl, micheals aj, et al. consequences of highdose steroid therapy for acute spinal cord injury. j trauma. 1997 feb;42(2):279–284. 9. gonzalez, m. e., francis, l. & castellano, o. (1998). antioxidant systemic effect of short-term cerebrolysin administration, j neural transm 53, 333-341. 10.gutmann b, hutter-paier b, skofitsch g, windisch m and gmeinbauer r (2002). in vitro models of brain ischemia: the peptidergic drug cerebrolysin protects cultured chick cortical neurons from cell death. neurotox res. 4:59-65. 11.haninec p, houst’ava l, stejskal l and dubovy p (2003). rescue of rat spinal motoneurons from avulsion-induced cell death by intrathecal administration of igf-i and cerebrolysin. ann anat. 185:233-8. 12.hurlbert rj. the role steroids in acute spinal cord injury: an evidence-based analysis. spine. 2001;26:3946. 13.jingmei rena, dana sietsmaa, shumei qiua, herbert moesslerb and seth p. finklestein cerebrolysin enhances functional recovery following focal cerebral infarction in rats; restorative neurology and neuroscience 25 (2007) 25–31 25. 14.lombardi vr, windisch m, garcia m and cacabelos r (1999). effects of cerebrolysin on in vitro primary microglial and astrocyte rat cell cultures. methods find exp clin pharmacol. 21:331-8. 15.mallory m, honer w, hsu l, johnson r, rockenstein e and masliah e (1999). in vitro synaptotrophic effects of cerebrolysin in nt2n cells. acta neuropathol (berl). 97:437-46 16.panisset, m., gauthier, s., moessler, h., windisch, m. & group, c. s. (2002). cerebrolysin in alzheimer’s disease: a randomized, double-blind, placebocontrolled trial with a neurotrophic agent, j neural transm 109, 1089-1104. 17.qian t, guo x, levi ad, vanni s, shebert rt, sipski ml. high-dose methylprednisolone may cause myopathy in acute spinal cord injury patients. spinal cord. 2005 apr;43(4):199–203. 320, 1999. 18.ruether, e., husmann, r., kinzler, e., diabl, e., lingler, e., spatt, j., et al. (2001). a 28 week, doubleblind, placebo-controlled study with cerebrolysin in patients with mild to moderate alzheimer’s disease, int clin pschopharm 16, 253-263. 19.safarova er, shram si, grivennikov ia and myasoedov nf (2002). trophic effects of nootropic peptide preparations cerebrolysin and semax on cultured rat pheochromocytoma. bull exp biol med. 133:401-3. 20.satou, t., itoh, t., tamai, y., ohde, h., anderson, a. j.&hashimoto, s. (2000). neurotrophic effects of fpf-1070 (cerebrolysin) on cultured neurons from chicken embryo dorsal root ganglia, ciliary ganglia, and sympathetic trunks, j. neural transm. 107, 1253-1262. 21.schauer e, wronski r, patockova j, moessler h, doppler e, hutterpaier b and windisch m (2005). neuroprotection of cerebrolysin in tissue culture models of brain ischemia: post lesion application indicates a wide therapeutic window. j neural transm 22.schwab, m., antonow-schlorke, i., zwiener, u. & bauer, r. (1998). brain derived peptides reduce the size of cerebral infarction and loss of map-2 immunoreactivity after focal ischaemia in rats, j neural transm 53, 299-311. 23.schwab, m., schaller, r., bauer, r. & zweiner, u. (1997). morphofunctional effects of moderate forebrain ischaemia combined with short-term hypoxia in rats – protective effects of cerebrolysin, exp toxic pathol 49, 29-37. 24.tatebayashi, y., lee, m. h., li, l., iqbal, k. & grundke-iqbal, i. (2003). the dentate gyrus neurogenesis. a therapeutic target for alzheimer’s disease, acta neuropathol 2003, 225-232. 25.weaver lc, gris d, saville lr, oatway ma, chen y, marsh dr, hamilton ef, dekaban ga, methylprednisolone causes minimal improvement after spinal spinal cord injury in rats, contrasting with benefits on an anti-integrin treatment, j neurotrauma, 2005, dec; 22 (12) 1375-87 26.wronski, r., tompa, b., hutter-paier, b., crailsheim, k., friedrich, b. & windisch, m. (2000). inhibitory effect of a brain derived peptide preparation on the intracellular calcium ca++dependent protease, calpain, j neural transm 107, 145-157. microsoft word 13xchiriac_ruptured romanian neurosurgery (2013) xx 4: 397 400 397 ruptured intracranial mycotic aneurysm of the distal middle cerebral artery – case report a. chiriac, a. iordache, n. dobrin1, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi introduction mycotic aneurysm represents a rare but serious clinical condition characterized by significant morbidity and mortality. the most common causative pathogens of mycotic aneurysm are staphylococcus aureus and salmonella species. also, other bacteria’s like pseudomonas spp., campylobacter fetus, streptococcus spp., clostridium spp., and corynebacterium spp. and klebsiella pneumoniae have been noted as possible pathogens. this neurovascular entity develops as a consequence of vessel wall necrosis due to a massive presence of bacterial emboli into the systemic circulation. multiple treatment modalities are currently available and consist in conservative antibiotherapy, surgical closure or endovascular occlusion. we report a patient with ruptured mycotic aneurysm successfully treated by a combined treatment (surgical hematoma evacuation and conservative antibiotherapy). case presentation a 63-year-old male presented with a one week history of headache, vomiting and an episode of short time lost of conscious. he performs a cranio-cerbral ct scan with no pathological imagistic signs (figure 1). he was addressed to the medical clinic for infectious diseases where the lumbar puncture shows a high level of cerebrospinal fluid leucocytes. also, the blood leucocytes formula was highly modified. the patient was immediately admitted with the suspicion of meningitis with possible septic status. in the next two days he developed high-grade fever with delirium and strong headache episodes. in this situation a double antibiotic therapy was initiated. four days after admission, the patient developed altered sensorium and conscious. he was immediately addressed to our neurosurgical clinic. on clinical examination, the patient was febrile, tachypneic, disoriented and not obeying verbal commands. his motor examination revealed slight paucity of movements and tone on left side. soon after he experienced a precipitous decline in neurological status, becoming only responsive to the pain. he stopped spontaneously moving his left side with associated hyperreflexia and a positive babinski sign on the left. repeat ct scan showed an extensive increased right intracerebral haemorrhage with ventricular efraction and local mass effect (figure 2). a helical ct angiogram performed in emergency showed no vascular pathological signs (figure 3). 398 chiriac et al ruptured intracranial mycotic aneurysm figure 1 initial diagnostic cerebral ct scan figure 2 diagnostic cerebral ct scan after neurological deterioration emergent evacuation of the intrecerebral hematoma with external decompression was performed on the same day. no fresh hematoma or hemosiderin pigmentation was observed in the subarachnoid space (right sylvian fissure) and a ruptured aneurysm could not be identified in the hematoma cavity. figure 3 helical ct angiogram showing no vascular pathological signs figure 4 postoperative cerebral ct scan showing partially evacuation of intracerebral hematoma a postoperative control ct scan was performed the next day showing a partially evacuation of right hemisphere hematoma (figure 4). the patient remained haemodynamically stable on intravenous antibiotics and subsequent sets of blood cultures had no growth. his mental status improved but his dense left hemiparesis still persisted. romanian neurosurgery (2013) xx 4: 397 400 399 figure 5a dsa in ap exposure showing an aneurysm on distal m2 segment of right middle cerebral artery figure 5b dsa in profile exposure showing an aneurysm on distal m2 segment of right middle cerebral artery four vessel digital substraction angiography was performed for better visualization of the suspected arteriovenous malformation. the right carotid angiogram showed an irregular aneurysm arising from distal m2 segment of right middle cerebral artery (figure 5 a, b) and measured approximately 5 millimeters. signs of vasospasm were also identified on both m2 segment of right middle cerebral artery. the remainder of the angiogram did not revealed any abnormality. a decision was made to continue antibiotic therapy and repeat the digital substraction angiography. the digital substraction angiography performed three weeks later revealed the total disappearance of the distal m2 aneurysm with no more sings of vasospasm (figure 6 a, b). finally, the patient was discharged to a recovery clinic two weeks later with only a slight left side hemiparesis. discussion intracranial infectious aneurysms are rare vascular lesions and were first reported by church in 1876 and account for 0.75.4% of all intracranial aneurysms. they are mainly located on the middle cerebral artery or its distal branches in up to 70% of the cases, less commonly on the anterior or posterior cerebral arteries. their evolution is unpredictable even after commencement of antibiotic therapy. the mycotic aneurysms can either regress, develop de novo, or rupture. variable outcomes have been reported (1), with a mortality rate of up to 83% (2). medical therapy is the first step in the management of mycotic aneurysms and consisting of long-term antibiotic therapy. however, surgery or endovascular therapy could be indicated in patients with intracerebral haematoma with significant mass effect or a possible vascular anatomical way to the lesion. to efficiency of medical therapy is determined by serial follow-up angiographic studies. the evolution of mycotic aneurysms with antibiotic therapy is unpredictable, they may regress, disappear, persist, enlarge or rupture. their good responses to antibiotic therapy are indicated by regression in the size of the aneurysm or complete resolution of the aneurysms.[2,3,4,5,6] 400 chiriac et al ruptured intracranial mycotic aneurysm figure 6a dsa control in ap exposure showing total disappearance of the distal m2 aneurysm figure 6b dsa control in profile exposure showing total disappearance of the distal m2 aneurysm conclusions our protocol is consisting in medical management for patients with aneurysms that have not yet ruptured or have no response to the antibiotics therapy. the medical therapy should be followed closely with serial cerebral angiograms. surgical treatment should be performed emergently in the setting of intraparenchymal hemorrhage or increased intracranial pressure. endovascular intervention should be based especially on the involvement of eloquent vascular territory anatomy. references 1. haruki yamakawa, tatsuaki hattori, tetsuya tanigawara, yukiko enomoto, akio ohkuma (2003) ruptured infectious aneurysm of the distal middle cerebral artery manifesting as intracerebral hemorrhage and acute subdural mematoma – case report , neurol med chir (tokyo) 43:541 – 545; 2. north-coombes d., schonland m. m. (1974) cerebral mycotic aneurvsma case report s a. medical journal, 1808 – 1810; 3. raut abhijit a, ghatge sharad b, nagar arpit, narlawar ranjeet s, ahmed nadeem, limaye uday l (2003) mycotic aneurysm of posterior cerebral artery: management by endovascular glue embolization, the journal of radiology, 5:78-82; 4. rene´ chapot, emmanuel houdart, jean-pierre saint-maurice, armand aymard, charbel mounayer, guillaume lot, jean-jacques merland (2002) endovascular treatment of cerebral mycotic aneurysms, radiology 2:389-396; 5. antonio v. salgado, anthony j. furlan, thomas f. keys (1987) mycotic aneurysm, subarachnoid hemorrhage, and indications for cerebral angiography in infective endocarditis stroke 1987, 18:1057-1060; 6. wai-kit lee, peter j. mossop, andrew f. little, gregory j. fitt, john i. vrazas, jenny k. hoang, oliver f. hennessy (2008) infected (mycotic) aneurysms: spectrum of imaging appearances and management, radiographics, 28:1853–1868; 7. ahsan h, ajmal f, saleem m f, sonawala a b (2009) cerebral fungal infection with mycotic aneurysm of basilar artery and subarachnoid haemorrhage, singapore med 50(1) : e22; 8. isabel kuo, theodore long, nathan nguyen, bharat chaudry, michael karp, nerses sanossian (2010) ruptured intracranial mycotic aneurysm in infective endocarditis: a natural history case reports in medicine 10: 897-904; 9. philip j peters, taylor harrison, jeff rey l lennox (2006) a dangerous dilemma: management of infectious intracranial aneurysms complicating endocarditis, lancet infect dis 6:742–48. microsoft word 17.dobrovatb_orbitaltrauma_f.docx romanian neurosurgery (2011) xviii 4: 525 532 525 orbital trauma: from anatomy to imaging patterns – a pictorial review b. dobrovăţ1, r. popescu1, a. nemtoi1, o. ladunca1, d. haba2 1phd student in radiology, “gr.t. popa” umph, iasi 2radiology clinic, “prof. dr. n. oblu” clinic and emergency hospital iasi abstract objective: in assessing the patients with orbital trauma, a basic knowledge of anatomy of this region is necessary to determine the gravity and the extent of traumatic injury. since the development of high resolution ct, significant progress has been made for the evaluation of orbital trauma, adding more sensitivity to the plain x-ray method. other imaging methods that can be useful is ultrasonography and mri. the objective of this article is to review the orbital anatomy correlated with the common ct imaging patterns, and to establish the modality of choice in assessing orbital trauma. methods: we retrospectively analyzed 297 patients with facial trauma who were submitted to spiral ct scanning. the ct images were interpreted using the following protocols: axial, multiplanar reconstruction (mpr), 3d images and association of axial/mpr/3d images. we evaluated the anatomical sites of lesions, dividing them according to the orbital walls: lateral; medial; superior (roof) and inferior (anterior, medial). results: in our study 35% of patients who suffered facial trauma had ocular or orbital injuries. most frequent site of orbital fractures was the medial wall. association of axial/mpr images interpretation increase the sensitivity of ct diagnosis compared with only axial protocol. conclusions: facial traumatized patients with clinical suspicion of orbital injuries are usually first evaluated with spiral ct, the best protocol is to obtain thin-section (1-3 mm) axial ct scans and then performing multiplanar reformation (specially coronal reformation is very useful). knowledge of diverse imaging patterns of potential injuries is essential to make a fast and accurate diagnosis of post-traumatic orbital injury. keywords: computer tomography, fracture, multiplanar reconstruction (mpr), orbital trauma background trauma to the eye is the cause of blindness in more than half a million people worldwide and of partial loss of sight in many more, and it is often the main cause of unilateral loss of vision in developing countries. for example, in the united states orbital trauma occurs in approximately 3% of all emergency department visits. orbital injuries are often seen in patients with multiple traumas from traffic accidents, assault, falls from height, gunshot. a basic knowledge of the potential injuries to the eye and of the anatomy of 526 b. dobrovăţ et al orbital trauma this region is necessary to determine the gravity and the extent of traumatic traumatic injury. imaging options computed tomography (ct) is the method of choice for evaluating orbital trauma and it is useful for evaluating bone fractures, soft tissue injury and foreign body detection. ct is a fast method to perform, readily available, no special need for patient preparation, the eye movement do not degrade the image acquisition and has no risk if metallic fragment are suspected. ct has been shown to be more accurate than radiography in detecting fractures. when fractures are present, three-dimensional reformation is a useful tool to guide treatment. other methods may be useful for evaluating orbital trauma: radiography has a sensitivity of 64%–78% for a fracture, but it has very low sensitivity for soft-tissue injuries; ultrasonography (us) is very useful for evaluating the globe and its contents; but us is contraindicated if a ruptured globe is suspected and additionally is operator dependent and offers no information about boune trauma; magnetic resonance (mr) imaging may be difficult to perform and it is contraindicated if there is a possibility that a metallic fragment is present. methods the study is a retrospective analysis of 297 patients diagnosed as having head trauma hospitalized between 2009 and 2010 at “prof. dr. nicolae oblu” hospital, iasi. the patients were submitted to spiral ct scanning. and ct images were interpreted using the following protocols: axial, multiplanar reconstruction (mpr), 3d images and association of axial/mpr/3d images. we evaluated the anatomical sites of lesions, dividing them according to the orbital walls: lateral; medial; superior (roof) and inferior (anterior, medial). discussion – from anatomy to traumatic ct patterns the orbit is a pyramidal space formed by seven bones: frontal, zygomatic, maxillary, ethmoidal, sphenoid, lacrimal, palatine. the paired orbital cavities lie on each side of the midsagittal plane of the skull on close relation to the nasal sinus and cranial cavities. the volume of each adult orbit is about 30 cc. the orbital entrance averages about 35 mm in height and 45 mm in width.. in adults, the depth of the orbit varies from 40 to 45 mm from the orbital entrance to the apex. a b figure 1 ct axial a and coronal b view of the orbit romanian neurosurgery (2011) xviii 4: 525 532 527 figure 2 bony orbit anatomy: 1 sphenoid, 2 zygomatic, 3 maxillary, 4 lacrimal, 5 ethmoidal, 6 frontal, 7 palatine the medial wall is approximately rectangular and it is formed by 4 bones: the frontal process of the maxilla (that forms the medial orbital rim), the lacrimal bone, the orbital plate of the ethmoid, and the lesser wing of the sphenoid. at its anterior aspect, it contains the lacrimal fossa which is bounded by the anterior and posterior lacrimal crests. the lacrimal sac is intimately related to the medial canthal tendon, which is a major supporting structure of the superficial tissues of the medial orbital region. the vast majority of the medial wall is comprised of the lamina papyracea. a paperthin bone overlying the ethmoid sinus that facilitates the infection spread in cases of ethmoid sinusitis, into the orbit; it is extremely thin, varying from 0.2 to 0.4 mm in thickness. the most posterior part of the medial wall is formed by the thick bone of the sphenoid body, adjoining the optic canal. the medial wall articulates with the roof at the fronto-ethmoid suture and it articulates with the the floor at the maxillo-ethmoid suture. figure 3 medial orbital wall is formed by: 1 frontal process of the maxilla, 2 lacrimal bone, 3 lamina papyracea, 4 sphenoid body the lamina papyracea fractures easily in blunt orbital trauma and in the course of ethmoid sinus surgery, exposing the orbit to the risk of inadvertent surgical injury. medial orbital wall trauma is strongly related with diploplia due to the mechanical entrapment of the medial rectus muscle (recognized on ct by displacement of the muscle into the fracture site, with or without bone displacement). ct scan also localizes the fragments of the fractured lamina papyracea even if the orbital sinus adjacent to the fracture is opacified. a degree of medial displacement of the lamina papyracea can be present, and the ethmoidal sinuses often are hyperdense due to edema and blood accumulation. the orbital floor is formed mainly by the orbital plate of the maxilla and with contributions from the zygoma anterolaterally and the palatine bone at its most posterior limit. the orbital floor is the roof of the maxillary sinus. in its posterolateral two-thirds, the floor is separated from the lateral wall by the inferior orbital fissure through which the maxillary division of the trigeminal nerve enters the orbit. 528 b. dobrovăţ et al orbital trauma a b figure 4 important structures on medial wall a axial nonenhanced ct image shows the nomal anatomy of lamina papyracea, and b on coronal view, the nasolacrimal canal a b figure 5 fractures of the medial orbital wall a axial nonenhanced ct image and b the coronal view show the displacement of the lamina papyracea with blood acumulation in adiacent ethmoidal cells an important structure is represented by the the infraorbital groove which is the location of infraorbital nerve that supplies sensation to check and ipsilateral upper alveolus and teeth. medial to the infraorbital nerve, the orbital floor is relatively thin and fractures easily. romanian neurosurgery (2011) xviii 4: 525 532 529 a b figure 6 a the orbital floor, b the infraorbital groove on sagital and coronal ct views orbital floor fractures can occur isolated, but they are also associated with le fort ii fractures (orbital floor fractures) and noe fractures (medial orbital wall fractures). orbital floor fractures may result when a object, which is of equal or greater diameter than the orbital aperture, hits the eye, and the resultant force is transmitted throughout the orbit causing a fracture of the orbital floor. the imaging study of choice is ct scan, with axial and coronal reconstruction ( thin cuts 2-3 mm with specific attention to the orbital floor and optic canal). the lateral wall is the thickest of the orbital walls and is formed by the greater wing of sphenoid posteriorly and the zygoma anteriorly. it is separated from the floor by the inferior orbital fissure and from the roof by the superior orbital fissure (posteriorly) and the frontosphenoid suture. a b c figure 7 fractures of the orbital floor. a sagital nonenhanced ct image shows a orbital floor fracture without evidence of entrapment of the inferior rectus muscle. b coronal nonenhanced ct image shows a left orbital floor fracture. the inferior rectus is displaced inferiorly into the maxillary sinus. c axial nonenhanced ct image shows the orbital fat herniation into the maxillary sinus 530 b. dobrovăţ et al orbital trauma a b figure 8 a lateral orbital wall is formed by: 1 zygoma and 2 greater wing of sphenoid, b axial nonenhanced ct image shows the lateral wall (with yellow the sphenoid and with green zygoma) in its posterior part, the greater wing of sphenoid is interposed between the middle cranial fossa and the orbit. during lateral orbitotomy, the cut is usually made just above the frontozygomatic suture, at which point the middle cranial fossa is in close proximity. a b figure 9 fractures of the orbital walls. a coronal and b axial nonenhanced ct image show fractures of the zygomatic bone that forms external wall of orbit the orbital roof is formed by the frontal bone with a minimal contribution from the lesser wing of sphenoid. it forms the floor of the anterior cranial fossa. the orbital roof is strong and rarely fractures. the lacrimal gland is located in a fossa in the anterolateral aspect of the roof. figure 10 a schematic representation of the orbital superior wall. b sagital and axial nonenhanced ct show the supraorbital notch which is the location of the homonym nerve romanian neurosurgery (2011) xviii 4: 525 532 531 isolated fractures of the orbital roof are uncommonly seen in the absence of a fracture of the superior orbital rim. figure 11 coronal nonenhanced ct image shows a fracture of the midportion of the orbital roof with displacement of the fracture fragments intraorbital and into the cranial fossa a b figure 12 a and b 3d reconstructed and coronal views that show an important frontal bone fracture that is extended to the superior orbital wall conclusion facial traumatized patients with clinical suspicion of orbital injuries are usually first evaluated with spiral ct, the best protocol is to obtain thin-section (1-3 mm) axial ct scans and then performing multiplanar reformation (specially coronal reformation is very useful). knowledge of diverse imaging patterns of potential injuries is essential to make a fast and accurate diagnosis of post-traumatic orbital injury. references 1. anderson je. grant’s atlas of anatomy. baltimore, md: williams & wilkins; 1978 2. bord sp, linden j. trauma to the globe and orbit. emerg med clin north am 2008;26:97–123. 3. cooper pw, kassel ee, gruss js. high-resolution ct scanning of facial trauma. ajnr am j neuroradiol 1983;4(3):495–498. 4. daffner rh. imaging of facial trauma. semin musculoskelet radiol 1998;2(1):65–82. 5. daniels dl, pech p, kay mc, et al. orbital apex: correlative anatomic and ct study. ajnr am j neuroradiol 1985;6:705–710 6. daniels dl, rauschning w, lovas j, et al. pterygopalatine fossa: computed tomographic studies. radiology 1983;149:511–516 7. gassner r, tuli t, hachl o, rudisch a, ulmer h. cranio-maxillofacial trauma: a 10 year review of 9,543 cases with 21,067 injuries. j craniomaxillofac surg 2003;31(1):51–61. 8. grant jh 3rd, patrinely jr, weiss ah, kierney pc, gruss js. trapdoor fracture of the orbit in a pediatric population. plast reconstr surg 2002;109(2): 482–489; discussion 490–495. 9. gruss js, mackinnon se. complex maxillary fractures: role of buttress reconstruction and immediate bone grafts. plast reconstr surg 1986;78(1):9–22. 10. iida s, kogo m, sugiura t, mima t, matsuya t.retrospective analysis of 1502 patients with facial fractures. int j oral maxillofac surg 2001;30(4):286– 290. 11. iinuma t, hirota y, ishio k. orbital wall fractures:conventional views and ct. rhinology 1994;32:81–83. 532 b. dobrovăţ et al orbital trauma 12. laine fj, conway wf, laskin dm. radiology of maxillofacial trauma. curr probl diagn radiol 1993;22(4):145–188. 13. markowitz bl, manson pn, sargent l, et al. management of the medial canthal tendon in nasoethmoid orbital fractures: the importance of the central fragment in classification and treatment. plast reconstr surg 1991;87(5):843–853. 14. rene c, rose ge, lenthall r, moseley i. major orbital complications of endoscopic sinus surgery. br j ophthalmol 2001; 85: 598–603. 15. rhea jt, rao pm, novelline ra. helical ct and three-dimensional ct of facial and orbital injury.radiol clin north am 1999;37:489–513. 16. simonton jt, garber pf, ahl n. margins of safety in lateral orbitotomy. arch ophthalmol 1977; 95: 1229– 1231. 17. who geneva. strategies for the prevention of blindness in national programmes. a primary health care approach, 2nd edn. who library cataloguing: england, 1997, pp 74–76. 18. williams pl, warwick r, dyson m, bannister lh, eds. gray’s anatomy. 35th ed. london: churchill livingstone; 1989:346–347 19. wolff e, ed. anatomy of the eye and orbit. 7th ed. philadelphia, pa:wb saunders; 1976 20. yeh s, foroozan r. orbital apex syndrome. curr opin ophthalmol 2004; 15: 490–498 21. zide bm, jelks gw. surgical anatomy of the orbit. new york, ny: raven press; 1985 doi: 10.33962/roneuro-2022-090 letter to editor the practice of empathy in neurocritical care an important aspect ebtesam abdulla, amit agrawal, rafael cincu, tariq janjua, luis rafael moscote -salazar romanian neurosurgery (2022) xxxvi (4): pp. 494-495 doi: 10.33962/roneuro-2022-090 www.journals.lapub.co.uk/index.php/roneurosurgery letter to editor the practice of empathy in neurocritical care an important aspect ebtesam abdulla1, amit agrawal2, rafael cincu3, tariq janjua4, luis rafael moscote-salazar5 1 department of neurosurgery, salmaniya medical complex, manama, bahrain 2 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india 3 department of neurosurgery, general university hospital, valencia, spain 4 department of critical care medicine, physicians regional medical center, naples, fl, usa 5 colombian clinical research group in neurocritical care, bogota, colombia the dehumanization of medicine has been a subject of debate in recent years with its implications. the dehumanization of medicine has repercussions for the patient, the doctor, and the health team. for the doctor-patient relationship to be successful, it requires an empathetic neurointensivist to the patient's needs. physicians have to communicate and understand patients’ needs, directions, beliefs, and expectations in order to help them therapeutically. through empathy, physicians manage to make adequate professional judgments with an understanding of patient experiences and develop moral behaviors. empathy is defined as a process of the cognitive order with positive repercussions for the doctor [1]. neurocritical care practice is firmly supported by numerous scientific and technological advances. scientists hypothesized that empathy is based on the interaction of its affective and cognitive components [2].it is basically, how to perceive others’ emotions, mentalize the perceived input, and execute mature functions [3]. while treating patient in neurocritical care units particularly in emergency scenarios for example a patient with severe brain injuries, the patient not only the patient himself might be in a position to make decision also many a times family members may not be immediately to make decisions for the patient. in these situations, team members need training, experience, and direction in order to demonstrate empathy for the needs of patients. for treatment consent, neurointensivists keywords empathy, neurocritical care corresponding author: ebtesam abdulla department of neurosurgery, salmaniya medical complex, manama, bahrain dr.ebtesam@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 495 the practice of empathy in neurocritical care an important aspect must describe, with empathy, in the patient's file the reason for every therapy or operation requiring permission for which consent cannot be acquired. waiting for formal permission may delay therapy, care effects, and the end result. to provide effective therapy direction to families with a language barrier, it is necessary to comprehend their thinking. empathy teaches us those patients are highly intelligent in their languages and cultures, regardless of the severe neurological crisis they are experiencing. in contrast, physician burnout is an enduring condition that will likely worsen over time. neurointensivists have the same difficulty, and the current covid-19 epidemic has not improved the situation. there is a greater need for experienced intensivists to be reminded of the need for empathy in neurocritical care and for novice intensivists to get training in this area. a formal patient survey has aided in providing input for the empathy evaluations and development programs [4,5] on the medicolegal side of medical practice, there is a quantifiable effect. since it is a cognitive process, doctors must be multipliers of empathetic behaviors, as empathy can be taught. our icus and neurosurgical teams have a tremendous duty to foster an attitude of empathy. formal workshops [6] and educational seminars may be of assistance. a system to include and impart culture of empathy reated training in education needs to be in place, also more research needs to be performed particularly address the issues faced in critical care settings to find out what can make involved professionals more empathetic. references 1. mercer sw, reynolds wj. empathy and quality of care. br j gen pract. 2002 oct;52 suppl(suppl):s9-12. 2. van dongen jdm. the empathic brain of psychopaths: from social science to neuroscience in empathy. front. psychol. 2020 11:695. 3. preston sd, and de waal fbm. empathy: its ultimate and proximate bases. behav. brain scence. 2022 25, 1–72. 4. howick j, steinkopf l, ulyte a, roberts n, meissner k. how empathic is your healthcare practitioner? a systematic review and meta-analysis of patient surveys. bmc med educ. 2017 aug 21;17(1):136. 5. stewart r, hobbs k, dixon k, et al. perceptions of quality of communication in family interactions in neurocritical care. health sci rep. 2021;4:e411. doi: 10.1002/hsr2.411 6. kang es, genova td, howick j, gottesman r. adding a dose of empathy to healthcare: what can healthcare systems do? j eval clin pract. 2022 jun;28(3):475-482. microsoft word 7.rajendra.docx 294 shrestha et al giant cavernous malformation in the child giant cavernous malformation in the child. case presentation rajendra shrestha1, reeka pradhan2, you chao1 1department of neurosurgery, west china hospital, sichuan university 2international medical school, tianjin medical university, china abstract cerebral cavernous malformations (ccms) are rare lesions that occurs 5 to 13% of all intracranial vascular malformations, develop in 0.02-0.13% of the population. extra axial cavernous malformations are even more rare and estimated to be 0.4 to 2% of all the intra cranial cavernous hemangiomas. ccms that are greater than six cm in size have been described as “giant” in the literature. we report ten year-old male who presented with right lower limb weakness and recurrent seizure disorder. the computed tomography and the magnetic resonance imaging scans demonstrated giant vascular malformation (10cm x 8cm x 6cm) on left parietal lobe. surgical excision of a giant cavernous malformation (gcm) was performed with good surgical skills. to the best of our knowledge, such large gcms are extremely rare lesion seen in neurosurgical practice. key words: cavernous malformation, cavernoma, child, surgery introduction the cavernous malformation (cm), also known as cavernous hemangioma, cavernoma, angioma and cavernous angioma, a well circumscribed, benign vascular hamartoma consisting of irregular thick and thin walled sinusoidal vascular channels located within the brain but lacking intervening neural parenchyma, large feeding arteries or large draining veins. even though there are many names for this phenomenon in world literature, most of these lesion are small and only become clinically significant when they induce seizures, hemorrhage or neurological deficit (2, 7). these lesions have been diagnosed more frequently in the pediatric population. we report a case of giant cavernous malformation (gcms) (10cm x 8cm x 6cm) associated with seizure and hemiparesis which, according to the best of our knowledge, has not been documented previously in the literature. case report a ten year-old-male presented with right lower limb weakness for five years. he was diagnosed with a case of vascular malformation in local hospital a couple of years back but was denied surgical intervention due to fearfulness. he had developed recurrent seizure over the course of two months and referred to our hospital for further management. on admission, patient vitals and parameter were within normal. neurological examination revealed that his right lower leg had grade 4 medical research council (mrc). his upper limbs were normal. bladder and bowel function were not affected. computed tomography (ct) scan revealed mixed density lesion on left parietal region (figure 2a). romanian neurosurgery (2012) xix 4: 294 – 298 295 a b figure 1 axial image t1 (a) and t2 (b) weighted mri showing gcms a mixed signal mass with areas of t2 hypo-intensities suggestive of haemosidren and/or calcification the magnetic resonance imaging (mri) scans demonstrated vascular malformation on left parietal lobe (figure 1a, b). dsa did not illustrate any lesion (figure 2b). after admission, left temporo-parietal craniotomy was done and it was found that the dura was not tense, with no signs of a high intracranial pressure as there was no outward brain swelling. a b figure 2 (a) computed tomography (ct) scanning showing a mixed density lesion in the left parietotemporal region (b) cerebral angiogram of the left carotid artery, no evidence of lesion after opening dura, 10cm x 8cm x cm blue-purple colored mulberry-like lesion tumor down to reach the lateral ventricle was revealed (figure 4a). tumors and brain tissue along the border excised and maintained hemostasis carefully. a complete resection tumor was performed without complication and sent for histopathological examination. post 296 shrestha et al giant cavernous malformation in the child operative event was uneventful and hpe revealed cavernous malformation (figure 4b). and patient transferred to rehabilitation centre. patient did not notice seizure and also good recover in his right lower limb after one month of follow up ct scan (figure 3). figure 3 after one month of follow-up, plain ct scan showing complete excision of the giant ccm a b figure 4 (a) per-operative picture showing gcms (10cm x 8cm x 6cm (b) histopathological examination of the gcms (h&e stain) showing thin walled vascular channels and various organizing thrombi within the cavernous vascular spaces (h&e, ×50) discussion the first comprehensives studies of cms were by cushing and bailey (1928) and dandy (1928) who described a few cases of epilepsy in which large cavernoma were found during exploratory operation, usually for suspected tumour. these lesion natural history and management are being discussed since 1980 in the english literature 8. to date, only a small number of cases have been reported. cms comprise 5-13% of cns vascular malformation; develop in 0.02-0.13% of the population. cms are found throughout the central nervous system in which 48-86% are supratentorial, 4-35% brainstem, 5-10% basal ganglia. they can occur in two types: a sporadic and hereditary. the latter may be transmitted as an autosomal dominant trait which is characterized by multiple lesions. however, the former one, sporadic, is more romanian neurosurgery (2012) xix 4: 294 – 298 297 common as single lesion (7). cms vary in size from a few millimeters to a few centimeters. according to the lawton et al. cms can be defined as giant cms when cavernoma with diameter greater than six cm (5). they are rare in the literatures as we couldn’t found such a big size in literature till date. differential diagnoses include meningioma, arteriovenous malformation, metastasis, infection, and other tumors. the presence of large amounts of hemoglobin degradation products such as methemoglobin, hemosiderin and ferritin around the malformation, seen both pathologically and radiologically with mri, provides evidence of multiple previous episodes of microscopic hemorrhage (3). ct often reveals a hyperdense lesion that enhances little or not at all with contrast administration. these lesions are not visible on angiography and represent the largest percentage of angiographically occult vascular malformations. they usually have little to none of either surrounding edema or mass effect. mri is the diagnostic tool of choice owing to its sensitivity and specificity for these lesions. (1, 9, 10, 13) the clinical presentations of these lesions are variable ranging from headaches to fatal hemorrhage. usual size lesions are usually revealed as incidental findings during investigations for unrelated symptoms. the usual symptoms of a cavernoma are seizure, acute onset of a severe headache, progressive neurologic deficit, hemorrhage and hydrocephalus (7, 9, 12). our case is more interesting as such giant cms not yet present in literature. in our best knowledge, the growth mechanism for these lesions acute or chronic massive hemorrhage, intraluminal thrombosis with recanalization and organization, angiogenesis proliferation with new capillaries, immunohistochemical demonstrated proliferation, nidus growth by new caverns formation, vascular smooth muscle proliferation (3, 4, 8). the treatment of cm still represents a challenge which lesions and in what patients an operation is indicated, because the natural history of these lesions is relatively poorly understood. surgical extirpation of such a lesion is relatively straightforward because there is usually a gliotic plane with evidence of hemosiderin from old hemorrhage around it. bleeding is much less of a problem with cavernous malformations than with arteriovenous malformations even gcms, because there are never large feeding vessels or draining veins. gamma knife surgery shows some promise role by reducing the size of the lesion especially in locations like deep in the brain, brainstem and basal ganglia6. microsurgical resection is the state of the art treatment in all patients whose cm is symptomatic, isolated, and localised in noneloquent regions of the brain (3, 4, 11, 12). our rare case of gcm was also completely removed by microsurgical treatment with rewarding outcome. conclusion microsurgical resection is ideal treatment since the cavernoma is well circumscribed and lacks attachment to the surrounding brain. however, prompt diagnosis and treatment of large intracranial tumors require sound knowledge of neuroanatomy, neuroradiology and good surgical skills. references 1. becker dh, townsend jj, kramer ra, newton th: occult cerebrovas-cular malformations. a series of 18 histologically verified cases with negative angiography. brain 102:249 –287, 1979. 2. delcurling jr o, kelly jr dl, elster ad, craven te: 298 shrestha et al giant cavernous malformation in the child an analysis of the natural history of cavernous angiomas. j neurosurg 1991, 75: 702-8. 3. dong wuk son, sang weon lee, chang hwa choi: giant cavernous malformation: a case report and review of the literature; j korean neurosurg soc 43: 198-200, 2008. 4. kim ds, park yg, choi ju, chung ss, lee kc: an analysis of the natural history of cavernous malformations. surg neurol 48 : 9-17, discussion 1718, 1997. 5. lawton mt, vates ge, quinones-hinojosa a, mcdonald wc, marchuk da, young wl: giant infiltrative cavernous malformation: clinical presentation, intervention, and genetic analysis: case report.neurosurgery 55 : 979-980, 2004. 6. liu kd, chung wy, wu hm, shiau cy, wang lw, guo wy, pan dh: gamma knife surgery for cavernous hemangiomas: an analysis of 125 patients. j neurosurg 102 [suppl]:81 86, 2005. 7. mark s. greenberg (2010): handbook of neurosurgery seventh edition; new york: thieme, page 1106-1107. 8. m. gorgan, angela neacsu, narcisa bucur, v. pruna et. al: update on the natural history of infratentorial cavernous malformations; romanian neurosurgery (2011) xviii 4. 9. ratul raychaudhuri, h. huntington batjer, issam a. awad: intracranial cavernous angioma: a practical review of clinical and biological aspects; surgical neurology 63 (2005) 319 328. 10.rigamonti d, drayer bp, johnson pc, hadley mn, zabramski j, spetzler rf. the mri appearance of cavernous malformations (angiomas). j neurosurg 1987;67:518 24. 11.samii m, eghbal r, carvalho ga, matthies c: surgical management of brainstem cavernomas. j neurosurg 95:825 832, 2001. 12. s. bigi, a. capone mori, m. steinlin, l. remonda, h. landolt, e. boltshauser, cavernous malformations of the central nervous system in children: presentation, treatment and outcome of 20 cases: european journal of paediatric neurology 15 (2011) 109 116. 13. tomlinson fh, houser ow, scheithauer bw, sundt jr tm, okazaki h, parisi je. angiographically occult vascular malformations: a correlative study of features on magnetic resonance imaging and histological examination. neurosurgery 1994;34:792 9 [discussion 799-800]. doi: 10.33962/roneuro-2021-085 cerebral amyloid angiopathy: early presentation in a patient with prior neurosurgical interventions. case report alec clark, arnav barpujari, brandon lucke-wold, ken porche, dimitri laurent, matthew koch, matthew decker romanian neurosurgery (2021) xxxv (4): pp. 499-502 doi: 10.33962/roneuro-2021-085 www.journals.lapub.co.uk/index.php/roneurosurgery cerebral amyloid angiopathy: early presentation in a patient with prior neurosurgical interventions. case report alec clark1, arnav barpujari2, brandon lucke-wold3, ken porche4, dimitri laurent5, matthew koch6, matthew decker7 1 medical student, university of central florida, usa 2 undergraduate student, university of florida, usa 3 md, phd, mcts, pgy4 neurosurgery resident, university of florida, usa 4 md, pgy5 neurosurgery resident, university of florida, usa 5 md, pgy6 neurosurgery resident, university of florida, usa 6 md, assistant professor, department of neurosurgery, university of florida, usa 7 md, mba, mph, assistant professor, department of neurosurgery, university of florida, usa abstract background: cerebral amyloid angiopathy (caa) has classically been described as a disease of the elderly. genetic predisposition has been linked to the apoe e3/e3 allele. evidence suggests that brain insult in the form of injury, prior surgical intervention, or radiation can exacerbate the clearance of toxic proteins in patients susceptible to caa. case: we describe a unique case of caa in a 30-year-old male who had prior surgical interventions for spina bifida, chiari malformation, and hydrocephalus as a child. conclusions: the case is used to teach important components regarding diagnosis, clinical suspicion, and highlight the need for further investigation regarding the emerging role of the glymphatic system and its role in clinical pathology. background ce re b ra l am ylo id an gio pa th y (c aa ) is c h arac te riz e d by th e accumulation of amyloid fibrils along the walls of small to mediumsized arterial blood vessels (1). the pathogenesis of caa remains unknown; however, in most cases of disease presentation, it is presumably caused by an irregular production or diminished clearance of amyloid beta protein (aβ) (1). as a result, there is a significant buildup of aβ protein levels, ultimately leading to its aggregation along the walls of small and medium sized leptomeningeal and cortical arteries (1). impaired vasodilation and alteration in vascular reactivity have been keywords cerebral amyloid angiopathy, glymphatic system, cranial surgery, haemorrhagic stroke corresponding author: brandon lucke-wold department of neurosurgery, university of florida, usa brandon.luckewold@neurosurgery.ufl.edu copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 500 alec clark, arnav barpujari, brandon lucke-wold et al. identified as early markers of the disease (1). collectively, these phenomena bring about oxidative stress, which further propagates the accumulation of aβ (1). a study conducted by yamada et al., investigating amyloid deposition in the brain of human subjects between the ages of 55 to 101 found that the incidence of amyloid deposition increases over time with advancing age. as such, caa is considered a disease of the elderly (2). little is known however if prior intracranial surgery can accelerate caa in predisposed individuals. surgical intervention has the potential to damage healthy brain tissue and can lead to neuroinflammation, which has been postulated to accelerate amyloid pathology. specifically, early surgical interventions can damage the blood-brain barrier (bbb), inhibit neurogenesis in the hippocampus, and lead to neural progenitor cell death. in patients without genetic predisposition for caa, it has been postulated that the glymphatic system helps regulate neuroinflammation and clear toxic protein aggregates. in patients with apoe e3/3, this system may become overwhelmed with insult and result in malfunction (3). additionally, vascular changes may involve early damage to vascular endothelial cells (3). a study conducted by sugihara et al. employed immunohistochemistry to examine 123 autopsy brains from patients aged 30 to 59 (4). in their findings, sugihara and colleagues report that the prevalence of cerebral aβ deposits was two times higher in the patients who had received brain surgical interventions (27.8%) as compared to those who had not (14.8%) (4). moreover, findings from this study also demonstrate that amyloid angiopathy was significantly more evident (p < 0.05) (4). this case report highlights a 30-year-old male who had early childhood surgical intervention for spina bifida, chiari malformation, and hydrocephalus who subsequently developed early onset caa. we postulate potential mechanisms that may have contributed and warrant further investigation. case this case report is of a 30-year-old male who had shunted hydrocephalus, chiari decompression, spina bifida, seizures, and cerebral palsy. he presented originally at age 29 with a right frontoparietal hemorrhagic stroke with multiple other small intracranial hemorrhages including a left thalamic hemorrhage. he required a right decompressive hemicraniectomy with subsequent cranioplasty. workup at that time for col4a and aortopathy was negative. diagnostic angiography was negative for vascular lesion. he was eventually discharged to rehab and made good clinical improvement with return to baseline functioning. figure 1. prior encephalomalacia from previous right frontoparietal intraparenchymal hemorrhage. new acute left frontal hemorrhagic stroke. figure 2. mri/mra consistent with cerebral amyloid angiography but not vasospasm. swi imaging with classic presentation for caa. 15 months after initial hemorrhage he developed symptoms of staring into space, right sided weakness, and aphasia. a left frontal intracranial hemorrhage was noted (figure 1). patient was admitted for further workup. electroencephalography was done with abundant left frontal rhythmic delta activity but no seizures. shunt tap was performed with no infectious or autoimmune etiology including negative findings for meningitis, jc virus, varicella, fungal infection, malignancy panel, antiphospholipid battery, and anca. he was taken for diagnostic angiography where non-specific vasculopathy was noted. magnetic resonance imaging with vasculitis protocol was done and concerning for caa (figure 2). rheumatology was consulted and ct chest, 501 cerebral amyloid angiopathy abdomen, and pelvis (cap) was negative for vasculitis. brain biopsy was completed and pathology was consistent with cerebral amyloid angiopathy and not acute vasculitis. apoe testing was positive for homozygous apoe e3/e3. he was discharged to long-term rehab and has been improving in strength and function. he remains nonverbal but is able to eat with assistance and smiles with family. discussion caa is associated with the accumulation of aβ protein along the blood vessel walls in the brain. it is typically a disease presenting in elderly patients. early-onset disease is generally associated with hereditary forms of caa (5). however, history of prior brain surgery and/or radiation has also previously been shown to be associated with caa in younger patients aged 30-59 (4). there are relatively few reported cases of biopsy-confirmed caa years after initial surgical intervention. no cases have been associated with a specific childhood spina bifida, chiari malformation, or shunted hydrocephalus. however, there has been documented vascular pathology after brain tumor radiation therapy that coincides with diagnostic criteria for cerebral amyloid angiopathy-related inflammation (caa-ri), a subtype of caa (6). roongpiboonsopit et al. demonstrated evidence of cerebral microbleeds (cmbs) in 18/27 patients followed for a median of 4.1 years after craniospinal intervention (7). five of these patients were children (median age 6.3 years). cmbs were primarily found in a lobar distribution which overlaps with the diagnostic criteria for caa-ri, which suggests pathological and potentially functional similarity to caa pathogenesis (6). the exact correlation between history of prior cranial intervention and caa remains unclear. a possible mechanism is decreased clearance of aβ protein. cerebral aβ proteins are cleared through para-vascular pathways (8). the more recently discovered glymphatic system uses peri-vascular channels to facilitate excretion of central nervous system waste products, and has been suggested to play a direct role in aβ protein clearance (9, 10). early surgical intervention could theoretically impair lymphatic aβ clearance, leading to an acceleration of caa. mcrobb et. al suggest another mechanism of early onset caa is the downregulation of adam10, a protein that modulates the production of aβ protein in the brain (11). both of these topics warrant further investigation in pre-clinical studies with subsequent validation from clinical patient samples. conclusion in summary, decreased clearance of aβ protein by impaired glymphatic systems and downregulation of protein modulators may be a contributor to the pathogenesis of caa and should be carefully considered in patients with apoe e3/e3 allele who had prior cranial interventions. other sources of increased aβ production should also be investigated. list of abbreviations: amyloid beta (aβ), blood brain barrier (bbb), cerebral amyloid angiopathy (caa), cerebral microbleeds (cmb), chest, abdomen, and pelvis (cap) references 1. gatti l, tinelli f, scelzo e, arioli f, di fede g, obici l, et al. understanding the pathophysiology of cerebral amyloid angiopathy. int j mol sci. 2020;21(10). 2. yamada m, tsukagoshi h, otomo e, hayakawa m. systemic amyloid deposition in old age and dementia of alzheimer type: the relationship of brain amyloid to other amyloid. acta neuropathol. 1988;77(2):136-41. 3. turnquist c, harris bt, harris cc. radiation-induced brain injury: current concepts and therapeutic strategies targeting neuroinflammation. neurooncol adv. 2020;2(1):vdaa057. 4. sugihara s, ogawa a, nakazato y, yamaguchi h. cerebral beta amyloid deposition in patients with malignant neoplasms: its prevalence with aging and effects of radiation therapy on vascular amyloid. acta neuropathol. 1995;90(2):135-41. 5. zhang-nunes sx, maat-schieman ml, van duinen sg, roos ra, frosch mp, greenberg sm. the cerebral betaamyloid angiopathies: hereditary and sporadic. brain pathol. 2006;16(1):30-9. 6. wu jj, yao m, ni j. cerebral amyloid angiopathy-related inflammation: current status and future implications. chin med j (engl). 2021;134(6):646-54. 7. roongpiboonsopit d, kuijf hj, charidimou a, xiong l, vashkevich a, martinez-ramirez s, et al. evolution of cerebral microbleeds after cranial irradiation in medulloblastoma patients. neurology. 2017;88(8):78996. 8. van veluw sj, hou ss, calvo-rodriguez m, arbel-ornath m, snyder ac, frosch mp, et al. vasomotion as a driving force for paravascular clearance in the awake mouse brain. neuron. 2020;105(3):549-61 e5. 502 alec clark, arnav barpujari, brandon lucke-wold et al. 9. jessen na, munk as, lundgaard i, nedergaard m. the glymphatic system: a beginner's guide. neurochem res. 2015;40(12):2583-99. 10. braun m, iliff jj. the impact of neurovascular, blood-brain barrier, and glymphatic dysfunction in neurodegenerative and metabolic diseases. int rev neurobiol. 2020;154:413-36. 11. mcrobb ls, mckay mj, gamble jr, grace m, moutrie v, santos ed, et al. ionizing radiation reduces adam10 expression in brain microvascular endothelial cells undergoing stress-induced senescence. aging (albany ny). 2017;9(4):1248-68. microsoft word ballaledia_contusion_f.docx romanian neurosurgery (2012) xix 1 contusion injuries of the optic nerve first results in thirty observations ledia balla1, n. ianovici2 1phd student in neurosurgery, “gr.t. popa” umph, iasi 2neurosurgery, clinical emergency “n. oblu” hospital, iasi abstract the paper presents the first results of thirty cases of contusion injuries of optic nerve : an analysis of symptoms and the aspect of visual impairment. indirect injury may damage the optic nerve and this leads to optic nerve contusions. in such cases, the fractures of the base of the skull, involving or not the optic canal, immediately leads to uni or bilateral blindness, stationary or slightly regressive. keywords: optic nerve, visual impairments i have chosen 30 observations and i have studied the patients’ symptoms presented at admission in the clinic in relation to the classical symptoms of the traumatic lesions to the optic nerve described in the literature. the signs or symptoms of traumatic head injuries like dizziness or coma make it impossible to establish the diagnosis during the first hours or days. in terms of cerebral involvement, 21 cases presented simple commotions and 9 cases presented brain contusions followed by coma and late blindness. sometimes, the ophthalmic examination can be difficult to perform due to the localization of the contusion (edema presented in 5 cases). the aspect of visual impairment is different. juge makes the following classification: visual impairments contemporary with the trauma late visual impairments visual impairments contemporary with the trauma may be divided into: 1. immediate unilateral blindness – in 19 cases. for all authors, this is the most frequent emergency (60 – 80%). in these cases, blindness is located on the same side as the trauma. the main signs are: lack of light perception, mydriasis associated with lack of photomotor reflex, and conservation of the consensual reflex. all these were highlighted in 15 cases: in 3 cases – rfm and rc are present in 5 cases – rfm is absent and rc is present in 8 cases – rfm and rc are absent for 2 observations i used a useful notion of semiology, namely the homolateral association of touching the optic nerve and the common oculomotor, association which makes it difficult to establish the diagnosis because in this case there is direct photomotor reflex and abolished consensual reflex on the injured side, and direct photomotor reflex kept and abolished consensual reflex on the healthy side. ledia balla, n. ianovici contusion injuries of the optic nerve 2. bilateral visual impairments – 4 cases. it manifested by blindness in one eye and decrease of visual acuity. fundus examination remains normal for a long time, but after the fifteenth day optic atrophy can be observed. 3. partial visual impairments – immediately after the injury has taken place, in 5 cases. they manifested by decrease of visual acuity in the eye situated on the same side as the injury. late impairments 1. secondary impairments – several hours or days after the injury has taken place. in the studied series, a case presented a decrease of visual acuity (in the left eye) 12 hours after the injury. 2. late impairments – weeks or months after the injury has taken place and have more or less a progressive evolution. the decrease of visual acuity is frequent, the perimetric anomalies are constant, and the fundus examination is normal; sometimes papilloedema and optic atrophy can be observed. during this study, i have met a case in which 2 months after the injury blindness installed progressively in the right eye and there was also a decrease of visual acuity in the left eye. after 6 months, the fundus examination revealed optic atrophy. when we talk about late impairments, we must take into account the possibility of producing a new injury of a different kind as well as the possibility of simulation or excessive fear which is part of the curing process of the injured people. the spontaneous evolution of the impairments shows that they can be transitory, permanent or aggravated (belloni). observation: b.a., aged 45, suffered a head injury left frontal impact three weeks before the admission. immediately after the injury had taken place, he observes a decrease of visual acuity in the left eye which gradually gets better. radiologic examination: suspected left orbital roof fracture, without involving the optical holes. unilateral immediate complete blindness which evolves spontaneously is usually permanent and leads to atrophy within 3 or 4 weeks. ophthalmologic examination case visual acuity fundus examination rfm rc 0 1 2 3 4 5 6 7 8 9 10 1 ai 19 ii re = 0 19 ii pale papilla 2 sp le – nd normal 3 rp 21 iv le p m m 23 iv pd la 20 cm 5 v le pmm 21 iv normal 5 v papillary discoloration + + 4 av le = 0 normal cannot be taken 5 cd 30 xii re = 0 8 i re = 0 30 xii partial discoloration 8 i optic atrophy absent absent 6 pc 6 xi le pd at 50 cm 6 xi temporary discoloration + + 7 us re 0 re atrophy romanian neurosurgery (2012) xix 1 8 ca 30 xii 10 ii le = ¼ re = pmm 30 xii papilla temporary discoloration 10 ii re atrophy le temporary discoloration 9 cg le = 0 normal 10 ec 9 i le = 0 13 i le = 0 19 i le = 0 9 i papilla with deleted edges 13 i papilla with deleted edges 19 i papillary discoloration absent + 11 zi le = 0 atrophy absent absent nerve iii paralysis 12 pv 20 ii re = 0 26 ii re = 0 11 iii re = 0 20 ii normal 26 ii temporary discoloration 11 iii optic atrophy absent 20 ii present 26 ii absent 13 ca 18 x re = 0 le = 1/3 23 x re = 0 le = 1/3 18 x physiological section n.o. 23 x dilacerated papilla absent absent nerve iii paralysis 14 gp re = 0 normal atrophy 15 bp le = 0 re = pmm atrophy 16 pm re = 0 re atrophy 17 rv 14 x 17 x re = 0 27 x od = 0 14 x normal 17 x papillo retinal edema 27 x atrophy intraoperative nerve iii paralysis 18 cv re = 0 le = nd normal absent + 19 dm 22 ii re pmm le nd 4m papilloedema 20 da re with no perception of light nasal pale papilla absent absent 21 ap 29 xii le sees 1 m 22 xii le sees 4 m atrophy 22 rc re = 0 re atrophy absent present 23 bc 13 xi le = 0 19 xi le = 0 13 xi le 19 xi le atrophy 24 td 23 xii re = 0 3 i re = 0 23 xii normal 3 i temporary discoloration absent present 25 frs 22 i le = 0 25 i vague perception of light 25 i normal outlined outlined 26 mi re = 0 absent absent 27 hv 8 i re = pmm 24 i re = 0 8 i normal 24 i normal absent absent 28 re re = 0 normal 29 dd 26 i le = 0 26 i normal absent absent 30 ip 30 i re = 0 30 i normal absent absent ledia balla, n. ianovici contusion injuries of the optic nerve preoperative examinations case blindness rfm mydriasis response external muscles pev fundus examination interval between time of injury and timing of intervention fracture 1 da right eye absent + present normal  right eye – nasal papilla with a slight tightening of the margins.  the rest in normal 7 days 2 ca right eye absent + absent paralysis iii  right eye – nasal papilla with total dilacerations and irregular margins.  traumatic chorioretinitis 3 ai left eye normal  left eye – the papilla was pale 30 days 4 sp left eye – installed progressively 24 hours after the injury normal 7 days conclusions indirect injury may damage the optic nerve and this leads to optic nerve contusions. in such cases, the fractures of the base of the skull, involving or not the optic canal, immediately leads to uni or bilateral blindness, stationary or slightly regressive. after imagistic examination, the fracture path can be visible or not at the level of the optic canal or hole, with no bone fragment compression. references 1. akor c and all ophtalmic plastic and reconstructive surgery journal 2003, 19.5, 466-469 2. andrews dw and all neurosurgery 2002, 51.4, 890 3. castros s and all rev.otoneuroopht. 1960, 32, 57-64 4. juge p. doctoral theses paris 1955 5. katzen j.t and all journal of trauma 2003,54.5, 1026-34 6. lazorthes g, and all ann oculist 1962, 121, 361 7. rocchi g and all surg.neural 2005, 63, 554-564 8. strieff e-b rev. oto-neuro-opht. 1951, 4, 321 9. turner v brain 1942, 66140151 microsoft word iacobg_microsurgicalremoval_f g. iacob et al microsurgical removal of posterior petrosal and petroclival meningiomas microsurgical removal of posterior petrosal and petroclival meningiomas: a report of 8 cases g. iacob, m. craciun, silvia tene clinic of neurosurgery, universitary hospital bucharest românia “meningiomas involve us all in a never – ending quest for technical improvement and less disruptive surgical approaches” gazi yasargil (28) abstract background: posterior petrosal and petroclival meningiomas are rare, benign tumors, representing difficult tumours to be treated by microsurgery: for often significant space-occupying effect, brain stem compression, frequent tight brain stem adherence, as well as encasement of the basilar artery, its perforators and cranial nerves. methods: we report our experience referring on 6 cases of posterior petrosal and 2 cases of petroclival meningiomas operated in the last 5 years; retrospectively analyzed, including: the history, clinical data, imaging studies, surgical & histological records, follow-up records. all patients were woman, the main age was 56 years (range 34-72 years). bony changes at the petrous apex was seen in one case with petroclival meningioma. results: gross total resection was achieved in 7 of 8 patients simson gr.1-2., using a conventional retromastoid, retrosigmoid approach and in one case a petrosal approach. retromastoid retrosigmoid approach was preferred approach for removing posterior petrous meningiomas, used also in one case of petroclival meningioma; especially if preoperative hearing is intact. in all cases the establishment of an arachnoid plane was critical for separating the tumor from the cerebellum and brainstem as well as microdissection of the neurovascular structures. once the tumor was excised, its dural attachment was removed or coagulated and hyperostotic bone was drilled away. tumor histology was fibrous, meningothelial and psammomatous meningioma. after surgery two patients had a transitory palsy of the third (extrinsec) and the seventh nerve, installed immediately after operation, but one patient with a petroclival meningioma operated using the posterior petrosal approach died after a hemorrhagic infarct in the midbrain. no recurrence or progression of disease occurred one year after. conclusions: a variety of techniques have been advocated for complete resection of posterior petrosal and petroclival meningiomas, with minimal brain retraction. for each case planning the safest approach should be sustaind on: detailed radiologic studies to define tumor size, location and extensions, the attachment of the tumor to the dura overlying the posterior face of the petrous apex, tumor encasement of the basilar and pontine perforators, venous anatomy delineation (especially the anatomy of the vein of romanian neurosurgery (2011) xviii 2 labbé). the consistency of the tumor, the operative distance to the tumor and neurovascular structures, minimal brain retraction, good visualization and lighting. the posterior petrosal approach is safe for total removal of clival and petroclival tumor, also for selected cases of petroclival meningioma even a retromastoidretrosigmoid approach can be suitable. keywords: skull base tumor, posterior fossa tumor, posterior petrosal and petroclival meningioma introduction taking account on the point of dural attachment, concerning to the internal auditory meatus and the direction of cranial nerve displacement, which can significantly determine surgery induced morbidity there are several distinct meningiomas (1) (3) (12) (17) (19): petrosal meningioma a hetrogenous group of meningioma in regards to tumor histology, surgical considerations, operative risks and outcome that originate anterior, superior to the internal auditory meatus and posterior to it; petroclival meningioma refer to meningioma that originate in the upper two-thirds of the clivus, at the petroclival junction, near the spheno-occipital synchondrosis, disposed partly supratentorial and partly infratentorial; arise medial to the trigeminal nerve, displace often the brain stem and the basilary artery to the opposite side; clival meningioma originate from the midclivus at the upper two-thirds, encasing typically the basilar artery and its perforators. if these tumors are fibrous and nonsuckable, it’s the most formidable to expose and disect; sphenopetroclival meningioma are the most extensive, invading the cavernous sinus (unilateral or bilateral), sella turcica, sphenoid sinus, involving the bony clivus and the petrous apex. material and methods we report our experience referring on 6 cases of posterior petrosal and 2 cases of petroclival meningiomas operated in the last 5 years; retrospectively analyzed, including: the history, clinical data, imaging studies, surgical & histological records, follow-up records. the main age was 56 years (range 34-72 years), our patients were 6 female, 2 male. the onset of clinical symptoms of our series was insidious: mean 3 month 2 years before admission, with: headaches, dizziness, facial pain and numbness, hearing loss, tinnitus, in one case cerebellar dysfunction and gait ataxia. in one case the patient was admitted for severe ataxia, diplopia, papilledema, with moderate hydrocephalus. imaging studies were based on: native and contrast cerebral ct scan demonstrate: tumor topography, brain stem compression, hyperostosis at the petrous apex in one cases with petroclival meningioma. in one case of a petroclival meningioma a moderate hydrocephalus was recorded. arteriography was performed in all cases to proof the blood supply coming from dural attachment, tumoral blush and the venous stage, especially to delineate to each patient the basal temporal veins, the vein of labbé, their relationship to the superior petrosal sinus, sigmoid sinus with jugular bulb location. cerebral mri using t1, t2, – weighted sequences, fse/stir, tof and resonance venography (mrv) were made to define: tumor (hypointense on t1 – weighted g. iacob et al microsurgical removal of posterior petrosal and petroclival meningiomas sequences, isointense on t2 – weighted sequences, with homogeneous enhancement after iv gd administration), tumor size (between 35 and 6o mm, mean 43,8 mm), tumor origin (6 posterior petrous and 2 petroclival areas). according to the site of tumor origin in reference to the internal auditory meatus we have had: 4 posterior petrous meningiomas, 1 superior petrous meningiomas and 1 ventral petrous meningiomas; involvement of the internal auditory canal by the tumor was detected in 2 cases of posterior petrous meningioma; tumor compression on brain stem and ipsilateral cerebellum in all cases, arachnoid brain stem invasion in 1 case, no tumor extension on temporal bone, sella turcica, sphenoid and cavernous sinus, tumor consistency on t2 details (7 cases of soft tumor and one case of firm petroclival tumor), peculiar venous drainage of the temporal lobe (the vein of labbé and basal temporal veins, bilateral demonstration of the superior petrosal, transverse and sigmoid sinuses), ventricular size and topography (in one case a moderate hydrocephalus was recorded). gross total resection, simson gr. 1-2, using microdissection of tumor and neurovascular structures was achieved in 7 of 8 patients, using a conventional retromastoid, retrosigmoid approach and in one case a petrosal approach. retrosigmoid approach was preferred approach for removing posterior petrous meningiomas, used also in one case of petroclival meningioma of a patient with intact preoperative hearing. this approach has the following advantages: hearing preservation, early drainage of cerebrospinal fluid cisterns allowing cerebellar relaxation. in all cases the establishment of an arachnoid plane was essential for separating the tumor from the cerebellum, compressed brainstem and nerves; suited by intracapsular removal; as well as microdissection of the neurovascular structures. tumor histology in petrous meningioma was: 3 fibrous, 1 meningothelial and 1 psammomatous meningioma. after tumor excision, its dural attachment is removed or coagulated and hyperostotic bone is drilled away. in one case of a petroclival tumor, a posterior petrosal approach (presigmoidian) was used; cutting the superior petrosal sinus respecting the labbé vein, splitting the tentorium. tumor histology in petroclival meningioma was fibrous and meningothelial meningioma. after surgery two patients had a transitory palsy of the third (extrinsec) and the seventh nerve, installed immediately after operation, but one patient died after a hemorrhagic infarct in the midbrain. no recurrence or progression of disease occurred after operation. illustrative cases 1. female, age 62, posterior petrosal meningioma, approach retromastoid, retrosigmoid total resection, hystologic diagnosis: meningothelial meningioma; vii & viii cranial nerves preserved, postop. no deficit (figure 1) 2. female, 44 years old, petroclival meningioma, mild headache, vertigo, left hypoesthesia v1 & v2, left hypoacusia, facial numbness & paraesthesiae insiduous installed 3 months ago, approach retromastoid, retrosigmoid, subtotal resection. a tumor residual 1/1 cm was related to cavernous sinus posterior involvement and bony invasion at the petrous apex. postop. anacusia, transitory palsy of the third (extrinsec) nerve, left facial paresis, despite cn vii, viii preserved (figure 2) romanian neurosurgery (2011) xviii 2 a b c d figure 1 posterior petrosal meningothelial meningioma: a preoperatory, b intraoperatory, c hystologic aspect, d postoperatory a b c d g. iacob et al microsurgical removal of posterior petrosal and petroclival meningiomas e f g figure 2 petroclival meningioma: a-b ct preop, c arteriography, d intraoperatory, e-g ct postoperatory a b c d e f g figure 3 petroclival meningioma: a-b ct preop, c mri preop, d arteriography, e intraoperatory, f fibrous meningioma, g ct postoperatory 3. female, 61 years old, petroclival meningioma, facial pain and numbness, hearing loss, tinnitus, cerebellar dysfunction and gait ataxia; petrosal approach, subtotal resection, hystologic diagnosis (fibrous meningioma), postop. the patient died after a hemorrhagic infarct in the midbrain. (figure 3) discussion posterior petrosal meningioma also known as meningiomas arising from the posterior surface of the petrous bone, cerebello-pontine angle meningioma, posterior fossa meningiomas type ii, iii, iv sekhar classification (1) (5) (13) (15) (17) (19) (26-27) represent a heterogeneous group of tumors in regards to surgical considerations, operative risks, outcome and tumor histology (5) (17) (27). posterior petrosal meningioma are relatively rare, account for approximately 8–23% of intracranial meningiomas or approximately 10–15% of the tumors in the cerebello romanian neurosurgery (2011) xviii 2 pontine angle versus 75% vestibular schwanoma, arise in more varied locations, usually larger than the average vs at presentation (17). according to the site of tumor origin in reference to the internal auditory meatus such tumors should be classified as: posterior petrous meningiomas, superior petrous meningiomas (the most common seventh-eighth cranial nerve complex is usually displaced anteriorly, cranially or caudally, the fifth nerve is frequently displaced cranially or anteriorly) and ventral petrous meningiomas.(5) (15) (17) posterior petrosal meningioma can be asymptomatic for a long period of time or be discovered during cranial imaging for other reasons. in general, clinical symptoms are insidious, lasted from 1 to 4 years. most frequent: facial pain, even on the contralateral side, due to mass effect, hemifacial spasm, facial numbness develop before eighth cranial nerve symptoms (17). if tumor arise near the internal auditory meatus hearing loss, tinnitus, disequilibrium are seen. otherwise if tumor is attached below the internal auditory meatus extending inferiorly near the jugular foramen swallowing difficulty, hoarseness could be seen. in late stages of the disease, depending on their size, symptoms of compression of the pons such as ataxia, gait imbalance, diplopia, papilledema, even obstructive hydrocephalus in 10–20% of these patients were observed (5) (13) (15) (26-27). high-resolution, thin-slice ct scan with bone window may show rarely focal or extended hyperostosis (spicula) in the petrous bone, suggesting the possible origin of the meningioma. the overall tumor size was 11–60 mm (17) (26-27). tumor involvement of the internal auditory canal could be detected in 25% of cases, even osseous hypertrophy ventral to the internal auditory canal at the site of tumor origin. on mri: tumor are well circumscribed, hypointense to isointense on t1 – weighted sequences and isointense to hyperintense on t2 – weighted sequences, with homogeneous enhancement after contrast (gadolinium) administration. t2 sequences are utile to define tumor contact to the brain stem with edema. since information of any possible contact with nerve and vascular structures is mandatory prior to surgical planning, (3d) mp-rage and 3d ciss sequences may be used. dural tail is frequently seen with meningiomas, both on the dura of the petrous bone and the tentorium, but it’s not specific: also some schwannomas and metastases may have dural tail caused by tumor infiltration and/or reactive changes (17). arteriography may show tumoral blush in huge tumors, blood supply comes from dural attachment, usually through branches of the artery of bernasconi-cassinari. embolization should be considered when this artery is particularly large (15). in the case of large tumors it’s possible to see intraor immediate postembolization swelling of the meningioma with cranial nerves ischemia risk. mra is used to define vascular anatomy of the venous system, especially the patency, the size and the ”dominance” of the sigmoid sinus. ct data can be fused with previous mri data for surgical neuronavigation. neuroophtalmologic evaluation, gait analysis, somatosensory and motor evoked potentials, neuropsychological testing, otologic examination and auditory brain stem evoked potentials should complete preoperative evaluation (17). petroclival meningioma are in general, g. iacob et al microsurgical removal of posterior petrosal and petroclival meningiomas rare, benign, deep located tumors of the skull base (3) (11) (14) (19) (22). disposed medial to cranial nerves v,vii, viii, ix, x. xi petroclival meningioma frequently extend to the cavernous sinus, middle cranial fossa, down to the magnum foramen; compress the brainstem, may infiltrate or involve the skull base bone, the dura mater. this tumor is accounting for 3 to 10 per cent of posterior fossa meningiomas, only 1,7 per cent of cushing and eisenhardt’s 205 meningiomas (3). most patient are woman, the average age is in the middle 40’s, with a very wide range. the typical presentation of the petroclival meningioma is that of an insidious onset, with slow, relentless growth, can become enormous before they become apparent clinically (14). the clinical presentation present: headache the most frequent complaint; cranial neuropathies with the fifth (even trigeminal neuralgia associated with contralateral posterior fossa tumors), eighth cranial nerves and facial nerve being the most frequently involved. the lower cranial nerves are involved in nearly one third, more rare cranial nerves iii, iv and vi, despite their proximity and ultimate involvement of tumor; mass effect on the cerebellum with cerebellar signs, which occur in nearly 70% of cases; brain stem compression expressed by long tract signs spastic paresis is reported in 15–57% of patients and somatosensory deficits reported in 15–20% of patients; increased intracranial pressure, either from the tumor mass or obstructive hydrocephalus (14). larger, symptomatic petroclival meningioma or those that show evidence of growth or aggressive features should be treated with surgical resection (still the gold standard of treatment), radiosurgery or conventional fractionated radiation therapy. if in pre microscopic era morbidity & mortality were estimated to ≥ 50%, the petrosal approach and total petrosectomy are the major advancement in total removal of petroclival meningioma, shortening the operative distance to 3 cm, intercepting early the vascular supply to the tumor, exposing the anterior and lateral aspects of the brain stem (11) (22). ct scan examination may reveal (6) bone erosion, hyperostosis, calcifications, a large tumor implantation, slightly hyperintense in comparison with the brain tissue; shows strong contrast enhancement, usually infiltrate the dura mater. high definition mri studies are essential for surgical planning, shows precisely the extension, dura mater infiltration “dura tail sign”, arachnoid invasion – edema in t2 weighted images, displacement and compression of normal structures, relationship of the lesion with vessels (mra), cranial nerves, brain stem (6) (23). by proton mr spectroscopy, meningiomas show marked elevation of the choline peak, very low or no naa, and presence of alanine (at 1.5ppm). dsa is performed when the tumor is seen to be highly vascularized on mri, also do define venous system anatomy (7). an ica balloon test occlusion is performed when the ica is involved. embolization of tumor feeders of the external carotid artery and the meningohypophyseal trunk (bernasconicassinari artery) is performed in selected cases of very highly vascularized tumors (14). for each case planning the safest approach should be sustained on (2) (4-5) (8-11) (14) (16-18) (21-22) (24-25) (29): a. patients age & general condition: preoperative hearing evaluation and deficits b. detailed radiologic studies ct, romanian neurosurgery (2011) xviii 2 high definition mri(fse/stir), ct – based neuronavigation fused images with the mri data, angiography, especially venous stage or magnetic resonance venography (mrv) to define: delination of patient’s anatomy concerning venous system anatomy: venous drainage of the temporal lobe (the vein of labbé, other basal temporal veins and their relationship to the superior petrosal sinus, tentorium, sigmoid sinus), bilateral demonstration of the transverse and sigmoid sinuses, jugular bulb location; tumor origin petrous and/or multiple clival areas attachment, also reference to the internal auditory meatus; tumor extension, cavernous sinus invasion may be a cause of subtotal removal, brain stem compression and arachnoid invasion, extension of dural attachments at the skull base, tumor encasement of the basilar and pontine perforators (in such cases is better to leave a small tumor piece to avoid brainstem infarction, tumor size – smaller the tumor, better the outcome ! significant factor influencing surgical morbidity and mortality, tumor consistency (see t2 details): soft or firm tumor (fibrous and nonsuckable), the operative distance to the tumor and neurovascular structures c. surgeon preferance approach, neuronavigation to create virtual surgical vectors to select a single corridor or a combined approach !; technique, skill and expertise, minimal brain retraction, a judicious application of cytoreductive surgery at the first operation, facilitated by the presence of an intact arachnoidal membrane separating the meningioma from the brain stem, the consistency of the tumor or whether tumor encasement of the basilar and pontine perforators exist; management of the vessels, especially venous structures, cranial nerves, brainstem; mentioning that the first operation provides the best and frequently the only opportunity for total removal, remaining a daunting task! according to sami experience (14) (19), surgery should be the treatment of choice for small petroclival meningiomas (up to 3 cm in diameter); the only chance of cure from this benign tumor. these small lesions can be totally removed (simpson’s grade 1) with preservation of the involved structures. d. technological: microscope, good visualization and lighting, microinstruments, high speed drill, cusa, electrophysiology (cranial nerve monitoring evoked potentials) a variety of techniques have been advocated for complete resection of posterior petrosal and petroclival meningiomas, with minimal brain retraction: suboccipital retrosigmoid (13) (17-18) (25), used mainly for tumors located in the posterior fossa with small extensions into the middle fossa and posterior cavernous sinus (the exposure could be enlarged removing the suprameatal tubercule and the petrous apex; petrosal approach (2) (4) (8) (10) (14) (22) (24) requiring only minimal retraction of the cerebellum, shortening the operative distance to the clivus by 3 cm, offering to the surgeon a direct line of sight to the lesion, also the anterior and lateral aspects of the brain stem, intercepting early in the operation the vascular tumor supply; presigmoid “minipetrosal” approach with variants of transpetrosal or combined approaches (16); combined suboccipitalretrosigmoid with the petrosal approach; subtemporal and retrosigmoid keyhole approach for extensive petroclival meningioma surgery (29). g. iacob et al microsurgical removal of posterior petrosal and petroclival meningiomas complete tumor removal should include: finding an arachnoid plane to separate the tumor from the cerebellum and brainstem; delicate microdissection of the meningioma at its origin from the nerves or their vasculature, internal decompression. once the tumor is excised, its dural attachment is removed or coagulated, the spiculae and hyperostotic bone is drilled away, to remove tumor nodules extending into this bone (14) (22). tumor resection should be made in the sense of „simpson grade 1” as defined by al-mefty et al. (1), especially concerning petrous meningiomas originating posterior to the internal auditory meatus, more fibrous, ingrowing into the internal acoustic canal, other foramina or its origin in the dural lining of these structures; good hemostasis on the origin of the meningioma. in the case of petroclival meningioma for small tumours, if tumor growth is detected on serial magnetic resonance imaging or treatment is desired by the patient, surgery should be the first choice. to patients with advanced age or significant co-morbidities tumor should be observed, in case of tumor growth radiosurgery is a solution. for medium sized tumours to symptomatic patients, surgery is mandatory. in large and giant petroclival meningiomas, tumour resection as radical as possible judged intraoperatively, with decompression of neural structures should be performed and in the case of growing tumour remnants, radiosurgery (20). reported rates of total removal (simpson i) of 86.1% in meningiomas around the posterior petrous bone with dural involvement around the iac – sami et al. and 55% gross total tumor removal (simpson’s grade i and ii) could be achieved in petroclival meningiomas; with a mortality rates between 0%–5% (14). generally better results are seen for the retromeatal tumors as compared to the premeatal tumors, although retromeatal tumors tend to be bigger than premeatal meningiomas (14) (17) (27). conventional radiotherapy, focused radiosurgical techniques, radiosurgery have been used as adjuvant therapy for tumor rests or primary treatment for small (up to 3 cm in diameter) petroclival meningiomas. adjuvant treatment with chemotherapy (hydroxyurea) or hormonal therapy (mifepristone) has been described, but the results were not satisfactory (14). surgical limitations especially in petroclival meningiomas, in spite of all advances in skull-base surgery for total excisions are: age factor (above 70 yrs !), large tumor, encasement of vb system, its perforators, cavernous sinus extension, cranial nerves involvement, brain stem edema (fse /stir mri) & arachnoid invasion. residual tumor growth should be treated by surgery or radiosurgery (4) (24). conclusions good results as measured by tumour control and preservation of quality of life can be achieved in posterior petrosal and petroclival meningiomas using a variety or combined techniques. for each case a judicious intraoperative judgement is mandatory. tumor size, consistency, tumor involvement and invasion of the cavernous sinus, cranial nerves, vessels, pia mater may limit surgical approach. in younger patients surgery should not be delayed because surgical morbidity relates positively with tumour size. in our series the posterior petrosal approach is a major advancement in the safe romanian neurosurgery (2011) xviii 2 and total removal of clival and petroclival tumor; but also the conventional suboccipital retromastoid-retrosigmoid approach can be suitable for a select group of petroclival meningioma providing a direct and early exposure of the lateral and inferior tumor extensions in relationship to the clivus, also the attachment of the tumor to the dura overlying the posterior face of the petrous apex. references 1. al-mefty o. – meningiomas of the posterior cranial base, in operative atlas of meningiomas, lippincottraven publishers 1998; part 3, 209-348 2. al-mefty o., fox j.l., smith r.r. petrosal approach for petroclival meningiomas, neurosurgery 1988; 22, 510-517 3. al-mefty o., smith r.r. clival and petroclival meningiomas, in al-mefty 0. meningiomas, raven press, new york, 1991; 517-537 4. bambakidis nc, kakarla uk, kim lj, nakaji p, porter rw, daspit cp, spetzler rf evolution of surgical approaches in the treatment of petroclival meningiomas: a retrospective review, neurosurgery 2008; 62:1182–1191 5. bassiouni h, hunold a, asgari s, stolke d. meningiomas of the posterior petrous bone: functional outcome after microsurgery, j neurosurg 2004; 100:1014–24 6. carvalho ga, matthies c, tatagiba m, eghbal r, samii m impact of computed tomographic and magnetic resonance imaging findings on surgical outcome in petroclival meningiomas, neurosurgery 2000; 47:1287–1294 7. deda h, erden i, yagmurlu b evaluation of petrosal sinus patency with 3-dimensional contrast-enhanced magnetic resonance venography in petroclival meningiomas for surgical strategy. surg neurol 2005; 64(suppl 2):s67–s71 8. erkmen k., pravdenkova s., al-mefty o. surgical management of petroclival meningiomas: factors determining the choice of approach, neurosurg focus 2005; 19(2) 9. goel a, muzumdar d. conventional posterior fossa approach for surgery on petroclival meningiomas: a report on an experience with 28 cases, surg neurol 2004; 62:3323–40 10.liu jk, gottfried on, couldwell wt. surgical management of posterior petrous meningiomas, neurosurg focus 2003; 14(6):article 7 11.mayberg m., symon, l. meningiomas of the clivus and apical petrous bone. j. neurosurg., 1986; 65, 160167 12.mayberg mr, symon ld meningiomas of the clivus and apical petrous bone: report of 35 cases. j neurosurg, 1986; 65:160–167 13.mehdorn h.m., buhl r.m. petrous meningiomas i: an overview, in lee j.h. – meningiomas, diagnosis, treatment and outcome, springer 2008; 47, 433-441 14.ramina r., fernandes b. y., neto m.c. – petroclival meningiomas: diagnosis, treatment and results, in ramina r., aguiar p., tatagiba m. samii’s essentials in neurosurgery, 2008; 13, 121-134 15.roberti f, sekhar ln, kalavakonda c, wright dc. posterior fossa meningiomas: surgical experience in 161 cases. surg neurol. 2001; 56:8–21 16.roche ph, fournier hd, sameshima t, fukushima t the combined petrosal approach. anatomical principles, surgical technique and indications, neurochirurgie 2008; 54:1–10 17.sade b. and joung h. lee j.h. – petrous meningiomas ii: ventral, posterior and superior subtypes, in lee j.h. – meningiomas, diagnosis, treatment and outcome, springer 2008; 48, 442-447 18.samii m, tatagiba m, carvalho ga. resection of large petroclival meningiomas by the simple retrosigmoid route, j clin neurosci 1999; 6:27–30 19.samii m., ammirati m. petroclival meningiomas, in: schmidek h.h. meningiomas and their surgical management, w. b. saunders co., 1991; 396-403 20.seifert v. clinical management of petroclival meningiomas and the eternal quest for preservation of quality of life, acta neurochir 2010; 152:1099–1116 21.sekhar l.n. et al. surgical excision of meningiomas involving the clivus: preoperative and intraoperative features as predictors of postoperative functional deterioration, j neurosurg. 1994; 81(6), 8608 22.sekhar, l. n., jannetta, p. j.petroclival and medial tentorial meningiomas. in: sekhar l.n., schramm v.s.jr.tumors of the cranial base: diagnosis and treatment, futura, mount kisco, new york 1987; 623-640 23.simis a, pires de aguiar ph, leite cc, santana pa jr, rosemberg s, teixeira mj peritumoural brain edema in benign meningiomas: correlation with clinical, radiologic and surgical factors and possible role on recurrence, surg neurol 2008; 70:471–477, discussion 477 24.tahara a, de santana pa jr, calfat maldaun mv, panagopoulosat, da silva an, zicarelli ca, pires de aguiar ph petroclival meningiomas: surgical management and common complications, j clin neurosci 2009, 16:655–65 g. iacob et al microsurgical removal of posterior petrosal and petroclival meningiomas 25.tatagiba m., acioly m.a. retrosigmoid approach to the posterior and middle fossae in ramina r., aguiar p., tatagiba m. samii’s essentials in neurosurgery, 2008; 14, 146 26.voss nf, vrionis fd, heilman cb, robertson jh. meningiomas of the cerebellopontine angle. surg neurol 2000; 53: 439–47 27.wu zb, yu cj, guan ss. posterior petrous meningiomas: 82 cases, j neurosurg 2005; 102:284–9 28.yasargil g meningiomas of the basal posterior cranial fossa. adv tech stand neurosurg 1980; 7:1–115 29.zhu w, mao y, zhou lf, zhang r, chen l combined subtemporal and retrosigmoid keyhole approach for extensive petroclival meningioma surgery: report of experience with 7 cases, minim invasive neurosurg 2007; 50:106–110 microsoft word rotarescuvirginia_psychotherapy_f.docx romanian neurosurgery (2012) xix 1 psychotherapy of hospitalized patients between option and necessity virginia rotărescu2, alexandru vlad ciurea1 1university of medicine and pharmacy “carol davila”, clinical emergency hospital “bagdasar-arseni”, bucharest, e-mail: rsn@bagdasar-arseni.ro 2clinical emergency hospital “bagdasar-arseni”, bucharest telephone: 0040722516345, e-mail: virginia.rotarescu@gmail.com abstract the existence of reciprocal psyche-soma influence requires a double relationship, medical and psychological; the consequences of poor communication include noncompliance to treatment and malpractice legal actions. this paper provides explanations which necessarily require psychosomatic approach of each patient, the patient reacting massively in psychological plan. delimitation of competence of various specialties is only for the benefit of the patient, who will be investigated and treated according to custom issues (“there are no diseases, only ill people”), imposing thus the integration of the psychologist in the therapeutic team. keywords: neurosurgical, psychotherapy, patient, quality of life, team, multidisciplinary the concept of “health genesis” and maintaining the health triggered the selfcare movement connected with the consumption in other areas of life. due to the improvement of means of investigation and to a more profound specialization, the hospitalized population is less willing to accept the treatment in a passive and uncritical mode; worldwide, there are registered increases in malpractice disputes that presses the hospitals and doctors to inform well the patients about their disease and treatment. this turns the patient from reactive into proactive and triggers its interest of asking questions in which to be responded by providing comprehensive and relevant information, feeling the need of self-assessment of alternatives. the psychological support strengthens the therapeutic act and can use means under the form of beneficial association to medication effects, but also under the form of remodeling some harmful behaviors for health and generating recurrence. man has the power to overcome the instinct and the desire, as well to overcome the motivation of obligation and duty, that i. kant called “rational will”. by the power to regulate his own behavior and to be responsible for his actions, the man gets the right to autonomy, whose value is inherent, intrinsic and infinite. the responsibility for his own decision may cause anxiety or may fail to childishness, but will never be compatible with passivity. recently, the sociologists have suggested that the current psychological environment from hospitals may be harmful to human health. thus, many people are terrified by virginia rotărescu, a.v. ciurea psychotherapy of hospitalized patients hospital because they associate it, on the one hand, with pain and death, and on the other hand they find the clinical atmosphere as frightening and decentralized; some people become angry in hospitals because they are restricted and infantilized by the system, while others become dependent and helpless, unable to make efforts to self-help in their own treatment. the question that must be asked is: “why are so many people stressed by the hospital environment?” first of all, patients are often very ill when they are hospitalized and the disease itself alienates and disorients. the illness produces changes in relations with the patients themselves, with their own bodies and with others. the concern that his own body became object of observation, that the symptoms may become worse, confusions regarding the present; uncertainty about the future undermines the ability to engage in planning, to feel competent, to make decisions, to engage in activities. these aspects of experiencing disease disorientation, isolation, suspension of normal activities, inability to communicate at a normal level are often accompanied by strong emotions such as fear, but also other variables and problematic psychological symptoms. dr. albert schweitzer said in his book “out of my life and thought” (norman cousins, 2011, p.188) the conviction at the time that “if he ever recovered he would never forget his own feelings while ill”; he would try as a doctor to give at least as much attention to the psychology of the patient as he did to a diagnosis. there is a “fellowship of those who tolerate the mark of pain” and those outside this fellowship have great difficulty in comprehending what lies behind the pain. “i know, that during my own illness in 1964, said norman cousins in his book anatomy of an illness (2011, p.188-189), my colleague patients at the hospital would talk about matters they would never discuss with their doctors. the psychology of the seriously ill put barriers between us and those who had the expertise and the abilities to nursing to us. i became convinced that nothing a hospital could provide in the way of technological marvels was as helpful as atmosphere of compassion”. (p.190) the stressful examinations or surgeries and, especially, its results can cause insomnia, nightmares and, in general, inability to concentrate; the hospital care can be very fragmented so that the patient may have contact with 30 different people. often, doctors have little time to waste with patients so that they may receive conflicting information as their search goes to everyone, including acquaintances, friends or other patients. “the central question to be asked about hospitals or about doctors for that matteris whether they inspire the patient with the confidence that he or she is in the right place; whether they enable him to have trust in those who seek to heal him; in short, whether he has the expectation that good things will happen” (cousins, 2011, p.191) the hospital is today a very complex organization, incorporating both historical trends as well as current innovations. sociologists have always been fascinated by the hospital's functions because there are so many and varied: it is a care facility, a treatment center, an institution of learning, research center and laboratory. due to the need of diagnosis and treatment there are necessary different perspectives of approach and specific professional skills. the need of integrative approach (bio-psycho-socio romanian neurosurgery (2012) xix 1 axiological) of the man explains the inclusion of elements of psychology in the composition of medical act, emphasis on psychology today based on recent notions of psycho-neurophysiology, endocrinology and immunology (dănăilă&golu, 2000, taylor, 1986). medical model based strictly on biological dimensions and with a reductionist character is outdated today because the doctor's role is limited to correction of some organic and functional disabilities by pharmacological or surgical ways; the diagnosis itself is determined less by historical data obtained from patients, being based more on imaging means and biochemical investigations. the recent western models, in which therapists work compulsory in team using “linked discipline”, require specialists in psychotherapy, psychologists, physiotherapists or even internists with studies in psychology to investigate and solve the problems of patients with psychosomatic pathology. also in our country, the interference zone between medicine and psychology begins to create a theoretical base and an application area which leads to optimization of medical act and to a worthy position of the human in pain (ciurea & col., 2007; rotărescu & col., 2007, 2006). dual relationship between doctor and patient medical and psychological and the reciprocal influence between psyche and soma necessarily impose the psychosomatic approach to any patient and of which objectives must be accepted by all doctors because the patient reacts massively in psychological plan (enătescu, 1981). the delimitation of the competence of various specialties is only for the benefit of the patient, who will be investigated and treated according to custom issues (“there are no diseases, only ill people”), imposing thus the integration of the psychologist in the therapeutic team (iamandescu, 1997). the clinical observations has managed to bring in the center of medical debate a number of psychological factors that participate directly or indirectly, to the onset and rhythm of the disease (going up to complications or death), often being factors of resistance to treatment or, on the contrary, it may increase. consideration of these factors is not only a goal but an absolute necessity in the medical economy. regarding the nature of suffering for which the patients present to medical consultation, on statistical level was set a percentage of 30% 40% as functional disorders, often psychosomatic (as an expression of acute or chronic stress) which by misinterpretation, may lead to extremist: either ignore of organic causes, or disregard the psychic factor and excessive use of medical assistance. even modern surgery, characterized by the speed of the exercise as well as by increasing the quality of life of the person who had been operated, is threatened by ignoring the existing psychological factor in any doctor-patient relationship; taking into account this factor will help the surgeon to grasp a series of features in which the operator act is accomplished with repercussions on the psyche of the patient but also with a series of positive implications of psycho-therapy attempts or in postoperative recovery dynamics. the psychologist will make a thorough examination, for information purposes, to assess how accurately the current mood is, personality type, ego strength, will and rationality potential deficit caused by the disease. it will work towards inferiority complex to prevent and avoid breaking the attitude of social contacts (obviously, especially to marrowy patients). virginia rotărescu, a.v. ciurea psychotherapy of hospitalized patients with the transition from normal to pathological, a change is being made in the balance of the personality and of the general mode of reporting and integration of the patient in the environment in which the patient is able to overestimate, underestimate or correctly evaluate their physical and mental possibilities, depending on its cultural level, previous to sickness emotional condition, hopes, promises, duration and degree of illness. in such situations, it becomes very important how the subject uses his self-image, especially in terms of feasibility when it comes to ranking or reshaping, the patient should review his future plans. mental disorder and disorientation will be the starting point of the first neurotic symptoms against which the doctor and psychologist must take immediate attitude for the recovery in time of the patients. the psyche deteriorates in the same time with the body and the motor rehabilitation, without a psychic one, give insufficient results; this is one of the reasons why the psychological study of the patients and their mental rehabilitation becomes a first order importance, being even harder to accomplish. most of us recognize that medicine is both art and science, and the most important knowledge to be learned or passed on in medicine is how the mind and body can invoke the hidden resources to cope some extraordinary challenges. building trust in the relationship with your body, is strengthened the conviction that the human mind can discipline the body, they can set goals, may in some way understand the capabilities and the decision to go forward. “however, some experts do not know enough to give a verdict condemning a man and need more attention to what they say to the patients they may be believed and that could be the beginning of the end”(cousins, 2011). all this arguments, sustained in this work, are strongly confirmed by the european norms for medicine in the affirmation of obligatory being there of the psychologist in the medical team. this data are officially confirmed like imperative necessity to the neurosurgical commission from the governmental department of health (ciurea a.v.). references 1. ciurea a.v., davidescu h.b., traumatologie craniocerebrală, editura universitară “carol davila”, bucureşti, 2007 2. ciurea a.v., ciubotaru v.gh., avram e., managementul modern în organizaţiile sănătăţiiperspective în serviciile de neurochirurgie, editura medicală, bucureşti, 2009 3. cousins n., anatomia unei boli. aşa cum a fost percepută de pacient, editura herald, bucureşti, 2011 4. dănăilă l., golu m., tratat de neuropsihologie, vol.i, editura medicală, bucureşti, 2000 5. enătescu virgil, dialogul medic-bolnav, editura dacia, cluj-napoca, 1981 6. iamandescu i.b, psihologie medicală, editura infomedica, bucureşti, 1997 7. rotărescu v., milea şt., ciurea a.v., the psychological intervention specific particularities for the early prevention in the families with a neuraxis injured parent-pilot study, lucrările conferinţei „centenarul psihologiei la universitatea din bucureşti, 26-29 octombrie 2006”, partea a ii-a, editura universităţii din bucureşti, 2007, p.891-903 8. rotărescu v., milea şt., ciurea a.v., quality of life in family with a parent central nervous sistem injured, lucrările conferinţei „centenarul psihologiei la universitatea din bucureşti, 26-29 octombrie 2006”, partea a ii-a, editura universităţii din bucureşti, 2007, p.877-889 9. rotărescu v., milea şt., oancea c., popa-mihalache e., the profile of the families refusing preventive services and the reasons for this refusals(romanian experience), revista de psihologie, tomul 52, nr.1-2, editura academiei române, bucureşti, ianuarie-iunie 2006, p.123-134 10.taylor e. shelley, health psychology, random house, new york, 1986 doi: 10.33962/roneuro-2021-090 aneurysmal subarachnoid haemorrhage in the context of a patient with traumatic brain injury william florez-perdomo, laura acevedo-aguilar, laura mass-hernández, michael gregorio ortega-sierra, j.a. jiménez-filigrana, luis jose payares-celins, roberto andrés ramos-cordoba, jorge alberto nuñez -gamez romanian neurosurgery (2021) xxxv (4): pp. 526-530 doi: 10.33962/roneuro-2021-090 www.journals.lapub.co.uk/index.php/roneurosurgery aneurysmal subarachnoid haemorrhage in the context of a patient with traumatic brain injury william florez-perdomo1, laura acevedo-aguilar2, laura masshernández2, michael gregorio ortega-sierra1,2, jhoyner alberto jiménez-filigrana3, luis jose payares-celins4, roberto andrés ramoscordoba5, jorge alberto nuñez-gamez6 1 colombian clinical research group in neurocritical care, latin american council of neurocritical care, cartagena, colombia 2 medical and surgical research centre, st mary´s medical group, cartagena, colombia 3 school of medicine, universidad el bosque, bogotá, colombia 4 school of medicine, universidad de sucre, sincelejo, colombia 5 school of medicine, universidad juan n. corpas, bogotá, colombia 6 school of medicine, universidad del sinú, cartagena, colombia abstract introduction: traumatic brain injury is a major public health problem worldwide, with higher incidence rates in lowand middle-income countries. in this context, the development of major complications has been evidenced, such as the formation of haemorrhages due to traumatic rupture of a cerebral aneurysm, which may threaten the patient's life and therefore require immediate medical and neurosurgical procedures. case: we present the case of a male patient in the fourth decade of life, who presented a closed head trauma with the consequent development of subarachnoid haemorrhage in the territory of the right middle cerebral artery secondary to traumatic aneurysmal rupture conclusion: one of the complications that can occur in the context of head trauma is the development of subarachnoid haemorrhage due to traumatic aneurysmal rupture. despite therapeutic options, these scenarios continue to be a challenge in lowand middle-income countries due to the lack of specialized tools in neurosurgical and neurorehabilitation areas. introduction traumatic brain injury (tbi) is a major public health problem worldwide [1], representing a significant cause of disability and mortality in the population of all ages along with a great socioeconomic impact, its main causes being falls and traffic accidents [2,3]. globally, it is estimated that keywords traumatic brain injury, subarachnoid haemorrhage, aneurysmal rupture, neurorehabilitation corresponding author: michael gregorio ortega-sierra medical and surgical research centre, st mary´s medical group, cartagena, colombia mortegas2021@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 527 aneurysmal subarachnoid haemorrhage in the context of a patient with traumatic brain injury between 60 and 70 million new cases of tbi occur each year, with high incidence rates that varies considerably between different parts of the world and have been increasing especially in lowand middle-income countries [4,5]. it has also been shown that a large number of these cases will develop complications that can threaten the patient's life and therefore require immediate medical and neurosurgical procedures [6]. among these complications is an increased risk of rupture of pre-existing cerebral aneurysms with the consequent formation of hemorrhages, due to the altered hemodynamics of cerebral blood flow in the context of neurotrauma [7]. the aim of this manuscript is to present a case of traumatic subarachnoid hemorrhage secondary to silent aneurysmal rupture and discuss aspects related to the limitations in the diagnosis and approach in lowand middle-income countries such as colombia. case description a 34-year-old male patient was admitted to the emergency department of a low-level hospital presenting closed head trauma secondary to a traffic accident as a motorcyclist, with scalp injury, headache, loss of consciousness, without convulsions, nausea or vomiting, muscle weakness, loss of sensation or visual disturbances. no personal or family medical pathological history. on physical examination on admission, the patient had a blood pressure of 100/70 mmhg, heart rate of 93 beats per minute, respiratory rate of 21 breaths per minute, oxygen saturation of 98% while breathing ambient oxygen, weight of 85 kilograms and height of 1.82 meters. in addition, he presented alcoholic breath. on neurological examination there was evidence of temporal and spatial disorientation, ocular opening when called, glasgow scale of 13, normal pupillary response, fundus without papilledema, normal venous and arterial pulses, normoreflexia, no muscle weakness and preserved sensation. initial paraclinical tests showed hemoglobin within normal limits. he did not present neurological deterioration, however, due to a history of alcohol consumption, a simple cerebral computed tomography was requested, which showed subarachnoid hemorrhage in the right middle cerebral artery territory in segment m2, with the presence of blood in the interhemispheric cistern and in the perimesencephalic cisterns with intraparenchymal hematoma in the sylvian valley (figure 1). due to the location of bleeding, aneurysmal hemorrhage is suspected. it was decided to refer to the neurosurgery department, who indicated cerebral angiography with endovascular management of aneurysm, where a ruptured aneurysm of m2 segment of 6 mm in diameter was found (figure 2). it is managed endovascularly with coils, no flowdiversifying stents were placed. during his stay in the icu, the patient showed no neurological deterioration, no evidence of rebleeding or vasospasm; however, he presented cough, deterioration of the ventilatory pattern with bilateral pulmonary rales and fever with a temperature of 39°c. antibiotic management with ampicillin/sulbactam 3 grams intravenously every 8 hours is indicated. she presented positive rt-pcr for sars-cov-2. patient died 3 days later due to covid19 pneumonia. figure 1. computed axial tomography of the brain without contrast 2 hours after trauma. discussion tbi is a major cause of morbidity and mortality worldwide [1]. incidence rates vary significantly in different parts of the world, with a greater burden in lowand middle-income countries [2,4]. likewise, the highest incidence occurs in adolescents and young 528 william florez-perdomo, laura acevedo-aguilar, laura mass-hernández et al. adults and in the population over 65 years of age, with the most frequent responsible events being traffic accidents and falls, respectively [3]. figure 2. angiography showing right middle cerebral artery aneurysm. a: before endovascular management. b: aneurysm with total occlusion (100%). most of the patients with tbi will develop serious complications that demand immediate medical and surgical measures in order to safeguard the patient's life [6]. traumatic aneurysmal rupture is one of the complications to be taken into account since trauma can cause various cerebrovascular damages that can affect the integrity of a pre-existing cerebral aneurysm, leading to subsequent hemorrhage formation [7]. aneurysmal subarachnoid hemorrhage, as described in our case, represents a serious and complex phenomenon in which there is extravasation of blood into the subarachnoid space as a consequence of an aneurysm rupture [8]. in this context, it is extremely important to provide an adequate and timely multidisciplinary approach in order to achieve satisfactory results [9]. considering the above, early management, during the first 24 hours, of aneurysmal subarachnoid hemorrhage, will be directly related to a better prognosis, reduction of neurological involvement, and possible complications associated with this medical emergency, such as rebleeding, cerebral vasospasm, arrhythmias, pulmonary edema, among many others [10,11]. the initial approach to patient management should consist first of support and monitoring of vital signs, assessing the need for airway intervention to protect oxygen saturation [12] and then establishing the appropriate treatment to stop bleeding, through two options, either by placing clips at the neck of the aneurysm in a craniotomy or through endovascular treatment consisting of embolization of the lesion by means of platinum coils, as in our case [11]. clipping surgery is indicated in patients with large intraparenchymal hematomas, middle cerebral artery aneurysms, wide neck aneurysms, and in patients who are unlikely to comply with long-term follow-up [13]. while endovascular treatment is preferred in patients older than 70 years, in severe aneurysmal subarachnoid hemorrhages and basilar artery aneurysms [14]. in order to establish the differences between endovascular treatment and clipping surgery, several studies have shown a lower percentage of mortality and disability at one-year follow-up in those patients managed with endovascular therapy compared to clipping surgery [15], while on the other hand, the latter has shown a slightly lower rebleeding rate. because of this evidence, both procedures are considered valid and the choice of one or the other goes hand in hand with the individualization of each patient [16]. however, it should be noted that, although low and middle-income countries, especially in latin america, have the highest mortality and disability figures associated with trauma, it is in these countries where neurosurgical interventions, as well as scientific studies and advances in the areas of neurology and neurorehabilitation, continue to be a challenge for the future [17]. the prognosis of a patient suffering an aneurysmal subarachnoid hemorrhage depends on multiple factors such as the patient's comorbidities, age, bleeding volume, early management, and above all the state of consciousness, in fact 15-25% of patients are left with neurological sequelae [9]. the rehabilitation process is very dynamic, motor and psychomotor recovery often occurs after the first six months, but verbal memory and other cognitive aspects may require much more time, even after the first year [18]. according to the pan american health organization, only 3% of people with neurological disabilities in latin america have access to neurorehabilitation services, as a consequence of a significant lack of resources due to underfunding and poor infrastructure of the health systems in these countries [19,20]. thus, based on this problem, it is of vital importance to establish support and funding strategies that allow the advancement of neuroeducation and neurorehabilitation in lowand 529 aneurysmal subarachnoid haemorrhage in the context of a patient with traumatic brain injury middle-income countries, in order to maintain and rehabilitate the patient's functionality and thereby reduce the high percentages of disability caused by neurotrauma [19,21,22]. as an example, it would be of great importance the implementation of robotic neurosurgery in these countries, being an innovative tool that has allowed a great advance in developed countries in the context of diagnostic and therapeutic approaches, providing great satisfactory neurosurgical results along with the consequent reduction of patients with disabilities due to greater ease in the course of neurorehabilitation [17]. conclusions aneurysmal subarachnoid hemorrhage is one of the complications that can occur after traumatic brain injury. this entity leads to a rather late recovery process of psychomotor and cognitive abilities of patients, so early diagnosis and management are the fundamental basis for achieving more satisfactory results. however, despite the different therapeutic options currently available, high morbidity and mortality rates continue to occur, especially in low and middle-income countries, as a consequence of deficits in access to adequate neurosurgical and neurorehabilitation tools. references 1. maas a. traumatic brain injury: changing concepts and approaches. chinese journal of traumatology. 2016; 19:3-6. 2. nguyen r, fiest km, mcchesney j, kwon cs, jette n, frolkis ad, et al. the international incidence of traumatic brain injury: a systematic review and meta-analysis. can j neurol sci. 2016; 43:774-785. 3. galgano m, toshkezi g, qiu x, russell t, chin l, zhao lr. traumatic brain injury: current treatment strategies and future endeavors. cell transplantation. 2017; 26(7): 1118-1130. 4. maas air, menon dk, adelson pd, andelic n, bell mj, belli a, et al. traumatic brain injury: integrated approaches to improve prevention, clinical care, and research. the lancet neurology. 2017; 16(12):987-1048. 5. dewan mc, rattani a, gupta s, baticulon re, hung yc, punchak m, et al. estimating the global incidence of traumatic brain injury. j neurosurg. 2019; 130:1080-1097. 6. ortega jm, lomillos n, choque b, tamarit m, poveda p, lópez mr, et al. traumatismo craneoencefálico leve. rev argent neuroc. 2017; 31(3):139-150. 7. razaghi r, biglari h, karimi a. risk of rupture of the cerebral aneurysm in relation to traumatic brain injury using a patient-specific fluid-structure interaction model. computer methods and programs in biomedicine. 2019; 176:9-16. 8. ortega jm, calvo m, lomillos n, choque b, tamarit m, poveda p, et al. hemorragia subaracnoidea aneurismática: avances clínicos. neurol arg. 2017; 9(2):96-107. 9. hoyos-castillo jd, moscote-salazar lr. hemorragia subaracnoidea aneurismática con mal grado clínico: revisión clínica. revista mexicana de neurociencia. 2016; 17(1):1-113. 10. galofre-martínez mc, ordosgoitia-morales j, ripollzapata v, morales-núñez ma, corrales-santander hr, moscote-salazar lr. manejo neurointensivo de la hemorragia subaracnoidea aneurismática. revista cubana de medicina intensiva y emergencias. 2020; 19(3):e523. 11. vivancos j, gilo f, frutos r, maestre j, garcía-pastor f, quintana f, et al. guía de actuación clínica en la hemorragia subaracnoidea. sistemática diagnóstica y tratamiento. sociedad española de neurología. 2014. 29(6):353-370. 12. flores ka, quiñonez kj, flores dl, cárdenas ca. actuación clínica en la hemorragia subaracnoidea. recimundo. 2020; 4(1):256-267. 13. sharma d. perioperative management of aneurysmal subarachnoid hemorrhage. anesthesiology. 2020; 133:1283–305. 14. brenes mj, romero a, jiménez m. abordaje de hemorragia subaracnoidea. revista médica sinergia. 2020; 5(10):e589. 15. sabogal-barrios r, cabrera-gonzáles a, de lima-zea a, lambertinez-alvarez i, pérez-calvo c, pájaro-galvis n. hemorragia subaracnoidea aneurismática. archivos de medicina. 2020; 16(6):17. 16. lindgren a, vergouwen md, van der schaaf i, algra a, wermer m, clarke mj, et al. endovascular coiling versus neurosurgical clipping for people with aneurysmal subarachnoid haemorrhage. cochrane database syst rev. 2018; 8(8):cd003085. 17. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, moshiur rahman md, pachecohernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. 18. hammer a, ranaie g, yakubov e, erbguth f, holtmannspoetter m, steiner hh. dynamics of outcome after aneurysmal subarachnoid hemorrhage. aging. 2020; 12(8). 19. ortega-sierra mg, durán-daza rm, carrera-patiño a, rojas-nuñez ax, charry-caicedo ji, lozada-martinez id. neuroeducation and neurorehabilitation in the neurosurgical patient: programs to be developed in latin america and the caribbean. journal of neurosurgical sciences. 2021. 20. ashfaq a, lazareff j. language and style: a barrier to neurosurgical research and advancement in latin america. surg neurol int. 2017; 8:308. 530 william florez-perdomo, laura acevedo-aguilar, laura mass-hernández et al. 21. muñoz-baez k, del castillo am, garcía-araujo hj, padrónechenique cj, martínez-bohórquez jm, lozada-martínez id, et al. latin american collaboration in global neurosurgery: challenges and difficulties persist. international journal of surgery open. 2021; 33:100355. 22. mila-grande jc, granadillo-daza ri, agudelo-rios da, lozada-martinez id. regarding: management of unfavorable outcome after mild traumatic brain injury: review of physical and cognitive rehabilitation and of psychological care in post-concussive syndrome. neurochirurgie. 2021; s0028-3770(21)00165-x. microsoft word 4.rotariud_malignanttransformation romanian neurosurgery (2010) xvii 4: 403 – 412 403 malignant transformation of low grade gliomas into glioblastoma a series of 10 cases and review of the literature d. rotariu1, s. gaivas1, z. faiyad1, d. haba2, b. iliescu1, i. poeata1 departments of neurosurgery1 and radiology2 , “gr.t. popa” university of medicine and pharmacy, iasi, romania abstract background: diffuse infiltrative low-grade gliomas (lgg) of the cerebral hemispheres in the adult are tumors with distinct clinical, histological and molecular characteristics. who (world health organization) classification recognizes grade ii astrocytomas, oligodendrogliomas and oligoastrocytomas. conventional mri is used for differential diagnosis, guiding surgery, planning radiotherapy and monitoring treatment response. advanced imaging techniques are increasing the diagnostic accuracy. lowgrade gliomas have been documented to undergo transformation into high-grade gliomas, and the time interval of this transformation has been reported to generally occur within 5 years in about 50% of patients diagnosed with low-grade gliomas. methods: we have reviewed all adult patients operated on for hemispheric glioblastoma at n oblu hospital in iasi between 2006 and 2009 and in particular those patients with secondary glioblastoma. results: from the total 110 cases of glioblastoma, ten of them were secondary to malignant transformation of an previously operated low grade glioma. of the 10 patients with secondary glioblastoma, the initial histology was: gr ii astocytoma in 6 cases, oligoastocytoma in 2 cases and in oligodendroglioma in 2 cases. the mean patient age was 46.1± 0.9 years and the most frequent symptom was represented by seizures 70%, the mean time from the first symptom to diagnosis was 11,2 months. 40% of the cases had subtotal resection and 60% had total resection (defined by the surgeon at the time of operation). 5 patients received radiotherapy postoperatively, 2 received both radio and chemotherapy and 3 had no adjuvant treatment. in our series the median time to malignant transformation was 32,5 months. conclusions: younger age, normal neurological examination and oligodendroglial histology are favorable prognostic factors, total/near total resection can improve seizure control, progressionfree and overall survival, mean while reducing the risk of malignant transformation. early post-operative radiotherapy improves progression free but not overall survival. chemotherapy can be useful both at recurrence after radiotherapy and as initial treatment after surgery to delay the risk of late neurotoxicity from large-field radiotherapy. keywords: astrocytoma, low-grade glioma, glioblastoma, oligodendroglioma, malignant transformation 404 d. rotariu et al malignant transformation of low grade gliomas low-grade gliomas are primary brain tumors classified as grade i and ii by the who grading system (14, 27) and occur primarily in children and young adults. the most common lggs are the who grade i pilocytic astrocytomas and the who grade ii diffuse astrocytomas (include fibrillary, gemistocytic and protoplasmic variants), oligodendrogliomas, and mixed oligoastrocytomas. it is important to separate gemistocytic astrocytoma, because it is more prone to malignant progression patients with low-grade gliomas have a more favorable prognosis than patients with high grade glioma the median survival for patients with low-grade gliomas is between 5 and 10 years (6, 9, 10, 13, 19) compared with a survival of only 14 months in patients with malignant glioma (gbm) (28). despite this more favorable prognosis, patients with lggs may survive for up to 20 years, in 50–75% of patients with lowgrade gliomas the tumors grow continuously and tend to progress to a higher grade, leading to neurological disability and ultimately to death (8, 24) in adults there are numerous prognostic factors reported in various prospective studies that have been shown to affect survival in patients with lgg, the most consistent are histological type, patient age, extent of resection (using postoperatively mri imaging), and tumor size. pilocytic astrocytomas, regardless of site (cerebral hemispheres, cerebellum, or spinal cord), are associated with a 10-year patient survival rate of ~ 80%, (6, 11, 14) but the rate is 100% in the subset of patients with brain tumors who undergo gtr. (3, 22) within the diffuse lgg group there is a significant difference in patient outcome based on histological tumor type. the factors consistently shown to be associated with improved survival8 for patients with gliomas are younger age, (13, 23) higher kps scores, (18) oligodendroglioma pathology, (17) postoperative radiation therapy, (25) and gtr. (1, 15, 26) the only factors that have been consistently shown to be associated with tumor recurrence (8) or malignant degeneration are preoperative contrast enhancement, (11, 12) tumor size, (1, 11) and str. (1, 3) methods we have analised all the patients operated on at 3rd neurosurgical department in n oblu hospital for malignant glioma between 2006 and 2009 and from the total of 110 cases ten percent of the malignant glioma were secondary to a malignant transformation of a low grade glioma. our point of interest was represented by the patients with initial diagnostic of low grade gliomas.. patients ≥ 18 years old with tissue-proven diagnosis of a hemispheric who grade i or ii glioma (fa, oligodendroglioma, or mixed glioma) (14) at the initial diagnosis, supratentorial tumor location and adequate (> 6 months) clinical follow-up and imaging reports were included in the study. patients with, who grade iii or iv glioma including anaplastic astrocytoma, glioblastoma multiforme, anaplastic oligodendroglioma, or anaplastic mixed oligoastrocytoma at the initial operation; nonsupratentorial tumor location including optic chiasm, optic nerve(s), pons, medulla, cerebellum, or spinal cord; prior malignancy unless disease free ≥ 5 years were excluded. romanian neurosurgery (2010) xvii 4: 403 – 412 405 the clinical, operative, and hospital course records were reviewed. information collected from clinical notes included patient demographics, age, presenting symptoms and signs, the interval between the first symptom and diagnostic, preand postoperative neuroimaging, extent of resection, postoperative neurological function, adjuvant therapy (radiotherapy and chemotherapy)medication history such as steroids and anticonvulsants. preoperative mr images, including t1weighted images with and without contrast enhancement as well as t2-weighted images (and flair images when available), were required. the preoperative tumor presence or absence of contrast enhancement was recorded. perioperative death was defined as death within 30 days of surgery. tumor recurrence was defined as any definitive evidence of tumor recurrence or progressive growth on mr imaging as per the neuroradiology reports. malignant degeneration was defined as either a notable increase in tumor contrast enhancement and/or a histopathologically proven malignant degeneration in tissue acquired during biopsy or resection (who grade iii or iv). results from all of low grade gliomas operated on between 2006 – 2009 ten of them have suffered malignant transformation. all the patients have underwent primary and secondary resection, 60 percent of the cases were secondary to grade ii astrocytomas (diffuse astrocytoma), 20 percent were secondary to oligodendroglioma and another 20 percent were secondary to oligoastrocytoma. the mean patient age was 46.1± 0.9 years, and 8 (80%) patients were male. the initial symptom was represented by seizures in 7 cases followed by motor impairment in 2 cases and rise intracranial hypertension in 1 case. the mean time from the initial symptom to diagnosis was 11.2±1.6 months. in our series 80% of the tumors were limited to a single cerebral lobe and in 20% there were involved 2 lobes, the most frequent affected lobe was the frontal lobe (6 cases) followed by the parietal lobe (5 cases). all of our cases had involvement of functional structures , in 6 cases there were functional areas involved, 2 cases involved the bazal ganglia and another 2 cases involved vascular structures (cavernous sinus, carotid artery). as treatment 4 patients had subtotal surgical resection and 6 total resection (as defined by the neurosurgeon at the time of surgery) . the main complication was represented by hematoma in the tumoral bed wich was observed in 30% of the cases. 50% had radiotherapy postoperatively 20% had both radio and chemotherapy while 30% recived non of them. the median time to malignant transformation in our series was 32.5 months. (figure 1 and table 1) figure 1 time to malignant transformation 406 d. rotariu et al malignant transformation of low grade gliomas table 1 characteristics of malignant transformed low grade gliomas series case 1 case 2 case 3 case 4 case 5 case 6 case 7 case 8 case9 case 10 sex m m m f m m m m m f age 42 41 37 55 59 45 60 39 50 33 1st sign seizures seizures seizures left hemiparesis seizures partial seizures jacksonian seizures olfactive seizures right hemiplegia ricp sindrome t to dg (months) 2 36 30 1 2 2 10 3 `2 1 loc f ftp f p p p f fti p fti funct areas 1 1 1 1 1 1 bazal ganglia 1 1 vascular srtucture 1 1 biopsy str 1 1 1 1 gtr 1 1 1 1 1 1 dg ap gr ii astrocytoma gr ii astrocytoma gr ii astrocytoma oligodendroglioma oligodendroglioma gr ii astrocytoma oligoastrocytoma oligoastrocytoma gr ii astrocytoma gr ii astrocytoma postop complic meningitis local hematoma local hematoma local hematoma rxt 1 1 1 1 1 rtx+cht 1 1 cht reinterve ntion (months) 52 29 28 23 84 40 16 54 36 21 pfs (months) 48 23 27 21 84 40 16 42 36 21 ap at reintervention gbm gbm gbm gbm gbm gbm gbm gbm gbm gbm momonths, f-frontal, p-parietal, t-temporal, i-insular, gbm-glioblastoma multiforme, pfsprogression free survival, dg apanatomopathological exam, t to dg-time to diagnosis, rxt-radiotherapy, chtchemotherapy, str-subtotal resection, gtr-gross total resection next we will present two eloquent cases from our series: case i 33 y o female presented for seizures for about 6 months, the mri scan (figure 2a) show a hipointense ftp lesion without contrast enhancement, she was operated using a pterional approach with subtotal resection, and the anatomopathological result was gr ii astrocytoma. the patient went for romanian neurosurgery (2010) xvii 4: 403 – 412 407 radiotherapy and she had 6 cure of linac. at 9 months the patient was asymptomatic and the mri study show a stabile lesion with no signs of progression or contrast enhancement (figure 2b), the same aspect is observed at 21 months postoperatively (figure 2c). at 22 months postop she came for right brachial monoparesis and depression the mri scan show 2 areas of contrast enhancement (figure 2d) and programmed for a pet scan wich was performed 1 month later wich show an hipermatabolic are in the right temporal pole (figure 2e). she went for a second surgery with subtotal resection of the lesion and the anatomopathological result was glioblastoma multiforme. postop the patient had a difficult evolution and the ct scan 1 month later showed a multicentric localization with involvement of both cerebral hemispheres (figure 2 g-h). case ii 42 y old male presented for seizures for over 2 months and rised icp syndrome, the ct scan with contrast enhancement show the lesion without contrast enhancement in the left frontal pole (figure 3a), the patient was operated on (gtr) and the histology was gr ii astrocytoma, he went for radiation therapy (6 cure of linac), at 4 months the patient was asymptomatic and the mri exam show no signs of recurrence (figure 3b), at 12 months the patient had no neurological impairment and the mri show a stable aspect with a hyperintense lesion in t2 in the left frontal pole (figure 3c) (scar secondary to surgery and radiotherapy) and we decided to go for surveillance and the mri at 30 months postoperatively show no signs of progression or recurrence, same aspect as previous mri exam) (figure 3d). figure 2 a. axial t1weighted contrast enhanced mri image show ftp area of hiposignal without contrast enhancement, b. and c. images obtained 9 and 21 months later at the same patient after surgery and 6 cure of linac stable images, d. axial mri images at 22 months are sowing 2 areas of contrast enhancement which weren’t present on the previous exam, e. pet scan is showing an area of hipermetabolism in the right temporal lobe and f. the correspondent images on t1-weighted with contrast enhanced mri image g. and h. at 23 months after second surgery ct images obtained 1 month later show involvement of both cerebral hemispheres 408 d. rotariu et al malignant transformation of low grade gliomas figure 3 a. computer tomography with contrast enhancement show a izointense lesion without contrast enhancement without mass effect and surrounded by edema, b. mri t2 axial image hyperintense area in the left frontal lobe at 4 months postoperatively and after radiotherapy, c. mri exam at 12 months t2 axial shows a stable hyperintense lesion in the left frontal pole surrounded by minimum edema (arrow), d. t2 axial at 30 months the lesion is stable with disappearance of edema, e. mri exam at 52 months t1 with contrast enhancement show a hypointense lesion (thick arrow) in the left frontal pole and a thin rim of contrast enhancement (thin arrow) but at 56 months the patient presented for memory impairment, the mri exam with contrast enhancement (figure 3e) showed in t1 a hypointense lesion located within 2 cm from the previous tumoral bed with a thin rim of contrast enhancement without perilesional edema, we decided for reintervention and the patient was operated on using the old approach with gross total removal appreciated by the surgeon at the time, the histology this time was glioblastoma multiforme and he was sent to the oncology clinic for chemotherapy (temozolamide) and further surveillance. discussion the annual incidence of low grade glioma is about 4700 cases per year (27), which makes them onethird as common as their higher grade counterparts.4 this relatively low incidence has prevented the development of standardized treatment protocols. (2, 22) treatment may include surveillance, biopsy, surgery, radiotherapy, or chemotherapy, and varies among different centers, location, and clinical presentation. (22) the majority of these tumors undergo recurrence or malignant transformation over time. the results vary among different studies with a 5 year progression from 50 to 70% and malignancy-free survival rates from 30 to 70%. (6, 13, 17, 18, 25) some patients have tumors that remain indolent for a couple of years, in our study only one patient had a pfs of 84 months, whereas others rapidly recur and progress leading to neurological deterioration and subsequent death. this heterogeneity in patient evolution has led to the necessity of identification of certain factors associated with survival, recurrence, and malignant development for patients undergoing resection of a low-grade glioma. the factors consistently known to be associated with improved survival include: 1. younger age (patients < 40 years) (13, 23). in our series 3 patients were younger than 40 years but they didn’t had a better prognostic than the group of patients older than 40 years this is due the fact that we had a small and non-homogenous series. 2. higher kps score, (18) 3. oligodendroglioma pathology, patients with fas and oligodendrogliomas have similar rates of recurrence and/or progression although patients with fas had a greater propensity to develop into higher romanian neurosurgery (2010) xvii 4: 403 – 412 409 grade tumors than patients with oligodendrogliomas, this may be due to the fact that fas are primarily composed of aberrant astrocytes, which have a greater tendency to undergo malignant degeneration (17, 27) 4. postoperative radiation therapy, (25) although improved pfs was demonstrated for patients treated with immediate rt, this did not translate into improved os. besides prolonging the time to tumor progression, rt has several other potential benefits, such as symptom control, particularly epileptic seizures (27). in our series 5 patient received radiotherapy and another 2 received both radio and chemotherapy but with no impact among pfs and 5. gtr (< 1 cm residual tumor), the first report of outcome based on an mr imaging based assessment of surgical resection for lgg was reported by berger et al. (1) in a series of 53 patients from the university of washington. the extent of resection (based on the volume of residual disease) and tumor size were inversely correlated with the likelihood of tumor recurrence, time to recurrence, and tumor grade at the time of recurrence, recent studies have shown that gross total resection independently decrease the risk of malignant transformation, that suggest that gtr should be pursued when these tumors are amenable to radical resection. (1, 8, 15, 26) a critical point is a precise definition of total resection that for lggs that do not enhance implies removal of all the hyperintense regions on t2 or flair images and thus can only be determined by comparing preoperative and post-operative tumor volumes on mri, respecting this standard even with intraoperative mriguided surgery, total resection is achieved in no more than 36% of patients (24). gtr was achieved in 6 cases of our series but it was appreciated by the surgeon, without an immediate postoperatively mri to confirm the extent of resection and these may also explain the short period until malignant transformation, comparatively with the data existing in the literature. the only factors that have been consistently shown to be associated with tumor recurrence or malignant degeneration are: 1. preoperative contrast enhancement, (8, 11, 12, 27) which occurs where the blood-brain barrier is disturbed primarily in tumor areas, (2, 3) contrast enhancement imaging often suggests a high-grade glioma, but it can also be present in 15–40% of patients with low grade gliomas. (7, 11, 23) the prognostic implications of contrast enhancement have been controversial and primarily limited to survival studies. (11, 14, 16, 17, 20) studies on contrast enhancement and recurrence remain relatively unknown and understudied. (17, 29) contrast-enhancing low-grade gliomas may behave more like their higher grade, contrast-enhancing counterparts, which means that they are more likely to recur following resection. these tumors may therefore benefit from more aggressive and/or earlier use of adjuvant therapies. 2. tumor size, the risk of recurrence increases 1.3 times for each centimeter increase in size and is independent of the extent of resection, tumor sizes ≥ 3 cm have the greatest statistical significance, with a 3.5 fold increased risk of tumor recurrence. larger low-grade gliomas, like malignant gliomas, (21) may have more microsatellite lesions and individual cell invasion, as well as more residual cells following resection, as a consequence of having a larger tumor mass. (21) these 410 d. rotariu et al malignant transformation of low grade gliomas factors may not only predispose to tumor recurrence, but suggest that earlier treatment while the tumor is smaller will delay recurrence, presumably by decreasing the number of invading and/or residual cells that escape the tumor mass, which may eventually transform to a malignant phenotype, 3. str. (1, 3) and 4. molecular abnormalities (27) james l. frazier reported in 2009 2 cases of rapid malignant transformation (12 weeks) in patients operated on for low grade astrocytomas , which didn’t enhance on the initial mri and confirmed by anatomopathological exam and imunohistochemestry low value of ki 76, but both cases had, overexpresion of edgf and absence of p53 mutation, molecular abnormalities seen in primary glioblastomas which may suggest possible risk factors for rapid malignant transformation. current recommendations according to guidelines on management of low-grade gliomas elaborated by efns: european federation of neurological societies and eano: european association for neurooncology and published in european journal of neurology june 2010 27 are: “• astrocytomas, oligodendrogliomas and oligoastrocytomas are diagnosed using morphological criteria according to who classification (level a). • combined loss of 1p/19q is a marker in favor of the diagnosis of oligodendroglioma or oligoastrocytoma (level b). • mri with contrast enhancement is the gold standard to monitor lgg after surgery: an mri examination every 6 months might be enough, unless the physicians think otherwise (good practice point). • mrs is useful for the differentiation of lgg from non-tumoral lesions, preoperative definition of extent and guiding stereotactic biopsies (level c). • dsc-mri can be employed in the follow-up to predict malignant transformation (level c). • pet with fdg is useful for detecting malignant transformation in astrocytomas (level c) and for differentiation between radiation necrosis and tumor recurrence (level b) • pet with met is useful for differentiation of lgg from non-tumoral lesions (level b), guiding stereotactic biopsies (level b), pre-treatment evaluation (level b) and monitoring treatment (level c). • prophylactic aeds must not be used before any epileptic seizures have occurred (level a). • aeds should be started after the first seizure (level a). aeds should be individualized according to seizure type, comedication, comorbidity and patient preferences (good practice point). • in patients who need a treatment with chemotherapeutics, non-eiaeds are to be preferred (level b). • surgical resection represents the first treatment option, with the goal to maximally resect the tumor mass whenever possible, whilst minimizing the postoperative morbidity (level b). • the identification of the eloquent cerebral areas, which have to be preserved during surgery, is performed through preoperative neuroimaging modalities (functional mri, fiber tracking) and intraoperative brain mapping techniques (level b), and awake surgery could improve the results (level c). romanian neurosurgery (2010) xvii 4: 403 – 412 411 • when surgery is not feasible (because of tumor location, extension or comorbidities), a biopsy (either stereotactic or open) should be performed to obtain a histological diagnosis (good practice point). • for patients with unfavorable prognostic factors (older age, incomplete or no resection, existing neurological symptoms), an adjuvant treatment is indicated at any time (level b), and this is more commonly rt (good practice point). • a total rt dose of 50.4–54 gy in fractions of 1.8 gy represents the current standard of care (level a). modern rt techniques (conformal dose delivery or intensity modulated techniques) should preferably be used (level b). • younger patients (<40 years of age) with (nearly) complete resection and tumors with an oligodendroglial component have a more favorable prognosis and can be observed after surgery (level b), but close follow-up is needed (good practice point). • chemotherapy is an option for patients with recurrence after surgery and radiation therapy (level b). • chemotherapy is an option as initial treatment for patients with large residual tumors after surgery or unresectable tumors to delay the risk of late neurotoxicity from large-field rt, especially when 1p/19q loss is present (level b). • neuropsychological tests, at diagnosis and during the follow-up, can be useful, being selected according to the needs of the clinical setting (good practice point). the neuropsychological tests must have standardized materials and administration procedures, published normative data, moderate to high test–retest reliability, brief administration time (30 – 40 min) and be suitable to monitor changes over time (good practice point). • cognitive rehabilitation can be helpful (level b)” conclusions patients with low-grade gliomas have a more favorable prognosis than patients with high grade glioma. despite this, the majority of patients with low-grade gliomas suffer either tumor progression or degeneration into to a more malignant lession (8) in our series the median to malignant transformation was 32,5 months which is comparable with the data existing in the literature (32 months (8)). younger age, normal neurological examination, oligodendroglial histology and 1p loss (we don’t have the possibility to evaluate molecular markers) are favorable prognostic factors. early post-operative radiotherapy improves progression free survival but not overall survival. chemotherapy can be useful as initial treatment after surgery or at recurrence after radiotherapy. references 1. berger ms, deliganis av, dobbins j, keles ge: the effect of extent of resection on recurrence in patients with low grade cerebral hemisphere gliomas. cancer 74:1784–1791, 1994 2. chang ef, potts mb, keles ge, lamborn kr, chang sm, barbaro nm, et al: seizure characteristics and control following resection in 332 patients with low-grade gliomas. j neurosurg 108:227–235, 2008 3. claus eb, horlacher a, hsu l, schwartz rb, delloiacono d, talos f, et al: survival rates in patients with low-grade glioma after intraoperative magnetic resonance image guidance. cancer 103:1227–1233, 2005 4. davis fs: epidemiology of brain tumors. expert rev anticancer ther 7:s3–s6, 2007 5. donato v, papaleo a, castrichino a, banelli e, giangaspero f, salvati m, et al: prognostic implication of clinical and pathologic features in patients with glioblastoma multiforme treated with concomitant radiation plus temozolomide. tumori 93:248–256, 2007 412 d. rotariu et al malignant transformation of low grade gliomas 6. gannett de, wisbeck wm, silbergeld dl, berger ms: the role of postoperative irradiation in the treatment of oligodendroglioma. int j radiat oncol biol phys 30:567–573, 1994 7. ginsberg le, fuller gn, hashmi m, leeds ne, schomer df: the significance of lack of mr contrast enhancement of supratentorial brain tumors in adults: histopathological evaluation of a series. surg neurol 49:436–440, 1998 8. kaisorn l.chaichana, matthew j.mcgirt ,john laterra, alessandro olivi, and alfredo quiñoneshinojosa: recurrence and malignant degeneration after resection of adult hemispheric low-grade gliomas: j neurosurg 112:10–17, 2010 9. janny p, cure h, mohr m, heldt n, kwiatkowski f, lemaire jj, et al: low grade supratentorial astrocytomas. management and prognostic factors. cancer 73:1937– 1945, 1994 10. keles ge, lamborn kr, berger ms: low-grade hemispheric gliomas in adults: a critical review of extent of resection as a factor influencing outcome. j neurosurg 95:735–745, 2001 11. kreth fw, faist m, rossner r, volk b, ostertag cb: supratentorial world health organization grade 2 astrocytomas and oligoastrocytomas. a new pattern of prognostic factors. cancer 79:370–379, 1997 12. kreth fw, faist m, warnke pc, rossner r, volk b, ostertag cb: interstitial radiosurgery of low-grade gliomas. j neurosurg 82:418–429, 1995 13. leighton c, fisher b, bauman g, depiero s, stitt l, macdonald d, et al: supratentorial low-grade glioma in adults: an analysis of prognostic factors and timing of radiation. j clin oncol 15:1294–1301, 1997 14. lote k, egeland t, hager b, stenwig b, skullerud k, bergjohnsen j, et al: survival, prognostic factors, and therapeutic efficacy in low-grade glioma: a retrospective study in 379 patients. j clin oncol 15:3129–3140, 1997 15. north ca, north rb, epstein ja, piantadosi s, wharam md: low-grade cerebral astrocytomas. survival and quality of life after radiation therapy. cancer 66:6–14, 1990 16. pallud j, devaux b, nataf f, roux fx, daumasduport c:spatial delimitation of low grade oligodendrogliomas. neurochirurgie 51:254–259, 2005 17. philippon jh, clemenceau sh, fauchon fh, foncin jf: supratentorial low-grade astrocytomas in adults. neurosurgery 32:554–559, 1993 18. piepmeier jm: observations on the current treatment of lowgrade astrocytic tumors of the cerebral hemispheres. j neurosurg 67:177–181, 1987 19. piepmeier j, baehring jm: surgical resection for patients with benign primary brain tumors and low grade gliomas. j neurooncol 69:55–65, 2004 20. piepmeier j, christopher s, spencer d, byrne t, kim j, knisel jp, et al: variations in the natural history and survival of patients with supratentorial low-grade astrocytomas. neurosurgery 38:872–879, 1996 21. price sj, jena r, burnet ng, carpenter ta, pickard jd, gillard jh: predicting patterns of glioma recurrence using diffusion tensor imaging. eur radiol 17:1675– 1684, 2007 22. schiff d, brown pd, giannini c: outcome in adult low-grade glioma: the impact of prognostic factors and treatment. neurology 69:1366–1373, 2007 23. shaw e, arusell r, scheithauer b, o’fallon j, o’neill b, dinapoli r, et al: prospective randomized trial of lowversus high-dose radiation therapy in adults with supratentorial low-grade glioma: initial report of a north central cancer treatment group/radiation therapy oncology group/eastern cooperative oncology group study. j clin oncol 20:2267–2276, 2002 24. shaw g, brian berkey,w.coons, dennis bullard, david brachman,c. buckner, et all: recurrence following neurosurgeon-determined gross-total resection of adult supratentorial low-grade glioma: results of a prospective clinical trial: j neurosurg 109:835–841, 2008 25. shibamoto y, kitakabu y, takahashi m, yamashita j, oda y, kikuchi h, et al: supratentorial low-grade astrocytoma. correlation of computed tomography findings with effect of radiation therapy and prognostic variables. cancer 72:190–195, 1993 26. smith js, chang ef, lamborn kr, chang sm, prados md, cha s, et al: role of extent of resection in the long-term outcome of low-grade hemispheric gliomas. j clin oncol 26: 1338–1345, 2008 27. soffietti r, baumert b.g, bello l, von deimling a, duffau h, frénay m et al : guidelines on management of low-grade gliomas: report of an efns–eano* task force: european journal of neurology 2010, 17: 1124– 1133 28. stupp r, mason wp, van den bent mj, weller m, fisher b, taphoornm mj, et al: radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. n engl j med 352:987–996, 2005 29. van veelen ml, avezaat cj, kros jm, van putten w, vecht c: supratentorial low grade astrocytoma: prognostic factors, dedifferentiation, and the issue of early versus late surgery. j neurol neurosurg psychiatry 64:581–587, 1998 microsoft word 5tascu_surgicaldecompression 264 tascu, florea surgical decompression of arachnoid cysts surgical decompression of arachnoid cysts: a study on 44 pediatric patients a. tascu1, simona mihaela florea2 1assist. prof. at the universtity of medicine and pharmacy “carol davila”, head of the 1st neurosurgical departmpent at the clinical emergency hospital “bagdasararseni”, bucharest, romania 2student, universtity of medicine and pharmacy “carol davila”, bucharest, romania abstract background: there are yet to clarify some aspects regarding the surgical indications and surgical methods that are at choice for treating acs. the purpose of the study is to contribute to the ongoing debate on the most appropriate treatment. materials and methods: we included in the study 44 pediatric patients (aged < 18 years), operated for acs in the neurosurgery i department, of the emergency clinical hospital “bagdasararseni” in bucharest, during the period january 2003 to december 2012. the surgical methods were either a craniotomy or cyst shunting. the information regarding these patients was retrospectively assessed based on their clinical and imaging records, and cross checked with the or protocols. treatment efficiency was evaluated considering postoperative clinical status, imaging appearance and postoperative complications. results: 84.1% of the patients reported postoperative disappearance or reduction of symptoms, while 13.6 had the same complaints as prior surgery. only one patient experienced worsening of symptoms. follow-up imaging showed cyst disappearance in 29.5% patients and cyst reduction in 61.4% patients. 9.1% had no change in cyst volume. craniotomy correlated with a better imaging appearance (p=0.02). there was no correlation between improved clinical status and cyst fluid reduction (p=0.6). 9 patients (20.4%), all with temporal cysts, experienced postoperative complications, and 7 of them (15, 9%) needed surgery. there was no severe or permanent dysfunction in any of the patients. 42.8% of the cyst shunting patients suffered postoperative complications, whereas only 10% of the craniotomy patients did. conclusion: cyst decompression results in significant clinical improvement and it can be performed with little risk for severe complications. craniotomy seems to be a better surgical treatment option than cystoperitoneal shunt, with a better neuroimaging appearance and a lower complications rate. key words: arachnoid cyst, pediatric, shunting, craniotomy introduction arachnoid cysts (acs) are benign congenital malformations, formed by the splitting or duplication of the arachnoid membrane, allowing a clear fluid romanian neurosurgery (2013) xx 3: 264 – 270 265 resembling normal cerebrospinal fluid to fill in the space crated (1, 2, 3). they are due to an increased pulsation of the cerebrospinal fluid (csf) (4, 5). they count for approximately 1% of the intracranial pathology, being most frequently located in the middle cranial fossa (about half of the acs) and the cerebellopontine angle (cpa) (2, 3, 4, 6), and they appear to affect more males than females (7, 8). the clinical presentation of acs is variable, depending on the cyst location and the importance of the mass effect exerted on the surrounding nervous structures (1, 2, 6, 9-11). most of the patients present with nonspecific symptoms such as headache, dizziness or balance impairment, or symptoms of increased intracranial pressure (3, 6). the positive diagnosis is set through cerebral imaging (ct scan or mri), and it reveals a sharply demarcated, non-enhancing, extra-axial cyst, with density/signal similar to the csf (12, 13). the main procedures to treat arachnoid cysts are stereotactic punction, cystoperitoneal shunting, craniotomy followed by radical resection and marsupialisation of the cyst in the subarachnoid space and neuroendoscopic fenerstration of the cyst. the surgical indications for acs, as well as the surgical procedures elected remain a controversial subject (1, 2, 8, 15, 14-22). arachnoid cysts can complicate with rupture/hemorrhage, especially encountered in large cysts and mostly associated with minor head trauma in the last month (1, 2, 20, 23, 24). material and methods patients characteristics: the study includes 44 patients, 30 boys (68%) and 14 girls (32%) sex ratio b:g≈2, 14:1 that had been operated in our department either by craniotomy or cystoperitoneal shunting. mean age at admission was 9.36 years (median=9.5, range 1-17). mean follow-up period was 17.3 months (range 3-62). study type and database: the present study is a retrospective, observational, analytic study that includes all pediatric patients (age <18 years) operated for an arachnoid cyst during the period january 2003 to december 2012, in the 1st neurosurgery department of the clinical emergency hospital “bagdasar-arseni” in bucharest. the patient information was extracted from the clinical and imaging records in the department’s database, and cross checked with the or protocols. the patients complete medical records offered information on: demographic data, subjective complaints, clinical finding at admission and during the in hospital period, imaging aspect, dimensions and location of the acs, galassi type for sylvian fissure cysts, complications present at admission, type of surgical procedure, postoperative neuroimaging either following the first 72 hours after surgery or at follow-up, 3 months from surgery. criteria for surgical treatment: symptoms related to the cysts were found in 41 patients (93%), while 2 other patients were asymptomatic, but with galassi type iii acs, exerting a significant mass effect on the adjacent brain structures. one patient had a large chronic subdural hematoma, asymptomatic, that was diagnosed during a check-up, after a history of repeated head trauma in the past month. decompression method: most of the patients (68%) were performed a craniotomy under general anesthesia, cyst membrane excision in the parts where it wasn’t adherent to the brain matter. the large bridging veins that presented the risk 266 tascu, florea surgical decompression of arachnoid cysts of rupture and hemorrhagic complications postoperatively were coagulated. the normal csf flow was reestablished by fenestrations that create communications with the posterior cranial fossa and the basal cisterns. the rest of the patients included in the study (32%) had a cystoperitoneal shunt, that drained the fluid in the cyst into the peritoneal cavity, thus relieving the pressure inside the cyst. this procedure was also performed under general anesthesia. treatment evaluation: the efficiency of the surgical treatment performed on each patient was evaluated considering 3 parameters the clinical presentation postoperative (cuantified by the clinical outcome status = cos scale), the neuroimaging aspect at the 3 months postoperative examination (evaluated by the imaging outcome aspect = ioa scale), and the presence of postoperative complications or reoperation due to complications or failure of the primary intervention. the cos and ioa categories are detailed in table 1. statistical analysis: the statistical data was analyzed with office 2007 excel and cdcs epi info 7 for windows. the contingency tables statistical significance was analyzed with persons chi square test and fisher exact (p level was 0.05, confidence interval – ci=95%). results cyst location: inside the patients group included in our study, most of the patients (82%) had a sylvian fissure cyst, followed by frontal arachnoid cysts (14%) and pca arachnoid cysts (4%). details on cyst locations are presented in table 2. no other cyst locations presented criteria for surgery. main clinical symptoms: with the exception of 3 patients, all patients presented with symptoms related to the cyst. the most frequently encountered symptoms were headache (90.9%), epilepsy (29.55%) and dizziness/balance impairment (29.3%). one patient presented a with motor deficiency in the right side of the body, and two patients complained of personality changes. table 3 summarizes the frequency of symptoms categorized by cyst location. table 1 cos and ioa cos cos1: no or minor postoperative symptoms cos2: relief of the symptoms presented preoperatively cos3: no change in the clinical presentation postoperatively cos4: more complaints postoperatively ioa ioa1: cyst no longer visible ioa2: decreased cyst volume ioa3: no change in cyst volume table 2 cyst location location side number of patients percentage of patients temporal left right 14 12 31.82% 27.28% frontal left right bilateral 3 2 1 6.82% 4.54% 2.27% cpa left 2 4.54% romanian neurosurgery (2013) xx 3: 264 – 270 267 table 3 main clinical symptoms by cyst location location symptom sylvian fissure frontal lobe cpa total headache 36 (81.8%) 2 (4.55%) 2 (4, 55%) 40 (90.9%) epilepsy 10 (22.73%) 3 (6.82%) 0 13 (29.55%) dizziness/balance impairment 9 (20.45%) 1 (2.3%) 2 (4.55%) 12 (29.3%) personality changes 1 (2.3%) 1 (2.3%) 0 2 (4.55%) hemiplegia 1 (2.3%) 0 0 1 (2.3%) table 4 postoperative complications/reoperation due to complications or treatment failure complication cyst shunting patients craniotomy patients overall infectious 1 (7.1%) 1 (3.3%) 2 (4.5%) subdural hematoma 0 1 (3.3%) 1 (2.3%) epidural hematoma 0 1 (3.3%) 1 (2.3%) revision of shunt 4 (28.6%) 0 4 (9.1%) new shunt^ 1 (7.1%) 0 1 (2.3%) reoperation* 5 (35.7%) 2 (6.6%) 7 (15.9%) all complicatios 6 (42, 8%) 3 (10%) 9 (20.4%) ^one of the patients developed secondary hydrocephalus and needed an aditional ventricular shunt *not all complications required surgical treatment a b 268 tascu, florea surgical decompression of arachnoid cysts c figure 1 sylvian fissure cysts galassi classification : a. type i: biconvex, located in the anterior temporal tip b. type ii: insula is completely open; rectangular shape; it involves proximal and intermediate segments of sylvian fissure c. type iii: involves entire sylvian fissure; important mass effect a b figure 2 surgical treatment : a. cyst shunting; b. craniotomy intracranial hemorrhage in patients with arachnoid cysts: 16 patients (31.8%) presented a hemorrhagic complication at admission (14 of them had a subdural hematoma and 2 presented with hemorrhage into the cyst. minor head trauma in the last month was a common finding among them (81.25%). data statistical analysis showed that a history of minor head trauma in the past month is a risk factor for hemorrhagic complications of acs – odds ratio (or)=56.33, p=0.000004, ci=(6.72, 636.86). clinical outcome status: 37 patients (84.1%) either no/minor complaints or the relief of symptoms postoperatively (a cos1 or cos2). 13.6% of the patients had no change in the clinical status after surgery (cos3), while only one patient complained of worse clinical status postoperatively (a cos4). the patient with the cos4 was one of the asymptomatic patients, with a compressive type iii cyst and complained of romanian neurosurgery (2013) xx 3: 264 – 270 269 headache/dizziness (the symptoms were no longer present 1 month later , at check-up). there is no significant statistical evidence that any of the two procedures results in a better clinical outcome (cos1/2) p=0.8. imaging outcome aspect: 90.9% of the patients (40/44) showed either cyst disappearence (ioa1) or cyst reduction (ioa2) at the 3 month neuroimaging examinations, while 9.1% (4/44) showed no change in cysts dimensions (ioa3). all the ioa3 subgroup patients where operated by cystoperitoneal shunting. craniotomy appears to result in a better neuroimaging aspect at 3 months (p=0.02). there is no correlation between a good clinical outcome and cyst reduction/disappearance in imaging examination (p=0.6). postoperative complications/reoperation due to complications or treatment failure: 42.8% of the patiets treated by cystoperitoneal drainage presented complications/reinterventions due to failure of primary treatment, whereas only 10% of the patients where a craniotomy was performed presented with postperative complications. the type of complications for each of the two surgical procedures is detailed in table4. however, the overall complications/reoperations due to failure of primary treatment rate of 20.4% and the lack of any severe or permanent postop deficiencies prove that surgery is an apropriate treatment for arachnoid cysts. statistical analysis of the data proved that craniotomy is a risk factor for postoperative complications/reoperations – rr=4.3 (relative risk), rd=32.8% (risk difference), p=0.019. discussion our study results regarding the sex distribution, cyst location and symptoms frequency is similar to the data cited in the international specialized literature (1-11). there was a high percentage of patients that presented with hemorrhagic complications, the numbers rising the question whether or not acs diagnosed in children should be operated on even though they are not symptomatic, considering the risk of bleeding associated with a history of head trauma and large arachnoid cysts (23, 24). the majority of patients that underwent surgical treatment had a good clinical and neuroimaging outcome and most of the patients had no complications and/or reoperations. plus, none of the complications implies any severe/permanent dysfunction in any of the patients operated. failure of treatment is associated more with cyst shunting than craniotomy, mostly because of the undershunting complications/reoperations that appear in most of the shunt dependant patients. conclusions we clearly demonstrated that a history of minor head trauma in the past month represents a risk factor for cyst hemorrhage. another conclusion is that surgical treatment of arachnoid cysts improves patients clinical symptoms, with little risk of severe postoperative complications, proving that surgery is an appropriate modality to improve patients quality of life, without causing damage. also, craniotomy has a better neuroimaging outcome and a lower risk of complications than cyst shunting, making it the best procedure of the two. the high rate of reoperations associated with cyst shunting indicates that shunt dependence is a problem that we should avoid whenever possible. 270 tascu, florea surgical decompression of arachnoid cysts references 1. youmans, julian r, md. neurological surgery:a comprehensive reference guide to the diagnosis and management of neurosurgical problems. 4th ed. philadelphia: saunders, 1996. 2. samii m, de carvalho ga, hinojosa m. arachnoid cysts of the posterior fossa. [ed.] ricardo ramina, paulo henrique pires agiular and marcos tatagiba. samii's essentials in neurosurgery. berlin: springer, 2008, 20, pp. 215-220. 3. ah, kaye. essential neurosurgery, 3rd ed. s.l.: blackwell publishing, 2005. 4. brooks ml, mater dp, sataloff rt, et al. intracanalicular arachnoid cyst mimicking acoustic neuroma: ct and mri. 16, 1992, comp med imag graph, pp. 283-285. 5. haberkamp tj, monsell em, house wf, et al. diagnosis and treatment of arachnoid cysts of the posterior fossa. 103, 1990, otolaryngol head nack surg, pp. 610-614. 6. greenberg, mark s., m.d. handbook of neurosurgery, 6th edition. new york: thime, 2006. 7. helland ca, lund-johansen m, wester k. location, sidedness, and sex distribution of intracranial arachnoid cysts in a population-based sample. nov 2010, journal of neurosurgery, vol. 113, pp. 934-939. 8. kang jk, lee ks, lee iw, et al. shunt-independent surgical treatment of middle cranial fossa arachnoid cysts in children. 2, feb 2000, childs nerv syst, vol. 16, pp. 111-116. 9. de volder ag, michel c, thauvoy c, et al. brain glucose utilisation in aquired childhood aphasia associated with a sylvian arachnoid cyst: recovery after shunting as demonstrated by pet. 1994, j neurol neurosurg psychiatry, vol. 57, pp. 296-300. 10. raeder mb, helland ca, hugdahl k, et al. arachnoid cysts cause cognitive dificits that improve after surgery. 2005: s.n., neurology, vol. 64, pp. 160162. 11. mayr u, aichner f, bauer g, et al. supratentorial extracerebral cysts of the middle cranial fossa. a report of 23 consecutive cases of the so called temporal lobe agenesis syndrome. stuttgart: s.n., 1982, neurochirurgia, vol. 25, pp. 51-56. 12. osborn, anne g et al. diagnostic imaging brain. 1st ed. salt lake city, utah: amirsys, 2004. 13. kornienko, valery n. and pronin, igor n. diagnostic neuroradiology. berlin: springer, 2009. 14. auer lm, gallhofer b, ladurner g, et al. diagnosisi and treatment of middle fossa arachnoid cysts and subdural hematomas. 3, march 1981, journal of neurosurgery, vol. 54, pp. 366-369. 15. helland ca, wester k. a population-based study of intracranial arachnoid cysts: clinical and neuroimaging outcomes following surgical cyst decompression in children. 5 suppl, nov 2006, j neurosurg, vol. 105, pp. 385-390. 16. ciricillo sf, cogen ph, harsh gr, et al. intracranial arachnoid cysts in children. a xomparison of th effects of fenestrating and shunting. 2, feb 1991, j neurosurg, vol. 74, pp. 230-235. 17. kim sk, cho bk, chung yn, et al. shunt dependancy in shunted arachnoid cyst: a reason to avoid shunting. 4, oct 2002, pediatr neurosurg, vol. 37, pp. 178-185. 18. di rocco c, tamburrini g, caldarelli m, et al. prolonged icp monitoring in children with sylvian fissure arachnoid cysts. 6, dec 2003, minerva pediatr, vol. 55, pp. 583-591. 19. harsh gr iv, edwards ms, wilson cb. intracranial arachnoid cysts in children. 1986, j neurosurg, vol. 64, pp. 835-842. 20. van der meche fg, braakman r. arachnoid cysts in the middle cranial fossa: cause and treatment of progressive and non-progressive symptoms. 1983, j neurol neurosurg psychiatry, vol. 46, pp. 1102-1107. 21. sommer ie, smit lm. congenital supratentorial arachnoid and giant cysts in children: a clinical study with arguments for a conservative approach. 1997, childs nerv syst, vol. 13, pp. 8-12. 22. sato h, sato m, katayama s, et al. effective shuntindependent treatment for primary middle fossa arachnoid cyst. 1991, childs nerv syst, vol. 7, pp. 375381. 23. sprung c, armbruster b, koeppen d, et al. arachnoid cysts of the middle cranial fossa accompanied by subdural effusieon-experience with 60 consecutive cases. 1, wien: s.n., jan 2011, acta neurchir, vol. 153, pp. 75-84. 24. cress m, kestle jrw, holubkov r, et al. risk factors for pediatric arachnoid cyst rupture/hemorrhage: a case-control study. 5, may 2013, neurosurgery, vol. 72, pp. 716-722. romanian neurosurgery (2019) xxxiii (4): pp. 400-403 doi: 10.33962/roneuro-2019-065 www.journals.lapub.co.uk/index.php/roneurosurgery gamma knife radiosurgery: effect on corticotropin-secreting pituitary adenoma dan nicolae paduraru1,2, raluca ciunt3, andra morar4, laura maria dragomir3, carla scânteie3, alexandra bolocan1,2, octavian andronic1,2, cristina ghervan3,5, bogdan socea2,6, mara carsote7, ana valea3,5 1 general surgery department and emergency iii, university emergency hospital of bucharest, romania 2 carol davila university of medicine and pharmacy, bucharest, romania 3 endocrinology department, county clinical emergency hospital, cluj-napoca, romania 4 clinical hospital of infectious diseases, cluj-napoca, romania 5 iuliu hatieganu university of medicine and pharmacy & county clinical hospital, cluj-napoca, romania 6 clinical emergency hospital “sf. pantelimon”, bucharest, romania 7 c.i. parhon national institute of endocrinology, bucharest, romania abstract introduction: cushing's disease (cd) is a complex endocrine disorder characterized by an increased risk of recurrence and persistence of hypercortisolism after initial transsphenoidal adenomectomy, a situation requiring alternative therapeutic measures. case presentation: a 21-year-old female patient was admitted for weight gain with centripetal fat distribution, transient headache, hair thinning and psycho-emotional lability. clinical examination revealed round facies, acne, purple-red striae, hirsutism with a ferriman-gallwey score of 20. the hormonal profile revealed high serum cortisol (of 283.1 ng/ml, normal:70-225 ng/ml) and high acth (adrenocorticotropic hormone) levels (of 260.6 pg/ml, normal: 7.2-63.3 pg/ml). the pituitary mri (magnetic resonance imaging) examination found a 4.3/4.4/6.2mm left paramedian microadenoma. the persistence of hypercortisolism after adenomectomy required gkrs (gamma knife radiosurgery). four months after radiosurgery, complete remission of the disease was achieved and it was maintained at the last evaluation. at present, the patient is 20 weeks pregnant. conclusions: gamma knife radiosurgery offers a high control rate of pituitary adenomas and a reasonable rate of remission of residual hypercortisolism after neurosurgical treatment. after surgery or gkrs, periodic monitoring is necessary for patients with cd due to the risk of pituitary insufficiency or relapse. keywords cushing's disease, radiosurgery, gamma knife corresponding author: mara carsote c.i. parhon national institute of endocrinology, bucharest, romania carsote_m@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 401 gamma knife radiosurgery introduction cushing’s disease is a complex disorder, characterized by a series of symptoms such as central obesity, hypertension, diabetes, as well as psychiatric and neurocognitive changes, caused by an acth–secreting pituitary adenoma leading to cortisol hypersecretion [1]. the gold standard treatment for cd is transsphenoidal surgical excision of the tumour, which is often curative. however, there is a failure rate of 10 to 35% in reaching complete remission, while a proportion of patients also experience disease recurrence in time [2-6]. a second-line treatment used to achieve control of hypercortisolism is represented by targeted radiation of the sellar adenomatous tissue, the most reliable therapy being gkrs [7,8]. case presentation a 21-year-old female smoker, without significant past medical history, was admitted for weight gain of 20 kg in the past two months with centripetal distribution, transient headache, hair thinning, sleeping disorders and psycho-emotional lability. clinical examination revealed height of 160 cm, weight of 76 kg, bmi (body mass index) of 29.68 kg/m2, blood pressure of 125/85 mmhg, heart rate of 64bpm, round facies, acne, purple-red striae and hirsutism with a ferriman-gallwey score of 20. the hormonal profile showed high serum cortisol levels of 283.1 ng/ml (normal: 70-225 ng/ml) with maintained circadian rhythm, high 24-hour urine free cortisol (ufc) of 456.61g/24h (normal: 50-190 g/24h), non-suppression of cortisol after the 1 mg dxm (dexamethasone) suppression test (of 145.9 ng/ml, normal 18 ng/ml), adequate suppression after the two-day, 8 mg dxm test, high acth level of 260.6 pg/ml (normal: 7.2-63.3 pg/ml), high levels of dheas (dehydroepiandrosterone-sulfate) and testosterone (table 1). pituitary function tests showed normal plasma gonadotropin levels, normal prl (prolactin) and tsh (thyroid stimulating hormone) of 0.51µui/ml with low ft4 (free thyroxine) of 0.86 ng/dl (normal: 0.89-1.76 ng/dl). there were no changes in biochemical parameters. pituitary mri (magnetic resonance imaging) examination described a left paramedian microadenoma of 4.3/4.4/6.2 mm in diameter. treatment with 25 µg tyroxine daily was initiated. transsphenoidal adenomectomy was performed one month later. a massive intraoperative haemorrhage did not allow the removal of the tumour, therefore gkrs at a dose of 25 gy was performed three weeks later. four months after radiosurgery, complete remission of the disease was achieved, which was maintained at the one-year post-radiosurgery evaluation (tabel 1). mri revealed the cystic transformation of the pituitary microadenoma. at present, the patient is 20 weeks pregnant. parameter before surgery after radiosurgery normal limits units morning plasma cortisol 283.1 176.2 70-225 ng/ml plasma cortisol 11pm 148.9 74.9 50-165 ng/ml 24-h urinary cortisol 456.61 52.8 50-190 g/24h acth 260.6 43.14 7.2-63.3 pg/ml morning plasma cortisol* 145.9 9.1 < 18 ng/ml morning plasma cortisol** 94.7 <50*** ng/ml dhea-s 8.19 2.79 0.9-3.6 µg/ml testosterone 1.22 0.66 0.3-1 ng/dl tsh 0.51 0.297**** 0.4-4 µui/ml ft4 0.86 0.96**** 0.89-1.76 ng/dl table 1: the endocrine parameters of a 21-year-old female patient diagnosed with cushing’s disease: before surgery and postgamma knife radiosurgery. *after the 1mg overnight dexamethasone suppression test; **after the two-day, 8 mg dexamethasone suppression test;***more than50% reduction; 24-h= 24-hours; acth= adrenocorticotropic hormone; dhea-s= dehydroepiandrosterone-sulfate; tsh=thyroid stimulating hormone; ft4=free thyroxine; ****25 µg/day thyroxine therapy. 402 dan nicolae păduraru, raluca ciunt, andra morar et al. figure 1: preoperative contrast-enhanced pituitary mri of a 21year-old woman diagnosed with cushing’s disease: microadenoma measuring 4/6.5mm. coronal plane. discussions cushing's disease remains a challenge in clinical practice, both in terms of diagnosis and treatment, especially for young patients [9-12]. transsphenoidal adenomectomy, the first-line therapeutic option, is not always curative. consequently, all patients should be informed that recurrence can occur in a delayed fashion and that annual endocrine testing should be done to track and confirm disease status [11-13]. in our patient’s case, the failure of transsphenoidal adenomectomy was due to an intraoperative complication consisting of massive haemorrhage in the nasal mucosa. considering the age of the patient and the desire to obtain a pregnancy, gkrs was recommended. the low risk of pituitary insufficiency and the relatively rapid remission of hypercortisolism are the main arguments for gkrs in persistent postoperative cd [14]. in this case, after gkrs, the secondary hypothyroidism persisted and was adequately controlled by thyroxine replacement therapy. generally, the secretor pituitary tumours are approached by neurosurgery, medical therapy in cases like acromegaly, prolactinoma (in this particular situation medical therapy is usually the first line), and cushing’s disease while radiotherapy remains a final option due to slow rate of response and the risk of associated hypopituitarism [16,17,18]. in this particular case the effect was rapidly observed. the non-secretor pituitary tumours are referred to surgery only if mass effect is positive [19,20]. as final option in cushing’s disease one time or two times bilateral adrenalectomy is done knowing the risk of lifelong adrenal insufficiency [21,22]. menstrual disorders and infertility are common in cd patients [15]. in our patient’s case there were no changes in ovarian function before gkrs, except for a higher level of testosterone. the normalization of cortisol, testosterone and deas levels in less than 6 months after gkrs allowed spontaneous pregnancy. considering the therapy used in this case, it is advisable to carefully monitor pituitary function throughout pregnancy. conclusions gamma knife radiosurgery offers a high control rate of pituitary adenomas and a reasonable rate of remission of residual hypercortisolism after neurosurgical treatment. close follow-up is necessary for patients with cd due to the risk of possible relapse and pituitary insufficiency after surgery or gnrs. acknowledgements: there in no conflict of interest. we thank the patient for her consent. references 1. mehta gu, lonser rr. (2017). management of hormonesecreting pituitary adenomas. neuro-oncol, 19(6), 762–773. 2. lonser rr, wind jj, nieman lk, weil rj, devroom hl, oldfield eh . (2013). outcome of surgical treatment of 200 children with cushing’s disease. j clin endocrinol metab, 98(3), 892–901. 3. hofmann bm, hlavac m, martinez r, buchfelder m, müller oa, fahlbusch r. (2008). long-term results after microsurgery for cushing disease: experience with 426 primary operations over 35 years. j neurosurg, 108(1), 9– 18. 4. semple pl, vance ml, findling j, laws er. (2000). transsphenoidal surgery for cushing’s disease: outcome in patients with a normal magnetic resonance imaging scan. neurosurgery, 46(3), 553–558. 5. ciric i, zhao jc, du h, findling jw, molitch me, weiss re, refetoff s, kerr wd, meyer j. (2012). transsphenoidal surgery for cushing disease: experience with 136 patients. neurosurgery, 70(1), 70–81. 6. rutkowski mj, breshears jd, kunwar s, aghi mk, blevins ls. (2018). approach to the postoperative patient with cushing’s disease. pituitary, 18(2), 232-7. 7. beauregard c, dickstein g, lacroix a. (2002). classic and 403 gamma knife radiosurgery recent etiologies of cushing’s syndrome: diagnosis and therapy. treat endocrinol, 1(2), 79-94. 8. sheehan jp, xu z, salvetti dj, schmitt pj, vance ml. (2013). results of gamma knife surgery for cushing’s disease, j neurosurg, 119(6), 1486–1492. 9. chen jc, amar ap, choi s, singer p, couldwell wt, weiss mh. (2003). trans-sphenoidal microsurgical treatment of cushing disease: postoperative assessment of surgical efficacy by application of an overnight low-dose dexamethasone suppression test. j neurosurg, 98(5), 967– 973. 10. hammer gd, tyrell jb, lamborn kr, et al. (2004). transsphenoidal microsurgery for cushing’s disease: initial outcome and long-term results. j clin endocrinol metab, 89(12), 6348–6357. 11. dallapiazza rf, oldfield eh, jane ja jr. (2015). surgical management of cushing’s disease. pituitary, 18(2), 211216. 12. raff h. (2013). update on late-night salivary cortisol for the diagnosis of cushing’s syndrome: methodological considerations. endocrine, 44(2), 346-9. 13. petersenn s, beckers a, ferone d, van der lely a, bollerslev j, boscaro m, et al. (2015). therapy of endocrine disease: outcomes in patients with cushing’s disease undergoing transsphenoidal surgery: systematic review assessing criteria used to define remission and recurrence. eur j endocrinol, 172(6), r227-39. 14. jagannathan j, sheehan jp, pouratian n, laws er, steiner l, vance ml. (2007). gamma knife surgery for cushing’s disease. j neurosurg, 106(6), 980-7. 15. paduraru dn, albu se, carsote m, valea a. (2016). adrenal cushing’ s syndrome in a female with ovarian cancer. arch balk med union, 51(3), 410-412. 16. valea a, ghervan c, carsote m, morar a, iacob i, tomesc f, pop dd, georgescu c. (2015). effects of combination therapy: somatostatin analogues and dopamine agonists on gh and igf1 levels in acromegaly. clujul med, 88(3), 3103, doi:10.15386/cjmed-435. 17. valea a, carsote m, ghervan c, georgescu c. (2015). glycemic profile in patients with acromegaly treated with somatostatin analogue. j med life, 8 (spec issue), 82-6. 18. poiana c, chirita c, carsote m, hortopan d, goldstein a. (2009). galactocele and prolactinoma a pathogenic association? maturitas, 62(1), 98-102, doi:10.1016/j. maturitas.2008.10.015. 19. carsote m, chirita c, dumitrascu a, hortopan d, fica s, poiana c. (2009). pituitary incidentalomas how often is too often? j med life, 2(1), 92-7. 20. gheorghisan-galateanu aa, carsote m, valea a. (2017). incidentaloma: from general practice to specific endocrine frame. j pak med assoc, 67(6), 917-922. 21. poiană c, chiriţă c, carşote m, hortopan d, ioachim d, corneci cm, stănescu b. (2013). adrenal and pituitary incidentalomas in a case of cushing's syndrome. chirurgia (bucur), 108(6), 886-91 22. paduraru dn, nica a, carsote m, valea a. (2016) adrenalectomy for cushing's syndrome: do's and don'ts. j med life, 9(4), 334-341. microsoft word 14selectedabstracts romanian neurosurgery (2011) xviii 2: 205 – 229 205 1st regional congress of neurosurgery in the danubecarpathian region neurosurgical controversies 26th 27th may 2011 abstracts predictive outcome factors by open surgery in intracranial aneurysms (ia). an experience of 628 cases a.v. ciurea, a. tascu1, a. iliescu1, f.m. brehar1, r. rizea1, a. spatariu 1st clinic of neurosurgery “bagdasar arseni” clinical hospital “carol davila” medical school, bucharest, romania background: the intracranial aneurysm (i.a.) has a prevalence between 0,2-7,9% in the literature. the variability depends of hospital referral, neuroimaging findings and autopsy pattern. the pathology of intracranial aneurysms is a dominant element in neurosurgical activity, because of the multiple preoperative and management problems. ia affect mainly the active age (40 and 60 years old) and the male sex. generally the incidence in usa is 10-28/100.000 (official data). the etiology of ia may be: congenital, (aneurysms appear due to a defect of the muscular layer of the arterial wall), arterial hypertension, neoplastic disease, atherosclerosis, inherited diseases, trauma, infection (mycotic an.), unknown causes. in all the cases of aneurysm ruptures, some of the following are incriminated as risk factors: cigarette smoking, alcohol excess, life stress. the cerebral circulation must be evaluated in totality and aneurysms in particular and the accuracy management is necessary for limitation of important lifethreatring complication (rebleeding and ischemic stroke). material & methods: the authors present a study about 628 consecutive operated patients with intracranial aneurysms, operated in first neurosurgical department between 1997december 2010 – 14 years (40 children and 588 adults). most cases (286 case 45,5%) were between 41 and 50 years old. male is the preponderent sex 427 cases (68%) (2,1 : 1). the symptoms were dominated by: headache (98%), stiffneck (94%) and focal neurologic deficit (71%) etc. most patients were hunt and hess grade ii (230 cases, 36,7%) and hunt and hess grade 3 (97 cases, 15,4%) at admission. the associated pathology was: systemic arterial hipertension (471 cases, 75%) and obesity/hypercolesterolemia (214 cases, 34,1%), ischemic cardiopathy (100 cases,16%), diabetus melitus (100 cases,16%), chronic alcoholism (82 cases,13%), ischemic stroke (75 cases,12%), atrial fibrilation (63 cases, 10%), miscellanea (88 cases, 14%, anticoagulant therapy). the main investigations were: ct scan, ds angiography. actually, the most important were 3d ds angiography and 3d ct angioct. the common localization of intracranial aneurysms was the anterior communicating artery 183 cases (29,1%); the other locations 206 abstracts 1st regional congress of neurosurgery in the danube-carpathian region were: medium cerebral artery 157 cases (25%), posterior comunicating artery 107 cases (17%), internal carotid artery 84 cases, (13,3%), basilar top artery cases 21 (3,3%) and vertebral artery 11 cases (1,8%). multiple aneurysm represent in our data 65 cases (10,3%). all cases were operated, as soon as possible after the subarachnoid hemorrhage (sah) and ia angiography diagnosis. “early surgery” eliminates the risk of re-bleeding and facilities the treatment of vasospasm which peak is between 6-8 days post sah. from all complications two are very critical for life and morbidity: aneurysm rebleeding and cerebral ischemia. the authors present by personal experience the outcome predictive factors : age (up to 65 and under 5 years) associated pathology (arterial hypertension 491 cases (78,1%)), obesity and hypercholesterolemia 214 cases (38,3%), ischemic cardiopathy 107 cases (17%), diabetus mielitis 11 cases (16%) and so on, subarachnoid hemorrhage diffusion (according to the fisher scale), aneurysm particularities – number, shape, size, association with avms, aneurysm timing of operation, brain relaxation (hyperventilation and csf drainage) aneurysm rerupture, peroperatory vasospasm, icu facilities, possibilities of coiling treatment, early neuroprotection and neurorehabilitation. the glasgow outcome scale (gos) in our data (at 6 months postoperator) shows: good recovery 421 cases (67%), moderate disability 148 cases (23.5%), severe disability 31 cases (4.9%), persistent vegetative state 7 cases (1.1%), death 21 cases (3.4%). conclusions: ia represents an important neurosurgical challenge. also ia by the rupture and complication is the real lifethreatering diseases. clincal features are dominated by sah & neurological signs (hunt and hess scale-1968, was perfectly useful). complete vascular exclusion is the treatment of choice by open microsurgical approach or endovascular embolization. the important measures to avoid rebleeding and cerebral ischemic stroke in intracranial aneurysms are perfect evaluation and early approach, perfect aneurysm dissection and neuroprotective measures (pre, intra and postoperatory). neuroprotective agents – useful to avoid cerebral ischemic stroke the timing of aneurysm surgery is one of the key of avoidance lifethreatring complication. recent diagnostic and therapeutic management of gliomas with special emphasis on 3t intraoperative mr (239 cases) f. kramář, d. netuka, t. belšan1, v. beneš, s. ostrý, m. mohapl, d. hořínek, v. masopust dept. of neurosurgery and 1dept. of radiology central military hospital, prague, czech republic brain gliomas are the most frequent primary brain tumors. they include a variety of histological subtypes and diagnostics is based on histological classification which relies on morphological findings in the tumor tissue. the treatment is still complicated and not as successful as one would expect. however, in last years new diagnostic and treatment methods were introduced. in nonrandom chromosomal abberations and gene mutations were found in last decade. as a one of first steps in tumorigeneses mutation of idh1/2 was revealed in low-grade gliomas. duplication of braf gene was found in pilocytic astrocytomas. new chemotherapeutic agents are constantly put in trials, temozolomide has become the “golden“ standard in the treatment of romanian neurosurgery (2011) xviii 2: 205 – 229 207 malignant gliomas. the extent of resection of glioma seems to be a very important factor in progression-free and overall survival not only in high-grade but also in low-grade gliomas. methods: since april 2008 the imageguided surgical suite is routinely used for glioma surgery. the suite is directly connected with 3.0t mr scanner (ge) by rail-based transfer system (maquet) and capable to perform intraoperative mr examination (imri). a consecutive series of 213 patients undergoing surgery with imri is presented. all patients signed an inform consent for imri examination. patient´s head is fixed in 3.0t mr compatible headholder. surgery may be interrupted according to neurosurgeon decision at any moment and imri is then performed. the imri takes about 15-20 minutes depending on the mr examination protocol. results: since april 2008 to december 2010, 213 glioma patients underwent 239 surgeries (200 resections, 38 stereobiopsies, 1 tumor cyst puncture) with imri. we have performed a prospective study to evaluate the safety and efficacy of imri in this consecutive series. in 101 patients the radical resection was intended and it was achieved in 80 (80%). unexpectedly, in the group of non-intended radical resection in 10 cases of 99, radical resection was achieved. in total in 90 of 200 cases the tumor was radically resected (mr radicality), in 45% of all resections. in comparison with our older series the radicality ratio doubled (from 22% in 2006 to 45% in 2010). imri changed the surgery strategy in 25% of all cases, the resection continued after the imri. the goal of resection was achieved in 177 surgeries, in 23 cases the resection could have been more extensive by retrospective analysis. mortality in the series was 2,9% (7 patients), most common cause of death was haematoma (5 cases). morbidity was 26,7% (64 patients – any kind of complication) but serious worsening was observed only in 7,1% (17 patients.). total mm was thus 10% (9 haematomas, 15 neurological worsenings). conclusions: one of the new “most challenging” tools in gliomas seems to be intraoperative mr examination. it is a valuable method for gliomas, eficient and safe. in our experience the resection radicality increased more than twice with imri. the morbidity/mortality rate is slightly higher in our series, but still acceptable. treatment of supratentorial low-grade gliomas: surgical versus conservative istván nyáry semmelweis university, budapest, hungary the management of low grade glioma is one of the most controversial areas in clinical neuro-oncology. there are numerous communications outlining the difficulties in management of these lesions. indeed, the principal questions about their management remain unanswered. however, the concept of management of low grade gliomas is not unitary but much more a composite of different challenges depending on the clinical presentation, signs, neuroradiology, perspectives of neurologists, the opinion of the neurosurgeon, and perhaps most importantly, the aspirations of the patient. it is true therefore that in many patients there will be a dilemma about what is considered optimal management since there is no good evidence base to underpin any single management undertaken. conversely, however, there are many groups of patients with various low grade gliomas in whom management decisions 208 abstracts 1st regional congress of neurosurgery in the danube-carpathian region are made more easily and pragmatically. in this presentation, the current approaches to different low grade gliomas presenting with different symptom complexes in different regions of the brain will be reviewed and the rationale for decision making discussed. under the recent world health organization classification of primary intracranial tumors, low grade gliomas would encompass grade i and grade ii neuro-epithelial tumors. the more common grade i tumors are pilocytic astrocytoma, dysembryoblastic neuroepithelial tumors (dnet), pleomorphic xantho-astrocytoma (pxa), neurocytoma, and ganglioglioma. the more common grade ii tumors include astrocytoma, oligodendroglioma, and mixed oligoastrocytoma. this spectrum of neuropathological entities is important since the grade i tumors generally can be cured by surgical excision and their symptoms very often alleviated. in turn, with the grade ii tumors, these are generally incurable but have median survival times of > 5 years. tumors with oligodendodrial components generally do better than astrocytomas. basically, there are three treatment options for a low-grade glial tumors: surgery to remove the tumor, radiation therapy to shrink the tumor, observing the tumor to monitor changes until treatment is necessary. low-grade gliomas tend to grow very slowly and may not cause any signs or symptoms for years. because of this, simply monitoring the tumor with scans is a very reasonable approach. in such cases, treatment is delayed until the tumor appears to be growing or gives rise to problems. tumor location plays a key role in determining treatment. if the tumor is in a critical area, surgery will be a challenge and may cause significant and permanent brain damage, in these cases surgery also becomes a branching point in the therapeutic algorithm. special care is needed for the identification of eloquent in the surgery of tumors located near speech-eloquent or primary motor brain areas, along with special techniques of removal. usually, when the tumor can be safely removed, surgery is considered to be the best treatment. 30 – 40 % of pediatric primary brain tumors are low grade glioma. their annual incidence is calculated to be 10 –12 per 1.000 000 children under the age of 15 years in western countries. these tumors occur at all ages with a mean age at diagnosis or operation between 6 and 8 years. therefore, special reference is made to the management of pediatric cases. glioma surgery and neuronavigation are there any controversies? y. enchev1, b. iliev1, s. chakarov1, g. mitev1, v. karakostov2, k. romansky2, m. marinov2, v. bussarsky2 1department of neurosurgery, university hospital “sv. marina”, medical university-varna, bulgaria 2department of neurosurgery, university hospital “sv. ivan rilsky”, medical university-sofia, bulgaria aim: the purpose of the current study was to analyze prospectively the effect of neuronavigation on some intraoperative neurosurgical parameters at intracranial gliomas and to specify the indications for the application of neuronavigation in glioma cases. material and methods: the study included 58 patients with cranial gliomas treated neurosurgically with neuronavigational assistance. seven of the patients, who underwent biopsy as a standalone procedure (1 case through burr whole and 6following craniotomy), were analyzed separately as well as one case with a romanian neurosurgery (2011) xviii 2: 205 – 229 209 mesencephalic glioma, treated neuroendoscopically, was discussed in a neuroendoscopy group. the accomplished study on the rest 50 cases was prospective, evaluating the neuronavigational impact on the parameters: “skin incision”, “craniotomy”, “anatomical orientation”, “dissection guiding”, “tumour localization”, “assessment of the extent of resection” and “duration of surgery”. the patients were examined and followed-up in a standard manner. results: in the series, by means of neuronavigation, the gliomas were removed gross totally in 26 cases, subtotallyin 13 and partiallyin 11. no any procedurerelated morbidity and mortality were identified. in the cases with gross total tumour removal the navigation was evaluated as particularly useful for determination of the border tumouredematous brain tissue and for localization of potential tumour residuals. at the patients with subtotally and partially excised tumours, the preoperatively planned volume of surgical activity was accomplished. thus, the navigational guidance was assessed as necessary exactly for determination of the borders of the marked for extirpation volume of the tumour, in order to avoid the eloquent brain zones and the relevant neurological deficit. conclusion: in the resection of brain gliomas the neuronavigation optimizes the surgical approach, outlining their interrelations to the skull landmarks and to the neighboring critical neurovascular structures. in consequence, neuronavigation may improve the early surgical results by precise localization, reliable dissection guiding and increased radicalism. the neuronavigational guidance, as a rule, is indicated in glioma cases because of its versatile benefits. arguments in favor of intraoperative ultrasonography in gliomas v. pasca, m. rus, şt.i. florian department of neurosurgery, cluj-napoca intraoperative ultrasonography is a means of investigation in real time, widely available, relatively inexpensive and nonconstraining. it is used to localize subcortical and deep lesions, define tumor margins, evaluate the tumor resection and determine the surgical complications. the transducer can be put into practice repeatedly within different stages of the operation. color and power doppler bmode sonography offers the possibilities of intraoperative control of neurosurgical procedures, recognition of tumor vascularisation, which thus helps avoiding unnecessary bleeding and preserves the vessels in contact with the tumor. ultrasonography estimates the unclear boundary between the tumor and brain edema, and comes in the aid of operative approach’s planning. the quality of ultrasonography improves with newer technologies, higher frequencies. the major drawback of ultrasonography is that it cannot be applied in order to acquire images through substances of high density (bone). why the current standard multimodal treatment failed? the glioma stem cells paradigm şt.i. florian1, o. soritau2, c. tomuleasa1, d. cernea2, a. cocis2, c. abrudan2 department of neurosurgery, cluj-napoca objective: angiogenesis is an important prognostic factor associated with tumor growth and progression. starting from personal clinical observations in some cases of re-intervention for recurrence in patients 210 abstracts 1st regional congress of neurosurgery in the danube-carpathian region treated with temozolomide (tmz), regarding to the development of particular aspects of angiogenesis, specific tumor angiogenic characteristics were investigated, to identify the most suitable prognostic factor in generating multimodal therapy protocols. material and methods: fresh tumor biopsies were processed for obtaining established cell lines and for development of a three dimensional (3d) functional angiogenesis assay in fibrin-gel matrix supplemented with serum-free growth medium, in presence of tmz and antiangiogenic or pro-angiogenic factors (bevacizumab, sunitinib, vegf, egf and pdgf). chemosensitivity for tmz of isolated tumor cells was determined by mtt test. genes implicated in angiogenesis were evaluated at mrna level by real-time pcr in tumor tissue and peritumoral tissue as control: vegf, pdgf, tnf-α, icams, ctgf, epcr. microvascular density (mvd) was also determined using a protocol adapted after weidner’s method. results: in 14 established cell lines, tumor cells tested by mtt assay shown sensitivity for tmz in 60% of cases. spontaneous angiogenesis was observed in most of the tumor explants tested and the development and spreading of capillary structures were enhanced in presence of tmz in 11 from 19 cases ( 57.8%). mvd values varied between 22-130, with a median value of 83.6. enhanced angiogenic potential in 3d model was correlated in 4 cases with higher mdv results (mdv>90) (21%) and in 5 cases with an increased expression of proangiogenic genes(26%). higher levels of vegf and pdgf mrna were observed in 47% of tumors. conclusions: a great individual variability was observed in tumor cells sensitivity to tmz and in angiogenic potential of gm, suggesting that these processes are controlled by multiple factors, mainly by the presence of growth factors such as vegf and pdgf, but in correlation with other variable local factors from the vascular niche. tmz enhanced angiogenesis in some tumors, probably by selection of cancer stem cells. a complex evaluation of each tumor can indicate the best choice of further therapy. individualized treatment strategies in pediatric low-grade gliomas (microsurgery vs stereotactic biopsy and brachytherapy) a. peraud, j.c. tonn, f.w. kreth neurochirurgische klinik und poliklinik, klinikum großhadern, ludwig-maximilians-universität, marchioninistrasse 15, 81377 münchen objective: in search for optimized treatment conditions for children with who grade i and ii gliomas not accessible to complete resection, brachytherapy (bt) has been proven to be beneficial. bt with temporary iodine-125-seeds provides precise radiosurgical planning sparing surrounding normal tissue. the results in 29 pediatric cases treated with bt after partial tumour resection or with bt alone, are presented. methods: 15 boys and 14 girls were included in the present study. mean age at the time of bt was 9 years. tumour location was hypothalamic/suprasellar in 9, lobar in 8, deep in 6, within the brainstem in 4, and in the cerebellum in 2 children. histology revealed 18 pilocytic astrocytomas, 9 fibrillary astrocytomas, one ependymoma and one ganglioglioma. partial resection with subsequent bt was performed in 12 cases, 17 tumours were stereotactically biopsied and implanted with iodine-125-seeds. results: mean follow-up time was 33 romanian neurosurgery (2011) xviii 2: 205 – 229 211 months. ten tumours showed complete regression 6 to 40 months after seed implantation, tumours decreased in size in 18 children 2 to 16 months after bt. two children developed space occupying radionecrosis which had then to be resected leading to neurological improvement. one boy died due to tumour progression of his who grade ii astrocytoma. twelve children even experienced an improvement of their previous neurological deficits. conclusions: brachytherapy is a safe and effective method even in the younger patient group under 3 years of age. microsurgery in combination with bt or bt as single treatment provides excellent surgical outcome, good tumour control and low morbidity. new facts on epidemiology and prevention in traumatic brain injury in germany wolf-ingo steudel klinik für neurochirurgie, universität des saarlandes, homburg/saar, germany introduction: the purpose of epidemiology is disease control and prevention. a review of the data published on the epidemiology of traumatic brain injuries (tbi) reveals that the data of almost all studies are drawn from local or regional series. nationwide data are rarely available. in germany, there has been a nationwide mortality register since 1898 and since 1994 all hospitals provide data on all admissions. in addition, the whole country is divided in trauma centres which provide data since 1995. methods: all head injuries between 1972 and 2009 were analysed according to icd-9 and after 1998 according to the updated icd-10.the data were provided by the federal bureau of statistics. the data of hospitalized cases and fatal cases were correlated with population data to calculate incidences and mortality rates. age-group specific data as well the specific situation after the reunification were also available and analysed. results: the incidence rate of fatal head injuries in germany decreased continuously from 27.2/100 000 in 1972 to 8.3/100000 in 2006.the mortality is highest inside the group older than 75 years. after the reunification in 1989 the number of fatal head injuries showed a temporary increase till 1994.the number of patients treated in-hospital increased from 266 944 in 1995 to 316 573 in 2006. the majority of hospitalized patients suffered minor head injuries. there is an increase in the number of vehicles and motorcycles on german roads and highways (in 2002 over 53 millions vehicles and 3.6 millions motorcycles), but a marked decrease of severe traffic accidents. the number of surgical procedures is highest in the age group 70 till 75 years. conclusions: analysis of the data of all german hospitals reveals surprising views of incidence, morbidity and mortality rates of head injuries in this country. rapid changes in motorization during the reunification period cause an increase of severe head injuries. prevention by laws and technical standards are very important. less head injuries caused by traffic accidents occur due to the increasing age of the population. but with increasing age more severe accidents occur at home. 212 abstracts 1st regional congress of neurosurgery in the danube-carpathian region seven years experience in 3d custommade implants for craniofacial bone defects reconstruction h. rotaru1, şt.i. florian2, h. stan2, gr. băciuţ1, r. schumacher3, h. f. zeilhofer4, h. chezan5, m. băciuţ1, c. dinu1, s.g. kim6, p. kiss2 1department of cranio-maxillofacial surgery, “iuliu hatieganu” university of medicine and pharmacy, cluj-napoca, romania; 2department of neurosurgery, “iuliu hatieganu” university of medicine and pharmacy, cluj-napoca, romania; 3department of medical rapid prototyping, fachhochschule nordwestschweiz, muttenz, switzerland; 4hightech research center of cranio-maxillofacial surgery, university hospital of basel, basel, switzerland; 5national rapid prototyping laboratory, technical university, cluj-napoca, romania; 6department of oral and maxillofacial surgery, college of dentistry, gangneung-wonju national university, gangneung, korea background and objectives: the posttraumatic or postoperative cranio-facial bone defects have functional and esthetical impairments among involved patients that can not be underestimated. for this reasons reconstruction of cranio-facial defects, a step in multimodal rehabilitation treatament, is mandatory. in the last years, the development of rapid-prototyping technologies offers the possibility of reconstructing some of the bone defects with custom-made craniofacial implants from alloplastic materials. this paper present our seven years experience in using these modern technologies. material and method: different bone defects of neural or visceral skull were morphological and functional rehabilitated using custom-made implants of polymethylmethacrilate or polyethylmethacrilate-hydroxyapatite. the implants were produced by threedimensional modeling, rapid-prototyping and casting into silicone-rubber molds. results: produced for each specific case, the custom-made implants adapted perfectly into the bone defects, assuring an excellent morphological and functional rehabilitation. due to the preoperative modeling, the time spent into the operation was significantly decreased. there were no adverse effects to the materials used. the process of producing custom-made craniofacial implants still involves an expensive technology which limits their use to complex cases but the future will expand the use of these technologies to ordinary cases. conclusions: the possibility of producing custom-made implants opened a new era in the reconstructive surgery of the craniofacial area. despite of some disadvantages linked to the high costs of production, the advantages of their clinical use proved to be multiple. surgery of the tumours of the third ventricle, our attitude juraj šteňo department of neurosurgry, comenius university, bratislava, slovakia neural structures composing the walls and the floor of the third ventricle participate at important functions, first of all maintenance of the homeostasis, memory mechanisms and visual functions. gradual involvement of the structures by enlarging tumour may be compensated for a certain time period. surgical manipulation with damaged neural structures during exposure of the tumour and its removal may cause serious worsening of the patient’s condition. therefore in past the main goal of surgery was biopsy and reopening or shunting the cerebrospinal fluid spaces. romanian neurosurgery (2011) xviii 2: 205 – 229 213 improvement of imaging diagnostic methods and microsurgical techniques enabled to reach almost any region of the brain without causing permanent neurological deficit. sufficient exposure of the tumour and its relationships with surrounding structures may thus be reached. surgeon thus can determine optimal extent of surgery and under favourable anatomical conditions may remove the tumour radically without jeopardizing the patient. in our series of more than one hundred patients this could be reached in two thirds of them with surgical mortality below 3%. the extent of tumour resection varied according to the location of the tumour and its histological nature. in our series we did not include patients with the tumours located predominately inside the lateral ventricles extending into the cavity of the third ventricle through a dilated foramen of monro or the patients with the tumours growing within the lateral wall of the ventricle, i. e. in the thalamus (paraventricular tumours). according to the relationships of the tumour to the ventricular cavity and to its floor three types of lesions were distinguished: basal tumours (intraventricular or intraventricular and extraventricular craniopharyngiomas, gliomas) occupying predominately basal part of the ventricle involving its floor, oral tumours (colloid cysts, gliomas) occupying predominately superior part of the ventricular cavity sparing the ventricular floor, and caudal tumours (pineocytomas, pineoblastomas, embryonic cell tumours, gliomas) growing in the posterior part of the ventricle. during the resection of the basal tumours we made every effort not to damage the optic chiasm and the hypothalamus. the goal could be achieved by choosing an appropriate surgical approach and the optimum extent of tumour resection: a) a part of a craniopharyngioma involving the hypothalamic structures within the floor and the walls of the third ventricle was left alone, b) anterior part of basal gliomas infiltrating the chiasm was not resected; only posterior-superior part of the tumour which occluded the third ventricular chamber and not infiltrated its lateral walls was removed. the most endangered structure during removal of the oral tumours is fornix. care must be taken to preserve it in order to avoid severe memory disturbances. whenever possible we avoided manipulation with both halves of the fornix; we always try to remove the tumour through one foramen of monro and use the other only for assessing the completeness of resection if necessary. oral gliomas did not involve the ventricular floor and could be safely completely resected in majority of patients. the most favourable anatomical conditions from surgical point of view were encountered in patients with caudal tumours which could be removed radically in a great majority of patients including those with gliomas. controversies in craniopharyngiomas. total or partial removal? a.v. ciurea, a. tascu, d. talianu, f. brehar, a. giovani 1st clinic of neurosurgery “bagdasar arseni” clinical hospital “carol davila” medical school, bucharest, romania objectives: craniopharyngiomas (cph) are benign slow-growing intra-cranial calcified tumors, preponderant in children. cph expand in the pituitary stalk axis, from the sphenoid body to the third ventricle. mri improves the anatomical location, the tumor diagnosis and the 214 abstracts 1st regional congress of neurosurgery in the danube-carpathian region operative strategy. microsurgery represents the main treatment option in spite of major difficulties. the goal of this study is to analyze the outcome of a series of 122 cph cases of pediatric population, treated surgically. methods: authors performed a retrospective analysis of 122 consecutive children (0 – 16 year old) with cph diagnosed and operated at the “bagdasararseni” clinical hospital, bucharest, during a period of 20 years (1991 – 2010). in this cohort of children, males were slowly preponderant (64 boys and 58 girls), affecting predominantly the age group 7 – 10 y.o. (49 cases – 40.2%). clinical features consisted of visual impairment (85 cases 69.6%), endocrine dysfunction (99 cases 81.3%) and increased icp syndrome (82 cases 67%). visual and endocrine symptoms prevailed. headache, was frequently encountered 106 cases (86.6%). hydrocephalus was present preoperatively in 31 cases (25,4%) and was dealt with vp shunt before definitive tumor therapy in 15 cases (12.3%). the essential neuroimaging findings is actually mri. no dsa investigation was carried out routinely. pathology: the adamantinous type was preponderant in children (111 cases91.1%). all the cases were followed up during a period going from 6 months to 15 years. in our series, in children, the most frequent location of cph was the suprasellar retrochiasmatic region (89 cases – 73.2%). pathologically, combined forms (cystic forms with calcifications) are prevalent: 65 cases (53.6%). a personal craniopharyngiomas grading scale was presented. in children, surgical approach was adapted to the tumor location: bilateral subfrontal (42 cases–34.4%), unilateral frontal (26 cases-21.4%), and pterional (24 cases–21.4%), followed by midline interhemispheric (21 cases–16.9%), transcallosal (3 cases–2.7%) and combined (6 cases-5.3%). actually, the fronto-lateral and pterional approach were preponderant surgical strategy both in children and adults. results: in children: the total removal of the cph was the goal of the surgery, but this was achieved in only 65 cases (54.4%), because of the risk of functional impairment or possible operative mortality. in 11 cases (8.9%) we performed near-total resection, in 41 cases (33.9%) partial resection, and 5 cases (4.1%) were biopsies. we performed biopsy with cyst evacuation only on giant, extremely compressive forms, in which the tumor collapse was accompanied by cardiac bradycardia. hydrocephalus was present in 32 cases (26.2%). no intraoperative death occurred. in the first month, there were 6 deaths (4.9 %), due to hypothalamic injury, in each case total removal having been attempted. the real recurrences occurred in 22 cases from 66 cases of total removal (33.3%); tumor regrowth was noticed in 44 cases (77.2%) from a total of 57 cases with remnant tumor (near-total, partial and biopsies). the actual treatmnent target the cystic craniopharyngiomas which is prevalent on children. in this situation, have tried: catheter on cyst and evacuation of the cyst in omaya reservoir, which is needle periodically; chemotherapy with bleomycin intracystic with disadvantages of allergy to this drog and multiple adherent, intracystic application of isotope of: phosphorus-32; rhenium-186; yttrium-90 completelly prohibited today and finally application of interferon alfa with some good results. the procedure consists in intracystic catheter placed by: 1.single burr hole using neuronavigation, 2. endoscopically, 3. romanian neurosurgery (2011) xviii 2: 205 – 229 215 positioning by craniotomy or 4. subcutaneous ommaya reservoir (3,000,000 iu/day for 12 days) + cyst fluid aspiration. gamma kinfe surgery (gks) was performed in 7 cases in children, all with reccurences, but the results remain disputable because the tumoral chist pression asked a surgical approach. neuropsychological assessments revealed no altered iq at individual level. the intracranial hypertension (icp) and the tumor localization determine attention deficits. extended tumor localization determines the deficient mental control and the apathy. the reccurent tumors determine psychological dysfunction: attention, memory and the orientation. the depression is dependent by age old of the patients and the qol is dependent by the tumor localization. psychosocial reinsertion is affected by memory dysfunction, medium moodiness and the forceless ego. a good rehabilitation recorded in 50% patients who underwent counseling before neurosurgical interventions. conclusions: surgical treatment remains the main option, but the important number of complications, regrowths and recurrences prove the necessity of a multidisciplinary approach: microsurgery, radiosurgery and endocrinological treatment. total or partial removal depends on the tumoral volume and hypothalamic adherences. actually the authors advocate for partial removal with adjuvant therapies. the adamantinomas type was very important in reccurences and regrowths of cph. also, the authors present a cph scale which facilitates the perfect location, surgical approach and outcome in this kind of tumor. orbital exenterations actual point of view ioan szabo, bianca szabo purpose: to determine the clinical indications and surgical approaches in the orbital exenterations. methods: retrospective case review of 46 exenterations performed in cluj county emergency hospital, romania, 1990 and 2011. reviewed data indications for exenteration, histopathologic diagnosis, and recurrences on follow-up. results: secondary intraorbital spread of malignant adnexal tumors was the most common indication for exenteration (24of 46). among these, the site of the primary neoplasm was the eyelid in 18 cases. exenteration was total in 10 cases, subtotal in 7 cases, and extended in 28 cases and bilateral in 1 case. in 5 cases, a dermis-fat graft was used for socket reconstruction; 3 cases were allowed to granulate spontaneously, subtotal exenteration posthesis in 12 cases, ti dynamic mesh in 39 cases. the average healing time was 21 weeks, (range, 4–6 months) for spontaneous granulation, and 6 weeks (range, 4–8 weeks) for dermis-fat grafts, 2 weeks in exenteration prosthesis and ti dynamic mesh. survival of the patients in the first year after exenteration (43 of 46) 93,4%. long term folow up 11 recurrences (23.9%). 13 patients (28,2%) died in the first 5 years after exenteration for agressive tumors. conclusions: the first year is the most important period for follow-up of local recurrences, but systemic examination is needed for the longer follow-up. the exenteration prosthesis and plastia with dynamic mesh significantly reduce the healing time and ameliorte the aesthetic aspect. 216 abstracts 1st regional congress of neurosurgery in the danube-carpathian region new diagnostic techniques in developmental abnormalities of cerebral venous evolution swi (susceptibility weighted imaging) stanca ples, horia ples, gabriela catau diagnostic imaging center neuromed timisoara neurosurgical departament, county hospital timisoara dva (developmental venous anomalies) are congenital cerebrovascular anomalies. this pathology was detected since new imaging tehniques have developed, tehniques in which slow flow vessels and any trace of hemosiderine can be seen. this new tehnique is called swi (susceptibility weighted imaging). our study is a preliminary study of 44 cases with different types of venous angiomas, with different situations, types and clinical manifestation. we detected also the presence in the same time of 30% cases of asociated cavernous angiomas. examination was made with siemens1,5 t avanto mr, we used: t1-tse 2 d, t1 mprage 3 dwe with gadolinium, t2 tse, t2 flair, swi. conclusions: the development of new mr techniques alowes to detect this new pathology of dva, to evaluate the complexity and the treatment of this cerebral vascular anomalies. clip or coil: treatment of mcaaneurysms after isat u. kehler, m. brunken dept. of neurosurgery, asklepios klinik hamburg altona, germany after the isat-study a substantial change of aneurysm treatment away from clipping towards coiling was observed. however, the long-term results concerning the clinical outcome do not show an advantage but a higher rebleeding rate in the coil group. we evaluated our middle cerebral arteryaneurysms from 2007 to 2010: 105 patients were treated, 58 were admitted with a subarachnoid hemorrhage. clinical results in the clip group were favorable although not showing statistical significance. mortality rate in the clipgroup with sah was 9% respective 25% in the coil-group. no mortality in unruptured mca aneurysms was observed in either group. the microsurgical approach for mcaaneurysms is also after isat a very good approach and seems to be superior in many cases. however, in every case, an individual approach should be discussed by the vascular team – independent to any vanity to realize the best result for the patient. aneurysm treatment in europe: an internet survey bradac ondrej introduction: aneurysm (an) treatment appears to differ from country to country and even from centre to centre. we therefore decided to conduct a survey, better to understand ‘state of the art’ aneurysm treatment in europe. aims: primary aim was to understand the roles of clipping and coiling in aneurysm treatment. design and methods: an interactive form was sent to major european neurosurgical centres. the responses relating to an location, status (ruptured/unruptured) and treatment modality were divided with regard to the volume of cases and centres geographical location. results: responses were received from 99 european centres. main finding was that clipping was used significantly more often in eastern europe than in the rest of europe to treat ruptured ans of anterior romanian neurosurgery (2011) xviii 2: 205 – 229 217 circulation (median 90% acomaans in eastern vs. 30% in rest of europe, 100% of mcaans vs. 70%, 90% pcomaans vs. 30%, 80% icaans vs. 20%). almost all ruptured ans across all locations are treated actively. the treatment of unruptured aneurysms of anterior circulation is similar. the median relating to observed unruptured ans across the europe was 10%. posterior circulation ans are treated predominantly by coiling, regardless of aneurysm status or geographical location. the average number of coilers vs. surgeons per centre was 2.5:3.0 in western , 1.9:3.6 in southern, 1.9:4.3 in eastern and 2.7:3.1 in northern europe. conclusions: the way in which intracranial aneurysms are treated appears to correlate with the economic development of european countries. it is probably also affected by the lack of experienced coilers in eastern europe. new endovascular treatment options for intracranial aneurysms based on flow dynamics and flow related biology i. szikora1, á. ugron2, gy paal2, zs berentei1, m. marosföi1, i. gubucz1 1national institute of neurosciences, budapest, hungary 2university of technology and economics, budapest, hungary the clinical benefits of endovascular treatment for intracranial aneurysms have been proved by multiple studies. although the endovascular approach provides better clinical outcome, its long-term stability is inferior as compared to open surgery. until recently, all endovascular techniques were entirely based on the mechanical obstruction of the aneurysm cavity as it is seen on angiographic images. treatment plan was purely based upon the geometry and the underlying hemodynamic conditions were not taken into consideration. in order to design more effective treatment methods, better understanding of the disease process is inevitable. with the combination of modern imaging technology and computer science, the local flow dynamics can be studied in vitro in real human aneurysms. it is well known, that intracranial aneurysms grow at arterial sections exposed to high hemodynamic load. computed fluid dynamics (cfd) simulation demonstrates that the most important hemodynamic factor in aneurysm initiation is high wall shear stress (wss) and even more importantly high spatial wss gradient. inside the aneurysms, high wss areas seem to induce further aneurysm growth, while low wss sections are prone to wall degeneration and may lead to rupture. understanding of the local hemodynamics initiated the development of new therapeutic methods. instead of attempting a mechanical obstruction while leaving the surrounding flow dynamics unchanged, these techniques aim to modify to local flow conditions in a way that favor aneurysm thrombosis. for sidewall and fusiform aneurysms, intravascular flow diverters are now regularly used and achieve a rate of over 90% thrombosis in large and giant aneurysms at 6 months and 1 year. further, this technique makes the aneurysms to collapse, effectively alleviating mass effect and compression syndromes. for bifurcation aneurysms, intrasaccular flow diverters are being developed that demonstrates promising early results in clinical application as of today. conclusion: understanding the interaction between flow and biology may help to develop treatment techniques that achieve true arterial reconstruction and high longterm stability. 218 abstracts 1st regional congress of neurosurgery in the danube-carpathian region brainstem cavernomas treated microsurgically and radiosurgically e. knosp, k. kitz, j. frischer dept. neurosurgery medical university vienna, austria the purpose of this retrospective study was to compare the long-term outcome of brainstem cavernomas after microsurgical or radiosurgical treatment in our institution. microsurgical resection of a cm was performed in 21 patients and 26 patients had been treated by gamma knife surgery. all cavernomas of the rs group were deep seated. following the classification of schefer and valavanis most lesions were classified as type ii (11.55%) and type i (6.30%). the most common localization was pons (50%), followed by thalamus (30%). neurological improvement was found in 66% after microsurgery (ms) and 50% after gamma knife radiosugery (gk), unchanged in11% after ms 25% after gk. deterioration ocurred in 22% after ms and in 25% after gk. one patient died after rebleeding after gk treatment. reduction of bleeding rates was achieved in both groups (p< 0.001) and neurological improvement was also found in both groups applying the modified rankin scale ( 0.9 after surgery and 0.5 after radiosurgery). conclusion: our experience show, that brainstem cavernomas can be treated with low morbidity and mortality. during a long-term follow-up both, microsurgery and gamma knife radiosurgery, are effective to reduce significantly the rebleeding rates. predictive outcome factors by open surgery in intracranial aneurysms (ia). an experience of 628 cases. a.v. ciurea, a. tascu1, a. iliescu1, f.m. brehar1, r. rizea1, a. spatariu 1st clinic of neurosurgery “bagdasar arseni” clinical hospital “carol davila” medical school, bucharest, romania background: the intracranial aneurysm (i.a.) has a prevalence between 0,2-7,9% in the literature. the variability depends of hospital referral, neuroimaging findings and autopsy pattern. the pathology of intracranial aneurysms is a dominant element in neurosurgical activity, because of the multiple preoperative and management problems. ia affect mainly the active age (40 and 60 years old) and the male sex. generally the incidence in usa is 10-28/100.000 (official data). the etiology of ia may be: congenital, (aneurysms appear due to a defect of the muscular layer of the arterial wall), arterial hypertension, neoplastic disease, atherosclerosis, inherited diseases, trauma, infection (mycotic an.), unknown causes. in all the cases of aneurysm ruptures, some of the following are incriminated as risk factors: cigarette smoking, alcohol excess, life stress. the cerebral circulation must be evaluated in totality and aneurysms in particular and the accuracy management is necessary for limitation of important lifethreatring complication (rebleeding and ischemic stroke). material & methods: the authors present a study about 628 consecutive operated patients with intracranial aneurysms, operated in first neurosurgical department between 1997 december 2010 – 14 years (40 children and 588 adults). most cases (286 case 45,5%) were between 41 and 50 years old. male is the preponderent sex 427 cases (68%) (2,1 : 1). the symptoms were dominated by: headache (98%), stiffneck (94%) and focal neurologic deficit (71%) etc. most patients were hunt and hess grade ii (230 cases, 36,7%) and hunt romanian neurosurgery (2011) xviii 2: 205 – 229 219 and hess grade 3 (97 cases, 15,4%) at admission. the associated pathology was: systemic arterial hipertension (471 cases, 75%) and obesity/hypercolesterolemia (214 cases, 34,1%), ischemic cardiopathy (100 cases,16%), diabetus melitus (100 cases,16%), chronic alcoholism (82 cases,13%), ischemic stroke (75 cases,12%), atrial fibrilation (63 cases, 10%), miscellanea (88 cases, 14%, anticoagulant therapy). the main investigations were: ct scan, ds angiography. actually, the most important were 3d ds angiography and 3d ct angioct. the common localization of intracranial aneurysms was the anterior communicating artery 183 cases (29,1%); the other locations were: medium cerebral artery 157 cases (25%), posterior comunicating artery 107 cases (17%), internal carotid artery 84 cases, (13,3%), basilar top artery cases 21 (3,3%) and vertebral artery 11 cases (1,8%). multiple aneurysm represent in our data 65 cases (10,3%). all cases were operated, as soon as possible after the subarachnoid hemorrhage (sah) and ia angiography diagnosis. “early surgery” eliminates the risk of re-bleeding and facilities the treatment of vasospasm which peak is between 6-8 days post sah. from all complications two are very critical for life and morbidity: aneurysm rebleeding and cerebral ischemia. the authors present by personal experience the outcome predictive factors : age (up to 65 and under 5 years) associated pathology (arterial hypertension 491 cases (78,1%)), obesity and hypercholesterolemia 214 cases (38,3%), ischemic cardiopathy 107 cases (17%), diabetus mielitis 11 cases (16%) and so on, subarachnoid hemorrhage diffusion (according to the fisher scale), aneurysm particularities – number, shape, size, association with avms, aneurysm timing of operation, brain relaxation (hyperventilation and csf drainage) aneurysm rerupture, peroperatory vasospasm, icu facilities, possibilities of coiling treatment, early neuroprotection and neurorehabilitation. the glasgow outcome scale (gos) in our data (at 6 months postoperator) shows: good recovery 421 cases (67%), moderate disability 148 cases (23.5%), severe disability 31 cases (4.9%), persistent vegetative state 7 cases (1.1%), death 21 cases (3.4%). conclusions: ia represents an important neurosurgical challenge. also ia by the rupture and complication is the real lifethreatering diseases. clincal features are dominated by sah & neurological signs (hunt and hess scale-1968, was perfectly useful). complete vascular exclusion is the treatment of choice by open microsurgical approach or endovascular embolization. the important measures to avoid rebleeding and cerebral ischemic stroke in intracranial aneurysms are perfect evaluation and early approach, perfect aneurysm dissection and neuroprotective measures (pre, intra and postoperatory). neuroprotective agents – useful to avoid cerebral ischemic stroke the timing of aneurysm surgery is one of the key of avoidance lifethreatring complication. controversies in ruptured aneurism timing i. poeata, z. faiyad, s. gaivas a. chiriac, bogdan chirita aneurismal subarachnoid hemorhage was and still is in our days a subject of large debate and controversies. historical periods in this field evolved from controversies: surgery – conservative treatment, macrosurgery – microsurgery, delayed surgery – early surgery, open approach – 220 abstracts 1st regional congress of neurosurgery in the danube-carpathian region endovascular approach. hunt and hess scale was created to differentiate class of patients suitable for early surgery in anesthetic and surgical conditions offered in the 70’s. despite initially aged patients and high score patients were considered for delayed surgery, during the next years technical advances in more and more hospitals modified this limit toward an early aneurismal occlusion. in this paper we analyze 170 ruptured aneurisms operated on in a period of 24 months (01.01.2009 – 31.12.2010). the analyses criteria were: time of admission, time of surgery, h&h grade, aneurism position and morphology, associated hematomas or hydrocephalus, age, associated medical conditions, especially hbp, complications and results. only 50% of the patients were submitted to an early surgery (first 3 days after rupture). the reason of delayed surgery was in range: delayed admission, high clinical grade, medical comorbidities, age of the patient. the protocol changed during these two years toward a more active attitude especially concerning early surgery in elderly people. our hospital protocol together with endovascular treated cases and the literature review are also emphasized. mini-invasive instrumented stabilization of lumbar and thoracolumbar spine vaněk p department of neurosurgery, charles university 1st faculty of medicine and central military hospital prague, czech rep. minimally invasive spine surgery (miss) represents a growing collection of surgical techniques that allow surgeons to perform spinal procedures through smaller incisions. the primary goal of miss is to limit damage to the soft tissue envelope of the spine, thereby diminishing postoperative pain and allowing an earlier return to normal activities. other advantages of miss include reduced blood loss, shorter hospitalization and quicker rehabilitation. miss procedures generally depend in part on the use of specialized surgical equipment including operative microscopes, endoscopes, cannulated screw technology, tubular retraction systems, fiber optic lighting and image guidance technology.it is an important not to compromise the goals of the surgical procedure when performing a miss approach. as with traditional spinal surgery, adequate decompression of the neural elements and meticulous preparation of a spinal fusion bed should be achieved. the objective of our study was to compare the efficacy of three techniques of instrumented transforaminal lumbar interbody fusion (tlif) in the treatment of low grade degenerative instability of lumbar spine. we conducted a prospective study with mean follow up 26 months. eighty-five patients (39 men and 46 women) were enrolled into study. twenty-seven patients (group 1) were treated by standard median approach with subperiosteal separation of muscles and 38 by two paramedian wiltse transmuscular incisions (group 2). interbody fusion was done by unilateral insertion of cage after total or partial resection of facet joint. srews were inserted according the method advocated by weinstein in both groups. twenty patients (group 3) were instrumented by percutaneous screw system a way for interbody fusion was done through tubular retractor. decompression of spinal canal romanian neurosurgery (2011) xviii 2: 205 – 229 221 was done by one side partial hemilaminectomy and undrecutting of opposite side. operation time, blood losses, number of complications, accuracy of pedicle insertion were evaluated. post operative pain profiles were measured each day during the first week after surgery by visual analoque scale (vas). vas and oswetry disability index (odi) were filled during outpatient controls 6 weeks, 3 and 6 months, one and two years after sugrery. overall patient´s satisfation and fusion were assesed 2 years after surgery. there were no significant diference in operation time among these three groups (p>0.05). in group 2 and 3 blood losses were less significantly compared to group 1 (p<0.05). first week post operative pain profile meassured by vas was significantly different for groups 2 and 3 compared to group 1. (p<0.05) patients from group 2 and 3 were less painful and no significant differencebetween these groups were found. no significant difference in values of vas and odi were found during the rest of follouw up. overal satisfaction was without any significant difference among the groups after two years of follow up.(p>0.05) we have concluded that long term clinical and radiological results after instrumented tlifs in degenerative lumbar spine instability are not related to extend of surgical approach. less invasive technique can offer more convenient pain profile during the first days after surgery. less invasive instrumented tlif looks to be viable alternative to standard techniques in treatmet of low grade lumbar spine instability. after familiar adoption of miss technique on the field of the degenerative lumbar spine instability we have decided to expore potential of mis in the tratment of other patologies. in the next pilot study we treated 15 patients with thoracolumbar fractures type a, according ao classification). we observed one screw malpozition, without any clinical consequences, no other periprocedural complication, no wound complication, no hardware failure and no lost of corresction during one year follow up. miss technique was used in the treatment of couple low back pain cases from the posterior approach and as aditional posterior instrumentation after anterior procedure too. finally, after five years lasting experinece with miss, we can conclude that low grade slips on the lumbar spine, thoracolumbar fractures type a or b, low back caused by ddd, some spinal tumors and inflamations could be recommended for this treatment. complex deformities, thoracolumbar fractures type c and high grade slips still present suboptimal indication. controversies in anterior cervical discectomy i. poeata, c. popescu, z. faiyad, s. gaivas, b. costachescu, b. iliescu herniated cervical disc in still a subject of acute controversies to our days. in our hospital we are routinely doing two different kinds of surgery by two different teams witch are among the authors. one attitude is microsurgical simple discectomy and osteophytes resection. the other attitude consists in discectomy and instrumentation, most often with intracorporeal polymeric cages. we analyze 30 consecutive cases operated on with the first protocol and 30 consecutive cases operated on with the second protocol. symptomatology, imagistic aspect, cervical stability evaluated through flexion 222 abstracts 1st regional congress of neurosurgery in the danube-carpathian region extension radiography, post-operative immobilization, complications and outcomes were evaluated for all these cases. a bias consisting in applying the protocol with implants exists because all the cases with instability were treated by this method but this condition was met in only two cases. we present illustrative cases and surgical videos. no significant differences were observed between the two groups with a two month post-operative control. some literature data are also reviewed. in our experience the two procedures seem to be equivalent in short term results and seem to be a personal preference of the surgeon. treatment options in recurrent highgrade gliomas dana cernea1, şt.i. florian2, v. bogdan1, magda petrescu3, vasile popita1, renata zahu1, ioana sicoe1 1oncology institute “ion chiricuta” cluj napoca; 2university of medicine and pharmacy cluj-napoca; 3county hospital cluj napoca, romania glioblastoma is the most common malignant primary brain tumor in adults. the current standard of care is maximal safe neurosurgical resection followed by radiation treatment to the involved brain with concurrent and adjuvant temozolomide . despite aggressive treatment, local tumor recurrence or progression develops in most patients in less than 1 year. there are limited options for salvage therapy: re-operation (if possible and clinically appropriate); re-irradiation (if no other options or small volume recurrence); local –therapy in conjunction with re-operation or investigational therapy); chemotherapy; targeted therapy (i.e., bevacizumab) or investigational therapy. there is a heterogeneous population at recurrence: 15% of patients are not able to receive further treatment, 9% refuse further treatment, 13% will receive second surgery or radiotherapy but not systemic therapy and 52 % progressed and will receive subsequent systemic therapy. the results of these different treatment options are poor: os between 6, 9 and 7 month with 6-months pfs between 9 and 19%. prospective studies, investigational therapies, best in clinical trials, are needed for these patients with poor neurological status and reduce expectance of life. alternative approaches to adjuvant chemotherapy for who grade iii and iv malignant gliomas ciprian tomuleasa, olga soritau, mihaela aldea, magda petrescu, dana cernea, bobe petrushev, horatiu ioani, adriana cocis, alexandru irimie, gabriel kacso, ioan stefan florian introduction: malignant gliomas remain one of the most devastating disease known to man and affects more than 17.000 patients in the united states alone every year. this malignancy infiltrates the brain early in its course and makes complete neurosurgical resection almost imposible. recent years have brought significant advanses in tumor biology, including the discovery that many cancers, including gliomas, appear to be supported by cells with stem-like properties. in the current study we have investigated the effects of combining metformin or arsenic trioxide with the temozolomide-based standard treatment-of-care chemotherapy. materials and methods: the subjects of the current study were eight patients with newly diagnosed high-grade gliomas, romanian neurosurgery (2011) xviii 2: 205 – 229 223 operated at the department of neurosurgery clinical university emergency hospital from cluj napoca. tumor tissue cultures were performed, characterized using immunofluorescnece microscopy and pcr analysis for cd133, cd90, gfap, nanog, sox2, neurofillamnet and aldh1 and the sensitivity to metformin, egf and temozolomide tested. microvascular density assay was performed on the tumor samples. low concentrations of arsenic trioxide or metformin were added in culture and cell proliferation was assessed. results: seven of the eight cases had a positive correlation between the number of the endothelial cells, the phenotype of the isolated tumor cells and the response to adjuvant chemoradiotherapy. the isolated tumor cells had a stem-like behaviour being resistant to conventional drugs. in most cases there was no statistical significant difference between temozolomide alone and temozolomide plus egf arms, but there was a important difference between temozolomide alone and temozolomide plus metformin arms in six of the cases. low concentrations of arsenic trioxide also lead to morphologic differentiation,with fewer stem cells in go state and differentiation-associated cytochemical features, like increased sensitivity to cytostatic drugs and radiotherapy. conclusion: new drugs and tergeted molecular therapies are important for future therapeutics, but sometimes we must not exclude drugs already used in the clinic that might have notable results. such is the case in the current paper, where exposure before conventional postoperative chemoradiotherapy for glioblastoma increased treatment efficacy. further in vivo experiments on laboratory animals and analysis of absorbtion rate and side effects are required. hormonal impact on malignant glial tumors gheorghe ungureanu1, cristian berce2, olga soritau3 1university of medicine and pharmacy “iuliu hatieganu” cluj 2university of agricultural sciences and veterinary medicine cluj 3the oncology institute “prof. dr. ion chiricuta” cluj background: glial tumors comprise about 40% of all the primary central nervous system tumors, out of wich glioblastoma multiforme(gbm) represent one half. the way these tumors are influenced by the hormonal status of the patient is still an unknown, although numerous supositions have been made. estrogen has been shown to have a stimulatory effect through the er-d5, although some studies suggest it’s protective role, oxitocin and progesterone have been considered to have an antiproliferative effect while prolactine inhibitors could be a metamorphic therapy for gbm. populational studies show a smaller incidence for high grade gliomas(hgg) in the female population. our purpose was to assess the way the hormonal status of female patients could influence the behaviour of hgg. material and method: our study was divided in two. the first part was a retrospective study on 113 cases of hgg from the neurosurgical department of cluj county emergency hospital. cases were analised to find differences between appearance, clinical behaviour and evolution of hgg in active hormonal female patients, and other patients. the other part was an in-vitro study on two lines of gbm cells and one tumor stem cell line that were cultivated and treated with doses of: 1ng/ml estrogen, 2,2ng/ml oxytocine, 25ng/ml progesterone, 1ng/ml bromocriptin, 1,5ng/ml testosterone,and 224 abstracts 1st regional congress of neurosurgery in the danube-carpathian region then. proliferation rate was analised using mtt assay. results: the incidence of hgg cases in female patients <51y in our group was the smallest(17,69%). hgg appeared 7 and 8y earlier in male patients versus female patients. the clinical symptoms evolved slowest (14.45weeks) in female patients<51y. reccurence occurred in this grup in a median time of 18.28 months vs.9.85 months in female patients >51y. median survival was significantly different between female patients under and over 51y (p<0.05), but not significantly different vs. male patiens<51 y. the 24 hours mtt assay for the gbm cell culture showed the smallest rate of proliferation for estrogen and the highest for testosterone, progesterone had a smaller proliferative effect than the controll culture, and the other hormones had a more intense proliferative activity. in the stem cell cultre all hormones had a proliferative activity close to the control. conclusion: hormones could influence the growth pattern of hgg and their clinical evolution. our study suggests that hormones could be a factor that improve the way these tumors evolve in the female population, but that survival is only influenced by the patient’s age. from internal to external validity in rcts dafin f. muresanu department of neurology, university cfr hospital faculty of medicine, university of medicine and pharmacy “iuliu hatieganu ” cluj -napoca, romania the last decade has been very fertile in the development of both neurosciences and evidence based medicine (ebm), even if sometimes they did not go hand in hand. evidence based medicine is a concept that tries to build clinical decisions based on empirical knowledge collected from randomized control trials (rcts). rcts were designed in order to avoid systematic sampling errors. randomised controlled trials (rcts) and systematic reviews are the most reliable methods of determining the effects of treatment. clinicians have to make decisions about individuals, and how best to use results of rcts and systematic reviews. this has generated considerable debate. they key issue remains to what extent the overall results of trials can properly inform decisions at the bedside or in the clinic. rcts must be internally valid (i.e., design and conduct must keep to a minimum the possibility of bias), but to be clinically useful the result must also be relevant to a definable group of patients in a particular clinical setting; this is generally termed external validity, applicability, or generalisability. as we can see from the genomic, transcriptomic and proteomic studies of post lesional regulations, the biological reality of the nervous system is extremely complex and rather individualistic (neurotrophicity, neuroplasticity and neurogenesis responses). therefore, due to patients’ heterogeneous responsivity in clinical practice, the approach of neurorehabilitation should be more individualistic, with better chances to manage complex situations. this presentation will analyze the concepts of internal and external validity of rcts and why rcts model is difficult to be applied to neurorehabilitation clinical trials. romanian neurosurgery (2011) xviii 2: 205 – 229 225 wrong side in neurosurgery a.v. ciurea1, d. mohan2, a. giovani1 1ist neurosurgical clinic bagdasar arseni hospital rsn@bagdasar-arseni.ro 2oradea county hospital mohan_dumitru@yahoo.com a very important problem of bioethics in surgery in general an in neurosurgery as our concern is wrong side surgery. this kind of mistake is more common in specialties where patients are operated immediately and in departments with a big number of interventions, like orthopedics but in neurosurgery also this kind of mistake has been reported. in us alone there are 1,300 to 2,700 wrong-site procedures annually in neurosurgery. in order to address this problem, the neurosurgical departments need guidelines to prevent wrong-site surgery. these guidelines should include to verifying the surgical procedure to be performed, marking the surgical site in advance; taking a “time out” immediately prior to starting the operation, during which team members verify that they’ve got the right patient, and confirming that medical records and scans are not reversed and match the marked surgical site. this preoperative check-up of the operative field should be performed by at least two doctors. it is also indicated that a ct scan or mri should be performed immediately postoperative to confirm the correct cure of the pathology. wrong side surgery even just an incision without the craniotomy represents a serious mistake and should be avoided new versus classic in brain protection and recovery dafin f. muresanu chairman and professor of neurology, department of neurology, university cfr hospital, cluj napoca, românia; vice dean of the faculty of medicine, “iuliu hatieganu” university of medicine and pharmacy, cluj-napoca, romania the old concept that neuroprotection means suppressing pathophysiological processes, the idea that a single mechanism molecule might be effective in clinical practice are obsolete today, and represents the root cause of failure. the effects of etiological agents on the brain traditionally are conceived as a linear sum of independent pathophysiological processed (excitotoxicity, inflammation, apoptosis-like, oxidative stress, misfolding protein, etc.) generating the pathways of pathological cascades in acute and chronic disorders. the pathway approach has produced a very detailed understanding of molecular changes in the postlesional brain but it possesses blind spots that are critically related to the failure of pharmacological neuroprotection treatment in neurodegenerative disorders. this is due to the simplistic way of understanding the neurobiological processes supporting brain protection and recovery and pathophysiological mechanisms. the failure of modifying disease therapies in many pathological conditions is measuring the failure of the reductionistic approach to the problem. every lesion in the nervous system initially triggers an endogenous neuroprotective reaction followed by an endogenous repair process, combining neurotrophicity, neuroprotection, neuroplasticity and neurogenesis, overlapping and acting under genetic control to generate endogenous defense activity (eda) which continually counteracts pathophysiological processes damage mechanism (dm). 226 abstracts 1st regional congress of neurosurgery in the danube-carpathian region all these biological processes are initiated and regulated by biological molecules. neurotrophic factors are probably the best example in this respect. they are acting in a pleiotropic neuroprotective way against pathological cascades. the same molecules, due to a complex genetically regulated process, are able to regulate further on neurotrophicity, neuroplasticity and neurogenesis as well. therefore, they have not only pleiotropic neuroprotective activity but also multimodal mechanism of action. beside the concept and therapeutical effects of pleiotropic multimodal molecules, this presentation will give an overview on particular aspects about new randomized controlled trials in the field. long-term effect of thalamic and subthalamic deep brain stimulation on motor symptoms of parkinson's disease istván valálik st. john’s hospital, department of neurosurgery, budapest, hungary we report the long-term effect of unilateral and bilateral thalamic (vimdbs), and bilateral subthalamic deep brain stimulation (stn-dbs) on patients with parkinson’s disease (pd). 52 consecutive patients with severe „onoff” fluctuation underwent ct-guided stereotactic impantation of model 3389 electrodes and kinetra or activa pc (medtronic inc) neurostimulator systems with mean follow-up of 47.6±25.1 (13114) months. additional 19 tremordominant patients had unilateral and 11 patients had bilateral vim-dbs with a mean follow-up of 43.5±14.8 (14.2-101.4) months and 29.5±8.2 (14.1-45.2) months respectively. clinical evaluation included hoehn-yahr stage (h-y), unified parkinson’s disease rating scale (updrs), and the schwab and england scale for activity of daily living (s&e). the drug therapy follow-up was based on levodopa equivalent daily dose (ledd). the bradykinesia was quantitatively measured with passive marker-based analyser of motions (pam) with a computer based scoring system, the proximal movements assessed with the pointing test (pt) and the distal movements with the finger tapping test (ftt). the tremor was measured with pam and computerized digital spiral drawing test (dsdt). after stn-dbs the „off” state h-y stage showed a 32%, the s&e an 86%, the tremor an 80%, the rigidity a 52.5%, the bradykinesia a 46.5%, and the fluctuation a 48.3% improvement. the on dyskinesia was reduced by 76.5%. the ledd was 553±453 mg and 32% lower than at the baseline. the pt score was measured in 24 patients in medication „off” state stimoff and stimon, and improved significantly (p=0.001) and uniformly on the left side from 0.52±0.28 to 0.84±0.39, and on the right side from 0.50±0.27 to 0.85±0.35. the ftts significantly (p=0.001) improved from 3.8±3.0 to 11.0±8.9 on the left side and from 4.1±3.5 to 12.6±9.0 on the right side. unilateral vim-dbs showed a 84.3% improvement on tremor score, and had a long lasting effect. in long-term, the reduction of improvement on rigidity and bradykinesia was observed. the changes of axial symptoms were minimal or could not be observed. bilateral vim-dbs showed an 82.9% of tremor, a 41.7% of rigidity and a 29.3% of bradykinesia improvement. in long-term the postural stability, gait and speech remained without significant changes in both stimoff and stimon romanian neurosurgery (2011) xviii 2: 205 – 229 227 conditions. the ledd increased by 7% to 318±282 mg after unilateral vim-dbs, and increased by 10% to 461±109 mg after bilateral vim-dbs. pam tremorometry showed a reduction of rest tremor by 94% and postural tremor by 90%. dsdt showed a 76.2% regression of kinetic tremor on the contra-lateral to surgery side. frequency domain had trend to change toward physiologic values. based on the clinical scales and quantitative measurements, stn-dbs, in both short and long-term, substantially alleviates all main motor symptoms of pd. vim-dbs, according to the clinical scales and quantitative measurements, is highly effective in tremordominant pd patients equally for both unilateral and bilateral tremor. the endovascular therapy of the cerebral aneurysms as an alternative to neurosurgery. the first 132 endovascular treated cerebral aneurysms st. dima1, l. marginean1, i. szikora2 1nova vita san hospital tg. mures 2neuroscience institut budapest introduction: since may 2005 we started to treat the intracranial aneurysms endovascular way as an alternative minimum invasive to the classic neurosurgery treatment. methods: an all-inclusive retrospective review of every patient who underwent coils embolization (stent or balloon assisted included) of saccular aneurysms from may 2005 to april 2011 was performed. goals: we studied the patients’ demographics, clinical presentation, aneurysm size and configuration, type of coils used for embolisation, the percentage of compactation and recanalization (especially in patients that presented with subarahnoid hemorrhage), the immediate complications due to our procedure. results: a total of 123 patients (49 men and 64 women) and 132 aneurysms were treated. a total of 108 patients (41 men and 55 women) underwent follow-up femoral cerebral angiograms (mean follow-up was 25 months and the longest was at 37 months). 6 patients required intra-arterial abciximab or integrilin due to thrombus formation. 4 patients had aneurysm rupture while the coil was being advanced. 12 patients were treated during vasospasm peak. 8 patients had recanalization at 12 months follow-up. discussion: the average hospitalization period was 4 days (between 38 days and 1 day). there is a close relation between hunt and hess scale score before the treatment and post interventional neurological status. the vasospasm due to subarahnoid hemorrhage, although treated endovascular, remains a threatening of the patient’s neurological status. conclusions: treatment of cerebral aneurysms with endovascular embolization with coils is a safe and durable option. the risk of recanalization or rerupture in our cohort is small compared to series that have been published elsewhere. larger series of patients treated with this method may support better our evidence. clipping aneurysmssome arguments in favor of surgery şt.i. florian, zorinela andrasoni, d. tusnea objective: our objective is to determine the value of the surgical treatment in experienced hands compared to the literature data regarding open-surgery, and the endovascular strategy in incidentally discovered intracranial aneurysm. 228 abstracts 1st regional congress of neurosurgery in the danube-carpathian region material and methods: we designed a retrospective study based on our series of 49 cases with h&h 0 and 1 of intracranial aneurysm out of the total of 458 patients who underwent open-surgery for intracranial aneurysms. results: during a fourteen years’ period, from the total of 458 cases treated by the authors for aneurismal pathology, 49 patients underwent open-surgery for nonruptured intracranial aneurysms, in all cases definitive clipping being achieved. we reviewed the results using the karnofsky performance status score and glasgow outcome scale, and we correlated these with the general and neurological status at admission, aneurismal localizations, associations, morphology and intraoperative particularities. from our series of 49 patients admitted with hunt & hess grade 0 and 1a, 83.7% were neurologically intact after surgery; only one patient was classified as gos 3 immediately post surgery. in general, the outcome depended on the general status, age, the localization and the morphology of the aneurysm, associated aneurysms and co-morbidities. conclusions: our results and comparisons show that open-surgery is in the most cases a very viable, if not the best option in the treatment of incidentally discovered intracranial aneurysms, conditioned by the fact that the surgical team must be an experienced one, and there must be an optimal collaboration between the surgeon, anesthesiologist and neurologist. aneurysm clipping vs coil occlusion is still a controversies a. chiriac, i. poeata, z. faiyad, n. dobrin background: the aneurysmal subarachnoid haemorrhage (sah) is one of the most devastating disease whose management still raises a lot of controversies between neurovascular specialists. the actual standard treatments in the last decade are both surgical clipping of the aneurysm neck and aneurysm sac occlusion with detachable coils. the objective of this study is to weigh evidence for the efficacy of endovascular coiling compared with microsurgical clipping in patients with aneurysmal subarachnoid haemorrhage. methods: we retrospectively reviewed the charts, procedural reports and imaging of patients who underwent surgical clipping or embolization for cerebral aneurysms in two medical centers between january 2004 and december 2009. in one center clipping is the standard procedure and embolization is in the other one. the all patients and procedural dates were statistically analyzed and correlated. results: the study group include 297 patients with coil occlusion and 406 patients treated by microsurgical clipping. the basic characteristics of patients in treatment groups were close in terms of location and size of aneurysm, severity of bleeding and clinic evaluation on various scales. hypertension and ekg modifications (25.4%) were the most commonly risk factor. 9% patients were hunt and hess grade i, 21% grade ii, 42% grade iii, 25% grade iv, and 3 grade v. 8% patients to endovascular group and 1.2% to surgical group show aneurysm repermeabilization. the periprocedural technical complication rate associated with coiling was 7.2% vs 9.5% with clipping. follow-up angiographic results were better with clipping, as total aneurysm occlusion was 91.3% vs 67.6% with coiling. the incidence of clinic vasospasm was 20.4% with coiling vs 25.4% with clipping, whereas the incidence of shunt-dependant hydrocephalus was 5% higher in embolization group. romanian neurosurgery (2011) xviii 2: 205 – 229 229 conclusion: continuous improvement of practical experience and a good selection of patient based on optimal criteria correlated with the rapidly evolving of treatments technology will definitely determine a better outcome results in patients treated for aneurismal sah, in the near future. the usefulness of intraoperative microvascular doppler sonography in cerebral aneurysm surgery th. birbilis, e. theodoropoulou, k. kontogiannidis, e. karakosta, a. birbili, g. matis department of neurosurgery, democritus university of thrace medical school, university hospital of alexandroupolis, greece aims: to evaluate the usefulness of intraoperative microvascular doppler sonography (mds) in cerebral aneurysm surgery. material and methods: for 28 patients (12♂, 16♀, mean age 59.5 years) who underwent surgery for the treatment of 34 intracranial aneurysms, mds with 16and 20-mhz microprobe (tip 1mm & 2mm) was used before and after clipping, to confirm the complete obliteration of the aneurysm. postoperative angiography was performed to assess the complete occlusion of the aneurysm and the patency of adjacent vessels. the findings of mds were analysed and compared with the postoperative angiography. results: the 1-mm microprobe was able to insonate all vessels of the circle of willis and their major branches; furthermore, perforating arteries were reliably insonated. the mean duration of mds investigations was 5.3 minutes. for 7 patients (20,5%), mds exposed parent artery or branching artery stenosis or occlusion and guided the immediate adjustment of aneurysm clip placement. in addition, mds demonstrated that 4 out of the 34 aneurysms failed to be complete occluded (11,7%). in two cases, a repositioning of the clip was performed and in the other two cases a second clip application became necessary for the complete occlusion of the aneurysms. there were no complications of microvascular doppler probe use. conclusions: intraoperative mds is a safe, instantaneous, effective, reliable, and costeffective method for documenting the patency of parent vessels, arterial branches, and major perforators and the complete occlusion of cerebral aneurysms. this technique can be reliably used, in many instances, instead of intraoperative angiography for the surgical treatment of aneurysms. microsoft word 11prunavgiant.doc 214 v. pruna et al giant extracranial liposarcoma giant extracranial liposarcoma – case report v. pruna, narcisa bucur, angela neacsu, a. giovani, anca buliman, m. gorgan first neurological clinic, fourth department of neurosurgery clinic emergency hospital “bagdasar-arseni” bucharest abstract objective: anaplastic liposarcoma of the head is an extremely rare entity. seventyseven cases of head and neck liposarcomas have been reported in the world literature since 1911. radical surgery is the form of treatment advised. clinical presentation: authors report the case of a 62 years old female patient admitted in our institution for a giant extracranial tumor (122/88 mm), developed insidious over a period of 3 years and neglected. the patient agreed surgery only for the epicranial tumor. the lesion was completely removed. postoperatory outcome was excellent concerning this tumor, although the histopathological result was not that great: high anaplastic liposarcoma. conclusion: liposarcoma of the scalp is rare. diagnosis is made histologically. the histopathologic variant influences clinical behavior and prognosis. the treatment of choice is wide surgical excision. keywords: giant tumors, anaplastic liposarcoma, surgical technique liposarcoma is a malignant mesenchymal neoplasm that arises from adipose tissue, most commonly in the retroperitoneum and lower extremities. liposarcoma of the head and neck is rare, representing 5% to 9% of cases in large series (2). common sites of occurrence in the head and neck region include the larynx, hypopharynx, oral cavity, orbit, scalp and soft tissues of the neck. liposarcomas rarely arise from a preexisting lipoma. liposarcoma tumors are the most radiosensitive soft-tissue tumors. the gross appearance of the tumor depends on the histologic type, degree of vascularity, presence of necrosis, and amount of mature fat and fibrous tissue. the tumor appears as a smooth, lobulated, or nodular mass, and in most instances, it is well encapsulated. however, the appearance of an encapsulated tumor may be misleading, because daughter nodules are often present around the main mass. complete excision is not always possible because of the close association of the tumor with vital structures; therefore, the recurrence rate is high. case presentation authors report the case of a 62 years old female patient admitted in our institution for a giant extracranial tumor, insidiously developed over a period of 3 years and neglected. she decided to underwent surgery for esthetic consideration in first place, neurological status being normal. a giant epicranial medial-occipital mass (122/88 mm) (figure 1) and two other masses: left parietal (25/20 mm), and left romanian neurosurgery (2010) xvii 2: 214 – 218 215 cerebellopontine angle (18/12 mm) was seeing on ct scan (figure 2). on irm cerebral the lesions was isodense in t1 and t2 weighted (figure 3). the patient agreed surgery only for the epicranial tumor, for cosmetic reason. the lesion was completely removed; care must be tacked to avoid excessive scalp removal or potential necrosis, and a good hemostasis was performed for prevent bleeding. postoperative outcome was excellent concerning this tumor, the wound healed normaly. but the histopathological result was not that great: high anaplastic liposarcoma, with large necrotic, mixomatous and undifferentiated areas associated with fibrosarcomatous cells. the case remains in observation for the other two intracranial tumors and the patient referred to oncologist. discussion liposarcoma can easily be misdiagnosed clinically; its relatively indolent course lead to often mistakes for lipoma (7), cyst or benign soft tissue tumors. nonetheless, many authors report difficulty in distinguishing these entities (3) and therefore histopathology is required for an appropriate diagnosis (11). the histologic characteristics that distinguish liposarcoma from intramuscular lipoma include the presence of cellular pleomorphism, mitotic activity, lipoblasts, and vascular proliferation (5). currently, the world health organization distinguishes the four variants proposed by enzinger and weiss based on developmental stage of the lipoblasts and overall degree of cellularity and pleomorphism. these four entities are described as well-differentiated, myxoid, round-cell and pleomorphic. the who also recognizes a fifth variant, dedifferentiated, to describe changes occurring within well-differentiated liposarcoma that correspond with more aggressive clinical behavior and poor outcome (9). patients with welldifferentiated and myxoid type tumors have higher 5-year survival rates and lower recurrence rates than patients with pleomorphic and round-cell types. 1a 1b figure 1 a, b preoperative photographs 216 v. pruna et al giant extracranial liposarcoma 2a 2b 2c figure 2 ct brain. a intracranial tumor plated on the rear face of the left temporal cliff, 18/12 mm; b, c shows a giant epicranial occipital tumor mass (122/88 mm), spontaneous homogeneous, well defined, without reactive changes of the bone. 3a 3b romanian neurosurgery (2010) xvii 2: 214 – 218 217 3c 3d 3e figure 3 irm cerebral shows 2 lesions: left parietal (25/20 mm) and rear face of the temporal cliff (18/12 mm). a, c, axial t1 weighted image; b, d, axial t2 weighted image; e, sagittal t1 weighted image. 4a 4b figure 4 postoperative pictures. a, ct scan; b, postoperative photograph of the lesion. the incidence of metastasis is also correlated with histologic type. wide surgical excision is the treatment of choice for liposarcoma. recurrence rate increases from 17% to 80% with incomplete excision (8), as may occur when tumors are mistakenly believed to be benign lipomas (4). although grossly these tumors appear to be encapsulated, they extend by infiltration; the likelihood of nearby satellite nodules necessitates wide excision (1). lymph node dissection is not indicated unless there is concrete evidence of 218 v. pruna et al giant extracranial liposarcoma metastasis, since the likelihood of nodal metastases in this disease is so rare (9). nonsurgical treatment modalities are of limited use in liposarcoma. the use of radiation therapy or chemotherapy remains controversial (10). prognosis of liposarcoma is influenced by three factors: histologic variant, adequacy of surgical excision, and location of the tumor (10). golledge et al (6) found a relatively favorable prognosis for liposarcoma of the scalp, face and larynx as compared with the oral cavity, pharynx and neck. the role of tumor size in prognosis is unclear. conclusion in conclusion, liposarcoma of the scalp is rare. diagnosis is made histologically. the histopathologic variant influences clinical behavior and prognosis. the treatment of choice is wide surgical excision. the scalp region represents a risk factor to the patient because the diagnosis is usually made late. references 1.collins bt, gossner g, martin ds, boyd jh: fine needle aspiration biopsy of well differentiated liposarcoma of the neck in a young female. a case report. acta cytol 43:452-456, 1999. 2.enterline ht, culberson jd, rochlin db, brady lw: liposarcoma. a clinical and pathological study of 53 cases. cancer 13:932-950, 1960. 3.evans hl, soule eh, winkelmann rk: atypical lipoma, atypical intramuscular lipoma, and well differentiated retroperitoneal liposarcoma: a reappraisal of 30 cases formerly classified as well differentiated liposarcoma. cancer 43:574-584, 1979. 4.fusetti m, silvagni l, eibenstein a, chiti-batelli s, hueck s: myxoid liposarcoma of the oral cavity: case report and review of the literature. acta otolaryngol (stockh) 121:759-762, 2001. 5.garavaglia j, gnepp dr: intramuscular (infiltrating) lipoma of the tongue. oral surg oral med oral pathol 63:348-350, 1987. 6.golledge j, fisher c, rhys-evans ph: head and neck liposarcoma. cancer 76:1051-1058, 1995. 7.larson dl, cohn am, estrada rg: liposarcoma of the tongue. j otolaryngol 5:410-414, 1976. 8.mcculloch tm, makielski kh, mcnutt ma: head and neck liposarcoma. a histopathologic reevaluation of reported cases. arch otolaryngol head neck surg 118:1045-1049, 1992. 9.newlands sd, divi v, stewart cm: mixed myxoid/round cell liposarcoma of the scalp. am j otolaryngol 24:121-127, 2003. 10.pack gt, pierson jc: liposarcoma; a study of 105 cases. surgery 36:687-712, 1954. 11.wescott wb, correll rw: multiple recurrences of a lesion at the base of the tongue. j am dent assoc 108:231-232, 1984. microsoft word 2_adamdanil_posttraumaticex 138 adam posttraumatic extracerebral fluid collections posttraumatic extracerebral fluid collections danil adam associate professor, department of neurosurgery “carol davila” university of medicine and pharmacy, bucharest, romania emergency clinical “st. pantelimon” hospital, șos. pantelimon 240, sect.2 bucharest, romania, e-mail: adam_danil@yahoo.com abstract objective: posttraumatic extracerebral fluid collections represent a heterogeneous group of conditions that have different terminologies but the same clinical and imaging features, benefiting from the same therapeutic modalities. between hygroma/hydroma and serous meningitis there is only a topographic difference that has no influence regarding the therapeutic decision or the patient’s outcome. posttraumatic extracerebral fluid collections present themselves as a unitary group which benefits from a unitary management, regardless the given terminologies. this 5 years study reviews the experience, treatment and outcome of patients with such conditions. method: a retrospective analysis of data collected from 46 patients with posttraumatic extracerebral fluid collections is presented. asymptomatic patients or those with mild symptoms were conservatively treated (n=27). surgical evacuation was performed in cases of intracranial hypertension or neurological worsening (n=19). results: clinical results are presented using the glasgow outcome scale (gos). regarding the group of patients treated conservatively, good results were obtained (gos score 4 or 5) in 81.4 % of the cases. regarding the surgical treated group of patients, good results were obtained in 73.6% of the cases. the mortality rate was 18.5%, and 26.3% respectively. conclusions: although several different names can be found in literature, posttraumatic extracerebral fluid collections present themselves as a unitary group, with good outcome after conservative or surgical treatment. the therapeutic decision is made regarding the neurological status and the clinical evolution, which can be correlated with some imaging features. key words: hygroma, hydroma, serous meningitis, posttraumatic extracerebral fluid collections. introduction posttraumatic intracranial fluid collections have rarely been reported in the neurosurgical literature, although, with the implementation of modern imagery, their incidence has increased significantly. they represent a heterogeneous group of fluid collections which can be localized in the subdural space (hygroma, hydroma) or in the subarachnoid space (serous meningitis). with a different pathophysiology, the two entities appear confounding on modern images. this review focuses on subdural romanian neurosurgery (2013) xx 2: 138 – 147 139 hygromas and serous meningitis and discusses clinical features and surgical treatment which are common to both conditions. patients and methods all patients with posttraumatic extracerebral fluid collections diagnosed and treated in our institution were included in this study. the patient’s data was collected from hospital records and was retrospectively analyzed (table 1). the following clinical information was collected: age, sex, gos score at admission, mechanism of injury, signs and symptoms and comorbidities. the patients were investigated via ctscan at admission, which was repeated during hospitalization in case of worsening and also in postoperative period. there were taken into consideration: the size of the fluid collection, the midline shift and the coexisting brain injuries. the treatment of the fluid collections was conservative for asymptomatic patients or for those with mild symptoms, with analgesics and hydration. it was administered in the neurosurgery ward or intensive care unit, depending on associated diseases requiring specific treatment. surgery was performed in cases of intracranial hypertension associated with altered consciousness, under general anesthesia by orotracheal intubation. the skull opening was performed with a trephine of 4.5 centimeters in diameter. after a star-shape opening of the dura mater and evacuation of the fluid under pressure, spontaneous and by suction, the dura mater was partially closed, the bone flap was restored and an epidural drain was left for 24-48 hours. table 1 patients characteristics total cases: 46 age (years) no % mean 68 range 16-94 sex male 36 78.2 female 10 21.8 mechanism of injury fall from the same level 22 47.8 fall from another level 4 8.7 car accident 7 15.2 traumatic brain injury secondary to i 2 4.3 unknown 11 23.9 signs and symptoms at admission headache and dizziness 20 43.4 psychomotor agitation 10 21.7 loss of consciousness for short i d f i 10 21.7 hemiparesis 8 17.3 dysarthria 7 15.2 temporo-spatial disorientation 7 15.2 balance disorders 6 13 otoragie 6 13 gcs 15-13 19 41.3 12-19 7 15.2 8-7 4 8.7 unspecified 16 34.7 comorobidities arterial hypertension 16 34.7 chronic alcoholism and smoking 15 32.6 chronic ischemic heart disease 7 15.2 cpod 5 10.8 ischemic stroke 5 10.8 cas 3 6.5 diabetis 4 8.7 cirrhosis 4 8.4 seizures 2 4.3 hemorrhagic stroke 1 2.2 gcs-glasgow coma scale, cpodchronic pulmonary obstructive disease, cas-cerebral athero-sclerosis 140 adam posttraumatic extracerebral fluid collections ct-scan was repeated in postoperative period and also before discharge in all cases, even if the patient was not operated. the patient’s clinical outcome was recorded on gos scale 3 months later, when he came at a follow-up visit. results forty-six patients with posttraumatic extracerebral fluid collections were diagnosed and treated over a 5-year period. irrespective of subdural or subarachnoid topography of fluid, the patients had similar clinical and radiological features. there were patients treated conservative (group a) and patients treated by surgery (group b). there were no differences in treatment modalities regarding the topography of fluid. demographics there were a total of 46 patients. there were 36 males and 10 females. the youngest patient was 16 years old and the oldest was 94 years old. the average age of patients with posttraumatic extracerebral fluid collections was 68 years. the distribution per decade of age is presented in table 2. radiological data brain ct scans were obtained from patients preoperative and postoperative. ct-scan revealed a simple fluid collection, not associated with brain injuries, in 6 cases. brain injuries associated with fluid collection, shown on the ct scan are presented in table 3 and in figures 1-5. table 3 brain injuries associated with fluid collections associated lessions no. % hemorrhagic contusions 25 54.3 skull fracture 12 26 cerebral atrophy 11 23.9 epidural hematoma 2 4.3 intraparenchymatous hematoma 4 8.7 subdural hematoma acute 3 6.5 chronic 9 19.6 table 2 distribution per decade of age 10-19 20-29 30-39 40-49 50-59 60-69 70-79 80-89 90-99 total f 1 2 5 2 10 m 3 2 4 7 13 6 1 36 total 1 3 2 4 9 18 8 1 46 romanian neurosurgery (2013) xx 2: 138 – 147 141 figure 1 male, 74, with head trauma caused by accidental 2 meter fall on the stairs, with bilateral hygroma right > left (a). a week after the evacuation of the hygroma in the left side a growth of extracerebral collection in the right side is observed (b); after 3 weeks it transformed into a chronic subdural hematoma 18 mm thick; the midline shifted 4 mm towards the left side (c). note that the hygroma from the right side was associated with hemorrhagic cortical contusions (complex hygroma). figure 2 male, 60, with head trauma caused by accidental fall from the same level. cerebral ct scan highlights extracerebral fluid collection, bilateral, 12 mm on the right side and 8 mm on the left side, without associated cerebral damage (simple bilateral hygroma). figure 3 male, 81, with head trauma caused by fall from the same level. cerebral ct scan in axial plane highlights: bilateral subdural hematoma (a). two weeks after surgery it is observed that the collection on the right side disappeared and that a hygroma developed on the left side (b). 142 adam posttraumatic extracerebral fluid collections figure 4 male, 73, with head trauma caused by fall from the same level. cerebral ct scan at admission highlights a small extracerebral fluid collection on the right side (a), which increased in dimensions after a week (b); two weeks later cerebral ct in axial and coronal planes highlights a right-sided chronic subdural hematoma and on the left side a chronic sdh formed from fluid associated with an underlying hygroma with clear-colored fluid during surgery (c) and (d). postoperatory ct scan shows brain expansion after the surgical evacuation of blood and fluid collections (e). figure 5 a 16 year old patient with head trauma caused by car accident. ct scan in axial plane (a), shows multiple cerebral concussions at admission: bifrontal and temporoparietal right-sided underlying a cranial fracture. after 3 weeks the cerebral ct scan in axial plane shows a development of left-sided frontoparietal and right sided frontal, 4 mm thick extracerebral fluid collections. the fluid collection was unilateral in 21 cases and bilateral in 25 cases. the fluid collection development appeared at a variable interval from the traumatic injury, between 24 hours and 50 days. the relationship between the size of the fluid collection, midline shift, applied treatment and outcome was followed. regarding the patients with conservative treatment, the size of the fluid collection in the axial plane was between 4 and 14 mm and the midline shift oscillated between 0 and 7 mm. there were 8 patients with 0 mm midline shift, 4 patients with 3 mm midline shift, 7 patients with 4 mm midline shift and 1 patient with 7 mm midline shift. in 10 cases, the midline shift was not mentioned. in 6 cases, the size of the fluid collection was not mentioned. in 13 cases regarding the group of patients treated conservatively, the hygroma was bilateral. the medical treatment was applied to 27 patients. regarding the patients who underwent surgery, the size of the fluid collection in the axial plane varied between 6 and 18 mm and the midline shift varied between 0 and 4 mm, but in most cases the midline shift was not mentioned. the decision to operate was made when neurological deterioration occurred. in 12 cases regarding the group of patients who underwent surgery, the hygroma was bilateral. 19 patients underwent surgery. among these, in 12 patients the fluid evacuated after dura incision was citrine, in 2 cases it was clear and in 5 cases the color was not mentioned. in 7 patients it was observed the existence of a vascularised parietal subdural membrane, with a variable thickness, about 1mm, unaccompanied by the existence of a visceral membrane. romanian neurosurgery (2013) xx 2: 138 – 147 143 clinical outcome the outcome regarding patients with intracranial fluid collections is presented in table 4. table 4 outcome according to gos (glasgow outcome scale) gos characteristics group a group b no. % no. % good recovery 19 70.3 12 63.1 moderate disability 3 11.1 2 10.5 severe disability vegetative state death 5 18.5 5 26.3 the causes of death, regarding the group of patients treated conservatively, were: liver failure associated with decompensated diabetes (1 case), exacerbation of chronic kidney disease (1 case), bronchopneumonia (1 case), and severe traumatic brain injury (2 cases). in the surgical group, 2 patients died because of pulmonary complications (bronchopneumonia), 1 patient died because of an ischemic stroke and 2 died because of the association of the hygroma and a subdural hematoma. discussions there is a terminological ambiguity regarding the designation of extracerebral fluid collections. subdural collections of fluid other than blood are referred to as sudural hygromas or hydromas. the term subdural hydroma was first reported by mayo [1] in 1894, but subsequently evolved into subdural hygroma or subdural effusion. described initially by payr [2] in 1916, the hygroma was separated as a nosologic entity under this name by dandy [3] in 1932. there is considerable confusion about these entities. in greek “hygros” means “wet”. the hygroma represents a fluid collection circumscribed in the subdural space, containing a xantocorm liquid which is bounded by a neomembrane [4]. in the case of hydroma, the liquid is clear and the membrane is missing. the serous meningitis is a circumscribed or diffuse accumulation of fluid located in the subarachnoid space. it is often confused with external hydrocephalus. between serous meningitis and hygroma/ hydroma there is only a difference of topography. although the fluid collections were identified at almost any age, there is a net movement of their occurrence over the age of 60. the youngest patient in our series was 16 years old and he was involved in a car accident. mayo reported the case of o 12 year-old boy who, secondary to head trauma, developed o fluid collection overlying the left cerebral hemisphere. the mechanism as well as the chronic subdural hematoma (sdh), the hygroma develops in the subdural space. chronic sdh derives from a subdural hygroma and vice versa. the cerebrospinal fluid leaks through an arachnoid breach detaching the dural border cells layer and produces a subdural collection. naffziger [5] discovered an arachnoid membrane rupture in 1924. as well as the chronic sdh, hygroma has a membrane. it forms as a result of an inflammatory reaction which follows the initial injury. the inflammatory reaction is characterized by cellular proliferation in the 144 adam posttraumatic extracerebral fluid collections dural border layer with formation of granulation tissue along with collagen fibers and blood vessels. the neo-formation membrane facing the arachnoid mater is avascular. the parietal side contains blood vessels. the subdural hygroma may evolve in a chronic sdh. also the hygroma may represent the final stage of chronic sdh when the fluid is watery, contains no blood and is similar to the cerebrospinal fluid (csf). in rare cases hygroma coexists with chronic sdh. serous meningitis is a fluid, compressive subarachnoid collection which causes intracranial hypertension. it is common in elderly adults and it develops in cases of external hydrocephalus and cerebral atrophy and it is bilateral in the majority of cases. the fluid collection fills the space between the atrophic brain and the arachnoid. the tearing of the arachnoid is generated by kinetic energy and shear stress caused by the trauma. the hygroma increases in volume due to a valve mechanism in the arachnoid breach which allows unidirectional csf flow from the subarachnoid space towards the outside when cough or sneeze occur or as a result of arterial pulse. the interface tear between the dura mater and the arachnoid can also be a result of surgery [6]. this explains how hygroma can be secondary to a decompressive craniotomy or to a chronic subdural hematoma evacuation. according to schneider [7], the subdural fluid is a plasma exudation resulting from high permeability of some blood vessels from the dura mater. the trauma was mentioned in all of the cases in our series of 46 patients while the type of trauma was specified in 75% of the patients. the most frequent head traumas were those with the same level fall (n=22) occurring in elderly patients. in a single case the trauma was associated with a blood disorder secondary to thrombocytopenia. in elderly persons hygroma as well as chronic sdh may develop after a minor head trauma. occurrence fluid collections after head trauma have an occurrence of 5 to 21% [8, 9, 10] reaching 25-30% secondary to a decompressive craniotomy [11, 12]. signs and symptoms the clinical picture of intracranial fluid collection is nonspecific. the signs and symptoms can be assigned to the trauma and not to a specific clinical entity. liquid collections occurred both as a result of minor head trauma and also secondary to severe head trauma. in addition to cases with mild symptoms there were also cases presenting symptoms which progressed to worsening, the headache increasing in intensity. moreover, some patients presented psychomotor agitation (21,7%) or were confused, disoriented (15%). medical history such as cerebral arteriosclerosis or stroke were factors in increased brain atrophy regarding the elderly; in addition we can observe that smoking and alcohol consumption are also risk factors, each found in 32% of patients with intracranial fluid collections. radiological investigations subdural fluid collections can be routinely detected through computerized tomography scans. the ct-scan revealed the extracerebral collection as hypodense, with a density similar to csf, unior bilateral. in our romanian neurosurgery (2013) xx 2: 138 – 147 145 series of patients we came across bilateral collections in 54% of the cases. in the axial plane the dimensions of the fluid collections varied between 4 and 15 mm. however, the midline shift did not increase accordingly either as a result of the bilateral collection or because it developed overlying an atrophic brain in elderly persons. the either surgical or conservative treatment was performed according to clinical status at admission or to its following evolution, as well as according to the axial dimensions of the fluid collections; the midline shift was a minor contributing factor for surgical treatment. the majority of the patients were treated conservatively and showed improvement as a result of hydration and neuroprotective treatment. hydration along with intracranial hyper-tension allowed the fluid collections to resolve spontaneously along with brain expansion. 41% of the patients underwent surgical evacuation of the fluid collections. the surgery was a trephine craniotomy 4,5 cm in diameter, star shaped section of the dura mater and under pressure evacuation of the subdural fluid. ct-scan images revealed different aspects: •complex unilateral hygroma •simple bilateral hygroma •complex bilateral hygroma which after the evacuation of fluid collections from one side became a chronic subdural hematoma of the opposite side •chronic bilateral subdural hematoma; a unilateral hygroma occurred after its evacuation •initially small hygroma which became thicker – sdh occurred on one side and on the opposite side chronic sdh was associated with an underlying hygroma the ct-scans highlighted the extracerebral fluid collection/collections and any potential brain damage but they did not differentiate between a hygroma, hydroma, serous meningitis or the final phase of a chronic sdh. differential diagnosis there have been attempts to differentiate subdural hygroma from chronic sdh based upon fluid characteristics. the hygroma fluid contains prealbumin found in csf but not in subdural hematoma [13]. the hygroma fluid has a content of less than 106 rbcs/ml while in the subdural hematoma the quantity of rbcs/ml (red blood cells /ml) is bigger [14]. management and outcome the majority of the extracerebral subdural collections is asymptomatic and progressively or spontaneously disappears. regarding post decompressive craniotomy hygroma, aarabi et al [12] observed that the hygromas appear in the first postoperatory week; they reach maximum volume in the 4th week and disappear around the 17th week. as far as the symptomatic hygromas are concerned, the clinical improvement advocates in favor of conservative treatment. patients with complex hygromas require clinical and imagistic follow-ups and a symptomatic treatment of underlying cerebral damage. operative decision making is based upon change in the patient’s state of consciousness associated with growth of hygroma. 146 adam posttraumatic extracerebral fluid collections mass effect defined by a midline shift bigger than 5mm is not always a good indicator of surgery; hygromas are of high occurrence among the elderly, along with cerebral atrophy and external hydrocephalus. a cerebral damage with an edema may create a false impression of subdural fluid collection on the initial ctscans. one of the patients in our series had a 7mm shift and evolved favorably under conservative treatment. furthermore, among the group that underwent surgery there were patients with a shift smaller than 5mm and required surgery. the surgery was in all cases a trephine craniotomy with a diameter of 4.5 cm. this allowed a better view of the operative field and an accurate hemostasis of the dura and parietal membrane. the general mortality of the entire series was 21.7% 18.5% in the medical group and 26.3% in the surgical group (figure 6). causes of death were the pre-existing medical conditions that were uncompensated by occurrence of pulmonary complications in elderly patients or cerebral ischemic complications. two patients who were medically treated deceased after suffering severe head trauma. mortality is more related to additional brain lesions or to systemic complications during hospitalization than to hygroma itself. conclusions posttraumatic extracerebral fluid collections can be generally found under varied terminologies. there are no differentiating imagistic aspects and no characteristic symptomatology for hygroma, hydroma or serous meningitis; thus, a terminological uniformity is necessary in the form of extracerebral fluid collections or plainly, hygroma. hygroma diagnosis is performed through ct-scans of all of the patients with craniocerebral trauma at admission and depending on the evolution, scans are repeated during hospitalization and at discharge. the majority of patients whose ctscans show extracerebral fluid collections are asymptomatic and the fluid collections are eventually spontaneously resolved. surgery is indicated when the clinical picture shows neurological damage. evacuation of subdural fluid collections can be performed through various methods. we prefer trephine craniotomy which allows a better view and an accurate hemostasis. mortality is in most cases caused by associated cerebral damage or systemic complications. romanian neurosurgery (2013) xx 2: 138 – 147 147 figure 6 mortality rate references 1. mayo ch. a brain cyst: the results injury causing aphasia, hemiplegia, etc. evacuation; complete recovery. ny med j. 1894; 59:434,. 2. payr e. meningitis serose bei und nach schadel verlezungen (traumatica). med klin. 1916; 12: 841-846. 3. dandy we. chronic subdural hydroma and serous meningitis (pachymeningitis serosa; localise external hydrocephalus). in: lewis d (ed): practice of surgery, hagerstom, maryland w. f. prior 1932, p. 306-314. 4.arseni c, oprescu i. neurotraumatologie, editura didactică si pedagogică, bucuresti 1983, p. 163. 5. naffziger hc. subdural fluid accumulations following head injury. jama 1924; 82: 1751-1752. 6. pardes i, cicuendes m, delgado am, et al. normal pressure subdural hygroma with mass effect as a complication of decompressive craniectomy. surg neurol int 2011; 2:88. 7. schneider rc. head injuries in infancy and childhood. surg. clin. north arm. 1961; 41: 1255. 8. born jd, hans p, flandroy p, et al. incidence and treatment of subdural hygroma in severe head injuries. acta anaesthesiol belg. 1984; 84: 174-182. 9. ohno k, suzuki r, masaoka h, et al. chronic sundural haematoma preceded by persistent traumatic subdural fluid collection. j neurol neurosurg psychiatry 1987; 50: 1694-1697. 10. lee ks, bae wk hg, yun ig. the fate of traumatic subdural hygroma in serial computed tomographic scans. j. korean med sci 2000; 15: 560-568. 11. yang xf, wen l., shen f, et al. surgical complications secondary to decompressive craniectomy in patients with a head injury: a series of 108 consecutive cases. acta neurochir (wien) 2008; 150: 1241-1247. 12. aarabi b, chesler d, maulucci c, et al. dynamics of subdural hygroma following decompressive craniectomy: a comparative study. neurosurg focus 2009; 26(6): e8. 13. greenberg sm. handbook of neurosurgery, thrid edition, greenberg graphics, inc. lakeland, florida, 1993, p. 546. 14. samandouras g. the neurosurgeon’s handbook. oxford university press inc, new york, 2010, p. 689. microsoft word 13surgeonoftheyear_f 116 surgeon of the year 2012 surgeon of the year 2012 “i believe that for every patient the surgeon of the year is the surgeon who operates him/her”. the motto is quoted from prof. dr. ioan stefan florian’s speech, when the distinction of “surgeon of the year 2012” was handed over to him at the healthcare gala (gala sanătăţii), event organized at the house of parliament in bucharest, on the 5th of december, 2012. prof. dr. ioan stefan florian, president of the senate of the university of medicine and pharmacy “iuliu hatieganu” clujnapoca since 2011, former president of the romanian society of neurosurgery in the period of 2010-2012, in the present pastpresident of it, member of the executive board of the society, received the distinction of “surgeon of the year 2012”. nominated and elected from all romanian surgeons, this distinction is to confirm his professional value and results. with an impressive surgical experience numbering more than 10.000 surgeries, among which 3012 brain lesions operated within the last 12 months, one of the most numerous series of brain stem lesions, intramedullary tumors, avm's, and more than 700 aneurysms operated along his career, he is the neurosurgeon who first introduced in romania the “single stage single opening” technique in the surgical treatment of multiple aneurysms, the first reported direct approach on a brain stem tumor, the translabirintic approach for acoustic neurinoma together with prof. dr. silviu albu (e.n.t. department), the endoscopic – endonasal approach for pituitary adenomas, and pioneered many other surgical approaches in brain and spinal surgery. as recognition of his didactic activity and purely based on the appreciation of students, he was elected professor bologna in 2010 by the students of the university of medicine and pharmacy “iuliu hatieganu” cluj-napoca. prof. dr. ioan stefan florian participated at many national and international scientific events, giving lectures. in 2011 he was invited to sustain a presentation within the section video with masters at the 14th wfns interim meeting & 15th brazilian society of neurosurgery congress of continuous education, in recife, brazil. romanian neurosurgery (2013) xx 1: 116 117 117 later, in 2012 he was invited to give a lecture at the 9th asian congress of neurological surgeons, within the section entitled “best oral presentations” held in istanbul, turkey. among the awards received by him just a few are mentioned, such as the distinction of the sanitary order in grade of commander accorded to civil citizens by ion iliescu, president of romania in 2004; “prof. dr. ion chiricuta” award in 2007, the award of the faculty of medicine of umf “iuliu hatieganu” cluj-napoca for surgical specialities. prof. dr. ioan stefan florian is member of many national and international societies, being the general secretary of euroacademia multidisciplinaria neurotraumatologica (emn), individual member of the european association of neurosurgical societies (eans), individual member of the congress of neurological surgeons (cns), and also the romanian ambassador to the dandy assembly together with prof. dr. a.v. ciurea. “labor omnia vincit improbus” as written on the logo of the department of neurosurgery from clujnapoca and it is one of the principles that prof. dr. ioan stefan florian and the department he runs, respect and apply. microsoft word 17review romanian neurosurgery (2011) xviii 1: 103 – 104 103 the management of the hospital unit a.v. ciurea, v.g. ciubotaru, e. avram (2010, editura universitară, bucharest, 310 p.) healthcare is a priority in all civilised countries. the right to healthcare is guaranteed by constitution and the gross domestic product allocated to this domanin is greatly variable from country to country. in france, for example, healthcare recieves an astonishing 11% of the gdp, having insured in this way it’s efficiency as many analysts consider it to be the best healthcare system in the world. fund allocation has to be strenghtened by a good management. monitoring, distribution of the expenses and their control as well as setting proper running parameters are tasks carried out at ministry level. finances and management insure efficiency in all the branches of the healthcare system with an special interest in preventive medicine, primary, secondary and tertiary medicine, research institutes, the approach on major health issues such as rare pathologies, dangerous diseases, strokes, trauma, vascular diseases and so on. for the proper functioning of the system it is necessary that financing and hospital managment are correctly callibrated. at hospital level a great emphasis is placed on managerial training. a tight cooperation with local healthcare authorities such as health departments is required. furthermore, a great importance is granted to the activity control mechanisms that are converted into parrameters for a better quantification : the bed usage index, the mixed case index, the adresability, the utilities usage index, the complications occurence percentage, nosocomial infections occurence percentage etc. the hospital unit is a important phalanx in preserving the health of the population. it’s the place where curative treatment is underwent. the leaders of the hospital unit must have a proper medical training, adequate managerial knowledge as well as administrative capabilities. many clinincs bind together appropriate medical education with a superior level medical practice. the modern healthcare systems add in advanced investigative technologies and minimally invasive instruments and techniques offering young doctors solid 104 a.v. ciurea et al the management of the hospital unit grounds for personal development. the management of the hospital unit is in full consolidation due to the current european demands transfigured by the ministry of health as demanded criteria published in special medical literature. furthermore, healthcare leading personnel are supplied with a variety of training courses in management that aim amongst others in developing teamwork, leadership, quality management, project management, administration etc. the work “the management of the hospital unit” is the latest appearance in what regards institutional organization. edited under the supervision of a.v. ciurea md, phd, msc, and colaborators. the editors believe that focusing towards hospital units has the best results in what regards healthcare management in the actual context. a proactive management is imperative. each decisional factor (unit leaders) should develop his own hospital unit and solve local conflicts without waiting support from outranking authorities. the editors consider that „we must relaunch ourselves, in this historical crisis moment, a time when society blames us and invites us to go serve other healthcare systems [...] we have to refreshen ourselves, take care of our patients and lead those who we outrank on the right path – fulfilling our duty and our destiny” this work contains contributions from several doctors, psychologists and sociologists already appreciated in practice and fields such as medical and managerial literature. contributions worthy of mentioning are those of prof. cary l. cooper, prof. ivan robertson and prof. gordon tinline from the lancaster university in the united kingdom. each chapter analizes a series of actual realities and suggests a broad spectrum of internal remedies at unit level. the first part chapters approach the organizing and the proper running of the hospital unit or department: the hospital unit management in the context of actual challenges in the romanian healthcare system, management through objectives in the neurosurgical clinic, running the clinic unit, from stress to welfare in the health system, health risks and security risks at work. the second part approaches the human resources management, the updating of personnel training programs, satisfaction at work, personnel policies principles in hospital units, the flexibility and relocation of the medical personnel. the third part underlines aspects of the relationship between healthcare personnel and the patient, including the patient’s familly as well: the theory of trust in the doctorpatient relationship, the trust in medical assistance, medical personnel and the terminally-ill patient, the terapeutical relationship with the elder patient, psychological aspects of cancer in adults. this work’s main goal is internal mobilization and challenging all doctors to propoze local managerial solutions. in a deliberate way, the authors don’t approach issues connected to managment of services. they concentrate only on organizational issues. this work’s purpose is to deffinitivate the editorial efforts done by proffesor a.v. ciurea and his collaborators during years past, and acts as a liaison from system and organizational management to departmental management. al. constantinovici md, phd member of the romanian academy of medical sciences doi: 10.33962/roneuro-2021-052 essentials of cerebral fat embolism syndrome. a hidden enemy in trauma ivan david lozada-martínez, michael gregorio ortega-sierra, m.d. del pilar zambrano-arenas, natalia páez-escallón, darwin gabriel perea-martínez, yuly sofia caldera-arrautt, kevin solis-bazza, d.a. betancourt-cundar, h. jose gonzalez-garces, a.m. manríque-gualdron, feraz fady zaghab-zgieb, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (3): pp. 316-320 doi: 10.33962/roneuro-2021-052 www.journals.lapub.co.uk/index.php/roneurosurgery essentials of cerebral fat embolism syndrome. a hidden enemy in trauma ivan david lozada-martínez1,2,3, michael gregorio ortega-sierra4, maría daniela del pilar zambrano-arenas5, natalia páezescallón5, darwin gabriel perea-martínez6, yuly sofia caldera-arrautt7, kevin solis-bazza8, duvan alexander betancourt-cundar9, hernando jose gonzalez-garces6, andrés mauricio manríquegualdron10, feraz fady zaghab-zgieb11, luis rafael moscote-salazar1,2 1 medical and surgical research center, university of cartagena, cartagena, colombia 2 colombian clinical research group in neurocritical care, university of cartagena, cartagena, colombia 3 global neurosurgery committee, world federation of neurosurgical societies, latin american chapter 4 medical and surgical research center, corporación universitaria rafael nuñez, cartagena, colombia 5 school of medicine, universidad el bosque, bogotá, colombia 6 school of medicine, universidad de santander, bucaramanga, colombia 7 school of medicine, universidad de cartagena, cartagena, colombia 8 school of medicine, corporación universitaria rafael nuñez, cartagena, colombia 9 school of medicine, universidad de antioquia, medellín, colombia 10 school of medicine, fundación universitaria juan n. corpas. bogotá, colombia 11 school of medicine, universidad de la sabana, bogotá, colombia abstract fat embolism syndrome typically appears after an asymptomatic period of 24 to 72 hours and is typically manifested by the clinical triad of respiratory failure, neurological manifestations and petechiae, together with analytical alterations such as anaemia and thrombopenia. respiratory distress is the most common symptom. cerebral fat embolism is an incomplete form of fat embolism, which does not meet all the diagnostic criteria; in fact, it may appear without the presence of respiratory failure; therefore, its early diagnosis is a challenge in the trauma patient. keywords cerebral fat embolism, trauma, diagnosis, narrative review corresponding author: ivan david lozada-martinez medical and surgical research center, university of cartagena, cartagena, colombia ivandavidloma@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 317 essentials of cerebral fat embolism syndrome introduction fat embolism syndrome occurs when fat enters the circulation and may embolize and may or may not present clinical manifestations [1,2]. it is a potentially serious complication of fractures, with a reported incidence of 0.5 to 3.5% in isolated fractures of the long bones and 5 to 10% in patients with polytrauma. [3,4] the mortality rate is 5 to 15% [5]. due to its association with polytrauma, it is much more frequent in the third and fourth decade of life [5,6]. it has also been associated, but to a lesser extent, with non-traumatic conditions such as orthopedic procedures, bone marrow transplants, extensive burns, closed-chest cardiac massage, acute pancreatitis, liposuction, parenteral lipid infusion, fatty liver, diabetes mellitus, osteomyelitis, rupture of a tarlov's cyst, and other non-traumatic conditions [5,7,8], or even more rarely, a case was reported after chest surgery in a patient with empyema [9]. this complication can target the vascularization of the brain and generate severe ischemic accidents. considering the potential of this pathological condition to negatively impact the integrity of the central nervous system, and that it is little known by medical students and primary care physicians, the aim of this review is to present basic concepts about its pathophysiological mechanism, important aspects for its early detection and approach. pathophysiological mechanisms of cerebral fat embolism cerebral fat embolism is caused by lipid droplets that travel through the bloodstream, subsequently blocking small vessels, especially at bifurcations [1,3,10]. this occurs in patients with long bone fractures, so it implies that there is bone trauma with exposure of the medullary fat, and that fat emboli subsequently enter the venous system [3,6,11,12,13]. they all travel into the pulmonary circulation and in the presence of right-to-left shunts pass into the systemic circulation [14]. there are several hypotheses that attempt to explain the pathophysiological mechanism of this disease. mechanical theory approximately 100 years ago, specifically in 1924, an author by the name of gauss posited that bone marrow adipose cells could access venous sinusoids due to increased intramedullary pressure following trauma [1]. these adipose cells have proinflammatory and prothrombotic attributes [15]. as the venous system travels back toward the heart, they precipitate platelet adhesion and increased fibrin production, forming an embolus and increasing the risk of embolizing the pulmonary arterial circulation when the vessels form capillaries [16]. capillary obstruction triggers interstitial bleeding, edema, alveolar collapse and reactive vasoconstriction. massive fat emboli can also cause macrovascular obstruction and shock. even in special cases such as in the permanence of a patent foramen ovale, fat cells can enter the arterial circulation [17]. biochemical theory another hypothesis put forward is biochemical. this supports the fact that the clinical manifestations of fat embolism are caused by a proinflammatory state [1]. bone marrow adipose cells are broken down by tissue lipases to form glycerol and toxic free fatty acids, which cause injury to pneumocytes and pulmonary endothelium, triggering a cascade of proinflammatory cytokines that lead to respiratory failure [18-20]. this theory helps to explain the cases of non-traumatic fat embolism. experiments in animal models support this hypothesis [1]. however, these results are derived from general concepts. the toxic properties of free fatty acids were demonstrated around 1950 [1]. since then, fatty acid infusions have been used in animal models to induce embolism-like changes in the circulation and lung. an example of this is the use of triolein to induce fat embolism syndrome and investigate a "second hit" phenomenon in rat models. lung damage after injection of another toxin has been found to be worse in rats that had a history of this clinically resolved triolein-induced syndrome than in rats that were exposed to the toxin alone [1]. however, it would be interesting to continue with this type of research to determine the precise degree of severity of pulmonary involvement and, specifically, of brain damage. clinical presentation as previously mentioned, clinical manifestations are usually delayed from 24 to 72 h, and some authors speak of an onset from 12 to 72 hours [21,22]. however, only one case of hyperacute cgd has been reported, whose clinical signs appeared 2 hours after an automobile accident, where the patient reported 318 ivan david lozada-martínez, michael gregorio ortega-sierra, m.d. del pilar zambrano-arenas et al. fractures of the right femur, tibia and fibula, in addition to non-specific symptoms during the first hours, the subsequent development of the symptoms was of bad prognosis for the patient, with almost no improvement after a few days [23,24]. typical symptoms of fat embolism syndrome include respiratory failure, cerebral dysfunction and petechial rash. respiratory manifestations appear in almost 100% of patients, neurological symptoms are usually transient appearing in 80% and petechial exanthema in 20 to 50% of cases and is the most specific, but the most delayed sign [25,26]. clinically, the syndrome can be variable from headache to diffuse encephalopathy, lethargy, convulsion, coma, pyramidal symptoms, aphasia, visual and auditory hallucinations, sexual hallucinations, aggressive behavior and pupillary paresis [2,27]. other manifestations described are renal failure, myocardial depression, jaundice and fever. patients with pure cerebral fat embolism have no respiratory symptoms and a history of cranioencephalic trauma [2,28]. diagnostic approach the clinical evolution of the patient must be considered, i.e., that he/she presents respiratory and neurological alterations and, in some cases, cutaneous petechiae after a fracture of long bones, orthopedic surgeries, or due to non-traumatic causes such as sickle cell anemia, which produces infarcts in the bone tissue. on the other hand, the use of imaging is one of the best methods to confirm the diagnosis, and thus exclude other clinical impressions such as diffuse axonal injury [1,2,29,30]. magnetic resonance imaging (mri) is considered the method of choice for diagnosis, because it is able to capture the lesions that occur in the brain. mri can commonly show a characteristic pattern of microemboli in the gray and white matter or cytotoxic edema, evidencing "lesions" by dots in the gray matter that form an image similar to a star field in t2 and dwi [1,2]. this pattern is true in most cases, varying in time the number of lesions that may appear, i.e., an mri performed during the first hours of neurological dysfunction may or may not show lesions in white matter, but a star field pattern may be present. another pattern found in dwi and t2 sequences, and whose significance is associated with a worse prognosis, corresponds to confluent bilateral periventricular and subcortical cytotoxic edema. finally, t2/flair sequences may show areas of hyperintensity probably associated with vasogenic edema [1,2,31]. therapeutic approach treatment is essentially coadjuvant; when one of these cases occurs, it is common to use heparin, dextran, aspirin, albumin and steroids, which are ineffective in treating the disease. currently, case reports have opted to include statins in their list, due to their anti-inflammatory mechanism rather than their cholesterol-lowering action; where the use of high doses of the drug had a result considered satisfactory, improving neurological functions. however, there is a lack of studies to support it [1,2]. in the case of patients with cerebral embolism, care of neurological manifestations and complications focuses on frequent neurological observation. these patients may develop cerebral edema which, although manageable, increases the risk of morbidity, mortality and disability [29-31]. continuous monitoring of intracranial pressure should be performed in these cases. although clinical diagnosis is still considered the preferred diagnostic method for this syndrome, studies have shown that mri is useful, in cases where there is no head trauma, to assess the severity of cerebral fat embolism and to predict the functional prognosis. in general, sedation and neuromuscular blockade for trauma patients should be titrated so as to keep the patient comfortable, without affecting their serial neurological examinations and, in addition, allowing them to tolerate mechanical ventilation [1,2,29,31]. prognosis usually, almost 80% of patients experience spontaneous resolution of symptoms, however, 3% to 8% die. it has been described that the prognosis could be associated to the promptness with which the symptoms appear, suggesting that when presenting in less than 12 hours, the morbimortality is higher [1-6]. conclusions cerebral fat embolism or fat embolism syndrome is a disorder characterized by the appearance of respiratory, neurological and cutaneous dysfunction symptoms (petechiae) frequently found in people who have suffered long bone and pelvic fractures. this pathology requires an adequate diagnosis and 319 essentials of cerebral fat embolism syndrome treatment, in order to reduce the morbimortality associated with it, even though there is no treatment oriented to the cause of it. for the time being, few changes have been described in the literature for this disorder, however, small trials are beginning to make inroads in terms of therapies that may be considered effective in the future. references 1. timon c, keady c, murphy cg. fat embolism syndrome a qualitative review of its incidence, presentation, pathogenesis and management. malays orthop j. 2021; 15(1):1-11. 2. vetrugno l, bignami e, deana c, bassi f, vargas m, orsaria m, et al. cerebral fat embolism after traumatic bone fractures: a structured literature review and analysis of published case reports. scand j trauma resusc emerg med. 2021; 29(1):47. 3. zakhari n, castillo m, torres c. unusual cerebral emboli. neuroimaging clin n am. 2016; 26(1):147-63. 4. manousakis g, han dy, backonja m. cognitive outcome of cerebral fat embolism. j stroke cerebrovasc dis. 2012; 21(8):906.e1-906.e3. 5. chen pc, hsu cw, liao wi, chen yl, ho ch, tsai sh. hyperacute cerebral fat embolism in a patient with femoral shaft fracture. am j emerg med. 2013; 31(9):1420.e1-1420.e3. 6. campo-lópez c, flors-villaverde p, calabuig-alborch jr. fat embolism syndrome after bone fractures. rev clínica española. 2012; 212(10):482–7. 7. haggis p, davis bj, leary ts, wimhurst ja. a good outcome following cerebral fat embolism. inj extra. 2009; 40(8):147–8. 8. duja cm, berna c, kremer s, géronimus c, kopferschmitt j, bilbault p. confusion after spine injury: cerebral fat embolism after traumatic rupture of a tarlov cyst: case report. bmc emerg med. 2010; 10(1):18. 9. lee sc, yoon jy, nam ch, kim tk, jung ka, lee dw. cerebral fat embolism syndrome after simultaneous bilateral total knee arthroplasty. a case series. j arthroplasty. 2012; 27(3):409–14. 10. scarpino m, lanzo g, cappelli f, moretti m, misuri g, voltolini l, et al. cerebral fat embolism after videoassisted thoracic surgery. ann thorac surg. 2016; 102(5):e409–11. 11. zhou y, yuan y, huang c, hu l, cheng x. pathogenesis, diagnosis and treatment of cerebral fat embolism. chinese j traumatol. 2015; 18(2):120–3. 12. aman j, van koppenhagen l, snoek am, van der hoeven jg, van der lely aj. cerebral fat embolism after bone fractures. lancet. 2015; 386(10001):e16. 13. bugnitz cj, cripe lh, lo wd, flanigan km. recurrent fat embolic strokes in a patient with duchenne muscular dystrophy with long bone fractures and a patent foramen ovale. pediatr neurol. 2016; 63:76–9. 14. kuo kh, pan yj, lai yj, cheung wk, chang fc, jarosz j. dynamic mr imaging patterns of cerebral fat embolism: a systematic review with illustrative cases. ajnr am j neuroradiol. 2014; 35(6):1052-7. 15. godoy da, di napoli m, rabinstein aa. cerebral fat embolism: recognition, complications, and prognosis. neurocrit care. 2017; 29(3):358-365. 16. kawati r, larsson a. brain death due to fat embolism could moderate hypercapnia and prone position be blamed for the tonsillar herniation? ups j med sci. 2013; 118(4):276–8. 17. whalen ld, khot sp, standage sw. high-dose rosuvastatin treatment for multifocal stroke in traumainduced cerebral fat embolism syndrome: a case report. pediatr neurol. 2014; 51(3):410–3. 18. garcía-estévez da, castro-menéndez m, canal-pérez mg. síndrome de embolia grasa cerebral: un caso clínico desencadenado tras una fractura humeral y sin distrés respiratorio asociado. rev neurol. 2014; 60(1):45–6. 19. fernández-torre jl, burgueño p, ballesteros ma, hernández-hernández ma, villagrá-terán n, de lucas em. super-refractory nonconvulsive status epilepticus secondary to fat embolism: a clinical, electrophysiological, and pathological study. epilepsy behav. 2015; 49(2015):184–8. 20. hsu tl, li tc, lai fp, ouhyoung m, chang ch, wang ct. late-onset isolated cerebral fat embolism syndrome after a simple tibial plateau fracture: a rare case report. j int med res. 2021; 49(7):3000605211028415. 21. di bari s, bisulli m, russo e, bissoni l, martino c, branca vergano l, et al. preoperative vena cava filter placement in recurrent cerebral fat embolism following traumatic multiple fractures. scand j trauma resusc emerg med. 2021; 29(1):86. 22. schnadthorst pg, rieder n, springer m, schulze c. cerebral fat embolism syndrome after polytrauma : complication after fracture treatment of several long bones of the lower extremities. unfallchirurg. 2021. online ahead of print 23. hoiland rl, griesdale de, gooderham p, sekhon ms. intraparenchymal neuromonitoring of cerebral fat embolism syndrome. crit care explor. 2021; 3(5):e0396. 24. hadden wj, herritt b, hoang r, milroy c, hooper j, wilkin g. fatal cerebral fat embolism after pelvic and multiple long bone fractures without associated lung injury: a case report. jbjs case connect. 2020; 10(4):e2000127. 25. sangani v, pokal m, balla m, merugu gp, khokher w, gayam v, et al. fat embolism syndrome in sickle cell βthalassemia patient with osteonecrosis: an uncommon presentation in a young adult. j investig med high impact case rep. 2021; 9:23247096211012266. 26. josan es, zaietta ga, hoskere gv. the devastating starfield pattern of cerebral fat embolism. neurol india. 2021; 69(2):538-539. 27. wang hc, yu n, wang x, dong r, long x, feng x, et al. cerebral embolism as a result of facial filler injections: a literature review. aesthet surg j. 2021; sjab193. 320 ivan david lozada-martínez, michael gregorio ortega-sierra, m.d. del pilar zambrano-arenas et al. 28. giyab o, balogh b, bogner p, gergely o, tóth a. microbleeds show a characteristic distribution in cerebral fat embolism. insights imaging. 2021; 12(1):42. 29. fowler jb, fiani b, sarhadi k, cortez v. cerebral fat embolism in the absence of a long bone fracture: a rare case report. surg neurol int. 2021; 12:78. 30. wang w, chen w, zhang y, su y, wang y. post-traumatic cerebral fat embolism syndrome with a favourable outcome: a case report. bmc neurol. 2021; 21(1):82. 31. huang ch, hsieh mh. isolated cerebral fat embolism syndrome: an extremely rare complication in orthopaedic patients. anz j surg. 2021. online ahead of print. microsoft word 13gheorghitaeva_anesthesia.doc 348 eva gheorghita et al anesthesia by electro acupuncture in neurosurgery anesthesia by electro acupuncture in neurosurgery eva gheorghita, g. litarczek, m. trifu, o. rata, j. ciurea, r.m. gorgan emergency clinical hospital bagdasar arseni, bucuresti abstract given the fact that in neuroanesthesia the choice of anesthetic substances must take into account the effect they have over the cerebral substance, we felt that using as few drugs as possible eliminates their shortcomings, improving the intraoperative conditions as well as the outcome of the surgical intervention. for this purpose, we have used anesthesia through electro acupunctural stimulation associated to hypnosis, drug relaxation under controlled breathing on a group of 12 patients, from which 10 patients had undergone brain surgery and 2 patients had undergone surgery for herniated disc. the outcomes showed the better effect of this method than that of the classical, the patients showing excellent intraoperative hemodynamic stability, relaxed brain, without the need to use depleted substances, rapid awakening with a much better postoperative analgesia. keywords: electroacupuncture, electrostimulation by acupuncture, neuroanaesthesia. introduction acupuncture is probably the oldest therapeutic method used worldwide nowadays. the beginning of this therapy is very old, since before our era in china. surgical anesthesia technique was used for the first time ever in china in 1958 for a dental extraction. only after 10 years of experimentation on a large number of cases in various fields of surgery appear the first communications. in 1969 professor n. gheorghiu published the first gynecological operations performed under acupunctural anesthesia. since 1970, appear many communications on acupuncture anesthesia in a number of countries and the method and its results are discussed in a series of congresses of anesthesia. the browse of the literature has shown that up until the present there is absolutely no consensus on the effectiveness of acupuncture in the current practice of anesthesia. the encountered views ranged from the rejection of the method to accepting it only as a placebo or hypnosuggestive and efficient method up until proving its real efficiency . surgical anesthesia by acupuncture technique is present in the speciality literature under the most various aspects starting with very optimistic reports submitted by the chinese authors, promoters of the method and some european and american authors and ending with the relative observations made by other authors who failed to reproduce the technique and to create good satisfactory conditions for the deployment of the operatory action. after many years of research and debates,it is considered today that the romanian neurosurgery (2010) xvii 3: 348 – 353 349 analgesic effect of acupuncture is a certainty. in romania, this method was used by prof. dr. n. gheorghiu, who published in 1969 the employment of this technique in gynecological interventions. starting with the 1980, electroacupunctural anesthesia is applied in our country by prof. dr. g. litarczek, fundeni hospital, then in other hospitals. however, there is no single theory yet to explain the complex mechanism of action of acupuncture. studies by melzack (22) have shown that acupuncture points correlate with trigger points used in classical medicine to inject some substance (anesthetics). other studies have demonstrated the existence of some special electrical properties at the level of the acupunctural points, the electric stream passing much easier at this level (3.19). by stimulating the acupunctural points, in the body appear many neurological and neuro-umoral changes. researches showed that the stimulation of certain acupuncture points edit nerve transmission in painful areas of the spinal cord and thalamus. there are several theories which confirm the different mechanisms of action. 1.the gate theory explains the effect of acupuncture as: the painful excitation is transmitted in the gelatinous substance of the spinal cord, led through the thin nerve fibers. thicker nerve fibers have inhibitory effect on pain by closing the gate at the spinal level,in the gelatinous substance. melzack suggests that acupuncture stimulates the thick myelinated nerve fibers, thus closing the gate. this theory can not explain the complex mechanism of action of acupuncture but it is certain that acupuncture works in part by blocking the gate 2. another theory, demonstrated by studies, shows the increase of the level of endorphins in several parts of central nervous system after acupuncture stimulation (25, 12, 1). this is confirmed by research showing that the effect of acupuncture can be blocked by injecting opioid antagonist substances. recent studies show that opioid antagonists do not interfere with acupuncture analgesia, considering that betaendorphin release is caused by stress and not by acupuncture. other studies have shown otherwise, so not even the endorphins theory explains enough the mechanism of action of this technique (21.5). 3. on the other hand, it is known that the monoaminergic system has an action of pain modulation. research has shown that the monoaminergic system’s antagonistic substances decrease the analgesic effect of electroacupuncture (7). north and collaborators have shown that the stimulation of adrenoreceptors α2 increases the driving speed of the neurons in the posterior horn, causing hiperpolarization and decreasing excitability, with analgesic effect (23). also has been found that synthesis and release of serotonin and norepinephrine in the cns is stimulated by electroacupuncture. other studies have shown the role of adrenergic descending pathways in modulating nociception. spinal administration of norepinephrine or electrical stimulation of the central noradrenergic cells induce strong antinociception. locus ceruleus in the brainstem is the largest cell group composed of catecolaminergic neurons. by 350 eva gheorghita et al anesthesia by electro acupuncture in neurosurgery empowering them antinociception decreases after intrathecal injection of alpha2 antagonists, but not of alpha1 antagonists.in conclusion, analgesia is mediated by alpha2 adrenereceptors (14). anon and collaborators have shown the antishock effect of acupuncture, demonstrating on experiments with dogs, that after a massive bleeding using acupuncture anesthesia, the animals had a significantly higher survival rate (2). therefore, it appears that the analgesic effect of acupuncture in various conditions may be mediated by different mechanisms. it is also possible that stimulation of various points to lead to different mechanisms of action. there are two methods used to achieve electro acupunctural anesthesia: 1. vigil surgical acupunctural analgesia technique; 2. hipoanalgesic technique by electroacupuncture hyperstimulation. in the vigil technique, the patient is awake and manual or electrical underlined stimulation is used. the technique of hypnoanalgesia by electroacupuncture hyperstimulation is using hypnotics (propofol, midazolam) and muscle relaxants,orotraheal intubation and mechanical ventilation. for analgesia in major surgical interventions electric supraliminar stimulation is exclusively used. material and method this work is based on general anesthesia performed by technical hipnoanalgetic electroacupuncture on 12 patients who underwent neurosurgical intervention. of these, 10 patients with the brain surgery (9 patients with brain tumor, 1 patient epilepsy surgery) and 2 patients with lumbar disc hernia. for electrical stimulation was used the chinese device dz 22 and romanian device eco 001. before surgery, patients were explained the technique used and required written consent to perform anesthesia. the technique used was: trained patients were sedated in the morning and in the evening with: one tablet diazepam 10mg or midazolam 7mg and 0.3 to 0.4 mg / kg clonidine; the patient was brought in the operating room where have been mounted least three peripheral venous lines, and possibly a central one, with saline infusion; monitoring was started ecg, bp (blood pressure), p(pulse), spo2, were fitted the needles of acupuncture in points l6 and li4 bilaterally with an electronic detector of acupuncture points; then the electrical stimulation device (figure 1) was set to 5hz frequency on the left oscillator and 100-120 hz on the right one; the needles were connected to the device , two for each hand at each of the two channels; injectomats were prepared with propofol and / or midazolam, related to the venous line; figure 1 the electrical stimulation device romanian neurosurgery (2010) xvii 3: 348 – 353 351 the induction was started with curare of protection, then 2mg/kg propofol, succinylcholine 1 mg / kg; orotraheal intubation was performed , the patient was connected to the o2 + air flow 1 / 1; electrical stimulation has been started, producing alternative unloadings of two frequences: 5-10 hz and 90-130 hz; propofol infusion was started with 1-3 mg / kg / hr and / or midazolam 0.05 to 0.1 mg / kg / hr; curare administration continued in bolus; current voltage was gradually increased incentive to limit supported by the pacient, about 40v; have implanted two more pins at the ends of the incision, which is stimulated by 100-120 hz; stimulation lasted 30 minutes before the start of surgery and continued until its completion; in the end of the intervention were stopped hypnotic drugs and electric stimulation; the curare has been antagonized. results the method of electroacupunctural anesthesia under hypnosis and relaxation has proven effective in all cases studied. in one of the cases, in the middle of surgery we found increased bp and p, when in fact stimulation device failed, then the patient was administered opiate to continue the surgery. we found difficulties in monitoring bis, artifacted by surgical maneuvers in the brain. analyzing hemodynamic parameters in all patients we found a trend of increasing bp and p within acceptable limits (5-10% of initial value), which was maintained throughout surgery (figure 2, figure 3). no patient has required extra analgesic; excellent hemodynamic stability, warm periphery; awakening was quick, no chills, vomiting or respiratory depression danger. no patient required analgesic medication in postoperative, enjoying prolonged post acupunctural analgesia. resumption of spontaneous micturition was swift. discussions in the case of neurosurgical interventions, painful periods are only related to the skin incision and suture of the teguments, meninges and periosteum, and also these patients do not require relaxation only for intubation and mechanical ventilation. 1 2 :0 0 :0 0 a m 1 2 :3 0 :0 0 a m 1 :0 0 :0 0 a m 1 :3 0 :0 0 a m 2 :0 0 :0 0 a m 2 :3 0 :0 0 a m 3 :0 0 :0 0 a m 3 :3 0 :0 0 a m 2 6 10 0 20 40 60 80 100 120 m ap (m m hg ) t i m e (m i n ) p a tie n ts figure 2 variation of blood pressure (bp) 0: 00 0: 30 1: 00 1: 30 2: 00 2: 30 3: 00 3: 30 1 4 7 10 0 10 20 30 40 50 60 70 80 90 100 hr (b/m in) tim e (m in) p a tie nts g figure 3 variation of heart rate 352 eva gheorghita et al anesthesia by electro acupuncture in neurosurgery given the fact that in neurosurgical pathology we are dealing with patients who have low cerebral compliance, a particular importance is the maintenance of the cerebral circulation autoregulation, and its reactivity to paco2. avoiding the use of nitrous oxide, halogenated substances, as well as the opioids,it is a great advantage to not emphasize the increase of intracranial pressure during the operation. the usage of propofol and/or midazolam have ensured a cerebral protection. i emphasize the fact that in the presented casuistry no patient required intraoperative depletive treatment, in all cases the brain was relaxed, without edema, facilitating surgical maneuvers and avoiding risk making cerebral ischemia secondary to these maneuvers. we observed hemodynamic sensitivity of these patients to major volemic loses. hypovolemia could be avoided by careful monitoring and adequate volemic filling pending the loses. a great advantage is also the probability to awaken the patient during the surgical intervention maintaining analgesia taking into account the fact that in neurosurgery the so-called "awake craniotomy" technique is becoming increasingly used in the surgical approach of motor and speech areas, in the epilepsy surgery and parkinson disease. rapid postoperative awakening is a great advantage in neurosurgery for the neurological evaluation,it can be made immediately, and could act quickly if there is clinical examination and then by fast ct appearance of postoperative hematoma. also, the absence of postoperative pain and chills does not expose the patient to increased risks of cerebral edema due to icp by hypoxia, hypercapnia, high respiratory pressure. the literature data shows that hyperstimulation made by electroacupuncture realises analgesia and blockade of thermoregulatory reaction by direct interference with the central nervous mechanisms involved in making a reaction to nociception and cold (litarczek). the occurrence of postoperative vomiting also increases the risk of increased icp. it is described in the specialty literature that the l6 point stimulation significantly reduces postoperative nausea and vomiting, a stronger effect, compared with prophylactic anti-emetic medication (8.9). numerous studies (27,15) showed the effect of stimulating the immune system both cellular and humoral, which is a big advantage compared with traditional general anesthesia. hemodynamic stability both at the microcirculation and macrocirculation level is another important advantage of this anesthetic technique. after a few hours postoperative we have found an analgesic effect without having to be given special medication for pain, this being found by other studies also (4). the only disadvantage of this technique would be the prolongation of the induction time until the beginning of surgery with about 30 minutes, needed to install analgesia after starting stimulation. some authors consider that the application of this method in neurosurgery is very useful, because of avoiding the use of drugs that interfere with the selfregulation of cerebral circulation and its reactivity to paco2 and to avoid cerebral vasodilatation with increased intracranial pressure. romanian neurosurgery (2010) xvii 3: 348 – 353 353 conclusions excellent hemodynamic stability obtained using this technique helps to avoid the occurrence secondary cerebral ischemia lesions. lack of favorable effects of increased intracranial pressure by eliminating the use of substances (volatile anesthetics, gas, opioids) and possible intraoperative awakening to maintain analgesia is a real advantage in neurosurgery. fast awakening , without chills, nausea, vomiting, allow early neurological assessment and avoid the occurrence of cerebral edema immediately after surgery, anesthesia costs of eliminating the use of several drugs are other advantages. the only disadvantage would be the prolongation of anesthetic induction time needed about 30 minutes required for analgesia. in conclusion, acupunctural hipoanalgezia is an anesthetic technique that is suitable for wide use in neurosurgical interventions. references 1. alisov ap et al. the content of beta – endorphin, met-enkephalin and acth in the blood plasma during electric and drug anesthesia. anestesiol reanimatol.(3): 9-14; 1996 may-jun. 2. anon, journal of chinese medicine 2:261; 1974. 3. becher et al. transactions on biomedical engineering p.533;1975. 4. bourdall-badie et al. long – lasting anaesthesia advantages of electroanaesthesia. anesth analg.; 37 (910): 523-6; 1980. 5. chapman cr, colpitts ym, benedetti c, kittaef r, gehrig jd. evoked potential assessment of acupunctural analgesia:attempted reversal with naloxone. pain. 9:183-197; 1980;. 6. cheng rss, pomeranz b monoominergic mechanism of electroacupuncture analgesia. brain res. 215:77-79; 1981. 7. cheng rss, pomeranz b. monoaminergic mechanism of elecroacupuncture analgesia. brain res. 215:77-92; 1981. 8. dundee jw, mcmillan cm. p6 acupuncture and postoperative vomiting. br j anaesth. 68:225-6; 1992. 9. dundee jw, ghaly rg, bill km, chestnutt wn, fitzpatrick ktj, lynas aea. effect of stimulation of the p6 anti-emetic point on postoperative nausea and vomiting. br j anaesth 63:612-18; 1989. 10. fuhazawa y, moeda t, koshioha s. the pharmachological mechanism of electroacupuncture. curr opin investig drug. 10(1):62-9; 2009. 11. graftieaux jp et al. electro-anaesthesia during neurosurgery. anesth analg 38 (3-4): 113-7; 1981. 12. han js, terenius l. neurochemical basis of acupuncture analgesia. annu rev pharmacol toxicol. 22:193-220; 1982. 13. harbach h et al. minimal immunoreactive plasma beta-endorphin and decrease of cortisol at standard analgesia or different acupuncture techniques. eur j anaesthesiol. 12:1-7; 2006. 14. jones sl, gebhart gf. characterization of coeruleospinal inhibition of the nociceptive tail-flick reflexin the rat: mediation by spinal α2-adrenoreceptors. brain res. 364:315-330; 1986. 15. kim sk et al. a parametric study of the imunomodulatory effects of electroacupuncture in dnp-klh immunized mice. evid based complement alternat med. 2009 nov 9. 16. lin jg, chen wl. acupuncture analgesia: a review if its mechanism of actions. am j chin med 36(4):63545; 2008. 17. litarczek g, ghertrude harsovescu, a popa. locul acupuncturii in anestezia chirurgicala moderna. chirurgia.35/5: 393-400; 1986. 18. litarczek g, v candea, a popa, i tintoiu, v stingaciu – hipnoanelgezia prin hiperstimulare electrica in puncte de acupunctura, ca metoda anestezica in chirurgia pe cord deschis. chirurgie. 37/1:63-72; 1988. 19. lykken dt, venables ph. direct measurement of skin conductance:a proposal for standardization, psychophysiology.;8:656-672; 1971. 20. mayer dj, price dd, rafii a. antogonism of acupuncture analgesia in man by the norcotic antagonist naloxone.brain res.121: 368-372; 1997. 21. mclennan h, gilfillan k, heap y. some pharmacological observations on the analgesia induced by acupuncture in rabbits.pain. 3:229-238; 1977. 22. melzack et al. science 150:197; 1965. pain 1:463; 1975. 23. north ra, yoshimura m. the action of noradrenaline on neurone of the rat substantia gelatinosa in vitro.j. physiol. 349: 43-55; 1984. 24. pomeranz b, chiu d, naloxone blockade of acupuncture analgesia:endorphin implicated. life sci.19:1757-1762;1976;. 25. sjolund b, trienius l, eriksson mbe. increased cerebrospinal fluid levels of endorphins ofter electroacupunture. acta phys scand 100:383-4; 1977. 26. takeshige c, sato t, mera t, hisamitsu t, fang j. descending pain inhibitory system involved in acupuncture analgesia. brain res bull. 29: 617-634; 1992. 27. yamaguchi n et al, acupuncture regulates leukocyte subpopulations in human peripheral blood. euid based complement alternat med.4(4): 447-453; 2007. microsoft word 5adamdanilnucleoplasty.doc romanian neurosurgery (2010) xvii 2: 159 – 165 159 nucleoplasty – general overview danil adam1, evgheni pevzner2, reuven gepstein2 1neurosurgical clinic, st. pantelimon clinical emergency hospital, bucharest, romania 2meir hospital, tel aviv, israel abstract the management of disc protrusion is multidisciplinary. in the midway between conservative treatment and open surgery are minimal invasive procedures. nucleoplasty is a new treatment of discogenic leg pain using bipolar radiofrequency device for vaporising a small volume of nucleus pulposus. percutaneous removal of nuclear tissue is thought to lower nuclear pressure, thereby reducing nerve root tension and allowing retraction of the protrusion. causes of discogenic pain are discussed. indications of the procedure and surgical technique and the literature results are presented. keywords: coblation, disc protrusion, discogenic pain, nucleopasty. introduction the chronic low back pain is the most frequent illness in modern societies, having serious financial and social consequences. disc sciatalgy affects almost 10.106 persons every year, with an estimated cost of over 20x109 $ (carey and col. 1995). the traditional treatment of low back pain, which appears frequently in association with leg pain includes: bed rest, immobilizing the spinal column, physiotherapy and the prescription of opioid medicines or nsaids. although this is the routine treatment, it may not be the optimal solution: patients could develop intolerance towards opioids, the nsaids have secondary, potentially dangerous effects, and physiotherapy may be ineffective. when the symptoms don’t respond to traditional treatment, other, more aggressive therapies must be taken into consideration, including the percutaneous disc decompression, minimally invasive. the surgical hld treatment by standard, open discectomy is indicated for patients with big, uncontained herniations and/or for patients with disc sequestration. carragee and col. (2001) reported that for patients with contained hd that measure less than 6 mm in ф ap, the post discectomy success rate was of only 24% as compared to 98% for patients with hd greater than 9 mm ф ap. the general tendency in spinal surgery was reductionist and minimalist in order to reduce the patient's trauma and in order to create alternatives to the open surgical procedures. in the last decades there have been imagined and applied several disc pain minimally invasive techniques for discogenic pain among which: 1975 hijikata – percutaneous discectomy 1984 – onik automated percutaneous disc decompression 1986 – choy/ascher – laser 160 danil adam et al nucleoplasty percutaneous disc decompression 2000 – saal – idet: intradiscal electrothermal annuloplasty 2000 – arthrocare nucleoplasty/ coblation the minimally invasive intradiscal percutaneous techniques aim at clearing off the discal material which is supposed to produce lombalgy and/or radiculopathy. percutaneous discal decompression is based on the principle of producing a small drop in volume in a closed hydraulic space as the intact disc is (including the contained disc hernia), which produces a pressure drop and reduces or eliminates thus pain. by reducing intradiscal pressure, the disc synthetesises a smaller quantity of inflammatory mediators, reduces its volume and initiates the healing process. all percutaneous discectomy techniques have in common the main purpose of clearing off a portion of the nucleus pulposus by laser energy or thermal ablation. causes of discogenic pain small protrusions produce at the same time axial pain (lombalgy) and radicular pain, as a consequence of raised pressure on the external annulus that contains nervous terminations and of neural inflammation. discogenic pain is caused partially by inflammatory chemical substances like: matricial metalloproteinaes, the prostaglandin pge2, interleukins, tnf, ph changes and by an influx of inflammatory cells given by chemical signals that appear in the degenerated disk. the anatomic structure in which these substances are produced must be cleared away as thoroughly as possible. the minimal change of the offending disc geometrical anatomy may be sufficient in the treatment of hd and the more elaborated treatments (fusion, artificial disk) may no longer be necessary. david choy, in 1997 reports the case of an acrobatic pilot with a sciatic ldh, whose pain became more acute when he was redressing from a dive with a force of 6g. the pilot observed that the pain was ameliorated immediately when he went up to 3000 m and executed a looping, producing a force of -3g. in the first situation, the centrifugal force raises the body weight by 6x gravitation. in the second, when the plane flies making a downwards curve, the body weight is 3 times diminished. this demonstrates that discogenic pain is due to a mechanical/pressure mechanism rather than to a chemical mechanism. nerve edema can be induced by pressure of only 50mmhg for 2 minutes. compression of the nerve root could in fact by disc protrusion contribute to low back pain. (takahashi et al. 1999) nucleoplasty alters the expression of inflammatory cytokines in the degenerated disks, leading to the dropping of il-1 and the rising of il-8. because il-8 has an anabolic effect, nucleoplasty can initiate a repair response in the disc. nucleoplasty nucleoplasty was introduced in clinic in july 2000. nucleoplasty is a new procedure, minimally invasive, that uses radiofrequency energy in order to clear away material from the nucleus pulposus and to create channels tubes in the disc. nucleoplasty uses the technique of controlled ablation in order to ablate and coagulate the soft tissue, combining both accesses to clear off a part of the disc. during coblation, the energy of rf (radio romanian neurosurgery (2010) xvii 2: 159 – 165 161 frequency) converts the fluid in the nucleus pulposus into a layer of ionized steam, called ‘plasma’. these full particles (excited ions) disintegrate the connections between disc molecules, and the disc interior is transformed into hydrogen and oxygen. these gases are eliminated through the cannula introduced percutaneously in the disc. during ablation the nucleus temperature reaches 45-55o c and during thermal coagulation the temperature rises to 70 o c. thus, the soft tissue dissolves itself and the healthy nearby tissue is kept integrally. by creating a series of channels in the disc the pressure exercised y the contained disc hernias on the nervous root is reduced. nucleoplasty is a simple procedure, that doesn't involve complications. table 1 inclusion/exclusion criteria for percutaneous disc nucleoplasty inclusion criteria exclusion criteria • sciatalgy ≥ lombalgy • contained disc protrusion (mri) • failure of traditional therapy for 6 weeks • the disk height ≥ 75% as compared with the adjacent ones • contained hd with ф ap ≤ 6mm • complete annular fracture • excluded or sequestred disc • fracture, tumour or spinal infection at the suspected level • the disk height < 25% as compared to adjacent levels (discal collapse) • severe canal stenosis • signifiant scoliosis • segmentary instability • psychiatric disorders • coagulopathies • more than 2 simptomatic levels nucleoplasty action mechanism by nuclear tissue ablation, using thermal energy, we obtain a decrease of intranuclear pressure, the tension exercised by the protruded nuclear material on the nervous root drops, this one having the possibility to come back in the interior of the disc. the back pain and the leg pain are explained through several mechanisms: the theory referring to the pressure exercised on the nervous root is one of these mechanisms. chen and le showed that by creating 6 channels in the intervertebral disk nucleus on a dead body, the intradiscal pressure dropped by 100% at young dead persons. on the other hand, in degenerated disks, the fall was insignificant. carragee and col (2003) obtained better results by removing through open surgery less nuclear material. although the rate of recurrent herniations was greater in this group, the surgical result measured by the degree of satisfaction, pain and function was superior. the more discal material is ablated, the more the height of the disk diminishes, a "bulge" appears and the stress on the discal annulus grows. the nuclear tissue is ablated using bipolar radiofrequency energy with high voltage (100-300v) and with a frequency of 120khz. this current creates a plasmatic field thick of approximately 75μm, composed of very ionised particles that have sufficient energy to break the organic molecular connections in the disk nucleus tissue and to vaporize thus this tissue. the coblation produces the normothermal molecular dissociation. the water content of the nucleus pulposus varies between 50-89%, being 162 danil adam et al nucleoplasty dependant on age and dropping with age. through nucleoplasty one reduces at a minimum level the volume of the nucleus pulposus and the intradiscal pressure. the reducing of pressure creates a pressure gradient that leads to the migration of the portion of nucleus that is herniated and to its removal from the nervous root that it constricts. this approach is based on the principle according to which in a closed, intact hydraulic space, the water being impossible to compress, a small change of volume will lead to a disproportionately big pressure change. the implosion theory another purpose of the central nuclear decompression is to create spaces inside the disk in which the protruded/herniated fragment can recede reducing the pressure on the nervous root and the annulus. there are few evidences to maintain this theory. the chemical theory: in a discal cells culture, coblation led to the augmentation of inflammatory mediators in the normal cells of the annulus and nucleus, but in the abnormal nuclear cells, it led to a fall of inflammatory mediators. surgical technique the anesthesia the nucleoplasty can be made under local anesthesia. the patient remains awake and thus he can tell the doctor when he feels a pain caused by the nerve irritation. the disadvantage of such type of anesthesia is that the patient doesn’t maintain the correct position on the surgical table. for avoiding this drawback, local anesthesia is supplemented with i.v sedation using propofol. general anesthesia is not indicated because inadvented lesion of the nerve root is not evident. antibiotics are given i.v, preoperative and 12 hours postoperative, using cephasilyn 1gr/dose. positioning the patient is placed in lateral decubitus position on the healthy side with his knees and his thighs bent. the head rests on a pillow. in the access of the disk l5-s1, in order to facilitate the approach, a pillow is placed under the basin in order to generate a scoliosis. the surgical table must be fluoroscopically compatible and to allow easy access for the c-arm in order to get ap and lateral images. on the skin is marked the iliac crest, the regarded discal space at the level of the posterior median line (figure 1). the c-arm is tilted towards the head or the legs till it’s obtained a fluoroscopically clear image of the discal space with the endplates perfectly parallel. the level of interest and the angle of access of the cannula in the disc are verified fluoroscopically. surgical steps the skin puncture is done at a distance of 8-11 cm from the median line, with a needle of 17 gauge that is introduced under fluoroscopic control at the junction between the annulus and nucleus, on the symptomatic side. a radiofrequency electrode calted spine wand is introduced then on this needle, overrunning the needle end by 5 mm. romanian neurosurgery (2010) xvii 2: 159 – 165 163 figure 1 skin markers figure 2 the catheter is introduce percutaneously into the discal space figure 3 intraoperative fluoroscopic image which show the catheter position into the l5-s1 disc space table 2 complications open nucleoplasty ▪ the damaging of the recurrent laringeous nerve ( 11%) ▪ the damaging of the vertebral artery (0.3 %) ▪ the damaging of the cervical roots ▪ the dysphagia (50%) ▪ pain in the place of the pin prick (76%) ▪ paresthesias (26%) ▪ the growing pain intensity (15%) ▪ discitis (1.3%) ▪ the damaging of the nervous structures (1%) ▪ the intradiscal break of the electrode (0.5%) on the proximal side of the caterer, the starting point has a circumferential marker. the caterer advances from the starting point to the junction between the anterior part of the annulus and the nucleus and a new marker (stop marker) is made on the caterer in order not to overrun this final position (figure 2 & 3). the discal decompression process includes the caterer’s progression into the ablative sequence, with a speed of 0.5 cm/sec then its retraction in the coagulation sequence with the same speed. by repeated ablation and coagulation several channels are created, with ф=1mm in the clock positions 2, 4, 6, 8, 10 and 12. at the end, the needle and the caterer are extracted and the puncture place is sterilely bandaged. at the end of the procedure an epidural injection with depo-medrol is done. the intervention takes 15 minutes. the patient is discharged after 2 hours. he can resume his activities in 2-3 days. for 14 days he must continue a treatment with nsaids: arcoxia. complications the complications of nucleoplasty, in comparison with standard disc herniation procedure are presented in table 2. 164 danil adam et al nucleoplasty bhagia et al (2006) reported the short term side effects and complications after nucleoplasty in 49 patients. the most common side effects at 24 hours post-procedure was soreness at the needle insertion side (76%), new numbness (26%), increased intensity of pre-procedure back pain (15%) and new areas of back pain (15%). at 2 weeks, no patient had soreness at the needle insertion site or new areas of back pain; however, new numbness was present in 15% of patients. two patients (4%) had increased intensity of preprocedure back pain. the authors concluded that nucleoplasty produced statistically significant reductions in visual analog scale (vas) score, for back pain and leg pain. the classical operation is accompanied by many types of complications, some of which may be permanent. the dysphagia and the paralysis of the recurrent laringeous nerve are the most frequent. the nucleoplasty’s complications are less important and can be remitted with antiinflammatory medication. the advantages of this method are: percutaneous access, local anesthesia and intravenous sedation, reduced operating time (10-15 minutes), avoiding (avoidance) epidural scarring risk. the procedure can be repeated at the same level or at adjacent levels. and np doesn’t contraindicate the open surgery if the results obtained are satisfactory. results the discal nucleoplasty is a relatively new technique and that is why literature contains few references to this subject. in 2005, marin published a retrospective study where he shows that he got 80% ameliorations of the vas score at 6 and 12 months. singh and col 2002 analyzed the results obtained by using nucleoplasty at 67 of his patients with ldh. one year after, 80% of the patients demonstrated a statistically significant amelioration of the numeric scores of pain. in another study published in 2004, he got a pain amelioration greater than 50% after 1 year, in 80% of the 49 patients treated. gerszten et al (2006) in a prospective, nonrandomised cohort study, using nucleoplasty-based percutaneous disc decompression, in patients with symptomatic contained disc herniations, concluded that nucleoplasty is safe and improves qol. yakovlev et al (2007) assessed the effect of nucleoplasty on pain and opioid use in improving functional activity in patients with radicular or axial low back pain secondary to contained herniated discs. reported pain and medication was improved at 1,3,6 and 12 months following nucleoplasty. these were ni complications associated with the procedure and continued improvements were observed over time. mirzai, in 2007, demonstrated a medium reduction of the vas score from 7,5 to 2,1 6 months after operating 52 patients. favourable results were also obtained in the case of cervical nucleoplasty (li, 2008; birnbaum, 2009). the results reported up to the present day show that nucleoplasty is associated with a significant decrease of pain and an amelioration of life quality. after nucleoplasty, the chronic back pain is reduced with about 50%. nucleoplasty is indicated especially in the treatment of leg pain. romanian neurosurgery (2010) xvii 2: 159 – 165 165 conclusions nucleoplasty: is attractive because it’s simple, relatively safe procedure and destroys a minimum of discal tissue. the disc height is generally maintained. the discal collapse is reduced slowly, allowing the body to adapt. references 1.bhagia s, slipman cw, nirschl m, et al: side effects and complications after percutaneous disc decompression using coblation technology. american journal of physical medicine & rehabilitation. 2006; 85(1): 6-13. 2.birnbaum k: percoutaneous cervical disc decompression. surg radiol anat 31: 379-387, 2009. 3.carey ts, garrett j, jackman a, et al: the outcomes and costs of care for acute low back pain among patients seen by primary care practitioners, chiropractors and orthopedic surgeons. the north carolina back pain project. n engl j med 333: 913-917, 1995. 4.carragee e, suen p, han m: scanning in patients with sciatica predict failure of open limited discectomy, in proceedings of the international society for the study of lumbar spine (issls). scotland, 2001. 5.choy ds, ascher pw, ranu hs, et al: intradiscal temperature study of percutaneous disc decompression with nucleoplasty in human cadavers, in nass meeting of the americas. new york: lippincott williams @ willkins, 2002. 6.choy dsj: positive and negative gravitational forces and herniated disc sciatic pain. n engl j med 337:19, 1997. 7.hijikata s, zamagishi m, nakagama t, et al: percoutaneous diskectomy: a new treatment method for lumbar disc herniation. j toden hosp 5: 5-13, 1975. 8.li j, deng-iu y, zhang z: percoutaneous cervical nucleoplasty in the treatment of cervical disc herniation. eur spine j 17: 1664-1669, 2008. 9.marin fz: cam versus nucleoplasty. acta neurochir suppl 92: 11-114, 2005. 10.mirzai h, tekin i, yaman o, et al: the results of nucleoplasty in patients with lumbar herniated disc: a prospective clinical study of 52 consecutive patients. spine j 7: 88-93, 2007. 11.onik g, helms ca, ginsburg lh et al: percoutaneous lumbar discectomy using a new aspiration probe. ajr am j roentgenol 144: 1137-1140, 1985. 12.p. c. gerszten, w. c. welch and j. t. king jr.: quality of life assessment in patients undergoing nucleoplasty-based percutaneous discectomy. journal of neurosurgery: spine (2006) 4: 36-42. 13.saal ja, saal js: intradiscal electrothermal treatment for chronic discogenic low back pain: a prospective outcome study with minimum 1-year follow-up. spine 25: 2622-2627, 2000. 14.singh v, piryani c, liao k, et al: percoutaneous disc decompression using coblation (nucleoplasty tm) in the treatment of chronic discogenic pain. pain physician 5: 250-259, 2002. 15.takahashi k, shima i, porter rw. nerve root pressure in lumbar disc herniation. spine 1999; 24: 2003-2006 16.yakovlev alexander, mazin al tamini, liang hong, eristavi maria: outcomes of percutaneous disc compression utilizing nucleoplasty for the treatment of chronic discogenic pain. pain physician 2007, 10, 319327. microsoft word 14chiriaca_ruptured_f 340 a. chiriac et al intracranial aneurysm and carotid occlusive diseases ruptured intracranial aneurysm associated with bilateral carotid occlusive diseases and venous angioma: a case report a. chiriac, j. baldauf1, h.w. schroeder1, z. faiyad, a.şt. iencean, i. poeată clinic of neurosurgery, “gr.t. popa” university of medicine and pharmacy iasi, romania 1klinik für neurochirurgie, ernst-moritz-arndt-universität greifswald, germany abstract coexistence of a ruptured intracranial aneurysm with an internal carotid arteries carotid artery occlusion, a contralateral internal carotid artery stenoses and a intracranial venous angioma is infrequent and it suppose a complicate diagnosis and therapeutic management of either disease. we report a case who underwent a first successful microsurgical clipping of the intracranial aneurysm followed by a right carotid artery angioplasty with stenting after two months. introduction a patient with coexistence of ruptured intracranial aneurysm, a carotid artery occlusion, an opposite carotid artery stenoses and brain venous angioma is a very rare clinical situation. ito m. and collaborators describe in there article a similar case but with multiple aneurysms. this special clinical situation is rarely found due to specialist attention focused on one of the two types of injuries, but also as a result of angioct use as first intent of imaging exploration detrimental to femoral catheter angiography. thus, many specialists do not perform a complete cerebral angiographic exploration for suspected stenosis and / or carotid occlusion, and most of neurosurgical centers use angioct exploration for diagnosis and interventional planning of intracranial aneurysms. coexisting of a ruptured intracranial aneurysm and a stenosis and / or carotid occlusion is a special situation where the therapeutic needs it requires a high performs. the extremely low number of these situations and the relatively results obtained led us to present this case. case presentation pacient t. d., male, 45 years old describe onset of symptoms by sudden sleep violent headache followed by nausea, vomiting. the patient had initial addressed to suceava hospital, where the symptoms were initially interpreted as heatstroke. so he was sent at home with medication treatment. because over the next seven days the headache persists the patient carry out a cerebral ct-scan which shows a sah (figure 1). he is directed to neurosurgery iasi. on admission he was in grade ii (hunt & hess scale). first, a cerebral angiomri was performed, reveling a possible anterior communicating artery aneurysm as source of subarachnoid hemorrhage. due to, an unclear image a femoral catheter angiography was performed next day. cerebral angiography exposed an occlusion of left internal carotid artery (figure 4a), a romanian neurosurgery (2011) xviii 3: 340 – 343 341 70% stenosis of right internal carotid artery, a t-insular venous anomaly and confirmed the antcoa aneurysm. cross filling was good, being provided from both carotid and vertebral territory through the anterior and posterior communicated segment (figure 2 a, b, c). after 7 days of standard treatment the patient was submitted to surgery. aneurysm was approached through a right pterional craniotomy with sylvian fissure dissection, carotid and suprachiasmatic cisterns opening, a minimum gyrus rectus resection and highlighting of a1, a2, bilateral recurrences. aneurysm is looking extremely thin, polilobate, brittle fragile except the two main lobes. figure 1 ct cerebral showing a sah figure 2 a 3d reconstruction of angiomri showing an acoa aneurysm; b ce mri and c dsa it has buds adjacent to the neck. the difficult dissection of the lateral aneurismal lobe, which is oriented to the left and adherent especially to left recurrent artery, cause a small bleeding of it. finally, a good obliteration of the aneurysm was achieved by using a lateral angulated yasargil clip with maintaining patency in all vessels exposed. the aneurysm was clipped with temporary clip control on both a1, lasting for less five minutes. post-operative course was good with no neurological events (figure 3). concerning the stenosis of right internal carotid artery the decision was to treated conservatively. the patients suffer a jacksonian seizure followed by a left hemiparesis two months later. the patient was hospitalized and a new cerebral ct scan and angiography was performed. no signs of ischemic lesions were documented and a carotid angioplasty and stenting has been suggested. the procedure was performed by o right femoral access using an 8fr sheath. first, an umbrella filters was placed 10 cm above carotid bifurcation as embolic protection device. an 8/30 mm tapered xact carotid stent (abbott) was used for stenotic portion dilatation of carotid artery. afterwards, the umbrella filters was retracted and a control injection was performed. the patient was discharge at home 3 days later. figure 3 dsa pre and post microsurgical clipping of acoa aneurysm a b c 342 a. chiriac et al intracranial aneurysm and carotid occlusive diseases figure 4 dsa showing a left ica occlusion; b right ica stenosis; c right ca dilated with stent the neurological symptoma thology remitted completely two weeks later (figure 4 b, c). discussion ruptured intracranial aneurysm coexisting with this type of bilateral stenotic and / or occlusive carotid lesions is a rare situation that raises a therapeutics issue. presence of this situation was appreciated by navaneethan sd and collaborators at 3% of total patients with intracranial aneurysms(5). the decision of initially intracranial aneurysm clipping before carotid dilation involves the risk of stroke because of decreased blood flow due to spasm, or to necessity of using temporary clips to control the final positioning of definitive clip on the aneurysm neck. on the other hand, stent carotid dilation before aneurysm clipping involves a risk of aneurysm rupture (specially to already ruptured aneurysm) due to increased flow in the territory of aneurysm location, or due to the need to initiate an on antiplatelet therapy and maintained anticoagulation. thus, the decision on which of the two treatments should be applied first, a balancing between the risk of a stroke and the outbreak of an aneurysm rupture should be made. in case of diagnosed unruptured aneurysms to a patient who suffered a stroke a carotid stent dilation is recommended followed by a microsurgical aneurysm clipping. if the patient is addressed for the cause of aneurysmal subarachnoid hemorrhage is preferable to achieve a first microsurgical clipped aneurysm and a carotid stenting thereafter(5). another option in this situation is represented by the achievement in the same therapy endovascular sessions a coil aneurysm occlusion and carotid stenting. even if the endovascular therapy allows a safety and definitive exclusion of intracranial aneurysms, this technique requires advancing of different microcatheters and wires through the carotid axis. it is well known the serious embolic complications risks of this maneuvers in the presence of a severe carotid stenosis. however, despite the increased use of these procedures, the informations regarding their influence in clinical practice are poor of clinical evidence. another theory newly disputed was the influence of different type of carotid stenotic disease on the aneurysmal development and rupture. it was stated that influence of stenotic ica anomalies in the pathogenesis of intracranial arterial aneurysms is due to increased of hemodynamic stress on the side opposite to the carotid lesion. the combination of the hydrodynamic theory, suggested by spallone and cantore study, with other possible factors, might lead to a better understanding of the mechanism underlying development of human cerebral arterial aneurysms. in their series of 76 a b c romanian neurosurgery (2011) xviii 3: 340 – 343 343 aneurysm patients, stenotic ica anomalies were mostly either located or more pronounced on the side opposite the aneurysm (in 22 as opposed to 11 on the same side, p < 0.004)(7). also, shumann and col. have presented in their article the role of xenon/ct cerebral blood flow (cbf) measurements as diagnostic tool in a case of bilateral ica stenosis associated with asymptomatic ipsilateral infraclinoidal ica aneurysm. the cbf measurements including testing of the cerebrovascular reserve capacity (crc) have demonstrated a compromise of cbf within the anterior circulation of the affected side(6). despite that, guidelines of intracranial aneurysm and carotid stenosis diagnosis and treatment are well known, a major impact on these points of view could be noted due to interdisciplinary implication (neurosurgeons, vascular surgeons, interventional cardiologists, interventional radiologists, neurologists). the usually investigation by eco-color doppler and cerebral ct doesn’t allow the necessary informations needed for carotid intervention. on the other hand, femoral catheter angiography is not a common alternative, due to its great invasivity and iatrogenic risk of complex examinations. the increased sensitivity and specificity of head and neck angio mri, plus its non invasive characteristic had a significant diagnostic impact in these special situations. in these cases, the mri pattern allows defining sufficient information for procedure planning. conclusions the incidental presence of bilateral ica occlusion daises and intracranial aneurysm need a careful attention for treatment planning. optimal and safety application of new diagnosis and treatment techniques to such complex vascular conditions can lead to an excellent outcome for these patients. references 1. bidziński j., bonicki w., kolity g. v. zaręba a. (1989) ruptured intracranial aneurysm associated with spontaneous occlusion of internal carotid artery, acta neurochirurgica, vol. 100, nu. 1-2:43-45; 2. espinosa g., dzieciuchowicz1 l.,grochowiczl. (2009) endovascular treatment of carotid stenosis associated with incidental intracranial aneurysm, annals of vascular surgery, vol. 23, (5):688.e1-688.e5; 3. ito m, sato k, tsuji o, wachi a, naito s. (1994) multiple aneurysms associated with bilateral carotid occlusion and venous angioma: surgical management risk-case report. j clin neurosci. vol. 1(1):62-8; 4. liang-der jou, h. shaltoni, h. morsi, m. mawad (2010) hemodynamic relationship between intracranial aneurysm and carotid stenosis: review of clinical cases and numerical analyses, neurological research, vol. 32 (10):1083-9; 5. navaneethan sd, kannan vs, osowo a, shrivastava r, singh s. (2006) concomitant intracranial aneurysm and carotid artery stenosis: a therapeutic dilemma., south med j., 99(7):757-8; 6. shumann m. u., mirzai sh., samil m., vorkapic p. () xenon/ct cbf measurements as valuable diagnostic tool in a case of bilateral occlusive cerebrovascular disease associated with intracranial aneurysm, acta neurologica scandinavica, vol. 93 (s166):104-109; 7. spallone a., cantore g. (1981) the role of extracranial carotid abnormalities in the genesis of cerebral aneurysms, j neurosurg. vol. 55(5):693-700. microsoft word stiljandaja_aretrospevtive_f.docx romanian neurosurgery (2012) xix 1 a retrospective and anatomopathological study of 40 orbital tumors daja stiljan1, n. ianovici2 1phd student in neurosurgery, “gr.t. popa” umph, iasi 2neurosurgery, “n. oblu” clinical emergency hospital, iasi abstract in casuistry of the neurosurgery clinic in iasi i recorded 40 observations of orbital tumors over a period of 20 years. the anatomopathological analysis of our observations has shown us a great variety of intraorbital processes occurring especially in small children with optic nerve glioma which lead to malignant tumors with age. keywords: orbital tumor, optic nerve glioma. the information from the anatomopathological study revealed that optic nerve gliomas are age specific for children. our study comprised 8 cases of gliomas in children (61.5%). this type of tumor is specific to children aged 12 – approximately 75% – proportionally more common in young children. our statistics revealed 6 cases in children under 10 years old and 2 cases in children over 10 years old – 11 and 14 years respectively. table i the anatomopathological types of 40 observations anatomopathological type number optic nerve glioma 6 optic chiasm glioma 4 meningioma 1 reticulosarcoma 2 fibrosarcoma 2 lacrimal gland, mixed tumor 1 neurinoma 2 epidermoid cyst 2 angiofibroneuroma, av angioma 3 multiforme sarcoma 4 melanoma 3 intraorbital bone neoformations 4 other intraorbital tumors 3 table ii the anatomopathological types of 13 observations of tumors in children out of the 40 observations anatomopathological type number meningioma 1 optic chiasm glioma 3 optic nerve glioma 5 angiofibroneuroma 1 reticulosarcoma 1 retinoblastoma 1 fibrosarcoma 1 discussion and conclusion the diagnosis of an optic nerve glioma should lead to a search for the stigmata of von recklinghausen’s neurofibromatosis, since this type of tumor is frequently associated with optic nerve glioma. in our study i found a case of optic nerve glioma associated with von recklinghausen neurofibroma. meningioma is rare in children. there was only one case of optic nerve meningioma which occurred in a 13-year daja stiljan, n. ianovici study of 40 orbital tumors old girl. in the study of 13 cases of orbital tumors, reticulosarcoma occurred only in one child. the evolution of children with this type of tumor is totally different from the evolution of adults. the anatomopathological and clinical study of 13 orbital tumors in children gave the following age group distribution: 0 – 2 years old, 3 cases 2 – 5 years old, 4 cases 5 – 10 years old, 3 cases 10 – 16 years old, 3 cases as it can be seen from our statistics and according to ingalls’ own statistic, the first decade of life gave the highest number of orbital tumors. in the study of 40 cases, in 24 cases the most common location is intraorbitary, in 6 cases the optic nerve, in 4 cases the optic chiasm, in 5 cases retrobular, and in 1 case the lacrimal gland. as a conclusion, the anatomopathological analysis of our observations has shown us a great variety of intraorbital processes occurring especially in small children with optic nerve glioma which lead to malignant tumors with age. references 1. castillo, bv jr. andkaufman, l. ”pediatric tumors of theeyeand orbit” pediatric clinics of north america, 50(1): 149-172, 2003; 2. cernea paul ”treaty of ophthalmology”, ed. medicala, bucuresti 1997; 3. onisim ligia – ph.d. thesis, umf bucuresti 2006; 4. szabo ioan, szabo bianca – ”neurosurgical approach of the primary intraorbital tumors”, ed. dacia, cluj napoca 2004 a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 464-469 doi: 10.33962/roneuro-2019-073 www.journals.lapub.co.uk/index.php/roneurosurgery rapid spontaneous resolution of traumatic acute subdural hematoma: a case series and review of literature gautam sachidanand, shringi prashant government medical college, kota rajasthan, india abstract introduction: acute subdural hematoma (asdh) is the most common type of traumatic intra -cranial hematoma accounting for 24% cases of severe head injuries and caries highest mortality. the mortality rates are seen to be ranging from 40% to 90%, diagnosed on computed tomography (ct) as extra axial, hyperdense, crescent lesion between the dura and brain parenchyma1. acute sdh is an acute space occupying lesion to increase intracranial pressure (icp), and is often complicated by co-existing intracranial lesions, including a variety of diffuse injuries, contusional hematomas, and edema. acute subdural post-traumatic hematoma’s (sdh) continue to have a distressingly high morbidity and mortality.2 clinical factors like presenting gcs, pupils, time to operative interval, hemodynamics and co-morbidities, plays a critical role in overall outcome from acute subdural hematoma.3careful monitoring of the neurological status is mandatory even for selected acute sdh patients with intact consciousness and no brain shift because of the possibility of the unexpected worsening. spontaneous resolution of an acute sdh has been reported in rare cases. we report a case series of spontaneous rapid reduction of acute sdh, also we discuss the prognosis of each patient according to a clinicoradiological prognostic score developed by gautam and sharma3 as well as mechanisms related to the rapid resolution of acute sdh. case series case 1 40 year old male presented with history of rta followed by loss of consciousness for 30 min and one episode of vomiting , on admission in emergency department glasgow coma score (gcs) was e3v3m5, both pupils were reactive to light , computed tomography (ct) scan shows acute sdh in right temporoparietal lobe (fig 1: a). we assess this patient according to gautam and sharma score as score is 8 and this patient was managed conservatively. repeat ncct head done after 24 hrs showed acute sdh was completely resolved (fig 1:b) patient improved and discharge on gcs of e4v5m6. keywords traumatic, acute, subdural hematoma corresponding author: s. n. gautam associate professor and head department of neurosurgery government medical college, kota rajasthan, india drsachidanandkgautam@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 465 rapid spontaneous resolution of traumatic acute subdural hematoma figure 1 (a): ct scan at admission-shows right temporoparietal sdh. figure 1 (b): (ct scan after 24 hrs shows rapid resolution of sdh. case 2 38 year old male admitted in emergency department with history of rta with 2-3 episode of vomiting but without any history of loss of consciousness, gcs was e4v5m6.on admission ncct head shows acute left temporoparietal sdh( fig 2), his score was 8 on gautam and sharma score and we managed this patient conservatively.ncct head done after 24 hrs which showed significant reduction/resolution in left temporoparietal sdh. he was discharge asymptomatically. figure 2: ct scan (a) shows left temporoparietal sdh; (b) shows repeat ct head reduction of left temporoparietal sdh. case 3 17-year-old male presented with history of rta followed by loss of consciousness, on admission in emergency department patient was intubated, glasgow coma score (gcs) was e1vtm5, both pupils were reactive to light computed tomography (ct) scan shows acute sdh in right frontotemporoparietal lobe (fig3). we assess this patient according to gautam and sharma score that was 7 and we also managed this patient conservatively. 466 gautam sachidanand, shringi prashant repeat ct head was done after 24 hrs which showed complete resolution of acute sdh. after 8 hrs of admission this patient was extubated and within 2 days he was oriented and following all commands, discharge on gcs of e4v5m6. figure 3: (a) ncct head shows right frontotemporal sdh; (b) ncct head after 24 hrs shows complete resolution of hematoma. case 4 25-year-old male presented after a road traffic accident with a brief loss of consciousness and minor facial injury. his condition declined in the emergency room necessitating a head computed tomogram (ct). at that point the patient was conscious but disoriented, his pupils were reacting and symmetric, was following commands, was able to say some words and he had movements in all extremities on verbal commands, glasgow coma scale of 14 (e4v4m6). the scan demonstrated a large (1.1cm) right sided asdh with significant mass effect and midline shift towards left side (fig.4a). past medical history is not significant for chronic illness. but his gautam and sharma score was 8 so we managed this patient conservatively; patient was started on manitol and was admitted for observation in neurosurgical icu. overnight the patient was remained in same neurological status and no deterioration in consciousness. repeat head ct (fig.4b) performed approximately 24 hrs post admission revealed resolution of hematoma with no midline shift. the patient remained stable and was discharged home without operative intervention with advice of close follow up. figure 4 (a): head ct scan shows large right temporoparietal sdh with midline shift. figure 4 (b): repeat ct scan of head resolution of hematoma. 467 rapid spontaneous resolution of traumatic acute subdural hematoma case 5 14-year-old female presented in emergency room in state of unconsciousness due to road traffic accident with history of ear and nose bleed and history of vomiting, urgently ncct head was done which showed left temporoparietal acute sdh with midline shift less then 5mm (fig 5a). on examination her gcs was e1v1m3, her breathing was irregular, both pupils were symmetrical and reactive to light. she was shifted in critical care unit, intubated and put on ventilator her gautam and sharma score was calculated that was 6. managed this patient conservatively, treated with manitol, higher antibiotics like meropenam and amikacin for associated injuries and aspiration pneumonitis. repeat ncct head after 48 hours which showed complete resolution of hematoma, continue treated patient conservatively ,patient wean off from ventilator on day 4 of admission and following verbal commands on day 5 ,subsequent repeated ct head were also normal(fig 5b). she was discharged after 8 days of hospitalization with gcs of 15. figure 5 (a): shows left temporoparietal subdural hematoma with midline shift (5b): shows complete resolution of hematoma. case 6 22 year old male presented in emergency department with history of loss of consciousness followed by road traffic accident ,there was also history of vomiting and right ear bleed present .on admission his gcs was e2v1m5 ,irritable , both pupils were symmetrical in size and reactive to light .urgent ncct head was done which shows right frontotemporoparietal acute subdural hematoma(fig 6a). gautam and sharma score was calculated after ct scan which was 8 and we decided to manage this patient conservatively started on manitol and supportive treatment. ct head was repeated after 24 hrs which shows complete resolution of acute sdh(fig 6b). after 6 days of treatment patient improved significantly and discharged on gcs of e4v5m6. figure 6 (a): ncct head shows right frontotemporoparietal acutesdh with midline shift; 6 (b) repeat ncct shows complete resolution of sdh 468 gautam sachidanand, shringi prashant prognostic factors score 0 score 1 gcs on arrival in hospital <8 >9 hematoma thickness (in mm)in ncct head on arrival >5 <5 presence and/ or degree of midline brain shift (in mm) in ncct head on arrival >5 <5 increase in midline shift and thickness of hematoma in repeatncct head after 6 hrs yes no pupil abnormality yes no age >60 <60 availability of ot, neurointensive care,ct and other facilities no yes co-morbidity and associated trauma yes no time to arrival in tertiary centre (in hours) <6 hr >6hr drop of gcs in subsequent examination >2 <2 gautam and sharma clinic-radiological prognostic score (0 to 10) low score – favours poor prognosis high score – favours good prognosis, operative intervention not required discussion acute subdural hematomas are usually neurosurgical emergencies. small sized hematoma in good neurological grade patients can be managed conservatively. rapid spontaneous resolution of an acute subdural hematoma is seldom reported. diagnosis of patients with acute sdh likely to resolve rapidly can avoid unnecessary surgery in some cases4. large asdh 10 mm or midline shift greater than 5mm on a computed tomography (ct) scan are considered neurosurgical emergencies5. there are reports of spontaneous resolution of the asdh with various theories as to why this phenomenon occurs, radiologic characteristics can be helpful in determining which asdh is mostly likely to spontaneously resolve. as clearly illustrated in this case series that utilizing a neurological score which is based upon patient clinical profile at the time of arrival to hospital and radiological assessment of consecutive ct scan of head i.e. clinicoradiological prognostic score in making that determination is critical in avoiding an unnecessary craniotomy. wen et al.6,7 reviewed the literature and identified 19 cases of spontaneous rapid resolution of asdh. based on their review, most patients who developed rapid resolution shared 5 characteristics: (1) transitory coma lasting no longer than 12 h, (2) exclusion of cerebral contusion, (3) band of low density between the skull and the hematoma on (ct) imaging, (4) thin width which is widely distributed, and (5) glasgow coma scale >8 on admission. two possible mechanisms have been proposed, first, the hematoma may be diluted by flow of cerebrospinal fluid (csf) through the arachnoid tear, followed by retrograde flow into the subarachnoid space. this is supported by the presence of a low-density band between the asdh and the inner table of the skull on ct scan. transient neurological deterioration with subsequent dramatic improvement may be related to csf influx and efflux within the subdural space. the prominent subarachnoid space with cerebral atrophy may facilitate dilution of asdh. second, the compression and redistribution of the hematoma can be induced by cerebral swelling and increased icp. according matsuyama et al spontaneous resolution of the asdh depends on both dilution due to csf participation and redistribution of the blood8. conclusion it is well noted that a large asdh and a deteriorated neurological examination should lead to emergent craniotomy. spontaneous resolution of asdh is a rare phenomenon with only a few reported cases in the literature. by using a clinicoradiological prognostic score one can make a decision of conservative management to avoid an unnecessary craniotomy on patients having high scores. simple anti edematous drugs, close monitoring of the neurological examination and observation with repeat imaging can result in avoidance of emergency craniotomy in young patients with good neurological status. references 1. clinical study of acute subdural haematoma – a level i trauma care centre experience. prahaladu p et al. int j res 469 rapid spontaneous resolution of traumatic acute subdural hematoma med sci. 2017 mar;5(3):857-862. doi:http://dx.doi.org/10. 18203/2320-6012 2. surgical management of traumatic acute subdural hematoma in adults: a review. neurol med chir (tokyo). 2014 nov; 54(11): 887–894. doi: 10.2176/nmc.ra.20140204. 3. a clinicoradiological scoring for management of acute subdural hematoma: a prospective study, sachidanand gautam , anubhav sharma , s.c. dulara. romanian neurosurgery (2018) xxxii 2: 359 365 | 359. doi: 10.2478/romneu-2018-0045 4. yadav yad ram et al . rapid resolution of acute subdural hematoma : a case report and review of literature indian journal of neurotrauma (ijnt) 2011, vol. 8, no. 1, pp. 45-48 5. spontaneously rapid resolution of acute subdural hemorrhage with severe midline shift. dong-won shin et al . j korean neurosurg soc. 2013 nov; 54(5): 431–433. doi: 10.3340/jkns.2013.54.5.431 6. wen l, liu wg, ma l, zhan ry, li g,yang xf. spontaneous rapid resolution of acute subdural hematoma after head trauma: is it truly rare. irish j med sci 2009;178:367–71. 7. rapid resolution of acute subdural hematoma in child with severe head injury: a case report.park et el, j med case rep. 2013; 7: 67. doi: 10.1186/1752-1947-7-67 8. rapid resolution of symptomatic acute subdural hematoma: case report. takeshi matsuyama et al.surgical neurology;1997;48:193-6 doi: 10.33962/roneuro-2022-030 invasive tumours of third ventricle. the possibilities of endoscopic transventricular surgery dmytro s. teslenko, orest i. palamar, andriy p. huk, dmytro i. okonskyi, oleksandr s. usatov romanian neurosurgery (2022) xxxvi (2): pp. 164-167 doi: 10.33962/roneuro-2022-030 www.journals.lapub.co.uk/index.php/roneurosurgery invasive tumours of third ventricle. the possibilities of endoscopic transventricular surgery dmytro s. teslenko, orest i. palamar, andriy p. huk, dmytro i. okonskyi, oleksandr s. usatov romodanov neurosurgery institute. department of endoscopic and craniofacial neurosurgery, ukraine abstract despite the rapid development of neurosurgery in the 21st century, the invasive (secondary) tumours of the third ventricle have always presented a highly sophisticated challenge in terms of surgical treatment. the question of radical resection of these tumours remains debatable, considering the high risk associated with the possibility of disability, the expected duration and the postoperative quality of life. we conducted a retrospective study of patients with invasive third ventricular tumours that have been treated in our department from 2015 to 2020 reviewing preand postoperative clinical and radiological data for 21 cases. the treatment options in all 21 cases included an endoscopic frontal transcortical transventricular transforaminal-transchoroidal tumour removal, achieving gross total and subtotal resection in 86% of the interventions, followed by adjuvant treatment (radiation therapy in all cases, and chemotherapy – for high-grade tumours). an endoscopic third ventriculocisternostomy was performed in cases with partial tumour removal in order to improve the csf flow. neurological deficits included permanent hemiplegia – in 3 patients (15%), permanent hemianopia – in 2 patients (10%), transient shortterm memory impairment – in 3 patients (15%) with regression in 2-4 weeks after surgery. there was no postoperative lethality. maximal postoperative survival in our patients with high-grade tumours was 16 months; patients with low-grade tumours are still under supervision. endoscopic frontal transcortical transventricular transforaminal-transchoroidal approach to resection of third ventricular tumours is an effective surgical modality, that maximizes the possible resection volume with minimal occurrence of postoperative complications, therefore can be recommended for the routine treatment of the aforementioned pathology. introduction despite the rapid development of neurosurgery in the 21st century, surgery of invasive (secondary) tumors of the third ventricle, which are malignant in most cases, remains far from a solution [1-9]. usually, the zone of primary growth of invasive third ventricular tumors is located in functionally important areas of the brain [2,3-9]. the questions of the radical removal of these tumors [4,7-9] remain debatable, taking into account the possible disability of patients [3-7,9], the expected duration and the postoperative quality of life [1,4,7,12]. keywords endoscopic transventricular, invasive tumors, secondary tumors, thalamus, third ventricle, transforaminal, ventriculocisternostomy corresponding author: dmytro s. teslenko romodanov neurosurgery institute. department of endoscopic and craniofacial neurosurgery, ukraine info@pituitary.com.ua copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 165 invasive tumours of third ventricle materials and methods from 2015 to 2020, we have treated 43 patients with tumors of the third ventricle, 21 of which were invasive tumors with predominant growth from the thalamus. all patients underwent complete endoscopic resection using the frontal transcortical transventricular transforaminal approach. if the size of the interventricular foramen was inadequate for the endoscopic intervention, it was expanded by dissection of the anterior portions of the choroid plexus (fig. 1). figure 1. step-like expansion of the interventricular foramen by dissecting the anterior portions of the choroid plexus: the interventricular foramen is circled in red; the yellow arrow indicates the choroid plexus; the green arrow indicates an invasive third ventricular tumour. preoperative neurological status of patients: nonfocal symptoms were present in all patients, central hemiparesis (up to 2/5 points) in 5 patients, impaired short-term memory in 6 patients. occlusive hydrocephalus was diagnosed in all cases. all patients underwent an endoscopic removal by a frontal transcortical transventricular transforaminal approach, and in 11 cases an additional endoscopic third ventriculocisternostomy was performed. results radicality of surgical removal of invasive tumors (fig. 2): gross total resection (removal within healthy tissues) 2 patients. subtotal resection (removal of up to 90% of the tumor) 16 patients. partial removal 3 patients. partial removal was performed in the cases where an excessive bleeding from the tumor was observed. endoscopic third ventriculocisternostomy was conducted in 11 cases with a bleeding tumor and limited removal radicality. figure 2. radical removal of invasive third ventricular tumors: (gtr gross total resection (total) removal of the tumor within healthy tissues; str subtotal resection subtotal (up to 90%) removal of the tumor; pr partial removal. histological distribution: low grade tumors (who grade 2 fibrillar astrocytoma) 3 cases; high grade tumors (who grade 3-4 anaplastic astrocytoma (fig. 3), anaplastic oligoastrocytoma (fig. 4), glioblastoma) 18 cases. the maximum size/diameter of the tumor reached 6.2 cm. a. b. 166 dmytro s. teslenko, orest i. palamar, andriy p. huk et al. figure 3. preoperative brain mri (a) and 3 months after surgery (b). total removal of the tumor of the left thalamus (histological diagnosis – anaplastic astrocytoma, who grade 3). hydrocephalus regressed in the postoperative period. a. b. figure 4. preoperative brain mri (a) and 3 months after surgery (b). total removal of an invasive tumor in the posterior portions of the third ventricle (histological diagnosis – anaplastic oligoastrocytoma, who grade 3). hydrocephalus regressed in the postoperative period. postoperative condition: the postoperative karnofsky performance status in all patients was 70 points or more. postoperative neurological deficit: permanent hemiplegia – in 3 patients (15%), permanent hemianopia – in 2 patients (10%), transient short-term memory impairment – in 3 patients (15%) with a regression in 2-4 weeks after surgery. in all patients, nonfocal symptoms regressed. after surgical treatment all patients received adjuvant treatment (radiation therapy in all cases, chemotherapy – for high-grade tumors). maximal postoperative survival in our patients with high-grade tumors was 16 months, patients with low-grade tumors are still under supervision. there was no postoperative lethality. discussion the problem of radical gross total resection of invasive tumors of third ventricle is deeply connected to their site of origin, as they predominantly arise from the thalamus. a greater resection volume may jeopardize the integrity of this critical neurostructure, thus leading to a postoperative neurological deficit and disability. previously, microsurgical technique for resection of third ventricular tumors has been performed with the use of operative microscope. the rapid development of neuroendoscopy in the last 20 years has provided new minimally invasive options for treatment of ventricular pathology, therefore opening new prospects for surgical resection of invasive tumors of third ventricle. shorter operative time period, minimal invasiveness and better visualization of deep-seated ventricular structures are considered to be the main advantages of neuroendoscopy over microsurgery, although the traditional microsurgery retains its edge in bleeding control [1, 3, 4, 5, 8]. the endoscopic frontal transcortical transventricular transforaminal approach has been used in surgical resection of third ventricular tumors in many institutions worldwide [3, 4, 5, 8]. this approach provides the possibility to utilize a natural pathway such as the foramen of monro in order to reach third ventricle through established anatomical landmarks, especially in the setting of hydrocephalus, which is habitually present in patients with invasive third ventricular tumors [8]. achieving gross total and subtotal resection was possible in 86% of the interventions, with minor postoperative complications. other authors, such as tawk rg et al. [8] have reported similar results, achieving complete and near complete resection in 84% of the cases. various endoscopic modalities could be used, when approaching the third ventricular invasive tumors [11]. the endoscopic endonasal approach has similar radical resection success and an etv procedure could be performed, but it is believed to be associated with higher risk of infectious complications, such as meningoencephalitis, and hormonal disorders (diabetes insipidus, obesity etc.) [10, 12]. the authors believe, that the use of endoscopic frontal transcortical transventricular transforaminal approach in patients with invasive third ventricle tumors and obstructive hydrocephalus may appear to be an effective alternative to microsurgical resection using an operative microscope, although more clinical studies have to be conducted in order to confirm the clinical efficacy of the endoscopic frontal transcortical transventricular transforaminal approach. [1-12]. 167 invasive tumours of third ventricle conclusions 1. minor functional disorders and high life expectancy in invasive high-grade tumors make it possible to recommend frontal endoscopic transcortical transventricular transforaminaltranschoroidal approach as an effective method of surgical treatment of these tumors. 2. to prevent the development of a postoperative obstructive hydrocephalus by a blood clot, intraventricular hemorrhages, obstruction of cerebral aqueduct, in patients with invasive third ventricular tumors, it is advisable to perform intraoperative third ventriculocisternostomy. disclosures the authors declare no funding sources or conflict of interest concerning the materials or methods used in this study or the findings specified in this paper. references 1. ahmed si, javed g, laghari aa, bareeqa sb, aziz k, khan m, samar ss, humera ra, khan ar, farooqui mo, shahbaz a. third ventricular tumors: a comprehensive literature review. cureus. 2018 oct 5;10(10):e3417. doi: 10.7759/cureus.3417. pmid: 30542631; pmcid: pmc6284874. 2. chibbaro s, di rocco f, makiese o, reiss a, poczos p, mirone g, servadei f, george b, crafa p, polivka m, romano a. neuroendoscopic management of posterior third ventricle and pineal region tumors: technique, limitation, and possible complication avoidance. neurosurg rev. 2012 jul;35(3):331-38; discussion 338-40. doi: 10.1007/s10143-011-0370-1. epub 2012 jan 19. pmid: 22258494. 3. iacoangeli m, di somma lg, di rienzo a, alvaro l, nasi d, scerrati m. combined endoscopic transforaminaltranschoroidal approach for the treatment of third ventricle colloid cysts. j neurosurg. 2014 jun;120(6):14716. doi: 10.3171/2014.1.jns131102. epub 2014 mar 7. pmid: 24605835. 4. chibbaro s, champeaux c, poczos p, cardarelli m, di rocco f, iaccarino c, servadei f, tigan l, chaussemy d, george b, froelich s, kehrli p, romano a. anterior transfrontal endoscopic management of colloid cyst: an effective, safe, and elegant way of treatment. case series and technical note from a multicenter prospective study. neurosurg rev. 2014 apr;37(2):235-41; discussion 241. doi: 10.1007/s10143-013-0508-4. epub 2013 dec 19. pmid: 24352893. 5. ibáñez-botella g, domínguez m, ros b, de miguel l, márquez b, arráez ma. endoscopic transchoroidal and transforaminal approaches for resection of third ventricular colloid cysts. neurosurg rev. 2014 apr;37(2):227-34; discussion 234. doi: 10.1007/s10143014-0529-7. epub 2014 feb 14. pmid: 24526368. 6. oppido pa, fiorindi a, benvenuti l, cattani f, cipri s, gangemi m, godano u, longatti p, mascari c, morace e, tosatto l. neuroendoscopic biopsy of ventricular tumors: a multicentric experience. neurosurg focus. 2011 apr;30(4):e2. doi: 10.3171/2011.1.focus10326. pmid: 21456929. 7. roth j, constantini s. combined rigid and flexible endoscopy for tumors in the posterior third ventricle. j neurosurg. 2015 jun;122(6):1341-6. doi: 10.3171/2014.9.jns141397. epub 2015 mar 27. pmid: 25816082. 8. tawk rg, akinduro oo, grewal ss, brasiliense l, grand w, grotenhuis a. endoscopic transforaminal transchoroidal approach to the third ventricle for cystic and solid tumors. world neurosurg. 2020 feb;134:e453e459. doi: 10.1016/j.wneu.2019.10.099. epub 2019 oct 24. pmid: 31669244. 9. brusius cv, bianchin mm, mira jm, frigeri t, kruger m, grudtner mc, lenhardt r, maschke s, wolfsberger s. single burr-hole extended transforaminal approach for concurrent endoscopic surgery in the third ventricle posterior to the foramen of monro and ventriculostomy: clinical series and planning steps. world neurosurg. 2021 jun;150:e1-e11. doi: 10.1016/j.wneu.2021.01.067. epub 2021 feb 12. pmid: 33582291. 10. youngbeom se, yong hwy kim, jung hee kim, doo-sik kong, yun-sik dho, ho kang, kyung-min kim, jin wook kim, chul-kee park outcomes of the endoscopic endonasal approach for tumors in the third ventricle or invading the third ventricle j clin neurosci. 2021 aug; 90:302-310. doi: 10.1016/j.jocn.2021.06.012. epub 2021 jun 21. 11. changfu zhang, zhengcun yan, xiaodong wang, yuping li, hengzhu zhang quantitative analysis of exposure and surgical maneuverability of three purely endoscopic keyhole approaches to the floor of the third ventricle j neurosurg sci. 2021 sep 21. doi: 10.23736/s03905616.21.05455-2. pmid: 34545733 pmid: 34275567 12. bolin liu, tao zheng, wenhai lv, yuanzhi huang, baofu li, baoying chen, binrong wang, shiming he endoscopic endonasal transsphenoidal approach for third ventriculostomy in the management of obstructive hydrocephalus j craniofac surg. 2021 oct 1;32(7):e609e612. doi: 10.1097/scs.0000000000007613 epub 2021 feb 12. pmid: 33710059. 7zentenomarco_vein romanian neurosurgery (2014) xxi 2: 195 201 195 vein of galen malformation: what to do when vascular access is not feasible? marco zenteno1, luis rafael moscote-salazar2, jorge santos-franco3, angel lee4 1instituto nacional de neurología y neurocirugía “manuel velasco suarez”, mexico 2universidad de cartagena, colombia 3centreo medico imss la raza, méxico 4hospital ángeles del pedregal, méxico abstract background: the vein of galen aneurysmal malformation (gvam) is a rare congenital vascular lesion, with high morbidity and mortality without treatment, endovascular management is the best alternative available today. aim: the purpose of this work is to report the case of a female patient with imaginological and angiographical diagnosis of gvam, which was difficult for endovascular managent alone, due to this was decided an alternative endovascular direct access guided by stereotactic assistance. case report: we report the case of an infant with imaging and angiographic diagnosis of gvam, with absence of the vein access through classical embolization could be done, complicating and making difficult for endovascular management alone, hence was decided an alternative endovascular direct access guided by stereotactic assistance, ensuring total embolization of the lesion with coils. the patient progressed satisfactorily. discussion: vgam generally represents only 1% or less of total cerebral vascular malformations, but in pediatrics may be as high as 30%. the malformation is occupying the subarachnoid space of the velum interpositum and the quadrigeminal cistern. it is characterized by the presence of the vein embryonic precursor of the vein of galen, and abnormal arterial shunts from arteries normally developed but extremely dilated. mortality rate is high in these patients without treatment, developing hydrocephalus and cerebral complications related to the occupying mass that could drive to epilepsy, serious cognitive sequelae, intracerebral emorrhage and death within the possibilities. heart failure is often a common complication. to our knowledge this is the first report of the use of stereotactic assistance in the endovascular therapeutic management of vgam. conclusions: in cases where clasical venous access cannot be achieved as in the case we report, further technical assistance can be obtained with stereotactic guidance, making easier the procedure, remembering 196 zenteno et al vein of galen malformation that without therapy, vgam result in lifethreatening hydrocephalus and/or intracranial hemorrhage, rapidly driving to death. key words: vein of galen aneurysmal malformation, endovascular management, stereotactic approach. introduction the vein of galen aneurysmal malformation (vgam) is a rare cerebral vascular malformation firstly reported by steinhel and cited by dandy 1919, (1, 2) with a prevalence of less than 1/25,000 deliveries. (3) vgam are responsible for about 1% of all the vascular malformations and about 30% of the pediatric vascular malformations. (4, 5) they are characterized by the abnormal persistence of the markowski’s median porencephalic vein which, fueled by primitive embryonic meningeal arteries, becomes in the blood collector of this malformation. (6) two different subtypes of vein of vgam can be distinguished, including the choroidal and mural types. patients with the choroidal type have multiple arterial feeders draining on multiple different locations into the dilated median prosencephalic vein, and usually present with heart failure as newborns; the mural type is characterized by the confluence of all arterial feeders in one terminal fistula, which drains into the prosencephalic vein, and its presentation is later in infancy with macrocephaly or failure to thrive, which may be associated with mild cardiac failure or asymptomatic cardiomegaly. (7) borthne and coworkers (8) used a different classification, see table 1. vgam can be classified also as a “true” vein of galen aneurysmal malformation or a “false”. (9) a “true” vgam involves a dilated median prosencephalic vein of markowsky receiving drainage from multiple arteriovenous shunts. a “false” vgam involves an arteriovenous malformation that drains into a tributary of the vein of galen, resulting in its overload and dilatation. the vasculature of vgams is very complex with choroidal arteries as the main feeding arteries. they form a fistula or multiple fistulae with the embryologic precursor of the galenic vein, the median prosencephalic vein. this dilated embryogenetic vein drains through the socalled falcine sinus which is in the embryogenesis the forerunner of the straight sinus into the superior sagittal sinus. (5) to note, high-flow arteriovenous malformation and fistula are commonly treated by using an endovascular approach with a variety of materials, such as detachable coils. we present the case of a female patient with imaginological and angiographical diagnosis of gvam, which was difficult for endovascular managent alone, due to this was decided an alternative endovascular direct access guided by stereotactic assistance. table 1 vgam classification by borthne et al (8) type characteristics i direct fistulae to the pouch (median prosencephalic vein). ii indirect arteriolovenous fistulae through an intervening tangle of vessels (nidus) between the arteries and the vein. iii combination of types i and ii: mixture of direct arteriovenous and arteriolovenous fistulae. romanian neurosurgery (2014) xxi 2: 195 201 197 case report a child of 24 months presented with macrocania. antenatal assessments revealed aneurysmal malformation of the vein of galen. endovascular management was decided by conventional technique but vascular access was not possible through the posterior cerebral arteries. the procedure was performed one week after direct approach to the aneurysm of the vein of galen by stereotactic guidance (leksell frame), is placed a stereotactic frame and direct approach was performed by parietal craniotomy, a complete embolization was performed in the aneurysmal malformation of the vein of galen with coils. (figure 1 a, b, c, d, e) the child tolerate the procedure and was followed by an interval of six months. 198 zenteno et al vein of galen malformation romanian neurosurgery (2014) xxi 2: 195 201 199 figure 1 discussion in this report we present the case of a vgam with absence of the vein access through classical embolization could be done, complicating and making difficult for endovascular management alone, hence was decided an alternative endovascular direct access guided by stereotactic assistance, ensuring total embolization of the lesion with coils. patient evolution was remarkable. the malformation develops between the 6th and 11th weeks of gestation after the development of the circle of willis. with the development of the basal ganglia, primitive internal cerebral veins form and fuse in the midline to form the vein of galen and straight sinus, replacing the median prosencephalic vein as the main venous drainage of the choroid plexus. the caudal remnant of the median prosencephalic vein becomes part of the vein of galen complex. persistence of the median prosencephalic vein is a common finding in vein of galen malformations. (10) the presence of a persistent falcine sinus (which normally regresses as the straight sinus develops) is also indicative of the arrested venous development that commonly occurs in the setting of a vein of galen malformation. (10) thus vgam result from the development of an arteriovenous connection between the primitive choroidal vessels and the median prosencephalic vein of markowski. the abnormal flow through the connection retards the normal involution of this embryonic vein and thus prevents the development of the vein of galen. (6, 11) the most obvious feature is a midline intracranial vascular fistula with aneurysmal dilation of the vein of galen. (12) although diagnosed principally in the pediatric age group, may not be revealed until adulthood. patients with vgam have varying age-related clinical presentations. clinically, vein of galen aneurysmal dilation usually presents in childhood or young adulthood and shares clinical manifestations with other deep-seated arteriovenous malformations. hydrocephalus as a presenting sign of vgam usually occurs secondary to impaired cerebrospinal fluid (csf) resorption due to venous hypertension. cerebral venous circulation often is reversed and rerouted toward the cavernous sinus and ophthalmic veins (producing dilation of facial veins or epistaxis) or to the basisphenoid sinus and pterygoid veins. (7) management is a major therapeutic problem, currently, interventional 200 zenteno et al vein of galen malformation neuroradiology is the therapeutical method of choice for vgam, (14) which is influenced by vgam’s classification: the mural type can be treated via a transarterial or a transvenous approach, whereas, the choroidal type can be treated only via a transvenous approach, however, when classicao vein acces to the vgam it is necessary to recur to alternative approaches or techniques, as we present here. despite neuroradiological intervention has been shown to control cardiac failure when present, there is a perception that neurological outcome in survivors is poor. (13) lasjaunias et al., (15) reported that 216 patients were treated with endovascular embolization, from which, 23 died despite or because of the embolization (10.6%). twenty out of the 193 (10.4%) surviving patients were severely retarded, 30 (15.6%) were moderately retarded, and 143 (74%) were neurologically normal on follow-up. their data demonstrated that most treated children survive and undergo normal neurological development, as in our case, with the extra help of stereotactic guidance; the endovascular management was achieved without complications. to our knowledge this is the first report of the use of stereotactic assistance in the endovascular therapeutic management of vgam. complications regard the endovascular approache are scarce, hyodo et al (16) reported the case of vgam in which coil migration was observed during the endovascular procedure. significant risk exists for either proximal or distal coil migration because of rapid flow. the cause of migration may be due to a size mismatch between the embolised coils and the caliber of the parent artery, probably due to redilatation of a constricted artery. another possible mechanism is mechanical vasospasm due to catheter manipulation in the early stage of the endovascular procedure. (16) conclusions aggressive medical treatment of complications secondary to vgam and urgent endovascular intervention has produced encouraging results, although early diagnosis remains a challenge. with more and more technological advances in the developments in the field of interventional neuroradiology and availability of better postprocedure intensive care, these once nontreatable conditions with a very high mortality rate are now potentially curable using interventional neuroradiological techniques with excellent clinical results, low complication rate and very low morbidity and mortality. in cases where clasical venous access cannot be achieved as in the case we report, further technical assistance can be obtained with stereotactic guidance, making easier the procedure, remembering that without therapy, vgam result in lifethreatening hydrocephalus and/or intracranial hemorrhage, rapidly driving to death. references 1. dandy w. experimental hydrocephalus. ann surg [internet]. 1919 aug [cited 2013 oct 14];70(2):129–42. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=1410318&tool=pmcentrez&rendertype=abstract 2. dandy w. cerebrospinal fluid. absorption. chicago: american medical association; 1929. p. 2012. 3. lasjaunias p, hui f, zerah m, garcia-monaco r, malherbe v, rodesch g, et al. cerebral arteriovenous malformations in children. management of 179 consecutive cases and review of the literature. childs nerv syst [internet]. 1995 feb [cited 2013 oct 14]; romanian neurosurgery (2014) xxi 2: 195 201 201 11(2):66–79; discussion 79. available from: http://www.ncbi.nlm.nih.gov/pubmed/7758015 4. casasco a, lylyk p, hodes je, kohan g, aymard a, merland jj. percutaneous transvenous catheterization and embolization of vein of galen aneurysms. neurosurgery [internet]. 1991 feb [cited 2013 oct 14];28(2):260–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/1997895 5. fellner f, fellner c, böhm-jurkovic h, blank m, bautz w. mr diagnosis of vein of galen aneurysmal malformations using virtual cisternoscopy. comput. med. imaging graph. [internet]. 1999 oct;23(5):293–7. available from: http://www.sciencedirect.com/science/article/pii/s08956 11199000270 6. raybaud ca, strother cm, hald jk. aneurysms of the vein of galen: embryonic considerations and anatomical features relating to the pathogenesis of the malformation. neuroradiology [internet]. 1989 jan [cited 2013 oct 14];31(2):109–28. available from: http://www.ncbi.nlm.nih.gov/pubmed/2664553 7. abe t, matsumoto k, kiyota k, tanaka h. vein of galen aneurysmal malformation in an adult: a case report. surg. neurol. [internet]. 1996 jan;45(1):39–42. available from: http://www.sciencedirect.com/science/article/pii/009030 1995003401 8. borthne a, carteret m, baraton j, courtel j, brunelle f. vein of galen vascular malformations in infants: clinical, radiological and therapeutic aspect. eur radiol [internet]. 1997 jan [cited 2013 oct 14];7(8):1252–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/9377511 9. lasjaunias p, rodesch g, pruvost p, laroche fg, landrieu p. treatment of vein of galen aneurysmal malformation. j neurosurg [internet]. 1989 may [cited 2013 oct 14];70(5):746–50. available from: http://www.ncbi.nlm.nih.gov/pubmed/2709115 10. davidson as, morgan mk. the embryologic basis for the anatomy of the cerebral vasculature related to arteriovenous malformations. j. clin. neurosci. [internet]. 2011 apr;18(4):464–9. available from: http://www.sciencedirect.com/science/article/pii/s09675 8681000843x 11. gupta vb, choudhary h, rastogi h, singh vp. intracranial arteriovenous malformation in an infant— vein of galen malformation. apollo med. [internet]. 2011 dec;8(4):307–9. available from: http://www.sciencedirect.com/science/article/pii/s09760 01611600148 12. chen m-y, liu h-m, weng w-c, peng s-f, wu e-t, chiu s-n. neonate with severe heart failure related to vein of galen malformation. pediatr. neonatol. [internet]. 2010 aug;51(4):245–8. available from: http://www.sciencedirect.com/science/article/pii/s18759 57210600472 13. nelson m, dickinson df, wilson n. transtorcular coil embolisation of malformations of the vein of galen-rapid resolution of heart failure in neonates. int j cardiol [internet]. 1988 mar [cited 2013 oct 14];18(3):437–41. available from: http://www.ncbi.nlm.nih.gov/pubmed/3360528 14. angelkova n, kuturec m, lekovska o, duma f, damjanovski g, avramovska vs. p244 vein of galen malformation. eur. j. paediatr. neurol. [internet]. 2009 sep;13, supple(0):s97. available from: http://www.sciencedirect.com/science/article/pii/s10903 79809703022 15. lasjaunias pl, chng sm, sachet m, alvarez h, rodesch g, garcia-monaco r. the management of vein of galen aneurysmal malformations. neurosurgery [internet]. 2006 nov [cited 2013 oct 8];59(5 suppl 3):s184–94; discussion s3–13. available from: http://www.ncbi.nlm.nih.gov/pubmed/17053602 16. hyodo a, yanaka k, kato n, nose t. coil migration during endovascular treatment in a patient with galenic arteriovenous malformation. j. clin. neurosci. [internet]. 2002 sep;9(5):584–5. available from: http://www.sciencedirect.com/science/article/pii/s09675 86802909744. doi: 10.33962/roneuro-2021-057 indirect revascularization in an iraqi child with moyamoya disease samer s. hoz, aktham o. al-khafaji, zahraa f. al-sharshahi, mohammed a. alrawi romanian neurosurgery (2021) xxxv (3): pp. 339-344 doi: 10.33962/roneuro-2021-057 www.journals.lapub.co.uk/index.php/roneurosurgery indirect revascularization in an iraqi child with moyamoya disease samer s. hoz1, aktham o. al-khafaji2, zahraa f. al-sharshahi1, mohammed a. alrawi1 1 department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 college of medicine, university of baghdad, baghdad, iraq abstract background: moyamoya disease (mmd) is a rare cerebrovascular disease characterized by bilateral stenosis starting at the supraclinoid internal carotid artery (ica), with the development of a collateral network of vessels. it is an established cause of stroke in the pediatric age group. despite its increasing prevalence in various parts of the world, it remains largely underrecognized in the middle east, particularly in iraq. this is the first case of mmd in an iraqi patient undergoing surgery. case description: a 12-year-old boy presents with a 3-months history of progressive behavioural changes. mri revealed diffuse infarcts of different ages. mra and ct angiography revealed extensive asymmetrical steno-occlusive changes of the supraclinoid icas extending into the anterior and middle cerebral arteries, with the development of a collateral network in the basal ganglia. indirect revascularization of the right side by encephaloduroarteriomyosynangiosis (edams) was performed. the clinical status of the patient improved during the follow-up and the mra showed a re-establishment of the blood flow to the mca. conclusion: mmd should be recognized as a cause of stroke or recurrent tias in the iraqi population, particularly in pediatric patients. edams is an effective revascularization procedure with good results in pediatric patients. introduction moyamoya disease (mmd) is a rare chronic idiopathic neurovascular disorder characterized by progressive bilateral steno-occlusive changes starting at the supraclinoid internal carotid artery (ica) and extending distally to involve proximal parts of the anterior & middle cerebral arteries (aca & mca) [1]. the resulting hypoxia leads to the development of a compensatory network of dilated vasculature at the basal ganglia, giving the characteristic moyamoya (japanese for "puff of smoke") appearance on cerebral angiography [2]. first described in 1957 as “hypoplasia of the bilateral internal carotid arteries” [29], the term “moyamoya” was coined in 1969 by suzuki and takaku [2]. originally, this disease entity was thought to be unique to east asian populations, particularly japan. however, it has keywords internal carotid artery, stenosis, moyamoya, revascularization, edams corresponding author: zahraa f. al-sharshahi department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 340 samer s. hoz, aktham o. al-khafaji, zahraa f. al-sharshahi et al. increasingly been identified in western populations [3, 4], and has become a recognized cause of stroke in pediatric patients [5]. nevertheless, it remains a rare entity with varying prevalence across ethnic groups, ranging from 6 per 100,000 in japan to a tenth of that in europe [3, 4, 16-18]. it has a female predominance, with the female-to-male ratio ranging between 2:1 and 4:1 [16,19]. some individual case reports and small series of mmds have been reported in middle eastern individuals [6-14], but there are no large series or long-term studies available in the literature. only one case of moyamoya syndrome in an iraqi patient has been reported in the literature, in which surgical revascularization has not been performed [15]. to the best of our knowledge, this is the second case report of mmd in an iraqi patient and the first to be successfully treated by cerebral revascularization. case presentation a 12-year-old boy was brought by his parents, who described a 3-month history of progressive behavioral changes and decreased school performance. his physical and neurological examination was unremarkable. routine blood and urine investigations were normal. magnetic resonance imaging (mri) showed signs of diffuse cortical and deep matter infarcts, as well as an old frontal infarct (figure 1). figure 1. axial mri of the brain. a-b: t2-weighted & flair images showing diffuse high signal intensities in the cortical and deep frontoparietal peri-ventricular regions. a large frontal porencephalic cyst, probably caused by an old infarct, can be seen as well. c: dwi image of the brain showing restricted flow in the abovementioned areas. magnetic resonance angiography (mra) & computer tomographic angiography (cta) (figure 2) revealed asymmetrical steno-occlusive changes of the anterior circulation with an extensive deep collateral network at the basal ganglia. these modalities showed generalized stenosis of the intracranial right ica with severe near-occlusive narrowing of its supraclinoid segment extending to the first few millimeters of the right aca & mca. the left supraclinoid ica is completely occluded with obliteration of its proximal intracranial segments, and the proximal parts of the left aca and mca are completely occluded. the vertebrobasilar system and the posterior cerebral arteries (pcas) were normal with no signs of stenosis, and the posterior communicating artery (pcom) was intact on both sides, providing flow to the mcas. as an endovascular facility was inaccessible at our center, no catheter angiography was performed. figure 2. brain mra (a) and cta (b) showing asymmetric stenosis of the anterior circulation with an extensive vascular network at the basal ganglia. the right ica shows stenosis with near-occlusive narrowing of its supraclinoid segment extending to a few millimeters of the right aca & mca. figure 3. revascularization by edams. a-b: a linear incision is made along the course of the sta (dashes) with the aid of doppler u/s and the artery is dissected and mobilized. c-d: a 5x5 cm craniotomy is created underlying the sta, and the dura opened and reflected in a cruciate fashion, with special care to preserve the middle meningeal artery. e: the sta and strips of temporalis muscle are sutured to the cortical surface adjacent to cortical mca branches (star). f: reimplantation of the bone 341 indirect revascularization in an iraqi child with moyamoya disease flap after creating opposing notches (stars) to accommodate passage of the sta with its perivascular tissues. a definitive diagnosis of asymmetrical mmd was made based on mri and mra criteria, and the patient underwent a right-sided extracranial-intracranial (ec-ic) bypass. indirect revascularization was performed by encephalo-duro-arterio-myo-synangiosis (edams), demonstrated in figure 3. a linear incision was made along the course of the sta with the aid of doppler u/s, after which the sta was dissected along with its perivascular tissue, and mobilized to allow safe drilling of 4 burr holes to make a 5 by 5 cm craniotomy. the dura was then opened and reflected in a cruciate fashion, with special care to preserve the middle meningeal artery (mma). afterwards, the sta was laid on & sutured to the cortical surface adjacent to cortical mca branches. strips of temporalis muscle were also reflected and attached to the cortex around the sta. the bone flap was reimplanted after preparation by creating opposing burr hole notches to accommodate the passage of the sta with its perivascular tissues. figure 4. mra performed 6 months following indirect revascularization (edams) of the right side shows establishment of collateral blood flow from the sta to the frontal and parietal cortical territory of the mca (circle). there were no surgical complications, and the postoperative recovery was uneventful. the patient was discharged home with protective headgear at day eight postoperatively, and the parents were informed of the need to perform left-sided revascularization. at his six-month follow-up appointment, the parents reported a noticeable improvement in the patient’s behavior and school performance. the follow-up mra confirmed the reestablishment of collateral blood flow to the right mca (figure 4). discussion moyamoya disease versus syndrome an important distinction when discussing moyamoya phenomena is differentiating moyamoya disease from moyamoya syndrome. mmd is characterized by bilateral, albeit sometimes asymmetrical, changes in the icas and eventually acas and mcas. when these changes are coupled with certain well-documented associated conditions, or when the changes occur unilaterally, it is referred to as moyamoya syndrome [5]. bilateral disease eventually develops in 40% of those with unilateral vasculopathy. our patient presented with bilaterally diseased cerebral circulation, with no associated risk factors and physical exam and laboratory investigations revealed no findings. therefore, his condition is classified as moyamoya disease. presentation mmd has a bimodal age distribution of disease onset (with peaks at ages 5-9 and 45-49) [19]. pediatric patients are more likely to present with ischemic symptoms such as stroke, transient ischemic attacks (tias), or seizures. hemorrhagic presentations are seen in both age groups, albeit at a much higher rate in adults [16, 20]. our pediatric patient presented with ischemic symptoms that are consistent with established patterns in patient presentation. diagnosis diagnosis of mmd is generally based on clinical and radiological characteristics. mmd should be in the differential diagnosis of any patient presenting with neurological deficits or unexplained symptoms attributable to cerebral ischemia, particularly in the pediatric age group. diagnosis can be confirmed by radiological evaluation, primarily with mri, mra and catheter angiography. specific mri sequences can detect cerebral infarction in its early and late stages, as was the case with our patient. flair imaging also 342 samer s. hoz, aktham o. al-khafaji, zahraa f. al-sharshahi et al. enables the detection of chronic hypoxia, which manifests as linear high signals along the cortical sulci; the so called “ivy sign” [21]. a highly suggestive finding on t1 & t2-weighted images is the absence of ica, aca and mca signal voids on the affected side, and the appearance of tortuous signal voids at the level of the thalamus and the basal ganglia, brought about by the development of collateral vessels in that region [22]. catheter angiography is the most valuable tool for definitive diagnosis of mmd by detecting the steno-occlusive changes in the supraclinoid ica extending to the aca and mca, and can visualize the leptomeningeal and/or basal collateral networks; the moyamoya or “puff of smoke” vessels. it also allows staging of the disease using the suzuki grading system [2]. due to concerns about cost, invasiveness and availability of catheter angiography, criteria have been established for diagnosing mmd based on mri and mra alone [23]. this criteria establishes a definitive diagnosis of mmd based on three conditions; namely the documentation of stenosis or occlusion at the terminal portion of the ica and the proximal portions of the aca and mca on mra, an abnormal vascular network in the basal ganglia seen on mra or mri, and the observation of the abovementioned two points bilaterally. in pediatric patients, the latter condition is not necessary for a definitive diagnosis. a staging system based on mra findings alone has also been proposed [24], and is summarized in table 1. using that system, our case would be categorized as grade ii. this corresponds to grade iii in the catheter angiography-dependent suzuki grading system (stenosis of the aca and mca with patent pcom and extensive collateral network at the basal ganglia). table 1. mra-based grading system for mmd [24] vessel changes score ica • normal 0 • stenosis of c1 1 • discontinuity of c1 signal 2 • invisible 3 mca • normal 0 • stenosis of m1 1 • discontinuity of m1 signal 2 • invisible 3 aca • normal a2 and its distal signal 0 • a2 and its distal signal decrease 1 • invisible 2 pca • normal p2 and its distal signal 0 • p2 and its distal signal decrease 1 • invisible 2 total 0-10 0-1: grade 1; 2-4: grade 2; 5-7: grade 3; 8-10: grade 4 treatment the mainstay of treatment for mmd is surgical revascularization using intact sta as an alternative source of blood flow. this has been shown to be a safe and effective treatment option that has reduced the incidence of strokes and tias in patients with mmd, with 96% of them having a 5-year stroke-free period and enhanced day-to-day activities [20, 23, 25]. there are no established surgical indications for patients with mmd, and some authors encourage surgical intervention in asymptomatic cases as neurological status at the time of surgery is stated to be the most significant predictor of long-term outcomes [20]. surgery consists of direct sta-mca bypass, indirect bypass techniques or a combination of both, with each modality having its own benefits and pitfalls. direct revascularization provides an immediate augmentation of cerebral blood flow to the stenotic arteries, but due to the technical difficulties in anastomosing small-caliber vessels, its use is limited in pediatric patients. on the other hand, indirect revascularization is a less technically demanding technique, in which highly vascular tissues are approximated to the cortical surface to promote angiogenesis and enable the passive development of collateral ec-ic vessels. this offers excellent long-term outcomes comparable to those of direct revascularization, but improvement in cerebral blood flow is delayed and collateral vessels might take up to 3-4 months to develop [23]. many techniques of indirect revascularization have been developed since the description of the disease in 1969, including encephalodurosynangiosis (eds), encephalomyosynangiosis (ems), encephaloduroarteriosynangiosis (edas), edams, omental flaps transplantation, and placement of multiple burr holes [1]. 343 indirect revascularization in an iraqi child with moyamoya disease we have reported the first case of mmd in an iraqi patient to be successfully treated, using the edams procedure of indirect revascularization. the aim of this procedure is to nourish the frontal and parietal cortical territories of the mca. it combines the edas and ems techniques thus maximizing the amount of vascular tissue involved in the synangiosis [26]. the very small size of the sta in our patient rendered direct bypass non-feasible. however, due to the long course of the vessel, its re-routing into the cortical surface was possible. long-term follow-up data has shown edams to be a safe and effective treatment modality for adults and older children with mmd [27, 28]. the reporting of such rare cases in the iraqi population should warrant higher vigilance and the consideration of mmd as differential diagnosis in patients presenting with ischemic stroke, particularly children. conclusion we present the second case of moyamoya disease in an iraqi patient and the first to be successfully treated by indirect surgical revascularization, using the edams technique. the article emphasizes the importance of recognizing this disease as a cause of stroke or recurrent tias in the iraqi population, particularly in the pediatric age group. abbreviations aca: anterior cerebral artery acom: anterior communicating artery cta: computer tomographic angiography dwi: diffusion-weighted imaging ec-ic: extracranial-intracranial edams: encephaloduroarteriomyosynangiosis edas: encephaloduroarteriosynangiosis eds: encephalodurosynangiosis ems: encephalomyosynangiosis flair: fluid attenuation inversion recovery ica: internal carotid artery mca: middle cerebral artery mma: middle meningeal artery mmd: moyamoya disease mra: magnetic resonance angiography mri: magnetic resonance imaging pca: posterior cerebral artery pcom: posterior communicating artery sta: superficial temporal artery tia: transient ischemic attack u/s: ultrasonography. authors' contributions s.s.h: data collection a.o.a: manuscript drafting z.f.a: manuscript revision m.a.a: manuscript revision references 1. scott rm, smith er. moyamoya disease and moyamoya syndrome. new england journal of medicine. 2009 mar 19;360(12):1226-37. 2. suzuki j, takaku a. cerebrovascular moyamoya disease: disease showing abnormal net-like vessels in base of brain. archives of neurology. 1969 mar 1;20(3):288-99. 3. kainth d, chaudhry sa, kainth h, suri fk, qureshi ai. epidemiological and clinical features of moyamoya disease in the usa. neuroepidemiology. 2013;40(4):2827. 4. kraemer m, schwitalla jc, diesner f, aktas o, hartung hp, berlit p. clinical presentation of moyamoya angiopathy in europeans: experiences from germany with 200 patients. journal of neurology. 2019 jun 1;266(6):1421-8. 5. smith er, scott rm. moyamoya: epidemiology, presentation, and diagnosis. neurosurgery clinics. 2010 jul 1;21(3):543-51. 6. elagouza ia, habib ma. moyamoya disease in children: an egyptian experience. egyptian journal of pediatrics. 2016 dec;394(5964):1-5. 7. jabbour r, taher a, shamseddine a, atweh sf. moyamoya syndrome with intraventricular hemorrhage in an adult with factor v leiden mutation. archives of neurology. 2005 jul 1;62(7):1144-6. 8. sencer s, poyanlı a, kırış t, minareci ö. recent experience with moyamoya disease in turkey. european radiology. 2000 mar 1;10(4):569-72. 9. al-hawsawi zm, al-zaid ma, barnawi ai, yassine sm. fanconi anemia associated with moyamoya disease in saudi arabia. saudi medical journal. 2015;36(2):233. 10. abuoliat za, alfarhan ba, alshahrani aa, alfarhan aa, almuntashri ma, alotaibi n. atypical location of intracerebral hemorrhage in moyamoya disease. cureus. 2017 dec;9(12). 11. habib hs. moyamoya disease presenting with ischemic stroke in association with diabetic ketoacidosis. journal of pediatric neurology. 2013 jan 1;11(1):39-42. 12. sabti k, hajj ba, hwang jm, traboulsi ei, reid j. congenital third nerve palsy, moyamoya disease and optic nerve head staphyloma. british journal of ophthalmology. 2005 jun 1;89(6):778-9. 13. el beltagi ah, el-sheikh a, el-saif r, norbash a. ivy sign in mildly symptomatic β-thalassemia intermedia, with development of moyamoya disease. the neuroradiology journal. 2014 feb;27(1):23-8. 14. ashrafi f, behnam b, yazdi hr, ahmadi ma, sarraf p. a child with moyamoya disease: case report. international clinical neuroscience journal. 2015 aug 1;2(2):74-6. 344 samer s. hoz, aktham o. al-khafaji, zahraa f. al-sharshahi et al. 15. mohamad aj, abood sh. moyamoya syndrome. iraqi journal of medical sciences. 2007;5(3):102-7. 16. kuriyama s, kusaka y, fujimura m, wakai k, tamakoshi a, hashimoto s, tsuji i, inaba y, yoshimoto t. prevalence and clinicoepidemiological features of moyamoya disease in japan: findings from a nationwide epidemiological survey. stroke. 2008 jan 1;39(1):42-7. 17. kossorotoff m, herve d, toulgoat f, renaud c, presles e, chabriat h, chabrier s. paediatric moyamoya in mainland france: a comprehensive survey of academic neuropaediatric centres. cerebrovascular diseases. 2012;33(1):76-9. 18. yonekawa y, ogata n, kaku y, taub e, imhof hg. moyamoya disease in europe, past and present status. clinical neurology and neurosurgery. 1997 oct 1;99:s5860. 19. baba t, houkin k, kuroda s. novel epidemiological features of moyamoya disease. journal of neurology, neurosurgery & psychiatry. 2008 aug 1;79(8):900-4. 20. scott rm, smith jl, robertson rl, madsen jr, soriano sg, rockoff ma. long-term outcome in children with moyamoya syndrome after cranial revascularization by pial synangiosis. journal of neurosurgery: pediatrics. 2004 feb 1;100(2):142-9. 21. fujiwara h, momoshima s, kuribayashi s. leptomeningeal high signal intensity (ivy sign) on fluidattenuated inversion-recovery (flair) mr images in moyamoya disease. european journal of radiology. 2005 aug 1;55(2):224-30. 22. houkin k, aoki t, takahashi a, abe h. diagnosis of moyamoya disease with magnetic resonance angiography. stroke. 1994 nov;25(11):2159-64. 23. hashimoto n, tominaga t, miyamoto s, nagata i, houkin k, suzuki n, koizumi a, nogawa s, nakagawara j, kitagawa k, kuroda s. guidelines for diagnosis and treatment of moyamoya disease (spontaneous occlusion of the circle of willis). neurol med chir (tokyo). 2012;52(5):245-66. 24. houkin k, nakayama n, kuroda s, nonaka t, shonai t, yoshimoto t. novel magnetic resonance angiography stage grading for moyamoya disease. cerebrovascular diseases. 2005;20(5):347-54. 25. fung lw, thompson d, ganesan v. revascularisation surgery for paediatric moyamoya: a review of the literature. child's nervous system. 2005 may 1;21(5):35864. 26. kinugasa k, mandai s, kamata i, sugiu k, ohmoto t. surgical treatment of moyamoya disease: operative technique for encephalo-duro-arterio-myo-synangiosis, its follow-up, clinical results, and angiograms. neurosurgery. 1993 apr 1;32(4):527-31. 27. sahoo ss, suri a, bansal s, devarajan sl, sharma bs. outcome of revascularization in moyamoya disease: evaluation of a new angiographic scoring system. asian journal of neurosurgery. 2015 oct;10(4):252. 28. riordan cp, storey a, cote dj, smith er, scott rm. results of more than 20 years of follow-up in pediatric patients with moyamoya disease undergoing pial synangiosis. journal of neurosurgery: pediatrics. 2019 mar 1;23(5):586-92. 29. takeuchi k, shimizu k. hypoplasia of the bilateral internal carotid arteries. brain nerve, 1957. 9; 37-43. 17taha_riskfactors romanian neurosurgery (2014) xxi 1: 113 123 113 risk factors for re-bleeding of aneurysmal subarachnoid hemorrhage: systemic review and meta analysis alfotih gobran taha, fang cheng li, xin ke xu, shang yi zhang sun yat sen memorial hospital, neurosurgery department, sun yat sen medical university, guang zhou, guang dong province, people’s republic of china abstract objective: the mortality of re-bleeding is high and patients surviving are usually in poor clinical condition and have a worse outcome than patients with single bleed. we performed an update systemic review and meta-analysis to determine the most common risk factors for re-bleeding in aneurysmal subarachnoid hemorrhage patients. method: we reviewed all publications on the risk factors of the re-bleeding or rerupture of already bled intracranial aneurysms. this meta analysis included studies published from the year 2000 until 2013. pooled mean difference was calculated for the continuous variables (age), and pooled odds ratio (or) was calculated for categorical factors. heterogeneity was tested first. if it is significant (p<0.05), random effect model was applied, otherwise, fixed model was used. software review manager was used to find pooled effects and perform significant test for each potential risk factor. results: we identified 174 articles. only 7 retrospective studies had met the inclusion criteria, with 2470 patients, 283 patients had aneurysmal re-bleeding. the weighted average rate of re-bleeding is 11.3% with 95% confidence interval [ci]: 10.1-12.6. statistically significant risk factor for re-bleeding were sex (or 1.46; 95% ci: 1.11, 1.92), high systolic blood pressure [sbp] (or 2.52; 95% ci: 1.40, 4.53), aneurysm size (or 3.00; 95% ci: 2.064.37), clinical condition (hunt & hess) (or 4.94; 95% ci: 2.29, 10.68), and fisher grade (or 2.29; 95% ci: 1.45, 3.61). conclusion: sex, high sbp, high fisher grade, aneurysm size larger than 10 mm, and patients with poor clinical condition (hunt & hess) were independent risk factors for aneurysmal re-bleeding. the importance of early aneurysm intervention should be emphasized to eliminate the risk of re-bleeding and poor outcome. key words: cerebral aneurysm, subarachnoid hemorrhage, re-bleeding, risk factor, meta-analysis. 114 taha et al risk factors for re-bleeding of aneurysmal subarachnoid hemorrhage introduction 10-15% of patients with aneurysmal sah die before reaching medical care [1]. a further 5% die within the first 24 hours of sah. by the 30th day of sah, the overall case fatality rate increases to nearly 50% [1] [2]. of the survivors 25–30% of patients re-bleed within the first four weeks from the sah. after the first six weeks of sah, the re-bleeding rate is about 4% per year. 50~90% of re-bleeding episodes occur in the first 6 hours after the primary bleed [3] [4]. mortality is reported to be as high as 75%~80% in patients who re-bled from their aneurysm [5] [6] [7] [8]. the rate of re-bleeding will be high if the aneurysm left untreated. 25% die as a result of medical complications of sah [9], like neurogenic pulmonary edema and neurogenic stunned myocardium. for these reasons, early detection and accurate evaluating the incidence of re-bleeding, predictors for re-bleeding is mandatory. factors associated with aneurysm rebleeding are still controversial. re-bleeding can occur before the patients are admitted or during transfer to the hospital [10] [11]or after hospitalization. in this study we included parameters that were available after admission. we had reviewed 9 factors that may have significant impact on re-rupture after primary bleeding. these findings could give neurologists, neurosurgeons, and health care providers with most common risk factors for re-bleeding in subarachnoid hemorrhage patients. method we reviewed all publications on the risk of the re-bleeding or re-rupture of already bled intracranial aneurysms. this meta analysis included studies published from the year 2000 until 2013.we performed a medline, embase, cochrane, web of science search. the following keywords were used in different combination: cerebral aneurysms, intracranial aneurysms, re-bleeding, re-rupture, recurrent hemorrhage, risk factors. we searched the reference lists for all relevant publications for additional studies, and the references of the publications thus found were checked again. inclusion criteria: 1patients with sah due to aneurysmal re-rupture after previous bleeding, proved by imaging studies such as magnetic resonance image (mri), computed tomography angiography (cta), digital subtraction angiography (dsa). 2studies comparing multi risk factors in re-bleeding and non re-bleeding groups such as: sex, age, clinical conditions at admission (hunt & hess), hypertension, location of aneurysm, multiple aneurysms, size of aneurysm, fisher grade, external ventricle drainage (evd). exclusion criteria: 1fewer than 20 patients were included, because smaller studies are more likely to suffer from selection bias. 2multiple reports were published for the same study population. 3-the article was a review, a case report, or editorial. 4sah due to romanian neurosurgery (2014) xxi 1: 113 123 115 non aneurysmal pathology (trauma, avm, etc.). 5-non english language articles. data extraction: two reviewers independently extracted data from the studies that met the inclusion criteria. information was extracted on patient, aneurysm characteristics, pre-operative treatment. in case of disagreement between the 2 reviewers, consensus was reached by joint review. the location of the aneurysms was classified as follows (1): anterior circulation: anterior communicating artery, internal carotid artery, anterior cerebral artery, middle cerebral artery, posterior communicating artery. (2) posterior circulation: vertebral artery, basilar artery, posterior cerebral artery. because in the studies different cut points were used for aneurysm size, we made the following categories: ≥10mm and < 10mm. others factors were classified as follow: hunt & hess: iv-v and i-ii-iii, fisher grade: ≥3 and < 3. measurements index: age, sex, hypertension, aneurysm location, multiple aneurysms, size, hunt & hess, fisher grade and external ventricle drainage. data analysis: 1. data (9 factors) were extracted from the 7 papers and entered into excel sheet. 2. software review manager was used to find pooled effects and perform significant test for each potential risk factor. 3. pooled mean difference was calculated for the continuous variables (age), and pooled odds ratio was calculated for categorical factors. 4. heterogeneity was tested first. if it is significant (p<0.05), random effect model was applied, otherwise, fixed model was used. results we identified 174 articles. only7 retrospective studies had met the inclusion criteria, with 2470 patients, 283 patients had aneurysmal re-bleeding (table 1). and we made a quality evaluation to every research by use of the newcastle-ottawa scale (nos). results of quality evaluation shown most of seven researches had high quality (table 2). the weighted average rate of re-bleeding is 11.3% with 95% confidence interval: 10.112.6. meta-analysis result sex (or 1.46; 95% confidence interval [ci]: 1.11, 1.92), high systolic blood pressure [sbp] (or 2.52; 95% ci: 1.40, 4.53), aneurysm size (or 3.00; 95% ci: 2.06-4.37), clinical condition (hunt & hess) (or 4.94; 95% ci: 2.29, 10.68), and fisher grade (or 2.29; 95% ci: 1.45, 3.61). whereas age, aneurysm location, multiple aneurysms and external ventricular drainage (evd) in this analysis are not significant risk factors for rebleeding in aneurysmal sah patients (table 3). 116 taha et al risk factors for re-bleeding of aneurysmal subarachnoid hemorrhage tabel 1 overview of the 7 included studies author publication year patient no# rebleeding rate study period (year) design diagnosis of rebleeding journal details of patient selection total rebleed no-rebleed kc cha et al. 2010 492 38 454 8.4% 12 (1995-2007) retrospective ct j. korean neurosurg soc no beck et al. 2006 237 23 214 10.7% 3 (1999-2002) retrospective ct stroke no lie mei guo et al. 2013 326 70 256 27.3% 9.3 (2002-2010) retrospective ct or lumbar puncture world neurosurg no cong w. et al. 2012 458 63 395 15.9% 3 (2005-2008) retrospective ct turkish neurosurgery yes naidech et al. 2005 574 40 534 7.5% 6 (1996-2002) retrospective ct arch neurol yes ohkuma et al. 2001 273 37 236 15.7% 10 (1989-1998) retrospective ct stroke yes wu tc. et al. 2012 110 12 98 12.2% 3 (2007-2010) retrospective ct j. comput assist tomogr yes total 2470 283 tabel 2 the risk factors of the studies and quality evaluation in the meta-analysis authors risk factor scores kc cha et al. a b c d e f g h 7 beck et al. a b f h i 8 lie mei guo et al. a b c d f g h 8 cong w. et al. a b c d e g 8 naidech et al. g i 8 ohkuma et al. a b c d g 7 wu tc. et al. a b c d f h 7 tabel 3 meta – analysis factor number of studies heterogeneity chi-squared models of meta-analysis pooled or/odd ratio 95%ci z p p i2(%) age (mean) 6 0.009 67 random 1.72 -1.61-5.04 1.01 0.31 sex male vs. female 6 0.61 0 fixed 1.46 1.11-1.92 2.71 0.007 hypertension 4 0.01 72 random 2.52 1.40-4.53 3.08 0.002 romanian neurosurgery (2014) xxi 1: 113 123 117 location anterior circulation vs. posterior circulation 5 0.83 0 random 1.59 0.72-3.48 1.15 0.25 multiple aneurysms 2 0.12 58 fixed 1.11 0.58-2.09 0.31 0.76 size ≥10mm vs. < 10mm. 4 0.11 50 fixed 3.00 2.06-4.37 5.74 0.00001 hunt-hess grade iv-v vs. i-ii-iii 5 0.0001 83 random 4.94 2.29-10.68 4.07 <0.0001 fisher grade ≥3 vs. ＜3 4 0.34 11 fixed 2.29 1.45-3.61 3.55 0.0004 external ventricular drainage (evd) 2 0.03 78 random 2.96 0.86-10.22 1.72 0.09 meta-analysis result 1. re-bleeding and age: there are 6 studies describing age and re-bleeding. pooled effects: or (95% ci): 1.72 (-1.61, 5.04), p-values for pooled effect: 0.31, p ˃0.05, there is no statistical difference between the subgroups. 2. re-bleeding and sex: there are 6 studies describing sex and re-bleeding. pooled effects: or (95% ci): 1.46 (1.11, 1.92), p-values for pooled effect: 0.007, p＜0.05, there is significant statistical difference between the subgroups. study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: chi² = 3.60, df = 5 (p = 0.61); i² = 0% test for overall effect: z = 2.71 (p = 0.007) events 21 11 31 32 0 17 6 118 total 38 23 70 63 0 37 12 243 events 161 87 99 147 0 73 33 600 total 454 214 256 395 0 163 65 1547 m-h, fixed, 95% ci 2.25 [1.15, 4.38] 1.34 [0.56, 3.17] 1.26 [0.74, 2.15] 1.74 [1.02, 2.97] not estimable 1.05 [0.51, 2.15] 0.97 [0.28, 3.32] 1.46 [1.11, 1.92] rebleeding no-rebleeding odds ratio odds ratio m-h, fixed, 95% ci 0.2 0.5 1 2 5 female male study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) heterogeneity: tau² = 10.43; chi² = 15.33, df = 5 (p = 0.009); i² = 67% test for overall effect: z = 1.01 (p = 0.31) mean 51.7 52 58.2 55 0 61.2 57 sd 11.22 15.8 8.99 20 0 12.1 18 total 38 23 70 63 0 37 12 243 mean 53.69 53.6 52.07 53 0 58.6 56.5 sd 12.06 13.7 10.15 17 0 12.3 15.6 total 454 214 256 395 0 236 98 1653 iv, random, 95% ci -1.99 [-5.73, 1.75] -1.60 [-8.31, 5.11] 6.13 [3.68, 8.58] 2.00 [-3.22, 7.22] not estimable 2.60 [-1.60, 6.80] 0.50 [-10.14, 11.14] 1.72 [-1.61, 5.04] rebleed no-rebleeding mean difference mean difference iv, random, 95% ci -10 -5 0 5 10 bleeding patient young bleeding patient old 118 taha et al risk factors for re-bleeding of aneurysmal subarachnoid hemorrhage 3. re-bleeding and hypertension: there are 4 studies describing hypertension and re-bleeding. pooled effects: or (95% ci): 2.52 (1.40, 4.53), p-values for pooled effect: 0.002, p＜0.05, there is significant statistical difference between the subgroups. 4. re-bleeding and aneurysm location: there are 5 studies describing aneurysm location and re-bleeding. pooled effects: or (95% ci): 1.59 (0.72-3.48), p-values for pooled effect: 0.25, p˃0.05, there is no significant statistical difference between the subgroups. 5. re-bleeding and multiple aneurysms: there are 5 studies describing multi aneurysm and re-bleeding. pooled effects: or (95% ci): 1.11 (0.58, 2.09), p-values for pooled effect: 0.76, p˃0.05, there is no significant statistical difference between the subgroups. study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: chi² = 2.38, df = 1 (p = 0.12); i² = 58% test for overall effect: z = 0.31 (p = 0.76) events 1 0 0 12 0 0 0 13 total 38 0 0 54 0 0 0 92 events 38 0 0 60 0 0 0 98 total 454 0 0 375 0 0 0 829 m-h, fixed, 95% ci 0.30 [0.04, 2.22] not estimable not estimable 1.50 [0.75, 3.02] not estimable not estimable not estimable 1.11 [0.58, 2.09] experimental no-rebleeding odds ratio odds ratio m-h, fixed, 95% ci 0.02 0.1 1 10 50 favours [experimental] favours [control] study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: chi² = 0.89, df = 3 (p = 0.83); i² = 0% test for overall effect: z = 1.15 (p = 0.25) events 38 0 66 46 0 35 11 196 total 38 0 70 42 0 37 12 199 events 438 0 230 359 0 225 87 1339 total 454 0 256 315 0 236 98 1359 m-h, fixed, 95% ci 2.90 [0.17, 49.23] not estimable 1.87 [0.63, 5.53] not estimable not estimable 0.86 [0.18, 4.02] 1.39 [0.16, 11.83] 1.59 [0.72, 3.48] experimental no-rebleeding odds ratio odds ratio m-h, fixed, 95% ci 0.05 0.2 1 5 20 others aca/mca/ica/acoma/pcoma study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: tau² = 0.26; chi² = 10.70, df = 3 (p = 0.01); i² = 72% test for overall effect: z = 3.08 (p = 0.002) events 16 0 44 32 0 26 0 118 total 38 0 70 63 0 37 0 208 events 159 0 65 142 0 100 0 466 total 454 0 256 395 0 236 0 1341 m-h, random, 95% ci 1.35 [0.69, 2.64] not estimable 4.97 [2.84, 8.71] 1.84 [1.08, 3.14] not estimable 3.21 [1.52, 6.81] not estimable 2.52 [1.40, 4.53] rebleeing no-rebleeding odds ratio odds ratio m-h, random, 95% ci 0.1 0.2 0.5 1 2 5 10 no hypertension hypertension romanian neurosurgery (2014) xxi 1: 113 123 119 6. re-bleeding and size: there are 4 studies describing aneurysm size and re-bleeding. pooled effects: or (95% ci): 2.91 (1.62, 5.22), p-values for pooled effect: 0.0003, p<0.05, there is significant statistical difference between the subgroups. 7. re-bleeding and hunt & hess: there are 5 studies describing hunt & hess and re-bleeding. pooled effects: or (95% ci): 4.94 (2.29, 10.68), p-values for pooled effect: 0.0001, p < 0.05, there is significant statistical difference between the subgroups. 8. re-bleeding and fisher grade: there are 4 studies describing fisher grade and re-bleeding. pooled effects: or (95% ci): 2.29 (1.45, 3.61), p-values for pooled effect: 0.0004, p<0.05, there is significant statistical difference between the subgroups. study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: chi² = 3.37, df = 3 (p = 0.34); i² = 11% test for overall effect: z = 3.55 (p = 0.0004) events 36 20 47 0 0 0 11 114 total 38 23 70 0 0 0 12 143 events 329 160 140 0 0 0 80 709 total 454 211 256 0 0 0 98 1019 m-h, fixed, 95% ci 6.84 [1.62, 28.83] 2.13 [0.61, 7.44] 1.69 [0.97, 2.95] not estimable not estimable not estimable 2.48 [0.30, 20.41] 2.29 [1.45, 3.61] rebleeding no-rebleeding odds ratio odds ratio m-h, fixed, 95% ci 0.02 0.1 1 10 50 fisher grade <3 fisher grade >=3 study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: tau² = 0.63; chi² = 23.51, df = 4 (p = 0.0001); i² = 83% test for overall effect: z = 4.07 (p < 0.0001) events 33 0 31 12 26 24 0 126 total 38 0 70 63 40 37 0 248 events 123 0 65 46 133 40 0 407 total 454 0 256 395 532 236 0 1873 m-h, random, 95% ci 17.76 [6.78, 46.53] not estimable 2.34 [1.35, 4.05] 1.79 [0.89, 3.59] 5.57 [2.83, 10.98] 9.05 [4.25, 19.26] not estimable 4.94 [2.29, 10.68] rebleeding no-rebleeding odds ratio odds ratio m-h, random, 95% ci 0.05 0.2 1 5 20 score <=iii score >iii study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: tau² = 0.17; chi² = 6.04, df = 3 (p = 0.11); i² = 50% test for overall effect: z = 3.58 (p = 0.0003) events 10 13 52 0 0 0 7 82 total 38 23 70 0 0 0 12 143 events 96 55 105 0 0 0 27 283 total 451 214 256 0 0 0 98 1019 m-h, random, 95% ci 1.32 [0.62, 2.81] 3.76 [1.56, 9.06] 4.15 [2.30, 7.50] not estimable not estimable not estimable 3.68 [1.08, 12.60] 2.91 [1.62, 5.22] experimental no-rebleeding odds ratio odds ratio m-h, random, 95% ci 0.05 0.2 1 5 20 size small (<10) size large (>=10) 120 taha et al risk factors for re-bleeding of aneurysmal subarachnoid hemorrhage 9. re-bleeding and evd: there are 2 studies describing evd and re-bleeding. pooled effects: or (95% ci): 2.96 (0.86-10.22), p-values for pooled effect: 0.09, p˃0.05, there is no significant statistical difference between the subgroups. discussion 10-15% of patients with aneurysmal sah die before reaching medical care [1]. a further 5% die within the first 24 hours of sah. by the 30th day of sah, the overall case fatality rate increases to nearly 50% [ 1, 2]. of the survivors 25–30% of patients re-bleed within the first four weeks from the sah, of these; approximately 70% die after the re-bleed [5]. after the first six weeks of sah, the re-bleeding rate is about 4% per year. 50~90% of re-bleeding episodes occur in the first 6 hours after the primary bleed [3] [4]. the re-bleeding rate in this meta analysis between: 7.5%~27.3%. the weighted average rate of re-bleeding is 11.3% with 95% confidence interval [ci]: (10.1, 12.6)%. 1-age and sex: advanced age people has poor outcome after sah [12]. several studies have reported that old people has higher tendency to re-bleed than the control cases [12]. naidech et al. and cong w. et al. suggested that age was not associated with re-bleeding [13] [14]. in our study we did not find significant difference between rebleeding and non re-bleeding groups. our analysis showed that re-bleeding risk for males was significantly higher than for females. this finding was quite different from other reports claim that female patients are high risk factor [15]. 2-hunt &hess grade: the patient's clinical and neurological condition on admission was evaluated by famous hunt and hess grade system [16]. several studies reported that poor hunt and hess grade was significantly relate to aneurysmal re-bleeding [4] [5] [13] [17] [18 ] [19]. our result does not differ from these studies. one study by inagawa et al. could not find relation between poor hunt and hess and re-bleeding [20]. this may due poor condition patients were frequently intubated, sedated, and therefore difficult to diagnosis clinically. 3-high sbp: naidech et al found that hypertension is study or subgroup kc cha 2010 beck 2006 lie mei2013 cong w2012 naidech 2005 ohkuma 2001 wu 2012 total (95% ci) total events heterogeneity: tau² = 0.63; chi² = 4.65, df = 1 (p = 0.03); i² = 78% test for overall effect: z = 1.72 (p = 0.09) events 0 15 0 0 29 0 0 44 total 0 23 0 0 40 0 0 63 events 0 118 0 0 175 0 0 293 total 0 214 0 0 534 0 0 748 m-h, random, 95% ci not estimable 1.53 [0.62, 3.75] not estimable not estimable 5.41 [2.64, 11.08] not estimable not estimable 2.96 [0.86, 10.22] rebleeding no-rebleeding odds ratio odds ratio m-h, random, 95% ci 0.02 0.1 1 10 50 without drainage with drainage romanian neurosurgery (2014) xxi 1: 113 123 121 not associated with re-bleeding after subarachnoid hemorrhage. in a large study reported that the re-bleeding rate is 6.9% after admission to the hospital, but did not find relationship to blood pressure [21]. many other studies found that high blood pressure after the initial sah can lead to the risk of re-bleeding [4] [17] [22]] [23]. ohkuma found that re-bleeding is more common in patients with high systolic blood pressure more than160mmhg [4]. our analysis shows high systolic blood pressure is a major risk for re-bleed in sah patients. 4-fisher grade: the amounts of clot in the subarachnoid space demonstrated on initial ct scan. patients with intracerebral or intraventricular hematoma usually present with poor clinical condition (high h&h grade) and high blood pressure on admission. this may be can lead to early re-rupture of aneurysm. reynold et al. reported higher incidence of intracerebral hematoma in patients with signs of repeated aneurysm rupture [24]. the high incidence of this bleeding pattern may substantially contribute to poor clinical condition of patient with repeat sah. inagawa et al and lie -mei guo et al did not find any correlation between fisher grade and re-bleeding [23] [20]. this is differ from our study which shows fisher grade is a risk factor for re-bleeding. 5-external ventricular drainage (evd): acute hydrocephalus is a common complication after aneurysmal sah, needs emergent cerebral spinal fluid (csf) drainage. often results in improvement in patient clinical condition. there are many conflicting studies that assumed csf drainage can lead to re-bleeding [13] [25] [26]. the most accepted theory is that, csf drainage in patients with unsecured, recently rupture aneurysm may increase the transmural pressure across the aneurysm wall, and this may lead to increasing likelihood of re-bleeding [27]. beck et al did not find strong correlation between external ventricular drainage and re-bleeding [28]. in this analysis we did not find that evd a risk factor for re-bleeding in aneurysmal sah patients. 6-aneurysm location: previous studies showed the location of the aneurysm was implicated in aneurysmal re-bleeding [3] [28], especially in the anterior communicating artery (acoma), and posterior communicating artery (pcoma) [29]. cong w. et al study showed posterior circulation aneurysm patient is in higher bleeding risk than those in the non-posterior circulation [14]. the present study revealed that the aneurysm location was not a risk factor for re-bleeding. this result agrees with previous studies by lei-mei guo and wu et al [23] [30]. 7-aneurysm size: most of studies emphasize that aneurysm size is a major risk for initial rupture [31] [32]. lei-mei guo et al found that the probability of re-bleeding in 122 taha et al risk factors for re-bleeding of aneurysmal subarachnoid hemorrhage patients with aneurysms larger than 10 mm was 1.624 fold greater than those with aneurysms of 10 mm or less [23], but this result is not consistent with other studies [22] [17]. in this analysis we found that aneurysm size has a significant risk on re-bleeding. 8-multiple aneurysm: patients with several aneurysm have more fragile vessels wall, that's may prone to form multiple aneurysms or prone to rebleeding after the aneurysm has already ruptured. some studies showed there was no significant difference between rebleeding and non re-bleeding in patients who harboring multiple aneurysms [14]. but beck et al. reported multiple aneurysms patients have a risk of rebleeding [28]. in our analysis we did not find any correlation between multiple aneurysms and re-bleeding. conclusion sex, hypertension, hunt and hess grade, aneurysm size, and fisher grade are major risk for re-bleeding in aneurysmal subarachnoid hemorrhage patients. we did not find any correlation between age, evd, aneurysm location and multiple aneurysms and aneurysm re-bleeding. we advocate early surgery for primary ruptured aneurysm in good clinical condition patients to eliminate the risk of re-bleeding. maintained systemic blood pressure in a moderate hypertensive range (140 to 160 mmhg) also can prevent early re-rupture of the aneurysm. limitation of this study all the studies are retrospective, the data quality could not be monitored. only few studies described inclusion and exclusion criteria, each study has different study objective, and diagnostic criteria could be different from hospital to hospital. risk factors studied vary from study to study, with different focus. correspondence address alfotih gobran taha sun yat sen memorial hospital, neurosurgery department, sun yat sen medical university p. o. box 510120, guangzhou, guangdong province, people’s republic of china tel: 008613066381670 email: gta_alfotih@yahoo. com references 1. pobereskin lh. incidence and outcome of subarachnoid haemorrhage: a retrospective population based study. j neurol neurosurg psychiatry. 2001; 70: 340–343. 2. hop jw, rinkel gj, algra a, et al. case-fatality rates and functional outcome after subarachnoid haemorrhage: a systematic review. stroke.1997; 28: 660– 664. 3. tanno y, homma m, oinuma m, et al.rebleeding from ruptured intracranial aneurysms in north eastern province of japan: a cooperative study. j neurol sci.2007; 258: 11-16. 4. ohkuma h, tsurutani h, suzuki s.incidence and significance of early aneurysmal rebleeding before neurosurgical or neurological management. stroke. 2001; 32: 1176-1180. 5. rosenorn j, eskesen v, schmidt k, et al. the risk of rebleeding from ruptured intracranial aneurysms. j neurosurg.1987; 67: 329–332. 6. ameen aa, illingworth r.anti-fibrinolytic treatment in the preoperative management of subarachnoid haemorrhage caused by ruptured intracranial aneurysm. j neurol neurosurg psychiatry.1981; 44: 220–6. 7. kassell n, torner j, haley c jr, et al. the international cooperative study on the timing of romanian neurosurgery (2014) xxi 1: 113 123 123 aneurysm surgery part 1: overall management results. j neurosurg.1990; 73: 18-36. 8. kassell n, torner j, jane j, et al. the international cooperative study on the timing of aneurysm surgery. part 2: surgical results. j neurosurg.1990; 73: 37-47. 9. solenskin j, haley ec, kassell nf, et al. medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. participants of the multicenter cooperative aneurysm study. crit care med.1995; 23: 1007-17. 10.biller j, toffol g j, kassell n f, et al. spontaneous subarachnoid hemorrhage in young adults. neurosurgery. 1987; 21: 664-7. 11.sakaki t, morimoto t, hoshida t, et al.rebleeding during transport of patients with a ruptured intracranial aneurysm. j stroke cerebrovasc dis. 1999; 8: 38-41. 12.lanzino g, kassell nf, germanson tp, et al. age and outcome after aneurysmal subarachnoid hemorrhage: why do older patients fare worse? j neurosurg. 1996; 85: 410-418. 13. naidech am, janjua n, kreiter kt, et al. predictors and impact of aneurysm rebleeding after subarachnoid hemorrhage. arch neurol. 2005; 62: 410–6. 14. cong w, zhongxin z, tiangui l, et al. risk factors for rebleeding of aneurysmal subarachnoid hemorrhage based on the analysis of on-admission information. turk neurosurg.2012; 22 (6): 675-81. 15.jamous ma, nagahiro s, kitazato kt, tamura t, et al. role of estrogen deficiency in the formation and progression of cerebral aneurysms. part ii: experimental study of the effects of hormone replacement therapy in rats. j neurosurg 2005; 103: 1052-1057. 16. hunt we, hess rm. surgical risk as related to time of intervention in the repair of intracranial aneurysms. j neurosurg.1968; 28 (1): 14-20 17. fujii y, takeuchi s, sasaki o, minakawa t, koike t, tanaka r. ultra-early rebleeding in spontaneous subarachnoid hemorrhage. j neurosurg.1996; 84: 35-42. 18. hijdra a, vermeulen m, van gijn j, et al. rerupture of intracranial aneurysms: a clinicoanatomic study. j neurosurg.1987; 67: 29-33. 19. roganovic z, pavlicevic g, tadic r, et al. risk factors for the onset of vasospasm and rebleeding after spontaneous subarachnoid hemorrhage. vojnosanit pregl. 2001; 58: 17-23 [in serbian]. 20. inagawa t, kamiya k, ogasawara h, et al. rebleeding of ruptured intracranial aneurysms in the acute stage. surg neurol. 1987; 28: 93-99. 21.kitsuta y, suzuki n, sugiyama m, et al.changes in level of consciousness and association with hyperglycemia as tool for predicting and preventing rebleeding after spontaneous subarachnoid hemorrhage. prehosp disaster med.2006; 21: 190-195. 22. cha kc, kim jh, kang hi, et al. aneurysmal rebleeding: factors associated with clinical outcome in the rebleeding patients. j korean neurosurg soc. 2010; 47: 119–23. 23. guo lm, zhou hy, xu jw, et al. risk factors related to aneurysmal rebleeding. world neurosurgery.2013; 76: 292-298. 24. reynolds a, shaw cm. bleeding patterns from ruptured intracranial aneurysms: an autopsy series of 205 patients. surg neurol.1980; 15: 232-5. 25. mehta v, holness ro, connolly k, walling s, hall r. acute hydrocephalus following aneurysmal subarachnoid hemorrhage. can j neurol sci. 1996; 23: 40–45. 26. rajshekhar v, harbaugh re. results of ventriculostomy with external ventricular drainage for acute hydrocephalus following subarachnoid hemorrhage. acta neurochir (wien). 1992; 115: 8–14. 27. paré l, delfino r, leblanc r. the relationship of ventricular drainage to aneurysmal rebleeding. j neurosurg.1992; 76: 422–427. 28. beck j, raabe a, szelenyi a, et al. sentinel headache and the risk of rebleeding after aneurysmal subarachnoid hemorrhage. stroke.2006; 37: 2733–7. 29. nibbelink dw, torner jc, henderson wg.intracranial aneurysms and subarachnoid hemorrhage. a cooperative study. antifibrinolytic therapy in recent onset subarachnoid hemorrhage. stroke.1975; 6: 622-629. 30. wu tc, tsui yk, chen ty, et al. rebleeding of aneurysmal subarachnoid hemorrhage in computed tomography angiography: risk factor, rebleeding pattern, and outcome analysis. j comput assist tomogr. 2012; 36 (1): 103-8. 31. prestigiacomo cj, he w, catrambone j, et al. predicting aneurysm rupture probabilities through the application of a computed tomography angiographyderived binary logistic regression model. j neurosurg.2009; 110: 1-6. 32. salary m, quigley mr, wilberger je jr. relation among aneurysm size, amount of subarachnoid blood, and clinical outcome. j neurosurg.2007; 107: 13-17. microsoft word seferisch_hearing_formatat charalampos seferis hearing outcome following γ-knife treatment hearing outcome following γ-knife treatment of vestibular schwannomas. a series of 33 cases charalampos seferis hygeia hospital, athens, greece, phd student in neurosurgery, university of medicine and pharmacy “gr.t. popa” iasi abstract due to the progress in neuro-imaging vestibular schwannomas (benign tumors rooting from scwann cells of vestibular nerve) witness an increase in incidence in the last decade. despite the advances in operating techniques and intraoperative technologies used surgery still presents a rate of morbidity and mortality. gammaknife became a therapeutic alternative for selected cases of vestibular schwannomas. however, the results of gamma-knife radiosurgery showed an influence on the audiograms of the patientstreated with this technique. the goal of our study is to assess the measure in which gamma-knife treatment influences the neuro-otologic behavior of these tumors. we study a series of the 33 consecutive cases which completed a 24 months follow-up after gamma-knife treatment. we use a neuroimagistic and neuro-otologic protocol aproved by our institution. 24 patients didn’t show a deterioration of the audiogram. among these 11 report an unmodified hearing function, while 11 describe an improvement in hearing (we excluded the cases with complete hearing loss. we manage to show that strictly following the patient selection criteria for gamma-knife treatment, radiosurgery is a safe treatment option for the patients with small to medium-sized vestibular scwannomas. keywords: audiogram, gamma-knife, radiosurgery, vestibular schwannoma introduction analyzing the results of gamma-knife treatment on patients with vestibular schwannomas (within a 4 years monitoring period) we observed certain changes in audiograms. the goal of the present study is to have a measure of photonic radiation treatment effect on the neuro-otologic behavior of these benign tumors. histologically, vestibular schwannomas are benign tumors that grow from the schwann cells of the 8th cranian nerve. due to improved neuroimaging the incidence of vestibular schwannomas within the general population increased. however, despite the advances in introperatory techniques, surgery still carries a risk for morbidity and mortality. depending on tumors characteristics vestibular schwannomas can be treated by different methods, other than neurosurgery. radiosurgery is one of these non-invasive techniques that can be used to treat vestibular schwannomas. it uses gamma radiation (photons) and is known as “gamma-knife” or “γ-knife”. romanian neurosurgery (2011) xviii 2 materials and method we study a series of the 33 consecutive cases which completed a 24 months followup (at 6, 12, and 24 month) after gammaknife treatment. we use a neuroimagistic and neuro-otologic protocol aproved by our institution. we used a leskell 201 with 611c source (photonic unit) in the treatment procedure. the patients included in the study presented bilateral vestibular schwannomas with partial or total hearing loss. inclusion criteria were as follows: increase in overall dimansions of small to medium-sized tumors in patients older than 65 years of age increase in overall dimensions folowing partial surgical removal, independent of patient age poor general status patient’s decision to undergo gammaknife treatment following a in-depth discusion with his doctor. results for all the patients in the follow-up we looked exclusively at the neuro-otologic results, regardlessof age, sex, or tumor size before and after γ-knife. clinical evaluation of the patients outcome at each monitoring session the usual questions asked were: “how do you feel after the treatment?” and “how is your hearing?”. considering the possibility of answer subjectivity we decided for this study to use audiogram as a objective measure of radiation effect on neurootologic function. from the total number of patients, 4 (10.6%) declaired hearing deterioration, 21 (55.2%) indicated no change in hearing function, while 13 (34.2%) indicated an improvement in hearing. subjective perception aside we focus on the quantitative differences in audiograms from the time of the treatment up to two years follow-up. we notice that out of a total of 33 patients modified audiogram was obtained in 24 cases. in 15 cases the audiometric curve was shifted towards high frequences, while in 9 cases the cruve shifted towards lower frequencies. at a normal audiogram recording (10db) we measure the curve shift ith a 5db treshold. table 1 number of patients with changes on the audiogram modified audiogram unchanged audiogram 24 9 table 2 details for the patients that didn’t show a significant shift in audiogram patient t = 0 (2 khz) t = 24 m (2 khz) t = 0 (4 khz) t = 24 m (4 khz) change in hearing α 52 61 66 58 improvement β 36 34 20 19 no change c 50 48 60 61 no change d 100 100 100 100 total loss ε 50 48 60 61 improvement f 61 58 63 60 no change g 39 39 28 26 improvement h 52 50 59 55 no change i 92 90 88 83 total loss charalampos seferis hearing outcome following γ-knife treatment table 3 details for patients with improvements in audiogram patient t = 0 (2 khz) t = 24 m (2 khz) t = 0 (4 khz) t = 24 m (4 khz) change in hearing α 91 77 100 78 no change β 72 50 60 48 no change c 52 10 50 42 improvement d 44 20 40 20 improvement ε 72 66 55 58 improvement f 81 68 92 76 no change g 60 41 60 57 improvement h 42 16 46 38 improvement i 48 28 41 27 improvement j 82 74 59 49 improvement k 71 64 73 64 no change l 41 30 48 41 improvement m 83 50 69 60 improvement n 44 36 42 32 no change o 78 63 50 52 no change table 4 patients with audiogram deterioration patient t = 0 (2 khz) t = 24 m (2 khz) t = 0 (4 khz) t = 24 m (4 khz) change in hearing α 64 77 58 78 no change β 54 63 65 74 no change c 41 60 60 70 deterioration d 66 75 53 70 deterioration ε 52 58 50 62 no change f 53 61 60 73 deterioration g 66 71 58 66 no change h 63 72 60 68 no change i 50 63 48 61 deterioration discussion as described by our results only 9 out of 33 patients that underwent gamma-knife treatment showed changes in audiograms. furthermore, asked how is their perceived hearing function after the treatment, 5 patients responded that it wasn’t affected by the radiation therapy (patients with complete hearing loss prior to the treatment aside). from the 9 patients that didn’t manifest a significant change in their audiogram during the 24 months following gammaknfe treatment, acustic acuity remained unchanged in 4 cases (compared to the pretreatment acuity), while 3 of them showed an improvement in hearing. finally, from the 15 patients that showed a significant improvement their audiometric diagram (δdb> 5, with an interval from 6 db to 42 db at 2 khz, and from -3 db to 22 db at 4 khz, respectivelly), 7 of them reported an improvement in hearing while for the other 8 there was no change in hearing. romanian neurosurgery (2011) xviii 2 figure 1 patient k.a. left: audiogram in 2006 (34 yrs.) proir to γ-knife, 44 db at 2 khz, 41 db at 4 khz. right: audiogram in 2008 (36 yrs) at two years after the treatment, 20 db at 2 khz, 20 db at 4 khz figure 2 reference dose for the final therapeutic plan ( 12 gy = 68 %, vol= 34,7 mm2 ) conclusions from a total of 24 patients that dind’t show a significant change in audiograms, 11 of them report no modifications in hearing, while 11 describe an improvement in hearing (we disregard the cases with complete hearing loss). while these data do not show unequivocally that a change in audiogram („quantitative gain”) is equivalent to a perceived improvement in hearing („qualitative gain”) it shows however that complying to strict criteria of patient selection for gamma-knife therapy makes this therapy a safe one for treating small to medium sized vestibular schwannomas. this therapy insures the preservation of the existing auditory acuity and even a significant improvement in a number of cases. references 1. olivecrona h: acoustic tumors. j neurosurg 26:613, 1967. 2. house wf, hitselberger we: fatalities in acoustic tumor surgery, vol 2. baltimore, university park press, 1979, pp 235-264. 3. neely jg: is it possible to totally resect an acoustic tumor and conserve hearing? otolaryngol head neck surg 92:162-167, 1984. 4. tator ch, nedzelski jm: preservahon of hearing in patients undergoing excision of acoustic tumors and other cerebellopon tine angle tumors. j neurosurg 63:168-174, 1985. 5. neely jg: hearing conservation surgery for acoustic tumors: a clinical-pathologic correlative study. am. j otol 6:143-146, 1985. 6. gardner g, robertson jh: hearing preservation in unilateral acoustic neuroma surgery. ann otol rhinol laryngol 97:55–66, 1988. 7. lunsford ld, kamerer db, møller m: gamma knife: an alternative treatment for acoustic neurinomas. ann otol rhinol laryngol 97:631–635, 1988. 8. linskey me, lunsford ld, flickinger jc: radiosurgery for acoustic neurinoma: early experience. neurosurgery 26: 736–745, 1990. 9. norén g: gamma knife radiosurgery in acoustic charalampos seferis hearing outcome following γ-knife treatment neuromas, in haid c (ed): vestibular diagnoses and neurootological management of the skull base. gräfelfing: demeter verlag, pp 43–45, 1991. 10.kanzaki j, ouchi t, shiobara r, toya s: hearing preservation in acoustic neuroma surgery by the extended middle fossa method. otolaryngol suppl acta 487:22-29, 1991. 11.moskowitz n, long dm: acoustic neurinomas: historical review of a century of operative series. neurosurg q 1:2-18, 1991. 12.jenkins ha: hearing preservation in acoustic neuroma surgery. laryngoscope 102:125-128, 1992. 13.whittaker ck, luetje cm: vestibular schwannomas. j neuro surg 76:897-900, 1992. 14.fischer g, fischer c, remond j: hearing preservation in acoustic neurinoma surgery. j neurosurg 76:910-917, 1992. 15.norén g, greitz d, hirsh a, et al: gamma knife radiosurgery in acoustic tumors. acta neurochir suppl 58:104–107, 1993. 16.cerullo lj, grutsch jf, heiferman k, osterdock r: the preservation of hearing and facial nerve function in a consecutive series of unilateral vestibular nerve schwannoma surgical patients (acoustic neuroma). surg neurol 39:485-493, 1993. 17.post k, eisenberg mb, catalano pj: hearing preservation in vestibular schwannoma surgery: what factors influence outcome? j neurosurg 83:191-196, 1995. 18.samii m, matthies c: management of 1000 vestibular schwannomas (acoustic neuromas): hearing function in 1000 tumor resections. neurosurgery 40:248-260, 1997. 19.seo y, fukuoka s, nakagawara j, et al: effect of gamma knife radiosurgery on acoustic neurinomas. assessment by 99mtcdpta-human serum albuminand 201tlcl-single photon emission computed tomography. stereotact funct neurosurg 66 (suppl 1): 93–102, 1997. 20.prasad d, steiner m, steiner l: gamma surgery for vestibular schwannoma. j neurosurg 92:745–759, 2000. 21.meijer ow, wolbers jg, baayen jc, slotman bj: fractionated stereotactic radiation therapy and single high-dose radiosurgery for acoustic neuroma: early results of a prospective clinical study. int j radiat oncol biol phys 46:45-49, 2000. 22.flickinger jc, kondziolka d, niranjan a, et al: results of acoustic neuroma radiosurgery: an analysis of 5 years, experience using current methods. j neurosurg 94:1–6, 2001. microsoft word 20.catanam_reduction_f.docx 546 m. catana and m. gorgan reduction and fusion in spondylolisthesis reduction and fusion in grade iv l5-s1 spondylolisthesis. case presentation m. catana1, m. gorgan2 1phd student “grigore t. popa” umph, iasi 2i-st neurosurgical clinic, 4-th neurosurgical department, “bagdasar arseni” clinical university hospital, bucharest abstract grade iv spondylolisthesis in meyerding classification is a special pathology given the particular anatomy, biomechanics, clinical presentation or surgical options. the clinical presentation may include a vertebral instability syndrome with various degrees of presentation but also radicular syndromes and caudaequina syndrome. surgical treatment is a difficult attempt, and the available techniques are subject to controversy. the objectives of surgery are decompression of the neural elements, lumbar spine alignment, lordosys correction, with a normal disc space, and calibration of neural foramina. the gold standard is represented by reduction and fusion, but as an alternative option is “in situ” fixation, if the first attempt failed. keywords: grade iv spondylolisthesis, vertebral instability, reduction, fusion background with bipedal locomotion, the human skeleton, including the spine, suffered important changes. the centre of gravity moved forward, anterior to the lombosacral junction, and the physiological lumbar lordosis appeared, the intervertebral discs especially l5 were oriented forwards and downwards. in the same time the l5 neural arch had a reactive development and articular facets were oriented in a coronal plane being in this way adapted to their function to prevent anterior sliding. an anatomical defect at the level of “pars interarticulars”, called spondylolysis make this anterior movement possible, and the vertebral body slides anteriorly on the subjacent vertebra – spondylolisthesis. in 1782, herbiniaux, a belgian obstetrician first described a vertebral sliding. he was concerned with the pelvic outlet narrowing, as a consequence of an deformity at the lobo-sacral junction (12). the term spondylolisthesis was introduced by kilian in 1854 and comes from greeks pondylos (vertebra) andolisthesis (sliding) (6, 21, 22). case presentation a 16 years old male was admitted in our department in october 2010 with lumbalgia, walking deficit and bladder symptoms. the clinical exam showed a severe lumbar instability (less than 30 min. tolerance to standing upright), lumbar blockage with paravertebral muscle spasm. a caudaequina syndrome was diagnosed with bilateral sciatalgia, l5-s1 bilateral paresthesia, frankel d paraparesis, predominantly in bilateral l5 myotomes romanian neurosurgery (2011) xviii 4: 546 550 547 (asia 3), and bladder disturbances including dysuria and polakiuria. the diagnosis of a l5-s1 isthmic grade iv spondylolisthesis was confirmed on lumbar radiographs. the surgical treatment, consisted in dural sac and bilateral l5 intraforaminal roots decompression, followed by complete l5 discectomy and l5-s1 reduction and fusion with a peek cage, completed with bilateral l4-l5-s1 posterior fusion with transpedicular screws. the patient remained immobilised in bed for 3 days. lumbago and sciatica remitted immediately and the motor deficits and the bladder dysfunction remitted 4 to 6 weeks postoperative. lumbar blockage persisted for two more months. at 6 months follow up the patient was walking and running without difficulty, he had a good lumbar mobility and no lumbago or sciatica, also no motor deficits or bladder dysfunction. a control hyperflexion-hyperextension radiographs showed a good alignment of l4-l5 and s1 vertebral bodies, a normal lumbar lordosis, and normal discal space height with a tendency towards a vertebral block. surgical technique given the evolution of the symptomatology the only available treatment was surgery, with a defined purpose of treating the lumbalgia and alleviate the neurological suffering. the goals of the surgery were nerve roots decompression with reduction and fusion of spondylolisthesis, regaining the lumbar lordosis, and the discal space and neural foramina height (figures 1 and 2). we also thought of a second option of decompression and “in situ” fusion. figure 1 preoperative x-ray figure2 postoperative x-ray (3 months) a 12-15 cm midspinal lumbar incision was performed, and the muscles were slipped to give a good view of the transverses. a bilateral l5 spondylolysis was observed along with l5 and s1 spina bifida 548 m. catana and m. gorgan reduction and fusion in spondylolisthesis and elongated l5 articular spaces with a coronary orientation. the mobile l5 posterior arch was resected along with the articulars. the dural sac was elongated and severely compressed on l5 disc posterior margin. l5 roots were compressed in the foramina. the s1 vertebral plateau was rounded in its posterior part (figure 3). the l5 disc was bilaterally excised to reduce the resistance to the reduction of the listesis. progressive and controlled l5-s1 distraction was applied in order not to elongate the dural sac. the foramina were enlarged using a high speed drill. l5 pedicles were conserved and l5 roots were decompressed towards the laterovertebral space.the s1 plateau was modelled and its posterior margin exised for a better decompression of the dural sac. the adjacent l5 and s1 surfaces were prepared for intersomatic fusion. we proceded then to reduction introducing poliaxialtranspedicular screws in l4 and s1 pedicles. special long head screws designed for reduction were introduced in l5 pedicles. the rods were then bent to imitate the lumbar lordosis and were intentionaly cut 2 cm longer, for the subsequent distraction to be efficient. the distraction was performed with attention to the tension in the dural sac and l5 roots, in order to avoid elongation. figure 3 intraoperatorypicture the dural sac is compressed by the posterior margin of the l5 disc a pursueder was used for the reduction, using the rod as a grade i lever fixed at l4 and s1. in the same time l5 body was mobilised using a disc spacer introduced in the discal space. the intersomatic fusion using a lumbar peek cage filled with hidroxyapatite and autologous bone from the l5 posterior arch. after the cage was secured and the lordosis was corrected the screws were locked. discussion grade iv spondylolisthesis is associated with important changes in vertebral biomechanics and is a difficult problem for the surgeon. l5 body slippage puts stress on the anterior sacral plateau with possible fractures produced by the axial loading forces. in time the anterior margin of the plateau becomes round allowing the progression of the listesis. l5 takes a trapezoidal form with a posterior small base. l5 nerve root is thus pressed to the s1 superior plateau, not with the l5 inferior plateau. the most frequent deficit in these cases is l5 radiculopaty. the surgical treatment creates new bony contact surfaces, for a stable and solid fusion. this is possible only if the spondylolisthesis is reduced and vertebral plateaus come in contact. given the periradicular cicatriceal adherences reduction is often difficult and can worsen the neurological deficit produced by elongation. that is the reason that some surgeons prefer in situ fusion, that implies a good posterior bony synthesis which have, however, the risk of further progressing of spondylolisthesis. romanian neurosurgery (2011) xviii 4: 546 550 549 conclusion grade iv spondylolisthesis remains a challenging surgical problem and the best treatment is reduction and solid fusion, which can be accomplished if the anatomical and biomechanical changes associated to this condition are well understood, and the surgical fusion techniques are safely performed. references 1. baker dr, mcholick w. spondylolischisis and spondylolisthesis in children. j bone joint surg am 38:933-934, 1956; 2. boxall d, bradford ds, winter rb. management of severe spondylolisthesis in children and adolescents. j bone joint surg am 61:479-495, 1979; 3. crock hv, normal and pathological anatomy of thelumbar spinal nerve rootcanals, j of bone and joint surgery, 63b, no 4:487-490, 1981; 4. dick wt schnebel b: severe spondylolisthesis. reduction and internal fixatio. clin orthop 232:70-79, 1988; 5. fairbank jc, pynsent pb, the oswestry disability index, spine 25(22):2940-52, 1976; 6. fredrickson be, baker d, mcholick wj. the natural history of spondylolysis and spondylolisthesis. j bone joint surg 66a:699-707, 1984; 7. frobin w, brinckmann p, kramer m, hartwig e. height of lumbar discs measured from radiographs compared with degeneration and height classified from mr images. eur radiol. 11:263–269, 2001; 8. gill gg, manneng fg, while hl: surgical treatment of spondylolisthesis without spine fusion. j bone joint surg am 37:493-520, 1955; 9. gould d, et al.: visual analogue scale (vas), journal of clinical nursing, 10, 697-706, 2001; 10. harvell jc, hanley en: spondylolysis and spondylolisthesis, disorders of the pediatric spine: 561674, 1995; 11. hersinger rn, lang jr, macewen gd: surgical management of spondylolisthesis in children and adolescents. spine i:207-216, 1976; 12. herbiniaux g. traite sur divers accouchemens laborieux et sur les polypes de la matrice. brussels: jl de boubers, 1782; 13. hutton wc, cynon bm. spondylolysis. the role of the posterior elements in resisting the intervertebral compressive force. acta orthopscand 49:604-609, 1978; 14. jackson dw, wiltse ll, cirincione rj. spondylolysis in thefemalegymnast. clin orthop 117:68-73, 1976; 15. junghanns h. spondylolisthes enohne spalt im zwischengelenkstuck, arch of orthop 29:118127,1930; 16. lambl d. zehn thesenuber spondylolisthesis. zentralbl gynak 9:356-357, 1885; 17. lehmann tr, spratt kf, tozzi je, et al. long-term follow-up of lower lumbar fusion patients. spine (phila pa 1976). 12:97–104, 1987; 18. leon l, wiltse ll, winter rb: terminology and measurement of spondylolisthesis, j of bone and joint surg, 65a, 6:768-772; 19. matsunaga s, sakou t, morizono y, et al.: natural history of degenerative spondylolisthesis: pathogenesisand natural course of slippage. spine 16: 1204-1210, 1990; 20.mayerding hw. spondylolisthesis. surg gynecol obstet 54:371-377, 1932; 21.macafee pc, weiland dj, carlow jj: survivor ship analysis of pedicle spinal instrumentation. spine 16: s422-s427, 1991; 22.mcphee b: spondylolisthesis and spondylolysis. in youmans jr (ed): neurological surgery. philadelphia, wb saunders, pp 2749-2784, 1990; 23. neugebauer fl. the classic: a new contribution to the historyandetiology of spondylolisthesis. clin orthop 117:4-22, 1976; 24. ohmori k, suzuki k, ishida y: translaminopedicular screw fixation with bone grafting for symptomatic isthmic lumbar spondylolysis. neurosurgery 30:379-384, 1992; 25. osterman k, lindholm ts, laurent le: late results of removal of thelooses posterior element (gill’s operation) in thetreatment of lytic lumbar spondylolisthesis. clin osthop 117:121-128, 1976; 26. peek rd, wiltse ll, reynolds jb et al: in situ arthrodesis without decompression for grade-iii or iv isthmic spondylolisthesis in adultswhohave severe sciatica. j bone joint surgery am 71:62-68, 1989; 27. pizzutillo pd, hummer cd iii: nonoperative treatment for painful adolescent spondylolisis or spondylolisthesis. j pediatr orthop 6:311-316, 1986; 28. pizzutillo pd, mirenda w, macewen gd: postero lateral fusion for spondylolisthesis in adolescence. j pediatr orthop 6:311-316, 1986; 29. rowe gg, roche mb: the etiology of separate neural arch, j bone joint surg am 35: 102-110, 1953 30. saraste h: the etiology of spondylolysis. a retrospective radiographicstudy. acta orthopscand 56:253-255, 1985; 31. semon rl, spengler d. significance of lumbarspondylolysis in collegefootballplayers. spine 6:172-174, 1981; 32. simper lb: spondylolysis in eskimoskeletons. acta orthopscand 57:78-80, 1986; 33. rosenberg nj. degenerative spondylolisthesis: 550 m. catana and m. gorgan reduction and fusion in spondylolisthesis surgicaltreatment. clin orthop 117:112-120, 1976; 34. rosenberg nj, bargar wl, friedman b. the incidence of spondylolysis and spodylolisthesis in non ambulatory patients. spine 6:35-38, 1981; 35. vital jm, lavignolle b, grenier n, et al.: anatomy of the lumbar radicular canal, anatomia clinica, 5:141, 1983; 36. wenger dr, lee cs. spondylolisthesis in children andadolescents. semin spine surg 5:308-319; 1993; 37. wiltse ll, newman ph, mac nab i. classification of spondylolysis and spondylolisthesis. clin orthop 117:23-29, 1976; 38. wiltse ll, rothman slg. spondylolisthesis: clasification, diagnosisand natural history. semin spine surg i:78-94, 1989; 39.wiltse ll, widell eh jr, jackson dw: fatiguefracture: the basic lesion in isthmic spondylolisthesis. j bone joint surg 61b:301-305, 1979; 40.wynne-davies r, scott jh: inheritance and spondylolisthesis: a radiographic family survey. j bone joint surg br 61:301-305, 1979. microsoft word 18anuntdanube romanian neurosurgery (2011) xviii 1: 105 – 106 105 neurosurgical controversies in the danube – carpathian region the danube carpathian region is more than a part of europe from a geographical point of view; it could become even an interesting european concept. the danube played the role of a binder among the nations, who it met during its course, and less of a natural border; thus spreading from its spring until it spills in the black sea centuries of culture, experiences and ideas. the carpathians have preserved in their arc all these particular acquisitions. neurosurgery, yet a relatively young specialty may become the common language for the development of more intense collaboration in this region of europe. by organizing a congress of the countries from this geographical area we wish to identify the common points in the field of diagnosis, treatment and research, but especially to identify together the weakness, the existing controversies and maybe to find keys for the future. therefore the “neurosurgical controversies în the danube – carpathian region” held between 26th – 27th of may 2011, should constitute a commencement în this respect. the proposed topics of the congress are: past, present and future of the represented countries controversies in the treatment of the gliomas what's wrong in degenerative spine surgery? form internal to external validity in evidence-based medicine in neurosurgery quality of life in neurosurgery severe brain injurywhat's the best? clipping aneurismwhat's the future? new vs. classic in brain protection and recovery this congress may be the milestone and the beginning of a fruitful, long term collaboration, which is proudly hosted in cluj-napoca. prof. dr. ioan stefan florian president of the romanian society of neurosurgery 106 neurosurgical controversies in the danube – carpathian region the congress will be preceded by the german romanian course entitled “degenerative diseases of the spine. midline lesions” period: 24th – 25th of may 2011 course venue: grand hotel napoca, cluj-napoca, romania co-presidents: prof. dr. jurgen piekgermany prof. dr. ioan stefan florian – românia neurosurgical controversies in the danube-carpathian region controversies in the treatment of gliomas • treatment of supratentorial low grade gliomas: surgical vs. conservative • cost-efficiency report of new adjuvant tools in surgery of low grade gliomas intraoperative mri awake surgery intraoperative ultrasound surgical experience • the role of surgery in de novo glioblastoma multiforme • gross total removal • frameless stereotactic biopsy • conservative vs. aggressive treatment of recurrent glioblastoma severe brain injury-what's the best? • early vs. delayed decompression? • icp monitoring: useful or mandatory? the role of icp monitoring in severe brain injury the best way to decrease icp what's wrong in degenerative spine surgery • to fuse or not to fuse? • dynamic stabilization vs. rigid stabilization • surgery vs. conservative management • microsurgery vs. minimal invasive approach in lumbar disc hernia intracerebral midline lesions • transphenoidal vs. intracranial approach in suprasellar large masses • microsurgical transcallosal vs. endoscopic approach of the third ventricular lesions • supracerebellar infratentorial vs. occipital supratentorial approach in pineal region tumors • sitting vs. .prone position in posterior fossa surgery cerebro-vascular pathology • clipping vs. coiling in anterior circulation aneurisms • single stage vs. multiple stage surgery in multiple aneurisms • urgent vs. early vs. delayed surgery in ruptured aneurisms • observation vs. surgery in unruptured aneurisms • conservative vs. radiotherapy vs. surgery in incidental avm's • pre-surgical embolisation vs. direct approach in ruptured avm's • comatose patient with intracerebral hemorrhage: surgery vs. conservative treatment from internal to external validity in evidence based-medicine in neurosurgery new vs. classic in brain protection and recovery quality of life in neurosurgery: "how long" or "how good"? microsoft word 3ienceanst_emergency_f romanian neurosurgery (2013) xx 1: 29 33 29 emergency treatment principles in intracranial hypertension st.m. iencean1, a.st. iencean2, i. poeata1 1“grigore t. popa” university of medicine and pharmacy iasi 2emergency hospital “n. oblu” iasi as general principles the treatment of intracranial hypertension depends on the type of intracranial hypertension and on the stage of the illness. first the treatment is an etiologic one in order to remove the cause that has caused the intracranial pressure increase: intracranial masses producing elevated icp should be removed when possible. simultaneously, there is an attempt to stop the pathogenic mechanisms that impact on the nervous structures, and a symptomatic treatment is applied in order to reduce the intensity of the clinical syndrome. in the case of a patient with a suspicion of decompensating intracranial hypertension, one must perform and assess: • the complete evaluation of the patient with the acute ich syndrome: one must assess the consciousness level, the conscience state, the aspect of the pupils must be monitored and the glasgow score must be established, • the vital conditions: free aerial ways, respiration and the circulatory function; resuscitation operations are performed if needed, with oro-tracheal intubation, etc. in case of traumatisms, a cervical vertebralmedullar lesion must be excluded, and possible lesions with a vital risk must be revealed if they require an immediate solution. • the emergency exploration by a cranial-cerebral computer tomography establishes the diagnosis and the therapeutic option is decided. (2, 8, 12, 14, 16, 30) thus the first therapeutic actions are determined depending on the lesional characteristics: the expansive intracranial process (tumor, traumatic process), which has induced the ich syndrome is surgically extirpated in order to remove the supplementary pathogenic volume with a compressive effect (mass effect), and which leads to a brain edema. the expansive intracranial process that blocks the csf circulation paths with the production of an obstructive hydrocephalus and the ich syndrome requires at first the performance of a ventricular drainage and then, based on the characteristics of the lesion, there will be an intervention for its extirpation. in the blood blockage of the ventricular system in intracranial hemorrhages, with the occurrence of the ich syndrome due to obstructive hydrocephalus, the ventricular drainage is performed, and then the exploration and the treatment of the intracranial hemorrhage. the presence of a brain edema without any other lesion requires the antiedematous treatment in order to reduce the intracranial pressure, at the same time as maintaining the a cerebral perfusion pressure within normal limits by the 30 iencean et al emergency treatment principles in intracranial hypertension administration of mannitol, furosemide, dexamethasone, vasopressors, etc. in non-surgical multiple traumatic lesions, a pathogenic therapy is applied in order to decrease the intracranial pressure and stop the evolution of secondary traumatic lesions. • an appropriate cerebral perfusion pressure must be maintained in order to prevent the cerebral ischemia. pcp must be higher than 60 – 80 mm hg. • avoidance of the situations when the cerebral metabolism increases: avoidance of stimuli: aspiration strictly when needed, patient’s transportation, etc. hyperthermia must be vigorously discouraged: antithermic medication, muscular relaxing substances, cold packing up; the moderate hypothermia is an efficient procedure to decrease the cerebral metabolism and for cerebral protection. • the evaluation of the biological parameters with the urgent control of the sanguine glycemia; in the case of the neurosurgical patient with a normal carbohydrate metabolism, it is not recommended to use glucose solutions as this may worsen the brain edema or the cerebral ischemic lesions • the decrease in the arterial and intracranial venous sanguine volume by: head raising, which facilitates the venous drainage and increases the csf removal the hyperventilation decreases pco2 leading to an arterial vasoconstriction that decreases the cerebral sanguine volume at monitoring, in order to hinder at variations: correction of the arterial hypotension (decrease in the cerebral sanguine perfusion), as well as of the high blood pressure(increase in the intracranial pressure) pharmacologic methods to decrease the metabolism and the o2 needs with the reduction of the cerebral sanguine volume (thiopental 4-6 mg/kg or propofol 2-3 mg/kg), but with the cerebral perfusion pressure maintained within normal limits • the signs of ich decompensation – unilateral mydriasis – (the cerebral compliance has been exceeded) require urgent measures of icp decrease and in order to prevent a further icp increase: the occurrence of acute hydrocephalus (by any mechanism) imposes the csf drainage with a ventricular catheter, which rapidly decreases the intracranial pressure, in order to prevent the cerebral herniation, a hemi-craniectomy can be used with a partial resection of the temporal lobe, in cases of malign brain edema, which is resistant to medicine therapies, a hemicraniectomy can be performed with the removal of the cranial bone and the sectioning of the dura mater in order to allow the expansion of the cerebral parenchyma during the acute stage, in brainstem compressions, at the same time as the aggressive medication treatments, the decompression of the posterior cerebral fosse is performed by means of a sub-occipital craniectomy, completed by a ventricular drainage if there is also hydrocephalus. • in the case of an operated patient, with a post-surgery icp monitoring, the normalization of the intracranial pressure values is monitored, as well as the improvement of the cerebral circulation: if the cerebral perfusion pressure is below 70 mm hg, the correction treatment of the intracranial sanguine contribution is started, even if the icp is still high, by means of the administration of colloidal romanian neurosurgery (2013) xx 1: 29 33 31 solutions, intravenous vasopressors, etc. if the intracranial pressure has values of less than 20 mm hg and the cerebral perfusion pressure is above 70 mm hg, the patient is supervised, and the evolution of the icp and pcp values are monitored. if the intracranial pressure is higher than 20 mm hg, the agitated patient is sedated and the permeability of the respiratory paths is checked; the head is raised at 25 30 degrees from horizontal, which leads to a moderate icp decrease through an increase in the venous drainage. the icp normalization during these maneuvers does not require other therapeutic actions regarding the intracranial pressure. • in the case of the patient who has not been in a surgery, but who has an icp monitoring indication, one must survey and correct the intracranial pressure increases and the cerebral perfusion pressure decreases. the icp values of more than 20 mm hg require the agitated patient’s sedation and the check of the respiratory path permeability. the decreased value of the cerebral perfusion pressure requires the specific therapy for the maintenance of the cerebral circulation within normal limits. treatment scheme in traumatic acute intracranial hypertension the therapeutic stages for patients with traumatic brain injury and an acute ich syndrome aim to reduce the icp increases and to maintain the pcp within normal limits. the treatment is performed progressively, depending on the monitoring values of icp, pcp and of the other parameters. (2, 7, 8, 12, 14) • sedation and perhaps a moderate hyperventilation; this is applied as long as icp < 20 mm hg for the first 12 hours: sedatives paco2 is maintained at ≈ 35 mm hg in the case of mechanically ventilated patients when the icp value is above 20 mm hg, one must verify whether the increased pressure values are caused by the agitated state or if there is a mechanical obstruction that may cause the pressure increase. the patient who manifests a psycho-motor agitation is sedated, and, if icp decreases below 20 mm hg, the monitoring, as well as the pathogenic and symptomatic therapy in the intensive care ward are continued. • csf drainage with the ventricular catheter: if icp > 20 mm hg for more than 5 minutes, csf drainage is used whenever needed, as long as the operation proves to be efficient. • use of diuretics: if icp is maintained high above 20 mm hg for more than 5 minutes, the following procedures are used: osmotic diuresis: mannitol administration. ansa diuretics: furosemide is used the combination of these two diuretics is more efficient and is performed while monitoring of osmolarity and of the sanguine electrolytes. • hyperventilation with the maintenance of paco2 at values of 25 – 30 mm hg. hyperventilation causes cerebral vasoconstriction and the icp decrease by decreasing the cerebral sanguine flux. hyperventilation is applied intermittently and it is recommended on the second day after a severe cranial-cerebral traumatism. • hypertensive therapy for the increase in the systemic blood pressure, which can ensure a normal cerebral perfusion pressure if the intracranial pressure is increased. if cerebral contusion lesions are evident (areas of cerebral hemorrhage – hemorrhagic contusion), the systemic arterial pressure 32 iencean et al emergency treatment principles in intracranial hypertension can increase up to 150 – 170 mm hg; if there are no areas of cerebral contusion, the blood pressure can increase to 180 mm hg. • controlled hypothermia, maintaining an approximate temperature of 35 ° c. • administration of a hypertonic nacl solution with a concentration of 7.5 %. • surgical decompression: if the cerebral ct exploration shows that the cerebral edema is very important without revealing a compressive intracranial lesion, performing a large decompressive craniectomy, unilateral or bilateral, must be considered. • the anesthetic administration is performed with an electro-encephalic monitoring up to doses that diminish the eeg activity, using: non-barbituric hypnotic substances: etomidate, propofol. barbituric substances: phenobarbital, thiopental (barbituric coma). • trometamol administration (tham), which generates a partial decrease in co2 pressure and produces a cerebral vasoconstriction. the condition is for the reactivity of the cerebral vessels to co2 to be intact • the lumbar puncture of csf drainage is applied after the exhaustion of the other therapeutic means. the cerebral computer tomography exploration must reveal the presence of the basal cisterns and of the lateral ventricles. the risk of inducing a cerebral hernia by this operation, which is not recommended in intracranial hypertension, is considered to be smaller than the unfavorable evolution by the accentuation of the intracranial pressure increase. (12, 31) treatment scheme in intracranial hypertension of ischemic stroke the emergency treatment of the massive ischemic cerebral or cerebellar stroke, which may lead to an ich syndrome, includes: • securing the vital conditions: free aerial ways, respiration and circulatory function, in the circumstances of a critical condition or of a coma, • the intravenous administration of a recombined activator of tissue plasminogen (rtpa, rtpa) during the first three hours from the beginning of the stroke in a dose of 0.9 mg/kg; maximum 90 mg. (1, 13, 17, 18, 24) the intravenous administration of streptokinase or of other thrombolytic agents does not have the same effects as the rtpa administration. • if it is necessary, a progressive decrease in the systemic blood pressure is performed, • administration of osmotic diuretics (mannitol) if there are any signs of intracranial hypertension decompensation, • hyperventilation when intracranial hypertension decompensation and cerebra hernia occurrence are imminent, • cortico-therapy is not recommended in the treatment of the cerebral edema in cerebral ischemic stroke • surgical intervention if the ich decompensation occurs: decompression and the evacuation of a cerebellar stroke with a compressive effect on the brainstem, perhaps a ventricular drainage too, decompression and the evacuation of a massive cerebral hemispheric stroke, which can reduce the intracranial hypertension, but the surviving patients are left with major neurologic deficits. romanian neurosurgery (2013) xx 1: 29 33 33 corresponding author: a.st. iencean emergency hospital “n. oblu” iasi andrei_steffan@yahoo.com references 1. adelson pd, bratton sl, carney na, chesnut rm, du coudray he, et al the use of barbiturates in the control of intracranial hypertension in severe pediatric traumatic brain injury. pediatr crit care med. 2003; 4: s49-52. 2. adelson pd, bratton sl, carney na, chesnut rm, et al the role of cerebrospinal fluid drainage in the treatment of severe pediatric traumatic brain injury. pediatr crit care med. 2003, 4(3 suppl): s38-9. 3. adelson pd, bratton sl, carney na, chesnut rm, et al use of hyperosmolar therapy in the management of severe pediatric traumatic brain injury. pediatr crit care med. 2003; 4(3 suppl): s40-4. 4. adelson pd, bratton sl, carney na, chesnut rm, et al surgical treatment of pediatric intracranial hypertension. pediatr crit care med. 2003; 4(3 suppl): s56-9. 5. adelson pd, bratton sl, carney na, chesnut rm, et al the use of corticosteroids in the treatment of severe pediatric traumatic brain injury. pediatr crit care med. 2003; 4(3 suppl): s60-4. 6. adelson pd, bratton sl, carney na, et al critical pathway for the treatment of established intracranial hypertension in pediatric traumatic brain injury. pediatr crit care med. 2003; 4(3 suppl): s65-7. 7. allan r, chaseling r. subtemporal decompression for slit-ventricle syndrome: successful outcome after dramatic change in intracranial pressure wave morphology. report of two cases. j neurosurg. 2004; 101( suppl): 214-7. 8. battison c, andrews pj, graham c, et al randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. crit care med. 2005; 33(1): 196-202. 9. berger s, schwarz m, huth r. hypertonic saline solution and decompressive craniectomy for treatment of intracranial hypertension in pediatric severe traumatic brain injury. j trauma. 2002 53(3): 558-63. 10. coppage kh, sibai bm. treatment of hypertensive complications in pregnancy. curr pharm des. 2005; 11(6): 749-57. 11. cruz j, minoja g, okuchi k. major clinical and physiological benefits of early high doses of mannitol for intraparenchymal temporal lobe hemorrhages with abnormal pupillary widening: a randomized trial. neurosurgery. 2002, 51(3): 628-37. 12. demchuk am, burgin ws, christou i, et al. thrombolysis in brain ischemia (tibi) transcranial doppler flow grades predict clinical severity, early recovery, and mortality in patients treated with intravenous tissue plasminogen activator. stroke. 2001; 32: 89–93. 13. diener hc, ringelstein eb, von kummer r, et al. treatment of acute ischemic stroke with the lowmolecular-weight heparin certoparin: results of the topas trial: therapy of patients with acute stroke (topas) investigators. stroke. 2001; 32: 22–29. 14. donnan ga, davis sm. surgical decompression for malignant middle cerebral artery infarction: a challenge to conventional thinking. stroke. 2003; 34(9): 2307. 15. el-watidy s. bifrontal decompressive craniotomy in a 6-month-old infant with posttraumatic refractory intracranial hypertension. pediatr neurosurg. 2005; 41(3): 151-4. 16. figaji aa, fieggen ag, peter jc. early decompressive craniotomy in children with severe traumatic brain injury.childs nerv syst. 2003; 19(9): 666-73. 17. fraser jf, hartl r. decompressive craniectomy as a therapeutic option in the treatment of hemispheric stroke. curr atheroscler rep. 2005; 7(4): 296-304. 18. 18.georgiadis al, suarez ji. hypertonic saline for cerebral edema. curr neurol neurosci rep. 2003; 3(6): 524-30 19. gupta r, connolly es, mayer s, elkind ms. hemicraniectomy for massive middle cerebral artery territory infarction: a systematic review. stroke. 2004; 35(2): 539-43 20. iencean st m a new classification and a synergetical pattern in intracranial hypertension. medical hypotheses, 2002; 58(2): 159-63. 21. iencean stm brain edema a new classification. med hypotheses. 2003; 61(1): 106-9. 22. iencean stm, ciurea av intractranial hypertension, nova science publishers, new york, 2009. 23. kontopoulos v, foroglou n, patsalas j, et al decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered? acta neurochir (wien). 2002; 144(8): 791-6. 24. lee ag, pless m, falardeau j, et al the use of acetazolamide in idiopathic intracranial hypertension during pregnancy. am j ophthalmol. 2005; 139(5): 855-9. 25. owler bk, parker g, halmagyi gm, pseudotumor cerebri syndrome: venous sinus obstruction and its treatment with stent placement. j neurosurg. 2003; 98(5): 1045-55. 26. watling cj, cairncross jg. acetazolamide therapy for symptomatic plateau waves in patients with brain tumors. report of three cases. j neurosurg. 2002; 97(1): 224-6. doi: 10.33962/roneuro-2021-086 correlation of neutrophil lymphocyte ratio to clinical outcomes based on 6 months surveillance on traumatic brain injury patients at haji adam malik general hospital (2018-2020) nindi lizen, ridha dharmajaya, abdul gofar sastrodiningrat, mahyudanil romanian neurosurgery (2021) xxxv (4): pp. 503-507 doi: 10.33962/roneuro-2021-086 www.journals.lapub.co.uk/index.php/roneurosurgery correlation of neutrophil lymphocyte ratio to clinical outcomes based on 6 months surveillance on traumatic brain injury patients at haji adam malik general hospital (2018-2020) nindi lizen, ridha dharmajaya, abdul gofar sastrodiningrat, mahyudanil department of neurosurgery, faculty of medicine, universitas sumatera utara haji adam malik general hospital medan, indonesia abstract introduction: traumatic brain injury is a major cause of disability, death, and economic loss in many countries around the world. the annual incidence in the united states is reported to reach 1.7 million sufferers, in europe it is reported as 262 per 100,000 people per year, and in indonesia, the incidence is increasing by 1% every year. direct and indirect damage resulting from a traumatic brain injury can cause inflammation by activating glial cells and leukocytes, inducing the release of proinflammatory cytokines, and accelerating neurodegeneration and neuroinflammation. recently, the neutrophil-to-lymphocyte ratio (nlr) has been proposed to be a predictor of clinical outcomes for various neurological diseases such as stroke and traumatic brain injury. to put it simply, elevated nlr levels in patients with intracerebral haemorrhage were independently associated with worse clinical outcomes. researchers want to research the relationship between nlr and outcome based on 6 months gos in traumatic brain injury patients at haji adam malik general hospital medan. methods: an observational analytic study with a retrospective cohort design. samples were selected based on inclusion and exclusion criteria from a traumatic brain injury at h. adam malik general hospital medan in 2018-2020. results: the research data were normally distributed and analyzed by the pearson trial; the sig value was obtained. (2-tailed) of 0.798 (p > 0.05), which means there is no between nlr and 6 months gos outcome in traumatic brain injury patients. conclusion: there was no relationship between nlr and outcome based on gos 6 months of traumatic brain injury patients. introduction traumatic brain injury is a major cause of disability, death, and economic loss in many countries around the world.1 the annual incidence in the united states is reported to reach 1.7 million sufferers, in europe it is reported as 262 per 100,000 people per year, and in keywords traumatic brain injury, neutrophils, lymphocytes, nlr, glasgow outcome scale corresponding author: nindi lizen department of neurosurgery, universitas sumatera, indonesia nindi.prokami@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 504 nindi lizen, ridha dharmajaya, abdul gofar sastrodiningrat et al. indonesia, the incidence is increasing by 1% every year.2. based on riskesdas data in 2018 that the incidence of traumatic brain injury increases every year from 8.2% in 2013 to 9.2% in 2018. the highest prevalence is experienced by male patients (11%) with an average age of 15 – 24 years (12.2%) with the most locations in urban areas (9.4%). road traffic accidents still account for the highest proportion (31.4%) with motorcycle riders being the most common cause of traumatic brain injury (72.7%).3 the incidence of traumatic brain injury is also a problem faced by many neurosurgeons, especially in the city of medan. based on data from patients served by smf neurosurgery, h. adam malik hospital medan in 2013 – 2017, traumatic brain injury sufferers were still listed as the most patients with the highest number reported reaching 32.64% in 2014 and the lowest figure found to be 15.83% in 2014. 2017.4 direct and indirect damage resulting from a traumatic brain injury can cause inflammation by activating glial cells and leukocytes, inducing the release of proinflammatory cytokines, and accelerating neurodegeneration and neuroinflammation.5 recently, the neutrophil-tolymphocyte ratio (nlr) has been proposed to be a predictor of clinical outcome for various neurological diseases such as stroke and traumatic brain injury.[6] neutrophil lymphocyte ratio (nlr) is calculated as the ratio of neutrophil cell count to lymphocyte cell count in peripheral blood. nlr is an objective, readily available, inexpensive, and reproducible indicator of inflammation. nlr is also a sign of extensive secondary damage by neutrophils and their products to cerebral tissues and attenuation of cell-mediated immunity associated with systemic inflammation. its prognostic role has been investigated in various neurological disorders such as stroke, multiple sclerosis, and traumatic brain injury. [7] evidence has suggested that patients with higher neutrophil cell counts, and lower lymphocyte cell counts have worse clinical outcomes. in addition, a higher nlr ratio was also associated with a worse clinical outcome at 1 year after traumatic brain injury.[8] it has been found that nlr values in patients with severe traumatic brain injury on the first day of hospital admission are independent predictors of mortality and functional clinical outcome. the power of the nlr test to predict functional clinical outcome in these patients appears to be like the power of the glasgow coma scale (gcs). there is a reported good correlation between nlr and gcs, where higher nlr is associated with lower gcs. however, the association between nlr and mortality was thought to be weaker than that of gcs, indicating the superiority of the gcs in predicting mortality in patients with traumatic brain injury.[9] nlr examination has several benefits for predicting patient prognosis compared to gcs. first, the nlr is more objective than the gcs, and individual judgment is not involved in the nlr. second, the slightest change in the patient's general condition related to the disease may not be directly reflected by the gcs, but the nlr is able to describe these changes. third, gcs assessment is impaired if the patient is sedated or on mechanical ventilation. however, in emergency situations, nlr retrieval takes a long time, which is around 30-40 minutes to get results.[8] to put it simply, elevated nlr levels in patients with intracerebral hemorrhage were independently associated with worse clinical outcomes. researchers want to research the relationship between nlr, and outcome based on 6 months gos in traumatic brain injury patients at haji adam malik general hospital medan. methods this study was an observational analytic study with a retrospective cohort study design to assess the relationship between neutrophil lymphocyte ratio and clinical outcome based on 6-month gos in traumatic brain injury patients. neutrophil lymphocyte ratio data from non-operative traumatic brain injury patients who came to haji adam malik hospital in medan from 2018-2020 were compared to the clinical outcomes of patients based on the glasgow outcome scale (gos) at 6 months post-injury. the independent variable in this study was the neutrophil lymphocyte ratio of patients with nonoperative traumatic brain injury on the first day of coming to haji adam malik general hospital, medan, while the dependent variable included clinical outcomes of patients based on gos 6 months after injury. inclusion criteria to be used as research samples are non-operative brain injury patients, head ct 505 correlation of neutrophil lymphocyte ratio to clinical outcomes scan criteria have features of epidural hematoma, subdural hematoma, intraparenchymal hemorrhage, brain contusion, and subarachnoid hematoma, aged more than 10 years and less than 70 years, and have data neutrophils and lymphocytes on the first day of hospital admission. while the exclusion criteria in this sample were patients with penetrating brain injury, posttraumatic patients who had multiple injuries other than in the head region as evidenced by clinical and radiological findings, patients with a history of previous head injuries, patients with a history of comorbid diseases such as stroke, brain tumors, lung disorders. and heart disease, chronic kidney disease, and previous systemic infectious disease. sample is total sampling of the traumatic brain injury patients who were treated at haji adam hospital medan from 2018 to july 2020 who had met the inclusion and exclusion criteria. the study was conducted at h. adam malik hospital using medical record data of non-operative traumatic brain injury patients from 2018-2020. data collection was carried out after obtaining approval from the usu medical faculty ethics committee. before starting the research, the researcher asked for ethical clearance from the permanent committee for assessing research ethics, faculty of medicine, university of north sumatra. the data obtained were then collected for data processing using spss software version 25.0. to determine the characteristics of patients with traumatic brain injury and to determine the clinical outcome of patients 6 months after traumatic brain injury based on the glasgow outcome scale, categorical data is presented in the form of a frequency distribution of n (%), tables and graphs, and numerical data is presented in the form of mean ± standard deviation. or median. the mortality rate is presented in the form of a rate. to determine the relationship between neutrophil lymphocyte ratio (nlr) on clinical outcomes of patients based on 6-month gos in traumatic brain injury patients, pearson correlation test analysis was performed if the data were normally distributed, or spearman's rank test was performed if the data were not normally distributed. normality test using the kolmogorov-smirnov test (n>50), the data is said to be normally distributed if p>0.05. results in this study, 77 samples from the total sampling met the inclusion and exclusion criteria. the sample data are patients who experienced traumatic brain injury at haji adam malik hospital medan from 2018 2020. the description of the characteristics of the research sample is described as follows: table 1. distribution of samples by gender genders total percentage male 63 81,82% female 14 18,18% total 77 100% based on table 1, it was found that the male research sample amounted to 63 people with a presentation of 81.82% and the female research sample amounted to 4 people with a presentation of 18.18%. from these data, it was found that the male research sample was more than the female patient. table 2. sample distribution based on gcs gcs total percentage 13-15 29 37,66% 9-12 28 36,36% < 9 20 25,98% total 77 100% based on table 2 get the research sample with gcs 13-15 totaling 29 people with a percentage of 37.66%, research samples with gcs 9-12 totaling 28 people with a percentage of 36.36% and research samples with gcs < 9 totaling 20 people with a presentation of 25 ,98%. from these data, it was found that the study sample with gcs 13-15 was more than the gcs 9-12 and <9. table 3. sample distribution by trauma onset onset of trauma total percentage < 24 h 66 85,71% > 24 h 11 14,29% total 77 100% based on table 3, the research sample with trauma onset less than 24 hours was 66 people with a percentage of 85.71% and the study sample with trauma onset more than 24 hours amounted to 11 patients with a percentage of 14.29%. 506 nindi lizen, ridha dharmajaya, abdul gofar sastrodiningrat et al. the data normality test was performed using the kolmogorov-smirnov test. normality test was conducted to determine the difference test to be used next. table 4. sample normality data using the one-sample kolmogorov-smirnov test n 77 normal parametersa,b mean ,0000000 std. deviation 1,94132437 most extreme differences absolute ,318 positive ,274 negative -,318 test statistic ,318 asymp. sig. (2-tailed) ,000c from table 4, the results of the normality test of the research sample data with a significance value (p < 0.05) suggest that the data are normally distributed. data with normal distribution will be tested for pearson correlation. to determine the correlation between gcs and 6month gos outcomes in patients with traumatic brain injury at h. adam malik hospital medan, the pearson correlation test was performed. table 5. gcs correlation test results data with 6-month gos outcomes gcs gos g c s pearson correlation 1 ,783** sig. (2-tailed) ,000 n 77 77 g o s pearson correlation ,783** 1 sig. (2-tailed) ,000 n 77 77 ** correlation is significant at the 0.01 level (2-tailed). from table 5. obtained a sig. (2-tailed) value of 0.00 and a positive value on the pearson correlation, which means that there is a positive correlation between gcs and 6-month gos outcomes, with a p value of < 0.05. to determine the correlation between nlr and 6month gos outcomes in patients with traumatic brain injury at h. adam malik general hospital medan, the pearson correlation test was performed. table 6. nlr correlation test results data with 6 months gos clinical outcome nlr gos n l r pearson correlation 1 -,030 sig. (2-tailed) ,798 n 77 77 g o s pearson correlation -,030 1 sig. (2-tailed) ,798 n 77 77 from table 6. sig value is obtained. (2-tailed) of 0.798 (p > 0.05) which means that there is no correlation between nlr and 6-month gos outcomes in traumatic brain injury patients. conclusion the nlr correlation test has been carried out on the clinical outcome of traumatic brain injury patients based on 6 months gos which obtained a sig value. (2tailed) of 0.798 (p > 0.05) which means that there is no correlation between nlr and 6-month gos outcomes in traumatic brain injury patients. the results in this study are different another which stated that there is evidence of a correlation between high nlr and the worst functional clinical outcome and vice versa, lower nlr has a clinical outcome good functionality.9 an nlr value >15.63 at first hospital admission was a predictor of poorer clinical outcome and mortality at 28 days. chen et al also reported that nlr levels with a cut-off value of 18.16 were correlated with clinical outcomes with a sensitivity of 74.3% and a specificity of 72.9%.8 in this study, different results were obtained from previous studies, where there was no relationship between nlr and clinical outcomes of traumatic brain injury patients. it is suspected that many factors can influence the results of this study. one of the types of intracranial lesions that occur due to impact on the head is thought to affect the nlr value itself. nlr values were seen to be significantly higher in brain injury patients with diffuse axonal injury than in patients with cerebral edema, intracerebral hemorrhage, subdural or epideral hematoma, and subarachnoid hemorrhage. in this study sample, there were heterogeneous types of intracranial lesions which were thought to have an impact on the results of the study. thus, the same study can be carried out again with more homogeneous intracranial lesions from each study sample so that it can have maximum results.[10] 507 correlation of neutrophil lymphocyte ratio to clinical outcomes in addition to the type of intracranial lesion due to a blow to the head, the onset of trauma upon admission to the hospital and the time the patient's blood sample was taken were thought to also play a role in nlr levels. nlr levels peak in the first 24 hours of onset of traumatic brain injury. in the sample of this study, 14.29% of the sample with onset more than 24 hours after the incident of traumatic brain injury before routine blood tests were performed. this is thought to affect the results of this study.[6] the research sample size is also suspected to affect the results of this study. small differences in clinical outcomes can be statistically significant if the number of samples is very large. on the other hand, a very significant clinical difference may not be statistically significant if the sample is too small. many studies are not published because the results are not statistically significant even though they are clinically important.11 from this study obtained 77 samples from the total sampling that have met the inclusion and exclusion criteria. there are many complicating factors experienced by researchers so that the number of samples obtained is too small. thus, other methods in determining the number of research samples, such as using a probability formula with a high confidence interval, can be an alternative for the next research to obtain maximum research results. discussion: there was no relationship between nlr, and outcome based on gos 6 months of traumatic brain injury patients. further research is needed with a larger sample size to obtain optimal results. references 1. sastrodiningrat ag. traumatik brain injury: primary brain damage, secondary brain damage, management and neuro critical care. neurosurgery lecture notes. usu press. hal 125-182. usu press. 2. nguyen r, fiest km, mcchesney j, et al. the international incidence of traumatic brain injury: a systematic review and meta-analysis. can j neurol sci j can sci neurol. 2016;43(6):774-785. doi:10.1017/cjn.2016.290. 3. mahyudanil m, bajamal ah, sembiring rj, dharmajaya r. the effect of progesterone therapy in severe traumatic brain injury patients on serum levels of s-100β, interleukin 6, and aquaporin-4. open access maced j med sci. 2020;8(b):236-244. doi:10.3889/oamjms.20 20.3974 4. dharmajaya r. cidera kepala di rsup h. adam malik medan th. 2013-2017. trauma kepala. 2018th ed. usu press. 5. prins m, greco t, alexander d, giza cc. the pathophysiology of traumatic brain injury at a glance. dis model mech. published online january 1, 2013:dmm.011585. doi:10.1242/dmm.011585 6. sabouri e, majdi a, jangjui p, rahigh aghsan s, naseri alavi sa. neutrophil-tolymphocyte ratio and traumatic brain injury: a review study. world neurosurg. 2020;140:142-147. doi:10.1016/j.wneu.2020.04.185 7. zhao j-l, du z-y, yuan q, et al. prognostic value of neutrophil-to-lymphocyte ratio in predicting the 6month outcome of patients with traumatic brain injury: a retrospective study. world neurosurg. 2019;124:e411e416. doi:10.1016/j.wneu.2018.12.107 8. chen w, yang j, li b, et al. neutrophil to lymphocyte ratio as a novel predictor of outcome in patients with severe traumatic brain injury. j head trauma rehabil. 2018;33(1):e53-e59.doi:10.1097/htr.0000000000000320 9. siwicka-gieroba d, malodobry k, biernawska j, et al. the neutrophil/lymphocyte count ratio predicts mortality in severe traumatic brain injury patients. j clin med. 2019;8(9):1453. doi:10.3390/jcm8091453 10. lin y, wen l. inflammatory response following diffuse axonal injury. int j med sci. 2013;10(5):515-521. doi:10.7150/ijms.5423 11. sastroasmoro s, ismael s. dasar-dasar metodologi penelitian klinis. vol 2. 3rd ed. jakarta : sagung seto; 2010. microsoft word 5iacobg_lumbarl romanian neurosurgery (2013) xx 4: 333 341 333 lumbar l4-l5 ganglion cyst with hemicauda equina syndrome. report of a case and review of the literature gabriel iacob1, bogdan rotund2 1prof. phd, neurosurgery clinic, umph “carol davila” bucharest, university hospital bucharest, romania 2senior neurosurgeon, university hospital bucharest, romania abstract mostly associated with degenerative facet joints and spondylolisthesis, symptomatic lumbar juxta facet cysts ganglion and synovial cysts are uncommon lesions of the spine. they can mimic herniated discs, causing low back pain, radiculopathy or even cauda equina syndrome; also some of them are associated with spinal instability. referring to a case with hemicauda equina syndrome where microsurgical decompression was performed with very good result; alternative treatment solutions are discussed: conservative therapy for symptomatic lesions is often unsuccessful, spinal fusion should be made for those cases with spinal instability, although there are reports of spontaneous resolution of these cysts as well as the symptoms associated with them. key words: ganglion cyst, synovial cyst, juxtafacet cyst, degenerative spine disease, cauda equine syndrome, spinal fusion. introduction although juxtafacet cysts are lesions noted as incidental findings associated with spinal facet joints on imaging studies of the spine (computed tomography ct and magnetic resonance imaging – mri); in some patients, they may produce symptoms: nerve root and/or spinal cord compression (1-9). in the lumbar area juxta facet cysts are mostly associated with degenerative facet joints and spondilolisthesis, generating back and radicular pain. patients with extradural degenerative lesions associated with with cauda equina syndrome generated by a juxtafacet cyst are rare (10). despite histological differences between ganglion and synovial cysts, physicians refer to both entities as synovial cysts because there are no differences concerning treatment and prognosis (11-14). method a female aged 47 years old with a hemicauda equina syndrome, with intense left radiculopathy: left motor l5, s1 (-4) deficits and sensory disturbances, no bowel and bladder dysfunction, installed four days before admission. there was no history of trauma. before surgery the patient had received: simple and flexion x-p: normal, without associated spinal instability; lumbar spinal computed tomography: round, left, low density cyst at l4-l5, in contact with the left articular process, compressing l5 root. magnetic resonance imaging (figure 1) in t2 weighted sequences shows a left, epidural, hyperintense mass at l4-l5, compressing root and dura, in contact with 334 iacob and rotund lumbar l4-l5 ganglion cyst with hemicauda equina syndrome the left articular process and the bulging disc l4. on sagital t2 weighted sequences, the outer wall appear hypointense. the patient was operated using a left hemilaminectomy suited by a microsurgical resection of the lumbar cyst, sparing the facet joint, without surgery related complications. lateral left recess was adequately decompressed as the l5 and s1 nerve roots. it was one cyst, without attachment to the left articular process. the removed cyst were histologically evaluated. macroscopic findings (figure 2 a) has shown a spherical, 1.3 diameter cyst, slate gray-pink, renitent consistence, well delineated wall, containing on section a fibrous capsule limiting yellow, thick, jellylike, mucinous fluid. the microscopic findings (figure 2 b, c) has shown a wall cyst of fibrous connective tissue, a fluid with high concentration of albumin, globulin and hyaluronic acid, without hemorrhagic material or hemosiderin deposits; no synovial lining membrane was found. results patient postoperative period was uneventful; one week after, no pain, without neurologic deficits. 2 months after surgery, she has no pain, no instability and on a new mri, there was no case of a recurrent cyst. a b figure 1 a. lumbar spinal mri in t2 weighted sequences shows a left, epidural, hyperintense mass at l4-l5, compressing root and dura, in contact with the left articular process and the bulging disc l4. b. sagital t2 weighted sequences, the outer wall appear hypointense. romanian neurosurgery (2013) xx 4: 333 341 335 a b c figure 2 resected cyst, macroscopic and microscopic findings: a. macroscopic view of the cyst, b,c ganglion cyst wall (pseudocyst): absence of synovial cell lining with connective tissue and foci of myxoid degeneration discussion based on nabors classification for spinal meningeal cysts (15) there a three main groups: meningeal cysts: epidural without neural tissue, epidural with neural tissue – similar terms perineural or tarlov cysts, intradural (anterior, posterior or lateral of the thoracal spinal cord, leated to a trauma, a hemorrhage or inflammation with secondary arachnoiditis, communicants or non communicants) epidural, non meningeal cysts include juxta facet cysts (synovial and ganglionar cysts), traumatic pseudomeningocele intra or extraspinal, containing or not roots, also tumoral lesions with cysts: schwannomas, dermoids, pigmented villonodular synovitis, metastasis neuroenteric cysts: rare, intradural, anterior extramedullary, uni or polilobular, interesting several spinal segments, frequently associated with congenital spinal anterior vertebral anomalies also klippelfeil syndrome, diastematomyelia, spina bifida. ayberk von gruker in 1880 (cited by 6) in a postmortem examination, reported the first description of a spinal synovial cyst and baker 1885 (cited by 9) explain synovial cysts adjacent to articulations. vosschulte and börger (16) first described in 1950 spinal synovial cysts as entities found arising at or around the joint capsule of the spinal facets, that cause symptoms by compressing nerves and many years the terms: synovial cyst, ganglion cyst, pseudocysts were used synonymously. kao (17)(18) describe in 1968 and in 1974 proposed the term juxta-facet (juxta = near or nearby) cysts; including the entities of synovial and ganglion cysts to the spinal facet joints or arising from the ligamentum 336 iacob and rotund lumbar l4-l5 ganglion cyst with hemicauda equina syndrome flavum. distinction between these two types of cysts could be difficult, also clinically unimportant (9) (19) (20). hsu (21) reffer to intra-spinal facet cysts regardless of whether synovial lining cells present or not, but with similar clinical manifestation. although there are histological differences between synovial and ganglion cysts, their treatment and prognosis are identical. that is why they are grouped together as juxtafacet cysts or in the stricter sense of word “cystic formations of mobile spine” (=cyfmos), but in practice it is common for physicians to refer to both entities as synovial cysts (22). disposed near articulations, either attached or adjacent to spinal facet joints (1, 3-5, 7, 11, 12, 21-23), spinal synovial or ganglion cysts are relatively small lesions mean diameter 1 cm, found incidentally in all spinal segments: most frequently in the lumbar spine (88-99%), especially at the most mobile interspace l4-l5 (12), up to 8% arise in the thoracic region and 1 to 4% are commonly found in the cervical area (35, 24). although juxtafacet cysts are usually unilateral, they are found bilaterally, most commonly at the l4-l5 level, in up to 54% of patients in some series, associated with significant spinal instability and the potential need for spinal fusion. more precisely these cysts could be placed: ventromedial to the facets as in our case, dorsal to the facet joints (and often asymptomatic), in the interlaminar space, with facet attachment most common, without nerve root compression; dorsal midline – uncommon, with involvement of dura & the base of neural arch; at the interspinous ligament, clinically unimportant or attached to inner side of ligamentum flavum, without facet attachment. their occurrence and location seem to be associated with degenerative arthritis of facet joints in up to 90% and with spondylolisthesis in up to 100% of patients in some series (1, 2, 6-9, 21). on anatomo pathological grounds juxta-facet cysts are: synovial cysts represent a true cyst. they are small cystic growths that occur adjacent to and attached to synovial tissue– lined joints, such as the spinal facet joints with a narrow connecting pedicle, which connects their cystic centers to the cavities of their parent joints, lined by a true synovium, contain synovial fluid. they are not only found in the spine, but also in the knees, hips, and elbows. grossly, synovial cysts contain clear, serous or xanthochromic fluid and occasionally have calcifications within their walls. histologically, these lesions have a normal synovial lining, but they may also contain hemosiderin, giant cells or inflammatory cells. synovial cysts may also contain hemosiderin deposits (occasional hemmorhage) because they occasionally bleed within themselves, causing acute growth and exacerbation of symptoms; or even calcification (1-8, 22) ganglion cysts are pseudocysts, occur in moveable tissues (the most common site of ganglion cyst is wrist, also knees, feet and elbows), are similar in size to synovial cysts, but lack a true synovial lining, more spherical, have no or little attachment to joint; as a result of advanced degeneration of soft spinal tissue or from a synovial cyst after degeneration or destruction of synovial lining membrane due to a chronic trauma. grossly, ganglion cysts contain viscous, proteinaceous fluid. on histological examination, their walls are composed of well-vascularized fibrous connective tissue. cyst fluid is thicker and romanian neurosurgery (2013) xx 4: 333 341 337 more viscous than normal synovial fluid; it could be highly viscous, sticky, jelly-like mucinous fluid or clear; never contain hemorrhagic materials (21, 22). the etiology of jfc is unknown (1, 6, 12); several possibilities may play a role in the pathogenesis: synovial fluid extrusion through a defect or rupture in the joint capsule most likely theory, even by latent growth of a developmental rest. increased motion and chronic micro trauma are favorable factors myxoid degeneration and cyst formation in the collagenous connective tissue various sites fibroblasts proliferation with increased hyaluronic acid production and secondary cyst formation pluripotential, non specific mesenchymal cell proliferation depending on topography, juxtafacet cysts are crowding the spinal canal, compressing the spinal cord and causing myelopathy, neurogenic claudication. in the lumbar area, in consequence of a lumbar spine stress (exercise loading) in addition to a degenerative lesion of the soft lumbar tissue synovial and ganglion cyst are uncommon cause of dorso-lateral root compression, associated or not with lateral recess and spinal stenosis (6, 23). symptoms depend on the pattern of growth, especially at l4-l5: upward and anterior growth, compresses l4 root, downward extension and intraspinal expansion compresses l5 root, extraspinal, dorsal to the facet joints growth could be asymptomatic – majority. patients with juxtafacet cysts present insidiously or acutely, due to intracystic or epidural hemorrhage from the lesion (10, 25, 26) with one or more of the following conditions: lower back pain with dull ache in the back radiating to the hip, unilateral or bilateral radiculopathy, neurogenic claudication, lumbar extension is usually restricted but lumbar flexion is maintained, motor deficit (12%), sensory loss (26%) reflex changes (12), cauda equina syndrome. rarely hemorrhage occur into the cyst, mostly in the lumbar region with acute intractable radiculopathy that is the result of sudden increase in the cyst’s volume with hematoma. bleeding in the cyst is the result of spontaneous rupture of fragile neoangiogenic vessels of the cyst’s wall, although their rupture in traumatic events and anticoagulant therapy has so been reported causing an acute cauda equina syndrome (10). juxtafacet cysts were usually discovered incidentally during surgery before the advent of ct and mr imaging, but with the increasing use of neuroimaging in the evaluation and management of cases of degenerative disease of the spine, they are commonly seen on preoperative diagnostic studies. their presence and potential role as a generator of symptoms must be considered (1-4, 6, 7, 11, 12, 21-23). juxtafacet cysts were associated with disc herniations, other epidural mass, degenerative spinal instability as well as other elements of degenerative spine disease. diagnostic studies should include: dynamic flexion/extension x-ray, computed tomography (ct) and magnetic resonance imaging (mri). ct scans reveal juxtafacet cysts as a soft tissue low-density, round lesions adjacent to facets, occasionally with calcification within their outer walls at the articulation level, projecting into the epidural space postero-lateral after contrast we can see contours. on ct myelography, contrast material is typically not seen within the center of a juxtafacet cyst. 338 iacob and rotund lumbar l4-l5 ganglion cyst with hemicauda equina syndrome mri is the tool of choice for diagnosis of juxtafacet cysts (4), with a typical pattern consisting of a hyperintense center and hypointense rim, adjacent to the facet joints on t2-weighted sequences. their proteinaceous contents may appear hyperintense to cerebrospinal fluid. on t1weighted mr imaging sequences, juxtafacet cysts appear as hypointense masses, most commonly located dorsal to the neural elements in the lumbar spinal canal. in contrast, herniated discs are commonly located ventral to the neural elements. their outer walls may enhance weakly on both ct and mr imaging studies (12,14). in the mri myelography the lesion appeared as a round extradural posterolateral filling defect. in case of bleeding cysts there are different aspect of mri imaging; ex: for subacute hemorrhage in the cyst we can saw inhomogeneous/isointense centers, intracystic hemorrhage can be predicted radiologically by an mri (inhomogeneous center in t2-weighted images and irregular hyperintensity in t1-weighted images) (10, 23, 24), but there is no correlation with the acute onset of symptoms. because of similar aspect for synovial or ganglionar cysts on mri, it’s mandatory to precise that only histology may differentiate them (4, 21, 22). optimal treatment for juxta facet cysts is a matter of controversy (1, 6, 7, 11, 12, 19, 21, 27, 28, 30, 34, 35). although relevant reports in the international literature are increasing, the controversy about conservative versus surgical treatment and the need for concomitant fusion still exists. the optimal treatment is not known. there are several attitudes: conservative treatment has been proposed by certain authors, including: bed rest, symptomatic treatment: analgesic medications, spine stabilization exercises, lower-extremity stretching, orthopedic corsets with disappointing results (27). therefore there are observations that some of these cysts may decrease in size or collapse spontaneously, similar to symptomatic disc herniations, which can regress over time (28). there is four cases reports of cysts that resolved spontaneously (29, 30), but it is infrequent. another conservative procedures for management of intraspinal juxtafacet cysts are: percutaneous ct-guided puncture cyst aspiration plus intracystic injection of steroid drugs (31) associated with frequent recurrence, transforaminal epidural injections of steroid agents may be effective in temporary relieving the inflammatory component; however, enlarging a mass lesion with in the spinal canal may also be associated with risks of neural compromise. there is little information available on the efficacy and outcome with treatment of lumbar facet joint synovial cysts by percutaneous, fluoroscopic, facet joint steroid injections, with cyst distention and rupture with shortterm improvement or no improvement at all (32). several complications such as dural puncture, spinal nerve injury, bleeding, and infection have been reported (33). surgical resection is the treatment of choice for symptomatic juxtafacet cysts in all cases of intractable pain or neurologic deficit (1, 3, 5-9, 11-13, 19, 20, 34-37). under general anesthesia, in the prone position, a wide exposure is encouraged to achieve complete resection hemilaminectomy on the symptomatic side is performed, suited by partial medial facetectomy, excision of thickened ligamentum flavum, foraminotomy. there romanian neurosurgery (2013) xx 4: 333 341 339 are series of patients with juxta facet cysts treated with minimally invasive decompression in conjunction with hemilaminotomy and cyst excision through a serial dilator/tubular surgical retractor system (6, 36, 37). because their usual location is in the lateral recess, microscopic piecemeal excision of the compressing cyst involves decompression of the traversing nerve root at that level as well as the exiting root above, along with adequate de compression of the lateral recess without fusion (13, 36, 37). sometimes removal can be difficult, because juxtafacet cysts are often firmly adherent to the duramater; some authors recommend careful application of electrocautery to the facet joint to prevent recurrence (12). partial cyst resection may lead to recurrent lesions and to a return of symptoms (12, 20, 38, 39). for those cases with degenerative listhesis, with associated instability primary fusion after resection of these lesions should be considered (1, 3, 6-8, 11-13, 19, 21, 22, 3539). similar to a herniated disc, lumbar stenosis, or spondylolisthesis, these lesions are not the cause, but instead a manifestation of spinal instability that may or may not be clinically significant (34). many authors reported that no difference in surgical outcome was found between patients having fusion and those who did not have it, while others concluded that, a concomitant fusion procedure may be performed in selected cases (19, 20, 38, 39). métellus et al. (12) has concluded that there is no reliable criterion that allows the development of a symptomatic spinal instability to be predicted in patients with preoperative spondylolisthesis and therefore, fusion as a first line procedure is still debatable. others have mentioned an association between spinal cysts and spondylolisthesis/instability and better surgical outcomes in patients having fusion than in those who did not have it (20, 21). closure is done with a submuscular drain). using these technique, generally all patients got benefit (70% 80% good results up to 100%) (38), with few related complications (dural tears in up to 4% of primary surgeries and up to 12% of secondary surgical procedures), with very good surgical outcomes and short duration of hospitalization (three days) (39). conclusions juxtafacet cysts (ganglion or synovial) are uncommon lesions of the spine with unclear etiology: micro trauma, a manifestation of spinal instability, more frecquent in the lumbar area, especially at l4-l5 level, generating lumbar radicular pain or even cauda equine syndrome. mri is the neuroinvestigation tool of choice for diagnosis. medical management (even puncture of the cyst) is less successful than it is for a herniated nucleus pulposus, does not adequately improve symptoms in patients with intraspinal juxta facet cysts and radicular signs. microsurgical resection of the cyst is the best treatment strategy, a safe and effective treatment for those symptomatic intraspinal juxta facet cysts unresponding to conservative treatment, associated with excellent long-term outcome also very low morbidity. for surgical exposure and complete decompression of the neural elements, as little bone removal as is deemed necessary to allow safe dissection of adhesions to the duramater is sufficient. symptomatic patients due to mechanical instability before surgery or in cases where wide bone decompression was required, a fusion should be considered to solve 340 iacob and rotund lumbar l4-l5 ganglion cyst with hemicauda equina syndrome iatrogenic instability, never as a first line procedure. recurrences and surgical complications are rare. references 1.lyons m.k., atkinson j.l. et al. surgical evaluation and management of lumbar synovial cysts: the mayo clinic experience, j. neurosurg. 2000, 93(1 suppl): 537 2.tillich m., trummer m., et al. symptomatic intraspinal synovial cysts of the lumbar spine: correlation of mr and surgical findings, neuroradiology 2001, 43:1070–5 3.trummer m., flaschka g., et al. diagnosis and surgical management of intraspinal synovial cysts: report of 19 cases, j neurol neurosurg psychiatry 2001, 70:74–77 4.schmid g., willburger r., et al. lumbar intraspinal juxtafacet cysts. mr imaging and ct-arthrography, rofo 2002, 174:1247–52 5.nakamura s., miyauchi h., et al. spinal juxta-facet cyst : report of seven cases and review of the literature, clinical orthopaedic surgery 2004, 39, 1, 85-92 6.epstein n. lumbar synovial cysts: a review of diagnosis, surgical management and outcome assessment, j spinal disord tech 2004, 17:321–325 7.choudhri h.f., perling l.h. diagnosis and management of juxtafacet cysts, neurosurg focus 2006, 20 (3):e1, 1-4 8.ayberk g., özveren f., et al. lumbar synovial cysts: experience with nine cases, neurol med chir (tokyo) 2008, 48:298–303 9.lommers e., gillet p. – le cas clinique du mois: une cause inhabituelle de sciatalgie necessitant un traitement chirurgical: le kyste arthrosynovial lombaire, rev. med. liege, 2010, 65, 12: 665-668. 10.abolfazl r. – bleeding in a lumbar juxtafacet cyst with cauda equina syndrome: report of a case and review of the literature, wscj 2011, 2: 46-51 11.boviatsis e.j., stavrinou l.c., et al. spinal synovial cysts: pathogenesis, diagnosis and surgical treatment in a series of seven cases and literature review. eur spine j. 2008, 17:831–7 12.métellus p., fuentes s., et al. retrospective study of 77 patients harbouring lumbar synovial cysts: functional and neurological outcome, acta neurochir (wien) 2006, 148(1):47-54 13.deinsberger r., kinn e., ungersböck k. microsurgical treatment of juxta facet cysts of the lumbar spine, j spinal disord tech. 2006, 19(3):155-60 14.christophis p., asamoto s., et al. “juxtafacet cysts”, a misleading name for cystic formations of mobile spine (cyfmos), eur spine j. 2007, 16(9): 1499–1505 15.nabors mw, pait tg, et al. updated assessment and current classification of spinal meningeal cysts., j neurosurg. 1988, mar, 68(3):366-77 16.vosschulte k., borger g. – anatomische und funktionelle untersuchungen uber den bandscheibenprolaps, langenbecks arch chir 1950, 265: 329-355 17.kao c.c., uihlein a., bickelr w.h.lumbar intraspinal extradural ganglion cyst, j. neurosurg. 1968, 29: 168-72 18.kao c.c.,winkler s.s., turner j.h. synovial cyst of spinal facet, j.neurosurg 1974, 41: 372-6 19.pirotte b., gabrovsky n., massager n., et al. synovial cysts of the lumbar spine: surgery-related results and outcome. j neurosurg. 2003, 99(1 suppl):14–9 20.bydon a., xu r., et al. recurrent back and leg pain and cyst reformation after surgical resection of spinal synovial cysts: systematic review of reported postoperative outcomes, spine j. 2010, 10:820–6 21.hsu k.y., zucherman j.f. et al. lumbar intraspinal synovial and ganglion cysts (facet cysts). ten-year experience in evaluation and treatment. spine 1995, 20:80–9 22.christophis p., asamoto s., et al. “juxtafacet cysts”, a misleading name for cystic formations of mobile spine (cyfmos), eur spine j. 2007, 16(9): 1499–1505 23.doyle a.j., merrilees m. synovial cysts of the lumbar facet joints in a symptomatic population: prevalence on magnetic resonance imaging, spine 2004, 29:874–8 24.miwa m., doita m., et al: an expanding cervical synovial cyst causing acute cervical radiculopathy, j spinal disord tech 2004, 17:331–333 25.wait s.d., jones f.d. et al. symptomatic epidural hematoma caused by lumbar synovial cyst rupture: report of two cases and review of the literature, neurosurgery 2005, 56: e1157 26.wang y.y., mckelvie p, et al. trauma as a precipitant of haemorrhage in synovial cysts. j clin. neurosci. 2004, 11:436–439 27.shah r.v., lutz g.e. lumbar intraspinal synovial cysts: conservative management and review of the world's literature, spine j. 2003, 3:479–88 28.de beukelaar j.w., dallenga a., et al. juxta facet cyst of the lumbar spine: an uncommon cause of lumbar radiculopathy, ned tijdschr geneeskd. 2010, 154:a1673 29.swartz p.g., murtagh f.r. spontaneous resolution of an intraspinal synovial cyst. ajnr 2003, 24:1261– 1263 30.houten j.k., sanderson s.p., et al.: spontaneous regression of symptomatic lumbar synovial cysts. report of three cases, j. neurosurg 2003, 99 (2 romanian neurosurgery (2013) xx 4: 333 341 341 suppl):235–238 31.lim a.k., higgins s.j., et al. symptomatic lumbar synovial cyst: management with direct ct-guided puncture and steroid injection, clinradiol. 2001, 56:990–3 32.allen t.l, tatli y, lutz g.e. fluoroscopic percutaneous lumbar zygapophyseal joint cyst rupture: a clinical outcome study, spine j. 2009, 9:387–95 33.martha j.f., swaim b., et al. outcome of percutaneous rupture of lumbar synovial cysts: a case series of 101 patients, spine j. 2009, 9:899–904 34.epstein n. lumbar laminectomy for the resection of synovial cysts and coexisting lumbar spinal stenosis or degenerative spondylolisthesis: an outcome study, spine 2004, 29:1049–1056 35.el shazly a.a., khattab f.m. surgical excision of a juxtafacet cyst in the lumbar spine: a report of thirteen cases with long-term follow up, asian j. neurosurg. 2011, 6(2): 78–82 36.sandhu f.a., santiago p., et al: minimally invasive surgical treatment of lumbar synovial cysts. neurosurgery 2004, 54:107–112 37.oertel m.f., ryang y. et al. – microsurgical therapy of symptomatic lumbar juxta facet cysts. minim invasive neurosurg. 2003, 46(6): 349-353. 38.banning c.s., thorell w.e., et al. patient outcome after resection of lumbar juxtafacet cysts, spine 2001, 26:969–972 39.khan a.m, synnot k., et al. lumbar synovial cysts of the spine: an evaluation of surgical outcome, j spinal disord tech. 2005, 18:127–31 microsoft word iordachealin_intracranial_f.docx romanian neurosurgery (2012) xix 1 intracranial pressure monitoring in neurosurgery department in iasi – latest developments alin iordache1, raluca munteanu2, mihaela cosman2, dana-mihaela turliuc1 1“gr.t. popa” university of medicine and pharmacy, iasi 2“prof. dr. n. oblu” clinical hospital, iasi abstract severe head trauma remains an important public health issue and the intracranial pressure monitoring is useful in indicating the patients prognosis, variation especially elevated intracranial pressure were associated with a poor prognosis. we illustrate some cases where we insert the monitoring system (intraparenchymal or intraventricular) and the neurological evolution. keywords: intracranial pressure monitoring, severe head trauma, camino monitor. introduction the brain functions and survival depends on cerebral blood flow (cbf). this is a parameter difficult to estimate. in turn cbf depends on cerebral perfusion pressure (ccp) which is associated with intracranial pressure (icp-easier to quantify). in severe head trauma patients recent study suggested that elevated icp is more dangerous than changes in cpp. the normal range of icp varies with age (in adults < 10 -15 mmhg). in 2010 our department of neurosurgery made an important step in the management of head trauma patients when we introduced the intracranial pressure monitoring. (1, 7) icp monitoring was made according with guidelines: 1. neurologic criteria: severe head injury (gcs<= 8); 2. an abnormal admitting head ct (contusion, cerebral edema, hematoma with or without midline shift >5mm / cisterns compressed or absent ); 3. a normal ct but with more them 2 risk factors: age >40 yrs, decerebrate or decorticate posturing on motor exam (unilateral or bilateral ), systolic blood pressure <90mmhg (3, 11). there are different types of system for icp monitoring (6): 1. intraventricular catheter (icv) golden standard: advantages: good accuracy in measuring the pressure, allows therapeutic csf drainage; disadvantages: may be difficult to insert into displaced or compressed ventricles, obstruction of the fluid column (blood clot); 2. subarachnoid catheter: advantages: infectious and hemorrhagic complication are decreased (1 %); disadvantage: surface of brain may occlude lumen resulting in false readings; 3. intraparenchymal catheter: advantage: good accuracy in measuring the pressure; disadvantage: does not allow therapeutic csf drainage. alin iordache et al intracranial pressure monitoring in neurosurgery department in iasi material and methods in our study the major criteria for icp monitoring was gcs <8 were excluded those patients with intracranial surgical lesions who were operated. the intervention was important because most of the patients with severe head injury were forensic cases and from ethical point of view we had to evacuate any diagnosed lesions even though the icp was not increased. the system used for icp monitoring was camino spm-1 (figure 1a) made by integra. this type of monitor uses a transducer with optic fiber to record information, the reference point is the atmospheric pressure. we used intraventricular catheter 1104hm type (figure 1c) with optic fiber transducer and intraparenchymal catheter 1104b type (figure 1b) when the ventricles size were reduced. the ventricular catheter was placed in the frontal horn in the kocher’s point. a b c figure 1 a camino spm-1 system; b intraparenchymal catheter; c intraventricular catheter. the drainage system 1104hb and 1104b are sterile and disposable. the specialty literature shows that the incidence of infectious complication increases after 5-7 days of use. our monitoring study was a retrospective one , the author was directly involved in monitor placing and tracking patient progress. the study lot was formed by 10 patients. romanian neurosurgery (2012) xix 1 illustrive cases 1. female age 30 presents with a severe head trauma from a car accindent. other organic lesions are excluded by thoracoabdominal-pelvis ct scan. her neurologic status was gcs=4 with hyperextension of upper and lower left limbs and babinski sign positive bilateral. craniocerebral ct scan shows diffuse cerebral edema in the right hemisphere with mild subfalcine herniation, frontal subarachnoid hemorrhage (figure 2a) on the right side, multiple hemorrhagic petechiae lesions 23mm diameter located predominantly frontal bilatera (figure 2b) and left temporal bone fracture. transcranial doppler examination by temporal bone window reveals the presence of flow in both sylvian arteries and the flow speed beeing 60 cm / s bilaterally. the patient presents indirect radiological signs of diffuse axonal injury, but also presents the clinical features of intracranial pressure monitoring. a b figure 2 a subarachnoid hemorrhage b petechiae lesions regarding the small size of ventricles and cerebral edema predominantly on the right hemisphere we decided to place an intraparenchymatos catheter on the right side (figure 3). figure 3 the pressure transducer alin iordache et al intracranial pressure monitoring in neurosurgery department in iasi the initial value of icp was 25 mmhg and after administration of mannitol decrease, reaching at 18 mmhg. immediately postoperative neurological evolution shows some improvement. the patient has subsequently intracranial pressure values of 3 to 6 mmhg. ct examination was performed for radiological control. there is improvement of cerebral edema. during the second day neurological status deteriorates. another ct scan is performed which confirms the transducer drift (figure 4) and shows the emphasize of the petechiae lesions (figure 5). a b figure 4 a transducer present b transducer absent figure 5 hemorrhagic petechiae lesions he was intubated for 10 days, the neurological evolution was slightly favorable with discrete movement on her left extremities. at 6 month she recovered quite well with slight hemiparesis on the left side and the mri control showed no residual sequeles. 2. a 29 years old patient presents with a severe head trauma, thoracic contusion from a car accident. the neurological exam relieves areactive pupils, left ear otorrhea and gcs=5. cranio-cerebral ct scan shows subarachnoid hemorrhage, left temporal and right frontal hemorrhagic contusion, temporal bone fracture, diffuse cerebral edema (figure 6), subdural hematoma on the right hemisphere and anterior interhemispheric hematoma (figure 7a). the ventricular system appears slightly asymmetric with left side subfalcine herniation phenomena (figure 7b). the neurological status worsens and he become coma grade iv. we put a parenchymal catheter on the left side and a ventricular catheter in the right ventricle (figure 8). romanian neurosurgery (2012) xix 1 a b figure 6 a subarachnoid hemorrhage, temporal hemorrhagic contusion, left temporal bone fracture; b frontal hemorrhagic contusion with diffuse cerebral edema a b figure 7 a subdural hematoma on the right hemisphere and anterior interhemispheric hematoma; b mild ventricules asymetry with left side subfalcine herniation. alin iordache et al intracranial pressure monitoring in neurosurgery department in iasi a postoperative neurological status was stationary and he became a candidate for organs transplantation. b figure 8 a right intraventriclar catheter; b left intraparenchymal catheter disscutions we study a number of 10 patients all of them had gcs<8. the craniocerebral ct scan made on admission showed different types of lesions (figure 9). figure 9 cerebral lesion found at ct scan all the patients had another associated lesions (figure 10). cerebral lesions 27% 23%18% 18% 14% cerebral edema subdural hematoma hemorrhagic contusion subarachnoid hemorrhage petechiae hemorrhagic lesion romanian neurosurgery (2012) xix 1 figure 10 associated lesions the neurological status on addmision was gcs 6 – 3 (figure 11). figure 11 neurological status on admission figure 12 neurological status at discharge associated lesions 30% 30% 20% 20% basal skull fracture temporal bone fracture thoracic contusion upper limbs contusion neurological status on admission 30% 30% 40% coma grade ii coma grade iii coma grade iv neurological status at discharge 80% 20% death hemiparesis alin iordache et al intracranial pressure monitoring in neurosurgery department in iasi the number of patinets is not extensive. this has an objective reasons. the major impediment in achieving a more extensive study is the material one. intracranial pressure monitor system cost is still prohibitive for our health system which is between 500 and 700 €. another reason is the ethical and the same time – legal reason. patients with neurosurgical lesions (acute subdural hematoma, epidural hematoma, contusions with important mass effect) requires quick intervention and follow-up of intracranial pressure for such injuries would mean loss of valuable time. even that placing an intracranial pressure transducer is a minimally invasive surgical procedure it involves intraoperative risks that should be explained and detailed to patient attendants. in some cases attendants do not accept the surgical risks and the fact that the benefits would not be immediately remarked. most patients studied had as expected a poor outcome (figure 12). most studies conducted so far on patients with severe head trauma at presentation, after removing the effects of any sedation, continues to present a state of coma grade iii or grade iv and has a mortality reaching 90%. as mentioned above the statistical value data is questionable due to a relatively small number of cases (2, 4). after insertion of the pressure transducer patient should be monitored for early detection of intracranial complications especially for hemorrhage. for this it is necessary to perform cranio-cerebral computer tomography at short interval after catheter insertion (5). this may be because the neurological worsening in a patient that is already in coma, intubated and artificially ventilated is difficult to detect. all the patient from our study performed an ct scan within 12 hours of monitoring onset. intracranial pressure monitoring was done by direct reading of pressure values on the monitor display every 2 hours. in general the neurological evaluation is difficult in patients with severe head trauma. they may be evaluated at about 2-3 hours after sedation removal. this assessment was made daily. beside the icp we monitorised the temperature (10), arterial blood pressure and heart rate. the icp variation is shown below. figure 13 icp variation – patient no. 1 romanian neurosurgery (2012) xix 1 figure 14 icp variation – patient no. 2 conclusion icp monitoring is usually a safe technique complication rate remains low even in the context of the catheter placement by people with less experience. it is useful in indicating the patients prognosis icp variation especially elevated intracranial pressure were associated with a poor prognosis (8, 9). it supports the diagnosis of brain death, especially in cases where the series eeg is not conclusive. the indication for icp monitoring should be extended to patients who were operated for surgical removal of a traumatic brain lesion and who have other injuries that may lead to increased intracranial pressure. a favorable outcome can be achieved only in the context of good collaboration with intensive care services because variations (upward or downward) of the intracranial pressure must be declared and treated with medication or surgical intervention (14). those patients should be more intense monitorised and in special carefully manipulated because exist the risk of removing the catheter. lack of continuous monitoring makes difficult to change the conservative treatment into an aggressive surgical conduct in time. the evolution of patients who underwent intracranial pressure monitoring as well as other with severe head trauma was aggravated by respiratory infections (13). a bad outcome in patients with severe head injury who underwent icp monitoring was associated with significant variations in blood pressure. a factor with poor prognostic was the association with elevated blood glucose repeatedly (12). in the group of patients who did not have icp monitoring we observed an increased mortality and also an increased rate of complications associated with prolonged stay in intensive care department. the vital prognosis of patients with severe head trauma was only one element of the study and it was not neglected the functional aspect and the social impact associated with patient who survived. the role of this study is to create conditions for a better approach of those patients and this can be achieved only under the conditions of investigation and treatment protocols which must be mandatory but also feasible, adapted to current conditions of our hospital. one of the conclusions of the study is the fact that it is imperative to be reduced alin iordache et al intracranial pressure monitoring in neurosurgery department in iasi the duration between the event (craniocerebral trauma) and therapeutic intervention – icp monitor placement. another aspect with importance on vital prognosis for polytraumatized patients with craniocerebral components it is the necessity of specialized units, qualified, currently non-existent. severe head trauma remains an important public health issue and leaves space for fundamental research, imaging and epidemiological studies. references 1. a. i. r. maas, m. dearden, g. m. teasdale, r. braakman, f. cohadon, f. iannotti, a. karimi, f. lapierre, g. murray and j. ohman, et al. ebicguidelines for management of severe head injury in adults, acta neurochir (wien) (1997) 139: 286–294. 2. alkhoury f, courtney j. outcomes after severe head injury: a national trauma data bank-based comparison of level i and level ii trauma centers, am surg. 2011 mar;77(3):277-80. 3. arbour r. intracranial hypertension: monitoring and nursingassessment. crit care nurse 2004;24(5): 19-32; 4. cremer ol, van dijk gw, van wensen e, brekelmans gj, moons kg, leenen lp, kalkman cj. effect of intracranial pressure monitoring and targeted intensive care on functional outcome after severe head injury, crit care med. 2005 oct;33(10):2207-13; 5. glowacki m, budohoski k, marszalek p, walecki j, czernicki z. a non-invasive assessment of intracranial volume reserve by measuring cerebrospinal fluid volume with the aid of ct imaging, acta neurochir suppl. 2010;106:199-202; 6. kathryn ko, md, and alicia conforti, rn training protocol for intracranial pressure monitor placement by nonneurosurgeons: 5-year experience, the journal of trauma_ injury, infection, and critical care volume 55, number 3 480 -484; 7. mark s. greenberg handbook of neurosurgery, 5th edition, ed. thieme new york 2001 8. marshall l.f., gautille t., klauber m.r. – the outcome of severe closed head injury. report on the traumatic coma data bank. j. neurosurgery – 1991;75;s28-s36 ; 9. schoser bg, riemenschneider n, hansen hc. the impact of raised intracranial pressure on cerebral venous hemodynamics: a prospective venous transcranial doppler ultrasonography study. j neurosurg. 1999;91(5):744-749. 10.thompson hj, kirkness cj, mitchell ph hypothermia and rapid rewarming is associated with worse outcome following traumatic brain injury, j trauma nurs. 2010 oct-dec;17(4):173-7; 11.timmons sd. current trends in neurotrauma care, crit care med. 2010 sep;38(9 suppl):s431-44 ; 12.yang sy, zhang s, wang ml: clinical significance of admission hyperglycemia and factors related to it in patients with acute severe head injury. surg neurol 44:373–377, 1995 13.zeng t, gao l. management of patients with severe traumatic brain injury guided by intraventricular intracranial pressure monitoring: a report of 136 cases, chin j traumatol. 2010 jun 1;13(3):146-51; 14.zhang ly, yao yz, jiang dp, zhou j, huang xk, shen y, huang j. surgical treatment strategy for multiple injury patients in icu., chin j traumatol. 2011 feb 1;14(1):42-5; microsoft word 4chiriaca_multimodaltreatment.doc romanian neurosurgery (2010) xvii 3: 281 – 290 281 multimodal tretment of intracranial aneurysm a. chiriac, i. poeata, j. baldauf1, h.w. schroeder1 clinic of neurosurgery, “gr.t. popa” university of medicine and pharmacy iasi, romania 1klinik für neurochirurgie, ernst-moritz-arndt-universität greifswald, germany abstract aneurysmal subarachnoid hemorrhage (sah), despite improvements in imagistic and medical treatment, is still a serious disease with high rates of case mortality and morbidity (40%). technical planning and therapy options of patients with aneurismal sah have changed during the angioct and 3d angiography era, and long-term outcome has significantly improved during the past few decades. however, the outcome is still determined mainly by specialist experience and severity of initial bleeding or early rebleeding. keywords: aneurysm, surgical clipping, stent, coil, embolization introduction intracerebral aneurysms are of variable pathogenesis and usually the largest group is represented by saccular aneurysms formed at proximal cerebral vessel bifurcations. likely based on a focal vessel wall weakness, fragile out-pouchings typically develop in areas of high shear stress and at areas of the vessel tree where there is higher intravascular pressure (along the proximal intracranial branching of the internal carotid artery and less frequently of the vertebro-basilar system). initiation, growth and rupture of an aneurysm are likely driven by a combination of several factors, each contributing to a variable degree in each of the evolutionary steps of an aneurysm’s history. current treatment modalities include for open surgical treatment various techniques to reconstruct the artery (clips) or to reinforce the aneurysm wall (wrapping) or to bypass circulation of the vessel carrying an aneurysm (aneurysm trapping and bypass surgery). endovascular treatment is less invasive techniques that have been developed on the principles of aneurysm filling with coils or polymers or vessel occlusion (aneurysm trapping). more recently, vessel reconstruction with stents rather than aneurysm filling has been advocated as treatment. both coils and stent techniques aim to induce slowing of blood flow and initiation of thrombosis within the aneurysm. secondary vessel wall repair with scar tissue occurs within weeks. with small vessel wall defects, coil implantation seems to allow successful repair under this principle, provided that the lumen of the aneurysm pouch is suitable for coil introduction. with larger vessel wall defects in proportion to the vessel diameter (segmental defects), either the vessel mustbe occluded if tolerated by the patient, or the vessel is reconstructed with the use of stent implants. 282 a. chiriac et al multimodal tretment of intracranial aneurysm surgical techniques the goal of surgical treatment is usually to place a clip across the neck of the aneurysm to exclude the aneurysm from the circulation without occluding normal vessels. when the aneurysm cannot be clipped because of the nature of the aneurysm or poor medical condition of the patient, the following alternatives may be considered: 1. wrapping: although this should never be the goal of surgery, situations may arise in which little else is possible (eg, fusiform basilar trunk aneurysms). three situations can be described: to reinforce a residual or additional ectasia next to the clipped aneurysm, usually proximal to the clip; -to treat an arterial ectasia, so called preaneurysmal ectasia, which proved not clippable at surgery; and -to protect a nervous or vascular neighbouring structure which was compressed by the clip grip. several agents for wrapping techniques can be used. the agents include cotton, muscle, silastic sheet, gauze, teflon, adhesives (biobond, fibrin glue, and polyglactin 910 fibrin sealant), collagen-impregnated dacron fabric (dupont, wilmington, de) or other polymer plastic resins may be slightly better than muscle or gauze for this purpose (figure 1a,b). some studies demonstrate benefit with plastic or other polymer, but others show no difference from natural course. in one study with long-term follow-up, the protection from rebleeding during the first month was unchanged, but, thereafter, the risk was slightly lower than for the natural history. 2. trapping/bypass: effective treatment requires both distal and proximal arterial interruption with direct surgery (ligation or occlusion with a clip). treatment may also incorporate extracranial-intracranial (ecic) bypass to maintain flow distal to the trapped segment. the balloon occlusion test (bto) represents the main criteria for choosing an appropriate bypass conduit. figure 1 a angiography images of a pcoa infundibular aneurysm; b – intraoperative images of infundibulum and wrapping with muscle figure 2 high flow bypass external carotid arteryradial artery graft-middle cerebral artery (eca-ragmca) with aneurysm trapping romanian neurosurgery (2010) xvii 3: 281 – 290 283 during the study, three different conditions were evaluated: -good clinical tolerance during the occlusion test, no sign of hypoperfusion at diamox single positron emission computed tomography (spect); -good clinical tolerance, appearance of hypoperfusion at spect; -poor clinical tolerance. the ica can easily be occluded without bypass in the first condition. it is a routine to perform sta-mca bypass with low flow in the second condition. it is general to perform saphenous vein graft (eca-svg-m2) or radial artery graft (eca-rag-m2) is generally performed in the third condition (figure 2). bypass surgery included low flow bypass such as superficial temporal artery to middle cerebral artery (stamca) direct anastomosis and high flow bypass such as external carotid artery-radial artery graft-middle cerebral artery (ecarag-mca) bypass grafting and external carotid artery-saphenous vein graft-middle cerebral artery (eca-svg-mca) bypass grafting. the bypass surgery for posterior circulation aneurysms includes occipital artery-posterior inferior cerebellar artery (oa-pica) and sta-p2 anastomosis. 3. proximal (hunterian) ligation: proximal ligation has been used with some success for giant aneurysms, particularly of the vertebrobasilar circulation. advanced endovascular techniques, however, now offer better alternatives for such lesions. 4. microsurgical clipping: after performing a craniotomy, use microsurgical techniques with the operative microscope to dissect the aneurysm neck free from the feeding vessels without rupturing the aneurysm. final treatment involves the placement of a surgical aneurysm clip around the neck of the aneurysm, thereby obliterating the flow into the aneurysm. the goal at surgery is to obliterate the aneurysm from the normal circulation without compromising any of the adjacent vessels or small perforating branches of these vessels (figure 3a,b). the clips are manufactured in various types, shapes, sizes, and lengths and are currently manufactured to be mri compatible. intraoperative angiography is now frequently used as an adjunct to clipping and permits confirmation of aneurysm occlusion and patency of nearby vessels. the frequency of its use varies widely; however, many vascular neurosurgeons choose to use this technique selectively for difficult aneurysms. recently, a new technique called nearinfrared indocyanine green videoangiography (icga) has become popular as a novel less invasive way to assess aneurysm and blood-vessel patency during aneurysm surgery. after intravenous injection of the indocyanine green dye, an operating microscope equipped with appropriate software can within minutes detect blood flow within the vasculature using near infrared technology. the technique is less invasive than intraoperative angiography, but one disadvantage is that only vessels that can be seen by the operating microscope can be evaluated. the operative morbidity and mortality associated with clipping depends on whether the aneurysm has ruptured; ruptured aneurysms are more treacherous to operate on and morbidity is higher. the risk of surgery for unruptured aneurysms is estimated to be 4-10.9% morbidity and 13% mortality. many factors affect the morbidity rates, with larger aneurysms in certain locations and in older, less medically healthy patients faring less well. surgeon experience likely plays a role, with highvolume surgeons working in high-volume institutions likely having lower morbidity; the definition of high-volume, however, is a matter of controversy. 284 a. chiriac et al multimodal tretment of intracranial aneurysm a b figure 3a, b schematic and intraoperative images of mca bifurcation aneurysm clipped coiling technique the use of detachable coils is a safe and effective alternative to surgical clipping of intracranial aneurysms. at present there is a wide range of coils, but their basic principles are similar to that of bare gdcs and include 3d and 2d coils. variable degrees of stiffness are available, including standard, soft, and ultrasoft coils. many investigations are currently evaluating new coils, including biologically active coils, radioactive coils, and coated coils with a swelling hydrogel. the aim of these innovations is to promote intra-aneurysmal clot organization and fibrosis or to increase packing density, which is associated with a higher long-term occlusion rate. all endovascular procedures were performed under general anesthesia and systemic heparinization. a bolus infusion of heparin (30–40 iu/kg body weight) was followed by a continuous drip (1000–1500 iu/h), with the purpose of doubling the baseline activated clotting time. no patient was placed on of aneurysm – pattern vessel. special attention should be considered in aneurysm sac catheterization, because there is a risk of aneurysm perforation by the top of the microcatheter or microguidewire in time of manipulation. the first coils selected to use should by the coil which enables to obtain the widest 3d configuration when is detached. this will provide the basic skeleton for anchoring the following coils. aneurysm packing, by the use of an excelsior 10 microcatheter (target therapeutics), is obtained by forming a basket with one or more 3d coils that were subsequently filled with smaller 2d coils. in all cases, it’s recommended to pack the aneurysm with the same type of coils. soft, ultrasoft, or both soft and ultrasoft coils are used at the end of the procedure to complete aneurysm obliteration. in case of matrix coils, to avoid friction inside the microcatheter, the coils are placed in a saline solution for at least 60 seconds to hydrate the polymer completely. when packing difficulties (high frictions between coils, compartmentalization) with matrix coils were encountered because of their stiffness. in case of a coil helix migration into the parent vessel during coil positioning or due to an improper configuration for the next coil introduction, withdrawal of the coil and providing a new optimal configuration before deployment is recommended. with the successive introduction of the coils may become difficult to angiographical image the position of new coils introduced. however placement should be continued until the alignment of radio-opacity markers is obtained (on the metal guide on the delivery microcatheter) thus ensuring a safe detachment. a b figure 4 a, b schematic and angiographic images of basilar tip aneurysm coiled romanian neurosurgery (2010) xvii 3: 281 – 290 285 using fluoroscopy with digital subtraction, detachment of each coils can be traced in real time. after the desired position for the coils is achieved, the detachment device is connected to the proximal end of coils delivery guidewire, and the disconnection it tocks place within a 2-60sec depending on the type of disconnection mechanism (figure 4 a, b). after detachment, the delivery guidewire is withdrawn, and if necessary a new coils is added into the aneurysm until a dense packing of coil configuration is achieved. the coils mass so obtained will lead to a stagnation of blood flow in the aneurysm sac, a thrombosis triggering antiplatelet medication before treatment. technique of endosaccular coil placement procedure begins with a classic angiographic images acquisition. after obtaining the best working position, a roadmap image of the pattern vessel is performed and the aneurysm sac is selectively catheterized with a microcatheter with two radio-opaque coaxial markers. the catheter tip may be manually curved to fit the complex anatomical configuration phenomenon and aneurysm isolation from blood circulation through the formation of neo-endothelium over its neck. balloon-assisted technique the neck remodeling or balloon-assisted embolization technique originally described by moret et al has been used in the endovascular treatment of wide-necked aneurysms or in aneurysms with an unfavorable neck-to-fundus ratio in which a standard coil placement technique may be unsuccessful. the procedures begin with 7f and 6f femoral sheaths insertion into both femoral arteries, and a digital subtraction angiography is performed. the parent vessel is catheterized with a microcatheter (excel 14, excelsior 10–18, target/boston scientific, fremont, ca; rapid transit 18; cordis, miami lakes, fl) placed near the aneurysmal neck. the calibers of the parent arteries and the size of the aneurismal neck were approximately calculated, and a microballoon size is chosen on the basis of these calculations. a nondetachable balloon (sentry 10–15 mm, target/boston scientific, or hyperglide, micro therapeutics corp, irvine, ca) will be then advanced through the contra-lateral femoral sheath to the neck of the aneurysm. the microcatheter is advanced into the aneurysm dome, while the balloon is uninflated. finally, the balloon is carefully inflated to occlude the aneurysmal neck, while the tip of the microcatheter is in a location in the body of the aneurysm that is suitable for coil deposition. coils of appropriate diameter, length, and stiffness were deposited in the aneurysm dome and detached electrolytically. for balloon inflation, a 1-ml precision injector with threaded plunger syring (microtherapeutics) is used (figure 5a,b). a b figure 5 a, b schematic and angiographic images of ica aneurysm coiled by balloon-assisted technique 286 a. chiriac et al multimodal tretment of intracranial aneurysm the microballoon will never be inflated more than its nominal volume. the initial framing coil is deployed through the intraaneurysmal microcatheter, after which the balloon was deflated and 1 to 2 minutes were permitted to elapse before the coil is electrolytically detached so that stability (did not herniate out of the aneurysm sac into the parent artery) of its placement could be ascertained. if no coil movement was noted, the coil is detached and the balloon reinflated before deployment of the next coil. this process is repeated until the aneurysm is embolized as completely as possible. by the time the balloon was inflated at the end of the procedure, the microcatheter had always been withdrawn. stent and stent-assisted coil techniques surgical or endovascular occlusion of small aneurysm is difficult because of tearing or narrowing the parent vessel during clipping and insufficient saccular space to deploy coil. fusiform aneurysm is another difficult and dangerous type of vascular lesion due to its fragile wall and indistinct neck. initially the “deconstructive” methods, described as proximal occlusion or trapping, had been treatment of choice for fusiform aneurysm. begin with the development of stent material and technique, the new concept has been evolved recently into “endovascular bypass” or “endovascular reconstruction” which is enabled to preserve affected parent artery and perforators, and occlude aneurysm safely. compared with the deconstructive methods, the reconstructive ones may be more definitive and optimal treatment physiologically. the use of stents in intracerebral aneurysms treatment has two principles technique: sole stenting technique and stent-assisted coiling. sole stenting technique (stent placement across the neck of an aneurysm causes) is one of reconstructive methods based on hemodynamic flow diversion principle that can, on occasion, cause aneurysmal occlusion/thrombosis without the need to introduce coils (figure 6). stent-assisted coiling technique is a technique of using an intravascular stent to create a bridging scaffold followed by endovascular placement of coils through the interstices of the stent into a wide-necked or fusiform aneurysm. the most used stents specifically designed for intracranial treatment are neuroform stent (boston scientific), leo stent (balt), self-expanding nitinol stent (cordis enterprise), and electrolytically detachable solo stents. leo and cordis enterprise stents are of closed-cell design and neuroform stents are of open-cell design. the closed-cell design allows all coils to be placed within the aneurysm and outside the flow of the parent artery with stent-assisted coiling. figure 6 angiographic image of anterior choroidal artery aneurysm treated by sole stenting technique romanian neurosurgery (2010) xvii 3: 281 – 290 287 neuroform stents have the disadvantage of being non-retrievable and strut prolapse can occur in curved vasculature due to its open-cell design. both leo and enterprise stents can be retrieved or repositioned even after 90% of deployment; this allows safer and more precise deployment. a new stent with a more tightly constructed mesh, pipeline chestnut medical, designed to cause increased hemodynamic diversion relative to the neuroform or enterprise, is undergoing experimental investigation and has already been used effectively in several patients. before choosing the endovascular device to use, we had to resolve 2 technical issues: sharply define the required diameter of the device, and precisely determine whether a balloon-expandable stent (bes) or sirolimus-eluting stent (ses) was to be deployed. to solve the first issue, we chose a device with a diameter closest to the size of the diameter of the vessel to receive a stent. a bes is indicated if we hoped to modify the angle of the vessel and an ses when a modification of the laminar flow was deemed to promote aneurysm thrombosis. technique of stent deployment and endosaccular coiling by using magnified fluoroscopy and digital biplane road mapping, the microcatheter was navigated into the cerebral vessel, distally from the neck of the aneurysm which was passed with the aid of a 0.010or 0.014-inch guide wire (fasdasher; boston scientific/target or silver speed, medtronic mis, sunnyvale, ca). the stent is preloaded in a 3f delivery microcatheter. a separately packaged stabilizer is inserted through the hub of the stent delivery microcatheter until its tip abuts the stent. a b figure 7 a, b schematic and angiographic images of posterior comunicanting artery aneurysms coiled by stent-assisted technique the stabilizer is essentially a 2f microcatheter that can be placed inside the 3f stent delivery microcatheter over a 0.014-inch wire. the delivery microcatheter is placed coaxially through a 6-f guide catheter (envoy, cordis neurovascular; or guider, boston scientific/target). the microcatheter is exchanged over a long micro guide wire which is used to introduce the stent system. when using bess, we inflated the devices to their nominal pressure (8 atm in most cases). in case of ses system, the stent delivery microcatheter and stabilizer are advanced over an exchange wire as a unit and positioned until the aneurysm neck is centered between the ends of the stent. the stent is deployed by gently retracting the microcatheter while holding the position of the stent fixed with the stabilizer. this unsheathes the stent and allows expansion within the vessel. as the stent deploys, the four marker bands on each end define the endoluminal surface. after deployment of the stent, the stent system with the exchange wire is removed, and a microcatheter with a preshaped soft microguidewire (transend-14; boston scientific, fremont, ca) can be used to 288 a. chiriac et al multimodal tretment of intracranial aneurysm enter the aneurysm through the interstices of the stent. finally, detachable coils are introduced into the aneurysm and detached as usual until occlusion is achieved. after sufficient packing of the aneurysm, the microcatheter is pulled back. once the stent and coils were placed, ds angiography sequences were performed to assess the deployment of the stent (figure 7a,b); the patency of the parent vessel and of the perforating or adjacent vessels; the modification of the flow within the aneurysm; and the distal arterial tree. liquid embolic occlusion technique onyx (micro therapeutics, inc., irvine, ca) is a liquid embolic material designed for endovascular use. it is an ethylene vinyl alcohol copolymer dissolved in the organic solvent dimethyl sulfoxide (dmso). the mechanism of action consist in embolic material precipitation when it comes into contact with an aqueous solution with formation of a soft spongy polymer cast, initially with an outer layer, remaining semi-liquid centrally. as further material is injected into the cast, it fills the space into which it is injected, and then additional material breaks out through the outer layer of the existing cast. in the treatment of intracranial aneurysms, the material, as currently used, is constrained by the placement of a balloon over the neck of the aneurysm. the material solidifies completely over a period of about 10 minutes with diffusion of the solvent dmso. as part of the evaluation for the use of onyx during the procedure, a seal test was performed to determine whether the neck of the aneurysm could be satisfactorily occluded by the balloon. a gentle injection of contrast material was made into the aneurysm via the microcatheter with the balloon inflated; stasis of contrast material was seen when the aneurysm neck could be controlled without significant leakage. this also ensured that no adjacent side branches filled. if adequate control of the aneurysm neck could not be obtained with the balloon, the onyx treatment is not recommended. 20and 30-mm braided-shaft balloons (hyperglide; micro therapeutics, inc.) were available, and most recently the highly compliant hyperform balloon (micro therapeutics, inc.), designed to occlude bifurcation aneurysms, became available. these new devices have improved the range of aneurysms in which the neck could be satisfactorily occluded. procedural technique the technique begins with the placement of a highly compliant dmsocompatible occlusion balloon (equinox or hyperglide) in the parent vessel over the neck of the aneurysm. the balloon is left deflated while a dmso-compatible microcatheter (rebar, micro therapeutics, inc.) is placed within the aneurysm. a slow test injection through the microcatheter is made with the balloon inflated to ensure that the neck is controlled and a satisfactory seal is achieved with stasis of contrast material within the aneurysm. the microcatheter is then purged with saline, to clear any residue of contrast material, and primed with dmso with a volume to match the catheter dead space. onyx (hd 500) is then introduced into the microcatheter. once sufficient volume (usually 0.2 ml) of the material has been injected, onyx approaches the end of the microcatheter, and the balloon is inflated to the predetermined volume. onyx is romanian neurosurgery (2010) xvii 3: 281 – 290 289 injected at a rate of about 0.1 ml per minute by using the specifically designed cadence precision injector syringe (micro therapeutics, inc.), which operates by a screw thread. because of the viscosity of onyx, it accumulates around the tip of the microcatheter and gradually enlarges to form a kernel that stays attached to the end of the microcatheter. after each injection, the balloon is left inflated for another 3 minutes and then deflated to allow cerebral reperfusion for at least 2 minutes; then the cycle is repeated. with each injection, new portions of the aneurysm fill, and eventually the material flows down to the margins of the balloon and occludes the neck of the aneurysm (figure 8 a, b). when the material is in contact with the balloon, injection is slowed or stopped with brief 15–30-second pauses to minimize the risk of leakage into the parent artery and beyond the balloon. it is important to ensure that material covers the aneurysm neck to achieve complete and durable occlusion and reduce the risk of aneurysm regrowth that is sometimes observed with wide-neck large and giant aneurysms. the microcatheter position is not adjusted at all once injection has started. a b figure 8 a, b schematic and angiographic images of posterior comunicanting artery aneurysms occluded with onyx (red contour is the limit of aneurysm fillede by onyx) following angiographic confirmation of the complete or satisfactory occlusion of the aneurysm, the catheter syringe is decompressed by aspiration of 0.2 ml and a 10-minute pause is taken to allow complete solidification of the polymer with the balloon deflated. the balloon is then reinflated and the microcatheter is removed by gentle traction. conclusions most of the literature studies show that both deconstructivtion and reconstructive (microsurgical clipping and endovascular therapies) treatment techniques are highly effective at preventing acute rebleeding from ruptured aneurysms. it is increasingly clear that excellent results can be achieved with clipping and coiling, and that outcomes are better in centers with experience and expertise in both techniques. also, specific treatment strategies must be particularized, taking into consideration the patient’s age, neurological status, and medical comorbidities, as well as angioarchitectural aspects such as aneurysm location, size, geometry, neck to dome ratio, and intraluminal presence of thrombosis or calcification. it was already demonstrated that, even a densely packed aneurysms have a propensity to coil compaction and subsequent recurrence, necessitating longterm follow-up and possibly further treatment, even years after the initial procedure. recurrence after complete aneurysm clipping is extremely unlikely, and late invasive imagistic investigation is probably not necessary. however, if there is incomplete clipping or multiple aneurysm situation, continued surveillance is warranted. 290 a. chiriac et al multimodal tretment of intracranial aneurysm a multidisciplinary approach emphasizing honest and valid assessment of local expertise and unbiased collaboration between surgeons and interventionalists is critical to decision making and will lead to improved outcomes. references 1. moyle h, patel ab, intracranial aneurysms: endovascular treatment. mt sinai j med. 2010 may;77(3):279-85. 2. colby gp, coon al, tamargo rj, surgical management of aneurysmal subarachnoid hemorrhage. neurosurg clin n am. 2010 apr;21(2):247-61. 3. morales f, maillo a, hernández j, pastor a, caballero m, gómez moreta j, díaz p, santamarta d, evaluation of microsurgical treatment in a series of 121 intracranial aneurysms. neurocirugia (astur). 2003 feb;14(1):5-15. 4. gonzález-darder jm, pesudo-martínez jv, feliutatay ra, microsurgical management of cerebral aneurysms based in ct angiography with threedimensional reconstruction (3d-cta) and without preoperative cerebral angiography. acta neurochir (wien). 2001;143(7):673-9. 5. reid aw, reid db, roditi gh, imaging in endovascular therapy: our future. j endovasc ther. 2009 feb;16 suppl 1:i22-41. 6. zipfel gj, modern management of brain aneurysms and vascular malformations. mo med. 2008 sepoct;105(5):413-9. 7. jeong sm, kang sh, lee nj, lim dj, stent-assisted coil embolization for the proximal middle cerebral artery fusiform aneurysm. j korean neurosurg soc. 2010 may;47(5):406-8. epub 2010 may 31. 8. rohde s, bendszus m, hartmann m, hähnel s, treatment of a wide-necked aneurysm of the anterior cerebral artery using two enterprise stents in "y"configuration stenting technique and coil embolization: a technical note. neuroradiology. 2010 mar;52(3):2315. epub 2009 oct 21. 9. gil a, vega p, murias e, cuellar h, balloon-assisted extrasaccular coil embolization technique for the treatment of very small cerebral aneurysms. j neurosurg. 2010 mar;112(3):585-8. 10. malek am, halbach vv, phatouros cc, lempert te, meyers pm, dowd cf, higashida rt, balloonassist technique for endovascular coil embolization of geometrically difficult intracranial aneurysms. neurosurgery. 2000 jun;46(6):1397-406; discussion 1406-7. 11. park ek, ahn js, kwon do h, kwun bd, result of extracranial-intracranial bypass surgery in the treatment of complex intracranial aneurysms : outcomes in 15 cases. j korean neurosurg soc. 2008 oct;44(4):228-33. epub 2008 oct 30. 12. sanai n, zador z, lawton mt, bypass surgery for complex brain aneurysms: an assessment of intracranialintracranial bypass. neurosurgery. 2009 oct;65(4):67083; discussion 683. romanian neurosurgery (2019) xxxiii (2): pp. 101-104 doi: 10.33962/roneuro-2019-020 www.journals.lapub.co.uk/index.php/roneurosurgery continuous intracranial pressure monitoring in severe traumatic brain injury in children st.m. iencean1,2, a. tascu3,4, c.a. apetrei2, c. gheorghita5, tsz-yan milly lo6, ian piper7, a.st. iencean2 1 neurosurgery, “grigore t. popa” university of medicine and pharmacy, iasi, romania 2 neurosurgery, “prof. dr. n. oblu” clinical emergency hospital, iasi, romania 3 neurosurgery, “bagdasar-arseni” clinical emergency hospital, bucharest, romania 4 neurosurgery, “carol davila” university of medicine and pharmacy, bucharest, romania 5 neurosurgery, “sf. maria” children clinical emergency hospital, iasi, romania 6 university of edinburgh (child life & health) / royal hospital for sick children (paediatric critical care medicine), uk 7 brainit group coordinator, principal health care scientist, neurointensive care monitoring research, uk abstract we present the results of the romanian team for the multi-center grant “paediatric brain monitoring with information technology (kidsbrainit). using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety”, acronym kidsbrainit. children aged 2 to 16 years who require intensive care management after sustaining traumatic severe brain injury are included in this study in three neurosurgical hospital: "prof. dr. n. oblu" clinical emergency hospital iasi, "sf. maria" children clinical emergency hospital iasi and "bagdasar-arseni" clinical emergency hospital bucharest. continuous real-time intracranial pressure monitoring became a "gold standard" in tbi intensive-care management and icp-lowering therapy is recommended when icp is elevated above 20 mmhg or more. continuous icp and mean arterial blood pressure (map) monitoring allow calculation of cerebral perfusion pressure (cpp) and to establish of an optimal cpp. this study aims to improve the treatments and the outcomes in severe traumatic brain injury in children. introduction annually, over 50,000 new cases of cranio-cerebral trauma (tbi) occur in romania; road accidents are the main cause of cranial traumas, which often cause cognitive, affective and behavioural disorders, with a particular impact on families and society. world health organization keywords cerebral perfusion pressure, traumatic coma, intracranial pressure, paediatric brain monitoring, severe children brain injury corresponding author: a. tascu "carol davila" university of medicine and pharmacy, bucharest, romania tascu_alexandru@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 102 st.m. iencean, a. tascu, c.a. apetrei et al. estimated that up to 90% of head injuries that receive treatment are mild, of which moderate and severe injuries represent 10%. in the european union the yearly aggregate incidence of tbi hospitalizations and fatalities is estimated at 235 per 100,000. fortunately, tbi in children is much lower, without being able to make a reliable estimate because of research differences, but partial studies have shown that tbi in children represents about 14% of the total tbi. also, children have a higher incidence of increased intracranial pressure (icp) following tbi than adults (80% vs. 50%) and it is a major cause of morbidity and mortality in the paediatric age group. in this report of the multi-center grant “paediatric brain monitoring with information technology (kidsbrainit). using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety”, acronym kidsbrainit we present the results of our study for almost the past two years. material and methods three neurosurgical hospital: "prof. dr. n. oblu" clinical emergency hospital iasi, "sf. maria" children clinical emergency hospital iasi and "bagdasararseni" clinical emergency hospital bucharest participated in this study that included children aged 2 to 16 years who require intensive care management after sustaining traumatic severe brain injury. a total of 941 children with traumatic brain injury received medical care during 16 months in these three neurosurgical departments, including minor, medium and severe brain traumas. thirtyone patients needed intensive care and 9 children have been icp and blood pressure monitored, but only four patients were included in this scientific project. as presented in the previous report in two cases the values of icp were high and very high and cerebral decompression was performed; unfortunately, the initial clinical condition was extremely severe and evolution was not favourable in these cases. the third and fourth patients monitored showed elevated icp values up to 28-30 mm hg and 30 40 mm hg, which were medically treated. figure 1: case of children with severe tbi and continuous intracranial pressure monitoring results during 16 months in our three neurosurgical departments there were a total of 941 children with traumatic brain injury and 31 patients needed intensive care and 9 children have been icp and blood pressure monitored, but only four patients were included in this scientific project. the scientific report that on the mid-term results of this multicentre grant presented the three cases: two children 103 continuous intracranial pressure monitoring in severe traumatic brain injury in children with high and very high values of icp and cerebral decompression, but not favourable evolution and the case of the third patient monitored with elevated icp values up to 28-30 mm hg, medically treated with a favourable evolution. the four case had oscillating high icp values up to 30 45 mm hg, but the extremely severe initial clinical condition has made its evolution not favourable. discussion our number of 941 cases in 16 months should be interpreted by reference only for two areas in the country: two hospitals in iasi and one in bucharest, so it does not cover the entire our country. this number of cases of paediatric tbi vary across clinical and epidemiological studies and till now our number of cases with icp and cpp monitoring are few and a statistical analysis could not be conclusive, but all the cases from the centres included in the grant from the other countries were hoping to have a statistical significance. intracranial pressure and cerebral perfusion pressure monitoring are invasive methods but they assured an early detection of increased icp and disturbance of cerebral perfusion pressure in children with severe tbi. as we have mentioned in another material about this grant, the relationship between icp elevation and cpp values is known in the adult, but in the paediatric tbi the studies are not conclusive; so “chambers et al. proposed age stratified critical levels of cpp: in the age groups 2–6, 7–10, and 11–16 years, cpp values of 43 mmhg, 54 mmhg and 58 mmhg, respectively, were associated with normal values of icp and good outcomes”. within the partnership between the centres involved in the finalization of this scientific research it has been achieved a distribution of the research work packages/tasks by partner: (1) kids brainit infrastructure development; (2) multi-centre multinational patient recruitment into the project; (3) data extraction, central data-bank development and implementation; (4) outcome assessment (6 and 12 months); (5) data artefact detection and cleaning; (6) physiological data analyse; (7) novel technology substudy and (8) mri outcome sub-study. anonymised clinical and physiological data from different centres are uploaded successfully into the data-bank using a secure http data upload service which ensures secured and encrypted transfer of fully anonymised data only. there are 48 patients recruited successfully into the study to-date in all contributing centres. an important novel technology sub-study refers to the hybrid diffuse optical technology device, which is available for testing in barcelona and patients are recruited into this sub-study since barcelona open for recruitment in may 2018. in our recruited patients with icp and cpp monitoring the performed manoeuvres were drug therapy, csf drainage and decompressive craniectomy in accordance with modern therapeutic guidelines. treatment used sedatives, analgesics; hyperosmolar therapy as intravenous mannitol and hypertonic saline to control intracranial hypertension; mild hyperventilation; barbiturates, temperature control and prophylactic anticonvulsants. the routine steroid treatment in children with severe tbi is not conclusive; it has to be individualized and rather it is not indicated because the potential harm from infectious complications. decompressive craniectomy was performed for controlling intracranial hypertension and it was effective at icp reduction. conclusions the severe traumatic brain injury in children requires a multidisciplinary approach in each phase of management. the prompt diagnosis during the initial evaluation and then the multimodal monitoring must be followed by the management of intracranial hypertension. continuous icp and mean arterial blood pressure (map) monitoring allow calculation of cerebral perfusion pressure (cpp) and to establish of an optimal cpp. all of this has its role to minimize the pathophysiological damage to the brain. the goal of this study is to establish the best care for severe tbi children and to ensure a transfer to a wider clinical audience. acknowledgments this study is within the grant: “paediatric brain monitoring with information technology (kidsbrainit): using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety”, grant: cofund-neuron iii eranet kidbrainit, funding no.2 / 01/06/2017. references 1. tsz-yan milly lo. paediatric brain monitoring with information technology (kidsbrainit): using it innovations to improve childhood traumatic brain injury intensive 104 st.m. iencean, a. tascu, c.a. apetrei et al. care management, outcome, and patient safety. proposal application form era-net neuron, 2016. 2. iencean st m, tascu a, apetrei ca, gheorghita c,iencean a st. continuous intracranial pressure monitoring in severe traumatic brain injury in children. romanian neurosurgery, vol xxxii, sept 2018, supplement pp.73. 3. kannan, n., ramaiah, r., & vavilala, m. s. (2014). pediatric neurotrauma. international journal of critical illness and injury science, 4(2), 131–137. doi: 10.4103/2229-5151. 134152. 4. c.a. apetrei, c. gheorghita, a. tascu, a.st. iencean, tsz-yan milly lo, ian pipe, st.m. iencean paediatric brain monitoring with information technology (kidsbrainit) era-net neuron grant. romanian neurosurgery (2018) xxxii 2: 183 186 doi: 10.2478/romneu-2018-0024. 5. st.m. iencean, a. tascu, c.a. apetrei, c. gheorghita, tsz-yan milly lo, ian piper, a.st. iencean mid-term results in continuous intracranial pressure monitoring in severe traumatic brain injury in children era-net neuron grant romanian neurosurgery (2018) xxxii 4: 547 551 doi: 10.2478/romneu-2018-0070. 6. tsz-yan milly lo. paediatric brain monitoring with information technology (kidsbrainit): using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety. annual scientific progress report era-net neuron, april 2019. 7. guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents (second edition). pediatr crit care med 2012. 13, no 1 (suppl.). 8. chambers ir, jones pa, lo tym et al. critical thresholds of intracranial pressure and cerebral perfusion pressure related to age in pediatric head injury. j neurol neurosurg psychiatry 2006. 77(2): 234-240. 9. depreitere b, güiza f, van den berghe g, schuhmann m, maier g, piper i, meyfroidt g. pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in severe traumatic brain injury patients based on minute-by-minute monitoring data. j. neurosurgery 2014 jun; 120(6): 1451-1457. 10. güiza f, meyfroidt g, lo tym, jones pa, greet van den b, depreitere b. continuous optimal cpp based on minuteby-minute monitoring data: a study on a pediatric population. acta neurochir 2015. 11. guiza f, depreitere b, piper i et al. visualizing the pressure and time burden of intracranial hypertension in adult and paediatric traumatic brain injury. intensive care medicine 2015. 41(6): 1067-1076. 12. hutchison js, frndova h, lo tym et al. impact of hypotension and low cerebral perfusion pressure on outcomes in children treated with hypothermia therapy following severe traumatic brain injury: a post hoc analysis of the hypothermia pediatric head injury trial. dev neurosci. 2010; 32(5-6): 406-12. 13. suttipongkaset p, chaikittisilpa n, vavilala ms, lele av, watanitanon a, chandee t, krishnamoorthy v . blood pressure thresholds and mortality in pediatric traumatic brain injury. pediatrics. 2018;142(2). 14. centers for disease control and prevention. report to congress: the management of traumatic brain injury in children. national center for injury prevention and control; division of unintentional injury prevention, atlanta, ga; 2018. 15. olsen, mari et al. incidence and mortality of moderate and severe traumatic brain injury in children: a ten-year population-based cohort study in norway european journal of paediatric neurology, online may 2019. in press. 16. manfiotto m et al. decompressive craniectomy in children with severe traumatic brain injury: a multicentre retrospective study and literature review. world neurosurgery. available online 1 may 2019, in press. microsoft word 6moscotesalazar_transient romanian neurosurgery (2013) xx 3: 271 – 276 271 transient mutism and cerebellar ischemic stroke: case report luis rafael moscote-salazar1, hernando alvis-miranda1, angel lee2, hector farid escorcia3, sandra milena castellar-leones1 1universidad cartagena, colombia 2hospital angeles del pedregal, méxico d.f, méxico 3hospital universitario cari, barranquilla, colombia abstract the ischemic stroke is one of the most common conditions in our hospitals, representing 50% of revenues of neurology services. a variety of processes is cerebral ischemic myocardial cerebellum. cerebellar infarction is not a rare disease, representing between 2 to 4% of all cerebrovascular events in clinical and autopsy series, and their ratio is 4-5 times higher than cerebellar hemorrhage. although it is increasingly documented, it rarely recognized stills like a phenomenon. mutism occurs primarily in children and occasionally in adults as a well-recognized complication of posterior fossa surgery. rarely been reported transient mutism associated with cerebellar infarction as isolated episode. key word: stroke, transient mutism, neurosurgery. introduction cerebrovascular diseases are a major cause of death in the world. the health report in the world, published by the world health organization 2003, cerebrovascular disease places fourth among those responsible for the global burden of disease for over 15 years, reaching the second in the population over 60 years. among the many presentations of ischemic cerebrovascular disease is ischemia cerebellum. the patient's neurological deterioration with cerebellar infarction is attributed to edema. medical management includes steroids, mannitol, barbiturates and hyperventilation. the symptomatology correspond to the classical cerebellar data. we present an unusual case characterized by sudden onset mutism in the context of cerebellar infarction progressing to acute hydrocephalus resolved by placement of a ventriculo peritoneal shunts case report a man of 55 years with a history of hypertension uncontrolled blood enters the emergency department by moderate headache clinical picture and language disturbance. no history of drug use. occasional alcohol consumption.the story did not report symptoms of anxiety or depression. neurological examination the patient was silence. biochemical tests were normal. imaging studies were performed which showed the presence of a cerebellar infarction. (figure 1) after 24 hours, the patient has neurological impairment whereby framework are images and acute hydrocephalus evidence, decides to place ventriculoperitonealshunt. the patient presented 24 hours disappearance of mutism and responded to commands. was discharged after 15 days. 272 moscote-salazar et al transient mutism and cerebellar ischemic stroke figure 1 irm postoperative reveals a cerebellar stroke romanian neurosurgery (2013) xx 3: 271 – 276 273 discussion cerebellar mutism (cm) is a form of severe dysarthria marked by profound impairment of fluency, articulation, and modulation of speech (1), resulting in the absence or marked pause of verbal output (2, 3) that is, anarthria (4). it only applies for cases whereby lesions of the cerebellum are associated with the onset of the mutism and do not have corresponding long tract signs, supra, cranial nerve palsies (5) or impaired consciousness (5, 6). the first mention of cm as a distinct clinical entity was reported in 1985 by rekate et al (7) and yonemasu (8).particularly, holmes noted that lesions of thecereballar hemispheres alone were enough to cause dysarthria, but when the vermis was involved, appears a greater difficulty in phonation and articulation (9, 10). although it is increasingly documented, it stills like a rarely recognized phenomenon (11). mutism occurs primarily in children and occasionally in adults as a well-recognized complication of posterior fossa surgery (4, 5).in general, mutism caused by intracranial surgical intervention has been described in the following areas (12): broca’s area;the anterior cingulate area;the descending tracts bilaterally;the mesencephalic reticular formation; after callosotomy for medically intractable epilepsy;the supplementary motor area; and in the midline cerebellar structures (13). have been reported that there are many lesions and locations within the posterior fossa that create a pathologic consequence related to speech disorders (14). continuously growing insights in the neuroanatomy of cerebellum, evidence from functional neuroimaging, neurophysiological research and advancements in clinical and experimental neurosychology contributed to the view that human cerebellum participates in a much wider range of functions than conventionally accepted (15, 16). the most common feature of cm is its transient nature, which has been explained by cerebral vasospasm (17). nevertheless, turgut (18) speculated that hydrocephalus, rather than the vasospasm, is a possible exacerbating factor in the development of cm, due to the delayed transient ischemia secondary to that process occurs after surgery on the cerebellum but not in other parts of the brain, possibly owing to the existence of more sensitive purkinje cells (11). cm is often associated with a particular behavior characterized by irritability and disturbances in socialization and communication ranging from emotional lability to autistic withdrawal (19-23). coplin et al. (24) in 1997, made the first report of transient mutism in an adult with neither tumor nor brainstem infarction, they presented a case of transient mutism of four month long in a patient after cereberal hemorrhage, the patient cannot return to his normal speech. his speech was characterized by great effort, ataxic dysarthria, and strained voice, with pitch often higher than normal. this documents the importance of cerebellar structures for initiation and production of speech in adulthood. marien et al. (16) present the case of a 73-years old patient with ischaemic lesion in the vascular territory of the right arteriacerebellaris superior, that induced a prefrontal aphasic syndrome and an agrammatism. the patient acutely developed cerebellar and brainstem symptoms. cerebellar involvement 274 moscote-salazar et al transient mutism and cerebellar ischemic stroke reflected by slight dysarthric speech problems and right-sided dysdiadochokinesia, dysmetria, and rebound phenomena. six months postonset, a dysarthric syndrome was found which cardinal features consisted of: articulatory imprecisions; phoneme iterations and syllable repetitions; irregular articulatory breakdowns and intervals; and slow rate. no stress aberrations, vowel prolongations, vowel distortions, harsh voice quality, loudness alternations, rate variability, altered nasality, voice tremor, task-dependency or audible inspiration were noted. given the presumed common substrate of an articulatory timing deficiency, the constellation of the dysarthric symptoms in this patient, the authors corroborated the view that temporal dysregulation might act as the primary component in impaired motor planning of speech after cerebellar lesions. mewasingh et al. (4), described the cases of two children who developed transient cm accompanied by a characteristic behavior associated with non-surgical causes.ischemic cerebellar infarction caused by hemolytic–uremic syndrome in one child and cerebellitis in the other. in both children, anarthria was followed by dysarthria. the two cases presented a behavioral pattern similar to that in postoperative mutism [classically transient, with lack of cranial nerve dysfunction and long-tract signs, comprehension remains unaffected,a period of intact speech usually occurs and lasts from a few hours to several days (1, 13, 20, 25-31)]. there is one case reported of transient mutism related to ischemic process secondary to traumatic injury of the vertebral artery, not located in cerebellum but in brain stem (32). most cases of cm described in the literature occur in children undergoing posterior fossa surgery for medulloblastoma or astrocytoma; but it is also described in adults after resection of a posterior fossa tumor such as hemangioblastoma or posterior circulation infarction or hematoma. cerebellum is part of a network of cerebello–cerebral/cerebro-cerebellar connections that process and mediate complex social and cognitive behaviors (19, 21, 33), its role in speech has expanded to include the cognitive component of speech generation, including the internal generation of words, choice of words, rehearsal of speech, timing of speech, and vocal intonations used during speech production (5, 34-38). human brain functional anatomy investigations by pet activation, magnetic resonance imaging and cerebral blood flow studies convincingly demonstrate the participation of cerebellar structures in non-motor tasks such as the mental association of a word with its use, mental arithmetic, mental imagery and stereognosic and associative procedural learning (15, 16). the orofacial muscles are coordinated by the paravermal regions of the cerebellum during speech, probably, the loss of coordination in those muscles movements is primarily responsible for the development of mutism (5). van mourik et al (39) observed that the time course of mutism can be characterized by the recovery of simple orofacial movements, and the recovery of complex orofacial movements coincides with the disappearance of mutism. our case represents a rare presentation of ischemic phenomena of cerebellar mutism should be considered as a possible romanian neurosurgery (2013) xx 3: 271 – 276 275 form of disease onset cerebellar ischemic stroke. correspondence: dr. luis rafael moscote-salazar, university of cartagena, cartagena de indias, colombia, southamerica. e-mail: mineurocirujano@aol.com references 1.nagatani k, waga s, nakagawa y. mutism after removal of a vermian medulloblastoma: cerebellar mutism. surg neurol. 1991 oct;36(4):307-9. pubmed pmid: 1948632. epub 1991/10/01. eng. 2.altshuler ll, cummings jl, mills mj. mutism: review, differential diagnosis, and report of 22 cases. the american journal of psychiatry. 1986 nov;143(11):1409-14. pubmed pmid: 3777229. epub 1986/11/01. eng. 3.geschwind n. current concepts: aphasia. the new england journal of medicine. 1971 mar 25;284(12):6546. pubmed pmid: 5545606. epub 1971/03/25. eng. 4.mewasingh ld, kadhim h, christophe c, christiaens fj, dan b. nonsurgical cerebellar mutism (anarthria) in two children. pediatric neurology. 2003 1//;28(1):59-63. 5.ozgur bm, berberian j, aryan he, meltzer hs, levy ml. the pathophysiologic mechanism of cerebellar mutism. surgical neurology. 2006 7//;66(1):18-25. 6.gelabert-gonzalez m, fernandez-villa j. mutism after posterior fossa surgery. review of the literature. clinical neurology and neurosurgery. 2001 jul;103(2):111-4. pubmed pmid: 11516555. epub 2001/08/23. eng. 7.rekate hl, grubb rl, aram dm, hahn jf, ratcheson ra. muteness of cerebellar origin. archives of neurology. 1985 jul;42(7):697-8. pubmed pmid: 4015467. epub 1985/07/01. eng. 8.yonemasu y. cerebellar mutism and speech disturbance as a complication of posterior fossa surgery in children. 13th annual meeting of the japanese society for pediatric neurosurgery; tsukuba, japan1985. 9.holmes g. the croonian lectures on the clinical symptoms of cerebellar disease and their interpretation. lecture ii. 1922. cerebellum (london, england). 2007;6(2):148-53; discussion 1. pubmed pmid: 17566247. epub 2007/06/15. eng. 10.holmes g. the symptoms of acute cerebellar injuries due to gunshot injuries. brain. 1917 december 1, 1917;40(4):461535. 11.turgut m. re: the pathophysiologic mechanism of cerebellar mutism (ozgur et al. surg neurol 2006;66:18-25). surgical neurology. 2007 7//;68(1):117. 12.tahta k, cirak b, pakdemirli e, suzer t, tahta f. postoperative mutism after removal of an anterior falcine meningioma. journal of clinical neuroscience. 2007 8//;14(8):793-6. 13.ersahin y, mutluer s, cagli s, duman y. cerebellar mutism: report of seven cases and review of the literature. neurosurgery. 1996 jan;38(1):605;discussion 6. pubmed pmid: 8747952. epub 1996/01/01. eng. 14.lechtenberg r, gilman s. speech disorders in cerebellar disease. annals of neurology. 1978 apr;3(4):285-90. pubmed pmid: 666268. epub 1978/04/01. eng. 15.mariën p, saerens j, nanhoe r, moens e, nagels g, pickut ba, et al. cerebellar induced aphasia: case report of cerebellar induced prefrontal aphasic language phenomena supported by spect findings. journal of the neurological sciences. 1996 12//;144(1–2):34-43. 16.marien p, engelborghs s, pickut ba, de deyn pp. aphasia following cerebellar damage: fact or fallacy? journal of neurolinguistics. 2000 7/15/;13(2–3):145-71. 17.al-anazi a, hassounah m, sheikh b, barayan s. cerebellar mutism caused by arteriovenous malformation of the vermis. british journal of neurosurgery. 2001 feb;15(1):47-50. pubmed pmid: 11303661. epub 2001/04/17. eng. 18.turgut m. transient "cerebellar" mutism. child's nervous system : chns : official journal of the international society for pediatric neurosurgery. 1998 apr-may;14(4-5):161-6. pubmed pmid: 9660116. epub 1998/07/11. eng. 19.riva d, giorgi c. the cerebellum contributes to higher functions during development: evidence from a series of children surgically treated for posterior fossa tumours. brain. 2000 may;123 ( pt 5):1051-61. pubmed pmid: 10775549. epub 2000/04/25. eng. 20.pollack if. posterior fossa syndrome. international review of neurobiology. 1997;41:411-32. pubmed pmid: 9378600. epub 1997/01/01. eng. 21.gordon n. mutism: elective or selective, and acquired. brain & development. 2001 mar;23(2):83-7. pubmed pmid: 11248456. epub 2001/03/15. eng. 22.sharkey l, mcnicholas f. 'more than 100 years of silence', elective mutism: a review of the literature. european child & adolescent psychiatry. 2008 aug;17(5):255-63. pubmed pmid: 18357427. epub 2008/03/22. eng. 23.steinhausen hc, juzi c. elective mutism: an analysis of 100 cases. journal of the american academy of child and adolescent psychiatry. 1996 may;35(5):606-14. pubmed pmid: 8935207. epub 1996/05/01. eng. 276 moscote-salazar et al transient mutism and cerebellar ischemic stroke 24.coplin wm, kim dk, kliot m, bird td. mutism in an adult following hypertensive cerebellar hemorrhage: nosological discussion and illustrative case. brain and language. 1997 10/1/;59(3):473-93. 25.dietze dd, jr., mickle jp. cerebellar mutism after posterior fossa surgery. pediatric neurosurgery. 1990;16(1):25-31; discussion pubmed pmid: 2133406. epub 1990/01/01. eng. 26.koh s, turkel sb, baram tz. cerebellar mutism in children: report of six cases and potential mechanisms. pediatr neurol. 1997 apr;16(3):218-9. pubmed pmid: 9165512. pubmed central pmcid: pmc3399684. epub 1997/04/01. eng. 27.van dongen hr, catsman-berrevoets ce, van mourik m. the syndrome of 'cerebellar' mutism and subsequent dysarthria. neurology. 1994 nov;44(11):2040-6. pubmed pmid: 7969956. epub 1994/11/01. eng. 28.aguiar ph, plese jp, ciquini o, marino r. transient mutism following a posterior fossa approach to cerebellar tumors in children: a critical review of the literature. child's nervous system : chns : official journal of the international society for pediatric neurosurgery. 1995 may;11(5):306-10. pubmed pmid: 7648574. epub 1995/05/01. eng. 29.asamoto m, ito h, suzuki n, oiwa y, saito k, haraoka j. transient mutism after posterior fossa surgery. child's nervous system : chns : official journal of the international society for pediatric neurosurgery. 1994 may;10(4):275-8. pubmed pmid: 7923241. epub 1994/05/01. eng. 30.d'avanzo r, scuotto a, natale m, scotto p, cioffi fa. transient "cerebellar" mutism in lesions of the mesencephalic-cerebellar region. acta neurologica. 1993 aug;15(4):289-96. pubmed pmid: 8249672. epub 1993/08/01. eng. 31.mariën p, de smet hj, wijgerde e, verhoeven j, crols r, de deyn pp. posterior fossa syndrome in adults: a new case and comprehensive survey of the literature. cortex. 2013 1//;49(1):284-300. 32.ersahin y. transient mutism after brain stem infarction. acta neurochirurgica. 1999;141(9):1020. pubmed pmid: 10610613. epub 1999/12/28. eng. 33.mewasingh ld, christiaens f, aeby a, christophe c, dan b. crossed cerebellar diaschisis secondary to refractory frontal seizures in childhood. seizure : the journal of the british epilepsy association. 2002 dec;11(8):489-93. pubmed pmid: 12464508. epub 2002/12/05. eng. 34.ackermann h, mathiak k, ivry rb. temporal organization of "internal speech" as a basis for cerebellar modulation of cognitive functions. behavioral and cognitive neuroscience reviews. 2004 mar;3(1):14-22. pubmed pmid: 15191639. epub 2004/06/12. eng. 35.decety j, sjoholm h, ryding e, stenberg g, ingvar dh. the cerebellum participates in mental activity: tomographic measurements of regional cerebral blood flow. brain research. 1990 dec 10;535(2):313-7. pubmed pmid: 2073609. epub 1990/12/10. eng. 36.ivry r, fiez j. cerebellar contributions to cognition and imagery. 2nd ed. gazzaniga m, editor. cambridge, ma: mit press; 2000. 37.ivry r, justus t, middleton c. the cerebellum, timing, and language: implications for the study of dyslexia. wolf m, editor: york press; 2001. 38.lotze m, montoya p, erb m, hulsmann e, flor h, klose u, et al. activation of cortical and cerebellar motor areas during executed and imagined hand movements: an fmri study. journal of cognitive neuroscience. 1999 sep;11(5):491-501. pubmed pmid: 10511638. epub 1999/10/08. eng. 39.van mourik m, catsman-berrevoets ce, van dongen hr, neville bg. complex orofacial movements and the disappearance of cerebellar mutism: report of five cases. developmental medicine and child neurology. 1997 oct;39(10):686-90. pubmed pmid: 9352731. epub 1997/11/14. eng. microsoft word 3_ienceanst_csf 148 iencean et al csf phosphorylated neurofilament biomarker of sci csf phosphorylated neurofilament subunit nf-h (pnf-h) levels are biomarkers of spinal cord injury st.m. iencean1, didona ungureanu1, al. tascu2, b. costachescu1, a.st. iencean3, i. poeata1 1“grigore t. popa” university of medicine and pharmacy iasi 2“carol davila” university of medicine and pharmacy bucharest 3emergency hospital “prof. dr. n. oblu” iasi abstract several studies showed that the phosphorylated form of the neurofilament subunit nf-h (pnf-h) are related to neuronal injuries and its detection provide information about the presence and degree of neuronal loss. neurofilaments are three subunits, namely nf-l, nf-m and nf-h. the phosphorylated neurofilament subunit nf-h (pnf-h) is present into serum and csf in significant amounts following neuronal injury and may be detected. the pnf-h can be a biomarker of the neuronal injuries and its detection allows the monitoring neuronal pathology and may provide diagnosis and prognosis in humans. we are interested in pnf-h as biomarker of neuronal injury in spinal cord injury and we used a pnf-h elisa test capable of detecting the levels of phosphorylated nf-h (pnf-h) to patients with spinal cord injury. we studied the pnf-h levels in csf in two patients with spinal cord injury (sci) and for normal values of pnf-h we determined the csf pnf-h level from individuals without neurological damage. the pnf-h values of csf from the two patients with sci were 5-10 times higher than the normal and its higher values were related to an unfavorable outcome. in conclusion, although the number of cases is very low only two, in the context of experimental studies in animals with sci, we can say that pnf-h is marker in sci in humans and its increased values are consistent with an unfavorable outcome. key words: biomarker, phosphorylated neurofilament subunit, spinal cord injury. introduction three major subunits of neurofilaments are namely heavy (nf-h), medium (nfm) and light (nf-l) subunits on the basis of molecular weight and these neurofilament are concentrated in large motor axons. the phosphorylated neurofilament subunit nf-h (pnf-h) is present into csf in significant amounts following neuronal injury and may be detected. several studies showed the pnfh is a biomarker of the neuronal injuries and its detection allows the monitoring neuronal pathology and we wished to study the pnf-h levels in csf as biomarker of neuronal injury in spinal cord injury. we measured pnf-h concentration by elisa test in csf in two spinal cord injury patients and and we correlated the values of pnf-h with the clinical evolution, also we measured the normal romanian neurosurgery (2013) xx 2: 148 – 150 149 values in samples obtained by lumbar puncture from individuals without neurologic disorders. cases presentation case 1 a 50-years old man with acute cervical spine injury and tetraplegia after a motor vehicle accident was admited 3 hours after the accident. radiology and cervical ct showed a bilateral c5-c6 facet dislocation and anterior luxation. (figure 1) the patient had marked vegetative disorders (neurogenic shock, respiratory failure, priapism etc.) and the treatment in intensive care unit included high doses of methylprednisolone and cervical spinal traction to reduce the luxation. unfortunately evolution was unfavorable with death in 3 days. case 2 a 53-years old man with acute cervical spine spine injury with tetraplegia after fall from a horse cart was admited 5 hours after the accident. radiology and cervical ct showed a unilateral c4-c5 dislocation with subluxation and spinal cord compresion. immediate surgical treatment consisted of anterior cervical approach with reduction and decompresion and stabilsation with autologous iliac crest bone graft. favorable evolution with csf samples obtained before surgery and each day for four days postoperatively. results we determined the normal level of pnf-h in samples obtained by lumbar puncture from five individuals without neurologic disorders and its values are similar to the normal level set by petzold and shaw in 2007: 0 ng/ ml to 0.9 ng/ml. figure 1 case 1 c5 c6 luxation and tetraplegia table 1 values of pnf-h in csf (ng/ml) day 1 day 2 day 3 day 4 day 5 case 1 9.3 10.9 9.3 case 2 4.5 5.5 5.9 6.5 5.6 normal 1 0.2 0.2 normal 2 0 normal 3 0 normal 4 0.9 0.9 normal 5 0.1 0.1 the normal values and the values of pnf-h in the two cases are shown in the table 1. the normal level of pnf-h in human csf was set less than or equal to 0.94 ng/ml (petzold and shaw, 2007). discussion and conclusion there are only two cases of spinal cord injury with csf phosphorylated 150 iencean et al csf phosphorylated neurofilament biomarker of sci neurofilament subunit nf-h (pnf-h) levels measurement. the normal values of pnf-h from five individuals without neurologic disorders are similar to the normal level set by petzold and shaw in 2007: less than or equal to 0.94 ng/ml. the pnf-h values of csf from the two patients with sci were 5-10 times higher than the normal. the case 1 of spinal cord injury with severe evolution and death had ten times higher values of pnf-h than the normal and the case 2 with favorable evolution had only five or six times higher of pnf-h values than the normal. there are several studies on the phosphorylated form of the neurofilament subunit nf-h (pnf-h) related to neuronal injuries but few data on pathological values of pnf-h in csf in patients with spinal cord injury. although there are only two cases, the results are similar to the experimental data, but it need analysis of a statistically significant number of cases in order to confirm the value of biomarker pnf-h in spinal cord injury. in conclusion the phosphorylated form of the neurofilament subunit nf-h (pnfh) is biomarker in sci in humans and its increased values are consistent with an unfavorable outcome. this study about acute traumatic spinal cord injury is the subject of the grant: “immediate neuroprotective therapy in acute traumatic spinal cord injury”, that won the 2011 national competition of national research council (cncs), ideas, grant number: pn-ii-id-pce-2011-30569, funded by cncs – uefiscdi romania. corresponding author: a.st. iencean neurosurgery, “prof. dr. nicolae oblu” hospital iasi, andrei_steffan@yahoo.com references 1. gerry shaw, cui yang, rebecca ellis, kevin anderson, j. parker mickle et all. hyperphosphorylated neurofilament nf-h is a serum biomarker of axonal injury biochemical and biophysical research communications 336 (2005) 1268–1277 2. axel petzold, gerry shaw comparison of two elisa methods for measuring levels of the phosphorylated neurofilament heavy chain j of immunological methods 319 (2007) 34–40 3. şt.m. iencean, i. poeată, gh. solcan, dana turliuc,e.c. popescu, b. costăchescu, a.şt. iencean: news and views of neuroprotection in complete traumatic spinal cord injuries, romanian neurosurgery, 2011, vol xviii,4;412 420 4. st.m. iencean, i. poeata, didona ungureanu, d. cuciureanu,b. costachescu, al. chiriac. traumatic spinal cord injuries: neuroprotection and recent outcomes romanian neurosurgery, 2012, vol xix,3; 210216 5. d de jong, r w m m jansen, y a l pijnenburg, w j a van geel, g f borm, h p h kremer, m m verbeek: csf neurofilament proteins in the differential diagnosis of dementia j neurol neurosurg psychiatry 2007;78:936–938 6. johannes brettschneider, axel petzold, sigurd d. sußmuth, g b. landwehrmeyer et all. neurofilament heavy-chain nfh in cerebrospinal fluid supports the differential diagnosis of parkinsonian syndromes movement disorders, vol. 21, no. 12, 2006 7. melissa m. gresle, helmut butzkueven, and gerry shaw neurofilament proteins as body fluid biomarkers of neurodegeneration inmultiple sclerosis multiple sclerosis international, volume 2011, article id 315406, 7 8. stephen b lewis, regina a wolper, lynn miralia, cui yang and gerry shaw detection of phosphorylated nf-h in the cerebrospinal fluid and blood of aneurysmal subarachnoid hemorrhage patients j of cerebral blood flow & metabolism (2008) 28, 1261 9. kevin j. anderson, stephen w. scheff, kelly m. miller, kelly n. roberts, et all. the phosphorylated axonal form of the neurofilament subunit nf-h (pnf-h) as a blood biomarker of traumatic brain injury j of neurotrauma, 2008, 25 : 1079 1085 10. petzold a, keir g, warren j, fox n, rossor mn. a systematic review and meta-analysis of csf neurofilament protein levels as biomarkers in dementia. neurodegener dis. 2007;4(2-3):185-94. microsoft word 14pascav_theroleof.doc 354 v. pasca et al intraoperative ultrasonography in low-grade gliomas the role of the intraoperative ultrasonography in low-grade gliomas. case report v. pasca1, şt.i. florian1,2, andreea magyoros1 1cluj county emergency hospital, neurosurgical department 2university of medicine and pharmacy “iuliu hatieganu” cluj-napoca abstract objective: use of intraoperative ultrasound for localizing tumors and determining the extent of resection. materials and methods: we report two patients diagnosed with brain tumors that underwent intraoperative ultrasonoghraphy in localizing and defining the borders of tumors and assessing the extent of their resection. discussions: intraoperative ultrasound brain scanning is extremely useful to detect the cerebral lesion, the relationships with the nearby structures, the estimation of vascularization, the grade of resection and other associated lesions. the tumor image is different from the normal anatomical cns structures, and some features like soft or hard tissue, cystic or necrotic areas can be visualized. conclusion: cerebral intraoperative ultrasound is a benefit for the surgical act, thus being the neurosurgeon’s “deep-seated eye”. keywords: low grade glioma, ultrasonography mode b, doppler backround medical practice requires a correlation of clinical aspects, imaging and treatment methods in order to have a successful outcome. in the neurosurgical field, approaching the intracranial lesion is more challenging than in other surgical specialties because the cranial vault can not be “squeezed” as the neurosurgeon would like to do it. in corticalized brain tumors the approach is easy. the maximum usage of ultrasound takes place during gliomas and metastases operations because of their subcortical deep-seated localization, where the need to pinpoint the tumor site is important so that a major brain damage to be avoided. ct scan and mr imaging are utilized to diagnose brain lesions. intraoperatively, the mri and ultrasound scanning are the tools used to localize the lesions. intraop. mri is of a higher sensitivity and can be correlated with the preop. mr images but, it’s still expensive, needing a special equipment and a quite long examination time. the real-time bmode and doppler sonography is easy, fast, reproducible, inexpensive and relatively simple equipment (1,5). one of the limitations of the intraoperative ultrasonography is that it is difficult to correlate with the preoperative examinations (ct, mri ), because the slices are different and the quality of the image somehow is poorer. however, some lesions are highly visible in ultrasound without requiring contrast enhancement. romanian neurosurgery (2010) xvii 3: 354 – 358 355 this study, supported by two clinical case presentations, highlights both the usefulness of the intraoperative ultrasound for lesion site and the quality of the echographic images. material and methods case one (figure 1 a, b, c, d) patient bc, a 36 years old male, admitted with headaches, vomiting, right omonime hemianopsy. the native and contrast enhanced cerebral ct scan revealed a hypodense lesion in the left occipital lobe with slight post contrast enhancement. t1 weighted mri images showed a decreased signal intensity lesion with distortion of the nearby structures and low contrast enhancement. on t2weighted images the lesion is of low signal intensity and with ill-defined tumor margins. intraoperative ultrasound was performed for tumor location and its relationships with the surrounding anatomical structures. the sonographic image was of a homogenous, hyperechogenic lesion, poor delineated with the aspect of an amphora with the neck oriented upwards. the cortical sulcus for the optimal approach to the tumor was also visualized and the doppler mode unveiled a low-grade tumor vascularization. macroscopically, a grey, friable, poorly defined, poorly vascularized and infiltrative tumor was removed. after ablation, the ultrasound was used to asses the extent of resection at the end of surgery. there was a clear boundary between the tumor and the cerebral edema and no signs of hemorrhage or ischemic lesions after surgery. figure1 a preoperative b mode ultrasonography figure 1 b b mode ultrasonography: for the tumor and reper figure 1 c postoperative ultrasonography 356 v. pasca et al intraoperative ultrasonography in low-grade gliomas figure 1 d mri cerebral figure 2 a preoperative ultrasonography figure 2 b postoperative ultrasonography highlighting zone resection and the tumoral rest figure 2 c doppler ultrasonography figure 2 d mri cerebral case two (figure 2 a, b, c, d) female patient, ma, 29 years old admitted in our department with partial seizures, dromomania, moderate intracranial hypertension syndrome, without papillary stasis at the romanian neurosurgery (2010) xvii 3: 354 – 358 357 ophthalmoscope examination. on the ct scan a hypointense lesion in the left temporal lobe with poor enhancement after contrast administration and displacement of the neighboring structures was detected. the mri t1-weighted images showed the left temporal lobe lesion, hypointense, poorly defined margins, with little contrast enhancement and with the corresponding mass effect. in t2-weighted imaging, the lesion has a moderate signal intensity and cerebral edema around the tumor mass. during surgery, the echographic imaging helped in localizing and defining the margins of the tumor. the tumor echoimage was hyperdense, homogenous with no well defined borders, poorly vascularized and with a moderate mass effect. after evaluating the cortical sulci above the tumor and the depth of the tumor, an ash-grey colored, friable, lowgrade vascularized and poorly defined mass lesion was removed. postoperatively, the resection control was done with the realtime b mode ultrasound. discussions astrocytomas are intraaxial, infiltrating brain tumors with a poor blood supply. according to the who grading system there are three types: who grade i corresponds to pilocytic astrocytoma, who grade ii corresponds to low-grade (diffuse) astrocytoma, who grade iii corresponds to anaplastic astrocytoma. grade ii astrocytoma appears as a poorly defined, homogeneous, infiltrating, low blood supply, usually unilocular lesion. astrocytomas of the cns arise in the subcortical areas and the regional effects include compression, invasion, and destruction of the brain parenchyma, leading to cortical surface flattening and altered cortical vascularization. sonographically, the lesion is hyperechoic, homogenous with ill-defined margins and perilesional edema which is seen as less echo-intense than the tumor. the mass effect on the surrounding cns structures is evident and the cortical sulci are left in place, the tumor extending along the arcuate fibers (7, 8 and 9). on the doppler mode the tumor vascularization is poor and the blood supply to the surrounding brain is affected according to the tumor localization. there are no intratumoral cysts or necroses which are seen as hypo or anechogenic areas. as keles et al. stated,(6) the main advantage is that the intraoperative ultrasound is a real time examination performed on certain anatomical features of each operative field. as it requires a certain pressure on the cortex during ultrasound examination, the brain structures and the image of the lesion are slightly modified from that of ct or mri investigations but, with all those the relationship between them remains the same. brain ct and mri studies are useful to pinpoint brain injuries and their effect on nearby structures, giving an overview of the intracranial content and details of lesion. the drawback is that they are not “live” examinations. intraoperative cerebral ultrasonograghy uses ultrasonic waves to highlight the injury. images are formed by analyzing the reflected waves from interfaces situated at different distances from the transducer (5). using distinct physical principles the echo images are different according to one of the three modes used in ultrasonography. intraoperative cerebral echography is a complementary examination for detecting the mass lesion in order to obtain the most easy and safe surgical approach (2,4). after 358 v. pasca et al intraoperative ultrasonography in low-grade gliomas tumor excision, the cerebral sonography is useful in assessing the extent of the resection, the anatomical relationship and the existence of some of the surgery produced injuries like hemorrhage, cerebral ischemia. ultrasound b-mode doppler sonography enables the estimation of tumoral and perilesional vascularization and the pulsed doppler specifies if the vessels are of arterial or venous type. signs like cortical blood supply, flattening of the cortical sulci, changing in the consistency of brain parenchyma at light palpation are indirect marks of a tumoral mass, and they are only clues in the whole surgical planning. b-mode real-time linear sonographic scanning can be used to identify and localize the margins of the lesion, the degree of the vascularization, the relationship to the surrounding neurovascular structures and cortical grooves, the type of the mass ( cystic, parenchymatous or mixt), size and the depth of the lesion(3). conclusion real-time b-mode intraoperative ultrasound is a complementary, convenient and user-friendly method for identifying, localizing, characterizing the pathological aspects, assessing the extent of tumor resection, pointing the relationships with surface and deep cerebral structures and, recognizing surgical complications at the time of tumor removal (hemorrhage, ischaemia, edema). the intraoperative ultrasound scanning is a useful medical tool, which doesn’t exclude the ct and mri examinations, and needs a good understanding of ultrasonography and anatomy. it is considered as the neurosurgeon’s “deep-seated” eye. references 1.dudea s.m., badea r. „manual de ultrasonografie vasculara doppler” editura mededicala universitara „iuliu hatieganu” cluj-napoca 2001. 2.keles g.e., lamborn k. r, berger m.s., „coregistration accuracy and detection of brain shift using intraoperative sononavigation during resection of hemisferic tumors” neurosurgery 53:556-564, 2003. 3.litofsy n.s., bauer a.m., kasper r.s., „image guided resection of high-grade glioma: pacient selection factors and outcome” neurosurgical focus, 2006. 4.lopez-hernanades f., hernanadez-palazon j., reuspintado m, „craniotomia guada por ultrasonografia bidimensional para exeresis de tumor cerebral supratentorial” neurocirugia 2008, 19: 530-536. 5.mircea p.a., dudea.s.m., badea r. „ecografie generala” tipografia umf. „iuliu hatieganu” clujnapoca 2000 6.nikas d.c, hartov a., lunn k., rick k., paulsen k., roberts d.w., „coregistered intraoperative ultrasonography in resection of malignant glioma” neurosurgery focus 14(2): article 6, 2003. 7.solhelm o., selbekk t. et col. „intraselar ultrasound in transsfenoidal surgery: a novel technique” neurosurgery 2010 66(1), 173-186. 8.tirakotai w, miller d, heinze s, benes l, bertalanffy h, sure u. „ a novel platform for image – guided ultrasound”, neurosurgery 58: 710-718, 2006. 9.unsgaarg g. „ brain operation guided by realtime two dimensional ultrasound: new possibilities as a result of improved image quality” neurosurgery online, vol.51, n.2, aug.2002, 402-412. microsoft word 5.iliescub_mrtractography romanian neurosurgery (2010) xvii 4: 413 – 420 413 mr tractography for preoperative planning in patients with cerebral tumors in eloquent areas b. iliescu1, d. negru2, i. poeata2 1“prof. dr. n. oblu” emergency clinical hospital, neurosurgery department, iasi 2“gr.t. popa” university of medicine and pharmacy, iasi abstract resection of the maximum amount of tumoral tissue while preserving the function of the brain within or neighboring the tumor region established itself as a fundamental goal of modern oncologic neurosurgery. a major step in preoperative mapping of eloquent cerebral cortex was taken reliably through the use of functional magnetic resonance imaging. however it does not provide any information about the white matter tracts that may be affected by invasive, intrinsic brain tumors. the advances in diffusion-tensor (dt) imaging techniques have been used to map white matter tracts in the normal brain. the aim of this study was to demonstrate the role of dt imaging in preoperative mapping of white matter tracts in relation to cerebral neoplasms and the way it can influence the operative decision in our practice. ten patients with brain malignancies within or neighboring eloquent cortical areas (nine glioblastoma and one grade two astrocytoma) underwent dt imaging examinations prior to tumor excision. anatomical information about white matter tract location, orientation, and projections was obtained in every patient. depending on the tumor type and location, evidence of white matter tract edema (one patient), infiltration (one patient), displacement (five patients), and disruption (three patients) could be assessed with the aid of dt imaging in each case. diffusion-tensor imaging allowed for visualization of white matter tracts and was found to be beneficial in the surgical planning for patients with intrinsic brain tumors. the authors’ experience with dt imaging indicates that anatomically intact fibers may be present in abnormal-appearing areas of the brain. whether resection of these involved fibers results in subtle postoperative neurological deficits requires further systematic study. keywords: cerebral eloquent areas, glioblastoma, mr tractography introduction resection of the maximum amount of tumoral tissue while preserving the function of the brain within or neighboring the tumor region established itself as a fundamental goal of modern oncologic neurosurgery. taking into account that most patients with tumors in eloquent areas such as the motor cortex present with no or mild neurological deficits, it is fundamental to have a precise representation of the relationship between the neoplasic mass and the normal brain structures, in order to achieve a maximal resection of the tumor without causing neurological deterioration. in glioblastoma cases it is considered that an area of 2-3 cm around the tumor is infiltrated by tumor cells at the moment of 414 b. iliescu, d. negru, i. poeata mr tractography for preoperative planning diagnosis14. in most cases an extensive resection cannot be performed without inflicting serious neurological deficits. however, even an extensive resection does not prevent tumor relapse. however, a complete resection is clearly correlated with a longer survival (1, 11). tractography is one of the methods that can ensure achieving this goal. although routine structural mr images can accurately demonstrate brain tumors, as well as important information on the relationship of the tumor with crucial brain structures (such as blood vessels) they fall short in providing precise information on the involvement and integrity of the white matter tracts in the immediate region surrounding tumors. the high-intensity signal often seen in the white matter adjacent to a tumor on t2-weighted or flair images may represent either tumor extension or edema in the surrounding normal white matter tracts. however, more detailed information on the relationship between the expanding mass and white matter tracts is one of the important facts to be taken into account in planning the treatment of patients with eloquent areas brain tumors. several functional approaches such as fmri and intraoperative electrophysiological mapping are used in the presurgical localization of eloquent cortex neighboring brain tumors (7, 13). functional mr imaging allows for the identification of important functional areas of the cerebral cortex that may be invaded by a neoplasm. this imaging modality focuses on cortical structures but does not provide information about subcortical gray matter and white matter, which in many instances may be involved in invasive, intrinsic brain tumors. diffusion tensor imaging (dti) can provide a wealth of information on the white-matter tracts using diffusion anisotropy maps (16). using directional information, the white matter tract organization is represented using directionally color-coded maps within the whole brain volume regardless of its structural integrity (15). in this study, we look at the role of dt imaging in characterizing the integrity of white matter tracts in patients with eloquent areas brain tumors and its implications in planning the appropriate treatment of these tumors. materials and method ten patients with intracranial eloquent areas neoplasms were selected for the study. patients ranged in age from 28 to 66 years of age (mean age 54 years). postoperatively histology showed glioblastoma in 8 cases, grade two astrocytoma in one case, and pilocytic astrocytoma in one case. the location of the lesions was the left temporal lobe in one patient, frontal lobe in two, insula in four, and parietal region in three. the dominant symptom at presentation was seizures (six patients), followed by paresis (hemi or monoparesis) in four patients, and motor aphasia in four patients. increased intracranial pressure was manifest in three patients (figure 1). magnetic resonance imaging studies were performed on a standard 1.5-tesla mr imaging scanner (philips achieva) with a standard quadrature birdcage head coil. dt mr imaging studies were performed as part of the presurgical tumor imaging protocol. as part of an approved institutional review board protocol, informed consent for the dt imaging portion of the study was obtained from each patient prior to scanning. romanian neurosurgery (2010) xvii 4: 413 – 420 415 a b figure 1 a. tumor localization for cases that underwent tractogrphy. b. white matter tracts findings in dti studies (percent of cases) color-coded dt imaging maps were analyzed. in every patient the tumors were isolated to one hemisphere, allowing for comparison between the affected tracts in the hemisphere in which the tumor was located and the contralateral control hemisphere. white matter tracts were then characterized as follows: displaced if they maintained normal anisotropy relative to the corresponding tract in the contralateral hemisphere but were situated in an abnormal location or with an abnormal orientation on color-coded orientation maps; edematous if they maintained normal anisotropy and orientation but demonstrated high signal intensity on t2weighted mr images; infiltrated if they showed reduced anisotropy but remained identifiable on orientation maps; and disrupted if anisotropy was markedly reduced such that the tract could not be identified on orientation maps. for tracts categorized as infiltrated, we did not attempt to determine whether anisotropy was reduced as a result of vasogenic edema, infiltration by the tumor, or a combination of these two factors. such a distinction may not be possible with dt imaging alone and is the subject of ongoing study by our group. results we were able to identify the extent of white matter tracts involvement in all patients using color-coded dt imaging maps and 3d reconstructions. normal white matter tracts were depicted contralaterally in all patients. the white matter findings were characterized for each patient. white matter involvement by mass occupying lesion was classified according to the criteria of displacement, infiltration, disruption, or edema in relation to the contralateral side. five large white matter pathways in five patients had deviated from their normal anatomical position when compared with fiber tracts in the contralateral hemisphere. the superior longitudinal fasciculus deviated in a medial or lateral direction in five of the five patients. the corticospinal tracts were deviated in three patients. the location of displacement varied depending on the location of the lesion (figure 2). deviation was seen in the corona radiata. lateral deviation of the fibers streaming within the inferior longitudinal fasciculus of the temporal lobe was demonstrated in one 416 b. iliescu, d. negru, i. poeata mr tractography for preoperative planning patient who developed a lesion towards the pole of the temporal lobe. evidence of white matter tract edema was seen in one patient (one glioblastoma case). in this patient, dt imaging reconstruction showed reduced anisotropy without displacement of white matter architecture, suggestive for tumor invasion (figure 3). diffusion-tensor imaging revealed evidence of white matter tract disruption in three patients. a b c figure 2 case of white matter tracts displacement. a. preoperative computer tomograph befre (left and after (right) contrast administration showing the parietal tumor (glioblastoma). b and c. 3d reconstruction dti showing displacement of the tracts surrounding the tumor the anterior aspect of the inferior longitudinal fasciculus in the left temporal lobe was obliterated by a glioblastoma. in the second case, a large temporo-insular glioblastoma produced a trimming of the anterior-posterior-directed fibers as well as romanian neurosurgery (2010) xvii 4: 413 – 420 417 projection fibers especially in the corticospinal tract and anterior thalamic radiation (figure 4), particularly evident when compared to the intact fibers in the contralateral hemisphere. in one case diffuse edema was seen along the peripheral edges of the tumor. in the patient with a glioblastoma, edema along the periphery of the temporal lobe involved the optic radiations in the parietal and temporal regions. the edema pattern, with edema interesting the fiber pathways of the optic radiations, was demonstrated on t2weighted images as well. dt imaging visualized the anterior/posterior fibers of the optic radiations in their normal anatomical position in relationship to unaffected fibers in the contralateral parietal and occipital lobes. a b figure 3 case of white matter tracts invasion a. t1-weighted(left) and enhanced t1-weighted (right) preoperative r image showing the parietal tumor (glioblastoma) b. 3d reconstructions dti showing edema of the tracts neighboring the tumor. a b c figure 4 case of white matter tracts disruption a. t1weighted(left) and enhanced t1-weighted (right) preoperative r image showing the temporal tumor (glioblastoma) b. 2d dti image showing the disruption of the tracts within the area of the tumor c. 3d dti reconstruction showing the same disruption of the tracts in the cerebral volume occupied by the tumor. 418 b. iliescu, d. negru, i. poeata mr tractography for preoperative planning discussion cerebral tumors may involve both functional cortical gray and white matter tracts. in order to achieve a good neurological outcome, the resection of these lesions requires a detailed understanding of functional anatomical relationships to cortical areas and adjacent white matter connections. this is of paramount importance when the tumor develops within or near an eloquent cortical area in the dominant hemisphere in which motor, sensory, speech, and cognitive functions are situated. understanding the location of the lesion in relation to the surrounding eloquent tissue represents a critical element in developing an operative plan. many diagnostic modalities are currently used to define eloquent regions of the brain. standard mr imaging, positron emission tomography, magnetoencephalography, and fmri are some of the tools used to investigate the location of functional cortical areas (2, 8). a thorough preoperative delineation of the tumor and a precise mapping of functional areas helps in determining critical relationships of the lesion to the surrounding cortical function. the resulting images can then be used within frameless stereotactic algorithms, allowing for the planning of optimal surgical approaches and determining the degree and volume of tumor resection (10). the goal of using these various mapping techniques is to delineate functional areas so that they can be preserved during surgical resection. maximal surgical tumor resection has been shown to correlate with longer patient survival and improved long-term functional status (11), representing the main predictor of patient outcome. current data shows that tumors that grossly invade areas of functional cortex may still retain functional fiber tracts within the pathological tissue. diffusion-tensor imaging provides information for tract identification when the white matter tracts are displaced by tumor. pathological states may affect the dt imaging measurements of intrinsic white matter pathways. wieshmann and colleagues (16) reported the case of one patient with a tumor in the right frontal lobe who presented with left hemiparesis. diffusion-tensor imaging documented deviation of fibers in normal-appearing white matter in relation to the anterior commissure – posterior commissure line when compared with measurements in normal patients. diffusion-tensor imaging represents a valuable preoperative diagnostic tool for evaluating expansive lesions within or close to vital cortical and subcortical structures. ten cases are analyzed in this study to demonstrate how dt mapping brings complementary information that helps elucidating the complex relationships between the tumor and its surrounding cerebral tissue. evidence of intact fiber bundles traversing areas of tumor invasion was apparent in two patients. other patients demonstrated displacement of white matter fibers from their normal anatomical position. in one patient with glioblastoma located centrally within the left hemisphere, the lesion displaced the corticospinal tracts within the corona radiata medially and anteriorly. knowledge of this displacement assisted in preoperative planning by informing the surgeon of the tract’s shifted location, thus allowing for adaptation of the surgical corridor to avoid destruction of the communicating white matter bundles. in this instance the tumor was approached from a temporal posterior direction, romanian neurosurgery (2010) xvii 4: 413 – 420 419 allowing for aggressive resection of the tumor while avoiding the anteriorly deviated motor fibers. this resulted in postoperative improvement of the patient’s hemiparesis, presumably due to the elimination of pressure on the corticospinal tracts. conclusions the effect of cerebral neoplasms on white matter pathways is not precisely understood with the aid of standard diagnostic modalities. diffusion-tensor imaging allowed for the identification of multiple viable white matter pathways within hemispheres involved by tumor. in this initial series of patients the information provided by dt imaging further defined precise relationships between cortical and subcortical white matter structures and cerebral neoplasms. involvement of white matter tracts represents an important piece of information in planning the surgical approach and in evaluating the extent of a safe resection in patients with intrinsic brain tumors. our experience with dt imaging indicates that anatomically intact fibers may be present in abnormalappearing areas of the brain. careful preoperative planning has to be complemented by intraoperative mapping and monitoring of eloquent cortical areas in order to insure a good neurological outcome of the surgery and valid functional prognostic. in planning these surgeries an equal importance should be attributed to the blood vessels that supply salient areas or tracts with significant functional value. references 1. ammirati m, vick n, liao yl, et al: effect of the extent of surgical resection on survival and quality of life in patients with supratentorial glioblastomas and anaplastic astrocytomas. neurosurgery 21:201–206, 1987 2. atlas sw, howard rs ii, maldjian j, et al: functional magnetic resonance imaging of regional brain activity in patients with intracerebral gliomas: findings and implications for clinical management. neurosurgery 38:329–338, 1996 3. bittar rg, olivier a, sadikot af, et al: cortical motor and somatosensory representation: effect of cerebral lesions. j neurosurg 92:242–248, 2000 4. cosgrove gr, buchbinder br, jiang h: functional magnetic resonance imaging for intracranial navigation. neurosurg clin n am 7:313–322, 1996 5. doran m, hajnal jv, van bruggen n, et al: normal and abnormal white matter tracts shown by mr imaging using directional diffusion weighted sequences. j comput assist tomogr 14:865–873, 1990 6. giese a., westphal m. glioma invasion in the central nervous system. neurosurgery 39:235–252, 1996 7. grafton st, woods rp, mazziotta jc, et al: somatotopic mapping of the primary motor cortex in humans: activation studies with cerebral blood flow and positron emission tomography. j neurophysiol 66:735– 743, 1991 8. handler t, et. al. delineating gray and white matter involvement in brain lesions: three-dimensional alignment of functional magnetic resonance and diffusion-tensor imaging. j neurosurg 99:1018–1027, 2003. 9. krings t, reinges mht, thiex r, gilsbach jm, thron m. functional and diffusion-weighted magnetic resonance images of space-occupying lesions affecting the motor system: imaging the motor cortex and pyramidal tracts. j neurosurg 95:816–824, 2001. 10. lehericy s, duffau h, cornu p, et al: correspondence between functional magnetic resonance imaging somatotopy and individual brain anatomy of the central region: comparison with intraoperative stimulation in patients with brain tumors. j neurosurg 92:589–598, 2000 11. mcdonald jd, chong bw, lewine jd, et al: integration of preoperative and intraoperative functional brain mapping in a frameless stereotactic environment for lesions near eloquent cortex. technical note. j neurosurg 90:591–598, 1999 12. mcgirt m.j., chaichana k.l., gathinji m., attenell f.j., than k., olivi a., weingart j.d., brem h., quiñones-hinojosa a. independent association of extent of resection with survival in patients with malignant brain astrocytoma. j neurosurg 110:156–162, 2009 13. mueller wm, yetkin fz, hammeke ta, et al: functional magnetic resonance imaging mapping of the motor cortex in patients with cerebral tumors. neurosurgery 39:515–521, 1996 420 b. iliescu, d. negru, i. poeata mr tractography for preoperative planning 14. nagano n, sasaki h, aoyagi m, hirakawa k: invasion of experimental rat brain tumor: early morphological changes following microinjection of c6 glioma cells. acta neuropathol 86:117–125, 1993 15. pajevic s, pierpaoli c: color schemes to represent the orientation of anisotropic tissues from diffusion tensor data: application to white matter fiber tract mapping in the human brain. magn reson med 42:526–540, 1999 16. pierpaoli c, jezzard p, basser pj, et al: diffusion tensor mr imaging of the human brain. radiology 201:637–648, 1996 17. roux fe, boulanouar k, ranjeva jp, et al: cortical intraoperative stimulation in brain tumors as a tool to evaluate spatial data from motor functional mri. invest radiol 34:225–229, 1999 18. wieshmann uc, symms mr, parker gj, et al: diffusion tensor imaging demonstrates deviation of fibers in normal appearing white matter adjacent to a brain tumor. j neurol neurosurg psychiatry 68:501– 503, 2000. microsoft word 7chiriac_mecanical.doc 226 chiriac et al mechanical failures of ventriculo-peritoneal shunts mechanical failures of ventriculo-peritoneal shunts a. chiriac, i. poeata, b. iliescu1 “gr. t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract ventriculo-peritoneal (vp) shunt placement represents the most widely accepted form of treatment for most patients with hydrocephalus. despite significant improvements in vp shunt procedures, various complications remain a common situation. the diagnosis of shunt failure can be confounded by a variety of factors, mechanical failure being the most common cause of multiple shunt revisions in a lifetime. a better understanding of mechanisms of shunt failure will cause an improvement in the management of this neurosurgical procedure. key words: vp shunt, shunt malfunction, mechanical failure. the defining mechanical shunt failure is not easy, and yet the literature is often quite ambiguous. numerous groups of patients with shunt failures that have been reported in the literature are difficult to interpret or to compare due to several reasons: the debate regarding what constitutes a failure of the shunt, and types of statistical analyzes applied to these series. while problems that are directly related to the shunt (as obstruction) are universally known as shunt complications, the problems due to its imperfect functioning (headache in different positions, subdural collection) are sometimes more difficult to interpret. in terms of shunt malfunction, any issues that require further operation seems to be the reasonable definition of shunt complications. in fact, we can extend this concept, and say that any subsequent surgical procedure to hydrocephalus treatment is a complication of the shunt (this includes also deaths to the failures category where no intervention has occurred). in reality the shunt failure causes are in direct relationship with it arises, on the other hand un improperly connected connector or improper shunt placement will occur immediately, while a problem due tube degeneration or fracture can take many years. because shunt complications are closely related to the time of surgery, constant supervision is required over time to adequately assess the likelihood of each failure at various time points after surgery. regarding the incidence of shunt failure we found that the risk of these is maximum in the first months of operation, estimated at a percentage of 18% to 40% after surgery. later, after this critical period, the risk remains around 4-5% per year (proper functioning time of it is being at least five years). an analysis of timing of shunt failures appearances in pediatric case series show significant differences. if some types of shunt failures tend to happen sooner or later after surgery for other risk period is slightly lower or something more long. for romanian neurosurgery (2012) xix 3: 226 229 227 a given type of failure causing factors are not always the same, for example ventricular catheter may be blocked immediately after surgery by a blood clot in the ventricles or later by choroid plexus adhesion. it is also likely that these factors differ in adult patients to children. many variables and interactions between various factors that appear in shunt failure analyzes studied in the literature makes the statistical interpretation of the results to be questionable. main types of mechanical failure rates are shown in figure 1. shunt obstruction as shown in studies of literature, shunt obstruction accounts for almost half of all shunt complications, especially in pediatric series. this percentage is lower in adults, but still significant. is interesting to note that the risk for shunt obstruction varies strongly related to time, the risk being higher in the immediate postoperative period. literature mentions that the report series of patients studied, the likelihood of shunt obstruction was approximately 7% in the first month after surgery and then decreased to 2-4% in the next four months. after the fifth month, the likelihood of complications was less than 0.5% per month for the next ten years. these variable results on the risk of failure resulting from obstruction causes are typically occurring in some periods. impurities, blood clots in the csf or wrong ventricular catheter placement are causes of quick obstruction, while developing choroid plexus, ependimar resection or immunological reactions are causes of late obstruction. the shunt may be obstructed at three different levels: the entry point (proximal obstruction); at the valve system (valve obstruction); the distal end (distal obstruction). factors that influence these obstructions are still investigated, but however an analysis of potential causes of these types of failures can be made. proximal obstruction chemically inert catheter that stays in a primary cavity (clean) by liquid (pure water) has no reason to obstruct. however, silicone catheters are not completely inert csf may contain impurities or tissue and the ventricular cavity can be so contracted at the contact point of the catheter and the wall or choroid plexus that these structure that are floating in csf can be naturally driven along catheter csf flow in the proximal direction (figure 2). components of csf. cellular impurities or blood clots favor blocking of distal holes or lumen of the ventricular catheter. an external drainage or repeated lumbar punctures may be a temporary solution to this problem. ventricular catheter location. this is probably one of the oldest controversies in the treatment of hydrocephalus. conventional ventricular catheter should be placed in front of monro foramen to avoid choroid plexus. however, a frontal ventricular catheter introduced through the occipital horn can be pulled back to choroid plexus due to increased head in children or ventricular collapse, causing migration of catheter surrounding parenchymal tissue. moreover, there are some near choroid plexus tissue that can bloc the catheter (ependymal cells, glial tissue, connective and leptomeningeal tissue). statistical studies in the literature have shown that proximal catheter placement in the frontal horn of lateral ventricle has a lower obstruction rate than those placed in the occipital area. in pediatric series an 228 chiriac et al mechanical failures of ventriculo-peritoneal shunts analysis of proximal obstruction by positioning instead showed some catheter obstruction to its placement in the posterior ventricle through the occipital area and when he was pushed in the direction of the frontal horn. in fact, there is probably not ideal catheter tip placement, the lowest risk being the largest ventricular area after decompression by drainage, varying from one patient to another. other factors involved in obstruction include catheter stiffness and method of his holes opening. due to elasticity silicone rubber catheter does not remain rigid at a right angle, tending to straighten to the ventricular wall. there is no evidence that special catheter tip designs are able to prevent obstruction, plus they can cause choroid plexus farm attaching the tubing. valve system obstruction the second component of obstruction risk is the valve system. very few obstructions are due to bad manufacturing of valve device, these being tested before implantation. besides these manufacturing issues, valves are flow restriction creates areas more or less dependent on valve type and dead spaces that can facilitate the accumulation of dirt and colonization of tissue that eventually lead to obstruction. limitation of supra drainage obtained through a severe restriction of flow can increase the risk to block the valve. valve obstruction can occur in different circumstances, so, it can occur as a result of active phenomena (bacterial proliferation, the development of immune reactions) or passive phenomena (accumulation of impurities). valve obstruction can be prevented by improving valves designs in the sense of avoiding dead spaces (figure 3). figure 1 percentage distribution of vp shunt failures figure 2 proximal catheter occlusion figure 3 valve occlusion distal obstruction risk of distal obstruction varies with shunt position and distal catheter's design. distal catheter openings with closed end carry a risk of obstruction. existence of dead space below the hole leading to the accumulation of impurities that causes catheter pulling. risk of this type of obstruction is not currently to open-ended catheters (figure 4). romanian neurosurgery (2012) xix 3: 226 229 229 figure 4 distal catheter occlusion distal partial obstructions may be due to reduced absorption capacity of the peritoneal cavity. most of these phenomena have clear origin (peritoneal infection, localized tumors), however many cases still remain unclear (immune reaction to drainage device). conclusions in conclusion, aside from advanced techniques, specialists should try to get a good compromise as in terms of patient and system status are guided by the following: trying to shunt a pure and clear csf can mean the use of alternative methods such as external ventricular drainage or transient drainage portion in patients who showed impurities during diagnosis of hydrocephalus; proximal catheter tip location in place that is expected to remain the most widely after ventricular decompression; selection of appropriate features for flow pressure is to limit as much as possible the phenomenon of overdrenage and avoid placing the catheter in a collapsed cave; shunt checking and particularly the valve in regarding the presence of impurities or clots and verification of normal flow before distal catheter insertion into drainage cavity. references 1. cochrane dd, kestle jr. the influence of surgical operative experience on the duration of first ventriculoperitoneal shunt function and infection. pediatric neurosurgery 2003; 38: 295-301; 2. choudhury ar. avoidable factors that contribute to the complications of ventriculoperitoneal shunt in childhood hydrocephalus. childs nerv syst 1990; 6: 346349; 3. ivan lp, choo sh, venturegra ecg: complications of ventriculoatrial and ventriculo periotoneal shunts in anew children's hospital canjsurg 1980; 23: 566-568.2; 4. george a. alexiou, ilias manolakos, neofytos prodromou: ventriculo-peritoneal shunt infection caused by brucella melitensis : letters to the editor: pediatr infect dis j. 2008 dec; 27 (12) : 1120; 5. joseph h. piatt, jr, hugh j.l. garton :clinical diagnosis of ventriculoperitoneal shunt failure among children with hydrocephalus: pediatr emerg care: 2008 april; 24 (4) :201-210; 6. mclaurin rl. ventricular shunts: complications and results,in: pediatric neurosurgery. 2nd ed. saunders,philadelphia ;1989. pp. 229; 7. pandey p, suri a, singh a, mahapatra a : brain abscessan unusual complication of ventriculoperitoneal shunt: indian j pediatr: 2003 oct; 70 (10): 833-4; 8. samuel r. browd, brian t. ragel, oren n. gottfried, john r. w. kestle : failure of cerebrospinal fluid shunts :part i:obstruction and mechanical failure: pediatr neurol. 2006 feb; 34 (2): 83-92. microsoft word 4shettyrohanunruptured.doc 34 romanian neurosurgery (2010) xvii 1: 34 45 unruptured arteriovenous malformations of brain an overview rohan shetty, yoko kato, takeya watabe, daikichi oguri, junpei oda, sadato akiyo, motoharu hayakawa, hirotoshi sano department of neurosurgery fujita health university hospital dengakugakubo, aichi-ken japan -4701192 email:shettyrohanadi@yaho.co.in abstract arteriovenous malformations are congenital lesions that occur most commonly in the supratentorial region. these space-occupying vascular lesions consist of multiple arteries and veins, connecting as a fistula without an intervening normal capillary bed. typically, avm’s are single lesions, except when associated with hereditary hemorrhagic telangiectasia. the histology includes clusters of normal or dilated arteries and abnormal veins with calcification and occasionally some prior haemorrhage. keywords: grading, hemorrhage, re haemorrhage, seizures, unruptured arteriovenous malformation introduction arteriovenous malformations (avm) of the brain are congenital vascular lesions that account for approximately 2%3% of all hemorrhagic strokes[1]. despite the relative rarity of the disease (with an estimated current detection rate of approximately 1/100 000 person-years) avms pose a significant neurological problem because patients are mostly young and otherwise healthy. moreover, the availability of noninvasive imaging has rapidly increased the detection of incidental avm’s. the complex cerebrovascular anatomy of avm’s makes them a challenge to treat, and the treatment itself carries significant risks. to evaluate the possible benefit of a risky treatment, one needs to understand the natural history and prognosis of the disease. the complexity of avm’s makes them a rather heterogeneous group of lesions in terms of various factors possibly affecting the risk of rupture and subsequent hemorrhagic stroke. over the past several decades, several groups have contributed to our knowledge of the haemorrhage risk associated with untreated avm’s. however, the development of therapeutic strategies has made it increasingly rare that a large proportion of patients would be followed conservatively. rohan shetty et al unruptured avm 35 clinical presentation the most common presentation in unruptured avm’s is focal or generalized seizures, which occur in 25% of patients. other presentations include headache in 15% of patients, which may mimic migraine, focal neurologic deficit, and pulsatile tinnitus. rarely, a deficit may be caused by a “steal” phenomenon of blood through the fistula, which deprives some surrounding neurons of required blood. the lesions are distinctly uncommon in children; presentations include congestive heart failure and large head due to hydrocephalus. headache not due to hemorrhage is the presenting symptom in 7% to 48% of patients [11]. no distinctive type, frequency, persistence, or severity occurs. earlier speculations have proved unfounded for a pattern differentiated from classical or common migraine, or that recurrent unilateral headache reflects an underlying avm [12]. response to medication has not been systematically studied, and although some reports state improvement in headache [13], proof is lacking that patients under optimal medical headache management require invasive treatment of their symptoms. some reference to focal neurologic deficits without signs of underlying hemorrhage has been reported in 1% to 40%, with this large range reflecting non uniformity of definitions. only a few patients (4% to 8%) have well documented progressing neurologic deficits [11]. once considered common, progressing syndromes were thought to be caused by “stealing” (ie, cerebral artery hypotension leading to ischemia in brain tissue adjacent to the lesion) [14,15]. arteriovenous malformations sometimes induce remarkable degrees of cerebral arterial hypotension, but evidence is lacking for a causal link with symptoms[11]. as of today, no definite information exists that may warrant invasive avm treatment on the assumption of a clinical relevant intracranial steal caused by an unruptured avm [16]. venous hypertension or mass effect of the nidus offers alternative explanations for progressing focal neurologic deficits [17]. the natural history of unruptured avm’s seems more favorable than for those discovered after initial haemorrhage. the average risk of bleeding from an unruptured avm (1.2% per year) seems to be about 5 times lower as compared with already ruptured malformations (5.6% per year). the bleeding risk seems to be particularly low in the most frequent subgroup of patients harbouring lobar avms with superficial venous drainage (0.9%peryear). finally, although some instances of avm rupture may indeed be disastrous, there seems to be a far lower morbidity and mortality than after intracerebral bleeding from other causes. haemorrhage: peak age for haemorrhage is between age of 15 -20 yrs with a mortality of 10% & a morbidity of 30 -50 % from each bleed. haemorrhage was related to avm size with small avm’s presenting more often with bleed than do large ones. larger avm’s more often presented with seizures merely because of involvement of the cortex. so conclusion is that small avm’s are more 36 romanian neurosurgery (2010) xvii 1: 34 45 lethal than larger ones. among patients who present with haemorrhage, the risk of recurrent haemorrhage is elevated early; the risk during the first year is between 6% and 17% and then decreases to a baseline level by the third year. after a second haemorrhage, the risk of another recurrent haemorrhage maybe even higher during the first year, up to 25%.clinical and imaging features at the time of initial diagnosis of an avm may predict future haemorrhage risk. from a clinical standpoint, prior haemorrhage is a strong predictor of haemorrhage. on imaging, small avm diameter or small volume may be predictive, but this has not been noted consistently. the venous drainage system may be particularly important, with deep venous drainage a potential predictor of haemorrhage. impaired venous drainage and a single draining vein also have been predictive of hemorrhage. in the arterial system of the periventricular or intraventricular area, the risk of haemorrhage may be increased by the presence of very distal aneurysms on the small feeding arteries (the so-called intranidal aneurysms), the presence of multiple aneurysms, and arterial supply via middle cerebral artery perforators. the presence of any non-nidal aneurysms also may increase the risk of haemorrhage. developments in the field of genetic research and biomarkers,with the goal of identifying patients with increased avm hemorrhage risk, are ongoing. initial results show associations of the tumor necrosis factor (tnf)-�-238 ag genotype [35 ], the interleukin (il)-6174gg genotype with high expression of il-6 protein in brain avm tissue [36], and an abnormal balance of matrix metalloproteinase (mmp)-9 and tissue inhibitors of metalloproteinases (timp) in the avm with increased probability of avm hemorrhage [37].whether mechanisms involved will be helpful in the decision process of avm treatment remains unsettled rebleeding: rebleeding rate in the first year after haemorrhage was 6% in one series and 18% in another series. in another large series ( ) the annual rate was 4% regardless of type of presentation. rebleeding rate declined at 2% per year after 10 years. life time risk of haemorrhage age at presentation estimated years of life 1% annual risk 2 % annual risk 3% annual risk 0 76 53 78 90 15 62 46 71 85 25 52 41 65 79 35 43 35 58 73 45 34 29 50 64 55 25 22 40 53 65 18 16 30 42 75 11 10 20 28 85 6 5.8 11 17 rohan shetty et al unruptured avm 37 seizures: seizures not caused by hemorrhage are the mode of initial presentation in 16% to 53% of cases. grand mal attacks occur in 27% to 35%, with the remainder being partialor partial complex seizures [51]. few reports document seizure frequency, but response to antiepileptic medication appears satisfactory [52]. patients with intractable seizures under conservative management do exist but data on their frequency are scarce. improvement of seizures in over 50% of these patients after stereotactic radiotherapy was reported in a small recent series [53]. the younger the patient at the time of diagnosis, higher the risk of developing convulsions. 20 years risk age 10-19 ---44% risk age 20-29 ----31% risk age 30-60 ----6% risk no avm found incidentally or presenting with neurological deficits developed seizures. avm’s and aneurysms: fifty eight percent of patients with avm’s have aneurysms. 75% of aneurysms are located on the major feeding artery. aneurysms also may form within the nidus or on the draining veins. categories of aneurysms associated with avm’s: type aneurysm location 1 proximal on ipsilateral major feeding artery 1 a proximal on major artery related but contralateral to avm 11 distal on superficial feeding artery 111 proximal or distal on deep feeding artery (bizarre ) 1v on artery unrelated to avm investigations unenhanced computed tomography has relatively low sensitivity, with calcification and hypointensity may be visualised; however, with the use of contrast enhancement, the arteriovenous system may be seen. computed tomographic angiography [cta] provides better vascular detail than magnetic resonance angiography [mra]. magnetic resonance imaging [mri] is more sensitive, with findings such as flow voids and hemosiderin deposition on t1-weighted and t2weighted imaging. magnetic resonance angiography (mra) can provide additional information regarding relation of avm to surrounding cerebral structures. additional information can be obtained with the use of functional mri, to identify eloquent brain tissue, and diffusion-tensor imaging to identify different important white matter tracts. angiography remains the standard by which to evaluate the architecture of the avm, including presence or absence of associated aneurysms, presence or absence of venous outflow obstruction, and pattern of venous drainage. three dimensional mra and three dimensional angiography may provide additional detail to guide interventional treatment. grading: spetzler martin avm grading system [20] graded feature points size small (< 3 cms ) medium (3-6 cms) large (>6 cms ) 1 2 3 eloquence of adjacent brain non eloquent eloquent 0 1 patten of venous drainage superficial only deep 0 1 38 romanian neurosurgery (2010) xvii 1: 34 45 a separate grade 6 is reserved for untreatable lesions, (by any means) resection of these would almost unavoidably be associated with disabling deficit or death. discussion patients harbouring brain avm’s are at a life long risk for haemorrhagic stroke, the natural history is poorly understood. natural history & predictive features of haemorrhage was studied at toronto western hospital on 678 consecutive patients & were followed for 1931. 7 patient years [50]. the rate of haemorrhage over long term follow up was recorded. the impact of baseline clinical & radiographic features & partial treatment on time to haemorrhage were analyzed using survival analysis. neurologic outcome after haemorrhage was assessed using glasgow outcome score. haemorrhage risk was 4.61% per year for entire cohort, 7.8 % per year for brain avm”s with haemorrhagic presentation 4.61 % for brain avm”s with seizure presentation, 3.99 % for patients not harbouring aneurysms, 6.93 % for patients harbouring aneurysms, 5.42 % for patients with deep venous drainage. haemorrhagic presentation was significant independent predictor of future haemorrhage.. haemorrhage risk was unchanged in patient who underwent partial arteriovenous embolisation. so they concluded that brain avm”s presenting with haemorrhage, deep venous drainage, or associated aneurysms had twofold likelihood of future haemorrhage. so aggressive short term management ie; total embolisation / microsurgery was suggested for patients harbouring high risk lesions & therapeutic approaches with longer obliteration times targeted at patients harbouring low risk natural history of haemorrhage. in a study conducted between july 1997 & 2003, 73 consecutive patients with grade iv & grade v avm”s were evaluated prospectively at barrow neurosurgical institute [32].treatment recommendations were classified as complete treatment, partial treatment & no treatment. retrospectively haemorrhage rates associated with these treatment groups were also calculated. in the prospective portion of the study [intention to treat analysis ], no treatment of avm”s was recommended for 75 % of patients and partial treatment for 10 % of patients. aneurysms associated with an avm were obliterated by surgery or endovascular treatment in 10 % patients & complete surgical removal of avm for 5% of the patients. the overall haemorrhage rate for grade iv & grade v avm”s was 1.5% per year. the annual risk of haemorrhage was 10.4 % among patients who previously received incomplete treatment compared with patients without previous treatment. hence they concluded that haemorrhage risk was comparatively less [1.5 % ] for grade iv & grade v avm”s than for grade i to grade iii avm”s. so authors recommended no treatment be given for grade iv & grade v avm”s. partial treatment was discouraged for the fact that it worsened the natural history of an avm. the authors did not support palliative treatment of avm except in specific circumstances of arterial rohan shetty et al unruptured avm 39 or intranidal aneurysms or progressive neurological deficits related to vascular steal. complete treatment was recommended for patients with progressive neurological deficits caused by haemorrhage of the avm. relatively low combined morbidity & mortality rates for grade iv & grade v avm”s of 17 % & 22 % respectively was reported. mahesh.v.jayaraman et al[41] studied on 61 patients retrospectively with grade iv & grade v avm”s. they reviewed the demographic, angiographic features, presenting symptoms & time of all haemorrhage events before or after treatment initiation. the annual pretreatment haemorrhage rate of 10.4 % was higher for all patients with 13.9% for patients with haemorrhagic presentation and 7.3% for patients with non haemorrhagic presentation. post treatment haemorrhage rates were 6.1% per year for all patients, 5.6% for patients presenting with haemorrhage and 6.4% in patients with non haemorrhagic presentation. based on this data they concluded that grade iv and grade iv avm”s warranted treatment and initiation of treatment did not increase the risk of haemorrhage. initiation of treatment in haemorrhagic group lowered the risk of re haemorrhage to levels with those of non haemorrhagic presentation. [patients with grade iv and grade v avm’s with prior haemorrhage are at a higher risk of recurrent haemorrhage] risk factors for subsequent haemorrhage in patients with cerebral arteriovenous malformations was studied by s.yamada et al[38] on 305 consecutive patients with avm’s between 1983 &2005. patients were followed up until the first haemorrhage, start of any treatment or end of 2005. possible risk factors that were investigated included age at initial diagnosis, sex, type of initial presentation, size and location of avm, nidus and venous drainage pattern. they reported an annual bleeding rate in haemorrhagic group was 6.8% after haemorrhage and the rate decreased in 5 years to 1.72 %. in the non haemorrhagic group annual bleeding rate of 3.12 % was reported. patients presenting with headache annual bleeding rate of 6.48% was reported and for asymptomatic presentation annual bleeding rate was 6.44%. conversely patients presenting with seizures had an annual bleeding rate of 2.20 % and with patients with neurological deficits had a bleeding rate of 1.73 %. a significant three fold increase of rebleeding was reported for children, female, and deep seated avm patients. the increased risk was highest among this group in the first year after initial haemorrhage and there after gradually reduced. ian. g. fleetwood et al[33] from loma linda university studied on cohort of 96 patients retrospectively with the avm’s in the basal ganglia and thalamus with respect to tendency of the lesions to bleed between the time of detection and their eventual successful management. mean age at diagnosis was 22.7 years and 51% were male patients. intracranial haemorrhage was the event leading to clinical detection in 71. 9 % of patients and 85.5% of these were left with hemiparesis. after diagnosis twety five 40 romanian neurosurgery (2010) xvii 1: 34 45 patients had bled a total of 49 times. the risk of haemorrhage after detection of an avm of basal ganglia or thalamus was 9.8% per patient per year. hence they concluded that rate of haemorrhage in patients with avm’s of thalamus and basal ganglia are much higher at 9.8% compared to avms in other locations [24% per ]year.they also concluded that risk of incurring a neurological deficit with each haemorrhagic event was high hence treatment was recommended for these patients. at the university of toronto avm study group assessed patients with large and deep avm’s for their risk of future haemorrhage since 1989 and concluded that patients with avm’s large size and deep location in the brain were the most important and significant factors associated with higher risk of future hemorrhagic events [31]. long-term follow-up study was done in an unselected, consecutive patient population with avm’s admitted to the department of neurosurgery at helsinki university central hospital between 1942 and 2005[50]. patients with untreated avm’s were followed from admission until death, occurrence of avm rupture, initiation of treatment, or until the end of 2005. patients with at least 1 month of follow-up were included in further analysis. annual and cumulative incidence rates of avm rupture as well as several potential risk factors for rupture were analyzed. two hundred and thirty eight patients with a mean follow-up period of 13.5 years were included (range, 1 month–53.1 years). the average annual risk of hemorrhage from avms was 2.4%. the risk was highest during the first 5 years after diagnosis, decreasing thereafter. risk factors predicting subsequent avm hemorrhage in univariate analysis were young age, previous rupture, deep and infratentorial locations, and exclusively deep venous drainage. previous rupture, large avm size, and infratentorial and deep locations were independent risk factors according to multivariate models. jae h choi et al[42]; studied on morbidity from spontaneous haemorrhage of untreated brain arteriovenous malformation. in a group of 241 consecutive avm patients from prospective columbia avm data bank initially presenting with haemorrhage in comparison to 84 non –avm patients with intracerebral haemorrhage from northern manhattan study [nomas ] served as control group, it was concluded that haemorrhage either at initial presentation or during follow up of untreated avm’s carried lower morbidity than intracranial hemorrhages from other causes. retrospective evaluvaton of outcomes in 46 unruptured avm’s & rate for bleeding during the follow up period was done by uno masaki et al[28]. in 18 of 22 patients in grade i & ii avm’s were surgically excised and the outcome was good. six of 9 patients in grade iv & v were conservatively treated. for patients in grade iii various treatments were performed according to the location of the avm, and their outcomes were favourable. rate of surgical complication was 15.3 % in26 unruptured avm’s. based on this data they concluded to rohan shetty et al unruptured avm 41 aggressively treat patients with grade i & grade ii.[uno masaki et.al] crawford p m et al[7] studied on unoperated avm’s with a mean follow up of 10.4 years. they concluded that there was a 42% risk of haemorrhage, 18% risk of epilepsy & 27% risk of neurological deficits by 20 years after diagnosis in unoperated patients. figure 1 a figure 1 b conclusion the behaviour of brain arteriovenous malformations (avms) remains difficult to predict. host, environmental, and gene susceptibility factors may influence the clinical manifestation. the complication with the most significant clinical sequelae is intracranial haemorrhage. figure 1 c figure 1 mri and angiography of a patient with of unruptured right frontal arteriovenous malformation (from emergency hospital “prof dr n oblu ”iasi, romania, dr n dobrin’s collection) slowly accumulating data suggest that once the process of bleeding starts, the lesion appears to become destabilized and susceptible to more bleeding [23,24]. therefore, the indication for treatment of ruptured avm’s is generally not under dispute. unruptured avm’s whatever the treatment technique, the crude 42 romanian neurosurgery (2010) xvii 1: 34 45 proportion of treatment-associated morbidity usually ranges around 10% in the most recent reports, but this seems acceptable given the persistent risk of potentially devastating bleeding from an untreated avm. when it comes to unruptured brain avm’s, however, the long-assumed benefit of interventional therapy seems to have become less clear. current natural history data from the columbia avm database, the ucsf avm study project, and the scottish intracranial vascular malformation study suggest the annual risk of spontaneous haemorrhage may be as low as 1% for unruptured avm’s [25,26]. in addition, the growing availability of mr imaging has led to a substantial increase in the incidental detection of unruptured malformations ranging between 54% and 62% of all diagnosed avm’s in modern population-based data-sets [25,26]. in the light of these figures, neurovascular teams face the clinical dilemma of how to balance the inherent risk of intervention against the potentially low haemorrhage rates in patients harbouring an unruptured brain avm[5] these figures raise concern that invasive treatment may be connected with an unfavourable benefit vs. risk ratio to the degree that some have become reluctant to recommend interventional therapy for many patients presenting with an unruptured avm. evidence-based guidelines give non intervention as one option in avm management [27]. although current clinical practice favours intervention in most patients, some clinicians understandably prefer to undertake intervention in specific subgroups of patients who are likely to benefit from the intervention. besides haemorrhagic presentation, predictors of avm haemorrhage during natural history follow-up include increasing age, deep brain location, associated aneurysms, and exclusive deep venous drainage [5,10]. by contrast, the risk of spontaneous haemorrhage may drop below 1% per year in avm’s without these risk factors [24]. these characteristics may guide the neurovascular team during case assessment and patient counselling, but the fact that the same factors not only increase the natural history risk but also the hazard of intervention, clearly adds to the complexity. careful explanation and sufficient time is given to patients as be the need, because they are often otherwise healthy young adults who are actively involved in their working and family life. although data from randomised trials to guide the choice of treatment are lacking, surgical resection, radiosurgery, embolisation, or a combination of these is appropriate for avm’s that are grade i to iii. the choice of treatment will depend on the specific features of the lesion, with consideration of the, age of the patient, presence or absence of bleeding and associated aneurysm, diameter and location of associated aneurysms, and pattern of venous drainage. grade i and grade ii surgery is recommended and consideration of endovascular embolisation followed by microsurgery is recommended for grade iii [27]. consideration of radio surgery is recommended for lesions that may be associated with an increased risk of surgical complications, owing to their rohan shetty et al unruptured avm 43 anatomical location or feeding vessel anatomy, in particular for lesions in the eloquent area. grade iv and grade v lesions palliate treatment is suggested for lesions with intranidal or arterial aneurysms or progressive neurological deficits related to vascular steal[32]. complete treatment is recommended for patients with progressive neurological deficits caused by haemorrhage of the avm. [because of the risks of treatment, grade iv and grade v lesions are generally not treated. american stroke association recommendation-2001]. lacking randomized studies on avm treatment, there is considerable uncertainty in the existing clinical literature on indications for invasive treatment in these patients. the best way to address the issue is a randomized clinical trial. the currently launched a randomized trial of unruptured brain avms (aruba) is a randomized, multicenter, international trial comparing outcome of invasive avm treatment with conservative management in patients with unbled avm’s. aruba is investigating whether treatment for consenting adults aged ≥18 years, with an unruptured brain avm that is potentially treatable, over a minimum follow up period of five years, based on outcome assessments by treating physicians. we will have to wait for fresh data from this study for enhancing our knowledge on management of unruptured avm’s for serving mankind. references 1. brown rd jr md, kelly.d.fleming md. natural history & management of intracranial vascular malformations mayo clinic proc feb 2005;80[2]; 269281 2. mccormick wf. pathology of vascular malformations of the brain. in: wilson cb, stein bm, eds. intracranial arteriovenous malformations. baltimore, md: williams & wilkins; 1984:44-63. 3. brown rd jr, wiebers do, torner jc, o’fallon wm. incidence and prevalence of intracranial vascular malformations in olmsted county, minnesota, 1965 to 1992. neurology. 1996;46:949-952. 4. kucharczyk w, lemme-pleghos l, uske a, brantzawadzki m, dooms g, norman d. intracranial vascular malformations: mr and ct imaging. radiology. 1985;156:383-389. 5. brown rd jr, wiebers do, forbes g, et al. the natural history of unruptured intracranial arteriovenous malformations. j neurosurg. 1988;68: 352-357. 6. wilkins rh. natural history of intracranial vascular malformations: a review. neurosurgery. 1985;16:421430. 7. crawford pm, west cr, chadwick dw, shaw md. arteriovenous malformations of the brain: natural history in unoperated patients. j neurol neurosurg psychiatry. 1986;49:1-10. 8. graf cj, perret ge, torner jc. bleeding from cerebral arteriovenous malformations as part of their natural history. j neurosurg. 1983;58:331-337. 9. ondra sl, troupp h, george ed, schwab k. the natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. j neurosurg. 1990;73:387-391. 10. mast h, young wl, koennecke hc, et al. risk of spontaneous haemorrhage after diagnosis of cerebral arteriovenous malformation. lancet. 1997;350:10651068. 11. kondziolka d, mclaughlin mr, kestle jr. simple risk predictions for arteriovenous malformation hemorrhage. neurosurgery. 1995;37:851-855. 12. forster dm, steiner l, hakanson s. arteriovenous malformations of the brain: a long-term clinical study. j neurosurg. 1972;37:562-570. 13. hartmann a, mast h, mohr jp, et al. morbidity of intracranial hemorrhage in patients with cerebral arteriovenous malformation. stroke. 1998;29:93 14. miyasaka y, yada k, ohwada t, kitahara t, kurata a, irikura k. an analysis of the venous drainage system as a factor in hemorrhage from arteriovenous malformations. j neurosurg. 1992;76:239-243. 15. kader a, young wl, pile-spellman j, et al. the influence of hemodynamic and anatomic factors on hemorrhage from cerebral arteriovenous malformations. neurosurgery. 1994;34:801-80 44 romanian neurosurgery (2010) xvii 1: 34 45 16. batjer h, samson d. arteriovenous malformations of the posterior fossa: clinical presentation, diagnostic evaluation, and surgical treatment. j neurosurg. 1986;64:849-856. 17. drake cg. cerebral arteriovenous malformations: considerations for and experience with surgical treatment in 166 cases. clin neurosurg. 1979;26:145208. 18. heros rc, korosue k, diebold pm. surgical excision of cerebral arteriovenous malformations: late results. neurosurgery. 1990;26:570-577. 19. sundt tm jr, piepgras dg, stevens ln. surgery for supratentorial arteriovenous malformations. clin neurosurg. 1991;37:49-115. 20. spetzler rf, martin na. a proposed grading system for arteriovenous malformations. j neurosurg. 1986;65:476-483. 21.hamilton mg, spetzler rf. the prospective application of a grading system for arteriovenous malformations. neurosurgery. 1994;34:2-6. 22. mclaughlin mr, kondziolka d, flickinger jc, lunsford s, lunsford ld. the prospective natural history of cerebral venous malformations. neurosurgery. 1998;43:195-200. 23. graf cj, perret ge, torner jc (1983) bleeding from cerebral arteriovenous malformations as part of their natural history. j neurosurg 58:331–337 24. stapf c, mast h, sciacca rr et al (2006) predictors of hemorrhage in patients with untreated brain arteriovenous malformation. neurology 66:1350–1355 25. al-shahi r, bhattacharya jj, currie dg et al (2003) prospective, population-based detection of intracranial vascular malformations in adults: the scottish intracranial vascular malformation study (sivms). stroke 34:1163–1169 26. stapf c, mast h, sciacca rr et al (2003) the new york islands avm study:design, study progress, and initial results. stroke 34: e29–33 27. ogilvy cs, stieg pe, awad i et al (2001) recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the stroke council, american stroke association. circulation 103:264 28. uno masaki. et al journal of surgery for cerebral stroke vol 34 (3) 157-162 2006 29. stiver, shirley i. neurosurgery vol 46(14);811-819 april 2000 30.harbaugh, kumberly s et al. neurosurgery vol34 (4) 1994. 31.stefani m a,porter pj,et al large and deepbrain arteriovenous malformationsare associated with risk of future haemorrhage. stroke2002;33:1220-1224. 32. han pp, ponce fa spetzler rf. intention to treat analysisof spetzler –martin grade ivand v arteriovenous malformations:natural history and treatment paradigm. j neurosurgery 2003;98: 3-7 33.33.fleetwood ig,marcellus ml et al. deep arteriovenous malformations of the basal ganglia and thalamus:natural history.j neurosurgery 2003 ;98 :747750 34. mohr jp, stapf c, sciacca rr, et al.: treatment outcome versus natural history risk inpatients with unruptured brain arteriovenous malformation [abstract]. neurology 2004 35. achrol as, pawlikowska l, mcculloch ce, et al.: tumor necrosis factor-alpha-238g>a promoter polymorphismis associated with increased risk of new hemorrhage in the natural course of patients with brain arteriovenous malformations. stroke 2006, 37:231–234. 36. chen y, pawlikowska l, yao js, et al.: interleukin-6 involvement in brain arteriovenous malformations. ann neurol 2006, 59:72–80. 37. hashimoto t, wen g, lawton mt, et al.: abnormal expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in brain arteriovenous malformations. stroke 2003, 34:925–931 38.yamada s, takagi y et al risk factors for subsequent haemorrhage in patients with cerebral arteriovenous malformations j neurosurgery2007;107:965-972 39. han pp, spetzler r f et al,intention to treat aanalysis of spetzler –martin grade iv & grade v avm j neurosurgery 2003 ;98: 3-7 40. hartman a, mast h, stapf et al treatment of avm of brain. curr neurol rep 2007;7:28 34 41. jayaraman m v, marcellus ml, et al haemorrhage rate in spetzler martin grade iv – grade v arteriovenous malformation: is treatment justified stroke 2007 ;38:325-329. 42. choi j h mast h,et al clinical outcome after first & recurrent haemorrhage in patientswith untreated brain arteriovenous malformations. stoke 2006 ;37:12431247. 43. mansmann u, meisel j, brock m, et al.: factors associated with intracranial hemorrhage cases of cerebral arteriovenous malformation. neurosurgery 2000, 46:272–279. 44. osipov a, koennecke hc, hartmann a, et al.: seizures in cerebral arteriovenous malformations. type, clinical course, and medical management. intervent neuroradiol1997, 3:37–41. 45. mast h, mohr jp, osipov a, et al.: ‘steal’ is an unestablished mechanism for the clinical presentation of cerebral arteriovenous malformations. stroke 1995, 26:1215–1220. rohan shetty et al unruptured avm 45 46. turjman f, massoud, tf,vineula f et al correlation of angioarchitectural features of cerebral arteriovenous malformations with clinical presentation of haemorrhage. neurosurgery,1995;37:856-60. 47.robert m friedlander arteriovenous malformations of the brain n eng journal of med 356;26:27042711. 48. leodante da costa,m christoperwallace et al the natural history & predictive features of haemorrhage of brain arteriovenos malformations. stroke 2009;40:100105 49. marco. a. stefani, philip. j. porter et al natural history & predictive features of haemorrhage of brain arteriovenous malformations stroke 2002;33:12201224. 50. j.hernesniemi et al natural history of brain arteriovenous malformations. neurosurgery.vol 63;5: nov 2008. 51. hofmeister c, stapf c, hartmann a, et al.: demographic, morphological, and clinical characteristics of 1289 patients with brain arteriovenous malformation. stroke 2000 31:1307–1310 52. osipov a, koennecke hc, hartmann a, et al.: seizures in cerebral arteriovenous malformations. type, clinical course, and medical management. intervent neuroradiol 1997, 3:37–41. 53. schauble b, cascino gd, pollock be, et al.: seizure outcomes after stereotactic radiosurgery for cerebral arteriovenous malformations. neurology 2004, 63:683– 687. microsoft word 6ivanovmarcelneuronavigation.doc 166 m. ivanov et al percutaneous treatment of trigeminal neuralgia neuronavigation in the percutaneous treatment of trigeminal neuralgia. technical note m. ivanov1, andrew brodbelt2, n. ianovici3, a.v. ciurea4, i. poeata5, f.m. gramada2 1neurosurgery, plymouth hospitals nhs trust, derriford hospital, plymouth, uk 2neurosurgery, walton centre for neurology and neurosurgery, liverpool, uk 3neurosurgery, clinical emergency “n. oblu” hospital, iasi, romania 4neurosurgery ,clinical emergency hospital “bagdasar arseni”, bucharest, romania, 5neurosurgery ,university of medicine and pharmacy “gr.t.popa”, iasi, romania abstract objective: to describe neuronavigationguided percutaneous radiofrequency thermocoagulation in the treatment of trigeminal neuralgia. methods: neuronavigation guided percutaneous radiofrequency thermocoagulation of the gasser ganglion was used in nine patients with trigeminal neuralgia who developed resistance to drugs used in the treatment of tn or have had adverse effects due to drug toxicity. the age of the patients was between 62 and 78 years. results: all patients had immediate pain relief after thermocoagulation guided by neuronavigation. neuronavigation allowed visualization of instrument position in relation to target and the related anatomical structures. the technique helped preoperative planning of the optimal trajectory for needle insertion. there were no complications of the procedure. conclusion: image guided percutaneous thermocoagulation in the treatment of trigeminal neuralgia is a safe and promising procedure. the technique has reduced the risk of postoperative complications caused by “hunting” of the foramen ovale. keywords: neuronavigation, image guided surgery, trigeminal neuralgia, minimally invasive surgery, frameless stereotaxy. introduction idiopathic trigeminal neuralgia has an incidence of 3-5 cases in 100 000. it is characterized by spontaneous facial pain that is either predominantly episodic (as in tn1) or constant (as in tn2) in nature. pain distribution is unilateral and follows the sensory distribution of the trigeminal nerve, typically radiating to the maxillary (v2) or mandibular (v3) area. since the description by hartel in 1912 of transovale trigeminal rhizotomy a number of treatment options have been described. in patients unsuitable for microvascular decompression, selective interruption of the nociceptive fibres in most cases can provide pain relif18. glycerol11,14, phenol19 or alcohol infiltration, radiofrequency thermocoagulation6, balloon compression 2, 4, 9, 17, stereotactic radiosurgery 7, 8, 15, 16, peripheral nerve10 block or rhizotomy 3, 13 – have all been used. currently radiofrequency thermocoagulation, balloon compression and stereotactic radiosurgery are the most common ablative methods used. recent published reports suggest that between romanian neurosurgery (2010) xvii 2: 166 – 170 167 these radiofrequency thermocoagulation is more efficient in treating the pain syndrome, but is associated with a higher risk of complication5. most methods use a percutaneous approach to the foramen ovale, using x-ray guidance. accuracy depends on individual anatomy, the surgeon’s experience and the quality of imaging. a number of complications caused by “hunting” of the foramen ovale have been described. reports of ct guided targeting of the foramen ovale has shown reduced complications. we present our experience on the first 9 cases of trigeminal neuralgia treated in our hospital using the navigation guidance with a drf (dynamic reference frame) fixed to the patient’s forehead. methods subjects nine patients diagnosed with idiopathic (burchiel tn1 and tn2) trigeminal neuralgia were treated in the iasi neurosurgical centre using percutaneous thermocoagulation guided by neuronavigation. an mri scan was performed in all the cases to exclude an intracerebral lesion and a ct scan was used for preoperative planning, 3d rendering and integration of imaging into neuronavigation system. for navigation a radionics (2003) frameless neuronavigation system was used. radiofrequency thermocoagulation was performed using a radionics rfg-3cf generator (tew kit, radionics, burlington, ma). stimulation at 50 hz, 1 ms, and 0–0.3 volts was applied. the lesion was made at 60°c–70°c for 60-90 s. technique description image acquisition and preoperative planning. a helical ct scan with maximum 2 mm thickness was performed in all patients. images were transferred to the navigation station and a 3d reconstruction of the skull base contouring the foramen ovale and adjacent critical structures (carotid artery, cavernous sinus etc. – figure 1) was obtained. the target (upper postero-medial margin of the foramen ovale) and entry point (approximately 2-3 cm lateral to the ipsilateral labial commissura) was then planed. the obtained trajectory of the needle is verified in “probe’s eye” or in the “probe view” window of the neuronavigation system, avoiding bony elements and important soft tissue structures, allowing adjustment as required. intraoperative patient’s registration all the patients received premedication with atropine (0,5 mg intramuscular) and light sedation with midazolam. heart rate, blood pressure and blood oxygen saturation were monitored. a dynamic reference frame (drf) was applied to the forehead of the patient. it was attached with an elastic velcro band (radionics) and remained in a fixed position relative to the head during the entire procedure. as an alternative (eg. with medtronic stealth equipment) the reference point can be attached using a suction cup (figure 2) or adhesive material as in em guided procedures. the patient was registered using either surface matching, fiducials or anatomical landmarks. to achieve a better accuracy either a higher number of fiducials and anatomical landmarks (>15) or more extensive surface matching of the face contours was performed. no details of registration error were recorded, but from the literature we assumed this to be in a range of 1-3 mm. 168 m. ivanov et al percutaneous treatment of trigeminal neuralgia a b figure 1 a neuronavigation screenshot shows the needle position in relation to the foramen ovale and related anatomical structures; b drawing and 3d ct rendering (c) of the skull base and foramen ovale a b figure 2 a dynamic reference frame fixed on the patient’s forehead before registration; b the universal instrument recognition (uir) tool attached to the needle makes the tip of the instrument "visible" by the navigation system romanian neurosurgery (2010) xvii 2: 166 – 170 169 the cannula used with a stylet was attached to the universal instrument registration tool (uir) and registered. after aseptic field preparation and draping the previously established entry point is marked. a small perforation of the skin with 11 blade is made. the needle attached to the uir tool is guided by the neuronavigation up to the medial border of foramen ovale, avoiding the oral cavity (figure 2). the patient usually has ipsilateral masseter contraction and winces at this point. csf fluid may also be obtained in some cases. at this point stimulation of the trigeminal nerve can be performed for localization of the affected branch and eventually fine needle readjustment. a dose of propofol 1% (1 mg/kg) is administered and three sequential lesions, produced by 60to 80 second applications, are performed by increasing the temperature by 5°c each time starting with 60°c. at the end of the procedure the patient should feel hypoaesthesia in the corresponding dermatome of the trigeminal nerve. results in our series no procedure-related complications have been noticed in patients where neuronavigation-guided percutaneous radiofrequency thermocoagulation was performed. all patients had good immediately postoperative and at one year follow-up pain control. patient registration time was between 7 and 20 minutes (mean 12 minutes). overall length of time for the procedure was between 22 and 49 minutes (mean 29). it was higher in earlier cases and lower in later cases as learning curve is rapid. discussions ablative or compressive procedures targeting the gasserian ganglion continue to play an important role in the management of trigeminal neuralgia. localization of the foramen ovale can be difficult due to imaging quality (improved by biplanar radiology systems), operator inexperience and anatomical variations. the optimal target within foramen ovale is its posterior part. complication rates due to inaccurate targeting are described as being 5%-7%. optic nerve lesion, intracranial haemorrhage, carotid artery injury, carotico-cavernous fistula, lesion of other cranial nerves (oculomotor, trochlear, abducens) with secondary diplopia and facial haematoma are all described1. advantages of using neuronavigation include precision in localization of the foramen ovale, visualization of adjacent vascular and soft tissue structures, no irradiation of theatre personnel and no need for the radiographer in theatre. also it aids trainees and less experienced surgeons in intraoperative orientation and planning. the imaging is given simultaneously both in 3d and in classical sagittal, coronal and transversal planes 12, 20. disadvantages include the need for helical ct scan for preoperative planning and intraoperative guidance; slight initial increase to the length of surgery (short learning curve). a flexible needle risks inaccuracy if distortion occurs during passage through the soft tissues, this can be avoided by using a rigid stylet or cannula to guide the needle to the target. addition of a localizer may reduce the effective length of the needle, requiring either a longer needle/stylet or changes in the design of the localizer. 170 m. ivanov et al percutaneous treatment of trigeminal neuralgia conclusions neuronavigation guided approaches to the foramen ovale for the treatment of trigeminal neuralgia improves target visualization and potentially reduce the risk of complications. it is simple and precise. the preliminary results are encouraging. the future studies of a larger series of patients with longer follow-up will provide more detail about the efficiency and complications of this technique. references 1.headaches, cranial neuralgias, facial pain, classification and diagnostic criteria. international headache society]. rev prat 40:416-426, 429-450, 1990 2.belber cj, rak ra: balloon compression rhizolysis in the surgical management of trigeminal neuralgia. neurosurgery 20:908-913, 1987 3.cetas js, saedi t, burchiel kj: destructive procedures for the treatment of nonmalignant pain: a structured literature review. j neurosurg 109:389-404, 2008 4.cheshire wp: trigeminal neuralgia: for one nerve a multitude of treatments. expert rev neurother 7:15651579, 2007 5.kanpolat y, berk c, savas a, et al: percutaneous controlled radiofrequency rhizotomy in the management of patients with trigeminal neuralgia due to multiple sclerosis. acta neurochir (wien) 142:685689; discussion 689-690, 2000 6.kanpolat y, savas a, bekar a, et al: percutaneous controlled radiofrequency trigeminal rhizotomy for the treatment of idiopathic trigeminal neuralgia: 25-year experience with 1,600 patients. neurosurgery 48:524532; discussion 532-524, 2001 7.kondziolka d: functional radiosurgery. neurosurgery 44:12-20; discussion 20-12, 1999 8.kondziolka d, lunsford ld, flickinger jc: the application of stereotactic radiosurgery to disorders of the brain. neurosurgery 62 suppl 2:707-719; discussion 719-720, 2008 9.lee st, chen jf: percutaneous trigeminal ganglion balloon compression for treatment of trigeminal neuralgia--part i: pressure recordings. surg neurol 59:63-66; discussion 66-67, 2003 10.long dm: surgical therapy of chronic pain. neurosurgery 6:317-328, 1980 11.lunsford ld: glycerol rhizotomy for trigeminal neuralgia. j neurosurg 66:151-152, 1987 12.mandat t, brozyna b, krzymanski g, et al: an image-guided, noninvasive method of cannulation of the foramen ovale for awake, percutaneous radiofrequency rhizotomy. j neurosurg 111:1223-1225, 2009 13.morello g, bianchi m, migliavacca f: combined extra-intradural temporal rhizotomy for the treatment of trigeminal neuralgia. results in 409 patients. j neurosurg 34:372-379, 1971 14.north rb, kidd dh, piantadosi s, et al: percutaneous retrogasserian glycerol rhizotomy. predictors of success and failure in treatment of trigeminal neuralgia. j neurosurg 72:851-856, 1990 15.richards gm, bradley ka, tome wa, et al: linear accelerator radiosurgery for trigeminal neuralgia. neurosurgery 57:1193-1200; discussion 1193-1200, 2005 16.sheehan j, pan hc, stroila m, et al: gamma knife surgery for trigeminal neuralgia: outcomes and prognostic factors. j neurosurg 102:434-441, 2005 17.sweet wh: percutaneous methods for the treatment of trigeminal neuralgia and other faciocephalic pain; comparison with microvascular decompression. semin neurol 8:272-279, 1988 18.tew jm, jr., keller jt: the treatment of trigeminal neuralgia by percutaneous radiofrequency technique. clin neurosurg 24:557-578, 1977 19.wilkinson ha: trigeminal nerve peripheral branch phenol/glycerol injections for tic douloureux. j neurosurg 90:828-832, 1999 20.yang y, shao y, wang h, et al: neuronavigationassisted percutaneous radiofrequency thermocoagulation therapy in trigeminal neuralgia. clin j pain 23:159-164, 2007 microsoft word petrescuion_deepjudgement_f.docx romanian neurosurgery (2012) xix 1 deep judgement and distinguished competence in approaching medico-sanitary facilities management h.c. ion petrescu, camelia ştefănescu, camelia konrad recently, under the valuable editorial guidance of prof. alexandru v. ciurea phd.msc., vasile gh. ciubotaru with phd in medical sciences and eugen avram with a phd. in psychology, as well as together with the participation of important specialists in the field, the renowned work “management in medico-sanitary facilities’ was published by editura universitară publishing house. starting from a synthetic but significant topic on medical management progress in romania and the european territory, connoisseurs of these medical policies in management reveal, by their research, current challenges that medico-sanitary institutions must cope with. this is where the authors’ source of concern comes from– in the context of numerous reforms within the romanian societymedical forces action, especially the behaviour in the competition for medical performance. when we add to this complexity, as main element, the need for quality in education and medical studies, compulsory stages for building real resistance of romanian competition and performance, the overall generous objective of the thesis that we evaluate becomes general. the topic is important and current, having implications on management, in general, and, especially, on medico-sanitary facilities management. the authors summarize the scope and focus on identifying the actual state and proposal for measures on restructuring romanian medical management. the importance of this thesis is supported by the fact that it addresses an issue having significant influence, being direct and focused on the health-care, economic and social, legal and political environment in romania. at the same time, it lays the borderlines of many research disciplines in medical management. also, the paper deals with medical management both in an operational manner, as well as in a strategic manner . elaboration is, from many points of view, a pioneering work in management. the essential issues regarding medicosanitary facilities are emphasized and judiciously separated in three parts: management of the medico-sanitary system and facilities, leadership and human resources. within the chapters specific to each part, the medical management thinking and its components are specific and concerned by their own improvement, rising to the level of useful management applications. this thesis is an attempt to highlight success through accessible arguments, combined with scientific rigor and potential management processes. the work subject to our attention does not hesitate, rightfully, to argument that from practice, the actual state of medical performance, and the theoretical ideal which our society must achieve we have an important way to go. the work is drawn up according to the h.c. ion petrescu et al judgement and competence in medico-sanitary management requirements of academic research report produced, precisely based on the criteria of scientific investigation: 18 chapters, each concluded with interesting partial conclusions, a comprehensive set of conclusions and solutions, proposals and personal contributions of the authors: a well-built and well-presented editorial device, an important corpus of figures and tables, and a more than generous bibliography. numerous footnotes, references, comments and additions to bibliographic work shape a broad, welldesigned thesis, current by its thematic and valuable by its approach, having wellreasoned arguments and conclusions. this paper is harmoniously distributed into chapters and subchapters, according to its gradual approach, from technicalmethodological aspects, to compared analysis and then the consolidation of the evaluation system. designed in a very complex and interdisciplinary vision, the work is comprehensive in scope, and the issues addressed responds to real needs in the field in the context of existing or pending changes. hence the purpose of the paper, to draw the attention of ministerial, departmental and functional-level managers on the issues addressed in the practice of health-care professionals. subordinate to the overall goal, the paper focuses on theoretical and practical approach of many issues: systemic treatment of services and health programs and seeking european means for health certification and insurance; ethical components, social liability and efficiency in the romanian health system; subjects of managerial activity, insisting on manager responsibility in comparison to leaders and, especially, successful leaders, careful with competences and guidance activity. particularly impressive is the authors’ concern to approaching the human factor from the perspective of health-care service provider and beneficiary, by involving medical, managerial and psychological thinking. each of the 18 chapters explains in detail the theory related matter, usually in two sections: a short review of what we call "traditional" management theory and the other with comments on new theories emerged in the field. complex approaches of issues that can apply the theory in question are chosen, aspects highlighted in the preface signed by prof. alexandru constantinovici phd. and in the foreword of prof. a. v. ciurea phd. msc. in turns, authors frequently take into account the implications of management strategies and health-care policies. our work appears to be complex, interesting, modern by research topics and solutions it proposes both by the academic environment, as well as medical practitioners in the national area. particularly interesting and useful is the way in which medical, economic, social, managerial, legislative, legal and political concepts are linked to specific health-care management issues that is not addressed in isolation, but as part of a macro-system which can provide a level of development in yet unpredictable future that would draw us near european union countries. the work is supported by extensive documentation and is based on numerous theoretical investigations and its theoretical, methodological and practical content presents itself as a corpus with rich informational support, a considerable scientific level, anchored in the reality of the eu domain. moreover, the work is well balanced, the romanian neurosurgery (2012) xix 1 transition from theoretical to practical problems appearing normal and real, and the registration of all efficiency issues aspects suggests a strong useful tool in health-care management. the teaching features of the work are obvious. they are meant to complement, supplement and reinforce the book text. numerous invitations to reflections on relevancy and concern for the real and significant problems are made. the area extends on the entire work and the problematic area has a logical sequence. key concepts are highlighted throughout the paper. the presentation style is distinctive and important ideas are well -defined and illustrated. special attention is given to constant terminology use throughout the entire paper. a logical device, having a scientific platform designed to build and able to achieve sustainable, explanatory and predictive contributions. quite useful in health facilities management literature are parts dealing with: quality of health-care services; implementation of european quality standards in the strategies and policies of romanian health-care providers; involving the diagnosis, debating ethical, financial efficiency and social issues, within the distinct features of the romanian health system and quartering on specific management of health-care units deserve special appreciation. our attention was drawn by: the concern for more flexible managerial and organizational structures, manager complex personality presentation, designed from the perspective of philosophy according to the octahedral model approach, linking leadership influence with the efficiency, effectiveness and access to success, satisfaction and reputation , the femalemanager under the “scrutiny" of a man, leadership style based on coaching. in dealing with the parties to which we referred above, the authors insist on some components of medical management on which we focus on. there are many issues raised by the authors, but we note, first that of management integrity in health-care activity, defined as providing services to citizens, patients entitled to receive it. this entitlement to services is in fact the cornerstone of the work, being extended simply according to the state fundamental law. as regards the other side of integrity, authors consider it to be the prevention of corruption. in other words, the integrity of health-care facilities management means public health-care entitlement services without disturbance of nature and corruption at any level or in any part. everything stems from organizational culture, being thoroughly supported throughout the paper. scientific and requirement terms correctly address in the paper human resources in the health system. the experience of european countries is generalized from school and university in the selection and integration of evaluation up to promotion, from motivation up to improvement for performance. the approach to human resources covering health-care facilities is very interesting, offering us a multitude of factographic information, sometimes surprising and consistently interesting, starting with the number and structure of staff, continuing with the status, but also the budget composition. case studies are excellently chosen as theme and provide new important solutions. h.c. ion petrescu et al judgement and competence in medico-sanitary management health–care systems staff policies are thoroughly presented, with emphasis on the need for inspiration in the american the canadian and british medical education system. formal and informal labour groups are approached in structural and dynamic ways, insisting on excellence training requirements, prevention of conflicts and need for training specialists for stress treatment. and last but not least, the need and role of psychologists in health facilities is highlighted, bowing to the appreciation that in the xxist century psychology, in general, and the three branches of work, industrial and organizational psychology will have to focus on solving problems globalization and europeanization in the field of professional practice. the authors face their well systematized theoretical and methodological acquiring during their entire works with the practical space of health-care facilities, which is an interesting exercise, good for the creation of the entire creative space. as a whole, the book is a valuable medical management research conducted so far in romania and within the european union, presented as a reference document for future research. authors demonstrate scientific competence, theoretical and practical management skills in the field of medical management and prove to be true researchers, having real skills in investigating management processes and phenomena, and the paper makes an important contribution to the development of knowledge in national and european context. throughout the paper, editors and authors have submitted their almost irresistible, deeply rooted tendency, specific to scientists who use their creative energy in solving apparently unsolvable problems. they were seduced by the tempting problem and arrived to exciting components within the plan of scientific investigation and results presentation. therefore, we take advantage of this opportunity in order to congratulate the publishers and authors and to assure them of the benefits given by such scientific gift. 8harishapn_massive 202 harisha et al massive spontaneous corpus callosal hemorrhage massive spontaneous corpus callosal hemorrhage with intraventricular extension p.n. harisha1, v. umamaheshwar reddy2, amit agrawal3, gopal kodali4 1assistant professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 3professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 4resident of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract spontaneous hemorrhage into the corpus callosum with intraventricular extension is uncommon. in the present article we describe a case 60 year female who had massive hemorrhage along the corpus callosum involving genu, body of corpus callosum and extending on ventral as well as dorsal aspect of the corpus callosum with intraventricular extension and areas of hypodensities in the body of the corpus callosum and adjacent cerebral cortex. in this case the subarachnoid and corpus callosal hemorrhage probably resulted from the ruptured aneurysms of the anterior cerebral artery. key words: corpus callosal hemorrhage, corpus callosal infarct, intra-ventricular bleed, distal anterior cerebral artery. introduction spontaneous hemorrhage into the corpus callosum with intraventricular extension is rare with only few reported cases in literature. (1-3) in the present article we describe a case of massive spontaneous corpus callosal hemorrhage with poor outcome. case report a 60 year old female presented to emergency department with the history of two episodes of projectile vomiting which was followed by loss of consciousness of one day duration. she was not a known hypertensive or diabetic. she had intermittent mild headaches that responded to mild analgesics. she also had 2-3 episodes of syncope from which she spontaneously recovered without any focal deficits and did not seek medical attention. at the time of examination in emergency room her blood pressure was 90/70 mm/hg. she was in altered sensorium (gcs was e1v2m4), pupils were mid-dilated and sluggishly reacting. blood investigations including coagulation profile were within normal range. romanian neurosurgery (2014) xxi 2: 202 205 203 as she had labored breathing, endotracheal intubation was performed and ventilator was connected. her ct scan plain axial images showed massive hemorrhage along the corpus callosum involving genu, body of corpus callosum and extending on ventral as well as dorsal aspect of the corpus callosum. hemorrhage was extending into the lateral, third and fourth ventricles. there were areas of hypodensities in the body of the corpus callosum and adjacent cerebral cortex (figures 1 and 2). because of poor general condition and neurological status she could not be further investigated and succumbed to massive intracranial hemorrhage. figure 1 ct scan plain axial (a and b) and coronal images showing massive hemorrhage along the corpus callosum involving genu, body of corpus callosum and extending on ventral and dorsal aspect of the corpus callosum and into the ventricles, there are areas of cortical hypodensities superior and lateral to the corpus callosum (? infarcts) figure 2 ct scan sagittal images showing the details and extension of the hemorrhages i.e. massive hematoma in the corpus callosum, intraventricular extension (lateral, third and fourth ventricles) with areas of cortical hypodensities discussion corpus callosum is supplied by the pericallosal branch of the anterior cerebral artery (main vas-cular supply to the body), subcallosal and me¬dial callosal arteries, branches of the anterior com-municating artery (main supply for the anterior portion of the corpus callosum) and the posterior pericallosal artery (branch of the posterior cerebral artery) supplies the splenium. (4) a 204 harisha et al massive spontaneous corpus callosal hemorrhage number of lesions including aneurysms of the pericallosal artery, giant aneurysms, traumatic brain injury, arteriovenous malformations, intracranial infections and intracranial tumors have been implicated as the cause of spontaneous hemorrhage into the corpus callosum. (1, 2, 4-9) however in spite of all the investigations there may not be any detectable underlying pathology. (1) subarachnoid hemorrhage resulting from the ruptured aneurysms of the anterior cerebral artery or the pericallosal artery can cause hematomas in the corpus callosum. (2, 3) the highest amount of blood is seen in the distal interhemispheric fissure, pericallosal cistern, and lam¬ina terminalis cistern. (10) the blood can pass through the lamina terminalis into ventricles and the septum pellucidum and thus appearing on the ventral as well as dorsal aspect of the anterior corpus callosum. (2, 3) the reported incidence of intraventricular hemorrhage is 25-30% of the patients and ivh is more frequently reported with ruptured a2as and a3 segment aneurysms. (11) the prognosis depends on the size of the hematoma and the prognosis is poor for patients with larger hemorrhages. (9) patients with smaller hemorrhages without any underlying pathology can recover with conservative management. (1) conclusion corpus callosum is very unusual site for spontaneous intracerebral hematoma, numerous etiological factors like aneurysms of the pericallosal artery, giant aneurysms, traumatic brain injury, arteriovenous malformations, intracranial infections and intracranial tumors have been implicated for this uncommon site of bleed. corpus callosal hemorrhage can dissect into ventricles through the lamina terminalis. correspondence: dr umamaheswara reddy v assistant professor of radiology department of radiology narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: mahesh.rd2112@gmail.com mobile+91-9959632228 references 1. roditis s. spontaneous hematoma of the septum pellucidum and corpus callosum: a case report. romanian neurosurgery 2011;xviii:344-348. 2. fitsiori a, nguyen d, karentzos a, delavelle j, vargas m. the corpus callosum: white matter or terra incognita. british journal of radiology 2011;84:5-18. 3. jackson a, fitzgerald j, hartley r, leonard a, yates j. ct appearances of haematomas in the corpus callosum in patients with subarachnoid haemorrhage. neuroradiology 1993;35:420-423. 4. türe u, yasargil mg, krisht af. the arteries of the corpus callosum: a microsurgical anatomic study. neurosurgery 1996;39:1075-1085. 5. ogura k, yamamoto i, hara m, suzuki y, nakane t, watanabe m. computerized tomography of the traumatic hematoma in the corpus callosum.--report of 2 cases]. no shinkei geka neurological surgery 1982;10:1299. 6. shigemori m, kojyo n, yuge t, tokutomi t, nakashima h, kuramoto s. massive traumatic haematoma of the corpus callosum. acta neurochirurgica 1986;81:36-39. 7. park d-h, chung y-g, shin i-y, lee j-b, suh j-k, lee h-k. thrombosed giant aneurysm of the pericallosal artery with inconclusive findings of multiple neuroimaging studies. neurologia medico-chirurgica 2008;48:26-29. romanian neurosurgery (2014) xxi 2: 202 205 205 8. lehecka m, porras m, dashti r, niemelä m, hernesniemi ja. anatomic features of distal anterior cerebral artery aneurysms: a detailed angiographic analysis of 101 patients. neurosurgery 2008;63:219-228; discussion 228. 9. lehecka m, dashti r, lehto h, kivisaari r, niemelä m, hernesniemi j. distal anterior cerebral artery aneurysms: springer, 2010. 10. stewart c, lurito j. ruptured pericallosal aneurysm causing hemorrhage along the fornix. neuroradiology 2002;44:993-995. 11. dashti r, hernesniemi j, lehto h, et al. microneurosurgical management of proximal anterior cerebral artery aneurysms. surgical neurology 2007;68:366-377. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 470-472 doi: 10.33962/roneuro-2019-074 www.journals.lapub.co.uk/index.php/roneurosurgery induced epidural haematoma sherief ahmed el anany, abd elghany elshamy mansoura university, egypt abstract background: a novel case of epidural haematoma caused by general surgery case presentation: fifty-four years male patient was admitted at mansoura emergency hospital with glasgow coma scale 4 on ventilator. rapid evacuation of edh was done and the gcs became 9 conclusion: rapid accumulation of epidural haematoma is fatal and may lead to death. background an epidural hematoma (edh) is an extra-axial collection of blood within the potential space between the outer layer of the dura mater and the inner table of the skull. it is confined by the lateral sutures (especially the coronal sutures) where the dura inserts. it is a life-threatening condition, which may require immediate intervention and can be associated with significant morbidity and mortality if left untreated. rapid diagnosis and evacuation are important for a good outcome . it occurs in approximately 10% of traumatic brain injuries (tbi) requiring hospitalization. both by traumatic and non-traumatic mechanisms can cause an epidural hematoma. the majority of cases related to a traumatic mechanism are a result of head injury due to motor vehicle collisions, physical assaults, or accidental falls (1). non-traumatic mechanisms include the following: • infection/abscess • coagulopathy • haemorrhagic tumours • vascular malformation most epidural hematomas result from arterial bleeding from a branch of the middle meningeal artery. the anterior meningeal artery or dural arteriovenous (av) fistula at the vertex may be involved. up to 10% of edhs are due to venous bleeding following the laceration of a dural venous sinus. (1) a novel and rare case in our practice had been developed showing induced epidural haematoma from left temporal soft mass, eroding keywords epidural haematoma, induced, iatrogenic, hepatocellular carcinoma, disturbed conscious level corresponding author: sherief ahmed el anany mansoura university, egypt dr.sherief89ahmed@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 471 induced epidural haematoma bone metastasis in skull, extending to subgalea and compressing the dura. the aim of this case can be used as a guidance for every practitioner to be cautious when dealing with any head swelling. case presentation fifty-four years male patient admitted at mansoura emergency hospital with gcs 4 on ventilator . urgent ct brain was done and showed large epidural hematoma with extra bony lesion (figure.1). before that incident with three hours, the patient was fully conscious and he visited outpatient clinic where a general surgeon tried to aspirate left temporal soft lesion, causing skin swelling, doughted that it was subgaleal haematoma . operation a left pteriyonal approach was done then a craniotomy with four burr holes. the soft lesion was excised completely with evacuation of edh (figure.2) and the bone was repositionned with closure of skin. the lesion was sent to histopathological analysis and showed hepatocellular carcinoma. the patient remained in icu with gcs 9 postoperative one week then died. conclusion epidural hematoma is a relatively common presentation to the emergency department, and if not diagnosed is associated with a high mortality. the condition is best managed by a multidisciplinary team that includes the emergency room physician, the trauma team, radiologist, neurologist, neurosurgeon, intensivist and the icu nurses. the condition has been associated with mortality rates in excess of 15%. every practitioner not related to neurosurgery should be careful when dealing with any case with head swelling and refer the case to a specialist avoiding iatrogenic death of patient. figure 1: pre-operative ct brain explaining large edh with bony erosion and extra dural lesion figure 2: post-operative ct brain explaining large edh with bony erosion and extra dural lesion totally removed 472 sherief ahmed el anany, abd elghany elshamy list of abbreviation gcs : glasgow coma scale icu : intensive care unit edh : epidural haematoma tbi : traumatic brain injuries ct : computerized tomography av : arterio venous declarations acknowledgement no other person contributed to this article funding nothing to disclose authors’ contribution the corresponding author and co-authors performed all of the procedures, clinical assessment, follow-up of patients, collection of results and are responsible for the study conception and design. consent for publication this study reported no personal data for any patients; informed consents were obtained for all patients included in this study for the publishing of results. none of the patient involved in this study had declined the publication of study results. competing interests no conflict of interests. availability of data materials raw data are available references khairat a, waseem m. epidural hematoma. [updated 2018 nov 15]. in: statpearls [internet]. treasure island (fl): statpearls publishing; 2019 jan. available from: https://www.ncbi.nlm.nih.gov/books /nbk518982/. microsoft word 6abrudancsurgeryofhigh 38 c. abrudan et al surgery of high grade gliomas surgery of high grade gliomas pros in favor of maximal cytoreductive surgery c. abrudan1,2, adriana cocis2, dana cernea3, b. suciu2, marilena cheptea3, i.șt. florian1,2 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery 2cluj county emergency hospital, department of neurosurgery 3“prof. dr. i. chirircuta” oncology institute cluj-napoca abstract background: malignant glioma is the most common primary brain tumour in adults. more and more studies are focused on the role of surgery in prolonged median of survival and survival at two years. the purpose of this study is to add some arguments in favour of radical surgery in malignant glioma. material and methods: the study is based 433 cases of high grade cerebral glioma operated between 01.01.2000-31.12.2009 at the department of neurosurgery, cluj county emergency hospital. we analyzed age, gender, type and duration of symptoms, type of surgery, pathological diagnosis and the correlation of these factors with overall survival. data for long term follow up were available for 266 patients. results: the results shows, according to their histological features, the fallowing dispersions: astrocitomas grade iii (28%), glioblastoma multiforme (64%), high grade oligodendrogliomas (5%) and high grade ependimomas (3%). the global survival rate was 47 % at 12 months, 26,3% at 18 months and 16,7% at 24 months. the age and type of surgery are prognostic factors that significantly influenced the survival at 12, 18 and 24 months (9,3 months age <65 years versus 7,1 months age >65 years; 9,2 months gtr versus 6,4 months str-at 12 months monitoring; 11,7 months age <65 versus 7,7 months age >65; 11,5 months gtr versus 7,1 months str-at 18 months monitoring; 12,8 months age <65 versus 8 months age >65; 12,6 months gtr versus 7,5 months str –at 24 months monitoring). conclusions: our study shows that long term postoperative outcome after radical surgical resection are better than the results of either partial resection or simple biopsy; in terms of duration of survival (the difference of mean survival at 12, 18 and 24 months monitoring was 2,8 months, 4,4 months and 5,1 months respectively in favour of patients with gross total removal) . keywords: anaplastic astrocitoma, anaplastic ependymoma, glioblastoma multiforme, gross total removal (gtr), high grade glioma, malignant oligodendroglioma, subtotal removal (str). introduction high grade gliomas are aggressive cancers. the world health organization grading system recognizes grade iii and grade iv primary brain tumors of astrocytic, romanian neurosurgery (2011) xviii 1: 38 – 53 39 oligodendroglial or mixed lineage. despite advances in surgical techniques, and improvement in radiation treatment and chemotherapy, the median survival of these patients has changed little over the last decades. identification of these tumours is usually easy by symptoms such as headaches, seizures or focal weakness or numbness, with imaging findings of an enhancing mass lesion. there are two major aspects of gliomas biology that contributes to its poor prognosis: the formation of new blood vessels through the process of angiogenesis and the invasion of glioma cells. the most severe form, glioblastoma multiforme, has a marked and diffuse infiltration through the normal brain parenchyma. health-related quality of life of these patients has always been poor. patients with a presumed primary brain tumour from clinical examination and radiological investigation have two initial surgical management options: biopsy or resection [25,26]. the goals of surgery for malignant glioma, as postulated by shapiro [28], are as follow: (1) the establishment of a histological diagnosis. (2) tumor cytoreduction for: (a) improvement in neurological status by reduction of increased intracranial pressure, and (b) possible change in tumor kinetics. in the recent eortc trial [32] surgery seems to have no prognostic role concerning the survival rate. latest studies are focused on the role of surgery in prolonged median of survival and survival at two years. the purpose of this study is to add some arguments in favour of surgery and especially of the radical surgery in malignant gliomas. patients and methods this is a retrospective study of a single centre, single surgeon and represents the last ten years of the senior author. the study is based on 433 cases of high grade cerebral gliomas operated between 01.01.2000 and 31.12.2009. at the neurosurgical department of cluj county emergency hospital. patients considered for the study were adults and children aged from 6 to 82 years old with the initial diagnosis of a malignant glioma. all the tumours were operated and gross total removal was the goal in all of the cases. the extent of surgery was reported by the neurosurgeon as partial or total removal, and confirmed on enhanced ct or mri in the first 24-48 postoperative hours. the tumours were histological proven high grade gliomas. data for long term follow up were available for 266 patients. the following statistic methods have been used for group description: descriptive: the distribution value (mean ± standard deviation, confidence interval, min/max values, contingency tables and frequencies. analytical: the survival analysis and the disease free interval depending on age, pathological diagnostic, surgical procedure/resection type through kaplanmeier method and the evaluation of a difference of survival existence between groups through log-rank test. the group of 266 patients have been split for the analysis of survival from surgery to 12, 18 and 24 months as it follows: for observing the disease free interval at 12 months all the 266 patients were included in the group 40 c. abrudan et al surgery of high grade gliomas for observing the disease free interval at 18 and 24 months 228 patients were included (patients operated in 2009 have been excluded). all analyses were done with spss. results between the 1st t of january 2000 and the 31st of december 2009, 433 malignant glioma have been operated. from all the cerebral tumour cases operated in this period (1861 cases) malignant gliomas represent 23.26%. in this period the temporal distribution of cases varied, the peaks being present in 2005 (79 cases out of 238 operated tumours) (figure 1) the patients were aged between 6 and 82 years old. most of the malignant glioma cases have been recorded in the fifth decade. from pathological point of view the glioblastoma multiforme was met in most of the cases (64%), followed by anaplastic astrocytoma (28%). the malignant oligodendroglioma and anaplastic ependymoma were met in 5%, 3% respectively. the most frequent symptom of the patients while they were admitted in our hospital was the increased intracranial pressure (icp) (78%) followed by focal weakness, seizures (18.9%), and aphasia (11.5%). the interval between the debut of symptoms and admission in the hospital was one month for 39% of cases. an evolution of symptoms longer than 6 months has been met for 12% cases (figure 3). the anaplastic astrocytoma have been diagnosed in 123 cases (28% of all the malignant glioma). having males as majority (62%) and the peak incidence between 40-49, the total removal has been reached in 83, 10% of the cases. 0 50 100 150 200 250 300 350 2000 2002 2004 2006 2008 temporal distribution of cases cerebral tumors high grade gliomas figure 1 distributions of cases in the studied interval hp  types   64% 28% 5% 3% g bm anaplastic  astrocitomas anaplastic  oligodendrog liomas anaplastic  ependimomas figure 2 pathological distribution of malignant gliomas in the present study interval between onset of symptoms and admission 0% 5% 10% 15% 20% 25% 30% 35% 40% 45% 1 week 2 weeks 1 month 2 months 3 months 4 months 6 months > 6 months figure 3 interval between onset of symptoms and admission gender distribution male female romanian neurosurgery (2011) xviii 1: 38 – 53 41 peak age is in the fourth decade 0 5 10 15 20 25 30 35 40 0-9 10 19 2029 3039 4049 5059 6069 7079 >80 number of cases figure 4 gender and age distribution of anaplastic astrocitoma cases the lobar localization of the tumour was met in 61.4% (figure 5.) of the cases, and in 30.1% of the cases it was multilobar. the posterior fossa localisations and the intraverticular one were met at 6%, and 2.5% respectively. the glioblastoma multiforme was met in 276 cases (64% from all the malignant tumours). the sex distribution has shown a majority of males (55.5%). unlike the anaplastic astrocitoma the most affected ages were between 50-59 (100 cases)(figure 6). the gross total removal has been obtained in 87,5% cases. the lobar localization has been considered as majority in this case (58,6%), the glioblastoma multiforme with multilobar localization being met in 36,8% of the cases. there were descriptions of the localizations at the callosal (1,8%) (figure 7), posterior fossa (1,4%) and ventricles (1,4%). the malignant oligodendrogliomas and anaplastic ependymomas were met in 5%, 3% respectively. in both situations there have been a male majority and the most affected was the fifth decade of life. the total removal was reached in most of cases. the global survival rate for 266 patients included in our study was 47 % at 12 months, 26,3% at 18 months and 16,7% at 24 months. (table 1) figure 5 preoperative enhanced mri and postoperative contrasted ct scan of a lobar anaplastic astrocytoma peak age is in the fifth decade 0 20 40 60 80 100 120 0-9 10 19 20-29 30-39 40-49 50-59 60-69 70-79 >80 n um be r of c as es figure 6 age distribution of glioblastoma cases 42 c. abrudan et al surgery of high grade gliomas table 1 overall survival at 12, 18 and 24 months disease free interval number of patients global survival rate survival mean rate (months) survival median rate (months) 12 months 266 47% 8,87 months ci-95%: 8,41-9,43 11 18 months 228 26,3% 10,96 months ci-95%: 10,20-11,72 11 ci-95%: 9,91-12,08 24 months 228 16,7% 11,96 months ci-95%: 11,01-12,91 11 table 2 disease free interval regarding the age, type of surgery and pathological findings disease free interval log rank (mantel-cox) factor: age (<65 years/ ≥65 years) log rank (mantel-cox) factor: type of surgery (gross total removal/subtotal removal) log rank (mantel-cox) factor: histopatholgical diagnosis log rank (mantel-cox) factor: gender 12 months 0,000 0,000 0,090 0,296 18 months 0,000 0,000 0,122 0,836 24 months 0,000 0,000 0,031 0,756 the age and type of surgery are prognostic factors that significantly influenced the survival at 12, 18 and 24 months, meanwhile the pathological diagnostic significantly influenced the survival only at 24 months (table 2) figure 7 preoperative enhanced mri and postoperative ct scan of a completely removed glioblastoma multiforme of corpus callosum romanian neurosurgery (2011) xviii 1: 38 – 53 43 from all 266 cases, the gross total removal (gtr) was reached in 229 patients, while the subtotal removal (str) of tumours was performed in 37 cases. there has been a significant difference between expected frequencies and the observed ones in resection type that concerns survival. at 12 months monitoring, the survival was around 9,2 months in patients with gtr, with a confidence interval between 8,7 and 9,7, meanwhile in the str group the survival mean was 6,4 months, with a confidence interval of 95% from 5,2 to 7,7. (table 3, figure 8) table 3 mean survival time at 12 months monitoring in patients with gtr and str respectively type of surgery mean(a) estimate std. error 95% confidence interval lower bound upper bound gross total removal 9,263 ,244 8,784 9,741 subtotal removal 6,478 ,640 5,223 7,734 overall 8,875 ,236 8,413 9,337 figure 8 type of resection as a prognostic factor at 12 months monitoring similar findings are found at 18 months interval monitoring , the survival mean for patients with gtr has been of 11.5 months (with a confidence interval of 95% from 10,7 to 12,4), significantly higher than survival rate for str group (7,1 months, with confidence from 5,5 to 8,7, p<0,005) (table 4, figure 9). the survival monitoring at 24 months also highlighted a significant difference of survival between gtr and str groups (p< 0,005). the survival mean at gtr group was of 12,6 months, compared to the 7,5 months one for the str group (table 8, figure 4). figure 9 mean and median survival time and survival graphic at 18 months depending on the type of surgery figure 10 mean and median survival time at 24 months depending on the type of surgery 44 c. abrudan et al surgery of high grade gliomas table 4 mean survival time for 18 months monitoring type of surgery mean(a) median estimate std. error 95% confidence interval estimate std. error 95% confidence interval lower bound upper bound lower bound upper bound gross total removal 11,592 ,414 10,780 12,405 12,500 ,673 11,182 13,818 subtotal removal 7,133 ,822 5,522 8,744 6,000 ,849 4,337 7,663 overall 10,966 ,388 10,205 11,727 11,000 ,552 9,917 12,083 table 5 mean survival time at 24 months monitoring type of surgery mean(a) median estimate std. error 95% confidence interval estimate std. error 95% confidence interval lower bound upper bound lower bound upper bound gross total removal 12,694 ,521 11,673 13,715 12,500 ,673 11,182 13,818 subtotal removal 7,508 ,998 5,551 9,464 6,000 ,849 4,337 7,663 overall 11,966 ,484 11,018 12,915 11,000 ,552 9,917 12,083 for determining the role of age as a prognostic factor all the 266 patients were split in 2 groups: one under 65 years old and another one above 65. the first group contained 213 patients and the second one 53 patients. the survival rate had been observed at 12, 18 and 24 months. in all situations a statistic association has been found between age and survival. the younger patients had a better survival than the ones over the age of 65 (table 6,7 and 8). meanwhile in the under 65 years of age romanian neurosurgery (2011) xviii 1: 38 – 53 45 group the mean survival was of 9,3 months (with lower bound at 8,802 and the upper bound at 9,797), in the group over 65 the mean survival was of 7,1 months with the lower bound at 6,113 and the upper bound at 8,228. the difference was more significant at the 18 months monitoring, with a difference of mean survival of 4 months in favour of the younger group. at the 24 months monitoring the difference was also significant, with a mean of 4,8 months in favour of the patient younger than 65. tables 6, 7 and 8 mean and median for survival time at 12,18 and 24 months age mean(a) median estimate std. error 95% confidence interval estimate std. error 95% confidence interval lower bound upper bound lower bound upper bound <65 years 9,300 ,254 8,802 9,797 . . . . =>65 years 7,171 ,539 6,113 8,228 8,000 1,211 5,626 10,374 overall 8,875 ,236 8,413 9,337 11,000 . . . age mean(a) median estimate std. error 95% confidence interval estimate std. error 95% confidence interval lower bound upper bound lower bound upper bound <65 years 11,714 ,420 10,891 12,537 12,500 ,715 11,098 13,902 =>65 years 7,750 ,825 6,133 9,367 6,500 1,366 3,823 9,177 overall 10,966 ,388 10,205 11,727 11,000 ,552 9,917 12,083 age mean(a) median estimate std. error 95% confidence interval estimate std. error 95% confidence interval lower bound upper bound lower bound upper bound <65 years 12,882 ,535 11,833 13,930 12,500 ,715 11,098 13,902 =>65 years 8,029 ,922 6,221 9,837 6,500 1,366 3,823 9,177 overall 11,966 ,484 11,018 12,915 11,000 ,552 9,917 12,083 46 c. abrudan et al surgery of high grade gliomas figure 11 survival graphic at 12, 18 and 24 months depending on age regarding de pathological findings, there is no statistical significant difference at 12 and 18 months monitoring (p=0.09 respectively p=0,122). for survival at 24 months, the survival mean for glioblastoma multiforme diagnosed patients was of 11,2 months, for the ones having anaplastic astrocytoma was of 11,9 months. patients with malignant oligodendrogliomas survived approximately for 16,1 months (with a confidence interval of 95% between 12,6 and 19,6) and the ones with malignant ependymoma for 17,1 months (p=0.031). (table 9) romanian neurosurgery (2011) xviii 1: 38 – 53 47 figure 12 survival functions depending on the pathological findings at 12, 18 and 24 hours monitoring table 9 mean and median survival time depending on pathological findings at 24 months monitoring pathological diagnostic mean(a) median estimate std. error 95% confidence interval estimate std. error 95% confidence interval lower bound upper bound lower bound upper bound anaplastic astocytoma 11,946 ,786 10,406 13,486 12,000 ,645 10,736 13,264 anaplastic ependymoma 17,100 3,889 9,477 24,723 . . . . glioblastoma multiforme 11,205 ,632 9,966 12,444 10,000 ,715 8,598 11,402 anaplastic oligodendrogliomas 16,167 1,795 12,648 19,685 17,500 2,635 12,335 22,665 overall 11,966 ,484 11,018 12,915 11,000 ,552 9,917 12,083 discussions the treatment of patients with highgrade gliomas remains a challenge for modern therapy. clear treatment guidelines regarding the extent of surgery, derived from randomized prospective studies in the literature do not exist, and there are some controversy regarding the best treatment for malignant brain tumours. the gold standard for high-grade gliomas includes combination of surgery, radiotherapy, and chemotherapy. high grade gliomas are widely infiltrative , fact them makes quite impossible to completely resect, even in cases of hemispherectomy, procedure that 48 c. abrudan et al surgery of high grade gliomas was pioneered by walter dandy in 1928[6]. in order to achieve the cure of this highly malignant tumours some other authors have been presented their results with hemispherectomy, although associated with a poor postoperative survival rate, but also with a recurrence of tumours in an interval of less than two years [ 3,6,12,23]. despite of impressive progress of the last two decades in terms of neuroimagistic diagnostic, despite of the new inraoperative tools namely neuronavigation, ultrasonography, awake neurosurgery or introperative mri, the nowadays neurosurgical results in malignant gliomas are still disappointing in terms of long term survival [17]. usually tumour recurrence occurs close to the resection margin, were the cell density is increased. outside of this region the cell density drops sharply as the distance from the resection cavity increases, an argument in favour of a wider resection margin which presumably could delay recurrence[1, 3]. in a review of literature ryken et al. [24] selected thirty qualitative papers, 10 prospective studies and twenty retrospective studies. five of the prospective studies provided class ii data [2, 15, 30, 31, 35] and one of the 20 retrospective studies provided class ii data [15]. all, but one of these better quality studies support extent of resection as a factor in improving survival in newly diagnosed adult patients with malignant glioma. of these only the study of levin published in 1985[17] failed to support extent of resection for glioblastoma, but did demonstrate a survival advantage in cases of anaplastic astrocytoma. of the remaining retrospective papers reviewed, all provided class iii data. fourteen studies of the nineteen provided data, which supported the concept of cytoreductive surgery in the initial management of malignant glioma. some of these reviewed studies are presented in summary. in 2003, metcalfe and grant provided an update on the cochrane report of 2000 on biopsy versus resection for malignant glioma [19]. after a search of over 2,100 documents, the authors failed to locate enough randomized data for analysis; therefore no conclusion could be drawn. a recommendation was made calling for randomized prospective study of this important issue. stummer et al.[31] describe a prospective study evaluating the extent of resection and its influence on survival employing 5-aminolevulinic acid, a fluorescent marker . focused on the novelty to the radical resection of gliomas using a fluorescent marker to aid in desection decision, the study underlines in subsidiary the advantage of gross total removal over de subtotal resection in terms of survival in multivariate analysis. in the same review of ryken [24], bricolo et al. are mentioned with a preliminary report of a prospective data collection on patients with presumed malignant glioma subjected to an aggressive surgical strategy and assessed postoperatively with ct scanning placing them either in a gross total resection or subtotal resection (10–15% remaining enhancement) group. while no statistical analysis is provided the authors report at 60% 1 year survival for their gross total resection group versus only 24% in the subtotal resection group. lacroix et al. [17] found that surgical resection of 98% or more of the contrastenhancing tumour volume is an romanian neurosurgery (2011) xviii 1: 38 – 53 49 independent variable associated with longer survival times in patients with glioblastoma multiforme. as a consequence their recommendation is that gross-total resection should be performed whenever possible for these patients, yet not at the expense of neurologic function or surgical complications. in the study of nitta et al. of 101 patients with malignant glioma including 68 patients with gbm and 32 with anaplastic astrocytoma who underwent operative procedures followed by a uniform radiotherapy and chemotherapy regimen [22], the authors found that in the glioblastoma group the patients undergoing gross total resection as judged by postoperative ct survived significantly longer than patients undergoing either a partial resection (less than 75%) or subtotal resection (75—less than 100%). they suggested that gross total excision might aid in the adjuvant therapy following surgical intervention. devaux et al.[7] in a retrospective study of 218 patients with newly diagnosed malignant glioma including 164 patients with grade iv tumours and 54 patients with grade iii tumours found that using a detailed surgical approach designed to achieve volumetric resection was of benefit in prolonging survival in grade iv patients even after adjustment for no clinical prognostic factors. as a result, it follows that the majority of the reviewed data supports maximal cytoreductive surgery. in our retrospective study of 266 cases that met inclusion criteria for statistical monitoring at 12, 18 and 24 months, the obtained data also supported maximal cytoreductive surgery in order to prolong survival of patients with malignant gliomas. in this study only gtr with str are compared, based on the senior author intraoperative impression and confirmed on immediate postoperative enhanced ct scan or mri. based on postoperative imaging we consider str any contrasted remnants visible on more than two adjacent slices from the initial volume of tumour. at 12 months monitoring, the survival was around 9,2 months in patients with gtr, with a confidence interval between 8,7 and 9,7, meanwhile in the str group the survival mean was of 6,4 months, with a confidence interval of 95% from 5,2 to 7,7. similar findings are found at 18 months interval monitoring, the survival mean for patients with gtr was of 11.5 months (with a confidence interval of 95% from 10,7 to 12,4), significantly higher than survival rate for str group (7,1 months, with confidence from 5,5 to 8,7, p<0,005). the survival monitoring at 24 months has also highlighted a significant difference of survival between gtr and str groups (p< 0,005). the survival mean at gtr group was of 12,6 months, comparing to 7,5 months for the str group. as it is shown, the difference increases from almost three months on the first period of monitoring (12 months) up to 5 months in the 24 months monitoring period. a median survival difference from three months up to five months between gtr and str represents findings that are consistently in favour of maximal cytoreduction, at least in our opinion. based on our data we consider our study a class iii recommendation. failure to demonstrate prolonged survival with class i data should not stop physicians from considering surgical resection thanks to the numerous other benefits of tumour removal. the obvious benefits from glioma 50 c. abrudan et al surgery of high grade gliomas resection are symptomatic relief from mass effect and obstructed cerebrospinal fluid. the tumoral mass produces compression of neural pathways and distortion of brain structure that contribute to both general symptoms and focal deficits and explain the neurological improvement following surgical resection. after surgery there are some global symptoms (headache, nausea, vomiting, general malaise) that show dramatic improvement (11). the partial reversal of neurological deficit is due to the relief of local compression (36). dexamethasone in dose of 16 mg per day has been proved an useful indicator of potential neurological improvement after glioma resection. patients who show improved functional status after steroid administration will be the one with improvement in quality of life after aggressive surgical resection, provided that there is low postoperative morbidity (20). a number of authors observed that partial tumour resection is associated with greater risk of postoperative neurological worsening than either radical excision or stereotaxic biopsy [5,14,25,29]. in the series of ciric et al [5] 97% of patients with gross total or nearly gross total resection had improved or stable postoperative neurological status; in contrast, postoperative neurological worsening occurred in 40% of patients with partial resection. in two other series fadul et al [8], vecht et al, [34] no significant difference was found in the incidence of neurological worsening following gross total resection compared to limited resection. these data from various studies suggest that radical tumour resection is associated with no greater or perhaps less risk of neurological compromise than with partial resection. in our experience we also could document a global improvement of neurological status in more than 85% of the gtr operated cases, with a less than 10% rate of neurological complications, and a mortality rate below 4%, large majority of them being patients with more than 70 years of age. related to age there are some studies that provide useful data regarding elderly patients, namely those over 65 [4,35]. in the latest study of chaichana (2010)[4] they found that patients who underwent surgical resection had median survival of 5.7 months, while patients who underwent needle biopsy without resection had median survival of 4.0 months. although modest in absolute terms, older patients did have significantly prolonged survival with aggressive resection as compared to needle biopsy, without an increase in surgical morbidity or mortality. their study demonstrates that older patients undergoing aggressive resection did not have an increase in surgical morbidity, and had prolonged survival as compared to matched older patients undergoing needle biopsy. older patients, as with younger patients, may therefore benefit from aggressive surgical resection, and aggressive resection should be considered for older patients who present with gbm. we are also in favour of aggressive surgery in patients older than 65, despite the fact that their median of survival is significantly lower than that of the younger patients. meanwhile in the under 65 years old group the mean survival was 9,3 months (with lower bound at 8,802 and the upper bound at 9,797), in the group over 65 the mean survival was 7,1 months with the lower bound at 6,113 and the upper bound at 8,228. the difference was more romanian neurosurgery (2011) xviii 1: 38 – 53 51 significant at the 18 months monitoring, with a difference of mean survival of 4 months in favour of the younger group (11,7 vs. 7,7 months), difference which is also maintained at the 24 months monitoring (12,8 versus 8,0 month). despite the fact that we compare only patients with gtr and str, without needle biopsy sampling, and considering the recent provided data from the chaichana's study, we can conclude that maximal cytoreduction surgery is recommendable in the elderly patients, mentioning also the fact that the mortality is higher in the group of patient over 65. the mechanical cytoreduction of the mass also obtains time for other therapeutic interventions (radiotherapy, chemotherapy, and immunotherapy). the reduced tumour burden has been shown to have a beneficial effect on cerebral blood flow and metabolism even at sites in the brain distant from tumour resection. one hundred grams of tumour mass is considered lethal for the average adult. along with surrounding edema, the tumoral mass accounts for 10% of the intracranial volume. for the neurologic symptoms to appear it generally takes 30 to 60 g of tumour or 3 to 6x1010 cell. 1 g of tumoral mass or 1x109 cell is thought to be left after a total resection of the gadolinium enhancing regions on magnetic resonance imaging. the adjuvant therapy of malignant glioma also contributes to tumoral reduction. while radiotherapy kills two logs of cell, chemotherapeutic regimens are thought to kill one to two logs of cell. the body’s immune mechanisms are believed to suppress tumour burdens less than 1x105 cells. despite these promising assertion , malignant glioma remains for the vast majority of patients an incurable disease (16). the efficacy of adjuvant therapy is increased when the tumour load is lower. a higher glioblastoma load increased chemotherapy resistance as it was demonstrated in an in vivo study. in order to achieve the same effect, a 4-fold increase in the glioblastoma load requires a 2-fold increase in the bcnu concentration (21). other argument in favour of open surgery is the accuracy of histological diagnosis, which is dependent on the size of the tissue sample. as a result of limited tissue samples, the stereotactic biopsy is associated with false negatives, with is estimated to be around 10% (27). a discrepancy rate of 38% between biopsy and subsequently resected specimens in 81 patients was reported by jackson et al (13). in 26% of cases, this discrepancy was found to affect the treatment. for the 38% of cases the prognosis was altered. concerning the pathological findings, not surprisingly in our study there is no statistical significant difference at 12 and 18 months monitoring (p=0.09 respectively p=0,122). for survival at 24 months, the survival mean for glioblastoma multiforme diagnosed patients was 11,2 months, for the ones having anaplastic astrocytoma was 11,9 months. patients with malignant oligodendrogliomas survived for approximately 16,1 months (with a confidence interval of 95% between 12,6 and 19,6) and the ones with malignant ependymoma 17,1 (p=0.031). finally surgical resection of large sample of tumour may serve as an aid in research. the collection of large human tumour samples allows for comprehensive molecular analysis and fingerprinting of each tumour [9,33] , which in turn may lead to the development of individually 52 c. abrudan et al surgery of high grade gliomas tailored molecular therapies. increasing evidence suggests that tumors of the central nervous system are derived from proliferatively active neural stem cells residing in defined neuropoietic niches of the adult brain. these cancer stem cells, also identified in other tumors, provide a reservoir of cells with self-renewal capabilities, can maintain the tumor by generating differentiated non-stem tumor cells and are responsible for recurrences after ablative neurosurgical therapy and chemoradiotherapy. the only way to successfully control recurrent malignant gliomas and even hope for a cure in the future is by combining standard chemotherapy with immunotherapy. despite the apparent improvements of current treatments, it should be realized that the characteristic brain tumor niche may provide recurrent gliomas an “escape mechanism” from anticancer treatments. thus, the use of targeted molecular therapy drugs may effectively inhibit or at least slow down cancer stem cell proliferation and stop the brain microenvironment from allowing furtive invasion and proliferation of highly aggressive malignant gliomas[9]. only through further understanding of the biology of gliomas can we hope to find a cure in the future. conclusion the review of the literature suggests that gross total resections for patients with malignant gliomas can improve both survival and quality of life. different studies show that early and long term postoperative outcome after radical surgical resection are better than the results of either partial resection or simple biopsy, in terms of neurological status and duration of survival. similarly, reoperation for recurrence of glioma offers reasonable extension of quality survival. our study provides a new argument in favour of gross total removal. we have shown that radical surgery improves the overall survival and total resection should be considered whenever possible. an aggressive cytoreduction is recommendable also in patients over the age of 65. total removal for patient with tumour recurrence does not change statistically significant the global survival comparing to partial removal but the quality of life sure benefits from it, by decreasing the intracranial pressure. acknowledgements this work was financially supported by a grant of the romanian ministry of research and education, project of exploratory research, contract idei 1161. references 1. albert fk, forsting m (2003) resection and prognosis. j neurosurg98(1):225–226; 2. ammirati m, vick n, liao yl, ciric i, mikhael m (1987). effect of the extent of surgical resection on survival and quality of life in patients with supratentorial glioblastomas and anaplastic astrocytomas. neurosurgery 21: 201 ± 206. 3. boon-chuan pang, wei-hwang wan, cheng-kiang lee, kathleen joy khu,wai-hoe ng. the role of surgery in high-grade glioma – is surgical resection justified? a review of the current knowledge:ann acad med singapore 2007;36:358-63. 4. chaichana k l, garzon-muvdi t, parker s, weingart jd, olivi a, bennett r, brem h, a quinones-hinojosa a. supratentorial glioblastoma multiforme: the role of surgical resection versus biopsy among older patients, ann surg oncol (2010) published on-line in 10 august 2010 5. ciric i, ammirati m, vick n, mikhael m (1987). supratentorial gliomas: surgical considerations and immediate postoperative results. gross total resection versus partial resection. neurosurgery 21: 21 ± 26. 6. dandy we. removal of right cerebral hemisphere for certain tumors with hemiplegia. jama 1928;90:823-5. 7. devaux bc, o’fallon jr, kelly pj (1993) resection, biopsy, and survival in malignant glial neoplasms. a romanian neurosurgery (2011) xviii 1: 38 – 53 53 retrospective study of clinical parameters, therapy, and outcome. j neurosurg 78(5):767–775 8. fadul c, wood j, thaler h, galicich j, patternson rh, jr, posner jb. morbidity and mortality of craniotomy for the excision of supratentorial gliomas. neurology 1988;38:1374–9. 9. florian is, tomuleasa c, soritau o, ioani h, irimie a, kacso g :cancer stem cells and malignant gliomas. from pathophysiology to targeted molecular therapy. accepted for publication in j buon jan. 2011 10.gardner we. removal of the right cerebral hemisphere for infiltrating glioma. arch neurol psychiatry 1932;67:787-9. 11. hentschel sj, lang ff. current surgical management of glioblastoma. cancer j 2003;9:113-25. 12. hillier wf jr. total left cerebral hemispherectomy for malignant glioma. neurology 1954;4:718-21. 13.jackson rj, fuller gn, abi-said d, lang ff, gokaslan zl, shi wm, et al. limitations of stereotactic biopsy in the initial management of gliomas. neurooncol 2001;3:193-200 14.kelly pj, daumas-duport c, scheithauer bw, kall ba, kispert db. stereotactic histologic correlations of computed tomographyand magnetic resonance imaging-defined abnormalities in patients with glial neoplasms. mayo clin proc 1987;62:450-9. 15.kiwit jc, floeth fw, bock wj (1996) survival in malignant glioma: analysis of prognostic factors with special regard to cytoreductive surgery. zentralbl neurochir 57(2):76–88 16.kole m and rock j. malignant glioma surgery: complication avoidance. neurosurgery quarterly 12(2002) (3):251–258 17. lacroix m, abi-said d, fourney dr, et al. a multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. j neurosurg 2001;95:190–8. 18.levin va, wara wm, davis rl et al (1985) phase iii comparison of bcnu and the combination of procarbazine, ccnu, and vincristine administered after radiotherapy with hydroxyurea for malignant gliomas. j neurosurg 63(2):218–223 19.metcalfe se, grant r (2003) biopsy versus resection for malignant glioma (cochrane review). the cochrane library 20.mitchell p, ellison dw, mendelow ad. surgery for malignant gliomas: mechanistic reasoning and slippery statistics. lancet neurol 2005;4:413-22. 21.ng wh, wan gq, too hp. higher glioblastoma tumour burden confers resistance to chemotherapeutic agent – in vitro evidence. j clin neurosci 2007;14:261-6. 22. nitta t, sato k prognostic implications of the extent of surgical resection in patients with intracranial malignant gliomas. cancer(1995) 75(11):2727–2731 23. rowe sn. mental changes following the removal of the right cerebral hemisphere for brain tumor. am j psychiatry 1937;94:605-14 24.ryken tc, frankel b, julien t, olson jj.surgical management of newly diagnosed glioblastoma in adults: role of cytoreductive surgery;j neurooncol (2008) 89:271–286 25.salcman m supratentorial gliomas: clinical features and surgical therapy. in: neurosurgery wilkins rj and rengachary ss (eds). second edition, mcgraw-hill book co., new york.1996, vol 1, pp 77788. 26.salcman m. glioblastoma and malignant astrocytoma. in: kaye ah, laws er, eds. brain tumors. new york: churchill livingstone; 1995:449–77. 27.sawaya r. extent of resection in malignant gliomas: a critical summary. jneurooncol 1999;42:303-5 28. shapiro wr. treatment of neuroectodermal brain tumors. ann neurol 1982;12:231–7. 29.shibamoto y (1994). influence of extent of surgery and tumor location on treatment outcome of patients with glioblastoma multiforme treated with combined modality approach. j neuro-oncol 21: 177 ± 185. 30. simpson jr, horton j, scott c et al (1993) influence of location and extent of surgical resection on survival of patients with glioblastoma multiforme: results of three consecutive radiationtherapy oncology group (rtog) clinical trials. int j radiatoncol biol phys 26(2):239–244 31. stummer w, pichlmeier u, meinel t, wiestler od, zanella f, reulen hj (2006) fluorescence-guided surgery with 5-aminolevulinic acid for resection of malignant glioma: a randomised controlled multicentre phase iii trial. lancet oncol 7(5):392–401 32. stupp r, mason wp, van den bent mj, weller m, fisher b, taphoorn mj, et al. radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. n engl j med 2005;352:987-96. 33. tomuleasa c., soriţău o., ciucă dr, ioani h, șuşman s, petrescu m, cernea d, kacsό g, irimie a, florian is: functional and molecular characterization of glioblastoma multiforme derived cancer stem cells, j buon. 2010 jul-sep;15(3): 583-91. 34. vecht cj, avezaat cj, van putten wl, eijkenboom wm, stefanko sz the influence of the extent of surgery on the neurological function and survival in malignant glioma. a retrospective analysis in 243 patients. j neurol neurosurg psychiatry (1990)53(6):466–471 35. vuorinen v, hinkka s, farkkila m, jaaskelainen j debulking or biopsy of malignant glioma in elderly people—a randomised study. acta neurochir (wien) (2003) 145(1):5–10 36. whittle ir, pringle am, taylor r. effects of resective surgery for leftsided intracranial tumours on language function: a prospective study. lancet 1998;351:1014-8. microsoft word 8.moraru.docx romanian neurosurgery (2012) xix 4: 299 – 308 299 neurological point of view bacterial spondylodiscitis: diagnostic challenges and therapeutic strategies igor moraru department of neurology, incomed medical center, balti, republic of moldova abstract spondylodiscitis has gained attention lately because of an alarming and progressive increasing of its incidence, reflecting the rise of percentage of the elderly and immunocompromised people, and the implementation in practice of advanced diagnostic methods. this review will focus on the etiology, diagnostic challenges, and treatment strategies in spondylodiscitis. the incidence of spondylodiscitis is currently 4-24/1 million, making up to 3-5 % of total osteomyelitis cases. it is approximately two times more common in men than in women. staphylococcus aureus is involved in 48 % 62.5 % of cases of spondylodiscitis. the clinical picture is dominated by spinal pain and stiffness, and increased erythrocytes sedimentation ratio and c-reactive protein are laboratory markers of spondylodiscitis. the most sensitive imaging method is magnetic resonance imaging. bacteriological examination is very important for proper and effective treatment, guiding the selection of the antibacterial regiment that has proven to be effective in about 75 % of patients. in other cases, surgical treatment may be used. the prognosis is favorable, except for those with comorbidities or noncompliance with treatment. key words: spondylodiscitis; discitis; disc infection. introduction infection of the intervertebral disc is a little studied problem, and which endangers in a significant extent the health and quality of life of patients if untreated. in the reason of a quasi-permanent association of the vertebral body inflammation, to define the disk infection further, “spondylodiscitis” term will be used. spondylodiscitis has gained attention lately because of an alarming and progressive increasing of its incidence, (1) reflecting the rise of number of the elderly and immunocompromised people, and the implementation in practice of advanced diagnostic methods. the absolute number of spondylodiscitis cases also increases progressively in close accordance with the raise in the number of spine interventions. (2) non-specificity of the clinical picture, clinical setting of appearance and the unfamiliarity of medical staff with this disease, often exclude spondylodiscitis from clinical reasoning of neurologists. (3) delayed diagnosis can have disastrous consequences for the patient, disability and permanent deformation of the spine being the possible scenario. the management of 300 moraru bacterial spondylodiscitis: diagnostic challenges and therapeutic strategies spondylodiscitis is also a subject of many controversies incited by the absence of clinical guidelines and treatment protocols. the incidence of spontaneous infectious spondylodiscitis has a bimodal distribution with peaks at ages under 20 years and in people after age of 50 years, (1) global values of incidence in developed countries varying in the range of 4-24 to 1 million populations (3) and make up from 3 % to 5 % of the total number of osteomyelitis. (4) the distribution by sex reflects a slight prevalence in men, their ratio to women being 1,5:1 (5, 6) or 2:1. (7, 8) the mean age of patients with postoperative spondylodiscitis tends to be lower than that of patients with spontaneous spondylodiscitis (60-69 versus 46-52 years). (7-9) spondylodiscitis is an inflammation of the intervertebral disc and neighboring vertebrae. the sequence of involvement in the process of these structures depends largely on their anatomical structure, chemical composition, and vascularization. there are three possible scenarios for the development of spondylodiscitis: primary infection of intervertebral disc by hematogenous spread of bacteria, vertebral body primary infection, or direct inoculation of the pathogen in the disc. the first mechanism is characteristic for spondylodiscitis in children, the rich vascularity of the intervertebral disc contributing to the precipitation of the pathogen at this level, often the infectious process being limited to this area, in which case we talk about pure discitis. also, such a development of the events may be possible in the elderly, (10) where the disc capsule, by virtue of degenerative processes, becomes vulnerable to microbial invasion. the second scenario is observed in adults. in such cases the intervertebral disc is largely avascular, and vascularization of the lamina terminalis has already begun to suffer from loss of intraosseous anastomoses, so that it creates the possibility of a primary infection of subchondral bone, which by destroying the lamina terminalis will propagate to adjacent intervertebral disc. (11) infection by direct inoculation is seen in iatrogenic spondylodiscitis. the propagation of germs in hematogenous spondylodiscitis can occur via arterial flow and, rarely, venous circulation. the source or site of entry of the infection is most often the skin (21 %), followed by the genitourinary (10 %) (5) and intestinal (12) tracts. however, in 53 % of cases of infection the site of entry remains unidentified. (5) diagnostic challenges the spondylodiscitis diagnosis rate at first visit to the physician is discouraging small, reaching only 39 % of cases. (5) given the non-specificity and nebulosity of symptoms at onset, the most common destination of visits of patients with spondylodiscitis is primary care units (66.7 %). (13) as a result, diagnostic failure worsens because of unawareness and reduced vigilance of physicians for this disease. the same is true for endocrinologists who have the mission to fight the prevailing background of spondylodiscitis diabetes mellitus. the time between the start of symptoms and the establishment of diagnosis in different studies ranged from 2 days to 12 months, (9, 14, 15) with an average of 4.3 months, (16) being higher in patients with postoperative spondylodiscitis. (8) one explanation is the similarity of clinical (pain) and laboratory (erythrocytes sedimentation rate (esr), c-reactive romanian neurosurgery (2012) xix 4: 299 – 308 301 protein (crp)) markers of spondylodiscitis and the normal postoperative changes. (17) achieving esr peak at day 5 of surgery and returning to normal in the first 3 weeks is a normal postoperative dynamic and any digression from this rhythm would raise suspicion. (18) given the prompt dynamic of changes of c-reactive protein (peak at day 3 and returning to normal in the first 2 weeks), this parameter may be more useful than esr in detecting early deviations from normal postoperative course. (18) in addition, the presence of neurological deficit in patients with spondylodiscitis increases confusion by directing the clinical reasoning to a post-operative relapse or failure of surgery, especially in the presence of pain with radicular distribution. (19) lack of fever in many patients with postoperative spondylodiscitis (8, 19) results in ignoring the infectious nature of observed changes. finally, the imaging changes in spondylodiscitis can be included in the normal postoperative picture, (20) although the identification of vertebral edema on mri has determined the usefulness of this method in differentiating between the two situations. (18) hazy clinical picture, slow evolution, and atypical symptoms (lack of systemic inflammatory reaction and fever) are responsible for the retard in the diagnosis of tuberculous spondylodiscitis, reaching an average of 6-8 months. (21, 22) for atypical and suspicious cases is recommended to repeat mri over 1-2 weeks, during which specific changes of spondylodiscitis can be delineated. (b2) (10, 21) etiology in the etiology of spondylodiscitis usually is involved a single organism, although multibacterial infection has been reported occasionally, especially on an immunocompromised or diseased background. (12) the most often isolated germ has been staphylococcus with a frequency of 48 % 62.5 %. (8, 9, 23) most of the community acquired staphylococci are sensitive to methicillin and about 30-40 % of nosocomial staphylococcal infections are methicillin-resistant. (24) next in frequency are gram-negative bacilli (4-30 %) and streptococci / enterococci (5-30 %). (21, 25, 26) gram-negative bacilli are commonly seen on an immunocompromised background or after infections of gastrointestinal or genitourinary tracts, (21, 24, 26) while anaerobic infections are more common in diabetic patients. (27) fungal infections are the cause of about 1 % of non-tuberculous spondylodiscitis in adults, the leading role played by candida albicans (21) and usually occur on a background prone to this type of infection such as immunosuppression, diabetes, broad-spectrum antibiotics or treatment in intensive care units. (21, 26, 28) brucella gain attention in certain geographical areas such as the mediterranean coast, where some studies have demonstrated involvement in 25-50 % of cases of spinal infection. (15, 22) the most common risk factor in developing spondylodiscitis is diabetes mellitus. (7, 13, 15) among other contributing factors are pathological states accompanied by immunosuppression (chronic alcoholism, (7, 9) prolonged steroidal or non-steroidal anti-inflammatory drug therapy, (8) intercurrent infections etc.), cardiovascular diseases, obesity, (4) crohn's disease, (12) cirrhosis, (29) cancer, (9) intravenous drug use (15) etc. clinical picture the clinical picture of spondylodiscitis often lacks conclusiveness and sometimes is 302 moraru bacterial spondylodiscitis: diagnostic challenges and therapeutic strategies confusing, unless pain and spinal stiffness is present. spontaneous nonspecific spondylodiscitis develop acutely, as opposed to specific infections that determine a blurred clinical picture and has a slow evolution. (30) in the course of postoperative spondylodiscitis, one can distinguish a clinically silent period following surgery, lasting on average 21 days and ranging from hours to months. (7) low back pain with inflammatory character (83-100 % of cases) (5, 8, 9) is the most common cause of visits to the physician, (14, 16) and sometimes is absent in patients with spontaneous spondylodiscitis. (8) the features of spondylodiscitis pain (the nocturnal character, resistant to painkillers and rest, (28) associated with morning stiffness and worsening at bed shaking – bed-shaking test (7)) has a diagnostic utility. pain intensity is less relevant, varying from moderate to severe. (7) pain usually is located in the affected region of the spine but can radiate into the buttocks, thighs, abdomen, or perineal region. (7) anatomical distribution of the infection has a downward character, lumbar region being involved in 38-70 % of cases. (5, 8, 9, 31) spinal stiffness, present in 77-100 % of cases, (5, 7, 9) aims to reduce the burden on anterior vertebral elements. (4) the systemic inflammatory syndrome is reflected by increased body temperature (observed in 50-97 % of cases), (5, 8, 9) profuse sweating, weight loss etc. the neurological deficit is present in most cases of postoperative spondylodiscitis and only in half of those with spontaneous spondylodiscitis. (8, 16) it is more common in cervical and thoracic locations of the infectious process (25) and in cases of tuberculous nature, (22) reflecting in an indirect way the causal relationship to the formation of paravertebral collections, (13) whose frequency was found to be increased in higher segments, (25, 32) and in patients with specific infectious. (30, 33, 34) investigations one of the first changed and the most faithful marker of spondylodiscitis is esr, which proved to be increased in 98-100 % of cases. (5, 7, 15) even if the esr did not correlate with severity of disease, (33) the dynamics of this parameter was found to be useful in assessing the response to the treatment. c-reactive protein is a marker as reliable as esr, some authors (35) considering it to be even more sensitive than esr, being increased in almost all cases (7, 15) of spondylodiscitis. the dynamics of these changes is more important than their absolute value, both to monitor the patient's clinical condition and to assess treatment efficacy. so, returning to normal esr and crp was observed on average 21 days (7) after the initiation of a successful treatment. leukocytosis is an inconstant parameter, with a frequency of 42-64 % of cases. (5, 25) the simplest and most accessible method of isolation of the infectious agent is blood culture. resultativity of blood culture is enhanced by the increased virulence of pathogens, (29) the spontaneous nature of spondylodiscitis, (8) the multiplicity of performed sowing (at least three), (a2) (4, 21) carrying out during fever peak or within 4 hours after puncture of the intervertebral disc, (26, 36) and is drastically reduced by prior antibiotic drugs therapy, in which cases is recommended to postpone the sampling for at least 2 weeks after cessation of antibacterial therapy. (a3) (21) given the low success rates of haemoculture in postoperative spondylodiscitis, (7) spilf guideline romanian neurosurgery (2012) xix 4: 299 – 308 303 recommends disco-vertebral biopsy in any suspicions of spondylodiscitis after intradiscal surgery. (a2) (21) urine, sputum, and samples from any site of entry are needed to detect possible sources of primary infection. (37) three successive failed inseminations is an indication for the use of disc puncture. the procedure is done under anesthesia and radiological (computerized tomography) guidance, (4) with a success rate of 60-70 %. (14, 26, 35, 38, 39) like blood culture, the disc puncture is compromised by prior antibiotic therapy. (21, 24) to increase the quality of the collected material, multiple sampling is recommended, two of the top terminal lamina, two of the bottom one and two from the intervertebral disc. (21) if the first disc puncture proves to be negative, it is recommended to repeat the procedure. (6, 40) open biopsy is necessary if percutaneous puncture and empirical treatment have both failed (28). serological investigations are not recommended to be performed routinely given their low success rate. (24) imaging 1. radiography usefulness of radiography in diagnosing spondylodiscitis in overall is low, and lies in highlighting the pinching of the intervertebral space and progressive subchondral sclerosis in association with an increased adjacent bone density, (33) which in the later stages can pass into geodes, compressions or vertebral collapse. broadening of the psoas shadow, mediastinum or retroperitoneal space is a sign of spreading of the infection to paravertebral tissues. (27) 2. computerized tomography in the first 2 weeks in 50 % of patients (21) computerized tomography (ct) reveals pinching and hipodensity of affected disc, erosion of the vertebral lamina and the vertebral body and soft tissue edema. (36, 38, 41) (figure 1) ct usefulness is evident in guiding the disc biopsies or drainage of paravertebral collections. (37) contrast administration will facilitate highlighting of paravertebral infiltration and fluid collection. (42) figure 1 computerized tomography (axial view) of the lumbar spine showing erosions of the vertebral lamina and the vertebral body. it is noticeable the sparing of the posterior elements of the vertebra figure 2 magnetic resonance imaging (mri) of the lumbar spine in a patient with spondylodiscitis: a. t1-weighted sequence showing destruction of lamina terminalis and vertebral edema; b. t2weighted mri revealing intradiscal hyperintensities (white arrow) and epidural abscess (black arrow); c. contrasting of intervertebral disc (arrowhead) on contrast-enhanced t1-weighted mri 304 moraru bacterial spondylodiscitis: diagnostic challenges and therapeutic strategies 3. magnetic resonance imaging magnetic resonance imaging (mri), considered to be the method of choice for early detection of changes in bacterial spondylodiscitis, (14, 21, 43) provides a number of criteria which are distinguished by high sensitivity and specificity: presence of epidural or paraspinal inflammation (sensitivity 97.7 %), contrasting of the intervertebral disc in t1-weighted sequences (sensitivity 95.4 %), hyperintensities or fluid signal intensities in the intervertebral disc in t2-weighted mri (sensitivity 93.2 %) and erosions and destructions of at least one vertebral lamina terminalis (sensitivity 84.1 %). (44) (figure 2, a, b, c) other signs include the disappearance of intranuclear hypodense slit in t2-weighted mri, epiduritis (epidural abscess) viewed as an epidural hypointensity in t1 and hyperintensity in t2-weighted images and paravertebral abscess (t1 hyperintense and t2 hypointense signals in the lateral vertebral regions). (9) anterior location of imaging changes in spontaneous spondylodiscitis and posterior situation of these changes in postoperative forms is a common regularity. (8) usefulness of mri in monitoring the progress and response to treatment of spondylodiscitis was discredited except in epiduritis and paravertebral abscess, imaging appearance of which correlated with clinical parameters and laboratory dynamics. (9) for patients in whom mri is contraindicated (i.e. implanted pacemaker), french guidelines recommend obtaining contrast scintigraphy followed by ct. (21) 4. other scintigraphy is not the method of choice, (45) while other authors consider it useful in the diagnosis of spondylodiscitis, especially in the elderly. (36) extreme usefulness of positron emission tomography (pet) with fluorine-18 fluorodeoxyglucose (18-f fdg) in revealing inflammatory process in the vertebral body (4) is counteracted by the high cost of this method and the inability to differentiate between a tumor and an inflammatory process. (45) differential diagnosis differentiating spondylodiscitis from the degenerative changes of modic i type is occasionally difficult, (46) given the similarity of imaging and clinical data. (46) intradiscal fluid hyperintensities in t2 sequences, the erosions and destructions of the lamina terminalis, and the formation of paravertebral collections, (44) is the mri picture that will lead us to the diagnosis of spondylodiscitis, given the rarity of degenerative origins of such changes. mri with diffusion and f-18 fdg pet are useful in this context by revealing inflammatory changes with a hyperintense in the first case (47) and hypermetabolic in the second, (4) appearance. coupling the imaging with the clinical (pain with inflammatory rhythm, fever, sweating) and laboratory (esr and crp increase) data, will increase the potential for discrimination between the two pathologies. however, one should not overlook the possibility of development of spondylodiscitis in a degenerated disc, (48) witch is one of the few situations when isolated discitis can develop in adults. the diagnosis of spondylodiscitis is sometimes evoked in the context of an injury other than infectious, such as seronegative spondyloarthritis, including ankylosing (49) and enteropathic (50) spondylitis. spondylodiscitis developed on this pathologic background is distinguished from the bacterial variant of the disease by romanian neurosurgery (2012) xix 4: 299 – 308 305 the absence of a localized pain and systemic inflammatory syndrome. in addition, the anatomical location of spondylodiscitis in ankylosing spondylitis is predominantly the lower chest segment and multiple levels of injury are more commonly seen than in the analogue of bacterial origin. (49) spondylodiscitis incidence in ankylosing spondylitis is estimated around 8 %. (49) treatment 1. general rules given the lack of prospective randomized trials, the treatment of spondylodiscitis remains controversial until today. (24) the success of conservative treatment was documented in approximately 73 % of patients with spondylodiscitis. (23) the crucial elements of a successful treatment of spondylodiscitis are the immobilization of the affected segment of the spine, antibiotics and (depending on the severity of disease) debridement and decompression of the spinal canal. (4) targeted antibacterial treatment is a fundamental element in the management of spondylodiscitis and identification of pathogens must precede always the elaboration of an individual treatment scheme, (4) except in cases of sepsis, with critical clinical status, neutropenia or severe neurological deficit, (37) which will require the use of empirical treatment. 2. selection of the antibiotics in the selection of the antibiotic, its ability to penetrate bone and intervertebral disc tissue should be taken into consideration, as is well known that fluoroquinolones, clindamycin, rifampicin, fusidic acid, and metronidazole reach remarkable bone concentrations. the penetrability of beta-lactams and glycopeptides is moderate, while aminoglycosides does penetrate bone even worse. (24) however, penetrability into the intervertebral disc correlates with antibiotic’s ion charge, negatively charged antibiotics such as penicillin being far less penetrating than the positively charged ones such as gentamicin. (51) in this framework of ideas, the ability of antibiotics to diffuse in disc tissue in decreasing order is as follows: clindamycin and aminoglycosides > quinolones and glycopeptides> penicillins and cephalosporins. (51) however, the value of such data in establishing antibacterial regime is unclear, once spilf guideline recommends as firstline treatment of staphylococcal infections penicillin and glycopeptides, (21) antibiotics that has been shown to penetrate moderately/poorly in disc tissue. (52) taking as support the result of bacteriologic exams, antibiotic selection within each therapeutic group will be guided by pharmacokinetic profile, ability to penetrate the disc and bone tissue, route of administration, toxicity, and cost. thus, greater oral bioavailability will favor the selection of cloxacillin over oxacillin for the treatment per os. (53) netilmicin was preferred among other aminoglycosides to treat infections with gram + bacteria, since the former has less ototoxicity while teicoplanin was preferred over vancomycin because of nephrotoxicity and more complicated use of second. (54) also, ciprofloxacin should be favored over other fluorchinolones in the treatment of infections caused by pseudomonas aeruginosa or other grambacteria, since it possesses the lowest minimum inhibitory concentration for these bacteria. (55) some authors recommend metronidazole for 306 moraru bacterial spondylodiscitis: diagnostic challenges and therapeutic strategies anaerobic etiology, (24, 56) while others plead in favor of clindamycin. (21) 3. duration of the treatment duration of parenteral antibacterial therapy has been adjusted depending on the level of c-reactive protein, normalization of this parameter in the first two weeks requiring parenteral treatment cessation, or its prolongation to 3 weeks otherwise. (43) switch to oral administration after achieving clinical improvement or normalization or considerable decrease of biological markers of inflammation (esr, crp, wbc) was a tactic favored by other authors. (4) oral bioavailability of clindamycin, fluoroquinolones, rifampicin and fusidic acid is high, (57) so they are a good choice for maintenance treatment, and are not recommended for the initial treatment because of the potential for developing resistant strains. (24) duration of oral antibiotic treatment is from 6 weeks to 3 months for nonspecific spondylodiscitis (23) and 2 times longer, (30) typically up to one year, (15) in tuberculous cases. paravertebral collections will sometimes require percutaneous or surgical drainage. surgery is rarely necessary and only in cases where spinal instability, (23, 32) progressive neurological deficit, (13, 23) failure of conservative treatment (4) or cauda equina syndrome (13) are present. antibacterial prophylaxis of spondylodiscitis is imperative after any intradiscal surgery. (58) prognostics residual symptoms may persist both after conservative and surgical treatment of spondylodiscitis. the recurrence rate of spondylodiscitis was reported to be between 0 % and 7 %. (59, 60) adverse outcomes are related to septic complications, (16) being more common in patients with a premorbid background such as diabetes. (31) conclusions spondylodiscitis is an issue whose importance on the one hand is often underestimated or missed and on the other hand is getting worse every year in the context of an increase in the number of spine interventions as well as in the prevalence of elderly and immunecompromised subjects. the diagnosis of spondylodiscitis is sometimes difficult, and knowledge of clinical features and atypical forms is essential for accurate and early diagnosis. at the forefront of the diagnostic labor in spondylodiscitis are imaging (mri) and bacteriologic exams. the keystone of an effective treatment of spondylodiscitis will be always the microbiological examinations and in cases where they fail it will be adjusted depending on the most likely etiology of the disease derived from the present clinical situation and guided by the results of previous clinical studies. references 1. espersen f, frimodt-møller n, thamdrup rosdahl v, et al. changing pattern of bone and joint infections due to staphylococcus aureus: study of cases of bacteremia in denmark, 1959–1988. rev infect dis 1991;13:347–58. 2. nakagawa h, kamimura m, takahara k, et al. optimal duration of conservative treatment for lumbar disc herniation depending on the type of herniation. j clin neurosci 2007;14:104-9. 3. gouliouris t, aliyu sh, brown nm. spondylodiscitis: update on diagnosis and management. j antimicrob chemother 2010;65 (suppl 3):11-24. 4. sobottke r, seifert h, fätkenheuer g, et al. current diagnosis and treatment of spondylodiscitis. dtsch arztebl int 2008;105:181-7. 5. jensen ag, espersen f, skinhøj p, et al. bacteremic staphylococcus aureus spondylitis. arch intern med 1998;158:509-17. 6. friedman ja. spontaneous disc space infections in adults. surg neurol 2002;57:81–6. romanian neurosurgery (2012) xix 4: 299 – 308 307 7. kutlay m, colak a, simsek h, et al. antibiotic and hyperbaric oxygen therapy in the management of postoperative discitis. undersea hyperb med 2008;35:42740. 8. dufour v, feydy a, rillardon l, et al. comparative study of postoperative and spontaneous pyogenic spondylodiscitis. semin arthritis rheum 2005;34:76671. 9. veillard e, guggenbuhl p, morcet n, et al. régression rapide des abcès paravertébraux et des épidurites au cours de l'évolution des spondylodiscites à germes banals. à propos de 16 spondylodiscites évaluées en irm. rev rhum 2000;67:219-28. 10. millot f, bonnaire b, clavel g, et al. la spondylodiscite à staphylococcus aureus par voie hématogène de l'adulte ne débute pas toujours dans le corps vertébral. rev rhum 2010;77:97-9. 11. wiley am, trueta j. the vascular anatomy of the spine and its relationship to pyogenic verteral osteomyelitis. j bone joint surg br 1959;41-b:796-809. 12. kroot ej, wouters jm. an unusual case of infectious spondylodiscitis. rheumatology 2007;46:1296. 13. asamoto s, doi h, kobayashi n, et al. spondylodiscitis: diagnosis and treatment. surg neurol 2005;64:103-8. 14. ben taarit ch, turki s, ben maiz h. [infectious spondylitis. study of a series of 151 cases]. acta orthop belg 2002;68:381-7. 15. faella fs, rossi m, pagliano p, et al. [non postoperative spondylodiskitis. our experience during the period 1990-2001]. infez med 2002;10:157-62. 16. fica a, bozán f, aristegui m, et al. [spondylodiscitis. analysis of 25 cases]. rev med chil 2003;131:473-82. 17.richter kj. clinical significance of the erythrocyte sedimentation rate in orthopaedic surgery. j bone joint surg am 1987;69:794b-. 18. silber js, anderson dg, vaccaro ar, et al. management of postprocedural discitis. spine j 2002;2:279-87. 19. bianco g, pompeo me, mastroianni c, et al. [nontubercular and non-brucellar spondylodiscitis: preliminary clinico-microbiologic analysis of 37 cases]. recenti prog med 2003;94:554-9. 20. boden sd, davis do, dina ts, et al. postoperative diskitis: distinguishing early mr imaging findings from normal postoperative disk space changes. radiology 1992;184:765-71. 21. societe de pathologie infectieuse de langue francaise (spilf). recommandations pour la pratique clinique: spondylodiscites infectieuses primitives, et secondaire un à geste intra-discal, sans mise en place de matériel. med mal infect 2007;37:573-83. 22. colmenero jd, jimenez-mejias me, sanchez-lora fj, et al. pyogenic, tuberculous, and brucellar vertebral osteomyelitis: a descriptive and comparative study of 219 cases. ann rheum dis 1997;56:709-15. 23. butler j, shelly m, timlin m, et al. nontuberculous pyogenic spinal infection in adults: a 12-year experience from a tertiary referral center. spine (phila pa 1976) 2006;31:2695-700. 24. grados f, lescure fx, senneville e, et al. suggestions for managing pyogenic (non-tuberculous) discitis in adults. joint bone spine 2007;74:133-9. 25. hadjipavlou ag, mader jt, necessary jt, et al. hematogenous pyogenic spinal infections and their surgical management. spine (phila pa 1976) 1976;25:1668-79. 26. vergne p, treves r. spondylodiscite bacterienne : etiologie, diagnostic, evolution, traitement. fran&#231;ais 1998;48:2065-71. 27. an hs, seldomridge ja. spinal infections: diagnostic tests and imaging studies. clin orthop relat res 2006;444:27-33. 28. govender s. spinal infections. j bone joint surg br 2005;87-b:1454-8. 29morrison r, naktin j. bacteremia, vertebral diskitis, and osteomyelitis in a man with cirrhosis. jaapa 2009;22:36, 8-9. 30. belghali s., ben fredj h, ben haj slama k, et al. les spondylodiscites infectieuses (spdi) a germes banals: étude comparative avec les spdi a germes spécifiques. rev rhum 2006;73:1126. 31. sapico fl, montgomerie jz. pyogenic vertebral osteomyelitis: report of nine cases and review of the literature. rev infect dis 1979;1:754-76. 32. han l, keiserrudin ma, jensen pl. atypical presentation of spontaneous discitis: case report. surg neurol 2004;61:142-3. 33.kemp hb, jackson jw, jeremiah jd, et al. pyogenic infections occurring primarily in intervertebral discs. j bone joint surg br 1973;55-b:698-714. 34. bhojraj s, nene a. lumbar and lumbosacral tuberculous spondylodiscitis in adults: redefining the indications for surgery. j bone joint surg br 2002;84b:530-4. 35. legrand e, massin p, levasseur r, et al. stratégie diagnostique et principes thérapeutiques au cours des spondylodiscites infectieuses bactériennes. rev rhum 2006;73:373-9. 36. lam ks, webb jk. discitis. hosp med 2004;65:280-6. 37. cottle l, riordan t. infectious spondylodiscitis. j infect 2008;56:401-12. epub 2008 apr 28. 38. gasbarrini al, bertoldi e, mazzetti m, et al. clinical features, diagnostic and therapeutic approaches to haematogenous vertebral osteomyelitis. eur rev med pharmacol sci 2005;9:53-66. 39. jiménez-mejías me, de dios colmenero j, sánchez-lora fj, et al. postoperative spondylodiskitis: 308 moraru bacterial spondylodiscitis: diagnostic challenges and therapeutic strategies etiology, clinical findings, prognosis, and comparison with nonoperative pyogenic spondylodiskitis. clin infect dis 1999;29:339-45. 40. gaudias j. considerations on antimicrobial therapy for pyogenic discitis. joint bone spine 2001;68:463-5. 41. varma r, lander p, assaf a. imaging of pyogenic infectious spondylodiskitis. radiol clin north am 2001;39:203-13. 42. maiuri f, iaconetta g, gallicchio b, et al. spondylodiscitis. clinical and magnetic resonance diagnosis. spine (phila pa 1976) 1997;22:1741-6. 43. ahmed r, douadi y, lescure fx, et al. étude des spondylodiscites infectieuses au chu d'amiens sur une période de 5 ans. rev med interne 2002;23:582. 44. ledermann hp, schweitzer me, morrison wb, et al. mr imaging findings in spinal infections: rules or myths? radiology 2003;228:506-14. 45. de winter f, van de wiele c, vogelaers d, et al. fluorine-18 fluorodeoxyglucose-positron emission tomography: a highly accurate imaging modality for the diagnosis of chronic musculoskeletal infections. j bone joint surg am 2001;83:651-60. 46. rahme r, moussa r. the modic vertebral endplate and marrow changes: pathologic significance and relation to low back pain and segmental instability of the lumbar spine. ajnr am j neuroradiol 2008;29:838-42. 47. eguchi y, ohtori s, yamashita m, et al. diffusion magnetic resonance imaging to differentiate degenerative from infectious endplate abnormalities in the lumbar spine. spine (phila pa 1976) 2011;36:e198-e202. 48. masamitsu t, hiroshi s, yoshiyuki y, et al. acute pyogenic discitis in a degenerative intervertebral disc in an adult. int med case rep j 2010;2010:77-80. 49kabasakal y, garrett sl, calin a. the epidemiology of spondylodiscitis in ankylosing spondylitis a controled study. rheumatology 1996;35:660-3. 50. calin a, robertson d. spondylodiscitis and pseudarthrosis in a patient with enteropathic spondyloarthropathy. ann rheum dis 1991;50:117-9. 51. riley lh 3rd, banovac k, martinez ov, et al. tissue distribution of antibiotics in the intervertebral disc. spine (phila pa 1976) 1994;19:2619-25. 52. darley es, macgowan ap. antibiotic treatment of gram-positive bone and joint infections. j antimicrob chemother 2004;53:928-35. 53. choutet p, desplaces n, evrard j, et al. traitement des infections ostéoarticulaires bactériennes en dehors des infections à mycobactéries. med mal infect 1991;21:546-50. 54. senneville e, legout l, corroyer b, et al. bon usage de la teicoplanine dans les infections ostéoarticulaires. med mal infect 2004;1:99-102. 55. perronne ch. traitement antibiotique des infections ostéo-articulaires en l'absence de matériel étranger : voies d'administration, surveillance et durée. med mal infect 21:505-12. 56. elgouhari h, othman m, gerstein wh. bacteroides fragilis vertebral osteomyelitis: case report and a review of the literature. south med j 2007;100:50611. 57. zeller v, desplaces n. antibiothérapie des infections ostéoarticulaires à pyogènes chez l'adulte : principes et modalités. rev rhum 2006;73:183-90. 58. brown e, pople i, de louvois j, et al. spine update: prevention of postoperative infection in patients undergoing spinal surgery. spine (phila pa 1976) 2004;29:938-45. 59. linhardt o, matussek j, refior hj, et al. long-term results of ventro-dorsal versus ventral instrumentation fusion in the treatment of spondylitis. int orthop 2007;31:113-9. 60. heyde ce, boehm h, el saghir h, et al. surgical treatment of spondylodiscitis in the cervical spine: a minimum 2-year follow-up. eur spine j 2006;15:1380-7. doi: 10.33962/roneuro-2021-084 endoscopic third ventriculostomy versus ventriculoperitoneal shunt for treatment of hydrocephalus in infants in a tribal population in india patel pratik bipinbhai, lodha krishna govind, jaiswal gaurav, gupta tarun kumar, yadav kaushal, rai abhinav kumar romanian neurosurgery (2021) xxxv (4): pp. 493-498 doi: 10.33962/roneuro-2021-084 www.journals.lapub.co.uk/index.php/roneurosurgery endoscopic third ventriculostomy versus ventriculoperitoneal shunt for treatment of hydrocephalus in infants in a tribal population in india patel pratik bipinbhai, jaiswal gaurav, lodha krishna govind, gupta tarun kumar, yadav kaushal, rai abhinav kumar department of neurosurgery, rnt medical college, udaipur, india abstract study design: prospective long term follow-up study background: hydrocephalus remains a common cause of admission in pediatric neurosurgery units. of the two prevalent modalities of treatment for hydrocephalus in infants, i.e., endoscopic third ventriculostomy and ventriculoperitoneal shunt, which one is a better option, especially in a tribal setting, is a matter of debate. aim: to determine and compare the effectiveness of endoscopic third ventriculostomy versus ventriculoperitoneal shunt for the treatment of infants in a tribal population. methods: a prospective follow-up study was carried out on 70 patients of hydrocephalus with age less than or equal to 12 months during a period of 7 years from august 2014 to june 2021. a detailed history, physical examination, and computed tomography scan were done in all the cases. based on patient condition, aetiology and parents’ choice, 30 patients were treated by endoscopic third ventriculostomy and 40 patients were treated by ventriculoperitoneal shunt. at enrolment, baseline clinical data were collected. postoperative data were collected, including assessments of complications and treatment failures. results: a total of 70 infants with hydrocephalus were enrolled in the study and out of them, 30 (42.86%) underwent etv and 40 (57.14%) underwent vp shunt for the initial treatment of their hydrocephalus. the mean age of patients was 6.4±1.2 months with a range of 18 days to 342 days. clinical improvement was shown in 76.67% and 70% in etv and vp shunt groups respectively. no significant difference (p=0.53) was observed in clinical outcomes in both groups. in the 1 to 6 months of age group, 07 (30.43%) clinically improved patients were from the etv group, while in the vp shunt group, 10 (35.71%) patients showed improvement. in the 7 to 12 months age group, 16 (69.57%) clinically improved patients were from the etv group and 18 (64.29%) patients were from the vp shunt group (p=0.69). association of treatment success with gender, term of gestation and aetiology of hydrocephalus was not statistically significant (p>0.05). out of 70 patients with hydrocephalus, postoperative complications such as infection, csf leak, haemorrhage and blockage were found in 09 (12.86%), 08 (11.43%), 05 (7.14%) and 08 (11.43%) patients respectively. a significant higher proportion of infection (p=0.043) and blockage (p=0.023) was found in the vp shunt group than in the etv group. keywords endoscopic third ventriculostomy, ventriculoperitoneal shunt, hydrocephalus, infants, tribal population, corresponding author: gaurav jaiswal department of neurosurgery, rnt medical college, udaipur, india pratik.krisha2020@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 494 patel pratik bipinbhai, lodha krishna govind, jaiswal gaurav et al. conclusion: treatment success was high in both procedures. vp shunt was found to be more successful than etv in terms of clinical outcome in both age groups. however, the results were statistically insignificant. a significantly higher proportion of complications was found with vp shunt than etv therefore greater benefits can be achieved using etv. thus, for a tribal population, where patient compliance is poor and healthcare accessibility, as well as regular follow-up, is difficult, a procedure like etv can be considered better than vp shunt. introduction hydrocephalus can occur at any age but is most common in infants and adults aged 60 and older.2 hydrocephalus in children remains one of the more common etiologies for admission in the pediatric neurosurgical units.6 hydrocephalus is characterized by excessive accumulation of cerebrospinal fluid (csf), leading to ventricular dilatation, raised intracranial pressure and may be accompanied by secondary brain parenchymal atrophy.8 the pathophysiology of hydrocephalus is complicated and remains unclear, which creates challenges in the management of patients.1 because of that, optimal treatment for infant hydrocephalus is yet to be definitively determined. two main surgical options exist namely: endoscopic third ventriculostomy (etv) and ventriculoperitoneal shunt.3 ventriculoperitoneal shunt remains the conventional treatment for hydrocephalus due to its relatively high safety features.8 recently, endoscopic third ventriculostomy was deemed to be indispensable for treating obstructive hydrocephalus, on account of least complications because it avoids foreign body associated infections.7,13,16 however there is ambiguity regarding the relative benefits of these two procedures. ventriculoperitoneal shunting is technically simple and has a lower rate of failure immediately after surgery than does etv, but it is more prone to failure over the long term and patients with shunt-dependent hydrocephalus may require urgent shunt-revision surgery due to obstruction of the shunt tubing or valve. in contrast, etv is technically more difficult than shunting, but it has the advantage that virtually all failures occur within 6 months, after which the risk of failure is low.9,15 nevertheless, it remains unclear as to which of these two is more beneficial to patients because both methods have advantages and disadvantages. in resource limited settings, especially in tribal area, there are economic, cultural and geographic barriers to accessing treatment. considering these factors, this study was planned to find out the effectiveness of endoscopic third ventriculostomy versus ventriculoperitoneal shunt in infants in a tribal population. aims and objectives to determine and compare the effectiveness of endoscopic third ventriculostomy versus ventriculoperitoneal shunt for treatment of infants in a tribal population. materials and method study design: prospective follow-up study conducted under the department of neurosurgery, rnt medical college, udaipur over a study period of 7 years (august 2014 to july 2021) for data collection, analysis and report writing, taking infants with hydrocephalus as the study population. inclusion criteria 1. patients of hydrocephalus with age ≤ 12 months. 2. both genders. 3. consenting parents. exclusion criteria 1. associated congenital anomalies such as spina bifida. 2. dysmorphic brain anatomical features. 3. known chromosomal abnormality. 4. associated intra-ventricular or intra-cerebral hemorrhage 5. non-consenting parents. method a prospective follow-up study was carried out on 70 patients of hydrocephalus with age ≤ 12 months and admitted in the neurosurgery department of rnt medical college during august 2014 to july 2021. a detailed history, physical examination, and computed tomography scan was done in all the cases. based on patient condition, etiology and parents choice, 30 patients were treated by endoscopic third ventriculostomy and 40 patients were treated by ventriculoperitoneal shunt. at enrolment, baseline clinical data were collected. postoperative data were collected, including assessments of complications and treatment failures. 495 etv versus vp shunt for treatment of hydrocephalus in infants follow-up following the initial intervention, patients were regularly followed as per departmental and surgeon’s practice with scheduled visits at post-op day 15, 1 month, 3months, 6months, 12 months and yearly thereafter. adverse events were documented. all the information was recorded in individual case record sheets. procedures 1. endoscopic third ventriculostomy etv was performed using a rigid pediatric endoscope (karl storz tuttlingen, germany), size 17f. the scope was introduced via anterior fontanels or a burr hole was placed just anterior to the coronal suture in the mid pupillary line in the patients with small fontanel. the floor of the third ventricle was punctured using a fogarty catheter and the fenestration was enlarged using a fogarty catheter balloon. successful creation of stoma was confirmed by appreciating clap sign as the indicator of establishing csf flow as well as visualization of basilar artery complex intraoperatively. 2. ventriculoperitoneal shuntthe vp shunt involved creating a burr hole in the frontal or parietal regions and cannulating the ventricle with a silastic catheter. this was then attached to a slit and spring valve mechanism and distal silastic tubing of a medium pressure ventriculoperitoneal (mpvp) shunt which ran subcutaneously to the peritoneal cavity. outcome success of procedure was defined clinically (by the criteria of improvement in the patient neurological status) and surgically (if no further csf diversion procedure required during the follow-up period of 1 year). treatment failure was consider if further csf diversion procedure was required or the patient dies. because of very low socioeconomic status and affordability issues radiological parameters were not used to assess the success of procedures. complications of procedure such as intra-operative bleeding, postoperative infections, csf leak and blockage leading to failure of procedure were evaluated and recorded. statistical analysis statistical analysis was performed with spss 20.0 (trial version). data was presented in form of tables and graphs. chi square test was used as test of significance and p value of <0.05 was considered statistically significant. ethical clearance enrollment of patients was started after taking ethical clearance from institutional ethic committee. written consent was taken from all the parents. results total 70 infants with hydrocephalus were enrolled in study and out of them, 30 (42.86%) underwent etv and 40 (57.14%) underwent vp shunt for the initial treatment of their hydrocephalus. mean age of patients was 6.4±1.2 months with range of 18 days to 342 days. male were 65.71% and female were 34.29%. ten (14.29%) infants born preterm and all of them have low birth weight (<2500gm). on the basis of clinical and radiological evaluation, cause of hydrocephalus was aqueductal stenosis among 51 (72.86%), arachnoid cyst among 06 (8.57%), dandy– walker cyst among 04 (5.71%) and tubercular meningitis among 03 (4.26%) patients. (table 1) table 1. characteristics of study participants. patients’ characteristics etv (n=30) vp shunt (n=40) total (n=70) age in months 1 -3 05 (16.67) 08 (20) 13 4 – 6 07 (23.33) 11 (27.5) 18 7 -12 18 (60) 21 (52.5) 39 gender male 20 (66.67) 26 (65) 46 female 10 (33.33) 14 (35) 24 term of gestation preterm 05 (16.67) 05 (12.5) 10 full term 25 (83.33) 35 (87.5) 60 etiology aqueductal stenosis 25 (83.33) 32 (80) 57 arachnoid cyst 02 (6.67) 04 (10) 06 dandy-walker cyst 02 (6.67) 02 (5) 04 tbm 01 (3.33) 02 (5) 03 clinical improvement was shown in 76.67% and 70% in etv and vp shunt groups respectively. no significant difference (p=0.53) was observed in clinical outcome in both groups. there were two mortalities in etv and three mortalities in vp shunt group and rest were required revision surgeries within one ear of follow-up. (table 2 & figure 1) table 3 depicts association of patient characteristics with treatment success of either 496 patel pratik bipinbhai, lodha krishna govind, jaiswal gaurav et al. procedure. in the 1 to 6 months of age group, 07 (30.43%) clinically improved patients were from the etv group, while in vp shunt group, 10 (35.71%) patients showed improvement. in 7 to 12 months age group, 16 (69.57%) clinically improved patients were from etv group and 18 (64.29%) patients were from vp shunt group (p=0.69). this suggested better results in vp shunt group compared to etv group, however the results are not statistically significant. (figure 2) association of treatment success with gender, term of gestation and etiology of hydrocephalus was not statistical significant (p>0.05). table 2. distribution of participants according to type of treatment and clinical outcome. clinical outcome etv vp shunt p value* successful 23 (76.67) 28 (70) 0.53 failure 07 (23.33) 12 (30) table 3. distribution of study participants according to clinical improvement. patients’ characteristics etv (n=23) vp shunt (n=28) p value* age in months 0.69 1 -6 07 (30.43) 10 (35.71) 7 -12 16 (69.57) 18 (64.29) gender 0.84 male 17 (73.91) 20 (71.43) female 06 (26.09) 08 (28.57) term of gestation 0.86 preterm 01 (4.35) 02 (7.14) full term 22 (95.65) 26 (92.86) etiology 0.99 aqueductal stenosis 21 (91.30) 23 (82.14) arachnoid cyst 01 (4.35) 02 (7.14) dandy-walker cyst 01 (4.35) 02 (7.14) tbm 0 (0) 01 (3.57) table 4. distribution of study participants according to clinical complications. clinical complications etv (out of 30) vp shunt (out of 40) total p value* infection 01 (3.33%) 08 (20%) 09 0.043 csf leak 06 (20%) 02 (05%) 08 0.11 hemorrhage 04 (13.33%) 01 (2.5%) 05 0.20 blockage rate 01 (3.33%) 07 (17.5%) 08 0.023 *chi square test was used as test of significance and p value of <0.05 was considered statistically significant. out of 70 patients of hydrocephalus, postoperative complication such as infection, csf leak, hemorrhage and blockage was found in 09 (12.86%), 08 (11.43%), 05 (7.14%) and 08 (11.43%) patients respectively. significant higher proportion of infection (p=0.043) and blockage (p=0.023) was found in vp shunt group than etv group. (table 4 and figure 3). figure 1. treatment outcome of study participants. figure 2. comparison of clinical improvement in etv and vp shunt as per age group of study participants. figure 3. comparison of complication rates in etv and vp shunt groups. numbers shown in figure are percentages. 76.67 23.33 70 30 successful failure etv vp shunt 30.43 69.57 35.71 64.29 1-6 months 7-12 months etv vp shunt 3.33 20 13.33 3.33 20 5 2.5 17.5 0 5 10 15 20 25 etv vp shunt 497 etv versus vp shunt for treatment of hydrocephalus in infants discussion the disturbance of csf formation, flow or absorption on account of obstacles, congenital or acquired, leads to an increase in overall csf volume in the central nervous system result in hydrocephalus. based on patient’s condition, two popular methods, etv and vp shunt are available for infants. the impact of etv compared to shunt on long-term outcome is not known and has been one of the most important questions in pediatric hydrocephalus. to compare effectiveness of these two procedures, a prospective follow-up study was conducted at neurosurgery department of rnt medical college. in present study, out of 70 infants with hydrocephalus, etv was performed in 30 (42.86%) and vp shunt was performed in 40 (57.14%) patients. mean age of patients was 6.4±1.2 months with range of 18 days to 342 days. male predominance was seen with 65.71%. abhaya v. kulkarni et al11 study 78 patients hydrocephalus and found mean age 5.1 months and male to female ratio of 1.29:1. out of 78 patients, 75.65% were treated by etv and 24.35% were treated by vp shunt. another study done by abhaya v. kulkarni et al10 on 100 patients of hydrocephalus and found mean age of patients was 3.1 (2.6 to 4.1) months and among them 39 were female. sarah c. jernigan et al8 conduct study on 872 infants (16.1%) initially underwent etv and 4544 (83.9%) underwent ventricular shunt placement. the median infant age was 37 days (iqr 11–122 days) with male predominance. in this study, most common cause of hydrocephalus was aqueductal stenosis (72.86%), followed by arachnoid cyst (8.57%), dandy–walker cyst (5.71%) and tubercular meningitis (4.26%). clinical improvement was shown in 76.67% and 70% in etv and vp shunt groups respectively with no statistical difference in success rate. pavlos texakalidiset et al14 study various study and published a meta-analysis report that also shows aqueductal stenosis as a common cause of hydrocephalus. in contrast to present study, abhaya v. kulkarni et al11 reported that etv success was 66.3% at 6 months and 64.1% at 36 months, while shunt success was 87.8 % at 6 months and 79.1 % at 36 months. these initial results suggest that shunting has a superior success rate compared to etv, although the success rate for both was relatively high. similar to this study, pawan goyal et al4 found 68% of success rate in cases underwent vp shunt and 42% success rate among etv group and there is no significant difference in success rate. treatment of choice was depending on many factors such as age, presence of complications, accessibility of treatment and follow-up. for a tribal population, where patient compliance is poor and healthcare accessibility, as well as regular follow-up is difficult, a procedure like etv can be considered better than vp shunt. in present study, association of treatment success was found insignificantly with age of patients, gender, term of gestation and etiology of hydrocephalus. significant higher proportion of infection and blockage was found in vp shunt group than etv group. overall rate of infection and hemorrhage was 6.4% and 5.1% in study of abhaya v. kulkarni et al11 although rate of infection and hemorrhage was not statistically different in both group. similar to present study, result of meta analysis done by liang lu et al12 showed significantly lower postoperative infection, hemorrhage and blockage rates in the etv group than vp shunt group. conclusion treatment success was high in both procedures (76.67% for etv and 70% for vp shunt). vp shunt was found to be more successful than etv in terms of clinical outcome in the in both age groups. however, the results were statistically insignificant. significant higher proportion of complication was found with vp shunt than etv therefore greater benefits can be achieved using etv. thus for a tribal population, where patient compliance is poor and healthcare accessibility as well as regular follow-up is difficult, a procedure like etv can be considered better than vp shunt. references 1. balthasar aj, kort h, cornips em, et al. analysis of the success and failure of endoscopic third ventriculostomy in infants less than 1 year of age. childs nerv syst 2007;23:151–5. 2. beuriat p-a, puget s, cinalli g, blauwblomme t, beccaria k, zerah m, sainte-rose c (2017) hydrocephalus treatment in children: long-term outcome in 975 consecutive patients. j neurosurg pediatr 20:10–18. 3. constantini s, sgouros s, kulkarni et al. a neuroendoscopy in the youngest age group. 2013: 79:s23 4. goyal p, srivastava c, ojha bk et al. a randomized study of ventriculoperitoneal shunt versus endoscopic third 498 patel pratik bipinbhai, lodha krishna govind, jaiswal gaurav et al. ventriculostomy for the management of tubercular meningitis with hydrocephalus. childs nerv syst (2014) 30:851–857. 5. jernigan sc, berry jg, et al. the comparative effectiveness of ventricular shunt placement versus endoscopic third ventriculostomy for initial treatment of hydrocephalus in infants. j neurosurg: pediatrics / volume 13 / march 2014: 295-300. 6. kalani my, turner jd, nakaji p. treatment of refractory low-pressure hydrocephalus with an active pumping negative-pressure shunt system. j clin neurosci. 2013;20:462-466. 7. koch-wiewrodt d,wagnerw et al. success and failure of endoscopic third ventriculostomy in young infants: are there different age distributions? childs nerv syst. 2006: 22:1537–1541. 8. kousi m, katsanis n. the genetic basis of hydrocephalus. annu rev neurosci. 2016;39:409-435. 9. kulkarni av, drake jm, kestle jr, et al. endoscopic third ventriculostomy vs cerebrospinal fluid shunt in the treatment of hydrocephalus in children: a propensity score-adjusted analysis. neurosurgery. 2010; 67: 588-93. 10. kulkarni av, schiff sj , kabachelor em et al. endoscopic treatment versus shunting for infant hydrocephalus in uganda. the new england journal of medicine 2017; 377:2456-64. 11. kulkarni av, sgouros s, leitner y, et al; international infant hydrocephalus study investigators. international infant hydrocephalus study (iihs): 5-year health outcome results of a prospective, multicenter comparison of endoscopic third ventriculostomy (etv) and shunt for infant hydrocephalus. childs nerv syst. 2018 dec;34(12):2391-2397. 12. lu l, chen h, weng s, xu y et al. endoscopic third ventriculostomy versus ventriculoperitoneal shunt in patients with obstructive hydrocephalus: meta-analysis of randomized controlled trials. world neurosurg: 2019: 129:334-340. 13. mixter w. ventriculoscopy and puncture of the floor of the third ventricle. boston med surg j. 1923;188:277-278. 14. texakalidis p, tora ms, wetzel js et al. endoscopic third ventriculostomy versus shunt for pediatric hydrocephalus: a systematic literature review and metaanalysis. child's nervous system (2019) 35:1283–1293. 15. warf bc, kulkarni av. intraoperative assessment of cerebral aqueduct patency and cisternal scarring: impact on success of endoscopic third ventriculostomy in 403 african children. j neurosurg pediatr. 2010;5:204-9. 16. warf bc, tracy s, mugamba j et al. long-term outcome for endoscopic third ventriculostomy alone or in combination with choroid plexus cauterization for congenital aqueductal stenosis in african infants. j neurosurg pediatr. 2012:10:108–111. 1adam_osteoporosis_brief 124 adam et al osteoporosis associated vertebral compression fractures brief communication osteoporosis associated vertebral compression fractures d. adam, ioana hornea, b.o. ene emergency "st. pantelimon" hospital, bucharest background osteoporosis is a degenerative bone disease characterised by bone loss or brittle bones. while the outside of the bone more or less stays the same, inside the bone substance disintegrates. the affected bone can cope with less strain than healthy bone. being a silent disease is often diagnosed when the patient breaks a bone. bone fractures can cause severe pain, restrict mobility and generally reduce the quality of life. the spine is commonly affected by osteoporotic fractures. the vertebral bodies of the thoracic and lumbar spine are under greatest degree of pressure. in most cases, the vertebral body becomes stronger by itself and the pain recedes with bed rest, pain killer and physical therapy. if the pain is severe and persistent surgical treatment should be considered: open surgery stabilisation or low invasive techniques. material and methods in 2008 we treated 5 patients with vertebral compression fractures: 3 males and 2 women, with ages between 40 and 72 years, by kyphoplasty (1 patient) and vertebroplasty (4 patients). preoperative diagnosis was performed based on plain x-rays and stir-weighted mri. vertebral augmentation is based on a minimally invasive approach to the vertebral body, transpedicular for the lumbar spine or parapedicular for the thoracic spine and cement injection using vertecem vertebroplsty by synthes and kyphoplasty kitt by kyfon, under c-arm control. the female patient 70 years old, is the first kyphoplasty case reported by neurosurgeons in romania. results at 3 hours after the procedure, all patients were pain-free. at 24 hours they resumed mobility and were discharged. in 1 patient we had a little cement leak lateral of the vertebral body. conclusions kyphoplasty and vertebroplasty are efficient methods for the treatment of vertebral compression fractures. increasing experience, associated with a careful selection of cases will diminish the risks of leakage and make the procedures safer. microsoft word 3.iacob_personalexperience_f.docx 400 g. iacob and m. craciun personal experience in lumbar spinal stenosis (lss) personal experience in lumbar spinal stenosis (lss) g. iacob, m. craciun clinic of neurosurgery, universitary hospital bucharest românia motto: “outcome may be improved through a more careful selection of patients and an adequate surgical decompression” deyo r.a. et al. (11) abstract objective: to investigate the effectiveness of our strategy in lumbar spinal stenosis. this is based on the following: precise clinical radicular description of the level of claudication by electrodiagnosis, fine neuroradiologic studies, microsurgical decompression, assessment of the factors which might influence the outcome. methods: the study was performed on 145 patients who underwent decompression in the last 8 years: 95 males, 50 females, mean age 65 yrs (50-81). comorbidities were carefully considered when choosing the surgical procedure, especialy in elderly patients; an initial conservative approach of 3 weeks was used for most patients. concerning etiology: 105 were degenerative, 16 post trauma, 24 others. our cases included: 48 cases of single, focal stenosis, 97 diffuse (52 cases in 2 levels and 45 cases in 3 or more levels); 50% were graded as severe and evolved within 6 weeks, 30% were graded severe to moderate and 20% were moderate after a 2 month evolution; 15 were central, 17 lateral, 13 foraminal and 100 mixed. precise clinical radicular description of the level of claudication by electrodiagnosis was used in all patients, mri studies – 115 patients, ct studies 30 patients, plain static x-rays of lumbar spine, dynamic flexion and extension x-rays of lumbar spine – all patients; disability degree evaluation: oswestry disability index, pain (visual analog scale and analgesic consumption), functional improvement (neurogenic claudication outcome score), walking performance and instability degree (pre-op and intraoperative) to all patients. we used a 4-5 cm incision for focal stenosis, 5-10 cm incision for 2-3 levels, carm for localization, high speed drill, cutting and diamond burrs, microscope, microinstruments, fenestration and medial facet undercutting to ensure an adequate root decompression. we excised the ligamentum flavum in the lateral recess which is often thickened. the lower lateral 6-12 mm of the lamina above and/or the superior lateral 3-9 mm of the lamina below were also resected to expose the root, the disc was excised and the posterior osteophytes were chiseled away with a fine micro chisel or diamond drill. in cases of focal stenosis we performed: foraminotomy, laminotomy, osteophytectomy, ligamentum flavectomy; diffuse/multilevel stenosis was approached as follows: laminotomies, foraminotomies, osteophytectomy, ligamentum flavectomy, medial facetectomy, fusion. in 24 cases we attempted a pedicle screw fixation and in romanian neurosurgery (2011) xviii 4: 400 411 401 two cases diam devices. no re-do surgery was required. results: one week after surgery, pain decreased in 87.9% of patients; nonsteroidal antiinflammatory drug consumption and analgetics decreased in 81%. two years after surgery, pain remained decreased in 79.8% of patients, neurogenic claudication outcome score decreased in 78.7% of patients and walking performance improved in 97.2% of patients. patients who underwent both multilevel decompression or single level decompression benefitted. conclusions: lss surgery is functional, never preventive; the initial management should be non-surgical except for severe cases. electrophysiological testing correlated with thorough neurological examination is more accurate than a radiological evaluation alone when choosing the roots to be decompressed. microsurgical selective decompression accomplishes a good balance between bony and soft tissue decompression, while also maintaining spinal stability. keywords: lumbar spinal stenosis (lss), microsurgical selective decompression introduction the recent increase in the diagnosis of lss resides not only in the improvement of neuroimagistic tools but also in the progressive degenerative changes in intervertebral joints and ligamentous structures in the elderly. the latter eventually leads to spinal canal and neural foraminal narrowing (11)(17)(27). despite progress in lumbar surgery on decompressive surgery and invasive fusion procedures, the risks and benefits of a surgical procedure in patients over 65 years old should be carefully considered (1) (5) (7) (10) (11) (16) (17) (20) (22) (33) (36). the purpose of this paper was to present our approach in a field where there are no specific recommandations for surgical procedures, especially in this age group. methods during the last 8 years, 145 patients underwent decompression and fusion for lss: 95 males, 50 females, mean age 65 yrs (50-81). patients with comorbidities were carefully weighted in the choice of a surgical procedure, especialy patients over 65 years. ekg, cardiac echography, spirometry, abdominal echography, thoracic and abdominal ct scans were performed. an initial conservative approach for 3 weeks was used in most patient. in 6 cases (4,13%) with cauda equine syndrome we performed an emmergency surgery. 115 cases presented symptomatic lumbar stenosis resulting from progressive degenerative changes in intervertebral joints and ligamentous structures. this led to spinal canal and neural foraminal narrowing. of these cases 23 patients had had previous lumbar surgery, 16 cases resulted post trauma, 2 presented spinal lipomatosis, 12 were constitutional. in 2 constitutional lss we found a cervical stenosis as well. our cases were classified as follows: 8 cases with single, focal stenosis, 97 diffuse (52 cases on 2 levels and 45 cases on 3 or more levels); 50% of cases with a severe evolution within 6 weeks, 30% severe to moderate and 20% moderate within 2 months; 15 were central, 17 lateral, 13 foraminal and 100 mixed. the diagnostic techniques that we employed (figure 1) were: clinical radicular description of the level of claudication by electrodiagnosis all patients, mri studies – 115 patients, ct studies 30 patients, 402 g. iacob and m. craciun personal experience in lumbar spinal stenosis (lss) plain static x-rays of lumbar spine, dynamic flexion and extension x-rays of lumbar spine – all patients, disability degree evaluation: oswestry disability index, pain (visual analog scale and analgesic consumption), functional improvement (neurogenic claudication outcome score), walking performance and instability degree (pre-op and intraoperative) in all patients. our strategy was clearly explained to each patient: surgery has no effect on focal or diffuse low back pain, stiffness, “degenerative” illnesses; surgical choices; the availability of resources and facilities in our institution; our surgical aims were to achieve a good life quality and to restore functional capacity exerted on neurovascular compression, no pain: neurogenic claudication and mono or pluri radicular resting or in efforts pain, no subjective signs and neurologic deficit during walking, anesthesia technique, possible complications. all data and medical team are specified in the informed consent. we used a 4-5 cm incision for focal stenosis, 5-10 cm incision for 2-3 levels, carm for localization, high speed drill, cutting and diamond burrs, microscope, microinstruments, fenestration and medial facet undercutting to ensure an adequate root decompression. we excised the ligamentum flavum in the lateral recess which is often thickened. the lower lateral 6-12 mm of the lamina above and/or the superior lateral 3-9 mm of the lamina below were also resected to expose the root, the disc was excised and the posterior osteophytes were chiseled away with a fine micro chisel or diamond drill. in cases of focal stenosis we performed: foraminotomy, laminotomy, osteophytectomy, ligamentum flavectomy; diffuse/multilevel stenosis was approached as follows: laminotomies, foraminotomies, osteophytectomy, ligamentum flavectomy, medial facetectomy, fusion. in 24 cases we attempted a pedicle screw fixation and in two cases diam devices. no re-do surgery was required. a b c romanian neurosurgery (2011) xviii 4: 400 411 403 d e f g h i j k l m n o figure 1 main investigations in lss: a-c electromyography for l5 motor deficit caused by a severe l4 stenosis, d-e plain static x-rays of lumbar spine in lss stenosis, f-i mri in central lss, j-k lss stenosis with disc herniation, l-m extension-flexion dynamic mri to a patient explored abroad, n-o axial rm in extension-flexion results one week after surgery, pain decreased in 87.9% of patients; nonsteroidal anti inflammatory drug consumption and analgetics lessened by 81%. two years after surgery, pain remained decreased in 79.8% of patients, neurogenic claudication outcome score decreased in 78.7% of patients and walking performance improved in 97.2% of patients. patients who underwent both multilevel decompression or single level decompression benefitted 404 g. iacob and m. craciun personal experience in lumbar spinal stenosis (lss) (figure 2). in patients over 65 years we attempted decompression only, while also including any combination of discectomy and laminectomy without fusion. medical complications occured in 7 patients (4,82%): acute myocardial infarction, respiratory failure, pulmonary embolism, bacterial pneumonia, aspiration pneumonia, pneumonia of unknown etiology, crural trombophlebitis, stroke and surgical complications in 11 patients (7,58%): wound complications (hemorrhage, hematoma or seroma), spondylodiscitis, csf fistula. previous spine surgery was associated with surgical complications: 3 spondylodiscitis, 2 csf fistula, 2 cases with wound hematoma to patients on oral anticoagulants. no patient was reoperated for recurrent symptoms. figure 2 a-b pre and c-d post operatory mri sagital and axial sections, in a 68 years old case with severe l4-l5 lss associated with a gr.1 l5-s1 spondilolystesis discussions lss is defined as a focal or diffuse (multilevel) narrowing of the lumbar spinal canal ± foramen ± lateral recess, causing nervous and vascular structures compression (16) (17). although lss had been described for over a century, it was first acknowledged as a distinct entity in 1954 by verbiest (32). lss is also known as a “loss of epidural reserve” and always it is important to elucidate the difference between “narrow” and “shrink” (27). lss is more frequently diagnosed due to improved neuroimagistic procedures (17); it could be primary (congenital) – in less of 5% of cases; in 10-20% congenital lss could be associated with a cervical stenosis too (17) and secondary (acquired) induced by non specific causes: degenerative changes (including central canal and lateral recess stenosis from posterior disk protrusion, zygapophyseal joint and ligamentum flavum hypertrophy, spondylolisthesis), specific: epiduritis, lipomatosis, neoplastic, iatrogenic changes result from surgical procedures such as laminectomy, fusion and discectomy; systemic processes that may be involved in secondary stenosis include: paget disease, fluorosis, acromegaly and ankylosing spondylitis. lss could be classified according to posture: static or dynamic lss according to ortostatic or sitting posture (35) (37) and anatomical criteria: central due to hypertrophic spurring, bony projection or ligamentum flavum/laminar thickening, medial – secondary to inferior articular process hypertrophy, lateral secondary to superior articular process hypertrophy, fleur de lis (clover leaf): laminar thickening with subsequent posterolateral bulging; on a level, segmentary (uni or bilateral), diffuse on/or several levels (16) (17). in our clinical study 115 patients presented progressive degenerative changes in intervertebral joints and ligamentous romanian neurosurgery (2011) xviii 4: 400 411 405 structures, leading to spinal canal and neural foraminal narrowing. of these 23 had had previous lumbar surgery, 16 resulted post trauma, 2 presented with spinal lipomatosis, 12 were constitutional. in 2 constitutional lss we found a cervical stenosis as well. our cases were classified as follows: 8 cases with single, focal stenosis, 97 diffuse: 52 cases on 2 levels and 45 cases on 3 or more levels; 50% of cases with a severe evolution within 6 weeks, 30% severe to moderate and 20% moderate within 2 months; 15 were central, 17 lateral, 13 foraminal and 100 mixed. lss pathophysiology explains several mechanisms of neural compression, pain and instability (12) (17). neural compression could occur anteriorly: disk protrusion or herniation, osteotic overgrowth: osteophytes and posteriorly: lamar & ligamentous hypertrophy, facet hypertrophy, synovial cyst, spinal lipomatosis, spondylolisthesis. pain is induced by: mechanical factors such as: venous congestion, ischaemia (+/ microcirculation anomalies), compression radiculopathy, instability. the release of citokines in inflammatory processes of facet joints (17) also triggers pain mechanisms, especially when the disc in involved (nucleus pulposus). the instability could be generated by the loss of discal integrity, ligamentous integrity, facetal integrity, supportive integrity, paraspinal and abdominal muscle tone and power; leading to: spondylolisthesis and scoliosis. lss includes mechanical instability without clinical signs and symptomatic instability with intermittent pain associated with clinical signs. instability was defined by panjabi (35) as: “the loss of the spine’s ability to maintain its patterns of displacement, under physiologic loads so there is no initial or additional neurologic deficit, no major deformity and no incapacitating pain”. the degenerative process cannot be prevented by diet, exercise, lifestyle; a slow progression appears to occur in all affected individuals. in addition no clear correlation has been found between lss and race, occupation, sex, body type, symptoms of stenosis. lss symptoms (17) may be: focal or diffuse low back pain and/or stiffness, radiculopathy, weakness, numbness or tingling of the legs, neurogenic claudication (up to 94%) leading to reduced walking capacity and mobility, rare cauda equina syndrome, rare bladder/bowel dysfunction. patients walk in flexion and prefer to sit and lean forward. physical examination findings (12)(17)(27) are insufficient when determining the presence or absence of lss; these may reveal: positive straight leg raising (55 84.2%), sensory impairment (51.2 – 63.6%), motor deficit (35.7 – 52.2%), reflex changes (36.7 – 51.8%). in our cases we found radicular signs in 125 patients especially in lateral, foraminal or mixted lss, motor deficits in 53 cases, sensory impairment in all cases, few anatomo-cinical correlations especially in segmentary stenosis (17). cauda equine syndrome was rare, in only 6 cases (4,13% of cases). no systematic worsening of lss symptoms was present, as the evolution was variable in each case. lss was assessed using the following neuroimagistic exams: plain static x-rays of lumbar spine with orientative value only; dynamic flexion and extension x-rays of lumbar spine to find an instability; ct lumbar scan indicated lss if canal surface was < 145 mm2, the saggital anteroposterior diameter < 12 mm if the axial section passed through the inferior part of 406 g. iacob and m. craciun personal experience in lumbar spinal stenosis (lss) the pedicles, the transverse diameter interarticular process was < 15 mm on a axial section passing through the discs, dynamic mri (37) involving saggital, axial or frontal sections of upright flexion and extension concerning surface, height and conflict nature; bone scan; ct myelogram (17). the diagnostic procedure was also based on: the precise clinical radicular description of the level of claudication by electrodiagnosis in all patients, mri studies in 115 patients, ct studies in 30 patients, plain static x-rays of lumbar spine, dynamic flexion and extension x-rays of lumbar spine, disability degree evaluation: oswestry disability index, pain (visual analog scale and analgesic consumption), functional improvement (neurogenic claudication outcome score), walking performance and instability degree (pre-op and intraoperative) in all patients. the natural evolution of all cases of lumbar spinal stenosis is not well understood. no correlation has been found between the time elapsed and the systematic progressive worsening. the evolution of lss within 49 months (17)(21) is variable. literature data disclosed that 70% of cases display unchanged symptoms. improvements also including the walking ability are present in 15% .worsening of symptoms occurs in 15% of cases. the 2006 cochrane database sys.rev (cited by 27) devised no specific recommendations although surgical treatment could alleviate pain and improve functional capacity. only 3 randomized prospective controlled trials have approached the surgical vs nonsurgical treatment (2) (24) (34).these revealed no short term correlation between the patient's outcome and the surgery timing: early vs late surgery. moreover an initial nonsurgical approach was advisable for most patients. only one third of patients with a surgical intervention also responded to non-surgical treatment. the latter rendered satisfactory results in 70% of cases at 6 months and 57% at 4 years follow up. the treatment choice in lss should consider the following: (2-7) (9) (16-18) (22) (27) (28): a medical treatment should precede the surgical one there is no recommendation referring to the timing of surgery, except motor deficit, cauda equina syndrome with bladder/bowel dysfunction. it is important to inform the patient about the difference between lumbar pain and the diagnosis of radicular syndrome and that surgery is not effective in lumbar pain. the number of nerve roots requiring decompression is often smaller than what appears in radiological studies. therefore surgical procedures should not be based on x-ray studies alone. the slow onset of neurogenic claudication is generated by an imbalance between the capacity of the spinal canal and its contents. this mostly involves a particular side and motion segment/s rather than multiple bilateral radiological levels. outcome could be improved by a careful selection of patients and an adequate surgical decompression. the latter implies a perfect correlation between the anatomical and clinical patterns as well as concordant results between the electrophysiological impairment test and the dermatomal pain distribution and myotomal muscle weakness after claudication. the evaluation for surgical treatment should regard each case individually. it romanian neurosurgery (2011) xviii 4: 400 411 407 should always consider the age, comorbidities, previous trials of conservative therapy and specific degree of stenosis (mri), neurological deficits and degree of disability (oswestry disability index, visual analog score for pain, walking distance, daily life activities), the degree of instability. other conditions for treatment evaluation include the patient's expectations (31) and the surgeon's experience. the latter could predict failure or intolerance to conservative therapy (34). patients selected for operation could be classified as follows (3) (4) (12) (17): a. incidental finding of lss including those with no limitation of life style and not worried about symptoms. patients in this category should be informed about lss findings and carefully monitored. treatment should be initiated for any comorbidities or other conditions responsible for symptoms of stenosis. low back pain could be treated with nsaid's, mainly selective cox 2 inhibitors. b. symptomatic lss with mild or moderate, persistent or worsening symptoms of neurogenic claudication and/or radiculopathy despite conservative therapy for at least 3 months (massage, ultrasound, tens, braces or supports, acupuncture, biofeedback, hot or cold packs, traction, or chiropractic manipulation gives symptomatic relief of radicular or low back pain, physical therapy avoid hyperextension and side bending, general reconditioning of spinal and abdominal musculature and ligaments), minimal comorbidities with radiologically proved severe stenosis, reducing walking distance and daily life activities: previous studies found poor correlations between symptoms and the degree of stenosis level b recommendation. better correlations were found between the severity of symptoms and the surgical outcome level b (17). in these patients there are options for early surgical management: the surgeon experience could predict failure of conservative therapy or to those requesting patients failing or intolerant to conservative therapy, patients with associated instability (see dynamic irm) and neurological deficit, rare in emergency for cauda equina syndrome (17). c. symptomatic lss in patients with comorbidities that increase the surgical risk such as pulmonary diseases, unstable cardiac status, morbid obesity, severe osteoporosis, extremely advanced age. in such cases a conservative treatment is desirable, to use adaptive techniques for restoring mobility, to utilize rehabilitation services (27). the surgical aims in lss are (3) (6) (7) (15) (17): to alleviate symptoms, restore functional capacity acting on neuro-vascular compression, no pain: neurogenic claudication and mono or pluri radicular resting or in efforts pain, no subjective signs and neurologic deficit during walking, to normalize daily life activities, to achieve a good quality of life. the patient should be well informed that surgery has no effect on focal or diffuse low back pain and/or stiffness (31), “degenerative” illnesses; he should be aware of the surgical choices and resources and facilities available in our institution as well as of the stabilization that could be required if facet and discal anatomy is compromised. the surgeon should choose the best operative technique, to avoid reintervention (and not for prevention), to continue with current best practice surgical expertise and experience for patient selection & for surgical skills. 408 g. iacob and m. craciun personal experience in lumbar spinal stenosis (lss) the surgical strategy in lss (17) (18): 1. decompression is not recommended in cases of dynamic stenosis: instability, hypermobility 2. the current surgical options are microsurgery “the gold standard” and endoscopy. (endoscopy guidelines ismiss – feb. 2008). microsurgery offers the following advantages when compared to macrosurgery (17) (23) (29): it minimizes tissue disruption, time of surgery, post operative morbidity, length of hospital stay; smaller incisions, less tissue trauma, minimal blood loss, earlier return to previous activities, easier operative approach in obese patients, local or regional anesthesia combined with conscious sedation can be used, less postoperative pain medication is required. 3. the roots to be decompressed: all roots should be decompressed in cases of central lumbar canal stenosis even with unilateral radiculopathy, during walking or effort(19); in cases of bilateral lateral recess stenosis with unilateral radiculopathy, at one level both roots should be decompressed; cases of multilevel lateral recess stenosis, with unilateral radiculopathy imply radical fenestration and foraminotomy with decompression on the symptomatic side and level only; foraminal stenosis requires the decompression of the affected root. 4.regarding stabilization our aims are: to treat patients with severe symptoms and radiographic evidence of excessive motion (greater than 4 mm translation or 10o of rotation) who fail to respond to nonsurgical treatment) (10) (14) (30) and to prevent postoperatory instability. stabilization should be limited (17), never systematic or for associated lumbar pains. we used stabilization in patients with pre-operatory instability (flexion-extension radiographs or dynamic mri), depending on the dimension of osteous resection, articular processes orientation – especially on anterior-posterior, to correct a deformity, to avoid hypermobility and to maintain lordosis and foraminal size. we performed stabilization in 24 cases, using pedicle screw fixation – medtronic tsrh-3d and in two cases diam devices. 5. the type of stabilisation to be used: arthrodesis and instrumentation could be performed using a rigid stabilization system with pedicle screw fixation in a classic procedure, percutaneously or with motion preservation: dynamic stabilization systems, facet arthroplasty: tfas® total facet arthroplasty system or with lumbar interspinous implants to unload the anterior column & reestablish the functional integrity of the posterior column: colfex, wallis, diam and x-stop. lss outcome (2) (3) (28) depends on age < 65 years, uniradicular deficit, simultaneous disc hernia, anatomic and clinical correlations of the root (s) to be decompressed, microsurgery, overall rating: improved (85%), some improvement (10%), no improvement (5%), worse (none). mean follow up at 24 months indicated: walking distance improvement (95%), leg pain improvement (85%), weakness and numbness improvement (70%), on daily life activities: normal 82%, modification on life/work style (13%), stopped working (5%). despite possible complication of diverse etiology: infectious, neurologic, mechanic most surgically treated patients would again choose surgery (1) (2) (4) (13) (20) (21). for recurrent symptoms (17), patient selection should be based on clinical, radiological (contrast studies, dynamic mri), electrophysiological studies (emg romanian neurosurgery (2011) xviii 4: 400 411 409 and ncs) of: residual stenosis at operative site due to inadequate first surgery, stenosis at adjacent levels to surgical site, new disc herniations, epidural and arachnoidal adhesions, instability and/or spondylolisthesis following first surgery. several techniques (7-9) (13) (17) (19) (20) (23) (25) (36) are used: partial decompressive lamino-arthrectomy uni/bilateral, complete facetectomy +/ discectomy; radical fenestration and foraminotomy, bilateral interlaminar fenestration and unroofing for the decompression of nerve roots through a unilateral approach, open door expansive lumbar laminoplasty, hemilaminotomy – arthrectomy with ligamentectomy & recess decompression, hemilamino arthrectomy several levels and unilateral lamino-foraminotomy, microendoscopic decompressive laminotomy, unilateral laminectomy for bilateral decompression, laminectomy – bilateral foraminotomy also known as “the recalibration” (it is mandatory to obtain consent for possible stabilization during the laminectomy procedure if facet and discal anatomy is compromised; 5% of laminectomies require stabilization in the end), the wiltse approach with foraminotomy for isolated foraminal stenosis. our technique consists of a 4-5 cm incision for focal, 5-10 cm incision for 2-3 levels, c-arm for localization, high speed drill, cutting and diamond burrs, microscope, micro-instruments, fenestration and medial facet undercutting to adequate root decompression, the ligamentum flavum in the lateral recess often thickened is excised, the lower lateral 6-12 mm of the lamina above and/or the superior lateral 3-9 mm of the lamina below were resected to expose the root, the disc is excised, posterior osteophytes are chiseled away with fine micro chisel or diamond drill. in 90 cases of one level focal stenosis we performed foraminotomy, laminotomy, osteophytectomy, ligamentum flavectomy; diffuse/multilevel stenosis on two levels (35 cases) and three levels (15 cases) required laminotomies, foraminotomies, osteophytectomy, ligamentum flavectomy, medial facetectomy. we have performed: foraminotomy in 138 cases, laminotomy in 112 cases, medial facetectomy in 47 cases, laminectomy in 16 cases. our results are comparable with literature data (17). one week after surgery, pain decreased in 87.9% of patients; nonsteroidal antiinflammatory drug consumption and analgetics decreased in 81%. two years after surgery, pain remained decreased in 79.8% of patients, neurogenic claudication outcome score decreased in 78.7% of patients and walking performance improved in 97.2% of patients. patients who underwent both multilevel decompression or single level decompression benefitted. in patients > 65 years we chosed decompression only, including any combination of discectomy and laminectomy without fusion. we have had medical complications in 7 patients (4,82%): acute myocardial infarction, respiratory failure, pulmonary embolism, bacterial pneumonia, aspiration pneumonia, pneumonia with unknown organism, crural trombophlebitis, stroke and surgical complications in 11 patients (7,58%): wound complications (hemorrhage, hematoma or seroma), spondylodiscitis, csf fistula. previous spine surgery was associated with surgical complications: 3 spondylodiscitis, 2 csf fistula, 2 cases with wound hematoma to patients on oral 410 g. iacob and m. craciun personal experience in lumbar spinal stenosis (lss) anticoagulants. no patient was reoperated for recurrent symptoms. conclusions lss surgery is functional and never preventive. the initial management of lss should be non-surgical, except for very severe cases with cauda equina syndroms. the choice of the roots to be decompressed should not be based on the radiological evaluation. better correlations with the neurological examination have been obtained for gold imaging standards such as mri and dynamic flexion and extension xrays as well as for electrophysiological testing. surgical interventions should be adapted to the unique patho-anatomical situation in the persistently symptomatic patient. selective decompression only at the neurological responsible level improved neurogenic intermittent claudication in the majority of patients. in addition unoperated radiological stenotic levels rarely became symptomatic on follow up. lss surgical aims are: to minimize tissue damage, minimally invasive decompressive techniques adapted to the unique pathoanatomical situation in the persistently symptomatic patient (more than 80% of cases may be spared from a more extensive surgery), balance bony and soft tissue decompression while maintaining spinal stability. stability should be limited, never systematic and never indicated for associated lumbar pains. logic dictates we should pursue and develop goals of minimally invasive surgery, anesthetic technique, supportive care and attempt to obtain evidence between conventional and newer techniques, to make more invasive surgery to old patients, for a better quality of life. references 1. aalto tj et al. preoperative predictors for postoperative clinical outcome in lumbar spinal stenosis: systematic review, spine 2006, 31:e648–e663 2. amundsen t, et al. lumbar spinal stenosis: conservative or surgical management? a prospective 10year study, spine 2000; 25:1424-35 3. atlas s.j. al. the maine lumbar spine study, part iii. 1-year outcomes of surgical and nonsurgical management of lumbar spinal stenosis, spine 1996; 21:1787-94. 4. atlas sj, et al. surgical and nonsurgical management of lumbar spinal stenosis: four-year outcomes from the maine lumbar spine study. spine 2000; 25:556-562. 5. atlas sj, et al. long-term outcomes of surgical and non surgical management of lumbar spinal stenosis : 8 to 10 year results form miane lumbar spine study. spine 2005 ; 30 : 936-43. 6. atlas sj, delitto a. spinal stenosis versus non surgical treatment. clin orthop relat res 2006; 443: 198-207 7. ausman j.i. spinal stenosis-what is the best treatment?, editorial, 2007 elsevier inc.2007.08. 8. benz rj et al. current techniques of decompression of the lumbar spine, clin orthop relat res 2001, 384:75–81 9. cavusoglu h, et al. midterm outcome after unilateral approach for bilateral decompression of lumbar spinal stenosis: 5-year prospective study. eur spine j 2007, 16:2133–2142 10. deyo r.a., gray d.t., et al. united states trends in lumbar fusion surgery for degenerative conditions. spine 2005;30:1441–1445. 11. deyo r.a., mirza s.k., al. trends, major medical complications, and charges associated with surgery for lumbar spinal stenosis in older adults, jama. 2010, april 7; 303(13):1259–1265 12.fritz jm, et al. lumbar spinal stenosis: a review of current concepts in evaluation, management, and outcome measurements. arch phys med rehabil 1998 jun; 79(6): 700-8 13.fritzell p, hagg o, nordwall a. complications in lumbar fusion surgery for chronic low back pain: comparison of three surgical techniques used in a prospective randomized study. a report from the swedish lumbar spine study group. eur spine j 2003;12:178–189. 14.fritzell p, hagg o, et al. and the swedish lumbar spine study group. 2001 volvo award winner in clinical studies: lumbar fusion versus nonsurgical treatment of chronic low back pain: a multicenter randomized controlled trial from the swedish lumbar spine study group. spine 2001;26:2521–2532. romanian neurosurgery (2011) xviii 4: 400 411 411 15.guiot b, et al. a minimally invasive technique for decompression of the lumbar spine. spine 2002, 27:432–438 16.iacob g. stenoza canalului vertebral lombar, medicina moderna, 2002, vol ix, nr.2, 58-63 17.iacob g., craciun m. lumbar spinal stenosis (lss): indications and operative treatment the “bucharest wiew”, german-romanian course, clujnapoca 24-25 may 2011 18.irwin z.n., hilibrand a., et al. variation in surgical decision making for degenerative spinal disorders. part i: lumbar spine. spine 2005;30:2208–2213. 19.iwatsuki k, yoshimine t, aoki m. bilateral interlaminar fenestration and unroofing for the decompression of nerve roots by using a unilateral approach in lumbar canal stenosis, surg neurol 2007;68:487-92 20.jakola et al. clinical outcomes and safety assessment in elderly patients undergoing decompressive laminectomy for lumbar spinal stenosis: a prospective study, bmc surgery 2010, 10:34 21.johnsson ke, uden a, rosen i. the effect of decompression on the natural course of spinal stenosis. a comparison of surgically treated and untreated patients. spine 1991; 16:615-619. 22.katz jn, et al. predictors of surgical outcome in degenerative lumbar spinal stenosis. spine 1999, 24:2229–2233 23.khoo l, et al. microendoscopic decompressive laminotomy for the treatment of lumbar stenosis, neurosurgery 2002, 51 [suppl 5]:s146–s154. 24.malmivaara a, slatis p, et al. for the finnish lumbar spinal research group. surgical or nonoperative treatment for lumbar spinal stenosis? a randomized controlled trial. spine 2007;32:1–8. 25.mariconda m, et al. unilateral laminectomy for bilateral decompression of lumbar spinal stenosis: a prospective comparative study with conservatively treated patients, j spinal disord tech 2002, 15:39–46 26.martin bi, et al. reoperation rates following lumbar spine surgery and the influence of spinal fusion procedures, spine 2007, 32:382–387 27.marty m. – canal lombaire etroit, retreci ou mixte, traitement conservateur ou chirurgical ?. 20e congres francais de rhumatologie 2007 28.north american spine society (nass). diagnosis and treatment of surgery for lumbar spinal stenosis. burr ridge (il): north american spine society (nass); 2007 jan., 262 29.oertel m, et al. long-term results of microsurgical treatment of lumbar spinal stenosis by unilateral laminotomy for bilateral decompression, neurosurgery 2006, 59:1264–1270 30.sonntag vkh, marciano ff. is fusion indicated for lumbar spinal disorders? spine. 1995;20(suppl):138s– 142s 31.verbeek j, et al. patient expectation of treatment for back pain. a systmatic review of qualitative and quantitative studies. spine 2004 ; 29 : 2309-18. 32.verbiest h. a radicular syndrome from developmental narrowing of the lumbar vertebral canal. j bone joint surg br 1954 ; 36-b : 230-7 33.weinstein j.n., lurie j.d., et al. united states trends and regional variations in lumbar spine surgery: 1992–2003. spine 2006;31:2707–2714. 34.weinstein j.n., tosteson t.d., et al. surgical versus nonsurgical therapy for lumbar spinal stenosis. n engl j med 2008;358:794–810. 35.white a.a., panjabi m.m. clinical biomechanics of the spine, 2nd ed, lippincott, philadelphia, pa, 1990 36.wilby m.j., seeley h., laing r.j. laminectomy for lumbar canal stenosis: a safe and effective treatment, br j neurosurg, 2006 dec;20(6):391-5 37.wildermuth s, et al. lumbar spine: quantitative and qualitative assessment of positional (upright flexion and extension) mr imaging and myelography. radiology 1998 ; 207 (2) : 391-8. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 411-416 doi: 10.33962/roneuro-2019-066 www.journals.lapub.co.uk/index.php/roneurosurgery nonsteroidal anti-inflammatory drugsinduced hypersensitivity reactions: algorithm for the diagnostic and management andrei gheorghe vicovan1,2, liliana veres1,2, andrei cucu3, dana turliuc3, cristina mihaela ghiciuc1 1 "grigore t. popa" university of medicine and pharmacy iași, romania 2 "sfântul spiridon" emergency clinical hospital iași, romania 3 "prof. dr. n. oblu" emergency clinical hospital iași, romania abstract the role of nonsteroidal anti-inflammatory drugs (nsaids) in neurosurgical practice is a secondary one, however they are still constantly involved in perioperative management of pain or in nonoperative management of acute radiculopathy. beside the well-known adverse reactions (adrs), the neurosurgeon practitioner should also take in account the drug hypersensitivity reactions (dhrs) of nsaids and be able to deal with it. the aim of this paper was to review the diagnostic and management steps for nsaids-induced hypersensitivity reactions. the actual stratification of nsaids-induced hypersensitivity reactions is based on understanding of the heterogeneity of immunological/non-immunological mechanisms of reactions and complexity of clinical manifestations. practically, this stratification allows the physician to assess suspicion of dhr, based on anamnesis and clinical analysis, and to consider further practical steps to manage and eventually confirm the diagnosis. drug allergies are considered only the dhrs for which a definite immunological mechanism (either drug-specific antibody or t cell) is demonstrated. in conclusion, clinical analysis and anamnesis of patient with nsaids-induced hypersensitivity reactions can be realized by any physician and could be enough to diagnose, but it is not sufficient to confirm the diagnosis. in vitro tests and oral provocation challenges may be necessary to be undertaken by an allergy specialist. introduction post-operative pain management in neurosurgery is very complex because the administration of some drugs might interfere with postoperative outcomes or with the neurological evaluation22. although the use of nonsteroidal anti -inflammatory drugs (nsaids) in neurosurgery has been restricted due to their platelet dysfunction and risk of intracerebral bleeding, the postoperative pain is a nociceptive type pain which responds well to nsaids17. furthermore, nsaids are keywords nonsteroidal antiinflammatory drugs (nsaid), drug hypersensitivity reaction, perioperative, diagnostic, management corresponding author: mihaela dana turliuc "prof. dr. n. oblu" emergency clinical hospital, iași, romania turliuc_dana@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 412 andrei gheorghe vicovan, liliana veres, andrei cucu et al. effective to reduce morphine requirements by 25%– 50% in a broad spectrum of postoperative (consequently decreasing adverse effects secondary to opioids administration) and for rescue analgesia in post-craniotomy pain management (may have even greater benefit when administered preemptively)8,22. the use of nsaids has been proved to be efficient also for the pain management after spine surgery19,21. besides perioperatory involvement, nsaids are often prescribed (for short term) in addition to muscle relaxants and oral corticosteroids for nonoperative management of acute cervical radiculopathy4,10. a recent study from the uk, conducted by marinho et al., in 2016, reported the use of mainly opioids (82%) by anesthesists, followed by paracetamol (56%) and nsaids (28%). diclofenac was the most commonly used nsaid for perioperative pain, followed by parecoxib and ibuprofen15. in a survey study of 31 neurosurgical units in great britain, 42% of these reported prescribing nsaids, with 19 % prescribing nsaids on a regular basis for post-craniotomy analgesia13. drug hypersensitivity reactions (dhrs) after nsaids administration are less taken into account by practitioners, because gastrointestinal bleeding, platelet dysfunction, increased bleeding times and cardiovascular risk are the most known and severe adverse drug reactions induced by nsaids6. depending on the method of assessment, the analyzed population and type of reaction, the general prevalence of nsaids hypersensitivity ranges from 0.6 to 6% and according to the online latin american survey on anaphylaxis (olasa), nsaids were the culprit agents in 73% of the druginduced anaphylaxis18. nsaids are frequently involved in dhrs because they are frequently prescribed at all ages. every practitioner should be aware that any drug can induce a dhr and the nsaids (especially ibuprofen) beside some antibiotics are more likely to be the culprit for immediate reactions such urticaria and anaphylaxis6. we propose a model of clinical approach for the neurosurgical patient with suspected nsaid hypersensitivity reaction. i. nsaids-induced hypersensitivity reactions diagnostic steps according to who (world health organization), adverse drug reactions induced by drugs are classified as: • a-type reactions: predictable and dose dependent, with a frequency of approximately 75%; • b-type reactions or dhr: unpredictable and dose-independent, with a frequency of approximately 25%; based on their mechanisms these are classified as: o immunologically mediated (allergic reactions): due to a specific ige or due to a t cell response o non-immunologically mediated (non-allergic reactions or cross-reactive): due to an increased release of cystenyl leukotrienes by inflammatory cells, secondary to the inhibition of cox-1 enzyme16; these are caused by changes of pharmacological pathways (e.g. inhibition of cyclooxygenase)14. in the general medical practice, when a drug allergic reaction is suspected, dhr is the used term, according to international consensus on drug allergy5. drug allergies are considered only the dhrs for which a definite immunological mechanism (either drug-specific antibody or t cell) is demonstrated. cross hypersensitivity represents the majority of dhrs induced by nsaids compared to specific immunological mediated-reactions (76 vs. 24%)14. based on the time-lapse between the last drug administration and the onset of the reaction, the dhrs of nsaids are classified as5: • immediate reactions (usually immediate to several hours after the drug exposure): o ige-mediated (immunological): ▪ single-nsaid-induced urticarial / angioedema / anaphylaxis (sniuaa) manifested as urticaria, angioedema and/or anaphylaxis induced by a single nsaid or by several nsaids belonging to the same chemical group in subjects that tolerate other chemically nonrelated nsaids and usually do not have a history of chronic urticaria or asthma → labeled as; o non ige-mediated (non-immunological or cross-reactive): ▪ nsaids-exacerbated respiratory disease (nerd) manifested as bronchial obstruction, dyspnea, and nasal congestion/rhinorrhea induced by aspirin or other nsaids in patients with an 413 nonsteroidal anti-inflammatory drugs-induced hypersensitivity reactions underlying chronic airway respiratory disease (asthma/rhinosinusitis/nasal polyps); ▪ nsaids-exacerbated cutaneous disease (necd) manifested as wheals and/or angioedema – induced by aspirin or other nsaids in patients with a history of chronic spontaneous urticaria; ▪ nsaids-induced urticaria/angioedema (niua) manifested as wheals and/or angioedema – induced by aspirin or other nsaids (at least two nsaids with different chemical structure not belonging to the same chemical group) in healthy subjects (without history of chronic spontaneous urticaria); • non-immediate reactions (usually more than 24 h after exposure): o single-nsaid-induced delayed hypersensitivity reactions (snidr) are t cell – mediated, manifested as cutaneous symptoms (exanthema), fixed drug eruption, drug reaction with eosinophilia and systemic symptoms, acute generalized exanthematous pustulosis, stevens-johnson syndrome/toxic epidermal necrolysis, severe organ-specific or systemic symptom – induced by a single nsaid. immediate to several hours after the drug exposure, as a chronological stratification, has limitations: the exact onset of initial symptoms might be hard to pinpoint; the route of administration can influence the time interval in which the reaction occurs. cofactors such as co-medications, food intake, alcohol and exercise, can speed up or slow down the onset or progression of a reaction2. nsaids-induced hypersensitivity nsaids-exacerbated respiratory disease (nerd) nsaidsexacerbated cutaneous disease (necd) nsaidsinduced urticaria/ angioedema (niua) single-nsaidinduced urticaria/ angioedema or anaphylaxis (sniuaa) single-nsaid-induced delayed hypersensitivity reactions (snidr) clinical manifestations? respiratory symptoms (bronchial obstruction, cough, wheezing dyspnea, and nasal congestion/rhinorrhea) wheals and/or angioedema urticaria, angioedema and/or anaphylaxis very diverse symptoms – from cutaneous symptoms (with different degree of severity) to severe organ-specific or systemic symptoms onset time of the reaction? 1-2 hours after drug intake, up to 24 hours (when reaction occurs within minutes or during the 1st hour there is highly susceptible for sniuaa or nerd/necd) more than 24 hours after drug intake history/relapse of symptoms? history of similar symptoms caused by other strong cox-1 inhibitor and/or history of good tolerance of selective cox2 history of reaction to more than one chemically unrelated cox-1 inhibitor history of cutaneous (urticaria and/or angioedema) and/or anaphylactic reactions to a single nsaid usually no typical history underlying chronic diseases? asthma and/or rhinosinusitis with nasal polyps episodes of spontaneous chronic urticaria / angioedema, unrelated to nsaids typical no underlying diseases table 1. diagnosis steps for nsaids-induced hypersensitivity 414 andrei gheorghe vicovan, liliana veres, andrei cucu et al. after the physician has gone through previous anamnesis and corroborates the obtained clinical data with dhrs classification represented in table 1, there is a high probability to clinically diagnose a dhr as follows: • the typical form of snidr can be clinically diagnosed (heterogenic reactions, mainly cutaneous symptoms, 24 h or more after last drug administration), but in clinical practice, in time-lapse between the intake of culprit drug and onset of delayed reactions other drugs are administrated, which can make the diagnosis assessment difficult; • nerd can be suspected when a patient with asthma and/or rhinosinusitis with nasal polyps accuses respiratory symptoms (cough, wheezing, dyspnea, nasal congestion, nasal discharge). the diagnosis of nerd is confirmed if he reports a history of similar symptoms after other strong cox-1 inhibitors and/or history of good tolerance of selective cox-2; • in the case of acute cutaneous symptoms (urticaria/angioedema) and/or anaphylactic symptoms after intake of nsaids, we have to distinguish between three subtypes of hypersensitivity: necd, niua or sniuaa. the detailed history of previous reactions establishes whether the patient is sensitized to a single drug or is the case of a cross-reactive type of nsaids hypersensitivity: o allergic type i reaction (sniuaa) is based on a history of cutaneous (urticaria and/or angioedema) and/or anaphylactic reactions to a single nsaid. o nonallergic type reaction (cross-reactive) is suspected in a patient with history of more than one chemically unrelated cox-1 inhibitor. the diagnosis of necd is based on history of episodes of spontaneous chronic urticaria/angioedema to several chemically unrelated nsaids. the diagnosis of niua is based on history of hypersensitivity cutaneous reactions to several chemically unrelated nsaids concomitant and a negative history of spontaneous urticaria/angioedema. the clinical reality may not always look like in the above description – 10% of patients with necd have respiratory symptoms (bronchoconstriction) that resembles the nerd23. moreover than this, concomitant rhino-conjunctivitis in patients with nsaid-induced cutaneous reactions are reported3. ii. nsaids-induced hypersensitivity reactions management the main indication in case of an already diagnosed nsaid dhr is the avoidance of drugs from the same family. however, the neurosurgeon has the possibility of an alternative nsaid related on type of dhr: • in the case of sniuaa, when the specific nsaid has been identified, it can be replaced by another nsaid with similar anti-inflammatory potency but an unrelated chemical structure; • in the case of nerd/necd, preferential cox-2 inhibitors (around 91 to 99% of patients with hypersensitivity nsaids tolerate meloxicam doses higher than 15 mg daily should be avoided) and highly selective cox-2 inhibitors (celecoxib with a rate of only 4% positive reactions and etoricoxib with a rate of reactions ranging from 2,9% to 4%) are generally well tolerated9,11,12; leukotriene-modifying drugs may bring benefits in correlation with standard chronic urticaria management1; • niua – avoidance of nsaids (desensitization done by allergolog). in case of patients who have taken multiple drugs (in addition to an nsaid), the administration of alternative drugs has to be suspended firstly; drugs continuously taken for months are not suspected (exception is angiotensin-converting-enzyme which can develop angioedema after months or even years of intake). particularly when a patient, with known dhr to a cox-1 inhibitor, needs urgently analgesic medication, the opioids should be recommended due to the differences in structure. also the selective cox-2 might be an alternative, but a benefit – risk analysis is imperative. iii. nsaids-induced hypersensitivity reactions with potential of severe progression in the case of a suspected dhr, a severe progression should always be taken into account. according to scherer k et. al and to the more recently task force report of european academy of allergy and clinical immunology, the severe progression could be 415 nonsteroidal anti-inflammatory drugs-induced hypersensitivity reactions indicated by the presence of some clinical signs [20,7] (table 2). immediate reaction (anaphylaxis) non-immediate reaction (delayed reaction) • severe urticaria • rapid onset of extensive pruritus (especially scalp and palmo-plantar) • angioedema of the oral mucosa (especially pharynx and larynx) • hypotension • conjunctivitis and rhinitis with flush on face and neck • dyspnea with bronchospasm (particularly in asthmatics) cutaneous symptoms: • hemorrhagic necrotizing lesions • centrofacial edema (diffuse erythematous swelling) • purpura • involvement of large body surfaces or erythroderma • painful skin • atypical target lesions • nikolsky sign positive • erosive stomatitis • mucositis (involving more than one mucosal area) symptoms suggesting internal organ involvement: • unexplained rapid onset of high fever (> 39 °c) • arthritis and arthralgias • disseminated lymphadenopathy table 2. clinical signs for a potential severe progression of nsaids-induced hypersensitivity reactions. iv. criteria to refer a patient with dhs to allergist first steps that include a clinical analysis and anamnesis of patient can be realized by a nonspecialist and could be enough to diagnose in some cases, but frequently nsaid hypersensitivity, is not sufficient to confirm the diagnosis (fig. 1). in vitro tests and oral provocation challenges may be necessary to be undertaken by an allergy specialist. figure 1. criteria to refer a patient with dhs to allergist up to 1/3 of patients with chronic spontaneous urticarial report exacerbations of cutaneous symptoms upon ingestion of nsaids. the level of sensitivity could temporary variate in relation to coexisting chronic spontaneous urticaria and consequently, sensitivity may decrease and even disappear – therefore reassessing the tolerance to nsaids is appropriate14. conclusions the neurosurgical practice implies often moderateto-severe postoperative pain in a multitude of procedures such as craniotomies for aneurysm clipping, craniotomies for tumor resections and epilepsy surgery, neuroradiological procedures and penetrating traumatic brain injury. post-operative pain management is very complex due to interference of drugs with postoperative outcomes or with the neurological evaluation22. nociceptive type pain responds well to nsaids, even their use in neurosurgery has been restricted due to the platelet dysfunction and risk of intracerebral bleeding17. diagnosing dhrs is a complex issue. clinical analysis and diagnostic of a dhr can be realized by any physician, but the confirmation of the diagnosis needs in vitro tests and oral provocation challenges which should be undertaken by an allergy specialist. if the nsaid-induced hypersensitivity is confirmed, • suspected dhr to nsaids and increased probability of the use of this group of drugs in the future • history of severe dhr (anaphylaxis or severe non-immediate cutaneous reaction). when is mandatory? • suspected, but not severe dhr to nsaids; no estimated nsaids use in the future. when is recommended? • 4–6 weeks after the complete resolution of all clinical symptoms (after 6–12 months, the results may be false negative7). when is the appropriate time-lapse for allergological investigations? 416 andrei gheorghe vicovan, liliana veres, andrei cucu et al. recommendations based on the current classification for drug avoidance, use of alternative nsaids, and other management modalities, including aspirin desensitization, can be implemented. references 1. asero r. leukotriene receptor antagonists may prevent nsaid-induced exacerbations in patients with chronic urticaria. ann allergy asthma immunol 2000;85:156-7. 2. bircher aj, scherer hofmeier k. drug hypersensitivity reactions: inconsistency in the use of the classification of immediate and nonimmediate reactions. j allergy clin immunol 2012;129(1):263–4. 3. caimmi s, caimmi d, bousquet pj, demoly p. how can we better classify nsaid hypersensitivity reactions? validation from a large database. int arch allergy immunol 2012;159:306-12. 4. childress ma, becker ba. nonoperative management of cervical radiculopathy. am fam physician 2016;93(9):74654. 5. demoly p, adkinson nf, brockow k et al. international consensus on drug allergy. allergy 2014; 69(4):420-37. 6. dona i, blanca-lopez n, cornejo-garcia ja, et al. characteristics of subjects experiencing hypersensitivity to non-steroidal anti-inflammatory drugs: patterns of response. clin exp allergy j br soc allergy clin immunol 2011;41(1):86–95. 7. doña i, caubet jc, brockow k, et al. an eaaci task force report: recognizing the potential of the primary care physician in the diagnosis and management of drug hypersensitivity. clin transl allergy 2018;8:16-9. 8. dunn lk, naik bi, nemergut ec, durieux me, postcraniotomy pain management: beyond opioids. curr neurol neurosci rep 2016;16(10):93-9. 9. dworzynski k, ardern jones m, nasser s. guideline development group; national institute for health and care excellence. diagnosis and management of drug allergy in adults, children and young people: summary of nice guidance. bmj 2014;349:g4852. 10. ghasemi m, masaeli a, rezvani m, et al. oral prednisolone in the treatment of cervical radiculopathy: a randomized placebo controlled trial. j res med sci 2013;18(1): s43-s46. 11. goksel o, aydin o, misirligil z, et al. safety of meloxicam in patients with aspirin/non steroidal anti inflammatory drug induced urticaria and angioedema. j dermatol 2010;37:973-9. 12. koschel d, weber cn, höffken g. tolerability to etoricoxib in patients with aspirin exacerbated respiratory disease. j investig allergol clin immunol 2013;23:275 80. 13. kotak d, cheserem b, solth a. a survey of post-craniotomy analgesia in british neurosurgical centres: time for perceptions and prescribing to change? br j neurosurg 2009; 23(5):538–42. 14. kowalski ml, asero r, bavbek s, et al. classification and practical approach to the diagnosis and management of hypersensitivity to nonsteroidal anti-inflammatory drugs. allergy 2013;68(10):1219–32. 15. marinho s, kemp h, cook tm, et al. cross-sectional study of perioperative drug and allergen exposure in uk practice in 2016: the 6th national audit project (nap6) allergen survey. br j anaesth 2018;121(1):146-158. 16. mastalerz l, setkowicz m, szczeklik a. mechanism of chronic urticaria exacerbation by aspirin. curr allergy asthma rep 2005;5:277-83. 17. masuda r, ajimi j, murata t. pharmacotherapy for neuropathic pain in japan. j nippon med sch 2017;84(6):258-267. 18. mota i; gaspar â, morais-almeida m. hypersensitivity to nonsteroidal anti-inflammatory drugs: from pathogenesis to clinical practice. rev port imunoalergologia 2018;26(3):207-20. 19. ortiz-cardona j, bendo aa. perioperative pain management in the neurosurgical patient. anesthesiol clin 2007;25(3):655-74. 20. scherer k, bircher aj. danger signs in drug hypersensitivity. med clin n am 2010;94(4):681–9. 21. svensson ci, yaksh tl. the spinal phospholipasecyclooxygenase-prostanoid cascade in nociceptive processing. annu rev pharmacol toxicol 2002;42:553–83. 22. vadivelu n, kai am, tran d, et al. options for perioperative pain management in neurosurgery. j pain res 2016;9:3747. 23. zembowicz a, mastalerz l, setkowicz m, et. al. histological spectrum of cutaneous reactions to aspirin in chronic idiopathic urticaria. j cutan pathol 2004;31:323-9. microsoft word 5ienceanst_intracranial_f romanian neurosurgery (2011) xviii 3: 279 – 285 279 intracranial hypotension şt.m. iencean neurosurgery, emergency clinical hospital “prof. dr. n. oblu” iaşi, romania abstract the intracranial hypotension is the decrease in the intracranial pressure caused by the decrease in the volume of the cerebrospinal fluid secondary to the csf loss. the intracranial hypotension is characterized by an orthostatic cephalea, not calmed by antalgics accompanied by nausea, vomiting, vertigos, diplopia, etc. the diagnosis is confirmed by a lumbar manometry and by the performed paraclinical explorations (cerebral ct, cerebral mri). the intracranial hypotension treatment is etiologic, and it consists in closing the csf fistula; pathogenic, which consists in recreating the normal csf volume, and symptomatic, which refers to the treatment of the symptoms related to intracranial hypotension. keywords: cerebrospinal fluid, csf fistula, intracranial hypotension, intracranial pressure introduction the intracranial hypotension represents the intracranial pressure decrease; it may be generated by the decrease in the volume of any of the intracranial components: the cerebral parenchyma, the cerebrospinal fluid, and the sanguine content and/or by the rapid removal of a pathologic volume under the circumstances of a pressure equilibrium achieved by the efficient compensating mechanisms (especially in the case of chronic subdural hematomas). the decrease in the volume of the cerebral parenchyma, by various mechanisms – senile cerebral atrophy, surgical resection, etc., does not generate first of all an intracranial hypotension syndrome, but there may be focal neurological symptoms depending on the suffering cerebral areas. the volume of the diminished cerebral parenchyma is progressively diminished by gliosis and/or by csf; therefore, the intracranial pressure is maintained at normal values. the decrease in the intracranial sanguine volume by arterial hypotension leads to the decrease in the cerebral perfusion pressure with ischemic phenomena; this may also lead to a decreased csf secretion, but the intracranial pressure decrease seems to be less important than ischemia. the surgical removal of a pathologic volume produces a sudden decrease in the endocranial volume and in the intracranial pressure, also known as the surgical cerebral-ventricular collapse, and which is rapidly compensated from a therapeutic point of view. once the neurosurgical intervention has been performed, the endocranial cavity is no longer a close environment, and there is no correspondence between the intracranial hypotension and the surgical cerebral collapse. therefore, of the three intracranial components, only the diminished volume of the cerebrospinal fluid intervenes in the generation of the intracranial hypotension. (figure 1). 280 şt.m. iencean intracranial hypotension figure 1 scheme of the meningeal layers figure 2 the ventricular system – schematic drawing the intracranial hypotension is, therefore, the decrease in the intracranial pressure caused by the decrease in the volume of the cerebrospinal fluid secondary to the csf loss (figure 2). the intracranial hypotension is characterized by an orthostatic cephalea, exacerbated by coughing, laughing, the valsalva maneuver, which is not calmed by antalgics and is accompanied by nausea, vomiting, vertigos, diplopia, etc. the diagnosis is confirmed by a lumbar manometry and by the performed paraclinical explorations (cisternography, cerebral ct, cranial-cerebral rmn). romanian neurosurgery (2011) xviii 3: 279 – 285 281 from a clinical perspective, the intracranial hypotension may be represented as: an acute form, with a violent symptomatology present in clinostatism, and which may evolve towards psychic disorders and the modification of the conscience state, a sub-acute form with absent symptoms or of a reduced intensity in clinostatism; they occur or they are exacerbated in orthostatism, a chronic, frequent form, with a symptomatology occurred in orthostatism, of smaller, bearable intensity and a tiresome feeling that may allow the development of an activity, but with a reduced efficiency though. etiology and pathogeny the decrease in the normal csf quantity in the cranial-spinal space may be generated by: • the persistence of a dural continuity solution and the most frequent causes are the following ones: operations involving the lumbar puncture: the exploratory lumbar puncture, myelography, myelo-ct, rachianesthesia, cranial-spinal traumatisms with the generation of a csf fistula, cranial-cerebral neurosurgical or spinal interventions, extremely rarely, by a spinal anteriorlateral csf fistula in thoracic surgery, • decrease in the csf secretion by various mechanisms (after radiotherapy, senile, etc.) • reduced csf quantity by a ventricular-peritoneal drainage, • the so-called “spontaneous” intracranial hypotension, when none of the above-mentioned causes is underlined, but the explorations prove the existence of several arachnoid fissures at the level of the spinal radicular sheath, or the case of the occult nasal csf fistula. • there have been cases of intracranial hypotension without the identification of a dural lesion in situations of dehydration, diabetic coma, uremia, or severe systemic illnesses. there are two theories concerning the mechanism leading to the intracranial hypotension symptomatology: the decrease in the volume of cerebrospinal fluid leads to movements of the endocranial structures with the traction of the formations that contain pain receptors: meninx, draining veins to sinuses, trigeminus, glossopharyngeal and vague nerves, as well as the first cervical spinal nerves. orthostatism increases the traction of these structures, emphasizing the symptomatology. the decrease in the csf volume leads to the intracranial pressure decrease and, therefore, according to the monro–kellie theory, a dilatation of the intracranial vascular structures is produced, which generated the accentuated cephalea in orthostatism. moreover, there is a dilatation of the spinal epidural veins, explaining the spinal radicular pains. it is currently considered that these two mechanisms are concomitant, they act together and they justify the symptomatology. clinical presentation the main symptom of the intracranial hypotension is the orthostatic cephalea: a cephalea that occurs or is emphasized in orthostatism. the characteristics of the cephalea vary from one patient to another, but the common element is the fact that it 282 şt.m. iencean intracranial hypotension is exacerbated in the orthostatic position, at a coughing effort, when laughing, etc., and it is not influenced by antalgics. vertigo is the nest symptom from the frequency point of view, vertigos that occur or are accentuated in orthostatism too. there may also be feelings of nausea, vomiting, tingles, facial paresthesias, and radicular pains at the level of the superior limbs, all of them being emphasized in orthostatism. the establishment of how severe the symptomatology is and of the etiology makes the distinction between the clinical forms: acute, sub-acute and chronic. in the chronic form of intracranial hypotension, symptoms are accentuated in orthostatism, and they diminish or disappear in clinostatism. sometimes, symptoms have a reduced intensity with the presence of an accentuated feeling of asthenia. based on the dominating symptom, there are forms which are mainly cephalalgic, vertiginous, paresthesic, with vegetative disorders, etc. in the sub-acute form, symptoms are manifested in the horizontal position, and they are exacerbated in orthostatism with an invalidating effect. the acute form is characterized by an accentuated symptomatology, which is present in clinostatism, with vomiting, to dehydration, photophobia, sometimes even convulsive crises. moreover, there may be psychic disorders or even modifications of the conscience state. the acute form is very rarely registered nowadays. explorations the intracranial hypotension diagnosis implies the corroboration of the clinical data with the anamnesis, as well as the performance of certain explorations that may exclude other pathology and confirm the intracranial pressure decrease. in the context of certain maneuvers that include the lumbar puncture (myelography, myeloct, rachianesthesia), the occurrence of a clinical syndrome that announces the intracranial hypotension does not require the performance of other investigations in the case of a patient who has already undergone a cranial-cerebral exploration. in the case of cranial-cerebral or spinal traumatisms, the investigations performed in order to establish the traumatic lesions underline the dural lesion. the occurrence of the symptomatology at temporal distance from a particular situation, which suggests the existence of a persistent dural fistula, requires the performance of certain explorations that may establish the diagnosis. it is considered that the testing of a patient with chronic cephalea by arranging him or her in a trendelenburg position, followed by the improvement of the cephalea, suggests a possible occult csf fistula and it requires supplementary explorations. the intracranial pressure measurement establishes the diagnosis, but it must be performed after the cranial-cerebral explorations that exclude another pathology. the cerebrospinal fluid has a quasi-normal composition; sometimes, there may be an increase in the cerebrospinal fluid proteins, lymphocytosis; erythrocytes may be present, with a xanthochromic aspect. the cranial-cerebral computer tomography may prove the erasure of the basal cisterns without the existence of a cerebral lesion. the cerebral nuclear magnetic resonance with a contrast substance may reveal: dura mater thickening, romanian neurosurgery (2011) xviii 3: 279 – 285 283 venous sinus dilatation, presence of certain subdural fluid collections, increase in the volume of the hypophysis gland, the movement of the brain downwards: the basal cisterns become smaller, there is an inferior motion of the optic chiasm, and sometimes the cerebellar amygdales descend. (figure 3) the presence and the intensity of these signs are in direct relation to the clinical gravity, and the improvement of the symptomatology is accompanied by the attenuation and erasure of the mnr modifications. the radioactive isotope cisternography allows the outlining of the csf fistulas: directly, by noticing the radio-isotopic accumulation outside the sub-arachnoid space, or indirectly, by the lack of outlining regarding the radio-isotope at the level of the cerebral convexity and the notification of the latter in urine or in the adipose tissue. the computer myelography (myeloct) allows the outlining of the csf spinal fistulas right at the level of the cranium base. treatment the intracranial hypotension treatment is: etiologic, and it consists in closing the csf fistula, pathogenic, which consists in recreating the normal csf volume, and symptomatic, which refers to the treatment of the symptoms related to intracranial hypotension. figure 3 a t1-weighted sagittal mri with general descent of the brain and sagging of the cerebellar tonsils through the foramen magnum and expansion of the sellar contents 284 şt.m. iencean intracranial hypotension as the intracranial hypotension syndrome frequently occurs after the lumber puncture, the pathogenic and symptomatic treatment is often in the foreground, waiting for the dural orifice produced by the lumbar puncture to become obstruent. the symptomatic treatment of cephalea consists in avoiding the orthostatism, having the patient resting in bed, and by the oral or intravenous administration of caffeine or theophyline. xanthins (theophyline) also increase the vascular resistance in the cerebral territory, reducing the circulation and diminishing the venous dilatation. bed rest decreases the csf pressure in the spinal dural sac and at the level of the remaining lumbar puncture orifice. the csf volume is recovered by oral and intravenous hydration, as well as by the administration of mineral corticoids. based on the registered evolution, one may appreciate whether the dural orifice of the lumbar puncture is maintained and if the csf loss persists. in this case, a “patch” applying operation is performed at the level of the dural puncture orifice. the epidural blood patch is achieved by an autologous blood injection in the epidural space at the level of the previously performed lumbar puncture, with very good results; this operation needs to be repeated only very rarely. the surgical solution of the csf fistula is applied from the very beginning in traumatic dural lesions (cranial-cerebral wound, vertebral-medullar wound, cranium base fracture with csf fistula, etc.), or the surgery may be temporized based on the intensity of the csf loss and on the fistula location, with therapeutic protection, supervising its spontaneous closure (in the csf fistula from the cranium base fracture). therefore postoperative csf leaks after brain surgery are initially managed conservatively with bed rest, stool softeners and a lumbar drain and persistence of the leak beyond 1 week indicates need for surgical repair. patients with postoperative csf leaks after endoscopic approaches are taken back to surgical repair immediately. there may also be surgical solutions for the spinal dural lesions remaining after the lumbar puncture only if none of the previously presented procedures has proven to be efficient. conclusions 1. the intracranial hypotension diagnosis implies the corroboration of the clinical data with the anamnesis, as well as the performance of certain explorations that may exclude other pathology and confirm the intracranial pressure decrease. 2. the intracranial pressure measurement establishes the diagnosis, but it must be performed after the cranialcerebral explorations that exclude another pathology. 3. the treatment of intracranial hypotension is etiologic, and consists in closing the csf fistula; pathogenic, which consists in recreating the normal csf volume and symptomatic, which refers to the treatment of the symptoms related to intracranial hypotension. the surgery for csf fistula is applied from the very beginning in traumatic dural lesions or the surgery may be temporized with therapeutic protection, supervising its spontaneous closure. romanian neurosurgery (2011) xviii 3: 279 – 285 285 references 1. albayram s, wasserman ba, yousem dm, et al: intracranial hypotension as a cause of radiculopathy from cervical epidural venous engorgement: case report. ajnr 23:618–621, 2002 2. alvarez-linera j, escribano j, benito-leon j, et al: pituitary enlargement in patients with intracranial hypotension syndrome. neurology 55:1895–1897, 2000 3. benamor m, tainturier c, graveleau p, et al: radionuclide cisternography in spontaneous intracranial hypotension. clin. nucl. med 23:150–151, 1998 4. binder dk, sarkissian v, dillon wp, weinstein pr. spontaneous intracranial hypotension associated with transdural thoracic osteophyte reversed by primary dural repair. case report. j. neurosurg spine. 2005;2(5):614-8. 5. brightbill tc, goodwin rs, ford rg: magnetic resonance imaging of intracranial hypotension syndrome with pathophysiological correlation. headache , 2000, 40:292–299 6. bruera o, bonamico l, giglio ja, et al: intracranial hypotension: the nonspecific nature of mri findings. headache , 2000, 40: 848–852 7. chen cc, luo cl, wang sj, et al: colour doppler imaging for diagnosis of intracranial hypotension. lancet,1999, 354:826–829 8. davenport rj, chataway sj, warlow cp: spontaneous intracranial hypotension from a csf leak in a patient with marfan’s syndrome. j. neurol. neurosurg psychiatry,1995, 59:516–519 9. dickerman rd, morgan j. pathogenesis of subdural hematoma in healthy athletes: postexertional intracranial hypotension? acta neurochir (wien). 2005;147(3):349-50 10.evan rw, mokri b: spontaneous intracranial hypotension resulting in coma. headache,2002, 42:159– 160 11.ferrante e, savino a. thunderclap headache caused by spontaneous intracranial hypotension. neurol.sci. 2005 ;26 suppl 2 12.fishman ra, dillon wp: dural enhancement and cerebral displacement secondary to intracranial hypotension. neurology,1993, 43:609–611 13.good dc, ghobrial m: pathologic changes associated with intracranial hypotension and meningeal enhancement on mri. neurology,1993, 43:2698–2700 14.hannerz j, dahlgren g, irestedt l, meyerson b, ericson k. treatment of idiopathic intracranial hypotension: cervicothoracic and lumbar blood patch and peroral steroid treatment. headache. 2006 mar;46(3):508-11 15.hong m, shah gv, adams km, et al: spontaneous intracranial hypotension causing reversible frontotemporal dementia. neurology ,2002,58:1285– 1287 16.iencean st m a new classification and a synergetical pattern in intracranial hypertension. medical hypotheses , 2002 ;58(2):159-63. 17.inenaga c, tanaka t, sakai n, et al: diagnostic and surgical strategies for intractable spontaneous intracranial hypotension. case report. j. neurosurg,2001, 94:642–645 18.kong ds, park k, nam do h, lee ji, kim js, eoh w, kim jh. clinical features and long-term results of spontaneous intracranial hypotension. neurosurgery. 2005 57(1):91-6 19.koss sa, ulmer jl, hacein-bey l: angiographic features of spontaneous intracranial hypotension. ajnr,2003, 24:704–706 20.kremer s, taillandier l, schmitt e, bologna s, moret c, picard l, bracard s. atypical clinical presentation of intracranial hypotension: coma. j.neurol 2005; 252 (11):1399-400 21.moriyama e, nishida a. intracranial hypotension.j. neurosurg. 2005;102(5):964-5. 22.schievink wi, akopov se. filum ependymoma mimicking spontaneous intracranial hypotension. headache. 2005 ;45(5):607-9. 23.schievink wi, maya mm, tourje j, moser fg. pseudo-subarachnoid hemorrhage: a ct-finding in spontaneous intracranial hypotension. neurology. 2005,12;65(1):135-7. 24.takahashi m, momose t, kameyama m, mizuno s, kumakura y, ohtomo k. detection of cerebrospinal fluid leakage in intracranial hypotension with radionuclide cisternography and blood activity monitoring. ann. nucl. med. 2005;19(4):339-43. doi: 10.33962/roneuro-2021-081 surgical smoke, neurosurgical practice and coronavirus: a few words of caution adesh shrivastava, noor-ul-huda maria, rakesh mishra, william florez-perdomo, amit agrawal, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (4): pp. 478-482 doi: 10.33962/roneuro-2021-081 www.journals.lapub.co.uk/index.php/roneurosurgery surgical smoke, neurosurgical practice and coronavirus: a few words of caution adesh shrivastava3, noor-ul-huda maria2, rakesh mishra6, william florez-perdomo4,5, amit agrawal3, luis rafael moscote-salazar1 1 centre of biomedical research (cib) faculty of medicine university of cartagena, colombia 2 punjab institute of neurosciences, lahore, pakistan 3 all india institute of medical sciences, bhopal, india 4 latin-american council of neurocritical care, colombia 5 south colombian university, neiva, colombia 6 national institute of mental health and neurosciences, bengaluru, india abstract surgical smoke also referred to as cautery smoke is a gaseous mixture produced during surgical procedures where there is ablation, cutting, coagulation, desiccation or vaporization of the tissue. in a true sense “surgical smoke” refers to surgically generated gaseous contents. the surgical smoke results from the destruction of bones and tissues, causing microscopic particles to get suspended in the environment. coagulation devices such as ultrasound, electrical instruments and laser generate nebulization of particles viral, carcinogens and toxic substances. [4, 6] the recent appearance of covid19 infection has emerged as a risk factor for surgical practice. surgical smoke contains particulate matter which passes the upper respiratory tract and gets deposited.7-9 the overall effect of surgical smoke is determined by the duration of the working hours in the operating room [5, 10] as well as safety measures adopted to protect from the surgical smoke. [5] the global pandemic of covid-19 has made surgeons rethink their strategies to maximize the safety of treating personnel. neurosurgery is not untouched by the current situation of this pandemic. there are many concerns including the safety of health care workers, poor availability of resources etc. many of the elective surgical procedures a r e p o s t p o n e d a l l r o u n d t h e g l o b e as a m e an s t o p r e v e n t transmission.[11] since the majority of neurosurgical illness is progressive and can transform from elective to emergency with time. also, like in other specialities, neurosurgery is benefitted with technological advances to maximize the efficacy and minimize keywords surgical smoke, coronavirus, neurosurgical practice corresponding author: luis rafael moscote-salazar department of neurosurgery, university of cartagena, colombia rafaelmoscote21@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 479 surgical smoke, neurosurgical practice and coronavirus the morbidity associated with neurosurgical procedures. there are concerns with the use of ultrasonic aspirator, drill system which potentially generates aerosols and surgical smoke. with ongoing pandemic, it is evident that these procedures cannot be postponed indefinitely and no alternative is yet available to ensure a better outcome. even in neurosurgical emergencies and neurooncological surgeries, it is of utmost importance to take cognizance of potential effects of surgical smoke and precautions while operating on patients who are suspected or proven covid-19 positive. neurological surgery comprises a versatile set of different surgical domains that include spinal surgery, cranial surgery, endoscopic surgery and minimally invasive surgical procedures which have their own biological and physical factors. since the surgical smoke has heterogenous composition, it is not clear which surgical procedure has more potential to generate smoke containing viral products as particulate matter. the surgical smoke thus generated consists of 95% water and 5% particulate matter consisting of chemical compounds, cell particles, bacteria, viruses and even drugs are taken by patients.[10, 12-15] several chemical compounds (≥ 80 different toxic chemicals) have been found in surgical smoke. [16, 17] which have the potential to cause cell damage. [1, 16] prolonged exposure to surgical smoke (with cumulative dose effect0 can cause mild symptoms like headache, irritability, mood changes to severe injuries like an injury to the lungs and in long term infections and a certain type of malignancies. 1, 9, 18 particulate matter in surgical smoke is mostly less than 5 um in size. [12, 19] although many regulatory bodies agree on the dangers of surgical smoke, the degree of hazard and methods to prevent is yet to be firmly established20. electrocautery generates heat which damages the cell membranes and generates smoke containing mostly water vapour which gets aerosolized in the operating room. [2, 8, 21], in addition, it chars the neighbouring cells. this causes further thermal necrosis and releases carbonized cell fragments and gaseous hydrocarbons.[22] the byproduct of diathermy coagulation and biochemicals present in the smoke depends on the settings of diathermy and the tissue being burnt with the gray matter being low particulate matter tissues. [1, 18, 23-27] similarly ultrasonic aspirators create aerosols by creating cavitation nuclei. the combined action of ultrasonic aspirators and diathermy electrocoagulation has potential to generate aerosols containing infective particulates. electrocautery produces more particulate matter than lasers and ultrasonic devices, but because the smoke generated by lasers and ultrasonic devices is colder and has more biohazard with the risk of transmitting infection [1, 26, 27] as the smoke and aerosols can be inhaled and gets deposited in the respiratory system.28 though, there is insufficient evidence for covid-19 transmission through surgical smoke, data, existing studies and expert opinion suggests it a theoretical risk.29, 30 a review was done based on the existing studies suggested the methods to mitigate the potential risk of surgical smoke and covid-19 transmission to or personnel. [29] the composition of this hazardous surgical smoke depends much on the type of surgical procedure, the duration, the devices/instruments used, the structure of the operating theatre, the expertise of the surgeon, the pathology operated upon and the precautionary measures taken during surgery. it is not hard to imagine that such surgical procedures carry the potential of a generation of heavy and potentially hazardous surgical smoke. while on the other hand, for brain surgery, a use of bipolar cautery, cusa, ultrasonic probe, generation of biological particle including tumours and again infectious matter, bone dust because of bone drilling and craniotomy flap elevation, neuronavigation and laser contribute in the generation of the surgical smoke. studies on biohazards of surgical smoke have shown the presence of viral dna, activated corynebacterium, hepatitis b, human papillomavirus. [1, 31-38] in a few studies, 80% of the surgical smoke from infected patients contained viral particles suggesting the potential risk of transmission to personnel in or. [39-41] bacteria and viruses can survive in the surgical smoke for up to 72 hours’[19] it has been shown that in aerosols sars-cov-2 can survive up to 3 hours and on the surfaces up to 72 hours.38 however, no data is yet available for transmission of sars-cov-2 through smoke produced in a surgical procedure. majority of the literature available is related to laparoscopic surgeries. [11, 42] even the biohazard potential is not very well established in other surgical specialities [42-44] sars-cov-2 has shown transmission potential through aerosols and fomites similar to sars-cov-1 in experimental conditions [38]. 480 adesh shrivastava, noor-ul-huda maria, rakesh mishra et al. to reduce the risk of transmission of sars-cov-2 through surgical smoke, preventive strategies suggested by zheng et al. seems appropriate and worth considering in neurosurgical patients.[11] chow et al have mentioned the method to convert existing or into negative pressure or.45 unilaminar airflow in or is effective in removing 97% of particulate matter of size more than or equal to 0.3 um.46 various filters can be used along with smoke evacuators in the or like, charcoal filters, coconut shell charcoal, ultralow particulate air (ulpa) filters.29 these filters can retain particles up to 0.1 um in size. different surgical societies all around the world have published guidelines involving comprehensive measures, changes in or and filtration systems aimed to prevent the established and hypothetical risk of transmission. [47-49] neurosurgical procedures are not immune to the production of surgical smoke given the usage of ultrasonic aspirators, high-speed pneumatic drills. in parallel to other surgical association, the neurosurgical community should assess the size of the risk to provide quality surgery to the patient and protection of the surgical team. the american national standards institute (ansi) has established strategies for smoke reduction during laser surgery. 50 in the current pandemic of covid-19, health care worker needs to have ppe and n95 masks. available masks to prevent inhalation of surgical masks and its health hazards include surgical mask, n85 masks and high filter masks.[51-53] surgical mask doesn’t provide tight face seal, positive pressure inside the facepiece and filter particulate matter less than 5 um in size and therefore may fail to protect from transmission of infective pathogens through surgical smoke.[21, 54] surgical masks my provide > 90% protection and has been in use for a century and n95 mask may not offer adequate protection in these potential contagious procedures and activated carbon filters in addition to n95 may be more appropriate. [21, 55-58] however, n95 masks have their own challenges which includes co2 build up, difficulty in breathing after a certain time and subjective symptoms of headache, light headedness etc. [59] in summary, there is an increased need to create awareness regarding the side effect of surgical smoke, to train an individual to minimize the exposure and develop facilities for the safe evacuation of the surgical smoke in the operation theatre and thus to safeguard the personnel’s in the operating theatre. [21] references 1. barrett wl, garber sm. surgical smoke: a review of the literature. is this just a lot of hot air? surgical endoscopy 2003;17:979-987. 2. mowbray n, ansell j, warren n, wall p, torkington j. is surgical smoke harmful to theater staff? a systematic review. surgical endoscopy 2013;27:3100-3107. 3. waddell aw. cultivating quality: implementing surgical smoke evacuation in the operating room. the american journal of nursing 2010;110:54-58. 4. carbajo-rodríguez h, aguayo-albasini jl, soria-aledo v, garcía-lópez c. surgical smoke: risks and preventive measures. cirugía española (english edition) 2009;85:274-279. 5. van giersbergen my, alcan ao, kaymakci s. investigation of surgical smoke symptoms and preventive measures in turkish operating rooms. international journal of health sciences and research 2019;9:138-144. 6. marsh s. the smoke factor: things you should know. j perioper pract 2012;22:91-94. 7. michaelis m, hofmann fm, nienhaus a, eickmann u. surgical smoke-hazard perceptions and protective measures in german operating rooms. int j environ res public health 2020;17:515. 8. fitzgerald je, malik m, ahmed i. a single-blind controlled study of electrocautery and ultrasonic scalpel smoke plumes in laparoscopic surgery. surgical endoscopy 2012;26:337-342. 9. liu n, filipp n, wood kb. the utility of local smoke evacuation in reducing surgical smoke exposure in spine surgery: a prospective self-controlled study. the spine journal : official journal of the north american spine society 2020;20:166-173. 10. ünver s, topçu sy, findik üy. surgical smoke, me and my circle. international journal of caring sciences 2016;9:697-703. 11. zheng mh, boni l, fingerhut a. minimally invasive surgery and the novel coronavirus outbreak: lessons learned in china and italy. annals of surgery 2020;publish ahead of print. 12. ulmer bc. the hazards of surgical smoke. aorn journal 2008;87:721-734; quiz 735-728. 13. fencl jl. guideline implementation: surgical smoke safety. aorn journal 2017;105:488-497. 14. tramontini cc, galvão cm, claudio cv, ribeiro rp, martins jt. [composition of the electrocautery smoke: integrative literature review]. rev esc enferm usp 2016;50:148-157. 15. gianella m, hahnloser d, rey jm, sigrist mw. quantitative chemical analysis of surgical smoke generated during laparoscopic surgery with a vessel-sealing device. surg innov 2014;21:170-179. 16. sisler jd, shaffer j, soo j-c, et al. in vitro toxicological 481 surgical smoke, neurosurgical practice and coronavirus evaluation of surgical smoke from human tissue. j occup med toxicol 2018;13:12-12. 17. king b, mccullough j. niosh health hazard evaluation report. heta# 2000-0402-3021. inova fairfax hospital, falls church, virginia 2006. 18. okoshi k, kobayashi k, kinoshita k, tomizawa y, hasegawa s, sakai y. health risks associated with exposure to surgical smoke for surgeons and operation room personnel. surgery today 2015;45:957-965. 19. benson sm, novak da, ogg mj. proper use of surgical n95 respirators and surgical masks in the or. aorn journal 2013;97:457-467; quiz 468-470. 20. york k, autry m. surgical smoke: putting the pieces together to become smoke-free: 1.6 www.aornjournal.org/content/cme. aorn journal 2018;107:692-703. 21. liu y, song y, hu x, yan l, zhu x. awareness of surgical smoke hazards and enhancement of surgical smoke prevention among the gynecologists. journal of cancer 2019;10:2788-2799. 22. pollock l. hazards of electrosurgical smoke. perioperative nursing clinics 2007;2:127-138. 23. ott de, moss e, martinez k. aerosol exposure from an ultrasonically activated (harmonic) device. j am assoc gynecol laparosc 1998;5:29-32. 24. karjalainen m, kontunen a, saari s, et al. the characterization of surgical smoke from various tissues and its implications for occupational safety. plos one 2018;13:e0195274. 25. petrusm b, patachiam, dumitrasdc. spectroscopic analysis of surgical smoke produced in vitro by laser vaporization of animal tissues in a closed gaseous environment. romrepphys 2015; 67(3):954-965. . 26. in sm, park dy, sohn ik, et al. experimental study of the potential hazards of surgical smoke from powered instruments. br j surg 2015;102:1581-1586. 27. weld kj, dryer s, ames cd, et al. analysis of surgical smoke produced by various energy-based instruments and effect on laparoscopic visibility. j endourol 2007;21:347-351. 28. limchantra iv, fong y, melstrom ka. surgical smoke exposure in operating room personnel: a review. jama surg 2019. 29. mowbray ng, ansell j, horwood j, et al. safe management of surgical smoke in the age of covid-19. br j surg 2020. 30. de leeuw ra, burger nb, ceccaroni m, et al. covid-19 and laparoscopic surgery, a scoping review of current literature and local expertise. jmir public health surveill 2020. 31. kwak hd, kim sh, seo ys, song kj. detecting hepatitis b virus in surgical smoke emitted during laparoscopic surgery. occup environ med 2016;73:857-863. 32. gloster hm, jr., roenigk rk. risk of acquiring human papillomavirus from the plume produced by the carbon dioxide laser in the treatment of warts. j am acad dermatol 1995;32:436-441. 33. choi sh, kwon tg, chung sk, kim th. surgical smoke may be a biohazard to surgeons performing laparoscopic surgery. surgical endoscopy 2014;28:2374-2380. 34. capizzi pj, clay rp, battey mj. microbiologic activity in laser resurfacing plume and debris. lasers surg med 1998;23:172-174. 35. hensman c, baty d, willis rg, cuschieri a. chemical composition of smoke produced by high-frequency electrosurgery in a closed gaseous environment. an in vitro study. surgical endoscopy 1998;12:1017-1019. 36. johnson gk, robinson ws. human immunodeficiency virus-1 (hiv-1) in the vapors of surgical power instruments. j med virol 1991;33:47-50. 37. zhou q, hu x, zhou j, zhao m, zhu x, zhu x. human papillomavirus dna in surgical smoke during cervical loop electrosurgical excision procedures and its impact on the surgeon. cancer manag res 2019;11:3643-3654. 38. van doremalen n, bushmaker t, morris dh, et al. aerosol and surface stability of sars-cov-2 as compared with sars-cov-1. n engl j med 2020;382:1564-1567. 39. baggish ms, poiesz bj, joret d, williamson p, refai a. presence of human immunodeficiency virus dna in laser smoke. lasers surg med 1991;11:197-203. 40. fletcher jn, mew d, descoteaux jg. dissemination of melanoma cells within electrocautery plume. american journal of surgery 1999;178:57-59. 41. sood ak, bahrani-mostafavi z, stoerker j, stone ik. human papillomavirus dna in leep plume. infect dis obstet gynecol 1994;2:167-170. 42. pawar t, pokharkar a, gori j, et al. the technique and justification for minimally invasive surgery in covid-19 pandemic: laparoscopic anterior resection for near obstructed rectal carcinoma. j laparoendosc adv surg tech a 2020;30:485-487. 43. ngaserin sh, koh fh, ong bc, chew mh. covid-19 not detected in peritoneal fluid: a case of laparoscopic appendicectomy for acute appendicitis in a covid-19infected patient. langenbecks arch surg 2020:1-3. 44. cicuttin e, cobianchi l, chiarugi m, catena f, coccolini f, pietrabissa a. detect to protect: pneumoperitoneum gas samples for sars-cov-2 and biohazard testing. surgical endoscopy 2020. 45. chow tt, kwan a, lin z, bai w. conversion of operating theatre from positive to negative pressure environment. the journal of hospital infection 2006;64:371-378. 46. spagnolo am, ottria g, amicizia d, perdelli f, cristina ml. operating theatre quality and prevention of surgical site infections. j prev med hyg 2013;54:131-137. 47. mintz y, arezzo a, boni l, chand m, brodie r, fingerhut a. a low cost, safe and effective method for smoke evacuation in laparoscopic surgery for suspected coronavirus patients. ann surg 2020. 48. the american college of surgeons. acs covid-19 and surgery march 24 aahwfoc-c-g. 49. https://www.sages.org/recommendations-surgicalresponse-covid-19/. tsoagaessrrsrtc-caa. 482 adesh shrivastava, noor-ul-huda maria, rakesh mishra et al. 50. bigony l. risks associated with exposure to surgical smoke plume: a review of the literature. aorn journal 2007;86:1013-1020; quiz 1021-1014. 51. coleman s. protecting yourself against surgical smoke. or nurse 2014;8:40-46. 52. lewin jm, brauer ja, ostad a. surgical smoke and the dermatologist. j am acad dermatol 2011;65:636-641. 53. fan jk, chan fs, chu km. surgical smoke. asian journal of surgery 2009;32:253-257. 54. bree k, barnhill s, rundell w. the dangers of electrosurgical smoke to operating room personnel: a review. workplace health & safety 2017;65:517-526. 55. georgesen c, lipner sr. surgical smoke: risk assessment and mitigation strategies. j am acad dermatol 2018;79:746-755. 56. jamal s, hassan m, farooqi m, ali s. surgical smokeconcern for both doctors and patients. indian j surg 2015;77:1494-1495. 57. oberg t, brosseau lm. surgical mask filter and fit performance. american journal of infection control 2008;36:276-282. 58. offeddu v, yung cf, low msf, tam cc. effectiveness of masks and respirators against respiratory infections in healthcare workers: a systematic review and metaanalysis. clinical infectious diseases : an official publication of the infectious diseases society of america 2017;65:1934-1942. 59. rebmann t, carrico r, wang j. physiologic and other effects and compliance with long-term respirator use among medical intensive care unit nurses. american journal of infection control 2013;41:1218-1223. microsoft word 12ienceanstmtwocases.doc romanian neurosurgery (2010) xvii 2: 219 – 224 219 two cases of bone marrow tissue implant into chronic cervical spinal cord injury st.m. iencean1, i. poeata2, gh. solcan3, n. ianovici1, a.st. iencean1 1neurosurgery, clinical emergency hospital “prof. dr. nicolae oblu” iasi, romania 2neurosurgery, faculty of medicine, “gr.t. popa” university of medicine and pharmacy iasi, romania 3faculty of veterinary medicine, university of agricultural sciences and veterinary medicine iasi, romania abstract two patients with chronic cervical spinal cord injury and quadriplegia underwent partial resection of the medular scar and implant of bone marrow tissue with a combination of drugs at the site of spinal cord injury. post-operatively they received a similar treatment in the neuromotor rehabilitation centre and were treated additionally with cerebrolysin . sensory improvements were noticed, but no significant motor improvements were observed twenty months afterwards. keywords: autologous bone marrow implant, sensory recovery, spinal cord injury, spinal scar spinal cord injury (sci) is a major medical problem worldwide and cervical spinal cord injuries can lead to quadriplegia and have devastating consequences for victims, families, and society in general. today there are no fully restorative treatments for spinal cord injury, but various cellular therapies have been tested in animal models. during the spinal cord injury there is a complete or an incomplete section; therefore there is a disrupted spinal cord or some types of contusion, compression, penetration or laceration of the spinal cord occur. spinal cord injury culminates in glial scarring, a multifactorial process that involves reactive astrocytes, microglia and macrophages, fibroblasts and schwann cells.(3,4,8,9) the scar is often oriented perpendicularly to the neuraxis and appears impenetrable. the scar also contains molecular inhibitors of axon growth. progressive expansion of the injury across more than one segment can also occur over months or years. therefore after spinal cord injury there are two types of lesions : complete disruption of the spinal cord or different types of scars. the scar of the spinal cord can be: a complete and impenetrable glial scar on the site of spinal cord injury, an incomplete scar and a posttraumatic syringomyelia or post-traumatic cysts on the site of spinal cord injury, a filiform connective scar of the two segments of damaged spinal cord. the glial scar, which is rich in growth inhibitors, as chondroitin sulfate proteoglycan (cspg), is a major impediment to axonal regeneration following injury. 220 st.m.iencean et al bone marrow tissue implant in spinal cord injury the inability to repair spinal cord damage is attributed to several factors: • the presence of inhibitory substances in the tissue that surrounds the lesion, • changes inside adult nerve fibres that make them unable to respond well to growth-inducing signals, • the formation of cysts at the injury site which growing fibres cannot cross, • the lack of nerve growth factors at the injury site, • the formation of scar tissue at the injury site with additional inhibitory substances. therefore any treatment must solve the above difficult problems.(7,13,14) there are no fully restorative treatments for spinal cord injury, but various rehabilitative therapies have been tested on animal models to improve functional outcomes after spinal cord injury. the stem cells based therapies are being tried in order to repair or replace tissues or cells damaged by injuries or diseases and to treat serious chronic diseases, such as spinal cord injuries. three therapeutic concepts are currently being envisaged: 1. transplantation of differentiated cells derived from stem cells. the source for the specific differentiated cell types could be embryonic or somatic stem cells including the patient’s own stem cells. 2. direct administration of stem cells directly to the patient; the stem cells will differentiate into the desired cell type . 3. stimulation of endogenous stem cells, induced by stimulating an individual’s own population of stem cells by administrating growth factors. stem cells are feasible candidates for cell therapy of spinal cord injury. (8,10,15) bone marrow cells are the subject of extensive interest because of their stem cell like characteristics and pluripotency. (11,16,18) there are more data supporting the beneficial effects of bone marrow cells in sci: 1. bone marrow contains multipotent adult progenitor cells that produce a variety of cell types, including neuroectodermal, mesodermal and endodermal cell types. 2. bone marrow cell transplants improve function recovery and differentiate into astrocytes, oligodendroglia and neural presursors in animal experiments. 3. bone marrow cell transplants facilitate remyelination of the spinal cord, appear to be neuroprotective and also promote regeneration in injured animal spinal cords. (21,22,24,25) neurotrophins and growth factors play an important role in development of the central nervous system and several neurotrophic factors induce neuroprotection in traumatic spinal cord injuries. (20) understanding the mechanisms by which adult stem cells produce growth factors and the effect of components of the spinal cord injury milieu to stimulate growth factor production and to promote spinal cord lesion repair are very significant issues. a combination of stem cells therapy with neurotrophins is a novel aspect of treatment in spinal cord injury and it will attenuate the neurological damage and could help restore the normal function of spinal cord. there are several similarities between the traumatic brain injuries and spinal cord injuries and there are also some similarities between the both their treatments. numerous studies have documented the neuroprotective and neurotrophic romanian neurosurgery (2010) xvii 2: 219 – 224 221 properties of cerebrolysin in traumatic brain injury. cerebrolysin is a standardized porcine brain-derived drug and it can pass through the blood-brain barrier. this paper presents the experience of two patients with traumatic chronic cervical spinal cord injuries with quadriplegia and the results of the microsurgical resection of the spinal scar and the implant of bonemarrow tissue in the site of the spinal cord lesion . methods two patients with chronic cervical spinal cord injury and quadriplegia voluntarily participated in this study. the cervical sci events occurred at least two years before this study. two physicians independently assessed the neurological injury status of each patient before and at regular intervals after the surgery. the surgical approaches and the implant were performed by the same neurosurgical team. the study protocol was approved by the ethics committee of the hospital “prof dr nicolae oblu“, iasi and the subjects gave informed consent. each patient underwent a cervical laminectomy to expose the site of the cervical spinal cord injury and a microsurgical partial resection of the medular scar and implant of autologous bone marrow tissue with a combination of drugs at the site of spinal cord injury. (figure 1) no postsurgery complications occurred. post-operatively the patients received a similar treatment in the neuromotor rehabilitation centre, also they received 5 10 ml/day for three to five months postoperatively. results two male patients were included in this study with the age of 26 and 33 years. sensory improvements were noticed, but no significant motor improvements were observed twenty months afterwards. (table 1). discussion the mechanisms of spinal injury are very important for the type of lesion of the spinal cord. when the spinal cord is injured, a number of events occur : injury of the neurons ( broken neural cell membranes, cut axons), blood vessels disruption, bleeding in the central grey matter, spinal cord edema and hypoperfusion of the spinal cord, the dura mater injury. the spinal cord injury is a complete lesion a disrupted spinal cord, or an incomplete lesion different types of compression or laceration of the spinal cord. a dura mater sheath lesion is followed by a fibroblastic reaction in the epidural tissue extended into the spinal cord with a connective scar, but maintaining the dural continuity can limit the formation of connective tissue scarring in the epidural space. (7) no case age f/m cervical sci level history of injury neurology cerebrolysin postoperatively outcome (m = months) 1 26 /m c4-c5 3y quadriplegia yes ; 5 ml/day 3 months 20 m : c7 2 33 /m c5-c6 3y quadriplegia yes ; 5 ml/day 3 months 22 m : c8 222 st.m.iencean et al bone marrow tissue implant in spinal cord injury the dural duraplasty following acute spinal cord laceration may improve cerebrospinal fluid flow by limiting meningeal fibrosis adjacent to the injury and minimize connective tissue scar formation. (9) the surgical treatment (ideally within eight hours of the injury occuring) must remove the tissues causing spinal cord compression, must correct a gross misalignment and must stabilize the spine. immediate surgery for spinal decompression including the duraplasty is of high importance for the prognosis and evolution of spinal cord injury. the secondary spinal cord injury is the damage that continues in the hours following trauma and consists of reduction in blood flow at the level of injury, excessive release of neurotransmitters (glutamate), inflamatory response, free radicals attack neurons and neuronal apoptosis. during this delayed secondary spinal cord injury the treatment may reduce the extent of disability, eg. methylprednisolone given within 8 hours of the injury occuring significantly improves recovery in humans. (2, 7,18,19) an efficient treatment in spinal cord lesions must combine several main approaches: minimising the initial damage and protecting surviving neurons neuroprotection, removing barriers: after the injury the scar tissue gradually fills the damaged area and it is an impenetrable barrier and it does not allow regenerating nerve fibres to pass through. blocking factors which inhibit neural regeneration, modulation of inflammatory response following spinal cord injury, preventing inhibition of regrowth, tissue engineering: biocompatible materials can form a bridge across the damaged region , stimulating and guiding – neurotrophic factors, replacing damaged cells – stem cells therapy, correctly reconnecting the damaged neural circuits inside and outside the spinal cord many researchers have tried to find effective strategies to improve outcomes after spinal cord injuries.(2,7,14,27,28) substances that limit secondary injury processes and promote repair and regeneration of the injured spinal cord such as monosialotetrahexosylganglioside (gm1), 4-aminopyridine (4-ap), [a potassiumchannel blocking agent], brain derived neurotrophic factor (bdnf) and glialderived neurotrophic factor (gdnf), also inhibitors of nogo (neurite outgrowth inhibitor) and mag (myelin-associated glycoprotein), have been studied. also transplanted tissues and cells, such as blood macrophages, bone marrow transplant with gm-csf, olfactory ensheathing cells, fetal tissues, stem or progenitor cells, appear to produce neurological improvements.(11,29) in pathological conditions eg. spinal cord injury, the neurotrophins promote survival and rescue nerve cells from death and promote neurite extension, neuronal survival and differentiation. in spinal cord injury, the neurotrophins are able to enhance axonal regeneration and reduce paraplegia. (23,24,25,26) some authors showed that the most efficient strategy for the acute complete transection of spinal cord was a combination of implantation of schwann cells, plus neuroprotective agents and growth factors administered in various romanian neurosurgery (2010) xvii 2: 219 – 224 223 ways, olfactory ensheathing cell (oec) implantation and chondroitinase administration.(2,3) other study concluded that combinations of interventions were needed to surmount the multiple barriers to recovery in spinal cord injury recovery.(20) two small studies noted sensory improvements in sci patients who underwent autologous bone marrow cell transplantation (bmt) in conjunction with granulocyte macrophage-colony stimulating factor (gm-csf) administration. (12,17) our study included two complete cervical sci patients and bone-marrow tissue obtained from the patient was implanted in conjunction with cerebrolysin as neurotrophic factor. the surgical procedure consisted of microsurgical dissection and partial removal of the spinal cord scar and implanting of the bonemarrow tissue into the spinal cord injury site. sensory improvements were noticed, but no motor improvements were observed twenty months afterwards. there are only few studies of the effect of cerebrolysin in nerve and spinal cord injuries in animal models (1,5,6) and a comparison of the efficacy of brain-derived neurotrophic factor (bdnf) and cerebrolysin treatment demonstrated that bdnf has more modest effects in functional recovery than cerebrolysin in nerve injury.(6) our results show that the cerebrolysin acted as a neurotrophic factor after the bone marrow implant and it was clinically effective in the long term treatment of one patient with chronic traumatic spinal cord injury. conclusion this is a preliminary study of the autologous bone marrow tissue implant into the lesioned cervical spinal cord and there are only two cases, but it is the first study about cerebrolysin in human cases of traumatic chronic cervical spinal cord injury. the bone-marrow tissue transplantation procedure has no complications. the post injury scar’s microsurgical partial removement may make the injury site more permeable to the axons attempting to re-grow through. this result is promising, but much follow-up work is needed to document the long-term benefits. the results are modest like everywhere else, yet but promising, compared to the lack of any effective therapeutic alternative. references 1.bunge mb. novel combination strategies to repair the injured mammalian spinal cord. j spinal cord med. 2008;31(3):262-9. 2. dallo jg, reichert bv, valladão júnior jb et all. differential astroglial responses in the spinal cord of rats submitted to a sciatic nerve double crush treated with local injection of cultured schwann cell suspension or lesioned spinal cord extract: implications on cell therapy for nerve repair. acta cir bras. 2007 ;22(6):485-94. 3. fernandez e, pallini r. connective tissue scarring in experimental spinal cord lesions: significance of dural continuity and role of epidural tissues.acta neurochir (wien).1985; 76 (3-4):145-8. 4. haninec p, houst'ava l, stejskal l, dubový p. rescue of rat spinal motoneurons from avulsioninduced cell death by intrathecal administration of igfi and cerebrolysin. ann anat. 2003;185(3):233-8. 5. haninec p, dubový p, sámal f et al reinnervation of the rat musculocutaneous nerve stump after its direct reconnection with the c5 spinal cord segment by the nerve graft following avulsion of the ventral spinal roots: a comparison of intrathecal administration of brain-derived neurotrophic factor and cerebrolysin. exp brain res. 2004;159(4):425-32. 6. hoang tx, havton la. novel repair strategies to restore bladder function following cauda equina/conus medullaris injuries. prog brain res. 2006;152:195-204. 7. hofstetter cp et al., marrow stromal cells form guiding strands in the injured spinal cord and promote recovery, proc natl acad sci usa ,2002, 99, 2199-2204 8. iannotti c, zhang yp, shields lb, han y et all. dural repair reduces connective tissue scar invasion and cystic cavity formation after acute spinal cord laceration injury in adult rats. j neurotrauma. 2006,23(6):853-65. 224 st.m.iencean et al bone marrow tissue implant in spinal cord injury 9. iencean st m, ciurea av. autologous bone marrow implant into traumatic chronic spinal cord injury. am j of neuroprotection and neuroregeneration, 2009, 1, 1, 73-77 10.kamei n, tanaka n, oishi y, ishikawa m, hamasaki t, et al. bone marrow stromal cells promoting corticospinal axon growth through the release of humoral factors in organotypic cocultures in neonatal rats . j neurosurg spine 6:412–419, 2007 11. knoller n, auerbach g, fulga v, zelig g, attias j, bakimer r, et al. clinical experience using incubated autologous macrophages as a treatment for complete spinal cord injury: phase i study results. j neurosurg spine 2005;3:173-81. 12.kwon bk, fisher cg, dvorak mf, tetzlaff w. strategies to promote neural repair and regeneration after spinal cord injury. spine. 2005 1;30(17 suppl):s313 13. lim pac, adela m tow recovery and regeneration after spinal cord injury: a review and summary of recent literature. ann acad med singapore 2007;36:49-57 14.lima c et al., olfactory mucosa autografts in human spinal cord injury: a pilot clinical study, journal of spinal cord medicine 2006, 29, 191-203, 15.ohta m et al., bone marrow stromal cells infused into the cerebrospinal fluid promote functional recovery of the injured rat spinal cord with reduced cavity formation, experimental neurology 2004, 187, 266-278 16.park hc, shim ys, ha y, yoon sh, park sr, choi bh, et al. treatment of complete spinal cord injury patients by autologous bone marrow cell transplantation and administration of granulocyte-macrophage colony stimulating factor. tissue eng 2005;11:913-22. 17.phinney dg, isakova i plasticity and therapeutic potential of mesenchymal stem cells in the nervous system. , curr pharm des. 2005 ;11 (10):1255-65 18.popovich pg, guan z, wei p, huitinga i, van rooijen n, stokes bt. depletion of hematogenous macrophages promotes partial hindlimb recovery and neuroanatomical repair after experimental spinal cord injury. exp neurol. 1999;158(2):351-65. 19.ratan rr, noble m. novel multi-modal strategies to promote brain and spinal cord injury recovery. stroke. 2009;40(3 suppl):s130-2. 20.schultz ss adult stem cell application in spinal cord injury, current drug targets, 2005, 6, 63-73 63 21.schwartz m, lazarov-spiegler o, rapalino o et all. potential repair of rat spinal cord injuries using stimulated homologous macrophages. neurosurgery. 1999 ;44(5):1041-5. 22.sharma hs. neurotrophic factors in combination: a possible new therapeutic strategy to influence pathophysiology of spinal cord injury and repair mechanisms. curr pharm des. 2007;13(18):1841-74. 23.sharma hs. a select combination of neurotrophins enhances neuroprotection and functional recovery following spinal cord injury. ann n y acad sci. 2007;1122:95-111. 24.sharma hs, ali sf, dong w et all drug delivery to the spinal cord tagged with nanowire enhances neuroprotective efficacy and functional recovery following trauma to the rat spinal cord. ann n y acad sci. 2007;1122:197-218. 25.sharma hs. new perspectives for the treatment options in spinal cord injury. expert opin pharmacother. 2008;9(16):2773-800. 26. sykova e, jendelova p. magnetic resonance tracking of transplanted stem cells in rat brain and spinal cord. neurodegener dis. 2006;3 (1-2):62-67 27.tsai ec, tator ch. neuroprotection and regeneration strategies for spinal cord repair. curr pharm des. 2005;11(10):1211-22 28.zhu j, wu x, zhanghl. adult neural stem cell therapy: expansion in vitro, tracking in vivo and clinical transplantation, current drug targets, 2005, 6, 97-110 97 29. zurita m vaquero j, bone marrow stromal cells can achieve cure of chronic paraplegic rats: functional and morphological outcome one year after transplantation, neuroscience letters, 2006, 410,10: 51-56 microsoft word 21.giovania_retrosigmoid_f.docx romanian neurosurgery (2011) xviii 4: 551 554 551 retrosigmoid approach for a ruptured pontine cavernous malformation, in a 10 years old pacient. case report a. giovani1 , a.v. ciurea2, angela neacsu, r.m. gorgan 1phd student in neurosurgery, “carol davila” umph, bucharest department of neurosurgery first neurosurgical clinic, ivth department of neurosurgery and 2first department of neurosurgery ; “bagdasar arseni” emergency clinical hospital, bucharest abstract brainstem cavernous malformations have a high risk of hemorrhage, ranging from 4 to 60%, this risk being even higher in children where larger lesions are encountered. even small hemorrhages can cause ,severe neurological symptoms because of the high density of cranial nerve nuclei and fiber tracts within the brainstem. the goal of surgical treatment is not only the improvement of neurological symptoms, but also preservation of the patient’s quality of life. we present a case of a 10 years old female pacient who presented after a 5 weeks conservative treatment with right sided weakness and loss of coordination, right hemihipoesthesia, she was diagnosed with a large left pontine cavernous malformation on mri. the cavernoma was resected using a retrosigmoidian approach , but a small remnant was left, when the surgery had to be stopped due to severe bradicardia. the neurological deficit improved at follow up. the choice of the surgical approach that allows the best exposure of the lesion is mandatory. in this case the lesion was evident on the surface of the brainstem and this facilitated its resection. traction on the tumor and coagulation near the cranial nerves nuclei should be avoided, but if bradicardia appears the surgery must be stopped. surgery is the best choice for the patients with symptomatic brainstem cavernomas that present with hemorrhage and neurological deficit, and its objectives should be complete removal and improvement of neurological deficit. keywords: brainstem cavernous malformations, cavernous angioma,, neural tracts, retrosigmoidian approach introduction cavernous malformations (cm) are benign angiographically occult vascular malformations with an estimated prevalence of 0,4-0,8% and 5-12% of all intracranial vascular lesions. brainstem cavernous malformations represent between 9-35% of all brain cavernous malformations, and most of them are localized in pons. brainstem cavernomas have a high risk of hemorrhage, ranging from 4 to 60%, this risk being even higher in children where larger lesions are encountered (1, 3, 5, 9). in the familial cases there is a higher incidence of multiple cavernomas 552 a. giovani et al retrosigmoid approach for pontine cavernoma cavernous malformations are treated conservative if they are asymptomatic and no hemorrhage is present, but if simptomatology appears, microsurgical resection is recommended. given the anatomic features of the brainstem, microsurgical resection of a brainstem cavernoma is amongst the most difficult neurosurgical procedures. macroscopically, they appear as mulberry-like heterogeneous masses. on t2-weighted magnetic resonance imaging (mri), hyper intense zones and partial contrast enhancement may be seen (5). cavernous malformations are clusters of dilated sinusoidal channels lined by a single layer of endothelium. in contradistinction to arteriovenous malformations, these lesions do not have smooth muscle or elastin in their lining, and they are angiographically occult even small hemorrhages can cause, severe neurological symptoms because of the high density of cranial nerve nuclei and fiber tracts within the brainstem. although some authors suggest conservative management or radiosurgery microsurgical resection of brainstem cavernomas has increasingly been performed to treat symptomatic patients, especially children given the high life expectancy . the goal of surgical treatment is not only the improvement of neurological symptoms, but also preservation of the patient’s quality of life (2, 6, 9). case presentation a 10 years old female patient presented after a 5 weeks conservative treatment with right sided weakness and loss of coordination, right hemihipoesthesia, iv and vii left cranial nerves deficit, with left blepharoraphy in the external third of the eyelids. the patient was conscious and hardly cooperative with a karnofsky score of 40. the eye exam showed bilateral horizontal nistagmus, with conjugate gaze deviation to the right, inferior corneal edema, and at ophtalmoscopy normal vessels and positive foveolar reflex. a ct scan showed a hematoma in the pons with discrete mass effect on iv ventricle. the angiography was unremarkable there was no indication fo avm or associated venous anomaly. the mri revealed a single irregular tumoral mass of 42/27/27 mm surrounded by a region evocative of hemoglobin products especially hemosiderin extended to the left 2/3 of the pons, the left cerebral peduncle, the left middle cerrebellar peduncle and the left cerrebellar hemisphere, with mass effect on the iv ventricle. a lateral park bench position was chosen to resect the lesion. a hockeystick incision was used, for a left suboccipital craniotomy. the lesion was subsequently resected using a retrosigmoid approach. the left cerebellopontine angle was entered under the operating microscope and the arachnoid cisterns dissected to allow retraction of the left cerrebellar hemisphere. after the hematoma is evacuated hemosiderin stain was identified on the pial surface surrounding the vi and vii nerve roots, the cavernous malformation is easily dissected from the surrounding gliotic plane using a blunt dissector. the cavernoma couldn't be completely resected leaving a small remnant attached to the pons after many attempts of complete ablation when the resection had to be interrupted due to severe bradicardia, this representing the particularity of the case. romanian neurosurgery (2011) xviii 4: 551 554 553 figure 1 preoperative mri showing a large pontine cavernoma with hemorhage and surrounding hemosiderin ring, the ivth ventricle is compressed the patient was extubated in the icu, 6h after the surgery and the first exam showed viii, ix and x left cranial nerves palsy. the motor deficit and the cranial nerves palsy showed partial remission at discharge on the 7th day postoperative. at 3 weeks follow up, nearly complete remission of the right hemi paresis and partial remission of the vi, vii, viii, ix and x left cranial nerves deficit were observed and the karnovsky score increased to 60. figure 2 3 weeks postoperative mri showing residual cavernoma in the left pons discussions and conclusion the main objective of this type of surgery is complete tumor removal without damaging the corticospinal tract, so that the patient should leave the operating room without any new neurological deficits. this objective can be best achieved by a sorrow planning of the surgery in order to pick the the most suitable approach, which avoids lesions of the cerebellar nuclei, too much traction on the cerebellum or on the cranial nerves, and most important, that avoids any lesions to the structures in the floor of the iv-th ventricle or to the corticospinal tracts. many approaches have been described that allowed a safe resection of brainstem cavernomas so the approach should be targeted on the location of the lesion in order to approach the cavernoma where it approaches the surface or appears on the 554 a. giovani et al retrosigmoid approach for pontine cavernoma surface of the brainstem as was the case here (7, 8, 10, 11). spetzler et all (1) published a series of 40 pediatric cases of brainstem cavernomas followed for a median of 30 months, 25% of them left with new neurological deficit and observed that the lesions are bigger in children than in adults, and also the regrowth rate from residual lesion is higher. also in our case the cavernoma was large but no regrowth was evident at 3 years follow up. this lesion was bulging in the cp angle and the nervous tracts were displaced antero and posteromedial so the approach to its surface was straightforward. also the hematoma made enough space in the cp angle to make this retrosigmoid approach the best choice (9). the best surgical approach differs according to the location of the cavernoma, many authors use complicated skull base approaches in order to have the best exposure of the lesion and surrounding neural structures, in this way having a comfortable resection. as much as possible, traction should be avoided with this kind of lesions, and the dissection should be done in a lateral to medial fashion using a blunt or sharp micro instruments as appropriate for the surgeon, avoiding traction on pons that can easily result in a low heart rate, much dangerous in children than in adults. bradicardia is a major indication for avoiding further resection. brain stem cavernomas are very difficult lesions to operate. surgery is indicated when these patients develop neurological deficit consecutive to hemorrhage, with the goal of complete resection and improvement of presenting symptoms on follow up. references 1. abla a.a., lekovic g.p., garrett m., wilson d.a., nakaji p., bristol r., spetzler r.f. cavernous malformations of the brainstem presenting in childhood: surgical experience in 40 patients, neurosurgery. 2010 dec; 67(6):1589-98; discussion 1598-9. 2. amin-hanjani s., ogilvy c.s., ojemann r.g., crowell r.m., risks of surgical management for cavernous malformations of the nervous system. neurosurgery 42:1220–1227, 1998. 3. bertalanffy h., benes l., miyazawa t., alberti o., siegel a.m., sure u., cerebral cavernomas in the adult: review of the literature and analysis of 72 surgically treated patients. neurosurg rev 25:1–53, 2002. 4. bertalanffy h., kühn g., scheremet r., seeger w., indications for surgery and prognosis in patients with cerebral cavernous angiomas. neurol med chir (tokyo) 32:659–666, 1992. 5. bertalanffy h., gilsbach j.m., eggert h.r., seeger w., microsurgery of deepseated cavernous angiomas: report of 26 cases. acta neurochir (wien) 108:91–99, 1991. 6. black p.mcl., moriarty t., alexander e., stieg p., woodard e.j., gleason p.l., martin c.h., kikinis r., schwartz r.b., jolesz f.a., development and implementation of intraoperative magnetic resonance imaging and its neurosurgical applications. neurosurgery 41:831–845, 1997. 7. françois p., ben ismail m., hamel o., bataille b., jan m., velut s., anterior transpetrosal and subtemporal transtentorial approaches for pontine cavernomas, acta neurochir (wien). 2010 aug; 152(8):1321-9; discussion 1329. epub 2010 may 4. 8. garber s.t., couldwell w.t., resection of an inferior pontine cavernous malformation using a farlateral transcondylar approach. 9. gorgan m., neacsu angela, bucur narcisa, pruna v., giovani a., dediu a., update on the natural hystory of infratentorial cavernous malformations, romanian journal of neurosurgery, 2011 xviii, nr 3. 10. ohue s., fukushima t., friedman a.h., kumon y., ohnishi t., retrosigmoid suprafloccular transhorizontal fissure approach for resection of brainstem cavernous malformation, neurosurgery. 2010 jun; 66 (6 suppl operative):306-12; discussion 312-3. 11. ohue s., fukushima t., kumon y., ohnishi t., friedman a.h., surgical management of brainstem cavernomas: selection of approaches and microsurgical techniques, neurosurg rev. 2010 jul; 33(3):315-22; discussion 323-4. epub 2010 apr 1. doi: 10.33962/roneuro-2021-087 congenital sphenoid wing defect with lateral angular dermoid presenting with csf leak after orbital surgery mohammad sarwar, laxminarayan tripathy, ejaz ahmed bari romanian neurosurgery (2021) xxxv (4): pp. 508-510 doi: 10.33962/roneuro-2021-087 www.journals.lapub.co.uk/index.php/roneurosurgery congenital sphenoid wing defect with lateral angular dermoid presenting with csf leak after orbital surgery mohammad sarwar1, laxminarayan tripathy1, ejaz ahmed bari2 1 medica institute of neurological diseases. medica superspecialty hospital, india 2 medica department of radiodiagnosis. medica superspecialty hospital, india abstract lateral angular dermoid may have associated bony defects which must be recognized before surgery. high-resolution 3-d ct scans and mris define these lesions very clearly. total excision with attention to the bony defect is usually curative. csf leak from the operative wound at the surgery or in the post-operative period signifies the intracranial connection or dural adhesion unnoticed by the ophthalmologist before surgery. introduction dermoid cysts are congenital benign tumours that originate from an embryonic ectodermal cell. angular dermoid present at the outer angle of eye, beneath or in close proximity to the eyebrow. various types of bony defects are associated with long standing dermoid in this location. congenital sphenoid wing dysplasia (swd) is a rare occurrence. it has a strong association with neurofibromatosis type i (nf-1)1, although it can occur alone. we present a case of a 3 years old male child presenting with orbital cellulitis, cerebrospinal fluid (csf) leak after orbital surgery for lateral angular dermoid with congenital sphenoid wing dysplasia, without any features of nf-1. case report a 3 years old male child presented with csf leak from wound near lateral canthus of right eye with suture breakdown and features of meningitis (fig 1a). he had history of recurrent right orbital swelling on crying since birth, and fowl smelling discharge from the swelling before surgery. excision biopsy of the swelling was reported to be a dermoid cyst. three-dimensional ct scan with ct-cisternogram showed a bony defect in the right sphenoid wing forming lateral wall of orbit (fig 1b) and csf pooling at lateral angle of orbit (fig 2a). mri revealed evidence of soft tissue thickening and fluid collection in extraconal compartment, keywords congenital sphenoid wing dysplasia, csf leak, lateral angular dermoid, sphenoid wing defect corresponding author: mohammad sarwar medica institute of neurological diseases. medica superspecialty hospital, india drsarwar262@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 509 sphenoid wing defect with angular dermoid with orbital and para-orbital cellulitis. we performed a right pterional craniotomy, excision of infected residual dermoid, wound debridement and csf fistula repair with the help of a rotated pedicled temporalis muscle graft and tisseel (fibrin) glue. in the immediate post-operative period, there was no csf leak (fig 2b). figure 1a. csf leak from operative wounds with breakdown of stitches (white solid arrows) figure 1b. 3dct of face showing a large bony defect in the greater sphenoid wing, involving the orbital rim and zygomatic arch on the right side (black arrow) figure 2a. ct cisternogram showing pooling and leakage of contrast at the defect site figure 2b. postoperative image discussion dermoid cysts are congenital benign tumours that originate from an embryonic ectodermal cell. these ectodermal cells are involved in neurulation during neural tube closure resulting in abnormal fusion. common sites of dermoid cysts are periorbital (zygomatico-frontal suture), nasal (fronto-nasal suture and rhinion), intraoral (floor of mouth), scalp (anterior fontanelle and cranial sutures) and postauricular2. angular dermoid occurs at the outer angle of eye, beneath or in close proximity to the eyebrows3. these tumours are ovoid, soft to firm, may be lobulated, containing a lipomatous element having a cystic nature. swd is a characteristic feature and one of the diagnostic criteria of nf-1. it occurs in 5-10% of the cases. features of nf-1 are six or more café-au-lait macules, 2 or more cutaneous/ subcutaneous neurofibromas or plexiform neurofibromas, axillary or groin freckling, optic pathway glioma, two or more lisch nodules in iris, bony dysplasia (swd, bowing or long bone +/pseudoarthrosis) and first degree relative of nf-11. swd can be an isolated finding also, like in our case, which is extremely rare. zygomatico-frontal suture defect has a strong association with orbital dermoid cyst4. n. sathananthan et.al reviewed ct scan of 70 patients (43 male and 27 female) who had a lesion palpable at outer canthus, and histologically proven dermoid cyst5. mean age of patients was 29 years. the lesion was always unilateral and 34 were on the left. the bone of the lateral wall and superotemporal angle of orbit showed following abnormalities, often in combination: pressure erosion in 61 cases, abnormal developmental shape 510 mohammad sarwar, laxminarayan tripathy, ejaz ahmed bari in 55, the dermoid cyst entering a tunnel or canal through the lateral wall in 24, a blind pit or crater in 15, and a cleft in 20. there are reports of unusual and interesting presentations of angular dermoids6,7,8. proptosis of eye with mastication was reported in a woman because of orbital mass communicating with the temporal fossa through a bony defect in lateral orbital wall; pressure by the temporalis muscle with mastication, on the dumb-bell shaped cyst caused the proptosis6. frontal headache and chewing related oscillopsia is reported in 60 years old man7. illusion of movement was due to mechanical displacement of retro-orbital cyst and eye by contraction of the temporalis muscle; removal of the cyst leads to complete remission of oscillopsia. history of blurring of vision of an eye with chewing is reported in a 29 years old lady with a dumb-bell dermoid cyst8. in this endoscopic era, direct surgical excision is an excellent approach, with a low complication rate and a very high aesthetic success rate, when performed through supra-eye brow or infraeyebrow approach9,10. proper anatomical delineation of the lesion and the bony defect with high resolution ct and mri imaging is extremely important as many of the angular dermoid have intracranial extension. involvement of a neurosurgeon in such cases is thus imperative and combined transcranial approach is done where indicated. conclusion lateral angular dermoid is associated with superolateral bony abnormality of orbital wall. congenital sphenoid wing dysplasia is a spectrum of bony defect. we present a case of congenital sphenoid wing dysplasia in a case of lateral angular dermoid presenting in post-orbital surgery csf leak. proper anatomical delineation of angular dermoid is extremely important as there are high chances of intracranial extension of the angular dermoid, and transcranial approach for complete excision for possible intracranial extension have to be kept in mind while dealing with angular dermoid. conflicts of interest: none declared. financial support and sponsorship: nil. references 1. neurofibromatosis. conference statement. national institutes of health consensus development conference. arch neurol. 1988 may; 45(5):575-8. 2. reissis d, pfaff mj, patel a, steinbacher dm. craniofacial dermoid cysts: histological analysis and inter-site comparison. yale j biol med. 2014; 87(3):349-357. published 2014 sep 3. 3. samuelson tw, margo ce, levy mh, pusateri tj. zygomaticofrontal suture defect associated with orbital dermoid cyst. survophthalmol. 1988 sep-oct; 33(2):12730. doi: 10.1016/0039-6257(88)90165-8. pmid: 3187895. 4. marston el, bland rw. angular dermoids. ama arch surg. 1958;76(3):467–468. doi:10.1001/archsurg.1958.01 280210137028 5. sathananthan n, moseley if, rose ge, wright je. the frequency and clinical significance of bone involvement in outer canthus dermoid cysts. br j ophthalmol. 1993 dec;77(12):789-94. doi: 10.1136/bjo.77.12.789. pmid: 8110674; pmcid: pmc504658. 6. whitney ce, leone cr jr, kincaid mc. proptosis with mastication: an unusual presentation of an orbital dermoid cyst. ophthalmic surg. 1986 may;17(5):295-8. pmid: 3725300. 7. knight rt, st john jn, nakada t. chewing oscillopsia. a case of voluntary visual illusions of movement. arch neurol. 1984 jan;41(1):95-6. doi: 10.1001/archneur.1984.04050130101034. pmid: 6689 898. 8. emerick gt, shields cl, shields ja, eagle rc jr, de potter p, markowitz gi. chewing-induced visual impairment from a dumbbell dermoid cyst. ophthalmic plast reconstr. surg. 1997 mar;13(1):57-61. doi: 10.1097/00002341-199703000-00010. pmid: 9076785. 9. gur e, drielsma r, thomson hg. angular dermoid cysts in the endoscopic era: retrospective analysis of aesthetic results using the direct, classic method. plastreconstr surg. 2004 apr 15;113(5):1324-9. doi: 10.1097/01.prs.0000111882.96242.7d. pmid: 15060343. 10. hachach-haram n, benyon s, shanmugarajah k, kirkpatrick wn. back to basics: a case series of angular dermoid cyst excision. j plastreconstraesthet surg. 2013 jan;66(1):57-60. doi: 10.1016/j.bjps.2012.07.030. epub 2012 aug 21. pmid: 22921308. 17amitagrawal_spinalcord romanian neurosurgery (2014) xxi 2: 241 242 241 spinal cord contusion and quadriplegia in a patient with klippel-feil anomaly amit agrawal professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) key words: cervical cord contusion, klippel-feil anomaly, minor trauma, klippelfeil syndrome. klippel-feil syndrome (kfs) patients are especially prone to cervical cord injury after a minor fall or a major traumatic episode. (1-9) a 43 year male patient presented with the history of road traffic accident. following that he was unable to move all four limbs. he had urinary retention for which he was catheterized. power in upper and lower limbs was grade 0/5. deep tendon reflexes were absent. there was sensory loss below c4. blood investigations were normal. figure 1 (a) lateral x-rays and (b) ct scan of the cervical spine showing c2-3 vertebral body fusion with waist formation figure 2 magnetic resonance image t2-weighted sagittal images showing a large contusion at c2-3 level in the spinal cord with canal stenosis and c3-4 disc prolapse causing the compression of the dural tube x-ray cervical spine showed klippel-fiel of c2-3 (figure 1). mri showed cord contusion at c3-4 level with disc prolapsed (figure 2). the patient underwent anterior cervical approach, cervical discectomy and fixation. he made minimal recovery in his motor power and was totally dependent for activities of daily living. the marked deformities in kfs patients 242 agrawal spinal cord contusion and quadriplegia result in mechanical distortion altering the compensatory properties of the spine to react to decelerating and rotatory forces thus increase the probability of spinal cord injury with trauma. (4, 6-9) there is multiple mechanisms those make the patients more prone for injuries. there is an increase incidence of spondylotic and discogenic changes at the junctional segments resulting from hypermobile segments adjacent to the fused vertebrae leading to cervical instability. (3-6, 9, 10, 5) this can result in symptomatic herniated cervical disc with spinal cord injury. (5, 6, 9, 10) apart from this there can be associated spinal canal stenosis, and, hence, increasing the likelihood to develop spinal cord injury in kfs patients even after minor trauma. (6, 11) management of kfs patients with spinal cord injury depends on the severity of symptomatic segmental instability, presence or absence of disc prolapsed and associated neurological deficits. (9, 12 13) in present case, the young adult patient had klippel-feil anomaly c2-3 segments, had disc prolapsed at c3-4 level level and canal stenosis at the fused segments made him prone for spinal cord injury even after trivial trauma. correspondence: dr amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.agrawal a, badve am, swarnkar n, sarda k. disc prolapse and cord contusion in a case of klippel-feil syndrome following minor trauma. indian journal of orthopaedics 2009;43:210-212. 2.hensinger rn, lang je, macewen gd. klippelfeil syndrome a constellation of associated anomalies. the journal of bone & joint surgery 1974;56:1246-1253. 3.guille jt, miller a, bowen jr, forlin e, caro pa. the natural history of klippel-feil syndrome: clinical, roentgenographic, and magnetic resonance imaging findings at adulthood. journal of pediatric orthopaedics 1995;15:617-626. 4.karasick d, schweitzer me, vaccaro ar. the traumatized cervical spine in klippel-feil syndrome: imaging features. ajr american journal of roentgenology 1998;170:85-88. 5.pizzutillo pd, woods m, nicholson l, macewen gd. risk factors in klippel-feil syndrome. spine 1994;19:2110-2116. 6.vaidyanathan s, hughes pl, soni bm, singh g, sett p. klippel-feil syndrome–the risk of cervical spinal cord injury: a case report. bmc family practice 2002;3:6. 7.matsumoto k, wakahara k, sumi h, shimizu k. central cord syndrome in patients with klippel-feil syndrome resulting from winter sports: report of 3 cases. am j sports med 2006;34:1685-1689. 8.strax te, baran e. traumatic quadriplegia associated with klippel-feil syndrome: discussion and case reports. archives of physical medicine and rehabilitation 1975;56:363-365. 9.samartzis d, lubicky jp, herman j, kalluri p, shen fh. symptomatic cervical disc herniation in a pediatric klippel-feil patient: the risk of neural injury associated with extensive congenitally fused vertebrae and a hypermobile segment. spine 2006;31:e335-338. 10.adeleye ao, akinyemi ro. cervical klippel-feil syndrome predisposing an elderly african man to central cord myelopathy following minor trauma. african health sciences 2010;10:302. 11.prusick v, samberg l, wesolowski d. klippel-feil syndrome associated with spinal stenosis: a case report. journal of bone and joint surgery american volume 1985;67:161-164. 12.tracy m, dormans j, kusumi k. klippel-feil syndrome: clinical features and current understanding of etiology. clinical orthopaedics and related research 2004;424:183-190. 13.neroni m, gazzeri r, galarza m, alfieri a. intradural cervical disc herniation in a klippel-feil patient. spine 2007;32:e608-e610. microsoft word 4.ienceanst_news_f.docx 412 şt.m. iencean et al news and views of neuroprotection of spinal cord injury news and views of neuroprotection in complete traumatic spinal cord injuries şt.m. iencean, i. poeată, gh. solcan1, dana turliuc, e.c. popescu, b. costăchescu, a.şt. iencean neurosurgery, “gr.t. popa” university of medicine and pharmacy iasi, romania clinic of neurosurgery, “prof. dr. nicolae oblu” hospital iasi, romania 1faculty of veterinary medicine, university of agricultural sciences and veterinary medicine iaşi, romania abstract spinal cord injury (sci) due to trauma has major functional, medical, and financial effects on the injured person, as well as an important effect on the individual's psychosocial well-being. these patients have not any treatment for their or tetraplegia and any therapeutical attempt can bring hope and can improve their quality of life. today methylprednisolone is a standard treatment option for an acute spinal cord injury but it is not a cure for a spinal cord injury. surgery is often necessary for decompression, to realign and to stabilize the spine. the experimental treatments had yet not results. in case of acute complete traumatic sci, steroid medication is insufficient and it is necessary to add new immediate procedures at the standard treatment performed today. treatment should be started immediately and must stop cell death, control inflammation and promote nerve regeneration (action to primary and secondary damage). keywords: methylprednisolone, neuroprotection, paraplegia, spinal cord injury microsoft word 7cruzortizventriculoperitoneal romanian neurosurgery (2013) xx 3: 277 – 281 277 ventriculoperitoneal shunt related meningioma: a case report g.a. cruz-ortiz1, a. samano-osuna1, m. jimenez-jimenez1, h.r. alvismiranda3, a. lee2, l.r. moscote-salazar1 1hospital juarez de mexico, mexico d.f. 2hospital angeles del pedregal. mexico d.f. 3universidad de cartagena, cartagena de indias, colombia abstract meningiomas are the most common primary, non-glial tumours of the brain and spine, and represent the most common extra-axial lesions. the typical meningioma is a dural-based, markedly enhancing extraaxial mass; they exhibit cortical buckling with trapped cerebrospinal fluid clefts or cortical vessels. there are factors strongly associated with risk of developing meningioma, as in the case of exposure to ionizing radiation, or exogenous or endogenous hormones, as in this case, the presence of shunt material as a foreign body may have contributed to oncogenesis on the basis of a chronic inflammatory reaction. the aim of this report is to present the clinical case of a meningioma, which enveloped the proximal catheter of ventriculoperitoneal shunt valve. key words: meningioma, ventriculoperitoneal shunt, oncogenesis. introduction meningiomas are the most common primary, non-glial tumours of the brain and spine, and represent the most common extra-axial lesions, accounting for 13-20% of all intracranial tumours (2). they are predominantly benign neoplasms that are derived from meningothelial cells [i.e., arachnoid cap cells (12)], almost all corresponding to grade i of the who histopathologic classification (10). less than 10% ever cause clinical symptoms (6). their incidence rates range from 1.2 to 11.5 per 100.000(19,9,5).the typical meningioma is a dural-based, markedly enhancing extra-axial mass; they exhibit cortical buckling with trapped cerebrospinal fluid clefts or cortical vessels (6). the most common locations include over the cerebral convexity, in the parasagittal region, or arising from the sphenoid wing (6). the aim of this report is to present the clinical case of a meningioma, which enveloped the proximal catheter of ventriculoperitoneal (vp) shunt valve. case report a 44 y.o. female patient, with prior history of basal arachnoiditis 12 years ago due to neurocysticercosis which left a residual bilateral amaurosis, plus ventriculoperitoneal shunt placing in the same year and 3 shunt revisions in the following four years due to hardware dysfunction.the current condition has 5month of evolution, consisting of holocraneal headache of gradual and progressive course, which partially decrease with analgesics and subsequently accompanied by intermittent episodes of 278 cruz-ortiz et al ventriculoperitoneal shunt related meningioma left predominance hypoesthesia and decreased strength on the same side. on examination, we observed that higher mental functions were kept, with glasgow coma scale (gcs) of 15 points; commitment of the ii cranial nerve, consisting in pale papilla with bilateral amaurosis; muscle strength 3/5 in the left hemibody and ipsilateral hyperreflexia and babinski. the patient presented astereoagnosia and left finger agnosia also. the cranial mri showed a right heterogeneous frontoparietal lesion on the hardware way, which on the gadoliniumt1wi phase showed homogeneous enhancement; flair with moderate perilesional edema (figure 1). a right fronto-parietal craniotomy was performed (figure 2a); evidencing a lesion of grayish-white appearance, rubbery consistency, regularly vascularized, which enveloped the catheter valve so both were removed entirely (figure 2b). the histopathological study reported a meningioma (figure 3). discusion meningiomas are benign tumours derived from the arachnoid villous structures of the meninges and are common in the central nervous system (8). histologically the meninges comprise many different cell types (18) including macrophages, dendritic cells, mast cells and fibroblasts (20), and it is known that meningothelial cells of the inner and outer layer of the arachnoid give rise to meningiomas (17).at computed tomography (ct), typical diagnostic features include a well-circumscribed, smooth mass with a broad dural attachment (6). in 75% of cases, the meningioma is hyperdense, with homogeneous enhancement after the administration of contrast material (6). figure 1 (a) brain mri showed a right heterogeneous frontoparietal lesion on the hardware way, which on the gadolinium-t1wi phase showed homogeneous enhancement;(b) flair with moderate perilesional edema romanian neurosurgery (2013) xx 3: 277 – 281 279 figure 2 (a)right fronto-parietal craniotomy, note the tumor cuddling the shunt hardware. (b) a lesion of grayishwhite appearance, rubbery consistency, and regularly vascularized, enveloped the catheter valve so both were removed entirely figure 3 the definitive histopathological study reported a meningothelial cell neoplasm arranged in spindleshaped beams, in parallel and intertwined with a collagen-rich matrix, conclusive of meningioma meningiomas have been described in the context of foreign bodies(14), radiation exposure(14,15,3), brain abscess(13,16), head injury (1), exogenous or endogenous hormones (11,4), among others. however, only ionizing radiation has been identified as an etiologic agent likely to be correlated with the occurrence of these tumors. the role of head trauma, viral infection, and sex hormones is less certain (9). in 1999, holthouse et al (7)reported the case of a 25-year-old man with a history of childhood cerebellar glioma treated by surgical removal, radiotherapy and a vp shunt presented with a 5 month history of frontal headaches. imaging revealed a mass surrounding the shunt, which was surgically removed but in this case the shunt was left in situ, unlike our case. the histopathological examination revealed an atypical and invasive meningioma; thus, to our knowledge the case we present is the first case of meningioma related to vp shunt hardware without prior radiation exposure. there are factors strongly associated with risk of developing meningioma, as in the case of exposure to ionizing radiation, 280 cruz-ortiz et al ventriculoperitoneal shunt related meningioma or exogenous or endogenous hormones, as in this case, the presence of shunt material as a foreign body may have contributed to oncogenesis on the basis of a chronic inflammatory reaction. competing interests none declared. funding none. ethical approval not required. abbreviations who: world health organization gcs: glasgow coma scale mri: magnetic resonance imaging vp: ventriculoperotoneal correspondence: dr. luis rafael moscote, universidad de cartagena, cartagena de indias, colombia. e-mail: mineurocirujano@aol.com references 1. annegers jf, laws er, kurland lt, grabow jd. head trauma and subsequent brain tumors. neurosurgery 1979; 4:203–6. available: http://www.ncbi.nlm.nih.gov/pubmed/460549. accessed 4 may 2013 2. buetow mp, buetow pc, smirniotopoulos jg. typical, atypical, and misleading features in meningioma. radiographics 1991; 11:1087–106. available: http://www.ncbi.nlm.nih.gov/pubmed/1749851. accessed 4 may 2013 3. daentzer d, böker dk. (radiation-induced meningioma 20 years after operation and high-dose irradiation of an ependymoma). zentralbl neurochir 1999; 60:27–32. available: http://www.ncbi.nlm.nih.gov/pubmed/10356722. accessed 4 may 2013 4. frassanito p, de bonis p, mattogno pp, novello m, anile c. hormonal therapy for fertility and huge meningioma: a purely random association? acta neurol belg 2012; 112:299–301. available: http://www.ncbi.nlm.nih.gov/pubmed/22426675. accessed 4 may 2013 5. gelabert-gonzález m, serramito-garcía r. (intracranial meningiomas: i. epidemiology, aetiology, pathogenesis and prognostic factors). rev neurol 2011; 53:165–72. available: http://www.ncbi.nlm.nih.gov/pubmed/21748714. accessed 4 may 2013 6. hallinan jtpd, hegde an, lim weh. dilemmas and diagnostic difficulties in meningioma. clin radiol 2013; available: http://www.ncbi.nlm.nih.gov/pubmed/23623578. accessed 4 may 2013 7. holthouse dj, robbins pd, lee ma. ventriculoperitoneal shunt related meningioma following excision and radiotherapy for glioma. j clin neurosci 1999; 6:347–348. available: http://www.sciencedirect.com/science/article/pii/s09675 86899900632. 8. iaconetta g, santella a, friscia m, abbate v, califano l. extracranial primary and secondary meningiomas. international journal of oral and maxillofacial surgery 2012; 41:211–217. available: http://www.sciencedirect.com/science/article/pii/s09015 02711014056. 9. longstreth wt, dennis lk, mcguire vm, drangsholt mt, koepsell td. epidemiology of intracranial meningioma. cancer 1993; 72:639–48. available: http://www.ncbi.nlm.nih.gov/pubmed/8334619. accessed 10 april 2013 10. louis d, scheithauer b, budka h, von deimling a, kepes j. meningiomas, in kleihues p, cavenee w (eds): pathology and genetics. tumours of the nervous system, who classification of tumors. iarc press: lyon, 2000, pp.176–84 11. markopoulos c, sampalis f, givalos n, gogas h. association of breast cancer with meningioma. eur j surg oncol 1998; 24:332–4. available: http://www.ncbi.nlm.nih.gov/pubmed/9725004. accessed 4 may 2013 12. marosi c, hassler m, roessler k, reni m, sant m, mazza e, et al. meningioma. critical reviews in oncology/hematology 2008; 67:153–171. available: http://www.sciencedirect.com/science/article/pii/s10408 4280800022x. 13. reichenthal e, rubinstein ab, shevach i, cohen ml. meningioma presenting at a site of a previously aspirated brain abscess. acta neurochir (wien) 1991; 109:142–4. available: http://www.ncbi.nlm.nih.gov/pubmed/1858532. accessed 4 may 2013 14. saleh j, silberstein hj, salner al, uphoff df. meningioma: the role of a foreign body and irradiation in tumor formation. neurosurgery 1991; 29:113–8; discussion 118–9. available: http://www.ncbi.nlm.nih.gov/pubmed/1870671. romanian neurosurgery (2013) xx 3: 277 – 281 281 accessed 4 may 2013 15. strojan p, popović m, jereb b. secondary intracranial meningiomas after high-dose cranial irradiation: report of five cases and review of the literature. int j radiat oncol biol phys 2000; 48:65–73. available: http://www.ncbi.nlm.nih.gov/pubmed/10924973. accessed 4 may 2013 16. sussman s, terbrugge kg, solt lc, deck jh. thorotrast-induced meningioma. case report. j neurosurg 1980; 52:834–7. available: http://www.ncbi.nlm.nih.gov/pubmed/7381542. accessed 4 may 2013 17. viswanathan a, demonte f. tumors of the meninges. handbook of clinical neurology 2012; 105:641–56. available: http://www.ncbi.nlm.nih.gov/pubmed/22230524. accessed 4 may 2013 18. weller ro. microscopic morphology and histology of the human meninges. morphologie 2005; 89:22–34. available: http://www.ncbi.nlm.nih.gov/pubmed/15943078. accessed 21 april 2013 19. wiemels j, wrensch m, claus eb. epidemiology and etiology of meningioma. j neurooncol 2010; 99:307–14. available: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=2945461&tool=pmcentrez&rendertype=abstract. accessed 11 march 2013 20. wieseler-frank j, jekich bm, mahoney jh, bland st, maier sf, watkins lr. a novel immune-to-cns communication pathway: cells of the meninges surrounding the spinal cord csf space produce proinflammatory cytokines in response to an inflammatory stimulus. brain behav immun 2007; 21:711–8. available: http://www.ncbi.nlm.nih.gov/pubmed/16989980. accessed 18 march 2013 microsoft word 10.craciunassorin_cervical_f.docx 456 sorin c. craciunas et al cervical arthroplasty or cervical fusion cervical arthroplasty versus anterior cervical decompression and fusion sorin c. craciunas1, mircea r. gorgan1, carmen m. cirstea2 1neurosurgery iv, “bagdasar-arseni” hospital, bucharest, romania 2departments of neurology and physical therapies, hoglund brain imaging center, kansas university medical center, kansas city, usa abstract background: anterior cervical decompression and fusion (acdf) is a common procedure in neurosurgical practice to manage the cervical cord/nerve roots compression by intervertebral disk herniation / osteophytic formation. however, cervical total disk replacement (tdr) progressively became a feasible alternative to acdf in surgical practice. this procedure is thought to have many advantages compared to classical acdf. the aim of the present study is to investigate if tdr is superior as outcome measures than acdf, by reviewing the published data available to date. methods: we searched several electronic databases up to december 2010. outcomes sought includes pain relief, functional capacity, quality of life, adjacent disk disease, secondary surgeries, kinematics/range of motion, return to work, adverse events, potential candidacy rate for surgery. we selected mainly randomized controlled trials. results: compared to acdf, tdr has superior or equal clinical outcomes, a lower incidence of adjacent disc disease (radiological +/clinical), lower rate of secondary revision surgeries, supplemental fixation or adjacent segment reoperation, superior spine kinematics, which is maintained over time, earlier return to work. on the other hand, the presented studies have shown that tdr exposes the patients to more frequent postoperative events and have an inferior candidacy rate compared to acdf. we did not have access to straight –forward economic data, but tdr seems to be more costly than acdf. conclusions: tdr already represents a well-established technique in the armamentarium to manage the cervical disc herniation, a method required to be handled by any surgeon involved in spinal care. keywords: cervical arthroplasy, cervical total disc replacement, bryan, prestige, prodisc-c, acdf background although anterior cervical discectomy and fusion (acdf) is the regular management for degenerative cervical disc disease, concerns regarding adjacent level degeneration and loss of motion have suggested that arthroplasty may be a better alternative. this procedure, which occurred quite recently in the armamentarium of therapies in spine surgery, became increasingly interesting for the medical community involved in spinal care. table 1 figures the rationale of using cervical tdr over classical acdf. romanian neurosurgery (2011) xviii 4: 456 464 457 table 1 rationale for cervical total disc replacement – comparison with acdf measurement acdf cervical total disc replacement (tdr) spinal segmental motion absent normal incidence of adjacent segment disease increased decreased intraoperative morbidity supplemental instrumentation anterior cervical plate none exposure equal equal operative time equal equal ( after learning curve) postoperative morbidity external immobilization rigid cervical collar none return to normal activity at least one month as early as 1-2 wks pseudarthrosis increased absent instrumentation failure minimal minimal cervical arthroplasy – historical timelines 1934 mixter and barr described operations for the removal of the ruptured intervertebral disc (lumbar) 1943 semmes and murphey published their landmark paper, “the syndrome of unilateral rupture of the sixth cervical intervertebral disc.” 1955 in 1955, robinson and smith briefly described anterior discectomies and interbody arthrodesis for cervical disc jan 1964 the first report of a cervical disc replacement south african medical journal 1966 fernstorm tried a method by placing a stainless steel ball into lumber and cervical disc center 1989 cummins-bristol disc 1990 bryan cervical disc 1991 – clinical trial initiated to investigate cummins-bristol disc 2002 – pilot study to investigate frenchay/prestige cervical disc 2002 – results of bryan cervical disc clinical trial were published 2007 – fda approval for prestige disc (medtronic, inc.) 2007 – fda approval for prodisc-c device (synthes, inc.) 2009 – fda approval for bryan cervical disc (medtronic, inc.) fda aproved devices at the moment, there are three fda approved devices for cervical disc arthroplasty: prestige st (medtronic), pro-disc-c (synthes) and bryan (medtronic) (see table 1). however, an increasing number of devices with this purpose are in various stages of institutional devices evaluation (ide) for fda approval: prestige lp cervical disc (medtronic); cervicore (stryker spine); pcm (nuvasive, inc); advent™ cervical disc (orthofix international n.v.); activ c disc prosthesis (b. braun/aesculap spine); neodisc (nuvasive, inc); discover™ artificial cervical disc (depuy spine, inc.); mobi-c (ldr spine usa); secure®-c cervical artificial disc (globus medical inc); kineflex-c (spinalmotion). clinicaltrials.gov reports 19 on-going ide trials concerning cervical disc prosthesis the prestige st cervical disc is a metal on metal device. it is made of stainless steel and contains two componentsa ball and a trough that articulate. it is attached to the cervical vertebrae with screws. it is manufactured from titanium ceramic composite material. a porous titanium plasma spray coating on the end plate surface facilitates bone in growth and long term fixation. the pro-disc –c cervical disc is a metal on polymer device. it has cobalt-chromium end plates with a central keel for anchorage 458 sorin c. craciunas et al cervical arthroplasty or cervical fusion to the vertebral bodies and a locking core of ultra high molecular weight polyethylene (uhmwpe) as a central polymer that provides a ball and socket articulation. in order to be compatible with tissue, the endplates are coated a titanium plasmapore. the bryan cervical disc is also a metal on polymer device. it is a single piece of a porous coated, clamshell shaped titanium endplates with a polycarbonate, polyurethane core. figure 1 the prodisc c device. the prosthesis a inserted on a patient at c4/c5 level – lateral view b figure 2 the bryan device. the prosthesis a inserted in vitro b and on a patient at c6/c7 level – lateral view c figure 3 the prestige device. the prosthesis a inserted in vitro b and on a patient at c5/c6 level – lateral view c, flexion d, extension e methods we performed a literature review in the following databases: the cochrane library and medline (national library of medicine). the review was limited to studies published between 2000 and 2010. the used keywords were: “cervical arthroplasty”, “cervical prosthesis”, “prodisc c”, “bryan”, and “prestige”. the search plan and the selection and quality ranking of the pertinent studies were carried out and analyzed separately by two persons in a first step and jointly synthesized and discussed in a second step. the studies that had been found were selected according to the quality criteria of the jadad score (2000) for randomized controlled trials (7, 8) and the checklist of downs and black (1998) for randomized and nonrandomized studies. only randomized controlled trials, comparing acdf vs cervical arthroplasty were included. 17 studies were identified. we tracked information about the following parameters: clinical outcome, romanian neurosurgery (2011) xviii 4: 456 464 459 adjacent disc disease, kinematics, secondary surgeries, return to work, adverse events. clinical outcome: tdr superior to acdf some studies reported superior results tdr vs acdf in terms of clinical outcome. garrido bj et al. investigated 47 patients randomly managed by acdf and tdr. at 48 months follow-up they found improved functional outcomes for ndi (neck disability index), neck/arm pain vas scores, and the sf-36 physical/mental health component scores for both the bryan arthroplasty and acdf cohorts. there has been no degradation of functional outcomes from 24 to 48 months for ndi, vas of neck and arm, and sf-36 (5). they found superior results for cervical arthroplasty group. heller jg et al. studied 563 patients (242 tdr vs 221 single-level acdf). at 24 months follow-up the investigational group patients treated with the artificial disc had a statistically greater improvement in the primary outcome variables: ndi score (p = 0.025) and overall success (p = 0.010) compared to acdf group (6). in another study, riina j et al. operated 19 patients randomly using tdr and acdf and follow them for 24 months. patients who underwent arthroplasty demonstrated greater improvement in neurologic function and neck pain than patients who underwent cervical discectomy and fusion (15). finally, sasso rc et al. managed 115 patients randomized in a 1:1 ratio to acdf or tdr. at 24 months follow up, the investigational group had statistically significant (p<0.05) improvements as assessed by the neck disability index, the neck pain score, and sf-36 physical component scores. the improvement in the mental component subscore values for the bryan and control groups was equivalent at 24 months (p=0.055). arm pain relief was similar in both groups (p=0.152) (17, 18). clinical outcome: no differences tdr vs acdf on the other hand, there are studies showing no differences in clinical outcome post acdf vs tdr. bhadra ak et al. studied 60 patients: (15 tdr, 15 plate and tricortical autograft, 15 plate, cage, and bone substitute, 15 cage only) at 31 months follow up. the clinical outcome in terms of vas of neck and arm pain and sf12 physical and mental score improvement (p=0.001) were comparable in all four techniques (3). in another study, buchowski jm et al. analyzed 199 patients: 106 patients (53%) tdr vs 93 (47%) acdf at 24 months follow up (4). patients in both the arthroplasty and arthrodesis groups had improvement following surgery; furthermore, improvement was similar between the groups, with no worsening of myelopathy in the arthroplasty group. kim sw et al. had 105 patients with 63 tdr placed in 51 patients and 54 patients operated with acdf, 26 single level , 28 double level at 19 months follow up (9). there was clinical improvement within each group in terms of vas and ndi scores from pre-op to final follow-up, but not significantly between the two groups for both single (vas p=0.8371, ndi p=0.2872) and double (vas p=0.2938, ndi p=0.6753) level surgeries. murrey d et al. operated 209 patients (106 acdf; 103 tdr) and follow them for 24 months (13). ndi and sf-36 scores, vas neck pain intensity and frequency as well as vas arm pain intensity and frequency were significantly less compared with presurgery scores at all follow-up visits for both the treatment groups (p<.0001). 460 sorin c. craciunas et al cervical arthroplasty or cervical fusion neurologic success (improvement or maintenance) was achieved at 24 months in 90.9% of prodisc-c and 88.0% of fusion patients (p=.638). however, at 24 months, there was a statistically significant difference in medication usage with 89.9% of prodisc-c patients not on strong narcotics or muscle relaxants, compared with 81.5% of acdf patients. 49 patients were randomly managed by nabhan a et al. with acdf or tdr (14). at 36 months followup, after both procedures, a significant pain reduction in neck and arm was observed, without significant differences between both groups. adjacent disc disease one major advantage claimed for tdr is the absence of adjacent disc disease. this condition occurs following acdf, due to the additional mechanical stress over the discs adjacent to the acdf site. two reports investigated the adjacent disc disease occurrence in tdr vs acdf. kim sw et al. studied 105 patients. 63 tdr were placed in 51 patients. a single level procedure was performed in 39 patients and a two-level procedure in the other 12 (9). fifty-four patients underwent acdf, 26 single level cases and 28 double level cases. mean follow-up was 19 months. statistically significant (p<0.0001 and p=0.0172) differences in the trend of intervertebral height measurements between the two groups were noted at all levels except for the anterior intervertebral height of single level surgeries at the upper (p=0.1264) and lower (p=0.7598) adjacent levels as well as posterior intervertebral height for double level surgeries at the upper (p=0.8363) adjacent level. radiological change was 3.5 times more observed for the acdf group. in another study the patients were treated with the affinity anterior cervical cage system (158) or the bryan artificial cervical disc (74) (16). follow-up period was 24 months. fusion was associated with a significant increase in x-ray film-based changes of adjacent-disc disease (p = 0.009, odds ratio [or] 2.44). in the cage fusion series, the incidence of symptomatic adjacent-level ddd was statistically greater than that in the group treated with the artificial disc (p = 0.018). secondary surgeries we also investigated the rates of secondary surgeries needed to fix complications such as: adjacent disc disease or pseudarthrosis. garrido bj et al. studied 47 patients randomly managed with acdf or cervical arthroplasy, at a follow up of 48 months. 6 additional surgeries were needed in acdf group (3 adjacent level, 1remote level and 2 for pseudarthrosis) and one surgery in tdr group for adjacent level (5). heller jg et al. investigated 563 patients (242 tdr vs 221 single-level acdf) and follow them for 2 years. there was no statistical difference between the 2 groups with regard to the rate of secondary surgical procedures performed subsequent to the index procedure (6). in another study (13), two hundred nine patients were randomized and treated (106 acdf; 103 prodisc-c). patients were assessed pre and postoperatively at six weeks, 3, 6, 12, 18, and 24 months. there was a statistically significant difference in the number of secondary surgeries with 8.5% of fusion patients needing a re-operation, revision, or supplemental fixation within the 24 month postoperative period compared with 1.8% of prodisc-c patients (p=.033). finally, in mummaneni et al. study five hundred forty-one patients with single-level cervical ddd and radiculopathy were enrolled at romanian neurosurgery (2011) xviii 4: 456 464 461 32 sites and randomly assigned to one of two treatment groups: 276 patients in the investigational group underwent anterior cervical discectomy and decompression and arthroplasty with the prestige st cervical disc system (medtronic sofamor danek); 265 patients in the control group underwent decompressive acdf. eighty percent of the arthroplasty-treated patients (223 of 276) and 75% of the control patients (198 of 265) completed clinical and radiographic follow-up examinations at routine intervals for 2 years after surgery. the arthroplasty group had a statistically significant lower rate of secondary revision surgeries (p = 0.0277) and supplemental fixation (p = 0.0031). rate of adjacentsegment reoperation was significantly lower in the investigational group as well (p = 0.0492, log-rank test) (11, 12). kinematics / range of motion one advantage of tdr vs acdf seems to be a better kinematics, with larger range of motion by keeping the operated vertebral segment mobil. the following studies were published in this regard. kim sw et al. studied 105 patients. 63 tdr were inserted in 51 patients. a single level acdf procedure was performed in 39 patients and a two-level procedure in the other 12. 54 patients underwent acdf, 26 single level cases and 28 double level cases. mean follow up period was 19 months. overall, rom and intervertebral height was relatively well maintained during the follow-up in the bryan group compared to acdf. regardless of the number of levels operated on, significant differences were noted for overall rom of the cervical spine (p<0.0001) and all other levels except at the upper adjacent level for single level surgeries (p=0.2872). statistically significant (p<0.0001 and p=0.0172) differences in the trend of intervertebral height measurements between the two groups were noted at all levels except for the aih of single level surgeries at the upper (p=0.1264) and lower (p=0.7598) adjacent levels as well as pih for double level surgeries at the upper (p=0.8363) adjacent level (9). radiological change was 3.5 times more observed for the acdf group. sasso rc et al. treated 463 patients (221 acdf and 242 tdr). the follow up was at 24 months. significantly more motion was retained in the disc replacement group than the plated group at the index level (sasso & best, 2008; sasso et al., 2008. the disc replacement group retained an average of 7.95 degrees at 24 months. the preoperative motion was 6.43 degrees and there was no evidence of degradation of motion over 24 months. in contrast, the average range of motion in the fusion group was 1.11 degrees at 3-month follow-up and gradually decreased to 0.87 degrees at 24 months. the preoperative motion was 8.39 degrees. murrey d et al., managed 209 patients (106 acdf vs 103 tdr). results show that at 24 months postoperatively, 84.4% of prodisc-c patients achieved a more than or equal to 4 degrees of motion or maintained motion relative to preoperative baseline at the operated level (13). nabhan a et al. studied 49 pts 1:1 randomized tdr vs acdf at a follow up of 36 months. the range of motion of the treated segment with prosthesis remained unchanged 3 years after surgery in comparison to the 1-year result (14). the prosthesis shows a significant segmental motion in contrast to the fusion group at each rsa examination time (p < 0.05). finally, mummaneni pv et al. investigated 541 patients (276 tdr vs 265 acdf) (11, 12). at 24 months the 462 sorin c. craciunas et al cervical arthroplasty or cervical fusion cervical disc implant maintained segmental sagittal angular motion averaging more than 7 degrees. in the investigational group, there were no cases of implant failure or migration. return to work one important issue to be taken into account is the professional outcome of this kind of patient following to tdr or acdf. we found three studies reporting this kind of data. heller jg et al. used bryan devices (6). 563 patients were enrolled (242 tdr vs 221 single-level acdf). they have data at 24 months follow-up. patients who received the artificial cervical disc returned to work nearly 2 weeks earlier than the fusion patients (p = 0.015). steinmetz mp et al.,(19) used prestige st and bryan devices. they studied 1004 patients and follow them for 24 months. at 6 weeks and 3 months, significantly more patients in the arthroplasty group were working compared with the fusion group. at 6 months and later, there was no significant difference in return-to-work rates. overall, patients returned to work at a median of 101 days after arthroplasty, compared with 222 days after acdf. mummaneni pv et al. analyzed 541 pts. 276 pts tdr (prestige st) vs 265 acdf(11, 12). the patients in the investigational group returned to work 16 days sooner than those in the control group. adverse events/ dysphagia two studies analyzed the adverse effects related to the cervical disk surgery, either by using acdf or tdr. mcafee pc et al., 2010 (10) used porous-coated motion (pcm) device in 151 patients and compared them with a control group of 100 acdf patients. the patients were followed for 12 months. the incidence of postoperative dysphagia and the long-term resolution of the dysphagia was greatly improved in the pcm group compared with the instrumented acdf control group. anderson pa et al., 2008 (1) reported four hundred sixty-three (463) patients having cervical radiculopathy and or myelopathy at a single level which were treated at 31 sites. a total of 242 patients received the disc and 221 patients had anterior cervical discectomy and fusion. all patients were evaluated before surgery and at 1.5, 3, 6, 12, and 24 months after surgery . no differences in overall medical events occurred between groups. surgically related events occurred more frequently in the investigational group secondary to more complaints of postoperative dysphagia and late medical events occurred more frequently in the investigational patients. however, the more severe world health organization grade 3 and 4 events occurred more frequently in the arthrodesis patients related to treatment of pseudarthrosis and persistent symptoms. significantly, more cervical spine reoperations occurred in the fusion group. only one spinal cord injury occurred and it was in the arthrodesis group and no patients had deep infection or death related to either procedure. potential candidacy rate for cervical tdr auerbach jd et al , 2008 (2) reviewed 167 consecutive patients who underwent cervical spine surgery. the authors used the published contraindications and indications listed in trials of four different cervical disc arthroplasty devices: prodisc-c (synthes spine, west chester, pa), prestige lp (medtronik sofamor danek, memphis, tn), bryan cervical disc prosthesis (medtronik sofamor danek, memphis, tn), and porous coated motion (pcm; romanian neurosurgery (2011) xviii 4: 456 464 463 cervitech, rockaway, nj). of the 167 patients (mean age 50.8 years, range 20-89 years) reviewed, 91.6% (153/167) had fusion surgery and 8.4% (14/167) had nonfusion surgery. 57 % percent (95/167) had absolute contraindications to cervical tdr, and within this group the average number of contraindications was 2.1 (sd=1.2, range 0-5). 43% (72/167) met the strict inclusion criteria, and had no exclusion criteria. if the indications were expanded to include treatment for adjacent segment disease (asd), an additional 4.2% (7/167) of the patients would have qualified as candidates for cervical tdr. this study is very interesting, highlighting the fact that acdf covers as surgical solution a larger group of patients than tdr. conclusions summarizing, compared to acdf, tdr has superior or equal clinical outcomes, a lower incidence of adjacent disc disease (radiological +/clinical), lower rate of secondary revision surgeries, supplemental fixation or adjacent segment reoperation, superior spine kinematics, which is maintained over time, earlier return to work. on the other hand, the presented studies have shown that tdr exposes the patients to more frequent postoperative events and have an inferior candidacy rate compared to acdf. we did not have access to straight –forward economic data, but tdr seems to be more costly than acdf. our final conclusion is that tdr already represents a wellestablished technique in the armamentarium to manage the cervical disc herniation, a method required to be handled by any surgeon involved in spinal care. abbreviations tdr – total disc replacement; acdf – anterior cervical decompression and fusion; ndi – neck disability index; vas visual analog scale; ddd – degenerative disc disease; rom – range of motion correspondence to dr. sorin constantin craciunas, address: emergency hospital “bagdasar-arseni” , no.1012, berceni street, sector 4, bucharest, e-mail: craciunassorin@yahoo.fr references 1.anderson pa, sasso rc, riew kd: comparison of adverse events between the bryan artificial cervical disc and anterior cervical arthrodesis. spine (phila pa 1976) 33:1305-1312, 2008. 2.auerbach jd, jones kj, fras ci, balderston jr, rushton sa, chin kr: the prevalence of indications and contraindications to cervical total disc replacement. spine j 8:711-716, 2008. 3.bhadra ak, raman as, casey at, crawford rj: single-level cervical radiculopathy: clinical outcome and cost-effectiveness of four techniques of anterior cervical discectomy and fusion and disc arthroplasty. eur spine j 18:232-237, 2009. 4.buchowski jm, anderson pa, sekhon l, riew kd: cervical disc arthroplasty compared with arthrodesis for the treatment of myelopathy. surgical technique. j bone joint surg am 91 suppl 2:223-232, 2009. 5.garrido bj, taha ta, sasso rc: clinical outcomes of bryan cervical disc arthroplasty a prospective, randomized, controlled, single site trial with 48-month follow-up. j spinal disord tech 23:367-371, 2010. 6.heller jg, sasso rc, papadopoulos sm, anderson pa, fessler rg, hacker rj, coric d, cauthen jc, riew dk: comparison of bryan cervical disc arthroplasty with anterior cervical decompression and fusion: clinical and radiographic results of a randomized, controlled, clinical trial. spine (phila pa 1976) 34:101107, 2009. 7.jadad ar, cepeda ms: evidence-based emergency medicine. ten challenges at the intersection of clinical research, evidence-based medicine, and pain relief. ann emerg med 36:247-252, 2000. 8.jadad ar, haynes rb, hunt d, browman gp: the internet and evidence-based decision-making: a needed 464 sorin c. craciunas et al cervical arthroplasty or cervical fusion synergy for efficient knowledge management in health care. cmaj 162:362-365, 2000. 9.kim hk, kim mh, cho ds, kim sh: surgical outcome of cervical arthroplasty using bryan(r). j korean neurosurg soc 46:532-537, 2009. 10.mcafee pc, cappuccino a, cunningham bw, devine jg, phillips fm, regan jj, albert tj, ahrens je: lower incidence of dysphagia with cervical arthroplasty compared with acdf in a prospective randomized clinical trial. j spinal disord tech 23:1-8, 2010. 11.mummaneni pv, burkus jk, haid rw, traynelis vc, zdeblick ta: clinical and radiographic analysis of cervical disc arthroplasty compared with allograft fusion: a randomized controlled clinical trial. j neurosurg spine 6:198-209, 2007. 12.mummaneni pv, robinson jc, haid rw, jr.: cervical arthroplasty with the prestige lp cervical disc. neurosurgery 60:310-314; discussion 314-315, 2007. 13.murrey d, janssen m, delamarter r, goldstein j, zigler j, tay b, darden b: results of the prospective, randomized, controlled multicenter food and drug administration investigational device exemption study of the prodisc-c total disc replacement versus anterior discectomy and fusion for the treatment of 1-level symptomatic cervical disc disease. spine j 9:275-286, 2009. 14.pitzen t, kettler a, drumm j, nabhan a, steudel wi, claes l, wilke hj: cervical spine disc prosthesis: radiographic, biomechanical and morphological post mortal findings 12 weeks after implantation. a retrieval example. eur spine j 16:1015-1020, 2007. 15.riina j, patel a, dietz jw, hoskins js, trammell tr, schwartz dd: comparison of single-level cervical fusion and a metal-on-metal cervical disc replacement device. am j orthop (belle mead nj) 37:e71-77, 2008. 16.robertson jt, papadopoulos sm, traynelis vc: assessment of adjacent-segment disease in patients treated with cervical fusion or arthroplasty: a prospective 2-year study. j neurosurg spine 3:417-423, 2005. 17.sasso rc, best nm: cervical kinematics after fusion and bryan disc arthroplasty. j spinal disord tech 21:1922, 2008. 18.sasso rc, best nm, metcalf nh, anderson pa: motion analysis of bryan cervical disc arthroplasty versus anterior discectomy and fusion: results from a prospective, randomized, multicenter, clinical trial. j spinal disord tech 21:393-399, 2008. 19.steinmetz mp, patel r, traynelis v, resnick dk, anderson pa: cervical disc arthroplasty compared with fusion in a workers' compensation population. neurosurgery 63:741-747; discussion 747, 2008. doi: 10.33962/roneuro-2022-031 clinico-radiological factors affecting visual recovery in pituitary tumours vivek kumar kankane, harshit agrawal, s.n. iyenger romanian neurosurgery (2022) xxxvi (2): pp. 168-174 doi: 10.33962/roneuro-2022-031 www.journals.lapub.co.uk/index.php/roneurosurgery clinico-radiological factors affecting visual recovery in pituitary tumours vivek kumar kankane, harshit agrawal, s.n. iyenger department of neurosurgery, g.r. medical college & jah groups of hospital gwalior (m.p.), india abstract objectives: it is a prospective, single institute, observational study: primary outcome measure; factors determining visual field improvement and secondary outcome measure; the relationship between severity of visual impairment and duration of symptoms. material and methods: it is a prospective, single institute, observational study that will be conducted between january 2020 and january 2022 in the department of neurosurgery at the g. r. medical college &j.a. group of hospitals, gwalior (m.p.), a tertiary centre in india. all patients were admitted to the neuro-surgery department & operated on basis of a ct scan of head/mri findings. patients with laboratory findings having hypopituitarism, diabetes insipidus (di), and hyperprolactinemia and willing to undergo endocrinological & visual field tests in inclusion criteria. data obtained from the study will be analyse by using appropriate statistical tests or methods results: at present, series most common age presentation (36.7%) between 21-30 years. in our study, of the total patients, 60% were males and 40% were females. the male to female ratio is 2:1 most common complaint of vision loss and only 50% had hormonal symptoms. in our study 46.7% patients have duration of symptoms < 6 months and 6/6 6/24 visual acuity was present in 73.3% patients & 13.3% had optic atrophy(primary/secondary), 43.3%patients had bi-temporal hemianopia. in our study suprasellar extension was present in 90% of patients & vascular invasion was seen in 26.7% of patients. conclusion: good results are seen in patients who have a lesser duration of symptoms, and good pre-operative visual acuity has improved the final visual outcome. post-operative visual recovery is most promising after 3 months to 1 year of surgery. immediate results of visual recovery should not be expected. most patients presented with larger adenomas had poor visual recovery as compared to small adenomas. patients who underwent endoscopic trans-nasal, trans-sphenoidal resection had better post-operative recovery. introduction pitutary adenomas account for 10-15% of all brain tumours, it is the third most frequently diagnosed brain tumour [1]. pitutary tumours can be clinically classified as functioning & nonfunctioning pituitary adenomas [2]. non-functioning pituitary adenomas are not usually associated with keywords pituitary adenoma, tumours, visual field defect, harmonal symptoms corresponding author: vivek kumar kankane department of neurosurgery, g.r. medical college & jah groups of hospital gwalior (m.p.), india vivekkankane9@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 169 clinico-radiological factors affecting visual recovery in pituitary tumours clinical syndromes related to hormone excess and may be discovered occasionally.[3] when they exert mass effects on surrounding tissues leading to visual impairments, headache and hypopituitarism and hydrocephalus.[4] the growing of pituitary tumors may compress the surrounding structures especially optic nerve, cause visual field defects including bitemporal hemianopia, visual disturbance. the frequency of visual field defects in pituitary adenomas varies from 37% to 96% in different studies.[5] the symptoms due to pituitary hormonal dysfunction are not the one for which the patient seeks medical attention. the presence of a visual field defect is one of the common indications for surgery in patients with pituitary tumors, and the degree of the visual field defect should be identified through a preoperative visual field examination, even if the patient does not complain of symptoms [6] if the tumor is accompanied by a visual field defect, it is clinically important to predict the prognosis for postoperative visual field recovery.[7] the typical visual field defect, bitemporal hemianopia, is due to anatomical compression of the optic chiasm, which contains the crossing nasal fibres of each optic nerve fibres.[8] materials and method study design it is a prospective, single institute, observational study will be conducted between january 2020 and january 2022 in the department of neurosurgery at the g. r. medical college &j.a. group of hospitals, gwalior (m.p.), a tertiary centre in india. the study protocol will be approved by the institutional ethics committee and written informed consent will be obtained from all participants. sample size 30 and above patients inclusion criteria 1. all patients admitted in neuro-surgery department & operated on basis of ct scan of head/mri findings. 2. patients with laboratory findings having hypopituitarism, diabetes insipidus (di), and hyperprolactinemia. 3. patients willing to undergo endocrinological & visual field tests. 4. patients with visual field defect induced by pituitary tumors. exclusion criteria 1. severe co-morbid illness 2. patients having past h/o of surgery or treatment adjacent to sellar lesion. 3. patients excluded who refused endocrinological evaluation. 4. patients not willing for operation. 5. patients less than 15 years of age. 6. cases with other causes of visual loss such as cataract, glaucoma, and retinal detachment. study protocol and data collection all patients of pituitary tumour admitted in department of neurosurgery. a written consent will be taken from the patient or their attendants for the study. details of demographics and detailed history of event, presenting symptoms and signs, laboratory parameters (serum prolactin, growth hormone, acth, tsh, cortisol) and imaging findings (size of tumour, invasion of surrounding structures) a contrast-enhanced magnetic resonance imaging (mri) of the sella was performed in all these patients preoperatively. the adenoma volume was calculated by the de chiro and nelson formula [volume = (sagittal × coronal × axial diameters) × π/6]. modified hardy's classification was used for staging (extension) and grading (degree of sellar destruction) of the pituitary adenomas. we also used knosp grading to document the parasellar extension, ophthalmologic evaluation (visual acuity, visual field, fundus) va was determined by the snellen's chart, and vf testing was performed by humphrey automated computerized perimeter, c76 panel (carl zeiss, germany). in patients with finger counting, hand movement, and only perception of light, the assessment of vf was done manually using confrontation test before surgery & after 1 month & 3 months of surgery will be noted. the results were recorded as follows: (i) no change, (ii) improved, and (iii) worsened. significant improvement/worsening was defined as any grade improvement or deterioration in the va and vf, based upon a 30% change to avoid interand intra-individual variation, according to john thomas smith's rule of the onethird. blindness was defined as absence of 170 vivek kumar kankane, harshit agrawal, s.n. iyenger perception of light. management of the patients will be planned and observe in terms of outcome. outcome measure 1. primary outcome measurefactors determining visual field improvement. 2. secondary outcome measurerelationship between severity of visual impairment & duration of symptoms. data analysis data obtained from the study, will be analyse by using appropriate statistical test or methods. data will be entered in microsoft word and analyzed using spss version 16.0 and epi info version 7.0. appropriate statistical test will be applied to analyze the data. results in present series (n=4 )13.3% patients were up to 20 yrs. of age, (n=11)36.7% between 21-30 years, (n=8)26.7% between 31-40 yrs., (n=5)16.7% were between 41-50 yrs. &(n=2) 6.7% between 51-60 yrs. our study of the total patient 30, (n=18)60% were males &(n=12) 40% were females. the male to female ratio is 2:1. in the present study (n=24)80% of patient had complaint of headache, vision loss was present in (n=25)83.3% of patients & features of raised icp were present in (n=15)50% of patients. in present study of total patients (n=30) only 50% had hormonal symptoms. acromegaly was present in (n=5)16.7% patients, amenorrhea was present in (n=2) 6.7% of patients. cushing feature was present in (n=3)10% patients. hirsutism was present in (n=4)13.3% patients. hypothyroidism was present in (n=1)3.3% patient in our study (n=14)46.7% patients have duration of symptoms < 6 months, 6 months -12 months (n=6) 20%, 1yr-2yr (n=3)10% & (n=7)23.3% had duration of symptoms more than 2 yr. visual acuity in our study 6/6 6/24 visual acuity was present in 73.3%(n=22) patients, 6/36 6/60 visual acuity was present in 13.3%(n=4) patient, hand movement was present in 6.7%(n=2), perception of light negative in 3.3% (n=1) & perception of light positive in 3.3% (n=1) patients. fundus in our study 70%(n=21) had normal fundus, 16.7%(n=5) had pale optic disc & 13.3%(n=4) had optic atrophy (primary/secondary). visual field in our study 43.3%(n=13) patients had bi-temporal hemianopia, normal field of vision in 33.3%(n=10), blind 13.3%(n=4), upper quadrantonopia was present in 6.7%(n=2) & total field loss in 3.3%(n=1). in our study hydodense lesion was seen in 66.7%(n=20) of patients, hyperdense lesion was seen in 6.7%(n=2) & hetrogenous lesion was seen in 23.3%(n=7). in our study 50%(n=15) were solid lesions, 30%(n=9) were cystic lesions & 20%(n=6) were mixed lesions. in our study vascular invasion was seen in 26.7%(n=8) of patients. in our study t1-w image 96.7%(n=29) were hypointense & 3.3%(n=1) were hyperintense & on t2-w image 100%(n=30) were hyperintense. in our study 100%(n=30) were macroadenoma pituitary tumours. suprasellar extension was present in 90%(n=27) patients & vascular invasion seen in 26.7%(n=8) patients. discussion pituitary adenomas can produce visual loss by compression of the optic chiasm or nerves. an extension of >10 mm above the seller diaphragm is necessary to compress the anterior visual system.[9][10] pituitary adenoma can be described as microadenoma, macroadenoma, and giant tumors based on size. microadenoma is a tumor less than 10 mm, while macroadenoma describes a tumor larger than 10mm. giant pituitary tumors are bigger than 40 mm. table 1. comparison of neurological complaints in various studies s. n o. study no. of patients visual impairment (%) headache (%) 1 khaled al dahmani et al (2016) 1005 76 62 2 elena valassi et al (2018) 51 51 34 171 clinico-radiological factors affecting visual recovery in pituitary tumours 3 pamela u freda et al (1999) 62 62 42 4 mukheraji kk et al (2016) 1007 87.5 87.3 5 amit padwal (2017) 80 46 53 6 present study 30 83.3 80 visual symptom is one of the major presenting manifestations of a pituitary macroadenoma causing considerable burden to patients and their families [11]. in present study [table1] vision loss (83.3%) was the most common symptoms followed by headache (80%) and followed by features of raised icp (50%) which is consistent with most of the studies of mukerji k k et al(2016)[12], khaled al dahmani et al(2016)[13],elena valassi et al(1999)[14], pamela u freda et al(1999)[15], amit padwal et al (2017)[16] table 2. comparison of harmonal symptoms in various studies study no. of patients acromegaly cushingoid 1 khaled al dahmani et al (2016) 1005 6% 0% 2 mukherji kk et al (2016) 1007 23.9% 8.6% 3 dong kyulee (2018) 102 18.3% 0% 4 present study 30 16.7% 10% the histologic diversity accounts for its ability to secrete a variety of hormones that include the growth hormone (gh), thyroid-stimulating hormone (tsh), adrenocorticotropic hormone (acth), folliclestimulating hormone (fsh), luteinizing hormone (lh), and prolactin (prl). the median lobe produces melanocyte-stimulating hormone (msh). the neurohypophysis is composed of the neural stalk and the neural lobe and functions as the primary storage site for antidiuretic hormone (adh) and oxytocin (ox). these hormones as well as other biologically active substances are released into the adjacent capillaries in response to hypothalamic nerve impulses [17,18,19]. hypersecretion of prolactin, growth hormone, acth and tsh produces corresponding clinical syndromes [19]. in present study 50%tumours were non functional which was not correlating with mukherji k k et al [12] were 68.8% were non functioning &dong kyu lee [20] were 80% were non functioning tumours.[table2]. in present study 16.7% presented with features of acromegaly being the most commonest followed by cushing features in 10% which is consistent with khaled al dahmani et al[13] 6%, mukherji kk et al[12] 23.9%, dong kyu lee [20] 18.3%. the most common consistent feature of these tumors is visual loss, a consequence of suprasellar growth and compression of anterior visual pathways. an asymmetric bitemporal hemianopia is the classically observed deficit, although other patterns of visual dysfunction commonly occur such as the junctional scotomas, monocular field defects, papilledema, optic atrophy and total blindness[21]. in the present study on fundoscopic examination (13.3%) patient had optic atrophy as a result of longstanding chiasmal compression from a pituitary macroadenoma.in a study by dhasmana et al[22] optic atrophy was seen clearly in 17% of patients with pituitary adenomas and all of them had significantly affected vision. mukherji k k et al [12] study too, had similar percentage (18.2%) of patients presented with optic atrophy and most of the patients had a poor visual acuity ranging from 6/36 -6/60 to no light perception.[table3] table 3. comparison of optic atrophy in various studies s. no. study optic atrophy % 1. dhasmana et al (2011) 17 2. mukherji et al (2016) 18.2 3. present study 13.3 from the surgical stand point sellar and parasellar masses such as pituitary tumors can be can be classified on the basis of their size and growth characteristics as determined by imaging studies.the most enduring classification is that devised by hardy and modified by wilson[23]. grade grading grade-0 microadenoma<1cm:no sellar changes grade-1 microadenoma<1cm:minor sellar changes grade-2 macroadenoma with diffuse enlargement 172 vivek kumar kankane, harshit agrawal, s.n. iyenger grade-3 macroadenoma with focal destruction grade-4 macroadenoma with extensive destruction of sella extrasellar extension stage-a extending to suprasellar cistern stage-b extending to third ventricle floor stage-c extending into the third ventricle stage-d extensive lateral intradural extension stage-e extensive lateral extradural extension. knosp classification mr imaging is the imaging mainstay of the sellar and parasellar regions. mr imaging has a better soft tissue resolution than computed tomography (ct) and is also not subjected to artifacts from surrounding bony structures.[24] in our study invasiveness of the lesion was assessed on mri by hardy &wilson classification & knosp classification. the evidence of carotid encasement in mri scan is defined invasion of cavernous sinus, in amit padwal et al [25] study of 93 patients, 50 patients had invasive adenoma and remaining 43 patients had non-invasive adenoma. this is in agreement with study done by amit padwal et al and ross & wilson [26] where grade-2 was most common finding. [table-4] table 4. comparison of hardywilson grading in various studies study no. of patients grading (most common grade 2) % amit padwal et al (2017 ) 93 2-58% ross & wilson (1988) 214 2-60% present study 30 2-47% ct is better than mr imaging for detecting calcifications, and can be used complementary to mr imaging if a primary bony lesion is suspected (eg, chordoma, chondrosarcoma) and also in defining the sphenoid sinus anatomy if endonasal/sublabial endoscopic or microscopic transphenoidal approach is planned [27,28].ct scan is also beneficial in detecting pituitary apoplexy which will have a hyperdense appearance. in our study, 29 cases showed hypointensity on t1 weighted image, while one case showed hyperintensity. all cases showed hyperintensity on t2 weighted image. these mri finding are supported by most of other studies, like pratisruti hui et al[29] & kushak gehlot et al [30], where similar results were obtained.[table5] table 5. comparison of mri in various studies study t1 mri t2 mri contrast kushak gehlot et al (2019) hypointense 84% hyperintense 9.2% hyperintensity -80% 75.9% pratisruti hui et al (2019) hypointense 100% hyperintensity -86% 92% present study hypointense 84% hyperintense 9.2% hyperintensity -100% 80% post-operative visual recovery played a significant role, post-operative assessment was done immediately post-operative, after 1 month & after 3 month of surgery. most of the patients showed visual recovery after 3 month. a ashish suri et al [31] showed visual improvement in 30% patients, apjit kaur et al [32] showed visual improvement in 44.8%, mukherji k k et al [12] showed improvement in 71.1% cases at 3 months which is similar to our study of 83.3% [ table-6]. table 6. comparison of post-op visual recovery study post-op visual recovery % ashish suri et al (2008) 30% apjit kaur et al 44.8% mukherji k k et al (2016) 71.1% our study 83.3% the minimally invasive transsphenoidal approach can be used effectively for 95% of pituitary tumors. 173 clinico-radiological factors affecting visual recovery in pituitary tumours exceptions are those large tumors with significant temporal or anterior cranial fossa extension. in such circumstances, transcranial approaches are often more appropriate. occasionally, combined transsphenoidal and transcranial approaches are used. nevertheless, some surgeons extend the basic transsphenoidal exposure in order to remove some of these tumors and avoid a craniotomy [33,34] conclusion good results are seen in patients who have lesser duration of symptoms, good pre-operative visual acuity have improved final visual outcome. in our study most cases of pituitary adenoma were functional, so patients with pituitary prolactinoma showed better visual recovery. post-operative visual recovery is most promising after 3 months to 1 year of surgery. immediate results of visual recovery should not be expected. most of patients presented with larger adenomas with supra-sellar & parasellar extension with encasement of internal carotid artery had poor visual recovery as compared to small adenomas. patients who underwent endoscopic trans-nasal, trans-sphenoidal resection had better post-operative recovery with less patient morbidity & less post-operative complications and lesser duration of post-operative hospital stay. references 1. zacharia be, bruce ss, goldstein h, malone hr, neugut ai, bruce jn. incidence, treatment and survival of patients with craniopharyngioma in the surveillance, epidemiology and end results program. neuro-oncol. 2012 aug;14(8):1070. 2. olsson ds, andersson e, bryngelsson il, nilsson ag, johannssong. excess mortality and morbidity in patients with craniopharyngioma, especially in patients with childhood onset: a population-based study in sweden. j clin endocrinol metab. 2015 feb;100(2): 467–74. 3. karavitaki n, brufani c, warner jt, adams cb, richards p, ansorge o, et al. craniopharyngiomas in children and adults: systematic analysis of 121 cases with long-term follow-up. clin endocrinol (oxf). 2005 apr;62(4):397–409. 4. pemberton ls, dougal m, magee b, gattamaneni hr. experience of external beam radiotherapy given adjuvantly or at relapse following surgery for craniopharyngioma. radiother oncol. 2005 oct;77(1):99– 104. 5. wijnen m, van den heuvel-eibrink mm, janssen ja, catsman-berrevoets ce, michiels em, van veelen-vincent mc, et al. very long-term sequelae of craniopharyngioma. eur j endocrinol. 2017 jun;176(6):755–67. 6. puget s, garnett m, wray a, grill j, habrand jl, bodaert n, et al. pediatric craniopharyngiomas: classification and treatment according to the degree of hypothalamic involvement. j neurosurg. 200 jan;106(1 suppl):3–12. 7. müller hl. craniopharyngioma. endocr rev. 2014 jun;35(3):513–43. 8. sterkenburg as, hoffmann a, gebhardt u, warmuthmetz m, daubenbüchel am, müller hl. survival, hypothalamic obesity, and neuropsychological /psychosocial status after childhood-onset craniopharyngioma: newly reported long-term outcomes. neurooncol. 2015 jul;17(7):1029–38. 9. hudson h, rissell c, gauderman wj, feldon se. pituitary tumor volume as a predictor of postoperative visual field recovery. quantitative analysis using automated static perimetry and computed tomography morphometry. j clin neuroopthalmol 1991;11:280-3. 10. shults wt. compressive optic neuropathies. in: miller nr, newman nj, editors. walsh and hoyt's clinical neuroophthalmology. 5th ed. baltimore: williams and wilkins; 1998. p. 657-8 11. dutta p, hajela a, pathak a, bhansali a, radotra bd, vashishta rk, et al. clinical profile and outcome of patients with acromegaly according to the 2014 consensus guidelines: impact of a multi-disciplinary team. neurol india. 2015;63:360-8. 12. visual outcome in in 2000 eyes following microscopic transsphenoidal surgery for pituitary adenomas: protracted blindness should not be a deterrent. dutta p, gyurmey, t,banshal r, pathak a,dhandapani s, rai a,bhansali a, mukherjee kk,. neurol india 2016;64:124753. 13. sellar masses : an epidemiological study. al-dahmani k, et al. can j neurol sci.2016mar;43(2):291-7. 14. current openion in endocrine & metabolic research.elena valssi, e resmini , 63-73,2018. 15. differential diagnosis of sellar masses, endocrionology & metabolism. palmela u fareda, kalmon d. clinics of north america. 28;1:1999, 81-117 16. evalution of factors affecting outcome in growth harmonr secreting pituitary adenoma. amit padwal, jagathal gangadharan, indian journal of neurosurgery2017;06(03):176-183. 17. wang s, nie q, wu z, zhang j, wei l. mri and pathological features of rathke cleft cysts in the sellar region. exp ther med. 2020 jan;19(1):611–8. 18. trifanescu r, ansorge o, wass ja, grossman ab, karavitaki n. rathke‟s cleft cysts. clin endocrinol (oxf). 2012 feb;76(2):151–60. 19. mahapatra ak: does optic nerve injury require decompression? j indian med assoc 88:82–84, 1990. 20. dong kyu lee, mi sun sung and sang woo park:factors influencing visual field recovery after transsphenoidal resection of pituitary adenoma.korean j ophthalmol.2018 dec;32(6):488-496. 174 vivek kumar kankane, harshit agrawal, s.n. iyenger 21. marchel a, bidzinski j, barczewska m, dziewiecke c. meningiomas of sella turcica: some clinical aspects. neurol neurochir pol 30:93–100, 1996 (pol). 22. dhasmana r, nagpal rc, sharmar, bansal kk, bahadur h. visual fields at presentation and after transsphenoidal resection of pituitary adenoma.j ophthalmic vis res 2011;6:187-91. 23. mcfadzean rm, doyle d, rampling r, teasdale e, teasdale g. pituitary apoplexy and its effect on vision. neurosurgery 29: 669–675, 1991 24. mcgirt mj, cowan ja jr, gala v, garton hj: surgical reversal of prolonged blindness from a metastatic neuroblastoma. childs nerv syst 21:583–586, 2005. 25. amit padwal, jagathal gangadharan “ evalution of factors affecting outcome in growth harmone-secreting pituitary adenoma” ijn,2017:06(03):176-183. 26. ross da, wilson cb, results of transsphenoid microsurgery for growth harmone secreting pituitary adenoma in series of 214 patients. j neurosurgery 1988;68(06): 854-67. 27. mcilwaine gg, carrim zi, lueck cj, chrisp tm: a mechanical therapy to account for bitemporal hemianopia from chiasmal compression. j neuroophthalmol 25:40–43, 2005. 28. mclarty dg, kermali w, makene wj: pituitary tumors and blindness: continuation of the pre-harvey-cushing era in developing countries. lancet 2:810–811, 1982. 29. accuracy of magnetic resonance imaging in evaluation of sellar & juxtra sellar tumours hui pratisutri,parida sasmita, mohanty jayshree, singh mamta, sarangi pradosh kumar 2019;3:1: 3-9. 30. aggrawal,n,kushal gehlot,nk kardam& a.khan.mri characterised of sellar & parasellar lesion & their clinical correlation. 2019 31. suri a, narang ks, sharma bs, mahapatra ak.visual outcome after surgery in patients with suprasellar tumours & pre-operative blindness. jneurosurg.2008 jan; 108(1):19-25. 32. apjit kaur, deepu banerji, devendra kumar, kartikey sharma. visual status in suprasellar pituitary tumours. indian j opthalmol 1995;43:131-4. 33. kaptain g.j., et al. transsphenoidal approaches for the extracapsular resection of midline suprasellar and anterior cranial base lesions. neurosurgery. 2001;49(1):94–100. 34. nimsky c., et al. intraoperative high-field magnetic resonance imaging in transsphenoidal surgery of hormonally inactive pituitary macroadenomas. neurosurgery. 2006;59(1):105–14. microsoft word 8dabija_lumbar.doc 230 dabija et al lumbar epidural lipomatosis in a patient with hodgkin lymphoma lumbar epidural lipomatosis in a patient with hodgkin lymphoma m. dabija1, 2, d. andronic2, c. gheorghita2, g. dumitrescu3 1“grigore t. popa” university of medicine and pharmacy, iaşi 2,3“prof. dr. n. oblu” clinical emergency hospital, iaşi 2neurosurgery department, 3anatomopathology department abstract spinal epidural lipomatosis (sel) is a pathological condition in which fat tissue is deposed in the spinal canal around the thecal sac in excess, causing neurological symptomatology (7, 9, 12). fat tissue is present in our body almost everywhere. when the normal quantity is exceeded is created a pathological situation. we present a 33 old man case with fat tissue excess deposited in lumbar spine canal. the pathological history of our patient includes a nodular form of stage ia hodgkin lymphoma diagnosed in 2011 for what he went combined radiochemotherapy. he also has ben diagnosed with grad i obesity. in last month he presented with rapidly progressive symptoms like lower back pain, paraparesis and sphincters dysfunctions. thoracic magnetic resonance imaging (mri) establishes a lumbar lipomatosis located in l3-s5 spinal canal. pathology results confirm the imagistic diagnostic. under surgery was performed a median laminectomy with fat tissue excision with good results in patient symptomatology. cortisone chronic therapy may lead to sel. however in our case, hodgkin lymphoma therapy appeared to be related to cortisone therapy. neurological symptomatically patients should be treated surgically. key words: lumbar pain; lipomatosis; hodgkin disease; radio-chemotherapy complications. introduction lumbar lipomatosis represents a pathological situation in which the fat tissue is deposed in excess in spinal canal (7, 8, 9). fat tissue is present in our body almost everywhere. in spinal canal has a protective roll for spine and nerves (5, 9). when is in excess it creates neurological symptomatology. lipomatosis is known to be a complication for chronic steroids therapy with neurological symptoms (8, 12). there were several other cases reported in which chronic steroids therapy lead to spinal lipomatosis (1, 10, 11, 15). another case of spinal lipomatosis was in a patient with cushing syndrome (1). we know that corticoids may influence the adipose tissue deposits. we present a similar case of a patient that was diagnosed with lumbar lipomatosis after he underwent radiotherapy with high doses of prednisone. case presentation a 33 years old patient presented at our clinic with rapidly progressive symptoms like lower back pain, paraparesis and romanian neurosurgery (2012) xix 3: 230 233 231 sphincters dysfunctions during the last month. from his medical history we know that he suffer an appendicectomy in 2009 that continued with abdominal pain and in 2010 he was diagnosed with inguinal adenopathy. in 2011 he suffer a surgery intervention to remove the nodular formation. the patient was diagnosed with stage ia nodular form of hodgkin lymphoma. the diagnosis was sustained by pathology result from the lesion. a petct was made to evaluate the lesion extension. the result was negative for any other lymphoma extension after first session of chemotherapy. he underwent combined radio-chemotherapy after surgery. he underwent 4 sessions of chemotherapy with r-chop (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) (17). the neurological symptoms starts after several months but in the last month they exacerbate rapidly affecting the motor functions and his quality of life. on the general exam we noticed that his body mass index (bmi) was 31 indicating grad i obesity. neurological exam revealed motor and sensory dysfunction on l3-s5 dermatomes with external popliteal sciatic (eps) paresis more evident on the left side and perineal paresis. he also had sphincter dysfunction with urinary problems. his clinical diagnosis was compressive myelopathy with cauda equine syndrome. the routinely laboratory and biochemical tests showed normally hematological parameters. the magnetic resonance imaging (mri) of lumbar spine (figure 1, figure 2, figure 3) whoever revealed highintensity fat within in the lumbar spinal canal. after preoperative planning our team managed to operate. figure 1 t1 mri lumbar column sagittal incidence figure 2 t2 mri lumbar column sagittal incidence a medial laminectomy l5and s1was performed with adipose tissue excision and nerve route decompression at the same levels. a tissue sample was taken for pathology. the result was positive for mature adipose tissue without lymphocyte infiltration (figure 4). 232 dabija et al lumbar epidural lipomatosis in a patient with hodgkin lymphoma figure 3 t2 mri lumbar column axillar incidence figure 4 histological examinations demonstrate nodular proliferation of mature fat cells symptoms were improved after surgery but the patient also needs kinesiology for full recovery. the diagnosed was lumbosacral lipomatosis, grad i obesity, and stage ia nodular form of hodgkin lymphoma. discussion spinal epidural lipomatosis (sel) is a pathological condition in which fat tissue is deposed in the spinal canal around the thecal sac in excess, causing neurological symptomatology (7, 9, 12). physiological the adipose tissue in spinal canal has a protective roll for spinal cord (5, 9). the adipose tissue thickness varies with spinal canal levels. in the cervical region the adipose tissue is almost inexistent. in thoracic region the distribution of epidural fat is patchy. in the lumbar region the epidural fat acquire it greatest volume (2, 9). the sel etiology is unknown (12) but there are some risks factors causing the adipose tissue to gather in excess. some of this includes cushing disease, obesity, epidural steroid injection, hypothyroidism, pituitary prolactinoma, renal transplants, rheumatoid arthritis, exogenous corticosteroid therapy, spinal anesthesia and idiopathic (1, 3, 4, 7, 10, 11, 12, 13, 14). off all this most common is exogenous corticosteroid therapy (11, 12, 16). spinal epidural lipomatosis could be found in patients with cushing syndrome and morbid obesity (1, 13, 14). there were some other cases in the literature of spinal epidural lipomatosis due to corticoid therapy (8, 11, 16). the best way to evaluate the adipose tissue in the spinal canal is by magnetic resonance imaging (mri) (2, 7, 8, 9, 10). borré (2) manage to evaluate the normal thickness of adipose tissue in the lumbar spinal canal and classify it in 4 grades. grade 0 represents the normal value of adipose tissue in lumbar region. lumbosacral epidural lipomatosis (lel) grade iii is symptomatic, grade ii only in 14.5% symptomatic and no symptoms in grade i (2, 7). although our patient had a grade ii lel (2), he had neurological symptoms that affect his quality of life. in our patient, signal intensity alterations were observed in lumbosacral level. the mri reveals massive adipose tissue in lumbosacral with highest thickness of 0.997mm (fig. 3). he suffers corticoid therapy after hodgkin lymphoma diagnostic. one of the steps of the stage ia hodgkin lymphoma protocol includes chemotherapy with r-chop (17). he underwent 4 sessions of chemotherapy in 4 moths period. pet-ct investigation did not confirm any dissemination after the first chemotherapy session. he underwent romanian neurosurgery (2012) xix 3: 230 233 233 radiotherapy with interferon (if) 20gy/ 10fr 2gy/ fr on iliac ganglions. his neurological symptoms appear 5 months after chemotherapy with rapidly developing in the last month. the patient was not on corticoid therapy on the time that symptomology increase and we did not find any connection between radiotherapy and spinal lipomatosis (3, 8, 11). there are various methods of therapy (1, 11, 13, 14, 15, 16). however is a matter of debate, what treatment is best for the patient. there were good results only with conservative treatment. however the treatment should be determined according to each case (1, 3, 10, 13, 14, 15, 16). in our case the patient has rapidly neurological symptoms evolution that required surgical treatment with nerve routs decompression. the differential diagnostic included spinal tumor, dural lymphoma and angiolipoma, which needed also surgery treatment (4, 6). after the surgery recommendations included loose weight and neurological rehabilitation. conclusion cortisone chronic therapy may lead to sel. however in our case, hodgkin lymphoma therapy led to cortisone complications. we did not find any radiotherapy implication in the literature. however the patient suffer for grad i obesity. neurological symptomatically patients should be treated surgically. references 1. alexander g l bodelier, wim groeneveld1, antonius n van der linden and harm r haak: symptomatic epidural lipomatosis in ectopic cushing’s syndrome. european journal of endocrinology (2004) 151 765– 769. 2. daniel g. borré, guillermo e. borré, flavioaude, gladys n. palmieri: lumbosacral epidural lipomatosis: mri grading. european radiologyjuly 2003, volume 13, issue 7, pp 1709-1721. 3. giuliozuccoli, nicolo` pipitone,nicola de carli,luigi vecchia, stefano c. bartoletti: acute spinal cord compression due to epidural lipomatosis complicated by an abscess: magnetic resonance and pathology findings. eur spine j (2010) 19 (suppl 2): s216–s219. 4. herbert b. newton, m.d. and arthur james: neurologic complications of systemic cancer. am fam physician (1999) feb 15; 59 (4): 878-886. 5. i.g. parkin and g. r. harrison: the topographical anatomy of the lumbar epidural space. j anat. (1985), 141, pp. 211-217. 6. jin hoon park, m.d., sang ryongjeon, m.d., seungchulrhim, m.d., sung woo roh, m.d., ph.d.: lumbar spinal extradural angiolipoma: case report and review of the literature, (2008), j korean neurosurgsoc 44: 265-267. 7. johan w. m. van goethem, luc van den hauwe, paul m. parizel: spinal imaging: diagnostic imaging of the spine and spinal cord: pp 200-208. 8. lisa m deangelis, jerome b posner: neurologic complications of cancer pp 101-131. 9. m. a. reina, c. d. franco, a. lópez, j. a. dé andrés and a. van zundert. clinical implications of epidural fat in the spinal canal. a scanning electron microscopic study. actaanaesth. belg. (2009), 60, 7-17. 10. per flisberg1, owain thomas1, bo geijer2 and ulf schött. epidural lipomatosis and congenital small spinal canal in spinal anaesthesia: a case report and review of the literature. journal of medical case reports (2009), 3:128. 11. r. gupta, md, frcp; a. n. kumar, md; v. gupta, md; sethu m. madhavan, md; s. k. sharma, md, phd.: an unusual cause of paraparesis in a patient on chronic steroid therapy. the journal of spinal cord medicine (2007), volume 30 number 1. 12. ralph m. buschbacher: rehabilitation medicine quick reference. spine pp. 66-67. 13. sang-beom lee, m.d., hyung-ki park, m.d., ph.d., jae-chil chang, m.d., ph.d., so-young jin, m.d., ph.d.: idiopathic thoracic epidural lipomatosis with chest pain. j korean neurosurgsoc 50 (2011): 130-133. 14. tetsuroohba, md, phd; toshiki saito, md, phd; nobuchika kawasaki, md, phd; shingo maekawa, md, phd; hirotakaharo, md, phd.:symptomatic spinal epidural lipomatosis with severe obesity at a young age. orthopedics (2011);volume 34, number 6. 15. a. c. w. borstlap, w. j. j. van rooij, m. sluzewski, a. c. m. leyten, g. beute: reversibility of lumbar epidural lipomatosis in obese patients after weightreduction diet. neuroradiology (1995), volume 37, issue 8, pp 670-673. 16. chung hong tok, shaleenkaur, afshingangi: symptomatic spinal epidural lipomatosis after a single local epidural steroid injection. cardiovascular and interventional radiology (2011), volume 34, issue 2 supplement, pp 250-255. 17. nccn clinical practice guidelines in oncology; hodgkin lymphoma, version 2.2012. microsoft word 4.rizear_3ddiffuse_f.doc 110 rizea et al 3d diffuse tensor imaging for preoperative planning 3d diffuse tensor imaging important acquisition in diagnostic and preoperative planning of intracranial lesions r.e. rizea, a.v. ciurea, g. onose hospital “bagdsar-arseni”, bucharest av. berceni, no. 10-12, sector 4, romania e-mail: rizea.radu.eugen@gmail.com, tel.: + 40 213343025 abstract diffusion tensor imaging (dti) is a mri technique that enables the measurement of the diffusion of water in tissue in order to produce neural tract images. dti allows clinicians to look at anisotropic diffusion in white-matter tracts, but it is limited in demonstrating spatial and directional anisotropy. advanced methods such as color coding and tractography (fiber tracking) have been used to investigate the directionality. the localization of tumors in relation to the white matter tracts (infiltration, deflection), has been one the most important initial applications. tractography potentially solves a problem for a neurosurgeon in terms of minimizing functional damage and determining the extent of diffuse infiltration of pathologic tissue to minimize residual tumor volume. in this way, tractography facilitates preoperative planning. tractographic images may help to clarify whether a tumor is compressing, abutting, or infiltrating the contiguous white-matter tracts. dti identify different tumor components, and to differentiate tumor invasion from normal brain tissue or edema. the recent development of dti allows for direct examination of the brain microstructure, and dti has become a useful tool for investigation of brain disorders such as stroke, epilepsy, ms, brain tumors, and demyelinating disorders. keywords: diffusion tensor imaging, neurosurgery, tractography. introduction diffusion tensor imaging (dti) is a mri technique that enables the measurement of the diffusion of water in tissue in order to produce neural tract images (figure 1). the idea of using diffusion data to produce images of neural tracts was first proposed by aaron filler & colleagues in march of 1991. several months later (1992) the first dti image showing neural tracts curving through the brain was produced. conventional magnetic resonance (mr) imaging has been the standard clinical tool to characterizing and localizing brain tumors. topical, mr imaging is used to determine the appropriate therapy and for neurosurgical planning if lesion resection is possible. however, even the most anatomically detailed mr imaging does not allow an assessment of specific white matter (wm) tracts. dti data can be used to visualize the major wm tracts of the brain [1..3]. dti is an mr technique that can indirectly evaluate the integrity of wm by measuring water diffusion and its directionality in three dimensions [4]. dti has been applied to differentiate edema from tumor, in patients with brain tumor for tumor characterization and to assess structural properties of the adjacent tracts [5..10]. romanian neurosurgery (2012) xix 2: 110 – 115 111 figure 1 the first images of tractography from our research project knowledge of the anatomical relationship between tumor and wm tracts could improve preoperative risk analysis and decrease the risk of wm tract injury during surgery. to minimize injury to the wm tracts adjacent to the tumor, knowledge of their structural integrity would be important. experimental the principal application of dti is in the imaging of white matter where the location, orientation, and anisotropy of the tracts can be measured. dti allows clinicians to look at anisotropic diffusion in white-matter tracts, but it is limited in demonstrating spatial and directional anisotropy. advanced methods such as color coding and tractography (fiber 112 rizea et al 3d diffuse tensor imaging for preoperative planning tracking) have been used to investigate the directionality. if diffusion gradients (i.e. magnetic field variations in the mri magnet) are applied in at least 3 directions (6 directions improves the accuracy) that describes the 3-dimensional shape of diffusion. the fiber direction is indicated by the tensor’s main eigenvector which can be color-coded, yielding a cartography of the tracts' position and direction: red for leftright, blue for superior-inferior, green for anterior-posterior. no consensus has been reached about an appropriate criterion standard for evaluation the accuracy of dti, and this technique is primarily investigational at present. tractography potentially solves a problem for a neurosurgeon in terms of minimizing functional damage and determining the extent of diffuse infiltration of pathologic tissue to minimize residual tumor volume. in this way, tractography facilitates preoperative planning. tractographic images may help to clarify whether a tumor is compressing, abutting, or infiltrating the contiguous white-matter tracts. dti identify different tumor components, and to differentiate tumor invasion from normal brain tissue or edema. dti has demonstrated a potential in distinguishing gliomas and solitary metastasis in the brain parenchyma. significantly higher mean diffusivity, compared with levels in normal-appearing white matter, have been demonstrated in the peritumoral regions of both gliomas and metastases. peritumoral mean diffusivity of metastases and meningioma is significantly higher than that of gliomas. some clinical applications of dti are in the tract-specific localization of white matter lesions such as trauma and in defining the severity of diffuse traumatic brain injury. the localization of tumors in relation to the white matter tracts (infiltration, deflection), has been one the most important initial applications. in surgical planning for some types of brain tumors, surgery is aided by knowing the proximity and relative position of tumor. the use of dti for the assessment of white matter in development, pathology and degeneration has been the focus of over 2,500 research publications since 2005. results and discussions tractography combined with functional mri may potentially help in preoperative planning of brain tumors by mapping areas of active infiltration. the recent development of dti allows for direct examination of the brain microstructure, and dti has become a useful tool for investigation of brain disorders such as stroke, epilepsy, ms, brain tumors, and demyelinating disorders. in the surgery of patients with brain tumors, preservation of vital cerebral function is as important as maximizing tumor resection. the associated morbidity of aggressive resections can be significantly reduced by carefully preservation of vital cerebral function, and the quality of life of these patients will be largely improved. simultaneously maximizing tumor resection can reduce the chance of recurrence of tumors and improve longer patient survival and long-term functional status [11,12]. for realizing these two goals, many imaging modalities were used to assess brain tumors, which include conventional mri, positron emission tomography, magnetoencephalography, and functional mri [13..15]. these tools were used to determine the relationship of tumors with surrounding cortical function areas but provide no information concerning the status of the eloquent white matter tracts. knowledge of the structural romanian neurosurgery (2012) xix 2: 110 – 115 113 integrity and location of eloquent white matter tracts relevant to cerebral tumors is crucial in neurosurgical planning, because damage to these clinically eloquent pathways can result in postoperatively neurological deficits as damage of functional cortical areas. it is very important for designing appropriate neurosurgical plan that determining the exact location of tumors relevant to eloquent white matter tracts. dti is an important progress in the field of mr imaging. it is the only imaging method that can visualize the 3d structures of white matter tracts in the brain in vivo. recently some researchers have reported that dti can be used to illustrate the relationship of clinical eloquent white matter tracts with brain tumors [16,17], and they were all restricted to preoperative studies. in general, cerebral tumor may alter the adjacent wm in three different ways: by (1) displacing the wm tracts but with relative preservation of the fibers, (2) infiltrating the wm tracts, and (3) disrupting of the wm tracts. intracranial tumors may involve both functional cortical gray and white matter tracts. resection of these lesions requires a detailed understanding of functional anatomical relationships to surrounding tissue and adjacent white matter connections. this is most critical in dealing with eloquent cortical regions in the dominant hemisphere in which motor, sensory, speech, and cognitive functions are situated. an understanding of the location of the lesion in relation to surrounding eloquent tissue assists the surgeon in developing an intraoperative plan. many diagnostic modalities are currently used to define eloquent regions of the brain. standard mr imaging, positron emission tomography, magnetoencephalography, and fmr imaging are some of the tools used to investigate the location of functional cortex areas. [18..22] these preoperative studies aid in identifying regions of the brain involved in the cortical activities of sensation, motor, and speech. preoperative targeting of these areas helps in determining critical relationships of lesion location and surrounding cortical function. the images can then be fused with frameless stereotactic devices, allowing for the planning of optimal surgical approaches and determining the degree and volume of tumor resection. [22] preoperative diagnostic studies still must be confirmed by intraoperative cortical mapping of functional areas in many cases. intraoperative cortical mapping has been shown to maximize the extent of tumor resection and to minimize the associated morbidity of aggressive resections. [23] the goal of using these various mapping techniques is to delineate functional areas so that they can be preserved during surgical resection. aggressive surgical resection of brain tumors has been shown to correlate with longer patient survival and improved long-term functional status. [24, 25] some neurosurgeons advocate the removal of cortical tissue appearing grossly abnormal during the operative procedure, that is, based on the premise that areas of functional tissue are either displaced or destroyed by infiltrative tumors. [26] researchers of other studies found that tumors that grossly invade areas of functional cortex may still retain functional fiber tracts within the pathological tissue. using intraoperative cortical stimulation, ojemann, et al., [27] limited the extent of resection by demonstrating gross invasion of tumor into cortical and subcortical structures. 114 rizea et al 3d diffuse tensor imaging for preoperative planning it is unclear if these fibers are displaced or obliterated by tumors. diffusion-tensor imaging provides information on the directionality of water molecules at the cellular level, thus indicating the orientation of fiber tracts. in tissue with an ordered microstructure, like cerebral white matter, orientation can be quantified by measuring its anisotropic diffusion. diffusion-tensor calculations permit the characterization of diffusion in heterogeneously oriented tissue. [28] the spatial orientation of myelinated fiber tracts can then be represented as distinct white matter maps in easily read, color-coded directional maps. [29] recently, various investigators have used directional diffusion information to create maps of white matter connectivity. [30..32] these techniques may be valuable for tract identification when the white matter tracts are displaced by tumor. diffusion-tensor imaging is a useful new preoperative diagnostic tool for evaluating lesions close to vital cortical and subcortical structures. knowledge of this displacement assisted in preoperative planning by informing the surgeon of the tract’s shifted location, thus allowing for adaptation of the surgical corridor to avoid destruction of the communicating white matter bundles. in this instance the tumor was approached from a frontal direction, allowing for aggressive resection at the frontal pole of the tumor while avoiding the posteriorly deviated motor fibers. this resulted in postoperative improvement of the patient’s hemiparesis, presumably due to the elimination of pressure on the corticospinal tracts. conclusions the recent development of dti allows direct examination, in vivo, of some aspects of brain microstructure. dti has already shown to be of value in studies of neuroanatomy, fiber connectivity, and brain development. it has become interesting for investigation of different brain pathology, such as cerebral ischemia, trauma, ms, presumed ad and cognitive impairment, epilepsy, brain tumors and metabolic disorders. however, further improvement in technique and stable postprocessing analyses is needed to increase the utility of dti in both research and clinical applications. acknowledgements this study was possible with support from national research project 42-149 “parteneriate in domeniile prioritare” 2008; “imagini ale traiectelor nervoase (diffusion tensor imaging) integrate unui model anatomic 3d instrument de diagnostic si tratament”. references 1. bammer r, acar b, moseley me (2003) in vivo mr tractography using diffusion imaging. eur j radiol 45:223–234 2. ciccarelli o, toosy at, parker gj, wheelerkingshott ca, barker gj, miller dh, thompson aj (2003) diffusion tractography based group mapping of major white-matter pathways in the human brain. neuroimage 19:1545–1555 3. mori s, van zijl pc (2002) fiber tracking: principles and strategies a technical review. nmr biomed 15:468–480 4. basser pj (1995) inferring microstructural features and the physiological state of tissues from diffusionweighted images. nmr biomed 8:333–344 5. field as, alexander al (2004) diffusion tensor imaging in cerebral tumor diagnosis and therapy. top magn reson imaging 15:315–324 6. field as, alexander al, wu yc, hasan km, witwer b, badie b (2004) diffusion tensor eigenvector directional color imaging patterns in the evaluation of cerebral white matter tracts altered by tumor. j magn reson imaging 20:555–562 7. field as (2005) diffusion tensor imaging at the crossroads: fiber tracking meets tissue characterization in brain tumors. ajnr am j neuroradiol 26:2168– 2169 8. nimsky c, ganslandt o, hastreiter p, wang r, benner t, sorensen ag, fahlbusch r (2005) romanian neurosurgery (2012) xix 2: 110 – 115 115 intraoperative diffusion-tensor mr imaging: shifting of white matter tracts during neurosurgical procedures— initial experience. radiology 234:218–225 9. stadlbauer a, nimsky c, gruber s, moser e, hammen t, engelhorn t, buchfelder m, ganslandt o (2007) changes in fiber integrity, diffusivity, and metabolism of the pyramidal tract adjacent to gliomas: a quantitative diffusion tensor fiber tracking and mr spectroscopic imaging study. ajnr am j neuroradiol 28:462–469 10. yu cs, li kc, xuan y, ji xm, qin w (2005) diffusion tensor tractography in patients with cerebral tumors: a helpful technique for neurosurgical planning and postoperative assessment. eur j radiol 56:197–204 11. ammirati m, vick n, liao yl, et al. effect of the extent of surgical resection on survival and quality of life in patients with supratentorial glioblastomas and anaplastic astrocytomas. neurosurgery 1987;21:201–6. 12. mueller wm, yetkin fz, hammeke ta, et al. functional magnetic resonance imaging mapping of the motor cortex in patients with cerebral tumors. neurosurgery 1996;39:515–21. 13. schreckenberger m, spetzger u, sabri o, et al. localisation of motor areas in brain tumour patients: a comparison of preoperative [18f]fdg-pet and intraoperative cortical electrostimulation. eur j nucl med 2001;28:1394–403. 14. quinones-hinojosa a, ojemann sg, sanai n, dillon wp, berger ms. preoperative correlation of intraoperative cortical mapping with magnetic resonance imaging landmarks to predict localization of the broca area. j neurosurg 2003;99:311–8. 15. fujiwara n, sakatani k, katayama y, et al. evokedcerebral blood oxygenation changes in false-negative activations in bold contrast functional mri of patients with brain tumors. neuroimage 2004;21:1464– 71. 16. witwer bp, moftakhar r, hasan km, et al. diffusion-tensor imaging of white matter tracts in patients with cerebral neoplasm. j neurosurg 2002;97:568–75. 17. clark ca, barrick tr, murphy mm, bell ba. white matter fiber tracking in patients with spaceoccupying lesions of the brain: a new technique for neurosurgical planning? neuroimage 2003;20: 1601–8. 18. atlas sw, howard rs ii, maldjian j, et al: functional magnetic resonance imaging of regional brain activity in patients with intracerebral gliomas: findings and implications for clinical management. neurosurgery 38:329–338, 1996 19. bittar rg, olivier a, sadikot af, et al: cortical motor and somatosensory representation: effect of cerebral lesions. j neurosurg 92:242–248, 2000 20. grafton st, woods rp, mazziotta jc, et al: somatotopic mapping of the primary motor cortex in humans: activation studies with cerebral blood flow and positron emission tomography. j neurophysiol 66:735– 743, 1991 21. lehericy s, duffau h, cornu p, et al: correspondence between functional magnetic resonance imaging somatotopy and individual brain anatomy of the central region: comparison with intraoperative stimulation in patients with brain tumors. j neurosurg 92:589–598, 2000 22. mcdonald jd, chong bw, lewine jd, et al: integration of preoperative and intraoperative functional brain mapping in a frameless stereotactic environment for lesions near eloquent cortex. technical note. j neurosurg 90:591–598, 1999 23. berger ms, ojemann ga: intraoperative brain mapping techniques in neuro-oncology. stereotact funct neurosurg 58: 153–161, 1992 24. ammirati m, vick n, liao yl, et al: effect of the extent of surgical resection on survival and quality of life in patients with supratentorial glioblastomas and anaplastic astrocytomas. neurosurgery 21:201–206, 1987 25. ciric i, ammirati m, vick n, et al: supratentorial gliomas: surgical considerations and immediate postoperative results. gross total resection versus partial resection. neurosurgery 21:21–26, 1987 26. kelly pj: volumetric stereotactic surgical resection of intra-axial 27. ojemann jg, miller jw, silbergeld dl: preserved function in brain invaded by tumor. neurosurgery 39:253–259, 1996 brain mass lesions. mayo clin proc 63:1186–1198, 1988 28. pierpaoli c, jezzard p, basser pj, et al: diffusion tensor mr imaging of the human brain. radiology 201:637–648, 1996 29. pajevic s, pierpaoli c: color schemes to represent the orientation of anisotropic tissues from diffusion tensor data: application to white matter fiber tract mapping in the human brain. magn reson med 42:526–540, 1999 30. basser pj, pajevic s, pierpaoli c, et al: in vivo fiber tractography using dt-mri data. magn reson med 44:625–632, 2000 31. conturo te, lori nf, cull ts, et al: tracking neuronal fiber pathways in the living human brain. proc nat acad sci usa 96: 10422–10427, 1999 32. stieltjes b, kaufmann we, van zijl pc, et al: diffusion tensor imaging and axonal tracking in the human brainstem. neuroimage 14:723–735, 2001 microsoft word 4_serbandaniel_management2013 romanian neurosurgery (2013) xx 2: 151 – 156 151 management of intramedullary astrocytomas daniel serban, florin exergian, r.m. gorgan “bagdasar-arseni” clinical emergency hospital, neurosurgery i, spinal surgery, bucharest abstract primitive imt represent 8-10% of all primary tumors of the spinal cord. only 24% of all cns tumors in adults are imt. adult astrocytomas are 25-35% of total imt (1). we prospectively analyzed clinical, imaging and pathological data from all consecutive patients operated for intramedullary tumors in our department (neurosurgery i clinic, ward ii) between january 2003 and august 2009 (80 months). all surgical interventions were performed by the same surgical team. we emphasized the technical difficulties raised by ablation of imt depending on the type of the tumor and postoperative neurological outcome. key words: intramedullary astrocytomas, surgery, postoperative neurological outcome. abreviations: cns – central nervous system, intramedullary tumors – imt, spinal cord sc. general data primitive imt represent 8-10% of all primary tumors of the spinal cord. only 24% of all cns tumors in adults are imt. sc tumors are much less common than intracranial tumors with an overall prevalence of approximately an intramedullary tumor for four intracranial tumors, with variations depending on the type of tumor. for example, the location intracranial/spinal for astrocytomas is approximately 10/1, while the same ratio for ependymomas varies from 3/1 to 20/1 depending on the histological type of ependymoma. in particular, mixo-papillary ependymomas are found more frequently in the sc (1). material and methods patients enrolled in the study were hospitalized and operated in the period 2003-2009 in neurosurgery i clinic, ward ii, "bagdasar-arseni" clinical emergency hospital for imt in various locations. 59 patients were included in the study, age between 15 and 70 years, 40% female sex ratio = 1.5. 62 surgeries were performed. all patients were operated on by the same surgical team, same main operator. result distribution in the series we have studied the distribution by frequency of pathological diagnoses found is the following: first place is occupied by ependymomas, which account for about half of all pathological types 29 cases (46.77%) on the second place are astrocytomas 15 cases ( 24.19%) third place hemangioblastomas 5 cases ( 8.06%) the fourth place two lipomas and a 152 seban et al management of intramedullary astrocytomas fibrolipoma summing 3 cases (4.83%) on the fifth place are cavernomas, meduloblastomas, gangliogliomas, schwanomas by 2 cases = 3.22% each, summimg 8 cases = 12.88% the sixth place epidermoid cyst and a metastasis 1 case = 1.61% each, totaling 2 cases = 3.22% note that the first three histological types, ependymomas, astrocytomas, hemangioblastomas adds up to approx. 80% of all imt in adults. all other seven histological types account for the remaining 20% analysis of tumor histology for astrocytomas revealed predominant who grades i and ii 11 cases, compared with grades iii and iv 4 cases. the most common subtype was fibrillary astrocytoma, 6 cases. figure 1 pathological types of astrocytomas a b figure 2 thoracic pilocitic astrocytoma, preoperative a – t1 image, dye examination b – t2 image preoperative diagnosis was made by mri in all cases, native examination and t1-dye examination. location: 2 cervical astrocytomas 13.33% (of total astrocytoma localization) 1 cervico-thoracic astrocytoma 6.66% 12 thoracic astrocytomas 80.00% most frequent location is the thoracic spine region 80%. astrocytomas occupied between 2 and 4 vertebral segments, with an average of 2.86 vertebral levels. romanian neurosurgery (2013) xx 2: 151 – 156 153 figure 3 astrocytomas location relative to the vertebral segments (abscissa c1 to l1 vertebral segments, the ordered number of cases each vertebral level) surgery anesthesia, patient positioning and wound opening, laminoplasty or laminectomy, opening and suspension of dura mater and arachnoid and wound closure are similar to surgery for any imt. myelotomy is more difficult for astrocytomas compared to the same maneuver for ependymomas (2). these problems are caused by the fact that astrocytomas are not developed in the midline, are imt with asymmetric development. in addition the sc may be "distorted", anatomical landmarks being no longer valid. whenever possible, it is recommended myelotomy in the posterior midline. finding solutions for posterior midline are coagulation and cutting tortuous veins usually found on the posterior surface of the sc and subsequent search for the posterior midline in the area where sc have anatomic appearance above and below the area of astrocytoma development. another solution is mielotomy in the dorsal root entry zone (drez) where the extension of the tumor is greater and neurological deficits are higher. as ultimate solution is used the myelotomy in the area where astrocytoma is closest to the posterior surface of the sc, the aim being to harm as little as possible the medullary tissue. astrocytoma biopsy to determine the degree of malignancy is the next step, which may be decisive for the further conduct of the surgeon. if biopsy results revealed low-grade astrocytoma, we always tempted total or almost total ablation of astrocytoma. although pathological results showed high-grade astrocytoma we was looking for an eventual cleavage plane and tried subtotal or nearly total ablation of astrocytoma. the same attitude was adopted in situations where polar cysts were encountered. we started to search for the cleavage plane between the tumor and normal medullary tissue, near the cysts. always be dissected with extreme caution, lateral sides of astrocytomas, which may come in contact with cortico-spinal tracts and the front of astrocytomas, that sometimes "stuck" anterior spinal artery. cortico-spinal tracts damage and/or anterior spinal artery lesions causes significant postoperative neurological deficits, most often irreversible (3, 4, 5). tumor ablation technique used was intratumoral partial ablation, emphasizing the "step by step" plan and finding the cleavage plane fragment by fragment. the internal pressure relief stitch was used in 2 cases when the astrocytoma extended for 4 vertebral levels. whatever type of tumor ablation, hemostasis was achieved by mild pressure, washing the wound with cold saline and wallpapering outstanding intramedullary cavity with surgicel. type of tumor ablation total ablation was possible in 2 cases (13.33%), a t2-t4 thoracic pilocytic astrocytoma and a fibrillary astrocytoma 154 seban et al management of intramedullary astrocytomas t9-t10, situations in which was possible to found a cleavage plane. nearly total ablation was performed in one case (6.66%), a pilocytic astrocytoma t11l1. the most common was subtotal ablation in 10 cases (66.66%) being imposed by the infiltrative nature of tumor formation (glioblastoma one case, 3 cases of anaplastic astrocytoma, diffuse infiltrative fibrillary astrocytoma grade ii / iii who one case) and unable to find a plane of cleavage between the imt and normal medullary tissue in the other cases (2). biopsy was chosen as a temporary solution in two cases (13.33%), in which intra-operative cardiovascular disorders were recorded, the primary surgeon’s decision was to minimize the duration of the intervention. pathological results were pilocytic astrocytoma in one case and fibrillary astrocytoma in the other. a second intervention was scheduled within the first 14 days postoperatively performing the almost total ablation in the first case and the subtotal ablation in the second case. figure 4 t1, sagital; t2, sagital pilocitic astrocytoma figure 6 types of tumor ablation intraoperative complications intraoperative bleeding was not significant except for one case; the thoracic astrocytoma was extended on 4 levels. in the two cases described above, in which biopsy was performed only at the first surgery, complications are caused by cardiovascular pathology that patients already had and were not related to location or type of excision of imt. postoperative complications no significant postoperative complications were recorded. a b figure 5 thoracic pilocitic astrocytoma, six months postoperative a t1 dye examination, image b – t2 image romanian neurosurgery (2013) xx 2: 151 – 156 155 discussion postoperative neurological evolution there were no significant neurologic deficits. additional motor deficit was averaging 1.2 points on asia scale and sensitivity disorders, except deep sensibility disorders, not widened. favorable evolution from both surgical and neurological point of view is related to the location of imt and the type of ablation. the tumors in low thoracic spinal cord had the lower critical risk (in our series there were no astrocytomas located above c4). the type of tumor resection is also extremely important: there were only 2 cases with total resection and 2 cases with subtotal resected tumors. in other words, if the imt location is "high" and/or tumor ablation attempt more radical (total or almost total), the vital and neurological risks and complications are higher (6, 7, 8, 9). postoperatively there has been no significant neurological worsening, no death registered. explanations are: type of ablation that was only in 2 cases total and in one case quasi total determined by the presence of cleavage plane; predominantly astrocytomas location in thoracic levels, 12 cases, only 2 locations cervical and 1 cervico-thoracic junction 1; surgery less "aggressive" if the pathological results were high-grade astrocytomas. type of tumor ablation should be adapted to histological subtype of astrocytoma and especially must take into account the existence or absence of a cleavage plane (8, 9). brotchi (2) in an article published in 1997 emphasizes that any surgical attitude addopted, if the astrocytoma is grade iii or iv, long-term results are similar. in these cases the surgeon's duty is to obtain a correct pathological result, to achieve decompression of the sc without affecting medullary tissue, without postoperative neurological deterioration. adjuvant treatment radiation radiation therapy has no indication for low-grade astrocytomas. all authors (2, 3, 4, 5, 6) agree that in pilocytic astrocytoma who grade i postoperative radiotherapy should not be done, just followed up the evolution by clinical and imaging surveillance. in these cases the neurological evolution, the risk of relapse and duration of postoperative survival are directly related to the type of tumor ablation, total or that sometimes occur after radiation: myelitis postirradiation and bone-marrow suppression. for high-grade gliomas, who grade iii and iv was made postoperative radiotherapy, fractionated doses of 50-54 gy in 24 sessions. for grade ii gliomas who histological with features of malignancy and recurrent gliomas grade ii radiotherapy was made with doses of 40-46 gy, fractionated in 20 sessions (10). postoperative radiotherapy was done in patients with who grade iii anaplastic astrocytomas (3 cases), glioblastoma who grade iv (1 case) and in who grade ii astrocytomas with anaplastic histological elements (1 case) in which we could not perform complete ablation. chemotherapy it was recommended as adjuvant therapy in the pediatric population because of disastrous side effects that radiation has on children. for adults was indicated in cases 156 seban et al management of intramedullary astrocytomas where astrocytomas are who grade iii and iv, imt resection was not complete, did not respond to radiotherapy and tumor recurrences were recorded or "tumoral growth" continues. etoposide was used initially, then temozolamide. temozolamide administered in doses of 150-200 mg./m2/day for 5 days a week for 4 weeks = a cycle (11). in the present series we did not have patients with postoperative chemotherapy. conclusions astrocytomas grade i could be completely or partially ablated. total or almost total ablation is due to the cleavage plane between imt and normal medullary tissue. in low-grade astrocytomas, where there plane cleavage is present, total or almost total ablation is the goal. astrocytomas grade iii and iv and part of grade ii astrocytomas (with anaplastic cells elements) were subtotally ablated because of their infiltrative nature. there were no major intraoperative complications, postoperative immediately and/or delayed. all cases of grade iii and iv astrocytomas have clear indication for postoperative radiotherapy. references 1. dolecek ta, propp jm, stroup ne, kruchko c. cbtrus statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2005-2009. neuro-oncol.2012;14 ( 5): v1-v49 2. brotchi j. intramedullary spinal cord astrocytomas: diagnosis and treatment. crit rev neurosurg. 1997;7:83–88. 3. cristante lhh. surgical management of intramedullary spinal cord tumors: functional outcome and sources of m8. grimm s., chamberlain m.c. adult primary spinal cord tumors. expert rev. neurother. 2009; 9(10) : 1487 – 95. 4. epstein f.surgical management of intramedullary spinal cord tumors : functional outcome and sources of morbidity (comment). neurosurgery.1994; 35: 76 5. chamberlain mc, tredway tl. adult primary intradural spinal cord tumors: a review. curr neurol neurosci rep. 2011; 11(3):320-8. 6. garcés-ambrossi gl, mcgirt mj, mehta va, sciubba dm, witham tf, bydon a, et al. factors associated with progression free survival and longterm neurological outcome after resection of intramedullary spinal cord tumors: analysis of 101 consecutive cases. clinical article. j neurosurg spine. 2009; 11:591–599 7. harrop js, ganju a, groff m, bilsky m. primary intramedullary tumors of the spinal cord, spine. 2009; 34,( 22s), s69–77 8. kim ms, chung ck, choe g, kim ih, kim hj. intramedullary spinal cord astrocytoma in adults: postoperative outcome. journal of neurooncology.2001; 52: 85–94 9. v benes v 3rd, barsa p, benes v jr, suchomel p. prognostic factors in intramedullary astrocytomas: a literature review. eur spine j .2009; 18:1397–1422 10. isaacson steven r. radiation therapy and the management of intramedullary spinal cord tumors. journal of neuro-oncology.2000, 47: 231–238 11. chamberlain m.c. temozolomide for recurrent low-grade spinal cord gliomas in adults. cancer. 2008;113(5):1019-1024. romanian neurosurgery (2019) xxxiii (2): pp. 105-109 doi: 10.33962/roneuro-2019-021 www.journals.lapub.co.uk/index.php/roneurosurgery tailored approach for the resection of planum sphenoidale meningiomas oana-mihaela punga1, cristiana-elena moisescu1, d. iftimie1, d. adam1,2 1 department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania abstract background and importance. planum sphenoidale meningiomas are relatively rare tumours that can grow to a considerable size before determining noticeable symptoms. modern imaging techniques can detect these tumours of varying size. surgical resection of planum sphenoidale meningiomas can be performed by adapting the approach to the size of the tumour. clinical presentation. a 56-year-old woman presented with a small (2 cm in diameter) planum sphenoidale meningioma that was resected through a frontal craniotomy performed with a 4,5 cm trephine at the level of the frontal sinus. the second case is that of a 55-year-old woman that presented with a large planum sphenoidale meningioma (5,6 cm in the antero-posterior plane and 5,5 cm craniocaudally) extending to the tuberculum sellae and sellar diaphragm, reaching the anterior wall of the third ventricle. in this case, a bifrontal craniotomy was performed with frontal sinus cranialization and resection of falx cerebri, achieving a simpson ii resection. both cases presented a favourable postoperative evolution, without any deficits and an excellent cosmetic result. conclusion. the approach for tumours of the anterior skull base must be tailored to the size of the tumour. a minimally invasive approach through the frontal sinus should not be avoided in cases with small tumours. introduction meningiomas are the most common primary intracranial tumours, arising from arachnoidal cells. they are benign, slow-growing tumours and the cognitive impairment as well as behavioural changes they can induce can easily be mistaken for dementia or depression1. planum sphenoidale meningiomas are relatively rare tumours that originate from the flat surface of the sphenoid bone, anterior to the optic chiasm. they are closely related to tuberculum sellae tumours but with a different clinical presentation. tuberculum sellae tumours determine early visual deficits even when lesions are small, due to their proximity to the optic chiasm. therefore, planum sphenoidale meningiomas can grow to a considerable size before determining keywords minimally invasive approach, planum sphenoidale meningiomas corresponding author: dragos iftimie “saint pantelimon” clinical emergency hospital, bucharest, romania iftimie.dragos@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 106 oana-mihaela punga, cristiana-elena moisescu, d. iftimie, d. adam noticeable symptoms2. modern imaging techniques can detect these tumours of varying size and surgical treatment is still the most commonly used treatment option. approaches that are used may vary depending upon tumour size and location, adjacent neurovascular structures and surgeon’s experience as well as preference3. clinical presentations case 1 a 55-year-old female, known with chronic viral hepatitis c and hypermetropic astigmatism with retinal angiosclerosis, was admitted in our department for headaches that appeared 3 months prior to presentation. the neurological examination was otherwise normal. a contrast mri examination revealed a 2 cm in diameter intracranial extra-axial tumour at the level of the planum sphenoidale, the radiological aspect suggesting a meningioma (figure 1). figure 1. axial (a), sagittal (b) and coronal (c) contrast mri images revealing a planum sphenoidale meningioma the approach was performed with a 4.5 cm trephine at the level of the frontal sinus (figure 2) and the tumour was completely resected, while preserving the integrity of the olfactory tract. postoperatively, the patient presented a favourable outcome with remission of headaches and no new neurological deficits. postoperative control mri confirmed total resection of the tumour (figure 3). figure 2. postoperative x-ray revealing the location of the craniotomy a b c a b 107 tailored approach for the resection of planum sphenoidale meningiomas figure 3. postoperative axial (a), sagittal (b) and coronal (c) images of t1 with contrast mri scan confirming the total resection of the tumour case 2 a 56-year-old woman was brought to the emergency department of our hospital for drowsiness and cognitive deterioration that began 3 months prior to presentation and progressively worsened. neurological examination revealed right anisocoria, no motor deficits, positive babinski on the left side and a gcs of 12 points. the emergency native ct scan showed an isodense frontal tumor with bilateral extension and significant perilesional edema. the contrast mri subsequently performed revealed a large extra-axial, isodense tumor with intense, homogenous enhancement, originating at the planum sphenoidale, imagistic features suggestive for a meningioma (figure 4). figure 4. t1 weighted with contrast mri in axial (a), sagittal (b) and coronal (c) planes that revealed a large planum sphenoidal meningiomas, 5.6 cm in the antero-posterior plane and 5.5 cm cranio-caudally this tumour was resected through a large bifrontal craniotomy (figure 5). after bone flap elevation and cranialization of frontal sinus, the dura mater was opened bilaterally and the anterior third portion of the superior sagittal sinus was ligated and resected. the tumour was completely removed with coagulation of dural insertion (simpson ii resection). figure 5. bifrontal craniotomy performed for the resection of the large planum sphenoidale meningioma postoperatively, the patient presented a favorable evolution with no new neurological deficits. the control ct showed complete removal of the tumor (figure 6) and the histopathological examination revealed a transitional meningioma (who grade i). figure 6: postoperative ct scans that confirm a total resection of the tumor discussions we presented two cases of planum sphenoidale meningiomas of different sizes, both operated through a bifrontal approach, with the extent of craniotomy adapted to tumor size. in both cases, a total tumor resection was achieved with no surgical morbidity. planum sphenoidale meningiomas can be resected using different surgical routes, each with its advantages and disadvantages, allowing the a c b c 108 oana-mihaela punga, cristiana-elena moisescu, d. iftimie, d. adam neurosurgeon to make decisions regarding the surgical strategy. the factors influencing it are: tumor size and its relationship to adjacent neurovascular structures, the patient’s symptoms and the neurosurgeon’s experience. there are various transcranial approaches to resect planum sphenoidale meningiomas: bicoronal subfrontal, unilateral subfrontal, pterional transsylvian, anterior interhemispheric, extended bifrontal, skull base techniques and fronto-temporal orbito-zygomatic4,5. the bifrontal craniotomy is generally used for most midline anterior cranial fossa lesions mainly because of the flexible operative working angles that it provides and for its generous exposure of the tumor6. when compared with bifrontal craniotomy, the pterional approach avoids the frontal sinuses, averting the necessity to sacrifice the anterior superior sagittal sinus. it does not imply the necessity to manipulate both frontal lobes. this approach also allows early identification of the optic apparatus, therefore facilitating its protection during tumor resection7,8. nakamura et al. compared in a series of patients, the bifrontal approach with frontolateral approaches, concluding that they prefer the frontolateral approaches that offer an adequate access to the tumor with less brain exposure while allowing a total tumor removal with a low morbidity rate9. also, a minimally invasive approach via a supraorbital incision and bone opening is also reportedly used quite frequently in removing these tumors10. another option is the endoscopic endonasal approach. in one study, ajlan et al. compared transcranial with endoscopic transnasal resection for anterior fossa tumors. while the transnasal endoscopic access associated fewer complications, the tumor resection rates were much lower compared to the transcranial approaches11. also, in a small single institution study, the endoscopic approach resulted in equal rates of resection with better outcomes and less trauma to the brain.12 however, in 2012 komotar et al. published a meta-analysis of 60 studies including over 1,000 patients with tuberculum sellae, planum sphenoidale or olfactory groove meningiomas resected either via an endoscopic or transcranial approach. the results indicated that patients had similar outcomes regardless of the approach with a higher rate of csf leaks associated to the endoscopic approach13. the transcranial approaches may be better suited for planum sphenoidale or tuberculum sellae meningiomas that are large, with significant lateral extension or vascular involvement. they offer better control and thus better tools to deal with vascular complications. ultimately, the optimal approach is predicated by the experience of the surgeon and the patient’s characteristics and should be determined on a case by case basis14. conclusions the approach for meningiomas of the anterior skull base must be tailored to the size of the tumor. a minimally invasive approach through the frontal sinus should not be avoided in cases with small tumors. references 1. chiang gsh, goh lg. olfactory groove and planum sphenoidale meningioma: dementia masquerade. can fam physician. 2017;63(4):288-291. http://www.ncbi.nlm. nih.gov/pubmed/28404703. accessed april 14, 2019. 2. fox d, khurana vg, spetzler rf. olfactory groove/planum sphenoidale meningiomas. in: meningiomas. london: springer london; 2009:327-332. doi:10.1007/978-1-84628784-8_34 3. schroeder hws. indications and limitations of the endoscopic endonasal approach for anterior cranial base meningiomas. world neurosurg. 2014;82(6):s81-s85. doi:10.1016/j.wneu.2014.07.030 4. estevão ia, camporeze b, matricardi g, et al. tuberculum sellae meningioma: is there an ideal approach? med express. 2017;4(4). doi:10.5935/medicalexpress.2017.04.03 5. lynch jc, gonçalves mb, pereira ce, melo w, temponi gf. the extended pterional approach allows excellent results for removal of anterior cranial fossa meningiomas. arq neuropsiquiatr. 2016;74(5):382-387. doi:10.1590/0004282x20160058 6. rhoton al. the anterior and middle cranial base. neurosurgery. 2002;51(suppl_4):s1-273-s1-302. doi:10.1097 /00006123-200210001-00007 7. mathiesen t, lindquist c, kihlström l, karlsson b. recurrence of cranial base meningiomas. neurosurgery. 1996;39(1):2-7; discussion 8-9. http://www.ncbi.nlm.nih. gov/pubmed/8805134. accessed april 14, 2019. 8. poppen jl. operative techniques for removal of olfactory groove and suprasellar meningiomas. clin neurosurg. 1964;11:1-7. http://www.ncbi.nlm.nih.gov/pubmed/5854772. accessed april 14, 2019. 109 tailored approach for the resection of planum sphenoidale meningiomas 9. nakamura m, struck m, roser f, vorkapic p, samii m. olfactory groove meningiomas: clinical outcome and recurrence rates after tumor removal through the frontolateral and bifrontal approach. neurosurgery. 2007;60(5):844-852. doi:10.1227/01.neu.0000255453.20602.80 10. arai h, sato k, okuda o, et al. transcranial transsphenoidal approach for tuberculum sellae meningiomas. acta neurochir (wien). 2000;142(7):751-757. doi:10.1007/s00701 0070089 11. ajlan am, choudhri o, hwang p, harsh g. meningiomas of the tuberculum and diaphragma sellae. j neurol surg b skull base. 2015;76(1):74-79. doi:10.1055/s-0034-1390400 12. bander ed, singh h, ogilvie cb, et al. endoscopic endonasal versus transcranial approach to tuberculum sellae and planum sphenoidale meningiomas in a similar cohort of patients. j neurosurg. 2018;128(1):40-48. doi:10.3171/ 2016.9.jns16823 13. komotar rj, starke rm, raper dms, anand vk, schwartz th. endoscopic endonasal versus open transcranial resection of anterior midline skull base meningiomas. world neurosurg. 2012;77(5-6):713-724. doi:10.1016/j.wneu.2011. 08.025 14. koutourousiou m, fernandez-miranda jc, stefko st, wang ew, snyderman ch, gardner pa. endoscopic endonasal surgery for suprasellar meningiomas: experience with 75 patients. j neurosurg. 2014;120(6):1326-1339. doi:10.3171/ 2014.2.jns13767. microsoft word 15tascua_giantasymptomatic.doc romanian neurosurgery (2010) xvii 3: 359 – 363 359 giant asymptomatic intracranial hydatid cyst in a 3 years old child – case report a. tascu, a.v. ciurea, iulia vapor, a. iliescu, f. brehar “bagdasar-arseni”clinical emergency hospital, bucharest, romania introduction objective although hydatid cysts are known commonly to affect the liver and lung, it can also affect the brain (1-2% of cases). brain involvement is more commonly seen in children (50-75% of intracranial hydatid cysts), and usually has intraparenchymal localization. in this paper we present a case of a 3 years old child diagnosed incidentally with a giant intracranial hydatid cyst. case presentation the patient was admitted in the hospital with a mild craniocerebral trauma, with an epicranial haematoma. the clinical and neurological examinations were normal. the ct scan of the brain revealed a giant solitary cystic lesion, located in the left frontoparietal lobe, with features suggestive of hydatid cyst. the removal of the cyst, without rupture, was performed using the dowling technique modified by aranainiguez. postoperatively the neurological exam was normal and the patient was asymptomatic at 7 months follow-up. conclusion the hydatid cyst usually enlarges slowly, but this is variable, the growth being higher in children, in whom it can reach giant dimensions without or with minimal symptoms. it is a benign lesion, and the removal of the cyst without rupture is very important. case presentation a three years old child was admitted in the hospital after a mild cranio-cerebral trauma. the neurological exam was normal and the local exam revealed a frontoparietal epicranial hematoma. the skull xrays showed a linear parietal fracture. the ct scan of the brain revealed a giant solitary cystic lesion, hypodense, nonenhancing, located in the left frontoparieto-occipital lobe, with the diameter 10 cm, and a midline shift of 1, 5 cm. the brain mri (figures 1, 2, 3) showed a cystic lesion hyperintense on the t2-weighted images (similar to csf) with a hypointense halo around the cyst capsule. the features were suggestive of hydatid cyst. the clinical exam, chest x-rays and abdominal ultrasound effectuated showed no signs of other localisations. routine laboratory tests were all normal. the serologic tests for hydatid disease were not performed. intraoperatively we used the dowling method modified by arana-iniguez. a large craniotomy was performed (figure 5 a). after that the dura mater was opened carefully taking care not to open the cyst because the cortex overlying the cyst was very thin (figure 5 b) a linear corticotomy was made (this must be no less than three quarters of the diameter of the cyst) (figure 5 c, d). saline solution (0, 9%) was used to dissect the cyst from the surrounding brain and to facilitate the hydatid removal (figure 360 a. tascu et al giant asymptomatic intracranial hydatid cyst 5 e, f). also is useful using the valsalva maneuvre and counterpressure to the surrounding brain. the hydatid cyst was removed without rupture (figure 6). the dura was closed in a watertight fashion after filling-up the remaining cavity (figure 5 g) with saline solution (0, 9%). the postoperative ct scan showed no signs of bleeding. the 7 months follow-up ct scan revealed a subdural liquid accumulation which was non-compressive, so we decided not to operate the patient and follow-up periodically (figure 5 a, b). figure 1 preoperative mri shows a cystic lesion hyperintense on t2-weighted images (similar to csf) with a hypointense halo around the cyst capsule figure 2 preoperative mri: t1 weighted images shows a cystic lesion. midline shift is 1,5 cm. also can be seen the epicranial haematoma romanian neurosurgery (2010) xvii 3: 359 – 363 361 figure 3 preoperative mrit2 weighted images, sagittal sections shows the compression of corpus callosum a b figure 4 (a, b) postoperative ct scan (7 months follow-up) shows a subdural collection, non-compressive a b c 362 a. tascu et al giant asymptomatic intracranial hydatid cyst d e f g figure 5 intraoperative images. alarge craniotomy ; bafter opening dura mater you can notice that cortex overlying the cyst is very thin; ccorticotomy must be at least ¾ of the diameter of the cyst; d counterpressure applied to surrounding brain is useful; e, f dissection of the hydatid cyst from surrounding brain is made using saline solution; gbig cavity which remains after the removal of the cyst sometimes can lead to subdural collections and porencephalic cysts. figure 6 hydatid cyst after removal without rupture discussion hydatid cyst is an anthropozoonosis caused by ecchinococcus granulosis. infection with the larval stage of the tapeworm causes hydatid cysts in humans. hydatid disease is endemic in the sheep and cattle-raising areas of the world (mediterranean countries, south america, middle east and australia). in romania, the disease is endemic in dobrogea, in the mountain areas, and in the towns located along the danube river. although hydatid cysts are known commonly to affect the liver and lung, it can also affect the brain (only 1-2% of cases). brain involvement is more commonly seen in children (50-75% of intracranial hydatid cysts), and usually has intraparenchymal localization. primary cysts are usually solitary, secondary cysts are usually multiple (from embolization of cardiac cysts that rupture or from iatrogenic rupture of cerebral cyst). ninety percent of the cases have solitary lesion, most frequently supratentorial, intraparenchymal, and in the middle cerebral artery territory. the cyst usually enlarges slowly, rates of approximately 1 cm per year are quoted, but this is variable, the growth being higher in children where it can reach a growth rate of 4, 5 cm every 6 months. there are debates about the presence of romanian neurosurgery (2010) xvii 3: 359 – 363 363 solitary brain hydatid cyst. some authors sustain the hypothesis that usually the cysts are multiple but due to the fact that the growth rate of intracranial hydatid cyst is higher than in other organs, at the moment of diagnose the others are too small to be detected clinically or radiological. sometimes hydatid cyst with other localisation can be diagnosed 20-30 years after the diagnosis and treatment of brain hydatid cyst. also, usually, the postoperative treatment includes the administration of drugs which can also inhibit the growth of other possible cysts. also the immune system can inhibit the growth of hydatid cyst in other organs, except the central nervous system due to the limited access to the immune system. the diagnostic tools include ct and mri (both may provide signs of a hydatid cyst specific enough to achieve a diagnosis) and serologic tests for hydatid disease, such as enzyme-linked immunosorbent assay or indirect hemagglutination. the ct images reveal a cystic lesion, round, without any surrounding edema and without enhancement. on t2-weighted mr images, the hydatid cyst appears as a cystic lesion with a hypointense halo around the cyst capsule. the main treatment is complete removal of the cyst without rupture. adjuvant therapy with mebendazole is recommended in cases with systemic disease, recurrence or when rupture of the cyst occurs during surgery. this can be done by using the dowling technique modified by aranainiguez. this consists of dissection of the cyst from the surrounding brain using a saline solution (0, 9%), also using the valsalva maneuvre and counterpressure to the surrounding brain. it is very important not to rupture the cyst. the main two complications of the rupture of the cyst are the anaphylactic reaction, and the contamination of the adjacent tissues with possible recurrence of multiple hydatid cysts. in the literature are reported recurrence rates of 19% and a mortality of 10,12%, morbidity 9, 8% and perioperative mortality of 8,48 %. when large cysts are removed, in the pediatric population, have been reported subdural collections and porencephalic cysts. in some cases if those lesions have mass effect it might be necessary the placement of a shunt. conclusions hydatid cyst usually is a slow growing lesion, but this is variable, the growth being higher in children in whom it can reach giant dimensions without or with minimal symptoms. it is a benign lesion and the removal of the cyst without rupture is the most important surgical goal. references 1.a leland albright, ian f pollack, p david adelson. principles and practice of pediatric neurosurgery: 1191-1192, 2009 2.farid radmenesh, farideh nejat. primary cerebral hydatid cyst: two cases report. iran j pediatrics, 18: 8386, 2008 3.j lunardi p, missori p, di lorenzo n, fortuna a. cerebral hydatidosis in childhood: a retrospective survey with emphasis on long-term follow-up. neurosurgery, 29 (4): 515-7, 1991 oct 4.mark s greenberg. hanbook of neurosurgery, 2006: 238-239 5.mehmet turgut, kemal benli, muzaffer eryilmaz. secondary multiple intracranial hydatid cysts caused by intracerebral embolism of cardiac echinococcosis: an exceptional case of hydatidosis. case report. j neurosurg, 86: 714-718, 1997 6.nur altinors, murad bavbek, hakan h caner, bulnet erdogan. central nervous system hydatidosis in turkey: a cooperative study and literature analysis of 458 cases. j neurosurgery, vol 93: 1-8, 2000 july 7.said hilmani, abderrazak bertal, abdelhakim lakhdar, ali ouboukhlik, abdenabi elkamar, abdessamad elazhari. craniocerebral hydatid cyst. case illustration. j neurosurg (1 suppl pediatrics), 105: 77, 2006 8.salaou ouman, ibrahiouin kadija, cheleaoiu abdemajid, hilmani said, et al. intracerebral hydatid cyst: about 1104 cases. african journal of neurological sciences, vol 26: 22-26, 2007 9.tazun y, kadioglu hh, izci y, et al. the clinical, radiological and surgical aspects of cerebral hydatid. pediatr neurosurg, 40 (4): 55-60, 2004 10.yusuf izci, yusuf tüzün, halil ibrahim seçer, engin gönül. cerebral hydatid cysts: technique and pitfalls of surgical management. j neurosurg, 24: 1-5, 2008 8agrawalamit_cladophialophora romanian neurosurgery (2014) xxi 1: 73 77 73 cladophialophora bantiana brain abscess masquerading cerebral tuberculoma in an immunocompetent host amit agrawal1, vissa shanthi2, k.v. murali mohan3, kishor v. hegde4, umamaheshwar reddy v.5 1professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2associate professor of pathology, department of pathology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 3professor of pathology, department of pathology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 4professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 5assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract phaeohyphomycosis is a term that collectively describes fungal infections caused by moulds and yeasts that have brown-pigmented cell walls (due to the presence of melanin). we report a case of 45 year female who had multiple coalescing lesions in the right basal ganglionic and thalamic region. based on the imaging and investigation findings a diagnosis of cerebral tuberculoma was suspected. histopathology of the excised specimen showed brown colored fungal hyphae surrounded by neutrophilic infiltrate. a diagnosis of phaeohyphomycosis caused by cladophialophora bantiana was made and accordingly antifungal treatment was started. brain abscess caused by cladophialophora bantiana in an immunocompetent host is relatively uncommon and usually associated with overall high mortality. the best outcomes have been reported in patients who receive both surgical excision of the abscess followed by systemic antifungal therapy. in view of its rarity of these lesions preoperative diagnosis is difficult particularly in an immunocompetent host and absence of other risk factors. key words: phaeohyphomycosis, cerebral, fungal infection, brain introduction phaeohyphomycosis infections is caused by dematiaceous fungi i.e., fungi that contain melanin in their cell walls. 1-3 cladophialophora bantiana usually causes brain abscess in immunocompromised hosts. (1-4) brain abscess caused by cladophialophora bantiana in an immunocompetent host is relatively 74 agrawal et al cladophialophora bantiana brain abscess uncommon. (1-3) in present article we discuss a case of brain abscess caused cladophialophora bantiana in an immunocompetent host which was masquerading cerebral tuberculoma. case report a 45 year female presented with the history of sudden onset of loss of consciousness for 10 minutes of 1 day back. while she regained the consciousness there was weakness of left upper and lower limbs, slurring of speech, difficulty in walking, moderate headache and multiple episodes of vomiting. there was no history of fever or seizures. there was no history of diabetes mellitus or any major illness in the past. at the time of examination she was conscious, dull and was obeying commands. pupils were bilateral equal and reacting to light. fundus showed mild papilledema and there was left upper motor neuron type of facial nerve palsy. there was weakness of left upper and lower limbs of grade 2/5 with exaggerated deep tendon reflexes. left plantar reflex was extensor and right was flexor. all the blood investigations were normal except raised esr (46 mm in 1st hour) and leukocytosis (18,000/mm3). test for hiv was negative. chest x-ray was normal. ct scan showed multiple coalescing lesions in the right basal ganglionic and thalamic region with significant perilesional edema and mass effect (figure 1). based on the imaging and investigation findings a diagnosis of cerebral tuberculoma was suspected and she was started on att and steroids. on 3rd admission she suddenly lapsed into altered sensorium (gcs-e1v1m2), right pupil became dilated and non-reacting. an urgent mri showed increase in cerebral edema and mass effect (figure 2). the patient was taken for emergency decompressive right frontal craniotomy and biopsy of the lesions. there was illdefined lesion with thin walled capsule with caseating material and yellowish nonfoul smelling pus. again an intraoperative diagnosis was tubercular abscess. following surgery the patient was kept on elective ventilation. she was continued on antiedema measures, anti-epileptics and was continued on att. there was no improvement in her condition. histopathology showed brown colored fungal hyphae surrounded by neutrophilic infiltrate. septate fungal hyphae were surrounded by neutrophilic infiltrate (figure 3). a diagnosis of phaeohyphomycosis caused by cladophialophora bantiana was made and accordingly antifungal treatment was started. however she did not respond to treatment and succumbed to the infection. discussion phaeohyphomycosis is a term that collectively describes fungal infections caused by moulds and yeasts that have brown-pigmented cell walls (due to the presence of melanin). (4) romanian neurosurgery (2014) xxi 1: 73 77 75 figure 1 (a, b and c) ct scan brain showing multiple coalescing lesions in the right basal ganglionic and thalamic region with minimal peripheral enhancement, significant mass effect and midline shift figure 2 (a, b and c) mri t2w sequences showing multiple ring shaped hyerintense lesions in right basal ganglionic and thalamic region with surrounding hypointense rim, extensive peri-lesional edema and mass effect figure 3 (a and b) brown colored fungal hyphae surrounded by neutrophilic infiltrate (h&e, x400), (c and d) septate fungal hyphae surrounded by neutrophilic infiltrate (pas, x400) cladophialophora bantiana has been implicated as a leading cause of cerebral phaeohyphomycosis, and is a soil-based neurotropic fungus, which has affinity to glial tissue. (2) although not clearly established, most probably the portal of entry is through respiratory tract. (2, 3, 5, 6) however, in the majority of patients of cerebral phaeohyphomycosis there may not be any evidence of sinus or lung disease. (7, 8) the exact pathogenesis of primary cerebral phaeohyphomycosis is presently unknown 9 and it has been suggested that the pathogenicity is primarily due to melanin (melanin is present in their cell walls and imparts the characteristic dark color to their conidia and hyphae) which scavenges free radicals produced by phagocytic cells. (2, 10, 11) clinically phaeohyphomycosis can present from solitary subcutaneous nodules to lifethreatening infections, brain abscess and disseminated disease. (3) as was seen in present case features of raised intracranial pressure (headache) followed by focal neurological deficits and/or generalized seizures are the most common presentation of cladophialophora brain abscess. (2, 3) because of its rarity it is difficult to make a pre-operative diagnosis of cerebral phaeohyphomycosis especially in an immunocompetent host. 3 a number of commoner disorders (i.e. tuberculosis, cysticercosis, demyelinating disorders, pyogenic abscess, toxoplasmosis, fungal infections, neurosyphilis, sarcoidosis, behcet disease, radiation encephalopathy, cerebral venous thrombosis and vasculitic disorders) including the immune status of the patient needs to be considered in the 76 agrawal et al cladophialophora bantiana brain abscess differential diagnosis of ring-enhancing lesions on neuroimaging. (12-14) as we confronted in the case, presently there are no specific initial clinical or laboratory feature that makes a preoperative fungal abscess diagnosis possible. (2, 3, 15) the diagnosis is only possible once the tissue is submitted for the histopathological or microbiological examination. (2, 3) because of the rarity of cerebral phaeohyphomycosis there are no standard guidelines for therapy and not many clinical trials comparing different treatment regimens. (2) the best outcomes were seen in patients who receive both surgical excision of the abscess followed by systemic antifungal therapy. (2, 5, 15) the combination of amphotericin b, 5-fc, and itraconazole has been suggested to improve survival; however only in few cases this triple combination is used. (1, 16-18) newer anti-fungal agents (voriconazole and itraconazole) have been found to be effective for the management of these unusual lesions. (19, 20) conclusion in summary, cerebral phaeohyphomycosis is associated with overall high mortality (around 70%) (2, 3, 15, 21) and the cladosporium bantianum species has been reported particularly to be more virulent with poorer outcome. 1 in view of its rarity of these lesions preoperative diagnosis is difficult particularly in an immunocompetent host and absence of other risk factors. till we find a better ways to diagnose such cases in advance we need to depend on histopathology and microbiological investigations of the tissue. address for correspondence: dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 references 1.borkar sa, sharma ms, rajpal g, jain m, xess i, sharma bs. brain abscess caused by cladophialophora bantiana in an immunocompetent host: need for a novel cost-effective antifungal agent. indian journal of medical microbiology 2008;26:271-274. 2.revankar sg, sutton da, rinaldi mg. primary central nervous system phaeohyphomycosis: a review of 101 cases. clinical infectious diseases : an official publication of the infectious diseases society of america 2004;38:206-216. 3.george ia, mathews ms, karthik r, et al. fatal cerebral abscess caused by cladophialophora bantiana. the journal of the association of physicians of india 2008;56:470-472. 4.surash s, tyagi a, de hoog gs, zeng js, barton rc, hobson rp. cerebral phaeohyphomycosis caused by fonsecaea monophora. medical mycology 2005;43:465472. 5.levin tp, baty de, fekete t, truant al, suh b. cladophialophora bantiana brain abscess in a solidorgan transplant recipient: case report and review of the literature. journal of clinical microbiology 2004;42:43744378. 6.goel a, satoskar a, desai ap, pandya sk. brain abscess caused by cladosporium trichoides. british journal of neurosurgery 1992;6:591-593. 7.sutton da, slifkin m, yakulis r, rinaldi mg. u.s. case report of cerebral phaeohyphomycosis caused by ramichloridium obovoideum (r. mackenziei): criteria for identification, therapy, and review of other known romanian neurosurgery (2014) xxi 1: 73 77 77 dematiaceous neurotropic taxa. journal of clinical microbiology 1998;36:708-715. 8.horré r, de hoog g. primary cerebral infections by melanized fungi: a review. stud mycol 1999;43:93. 9.brown jw, nadell j, sanders cv, sardenga l. brain abscess caused by cladosporium trichoides (bantianum): a case with paranasal sinus involvement. southern medical journal 1976;69:1519-1521. 10.casadevall a, rosas al, nosanchuk jd. melanin and virulence in cryptococcus neoformans. current opinion in microbiology 2000;3:354-358. 11.dixon dm, polak a, szaniszlo pj. pathogenicity and virulence of wild-type and melanin-deficient wangiella dermatitidis. journal of medical and veterinary mycology : bi-monthly publication of the international society for human and animal mycology 1987;25:97106. 12.garg rk, sinha mk. multiple ring-enhancing lesions of the brain. journal of postgraduate medicine 2010;56:307-316. 13.cortese i, nath a. case 11: a young woman with ring-enhancing brain lesions. medgenmed : medscape general medicine 2006;8:3. 14.omuro am, leite cc, mokhtari k, delattre j-y. pitfalls in the diagnosis of brain tumours. lancet neurology 2006;5:937-948. 15.deb s, khan ak, debasish b, subroto b. intracranial necrotizing granuloma caused by cladophialophora bantiana. neurology india 2005;53:335-336. 16.mcginnis mr, pasarell l. in vitro evaluation of terbinafine and itraconazole against dematiaceous fungi. medical mycology 1998;36:243-246. 17.walsh tj, goodman jl, pappas p, et al. safety, tolerance, and pharmacokinetics of high-dose liposomal amphotericin b (ambisome) in patients infected with aspergillus species and other filamentous fungi: maximum tolerated dose study. antimicrobial agents and chemotherapy 2001;45:3487-3496. 18.sharkey pk, graybill jr, rinaldi mg, et al. itraconazole treatment of phaeohyphomycosis. journal of the american academy of dermatology 1990;23:577586. 19.fica a, diaz m-c, luppi m, et al. unsuccessful treatment with voriconazole of a brain abscess due to cladophialophora bantiana. scandinavian journal of infectious diseases 2003;35:892-893. 20.lyons mk, blair je, leslie ko. successful treatment with voriconazole of fungal cerebral abscess due to cladophialophora bantiana. clinical neurology and neurosurgery 2005;107:532-534. 21.jayakeerthi sr, dias m, nagarathna s, anandh b, mahadevan a, chandramuki a. brain abscess due to cladophialophora bantiana. indian journal of medical microbiology 2004;22:193-195. 10amitagrawal_recurrent 212 agrawal et al recurrent extraventricular anaplastic ependymoma recurrent extraventricular anaplastic ependymoma with scalp metastasis amit agrawal1, k.v. murali mohan2, vissa santhi3, kishor v. hegde4, umamaheswara reddy v.5 narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 1professor of neurosurgery, department of neurosurgery 2associate professor of pathology, department of pathology 3professor of pathology, department of pathology 4professor of radiology, department of radiology 5assistant professor of radiology, department of radiology abstract extraneural metastasis from anaplastic ependymoma is uncommon. in a study from memorial sloan kettering cancer center where the authors reviewed 81 ependymomas cases (between 1956 and 1989) there were only five (6.2%) cases had extraneural metastases. we present a case of anaplastic ependymoma with scalp metastasis and discuss the possible mechanism of spread. in majority most of the cases of metastatic extracranial ependymoma patients have underlying progressive intracranial disease. although these patients receive standard treatment for the primary tumor (gross total resection and radiotherapy) and the management options for recurrences includes re-excision, focal reirradiation, stereotactic radiosurgery, or craniospinal radiotherapy for metastatic disease the long term outcome is not favorable. key words: anaplastic ependymoma, scalp metastasis, brain tumors. introduction anaplastic ependymomas probably arises from radial glial cells of the ventricular zone and is a relatively uncommon tumor which have a propensity for local recurrence with rarer incidence of extraneural metastasis (the lungs, lymph nodes, pleura, mediastinum, liver, diaphragmatic muscle, and bone). (1-6) scalp metastasis from anaplastic ependymoma is extremely rare. (5, 6) we present a case of anaplastic ependymoma with scalp metastasis and discuss the possible mechanism of spread. case report 45 year gentleman a case of recurrent left parietal anaplastic ependymoma who was operated on three occasions (first time in december 2010, 2nd time in june 2012 and 3rd time in april 2013) presented with multiple scalp swelling, headache and vomiting. preciously the tumor was managed with near total resections and he received radiotherapy and chemotherapy after the previous romanian neurosurgery (2014) xxi 2: 212 215 213 surgeries. he had residual right hemiparesis after at the second time of surgery which was pressing. there was no history of fever, loss of consciousness or seizures. his general and systemic examination was normal. neurologically he was conscious, alert and oriented to time place and person. he had mild aphasia and grade 3/5weakness of right upper and lower limbs. there was patchy loss of hair over scalp. there were multiple hard, nontender nodules over the scalp and along the previous craniotomy incisions site (figure 1). mri brain showed extensive recurrence of the tumor. post-contrast images showed that the tumor was extending along the trajectory of the incision and extending extracranially into the subgaleal plane (figure 2). figure 1 clinical photograph showing multiple scalp nodule near to the surgical incision site figure 2 post contrast mri t1w axial, sagittal and coronal images showing (a) recurrent tumor cyst in left parieto-occipital region with enhancing nodule, (b) in addition to the enhancing nodules in the cyst cavity there is large enhancing lesion in scalp and (c) multiple enhancing lesion are better visualized on coronal image 214 agrawal et al recurrent extraventricular anaplastic ependymoma figure 3 (a) sheets of tumor cells having round to oval nuclei with moderate amount of cytoplasm in the hemorrhagic background (h&e,x100) and (b) tumor cells having round to oval nuclei with most of them showing nuclear grooving. cells have moderate amount of cytoplasm and indistinct cell borders (h&e, x400) the patient underwent fine needle aspiration cytology (fnac) of the scalp lesions which showed sheets of tumor cells having round to oval nuclei with moderate amount of cytoplasm in the hemorrhagic background, most of them showing nuclear grooving and cells had moderate amount of cytoplasm and indistinct cell borders (figure 3). discussion in a study from memorial sloan kettering cancer center where the authors reviewed 81 ependymomas cases (between 1956 and 1989) there were only five (6.2%) cases had extraneural metastases. (4) in other reports articles most of the cases of metastatic extracranial ependymoma also had underlying progressive intracranial disease (resulting in poor outcome). (4, 5, 7) because of their proximity to the ventricular spaces ependymoma are prone to leptomeningeal dissemination. (5) it has been hypothesized that craniotomy and shunt placement disrupts the blood-brain barrier and promotes vascular seeding to distant sites in some but not all cases. (4, 8, 9) as was seen in present case proximity of the recurrent tumor to the surgical site suggests surgical seeding and scalp metastasis. (5) all the patients received standard treatment for the primary tumor (gross total resection and radiotherapy) and the management of recurrences included reexcision, focal re-irradiation, stereotactic radiosurgery, or craniospinal radiotherapy for metastatic disease with good survival rates (5year survival in up to 50% of patients). (3, 6, 10, 11) although chemotherapy has been found to delay progression in some cases and provides palliative relief, but has not been shown to increase survival. (11-14) correspondence: dr. amit agrawal (mch) professor, department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 romanian neurosurgery (2014) xxi 2: 212 215 215 andhra pradesh (india) emaildramitagrawal@gmail.com mobile+91 8096410032 references 1.fischer c, haque ss, huse jt, et al. extraneural ependymoma: distant bone, lung, liver, and lymph node metastases following bevacizumab. pediatric blood & cancer 2013;60:143-145. 2.kinoshita m, izumoto s, kagawa n, hashimoto n, maruno m, yoshimine t. long-term control of recurrent anaplastic ependymoma with extracranial metastasis: importance of multiple surgery and stereotactic radiosurgery procedures--case report. neurologia medico-chirurgica 2004;44:669-673. 3.donepudi sk, tennant pa, samant s. anaplastic ependymoma metastatic to the neck. laryngoscope 2009;119:s66-s66. 4.newton hb, henson j, walker rw. extraneural metastases in ependymoma. journal of neuro-oncology 1992;14:135-142. 5.chao mm, packer rj, myseros js, rood br. isolated extracranial recurrence of anaplastic ependymoma. pediatric blood & cancer 2011;56:317-318. 6.davis mj, hasan f, weinreb i, wallace mc, kiehl tr. extraventricular anaplastic ependymoma with metastasis to scalp and neck. journal of neuro-oncology 2011;104:599-604. 7.ferracini r, manetto v, poletti v, giangasparo f. a cerebral ependymoma with extracranial metastases. tumori 1984;70:389-392. 8.duffner pk, cohen me. extraneural metastases in childhood brain tumors. annals of neurology 1981;10:261-265. 9.rubinstein lj. development of extracranial metastases from a malignant astrocytoma in the absence of previous craniotomy. case report. journal of neurosurgery 1967;26:542-547. 10.merchant te, boop fa, kun le, sanford ra. a retrospective study of surgery and reirradiation for recurrent ependymoma. international journal of radiation oncology, biology, physics 2008;71:87-97. 11.zacharoulis s, moreno l. ependymoma: an update. journal of child neurology 2009;24:1431-1438. 12.bouffet e, capra m, bartels u. salvage chemotherapy for metastatic and recurrent ependymoma of childhood. child's nervous system : chns : official journal of the international society for pediatric neurosurgery 2009;25:1293-1301. 13.messahel b, ashley s, saran f, et al. relapsed intracranial ependymoma in children in the uk: patterns of relapse, survival and therapeutic outcome. european journal of cancer (oxford, england : 1990) 2009;45:1815-1823. 14.reni m, gatta g, mazza e, vecht c. ependymoma. critical reviews in oncology/hematology 2007;63:81-89. microsoft word nica_international_f.docx romanian neurosurgery (2012) xix 1 international neuroscience institute (ini) center hanovra. a new step in neurosurgery d.a. nica1, r. copaciu1, a.v. ciurea2 1neurosurgery clinic, “sf. pantelimon” clinical emergency hospital, bucharest, romania 2first neurosurgery clinic, “bagdasar-arseni” emergency hospital, bucharest, romania when you get in front of the building of the international neuroscience institute (ini) center in hannover you become instantly impressed with the way it was designed. the exterior aspect is that of a giant human brain and inside, the main pillar, represented by the elevators, resembles the brain stem (1) (figure 1). the ini center project was initiated by the distinguished professor madjid samii and it was designed and accomplished mainly by the siemens company. the first symbolic foundation brick was laid in december 1998 and after only 18 months, in july 2000, at the occasion of the world exposition in hannover, it was inaugurated in the presence of 1800 guests (2). the exterior and the interior space design (extremely functional) along with the department constitution was also suggested and coordinated by professor madjid samii. figure 1 exterior and interior design of ini center figure 2 prof. madjid samii prof. dr. med. dr. h. c. mult. madjid samii (figure 2) is the founder and president of the ini center. he was president of world federation of neurosurgical societies (wfns), doctor honoris causa of many universities and honorary member of romanian society neurosurgery (rsn). he headed the neurosurgical department of the nordstadt hospital hannover and the neurosurgical department of the medical school hannover until 2003. since then he is working exclusively at the ini clinic and research institute (2). throughout his entire career, prof. dr. madjid samii, has perfected and continues to perfect neurosurgical techniques, bringing an essential contribution in the approach of ponto cerebral angle and brain base tumors, leading as well the d.a. nica et al international neuroscience institute (ini) center hanovra department of “skull base surgery” of ini. through his imposing personality and his charisma, he succeeded to gather along his side a group of world renowned professors, each specialized on certain neurosurgical fields. figure 3 prof. amir samii figure 4 prof. helmut bertalanffy figure 5 prof. rudolf fahlbusch prof. dr. med. amir samii is the vicedirector of the neurosurgical center (figure 3). prof. dr. med. helmut bertalanffy is the director of neurovascular surgery department from 2010 (figure 4). he received his neurosurgical training from the albert-ludwigs university of freiburg im breisgau, germany, where he completed with honors a medical doctorate in 1986 and obtained the qualification as board certified neurosurgeon in 1990. in 1997 dr. bertalanffy was appointed to professor on a permanent basis by the state of hessen, germany, and served as professor and chairman of the depart­ment of neurosurgery of the philipps university of marburg for 10 years. in july 2007 he was appointed to chairman of the department of neurosurgery of the university of zurich, switzerland, where he served three and a half years in that position. in november 2010 he accepted the new position of director of the center for vascular neurosurgery at the prestigious international neuroscience institute in hannover, germany (3). prof. dr. med. rudolf fahlbusch is the director of neuroendocrine surgery department (figure 5). his major neurosurgical contribution to the sellar region tumors is internationally renowned (3). prof. dr. med. dieter hellwig is the director of stereotactic and functional neurosurgery department. prof. dr. med. wolfgang r. lanksch is the director of general neurosurgery department. prof. dr. med. shizno oi is the director of pediatric neurosurgery. romanian neurosurgery (2012) xix 1 prof. dr. med. anton valavanis is the director of interventional neurosurgery department. prof. dr. med. volker sturm is the director of stereotactic neurosurgery department. prof. dr. med. wolfgang draf, from the ent department of the medical university of hannover, is a close collaborator with the ini center, especially in border-line lesions. alongside these professors there are other well trained doctors, from different specialties (anesthetists, radiologists, psychiatrists, neurologists, neurophysiologists, anatomopathologists, psychologists, kinetic physiotherapists) who, through their contribution, assure the patients medical investigation and preparation for surgery, as well as postoperative recovery, at the highest level. the operating rooms are at the fifth floor, a total of six operating rooms, each fitted (beside the basic utilities) according to top standards: operative microscope, complete microsurgery instruments, cusa, neuronavigation (navi) and at least 3 screens for intraoperative viewing (for academic purposes) (3). figure 6 the structure of ini center the first operating room is fitted with mri theatre (1,5 tesla) for preoperative functional mri evaluation, intraoperative and postoperative navi controlled evaluation, being used especially in intracerebral lesions. for vascular lesions, one of the operating rooms is fitted with angiograph (dsa) for intraoperative evaluation and interventional neuroradiology. there are also 3 echo-doppler devices, 2 neurosurgical endoscopes, 2 more mri machines (1,5 and 3 tesla), computed tomography, 4 navi, 2 intraoperative electrophysiological evaluation devices, different stereotactic systems, one anesthetic endoscope and other utilities. also on the fifth floor is the intensive care unit. it’s worthy to note that the patients are from all around the world, with an impressive addressability. having the approval of prof. dr. madjid samii, i had the honor (among other trainees) to be under the direct guidance of prof. dr. helmut bertalanffy from 19th of july to 31st of july, as a “visiting doctor”. after the clinical and paraclinical preoperative evaluation, the data regarding each patient is subject for discussion with the whole clinic staff so that the surgical interventions are performed in the most accurate and efficient way. intraoperative, at the same time with the screen presentation of the microsurgical step, the surgery is being recorded in order to be analyzed afterwards and also for possible academic presentation in courses, national and international conferences and congresses. intraoperative the key moments of the surgery are pointed and explained by the professors to the group of viewing doctors. d.a. nica et al international neuroscience institute (ini) center hanovra there are no surgical maneuvers, approach, investigation or surgical step that remains unexplained to the smallest detail. in case there are questions or even inadequate answers from trainees, you are being presented with the right solution, thoroughly explained so that there are no uncertainties, without making the trainee look bad. after each surgical intervention, the operation is debated with the entire staff and with the doctors who came for upgrading their practice. the academic part is impressive, proof of that is the large number of doctors, all around the world, who come for training courses with the ini. i had the possibility to attend, as well as the other resident or specialist colleagues, the surgical interventions from each of the six operating rooms. in medium there are 5 daily surgical interventions, most having a high degree of difficulty. it’s impressive to realize how fast the 4-5 hours of surgery passes during, for example, an intervention for an acoustic neurinoma “from skin to skin”. this is the operative schedule of an “ordinary” day: operating room 1. diagnosis: right occipital glioma. approach and goal: posterior temporal-occipital craniotomy; total removal of the tumor. positioning: supine position. first operator: prof. lanksch. utilities needed: functional mri into or, operating microscope, navi, cusa operating room 5. diagnosis: right intracanalar acoustic neurinoma. approach and goal: right lateral suboccipital; decompression, ablation. positioning: semiseating position. first operator: prof. m. samii. utilities needed: operating microscope, cardiac echo-doppler, sep, aep, f-emg, cusa operating room 2. diagnosis: infradiafragmatic pituitary tumor. first operator: prof. fahlbusch. approach: transnassal-transsphenoidal. utilities needed: operating microscope. moderate bleeding. time 2-3 h operating room 6. diagnosis: lumbar disc recurrent herniation. operation: re intervention + discectomy. approach: lateral foramintomy. first operator: prof. m. samii. utilities needed: operating microscope operating room 3. diagnosis: left anterior-lateral peduncular giant cavernoma. approach and goal: left mediolateral suboccipital infratentorial supracerebellar; total removal of cavernoma. positioning: semi-seating position. first operator: prof. h bertalanffy. utilities needed: operating microscope, cardiac echo-doppler, sep, aep, emg (nn. iii, iv, vi, vii) losing only 100 ml of blood “from skin to skin”, short neurophysiologist intervention (only 2-3 times) and the real good follow-up (no neurological deficit) proves that in order to deal with such a lesion and with this kind of topography, one must have solid knowledge of regional topographic anatomy, experience, practice, dexterity and self-confidence characteristic to the education of a samurai, which professor hemult bertalanffy fully possesses. thanks to the clinic’s international professional, didactic and academic recognition, this project was followed in other countries, so that in 2010, when ini hannover celebrated a decade of activity, a new ini center was opened in pekin and romanian neurosurgery (2012) xix 1 this year in october another ini center will be opened, in teheran. i consider that the activity in this center represents, for every specialist, a mandatory step in professional training and i believe that ini center hannover leads were neurosurgery is concerned. references 1. prof. dr. ciurea, “hipocrate” magazine. may 2011. pg 80-81. 2. ini center 10 jahre, jubiliary edition. 3. www.ini-hannover.de. microsoft word mitricam_thevalue_f m. mitrică et al the value of fusion imaging the value of fusion imaging (pet – ct) in the diagnosis of vertebral and spinal tumors m. mitrică1, c. năstase1, c. mazilu2, i. codorean2 1neurosurgery clinic of "dr. carol davila" central universitary military emergency hospital, bucharest 2nuclear medicine service, "dr. carol davila" central universitary military emergency hospital, bucharest abstract fusion imaging (pet/ct), widely used in the developed countries, allows the identification of different lesions at the molecular level, enabling the emergence of a new field of advanced medicine "molecular imaging". for example, marking with a radiotrasor of a nucleic acid chain component allows the identification of the cancer at the molecular level and its treatment by radioimuno scintigraphic techniques. having a great sensitivity in the early detection of some lesions in a wide spectrum of pathology, nuclear medicine procedures are much sought by the clinicians. keywords: cancer, cyclotron, radionuclides, spinal tumors introduction cancer begins at subcelular molecular level by altering a gene that controls cell growth and behavior; in particular there is a marked increase in dna synthesis and an exaggerated local consumption of glucose as an energetic support for anarchic cell multiplication. these amendments are being “propagated” little by little, so that after a certain period of time (years) during wich the disease usually progresses asymptomatically , tissues or organs come to be involved. when the number of cancer cells is large enough to be detected visually by conventional techniques (x-ray, ultrasound, ct, mri), the disease has already passed the stage where it can be treated successfully. the challenge of medical activity is to detect cancer before the onset of clinical symptoms and dissemination in other organs and to establish an early effective treatment. cancer is one of the main causes of mortality in the world. recent statistical studies conducted under the auspices of the world health organization (who) show that 1 in 9 women will develop some form of breast cancer, 1 in 7 men will develop a form of prostate cancer, and 1 of 10 male will develop lung cancer. effective treatment depends mainly on early detection of tumor process (8). materials and methods when diagnosed by the methods existing today in our country, including the high performance imagistic explorations, cancer can not be cured. the established treatment surgery, chemotherapy or radiation may provide, in relation to the evolutive stage of the desease a survival not exceeding 4-5 years (2). medical imaging is a top field of romanian neurosurgery (2011) xviii 2 medicine that includes a group of modern medical techniques with different principles, which have in common the fact that provide diagnostic data through the image of the anatomical systems, internal organs or injuries. these imaging techniques can be grouped into: anatomical (structural) techniques: ultrasound, computed tomography (ct), magnetic resonance imaging (mri), angiography, digital radiography; functional (metabolic) techniques: planar scintigraphy, tomoscintigraphy (spect), monoclonal antibody imunoscintigraphy, positron emission tomography (pet). anatomic and metabolic imaging fusion: integrated pet-ct, spect-ct, pet-rm systems are high performance techniques that enable in a single view both the pathological metabolic process examination and its precise location by co-registering the two categories of information (13, 14). due to its increasingly large expansion and wide introduction into diagnostic and settlement protocols around the world, we will refer next to pet-ct technique. the pet-ct is an imaging technique that realizes the early detection of cancer by visualizing the excessive glucose consumption in the cancer cells (pet) and the anatomical location of the precise process by simultaneous pet and ct scanning. since 1991 over 2000-3000 equipments have been installed over the world. who estimates a need of approximately one pet equipment at 1 million inhabitants. pet technique is based on marking a normal constituent of the body (e.g. deoxiglucose, an analogue of glucose) with a positron emission radiotrasor ( 18f, 14c, 16o, 13n but usually 18f ) that after iv injection is distributed throughout the body, depending on the distribution properties of the radiolabeled constituent. once injected into the body, the positrons emitted by radionuclide decay migrate to short distance into the tissues, lose some of the energy, slow their motion, and annihilate after the collision with present electrons. the annihilation process will give two gamma photons emitted in opposite directions (1800), with an energy of 511 kev each. both radiations can then be detected by forming a ring of detectors around the patient so that it becomes possible mapping the distribution of positron-emitting isotope into the body. in this way can be studied the distribution of an extremely large number of substances whose metabolism is affected in various pathological conditions (2, 12, 13). by far the most widely used positron-emitting radionuclide is 18f coupled with deoxiglucose analogue of glucose. metabolically active cancer cells will capture the labeled glucose about 30-40 times higher than the adjacent healthy cells. the computerized system of the facility that detects the photons emitted from the positron annihilation with an electron, allows the space identification of the positronic radiotracer fixation place and also viewing the pathological process (9). the positron emitting radiotracers used for pet examination are included in the table below: positron emitting radiotracer physical t1/2 18f 110 min. 11c 20 min. 13n 10 min. 15o 2 min. m. mitrică et al the value of fusion imaging figure 1 fdg – pet normal appearance because of the short physical half-life, positron emitting radionuclides need to be produced on site in a medical cyclotron (baby cyclotron). there are positron emitting radionuclides produced in a generator, e.g. 68ga, which by coupling with different peptides allow to assess and conduct therapeutic setting for neuroendocrine tumors, but other clinical applications are currently in the research stage (10). the method was developed in the '70s (phelps and hoffman) and it has been used for two decades predominantly in the clinical research of various cellular processes at molecular level by incorporating the positronic isotop into different messenger molecules (enzymes, hormones, antibodies, peptides and oligonucleotide). imaging of apoptosis, neurotransmitters and neoangiogenesis have been translated from experimental evidence into clinical practice (figure 1). the remarkable progress in molecular imaging determined w. wagner jr. (from j. hoppkins clinic baltimore) to assert that "the molecular medicine has revolutionized modern medicine, the nuclear medicine comes to revolutionize molecular medicine". in 1998, townsend had the idea to combine (overlay) the metabolic pet images with the anatomic ct images, making accurate anatomical localization of the lesions through what is called "fusion image". the first integrated pet-ct equipments produced by major companies have been introduced into clinical practice around 2000, being widely accepted by the medical community. the pet-ct equipment through a single examination allows to obtain a fusion image that contains both metabolic information (pet) and precise anatomical details (ct). the pet-ct main indications are: detection and indication of the malignant or benign substrate of various tumors; determining the actual extension of malignant tumors, the preoperative and postherapeutic staging; -differentiating the postoperative fibrosis, the residual post irradiation tumor necrosis or the relapse; establishing the tumor prognosis compared with the level of glucose uptake and the histological grade; -directing the therapeutic surgical approaches: minimal surgery, ctguided percutaneous ablation, chemoembolization; -directing the selective biopsy by identifying viable component of the partially necrotic tumors (8). the necessary equipment includes: cyclotron for obtaining the positron emitting radioisotopes; radiopharmacy laboratory for radiolabelling the active molecules (fluorine deoxiglucose, 11c methionine, 11c thymidine, 18f deoxythymidine, 18f romanian neurosurgery (2011) xviii 2 choline, etc.). it is possible to purchase the radiotrasor from a radiopharmacy, but the latter must be at a reasonable distance from pet-ct unit because of the very short halflife of radionuclides and it is only possible for radiotrasors tagged with 18f (t1/2 = 110 min., compared to 11c with t1/2 = 20 min. or 15o with t1/2 = 2 min.!) (figure 2). the pet/ct scan combines the metabolic details of a pet scan (tumor cell activity, tumor viability etc.) with the anatomical details offered by a ct scan (size and location of tumor, mass, anatomical relationships etc.), giving a more accurate image than pet or ct used separately. the pet examination begins with intravenous injection of fdg (18-fluorine dezoxiglucose), a glucose-like substance which is attached to the f18 isotope. the metabolically active tissues or these with abnormally high rate of multiplication (tumors) consume much higher amounts of the radioactive sugar. the radiotracer accumulation leads to gamma rays emissions that are converted by computer into images. these images indicate "hot" areas signaling tissues with high metabolic activity (abnormal increased multiplication rate) because cancer cells consume more sugar / energy than other tissues or organs. the ct scan is based on the absorption in varying degrees of the xrays by the examined structures and on the computerized data processing to obtain the thin sections that can be reconstructed threedimensional reproducing detailed images of body structures. the entire examination usually takes 30 minutes, providing detailed and accurate information that enables physicians to provide a quick, correct and complete diagnosis. figure 2 the integrated pet-ct equipment figure 3 67 years old male patient. rx and ct examinations: solitary pulmonary nodule. the indication of pet-ct: assessing the malignant/benign substrate of the lesion. anatomopathological examination: small cell carcinoma m. mitrică et al the value of fusion imaging in oncology, the pet/ct investigation offers the ability to early diagnose, locate, monitor and control the development of cancer. with pet-ct, surgeons, oncologists and other specialists will be able to detect cancer more accurately, to assess recurrences, to make a complete and accurate staging, to assess the patient's likely response to therapy and to monitor more effectively the results of chemotherapy and radiotherapy. in oncology, pet-ct provides vital diagnostic information that allows monitoring of treatment outcomes and often helps avoid surgery (4). in neurology and neurosurgery, pet ct is used to identify areas of the brain that cause seizures and to determine whether surgery is a viable option. also, this technology allows diagnosis of alzheimer's disease at a stage when the disease can still be controlled with medication. before examination, patients are asked: not to eat nor drink anything (or to drink only plain water) at least 6 hours before the examination, because it could affect the results (the ban also refers to sugarfree chewing gum, mints, candies and drinks of any kind); if they take drugs, they should drink only as much water as it is necessary to swallow them; to minimize their physical activity on the day they are examined (gymnastics, jogging, etc.) as it might affect the capture of the radionuclide; to bring with them on the day they are examined previous ct scan, x-ray, scintigraphic or mri examinations, tumoral markers results, anatomo-pathological test results and hospital discharge papers they have (as written reports, images or cds); to announce in advance whether they are diabetic, to allow physician consultation on the preparation and conduct of examination; before the actual examination begins their blood glucose level is measured anyway. when recording high blood glucose levels which persist even after being taken measures to low them, the investigation can not be done; to announce whether they are febrile; to announce the existence or suspicion of pregnancy or nursing status; to call the physician if they have questions about the scheduled procedure (15). the examination will begin with a test to determine blood glucose level. patients will then receive an injection containing a small amount of radioactive glucose (radioactive sugar), which will be distributed throughout the body. the radiotracers used for pet/ct scan lose their radioactivity very quickly (within two to three hours) and only very small doses are injected. six to eight hours after injection, the remaining radioactivity is negligible. in most cases, patients will have to wait about an hour for radioactive drug to be distributed in the body. figure 4 78 years old woman with operated squamous cell lung adenocarcinoma (postpneumonectomy status). the indication of pet-ct: staging. pet-ct examination: tumoral relapse; right lung metastasis, on the front and left side of the t5 vertebral body romanian neurosurgery (2011) xviii 2 about 60 minutes after the injection, patients will go to the toilet to urinate. patients will be asked to stand still during the scan because movement can affect the outcome of the investigation. during the scan patients breathe normally. during the acquisition of the images they will not feel anything unusual, except table movements, as some areas of the body are scanned. throughout the examination the patients will be monitored by an operator and they may communicate with him through the microphone and through the cameras. the pet-ct scan takes between 20 and 30 minutes. the examination procedure may differ depending on the examined area (20). the risks and precautions during the examination are not negligible and should be known. except the restraint during the examination, there is recorded no special sensation like pain, annoying noises, temperature differences, etc. there were never reported unwanted side reactions after intravenous administration of fdg, required for carrying out the pet / ct examination. there are no contraindications for the fdg administration and only in cases of severe renal failure or high blood sugar level that not falls within lower values of 180-200 mgr/dl, the examination is not made, because these conditions make it impossible to correctly use the radiotracer. sometimes, intravenous injection of the substance can be difficult. in this case there is a catheter inserted in advance. any state of pregnancy, suspected or found, is a contraindication to the examination. in this case, the necessity of investigation should be determined by mutual agreement with the treating physicians. breast-feeding should be discontinued for at least 6 hours after completion of investigation. renal failure causes a reduction in quality of pet / ct scan images, although it is not a contraindication to perform the examination. patients wearing orthopaedic prostheses, pacemakers, implanted arterial or venous prostheses, etc., are not exposed to any risk, but it is appropriate to inform of their existence the physician that records the medical history (22). after the administration of fdg follows an average wait of 60 minutes to ensure optimal distribution of the substance into the body. the image acquisition time with pet – ct equipment is about 30 minutes, but in some cases may be extended, depending on the disease (e.g.melanomas) or on the pursuit of certain issues. the last part of procedure lasts about 15 minutes (16). the presence of the integrated pet-ct equipment in romania allows detection of cancer (and other diseases) to debut before the effective dissemination into the entire body, with maximum therapeutic efficiency (9). figure 5 37 years old female patient, presenting physical fatigue, low grade fever, left laterocervical swelling / the indication of pet / ct: diagnosticstaging. anatomo-pathological examination: hodgkin’s lymphoma m. mitrică et al the value of fusion imaging figure 6 39 years old female, presenting fever, physical fatigue, pruritus, palpable supraclavicular lymph nodes, thoracic pains. the indication of petct: staging. pet-ct examination: fdg uptake is observed in several coastal, vertebral and axillary lymph nodes outbreaks. supraclavicular lymph nodes biopsy: hodgkin’s lymphoma figure 7 51 years old male with non-hodgkin’s lymphoma with mediastinal, lung, spinal and cerebral dissemination, that followed multiple courses of chemotherapy. the indication of petct: evaluation 6 months after the last course of chemotherapy. pet-ct examination : axillary lymphatic dissemination after chemotherapy for non-hodgkin’s lymphoma the world health organization and the international agency for fight against cancer recommends a pet-ct facility at approx. 1-2000000 inhabitants (19). figure 8 43 years old female patient with right mastectomy 2 years ago for breast cancer, with vertebral, lung and liver metastatic diseminations. clinical issues: difuse bone pains, pronounced at sternal and verterbral level. the indication of petct : new staging cases presentation we present some clinical cases of patients treated in the neurosurgery clinic of "dr. carol davila" central universitary military emergency hospital and investigated petct at euromedic fundeni clinic (figure 8, 9, 10, 11, 12, 13, 14). before chemotherapy romanian neurosurgery (2011) xviii 2 after chemotherapy figure 9 67 years old female with metastatic breast cancer. the indication of pet-ct: assessing the response chemotherapy figure 10 52 years old male patient with lung cancer: multiple bone metastases in pet and pet / ct (thoraco-abdominal contrast ct scan in normal range) figure 11 t11 compression in 63 years old female with multiple osteoblastic lesions figure 12 63 years old female with breast cancer and secondary disseminations at t10 epidural and vertebral body and pedicle level m. mitrică et al the value of fusion imaging figure 13 52 years old female with colon cancer and metastatic process involving the t11 posterior body and posterior elements, with epidural extension figure 14 tumoral mass with epidural extension through the left t11 intervertebral foramen in a 51 years old female patient with lymphoma discussion the goal of surgery is to improve the quality of life as it is not always possible to cure the illness itself. it aims to: decompress the nerves trying to improve the patients neurological status; stabilize and relief pain, so the patient to be able to keep upright and walk; obtain a histo-pathological diagnosis followed by a specific oncological treatment (23). currently the vertebral and spinal pathology benefits from the contribution of new diagnostic techniques that have been developed and applied in the last two decades. generally these techniques are known as imaging techniques that have in common the fact that provide diagnostic information on the lesion substrate using computerized processed images. in the order of their clinical applicability have been imposed: magnetic resonance imaging (mri), computerized tomography (ct), tomoscintigraphy (spect) and positron emission tomography (pet-ct). these computerized techniques have revolutionized the neuroradiology replacing or restricting the applicability of conventional radiological diagnostic methods: plain or contrast radiography (myelography), conventional tomography and arteriography (22). pet-ct scan shows a lot of benefits compared with other commonly used imaging means: • determines how widespread the disease is; • indicates the location of the tumor to execute biopsy, surgical treatment or planning of treatment; • analyzes the response to and efficiency of the therapy; romanian neurosurgery (2011) xviii 2 • detects traces of residual disease or relapse; • helps to avoid invasive diagnostic procedures. being fully compatible with the oncological radiotherapy systems (micromultileaf, cyberknife, tomotherapy), pet / ct allows the urgent development of optimized treatment plans for selective irradiation of metabolically active tumoral tissue, fully preserving healthy tissues (8). conclusions the investigation and treatment of vertebral and spinal tumoral injuries is necessary to comply with the best neurosurgical conduct requirements. these requirements are imposed by current knowledge of acquisitions in the field of spinal surgery, as reflected in literature. their main purpose is to avoid the numerous errors and complications that may occur during treatment. meeting these requirements will bring more clarity to the doctor-patient relationship, particularly in cases where after the neurosurgical treatment occurre litigations related to the quality of the medical care (17). in spinal tumoral pathology the investigations are required to clarify the location and, if possible, the etiology of the lesion. the precise location dictates the approach path and the suspected etiology allows selection of an appropriate surgical technique. also, for the surgery decision is necessary that the location of the lesion to be consistent with the neurological symptoms, ie the location to explain the neurological syndrome (21). the patient should be exhaustively investigated, meaning not a lot of abusive and aimless investigations, but a full appropriate investigation protocol, to establish an accurate diagnosis. in line with current international standards, the methods of diagnosis in spinal pathology should focus on minimally invasive investigations that provide maximum information (12). references 1. aryanpur j, ducker t multilevel lumbar laminotomies: an alternative to laminectomy in the treatment of lumbar stenosis, neurosurg. 1999, 26: 429-433. 2. arseni c, simionescu m patologia vertebromedulara neurochirurgicala, ed.medicala1968,267-268. 3. black p., kaye a. – operative neurosurgery. churchill livingstone 2000; 879-898: 4. connelly s., mc khann g., huang j., chondhry t. – fundamentals of operatives techniques in neurosurgery. thieme 2001; 5. deshayes p, louvel jp le canal lombaire étroit, la rev pract (paris) nr.5, 1992, 569-572. 6. depalma a, rothman rh, lewinnek g, carole s. anterior interbody fusion for severe cervical disc degeneration. surg gynecol obstet. 1999; 134: 755-758. 7. flynn tb. neurologic complications of anterior cervical interbody fusion. spine. 1982; 7: 536-539. 8. fraser jf, härtl r. anterior approaches to fusion of the cervical spine: a metaanalysis of fusion rates. j neurosurg spine. 2007; 6: 298–303. 9. ganz jc lumbar spinal stenosis: postoperative results in terms of preoperative posture -related pain, j of neurosurgery1990,72:71-74. 10. greenberg ms handbook neurosurgery, vol 1, greenberg graphics, 1997, 207-213 11. henderson cm, hennesy r, shuey h. posterior lateral foraminotomy for an exclusive operative technique for cervical radiculopathy. a review of 846 consecutively operated cases. j neurosurg. 1983; 13: 504-512. 12. matz pg, ryken tc, groff mw, vresilovic ej, anderson pa, heary rf, holly lt, kaiser mg, mummaneni pv, choudhri tf, resnick dk. techniques for anterior cervical decompression for radiculopathy. j neurosurg spine . 2009; 11: 183–197. 13. matz pg, anderson pa, kaiser mg, holly lg, groff mw, heary rf, mummaneni pv, ryken tc, choudhri tf, vresilovic ej, resnick dk. introduction and methodology: guidelines for thesurgical management of cervical degenerative. journal of neurosurgery: spine. 2009; 11(2): 101-103. 14. michael g. fehlings, and babak arvin. surgical m. mitrică et al the value of fusion imaging management of cervical degenerative disease: the evidence related to indications, impact, and outcome. j neurosurg spine. 2009; 11: 97–100. 15. netter f. neurologic and neurosurgical disorders, second edition. the ciba geigy corp. 1992,184 189. 16. silvers hr, lewis pj decompressive lumbar laminectomy for spinal stenosis, j neurosurg,1993,78:695-701. 17. simpson jm, silveri cp, simeone fa, balderston ra. cervical disc disease and the keyhole foraminotomy: proven efficacy at extended long term follow-up. spine. 2008; 8(2): 115-120. 18. skalpe io, sortland o myelography, tano, 1989,57-61. 19. taveras jm neuroradiology, third ed. 1996,823825 20. tuite gf, stern jd, doran se outcome after laminectomy for lumbar spinal stenosis. part 1: clinical correlations, j neurosurg. 1994, 81: 699-706. 21. tervonen h, niemelä m, lauri er, bäck l, juvas a, räsänen p, roine rp, salmi t, vilkman e, aaltonen lm. dysphonia and dysphagia after anterior cervical decompression. j neurosurg spine. 2007;7: 124–130. 22. zdeblick ta, zou d, warden ke, mccabe r, kunz d, vanderby r. cervical stability after foraminotomy. j bone joint surg. 1992; 74: 22-27. 23. youmans j. r. – neurological surgery, fourth edition, w. b.saunderscompany,2000. microsoft word 6moscotesalazar_aproposal 342 moscote-salazar and alvis-miranda new pial arteriovenous fistulas grading scale a proposal for a new pial arteriovenous fistulas grading scale for neuroendovascular procedures and literature review luis rafael moscote-salazar1, hernando raphael alvis-miranda2 1department of neurological endovascular therapy, instituto nacional de neurología y neurocirugía; méxico city, méxico, mineurocirujano@aol.com 2universidad de cartagena, cartagena de indias, colombia abstract pial arteriovenous fistulas are an unusual type of cerebrovascular lesion. the vascular supply of this type of injury comes from cortical and pial vessels which are not located in the dura leaflets. with the aim to make a grading scale for this type of injury, we conducted a literature search using the keywords "pial arteriovenous fistulas", "embolization" associated with "outcome". angiographic and imagenological characteristics typically found in pial arteriovenous fistulas were taken and was developed a preliminary classification system that must be validated in future studies. pial arteriovenous fistulas are associated with a poor natural history and the establishment of an individualized therapeutic strategy can provide a good prognosis. the endovascular management of these lesions is safe and effective. key words: pial arteriovenous fistulas, embolization, outcome. introduction pial arteriovenous fistulas (pavf) are a rare type of intracranial arteriovenous lesions, with clinical relevance, (1, 2) that recently have been recognized as different from arteriovenous malformations (avm). (3) pavf differ from dural arteriovenous fistulas in that their arterial supply derive from pial and cortical arteries and they are not involved by the leaflets of the duramater. they can have one or multiple arterial conections with only one venous channel, without an intervening nidus or capillary. pavf can be located in any cerebral region, but usually shown preference for supratentorial regions. (4) pavf can be acquired traumatically, iatrogenically or can be congenital lesions. due to its unfavorable natural course, the conservatory management its associated with a mortality rate up to 63%. (5) because of the nidus abscense the shunt closure by endovascular or surgical approaches represents a satisfactory therapeutical procedures. (6) at presentation, can be hemorrhages, seizures, focal déficits, and heart failure in neonates, headache and symptoms of raised intracranial pressure, mass effect, palpable masses, cranial erosions and macrocephaly. this type of fistulas can receive diverse endovascular treatments, currently, due to the scarce cases reported, a classification pointing the type of endovascular approaches needed is absent. we propose a classification using factors already deemed as significant determinants of risk and outcome for endovascular pavf patients. the classification scheme proposed is very practical in clinical use. romanian neurosurgery (2013) xx 4: 342 350 343 methods a literature search was performed in several medical databases including medline, showing a total of 33 results using the keywords “pial arteriovenous fistulas”, “embolization”, associated with “outcome”. emphasis was given to the angiographic, imaginologic and hemodynamic characteristics found usually in pavf because these can be easily adapted to the management established for each particular patient; and was developed a preliminary grading scale that needs be applied in future studies to be validated. the resulting articles were assessed by considering factors such as: age, gender, clinical presentation, and aneurysm or varyx association. results from the search of 33 articles, emphasis was given to the angiographic, imaginologic and hemodynamic characteristics found usually in pavf because these can be easily adapted to the management established for each particular patient, as mentioned previously. 23 articles were found. in table 1 are summarized the main factors associated with impact on the natural course of pavf, that we consider determinant as variable for grading score. age hetts et al., (7) through a retrospective review of a neurointerventional database, identified 386 pediatric patients with intracranial avfs and avms, from which 25 had pavf. they found that pavf constituted 7.3% of pediatric intracranial vascular lesions with a nondural arteriovenous shunt; single-hole fistulas predominate later in childhood and more frequently presented with seizures, hemorrhage, or focal neurologic deficits. in pediatrics patients, the age is a relevant factor, in these same review by hetts et al.,(7) they found that patients ≤ 2 years of age compared with patients presenting at >2 years of age had more treatment procedures (p = .041), as in those harboring a multi-hole fistula versus those with a single-hole fistula (p = .003); patients ≤ 2 years of age were also more likely to have a multi-hole fistula (100% versus 25%, p = .0001) and to have a poor clinical outcome (54% versus 0%, p = .0052), defined as a pediatric mrs of ≥ 3. table 1. proposal grading scale for pavf variable characteristics value • calcification yes 1 no 0 • aferences unique 1 multiple 2 • location eloquent área 1 non-eloquent área 0 • associated avm yes 1 no 0 • varix >5cms 3 3-5cms 2 <3cms 1 no 0 interpretation: type i: 2-3; type ii: 4-6; type iii: 7-8. avm: arteriovenous malformation eloquent area: visual cortex, motor-sensitive cortex, hypothalamus, thalamus, intern capsule, brainstem, crux cerebri, or cerebellar nucleus. varix varix formation is a special finding in patients with pial avf. some reports suggest that the high pressure blood flow from arterial feeder directly into the venous drainage may result in venous varix formation. (8–12) yang et al., (13) determined that patients presented at younger age (≤15 years old) are more likely 344 moscote-salazar and alvis-miranda new pial arteriovenous fistulas grading scale to have varix in angiographic study (p<0.05) compared with the adult population, being the clinical presentation different in these two groups. younger patients are more likely to have symptom related to shunting effect; however, haemorrhage is the major presentation in older patients. furthermore, the absence of varix do have significant correlation with haemorrhage (p=0.001). however, it is necessarily to remember that patients with pavf may manifest differently according to their age and the existence of varix. this later might exerts a buffer effect to tolerate the high arterial flow pressure and consequently decrease the risk of bleeding. much less frequently, there is also an aneurysm of the feeding artery. (11) calcification it is important to consider the presence of associated calcification, which is more probable in pial than dural arteriovenous lesions. the mechanism of calcification in these lesions is a dystrophic process due to hypoperfusion caused by steal phenomenon or venous congestion over a long time,(2) when mural calcification is thick, it implies a longstanding course of cerebral damage. in these circumstances, even when is feasible the obliteration trough endovascular methods, alleviating the mass effect could be impossible; furthermore, perform first an endovascular approach, and in a second stage surgical removal could be tricky when compared to a single operation for occluding the accessible feeder artery and removing the mass simultaneously. another fact to consider is that the calcified shell would physically restrict approach and handling of endovascular devices.(2) arteriovenous malformation pavf inducing dural arteriovenous shunts (davs) have been proposed particularly in some high-flow pavf associated with davs upstream from their drainage into the dural sinus. (14) this could be caused by a similar sump effect created by the high-flow venous drainage of the pavf downstream. (15) the venous changes produced by high-flow pial avs on the venous sinuses, such as increased venous pressure or venous outflow obstruction, can also be triggering factors. (15) but this is not the situation in our cases, because they were high-flow davss anatomically closely related to the pial avfs that were upstream from the davss. the dominant shunts in our cases were highflow davs rather than pavf. (15) endovascular therapy of intracranial dural arteriovenous fistula may be curative but is often complex and carries definite risks. neurosurgical ligation of pial draining veins, with pre-operative embolization when safe, may be a relatively more controlled method to achieve complete cure. (16) location lesions in deep and eloquent locations can be associated with a high surgical risk for neurologic morbidity. (17) outcome lv et al., (17) reviewed the clinical and radiologic data of 16 patients with pavf who were treated endovascularly at the beijing tiantan hospital between 1998 and 2008. at the time of the last follow-up evaluation (range, 3–12 months; median, 7 months), 15 patients (93.75%) had a glasgow outcome score of v and 1 patient (6.25%) had a glasgow outcome score of iv. altogether, there were three perioperative complications (18.75%). during the follow-up period (range, 3–12 months; mean, 7.4 months), the overall morbidity rate was 6.25%. romanian neurosurgery (2013) xx 4: 342 350 345 hydrocephalus caused by venous thrombosis is the main complication, thus heparin should be given routinely after endovascular embolization. (17,18) pathophysiology although they account for only 1.6% of all avm are associated with a poor natural history. patients with pavf, and specially infants, are known to develop hydrovenous disorders that rapidly damage the surrounding brain, others alterations include subependymal or cortical atrophy, white matter calcification and delayed myelinization; thus early intervention is essential for optimal neurological and cognitive development. (4,19) intracranial pavfs differ from avm owing to the lack of nidus and from dural arteriovenous fistulas in that they derive their arterial supply from pial or cortical arterial vessels, and the lesion does not lie within the dural leaflets. (8) the abnormality from a pavf arises from its high-flow nature. the origin of pavfs can be traumatic, iatrogenic, or congenital. (4) congenital pavfs are usually present in childhood. pavf are considered to be congenital in nature. (20) however, there is little evidence that the pavf diagnosed in adults are present in the same form at birth. in addition, cases of de novo pavf have been reported. (21–24) little is known about the pathophysiological development mechanism ofthese lesions, but probably are produced by a misstep in the embryological development of the cerebrovasculature, (4, 25), also, abnormal angiogenesis and associated vascular growth factors and cytokines may play a role. (4) lasjaunias (19) proposed that the congenital event is primarily involving the vascular modeling and remodeling process at the cellular and structural level, affecting the endothelial cells at the venous side of the capillaries, resulting in a progressive dysfunction, and its manifestations will be related with the triggers, such as mechanical, hormonal, pharmacologic, hemodynamic, thermal, radiation, viral, infective, and metabolic factors. the frequency of venous varices and vessel ectasia, not to mention the association of syndromes that embrace angiodysplasia, (26) may reflect an inherent predilection of dysplastic elements toward the formation of such lesions. (4) the diverse nature and timing of the various triggers causes the different time and form of presentation of the abnormal arteriovenous shunts. the previous postulation can be applied to the acquired lesions, in which the trigger is applied for a certain length of time and had the same consequence on the target cells related to venous vascular remodeling. the pathogenesis of pavf also includes abnormal expression of various angiogenic factors such as vascular endothelial growth factor, basic fibroblast growth factor, and alpha transforming growth factor. (27–30) suppression of vascular cell growth modulators, including endoglin1, has also been found. (31) as have been learned from cases of acquired pavf following cerebral vein thrombosis (22), ischemia or hypoxia are important etiological factors. there is evidence that hypoxia is a powerful trigger for the up-regulation of angiogenic factors expression. (32) main clinical and angiographical characteristics the majority of avms occurring in the neonatal and infant period are vein of galen 346 moscote-salazar and alvis-miranda new pial arteriovenous fistulas grading scale malformations. nongalenic cerebral avm (or pial avm) have been reported to account for roughly 22 % of avms found in neonates and 35% of avms in infants. (1) the common presentations in neonates are systemic cardiac manifestations (54%), seizures (31%), hemorrhage (15%). in infants, hemorrhage (38%), hydrodynamic disorders (38%), cardiac manifestations (16%) and seizures (8%) are known to occur. (1) pavf produced in the first years of life can be associated with syndromes such as rendu-osler weber and klipeltrenaunay-weber síndromes. (33, 34) pavf can cause headaches, hemorrhage, seizures, focal neurologic deficits, and raised intracranial pressure. (18) flow and perfusion pressure through a pial av fistula is certainly high. impaired venous drainage in avms has been implicated in the risk of hemorrhage, but whether venous varices accompanied by pavf are associated with an increased risk of hemorrhage remains unclear. at present, four-vessel cerebral angiography is the gold standard diagnostic procedure which can distinguish nongalenic avfs from avms. (35) angiographic diagnostic criteria for avfs consist of: (36) 1. rapid circulation time because of high-velocity flow; 2. enlarged feeding artery; 3. direct filling of a large varix. therapeutical approaches therapeutic options of pial avf include surgical excision of lesion, surgical ligation of feeder and endovascular obliteration of feeders. in addition to standard microsurgical technique, additional measures such as induced hypotension, temporary clipping and pharmacological neuroprotection may be helpful. the anesthetic team should be ready in anticipation of severe blood loss and potential circulatory collapse, because preexisting venous hypertension may precipitate severe bleeding that does not respond to these and other standard hemostatic measures. the simple disconnection of the fistula should be the goal of therapy, (4) and attempts at excision of the varix may exacerbate parenchymal bleeding. hoh et al have summarized the literature from 1970 to 2000. there have been 79 patients reported to date. venous varices were found in 48 of 54 cases (89%). however, at that individual centre, only three out of nine were associated with varices. in their series, the concept of 'flowdisconnection' either endovascularly or surgically was advocated. (4) surgical disconnection involves either aneurysm clip application or cauterization of the feeding vessel. though this has been proven effective, some lesions are deep or surgically inaccessible and the risk of surgery can be very significant. as in this case, severe bleeding can be expected due to: (1) venous hypertension due to the high-flow system and, (2) hyperaemia from normal perfusion pressure breakthrough. unlike the case of nidus-type avm, the strategy of surgical disconnection without lesion resection was found to be sufficient for obliteration of the fistula. hence, excision of the varix is probably not required. (4) endovascular approach pavf are rare vascular lesions that require prompt treatment. as symptomatic patients managed conservatively have a romanian neurosurgery (2013) xx 4: 342 350 347 poor prognosis, radical treatment should be undertaken as soon as possible. (37) obliteration of the fistula by an endovascular route, avoiding the risks associated with craniotomy, should always be considered especially when the lesion is deep seated or the risk of neurological deficit with surgery is high. (4, 19, 38, 39) also should be considered the endoscopic intervention, that can be an effective and safe option for the treatment of this type of lesion. endovascular attempts are not always successful or safe. several technical difficulties in obliteration of the fistula have been described. endovascular embolization of the fistula may be complicated by migration of the embolization agent into a varix, to the lung or elsewhere in the cerebral vasculature. (4) newman et al., (40) described a novel endovascular treatment strategy that was used successfully to treat 2 pediatric patients with a pavf, a single-channel high-flow pavf was diagnosed in 2 male patients (6 and 17 years of age). both patients were treated with endovascular flow arrest using a highly conformable balloon followed by onyx infusion for definitive closure of the fistula. neither patient suffered a complication as a result of the procedure. at the 6-month follow-up in both cases, the simple discontinuation of blood flow had resulted in durable obliteration of the fistula and stable or improved neurological function; thus, the authors conclude that onyx can be delivered successfully into high-flow lesions after flow arrest to allow a minimally invasive and durable treatment for pavf. paramasivam et al., (41) reported that development of de novo dural arteriovenous fistula(s) following endovascular embolization of a prior highflow pavf is not an uncommon development. they are mostly asymptomatic and develop anywhere along the drainage of the fistula, maturing over time and diagnosed during follow-up studies, emphasizing the need for follow-up angiography. they can be effectively treated by endovascular embolization. localized refractory dural fistulas can be dealt with by radiosurgery. conclusions intracranial arteriovenous fistulas are vascular malformations in which clinical suspicion and prompt diagnosis, with a subsequent appropriate therapeutic approach, are crucial to avoid the development of irreversible neurological damage or even patient death because these lesions can be associated with heavy bleeding and high mortality rates. depending on their location and high-flow dynamics, these lesions can present treatment challenges for both endovascular and open cerebrovascular surgeons. disconnection of direct shunting, either by endovascular or surgically, is sufficient to achieve successful treatment; therefore, total resection of the lesion is unnecessary. we propose a pavf grading score, however a retrospective study is necessary to validate it. to our knowledge this is the first proposal for classifying pavf based on evidence. correspondence: dr. luis rafael moscote-salazar, universidad de cartagena, cartagena de indias, colombia. e-mail: mineurocirujano@aol.com 348 moscote-salazar and alvis-miranda new pial arteriovenous fistulas grading scale references 1. pillai a, rajeev k, unnikrishnan m. surgical management of a pial arteriovenous fistula with giant varix in an infant. neurol india [internet]. 2006 dec [cited 2013 sep 8];54(4):434–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/17114861 2. tabatabai saf, zadeh mz, habibi z, meybodi at, hashemi m. intracerebral atypical calcification in nongalenic pial arteriovenous fistula: a case report. cases j [internet]. 2008 jan [cited 2013 sep 7];1(1):335. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=2605763&tool=pmcentrez&rendertype=abstract 3. passacantilli e, pichierri a, guidetti g, santoro a, delfini r. surgical treatment of pial cerebellar arteriovenous fistulas with aneurysm of the main feeding artery. surg neurol [internet]. 2006 jan [cited 2013 sep 7];65(1):90–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/16378872 4. hoh bl, putman cm, budzik rf, ogilvy cs. surgical and endovascular flow disconnection of intracranial pial single-channel arteriovenous fistulae. neurosurgery [internet]. 2001 dec [cited 2013 sep 7];49(6):1351–63; discussion 1363–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/11846934 5. nelson k, lasjaunias p, berenstein a. endovascular embolization of congenital intracranial pial arteriovenous fistulas. neuroimaging clin n am. 1992;2:309–17. 6. lasjaunias p, manelfe c, chiu m. angiographic architecture of intracranial vascular malformations and fistulas--pretherapeutic aspects. neurosurg rev [internet]. 1986 jan [cited 2013 sep 7];9(4):253–63. available from: http://www.ncbi.nlm.nih.gov/pubmed/3614684 7. hetts sw, keenan k, fullerton hj, young wl, english jd, gupta n, et al. pediatric intracranial nongalenic pial arteriovenous fistulas: clinical features, angioarchitecture, and outcomes. ajnr am j neuroradiol [internet]. 2012 oct [cited 2013 sep 10];33(9):1710–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/22766672 8. kikuchi k, kowada m, sasajima h. vascular malformations of the brain in hereditary hemorrhagic telangiectasia (rendu-osler-weber disease). surg neurol [internet]. 1994 may [cited 2013 sep 8];41(5):374–80. available from: http://www.ncbi.nlm.nih.gov/pubmed/8009411 9. viñuela f, drake cg, fox aj, pelz dm. giant intracranial varices secondary to high-flow arteriovenous fistulae. j neurosurg [internet]. 1987 feb [cited 2013 sep 8];66(2):198–203. available from: http://www.ncbi.nlm.nih.gov/pubmed/3806202 10. giller ca, batjer hh, purdy p, walker b, mathews d. interdisciplinary evaluation of cerebral hemodynamics in the treatment of arteriovenous fistulae associated with giant varices. neurosurgery [internet]. 1994 oct [cited 2013 sep 8];35(4):778–82; discussion 782–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/7808630 11. carrillo r, carreira lm, prada j, rosas c, egas g. giant aneurysm arising from a single arteriovenous fistula in a child. j neurosurg [internet]. 1984 may [cited 2013 sep 8];60(5):1085–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/6716144 12. barnwell sl, ciricillo sf, halbach v v, edwards ms, cogen ph. intracerebral arteriovenous fistulas associated with intraparenchymal varix in childhood: case reports. neurosurgery [internet]. 1990 jan [cited 2013 sep 8];26(1):122–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/2294462 13. yang w-h, lu m-s, cheng y-k, wang t-c. pial arteriovenous fistula: a review of literature. br j neurosurg [internet]. 2011 oct [cited 2013 aug 20];25(5):580–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/21501060 14. valavanis a, yaşargil mg. the endovascular treatment of brain arteriovenous malformations. adv tech stand neurosurg [internet]. 1998 jan [cited 2013 sep 11];24:131–214. available from: http://www.ncbi.nlm.nih.gov/pubmed/10050213 15. lai cw, agid r, van den berg r, ter brugge k. cerebral arteriovenous fistulas induced by dural arteriovenous shunts. ajnr am j neuroradiol [internet]. 2005 may [cited 2013 sep 11];26(5):1259– 62. available from: http://www.ncbi.nlm.nih.gov/pubmed/15891194 16. pelz d, lownie s, fox a, rosso d. intracranial dural arteriovenous fistulae with pial venous drainage: combined endovascular-neurosurgical therapy. can j neurol sci. 1997;24(7):210–8. 17. lv x, li y, jiang c, wu z. endovascular treatment of brain arteriovenous fistulas. ajnr am j neuroradiol [internet]. 2009 apr [cited 2013 sep 7];30(4):851–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/19147710 18. gonzalez lf, chalouhi n, jabbour p, teufack s, albuquerque fc, spetzler rf. rapid and progressive venous thrombosis after occlusion of high-flow arteriovenous fistula. world neurosurg [internet]. 2012 oct 24 [cited 2013 sep 11]; available from: http://www.ncbi.nlm.nih.gov/pubmed/23103261 19. rodesch g, malherbe v, alvarez h, zerah m, devictor d, lasjaunias p. nongalenic cerebral arteriovenous malformations in neonates and infants. review of 26 consecutive cases (1982-1992). childs nerv syst [internet]. 1995 apr [cited 2013 sep 8];11(4):231–41. available from: http://www.ncbi.nlm.nih.gov/pubmed/7621485 20. lasjaunias p. a revised concept of the congenital romanian neurosurgery (2013) xx 4: 342 350 349 nature of cerebral arteriovenous malformations. interv neuroradiol [internet]. 1997 dec 20 [cited 2013 sep 11];3(4):275–81. available from: http://www.ncbi.nlm.nih.gov/pubmed/20678357 21. ozawa t, miyasaka y, tanaka r, kurata a, fujii k. dural-pial arteriovenous malformation after sinus thrombosis. stroke [internet]. 1998 aug [cited 2013 sep 11];29(8):1721–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/9707217 22. phatouros cc, halbach v v, dowd cf, lempert te, malek am, meyers pm, et al. acquired pial arteriovenous fistula following cerebral vein thrombosis. stroke [internet]. 1999 nov [cited 2013 sep 11];30(11):2487–90. available from: http://www.ncbi.nlm.nih.gov/pubmed/10548689 23. schmit bp, burrows pe, kuban k, goumnerova l, scott rm. acquired cerebral arteriovenous malformation in a child with moyamoya disease. case report. j neurosurg [internet]. 1996 apr [cited 2013 sep 11];84(4):677–80. available from: http://www.ncbi.nlm.nih.gov/pubmed/8613863 24. kader a, goodrich jt, sonstein wj, stein bm, carmel pw, michelsen wj. recurrent cerebral arteriovenous malformations after negative postoperative angiograms. j neurosurg [internet]. 1996 jul [cited 2013 sep 11];85(1):14–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/8683264 25. batjer h, samson d. arteriovenous malformations of the posterior fossa: clinical presentation, diagnostic evaluation and surgical treatment. neurosurg rev [internet]. 1986 jan [cited 2013 sep 8];9(4):287–96. available from: http://www.ncbi.nlm.nih.gov/pubmed/3614687 26. halbach v v, higashida rt, hieshima gb, hardin cw, dowd cf, barnwell sl. transarterial occlusion of solitary intracerebral arteriovenous fistulas. ajnr am j neuroradiol [internet]. 1989 [cited 2013 sep 7];10(4):747–52. available from: http://www.ncbi.nlm.nih.gov/pubmed/2505503 27. stapleton cj, armstrong dl, zidovetzki r, liu cy, giannotta sl, hofman fm. thrombospondin-1 modulates the angiogenic phenotype of human cerebral arteriovenous malformation endothelial cells. neurosurgery [internet]. 2011 may [cited 2013 sep 11];68(5):1342–53; discussion 1353. available from: http://www.ncbi.nlm.nih.gov/pubmed/21307796 28. kiliç t, pamir mn, küllü s, eren f, ozek mm, black pm. expression of structural proteins and angiogenic factors in cerebrovascular anomalies. neurosurgery [internet]. 2000 may [cited 2013 sep 11];46(5):1179–91; discussion 1191–2. available from: http://www.ncbi.nlm.nih.gov/pubmed/10807251 29. rothbart d, awad ia, lee j, kim j, harbaugh r, criscuolo gr. expression of angiogenic factors and structural proteins in central nervous system vascular malformations. neurosurgery [internet]. 1996 may [cited 2013 sep 11];38(5):915–24; discussion 924–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/8727816 30. uranishi r, baev ni, kim jh, awad ia. vascular smooth muscle cell differentiation in human cerebral vascular malformations. neurosurgery [internet]. 2001 sep [cited 2013 sep 11];49(3):671–9; discussion 679– 80. available from: http://www.ncbi.nlm.nih.gov/pubmed/11523679 31. rhoten rl, comair yg, shedid d, chyatte d, simonson ms. specific repression of the preproendothelin-1 gene in intracranial arteriovenous malformations. j neurosurg [internet]. 1997 jan [cited 2013 sep 11];86(1):101–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/8988087 32. shweiki d, itin a, soffer d, keshet e. vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis. nature [internet]. 1992 oct 29 [cited 2013 aug 12];359(6398):843–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/1279431 33. helmchen c, nahser hc, yousry t, witt tn, kühne d. [therapy of cerebral aneurysms and arteriovenous vascular malformations in hereditary hemorrhagic telangiectasia (rendu-osler-weber disease)]. nervenarzt [internet]. 1995 feb [cited 2013 sep 8];66(2):124–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/7715751 34. garcía-mónaco r, taylor w, rodesch g, alvarez h, burrows p, coubes p, et al. pial arteriovenous fistula in children as presenting manifestation of rendu-oslerweber disease. neuroradiology [internet]. 1995 jan [cited 2013 sep 8];37(1):60–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/7708192 35. upchurch k, feng l, duckwiler gr, frazee jg, martin na, viñuela f. nongalenic arteriovenous fistulas: history of treatment and technology. neurosurg focus [internet]. 2006 jan [cited 2013 sep 11];20(6):e8. available from: http://www.ncbi.nlm.nih.gov/pubmed/16819816 36. tomlinson fh, rüfenacht da, sundt tm, nichols da, fode nc. arteriovenous fistulas of the brain and the spinal cord. j neurosurg [internet]. 1993 jul [cited 2013 sep 11];79(1):16–27. available from: http://www.ncbi.nlm.nih.gov/pubmed/8315463 37. oshita j, ohba s, itou y, sakoda e, ishihara s. [case with intracranial pial arteriovenous fistulas]. no shinkei geka [internet]. 2011 dec [cited 2013 sep 7];39(12):1197–202. available from: http://www.ncbi.nlm.nih.gov/pubmed/22128276 38. hermier m, turjman f, bozio a, duquesnel j, lapras c. endovascular treatment of an infantile nongalenic cerebral arteriovenous fistula with cyanoacrylate. childs nerv syst [internet]. 1995 aug 350 moscote-salazar and alvis-miranda new pial arteriovenous fistulas grading scale [cited 2013 sep 8];11(8):494–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/7585691 39. de aguiar gb, conti mlm, veiga jce, jory m. giant intracranial pial arteriovenous fistula treated by endovascular intervention. minim invasive neurosurg [internet]. 2011 oct [cited 2013 sep 10];54(5-6):247–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/22278788 40. newman cb, hu yc, mcdougall cg, albuquerque fc. balloon-assisted onyx embolization of cerebral single-channel pial arteriovenous fistulas. j neurosurg pediatr [internet]. 2011 jun [cited 2013 sep 10];7(6):637–42. available from: http://www.ncbi.nlm.nih.gov/pubmed/21631202 41. paramasivam s, toma n, niimi y, berenstein a. de novo development of dural arteriovenous fistula after endovascular embolization of pial arteriovenous fistula. j neurointerv surg [internet]. 2013 jul [cited 2013 sep 10];5(4):321–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/22510457 microsoft word 7ciureaavourpolicy 54 a.v. ciurea et al intraventricular colloid cysts our policy in intraventricular colloid cysts. experience of 31 operated cases. a.v. ciurea, f.m. brehar, al. tascu, a. iliescu, d. talianu, r. rizea first neurosurgical department emergency clinical hospital “bagdasar-arseni”, bucharest abstract the colloid cyst of the third ventricle is a benign tumor situated in the anterior part of the third ventricle. this lesion represents less than 1% of the primary brain tumor being more common in young adults. because of its particular location, the colloid cyst can obstruct the monro foramen, producing intermittent intracranian hypertension with headache, vomiting and visual disturbances. thirtyone cases of colloid cysts have been operated using the microsurgical approach in the first neurosurgical department of emergency clinical hospital “bagdasararseni” between january 1995 and december 2008. the age of the patients was between 17 and 46 years, with a medium age of 31 years. the follow-up period was between 9 months and 7 years. in three cases tta approach has been performed. one of the cases developed a venous cerebral infarct after this procedure, but the patient had finally a good outcome. for 28 patients the transcortical approach has been performed. in all cases the total resection of the colloid cyst has been performed. of all 31 cases, one case presented a transitory hemiparesis, two cases showed negativist behavior, and three cases had transitory memory disturbances. there was no intraventricular hemorrhage after colloid cyst resection in our series. in conclusion, according to our policy, the microsurgical approach is the best treatment for third ventricular colloid cysts because of its main advantages compared with the endoscopic approach: the possibility of total resection of the cyst, the good control of the bleeding source during the procedure, and a better exposure of the anatomical landmarks. keywords: colloid cyst, obstructive hydrocephalus, microsurgical approach, neuro-endoscopy. introduction colloid cysts are among the most common benign tumors of the third ventricle and represents, according with literatury data, between 0.5 and 2% of all intracranial neoplasms (10, 11). a characteristic feature of the colloid cyst is its location at the anterior part of the third ventricle, which may produce the occlusion of the foramina of monro, resulting in biventricular hydrocephalus (11). this particular location reflects in a specific clinical picture which may include rapid neurological deterioration and even sudden death. (9, 19). the vast majority of colloid cysts reported in the literature are symptomatic and were therefore treated. the size of the cysts which is clinically significant is more than 1,5 cm in diameter (figure 1). romanian neurosurgery (2011) xviii 1: 54 – 59 55 figure 1 mri aspect of the colloid cyst of the third ventricle figure 2 ct scan showing colloid cyst located in third ventricle with obstructive hydrocephalus the main symptoms of the colloid cysts are: headache, gait disturbances, disturbed mentation, vomiting, blurred vision, incontinence and dizziness. the main signs are papilledema, gait disturbance, hyperreflexia, incoordination and nistagmus (10) the treatment of asymptomatic colloid cysts depends on individual characteristics and patients’options (12, 13). the major symptoms depend of the size of the colloid cysts and are usually related to the secondary hydrocephalus produced when they are large enough to occlude the monro foramen (figure 2). signs and symptoms may be also produced by compression of the nearby structures, like hypothalamus floor and fornix. sjovall et al postulated 100 years ago, that episodic intracranial hypertension crises could be produces by intermitent obstruction of monro foramen (20). sudden increased in size of the colloid cyst due to intracystic hemmorhage could be another mechanism which explain the neurological deficits (1). despite several cases which presented several neurological deficits related to the size of the cyst, sudden deterioration is rare for the most patients with colloid cysts, and the first symptoms are intermittent and nonspecific. (3). the cause of these deterioration is usually related to the obstruction of csf outflow due to particular location of the cyst. other authors suggested that sudden death is related rather to local compression of the wall of the third ventricle, thus compromising cardiovascular regulatory centers in the hypothalamus, than with acute obstructive hydrocephalus (16). probably, keeping in mind both hypothesis mentioned above, the mechanism in such cases is multifactorial (6). in cases with obstructive hydrocephalus, acute 56 a.v. ciurea et al our policy in intraventricular colloid cysts deterioration might be provoked by lumbar puncture, therefore a ct scan is mandatory before performing such a procedure (3). in the presence of associated obstructive hydrocephalus, there are two managemnt options. if there is an acute symptomatic hydrocephalus, a ventricular drainage should be performed in emergency. if the ventricular enlargment is not accompanied by sings and symptoms of intracranial hypertension, the presence of hydrocephalus ventricles could be advantageous, offering to the surgeon a natural corridor and enough room to reach the cyst and to remove the lesion. this situation is favorable for the transcortical approach. contrary, if the transcallosal route is chosen, one way is to implant a ventricular drain in order to avoid excessive retraction of the medial wall of the frontal lobe (11). in this paper the authors present their experience in 31 consecutive cases of colloid cysts operated using two microsurgical approaches. materials and methods thirty one cases of colloid cysts have been operated using the microsurgical approach in the first neurosurgical department between january 1995 and december 2008. the age of the patients was between 17 and 46 years, with a medium age of 31 years. there were 15 males and 16 females. the main symptoms were: headache in 28 cases (90,3%), ataxiain 12 cases (38,7%), vi-th nerve paresis in 9 cases (29,1%), memory impairment in 14 cases (45,2%), “ventricular seizures” in 18 cases (58,1%). other clinical signs consist in gatism in 4 cases (12,9%), nystagmus in 5 cases (16,1%), bilateral dismetria in 4 cases (12,9%), epileptic seizures in 11 cases (35,5%), psychic impairment in 5 cases (16,1%). twenty-eight cases (90,4%) have preoperative hydrocephalus and 3 cases (9,6%) were without hydrocephalus the follow-up period was between 9 months and 7 years. one case died in the emergency room and diagnosis has been established during necropsy (case nonincluded in our series). another case presented at the emergency room with intracranial hypertension syndrome. the ct scan showed signs of acute hydrocephalus. vp shunt has been performed in emergency and the patient’s symptoms improved significantly. the mr performed after surgical procedure identified a colloid cyst located in the third ventricle which had produced the obstructive hydrocephalus. treatment consisted in surgery in 31 cases (100%), respectively in tumour removal without vp shunt 29 cases (93,5%) and vp shunt (performed in emergency) and removal of the tumor in 2 cases (6,50%). there was no case for observation only. in three cases, tta approach has been performed. one of the cases developed a venous cerebral infarct after this procedure, but the patient had finally a good outcome. for 28 patients, the transcortical approach has been performed. the advantages of this approach consist in the excellent exposure of the cyst and surrounding important anatomical landmarks (internal cerebral vein, anterior septal vein, talamo-striate vein, choroid plexus, etc.), the resection of the cyst totally inclusive the cyst’s capsule and a very good control of any bleeding point. results and discussions in all cases total removal of the colloid cyst has been performed (figure 3 and figure 4). romanian neurosurgery (2011) xviii 1: 54 – 59 57 figure 3a figure 3a colloid cyst of the third ventricle. b postoperative aspect of all 31 cases, one case presented a transitory hemiparesis, two cases showed negativist behavior, and three cases had transitory memory disturbances. there was no intraventricular hemorrhage after colloid cyst resection in our series. immediate complications consist in intracerebral hemorrhage 1 case (3,2%), epileptic seizures in 11 cases (35,4%), of which partial seizures in 7 cases (22,5%) and generalized seizures in 4 cases (12,9%). figure 4a figure 4a colloid cyst of the third ventricle. b postoperative mr image which shows total resection of the cyst late complications were: obstructive hydrocephalus in 2 cases (6,4%), transitory left hemiparesis in 5 cases (16,1%), memory disorder in 8 cases (25,8%), negativism, apathy in 4 cases (12,9%). evolution of 31 cases operated were favorable in 30 cases (96,7%), worse in 1 case (3,3%) and no case of death (0 %). microsurgical approach should be the first treatment option. either transvers transcallosal approach (tta), or 58 a.v. ciurea et al our policy in intraventricular colloid cysts transcortical approach could be used to reach and resect the lesion totally. both approaches are effective and usually safe, although neither is without complications. the initial steps of the transcallosal are perhaps a bit more difficult and require meticulous microsurgical techniques. we do not prefer it, however this is the procedure of choice if ventricles are not enlarged. it allows a good visualization of the structures inside the ventricular system. on the other hand the trancortical approach have several advantages compared with transvers transcallosal approach. the minim invasive techniques consist in endoscopic, endoscope-assisted keyhole approaches and, less frequently nowadays, stereotactic aspiration of the cyst. colloid cysts, especially in patients with normal ventricles after shunting, can be treated with simple stereotactic aspiration (2). it should be mentioned that the content could be too viscous and difficult to aspirate (15) and, furthermore, part of the capsule may be left behind, causing recurrence of the lesion in an unacceptably high rate (8). more recently, endoscopic approach represents reasonable alternatives. however, there are many cases when portions of the capsule are left behind so the risk of recurrence still remains. despite of the technological advances, questions still remain regarding the advantages of open versus endoscopic in resection of colloid cysts. comparing a series of a single institution, horn et al. showed that in the endoscopic group the rate of residual or recurrent cysts was higher and the length of stay was slightly shorter (7). this study showed also, that severe complications such as hemiparesis and memory deficits can be associated with this minimal invasive approach. before the recent development of modern endoscopic technique, kelly et al proposed another minimally invasive approach which consisted in placing stereotactically a tube retractor through a frontal burr hole. other authors support the simultaneous approach of endoscopic and microsurgical strategies (4). as mentioned above, ventricular enlargement could be advantageous for the surgical approach, especially for transcortical approach. contrary, if the transcallosal route is chosen, a ventricular drain should be used intra-operatively in order to avoid excessive retraction of the medial wall of the frontal lobe (11). several authors who support the microsurgical approach of the colloid cyst of the third ventricle as the best therapeutically option (5, 14, and 18). m. sami consider also that third ventricle colloid cyst has a perfect microsurgical indication (17). in our opinion the microsurgical approach is the best treatment for third ventricular colloid cysts because it offers several advantages compared with the endoscopic approach, such as the possibility of total resection of the cyst, the good control of the bleeding source during the procedure, and a better exposure of the anatomical landmarks. our option is for the transcortical microsurgical approach because tta has and important risk of memory deficit and could produce deep vein lesions. the advantages of this approach consist in the excellent exposure of the cyst and surrounding important anatomical landmarks (internal cerebral vein, anterior septal vein, talamo-striate vein, choroid plexus, etc.), the resection of the cyst totally inclusive the cyst’s capsule and a very good control of any bleeding point. romanian neurosurgery (2011) xviii 1: 54 – 59 59 conclusion colloid cysts are rare benign lesions located in the anterior part of the 3rd ventricle in monro area. the patognomonic features are intracranial hypertension attacks and so called “ventricular seizures”. the presence of intracranial hypertension requires surgery in emergency. in conclusion, we think the microsurgical approach is the best treatment for third ventricular colloid cysts because of its main advantages compared with the endoscopic approach: the possibility of total resection of the cyst, the good control of the bleeding source during the procedure, and a better exposure of the anatomical landmarks. microsurgical approach should be the first treatment option. either transvers transcallosal approach (tta), or trancortical approach could be used to reach and resect the lesion totally. e-mail: felixbrehar@yahoo.com tel: +40213343025 abbreviations csf: cerebro-spinal fluid; tta: transvers transcallosal approach; vp: ventriculo-peritoneal references 1. beems t, menovsky t, lammens m (2006) hemorrhagic colloid cyst. case report and review of the literature. surg neurol 65: 84-86 2. bosch d a, rahn t, backlund e o: treatment of colloid cyst of the third ventricle by stereotactic aspiration, surg. neurol. 9: 15-8, 1978 3. buttner a, winkler pa, eisenmenger w, weis w (1997) colloid cyst of the third ventricle with fatal outcome: a report of two cases and review of the literature. int j legal med 110: 260-266 4. charampaki p, filippi r, welschehold s, et al. (2005) tumors of the lateral and third ventricle: removal under endoscope – assisted keyhole conditions. neurosurgery 57 (ons suppl 4): ons-302-ons-311 5. ciurea a.v., al. tascu, f. brehar, r. rizea, microsurgical procedures in intraventicular choloid cyst in neuroendoscopy era, al vi-lea congres national al asociatiei romane de chirurgie endoscopica, bucuresti, 11-14.11.2009. 6. hamlat a, pasqualini e, askar b (2004) hypothesis about the physiopathology of acute deterioration and sudden death caused by colloid cysts of the third ventricle. med hypotheses 63: 1014-1017 7. horn em, feiz-erfan i, bristol re, et al. (2007) treatment options for the third ventricular colloid cysts: comparison of open microsurgical versus endoscopic resection. neurosurgery 60: 613-620 8. lobo-antunes j, louis km, ganti sr (1980) colloid cysts of the third ventricle. neurosurgery 7: 450-455 9. lobosky jm, vangilder jc, damasio ar (1984) behavioural manifestations of third ventricular colloid cysts. j neurol neurosurg psychiatry 47: 1075-1080 10. mark s. greenberg, handbook of neurosurgery, thieme, 2006 11. marc sindou, practical handbook of neurosurgery, thieme, 2009 12. pollock be, huston j (1999) natural history of asymptomatic colloid cysts of the third ventricle. j neurosurg 91: 364-369 13. pollock be, shreiner sa, huston (2000) a theory on the natural history of colloid cysts of the third ventricle. neurosurgery 46: 1077-1083 14. r. l. jeffree and m. besser, colloid cyst of the third ventricle: a clinical review of 39 cases, journal of clinical neuroscience, volume 8, issue 4, july 2001, pages 328-331 15. rivas j j, lobato r d: ct – assisted stereotactic aspiration of colloid cyst of the third ventricle. j. neurosurg 62, 238 – 42, 1985 16. ryder j w, kleinschmidt b k, keller t s, sudden deterioration and death in patients with benign tumors of the third ventricle area. j. neurosurg. 64:216-23, 1986 17. sami m. et al. (2009), microsurgical approach of the colloid cyst of the third ventricle, romanian neurosurgical conference with international participation, sibiu, 30.09-03.10.2009. 18. sampath, raghuram md; vannemreddy, prasad md; nanda, anil md (2010), microsurgical excision of colloid cyst with favorable cognitive outcomes and short operative time and hospital stay: operative techniques and analyses of outcomes with review of previous studies, neurosurgery: february 2010 volume 66 issue 2 p 368–375; doi: 10.1227/01. neu.0000363858.17782.82 19. shaktawat sameer,walid d salman,zuhair twaij, and abdul al-dawoud, unexpected death after headache due to a colloid cyst of the third ventricle, world j surg oncol. 2006; 4: 47 20. sjovall e (1910) über eine ependymcyste embryonalen charakters (paraphyse?) im dritten hirnventrikel mit tödlichem ausgang. zugleich eine beobachtung wahrer lipochromer veränderungen mit auftreten von halbmondkörperchen. beitr pathol anat 47: 248-269 microsoft word 2gheorghita_considerations.doc romanian neurosurgery (2012) xix 3: 183 192 183 considerations on anesthesia for posterior fossa-surgery eva gheorghita, j. ciurea, b. balanescu emergency hospital bagdasar arseni, bucharest abstract neuroanesthesia is a special chapter of anesthesia, referring to surgery that is performed right at the site of action of anesthetic drugs, namely the central nervous system (cns). changes induced by general anesthesia on the cns are accompanied by changes in brain physiology, including cerebral blood flow (cbf), cerebral metabolic rate of oxygen (cmro2), cerebral perfusion pressure (cpp) and electrophysiological functions. in neuroanesthesia, posterior fossa surgery faces difficult challenges due to the peculiarities observed from an anatomical and physiological point of view, which also requires the patient to be put in a specific position prior to surgery. therefore, we have considered useful and detailed aspects of general anesthesia in this type of surgery, presenting data both from specialized literature and from personal experience of over 25 years. fundamentals of anatomy and physiology the posterior fossa contains vital nerve structures such as the brainstem, the cerebellum and the fourth ventricle. the brainstem is the most important area of the subtentorial space with a complex structure, representing the transitional area for the main ascending and descending nervous paths that cross each other belonging to the nervous system. the gray matter of the brainstem is represented by its own nuclei and origin nuclei of the cranial nerves. the brainstem contains numerous vital centers such as: • the respiratory center; • the cardiovascular center; • the swallowing center; • the center of vomiting, coughing, and/or hiccups; • the chewing center; • the salivary centers. the brainstem reticular substance plays an important role as it is involved in our sleep-wake state regulation, regulation of muscle tone, regulation of sensori-sensitive function and the regulation of our autonomic functions. reticular formation is a vast neural mass stretched all along the brainstem as an unspecific, polysynaptic path also containing the majority of neural network points, somatovegetative (respiratory, cardiovascular) and a series of extrapyramidal structures. the cerebellum is another important part of the posterior fossa, as it plays a essential role in regulation, coordination, and controlling voluntary and involuntary motor activity like balance and locomotion. the iv ventricle is a dilated region in the form of tent, located between the brain stem and cerebellum. it consists of the floor and ceiling. the fourth ventricle floor is the rhomboid fossa, posterior faces in 184 gheorghita et al anesthesia for posterior fossa-surgery correspondence to the bulbo-pontine area. this floor designs the bulbo-protuberanţial locum for vital centers, and thus poses high risks during surgical practices. the content skull consists of three components: • brain substance (80%); • blood volume (12%); • cerebrospinal fluid (csf) 8%; these sections performed in a pressure skull called the intracranial pressure (icp), with normal values between 8-15 mmhg. in pathological conditions, the volume of a compartment through various mechanisms (cerebral edema, hydrocephalus) or the emergence of a new compartment represented by a pathological process (hematoma, tumor, cyst, abscess) determines the increase in intracranial pressure. intracranial hypertension (ich) is accompanied by changes in blood circulation, drainage of csf, and decreased brain compliance, which is defined as relation volume /pressure. the relationship between cerebral hemodynamics, csf dynamics, cerebral perfusion pressure and mean blood pressure (tam), plays an important role in icp changes occurring in brain injury of any etiology. the cerebrospinal fluid (csf) is produced by the choroid plexus in the walls of the lateral ventricles and in the floor of the fourth and third ventricle; a small amount is produced in the perivascular spaces. the tissue compartment is the largest intracranial compartment consisting of neurons, glial cells and extracellular space. the main cause of increase in brain volume is the cerebral edema, which causes intracranial hypertension . the vascular compartment consists in arterial and venous blood and its volume changes as changes in cerebral blood flow by autoregulation (effect of paco2 and cmro2) however, venous volume change if the superior vena cava syndrome, venous sinus thrombosis is present or mechanical ventilation with positive end expiratory pressure (peep) occurs. cerebral vessels are anatomically (endothelial tight junctions) and physiological (mechanisms of self-regulation and chemo regulation) different from vessels outside the central nervous system. cerebral perfusion pressure is defined as the difference between map and icp. auto-regulation of cerebral blood flow is defined as the ability of the cbf to keep its constant values despite a wide variation of map(at normal value of pa o2 şipaco2) so long as the lime map varies between 50-120 mmhg(13). influence of the metabolic rate of oxygen. the brain is the organ with the highest metabolic rate, but its reserves in glucose and oxygen are limited. increased neuronal activity leads to increased neuronal metabolic rate and of cerebral blood flow in order to provide oxygen and glucose requirements. posterior fossa neurosurgical disorders are classified by: etiology tumor pathology traumatic pathology vascular pathology infectious pathology location median line syndrome cerebellar hemisphere-syndrome ponto-cerebellar angle syndrome brainstem syndrome depending on the location of the disease process, there is a large variety of clinical romanian neurosurgery (2012) xix 3: 183 192 185 symptoms, due to intracranial hypertension syndrome, cerebellar and vestibular disorders, movement disorders and susceptibility to onset of autonomic disorders which is a sign of serious prognostic and damage of vital centers, respiratory and cardiovascular (1, 5). ich syndrome, in most cases, is among the first element of diagnosis of the posterior fossa neurological disorders. it is represented clinically by headache, vomiting, visual disturbances (due to papilledema). this increase, even if slight, affects the brain function by two means: it lowers the cbf with secondary ischemia; it causes herniation of brain substance. after exhaustion of compensatory mechanisms herniation of the cerebral mass will take place, especially cerebellar tonsils through the "foramen magnum" with compression, constriction and twisting of the blood vessels and nervous paths of the brainstem impairing the brainstem vital functions coordinated at this level. neural damage due to cerebral ischemia in neurosurgical infratentorial pathology provides critical clinical forms, due to the presence of vital and neurovegetative centers that are in this area. appropriate means to avoid cerebral ischemia during surgery at this level is an important concern of the anesthetic and surgical team. anesthetic peculiarities the presence of vital nerve structures and limited space for surgical approach to the posterior fossa, explains the aforementioned challenges of surgery at this level, both for the surgeon and the anesthetist. along with the pathological and surgical maneuvers, anesthesia interacts with brain structures and functions. as a result, in addition to systemic hemodynamic stability in neuroanesthesia, the criteria for choosing the anesthetic technique is aiming to achieve the following: icp stability avoiding its growth; cbf and cmro2-reducing, maintaining physiological coupling; maintaining of self-control/regulation of cerebral circulation; maintaining cerebrovascular reactivity to changes in paco2; ensuring optimum cpp; possibility to monitor evoked potentials and electromyography; protection of the brain; rapid waking up for early postoperative neurological assessment. in order to fulfill these criteria, the following are of particular importance: -use of modern methods for monitoring all the vital functions; -positioning the patient on the operating table; -choosing appropriate anesthetic technique. in patient monitoring, both general and especially neuroanesthesia is inconceivable nowadays without modern methods of monitoring. patients undergoing surgery of the subtentorial area are subjects to blood loss, cardiac arrhythmias, blood pressure variations, air embolism, urinary losses, specific positioning causing difficult survey of the tracheal tube caused by difficult access also of the precordial area; therefore multimodally monitoring to assess appropriate the status of all vital organs is mandatory. taking into account the importance of systemic hemodynamic stability during 186 gheorghita et al anesthesia for posterior fossa-surgery neurosurgical interventions to ensurecpp, and that the infratentorial region-based surgical maneuvers may affect cardiovascular centers of the brainstem, systemic hemodynamic invasive and noninvasive monitoring (ecg, map, poulse,central venous pressure, precordial doppler) are mandatory. monitoring breathing for posterior fossa surgery requires a great amount of concentration in order to sustain the hemodynamic stability and icp. thus, inspiratory pressure should be as low as to not embarrass venous return and additional attention should be given to continuous monitoring of spo2, etco2, tidal volume, minute volume, blood gas analyst. intraoperativ neurophysiological monitoring has become standard of care in many neurosurgical procedures. the main modalities are: somatosensory evoked potentials(ssep),motor evoked potentials(mep), and electromyography(emg) (7). other monitored parameters are temperature, diuresis, blood glucose, hematocrit. patient positioning. a good surgical access, hemodynamic stability and optimal icp, need optimal patient selection position in order to perform surgery in the infratentorial area. this topic has been controversial over time, giving up certain positions, then returning to them. choosing one of the positions listed below is a decision taken by the anesthesiologist and neurosurgeon, taking into account: • neurosurgical pathology; • patient age; • preexisting diseases; • constitutional type; • method of surgical approach; • technical possibilities of monitoring; • proper operating facilities. main positions used in posterior l fossa surgery are: • ventral/prone position; • sitting position; • lateral position with her version of park bench position. the "prone" position is the oldest and most commonly used in posterior fossa surgery. the patient is laid face down and has his head flexed on a special head holder, legs slightly bent to prevent slippage from the operating table. benefits of this position are: • surgical access pretty good, both midline and lateral; • low risk of air embolism; • better hemodynamic stability with a minimal risk of hypotension. disadvantages: • amount of blood loss is bigger than in sitting position; • difficult access to the airway, precordial area and tracheal tube; • ischemia and risk of retinal bleeding due to compression in the orbital area; • danger of necrotic lesions of the face areas and other points of support, which can be avoided by careful placement. sitting position for the posterior fossa surgery is controversial due to its great advantages over the contradiction between intracranial pressure values and serious incidents generated by this position. benefits of this position: • good surgical access, with good viewing of the pontin cerebellar angle; • good csf and venous drainage with decreases of icp and intraoperative bleeding; • easier access to the airways. disadvantages: • hemodynamic instability, concerning romanian neurosurgery (2012) xix 3: 183 192 187 patients especially at extreme ages and impaired cerebral circulation due to hypovolemia; • distribution volume change causes respiratory inflation pressure if small peaks in the expense base ventilation and perfusion lung damage reversed distribution under the influence of hydrostatic pressure, are bases shint and tops dead space. for this reason, optimal peep must be used carefully; • risk of air embolism; • quadriplegia with cervical spinal ischemia; • orthopedic and skin problems. choice of anesthetic technique the preanesthetic checkup of the patient include the assessment of neurological and other organic systems disorders for establishing the right position on in the asa scale / anesthetic risk. the correct evaluation and possible treatment failures is of particular importance, given the undesirable effects of hemodynamic instability and hypercapnia on cbf and icp. sensitivity to sedatives and narcotics in neurosurgical patients require special attention in their use preanesthetic stage. danger of respiratory depression even at low doses of the substances mentioned above, the occurrence of hypoxia and hypercapnia, knowing the effects of hypoxia and hypercapnia if low brain compliance require keen surveillance induction of anesthesia is a critical time of any anesthesia because the period of apnea during intubation, risk of cough and hyperdynamic cardiovascular response to laryngoscopy and intubation maneuvers and the danger of hypotension and bradycardia when injecting certain drugs at this stage. danger of these shortcomings is much higher in patients with posterior fossa pathology due to low compliance with the ich syndrome and cause cerebral ischemia or engaging tonsils with brainstem compression. we note the importance of selecting anesthetic drugs used, taking into account their effects on cerebral and systemic hemodynamics and fineness of maneuvers performed during this period (2). exept ketamine, all drugs used in induction (thiopental, midazolam, propofol, etomidate) decrease more or lesscbf and cmro 2 depending on the dose, resulting in decreased icp and having cerebral protective effect (by decreasing cerebral oxygen consumption). maintenance of anesthesia. whilst selecting an anesthetic technique, we always wonder whether there is a perfect technique in order to perform modern neuroanesthesia and what the criteria is for choosing it. modern neuroanesthesia criteria are: • getting a relaxed brain; • systemic and cerebral hemodynamics monitoring, maintenance nomal levels of blood glucose and plasma osmolarity; • cerebral protection; • temperature control; • quick waking up. cerebral protection is achieved through the "state of anesthesia" itself. to protect from cerebral ischemia, propofol or thiopental avoid postoperative sequels. by following the above criteria we can say that all agents available today in certain combinations and doses may achieve a good neuroanesthesia, if used by a skilled anesthesiologist (young wl 1998). criteria for choosing anesthetic techniques after templehoff's scale (17)are 188 gheorghita et al anesthesia for posterior fossa-surgery valid today: • easy use; • rapid induction and awakening; • maintenance ppc and self-regulation; • prevention of icp growth; • maintenance of vascular reactivity to co2; • lack of systemic toxicity; • possibility of electrophysiological monitoring; • low cost. to meet these criteria there are many possible combinations. the anesthesiologist will have to choose a technique based on knowledge of the pharmacological characteristics of the available agents. a. total intravenous anesthesia short-term effects of anesthetics (like propofol, alfentanyl, remifentanyl, rocuronium) and new pharmacokinetic and pharmacodynamics studies have increasingly started using "total intravenous anesthesia"(tiva). in clinical practice, optimal conditions are obtained when the anesthetic agent concentration in the cns (site of action) is stable, and it depends on stable concentration in blood stream, however maintaining such constant concentrations is not possible unless certain procedures are carried out: by bolus, when there is a sudden increase in blood concentration, and a decrease in distribution and elimination. the following cns concentration remains longer in the blood compartment and maintenance of anesthesia will require an accurate titration of the drug. by manually controlled infusion, because you cannot get a steady blood concentration than hard as complex mathematical calculations required several times during anesthesia. a computer included in an automatic injection pump can easily perform these calculations. this creates so-called technique of intravenous target controlled infusion (tci). maintenance dose of opioids are different in neuroanesthesia. painful events in neurosurgery are at the start and end point of the intervention, which are: • laryngoscopy, tracheal intubation; • fixing the head in the headrest; • skin, periosteum, and dura matter incision; • suture of dura matter and scalp. as a result, higher analgesic doses are required for dura mater incision and suture. cerebral substance does not trigger pain when penetrated however. so between these two intervals, the patient requires more hypnosis and muscle relaxants than analgesia. we can say that neuroanesthetical doses of anesthetics are more individualized. b. pivot inhaled anesthesia (balanced) balanced anesthesia is a more ancient than tci and tiva and more commonly used today. it involves maintenance of anesthesia with an inhaled agent, associations at or not nitrous oxide and repeated injection of small doses of opioid analgesic and muscle relaxants, depending on the need. with increasing dose inhaled anesthetics decrease cerebral metabolism and causes cerebral vasodilation (8), so they have the potential to increase icp, threatening maintaining optimal cpp (11). however, inhaled agents react with the co2 in cerebral vessels, especially isoflurane (8), allowing their use in romanian neurosurgery (2012) xix 3: 183 192 189 neuroanesthesia by assigning a moderate hyperventilation to counter their effect of increasing the cbf(16). the cmro2 decrease and circulation auto-regulation is impaired with an increase of inhaled agent’s concentration. isoflurane protects brain through two mechanisms: • reducing excitatory neurotransmitters release by presynaptic mechanism, an effect comparable to hypothermia (k nakashima et al 1996); • decreasing neuronal metabolism by nontoxic mechanism, and lowering glucose takeover in neurons, an effect comparable to thiopental (4); it can induce an eeg isoelectric line at non-toxic concentrations (2mac). isoflurane can be an attractive opportunity to compete with the new trend of using tiva, tci. sevoflurane has a lower solubility coefficient than isoflurane, which makes it attractive for neuroanesthesy. cerebral effects (oncbf,cmro2, self, reactivity to paco2)are similar to isoflurane, but not irritating to the airways, and that lend itself to mask induction agent used mostly in young children and infants. sevoflurane is improving hemodynamic stability and decrease opioid and muscle relaxants dose as well, allowing a faster awakening and decreasing more the incidence of postoperative nausea and shivering. inhaled agents do not provide adequate analgesia and as a result require analgesic supplements especially to painful moments in neurosurgery. this is achieved with low doses of synthetic opioids injected during induction, the start of surgery, during surgery. opioids can be administered on continuous pace with automatic pump. the use of nitrous oxide is the most controversial in posterior fossa interventions. studies have shown its effect of increasing the cbf and even cerebral oxygen consumption (14). has also demonstrated its excitatory effect on the brain. it is advisable not to use nitrous oxide when somatic sensory evoked potentials are monitored. introduction using tiva was an important step in improving anesthetic technique for this type of surgery. using tci technology allows precise dosing of anesthetic drugs, necessary medication use is much lower, also the incidence of postoperative vomiting and shivering, quick awakening affording early postoperative neurological assessment (15). using sitting position allows a relaxed brain, does not require depletion treatment, offers minimal intraoperative bleeding and good surgical approach and reduces the risk of damage of the nerves structures. i have not met incidents of air embolism or hemodynamic instability problems. say that i have not used this position for small children, the elderly and cardiac patients with gcs less than 15 points. management of intraoperative fluids must take into account the maintenance of normovolemia primarily. it is allowed using intraoperative glucose solutions as glucose worsen cerebral edema and ischemic brain damage. mannitol remains diuretic of choice in reducing intraoperative brain edema and obtaining a convenient icp. it can lead to a transient increase in cerebral blood volume (vasodilator effect of hiperosmolality) and increased icp. this phenomenon does not occur when administered slowly, at least 20'-30'. manitol may accumulate in repeated doses. the rebound effect must be taken into account as doses that are used are 0.5-1g / 190 gheorghita et al anesthesia for posterior fossa-surgery kg (18). loop diuretics administered before mannitol may reduce cellular edema, but without affecting the extracellular fluid volume. the two diuretics work better together, but attention to urinary losses and electrolyte disorders. intraoperative problems posterior fossa surgery, concerning vital nerve centers during surgical manipulation provides the worst risk, which is represented by cardiovascular disorders. fourth ventricle floor stimulation can cause hypertension, bradycardia, tachycardia, and arrhythmia. if these problems required surgical maneuvers off, leading to normalize hemodynamic situation. pharmacological treatment is necessary in rare cases. the incidence of cardiovascular disorders is higher in patients with high icp. ventriculo-peritoneal drainage performed 1-2 weeks before surgical cure of the tumor decreases this risk. due to the patient position ventilation problems can arise (by sliding the tracheal tube). air embolism may be another intraoperative complication in sitting position. intraoperative bleeding requires monitoring losses and volume replacement with crystalloids and colloids, then blood transfusion (over 20% volume of blood loss). awakening allows immediate postoperative neurological assessing; clinical neurological examination is the best existing neuro-monitoring. immediate awakening is associated with lower cardiovascular and catecholamine changes, but there is a risk (sometimes quite small) the occurrence of hypoxia and hypercapnia (6). delayed awakening allows better control of oxygenation and co2 removal, but can be associated with delayed neurological examination and a stronger incentive to extubation (hypersympaticotone reaction). shivering increases o2 consumption and co2 production. all this is more serious in neurosurgical patient population, due to increased danger of icp occurrence and cerebral bleeding and ischemia. as a result, awakening in posterior fossa neuroanesthesia will be gentle, avoiding cough and shivering. the reversal of muscle relaxants and opioids will be after covering the patient. low doses of hypnotics, helps us to control the situation some studies shown that the primary extubation is generally feasible, except patients with highes asa score and a longer length of surgery. also, the patients not extubated in the operating room have a longer stay in the hospital (3). in conclusion, when consciousness is intact in the preoperative phase, surgery runs without any difficulties,it is recommended that the patient is awakened in the operating room. if consciousness is impaired preoperatively, if the operation time is prolonged if peroperative problems occur (cerebral edema, hemodynamic instability), delayed awakening is recommended. these recommendations of bracco d et al (1998) are confirmed by randomized trials with significant differences in mortality and morbidity of immediate or delayed awakening. postoperative complications since the posterior l fossa surgery that is performed with surgical maneuvers around romanian neurosurgery (2012) xix 3: 183 192 191 key vital centers monitoring of cardiovascular, respiratory, neurological, renal functions are particularly important in the postoperative period. risk of respiratory disorders, swallowing disorders, cardiovascular disorders, requires careful and continuous monitoring in the icu of these subjects. in the postoperative period, sedation, analgesia and cerebral protection are key elements to prevent growth of icp. choices of substances that produce lower of cbfand cmro 2 for sedation also provide cerebral protection (thiopental, midazolam, propofol). sedation will perform with blood gas monitoring, due to danger of respiratory depression. in most cases, these patients do not require analgesia; postoperative headache is usually caused by increased icp. therefore, prevention of ich prevents the headache. in case of cerebral edema, this is treated with depletion, sedation, adequate oxygenation and possibly minor analgesics. acute postoperative hematoma andhydrocephaluses are serious complications that require early detection and emergency surgery. to this end, close monitoring and repeated neurological examination every hour are tracking patient postoperatively. conclusions preserving neural function is a priority in neurosurgical interventions and especially in the posterior fossa level. current trends in neurosurgery using intraoperative microscope allows performance to the deepest and most sensitive areas of the brain structures. the safest way for reaching them without causing damage by mechanical traction through spreaders means to obtain a” relaxed brain” and compliant with the socalled "chemical methods", which actually represent the key to success by means of a modern anesthetic technique. hence the question: “what is the best anesthetic technique for this type of neurosurgical intervention?” from the above, we can conclude that the techniques described can be used to access the posterior fossa surgical pathology but only provided with appropriate multimodal monitoring. it should be noted that the choice of anesthetic technique depends on both the equipment and anesthetic team experience. in case of insufficient or inappropriate equipment it should be better to avoid this area of neurosurgical activity. the tci technique, using pharmacokinetic models, with control over blood concentrations of anesthetic substances might be preferred because it avoids the risks of over-or under dosing the anesthetic drugs, offering a rapid awakening that allows immediate neurological evaluation which is of extreme importance in this pathology. references 1. arseni c, constantinescu aji, maretzis sm, stancium,voinescu i. procesele expansive intracraniene ed. academiei rsr, bucuresti, 1973; 2. bozeman wp, idris ah. intracranial pressure changes during rapid sequence intubation:a swine model. j trauma 2005; 58:278-283; 3. cata jp, saager l, kurz a, avitsian r.successfulextubation in the operating room after infratentorial craniotomy: the cleveland clinic experience. j neurosurg anesthesiolog. 2011 jan;23(1):25-29; 4. cottrell je. brain protection in neurosurgery. asa annual refresher course lecturer 1997; 153; 5. danaila l . tratamentul tumorilor cerebrale. ed. academiei române, bucureşti 1993; 6. david m, hennes hj , oeltze jp , schafer m, mauer d, dick w . early extubation after elective craniotomy : prospestive evaluation for the frequency of reintubation 192 gheorghita et al anesthesia for posterior fossa-surgery . eur j anaesth 1998; 15( 17):72; 7. deiner s. highlights of anesthetic considerations for intraoperative neuromonitoring.semin cardiotorach vasc anesth. 2010mar;14(1):51-53; 8. drummond jc,todd mm.,scheller ms,shapiro hm. a comparison of the direct cerebral vasodilatating potencies of halothane and isoflurane in the new zeeland white rabbit. anesthesiology 1996; 65:426-467; 9. drummond jc,todd mm.the response of feline cerebral circulation to paco2 during anesthesia with isoflurane and halothane and during sedation with nitrous oxide.1985; 62:268-273; 10. engelhard k, werner c inhalational or intravenous anesthetics for craniotomies? pro inhalational.. curr opin anaesthesiol. 2006 oct;19(5):504-; 11. fraga m, rama maceiras p, rodino s et al. the effects of isoflurane and desflurane on intracranial pressure, cerebral perfusion pressure and cerebral arteriovenous oxygen content difference in normocapnic patients with supratentorial brain tumors. anesthesiology 2003;98:1085-1090; 12. gheorghita eva. anestezia in chirurgia fosei craniene posterioare.ed.medicala, bucuresti. 2010; 13. hall m.principles of critical care 1992; 14. hoffman we, charbel ft, edelman g, albrecht rf, ausman jl. nitrous oxid added to isoflurane increases brain artery blood flow and low requency brain electrical activity. j neurosurg anesth 1995; 7:8288; 15. miura y, kamiya k, kanazawa k, okada m, nakane m, kumasaka a, kawamae k.superior recovery profiles of propofol-based regimen as compared to isofluranebased regimen in patients undergoing craniotomy for primary brain tumor excision: a retrospective study. journal of anesthesia2012; 10.1007/s00540-012-1398-2; 16. newell dw, weber jp, watson r, aaslid r, winn hr. effect of transient moderate hyperventilation on dynamic cerebral autoregulation after severe head injury.neurosurgery.1996 jul;39(1):35-43; 17. tempelhoff r. the new inhalational anaesthetics desflurane and sevoflurane are valuable additions to the practice of neuroanaesthesia. j neurosurg anesth 1997; 9:69-71; 18. thenuwara k, todd mm, brian jej. effect of mannitol and furosemide on plasma osmolality and brain water. anesthesiology 2002; 96:416-421; 19. xing y,wang bg, mi wd, an jx,guo ql, huang xq.application of remifentanil in neurosurgical aesthesia: a multicenter study. zhonghua yi xue za zhi.2008 apr 29;88(27):1163-1167. microsoft word 13iacobggiant.doc romanian neurosurgery (2010) xvii 2: 225 – 230 225 giant atypical posterior fossa meningioma revealed by rhinorrhea g. iacob1, dana paula georgescu2, mihaela poparda3, m. craciun1, l. nicolae1 1clinic of neurosurgery, university hospital bucharest romania 2clinic of neuroradiology, university hospital bucharest romania 3neuropathology clinic, university hospital bucharest romania abstract objective and importance: cerebral supra or infratentorial tumors associated with chronic intracranial hypertension and hydrocephalus may rarely generate spontaneous, non-traumatic rhinorrhea. we report one case of this rare condition with a giant atypical left posterior fossa meningioma and right nostril rhinorrhea. clinical presentation: a 55-years-old woman was admitted for a 16-year history of headache, 1-year of right nostril rhinorrhea, which was exacerbated when the patient was standing or when she bent forward, ataxia, astasia-abasia. spontaneous rhinorrhea (no previous history of head trauma or meningitis) stopped suddenly a few days before admission, while cephaleea increased and her general condition worsened. native and contrast ct scan disclosed a giant extraaxial tumor: 7/9/8 cm, developed in the left posterior fossa, but also active, internal, supratentorial hydrocephalus. the anterior recess of the third ventricle was dilated; with a small discontinuity of the right spenoid sinus. intervention: the microsurgical resection of the tumor mass was subtotal, as confirmed by postop ct scan, induced by cardiac rhythm fluctuation and tensional oscillations. after the operation the patient became free of csf leakage and a direct approach for rhinorrhea was not needed. conclusion: a case of non-traumatic spontaneous rhinorrhea generated by a giant atypical left posterior fossa, atypical meningioma is described. using microsurgical resection, the tumor was subtotally removed, the patient improved and rhinorrhea didn’t recur. keywords: spontaneous rhinorrhea, posterior fossa meningioma, atypical meningioma cerebrospinal fluid rhinorrhea usually occurs after (1-4): trauma (fracture the anterior skull base, fracture of the petrous temporal bone in the presence of an intact tympanic membranae; in which csf in the middle ear drains to the nose), developmental defects of the ethmoid, sphenoid, frontal, petrous bones with the formation of a meningocele or meningoencephalocele with intact tympanic membrane iatrogenic causes: sequel of skull-base surgery, endoscopic sinus surgery, transsphenoidal pituitary surgery, translabyrinthine acoustic schwannoma and mastoid surgery with intact tympanic membrane, 226 g. iacob et al giant atypical posterior fossa meningioma destructive skull base lesions including neoplasms both benign and malignant empty sella radiation therapy. spontaneous rhinorrhea is seldom found in brain tumor, before treatment, when the dura and skull base bone are eroded by the tumor directly or by progressive chronic obstructive hydrocephalus induced by tumor development (5-7). in this second condition spontaneous rhinorrhea is generated under chronic high pressure by weakness of the arachnoid sheath accompanying the pituitary gland stalk or by lack of bone support under the diaphragma sellae (5). we present such a case, with a huge meningioma of the left posterior fossa. case report on january 2, 2010, a 55-years-old woman was admitted to our hospital with a 16-year history of headache, 1-year of right nostril rhinoliquorrhea that was exacerbated when the patient was standing or when she was bending forward, ataxia, astasia-abasia. one year earlier, based on cerebral ct scan, the patient had been diagnosed with a giant left posterior fossa tumor, secondary hydrocephalus and non-traumatic rhinorrhea in another institution, but refused operation. one week before admission spontaneous right nostril rhinorrhea stopped suddenly, cephaleea increased and her general condition worsened. she denied any history of head trauma or meningitis. her physical examination showed: an obese 115 kg woman, light nuchal stiffness, marked ataxia, dysarthria, decreased visual acuity in both eyes, left facial paralysis and hypoacusia, gr. ii horizontal nystagmus, bilateral babinski sign, no motor deficit. her mental status was alert. no rhinorrhea was remarked at admission, even when the patient leaned forward. ophthalmologic examination was normal: visual acuity, campimetry, fundus oculi. native and contrast ct scan (figure 1) revealed a giant extraaxial tumor: 7/9/8 cm, developed in the left posterior fossa which is entirely occupied, in contact with the left mastoid cells, extended over the median line and cranially over the temporal bone, pulling up the tentorium, with severe mass effect on the brain stem. the tumor had important parietal calcifications, even calcar septs; the tissular component didn’t enhance much with contrast. in the supratentorial compartment, there was an active internal hydrocephalus with transependimar resorbtion signs presented to the temporal horns of the ventricular system. the anterior recess of the third ventricle was dilated; with a small discontinuity of the right spenoid sinus. a median shift of 1 cm to the right at the level of third ventricle was described. on the 4th hospital day the tumor was operated. a combined middle fossaretrolabyrinthine approach, with the patient in the supine position, with head turned 450 towards right side was performed. the tumor surface was nodular, with soft consistence, red-grayish, highly vascular. the left posterior fossa tumor extended from foramen magnum up to the tentorium which was pushed upward. using microsurgical technique the tumor was subtotally resected, less a tumor remnant adherent to the brainstem and tentorium (simpson d resection) because of cardiac rhythm fluctuation and tensional oscillations reasons. romanian neurosurgery (2010) xvii 2: 225 – 230 227 a b c d e f g figure 1 cerebral ct scan: a-e a giant extraaxial tumor: 7/9/8 cm, developed in the left posterior fossa which is entirely occupied, in contact with the left mastoid cells, extended over the median line and cranially over the temporal bone, pulling up the tentorium, with severe mass effect on the brain stem. the tumor is native hyperdense, with important parietal calcifications, even calcar septs; also a large area of implantation on posterior fossa dura; f-g a small discontinuity of the right spenoid sinus was discovered (white arrow) explainig right nostril rhinorrhea, induced by progressive chronic obstructive hydrocephalus liated to tumor development figure 2 postoperatory ct scan: small tumor remnant, adherent to the brainstem and tentorium postoperative evolution was uneventful, without any recurring rhinorrhea, aspect confirmed by postoperative ct scan (figure 2). the patient was discharged on the 7th postoperative day neurologically improved and without any cerebrospinal fluid leakage. the pathology of the tumor was atypical meningioma grade ii (figure 3), diagnosis sustained on (8): increased mitotic activity 4 or more mitoses/10 high-power fields (40x) or 3 or more of the following histologic features: increased cellularity, small cells with a high nuclear/cytoplasmic ratio, prominent nucleoli, uninterrupted patternless or sheet-like growth, foci of necrosis. the tumor has also several calcifications. 228 g. iacob et al giant atypical posterior fossa meningioma a b c d e figure 3 atypical meningioma grade ii: a cellular atypia (he×10), b cellular polimorphism (he×10), c necrosis area (he×10), d necrosis area (vg×10), e atypical mitosis (he ×40) 4 weeks after operation the patient was alert, with litle ataxia. we recommended postoperative radiation therapy for two reasons: tumor patology the already mention criteria have been shown to correlate with 8-fold higher reccurence rates especially mitose and an elevated mib-1 index are often present in perinecrotic regions, necrosis usually occurs as small foci, sometimes surrounded by pseudopalisading (9) and the extent of surgical resection. discussion the term “spontaneous” cerebrospinal fluid leak was used as a clinical entity by miller in 1826 (10), referring to a nontraumatic cerebrospinal fluid fistula. in 1899 thompson (11) described a similar case. in 1947 coleman and trolard cited by (12) identify 14 cases. o’connell in 1953 (13) subdivided this condition in “primary spontaneous” or “idiopathic” csf leak when no cause could be found identifying over 75 cases in 1964 and “secondary spontaneous” fistula when a cause, usually a tumor was discovered or an anatomical defect which made the cribriform plate particularly vulnerable to the variations in the pressure of csf. later paillas – cited by (12) made a classification into congenital spontaneous fistula and medical fistula induced by tuberculous meningitis or pituitary adenoma with sella turcica erosion. ommaya 1968 (14) on certain 82 cases found in literature suggested that it would be more accurate the term “non-traumatic” cerebrospinal fluid fistula which could be subdivided into high pressure and normal pressure categories. rovit 1969 (15) on four cases identified high pressure csf rhinorrhea due to benign circumscribed mass lesions obstructing csf flow at the foramen of monro and obstructive hydrocephalus secondary to a parieto-occipital meningioma. romanian neurosurgery (2010) xvii 2: 225 – 230 229 in 1978 oblu, ianovici (12) identified several causes of non traumatic spontaneous cerebrospinal fluid leak: congenital: anterior skull base congenital defects especially to lamina cribrosa with or without meningoencephaloceles, craniostenosis (crouzon disease, oxycephaly), arnold chiari syndrome, hydrocephalus by congenital sylvius aqueduct stenosis tumoral: by direct mechanism (bone defect generated by compression or infiltration) or indirect mechanism (intracranial hypertension with internal hydrocephalus): pituitary, forth ventricle a.s.o. infectious parasitic diseases: sinus infections with osseous osteitis, tuberculous meningitis, osteomyelitis vascular: ethmoidal vessels thrombosis empty sella syndrome spontaneous csf rhinorrhea are less than 5% (12). cerebral tumors both supra or infratentorial may generate rhinorrhea as: parieto-occipital meningioma (16), tentorial meningioma (5), posterior falx meningioma (17), exophytic choroid plexus papilloma of the fourth ventricle (18), fourth ventricle ependymoma (19), macroprolactinomas (20), colloid cyst (21) a.s.o. a remote tumor as in our case a giant, atypical, left, posterior fossa meningioma could be revealed by rhinorrhea. second most common posterior fossa tumor after acoustic neuroma, posterior fossa meningioma are a very uncommon tumor group as compared to supratentorial meningiomas, representing 9-10% of all intracranial meningiomas (22), with multiple possible topography: cerebellar convexity, cerebello-pontine angle, tentorial, jugular foramen, petroclival, foramen magnum, iv ventricle, unclassified. the vast majority of these tumors present with an insidious onset of symptoms; for large tumors that compress the brain stem structures or the 4th ventricle, as in our case, ataxia, hydrocephalus or multiple cranial nerve palsies are the most common symptoms. frequently these tumors are discovered incidentally after brain imaging for other reasons. in our case the patient had a 16year history of headache, 1-year of right nostril rhinoliquorrhea, without previous head trauma or meningitis. diagnosis was made on clinical and cerebral ct grounds one year before, in another institution, but the patient refused operation. a giant left posterior fossa tumor with important parietal calcifications, secondary hydrocephalus and non-traumatic rhinorrhea was described. only when her general condition worsened, with increasing cephaleea as the spontaneous rhinorrhea stopped suddenly the patient accepted emergency operation. the native and contrast ct scan revealed a giant extraxial tumor: 7/9/8 cm, developed in the left posterior fossa which it occupied entirely, in contact with the left mastoid cells, extended over the median line and cranially over the temporal bone, pulling up the tentorium; with severe mass effect on the brain stem. supratentorial an active internal hydrocephalus with transependimar resorption sign was present to the temporal horns of the ventricular system. the anterior recess of the third ventricle was dilated; with a small discontinuity of the right spenoid sinus, also air-fluid level. a median shift of 1 cm to the right at the level of third ventricle was described. using microsurgical technique the 230 g. iacob et al giant atypical posterior fossa meningioma tumor was subtotally resected because of cardiac rhythm fluctuation and tensional oscillations reasons, less a tumor remnant adherent to the brainstem and tentorium (simpson d resection), without postoperative complications. in our case with a remote tumor we thought that high pressure cerebrospinal leak associated with focal atrophy on the right spenoid sinus may explain the symptoms. tumor removal with or without preoperative shunt may cure rhinoliquorrhea and a direct approach for it was not necessary. conclusion a case of non-traumatic spontaneous right nostril rhinorrhea generated by a giant atypical left posterior fossa, atypical meningioma is described. using microsurgical resection tumor was subtotally removed, the patient improved and rhinorrhea didn’t recur. references 1.robertson h.j.f. – cerebrospinal fluid leak, emedicine oct. 26, 2009 2.snow j.b.jr., ballenger j.j. – complications of skull base surgery, in ballenger’s otorhinolaryngology, 16th ed. hamilton, ontario, decker 2003, 508-36:684-7, 799. 3.pearson b.w. – cerebrospinal fluid rhinorrhea, in otolaryngology, 3rd ed. philadelphia: w.b.saunders co. 1991: 1899-909. 4.sautter n.b., batra p.s., citardi m.j. – endoscopic management of spenoid sinus cerebrospinal fluid leaks, ann otol.rhinol.laryngol ian 2008, 117, (1)32-9 5.guan jing-yu, tong xiao-jie, wei xue-zhong – spontaneous cerebrospinal fluid rhinorrhea in a patient with tentorial meningioma – case report, chinese medical journal 2007, 120(14), 1287-1288 6.benvenuti d., lavano a., corriero g., irace c., de divitiis e. – cerebrospinal rhinorrhea in a patient with a posterior cranial fossa tumor, neurosurgery 1987, 21, 742-744. 7.obana w.g., hodes j.e, weinstein p.r., wilson c.b – cerebrospinal fluid rhinorrhea in patients with untreated pituitary adenoma: report of two cases. surg. neurol. 1990, 33, 336-340 8.burger p.c., scheithauer b.w. – tumors of the central nervous system, afip atlas of tumor pathology, arp press, 2007 9.who classification of tumours of the central nervous system, 4-th edit., international agency for research on cancer, 2007 10.miller c. – case of hydrocephalus chronicus with some unusual symptoms and appearances on dissection, trans-med-chir. soc. edinb. 1826, 2:243-248. 11.thomson st. c. – the cerebrospinal fluid: its spontaneous escape from the nose. cited from cassell: london 1899 12.oblu n., ianovici n. – fistulele lichidiene cranionazale posttraumatice, junimea 1978, 120-125. 13.o’connell j.e.a. – the cerebrospinal fluid pressure as an etiological factor in the development of lesions affecting the central nervous system brain 1953, 76: 279-298. 14.ommaya a.k., dichiro g., baldwin h., pennybacker j.b. – non-traumatic cerebrospinal fluid rhinorrhea. j. neurol.neurosurg.psychiat 1968, 31: 214-225. 15.rovit r.l., schechter m.m., nelson k. – „high pressure cerebrospinal rhinorrhea” due to lesions obstructing flow of cerebrospinal fluid, jns 1969, 30, 4. 16.sang kun park, kyu chang lee, hun jae lee – „high pressure” cerebrospinal fluid rhinorrhea due to parieto-occipital meningioma, a case report, yonsei medical journal, 1977,18, 2, 160-165 17.liang c.l. et al. – non-traumatic cerebrospinal fluid rhinorrhea indirectly caused by remote brain tumor: a case report and review of the literature, clin neurol. neurosurgery 2001, 103(2), 83-86. 18.symss n.p. et al. – exophytic choroid plexus papilloma of the fourth ventricle presenting with cerebrospinal fluid rhinorrhea: a case report, surgical neurology 2009, 71, 705-708. 19.tan s.p. et al. – rupture of the lateral ventricle secondary to a fourth ventricle tumour resulting in an indirect nontraumatic cerebrospinal fluid fistula, neuroradiology 2003, 45 (1), 53-55. 20.de lacy p. et al. – is surgical intervention frequently required for medically managed macroprolactinomas ? a study of spontaneous cerebrospinal fluid rhinorrhea, surg.neurol. 2009, 72(5), 461-463. 21.kane p.j. et al. – cerebrospinal fluid rhinorrhea associated with colloid cyst, br. j. neurosurg. 1981, 5 (3), 317-320. 22.kaye a.h. – posterior fossa meningiomas, in marc sindou – practical handbook of neurosurgery, spinger – verlag, 2009, vol. 2, 181-198 microsoft word 6.turliucdana_managementofmild romanian neurosurgery (2010) xvii 4: 421 – 431 421 management of mild and moderate head injuries in adults dana turliuc, a. cucu universitatea de medicină şi farmacie “gr.t. popa” iasi “shock is a respite on the road with no return to death.” (john collins warren, 1842 renowned american surgeon of the 19th century) abstract introduction: craniocerebral trauma (cct) is a major cause of morbidity and mortality world wide. in romania, the trauma is the forth leading cause of mortality after vascular, neoplastic and digestive diseases and its coincidence continues to increase and this is explained by the development of transport infrastructure and by the increasing number of the motor vehicle and assaults. cct consequences lead most of the time to invalidity, so the patients find it difficult to integrate in society or to return to their jobs, and the economic costs are high. despite the fact that minor and moderate cct appear frequently, their classification and management remain surprisingly controversial and pose problems due to the lack of agreement on definitions, of universal standardized guidelines, of insufficient studies and most importantly the lack of medical logistics and medical legal environment. also, the absence of such guidelines increase the morbidity and mortality in patients with cct due to the lack of information and prompt diagnosis and have high economic costs because of diagnostic tests and unnecessary hospitalization. objectives: demonstrating the need for a protocol on minor and moderate management. material and methods: the study group included 91 patients (m/f 66/25) aged between 8 and 92 years, hospitalized in the clinic of neurosurgery in iasi in the period 2004-2009. the patients were clinically evaluated both at admission (gcs) and at discharge, imaging (ct) and it was followed up the etiology of cct and the present symptoms. keywords: minor cct, medium cct, gos, protocol, management. introduction head injuries (hi) are a major cause of mortality and morbidity in the world. in the united states, trauma is the 3rd cause of death after cerebral and cardiac vascular diseases and cancer (1); it has a worrying incidence of 200-400 cases per 100,000 inhabitants, of which mild head injuries represents a percentage of 80% (2). in romania, trauma is the 4th cause of death after cardiovascular diseases, cancer and digestive system diseases (3). studies conducted in the u.s. have shown that hi is the leading cause of death and disability in children and adults aged 144 years, and the moderate hi and severe hi are associated with an increased risk of alzheimer’s disease at 2.3 respectively 4.5 times higher than in healthy population. also, men are 2 times more likely than 422 d. turliuc, a. cucu management of mild and moderate head injuries in adults women to suffer an hi (4). unfortunately, the hi hospitalization rate increased from 75% in 100,000 inhabitants in 2002 to 87.9% in 2003 (5). development of infrastructure, industry, transport, increasing the number of vehicles, and military actions resulted in increasing the incidence of hi. hi consequences are more severe in women than in men. the hi consequences are more severe in women than in men. the cause of these differences is not exactly known, but several factors have been incriminated to be related to the mechanism of injury, treatment variability and to different premorbid states related to gender (6). purpose and objectives of hi management guidelines unfortunately, despite that mild head injuries are common, their classification and management remain surprisingly controversial being a constant dispute subject for physicians. as factors leading to these controversies, we can mention: the lack of agreement on definitions, the absence of standardized and valid universal guidelines for each country, insufficient studies in certain areas, lack of prospective randomized trials, and so forth (7). much of the variation in hi management strategies between the usa, canada, europe and australia is driven by local issues such as the availability of resources and the medico-legal envirtonment. thus the usa has higher rates of ct scanning for mild head injuries compared to canada, europe (8). clinical guidelines may reduce unnecessary tests and hospital admissions for patients with mild head injury as a helpful tool and not a substitute for medical thinking. they were designed for use by clinicians and neurosurgeons in both hi management, in major trauma services and also in regional and local hospitals. the main objective of these guidelines is to reduce morbidity and mortality of adult patients with hi and avoid unnecessary diagnostic tests and hospital admissions, especially in patients with mild head injuries. (9) definition of mild and moderate head injuries summary of closed head injury classification and outcome (10) mild moderate severe initial gcs 14-15 9-13 3-8 % of total 80 10 10 abnormal ct scan (%) 10-15 40-50 90 neurosurgical intervention 1-3 10-15 40-50 mortality (%) <1 10-15 20-80 good functional outcome (%) >90 50 10-50 a mild head injury is an injury suffered by a patient with a 14-15 glasgow coma score (gcs) who arrives to the hospital after an injury without penetration (with or without a history of consciousness or memory loss). for classification of hi, the glasgow scale is mostly used and evaluation should be made both initially and dinamically. although intubation and sedation interferes with gcs, and in some cases its accuracy is only 75%, this scale still remains an important universal code in medicine (11). doctors have proposed changes to the gcs score with an increased sensitivity to mild head injuries; for example, gcsextended (gcse) or gcs 15, which defines the degree of post-traumatic amnesia (pta) suffered by the patient. it’s normal value should be between 0-7. if the period of amnesia is more than three romanian neurosurgery (2010) xvii 4: 421 – 431 423 months, the score is 0, and if amnesia is present, the score is 7 (12). gcse has three risk categories based on the results of ct and symptoms: low-risk: no symptoms or previous symptoms of dizziness, headache, vomiting intermediate risk: loss of consciousness or post-traumatic amnesia high risk: severe headache, persistent nausea, vomiting ≥ 1 episode. (13) typical characteristics of mild head injuries: 1. direct blow to the head or the mechanism of acceleration / deceleration 2. transient loss of consciousness or amnesia * 3. transient changes of vigilance, behavior or cognitive function 4. rare neurosurgical intervention 5. post concussion symptoms are common 6. good long-term functional outcome * amnesia after a hi is a predictive factor of intracranial complications. retrograde amnesia is a more significant risk factor than anterograde amnesia. (14) risk stratification of hi is based on: 1. gcs on admission and for 2 hours post-injury 2. the duration of consciousness loss or amnesia 3. presence or absence of other specified risk factors most important clinical complications of mild head injuries clinicians and patients should be aware of both the risk of neurosurgical intervention, and the risk of cognitivebehavioural sequelae following mild head injury. they also need to consider that the absence of visible structural lesion on ct following mild head injury does not exclude the possibility significant cognitivebehavioural sequelae. acute life-threatening complications that require neurosurgical intervention are rare in mild head injury patients: low risk, 03% and high risk 0,5-6,5% of mild head injury. (15) post concussion symptoms are common in mild head injury patients and may have significant cognitive-behaviouralsocial impacts on both patients and their families. typical post concussion symptoms include: headaches dizziness fatigue memory impairment poor concentration behavioural changes social dysfunction up to 50% of patients with mild head injury may have significant post concussion symptoms that can persist several weeks. about 10% of patients with mild head injuries will have persistent disabling post concussion symptoms. 424 d. turliuc, a. cucu management of mild and moderate head injuries in adults the assessment of mild head injuries (1) mild head injury patients should have a minimum of hourly observations for 4 hours post injury. these observations include: -gcs -alertness/behavior/cognition -pupillary reactions -vital signs serial neurological observations should be continued on any mild head injury patients who fail to clinically improve at four hours post injury or who are found to have structural lesions requiring hospital admission. assessment for post traumatic amnesia (pta) should be performed on any mild head injury patients who fail to clinically improve at 4 hours post injury or who are found to have structural lesions requiring hospital admission. skull x-rays are not sufficiently sensitive to be used as a routine screening investigation to identify significant intracranial lesions.1 ct scanning is the most appropriate investigation for the exclusion of neurosurgically significant lesions in mild head injured patients. ct scanning is indicated for those mild head injury patients identified by structured clinical assessment as being at increased risk of intracranial injury. if structured clinical assessment indicates the risk of intracranial injury is low, the routine use of ct scanning is neither clinically beneficial nor cost effective. the need for ct scanning in mild head injuries (16) initial assessment: persistent gcs < 15 at two hours post injury focal neurological deficit clinical suspicion of skull fracture * prolonged loss of consciousness >5 min prolonged anterograde or retrograde amnesia >30 min post traumatic seizure repeated vomiting ≥ 2 occasions persistent severe headache known coagulopathy (coagulability disorders, spontaneous hemorrhage, anticoagulation with warfarin or other anticoagulants)** age >65 years (clinical judgment appropriate if no other risk factors present)   romanian neurosurgery (2010) xvii 4: 421 – 431 425 after a period of observation (4 hours post injury): any deterioration in gcs persistent abnormal mental status (abnormal alertness, behaviour or cognition) any patient who fails to clinically improve clinical judgment required if: age >65 years drug or alcohol ingestion dangerous mechanism/multi-system trauma dangerous mechanism of injury production (pedestrian accident, bicycle accident, ejection from vehicle, violent physical attack, traumatic fall of 1 m or more than 5 stairs, etc.) *** *the risk of developing an intracranial hematoma is 12 times higher in patients with skull fracture radiographically evident than in those without. (16) **although patients with coagulopathy are at increased risk of intracranial complications, recent studies have failed to recognize the importance of this link (2) ***the chalice study 2006 (children’s head injury algorithm) considers that a fall of more than 3 meters high is associated with more increased risk for the patient to develope an intracranial lesion. safe discharge of the patients (1) patients with hi can be discharged after a period of observation in the hospital, if they meet the clinical and social criteria: clinical criteria: normal mental status and behaviour with clinically improving minor post concussion symptoms after observation until at least 4 hours post injury no clinical risk factors indicating the need for ct scanning or normal ct scan if performed due to risk factors being present no clinical indicators for prolonged hospital observation such as: -clinical deterioration -persistent abnormal gcs or focal neurological deficit -persistent abnormal mental status or behaviour -persistent severe post concussion symptoms -persistent drug or alchohol intoxication -presence of known coagulopathy (relative criteria) -presence of multi-system injuries (relative criteria) -presence of intercurrent medical problems (relative criteria) -age> 65 years (relative criteria) social criteria: responsible person avaible to take patient home responsible person avaible for home observation patient able to return easily in case of deterioration written and verbal discharge advice able to be understood 426 d. turliuc, a. cucu management of mild and moderate head injuries in adults discharge advice criteria: discharge summary for primary doctor written and verbal head injury advice given to patient: -symptoms and signs of acute deterioration -reasons for seeking urgent medical attention -typical post concussion symptoms initial management of moderate head injuries (gcs 9-13) (1) standard care: initial assessment of abcdes and resuscitation early ct scanning to identify neurosurgically correctable focal intracranial haematomas period of ed observation prevention of secondary brain injury by avoiding hypoxaemia (o2 saturation < 90%) and hypotension (systolic bp <90) supportive care of abcde’s admit for prolonged hospital observation (24-48 hours) unless rapid clinical improvement, normal ct scan and absence of other risk factors early neurosurgical consult if not clinically improving and/or abdnormal ct scan routine post traumatic amnesia (pta) testing outcome: approximately 80% of moderate head injuries improve while 20% deteriorate and required management as per severe head injuries the majority of patients who suffer moderate head injuries will have some degree of cognitive-behavioural sequelae and should be considered for routine follow-up with a brain injury rehabilitation service or a neurologist hi patient transfer to a neurosurgery service patients with severe head injuries (gcs 3-8) patients with moderate head injuries (gcs 9-13), if: clinical deterioration abnormal ct scan normal ct scan but not clinically improving ct scan unavailable patients with mild head injuries (gcs 14-15), if: clinical deterioration abnormal ct scan normal ct scan but not clinically improving high risk mild head injury with ct scan unavailable   romanian neurosurgery (2010) xvii 4: 421 – 431 427 the transfer of patients with brain injuries is potentially dangerous if it is poorly done and, therefore (2), any hi must be correctly diagnosed so that, between the onset and neurosurgical intervention, no more than four hours should pass. (3) the purpose of this study was to demonstrate the necessity of a protocol in the management of minor and medium cct. methods and materials the study was based on a retrospective study on a group of 91 patients hospitalized in the clinic of neurosurgery in iasi in the period january 2005 – december 2009. the patients selected were aged between 8 and 92 years (the average age is 52) and the male-female ratio was 66:25 cases. the patients were clinically evaluated both at admission (gcs) and at discharge, imaging (ct), and it was followed up the etiology of cct, the present symptoms (headache, intracranial hypertension, impaired consciousness, and focal neurological deficit) and the duration of hospitalization. the patients who presented other organs’ involvement and systems, as well as patients who had preexisting medical conditions were excluded. results and discussions all the 91 patients were evaluated on admission by gcs: 35% were minor cct (gcs scale 14 and 15) and 65% were moderate cct (gcs scale 9-13). the predominance of moderate cct was convenient to us in our analysis to see if they have not been overrated by the neurosurgeons (figure 1). a percentage of 73% patients of our group were man (66 cases) and only 25% women. also, the literature confirms that the incidence of cct in men is twice higher than in women. if we take a look at every 10-year age group, we can observe a uniform distribution of the cases, except for those over 89 and under 9 years, which represents 3% of cct. 19% of the patients with cct belong to the 6th decade, followed by the low percentage of the 7th decade (17%), 5th (15%) and 2nd (14%). it seems that the highest incidence is met at patients aged between 50 and 80 and this represents half of the total number of tcc. the 14% percentage of cct for patients aged 20-29 could be explained by more intensive activities in this period. 428 d. turliuc, a. cucu management of mild and moderate head injuries in adults from the distribution of the etiology of cct, 41.7% of the patients were hospitalized for falling on same level, followed by those with car accidents and high level falling (approximately 21.9% and 19.7%). only 15 patients of a total of 91 came to the hospital as a consequence to physical aggression. in current practice, high level falling is usually associated with moderate or severe cct, while falling on same level is not associated with moderate or severe cct. this mantrap in which the patient’s age, the symptoms at admission / in dynamic or ct changes are not taken into account, but only the mechanism of cct, makes moderate cct to be overrated or even worse, minor overrated cct could lead to risks and adverse consequences for the patient. the prevalence of cct caused by falling on same level (41.7% of cct) was convenient in our analysis since this segment of etiologies of cct causes the most confusion. 56% of the patients had md at admission and 19% presented headache. only 9 patients (10%) displayed signs of ich. after ct scan, it has been discovered at about a quarter of all patients (24.18%) the presence of a subdural hematoma combined with other injuries, at 13.19% there signs of cerebral concussion and in an equal percentage of 11% there were patients with subdural hematoma, with concussion and cerebral laceration respectively. depending on their age, minor and medium cct have a similar distribution, except for some peaks of moderate cct in the 2nd and 5th decade. distribution of cases according to ct aspect romanian neurosurgery (2010) xvii 4: 421 – 431 429 after the correlation between the patient’s age and the results of the ct scan, the differences are statistically significant (p<0.01). that means that the patients of the same age, same type of injury have different ct scan results. after correlating the etiology with the symptoms, i have found significant statistical differences (p<0.05). this reveals that the etiology of cct has different symptoms. regardless the etiology of trauma, md has been prevailingly the main symptom, followed by headache and hemiparesis. after the correlation between the symptoms and the gcs evaluation, the differences are statistically significant (p<0, 01). the “error” is given by the fact that the gcs evaluation does not take into account the motor or speech deficits which could also influence the final result. there have not been significant statistical differences after the correlations made between the symptoms and the gos. at discharge, the majority of patients with md had gos 1, 2 or 3. at discharge, it has been discovered that most patients were evaluated with gos 2 (44%), followed by patients with gos 3 (29%) and gos 1 (23%). two patients with moderate cct died (gos 5). at discharge it has been discovered that most of the patients with minor cct (78%) had gos 1 and gos 2 (12, respectively 13 patients). in the case of moderate cct, only 15% (9 patients) of the patients recovered completely (gos 1), most of them with gos 2 (46%) and gos 3 (36%). most patients have gos 1, 2 and 3 respectively. 430 d. turliuc, a. cucu management of mild and moderate head injuries in adults regarding the average length of hospitalization, i have discovered that the medium is 14-15 days for minor cct and 15-42 days for medium cct. the average length of hospitalization extremely close as value raises issues, confirming once again the consequences of the lack of management guidelines: morbidity and mortality of patients with cct due to the lack of prompt recognition and diagnosis, of diagnostic tests and unnecessary hospitalizations and therefore, high economic costs. conclusions based on the results, i have discovered that minor cct evolution is influenced by the precocity of diagnosis, the elimination of unnecessary time for diagnosis and the establishment of proper treatment and this conduct can be set by introducing some protocols which can be adapted to real possibilities of each region. references 1. kaye andrew, essential neurosurgery, blacwell publishing, 2005:p.40 2. servadei f et al 2001, defining acute mild head injury in adults: a proposal based on prognostic factors, diagnosis and management, journal of neurotrauma, 18(7):p.657-664 3. zanoschi g 2003, sanatate publica si management sanitar, edit dan, 2003, p.112 4. langlois j, the epidemiology and impact of traumatic brain injury: a brief overview; journal of head trauma rehabilitation,2006, 21(5):p. 375-378 5. mmwr morb mortal wkly rep. 2007, 56:p.167-170. 6. arace e et al 2000, do women fare worse? a metaanalysis of gender differences in outcome after traumatic brain injury, neurosurg focus, 8 (1):p.1-9 romanian neurosurgery (2010) xvii 4: 421 – 431 431 7. narayan rk et al 2002, clinical trials in head injury, journal of neurotrauma, 19 (5):p.503-557 8. stiell ig et al 2002, variation in ed use of computed tomography for patients with minor head injury, annals of emergency medicine, 30(1): p.14-22 9. mower wr et al 2002, developing a clinical decision instrument to rule out intracranial injuries in patients with minor head trauma, annals of emergency medicine, 40(5):p.505-514 10. duncan r, 2007, adult trauma clinical practice guidelines-initial management of closed head injury in adult,ed.nsw institute of trauma and injury management:p.16 11. fearnside m et al, 1998, moderate head injury: a system of neurotrauma care, australia and new zeeland journal of surgery, 68 (1):p.58-64 12. batchelor j, 2002, a meta-analysis of gcs 15 headinjured patients with loss of consciousness or posttraumatic amnesia, journal of emergency medicine, 19:p.515-519 13. esther b, 2007, mild traumatic brain injury: an update for advanced practice nurses, journal of neuroscience nursing, 39(1):p.43-51. 14. yates d et al, 2007, head injury-triage, assessment, investigation and early management of head injury in infants, children and adults, national collaborating centre for acute care 2007:p.83 15. ibanez ja et al, 2004, reliability of clinical guidelines in the detection of patients at risk following mild head injury: results of a prospective study, journal of neurosurgery, 100 (5):p.825-834 16. hofman pa et al, 2000, value of radiological diagnosis of skull fracture in the management of mild head injury: meta-analysis, journal of neurology, neurosurgery & psychiatry, 68 (4):p. 416-422 17. saab m et al, 1996, warfarin and the apparent minor head injury, journal of accident and emergency medicine 13(3):p.208-209 18. andrews pjd et al, 1990,secondary insults during intrahospital transport of head-injured patients. lancet: p.327-330 19. farling pa et al, 2006, recommendations for the safe transfer of patients with brain injury, association of anaesthetists of great britain and ireland:p.4 a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 424-430 doi: 10.33962/roneuro-2019-067 www.journals.lapub.co.uk/index.php/roneurosurgery the supraorbital keyhole approach for clipping of anterior circulation ruptured aneurysms mostafa m. nabeeh ashraf a. ezz-el din neurosurgery department, mansoura university, egypt abstract introduction. the supraorbital approach has been demonstrated to be useful, particularly in minimization of brain retraction and exposure to air, decreases blood loss, surgical trauma, operative time and infection rates. while its shortcomings include difficult control of frontal air sinus, narrower surgical view and limited exposure of sylvian fissure. patients and methods. we retrospectively reviewed the files of patients who underwent clipping of anterior circulation aneurysms through the supraorbital keyhole approach at neurosurgery department, mansoura university between jan 2014 and may 2016. results. twenty-five consecutive patients harbouring aneurysm at anterior circulation underwent clipping through the supraorbital keyhole approach, sixteen acom artery aneurysms and nine cases of ica aneurysms table 1 show the location of aneurysms. eleven patients were males, and 14 were females. the ages ranged from 44 to 69 with a mean age of 61.9 years. all patients were presented with subarachnoid haemorrhage due to rupture of aneurysms in anterior circulation the hunt and hess grade was (1.50 ± 0.65) and fisher grade was (1.67 ± 0.45). the average operative time was 3.32 ± 1.14 hours. follow-up ranged from 1 to 16 months with a mean of 7 months conclusion. surgical clipping of some selected aneurysms of anterior circulation can be operated through minimally invasive supraorbital approach which minimize the dissection and retraction of the brain, reduce operative time and blood loss with small incision and good cosmetic results. introduction conventional approaches to anterior skull base lesions including anterior circulation aneurysms highly developed since the large skin incision and fronto-temporal craniotomy described by dandy to the less invasive pterional approach suggested by yasargil [25] till the minimally invasive eye brow incision with supraorbital keyhole craniotomy [15, 20, 21, 24]. the pterional approach is popular and widely accepted among neurosurgeon; it provides wide central exposure, direct access to whole length of sylvian fissure, adequate visualization of anterior and keywords supraorbital approach, ruptured aneurysm, keyhole concept corresponding author: mostafa m nabeeh lecturer of neurosurgery and deputy director of emergency hospital mansoura university, egypt sasamah2001@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 425 the supraorbital keyhole approach for clipping of anterior circulation ruptured aneurysms posterior circulation. however, pterional approach has disadvantages like longer operative time, blood loss, brain exposure, damage to frontal branch of facial nerve with subsequent facial asymmetry, temporalis wasting and interference with mandibular function [2, 9, 10, 11]. the supraorbital approach was early described and applied to a pituitary tumor by frazier in 1913[12], then it has been described for multiple types of intracranial pathologies including tumors excision, infection drainage, fractures and aneurysms clipping [4, 6, 20, 21]. jane et al, described the supraorbital approach for clipping of anterior circulation aneurysms for the first time in 1982[15]. the approach was refined and popularized by axel perneczky, the pioneer in the development of keyhole concept [24,21]. the supraorbital approach has been demonstrated to be useful, particularly in minimization of brain retraction and exposure to air, decreases blood loss, surgical trauma, operative time and infection rates. while its shortcomings include difficult control of frontal air sinus, narrower surgical view and limited exposure of sylvian fissure [14, 16, 19, 22]. complications related to the supraorbital approach may include cosmetic problems like visible scar or bone defects, damage to supraorbital nerve with frontal hypoesthesia, lost eyebrow elevation and csf rhinorrhea [3, 5, 6]. materials and methods in this report, we represent our experience in clipping of anterior circulation ruptured aneurysms through the supraorbital keyhole approach. we retrospectively reviewed the files of patients who underwent clipping of anterior circulation aneurysms through the supraorbital keyhole approach at neurosurgery department, mansoura university between jan 2014 and may 2016. only patients presented by subarachnoid hemorrhage due to ruptured aneurysm of anterior circulation and their aneurysms have clipped through supra orbital approach were included in this study. demographic data, hunt and hess grades, fisher grade, consciousness, aneurysm location, size, craniotomy size, operative time, blood loss, operative details, early post-operative follow up ct and cta before discharge, clinical and surgical complications and data from follow up visits were reviewed. operative technique a lumbar drain was used in all cases . the patients were placed in a supine position with the head fixed in a mayfield head holder, the neck extended and turned about 20º to the contralateral side .the skin incision placed in forehead crease extended from lateral edge of the supraorbital notch to the superior temporal line .then fascia and frontalis muscle were incised in the line of the skin incision and retracted up .a free 3×2 cm bone flap using a fine craniotome as basal as we can. in case the sinus was opened we extended the incision laterally to expose temporalis fascia which used with a pericranial graft to control frontal air sinus after cauterization and stripping of mucosa and adequate disinfection, and packing with gelfoam soaked with bovodin. after adequate exposure, the dura was opened in transverse fashion, the lumbar drain opened, the frontal lobe falls backward aided by the effect of gravity and with minimal retraction the circle of willis was identified, proximal control then clipping of the aneurysm. the incision above the eyebrow was sewn with a subcutaneous dissolving stitch. figure (1 a-d) figure 1. operative technique a) patient's head fixed to mayfiled fixator marking of skin incision and bone flap; b) minicraniotomy; c) closure of dura; d) closure of skin incision. results twenty-five consecutive patients harboring 426 mostafa m. nabeeh, ashraf a. ezz-el din aneurysm at anterior circulation underwent clipping through the supraorbital keyhole approach, sixteen a-com artery aneurysms and nine cases of ica aneurysms table 1 show the location of aneurysms. eleven patients were males, and 14 were females. the ages ranged from 44 to 69 with a mean age of 61.9 years. all patients were presented with subarachnoid hemorrhage due to rupture of aneurysms in anterior circulation the hunt and hess grade was (1.50 ± 0.65) and fisher grade was (1.67 ± 0.45). the average operative time was 3.32 ± 1.14 hours. follow-up ranged from 1 to 16 months with a mean of 7 months table 1. location of treated aneurysms location number anterior communicating 16 anterior cerebral 4 posterior communicating 3 ophthalmic 1 bifurcation 1 visualization and orientation of aneurysm neck was feasible through mini craniotomy in 24 cases (96%) in whom successful aneurysm clipping was possible. (figure 2, 3 and 4) in one patient, early aneurysm rupture obscures the field and procedure aborted after bleeding control then the patient was reoperated later through inter-hemispheric approach. table 2 summarizes the operative findings. figure 2. case of posterior communicating segment aneurysm aaneurysm identification btemporary clip application c application of permanent clip dremoval of temporary clip and dissection of dome. figure 3. case of anterior communicating artery aneurysm a opening of dura and sah and brain selling is identified b temporary clip application c&dapplication of permanent clip. figure 4. case of large anterior communicating artery aneurysm: a) opening of dura and sah and brain selling is identified; b) identification of aneurysm with wide neck; c) right angle fenestrated clip for reconstruction of anterior communicating artery; d) application of the first permanent clip; e) application of another fenestrated clip to reconstruct a.com artery. intra operative rupture occurred in two cases (8%); one carotid bifurcation aneurysm controlled by a temporary clip over proximal internal carotid artery. another one ugly large multi lobulated a.com aneurysm ruptured very early during frontal retraction. the dominant left anterior cerebral 427 the supraorbital keyhole approach for clipping of anterior circulation ruptured aneurysms couldn’t be controlled from the right supraorbital approach. this patient was planned for clipping through this approach according ct angiogram only while dsa revealed the complicated configuration of aneurysm. patient planned later for interhemispheric approach the aneurysm was clipped after the a1 segment of left anterior cerebral artery was proximally controlled before dissection of the aneurysm neck. table 2. operative findings total number 25 number clipped 24 mean operation time 190 minutes estimated blood loss 50-300 (100ml) size of aneurysm 7+3 mm size of craniotomy 3+1.7 × 2+1.2 mm lumbar drain 25 gyrus rectus subpial resection 4 post-operative hospitalization stay 2-18 (7) days table 3. post-operative ct and cta findings cta residual neck radiological vasospasm 0 6/25(24%) ct brain hemorrhage br contusion oedema infarction 1/25(4%) 2/25(8%) 3/25(12%) 3/25(12%) frontal air sinus was breached in 2 cases (8%) securing of sinus was done in both cases, one of those two cases was 60 years old patient developed csf rhinorrhea which needed reoperation the basal dura was successfully repaired with fascia lata graft. ct brain and cta routinely have done for all patients, table 3 summarize the of post-operative radiological findings. 9 patients (36%) suffered transient periorbital ecchymosis and oedema that resolved few days later. three patients (12%) showed post-operative transient deficit which improved later. two patients died in this study one patient died due to symptomatic vasospasm and another patient died before discharge from hospital after postoperative pneumonia. 23 patients were clinically followed-up for duration ranged from 3 to 30 months, 82.3% (19/23) of patients attained a favorable outcome (glasgow outcome scale iv or v), no re-bleeding was noted. as regard cosmetic outcome, the survived 23 patients were questioned for their subjective satisfaction about the esthetic outcome of their surgical incision on 3 months follow up visit. figure 5. nineteen patients (82.6%) were happy and satisfied about cosmetic outcome, while 4 patients were not satisfied; one female patient complained frontal hypothesia with denervation pain and itching lead to hyperpigmentation of forehead and alopecia behind hair line, figure 6. another patient complained depression of forehead with loss of forehead elevation and 2 patients were worry about hyper pigmented scar. figure 5. early and late cosmetic outcome figure 6. hyperpigmentation (blue arrow) and alopecia (white arrow) after injury of supraorbital nerve and denervation pain and itching. discussion the endovascular coiling for management of ruptured intracranial aneurysms are less invasive than surgical clipping and this made a challenge for surgical approaches to be less traumatizing, 428 mostafa m. nabeeh, ashraf a. ezz-el din otherwise, it won't be accepted by many patients as alternative option [1, 8, 13, 18]. surgical clipping of aneurysm provides visualization of vasculature and perforators, permanent secure of aneurysm, cleaning blood from subarachnoid spaces which decreases incidence of vasospasm and hydrocephalus, however, the international subarachnoid aneurysm trial (isat) study comparing both modalities showed marginal superiority for endovascular techniques for management of ruptured aneurysm [18]. one explanation for these results is the application of standard approaches so the approach related morbidity down the outcome of surgical cases [18]. supraorbital approach uses a smaller bone flap than others standard microsurgical approaches and minimize brain exposure, retraction, and traumatization, and possibly improve cosmetic results due to small incision, avoiding the injury of the frontal branches of facial nerve or the temporalis muscle and not interfere with mandibular function [7, 12, 17]. in this study we reported feasibility of clipping of ruptured anterior circulation aneurysms using the keyhole supraorbital craniotomy which proved by good results. our results of clipping 96% of aneurysms and 82.3% of patients attained favorable outcome support others conclusions [3, 5, 7, 16] that the supraorbital approach can be performed reliably and safely to clip ruptured anterior circulation aneurysms. however the fact that we spare the approach for certain selected aneurysms doesn't support its use for all anterior circulation aneurysms. the minimally invasive nature of this approache with less trauma, operative time and blood loss is suitable for relatively small aneurysms with simple configuration, and should be on the armamentarium of vascular neurosurgeon to be provided as option for some patients. narrower surgical view and limited exposure, unfamiliar view of anatomy especially of sylvian fissure which appeared laterally in the operative field. this make this approach not universe for all cases and not standard approach like pterional, but should be served for cases when the size and extent of exposure is enough for safe proximal control of parent vessel, appropriate dissection of the aneurysm neck and secure clip application [14, 16] we faced intraoperative early rupture of aneurysm in 2 cases (8%) in one patient we couldn’t clip the aneurysm a situation realized later and after doing dsa to be related to planning and selection of the aneurysm. madhugiri et al [17] in a systematic review of intraoperative rupture rates in suprabrow and pterional approaches, they analyzed a total number of 3039 ruptured aneurysms, 2848 aneurysms in the pterional group and 191 in the suprabrow group and they found the rate of intraoperative rupture is higher in suprabrow patients than pterional group 19.37% and 13.8% respectively. chalhouni et al [5] reported higher rate of intraoperative aneurysm rupture in the supraorbital group compared to pterional (10.6% vs 2.5%) they explained it as the lesser degrees of proximal control and the narrow available space for dissection and maneuverability of instruments, and advocated the supraorbital keyhole approach to be performed by neurosurgeons who have gained sufficient experience with the technique. exposure of frontal air sinus in 2 cases with persistent post-operative csf rhinorrhea in spite that we have planed the craniotomy on preoperative ct bone window for assessment of the penumatization of the frontal air sinus. we didn’t consider the supraorbital approach if there is large sinus that extends beyond the expected line of supraorbital nerve. the incidence of csf rhinorrhea after supra orbital approach in the literature is ranged between 0% and 9.1%. thaher etal.studied 350 patients of supraorbital keyhole craniotomy and reported 25.1% radiographic breaching of the frontal sinus and 2.3% developed csf rhinorrhea postoperatively [23]. in their report of 139 patients van lindert et al performed a supraorbital craniotomy for aneurysm clipping, craniotomy size was 2-3.5 cm in width and 1.5-2 cm in height. they reported no frontal sinus exposure and emphasized the importance of measurement of the frontal sinus on pre-operative images [24]. kim et al made wider craniotomy (4.5cm) and report one sinus exposure in their 10 approaches [16]. the two cases of mortality were of high hunt– hess and fisher grads, and we think their checkered post-operative course was related to their clinical condition and icu stay rather than to be related to the approach used for clipping. we routinely used lumbar drain inserted before 429 the supraorbital keyhole approach for clipping of anterior circulation ruptured aneurysms positioning of patient which opened after opening of dura for csf drainage which facilitate relaxation of the frontal lobe, we think it is of extremely important step because all of our patients presented by aneurysm rupture and brain swelling is expected and blood in subarachnoid spaces made opening of cisterns and drainage of csf of limited value however some report operating on ruptured aneurysm as early as 2 days through keyhole approach and found slow csf drainage from cistern is feasible [20]. others drain cerebrospinal fluid by intraoperative ventriculostomy at paine's point [6, 14, 16]. the small sample size, retrospective design of this study and selection of certain aneurysm size type and location are limitations of this report but we reported our experience of clipping the ruptured anterior circulation aneurys through this approach. despite few comparative studies comparing the approach to conventional ones still we need large size randomized blind trial to compare minimally invasive approaches to conventional open approach and to endovascular technique. conclusions surgical clipping of some selected aneurysms of anterior circulation can be operated through minimally invasive supraorbital approach which minimize the dissection and retraction of the brain, reduce operative time and blood loss with small incision and good cosmetic results. authors contributions this work was carried out in collaboration between the two authors. authors, designed the study, author, mostafa m. nabeeh wrote the protocol, managed the literature research, author ashraf ezz eldin revised the final manuscript. all surgical procedures were carried out by the same surgical team including the two authors. all authors read and approved the final manuscript. abbreviations ct: computerized tomography. cta: computerized tomography angiogram. dsa: digital subtraction angiogram. csf: cerebrospinal fluid. a. com: anterior communicating artery p. com: posterior communicating artery references 1. ausman ji: isat study: is coiling better then clipping? surg neurol 2003, 59:162-165. 2. aydin ih, takci e, kadioglu hh, et al.: pitfalls in the pterional approach to the parasellar area (review). minim invasive neurosurg 1995, 38:146–52. 3. beseoglu k, lodes s, stummerw, steiger hj, hanggi d. the transorbital keyhole approach: early and long-term outcome analysis of approach-related morbidity and cosmetic results. technical note. j neurosurg. 2011, 114(3):852-856. 4. bhatoe hs: transciliary supraorbital keyhole approach in the management of aneurysms of anterior circulation: operative nuances. neurol india 2009 sep-oct, 57(5):599606. 5. chalouhi n, jabbour p, ibrahim i, starke rm, younes p, el hage g, samaha e. surgical treatment of ruptured anterior circulation aneurysms: comparison of pterional and supraorbital keyhole approaches. neurosurgery. 2013 mar,72(3):437-41 6. chen h.-c. and tzaan w.-c: microsurgical supraorbital keyhole approach to the anterior cranial base. journal of clinical neuroscience 2010, 17 1510–1514 7. czirjak s, szeifert gt: surgical experience with frontolateral keyhole craniotomy through a superciliary skin incision. neurosurgery. 2001, 48(1):145-149; discussion 149-150. 8. diringer mn: to clip or to coil acutely ruptured intracranial aneurysms: update on the debate. curr opin crit care 11:121-125, 2005. 9. figueiredo eg, deshmukh p, nakaji p, et al.: the minipterional craniotomy: technical description and anatomic assessment. neurosurgery 2007, 61:256–64 10. figueiredo eg, deshmukh p, zabramski jm, et al.: the pterional-transsylvian approach: an analytical study. neurosurgery 2008, 62:1361–7. 11. figueiredo eg, welling lc, preul mc, sakaya gr, neville i, et al.: surgical experience of minipterional craniotomy with 102 ruptured and unruptured anterior circulation aneurysms. journal of clinical neuroscience 2016, (27) 34– 39 12. fischer g, stadie a, reisch r, et al.: the keyhole concept in aneurysm surgery: results of the past 20 years. neurosurgery. 2011, 68(1 suppl operative):4551;discussion 51. 13. flett lm, chandler cs, giddings d, gholkar a: aneurysmal subarachnoid hemorrhage: management strategies and clinical outcomes in a regional neuroscience center. ajnr am j neuroradiol 2005, 26:367-372, 14. jallo gi, bognár l: eyebrow surgery: the supraciliary craniotomy: technical note. neurosurgery 2006, 59 (1 suppl):157-158. 15. jane ja, park ts, pobereskin lh, winn hr, butler ab: the supraorbital approach: technical note. neurosurgery. 1982, 11(4):537-542. 16. kim y, yoo c j, park cw, kim mj, choi dh, kim yj, park k: modified supraorbital keyhole approach to anterior 430 mostafa m. nabeeh, ashraf a. ezz-el din circulation aneurysms. j cerebrovasc endovasc neurosurg. 2016, 18(1)5-11 17. madhugiri vs1, ambekar s, pandey p, guthikonda b, bollam p, brown b, ahmed o, sonig a, sharma m, nanda a: the pterional and suprabrow approaches for aneurysm surgery: a systematic review of intraoperative rupture rates in 9488 aneurysms. world neurosurg. 2013 dec, 80(6):8067. 18. molyneux a, kerr r, stratton i, sanderock p, clarke m, shrimpton j, holman r; isat collaborative group: international subarachnoid aneurysm trial (isat) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized trial. lancet 2002, 360:1267-1274. 19. ormond dr, hadjipanayis cg. the supraorbital keyhole craniotomy through an eyebrow incision: its origins and evolution. minim invasive surg 2013, 296469. 20. paladino j, pirker n, stimac d, et al.: eyebrow keyhole approach in vascular neurosurgery. minim invasive neurosurg 1998,41:200–3. 21. reisch r, perneczky a, filippi r: surgical technique of the supraorbital key-hole craniotomy. surg neurol. 2003, 59(3):223-227. 22. schick u, hassler w: the supraorbital approach—a minimally invasive approach to the superior orbit. acta neurochir (wien) 2009, 151:605-611. 23. thaher f, hopf n, hickmann ak, kurucz p, bittl m, henkes h, feigl g: supraorbital keyhole approach to the skull base: evaluation of complications related to csf fistulas and opened frontal sinus. j neurol surg a cent eur neurosurg. 2015 nov, 76(6):433-7 24. van lindert e, perneczky a, fries g, pierangeli e: the supraorbital keyhole approach to supratentorial aneurysms: concept and technique. surg neurol 1998 may, 49(5):481-9. 25. yasargil mg, fox jl: the microsurgical approach to intracranial aneurysms. surg neurol 1975 jan, 3(1):7-14. microsoft word 22.vaporiulia_supratentorial_f.docx romanian neurosurgery (2011) xviii 4: 555 563 555 supratentorial neuroectodermal tumor in a 4 years old child presented with intratumoral hemorrhage – case presentation and review of the literature iulia vapor1, a. taşcu, m.r. gorgan 1phd student in neurosurgery, “carol davila” umph bucharest faculty of medicine, departament of neurosurgery “bagdasar-arseni” clinical emergency hospital, bucharest, romania abstract brain tumors represent the most frequent solid malignancy in children and the first cause of cancer-related deaths in pediatric population. supratentorial neuroectodermal tumor (pnet) represents one of the most aggressive brain tumors at this age. incidence of s-pnet is 2-3% of all brain tumors in children, but reaches up to 20% of brain tumors in 0 3 years old children. although in the last years the outcome has improved, the prognosis remains dismal. we choose to present the case of a 4 years old child who was at presentation in a comatose state (gcs 4 points) with anisocoria (right pupil was mydriatic). the performed head ct-scan showed a right fronto-parietal tumor with intratumoral hemorrhage, maximal dimensions of 52/75/70 mm and a midline shift of 15 mm. the surgery was performed in emergency and we made a gross total resection. immediate postoperative ctscan confirmed the total resection. the histopathological diagnosis was s-pnet, this result being confirmed by immunochemistry. after neuromotor rehabilitation, at the 4 month follow-up visit the gos was md. the patient was also referred to the oncologist and was made chemotherapy and radiotherapy of the entire craniospinal axis. the tumor showed no signs of recurrence during 12 months of follow-up. keywords: s-pnet, child, prognostic introduction supratentorial pnet is one of the most aggressive brain tumors in the pediatric population. it represents 2-3% of all brain tumors in children, this percent rising up to 20% in the 0 3 years old population. due to the small incidence, the relative recent description of this entity (s-pnet was firstly described in 1973, while the first description of medulloblastomas dates from 1925) and the fact that in the who classification those tumors were discordant, there are few data in the literature concerning this subject when comparing with medulloblastomas. the highest incidence of s-pnet is at young age. signs and symptoms at presentation are seizures, signs of intracranial hypertension, focal neurologic deficits. although in the last years the management of these cases has improved, the outcome is very poor. 556 iulia vapor et al supratentorial neuroectodermal tumor case presentation history and presentation: a four years child was admitted in the clinic in coma, gcs 4 points, with anisocoria (right pupil was mydriatic). the patient had headaches, debuted 5 months before, and nausea vomiting for 3 days before admission in the hospital, those being diagnosed as gastrointestinal disorders. in the day of admission the child went to bed and did not wake up. before these 5 months, she had no history of medical problems. clinical and neurological examination: the patient was in coma, gcs 4 points, with anisocoria (right pupil was mydriatic), babinsky positive on the right side, hemodynamically stable, intubated orotracheal and mechanically ventilated (cpap). neuroimaging investigations: a brain ct-scan was performed, which revealed a fronto-parietal mass, heterogeneous, with areas of hemorrhage, without contrast enhancement and minimal surrounding edema, maximal dimensions of 52/75/70 mm and a midline shift of 15 mm (figure 1, 2). due to the neurological and clinical state we did not performed a preoperative brain mri. figure 1 preoperative native ct-scan romanian neurosurgery (2011) xviii 4: 555 563 557 figure 2 preoperative ct-scan with contrast enhancement operation: we operated the child in emergency. a fronto-parietal bone flap was made, dura mater, in tension, was incised semicircular with medial pedicle. we found a fronto-parietal tumor heterogenous, friable, with intratumoral hemorrhage, with a diameter of approximately 7 cm. we made gross total excision. at the end of the operation the brain was collapsed, pulsatile. dura mater was sutured in “water-tight” fashion, and the bone flap was fixated. the surgical intervention lasts 3 hours and 45 minutes and the blood loss was 300 ml. postoperative course: postoperative the child was transferred in the icu, intubated oro-tracheal and mechanically ventilated. postoperative brain ct-scan confirmed the gross-total resection, and showed no signs of postoperative hemorrhage (figure 3). the spinal mri showed no signs of dissemination. after 3 weeks she was transferred in a neuromotor rehabilitation centre (gos= sd). the histopatological diagnosis was pnet, which was confirmed by the immunohistochemical tests. the patient was referred to the oncologist. the oncologic treatment was chemotherapy and radiotherapy of the entire craniospinal axis. follow-up: at the one month follow-up visit the child’s neurological state had improved and brain mri showed no signs of tumor recurrence (figure 4). at the 4 months postoperative visit,gos was md – the child was conscious, with left hemiparesis (asia 4), with partial right third nerve palsy. brain mri (figure 5) showed no signs of tumor recurrence. 558 iulia vapor et al supratentorial neuroectodermal tumor figure 3 postoperative ct-scan figure 4 one month postoperative mri romanian neurosurgery (2011) xviii 4: 555 563 559 figure 5 four months postoperative mri figure 6 one year postoperative mri 560 iulia vapor et al supratentorial neuroectodermal tumor the next follow-up visits were made at one year postoperative and, also, the brain mri (figure 6) showed no signs of tumor recurrence and the neurologic status had improved. in the future for follow-up will be made a brain mri every 6 months, or faster if the neurological status impose so. discussions the entity of s-pnet was described for the first time in 1973 by hart and earl. over the time there had been divergences in classifying those tumors. for example in the who classification published in 1993, s-pnet and medulloblastomas were classified as embryonal tumors with multipotent differentiation. until the 2000 publication of the who classification, medulloblastomas were considered infratentorial pnet and until then, those two types of tumors were studied together. in the 2000 published who classification those entities were separated in two distinct subtypes of embryonal tumors. in the most recent who classification (2007) the tumors categorized as s-pnet were cns neuroblastomas, cns ganglioneuroblastomas, medulloblastomas and ependymoblastomas. due to those divergences there are relatively few studies focalized on s-pnet in the literature. s-pnets are malignant embryonal tumors which can be phenotypically poorly differentiated or can show different degrees of differentiation along neuronal, astrocytic and ependymal lines. tumors with neuronal differentiation are termed cns neuroblastomas, if also neuroplastic ganglion cells are present, the term is cns ganglioneuroblastoma. tumors presenting features of the embryonal neural tube formation are named medulloepitheliomas and those with ependymoblastic rosettes are termed ependymoblastomas. all those types of tumors (which in the previous classifications were different entities) are variants of cns pnets. in this classification is described an unusual pnet called “embryonal tumor with abundant neuropil and true rosettes” and can occur in the cerebrum, brain stem and cerebellum of young children. despite the progress made in the management of s-pnets the prognostic remains poor. the majority of studies included patients with tumors categorized as pnet before the last who classification.biswas and co. found a 5 years survival rate of 9% (study of 11 patients with s-pnet published in 2009).in the ccg 921 trial were included 44 patients with s-pnets and the pfs at 3 years was 33%, the factors of negative prognosis being metastatic disease (all patients with metastatic disease died) and young age. in german hit 88/89 and hit 91 trials were enrolled 63 patients with s-pnet and the 3 years pfs was 39,1%. s-pnets can disseminate via csf (cerebrospinal fluid) or can generate extraneural metastases. rubens and co. reported a case of a small child (23 months old) with lung metastases but with long survival. extraneural metastases are very rare, more frequent in medulloblastomas than in s-pnets. craniospinal metastases occur in approximately 17-27% of spnets and the presence of dissemination at the moment of diagnosis is a poor prognostic factor. this dissemination can be detected using csf cytology (lumbar or intracranial) or by using neuroimaging techniques (mri of full neuraxis). there is a percent of divergences between those methods of detecting craniospinal dissemination. however, most treatment romanian neurosurgery (2011) xviii 4: 555 563 561 protocols recommend the use of csf cytology obtained by lumbar tap. the positive cytology without mri findings of metastases can suggest an early stage of dissemination. terterov and co. found that mri findings are correlated with survival, whereas perioperative csf cytology does not. some studies try to evaluate with accuracy the best method for the diagnosis of craniospinal dissemination and the opportunity to avoid the irradiation of the entire neuraxis in cases of localized disease to avoid the post irradiation complications. in the case we presented that the child had no craniospinal dissemination, but the oncologist decided, in accordance with current protocols, to do irradiation of the entire craniospinal axis after chemotherapy. another factor that has impact on the survival is the grade of resection. usually those tumors are located in eloquent areas ant gross total resection cannot be accomplished. in the ccg 921 study authors found that the dimensions of the residual tumor is an important prognostic factor, but only in patients with localized disease. in the case which we presented the postoperative ct-scan confirmed the gross total resection and the 1, 4 and 12 months postoperative brain mri showed no signs of tumor recurrence. the good postoperative course is in accordance with the current literature (gtr and no signs of disseminated disease), but there may be other factors that contribute to that evolution. there is necessarily to continue the study of this entity in order to identify other prognostic factors and new treatment strategies to improve the survival period and the quality of life of pediatric patients with s-pnet. in ccg 921 and in the german hit trials gtr could be accomplished in just 40% of the cases of spnets. in those two studies the amount of residual tumor was not a prognostic factor, probably due to the small number of cases, but there was a tendency for a better survival in children with less residual tumor. another prognostic factor is the age. small children have a worse prognostic, although it is difficult to establish if age itself is a prognostic factor due to the fact that children younger than 3 years cannot undergo radiotherapy. in children younger than 3 years old, radiotherapy can cause significant late effects such as endocrine abnormalities, impaired axial growth, hearing impairment, neuropsychological dysfunction and secondary tumors. in the french society of pediatric oncology infant study, the median survival period in patients with s-pnet was 12 months and the 2 years pfs was 4%. the mri appearance of s-pnets is very heterogeneous. usually there are big lesions, without or with minimal surrounding edema, and can show cystic degeneration, necrosis, and intratumoral hemorrhage. in present the majority of studies referring to the s-pnets focus on the different strategies of chemotherapy and the identification of target molecules for adjuvant therapies. also new methods of treatment are developed. pinakin and co published a case of treatment of s-pnet located in right thalamus extended into the right midbrain, using magnetic-resonance-guided laserinduced thermal therapy, with good results at 6 months of follow-up. this method may be promising for tumors located in high-eloquent areas. 562 iulia vapor et al supratentorial neuroectodermal tumor conclusion we presented a case of a small child with s-pnet admitted in the hospital with intratumoral hemorrhage and poor neurological status, without signs of disseminated disease, but with good postoperative evolution after gross total resection, chemotherapy and irradiation of the entire neuraxis. although in the last years the survival period of those children has improved, is necessary to develop new strategies to improve the quality of life and survival in pediatric patients with spnets. abbreviations s-pnet = supratentorial neuroectodermal tumor; gcs = glasgow coma scale; ct = computed tomography; who = world health organization; cns = central nervous system; gos = glasgow outcome scale; md = moderate disability; icu = intensive care unit; pfs = progression free survival; csf = cerebrospinal fluid; gtr = gross total resection; mri = magnetic resonance imaging. references 1. behdad a, perry a. central nervous system primitive neuroectodermal tumors: a clinicopathologic and genetic study of 33 cases. brain pathol. 20(2):441-50. 2010. 2. biswas s, burke a, cherian s, williams d, nicholson j, horan g, jefferies s, williams m, earl hm, burnet ng, hatcher h. non-pineal supratentorial primitive neuro-ectodermal tumors (spnet) in teenagers and young adults: time to reconsider cisplatin based chemotherapy after craniospinal irradiation? pediatr blood cancer. 52(7):796-803. 2009 3. burger pc. supratentorial primitive neuroectodermal tumor (spnet). brain pathol. 16(1):86. 2006 4. burkhardt jk, kockro ra, dohmen-scheufler h, woernle cm, bellut d, kollias s, bertalanffy h. small supratentorial, extraaxial primitive neuroectodermal tumor causing large intracerebral hematoma. neurol med chir (tokyo). 51(6):441-4, 2011. 5. butturini am, jacob m, aguajo j, vander-walde na, villablanca j, jubran r, erdreich-epstein a, marachelian a, dhall g, finlay jl. high-dose chemotherapy and autologous hematopoietic progenitor cell rescue in children with recurrent medulloblastoma and supratentorial primitive neuroectodermal tumors: the impact of prior radiotherapy on outcome. cancer. 1;115(13):2956-63. 2009 6. dai ai, backstrom jw, burger pc, duffner pk. supratentorial primitive neuroectodermal tumors of infancy: clinical and radiologic findings. pediatr neurol. 29(5):430-4. 2003 7. fouladi m, chintagumpala m, laningham fh, ashley d, kellie sj, langston jw, mccluggage cw, woo s, kocak m, krull k, kun le, mulhern rk, gajjar a. white matter lesions detected by magnetic resonance imaging after radiotherapy and high-dose chemotherapy in children with medulloblastoma or primitive neuroectodermal tumor. j clin oncol. 15;22(22):455160. 2004 8. hong ts, mehta mp, boyett jm, donahue b, rorke lb, yao ms, zeltzer pm. patterns of failure in supratentorial primitive neuroectodermal tumors treated in children's cancer group study 921, a phase iii combined modality study. int j radiat oncol biol phys. 1;60(1):204-13. 2004 9. johnston dl, keene dl, lafay-cousin l, steinbok p, sung l, carret as, crooks b, strother d, wilson b, odame i, eisenstat dd, mpofu c, zelcer s, huang a, bouffet e. supratentorial primitive neuroectodermal tumors: a canadian pediatric brain tumor consortium report. j neurooncol. 86(1):101-8. 2008 10. kuhn sa, hanisch uk, ebmeier k, beetz c, brodhun m, reichart r, ewald c, deufel t, kalff r. a paediatric supratentorial primitive neuroectodermal tumour associated with malignant astrocytic transformation and a clonal origin of both components. neurosurg rev. 30(2):143-9; discussion 149. 2007 11. larouche v, capra m, huang a, bartels u, bouffet e. supratentorial primitive neuroectodermal tumors in young children. j clin oncol. 10;24(35):5609; 2006. 12. mcbride sm, daganzo sm, banerjee a, gupta n, lamborn kr, prados md, berger ms, wara wm, haas-kogan da. radiation is an important component of multimodality therapy for pediatric non-pineal supratentorial primitive neuroectodermal tumors. int j radiat oncol biol phys. 1;72(5):1319-23. 2008. 13. nordfors k, haapasalo j, korja m, niemelä a, laine j, parkkila ak, pastorekova s, pastorek j, waheed a, sly ws, parkkila s, haapasalo h. the tumourassociated carbonic anhydrases ca ii, ca ix and ca xii in a group of medulloblastomas and supratentorial primitive neuroectodermal tumours: an association of romanian neurosurgery (2011) xviii 4: 555 563 563 ca ix with poor prognosis. bmc cancer. 18;10:148. 2010 14. phi jh, kim jh, eun km, wang kc, park kh, choi sa, kim yy, park sh, cho bk, kim sk. upregulation of sox2, notch1, and id1 in supratentorial primitive neuroectodermal tumors: a distinct differentiation pattern from that of medulloblastomas. j neurosurg pediatr. 5(6):608-14. 2010 15. pinakin r. jethwa, m.d.1, jason h. lee, m.d.3, rachid assina, r.ph., m.d.1, irwin a. keller, m.d.3, and shabbar f. danish, m.d.2 treatment of a supratentorial primitive neuroectodermal tumor using magnetic resonance–guided laser-induced thermal therapy. technical note. j neurosurg pediatrics 8: 468475, 2011 16. pizer bl, weston cl, robinson kj, ellison dw, ironside j, saran f, lashford ls, tait d, lucraft h, walker da, bailey cc, taylor re. analysis of patients with supratentorial primitive neuro-ectodermal tumours entered into the siop/ukccsg pnet 3 study. eur j cancer. 42(8):1120-8. 2006. 17. prasad an. supratentorial pnet in a young child. indian j pediatr. 78(5):613-5. 2011 18. rubens j, gosiengfiao y, tomita t, jacobsohn da, fangusaro j. long-term survival in a pediatric patient with supratentorial primitive neuro-ectodermal tumor and extraneural metastasis at diagnosis. pediatr blood cancer.; 57(2):341-4. 2011 19. schmid i, stachel d, graubner ub, elsner r, schulze s, pöllinger b, goetz c, haas rj. [supratentorial primitive neuroectodermal tumor: a single center experience and comparison with the literature]. klin padiatr. 217(3):153-7. 2005 20. taylor re, donachie ph, weston cl, robinson kj, lucraft h, saran f, ellison dw, ironside j, walker da, pizer bl; children's cancer and leukaemia group cns tumour division. impact of radiotherapy parameters on outcome for patients with supratentorial primitive neuro-ectodermal tumours entered into the siop/ukccsg pnet 3 study. radiother oncol. 92(1):83-8. 2009 21. terterov s, krieger md, bowen i, mccomb jg. evaluation of intracranial cerebrospinal fluid cytology in staging pediatric medulloblastomas, supratentorial primitive neuroectodermal tumors, and ependymomas. j neurosurg pediatr. 6(2):131-6. 2011 22. timmermann b, kortmann rd, kühl j, meisner c, dieckmann k, pietsch t, bamberg m. role of radiotherapy in the treatment of supratentorial primitive neuroectodermal tumors in childhood: results of the prospective german brain tumor trials hit 88/89 and 91. j clin oncol. 1;20(3):842-9. 2002 23. visée s, soltner c, rialland x, machet mc, loussouarn d, milinkevitch s, pasco-papon a, mercier p, rousselet mc. supratentorial primitive neuroectodermal tumours of the brain: multidirectional differentiation does not influence prognosis. a clinicopathological report of 18 patients.histopathology. 46(4):403-12. 2005 24. von bueren ao, warmuth-metz m, schlegel pg, soerensen n, krauss j, roggendorf w, pietsch t, feiden w, graf n, pohl f, flentje m, kuehl j, rutkowski s. late complete remission of supratentorial primitive neuroectodermal tumor (cns-pnet) after multiple relapses. 56(3):503-5. 2011 microsoft word 6tataranuligiaendoscopic_bun.doc 52 romanian neurosurgery (2010) xvii 1: 52 63 endoscopic endonasal transsphenoidal approach in the management of sellar and parasellar lesions: indications and standard surgical technique (part i) ligia tataranu1, m.r. gorgan1, v. ciubotaru1, adriana dediu1, b. ene1, d. paunescu1, anica dricu2, v. pruna1 1neurosurgical clinic, “bagdasar-arseni” clinical emergency hospital, bucharest, romania; 2university of medicine and pharmacy, craiova, romania abstract transsphenoidal approaches have been used for a century for the resection of pituitary and other sellar tumors. in the past decade, however, the endoscopic endonasal transsphenoidal approach has been proposed as a minimally invasive procedure for the treatment of pathologies of the sellar region. this procedure introduces various advantages compared with the transsphenoidal microsurgical approach, such as an improved vision of the surgical field, less traumatism of the nasal structures and reduced complications. patients’ quick recovery, short hospital stays and minimal postoperative discomfort have been observed. more recently, the standard endoscopic endonasal technique has been extended to provide access to parasellar lesions. this expansion carries significant potential for the resection of skull base lesions. in this article, the authors review the indications of the endoscopic endonasal transsphenoidal approach and define the main phases of the standard surgical technique. preoperative evaluation, equipment, preoperative and postoperative care are presented. endoscopic endonasal technique is a safe and effective method for removal of most sellar and some parasellar masses, providing more complete lesion excision and reducing complications. keywords: endoscopy, minimally invasive surgery, parasellar lesion, pituitary tumor, sellar lesion, transsphenoidal surgery endoscopes have two advantages relative to operating microscopes: they provide a wide panoramic view of the surgical field through a narrow corridor as well as images of the surrounding anatomy, including various anatomical corners. endoscopes can be used to assist visualization during conventional microscopic surgery (endoscope-assisted microsurgery), to place an endonasal retractor during microsurgery (endoscopic sphenoidotomy) or as a sole visualizing tool during endoscopic endonasal transsphenoidal approach [1]. when the endoscope is used in transsphenoidal surgery, jho and alfieri (2000) recommend first to conduct endoscope-assisted microsurgery, followed by endoscopic sphenoidotomy assisted by a rhinologist, and then to proceed with the endoscopic endonasal transsphenoidal approach [1]. endoscope-assisted transsphenoidal microsurgery transsphenoidal microsurgical procedure can be performed through sublabial approach or endonasal route. ligia tataranu et al endoscopic endonasal approach 53 after a retractor is placed through rhinoseptal route, anterior sphenoidotomy is made, and the entire septa inside the sinus are removed, the endoscope is used to provide a panoramic view of the posterior wall of the sphenoidal sinus and to establish anatomical landmarks. radiological identification can not be used. in tumor resection phase, endoscope’s angled lenses provide direct visualization of hidden anatomical corners. therefore, the endoscope can be introduced intrasellar (to view lateral walls) or suprasellar. the retractor limits the simultaneous use of endoscope and surgical instruments. the endoscope-assisted microsurgery is efficient especially for macroadenomas with suprasellar or parasellar extension. in these particular cases, the precise localization of the tumor can be estimated and the remnant tumor tissue from the recesses can be identified and removed by using the endoscope guiding. in this way, the resection rate for secreting adenomas is improved; this type of adenoma needs total resection for complete cure. also, the endoscope provides the view of the walls of the cavernous sinuses and reduces the risk of injure at this level [2, 3]. endoscopic sphenoidotomy for endonasal placement of a transsphenoidal retractor transsphenoidal microsurgical procedure is preceded by an endoscopic sphenoidotomy made by a rhinologist using an endonasal route. afterwards, a transsphenoidal retractor is placed though endonasal route and the microsurgical approach can be performed [1]. this technique offers special advantages because endonasal approach and endoscopic sphenoidotomy avoid nasal packing, postoperative discomfort is minimal and patients recover fast. endoscopic endonasal transphenoidal approach endoscopic endonasal transsphenoidal approach is performed exclusively under endoscopic visualization. the endoscope provides wide panoramic views, optical zoom-in on surgical targets and visualization of various anatomical corners using its angled lenses. surgical instruments must be parallel with the endoscope. paraseptal approach (between middle turbinate and nasal septum) is used through patient’s natural nasal airpassage. unlike conventional approach, the endoscopic approach does not require transsphenoidal retractor, radiological identification, dissection of mucosa of nasal septum and nasal packing. endoscopic endonasal transsphenoidal approach can be difficult, and it must be performed by surgeons with experience in endoscopic surgery. neurosurgeons with no experience in using the endoscope require a learning period (the first 20 to 30 cases) [1, 4]. the endoscope is held in the surgeon’s nondominant hand and the surgical instruments are held in the other hand. the surgical instruments must be inserted parallel with the endoscope through a narrow natural corridor, respecting the anatomy. the surgical technique is improved by using a wide 54 romanian neurosurgery (2010) xvii 1: 52 63 variety of endoscope holders and specific instruments. indications the surgical indications for endoscopic endonasal transsphenoidal approach are similar to those for transsphenoidal microsurgery. this technique can be used for intrasellar lesions, intrasellar lesions with symmetric suprasellar extension, or lesions that extend into sphenoidal or cavernous sinus (when a massive tumor resection is needed, usually followed by radiotherapy). intrasellar lesions with asymmetric or polilobate suprasellar extensions require intracranial approach. sagital or lateral extended approach make it possible to treat lesions located in the tuberculum sellae, planum sphenoidale, clivus, or spheno-ethmoidal regions. endoscopic endonasal transsphenoidal approach is recommended in the treatment of: •pituitary tumors (adenomas and carcinomas); •craniopharyngiomas; •rathke’s cleft cysts; •germinoma located in the sellar or parasellar region; these tumors represent about 20% of all germ cell intracranial tumors [5]; these tumors can be approached by endoscopic endonasal transsphenoidal approach for decompression of the optic pathways and histological diagnosis [6]. •epidermoid tumors; •malignant tumors; •intrasellar arachnoid cysts; •empty sella; •clival tumors; •tuberculum sellae meningiomas or planum sphenoidale meningiomas; •cerebrospinal fluid spheno-ethmoidal fistulas [7]; •congenital, iatrogenic or posttraumatic meningoencephalocele of spheno-ethmoidal region [6]. endoscopic endonasal transsphenoidal approach is preferred for recurrent pituitary tumors that have been first treated through conventional transseptal transsphenoidal surgery because it is minimally invasive [8]. minimally invasive endoscopic endonasal transsphenoidal surgery provides easy and quick recovery; therefore, this procedure is recommended for sellar and parasellar lesions in children. it is essential to keep children’s anatomical and functional integrity to ensure their normal growth and nasosphenoidal ventilation [6]. several factors should be considered when contemplating this type of surgery. first, the amount of pneumatization of the sphenoid body is important. there are three types of adult sphenoid sinuses: the sellar type (86% of cases), which is fully pneumatized, the presellar type (11% of cases), with less pneumatization and the conchal type (3% of cases), without pneumatization, thus limiting access to the sella (figure 1). ligia tataranu et al endoscopic endonasal approach 55 figure 1 (a. b, c)types of pneumatization of the sphenoid body. a – sellar type; b – presellar type; c – conchal type active infection in the sphenoid sinus prevents any transsphenoidal pituitary surgery. if the septum is grossly deviated, a septoplasty may be performed prior to opening the sphenoid. rare contraindications include carotid arteries that project into the midline [9]. preoperative evaluation preoperatively, all patients should undergo clinical examination, endocrine testing, ophthalmological (visual field and acuity) and rhinological assessment, and radiological investigations. mri is the investigation of choice, because it provides better definition of tumors. gadolinium is given to help identify the tumor, as well as to delineate adjacent vessels, indicating the proximity to the tumor of such parasellar structures such as optic nerves, cavernous sinuses and internal carotid arteries. ct scanning (with bone window, high resolution coronal and axial scans, intravenous contrast and three-dimensional reconstruction) is performed for sellar and parasellar surgery to view nasal cavities and paranasal sinuses. also, ct scan images are useful to select the approach (right or left), to assess the pneumatization of the sphenoid, and the position of its septa. equipment endoscopic approach, when compared with standard transsphenoidal microsurgical approach, has two distinguishing characteristics that arise from the use of endoscope as the sole optic system and the absence of transsphenoidal retractor [10]. these require proper endoscopic equipment and specifically designed surgical tools. endoscope must function perfectly and offer good quality images. commonly used endoscopes are rigid scopes with 4 mm in diameter, 18 or 30 cm in length, equipped with zero, 30 and 45-degree lenses, according to different steps of the surgical operation. smaller endoscopes that are 2.7mm in diameter can be used, especially in children and in patients with very narrow nostrils. the endoscope must be introduced in a sheath, connected to a cleaning-irrigation system, and controlled by a manual or foot switch. the irrigation system permits cleaning of the distal lens, thus avoiding repeated entrances and exits from the nostril. an endoscope holder is used to provide stability to the endoscope during the sellar phase, thus freeing surgeon’s hands and providing a fixed image of the operating field. the c-arm fluoroscopy is used in particular cases (patients with presellar or conchal-type sphenoid sinuses). the use of the neuronavigation system (conventional or “augmented reality”) can be helpful to assist in the identification of the anatomic landmarks, particularly in patients with recurrent tumors [11, 12]. virtual neuroendoscopic system is used in learning and preoperative planning [13]. 56 romanian neurosurgery (2010) xvii 1: 52 63 surgical instruments are different from those used in a microsurgical approach, in which the bayonet shape is needed to avoid conflict between surgeon’s hands and microscope’s lenses. in the endoscopic approach, straight instruments are preferable as they can be inserted close to the endoscope along its axis. instruments are equipped with differently angled tips such that surgeons can manage all areas that become visible as a result of the wider view afforded by the endoscope. standardized surgical technique patients with preoperative hypopituitarism receive hormonal replacement therapy before their operation, and a single dose of hydrocortisone (100 mg) is administrated at surgery. prophylactic antibiotics composed of 1g cefazolin or occasionally 1g vancomycin and 80 mg gentamicin (if the patient is allergic to cefazolin) are administrated intravenously as a single intraoperative doze [14, 15]. figure 2 surgical setup and relative position of patient and surgeons. 1 – surgeon; 2 – cosurgeon; 3 – scrub nurse; 4 – tv monitor; 5 – c-arm image intensifier; 6 – anesthetic machine; 7 – instrument trays the operating team and equipment are positioned in an ergonomic setup (figure 2). the operation is performed under general anesthesia with orotracheal intubation. patients are placed supine and their torso is elevated about 10-20 degrees to reduce the venous pressure in the cavernous sinus. patient‘s head is put in a mayfield headrest and turned 10-20 degrees in an horizontal plane toward the surgeon. the inclination of the head in the vertical plane varies as a function of the anatomy of the lesion. if lesions are primarily in the sellar region or the clivus, the head is slightly flexed, whereas in lesions that extend toward the suprasellar region or the planum sphenoidale, the head of the patient is left in a neutral position slightly hyper extended. these variations of the head’s inclination are necessary to avoid surgical instruments interfering with patient’s thorax. the corneas are protected with ophthalmic ointment, and the eyelids are closed. the operating field (nasal cavities, nose and face) is prepared with 5% providoneiodine solution or 5% chlorhexidine gluconate. if fat graft material is used, abdominal fat is harvested through a 1-2 cm long infraombilical skin incision. once the patient is draped aseptically, the endoscope is assembled. standard technique includes three phases: nasal, sphenoid and sellar phase [10]. during nasal phase, the endoscope is introduced through the nostril and is advanced until it reaches the sphenoid ostium. ligia tataranu et al endoscopic endonasal approach 57 during the sphenoid phase, the nasal septum is separated from the sphenoid rostrum and anterior sphenoidotomy is performed, i.e. the entire septa inside the sphenoid sinus are removed and the anatomical landmarks are exposed. during the sellar phase, the sellar floor is opened, the lesion is removed, the sellar reconstruction is performed and the endoscope is pulled out. 1. nasal phase the side of the nasal cavity to be used is determined by the width of the nasal cavity and the side of the tumor. preferably, the wider side of the nasal cavity is used. the anatomy of nasal cavity can be altered by septal deviation, hypertrophy of nasal turbinates, scars or synechias (in recurrent tumors, when the first operation was conventional transseptal transsphenoidal microsurgery). in these situations, the other nostril will be used. occasionally, partial removal of the middle turbinate is necessary to improve access. sellar lesions can be approached both ipsilateral or controlateral, depending on the localization and extension of the tumor. thus, an inferior extension of the tumor (into the sphenoid sinus) or a lateral extension in the anterior inferior part of the cavernous sinus can be efficiently reached by ipsilateral nostril. on the other hand, it is advisable to approach through the controlateral nostril a laterally located microadenoma, an extension in the medial part of the cavernous sinus or an asymmetric suprasellar tumor, because an endonasal approach is a few degrees off midline and would easily lead to the controlateral sella (figure 3). figure 3 an inferior extension of the tumor (into the sphenoid sinus) or a lateral extension in the anterior inferior part of the cavernous sinus can be efficiently reached by ipsilateral approach (lesion a). an asymmetric suprasellar extension can be easily removed by controlateral approach (lesion b). some authors recommend adequate nasal vasoconstriction prior to surgery to ensure a minimal bleeding from nasal mucosa. the middle turbinate, the anterior wall of the sphenoid and the rostrum are infiltrated with 1% xiline and 1:200 000 adrenaline. cottonoids soaked in 1:10 000 adrenaline are then placed in the nose both sides [16]. other authors consider local vasoconstriction unnecessary [14, 17], but recommend correct analgesia and sometimes controlled hypotension [10, 14]. topical vasoconstriction reduces mucosal bleeding during surgery, but it is usually associated with postoperative bleeding when drugs cease their action [17]. zero-degree endoscope (4 mm in diameter, 18 cm in length) is introduced through the chosen nostril, tangential to the floor of the nasal cavity. the first structures to be identified are the inferior turbinate laterally and the nasal septum 58 romanian neurosurgery (2010) xvii 1: 52 63 medially. as the endoscope advances along the floor of the nasal cavity, it reaches the choana (communicating orifice with the nasopharynx). its medial margin is the vomer, which confirms the midline of the approach, and its roof is shaped by the inferior wall of the sphenoid sinus. lateral to the choana is the tail of the inferior turbinate. the head of middle turbinate, which is usually close to the nasal septum, can be observed above the inferior turbinate. the main surgical landmarks are the communicating orifice with the nasopharynx and the inferior margin of the middle turbinate. sometimes the superior turbinate mimics the middle turbinate. therefore, anatomical reference to the choana is essential to confirm the middle turbinate. the level of the inferior margin of the middle turbinate is just rostral to the nasopharynx in a vertical axis. the line drawn along the inferior margin of the middle turbinate extends posteriorly to about 1 cm inferior to the floor of the sella [14] (figure 4). figure 4 the line drawn along the inferior margin of the middle turbinate extends posteriorly to about 1 cm inferior to the floor of the sella. a – sagital section; b – coronal section. 1 – inferior turbinate; 2 – middle turbinate; 3 – projection of the choana; 4 – projection of the sella. the mucus conduit from the frontal sinus, anterior ethmoidal sinus, and maxillary sinus is through the hiatus semilunaris, which is laterally to the middle turbinate. posteriorly, the sphenoethmoidal recess, which is along the lateral margin of the anterior wall of the sphenoidal sinus, is a mucus conduit from the posterior ethmoidal sinus and sphenoidal sinus. during the operation, caution must be used not to damage these mucus pathways to prevent postoperative sinusitis [14, 17]. to enlarge the approach space, cottonoids soaked with isotone saline solution [14], with diluted adrenaline (1:100 000) or with xylometazoline hydrochloride [10] are positioned between the middle turbinate and the nasal septum. the head of the middle turbinate is delicately dislocated laterally. ligia tataranu et al endoscopic endonasal approach 59 then the cotton patties are removed and the endoscope is angled upward along the roof of the choana and the sphenoethmoidal recess until it reaches the sphenoid ostium, usually located approximately 1.5 cm above the roof of the choana. the sphenoid ostium is extremely variable in localization, size and shape. when the ostium is situated laterally, it can be covered by superior or supreme turbinate; in these cases, the superior and/or the supreme turbinate can be lateralized or removed. a csf leak can occur due to fracture of the lateral lamella or of the cribriform plate, on which these turbinates are inserted. if the sphenoid ostium is not visible and the sphenoid sinus is well pneumatized, an artificial orifice can be made between nasal septum and superior turbinate, at approximately 1.5 cm above the superior margin of the choana. 2. sphenoid phase once the sphenoid ostium is identified, coagulation of the mucosa of the anterior wall of the sphenoid sinus is performed. this serves to avoid arterial bleeding originating from septal branches of the sphenopalatine artery. the vomer is the landmark for the midline. a microdrill or a septal breaker is used to separate the nasal septum from the sphenoid rostrum [17]. submucosal dissection of anterior wall of controlateral sphenoidal sinus is made, such that the anterior wall is bilaterally exposed. the anterior sphenoidotomy about 1.5-2 cm is made with a microdrill or with kerrison punches (figure 5). the sphenoid rostrum is removed in fragments and not “en bloc”. it is mandatory to remove the anterior wall of the sphenoid widely, especially downward, before reaching the sella; otherwise, the instruments are not able to reach all the areas visible by the endoscope. caution must be used in the inferolateral direction, where the sphenopalatine artery or its major branches lies, to avoid arterial bleeding. the haemostasis is obtained by coagulation with bipolar forceps. in endoscopic surgery it is essential to have an operating field without bleeding. the mucosa is removed only in the anterior sphenoidotomy zone. figure 5 anterior sphenoidotomy – endoscopic view when the sellar lesion does not extend into the sphenoidal sinus, there is sufficient space to manoeuvre the endoscope and the instruments. if the sellar lesion invades the sphenoidal sinus, it is necessary to remove about 1 cm from the posterior part of nasal septum. one or more septa can be identified inside de sphenoid sinus. the images of the sphenoid sinus septations are revealed by the preoperative ct scan (in coronal and axial sections). these images are very useful, especially when the septa are implanted on the carotid prominences 60 romanian neurosurgery (2010) xvii 1: 52 63 and the sphenoid sinus is a presellar type. these septa must be removed as much as possible by cutting bone punches, avoiding detachment of the sphenoid mucosa unless adenomatous infiltration is evident or suspected. at this moment in the procedure, the landmarks inside the sphenoid sinus are identified (figure 6, 7). the sellar floor at the centre, the sphenoethmoidal planum above it, and the clival indentation below are visible. lateral to the sellar floor, the bony prominences of the intracavernous carotid artery and the optic nerve can be observed; between them, the optocarotid recess can be found. in 4% of the cases, the internal carotid artery and the optic nerve do not have bone protection [18]. in the presence of a presellar or a conchal sphenoid sinus, there will be a paucity of anatomic landmarks. the neuronavigation system is very useful in these situations. 3. sellar phase in this phase of the procedure, a longer endoscope (zero-degree angled lens, 4 mm in diameter and 30 cm in length) is used. the endoscope is mounted on the endoscope holder, such that surgeon’s both hands are free. figure 6 panoramic view of the posterior wall of the sphenoidal sinus. the endoscope holder is fixed at a certain distance from sella turcica to allow a comfortable use of the instruments. the opening of the sellar floor is performed with bone punchers or a microdrill and must be extended as required by the specific pathological process. the dura is incised in a midline position, in a linear, rectangular, or cruciate fashion (figure 8). the superior and the inferior intercavernous sinuses are usually compressed and obliterated in patients with macroadenomas, making the dural incision bloodless; in microadenomas, and especially in cushing disease, the entire sellar dura may be covered by one or two venous channels, which can bleed during the dural incision. to avoid this, these venous channels are secured and sealed with bipolar coagulation forceps or with small surgical clips placed across them. sometime, an ectatic carotid artery may be located within the sella. figure 7 schematic drawing of the panoramic endoscopic view of the posterior wall of the sphenoidal sinus. 1 – clival indentation; 2 – sella; 3 – tuberculum sella; 4 – bony protuberances covering the carotid artery; 5 – bony protuberances covering the cavernous sinus; 6 – optic protuberances. ligia tataranu et al endoscopic endonasal approach 61 the sellar phase of the endoscopic procedure must follow the already well defined rules of the microsurgical transsphenoidal approach. in cases involving microadenomas, the tumor is removed with a small ring curette from the suspected location suggested by mri images. while the tumor tissue is curetted out, the thin shell of normal pituitary tissue is shaved along the tumor cavity [17]. in cases of macroadenomas, the inferior part is excised first and then the lateral part of the tumor. an angled 30degrees or 40-degrees endoscope is advanced into the tumor cavity to see lateral parts and to verify the presence of any tumor remnants that are often imprisoned in the recesses created by the fall of suprasellar cistern. figure 8 endoscopic view. after the opening of the sellar floor, the dura mater is incised in a midline position and often tumor tissue spills over. the tumor remnants are removed with curved instruments. when the lesion extends toward the medial wall of the cavernous sinus, its removal can be accomplished under endoscopic control. the venous bleeding that might occur can be controlled by temporarily positioning haemostatic substances and cottonoids and by gentle compressing the medial wall of cavernous sinus and irrigating for a few minutes. attention must also be paid to the anterior superior and suprachiasmatic regions that are not situated on the surgical trajectory in the endoscopic approach. finally, the suprasellar part is progressively removed from the periphery of the diaphragm sella toward the centre; this way is avoided the premature release of the redundant diaphragm, which would obscure visualization of the lateral portions, into the operative field. after tumor’s removal, if the descent of the suprasellar portion of the lesion is not observed, it is useful to perform a valsalva maneuver, which may encourage protrusion of the suprasellar cistern into the sellar cavity. after intracapsular emptying of the tumor, its pseudocapsule can be dissected from the suprasellar cistern. attention must be taken not to rupture the arachnoid membrane that prevents cerebrospinal fluid (csf) leak. vector maneuvering of the surgical instruments during tumor resection should avoid any force that would apply traction to the pituitary stalk. traction injury to the pituitary stalk carries the risk of postoperative diabetes insipidus. the junction with normal pituitary tissue is identified and preserved. a sellar reconstruction is performed in selected patients with the purpose of reducing the dead space, creating a protective barrier, and preventing the descent of the chiasm into the sellar cavity. sellar repair is mainly indicated when the tumor resection cavity is large or a csf leak occurs intraoperative. various techniques are used: intradural and/or extradural closure of the sella and packing of the sella with or without 62 romanian neurosurgery (2010) xvii 1: 52 63 packing of the sphenoid sinus [14, 15, 17, 19-22]. postoperative, lumbar drainage is used to prevent or to treat a csf leakage. at the end of the procedure, haemostasis is obtained, irrigation is performed and the endoscope is removed gradually. generally, the sphenoid sinus is maintained empty without any foreign materials inside it. the middle turbinate is gently restored in a medial direction and contact with nasal septum is avoided to prevent the formation of synechias. packing of the nasal cavity for a few hours is not considered necessary, except for instances when a diffuse intraoperative bleeding from the nasal mucosa occurred, as it may happen in some acromegalic patients or in poorly controlled hypertensive patients [10]. standard endoscopic endonasal transsphenoidal approach uses a paraseptal route. the approach of the sphenoid rostrum is made between nasal septum and lateral luxated middle turbinate. the vomer and the nasal septum are detached from the sphenoid rostrum and moved controlateral. but this approach is very flexible. it can be adapted to different anatomical aspects, and can be used in various sellar and suprasellar lesions. some changes in the standard technique were made to optimize the surgical resection in minimally invasive conditions [23]. one could use a minimal approach (hemisphenoidotomy), a deep transseptal approach, an extended approach (superior, inferior or lateral) or a bilateral approach. postoperative care postoperative discomfort is minimal and the narcotic analgesics are rarely necessary. nasal drainage is also minimal. the use of the saline douches three times a day diminishes nasal crusting and prevents synechias. an ointment is also used with antibiotics for local applications in the nasal cavity three times a day. patients are kept on a five-day course of oral clarithromycin (1g/day) [14, 17]. postoperative risk for diabetes insipidus is high, so the patients are observed in a regular hospital room for two days [15]. the electrolytes are measured after the operation and the next morning. cortisol is also measured the following morning. when the cortisol level is higher then 15 ng/dl, postoperative steroids are unnecessary. patients with cortisol level less then 15 ng/dl are placed on hydrocortisone (20 mg every morning and 10 mg early night). patients with cushing’s disease are discharged with dexamethasone (1 to 2 mg/day) [14]. an endocrinological evaluation is necessary several weeks after the surgical procedure. if patients develop csf leak postoperatively, this is immediately repaired using an endoscopic technique. lumbar drainage can be useful. on postoperative day 15, patients undergo clinical evaluation and after three months clinical and neuroradiologic evaluation (mri scan with gadolinium). patients with hormone-secreting microadenomas are followed with interval endocrine testing. patients with macroadenomas and hormone nonsecreting adenomas are followed with interval mri scan of the brain. conclusions the endoscopic endonasal transsphenoidal approach has major advantages relative to the conventional microsurgery technique: provides an excellent view of the operating field, is less invasive, reduces the incidence of complications, and decreases the postoperative discomfort, the postoperative hospitalization, as well as the cost of patient treatment [24]. the ligia tataranu et al endoscopic endonasal approach 63 adaptability of the endoscopic transsphenoidal approach to different pathological conditions permits the best treatment of the various sellar and parasellar lesions, allowing an adequate surgical procedure (more or less invasive). correspondence to: ligia tataranu, md, phd, “bagdasar-arseni” clinical emergency hospital, sos. berceni 10-12, 041514 bucharest, romania e-mail: medic@neurochirug.ro; phone: +40744-375 000 references 1. jho hd, alfieri a, endoscopic transsphenoidal pituitary surgery: various surgical techniques and recommended steps for procedural transition. british journal of neurosurgery, 2000. 14(5): p. 432-440. 2.baussart b, aghakhani n, portier f, chanson p, tadie m, parker f, endoscope-assisted microsurgery for invasive endoand suprasellar pituitary macroadenomas: a consecutive retrospective study with 13 patients. neurochirurgie, 2005. 51(5): p. 455-463. 3.ellamushi h, powell m, endoscope-assisted transsphenoidal pituitary microsurgery, in the centre of the skull base. proceedings of the 4th european skull base society congress, fahlbusch r, buchfelder m, editor. 2000, einhorn-presse verlag. p. 192-199. 4.kenan k, ihsan a, dilek o, burak c, gurkan k, savas c, the learning curve in endoscopic pituitary surgery and our experience. neurosurgical revue, 2006. 29(4): p. 298-305. 5.jellinger k, primary intracranial germ cell tumours. acta neuropathol, 1973. 25: p. 291-306. 6.de divitiis e, cappabianca p, gangemi m, cavallo lm, the role of the endoscopic transsphenoidal approach in pediatric neurosurgery. child's nervous system, 2000. 16: p. 692-696. 7.kelley tf, stankiewicz ja, chow jm, origitano tc, shea j, endoscopic closure of postsurgical anterior cranial fossa cerebrospinal fluid leaks. neurosurgery, 1996. 39: p. 743-746. 8.cappabianca p, alfieri a, colao a, cavallo lm, fusco m, peca c, lombardi g, de divitiis e, endoscopic endonasal transsphenoidal surgery in recurrent and residual pituitary adenomas: technical note. minimally invasive neurosurgery, 2000. 43: p. 38-43. 9.couldwell wt, weiss mh, pituitary macroadenomas, in brain surgery, apuzzo mlj, editor. 1993, churchill livingstone: new york. p. 295-310. 10.cappabianca p, cavallo lm, de divitiis e, endoscopic endonasal transsphenoidal surgery. neurosurgery, 2004. 55(4): p. 933-941. 11.kawamata t, i.h., shibasaki t, hori t, endoscopic augmented reality navigation system for endonasal transsphenoidal surgery to treat pituitary tumors: technical note. neurosurgery, 2002. 50(6): p. 13931397. 12.lasio g, ferroli p, felisati g, broggi g, imageguided endoscopic transnasal removal of recurrent pituitary adenomas. neurosurgery, 2002. 51(1): p. 132137. 13.wolfsberger s, f.m., donat m, neubauer a, buhler k, wegenkittl r, czech t, hainfellner ja, knosp e, virtual endoscopy is a useful device for training and preoperative planning of transsphenoidal endoscopic pituitary surgery. minimally invasive neurosurgery, 2004. 47: p. 214-220. 14.jho hd, endoscopic transsphenoidal tumor surgery. operative techniques in neurosurgery, 2002. 5(4): p. 218-225. 15.jho hd, carrau rl, endoscopic endonasal transsphenoidal surgery: experience with 50 patients. journal of neurosurgery, 1997. 87: p. 44-51. 16.pell mf, atlas md, biggs nd, endoscopic pituitary tumor removal, in operative neurosurgery, kaye ah, black pm, editor. 2000, churchill livingstone: london. p. 715-722. 17.jho hd, alfieri a, endoscopic endonasal pituitary surgery: evolution of surgical technique and equipment in 150 operations. minimally invasive neurosurgery, 2001. 44: p. 1-12. 18.rhoton al, harris fs, renn wh, microsurgical anatomy of the sella region and cavernous sinus. clinical neurosurgery, 1977. 24: p. 54-85. 19.cappabianca p, cavallo lm, mariniello g, de divitiis o, romero acb, de divitiis e, easy sellar reconstruction in endoscopic endonasal transsphenoidal surgery with polyester-silicone dural substitute and fibrin glue: technical note. neurosurgery, 2001. 49(2): p. 473-476. 20.cappabianca p, cavallo lm, valente v, romano i, d'enza ai, esposito f, de divitiis e, sellar repair with fibrin sealant and collagen fleece after endoscopic endonasal trassphenoidal surgery. surgical neurology, 2004. 62(3): p. 227-233. 21.cappabianca p, c.l., esposito f, valente v, de divitiis e, sellar repair in endoscopic endonasal trassphenoidal surgery: results of 170 cases. neurosurgery, 2002. 51(6): p. 1365-1371. 22.kubo s, hasegawa h, inui t, tominaga s, yoshimine t, suture knot on the repair splint: a simple method to facilitate reconstruction of the sella turcica during endonasal endoscopic trassphenoidal surgery. technical note. journal of neurosurgery, 2005. 102(5): p. 938-939. 23.de divitiis e, cappabianca p, cavallo lm, endoscopic transsphenoidal approach: adaptability of the procedure to different sellar lesions. neurosurgery, 2002. 51(3): p. 699-707. 24.cappabianca p, alfieri a, colao a, ferone d, lombardi g, de divitiis e, endoscopic endonasal transsphenoidal approach: an additional reason in support of surgery in the management of pituitary lesions. skull base surg, 1999. 9: p. 109-117. microsoft word 8cucosliliana_epidemiological_f 300 liliana cucoş et al epidemiological issues related to parkinson’s disease epidemiological issues related to parkinson’s disease in romania liliana cucoş1 , c. iov2 , l. pendefunda3 1phd student umph “gr.t. popa” iaşi, 2nd neurology department, the emergency clinical hospital “prof. dr. n. oblu” iaşi, romania 2eng., phd, ma, trias microelectronics, research coordinator assistant umf “gr.t. popa” iaşi, romania 3umph “gr.t. popa” iaşi , 2nd neurology department, the emergency clinical hospital “prof. dr. n. oblu” iaşi, romania abstract the introduction of the advanced technologies into the medical field entails the increase in the average age of the population, fact which has as a major impact on the increase in the number of the medical disorders reported, cases which burden the medical system which is supposed to ensure medical assistance, at least of primary degree, to any particular situation. in this work, we bring forward the casuistry related to parkinson’s disease both at the level of romania and at the level of the moldavia region in order to estimate the effort which must be made towards identifying the model of optimal management to be used in order to minimize human and material costs when approaching this medical disorder. due to the high average age, the issues related to parkinson’s disease become more important as the occurrence rate is particularly high, around 60-65 years. keywords: epidemiology, parkinson’s disease, parkinsonian syndrome. introduction medicine has evolved from the simple procedures of symptomatic treatment to the management of the entire medical process which includes the treatment of the cause of the disease (9).the final diagnosis is not anymore just the result of interpreting anamnesis and evident clinical signs. the diagnosis is the result of a complex interdisciplinary activity. when talking about parkinson’s disease we mean diagnosis, treatment, results, costs, quality of life, etc (2). the management of parkinson’s disease requires that all data should be analyzed and considered followed by a decision liable to guarantee the optimal average for the patient and for the medical system of the completion of this process. treatment evolved from symptomatic approaches to focusing on cause and its removal (5) (13). at the beginnings of diagnosing parkinson’s disease, a long time ago, the signs such as tremor, muscle stiffness or loosing balance were classified as parkinson’s disease. these are evident clinical signs, evident at first sight. nowadays, it has been proved that parkinson’s disease means more than these three types of symptoms. in the equation are also included cognitive symptoms, dementia, depression, etc. (12) and specific romanian neurosurgery (2011) xviii 3: 300 – 305 301 management approach must be considered (4). the problem evolves from the fact that the increasing number of diagnostics increases the load on the health public system. the epidemiological data has a great impact on the managing such already public disease. method we are interested on the paper on the epidemiological impact of this disease. the literature was studied, some international data are presented. local data from the direction of public health is described as well. the aim is to create a good parkinson management model for our geographical area. as far as the case of romania is concerned, we will present as follows some epidemiological data which come from the direction for public health. for an average population of 21,544,036 persons during 2005-2009, figure 1 presents the average value according to the age groups in 20052009. considering the demographic information mentioned above, we present as follows the incidence of parkinson’s disease and of parkinson’s syndrome, the cases being reported by the family physicians. 0-1 1% 1-14 14% 15-64 70% 65 + 15% figure 1 the population of romania according to age groups, average values in 2005-2009 results figure 2 indicates the incidence of parkinson’s disease at the level of the population in romania during 2005-2009, according to age groups. out of the total population represented on the diagram, we can notice that most of the cases are reported for the age group over 65 years. in spite the fact most of the cases reported are included in the over 65 years group, this medical condition was revealed for the range 15-64 as well. we can notice that for the age groups 0-1 years and 1-14 years, there are no cases reported. for the age groups 15-64 years and 65+, the number of cases which were reported increased by almost 75% from 2005 to 2009. figure 3 presents the number of cases suffering from the parkinsonian syndrome reported for the period 2005-2009. there are less cases than parkinson’s disease reported for the same period and undergoing a fall from 2005 to 2009. the data we obtained allowed the distribution of the reported cases for the region of moldavia, according to counties. figure 4 and figure 5 present the incidence of parkinson’s disease and of parkinson’s syndrome for the period 2007-2009. the distribution is relatively equal for all the counties. only in 2007, the county of suceava reported an almost double incidence (per 100,000 inhabitants) in comparison with the average value of the other counties. 302 liliana cucoş et al epidemiological issues related to parkinson’s disease 0 1000 2000 3000 4000 5000 6000 2005 2006 2007 2008 2009 0-1 an 1-14 ani 15-64 ani 65 + ani figure 2 cases of parkinson’s disease reported according to age groups 1344 1898 352 358 400 0 200 400 600 800 1000 1200 1400 1600 1800 2000 an 2005 an 2006 an 2007 an 2008 an 2009 figure 3 the incidence of the parkinsonian syndrome for the period 2005-2009 (the number of cases) 37.86 12.53 25.02 24.81 23.54 65.17 33.75 31.21 0.00 10.00 20.00 30.00 40.00 50.00 60.00 70.00 bacau botosani galati iasi neamt suceava vaslui vrancea a 34.06 22.53 44.72 23.56 30.56 44.68 25.24 31.20 0.00 5.00 10.00 15.00 20.00 25.00 30.00 35.00 40.00 45.00 50.00 bacau botosani galati iasi neamt suceava vaslui vrancea b 35.58 45.81 44.26 35.44 32.49 40.37 30.70 32.35 0.00 5.00 10.00 15.00 20.00 25.00 30.00 35.00 40.00 45.00 50.00 bacau botosani galati iasi neamt suceava vaslui vrancea c figure 4 the incidence of parkinson’s disease calculated for the counties of moldavia for the year a 2007, b 2008 şi c 2009 2.24 0.45 3.95 0.98 0.35 0.97 0.80 13.87 0.00 2.00 4.00 6.00 8.00 10.00 12.00 14.00 16.00 bacau botosani galati iasi neamt suceava vaslui vrancea a 0.56 3.60 1.99 0.98 1.44 2.58 0.00 0.00 0.00 0.50 1.00 1.50 2.00 2.50 3.00 3.50 4.00 bacau botosani galati iasi neamt suceava vaslui vrancea b 1.69 3.63 2.33 1.47 1.44 1.15 0.44 1.04 0.00 0.50 1.00 1.50 2.00 2.50 3.00 3.50 4.00 bacau botosani galati iasi neamt suceava vaslui vrancea c figure 5 the incidence of the parkinsonian syndrome calculated for the counties of moldavia for the year a 2007, b 2008 şi c 2009 romanian neurosurgery (2011) xviii 3: 300 – 305 303 discussions the management of parkinson’s disease, one of the well-known neurodegenerative disorders (more than 1 million americans aged over 60 suffer from the disease (1)), the second only after alzheimer, has become a true challenge of the present times (14). it involves several stages as anamnesis, diagnosis, decision over the treatment and treatment administration and the identification and monitoring of results. 20% of 1 million persons suffering from parkinson’s disease in the united states of america do not present any of the classical signs of the disease, such as the resting tremor. that is why this aspect has determined over the years the false diagnosis of parkinson’s disease. for example, the essential tremor has been many times confounded with parkinsontype tremor. nevertheless, clinical studies (6) showed that the symptom that best describes this type of medical disorder is the resting tremor, the response asymmetry of one part in relation to the other and a good response to levodopa. this type of differential diagnosis is however not absolute. there are several parkinsonian symptoms. primary parkinsonism or parkinson’s disease is characterized by tremor, bradykinesia, stiffness and postural instability and from a pathological point of view, by losses of pigmented neurons of the black substance and eosinophilic cytoplasmic inclusions (lewy bodies). nevertheless, parkinsonism may be produced by injuries of basal ganglia in cerebrovascular diseases, infections and toxins, also known as secondary parkinsonism. as the images shows, the most cases are identified on the range of 65+, an important number occurs on the range of 15+64 years old and very few cases bellow 15 years old. most of the romanian population is squeezed on the range of 1564. if we correlate the numbers, it seems that the number of cases is important enough comparing the population age and ranges. the thing is that the high technology and opportunity of treatments increase these numbers also and this disease, if not yet, will become a problem of public health. that’s why, the preventive approach impose the early diagnostics of such medical condition. it is less costly to prevent than to treat. the thing is that the parkinson managements at this moment are quite limited for us. either we do not have enough data from the field or not affordable procedures are available. for the last about 30 years, levodopa was the most used efficient treatment. in spite of the very good results on the short time basis, the long term can add more issues on the patient. the motors symptoms could escalate. the neurosurgery using brain stimulators is an alternative for some patients (about 5%). using invasive procedures, certain brain areas are stimulated using electrodes. these electrodes are connected by cables to a controlling and processing box under the clavicle. this technique is quite efficient on managing the tremors, the rigidity and movement parkinson related disorders. there are restrictions though. this procedure cannot be proposed to the patients suffering of this illness for more than 5 years and can be applied only to those without neurological complications. if the age is not a selection item, the general health status must be pretty good. conclusions 1. parkinson’s disease is nowadays a complex medical disorder which does not 304 liliana cucoş et al epidemiological issues related to parkinson’s disease involve only problems related to the voluntary motor system, but it is also associated with non-motor and neuronal manifestations. due to this fact, aprroaching the disease over the past years evolved from the simple treatment to the management of the whole process of identification, control and monitoring. 2. the cost-related problems involved by the numerous medical disorders which society has to manage, require an approach which is superior to the classical allopathic approach according to which a disorder had a solution which could be solved. the diseases became complex or better said, in order to understand them better, interand multidisciplinarity are absolutely necessary. owing to this, the solutions evolved as well, from the simple curative drugs to the medical procedures for treatment, for the systemic approach of the disorders. the solutions are in their turn interand multidisciplinary. the aim of simply treating the disease evolved from the simple “recovery” to the improvement in the quality of life which, most of the time, becomes the main objective. the personal objective is that related to the quality of life while the social objective is that of minimizing the social impact of the individual on the society and that of the society on the individual. the relation is mainly a cost-related and efficiency-based relation. 3. the reported epidemiological data regarding parkinson’s disease and the parkinsonian syndrome point out a considerable incidence which should determine us to search for methods and models for the management of casuistry (8). an important issue is that case reporting is very much related to the specialist physician who diagnoses a case and especially to the preventive education of the patient who should see a doctor when the symptoms begin to manifest and not do this at a great distance in time when these symptoms lead to the patient’s immobility. even more so, considering the present economic situation due to the economic crisis we are passing through and whose duration we do not know, the early identification with the purpose of carrying out procedures for the management of the disease at the early stage, would save many resources and would relieve the system of health insurances as well as the system of social security of additional expenses. the model primarily used by patients is that of seeing the doctor when the medical disorders overwhelm them and prevent them from carrying out the daily activities. therefore, they get into a situation in which they are brought as medical urgencies to the hospital where the costs of recovery, treatment and monitoring are much higher than a process of prevention previously peformed would have involved. the reported casuistry for our country determines us to identify methods for raising the patients’ awareness to see the doctor in due time in order to maximize the therapeutic approach. correspondence author: cătălin iov e-mail: iovcatalin@yahoo.com references 1. brownlee h.j., parkinson disease in primary practice: keys to diagnosis and management, in consultant suppl., pp. s1-s7, september, 2008 2. chen j.j., lew m.f., siderowf a., treatment strategies and quality-of-care indicators for patients with parkinson’s disease, supplement to journal of managed care pharmacy, jmcp, vol. 15, no. 3, pp. s2-s19, april, 2009 3. cutson t.m., cotter laub k., schenkman m., pharmacological and nonpharmacological romanian neurosurgery (2011) xviii 3: 300 – 305 305 interventions in the treatment of parkinson's disease, physical therapy, vol. 75, no. 5, pp. 363-373, may, 1995 4. hagestuen r., wichmann r.l., johnson m.l., parkinson’s disease symptom management: an interdisciplinary approach, chapter 25 in rajesh pahwa, kelly e. lyons, william c. koller (eds.): handbook of parkinson’s disease, third edition, marcel deckker, inc., publishing house, isbn: 0-8247-4242-7, 2003 5. hanson m.r., gálvez-jiménez n., catechol-omethyltransferase inhibitors in the management of parkinson’s disease, seminars in neurology, vol. 21, no. 1, 2001 6. horstink m., tolosa e., bonuccelli u., deuschl g., friedman a., kanovsky p., larsen j. p., lees a., oertel w., poewe w., rascol o., sampaio c., review of the therapeutic management of parkinson’s disease. report of a joint task force of the european federation of neurological societies and the movement disorder society–european section. part i: early (uncomplicated) parkinson’s disease, european journal of neurology, 13: 1170–1185, 2006 7. keus s.h.j., hendriks h.j.m., bloem b.r., brederocohen a.b., de goede c.j.t., van haaren m., jaspers m., kamsma y.p.t., westra j., de wolff b.y., munneke m., clinical practice guidelines for physical therapy in patients with parkinson’s disease, in supplement to the dutch journal of physical therapy parkinson's disease, kngf guidelines for physical therapy in patients with parkinson's disease, vol. 114, issue 3, 5-53, 2004 8. lang a. e., lees a., editorial management of parkinson’s disease: an evidence-based review, movement disorders, vol. 17, suppl. 4, 2002 9. morley j.f., hurtig h.i., current understanding and management of parkinson disease, five new things, neurology clinical practice, 75(suppl 1):s9–s15, 2010 10. nutt j.g., wooten g.f., diagnosis and initial management of parkinson’s disease, n engl j med, 353, 10, 10211027, september, 8, 2005 11. parkinson’s disease diagnosis and management in primary and secondary care, nice clinical guideline 35, developed by the national collaborating centre for chronic conditions, june 2006 12. poewe w., gauthier s., aarsland d., leverenz j. b., barone p., weintraub d., tolosa e., dubois b., diagnosis and management of parkinson’s disease dementia, j clin pract, october, 62, 10, 1581–1587, 2008 13. rascol o., goetz c., koller w., poewe w., sampaio c., treatment interventions for parkinson’s disease: an evidence based assessment, lancet, 359: 1589–98, 2002 14. robinson r., parkinson’s disease, chapter in chamberlin s.l., brigham n. (eds.), the gale encyclopedia of neurological disorders, 646-651, 2005 microsoft word 5ciureaav_medulloblastoma.doc romanian neurosurgery (2010) xvii 3: 291 – 303 291 medulloblastoma – an overview a.v. ciurea, claudiu palade 1st neurosurgery clinic ,“bagdasar-arseni” emergency hospital abstract the authors intend to present in this paper the most actual trends and perspectives in the challenging field of medulloblastoma multimodal treatment. the data collected from the medical literature and augmented with personal experience, outline a scientifical and pragmatic conduct of medical thinking and action. the epidemiology, clinical presentation, neuroimaging modalities, pathology and therapy (surgical, xrt and chemotherapy) regardind this medical issue are thoroughly glanced and outlined. epidemiology medulloblastoma is a malignant and invasive embryonal tumor of the cerebellum, corresponding histologically to world health organization (who) grade iv, that has sometimes been referred to as an infratentorial primitive neuroectodermal tumor, or pnet. [21] although medulloblastoma is the most common histologic type of malignant central nervous system (cns) tumor in childhood (0 to 19 years), accounting for 17.2% of these tumors, they account for only 0.7% of all malignant cns tumors in adults (age ≥20). the incidence of this tumor steadily decreases with increasing age after a peak occurrence at age 6. it is estimated that only 29% of medulloblastomas occur in patients age 20 or older. this tumor rarely occurs after the age of 50. sixtytwo percent of patients are male (61% age <20 and 63% age≥20). important clinical features the clinical presentation of posterior fossa tumors is similar in adults and children, and many signs and symptoms are related to hydrocephalus caused by obstruction of cerebrospinal fluid (csf) flow by the tumor. early in the course of disease, complaints of nonspecific headache, fatigue, slight imbalance, and personality changes may occur. as the disease progresses, signs and symptoms of increased intracranial pressure predominate, especially headache. these headaches are usually present on awakening in the morning and improve or resolve after rising and as the day progresses. headaches may become persistent if the tumor is not diagnosed and treated. nausea and vomiting are also common. sixth cranial nerve palsies and diplopia, caused by increased intracranial pressure, are not uncommon. focal neurologic deficits caused by pressure on or infiltration of the brainstem, cranial nerves, or cerebellar structures also occur. dizziness or other cerebellar dysfunction occurs in most patients, and the pattern of deficits is related to the location of tumor in the posterior fossa. lesions occurring in the midline are likely 292 a.v. ciurea, claudiu palade medulloblastoma – an overview to cause truncal and gait ataxia, whereas limb ataxia is more common in lesions involving the lateral cerebellar hemispheres. other focal neurologic deficits such as hemiparesis, hearing loss, and seventh cranial nerve palsies occur less often. seizures are rarely seen in children or adults with pf tumors unless extension into the supratentorial cortex occurs. alterations of consciousness may occur late in the course of the disease. hemorrhage into the pf mass may cause acute loss of consciousness and coma. neuroimaging because of its exquisite contrast resolution, mri is the imaging modality of choice in the preoperative work-up for infratentorial tumors and for the evaluation of leptomeningeal metastasis. once medulloblastoma is suspected on imaging or confirmed cytologically or pathologically, mri of the brain and entire spine before and after administration of gadolinium contrast becomes necessary. the goal of this imaging is to determine whether there are demonstrable metastases in the craniospinal axis because of the significant impact these metastases have on management and prognosis.[2,28,38] figure 1 preoperative mri aspect –axial incidence (personal case) figure 2 preoperative mri aspect – sagital incidence (personal case) it is estimated that approximately one half of adult patients with medulloblastoma have their tumors originate peripherally in the cerebellum (paramedian and lateral locations). on rare occasions, a medulloblastoma presents as an exclusively extra-axial mass in the cerebellopontine angle and may be mistaken for a meningioma or vestibular schwannoma on computed tomography (ct) and mri scans.[2,38] adult medulloblastoma is typically heterogeneous on ct and can appear hypodense or hyperdense to gray matter and have variable patterns of enhancement.[2,6] the more common peripheral tumors are poorly enhanced with contrast, whereas the less common vermian central tumors tend to be intensely enhanced with contrast. on mri, tumors show hypointense signal on t1 and hyperintense signal on t2 weighted images. contrast-enhanced t1 sequences best demonstrate the heterogeneity of these tumors. small cysts are commonly encountered in the peripheral tumors, whereas a predominantly cystic medulloblastoma is rare.[6,34,38] melanotic medulloblastoma is a rare form of medulloblastoma that can potentially demonstrate high t1 signal on romanian neurosurgery (2010) xvii 3: 291 – 303 293 the unenhanced t1 sequences.[22,60] this high signal can suggest or be confused with hemorrhage. a rare entity in the adult literature, “lipidized” or “lipomatous” medulloblastoma has been provisionally reclassified by who as cerebellar liponeurocytoma (9506/1) and can also demonstrate high signal on unenhanced t1 sequences. mri of the brain and spine is useful in assessing response to treatment, stability, tumor progression, and metastatic disease. mri of the entire spine with and without gadolinium contrast enhancement has become the study of choice for evaluating drop metastases. pathological aspects the gross appearance and histology of medulloblastoma occurring in adults overlap substantially with the features of pediatric medulloblastoma. the histology includes the five principal patterns: 1) undifferentiated or classic medulloblastoma, 2) desmoplastic nodular medulloblastoma, 3) medulloblastoma with neuroblastic or neuronal differentiation, 4) large cell or anaplastic medulloblastoma, 5) medulloblastoma with glial differentiation.[7,21] the other variant forms such as: 6) medullomyoblastoma and 7) melanotic medulloblastoma are rare in the adult population, [44,57] and they are the forms containing more heterogeneous differentiation. undifferentiated or “classic” medulloblastoma, consisting of patternless masses of monotonous small cells, comprises the majority of medulloblastomas in both adult and pediatric groups. figure 3 microscopic aspect of a medulloblastoma specimen (he stain) evidence of neuronal differentiation by hematoxylin and eosin (h&e) staining in some cases includes the formation of neuroblastic rosettes and, occasionally, the presence of ganglion cells. despite the common lack of evidence of differentiation by routine h&e staining, evidence of neuronal differentiation may be demonstrable by immunohistochemical staining for synaptophysin or other neuronal markers or by the electron microscopic demonstration of neurites, synaptic structures, or neurosecretory granules. the findings of necrosis, apoptosis, calcification, infiltrative behavior, intratumoral hemorrhage, and tumor extension into the overlying leptomeninges occur in both pediatric and adult cases. the nodular or desmoplastic variety, defined by the presence of prominent nodules or “pale islands” of tumor of lower cellularity in a background of collagen-rich, highly proliferative tumor, occurs more often in the older population.[1,23,33,45,56] a rare variant medulloblastoma with extensive nodularity and neuronal differentiation associated with a more favorable prognosis is more common in the pediatric population.[17,24] 294 a.v. ciurea, claudiu palade medulloblastoma – an overview medulloblastoma with neuroblastic or neuronal differentiation characterized by extensive nodularity and differentiation toward neurocytes or ganglion cells and referred to by some authors as “cerebellar neuroblastoma,” is an uncommon variant and occurs primarily in infants and very young children. large cell or anaplastic medulloblastoma, characterized by populations of larger, more pleomorphic tumor cells than those in classic medulloblastoma, is also an uncommon variant occurring predominantly in the pediatric population and is often associated with an unfavorable outcome. [16,25] glial rather than neuronal differentiation in medulloblastoma has been reported in up to one third of cases of medulloblastoma occurring in older individuals. mature glial cells, identified by the presence of eosinophilic cytoplasm and cell processes, may be difficult to identify in h&e-stained sections. by immunohistochemical staining for glial fibrillary acidic protein (gfap), immunoreactive fibrillated cells can be identified in most pediatric [11] and adult medulloblastomas, typically in a perivascular location or at the periphery of the tumor. although such cells have commonly been considered entrapped reactive astrocytes rather than tumor cells, similar cells have been observed in metastatic medulloblastoma in nonbrain sites, suggesting that they are actually tumor cells. glial differentiation in tumor cells, usually defined by the finding of glial fibrillary acidic protein-immunoreactivity in the perikaryon or short cell processes of cells with distinctively neoplastic nuclear features, has been described in a small percentage of medulloblastomas, particularly in the adult population. gfapimmunoreactive cells have also been noted within the nodules and in the internodular tumor cell population of desmoplastic nodular medulloblastomas. studies investigating the prognostic significance of glial differentiation have yielded contradictory results.[11,29,35] in the pediatric population, suggestions of correlations between genetic markers and prognosis such as cytogenetic studies of chromosome 17 and others, p53 overexpression, studies of erbb2 receptors, high trkc receptor expression, amplification of myc, and abnormalities in the sonic hedgehog (shh)–ptch pathway have been noted, with the best correlations occurring in the large cell– anaplastic variant.[17,42,65] in adult medulloblastoma, a recent study correlated overexpression of mdm2 with shorter survival. [27,28] more recently, cdna-based geneexpression profiling has demonstrated that medulloblastomas are distinct from primitive neuroectodermal tumors and that the “classic” and desmoplastic subtypes are distinct.[54] these studies confirmed earlier observations about high trkc receptor expression and amplification of myc. these studies have also strongly supported the hypothesis that medulloblastomas are derived from cerebellar granular cells through the activation of the shh pathway and suggested various novel prognostic markers related to shh pathway activation. however, more extensive investigation will need to be carried out to verify the utility of the various genetic and molecular markers in assessing prognosis, especially in the forms of medulloblastoma more commonly encountered in the adult population such as romanian neurosurgery (2010) xvii 3: 291 – 303 295 desmoplastic nodular medulloblastoma. furthermore, a parallel between pediatric and adult tumors cannot be assumed. tumor staging the chang staging system , which was published in 1969, evaluates tumor size, local extension, and the presence or absence of metastases.[10] the tumor (t) staging portion of the staging system may no longer have the same prognostic value that it once had. several pediatric studies have shown that the amount of residual disease, age, and m stage are more predictive of outcome than t stage.[39,66] it was initially based on the surgeon’s intraoperative observations; however, in the modern era of neuroimaging, preoperative and postoperative scans provide similar if not better information. chang staging system for metastasis (m staging portion) stage definition m0 no evidence of gross subarachnoid or hematogenous metastasis m1 microscopic tumor cells found in cerebrospinal fluid m2 gross nodular seedings demonstrated in the cerebellar, cerebral subarachnoid space, or in the third or lateral ventricles m3 gross nodular seeding in spinal subarachnoid space m4 extraneuroaxial metastasis the chang metastasis (m) stage (m0 denotes local disease only, m1 denotes positive csf cytology, m2 denotes tumor present beyond the primary site but within the brain, m3 denotes gross nodular seeding in the spinal subarachnoid space, and m4 denotes extracranial spread) has consistently been related to outcome in pediatric studies, although this is less clear in adult series. evaluation for the purpose of staging includes preoperative mri scans of the cranial vault and entire spine. csf sampling should be performed before surgery or 10 to 14 days postoperatively to avoid a false positive related to surgery. postoperative mri scans of the brain should be obtained within 24 to 48 hours after resection to minimize postoperative imaging changes and accurately evaluate the extent of resection. if a preoperative mri scan of the spine was not performed, it should be performed 2 weeks after surgical resection to allow for resolution of postoperative blood and protein artifacts that may be misinterpreted as metastatic tumor. over the past 10 to 15 years, sequential studies carried out by the children’s cancer group (ccg) and the pediatric oncology group (pog)[18,19,49,51] have revealed two risk categories defined by age, extent of surgical resection, and m stage. patients are considered to be average or standard risk if they are older than 3 years, have no more than 1.5 cm2 of residual tumor after surgical resection, and have no csf or spinal involvement (m0).(66) all other pediatric medulloblastoma patients are considered to be poor or high risk. although recent data suggest that a histologic variant showing moderate to severe anaplasia may have an adverse prognosis in pediatric tumors,16 this and other possible genetic and histopathologic prognostic variables have not yet been used in prospective risk categorization, and need to be verified in other studies.[17,27,28,42,65] 296 a.v. ciurea, claudiu palade medulloblastoma – an overview surgical treatment surgery plays an integral and important role in the management of adults with medulloblastoma. the goals of surgical therapy are threefold: histologic diagnosis, maximal safe tumor resection, and restoration of patency of csf pathways. because medulloblastomas commonly present with some degree of hydrocephalus, the first surgical decision often pertains to management of this condition. tumor resection alleviates hydrocephalus in up to 90% of patients in most modern series,[63] and avoids shunt-related complications such as upward herniation of the brainstem, intratumoral hemorrhage, and csf dissemination. thus prompt, definitive surgical resection with use of steroids to control edema is preferred to a staged approach of shunting followed by resection. if steroids fail or urgent ventricular drainage is required, a nondominant ventriculostomy is preferred over a shunt, because it allows more precise control of intracranial pressure and drainage. care should be taken to measure opening pressure and drain slowly at 20 cm of csf or higher, and resection should be accomplished promptly. numerous studies have demonstrated the relationship between extent of resection and prognosis [41]; thus optimization of the surgical procedure is critical. this is achieved in part by meticulous preoperative preparation and by using stereotactic computer-aided navigation (can) tools, intraoperative ultrasound, and in some cases, brainstem evoked-potential monitoring. figure 4 patient positioning (prone position) – routinely used by the senior author surgery is more often performed with patients prone to avoid the risk of air embolism and subdural hematoma associated with sitting. the patient is managed preoperatively with antibiotics, corticosteroids, mannitol, and moderate hyperventilation. a ventriculostomy is usually performed at the time of surgery if it has not already been performed and is managed as noted previously. after a generous craniotomy or craniectomy centered over the tumor, the cisterna magna is opened to drain csf. although invasive, the tumor usually is surrounded by a pseudocapsule facilitating identification and removal from the surrounding brain. can and ultrasound are also helpful in this regard. using microsurgical techniques, the tumor is internally debulked using an ultrasonic aspirator and a self-retaining retractor to minimize cerebellar retraction. the surgeon must anticipate the location of critical structures such as the posterior inferior cerebellar artery, inferior vermian veins, cranial nerves (in the case of laterally romanian neurosurgery (2010) xvii 3: 291 – 303 297 placed tumors), the dentate nuclei, the cerebellar peduncles, and the floor of the fourth ventricle. often, the tumor can be gently peeled from these structures without damaging the pial membrane. the surgeon places cottonoids along the cisterna magna and along the roof and floor of the fourth ventricle to prevent iatrogenic dissemination of tumor along csf pathways as these structures are exposed. invasive tumor is aggressively resected from the cerebellum and, if required, a single cerebellar peduncle. however, aggressive resection of tumor invading the floor of the fourth ventricle or the second cerebellar peduncle is avoided to reduce unacceptable postoperative morbidity. after as complete a gross resection consistent with good neurologic function has been achieved, the resection cavity is reinspected using microscopic magnification, can, and ultrasound to identify and then resect any residual tumor, cerebellar hematoma, or retraction injury. meticulous hemostasis minimizes postoperative nausea, vomiting, and hydrocephalus. a watertight closure of the dura is performed using tisseal or fibrin glue to avoid csf leak, pseudomeningocele, and chemical meningitis. postoperatively, the ventriculostomy is drained until the blood clears, and then the patient weaned from ventricular drainage if possible. postoperative mri with and without contrast is done within 48 hours postoperatively, both as a baseline and to assess extent of resection. mri of the spinal axis should be performed approximately 2 weeks after surgery if it has not been done preoperatively. (figure 5-personal case) figure 5 (postoperative aspectct scan same personal case shown in fig 1&2) if significant resectable residual neoplasm is seen or the patient requires a ventriculoperitoneal shunt, prompt reoperation is indicated to avoid delay of postoperative radiation therapy and chemotherapy. operative mortality should be well under 1%; morbidity is 5% to 10% in most series.[41] most common complications are transient, including ataxia, nystagmus, and dysmetria. cranial nerve palsies are related to manipulation along the floor of the fourth ventricle. cerebellar mutism may also be induced by damage to the dentate nuclei. it is advisable to wait 10 to 14 days after surgery before beginning radiation therapy to ensure adequate wound healing and minimize the possibility of wound dehiscence. radiation therapy when radiation therapy is used in newly diagnosed patients, the standard dose delivered to the craniospinal axis is 35 to 36 gy if patients have no evidence of neuraxis dissemination (m0). the pf is then boosted for an additional 18 to 20 gy so that the total dose to the pf is approximately 54 to 56 gy. if csf cytology is positive (m1), the recommended dose to 298 a.v. ciurea, claudiu palade medulloblastoma – an overview the csa according to the pediatric experience is still only 36 gy. if nodular disease in the subarachnoid space (m2 or m3) is present, a boost is delivered immediately following csi to the site of the original metastatic disease (m2 to m3) up to a total dose of 45 gy. the fractionation scheme used most often is 1.8 gy daily, 5 days per week. the current standard therapy is to boost the entire pf to a total dose of 54 to 55.8 gy at a fractionation of 1.8 gy per day using high-energy photons (x-rays). there are no convincing data that administering higher doses to the pf by conventional fractionation or hyperfractionated treatment schedules improves outcomes,[55] although boosting residual disease with a stereotactic radiosurgical boost has shown promise in a limited number of patients.[52,64] the duration of radiation therapy may also influence outcomes. taylor et al[61] showed a statistically significant reduction in overall survival and efs if the time from the first radiation treatment to the last radiation treatment was more than 50 days. in this study, there was no difference in the mean or median duration of radiation therapy between those patients treated with radiation therapy alone and those treated with chemotherapy followed by irradiation. it is advisable to complete radiation therapy without breaks. complications associated with radiation therapy can be divided into two time frames: acute effects occurring during or shortly after treatment, and late effects occurring months to years after completion of treatment. acute side effects in adults are usually more pronounced than in children and consist of nausea, vomiting, fatigue, alopecia, skin erythema, significant bone marrow suppression, soreness in the back of the throat with resultant dysphagia, transient loss of taste, transient xerostomia, and occasionally wound dehiscence (usually when there is not an adequate 10to 14-day interval between surgery and initiation of radiation therapy). late effects are generally less prominent in adults than in children and include potential pituitary dysfunction, possible infertility, effects on cognition, and possible induction of second malignancies. although the neurocognitive effects in treated adults have not been studied as extensively as in children, there are data to suggest that cranial doses of 30 to 36 gy may have an impact on cognitive function in survivors, especially on memory, reasoning, visualspatial ability, and arithmetic calculation skills.[40] chemotherapy the usefulness of chemotherapy has been established in the pediatric medulloblastoma population. however, for adults with medulloblastoma, the role of chemotherapy is not yet established. the most commonly used regimen is the packer regimen, which consists of weekly vincristine during csi and eight cycles of ccnu, cisplatin, and vincristine (ccv) after csi for children with medulloblastoma. this has become the standard against which all other chemotherapy regimens are measured.[49] there has not been a preradiation chemotherapy combination used in a randomized trial that has shown better efficacy as measured by overall survival or progression-free survival, although a recently reported study by taylor et al describes efs at 5 years that is comparable. [61] romanian neurosurgery (2010) xvii 3: 291 – 303 299 the most notable dose-limiting side effects of this ccv-chemotherapy combination are peripheral neuropathy, hearing loss, renal insufficiency, and myelosuppression. as with most chemotherapy regimens, occasional patients succumb to overwhelming infection. less serious side effects include nausea, vomiting, constipation, obstipation, and elevated transaminases. hundreds of children have been treated with this combination, but there is little in the literature to describe the tolerance that adults have to the same combination. whereas the thrust of recent pediatric trials has been to add chemotherapy to decrease the dose of craniospinal axis radiation and thereby decrease the harmful effects of radiation on neurocognitive and endocrine function such as low full-scale intelligence quotients (iqs) and short stature, there has not been a comparable effort in treating adults for several reasons. these reasons include the fact that there is an approximate 60% 5-year progression-free survival rate with surgery and csi alone [8] a belief that there is less harm to giving standard radiation doses to adults than children, and a less convincing case for a survival benefit to receiving chemotherapy as part of initial therapy. as a result, there is a perception among many clinicians that one can safely rely more on radiation and omit chemotherapy. however, there has been little formal investigation of neuropsychologic sequelae in adults who are long-term survivors of medulloblastoma. in the largest series of adult patients reported to date, a retrospective analysis involving 156 patients treated at 13 institutions in france, carrie et al concluded that 5and 10-year efs rates of 61% and 48%, respectively, were similar to those observed in children. their ultimate conclusion was that radiation therapy at the usual dose without chemotherapy should be considered the standard postoperative treatment in adults with medulloblastoma. greenberg et al [30] retrospectively analyzed a group of adults diagnosed between 1991 and 1997 who were treated at one of three institutions with chemotherapy consisting of the packer regimen51 or a pog protocol consisting of preradiation chemotherapy with cycles of cisplatin and etoposide alternating with cyclophosphamide and vincristine15 followed by csi. there is agreement among those who have written about the management and treatment of medulloblastoma in adults that patients should have maximal safe tumor resection followed by csi. the role of and type of chemotherapy that should be employed and when it should be used remains less clear. most neuro-oncologists would agree that patients with poor-risk medulloblastoma should also be treated with chemotherapy as part of initial therapy, but there is not agreement about its use in average-risk patients. there is a suggestion that combinations of cyclophosphamide or ifosfamide plus carboplatin or cisplatin plus vincristine with or without etoposide may be as effective and less toxic to adults than the packer ccv regimen. clinical trials in the adult population would help clarify the role of chemotherapy, especially in patients with average-risk disease. 300 a.v. ciurea, claudiu palade medulloblastoma – an overview outcome the ability to categorize patients by risk factors has led to specific tailoring of treatment for the pediatric population,[66] and it is against these results that adult studies need to be compared. since the initial encouraging reports describing the use of combination chemotherapy and reduced-dose radiation therapy by packer et al [51] in the early 1990s, this approach has become the standard of care at most pediatric institutions. in 1999, packer et al [49] reported the results of a ccg study using a reduced craniospinal dose (23.4 gy) of irradiation given with weekly vincristine followed by chemotherapy consisting of ccnu, vincristine, and cisplatin for eight cycles following csi for average-risk patients between the ages of 3 and 10 years. the total dose to the pf remained at 55.8 gy. the progression-free survival rates were 86% at 3 years and 79% at 5 years, which were more favorable than historical comparisons from previous ccg or pog studies. in 2003, taylor et al [61] reported the results of a european prospective randomized trial in which pediatric patients with m0 and m1 disease were randomized to radiation therapy alone versus preradiation therapy chemotherapy with vincristine, etoposide, carboplatin, and cyclophosphamide. the radiation therapy consisted of 35 gy csi in 1.67 gy daily fractions followed by a pf boost of 20 gy for a total pf dose of 55 gy in both treatment arms. the efs was superior in the patients who received preradiation chemotherapy, with efs at 5 years of 74% versus 59.8% in the patients who received radiation therapy alone. improvements in imaging modalities, surgical techniques, and the precision of radiation therapy delivery, as well as the addition of systemic chemotherapy over the past 2 decades, have contributed to the increased overall survival in pediatric series. it is more difficult to assess improvement in the outcome of adults with medulloblastoma because of the paucity of patients and lack of prospective or randomized adult trials. it is most likely that the improvement in survival of these groups is related most to the improvements in surgical techniques, radiation therapy, and imaging and probably less to the improvements in the addition of chemotherapy, at least in the adult population. conclusions medulloblastoma represent an important therapeutical problem of pediatric neurosurgical pathology. mri of the head and spine represent an efficient and early diagnostic procedure. there is a high probability of csf dissemination in medulloblastoma natural history. the autors emphasize the role of the multimodal therapy. severe prognosis is expected in this condition overall survival ranges from 25% to 84% at 5 years with 10-year survival rates ranging from 35.6% to 51%. [44,45,46] correspondence to: rsneurosurgery@gmail.com claudiu_palade@yahoo.com references 1. abacioglu u, uzel o, sengoz m, et al: medulloblastoma in adults: treatment results and prognostic factors. int j radiat oncol biol 54:855–860, 2002. romanian neurosurgery (2010) xvii 3: 291 – 303 301 2. becker rl, backer ad, sobel df: adult medulloblastoma: review of 13 cases with emphasis on mri. neuroradiology 37:104–108, 1995. 3. berman dm, karhadkar ss, hallahan ar, et al: medulloblastoma growth inhibition by hedgehog pathway blockade. science, 297:1559–1561, 2002. 4. bloom hjg, wallace mb, henk jm: the treatment and prognosis of medulloblastoma in children: a study of 82 verified cases. am j roentgenol rad ther nucl med 105:43–62, 1969. 5. bourgouin pm, tampieri d, grahovac sz, et al: ct and mr imaging findings in adults with cerebellar medulloblastoma: comparison with findings in children. am j radiol 159:609–612, 1992. 6. burger pc, scheithauer bw, vogel fs: surgical pathology of the nervous system and its coverings. new york, churchill livingstone, 2002. 7. carrie c, lasset c, alapetite c, et al: multivariate analysis of prognostic factors in adult patients with medulloblastoma. cancer 74:2352–2360, 1994. 8. chan aw, tarbell nj, black pm, et al: adult medulloblastoma: prognostic factors and patterns of relapse. neurosurgery, 47:623–632, 2000. 9.. chang ch, housepain em, herbert cj: an operative staging system and a megavoltage radiotherapeutic technic for cerebellar medulloblastomas. radiology 93:1351–1359, 1969. 10. ciurea av: medulloblastomas in ciurea av: treatise of neurosurgery (eds), medical publishers house, bucharest, 2010 11. ciurea av, constantinovici a: medulloblastoma in practical handbook of neurosurgery, medical publishers house, bucharest, 1998 12. coffin cm, mukai k, dehner lp: glial differentiation in medulloblastomas. am j pathol 7:555–565, 1983. 13. cushing h: experience with the cerebellar medulloblastomas. acta pathol microbiol scand 7:1– 86, 1930. 14. cutler ec, sosman mc, vaughan ww: the place of radiation in the treatment of cerebellar medulloblastomata. am j roentgenol rad ther nucl med 35:429–445, 1939. 15. douglas jg, barker jl, ellenbogen rg, geyer jr: concurrent chemotherapy and reduced-dose cranial spinal irradiation followed by conformal posterior fossa tumor bed boost for averagerisk medulloblastoma: efficacy and patterns of failure. int j radiat oncol biol phys 58:1161–1164, 2004. 16. duetsch m, thomas prm, krischer j: results of a prospective randomized trial comparing standard dose neuraxis irradiation (3,600 cgy/20) with reduced neuraxis irradiation (2,340 cgy/13) in patients with lowstage medulloblastoma. pediatr neurosurg 24:167–177, 1996. 17. duffner pk, horowitz me, krischer jp, et al: postoperative chemotherapy and delayed radiation in children less than three years of age with malignant brain tumors. n engl j med 328:1725–1731, 1993. 18. eberhart cg, kepner jl, goldthwaite pt, et al: histopathologic grading of medulloblastoma. cancer 94:552–560, 2002. 19. ellison d: classifying the medulloblastoma: insights from morphology and molecular genetics. neuropathol appl neurobiol 28:257–282, 2002. 20. evans ae, jenkin rdt, sposto r, et al: the treatment of medulloblastoma. j neurosurg 72:572– 582, 1990. 21. freeman cr, taylor re, kortmann r, et al: radiotherapy for medulloblastoma in children: a perspective on current international clinical research efforts. med pediatric oncology 39:99–108, 2002. 22. frost pj, laperriere nj, shun wong c, et al: medulloblastoma in adults. int j radiat oncol biol phys 32:951–957, 1995. 23. giangaspero f, bigner sh, kleihues p, et al: medulloblastoma. in kleihues p, cavenee wk (eds): pathology and genetics of tumors of the nervous system. lyon, france, iarc press, 2000. 24. giangaspero f, cenacchi g, roncaroli f, et al: medullocytoma (lipidized medulloblastoma). am j surg pathol 20:656–664, 1996. 25. giangaspero f, chieco p, ceccarelli c, et al: “desmoplastic” versus “classic” medulloblastoma: comparison of dna content, histopathology and differentiation. virchow arch 418:207–214, 1991. 26. giangaspero f, perilongo g, fondelli mp, et al: medulloblastoma with extensive nodularity: a variant with favorable prognosis. j neurosurg 91:971–977, 1999. 27. giangaspero f, rigobello l, badiali m, et al: large cell medulloblastoma: a distinct variant with highly aggressive behavior. am j pathol 16:687–693, 1992. 28. gilbertson r, wickramasinghe c, herman r, et al: clinical and molecular stratification of disease risk in medulloblastoma. br j cancer 85:705–712, 2001. 29. giliemorth j, kehler u, knopp u, et al: a multifocal cerebellar and supratentorial medulloblastoma in an adult. acta neurochir (wien) 140:723–724, 1998. 30. giordana mt, duo d, gasverde s, et al: mdm2 overexpression is associated with short survival in adults with medulloblastoma. neuro-oncology 4:115– 122, 2002. 31. giordana mt, schiffer p, lanotte m, et al: epidemiology of adult medulloblastoma. int j cancer 80:689–692, 1999. 32. goldberg-stern h, gadoth n, stern s, et al: the prognostic significance of glial fibrillary acidic protein staining in medulloblastoma. cancer 68:568–573, 1991. 302 a.v. ciurea, claudiu palade medulloblastoma – an overview 33. greenberg hs, chamberlain mc, glantz mj, et al: adult medulloblastoma: multiagent chemotherapy. neuro-oncology 3:29–34, 2001. 34. haie-meder c, song py: medulloblastoma: differences in adults and children—regarding frost et al: ijrobp 32: 951–957; 1995 and prados et al: ijrobp 32:1145–1152; 1995. int j radiat oncol biol phys 32:1255–1257, 1995. 35. hernan r, fasheh r, calabrese c, et al: erbb2 upregulates s100a4 and several other prometastatic genes in medulloblastoma. cancer res 63:140–148, 2003. 36. hubbard jl, scheithauer bw, kispert db, et al: adult cerebellar medulloblastomas: the pathological, radiographic, and clinical disease spectrum. j neurosurg 70:536–544, 1989. 37. hyman ad, lanzieri cf, solodnik p, et al: cystic adult medulloblastoma. ct. j compute tomogr 10:139–143, 1988. 38. janss aj, yachnis at, silber jh, et al: glial differentiation predicts poor clinical outcome in primitive neuroectodermal brain tumors. ann neurol 39:481–489, 1996. 39. katsetos cd, herman mm, frankfurter a, et al: cerebellar desmoplastic medulloblastomas. afurther immunohistochemical characterization of the reticulinfree pale islands. arch pathol lab med 113:1019–1029, 1989. 40. kim jy, sutton me, lu dj, et al: activation of neurotrophin-3 receptor trkc induces apoptosis in medulloblastomas. cancer res 59:711–719, 1999. 41. koci tm, chiang f, mehringer cm, et al: adult cerebellar medulloblastoma: imaging features with emphasis on mr findings. ajnr: am j neuroradiol 14:929–939, 1993. 42. kortmann rd, kuhl j, timmerman b, et al: postoperative neoadjuvant chemotherapy before radiotherapy as compared to immediate radiotherapy followed by maintenance chemotherapy in the treatment of medulloblastoma in childhood: results of the german prospective randomized trial hit 91. int j radiat oncol biol phys 46:269–279, 2000. 43. kramer jh, crowe ab, larson da, et al: neuropsychological sequelae of medulloblastoma in adults. int j radiat oncol biol phys 38:21–26, 1997. 44. kunschner lj, kuttesch j, hess k, et al: survival and recurrence factors in adult medulloblastomas: the md anderson cancer center experience from 1978 to 1998. neuro-oncology 3:167–173, 2001. 45. leonard jr, cai dx, rivet dj, et al: large cell/anaplastic medulloblastomas and medullomyoblastomas: clinicopathological and genetic features. j neurosurg 95:82–88, 2001. 46. macdonald tj, brown km, lafleur b, et al: expression profiling of medulloblastoma: pdgfra and the ras/mapk pathway as therapeutic targets for metastatic disease. nat genet 29:143–152, 2001. 47. mahapatra ak, sinha ak, sharma mc: medullomyoblastoma: a rare cerebellar tumor in children. childs nerv syst 14:312–316, 1998. 48. malheiros sm, franco cm, stavale jn, et al: medulloblastoma in adults: a series from brazil. j neurooncol 60:247–253, 2002. 49. millot f, delval o, giraud c, et al: high-dose chemotherapy with hematopoietic stem cell transplantation in adults with bone marrow relapse of medulloblastoma: report of two cases. bone marrow transplant 24:1347–1349, 1999. 50. moots pl, jennings mt, bowen mg, et al: multiagent chemotherapy followed by craniospinal radiation (csrt) for adults with poor risk medulloblastoma (mbl) and ependymoma with subarachnoid dissemination (d.e.). neurology 50:a380 abstract, 1998. 51. moots pl, o’neill a, barger gr, et al: toxicities associated with chemotherapy followed by craniospinal radiation for adults with poor-risk medulloblastoma/pnet and disseminated ependymoma: a preliminary report of ecog 4397. annual meeting proceedings of the american society of clinical oncology, 23(abst 1573):125, 2004. 52. newton hb: review of the molecular genetics and chemotherapeutic treatment of adult and pediatric medulloblastoma. expert opin investig drugs 10:2089– 2104, 2001. 53. packer rj, goldwein j, nicholson hs, et al: treatment of children with medulloblastomas with reduced-dose craniospinal radiation therapy and adjuvant chemotherapy: a children’s cancer group study. j clin oncol 17:2127–2136, 1999. 54. packer rj, sutton ln, elterman r, et al: outcome for children with medulloblastoma treated with radiation and cisplatin, ccnu, and vincristine chemotherapy. j neurosurg 81:690–698, 1994. 55. packer rj, sutton ln, goldwein jw, et al: improved survival with the use of adjuvant chemotherapy in the treatment of medulloblastoma. j neurosurg 74:433–440, 1991. 56. patrice sj, tarbell nj, goumnerova lc, et al: results of radiosurgery in the management of recurrent and residual medulloblastoma. pediatr neurosurg 22:197–203, 1995. 57. peterson k, walker rw: medulloblastoma/primitive neuroectodermal tumor in 45 adults. neurology 45:440–442, 1995. 58. pomeroy sl, tamayo p, gassenbeek m, et al: prediction of central nervous system embryonal tumor outcome based on gene expression. nature 415:436– 442, 2002. romanian neurosurgery (2010) xvii 3: 291 – 303 303 59. prados md, edwards ms, chang sm, et al: hyperfractionated craniospinal radiation therapy for primitive neuroectodermal tumors: results of a phase ii study. int j radiat oncol biol phys 43:279–285, 1999. 60. prados md, warnick re, wara wm, et al: medulloblastoma in adults. int j radiat oncol biol phys 32:1145–1152, 1995. 61. ramsay da, bonnin j, macdonald dr, et al: medulloblastomas in late middle age and the elderly: report of 2 cases. clin neuropathol 14:337–342, 1995. 62. rao c, friedlander me, klein e, et al: medullomyoblastoma: a population-based study of 532 cases. cancer 65:157–163, 1990. 63. sarkar c, pramanik p, karak ak, et al: are childhood and adult medulloblastomas different? a comparative study of clinicopathological features, proliferation index, and apoptotic index. j neurooncol 59:49–61, 2002. 64. segal ra, goumnerova lc, kwon yk, et al: expression of the neurotrophin receptor trkc is linked to a favorable outcome in medulloblastoma. proc natl acad science usa 91:12867–12871, 1994. 65. soylemezoglu f, soffer d, onol b, et al: lipomatous medulloblastoma in adults. am j surg pathol 20:413–418, 1996. 66. taylor re, bailey cc, robinson k, et al: results of a randomized study of preradiation chemotherapy versus radiotherapy alone for nonmetastatic medulloblastoma: the international society of pediatric oncology/united kingdom children’s cancer study group pnet-3 study. j clin oncol 21:1581–1591, 2003. 67. thomas prm, deutsch m, kepner jl, et al: lowstage medulloblastoma: final analysis of trial comparing standard-dose with reduced-dose neuraxis irradiation. j clin oncol 18:3004–3011, 2000. 68. tomita t, rosenblatt s: management of hydrocephalus secondary to posterior fossa tumors. in matsumoto s, tamaki n (eds): hydrocephalus: pathogenesis and treatment. tokly, springer-verlag, 1991. 69. wolden sl, dunkel ij, souweidane mm, et al: patterns of failure using a conformal radiation therapy tumor bed boost for medulloblastoma. j clin oncol 21:3079–3083, 2003. 70. woo c, baldassarre s, lulu b, et al: the use of stereotactic radiosurgical boost in the treatment of medulloblastoma. int j radiat oncol biol phys 37:761– 764, 1997. 71. woodburn rt, azzarelli b, montebello jf, et al: intense p53 staining is a valuable prognostic indicator for poor prognosis in medulloblastoma/central nervous system primitive neuroectodermal tumors. j neurooncol 52:57–62, 2001. 72. zeltzer pm, boyett jm, finlay jl, et al: metastasis stage, adjuvant treatment, and residual tumor are prognostic factors for medulloblastoma in children: conclusions from the children’s cancer group 921 randomized phase iii study. j clin oncol 17:832–845, 1999. microsoft word 7iencean_preliminary romanian neurosurgery (2013) xx 4: 351 356 351 preliminary results of csf phosphorylated neurofilament subunit nf-h (nfp-h) as biomarkers of acute spinal cord injury st.m. iencean1, d. adam2, didona ungureanu1, al. tascu2, d. cuciureanu1, b. costachescu1, a.st. iencean3, i. poeata1 1“grigore t. popa” university of medicine and pharmacy iasi 2“carol davila” university of medicine and pharmacy bucharest 3neurosurgery iii, emergency hospital “prof. dr. n. oblu” iasi doi: 10.33962/roneuro-2021-091 multimodal neurological monitoring in neurotrauma. theoretical considerations for a practical approach randy reina-rivero, m.m. rodriguez-gutierrez, michael gregorio ortega-sierra, diego fernando jamioy-cabrera, juan felipe villegas-lora, d.m. caycedo-montiel, juan david balanta-perea, richard adrian vergara-trujillo, fernando bellera, yelson alejandro picón -jaimes romanian neurosurgery (2021) xxxv (4): pp. 531-537 doi: 10.33962/roneuro-2021-091 www.journals.lapub.co.uk/index.php/roneurosurgery multimodal neurological monitoring in neurotrauma. theoretical considerations for a practical approach randy reina-rivero1, maria manuela rodriguez-gutierrez2, michael gregorio ortega-sierra3, diego fernando jamioy-cabrera4, juan felipe villegas-lora5, daniela margoth caycedo-montiel6, juan david balanta-perea7, richard adrian vergara-trujillo7, fernando bellera8, yelson alejandro picónjaimes9 1 school of medicine, universidad de cartagena, cartagena, colombia 2 future surgeons chapter, colombian surgery association, bogotá, colombia 3 school of medicine, corporación universitaria rafael nuñez, cartagena, colombia 4 school of medicine, universidad surcolombiana, neiva, colombia 5 school of medicine, universidad del norte, barranquilla, colombia 6 school of medicine, universidad libre, barranquilla, colombia 7 school of medicine, universidad san martin, cali, colombia 8 department of neurosurgery, centro policlinico valencia, la viña, venezuela 9 valencian international university, santiago de chile, chile, colombia abstract multimodal neuromonitoring is used as an adjunct to clinical neurological examination, imaging and other diagnostic studies to obtain the most detailed information about the physiology of the brain. neuromonitoring has been a standard of care for patients presenting with traumatic brain injury in most critical care centres for the past several years. neuromonitoring is composed of multiple variables, which not only provides a better dynamic of the pathophysiology of the compromised brain but also how it might respond to the corresponding management procedures. although the clinical neurological examination is the standard for monitoring the neurocritical patient, the results obtained in the latter may be insufficient or inconclusive to detect or prevent secondary brain injury. therefore, multiple neuromonitoring tools have been developed to measure different physiological variables that can contribute to a better follow-up of patients with traumatic brain injury. these variables include cerebral blood flow, cerebral electrical activity, cerebral keywords intracranial pressure, critical care, traumatic brain injury, multimodality monitoring, cerebral blood flow corresponding author: michael gregorio ortega-sierra medical and surgical research centre, st mary´s medical group, cartagena, colombia mortegas2021@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 532 randy reina-rivero, maria manuela rodriguez-gutierrez, michael gregorio ortega-sierra et al. metabolism, cerebral oxygenation and cerebral pressure. thanks to monitoring as an adjuvant in critical care, it has been possible to avoid, identify and manage secondary brain injuries that commonly aggravate patients. this review aims to illustrate the main advantages and most recent recommendations regarding neuromonitoring based on the most current evidence. introduction the objective of patient management is the identification, prevention and treatment of secondary brain injuries that may aggravate the patient's outcome. understanding the mechanisms of brain injury and its pathophysiology are necessary for an adequate and patient-oriented treatment. as the primary damage, which represents direct mechanical damage, cannot be influenced therapeutically, the goal of treatment is the limitation of secondary damage (delayed non-mechanical damage). it is influenced by changes in cerebral blood flow (hypoand hyperperfusion), impaired cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. at this case, the neuromonitoring multimodal is useful to observe the alterations [1]. in this manuscript we describe the different tools used for multimodal neuromonitoring in traumatic brain injuries patients such as clinical examination, intracranial pressure, autoregulatory reserve, cerebral oxygenation, cerebral blood flow, cerebral microdialysis and electroencephalogram. icp measurement, clinical neurological examination along with computed tomography have been the main methods for monitoring tbi patients [2]. clinical examination is a key point of multimodal neuromonitoring; but despite its accuracy it can often be confounded by intravenous sedation or concomitant metabolic disturbances in the patient. in isolation, the clinical examination may be nonspecific and deterioration occurs because of late manifestations of secondary brain injury that could have been avoided with a more complete management of the patient through all the tools that neuromonitoring provides [3]. this review aims to illustrate the main advantages and most recent recommendations regarding neuromonitoring based on the most current evidence. methods a bibliographic search was carried out in the databases pubmed and science direct and in the google scholar search engine using the following terms: intracranial pressure; critical care, cranioencephalic trauma, multimodal monitoring, articles in english language were included, emphasizing the benefits obtained by performing neuromonitoring by means of the most determinant neurological variables that allow an adequate and complete analysis of brain functionality. the date of publication was not taken into account. a total of 245 articles were identified, including original articles, subject reviews, systematic reviews, letters to the editor, case reports and case series. 42 articles were selected that matched the goal of the article. results neurological assessment of all the modalities of neuromonitoring, the clinical examination of an awake and cooperative patient offers the most comprehensive assessment of the central nervous system (cns) function. despite the advances in neuroimaging and other diagnostic tools, the clinical examination performed by a trained staff is still the "gold standard" for the assessment of patients with tbi. this evaluation should include the examination of cns structures at risk in a given patient and a general description such as the documentation of the level of consciousness, for example, through the glasgow coma scale, motor responses to verbal stimuli and / or painful and the evaluation of brain stem reflexes [2]. despite being a fundamental component in neuromonitoring, the neurological examination has limitations that may diminish its effectiveness: 1) patients in the icu frequently present with an altered state or with diseases that substantially limit the information obtained clinically [2]; 2) neurological evaluations are often done at different times by different examiners resulting in different findings and relevant changes can go unnoticed; 3) the findings of the neurological examination are influenced by therapeutic interventions frequently done in the icu such as endotracheal intubation, use of hypnotics / sedatives, analgesics or neuromuscular blockers, among others [3]; therefore, clinical examination is insufficient to fully evaluate tbi patients and additional test is needed [4]. multimodal monitoring multimodal neuromonitoring (mnm) is used as a 533 multimodal neurological monitoring in neurotrauma complement to clinical neurological evaluation, diagnostic imaging, among other diagnostic methods to obtain the most complete documentation of the brain physiological, particularly of changes [5]. mnm integrates several variables, not only providing a better overview of the physiopathology of the injured brain ’but also how it responds to interventions. due to the vulnerability of neurocritical patients to suffer silent cerebral infarctions, mnm may timely diagnose deterioration and guiding the clinician to intervene before irreversible injuries take place. this is done by direct tissue monitoring, inserting probes into the cerebral parenchymal tissue through a trephine orifice and fixed by a cranial pin system. although the ideal location of the probe is not available, it is considered essential for the interpretation of the data and it is suggested to monitor brain tissue with a higher risk of secondary injury [3,6]. the mnm integrates many devices such as intracranial pressure (icp), cerebral oxygenation, cerebral blood flow, autoregulatory reserve, brain electrophysiology, cerebral oxygenation, cerebral microdialysis and electroencephalogram, and will be detailed below (table 1). table 1. procedures and variables of major importance in the neuromonitoring of patient with acute brain injury [1-7]. technique advantages disadvantages intracranial pressure ventricular catheter gold standard. technically difficult placement. measures global pressure. therapeutic drainage of cerebrospinal fluid. risk of hemorrhage. in vivo calibration. risk of infection. microsensor intraparenchymatous subdural placement. no in vivo calibration possible. easy to place with low procedural complication rate. measures localized pressure. low risk of infection. regular monitoring transcranial doppler non-invasive real time with good temporal resolution. measures relative rather than absolute cerebral blood flow (fsc). operator dependent. failure rate of 5 to 10% (absence of acoustic window). jugular venous oximetry evaluates the balance between oxygen supply (blood flow) and demand (metabolism). global and insensitive to regional changes. easy to perform. risk of venous thrombosis, hematoma, carotid puncture. po 2 of brain tissue the bedside gold standard for cerebral oxygenation monitoring. invasive measures regional oxygen tension, so usefulness depends on the location of the probe. assesses the balance between oxygen supply (fsc) and demand (metabolism). continuum. near infrared spectroscopy non-invasive real-time real-time of regional cerebral oxygenation in multiple regions of interest. depends on manufacturer's algorithms. signals affected by extracerebral tissue. microdialysis measurement of local brain tissue biochemistry. focal measurement. uncertain anomaly thresholds. early detection of hypoxic / ischemic injury. electroencephalography no invasive. expert interpretation required. at real time. correlates with ischemic and metabolic changes. affected by anesthetic/sedative agents. non-convulsive seizure / status epilepticus evaluation. intracranial pressure intracranial pressure (icp) and cerebral perfusion pressure (cpp) are the most commonly measured physiological brain parameters measured in the neurocritical care unit, and used in many treatment algorithms [7]. there is a large experience with icp monitoring in tbi patients, aneurysmal subarachnoid hemorrhage, ischemic stroke and intracerebral hemorrhage in neurocritical care [1]. normal icp is 7-15mmhg in adults in the supine position, varying according to age, body position and clinical condition [2]. the term "intracranial hypertension" depends on the pathology, but levels above 15mmhg are considered abnormal [7]. an 534 randy reina-rivero, maria manuela rodriguez-gutierrez, michael gregorio ortega-sierra et al. increase in brain volume activates the regulatory mechanisms, but an alteration of these produces an elevation of the icp, that is to say an increase of any component of the cranial vault demands a compensatory reduction of another to preserve a normal pressure [8]. the cerebrospinal fluid (csf) is fundamental for the compensatory space mechanism because it can be distributed to the spinal cord reservoir [9]. icp monitoring methods icp monitoring provides information on the state of cerebral self-regulation and is essential for the treatment of severe tbi. icp may be measured by parenchymal microtransducers or intraventricular catheters, the later considered the "gold standard" for icp monitoring [9,10]. in addition, subarachnoid and epidural devices are also used, but they are less precise [2]. intraventricular catheters are inserted into the lateral ventricles, and connected by fluid-filled tubing system to a pressure transducer [8,11]. this method allows to measure the global icp and allows medication administration and therapeutic drainage of csf. risks associated with iv catheters are hemorrhages [12] and ventriculitis, often managed by exchanging to catheters impregnated with antibiotic [13]. monitoring with intraparenchymal microtransducers the same precision as intraventricular catheters, lower infection rates, lower risk of hemorrhage, and can be easily placed providing continuous monitoring of the icp. however, it is limited by its inability to be recalibrated [9]. similar to clinical neuro examination, icp monitorization alone is not sufficient to diagnose all relevant physiological brain derangements generated by the brain injury [14]. other noninvasive icp monitoring techniques have been proposed as alternatives to direct icp measurement including transcranial doppler, eeg, pupillometry and ultrasound measurement of the diameter of the optic nerve sheath (dons) [15]. dons is an ophthalmological technique used to measure icp, because the optic nerve sheath is adjacent to the dura of the brain and contains csf that communicates with the cerebral subarachnoid components, so it can be useful as a means to detect indirectly the increase in the cip. the pupilometer measures icp indirectly by quantitatively evaluating pupillary reflex. there is no evidence that noninvasive measures of the icp has the same clinical utility as direct invasive monitors [15]. cerebral perfusion pressure cpp is a surrogate measurement of cerebral blood flow. cpp is the difference between mean arterial blood pressure and icp measured by invasive methods [2,16]. when cerebral autoregulation is normal, any increase in cpp causes compensatory vasoconstriction, reducing cerebral blood volume and icp [1]. however, when autoregulation is lost, elevated cpp (higher than 120mmhg) can cause an increase in brain flow causing cerebral hyperemia, edema and hypertensive encephalopathy [2]. monitoring both the icp and cpp is frequently done in patients with tbi, subarachnoid hemorrhage and intracranial hypertension [17]. vascular self-regulation vascular self-regulation is a fundamental brain protective mechanism from variations in cerebral blood flow, csf and blood pressure after tbi. this is evaluated using the index of reactivity to pressure (prx) which is the coefficient between the mean arterial pressure (map) and the icp. a negative prx indicates a preservation of self-regulation. on the other hand, when there is an increase in the volume of the cerebral vascular compartment, the icp is increased and we are talking about a positive prx, this indicates a deterioration of the self-regulation [18]. reactivity to cerebrovascular pressure is defined as the ability of vascular smooth muscle to respond to changes in transmural pressure and is determined by observing the response of icp to changes in blood pressure [19]. this index allows us to calculate the cerebrovascular reactivity and give value to the cerebral autoregulatory reserves [9,20]. in addition, cerebrovascular reactivity can be evaluated with the oxygen reactivity index which is the mobile correlation between tissue oxygen pressure (ptio2) and ppc. prx is considered a global measure of self-regulatory status, while orx represents regional self-regulation due to the focal nature of ptio2 [13,20]. cerebral blood flow maintaining adequate cerebral blood flow (cbf) is fundamental therapeutic target and is quantified by neuroimaging modalities including ultrasonography, 535 multimodal neurological monitoring in neurotrauma ct scan, positron emission tomography, and mri [9]. the advantage of these techniques is their good spatial resolution. limitation includes the need to transport the critically ill patient to the radiology department and are not continuous, providing information at a single point in time [21]. the ideal neuromonitoring demands continuous measurements that can be done at the bedside [3,11]. continuous "real-time" cbf monitoring is relatively new in neurocritical care and the technology is still being developed and refined. however, another modality, transcranial doppler (tcd) has been used to evaluate focal regions of the brain with thermal diffusion flowmetry [9]. transcranial doppler measures non-invasively the speed of blood flow by emitting and receiving high frequency energy in the form of waves. the change in frequency reflects the speed and direction of cerebral circulation [22]. it can be done at bedside but is limited for being operator dependent [9]. fluxometry by thermal diffusion allows the measurement, through a catheter inserted in the white matter, of the local cerebral blood flow. the catheter consists of 2 thermistors. one measures brain temperature and the other rises slightly at a temperature higher than the first [3,18]. the energy required to maintain the temperature difference between the two thermistors is proportional to the conductive properties of heat of the white matter [23], which remain constant as long as the catheter is correctly positioned and does not move, and the convective cooling of the cerebral blood flow, which is reported in conventional units of ml/100 g/min [3]. cerebral microdialysis: metabolic monitoring in real time the cerebral microdialysis is a technique that consists of extracting and quantifying the substances of the cerebral interstitial space. it is a laboratory tool introduced in the 90s and its clinical use approved in europe in 1995 and in the united states in 2002 [3]. the physiological premise to obtain tissue metabolites lies in the assumption that it is essential to know when the transition from an aerobic to an anaerobic metabolism occurs which results in an energy failure [24]. in practice, microdialysis focuses on markers of cerebral energy metabolism (glucose, lactate and pyruvate), neurotransmitters (glutamate) and cell damage markers (glycerol). measurements of glucose, pyruvate and lactate provide information on the relative contributions of aerobic and anaerobic metabolism to bioenergetics [25]. as for glycerol, it is a lipid component of neurons and its elevation is commonly associated with death / irreversible cellular ischemia. the increase in glutamate concentrations has been associated with hypoxia, ischemia and reduced brain tissue oxygenation (pbto2) or cpp [1,26]. electroencephalography several studies have shown that seizures are relatively common in patients with severe tbi., and are frequently non-convulsive, which may go unrecognized. prophylactic anti-seizure medication is indicated to all patients with severe tbi [27]. seizure identification after tbi has important implications for the management and prognosis of the patient [11]. the electroencephalogram has long been used to study electrical activity of the brain and diagnose seizures [16]. continuous electroencephalography (ceeg) is instrumental in diagnosing seizures [28]. late detection and treatment result in a significant decrease in the efficacy of anticonvulsant drugs. unrecognized seizures, particularly if prolonged (status epilepticus), may raise intracranial pressure, metabolic demand, excitotoxicity and worsen primary brain injury [29]. there are limitations for the use of ceeg in the icu. these include: 1) the availability of trained personnel to place the electrodes, 2) artifacts, and 3) the lack of trained professionals able to interpret the eeg in a timely manner. additionally, there is an inherent degree of variability between the different interpretations [30]. the invasive ceeg is also available to identify crises that are not visible using scalp electrodes. the use of this modality can provide greater sensitivity to detect crises and improve the signal-to-noise ratio when compared to surface electrical activity [31]. measuring cerebral oxygenation oxygenation is vital to cellular homeostasis and neuronal integrity, and can be used as a marker for tissues at risk of secondary injury. brain tissue oxygen (pbto2) and jugular venous oxygen saturation (sjvo2) allow continuous real-time evaluation of cerebral oxygenation [32]. 536 randy reina-rivero, maria manuela rodriguez-gutierrez, michael gregorio ortega-sierra et al. pbto2 provides information on 2 contexts: 1) it can evaluate oxygenation when there are normal values of ppc, and 2) it can diagnose cerebral hypoxia secondary to low perfusion when the ppc is within normal limits. the jugular venous oxygen saturation provides information on global cerebral oxygen. the catheter is placed in the dominant internal jugular vein and advanced to the upper part of the jugular bulb [33,34]. normal values range between 55 and 75%. lower values indicate increased oxygen extraction and risk of ischemia. the compensatory mechanisms for poor oxygen supply or an increase in demand is increased oxygen extraction [31]. in decompensated states, ischemia may occur while high sjvo2 indicates hyperemia, decreased metabolic demand or even cell death [3,35]. it is necessary to carry out a greater number of prospective multicenter studies, especially in lowand middle-income countries where there are still not enough specialized centers and high-quality mass training in neurological and neurosurgical monitoring, in order to improve the management of patients with neurotrauma and reduce the burden of neurological diseases [36-40]. in the same way, involve students and residents from early stages of their process, so that they are related to this type of recent techniques [41,42]. conclusions mnm integrates different equipments and measures that allow real-time monitoring of brain and identification of pathophysiological changes that occur after tbi. mnm allows early detection and compression of physiological changes caused by the injury, which will facilitate the determination of proper management of the neurocritical patient. references 1. cecil s, chen pm, callaway se, rowland sm, adler de, chen jw. traumatic brain injury advanced multimodal neuromonitoring from theory to clinical practice. crit care nurse. 2011; 31(2):25–37. 2. macas a, bilskienė d, gembickij a, žarskus a, rimaitis m, vilkė a, et al. multimodal neuromonitoring. acta medica litu. 2012; 19(3):180-186. 3. dries dj. textbook of neurointensive care. shock. 2004; 22(6):592. 4. makarenko s, griesdale de, gooderham p, sekhon ms. multimodal neuromonitoring for traumatic brain injury: a shift towards individualized therapy. j clin neurosci. 2016; 26:8–13. 5. egea-guerrero jj, gordillo-escobar e, revuelto-rey j, enamorado-enamorado j, vilches-arenas a, pachecosánchez m, et al. clinical variables and neuromonitoring information as predictors of brain-death development after severe traumatic brain injury, transplantation proceedings. 2012; 44(7):2050-2052. 6. raith ep, reddy u. neuromonitoring. anaesthesia & intensive care medicine. 2020; 21(6):275-281. 7. hemphill jc, andrews p, de georgia m. multimodal monitoring and neurocritical care bioinformatics. nat rev neurol. 2011; 7(8):451–60. 8. gilo arrojo f, herrera muñoz a, anciones b. hipertensión intracraneal aguda, neurología. 2010; 25(s-1):3-10. 9. smith m. monitoring intracranial pressure in traumatic brain injury. anesth analg. 2008; 106(1):240–8. 10. schmidt b, klingelhöfer j, clinical applications of a noninvasive icp monitoring method, european journal of ultrasound. 2002; 16(1-2):37-45. 11. garcía-lira jr, zapata-vázquez re, alonzo-vázquez f, rodríguez-ruz sg, medina-moreno mr, torres-escalante jl, monitorización de la presión intracraneal en traumatismo craneoencefálico severo, revista chilena de pediatría, 2016; 87(5):387-394. 12. lazaridis c, robertson cs. the role of multimodal invasive monitoring in acute traumatic brain injury. neurosurg clin n am. 2016; 27(4):509–17. 13. ko s-b. multimodality monitoring in the neurointensive care unit: a special perspective for patients with stroke. j stroke. 2013; 15(2):99–108. 14. al-mufti f, smith b, lander m, damodara n, nuoman r, el-ghanem m, et al. novel minimally invasive multimodality monitoring modalities in neurocritical care, journal of the neurological sciences. 2018; 390:184-192. 15. melhem s, shutter l, kaynar am, videtta w, petroni g, lujan s, et al. journal club critique. a trial of intracranial pressure monitoring in traumatic brain injury. crit care. 2014; 1–3. 16. ming-tao yang, multimodal neurocritical monitoring, biomedical journal. 2020; 43(3):226-230. 17. mcnett m, koren j, blood pressure management controversies in neurocritical care, critical care nursing clinics of north america. 2016; 28(1):9-19. 18. kirkman ma, smith m. multimodality neuromonitoring. anesthesiol clin. 2016; 34(3):511–23. 19. ding k, tarumi t, tomoto t, mccolloster m, le t, dieppa m, et al. impaired cerebral blood flow regulation in chronic traumatic brain injury, brain research. 2020; 1743:146924. 20. adam j. wells, peter ja. hutchinson. the management of traumatic brain injury. surgery (oxford). 2018; 36(11):613-620. 21. sankar sb, pybus af, liew a, sanders b, shah kj, wood lb, et al. low cerebral blood flow is a non-invasive biomarker of neuroinflammation after repetitive mild traumatic brain injury. neurobiology of disease. 2019; 124:544-554. 22. calviello la, zeiler fa, donnelly j, uryga a, de riva n, 537 multimodal neurological monitoring in neurotrauma smielewski p, et al. estimation of pulsatile cerebral arterial blood volume based on transcranial doppler signals. medical engineering & physics. 2019; 74:23-32. 23. roh d, park s. brain multimodality monitoring: updated perspectives. curr neurol neurosci rep. 2016; 16(6):56. 24. eiden m, christinat n, chakrabarti a, sonnay s, miroz jp, cuenoud b, et al. discovery and validation of temporal patterns involved in human brain ketometabolism in cerebral microdialysis fluids of traumatic brain injury patients. ebiomedicine. 2019; 44:607-617. 25. chamoun r, suki d, gopinath sp, goodman jc, robertson c: role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury. j neurosurg. 2010; 113:564–570. 26. young b, kalanuria a, kumar m, burke k, balu r, amendolia o, et al. cerebral microdialysis. critical care nursing clinics of north america. 2016; 28(1):109-124. 27. sandsmark dk, kumar ma, park s, levine jm. multimodal monitoring in subarachnoid hemorrhage. stroke. 2012; 43(5):1440–5. 28. montupil j, defresne a, bonhomme v. the raw and processed electroencephalogram as a monitoring and diagnostic tool. journal of cardiothoracic and vascular anesthesia. 2019; 33(s-1):s3-s10. 29. mete m, alpay s, aydemir i, unsal uu, collu f, özel hf, et al. therapeutic effects of lacosamide in a rat model of traumatic brain injury: a histological, biochemical and electroencephalography monitoring study. injury. 2021; 52(2021):713-723. 30. oddo m, villa f, citerio g. brain multimodality monitoring: an update. curr opin crit care. 2012; 18(2):111–8. 31. korbakis g, vespa pm. multimodal neurologic monitoring. handb clin neurol. 2017; 140:91-105. 32. domínguez-roldán jm, lubillo s, videtta w, llompart-pou ja, badenes r, márquez rivas j, et al. international consensus on the monitoring of cerebral oxygen tissue pressure in neurocritical patients, neurocirugía (english edition). 2020; 31(1):24-36. 33. rosenthal g, hemphill jc 3rd, sorani m, martin c, morabito d, obrist wd, et al. brain tissue oxygen tension is more indicative of oxygen diffusion than oxygen delivery and metabolism in patients with traumatic brain injury. crit care med. 2008; 36(6):1917-24. 34. yang mt. multimodal neurocritical monitoring. biomed j. 2020; 43(3):226-230. 35. rosenfeld jv, maas ai, bragge p, morganti-kossmann mc, manley gt, gruen rl. early management of severe traumatic brain injury. lancet. 2012; 380(9847):1088-98. 36. acevedo-aguilar l, gaitán-herrera g, reina-rivero r, lozada-martínez id, bohorquez-caballero a, paézescallón n, et al. pulmonary injury as a predictor of cerebral hypoxia in traumatic brain injury: from physiology to physiopathology. j neurosurg sci. 2021 nov 11. 37. blanco-teherán c, quintana-pájaro l, narvaez-rojas a, martínez-pérez r, garcía-ballestas e, moscote salazar l, et al. evidence-based medicine in neurosurgery: why and how? j neurosurg sci. 2021 aug 3. 38. miranda-pacheco ja, de santis-tamara sa, parra-pinzón sl, gonzález-monterroza jj, lozada-martínez id. medical interest groups and work policies as emerging determinants of a successful career: a student perspective correspondence. int j surg. 2021; 92:106020. 39. ortega-sierra mg, beltran-hoyos ge, benjumeavelásquez am, bossio-martínez im, lozada-martínez id. surgery interest groups in medical schools: mentoring factory. j surg res. 2021; 267:209-210. 40. ortega-sierra mg, charry-caicedo ji, orrego-torres at, rueda-ibarra l, lozada martínez id. breaking down barriers to surgical learning in times of covid-19: an initiative of future surgeons. eur surg. 2021: 1-2. 41. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. 42. lozada-martínez i, bolaño-romero m, moscote-salazar l, torres-llinas d. letter to the editor: 'medical education in times of covid-19: what's new in neurosurgery?'. world neurosurg. 2020; 143:603. microsoft word 4alvishernando_microglia_ff 34 alvis-miranda et al microglia: roles and rules in brain traumatic injury microglia: roles and rules in brain traumatic injury hernando raphael alvis-miranda, gabriel alcala-cerra1, luis rafael moscote-salazar1 university of cartagena, colombia 1neurosurgery abstract microglia are a special type of supporting cells in the nervous system. between the functions they perform are myelin production, structural support, regulation of extracellular fluid, glial scar formation among others. this cell type for its versatility, is also related to pathological events, where his multiple roles and the release of proinflammatory factors can contribute to understand especially in traumatic brain injury, as secondary injury and the healing process, important aspects the context of brain injury. key words: microglia, brain trauma injury, neurons, neurotrauma introduction the role of microglia in the neurotrauma has been under continuous debate, researches have been trying to state how microglia-mediated inflammation can contribute to recovery of function after trauma, or fell in secondary injury. microglia, are resident cells of the brain involved in regulatory processes critical for development, maintenance of the neural environment, injury, and repair (1). microglia derives from mesodermal precursor cells of hemapoietic lineage that populate the central nervous system (cns) in early development. resident microglia cells are turned over slowly, and are replenished throughout adult life by proliferation (2), and represent the resident macrophages of the cns, accounting for 10% of the adult glial cell population in the normal brain (3). morphologically distinct from neurons and astrocytes, these cells were classified by cajal in 1913 as a third element of cns (4). del río hortega made a further distinction between microglia and other glial cells in 1932. at that time the morphological classification of microglia allowed three kinds of states: ramified, intermediate forms, and ameboid (5). recent studies have evolved the classification to include a functional connotation like m1 and m2 phenotypes (6). these phenotypes, allows them to actively participate in pathological processes by changing their morphology, expressing various antigens and becoming phagocytic (7). microglia cells function as sentinels for innate immunity in the cns continually monitoring and screening the extracellular environment, walling off areas of the cns from foreign tissue, and removing damaged or dead cells (1), to achieve that, these cells express various sets of pattern recognition receptors (prrs) in response to pathogenassociated molecular patterns (pamps) that include toll-like receptors (tlrs; e. g: tlr-4) and inflammasomes (8). very often, microglia cells provide the first line romanian neurosurgery (2013) xx 1: 34 45 35 defense against invading germs, and interacting with neurons and other glial cells, they can be the first sense of critical changes in the neuronal activity. although microglial cells are thought to contribute to most pathological conditions, including cns infections, neuroinflammatory lesions, brain tumors, and neurodegenerative diseases, their exact role in cns development, homeostasis, and disease remains poorly understood (3). regarding to neurotrauma, exists a strongly investigated feature, and that is the histological evidence of a prominent microglial activation (9). currently there are many medical conditions under research because of the microglia activation in their pathological processes (10, 11, 12, 13). this review will explore the current concepts and researches on microglial responses to cns traumatic injury and also will be discussed the differential role of microglia. general response of microglia to injury for microglial activation no large amount of tissue damage is required; alterations of neural electric transmission or extracellular electrolyte composition and the release of soluble factors normally confined to the intracellular compartment are sufficient to trigger microglia cells activation. in the healthy mature cns, microglia have a ramified morphology, a small soma with fine cellular processes, this appearance has been associated with microglial “resting state”. when cns is insulted, either for trauma, infection, ischemia, neurodegenerative disease o an altered neuronal activity, microglia can evoke rapid and intense changes in their cell shape, gene expression and functional behavior, all these changes conjure the “microglial activation” (14), as will be discussed later more precisely, microglia cells respond by detecting lipopolysaccharide (lps) (8), beta-amyloid (aβ) (15), thrombin, ifn-γ, and other proinflammatory cytokines (16). in this late state, microglia suffer a morphological transformation, induction of a wide range of soluble factors, like cytokines, free radicals and nitric oxide, acquire a phagocytic phenotype (17) to clear tissue debris, damaged cells, or germs, and get physically associated with injured neurons. microglial activation may result in expression of mhc (18) antigens and costimulatory molecules and in the capacity of microglia to act as antigen presenting cells. microglial activation has key features: first, these cells react to all cns pathologies, no matter if they are acute or chronic. second, the response evoked is graded, and can range from very slight morphological changes accompanied by minor immunological activation, to the development of full-blown tissue macrophages with the associated expression of an entire battery of membrane bound and soluble immunologically relevant molecules (19). because of the “immune privilege” (20) of the cns, i. e., that the brain parenchyma has to protect itself from the potentially detrimental consequences of an immune reaction, the microglial activation is a highly regulated process. it is important to recognize the fact that microglia in “resting state”, actively scan and monitor the extracellular environment by pinocytosis (21), always ready to transform to a state of “activity”, in which microglia primarily serve for support and protection. so, the transition from a “resting” mode to an executive state thereby 36 alvis-miranda et al microglia: roles and rules in brain traumatic injury represents a shift in activities rather than “activation” phenomenon, then, there are no periods of inactivity. once microglial cell “activation” occurs, it starts with an emergency like response, such as defense oriented functions, i. e., combat an infection or to limit additional damage after injury. eventually, the activated population, convert to a repairoriented response, for tissue reparation. although much effort has been directed toward characterizing the fundamental properties of an activated microglial cell, surprisingly little is known about the intrinsic molecular mechanisms that program the functional state of these cells in either the healthy or the diseased cns (22), but these molecular mechanisms can be grouped to produce five stages: proliferation, migration, secretion of soluble products and electrophysiological changes. proliferation: irrespective of the type of cns lesion, microglial cells show an early proliferative response, usually proliferation indices, i. e., the number of actively proliferating microglial cells divided by the total number of microglial cells, peak around 3–5 days after a lesion (19). this proliferative response rapidly declines subsequently and approaches control levels 7-15 days after injury; but even after the zenith of the proliferation index, the total number of microglial cells can remain elevated, and depending on the type of injury, will still being significantly higher than pre-lesion values around a month after an experimental injury (23, 24, 25). the proliferation of microglial cells is triggered by damage to adjacent neurons, and deafferentation of central neurons by peripheral axotomy is a sufficient stimulus to induce it. a number of different factors have been shown to play important roles in the initiation of microglial proliferation but even actually is an incompletely answered world. in laboratory experiments have been demonstrated the presence of macrophagecolony stimulating factor (m-csf) as a driver of the cell cycle of microglia, inducing their proliferation (26). purinergic receptor p2x7 also controls microglial proliferation (27). others microglial mitogens are the granulocyte/monocyte colony-stimulating factor (gm-csf), brain-derived neurotrophic factor (bdnf), neurotrophin (nt)-3, il-1, il-5, and chemokines (e. g., fractalkine and its receptor cxc3cl1) (28, 29, 30, 31, 32, 33). in the other hand, the proliferation regulation or inhibition seems to be exerted by the transforming growth factor beta (tgf-β), mainly produced by activated astrocytes (34). in microglial cells proliferation, also are important the cell-cell interactions, particularly with neurons (35), which have key roles in delivery of regulatory signals, in part through the glycoprotein ox-2 (36). microglia are equippated with glutamate-, purinergic-, acetylcholine-, adrenergic-, dopamine-, neurokinin-, serotoninergic-, opioidand gamma-amino-butyric-acid-receptors, implicating that for their function is important the neuronal activity detection, but, microglia neurotransmitter receptor aren’t in a specialized region in close apposition to neurotransmitter release sites. spatial proximity to synapses can be attained transiently; the long-term association is not likely since microglia cells are highly motile in resting and activated states (21). neuron-microglia communication relies mostly on release of signaling molecules from extrasynaptic romanian neurosurgery (2013) xx 1: 34 45 37 axonal varicosities, as well as their diffusion from synapses. migration microglia processes are capable of rapid extension (≈1. 25 mm/min) towards sites of acute cns damage (37). the main candidate for a chemoattractant sensed by microglia is adenosine triphosphate [atp; involves g(i/o) proteins and the mitogenactivated protein kinase (mapk)/extracellular signal-regulated kinase (erk)-dependent pathway] (38) through microglial p2y12 receptors (39) and an outward potassium current (40). neuropeptides such as angiotensin ii, bradykinin (controlled by a g(i/o)-proteinindependent pathway), endothelin, galanin [induces microglial migration in a similar way to bradykinin, but induces intracellular ca(2+) mobilization by inositol-3, 4, 5trisphosphate (insp(3))-dependent ca(2+) release from the intracellular store] and neurotensin are also chemoattractants for microglia. the fact that there are different intracellular signaling cascades indicates that chemoattractants control distinct microglial functions. nitric oxide (no) also is an additional guidance cue involved in microglia migration. secretion of soluble factors these are derived mainly from the activated microglia, and consist of cytokines, proteases, free radicals and growth factors. proinflammatory cytokines, which are closely involved in various diseases (including trauma, ischemia, alzheimer's disease, epilepsy, and others), play important roles in the facilitation of activated microglia for astrocytic activation (34). among the most important cytokines is il-1 (41), showing neurotoxic actions, and stimulating astrocytes and other microglial cells in paracrine and autocrine way. its receptor is also founded both in neurons and glial cells. il-1 induces expression of other proinflammatory mediators like il-6 (42), and tnf-α (43), thus this interleukin seems to play a regulating role in the concert of cytokines, and binding results in activation of a series of intracellular adaptor molecules, mitogen activated protein (map) kinases and the transcription factor, nuclear factor kappa b (nf-kb), leading to changes in gene expression. the first cells to express il-1 are microglia, but other brain cells (astrocytes, invading immune cells, vascular cells and probably neurons) can also produce il-1 (41). once the microenvironment of the cns becomes activated, local cells also produce proinflammatory cytokines, chemokines and upregulate inmunomodulatory surface markers. these changes in turn decrease the stringency of the blood-brain barrier, allowing entry of other soluble factors and peripheral immune cells, including macrophages, natural killer cells and lymphocytes. proteases are also very important after cns injury, because they mediate tissue damage and invasion of blood-derived immunocompetent cells. a factor recognized as a potential neurotoxic microglial secretion product is tissueplasminogen activator (t-pa); it aggravates neuronal injury after ischemia (44). one key mediators of cytotoxicity in the cns secreted by microglia is no (45), this molecule displays a wide array of biological activities, ranging from cytotoxicity to neuroprotective effects and neurotransmission (46). no acts directly as neurotoxic via excitotoxic mechanisms (47). little is known about cellular mechanisms regulating reactive oxygen species (ros) production by activated microglia under 38 alvis-miranda et al microglia: roles and rules in brain traumatic injury pathological conditions, but, in microglia can produce ros in different ways, e. g., nadph oxidase, mitochondria or xanthine oxidase (48). phagocytic and cytotoxic functions of microglia are also triggered during cns injury. upon activation, microglia upregulate opsonic receptors including complement receptors (cr1, cr3, cr4) and fc gamma receptors (i, ii, iii), which enhance phagocytic activity by binding to complement components and immunoglobulin fragments respectively (36). electrophysiological changes in the ion channels relays key functions of microglial physiology, for example, deramification of microglial cells in culture was inhibited by blockade of nonselective cation channels, this suggest that cation influx through such channels increases the intracellular osmolarity with a subsequent osmotic entry of water and cell swelling (49), and the ramification, or the adquisition of a amoeboid shape, is likely o be associated with stretch-activated cl channels (50). also has been observed that voltageand/or ca2+-activated k+ channels regulate microglial proliferation (51), migration (52, 53), cytokine secretion (54, 55, 56), production of free radicals (57, 58, 59). strikingly, the intracellular conversion of pre-il-1b to biologically active il-1b is dependent for the decrease the cytoplasmic k+ concentration (60) and blockade of delayed outward rectifier k+ channels resulted in an inhibition of lplstimulated microglial il-1release (61). chloride channels have been found to be involved in microglial proliferation (62, 63), production of ros (64, 65), inos expression and nitric oxide production (66), migration (52), phagocytosis (67) and ramification (68). during nadph oxidase mediated respiratory burst of microglia are important the proton channels for charge compensation (69). calcium has been evidenced to participate in transmission of brain-damage signals to microglia through long-range waves, this type of waves is induced by glutamate and is independent of atp (70). what happens after activation is an even less known fact than the microglial activation. microglial activation when no longer needed, finishes being an unremarkable phenomenon, and not even much noticed, but, may be some residual effects (71). when being challenged again, the experienced microglia could behave differently, and this could explain some chronically related problems like agerelated dysfunction or a neurodegenerative process (72, 17). however this behavior could be a protective effect, because the affected cells have been prepared by the former activation to respond quickly and efficiently in a second injury. microglia: dual behavior? exists the concept of secondary neuronal damage, i. e., microglia-mediated inflammation fell in secondary neuronal injury, and is in part built over the base that immunocompetent cells can aggravate neuronal demise, but whether microglial cells have a dual role, supportive or detrimental in neurotrauma and in others cns acute or chronic pathologies has been the key question of almost a century. has been stated that microglial behavior depends on several factors: the kind of stress and damage signals, the duration/timing of an impact, the microenvironment, the interaction with other cell types and, interestingly, even the age of an organism (73). there are a romanian neurosurgery (2013) xx 1: 34 45 39 contrast between the potentially neurotoxic substances and the growth factors secreted by microglia, but it is impossible to predict the kind of microglia behavior (benefit or harm to surviving neurons) that will be induced by the lesion in an acute and chronic way. macrophages and microglia can be classified into at least two subsets with distinct molecular phenotypes and effector functions depending on the activation pathway. the “activated” proinflammatory m1 macrophages, activated by lps and by the proinflammatory cytokine ifn-γ, express cd86 and cd16/32 and produce high amounts of oxidative metabolites (no and superoxide), proteases and proinflammatory cytokines. they play a central role in host defense against pathogens and tumor cells, and they can also damage healthy cells such as neurons and glial cells. in contrast, m2 macrophages are ‘alternatively activated’, anti-inflammatory macrophages induced by il-4 and il-13, and they express cd206 and arginase 1. the latter downregulate inflammation and promote tissue remodeling/repair and angiogenesis (73, 6). as previously mentioned, microglia can both produce and respond to cytokines, these can be either neuroprotective [e. g. il-10, tumor growth factor (tgf)-β, tnf-α] and/or neurotoxic (e. g. il-1, tnf-α, ifn-γ) (74). at high levels tnf-α is neurotoxic, but at low levels it can be neuroprotective (75). in models that simulate chronic systemic inflammation has been shown that microglia in young mice protect dopaminergic neurons against lps, but in the old mice, microglia promote the death cell (76). beneficial responses almost all studies for evaluation of the role of microglia in pathological circumstances have been performed using in vitro cultured microglia, whereby there are limitations because those only shows one cell phenotype simulating a physiological or pathological condition, also, these models lacks of the microenvironmental interactions with other cells like neurons and astrocytes. thanks to the phagocytic function, microglia can enter damaged brain regions and remove toxic detritus, invading pathogens and cell debris. in case of stimulation of tlr by pathogens is induced a proinflammatory reaction but, in cases of brain injury, the recognizing of phosphatidylserine of the cell membrane of damaged neurons induces an antiinflammatory reaction (74). also in brain injury, microglial shows other beneficial activities like promoting protection to neurons (77), reestablishment of the neural environment (78), and has been evidenced that insufficient removal of myelin by microglia impairs the recruitment of oligodendrocyte precursor cells and induces an arrest of oligodendrocyte differentiation (78). some cytokines secrete by microglia have an important role in protection, il-6 can act on astrocytes and induce brain tissue repair (79), the il-10 is an inhibitory cytokine of microglial apoptosis (80) and the tgf-β also can be neuroprotective (81, 82, 83) and it is elevated after injury (84, 85). these pleiotropic cytokines have central roles in vascular remodeling, immune suppression, immune homeostasis and repair after injury (86, 87, 88, 89). furthermore, both tgf-β and il-10 inhibit macrophage and microglia activation by downregulating the expression of molecules associated with antigen presentation and production of proinflammatory cytokines, chemokines, and nitric and oxygen free radicals (90, 91, 40 alvis-miranda et al microglia: roles and rules in brain traumatic injury 92). microglia promote neuroplasticity and axonal regeneration, in addition to the monitoring and pruning of synapses (93, 94). microglia can modify neural networks in multiple ways: promoting neuronal cell death, influencing neural circuitry by neuroplastic reorganization or synaptic stripping (95). activated microglia also enhance angiogenesis (96, 97, 98). has been suggested that t cells, once activated (by encountering their relevant antigenpresenting cells), control the local innate response by activating resident microglia in a well-controlled way (99). they can also express neuroprotective proteins such as neurotrophins and glutamate transporters (100, 101). the latter transporters might help to reduce glutamate toxicity via uptake of glutamate. detrimental responses microglia have been implicated as a contributor to neuron damage, in models of excitotoxic cell death, phagocytic microglia contribute to neuronal degeneration and cell loss. microglia can release glutamate, this neurotransmitter is well known to trigger excitotoxic neurodegeneration and cell death of astrocytes and oligodendrocytes (102, 103, 104, 105). the exact mechanism leading to microglial overactivation is still not fully understood, but glial-neuronal crosstalk seems to be central (106), but because of activated microglia can release cytotoxic factors such as no and ros and secrete pro-inflammatory cytokines that can potentially damage neurons, oligodendrocytes or extracellular matrix structures directly or indirectly, i. e., activating astrocytes trough il-1-mediated neurotoxicity (107, 34, 108) have been considered as a “double-edged sword”, and inhibition of its functions have been beneficial in some circumstances (109, 110, 19, 111). evidence is available to show the presence of activated microglia and their ability to induce cell death in the immature white matter, both in oligodendrocytes precursors and in astrocytes (112, 113). the ros (no, hydrogen peroxide, superoxide) can kill invading microbes but also can induce neural damage and reactive gliosis (74). the intracellular ros derived from nadph oxidase play special roles in neurodegeneration for his dual functions (114, 115). the ros released extracellularly can be directly toxic for neurons, especially dopaminergic ones, and when intracellular ros concentrations raise, can alter the signaling cascade leading to microglia activation (116, 117, 118, 119). microglia have been related to the progressive nature of neurodegenerative diseases through their capacity to be chronically activated by neuron death and fuelling, a self-renewing cycle of microglial activation followed by further neuron damage (reactive microgliosis). this selfpropelling cycle in microglial cells is possibly mediated by intracellular ros and no when they become activated by lps (120). the activation of the prostaglandin e2 receptor of the prostaglandin e2 pathway can lead to microglia-induced paracrine neurotoxicity (121). the acute microglia response is not considered detrimental, but when it became persistent, i.e., chronic microglial activation, is considered to be the most damaging response of microglia to injury through the previously stated mechanisms, that in the interaction damaged neuronhyperactivated microglia create a selfpropagating feedback loop that leads to an aberrant prolonged microglial activation and to neuronal death, chronic progression and neurodegeneration. romanian neurosurgery (2013) xx 1: 34 45 41 correspondence: dr. luis rafael moscote-salazar, university of cartagena, cartagena de indias, colombia. e-mail: mineurocirujano@aol.com references 1. harry gj, kraft ad. microglia in the developing brain: a potential target with lifetime effects. neurotoxicology. 2012; 33: p. 191–206. 2. vilhardt. microglia: phagocyte and glia cell. the international journal of biochemistry & cell biology. 2005; 37: p. 17–21. 3. greter m, merad m. regulation of microglia development and homeostasis. glia. 2013; 61: p. 121– 127. 4. cajal sr. contribución al conocimiento de la neuroglía del cerebro humano. trab. lab. invest. biol. univ. madrid. 1913; 18: p. 225-315. 5. del rio hortega p. microglia. in penfield w, editor. citology & cellular pathology of the nervous system. new york; 1932. p. 483-534. 6. kigerl ka, gensel c, ankeny dp, alexander jk, donnelly dj, popovich pg. identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. the journal of neuroscience. 2009; 29(43): p. 13435–13444. 7. luo xg, chen sd. the changing phenotype of microglia from homeostasis to disease. translational neurodegeneration. 2012; 1(1): p. 1-13. 8. saijo k, crotti a, glass ck. regulation of microglia activation and deactivation by nuclear receptors. glia. 2013; 61: p. 104–111. 9. shitaka y, tran ht, bennett re, sanchez l, levy ma, dikranian k, et al. repetitive closed-skull traumatic brain injury in mice causes persistent multifocal axonal injury and microglial reactivity. j neuropathol exp neurol. 2011; 70(7): p. 551–567. 10. jovanović z. mechanisms of neurodegeneration in alzheimer's disease. med pregl. 2012; 65(7-8): p. 301-7. 11. stertz l, magalhães pv, kapczinski f. is bipolar disorder an inflammatory condition? the relevance of microglial activation. curr opin psychiatry. 2013; 26(1): p. 19-26. 12. shibata m. mechanisms underlying migraine chronification. rinsho shinkeigaku. 2012; 52(11): p. 1012-3. 13. derecki nc, cronk jc, kipnis j. the role of microglia in brain maintenance: implications for rett syndrome. trends immunol. 2012. 14. kettenmann h, hanisch uk, noda m, verkhratsky a. physiology of microglia. physiol rev. 2011; 91: p. 461–553. 15. mannix rc, whalen mj. traumatic brain injury,microglia, and beta amyloid. int j alzheimers dis. 2012;: p. 1-5. 16. dheen st, kaur c, ling ea. microglial activation and its implications in the brain diseases. curr med chem. 2007; 14: p. 1189-97. 17. ladeby r, wirenfeldt m, garcia-ovejero d, fenger c, dissing-olesen l, dalmau i, et al. microglial cell population dynamics in the injured adult central nervous system. brain research reviews. 2005; 48: p. 196– 206. 18. engel s, schluesener h, mittelbronn m, seid k, adjodah d, wehner hd, et al. dynamics of microglial activation after human traumatic brain injury are revealed by delayed expression of macrophage-related proteins mrp8 and mrp14. acta neuropathol. 2000; 100: p. 313–322. 19. hailer np. immunosuppression after traumatic or ischemic cns damage: it is neuroprotective and illuminates the role of microglial cells. progress in neurobiology. 2008; 84: p. 211–233. 20. galea i, bechmann i, perry h. what is immune privilege (not)? trends immunol. 2007; 28: p. 12–18. 21. nimmerjahn a, kirchhoff f, helmchen f. resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. science. 2005; 308(5726): p. 1314-1318. 22. minten c, terry r, deffrasnes c, campbell il, king n. ifn regulatory factor 8 is a key constitutive determinant of the morphological and molecular properties of microglia in the cns. plos one. 2012; 7(11): p. e49851. 23. jorgensen mb, finsen br, jensen mb, castellano b, diemer nh, zimmer j. microglial and astroglial reactions to ischemic and kainic acid-induced lesions of the adult rat hippocampus. exp. neurol. 1993; 120. 24. fujita t, yoshimine t, maruno m, hayakawa t. cellular dynamics of macrophages and microglial cells in reaction to stab wounds in rat cerebral cortex. acta neurochir. 1998; 140: p. 275–279. 25. hailer np, grampp a, nitsch r. proliferation of microglia and astrocytes in the dentate gyrus following entorhinal cortex lesion: a quantitative bromodeoxyuridine-labelling study. eur. j. neurosci. 1999; 11: p. 3359–3364. 26. yamamoto s, nakajima k, kohsaka s. macrophage-colony stimulating factor as an inducer of microglial proliferation in axotomized rat facial nucleus. j neurochem. 2010; 115(4): p. 1057-67. 27. bianco f, ceruti s, colombo a, fumagalli m, ferrari d, pizzirani c, et al. a role for p2x7 in microglial proliferation. j. neurochem. 2006; 99: p. 745–758. 28. ringheim ge. mitogenic effects of interleukin-5 42 alvis-miranda et al microglia: roles and rules in brain traumatic injury on microglia. neuroscience letters. 1995; 201: p. 131134. 29. ganter s, northoff h, männel d, gebickehärter pj. growth control of cultured microglia. j neurosci res. 1992; 33(2): p. 218-30. 30. yang h, feng gd, liang z, vitale a, jiao xy, ju g, et al. in vitro beneficial activation of microglial cells by mechanically-injured astrocytes enhances the synthesis and secretion of bdnf through p38mapk. neurochem int. 2012; 61(2): p. 175-86. 31. zhou lj, yang t, wei x, liu y, xin wj, chen y, et al. brain-derived neurotrophic factor contributes to spinal long-term potentiation and mechanical hypersensitivity by activation of spinal microglia in rat. brain behav immun. 2011; 25(2): p. 322-34. 32. zujovic v, benavides j, vigé x, carter c, taupin v. fractalkine modulates tnf-alpha secretion and neurotoxicity induced by microglial activation. glia. 2000; 29(4): p. 305-15. 33. verge gm, milligan ed, maier sf, watkins lr, naeve gs, foster ac. fractalkine (cx3cl1) and fractalkine receptor (cx3cr1) distribution in spinal cord and dorsal root ganglia under basal and neuropathic pain conditions. eur j neurosci. 2004; 20(5): p. 1150-60. 34. liu w, tang y, feng j. cross talk between activation of microglia and astrocytes in pathological conditions in the central nervous system. life sciences. 2011; 89(141–146). 35. panatier a, robitaille r. the soothing touch: microglial contact influences neuronal excitability. dev cell. 2012; 23(6): p. 1125-6. 36. yang i, han sj, kaur g, crane c, parsa at. the role of microglia in central nervous system immunity and glioma immunology. j clin neurosci. 2010; 17(1): p. 6-10. 37. parkhurst cn, gan wb. microglia dynamics and function in the cns. current opinion in neurobiology. 2010; 20: p. 595–600. 38. noda m, ifuku m, mori y, verkhratsky a. calcium influx through reversed ncx controls migration of microglia. adv exp med biol. 2013; 961: p. 289-94. 39. haynes se, hollopeter g, yang g, kurpius d, dailey me, gan wb, et al. the p2y12 receptor regulates microglial activation by extracellular nucleotides. nat neurosci. 2006; 9: p. 1512-1519. 40. wu lj, vadakkan ki, zhuo m. atp-induced chemotaxis of microglial processes requires p2y receptor-activated initiation of outward potassium currents. glia. 2007; 55: p. 810-821. 41. gibson rm, rothwell nj, le feuvre ra. cns injury: the role of the cytokine il-1. the veterinary journal. 2004; 168: p. 230–237. 42. li w, liu hd, you c, zhou ml, ling hp, shen w, et al. enhanced cortical expression of myeloid differentiation primary response protein 88 (myd88) in patients with traumatic brain injury. j surg res. 2012 nov 22. 43. john gr, lee sc, song x, rivieccio m, brosnan cf. il-1-regulated responses in astrocytes: relevance to injury and recovery. glia. 2005; 49(2): p. 161–76. 44. tsirka se. clinical implications of the involvement of tpa in neuronal cell death. j. mol. med. 1997; 75: p. 341–347. 45. nakamichi k, saiki m, sawada m, yamamuro y, morimoto k, kurane i. double-stranded rna stimulates chemokine expression in microglia through vacuolar ph-dependent activation of intracellular signaling pathways. j neurochem. 2005; 95(1): p. 27383. 46. zielasek j, hartung hp. molecular mechanismos of mircoglial activation. advances in neuroimmunology. 1996; 6: p. 191-222. 47. michikawa m, lim kt, mclarnon jg, kim su. oxygen radicalinduced neurotoxicity in spinal cord neuron cultures. j. neurosci. res. 1994; 37: p. 62–70. 48. schilling t, eder c. stimulus-dependent requirement of ion channels for microglial nadph oxidase-mediated production of reactive oxygen species. journal of neuroimmunology. 2010; 225: p. 190–194. 49. schilling t, lehmann f, ruckert b, eder c. physiological mechanisms of lysophosphatidylcholineinduced de-ramification of murine microglia. j. physiol. 2004; 557: p. 105–120. 50. eder c, klee r, heinemann u. involvement of stretch-activated clchannels in ramification of murine microglia. j. neurosci. 1998; 18: p. 7127–7137. 51. kotecha sa, schlichter lc. a kv1. 5 to kv1. 3 switch in endogenous hippocampal microglia and a role in proliferation. j. neurosci. 1999; 19: p. 10680–10693. 52. rappert a, biber k, nolte c, lipp m, schubel a, lu b, et al. secondary lymphoid tissue chemokine (ccl21) activates cxcr3 to trigger a clcurrent and chemotaxis in murine microglia. j. immunol. 2002; 168: p. 3221–3226. 53. schilling t, stock c, schwab a, eder c. functional importance of ca2+-activated k+ channels for lysophosphatidic acid-induced microglial migration. eur. j. neurosci. 2004; 19: p. 1469–1474. 54. caggiano ao, kraig rp. prostaglandin e2 and 4aminopyridine prevent the lipopolysaccharide-induced outwardly rectifying potassium current and interleukin1β production in cultured rat microglia. j. neurochem. 1998; 70: p. 2357–2368. 55. franciosi s, ryu jk, choi hb, radov l, kim su, mclarnon jg. broad-spectrum effects of 4aminopyridine to modulate amyloid β1-42-induced cell signaling and functional responses in human microglia. j. neurosci. 2006; 26: p. 11652–11664. romanian neurosurgery (2013) xx 1: 34 45 43 56. stock c, schilling t, schwab a, eder c. lysophosphatidylcholine stimulates il-1β release from microglia via a p2x7 receptor-independent mechanism. j. immunol. 2006; 177: p. 8560–856. 57. khanna r, roy l, zhu x, schlichter lc. k+ channels and the microglial respiratory burs. am. j. physiol. 2001; 280: p. c796–c806. 58. fordyce cb, jagasia r, zhu x, schlichter lc. microglia kv1. 3 channels contribute to their ability to kill neurons. j. neurosci. 2005; 25: p. 7139–7149. 59. kaushal v, koeberle pd, wang y, schlichter lc. the ca2+-activated k+ channel kcnn4/kca3. 1 contributes to microglia activation and nitric oxide dependent neurodegeneration. j. neurosci. 2007; 27: p. 234–244. 60. cheneval d, ramage p, kastelic t, szelestenyi t, niggli h, hemmig r, et al. increased mature interleukin-1beta (il-1beta) secretion from thp-1 cells induced by nigericin is a result of activation of p45 il1beta-converting enzyme processin. j. biol. chem. 1998; 273: p. 17846–17851. 61. caggiano ao, kraig rp. prostaglandin e2 and 4aminopyridine prevent the lipopolysaccharide-induced outwardly rectifying potassium current and interleukin1beta production in cultured rat microglia. j. neurochem. 1998; 70: p. 2357–2368. 62. schlichter lc, sakellaropoulos g, ballyk b, pennefather ps, phipps dj. properties of k+ and cl channels and their involvement in proliferation of rat microglial cel. glia. 1996; 17: p. 225–236. 63. novarino g, fabrizi c, tonini r, denti ma, malchiodi-albedi f, lauro gm, et al. involvement of the intracellular ion channel clic1 in microgliamediated β-amyloid-induced neurotoxicity. j. neurosci. 2004; 24: p. 5322–5330. 64. thomas mp, chartrand k, reynolds a, vitvitsky v, banerjee r, gendelman he. ion channel blockade attenuates aggregated alpha synuclein induction of microglial reactive oxygen species: relevance for the pathogenesis of parkinson's disease. j. neurochem. 2007; 100: p. 503–519. 65. milton rh, abeti r, averaimo s, debiasi s, vitellaro l, jiang l, et al. clic1 function is required for β-amyloid-induced generation of reactive oxygen species by microglia. j. neurosci. 2008; 28: p. 11488– 11499. 66. kjaer k, strøbaek d, christophersen p, rønn lc. chloride channel blockers inhibit inos expression and no production in ifnγ-stimulated microglial bv2 cells. brain res. 2009; 1281: p. 15–24. 67. ducharme g, newell ew, pinto c, schlichter lc. small-conductance clchannels contribute to volume regulation and phagocytosis in microglia. eur. j. neurosci. 2007; 26: p. 2119–2130. 68. eder c. ion channels in microglia (brain macrophages). am. j. physiol. 1998; 275: p. c327– c342. 69. thomas mp, chartrand k, reynolds a, vitvitsky v, banerjee r, gendelman he. ion channel blockade attenuates aggregated alpha synuclein induction of microglial reactive oxygen species: relevance for the pathogenesis of parkinson's disease. j. neurochem. 2007; 100: p. 503–519. 70. sieger d, moritz c, ziegenhals t, prykhozhij s, peri f. long-range ca2+ waves transmit brain-damage signals to microglia. dev cell. 2012; 22(6): p. 1138-48. 71. hanisch uk, kettenmann h. microglia: active sensor and versatile effector cells in the normal and pathologic brain. nat neurosci. 2007; 10(11): p. 138794. 72. block ml, zecca l, hong js. microglia-mediated neurotoxicity: uncovering the molecular mechanisms. nat rev neurosci. 2007; 8: p. 57–69. 73. czeh m, gressens p, kaindl am. the yin and yang of microglia. dev neurosci. 2011; 33: p. 199–209. 74. walter l, neumann h. role of microglia in neuronal degeneration and regeneration. semin immunopathol. 2009; 31: p. 513–525. 75. bruce aj, boling w, kindy ms, peschon j, kraemer pj, carpenter mk, et al. altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking tnf receptors. nat med. 1996; 2(7): p. 788-94. 76. sawada m, sawada h, nagatsu t. effects of aging on neuroprotective and neurotoxic properties of microglia in neurodegenerative diseases. neurodegener dis. 2008; 5: p. 254–256. 77. kiyama h. the fate of injured motor neurons and the behavior of surrounding glial cells. rinsho shinkeigaku. 2012; 52(11): p. 934-6. 78. kotter mr, li ww, zhao c, franklin rj. myelin impairs cns remyelination by inhibiting oligodendrocyte precursor cell differentiation. j neurosci. 2006; 26: p. 328–322. 79. streit wj, hurley sd, mcgraw ts, semplerowland sl. comparative evaluation of cytokine profiles and reactive gliosis supports a critical role for interleukin-6 in neuron-glia signaling during regeneration. j neurosci res. 2000; 61: p. 10–20. 80. strle k, zhou jh, broussard sr, venters hd, johnson rw, freund gg, et al. il-10 promotes survival of microglia without activating akt. j neuroimmunol. 2002; 122(1-2): p. 9-19. 81. dolga am, culmsee c. protective roles for potassium sk/k(ca)2 channels in microglia and neurons. front pharmacol. 2012; 3: p. 196. 82. rodríguez-martínez g, velasco i. activin and tgf-β effects on brain development and neural stem cells. cns neurol disord drug targets. 2012. 83. dobolyi a, vincze c, pál g, lovas g. the 44 alvis-miranda et al microglia: roles and rules in brain traumatic injury neuroprotective functions of transforming growth factor beta proteins. int j mol sci. 2012; 13(7): p. 821958. 84. mctigue dm, popovich pg, morgan te, stokes bt. localization of transforming growth factor-beta1 and receptor mrna after experimental spinal cord injury. exp neurol. 2000; 163: p. 220-230. 85. doyle kp, cekanaviciute e, mamer le, buckwalter ms. tgfβ signaling in the brain increases with aging and signals to astrocytes and innate immune cells in the weeks after stroke. j neuroinflamm. 2010; 7: p. 62. 86. dhandapani km, brann dw. transforming growth factor-beta: a neuroprotective factor in cerebral ischemia. cell biochem biophys. 2003; 39: p. 13-22. 87. pepper ms. transforming growth factor-beta: vasculogenesis, angiogenesis, and vessel wall integrity. cytokine growth factor rev. 1997; 8: p. 21-43. 88. bertolino p, deckers m, lebrin f, ten dijke p. transforming growth factor-beta signal transduction in angiogenesis and vascular disorders. chest. 2005; 128: p. 585s-590. 89. li mo, wan yy, sanjabi s, robertson ak, flavell ra. transforming growth factor-beta regulation of immune responses. annu rev immunol. 2006; 24: p. 99-146. 90. aloisi f, de simone r, columba-cabezas s, levi g. opposite effects of interferon-γ and prostaglandin e2 on tumor necrosis factor and interleukin-10 production in microglia: a regulatory loop controlling microglia proand anti-inflammatory activities. j neurosci res. 1999; 56: p. 571–580. 91. o’keefe gm, nguyen vt, benveniste en. class ii transactivator and class ii mhc gene expression in microglia: modulation by the cytokines tgf-β, il-4, il-13 and il-10. eur j immunol. 1999; 29: p. 1275– 1285. 92. frei k, lins h, schwerdel c, fontana a. antigen presentation in the central nervous system. the inhibitory effect of il-10 on mhc class ii expression and production of cytokines depends on the inducing signals and the type of cell analyzed. j immunol. 1994; 152: p. 2720 –2728. 93. gordon s. alternative activation of macrophages. nat rev immunol. 2003; 3: p. 23–35. 94. chen mk, guilarte tr. translocator protein 18 kda (tspo): molecular sensor of brain injury and repair. pharmacol ther. 2008; 118: p. 1–17. 95. perry vh, nicoll ja, holmes c. microglia in neurodegenerative disease. nat rev neurol. 2010; 6: p. 193–201. 96. ling l, zeng j, pei z, cheung rt, hou q, xing s, et al. neurogenesis and angiogenesis within the ipsilateral thalamus with secondary damage after focal cortical infarction in hypertensive rats. cereb blood flow metab. 2009; 29: p. 1538-1546. 97. jantaratnotai n, schwab c, ryu jk, mcgeer pl, mclarnon jg. converging perturbed microvasculature and microglial clusters characterize alzheimer disease brain. curr alzheimer res. 2010; 7: p. 625-636. 98. welser jv, li l, milner r. microglial activation state exerts a biphasic influence on brain endothelial cell proliferation by regulating the balance of tnf and tgf-β1. j neuroinflamm. 2010; 7: p. 89. 99. shaked i, porat z, gersner r, kipnis j, schwartz m. early activation of microglia as antigen-presenting cells correlates with t cell-mediated protection and repair of the injured central nervous system. journal of neuroimmunology. 2004; 146: p. 84–93. 100. nakajima k, honda s, tohyama y, imai y, kohsaka s, kurihara t. neurotrophin secretion from cultured microglia. j. neurosci. res. 2001; 65: p. 322– 331. 101. nakajima k, tohyama y, kohsaka s, kurihara t. ability of rat microglia to uptake extracellular glutamate. neurosci. lett. 2001; 307: p. 171– 174. 102. chang ml, wu ch, chien hf, jiang-shieh yf, wen cy. microglia/macrophages responses to kainateinduced injury in the rat retina. neurosci. res. 2006; 54(3): p. 202-212. 103. cho ih, hong j, suh ec, kim jh, lee je, lee s, et al. roles of microglial ikkbeta in kainic acid-induced hippocampal neuronal cell death. brain. 2008; 131(11): p. 3019-3033. 104. jim je, kwak se, jo sm, kang tc. blockade of p2x receptor prevents astroglial death in the dentate gyrus following pilocarpine-induced status epilepticus. neurol. 2009; 31(9): p. 982-8. 105. yenari ma, kauppinen tm, swanson ra. microglial activation in stroke: therapeutic targets. neurotherapeutics. 2010; 7: p. 78–391. 106. liu w, tang y, feng j. cross talk between activation of microglia and astrocytes in pathological conditions in the central nervous system. life sciences. 20011; 89(141–146). 107. chao cc, hu s, sheng ws, bu d, bukrinsky mi, peterson pk. cytokine-stimulated astrocytes damage human neurons via a nitric oxide mechanism. glia. 1996; 16(3): p. 276–84. 108. retamal ma, froger n, palacios-prado n, ezan p, sáez pj, sáez jc, et al. cx43 hemichannels and gap junction channels in astrocytes are regulated oppositely by proinflammatory cytokines released from activated microglia. j neurosci. 2007; 27(50): p. 13781-92. 109. microglial activation induced by brain trauma is suppressed by post-injury treatment with a parp inhibitor. journal of neuroinflammation. 2012; 9: p. 31. 110. kumar a, loane dj. neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. brain, behavior, and immunity. 2012; 26: romanian neurosurgery (2013) xx 1: 34 45 45 p. 1191–1201. 111. surace mj, block ml. targeting microgliamediated neurotoxicity: the potential of nox2 inhibitors. cell mol life sci. 2012; 69(14): p. 2409-27. 112. tahraouis sl, marret s, bodénant c, leroux p, dommergues ma, evrard p, et al. central role of microglia in neonatal excitotoxic lesions of the murine periventricular white matter. brain pathol. 2001; 11(1): p. 56-71. 113. dommergues ma, plaisant f, verney c, gressens p. early microglial activation following neonatal excitotoxic brain damage in mice: a potential target for neuroprotection. neuroscience. 2003; 121: p. 619–628. 114. choi sh, aid s, kim hw, jackson sh, bosetti f. inhibition of nadph oxidase promotes alternative and anti-inflammatory microglial activation during neuroinflammation. j. neurochem. 2012; 120: p. 292– 301. 115. groemping y, rittinger k. activation and assembly of the nadph oxidase: a structural. biochem j. 2005; 386: p. 401–416. 116. sedeek m, hébert rl, kennedy cr, burns kd, touyz rm. molecular mechanisms of hypertension: role of nox family nadph oxidases. curr. opin. nephrol. hypertens. 2009; 18: p. 122–127. 117. muller g, morawietz h. nitric oxide, nad(p)h oxidase, and atherosclerosis. antioxid. redox signal. 2009; 11: p. 1711–1731. 118. robinson jm. phagocytic leukocytes and reactive oxygen species. histochem. cell biol. 2009; 131: p. 465–469. 119. huh sh, chung yc, piao y, jin my, son hj, yoon ns, et al. ethyl pyruvate rescues nigrostriatal dopaminergic neurons by regulating glia activation in a mouse model of parkinson’s disease. j. immunol. 2011; 187: p. 960–969. 120. lijia z, siqi z, xiaoxiao w, chunfu w, jingyu y. a self-propelling cycle mediated by reactive oxide species and nitric oxide exists in lps-activated microglia. neurochemistry international. 2012; 61: p. 1220–1230. 121. kim yt, moon sk, maruyama t, narumiya s, doré s. prostaglandin fp receptor inhibitor reduces ischemic brain damage and neurotoxicity. neurobiol dis. 2012; 48(1): p. 58-65. 122. etemad s, zamin m, ruitenberg mj, filgueira l. a novel in vitro human microglia model: characterization of human monocyte-derived microglia. journal of neuroscience methods. 2012; 209: p. 79– 89. 123. ellis sl, gysbers v, manders pm, li w, hofer mj, müller m, et al. the cell-specific induction of cxc chemokine ligand 9 mediated by ifn-gamma in microglia of the central nervous system is determined by the myeloid transcription factor pu. 1. j immuno. 2010; 185(3): p. 1864-77. 124. bsibsi m, ravid r, gveric d, van noort jm. broad expression of toll-like receptors in the human central nervous system. j neuropathol exp neurol. 2002; 61(11): p. 1013-21. microsoft word 5.chiriaca_ourcenter_f.docx romanian neurosurgery (2011) xviii 4: 421 424 421 our center experience in carotid artery stenting a. chiriac, n. dobrin, i. nedelciuc, z. faiyad, i. poeată clinic of neurosurgery “gr.t. popa” university of medicine and pharmacy iasi, romania “prof. dr. n. oblu” clinical emergency hospital, iaşi, romania clinic of cardiology, “g. georgescu” cardiology institute, iasi, romania abstract carotid artery stenting becomes first intention treatment in atheromatous carotis artery stenosis. in this article we present our first experience in carotid artery stentig on 27 consecutive patients. demographic, clinic and angiographic dates are retrospectively review and technical success rate and postprocedural complication are statistically compared with literature trial studies. keywords: carotid stenosis, stroke, stents introduction cerebrovascular events due to atherosclerotic carotid artery disease represent 20 percent of all strokes. percutaneous transluminal carotid angioplasty with stent becomes today the most used therapy for atheromatous causes of stenotic and occlusive disease of the internal carotid artery. previously study trials have shown that the endovascular stenting treatment of carotid artery stenosis is an optimal therapy for carotid artery stenosis more that 70% in asymptomatic patients or more that 50% in symptomatic patients. in this study we report the efficiency, clinical and imagistic results in the stenting treatment of 27 consecutive patients with internal carotid artery stenosis. methods all 27 patients included in the study benefit of an endovascular carotid stenting for unilateral or bilateral carotid artery stenosis between may 2010 and october 2011. the first evidence of carotid stenosis was identified on non invasive test (doppler sonography, angio-ct and angiomri) in 20 patients and on invasive catheter angiography (in time of coronary and peripheral angiography) in 7 cases. careful neurological evaluation was performed in all patients before endovascular intervention, 24 hours after procedure and at the periodical control at 2 and 6 months by the same neurosurgeon specialists. preprocedural cerebral ct scans were performed for the patients with permanent or remitted neurological deficits after a previously stroke (between 6-12 months). postprocedural cerebral ct scan was only performed in the patients with neurological deficits installed after a stroke suffered at more than 2 weeks before the procedure. control catheter angiography was performed earlier than one year for the 3 patients who benefit from a bilateral carotid stenting in two steps and after one year in 5 patients. 422 a. chiriac et al our experience in carotid artery stenting stenting procedure before the procedure all patients received 100 mg acetylsalicylic acid and 75 mg clopidogrel for at least 3 days. 300 mg clopidogrel loading dose was administrated on the same day of the procedure for those patients with no antiplatelet medication. a dose of 5000 units of heparine was administrated during the procedure to maintain an optimal activated clotting time between 200 and 250. 75 mg clopidogrel and 100 mg acetylsalicylic acid were continued to be administrated for at least 6 months. for bradycardia and hypotension reaction prevention, potentially associated with carotid dilatation, 1 mg of atropine was intravenously administrated. arterial blood pressure, ekg and o2 saturation were continuously monitored during the procedures. all procedures were performed under local anesthesia with 5% lidocaine infiltrated at the access site. a standard retrograde trans-femural access through an 8f vascular sheath was used for all stenting procedures. selective common carotid artery angiographies were obtained with an 8f mach1, boston guiding catheter. the guiding catheters were advanced into the common carotid artery on support of a hydrophilic guide wire (0.035in, “j” peak, 150cm length). after that, an angiographic examination of the stenotic carotid lesion in an optimal projection (clearly exposure of the carotid bifurcation) was done. keeping this angiographic image as reference image on the secondary screen, an embolic protection device was thereafter employed. two different embolic protection device were used, the boston scientific filter wire “ez” in 6 patient and abbott emboshield nav6 embolic protection system in 14 patients. in 8 cases a predilatation procedure of the severe stenotic lesion with a 2.5/20 mm balloon was necessary for a safety embolic protection device passes (table 3). a self-expandable stent was placed over the atheromatouse lesion. a boston scientific stent “wallstent” was used in 8 cases and an abbott xact carotid stent system was used in 19 cases. 17 patients benefited by postdilatation for intra-stent blood flow optimization with a 5.5/30mm balloon. a final carotid angiographic exposure is performed (figure 1). all the patients were discharged at home at two days except 4 patients who were transferred to neurology. figure 1 angiography images with a ica stenosis b intrastent balloon postdilatation c ica dilatated with stent table 1 criteria for high-risk patients: pathologic criteria cases age over 80 years history of open heart surgery need for open heart surgery within 30 days 1 multi-vessel atherosclerosis 2 left ventricular dysfunction with ejection deficit fraction <40% old myocardial infarction with coronary stenting 3 severe bronchopulmonary disease severe renal diseas significant contralateral carotid artery disease 6 previous endarterectomy 12 romanian neurosurgery (2011) xviii 4: 421 424 423 table 2 demographic, clinic and angiographic dates criteria no. age (mean + sd) years 61 + 12 gender (male / female) 18 / 9 symptomatic / asymptomatic 15 / 13 hemiplegia / hemiparesis 3 / 4 aphasia – disartria 5 mean lesion length (mm) 18 mean severity of stenosis (%) 84 bilateral carotid disease > 70% 5 contralateral carotid occlusion 2 table 3 procedural characteristics and angiographic results characteristics no. embolic protection device (boston/abbott) 6 / 14 stent (boston/abbott) 8 / 19 predilatation 8 postdilatation 17 residual stenosis (mean + sd) 14 +6 results the demographic data of the study group shows an average age of 61 years (range from 48 to 72) and gender distribution of 18 men and 9 women. in terms of clinical aspects 12 patients were classified as high risk patients (6 suffered from significant contralateral carotid artery disease, 3 had old myocardial infarction with coronary stenting and 2 had multivessel atherosclerosis. one asymptomatic patient, who referred to us for carotid stenting treatment, required an open heart surgery in the following 30 days and one was known with left ventricular dysfunction with ejection deficit fraction under 40% (table 1, 2). good postdilatation results were obtained with residual stenosis less than 20% in al cases (the mean residual stenosis was 14%). no subintimal dissection, arterial disruption or contrast extravasations were noted. neurological examinations at two days and 2 months posinterventionl show no major modification comparative with the admission neurological status. mild headache, lightheadness, dizziness or minor discomfort at the neck level, remitted completely in 24 hours were observed in 4 patients. three patients showed episodes of significant bradycardia after balloon dilatation. new stroke or deaths were not encountered at 6 months after the procedure, except one patient who experienced a temporary aphasia at 4 month. discussion our experience concerning the carotid angioplasty with stent placement suggest that this technique it’s an efficient therapeutic alternative especially in those patients considered to be at higher risk for stroke. the short-term neurological and angiographic results of our patients series are well correlated with other largest series reports from the literature. data from the most recent randomized trials reported a technical success rate of 98.4%, a minor stroke rate of 2.7%, a major stroke rate of 1.49%, and a mortality rate of 0.88% (3). a rigorous comparison of the results provided by this study with those obtained from the published studies could not be done because of differences in patient’s number, neurological status at the admission and upper age limit. the european carotid stent trial (ecst) had reported an overall sever stroke and death rates of 7% in patients with symptomatic patients wile the 424 a. chiriac et al our experience in carotid artery stenting asymptomatic carotid atherosclerosis study (acas) had reported periprocedural stroke and death rates of 2.3% in lower-risk subset (3). although, in our patients study there was no statistic difference between symptomatic group and the asymptomatic group, our results been more close to those obtained in acas. some studies recommend the use of carotid protection device even if an intrstent balloon postdilatation is not necessary. although, these studies mention a periprocedural increased risk due to not using a carotid protection device and during balloon postdilatation, we have not encountered such problems. we believe that the use of a carotid protection device for carotid stenting without balloon postdilatation is not absolutely necessary, and a reduction of balloon inflation time will minimize the disruptions of cerebral blood flow, especially in patients with contralateral carotid occlusion. the technical success rate of our 27 consecutive carotid stenting procedures was 100%. the mean residual stenosis immediately after stent implantation was 14% indicating the feasibility of this procedure under optimal choice of materials and experienced specialist. conclusions the carotid artery stenting was proven to be an optimal treatment for most of the patients with symptomatic carotid stenosis or asymptomatic severe carotid stenosis (>70%). we need for a long-time study including a greater number of patients in order to make a correct statistical analysis with other multicenter studies. finally, our study could be a guide for the other neurosurgeon colleagues who wants to implement this treatment technique in their departments. references 1. brahmajee k. nallamothu, hitinder s. gurm, henry h. ting, philip p. goodney, mary a. m. rogers, jeptha p. curtis, justin b. dimick, eric r. bates, harlan m. krumholz, john d. birkmeyer (2011) operator experience and carotid stenting outcomes in medicare beneficiaries, jama, 306(12):1338-1343; 2. chaer ra, makaroun ms. (2008) evolution of carotid stenting: indications, semin vasc surg. jun; 21(2):59-63; 3.haji-zeinali ali-mohammad, kazemi-saleh davood (2006) an experience with angioplasty and stenting of carotid artery stenosis with embolic protection devices, arch iranian med 2006; 9 (2): 138 – 143; 4. knur r. (2009) carotid artery stenting: a systematic review of randomized clinical trials, vasa. nov; 38 (4): 281-91. 5. giovanni s, roberto g, francesco v, enrico p, sebastiano f, matteo s, alessio s, carlo ar, massimiliano dp, eleonora g. (2009) carotid artery stenting : a single-centre experience with up to 8 years> follow up. eur radiol 19:982-989; 6. namazi mo. hassan, mohammadi af., safi m., vakili h., saadat h., amini ad. (2010) carotid artery stenting: a single-center experience, j teh univ heart ctr 4 (2010) 188-193; 7. verzini f, cao p, de rango p, parlani g, maselli a, romano l, norgiolini l, giordano g. (2006) appropriateness of learning curve for carotid artery stenting: an analysis of periprocedural complications. j vasc surg 44:1205-1211; 8. yun ws, kwun wh, suh by. (2011) the early and mid-term results of carotid artery stenting in high-risk patients, j korean surg soc.apr;80(4):283-8. moscotesalazar_asystematicrew romanian neurosurgery (2014) xxi 2: 135 145 135 endovascular management of dural fistulas into the cavernous sinus. a systematic review luis rafael moscote-salazar1, marco zenteno2, jorge a santosfranco3, nancy carolina duarte-valdivieso4, hernando raphael alvis-miranda1, angel lee5 1universidad de cartagena, colombia 2instituto nacional de neurologia y neurocirugía “manuel velasco suarez”, mexico 3imss “la raza” mexico d.f, mexico 4chang gung memorial hospital, linkou, taiwan 5hospital angeles del pedregal, mexico abstract background: dural fistula to the cavernous sinus (dfcs) is an infrequent pathology that consists in the anomalous communication between the meningeal branches of the internal carotid artery (ica) and/or the external carotid artery (eca) and the cavernous sinus. aim: to perform a systematic review to evaluate clinical and imaging findings in dfcs, and current indications for treatment. methods: a literature search was performed in several medical databases using the keywords “intracranial dural fistula”, “carotid-cavernous fistula”, “endovascular treatment”, associated with “outcome”; resulting articles were assessed by considering factors such as: number of patients treated, type of material used, complications, and type of image technique used for diagnosis. results: 33 articles were selected, yielding: clinical and imaging: the symptoms are basically related to the type of venous drainage of the fistula. the combination of ocular symptoms and tinnitus is highly suggestive of dfcs. ocular symptoms are found in 80-97% of patients, while the tinnitus is present in up to 50% of cases. the imaging method for initial assessment of the dfcs is the magnetic resonance imaging. digital subtraction angiography is the method of choice to determine adequately the precise angioarchitecture of the injury and its drainage. this data is of vital importance in future decision making. treatment: currently are considered as indications for the management of dfcs: 1) rapidly progressive deterioration of visual function, 2) angiographic evidence of abnormal cortical venous drainage, 3) the hypoxic consequences in retina and optic nerve, and 4) ischemic keratitis; the most suitable materials for embolization of the dfcs are ca and pap. conclusion: dfcs stills being an uncommon cerebrovascular condition, with good outcomes from endovascular treatment. 136 moscote-salazar et al endovascular management of dural fistulas into the cavernous sinus key words: dural fistula; carotidcavernous fistulas; n-butil-cyanoacrylate; cavernous sinus. introduction intracranial arteriovenous fistulae are of two main types: carotid-cavernous fistulas (ccf) and dural arteriovenous fistulas. ccf is an infrequent pathology that consists in the anomalous communication between the meningeal branches of the internal carotid artery (ica) and/or the external carotid artery (eca) and the cavernous sinus. these belong to the indirect ccf. unlike direct ccf which are frequently evocated by trauma, (1–5) indirect ccf more commonly occur spontaneously, being rare the traumatic etiology. (5, 6) clinical manifestations generally follow a less severe course than direct ccf, being the ophthalmological symptoms and the presence of superior drainage, the most relevant data, mainly for provide an adequate therapeutic approach. currently the preferred management is the endovascular. in this article we present a systematic review about endovascular management of dural fistulas into the cavernous sinus. methods a literature search was performed in several medical databases including pubmed, embase, scopus, and google scholar; without restrictions or filters with regard to language or year of publication; showing a total of 33 results using the keywords “intracranial dural fistula”, “carotid-cavernous fistula”, “endovascular treatment”, associated with “outcome”. emphasis was given to the angiographic, imaging and hemodynamic characteristics found usually in dural fistulas to the cavernous sinus (dfcs); the resulting articles were assessed by considering factors such as: number of patients treated, type of material used, complications, and type of image technique used for diagnosis. etiology indirect ccf occurs typically and spontaneously in postmenopausal women, although they can occur also in other age groups as consequence of pregnancy, sinusitis or cavernous sinus thrombosis. (5–8). there is not a universal and convenient explanation regard its genesis, however, since houser et al demonstrated that thrombosis of the lateral and sigmoid sinus precede the formation of dural fistulas, many authors implied the thrombosis of the cavernous sinus as the natural precursor of the dfcs, pushing away the theory proposed by newton and hoyt, who pointed out as cause, the microtraumatisms over the delicate vessels of the carotid siphon (7). meyers et al (5), reported their 15 years’ experience in the management of 135 consecutive patients with diagnosis of dfcs, being none of traumatic etiology. therefore, the frank traumatic etiology of the dfcs is extremely rare. berenstein et al (9) in 1986, reported 11 cases of arteriovenous fistulas, and mention one of dfcs of traumatic origin. keltner et al (10) in 1987, described the case of traumatic indirect ccf within a total of 12 cases of ccf. higashida et al (11) in an extensive review of 213 traumatic ccf published in 1989, found 7 cases of indirect fistula to the cavernous sinus. jacobson et al romanian neurosurgery (2014) xxi 2: 135 145 137 (6), in 1996 reported two additional cases of traumatic indirect ccf. notably, jacobson and colleagues conclude that the recognition of traumatic origin allow an adequate choice of route and material to be used, we do not think that the traumatic history is a planning guide for management, we believe the choice of route and the material will be governed by the amount and type of tributaries that have the fistula, and venous drainage pattern, considerations that go far beyond agreement cited by other authors (6, 7, 10, 12). clinical and imaging findings clinical findings the symptoms are basically related to the type of venous drainage of the fistula, therefore: 1) anterior drainage into the superior ophthalmic vein originate ophthalmic symptoms, for example, exophthalmos and chemosis; 2) posteroinferior drainage into the petrosal sinus, basilar plexus and pterygoid plexus will produce murmurs, and deficit of some cranial nerves; 3) subsequent drainage into the superior petrosal sinus originates murmur; 4) cortical reflux into the sphenoparietal sinus and upper middle cerebral vein may cause infarction and hemorrhage; and 5) deep drainage into the deep middle cerebral vein and the uncal vein can trigger hemorrhages (13). these symptoms affecting intracranial and extracranial structures can be grouped into four patterns (14): a) orbital including chemosis, proptosis, eyelid edema and periorbital pain, b) cavernous with ptosis, diplopia, anisocoria and ophthalmoplegia, c) ocular with decreased visual acuity or increased intraocular pressure (> 20 mmhg or interocular difference greater than 5 mmhg), severe eye pain, glaucoma, and retinal hemorrhage, and d) cerebral, including cerebral venous congestion in the basal ganglia, brain stem or cerebellum promoting presence of epilepsy and hemorrhage. the combination of ocular symptoms and tinnitus is highly suggestive of dfcs. ocular symptoms are found in 80-97% of patients, while the tinnitus is present in up to 50% of cases. these symptoms are usually less dramatic than direct ccf, and rarely are lifethreatening. the flow of dfcs is usually much lower than the direct ccf, being the most important reason to present a less aggressive clinical spectrum, however there are reports of significant morbidity such as blindness and stroke (15,16). about 30 to 40% cases of indirect ccf present cerebral hemorrhage due to the rupture of dilated cerebral veins as a result of retrograde drainage. when dfcs is clinically suspected, the patient must be carefully examined for confirmatory signs. in the presence of an eye with engorged vessels, conjunctival erythema or proptosis is mandatory to auscultate the skull and facial bones searching for murmurs. usually the affected eye is ipsilateral to the fistula, however there are cases of bilateral symptoms due to the commitment of both cavernous sinuses because communication between them through intercavernous sinuses. imaging findings the imaging method for initial assessment of the dfcs is the magnetic resonance 138 moscote-salazar et al endovascular management of dural fistulas into the cavernous sinus imaging (mri). the findings include: 1) increased volume of the cavernous sinus; 2) loss of the interface between the cavernous sinus and the intracavernous portion of the ica, 3) dilation of the superior ophthalmic vein (17, 18). digital subtraction angiography (dsa) is the method of choice to determine adequately the precise angioarchitecture of the injury and its drainage. this data is of vital importance in future decision making. therefore, the angiographic evaluation must provide specific information regarding arterial tributaries, the precise site of shunt and the venous drainage pattern. in many cases this analysis can only be complete during the therapeutic phase. for this, it is recommended the angiographical evaluation in two phases: 1) diagnostic catheterization and 2) supraselective catheterization, which can be performed during treatment of the injury. some authors have emphasized the importance of non-invasive alternatives modalities such as helical ct-angiography (angio-ct) and magnetic resonance angiography (mra), which is supposed to characterize the injury angioarchitecture (18). however, even with the visualization of afferent vessels and draining veins, dsa only guides in analyzing how the different compartments involved are interrelated, and helps the understanding of the hemodynamics of the lesion, enabling better therapeutic approach. thus, the dsa still remains the gold standard for assessing dfcs. barrow et al (19) proposed an angiographic classification for ccf, revalidated by debrun et al (7), and widely used by diverse authors, see table 1. in the review of literature persists the trending of the predominance of the ccf type d over type c, being truly extraordinary the type b. table 1 barrow classification of dfcs type fistulous vessels characteristics a carotid artery to cavernous sinus direct, high flow, the most common b dural ica branches to cavernous sinus: -meningohypophyseal trunk (66%) -inferolateral trunk (30%) indirect, low flow c eca branches to cavernous sinus: -internal maxillary (67%) -middle meningeal (31%) -ascending pharyngeal (24%) indirect, low flow d both ica and eca branches indirect, the most common of low flow ica: internal carotid artery; eca: external carotid artery why and when to treat dfcs? from all dural fistulas, about 10% to 60% can present spontaneous resolution, and 25 to 50% are to the cavernous sinus, therefore have a much more benign course than direct ccf with a natural history that can lead to spontaneous healing. (10, 15, 16, 19–22) the cure occurring shortly after performing diagnostic angiography is not rare. many patients experience a period of worsening of symptoms, particularly ophthalmics, during the spontaneous healing process. (12, 23) for this reason the decision on the management of the dfcs is controversial. keltner, et al (10) treated by endovascular approach only 1 of the romanian neurosurgery (2014) xxi 2: 135 145 139 10 cases reported, while 7 were offered only ophthalmologic management with treatment for glaucoma, reporting good control, therefore conclude that these cases should not be subjected to definitive treatment. currently are considered as indications for the management of dfcs: 1) rapidly progressive deterioration of visual function, 2) angiographic evidence of abnormal cortical venous drainage, 3) the hypoxic consequences in retina and optic nerve, and 4) ischemic keratitis (5, 11, 12, 20). among the mechanisms involved in the worsening of dural fistulas are: 1) stenosis or thrombosis of the outflow, 2) increasing of the arterial blood flow, and 3) the emergence of a new fistula or enlargement of preexisting shunt (21, 24). in the days before the advent of neurological endovascular therapy, traditional surgery for the management of this condition was accompanied by a very high risk of thromboembolic events, almost always accompanied by cerebral ischemic disease and/or blindness (11). currently the endovascular therapy is considered as the treatment of choice for all types of ccf for the following reasons: 1) is performed under local anesthesia with the possibility of ongoing clinical evaluation of the patient for early detection of any complication, 2) is a low risk approach, 3) less time consumption during the procedure, 4) reaches surgically inaccessible sites, 5) more likely to conserve the ica blood flow, 6) fast recovery of the patient, and 7) there is always the possibility to repeat the procedure in case of initial failure or recurrence of the fistula (3–5, 7, 9, 11, 12, 20, 25) approach route the dfcs are arteriovenous or arteriovenous shunts, in these cases it is determined that occlusion of the venous portion is the treatment of choice (26–28) for this purpose transvenous route is usually the best access method for insertion and release of embolic material, with current predominant use of detachable coils. different routes have been described and used to reach the cavernous sinus, such as through lower petrosal sinus (contralateral or ipsilateral), basilar plexus, circular or intercavernous sinus, through the facial vein, the angular and superior ophthalmic veins or through the pterygoid plexus (5, 11, 20, 24, 25, 29–34). in a large retrospective study, mayers et al (5), summarizes 15 years of experience in the management of 135 dfcs patients treated transvenously, coils were used in 87% of cases, pieces of suture material in 13% and only in 3% of patients was used liquid adhesive material. they reported good long-term results in 97% of cases. cheng et al (25) reported the cases of 27 patients treated transvenously with gdc and fibered coils, where only one case was necessary to combine with the arterial line for administration of pap; in these same study, 89% of the cases experimented angiographic cure (25). retrospectively, klish et al, reported 11 cases of dfcs embolized by transvenous approach with coils, reaching a frequency of anatomical cure of 63%, however, they refer that all patients, including those who did not achieve such healing, showed improvement in their symptoms (20). reported complications of the transvenous approach with occlusion of 140 moscote-salazar et al endovascular management of dural fistulas into the cavernous sinus the cavernous sinus, the lesion of the vein access, the immediate and rapid increase of the ophthalmologic symptomatology and the injury of any of the oculomotor nerves caused either by over-packing of coils or induced thrombotic process itself within the sinus (10, 25). furthermore, it has been determined in the case of dural fistulas that sinus therapeutic occlusion with coils, and the subsequent thrombosis can activate angiogenic factors within the adjacent dural walls (22, 32, 35–37). in cases where it is not possible to exploit adequately the venous approach, the arterial approach can be useful (11, 12). ca is the material of choice in the arterial approach because allows better control of time and degree of polymerization modifying its dilution with the lipid contrast dye without starting with a total sacrifice of the circulation of the cavernous sinus, situation that makes it a more controllable material than pap. some authors not use the transvenous approach just for the likelihood of these complications plus it is expensive for the number of coils typically required to occlude the cavernous sinus, fact that in economic stringency environments becomes a major limiting factor in the decision making. one limitation of the arterial approach is the partial treatment of the fistula, particularly in type d cases, in which only were treated the fistulous pedicles of a single axis. this, in theory, perpetuates the fistula and may even increase the flow in other components, but our percentage of success and immediate and long-term cure is high. we think this is because the decision to embolize the pedicles of greater flow, and allow the passage of embolic material to the malformation own nest which could induce a progressive thrombosis of the compromised segments of the cavernous sinus, this thrombosis is seen further promoted by combination with manual compression maneuver of the carotid artery. hence can be avoided the nerve damage of oculomotor nerves or ophthalmologic deterioration that can be observed with the venous approach, and is a far less expensive method. satomi et al (24), have shown that partial treatment of dfcs, to what they have called palliative treatment, induces progressive changes in the pattern of venous drainage of the cavernous sinus with a trend towards very benign evolution with minimal ophthalmological commitment and almost no dilated cortical veins. another advantage observed with the arterial approach is the use of catheters guided by the flow, so far as possible avoids the use of microguides, which are to blame for vascular injury in case of venous approach. among the complications of trans-arterial route, viñuela et al (12) reported migration of the ca into distal branches of the middle cerebral artery, fortunately without much clinical implication, in addition to the transient increase in retroocular pain of one patient. embolization material viñuela et al (12) concluded that the most suitable materials for embolization of the dfcs are ca and pap. the use of ca is currently widespread in the management of arteriovenous malformations (avm), the opposite situation occurs in dfcs with few reports or small series. ca was first used as romanian neurosurgery (2014) xxi 2: 135 145 141 management of direct ccf in a case treated by bank et al (38) and in three cases managed by kerber et al (39) reported in 1978 and 1979, respectively in which is highlighted the conservation of the carotid flow which was established in a situation really encouraging, in a time when most endovascular and surgical techniques aimed to blood flow occlusion of the ica. it is noteworthy that the experience of the last authors was when acrylic was not approved by the fda for use in humans in northamerica. so was criticized and considered dangerous, and that the three cases described by kerber et al (39) presented some type of deficit arising from the migration of the substance or by the application of the microcatheter or the non-detachable ballon technique used to administrate the substance, although the deficit was transient and the evolution of the patients was good in the short and medium term. some authors like pierot et al (40), luo et al (3) and wang et al (41) reported their successful experience with ca in management of direct ccf of traumatic origin, partially treated or recurrent. berenstein et al (9) were first to use ca in the management of dfcs, which in turn was caused by trauma (9). from 10 cases described by keltner et al (10), only one was treated by endovascular technique with glue, precisely their single case secondary to trauma. viñuela et al (12) described a series of 16 spontaneous dfcs, of which four were treated with ac, 1 with ca and surgery, 1 with ca and particles, and 3 with only particles. from all cases only one was identified as "inadequate" healing. these authors conclude that the ca and the particles must be considered as the treatment of choice in the dfcs because allow superselective and more distal tributary vessels occlusion near the nest of the arterio-venous fistula, they consider that this may be sufficient to promote the cavernous sinus thrombosis with consequent total occlusion of the lesion. debrun et al (7) reported 132 cases of ccf, from which 32 were dfcs, of which 13 cases were treated only with ca, and the remaining with pap or a mixture of both. cure was obtained in 16 patients, whereas in the patients without early cure, some progressively improved, while others were lost to follow. it is necessary to emphasize that in this study the majority of indirect fistulas were type d (28 of 32 cases) and the authors conclude that they are the most difficult to treat because of the increased number of branches involved, which came from both ace and aci, hence adequate obliteration was more difficult to achieve, especially when considering that that occlusion of only ace flow can result in increased participation of the meningeal branches of the ica with much more difficult management in later stages (7). type d fistulas are more laborious, also require more mental exercise and can be disappointing for the endovascular specialist. for this reason some authors have considered to radiosurgery as a treatment option in selected cases, being combined with embolization or even with no pretreatment (42–46), however, more experience is needed with long-term outcomes to determine its efficacy and safety. 142 moscote-salazar et al endovascular management of dural fistulas into the cavernous sinus conclusions dfcs stills being an uncommon cerebrovascular condition, with good outcomes from endovascular treatment. currently the endovascular therapy is considered as the treatment of choice for all types of ccf, because good outcomes, and because traditional surgery is accompanied by a very high risk of thromboembolic events, almost always accompanied by cerebral ischemic disease and/or blindness. abbreviations: avm: arterio-venous malformation ca: cyanoacrylate. ccf: carotid-cavernous fistula. dfcs: dural fistula into the cavernous sinus dsa: digital substraction angiography eca: external carotid artery. gdc: guglielmi detachable coils. ica: internal carotid artery. mri: magnetic resonance imaging pap: polyvinyl-alcohol particles. correspondence: dr. luis rafael moscote-salazar, universidad de cartagena, cartagena de indias, colombia e-mail: mineurocirujano@aol.com references 1. kähärä veikko j, seppänen s, kuurne t, laasonen em. endovascular treatment of carotid-cavernous fistulae. acta neurol scand [internet]. 1998 oct [cited 2013 may 25];98(4):254–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/9808275 2. lewis ai, tomsick ta, tew jm. management of 100 consecutive direct carotid-cavernous fistulas: results of treatment with detachable balloons. neurosurgery [internet]. 1995 feb [cited 2013 may 25];36(2):239–44; discussion 244–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/7731502 3. luo c-b, teng mm-h, yen dh-t, chang f-c, lirng j-f, chang c-y. endovascular embolization of recurrent traumatic carotid-cavernous fistulas managed previously with detachable balloons. j trauma [internet]. 2004 jun [cited 2013 may 25];56(6):1214–20. available from: http://www.ncbi.nlm.nih.gov/pubmed/15211128 4. luo c-b, teng mm-h, chang f-c, lirng j-f, chang c-y. endovascular management of the traumatic cerebral aneurysms associated with traumatic carotid cavernous fistulas. ajnr am j neuroradiol [internet]. 2004 mar [cited 2013 may 25];25(3):501–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/15037481 5. meyers pm, halbach v v, dowd cf, lempert te, malek am, phatouros cc, et al. dural carotid cavernous fistula: definitive endovascular management and longterm follow-up. am j ophthalmol [internet]. 2002 jul [cited 2013 apr 24];134(1):85–92. available from: http://www.ncbi.nlm.nih.gov/pubmed/12095813 6. jacobson be, nesbit gm, ahuja a, barnwell sl. traumatic indirect carotid-cavernous fistula: report of two cases. neurosurgery [internet]. 1996 dec [cited 2013 apr 24];39(6):1235–7; discussion 1237–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/8938780 7. debrun gm, viñuela f, fox aj, davis kr, ahn hs. indications for treatment and classification of 132 carotid-cavernous fistulas. neurosurgery [internet]. 1988 feb [cited 2013 apr 24];22(2):285–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/3352876 8. alvis-miranda h, castellar-leones s, alcala-cerra g, moscote-salazar l. cerebral sinus venous thrombosis. j neurosci rural pr [internet]. 2013 [cited 2013 oct 25];4(4):427. available from: http://www.ruralneuropractice.com/text.asp?2013/4/4/4 27/120236 9. berenstein a, scott j, choi is, persky m. percutaneous embolization of arteriovenous fistulas of the external carotid artery. ajnr am j neuroradiol [internet]. 1986 [cited 2013 apr 24];7(5):937–42. available from: http://www.ncbi.nlm.nih.gov/pubmed/3096119 10. keltner jl, satterfield d, dublin ab, lee bc. dural and carotid cavernous sinus fistulas. diagnosis, management, and complications. ophthalmology [internet]. 1987 dec [cited 2013 apr 24];94(12):1585– 600. available from: http://www.ncbi.nlm.nih.gov/pubmed/3323984 11. higashida rt, halbach v v, tsai fy, norman d, pribram hf, mehringer cm, et al. interventional romanian neurosurgery (2014) xxi 2: 135 145 143 neurovascular treatment of traumatic carotid and vertebral artery lesions: results in 234 cases. ajr am j roentgenol [internet]. 1989 sep [cited 2013 apr 24];153(3):577–82. available from: http://www.ncbi.nlm.nih.gov/pubmed/2763958 12. viñuela f, fox aj, debrun gm, peerless sj, drake cg. spontaneous carotid-cavernous fistulas: clinical, radiological, and therapeutic considerations. experience with 20 cases. j neurosurg [internet]. 1984 may [cited 2013 apr 24];60(5):976–84. available from: http://www.ncbi.nlm.nih.gov/pubmed/6716167 13. kiyosue h, hori y, okahara m, tanoue s, sagara y, matsumoto s, et al. treatment of intracranial dural arteriovenous fistulas: current strategies based on location and hemodynamics, and alternative techniques of transcatheter embolization. radiographics [internet]. 2004 [cited 2013 may 25];24(6):1637–53. available from: http://www.ncbi.nlm.nih.gov/pubmed/15537974 14. suh dc, lee jh, kim sj, chung sj, choi cg, kim hj, et al. new concept in cavernous sinus dural arteriovenous fistula: correlation with presenting symptom and venous drainage patterns. stroke [internet]. 2005 jun [cited 2013 may 25];36(6):1134–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/15890994 15. lasjaunias p, chiu m, ter brugge k, tolia a, hurth m, bernstein m. neurological manifestations of intracranial dural arteriovenous malformations. j neurosurg [internet]. 1986 may [cited 2013 apr 24];64(5):724–30. available from: http://www.ncbi.nlm.nih.gov/pubmed/3701421 16. palestine ag, younge br, piepgras dg. visual prognosis in carotid-cavernous fistula. arch ophthalmol [internet]. 1981 sep [cited 2013 apr 24];99(9):1600–3. available from: http://www.ncbi.nlm.nih.gov/pubmed/7283811 17. kwon bj, han mh, kang h-s, chang k-h. mr imaging findings of intracranial dural arteriovenous fistulas: relations with venous drainage patterns. ajnr am j neuroradiol [internet]. 2005 [cited 2013 may 25];26(10):2500–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/16286391 18. tsai y-f, chen l-k, su c-t, lu t-n, wu c-c, kuo c-j. utility of source images of three-dimensional timeof-flight magnetic resonance angiography in the diagnosis of indirect carotid-cavernous sinus fistulas. j neuroophthalmol [internet]. 2004 dec [cited 2013 may 25];24(4):285–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/15662241 19. barrow dl, spector rh, braun if, landman ja, tindall sc, tindall gt. classification and treatment of spontaneous carotid-cavernous sinus fistulas. j neurosurg [internet]. 1985 feb [cited 2013 apr 24];62(2):248–56. available from: http://www.ncbi.nlm.nih.gov/pubmed/3968564 20. klisch j, huppertz hj, spetzger u, hetzel a, seeger w, schumacher m. transvenous treatment of carotid cavernous and dural arteriovenous fistulae: results for 31 patients and review of the literature. neurosurgery [internet]. 2003 oct [cited 2013 apr 24];53(4):836–56; discussion 856–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/14519216 21. satomi j, satoh k, matsubara s, nakajima n, nagahiro s. angiographic changes in venous drainage of cavernous sinus dural arteriovenous fistulae after palliative transarterial embolization or observational management: a proposed stage classification. neurosurgery [internet]. 2005 mar [cited 2013 apr 24];56(3):494–502; discussion 494–502. available from: http://www.ncbi.nlm.nih.gov/pubmed/15730574 22. makiuchi t, takasaki k, yamagami m, oda h, todoroki k, atsuchi m, et al. a case of sigmoid sinus dural arteriovenous fistula after treated cavernous dural arteriovenous fistula. interv neuroradiol [internet]. 1998 nov 30 [cited 2013 apr 24];4 suppl 1:219–22. available from: http://www.ncbi.nlm.nih.gov/pubmed/20673478 23. sergott rc, grossman ri, savino pj, bosley tm, schatz nj. the syndrome of paradoxical worsening of dural-cavernous sinus arteriovenous malformations. ophthalmology [internet]. 1987 mar [cited 2013 apr 24];94(3):205–12. available from: http://www.ncbi.nlm.nih.gov/pubmed/3587894 24. satomi j, van dijk jmc, terbrugge kg, willinsky ra, wallace mc. benign cranial dural arteriovenous fistulas: outcome of conservative management based on the natural history of the lesion. j neurosurg [internet]. 2002 oct [cited 2013 apr 24];97(4):767–70. available from: http://www.ncbi.nlm.nih.gov/pubmed/12405361 25. cheng k-m, chan c-m, cheung y-l. transvenous embolisation of dural carotid-cavernous fistulas by multiple venous routes: a series of 27 cases. acta neurochir [internet]. 2003 jan [cited 2013 apr 24];145(1):17–29. available from: http://www.ncbi.nlm.nih.gov/pubmed/12545258 144 moscote-salazar et al endovascular management of dural fistulas into the cavernous sinus 26. houdart e, saint-maurice j-p, chapot r, ditchfield a, blanquet a, lot g, et al. transcranial approach for venous embolization of dural arteriovenous fistulas. j neurosurg [internet]. 2002 aug [cited 2013 may 25];97(2):280–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/12186454 27. urtasun f, biondi a, casaco a, houdart e, caputo n, aymard a, et al. cerebral dural arteriovenous fistulas: percutaneous transvenous embolization. radiology [internet]. 1996 apr [cited 2013 may 5];199(1):209–17. available from: http://www.ncbi.nlm.nih.gov/pubmed/8633147 28. cognard c, gobin yp, pierot l, bailly al, houdart e, casasco a, et al. cerebral dural arteriovenous fistulas: clinical and angiographic correlation with a revised classification of venous drainage. radiology [internet]. 1995 mar [cited 2013 may 25];194(3):671–80. available from: http://www.ncbi.nlm.nih.gov/pubmed/7862961 29. hosobuchi y. electrothrombosis of carotidcavernous fistula. j neurosurg [internet]. 1975 jan [cited 2013 apr 24];42(1):76–85. available from: http://www.ncbi.nlm.nih.gov/pubmed/1110393 30. mullan s. treatment of carotid-cavernous fistulas by cavernous sinus occlusion. j neurosurg [internet]. 1979 feb [cited 2013 apr 24];50(2):131–44. available from: http://www.ncbi.nlm.nih.gov/pubmed/430123 31. teng mm, guo wy, huang ci, wu cc, chang t. occlusion of arteriovenous malformations of the cavernous sinus via the superior ophthalmic vein. ajnr am j neuroradiol [internet]. 1988 [cited 2013 apr 24];9(3):539–46. available from: http://www.ncbi.nlm.nih.gov/pubmed/3132828 32. yamashita k, taki w, nishi s, sadato a, nakahara i, kikuchi h, et al. transvenous embolization of dural caroticocavernous fistulae: technical considerations. neuroradiology [internet]. 1993 jan [cited 2013 apr 24];35(6):475–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/8377926 33. berkmen t, troffkin na, wakhloo ak. transvenous sonographically guided percutaneous access for treatment of an indirect carotid cavernous fistula. ajnr am j neuroradiol [internet]. 2003 sep [cited 2013 apr 24];24(8):1548–51. available from: http://www.ncbi.nlm.nih.gov/pubmed/13679268 34. bellon rj, liu ay, adler jr, norbash am. percutaneous transfemoral embolization of an indirect carotid-cavernous fistula with cortical venous access to the cavernous sinus. case report. j neurosurg [internet]. 1999 may [cited 2013 apr 24];90(5):959–63. available from: http://www.ncbi.nlm.nih.gov/pubmed/10223466 35. kubota y, ueda t, kaku y, sakai n. development of a dural arteriovenous fistula around the jugular valve after transvenous embolization of cavernous dural arteriovenous fistula. surg neurol [internet]. 1999 feb [cited 2013 apr 24];51(2):174–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/10029423 36. kurl s, vanninen r, saari t, hernesniemi j. development of right transverse sinus dural arteriovenous malformation after embolisation of a similar lesion on the left. neuroradiology [internet]. 1996 may [cited 2013 apr 24];38(4):386–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/8738104 37. nakagawa h, kubo s, nakajima y, izumoto s, fujita t. shifting of dural arteriovenous malformation from the cavernous sinus to the sigmoid sinus to the transverse sinus after transvenous embolization. a case of left spontaneous carotid-cavernous sinus fistula. surg neurol [internet]. 1992 jan [cited 2013 apr 24];37(1):30–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/1727080 38. bank wo, kerber cw, drayer bp, troost bt, maroon jc. carotid cavernous fistula: endarterial cyanoacrylate occlusion with preservation of carotid flow. j neuroradiol [internet]. 1978 dec [cited 2013 may 25];5(4):279–85. available from: http://www.ncbi.nlm.nih.gov/pubmed/755100 39. kerber cw, bank wo, cromwell ld. cyanoacrylate occlusion of carotid-cavernous fistula with preservation of carotid artery flow. neurosurgery [internet]. 1979 mar [cited 2013 may 25];4(3):210–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/460551 40. pierot l, moret j, boulin a, castaings l. endovascular treatment of post-traumatic complex carotid-cavernous fistulas, using the arterial approach. j neuroradiol [internet]. 1992 jan [cited 2013 may 25];19(2):79–87. available from: http://www.ncbi.nlm.nih.gov/pubmed/1629778 41. wang d, ling f, li m, zhang h, miu z, song q, et al. [refractory carotid-cavernous fistula: causes and countermeasures]. zhonghua wai ke za zhi [internet]. 1999 dec [cited 2013 may 25];37(12):754–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/11829946 romanian neurosurgery (2014) xxi 2: 135 145 145 42. hasuo k, mizushima a, matsumoto s, uchino a, uehara s, miyoshi m, et al. type d dural carotidcavernous fistula. results of combined treatment with irradiation and particulate embolization. acta radiol [internet]. 1996 may [cited 2013 may 25];37(3 pt 1):294– 8. available from: http://www.ncbi.nlm.nih.gov/pubmed/8845256 43. bitoh s, hasegawa h, fujiwara m, nakao k. irradiation of spontaneous carotid-cavernous fistulas. surg neurol [internet]. 1982 apr [cited 2013 may 25];17(4):282–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/7079953 44. hidaka h, terashima h, tsukamoto y, nakata h, matsuoka s. radiotherapy of dural arteriovenous malformation in the cavernous sinus. radiat med [internet]. 1989 [cited 2013 may 25];7(3):160–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/2587806 45. pierot l, poisson m, jason m, pontvert d, chiras j. treatment of type d dural carotid-cavernous fistula by embolization followed by irradiation. neuroradiology [internet]. 1992 jan [cited 2013 may 25];34(1):77–80. available from: http://www.ncbi.nlm.nih.gov/pubmed/1553043 46. guo wy, pan dh, wu hm, chung wy, shiau cy, wang lw, et al. radiosurgery as a treatment alternative for dural arteriovenous fistulas of the cavernous sinus. ajnr am j neuroradiol [internet]. 1998 [cited 2013 may 25];19(6):1081–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/9672015. 11mittal_lumbosacral 216 mittal et al lumbosacral myelocystocele lumbosacral myelocystocele: a case report r.s. mittal1, pankaj gupta2, ashok gandhi3, achal sharma4, vinod sharma5, varsha kumar6 1professor & head, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 2senior resident, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 3assist. professor, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 4professor, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 5assist. professor, dept. of neurosurgery, s.m.s. medical college, jaipur, rajasthan 6senior resident, dept. of pathology, sgpgims, lucknow, uttar pradesh abstract myelocystocele is a rare variety of spinal dysraphism that presents as a skin covered, midline, lumbosacral mass. many a time it is associated with other congenital anomalies but isolated myelocystocele is rarely associated with neurological deficit. mri is the modality of choice for preoperative diagnosis. a 3 years old female child presented with skin covered lumbosacral mass since birth. there was no associated neurological deficit. mri revealed single cyst, which was continuous with central canal of spinal cord. peroperatively, myelocystocele was found with tethering of cord. untethering of cord and repair of myelocystocele was performed with uneventful recovery. key words: myelocystocele, spinal dysraphism, myelomeningocele. introduction myelocystocele is a rare spinal cord anomaly comprising 5-8% of all cases of spinal dysraphism. (1, 2, 6) this results from defect in secondary neurulation. a terminal myelocystocele is composed of a low lying conus medullaris with cystic dilatation of the caudal central canal, a surrounding meningocele and a lipoma that extends from the conus to a subcutaneous fat collection. (5) the terminal cyst is lined with ependyma and dysplastic glial tissue and it does’nt communicate with subarachnoid space. (3, 4, 5) myelocystoceles are often associated with cloacal extrophy, omphalocele, bladder extrophy, ambiguous genitalia, imperforate anus, hemi-vertebrae, sacral agenesis and pelvic abnormalities. when all these abnormalities are present, the defect is called oeis complex (for omphalocele, bladder extrophy, imperforate anus and spinal defect) (4). myelocystoceles are only rarely associated with hydrocephalus or chiari ii malformation. (7) patients with myelocystocele have normal intelligence and are usually born without neurological deficit. therefore these defects must be identified early and repaired before romanian neurosurgery (2014) xxi 2: 216 219 217 the onset or progression of lower limb weakness. (6) case report a 3 yrs old female child presented with skin covered lumbosacral mass, which was present since birth. the swelling was gradually increasing in size. patient was born at full term, by normal vaginal delivery. no abnormality was reported in relation to the urination and defecation. developmental milestones, intelligence, head circumference and the neurological examination was essentially normal. the swelling was smooth, cystic, fluctuant and transilluminant, present over lumbosacral region measuring 8x8 cm. in size, covered with normal skin having well defined round borders. it was soft in consistency, dull on percussion and the cough impulse was present. mri showed single compartment cystic swelling that was in continuation of central canal of spinal cord. it was associated with lipomeningocele at s3-s4 region, low lying cord and thickened filum terminale. patient was operated electively. a vertical incision was given in midline and about 50 ml csf was drained. the cyst was explored, opened and found to be in continuation with the central canal. central canal of cord was found dilated (hydromyelia). cord was tethered over s1-s2 region and was low lying type. the peroperative diagnosis was myelocystocele. figure 1 t1w1 & t2w1 mri images of saggital cut of spinal cord is showing evidence of dilated terminal portion of central canal, continuing in cyst over sacral region,suggestive of myelocystocele figure 2 peroperative picture showing dilated central canal of cord (asterixis) with low lying cord and cord tethering (arrow) the detethering of cord done and water tight repair of myelocystocele defect performed. the postoperative recovery was uneventful. no evidence of csf leakage was there in postoperative period. 218 mittal et al lumbosacral myelocystocele the patient is under regular follow up and doing well. discussion the myelocystocele is an unusual and rare congenital malformation of spine. the overall incidence of neural tube defect is 1:1000 live births, but variable throughout world. (3, 5) cloacal extrophy occurs sporadically with an incidence of 1 in 200,000 to 400,000 live births. (4) no risk in siblings has been identified as no genetic association is there and myelocystocele occurs sporadically. (5) loperamide hydrochloride, diphenylhydantoin and retinoic acid has been associated with myelocystoceles. influenza vaccine has association with oeis complex. mri is the modality of choice for diagnosis of myelocystocele both in prenatal as well as postnatal period. (2, 6) the afp level is usually not elevated in pregnancy as myelocystoceles are skin covered lesions. but if there is concurrent omphalocele, then afp is elevated. (5, 7) mri can delineate cystic mass with septations in coronal view and can show continuation with central canal of cord in saggital view. (2) it can also detect other spinal cord anomalies like tethered cord, diastematomyelia, arnold-chiari malformations, syringocele etc. (2) it is very difficult to diagnose myelocystocele by ultrasonography in antenatal period. (2) myelocystoceles have been reported in cervical, thoracic and lumbosacral regions. (1, 6) cervical myelocystocele is infrequently associated with neurological deficit whereas terminal myelocystoceles are associated with more neurological problems. (6) the whole spinal axis including craniocervical junction should be imaged, atleast in saggital plane to evaluate other associated anomalies. (2) in contrast to meningomyelocele repair, which is repaired at birth, repair of myelocystocele is initiated after the early stages of repair of genitourinary abnormality, if present. (1, 3) ideally, repair of myelocystocele should be performed within first 6 months to minimize neurological loss from spinal cord tethering. (5, 7) a child with repaired myelocystocele must be monitored throughout life for symptoms and signs of retethering. (1, 6) to summarize, myelocystocele is a rare spinal dysraphism. our case was an isolated myelocystocele with no neurological deficits. mri can diagnose the condition very well and excellent outcome can be achieved by an early repair of the defect. footnotes: source of support: nil. conflicts of interest: none declared. correspondence address: dr. ashok gandhi (mch.) assist. professor (neurosurgery) deptt. of neurosurgery, s.m.s. medical college, jaipur, rajasthan, 302004. email: drpankaj.gupta@yahoo.co.in gandhineuro@gmail.com references 1. konya d, dagcinar a, akakin a, gercek a, ozgen s, pamir m. cervical meningocele causing symptoms in adulthood: case report and review of the literature. j spinal disord tech. 2006;19:531-3.[pubmed] 2. feltes ch, fountas kn, dimopoulos vg, escura ai, boev a, kapsalaki ez, et al. cervical meningocele in association with spinal abnormalities. childs nerv syst. romanian neurosurgery (2014) xxi 2: 216 219 219 2004;20:357-61. [pubmed] 3. andronikou s, wieselthaler n, fieggen ag. cervical spina bifida cystica: mri differentiation of the subtypes in children. childs nerv syst. 2006;22:379-84.[pubmed] 4. bilal mirza, nasir mahmood, lubna ijaz, tariq khawaja, imaran aslam, afzal sheikh. isolated terminal myelocystocele: a rare spinal dysraphism. apsp j case rep. 2011;jan-apr: 2: 3. 5. ramesh v, v chandra, phani m kumar. cervical myelocystocele: case report and review of literature. j pediatr neurosci. 2011; jan-jun: 6: 55-57. 6. ochiai h, kawano h, miyaoka r, nagano r, kohno k, nishiguchi t, et al . cervical (non-terminal) myelocystocele associated with rapidly progressive hydrocephalus and chiari type ii malformation--case report. neurol med chir (tokyo). 2010;50:174-7. 7. kumar r, chandra a, terminal myelocystocele. indian j pediatr. 2002;69:1083-1086.[pubmed] microsoft word 9petraru_cerebral.doc 234 petraru et al cerebral hemorrhage in chronic viral liver cerebral haematoma and diffuse cerebral hemorrhage in the context of chronic viral liver disease with severe metabolic disorder of hemostasis. observations on a series of 7 cases c. petraru1, v.b. buburuzan2, gh. balan3 1ph.d. student, “gr. t. popa” university of medicine and pharmacy, iasi, romania; gastroenterology department, county emergency hospital, bacau, romania 2neurosurgery department, county emergency hospital, bacau, romania 3clinic of gastroenterology and hepatology, “st. spiridon” emergency hospital, iasi, romania abstract the aim of our study was to describe some characteristics of a series of 7 cases with subdural (4), extradural (1) and intracerebral hemorrhage (2) associated with chronic hepatitis and liver cirrhosis in the context of long-term infection with b and c viruses. we collected data regarding hepatic dysfunction (alt, ast) and hemostatic disorder (blood platelet count, prothrombin time and howell test). in conclusion, patients with chronic and cirrhotic liver disease and a severe hemostatic syndrome should investigated neurosurgically in order to prevent intracerebral hemorrhage and hematoma. an important laboratory alarm signal could consider an important decrease of blood platelet count and a prolonged prothrombin time and a pathologic howell test. key words: viral chronic hepatitis, hemostasis, intracerebral hemorrhage, liver cirrhosis, subdural hematoma. introduction chronic subdural hematoma represents a common condition seen usually in the later stages of life (12). epidemiological data suggested that the incidence of chronic subdural hematoma and intracerebral hemorrhage did not decrease between 1980 and 2008. the overall incidence was 24.6%ooo per year (95 % confidence interval 19.7–30.7), ranging from 1.8 to 129.6. the incidence values were 15 % lower in women than men (overall incidence ratio 0.85, 95% ci 0.61-1.18). incidence ratios increased from 0.10 (95% ci 0.06-0.14) for people aged less than 45 years to 9.6 (6.6-13.9) for people older than 85 years. case fatality is lower in japan than elsewhere, increases with age, and has not decreased over time (2, 5, 13). chronic subdural hematoma is known to have a recurrence rate from 5% to 30%, reported by several studies, but authors din not established the recurrence criteria, yet. however, one of them could be the low blood platelet count and other signs in the context of liver or spleen disorders such as chronic hepatitis and cirrhosis due to viral infections (10, 14) many epidemiological studies tried to identify risk factors for intracerebral hemorrhage, in order to find targets for romanian neurosurgery (2012) xix 3: 234 238 235 preventive and therapeutical strategies. along with hypertensive vasculopathy and amyloid angiopathy, or warfarin use, authors highlighted that an important risk factor in these cases is the hemorrhagic syndrome in the context of a chronic liver dysfunction (3, 4, 6, 9). material and methods our study included a series of 7 cases admitted county emergency hospital of bacau, romania, department of neurosurgery, with diagnosis of subdural hematoma or intracerebral hemorrhage, between 2011 and 2012. the inclusion criteria contained also hepatitis or cirrhosis due to a chronic viral infection with b or c virus, with a low blood platelets count. the exclusion criterium considered patients without viral liver infections. the studied series included 5 males (3 from rural and 2 from urban area) and 2 females (both from rural area). the age range was 44 to 69, with a median=54 and an mean age=55.85 years. we considered clinical diagnosis and certain laboratory investigations such as: alt and ast (alanine and aspartate aminotransferases), blood glucose level, hemoglobin and blood platelet count, as well as the prothrombin time (quick-test) and howell test. results 1. clinical features of the studied series. chronic subdural hematoma was found in 4 patients (3 males and 1 female), one patient with extradural hematoma, and intracerebral hemorrhage in 3 cases (2 males and 1 female) (figure 1). patients suffering from cirrhosis were 5 (3 males and 2 females) and from chronic hepatitis – 2 males. liver disorder was given by b virus in 4 cases (all males) and c virus in 3 patients (1 male and 2 females). patients with chronic hematoma also suffered from b virus infection in 4 cases and c virus in 1 case, but intracerebral hemorrhage was observed only in patients with c virus (1 male and 1 female) (figure 2). figure 1 distribution of cases by type of lesions and sex figure 2 distribution of cases by type of lesions and type of liver viral infection 2. laboratory characteristics. liver disorder was highlighted by the alt levels which ranged between a minimum of 15 ui (female, subdural hematoma, chronic hepatitis with c virus) and a maximum of 73 ui (female, intracerebral hemorrhage, liver cirrhosis with c virus). besides, ast levels ranged between a minimum of 29 ui (male, intracerebral hemorrhage, chronic hepatitis with c virus) and a maximum of 56 (the same patient for maximum of alt). 236 petraru et al cerebral hemorrhage in chronic viral liver blood glucose levels over 120 mg/dl defined 4 males (all of them with hematoma) and 1 female (with intracerebral hemorrhage), with a maximum of 147 in a patient also suffering from diabetes mellitus type-1. hemoblobin levels ranged between a pathological minimum of 9.4 g/dl (male, subdural hematoma, liver cirrhosis due to b virus infection) and a normal maximum of 13.9 (female, intracerebral hemorrhage, liver cirrhosis with c virus). more important in our study context was blood platelet count that could explain a severe hemostatic syndrome in these patients. a minimum of blood platelet count (48,000/μl) registered in the same male patient with a minimum of hemoglobin, and a maximum (91,000/μl) in the same female patient with normal glucose level. we also took into account the prothrombin time (quick-test) and howell test. the quick-test maximum value in the studied series was of 21.5 sec. in a male case (the same patient with the lowest platelet count), followed by a value of 20.5 sec. found in a female patient with intracerebral hemorrhage and c viral liver cirrhosis (figure 3). the howell test values oscillated between the normal limits (70140 sec.) in all patients. evolution. all 7 patients recovered completely after surgical intervention and no death was noticed. some radiographic features are presented in figure 4 and figure 5 seen below. figure 3 distribution of cases by type of lesions and sex figure 4 blood present in the prepontine cisterns, willis polygon and sylvian valleys (arrow) (male, 63 years old, chronic hepatitis with b virus infection) figure 5 paracavernos hemorrhagic collection (arrow) (female, 61 years old, liver cirrhosis with c virus infection) romanian neurosurgery (2012) xix 3: 234 238 237 discussions akioka et al. (1) reported a series of 6 patients with acute spontaneous subdural hematoma, surgically treated between 1994 and 2003. for our study, the most important features of this series was mean age of 53.0 years (range 32-82), and the fact that medical history included hepatitis c. surgical intervention showed that the bleeding points were identified as ruptures of cortical arteries located near the sylvian fissure. the post-operative evolution showed that one patient completely recovered, one had a moderate deficit, two had severe deficits, one fell into a vegetative state, and one died. authors highlighted that an early surgical intervention is required for a good outcome. other research performed by hoya et al. (7) on patients with chronic liver disease and their risk of intracerebral hemorrhage noticed that the fatality was lower in this group than in the control group (without liver dysfunction). authors concluded that the hemostatic disorders seemed to be related to site of hemorrhage, but not to life prognosis in patients with liver disorders and evolution was worsened by nonneurological complications. in a study performed on 4515 hospitalized cirrhotic patients, between 1997 and 2006, huang et al. (8) analyzed the risk of spontaneous intracerebral hemorrhage focused on 36 cases with no history of stroke, head injuries, or cerebral arteriovenous malformations. authors noticed the patients’ features, the etiology (virus-related cirrhosis 0.3%, combined virusand alcohol-related cirrhosis 3%) and severity of cirrhosis, as well as hematoma location and prognosis. they concluded that spontaneous intracebral hemorrhage occurred especially in young males with mild-to-moderate liver cirrhosis, the etiology of liver dysfunction was related to the incidence of hemorrhage, and not to patients’ outcome, but severity of liver cirrhosis was associated with patients’ evolution but not with the incidence of hemorrhage. a cohort study included data collected from the national health insurance of taiwan and performed by lai et al. (11) during the year 1999 noticed that intracerebral hemorrhage developed in 1.3% of patients with liver cirrhosis, with an adjusted hazard ratio of 1.62 (95% ci, 0.85 to 3.10) for patients with liver cirrhosis to develop intracerebral hemorrhage compared with patients without liver cirrhosis. authors concluded that patients suffering from liver cirrhosis had a similar incidence rate of intracerebral hemorrhage with a trend of increased risk for intracerebral hemorrhage compared with the control group. conclusions patients with chronic and cirrhotic liver disease and a severe hemostatic syndrome should investigate imagistically at the cranial-cerebral level, when any “soft” neurological signs occur, in order to diagnose intracerebral hemorrhage and hematoma as soon as possible. an important laboratory alarm signal could consider an important decrease of blood platelet count and a prolonged prothrombin time and a pathologic howell test. chronic liver dysfunctions in the context of a long-term infection with b and c viruses represent important risk factors for neurosurgical conditions such as subdural hematoma and intracerebral hemorrhage. 238 petraru et al cerebral hemorrhage in chronic viral liver correspondence author dr. constantin petraru county emergency hospital no. 2, spiru haret street 600114 bacau, romania e-mail: drpetraru@yahoo.com references 1. akioka n, fukuda o, takaba m, kameda h, saito t, endo s. clinical investigation of acute spontaneous subdural hematoma cases. j stroke cerebrovasc dis 2007;16(3):109-13; 2. amin os, omer rt, abdulla aa, ahmed rh, ahmad o, ahmad s. recurrent, sequential, bilateral deep cerebellar hemorrhages: a case report. j med case rep 2011;5:360; 3. ariesen mj, claus sp, rinkel gj, algra a. risk factors for intracerebral hemorrhage in the general population: a systematic review. stroke 2003;34(8):2060-5; 4. depreitere b, van calenbergh f, van loon j. a clinical comparison of non-traumatic acute subdural haematomas either related to coagulopathy or of arterial origin without coagulopathy. acta neurochir (wien) 2003;145(7):541-6; 5. flaherty ml, haverbusch m, sekar p, kissela b, kleindorfer d, moomaw cj, sauerbeck l, schneider a, broderick jp, woo d. long-term mortality after intracerebral hemorrhage. neurology 2006;66(8):11826; 6. grønbæk h, johnsen sp, jepsen p, gislum m, vilstrup h, tage-jensen u, sørensen ht. liver cirrhosis, other liver diseases, and risk of hospitalization for intracerebral haemorrhage: a danish populationbased case-control study. bmc gastroenterol. 2008; 8: 16; 7. hoya k, tanaka y, uchida t, takano i, nagaishi m, kowata k, hyodo a. intracerebral hemorrhage in patients with chronic liver disease. neurol med chir (tokyo) 2012;52(4):181-5; 8. huang hh, lin hh, shih yl, chen pj, chang wk, chu hc, chao yc, hsieh ty. spontaneous intracranial hemorrhage in cirrhotic patients. clin neurol neurosurg 2008;110(3):253-8; 9. ikram ma, wieberdink rg, koudstaal pj. international epidemiology of intracerebral hemorrhage. curr atheroscler rep 2012;14(4):300-6; 10. ko bs, lee jk, seo br, moon sj, kim jh, kim sh. clinical analysis of risk factors related to recurrent chronic subdural hematoma. j korean neurosurg soc 2008;43(1):11-5; 11. lai ch, cheng py, chen yy. liver cirrhosis and risk of intracerebral hemorrhage: a 9-year follow-up study. stroke 2011;42(9):2615-7; 12. ramachandran r, hegde t. chronic subdural hematomas--causes of morbidity and mortality. surg neurol 2007;67(4):367-72; 13. van asch cj, luitse mj, rinkel gj, van der tweel i, algra a, klijn cj. incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. lancet neurol. 2010;9(2):167-76; 14. wilberger je. pathophysiology of evolution and recurrence of chronic subdural hematoma. neurosurg clin n am 2000;11(3):435-8. 9agrawalamit_primary2014 78 agrawal et al primary hypothyroidism masquerading pituitary macroadenoma primary hypothyroidism masquerading pituitary macroadenoma amit agrawal1, amareesh p. reddy2, g. malleswara rao3, umamaheswara reddy v.4 1professor of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2assistant professor of endocrinology, department of endocrinology, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 3professor of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 4assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract diffuse and reactive pituitary gland enlargement secondary to primary hypothyroidism is an uncommon occurrence and that can masquerade many pituitary disorders. in present article, we report a case of 19 year female severe hypothyroidism presenting with diffuse enlargement of pituitary gland and hyperprolactinemia and review the clinical importance of this entity. knowledge of this entity is very important to avoid unnecessary surgery and irreversible complications in this sub-group of patients. key words: pituitary hyperplasia, primary hypothyroidism, pituitary hyperplasia. introduction diffuse and reactive pituitary gland enlargement secondary to primary hypothyroidism is an uncommon occurrence and that can masquerade many pituitary disorders. (1-8) in present article, we report a case of severe hypothyroidism presenting with diffuse enlargement of pituitary gland and hyperprolactinemia. case report a 19 year female presented with headache of one year duration and one episode of seizures. there was history of galactorrhoea. there was no history of loss of appetite and cold intolerance. she had easy fatigability and no visual symptoms. her general and systemic examination was unremarkable. higher mental functions and cranial nerves were normal. motor and sensory examination was normal. deep tendon reflexes were sluggish. routine blood investigations were within normal range, except low level of hemoglobin (9.1 gm / dl). hormonal profile revealed raised thyrotropin stimulating hormone (tsh) romanian neurosurgery (2014) xxi 1: 78 81 79 (>100 microlu/dl, range 0.34-5.6) and low t4 (0.10 microgram/ml, range 0.61-1.12). prolactin was 200 iu/dl. magnetic resonance imaging (mri) of the brain showed a large diffuse sellar mass lesion, hypointense on t1w images and uniformly enhancing after contrast administration (figure 1 and 2). based on clinical features, investigation reports (increased tsh and prolactin secretion) and imaging findings a diagnosis of diffuse pituitary hyperplasia secondary to primary hypothyroidism was made. the patient was started on 100 microgram thyroxine. discussion pituitary hyperplasia is a process and ranges from the slight increase in the number of normal cells without much change in the tissue architecture to massive enlargement of the gland with significant alteration in both tissue architecture and morphology. (9) thyrotroph hyperplasia is the most common cause of pituitary enlargement in the context of untreated primary hypothyroidism. (2, 10) the incidence of pituitary hyperplasia in hypothyroidism ranges from 25% to 81% (11) and the incidence is high if the tsh levels are >50 microiu/ml. (12) it has been suggested that the primary uncontrolled hypothyroidism can be a precursor to pituitary hyperplasia. (2) low thyroxine levels in these patients results in the loss of negative control on hypothalamo-pituiatry-thyroid axis resulting in the increase of thyrotroph releasing hormone (trh) from hypothalamus which increases the thyroid stimulating hormone (tsh) from pituitary in an attempt to maintain the normal thyroxine levels (3, 7, 13-16) figure 1 mri brain axial images showing diffuse enlargement of the pituitary gland, it was hypointense on t1w images and diffusely enhancing after contrast administration figure 2 mri brain sagittal and coronal post-contrast images showing diffusely enhancement of pituitary gland 80 agrawal et al primary hypothyroidism masquerading pituitary macroadenoma as was seen in present case, trh also exerts a weak stimulatory effect on lactotroph cells resulting in mild to moderate hyperprolactinemia is expected. (13) because trh also has a weak stimulatory effect on lactotroph cells, mild to moderate hyperprolactinemia may also occur in about three-quarters of patients. (11) clinically the patients with pituitary hyperplasia can present with headache, visual symptoms and features of hypothyroidism. (1, 3, 7, 14) it is important to understand that the headache may be due to hypothyroidism, although the exact underlying mechanism is not clear. (7) in many cases pituitary hyperplasias may be clinically silent and focal pituitary hyperplasia can be an incidental finding at autopsy. 9 the diagnosis of pituitary hyperplasia can be difficult and it needs a high degree of clinical suspicion. (1-4, 6-8, 11, 12, 14, 15, 17) radiological investigations i.e. ct and mri with contrast administration will show the enlargement of pituitary gland. mri is superior to ct scan and a follow up imaging will further help to monitor the size of the gland. (4, 6, 18-22) detail thyroid functions are the mainstay of diagnosis as it will show decrease in the levels of serum t3 and t4 but greatly elevated serum tsh levels. (2, 3, 6) one the diagnosis of pituitary hyperplasia secondary to primary hypothyroidism is suspected the patients can be managed with adequate hormone replacement with l-thyroxine (25 to 300 mcg/day) and in most of the cases this will result in relief of symptoms and regression of pituitary hyperplasia within a few months. (1-4, 6-8, 11, 12, 14, 15, 17) in a selected group of patients where there is compression of the optic chiasm, does not respond to, or worsens under, thyroid hormone replacement or the diagnosis is in doubt surgery may be considered as an option. (23) although imaging findings will not distinguish between tsh-producing macroadenoma and hyperplasia of pituitary gland, only the follow up imaging and response to replacement therapy will support the diagnosis. (24) conclusion in summary, diffuse pituitary enlargement can be a manifestation of severe primary hypothyroidism and interpretation of a pituitary mass without an endocrine investigation can lead to unnecessary surgery (4, 5, 22, 25, 26). a knowledge of this entity is very important to avoid unnecessary surgery and irreversible complications in this sub-group of patients. address for correspondence dr amit agrawal professor of neurosurgery department of neurosurgery narayna medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 romanian neurosurgery (2014) xxi 1: 78 81 81 references 1. nicholas wc, russell wf. primary hypothyroidism presenting as a pituitary mass. journal of the mississippi state medical association 2000;41:511-514. 2. joshi as, woolf pd. pituitary hyperplasia secondary to primary hypothyroidism: a case report and review of the literature. pituitary 2005;8:99-103. 3. agrawal a, diwan sk. pituitary hyperplasia resulting from primary hypothyroidism. asian journal of neurosurgery 2011;6:99-100. 4. xu a-j, li t. [pituitary hyperplasia secondary to primary hypothyroidism in children: report of 8 cases]. zhongguo dang dai er ke za zhi = chinese journal of contemporary pediatrics 2010;12:17-20. 5. al-gahtany m, horvath e, kovacs k. pituitary hyperplasia. hormones-athens2003;2:149-158. 6. passeri e, tufano a, locatelli m, lania ag, ambrosi b, corbetta s. large pituitary hyperplasia in severe primary hypothyroidism. the journal of clinical endocrinology and metabolism 2011;96:22-23. 7. franceschi r, rozzanigo u, failo r, bellizzi m, di palma a. pituitary hyperplasia secondary to acquired hypothyroidism: case report. italian journal of pediatrics 2011;37:15. 8. kunjumohamed f. pituitary hyperplasia and hyperprolactinemia secondary to severe hypothyroidism. indian journal of medical specialities 2013;4. 9. horvath e, kovacs k, scheithauer bw. pituitary hyperplasia. pituitary 1999;1:169-179. 10.smallridge rc. thyrotropin-secreting pituitary tumors. endocrinology and metabolism clinics of north america 1987;16:765-792. 11.beck-peccoz p, brucker-davis f, persani l, smallridge rc, weintraub bd. thyrotropin-secreting pituitary tumors. endocrine reviews 1996;17:610-638. 12.khawaja nm, taher bm, barham me, et al. pituitary enlargement in patients with primary hypothyroidism. endocrine practice : official journal of the american college of endocrinology and the american association of clinical endocrinologists 2006;12:29-34. 13.yen pm. physiological and molecular basis of thyroid hormone action. physiological reviews 2001;81:10971142. 14.betônico ccr, rodrigues r, mendonça scl, jorge pt. [primary hypothyroidism mimicking pituitary macroadenoma]. arquivos brasileiros de endocrinologia e metabologia 2004;48:423-426. 15.young m, kattner k, gupta k. pituitary hyperplasia resulting from primary hypothyroidism mimicking macroadenomas. british journal of neurosurgery 1999;13:138-142. 16.koller kj, wolff rs, warden mk, zoeller rt. thyroid hormones regulate levels of thyrotropinreleasing-hormone mrna in the paraventricular nucleus. proceedings of the national academy of sciences of the united states of america 1987;84:73297333. 17.ehirim pu, kerr ds, cohen ar. primary hypothyroidism mimicking a pituitary macroadenoma. pediatric neurosurgery 1998;28:195-197. 18.okuno t, sudo m, momoi t, et al. pituitary hyperplasia due to hypothyroidism. journal of computer assisted tomography 1980;4:600-602. 19.pita jc, shafey s, pina r. diminution of large pituitary tumor after replacement therapy for primary hypothyroidism. neurology 1979;29:1169-1172. 20.sarlis nj, brucker-davis f, doppman jl, skarulis mc. mri-demonstrable regression of a pituitary mass in a case of primary hypothyroidism after a week of acute thyroid hormone therapy. the journal of clinical endocrinology and metabolism 1997;82:808-811. 21.wolansky lj, leavitt gd, elias bj, lee hj, dasmahapatra a, byrne w. mri of pituitary hyperplasia in hypothyroidism. neuroradiology 1996;38:50-52. 22.shimono t, hatabu h, kasagi k, et al. rapid progression of pituitary hyperplasia in humans with primary hypothyroidism: demonstration with mr imaging. radiology 1999;213:383-388. 23.simşek e, simşek t, savaş-erdeve s, erdoğmuş b, döşoğlu m. pituitary hyperplasia mimicking pituitary macroadenoma in two adolescent patients with longstanding primary hypothyroidism: case reports and review of literature. the turkish journal of pediatrics 2009;51:624-630. 24.eom ks, see-sung c, kim jd, kim jm, kim ty. primary hypothyroidism mimicking a pituitary macroadenoma: regression after thyroid hormone replacement therapy. pediatric radiology 2009;39:164167. 25.chan aw, macfarlane ia, foy pm, miles jb. pituitary enlargement and hyperprolactinaemia due to primary hypothyroidism: errors and delays in diagnosis. british journal of neurosurgery 1990;4:107-112. 26.riedl s, frisch h. pituitary hyperplasia in a girl with gonadal dysgenesis and primary hypothyroidism. hormone research 1997;47:126-130. doi: 10.33962/roneuro-2021-082 basic considerations on growth hormone deficiency in traumatic brain injury ivan david lozada-martinez, michael gregorio ortega-sierra, maría milagros daza-vega, leidy natalia cárdenas -hormiga, j.e. contreras-saldarriaga, carlos eduardo garcia-moron, juan santiago serna-trejos, jorge alberto nuñez -gamez, daniela gómez-murillo, mary elena rosero-burgos, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (4): pp. 483-489 doi: 10.33962/roneuro-2021-082 www.journals.lapub.co.uk/index.php/roneurosurgery basic considerations on growth hormone deficiency in traumatic brain injury ivan david lozada-martinez1, michael gregorio ortega-sierra2, maría milagros daza-vega3, leidy natalia cárdenas-hormiga4, jorge eduardo contreras-saldarriaga5, carlos eduardo garcia-moron6, juan santiago sernatrejos7, jorge alberto nuñez-gamez8, daniela gómez-murillo9, mary elena rosero-burgos10, luis rafael moscote-salazar1 1 colombian clinical research group in neurocritical care, universidad de cartagena, cartagena, colombia 2 medical and surgical research centre, corporación universitaria rafael nuñez, cartagena, colombia 3 school of medicine, universidad simon bolivar, barranquilla, colombia 4 school of medicine, universidad pedagógica y tecnológica de colombia, tunja, colombia 5 school of medicine, universidad de cartagena, cartagena, colombia 6 school of medicine, universidad libre, barranquilla, colombia 7 school of medicine, universidad libre, cali, colombia 8 school of medicine, universidad del sinú, cartagena, colombia 9 school of medicine, universidad de manizales, manizales, colombia 10 school of medicine, fundación universitaria san martín, pasto, colombia abstract growth hormone is responsible for stimulating the growth and differentiation of cells of various tissues and cell types contribute to protein synthesis and the mobilization of fatty acids. at the nervous system level, it stimulates the regeneration of neurons, astrocytes, endothelial cells, oligodendrocytes, and even neuronal myelination. traumatic brain injuries can alter the secretion of this hormone, due to the deformation of brain tissue and the alteration of neurometabolism by the subsequent ischemia. knowing the basic aspects of pituitary disorders in this type of patient allows early identification and management to avoid complications. introduction growth hormone (gh), synthesized in the adenohypophysis, is responsible for the stimu-lation of cell growth and differentiation, its keywords traumatic brain injury, growth hormone, deficiency, narrative review corresponding author: ivan david lozada-martinez colombian clinical research group in neurocritical care, universidad de cartagena, colombia ilozadam@unicartagena.edu.co copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 484 ivan david lozada-martinez, michael gregorio ortega-sierra, maría milagros daza-vega et al. synthesis and release is related to growth hormone releasing hormone (ghrh) which is responsible for stimulating the process of synthesis and release of gh, while somatostatin hormone is responsible for inhibiting the synthesis and release, thus performing a negative feedback. it has been shown that the highest serum levels of this hormone are found during sleep [1,2] gh secretion occurs in the form of pulses, and its serum concentrations may vary according to sex and individual conditions [3]. different brain injuries can alter gh metabolism, taking into account that different trauma mechanisms can produce damage to the brain parenchyma as inflamma-tory or ischemic damage [4,5]. considering the relevance and impact of neuroendocrine disorders on neurological integrity and quality of life, the aim of this review is to present basic concepts for the understanding and early detection of growth hormone deficiency in traumatic brain injury. growth hormone generalities gh is synthesized in the lateral zones of the adenohypophysis by somatotropic cells. this hormone is a protein consisting of 191 amino acids with an approximate weight of 22650 daltons. the synthesis and release of this hormone depends on two neurohormones loca-ted in the hypothalamus: ghrh and somatostatin [2,3]. the first one has a stimulating character, while the latter has an inhibitory character. its release is rhythmic and alterna-ting, occurring when the amount of ghrh in plasma predominates. the peaks of gh re-lease occur in the slow wave phase of sleep, with a maximum amplitude hypothalamic-pituitary rhythm [2]. growth hormone synthesis growth hormone synthesis is directly influenced by hypothalamic and peripheral factors which act on somatotrophs. both act by binding to specific receptors located on the surface of somatotroph cells [3,6]. ghrh binds to a metabotropic receptor, which are receptors with 7 transmembrane domains that couple to second messengers via g proteins, which upon ligand-induced activation causes intracellular stimulation of cyclic adenosine monophosphate (camp), leading to gh synthesis [2]. hypothalamic somatostatin has five receptor subtypes (sstr1-sstr5). among which sstr2 and sstr5 are responsible for signaling suppression of pituitary gh and thyrotropin secretion [7]. other regulators have been described, such as igf-1, which in addition to mediating the peripheral actions of gh, is also capable of inhibiting gh secretion. nutritional status can also influence the synthesis and secretion of gh, since it has been described that it can be increased in malnourished or fasting individuals [3,8]. although, in states of hyperglyce-mia, hormones such as leptin are able to inhibit gh secretion. it has also been found to be associated with ghrelin, which is an intestinal peptide responsible for the induction of gh secretion, its receptor is expressed in the anterior pituitary, this peptide is produced mainly in the stomach, although small amounts are obtained from intestinal tissue, pitui-tary, placenta and pancreas, it is of great relevance because it is a nutritional regulator of gh secretion, its function is to maintain blood glucose levels during starvation [3,8]. excretion gh excretion is pulsatile, its serum concentration can be detected if an ultrasensitive as-say is used. these pulses are regulated by the reduction of inhibition by somatostatin. therefore, serum gh measurement should be done in a 20-minute sampling during 24 hours, which would allow accurate assessment of serum gh concentrations; it was found that on average, serum gh during the night ranges between 1. 0 ± 0.2 ng/ml, while day-time concentrations average 0.6 ± 0.1 ng/ml in unimpaired adults; these levels may be lower in adults and obese persons, and higher during puberty and in neonates [2,8,9]. the maximum serum gh concentration ranges from 4.3 ± 0.7 ng/ml at night to 2.7 ± 0.5 ng/ml during the day, with the highest peak gh excretion occurring 1 hour after the onset of deep sleep. physical activity, trauma and septic states increase gh secretion in the ran-ge of 20 to 30 ng/ml (3). receptors gh acts by binding to a specific receptor which is a homodimer located mainly in the li-ver, and induces intracellular signaling through a phosphorylation cascade by the jak/stat pathway which are activators of signal transcription. its main action is to sti-mulate hepatic synthesis and secretion of igf-1, which contributes to cell growth and dif-ferentiation [2,3]. 485 basic considerations on growth hormone deficiency in traumatic brain injury the gh receptor is a 70 kd protein, belonging to the cytokine/hematopoietin superfamily. it consists of a single extracellular ligand-binding domain which spans the membrane and a cytoplasmic signaling component. circulating gh-binding proteins are fragments of the receptor that bind to gh [6]. it has been observed that a single gh molecule is able to form complexes with two gh receptor molecules, leading to rapid internal turnover and activation of the jak2 tyrosine kinase, which allows phosphorylation of several cyto-plasmic signaling molecules that determine cell proliferation and differentiated function [6]. on the other hand, it has been observed that stat proteins, which are cytoplasmic pro-teins, represent important signaling components for gh action. they are phosphorylated by jak2 and translocate directly to the cell nucleus, triggering ghspecific target gene effects at this level by binding to the nucleotide dna. within this group of proteins, it has been observed that stat 1 and 5 interact most directly with the gh receptor [10,11]. the function of this receptor can be directly inhibited by igf-1, as well as gh secretion, which is due to negative feedback [2,5]. gh receptor mutations have been described to be associated with partial or complete gh insensitivity and growth failure (laron dwarfism), which is associated with normal or high serum gh concentrations, decreased serum gh-binding protein concentrations, and decreased serum igf-1 concentrations [2,3]. physiological functions unlike the other hormones produced by the pituitary gland, growth hormone does not act in a specific gland, but in the whole organism. this hormone stimulates the growth and differentiation of cells of various tissues and cell types. its anabolic effects are remar-kable, stimulating protein synthesis and the mobilization of fatty acids for use as a source of energy [3,6]. it is also known to promote a diabetogenic state by decreasing glucose uptake by peripheral tissue, stimulating glucose secretion in the liver, and in turn insulin secretion [3]. in bone, it promotes protein deposition by bone growthinducing cells, con-tributes to the rapid growth of bone cell lines, and is known to stimulate the conversion of chondrocytes into osteogenic cells, resulting in the pre-dominance of the rate of bone ma-trix apposition over the rate of bone resorption [3,12]. at the level of the central nervous system, it has been proven that this hormone exerts important functions related to neuro-nal function and differentiation; its contribution to the regeneration of neurons, astrocytes, endothelial cells, oligodendrocytes, and even neuronal myelination has been studied. it has also been implicated in processes such as migration and survival of neurons [1]. the current concept of the diagnosis of growth hormone deficiency in the adult is based on the absence of growth hormone secretion following the administration of pharmacolog-ical agents, which normally trigger hormone secretion. this is due to the fluctuation of hormone over a 24-hour period. however, serum igf-1 levels lack diurnal fluctuation and reflect the action of gh. therefore, the usefulness of the latter has been investigated in the diagnosis of growth hormone deficiency [13]. in children in some cases, clinical risk factors are identified and taken into account, which may provide evidence of growth hor-mone deficiency, without the need for continuous stimulation testing. however, for con-firmation of the diagnosis in most countries of the world the latter test is required [14]. traumatic brain injury pathophysiology primary and secondary lesions in traumatic brain injury divide the pathophysiology of trauma into two distinct phases. the first phase is characterized by mechanical deforma-tion of brain tissue and the second by brain biochemical changes that occur from the time of injury and last from days to months. the first phase is produced by the forces of acceleration, deceleration, and impact forces, which will lead to loss of polarity of neurons, da-mage to blood vessels and axons. ischemia is explained in the alteration of the architectu-re and functionality of the blood vessels, evidencing compromise in terms of tissue perfu-sion due to the lack of vascular bed density, added to other physiological phenomena such as arterial hypotension due to the loss of intrinsic capillary regulation, deficit of nitric oxide production and excess of prostaglandins, which will promote vasoconstriction [4,5,15]. post-traumatic vasospasm is the result of an imbalance of vasodilator and vaso-constrictor factors, and is an aggravating factor of ischemia and hypoxia. due to 486 ivan david lozada-martinez, michael gregorio ortega-sierra, maría milagros daza-vega et al. the state of anaerobiosis, the increase in lactic acid will directly alter cell membrane permeability [4,5,15]. the water and electrolyte imbalance will contribute to the formation of cerebral edema, with subsequent endocranial hypertension. the second phase of traumatic brain injury will initiate an inflammatory cascade characterized by the presence of inflamma-tory cytokines and the presence of excitatory neurotransmitters that will alter calcium homeostasis and other electrolytes. the excess of intracellular calcium, together with an environment rich in inflammatory substances, will lead the neuron to the activation of internal pathways of selfdestruction, represented by proteases and caspases that will de-grade the cytoskeleton proteins, irreversibly activating programmed cell death, or earlier, necrosis, with subsequent release of inflammatory substances into the extracellular environment [4,5,15]. pathophysiology of hypopituitarism induced by traumatic brain injury although the exact pathophysiology of hypopituitarism following traumatic brain injury is unclear, several pathological mechanisms have been proposed as responsible for this dysfunction [16]. one of the main hypotheses is based on the argument of their anatomi-cal location. the pituitary gland, the hypothalamus and the vessels that irrigate these structures are fragile and vulnerable to significant changes in the characteristics of the environment in which they are located, which is the case in traumatic brain injury. me-chanical alterations secondary to trauma can lead to different situations such as edema, rupture of blood vessels, hematoma, increased intracranial pressure, displacement of the hypothalamus, tearing and fracture of bones that destabilize the function of the gland [5]. several studies have found genetic predisposition and immunity to be factors responsible for this condition. high levels of antihypophysis and antihypothalamic antibodies have been found in patients with this pituitary dysfunction after traumatic brain injury. tanri-verdi et al [17], showed a strong association between the presence of high titers of anti-pituitary antibodies and anti-thalamic antibodies five years after traumatic brain injury [17]. damage to the gland has been found, ranging from 26 to 86%, in patients who died after trauma. it is not uncommon to find infarcts in segments of the pituitary gland, such as anterior neocrosis of the gland in patients who died less than a week after traumatic brain injury. mechanisms such as ischemia and intracranial pressure may be responsible for this damage to the pituitary gland [15]. the vascular hypothesis is supported by imaging studies that have demonstrated severe pathological changes in relation to vascular injury. this hypothesis is also related to patterns of hormone loss, through studies showing that the most frequent hormone loss is somatotropin and gonadotropins, excreted in specific sites irrigated by pituitary portal vessels. the genetic polymorphism could also be associated with hypopituitarism [18]. medications used in the intensive care unit could be responsible for having an impact on endocrine function. growth hormone deficiency secondary to traumatic brain injury and its effect on quality of life the prevalence of hypopituitarism and quality of life in patients who survive traumatic brain injury is subject to factors such as skull fracture, duration of ventilatory support, initial imaging related to marshall's classification and coma [19]. although head trauma is common in certain high-risk occupations such as military service, a clear association between pituitary hormone dysfunction and head trauma in the military has not been established, but a long-term negative psychological effect may possibly be generated [14,20,21,22]. in a meta-analysis it was also analyzed that 12 months after a head trauma, about one third of patients were at high risk of suffering post-traumatic pituitary deficien-cy [23]. in a prospective study, it was recognized that in children, unlike adults, the prevalence of hypopituitarism after traumatic brain injury remains controversial [16]. however, it has been established that children after trauma suffer a challenge in terms of rehabilita-tion and reintegration to their life as it was prior to the traumatic injury. this finding is directly related to the severity of the brain injury, which in turn affects the resilience of children after trauma [24-28]. reduced growth hormone production in the context of pituitary dysfunction following head trauma is common. during a crossover, doubleblind, placebo-controlled study, physical changes, resting energy expenditure, fatigue, sleep 487 basic considerations on growth hormone deficiency in traumatic brain injury disturbance and neuropsycho-logical status were observed in 18 patients with growth hormone deficiency secondary to trauma. additionally, changes in anatomical features of the brain parenchyma were ob-served on mri scans of these patients. however, when growth hormone was replaced, al-terations in brain morphology and connectivity were evident, as well as a reduction in fatigue and other related symptoms [29,30]. growth hormone and its effect on bone mass loss induced by mild head trauma it has been demonstrated that recurrent mild head trauma exerts certain effects on the vol-ume of trabecular bone at different scales depending on the affected skeletal site. in con-trast, cortical bone is unaffected [31]; it is believed that this is due to several mechanisms among which are: the site where bone remodeling takes place, regulatory mechanisms of trabecular and cortical bone formation, the site of the trabecular bone formation and the cortical bone formation [32,33]). finally, neuroendocrine signals generated by trauma may affect trabecular bone formation and remodeling more than cortical bone formation and remodeling. findings showed that low-dose growth hormone treatment was useful, as it partially rescued the loss of trabecular bone mass, which had been caused by the combi-nation of trauma and immobility generated by trauma. however, more research in humans is needed to confirm these effects [34]. roles of gh/igf-1 in non-severe traumatic brain injury normally igf-1 exerts a neuroprotective and neurorepair mechanism after any brain inju-ry [35]. rapidly after cranioencephalic trauma gh/igf-1 levels are elevated, regardless of growth hormone status [36,37]. however, depending on which igf-1 allele is present in the neurocritical-posttraumatic patient, neuropsychiatric symptoms and feelings of dizzi-ness or lightheadedness may be present or become chronic, so the final outcome of the traumatic injury is variable [38-40]. alterations in the axis gh/igf-1 intestinal microbiota after traumatic brain injury the rapid expansion in the field of interaction between different systems such as gastroin-testinal, immune, endocrine, neurological in relation to the intestinal microbiota, has led to the conclusion that the microbiota has an influence on any of these systems [41-43]. this leads to the discussion of an axis currently known as the microbiota-gut-brain axis [44,45]. recent analyses have demonstrated a link between altered gut microbiota and altered neurocognitive, behavioral and neuropathological states [46-50]. growth hormone deficiency in subarachnoid haemorrhage and cerebral ischemia subarachnoid hemorrhage (sah) is a disease of acute onset and sudden onset consisting of three phases: acute rupture phase, vasospasm phase and recovery phase. the most fre-quent neuroendocrine abnormalities studied in sah are disorders of the hypothalamic-pituitary-adrenal axis [51,52]. endocrine disorders were found in 78% of patients with subarachnoid hemorrhage and in those with ischemic stroke. the most common findings were low igf-1 levels compatible with growth hormone deficiency (45%), followed by hypogonadism (39%), thyroid dys-function (36%) and hypo-reactivity to cortisol (33%) [53]. the pathophysiological mechanisms of endocrine disruption in patients with brain injury following subarachnoid hemorrhage are not clear, however, it is believed that hypothala-mic and pituitary injury secondary to hematoma compression, ischemic injury or elevated intracranial pressure would be a logical explanation for the endocrine disorders generated [53]. another explanation for these findings is the influence of proinflammatory cytoki-nes, such as il-6, tnf α, il1b, present in acute brain injury processes of various kinds, which may exert inhibitory or stimulatory effects on pituitary and hypothalamic hormones [54]. conclusions hypopituitarism secondary to brain lesions has not been fully described, it has been ob-served that traumatic brain lesions can deform the brain tissue and subsequently generate biochemical changes; permanent lesions have been explained due to the alteration in the form and function of blood vessels, finding a compromise in cerebral irrigation, as a consequence of this and taking into account the anatomical location, the pituitary is an organ susceptible to ischemic changes, which happens in 488 ivan david lozada-martinez, michael gregorio ortega-sierra, maría milagros daza-vega et al. brain lesions causing a hormonal loss, mainly of soma-totropin and gonadotropins, in conclusion, there is an alteration in the metabolism of gh. references 1. arce vm, devesa p, devesa j. role of growth hormone (gh) in the treatment on neural diseases: from neuroprotection to neural repair. neurosci res. 2013; 76(4):179–86. 2. tresguerres ja. fisiología humana. madrid: interamericana-mcgraw-hill; 2005. 3. brinkman je, tariq ma, leavitt l, et al. physiology, growth hormone. [updated 2021 may 7]. in: statpearls [internet]. treasure island (fl): statpearls publishing; 2021 jan-. available from: https://www.ncbi.nlm.nih.gov/books/nbk482141/ 4. kobeissy fh, editor. brain neurotrauma: molecular, neuropsychological, and reha-bilitation aspects. boca raton (fl): crc press/taylor & francis; 2015 5. popovic v, aimaretti g, casanueva ff, ghigo e. hypopituitarism following traumatic brain injury. growth horm igf res. 2005; 15(3):177-84. 6. tölli a, borg j, bellander bm, johansson f, höybye c. pituitary function within the first year after traumatic brain injury or subarachnoid haemorrhage. j endocrinol invest. 2017; 40(2):193–205. 7. fernandez-rodriguez e, bernabeu i, castro ai, casanueva ff. hypopituitarism after traumatic brain injury. endocrinol metab clin north am. 2015; 44(1):151–9. 8. cruz-lópez a de, garrido-aguirre e. disfunción hormonal en el paciente neurocrítico. revista mexicana de anestesiologia. 2015; 38:441–2. 9. klose m, feldt-rasmussen u. chronic endocrine consequences of traumatic brain inju-ry what is the evidence? nat rev endocrinol. 2018; 14(1):57–62. 10. ioachimescu ag, hampstead bm, moore a, burgess e, phillips ls. growth hormone deficiency after mild combat-related traumatic brain injury. pituitary. 2015; 18(4):535–41. 11. masel bs, urban rj. chronic endocrinopathies in tbi disease. j neurotrauma. 2015; 1(32):1902–10. 12. tritos na, biller bmk. current concepts of the diagnosis of adult growth hormone deficiency. rev endocr metab disord. 2021; 22(1):109-116. 13. lee j, anderson lj, migula d, yuen kcj, mcpeak l, garcia jm. experience of a pi-tuitary clinic for us military veterans with traumatic brain injury. j endocr soc. 2021; 5(4):bvab005. 14. builes ca, sierra j. hipopituitarismo postraumático: reporte de un caso. revista co-lombiana de endocrinología, diabetes y metabolismo. 2015; 2(4)55–9. 15. daskas n, sharples p, likeman m, lightman s, crowne ec. growth hormone secre-tion, fatigue and quality of life after childhood traumatic brain injury. eur j endocrinol. 2019; 181(3):331-338. 16. bellis a de, ulutabanca h, bizzarro a, sinisi aa, tanriverdi f, bellastella g, et al. a five year prospective investigation of anterior pituitary function after traumatic brain injury : is hypopituitarism long-term after head trauma associated with autoimmuni-ty ? j neurotrauma. 2013; 1433:1426–33. 17. tanriverdi f, schneider hj, aimaretti g, masel be, casanueva ff, kelestimur f. pi-tuitary dysfunction after traumatic brain injury : a clinical and pathophysiological ap-proach pituitary dysfunction after traumatic brain injury : a clinical and pathophysio-logical approach. endocr rev. 2015; 36(3):305-42. 18. bensalah m, donaldson m, labassen m, cherfi l, nebbal m, haffaf em, et al. preva-lence of hypopituitarism and quality of life in survivors of post-traumatic brain injury. endocrinol diabetes metab. 2020; 3(3):e00146. 19. ciarlone sl, statz jk, goodrich ja, norris jn, goforth cw, ahlers st, et al. neuro-endocrine function and associated mental health outcomes following mild traumatic brain injury in oef-deployed service members. j neurosci res. 2020; 98(6):1174-1187. 20. wilk je, herrell rk, wynn gh, riviere la, hoge cw. mild traumatic brain injury (concussion), posttraumatic stress disorder, and depression in u.s. soldiers involved in combat deployments: association with postdeployment symptoms. psychosom med. 2012; 74(3):249-57. 21. wilkinson cw, pagulayan kf, petrie ec, mayer cl, colasurdo ea, shofer jb, et al. high prevalence of chronic pituitary and target-organ hormone abnormalities after blast-related mild traumatic brain injury. front neurol. 2012; 3:11. 22. emelifeonwu ja, flower h, loan jj, mcgivern k, andrews pjd. prevalence of ante-rior pituitary dysfunction twelve months or more following traumatic brain injury in adults: a systematic review and meta-analysis. j neurotrauma. 2020; 37(2):217-226. 23. weil zm, karelina k. lifelong consequences of brain injuries during development: from risk to resilience. front neuroendocrinol. 2019; 55:100793. 24. wright t, urban r, durham w, dillon el, randolph km, danesi c, et al. growth hormone alters brain morphometry, connectivity, and behavior in subjects with fatigue after mild traumatic brain injury. j neurotrauma. 2020; 37(8):1052-1066. 25. mila-grande jc, granadillo-daza rl, agudelo-rios da, lozada-martínez id. regar-ding: management of unfavorable outcome after mild traumatic brain injury: review of physical and cognitive rehabilitation and of psychological care in post-concussive syn-drome. neurochirurgie. 2021; s0028-3770(21)00165-x. 26. rodriguez-zapata mf, valdes-moreno pl, baldoseamena y, lozada-martinez id. regarding: nutritional factors in sport-related concussion. neurochirurgie. 2021; s0028-3770(21)00164-8. 27. ortega-sierra mg, durán-daza rm, carrera-patiño sa, rojas-nuñez ax, charry-caicedo ji, lozada-martínez id. neuroeducation and neurorehabilitation in the 489 basic considerations on growth hormone deficiency in traumatic brain injury neurosur-gical patient: programs to be developed in latin america and the caribbean. j neurosurg sci. 2021. online ahead of print. 28. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neu-rosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. 29. hu y, liu x, chen x, chen t, ye p, jiang l, et al. differences in the functional con-nectivity density of the brain between individuals with growth hormone deficiency and idiopathic short stature. psychoneuroendocrinology. 2019; 103:67-75. 30. kesavan c, bajwa nm, watt h, mohan s. experimental repetitive mild traumatic brain injury induces deficits in trabecular bone microarchitecture and strength in mice. bone res. 2017; 5:17042. 31. zhou x, von der mark k, henry s, norton w, adams h, de crombrugghe b. chondro-cytes transdifferentiate into osteoblasts in endochondral bone during development, post-natal growth and fracture healing in mice. plos genet. 2014; 10(12):e1004820. 32. aghajanian, p, mohan s. the art of building bone: emerging role of chondrocyte-to-osteoblast transdifferentiation in endochondral ossification. bone res. 2018; 6:19. 33. kesavan c, bajwa nm, watt h, mohan s. growth hormone effects on bone loss-induced by mild traumatic brain injury and/or hind limb unloading. scientific reports. 2019; 9:18995. 34. aberg nd, brywe kg, isgaard j. aspects of growth hormone and insulin-like growth factor-i related to neuroprotection, regeneration, and functional plasticity in the adult brain. scientificworldjournal. 2006; 6:53-80. 35. madathil sk, evans hn, saatman ke. temporal and regional changes in igf-1/igf-1r signaling in the mouse brain after traumatic brain injury. j neurotrauma. 2010; 27(1):95-107. 36. walter hj, berry m, hill dj, logan a. spatial and temporal changes in the insulin-like growth factor (igf) axis indicate autocrine/paracrine actions of igf-i within wounds of the rat brain. endocrinology. 1997; 138(7):3024-34. 37. wang y-j, wong hs-c, wu c-c, chiang y-h., chiu w-t, chen k-y, et al. the fun-ctional roles of igf-1 variants in the susceptibility and clinical outcomes of mild traumatic brain injury. journal of biomedical science. 2019; 26:94. 38. marzo sj, leonetti jp, raffin mj, letarte p. diagnosis and management of post-traumatic vertigo. laryngoscope. 2004; 114(10):1720-3. 39. chamelian l, feinstein a. outcome after mild to moderate traumatic brain injury: the role of dizziness. arch phys med rehabil. 2004; 85(10):1662-6. 40. martin cr, mayer ea. gut-brain axis and behavior. nestle nutr inst workshop ser. 2017; 88:45-53 41. sundman mh, chen nk, subbian v, chou yh. the bidirectional gut-brainmicrobio-ta axis as a potential nexus between traumatic brain injury, inflammation, and disease. brain behav immun. 2017; 66:31-44 42. yuen kcj, masel be, reifschneider kl, sheffield-moore m, urban rj, pyles rb. alterations of the gh/igf-i axis and gut microbiome after traumatic brain injury: a new clinical syndrome? j clin endocrinol metab. 2020; 105(9):dgaa398. 43. rice mw, pandya jd, shear da. gut microbiota as a therapeutic target to ameliorate the biochemical, neuroanatomical, and behavioral effects of traumatic brain injuries. front neurol. 2019; 10:875. 44. sherwin e, dinan tg, cryan jf. recent developments in understanding the role of the gut microbiota in brain health and disease. ann n y acad sci. 2018; 1420:5-25 45. ghaisas s, maher j, kanthasamy a. gut microbiome in health and disease: linking the microbiome-gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases. pharmacol ther. 2016; 158:52-62 46. alkasir r, li j, li x, jin m, zhu b. human gut microbiota: the links with dementia development. protein cell. 2017; 8:90-102 47. cenit mc, sanz y, codoner-franch p. influence of gut microbiota on neuropsychiatric disorders. world j gastroenterol. 2017; 23:5486-5498 48. dash s, clarke g, berk m, jacka fn. the gut microbiome and diet in psychiatry: fo-cus on depression. curr opin psychiatry. 2015; 28:1-6 49. foster ja, mcvey neufeld ka. gut-brain axis: how the microbiome influences an-xiety and depression. trends neurosci. 2013; 36:305-312 50. kelly df, gonzalo it, cohan p, berman n, swerdloff r, wang c. hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. j neurosurg. 2000; 93:743-752 51. vespa pm. hormonal dysfunction in neurocritical patients. curr opin crit care. 2013; 19(2):107-12. 52. dimopoulou i, kouyialis at, orfanos s, armaganidis a, tzanela m, thalassinos n, et al. endocrine alterations in critically ill patients with stroke during the early recovery period. neurocrit care. 2005; 2(4):306–12. 53. mckeating eg, andrews pjd. cytokines and adhesion molecules in acute brain inju-ry. br j anaesth 1998; 80:77–84. 54. bornstein sr, chroussos gp. clinical review 104: adrenocorticotropin (acth)and non-acth-mediated regulation of the adrenal cortex: neural and immune inputs. j clin endocrinol metab 1999; 84:1729–1736. 8amitagrawal_falco romanian neurosurgery (2014) xxi 3: 299 302 299 falco-tentorial meningioma producing irreversible midbrain damage amit agrawal professor of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract meningiomas arising from the falcotentorial junction are the rarest subgroup of tentorial menigiomas. because of the distance from the brain surface and the surrounding deep cerebral veins these lesions are difficult and dangerous to treat surgically. a 45-year-old female presented with the history of progressive headache, disorientation, unsteadiness, and urinary incontinence for over 6 months. the patient developed difficulty in swallowing, and weakness of all four limbs for the last 7 days. ct scan brain plain and contrast showed a large well defined, homogenously enhancing mass lesion in the peineal region with compression of the upper brain stem and obstructive hydrocephalus. inspite of the good surgical decompression the patient did not do well. as described in the literature, the compression of the midbrain can cause severe respiratory disturbances with fatal outcome; probably the similar mechanism resulted in poor outcome in present case. as we noticed the diffuse hypodensity in midbrain on ct scan, similar findings have been described in literature in cases of transtentorial herniation with poorer outcome. key words: falcotentorial meningioma, midbrain, transtentorial herniation introduction meningiomas arising from the falcotentorial junction are the rarest subgroup of tentorial menigiomas. (1-5) because of the distance from the brain surface and the surrounding deep cerebral veins these lesions are difficult and dangerous to treat surgically. (6-9) case report a 45-year-old female presented with the history of progressive headache, disorientation, unsteadiness, and urinary incontinence for over 6 months. the patient developed difficulty in swallowing, and weakness of all four limbs for the last 7 days. she had multiple episodes of vomiting and was in altered sensorium for last three days. there was no history of fever or trauma. on neurological examination she was unconscious (gcs-e2v1, m3). pupils were bilateral equal and reacting to light. fundus 300 agrawal falco-tentorial meningioma producing irreversible midbrain damage showed bilateral papilloedema. extra ocular movements were restricted in all directions. she had spastic quadriparesis. her general and systemic examination was unremarkable. blood investigations were normal except low hemoglobin (8 gm %). ct scan brain plain and contrast showed a large well defined, homogenously enhancing mass lesion in the peineal region with compression of the upper brain stem and obstructive hydrocephalus (figures 1 and 2). figure 1 plain ct scan brain showing a large showing mass lesion in the pineal region with hydrocephalus figure 2 contrast ct scan brain showing the homogenous enhancement after contrast administration romanian neurosurgery (2014) xxi 3: 299 302 301 figure 3 post-operative follow up ct scan showing diffuse hypodensity involving the midbrain the patient was operated using a right interhemisheric parieto-occipital approach consisted of a unilateral parieto-occipital craniotomy exposing the ipsilateral torcula, superior sagittal sinus, transverse sinus and the occipital lobe. during surgery the major part of the tumor was found to be attached to the falco-tentorial junction and a near total excision of the lesion was performed. followed surgery initially patient improved in her sensorium (opening eyes to call), but there was no improvement in her other neurological parameters. at day two she again deteriorated in her sensorium and a repeat ct scan showed increase in the hydrocephalus and diffuse hypodensity in the midbrain (figure 3). the patient underwent right ventriculoperitoneal shunt, however she did not improve and continued to deteriorate. she expired on day six. histological examination demonstrated a fibroblastic type of meningioma. discussion the ideal surgical approach should allow prompt and gross total removal of falcotentorial meningiomas with minimum brain retraction and at the same time safeguard the galenic system and neighboring vital structures. (5, 10) although total total tumour excision is the goal, however it may not be possible in all the cases. (2, 10-12) to achieve the total excision many operative approaches have been described and include transcallosal, occipital transtentorial, infratentorial supracerebellar approaches and sitting, prone or concorde positions. (11) we used the parieto-occipital route to access the lesion in the present case, which has been described as the shortest way to reach epiphysis and falco-tentorial notch. (11, 13) uneventful postoperative courses without neurological deficits and an excellent outcome have been reported after complete removal of 302 agrawal falco-tentorial meningioma producing irreversible midbrain damage the tumor. (1-5) however, the inferior extension of the tumor can compress the deep veins and the brainstem, although occlusion of deep veins may not significantly influence the outcome. (12) as described in the literature, the compression of the midbrain can cause severe respiratory disturbances with fatal outcome, (14) probably the similar mechanism resulted in poor outcome in present case. as we noticed the diffuse hypodensity in midbrain on ct scan, similar findings have been described in literature in cases of transtentorial herniation with poorer outcome. (15) correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email dramitagrawal@gmail.com dramit_in@yahoo.com mobile +91-8096410032 references 1.asari s, maeshiro t, tomita s, kawauchi m, yabuno n, kinugasa k, ohmoto t. meningiomas arising from the falcotentorial junction. clinical features, neuroimaging studies, and surgical treatment. j neurosurg. 1995;82(5):726-38. 2.okami n, kawamata t, hori t, takakura k. surgical treatment of falcotentorial meningioma. j clin neurosci. 2001;8 suppl 1:15-8. 3.quiñones-hinojosa a, chang ef, chaichana kl, mcdermott mw. surgical considerations in the management of falcotentorial meningiomas: advantages of the bilateral occipital transtentorial/transfalcine craniotomy for large tumors. neurosurgery. 2009;64(5 suppl 2):260-8. 4.quinones-hinojosa a, chang ef, mcdermott mw. falcotentorial meningiomas: clinical, neuroimaging, and surgical features in six patients. neurosurg focus. 2003 ;14(6):e11. 5.majchrzak k, tymowski m. surgical treatment of the tentorial and falco-tentorial junction meningiomas. minim invasive neurosurg. 2009;52(2):93-7. 6.matsuda y, inagawa t. surgical removal of pineal region meningioma--three case reports. neurol med chir (tokyo). 1995;35(8):594-7. 7.nakayama k, miyasaka y, ohwada t, yada k. [meningioma in the pineal region--report of a case and review of the literature (author's transl)]neurol med chir (tokyo). 1980;20(3):265-71. (in japanese) 8.suzuki s, mizoi k, kato s, suzuki j: a successful removal of huge confluence meningioma. no shinkei geka 1988 ;16: 289-294. (in japanese) 9.toyota a, takahashi a, yoshida y, murakami t, saiki i, kanaya h: meningioma of pineal region. no shinkei geka 1990 ;18: 745-749. (in japanese) 10.raco a, agrillo a, ruggeri a, gagliardi fm, cantore g. surgical options in the management of falcotentorial meningiomas: report of 13 cases. surg neurol. 2004;61(2):157-64. 11.brotchi j, raftopoulos c, levivier m, dewitte o, pirotte b, vandesteene a, baleriaux d, noterman j. [lesions of the pineal and tentorial region. occipitoparietal approach in three-quarter prone position with infrasagittal craniotomy][article in french] neurochirurgie. 1991;37(6):410-5. 12.goto t, ohata k, morino m, takami t, tsuyuguchi n, nishio a, hara m. falcotentorial meningioma: surgical outcome in 14 patients. j neurosurg. 2006;104(1):47-53. 13.misu n, hirota t, tohyama k. [meningioma of the falco-tentorial junction developing into the pineal region. report of two cases][article in japanese] neurol med chir (tokyo). 1987;27(4):313-8. 14.topsakal c, kaplan m, erol f, cetin h, ozercan i. unusual arachnoid cyst of the quadrigeminal cistern in an adult presenting with apneic spells and normal pressure hydrocephalus--case report. neurol med chir (tokyo). 2002;42(1):44-50. 15.hattori t, yamakawa h, kobayashi h, niikawa s, ohkuma a. computed tomographic features of central descending transtentorial herniation--case report. neurol med chir (tokyo). 1990;30(1):51-3. doi: 10.33962/roneuro-2022-033 posterior fossa extradural hematoma clinical presentation and outcome. a single centre experience from india yadav kaushal, lodha krishna govind, jaiswal gaurav, gupta tarun kumar, patel pratik bipinbhai, kumawat suresh romanian neurosurgery (2022) xxxvi (2): pp. 181-185 doi: 10.33962/roneuro-2022-033 www.journals.lapub.co.uk/index.php/roneurosurgery posterior fossa extradural hematoma clinical presentation and outcome. a single centre experience from india yadav kaushal, lodha krishna govind, jaiswal gaurav, gupta tarun kumar, patel pratik bipinbhai, kumawat suresh department of neurosurgery, maharana bhupal government hospital & ravindra nath tagore (rnt) medical college, udaipur, rajasthan university of health sciences, jaipur (rajasthan), india abstract background: posterior fossa extra dural hematoma (pfedh) is a rare entity but certain crucial structures are supposed to be injured. because of limited space in the posterior fossa, a clinical small volume of hematoma can deteriorate patients. therefore, timely diagnosis and prompt intervention are required. objective: this study is done to analyse factors like demographic profile, mode of injury, clinical features in relation to pfedh and its management and how they influence the outcome. materials & methods: this is a retrospective analysis of patients who presented with pfedh from july 2016 to july 2021 at rnt medical college and m.b. group of hospitals udaipur, india. patients were evaluated on the basis of demographic profile, mode of injuries, gcs on admission & discharge, and associated radiological findings. result: a total of 25 patients with pfedh were included in this study. amongst these, 18 (72%) were males, and10 (40%) were less than 18 years of age. on admission 19 (76%) had gcs 13-15.22 (88%) patients underwent surgery and 3 (12%) were planned for conservative management. at 6-month follow-up, 22 (88%) patients had good outcomes with gos 3-5 and 1 was lost to follow up while 2 (8%) had poor outcomes with gos 1-2. conclusion: gcs on admission is a good predictor of outcome. the volume of edh was one of the key factors in deciding the line of management. pfedh can sometimes be rapidly fatal due to expansion of hematoma and compression of posterior cranial fossa space which leads to brain stem compression therefore time management is the most important factor for a good outcome. introduction extradural hematoma is said to be the most frequently encountered traumatic neurological pathology. but pfedh has only 4–7% incidence (1.2–15% in various studies for all age groups) of all extradural hematomas.1,2 edh comprises the most frequent traumatic spaceoccupying lesion of the posterior fossa.12 posterior fossa is unique keywords posterior fossa, extradural hematoma, edh corresponding author: yadav kaushal department of neurosurgery, rnt medical college, udaipur, india kaushalyadav460@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 182 yadav kaushal, lodha krishna govind, jaiswal gaurav et al. because it contains the brain stem and is smaller in volume than the supratentorial compartment of the cranium. though relatively infrequent in occurrence, early identification and immediate appropriate management of posterior fossa extradural hematoma (pfedh) is essential for successful neurotrauma management.4 in pfedh clinical progress may be silent and slow, but sudden deterioration may occur without significant warning signs. pfedh can present with quick clinical deterioration because of rapid increasing in size and may cause brain stem compression. management of pfedh is either surgical or conservative based on clinical condition and various other factors. conservative management has shown good results both in children and in adults in cases of traumatic posterior fossa extra dural hematoma. materials and methods this is a retrospective study from july 2016 to july 2021 at a tertiary care centre, r.n.t. medical college & m.b. group of hospitals, udaipur, rajasthan. this study includes 25 cases of traumatic extradural hematoma which were located in posterior fossa. patients were categorised on the basis age, sex, mode of injury, gcs on admission, ct findings, volume of pfedh, type of intervention and postoperative outcome. outcome was assessed by gos at discharge and at 6 months follow-up. results this study includes 25 cases of traumatic posterior fossa extradural hematoma taken over a period of 60 months from july 2016 to july 2021. the mean age of patients was 26.6 (5-48 years).18 (72%) were males amongst these .10 (40%) patients were below 18 years. rta was found to be the most common mode of injury amongst these patients 18 (72%). rest were either fall from height or assault. majority of these patients had gcs 13-15, 19 (76%) when presented to emergency department. 21 (84%) patients were brought within 1 hour of trauma. headache, vomiting and altered sensorium were few common symptoms found in most of these patients. all patients underwent non contrast ct brain and pfedh was found in all. pfedh was unilateral in 23 cases (92%). occipital bone fracture was found in 17(68%) patients f/b supratentorial extension in 3 (12%) patients, acute subdural hematoma in 1 (4%) patient, frontal contusion in 2 (8%), hydrocephalus and ivh was also present in 1 (4%) patient.volume of pfedh was >15 cc in 22(92%) patients and <15 cc in 3 (12%) patients. amongst these patients 22 (88%) underwent surgery and 3 (12%) were planned for conservative management. decesion was based on volume of pfedh and gsc at admission and associated injuries. incision and craniotomy were made as per the site and size of edh. all operated patients were subjected to early ncct brain postoperatively. on discharge 23 (92%) patients had gcs 13-15 and 2 (8%) had gcs of 9-12. patients who were admitted within 1 hour of trauma had better outcome at discharge, signifying the importance of very early intervention before deterioration. at 6 month follow up 22 (88%) had good outcome with gos 5, 1(4%) was lost to follow up and 2 (8%) eventually had poor outcome with gos 2. figure 1. ncct head showing extradural hematoma in posterior fossa on left side. figure 2. post-operative ncct head after evacuation of extradural hematoma. 183 posterior fossa edh: clinical presentation and outcome discussion post-traumatic posterior fossa extradural hematoma is a rare entity. incidence is 0.3% of all craniocerebral injuries, and 4-12% of all extradural hematomas.7 posterior cranial fossa lodges some important vital structures of brain, like brain stem. if pfedh is large, it can cause rapid fall in consciousness level and brain stem dysfunction. pfedhs have a venous origin in 85% of the cases and develop as a result of injury to the transverse or sigmoid sinuses secondary to occipital bone fracture.17 for pfedh, it takes longer to develop clinical picture and it is of vital importance to use imaging methods for early diagnosis. an acute extradural hematoma is seen as a biconvex hyperdense mass located between the duramater and the bone on ncct. an acute extradural hematoma is demonstrated as a localized extra-axial collection of blood between dura and inner table of skull bones on magnetic resonance imaging. imaging of dura as a line with very low signal intensity between the hematoma and brain parenchyma is pathognomonic for extradural hematoma. mr imaging modality is more sensitive in detection of parenchymal conditions or dural venous sinus thrombosis possibly associated with pfedh.13,14 still imaging of choice and the most commonly used method is ncct because of a short acquisition time, allowing demonstration of occipital fractures that are associated with great majority of pfedhs. it also defines the size and mass effects of the hematoma and also provide visualization of possible supratentorial conditions that are reported to be associated with half of the cases in the literature15,5 and mr imaging study is difficult in unstable trauma patients. among all the clinico-radiological parameters, volume of pfedh is the most important factor in deciding the line of management, as also suggested by prasad et al.6 occipital subgaleal haematoma and battle’s sign can be a clue to the diagnosis of pfedh. fracture of the occipital bone is an important sign and it necessitates close observation along with repeat ct scan later to diagnose these haematomas. change in gcs or severe headache with vomiting and new onset cerebellar signs are associated features that can help to have an idea of diagnosis. hydrocephalus may be observed in as high as 30% of cases on the ct scan. all the patients who required surgery in this study had volume of pfedh more than 15cc. this is similar to the observation of bozbuga et al.8 patients with pfedh should be operated based on radiological indications without waiting for clinical deterioration, in order to get a good outcome. paediatric patients with pfedh require surgery more often than adults because of smaller posterior fossa volume and elderly require surgery less often, as atrophic brain can accommodate more volume.10 admission gcs score is the single most important predictor of outcome, with gcs more than 8 having strong association with good outcome (gos 5). gcs at admission is found directly proportional to gcs at discharge, better the gcs i.e. >8 better the outcome seen. our study is also in line with this fact and is consistent with that reported by balik et al, jang et al and prusty et al.11,16 pfedh needs more urgent management, before irreversible brainstem herniation occurs. this requires vigilant paramedical and medical care right from the site of accident, early shifting to neurosurgical care, high index of suspicion in cases of occipital trauma and prompt management. conservative management can also be an option if the patient is asymptomatic and has good gcs. the patient should be kept under close monitoring in neurosurgical intensive care unit (icu). there are some case reports in the literature about these haematomas which resolved spontaneously without any intervention.3 3(12%) cases in our study were managed conservatively out of which 1(4%) did not report back at follow up of 6 month. in our study, pfedh was more common among male than female patients similarly prashant et al also showed in their study that more males suffered from head trauma as compared to females because of more exposure of males to traffic and outdoor activities than females.9 rta being the most common mode of injury in our study was in line with the studies bavil ms et al3and igun go et al.9 patients with associated intracranial findings, with mass effect over brainstem had lesser gcs score on admission, increased edh volume had increased hospital morbidity compared to other patients. occipital bone fracture was found in 68% patients which was in line with that reported by karasu et al. 184 yadav kaushal, lodha krishna govind, jaiswal gaurav et al. conclusions pfedhs are rare. early diagnosis and emergent evacuation lead to good outcome and also reduces morbidity. occipital bone fractures and associated injuries in form of supratentorial or infratentorial subdural hematoma, intraparenchymal hematoma or intraventricular haemorrhage can also be present. clinical progression of disease is silent and slow, but the deterioration is sudden and quick. it can lead to serious complications if not promptly diagnosed and treated. figure 3. distribution of radiological findings table 1. demographic data gender number of cases percentage male 18 72% female 7 28% age <18 10 40% >18 15 60% table 2. mode of injury rta 18 72% fall 6 24% assault 1 4% table 3. radiological findings occipital bone fracture 17 68% frontal contusion 2 8% acute subdural hematoma 1 4% infratentorial extension 0 0 supratentorial extension 3 12% hydrocephalus 1 4% intra ventricular hemorrhage 1 4% table 4. gcs at admission 13-15 19 76% 9-12 4 16% <8 2 8% at discharge 13-15 23 92% 9-12 2 8% <8 0 0 table 5. volume of pfedh <15 3 12% >15 22 88% table 6. management conservative 3 12% surgery 22 88% table 7. outcome based on gos outcome based on gos at discharge at 6 month gos 5 21(84%) 22 (88%) gos 4 2(8%) 1 (4%) gos 3 1 (4%) 0 gos 2 1 (4%) 1 (4%) gos 1 0 0 68% 8% 4% 12% 4% 4% occipital bone fracture frontal contusion acute subdural hematoma infratentorial extension supratentorial extension 185 posterior fossa edh: clinical presentation and outcome conflicts of interest the authors declare no conflict of interest. informed consent informed consent was obtained from all individual participants included in the study. references 1. ammirati m, tomita t. posterior fossa epidural hematoma during childhood. 2. asanin b. traumatic epidural hematomas in posterior cranial fossa. acta clin croat 2009;48:27 30. 3. bavil ms. autopsy findings in patients with severe head injury. res j med sci 2008;2(4):190. 4. berker m, cataltepe o, ozcan oe. traumatic epidural haematoma of the posterior fossa in childhood: 16 new cases and a review of the literature. br j neurosurg 2003;17:226 9. 5. bozbuğa, m., i̇zgi, n., polat, g., & gürel, i. (1999). posterior fossa epidural hematomas: observations on a series of 73 cases. neurosurgical review, 22(1), 34-40.1. 6. ersahin, y., & mutluer, s. (1993). posterior fossa extradural hematomas in children. pediatric neurosurgery, 19(1), 31-33, doi:10.1159/000120697. 7. garza-mercado r. extradural hematoma of the posterior cranial fossa. report of seven cases with survival. j neurosurg. 1983;59(4):664-72. 8. balik, v., lehto, h., hoza, d., sulla, i., & hernesniemi, j. (2010). posterior fossa extradural haematomas. central european neurosurgery-zentralblatt neurochirurgie, 71(04), 167-172, doi:10.1055/s-0030-1249046. 9. igun go. predictive indices in traumatic intracranial haematomas. east afr med j 2000;77(1):9. 10. jang, j. w., lee, j. k., seo, b. r., & kim, s. h. (2011). traumatic epidural haematoma of the posterior cranial fossa. british journal of neurosurgery, 25(1), 5561, doi:10.3109/02688697.2010.520759 11. prusty, g. k., & mohanty, a. (1995). posterior fossa extradural haematoma. journal of the indian medical association, 93(7), 255-8. 11. kang sh, chung yg, lee hk. rapid disappearance of acute posterior fossaepidural hematoma. neurol med chir (tokyo). 2005;45(9):462-3. 12. koc rk, pasaoglu a, menkii a, oktem s, meral m. extradural hematoma of the posterior cranial fossa. neurosurg rev 1998;21:52-7. 13. osborn ag. craniocerebral trauma, diagnostic neuroradiology. st. louis: mosby; 1994. p. 204 5. 14. pozzati e, tognetti f, cavallo m, acciarri n. extradural hematomas of the posterior cranial fossa. observations on a series of 32 consecutive cases treated after the introduction of computed tomography scanning. surg neurol 1989;32:300 3. 15. prasad gl, gupta dk, sharma bs, mahapatra ak. traumatic pediatric posterior fossa extradural hematomas: a tertiary-care trauma center experience from india. pediatr neurosurg 2015;50:250-6. 16. prashant g, atul k, amit d, kumkum g, madhu b, gouri g, et al. ct scan findings and outcomes of head injury patients: a cross-sectional study. j pak med stud 2011;1(3):78–82. 17. samudrala s, cooper pr. traumatic intracranial hematomas. in: wilkins rh, rengachary ss, editors. neurosurgery. 2nd ed. new york: mcgraw hill; 1996. p. 2797 807. microsoft word 5.rajendrash_recurrent_f.docx 116 shrestha et al recurrent intracranial epidural hematoma recurrent intracranial epidural hematoma following ventriculoperitoneal shunt in a child rajendra shrestha1, reeka pradhan2, ju yan1, you chao1 1department of neurosurgery, west china hospital, sichuan university, china 2international medical school, tianjin medical university, china abstract intracranial hematoma is commonly observed in neurosurgical practice. however, recurrent intracranial epidural hematoma following ventriculoperitoneal (vp) shunt is more of an exception than the norm. it is a rare but serious cause of morbidity and mortality in patients with vp shunt. however, treatment is very promising especially with surgical intervention in time. here we report a case of a ten-year-old girl who presented with chronic headache for a couple of years whose imaging features suggested a hydrocephalus with tonsillar herniation. initially, she developed right frontotemporal hematoma and then bilateral frontal epidural hematoma following a vp shunt. emergency decompression was done. keywords: epidural hematoma, hydrocephalus, intracranial, ventricularperitoneal shunt introduction intracranial epidural hematomas (edhs) accounts for approximately 2% of patients following head trauma and 5-15% of patients with fatal head injuries. 65-90% cases are associated with skull fractures4. edh following cerebrospinal fluid (csf) diversion for hydrocephalus is rare. we report our experience with edh after ventriculoperitoneal shunt (vps), management aspects and review of literature. case report a ten-year-old female child presented with intermittent headache for 2 years. she was diagnosed with and treated for sinusitis at a local hospital. however, it was severe with repeated vomiting for a couple of months. she was referred to our hospital for further management. there was no history of trauma, fever, any anticoagulation drug intake, or any other co-morbid disease seemingly responsible for such event as elaborated from history. on examination, there was no neurological deficit. magnetic resonance imaging revealed obstructive hydrocephalus as well as cerebellar tonsil herniation (figure 1 a and b). her blood profile was within the normal range. immunological investigations were also within normal limit. patient underwent right ventricular peritoneal shunting procedure. post operative computed tomography (ct) scan was performed as her gcs was altered and showed right fronto-parieto-temporal epidural hematoma (figure 2a). emergency frontoparieto-temporal craniotomy was done and dural tacked up sutures along the margin of craniotomy. 50 ml dark red blood clots, some of which was liquefied was found and evacuated. patient was put under close monitoring in icu. romanian neurosurgery (2012) xix 2: 116 – 119 117 post operative ct scan of craniotomy two days later showed just edh (figure 2b) but in a small amount so patient underwent strict observation. patient complained of headache a week after craniotomy. ct scan showed bilateral frontal huge epidural hematoma (figure 2c). a b figure 1 preoperative axial (a) and sagittal (b) section of mri showing hydrocephalus and tonsillar herniation a b c 118 shrestha et al recurrent intracranial epidural hematoma d figure 2 (a) non-contrast axial head ct after vps revealing right frontoparietto-temporal hypohyperdensity-epidural hematoma and a portion of the shunting apparatus with mass effect. (b) noncontrast head ct obtained after 2 days of second operation, revealing hematoma frontal region (c) head ct after 7 days of vps, revealing huge bilateral frontal epidural hematoma. (d)head ct after third operation showing normal ventricle with shunting apparatus bilateral frontal craniotomy was done and dura was tight sutured along site of craniotomy. about 70 ml dark calcified black blood, adhesion with dura was found and evacuated. this time patient recovered smoothly. post operative ct scan showed normal shaped ventricle without edh (figure 2d). discussion in 1902, cushing h. introduced ventricular drainage (vd) as a means of reducing intracranial pressure. since then, vd procedure has been frequently performed in neurosurgical practice. several intracranial subdural hematomas (sdh) after vps have been reported in the literature as a complication. to our knowledge, the first reported complication of vd was mentioned by schorste in 1942 (9). there are only few published reports of intracranial edh as a complication of vps. intracranial edh following csf diversion for hydrocephalus is an important cause of immediate deterioration and contributes to morbidity and mortality. their presentation is according to the size and location of hematoma, elevated intracranial pressure and midline shift. the computed tomography scan has played a significant role in the early detection and proper treatment of post operative intracranial hematoma. edhs are contact injuries resulting from blunt trauma to the skull and meninges. fractures, most often linear, are present in 30 to 91 per cent of patients with epidural hematomas (1). it is thought that the initial impact, with deformation or fracturing of the cranium, produces detachment of the dura directly beneath the site of the blow and injures blood vessels (most commonly branches of the middle meningeal artery). hemodynamic factors like vascular malformations of the dura mater and preoperative administration of anticoagulation or disorders of blood coagulation (spontaneous or iatrogenic), hypertension, effect of operative position to venous outflow are the mechanisms of edh. j. f. sanchis et al (1975) explained that neighborhood infection is also one of the causative factors for edh. in the literature, authors mentioned that mechanical factors like bridging vein tearing, dural detachment because of brain parenchyma displacement induced by csf (5, 6, 7). our case is interesting as edh developed adjacent and distant to the vp shunt in 24 hours and one week respectively. in our knowledge, the duramater is firmly attached at the cranial sutures in infants. sudden lowering of romanian neurosurgery (2012) xix 2: 116 – 119 119 intracranial pressure (icp) or rapid drainage of ventricular csf or gravitation flow of csf result in brain shrinkage from the skull. ultimately, detaching the collagenous fixations of the dura from the inner table of the skull may initially cause dural and diploic veins to bleed into the extradural pocket (7, 8). once bleeding has begun, the blood fills the pocket. experimental evidence indicates that arterial bleeding into the resulting pocket creates a hydraulic “water press” effect, progressively stripping away the dura from the skull and widening the perimeter of the hematoma (2). post shunt edh can be managed surgically and conservatively. the choice between a surgical or a nonsurgical treatment of post shunt edh requires the evaluation of various factors: volume, thickness, midline shift and amount of fresh blood present on ct scan (4), the age of the patient, and the clinical picture. huge acute or subacute collections in adults or in children with closed fontanelles usually require surgical treatment. however, in a series concerning a pediatric population, it was stated that asymptomatic edh may become symptomatic later on and that it is safer to treat all post shunt edh, whether symptomatic or not (1). our case is quite unique where a patient had presented primarily with extradural hematoma after vps and again gradually developed edh within one week after craniotomy. we performed craniotomy twice and evacuation of hematoma after dural tenting sutures along the margin to help hemostasis (3). she did well post operatively even after three consecutive operations and was discharged from the hospital in good condition. conclusion vps is a common neurosurgical interventional procedure. patients should be monitored closely post shunt, so intervention can be done immediately if any evidence of deterioration like sdh, edh and others. neurosurgeons must keep in mind that icp raised patients may present with such potentially fatal complication which can be successfully treated if diagnosed in time. correspondence to: dr. rajendra shrestha department of neurosurgery, west china hospital, sichuan university, 37 guo xue xiang, wuhou district, chengdu 610041, china e-mail: rajendra39@yahoo.com references 1. baykaner, k., alp, h., ceviker, n., et al.: observation of 95 patients with extradural haematoma and review of literature. surg. neurol., 30:339, 1988; 2. crooks, d. a.: pathogenesis and biomechanics of traumatic intracranial haemorrhages. virchows arch. a pathol anat histopathol, 418:479-83, 1991; 3. dandy we: surgery of the brain. lewis' practice of surgery, vol 12. hagerstown : wf prior, pp144-162 , 1945–dura srain; 4. dinesh k rajput, rohit kamboj, arun k srivastav, priyanka kaval, raj kumar, is management of spontaneous intracranial extradural hematoma in chronic renal failure is different with traumatic extradural hematoma case report and review of literature: indian journal of neurotrauma (ijnt), vol. 7, no. 1,pp.81-84, 2010; 5. fan xue zheng, you chao. spontaneous intracranial extradural hematoma: case report and literature review;neurology india; 57: 324-6, 2009; 6. j.f. sanchis, m. orozco, and j. cabanes: spontaneous extradural haematomas. j neurol neurosurg psychiat; 38: 577-80, 1975; 7. jin-soo jeon,in-bok chang,byung-moon cho,hokook lee, seung-koan hong, sae-moon oh, immediate postoperative epidural hematomas adjacent to the craniotomy site :vol.39,no.5 pp335-9, 2006; 8. marks sm, shaw md. spontaneous intracranial extradural hematoma. j neurosurg;57:708-9, 1982; 9. sengupta rp, hankinson j: extradural haemorrhage : a hazard of ventricular drainage. j neurol neurosurg psychiatry 35 : 297-303, 1972. microsoft word 6_chiriaca_onyxtreatment 164 chiriac et al onyx treatment of dural arteriovenouse fistulae onyx treatment of dural arteriovenouse fistulae. our first experience a. chiriac, b. iliescu1, n. dobrin1, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract intracranial dural arteriovenous fistulae (davf) with retrograde cortical venous drainage are uncommon lesions frequently associated with a poor prognosis if left untreated. the treatment of davfs with cortical venous drainage by endovascular occlusion of the entire arterial supply or the venous drainage is considered curative. we present our first endovascular experience with use of onyx via the arterial route in these aggressive fistulas. key words: dural arteriovenous fistulae; onyx embolization introduction cerebral vascular malformations like intracranial dural arteriovenous fistulas (davfs) are considered today dangerous lesions if left untreated, especially those with retrograde cortical venous drainage. because the natural history of untreated lesions is frequently associated with a poor prognosis, prompt treatment is indicated. dural arteriovenous fistulas are considered abnormal direct connection (fistula) between multiple meningeal arteries (arterial feeders) and a meningeal vein or dural venous sinus. the treatment of davfs with cortical venous drainage consist in occlusion of the all arterial supply or the venous drainage and can be done surgically, endovascularly, or by a combination of both approaches. endovascular treatment of total occlusion of a davf using a transarterial embolization it’s difficult as a result of this extreme rich anastomotic network of the dural/falcine plethora of feeding arteries, blood supply to cranial nerves, and extra intracranial anastomoses [1]. transvenous occlusion of the affected venous sinus could be effective in selected cases, especially when the venous sinus did not drain into cortical or deep veins. the endovascular occlusion of davfs via an arterial or venous route has usually included embolization with acrylic glue, particles, coils, or a combination. today, the use of onyx (ev3, irvine, california) via the arterial route has been reported as the optimal treatment choice. due to its longer precipitation time enabling prolonged injection time, the onyx offer a better penetration into a fistulous network. we report our initial experience with arterial injection of onyx in the endovascular treatment of a davf with retrograde cortical. technical procedure for a complete cure, the endovascular treatment is considered the primary modality of treatment of all davfs at most neurosurgical center. the liquid embolic agent, onyx 18 (ethylene vinyl alcohol romanian neurosurgery (2013) xx 2: 164 – 169 165 copolymer, ev3), is usually used for treatment of the patients with these lesions. the procedure is performed with the patient under general anesthesia on a biplane angiographic unit (axion artis; siemens medical solutions, erlangen, germany). unilateral or bilateral transfemoral approach involving the use of 5f–6f introducing sheaths permutes arterial catheterization. standard coaxial techniques ensure a secure guiding and control catheters positioning in the external, internal carotid or vertebral arteries. the guiding catheter is continuous flushing with saline solution for prevention of tromboembolic events. at the beginning a six-vessel complete selective angiography is performed to precisely determine the anatomic characteristics of the shunt, to obtain an optimal projection and to plan the treatment. after the diagnostic angiography was concluded, a 5f guiding catheter was used for the external carotid artery (eca) and 6f mpc envoy guide catheter (cordis endovascular, miami lakes, fla) for the internal carotid artery (ica) and vertebral artery (va) 6f) catheterization. an intravenous bolus of 5000 iu loading dose of heparin is administered to patient after guiding catheter placement and 1000 units per hour thereafter. superselective catheterization of the predominant feeding artery using a dimethyl-sulfoxide (dmso) compatible microcatheter (marathon, ev3, irvine, ca) (ultraflow, marathon, or echelon, ev3) coaxially advanced on a 0.008 inch microguidewire (mirage or x-pedion, ev3) is performed to reach the distal aspect of the pedicle supplying the davf as close as possible to the fistula. microcatheter angiography is then performed to confirm optimal position and to see the drainage of the fistula. special attention is taken to ensure that the distal tip of the catheter is in a straight segment of the feeding artery to facilitate catheter retrieval. the microcatheter is less likely to stick when placed in a straight rather than a tortuous segment of the vessel. the microcatheter is then flushed with 10 ml of normal saline and its “dead space” is subsequently filled with 0.25 ml of dmso, and the microcatheter hub is bathed with dmso forming a meniscus. onyx and dimethyl-sulfoxide (dmso) are drawn into 2 separate 1-ml syringes. dmso is injected slowly over 40 sec. the onyx vial is shaken on the onyx mixer for at least 20 min prior to its use. then, onyx 18 is slowly injected, initially 0.2 ml/s, without guidance, over approximately 40 seconds to avoid a rapid bolus of dmso in the cerebral circulation. subsequently under subtraction fluoroscopy or biplane roadmap guidance onyx injection is then slowly carried out using a “thumb-tapping” technique. in case of high flow fistulas a higher viscosity onyx 34 it better to be chose because the higher viscosity agent is felt to less likely pass through the fistulous connection. later in the course of the injection, once flow through the fistula is reduced, lower viscosity onyx 18 is used to facilitate greater penetration of the nidus of the fistula (figure 1 a, b). special attention is paid to maintain a gradual and progressive injection rate, while looking for any reflux of the embolizing agent, which would signal the surgeon to interrupt the injection. 166 chiriac et al onyx treatment of dural arteriovenouse fistulae figure 1: a microcatheterization of the davf; b – onyx occlusion of davf [12] if onyx penetrated the network of arterial feeders, the injection is continued until we suspected any of the three danger signs: 1) penetration of onyx into a cortical vein 2) when there is any reflux around the catheter tip or 3) if there is retrograde filling into pial feeder. in these situations we abort the injection for 30s to 120s to allow solidification of onyx in an attempt to change the direction of penetration in the network of interconnecting feeders. usually, reflux occurred several times before onyx would advance into the fistula site. a small amount of initial reflux is allowed, as it typically leads to the formation of a “plug,” which may subsequently facilitate antegrade flow of the embolic agent. excessive reflux, however, is avoided, since it may lead to the occlusion of normal vessels or make the microcatheter removal more difficult. the normal length of tolerated reflux is between 1.5 and 3 cm, depending on the vascular territory. in some cases with middle meningeal artery injection, more than a 5cm reflux was accepted. in other particular cases a feeding artery could be blocked with a microballoon (hyperform, ev3) to prevent reflux and promote advancement of onyx into the target sinus. protective balloons should be used in cases with highflow davfs with large supplies from the vertebal or the internal carotid arteries. flow control can be achieved with manual compression of the carotids or both the jugular vein and the carotid, or by balloon occlusion of the venous sinus. using this "waiting technique" to change the direction of filling of the fistula when a dangerous sign is identified is crucial to achieve complete obliteration of the fistula. whenever reflux appears, injection is stopped for sometime. when restarting the injection, it was helpful to employ roadmap techniques to rapidly identify the new site of onyx delivery to ensure a safe embolization. the procedure is considered terminated when reflux recurred and persisted and no onyx is entering the fistula feeding network or when angiography shows a complete fistula occlusion. the microcatheter is then pulled gently until it detached from their onyx cast. ultraflow microcatheters (ev3) could be stretched romanian neurosurgery (2013) xx 2: 164 – 169 167 until rupture in their distal flexible end, if they did not move. marathon microcatheters (ev3) are braided and stiffer, allowing much more force for retrieval before rupture could occur. patients are heparinized over 24–48 h and eventually kept on low molecular weight heparins for 1–2 weeks when we observed slowing down of territorial venous outflow or contrast stasis in various cortical veins. case report a 57 year-old woman presented in december 2012 for an episode of speech disturbances and right temporal hemianopsia. the patient declares a history of ten years of a sincron noise in the left ear associated with retroauricular throbbing pain. she was diagnosed in march 2012 with breast carcinoma and operated by total left mastectomy followed by chemotherapy and radiotherapy. neurological examination was normal except for pulsatile tinnitus. the patient initially underwent cerebral ct scan with enhancement that revealed low-density areas in left hemisphere regions, with several punctiform or vermicular enhancements (figure 2). digital subtraction angiography showed a dural fistula with supply from the tentorial artery, posterior auricular artery, middle meningeal artery, and occipital artery and draining into a left sigmoid sinus with multiple venous ecstasies in the left cerebral hemisphere (figure 3). figure 2 ct scan with several punctiform or vermicular enhancements figure 3 dsa showing a davf with cortical vein drainage figure 4 dsa image with onyx migration showing the perforation of microcatheter 168 chiriac et al onyx treatment of dural arteriovenouse fistulae figure 5 postprocedural angiography showing davf complete occlusion the patient initially underwent a left middle meningeal artery branch approach. when the dmso injection was performed a perforation of the microcatheter occurs due to a high pressure injection. the perforation of microcatheter was visualized when the injection of onyx was started and the glue migrated into the artery at the perforations sites. the injection was stopped with the retrieve of the microcatheter (figure 4). the posterior auricular branch was microcatheterized and the davf (fistula segment of left sigmoid sinus) was completely occluded with onyx. complete occlusion of the davf is confirmed by postprocedural angiography (figure 5). the patient was discharged seven day later with no neurological deficit. discussion the relationships between intracranial dural arteriovenous fistula, venous drainage patterns and clinical presentation were already presented in several studies. many researchers have attempted to identify the factors that predispose to the risk of aggressive davf symptoms. on the basis of their findings, it is now generally accepted that the venous drainage pattern of davfs is the most predictive factor.[5] intracranial davfs with retrograde cortical venous drainage are more aggressive lesions that have shown a much higher incidence of hemorrhage or venous infarction. usually, these lesions can present with intracranial hemorrhage, seizures, progressive neurologic deficit, intracranial hypertension, or dementia. although several classification systems have been developed to grade the risks of davfs, those devised by cognard et al and borden et al are the most widely used.[5] general approaches for the treatment of davfs include conservative treatment, radiation therapy, endovascular intervention, and surgery. treatment option is dependent on the grade of fistula and the clinical picture. in selected cases as davf without angiographic evidence of retrograde sinus or cortical venous drainage and presenting with a well-tolerated or non-disabling tinnitus conservative treatment can be effective. the simple carotid artery or occipital artery manual compression has been reported to occasionally lead to davfs obliteration. also, this may correspond to the natural history of the disease. the most frequently treatment of such fistulas primarily involves an endovascular approach, and if this fails, surgical or radiosurgical approaches are used. also, the combination of them is sometime an option. transarterial embolization of davf with embolic materials such as nbca, ethanol, coils, and particles didn’t bring satisfactory results especially for extensive lesions because only large feeding artery can be occluded. incomplete occlusion of the fistulas will result in recanalization of the davf from the multiple collateral arteries constituting the dural blood supply[1]. romanian neurosurgery (2013) xx 2: 164 – 169 169 onyx™ (ev3, irvine, ca, usa) is a liquid embolic material that is increasingly used via the arterial route in embolization of arteriovenous malformations. its properties of longer precipitation time enabling prolonged injection time, with potential of better penetration into a fistulous network make onyx the best option for complete davfs occlusion. onyx treatment for davfs with cortical venous drainage is encouraging and our case presentation confirms the good results reported recently by other authors [6]. the complications reported in the literature were the bleeding after incomplete occlusion, cerebral ischemia due to venous thrombosis and ischemic damage to the trigeminal and facial nerves. damage to these nerves may occur if onyx reflux extends proximally to the foramen spinosum level and occludes the cavernous and petrosal branches.[6] the annual mortality rate for cortical venous reflux may be as high as 10.4%, whereas the annual risk for hemorrhage or nonhemorrhagic neurologic deficits during follow-up are 8.1% and 6.9%, respectively, resulting in an annual event rate of 15%.[3] conclusions a better understanding of factors as drainage patterns, risk of aggressive symptoms and feasibility of recent technical advances is essential for the treatment of davfs. onyx embolization has revolutionised the endovascular treatment of davfs and become the primary treatment option for most cases. despite achieving a higher cure rates in single session with minimal complication, larger number of cases and longer follow up are required to determine the efficacy and safety of this technique. references 1. katsunari namba, yasunari niimi, joon k. song, alejandro berenstein (2009) onyx transarterial embolization of dural arteriovenous fistula for failed nbutyl cyanoacrylate treatment: case report, jnet 3:174180; 2. alexandros l. georgiadis, giuseppe lanzino, nazli janjua, jawad f. kirmani, adnan i. qureshi (2008) a case of dural arteriovenous fistula with retrograde intracranial venous flow, j vasc interv neurol; 1(1):913; 3. c. cognard, a.c. januel. n.a. silva, jr. p. tall (2008) endovascular treatment of intracranial dural arteriovenous fistulas with cortical venous drainage: new management using onyx, ajnr am j neuroradiol 29:235– 41; 4. w.j. van rooij, m. sluzewski (2010) curative embolization with onyx of dural arteriovenous fistulas with cortical venous drainage, ajnr am j neuroradiol 31:1516 –20; 5. hiro kiyosue, yuzo hori, mika okahara, shuichi tanoue, yoshiko sagara, shunro matsumoto, hirofumi nagatomi, hiromu mori (2004) treatment of intracranial dural arteriovenous fistulas: current strategies based on location and hemodynamics, and alternative techniques of transcatheter embolization1, radiographics 24:1637–1653; 6. josé e. cohen, john m. gomori, samuel moscovici, eyal itshayek (2011) dural arteriovenous fistula with cortical venous drainage: complete occlusion with onyx embolization, imaj 13:705-6; 7. e. william.adams (2007) intracranial dural arteriovenous fistulae, vol. 7, 3:10-12; 8. rashmi saraf, manish shrivastava, nishant kumar, uday limaye () intracranial dural arteriovenous fistulae, indian j radiol imaging, vol 20, 1:26-33; 9. chai eq, wang j. (2011) transarterial onyx embolization of sagittal sinus dural arteriovenous fistulae. neurol india 59:262-5. 10. chong bw, demaerschalk bm. (2008) unusual presentation of a dural arteriovenous fistula of the superior sagittal sinus and single modality therapy with onyx. radiology case reports 3:158; 11. ross c. puffer, david j. daniels, david f. kallmes, harr yj. cloft, giusepp e lanzino (2012) curative onyx embolization of tentorial dural arteriovenous fistulas, neurosurg focus 32(5):1-7. 12. alejandro m. spiotta, thinesh sivapatham, muhammad shazam hussain, ferdinand k. hui, shaye i. moskowitz, rishi gupta (2012) combined surgical and endovascular approach to a complex dural arteriovenous fistula involving the superior sagittal sinus and torcula, vol 21, 4:283–288. doi: 10.33962/roneuro-2021-092 tumefactive multiple sclerosis. a rare but serious variable in multiple sclerosis michael gregorio ortega-sierra, raul david delgado-marrugo, cristian camilo campo-bedoya, geraldine marín-pérez, rhonald gómez-caballero, bryan d. hernández-nieto, g.f. gutiérrez-castillo, john fredys bello-cordero, mónica alejandra torres-báez, rafael ricardo ramirez -morales, ivan david lozada-martinez, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (4): pp. 538-543 doi: 10.33962/roneuro-2021-092 www.journals.lapub.co.uk/index.php/roneurosurgery tumefactive multiple sclerosis. a rare but serious variable in multiple sclerosis michael gregorio ortega-sierra1, raul david delgado-marrugo2, cristian camilo campo-bedoya3, geraldine marín-pérez4, rhonald gómez-caballero5, bryan d. hernándeznieto6, gabriel fernando gutiérrez-castillo7, john fredys bello-cordero8, mónica alejandra torresbáez9, rafael ricardo ramirez-morales9, ivan david lozada-martinez1,10, luis rafael moscote-salazar10 1 medical and surgical research centre, future surgeons chapter, colombian surgery association, cartagena, colombia 2 school of medicine, universidad militar nueva granada, bogotá, colombia 3 school of medicine, universidad tecnológica de pereira, pereira, colombia 4 school of medicine, universidad cooperativa de colombia, medellín, colombia 5 school of medicine, universidad de ciencias aplicadas y ambientales, bogotá, colombia 6 school of medicine, universidad simón bolívar, barranquilla, colombia 7 school of medicine, universidad de boyacá, boyacá, colombia 8 school of medicine, fundación universitaria de ciencias de la salud, bogotá, colombia 9 school of medicine, universidad el bosque, bogotá, colombia 10 colombian chapter, latin american council of neurocritical care, cartagena, colombia abstract tumefactive multiple sclerosis is a rare variant of multiple sclerosis, characterized by the presence of brain lesions that may be solitary or multiple. considering that these lesions have a pseudotumoral appearance, it is a challenge to differentiate them from central nervous system neoplasms through neuroimaging. many cases are associated with the administration of monoclonal antibodies, and due to an increase in the incidence of cancer globally, it is expected that secondary to chemotherapeutic treatments, more and more cases may appear. taking into account the above, the objective of this review is to review aspects of usefulness in clinical practice, on the diagnosis and approach of this pathological condition keywords tumefactive multiple sclerosis, multiple sclerosis, demyelinating diseases, rare disease, neurosurgical disease corresponding author: michael gregorio ortega-sierra medical and surgical research centre, st mary´s medical group, cartagena, colombia mortegas2021@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 539 tumefactive multiple sclerosis introduction tumefactive multiple sclerosis (tms) is a rare variant of multiple sclerosis (ms) characterized by the presence of brain lesions that may be solitary or multiple with a diameter greater than or equal to 2 cm (1-5) these lesions are observed with a pseudotumoral appearance (6), larger than the typical ms plaques mimicking an intracranial neoplasm, infection or a non-demyelinating brain pathology (7). tms accounts for approximately 2.87% of all ms cases (1,7). magnetic resonance imaging (mri) shows ring enhancement (4,5) and perifocal edema (2,3,5), in addition, the presence of decreased cerebral blood volume (3), hypervascularity, increased vascular permeability and mass effect, make it difficult to make a differential diagnosis with abscesses and brain tumors (2, 8). the brain lesions present in this entity are known as "tumefactive demyelinating lesions (tdl) (9), which are best described in ms (10) and are mainly located in the cerebral white matter, specifically in the frontal and parietal lobe, but can appear in any part of the central nervous system (cns). rare tumefactive variants of ms are schilder's disease, acute marburg ms and concentric balo sclerosis (9). tdls in ms when presented as solitary lesions complicate the diagnosis due to their similarity to intracranial neoplasms, leading to misdiagnosis and therefore unnecessary intervention and treatments that put the patient's health at risk (5,10). to avoid misdiagnosis, better imaging techniques such as diffusion-weighted imaging (dwi), magnetic resonance spectroscopy (mrs), fluorodeoxyglucose positron emission tomography (fdgpet) (10), csf examination (8) and brain biopsy have been sought, the latter being the one that establishes definitive diagnosis (10). epidemiology the prevalence of tme is approximately 1 to 2 per 1000 cases diagnosed with ms (9-12) and a prevalence of tumor-type tdls of 3 cases per 1,000,000 inhabitants, with the female sex being the most affected. the presentation of ms at older ages is rare with approximately 0.6-0.75 of cases diagnosed after the sixth decade of life, increasing the difficulty in distinguishing tdls from brain tumors (11). tdls occur more frequently in asian countries with an incidence between 6.3-11.76%, probably due to ethnic differences with heterogeneous immunological backgrounds (10). kuan et al. in 2013 conducted a study in taiwan with 190 patients with ms diagnoses between the years 1985 and 2010, of which 12 were confirmed with tms, representing approximately 6.3% of ms patients, but this percentage does not represent the prevalence of the country because only patients who from a single medical center in tapei city were included (13). aetiology the causes that generate the appearance of tdl are not yet elucidated. however, a relationship has been found between the immature isoform of myelin basic protein (mbp) and the occurrence of extensive atypical demyelinating lesions in acute marburg ms and probably the role of this protein in the development of tdl. several isoforms may be involved in normal functioning and exposed to the process of protein degradation, leading to an increased likelihood of recurrence of tdls (10). localization tdls occur most frequently in the cerebral hemispheres (especially in the frontal and parietal lobe) (5), but can be observed in different components of the cns, such as segments of the cervical spine and the cervical spine (3). kuan et al. reported that 80% of the lesions were found at the supratentorial level, mainly in the periventricular and juxtacortical area and 40% in the spinal cord (13,14). clinical manifestations the clinical presentation of patients with tme can be polysymptomatic when the lesions are large and multiple (9). the symptoms originated by tdl can have an acute or subacute presentation (3) which depends on the location, size of the lesion and its mass effect (6,9). the clinical manifestations of tms include headache, cognitive abnormalities, mental confusion, seizures, apraxia, aphasia (1,3,4), increased intracranial pressure, vomiting, behavioral disturbances, visual disturbances, optic neuritis and hemiparesis (3,15,16). tdl often causes memory dysfunction, gerstmann's syndrome and in some patients, encephalopathies are observed (9). visual and somatosensory potentials with abnormalities can be observed in 33-60% of cases diagnosed with tms (1). generally, the signs and symptoms are not 540 michael gregorio ortega-sierra, raul david delgado-marrugo, cristian camilo campo-bedoya et al. associated with ms, which means that this entity is not considered in the differential diagnoses and a neoplasm or infection is suspected. however, even if there is a pre-existing diagnosis of ms, the probability of presenting a neoplasm or nonmyelinating pathology is not ruled out, which leads to suggest a biopsy to diagnose the pathology (11,17,18). diagnosis histologically, tdls show similarity to neoplasms by hypercellularity, gliosis, atypical reactive astrocytes, mitosis, permeabilized lymphocytes (6,11) necrosis, cystic changes (11) and creutzfeldt cells (9). in addition, abundant foamy macrophages containing myelin debris and relative axonal preservation are observed (11,18,19). although the biopsy allows a definitive diagnosis to be made, it has been reported that the trauma produced by the intervention for taking the sample generates neurological deficit and even death (11). however, in patients with uncertain diagnosis and who present a complex clinical picture, a biopsy is justified in order to generate a definitive diagnosis. misdiagnosis of tdl is estimated to be approximately 31% (9), leading to unnecessary interventions and treatment. it is important to distinguish ldt from a neoplasm in order not to expose the brain to inadvertent irradiation that aggravates tms (11). hamed, in the published case report of a patient with tms made the diagnosis based on: acute onset of the condition, cognitive impairment, multiple bilateral lesions on imaging studies, absence of cortical involvement, absence of mass effect, gadolinium enhancement, regression with corticosteroid, and lack of mri evidence of new lesions on follow-up (1,18,19). differential diagnosis the diagnosis of tdl in ms is a challenge due to its similarity with neoplasms, abscesses, acquired demyelinating disorders and vascular lesions (3). in order to achieve an adequate differentiation, imaging techniques have been used to avoid unnecessary biopsies that affect the patient's condition. mrs is a non-invasive imaging method that is useful for understanding biochemical alterations in various intracranial pathologies and according to studies is an important tool for the differential diagnosis of tms with brain tumors. mrs focuses on the metabolites n-acetyl aspartate (naa), choline, creatine, lp and lac; finding that when there is neuronal and axonal loss and impaired mitochondrial function, naa levels are low. the detection of elevated levels of choline, lp and lac are related to myelin degradation or cell renewal processes. kobayashi et al. found that in 2 of the 3 cases diagnosed with tms, decreased naa was observed and all 3 cases had in common that choline/creatine ratios were elevated in the peripheral areas associated with myelin degradation (2). it is important to take into account that gliomas can develop in patients with ms, which makes it impossible to determine that the lesions that appear in this pathology are ldt without performing studies that support the diagnosis, because tms can coexist with gliomas, which generates difficulties in making a differential diagnosis (9). butteriss et al. in a study diagnosed tms patients by using preoperative mri, who after surgery were found to be oligodendroglioma (8). a positive response to steroids (6) and the reduction of the size of the lesions in serial neuroimaging allows distinguishing the demyelinating nature of a tumefactive lesion from an abscess or neoplasm (3). however, challenges have been reported in diagnosing tms by mrs and pet, without biopsy and careful follow-up by serial mri with or without steroid treatment is usually sufficient to establish a diagnosis (8,20,21). on the other hand, although csf analysis has not shown statistical significance as a support for the diagnosis of tms, it has been observed that the presence of oligoclonal bands and elevated immunoglobulin g has allowed determining demyelinating processes (9,20,21). tumefactive variants of multiple sclerosis among the rare tumefactive variants of ms we find: acute marburg ms, schilder's disease and concentric balloon sclerosis. acute marburg multiple sclerosis was described in 1906 by otto marburg as an idiopathic inflammatory demyelinating disease of the cns characterized by large lesions of the cns. histologically, macrophage infiltration, generalized demyelination, axonal loss and areas of necrosis are observed. mutations have been observed in mbp leading to structural instability of myelin (9). it is a pathology caused by severe axonal loss that leads to 541 tumefactive multiple sclerosis rapid disability and can lead to death of the patient (1). myelinoclastic sclerosis, also called schilder's disease, was introduced in 1912 as a demyelinating disease with large lesions. however, this entity has not yet been fully elucidated and in some cases the term is used to refer to x-linked adrenoleukodystrophy. finally, concentric baló disease is an entity characterized by a pattern of concentric layers formed by damaged myelin tissue (1) and is known as an entity that presents rings of demyelination corresponding to areas of t2 hyperintensity on mri alternating with rings of normal myelination or partial remyelination corresponding to areas of t2 isointensity. these lesions can be located in the basal ganglia, cerebellum and in some cases spinal cord and optic nerve (9). imaging among the imaging techniques proposed for the diagnosis of tme are: mrs, dwi, perfusion-weighted imaging (pwi), apparent diffusion coefficient (adc) (6). tms poses multiple challenges in imaging studies, since the mass effect and perilesional edema do not allow differentiation from a brain tumor or infection, but observing a ring enhancement after gadolinium administration suggests an tdl (7). furthermore, it has been shown that when comparing mri enhancement regions with the respective areas on ct, hypoattenuation was specific to make an adequate distinction of tdl from glioma or lymphoma, but this differentiation was only applicable for these two tumor subtypes. in relation to brain abscesses, lesions in tms are centrally homogeneous on t2-w (6). furthermore, relative to brain abscesses and tumors the mass effect along with edema in tms are proportionally smaller relative to plaque size. it has been suggested that the lack of mass effect differentiates ms plaques from other space-occupying lesions (11,22,23). although there are no pathognomonic features for the diagnosis of ldt by imaging studies, features such as the presence of a hypointense ring in t2 around the lesion and the presence of white matter lesions typical of ms allow the diagnosis to be adequately directed (9). some of the lesions on tms are frequently enhanced on mri, but cases have been found where this pattern is not observed, suggesting that a lack of enhancement does not rule out tdl (12). in addition, within the characteristics of the lesions on mri are vascular structures crossing the center of the lesions in t2-w and marked reduction in blood flow perfusion compared to normal white matter (6,24,25). dwi is an imaging method for the measurement of water molecules. most lesions show variable adc values on dwi as a result of the pathological heterogeneity of ms lesions (2). most tdl demonstrate increased dwi and adc signals on mri, allowing differentiation of lymphomas with a water diffusivity restriction that makes them hyperintense on dwi and hypointense on adc maps. occasionally, acute demyelinating lesions may have areas of diffusion restriction with reduced adc values at the periphery of the lesion (6,23,25). mrs is an imaging method for the detection of biochemical alterations at the brain level, thus allowing improvements in the specificity of pathologies. when an increase in choline is observed due to elevated cell membrane turnover in ms during demyelination and inflammation processes, mrs is a method for the detection of biochemical alterations at the brain level, allowing for improved pathology specificity. naa is an important brain marker because it is found only in neurons (4). a relationship of tdls in ms and abnormal levels of choline, glutamate-glutamine and lactate has been found. in addition, an elevated choline/creatine ratio, increased lactate and an abnormal naa/creatine ratio allow suspicion of inflammatory processes or demyelination (5,7). however, mrs is of limited utility, because tdls present a similar pattern of increased choline/creatine and reduced naa/creatine as in brain tumors. on the other hand, fluorodeoxyglucose positron emission tomography may provide diagnostic clues (9). treatment there is still no standardized immunomodulatory treatment for tms. although within the pharmacological treatments we find methylprednisolone, beta interferons, plasma exchange, rituximab and natalizumab (1,9); the literature reports as first line treatment the use of high doses of steroids (9), due to the fact that in the majority of cases a positive response is obtained (6) and in some cases they are accompanied by surgical intervention (14). when patients do not respond to this, plasma exchange therapy is used. in cases 542 michael gregorio ortega-sierra, raul david delgado-marrugo, cristian camilo campo-bedoya et al. where an adequate response is not obtained, the use of rituximab or cyclosfamide is suggested (9). on the other hand, some studies have recommended avoiding the use of fingolimod because of reports of cases of tdl occurring with the use of this drug (9). prognosis and neurosurgical education the long-term prognosis depends largely on whether the patient has recurrent neurological disease. most patients who relapse will have lesions typical of ms, with a minority recurring in a tumefactive form. patients who develop ms after ldts have similar long-term disability as those with prototypical ms (9). in lowand middle-income countries, where there are limitations with respect to the availability of high-cost technology and access to specialized health services, it is necessary to design strategies to facilitate the early diagnosis and management of these patients (26-28). the theoretical training of primary care physicians and medical students is a low-cost strategy that allows those who, due to policies and agreements, must go to provide health care in marginalized areas, to suspect this condition and refer the patient to high complexity hospitals (29,30). the implementation of robotic neurosurgery and translational research are other aspects that would improve patient prognosis (31). neurosurgical education should be mainly focused on the physician, who is the one who should make the differential diagnosis. conclusions tumefactive multiple sclerosis is an infrequent disease, but it has a substantial negative impact on the functional capacity and quality of life of the affected person. it is necessary to have high quality imaging tools and suspicious clinical criteria to be able to suspect and differentiate this condition from other differential diagnoses, such as neoplasms of the central nervous system. more prospective multicenter studies are needed to more accurately characterize this condition. references 1. hamed sa. variant of multiple sclerosis with dementia and tumefactive demyelinating brain lesions. world j clin cases. 2015; 3(6):525-32. 2. kobayashi m, ono y, shibata n, kobayashi m, shimizu y, ohta k, et al. correlation between magnetic resonance imaging findings and pathological observations in tumefactive multiple sclerosis. the neuroradiology journal. 2009; 22:155-63. 3. ashrafi mr, tavasoli ar, alizadeh h, zare noghabi j, parvaneh n. tumefactive multiple sclerosis variants report of two cases of schilder and balo diseases. iran j child neurol. 2017; 11(2):69-77. 4. kaeser ma, scali f, lanzisera fp, bub ga, kettner nw. tumefactive multiple sclerosis: an uncommon diagnostic challenge. j chiropr med. 2011; 10(1):29-35. 5. kilic ak, kurne at, oguz kk, soylemezoglu f, karabudak r. mass lesions in the brain: tumor or multiple sclerosis? clinical and imaging characteristics and course from a single reference center. turk neurosurg. 2013; 23(6):72835. 6. conforti r, capasso r, galasso r, cirillo m, taglialatela g, galasso l. a challenging diagnosis of late-onset tumefactive multiple sclerosis associated to cervicodorsal syringomyelia: doubtful ct, mri, and bioptic findings: case report and literature review. medicine (baltimore). 2016; 95(36):e4585. 7. koppula r, degnan aj, ghassibi m, duggan p, jones r, levy lm. neuroimaging of tumefactive multiple sclerosis with atypical features. radiol case rep. 2012; 7(4):752. 8. yamada s, yamada sm, nakaguchi h, murakami m, hoya k, matsuno a, et al. tumefactive multiple sclerosis requiring emergent biopsy and histological investigation to confirm the diagnosis: a case report. j med case rep. 2012; 6:104. 9. frederick mc, cameron mh. tumefactive demyelinating lesions in multiple sclerosis and associated disorders. curr neurol neurosci rep. 2016; 16(3):26. 10. totaro r, di carmine c, splendiani a, torlone s, patriarca l, carrocci c, et al. occurrence and long-term outcome of tumefactive demyelinating lesions in multiple sclerosis. neurol sci. 2016; 37(7):1113-7. 11. lucchinetti cf, gavrilova rh, metz i, parisi je, scheithauer bw, weigand s, et al. clinical and radiographic spectrum of pathologically confirmed tumefactive multiple sclerosis. brain. 2008; 131(pt 7):1759-75. 12. yacoub h, al-qudahl z, lee h-j, baisre a, souayah n. tumefactive multiple sclerosis presenting as acute ischemic stroke. journal of vascular and interventional neurology. 2011; 4(2):21-3. 13. kuan yc, wang kc, yuan wh, tsai cp. tumefactive multiple sclerosis in taiwan. plos one. 2013; 8(7):e69919. 14. munarriz pm, castano-leon am, martinez-perez r, hernandez-lain a, ramos a, lagares a. tumefactive multiple sclerosis requiring emergency craniotomy: case report and literature review. neurocirugia (astur). 2013; 24(5):220-4. 15. french hd. tumefactive multiple sclerosis versus highgrade glioma: a diagnostic dilemma. surg neurol int. 2021; 12:199. 543 tumefactive multiple sclerosis 16. kumar s, datta ak, chakraborty u, pandit a, ray bk. tumefactive demyelination: a clinico-radiological dilemma. j r coll physicians edinb. 2021; 51(3):278-280. 17. sánchez p, chan f, hardy ta. tumefactive demyelination: updated perspectives on diagnosis and management. expert rev neurother. 2021; 21(9):1005-1017. 18. plowman rs, varma h. prognostic factors in tumefactive demyelinating lesions: a retrospective study. j neurol sci. 2021; 428:117591. 19. garcia jr, baquero m, bassa p, compte a, mourelo s, riera e. a false-positive case on brain 18f-choline pet/mr due to tumefactive multiple sclerosis. a case report. rev esp med nucl imagen mol (engl ed). 2021; s2253-654x(21)00055-x. 20. villarreal jv, abraham mj, acevedo jag, rai pk, thottempudi n, fang x, et al. tumefactive multiple sclerosis (tms): a case series of this challenging variant of ms. mult scler relat disord. 2021; 48:102699. 21. di gregorio m, torri clerici vla, fenu g, gaetani l, gallo a, cavalla p, et al. defining the course of tumefactive multiple sclerosis: a large retrospective multicentre study. eur j neurol. 2021; 28(4):1299-1307. 22. fereidan-esfahani m, tobin wo. cyclophosphamide in treatment of tumefactive multiple sclerosis. mult scler relat disord. 2021; 47:102627. 23. mamilly a, aslan a, adeeb n, al asfari a, cuellar h. tumefactive multiple sclerosis of the cervical spinal cord: a rare case report. cureus. 2020; 12(1):e6754. 24. mitsutake a, sato t, katsumata j, nakamoto fk, seki t, maekawa r, et al. tumefactive multiple sclerosis which initially presented with brainstem encephalitis with a long-term follow-up. mult scler relat disord. 2019; 32:2326. 25. zaheer k, ajmeri an, singh m, suliman ms, teka s. tumefactive multiple sclerosis, a rare variant presenting as multiple ring-enhancing lesions in an immunocompetent patient: a case report. cureus. 2018; 10(12):e3738. 26. ortega-sierra mg, prado-grajales v, martinez-imbett r, unás-perea k, lozada martinez id. research career in neurosurgery: a challenge for future neurosurgeons. j neurosurg sci. 2021 aug 3. 27. blanco-teherán c, quintana-pájaro l, narvaez-rojas a, martínez-pérez r, garcía-ballestas e, moscote salazar l, et al. evidence-based medicine in neurosurgery: why and how? j neurosurg sci. 2021 aug 3. 28. ortega-sierra mg, durán-daza rm, carrera-patiño sa, rojas-nuñez ax, charry-caicedo ji, lozada-martínez id. neuroeducation and neurorehabilitation in the neurosurgical patient: programs to be developed in latin america and the caribbean. j neurosurg sci. 2021 jun 10. 29. gaitan-herrera g, lozada-martínez i, acevedo-aguilar l, bohorquez-caballero a, moscote-salazar l. simulation as a tool to educate the patient about neurosurgical pathology. j neurosurg sci. 2021 jan 22 30. herrera-martinez mp, garcía-ballestas e, lozadamartinez i, torres-llinás d, moscote-salazar l. letter to the editor. creating the conditions for gender equality to end sexual harassment in neurosurgery. j neurosurg. 2021 feb 5:1-2. 31. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. microsoft word 8chiriaca_traumatic 282 chiriac et al traumatic intracranial aneurysms traumatic intracranial aneurysms a. chiriac, b. iliescu1, z. faiyad1, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract traumatic intracranial aneurysms are rare conditions that can be a result of vast head trauma. different aspects as history, etiology, histopathology, clinical manifestations, diagnosis and treatment options are discussed regarding the literature. a particular case of a pericalosal aneurysm is presented to highlight the importance of keeping in mind that this location can be a site of such aneurysms. introduction traumatic intracranial aneurysms are rare conditions and represents less than 1% of all intracranial aneurysms. (1) they can be a result of a penetrating or nonpenetrating head trauma and are most frequently located in the peripheral cerebral vasculature or close to the skull base. because traumatic aneurysms are fragile vascular lesions with high risks of rupture, early diagnosis and prompt treatment are essential. historical notes (2) in 1829, smith reported for the first time an autopsy-proven case of a middle meningeal artery aneurysm after head injury. later, in 1891, bollinger postulated that some instances of "delayed apoplexy" after head injury were due to the rupture of a traumatic aneurysm. although guibert in 1985 reported a case involving the infraclinoid internal carotid artery, birley and trotter in 1928 were the first who describe a case of an intracranial aneurysm after severe head injury. they were followed by tonnis and cairns in 1934 and 1942 who demonstrated the first case proven by angiography and provided a comprehensive description of these aneurysms. in 1949 krauland described an aneurysm formation after a depressed skull fracture and angiographically evidence of these lesions after a closed head injury were demonstrated in 1962 (hirsch et al 1962; burton et al 1968). beginning with 1970s the frequency of their diagnosis has decreased due to the application of computerized tomography (rather than traditional angiography) as the modality of imagistic evaluation of headinjured patients. conventional cerebral angiography remains the reference standard for the diagnostic work-up of intracranial aneurysms (dubey et al 2008). etiology traumatic intracranial aneurysms may result from vast but commonly causes as sports accidents, assault or traffic accidents (pedestrians or in vehicle passengers. they have been described in association with both blunt and penetrating trauma, with the former being more commonly reported. (5) several mechanisms have been found responsible for traumatic aneurysms formation. all involve either direct injury to the vessel or stretching of the vessel by adjacent forces. the mechanism of injury is closely related to the anatomical location of the involved artery. infraclinoid carotid and romanian neurosurgery (2013) xx 3: 282 – 288 283 basilar artery aneurysms are commonly associated with basilar skull fractures, which are explained by the close relation of these vessels with the skull base. in the supraclinoid segment the carotid artery is characterized by a transitions zone, from a relatively fixed structure in the skull base and cavernous sinus to a relatively mobile structure as it ascends in the cisternal spaces. there are hypothesis that, either movement of the supraclinoid segment against the anterior clinoid process or stretching of the carotid artery at this transition zone may leads to an aneurysm formation. (5) concerning the distal subcortical aneurysms occurrences there are predominantly along the anterior cerebral artery and its branches. the close relation of these vessels along much of their length to the falx cerebri has led some authors to the hypothesis that traumatic movement of the brain and vessels against the relatively fixed falx cerebri can lead to aneurysm formation. (5) in the same siuation, posterior cerebral artery aneurysms are thought to be the result of trauma of the vessel against the tentorium. (5) also, the distal cortical aneurysms may occur in association with linear or depressed skull fractures and dural lacerations, commonly involving the middle cerebral artery or aca. (5) it is believed that temporary or prolonged herniation of the cortical vessel up into the fracture defect leads to direct injury to the vessel wall. (5) ventureyra and higgins proposed 4 categories of the mechanism of causation of traumatic intracranial aneurysms, as closed head injuries, missile injuries, penetrating head injuries, and iatrogenic injury. in their review of 130 traumatic intracranial aneurysms in children, closed head injuries was found to constitute 72% of cases, missile injuries 16%, iatrogenic injury 8%, and penetrating head injury 4% of cases. minor closed head injuries without fracture or significant initial impairment of consciousness can also produce traumatic intracranial aneurysms. traumatic intracranial aneurysms due to closed head injuries can result from rapid deceleration causing sudden brain and artery movement producing vessel wall injury against stationary structures. (4) developments of iatrogenic traumatic aneurysms have been described by some authors after a variety of procedures, including endoscopic ventriculostomy, intranasal procedures, intracranial surgery, and repeated subdural taps. histopathology from histological point of view, traumatic aneurysms can be classified as true, false or mixed aneurysms. the classification is based on both the anatomy and mechanism of traumatic aneurysm formation. true aneurysms are characterized by incomplete mural injury of the intima and variable involvement of the internal elastic layer and media that produces a localized weakening of the vessel wall and aneurysm formation. false aneurysms are considered to be the most common histological type that results from disruption of all three layers of the vessel wall with formation of a contained hematoma outside the vessel. a false lumen formation then develops, creating an aneurysmal dilation. because the adventitia of the native vessel usually is intact, the phenomenon is being presumably secondary to flow dynamics against the weakened vessel wall. these are presumably the histological type associated with penetrating injuries. the third histological types, the mixed aneurysms, are initially true aneurysms that subsequently undergo a contained rupture forming hematoma and false lumen. the term of 284 chiriac et al traumatic intracranial aneurysms "mixed aneurysm" is used by some authors to describe saccular aneurysms that occur in association with dissection of the parent. (4, 5) however, because the most case reports contain little or no histological data, the relative incidence of these histological types is not well known. the histological classification is of little benefit in terms of clinical management because intervention is required regardless of the type or mechanism. ventureyra and higgins proposed a classification of paediatric traumatic intracranial aneurysms, into early onset (occurring within 4 weeks after injury) or late onset (occurring beyond 4 weeks). most reported cases of traumatic intracranial aneurysms presented with early onset. late onset manifestation in paediatric traumatic intracranial aneurysms, as in the present case is rare with only about 10 reported cases in literature till date. they often result from chi and manifest clinically as aneurysmal masses. (5) location the location of traumatic intracranial aneurysms varies, but these are commonly found in the anterior circulation. the majority of traumatic intracranial aneurysms occur in the supraclinoid segment of the carotid artery and along the anterior cerebral artery and its branches, particularly the pericallosal and callosomarginal arteries. however, reported locations are the vertebral artery, internal carotid artery, anterior cerebral artery, middle cerebral artery and middle meningeal artery. asari at al observed that the most common location for traumatic aneurysms was the middle cerebral artery, followed by the distal anterior cerebral artery. traumatic aneurysms of the skull base usually involve the petrous, cavernous and supraclinoid ica. petrous and cavernous ica traumatic aneurysms are usually associated with basilar skull fractures. supraclinoid ica aneurysm may form as a result of blunt arterial contusion by the anterior clinoid process or sudden stretching of the artery during impact and/or they may be associated with orbital roof or anterior clinoid process fractures. (3) clinical manifestations the clinical manifestations of traumatic intracranial aneurysms are usually similar with that of normal aneurysms. however, direct neural injuries and associated impairment of consciousness produced by head injury often mask the early symptoms due to traumatic intracranial aneurysms, leading to delayed diagnosis. typically, traumatic intracranial aneurysms range in size from 2 to 15 mm (salar et al 1978; achram et al 1980; (haddad et al 1991). most present 2 to 8 weeks after injury, but some present earlier and others are delayed by months or years (fleischer et al 1975; aarabi 1988; haddad et al 1991; ventureyra and higgins 1994). (3, 5) the most common symptoms include an acutely decreased level of consciousness, seizure, or focal neurological deficit. in a typical patient, the level of consciousness is initially depressed due to the trauma itself followed by a lucent period after which secondary deterioration occurs because of intracranial hemorrhage (sasaoka et al 1997) (2). imaging scanning usually demonstrates acute intracranial hemorrhage, which may be subarachnoid, intraparenchymal, intraventricular, or subdural depending on aneurysm location. (5) the average time from initial trauma to traumatic aneurysmal hemorrhage is approximately 21 days and is associated with a mortality rate as high as romanian neurosurgery (2013) xx 3: 282 – 288 285 50%. (5) patients with infraclinoid carotid artery aneurysms can present with cranial nerve deficits, diabetes insipidus, recurrent or massive epistaxis, unilateral blindness, or symptoms of a cavernous-carotid fistula. (5) a later compressive cranial nerve palsies may occur due to enlarging aneurysm, but an abducens palsy can be present within the first few days because of raised intracranial pressure (2). the epistaxis appears when a petrous or intracavernous internal carotid artery aneurysm is associated with a basal skull fracture ruptures. patients with supraclinoid carotid artery lesions can present with headache, memory disturbance, and progressive visual loss prior to rupture; such symptoms have been reported to occur for as long as 7 years prior to diagnosis. (5) some cases have presented with hydrocephalus, involving pericallosal aneurysms and with a distal cortical lesion. distal cortical aneurysms have unique characteristics that may make them more likely to be diagnosed prior to the occurence of hemorrhage. these aneurysms can lead to the development of a growing skull fracture that becomes physically palpable months to years after the injury. (5) buckingham and colleagues found 11 reported cases of distal cortical aneurysms associated with blunt trauma; seven of these patients (63. 6%) presented without hemorrhage and were diagnosed primarily with either on routine radiographic follow up or by evaluation of growing skull fractures. however, only 20. 5% (of 44) of blunt traumatic aneurysms were diagnosed prior to hemorrhage in more proximal locations. (2, 5) the otic hemorrhage is rare condition. in infants, a skull fracture may "grow" concomitant with the enlargement of an aneurysm because the skull sutures are not fused (endo et al 1980). the aneurysm may be asymptomatic and discovered incidentally in 10% to 20% of cases during neuroimaging. a recent case repot discloses acute sanguinous ventriculostomy output, suggesting underlying aneurysm rupture (dubey et al 2008). (2) diagnosis in the early part of the century, clinicians did not have access to the neuroimaging modalities such as ct and mr imaging. the direct diagnosis of a traumatic aneurysm could only be made on the angiography, in the operating room, or at autopsy (5). the diagnosis of traumatic intracranial aneurysms requires a high index of suspicion (3). suspicion should be made in all head injured or post-operative patients with delayed neurological deterioration, delayed haemorrhage, unexplained major arterial bleeding during evacuation of the haematoma, new or unexplained intracranial bleed, discrepancy between the amount of subarachnoid haemorrhage, intraventricular haemorrhage, facio-orbito-pterional injuries, penetrating fragments, especially if they cross the midline or traverse into another dural compartment. (5) possibility of emergency ct scanning has allowed clinicians to diagnose delayed intracranial hemorrhage due to traumatic aneurysmal rupture more rapidly and more frequently than previously possible. for patients suffering closed head injury immediate ct scanning should be undertaken as soon as possible. thus, cerebral angiography should be considered in patients with delayed neurological deterioration or with ct scan evidence of vascular injury. cerebral angiography is instrumental in the diagnosis of traumatic aneurysms and also helpful in differentiating them from congenital aneurysm. imagistic features on angiography such as absence or poorly defined neck, unusual sites (peripheral 286 chiriac et al traumatic intracranial aneurysms location other than at a branching point) or projections of the aneurysm, irregularly contoured aneurysmal sac, and delayed filling and emptying of the aneurysm could suggest a traumatic etiology. (4, 5) magnetic resonance angiography (mra) with time of flight (tof) mra alone or combined with standard spin-echo imaging should be considered in the diagnosis of spontaneous intracranial aneurysms especially in patients with history of trauma and recurrent epistaxis, visual loss, progressive cranial nerve palsy or an enlarging skull fracture. recently, ida et al (18) reported a 90% true-positive diagnostic rate in detection of traumatic intracranial aneurysm. however, so far no studies on efficacy of mri/mra in diagnosis of have been reported. (3, 4) more recent literature describe several cases in which patients with normal angiography subsequently present with delayed hemorrhage and have aneurysms that are then revealed on repeated studies. also, some authors of several large series recommend routine angiography 2 weeks after the injury to rule out the delayed aneurysm formation especially for penetrating injuries and particularly stab wounds. today, an earlier definitive diagnosis of traumatic intracranial aneurysm seems to be associated with a trend toward more aggressive surgical treatment, and better outcomes than in earlier cases. treatment options once diagnosed, traumatic intracranial aneurysms required an emergency management because they rarely regress and have a high incidence of rupture (as high as 67% in some studies). (3) the management is mainly directed to prevent recurrent hemorrhage and surgical repair and endovascular interventions. usually, the treatment approach is carried out on a case to case basis since atypical locations and variable anatomical features are often encountered. surgical techniques option includes aneurysmal clipping, aneurysm resection with or without arterial bypass, or trapping of the aneurysm. such treatment requires careful planning and evaluation such as preoperative test occlusion of the vessel in preparation for a trapping procedure. in case of impossibility clip obliteration of the aneurysm it may need to be trapped with an accompanying vascular bypass. thus, the surgical approach should allow easy acces to the superficial temporal artery or the saphenous vein for bypass grafting and also, a proximal and distal control. when aneurysm trapping or clipping is not possible wrapping with piece of muscle secured with clips may be employed. (3) the endovascular option should be considered in the difficult aneurysms. endovascular interventions may include embolization with liquid agents, detachable balloons, or coils which may require assistance with balloon or a stent placement. there are also situations when patient’s clinical condition may also limit treatment options. unstable patients that not be suitable to undergo general anesthesia, patients with active bleeding that cannot be treated by dual antiplatelet therapy for stent assisted aneurysm coil embolization are special cases that need combined treatment. fleischer and coworkers reported in 1975 a 41% mortality rate for patients with conservative treatment and a 18% mortality rate in surgically treated patients. if the surgical clipping has the advantages of definitive aneurysm occlusion, vascular reconstruction with parent artery preservation or mass effect removable, the endovascular techniques avoids prolonged anesthesia, minimizes manipulation of romanian neurosurgery (2013) xx 3: 282 – 288 287 adjacent vessels and structures, and allows immediate angiography control. (5) case presentation a 72-year-old woman slipped on ice and fell down from a steers one month prior to admission in this hospital. he was asymptomatic, except for headache and dizziness for 2 days. he was treated by a neurologist in a local hospital and was investigated by cranio-cerebral computed tomography with enhancement. imaging ct demonstrates no brain hemorrhage or vascular lesion (figure 1). after 1 month, she developed sudden onset of headache and vomiting in time of slipping followed by confusion syndrome. she was readmitted for the same and later referred to this hospital for further treatment. mri of brain (figure 2) revealed well defined lobulated hypo-intense lesion on t2-trim-dark-fluid and t2-tse sequences in the region of distal anterior cerebral artery. she improved gradually over next 7 days and was sent to our hospital for further treatment. at admission, she was conscious with a gcs of 14. a cerebral ct-angiography (figure 3) was performed and revealed a left sided anterior cerebral artery aneurysm just proximal to its bifurcation into callosomarginal and pericallosal arteries. a repeat native ct scan of brain revealed no hemorrhage or hydrocephalus. on the same day day, left frontal craniotomy and clipping of the aneurysm by inter-hemispheric approach was performed. by microdissection and concomitant retraction of the medial surface of the left frontal lobe, the pericallosal arteries were identified distally. they were followed towards to suspected site of aneurysm and proximal portion of the right pericallosal artery was identified. figure 1 initial ct scan (after head trauma) a b figure 2a, b t2-trim-dark-fluid and t2-tse sequences showing a vascular lesion in the region of distal anterior cerebral artery 288 chiriac et al traumatic intracranial aneurysms figure 3 3d ct angio reconstruction showing a a left sided anterior cerebral artery aneurysm figure 4 postoperative ct scan after having achieved proximal control, the aneurysm was dissected and the neck reconstructed with three yasargil clips for aneurysm complete occlusion. post operative period was uneventful and a ct scan was performed before discharge 7 days later (figure 3). conclusions traumatic intracranial aneurysms are rare, but must be considered in patients with acute neurological deterioration after closed head injury. usually they occur more commonly in children than adults. the appropriate management of these lesions may include surgical clipping, excision or trapping procedure and/or endovascular occlusion. references 1. jefferson t miley, gustavo j rodriguez, adnan i qureshi: traumatic intracranial aneurysm formation following closed head injury, journal of vascular and interventional neurology 2008; 1(3):79-82; 2. zachary h dodd, mitesh v shah, steven r levine: traumatic intracranial aneurysms, medlink neurology 2013; 3. deepak awasthi, greg dowd: lessons learned from a case of a traumatic intracranial aneurysm, http://www.medschool.lsuhsc.edu/neurosurgery/nervec enter/ traumatican.html. 4. raju b s, purohit a k, murthy s r, sundaram c, sanjay t: traumatic distal anterior cerebral artery aneurysm in a child: a case report. neurol india 2001;49:295; 5. paul s. larson, andrew reisner, dante j. morassutti, bassam abdulhadi, john e. harpring: traumatic intracranial aneurysms, neurosurg focus. 2000;8(1). alfotihgobran_embolization romanian neurosurgery (2014) xxi 3: 251 – 258 251 embolization of the middle meningeal artery effectively treats refractory chronic subdural hematoma: a systematic review alfotih gobran*, fang-cheng li, xin-ke xu, shang-yi zhang sun yat sen memorial hospital, neurosurgery department, sun yat sen medical university, p.o. box 510120, guangzhou, guangdong province, people’s republic of china abstract chronic subdural hematoma (csdh) formation mechanism is very complex, and has not entirely understood. it represents a frequent type of intracranial hemorrhage, and is very common disease in neurosurgery practice, especially in older patients. various surgical treatments have been proposed for the treatment of csdh. the rate of recurrence in csdh after surgery ranges from 5% to 30%, repeated surgery must be considered. but in some cases subdural collections are still persistent. endovascular embolization of the middle meningeal artery (mma) is an option for treatment of refractory csdh. we review all cases that were treated with embolization to assess the effect of this intervention. our review revealed 6 papers with a total enrollment of 14 patients were treated with mma embolization for refractory chronic subdural hematoma without any postoperative complication or recurrence. in this study we suggest mma embolization as an alternative for treatment of non-curable csdh, especially for old people with systematic diseases, who cannot tolerate repeat surgery. introduction chronic subdural hematoma (csdh) is a common neurological condition, particularly for older patients (1, 2), with an estimated incidence of 7.32 per 100,000 people per year for individuals above 70 years old (3). levels of mortality associated with csdh range from 1.5% to 8% (4). the pathogenesis of csdh formation remains unclear, although new imaging and molecular biology techniques have improved our understanding of these processes (5, 6). the rate of recurrence in csdh after surgery with any of actual techniques (burr-hole surgery with irrigation and drainage, twist drill, craniotomy) ranges from 5% to 30% (7, 8, 9). patients who have high risk factors for recurrence, especially with coagulopathy10 or under anticoagulant therapy (11), hematoma may be recur after the first intervention, and repeated surgery must be considered. the treatment options remains controversial. a number of techniques are used to manage recurring csdh, including burr hole plus drainage, repeated irrigation, the installation of reservoirs and aspiration 252 alfotih gobran et al arterial embolization to treat subdural hematoma (12), subdural peritoneal shunts (13), capsule removal with large craniotomy, and the endoscopic perforation of the septum (14). for elderly patients, however, efforts should be made to avoid the repeated application of invasive procedures. embolization of the middle meningeal artery (mma) is another treatment option for frequently recurring csdh. this procedure is often used to treat dural arteriovenous shunts or as a preoperative treatment for meningioma tumors. mma embolization was first used to treat csdh in 2000, preventing csdh recurrence in a patient with cirrhosis of the liver (15). here we have evaluated whether mma embolization effectively prevents the recurrence of hematoma in patients with csdh. a search of the literature revealed six reports concerning 14 patients. these patients were 55–87 years old and had follow-up periods of 3–18 months. none of the patients treated with mma embolization for refractory csdh experienced any postoperative complications or hematoma recurrence. this analysis suggests that mma embolization is an effective, alternative treatment for noncurable csdh, especially for older patients with systematic diseases who cannot tolerate multiple surgeries. methods to identify relevant case reports in the scientific literature, the medline, pubmed, embase, and isi web of science databases were searched using the key words “chronic subdural hematoma" combined with "recurrence" and "embolization" or "middle meningeal artery". only patients who received mma embolization for the treatment of recurrent csdh were included in the analysis. articles not available in english were excluded. after identifying relevant articles, all studies referenced by these manuscripts were also reviewed. our search identified six publications that describe outcomes for 14 patients treated with mma embolization. included studies were case series that presented class iii evidence. results among the 14 patients who met our inclusion criteria were 12 males and two females, with ages that ranged from 55 to 87 years (table 1). seven patients had suffered a previous head trauma; three patients had not experienced a trauma; trauma histories were not available for three patients; and for patient number 9 the history of head trauma was unclear. patients presented with symptoms that included abnormal behavior, disorientation, speech abnormalities, dementia, motor weakness, hemiparesis, gait disturbances, and loss of consciousness. three patients were taking the anticoagulant warfarin (coumadin), one patient had coagulopathy from cirrhosis of the liver, one patient was on hemodialysis because of chronic renal failure, one patient was receiving chemotherapy for peritoneal mesothelioma, one patient was receiving treatment for dentatorubral-pallidoluysian atrophy, one patient was suffering from alcoholism, and six patients had no previous medical histories. based on computed tomography scans, six patients had bilateral csdh, whereas eight patients had onesided csdh. romanian neurosurgery (2014) xxi 3: 251 – 258 253 table 1 patients’ characteristics author patient no. age sex head trauma? pre-treatment symptoms past medical history csdh on ct pre-embolization treatments embolization materials follow-up (months) major treatments other treatments mandai et al.15 1 59 m no loc, hemiparesis coagulopathy from cirrhosis of the liver 1) bilateral 2) mls burr hole, irrigation ommaya reservoir pva particles 7 hirai et al.27 2 81 m yes motor weakness, gait disturbance warfarin (aortic valve replacement) bilateral burr hole, irrigation irrigation pva particles, platinum coils 10 3 63 m yes abnormal behavior, disorientation warfarin (cardiomyopathy) right side burr hole, irrigation, drainage irrigation platinum coils unavailable ishihara et al.28 4 78 m yes unavailable hemodialysis (chronic renal failure) left side burr hole, drainage none 20% nbca 16 mino et al.29 5 73 m yes gait disturbance none bilateral burr hole, drainage irrigation gelatin sponge, gdc 6 6 79 m no speech disturbance, dementia none right side burr hole, drainage craniotomy gelatin sponge, gdc 6 7 65 m yes hemiparesis none left side burr hole, drainage none gelatin sponge, gdc 6 8 75 m yes gait disturbance none bilateral burr hole, drainage none gelatin sponge, gdc 6 tsukamoto et al.30 9 64 m unclear consciousness disturbance drpla bilateral burr hole, drainage steroids pva particles 18 hashimoto et al.31 10 79 m yes none peritoneal mesothelioma right side burr hole, irrigation none 16% nbca 3 11 55 m unavailable unavailable heavy drinker left side burr hole, irrigation none 20% nbca unavailable 254 alfotih gobran et al arterial embolization to treat subdural hematoma 12 87 m unavailable unavailable none left side burr hole, irrigation none 16% nbca unavailable 13 73 f unavailable unavailable none bilateral burr hole, irrigation none 18% nbca 200-μm pva particles unavailable 14 68 f no disorientation warfarin (cerebral infarction, pulmonary embolism) left side burr hole, irrigation none 20% nbca 4 csdh, chronic subdural hematoma; drpla, dentatorubral-pallidoluysian atrophy; gdc, guglielmi detachable coils; mls, midline shift; nbca, n-butyl 2-cyanoacrylate; loc, loss of consciousness; pva, polyvinyl alcohol table 2 factors associated with the recurrence of csdh* patient factors laboratory findings imaging findings surgical factors -age -sex -low gcs -low gos at discharge -hemodialysis -dementia -diabetes -epilepsy -aps or acs -chemotherapeutic agents -intracranial hypotension (csf shunt surgery) -hypertension -alcoholism -postoperative patient posture -liver dysfunction -renal failure -thrombocytepenia -coagulation-factor deficiency -brain atrophy -high and mixed-density csdh -bilateral csdh -midline shift more than 5 mm -width of the hematoma -cranial base hematoma -septum formation -duration of drainage -residual air after surgery *these factors are still controversial ac, anticoagulant; ap, antiplatelet; csf,crebrospinal fluid; gcs, glasgow coma scale, gos, glasgow outcome scale romanian neurosurgery (2014) xxi 3: 251 – 258 255 the first treatment that these patients received were: 1) burr hole plus drainage and irrigation, 2) burr hole plus drainage, or 3) burr hole plus irrigation. several techniques were also used to treat hematoma recurrence, namely an additional surgery, irrigation, an ommaya reservoir, and steroids. the materials used to embolize the mma were: polyvinyl alcohol particles, 16–20% n-butyl 2cyanoacrylate, gelatin sponges, and guglielmi detachable coils. no complications were reported after the mma embolization procedure. follow-up times ranged from 3 to 18 months, although follow-up times for patients 3, and 11–13 were not available. importantly, all 14 patients experienced no recurrences or enlargements of csdh following embolization of the mma. discussion csdh is one of the most common types of intracranial hemorrhage and it is associated with high levels of morbidity and mortality (1.5–8%) (4, 16, 17). patients with advanced age are more likely to have csdh because of atrophy of the brain parenchyma. this atrophy enlarges subarachnoid spaces, thereby stretching veins that bridge these spaces (18). stretched veins are more fragile and tend to rupture, releasing venous blood into the subdural space (19). men are twice as likely as women to have csdh because they experience more head injuries (20). single or double burr holes with closed drainage systems (with or without irrigation) are currently the treatments of choice for this condition, but many others techniques have been described (21). the recurrence of csdh following surgery is not uncommon, and can result from poor re-expansion of the brain, or inflammation and hemorrhage of the outer membrane (22). several factors are associated with csdh recurrence, including advanced age, a tendency to bleed, brain atrophy, alcohol abuse, kidney and liver diseases, diabetes, epilepsy, anticoagulants, chemotherapy agents, intracranial hypotension, hemodialysis, the density of the hematoma, the width of the hematoma, insufficient intraoperative drainage, postoperative accumulation of air in the subdural space, bilateral csdh, postoperative position, the glasgow coma scale, and the glasgow outcome scale (7, 11, 16, 17, 23–26) (table 2). analyses concerning these associations, however, have yielded inconsistent results. the treatment of recurrent csdh remains controversial and many techniques have been used to manage this condition, including burr holes plus drainage, repeated irrigations, the installation of reservoirs and aspiration (12), subdural peritoneal shunts (13), capsule removal with large craniotomy, endoscopic perforation of the septum (14), and mma embolization (15, 27–32). embolization of the mma to treat csdh was first reported by mandai et al. (15) for patients with coagulopathy (cirrhosis of the liver). application of this technique resulted in very positive patient outcomes. in one japanese article takahashi et al. (32) reported results concerning three patients with recurrent csdh that had been subjected to several unsuccessful drainage procedures. after mma embolization no hematoma 256 alfotih gobran et al arterial embolization to treat subdural hematoma enlargements were seen and all hematomas gradually and completely resolved (32). tanaka et al. (33) performed superselective angiography of the mma in a series of 35 patients. they found diffuse dilation of the mma and scattered networks of abnormal vasculature, which seemed to be macrocapillaries within the outer membrane (29, 33). to understand the relationship between the mma and the outer membrane in csdh, tanaka et al. (34) studied histological features of the outer membrane and observed many communicating arteries, i.e., arteries that originated from branches of the mma and then entered the outer membrane. they concluded that the mma provides nutrients to the abnormal membrane that surrounds the hematoma via these communicating arteries. as direct arterial pressure of the mma may rupture these communicating arteries, mma embolization may prevent or delay csdh recurrence. the most common materials used for the embolization procedure were: n-butyl 2cyanoacrylate, guglielmi detachable coils, polyvinyl alcohol particles, and gelatin sponges. using a low concentration of liquid n-butyl 2-cyanoacrylate increases the therapeutic effect by embolizing more peripheral vessels associated with the mma with a low risk of catheter adhesion (28, 31). to prevent the aberrant flow of blood into the ophthalmic artery, it is necessary to perform a pre-embolization study of the mma pathway and its anastomosis with the internal carotid artery through the inferolateral trunk, or the feeding vessel to the facial nerve. if there is anastomosis between the mma and the ophthalmic artery, embolization of the proximal mma using coils or gelatin sponges should be considered (31). here we have review 14 cases in which mma embolization was used to treat csdh. none of these patients had post-operative complications, csdh recurrence, or csdh enlargement. it should be acknowledged, however, that this review does not contain class i or class ii data, and that this analysis should be supplemented with more definitive data (e.g., randomized trials) when they become available. results to date indicate that embolization of the mma represents an effective option for treating recurrent csdh. it is is good option for patients who cannot tolerate invasive intervention such as repeated surgery (burr hole), capsule removal with large craniotomy or perforation of the septum with an endoscope. it can use as adjuvant therapy in treating recurrence of chronic subdural hematoma. acknowledgments: we thank dr. samir taha for his assistance throughout this study. correspondence gobran taha alfotih, md department of neurosurgery second affiliated hospital of sun yat-sen university guangzhou, guangdong, 510120, china e-mail: gta_alfotih@yahoo.com tel: +8613066381670 references 1. baechli h, nordmann a, bucher hc,gratzl o . demographics and prevalent risk factors of chronic subdural haematoma: results of a large single-center cohort study. neurosurg rev. 2004;27:263–266. romanian neurosurgery (2014) xxi 3: 251 – 258 257 2. forster mt, mathé ak, senft c, scharrer i, seifert v, gerlach r. the influence of preoperative anticoagulation on outcome and quality of life after surgical treatment of chronic subdural hematoma. j clin neurosci. 2010;17:975–979. 3. foelholm r, waltimo o. epidemiology of chronic subdural haematoma. acta neurochir (wien). 1975;32:247–250. 4. ramachandran r , hegde t .chronic subdural hematomas--causes of morbidity and mortality. surg neurol 2007; 67: 367-72. 5. könig sa, schick u, döhnert j, goldammer a, vitzthum he. coagulopathy and outcome in patients with chronic subdural haematoma. acta neurol scand 2003;107: 110-6. 6. hong hj, kim yj, yi hj, ko y, oh sj, kim jm. role of angiogenic growth factors and inflammatory cytokine on recurrence of chronic subdural hematoma. surg neurol 2009;71:161-5. 7. abouzari m, rashidi a, rezaii j, esfandiari k, asadollahi m, aleali h, abdollahzadeh m. the role of postoperative patient posture in the recurrence of traumatic chronic subdural hematoma after burr-hole surgery. neurosurgery. 2007;61:794–797. 8. santarius t, kirkpatrick pj, ganesan d, chia hl, jalloh i, smielewski p, richards hk, marcus h, parker ra, price sj, kirollos rw, pickard jd, hutchinson pj. use of drains versus no drains after burr-hole evacuation of chronic subdural hematoma: a randomised controlled trial. lancet. 2009; 374:1067-1073. 9. wilberger je. pathophysiology of evolution and recurrence of chronic subdural hematoma. neurosurg clin n am 2000;11:435-438. 10. ko bs, lee jk, seo br, moon sj, kim jh, kim sh.clinical analysis of risk factors related to recurrent chronic subdural hematoma. j korean neurosurg soc 2008;43:11-5. 11. torihashi k, sadamasa n, yoshida k, narumi o, chin m, yamagata s. independent predictors for recurrence of chronic subdural hematoma: a review of 343 consecutive surgical cases. neurosurgery 2008;63:1125-9. 12. sato m, iwatsuki k, akiyama c, kumura e, yoshimine t. implantation of a reservoir for refractory chronic subdural hematoma. neurosurgery 2001;48:1297-301. 13. vinchon m, noulé n, soto-ares g, dhellemmes p. subduroperitoneal drainage for subdural hematomas in infants: results in 244 cases. j neurosurg 2001;95:249-55. 14. hellwig d, kuhn tj, bauer bl, list-hellwig e. endoscopic treatment of septated chronic subdural hematoma. surg neurol 1996;45:272-7. 15. mandai s, sakurai m, matsumoto y. middle meningeal artery embolization for refractory chronic subdural hematoma: case report. j neurosurg 2000;93:686-8. 16. oishi m, toyama m, tamatani s, kitazawa t, saito m.clinical factors of recurrent chronic subdural hematoma. neurol med chir (tokyo) 2001;41:382-386. 17. yamamoto h, hirashima y, hamada h, hayashi n, origasa h, endo s. independent predictors of recurrence of chronic subdural hematoma : results of multivariate analysis performed using a logistic regression model. j neurosurg 2003;98:1217-1221. 18. roob g, fazekas f. magnetic resonance imaging of cerebral microbleeds. curr opin neurol 2000;13:69-73. 19. yamashima t, friede rl. why do bridging veins rupture into the virtual subdural space? j neurol neurosurg psychiatry 1984;47:121-7 20. sim yw, min ks, lee ms, kim yg, kim dh. recent changes in risk factors of chronic subdural hematoma. j korean neurosurg soc 2012; 52: 234-9. 21. markwalder tm .chronic subdural haematomas: a review.j neurosurg 1981;54: 637–645. 22. nagahori t, nishijima m, takaku a. histological study of the outer membrane of chronic subdural hematoma: possible mechanism for expansion of hematoma cavity. no shinkei geka 1993;21:697–701. 23. el-kadi h, miele vj, kaufman hh. prognosis of chronic subdural hematomas. neurosurg clin n am 2000;11:553-567. 24. amirjamshidi a, abouzari m, eftekhar b, rashidi a, rezaii j, esfandiari k, shirani a, asadollahi m, aleali h. outcomes and recurrence rates in chronic subdural haematoma. br j neurosurg 2007;21:272–275. 25. nakajima h, yasui t, nishikawa m, kishi h, kan m.the role of postoperative patient posture in the recurrence of chronic subdural hematoma: a prospective randomized trial. surg neurol 2002 ;58:385–387. 26. stanisic m, lund-johansen m, mahesparan r. treatment of chronic subdural hematoma by burr-hole craniostomy in adults:influence of some factors on postoperative recurrence. acta neurochir (wien) 2005;147:1249–1256. 27. hirai s, ono j, odaki m, serizawa t, nagano o. embolization of the middle meningeal artery for refractory chronic subdural haematoma. usefulness for 258 alfotih gobran et al arterial embolization to treat subdural hematoma patients under anticoagulant therapy. interv neuroradiol 2004;10suppl 2:101-4. 28. ishihara h, ishihara s, kohyama s, yamane f, ogawa m, sato a, matsutani m. experience in endovascular treatment of recurrent chronic subdural hematoma. interv neuroradiol 2007;13suppl 1:141-4. 29. mino m, nishimura s, hori e, kohama m, yonezawa s, midorikawa h, kaimori m, tanaka t, nishijima m. efficacy of middle meningeal artery embolization in the treatment of refractory chronic subdural hematoma. surg neurol int 2010;1:78. 30. tsukamoto y, oishi m, shinbo j, fujii y.transarterial embolisation for refractory bilateral chronic subdural hematomas in a case with dentatorubral-pallidoluysian atrophy. acta neurochir (wien) 2011;153:1145-7. 31. hashimoto t, ohashi t, watanabe d, koyama s, namatame h, izawa h, haraoka r, okada h, ichimasu n, akimoto j, haraoka j. usefulness of embolization of the middle meningeal artery for refractory chronic subdural hematomas. surg neurol int 2013;4:104. 32. takahashi k, muraoka k, sugiura t, maeda y, mandai s, gohda y, kawauchi m, matsumoto y. middle meningeal artery embolization for refractory chronic subdural hematoma: 3 case reports. no shinkei geka 2002;30:535-9. 33. tanaka t, fujimoto s, saitoh k, satoh s, nagamatsu k, midorikawa h. superselective angiographic findings of ipsilateral middle meningeal artery of chronic subdural hematoma in adults. no shinkei geka 1998; 26:339-47 34. tanaka t, fujimoto s, saito k, kaimori m.histological study of operated cases of chronic subdural hematoma in adults: relationship between dura mater and outer membrane. no shinkei geka 1997;25:701–705 romanian neurosurgery (2019) xxxiii (2): pp. 110-115 doi: 10.33962/roneuro-2019-022 www.journals.lapub.co.uk/index.php/roneurosurgery biomarkers of the brain injuries the future diagnosis standard in head trauma? brief literature review andreea elena bîrlescu1,2, bianca hanganu1, andreea alexandra hleșcu1,2, irina smaranda manoilescu1,2, beatrice gabriela ioan1,2 1 “grigore t. popa” university of medicine and pharmacy, dept. of legal medicine, iași, romania 2 institute of legal medicine, iasi, romania abstract acute head trauma is often a clinical challenge in diagnosing the brain damage, assessing its severity and prognosis, and establishing the optimal treatment. different patients, with brain damage of apparent comparable severity according to the imaging examination, may have different neurological evolution or different response to therapy. minor traumatic brain injuries can induce a brief loss of consciousness or confusion, are usually benign, but sometimes they cause persistent and progressive brain symptoms in the long run. however, at present, there are no reliable methods that can diagnose properly minor traumatic brain injuries. biomarkers of the brain injuries allow the monitoring of both physiological and pathological processes. the identification of such biomarkers could allow a better understanding of the pathological processes involved in traumatic brain injuries, their diagnosis, prognosis and may facilitate the establishment of a better treatment regimen for these patients. in this article, the authors make a brief review of the literature in which they analyse the biomarkers of the lesions of the various brain structures identified so far, which can be detected in biological fluids (blood, cerebrospinal fluid) and the advantages and limitations of their use in the current medical practice. introduction brain injury may be graded by glasgow coma scale score (gcs) in: severe trauma, characterized by a gcs score of less than or equal to 8 the cerebral coma equivalent; moderate trauma, characterized by a gcs score of 9-12 [1], of which 10% of patients will experience neurological deterioration and cerebral coma and minor trauma, where the gcs score is between 13 and 15 [2]. minor brain trauma can be characterized by the loss of consciousness of short durationup to 30 minutes, or confusion, retrograde amnesia to the traumatic event of up to 24 hours, headache, keywords biomarkers, brain injuries, head trauma, advantages, limitations corresponding author: andreea alexandra hleșcu “grigore t. popa” university of medicine and pharmacy, dept. of legal medicine, iași, romania andreea.velnic@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 111 biomarkers of the brain injuries the future diagnosis standard in head trauma? vomiting (unrelated to intracranial hypertension) and/ or transient focal neurological signs or convulsions [1]. most patients with minor brain trauma show favourable progression, but about 3% of cases have an unfavourable progression, with increased risk for intracranial haemorrhage and diffuse axonal injuries, the promoters of cognitive, motor and psychosocial deficits [2]. the morbidity associated with cerebral traumatic injuries (even minor) is considerable. studies have shown that between 1 and 20% of patients with minor traumatic brain injuries develop persistent physical, cognitive and behavioural disorders [3], such as chronic dizziness, fatigue, headache, and amnesia. it is also important that in the clinic, minor brain injuries are more common than stroke, dementia and epilepsy, indicating their high prevalence and justifying the efforts to diagnose and treat them as accurately as possible. despite substantial efforts to clarify and improve the diagnostic criteria for minor traumatic brain injuries, compared to moderate and severe brain injuries, the former often remain a diagnostic challenge. this is largely due to the rapid resolution of acute signs and symptoms after a simple rest and the absence, in many cases, of objective neuroimaging evidence. current diagnosis regimens for minor traumatic brain injuries often face the difficulty of differentiating them from non-traumatic pathologies that may exhibit a similar symptomatology. currently, the gold standard for diagnosing and establishing the therapeutic management of traumatic brain injuries is the computer tomography (ct) exam. it allows the detection of various traumatic head injuries, such as cranial fractures, extraand subdural hematomas, subarachnoid haemorrhage, cerebral contusion and laceration, cerebral edema, etc. with increased sensitivity and specificity and by using it in the clinic as a routine exam, the head ct scan surpassed the simple head radiography [1]. however, the head radiography retains its importance in the initial classification of traumatic brain injuries as complicated injuries (radiographically proven) or uncomplicated injuries (negative radiography), and thus contributes to establishing the necessary further investigations, such as ct scan or mri, and the therapeutic management (hospital admission with or without surgery). despite the superior results from classical x-rays, modern imaging modalities such as ct scan and mri are costly and entail a number of risks, including the risk of irradiation and the risk associated with the administration of the contrast substance [3]. also, in many cases, minor traumatic brain injuries cannot be detected by ct scan. under these circumstances, an additional diagnostic tool is necessary to detect patients at risk of developing further complications. biomarkers of cerebral lesions pathophysiological background research on biomarkers of neuronal lesions began after the 1950s, and their interest has increased significantly over the past 25 years. biomarkers, also called biological markers, are natural characteristics that can be measured and interpreted objectively as indicators of biological processes or responses to therapeutic interventions [4]. biomarkers are indicators of physiological, pathological or pharmacological processes. each organ system has more or less specific biomarkers, and their analysis, either isolated or joined to other clinical investigations, allows monitoring of an individual's health status [2]. from the pathophysiological point of view, due to the brain injuries, the neuronal and astroglial network loses its structural integrity, cellular membranes are affected and secondary to these events, biomarkers are released in the cerebrospinal fluid and in blood, allowing for the diagnosis and prognosis of brain injuries [5]. traumatic mechanical forces can determine cell damage due to shear, rupture and stretching of neurons, axons, glial cells and blood vessels, and the lesion will induce biochemical changes such as excitotoxicity, necrosis and apoptosis, oxidative stress and inflammation. similar pathophysiological changes can also be seen in disorders induced by acute pathological brain injury such as stroke. sensitive and specific biomarkers that reflect the brain damage can provide important information about the pathophysiology of traumatic brain injuries and can predict abnormal ct results and/ or the development of residual deficits in patients suffering from minor traumatic brain injuries. biomarkers could be diagnostic criteria for traumatic brain injuries and could be a valuable adjuvant to clinical and routine imaging. in particular, the possibility of using biomarkers in patients with minor 112 andreea elena bîrlescu, bianca hanganu, andreea alexandra hleșcu et al. traumatic brain injuries could provide a rapid, differential, non-invasive and cost-effective diagnostic test to guide appropriate patients’ triage and their early management [6]. biomarkers of brain injuries – promising results a wide range of proteins, of different origins and resulting from various pathways, have been studied as biomarkers for diagnosis and prognosis of brain injuries. however, the performance of many of these biomarkers has not been studied in the case of minor traumatic brain injuries [7]. at the level of the central nervous system, the lesion biomarkers studied to date are s100beta, glial fibrillary acidic protein (gfap), neuronspecific enolase (nse), alpha ii spectrin, tau protein, ubiquitin c-terminal hydrolase l1 (uch-l1), fattyacid-binding proteins (b-fabp, h-fabp) and il-10. among the listed biomarkers, the most studied are s100 beta and neuronspecific enolase (nse), the values of which increase in hypoxic conditions, starting on the 2nd post-traumatic day and normalize at about 4 days after the trauma [2]. s100 beta is a dimer that binds cell calcium, is involved in cellular differentiation and neuronal proliferation and has a life span of about 2 hours. there are 19 types of such dimers, of which s100a1 (in skeletal muscles, heart, and kidneys), s100a1b (in astrocytes), s100b (in astrocytes and schwan cells) and s100bb (in astrocytes). the low molecular weight of 21kda allows the s100beta dimers to easily cross the blood-brain barrier, so that in brain injuries high levels of s100beta are found in the blood. unlike the nse, the plasma level of s100beta is not affected by hemolysis, 21.2 micrograms/ liter suggesting the installation of anoxic coma, and 15.2 micrograms/ liter indicates neuronal recovery. neuronspecific enolase (nse) is an isoform dimer involved in glucose metabolism, which is normally not found in the peripheral blood. in patients with stroke, the nse value increases, with higher values for patients with irrecoverable traumatic brain injuries compared to patients with favourable progression. decreasing nse values at 24-48 hours after the trauma usually indicates a good prognosis, while a value greater than or equal to 30 micrograms/ liter, 48 hours post-trauma, predicted death in 100% of the cases. as mentioned above, nse values are influenced by hemolysis, which does not allow its determination in peripheral blood. apart from brain lesions, other sources of nse may also be small cell carcinomas, neuroblastoma, haemorrhagic shock, femoral fracture, ischemia and local reperfusion. glial fibrillary acidic protein (gfap) is a monomer, being an intermediate protein derived from astroglial cells. gfap has increased specificity for neuronal tissue, with high values in degenerative brain diseases, cerebral infarction, severe brain injury, and axonal injuries. gfap is a predictive indicator for the recovery of anoxic cerebral coma, but studies conducted so far on this monomer are contradictory, and further research is needed on post-mortem biological products. ubiquitin c-terminal hydrolase l1 (uch-l1) is a compound that plays a role in the elimination of oxidized neuronal proteins under both normal and pathological conditions. initially, it was used as a histological marker for neurons. recently, uch-l1 has been found to have elevated values in the cerebrospinal fluid after a traumatic brain injury, which can be immediately detected posttraumatically, with elevated values lasting for about one week [2]. both s100b and the combination of gfap and uch-l1 were promising in screening for ct positivity/ negativity among patients with acute traumatic brain injury [8]. alpha ii spectrin is a major component of the cortical membrane of the cytoskeleton, being present in axons and presynaptic terminations. it is a marker for apoptosis and necrosis in the posttraumatic initial stages and has high values in moderate and severe brain injuries [2]. tau is a microtubule associated protein, which is necessary to maintain the structural integrity of the axons. tau proteins have also other functions, such as nerve impulse transmission, synaptic activity, cellular proliferation, neurobiological development and neuroplasticity. phosphorylation of tau proteins is a normal metabolic process, while in both aging and neurodegenerative diseases, tau proteins undergo hyper-phosphorylation, which determines their aggregation as fibrillar deposits. post mortem studies on human corpses described different patterns of taunting, depending on the pathological phenotype. recent studies also highlight the uniqueness of pathological models, including a model attributed to repetitive cerebral trauma, 113 biomarkers of the brain injuries the future diagnosis standard in head trauma? although clinical correlations were relative [9]. fatty-acid-binding proteins (fabps) are nonenzymatic cytoplasmic proteins involved in intracellular buffering and transport of fatty acids. these are 9 distinct protein types, each named after the tissue in which it was first detected. fabps are rapidly released into circulation from the injured cells and are eliminated by the kidney, with a half-life of about 20 minutes. b-fabp was first identified in the rodent brain where it has a variable concentration depending on the animal’s age (stage of development). thus, in adult mice, b-fabp is usually produced at low concentrations and is detected only in glial cells of the white matter. unlike b-fabp, h-fabp is also detected in neurons of the gray matter. b-fabp and h-fabp proteins have different brain tissue distribution, with the highest concentrations in the frontal lobe. however, in all brain structures it was observed that the level of hfabp concentration is about 10 times higher than the b-fabp concentration. studies show that these two proteins have greater susceptibility to minor cerebral lesions than the currently used markers, s100b and nse respectively [10]. diagnostic relevance of biomarkers of cerebral injuries to date, biomarkers of cerebral injuries have been detected in cerebrospinal fluid and in peripheral blood. it has been found that in cases where the blood-brain barrier is intact, cerebral proteins are only present in small amounts in blood. the condition of the blood-brain barrier has, therefore, an important influence on the concentration of those proteins in the blood, which should be considered for the interpretation of the cerebral lesion-specific biomarkers [7]. the cerebrospinal fluid is in direct contact with the extracellular matrix of the brain, and its composition reflects the biochemical changes occurring in this organ. for these reasons, the cerebrospinal fluid could be an optimal source of brain damage biomarkers. several cerebral lesion specific biomarkers have already been described, including proteins that indicate the integrity of the blood-brain barrier and neuro-inflammation, as well as axonal, neuronal and astrogial lesions. some proteins that are expressed in the central nervous system are also detectable in peripheral blood, albeit at very low concentrations due to their dilution in the much larger volume of the extracellular plasma and matrix of peripheral tissues. because peripheral blood sampling is much easier in practice than the collection of the cerebrospinal fluid, a series of cerebrospinal fluid biomarkers specific for minor traumatic brain injuries have also been evaluated in the peripheral blood. the low concentration of potential biomarkers in the peripheral blood is, however, a technical limitation on the use of most standard immunological tests. however, the number of potential biomarkers of cerebral lesions in the peripheral blood studied is steadily increasing as the analytical tools for detecting them become more and more sensitive [11]. studies have shown that unique biomarkers do not have the specificity and sensitivity required for their use as diagnostic tools. for a biomarker to be useful its sensitivity and specificity should be very high to ensure diagnosis and prognosis assessment without the need for a ct brain exam. so far, most research on biomarkers of minor traumatic brain injuries has been performed with unique biomarkers. the combination of different biomarkers has been suggested to enhance the diagnostic performance. several studies have shown that combinations of biomarkers significantly increase diagnostic performance in various pathologies, such as sleep disorders, post-stroke subarachnoid haemorrhage, lung cancer or differentiation of post-traumatic brain injuries from other types of lesions. furthermore, it has been suggested that some combinations of different clinical parameters, such as the age and types of biomarkers, e.g. inflammatory proteins, can improve the classification of lesions [7]. in a multicentre study, 13 cerebral biomarkers, all previously investigated in patients with stroke, were evaluated for their ability to correctly classify patients with minor traumatic brain injury, ct positive and ct negative, with a gcs score of 15 and showing at least one clinical symptom. of the 13 biomarkers, the hfabp and il 10 proteins were the best single markers. these were further compared and combined with the better-studied s100b and gfap markers. h-fabp was the best single marker, but when combined with gfap, the overall performance increased from 32% to 46%, with a sensitivity of 100%. proteins have been shown to be released from various types of injured cells. s100b and gfap 114 andreea elena bîrlescu, bianca hanganu, andreea alexandra hleșcu et al. were derived from astrocytic lesions, h-fabp from endothelial cells and neuronal cellular bodies, while il10 is expressed by monocytes and macrophages [7]. detection of cerebral lesions by the serum biomarkers is not a standard procedure in current clinical practice, although several proteins, such as s100b, nse, myelin basic protein and gfap show promising results [10]. some biomarkers, such as s100b and gfap, have been extensively studied in the blood of patients with minor traumatic brain injuries, but so far none seem to provide sufficient information [7]. difficulties and limitations in the study of biomarkers of brain injuries the main difficulty facing biomarkers for brain damage is to know whether the measured proteins really come from the brain injuries. as shown above, regardless of their origin, single biomarkers do not have sufficient performance to be transformed into diagnostic tools. biomarker combinations, however, have been shown to enhance diagnostic performance when proteins of different origins and pathways are combined, due to the complexity of the nervous system and the heterogeneity of the traumatic brain injuries [7, 8]. there are also other obstacles to the development of a series of blood biomarkers for minor traumatic brain injuries. the blood-brain barrier prevents the evaluation of the biochemical changes in the brain by using biomarkers in the blood, but this is possible, however, in the case of loss of blood-brain barrier integrity, which occurs in severe brain lesions. in addition, some potential biomarkers suffer a proteolytic degradation in the blood, and their levels may be affected by clearance in the blood through the liver or kidneys. the accuracy of immunoassays may also be affected by the binding of biomarkers to carrier proteins and extra-cerebral sources of biomarkers [12]. biomarkers of the cerebral injuries have different delivery patterns, and this has limitations on their practical use. as a result, clinical applicability may be limited by the type of brain injury (traumatic, stroke, hypoxia-ischemia). another important limitation in the analysis of cerebral biomarkers is their ambiguity in multiple lesions. despite the current limitations in the study and application of biomarkers of cerebral lesions in the current medical practice, biomarkers could be used in the future as an adjuvant, supplementing the traditional and neuro-imaging examination in the diagnosis and prognosis of patients with traumatic brain injuries [4]. conclusions traumatic brain injuries may raise clinical challenges due to the diagnostic difficulties and the lack of specific prognostic tools. a special place in the traumatic pathology of the brain is occupied by minor traumatic brain injuries that, although characterized by immediate mild signs and symptoms, can induce long-term brain pathology with increased disability potential. biomarkers of cerebral injuries may be a new diagnostic standard for traumatic brain injuries, and in particular, minor ones that often cannot be detected by cerebral ct. however, further studies are needed to identify the biomarkers or combinations of biomarkers with the highest sensitivity and specificity for cerebral injuries. references 1. popescu i, florian is, poeată i. tratat de neurochirurgie. bucurești: editura academiei române, 2014. 2. chirica vi. useful markers to assess traumatic and hypoxic brain injury. rom j leg med. 2017; 25: 146-151. 3. sharma r, rosenberg a, bennet er, laskowitz dt, acheson sk. a blood-based biomarker panel to risk stratify in mild traumatic brain injury. plos one. 2017; 12(3): e0173798. 4. toman e, harrisson s, belli t. biomarkers in traumatic brain injury: a review. journal of the royal army medical corps. 2016; 162(2):103-108. 5. mondello s, schmid k, berger rp, kobeissy f, jeromin a, italiano d, buki a. the challenge of mild traumatic brain injury: role of biochemical markers in diagnosis of brain damage. med res rev. 2014 may; 34(3):503-531. 6. http://www.traumaticbraininjury.com/understandingtbi/what-are-the-causes-of-tbi/ 7. mrozek s, dumurgier j, citerio g, mebazaa a, geeraerts t. biomarkers and acute brain injury: interest and limits. crit care. 2014; 18:220. 8. pelsers mmal, hanhoff t, van der voort d et all. brain and heart type fatty acid binding proteins in the brain: tissue distribution and clinical utility. clin chem. 2004; 50(9): 15681575. 9. posti jp, takala rsk, lagerstedt l et all. correlation of blood biomarkers and biomarker panels with traumatic findings 115 biomarkers of the brain injuries the future diagnosis standard in head trauma? on computed tomography after traumatic brain injury. j neurotrauma. 2019, apr 5. [epub ahead of print]. 10. lagerstedt l, egea-guerrero jj, bustamenate a et all. combining h-fabp and gfap increases the capacity to differentiate between ct-positive and ct-negative patients with mild traumatic brain injury. plos one. 2018, jul 9; 13(7):e0200394. 11. zetterberg h, smith dh, blennow k. biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood. nat rev neurol. 2013 apr; 9(4): 201–210. 12. castellani rj, perry g. tau biology, taupathy, traumatic brain injury and diagnostic challenges. j alzheimers dis. 2019; 67(2): 447–467. microsoft word 16costind_combined.doc 364 d. costin et al combined mechanism glaucoma and grave's ophtalmopathy combined mechanism glaucoma asociated with grave's ophtalmopathy. case report d. costin1, c. constantin2, m.p. bucatariu2, a. al mousa1, andreea dana moraru3 1university of medicine and pharmacy “gr. t. popa” iasi, 2nd ophthalmological clinic, clinical emergency neurosurgical hospital 22nd ophthalmological clinic, clinical emergency neurosurgical hospital iasi 31st ophthalmological clinic, clinic emergency hospital “sf. spiridon” iasi abstract a 69-year-old female presented marked vision loss in both eyes, intense photophobia and ocular pain. the patient had long history of uncompensated glaucoma, graves ophtalmopathy, treated for several years with topical medication without normalizing the intraocular pressure. the patient undergo orbital decompression for grave’s ophtalmopathy which ameliorated the exophthalmia. visual assessment showed 0,08 best corrected visual acuity (bcva) in the right eye respectively 0 in the left eye, posterior chamber pseudophakic implant both eyes, posterior capsular opacification left eye. the intraocular pressure was 18-25 mmhg in the right eye, respectively 14-19 mm hg under topical medication. the cup-disc ratio was 0.8 in the re respectively 0.9-1 in the le. the visual field assessment in the re showed relative central scotoma, complete lower arcuate (bjerrum) scotoma, generalized depresion of vf. we performed re trabeculectomy with 5 fluorouracil and collagen implant (ologen®), with good postoperative evolution. the visual acuity improves significantly to 0.1, the iop after a month was 15 mm hg. the onset, symptomatology and general clinical context of the patient determined the focus on the neuro-ophthalmological aspect of the case, even if that meant that the control of the glaucoma, at times obviously inefficient, would remain second, from the perspective of its importance. keywords: combined mechanism glaucoma, compressive ischemic optic neuropathy, grave's orbitopathy, collagen implant. thyroid orbitopathy is an immunological disorder that affects the orbital muscles and fat. hyperthyroidism is seen with orbitopathy at some point in most patients, although the two are commonly asynchronous. middle-aged adults (30–50 years) are affected most frequently, the disease is seen in women more commonly than in men, in a ratio of 3-4:1, it is always a bilateral process but is often asymmetrical and multiple muscles are involved simultaneously, most commonly the inferior and medial rectus.[10] symptoms and signs include dry eyes, conjunctival injection, lid retraction, exophthalmos, diplopia, corneal exposure, and rarely optic nerve compression. graves’ romanian neurosurgery (2010) xvii 3: 364 – 373 365 disease usually runs a progressive course for 3–5 years and then stabilizes. primary open angle glaucoma is associated with graves ophthalmopathy (go) in 5-24% of the cases. there are studies who support the association of go with normal tension glaucoma. case report a 69-year-old female presented marked vision loss in both eyes, intense photophobia and ocular pain. the history shows that the patient was diagnosed in may 2001 with hypothyroidism, treated with levothyroxinum (eutirox®). in march 2003 she presented with signs of exophthalmia, the analyses certified the hyperthyroidism. in may 2003 the patient complained of visual loss in left eye (le), over a two month period associated with moderate exophthalmia, visual loss in right eye (re) with slower progression. in july 2003 the patient was diagnosed with basedow grave’s disease and thyroid ophthalmopathy. the visual assessment showed best corrected visual acuity (bcva) 0.04 in the re, respectively hand motion (hm) in the le. the computertomography: bilateral exophthalmia with hypertrophy of ocular extrinsic muscles and infiltration of the retrobulbar fat tissue. the intraocular pressure (iop) was 30 mm hg in both eyes. the ophtalmoscopy revealed precise contour optic disk with normal coloration. the patient presented marked ophtalmoplegia with extremely limited ocular motility. the patient was recommended latanoprostum, brinzolamide and timolol (xalatan®, azopt® and timolol®). for the thyroid ophthalmopaty the patient received repeated methylprednisolone therapy (solumedrol®). in september 2003, the patient with basedow grave’s disease was treated with antithyroid drugs, the bcva was 0.04, respectively hm. the iop remained 30 mm hg even under topical medication: latanoprostum, brinzolamide and timolol (xalatan®, azopt® and timolol®). in october 2003 for marked visual loss and following the ct scan which revealed marked optic nerve tumefaction at the level of the bilateral optic channel, the patient undergo surgery treatment, re decompression of the optic nerve in the optic channel and orbital fat resection, which led to the amelioration of exophthalmia. in november 2003, the follow-up mentions “a slight sight improvement”, without specifying any particular values, after the serious sight aggravation, immediately after the surgery. in february 2004 the patient’s diagnostics were malignant basedow grave’s disease, grave’s ophtalmopathy, compensated glaucoma both eyes, optic atrophy, left eye total optic atrophy, incipient cortisone cataract both eyes, iatrogenic cushing’s syndrome, diabetes mellitus, dyslipidemic syndrome. the visual assessment showed the bcva 0.06, in the re respectively no perception of light (npl) in the le. the iop was 18 mm hg, respectively 19 mm hg under treatment with latanoprostum, brinzolamide and timolol (xalatan®, azopt® and timolol®). the ophthalmoscopy revealed discolored, moderately swollen optic disks, no cupping. the visual field (vf) assessment showed isolated areas of light sensitivity in the 300 central area. this seems to be a glaucoma via orbital compression: latanoprostum 366 d. costin et al combined mechanism glaucoma and grave's ophtalmopathy (xalatan®) is no longer used for the treatment. the iop continues to be treated with timolol and brinzolamide (timolol® and azopt®), remaining at the same values. the general recommended treatment was piracetam® and difrarel®. in march 2004, the bcva was 0.016, the iop 19-20 mm hg under timolol and brinzolamide (timolol® and azopt®), constriction of the visual field. one tablet of acetazolamidum (ederen®) and two tablets of nicergoline (sermion®) were added. the mri exam revealed muscular hypertrophy, more important in the posterior half of the muscular body, at which level the optic nerves are compressed in their trajectory to apex of orbit. in june 2004, the bcva was 0.033 and npl, the iop 17-31 mm hg under timolol and brinzolamide (timolol® and azopt®). an interdisciplinary examination concluded that this is a compression glaucoma (“pseudo-glaucoma”), for which the recommended treatment is: acetazolamidum, timolol and brinzolamide (ederen®, timolol®, azopt®), prednisone 80mg/day for 3 weeks, after which the dose will be decreased. in august 2004 the right eye cataract undergo surgery, was performed phacoemulsification with posterior chamber pseudophakic implant (pc iol), with favorable evolution. in november 2004, the patient presented dysthyroid orbitopathy, secondary glaucoma, ischemic optic neuropathy in both eyes, antiphospholipid syndrome and dyslipidemia. the patient continues the same treatment, with timolol and brinzolamide (timolol®, azopt®) – the iop values are not measured. the mri exam revealed optic nerve with reduced thickness (≈2 mm re, ≈1.5 mm le); hypertrophy of the extrinsic muscles. the successive hospitalizations of april 2005, june 2005, and july 2005 confirm the antiphospholipid syndrome as being secondary to toxoplasmosis. the patient is under periodic treatment with cerebrolysin®, sulodexide (vesselduef®). in aprilie 2005 the patient was operated for cataract, with a pc pseudofakic implant in the left eye. over the period 2005-2008, the patient was treated with cerebrolysin®, sulodexide (vesselduef®). treatment with timolol and brinzolamide continues, without the monitorization of iop. in may 2008 the patient was examined at the rothschild clinic. the bcva in the re was 0.02 and hm in the le. the patient presented exotropia of the left eye. the iop was 19 mm hg in the right eye, respectively 23 mm hg in the left eye. in both eyes the patient presented pseudofakic implant. the ophtalmoscopy revealed white optic disks. the visual field revealed a paracentral residual island, only in the right eye. the visual evoked potentials showed a persistency of a flash response in the right eye, a low vep in the left eye. the oct scan, performed in october 2008 revealed in the right eye: major optic atrophy with a retinal nerve fiber layer less than 50 μ thickness. the mri scan showed thick and non-inflamed extraocular muscles in both eyes, with discrete compression at the level of the apex. the main conclusions at the rothschild clinic were: considering the serious nature of the disease and its long history, a orbital decompression might be useful, without a guaranteed favorable outcome; it is necessary to reduce the iop, the recommended treatment was romanian neurosurgery (2010) xvii 3: 364 – 373 367 latanoprostum (xalatan®) and brinzolamide (azopt®). although a surgical orbital decompression was recommended, the clinic where the patient was hospitalized refused to perform the surgery. over the period 2008-2009, the patient continues the treatment with: sulodexide (vesselduef®), cerebrolysin® and topical treatment with latanoprostum (xalatan®), dorzolamide and timolol (cosopt®). visual discomfort becomes more intense, being dominated by marked photophobia. in november 2009 the patient was examined in an ambulatory department. the bcva was 0.02 in the re and npl in the le. the iop was 40 mm hg, in the right eye, respectively 24 mm hg in the left eye under the treatment with latanoprostum (xalatan®), dorzolamide and timolol (cosopt®). it was recommended for the patient to be hospitalized, and the topical treatment was changed with bimatoprost and timolol (ganfort®). the patient arrived in our department in december 2009. the visual assessment revealed the bcva in the right eye 0.02, the left eye 0 (npl). at the slit lamp exam: pc pseudofakic implant in both eyes, posterior capsular opacification in the left eye. intraocular pressure in the right eye was 18-25 mm hg, respectively 14-19 mm hg in the left eye (circadian curve) under bimatoprost and timolol (ganfort®). the iop correction was -1 mm hg (pachymetry=551 μ, herndon formula, ocuscan rxp®) the gonioscopy: open angle – lower third degree, 2nd-3rd degree nasal and temporal, upper second degree. ophtalmoscopy: cup-disc ratio 0.8 in the right eye and 0.9-1 in the left eye, choroidal folds at the posterior pole in the left eye. figure 1 slit lamp photo of the right eye figure 2 slit lamp photo of the left eye figure 3 fundus examination of the right eye 368 d. costin et al combined mechanism glaucoma and grave's ophtalmopathy figure 4 fundus examination of the left eye figure 5 choroidal folds in the left eye the perimetrical assessment: the right visual field revealed relative central scotoma, complete lower arcuate (bjerrum) scotoma, generalized depresion of vf. the general examination revealed the associated diseases: arterial hypertension, painless chronic ischemic cardiopathy, first degree of obesity and hypothyroidism. the ophthalmic diagnoses were: combined mechanism glaucoma both eyes, compressive ischemic optic neuropathy, optic atrophy, total left eye optic atrophy. we decided to perform a trabeculectomy with addition of 5-fluorouracil and collagen implant (ologen™). ologen™ is a biodegradable and implantable scaffold collagen matrix implant. it's function is to induce a regenerative non-scarring wound healing process without the use of anti-fibrotic agents. the matrix improves regeneration and tissue re-modeling, preventing scar formation. the implantation of ologen™ is a simple process requiring that the ophthalmologist perform the operation based on traditional methods and techniques with minimal changes to suture techniques (such as the trabeculectomy). ologen™ is implanted over the scleral flap, with the surgeon making sure to carefully suture both tenon's capsule and conjunctiva over the ologen making a water tight seal of the wound. before surgery we maintained the ocular hypotonia with topical medication bimatoprostum and timolol (ganfort®) and systemic osmotic manitolum (manitol®). we also began the neuroprotective treatment with pentoxifyllinum (pentoxifilin®) and cerebrolysin®. the surgery consists of subconjunctival anaesthesia at 10-11 mm posterior to the limbus, we perform the lift of the conjunctiva. the incision is made at 9 mm posterior to the limbus, having a length of 9 mm. we make a square conjuctival flap with the length of 9 mm. we perform a carefully diathermia and clean the sclera of any tissue (tenon’s capsule or episclera). the 5 fluorouracil is then applied for 2 or 3 minutes. after this we make the scleral flap, the trabeculectomy and peripheral iridectomy. we suture the sclera and apply 5 fluorouracil 1 or 2 minutes. the collagen implant (ologen ™) is implanted over the sclera flap with tight seal of the wound. romanian neurosurgery (2010) xvii 3: 364 – 373 369 for the next day the patient wear a slightly compressive patch.[4] immediately after the surgery the bcva in the re was 0.02, and iop was 14-16 mm hg under dorzolamidum and timolol (cosopt®). the bcva in the le was 0 and the iop was 17 mm hg under bimatoprost and timolol (ganfort®). the patient was administered pentoxifyllinum and cerebrolysin and, at discharge the patient was recommended treatment with: nicergoline (sermion®), lutein, omega 3 (lutein-omega 3®), and she remained under treatment with topic hypotensors (cosopt® and ganfort®) and also indomethacin (indocollyre®). the patient was treated, at home, with cerebrosylin. the patient’s follow-up after a month revealed the bcva in the re 0.1. at the slit lamp exam: discreetly congestive filtration bleb, minor corneal oedema, average depth of the anterior chamber, free iridectomy; functional filtration bleb at gonioscopy. the fundus exam revealed a discrete macular oedema. the iop was 15 mm hg, corrected with a 4 mm hg factor (pachymetry was 586 μm). the visual field shows extension of the deficit, with increase in the density of the central scotoma (aspect of altitudinal visiual fiel defect). we recommended topical treatment with bimatoprost (lumigan®), indomethacin (indocollyre®) and systemic treatment with pentoxifyllinum for 10 days and cerebrolysin for 5 days. in march 2010 the bcva in the re was 0.125, the iop 16-17 mmhg under treatment with bimatoprost (the internist advised against the use of timolol because the patient registered cardiac side effects), a reduction of the density of the central scotoma, free central zone and reduction of the extension of the altitudinal vf defect. figure 6 ologen ™ implant figure 7 slit lamp exam: filtration bleb figure 8 gonioscopy: patent filtration bleb 370 d. costin et al combined mechanism glaucoma and grave's ophtalmopathy 9 a 9 b figure 9 visual field evolution we recommended interruption of the anti-glaucoma topical medication, continuation of the treatment with nicergoline (sermion®) and luteinomega3®, periodical treatment with cerebrolysin and pentoxifyllinum, topical treatment with indomethacin (indocollyre®), if necessary, examination after a 3 months period. a. the diagnosis romanian neurosurgery (2010) xvii 3: 364 – 373 371 • combined mechanism glaucoma • via compression • primary open angle glaucoma • compressive ischemic optic neuropathy b. the treatment • medical • surgical c. therapeutic strategies • priority of treatment of the diseases d. behavior in the cases with multiple risk factors a. combined mechanism glaucoma it is known that the 1 mm hg increase of the pressure in the episcleral veins determines the increase of iop by approximately 1 mm. [5] graves ophthalmopathy is the most frequent cause of obstructive mechanisms that generate the pressure increase in the episcleral veins. the iop also increases via the pressure rise in the episcleral veins and via the trabecular blockage, through the increased deposit of muccopolysaccharides in the trabecular system. [2] the compression of the globe is also exercised via the fibrotic extraocular muscles, with increased volume, in certain positions of the sight. the pressure increase in the episcleral veins is a sure fact, for the mri and the ct scans revealed modifications of the orbital elements (oculomotor muscles, orbital fat). at present, the le seems to suffer from a certain extent of orbital compression (revealed by the choroidal folds at the posterior pole) and the eye is more seriously affected. primary open angle glaucoma primary open angle glaucoma is associated with graves ophthalmopathy in 5-24% of the cases.6 there are studies who support the association of go with the normal pressure glaucoma. [1] we thought about the existence of a poag either simultaneously with or before the thyroid disease, because of the following reasons: the existence of relatively high iop values (even if measured with the schotz tonometer) from the occurrence of the disease. the severe decrease of visual acuity made us think about the preexistence of a disease at the level of the optic nerve. we must not forget that the iop also increases in go via the trabecular blockage, and that the patient also suffered from insufficiently controlled thyroid disease, about 2 years before the triggering of the acute phenomena. there is a genetically related predisposition between glaucoma and thyroid diseases. counter-arguments: lack of documentation related to the assessment of the aspect of the optic disk (c/d ratio) lack of documentation related to the modifications of the vf compresive ischaemic optic neuropathy in this case, severe orbital compression determined, on the one hand, the increase of intraocular pressure, with the impairment of the perfusion of optic nerve head and on the other hand, the impairment of the blood flow in the orbit, at the level of the optic nerve. the optic nerve oedema may have not occurred following the increased values of iop. anyhow, the stasis of the axoplasmic flow compressed the on in the optic channel. b. treatment medical treatment of glaucoma it seems that, in these circumstances, the topical medication did not manage to 372 d. costin et al combined mechanism glaucoma and grave's ophtalmopathy control the evolution of the glaucoma and not even the iop values. surgical treatment of glaucoma the therapeutic target should have been established at a lower level and the surgical intervention should have occurred earlier. the surgery (in the absence of an artificial drainage device) was meant to be as radical as possible, but also safe. medical treatment of compressive ischemic optic neuropathy treatment with cerebrolysin (especially) and vasodilator drugs, in association with sulodexide (not performed after the surgery) proved its efficiency. the sustained neuroprotective treatment contributed to the post-operative improvement of va and vf. we consider that such a neuroprotective treatment is of great interest in all the diseases that target the on, either directly or indirectly. antiedematous treatment with intravenous acetazolamide would have also been useful. surgical treatment of compressive ischemic optic neuropathy the first decompression had a relatively limited effect. the intervention was the only viable solution in the given situation. the subsequent evolution of the disease seems to have shown that a second decompression would have not had better results. this was also the decision of the neurosurgeons that were requested to perform a second intervention. we must underline the importance of neuroprotective medication as adjuvant therapy in all these situations. c. therapeutic strategies we consider that an equidistant approach of the components of eye impairment would have been appropriate in this case. if, in the case of the on, the surgical intervention was choosen hastily, maybe this is how it should have with the glaucoma. there may have been constraints as concerns the decision of performing the glaucoma surgical intervention, associated with the discovery and exposure of the filtration bleb because of the exophthalmia; an artificial drainage system would definitely have been a good solution at any given time. the modest result of the laminectomy may have reduced the hopes, associated with the benefits of glaucoma surgery. d. behavior in the cases with multiple risk factors analysis of each disease, with the evaluation of the impact on the target segments. analysis of the interactions of the diseases and of the most exposed areas following the combined action of risk factors. overall analysis of the general etiopathogenic context. conclusions the open-angle glaucomas are chronic, progressive optic neuropathies, that have in common characteristic morphological changes at the optic nerve head and retinal nerve fibre layer in the absence of other ocular disease or congenital anomalies. progressive retinal ganglion cells death and visual field loss are associated with these changes. [8,9] it is much easier to make accurate assessment by analyzing at the end, a long sequence of data and information that become complete and clear, along the way. unfortunately, most of the times we have to choose the best solution at that very romanian neurosurgery (2010) xvii 3: 364 – 373 373 moment and we can only hope that there will be only few cases, when this solution does not turn out to be the best. references 1.behrouzi z, rabei hm, azizi f, daftarian n, mehrabi y, ardeshiri m, mohammadpour m. prevalence of open-angle glaucoma, glaucoma suspect, and ocular hypertension in thyroid-related immune orbitopathy , j glaucoma. 2007 jun-jul;16(4):358-62. 2.bradley, elizabeth a. md graves ophthalmopathy, current opinion in ophthalmology:,october 2001 volume 12 issue 5 pp 347-351 3.carter k d, frueh b r, hessburg t p, musch d c. long-term efficacy of orbital decompression for compressive optic neuropathy of graves' eye disease. ophthalmology 1991; 98: 1435–1442 4.dimitris papaconstantinou, ilias georgalas, efthimios karmiris, andreas diagourtas, chrysanthi koutsandrea, ioannis ladas, michalis apostolopoulos and gerasimos georgopoulos. trabeculectomy with ologen versus trabeculectomy for the treatment of glaucoma: a pilot study,acta oftalmologica, vol. 88, issue 1, pages 80-85, 2009 5.onur konuk, zafer onaran, suna ozhan oktar, cem yucel and mehmet unal intraocular pressure and superior ophthalmic vein blood flow velocity in graves’ orbitopathy: relation with the clinical features, graefe’s archive for clinical and experimental ophtalmology, vol. 247, no. 11, nov.2009 6.rachel kalmann, maarten ph mourits prevalence and management of elevated intraocular pressure in patients with graves’ orbitopathy, br j ophthalmol 1998;82:754-757 doi:10.1136/bjo.82.7.754 , 1998 7.walsh t j. optic nerve field defects. visual fields. examination and interpretation, t j walsh. am acad ophthalmol, san francisco 1990; 137–149 8.terminology and guidelines for glaucoma (3rd edition), european society of glaucoma, 2010 9.tuulonen a, airaksinen pj, brola e, forsman e, friberg k, kaila m, klement a, makela m, oskala p, puska p, sioranta l, teir h, uusitalo h, vainio-jylha e, vuori ml. the finnish evidence/based guideline for open-angle glaucoma. acta ophtalmol scand. 2003;81:3-18 10.yanoff & duker: ophthalmology, 3rd ed. microsoft word 14florianistgiant.doc romanian neurosurgery (2010) xvii 2: 231 – 237 231 giant hyperostosis secondary to a neglected pott’s puffy tumour. surgical repair with ct-assisted cranioplasty case report i.st. florian1,2, h. rotariu3, b. suciu2 1university of medicine and pharmacy “iuliu hatieganu “ clujnapoca, romania, neurosurgical department 2cluj county clinical emergency hospital, neurosurgical department 3cluj county clinical emergency hospital, cranio-maxillofacial department abstract this paper presents a case with several particularities: severe intracranial hypertension due to a bifronto-parietal hyperostosis secondary to a pott’s puffy tumor previously improper treated; chronic (18 years) intermitent epidural-cutaneous fistula ; ctassisted cranioplasty for the largest cranial vault defect ever performed in our department, made with custom made cranial implants (pema combined with hydroxyapatite) prepared in a siliconerubber mould. keywords: pott’s puffy tumor, hyperostosis, craniectomy, ctassisted cranioplasty introduction sir percivall pott described pott’s puffy tumour in 1768 as a local subperiosteal abscess due to frontal bone suppuration resulting from trauma. pott reported another case due to frontal sinusitis in 1775. the pott’s puffy tumor is a subperiosteal abscess of the frontal bone associated with an underlying osteomyelitis. the most common cause is frontal sinusitis, with head injury coming on second place (1). the direct spread from erosion of the outer table can result in a subperiosteal abscess. similar erosion through the inner table can cause an epidural abcess. such an abscess could then erode through the dura, and cause a subdural empyema or intraparenchimatous abcess. (1,2). most of the patients presented with an indolent forehead swelling with or without systemic septic features, which were often mistaken for a ‘simple scalp abscess’ or ‘infected sebaceous cyst’. simple drainage results in recurrent collection or complications from spreading infection. the pott’s puffy tumor is most often caused by streptococcus and staphylococcus species, or by anaerobic organisms. however, multiple organisms are frequently involved simultaneously. in cases involving the intracranial spread of infection, anaerobes are more common (1). material and methods a 47 year-old man was admitted in our department in 1985 with an enlarging mass on his vertex. physical examination revealed a soft fluctuant, non-tender swelling on the vertex with active signs of inflammation and headache. the patient had a history of severe local trauma several years before admission. because there was no 232 i.st. florian et al giant hyperostosis secondary to a pott’s puffy tumour intracranial involvement, external drainage of the subperiostal collection was the treatment of choice, followed by 6 weeks of culture-guided antibiotherapy. two years later a spontaneous right frontal fistula developed at the site of previous external drainage. axial ct revealed an enhancing subgaleal mass in the vertex region, associated with an adjacent epidural collection, conducting to a definitive diagnosis of pott’s puffy tumour. at surgery, a small trephination encircling the fistulous channel and epidural drainage of the pus was performed. a 6-week course of intravenously culture-guided antibiotics was administered in postoperative period. 18 year later the patient was readmitted in our department with signs of local infection, intermittent opening of the former fistula and symptoms of increased intracranial pressure. on mri a massive endocranial bifronto-parietal hyperostosis with mass effect on the adjacent brain was discovered (figure 1). at surgery, in general anesthesia, large craniectomy was planned by a standard bicoronal skin incision. as the scalp was reflected copious malodorous pus was drained. the scalp in the subgaleal plane was adherent to the underlying bone secondary to massive amounts of granulation tissue, which formed the puffy tumor. this granulation tissue was removed progressively, and a large bifronto-parietal craniectomy was performed until the normal osseous architecture was met at every border of the craniectomy. the pathological bone was removed in one piece; the endocranial surface presented an important hyperostosis, with an irregular surface (figure 2). the postoperative course was uneventful and the patient was discharged without any neurological deficit. follow up controls showed no local signs of infection, the trajectory of the former fistula being completely occluded. after one year the patient presented a mild “trephined syndrome” and, in order to eliminate the drawbacks of a craniectomy status, (figure 3) a custom made cranioplasty was planned. the protocol for custom made cranial plates starts with the ct 3d reconstruction based on a spiral ct scan of the head, from frankfurt horizontal-line to vertex with 0 tilt, and continuous axial slices (2 mm thick). figure 1 cranial mri: massive endocranial bifrontoparietal hyperostosis with mass effect on the adjacent parenchyma romanian neurosurgery (2010) xvii 2: 231 – 237 233 figure 2 one piece craniectomy of the affected bone. note the thickness irregularities of the inner table using mirroring procedures, superimposition, and algebraic boolean operations a virtual 3d model of the cranioplasty was obtained in order to fit with osseous defect. using selective laser sintering (sls) for rapid prototyping, both virtual models (defect and plate) were transformed into real models of polyamide. after a small manual processing, the plate fitted perfectly into the defect (figure 4). the pattern of the cranioplasty plate made of polyamide (by sls) was used in order to make a silicone rubber mould. figure 3 the cranial aspect after craniectomy the plate was prepared by a radiopaque bone cement of polymethylmethacrylat and polyethylmethacrylate combined with hydroxyapatite, and the paste was casted in the silicone rubber mould and pressed into form (5). after unmoulding, any excess of material was drilled away, and 5 mm diameter holes were placed on the entire surface in order to prevent development of 234 i.st. florian et al giant hyperostosis secondary to a pott’s puffy tumour a postoperative epidural haematoma, and to help fixation. with more than 72 hours before surgery, ethylene-oxide sterilization was applied on the plate. using the same bicoronar incision in general anesthesia, the patient underwent surgery. during the surgery the most difficult time was the maintenance in the subgaleal plane in a thick scar tissue, in order not to produce any additional lesion on the scalp or on the dura mater. the entire bony defect was exposed, and deperiosted for fixation. the plate was applied, perfectly fitting at every margin. using 2.0 silk wires the plate was circumferentially fixed (figure 5) without any intraor postoperative complications. figure 4 using selective laser sintering (sls) for rapid prototyping, both virtual models (defect and plate) were transformed into real models of polyamide. after a small manual processing, the plate fitted perfectly into the defect a b figure 5 intraoperative aspects before (a) and after cranioplasty (b) the patient was discharged on the eighth postoperative day with a very good functional and esthetic aspect of the cranial vault (figure 6). discussion in cases of pott’s puffy tumour most patients are presenting with an indolent romanian neurosurgery (2010) xvii 2: 231 – 237 235 forehead swelling with or without systemic septic features, which were often mistaken for a ‘simple scalp abscess’ or ‘infected sebaceous cyst’. simple drainage will result in recurrent collection or complications from spreading infection. the condition requires open drainage with adequate soft tissue and bony debridement. intracranial complications include extradural empyema, subdural empyema, brain abscess, and venous or sinus thrombosis. streptococcus milleri is the most common organism related to chronic sinusitis reported in the literature. staphylococcus, bacteroides or mixed growth have also been reported. figure 6 postoperative aspects 7 days after cranioplasty however, the bacteriology will be different from acute sinusitis (streptococcus pneumoniae or haemophilus influenzae)(14). the cornerstone of treatment for the pott puffy tumor is surgery (1). the goals are to drain all associated abscesses, send the fluid for gram staining and culture, and remove all of the osteomyelitic bone until the limits of craniectomy meets normal osseous architecture. large cranial defects produce not only aesthetic, but also functional alterations. (6,7). one very important particularity in this case is the endocranial hyperostosis, reactive to chronic osteomielytis. although it is well known that the osteomielitis is radiologically described as an osteolityc lesion, in this particular case the chronic infection produced an osteogenical reaction probably due to the periosteum capacity to react to different stimuli by producing osseous tissue. until now no other case with such an osseous reaction was described. although the pott puffy tumor is rarely seen in the era of antibiotics, a delayed or missed diagnosis can lead to such associated complications as epidural abscess, subdural empyema, sinus thrombosis, and intraparenchymal abscess. an optimal outcome is best attained with early diagnosis followed by aggressive treatments. another particular aspect of the reported case is the 18 years patient’s tolerance to a chronic infection on the calvaria without any neurological or general clinical impairment, except the last month before readmission when increased intracranial pressure syndrome developed. considering the cranioplasty, the threedimensional imaging and rapid prototyping techniques associated with the use of 236 i.st. florian et al giant hyperostosis secondary to a pott’s puffy tumour alloplastic materials allow manufacture of a cranioplasty plate preoperatively. the defect is repaired symmetrically even in thickness. various materials have been used to fill defects in the cranial vault, such as titanium, xenografts, autografts, and allografts (8). a good synthetic material must be: biocompatible, inert, low or even non-thermal conductive, capable of generating no artifacts on ct and mri, of the same weight as the bone or even lighter, strong enough to resist functional stress, simple to work with and not expensive. acrylates are fulfilling these demands. polymethylmethacrylate (pmma) is one of the most used for material for cranioplasty. polyethylmethacrylate (pema) offers some advantages over pmma, such as greater elasticity, lower polymerization temperature, easiness in processing. when pema is combined with hydroxyapatite the advantages are even better: physical resistance similar to bone, formation of collagen bridges between bone and hydroxyapatite (9,10). it is difficult to produce a symmetric, accurate implant presurgically, or at the time of surgery when the defect is greater than 50 cm2 (11).the method presented here used a silicone rubber mould. compared to plaster, the main advantage of silicone rubber is that it allows preservation of very thin details of the plate (e.g. margins) during unmolding. preserving the thin margins of the plate provided a better stabilization and there was no need of rigid fixation. the latter could prevent secondary damage to the brain during drilling and screwing (9). conclusion surgical intervention is the treatment of choice in pott’s puffy tumor. a thorough debridement of granulation, removal of the infected bone and underling epidural granulations, drainage of pus are mandatory. to repair large skull defects one can choose either to reconstruct the vaults strictly intra-operatively, or to prepare a so called “custom made cranial implant,” prior to the operation. the disadvantages of intra-operative repair are the timeconsuming, the increasing risk to the patient, insufficient protection from trauma and infection, often resulting in suboptimal cosmetic result. however, custom made cranioplasty implants have the advantages of a reduced operative time, less invasive surgery, improved cosmetic results, faster recuperation, and reduced costs due to short a operative time (9,12,13). references 1.laurence davidson, m.d., and j. gordon mc comb, m.d. epidural–cutaneous fistula in association with the pott puffy tumor in an adolescent. case report. j neurosurg (3 suppl pediatrics) 105:235–237, 2006. 2.ramos a, rayo ji, martin r, pardal jl, gomez jl, del canizo a. epidural empyema; a complication of frontal sinusitis. acta otorrinolaringol esp. 1989 novdec;40(6):451-3. 3.ç. evliyaoglu; g. bademci; e. yucel and s. keskil. pott’s puffy tumor of the vertex years after trauma in a diabetic patient: case report. neurocirugía vol.16 no.1 murcia feb. 2005. 4.marquardt, g., schick, u., moller-hartmann, w.: brain abscess decades after a penetrating shrapnel injury. br j neurosurg 2000; 14: 246-248 5.h. rotaru, s. bran, g. bǎciuţ, m. bǎciuţ, c. dinu, h. stan, h. chezan, s.g. kim, d. munteanu and p.berce. silicone-rubber moulding of custom-made cranioplasty plates. xviii congress of the european asociation for cranio-maxillo facial surgery. barcelona (spain), september 12-15, 2006durand jl, renier d, marchac d. the history of cranioplasty. ann chir plast esthet. 1997 feb;42(1):75-83. 6.dujovny m, aviles a, agner c, fernandez p, charbel ft: cranioplasty: cosmetic or therapeutic? surg neurol 47: 238-241, 1997. 7.dujovny m, agner c, aviles a.: syndrome of the trephined: theory and facts. crit rev neurosurg 24: 271-278, 1999. romanian neurosurgery (2010) xvii 2: 231 – 237 237 8.durand jl, renier d, marchac d: the history of cranioplasty. ann chir plast esthet 42: 75-83, 1997. 9.horatiu rotaru, mihaela bǎciuţ, horatiu stan, simion bran, horea chezan, alexandru iosif, mircea tomescu, seong-gon kim, alexandru rotaru, grigore bǎciuţ. silicone rubber mould casted polyethylmethacrylate-hydroxyapatite plate used for repairing a large skull defect. journal of craniomaxillofacial surgery (2006) 34, 242-246. 10.florian st, sima v, tomescu m: placa pem-ha pentru cranioplastie. quo vadis, 2, :21-22, 1998. 11.van putten mc jr, yamada s. alloplastic cranial implants made from computed tomographic scangenerated casts. j prosthet dent. 1992 jul;68(1):103-8. 12.rotaru ah: avantajele si dezavantajele utilizarii modelelor tridimensionale medicale. in: rotaru ah: reconstructii si modele tridimensionale medicale. ed. casa cartii de stiinta, cluj-napoca, 2001. pp. 99-100. 13.yacubian-fernandes a, laronga pr, coelho ra, ducati lg, silva mv. prototyping as an alternative to cranioplasty using methylmethacrylate: technical note. arq neuropsiquiatr. 2004 sep;62(3b):865-8. epub 2004 oct 5. 14.kung sw, chan dtm, suen py, boet r, poon ws; pott’s puffy tumour; hong kong med j vol 8 no 5 october 2002. microsoft word 14selectedabstracts romanian neurosurgery (2013) xx 4: 401 – 435 401 selected abstracts of the 39th congress of the romanian society of neurosurgery with international participation, bucharest, september 18th 21th 2013 intracranial vascular malformation a surgical point of view i.s. florian1,2, s.v. trifoi2, p. kiss2 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery 2cluj county emergency hospital, department of neurosurgery introduction: in this paper we want to describe our surgical experience and strategy in the field of intracranial vascular malformation and the current management of these lesions, in the absence of endovascular preoperative embolisation or neuronavigation facilities. patients and methods: the retrospective analysis of 192 intracranial vascular malformations admitted and surgically treated in our department between june 1996 and november 2012. from all intracranial vascular malformations 66% (127) are arteriovenous malformations, and 34% are cavernomas (65 cases). the diagnosis was established based on clinical findings, ct, mri, angiography, and confirmed with pathological findings. we recorded a minor male preponderance (54% for avms and 58% for cavernomas). the peak incidence has been found in the 5th decade. results: the major clinical findings were: hemorrhage, seizures, progressive neurological deficit, and headache and according to spetzler-martin grading system most cases of avms were grade ii and iii (65%). all the cases included in the study ware treated surgically. for arteriovenous malformation, postoperative complications were: transient neurological deficits (11%), hydrocephalus (9%), and re-bleeding (9%). the outcome was gos 5 and 4 in 86% of the cases. in 20% of the cases, the avms had associated aneurisms, treated in the same operatory session. for cavernomas, postoperative complications were predominantly seizures and neurologic deficits (each 11%), and then hydrocephalus, and re-bleeding. the outcome was good (gos 5 and 4) in 77% of the cases. the mortality rate for the entire series was 1.53% (meaning a case with multiple cavernomas). conclusions: the best treatment of an intracranial vascular malformation is surgical resection, subtotal resection being in our opinion not a good option in surgery. key words: intracranial vascular malformation, surgical resection. current aspects in the surgical treatment of avms – analysis of a personal series of 26 cases treated surgically and pathologically confirmed in 3 years i. poeata1,2, al. chiriac1, f. ziyad1, n. dobrin1, smaranda predoaica1, antonia nita1 1emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania 2gr.t. popa university of medicine and pharmacy, neurosurgery, iasi, romania 402 abstracts 39th congress of the romanian society of neurosurgery introduction: microsurgical treatment of avms changed in the last years due to access to gamma-knife and the development of endovascular techniques in our department in iasi. patients and methods: we analyze 26 cases of avm treated surgically and confirmed by imagistic and anatomo-pathological studies in the 07.2010-06.2013 period. results: we looked at: spetzler grade, presentation, previous treatments, localization, preop and postoperative clinical status, preand postoperative imagistic, complications. conclusions: microsurgical resection plays still a major role in the definitive treatment of avms either as a single treatment or in conjunction with endovascular techniques or gamma-knife radiosurgery in complex cases. key words: avm, microneurosurgery, treatment microsurgical management of brain arteriovenous malformations: longterm outcome and results m.r. gorgan1,2, narcisa bucur2, angela neacsu2, aurelia mihaela sandu2,3, f.m. brehar1,2, v.m. pruna2,3, d. martin2, a. giovani2, o. zamfir2, anamaria gheorghiu2 1clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 2fourth department of neurosurgery, emergency clinical hospital bagdasar-arseni 3ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: brain arteriovenous malformations (avms) are congenital complex network of dysplastic vessels. material and method: we retrospectively reviewed medical records of patients with brain avms operated from 1998 to 2013, in the fourth department of neurosurgery, emergency clinical hospital bagdasararseni. results: fifty-three patients with brain avms underwent surgery. mean age was 37.58 years, varying from 17 to 85 years. eight patients (15.1%) had avms spetzlermartin grade i, 12 patients (22.6%) grade ii, 21 patients (39.6%) grade iii, 7 patients (13.2%) grade iv and 5 patients (9.4%) grade v. fourty-six patients (86.8%) had supratentorial and 7 (13.2%) had infratentorial lesions. we performed total resection of avms in 39 cases (73.6%). fourteen patients (26.4%) had residual nidus. patients with residual nidus were referred to stereotactic radiosurgery with good outcome. thirty-four patients (64.2%) presented increased modified rankin score (mrs) following surgery, in 6 cases (11.3%) mrs remained unchanged and 13 patients (24.5%) presented decreased mrs. mortality rate was 9.4%. long term followup showed excellent quality of life in 22 patients (45.8%), good quality of life 10 cases (20.8%), mediocre quality of life in 8 patients (16.7%) and a poor quality of life in 8 cases (16.7%). conclusions: microsurgery is the treatment of choice in avms. surgical results are excellent, with low morbidity rate. patients with poor surgical results belonged to the group admitted with severe altered state of consciousness, massive hematomas, acute brainstem dysfunction. if for any reason part of the nidus cannot be safely surgical resected, stereotactic radiosurgery can provide definitive cure. key words: arteriovenous malformation, microsurgery, outcome. romanian neurosurgery (2013) xx 4: 401 – 435 403 current protocol of brain glioma treatment in the neurosurgery clinic of iasi – a retrospective study of 341 cases b. iliescu, d. rotariu, c. apetrei, f. ziyad, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi, neurosurgery, romania introduction: multidisciplinarity, multimodality, and maximal safe resection are the current standard in the therapeutic approach towards brain glioma. although an increasing body of biological data raises promising new possibilities for targeted treatment microsurgical resection, radiotherapy, and chimiotherapy still represent the main line of defense against this pathology. however, new technical developments and clinical evidence impose significant changes in the protocols and therapeutic approach. patients and methods: we have analyzed a series of 341 cases of gliomas which were diagnosed and surgically treated between march 2010 and march 2013 following the current diagnostic and therapeutic protocols, including functional imaging, microsurgical resection, intraoperative neuronavigation and ultrasound, and awake surgey for eloquent areas tumors. we have excluded the patients without histological confirmation and patients with infratentorial lesions or the age under 18. results: in our series we have observed a slight predominance in males 55.4 %. the main symptom besides headache was the impairment of the motor function observed in 36.3 % cases and seizures in 30.9% cases. the preponderant age group was between 51 and 60 years of age (31% ). the complete resection was obtained in 35.4% of cases and in other 61.8% of cases radical surgery was not possible because of the tumor infiltration in basal ganglia (21.8%), eloquent areas (49%), and invasion of vascular structures (13.6%). the main complications were: hemorrhage in the tumoral resection bed (13.6%). all patients were directed, after recovery from surgery, to the oncology department for adjuvant therapy (rxt/cht). in 36 patients there was a second operation for recurrence and the average time for re-intervention was 15,6 months. conclusions: early imaging diagnosis, using high sensitive mri exams, and maximal safe microsurgical resection are in our series the factors that significantly improve the outcome of brain gliomas aided by a coherent adjuvant therapy plan. nonetheless, complete cure is difficult to assess and needs long periods of follow-up. we present the most interesting cases of our series and discuss the advantages and disadvantages of our current therapeutic and surveillance protocol for brain gliomas. key words: glioma, microsurgery, treatment. low grade gliomas surgery how i do it i.s. florian1,2, a. baritchii1, a. iosif2, z. andrasoni3 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery 2cluj county emergency hospital, department of neurosurgery introduction: low grade gliomas include numerous histopathological types with varying peculiarities considering evolution, diagnosis, imaging and treatment. despite their slow growing nature, they are not in most of the cases benign tumors, malignant 404 abstracts 39th congress of the romanian society of neurosurgery transformation being described in all histopathological types. the aim of this study is to highlight some of the elements concerning the role of surgery in the treatment of low grade gliomas patients and methods: we present a retrospective study of 400 low grade gliomas, representing 40,1 % of 997 operated by the main author (prof. dr florian) between 01.01.2000 and 31.12.2012, accounting for 33,18% out of the total of 3004 tumors operated within the same interval. 224 cases of low grade gliomas met the inclusion criteria for multivariate statistical analysis in order to define the role of radical surgery in low gliomas treatment. results: from a total of 400 low grade gliomas cases pilocytic astrocitomas represent 23,5 % (94 cases), grade ii gliomas (astrocitomas, mixed gliomas) represent 44,5% (178 cases), oligodendrogliomas 10,7% (43 cases) and ependimomas (grade i and ii) 15,25% (61 cases). gross total removal was achieved in 88% of the cases. the improvement of the kps scale is significantly higher (p< 0,05) in patients with gross total removal of the tumor. conclusion: the extent of removal independently influences the outcome, but no correlation with malignant transformation could be established. radical surgery must be the goal of the treatment of all cerebral gliomas. key words: low grade gliomas, radical surgery, outcome, prognosis. current surgical treatment and prognosis of s u pratentorial low grade gliomas in adults v. ciubotaru1, d. paunescu1,2, ligia tataranu1,2, m. chelsoi1, anica dricu3 1neurosurgical clinic, “bagdasar-arseni” clinical hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania 3division of biochemistry, university of medicine and pharmacy, craiova, romania introduction: the importance of surgical resection for adult patients with supratentorial low-grade glioma (lgg) remains controversial. material and methods: from june 2003 to june 2013, 84 adult patients with supratentorial low-grade gliomas were treated at “bagdasar-arseni” clinical hospital (neurosurgery clinic iii). all patients underwent surgical intervention: gross total resection in 24 patients (>90%), subtotal resection (<90%) in 53 patients and biopsy in 7 patients. this retrospective study assessed whether the extent of resection was associated with improved of survival and malignant transformation. the challenge for an optimal management of these patients is to find the balance between an optimal survival and the preservation of neurological function including cognition. results: in our group, histological subtypes were as follows: oligoastrocytoma in 22 patients (26 %), diffuse astrocytoma in 26 patients (31 %) and oligodendroglioma in 36 patients (43 %). median preoperative tumor volumes were 46.2 cm3 (between 8.3 and 174 cm3) and postoperative 5.8 cm3 (between 0 and 132.2 cm3). patients were divided into two groups by the resection grade: ≥90% and <90%. overall survival romanian neurosurgery (2013) xx 4: 401 – 435 405 and malignant transformation were analyzed. better survival rate was correlated with increased excision for diffuse astrocytoma but not for oligodendroglioma (which are sensitive to chemotherapy). malignant transformation occurred in 11 patients (9 of the patients given postoperative radiotherapy) of subtotal resection group (9 male and 2 female). conclusions: overall survival is significantly better and malignant transformation is reduced in patients with excision higher then 90%. key words: low-grade glioma, biopsy, surgery, overall survival, malignant transformation. supratentorial low grade gliomas new achievments in diagnostic and treatment a.v. ciurea1, v. ciubotaru2, i. ogrezeanu2, m. lisievici3, i. luca-husti1, h. moisa4 1sanador medical center, department of neurosurgery, 2“bagdasar-arseni” clinical hospital, department of neurosurgery 3“bagdasar-arseni” clinical hospital, department of neuropathology 4“carol davila” university of medicine and pharmacy, bucharest, romania, av. berceni 10-12, sector 4, cod 041915, bucharest introduction: low grade gliomas (lgg) are slow growing tumors. the aim of the treatment is to simultaneously combine an optimal extension of resection by preservation of functional integrity with correct grading of tumor malignancy and the adequate adjuvant therapies in order to achieve a long survival, with a good postoperative quality of life. there are some important questions regarding lgg: what is the delimitation of lgg? what are the therapeutical decisions: observation, surgical removal or biopsy? does surgical removal alone ever cure lgg? if recurrences appear, is another surgery recommended? what is the efficiency of radiotherapy and chemotherapy in lgg recurrences? what are the indications of gamma knife surgery (g.k.s.)? materials and method: our experience in a series of 160 adult patients with supratentorial lgg, operated over a period of 11 years (january 2002 december 2012) is presented, focusing on the newest achievements in the diagnosis of gliomas (neuroimaging, immunohistochemical analysis of tumor specimens), surgical treatment (intraoperative electrophysiology) and adjuvant therapies (oncological protocols). preoperative diagnosis was based on 1t mri images. microsurgical resection was performed in all cases: total removal 79 cases (49,3 %), partial removal 81 cases (50,6 %), with no perioperative mortality. the outcome at 6 month (gos): good recovery 135 cases (84,3%), moderate disability 21 cases (13,1%), severe disability 4 cases (2,5%). the follow-up period was between 12 months – 9 years with the medium range of 4,5 years. histological grading was assessed by classical pathologic examination and showed: fibrilary astrocytomas in 102 cases, oligodendriogliomas in 26 cases, oligoastrocytomas in 21 cases, dysembryoplastic neuroepithelial tumor in 5 cases, protoplasmic astrocytoma in 4 cases, ganglioglioma in 2 cases. in our data at 5 years postoperative we find: 11 patients were lost, recurrences to grade iii-iv in 49 cases, regrowth grade ii-iii in 53 cases and 47 cases remain in evidence (grade ii). the total number of regrowth-recurrences cases 406 abstracts 39th congress of the romanian society of neurosurgery is 102 (63,8%). it is very important to perform a check-up mri exam every 6 months. lgg causing long-standing and medically refractory epilepsy are more likely to be associated with multiple epileptogenic foci, therefore intraoperative electrocorticography was used for tailoring the resection, together with intraoperative localization of central sulcus using somatosensory evoked potentials in tumors localized around the central area. intraoperative electrophysiological monitoring was performed in 31 cases. because actually, the final diagnosis requires immunohistochemistry and also, study of the molecular biology of these tumors is an important step for understanding the genesis and biological behavior of these diseases, in the last years of the study we have performed also immunohistochemical analysis of the tumor specimens. we have studied in order to identify, quantify and compare, in a series of 37 cases of glioma surgical specimens (low grade and high grade gliomas), previously classified concerning their histological grade (who), the following immunohistochemical markers: ki-67 proteins and pcna (markers of the cellular proliferation), p53 (product of the tumor suppressor gene tp53), cd 34, vegf, vegfr2, bfgf (markers for angiogenesis). surgical specimens were immunostained for p53 (clona do-7, biogenex usa); ki-67 (mib-1; 1:50, dakoglostrup, denmark) and proliferating cell nuclear antigen (pcna; 1:10, pc10 dakote). proliferative activity (nuclear immunostain) was measured. p53 immunoreactivity was positive in all grade iii and iv gliomas, and in 50% of low grade gliomas. with a median of 12% and 24% for mib-1 and pcna respectively, for all neoplasms in the study, the mean percentage positive nuclear area for mib-1 and pcna was 3.06% and 13.11% in lowgrade (ii) astrocytomas, 14.34% and 29.68% in highgrade (iii) astrocytomas, and 18.77% and 44.11% in glioblastoma multiforme (grade iv). one-way analysis of variance showed a significant correlation between the histological grade and mib-1 and between the histological grade and pcna. isolated cases of low grade gliomas with high mib and pcna percentage were noticed. cd34, vegf, vegfr2 and bfgf expression were determined by immunohistochemistry (cd34, clone q band, immunotech; vegf, sc-152, santa cruz bioth.; vegfr2, sc-7269, santa cruz bioth; bfgf, bfgf88, biogenex). immunoreactivity for cd34 was positive in all types of the tumors. immunoreactivity for vegf, vegfr2 and bfgf was seen in both endothelial cells and tumor cells, with increased levels in more aggressive tumors, comparing with normal tissue where immunoreactivity was present only in endothelial cells. conclusions: lgg could be treated only surgically. we advocate the idea, that patients with lgg and medically refractory epileptic seizures, may undergo tailored resections. incompletely resected tumors may be managed with irradiation in the tumor bed, or by observation alone. proliferation in gliomas, measured as mib1 and pcna, correlates significantly with histological grade, providing useful additional information for diagnosis evaluation of the tumor recurrence susceptibility. angiogenesis markers could indicate the invasiveness tendency of the tumor. correlated with the proliferation romanian neurosurgery (2013) xx 4: 401 – 435 407 markers, they express the aggressive tendency of the tumor and consequently, the prognosis. as a result, the correct treatment and prognosis of the case could be evaluated, especially in lgg where the indication of radiotherapy is debatable. despite the optimism associated with prognostic in lgg, these tumors usually recur, having a higher grade of malignancy. we consider that new, even more aggressive treatment protocols are needed for their management. key words: low grade gliomas, supratentorial, microsurgery, intraoperative electrophysiology, immunohistochemistry, neuro-oncology, gamma knife surgery (g.k.s.) therapeutical decision in pediatric low grade gliomas; our opinion based on 408 cases a. tascu1,2, l. nuteanu1, r.e. rizea1,2, a. iliescu1, c. pascal1, iulia vapor1, a. enache1 11-st neurosurgery clinicpediatric department, emergency hospital „bagdasar-arseni”, bucharest, romania, av berceni 10-12 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: low grade gliomas (lgg) are slow growing tumors. surgery realise citoreduction and establish the tumoral grading. there are some important points: delimitation of lgg; therapeutical decision: observation, surgery or biopsy; in recurrences, surgery ? radiotherapy (gamma-knife ?) ? chemotherapy ? our goals are to evaluate the necessary factors for the therapeutical decision. patients and methods: department’s 408 cases of lgg (including spinal) and literature were used. we consider: pilocytic astrocytoma (62.99 %), fibrillary astrocytoma (15.44 %), ganglioglioma (11.03 %), gangliocytoma (1.71 %), oligodendroglioma (1.96 %), oligoastrocytoma (4.9 %), pleomorphic xanthoastrocytoma (0.49 %), dysembrioplastic neuroepithelial tumor (1.23 %), ependimoma (0.24 %); 0 central neurocytomas, subependymal giant cell astrocytomas, choroid gliomas of the third ventricle. results: in our serie, gos was: gr 87.25 %, md 9.55 %, sd 2.2 %, d 0.98 %. recurrencies at 5 years were 7.35 % and at 10 years 7.59 %. surgical resection was 49.26 % total and 50.73 % subtotal. conclusions: we advocate as much as possible surgical resection, without new deficits, even in critical areas (for focal tumors). observation or biopsy is indicated only for particular cases. in recurrences, surgery, radiotherapy and chemotherapy should be considered. in the future, molecular biology will help the prognosis and therapy. key words: low grade gliomas, pediatric, therapy. cerebellar pilocytic astrocytomas in children – a continous challenge a. tascu1,2, iulia vapor1, mihaela florea3, l. nuteanu1, c. pascal1, a. iliescu1 11-st neurosurgery clinicpediatric department, emergency hospital „bagdasar-arseni”, bucharest, romania, av berceni 10-12 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3student of university of medicine and pharmacy “carol davila”, bucharest introduction: posterior fossa piloctytic astrocytomas represent approximately 2740% of pediatric posterior fossa tumors. 408 abstracts 39th congress of the romanian society of neurosurgery these are benign tumors with a natural history of slow growth, this leading to a delay of diagnosis. usually at the time when the child is referred to the neurosurgeon the tumor has big dimensions, usually accompanied by hydrocephalus. material and method: we present our experience in 107 cases of pediatric posterior fossa pilocytic astrocytomas treated in our department from january 2003 to december 2012. the average age at the time of diagnosis was 9,05 years. the period from the setting of signs and symptoms until the moment of diagnosis was 1day to 2 years (mean period 2 months). results: hydrocephalus was present in 87% of cases. gross total resection was accomplished in 80,38% of cases (evaluation based on postoperative irm). outcome was favorable in 95,33% of cases. conclusions: according to the benign course of most cases of pediatric posterior fossa pylocitic astrocytomas, the goal of surgery is achieving maximum resection of tumor without producing new neurological deficits. key words: piloctytic astrocytoma, posterior fossa, child. analysis of 136 patients with intracranial glioblastoma: clinical characteristics, management and prognostic factors ligia tataranu1,2, adriana dediu1,2, v. ciubotaru1, alisa popescu3, anica dricu4 1neurosurgical clinic, “bagdasar-arseni” clinical hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania 3neurological department, university of medicine and pharmacy, craiova, romania 4division of biochemistry, university of medicine and pharmacy, craiova, romania introduction: gioblastomas are the most common primary brain tumours in adults. these tumours have an aggressive behaviour with a median survival after diagnosis about one year. the main therapeutic methods for this pathology are surgical resection, radiotherapy and chemotherapy. material and methods: between june 2010 and july 2013, 136 consecutive patients were diagnosed with intracranial glioblastoma and surgically treated in our neurosurgical department from emergency clinical hospital “bagdasar – arseni” bucharest, romania. adequate follow-up was obtained for all patients of the study. there were 54 women (39.8%) and 82 men (60.2%) with age between 30 and 78 years old. the mean age at admission was 56.4 years. results: there were 133 supratentorial tumors, 2 brainstem tumors and one tumor located in the left cerebellar hemisphere. from the 133 supratentorial tumors, 26 were frontal (19.1%), 28 in the temporal lobe (20.5%), 6 in the parietal lobe (4.4%), 3 in the occipital lobe (2.2%), 8 in the basal nucleus (5.8%), 62 tumors were located in more than one lobe, sometimes with invasion in the corpus callosum. of the 129 supratentorial tumors that were lateralized, 44.1% were located in the left hemisphere (60 patients) and 50.7% in the right hemisphere (69 patients). in two patients we found another associated tumors: one had a meningioma diagnosed and treated 2 years before the glioblastoma was diagnosed and the other patient had a tumor in the left ponto-cerebellar angle. fourteen patients had needle biopsy, one patient had biopsy romanian neurosurgery (2013) xx 4: 401 – 435 409 during open surgery, for 118 the tumor was resected during surgery and 3 patients were untreated surgically. the histopathological examination confirmed the diagnosis of glioblastoma in operated patients; in one case sarcomatos elements were also observed. conclusions: patients with glioblastoma who underwent radical excision of the tumour followed by adjuvant radiotherapy and temozolomide have an improved survival compared to patients undergoing biopsy or subtotal resection. in conclusion, younger age, small tumors, gross or near total resection, radiotherapy and temozolomide therapy are factors that predicte prolonged survival. the findings of this study may help guide treatment and prognosticate survival for patients with glioblastomas. key words: glioblastoma, biopsy, surgery, radiotherapy, chemotherapy. prognostic factors and survival following surgery for malignant glioma c. toader1,2, m. stroi2 1clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 2national institute of neurology and neurovascular diseases bucharest, neurosurgery, romania introduction: despite the remarkable advances in surgical techniques, adjuvant treatment strategies and the use of the operating microscope, malignant brain glioma remains a serious disease that is never cured. even if the modern diagnostic and surgical procedures contributed to the reduction of the perioperative morbidity and mortality rates in malignant gliomas, the odds of significant long term survival has remained poor and stable for the last three decades. patients and methods: a retrospective study evaluated 120 consecutive patients diagnosed with malignant supratentorial glioma who underwent surgery at the vascular neurosurgical department of the national institute of neurology and neurovascular diseases between april 2008-july 2012. there were 72 women and 48 men; age range 21-78 years, mean 52 years. patient were followed-up until death or up to 14 months after enrollment in the study and survival data were correlated with the histopathological grade and location of the tumor, the extent of surgery, the patient”s performance status, the applied adjuvant therapies, complications, tumor recurrences, the time interval from the onset of symptoms to diagnosis and surgical treatment. the postoperative quality of life was assessed with the help of the kps. survival curves were calculated by the kaplan meyer method to account for varying periods of follow-up. results: in multivariate analyses, the extent of resection, age 65 years or younger and a kps score of 70 or great, and anaplastic oligodendroglioma were associated with a prolonged survival time for patients with malignant gliomas. multifocal glioblastoma and anaplastic glioma apparently arose de novo are associated with poor prognostic. conclusions: this study provide evidence to support tumor grade, the extent of resection, patient” age and patient”s functional status as prognostic factors for survival in patient with malignant glioma. key words: malignant glioma,survival, resection, prognostic. 410 abstracts 39th congress of the romanian society of neurosurgery prognostic factors of the microsurgical treatment for recurrent glioblastomas f. m. brehar1,2, r.m. gorgan1,2, narcisa bucur1, angela neacsu1, v.m. pruna1,3, aurelia mihaela sandu1,3 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: glioblastoma is the most common malignancy of the central nervous system with a poor outcome because of its tendency for recurrences. there are divergent opinions regarding the management of glioblastoma recurrence. patients and methods: the authors of this study present a series of 198 surgical procedures performed for glioblastoma recurrences in 156 patients admitted in our clinic between january 1998 and july 2013. the majority of patients (126 cases) underwent one operation for recurrences, 21 patients have been operated for two times (first and second recurrence), 6 patients for three times and 3 patients for four times. results: the surgical mortality in this series was 1,2 % and morbidity (new neurological deficits postoperatively) was 9,5%. the medium survival time for recurrent glioblastoma was 30 weeks. the authors correlated the medium survival time, mortality and morbidity with the following preoperative parameters: age, karnofsky performance status (kps) preoperative score, tumor location (dominant or nondominat hemisphere) and extension (lobar vs multilobar). several preoperative criteria were found to be predictive for a better outcome in operated recurrences of glioblastoma: age<70 years, kps score>80 and location in nondominant hemispheres. conclusions: tumor resection should be considered for the following cases of glioblastoma recurrences: age<70 years, tumor location in non-dominant hemispheres and symptoms related to tumor mass-effect. careful selection of the patients, based on analysis of several specific preoperative criteria (age, kps score, location, mass-effect), is important in order to obtain a better outcome and a good quality of life. key words: recurrent glioblastoma, prognostic criteria, mortality, morbidity. nestin expression in biopsy samples correlates with the invasive phenotype of cerebral gliomas f.m. brehar1,2, d. arsene3, m. lisievici1, m.r. gorgan2 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3institute of cerebro-vascular diseases, bucharest introduction: new evidences suggest that cancer stem cells (cscs) play an important role in malignant gliomas invasion. nestin is one of the most used markers for cscs. the aim of this report was to analysis the relation between nestin expression in biopsy samples and gliomas invasion. patients and methods: serial stereotactic biopsies have been performed for 49 patients, admitted in our institution between september 2010 and april 2013 with cerebral gliomas, using leksell stereotactic system (elekta, sweden). all tissue samples included in study were from brain-tumor interface and were formalin fixed and paraffin embedded. immunohistochemistry was performed romanian neurosurgery (2013) xx 4: 401 – 435 411 using the envision+ dual link system peroxidase kit (dako, carpinteria, ca, usa) and primary antibodies anti nestin (santa cruz biotechnology, ca, usa, dilution 1:50). statistic analysis was performed using spss version 19. results: in forty cases (81,6%) the tissue samples presented three distinct areas: tumor area, intermediate area and distant areas. in nine cases (18,4%) only tumor tissue could be identified. there was a statistically significant correlation between the invasiveness of tumors (assesed by preoperative mr investigations) and the intensity of nestin expression for each area of the samples, as follows: nestin in tumor area (p=0,046), nestin in intermediate area (p=0,001) and nestin in distant area (p=0,011). conclusions: our results support the hypothesis that cscs promote gliomas invasion. moreover, nestin could be a clinically relevant marker associated with the infiltrative phenotype of cerebral gliomas. acknowledgments: this work was supported by grant no.28487/30.10.2012 of university of medicine and pharmacy “carol davila”, bucharest, romania. key words: nestin, gliomas, stereotactic biopsy, invasion. surgical approaches in lateral ventricle tumors m. radoi, l. danaila, f. stefanescu, r. vakilnejad, d.a. petrescu, s. suditu national institute of neurology and neurovascular diseases bucharest, neurosurgery, romania introduction: tumors of the lateral ventricle are rare lesions including a large variety of benign or malignant tumors and cyst formations. the purpose of this study is to discuss the factors that affected the preference for transcallosal or transcortical approach. patients and methods: it was a retrospective series that comprised 26 consecutive patients who underwent operation for lateral ventricle tumors between 2006-2013. the main clinical symptoms and signs were associated with the localization and size of the tumors. cerebral computed tomography and magnetic resonance imaging were used to determine the location and expansion of each tumor. the transcortical approach was used in 15 patients and the transcallosal approach was used in 11 patients. results: total tumor resection was achieved in 19 patients. most frequent histologic tumor’s type were glioblastoma (5), choroid plexus papilloma (5), ependymoma (4) and meningioma (4). signs of increased intracranial pressure were most dominant. one patient died because of postoperative intraventricular hemorrhage. additional neurological deficits were seen in 3 patients and postoperative seizure occurred in one patient. two patients, one with postoperative hydrocephalus and the other with postoperative epidural hematoma required reoperation. 15 of 26 patients received postoperative radiotherapy. the mean duration of postoperative evaluation was 24,32 (range 5-92). we reoperated 2 patients due to recurrence. conclusions: the nature, size, location and vascularization of intraventricular tumors are the most important elements influencing the choice of surgical approach. surgeons must evaluate all these factors and prefer the short and safe way to remove the tumor. 412 abstracts 39th congress of the romanian society of neurosurgery key words: transcortical approach, transcallosal approach, prognostic factors. management of intramedullary astrocytomas d. serban, f. exergian, c. zamfir, n. calina, g. checiu, m. podea clinical hospital “bagdasar-arseni”, spine surgery, bucharest, romania introduction: primitive imt represent 810% of all primary tumors of the spinal cord. only 24% of all cns tumors in adults are imt. sc tumors are much less common than intracranial tumors with an overall prevalence of approximately an intramedullary tumor for four intracranial tumors, with variations depending on the type of tumor. for example, the location intracranial/spinal for astrocytomas is approximately 10/1, while the same ratio for ependymomas varies from 3/1 to 20/1 depending on the histological type of ependymoma. in particular, mixo-papillary ependymomas are found more frequently in the sc (1). patients and methods: patients enrolled in the study were hospitalized and operated in the period 2003-2009 in neurosurgery i clinic, ward ii, “bagdasar-arseni” clinical emergency hospital for imt in various locations. 59 patients were included in the study, age between 15 and 70 years, 40% female sex ratio = 1.5. 62 surgeries were performed. all patients were operated on by the same surgical team, same main operator. results: we prospectively analyzed clinical, imaging and pathological data from all consecutive patients operated for intramedullary tumors in our department (neurosurgery i clinic, ward ii) between january 2003 and august 2009 (80 months). all surgical interventions were performed by the same surgical team. we emphasized the technical difficulties raised by ablation of imt depending on the type of the tumor and postoperative neurological outcome. conclusions: astrocytomas grade i could be completely or partially ablated. total or almost total ablation is due to the cleavage plane between imt and normal medullary tissue. in low-grade astrocytomas, where there plane cleavage is present, total or almost total ablation is the goal. astrocytomas grade iii and iv and part of grade ii astrocytomas (with anaplastic cells elements) were subtotally ablated because of their infiltrative nature. there were no major intraoperative complications, postoperative immediately and/or delayed. all cases of grade iii and iv astrocytomas have clear indication for postoperative radiotherapy. key words: intramedullary astrocytomas, surgery, postoperative neurological outcome. the first year experience in the spinal instrumentation neurosurgery from microneurosurgery to the spinal neurosurgery g. zapuhlih1, s. borodin1, al. bostan1, m. andronic1, v. frumusachi2, a. marin3 1department of neurosurgery, institute of neurology and neurosurgery, chisinau, moldova 2department of neurology, institute of neurology and neurosurgery, chisinau, moldova 3department of neuroradiology, institute of neurology and neurosurgery, chisinau, moldova introduction: increasing incidence of spinal column pathology as trauma, tumor and degenerative disease led to “explosion” romanian neurosurgery (2013) xx 4: 401 – 435 413 of spinal fusion surgery in our country. analysis of own experience in diversity of spinal fusions using same company implants and screws. patients and methods: retrospectively, we analyzed 18 spinal fusion cases, performed in the neurosurgical clinic of the institute of neurology and neurosurgery, chisinau, moldova from november 2012 to september 2013. results: from all spinal column pathology 8 cases were traumatic and 10 were degenerative. topographical level of the lesion was: lumbar spine pathology 13 cases, of which 10 cases were nontraumatic pathology, 3 cases traumatic one. in cervical and thoracic segment all cases were exclusively traumatic, 2 case at cervical level, 3 cases at lower thoracic level. depending on the type of spinal fusion were performed: 10 cases of transpedicular isolated fusion, of which 6 cases with fixation in 2 levels, 1 case of spinal fixation in 3 levels and 3 cases with fixation in 4 levels.. exclusively in neurosurgical practice from republic of moldova were performed cervical fusion with add plus and intersomatica golden gate plates. conclusions: in all cases we obtained good anterior and posterior compartments fusion. key words: spinal instrumentation surgery. incidental durotomy in lumbar spine surgery: incidence, risk factors and management d. adam1,2, t. papacocea1,2, r. iliescu1, ioana hornea1, cristina moisescu1 1“carol davila” university of medicine and pharmacy neurosurgery, bucharest, romania 2emergency clinical “st. pantelimon” hospital, neurosurgery, bucharest, romania introduction: incidental durotomy is a common complication of lumbar spine operations for degenerative disorders. its incidence varies depending on several risk factors and regarding the intra and postoperative management, there is no consensus. the aim is to present our experience with incidental durotomy in patients who were operated on for lumbar disc herniation, lumbar spinal stenosis and revision surgeries. methods: between 2009-2012, 1259 patients were operated on for degenerative lumbar disorders. for primary operations, the surgical approach was mini-open, interlamar, unior bilateral, as for recurrences, the removal of the compressive element was intended: the epidural scar and the disc fragment. there were operated on 863 patients (67.7%) for lumbar disc herniation, 344 patients (27.3%) for lumbar spinal stenosis, and 52 patients (5%) for recurrences. the operations were performed by neurosurgeons with the same professional degree but with different operative volume. results: unintentional durotomy occurred in 20 (2.3%) of the patients with herniated disc, in 14 (4.07%) with lumbar spinal stenosis and in 12 (23%) with recurrences. the most frequent risk factors were: obesity, revised surgery and the physician’s low operative volume. intraoperative dural fissures were repaired through suture (8 cases), by applying muscle, fat graft or curaspon, tachosil, fibrin glue. four cerebro-spinal fluid (csf) fistulas were repaired at reoperation. conclusions: incidental dural fissures during operations for degenerative lumbar disorders must be recognized and immediately repaired to prevent complications such as csf fistula, 414 abstracts 39th congress of the romanian society of neurosurgery osteodiscitis and increased medical costs. preventing, identifying and treating unintentional durotomies can be best achieved by respecting a neat surgical technique and a standardized treatment protocol. key words: durotomy, dural tear, csf fistula. lumbar l4-l5 ganglion cyst with cauda equina syndrome. report of a case g. iacob clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest, suub, bucharest, romania introduction: although juxtafacet cysts are lesions noted as incidental findings associated with spinal facet joints on imaging studies of the spine (computed tomography ct and magnetic resonance imaging – mri); in some patients, they may produce symptoms methods: a female aged 47 years old was admitted for an acute cauda equina syndome induced by a ganglion facet cyst. diagnosis was sustained on spinal lumbar mri and dynamic flexion/extension x-rays. results: the patient got benefit from microsurgery, with excellent outcome, with no surgery-related complications six months after operation and no fusion. conclusions: mostly associated with degenerative facet joints and spondylolisthesis, symptomatic lumbar juxta facet cysts ganglion and synovial cysts are uncommon lesions of the spine. they can mimic herniated discs, causing low back pain, radiculopathy or even cauda equina syndrome. key words: ganglion cyst, synovial cyst, juxtafacet cyst, spinal fusion, degenerative spine disease, cauda equine syndrome the value of diffusion tensor mr imaging in cervical trauma assessment m. dabija, b. iliescu, b. chirita, d. andronic, i. poeata “prof. dr. n. oblu” clincial emergency hospital, 1st neurosurgery, iasi, romania introduction: mr imaging, with its high soft-tissue resolution, has been established as the gold standard in evaluating the extent of spinal cord structural damage in cases with spinal cord trauma. however, the conventional mr imaging offers poor data concerning the microstructure of the spinal cord, such as fiber tracts of the white matter. the advent of diffusion tensor imaging made it possible to analyze the level of integrity of functional structures represented by the white matter tracts. patients and methods: we present our initial experience of using a complex imaging protocol that includes dti sequences in the cases with cervical spine trauma. we analyze the clinical and imaging characteristics of 17 patients that suffered traumatic injuries of the cervical spine from various causes. results: clinically we established the asia score for each individual case. from the imaging data we studied the t2 and flair-weighted images and looked at the signal intensity abnormalities. correlations were established between the three different measures. we discuss the prognostic value of each measure separately and in conjunction. conclusions: our current data suggest that dti has a better correlation with the romanian neurosurgery (2013) xx 4: 401 – 435 415 clinical status of the patient, offers a better explanation for the degree of neurological deficit, and, most importantly has a much better prognostic value.for the outcome of the cervical spine trauma that affects the spinal cord. key words: cervical, trauma, diffusion tensor mri, outcome. traumatic pathology of the thoracic and lumbar spine t. maior cluj county emergency hospital department of neurosurgery, cluj-napoca, romania introduction: traumatic pathology of the thoracic and lumbar spine is easy to be surgically solved. surgery itself does not represent a real surgical challenge, but the true challenge regarding this pathology is related to the decision making process. the paper presents the surgical treatment protocol in trauma pathology located in dorsal and lumbar spine area. aspects related to vertebral body surgery, lengths and type of instrumentation, reason of treatment, and pitfalls in trauma surgery are discussed. methods: 180 of cases were studied with at least one year post-op follow-up, operated according to the same criteria. the treatment algorithms area presented, including some representative cases of posterior approaches, and of combined (anterior and posterior) approaches. all presented cases are from the author’s personal archive and underwent surgery using the same system of stabilization and the same technique. results: obvious advantages of the transpedicualr stabilization, ligamentotaxis and the reconstruction of the vertebral body. images of illustrated cases are presented. conclusions: based on our expereince short intrsumentations, good restoration of the sagital balance, vertebral body reconstruction are key facts in order to obtain good long term results in spine traumatic pathology. key words: transpedicular posterior instrumentation, ligamentotaxis, short instrumentations. treatment of traumatic spinal cord injuries tested by csf phosphrylated neurofilament subunit nf-h (pnf-h) levels st.m. iencean1, a. tascu2, a.st. iencean1,3, i. poeata1,3 1gr.t. popa university of medicine and pharmacy, iasi, neurosurgery, iasi, romania 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania introduction: several studies showed that the phosphorylated form of the neurofilament subunit nf-h ( pnf-h) are related to neuronal injuries and its detection provide information about the degree of neuronal loss. the phosphorylated neurofilament subunit nfh ( pnf-h ) is present into csf in significant amounts following neuronal injury and may be detected. the pnf-h could be a biomarker of the neuronal injuries and its detection might provide prognosis in humans. methods: we used a pnf-h elisa test capable of detecting the levels of phosphorylated nf-h (pnf-h) to patients with spinal cord injury. we studied the pnf-h levels in csf in patients with spinal cord injury (sci) and for normal 416 abstracts 39th congress of the romanian society of neurosurgery values of pnf-h we determined the csf pnf-h level from individuals without neurological damage. results: the normal values were: 0 to 0.9 ng/ml and the pathological values were till 10.9 ng/ml. the pnf-h values of csf from the patients with sci were 6 10 times higher than the normal and its higher values were related to an unfavorable outcome. conclusions: in conclusion the phosphorylated form of the neurofilament subunit nf-h ( pnf-h) is biomarker in sci in humans and its increased values are consistent with an unfavorable outcome. key words: biomarker, phosphorylated neurofilament subunit pnf-h, spinal cord injury. our experience with cerebral hemangioblastomas: neurosurgical management and results m.r. gorgan1,2, narcisa bucur1, angela neacsu1, aurelia mihaela sandu1,3, f.m. brehar1,2, v.m. pruna1,3, d. martin1, a. giovani1, o. zamfir1, anamaria gheorghiu1 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest background: hemangioblastomas are highly vascular, well-defined, cystic, cystic with mural nodule or solid, benign tumors, occurring sporadically or in von hippel lindau disease. material and method: we retrospectively reviewed medical records of adult patients, admitted and operated into the fourth department of neurosurgery, emergency clinical hospital bagdasar-arseni with positive histopathological diagnosis of hemagioblastoma. results: from 1998 to 2013, 39 patients with brain hemangioblastomas were admitted in our department. in 31 patients hemangioblastoma (79.5%) occurred sporadically and 8 cases (20.5%) had von hippel-lindau disease. there were 22 males (56.4%) and 17 females (43.6%). mean age was 44.38, varying from 18 to 73 years. in 33 patients (84.6%) the tumor was located into the posterior fossa and in 6 cases (15.4%) the tumor was supratentorial. the tumor was intraaxial in 35 patients (89.74%) and extraaxial in 4 cases (10.26%). patients underwent 67 surgical procedures: 39 underwent primary tumor surgical resection, 10 patients underwent second surgery for tumor recurrence, 4 patients underwent third surgery for tumor recurrence, 8 patients required a ventriculoperitoneal shunt for hydrocephalus, 2 patients underwent shunt revision and 4 patients required surgery for complications, posterior fossa compressive cyst requiring cystic-ventriculoperitoneal shunt, cerebral abscess, extradural hematoma and intraparenchymatal hematoma. all 10 patients (25.6%) with tumor recurrence had subtotal resection. morbidity rate was 12.82% and mortality was 2.56%. twenty eight (71.79%) patients had favorable longterm outcome. conclusions: the most common location for hemangioblastomas was posterior fossa. subtotal resection is associated with tumor recurrence. total resection ensures a favorable long-term and a recurrence-free outcome. hydrocephalus is the most frequent associated pathology. key words: hemangioblastoma, posterior fossa tumor, surgery. romanian neurosurgery (2013) xx 4: 401 – 435 417 the role of the microsurgical treatment within the multimodal therapy of brain metastases from lung cancer r.m. gorgan1,2, narcisa bucur1, angela neacsu1, aurelia mihaela sandu1,3, v.m. pruna1,3, f. m. brehar1,2 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: cerebral metastases of pulmonary origin represent a pathology with an increasing incidence and a severe prognosis. often patients come to the neurosurgeon with multiple cerebral metastases and a surgical decision has to be taken based on the benefits and the risks of the microsurgical treatment. patients and methods: the authors present a series of 78 patients with cerebral metastases with pulmonary origin operated in our clinic between 2006 and 2012 and detailed the therapeutic strategies in relation with the location and number of metastases. results: there were 20 women (25, 6 %) and 58 men (74, 4%) with a mean age of the series of 55,44 years (±sd 10,46). there was no surgical mortality in this series and no additional neurological deficits postoperatively. 62 patients had one metastasis. the surgical resection was total for all cases with single cerebral metastases. 10 patients had 2 cerebral metastases. in 3 patients both cerebral metastases have been removed by a singlestage surgical approach. in 7 patients the larger metastasis has been totally removed and for the smaller one the gamma-knife has been performed. six patients had three or more metastases. in all these cases the largest, life threatening metastasis has been removed and for smaller lesions, gamma-knife has been performed. conclusions: single symptomatic cerebral metastases have the following surgical indications: age<75 years, karnofsky performance status (kps)>70, stable primary cancer, midline-shift and the presence of a perilesional hypodens area on ct scan of minimum 3 cm. patients with multiple cerebral metastases and one symptomatic and surgical accessible lesion have also the same neurosurgical indications. in these cases, neurosurgical procedure removed the life-threatening lesion, while gamma-knife therapy provided a long term control of the remaining smaller lesions. key words: cerebral metastases, microsurgical treatment, mortality. surgery in superior sagittal sinus meningiomatosis case report a. st. iencean1, b. secara1, f. ziyad1, st. m. iencean1,2, i. poeata1,2 1emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania 2gr.t. popa university of medicine and pharmacy, neurosurgery, iasi, romania introduction: multiple meningiomas attract a lot of interest because of their relative rarity, unclear aetiology and the problems related to proper management strategy. patients and methods: we describe a case of 58 years old female that presented with slowly progressive right hemiparesis for 2 years, aphasia for 2-3 months that improved under medical treatment, left crural paresis for 10 days and signs of intracranial hypertension. the mri imaging showed multiple nodules: right parasagital precoronar, right paracentral, bilateral 418 abstracts 39th congress of the romanian society of neurosurgery parasagital pre-lambdoidal. also, the seldinger angiography show total obstruction of sinus at the level of precoronar nodule and partial at the level of pre-lambdoidal nodules and the possibility of venous drainage through venous ducts in the periphery of lambdoidal tumors. the surgey consisted in parasagittal bilateral bone flap, mainly on the right side, resection of the pre-coronar and paracentral nodules; intracapsular resection of the prelambdoidal nodules with keeping some patent venous ducts in the thickness of tumoral capsule and partial resection of the nodule invading the sss. results: the patient had a very good postoperative evolution (karnofsky 70 to 90), the signs of intracranial hypertension dissapeared and she improved the hemiparesis and the walking ability. conclusions: radical resection of meningiomas invading the superior sagittal sinus (sss) presents several hazards. some surgeons consider sss invasion a contraindication for complete resection, and others advocate total resection with venous reconstruction. key words: meningiomatosis, surgical approach, superior sagittal sinus. sixth nerve palsy secondary to craniocerebral trauma options of treatment violeta ioana pruna1,5, ligia tataranu2,3, daniela cioplean1, v.m. pruna2,4, m.r. gorgan2,3 1oftapro clinic, bucharest, romania 2clinical hospital “bagdasar-arseni”, bucharest 3clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 4ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest 5ph.d. student in ophtalmology university of medicine and pharmacy “carol davila”, bucharest introduction: due to it’s long intracranial course, sixth nerve is one of the most common affected cranial nerves in cranial cerebral trauma. it may be damaged either by direct mechanism (skull base fractures) or indirectly, by raised intracranial pressure, which compress the nerve at the angle over the tip of the petrosum bone. neuromuscular dysfunction may be partial (paresis) or complete (palsy) and significantly reduces the quality of the patient’s life, by diplopia and confusion. a waiting period of 6 months to one year prior to strabismus surgery must be considered, in order to assess the chance of spontaneous recovery. treatment may be conservative or surgical, depending on the residual neuromuscular function and time elapsed from the injury. material and methods: authors reviewed the files of 17 patients admitted into oftapro clinic with sixth nerve palsy, secondary to cranial cerebral trauma, produced by car crash (13 cases) and falls from height (4 cases). 12 patients had unilateral, and 5 patients had bilateral sixth nerve paralysis. in terms of neural muscular dysfunction degree, 12 patients manifested complete sixth nerve palsy, and in 5 cases, the deficit was partial. 9 of the patients underwent surgery alone, botulinum toxin injection alone worked in one case, 5 cases needed combined therapy (surgical, btxa, and prismatic correction) and 2 cases showed spontaneous recovery in time. results: good ocular alignment or slightly under correction, with restoration of binocular vision (with or without prismatic correction) was obtained in all cases, except one, in whom ocular romanian neurosurgery (2013) xx 4: 401 – 435 419 misalignment persisted, despite surgery and btx-a injection (the patient refuses the idea of reintervention). surgical success was defined as orthoptic ocular alignment in primary position or residual esotropia less than 12 pd (prism diopters), with ability of the eye to move at least at the median line (abduction – 4), associated with binocular vision recovery. conclusions: sixth nerve palsy has multiple therapeutic options, depending primarily on the degree of residual neuromuscular function. good functional results can be obtained if different procedures are applied specifically for each case. a good interdisciplinary collaboration is mandatory for functional recovery of these patients. key words: sixth nerve palsy, cranial cerebral trauma, binocular vision, diplopia. normal pressure hydrocephalus active and passive pathogenetic mechanisms st. m. iencean1, a. tascu2, i. poeata1,3, a. st. iencean3, m.r. gorgan2 1gr.t. popa university of medicine and pharmacy, iasi, neurosurgery, iasi, romania 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania introduction: normal pressure hydrocephalus (nph) is characterized by normal csf pressure, less than 18 cm h2o, classical clinical triad: gait disturbance, dementia and incontinence in patients with communicating hydrocephalus on ct or mri. patients and methods: we analyzed retrospectively the nph hospitalized patients in three neurosurgical centers between january 2008 and december 2011. there were only 41 selected cases of patients with nph, including 24 patients with secondary nph and 17 patients with idiopathic nph. results: ventriculoperitoneal shunt was performed in all 24 patients with secondary nph and at 9 patients with idnph. the short-term and long-term results were good and very good for cases of secondary nph and good in 60% and poor in 40% in cases of idnph. conclusions: we can consider that secondary nph and some cases of idiopathic nph with repeated small increases of icp, with transependymal migration of csf and hydrocephalus causes clinical triad because of the open glialependymal barrier, as an active normal pressure hydrocephalus and the shunt has good results ; and other cases of idnph have not increases of intracranial pressure, no transependymal migration of csf and there are pre-existing periventricular deep lesions that causes clinical triad, as a passive hydrocephalus, this is a passive normal pressure hydrocephalus. key words: normal pressure hydrocephalus, idiopathic normal pressure hydrocephalus. preliminary results in epilepsy surgery j. ciurea1, ioana mandruta2, teodora coman1, nicoleta diaconu1, a. rasina1, mirela renta1, ana ciurea1, g. gari1, a. barborica3 15th dept. of functional neurosurgery , clinical hospital “bagdasar-arseni”, bucharest 2univ. mun. hospital, neurology, epilepsy center, bucharest, romania 3univ. of physics, magurele, romania introduction: the objective is to investigate results after electrophysiologial 420 abstracts 39th congress of the romanian society of neurosurgery diagnosis and resective epilepsy surgery in department of functional neurosurgery. patients and methods: all patients were referred to our center after careful assessment by a dedicated epilepsy team from another hospital. the first step was implantation of deep brain electrodes for a tailored well planed resection. there were 12 procedures. identification of vessels was performed by mr enhancement studies in dedicated idl environment. ct scans were used for postoperative assessment. a total of 40 procedures were performed in the last 2 years of which there were 4 lobectomies 7 lezionectomie with electrocorticography, 5 supraselective amigdalohypocampectomies, and one reposition of electrodes. all patients had been prospectively followed in the dedicated epilepsy center. results: in the short term, all patients were seizure-free or improved significantly postop, one patient developed an ischemia. the fusion of preoperative and postoperative images aloud confirmation of precision electrode placement. the resection was selective due to electrophysiology and the final results were analyzed on pre and post operative imaging. conclusions: almost all patients are seizure-free or improved since surgery. many patients who gain seizure freedom can successfully discontinue antiepileptic drugs in future. key words: epilesy, surgery deep brain electrodes. actual tendencies in the management of spontaneous intracerebral hematoma – analysis of a series of 100 cases and review of the literature i. poeata1, c. apetrei2, b. iliescu2, z. fayad2, s. predoaica2, al. chiriac2 1gr.t. popa university of medicine and pharmacy, iasi, neurosurgery, iasi, romania 2emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania introduction: non-traumatic intracerebral hematoma may be the result of an avm rupture discoverable n routine angiography. in other cases the clinical and imagistic data suggest the possibility of hematoma in the context of hypertension of amyloid angiopathy. besides these there are a number of other possible causes: anticoagulation, hemorrhagic infarction, hemorrhagic tumors, cryptic avms. patients and methods: the goal of this paper is to analyze the shifts in the diagnosis and therapeutic approach with the advent of mri as the main diagnostic tool, in the context of multiple angiographic diagnosis options, continuous improvement of neuroanesthesiology and intensive care, improved surgical techniques, better intraoperative localization and hemostasis. in the same time we look at the change in attitude in favor of a more conservative approach for a vast portion of these cases, while the complexity of the cases increased due to an aging population and the increased life expectancy with additional comorbidities. we analyzed retrospectively 100 consecutive cases with ich admitted recently in the department of neurosurgery in iasi. results: the following pathologies were encountered: hypertension in 74 cases, ruptured intracranial aneurysms in 7 cases, cavernomas in 5 cases, avm in 2 cases, amyloid hematoma in 2 cases, anticoagulation in 2 cases, hemorrhagic infarction in 2 cases, hemorrhagic tumor in 1 case, while 5 cases had no discoverable cause. surgical removal of the hematoma was performed in 28 cases, 12 of which romanian neurosurgery (2013) xx 4: 401 – 435 421 were treated in the same procedure for the underlying vascular lesion (aneurysm clipping, cavernoma or avm nidus resection). in one case the aneurysm was embolyzed and the hematoma treated conservatively. 3 cases had a evd performed and one case necessitated decompressive craniectomy. conclusions: in the diagnosis the main dilemma consists in how far the investigations should go in order to discover a etiology underlying the hemorrhage. the treatment is constrained by the decision of surgical evacuation of the hematoma. whilst additional data was made available it is still a multifactorial decision and it is more often than not influenced by the personal preference of the surgeon in charge of the case. key words: intracerebral hematoma, spontaneous, treatment, diagnosis. neurosurgical management of anterior circulation cerebral aneurysms c. toader1,2, m stroi2 1clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 2national institute of neurology and neurovascular diseases bucharest, neurosurgery, romania introduction: ruptured intracranial aneurysms are major neurosurgical urgencies that have a poor natural history with regard to rebleeding and should be treated as soon as possible. patients and methods: we present our surgical experience in 83 patients who presented 99 anterior circulation cerebral aneurysms, who underwent surgery at the vascular neurosurgical department of the national institute of neurology and neurovascular diseases between july 2010 august 2013. there were 38 male and 51 women. age range 26-78 years, mean 54 years. anterior communicating artery aneurysms were encountered the most frequent (32 patients). 24 patients were diagnosed with middle cerebral artery aneurysms. one patient had unruptured ophthalmic artery aneurysm.11 patient harbored posterior communicating artery aneurysms. the rest of the patients presented anterior circulation intracranial aneurysms as follows: anterior choroidal aneurysms (2 patients), carotid artery bifurcation aneurysms (4 patients), distal anterior cerebral artery aneurysms (6 patients), cavernous carotid artery aneurysms (3patients ). large and giant aneurysms were encountered in 13 patients. 16 patients harbored multiple aneurysms. two patients had 5 aneurysms. results: we analised the rate of morbidity and mortality and complications related to each type of eneurysm. the overall mortality was 9% and the morbidity was 27%. conclusions: aneurysms surgery is and should remain an important element of neurosurgical culture, even as endovascular techniques advance in popularity and sophistication. modern aneurysms techniques offer excellent solutions and must be saved for those aneurysms that require them. key words: aneurysms, clipping, subarachnoid hemorrhage, outcome 422 abstracts 39th congress of the romanian society of neurosurgery superior cerebellar artery ruptured aneurysms treated by endovascular or surgical techniques – case discussion m. radoi1, st. dima1, f. stefanescu1, l. marginean2 1national institute of neurology and neurovascular diseases bucharest, neurosurgery, romania 2nova vita hospital tg mures, angiography, tg. mures, romania introduction: in the last decade, aneurysms of the cerebral posterior circulation were more feasible to endovascular treatment due to the challenging position of these aneurysms for surgical clipping. we reported two particular cases of a distal superior cerebellar artery ruptured aneurysm treated by endovascular and, respectively, surgical techniques. methods: occlusion of the aneurysms was achieved by endovascular placement of two stents, and, in the other case, by surgical clipping. results: in both cases, the aneurysm was excluded from circulation. six months, and respectively, twelve months follow-up control angiography demonstrate complete occlusion of the aneurysms. no focal neurological deficits of the both patients were recorded. conclusions: in experienced hands and in selected cases surgery of aneurysms developed in challenging surgical positions could be as successful and efficient as endovascular therapy. key words: aneurysm, endovascular, surgery. our last 10 years experience in treatment of tuberculum sellae meningiomas ligia tataranu1,2, v. ciubotaru1, b. dumitrescu1, anica dricu3 1neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania 3university of medicine and pharmacy, craiova, romania introduction: tuberculum sellae meningiomas present a close relationship with anterior visual pathways, the arteries of the anterior circulation and the hypothalamus. the authors report on a series of surgically treated tuberculum sellae meningiomas, resection being achieved by different approaches. material and methods: a retrospective study was conducted on 24 consecutive patients with tuberculum sellae meningiomas, operated on at the 3rd neurosurgical clinic, “bagdasar – arseni” clinical hospital bucharest, between january 2002 and july 2012. the mean age of the 19 women and 5 men enrolled in the study was 51 years (range 21 – 75 years). the follow-up period ranged from 3 to 85 months (median: 46 months). results: the main presenting symptom was visual compromise in 83.3 % of the patients (20 cases). in addition, preoperative hormonal abnormalities were highlighted in 25 % of the patients (6 cases). mri and angio mri were the main radiological exams. in terms of surgery, a frontolateral approach was used in 21 patients (87.5 %) and an endoscopic endonasal extended transsphenoidal approach for the rest of the romanian neurosurgery (2013) xx 4: 401 – 435 423 3 patients (12.5 %). quick access to the tumor was achieved through these approaches; they were also minimally invasive with less brain exposure, therefore complications were being kept to a minimum. radical tumor removal was possible in all but 2 patients (91.7 %). postoperatively, vision improved in 19 patients (79.2 %), did not change in 4 patients (16.7 %) and worsened in one patient (4.2 %). no perioperative mortality was recorded. conclusion: the surgical treatment’s goal in the majority of patients with tuberculum sellae meningiomas is total resection. usually, this can be safely accomplished, with minimal postoperative complications and morbidity. the most important factors that influence the treatment strategies are the extent and duration of visual symptoms, the size of the tumor and the encasement of the anterior cerebral artery complex. key words: tuberculum sellae meningiomas, frontolateral approach, endoscopic endonasal, extended transsphenoidal approach. gasserian cystic schwanoma with intracavernous extension and skull base destruction. a microscopic extradural middle fossa approach v. munteanu, r. stanescu neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania backround: trigeminal schwannomas account for less than 8% of intracranial schwannomas. they originate within the ganglion, nerve root, or 1 of the 3 divisions of the trigeminal nerve. about 50% of these tumors are limited to the middle fossa, while 30% extend into the posterior fossa and 20% are dumbbell-shaped and extend into both fossae. diagnosis is best established with mri. the differential diagnosis includes meningioma, vestibular schwannoma, epidermoid lesions, and primary bone tumors of the skull base. methods: a 60 years old female pacient was admitted for numbness in the left trigeminal v b region. irm study revealed an extranevraxial left temporal tumor invading the cavernous sinus, cavum mecheli and the sphenoidal sinus. ophtalmologic examamination showed papiledema. results: surgery was performed and a predominent chystic tumor with solid component was identified and resected. postoperative neurological evolution was favorable marked only by a csf fisutla has been treated by instaling a lumbar drainage for 5 days. after the microdecompresion the pain has completely dissapear. histophatological exam was schwanoma antoni a. conclusion: extranevraxial skull baze schwanomas can be surgically removed safelly. csf fisula can be a compication that can be treated conservatively. key words: schwanoma, skull base, middle fossa approach. surgical treatment in huge foramen magnum tumor in children – case report b. secara1, a. st. iencean1, f. ziyad1, st. m. iencean1,2, i. poeata1,2 1emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania 2gr.t. popa university of medicine and pharmacy, neurosurgery, iasi, romania introduction: we present the clinical, imagistic, surgical findings and the outcome 424 abstracts 39th congress of the romanian society of neurosurgery at a 12-years old girl with huge foramen magnum tumor. patients and methods: a 12-years old girl presented with progressive proximal upper right extremity paresis for 3 weeks and spastic tetraparesis mainly on the right side for 3 days. mri imaging showed a huge foramen magnum gadolinium-enhancing lesion that compressed and displaced the spinal cord. the surgery consisted in suboccipital craniectomy with c1 laminectomy, c2 laminoplasty and microsurgical resection of the tumor. results: after surgery the patient made good neurological improvements, and the postoperative mri showed the resolution of spinal cord compression at cervical level. the anatomopathological report was meningothelial meningioma with many psamomatous bodies. conclusions: meningiomas are relatively uncommon in childhood. the intraoperative appearance of the tumor with the extent in the c2 foramen suggested a neurinoma. the recent onset and rapid progression are discordant with the tumoral size and the fast recovery. key words: meningioma, foramen magnum tumor, children. radio-induced neurosurgical brain lesions m.r. gorgan1,2, narcisa bucur1, angela neacsu1, aurelia mihaela sandu1,3, f.m. brehar1,2, v.m. pruna1,3, d. martin1, a. giovani1, o. zamfir1, anamaria gheorghiu1 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: radio-induced neurosurgical brain lesions occur inside previously radiation area, are not present at the time of radiotherapy, occur after a sufficiently long period of time following radiotherapy, have different histopathological diagnosis compare with the primary tumor and patients lack genetic predisposition for second tumor occurrence. radio-induced neurosurgical brain lesions are: meningiomas, vestibular schwannomas, gliomas, cavernomas, etc. material and method: we report 4 cases with radio-induced brain lesions, admitted into the fourth department of neurosurgery, emergency clinical hospital bagdasararseni. results: all 4 patients were males. primary disease was third ventricle tumor in 3 cases and scalp trichophytia in one case. three patients underwent surgery with tumor resection and were referred to adjuvant conventional whole-brain radiotherapy. one patient suffered from scalp trichophytia and was treated with scalp radiation. time to diagnosis of radioinduced brain lesion was 13, 17, 17, and 30 years following radiotherapy. two patients presented supratentorial meningiomas and two presented cerebellar hemisphere cavernomas. patients with meningiomas, were symptomatic, presented large tumors and required life-saving surgery. other imaging findings were diffuse brain atrophy and leukoencephalopathy. conclusions: radiotherapy can cause long-term complications and can induce new brain lesions development inside the radiation area. meningiomas and cavernomas may be radio-induced brain lesions and may occur following previous romanian neurosurgery (2013) xx 4: 401 – 435 425 radiotherapy. meningiomas grow to large size, requiring surgery. key words: radiotherapy, long-term complications, meningioma, cavernoma. endoscopic transnasal approach for pituitary adenoma – preliminary experience d. rotariu, f. ziyad, i. poeata ”gr. t. popa” university of medicine and pharmacy, iasi, neurosurgery, romania introduction: pituitary adenomas account for 10-15% of all brain tumors. the current approach to this sellar lesion is the transnasal endoscopic approach. we present our preliminary experience and results using this approach in the treatment of sellar region tumor. methods: we have included all patients with pituitary adenoma operated on using the endoscopic transnasal approach in the 3rd neurosurgical department of neurosurgery at “prof dr n oblu” clinical emergency hospital, iasi, romania since the introduction of the technique (may 2013). results: 6 cases (3 males and 3 females) were operated on using the endoscopic transnasal approach in the last 3 months. 4 of the patients had non secreting pituitary adenoma and 2 of them had prolactinomas with signs of pituitary apoplexy. the mean volume of the lesions was 13.52 cm3 (range 3.85-28.6cm3). cavernous sinus was invaded in 4 cases, 3 cases had type c supraselar extension and in 4 cases the sellar floor was invaded. all the patients had single nostril approach (right side) and 3 of them had a deviated nasal septum on the side of the approach. the sphenoid sinus had a simple structure (one single septum) in 4 cases and 2 had complex structure (3 septum). the mean time of procedure was 181 minutes (range 145 230). one single case, the first one, needed reconversion to microsurgery in order to control bleeding. gross total removal was achieved in one case and subtotal in the other 5 (but with no signs of compression on the adjacent structures). the pituitary gland was identified intra operatively and preserved in 5 cases, postoperatively no patient had new endocrine insufficiency. the main complication was represented by transitory diabetes insipidus in 2 cases, with no cases of infection or csf leak. conclusions: the transnasal endoscopic approach is a safe and efficient procedure for treatment of pituitary adenomas, with a low rate of surgical complication, and with high rates of endocrine function preservation given the high optics, which permit the identification and preservation of the normal pituitary gland. anyhow the duration of surgery is comparable to the microsurgical trans sphenoidal approach and will continue to lower with further gain of experience. key words: pituitary adenoma, endoscopic transsphenoidal approach. apoplexy in a recurrent pituitary adenoma – case report adriana dediu1,2, ligia tataranu1,2, v. ciubotaru1, violeta pruna3, m.r. gorgan1,2 1neurosurgical clinic, “bagdasar-arseni” clinical hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania 3“oftapro” clinic, bucharest, romania background: pituitary apoplexy is a clinical syndrome characterized by abrupt onset of severe signs of intracranial 426 abstracts 39th congress of the romanian society of neurosurgery hypertension, visual impairment, restriction of visual fields, paresis of ocular muscles, nausea, vertigo, meningismus, and/or decreased level of consciousness. the clinical syndrome is consequent to subarachnoid extravasation of blood and dural irritation, cranial nerve and hemispheric compression from lateral or superior extention of necrotic and/or hemorrhagic material, endocrine abnormalities from acute pituitary dysfunction. standard therapy of pituitary apoplexy includes decompression via transsphenoidal route and high-dose steroid treatment. case report: we report a case of a 29-year old woman with a history of transsphenoidal hypophysectomy for a prolactinoma 7 years ago and currently on bromocriptine and glucocorticoid and thyroid hormone replacement, who presented with galactorrhea, sudden severe headache, nausea, vomiting, diplopia and visual impairment on both eyes. computer tomography and contrastenhanced magnetic resonance imaging of the head proved a large sellar tumor with extension to the suprasellar region with intratumoral hemorrhagic zones. the treatment of choice was resection of the sellar mass by transsphenoidal approach. histological examination revealed a pituitary adenoma mostly acidophil, with intratumoral hemorrhage, highly suggestive for pituitary apoplexy. the outcome was favorable and the patient was discharged in a good condition but with necessity for hormonal replacement as a treatment of pituitary insufficiency. conclusions: pituitary apoplexy remains a potentially life-threatening disease. this case demonstrates that apoplexy can occur and should be suspected even in a patient with a previous history of hypophysectomy. key words: pituitary adenoma, pituitary apoplexy, transsphenoidal approach. colloid cyst – an unusual location. case report d. păunescu1,2, ligia tataranu1,2, v. ciubotaru1, m.r. gorgan1,2 1neurosurgical clinic, “bagdasar-arseni” clinical hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania background: colloid cysts represents 0.2 2% of brain tumors and less than 1% of symptomatic brain tumors. they are found throughout the neuroaxis but over 99% of them develop in the third ventricle. colloid cysts of the pituitary gland are very rare pathological lesions occurring in sellar region. case presentation: a 67-year-old woman presented to the endocrinology department with a 3-months history of frontal and retroocular persistent headache. no focal neurological deficits and no signs of intracranial hypertension were present and hormonal biomarkers were in normal range. magnetic resonance imaging (mri) of the brain showed a relatively homogeneous sellar mass extended superiorly into the suprasellar cistern and impinge on the optic chiasm. visual field examination shows optochiasmatic syndrome. tumor removal proceeded in a standard way by transsphenoidal approach and the pathologic examination confirmed the diagnosis of colloid cyst. at the 3rd month followup visit the patient did not show any endocrinological or focal neurological deficits. mri brain images romanian neurosurgery (2013) xx 4: 401 – 435 427 revealed total resection of colloid cyst and no compression on opic chiasma. conclusions: the absolute differentiation of pituitary macroadenomas from rare nonpituitary origin sellar tumours is often not possible prior to invasive therapeutic or diagnostic procedures. key words: colloid cyst, transsphenoidal approach. glucose and insulin expression in various types and grades of brain tumors oana alexandru1, l. ene1, ligia tataranu2, v. ciubotaru2, alisa popescu1,3, ada maria georgescu4, v. pruna2, anica dricu3 ¹department of neurology, university of medicine and pharmacy, craiova, romania 2neurosurgical clinic, „bagdasar-arseni” clinical hospital, „carol davila” university of medicine and pharmacy, bucharest, romania 3division of biochemistry, university of medicine and pharmacy, craiova, romania 4“medico science” srl, craiova, romania introduction: in the last years, many authors suggest the existence of an association between different components of metabolic syndrome and various cancers. two important components of metabolic syndrome are hyperglycemia and hyperinsulinemia. both of them had already been linked to increased risk of cancers: pancreas, breast, endometrial or prostate. however the correlation of the glucose and insulin level with various types and grades of brain tumors remains unclear. material and methods: in this article we analyzed the values of plasma glycemia and insulin in 267 patients consecutively diagnosed with various types of brain tumors. results: our results showed no correlation between the glycemia and brain tumor types or grades. high plasma levels of insulin were found in brain metastasis and astrocytomas while the other types of brain tumors (meningiomas and glioblastomas) had lower levels of the peptide. the expression of insulin was also higher in brain metastasis and grade 3 brain tumors compared with the grades 1, 2 and 4 brain tumors. key words: insulin level, brain tumor, astrocitoma, glioblastoma, meningioma, brain metastasis. spinal associated with von recklinghausen’s disease k. istvan clinical emergency hospital, neurosurgery, tg. mures, romania introduction: the neurofibromatosis type 1 (nf1) was first described by von recklinghausen and festscher, and has been known as the von recklinghausen’s disease also. it is inherited as an autosomal dominant trait, therefore, is a hereditary condition. at least eight forms of neurofibromatosis have been recognized, but the most common is the (nf1), with a prevalence of 1:2200 to 3000 births. when associated with von recklighausen’s disease, the tumors are usually multiple, and may occur at numerous levels of the spinal cord. the signs and symptoms of this condition vary widely among affected people. the most common sign on the skin are multiple neurofibromas that can occur anywhere in the body. another highly characteristic feature on the skin is the presence of café au lait (coffee with milk) pigmentation. lisch 428 abstracts 39th congress of the romanian society of neurosurgery nodules (pigmented hamartomas of the iris), translucent brown-pigmented spots on the iris, are found in nearly all affected individuals. bone lesions, cardiovascular and neurological abnormalities are others manifestations of this disease. abnormalities that involve neurological system includes central nervous system tumours, macrocephaly, mental deficiency, seizures, short statute and scoliosis. patients and methods: a 32 years-old female patient was referred to our department, due to full motor loss (immobilized to bed), localized at the level of the inferior members and urinary and defecation disfunctions. in general physical examination we notice the presence of papules, subcutaneous nodules and café au lait pigmentation in many parts of the body. after mri-examinaton we observed the presence, of subdural tumoral lesions at the l2-l5 levels. complete resection of the lesions was performed, through a l2-l5 laminectomy, confirming the initial diagnosis. thoracic and abdominal ct also showed multisistemic involvance. the general clinical, imagistic and intraoperative findings, completed with the histopathological examination confirmed the diagnosis of von recklinghausen’s disease. a modest neurological improvement was observed during the initial postoperative course. the patient could walk independently 5 days later, with the preservation of urinary and defecation functions. postoperative follow-up was difficult in this case, she came back to our institute one year after surgery. clinical signs were bilateral cervicobrachialgia, paraparesis, bilateral sensitive radiculopathy c3c7 levels. mri showed multiple subdural, extramedullary tumoral masses at the c2-c6 levels, with intraforaminal extension. a c2-c6 laminectomy was performed with the microscopical resection of the tumoral masses. after surgery the patient had favorable outcome with the remission of preoperative clinical signs. results: the best results are obtained with patients showing minimal neurological deficits during the pre-operative period. little improvement may be expected from the patients who develop complete transection syndrome during the postoperative period. conclusions: is one of the few genetic diseases, which requires neurosurgical implications. prenatal diagnosis is possible, but difficult. there is about a 5% increase in risk for various cancers, including brain tumor. plexiform neurofibromas can become malignant. there is also an increased rate of scoliosis in nf1, with progresses around the time of pubert. key words: von recklinghausen’s disease, neurofibromatosis 1, neurofibroma. cerebral avm-related intracranial hemorrhageclinical considerations anca smaranda natalia predoaica1, b. iliescu2, z. fayad1, al. chiriac1, d. rotariu1, i. poeata1,2 1emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania 2gr.t. popa university of medicine and pharmacy, neurosurgery, iasi, romania introduction: arteriovenous malformations (avms), part of intracranial vascular malformations group, are leading cause of intracerebral haemorrhage in young adults and the most common presenting symptom for patients with avms is brain hemorrhage that can cause devastating neurological deterioration. romanian neurosurgery (2013) xx 4: 401 – 435 429 patiens and methods: between 2009 and 2013, medical records of 44 patients reffered to university hospital “n. oblu” iasi, presented with intracranial hemorrhage caused by cerebral arteriovenous malformation (avm), which was diagnosed by ct scan factors followed in terms of their influence on the level of consciousness at admission were: volume of intraventricular hematoma, acute hydrocephalus, intraparenchymal hematoma. results: diagnosis of avms was confirmed with mra, angio ct scan, and/or seldinger angiogram. nineteen patients had intraparenchymal supratentorial, five had intraparenchymal posterior fossa, twenty had intraventricular hemorrhage clinical status ranged from mild impairment to profound coma. conclusions: all factors we follow significantly contributed to the development of serious disturbance of consciousness in the acute stage following intracranial hemorrhage. left untreated, can cause a progression of symptoms that can lead to permanent disabilities or death. key words: cerebral arteriovenous malformations, intracranial hemorrhage. posttraumatic epicranian arteriovenous fistula – case report m.r. gorgan, f.m. brehar, aurelia mihaela sandu, v.m. pruna, anamaria gheorghiu fourth department of neurosurgery, emergency clinical hospital bagdasar-arseni posttraumatic arterio-venous fistulas are rare lesions which occur at various periods of time after the initial traumatic injury. epicranian locations are usually related to open wound injuries of the scalp which involve major feeding arteries of the scalp. the authors of this presentation report the case of a 28 year-old male which presented an open injury of the scalp with the involvement of the right superficial temporal artery. the wound was treated in another department. at one month after the initial injury, patient presented tinnitus and right hemicrania. patient was admitted in our department and local exam revealed a subcutaneous pulsatile right temporal mass and right temporal bruit. patient had no neurological deficits. cerebral angiography (which included external carotid catheterization) showed an arteriovenous fistula between right superficial temporal artery and right external jugular vein. we chose to treat surgically this lesion due to its superficial and accessible location. a linear right temporal preauricular incision was performed and after subcutaneous dissection, an arterioven ous fistula with feeders from right superficial temporal artery was found, located superficial to temporal muscle fascia. total resection was performed. postoperative cerebral angiography showed total removal of the lesion. patient was discharged with no neurological deficits. tinnitus and bruit remitted completely. posttraumatic epicranian arteriovenous fistulas are rare lesions which are suitable to surgical resection due to their superficial and accessible location. key words: arteriovenous fistula, posttraumatic, surgical resection. 430 abstracts 39th congress of the romanian society of neurosurgery complications related to severe cerebral vasospasm after aneurysmal subarachnoid hemorrhage d.a. petrescu, l. danaila, st. dima, otilia petrescu, c. preoteasa, s. suditu national institute of neurology and neurovascular diseases bucharest, neurosurgery, romania introduction: vasospasm is a common complication that may occur after aneurysmal subarachnoid hemorrhage. irritating blood breakdown products cause the walls of an artery to contract and spasm. the prolonged smooth muscle contraction involves some alteration in the structure of the arterial wall (hypertrophy, fibrosis, degeneration), that reduces blood flow to a specific vascular territory causing a secondary stroke. patients and methods: our study includes 1294 cases of cerebral aneurysms, diagnosed angiographic (38,64%), out of 3348 cerebral angiographies, performed in neurosurgical department of national institute of neurology and neurovascular diseases, during a period of 5 years. of all discovered aneurysms, 1186 (91,65%) were broken and they started with subarachnoid and/or cerebral hemorrhage. the remaining 108 (8,35%), were incidentally detected during investigations for other diseases. 1242 (95,98%) of all detected aneurysms were treated with surgical clipping and only 28 (0,84%), were treated with endovascular procedures. the remaining 24 (0,71%) were not treated, either because of refusal, or because bad conditions that resulted in death. a total of 423 cases with broken aneurysms (35,66%) had a deterioration of awareness and neurological deficits, secondary outbreaks of cerebral hemorrhage and/or angiographic demonstrated vasospasm. the vasospam was present in a number of 318 cases (26,81%). the meaning of the present paper, we have defined the severe vasospasm, that change of vascular diameter, angiographic, demonstrable, responsible exclusively for major neurological deficits, stable and irreversible after the conventional therapy applied in accordance with medical protocols, which led to the invalidity or death. results: 129 patients (10,88%) had a good recovery, after correct treatment of vasospasm with nimodipine in continuous intravenous perfusion or local intra arterial, 113 (9,53%) survived with a minimal disability, 50 (4,21%) survived with major focal neurological deficits and 26 (2,19%) died. both, the correct treatment of aneurysms and the postoperative presence of vasospasm were angiographic demonstrated in all cases. conclusions: recovery and prognosis are highly variable and largely dependent on the severity of the initial vasospasm. key words: cerebral aneurysm, subarachnoid hemorrhage, vasospasm, cerebral angiography. subarachnoid haemorrhage in multiple intracranial aneurysms v. munteanu, r. stanescu, diaconu nicoleta neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania backround: intracranial aneurysms are common and are located on the large arteries of the circle of willis and its branches. autopsy series uncover them in 0.4–3.6% of individuals, whereas cerebral romanian neurosurgery (2013) xx 4: 401 – 435 431 angiography documents incidental aneurysms in 3.7–6.0% of patients. therefore, roughly 2% of all individuals harbor aneurysms. approximately 80–85% of these lesions are in the anterior cerebral circulation, and the rest are in the posterior circulation. cerebral aneurysms are multiple in 25% of cases methods: case a – a 51 years old woman was admitted for headache, dysarthria, severe episthaxis, and balance disorder. case b a 64 years old man was admitted for headache, neck pain, balance disorder and vomiting. results case a four-vessel angiography disclosed sacular aneurysm at the bifurcation of the left mca, with maximum diameter of 4.46 mm and neck of 2.36, and another one aprox. 3mm distance from the first aneurysm anterior oriented with maximum diameter of 4.73mm, neck of 2.27mm. case bfour vessel angiography disclosed ruptured aneurysm with daughter sac inserted at the origin of the left pericalosal artery, with 3,9/3.5mm diameter, 2mm neck. in both cases ct scan revealed sah. conclusion: familial aneurysms are generally larger at time of rupture and more likely to be multiple than sporadic aneurysms. the development of large and multiple aneurysms may be related to genetic factors that determine defects of the arterial wall. key words: intracranial ruptured aneurysms, four-vessel angiography, sah, genetic factors. surgical treatment of basilar apex aneurysm-case presentation a. spatariu1, c. pascal1, p. petrescu1, barari1, al. tascu1,2 11st neurosurgical department bagdasar arseni hospital bucurest. romania 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest posterior circulation aneurysms represent a special challenge to neurosurgeons because of the deep location and intimate reports with brainstem, cranial nerves and perforating arteries. despite progress in neurosurgical techniques, neuroanastesiology, neuroradiology, the surgical treatment of basilar apex aneurysms shows a higher morbidity and mortality than aneurysms of anterior circulation. the inability to perform microsurgical clipping of basilar apex aneurysms has led to the development of other treatment modalities such as endovascular therapy. however, endovascular coil occlusion is less durable than microsurgery, as shown by its higher rates of aneurysm recanalization and regrowth and microsurgery provided better outcome in some specific basilar apex aneurysms. in this paper we present the case of a patient with subarachnoid hemorrhage hunt & hess1becouse of a rupture of basilar apex aneurysm susccessfuly treated by microsurgical clipping using a subtemporal route. outcome was assessed by glasgow outcome scale : gos-gr. 432 abstracts 39th congress of the romanian society of neurosurgery bibliography: angiographic and clinical results in 316 coil-treated basilar artery bifurcation aneurysms. henkes h, fischer s, mariushi w, weber w, liebig t, miloslavski e, brew s, kühne d j neurosurg. 2005 dec; 103(6):990-9. schievink wi, wijdicks ef, piepgras dg, chu cp, o'fallon wm, whisnant jp.the poor prognosis of ruptured intracranial aneurysms of the posterior circulation. j neurosurg. 1995 may; 82(5):791-5. bavinzski g, killer m, gruber a, reinprecht a, gross ce, richling b.treatment of basilar artery bifurcation aneurysms by using guglielmi detachable coils: a 6-year experience. j neurosurg. 1999 may; 90(5):843-52. eskridge jm, song jk. endovascular embolization of 150 basilar tip aneurysms with guglielmi detachable coils: results of the food and drug administration multicenter clinical trial.j neurosurg. 1998 jul; 89(1):81-6. vallee jn, aymard a, vicaut e, reis m, merland jj. endovascular treatment of basilar tip aneurysms with guglielmi detachable coils: predictors of immediate and long-term results with multivariate analysis 6-year experience. radiology. 2003;226:867–879. volumetric assessment of intracranial aneurysms from 3d rotational angiography al. chiriac, b. iliescu, f. ziyad, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi, neurosurgery, romania introduction: the 3d rotational angiography is an increasingly used method for cerebral aneurysms treatment planning. volume measurement techniques of intracranial aneurysms from 3d rotational angiography vary on different factor settings and, therefore, are operator-dependent. methods: in this study we evaluate the application and the precision of ellipsoidal approximation (mathematics and computer technique) and software methods to measure intracranial aneurysms volume starting from planar (dr and sd) and 3dimensional (3d) angiographic images. retrospective assessment of aneurysm volume was achieved with two measurement methods by using twodimensional copies or 3d reconstruction images (digital or printed form in sagittal and coronal angiography section) obtained with a siemens artis angiograph with rotational digital subtraction possibilities. the reliability of the methods was statistically compared in a clinical setting of 42 angiograms and 100 measurements performed by the same users. results: based on statistical analysis obtained from the friedman test we found statistically significant differences at p £ 0,05 threshold between the three techniques of analysis [?2 (2) = 8.714, p = 0.013] conclusions: this study suggests that both techniques could be used for clinical applications with similar efficiency results. key words: aneurysm, 3d rotational angiography. romanian neurosurgery (2013) xx 4: 401 – 435 433 the effect of epidural instillation of dexamethasone on local scaring tissue after lumbar microdiscectomy g. vasilescu, v. ciubotaru, b. ghinguleac, a. spatariu neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania background: lumbar disc herniation is a pathological condition that appears in 1% to 3% of the general population, being influenced by age, usually between 30 and 50 years, gender, male to female ratio is higher in male (2:1), working conditions, with higher incidence on patient who have an intense physical work, professional drivers etc. in the literature the overall recurrence rate is around 7 to 12% of the total cases operated by microdiscectomy. in the senior authors series the recurrence rate is 3.5%. methods: the authors have analyzed the incidence of local compressive tissue after lumbar disc herniation microdiscectomy requiring surgical removal comparing the patients where dexamethasone was used intraoperative and those where corticoid instillation was not performed. length of the surgical procedure, difficulty of dissection and the volume of the compressive/adherent epidural tissue were chosen as the comparison criteria. results: as a result of corticoid epidural instillation after microdiscectomy the adherential scaring process is reduced dramatically with the condition of performing a proper foraminectomy when the genuine microdiscectomy is done. the overall volume of compressive scar requiring surgical removal after microdiscectomy was not influenced by the use of dexamethasone and may depend on personal factors. the duration of the surgical procedure, the ease of the dissection process itself and the much lower occurrence of dural tear are the main benefits of the epidural corticoid instillation. conclusion: the epidural instillation of one vial of dexamethasone after microdiscectomy represents a simple gesture devoid of risk that is useful for those cases where a second surgical decompressive procedure is needed. key words: epidural instillation, dexamethasone, microdiscectomy. lumbar-pelvic stabilization using iliac screws in a case of a lumbar-sacral giant tumor m. catana1, v.m. prună1,2, m.r. gorgan1,3 1clinical hospital “bagdasar-arseni”, bucharest, romania 2ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: the first lumkmbar-pelvic stabilization was described in 1982 by allen and ferguson. indications for sacroiliac fixation include lumbosacral destructive processes (tumors, infections, trauma), pseudoarthrosis l5-s1, l5-s1, high grade spondylolisthesis, symptomatic lumbar spine deformities. symptoms consist in pain (in about 96% of cases), radiculopathy or cauda equine syndrome. the investigation of choice is the mri with sagittal, coronal and axial acquisitions. case presentation: a 58 y.o. woman, with breast cancer, was admitted in our clinic with low back pain, bilateral l5-s1 sciatica and cauda equina syndrome, frankel d. lumbar spine mri shows a spinal tumor 434 abstracts 39th congress of the romanian society of neurosurgery that destroyed the l5, s1 vertebral bodies, causing severe l5, s1 nerve roots and dural compression. the surgical treatment was performed by a total l5 vertebrectomy and partial s1 (involved by tumor) and the spinal canal and the neuroforamina was decompressed. spinal reconstruction was achieved using acrylic cement with contention in vertebral body l4 and s2 segment of the sacrum. surgical stabilization was performed with titanium polyaxial screws into l3-l4s1 bilateral pedicles and two titanium screws (with a length of 90 mm) in both iliac wings. we used the zodiac spinal fixation system by alfa tech. the technique of the placement of iliac screws after the posterior superior iliac spines (psis) were identified, the iliac screws insertion points were located at about 1 cm inferior to the psis and 1 cm proximal to the distal edge of psis. the screws were about 90 mm in length and 8.5 mm in diameter. the two iliac screws were connected to the system via two connectors. postoperative outcome was favorable and local pain disappeared. neurological deficits begin to improve and the spinal stability was achieved. no postoperative complications. hystological examination: metastasis of adenocarcinoma (possible breast cancer).the patient was discharged 8 days postoperatively. conclusions: the lumbar-pelvic fixation is a relatively easy technique, and stabilisation with transiliac screws is sometimes necessary, when the tumor invades the lumbar-sacral junction and the spinal stability was definitely compromised. key words: lumbar-sacral junction, vertebral tumor, lumbar-pelvic fixation. titanium expandable cage – an excelent choice for the surgical treatment of cervical spinal metastasis m. catana1, v.m. prună1,2, m.r. gorgan1,3 1clinical hospital “bagdasar-arseni”, bucharest, romania 2ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: spinal metastases are the most common malignant lesions of the spine (over 94 %). clinical symptoms consist in neck pain (90%) and various degrees of motor deficits (over 50% of patients). the most common type are osteolytic when osseous destruction can lead to fracture of the vertebral body, spinal instability and deformity of the spine. because the majority of cervical metastases develops in the vertebral body, the anterior cervical approach is most suitable for surgery. the surgery goals are: decompression of spinal cord, spinal reconstruction and spinal stability. cervical spine reconstruction after corporectomy can be done using several methods, such as: bone graft, bone cement, titanium mash, expandable cage. the expandable cages are cylindrical devices, with different shapes and sizes which facilitates stability of the spine. the cage can be filled with bone allograft or bone substitute. case presentation: a 69 y. o. woman, was admitted in our clinic for neck pain, incomplete tetraplegia, with c6 level (frankel d). cervical mri reveals a c6 vertebral body tumor, with spinal cord compression and vertebral collapse. no history of neoplasticdisease, but the ct scan of the thorax showed an expansive process in the right inferior lobe. no other romanian neurosurgery (2013) xx 4: 401 – 435 435 lesions in the brain or abdominal cavity. the surgery was performed by an anterior cervical approach with c6 corporectomy, spinal cord decompression and spinal reconstruction using titanium expandable cage (cage-loc by biotek), filled with bone substitute (synthetic phosphocalcic hydroxyapatite nanogel). extension mechanism was secured by 2 screws that block the mechanism extension. pathological examination found metastatic adenocarcinoma, probably pulmonary origin. postoperatively the patient's evolution was favorable, drainage was suppressed at 24 hours after surgery. second day, she was mobilized. she was discharged at 7 days after surgery. conclusions: fully ablation of the cervical spinal metastasis can be easily performed through a cervical anterior approach. once the corporectomy was done, reconstruction of the vertebral body and spine stabilization are mandatory. the expandable cages represent an excellent and safe option for the vertebral reconstruction. key words: spinal metastasis, cervical vertebral body, expandable cage. microsoft word 11.rotariud_pituitary_f.docx romanian neurosurgery (2011) xviii 4: 465 475 465 pituitary adenoma, therapeutic approach and surgical results d. rotariu1, s. gaivas1, z. faiyad2, a.st. iencean2, i. poeată3 1phd student “gr.t. popa” university of medicine and pharmacy iasi 23rd department of neurosurgery “prof.dr. n. oblu” clinical emergency hospital, iasi 3“gr.t. popa” university of medicine and pharmacy iasi abstract objectives: pituitary adenoma represents the most frequent tumour encountered in the sellar region. we have proposed to review the principles of diagnosis and treatments and to analyze their standard protocol of approaching pituitary lesions. material and method: we have retrospectively analyzed the cases of pituitary adenoma between jan 2006 and dec 2010, we studied presenting symptoms, hormonal status, local extension, surgical approach, tumor histology, type of resection, tumor volume, cavernous sinus invasion, surgical corridors, recurrence rate, intra operative and postoperative complications results: 72 patients were included in the study, with no significant difference between sexes, the pathology was dominated by pituitary macro adenomas in 47 cases, regarding the hormonal status 51.3% were non secreting pituitary adenomas, the rate of operability in our series was 65.2%, the surgical indication has been given mainly by the hormonal status and involvement of the optic apparatus which in our series was 51%, the invasion of the cavernous sinus has been appreciated according the knosp criteria (7) and grade 3 and 4 was present in 44% of the cases. the most used surgical approach was the pterional approach in 83% and the remaining 17% by the transsphenoidal approach. the most frequent surgical corridor was represented by the prechiasmatic route in 54%, gross total resection was achieved in 51%. the most frequent postoperative complication encountered in our series was represented from systemic complication the meningitis 13%, as for endocrine complication it was represented by transitory diabetes insipidus in 23.4% and siadh in 4.2% (2 cases). the follow up at 3 months showed no cases of early recurrence, from the group of patient with str 6 were sent to radiotherapy. the follow up at 1 year has comprised 3 deaths, 3 cases of hydrocephalus treated with ventriculoperitoneal derivation, 19 cases were with no imagistic or clinical symptoms of tumour and 22 presented with imagistic evidence of stable residual tumour with no clinical symptoms. conclusions: the main surgical indication in pituitary adenomas is represented by the secreting hormonal status of the patient (excepting prolactin secreting tumours) and the impairment of the vision. the most frequent surgical approach was represented by the transcranial (pterional) approach due to the large dimensions and invasiveness of the tumours presented in our series but also the 466 d. rotariu et al pituitary adenoma surgical team preference (in the absence of intracranial endoscopy at those times). keywords: pituitary adenoma, pituitary apoplexy, prolactinoma, sellar region. introduction sellar tumours have a large histological variability and represent approximately 1015% of all intracranial neoplasms, from them pituitary adenomas represent 95% of lesions. pituitary adenomas can be classified according their size in micro adenomas (<10mm), macro adenomas (>10mm) and giant adenomas (>40mm) (20). according to their functional status pituitary adenomas are classified as non secreting pituitary adenomas (nspa) or as secreting pituitary adenomas (spa) with different subtypes depending on the secreted hormone (prolactin/growth hormone etc). at presentation there are three main types of complaints: 1. symptoms caused by tumor dimension with compression to the adjacent structures (optic chiasm/ diencephalon/cavernous sinus) (24) 2. symptoms produced by abnormal secretion of hormones insufficiency/hyper secretion (acromegaly/cushing’s disease) 3. incidental findings – patient explored for some other pathology (6, 8). a particular clinical presentation is represented by pituitary apoplexy with altered level of consciousness, intracranial hypertension signs, blindness caused by sudden expansion of tumor volume secondary to intratumoral hemorrhage/infarction and with clear surgical indication (18, 24). the actual management of those tumors varies from surveillance, medical treatment, surgery or a combined approach; however surgery remains the main therapeutic method (25). material and method we have retrospectively analyzed all cases of pituitary adenomas which were addressed to the 3rd neurosurgical department at n. oblu hospital between jan 2006 and dec 2010, during this period of time eighty three patients were consulted and 72 cases were included in the study, we have excluded the patients younger than eighteen years old, patients with previous surgery for pituitary adenomas and patients who refused the proposed therapeutic method according to our protocol (figure 1 and 2). all patients underwent clinical neurological evaluation: significant neurological deficits were notes (3rd nerve palsy, signs of hydrocephalus, altered level of conscious, visual impairments) and the time interval from beginning of symptoms to presentation. imagistic evaluation consisted in contrast enhanced mri with details upon the sellar region. tumor dimension was recorded and also the invasion into the adjacent structures (3rd ventricle/sphenoid sinus) invasion of the cavernous sinus was assessed according to knosp classification, routinely the surgical site was analyzed by ct in the first day postoperatively and then by contrast enhanced mri at 3 and 12 months. unoperated patients were imagistic followed up using contrast enhanced mri at 12 months. endocrine evaluation consisted in evaluation for free cortisol, acth, prl, gh, tsh, ft4, to assess for endocrine derangements, except 2 cases who presented with pituitary apoplexy. ophthalmologic evaluation consisted in visual acuity determination and perimetry. the patients were assessed for treatment according to the tumor size, endocrine romanian neurosurgery (2011) xviii 4: 465 475 467 status and visual disturbance using the following algorithms, treatment options in our series were represented by surveillance, medical treatment and surgery. there were two main surgical techniques: trans sphenoid or trans cranial approach, we have noted the surgical corridors used during intervention, the degree of resection by surgeon intra operative appreciation and on ct scans performed on the 1st day postoperatively, the postoperatively complications (local/systemic). results we have included in our study a number of 72 patients who presented for pituitary adenoma pathology. the cohort was composed of 39 females and 33 males, with a mean age of 50.0 years (ranged 16-75 years). our series contains a number of 25 cases of micro adenomas from which 6 undergone surgical resection and 47 cases of macro adenomas, with 41 cases operated on. the majority of patients who underwent resection sought medical attention for symptoms related to visual impairment (51%). the remaining patients complained of severe headaches (19%), symptoms related to hormone production (16%) or cranial nerve palsy/epileptic seizures (7% both). 15% of our patients presented with pituitary apoplexy confirmed by the mr imaging and the intra operative aspects. figure 1 therapeutic approach in pituitary micro adenomas (<10mm) according to their endocrine functioning status. microadenoma <10 mm hormone hypersecretion prolactinoma dopamine antagonist other (gh, acth, tsh) transphenoidal surgery no hormone hypersecretion no mass effect clinical reassessment mri at 1,2,5 years no change conservative treatment tumor growth visual simptoms pituitary insufficiency surgery 468 d. rotariu et al pituitary adenoma figure 2 therapeutic approach in pituitary macro adenoma (>10mm) according to their functional endocrine status and their effect upon intracranial optic structures preoperative imaging revealed micro adenomas in 34.7% and macro adenomas (diameter large than 10 mm) in 65.3%. invasion of the cavernous sinus was appreciated using the knosp criteria (7) and was grade 2 in 35%, grade 3 in 27% and grade 4 in 17 %, the suprasellar tumor extension was detected in 58.3%. in our cohort none of the patients had undergone previous resection. regarding the hormonal status our series contains 51.3% cases of nonfunctioning adenomas, 37.5 % presented with secreting adenomas from which 55.5% (15 cases) of gh secreting adenomas and 37,7% prolactinomas (10 cases). surgical results in our series 47 patients (65.2%) underwent surgical resection, from them 39 incidental macroadenoma complete hormonal lab test for rulling out a hypersecretion + ophthalmological consultation proven hypersecretion usual treatment for secretant macroadenomas no hypersecretion visual simptoms? yes prolactin measurement > 200 ng/ml dopamine antagonist < 200 ng/ml surgery no follow-up mri volume growth yes surgery (eventually monitoring) no romanian neurosurgery (2011) xviii 4: 465 475 469 operations (83%) were performed using a transcranial route (pterional approach), the rest of the operated patients (8 cases) had a sublabial transsphenoidal approach. the unoperated patients (25 cases) 34.8% beneficiated from conservatory treatment (dopaminergic agonists) in 12 cases (48%), imagistic surveillance in 11 patients, and 2 patients were sent to gamma knife according to their preference. the mean time for surgical intervention was 3h30’ with no clear difference between the transcranial and transsphenoidal approaches. the degree of resection in our series was noted according to the subjective intraoperative appreciation and objectively sustained on the 1st day ct scan, as result we have obtained gross total resection (gtr) in 51% of operated cases. the most frequent surgical corridor used was represented by the pre chiasmatic route in 54 % and opticocarotidian route in 24%, the transsphenoidal route was used in 12 % of the cases while the translaminaterminalis and carotidooculomotor route were used in 6% and 4% respectively the surgical complications were divided into systemic complications and were represented by meningitis in 6 cases, as for local surgical complications we had 16 cases of hematomas in the surgical bed from them only 1 necessitating evacuation and 2 cases of csf leak 1 spontaneous closed. the postoperative status was assessed and revealed no endocrine deficiency in 60 % cases, transitory diabetes insipidus in 23.4 %, 4.2% had siadh and 6% had panhypopituitarism. the outcome of patients operated on for pituitary adenomas consisted in 2 per operative deaths (death in the first 30 days after surgery – 1 case of pulmonary embolism and another of severe water electrolytes imbalance), 4 cases had no amelioration of visual symptoms, and 1 patient had a new neurological deficit (left hemiparesis); the rest of the patients had a good surgical outcome. at three months follow up we had one early recurrence (ap: adenocarcinoma), 22 patients had no imagistic evidence of intracranial tumor, from the group of patients with residual tumor 6 were sent to radiotherapy and the rest were symptom free and kept under surveillance. the follow up at 1 year comprised contrast enhanced mri evaluation and clinical neurological examination, 19 patients had no imagistic or clinical evidence of residual tumor, in 21 patients the imagistic evaluation detected residual tumour but without clinical symptoms, this category of patients being kept under imagistic and endocrine surveillance, we had three recurrences and the treatment was represented by surgery. the mortality in our group at 1 year was 6.3% (3 patients), as late complications we had 3 cases of hydrocephalus 2 in the group of gtr an 1 in the group of stg – all treated with ventriculoperitoneal derivation. table 1 early complications in 47 patients operated for pituitary adenoma type of complication no. of patients % treatment meningitis 6 (13) antibiotics blood collection 16 (34) evacuation (1) csf leak 2 (4.2) surgical closure (1) transitory di 11 (23.4) desmopresin siadh 2 (4.2) water restriction panhypopituitarism 3 (6.3) hormone replacement 470 d. rotariu et al pituitary adenoma a b c figure 3 t1 contrast enhanced irm coronal a and axial b sections showing a hypo intense, non enhancing lesion, in the left pituitary gland c ct scan in the 1st day after transsphenoidal surgery in a 60 y o female with acromegaly and gh 47.8μg/l a b c d e f figure 4 mri examination t1 with contrast enhancement axial (a)/sagital (c) and t2 axial showing a sellar and suprasellar mass hyperintense in t1 and axial t2 (b) with inhomogeneous contrast enhancement suggestive for pituitary apoplexy, (d) ct scan on 1st day postoperatively (transcranian) in the same 50y old f patient in treatment with dostinex® for a known prolactinoma who presented with visual loss and impaired consciousness. (e) and (f) t1 contrast enhanced mri at 3 months showing a residual tumor in the left cavernous sinus. romanian neurosurgery (2011) xviii 4: 465 475 471 discussion our experience has brought us to the conclusion that the treatment of pituitary adenomas should be multidisciplinary, namely, endocrinological, surgical and radiotherapeutical. the order in which treatment is applied is dependent on the tumour size, hormonal status of the patient and the clinical condition of the patient. the goals of surgery are to remove the tumor, relieve the mass effect, improve visual abnormalities, reduce hormone hypersecretion to normal levels, and preserve normal pituitary function (16), surgery is the first-line treatment in pituitary adenomas with compression upon optic structures and visual impairment and in all actively secreting adenomas except prolactinomas (16). either transcranial or transsphenoidal approaches can be adopted in the surgical treatment of pituitary adenomas, in our cohort the most used surgical approach was transcranial (pterional) due to the preference of the operative team and due to the complexity of the cases (cs invasion knosp 3 and 4 in 40%) in our series cavernous sinus invasion was directly correlated with str, safe complete resection of tumor lateral to the carotid artery remaining nearly impossible with no regards to the surgical corridor used (3, 22, 23), also the suprasellar extension of the tumor (58.3% in our series), recommend considering the transcranial approach as the natural choice unless the tumour suspected to be hemorrhagic (1, 4). in reality, surgery is very effective in relieving the mass effect; however, most patients harboring a large lesion will require additional treatment to produce hormonal remission and prevent regrowth of residual tumor, and many will require hormone replacement therapy to reestablish a normal hormonal balance (3, 8, 27). radiation treatment (conventional, stereotactic, or protonbeam) of the pituitary is most commonly used as an adjunctive treatment after incomplete tumor resection (19). radiotherapy reduces the risk of residual tumor enlargement and offers the chance of permanent control of hormone hyper secretion, in our series 6 patients of 23 with incomplete resection were treated using stereotactic radiation therapy. in our cohort the rate of gross total resection was achieved in only 51% of the cases that is lower than literature data (1, 23). surgical indication is also guided by the functional status of the pituitary adenoma, all secreting pituitary adenomas have surgical indication except prolactinomas, in which the first line of treatment is oral administration of a dopamine agonist, such as cabergoline, bromocriptine, or pergolide (8, 16) (more than 90% of patients respond to this treatment with reduction in the serum prl level and with tumor shrinkage). it is known that approximately 60% of patients with a gh-producing tumor are found to harbor a macro adenoma that is often invasive, making its complete removal unlikely this is the reason we prefer to operate gh secreting pituitary adenomas at moment of diagnosis, without previously use of somatostatin analog (attitude that is still a controversy in the literature) (8, 16). on the other hand there is a clear surgical indication for acth secreting adenomas, in which there is no effective medical therapy to reduce acth production or decrease tumor size, surgical removal of the lesion being the first choice of therapy. if the surgery is not successful, pituitary 472 d. rotariu et al pituitary adenoma irradiation should be considered and medical therapy with ketoconazole. as for non functional adenomas, there is no effective medical treatment, surgery being the primary therapeutic option according to their volume and clinical symptoms (15). another clear surgical indication, given by the clinical status of the patient, is represented by pituitary apoplexy – surgical emergency (comprises visual deficits, ophthalmoplegy, hypopituitarism, altered levels of consciousness) the apoplexy rate in our group was 15%, greater than data in the literature (10%) (1, 12), the apoplexy was encountered only in macro adenomas in our series from which 13 were non functional macro adenomas and 2 were gh secreting adenomas. in the literature there are several theories concerning the precipitating factors in apoplexy, biousse et al. divide this factors in: 1) factors associated with reduced blood flow, 2) acute increase in blood flow, 3) stimulation of the pituitary gland, and 4) the anticoagulated state (2, 12) however in our series we did not managed to identify precipitating factors such as (surgical intervention, postpartum status, radiotherapy, head injury) (2, 12, 18). regarding the postoperative complications, the most frequent was represented by meningitis 13%, the rate of csf leaks was encountered in only 2 cases both after transsphenoid surgery from which one was closed spontaneously. one particularity of our operated pituitary adenoma is represented by the packaging of the pituitary fosa after tumor removal with pure alcohol for 3 minutes in order to destroy the remnant of any neoplasic cells; also all of our patients beneficiated from glucocorticoid therapy (prednisone acetate) administrated pre operatively 25mg/day in a fractionated fashion and continued in the post operatively with progressively decreasing doses. this attitude is due to the fact that patients undergoing pituitary adenoma surgery may be prone to hypocortisolic states due to pre-existing or newly developed hypothalamic-pituitaryadrenal axis impairment, in order to avoid potentially life threatening hypocortisolic states which may appear in patients with hpa impairment, adequate corticoid replacement therapy is considered mandatory (5, 10). of course in the literature there is no consensus regarding these attitude because some authors administer peri-operative corticoid replacement medication regardless of the pre-operative hpa integrity while others limit peri-operative corticoid substitution to patients with impaired hpa. also, the reported dosages of corticoids administered per operatively differ (5, 10, 17). postoperatively endocrine status showed transitory diabetes insipidus in 23.4% from which 4.2% developed the second phase of diabetes insipidus, siadh, it is very important to make the difference between these two conditions with similar clinic manifestations because the treatment is completely different. none of our patients developed the third phase of diabetes insipidus, the permanent phase. there are several theories regarding the post operative fluid balance disorders such as: mobilization of previously third space softtissue fluid especially in patients harboring gh secreting tumors, baseline elevations in the levels of renin, angiotensin, atrial natriuretic peptide, and arginine vasopressin in patients with acromegaly have been implicated in this phenomenon, and their reduction after surgery likely contributes to romanian neurosurgery (2011) xviii 4: 465 475 473 the diuresis experienced by patients via a reduction in sodium retention (26). there is well known the triphasic response of the diabetes insipidus,1) the first phase of diabetes insipidus is initiated by a partial or complete pituitary stalk section, which severs the connections between the cell bodies of avp-secreting neurons in the hypothalamus and their nerve terminals in the posterior pituitary gland, which prevents avp secretion this phase is usually treated with single doses of parenteral desmopressin in order to decrease polyuria and minimize the occurrence of hyponatremia due to overtreatment, 2) the second phase is dominated by the inappropriate antidiuresis, which is caused by uncontrolled release of avp from either degenerating posterior pituitary tissue, or from the remaining magnocellular neurons whose axons have been severed, 3) the third phase develops if >80-90% of the avpsecreting neuronal cell bodies in the hypothalamus have degenerated and which results in permanent diabetes insipidus ; these patients being best managed with long-term administration of intranasal or oral desmopressin (9) in our protocol we follow up clinical and imagistic the operated patients at 3 months, in order to avoid irm artifacts after per operative administration of corticosteroids (used to avoid pituitary insufficiency). results at 3 months showed one early recurrence (with tumor regrowth and significantly clinical symptoms the patient was re operated and the histology showed pituitary adenocarcinoma κi 67 18% (21)), 22 patients had no imagistic evidence of intracranial tumor, from the group of patients with residual tumor 6 were sent to radiotherapy and the rest were symptom free and kept under surveillance. gamma knife surgery is a commonly used adjunctive treatment for patients with a residual or recurrent adenoma, or in patients with persistent hormone hypersecretion. decreasing the adenoma volume by resection and temporarily withholding pituitary suppressive medications seem to be prudent approaches prior to radiosurgery (13, 14). we have sent to radiotherapy only the cases with significant mass lesions and especially non functional pituitary adenomas (3) in which is known the lack of medical treatment. the endocrine status at three months was represented by the presence of panhypopituitarism in 6% (treated with hormonal substitution) of the cases with no other endocrine deficits. the visual symptoms had no improvement in 4 patients (16.6% of patients who were operated on and presented with visual impairment) but with no cases of worsened vision. in a recent paper schramm and coworkers published the results of visual outcome in patients with pituitary adenomas and preoperative chiasma syndrome, according to them the syndrome completely regressed in 42.9%, improved in 38.3%, remained unchanged in 11.2% and worsened in 7.4% of the patients postoperatively (11) it is also believed that visual acuity improvement is significant during the first two postoperative weeks, with no further significant improvement after this period while visual field defects significantly improve during the first two weeks postoperatively and continue to improve for the first three months but no later than that; this affirmation given the idea that maximum visual improvement after 474 d. rotariu et al pituitary adenoma pituitary surgery is at three months postoperatively (11). results after 1 year follow up showed 19 patients with no imagistic or clinical evidence of residual tumor, in 20 patients the imagistic evaluation detected minimal residual tumour but without clinical symptoms, this category of patients being kept under imagistic and endocrine surveillance, we had three recurrences and the treatment was represented by surgery, the mortality in our group at 1 year was 6.3% (3 patients 2 per operatively deaths first month following surgery and 1 after 6 months with no relation to the surgery). late complications in our series were represented by the appearance of hydrocephalus, we had three cases of hydrocephalus at 1 year follow up who presented with hakim-adams syndrome and without any imagistic sign of obstruction, all of them being treated with ventriculoperitoneal derivation 1 case presented with hydrocephalus at the time of diagnostic and the condition did not remitted after surgery but the other two cases developed the hydrocephalus post operatively. conclusions in our series the main surgical approach was the transcranial (pterional) route due to the complexity of the cases (large tumors with extension into the suprasellar region and into the cavernous sinus) and the preference and experience of the operating team. the packaging of the sella with pure alcohol after protecting the optic structures seems to be a safe procedure with no contribution to visual deterioration, the rate of pituitary apoplexy is greater than the rate cited in the literature with no predisposing factors identified that should represent a signal of alarm because pituitary apoplexy represent a life threatening condition that must be recognized and needs adequate urgent treatment. pituitary adenoma remains a pathology with lot of controversies and in which further randomized studies are need in order to clarify them although usually the operation is not the end of the problem, given the potential need for hormone treatment before and after surgery, additional treatment such as pituitary radiation therapy, and the risk for recurrence. patients with pituitary lesions require lifelong follow up by all physicians (endocrinologist, neurosurgeon, and radiation oncologist) involved in their care. a coordinated, multidisciplinary approach to the care of these patients should result in successful care and optimal outcomes. references 1. benjamin r., randall william, t. couldwell: apoplexy in pituitary micro adenomas acta neurochir 152:1737–1740, 2010 2. biousse v, newman nj, oyesiku nm: precipitating factors in pituitary apoplexy. j neurol neurosurg psychiatry 71:542–545, 2001. 3. fahlbusch r, buchfelder m: present status of neurosurgery in the treatment of prolactinomas. neurosurg rev 8: 195-205, 1985 4. guidetti, b. fraioli, and g. p. cantore: results of surgical management of 319 pituitary adenomas acta neurochir (wien) 85:1 t7-124, 1987 5. inder wj, hunt pj: glucocorticoid replacement in pituitary surgery: guidelines for peri-operative assessment and management j clin endocrinol metab 87: 2745–2750, 2002 6. jackson imd, noren g: role of gamma knife therapy in the management of pituitary tumors. endocrinol metab clin n am 28:133–142, 1999 7. knosp e, steiner e, kitz k, matula c: pituitary adenomas with invasion of the cavernous sinus space: a magnetic resonance imaging classification compared with surgical findings. neurosurgery 33:610–618, 1993 8. jane j a jr, laws, e r jr: surgical management of pituitary adenomas. singapore med j.; 43(6) : 318-323, 2002 romanian neurosurgery (2011) xviii 4: 465 475 475 9. jennifer a. loh; joseph g. verbalis: diabetes insipidus as a complication after pituitary surgery nat clin pract endocrinol metab 3(6):489-494, 2007 10. kristof r. a., m. wichers, d. haun, l. redel, d. klingmu¨ ller, j. schramm: peri-operative glucocorticoid replacement therapy in transsphenoidal pituitary adenoma surgery: a prospective controlled study acta neurochir (wien) 150: 329–335, 2008 11. kristof rudolf andreas, daniel kirchhofer, daniel handzel, georg neuloh, johannes schramm, christian-andreas mueller, nicole eter: pre-existing chiasma syndromes do not entirely remit following transsphenoidal surgery for pituitary adenomas acta neurochir 153:26–32, 2011 12. nawar r, abdelmannan d, selman w, arafah b: pituitary tumor apoplexy: a review. j intensive care med 23:75–90, 2008 13. sheehan j.p., m.d., ph.d., douglas kondziolka, m.d., john flickinger, m.d., and l. dade lunsford, m.d : radiosurgery for residual or recurrent nonfunctioning pituitary adenoma j neurosurg (suppl 5) 97:408–414, 2002 14. sheehan j.p., m.d., ph.d. nader pouratian, m.d. ph.d. ladislau steiner, m.d. ph.d. edward r. laws, m.d. and mary lee vance, m.d. gamma knife surgery for pituitary adenomas: factors related to radiological and endocrine outcomes j neurosurg 114:303–309, 2011 15. tanaka y, hongo k, tada t, sakai k, kakizawa y, kobayashi s: growth pattern and rate in residual nonfunctioning pituitary adenomas: correlations among tumor volume doubling time, patient age, and mib-1 index. j neurosurg 98:359–365, 2003 16. vance mary lee, m.d. treatment of patients with a pituitary adenoma: one clinican’s experience neurosurg focus 16 (4): article 1, 2004 17. vogeser m, felbinger tw, reoll w, jacob k cortisol metabolism in the post-operative period after cardiac surgery. exp clin endocrinol diabetes 107: 539–546, 1999 18. wakai s, fukushima t, teramoto a, sano k: pituitary apoplexy: its incidence and clinical significance. j neurosurg 55:187–193, 1981 19. wilson cg: neurosurgical management of large and invasive pituitary tumors, in tindall gt, collins wf (eds): clinical management of pituitary disorders. new york: raven press, pp 335–342, 1979 20. wolfsberger s, knosp e: comments on the who 2004 classification of pituitary tumors. acta neuropathol 111:66–67, 2006 21. wolfsberger s, wunderer j, zachenhofer i, czech t, böcher-schwarz hg, hainfellner j, et al: expression of cell proliferation markers in pituitary adenomas— correlation and clinical relevance of mib-1 and antitopoisomerase-iialpha. acta neurochir (wien) 146:831–839, 2004 22. woosley re: multiple secreting microadenomas as a possible cause of selective transsphenoidal adenomectomy failure. j neurosurg 58: 267±269, 1983 23. yokoyama s, hirano h, moroki k, goto m, imamura s, kuratsu ji: are nonfunctioning pituitary adenomas extending into the cavernous sinus aggressive and/or invasive? neurosurgery 49:857–863, 2001 24. yonezawa k, tamaki n, kokunai t: clinical features and growth fractions of pituitary adenomas. surg neurol 48: 494–500, 1997 25. zada g, kelly df, cohan p, wang c, swerdloff r: endonasal transsphenoidal approach for pituitary adenomas and other sellar lesions: an assessment of efficacy, safety, and patient impressions. j neurosurg 98:350–358, 2003 26. zada gabriel, m.d. walavan sivakumar, b.a. dawn fishback, p.a.-c.peter a. singer, m.d.and martin h. weiss, m.d. significance of postoperative fluid diuresis in patients undergoing transsphenoidal surgery for growth hormone–secreting pituitary adenomas j neurosurg 112:744–749, 2010 27. zhang x, fei z, zhang j, fu l, zhang z, liu w, chen y: management of nonfunctioning pituitary adenomas with suprasellar extensions by transsphenoidal microsurgery. surg neurol 52:380–385, 1999. microsoft word 23.munteanuvalentin_multiple_f.docx 564 valentin munteanu et al intrafamilial multiple intracranian aneurysms multiple little intracranian aneurysms as familial inheritance valentin munteanu1, mircea r. gorgan2, radu stanescu3, vasile ciubotaru4 1phd student in neurosurgery, “carol davila” umph, faculty of medicine, departament of neurosurgery 2professor of neurosurgery, “carol davila” umph, “arseni – bagdasar” hospital 3resident in neurosurgery, “bagdasar arseni” hospital, bucharest 4senior neurosurgeon, “bagdasar arseni” hospital, bucharest abstract in this particular case, the authors have studied a family in wich two of the members on the same genetic line-mother and daughter have suffered intracranial bleeding from ruptured aneurysm. the congenital nature and the patterns of inheritance of the disease are discussed. the indications for elective investigation of the asymptomatic relatives and surgical prophylaxis on asymptomatic aneurysms are also discussed. material and method: two cases, same hereditary line, same nosocomial pattern, rare case of multiple intracranial aneuysms. surgical treatment of ruptured and unruptered aneurysm, same part, same time. results: operated pacient done well without neurological deficits after one year. conclusions: making good judgment based on complete investigations lead to a good aoutcome. further investigations on family hereditary aneurismal lesions should be perform. keywords: multiple intracranial aneurysms, familial aneurysms, asymptomatic aneurysms, surgery introduction familial intracranial aneurysms are uncommon. multiple familial intracranial aneurysms are much more uncommon. according to our review of the literature, only few families are known to have more than one of their members with multiple aneurysms. our report describes a family in which mother and daughter had multiple intracranial aneurysms. case report a 39-year-old woman was admitted in our neurosurgical department. the night prior to admission he awoke, complaining of severe headache accompanied by vomiting and followed by loss of consciousness lasting about ten minutes. on admission the patient was conscious but with severe headache and confused. neurological examination revealed only neck stiffness. blood pressure was 160/80 mmhg. laboratory data were normal. lumbar puncture show bloody spinal fluid under elevated pressure. a ct scan was perform one hour after the onset of headache at the first hospital where she has been addressed to, and it was repeated three hours later, at the arrival in our department. on all ct scan images it was the same subarachnoidian hemorrhage picture, unchanged. romanian neurosurgery (2011) xviii 4: 564 568 565 figure 1 ct scan with minimal subarachnoid hemorrhage predominant on the left side four-vessel angiography disclosed multiple intracranial aneurysms, atotal of 6 aneurysms. on the right side 1,78 mm c6-carotid aneurism with 3,86 neck, under the pcoa origin, aneurismal dilatation also at the c6 – carotid level nearby the ophthalmic origin, aneurismal dilatation at the pcoa origin. on the left side aneurism with 2,2 maximal diameter and 3,45 mm neck at the ica bifurcation, ruptured aneurism at the mca bifurcation, with daughter sac 4,3-3,39 and 2,74 neck, aneurismal dilatation at the pcoa origin. also we perform angio-ct wich we believe not only disclosed the number and pattern of the aneurysms but, make the surgical plans more accurate. in this case particulary we have to find and choose the side where the bleeding was and wich aneurism has been bled, and base on all data we choose that the ica bifurcation aneurism bled, being the only one ruptured, but we judged that also the mca bifurcation aneurism is at high risk of rupture so we decide to operate on the left side. figure 2 four vessels cerebral angiography is routinely perform, but is very usefull in multiple aneurysms a 3d image of the lesions 566 valentin munteanu et al intrafamilial multiple intracranian aneurysms figure 3 in the 3d images all the details of multiples intracranial aneurysms can be appreciated and a precise surgical approach can be done romanian neurosurgery (2011) xviii 4: 564 568 567 figure 4 angio ct with very clear aspect of the aneurysms size and location the patient underwent surgery through a left fronto-pterional approach, and two of the aneurysms were successfully clipped the aneurism situated at the level of the ica bifurcation wich was the one who bled, and the aneurism situated at the level of the mca bifurcation. the postoperative course was of an improving neurological status but with motor aphasia lasting about three weeks, which recovered partially during the hospitalization. overall now the patient is well, without any other neurological deficit. for the mother case, the data has been received by family anamnestic interview wich disclosed severe intracranial hemorrhage with gcs 6 at presentation 23 years ago, operated after she has been diagnosed on angiography with multiple intracranial aneurisms but unfortunately died 4 days after one bled carotid aneurism has been clipped. our patient has been operated one year ago but because of some personal, social issues, did not come back to allow us to make proper angiographic controls, only telephonic survey has been done. discussion the congenital nature of intracranial aneurysms is generally assumed, and seems to be due to a maldevelopement of the embryonic vasculature resulting in a deficiency of the elastic layer at the bifurcation of a vessel (1, 3). whether hereditary factors play a role in the origin of cerebral aneurysms is still uncertain. intracranial aneurysms are not uncommonly associated with congenital malformations and other disorders, such as polycystic kidneys, arteriovenous malformations, coarctation of the aorta, ehlers-danlos syndrome, fibromuscolar hyperplasia of arteries, and possibly other connective tissue diseases (3). a very interesting part of these pathology is because there are cases reported of familial aneurysms located in identical positions on the same side of the head. there are identical twins wich have been reported having multiple intracranial aneurysms; these findings suggest that 568 valentin munteanu et al intrafamilial multiple intracranian aneurysms hereditary factors do have a specific role in some exemples of familial aneurysms, an autosomal dominant inheritance, with variations in penetrance, seems to offer the best explanation and a detailed prospective study of the families with more than one member having intracranial aneurysms would be very helpful to be studied in the future (4). there is still disagreement as to whether a relative of a patient affected by intracranial aneurysms has an increased risk of having an asymptomatic aneurysm. it has been stated that there is not any increased risk to a relative (2, 5, 7). however, review of the literature indicates that there are many reported cases in which the presence of an intracranial familial aneurysm, although strongly suspected, was not verified by angiography, surgery, or autopsy. also, in some well-documented families, members are reported suddenly dead in whom the likely presence of ruptured intracranial aneurysms remained unexplored due to a lack of post-mortem examination. these findings suggest that the actual incidence of familial aneurysms is very likely to be higher than has been reported. another important dispute concerns the indication for cerebral angiography on asymptomatic members and surgical prophylaxis for asymptomatic aneurysms found by elective investigation. asymptomatic familial aneurysms found by elective angiography have been reported and well documented (2, 6). in view of the good results of the surgical treatment of intact cerebral aneurysms, in japanese studies (5, 7) it has been suggested that elective investigation of the asymptomatic members should be considered when there are already two or more individuals affected in a family. we consider that is not possible, at least yet to justify and perform cerebral angiography on all asymptomatic relatives. we think that families in wich a pacient with multiple aneurisms has been disclosed, all relatives on the direct hereditary line shoud be advise of being alert of any new symptoms that will possibly appear and notice their physician. elective investigation should be performed as soon as any warning signs, even headaches, appear. it should be done periodically neurological examinations of the asymptomatic members in order to prevent, if possible, bleeding by trying to disclose any early neurological warning signs. references 1. unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention. international study of unruptured intracranial aneurysms investigators. n engl j med 339:1725-1733, 1998. 2. campi a, ramzi n, molyneux aj, summers pe, kerr rs, sneade m, yarnold ja, rischmiller j, byrne jv: retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the international subarachnoid aneurysm trial (isat). stroke 38:1538-1544, 2007. 3. harris pc, ward cj, peral b, hughes j: polycystic kidney disease. 1: identification and analysis of the primary defect. j am soc nephrol 6:1125-1133, 1995. 4. hassler o: morphological studies on the large cerebral arteries, with reference to the aetiology of subarachnoid haemorrhage. acta psychiatr scand suppl 154:1-145, 1961. 5. kaminogo m, yonekura m, shibata s: incidence and outcome of multiple intracranial aneurysms in a defined population. stroke 34:16-21, 2003. 6. molyneux aj, kerr rs, birks j, ramzi n, yarnold j, sneade m, rischmiller j: risk of recurrent subarachnoid haemorrhage, death, or dependence and standardised mortality ratios after clipping or coiling of an intracranial aneurysm in the international subarachnoid aneurysm trial (isat): long-term follow-up. lancet neurol 8:427-433, 2009. 7. quinones-hinojosa a, gulati m, singh v, lawton mt: spontaneous intracerebral hemorrhage due to coagulation disorders. neurosurg focus 15:e3, 2003. microsoft word 7.costachescub_modernmanagement.doc 432 b. costachescu, c.e. popescu modern management in vertebral metastasis modern management in vertebral metastasis b. costachescu, c.e. popescu department of neurosurgery, division of spine surgery, university of medicine and pharmacy “gr. t. popa”, iasi abstract vertebral metastases (vb) remain a real challenge in spine surgeons. recent advancements in surgical techniques and oncological management allow a more aggressive approach of the patient with such a pathology, with better results in terms of decreasing pain, improvement of the quality of life. the aim of this paper is to review the optimal surgical planning in metastatic spinal tumors. keywords: vertebral metastases, surgery, surgical staging system, preoperative prognostic score introduction it is well known that the liver and lungs are the most common distant sites for carcinoma. bone – vertebral column is the third site affected (1). the most common primary malignancy is prostate cancer for men, followed by lung and colon cancer (incidence ranging from 160.4 to 65.0 cases per 100,0000; for women the first cause for vertebral metastases is the breast cancer, followed by the same malignancies as in men (incidence ranging from 128.9 to 47.0 cases/ 100,000). the primary spinal tumors are rare as comparing with metastases (2). recent advancement of oncological management improved the survival rate of patients with malignancies, including the ones with vertebral metastases; so spinal surgeons are faced very often with such of patients and they have to decide which is the best way to deal with this kind of pathology. vertebral metastases occur in all age groups, with the highest incidence between age 40 and 65 years (3). improvement in cancer management leads to increasing survival rate, thus to more patients with spinal secondary lesions. cancers of breast, renal, lung, prostate are the most frequent primary lesions which will develop spinal secondary lesions (4). classic autopsy studies of willis (5) have demonstrated that the size of vertebrae is related with secondary lesions. thus the most affected is lumbar region followed by thoracic spine and rare cervical spine. despite this, today the studies show that the most affected is thoracic spine (60% to 80%), followed by the lumbar spine (15% to 30%), and finally the cervical spine (less than 10%) (6), probably related to the smaller size of thoracic spinal canal. in transverse plan of vertebrae the most affected site is the vertebral body (85%), paravertebral spaces (10-15%), epidural space (<5%), intradural/intramedullary (7). even today we can encounter physicians considering the appearance of a spinal metastasis to be the death “signature” for patients with carcinoma. advances in imaging, early diagnosis, new surgical techniques – more aggressive, associated with oncological treatment allow to improve the management of this patients “too sick to be treated”. romanian neurosurgery (2010) xvii 4: 432 – 437 433 treatment the three basic treatment modalities in vertebral metastasis are chemotherapy, radiotherapy and surgery. chemotherapy includes antitumor medication, steroids and biphosphonates.it is very important to know the sensitivity of the tumor to chemotherapy prior to treatment. krakoff defines three types of tumoral sensitivity to chemotherapy (8): higly sensitive 1. childhood cancers like acute lymphocytic leukemia, wilms tumor, ewing’s tumor, retinoblastoma, and rhabdomyosarcoma. 2. hodgkin’s lymphoma. 3. carcinoma of the testis. 4. choriocarcinoma. 5. burkitts tumor. 6. acute promyelocytic leukemia. in many centers chemotherapy is considered the primary treatment for patients with these tumors even in the presence of epidural compression (9): moderately sensitive 1. adenocarcinoma of breast. 2. non-hodgkin’s lymphoma. 3. lung cancer. 4. osteosarcoma. 5. adult myeloid and lymphocytic leukemia. 6. carcinoma of the prostate. 7. colorectal carcinoma. 8. female cancers of the ovary, endometrium, and cervix. minimally sensitive 1. endocrine gland cancers. 2. malignant melanoma. 3. hepatocellular carcinoma. 4. renal carcinoma. 5. pancreatic carcinoma. steroids are used for the control of biologic pain and vasogenic edema to help stabilize neurologic dysfunctions in pre and postoperative periods. biphosphonates tend to inhibit osteoclast reabsortion of bone matrix and decrease bone turnover. there are three generations of biphosphonate currently available. radiation therapy (rt) remained an important tool in these patients treatment. since 1970’s rt replaced laminectomy as first-line therapy for patients with spinal metastasis and cord compression. recent studie (10) have confirmed the utility of rt for the treatment of patients with spinal metastasis. the standard rt treatment for palliation of spinal metastasis is a total dose of 3000 gy; higher doses increases the risk for pathologic myelopathy and functional spinal cord transection. today new radiation techniques are available: intraoperative rt, 3-d conformal rt, and intensity-modulated rt. all these techniques may permit the delivery of a higher dose of radiation to a target tissue while maintaining the dose to the spinal cord at a much lower level. surgical management surgical treatment of vertebral metastases is a real challenge for a spine surgeon. there are many strategies currently available for this disease, starting with observation to aggressive en bloc spondilectomy. furthermore, it is not enough to asses the patient only from the surgical point of view, it’s mandatory to asses the stage of his cancer, needing a multidisciplinary team. patients with spinal metastases are often compromised and at higher risk for surgical and medical complications after aggressive treatment. mclain (11) identifies the steps for a successful surgical plan: 1. identify and characterize the tumor. 434 b. costachescu, c.e. popescu modern management in vertebral metastasis 2. classify the tumor as stage and extension. 3. identify an indication for surgery relative or absolute. 4. review the non-operative options. 5. review the options for resection and reconstruction. 6. determine the role of adjuvant therapy. there is no clear cut indications for surgery in vertebral metastases; however, there are some circumstances accepted as surgical candidates (12), (13): 1. unknown or impossibility to establish the histological diagnosis 2. neurological compression owing to pathological fracture with bony impingement, vertebral collapse more than 50% of vertebral height, kyphosis more than 50º; 3. mechanical instability with severe pain or impending neurological injury. 4. tumor progression in face of, or following radiotherapy. 5. known radio-resistant tumor. 6. resectable solitary metastasis in patient with potential long-term survival. there are also some relative contraindications: 1. longstanding complete paralysis (more than 24 hrs) 2. highly radiosensitive tumor (lymphoma, myeloma) 3. multiple levels of involvement 4. poor life expectancy (less than 3 months) 5. extreme medical comorbidities an important issue is timing of surgery, especially for the patients with neurological deficits. complete paralysis has less chances to recovery after 24 hours. however, surgery is indicated in patients with partial neurological deficits appeared for 3 days or less (14). terminology and surgical staging/preoperative prognostic score it is necessary to establish some definitions in order to describe the degree of tumoral resection in spine. the surgery of musculoskeletal tumors delineates the resection as intralesional, marginal, wide, and radical margins. in spine surgery this radical margins are very difficult to achieve due to presence of neural elements. that’s why the applications of the oncological staging systems for long bones such as enneking system for the surgical staging of bone and soft-tissue tumors is difficult (15). there are many surgical staging systems, and prognostic systems designed to evaluate each patient in order to choose the optimal surgical treatment. in 1997, weinstein, boriani and biagini describe the terms of surgical resection and surgical staging system (wbb) (16): “curettage” – piecemeal removal of the tumor – intralesional procedure “en bloc” – removal of the tumor in one piece, alltogether with a layer of healthy tissue. the piece has to be sent to histological studies to define “intralesional”, “marginal” or “wide” (15) as shown in figure 1. “radical resection” – en bloc removal of the tumor and the whole compartment of tumor origin. this is practically impossible in spine tumor due to presence of nervous tissue. “ palliation” – surgical procedure with a functional purpose – spinal cord decompression, fracture stabilisation +/ partialor piecemeal resection of the tumor leading to control the pain, improvement of neurological deficit. romanian neurosurgery (2010) xvii 4: 432 – 437 435 figure 1 types of surgical resection figure 2 wbb surgical staging for spine tumors in axial plane the vertebra is divided in 12 radiating zones and 5 layers (from a to e). ( from wbb surgical staging system, 1997) there are 3 methods for performing en bloc exicisions depending of tumor’s location (16): • vertebrectomy (marginal/wide en bloc excision of the vertebral body) – tumor is located in zones 4 to 8 or 5 to 9, and at least one pedicle is free from tumor. • sagittal resection (marginal/wide) tumor is located in zones 3 to 5 or 8 to 10, which means that it is situated eccentrically within the body, pedicle, transverse process. • resection of posterior arch resection (marginal/wide) tumor is located in zones 10 to 3. although wbb system is designed for primary spine tumors, it can be successfully used for spine metastases. in 2001 tomita discloses his results using another scoring system for spinal metastases using 3 prognostic factors (17) as shown in table 1. 1) grade of malignancy (slow growth 1 point; moderate growth 2 points; rapid growth – 4 points), 2) visceral metastases (no metastasis 0 points; treatable 2 points: untreatable 4 points), 3) bone metastases (solitary or isolated 1 point; multiple – 2 points). prognostic score between 2 and 10. en bloc resecn intralesional – the cut is within the tumor marginal – dissection along the psudocapsule of tumor wide – the cut is outside the pseudocapsule, removing the tumor with a layer of healthy tissue 436 b. costachescu, c.e. popescu modern management in vertebral metastasis another scoring system was proposed by tokuhashi (18). it is a preoperative prognostic scoring system taking into account six variables in order to evaluate life expectancy of the patients (table 2). aggressive surgery is reccomended for patients having a score of 9 or more and palliative surgery for scor of 5 or less. hecht (19) describes surgical strategies according to life expectancy and surgical staging using tomita and tokuhashi scores. (table 4) table 1 tomita preoperative prognostic score table 2 tomita’s local extension of lesion table 3 tokuhashi prognostic scoring system general status score metastases to major internal organs score general condition (karnofsky) 10-40 50-70 80-100 0 1 2 nonremovable removable none 0 1 2 no of extraspinal bone metastases >3 2 1 0 1 2 lung, stomach kidney, liver, uterus thyroid, prostate, breast, rectum 0 1 2 no of metastases in the spine >3 2 1 0 1 2 neurological deficit complete incomplete none 0 1 2 tokuhashi score 0-4 5-8 9-12 life expectancy <3 months <6 months >6 months table 4 surgical strategies according to life expectancy and tomita and tokuhashi scores tokuhashi score life expectancy tomita scoring system surgical technique 0-4 <3 months 1-7 laminectomy +fixation 5-8 3-6 months 1-7 posterior decompression + fixation +reconstruction 9-12 >6 months 1-3 4-6 7 en bloc resection +reconstruction 360° intralesional vertebrectomy+ reconstruction 360° posterior decompression and fixation romanian neurosurgery (2010) xvii 4: 432 – 437 437 discussion the management of patients with spinal metastases is frequently a challenging task, with many risks. in the past the treatment was radiation therapy associated or not with laminectomy; but laminectomy alone leads to secondary aggravation of the neurological deficit due to increased spine instability. therefore, more sofisticated techniques were developed for this kind of lesions including anterior/anterolateral approaches combined or not with posterior approaches, tumor removal in different ways, associated with reconstruction and stabilisation. this techniques allowed a more aggressive tactics, improving the survival rate and the quality of life. this more extensive /aggressive surgical technique prolonge significantly the survival rate – 18,8 month for en bloc resection compared with 3,7 month for palliative surgery (4). the most important issue in dealing with spine metastases is a proper assessment. it can be done using surgical staging systems and preoperative prognostic scores as described above. however, there is a lack of standardization of the surgical terms sometimes is used the same term for different surgical procedures (20). using this instrument it is possible to choose the optimal treatment for the patient (avoiding overtreatments or undertreatments patient too sick to be treated). references 1. harrington k.d. metastatic disease of the spine. j bone jointsurg am 68:1110–1115, 1986. 2. cdc united states cancer statistics review, 19752007, www.seer.cancer.gov./statistics/. 3. perrin r.g., laxton a.w. metastatic spine disease: epidemiology, pathophysiology, and evaluation of patients. neurosurg clin n am 2004; 15: 365–373). 4. a. ibrahim et al.j. neurosurg.: does spinal surgery improve the quality of life forthose with extradural (spinal) osseous metastases? an international multicenter prospective observational study of 223 patients, spine / volume 8 / march 2008). 5. willis (willis r.a.: the spread of tumours in the human body, ed2. london: butterworth, 1952) 6. agarawal j.p., swangsilpa t., van der linden y., et al. the role of external beam radiotherapy in the management of bone metastases. clin oncol (r coll radiol) 2006; 18: 747–760. 7. bryne t.n. spinal cord compression from epidural metastases n engl j med. 1992 aug 27;327(9):614–619. 8. krakoff i.h. systemic treatment of cancer. ca cancer j clin 1996; 46:137–141.) 9. bilsky m., vitaz t. metastatic spine tumors, in benzel ec: spine surgery, sec. ed., elsevier, 2005. 10. maranzano e., latini p.: effectiveness of radiation therapy without surgery in metastatic spinal cord compression: final results from a prospective trial. int j rad onc biol phys 32(4): 959-967, 1995. 11. robert mclain, the role of surgical therapy, in robert mclain, cancer in the spine, a comprehensive care, 2006 humana press inc. 999 riverview drive, suite 208 totowa, new jersey 07512. 12. w. bradley jacobs et al evaluation and treatment of spinal metastases: an overview, neurosurg focus 11 (6):article 10, 2001. 13. robert mclain, the role of surgical therapy, in robert mclain, cancer in the spine, a comprehensive care, 2006 humana press inc. 999 riverview drive, suite 208 totowa, new jersey 07512. 14. christian hessler et al., dynamics of neurological deficit after surgical decompression of symptomatic vertebral metastases spine volume 34, number 6, pp 566–571©2009, lippincott williams & wilkins). 15. enneking w.f. et al., a system for the surgical staging of musculoskeletal sarcomas, clin. orthop, 1980, 153, 106-20. 16. boriani s., weinstein j., biagini r., primary bone tumors of the spine:terminology and surgical staging., spine 22:1036–1044, 1997. 17. tomita k. akamarut. al surgical strategy for spinal metastasesspine, vol 26, no.3, 298-306, 2001. 18.tokuhashi y., toriyama s. et al, scoring system for the preoperative evaluation of metastatic spine tumor prognosis – spine, 1990, 15, pg: 1110-1113. 19. a. hecht and al.metastatic disease in j. frymoyer, the adult and pediatric spine, third edition, lippincott williams&wilkins, 2004. 20. cloid j., ames c. et al, en bloc resection for primary and metastatic tumors of the spine: a systematic review of the literature, neurosurgery, vol. 67, no. 2, august 2010). microsoft word 10inmemoriam.doc romanian neurosurgery (2012) xix 3: 239 239 in memoriam dr. i.f. vesa (1948-2011) it gives us great sadness to inform the readers of the romanian journal of neurosurgery about the loss of our distinguished colleague and friend, dr. i. f vesa, who passed away on august 17, 2011. born in 1948 in the village of zam, romania, dr. i. f vesa saw daylight in a rich county full of ancient tradition and honor, called “motilor country”. he attended high school in deva and graduated from the “carol davila” university school of medicine in bucharest in 1968, after which he began his medical practice in various hospitals in bucharest. since 1975 dr. i. f vesa trained in neurosurgery as a resident at the bagdasararseni hospital, in bucharest, for six years until 1981. dr. i. f vesa has trained and worked at this clinic with prof. c arseni and his coworkers; he had a good work relationship with dr.m ghitescu, a senior neurosurgeon at that time, who became gradually one of his mentors. starting with the year 1981 dr. i. f. vesa practiced the art of medicine as a neurosurgeon at st. andrew hospital in galati with dr. grigorovici (who was also trained in the neurosurgery clinic at bagdasar-arseni hospital). in 1981 dr. i.f. vesa became head of the department, until 2008. he was not only a pioneer of neurosurgery in galati but he also showed authentic leadership qualities that allowed him to become the director of st. andrew hospital there from 1991 to 1997/ dr. i.f. vesa was a good colleague, a generous man with a strong character who never forgot the moral principles which he was educated with. a proud man of the “apuseni mountains” , dr. i.f. vesa was a fighter throughout his life, succeeding in all challenges offered by his destiny. he fought the disease for years without making his medical condition public, but his generous heart suddenly stopped. although he left us, dr. i.f. vesa will always remain in the conscience of those who knew him, and hopefully in memory of readers of romanian neurosurgery. may he rest in peace! c. mihalache prof. a.v. ciurea “sfantul andrei” clinic hospital galati “bagdasar-arseni” clinic hospital bucharest 17moscote-salazar_remote romanian neurosurgery (2014) xxi 3: 349 352 349 remote supratentorial hemorrhage after posterior fossa surgery: a brief case report luis rafael moscote-salazar1, gabriel alcalá-cerra1, hernando raphael alvis-miranda2, omar ramírez3, willem guillermo calderón-miranda4, andrés m. rubiano5 1neurosurgeon, universidad de cartagena, colombia 2physician, universidad de cartagena, colombia 3neurosurgeon, universidad el bosque, colombia 4physician, universidad del magdalena, colombia 5neurosurgeon, hospital universitario de neiva, colombia abstract the supratentorial hemorrhage after posterior fossa surgery is an unusual but delicate complication that carries high mortality and morbidity. a 50 year old woman presented vertigo 6 months of evolution, which worsened in the last 2 months accompanied by ataxia. she showed left cerebellar signs, had no focal motor or sensory deficits. a brain mri identified cerebellopontine angle lesion with mass effect. the patient was treated on suboccipital craniectomy and resection of right posterior fossa tumor, the histopathological diagnosis was consistent with typical meningioma. (who class i). the postoperative period was satisfactory. a month later, presented clinical symptoms of right-sided hemiparesis, brain ct revealed left frontal supratentorial hematoma, receiving conservative management. patient was discharged after 10 days. reports in the literature on this rare complication, detailed cases where the hematoma was presented in hours to days. to our knowledge this is the first report in the literature of supratentorial hemorrhage and posterior fossa surgery one month after the surgical procedure has been performed. key words: meningioma, posterior fossa surgery, supratentorial hemorrhage, neurosurgery introduction remote supratentorial hematoma after posterior fossa surgery for the removal of a space-occupying lesion is a rare but dramatic and dreaded complication, carrying significant morbidity and mortality. we describe a rare complication of extensive supratentorial hemorrhage following posterior fossa surgery; review the relevant 350 moscote-salazar et al remote supratentorial hemorrhage after posterior fossa surgery literature and discus the possible cause of hemorrhage in the present case. case report a 50-year-old woman had a history of headache and progressive ataxia over 1 year. neurological examination showed a horizontal nystagmus, a slight gait ataxia, right dysmetria and bilaterally papilledema. ct scan also revealed a right meningioma of 6x5x5,5 cm in size in the right posterior fossa with moderate hydrocephalus (figure 1). preoperative right carotid and right vertebral artery angiographic scan has been done. the patient underwent suboccipital craniectomy in sitting position and ventricular drainage has been performed to prevent air embolism. so intraoperative course was uneventful and tumor removed totally [figure 2]. in early postoperative neurological examination was normal but after six hours she became somnolent and developed a hemiplegia on the left site. a new ct scan revealed a hyperdense lesion of 2x1,5x4 cm in size in the right frontoparietal region [figure 3]. the patient was treated conservatively and the patient's neurologic state improved in five days. ct scan revealed a hypodense lesion in the right fronto-parietal region in subsequent second month. discusion supratentorial intracerebral hemorrhage is uncommon after posterior fossa surgery. figures 1 and 2 preoperative brain t1w mri contrast images showing large posterior fossa tumor on right side with mass effect figure 3 postoperative ct scan revealed a hyperdense lesion of 2x1,5x4 the mechanism for producing the bleeding is not entirely certain, but it is proposed that in the case where the sitting position is used, a romanian neurosurgery (2014) xxi 3: 349 352 351 decrease of cerebral blood flow and then cerebral ischemia occurs. by switching the position after surgery hyperperfusion areas leads to bleeding in ischemic areas. heines et al reported 5 supratentorial hemorrhages after posterior fossa surgery in 825 patients firstly. the patients had neither coagulopathy nor predisposant factors. [1,2] table 1 summary of published supratentorial intracerebral hemorrhage after posterior fossa surgery author and year age/gender diagnosis localization pop interval sequela haines, 1978 65/f 55/f 41/f 64/f 62/f neuralgia v right neuralgia ix right neuralgia v right an. painful right schwanoma viii left right occipital ringht basal ganglia right frontoparietal left frontal intraventricular 4 hrs 45 min inmediate 18 horas inmediate - standefer, 1984 59/- meningioma basal ganglia 7 days - harders, 1985 44/f 51/f 58/m meningioma schwnoma viii meningioma left frontoparietal bilateral frontal left parietal - - - - seiler, 1986 66/f 64/f 59/f schwnoma viii right right meningioma right schwnoma right parietal left parietal right occipital inmediate 3 hrs 24 hrs - kalfas, 1988 ----- bucciero, 1991 46/f hemangioblastoma left temporoparietal 6 hrs - prieto, 1993 45/f left schwnoma viii left frontoparietal 16 hrs - tondon, 2004 30/f 50/f schwannomas astrocitoma left parietaloccipital basal ganglia 24 hrs 6 hrs died died kalkan, 2006 63/f meningioma -6 hrs - agrawal, 2010 47/f --right temporal 3 hrs - moscote, 2014 50/f meningioma left frontal 30 days right hemiparesis f: female m: male our patient underwent tumor resection in the benck park position. no ventricular drain was placed. in the preoperative and postoperative periods coagulation parameters were normal. the values of blood pressure preoperatively, intraoperatively and postoperatively were normal. bleeding was probably caused by the rupture of perforating veins of the basal ganglia or in the subependymal region. 352 moscote-salazar et al remote supratentorial hemorrhage after posterior fossa surgery conclusion the supratentorial hemorrhage after posterior fossa surgery is an unusual but delicate complication that carries high mortality and morbidity. reports in the literature on this rare complication, evidence cases where the hematoma was presented in hours to days. (3, 4, 5, 6, 7, 8, 9, 10). to our knowledge this is the first report in the literature of supratentorial hemorrhage and posterior fossa surgery one month after the surgical procedure has been performed. correspondence dr. luis rafael moscote-salazar, universidad de cartagena, cartagena de indias, colombia, e-mail: mineurocirujano@aol.com references 1. tondon a, mahapatra ak. superatentorial intracerebral hemorrhage following infratentorial surgery. j clin neurosci. 2004;11:762–5. [pubmed] 2. haines sj, maroon jc, jannetta pj. supratentorial intracerebral hemorrhage following posterior fossa surgery. j neurosurg. 1978;49:881–6. [pubmed] 3.kalkan e, eser o. supratentorial intracerebral haemorrhage following posterior fossa operation. neurol india. 2006;54:220–1. 4. bucciero a, quaglietta p, vizioli l. supratentorial intracerebral hemorrhage after posterior fossa surgery: case report. j neurosurg sci. 1991;35:221–4. [pubmed] 5. harders a, gilsbach j, weigel k. supratentorial space occupying lesions following infratentorial surgery early diagnosis and treatment. acta neurochir (wien) 1985;74:57–60. [pubmed] 6. vrettou cs, stavrinou lc, halikias s, kyriakopoulou m, kollias s, stranjalis g, et al. factor xiii deficiency as a potential cause of supratentorial haemorrhage after posterior fossa surgery. acta neurochir (wien) 2010;152:529–32. [pubmed] 7. wolfsberger s, gruber a, czech t. multiple supratentorial epidural haematomas after posterior fossa surgery. neurosurg rev. 2004;27:128–32. [pubmed] 8.pandey p, madhugiri vs, sattur mg, devi bi. remote supratentorial extradural hematoma following posterior fossa surgery. childs nerv syst. 2008;24:851–4. [pubmed] 9. seiler rw, zurbrugg hr. supratentorial intracerebral hemorrhage after posterior fossa operation. neurosurgery. 1986;18:472–4. [pubmed] 10. agrawal a, kakani a, ray k. extensive supratentorial hemorrhages following posterior fossa meningioma surgery. j surg tech case rep. 2010 juldec; 2(2): 87–89. microsoft word seferisch_imaging_formatat charalampos seferis imaging of vestibular schwannomas following γ-knife treatment imaging of vestibular schwannomas following γ-knife treatment – a series of 79 cases charalampos seferis hygeia hospital, athens, greece, phd student in neurosurgery, university of medicine and pharmacy “gr.t. popa” iasi abstract gamma-knife became an established therapeutic alternative for selected cases of vestibular schwannomas (benign tumors rooting from scwann cells of vestibular nerve). however, the long term results and effects on the tumor and surrounding brain are still a matter of research. we analyze the imagistic findings in the patients with vestibular scwannomas treated with gamma-knife radiosurgery in the gammaknife department, hygeia hospital, athens. we performed radiosurgery on 79 cases of vestibular scwannomas. 23 of them were first operated with incomplete resection and had gamma-knife performed on residual tumor. of all cases, one patient died 4 years after the treatment, while 4 cases didn’t comply with the follow-up protocol and were excluded from the study. the other cases underwent a follow-up protocol with mri sudies at 6, 12, 18, and 24 months following the gamma-knife session. we looked at the tumoral volume, and the evolution of the tumor in relationship with the iradiation dise and isodose curve. our results confirm the landmark results of karolinska an pittsburg studies. we show that small gamma-knife doses are suitable for a satisfactory control of tumoral volume. stereotactic mri imaging and multiple doses programs are the main factors contributing to these results. keywords: vestibular schwannoma, radiosurgery, gamma-knife, mri introduction histologically, vestibular schwannomas are benign tumors that grow from the schwann cells of the 8th cranian nerve. due to improved neuroimaging the incidence of vestibular schwannomas within the general population increased. however, despite the advances in introperatory techniques, surgery still carries a risk for morbidity and moratality. depending on tumors characteristics vestibular schwannomas can be treated by different methods, other than neurosurgery. radiosurgery is one of these non-invasive techniques that can be used to treat vestibular schwannomas. it uses gamma radiation (photons) and is known as “gamma-knife” or “γ-knife”. we analyze the imagistic findings in the patients with vestibular scwannomas treated with gamma-knife radiosurgery in the gamma-knife department, hygeia hospital, athens. our results point to the fact that using small doses of radiation (similar to those used in the reference series from karolinska and pittsburg) can control the volume of the lesion as shown by the follow-up controls results. stereotactic mri and a romanian neurosurgery (2011) xviii 2 multiple dosage program seem to be the main factors in achieving this result. according to published results the method can fail if the doctor decides not to partially exclude the lesions localized ar superior limit of the treated region. materials and method in the last six years (february 2004 – september 2010) 79 cases of vestibular schwannomas have been treated with gamma-knife radiosurgery in our unit. 23 patients have undergone surgery prior to gamm-knife, and had radiosuergery as an adjuvant therapy on remnant tumor. one patient died 4 years after the gamma-knife treatment because of pre-existing cardiac co-moribidities. 4 patients failed to comply woth the follow-up rpotocol and were excluded from our study. 2 patients declaired that their quality of life deteriorated as a result of radiosurgery. to study the effects of radiation therapy the patients had to comply with a follow-up protocol that included mri studies at 6, 12, 18, and 24 months after the treatment. the goal of follow-up was to monitor the volume of the schwannoma and to analyze the imagistic aspects as a result of gammaknife therapy. the radiation dose (gy) and radiation isodose curve have been measured in relationshipwith their effect in controling the progress of the tumors. the average age of the patients included in our study was 55 years (22-74). out of 79 cases 9 presented intracanlicular tumors, 19 developed intracanalicular and cisternal tumors, while 51 presented with tumors occupying the cerebello-pontine cistern (table 1.). the main tumor volume (vm) was 4.72 cm3 (0.2-19.3 cm3). the female to male ration was 51:28. table 2 characteristics of the 79 vestibular schwannoma patients that underwent gamma-knife surgery parameters values median age (interval) 55 (27 74) female to male ratio 51:28 tumor localization intracanalicular cerebello-pontine cistern both cisternal and intracanalicular 9 51 19 previously treated 23 medium colume in cm3 (interval) 4,72 (0,2019,3) gamma-knife therapy particularities gamma-knife radiosurgery is base on four principles: 1. “target” localization, using neuroimagistic techniques, a stereotactic frame, and computer software to record and alter imaging data. 2. computing lesion volume 3. determining the distribution of radiation dose 4. radiotherapy during a radiosurgery session the median of isodose curve was 48.25%, with an interval of 40-54%. target localization is extremely important and excluding important cranial structures from being exposed to the gamma radiation (such as cranial nerves, cerebellum, and of course brain stem). during treatment average marginal dose was 12.09 gy (11 – 14 gy), and maximal average dose was 19.83 gy (20.5 – 29.9 gy). average tumor volume of treated charalampos seferis imaging of vestibular schwannomas following γ-knife treatment schwannomas was 4.72 cm3 (0.2 – 19.3 cm3). to protect the undefined segments of the facial and trigeminal nerves that are prone to be included in the designated lesion volume, we administered in these areas doses below 13 and 15 gy respectively. in two cases where the tumor had an occupying effect involving the brainstem the same dose didn’t reach more than 10 gy. all patients responded well to the treatment and were released the next morning after treatment completion. none reported neurological problems during hispitalization (such as epileptic seizures). headache was present in 12 cases, most likely due to the steretactic frame. to address these headaches patients were given oral pain killers for a short period of time (2-3 days) in the period following their release. follow-up all patients, with one exception, underwent mri imaging 6 months after the treatment. six of them didn’t present for the next follow-up session, at 12 months. mri evaluation criteria included: •changes in the volume of the vestibular schwannoma •neuro-imagistic findings like: loss of central enhance (necrosis), local swelling through the cerebral ventricular system. results the average follow-up period was of 24 months (1 – 51). 84.2% of the patients performed at least one mri exploration at 6 months. mri evaluation the solid part of the tumor reacted satisfactory to gamma-knife iradiation. as documented by the mri images in the first six months this response takes the shape of a central region of necrosis (seen in t1). acording to published data this phenomena is noticed from the first month (or later than 23 months) and can extend within the tumor in the next 10 months (or even later than 60 months) after the treatment. a small percentage of the patients (11,8%) showed a swelling of the lesion. mri findings at first follow-upmatch those reported in the literature in 34 cases. only 2 cases showed a significant change in lesion volume in the 24 months period following gamma-knife therapy (from 0.71 cm3 to 1.1 cm3, and from 19.3 cm3 to 23.1 cm3), while the maximum reduction in tumor volume recorded in our series was from 12.4 to 2.7 cm3. discussion optimal radiation dosage for tumor control optimal radiation dosage for vestibular schwannoma control is still a matter of debate. a review of the literature showed a tendency to decreasing prescription dosage from 25-100 gy used in the initial studies to 13 gy in the current protocols. nóren, et al. have prescribed dosages of 25-35 gy to the tumor periphery to ensure stopping tumor growth. however, high dose radiation has led to high morbidity due to facial and trigeminal nerve damage. in addition, possible preservation of hearing may be compromised when using a high dosage. first of all, a reduced radiation dose lowers the probability of cranial nerve neuropathy. second of all, small doses have a better chance, at least in theory, to preserve hearing close to preoperative levels. third of all, a lower dose should theoretically reduce or minimize the degree of swelling of the tumor that may occur after treatment. romanian neurosurgery (2011) xviii 2 figure 1 left: male, 62 yrs. old, before therapy. dose 12gy (45%), volume 3,4 cm³. right: control at 6 months (central necrosis) figure 2 upper left: male, 73 yrs., before therapy. dose 11 gy, tumor volume 5.6 cm³. at 24 months after gamma-knife tumor volume 3,1 cm³ (lower right). dimensions before therapy: 3 cm x 2 cm, and after therapy: 2 cm x 1,4 cm. charalampos seferis imaging of vestibular schwannomas following γ-knife treatment figure 3 female, 44 yrs., before therapy. dose 11 gy (50%). after 6, 12, and 24 months respectively. tumor volume before therapy 12,4 cm³, 24 months after therapy 3cm³. larson et al. proposed the use of a single dose of 13.5 gy, given the biological effect of delayed tissue response. flickinger and ass. have questioned whether or not the tumor control rate could be reduced by a dose smaller than 13 gy. in this study, we had satisfactory results in patients treated with a median marginal dose of 12.09 gy (11-14 gy). thus, in our experience it is possible to obtain satisfactory long-term control of the tumor at a marginal dose less than 11 gy. tumor control rate was in no way worse than those reported in earlier series, where significantly higher doses were used. optimal dosage for preservation of cranial nerves it has been suggested that the facial nerve tolerates marginal doses up to 15 gy, but doses above 14 gy have been shown to lead to a significant increase in neuropathy incidence, particularly in the patients with large tumors. in the early days of radiosurgery, subjective numbness or hypoesthesia has been reported as major complication of trigeminal nerve radiation damage. the incidence was as high as 19% in both karolinska and pittsburgh series. the large tumoral volume and high radiation doses used corroborate to this undesirable consequence of radiation therapy. the incidence of trigeminal neuropathy was reduced to 4% transient neuropathy and 1.6% persistent neuropathy in charlottesville exerience, where the average marginal dose used was 13.2 gy. in the present series, no patient developed any kind of sensory deficit. preservation of hearing has become the main concern in advanced radiosurgery. in this study, 43 of 60 patients with good preoperative hearing, maintain a functional hearing during a romanian neurosurgery (2011) xviii 2 follow-up period of 21 months. numerous studies have reported a total rate of 33-55% of hearing preservation in a 2-4 years period after treatment. a definite inverse correlation exists between the dimensions of the tumor and the probability of hearing preservation. prasad and colleagues have reported a marginal inverse correlation between the dose used and the likelihood of hearing preservation, especially manifest at a dose higher than 13 gy. in our series, neither the volume of the tumor nor the marginal dose appear to play a critical role in postoperative hearing preservation. in contrast, pure tone audiometry before gamma knife surgery seems to be a good possible measure for evaluating the results. loss of central contrast enhance loss of central enhancing on mri imaging was observed in 54% of patients of prasad et al., 70% of nóren, et al. and 63% of flickinger, et al series. in this study, this phenomenon was observed in 63.3% of cases. this is a common observation after radiosurgery. more research is required to clarify the pathogenesis. backlund reported that tumor necrosis was found in a histological study, which corresponds to the central region of enhanced mri image. seo, et al. showed using scanning with 99tc (human serum albumin dietulenetriamin pentaacetic acid-photon) positron emission computed tomography reduced vascularization of vestibular schwannoma 1 to 2 years after radiosurgery,. spiegelman and colleagues have suggested that ischemia was produced by tumor associated acute edema. fukoka and colleagues suggested that apoptosis may be a possible mechanism. based on these observations, it is aceeptable to consider that the loss of radiological central enhancing is a reliable indicator of longterm good control. this hypothesis, however, requires additional data from more patients and longer-term follow-up. failed treatment in no case was there any evidence of active tumor growth. it has to be considered that labyrinth schwanomas can swell without regrowing after radiosurgery. it is suggested that the modest doses currently in use may reduce this tendency. conclusions using small doses of radiation (similar to those used in the reference series from karolinska and pittsburg, smaller than the usual doses used in other gamma-knife units) can control the volume of the lesion as shown by the follow-up controls results. stereotactic mri and a multiple dosage program seem to be the main factors in achieving this result. according to published results the method can fail if the doctor decides not to partially exclude the lesions localized ar superior limit of the treated region. references 1. andrews jc, wackym pa, canalis rf: translabyrinthine approach to the cerebellopontine angle and internal auditory canal. in samii m, cheatham m, becker dp (eds): atlas of cranial base surgery. philadelphia, wb saunders, 1995, pp 18-23. 2. atkinson wj: anterior inferior cerebellar artery. j neurol neurosurg psychiatry 12:137-151, 1949. 3. backlund eo: stereotactic radiosurgery in intracranial tumors and vascular malformations. adv tech stand neurosurg 6:3–37, 1979. 4. burger pc, scheithauer bw, vogel fs: surgical pathology of the nervous system and its coverings. new york, churchill livingstone, 1991. 5. cairns h: acoustic neurinoma of the right cerebellopontine angle: complete removal. spontaneous recovery from postoperative facial palsy. proc r soc med 25:7-12, 1931. 6. cerullo lj, grutsch jf, heiferman k, osterdock r: the preservation of hearing and facial nerve function in a consecutive series of unilateral vestibular nerve charalampos seferis imaging of vestibular schwannomas following γ-knife treatment schwannoma surgical patients (acoustic neuroma). surg neurol 39:485-493, 1993. 7. chung wy, pan hc, guo wy, et al: protection of visual pathway in gamma knife radiosurgery for craniopharyngiomas. stereotact funct neurosurg 70 (suppl 1):139–151, 1998. 8. cross jp: unilateral neurilemmomas of the vii-th cranial nerve: then and now. am j otol 3:28-34, 1981. 9. cushing h: tumors of the nervus acusticus and the syndrome of the cerebellopontine angle. philadelphia, wb saunders, 1917. 10. dandy we: an operation for the total removal of cerebellopontine (acoustic) tumors. surg gynecol obstet 1:129-148, 1925. 38 11. dandy we: removal of cerebellopontine (acoustic) tumors through a unilateral approach. arch surg 29:337-344, 1934. 12. dandy we: results of removal of acoustic tumors by the unilateral approach. arch surg 42:1026-1033, 1941. 13. dituuio mv, malkasian d, rand rw: a critical comparison of neurosurgical and otolaryngological approaches to acoustic neuromas. j neurosurg 48:112,1978. 14. ebersold mj, hamer sg, beatty cw, et al: current results of the retrosigmoid approach to acoustic neurinoma. j neurosurg 76:901-909, 1992. 15. fischer g, fischer c, remond j: hearing preservation in acoustic neurinoma surgery. j neurosurg 76:910-917, 1992. 16. flickinger jc, kondziolka d, lunsford ld: dose and diameter relationships for facial, trigeminal, and acoustic neuropathies following acoustic neuroma radiosurgery. radiother oncol 41: 215–219, 1996. 17. flickinger jc, kondziolka d, niranjan a, et al: results of acoustic neuroma radiosurgery: an analysis of 5 years, experience using current methods. j neurosurg 94:1–6, 2001. 18. foster dmc, kemeny aa, pathak, et al: radiosurgery: a minimally interventional alternative to microsurgery in the management of acoustic neuroma. br j neurosurg 10:169–174, 1996. 19. fukuoka s, oka k, seo y, et al: apoptosis following gamma knife radiosurgery in a case of acoustic schwannoma. stereotact funct neurosurg 70 (suppl 1):88–94, 1998. 20. gantz bj, wackym pa: facial nerve abnormalities. in bumstead r, smith j (eds): pediatric facial plastic and reconstructive surgery. new york, raven press, 1993, pp 337-347. 21. gardner g, robertson jh: hearing preservation in unilateral acoustic neuroma surgery. ann otol rhinol laryngol 97:55–66, 1988. 22. glasscock me, poe ds, johnson gd: hearing preservation in surgery of cerebellopontine angle tumors. in fisch u, valavanis a, yasargil m (eds): proceedings of the sixth international symposium of neurological surgery of the ear and skull base. zurich, kugler & ghediru, 1988, pp 207-216. 23. hardy rwj, kinney se, lueders h, lesser rp: preservation of cochlear nerve function with aid of brain stem auditory evoked potentials. neurosurgery 11:16-19, 1982. 24. horrax g, poppen jl: experiences with the total and intracapsular extirpation of acoustic neuromata. ann surg 110:513-524, 1939. 25. horrax g: a comparison of results after intracapsular enucleation and total extirpation of acoustic tumors. j neurol neurosurg psychiatry 13:268-270, 1950. 26. house jw, brackmann de: facial nerve grading system. otololaryngol head neck surg 93:146–147, 1985. 27. house wf, hitselberger we: fatalities in acoustic tumor surgery, vol 2. baltimore, university park press, 1979, pp 235-264. 28. house wf: case summaries. arch otolaryngol 88:586-591, 1968. 29. house wf: monograph i: transtemporal bone microsurgical removal of acoustic neuromas. arch otolaryngol 80:587-756, 1964. 30. house wf: monograph ii: acoustic neuroma. arch otolaryngol 88:576-715, 1968. 31. house wf: trarislabyrinthine approach, vol 2. baltimore, university park press, 1979, pp 43-87, 12:137-151, 1949. 32. jackler rk, brackmann de (eds): neurotology. st. louis, mosbyyear book, 1994. 33. jenkins ha: hearing preservation in acoustic neuroma surgery. laryngoscope 102:125-128, 1992. 34. kanzaki i, kunihiro t, o-uchi t, et al: preservation of facial i nerve function in acoustic neuroma surgery by extended middle fossa approach. acta otolaryngol suppl 487:36-40, 1991. 35. kanzaki j, ouchi t, shiobara r, toya s: hearing preservation in acoustic neuroma surgery by the extended middle fossa method. otolaryngol suppl acta 487:22-29, 1991. 36. kaplan el, meier p: nonparametric estimation from incomplete observations. j am stat assoc 53:457– 481, 1958. 37. kartush jm, lundy lb: facial nerve outcome in acoustic neuroma surgery. oaolaryngol clin north am 25:623-647, 1992. 38. kondziolka d, lunsford ld, mclaughlin mr, et al: long-term outcomes after radiosurgery for acoustic neuromas. n engl j med 339:1426–1433, 1998. 39. kwartler ja, luxford wm, atkins j, shelton c: facial nerve monitoring in acoustic neuroma surgery. otolaryngol head neck surg 104:814-517, 1991. 40. lalvvani ak, butt fy, jackler rk, et al: facial nerve outcome after acoustic neuroma surgery: a study from the era of cranial nerve monitoring. otolaryngol head neck surg 111:561-570, 1994. romanian neurosurgery (2011) xviii 2 41. larouere mj, niparko jk, gebarski ss, kemink jl: three-dimensional x-ray computed tomography of the temporal bone as an aid to surgical planning. otolaryngol head neck surg 103:740-747, 1990. 42. larson da, flickinger jc, loeffler js: the radiobiology of radiosurgery. int j radiat oncol biol phys 25:557–561, 1993. 43. linskey me, lunsford ld, flickinger jc: neuroimaging of acoustic nerve sheath tumors after stereotactic radiosurgery. ajnr am j neuroradiol 12:1165-1175.1991. 44. linskey me, lunsford ld, flickinger jc: neuroimaging of acoustic nerve sheath tumors after stereotaxic radiosurgery. ajnr am j neuroradiol 12:1165–1175, 1991. 45. linskey me, lunsford ld, flickinger jc: radiosurgery for acoustic neurinoma: early experience. neurosurgery 26: 736–745, 1990. 46. list cf: die operative behandling die acoustic neurinoma mit drei ergebrisse. arch u klin chir 171:282-325, 1932. 47. lunsford ld, kamerer db, møller m: gamma knife: an alternative treatment for acoustic neurinomas. ann otol rhinol laryngol 97:631–635, 1988. 48. lye rh, dutton j, ramsden rt: facial nerve preservation during surgery for removal of acoustic nerve tumors. j neurosurg 57:739-743, 1982. 49. mafee mf, kumar a, valvassori ge, et al: diagnostic potential of ct in neurological disorders. laryngoscope 95:505-514,1985. 50. mckenzie kg, alexander ej: acoustic neuroma. clin neurosurg 2:21-36, 1955. 51. moller ar, janetta pj: preservation of facial function during removal of acoustic neuromas. j neurosurg 61:757-760, 1984. 52. mrazek j, fisur z, mazkora d: diagnosis, size, and operation results in 41 acoustic neurinomas. neoplasma 35:467-474, 1988. 53. nedzelski jm, tatar ch: hearing preservation: a realistic goal in surgical removal of cerebellopontine angle tumors. j otolaryngol 13:355-360, 1984. 54. neely jg: hearing conservation surgery for acoustic tumors: a clinical-pathologic correlative study. am j otol 6:143-146, 1985. 55. neely jg: is it possible to totally resect an acoustic tumor and conserve hearing? otolaryngol head neck surg 92:162-167, 1984. 56. norén g, arndt j, hindmarsh t: stereotactic radiosurgery in cases of acoustic neurinoma: further experiences. neurosurgery 13: 12–22, 1983. 57. norén g, greitz d, hirsh a, et al: gamma knife radiosurgery in acoustic tumors. acta neurochir suppl 58:104–107, 1993. 58. norén g: gamma knife radiosurgery in acoustic neuromas, in haid c (ed): vestibular diagnoses and neurootological management of the skull base. gräfelfing: demeter verlag, pp 43–45, 1991. 59. ogunrinde ok, lunsford ld, kondziolka, et al: cranial nerve preservation after stereotactic radiosurgery of intracanalicular acoustic tumors. stereotactic funct neurosurg 64 (suppl 1): 87–97, 1995. 60. olivecrona h: acoustic tumors. j neurosurg 26:613, 1967. 61. olivecrona h: analysis of results of complete and partial removal of acoustic neuromas. j neurol neurosurg psychiatry 13: 271-272, 1950. 62. poole jl, pava aa: the early diagnosis and treatment of acoustic nerve tumors. springfield, il, charles c thomas, 1957. 63. poole jl: suboccipital surgery for acoustic neurinomas: advantages and disadvantages. j neurosurg 24:483-492, 1966. 64. post k, eisenberg mb, catalano pj: hearing preservation in vestibular schwannoma surgery: what factors influence outcome? j neurosurg 83:191-196, 1995. 65. prasad d, steiner m, steiner l: gamma surgery for vestibular schwannoma. j neurosurg 92:745–759, 2000. 66. prasad s, hirsch be, kamerer db, et al: facial nerve function following cerebellopontine angle surgery: prognostic value of intraoperative thresholds am j otol 14:330-333, 1993. 67. rand rw, kurze t: case reports and technical notes: preservation of vestibular, cochlear and facial nerves during microsurgical removal of acoustic tumors—report of two cases. j neurosurg 28:158-161, 1968. 68. rand rw: microneurosurgery for acoustic tumors. in microneu rosurgery. st. louis, cv mosby, 1969, pp 126-155. 69. samii m, matthies c: management of 1000 vestibular schwannomas (acoustic neuromas): hearing function in 1000 tumor resections. neurosurgery 40:248-260, 1997. 70. samii m, matthies c: management of 1000 vestibular schwannomas (acoustic neuromas): the facial nerve-preservation and restitution of function. neurosurgery 40:684-694, 1997. 71. samii m, matthies c: management of 1000 vestibular schwannomas (acoustic neuromas): surgical management and results with emphasis on complications and how to avoid them. neurosurgery 40:11-21, 1997. 72. samii m, matthies c: management of 1000 vestibular schwannomas (acoustic neuromas): surgical management and results with an emphasis on complications and how to avoid them. neurosurgery 40:11–23, 1997. 73. sampath p, holliday mj, brem h, et al: facial nerve injury in acoustic neuroma (vestibular schwannoma) surgery: etiology and prevention. j neurosurg 87:6066, 1997. charalampos seferis imaging of vestibular schwannomas following γ-knife treatment 74. sampath p, holliday mj, brem h, et al: facial nerve injury in acoustic neuroma (vestibular schwannomas) surgery: etiology and preservation. j neurosurg 87:60– 66, 1997. 75. sampath p, holliday mj, brem h, et al: prevenhon of facial nerve injury in vestibular schwannoma surgery. neurosurg focus 5:4, 1998. 76. sampath p, rhines ld, goel r, long dm: cranial nerve preservation in vestibular schwannoma (acoustic neuroma) surgery. crit rev neurosurg 8:86-96, 1998. 77. selesnick sh, jacker rk: the changing clinical presentation of acoustic tumors in the mri era. laryngoscope 103:431–436, 1993. 78. seo y, fukuoka s, nakagawara j, et al: effect of gamma knife radiosurgery on acoustic neurinomas. assessment by 99mtcdpta-human serum albuminand 201tlcl-single photon emission computed tomography. stereotact funct neurosurg 66 (suppl 1): 93–102, 1997. 79. spiegelmann r, lidar z, gofman j, et al: linear accelerator radiosurgery for vestibular schwannoma. j neurosurg 94:7–13, 2001. 80. sterkers jm, morrison ga, sterkers o, badr eldine mmk: preservation of facial, cochlear, and other nerve functions in acoustic neuroma treatment. otolaryngol head neck surg 110:146-155, 1995. 81. sterkers jm, morrison ga, sterkers o, el-dine mm: preservation of facial, cochlear, and other nerve functions in acoustic neuroma treatment. otolaryngol head neck surg 110:146-155, 1994. 82.tator ch, nedzelski jm: preservahon of hearing in patients undergoing excision of acoustic tumors and other cerebellopon tine angle tumors. j neurosurg 63:168-174, 1985. 83. tos m, thomsen j: ten years’ experience with translabyrinthine acoustic neuroma surgery in denmark. acta otolaryngol suppl 449:2s-24, 1988. 84. varlotto jm, shrieve ds, alexander e iii, et al: fractionated stereotactic radiotherapy for the treatment of acoustic neuromas: preliminary results. int j radiat oncol biol phys 36:141–145, 1996. 85. wackym pa, andrews jc: middle cranial fossa approach. in samii m, cheatham m becker dp (eds): atlas of cranial base surgery. philadelphia, wb saunders, 1995, pp 26-31. 86. wackym pa, linthicum fh jr: diabetes mellitus and hearing loss: clinical and histopathological relationships. am j otol 7: 176-182, 1986. 87. wackym pa, rice dh, schaefer sd (eds): minimally invasive surgery of the head, neck, and cranial base. philadelphia, lippincott williams & wilkins, 2002, pp 1-559. 88. whittaker ck, luetje cm: vestibular schwannomas. j neuro surg 76:897-900, 1992. 89. yasargil mg, fox jl: the microsurgical approach to acoustic neurinomas. surg neurol 2:393-398, 1974. 90. yasargil mg, smith rd, gasser jc: microsurgical approach to acoustic neurinomas. adv tech stand neurosurg 4:93-197, 1977. 91. yasargil mg: a legacy of microneurosurgery: memoirs, lessons, and axioms. neurosurgery 45:10251091, 1999. microsoft word 8gramadafmmanagement 60 f.m. gramada et al management of unknown origin cerebral metastases management of unknown origin cerebral metastases f.m. gramada1, anca indrei2, st.m. iencean1, i. poeata3, gabriela dumitrescu4, l. miron5 1neurosurgical department, emergency hospital “n. oblu” iasi 2department of anatomy and embriology, “gr.t. popa” u.m.ph. iaşi 3neurosurgery, “gr.t. popa” university of medicine and pharmacy iaşi 4pathological department, emergency hospital “n. oblu” iasi 5oncologic department, emergency hospital “sf. spiridon” iasi abstract aim: the present study attempts to determine the steps for obtaining the etiological diagnosis of brain metastases with unknown origin. material and methods: a total of 190 patients with brain metastases diagnosed in the department of neurosurgery in emergency hospital ”n. oblu” iasi between 2007-2010 were included in this study. the clinical characteristics and pathological features were analyzed. results: there were 102 males and 88 females with a m:f ratio of 1.15:1. the median age of patients was 47.07 years (range 31-77 years). females patients were older (mean age 57.21 years) than males patients (49.15 years). 154 patients (81.05%) had single brain metastasis, and 36 patients (18.95%) had more than two. the lesions were supratentorial in 142 patients (74.73%), infratentorial in 18 (9.47%), and both infratentorial and supratentorial in 30 patients (15.78%). surgical treatment involved complete resection in 47.9% of cases, subtotal resection in 26.8%, and biopsy alone in the remainder (25.3%). brain metastases originating in lung cancer represented the most common type (47.39%), followed by those from breast cancer (19.79%), then those from skin (melanoma) (8.33%), genitourinary carcinoma (6.30%), and gastrointestinal carcinoma (2.62%). in 16.31% of cases, the primary tumor remained unknown, despite extensive investigation. conclusion: the primary cancer leading to brain metastases can be detected either by obtaining a sample of tumoral tissue through a neurosurgical operation on the intracerebral tumor (total ablation or stereotactic biopsy) with histopathological examination, or by additional tests of the whole body. taken into consideration the results of our own study, the management of the patients with brain metastases should include a thoracic ct scan or anteroposterior and lateral chest x-ray, clinical breast examination and mammography, abdominal ultrasound exploration, and skin, kidney and prostate examination. with the most sophisticated methods of diagnosis in approximately 16% of cases the origin of metastasis remains unknown. the identification of the primary site by the neuropathologist after stereotactic biopsy would clearly be advantageous. keywords: brain metastases, cerebral cancer treatment, stereotactic biopsy, tumoral type romanian neurosurgery (2011) xviii 1: 60 – 67 61 of all intracranial neoplasms, brain metastases represent 13.5-41% of all cases (4). although most of these metastatic brain tumors can have a known primary site such as lung or breast carcinoma, there remaines a number of cases in which a thorough search failed to identify the primary site even at autopsy (26). brain metastases of unknown origin become more frequently a problem for neurosurgeons as the expansion of computed tomograph (ct) network makes possible a cranio cerebral exploration for any patient with neurological symptoms (20). intraparenchymal metastases are usually well-defined round masses, often with nodular or ring enhancement (due to central necrosis) and with peritumoral edema. if multiple masses are seen, the diagnosis is much easier (4). magnetic resonance imaging (mri) with gadolinium is more sensitive than computed tomography for confirming the presence of brain metastases (18). it reveals single brain metastases in 1/3 of cases and multiple tumors in the remainders (28). thus, for patients complaining of indistinctive symptoms such as headache, dizziness, nausea or vomiting, a ct scan can provide the surprising discovery of a brain tumor which proves to be a metastasis after completion of exploration. from a clinically point of view, such a brain tumor can manifest through a major inaugural neurological symptom, such as localized or generalized seizures. the third situation is the discovery of such a brain tumor through a ct screening. in all these cases the patients did not complain of any other organ symptoms and they haven’t been registered with a cancer (1). this report details the experience at the neurosurgery department of “prof. dr. n. oblu” clinic emergency hospital, iasi, in the management of patients in whom the only evidence of malignancy at presentation was the metastatic disease of the brain. the aim of the present study was to evaluate this patient group in order to develop guidelines for further diagnostic and treatment procedures. material and method between 2007-2010, 190 consecutive patients with brain metastases, but with unknown primary site and no other evidence of metastases were treated in the neurosurgery department of “prof. dr. n. oblu” clinic emergency hospital, iasi. all the patients were admitted in the hospital due to a previous general and neurological screening. imaging investigation (ct or mri) confirmed the diagnosis of a brain metastasis and gave information about their number. surgical removals or stereotactic biopsies were carried out in all of them. a search for the primary site of the tumor was made in each case during hospital stay. these included detailed history taking, thorough physical examination, routine chest radiographs, urine and blood investigations. also, tissue samples taken through surgical removal or stereotactic biopsy have been processed in the department of pathology of the same hospital using the standard histopathological technique. microscopical examinations have been done in all cases in order to determine the tumoral type of cerebral neoplasia and to identify the primary cancer due to some histopathological similarity between metastases and their “parental” malignancies. 62 f.m. gramada et al management of unknown origin cerebral metastases results personal experience in the neurosurgery service of the hospital “n. oblu” iasi showed that in a three years period of time have been diagnosed 190 patients with cerebral metastasis. there were 102 males and 88 females with a m:f ratio of 1.15:1. the mean age of entire population was 47.07 years with a range of 31 – 77 years. females ranged in age from 49 to 77 years with a mean of 57.21 years, whereas males had a mean age of 49.15 years with a range of 31 to 75 years. the highest incidence of brain metastases was in the sixth and seventh decades of life (table 1). brain ct was performed in 135 patients (71.05%), mri in 36 patients (18.94%), and ct plus mri in 19 (10%). 154 patients (81.05%) had single brain metastasis, and 36 patients (18.95%) had more than two. the lesions were supratentorial in 142 patients (74.73%), infratentorial in 18 (9.47%), and both infratentorial and supratentorial in 30 patients (15.78%). surgical treatment involved complete resection in 47.9% of cases, subtotal resection in 26.8%, and biopsy alone in the remainder (25.3%). primary malignancies were diagnosed after surgical removal. taken all cases together, brain metastases originating in lung cancer represented the most common type (47.39%) (figures 1 and 2), followed by those from breast cancer (19.79%), then those from skin (melanoma) (8.33%) (figure 3), genitourinary carcinoma (6.30%), and gastrointestinal carcinoma (2.62%). in 16.31% of cases, the primary tumor remained unknown, despite extensive investigation (table 2). table 1 brain metastases frequency by patients' age age (years) 30-39 40-49 50-59 60-69 70-79 total no. of cases 12 23 65 74 16 190 percentage 6.31% 11.97% 34.21% 38.54% 8.33% 100% table 2 brain metastases frequency by primary cancer site organ of origin lung breast skin colo rectum stomach testicul prostate kidney unknown no. of cases 91 38 16 3 2 3 7 2 31 per –centage (%) 47.39 19.79 8.33 1.57 1.05 1.57 3.68 1.05 16.31 figure 1 smear of a brain metastasis originating in an epidermoid squamocelullar carcinoma of the lung (toluidine blue, 10x20) figure 2 microphotograph of the microscopic features of a brain metastasis originating in a papillary carcinoma of the lung (hematoxylin&eosin, 10x10) romanian neurosurgery (2011) xviii 1: 60 – 67 63 figure 3 histologic features of a brain metastasis from an epithelioid melanoma of skin (hematoxylineosin, 10x20) discussion in 33-66% of patients, solitary cerebral metastasis give rise to the symptoms preceding even the primary lesion. furthermore, in a significant number of cases the primary malignancy can not be diagnosed during life and in some cases remains unknown even at autopsy (26). the incidence and primary source of brain metastases vary with patient age. the highest incidence of brain metastases (over 60%) is observed in patients 50 to 80 years old. in our study, the highest incidence of all cerebral metastases (72.75%) appeared in a younger group of patients (50-69 years) and the peak incidence (38.56%) was encountered in the sixth decade (50-59 years). in the present research, there is no predilection of brain metastases for males or females. the histology of the primary cancer appears to be the major dictator of the frequency and pattern of intracranial extension. virtually, any type of cancer has the ability to produce brain metastases. however, in decreasing relative frequency, lung cancer, breast cancer, melanoma, renal cancer, and colon cancer account for most brain metastases (27). in 1889, an english pathologist, stephen paget, analysed the organ distribution of metastases produced by different human neoplasms in order to determine the pattern of metastasis process. he concluded that certain tumor cells (the “seed”) had a specific affinity for the milieu of certain organs (the “soil”) because metastases resulted only when the seed and soil were compatible (9). it is consider that 30% to 60% of brain metastases originate from lung cancer (12). breast cancer ranks second to lung cancer as the most frequently occurring primary tumor in patients with brain metastases. among women, breast cancer is the most common cause of brain metastasis, resulting in 5% to 30% of all brain metastases (7). melanoma ranks third among primary tumors giving rise to brain metastases. of patients with brain metastases, approximately 5% to 21% will have melanoma as their primary tumor (29). metastatic brain tumors from colorectal cancer are relatively rare, with a reported frequency of 1.8% to 4.8% of all metastatic brain metastases (24). brain metastases from gastric cancer are extremely rare. patients with gastric cancer account for less than 1% of all cases of brain metastases in autopsy and clinical series (27). intracranial metastases from prostate cancer are rare (0.6% to 4.4% of cases) (8). the incidence of brain metastases in patients with testicular cancer ranges from 2% to 25% in clinical series and was 20.7% in an autopsy series. however, brain metastases are extremely rare in surgical series of patients with testicular cancer (2%) (27). the incidence proportion of metastatic brain tumors from renal cancer in patients with primary renal tumors ranges from 5.5% to 11% (16) in 1999, 64 f.m. gramada et al management of unknown origin cerebral metastases taddei et al. investigated a group of patients with brain metastases with clinical characteristics similar with our study. in their group, made up of 211 patients with age ranging from 33 to 79 years, lung tumors (47%) and breast tumors (9%) were the most frequently responsible for brain metastases. in 17% of patients, the primary lesion was unknown (33). in our study, most of the patients with an identified underlying malignancy had a primary lung cancer (49.69%). this cancer also ranked first in other studies, although le cesne et al found gastrointestinal tumours to be the most frequent (6). there are two possibilities to discover the location of primary cancer: • neurosurgical intervention and sampling of tumoral tissue in order to determine the histopathological features of tumoral architecture and tumoral cells; • general clinical examination and laboratory tests for discovery of primary neoplasm. neurosurgical intervention may be classical ablation of the tumor or stereotactic biopsy. total ablation intervention addresses to patients who have a good general state, single metastases, which is located in a non-eloquent area. in cases with multiple metastases total removal will address to the voluminous formation with herniation tendency. indications for stereotactic biopsy refer to patients with deterioration of the general state, and with multiple metastases located in eloquent areas (rolando area, central gray nuclei, corpus callosum, and brain stem). to obtain a valuable result it is necessary to make multiple samples within the tumor. as a consequence, fine needle biopsy could be a source of errors. after completing all explorations, including neurosurgical intervention, the discovery of the initial site of the primary cancer could rise to 85%. pavlidis et al. (25) found that primary neoplasias remain unknown in 3% of all cases of cancers and greco and hainsworth (15) reported even less (2% of all cases). in our study, the primary site remained unknown in 16.44%patients, that represents a comparable group with those in other studies, in which the underlyning malignancy could not be detected in 15%50% of the patients with brain metastases. to have certainty it is mandatory to see a well-differentiated tumoral tissue that repeats the architecture of the tissue where the cancer developed initially. for poorly differentiated tumors, the origin of neoplasia couldn’t be identified. moreover, there are two situations: in some cases existed similarity between the microscopic appearances of the brain metastasis and those of primary cancer, but in other cases the histopathological features of the brain metastasis does not coincide with those of the primary cancer. so, surgical intervention can offer a tumor sample that will be analyzed by the neuropathologist who could identify the histological type and the location of the primary cancer, but when there are poorly differentiated tumoral cells, than the pathological diagnosis could be difficult. in these cases it is necessary to use further investigations such as immunohistochemistry, electron microscopy and genetic analysis. a second possibility to identify the origin of a brain metastasis is to explore the whole body when there isn’t the necessity of an emergency operation for decompression. this is the situation of small brain metastases, with no tendency of herniation and no signs of intracranial romanian neurosurgery (2011) xviii 1: 60 – 67 65 hypertension. the easier examination and more comfortable for the patient is a positron emission tomography (pet scan), but it has high costs. a study comprising 3000 asymptomatic subjects have been found the existence of at least one brain metastasis in 3% of cases. brain metastases with unknown origin can be detected with fluorodezoxyglucoze 18 (18f) which allowed the discovery of the primary cancer in 29% of cases (19, 22, 23). if there isn’t pet scan in the hospital, then it can be used classical explorations (radiograph, ct, mri, laboratory testing). the ranking of these explorations could be based on statistics which showed how often can be encounter an organ as the origin of the primary cancer which can lead to a brain metastasis. taken into consideration statistics from the literature (21) and the results of our own study, the management of the patients with brain metastases should include a thoracic ct scan or anteroposterior and lateral chest x-ray, clinical breast examination and mammography, abdominal ultrasound exploration, and skin, kidney and prostate examination. the treatment of brain metastases have to be complex in order to provide the longest survival for the patients (figure 4). so, the management of brain metastases represents a formidably challenge. the first place in the panoply of treatment methods is neurosurgical complete removal of single metastases. the second method is the whole brain radiotherapy with or without pharmacological agents (such as motexafin gadolinium) which enhance the effect of radiation on brain metastases remnants (10). another possibility for intracerebral metastases treatment is stereotactic radiosurgery which use several types of radiation-therapy devices: cobalt-60–based machines, linear accelerators, and cyclotrons, which use gamma rays,x-rays, and proton, respectively (32). it can be used also brachytherapy with iodine 125 (17) or laser induced thermal therapy (31). the goal of discovering the site of primary cancer would be the use of a specific type of chemotherapy for achieving cure of cerebral metastases. unfortunately it should be noted that the existence of blood-brain barrier prevents chemotherapy drug action (9). however, there are studies (3) indicating the size reduction of brain metastases in some cases with lung or breast origin after using temozolomide, efaproxiral, metoxafin (13). in carcinomatous meningitis we can use intrathecal cytarabin and methotrexate (5). the maximum dose intravenous methotrexate also can be used (14). when brain metastases are discovered, it should be initiated a symptomatic corticosteroid therapy and treatment for prevent seizures or thromboembolism. after interdisciplinary cooperation, primary cancer should be treat in tandem and in function of vital emergency. complex treatment of cerebral metastases provides the longest survival. the median survival of patients with cerebral metastases would be 7 months when they are treated with whole brain radiotherapy, 15 months when radiosurgery is associated, 14 months when radiosurgery is used alone, 14 months when brain radiotherapy is associated with surgical ablation, and 21 months when all three treatment methods are used together (2, 11, 30, 34). 66 f.m. gramada et al management of unknown origin cerebral metastases algorithm of diagnosis and treatment unknown origin cerebral metastasis high ger of engagement little danger of engagement ablation of dangerous metastasis emergency pet-ct/general examination solitary metastasis surgery available ablation multiples metastasis surgery non-available stereotactic biopsy radiosurgery treatment of origin cancer; radiotherapy +/chemotherapy symptomatic treatment figure 4 algorithm of diagnosis and treatment for unknown origin cerebral metastases depending on the number of cerebral metastases, it is noted that single metastasis treated by surgical ablation and radiotherapy has a median survival time of 13 months while those multiple will have a median survival time of 7 months, with 0% survival at 2 years. surgical ablation combined with radiosurgery offers an average survival of 10 months (15% surviving at 2 years). conclusions the discovery of a brain metastasis in a routine computed tomography examination or for minor neurological symptoms become more frequently. the primary cancer leading to brain metastases can be detected either by obtaining a sample of tumoral tissue through a neurosurgical operation on the intracerebral tumor (total ablation or stereotactic biopsy) with histopathological examination, or by additional tests of the whole body. taken into consideration the results of our own study, the management of the patients with brain metastases should include a thoracic ct scan or anteroposterior and lateral chest x-ray, clinical breast examination and mammography, abdominal ultrasound exploration, and skin, kidney and prostate examination. with the most sophisticated methods of diagnosis in approximately 16% of cases the origin of metastasis remains unknown. the identification of the primary site by the neuropathologist after stereotactic biopsy would clearly be advantageous. references 1. abd-el-barr m. m., rahman m., rao g.: investigational therapies for brain metastases; neurosurg. clin n. am.; 2011, 22(1), 87-96 2. agboola o., benoit b., cross p et al.: prognostic factors derived from recursive partition analysis (rpa) or radiation therapy oncologic group (rtog) brain metastases trials applied to surgically resected and irradiated brain metastatic cases., int jj rradiol oncol biol phys, 1998;42(1),155. romanian neurosurgery (2011) xviii 1: 60 – 67 67 3. van den bent m. j.: the role of chemotherapy in brain metastases. eur j cancer; 2003;39(15);2114. 4. berry m, suri s, chowdhury v, mukhopahyay (eds.), diagnostic radiology. neuroradiology including head and neck imaging, second edition, jaypee bothers medical publishers, india, 2006, pp. 334-353 5. bleyer w. a., poplack d. g.: intraventricular versus intralumbar methotrexate for central-nervous-system leukemia: prolonged remission with the ommaya reservoir. med pediatr oncol; 1979;6(3)207. 6. le cesne a, le chevalier t, caille p, métastases de cancer à point de départ inconnu: enseignement de 302 autopsies, la press médicale, 1991; 20:1369-73) 7. cheng x, hung mc, breast cancer brain metastases, cancer metastasis rev, 2007, 26:635 8. erasmus ce, verhagen wi, wauters ca, van lindert ej,: brain metastasis from prostate small cell carcinoma: not to be neglected, can j neurol sci, 2002, 29:375-377 9. fidler i. j., balasubramanian k., lin q., kim s. w., kim s. j.: the brain microenvironment and cancer metastasis. molcells, 2010 ;30(2);93-8. 10.francis d, richards gm, forouzannia a, mehta mp, khuntia d, motexafin gadolinium: a novel radiosensitizer for brain tumors, expert opin pharmacother, 2009, 10(13):2171-80 11.gaspar i., scott c., rotman m. et al: recursive partitioning analysis (rpa) of prognostic factors in three radiation therapy oncology group (rtog) brain metastases trials. int j radiol oncol bbiol phys; 1997;37(4),745. 12.ghaffarpour m, firouzbakhsh sh, glichnia omrani h, mansoorian b, neurologic manifestations as the presenting symptoms un lung cancer. , acta medica iranica, 2002, 40(3):198-202 13.giorgio cg, giuffrida d, pappalardo a, russo a, santini d, salice p. et al. oral temozolomide in heavily pre-treated brain metastases from non-small cell lung cancer phase ii study, lung cancer 2005, 50(2):247-254 14.glanz m. j., cole b. f., recht i. et al. : high-dose intravenous methotrexate for patients with nonleukemic leptomeningeal cancer : is intrathecal chemotherapy necessary ? j clin oncol. 1998;16(4)1561 15.greco f. a., hainsworth j. d.: cancer of unknown primary site in de vita, helman, and rosenberg’s: cancer principles & practice of oncology, 8th edition, 2008, vol ii, pp 2363-2387 16.harada y, nonomura n, kondo m et al, clinical study of brain metastases of renal carcinoma, eur urol 1999, 36:230 17.huang k, sneed pk, kunwar s, kragten a, larson da, berger ms, chan a, pouliot j, mcdermott mw, surgical resection and permanent iodine-125 brachytherapy for brain metastases, j neurooncol, 2009, 91(1) :83-93 18.jin j, zhou x, liang x, huang r, chu z, jiang j, zhan q., a study of patients with brain metastases as the initial manifestation of their systemic cancer in a chinese population. j neurooncol. 2010 oct 27. http://www.ncbi.nlm.nih.gov/pubmed/20978821 19.kruger s., mottaghy f. m., buck a. k., maschke s., kley h., frechen d., wibmer t., reske s. n., pauls s.: brain metastsis in lung cancer. comparision of cerebral mri and 18-fdg-pet/ctfor diagnosis in the initial staging; nuklearmedizin, 2010, 17,50(2) 20.larson d. a., rubenstein j., mcdermott. m. w.: metastatic cancer to the brain, in devita vt jr., lawrence ts, rosenberg sa, devita, hellman, and rosenberg’s: cancer. principles & practice of oncology, 8th edition, 2008, vol. ii, lippincott williams & wilkins, usa, pp. 2461-2475. 21.lassman a. b., deangelis i. m.: brain metastases. neurol clin; 2003;21(1),1. 22.lengyel z., szakall s., kajary k., toth g., molnar p.: pet/ct in malignant diseases and our experiences since 2005; 1-st international symposium of oncologic imaging focusing on pet/ct; felix; 30-31.10.2009, pg. 35-36 23.mansi l., cuccurulo v., rambaldi p. f., cascini g.: background of pet-ct imaging in oncology;1-st international symposium of oncologic imaging focusing on pet/ct; felix; 30-31.10.2009, pg.10. 24.patanaphan v, salazar om, colorectal cancer : metastatic patterns and prognosis, south med j, 1993, 86:38 25.pavlidis n., briasooulis e., hainsworth j. et al: diagnostic and therapeutic management of cancer of an unknown primary., eur j cancer; 2003;39(14),1990 26.salvati m, cervoni l, raco a, single brain metastases from unknown primary malignancies in ctera , journal of neuro-oncology, 1995, 23: 75-80 27.sawaya r, intracranial metastases: current management strategies, blackwell, futura, 2004, p. 20 28.schellinger pd., meinck hm, thron a.. diagnosti accuracy of mri compared to ct in patients with brain metastases, j neurooncol;1999;44(3);275. 29.sloan ae, nock cj, einstein db, diagnosis and treatment of melanoma brain metastases: a literature review, cancer control 2009, 16:248 30.sneed p. k., suh j. h., goetsch s. j.,et al: a multiinstitutional review of radiosurgery alone vs. radiosurgery with whole brain radiotherapy a the initial management of brain metastases. int j radiol oncol biol phys; 2002;53(3);519. 31.stafford rj, fuentes d, elliott aa, weinberg js, ahrar k, laser-induced thermal therapy for tumor ablation, crit rev biomed eng, 2010; 38(1):79-100 32.suh jh, stereotactic radiosurgery for the management of brain metastases, n engl j med 2010; 362:1119-1127 33.taddei gl, moncini d, raspollini mr, mennonna p, et al. metastatic brain tumors, pathologica 1999, 91(1):13-17 34.tendulkar f.d., liu s. w., barnett g. h. et al.: rpa classification has prognosti significance for surgically resected single brain metastases. int j radiol oncol biol phys 2006;66(3)1990. 404 not found 10pankajgupta_long2014 82 gupta et al long segment dorsolumbar spinal arachnoid cyst long segment dorsolumbar spinal arachnoid cyst: a case report pankaj gupta1, nityanand gopal2, varsha kumar3 1registrar, department of neurosurgery, sawai man singh medical college, jaipur, rajasthan 302004 2associate professor, p.g. department of surgery, m.l.n. medical college, allahabad, uttar pradesh – 211001 3senior resident, department of pathology, sanjay gandhi post-graduate institute of medical sciences, lucknow, uttar pradesh 226014 abstract congenital spinal intradural arachnoid cyst involving almost the entire spine is very rare. we report a case of 15 years old boy, who presented with progressive spastic paraparesis with gait instability for last 4 months. mri spine revealed thoracolumbar arachnoid cyst extending from d4 to l3 segment. complete surgical excision of arachnoid cyst and laminoplasty was done. patient recovered completely and histopathological examination of specimen confirmed the diagnosis of arachnoid cyst. introduction arachnoid cysts are pouches of csf, found within subarachnoid space. they are of two types, primary spinal intradural arachnoid cysts are uncommon congenital lesions that arise during development from the splitting of arachnoid membrane, which contains csf like fluid. although the exact pathogenesis is unclear but they may result from an alteration and enlargement of the arachnoid trabeculae because of valve like mechanism. secondary arachnoid cysts result from trauma, meningitis, arachnoiditis or may be iatrogenic following spinal anaesthesia. it may be associated with congenital meningocoele, syringomyelia, neurofibromatosis, marfan syndrome or corpus callosal agenesis.according to medical literature, very rarely it may run in families as an autosomal recessive trait. (2) the most common location of arachnoid cyst in spine is thoracic segment, dorsal to the spinal cord, while in brain it is middle cranial fossa. (3) although it is congenital in origin but most common age of presentation is between 30 to 50 years of age, with slight female predominance. (4,5) spinal arachnoid cysts almost always communicate with intrathecal subarachnoid space through a small defect in the dura. usually they are asymptomatic and rarely they can cause spinal cord compression, romanian neurosurgery (2014) xxi 1: 82 84 83 producing local/radicular pain, paraparesis/paraplegia, sensory disturbances, gait instability/ataxia and sphincter disturbances. rarely they may present with intracystic haemorrhage or with intracranial hypotension due to spontaneous cyst rupture. (5) case report a 15 years old boy presented to the neurosurgery opd with chief complaints of weakness, numbness of both lower limbs and instability during walking for last 4 months. the onset of symptoms was insidious and gradually progressive in nature. there was no history of trauma, spinal surgery, infection or spinal anaesthesia. on examination spastic paraparesis was present. motor power of both lower limbs was 4/5 at hip and knee and 3/5 at ankle and toes. deep tendon reflex was bilaterally brisk and babinski’s sign was present. no clinical evidence of neurofibromatosis was present. mri of spine revealed intradural-extramedullary, multiloculated, large, cystic lesion extending from d4 to l3 segment, which was hypointense to cord on t1w1 and hyperintense on t2w1. lesion was isointense to csf, showing restriction on dwi images. there was no enhancement on contrast study. the cord compression was most marked from d9 to l3 region. patient was operated electively and d4 to l3 segment open door laminoplasty done. dura was tense and bulging. vertical midline durotomy done. on opening the arachnoid layer, csf escaped out under high pressure and the cyst filled with csf became visible. the cyst was large, multiloculated, covering the dorsal aspect of spinal cord, extending from d4 to l3 segment and was producing cord compression, which was evidenced by thinning of cord and absence of cord pulsation. the cystic membrane was exposed and resected in piecemeal. after excision of cyst the dorsal portion of the cord gradually regained its normal diameter and adequate cord pulsation returned back. water tight dural repair was done using and no csf leak was observed peroperatively. the postoperative period was uneventful. patient recovered almost completely and the power of both lower limbs was 5/5 on postoperative day 4. patient could walk on postoperative day 8, without gait instability. histopathological examination of the resected specimen confirmed the diagnosis of arachnoid cyst. on regular follow up, the boy could walk and run without difficulty. till date patient has no complaints suggestive of recurrence of arachnoid cyst. discussion spinal intradural arachnoid cyst is an uncommon entity and it rarely leads to symptomatic spinal cord compression. to the best of our knowledge, baysefer et al. (2001) has reported such a giant arachnoid cyst in a 2 years old boy, extending from d3 to l1 segment. (2) 84 gupta et al long segment dorsolumbar spinal arachnoid cyst figure 1 mri saggital and axial section of spine showing intradural-extramedullary, multiloculated, large, cystic lesion extending from d4 to l3 segment, which is hypointense to cord on t1w1 and hyperintense on t2w1. the lesion is isointense to csf. the conservative management is reserved for asymptomatic patients of spinal arachnoid cyst, while complete neurosurgical excision is the treatment of choice in symptomatic cases. extensively giant cysts, ventrally located cysts, or cysts densely adhered to the cord can be treated by partial resection and fenestration of the cyst, so that it can freely communicate with subarachnoid space. (2,5) other options of treatment are cystoperitoneal shunt, cystopleural shunt, cystoarachnoid shunt, marsupialisation, endoscopic/laser fenestration and reservoir placement. (1) simple aspiration of cyst is associated with unacceptable high recurrence rate, so it is not a recommended treatment modality. (2) the role of pharmacotherapy is limited to symptomatic relief only. footnotes: source of support: nil conflicts of interest: none declared correspondence address: dr. nityanand gopal(mch) associate professor neurosurgery p.g. department of surgery swaroop rani nehru hospital moti lal nehru medical college allahabad uttar pradesh 211001. email id: drpankaj.gupta@yahoo.co.in, nnggopal@yahoo.co.in references 1. alvisi c, cerisoli m, giulioni m, guerra l; longterm results of surgically treated congenital intradural spinal arachnoid cysts. journal of neurosurgery; 67(3):333–335, 1987. 2. baysefer a, lzci y, erdogan e; lateral intrathoracic meningocele associated with a spinal intradural arachnoid cyst. pediatric neurosurgery; 35(2):107–110, 2001. 3. elsberg ca, dyke cg, brewer ed; bull. neurol. inst. n.y., iii, 395, 1934. 4. lee hj, cho dy; symptomatic spinal intradural arachnoid cysts in the pediatric age group: description of three new cases and review of the literature. pediatric neurosurgery; 35(4):181–187, 2001. 5. wang my, levi ad, green ba; intradural spinal arachnoid cysts in adult. surgical neurology; 60(1):49– 56, 2003. 14jaiswal_traumatic acute 478 jaiswal et al traumatic acute posterior fossa subdural hematoma traumatic acute posterior fossa subdural hematoma – a case report and review of literature manish jaiswal, i. vijay sundar, ashok gandhi, devendra purohit, r.s. mittal department of neurosurgery, sms medical college and hospital jln marg, jaipur (302004), rajasthan, india abstract: traumatic subdural hematomas of the posterior fossa are rare but dangerous neurosurgical emergencies that require prompt diagnosis and management to avoid the uniformly poor outcome. we present a case of a teenager with severe tbi and acute subdural hematoma of the posterior fossa that deteriorated rapidly before surgery but eventually made a good recovery. we also the review the literature concerning traumatic posterior fossa subdural hematomas [pfsdh]. key words: acute subdural hematoma; posterior fossa sdh; head injury. introduction acute pfsdhs are rare manifestations of traumatic brain injury with a reported incidence of 0.21% to 0.27% [1, 2]. they are classical neurosurgical emergencies as they can cause abrupt deterioration and death from brainstem compression. case report a 16 year old male presented to the emergency department with history of unconsciousness following road traffic accident. on examination patient was comatose with glasgow coma score (gcs) of e1v2m4. pupils were bilaterally 4mm and sluggishly reactive. patient was intubated and an immediate computed tomography scan (ct scan) brain was performed which showed hyper-dense blood in posterior fossa region between cerebellar hemispheres with maximum thickness more than 1 cm causing pressure on fourth ventricle (figure 1). patient was immediately shifted to operation theatre where posterior fossa craniectomy and foramen magnum decompression was done. dura was tense and bluish (figure 2). durotomy and evacuation of acute sdh was done. to accommodate cerebral edema dura was left open. patient was shifted to neurosurgical icu and kept under intensive monitoring and elective ventilation. he gradually recovered over the next 48 hours and was extubated on the third day. patient was eventually discharged at 10th post-operative day at which time he was conscious. at last follow up of two months from surgery patient is doing well and is ambulatory without support. romanian neurosurgery (2014) xxi 3: 478 – 481 479 figure 1 ct scan showing hyper-dense blood in posterior fossa region causing pressure on fourth ventricle figure 2 posterior fossa craniectomy and foramen magnum decompression showing bluish and tense duramater discussion pfsdhs constitute the rarest type of posterior fossa traumatic hematomas, accounting for approximately 10% of posterior fossa traumatic lesions and is roughly 0.3 to 0.8% of supra-tentorial subdural hematomas (1, 2, 3). d’avella et al (1) classified patients with posterior fossa subdural hematomas into two groups. 1: conscious patients with hematomas not more than 1cm with no signs of pressure effects on the brainstem, fourth ventricle or basal cisterns and 2): patients with hematomas larger than 1 cm, signs of mass effect on the brainstem, fourth ventricle or basal cisterns. urgent surgery was recommended in the latter group. clinical features are diverse and unpredictable ranging from coma or significant depression of consciousness [4] to almost conscious patients. the clinical course during the initial 24 48 hours is more important (1, 4). progressive or sudden clinical deterioration has been observed frequently within the first several hours after injury. typical ct finding of pfsdh is the presence of high attenuation extra-cerebellar/ retrocerebellar collection in a concave-convex shape (1). occipital fracture, hydrocephalus and subarachnoid hemorrhage could be seen in these patients (1, 4, 5). impact in the region of posterior fossa frequently produces contrecoup lesions supratentorially in the frontal and/ or temporal region which are common findings in traumatic pfsdh [6]. delayed or evolving hemorrhagic lesions of the posterior 480 jaiswal et al traumatic acute posterior fossa subdural hematoma fossa have been reported (7) thus emphasizing the need for close monitoring which may include daily ct scans until the lesion stabilizes. ct scan plays an even more important role in the absence of clinical deterioration. ct parameters such as thickness of hematoma, appearance of the cisterns surrounding the brainstem, and coexisting posterior fossa lesions aid decision making (1, 8). the thickness of hematoma, although reflecting only in part the course of the disease, is an important parameter since large hematomas generally need prompt evacuation, whatever the clinical status of the patient. possible brainstem damage which may co-exist with pfsdh may be responsible for the discrepancy that is sometimes noted between the thickness of the hematoma and the clinical condition (5, 6). management of pfsdh is individualized rather than algorithmic. the general concept is that an acute posterior fossa subdural hematoma is a neurosurgical emergency as it may cause brainstem compression and acute fourth ventricle obstruction, worsening clinical features and death. d’avella et al performed a clinicoradiological analysis of 24 patients of traumatic pfsdh of which 19 were operated upon [1]. they found a high percentage of favorable outcome in the group with initial gcs>, or = 8 whereas a uniformly poor outcome was noted in the group with initial gcs<8. they found that only gcs score had independent prognostic significance. park et al published their experience of six operated cases of pfsdh and noted that of the four patients with initial gcs of 13 or above three patients deteriorated within 24 hours from trauma. patients with thick hematomas and deteriorating clinical status need urgent surgery as do patients with the radiological signs of pressure effects on the fourth ventricle or brain stem or the surrounding cisterns, even when the patient has no neurological deficits (4). conservative approach may be advocated in pfsdhs which are less than or equal to 1 cm in thickness with no pressure effect on the brain stem and fourth ventricle and no signs of neurological deficit (9). the rest need close neurosurgical monitoring because of the danger of delayed increase in hematoma or fall in conscious level. the standard surgical treatment consists of evacuation of the hematoma by suboccipital craniectomy and durotomy (4). the most important prognostic factor in pfsdh is the clinical condition of the patient at the time of surgery (4, 9, 10). patients with a glasgow coma scale score less than 8 have a high percentage of bad outcome and patients with a glasgow coma scale of 8 or more have better chance of recovery (1). early ct scanning is very important as it not only provides data for immediate decision making but also serves as a control to evaluate the progression of the hematoma within the first 24 hours in conservatively managed patients (1). early diagnosis before neurological deterioration develops and a prompt surgical evacuation of hematoma lead to satisfactory outcome in the treatment of pfsdh patients. romanian neurosurgery (2014) xxi 3: 478 – 481 481 conclusion pfsdh is a relatively rare manifestation of traumatic brain injury which can have various presentations. the possibility of a progressive course of the lesion or a delayed hematoma should be kept in mind even if initial ct is normal. the most important factor determining the prognosis is level of consciousness just before surgery. early diagnosis by an early ct scan and a prompt surgical evacuation lead to excellent recovery in patients with pfsdh. we recommend urgent posterior fossa craniectomy and durotomy if the patient has poor initial gcs, deterioration in gcs during hospital stay, initial ct scan showing pressure on fourth ventricle or hematoma more than 1 cm thick. during surgery it is advisable to accommodate cerebral edema by leaving the dura open or by duraplasty. in all cases pre and post-operative intensive neurosurgical monitoring is mandatory. correspondence manish jaiswal a 33/48 a 2, omkareshwar, varanasi, 221001, uttar pradesh, india phone – 091-9799980494 email – manishmlnmc@gmail.com references 1. d’avella d, servadei f, scerrati m, tomei g, brambilla g, massaro f, et al: traumatic acute subdural hematomas of the posterior fossa: clinicoradiological analysis of 24 patients. acta neurochir (wien) 145:1037-1044, 2003 2. karasawa h, furuya h, naito h, sugiyama k, ueno j, kin h: acute hydrocephalus in posterior fossa injury. j neurosurg 86: 629-632, 1997 3. dirim bv, oruk c, erdogan n, gelal f, uluc e: traumatic posterior fossa hematomas. diagn interv radiol 11: 14-18, 2005 4. hecimovic i, blagus g, kristek b, rukovanjski m, vrankovic d: successful treatmentof traumatic acute posterior fossa subdural hematoma: report of two cases. surg neurol 51: 247-251, 1999 5. kim yd, park hk, chang jc, cho sj, choi sk, byun pj: traumatic intracerebellar hematomas. j korean neurosurg soc 37: 213-216, 2005 6. vrankovic d, splavski b, hecimovic i, kristek b, dmitrovic b, rukovanjski m, et al: anatomical cerebellar protection of contrecoup hematoma development. analysis of the mechanism of 30 posterior fossa coup hematomas. neurosurg rev 23: 156-160, 2000 7. servadei f, nanni a, nasi mt, zappi d, vergoni g, giuliani g, et al: evolving brain lesions in the first 12 hours after head injury: analysis of 37 comatose patients. neurosurgery 37: 899-907, 1995 8. servadei f: prognostic factors in severely head injured patients with subdural haematoma’s. acta neurochir (wien) 139: 273-278, 1997 9. ashkenazi e, carmon m, pasternak d, israel z, beni l, pomeranz s: conservative treatment of a traumatic subdural hematoma of the posterior fossa in a child: case report. j trauma 36: 406-407, 1994 10. motohashi o, komeyama m, shimosegawa y, fujimori k, sugai k, onuma t: single burr hole evacuation for traumatic acute subdural hematoma of the posterior fossa in the emergency room. j neuro-trauma 19: 993-998, 2002 a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 431-437 doi: 10.33962/roneuro-2019-068 www.journals.lapub.co.uk/index.php/roneurosurgery adeloye-odeku disease in irrua, south-south nigeria. the experience so far in a rural neurosurgical setting e. morgan1, c.o. okwumezie2, g.c. akasike1, e a. morgan1 1 neurosurgery unit, department of surgery, irrua specialist teaching hospital, irrua, edo state, nigeria 2 department of orthopaedics, irrua specialist teaching hospital, irrua, edo state, nigeria 3 department of surgery, irrua specialist teaching hospital, irrua, edo state, nigeria abstract first described in a publication by two nigerian neurosurgeons, adeloye a and odeku el, in 1971, adeloye-odeku disease is a solitary congenital subgaleal inclusion dermoid cyst of the anterior fontanelle. this rare lesion, which makes up about 0.10.5% of all cranial tumours and 0.2% of all inclusion cysts, was initially thought to be found only in africans. however, further reports have shown it to have a universal occurrence, as it has been reported in caucasians, chinese, indians, and other part of the world. this lesion is also known as congenital inclusion dermoid cyst (cids), is a benign slow-growing lesion, and if untreated, may persist to adult life. this article gives a highlight of the disease and its management and goes further to report 3 cases of this rare benign lesion seen in irrua, south-south nigeria, a rural, low-resource tertiary health institution. incidentally and interestingly, all three cases presented within three consecutive months (january-march, 2019) at the neurosurgery outpatient clinic. being uncomplicated cases, private and group counselling was done. the parents of the patients were much more reassured and relieved from their anxieties seeing others with similar problem. they were all worked up for surgery at different dates, had excision of the cysts with no complication and are currently being followed at the outpatient clinic. introduction adeloye-odeku disease, also known as congenital inclusion dermoid cyst (cidc), is a solitary congenital subgaleal inclusion dermoid cyst of the anterior fontanelle. it is named after adeloye a and odeku el, who first reported it in 1971, presenting series of 18 patients seen at the university college hospital, ibadan. they also published a full description of the cyst and its management.1 keywords adeloye-odeku, congenital, inclusion dermoid, cyst, anterior fontanelle corresponding author: eghosa morgan neurosurgery unit, department of surgery, irrua specialist teaching hospital, irrua, edo state, nigeria morganeghosa@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 432 e. morgan, c.o. okwumezie, g.c. akasike et al. cidc is an inclusion dermoid, a developmental anomaly in which displaced dermal elements are included in the neuroaxis along the embryonic fusion line. in this case, it occurs under the epicranial aponeurosis over the anterior fontanelle. surgical excision, preferably enucleation, is curative for this disease, and no recurrence has been reported so far. epidemiology following its first report from patients in nigeria in 1971, it was initially thought to be an african disease.2 however, subsequent publications from various parts of the world have shown the cyst to be multiracial and to have a universal occurrence.3,4,5,6 the cyst accounts for 0.1 -0.5% of all cranial tumours6 and 0.2% of all inclusion cysts.7 although present at birth, its initial small size draws little or no attention. hence, most cases are seen after the age of 3 months. if left untreated, it may persist till adult life as already reported.8,9 aetiopathogenesis the disease is caused by a developmental anomaly in which displaced dermal elements are included in the neuroaxis along the embryonic fusion line around the epicranial aponeurosis over the anterior fontanelle. this forms a slow-growing inclusion dermoid with no intracranial connection. the cyst has a fibrous tissue wall lined by stratified squamous epithelium and it contains mainly a clear and colourless fluid with striking resemblance with cerebrospinal fluid (csf) but with much smaller quantity of sugar and protein. the fluid may be mixed with cholesterol crystal, sebaceous materials and desquamated epithelial cells. these may form clumps or floccules floating over the surface of the fluid or line the inner wall, giving it a rather rough and shaggy appearance.10 clinical features the history is usually that of a slow-growing swelling over the anterior fontanelle present since birth. the swelling is oval, spherical, non-tender, fluctuant, with intact overlying skin. it transilluminates brilliantly but does not show transmitted cough impulse due to no intracranial communication. the size of the cyst varies with the age of the patient at the time of the diagnosis.4 however, a range of 1-7cm have been recorded.6 the lesion is loosely attached to the overlying aponeurosis and underlying pericranium and the absence of cough impulse differentiates it from a meningocoele or encephalocoele. differential diagnoses the differential diagnoses of this condition include encephalocoele, meningocoele, sebaceous cyst, lipoma, haemangioma, cephalohaematoma. however, cidc is differentiated from the above by its clinical features and this is corroborated by the findings of appropriate radiological and laboratory investigations employed. management usually, the patient is stable with an uncomplicated lesion, presenting at the clinic. a good history is taken and clinical examination done and all findings documented. necessary radiological and laboratory investigations are carried out. counseling is done and this should cover the pathology, its cause and course, investigations required, treatment options and possible complications. informed consent is obtained appropriately and the patient is worked up for excision thereafter. the cyst is excised completely and sent for histology so as to get a confirmatory tissue diagnosis. patient is the followed up appropriately. investigations radiological investigations to identify the location, size, nature and possible contents of the cyst and find out if there is any intracranial communication. they also serve as a guide for the surgeon intra-operatively. they include: transfontanelle ultrasound scan /ultrasound scan of the mass this is much used for this condition in low economic regions where there is no computed tomography (ct)/ magnetic resonance imaging (mri) scan or, even if present, patient cannot afford them as seen irrua. the scan usually reveals a cystic mass with homogenous or heterogenous echogenicity, well circumscribed, and lying over the anterior fontanelle with no intracranial extension. 433 adeloye-odeku disease in irrua, south-south nigeria computed tomography (ct)/ magnetic resonance imaging (mri) scan these outline the lesion and confirm the cyst. usually, a well-defined extracranial, subcutaneous fluid-density cyst over the anterior fontanelle is seen. it also gives the opportunity to visualize intracranial contents and usually there is no intracranial extension. body fluid investigations necessary for preoperative work up to assess patient’s fitness for surgery include: full blood count, serum electrolyte, urea, creatinine, and random blood glucose/ fasting blood glucose (especially for diabetics). histology and cyst fluid analysis this is done post excision of the cyst. it confirms the diagnosis and rules out malignancy. the usual finding is that of cyst wall connective tissue lined by stratified squamous epithelium while the cyst fluid is clear with varying amount of glucose, protein, potassium,sodium,urea and ldh. some cysts will contain sebaceous glands, hair follicles, etc, in the adnexial layer. treatment surgery is the mainstay of treatment. this involve enucleation of the lesion through a transverse scalp incision, usually under general anaesthesia, is curative for the disease. care is taken to avoid injury to the underlying dura if fontanelle is still patent, and the cyst is delivered without capsular rupture. redundant scalp may be excised and the wound closed appropriately, bearing in mind the need to achieve satisfactory aesthetic outcome. complications these are usually rare. however, some of the possible complications include: cyst rupture and secondary infection if left untreated. dura breach with resultant csf leak as a complication of surgery. there is however no report of such in the literatures reviewed. surgical site infections may be seen. the irrua experience so far (case series) case i a 4-month old male infant who was brought to the outpatient clinic with a painless, progressive scalp swelling over the anterior fontanelle which has been present since birth. no associated skin changes or discharge. no neurological symptoms or deficits. no swellings in other parts of the body. developmental milestones were achieved at the appropriate time for age and patient was up to date with the immunization schedule. no family history of such swellings. pregnancy, birth and neonatal history were uneventful and mother was delivered via a spontaneous vaginal delivery. birth weight is 2.8kg. examination revealed a 6cm diameter hemispherical mass over the anterior fontanelle which was cystic, non-tender, smooth, and non-pulsatile. there was no differential warmth and no cough impulse. it was loosely attached to the overlying skin and underlying pericranium and transilluminates well. other examinations revealed normal findings. transfontanelle ultrasound done revealed a well circumscribed cystic mass overlying the anterior fontanelle, containing dependent echogenic debris. it measures 8.76cm3. underlying brain is normal and there is no intracranial extension of the mass. a diagnosis of adeloye–odeku disease was made and the parents of the patient were counseled for surgery. informed consent was obtained and preopereative work up done. routine blood investigations were normal. he had enucleation of the cyst via a transverse scalp incision under general anaesthesia. intraoperative finding was a 6cm diameter oval cystic mass underneath the aponeurotic layer of the scalp over the anterior fontanelle. the tissue was sent for histology. wound was closed with absorbable vicryl and patient did well postoperatively. he was discharged on the 2nd day post -operative and followed up in the outpatient clinic. histology report revealed an ovoid cystic mass with shining grey-brown capsule measuring 3x2x2cm on macroscopy. cut surface revealed a cystic cavity containing clear-white jelly substance. microscopically, the sections showed a benign cystic lesion, containing keratinous debris and lined by keratinized stratified squamous epithelium with focal areas of attenuation. the wall is composed of fibrocollageneous stromal element with several skin adnexial structures. a histologic diagnosis of scalp mass: dermoid cyst, was made. the patient is currently being followed up on outpatient basis and is doing fine with no complication or recurrence so far. 434 e. morgan, c.o. okwumezie, g.c. akasike et al. case ii a 22-month old female child with progressive painless scalp swelling over the anterior fontanelle present since birth. no associated neurological deficits. no skin changes or discharge for the swelling. no other swelling in any other part of the body. pregnancy, birth and neonatal history were uneventful. developmental milestone was attained at appropriate time and the child will be properly immunized for age. examination reveals a 4cm diameter spherical swelling over the anterior fontanelle which was nontender, cystic, with no differential warmth. it was loosely attached to the underlying structure and overlying skin and transilluminates. other examinations were normal. a clinical diagnosis of sub galeal dermoid cyst was made. transfontanelle uss done revealed a cystic sub periosteal lesion measuring 19.9 x 19.2 x 78mm located in the midline between the outer and inner table of the frontal bone. there is no demonstrable communication with the csf or brain meninges. both lateral, third and fourth ventricle are normal in size and outline. no sonographic evidence of intraventricular hemorrhage, mass or hydrocephalus. the brain parenchyma appears normal sonographically with normal grey and white matter differentiation. the parents were counseled for surgery and informed consent was obtained. preoperative investigation was normal. she subsequently had excision biopsy done under general anesthesia via a transverse scalp incision. the intra-operative finding was that of 3cm diameter ovoid cyst in the subgaleal layer of the scalp. the sample sent for histology and the wound closed with absorbable vicryl, both deep and subcuticular layer. post-operative condition was satisfactory and patient was discharged on the second day post-op. histology report revealed: macroscopically, an encapsulated cystic mass that is grayish-white, weighing less than 50g, measuring 1.9 x 1.5 x 1.0cm. sections showed a cystic lesion lined by stratified squamous epithelium with lamellated keratin in the cavity. the lining epithelium is in connection with a pilosebaceous unit in some areas while in the other area by sebaceous gland. the wall is extensively fibrocollagenous with collagenization in some areas and fibrosis and hemorrhage in other areas. histological diagnosis of scalp mass-epithelial inclusion cyst was made. no evidence of neoplasm. the patient is currently being followed up on outpatient basis with no complication or recurrence so far. case iii a 7-month old female infant with a small painless scalp swelling on the anterior fontanelle noticed since birth. the swelling was progressively increasing in the size, though slowly. no associated overlying ulcer or discharge. no swelling in other parts of the body and no family history of such swelling. no neurological deficit. the pregnancy, birth and neonatal history were normal. no delayed developmental milestones and she was up to date with the immunization schedule. examination revealed a localized spherical swelling on the anterior fontanelle of about 5cm diameter. it was non-tender, well defined, and cystic, with no differential warmth. not attached to the overlying skin and transilluminates. other findings were grossly normal. a clinical diagnosis of adeloyeodeku disease was made. transfontanelle uss requested revealed a thickwalled echogenic collection with amorphous intra lesional solid components that appear villiform, overlying the anterior fontanelle. the collection measures about 23.0cm3. there is no communication between the collection and the intracranial structures. intracranial structures appear grossly normal. the parents were counseled for surgery (excision biopsy) and with informed consent obtained, she was worked up for surgery. preoperative investigations were normal. she had enucleation of the cyst via a transverse scalp incision under general anaesthesia and the inra-operative findings was a 4cm diameter cystic mass underlying the aponeurosis over the anterior fontanelle and overlying the dura. the tissue was sent for histology and wound closed with absorbable vicryl and dressed appropriately. the post-operative condition of the patient was satisfactory and she was discharged on the second day post op. the histology report revealed: macroscopically, a spherical grayish-white cystic tissue measuring 3x2x2cm. cut surface revealed a colourless fluid, a cystic wall coated with whitish friable material with interspersed shaft. microscopically, histologic 435 adeloye-odeku disease in irrua, south-south nigeria sections showed a benign cystic lesion which contains keratin debris and surrounded by a wall made up of fibrocollagenous with collagenization in some areas and fibrosis and hemorrhage in other areas. a histological diagnosis of anterior fontanelle swelling: benign inclusion cystic was made. the patient is currently being followed up on outpatient basis and is doing well with no complications or recurrence so far. figure 1. preoperative photograph of case ii figure 2. intraoperative, showing lesion being excised figure 3. post excision figure 4. just after wound closure figure 5. at first follow up visit post op 436 e. morgan, c.o. okwumezie, g.c. akasike et al. summary of cases three cases of this rare lesion were seen within three consecutive months and they involved two females and a male child, all within the age range of 422months. the scalp swellings, which had been present since birth in all cases, were of sizes ranging between 46cm diameters, located over the anterior fontanelle, non-tender, cystic, smooth, transilluminate, loosely attached to the underlying structure and overlying skin, with no positive cough impulse. none of them was ulcerated and there was no discharge from any. clinical diagnoses of adeloye-odeku disease was made in all three cases and they had radiological investigations done to properly further define the lesions, especially their location, size, content, and if they communicate with the intracranial structures. with no intracranial communications confirmed, the parents were counseled and informed consent obtained. thereafter, all three patients had enucleation of the lesions via a transverse scalp incision under general anaesthesia. there were no intra or post-operative complications. histology reports of these lesions gave confirmatory tissue diagnosis of dermoid cyst, epithelial inclusion cyst, and benign cystic teratoma respectively. all were in keeping with adeloye-odeku disaease-congenital inclusion dermoid cyst over the anterior fontanelle. all three patients are currently being followed up with no complications or recurrence recorded so far. discussion adeloye-odeku disease still remains a rare lesion though reports have shown its universality in occurrence and its multiracial prevalence1,2,3,4,5,6,7,8,9,11,12,13,14 as against the initial thought of it being an african disease1,2,3,4,5,6,7,8,9,. so far, over 229 cases of this condition has been reported in literature until 2003.4 nevertheless, a report by dadlani et al suggest that its occurrence may be underreported and under-calculated due to observed non-uniformity in the nomenclature of the disease in various medical literatures and its management, in some cases, by other specialties (paediatric surgeons, general and plastic surgeons).11 our report may give some credibility to the above as the 3 cases were seen within 3 months in a nascent neurological unit, just in less than 2 years of its existence. currently, the lesion accounts for 0.1-0.5% of all cranial tumours and 0.2% of all inclusion cysts.6,7 aesthetic appearance and anxiety over the cause of the swelling are the main reasons for seeking surgical intervention by parents12. this was clearly evident in the response given by the parents of the children in this index report during consultation. all three couples saw the lesion as a form of deformity and were worried about what could be therein. all three lesions in our report were present since birth, slow growing and with sizes ranging from 46cm, in keeping with the range reported in other studies.7 our report involved 2 females and a male child, though no sex predilection has been established in this disease. while some reports have male preponderance2,3,6,7 others reveal the disease to be more in females.3,14 the three cases in this report have the classical clinical features of the disease in keeping with other reported cases. there was, however, a major challenge in the radiological investigations to confirm the nature and extent of the lesion. in our report, transfontanelle ultrasound scan was used in place of ct and mri scan due to financial constraints on the part of the parents of the patients who unfortunately have no health insurance. nevertheless, we were able to establish the location, size and nature of the cyst and non-communication with intracranial structures via the uss done. all three patients had excision of the cysts (enucleation) under general anaesthesia with no complications. the histology of the cysts in all 3 cases in our report showed benign cystic lesions lined by stratified squamous epithelium and containing skin appendages like hair follicles, sweat and sebaceous glands in the adnexial layers. this is in keeping with other reported cases.5,6,9 two of our reported cases (1st and 3rd) revealed the content of the cyst to be clear, colourless fluid consistent with published cases5,15,16,17. however, further biochemical evaluation of its contents could not be carried out due to the technical limitations of our facility. nonetheless, the histology reports confirm all three cases to be dermoid cysts and ruled out any malignancy. all three patients are currently being followed up with no complications or recurrence so far and with satisfactory aesthetic outcome. 437 adeloye-odeku disease in irrua, south-south nigeria conclusion adeloye-odeku disease, first reported in nigeria, and currently shown to be universal, remains a rare benign lesion of interest to the neurosurgeon. total surgical excision is curative of the disease as shown in all reports.these case series have added credence to the above and has shown its successful management in a rural, low-resource setting. references 1. adeloye a, odeku el. congenital subgaleal cysts of the anterior fontanelle in nigerians. arch. dis child. 1971. pg 95-96. 2. peter jc, sinclair-smith c, de villiers jc. the congenital bregmata dermoid: an african cyst? br j neurosurg. 1992;6(2):107-114 3. parizek j, nemecek s, nemeckova j, cernoch z, serci m. congenital dermoid cyst over the anterior fontanelle: report on 13 cases in czechoslovak children. child’s nerv syst. 1989;5:234-237 4. aquino h. congenital dermoid inclusion cyst over the anterior fontanelle. arq neuropsiquitr 2003; 61:448-452 5. kanamaru k, waga s. congenital dermoid cyst of the anterior fontanelle in a japanese infant. surg neurol. 1984.pp287-290. 6. asalan o. congenital dermoid cyst of the anterior fontanelle in turkish children-four case reports. neurol med chir. 2004;44:150-152 7. carvalho gt, faqundes-pereyra wj, marques ja, dantas fl, sousa aa. congenital inclusion cyst of the anterior fontanelle. surg neurol. 2001;56:400-405 8. ojikutu na, mordi vpn. congenital inclusion dermoid cyst located over the region of the anterior fontanelle in adult nigerians. j neurosurg. 1980;52:724-727 9. castro ra, ribeiro filho ade, vv silva. dermoid cyst of the anterior fontanelle in adults: a case report. neuropsiquiatr 2007; 65(1): 170-172. 10. archampong eq, naaeder sb, ugwu b. baja’s principles and practice of surgery, including pathology, in the tropics. 5th edition, vol ii (2015), chapter 52, pg 1112. 11. dadlani r, furtado s, ghosal n, hedge a. adeloye-odeku disease: an african disease in an indian child? turkish neurosurgery 2012 ; 22: 515-520 12. algahtany ma, binitie op. adeloye-odeku disease in aseer region of saudi arabia. j west afr coll surg 2011 janmar; 1(1): 113-120 13. fermin s, fernandez-guerra ra, lopez-carnacho o, alvarez r. congenital dermoid cyst of the anterior fontanelle in mestizo-mulatto children. child’s nerv syst. 2001; 17: 353-355. 14. pannell bw, hendrick eb, hoffman hj, humphreys rp. dermoid cysts of the anterior fontanelle. neurosurgery 1982; 10: 317-323. 15. tateshima s, numoto rt, abe s, yasue m, abe t. rapidly enlarging dermoid cyst over the anterior fontanelle: a case report and review of the literature. child’s nerv syst. 2000; 16: 875-878. 16. agrawal a, pratao a, sinha ak, agrawal b, thapa a, bajrachanya t. epidermoid cyst of anterior fontanelle with clear contents. surg neurol. 2007; 68(3): 313-315 17. majed m, nejat f, el khashab m. congenital dermoid cyst of the anterior fontanelle. indian j plast surg. 2008; 41: 238240. 22book romanian neurosurgery (2014) xxi 4 547 book presentation: atlas of ct angiography gratian dragoslav miclaus, horia ples springer international publishing, 2014 the "atlas of ct angiography" by romanian authors gratian miclaus and horia ples published by springer international publishing, 2014 is an editorial event based on the professional value of the authors. the two first chapters cerebral angiography and carotid angiography show the most important cranio-cerebral and cervical lesions. the images are significant and very good, authors used the subtraction of the bone, allowing the evaluation of the arterial cerebral circulation, without the presence of the bony structures. also, the authors make use of the 3d vrt reconstructions without the bone subtraction, for the optimal planning of the craniotomies. this book is a success of the team of neurosurgeons and neuroradiologists from timisoara and naturally for romania. giovania_clipreconstruction romanian neurosurgery (2014) xxi 2: 161 165 161 clip reconstruction of a large right mca bifurcation aneurysm. case report a. giovani1, angela neacsu, ana gheorghiu, r.m. gorgan department of neurosurgery clinical hospital bagdasar-arseni, bucharest 1student abstract we report a case of complex large middle cerebral artery (mca) bifurcation aneurysm that ruptured during dissection from the very adherent mca branches but was successfully clipped and the mca bifurcation reconstructed using 4 yasargill clips. through a right pterional craniotomy the sylvian fissure was largely opened as to allow enough workspace for clipping the aneurysm and placing a temporary clip on m1. the pacient recovered very well after surgery and was discharged after 1 week with no neurological deficit. complex mca bifurcation aneurysms can be safely reconstructed using regular clips, without the need of using fenestrated clips or complex by-pass procedures. key words: mca bifurcation; yasargil clips; clip reconstruction. introduction the mca aneurysms represent 20-25 % of all intracranial aneurysms. given their complex anatomy including broad necks, trifurcated anatomy and the high risk to occlude a small branch whose origin cannot be seen on angiography when detaching the coils these aneurysm are considered unfavorable for endovascular treatment. because they are easy to reach in the sylvian fissure and in that region the fissure is large enough to allow complex reconstruction and bypass techniques if necessary the best treatment for these lesions is surgical clipping. several studies showed the surgical results to be superior to endovascular results. (3, 4) this article reports the reconstruction of mca branches by applying several parallel clips to a large mca aneurysm that could not be dissected and ruptured while being dissected from one of the branches. (6, 7, 12) case report a 59 years old right handed woman with multiple associated pathology including basocellular nose carcinoma operated 2 years prior, glaucoma, diabetes mellitus, and psychiatric symptoms including depression and bipolar disorder, presented for intense headache worsened over the last two weeks. the patient had a two years history o intermittent headache. a ct angiography 1 week prior admission indicated the presence 162 giovani et al clip reconstruction of a large right mca bifurcation aneurysm of a right mca bifurcation aneurysm. the lesion was confirmed on the angiography but the neck was very difficult to describe because of 4 branches of the mca surrounding the aneurism given the very close. this aspect was probably due to the bifurcation of each of the 2 m2's immediately after emergence from m1. no subarachnoid hemorrhage was visible on ct so it was an incidental discovery. the rotational angio ct in our department was more useful than the angiography because it showed the relation of the aneurysm with the mca branches whereas on angiography the branches superimposed on the contour of the aneurysm and the neck could not be distinguished. the patient was positioned supine with the head rotated 45° to the left. a right frontotemporal standard craniotomy was performed. after the dural incision the sylvian fissure was opened from distal to proximal. the m1 was identified with a large bilobulated aneurysm at its bifurcation. immediately after origin from m1 both m2 bifurcated and all 4 branches engulfing the aneurysm prevented the operator to gain access to the neck. a very adherent branch separated the two lobes of the aneurysm. when attempting to dissect the dome from this branch, given the very thin wall at this level, a punctiforme hole was created in the aneurysm but the wall did not tear. a temporary clip was applied on m1 and removed 1 minute later after a definitive curved clip was applied on the hole in the aneurysm and the bleeding stopped. figure 1 preop. angiograpgy and angio-ct the aneurysm was next reconstructed using two more curved clips on the bigger (frontal) lobule with care to spare the frontal m2 branch adherent to the dome. than the temporal lobule was reconstructed with a 4th clip applied between two temporal branches. (figures 1 and 2). no retractor was needed during surgery, the suction tube was used as a retractor (1). also the importance of sylvian fissure opening should be stated. before closure the arterial pressure was raised to make sure there was no bleeding, and the clipping was controlled with a doppler probe to make romanian neurosurgery (2014) xxi 2: 161 165 163 sure no mca branch is occluded and no aneurism remnant was left. the dura was closed and circullary suspended to the fascia, the bone flap fixed in place with separated sutures and the scalp closed. a b c d e f figure 2 a. tight adherent branch dissection; b. rupture of the aneurysm; c. first clip including the rupture site; d. second clip inserted under a frontal branch; e. third clip on the small temporal aneurysm lobule; f. fourth curved clip to include the rest of the aneurysm the patient showed no neurological deficit after the surgery and she was discharged 7 days after surgery. the postoperative angiography showed a good flow in the right mca peripheral branches and the disappearance of the aneurysm. figure 3 graphic depiction of the dissection and clipping starting with freeing the dome from the highly adherent branches on its surface followed by rupture and clip reconstruction 164 giovani et al clip reconstruction of a large right mca bifurcation aneurysm figure 4 postoperative angiography and angio-ct discussion treatment of complex mca bifurcation aneurysms represents a challenge both for the endovascular surgeon given the broad neck and for the neurosurgeon given that major branches of mca can be adherent to the aneurism wall. the purpose of surgery is exclusion of the aneurysm from circulation, with preservation of normal vascular anatomy while minimizing the risk of recurrence at the clipping site. (9, 10, 11) the latter is achieved by appropriate placement of the clips used to reconstruct the aneurysm without letting any dog ears, and this can be difficult to achieve in cases where the clip slides on atheromatous vessels. it is very important to control the clipping in order to make sure that no branch is occluded and there is no aneurysm remnant. even though it is not available in our service indocyanine-green is very usefull as a proof that the perfusion of the branches distal to the aneurysm is adequate. we reconstructed the aneurysm using 4 yasargil clips two straight and two curved applied in such a fashion as to clip the base of the aneurysm without injuring or obliterating the branches that crossed on the surface of the aneurysm. (4, 5, 8) in cases where the branches cannot be dissected from the fragile aneurysm wall, using fenestrated clips alone or stacked together to create tubes around the branch should be considered. (13) unfortunately we had no such clips available for this surgery. in gigant aneurysms or in those large unclipable, more difficult repair techniques including excision of the aneurysm and reanastomosing the vessels, or simply resuturing the arterial wall after resecting the aneurysm with or without a high flow or a low flow bypass are to be taken into account (2, 5). of note is also the technique of bipolar shrinkage of the aneurysm which makes it smaller, more easily to dissect from the adherences and more clipable. this technique though is very risky in aneurysms with very thin walls and in those very adherent to the romanian neurosurgery (2014) xxi 2: 161 165 165 branches. the technique used is a good option for clipping large mca bifurcation aneurysms whose dome and neck cannot be fully dissected from the adherences. correspondence giovani andrei m.d. phd stud. department of neurosurgery clinical hospital bagdasar-arseni, bucharest e-mail: giovani.andrei@gmail.com references 1. robert f. spetzler, m.d., and nader sanai, m.d. 2012. the quiet revolution: retractorless surgery for complex vascular and skull base lesions. clinical article. j neurosurg 116:291-300. 2. mrak, goran; paladino, josip; stambolija, vasilije; jacob nemir; laligam n. sekhar. 2014. treatment of giant and large fusiform mca aneurysms with excision and interposition radial artery graft in a four year old child. neurosurgery. , 10:172-177 3. ulm, arthur j.; fautheree, gregory l.; tanriover, necmettin, 2008, microsurgical and angiographic anatomy of middle cerebral artery aneurysms: prevalence and significance of early branch aneurysms; more; neurosurgery. 62(5):ons344-ons353. 4. rodríguez-hernández, ana; gabarrós, andreu; lawton, michael t.; 2012; contralateral clipping of middle cerebral artery aneurysms: rationale, indications, and surgical technique neurosurgery. 71():ons116-ons124. 5. nossek, erez; costantino, peter; eisenberg, mark; more ;2014 ; internal maxillary artery to middle cerebral artery bypass: infratemporal approach for subcranial intracranial (sc-ic) bypass neurosurgery., post acceptance, 10 march 2014 6. michel bojanowski, m.d., robert f. spetzler~ m.d., and l. philip carter, m.d. 1988. reconstruction of the mca bifurcation after excision of a giant aneurysm technical note. j neurosurg 68:974-977, 7. yuichiro tanaka, m.d., shigeaki kobayashi, m.d., kazuhlko kyoshima, m.d., and kenichiro sugita, m.d. 1994; multiple clipping technique for large and giant internal carotid artery aneurysms and complications: angiographic analysis; j neurosurg 80:635-642. 8. leena kivipelto, m.d., ph.d., mika niemelä, m.d., ph.d., torstein meling, m.d., ph.d., martin lehecka, m.d., ph.d., hanna lehto, m.d., and juha hernesniemi, m.d., ph.d. ;feb 2014; bypass surgery for complex middle cerebral artery aneurysms: impact of the exact location in the mca tree: clinical article journal of neurosurgery / vol. 120 / no. 2, pages 398-408 9. daniel l. surdell, m.d., ziad a. hage, m.d., christopher s. eddleman, m.d., ph.d., dhanesh k. gupta, m.d., bernard r. bendok, m.d., and h. hunt batjer, m.d.; feb 2008 ; revascularization for complex intracranial aneurysms . neurosurgical focus / vol. 24 / no. 2, page e21 10.clatterbuck, richard e.; galler, robert m.; tamargo, rafael j ; october 2006; orthogonal interlocking tandem clipping technique for the reconstruction of complex middle cerebral artery aneurysms.; neurosurgery. 59(4):ons-347-ons-352,. 11.rodríguez-hernández, ana; lawton, michael t.; june 2012; flash fluorescence with indocyanine green videoangiography to identify the recipient artery for bypass with distal middle cerebral artery aneurysms: operative technique neurosurgery. 70():ons209-ons220. 12.heros, roberto c.; fritsch, michael j. surgical management of middle cerebral artery aneurysms neurosurgery. 48(4):780-786, april 2001. 13.yang, isaac m.d., ph.d.; lawton michael t. m.d. 2008; clipping of complex aneurysms with fenestration tubes: application and assessment of three types of clip techniques; neurosurgery: volume 62 issue 5 p ons371-ons379. microsoft word 3craciunas_longitudinal.doc romanian neurosurgery (2012) xix 3: 193 202 193 longitudinal volumetric mri study of pituitary gland following severe traumatic brain injury sorin c. craciunas1,*, carmen m. cirstea1,2,4, hung-wen yeh3, lewis hutfles1, joann lierman1, allan schmitt1, william m. brooks1,4 1hoglund brain imaging center; departments of 2physical therapy & rehabilitation science, 3biostatistics and 4neurology, university of kansas medical center, kansas city, kansas, usa *current address: neurosurgery unit iv, bagdasar arseni hospital, bucharest, romania abstract purpose: previous studies have suggested that the hypopituitarism following traumatic brain injury (tbi) is more prevalent than traditionally thought. the objective of this study was to characterize longitudinal mri morphometric changes of pituitary gland in patients with severe tbi. materials and methods: fourteen patients who had suffered a severe tbi (glasgow coma score=3 8) underwent mri at three time points: time 1 (mean=31. 5 days), time 2 (98. 0) and time 3 (185. 5). the pituitary gland volume was quantified by manually tracing on t1-weighted magnetic resonance images. data from tbi patients were compared to 14 ageand sexmatched uninjured controls. the relationships between pituitary volumetric measures and patient demographics, length of respiratory support and coma, and presence of intracranial hemorrhage or skull fractures were also analyzed. results: following tbi, the pituitary volumes were significantly greater at all three time points: time 1: median=665mm3, range=460-830mm3, p=0. 007; time 2: 694mm3, 467-866mm3, 0. 007; and time 3: 655mm3, 444795mm3, 0. 015, compared with controls (504mm3, 433-591mm3). at time 1, pituitary volume was increased in 10 out of 14 patients. of these, early pituitary enlargements persisted up to six months in nine patients. pituitary enlargements were negatively correlated with gcs, but not with other variables. conclusion: following a severe tbi, early pituitary enlargement found in most of our patients persisted in the chronic phases. our data suggest a potential role of mri morphometry in early prediction of pituitary dysfunction following head trauma, but further studies including hormonal measurements are necessary for validation. key words: neuroimaging, traumatic brain injury, hypopituitarism introduction traumatic brain injury (tbi) represents a major cause of mortality and long-term morbidity. in the united states alone, each year approximately 1. 4 million people sustain a tbi(17) with an estimated cost of $60 billion. (10) at present, there are at least 5. 3 million tbi survivors, about 2% of the u. s. population, with long-term disabilities. (33) 194 craciunas et al mri study of pituitary gland after severe tbi although pituitary damage following tbi was reported as early as 1918,(7) interest in this clinical entity has grown with recent studies consistently reporting a high-risk of hypopituitarism, determined by endocrine testing, with an incidence of 30-70% following tbi. (1-3, 5, 12, 18, 28) despite this incidence, pituitary function testing has not become routine for patient management after tbi. since the pituitary gland has the role of “endocrine brain”, we could speculate that the failure to diagnose post head trauma hypopituitarism (phth) might contribute considerably to morbidity and mortality in tbi patients. consequently, the signs and symptoms of phth might be overlooked and could be interpreted as being post-tbi cognitive/behavioral sequelae. for example, clinical complaints such as headache, irritability, poor concentration and memory, depression, fatigue, decrease in libido, although considered symptoms of postconcussional syndrome, can also result from hypopituitarism, particularly of growth hormone (gh) deficiency. (9, 19, 21, 24) hormonal substitution therapies are used successfully for non-traumatic hypopituitarism and it has been suggested that tbi-mediated hypopituitarism might also benefit from appropriate hormonal supplements. (9, 21) numerous attempts have been made to define criteria or to identify high-risk factors that indicate the need for endocrine testing post head trauma,(1, 3, 4, 13, 14, 18, 24, 26, 28, 30, 31) but no valid prognostic index has been found to be sufficiently accurate. since imaging investigations (ct, mri) are mandatory in the management of most tbi patients, the identification of a quantitative neuroimaging biomarker of phth might be a reliable and costeffective tool to determine which tbi patients require endocrine testing and follow-up. the major goal of the present study was to quantify pituitary volume changes in the first six months after tbi. the relationship between pituitary volume changes, measured from mri, and clinical factors of tbi severity (e. g. , skull fractures, length of coma) was also studied. we focused on severe tbi, since this group has a high-risk for developing phth, and on the first six months post-tbi when pituitary hormonal alterations are dynamic. (11, 15, 23, 30, 31) materials and methods participants fourteen tbi patients (4 women; age median=23yrs, range=16-47yrs) participated. inclusion criteria were: severe tbi (glasgow coma score, gcs<8); age: 18-55 years; and body mass index: 17-30 kg/m2 (see table 1). exclusion criteria were: previous and/or penetrating tbi; preexisting neurological and/or endocrinological disease; systemic conditions, such as chronic metabolic disturbance, hepatic failure, uremia, kidney transplant, uncontrolled diabetes; major substance abuse; and treatment with neuroleptic or antiepileptic drugs prior to the event. the severity of tbi was based on gcs assessment at 24 hours post-tbi(32) to minimize the possible effect of confounding factors that could overestimate the severity of trauma at emergency room (i.e., illicit drugs, sedation, alcohol). histories for each patient, including the injury type, estimated severity and patient condition at presentation (from family interviews, medical chart reviews, emergency room notes, police reports) were obtained. neurologic signs, vital romanian neurosurgery (2012) xix 3: 193 202 195 functions, history of resuscitation, degree of skeletal and visceral injury, cranio-cerebral lesions (skull fractures, posttraumatic intracranial hemorrhage/hematoma), anesthesia, respiratory support, and coma days were also recorded. fourteen ageand sex-matched uninjured controls (4 women; 24. 5yrs, 1847yrs) without history of neurological and endocrinological disorder or drugs/alcohol abuse were recruited. all participants were informed of the experimental procedures and gave their written consent to this study that was approved by the local institutional review board. mri assessment and analysis magnetic resonance imaging was carried out using a 3 tesla siemens allegra scanner (siemens medical solutions, erlangan, germany). we studied tbi patients at one month, when they were clinically stable for transport to our outpatient imaging facility (time 1: actual mean=31. 5 days), three (time 2=98. 0 days) and six months (time 3=185. 5 days) post-injury. a 3d axial t1weighted series (magnetization-prepared rapid gradient echo mprage, tr=1520ms, te=4. 38ms, ti=900ms, flip angle=8 degree, 256x156mm2 matrix, 1. 5mm slice thickness) was collected. we paid careful attention to patient positioning at each time point by using the reference landmarks as described previously. (6) anterior and posterior pituitary gland was outlined manually on the t1-weighted images and the volume quantified by multiplying the traced area in each slice by the slice thickness and summing over all slices (medinria v2. 0. software, inria, sofia antipolis, france). the pituitary boundaries were drawn on the axial slices (figure 1a and b), with confirmation on the simultaneously displayed sagittal and coronal planes (3d reconstruction, figure 1c and d), by a neurosurgeon. mri data were analyzed blinded to group and time point. accuracy and reproducibility of pituitary volume measurements to verify the anatomical accuracy of tracing, one investigator traced the pituitary boundaries on six randomly selected image sets. then, a second investigator compared the tracings with an anatomic atlas (22). in the case of inaccuracy the tracing was reexecuted. this cycle was repeated until agreement was reached. to determine intra-rater reliability, 10 pituitary image sets were traced by one investigator on two different occasions separated by 7-10 days. the second tracing was executed without reference to the first. figure 1 measurement of pituitary gland volume. (a) outline of pituitary gland shown on complete axial t1-weighted slice (tr=1520ms, te=4.38ms, ti=900ms, flip angle=8 degree). (b) magnified view of a showing detailed anatomy. (c) and (d) corresponding sagittal and coronal views that are viewed simultaneously while tracing to ensure accurate boundaries the intra-rater reproducibility was extremely high (spearman coefficient r=1. 00; p<0. 0001). 196 craciunas et al mri study of pituitary gland after severe tbi to determine inter-rater reliability, one investigator traced the pituitary boundaries on eight randomly selected image sets. a third investigator then traced these pituitary image sets without reference to the results of the previous investigator. the reliability between these independent raters was high (spearman r=0. 81; p<0. 02). statistical analysis since the sample size was small, we used nonparametric methods obviating the need for assumptions of normal distributions in pituitary volume measurements. analysis focused on one outcome measure (pituitary volume) and five variables (gcs at 24 hours; number of days on ventilator support; number of days of coma; intracranial hemorrhagic lesions, where 1=present and 0=absent; and skull fractures, where 1=present and 0=absent). the between-group comparisons at each time point were conducted by the wilcoxon rank-sum/mann-whitney u test whereas the within group (tbi) comparisons were conducted by the wilcoxon signed-rank test. to address the question of whether presence of overt injury was associated with pituitary volumes, we divided the tbi group based on the presence of either hemorrhage or skull fracture. we then used the wilcoxon rank-sum test to determine whether pituitary volumes were different for any subgroup at any time point. the relationships between pituitary volumes and clinical injury severity variables were estimated by the spearman’s correlation coefficients between the pituitary volume at each time point and each of the five variables. finally, we divided the tbi group according to their pituitary volume at time 1. we considered any pituitary volume that fell within the normal range of our healthy group mean to be normal and volumes that fell outside this range as abnormal. we then repeated the aforementioned analyses for the abnormal and normal tbi subgroups separately. all hypothesis testing was 2-sided and we did not attempt to control the experiment-wise type i error rate. the significance level was set at α = 0. 05. results patient characteristics the causes of injury included motor vehicle accident (n=10), fall (2), and assault (2) (see table 1), resulting in a severe tbi (gcs at 24 hours ranged from three to seven; seven patients had a gcs of three) with length of coma ranging between two and eight days (median=3. 5 days). all patients received oro-tracheal intubation and ventilator support (median=5. 5 days, range=2–19 days). associated intracranial hemorrhagic lesions were present in 71% (10/14) of patients and fractures of skull vault in 43% (6/14). no patient had a skull base fracture. half of the patients (n=7) presented with multiple trauma, including hemoand/or pneumothorax (six patients), fractures (vertebral, pelvis, extremities), spleen laceration, and kidney contusion. pituitary volume measurements the pituitary volume measurements were summarized by medians and ranges for each group and each time point (table 2). compared with uninjured controls, the pituitary volumes in tbi survivors were significantly greater at all time points (see table 2 and figure 2). romanian neurosurgery (2012) xix 3: 193 202 197 table 1 demographic and clinical data of tbi survivors patient age/ sex bmi tbi cause gcs (24hr) intracranial hemorrhage skull fracture coma length (days) respirator support (days) 1 41/m 23.6 mva 3 5 6 2 16/m 23.3 mva 3 + + 6 11 3 47/m 21.5 assault 3 + + 8 10 4 24/m 22.8 fall 3 + 2 4 5 20/f 19.9 mva 3 3 3 6 21/f 25.0 mva 3 + 7 15 7 18/m 21.5 mva 3 + + 3 5 8 27/f 28.8 mva 5 + + 1 2 9 24/m 22.2 mva 6 3 14 10 22/m 19.2 mva 6 + + 5 5 11 21/m 23.0 mva 6 + 3 7 12 47/f 22.0 assault 6 + 2 2 13 26/m 25.4 mva 7 + 6 19 14 22/m 22.1 fall 7 + 4 4 note. bmi = body mass index; f = female; gcs = glasgow coma score; m = male; mva = motor vehicle accident; + = present. patients are ranked according to glasgow coma score. overall, these values suggest that following tbi, pituitary volumes are higher than normal (uninjured control vs. time 1; p=0. 007), followed by further enlargement up to three months (time 2 vs. 1; p=0. 09) and finally apparent return toward normal range at six months post tbi (time 3 vs. 2; p=0. 02; table 2 and figure 2). at time 1, 10 of the tbi patients (71%; tbi patients # 3-7 and 9-13 in the table 2) had pituitary volumes outside the normal range of the uninjured group. in this tbi subgroup (abnormal tbi subgroup), the median pituitary volume increased slightly from 718 to 753mm3 at time 2 (time 2 vs. 1, p=0. 06) and decreased to 673mm3 at time 3 (time 3 vs. 2 and 1, p=0. 01 and 0. 16 respectively). although the pituitary volumes decreased between times 2 and 3, the volumes measured at time 3, nonetheless, remained above the uninjured group range in nine of the patients. 198 craciunas et al mri study of pituitary gland after severe tbi table 2 pituitary volumes (mm3) in tbi survivors and healthy controls subject tbi patients uninjured controls time 1 time 2 time 3 1 499 513 507 433 2 460 481 486 501 3 739 866 659 499 4 711 760 743 571 5 830 811 795 504 6 794 781 740 548 7 761 820 659 529 8 584 528 504 494 9 725 706 550 456 10 645 654 617 492 11 662 683 651 512 12 668 747 688 504 13 615 666 693 576 14 470 467 444 591 median 665‡ 694‡ 655† 504 range 460 830 467 866 444 795 456 591 mean±sd 654 ± 118 677 ± 133 624 ± 109 521 ± 45 note. † p < 0.05; ‡ p < 0.01 compared with uninjured controls. patients 1, 2, 8, and 14 remained within the normal range throughout the study period. the four patients (# 1, 2, 8, and 14) with pituitary volumes within the normal range at time 1 (normal tbi subgroup) did not show significant progression over time (median=465, 497, and 485mm3 at times 1, 2, and 3, respectively). figure 2 median and range pituitary volumes (mm3) in uninjured (open square) and tbi (filled square) groups. in the tbi group, pituitary volumes were measured at three time points: time 1 (one month-post tbi), time 2 (three months) and time 3 (six months). asterisks (*) indicate significant differences between tbi and healthy groups, and carat (^) between time 3 and time 2 in tbi group (p < 0.05). correlations between pituitary volume measurements and clinical variables although, for the entire tbi group, the pituitary volume at all time points was negatively correlated with the gcs, none of these correlations was significant (p=0. 16, 0. 10, and 0. 33 at times 1, 2, and 3 respectively). however, for the abnormal tbi subgroup, we found stronger correlations at all time points (time 1: r=0. 84, p=0. 002; time 2: r=-0. 87, p=0. 001; time 3: r=-0. 46, p=0. 18; see figure 3). for both the whole tbi group and the abnormal subgroup, correlations between pituitary volume and number of coma days or ventilator support days did not reach statistical significance at any time point. no significant difference was found between the patients with and those without intracranial hemorrhagic lesions or skull fractures. romanian neurosurgery (2012) xix 3: 193 202 199 discussion we found substantially larger pituitary volumes in the majority of survivors of severe tbi compared with uninjured controls. we interpret the larger volumes as indicating injury-related enlargement. moreover, in these patients, the pituitary volume tended to increase until three months. although there was some indication of recovery by six months postinjury, pituitary volume in all but one patient remained above the normal range. in contrast, none of the patients with pituitary volumes in the normal range at one month post-injury presented with pituitary enlargement over the same period. our findings are consistent with recent reports of pituitary enlargement in the acute (0-7 days) phase of moderate to severe tbi(20). however, an association between increased pituitary volume and pituitary dysfunction following tbi is still to be elucidated. the hypothalamus-pituitary axis can be directly or indirectly altered by tbi. hypoxia, edema, intracranial hemorrhage or increased intracranial pressure,(8) subsequent to trauma of either pituitary, hypothalamus, stalk, or other brain regions are potential mechanisms underlying such dysfunction. histological studies of tbiinduced alterations of this axis have found various degrees of pituitary hemorrhage, ischemic necrosis, fibrosis and/or thrombosis. (1, 24-26) however, the most prevalent mechanisms associated with pituitary dysfunction seem to be hemorrhage and ischemia. (13) to date, no correlations between the type or extent of histological pituitary alterations and characteristics of trauma, such as mechanism, extension and type of brain injuries, or skull fractures, have been reported,(24) although one study found no histological changes in 14 to 74% of tbi cases. (26) in addition, pituitary dysfunction might be secondary to other tbi-related factors, such as cardiac arrest and medications used post-tbi (e. g. , etomidate, heparin, anticonvulsants, benzodiazepines). (8, 24) furthermore, an autoimmune process involving hypothalamic-pituitary region triggered by head trauma might play a role in the development of pituitary dysfunction post tbi. (29) the trend toward normalization of pituitary volume at six months post-tbi was also suggested at 12 months follow-up. (20) recently, an integrative neuroimaging/hormonal study of chronic (17±15 yrs) tbi patients reported pituitary gland volume changes in 80% of patients with hypopituitarism, and in only 29% without,(27) with loss of volume or empty sella the most common abnormality seen. taken with those of other studies, (20, 30) our data raise the question of whether the reductions of pituitary volumes seen in the chronic phases of tbi represent true recovery or whether it is a step toward further deterioration (i. e. , atrophy) as suggested by schneider et al. (27) further studies over an extended period might answer this question. nevertheless, over a period of 3 years post-tbi,(31) a recovery of pituitary function was reported in most patients with worsening or new onset of hypopituitarism rarely occurring. in our patients, the pituitary volume was correlated with tbi severity i. e., low gcs at 24 hours predicted larger volume (see figure 3). although our result is consistent with previous findings that gcs at the emergency room predicts the development of phth, (12) other studies reported no association between gcs and the prevalence of phth. (3, 18) 200 craciunas et al mri study of pituitary gland after severe tbi figure 3 correlations between pituitary volumes at one (time 1), three (time 2) and six (time 3) months post-tbi and glasgow coma score 24 hours post-event in the tbi abnormal subgroup (n=10) that presented with significantly largely pituitary gland volume at time 1 compared to the uninjured group. several risk factors associated with injury severity have been identified in the context of phth. one of these is presence of skull base fracture. (28) however, none of our patients presented with skull base fracture. in contrast, some of our patients sustained fractures of the cranial vault. however, the presence of cranial vault fractures was not correlated with pituitary volume changes. another risk factor for hypopituitarism is the presence of subarachnoid hemorrhage, (2, 5, 16) which might indicate the need for follow-up to detect delayed hypopituitarism. (19) however, we found no relationship between the presence of intracranial hemorrhagic lesions and pituitary enlargement. finally, we found no significant correlation between pituitary enlargement and length of ventilator support at any time point. the present study has some limitations: (i) we focused on severe tbi patients who survived for six months after the event, which might contribute a selection bias i. e., the event was serious enough to induce a severe, but not terminal, tbi; (ii) we acquired the imaging data in the axial, rather than the commonly-used coronal, plane. however, we used the same 3d reconstruction to obtain reference coronal and sagittal images in survivors and uninjured controls and do not expect bias from this source; (iii) although the small sample size might limit the generalizability of our results, this approach may be used to determine post-traumatic morphometric pituitary changes. however, in the absence of hormonal determination, any attempt to suggest the presence of hypopituitarism remains speculative. longitudinal endocrinological studies have shown that phth occurs mainly in the acute phase of tbi, but later appearance has been also described. giordano et al. (11) reported that pituitary insufficiency at three months posttbi persisted at 12 months follow-up in patients with multiple hormonal dysfunctions, but recovered in those with only isolated hormonal dysfunction. additionally, 5% of cases with initially normal pituitary function presented with subsequent pituitary insufficiency. this is further confirmed by the recently reported appearance of new phth cases at 12 and 36 months post-tbi. (30), (31) in contrast, a prospective study (15) suggests that recovery of phth is the sole tendency in tbi patients at 12 months, with no new insufficiencies reported during that time period. thus, the functional (hormonal) profile of the pituitary gland seems to be quite dynamic following tbi, and a combined, imaging and hormonal, approach might increase the understanding of the mechanisms underlying hypopituitarism following head trauma. since the sub-acute stage (one month post) represents a potentially rich set of restorative therapy targets, these results would be especially useful for prospectively predict patient risk for developing romanian neurosurgery (2012) xix 3: 193 202 201 hypopituitarism. our results might help clinical decision-making and determining individual treatment strategies. summary statement/conclusions larger pituitary volumes were found at one month after injury in the majority of survivors of severe tbi compared with uninjured controls, with elevated, or normal, pituitary volumes at three or six months predicted by the volumes observed at one month after injury. conflict of interest authors stated no financial, personal, or professional conflicts of interest regarding this manuscript. sources of support: this work was supported by national institutes of health grants ns039123 to w. m. b. and hd02528 to the university of kansas. the hoglund brain imaging center is supported by c76 hf00201 and a grant from forrest and sally hoglund. w. m. b. is also supported by hd050534, ag029615, ag026374, ag026482, dk080090, and rr015563. c. m. c. is supported by the american heart association. corresponding author: sorin c. craciunas m. d. , ph. d. staff neurosurgeon, neurosurgery unit iv, bagdasar-arseni hospital, 10-12, berceni avenue, bucharest, romania e-mail: craciunassorin@yahoo. fr references 1. agha a, thompson cj: anterior pituitary dysfunction following traumatic brain injury (tbi). clin endocrinol (oxf) 64:481-488, 2006. 2. aimaretti g, ambrosio mr, di somma c, fusco a, cannavo s, gasperi m, scaroni c, de marinis l, benvenga s, degli uberti ec, lombardi g, mantero f, martino e, giordano g, ghigo e: traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury. clin endocrinol (oxf) 61:320-326, 2004. 3. aimaretti g, ghigo e: traumatic brain injury and hypopituitarism. scientificworldjournal 5:777-781, 2005. 4. benvenga s, campenni a, ruggeri rm, trimarchi f: clinical review 113: hypopituitarism secondary to head trauma. j clin endocrinol metab 85:1353-1361, 2000. 5. bondanelli m, de marinis l, ambrosio mr, monesi m, valle d, zatelli mc, fusco a, bianchi a, farneti m, degli uberti ec: occurrence of pituitary dysfunction following traumatic brain injury. j neurotrauma 21:685-696, 2004. 6. brooks wm, friedman sd, stidley ca: reproducibility of 1h-mrs in vivo. magn reson med 41:193-197, 1999. 7. cyran e: pituitary damage due to basal skull fracture (in german). deutsche medizinische wochenschrift 44:1261, 1918. 8. dusick jr, wang c, cohan p, swerdloff r, kelly df: chapter 1: pathophysiology of hypopituitarism in the setting of brain injury. pituitary, 2008. 9. estes sm, urban rj: hormonal replacement in patients with brain injury-induced hypopituitarism: who, when and how to treat? pituitary 8:267-270, 2005. 10. finkelstein e cp, miller t and associates: the incidence and economic burden of injuries in the united states. new york (ny): oxford university press; , 2006. 11. giordano g, aimaretti g, ghigo e: variations of pituitary function over time after brain injuries: the lesson from a prospective study. pituitary 8:227-231, 2005. 12. kelly df, gonzalo it, cohan p, berman n, swerdloff r, wang c: hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. j neurosurg 93:743752, 2000. 13. klose m, feldt-rasmussen u: does the type and severity of brain injury predict hypothalamo-pituitary dysfunction? does post-traumatic hypopituitarism predict worse outcome? pituitary, 2008. 14. klose m, juul a, poulsgaard l, kosteljanetz m, brennum j, feldt-rasmussen u: prevalence and predictive factors of post-traumatic hypopituitarism. clin endocrinol (oxf) 67:193-201, 2007. 15. klose m, juul a, struck j, morgenthaler ng, kosteljanetz m, feldt-rasmussen u: acute and longterm pituitary insufficiency in traumatic brain injury: a prospective single-centre study. clin endocrinol (oxf) 67:598-606, 2007. 16. kreitschmann-andermahr i: subarachnoid 202 craciunas et al mri study of pituitary gland after severe tbi hemorrhage as a cause of hypopituitarism. pituitary 8:219-225, 2005. 17. langlois ja r-bw, thomas ke. : traumatic brain injury in the united states: emergency department visits, hospitalizations, and deaths. centers for disease control and prevention, nation center for injury prevention and control, 2006. 18. lieberman sa, oberoi al, gilkison cr, masel be, urban rj: prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury. j clin endocrinol metab 86:2752-2756, 2001. 19. lorenzo m, peino r, castro ai, lage m, popovic v, dieguez c, casanueva ff: hypopituitarism and growth hormone deficiency in adult subjects after traumatic brain injury: who and when to test. pituitary 8:233-237, 2005. 20. maiya b, newcombe v, nortje j, bradley p, bernard f, chatfield d, outtrim j, hutchinson p, matta b, antoun n, menon d: magnetic resonance imaging changes in the pituitary gland following acute traumatic brain injury. intensive care med 34:468-475, 2008. 21. masel be: traumatic brain injury induced hypopituitarism: the need and hope of rehabilitation. pituitary 8:263-266, 2005. 22. moeller tb, reiff e: pocket atlas of sectional anatomy: head and neck. thieme, 2007. 23. popovic v, aimaretti g, casanueva ff, ghigo e: hypopituitarism following traumatic brain injury. growth horm igf res 15:177-184, 2005. 24. powner dj, boccalandro c, alp ms, vollmer dg: endocrine failure after traumatic brain injury in adults. neurocrit care 5:61-70, 2006. 25. salehi f, kovacs k, scheithauer bw, pfeifer ea, cusimano m: histologic study of the human pituitary gland in acute traumatic brain injury. brain inj 21:651656, 2007. 26. samadani u, reyes-moreno i, buchfelder m: endocrine dysfunction following traumatic brain injury: mechanisms, pathophysiology and clinical correlations. acta neurochir suppl 93:121-125, 2005. 27. schneider hj, samann pg, schneider m, croce cg, corneli g, sievers c, ghigo e, stalla gk, aimaretti g: pituitary imaging abnormalities in patients with and without hypopituitarism after traumatic brain injury. j endocrinol invest 30:rc9-rc12, 2007. 28. schneider m, schneider hj, yassouridis a, saller b, von rosen f, stalla gk: predictors of anterior pituitary insufficiency after traumatic brain injury. clin endocrinol (oxf) 68:206-212, 2008. 29. tanriverdi f, de bellis a, bizzarro a, sinisi aa, bellastella g, pane e, bellastella a, unluhizarci k, selcuklu a, casanueva ff, kelestimur f: antipituitary antibodies after traumatic brain injury: is head traumainduced pituitary dysfunction associated with autoimmunity? eur j endocrinol 159:7-13, 2008. 30. tanriverdi f, senyurek h, unluhizarci k, selcuklu a, casanueva ff, kelestimur f: high risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma. j clin endocrinol metab 91:2105-2111, 2006. 31. tanriverdi f, ulutabanca h, unluhizarci k, selcuklu a, casanueva ff, kelestimur f: three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study. clin endocrinol (oxf) 68:573-579, 2008. 32. teasdale g, jennett b: assessment of coma and impaired consciousness. a practical scale. lancet 2:8184, 1974. 33. thurman dj, alverson c, dunn ka, guerrero j, sniezek je: traumatic brain injury in the united states: a public health perspective. j head trauma rehabil 14:602-615, 1999. microsoft word 12.selectedabstracts.doc romanian neurosurgery (2010) xvii 4: 461 – 508 461 the 7th national congress of the romanian society of neurosurgery with international participation 28 september 2 october, cluj napoca abstracts undue effects following gamma surgery for cerebral avms l. steiner the first avm managed with the gamma knife was by steiner in april 1970, and up to 2009, he used the procedure in oyer 2,500 cases of avms and dural fistulas in the department of neurosurgery, karolinska hospital, stockholm; clinica del sol, buenos aires, argentina; university of pittsburg medical center, pittsburgh, pa, and university of virginia, charlottesville, va, usa. in the early stages of our avm project, patients were subjected to a rigorous protocol of repeated angiograms. later with the advent of mr1, angiography was not performed until the nidus was no longer visible on mri performed at six month intervals for two years and then on an annual basis. of the more than 2,500 cases, 1,500 gamma procedures in a total of 1,309 patients with avms or fistulae were treated by steiner at the lars leksell center for gamma surgery, university of virginia, charlottesville, va. the present study aims to analyze the radiation induced imaging changes, venous thrombosis, delayed cyst formation, and secondary tumor occurrence including only the series of patients treated in charlottesville. the severity of radiation induced changes on images and associated neurological deficits varied ranging from asymptomatic, a few millimeters increased t2 signal surrounding the treated nidus to massive brain edema with symptoms and signs of increased intracranial pressure. from 1426 gamma procedures performed for avm patients with follow-up mr i available for analysis, 34% of patients developed radiation induced changes. among them, 58% had mild (a few millimeters of increased t2 signal surrounding the nidus), 34% had moderate (compression of ventricle and effacement of sulci) and 8% had severe (midline shift) radiation induced changes. the mean time to the development of radiation induced changes was 13 months after gks, and the mean duration of the changes was 22 months. larger nidus volumes, nidi with a single draining vein and nidi without prior hemorrhage or surgery were associated with a higher risk of radiation induced changes. one hundred and twenty two (8.7%) patients developed headache (33 patients), worsening or new seizures (16 patients) or neurological deficits (73 patients) associated with radiation induced changes. patients with severe radiation induced changes, nidi at eloquent areas, mid nidi with prior embolization were more likely to develop symptoms. twenty six patients (1.8%) had permanent neurological deficits/radiation necrosis. 462 abstracts the 7th national congress of rsn twelve patients were found to have early thrombosis of draining veins accompanied with the radiation induced changes/brain edema. the incidence was 1% (12 out of 1256 patients). the venous thrombosis and radiation induced changes occurred 6 to 25 months (mean 13 months) following gks. three patients were asymptomatic upon the image findings of venous occlusion and brain edema, three experienced headache, one had seizure and headache and five developed neurological deficits. the radiation induced changes from occlusion of the prominent draining veins tended to be extensive and were more likely to associate with symptoms. patients with neurological deficits were treated with corticosteroids; two of the patients recovered completely, one still had slight hemiparesis, one had short-term memory deficits, and one died from massive intracerebral hemorrhage. on follow-up images, eight nidi obliterated on angiograms, two obliterated based on mri, two remained patent. cyst formation is a rare complication following gks. those developed after resolution of previous hemorrhages or fluid cavities from encephalomalacia after surgeries were not considered as complications related to gks. from our 1275 patients with followup mri available, we found a total of 21 patients (1.6%) developing a cyst after a mean of 7.9 years post-gks. five cysts were found in 702 patients (0.7%) with followup shorter than 5 years, eight cysts in 308 patients (2.6%) with follow-up between 5 and 10 years, and another eight cysts in 265 patients (3.0%) with follow-up between 10 and 20 years. of the 21 patients, 19 had regular mri follow-up and 15 (79%) of them had radiation induced changes before the development of cysts. six patients had large cysts and 3 of them were symptomatic requiring surgery. two cases underwent craniotomy and drainage of the cyst. the cyst wall showed no evidence of neoplasia. two secondary meningiomas in 1275 avm patients were detected. follow-up mri performed over a period of at least 10 years was available in 265 patients. if conservatively estimated that radiosurgically induced secondary neoplasia occurred in two cases during a 2,650 person years or 75 in 100,000 person years, there is a 0.8% chance that a radiation induced tumor may develop within 10 years following gamma surgery. microsurgical repair of intracranial aneurysms in the era of endovascular treatment what is left for microsurgery? istván nyáry department of neurosurgery, semmelweis university, hungary objective: since the advent of endovascular treatment of intracranial vascular malformations including cerebral aneurysms, majority of cases will be treated in this arm of treatment modalities, due to the less invasiveness brought about by avoiding craniotomy. however, considerable number of aneurysms still remain for microvascular repair. this paper do not intend to tackle still persisting controversies in the clip or coil debate, instead it aims to identify and explore the group of cases in the praxis of a busy centre, where neurosurgeons and interventionists work together, and endovascular is the first choice for treatment. following the above mentioned approach, three major entities romanian neurosurgery (2010) xvii 4: 461 – 508 463 can still be elected for intracranial repair: aneurysms not or less amenable for endovascular treatment, giant aneurysms, and clipping after insufficient obliteration by coiling. methods: patient material of our service comprises around two hundred aneurysm cases each year, two third / one third distributed between the endovascular and microsurgical treatment modality. all operated aneurysm patients are worked up within the budapest aneurysm registry, now containing more than five thousand cases. results and surgical strategy: aneurysms less amenable for endovascular obliteration with continuous development of endovascular technologies, virtually all kinds of vascular pathologies can be tackled by this method. still, if well trained interventionist and surgical teams work together, the pressure to perform is less and those cases can be left for craniotomy which are less favorable for endovascular treatment. determinants for this group are: localization (e.g. middle cerebral artery bifurcation), and morphology of the aneurysm (wide neck, involvement of bifurcation into the neck, fusiform aneurysms). from surgical point of view, following difficulties need to cope with: sclerotic, stiff neck, rendering calamitous to model the neck appropriately for clipping; if primary vessels virtually offspring from the sack, due to widening of the bifurcation, reconstruction of the bifurcation itself is necessary by clipping; similarly, special challenge to reconstruct normal anatomy by clipping in cases of fusiform aneurysms. giant aneurysms: aneurysms with a diameter greater than 2.5 cm comprise this group (locksley 1966). frequency of giant aneurysms is around 5-6% with respect to all aneurysm occurrences, and outcome of untreated cases is rather bleak: 80% lethal or with severe symptoms within five years. they may bleed or are presented with symptoms of a space occupying lesion. the virtually arbitrary limit of 2.5 cm, however, has a profound meaning that may also be considered as definition for giant aneurysms. considering intracranial geometry (diameter of major vessels, measure of the intracranial space in the surrounding of the aneurysm) this is the size, when due to bulging of the sack, the neck cannot be seen at exposure, regardless the size of craniotomy. from this condition immediately stems the first difficulty during surgery: in order to come close to the neck for clipping, the sack needs to be diminished. different surgical strategy and technology is necessary to achieve this goal, depending whether the sack is partially thrombosed or not. proximal control of blood supply is a must (temporary clipping, intracarotid inflatable balloon), and depending on collateral circulation establishment of high-flow venous graft anastomosis before the direct attack on the aneurysm can be useful, as well. remodeling of the neck either by clipping using special and sometimes big clips or by micro suturing is more often needed than with other aneurysms. because of the rather difficult and sometimes calamitous surgery inherent with this type of lesions, preoperative knowledge of exact vascular morphology and functional state of circulation is absolute necessary. modern imaging techniques (3d reconstruction) provides great help. clip after coil: even the best endovascular procedure may leave partial filling of the sack, that may increase with time due to the water hammer effect, or perforation and re 464 abstracts the 7th national congress of rsn bleeding occurs either at the procedure or later. although, number of unwanted complications remains a small fraction as compared to the whole number of endovascular procedures, still the frequency of craniotomies increases with the increasing number of endovascular obliterations. from a surgical point of view, when clipping a coiled sack, difficulty stems from the fact, that the packed aneurysm needs to be evacuated, because the rigidly elastic coil material in most cases prevents satisfactory placement of the clip on the neck. conclusion: it seems, that microsurgical repair still remains an eligible treatment modality, in spite of the preponderance of endovascular techniques. question is the training for these rather difficult surgical interventions, because, paradoxically the per se more complicated cases are left for microsurgery. concentrating delicate cases into expert major centers can be the solution in order to assure sufficiently high number of procedures needed to gain appropriate exercise and opportunity for training. endoscopic assisted surgery in skull base tumours: results with 282 cases j. oertel the indication for endoscopic assisted surgery in skull bases processes is under controversial discussion. experienced skull base surgeons often consider the endoscope to be unnecessary while a younger generation of surgeons counts on the value of the endoscope in such procedures. here, we present our series of endoscope assisted procedures performed since february 2003. during the investigated time period, a total of 282 skull base cases were operated on with application of the endoscope. the endoscope was not routinely applied but only when it was felt to be helpful in each individual case. the application of the endoscope was evaluated with respect to the frequency and the duration of the assistance and with respect to the subjective value for the individual surgeon. all patients were postoperatively followed. in all cases, an early postoperative mri was performed for resection control. the 285 skull base cases consisted of 128 vestibular neurinomas, 4 trigeminal neurinomas, 20 planum sphenoidale meningiomas, 16 cerebello pontine angle meningiomas, 10 arachnoid cysts, 18 craniopharyngiomas, 14 pineal lesions, 22 aneurysms, 10 hemifacial spasms, 21 trigeminal neuralgias, 8 epidermoids, and 3 others. overall the endoscope was considered to be helpful in 225 of 282 cases (80%). it was considered to be indispensable in 39 cases (14%). in vestibular neurinomas, the endoscope was used for inspection in 105 cases (82%) and for endoscopic assistance in 23 (18%). the technique was considered to be indispensable in high jugular bulb and deep intrameatal tumour. the endoscope was considered helpful in 93 (73%) and indispensable in 19 (15%). in craniopharyngiomas, the endoscope was used for inspection in fourteen cases (78%) and for endoscopic assistance in 4 (22%). the endoscope was considered helpful in 14 (78%) and indispensable in 4 (22%). one transient oculomotor palsy occurred possibly due to the light source temperature. in hemifacial spasm, the endoscope was used in 100% for inspection and was considered to be helpful in all cases. in aneurysms, the endoscope was applied for inspection in 22 cases (100%). it romanian neurosurgery (2010) xvii 4: 461 – 508 465 was considered to be helpful in 16 (72%) and indispensable in 6 (28%). it was particularly helpful in pcom, ba, and a1 aneurysm surgery to excluded clipping of perforators. in all, the authors consider endoscopic assistance a valuable tool in selected cases of skull base procedure with being indispensable in a small subgroup of these procedures.functional results of vestibular schwannoma surgery after radiation treatment marcos tatagiba tübingen, germany. introduction: radiosurgery has been increasingly used as alternative treatment for vestibular schwannomas (vs), particular the small ones. there is a controversial discussion whether radiated vs may be more difficult to be removed because of the fibrous changes caused by irradiation. aim of this retrospective study war to show the functional results of facial nerve preservation following vs surgery after failed radiation treatment. method: among 360 surgical cases of vs, a total of 9 patients had received previous radiation. all 9 patients showed growing tumours at mri studies. all patients underwent tumour removal via retrosigmoid approach. postoperative facial nerve results were classified after housebrackmann grading system. results: in the total series of 360 vs, complete tumour removal was achieved in 97.8% of the cases, and facial nerve was preserved in 98.5% of the cases. among the 9 patients with previous radiation, 4 patients had incomplete tumour removal. postoperative facial nerve was classified as follows: grade i-ii: 4 patients, grade iii: 3 patients, grade v: 2 patients. conclusion: surgical emoval of vs after radiosurgery was shown to be more difficult than non-radiated cases.although tumour removal does not necessarily result in facial palsy, there is a significant risk o injury the facial nerve in these cases. patients who require microsurgical tumour removal need a more conservative approach compared to non-radiated patients. functional results of vestibular schwannoma surgery after radiation treatment m. s. tatagiba introduction: radiosurgery has been increasingly used as alternative treatment for vestibular schwannomas (vs), particular the small ones. there is a controversial discussion whether radiated vs may be more difficult to be removed because of the fibrous changes caused by irradiation. aim of this retrospective study war to show the functional results of facial nerve preservation following vs surgery after failed radiation treatment. method: among 360 surgical cases of vs, a total of 9 patients had received previous radiation. all 9 patients showed growing tumours at mri studies. all patients underwent tumour removal via retrosigmoid approach. postoperative facial nerve results were classified after housebrackmann grading system. results: in the total series of 360 vs, complete tumour removal was achieved in 97.8% of the cases, and facial nerve was preserved in 98.5% of the cases. among the 9 patients with previous radiation, 4 patients had incomplete tumour removal. postoperative facial nerve was classified as follows: grade i-ii: 4 patients, grade iii: 3 patients, grade v: 2 patients. conclusion: surgical emoval of vs after radiosurgery was shown to be more 466 abstracts the 7th national congress of rsn difficult than non-radiated cases.although tumour removal does not necessarily result in facial palsy, there is a significant risk o injury the facial nerve in these cases. patients who require microsurgical tumour removal need a more conservative approach compared to non-radiated patients. strategies in surgery for anterior skullbase meningeomas: endoscopic or microscopic endonasal or transcranial? h.w.s. schroeder endoscopic endonasal skullbase surgery has been increasingly used to approach frontal skullbase meningeomas. the endonasal approach has several advantages compared to the transcranial approach, but also many limitations. larger meningeomas of the anterior skullbase often involve cerebral blood vessels and olfactory and/or optic nerves. dissection of these adhesions seems to be safer via a craniotomy than from below. furthermore, often tumor extensions growing along the dura over the extent expected from preoperative mr imaging is found during surgical exploration. we use 3 standard approaches for anterior skullbase meningeomas: for large tumors the frontolateral, for medium-sized tumors the supraorbital, and for very small tumors the endonasal approach. details regarding surgical technique and patient selection are provided. controversies in multimodal management of pineal tumors (experience of 87 cases) a.v. ciurea1, a. tascu1, m. lisievici2, f. brehar1, r.e. rizea1, carmen radoslav3 1neurosurgical clinic, 2neuropathology department, 3neuro-intensive care unit “prof. bagdasar-arseni” clinical hospital, bucharest, romania background: tumor of the pineal region is more common in children (3-8% of primary brain tumours) than in adults (1%). germ cell tumors (gtc) are dominating in this area, followed by pineal ccell tumors, glial tumors and miscellaneous material and method: the authors reviewed diagnostic problems, management, therapeutical strategies and outcome in 87 cases of pineal area tumors admitted over a period of 15 years (2000 – 2010). the series comprises 51 male and 36 female patients, ranging in age from 0 to 59 years (median age 26 y.o.). the clinical features were represented by intracranial hypertension (72 cases – 84.7 %), parinaud syndrome (59 cases – 70.2 %), convergence palsy (18 cases – 21.4 %), ataxia (30 cases – 34.5%), seizures (16 cases – 19 %), endocrine disturbances precocious puberty (13 cases – 15.4 %), consciousness disturbances (10 cases, 11.9%). diagnostic evaluation consisted of a medical history, physical & neurological examination, neurodiagnostic findings (ct and mri scan) and studies of serum and csf tumor markers. hydrocephalus was associated in 70 cases (80.4 %). generally, gct, ependymomas and pineal cell tumors metastasize easily through the csf (“drop metastases”). in that situation the all cns will be evaluated by mri scan preoperative and postoperative. surgical strategy: 84 (96.5%) cases were microsurgically approached, via the occipital transtentorial approach (72 cases) (82.7%) or supracerebellar infratentorial approach (12 cases) (13.8%). three cases romanian neurosurgery (2010) xvii 4: 461 – 508 467 (3.4%) in our data receive stereotactic procedures, followed by neurooncological therapy. histological diagnosis has revealed gct in 40 cases (46%), pineal cell tumors in 16 cases (19 %), glial cell tumors in 27 cases (32 %) and miscellaneous tumors in 4 cases (4,6 %). total removal of the tumor was achieved in 22 cases (25.2 %), near total removal in 23 cases (26.4 %), partial removal in 33 cases (37.9 %); open biopsy was undertaken in 8 cases (9,1 %) and stereotactic biopsy in 3 cases (3,4%). postoperatory mortality: four deaths in the first six months (4.8 %). the postoperative complications included: ocular movement disorders (28 cases – 33.3 %), alterated consciousness (19 cases – 22.6 %), seizures (18 cases – 21.4 %), ataxia (15 cases – 17.8 %), pupillary abnormalities (15 cases – 17.8 %) and others. the majority of these complications were transient. forty-one (47.1%) patients received craniospinal irradiation and two (2.3%) followed focused radiotherapy (g.k.s.). radiation therapy was done always after the pathological diagnosis. craniospinal irradiation was administered only to those patients with the disease involving more than one intracranial site, demonstrated meningeal seeding or positive csf cytology. chemotherapy (cisplatin & bleomycin & actinomycin d) was received in 43 cases. the glasgow outcome scale (gos) at 6 months shows: good recovery 49 cases (56.3%), moderate disability 22 cases (25.2%), severe disability 11 cases (12,6%), persistent vegetative state 1 cases (1.1%), and death 4 cases (4.6%). conclusion: pineal tumors represent a therapetical challenge for neurosurgeons. on the basis of this review, the authors consider that the outcome depends both by the histological type of tumor and the modality of treatment applied. there is no one surgical approach superior to others, but the stereotactic approach is one of the good and minimal invasive option for obtain enough material for pathological diagnosis. the deep cerebral veins are not a major obstacle for operation in these regions. keywords: pineal area tumors, mri, microsurgery, stereotactic biopsy, germ cell tumors and gamma knife surgery abreviation: pa = pineal area; pbt = pediatric brain tumors; gct = germ cell tumors; g.k.s. = gamma knife surgery; g.o.s. = glasgow outcome scale; csf = cerebral spinal fluid; cns= central nervous system endoscopic options in intraventricular tumours j. oertel, h. w.s. schroeder, m.r. gaab kliniken für neurochirurgie, universität mainz, universität greifswald und krankenhaus hannover nordstadt, germany intraventricular lesions represent ideal candidates for neuroendoscopic approaches. here we present our data since february 1993. one-hundred-twenty-one lesions consisted of 30 colloid cysts, 28 gliomas, 9 craniopharyngiomas, 5 subependymomas, 9 intraventricular arachnoid, 8 pineal cysts, 5 metastases, 3 glial scars, 3 plexus papillomas, and 18 others. in one case, no histologic diagnosis was achieved. in two cases, only a ventriculitis was found. follow up was performed up to 9 years. there was no emergency stopping of any endoscopic procedure. in three cases of colloid cysts venous rebleeding occurred, 468 abstracts the 7th national congress of rsn and in one case, a switch to microsurgery was done. in two other cases, the endoscopic technique was abandoned because of tumour size, and the tumour resection was continued microsurgically. mean surgical time scored 90 minutes (range 30 to 240 minutes). cystic lesions were evacuated and membranes fenestrated. in three colloid cysts, capsule remnants were left at the roof of the third ventricle. in these three cases, no recurrent growth was observed (fu up to 93 months). a complete resection was performed in small solid tumours in two cavernomas, three plexus papillomas, two medulloblastomas, and one subependymoma. larger astrocytomas was decompressed. an endoscopic biopsy was performed in 38 cases. csf flow was restored by 39 ventriculostomies and 9 septostomies. the csf flow restored in all cases. one meningitis, one permanent mental syndrome, one transient trochlear nerve palsy as well as one transient mental syndrome occurred. in all, the endoscopic technique represents a safe and effective therapeutic option in intraand paraventricular lesion. particularly in association with csf flow disturbances, neuroendoscopy is an ideal technique for such lesions. endoscopical versus microsurgical treatment of pineal region tumors g. zapuhlih, r. safta department of neurosurgery, institute of neurology and neurosurgery, republic of moldova objective: tumors of the pineal region represent a diverse collection of tumors with a variety of natural histories. the authors evaluate their results in the management of patients with tumors in the pineal region methods: this is a retrospective clinical evaluation of 14 patients with primary tumors of the pineal region treated by microsurgery and endoscopy. there were 5 pineocytoma, 4 pineoblastomas, 3 lowgrade gliomas, one germinoma and one teratoma. there were 8 male and 6 female patients. their median age was 15.5 years (range 3-49 years). in 1 case the endoscopic procedure represented the only surgical treatment (with total removal of a pineocytoma) . in 13 cases, microsurgical removal of the lesions and/or etv or ventriculo-peritoneal shunts placement were performed for the management of hydrocephalus. results: all neoplasms were treated surgically with good results. the etvc was successfully performed without complication in 5 patients and a ventriculoperitoneal shunt was done in four. a total tumor removal was achieved in 9 operations, subtotal in 4 and partial in 1. conclusions: early surgical resection combined with etv or diversion of cerebrospinal fluid is effective in the treatment of pineal lesions. the endoscopic management of patients with pineal region tumors affords a minimally invasive way to obtain resolution of obstructive hydrocephalus by endoscopic third ventriculostomy (etv and tissue diagnosis) and sometimes can be an only surgical treatment. when a direct microsurgical approach is indicated, the choice among the surgical approaches depends on the size and the location of the lesion in the pineal area and its relation to the ventricular system. romanian neurosurgery (2010) xvii 4: 461 – 508 469 suboccipital supracerebellar approach for pineal region tumors i. poeata, z. faiyad, s. gaivas, b. iliescu, al. chiriac the rarity of pineal region tumors and repeated changes in their histopathological diagnostic criteria makes the study of their biological behavior and clinical outcomes difficult. furthermore, the difficulty of preoperative imagistic differential diagnosis imposes a surgical approach to these lesions, including for symptomatic cystic lesions. the deep-seated location of pineal region tumors and their associations with critical structures make their surgical resection technically challenging. we analyze the surgical techniques and results of the suboccipital-supracerebellar approach for pineal region tumors together with the results in the pathological study of these lesions. in our series of pineal region lesions 11 were operated through this approach using prone position. we present the advantages in visualizing the pineal region and its surrounding structures using this approach and the technical challenges and pitfalls. our experience suggests that the suboccipital-supracerebellar approach provides a good way of access to the pineal region and allows for a good control of the tumor and of the important neighboring structures. supracerebellar infratentorial approach for pineal region tumors st. i. florian, h. stan, bianca pintea, c. pirjol, andreea mogyoros background: pineal region tumors represent a heterogeneous group of tumors as origin (at least 17 different subtypes) which are deep-seated, uncommon; tend to enlarge the gland and be locally invasive; occasionally seed the neuraxis or cause obstructive hydrocephalus or parinaud’s syndrome. they represent about 1% of all brain tumors, but account for 3% to 8% of the intracranial tumors in children. the purpose of this material is to present our experience in treating patients presenting these lesions. material and methods this review consist in a retrospective study of 25 cases of tumors located in pineal region area, diagnosed and operated in 1st neurosurgical department of county emergency hospital cluj-napoca, january 1998 to june 2010, from a total of 2370 patients with intracranial tumors. from this 25 patients, 24 were surgically treated, one receiving ventriculo-peritoneal shunt followed by radiation therapy with good response. results: in 18 cases (72%), total removal of the tumor was achieved; 4 cases (16%) underwent subtotal removal and 2 biopsy. histological features correspond with already published data. groups marked: pineal parenchymal tumors 2 cases (8%), glial tumors – 9 cases (36 %), germ cell tumors – 3 cases (12%), meningeoma 6 cases (24 %), metastases 3 cases (12 %), and 1 case of tumor with ependimar cells. gender distributions: 63% female, versus 37% male. most common presentations were headache, nausea, and vomiting caused by obstructive hydrocephalus, respective parinaud syndrome, nistagmus, ataxia and dismetrie. in 9 cases (36%) csf shunting was requested for obstructive hydrocephalus, both preoperative – 6 cases and postoperative – 3 cases; this was achieved either by ventriculocisternostomy: 3 cases or ventriculoperitoneal shunting: 6 cases. surgical approach was most 470 abstracts the 7th national congress of rsn commonly infratentorial supracerebellar 16 cases (64%), and combined infratentorial-occipital transtentorial – 3 cases (12%); subchoroidal approach and endoscopic biopsy were used for the rest of the cases. for almost all cases, we used the sitting position. complete removal of the tumor was achieved in 18 cases, subtotal in 4 cases; 2 cases was approach by endoscopic biopsy and one case treated only with radiotherapy. postoperative karnovsky score was 70 to 100. a single case was noted as deceased, due to acute postoperative cerebellar edema. conclusions: infratentorial supracerebellar approach was the most commonly used in our series. as well as the occipital transtentorial approach, this allow a relatively easy access to the pineal region and good intra-operative comfort for the surgeon. malignant tumors should undergo aggressive resection followed by radiotherapy and/or chemotherapy while pure germinomas, which are exquisitely radiosensitive, should be treated by conventional radiother the anatomical and functional spinal balance in vertebral tumors after surgical resection and reconstruction p.p. varga aims: the primary goal of the surgical intervention in primary spine tumor care is to perform „en bloc” resection and obtain tumor-free surgical margins. at the same time, the functional outcome and the quality of life of the patients are highly depends ont he definitive neurological deficits and the possibilities of the soft tissue and bony reconstructions. in this lecture we summaries the basic principles and our institutional policy of the spinal balance restauration supporting the goals adressed below. materials and methods: during the last 12 years we use a complex prospective database of the primary tumors operated int he ncsd. 320 cases are listed, and among them in 205 cases we performed reconstruction after the tumor resection. in this study we analyse the different techniques in different spinal levels, particularly the sacral resections and lumbopelvic reconstructions. results: in this prospective cohort the best results could be expected from the reconstruction of the entire biomechanical enviroment of the affected segments. total segment resection and total sacrectomy gives the best functional results if anterior support and posterior stabilization are applied including proper bone grafting and soft tissue reconstruction (fascia, muscles and skin flaps). most comon complications are deep wound infection int he early postoperative period and stress failure of the implants for a longer follow up. conclusion: as a result of the proper oncological resection of the primary spinal tumors often destroys the stability of the affected section of the vertebral coloumn making the functional result of the surgery less favourable. particularly after sacral tumor resections the neurological deficits should be considered prior the surgery int he planning process of the rehabilitation and the patient consent. proper data collection and multicentric collaboration could improve the accuracy of the evolution of the long term results after this procedures. romanian neurosurgery (2010) xvii 4: 461 – 508 471 craniocervical stabilization techniques m. zileli introduction: cranicoervical instability may be due to trauma (odontoid fracture, ligamentous injuries, combined c1-c2 fractures), rheumatoid arthritis, congenital abnormalities, tumors and iatrogenic. there are many surgical techniques used for stabilization of the craniocervical junction: odontoid screw fixation, c1-c2 wire fixation, c1-c2 transarticular screw fixation, c1-c2 segmental screw fixation and occipito-cervical fixation. aim: this paper will summarize the craniocervical stabilization techniques and their results. method: in a 10 years period we performed 162 upper cervical fixations for instability. the methods we used were occipitocervical fixation (103), c1-c2 wiring (24), c1-c2 screw fixation (20), halifax clamp fixation (2), odontoid screw fixation (11) and c2-clivus anterior plate fixation (2). we reviewed the surgical results, fusion rates and complications of these techniiques. conclusions: the anatomy of this region requires attention during all these techniques. vascular, cranial nerve and spinal cord anatomy have all unique features. to decrease the complication rate and provide solid union, special attention is necessary to biomechanics of this region. keywords: craniocervical stabilization, odontoid fracture, occipitocervical fixation, basilary invagination extensive vertebral resection in spine tumor pathology. our perspective and experience t. maior, st.i. florian, c. pirjol, d. fetche1 cluj county emergency hospital, department of neurosurgery university of medicine and pharmacy “iuliu hatieganu” cluj-napoca aims: spinal instrumentation currently allows gross-total resection and reconstruction in cases of malignancies at all levels of the spine. in the past, the goal of surgery was mainly limited to providing histological diagnosis, neural decompression, and palliation of pain. now, it is technically feasible to resect tumors completely from all levels of the spine, while simultaneously restoring stability by reconstruction of the resected segments. our series included those cases in which the surgical management comprised combined approaches, anterior and posterior, associated with instrumentation on several levels. cases approached only for decompression (without instrumentation) were not considered. major indications for anterior– posterior resection followed by instrumentation included three-column involvement, high-grade instability, involvement of contiguous vertebral bodies, and solitary metastases. material and method: we will discuss the results obtained in 92 patients who underwent surgery for primary and metastatic spinal tumors, over a 5-year period (2005-2010) in our department. the surgical approach was chosen taking into consideration the histological type of tumor and the degree of instability. in order to classify the cases, we used the 472 abstracts the 7th national congress of rsn instability scale based on the degree of involvement of the three stability pillars (described by denis). 45 patients were operated through combined anterior and posterior approaches. in 18 cases we performed only anterior approaches (14 cases with tumors located in the cervical region). i did not perform any “en block” resections, only piecemeal resections. in all anterior approaches i was assisted by a general or cardiovascular surgeon. results: postoperatively, a significant neurological improvement was recorded in 74 patients. the overall median survival period was 16 months, and 46% of patients survived up to 2 year. 25% suffered postoperative complications. conclusion: despite the high incidence of complications, the majority of patients reported improvement in their quality of life at follow-up review. blood loss was significantly lower in anterior approaches. the outcome is better in the cases where complete resection was possible through combined anterior and posterior approaches. en block resection is superior to piecemeal resection in terms of recurrence risk. stereotactic management strategies for low-grade gliomas f.w. kreth supratentorial world health organization grade ii gliomas constitute a heterogeneous group of neoplasm, some of which are associated with early tumor progression and malignant behaviour. outcome is powerfully influenced by clinical and molecular-genetic parameters leading to highly divergent outcome measurements independent of any applied treatment strategie: 10 year survival ranges from as low as 6% to as high as 55%. accordingly, risk adjusted tailored treatment concepts for well defined subpopulations have increasingly gained influence. given the fact that only a selected number of these tumors are suitable for complete tumor resection and that the prognostic impact of incomplete resection is not well substantiated, minimal invasive tumor characterization by biopsy might play an essential role for risk adjusted treatment planning of these complex tumor entities. here we show that the still new method of molecular stereotacic biopsy technique guided by molecular/metabolic imaging such as positron emission tomography is a safe and powerful tool for tumor characterization in eloquently located gliomas not suitable for complete tumor resection: we demonstrate that the status of important prognostic/predictive biomarkers (such as tp35-, mgmt promoter methylation-, idh1-, loh 1p/19q-status) can be reliably and safely obtained using size adjusted molecular-genetic techniques. the success rate of these molecular-genetic analyses lies in the range of > 98%. we further show that the risk of the molecular stereotactic procedure still remains extremely low in experienced hands (< 1%) and is not influenced by tumor location. we further demonstrate that stereotatic iodine-125 brachytherapy alone or in combination with tumor resection is an attractive treatment concept for selected patients with circumscribed eloquently located glioma. thus, the modern role of stereotactic techniques for modern management strategies of low-grade gliomas is underscored. romanian neurosurgery (2010) xvii 4: 461 – 508 473 surgery of high grade gliomas-pro\'s in favor of gross total removal (2010) – personal experience st.i. florian1,4, c. abrudan1,4, cernea dana2, petrescu magda3, b. suciu4, adriana cocis4 1university of medicine and pharmacy „iuliu hatieganu” cluj-napoca; 2cluj county emergency hospital, department of neurosurgery 3“prof. ion chiricuta” oncology institute, cluj-napoca 4cluj county emergency hospital, department of pathology background: malignant glioma is the most common primary brain tumor in adults. even with aggressive treatment using surgery, radiation and chemotherapy, median reported survival arround one year. in the recent eortc trial surgery seas to have no prognostic role concerning the survival rate. in the last years more and more studies are focused on the role of surgery in prolonged median of survival and survival at two years. the purpose of this study is to add some arguments in favor of surgery and especially of the radical surgery in malignant glioma. material and methods: this is a retrospective study of a single centre single surgeon and represent the the last eleven years of the main author. the study is based 433 cases of high grade cerebral glioma operated between 01.01.2000-01.01.2010 at the neurosurgical clinic of cluj-napoca university hospital. all the tumors were operated and total removal was the goal in all the cases. we analyzed age, gender, duration of symptoms, type of surgery, interval from surgery to radiotherapy, total dose received, type of chemotherapy and the correlation of these factors with overall survival. results: the results shows, according to their histological features, the fallowing dispersions: astrocitomas grade iii (28,4%), glioblastoma multiforme (63,7%), high grade oligodendrogliomas (5%) and high grade ependimomas (2,8%). age was ranged between 6 to 82 years. considering de gender, 56,2% were male and 43,8% female. in a clinical point of view icreased intracranial pressure was the major sign, followed by motor deficits, languege impairment and behavioral changings. gross total removal of the tumor was achieved in more than 90% of the cases and the mortality was arround 3%, large majority of the deceased cases being more than 70 years of age. data for long term follow up were available for 123 patients. conclusions: glioblastoma multiforme is the most frecvent tip of glioma operated. the most important for a good outcome of the surgical treatment is the extent of resection. standard treatment for high grade gliomas including gross total removal surgery followed by concomitant radiochemotherapy and adjuvant chemotherapy with temodal should be considered for all patients. despite advances in multimodal treatment, the overall prognosis remains poor keywords: glioma, glioblastoma multiforme, astrocitoma, oligodendroglioma, ependimoma possibilities and limits in malignant gliomas treatment with the actual therapeuthic methods, a retrospective study of 110 cases treated between 2006 and 2009 i. poeata, z. faiyad, d. rotariu, s. gaivas, b. iliescu, a. iencean attempt to complete resection in high grade gliomas are limited by difficulty in 474 abstracts the 7th national congress of rsn preserving functional structures in the unclear peritumoral infiltrative area as well as deep located vital area with perforator vessels type irrigation. sacrificing functional areas is not acceptable for lesions wellknown for their constant reccurency tendences. we have analyzed a series of 110 cases of glioblastoma wich were operated on between january 2006 and december 2009 using the actual therapeutic methods wich include microsurgical resection, intraop echography, neuronavigation, cusa and awake surgey for eloquent areas. we have excluded the patients without histological confirmation and patients with infratentorial lesions or age under 18. in our series we have observed a slight predominance in males 55.4 %, the main symptom was the impairment of the motor function observed in 36.3 % casese and seizures in 30.9% cases. the preponderent age groupe was between 51 and 60 age with 31% of the cases. the complete resection was obtained in 35.4% of cases and in other 61.8% of cases radical surgery was not possible because of the tumor infiltration in basal ganglia in 21.8% of the cases, eloquent areas in 49% of cases and invasion of vascular structures 13.6% of the cases. the main complications in patients operated for gbm was the hemorrhage in the tumoral bed in 13.6% of the cases. we have followed up the pacients using mri examination with contrast enhancement and neurological exam at 2,6 and 12 months postop. the patients were directed to the territorial oncology department for adjuvant therpy (rxt/cht), from all of our series only 60 patients have come back for reevaluation and from those only 43 patients have done adjuvant therapy. in 25 patients there was a second operation for recurrence and the average time for re-intervention was 15,6 months. early imagistic diagnosis, using high sensitive mri exams, and complete microsurgical resection seem to improve the outcome of malignant gliomas together with radiotherapy and chemotherapy, but complete cure is difficult to confirm and needs long period of follow-up. some interesting cases together with our therapeutic and surveillance protocol in glioblastoma are presented. keywords: glioblastoma, high grade glioma, malignant glioma image guided stereotactic biopsy for infiltrative, multicentric and deepseated cerebral gliomas f.m. brehar1, a.v. ciurea1, r.m. gorgan1, m. lisievici2, a. tascu1, r. rizea1 1first neurosurgical clinic 2department of pathology “bagdasar-arseni” emergency clinic hospital, bucharest, romania aims: despite the recent advances achieved in neuroimaging techniques and microsurgical approaches, the infiltrative cerebral gliomas remain a neurosurgical challenge. in this paper, the authors present their experience in 54 stereotactic biopsies performed for infiltrative, multicentric and deep-seated low-grade and high-grade cerebral gliomas. matherial and methods: fifty-four patients with infiltrative, multicentric and deep-seated gliomas have been enrolled in this study. the median age was 42 years. the stereotactic and neuroimagistic tools used for these procedures include the leksell stereotactic system and the latest software: stereotactic planning system (sps), ntps 8.2. results: the histopatological results for these lesions were: 26 cases of grade iv romanian neurosurgery (2010) xvii 4: 461 – 508 475 gliomas (glioblastoma) (48,1%), 8 cases of grade iii gliomas (anaplastic astrocytoma) (14,8%), 14 cases of grade ii fibrillary astrocytomas (25,9%) and 6 cases of grade i astrocytomas (11,1%). in 8 cases (14,8%) the immunohistochemistry has been performed in order to obtain a more precise histopathological result (for tumor grading). in this series the mortality was 0%, with no cases of clinical significant hemorrhages after biopsy procedure. minor bleeding at the biopsy site was revealed by the postbiopsy ct scan in 10 patients (18,5%). temporary increasing of neurological deficits has been noticed in 6 patients (11,1%). as soon as the histopathological results have been assessed, the patients have been advised to undergo specific oncological treatment in accordance with the degree of malignancy of the tumors. conclusions: in conclusion, the image guided stereotactic biopsy represents now a safe method for establishing a precise histopathological diagnosis, which may influence the therapeutically management of the patient. keywords: stereotactic biopsy, mass lesions, gliomas current status of endoscope-assisted microsurgery h.w.s. schroeder endoscope-assisted microsurgery is a surgical technique which combines the use of the microscope and the endoscope. both optical tools have advantages and disadvantages. the microscope provides excellent visualization of superficial structures and, more importantly, a stereoscopic view. however, areas behind bony corners or neurovascular structures cannot be visualized. the endoscope brings the eye close to the area of interest which has advantages in deep and small surgical corridors. because of the wide-angle optics, the endoscope gives a nice panoramic overview and furthermore, with angulated endoscopes looking and working around a corner is possible. in many skullbase surgeries, the combination of microscopic and endoscopic visualization is helpful. most of the surgery is done under microscopic view. however, areas which cannot be visualized in straight line with the microscope are approached using the endoscope. in vestibular schwanomma surgery, the endoscope is used to inspect the fundus of the internal auditory canal. in epidermoids which may spread extensively along the subarachnoid spaces, endoscopes aid in inspecting the subarachnoid space in other surgical compartments. extensions of skullbase meningeomas entering the canals of the cranial nerves, can be removed under endoscopic view. the endoscope-assisted microsurgical technique enables a safe tumor removal when tumor parts are not visible in a straight line. the need for neurovascular retraction and skullbase drilling can be reduced. tumor extension into adjacent compartments can be removed via the same approach without enlarging the craniotomy. best treatment in intracranian arahnoid cysts (acs) a.v. ciurea, a. tascu, d. talianu, f. brehar , r. rizea, a. spatariu introduction: also known as leptomeningeal cysts, arachnoid cysts(acs) are congenital, benign, nonneoplatic, extraxial, lesion that arise during 476 abstracts the 7th national congress of rsn development from splitting of arachnoid membrane. distinct from posttraumatic cysts and unrelated to infection. bright (1831) describe the intraarahnoidian origin of these lesions, starkman et all (1958) proposed that the asociated temporal hypoplasia is secandary to cyst expansion and pressure on the temporal operculum. acording to di rocco et all (2010), acs are developmental defect, that occurs within the first three months of gestational life, in the duplication or splitting of the arachnoid layers, and are related to abnormalities of csf flow. location: in 50% intracranian araschnoid cyst involve the sylvian fissure/middle cerebral fossa.acording to gallasi et all. (1980) sylvian acs can be classified into three subgoups acordint to cysts dimensions and extensions. other common locations are: cp angle, the quadrigeminal cistern ,the retrocerebelar area and the sellar/supraselar region. less commonly acs can develope within the interhemisferic fissure and cerebral convexity. clinical findings: acs become symptomatic mainly during childhood and adolescence, depending on the location of the cyst not to it’s dimension. asymmetrical macrocranian or a focal bulging of the skull in the temporal region is the most common symptom, headaches, focal neurological symptoms, epilepsy and sings of increased intracranial pressure. in suprasellar acs endocrine disfunctions (60% of cases), hydrocephalus (40% of cases probably due to compression of the third ventricle) and visual impairment are the most common presenting symptoms. terapeutical options: observation many authors recommend not treating arachnoid cysts that do not cause mass effect or symptoms, regardless of their size and location. multimodal surgical treatment consisting of shunting the cyst into peritoneum, craniotomy (microsurgery) with fenestration and cystwall excision, endoscopic fenestration or stereotaxic suction. patients and methods: the authors study 317 cases of arachnoid cysts, admited in 1st neurosurgical clicin, pediatric neurosurgery departament betweem january 2002-january 2010 (8 years). admission criteria was: patients diagnosed, treated and fallowed in 1st neurosurgery clinic. results: localisation of acs : sylvian fissure 172 cases(54%), cp angle 38 cases(12%), sellar and suprasellar region 32 cases(10%), pineal area 28 cases(9%), retrocerebelar 28 cases (9%) and interhemisferic 19 cases(6%). the most common clinical finding was the focal bulging of the skull 62% (196 cases), irritability 51%(162 cases), epilepsy 32%(101 cases) minor focal neurological symptoms 18%(57 cases), cranial nerves palsy 11%(35 cases) and increased intracranial pressure syndrome in 13%(41 cases). elected treatment was observation in 40 de cases(12,6%), unishunt cysto-peritoneal drainage 162 cases (51,4%), low pressure valv cysto-peritoneal shunt in 20 cases(6,3%). endoscopic procedure in 31 cases (9,7%) and in 64 cases (20,1%) microsurgucal approach with cystwall excision and fenestration. conclusions: acs are very frequent congenital cerebral malformation, more than 80% of them are incidental findings being completely asymptomatic. treatment is recommended only in romanian neurosurgery (2010) xvii 4: 461 – 508 477 symptomatic acs by focal neurological deficits, skull deformities, signs/symptoms related to increased icp and seizures not responsive to medical treatment. current series of 317 cases constitute a uniform cohort because cases are diagnosed, treated and followed in a single pediatric neurosurgical service. choice of treatment was performed very carefully to obtain the best clinical outcome and to reduce the size of the cyst. keywords: arachnoid cyst, congenital lesion, temporal hypoplasia, gallasi clasification, microsurgical fenestration, cystwall excision, endoscopic approach, stereotaxic suction, cyst shunting, symptomatic cyst increased intracranial pressure. anterior meningo encephaloceles. techniques and results f.x. roux1, p. page1, marie-christine djian² 1department of neurosurgery 2department of neuro anaesthesiology centre hospitalier sainte-anne, paris, france the authors present their experience concerning anterior meningoencephaloceles in children. 80 patients, aged 11 months to 18 years, were treated between 1999 and 2009. 75 were native from cambodia, 5 from africa (congo). the pre operative evaluation was based on clinical data, ct-scan and/or mri. all the operated children presented with a good neurological and cognitive state with an global normal psychomotor development. the authors detail the surgical techniques: 42 patients were operated through a double bifrontal and transfacial approach. most of these procedures were intradural, 38 were operated through a sub fronto orbito nasal approach (sfon) which has the advantage of allowing an epidural and shorter procedure. the few pathological data we obtained confirmed that the removed tissues were made of gliosis without any neurons in the examined samples. the post-operative and long term results are detailed: mortality: 2 cases (2.5%) meningitis: 3 cases, cured by antibiotherapy csf leakage: 4 cases, treated only by lumbar puncture intracranial hypertension due to an arachnoid cyst which was treated by a cysto peritoneal shunt aesthetic results were considered as fine for 77 patients. 3 had to undergo a second procedure for a craniofacial correction. rare cns tumors in children j.c. marchal rare tumors in chilhood are either really rare and specific of children or tumors common in adult but rare in childhood. they are made up of 5 clusters of entities: 1. neuronal, neuronal/glial tumors 2. pleomorphic xanthoastrocytomas 3. meningiomas 4. rare familial syndromes 5. metastasis interestingly, amongst the neuronal, neuronal/glial tumors, gangliocytoma, ganglioglioma, and desmoplastic infantile astrocytomas/gangliomas are quite are but must be recognized because their diagnosis is difficult and can lead to mistakes for 478 abstracts the 7th national congress of rsn tumors the prognosis of which is good provided the surgery is undertaken early. pleomorphic xantho astrocytomas are responsible for 4% of temporal lobe epilepsy, are theoretically benign but have a risk of anaplastic transformation. primitive meningiomas are uncommon in childhood. they have to be separated of the “second tumor” occurring after encephalic radiation therapy. amongst the familial tumor syndromes involving the cns phakomatosis are usual and well known contrary to the li fraumeni, cowden, turcot and gorlin syndromes. finally the cns metastases in children occur rarely and have specific primitive cancer location. the anatomy of the white matter of the telencephalon n. krayenbühl introduction: the fiber dissection technique developed by dr. klingler in the 1930s in basel to study the white matter anatomy of the brain has been revitalized in neurosurgery in the last few years. due to the advances in neuroimaging with the development of the fiber tracking (dti) technique, the white matter fiber tracks can nowadays been visualized and influenced the planning in neurosurgical procedures. material and methods: the different major white matter bundles of the telencephalon were dissected in anatomical specimens from the medial and lateral aspect and put in correlation with dti images. the importance and application of the knowledge of this anatomy in planning surgical procedures is analyzed in some clinical cases. conclusions: with the knowledge of the white matter anatomy gained by the fiber dissection technique the advances in preoperative planning can be applied more effectively. surgery for intractable epilepsy in eloquent areas b. devaux temporal lobe surgery is the most widely used procedure for intractable partial epilepsy – between 60 and 75% of surgical procedures – because of the high frequency of mesial temporal epilepsy as well as excellent outcome, with a seizure relief in 60 to more than 80% of patients. however, in experienced centers, 20 to 25% of patients have their seizures originating from an eloquent area of the brain : sensorimotor region, language areas, occipital and parietal lobes, or insular cortex. in these cases, surgical resection of epileptogenic cortex or lesion is challenging, with a risk of seizures recurrence related to en incomplete resection and a risk of unacceptable postoperative functional deficit. over a 15-years period, 89 patients (20,5% of all epilepsy surgery cases) presenting with focal epilepsy of the sensorimotor region (48), language areas (8), parietal or occipital lobes (25) and insula (8), were operated. preoperative investigations include clinical tests with seizures analysis, video-eeg recordings, high-definition imaging studies, neuropsychological tests and psychiatric assessment. magnetic resonance imaging was normal in 25 cases (28%). 70 patients underwent depth electrode implantation and seizure monitoring (seeg) for improved epileptogenic zone identification and surgical planning. a resection guided with neuronavigation romanian neurosurgery (2010) xvii 4: 461 – 508 479 and cortical/subcortical stimulations was performed in 83 patients and 6 patients underwent multiple stereotactic thermocoagulations. ten patients were reoperated as a consequence of seizure recurrence. neuropathological examination of resected tissue (n=83) revealed an epileptogenic lesion in 73 patients (88%): atrophic scar (11 cases with infantile hemiplegia), focal cortical dysplasia (41), indolent tumors (17), other (4). immediate postoperative deficit or worsening was observed in 61 % of patients, 54% of whom recovered within one week to one month. a minor and moderate to severe functional deficit persisted in 20% and 8% of these patients respectively. with a one-year or more follow-up (mean: 3,6 yrs) in 74 patients, 72% were seizure-free (engel’s class i). multivariate analysis found that seizure outcome was significantly correlated to etiology – seizure-free outcome was observed in 93% of patients with a focal cortical dysplasia, while seizure freedom was observed in 40 % only of patients with cryptogenic epilepsy but no significant correlation with lesion or epileptogenic zone location and seizure outcome was found. surgery in eloquent cerebral areas is feasible and allows for excellent seizure outcome and minimal permanent morbidity in most patients harboring an epileptogenic lesion. functional recovery observed after resection in eloquent regions is related to abnormal organization of functional cortex as well as to mechanisms of functional cortical reorganization. careful preoperative investigations ensure identification of epileptogenic cortex or lesion while adequate surgical tools help identifying functional structures and their preservation. towards a unified theory in brain lesion and recovery d. muresanu the old concept that neuroprotection means suppressing pathophysiological processes, the idea that a single mechanism molecule might be effective in clinical practice are obsolete today, and represents the root cause of failure. the effects of etiological agents on the brain traditionally are conceived as a linear sum of independent pathophysiological processed (excitotoxicity, inflammation, apoptosis-like, oxidative stress, etc) generating the pathways of pathological cascades (ischemic, traumatic, neurodegenerative). the pathway approach has produced a very detailed understanding of molecular changes in the postlesional brain but it possesses blind spots that are critically related to the failure of neuroprotection. this has influenced the simplistic way of understanding the concepts and as well, all attempts at clinical neuroprotection. the idea that a system is a linear sum of its component parts is called “superposition”, and the associated approach is called “reductionism”. the failure of clinical neuroprotection, recovery and modifying disease therapies in many chronic conditions, is measuring the failure of the reductionistic approach to the problem. the pathways can and do interact in a variety of fashions, via cross-talk, positive and negative feedback, etc, but the pathway heuristic itself offers no formal means of understanding such interactions. the expectation of discovering the magic cell 480 abstracts the 7th national congress of rsn death pathway x has affected experimental designs of neuroprotection studies. the causality demonstrated by the application of the plus/minus strategy is ultimately an illusion. to overcome the limits of the pathway view of cell function, a different approach is needed. such an approach is provided by network concepts applied to complex systems. the bistable model based on these assumptions seems to be a better instrument for a successful translational approach in brain lesion and recovery. trigeminal neuralgia management. an unsolved subject j. ciurea, t. cornel, b. balanescu, teodora coman, a. rasina the 5th dept. of functional neurosurgery, clinical emergency hospital” bagdasar arseni” bucuresti, romania introduction: more than 100 related references were published in literature this year according to a most recent pubmed search. from vascular decompression to percutaneous trigeminal ganglion approach including radiofrequency, balloon compression, glycerol injection, even to injection of botulinum toxin a in trigger zone, all those myriade techniques argue for an unsolved standard method. particular problems rise the postherpetic neuralgias and multiple sclerosis secondary trigeminal neuralgia. the published data are on small or relative small groups of patients, many of them retrospective, with a different followup from a center to another. there are only few data on life quality compared pre and postoperative. materials and methods: during the last 14 years, there were hundreds of patients presenting trigeminal neuralgia treated by us. our policy is direct approach of the cause in case of mass lesion evidence. radiofrequency at foramen ovale is usually the first step in essential neuralgia, mostly in old patients, followed by neurovascular decompression. direct hands free foramen ovale approach is the rule. we did not use neuronavigation or ct scan for aiming the target. instead we count on fluoroscopy and neurophysiology. results: our detailed results were presented elsewhere. there were no major complication despite the anatomical challenges for both procedures, radiofrequency and decompression. when compared to others, the results are in range. no suicidal attempt was recorded after surgery. most of gasser radiofrequency patients are discharged after no more than 12 to 24 hrs. postsurgery, the amount of medication is lower but do not cut to null. discussions: those techniques proved time efficient. in other words the effects are immediate. radiofrequency is supraselective when compared to gammaknife, compression and glycerol. not neglectable at all, radiofrequency is less expensive then others. when compared to “open sky vascular decompression”, the risks of radiofrequency are less mainly in cardiac old patients. the abundance of published literature data is mind challenging. it depends on local economical conditions, center size and referral area and last but not least by neurosurgeon training and expertise. conclusions: radiofrequency at foramen ovale lesioning in a first intention technique in most of our patients and a unique indication in old cardiac patients. it can be effective in case of second or even third recurrences. vascular decompression is our romanian neurosurgery (2010) xvii 4: 461 – 508 481 second chronological choice in selected patients. it is obvious that large prospective randomized multi centric studies are necessary for the next future practice standards. neurosurgeons perspective on hrqol following brain damage could we apply qolibr, the tbi assessment tool, for tumour patients? k. von wild objective: today, increasingly more patients will survive even severest brain lesions thanks to modern neurosurgical techniques, neuro-intensive care and early neurosurgical rehabilitation that, however, might be on the price of long lasting impairments of higher cortical functioning with physical, mental cognitive, and behavioral disabilities causing .social restrictions long run. mentalcognitive and behavioural disabilities are more persistent and constitute more of a handicap than do focal neurological signs. physical and mental disabilities combine to produce the social or overall outcome and reintegration. gose and sf 36 assess only the functional impairment and disability. qolibri has been shown to be able to assess the individuals overall outcome by self assessment for the first time. methods: functional impairments after primary, secondary and following brain damage refer to loss of structures and functions. therefore, disabilities refer to limitations of functioning social restrictions. functioning is an umbrella term encompassing all body functions, activities and participation. treatment has to be focused on neuroprotection, brain plasticity, and functional restoration. acute neurosurgical care and neurorehabilitation both will need a multidisciplinary team approach. qolibri for tbi can be assessed by self report. results: qolibri was demonstrated to be the first tbi-specific measure for self assessed hrqol. it provides information about patients’ subjective views of their own lives. it complements traditional measures of disability and recovery (sf 36) by capturing life satisfaction rather than health function while being sensitive to disability and mental health, demographic and socioeconomic factors at the same time. assessment time 15 min (85%). conclusion: obviously the impairment of mental-cognitive and neurobehavioral functioning and not loss of physical skills cause patients’ loss of life transactions and final outcome main predictors for hrqol are depression, help needed, health complaints, anxiety, disability. this might be also true for tumour and vascular lesions pathology and others in neurosurgery. cerebrolysin – important neuroprotection therapeutic factor to improve outcome in sbi a.v. ciurea1, d. muresanu4, eva gheorghita3, g. onose2, f. brehar1, a. spatariu1 1neurosurgical clinic, 2neurorehabilitation department, 3icu clinic hospital “bagdasar – arseni”, medical university „carol davila”, bucharest, românia; 4chairman department of neurology, university of medicine and pharmacy “iuliu hatieganu”, cluj napoca, romania traumatic brain injury (tbi) represent a very important cause of disease in all countries. tbi delimitation was performed by teasdale and jennett (1974), in glasgow 482 abstracts the 7th national congress of rsn coma scale (gcs), important standard in the assessment of these brain lesions: minor (13-15), moderate (12-9), severe (8-3). this standard (“golden”) scale in tbi was established by motor (1-6p.), verbal (1-5p.), eyes (1-4p.) response at external stimulus. for children (0-16 years) in all hospitals was children coma scale (ccs), also quantification 3-15 points. severe brain injuries (gcs 3-8) represent an important cause of mortality and morbidity, especially in patients with active period of live (20-40 years old). material and method: including criteria: the authors studied non selected consecutive 88 patients with sbi (between 6 – 66 years old), 53 male and 35 female in period 2006-2009 (4 years) at the hospital “bagdasar-arseni”, bucharest. the distribution by age was children 30 cases (34,1%) and adults 58 cases (65,9%). the most frequent cause of sbi is represented by the car accidents (car to pedestrian, passenger vehicle) 58 cases (65,9%), followed by falls different higher 23 cases (26,1%) domestic accidents 4 cases (4,5%) and sport traumas 3 cases (3.4%). all intracranial hematomas were operated in the first 6 hours after admission. excluding criteria: all patients in sbi status with multiple traumas with or without intracranial hematomas. all 88 cases were monitoring in intensive care unit (icu). at admission gcs 3-4 was 26 cases (29,5%), gcs 5-6 was 25 cases (28,4%), gcs 7-8 was 37 cases (42%). in all cases the admission ct scan was performed immediately ; the following ct scan was performed at 24, 48, 72 hours and after 1 week to verified the brain lesion and intracranial mass lesion. in 30 cases (34,1%) intracranial mass lesions undergone to the operative procedures: extradural hematoma 14 cases (15,9%), subdural hematoma 10 cases (11,3%), intraparenchimal hematoma 6 cases (6,8%). additional in 10 cases (11,3%) we report penetrated head injury. also, ct scan showed hemorrhagic contusion 23/88 (26,1%) sah in 27/88 cases (30.7%), hypodense (ischemic aria lesion in 25/88 cases (28.4%), cerebral edema 40/88 cases (45.5%) and dai 19/88 cases (21,6%); dai was diagnosis only by mri and the first week post-injury. in our data surgical evacuation of mass lesions was performed as needed, but only five decompression craniotomy was done. in our study no mortality was registered in the group of icp < 20 mmhg, all the 28/88 cases (31.8%) which died had the icp > 20 mmhg. in the literature there are studies which correlate the gos with gcs, metabolic, hematological, radiological and clinical profiles. important predictor’s factors are: patient age, associated pathology and drugs, transport & hospital facilities, multiple trauma, gc scale score at admission, ct scan abnormalities and early neuroprotection & neurorehabilitation. in our experience the cerebrolysin is a significant improvement in sbi. cerebrolysin (mixture of low molecular polypeptide, extracted from pig brain) increase motor function, enhance the cognitive performances, increase memory & attention, improve of brain bioelectrical activity. in all cases, admitted in i.c.u cerebrolisyn –as neuroprotective therapy was early administrated, in the first 24-48 hours. also early neurorehabilitation represent an important therapeuticall factor in global outcome. in our data glasgow outcome scale romanian neurosurgery (2010) xvii 4: 461 – 508 483 (gos): good recovery was in 27 cases (30,68%), moderate disability 13 cases (14,7%), severe disability 22 cases (25%), vegetative state 6 cases (6,8%), death 20 cases (22,7%). at admission gcs 7-8 was preponderent 37 cases (42%) which it was in concordance with the global outcome. the psychological support in all sbi will be necessary to obtain social, familial and professional integration. the control study (22 cases – gcs: 38pct) was realized in the same period; the gos in control study : good recovery was in 5 cases (22,7%), moderate disability 3 cases (13,6%), severe disability 4 cases (18,2%), vegetative state 2 cases (9,1%), death 7 cases (31,8%). the statistical comparative data show strong association between cerebrolysin treatment and global outcome.( chi-square test : p<0,001) conclusions: sbi represent an important medical and neurosurgical problem. many therapeutical factors may improve the outcome in sbi (early neuroprotection, neuroplasticity, neuroregeneration, neurorehabilitation and psychological support). keywords: traumatic brain injury (tbi), gcs, severe brain injury (sbi), dai, icp, neuroprotection, cerebrolysin, neurorehabilitation, outcome, gos. purified brain proteins and amino acids (of porcine origin) in the treatment of traumatic brain injuries st.i. florian1,2, a. blaga2, zorinela andrasoni2, monica scutariu2 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca 2cluj county emergency hospital, department of neurosurgery aims: to assess the benefits of cerebrolysin treatment for traumatic brain injuries. material and methods: this is a retrospective study conducted over a period of 5 years. between the 1st of january 2004 and the 31st of december 2008 1279 patients were admitted in our department with close traumatic brain injuries (with no politrauma). for these patients, 14 parameters were recorded: age, sex, gcs (motor, eyes and verbal response), mechanism of injury, symptoms, brain injuries as seen on cerebral ct scan, days of hospitalization, first day of infusion, ml. per day and the outcome at the 10th and the 30th day. the outcome was appreciated using two scales: the rankin scale and the glasgow outcome scale (where 1 means good recovery and 5 is death). cerebrolysin is a mixture of lowmolecular-weight peptides and amino-acids derived from pigs’ brain tissue with neuroprotective and neurotrophic properties. the primary indication is for neurological degenerative diseases therapy but it is also used for neural regeneration after traumatic brain injuries. from these 1279 patients, 184 received perfusion cerebrolysin. the daily dose of cerebrolysin was 20 to 30 ml. and the period of time ranged from 5 to 30 days of treatment, during their admission in our department or after. the outcome was compared in terms of statistical significance between the patients, who received cerebrolysin and those who did not received. for statistics we used epi info 3.5.1(www.cdc.gov). results: in the group of patients who did not received cerebrolysin (with an average gcs at admission time of 11.463) the 484 abstracts the 7th national congress of rsn average gos at day 30 was 1.826 while in the cerebrolysin patients’ group (average gcs at admission 10) the outcome average was 1.641. in terms of rankin outcome scale the average values were 1.512, respectively 1.434 for the patients who received cerebrolysin. conclusions: cerebrolysin can be a useful adjuvant drug in the treatment of traumatic brain injuries. minimal invasive approaches of dorsal spinal canal lesions ventral-located: usefulness of 3d fluoroscopy g. gambardella, o. gervasio, c. pecora, a. fede lesions in the ventral dorsal spine present considerable difficulties in the surgical treatment for anatomical imperviousness of the access routes. since about ten years we’re using a minimally invasive approach with microsurgical technique, as described in our previous work. to date we have used that technique for treatment of 15 meningiomas, 4 neurinomas, 2 small metastases and 6 disc herniations, with better surgical outcome. we therefore support a review of the literature and illustrate the advantages of fluoroscopy with 3d reconstructions on the timing and complexity of surgical procedure, using a ziehm vision vario 3d and a radiolucent operating table, that provide a valuable aid in positioning the fixation and in anatomical planes dissection, much to increase safety and decrease intraoperative risk to the patient. decision making in cervical spine metastases e. popescu, b. costachescu nearly 10% of spinal metastases arise in the cervical region. breast, lung and prostate cancers are the most common primary tumors that spread to the spine. the early diagnosis and treatment of metastatic spine tumors is essential to reducing pain, preserving neurologic function, and improving quality of life. during a 5-year period (2002-2006) we treated a number of 22 patients with metastatic cervical spine tumors. general principles of treatmet and results are presented in this paper. the thoracic-lumbar burst fracture – posterior-lateral approach with vertebroplasty “eggshell” d. serban, fl. exergian and collaborators department of spine surgery of “bagdasar-arseni” clincal hospital of urgency bucharest burst fracture is a complex lesion of vertebral column, and the frequency at the level thoracic-lumbar is high. despite the biomechanical concept that we use, 2 or 3 columns (holdsworth or dennis concept), it is difficult to categorize this lesion, and in consequence to apply a treatment that can address to all pathological aspects of this kind of fracture (anterior and posterior column). with the years the collective of the department of spine surgery of clinical hospital of urgency “bagdasar-arseni” bucharest, has perfected the technique for approaching the burst fracture, reaching at the present form. the technique is a modified posterior-lateral approach, that succeeds to rebuild the fractured vertebral body by a vertebroplasty with poliacrilic cement named “eggshell” with correction of the spine angulation’s, to decompress the neurological elements of spine by direct romanian neurosurgery (2010) xvii 4: 461 – 508 485 visual control, to resolve the lesions of fractured neural arch and to assure the reaxetion of spine by short posterior osteosinthesis. aims of study: to make knowable the technique and to evaluate, clinic and imagistic, the results obtained with this new approach. materials and metods: we have collected the dates from the casuistic of the department of spine surgery of clinical hospital of urgency “bagdasar-arseni” bucharest on the period july 2009, the beginning implantation’s of the technique, until july 2010. pre and postoperator, at 6 days and 2 months, it was measured the neurological deficit with the asia scale, the degrade angulation’s on simple radiographies, compression’s on vertebral rmn and reconstruction’s of vertebral body on ct. results: in study was included 37 patients with the burst fractures at the levels t11-l2 of spine. preoperator all patients have presented neurological deficit ranged from frankel b to frankel d, the grade of compression was greater then 30% of anterior-posterior diameter of vertebral canal and that of angulation’s greater then 200. postoperator all patients were mobilized rapidly and have improved the neurological deficit at 2 months, the correction of angulation’s was realized significantly to all patients and was maintained at 2 months. conclusions: the technique has proved to be a reliable one, permitting rapidly mobilization of patients, with the favorable results at 2 months to regain the neurological state and anatomicphysiologic, close to normal, status of a functional spine. in the future is necessary to evaluate the efficiency of the technique for a greater follow-up period of time and to compare with others techniques used to approach burst fracture. chronic cervical spinal cord injury and bone marrow tissue implant st.m. iencean1, gh. solcan2, a.st. iencean1 1neurosurgery, emergency hospital “n. oblu” iasi 2faculty of veterinary medicine, university of agricultural sciences and veterinary medicine iasi, romania spinal cord injury (sci) is a major medical problem worldwide. spinal cord injuries can lead to paraplegia or quadriplegia and have devastating consequences for victims, families, and society in general. although there are no fully restorative treatments for spinal cord injury, various rehabilitative and cellular therapies have been tested in animal models. stem cells are feasible candidates for cell therapy of spinal cord injury. bone marrow cells are the subject of extensive interest because of their stem cell like characteristics and pluripotency. there are more data supporting the beneficial effects of bone marrow cells in sci: bone marrow contains multipotent adult progenitor cells; bone marrow cell transplants improve function recovery and differentiate into neural presursors in animal experiments and bone marrow cell transplants facilitate remyelination of the spinal cord. we present the experience of two patients with traumatic chronic cervical spinal cord injuries with quadriplegia and the results of the microsurgical resection of the spinal scar and the implant of bonemarrow tissue in the site of the spinal cord lesion. each patient underwent a cervical laminectomy to expose the site of the 486 abstracts the 7th national congress of rsn cervical spinal cord injury and a microsurgical partial resection of the medular scar and implant of autologous bone marrow tissue with a combination of drugs at the site of spinal cord injury. no postsurgery complications occurred. sensory improvements were noticed, but no significant motor improvements were observed twenty months afterwards. this is a preliminary study of the autologous bone marrow tissue implant into the lesioned cervical spinal cord.the bone-marrow tissue transplantation procedure has no complications. the post injury scar’s microsurgical partial removement may make the injury site more permeable to the axons attempting to regrow through. this result is promising, but much follow-up work is needed to document the long-term benefits. current stage of cell stem implant into traumatic spinal cord scar st.m. iencean1, i. poeata2, a.st. iencean1 1neurosurgery, emergency hospital “n oblu” iasi 2neurosurgery, faculty of medicine, “gr.t. popa” university of medicine and pharmacy iasi, romania spinal cord injury can lead to paraplegia or quadriplegia. spinal cord injury is heterogeneous and can result from contusion, compression, penetration or maceration of the spinal cord. spinal cord injury culminates in glial scarring, a multifactorial process that involves reactive astrocytes, glial progenitors, microglia and macrophages, fibroblasts and schwann cells.the scar is often oriented perpendicular to the neuraxis and appears impenetrable. the scar of the spinal cord can be: a complete and impenetrable glial scar on the site of spinal cord injury, an incomplete scar and a posttraumatic syringomyelia or cysts on the site of sci a filiform connective scar of the two segments of damaged spinal cord. the inability to repair spinal cord damage is attributed to several factors: the presence of inhibitory substances around the lesion , the adult nerve fibres become unable to respond to growth-inducing signals, the formation of cysts at the injury site, the lack of nerve growth factors at the injury site and the formation of scar tissue. three therapeutic concepts are currently being envisaged: transplantation of differentiated cells derived from stem cells; direct administration of stem cells to the patient in such a way that they would colonise the correct site of the body; stimulation of endogenous stem cells. cellular transplantation after spinal cord injury has several aims: to bridge any scar, cysts or cavities, to replace dead cells and to create a favourable environment for axon regeneration. a variety of adult stem cells have been implanted in animal models of spinal cord injury: olfactory ensheathing cells, bone marrow derived stem cells, cultured spinal cord stem cells etc. an efficient treatment in spinal cord lesions must combine more main approaches: neuroprotection, removing barriers: after the injury the scar tissue gradually fills the damaged area and it is an impenetrable barrier and it does not allow regenerating nerve fibres to pass through, blocking factors which inhibit neural regeneration, modulation of inflammatory response following spinal cord injury, preventing inhibition of regrowth, tissue engineering: biocompatible materials can form a bridge across the romanian neurosurgery (2010) xvii 4: 461 – 508 487 damaged region, stimulating and guiding neurotrophic factors, replacing damaged cells stem cells therapy correctly reconnect the damaged neural circuits inside and outside the spinal cord a combination of stem cells therapy with neurotrophins is a novel aspect of treatment in spinal cord injury and it will attenuate the neurological damage and could help restore the normal function of spinal cord. the surgical management of gliomas located in functionnally eloquent brain areas j.m. derlon, b. drouler, e. olivier chu (university hospital), caen, france introduction: the prognosis of gliomas, either of low or high grades, is improved when a complete or large surgical resection has been performed as a 1st therapeutic step. however, many gliomas – and especially those of grades ii or iii – are located close to eloquent brain areas, involved in sensory-motor or language functions. in order to remove them with a low risk of post-operative neurological deficit, 3 important conditions must be fulfilled: an accurate pre operative neuro imaging assessment, with anatomical and functional imaging; a good neuronavigation system; and an intra operative electrophysiological management in order to localize functional eloquent areas, and subcortical tracts. material and methods: since 1996, we have investigated then operated patients, most of them having gliomas grade who ii or iii, located in or close to eloquent areas, in the following way: a full anatomical mri, functional mri in all cases of glioma close to language areas, and a few of those close to motor areas, and orthophonic and neuropsychological assessment when necessary. anaesthesia depended about the functional area which was threatened : general anaesthesia was allowed for monitoring the motor function, but should be performed without curare ; but local anaesthesia is imperative for monitoring the language function, when functional mri has shown activation close to the tumor. the main intra operative complication of the stimulation was the occurrence of seizures, a risk which may be lowered by using a monopolar instead of a bipolar stimulating electrode, in the case of motor monitoring, and controlled by irrigating the cortex with iced serum. results: this management allowed large or subtotal tumour removal in about 80% of the patients, with a low rate of permanent neurological disorder, and long survival without recurrence. conclusion: when a glioma is located in or close to a cortical eloquent brain area, it should not be considered as a candidate for only needle biopsy, but carefully investigated and managed for a large removal. 488 abstracts the 7th national congress of rsn prognostic genetic markers in malignant gliomas r. ketter1, wemmert silke2, w.i. steudel1, urbschat steffi1 1department of neurosurgery, 2department of otolaryngology, saarland university, homburg/ saar, germany glioblastomas are the most frequent and malignant brain tumors in adults. surgical cure is virtually impossible and despite of radiation and chemotherapy the clinical course is very poor. epigenetic silencing of mgmt has been associated with a better response to temozolomide-chemotherapy. we previously showed that temozolomide increases the median survival time of patients with tumors harbouring deletions on 9p within the region for p15(ink4b), p16(ink4a), and 10q (mgmt). the aim of this study was to investigate the methylation status of p15, p16, 14arf and mgmt in glioblastomas and to correlate the results with the clinical data. only patients with kps > 70, radical tumor resection, radiation and temozolomide-chemotherapy after recurrence were included. we observed promoter methylation of mgmt in 56% (15/27) and of p15 in 37% (10/27) of the tumors, whereas methylation of p16 and p14arf were rare. interestingly, methylation of p15 emerged as a significant predictor of shorter overall survival (16.9 vs. 23.8 months, p=0.025), whereas mgmt promoter methylation had no significant effect on median overall survival under this treatment regimen (22.5 vs. 22.1 months, p=0.49). in the presence of other clinically relevant factors, p15 methylation remains the only significant predictor (p=0.021; cox regression). although these results need to be confirmed in larger series and under different treatment conditions, our retrospective study shows clear evidence that p15 methylation can act as an additional prognostic factor for survival and underlines that this tumor suppressor, involved in cell cycle control, can act as an attractive candidate for therapeutic approaches in glioblastomas. the role of intraoperative cerebral echography v. pasca1, andreea mogyoros1, st.i. florian1,2 1clinical of neurosurgery cluj-napoca 2university of medicine “iuliu hatieganu’' cluj-napoca objective: the intraoperative cerebral ultrasonography can be used to localize brain lesions, their relationships with the surrounding neurovascular structures, the grade of vascularization, the extent of the surgical resection and the existence of any possible postsurgical complications. materials and methods: in our study we used a siemens sonoline sienna 3.5 mhz (sectorial transducer)/5 mhz (liniar transducer), pulsed and color doppler ultrasound in b–mode to evaluate 30 patients diagnosed with different brain tumors. there were 17 males and 13 females with various supratentorial lesions (meningiomas, astrocytomas, glioblastomas, metastasis, vascular malformations, dermoid cyst, lymphomas, tuberous sclerosis, intracerebral hemorrhage and cerebral ischemia). analysing the echographic images we were able to detect the tumor site, to see its echogenicity and to control the margins of resection. results: with intraoperative cerebral sonography we were able to identify and romanian neurosurgery (2010) xvii 4: 461 – 508 489 localize the brain tumors, to assess the blood supply of the lesion and the relations with the nearby anatomy and to verify the extent of tumor removal. conclusions: the real-time intraoperative cerebral ultrasound is a complementary examination and brings important information that can enhance the surgical outcome. induction of differentiation inhibits the tumorigenic potential of glioblastoma cancer stem cells f.m. brehar, a.v. ciurea, r.m. gorgan, a. tascu, coralia bleotu, otilia zarnescu clinical hospital “bagdasar-arseni”, bucharest aims: isolation and characterization of cancer stem cells (cscs) from human glioblastoma opened new perspectives in primary brain tumors research and offered an alternative experimentally approach for this severe disease. the authors of this study successfully inhibited the tumorigenic potential of cscs isolated from glioblastoma samples, using a combination of differentiation induction factors. material and methods: tumors from patients with confirmed glioblastoma multiforme (gbm) were mechanically and enzymatically dissociated and grown in neural stem cell expansion medium to generate neurospheres (dmem supplemented with 10-20ng/ml fgf; 10-20 ng /ml egf; 1x b27; 1xn2). the in vivo tumorigenic potential of glioblastoma cell cultures (neurospheres) was assessed by intracranial injection of glioblastomaderived csc into the right striatum of cd1 nude mice. then, induction differentiation factors like bdnf, nt-3 and transretinoic acid have been added in cscs cultures. the changes in stem cell markers, matrixmetalloproteases, cadherins and notch patway expression have been assessed. cscs exposed to the differentiation factors have been inoculated in nude mice and their tumorigenic potential has been evaluated. results: some of the initiated cultures formed the free-floating structures generated by these cells in vitro, the “neurospheres”, considered to be a characteristic feature of tumor neural stem cell, which were morphologically and functionally heterogeneous. the authors of this study successfully developed tumor xenografts in nude mice using these primary cultures. the using of serum-free culture for selection (neurosphere assay) allowed the selection of cscs containing subpopulation that were able to reproduce original tumour aspect in orthotropic xenografts. the expression of genes regulating neurogenesis on notch pathway (dll1, dtx1, heyl, jag1, neurl, notch2, pax5) were increased from 1.5 to 6 times. the stemness biological feature was correlated with increased of same metalloproteases, cadherins, catenin and with tumour contra-lateral invasion. the expression of stem cells markers, metalloproteases and cadherins decreased after exposure of the cscs cultures to the differentiation induction factors. in vivo experiments demonstrated also the inhibition of tumorigenic potential of cscs cultures exposed to the differentiation factors. conclusions: serum-free culture allowed the selection of a subpopulation containing cscs with increased tumorigenic potential. cscs cultures showed a decrease in the expression of stem cells markers and lost their tumorigenic potential, when they were exposed to a specific combination of differentiation induction factors. 490 abstracts the 7th national congress of rsn malignant transformation of low grade gliomas into glioblastoma a series of 10 cases d. rotariu, s. gaivas, z. faiyad, d. haba, b.iliescu, i. poeata low-grade gliomas of the central nervous system constitute 15 to 35% of primary brain tumors. although this category of tumors encompasses a number of different well-characterized entities, lowgrade tumors constitute every tumor not obviously malignant at initial diagnosis. we present a series of 10 cases of low grade astrocytomas, confirmed by hystological exam, operated between 2006 and 2009 wich have suffered malignant transformation into glioblastomas during postop surveillance. the average time of transformation from low grade glioma to high grade glioma was 37,5 months. in patients with subtotal resection the average time to malignisation was 26 months while in patients with total resection was 41,3 months. in our series 3 patients have no adjuvant therapy in 5 patients surgery was followed by rxt and 2 have made both rxt and cht. in those with no adjuvant therpy the free symptom period was 29,3 months and in those in wich surgery was followed by adjuvant therapy the free symptom period was 38.5 months. conclusions: in our series the complete resection and the adjuvant rxt and cht in the treatment of low grade gliomas has delayed the time to malignisation. the series is to short to have statistical significance in this controversial subject in the literature. some interesting cases together with our surveillance protocol in glioma are presented. electrophysiological mapping using background multi-unit activity and local field potentials for targeting subthalamic nucleus a. barborica1, j. ciurea2, a. rasina2, c. tancu2, b. balanescu2 1fhc inc, bowdoin me, usa 2bagdasar-arseni hospital, bucharest, romania aim: to investigate the use of background neuronal activity as a method to improve the accuracy of the target localization for the implantation of deep brain stimulation (dbs) electrodes in the treatment of parkinson disease. material and methods: between january 2009 and january 2010, fifteen patients with advanced parkinson disease underwent bilateral implantation of dbs electrodes in the subthalamic nucleus (stn) under local anesthesia. anatomical direct targeting was refined based on electrophysiological functional mapping, using a fhc guideline 4000 microrecording system. the functional mapping included recording neuronal activity using microelectrodes and performing electrical stimulation. on targeting 12 out of 30 stn, short 2-second segments of data were recorded periodically along the entire electrode trajectory on three simultaneous tracks (typically). neuronal activity in the frequency band 500 to 6000hz was recorded, then separated into single and multi-unit activity (mua) using an unsupervised wavelet thresholding algorithm. on the initial trajectory, we also simultaneously recorded lfp’s in the band 0.5 to 100hz. results: the mua power showed a significant enhancement in the target region compared to the baseline with a factor of 3.07±1.47 (mann-whitney u-test p the mean improvement of patients according to romanian neurosurgery (2010) xvii 4: 461 – 508 491 the updrs scale (iii section) was 65% at 6 months follow-up. conclusions: background multi-unit neuronal activity recording can be used as a method to refine the anatomical targeting of the stn in patients with parkinson disease. partial tibial neurotomy as combined neurosurgical treatment in residual spastic foot in children a. rasina1, b. balanescu2, c. tancu1, teodora coman1, j. ciurea1 1the 5th dept. of functional neurosurgery, clinical emergency hospital” bagdasar arseni” bucuresti, romania 2umf “ carol davila” introduction: tibial neurotomy is indicated for the treatment of spastic varus plantar flexion (equinus deformity) with or without claw toes. it consists in partial sectioning of one or several motor branches (considered responsive for spasticity and identified by electrical stimulation) after their entire exposing at the popliteal fossa and the nerve epineurium opening (i.e. the nerve fascicles to gastrocnemius and soleus, tibialis posterioris, popliteus, flexor hallucis longus and flexor digitorum longus). aim: to prove the clinical and functional benefits of tibial neurotomy after other surgical procedures performed, even neurosurgical, but especially orthopedic in our country circumstances where traditionally is first considered. method: a total of 18 cases with secondary partial tibial neurotomy after other surgical procedures (2 cases of intratecal baclofen pump, 4 cases of dorsal rhizotomy and 12 cases of achile tendon surgery), all cases in the ambulatory children with equinovarus secondary of the cerebral palsy, between 8 and 16 years old, when the gait is mature. the clinical examination includes observation of posture and gait, assessment of passive range of motion, quantification of the degree of spasticity using ashworth and tardieu scales. we used the test by tibial nerve block using local anaesthetics, such as long-lasting bupivacaine which mimiked the outcome of selective neurotomy, in according with the recording of the ankle angle amplitude by goniometry. motion analysis using an optoelectronic system is coupled with the evaluation by electrophysiological h reflex recordings. this studies prove the motion pattern modifications during all phases of gait (early-, midand latestance, swing) with resulting instability of the whole body. conclusions: this surgical procedure cannot be performed in isolation but it must be integrated into a long-term rehabilitation programme that is acceptable for the patient over time. the place of neurosurgery in the treatment of spasticity continues to be studied and refined. when combined with orthopedic and medical approaches, and when the properly selected neurosurgical approach is combined with the properly selected patient, it may offer important advantages to people with spasticity attempting to optimize their function in the community and their activities of daily living. the cases presented demonstrates the good surgical indication of the combined selective tibial neurotomy in residual foot spasticity after other treatments, even surgical. 492 abstracts the 7th national congress of rsn ent and neurosurgical combined approach of extended skull base tumours intraoperative neuromonitoring role teodora coman1, r. c. popescu2, c. tancu1, b. balanescu3, a. rasina1, j. ciurea1 1the 5th dept. of functional neurosurgery, clinical emergency hospital” bagdasar arseni” bucuresti, românia; 2ent dept. coltea hospital 3umf “ carol davila” aim: the challenging large skull base tumours extended upwards and downwards can benefit of multidisciplinary team approach including neurosurgeon, ent surgeon and neurophysiologist. this is justified by large safe resection and less cranial nerve dysfunction. patients and methods: a total of three patients will be presented as examples. a 70 years old lady presenting a right sphenoid wing meningioma with an eight years postoperative invasion in orbit and maxillary invasion was successfully solved in a three steps surgery.another 50 years lady presenting a right spheno-orbital osteomeningioma underwent surgery via frontotemporal approach followed by a total tumour resection. a 57 yrs. old patient presenting a large glomus jugulare tumour was operated through a retro and trans mastoidian approach. the most frequently monitored motor nerves were facial and trigeminal nerve. auditive and visual evoked potentials were used in certain situations. results: a total tumour removal was performed in all cases. intraoperative monitoring allows a degree of surgical comfort by providing immediate information regarding the status of the nerves or central pathways. the amplitudes of emg recordings was maintained in the physiological range referred to baseline. the latency of evoked potentials was monitored in order not to exceed 1 ms. there were no supplementary postoperative cranial nerves deficits. conclusion: the multidisciplinary approach associated with neuromonitoring allowed a proper surgical management of extensive head lesions as revealed by our cases and literature. pituitary tumor apoplexy – surgical management and prognosis ligia tataranu1, v. ciubotaru1, m. gorgan1, eva gheorghita2, d. paunescu2 the 5th dept. of functional neurosurgery, clinical emergency hospital” bagdasar arseni” bucuresti, romania 1ent dept. coltea hospital 2umf “ carol davila” objective: the most urgent indication for surgery in pituitary adenomas relates to instances of pituitary tumor apoplexy, caused by ischemic necrosis or sudden hemorrhage into a preexisting sellar mass, followed by expansion of sellar contents. the authors review the current standard of management in pituitary apoplexy and present their personal experience. material and methods: the authors analyze a group of 28 patients with symptomatic pituitary tumor apoplexy, who presented to emergency clinical hospital “bagdasar – arseni” bucharest between january 2008 and december 2009. patients were followed for up 2 years (range = 4 months – 2 years). the retrospective study identifies 16 male and 12 female patients with pituitary apoplexy (mean age = 53.3 years, range = 28 – 80). only 6 (21.4 %) patients had previously known pituitary tumors. romanian neurosurgery (2010) xvii 4: 461 – 508 493 results: headache (92.9 %) was the most common presenting symptom, followed by nausea (78.6 %) and visual dysfunctions (reduced visual acuity – 57.1 %, visual field defect – 75.0 % and oculomotor palsy – 14.3 %). ct and mri were used for anatomical evaluation preoperatively and postoperatively. 22 (78.6 %) patients had partial or pan-hypopituitarism at presentation. 18 (64.3 %) patients had nonfunctioning adenoma, 2 (7.1 %) had prolactinoma, 7 (25.0 %) had somatotroph adenoma and 1 (3.6 %) had corticotroph adenoma. an urgent neurosurgical decompression via a transsphenoidal approach was performed in all cases. improvement in visual acuity occurred in 92.9 % of patients operated on within the first week, but only in 46.4 % of patients operated on with a greater delay. none of the 22 patients with hypopituitarism had a full endocrine recovery. steroid replacement during the acute stage was necessary. long-term hormone replacement was necessary in some cases (steroid hormone – 60.7 %, thyroid hormone – 42.9 %, testosterone – 25.0 %, desmopressin – 7.1 %). conclusions: the authors advocate urgent transsphenoidal surgical decompression for all patients with pituitary apoplexy, to save life and improve vision and to have a chance at regaining pituitary function. early surgery, within the first week, leads to a better visual outcome when compared with later surgery. still, oculomotor palsies improve even if surgery is delayed. current management of pineal region lesions – an analysis of a personal series of 34 cases. the third’s neurosurgical department of nicolae oblu hospital experience in tumors of the third’s ventricle i. poeata, c. apetrei, b. iliescu tumors of the third ventricle are rare, representing less then 1% of intracranial lesions. even though most of them are benign, the management of these lesions is difficult. to make the difference between an incidental inoffensive lesion and a lesion with possible life-threatening complication sudden death caused by acute hydrocephalus -, is some time difficult. symptoms occur usually in adults, with episodes of headache, weakness of the limbs, and loss of consciousness. mri is the imagistic method of choice. we present our experience in the neurosurgical management of these lesions in the last five years: 2006 – 2010. 24 patients with third ventricle lesions were admitted and 14 of them underwent surgical treatment. we preferred the interhemispheric transcalosal approach for most of the lesions with other approaches chosen for the rest. the remaining cases were considered incidental inoffensive lesions in which we decided imagistic follow up. the histology of the tumors was: colloid cysts (6), astrocytoma (3), craniopharyngioma (2), pinealoblastoma (1), glioblasoma (1), meningioma (1). patients with third ventricle tumors are at risk for developing impairments in memory, executive function, and fine manual speed and dexterity, which are domains associated with frontal subcortical functions. 494 abstracts the 7th national congress of rsn current management of pineal region lesions – an analysis of a personal series of 34 cases i. poeata, c. apetrei, b. iliescu pineal region tumors comprise of heterogeneous group of neoplasms with different histological origin growing from the pineal gland itself or from structures adjacent to the pineal region. these tumors are rare and account for 0.4 to 1.0% of intracranial tumors in adults. the treatment options for the different pineal region tumors vary according to their histological nature. however, with the exception of germinomas which can be nowadays cured by low-dose radiotherapy and chemotherapy and only require a biopsy for diagnosis, surgery still plays a central role in the management of most of the other pineal region tumors followed or not by adjuvant radiotherapy, chemotherapy or a combination of both. we follow the therapeutic options in our series of 34 pineal lesions series, including the cases with symptomatic pineal cysts. the most common clinical syndromes included: paroxysmal headache with gaze paresis; chronic headache, gaze paresis, papilledema, and hydrocephalus, or pineal apoplexy with acute hydrocephalus. surgical intervention was performed in 11 cases, the goal being complete tumor removal. complete tumor removal is desirable; however, subtotal resection is preferable if the tumor cannot be easily separated from the quadrigeminal plate. the remnant tumoral tissue can be considered for adjuvant radio or chemotherapy. ventricular shunting should be reserved for patients with persistent hydrocephalus after cyst resection. supratentorial ventricular tumors a surgical perspective st. i. forian2, c. abrudan1,2, a. oslobanu1,2, zorinela andrasoni2, m. danciut2 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca 2cluj county emergency hospital, department of neurosurgery aims: brain tumors located in the ventricles represent 1,4% from all primary central nervous system tumors. from a surgical point of view, the profound location and the necessity to intersect normal brain tissue with minimal functional alteration, the abundant vascularisation which interfere with normal vasculature, and also large dimensions of tumors, altogether represent problems that must be solved by neurosurgeon. this study consists in a retrospective analysis of 61 cases of intraventricular supratentorial tumors diagnosed and operated in an 12 years period. material and methods: we retrospectively present the indications, results, outcome and specific characteristics of 61 patients diagnosed with intraventricular supratentorial tumors . results: supratentorial intraventricular tumors represent 2,54 % out of 2398 intracranial tumors operated by author between january 1998 and september 2010. our peak incidence is in the first and sixth decades of life. in a surgical perspective, our strategy is: tumors located in the lateral ventricle are approached by a transcortical route; tumors located in the third ventricle are approached transcallosal or subfrontal trans-laminaterminalis if there is an intraventricular extension from a sellar tumor. vp-shunt is reserved only for cases of romanian neurosurgery (2010) xvii 4: 461 – 508 495 persistence of symptomatic hydrocephalus after tumor removal, or in cases in which the direct approach was refused or considered too dangerous related to the clinical status of the patient. temporary external ventricular drainage (first 4 to 5 postoperative days) is largely used after transcallosal or transcortical approach. considering this we used the transcalosal approach in 57% of the cases, in 28.2% a transcortical approach was performed, in 9.8% of the cases a subfrontal translamina terminalis approach was chosen and in 5% a neuroendoscopic approach was performed. in 86 % of the cases, we managed to obtain total removal. recurrences occurred in 11% of the cases. pathological examination revealed a variety of findings: 21.3% astrocitomas, 13.1% malignant gliomas, 11.5% ependimomas, 16.4 % craniopharingyomas, 4,9% choloid cysts, 13.1 % meningiomas and 19.7% neurocytomas, metastases, choroid plex papilomas, gangliolgliomas and pituitary adenomas. postoperative complications consisted in persistent symptomatic hydrocephalus (6 cases), intraventricular bleeding and/or edema in other four cases. the surgical results were very good and good (gos 5 and 4) in 48 cases, 11 cases with moderate disability (gos 3) and 2 cases died (one case with multiple metastases and one case with pulmonary embolism). conclusions: complete neuroimagistic evaluation, a proper surgical approach, progressive debulking of tumor with great attention to preserve normal vasculature, external ventricular drainage in order to prevent acute hydrocephalus are the key points for good surgical results. keywords: intraventricular supratentorial tumors, transcortical approach, transcallosal approach, hydrocephalus. temozolomide-loaded gold nanoparticles as an alternative chemotherapy option for inoperable recurrent malignant gliomas c. tomuleasa, anamaria orza, olga soritau, g. kacso, adriana cocis, h. ioani, m. diudea, al.s. biris, st.i. florian iuliu hatieganu university of medicine and pharmacy from cluj napoca ion chiricuta oncology institute from cluj napoca faculty of chemistry and chemical engineering, babesbolyai university, cluj-napoca applied science department, arkansas nanotechnology center, united states of america high grade malignant gliomas are considered today to be incurable diseases despite neurosurgical intervention followed by adjuvant chemo radiotherapy. this because of a small population of stem-like cells that allow the tumor to acquire resistance to conventional therapy and invade the surrounding nervous tissue. the aim of the current study was to evaluate in vitro the antitumor efficacy of temozolomide-loaded gold nanoparticles (gnps) in hope to provide a new approach to treat brain cancer with minimal toxicity and an increased efficacy profile. gnps stabilized with a monolayer of poly(l-aspartate-cytostatic drug) was synthesized as a tumor targeted drug delivery carrier. the drug (temozolomide, bevacizumab) was covalently conjugated onto the hydrophobic inner shell by acidcleavable hydrazone linkage. the aupoly(l-aspartate-drug) gnps formed stable unimolecular micelles in aqueous solution. transmission electron microscopy, uv-vis spectroscopy and nuclear magnetic resonance analysis were employed to characterize the morphological, optical and structural properties of these metallic 496 abstracts the 7th national congress of rsn nanostructures. the chemical structures formed by gnps and cytostatics were then added in culture, testing the sensitivity of glioma-derived cancer stem cells. gnps facilitated the activity of the alkylating drug to reverse the resistance of cancer stem cells to temozolomide, offering a new chemotherapy strategy for patients diagnosed with unresectable recurrent malignant gliomas. as intrinsec and acquired resistance to chemotherapeutic drugs is a major obstacle in the clinical treatment of recurrent glioblastoma multiforme and the complete mechanisms for multidrug resistance remain unclear, the development of alternative therapeutic strategies may contribute to a better approach of this lethal disease. arsenic trioxide sensitizes brain cancer stem cells to chemoradiationa differentiation therapy model for glioblastoma c. tomuleasa, olga soritau, g. kacso, eva fischer-fodor, adriana cocis, h. ioani, magda petrescu, dana cernea, st. i. florian iuliu hatieganu university of medicine and pharmacy, cluj napoca, romania glioblastoma multiforme still has a very dismal prognosis despite complete resection followed by adjuvant chemoradiation. the aim of the current study was to evaluate in vitro the antitumour efficacy of arsenic trioxide in combination with ionizing radiation plus temozolomide and bevacizumab against glioblastoma cultured stem like cells, as possible way to increase the therapeutic index. material and methods: stem-like tumor cells isolated from a glioblastoma multiforme biopsy were established by cell proliferation assays and up-regulation of stem cell markers, as proven by reverse transcription – polymerase chain reaction. low concentrations of arsenic trioxide were added prior to temozolomide, bevacizumab and ionizing irradiation. results: molecular analysis show that cells express cxcr4, oct-3/4 and gapdh when compared to placental mesenchymal stem cells, as well as nestin, gfap and neurofillament protein. low concentrations of arsenic trioxide lead to morphologic differentiation,with fewer stem cells in go state and differentiation-associated cytochemical features, like increased sensitivity to cytostatic drugs and radiotherapy. conclusion: arsenic trioxide exposure before conventional postoperative chemoradiotherapy for glioblastoma might increase treatment efficacy. further in vivo experiments on laboratory animals and analysis of absorbtion rate and side effects are required. the role of intraoperative cerebral echography fronto temporal approach in sellar and parasellar meningiomas g. mild, d.tusnea, i.st. florian although the most of the meningiomas are histologically benign tumors, in the case of sellar are parasellar localization, because of the difficulty to approach them, they where considered quasi malign. there was a period in the neurosurgery, when the surgeons strived for large bone resections, but achieved still incomplete excisions. the aim of this paper is to demonstrate, that even in the absence of high technology, but with vast experience, well aimed romanian neurosurgery (2010) xvii 4: 461 – 508 497 approaches, and with delicate maneuvers in most of the cases it is possible to perform smaller bone resections and total macroscopic excisions. material and methods: a retrospective analysis was performed on data obtained in 134 consecutive patients with sellar and parasellar meningiomas who underwent resection between january 1998 and june 2010, from a total of 549 surgical interventions for intracranial meningiomas (498 new cases, the rest of the operations being made for recurrences or for multiple meningiomas) results: we recorded a female predominance, with an pick incidence in the fifth decade. in the medial group of paraclinoid meningiomas (tubercullum sellae, sellar diaphragm, clinoidal and spheno-cavernous meningiomas) we recorded 69 cases, mean while in the lateral group (sphenoid wing) we encounter 65 cases. the grade of removal was as it follows: simson i79 cases (59%), simson ii-42 cases (31%), simson iii7 cases (5,5%), simson iv -6 cases (4,5%) . concerning the pathology the most frequent types were transitional, meningothelial and fibroblastic. in the entire series we noted some local postoperative complications: hematomas , wound infections, cerebral edema, csf fistula; and also some neurological complications: transient motor deficit, visual worsening, oculomotor palsies, transient diabetes insipidus, cerebral infarction, hydrocephalus. the mortality rate for the entire series was 1% (1 case). conclusion: most paraclinoidal meningiomas can be removed completely and safely. the most used surgical approach is the standard fronto-temporal approach. in our opinion there is no reason for large bone removal except for cases invading the cavernous sinus and optic canal. when complete tumor removal is not advisable for whatever reason, the strategy of a subtotal tumor removal followed by radiation therapy can be used. keywords: parasellar meningioma, surgery, fronto-temporal approach magnetic resonance tractography for pre-surgical planning in eloquent areas tumors b. iliescu, d. negru, s. gaivas, i. poeata tumors in eloquent areas of the brain pose a particular challenge to neurosurgery, in terms of tumor removal without inflicting new neurological deficit. careful pre-surgical planning plays a crucial role in approaching these tumors safely. knowledge of the relationship between the expanding mass and white matter tracts is one of the important facts to be taken into account in planning this surgery. diffusion tensor imaging (dti) can provide a wealth of information on the white-matter tracts using diffusion anisotropy maps. we analyze our series of first 10 patients, 5 males and 5 females, with salient areas infiltrative tumors (postoperatively glioblastoma multiforme in 8 cases), the role of tractography in providing information on the white matter tracts implication in the pathological process and in planning the right approach and extent of tumor removal. all patients underwent appropriate microsurgical tumor resection with preservation of the documented intact tracts, and preoperative neurological function. our initial experience strongly supports the view that tractography offers essential information in planning a safe surgery for the tumors in eloquent brain areas. 498 abstracts the 7th national congress of rsn gigantic expandable tumors in advanced stages in the periorbital region i. szabo, p.a. kiss, v.r.n. gunness cluj county emergency hospital, department of neurosurgery aims: surgical management of orbital tumor requires frequently an approach of the tumor of considerable dimension which concerns as much the periorbital region and the structures from the orbit as well. according to the data accepted in the literature we defined a gigantic tumor in advanced stage, after the following two principle criteria: 1. tumor dimensions, maximum diameter of tumor over 8 cm. 2. extension of the tumor to a structure of vital functional importance: eyeball, optic nerve, middle ear. material and methods: in our study, we took a sample of 48 cases of orbital and periorbital regional tumors. we did a retrospective study, concerning: sex, age, histopatologic structure, and treatment methods. results: from a number of 623 cases with surgical orbital and periorbital pathology, the total number of expandable gigantic tumors in the study in advanced stage was of 48 cases; from these 17 cases were malignant, 25 cases were benign tumors, one case was a pseudotumor, 4 cases of inflammation and non specific infection, and one case of parasites. conclusion: •expansive gigantic masses in advanced stages in periorbital region are frequent. •in most of the cases there was a disruption which is incompatible with ocular function. •from the surgical procedures that were carried out, extended orbital exenteration was more frequent. •to find a solution for these cases a multidisciplinary collaboration is needed. intraorbital hypertension: clinical features, diagnosis, treatmentnecessary knowledge for any m.d. i. szabo, g. ungureanu, g. mild neurosurgical department, cluj county emergency hospital intraorbital hypertension (ioh) is a potential sight threatening event. according to the time of the onset it can be acute and chronic. acute ioh is comonly known as orbital compartment syndrome(ocs). ocs is a rare, uncommon surgical emergency and can be caused by orbital hemorrhage, infections, emphysema, cellulitis, edema. chronic ioh is most frequently caused by intraorbital expansive processes e.g tumors, pseudotumors, grave’s disease. matherial and methods: 79 cases with diseases that involved ioh treated in the neurosurgery department of the cluj county emergency hospital were analised, from wich 7 cases of ocs. the main cause for chronic ioh were tumors. the causes of ocs were posttraumatic foreign objects (3 cases), intraorbital hematoma (2 cases), orbital emphysema (1 case), orbital cellulitis (1 case). results: patients with chronic ioh presented for proptosis, pain, diplopia, tearing, visual loss. patients with ocs presented for pain, visual loss, limited eye movement, protrusion. surgical and medical treatment were indicated in all cases, mentioning that in ocs surgery was an immediately emergency. medical treatment was made with hyperosmotic romanian neurosurgery (2010) xvii 4: 461 – 508 499 agents (manitol), carbonic anhydrase inhibitors (acetazolamide), corticosteroids. in ocs medical treatment is auxiliary to surgical treatment, witch is urgent. the aim of surgery for orbital tumors was the total macroscopic removal. in ocs lateral canthotomy and cantholysis are needed. the aim is to prevent optic nerve atrophy, retinal compromise or blindness. discussion: the treatment for chronic ioh should be made by specialists in ophthalmology, orbital and ophthalmic surgery. the diagnosis is clinical and using imagistic methods. acute ioh is rare, but when it occurs is a surgical emergency. lateral canthotomy and cantholysis are simple maneuvers, but vision saving procedures, and should be made by the first doctor that treats the patient. diagnosis is clinical! conclusions: chronic ioh when diagnosed, should raise the suspicion of an underlying tumoral process. surgical treatment for acute ioh must be done in emergency to prevent vision loss. management of high grade gliomas: current strategies and dilemas narcisa bucur, angela neacsu, v.m. pruna, anca buliman, g.m. gorgan clinic emergency hospital bagdasar-arseni bucharest, first neurosurgical clinic, fourth neurosurgical department objective: malignant glioma is the most common primary intra-axial tumor of the central nervous system. despite recent therapeutic advances in glioma treatment, the outcome of glioma remains disappointing. the oncologic principle of total tumor resection achieved by complete excision with clear margin is harder to achieve in glioma surgery due to potential neurological deficits that may be incurred wide margin resection, especially when the tumor is situated near the eloquent cortex. the goals of surgical resection in high grade gliomas are supposed to improve survival outcome, symptomatic control, massive cytoreduction, histological diagnosis and an adequate quality of life for the surviving period. methods: authors analyze a large case series of high grade gliomas 347 cases, operated in the fourth neurosurgical department, between 2001 2010 by a team conducted by author, following the same principles of surgery, in which, for every case, the surgical decision was made on the principle of analysis risks versus benefits criteria. results: from this series, 347 (86,31%) were high grade glioma (glioblastomas primary or secondary, anaplastic astrocytomas, anaplastic oligodendrogliomas, and anaplastic oligoastrocytomas), the rest of 55 (13,68%) being low grade gliomas. the relationship between possible risks and potential benefits of the treatment was based on the evaluation of: tumor localization and size (dominant or nondominat hemisphere, deep or superficial), tumor extension (lobal, multilobar, bilateral), mass effect with midline shift, age, associated diseases, karnofsky preoperative score (more than 70, less than 70), estimated possibility of total or near-total resection. according to these criteria, massive cytoreduction was achieved and patients were referred for oncologic reduction and adjuvant therapy. the medium survival time for malignant astrocytoma was 24 months, and for glioblastoma was 16 months, surgical standard mortality was 1,99 % (8 cases), morbidity was 7,21% (29 cases). 500 abstracts the 7th national congress of rsn conclusions: tumor resection should be considered for histological confirmation, cytoreduction and alleviate mass effect. aggressiveness of tumor resection is limited by the risk of new neurological deficits witch delay further radiotherapy or chemotherapy. adjuvant intraoperative procedures to facilitate safe tumor resection should be encouraged. despite malignant gliomas prognosis did not change in the last 20 years, the short term benefits of surgical resection should be all times keep in mind. neuroprotective effect of hypothermia in severe traumatic brain injury eva gheorghita, oana rata, m. trifu, v. pruna bagdasar-arseni emergency hospital, bucharest, romania the use of induced hypothermia as a neuroprotection method is rather an old technique it was abandoned for a period of time, then has been retaken for the past 1015 years. objectives: clinical study results regarding induced hypothermia are conflicting. thus the authors proposed themselves study the efficience of hypothermia in the management of sever skull and brain injury. material and method: the study followed the effects of slight hypothermia (t=34,535,5۫ c) in 10 patients with severe brain and skull injuries (gcs=3-7p) comparatively to a witness lot (group) of 12 patients with normal temperature and the same diagnostic. in the study there were not included the patients with brain death, hypoxia and hypotension >30\', and also the patients in which we could not estimate the timing of the injury.were included patients between 17 and 55 years old, 14 being males and 8 females. results: mean hospitalisations time in the intensive therapy was similar for the 2 groups. comparing the survival rates, these were higher in the hypothermia lot, 60% versus 50%. we must emphasire that the higgest survival rate was in the group with a gcs of 5-7 p in both lots. the incidence of bradicardia and hypothension was bigger in the hypothermia lot, 25% versus 8,33%, needing in some cases inotropic and vasopressor therapy. coagulation disturbances (↓plt, ↓pa) were noticed in the vast majority of the patients who belonged to the hypothermic group, without clinical signs of bleeding. infection complications were also more frequent in the hypothermie lot, especially lung and urinary infections. conclusions: hypothermia is a very good neuroprotection method in brain injuries, with respect to some prerequsiter: to be started immediately after the primary brain injury; the patients must benefit of a very close monitoring to prevent and fight against the early hypothermia side effects; cooling and reheating must be done very slowly (5-12 hours); if hypothermia cannot be achived, at least we must obtain normal temperatures. keywords: hypothermia, brain injuries, monitoring, brain protection. romanian neurosurgery (2010) xvii 4: 461 – 508 501 pediatric guidelines for the management of severe traumatic brain injury eva gheorghita, cristina bucur, luminita neagoe, v. pruna bagdasar-arseni emergency hospital, bucharest, romania sever traumatic brain injury is associated with a significant morbidity and mortality. the primary goal in treating any pediatric patient with severe traumatic brain injury (tbi) is the prevention of secondary insults due to hypotension, hypoxia, hypercarbia, anemia, hyperglycemia and cerebral oedema. the therapeutic management of critically ill children with tbi requires a precise assessment of the brain lesions but also of potentially associated extra-cranial injuries. corect management according to new therapeutic guides, consequent to recent studies, is an important goal in order to improve the outcome in this pathology. on the oder hand, one of the major goals of resuscitation in these children is aimed at protecting against secondary brain insults (sbi). in this paper, the authors propose new therapeutic options in the management of tbi. it is a synthetic approach of our vast experience achieved in this domain. keywords: tbi, child, therapeutic management the main osmolarity disorders in the cerebral pathology eva gheorghita, cristina bucur, luminita neagoe, v. pruna bagdasar-arseni emergency hospital, bucharest, romania the relationship between the cerebral pathology and the fluid equilibrium of the body is a bidirectional one. various cerebral affections have effects over volemia, but reversely as well, changes of intracellular hydration (edema or dehydration) make a mark on the state of consciousness and on the neurological status. perioperative fluid administration, mannitol use, syndrome of inappropriate antidiuretic hormone and cerebral saltwasting syndrome are potential causes of hyponatremia. enteral tube feeding, osmotic diuresis and insipid diabetes are potential causes of hypernatremia. cerebral pathology which modifies the proper release of antidiuretic hormone (adh) and the feeling of thirst will have the most diverse and nocuous effects over the body’s hydration state, over the structure of the various fluid compartments that will lead, by themselves, to the alteration of the state of consciousness and to the wide extension of the neurological consequences of the initial cerebral pathology, no matter its kind (vascular, malign, traumatic and ischemic). the therapy for these disorders of osmolarity is specific for the various illnesses producing them, but it is also oriented to general therapy towards maintaining the fluid balance, on one side, and towards the correction of the sodium capital on the other side. keywords: osmolarity, hypersodemia, hyposodemia, mannitol, insipid diabetes, syndrome of inappropriate secretion of adh, cerebral salt-wasting syndrome, cerebral oedema, water balance. 502 abstracts the 7th national congress of rsn tci anaesthesia in neurosurgery eva gheorghita1, m. trifu1, oana rata1, cristina berteanu1, daniela ionescu2, m. gorgan1, a. v ciurea1 1clinical emergency hospital bagdasar arseni, bucharest, romania 2university of medicine and pharmacy cluj-napoca, romania aims: target controlled infusion (tci) have been launches as simple, accurate and reliable delivery systems of intravenous drugs. tci pump function using a programme based on a pharmacokinetic/pharmacodynamic model. the anesthetist sets the desired target blood or effect site concentration and the tci pump adjusts the rate of delivery of anesthetic agent according to that models. this method was not used until now in romania for neurosurgery. for patients undergoing neurosurgery it is desirable to have stable and easily controllable hemodynamics. rapid postoperative recovery is essential to asses neurological function. material and methods: our study was designed to analyse two different techniques of anesthesia, tci with propofol and remifentanil versus conventional balanced anesthesia sevoflurane remifentanil. we study two lots of patients admitted for cranial or spinal surgery who recived this different types of anesthesia. during the surgery we correlated the level of analgesia with the recommended doses and we registred their variations. the awakening quality was evaluated using the observer assesment of alertness / sedation (oaas) score. we measured the hypnotic effect of anesthetics using bispectral index (bis) for 26 patients. had been monitored recovery times. results and conclusions: tci with propofol / remifentanyl is similar to sevoflurane / remifentanyl with regard to hemodynamic stability. time to extubation was significantly shorter in tiva while cognitive functions and level of consciousness were better in tiva-tci group also. the study was funded by the research grant 41025-cnmp giant, atypical, left, posterior fossa meningioma revealed by rhinorrhea g. iacob1, dana paula georgescu2, m. craciun1, l. nicolae1 1clinic of neurosurgery, universitary hospital bucharest romania 2clinic of neuroradiology, universitary hospital bucharest romania objective and importance: cerebral supra or infratentorial tumors associated with cronic intracranial hypertension and hydrocephalus may rarely generate spontaneous, non-traumatic rhinorrhea. we report one case of this rare condition with a giant, atypical, left, posterior fossa meningioma. clinical presentation: a 55-years-old woman was admitted for a 16-year history of headache, 1-year of rhinorrhea, which flow exacerbated when the pacient is standing or she bent forward, ataxia, astasiaabasia. spontaneous rhinorrhea (no history of head trauma or meningitis) stoped suddenly before admission, cephaleea increased, his general condition worsened. native and contrast ct scan disclosed a giant, extraxial, tumor: 7/9/8 cm, developed in the left posterior fossa, but also active, internal, supratentorial hydrocephalus. the anterior recess of the third ventricle was dilated; sella turcica is global ballonised, romanian neurosurgery (2010) xvii 4: 461 – 508 503 with a small disappearance of the floor in its anterior portion. intervention: the tumor mass was subtotal removed for cardiac rhythm fluctuation and tensional oscilations, confirmed by postop ct scan. after the operation, the patient became free of leakage, a direct approach for rhinorrhea was not needed. conclusion: a case of non-traumatic, spontaneous, rhinorrhea generated by a giant atypical left posterior fossa, atypical meningioma is described. using microsurgical resection tumor was subtotally removed, the patient improved and rhinorrhea don’t recurred. keywords: posterior fossa meningioma, spontaneous rhinorrhea large and giant vestibular schwannomas g. iacob, m. craciun, m. stoiceanu clinic of neurosurgery, universitary hospital bucharest romania background: the main objective in treating large and giant vestibular schwannomas (vs) (large diameter exceeding 3.5 cm and giant diameter exceeding 4.5 cm) is their complete removal without significant morbidity. our experience on 7 cases (4 females, 3 males, mean age 42.5 years) with marked brainstem compression, operated between 2004-2009 focuses on factors influencing recurrence and morbidity, especially related to facial nerve function. these patients were included in a series of 32 consecutive vestibular schwannoma excisions. methods: this report is a retrospective analysis of the surgical outcome of 7 patients with large and giant vs using the retrosigmoid-transmeatal approach. several prognostic factors were evaluated: patient age, tumor size and consistency, extent of surgical removal, concurring hydrocephalus, hearing loss, facial nerve function, trigeminal nerve deficits, cranial nerve vi, ix and x palsy, tongue edema, ataxic gait and motor deficits. results: the mean age was 42.3 years, the mean tumor diameter was 51.8 mm. there were no deaths and the tumors were histologically benign. extensive microscopic tumor resection was performed in 5 cases related to solid tumor’s consistency. preoperatively hearing loss and high intracranial pressure were encountered in all patients. 4 patients had cerebellar ataxia. facial anatomical continuity was preserved in 6 cases with solid tumor consistency; 4 patients had a preoperative facial palsy, a good facial nerve function was achieved in 3 cases – housebrackmann grade i/ii. we have met other distinctive signs: cranial nerve v hypoesthesia, vi, ix and x palsy, tongue edema in 2 cases with slight contralateral motor deficit. all patients were clinical and mri monitored at 3, 6 and 12 months postoperatively. conclusion: total resection associated with a low morbidity rate is possible, avoiding recurrence, reintervention and severe scar tissue. in cases with subtotal resection, radiosurgery is recommended to improve outcome. keywords: large and giant vestibular schwannomas (vs), surgical approach, facial nerve function 504 abstracts the 7th national congress of rsn gelastic seizures in a patient with right gyrus cinguli astrocytoma l. nicolae1, g. iacob1, b. popescu2, mihaela poparda3 1clinic of neurosurgery, university hospital bucharest românia; 2clinic of neurology, university hospital bucharest românia; 3neuropathology clinic, university hospital bucharest romania abstract: objective and importance: gelastic seizure (gs) also known as “gelastic epilepsy” is a rare type of seizure associated with several different conditions such as tumors hypothalamic hamartromas, tuberous sclerosis, hemangiomas, post infectious foci, cortical temporal dysplasia we report one case of this rare condition generated by a right gyrus cinguli gr.ii astrocytoma. clinical presentation: a 27 years, old male, right handed, was admitted for a 2 years history of very frequent gelastic seizures accompanied sometimes by simple motor partial seizures in both arms, more often being involved his left arm, without impairment of his consciousness state. his neurological examination was normal. diagnosis was made on native ct scan: minimal hypodense frontal right paramedian lesion, cerebral mri showed a small right, parenchymal, homogeneous lesion (16/22/15mm), well delimited, involving gyrus cinguli, without perilesional edema and mass effect, hyperintense both on t1 and t2 mr sequences, non-enhancing after gadolinium. the cerebral lesion was also documented on eeg and video-eeg recordings. using an interhemispheric microsurgical approach, above the corpus callosum and the right pericallosal artery, at the level of gyrus cinguli, a yellow-gray, infiltrative tumour, having a moderate vascularisation had been identified and totally removed. the anatomo-pathological analysis revealed a grade ii astrocytoma. the patient recovered very well, without deficits, no gelastic seizures or epileptic manifestations; three months after operation he is still free of seizures. conclusion: a case of gelastic seizures accompanied by simple motor partial seizures in both arms, without impairment of his consciousness state induced by a grade ii right gyrus cinguli astrocytoma is described and documented by radiological and electrophysiological studies. using microsurgical resection, the tumor was totally removed, the patient clinical condition improved. without an affective connotation as in temporal or hypothalamus topography, gelastic seizures are not patognomonic for hypothalamic hamartomas and in the case of frontal localization of the lesion they can be associated with motor involvement of the limbs as in our case. keywords: gelastic seizures (gs), dacrystic seizures (ds), epilepsy surgery, gyrus cinguli, cerebral astrocytoma considerations about hemangioblastomas of the central nervous system v. pruna, narcisa bucur, angela neacsu, m.r. gorgan first neurosurgical clinic, fourth neurosurgical department, clinic emergency hospital “bagdasararseni” bucharest objective: hemangioblastoma of the central nervous system are benign tumors that may occur sporadically or in association with von hippel-lindau disease. is the romanian neurosurgery (2010) xvii 4: 461 – 508 505 most common primary intra-axial tumor in the adult posterior fossa. von hippellindau disease (vhl) is a multisystem neoplastic disorders characterized by a tendency to develop hemangioblastomas of the retina, brain and spinal cord, renal clear cell carcinoma, pheochromocytomas, endolymphatic sac tumors, and others. methods: the surgical database of our institution was searched to identify all patients with histologically verified hemangioblastomas occurring from 20052010. the medical, radiological, surgical and pathology records from these patients were analyzed. results: we analyzed 25 patients (12 female and 13 male) which presented with cns hemangioblastomas. twenty-two (88%) patients had sporadic hemangioblastomas and three (12%) patients suffered by vhl syndrome. one (4%) patient with hemangioblastoma died as a result of late medical complications. seven (28%) patients developed obstructive hydrocephalus. the two (8%) patients underwent gamma knife radiosurgery – one patient with a right eye hemangioblastoma and one patient for a left parietal hemangioblastoma. conclusions: surgical treatment may be curative in cases of sporadic hemangioblastomas and pre-operative gamma-knife radiosurgery may help reduce the tumor size. because patients with vhl syndrome are at risk for development of new lesion, they require lifelong follow-up. keywords: hemangioblastoma, von hippel-lindau disease, gamma-knife radiosurgery microsurgical resection for arteriovenous malformation – series of 121 patients v. pruna, narcisa bucur, m.r. gorgan, anca buliman first neurosurgical clinic, fourth neurosurgical department, clinic emergency hospital “bagdasararseni” bucharest objective: the arteriovenous malformations (avm) are congenital lesions and represent an abnormal collection of blood vessels wherein arterial blood flows directly into draining veins without the normal interposed capillary beds. the goal of the treatment of brain arteriovenous malformation (avm) is to perform a complete resection/obliteration to eliminate the risk of secondary hemorrhage, as bleeding means high rates of morbidity and mortality, with shortened survival expectancy. multimodal therapy is often necessary to obtain complete occlusion of malformation with optimum results. methods: the authors analyzed 121 patients (66 female and 55 men) with brain avm admitted in our clinic between 2001 to 2010, whose data were collected retrospectively from the electronic database and image archive. results: 57 cases (47,1%) have undergone surgery, eight cases (6,6%) were treated by embolization, 22 cases (18,1%) were treated with gamma-knife radiosurgery, 4 patients received combination therapy (surgery + radiosurgery) and 29 patients (23,9%) remained in clinical observation. according to spetzler-martin scale series of patients fit the following profile: 19 cases (15,7%) in grade i, 29 cases (23,9%) in grade ii, 36 cases (29,7%) in grade iii, 23 cases (19%) in grade iv, 11 cases (9%) in grade v and three 506 abstracts the 7th national congress of rsn cases (2,4%) in grade vi. 16 (13,2%) patients who died (14 (11,5%) unoperated because very serious neurological condition and 2 (1,65%) have been charged in palliative surgery or simple external ventricular drainage of hematoma evacuation). conclusions: avm locations in eloquent areas, according to spetzler-martin scale as well as a deep avm location are risk factors in the treatment of asymptomatic avm. morbidity is low surgical resection of an avm when located in non-eloquent area. bleeding remains the most disabling and the dreaded event in the evolution and natural history of an avm. surgical resection is the treatment of choice in selected patients, with increased rates of cure with low morbidity and mortality. keywords: arteriovenous malformation, spetzler-martin grading system, surgical treatment, embolization management of the third ventricle tumors v. pruna, narcisa bucur, m.r. gorgan first neurosurgical clinic, fourth neurosurgical department, clinic emergency hospital “bagdasararseni” bucharest objective: tumors of the third ventricle are often benign and grow slowly. there are multiple surgical approaches (transcallosal, subfrontal, interhemisferic, pterional, etc.) but all attempts to use the pathway around the brain that least disturb and minimally displace normal anatomy. most commonly postoperative complications are hydrocephalus, seizures and cognitive deficits. methods: 21cases of third ventricle tumors treated in fourth neurosurgical department in clinical emergency hospital “bagdasar-arseni”, bucharest between 2005 – 2010. the authors analyzed data that they had collected to study the clinic pathological aspects and review the presentation, imaging, and management of these tumors. results: nine of these 21 patients were men and twelve were women. raised intracranial pressure (icp) was presented in 12 (57,14%) patients, and the preoperative diagnoses were confirmed on neuroimaging studies. a gamma-knife radiosurgery was performed in 2 (9,52%) patients and a direct surgical approach was performed in 15 (71,42%) patients. one (4,76%) patient received chemoteraphy. six (28,57%) patients received no treatment. the mortality in the our series is 14,2%. conclusions: approaches to the third ventricle are difficult and potentially dangerous procedures. the complications are very specific to the type of tumor and its location. the histopathological features are varied, although most of the tumors in the study were infiltrative gliomas. keywords: third ventricular tumors, glioma, surgical approach, chemoterapy subacute subdural hematioma c1-c2. the experience of department of neurosurgery, clinical emergency hospital constanta d. balasa1, d.m. schiopu1, al. tunas1, m. bardas2, gabriela butoi2 1department of neurosurgery clnnical emergency hospital constanta 2department of radiology medimar constanta male, 54 years old, admited in emergency at department of neurosurgery clnnical emergency hospital constanta for pain in the neck slight tetraparesis, more on the right side, pain in the left shoulder. romanian neurosurgery (2010) xvii 4: 461 – 508 507 ct scan of the head and the cervical spine: indefinite for the diagnosis. mri of cervical spine: subdural lesion c1-c2 predominantelly on the right side (posible hasematoma) surgical treatment: laminectomy c1-c2, predominant on the right side, microsurgical aspiration of the haematoma. postoperative status: disappearance of tetaparesis. it rested a slight pyramidal syndrome more specifically crural on the right side. postoperative neurosurgical supervision: 4 months conclusion: subdural c1-c2 haematoma is a very rare lesion surgical treatment is mandatory for healing and a good neurological evolution mri was the only investigation who diagnose the lesion and give the neurosurgical team the dates optimal for a good surgical strategy. metastatic spine disease – management options s.c. craciunas, m.c. catana, eva gheorghita, anca buliman, m. r. gorgan neurosurgery unit iv, bagdasar-arseni hospital, bucharest, romania background: spine metastases represent a growing problem in cancer patients and have a potential to cause significant functional impairment or even death. left untreated, the clinical course of spine metastases is toward progressive loss of motor, sensory and autonomic function. objectives: to assess the demography, neurological status, histopathology and short-term outcomes of surgery in spine metastatic patients. methods: data from forty-four patients with spine metastases admitted and operated in neurosurgery unit iv – bagdasar-arseni hospital, from 2005-2010, were retrospectively reviewed. demographical and clinical data were reported, along with the short-term outcomes following the surgery. the extent of the spinal metastases was preoperatively assessed on appropriate imaging studies and technically suitable and feasible surgery was performed, such as vertebrectomies, piecemeal thorough excision, curettage, or palliative surgery. results: the majority of spinal tumors (72%) operated in our unit were metastases. the incidence among males has been double compared to females. the mean age was 56.7 years. lung and breast were the primary cancers involved the most (18% and 16 % respectively). however, at the time of admission, only 34 % of patients had diagnosed a malignancy, and for another 16 % of them, the primary cancer was diagnosed over the admission interval. in 39 % of cases, the primary source of metastasis has not been detected even following the conventional histopathological analysis. solitary metastases have been found in almost half of patients. thoracic region was involved the most, followed by lumbar spine. local pain was present in all cases. in addition, 45% of patients presented symptoms of spinal cord/ cauda equina compression. the rest of them exhibited signs of nerve roots compression only. sphincter troubles were noted in 36% of cases. 70% of patients were able to walk at the time of surgery. synchrone metastases were observed in 25 % of cases, most of them involving other bones. all patients had a good short-term postoperative outcome, with better pain control, ambulation and neurological improvement. only one complication was reported, an epidural hematoma, that has been evacuated in emergency and the 508 abstracts the 7th national congress of rsn patient recovered with no additional deficits. conclusions: surgery is playing a key role in the management of spinal metastases patients, with good short-term results and low complications rate. nevertheless, selecting the suitable patients for surgery and choosing the proper operation for metastatic spinal tumors is often difficult, and depends on many factors, especially the life expectancy and the balance of the risk of surgery against the likelihood of improving quality of life. thoracic spinal stenosis c. matei, l. tanase department of neurosurgery, emergency clinical county hospital, sibiu, romania introduction: the presence of the stenosis in the thoracic region with its related clinical manifestations has only been recently appreciated. thoracic spinal stenosis due to ossified ligamentum flavum is less common than cervical or lumbar spinal stenosis and it has been documented to occur predominately in japanese population. in non-east asian populations there are only few cases in the literarature. material and method: in this article the authors describe a case of a patient with 59 years of age admitted in our department with slowly progressive thoracic myelopathy. irm and ct of the spine revealed posterior thoracic stenosis, due to ossified ligamentum flavum. the patient was undergone to surgery, consisting of laminectomy and resection of ossified ligamentum flavum. histologically ossifification of the ligamentum flavum was identified by completely ossified bone. postoperative the patient has a favorable course and was discharged after seven days with gos 5. conclusions: thoracic ossified ligamentum flavum develops in the lower thoracic spine in middle-aged men, very rare in non east asian populations. generally the diagnosis and treatment is delayed due to long-delayed onset of symptoms and many cases are complicated by the presence of multiple spinal lesions. until now, no clear therapeutic guideline and no evidence based data are available. doi: 10.33962/roneuro-2022-009 spontaneous height restoration of cervical traumatic non-pathological vertebral compression fracture. short report khelifa adel, aichaoui fayçal, berchiche lakhdar, morsli abdelhalim romanian neurosurgery (2022) xxxvi (1): pp. 49-51 doi: 10.33962/roneuro-2022-009 www.journals.lapub.co.uk/index.php/roneurosurgery spontaneous height restoration of cervical traumatic non-pathological vertebral compression fracture. short report khelifa adel, aichaoui fayçal, berchiche lakhdar, morsli abdelhalim algiers university/faculty of medicine; and department of neurosurgery, mohamed lamine debaghine university hospital (beo), algiers algeria abstract spontaneous regaining of radiological normal shape with vertebral compression fracture is very uncommon in the cervical spine; conducting confusion regarding the presence of a potentially surgical lesion. we report the case of 48 years old man without past medical history who presented post traumatic compression fracture that resolved spontaneously after transcranial traction. the patient was operated on with a good outcome. this report aims to confirm the presence of such phenomena already reported in the dorso-lumbar spine. introduction vertebral compression fracture is a common lesion in the cervical spine trauma; characterized by a loss of the vertebral height. spontaneous regaining of the initial radiological normal shape is very uncommon in the cervical spine; conducting to confusion regarding the presence of potentially surgical lesion. case report the patient is a 48 years old man without past medical history victim of road traffic accident. the clinical exam at the admission found a conscious patient without neurologic deficiency presenting neck pain. the patient is scored e on the asia impairment scale. initial x-rays performed in standing position objectified c6-c7 bilateral facet joint dislocation and distraction; with anterior compression fracture of the c7 body causing an angulation of 40°; without body listhesis; resulting in a significant regional kyphosis (figure a). with slight careful distraction-extension movement while putting the cervical collar the spine ct performed in supine position objectified partial facet joint reduction (figures b, c and d). cervical spine mri objectified no significant intervertebral disk hernia and no spinal compression (figure e and f). the patient was put under transcranial traction using gardner keywords cervical spine, neuro-trauma, compression fracture, height restoration corresponding author: khelifa adel department of neurosurgery, mohamed lamine debaghine university hospital (beo); algiers algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 50 khelifa adel, aichaoui fayçal, berchiche lakhdar, morsli abdelhalim wellstongs, gradually to 6 kg (1/10 the boy weight). impressionably per-operativefluoroscopy at the operating room objectified not only a total reduction offacet joint dislocation, but also c7 spontaneously regained totally a normal height. through a smith robinson approach; a c6-c7 and c7-d1 discectomy were performed with partial corpectomy of c7, autografting and c6-d1 fixation. postoperatively, the patient preserved his neurologic integrity. a: initial lateral x-rays; showing the degrees of angulation caused by c7 compression lesion and the arrow is showing the amount of facet joint initial dislocation. b: sagittal ct, the arrow is showing the slight improvement in vertebral height in supine position. c&d: parasagittal ct passing through left and right facet joints, the arrow is showing the partial reduction of facet joint dislocation. e&f: spinal mri in sagittal t1 and t2 wis, the arrow is showing the pre-vertebral hematoma. g: peroperative lateral fluoroscopy, the arrow is showing a total reduction of c7 body height. h: post-operative lateral x-rays. discussion mckiernanet al.described on dorso-lumbar levels; the phenomena of “dynamic mobility of vertebral compression fractures” in osteoporotic patients where a postural height reduction was noted in many patients candidates for vertebroplasty[1]. in our case -although a slight normalization in vertebral height was noted in ct performed in supine position compared to x-rays performed in standing positionwe explain height restoration by the transcranial traction force applied on the superior end plate of the inferior vertebra transmitted by an undamaged disk. in fact, based on the relatively healthy disk aspect on mri, the absence of body listhesis and the per-operative harmonious aspect of the disk; we think that the relatively integrity of the disk contributed to this phenomena. in the presented case the compression fracture was associated with bilateral facet joint dislocation and thoughthe mechanism is hyperflexion, posterior distraction and anterior compression[2]. in such cases closed reduction with transcranial traction is highly indicated; and giving the absence of significant disk hernia it is without risks. although the patient is neurologically intact and kyphosis has been corrected; the lesion is still highly instable, giving the facet joint dislocation[2], sign of sever ligamentous damage [3].with reduced bilateral facet joint dislocation, anterior fixation is our choice; it offers the possibility of rigid fixation with both arthrodesis and osteosynthesis, allows to perform a discectomy and especially in that case to perform a corpectomy. in fact although preoperative x-rays body aspect seemed to be normal we insisted on corpectomy and body reconstruction using graft, because we think that histological architecture of the body has been severely damaged and though will not be able to support the force transmitted by head and neck weight. we find this rational in dorso-lumbar compression fractures where vertebroplasty is performed with best outcome in patients with spontaneous height reduction after hyperextension positions [1, 4] conclusion in this report we confirm the presence of spontaneous height restoration of compression fractures in cervical spine. this radiological normalization should not hold back body replacement in case of surgical management. funding none. references 1. mckiernan f, jensen r, faciszewski t. the dynamic mobility of vertebral compression fractures. j bone miner res. 2003 jan;18(1):24-9. doi: 10.1359/jbmr.2003.18.1.24. pmid: 12510802. 2. a sayadipour. d g anderson.s mlyavykh. o perlmutter. ar vaccaro.subaxial cervical spine injuries. in: benzel, edward c. spine surgery 2-vol set e-book: techniques, 51 spontaneous height restoration of cervical traumatic non-pathological vertebral compression fracture complication avoidance, and management (expert consult-online). elsevier health sciences, 2012. 3. mclain rf, aretakis a, moseley ta, ser p, benson dr. subaxial cervical dissociation. anatomic and biomechanical principles of stabilization.spine (phila pa 1976). 1994 mar 15;19(6):653-9. doi: 10.1097/00007632-19940300100003. pmid: 8009329. 4. yang jj, koo kh, kim k, park s. efficacy of postural reduction of vertebral compression fracture with extension lateral radiograph before vertebroplasty.world neurosurg. 2020 nov;143:e430e441. doi: 10.1016/j.wneu.2020.07.188. epub 2020 aug 1. pmid: 32750516. microsoft word 6.okezieobasi_calvarial_f.docx 120 kanu et al calvarial hemangioma causing seizure disorder calvarial hemangioma causing seizure disorder: a case report with review of literature okezie obasi kanu1, omotayo a. ojo1, olufemi bankole1, abimbola olaniran1, charles anunobi2, sarajudeen oladele arigbabu1 1neurosurgery division, department of surgery 2department of pathology lagos university teaching hospital, surulere, lagos state, nigeria abstract calvarial hemangiomas are rare benign tumours of the skull bone for which seizure as a presentation is unusual; neurological deficits are uncommon. we report a case of cavernous hemangioma of the parietal bone causing seizure disorder in a 47 year old man. the tumor was removed enbloc with satisfactory methylmethacrylate cranioplasty. pathological examination confirmed the diagnosis. patient received short course of antiepileptic drugs with satisfactory recovery. this case demonstrates that seizure disorder can occur in calvarial haemangiomas as a rare complication. a review of relevant literature is included herein. keywords: cavernous hemangioma, calvarium, epilepsy, seizure disorder introduction intraosseous cavernous haemangiomas are rare benign tumors that constitute 0.7% to 1% of all bone tumors. they are commonly seen along the vertebral column especially in the thoracic spine (1, 2, 27). calvarial cavernous haemangioma is very rare, constituting about 0.2% of all benign neoplasms of the skull (19, 23). hemangiomas arise from the intrinsic vasculature of the bone, and in the skull, the diploe. neurological deficit from calvarial haemangiomas is not common and seizure disorder from calvarial hemangioma is rare (19). the authors present a case of calvarial haemangioma of the parietal bone causing seizure disorder. case report a 47 year old male teacher was seen in 2007 on account of right-sided parietal swelling of 5 months duration. swelling gradually increased in size and became painful 2 months prior to presentation. pain was dull in nature, non-radiating, relieved by analgesic but no known aggravating factor. no history of trauma to the head and no similar swellings in other parts of the body. the patient had two episodes of left-sided partial seizures with secondary generalization a week prior to presentation with associated post-ictal sleep. there was no fever or history suggestive of thyrotoxicosis. examination revealed a swelling over the right parietal prominence measuring ≈4cm x 4cm, tender but not differentially warm. it had bony hard consistency, appeared to be in continuity with the bone and was not attached to the overlying skin. romanian neurosurgery (2012) xix 2: 120 – 123 121 emptying sign was negative and there was no bruit. there were no enlarged peripheral lymph nodes, and no other abnormal findings on general and neurologic examination. skull x-ray showed a well circumscribed radiolucent lesion in right parietal bone with a sclerotic rim (figure 1 a, b). ct scan of the brain revealed a mixed density lesion on the right parietal bone and discontinuity of the cortical surface on the outer table of the skull in the lytic portion of the tumor (figure 1 c-e). a right parietal craniectomy was performed with excision of a rim of normal bone. findings at surgery included a fleshy well circumscribed tumour of the bone, expansile in nature and vascular, compressing on the dura but not attached to it. surrounding bone was thickened in the parietotemporal region. tumour was not attached to overlying skin (figure 2 b d). cranioplasty was performed with methylmethacrylate. figure 1 radiological features of the lesion; a-b show web-like trabecular pattern or sunburst appearance on skull radiograph. c-e: ct images showing expansile bony lesion with compression of the underlying brain (c-d) and erosion of both outer and inner tables of the skull (e) figure 2 perioperative images of the lesion as described in the text. the resultant bony defect (c) was replaced with methylmethacrylate. histological section showed interconnecting trabeculae of bone within which are numerous dilated large caliber thin walled blood vessels lined by flat endothelial cells. few of these vascular channels showed branching. features are consistent with cavernous haemangioma. anti-epileptic drugs (epanutin, pfizer pharmaceuticals) was continued in the post-operative period and discontinued after one year seizure-free period. patient has remained neurologically intact. discussion intraosseous hemangiomas occur in patients of all ages with a peak incidence about the 4th decade (7, 12, 13, 27). they are commoner in females than males (4, 7, 16, 27). haemangiomas are slow-growing and as such takes months to years before symptoms manifest (3). depending on location, signs and symptoms vary, but neurological deficits due to intracranial 122 kanu et al calvarial hemangioma causing seizure disorder expansion is rare (19). common clinical features include pain and bony deformity with occasional pathological fractures (20, 26). lesions in the temporal region may cause facial nerve paralysis, hearing loss or vestibular symptoms (9, 11, 16, 21). seizure disorder as seen in our patient is an uncommon manifestation of calvarial haemangiomas. to the best of our knowledge and available literature, this is the first recorded case of calvarial haemangioma causing seizure disorder. haemangiomas of the maxillary and mandibular regions cause excessive bleeding during surgery or tooth extraction (23). loss of vision, pain and proptosis are seen in lesions involving the orbit (15). haemangiomas usually produce a radiating lattice-like or web-like trabecular pattern giving the typical “sunburst” appearance on radiographs. this is usually due to initial osteoclastic activity and a secondary osteoblastic remodeling with trabecular bone (16). this feature is not always present in all cases. most of the lesions often expand outwards leaving the inner table intact (21, 23) but the lesion in our patient involved both inner and outer tables of the skull with resultant compression of the brain and probably irritation of the underlying meninges (figure 1 a, b) this, in our consideration contributed to the seizure disorder noted in this patient. cavernous hemangiomas may resemble other tumors of the skull, making diagnosis uncertain until surgical excision and histology (24). such lesions include osteoma, osteosarcoma, aneurismal bone cyst, giant cell tumor, fibrous dysplasia, intraosseous meningioma, metastatic disease, paget disease, dermoid or epidermoid cyst and acoustic schwannoma (5, 8, 14, 16, 26). the current treatment of choice for cranial hemangioma is enbloc surgical resection (3, 13, 15, 16, 18, 19). the removal of a rim of normal bone is recommended to prevent recurrence (13, 19, 22). cranioplasty with methylmethcrylate yields satisfactory cosmetic results (8, 21), as in our patient. curettage and radiation have also been used in treating this lesion (25). gamma-knife has also been used to treat cavernous hemangioma with satisfactory results (17). there is a risk of malignant transformation following radiotherapy (10). radiotherapy is therefore reserved for unresectable lesions, partially resected tumors and in patients who reject surgical therapy (6, 13, 21, 22). anti epileptic drug becomes necessary in any patient like ours who develop seizures and such patient should be followed up till seizure abates and drug discontinued. conclusion intraosseus calvarial hemangiomas are rare slow-growing tumors with varied clinical features based on location. we report this first case of calvarial haemangioma causing seizure disorder. surgical enbloc resection with margin of normal bone provides cure and cranioplasty with methylmethacrylate produces satisfactory results. acknowledgements the authors are grateful to dr. njideka okubadejo and dr. edamisan temiye for their critical review of this manuscript and useful suggestions. dr. adaeze igwilo helped with the final preparation of the manuscript. romanian neurosurgery (2012) xix 2: 120 – 123 123 correspondence okezie obasi kanu, mbbs, fwacs neurosurgery secretariat, room 219, department of surgery, lagos university teaching hospital pmb 12003, surulere, lagos state, nigeria e-mail: drkanu@gmail.com telephone:+234 806 891 8462 (mobile) +234 802 300 1347 (alt mobile) references 1.acosta fl, jr., dowd cf, chin c, tihan t, ames cp, weinstein pr: current treatment strategies and outcomes in the management of symptomatic vertebral hemangiomas. neurosurgery 58:287-295; discussion 287-295, 2006. 2.acosta fl, jr., sanai n, chi jh, dowd cf, chin c, tihan t, chou d, weinstein pr, ames cp: comprehensive management of symptomatic and aggressive vertebral hemangiomas. neurosurg clin n am 19:17-29, 2008. 3.ajja a, oukacha n, gazzaz m, akhaddar a, elmostarchid b, kadiri b, oukabli m, boucetta m: cavernous hemangioma of the parietal bone. a case report. j neurosurg sci 49:159-162; discussion 162, 2005. 4.bastug d, ortiz o, schochet ss: hemangiomas in the calvaria: imaging findings. ajr am j roentgenol 164:683-687, 1995. 5.buhl r, barth h, dorner l, nabavi a, rohr a, mehdorn hm: de novo development of intraosseous cavernous hemangioma. j clin neurosci 14:289-292, 2007. 6.chuang cc, jung sm, yang jt, chang cn, pai pc: intrasellar cavernous hemangioma. j clin neurosci 13:672-675, 2006. 7.clauser l, meneghini f, riga m, rigo l: haemangioma of the zygoma. report of two cases with a review of the literature. j craniomaxillofac surg 19:353-358, 1991. 8.dogan s, kocaeli h, sahin s, korfali e, saraydaroglu o: large cavernous hemangioma of the frontal bone. neurol med chir (tokyo) 45:264-267, 2005. 9.dufour h, fesselet j, metellus p, figarella-branger d, grisoli f: cavernous hemangioma of the sphenoid sinus: case report and review of the literature. surg neurol 55:169-173; discussion 173, 2001. 10.fredrickson jm, haight js, noyek am: radiationinduced carcinoma in a hemangioma. otolaryngol head neck surg 87:584-586, 1979. 11.gavilan j, nistal m, gavilan c, calvo m: ossifying hemangioma of the temporal bone. arch otolaryngol head neck surg 116:965-967, 1990. 12.haynes r, sobel df, holeman g: cranial arteriovenous hemangioma in a neonate. ajnr am j neuroradiol 8:916-918, 1987. 13.heckl s, aschoff a, kunze s: cavernomas of the skull: review of the literature 1975-2000. neurosurg rev 25:56-62; discussion 66-57, 2002. 14.hoffmann df, israel j: intraosseous frontal hemangioma. head neck 12:160-163, 1990. 15.hook sr, font rl, mccrary ja, harper rl: intraosseous capillary hemangioma of the frontal bone. am j ophthalmol 103:824-827, 1987. 16.khanam h, lipper mh, wolff cl, lopes mb: calvarial hemangiomas: report of two cases and review of the literature. surg neurol 55:63-67; discussion 67, 2001. 17.kida y, kobayashi t, mori y: radiosurgery of cavernous hemangiomas in the cavernous sinus. surg neurol 56:117-122; discussion 122-113, 2001. 18.kumar na, ranganadham p, bhaskar g, chowdhury ar: multiple calvarial cavernous haemangiomas: case report and review of the literature. neuroradiology 38 suppl 1:s83-85, 1996. 19.liu jk, burger pc, harnsberger hr, couldwell wt: primary intraosseous skull base cavernous hemangioma: case report. skull base 13:219-228, 2003. 20.mccarthy ef, frassica fj: pathology of bone and joint disorders with clinical and radiographic correlation. philadelphia, saunders, 1998. 21.naama o, gazzaz m, akhaddar a, belhachmi a, asri a, elmostarchid b, elbouzidi a, kadiri b, boucetta m: cavernous hemangioma of the skull: 3 case reports. surg neurol 70:654-659, 2008. 22.peterson dl, murk se, story jl: multifocal cavernous hemangioma of the skull: report of a case and review of the literature. neurosurgery 30:778-781; discussion 782, 1992. 23.rothstein j, maisel rh, miller r, tubman d: mixed cavernous and capillary hemangioma of the frontal bone. ear nose throat j 64:481-485, 1985. 24.sarac k, biliciler b, vatansever m, aladag ma, colak a: unusual frontal osteoma, mimicking a haemangioma. neuroradiology 38:458-459, 1996. 25.shibata s, mori k: effect of radiation therapy on extracerebral cavernous hemangioma in the middle fossa. report of three cases. j neurosurg 67:919-922, 1987. 26.suzuki y, ikeda h, matsumoto k: neuroradiological features of intraosseous cavernous hemangioma--case report. neurol med chir (tokyo) 41:279-282, 2001. 27.yoshida d, sugisaki y, shimura t, teramoto a: cavernous hemangioma of the skull in a neonate. childs nerv syst 15:351-353, 1999. 10amitagrawal_developing romanian neurosurgery (2014) xxi 3: 307 312 307 developing a traumatic brain injury registry: lessons learned from difficulties amit agrawal1, m. veera prasad2, s. satish kumar3, b.v. subrahmanyan4, p.n. harisha5, g. malleswara rao1 1professor of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india); 2associate professor: department of hospital administration, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india); 3associate professor of emergency medicine, department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india); 4professor of forensic medicine, department of forensic medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india); 5assistant professor of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract aim: the aim of present article is to share our experiences and lessons learned from a pilot study which was conducted to collect data to serve as a model in establishing a multicenter registry on traumatic brain injury patients. methods: the present study was conducted from december 2013 to june 2014 in the department of neurosurgery and department of accident and emergency medicine. all patients with the diagnosis of traumatic brain injury (as per the criteria laid by international classification of disease injury codes icd 10) were enrolled in the study. variables were identified as per the international norms and the data points were selected which included demographic details, pre-hospital characteristics, clinical details in emergency room, injury details, course during hospital stay, treatment and disposition. the data were categorized into master data, data related to pre-hospital events including pre-hospital care, data related to emergency room care offered in the emergency department, data related to hospital stay and patient course, outcome and follow up. results: a total of 231 patients were admitted with the diagnosis of traumatic brain injury. there were 79.1% male and 20.5% female patients. mean age was 37.19 years (sd±17.02 years, range 4-87 years). mean hospital stay was 3.66 days (sd±4.46 days, range-1-21 days). data were collected daily for all the admitted patients on previous day fulfilling the inclusion criteria. the proforma was easy to comprehend and it was easy to fill. conclusion: we found that a well-designed proforma based under supervision data collection in a relatively low volume trauma 308 agrawal et al developing a traumatic brain injury registry: lessons learned from difficulties center. we found that a well-designed proforma based under supervision data collection in a relatively low volume trauma center and at regular intervals can be costeffective which can be managed by personnel with basic training. key words: traumatic brain injury, trauma registry, injury introduction a registry is defined as a systematic collection of a clearly defined set of health and demographic related data for patients with specific health characteristics which are held in a database for a predefined purpose. (1) the role of databases is being increasingly recognized for the improvement of trauma care in healthcare environment. (2) thus it is becoming more and more important that the hospitals who involve in the management of injured patients should have some mechanism of trauma data management. (3) many instruments have been developed in europe and north america but these have limited value elsewhere. (4-8) the aim of present article is to share our experiences and lessons learned from a pilot study which was conducted to collect data to serve as a model in establishing a multi-center registry on traumatic brain injury patients. material and methods the present study was conducted from december 2013 to june 2014 in the department of neurosurgery and department of accident and emergency medicine of the narayana medical college and hospital (nmch) in nellore, india. nmch is a 1200 bed tertiary care center, with a training program in emergency medicine and has 24hours facilities to manage traumatic brain injury cases with a team comprising of emergency physicians and residents from anesthesia and neurosurgery. all patients with the diagnosis of traumatic brain injury (as per the criteria laid by international classification of disease injury codes icd 10) presenting to the departments of neurosurgery and emergency medicine were included in this study. the data were collected from patients medical records; doctors' and nurses' notes records which included laboratory, radiology, and operative findings. the medical records of traumatic brain injury patients were reviewed by the treating physician and the data were obtained by a research assistant who was trained in abstracting data from medical records and was familiar with icd-10 injury codes, (9) ais and injury severity scoring. (10) variables were identified as per the international norms and the data points were selected which included demographic details, pre-hospital characteristics, clinical details in emergency room, injury details, course during hospital stay, treatment and disposition. (1113) the data were categorized into master data, data related to pre-hospital events including pre-hospital care, data related to emergency room care offered in the emergency department, data related to hospital stay and patient course, outcome and follow up. (14) this pilot study protocol was approved by the institutional ethics review committee. romanian neurosurgery (2014) xxi 3: 307 312 309 statistical analysis data were presented as the mean and standard deviation for continuous variables and as a percentage for categorical variables. statistics were calculated using pspp statistical software. (15) results a total of 231 patients were admitted with the diagnosis of traumatic brain injury. there were 186 (79.1%) male and 48 (20.5%) female patients. mean age of the patients was 37.19 years (sd±17.02 years, range 4-87 years). mean hospital stay was 3.66 days (sd±4.46 days, range-1-21 days). most of the patient made good recovery (82.9%) and were discharged to home (table 1). the proforma was easy to comprehend and it was easy to fill. data were collected daily for all the admitted patients on previous day fulfilling the inclusion criteria. table 1 example summary of glasgow outcome scale at discharge and discharge destination from hospital glasgow outcome scale at discharge death 6 (2.6 %) good recovery 194 (82.9 %) moderate disability 26 (11.1 %) severe disability 8 (3.4 %) discharge destination from hospital home 196 (83.7 %) other hospital 33 (14.1%) plastic surgery 1 (0.4 %) discussion development of trauma data registry particularly multicenter data registry needs a well-planned, systematic and step-wise approach. (13, 16-19) the approach needs to be comprehensive but with a short proforma, well defined inclusion and exclusion criteria, user friendly electronic database (which facilitate multi-center data collection), deployment of data entry personnel’s and finally team to perform data analysis and data reporting. (13, 19) before we started the whole process we discussed the factors and obstacles which are faced when conducting research in developing countries have already been discussed in the literature. (3, 20) it was recognized that there may not be any appreciation, there will be hardships in securing funds and it will be difficult to hire good data entry assistants. (19) however, our team took this as a challenge and decided to overcome all the hurdles and we could complete the first stage successfully. requirements the successful registry depends on good patient records, documentation of all relevant information, and availability of trained personal, adequate funding and institutional support. (3, 19, 21-27) a secure source of funding, a well-defined patient population, a minimum data set, adequate staffing and training, and a means to estimate the completeness and accuracy of case reporting remain critical operational imperatives. (28) data collection it has been recognized that successful establishment of registry depend on a concise 310 agrawal et al developing a traumatic brain injury registry: lessons learned from difficulties data entry form, a user-friendly secure and accessible web-based database system. (19) the design of a trauma database is correctly identify the defined population (3, 29, 30) and to overcome this we used icd (10) as the standard to identify the tbi cases. one the cases are identified the next step is to design a valid, reliable and efficient data set to collect required information. (21) standardized proforma not only can act as an educational tool for doctors not to miss any injuries but it also can help in improved medical documentation of tbi patients. (31) careful selection and definition of each data point is essential (21) and it is important to understand that too little data will be of limited value and too much data will be time-consuming and expensive to collect. (19) future a well-designed database can be used to pool multi-center trauma data for epidemiologic reports, to compare effectiveness of care among centers and to evaluate the performance improvement indicators. (3) commercial available data collection programs are expensive which needs training, updates and maintenance which make these commercial products inaccessible for many low and middle income countries. (21) it has created a need to locally develop electronic trauma registry software which can be used in our hospital settings. (23, 24, 32) it is of utmost importance to understand the step to develop such a data collection system which needs a suitable and concise data entry form, a database and secure online electronic form, well trained personals to extract and enter data and most importantly personals to analyze and interpret data. (19) limitations the present pilot study was conducted at a single tertiary-care teaching institution and our study circumstances may not reflect the exact situation in many of the hospitals of our country (lack of adequate facilities to handle patients with tbi). it has been learned that a public health approach in the design of trauma registries adds a level of completeness to the research and a staged approach is mandatory to refine data form and to reduce the total number of data elements. (19) in agreement of the literature the current hospital-based tbi registry is not representative of all injuries in the population as we did not take into account those patients who did not survive to reach our hospital, did not seek hospital treatment for minor injuries or were treated elsewhere. (28) conclusions we found that a well-designed proforma based under supervision data collection in a relatively low volume trauma center and at regular intervals can be cost-effective which can be managed by personnel with basic training. we believe that the information collected will help to better understand the epidemiology of traumatic brain injury in developing countries and will help in injury control, research, education, acute care, and resource allocation. (33) we also believe that the present study is a beginning to fulfill the existing gap for data collection in the field of traumatic brain injury in developing countries. in near future we are in process to romanian neurosurgery (2014) xxi 3: 307 312 311 convert the paper based data collection form into an electronic data base and interfaces to these databases. after successful completion of first pilot phase we are planning to convert the paper based proforma into electronic database to facilitate easy data entry and data retrieval. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.solomon dj, henry rc, hogan jg, van amburg gh, taylor j. evaluation and implementation of public health registries. public health reports (washington, dc: 1974) 1991;106:142-150. 2. spott ma. basic protection of trauma registry information. journal of trauma nursing: the official journal of the society of trauma nurses 2000;7:16-18. 3. nwomeh bc, lowell w, kable r, haley k, ameh ea. history and development of trauma registry: lessons from developed to developing countries. world journal of emergency surgery: wjes 2006;1:32. 4. gabbe bj, cameron pa, wolfe r. triss: does it get better than this? academic emergency medicine: official journal of the society for academic emergency medicine 2004;11:181-186. 5.zafar h, rehmani r, raja aj, ali a, ahmed m. registry based trauma outcome: perspective of a developing country. emergency medicine journal: emj 2002;19:391394. 6. podang j, singhasivanon p, podhipak a, santikarn c, sarol jn, ancheta ca. primary verification: is the triss appropriate for thailand? the southeast asian journal of tropical medicine and public health 2004;35:188-194. 7. onwudike m, olaloye oa, oni oo. teaching hospital perspective of the quality of trauma care in lagos, nigeria. world journal of surgery 2001;25:112-115. 8. talwar s, jain s, porwal r, laddha bl, prasad p. trauma scoring in a developing country. singapore medical journal 1999;40:386-388. 9.icd-10 version:2010 [online]. available at: http://apps.who.int/classifications/icd10/browse/2010/e n. 10. greenspan l, mclellan ba, greig h. abbreviated injury scale and injury severity score: a scoring chart. the journal of trauma 1985;25:60-64. 11. who | injury surveillance guidelines [online]. available at: http://www.who.int/violence_injury_prevention/publica tions/surveillance/surveillance_guidelines/en/. 12. tbi standards ninds common data elements [online]. available at: http://www.commondataelements.ninds.nih.gov/tbi.as px#tab=data_standards. 13. morris sc, manice n, nelp t, tenzin t. establishing a trauma registry in bhutan: needs and process. springerplus 2013;2:231. 14. burkhardt m, nienaber u, holstein jh, et al. trauma registry record linkage: methodological approach to benefit from complementary data using the example of the german pelvic injury register and the traumaregister dgu((r)). bmc medical research methodology 2013;13:30. 15. pspp gnu project free software foundation [online]. available at: http://www.gnu.org/software/pspp/. 16. agrawal a. injury surveillance or trauma registry: need of hour and time to start. the indian journal of neurotrauma 2011;8:37-39. 17. agrawal a. a critical appraisal of neurotrauma and neurocritical care perspectives of traumatic brain injuries in indian scenario. the indian journal of neurotrauma 2013;10:38-42. 18. joshi a, agarwal a, pal r, et al. the 2014 academic college of emergency experts in india′s indo-us joint working group (jwg) white paper on "developing trauma sciences and injury care in india". international journal of critical illness and injury science 2014;4. 19. shaban s, eid ho, barka e, abu-zidan fm. towards a national trauma registry for the united arab emirates. bmc research notes 2010;3:187. 20. abu-zidan fm, rizk dee. research in developing countries: problems and solutions. international 312 agrawal et al developing a traumatic brain injury registry: lessons learned from difficulties urogynecology journal and pelvic floor dysfunction 2005;16:174-175. 21. rutledge r. the goals, development, and use of trauma registries and trauma data sources in decision making in injury. the surgical clinics of north america 1995;75:305-326. 22. moore l, clark de. the value of trauma registries. injury 2008;39:686-695. 23. mehmood a, razzak ja. trauma registry--needs and challenges in developing countries. jpma the journal of the pakistan medical association 2009;59:807-808. 24. schuurman n, cinnamon j, matzopoulos r, fawcett v, nicol a, hameed sm. collecting injury surveillance data in lowand middle-income countries: the cape town trauma registry pilot. global public health 2011;6:874-889. 25. cameron pa, finch cf, gabbe bj, collins lj, smith kl, mcneil jj. developing australia's first statewide trauma registry: what are the lessons? anz journal of surgery 2004;74:424-428. 26. agrawal a, galwankar s, kapil v, et al. epidemiology and clinical characteristics of traumatic brain injuries in a rural setting in maharashtra, india. 2007-2009. international journal of critical illness and injury science 2012;2:167-171. 27. agrawal a, kakani a, baisakhiya n, galwankar s, dwivedi s, pal r. developing traumatic brain injury data bank: prospective study to understand the pattern of documentation and presentation. the indian journal of neurotrauma 2012;9:87-92. 28. pollock da, mcclain pw. trauma registries. current status and future prospects. jama: the journal of the american medical association 1989;262:2280-2283. 29. bergeron e, lavoie a, moore l, bamvita j-m, ratte s, clas d. paying the price of excluding patients from a trauma registry. the journal of trauma 2006;60:300-304. 30. mann nc, guice k, cassidy l, wright d, koury j. are statewide trauma registries comparable? reaching for a national trauma dataset. acad emerg med 2006;13:946953. 31.wallace sa, gullan rw, byrne po, bennett j, perezavila ca. use of a pro forma for head injuries in the accident and emergency department--the way forward. j accid emerg med 1994;11:33-42. 32. schultz cr, ford hr, cassidy ld, et al. development of a hospital-based trauma registry in haiti: an approach for improving injury surveillance in developing and resource-poor settings. the journal of trauma 2007;63:1143-1154. 33. american college of surgeons: trauma programs: ntdb [online]. available at: http://www.facs.org/trauma/ntdb/. microsoft word 9iencean_early romanian neurosurgery (2013) xx 3: 289 – 292 289 early therapies for acute traumatic spinal cord injury st.m. iencean1, al. tascu2, a.st. iencean3, i. poeata1 1“grigore t. popa” university of medicine and pharmacy iasi, romania 2“carol davila” university of medicine and pharmacy bucharest, romania 3“n. oblu” emergency hospital iasi, romania abstract early therapies for acute traumatic spinal cord injury has some key points: 1. immediately or soon after the injury is recommended a hemodynamic support to maintain mean arterial pressure at 85 – 90 mmhg and monitoring in an intensive care unit for the first week after spinal cord injury. 2. immediate surgery for spinal cord decompression is of high importance for the prognosis and evolution of spinal cord injury. 3. the recommendation is to treat all patients with spinal cord injury according to the local protocol, methylprednisolone is not standard of care anymore, it is a treatment option that should only be undertaken with knowledge of the potential complications. key words: methylprednisolone, spinal cord injury. in april in canadian medical association journal was published an excellent review of the acute traumatic spinal cord injury problem: "emerging therapies for acute traumatic spinal cord injury" written by jefferson r. wilson, nicole forgione and michael g. fehlings (cmaj, vol. 185 no. 6, pp.485 492, 2013). in the beginning the article show the incidence and prevalence of traumatic spinal cord injury in canada; for us this is a serious problem! we have not a situation of these cases in romania, therefore we have not a national perspective on the incidence and prevalence of spinal cord injury in our country. neurosurgical and neurorehabilitation departments must keep track of cases of spinal trauma and each statistic should be centralized. following the protocols developed for the spinal cord injury patients the care on the first 72 hours of injury are the most important and all must prevent secondary complications. after a good triage protocols and trauma systems of care, including prehospital triage, spinal stabilization during emergency transport and early immobilization of all patients with a potential spinal injury, patient arrives at the spinal cord injury center. initial prehospital management of traumatic acute spinal cord injury is crucial for the morbidity and mortality following acute spinal cord injury. the radiographic evaluation of patients following spinal cord injury consists of the images of the entire spine and to perform mri of the known or suspected ares of spinal cord injury. in the spinal cord injury center the patient receives “aggressive medical and surgical methods to maintain cord perfusion, avoiding complications, decompressing the spinal cord and restoring stability.” (citare emerging). the 290 iencean et al early therapies for acute traumatic spinal cord injury authors recommend to maintain mean arterial pressure at 85 – 90 mmhg and monitoring in an intensive care unit for the first week after spinal cord injury. these recommendations are consistent with recommendations of the american association of neurological surgeons: that patients’ mean arterial pressure must be maintained at 85–90 mmhg for the first 7 days after injury, published since 2002, in article: “blood pressure management after acute spinal cord injury” neurosurgery. also “when volume replacement is inadequate to achieve this goal, intravenous vasopressor medications may be introduced. patients, particularly those with severe cervical injuries, should receive treatment in an intensive care unit (icu) with continuous cardiac, hemodynamic and respiratory monitoring for the first 7–14 days after injury. in observational studies, the standardized admission of patients with spinal injuries to an icu has been associated with reduced mortality and morbidity, in addition to improved neurologic recovery.” (citare emerging ). the surgical treatment (ideally within eight hours of the injury occuring) must remove the tissues causing spinal cord compression, must correct the misalignment and must stabilize the spine. immediate surgery for spinal cord decompression is of high importance for the prognosis and evolution of spinal cord injury. stascis, the surgical timing in acute spinal cord injury study, was a prospective study that compares patients who underwent either early (< 24 h after injury) or late ( ≥ 24 h after injury) surgical decompression and the results were early surgery were associated with better neurologic recovery at 6 months. figure 1 c5 cervical spinal fracture with traumatic acute spinal cord hemorrhage, tetraplegia figure 2 t 10 fracture with traumatic acute spinal cord injury, paraplegia romanian neurosurgery (2013) xx 3: 289 – 292 291 thefore the conclusion is that: “decompressive surgery within 24 hours after injury has been shown to be safe and feasible; in prospective nonrandomized trials, it has been associated with improved rates of neurologic recovery.” there are still other drugs which can be used and the recommendation is to treat all patients with spinal cord injury according to the local protocol. if steroids are recommended, they should be initiated within 8 hours of injury with the following steroid protocol: methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the bolus. methylprednisolone is not standard of care anymore, “optional at best, although could still be considered in view of the lack of other treatment options”. other drugs with therapeutic potential in acute spinal cord injury are: naloxone, an opioid antagonist that blocks the neurotoxic effects of the endogenous opioid. nimodipine, as a l-type calciumchannel blocker and it prevents activation of calciumdependent apoptotic enzymes and blocks presynaptic release of glutamate minocycline promotes functional recovery, enhances axonal survival, and reduces injury-site lesion size. gm-1 ganglioside (sygen) decreases injury-induced, over-release of damageperpetuating excitatory substances. riluzole, a sodium-channel blocker used for the treatment of amyotrophic lateral sclerosis (als), in which it reduces motor neuron degeneration and in preclinical models of spinal cord injury it decreases secondary injury by blocking pathological activation of sodium channels and reducing the release of neuronal glutamate. erytropoietin has neuroprotective effects and contributes to neurons regeneration neotrofin stimulat es growth-factor production, enhances proliferation of cns stem cells, and protects neurons from the release of excitatory substances. the implant in the site of spinal cord injury or the transplantation of stem cells and autologous non–stem cells has been studied in preclinical injury models. the cellular subtypes used for this purpose include: bone marrow–derived stem cells, olfactory ensheathing cells, schwann cells, activated autologous macrophages, tissue-derived adult neural stem cells. the results are promising, but further studies are needed on larger groups of patients with spinal cord injury. conclusions the patient with spinal cord injury must reach in the spine surgery service as early as possible to evaluate the need for immediate decompression and stabilization surgery. methylprednisolone is not standard of care anymore, optional at best, although could still be considered in view of the lack of other treatment options. the patient with spinal cord injury must admitt to an intensive care unit with continuous cardiac, hemodynamic and respiratory monitoring for the first 1–2 weeks. this article about early treatments in acute traumatic spinal cord injury is part of the grant: “immediate neuroprotective therapy in acute traumatic spinal cord 292 iencean et al early therapies for acute traumatic spinal cord injury injury”, that won the 2011 national competition of national research council (cncs), ideas, grant number: pn-ii-id pce-2011-3-0569, funded by cncs – uefiscdi romania corresponding author: a.st. iencean neurosurgery, “prof. dr. nicolae oblu” hospital iasi, andrei_steffan@yahoo.com references 1. wilson jr, forgione n, fehlings mg emerging therapies for acute traumatic spinal cord injury can maj, vol. 185 no. 6, pp.485 492, 2013 2. st.m. iencean, i. poeata, didona ungureanu, d. cuciureanu,b. costachescu, al. chiriac, traumatic spinal cord injuries: neuroprotection and recent outcomes romanian neurosurgery (2012) xix 3: 210 216 3. marklund niklas: spinal cord regeneration – current and future treatment options for traumatic spinal cord injury, eans training courseleeds, 26 – 30 august 2012 4. bunge mb. novel combination strategies to repair the injured mammalian spinal cord. j spinal cord med. 2008;31(3):262-9; 5. noonan vk, fingas m, farry a, et al. the incidence and prevalence of spinal cord injury in canada: a national perspective. neuroepidemiology 2012;38:21926. 6. furlan jc, noonan v, cadotte dw, et al. timing of decompressive surgery of spinal cord after traumatic spinal cord injury: an evidence-based examination of pre-clinical and clinical studies. j neurotrauma 2011;28:1371-99. 7. fehlings mg, vaccaro a, wilson j, et al. early versus delayed decompression for traumatic cervical spinal cord injury: results of the surgical timing in acute spinal cord injury study (stascis). plos one 2012;7:e32037. 8. bracken mb, shepard m, holford t, et al. administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. results of the third national acute spinal cord injury randomized controlled trial. national acute spinal cord injury study. jama 1997;277:1597-604. 9. yoon sh, shim ys, park yh, et al. complete spinal cord injury treatment using autologous bone marrow cell transplantation and bone marrow stimulation with granulocyte macrophage-colony stimulating factor: phase i/ii clinical trial. stem cells 2007; 25: 2066-73. 10. syková e, homola a, mazanec r, et al. autologous bone marrow transplantation in patients with subacute and chronic spinal cord injury. cell transplant 2006;15:675-87. 11. hugenholtz h, cass d, dvorak m. high-dose methylprednisilone for acute closed spinal cord injury only a treatment option. can j neurol sci 2002; 3:22735. 12. fehlings mg, wilson jr, frankowski rf, et al. riluzole for the treatment of acute traumatic spinal cord injury: rationale for and design of the nactn phase i clinical trial. j neurosurg spine 2012;17:151-6. 13. lammertse dp, jones la, charlifue sb, et al. autologous incubated macrophage therapy in acute, complete spinal cord injury: results of the phase 2 randomized controlled multicenter trial. spinal cord 2012;50:661-71. 14. iencean st m, ciurea av. autologous bone marrow implant into traumatic chronic spinal cord injury. am j of neuroprotection and neuroregeneration, vol 1, no 1,. pp. 73-77, 2009. microsoft word 9zenteno_useheparin romanian neurosurgery (2013) xx 4: 369 374 369 use of heparin in neurointervention: a review of the literature m. zenteno1, l.r. moscote-salazar2, h. alvis-miranda3, a. lee4 1professor of neurological endovascular therapy, departamento de terapia endovascular neurológica, instituto nacional de neurología y neurocirugía, universidad nacional autónoma de méxico; strokeunit, hospital ángeles del pedregal. 2department of neurological endovascular therapy, instituto nacional de neurología y neurocirugía; méxico city, méxico, mineurocirujano@aol.com 3universidad de cartagena, cartagena de indias, colombia 4department of neurosurgery, instituto nacional de ciencias médicas y nutrición salvador zubirán; strokeunit, hospital ángeles del pedregal, méxico city, méxico abstract background: the use of heparin is routine in endovascular procedures as a strategy in many centers that perform neurointerventional procedures to prevent occlusion of the catheters, but the use of this drug carries risks such as heparininduced thrombocytopenia. objective: the purpose of this paper is to present a review of the literature. material and methods: we conducted an extensive search and review of published papers about heparin and neurointerventional procedures. results: the evidence in the literature is weak in relation to the use of heparin and the reduction of embolic effects associated with their use in endovascular procedures. conclusion: the evidence on the use of heparin for the prevention of thromboembolic events in endovascular procedures are of low quality. there is insufficient evidence to conclude a potential benefit of heparin is useful in neurointerventional procedures. prospective studies are needed to determine the effectiveness of heparin and avoid exposing patients to potential risks. key words: heparin, neurointervention, neuroangiography, arterial catheters. introduction during neurointerventional procedures, the use of catheters is a key step in the realization of the same, many international centers have traditionally used heparin infusion in order to prevent the formation of clots inside the devices; this potential thrombus can migrate to different parts of the body and cause injury. complications of angiography and endovascular procedures, whichhave historically been used for the diagnosis and treatment of neurovascular diseases, have rarely been described in the literature.the most frequent complication reported in the literature is bruising during these procedures. complications derived from angiographic procedures such as anaphylaxis and death account for 0.03 % and 0.06 %, respectively. uses of heparin heparin is the anticoagulant most frequently used in hospitalized patients in many neurosurgical centers. in 370 zenteno et al use of heparin in neurointervention industrialized nations, there are applied 80 million doses annually. the use of heparin is directed to maintain the integrity of catheters used in endovascular therapy. currently the use of low molecular weight heparins is to prevent venous thromboembolism. heparin is a mucopolysaccharide acid with variable molecular weight (4.000 to 40.000da). since 1935, high-molecular weightsheparins have been usedto inhibit platelet activityalso. heparin acts in vitroas antithrombininhibitor, activating the plasma, which disables the thrombin and factor xa, then is metabolized byfast ndesulfation after administration in the body. usually heparin and similar products cause immunologically mediated thrombocytopenia, which usually occurs between the 5th and the 10th day. usually the action of heparin is reversed by protamine sulfate, being the only agent that can stop heparin anticoagulation;complications of the use of protamine include systemic arterial hypotension, pulmonary arterial hypertension, bradycardia and oxygen consumption declination. kaufmann et al. evaluated and analyzed the complications of diagnostic angiographyin 19826 consecutive patients, in that work thrombotic events were only 9 (0.05%). neurological complications occurred within the first 24 hours of angiography in 2.63% of patients. (1)it has been reported the presentation of intracerebral hemorrhage associated to endovascular procedures in which heparin was used. (2) the vasodilatory effects of heparin have been reported due to rapid administration, in the form of boluses. therapeutic uses venous thromboembolism: heparin have beenextensively used for prevention of venous thromboembolism, a fixed dose of heparin of 5000 iu subcutaneously administered, every 8 hours reduce from 60 to 70% the risk of venous thrombosis and decrease in mortality of 0.2% compared with control groups which evidenced a mortality of 0.7%. (5). heparin has been used for many therapies along neurointervensionism evolution, such as aneurisms, (3, 4)atherothrombotic vertebrobasilar occlusion, (5) as part of the reperfusion strategies for acute ischemic stroke, (6–11) for free-floating carotid thrombus, (12) cerebral venous sinus thrombosis, (9, 13) primary stent revascularization, (14) among others.heparin is recommended during interventions due to the use of multiple intravascular tools in procedures that can last several hours. (3) currently, neurointerventional procedures are performed under therapeutic heparinization even in cases of ruptured aneurysms to prevent thromboembolic events. (15) due to the fact that many published multicenter studies about the use of anticoagulants have left the doses to the judgment of the investigators, these had notbeen reported. however, doses reported by major monocenter studies (16–18) have been of initial boluses ranging from 3000 to 5000 iu followed by 20-40 iu/kg/h continuously to maintain a monitored activated clotting time (act) between 200 and 300 seconds. (3) protocols vary largely, and often comprise a standardized loading dose and no specified controls. in other kind of endovascular procedures, after a baseline act is obtained, intravenous heparin (70 iu/kg) is romanian neurosurgery (2013) xx 4: 369 374 371 generally given to a target prolongation of approximately 2 to 3 times the baseline value. then heparin can be given continuously or as an intermittent bolus with hourly monitoring of act. (19) only 69% of the surveyed members of the world federation of interventional and therapeutic neuroradiology (wfitn), uses heparin intraoperatively and in a continuous fashion. (3) the wfitn recommends a 5000 iu bolus, then 1000 iu/h continuously, with (monitored) act at about 200s. nevertheless, there are many recommendations for heparin use outside the field of interventional neuroradiology that may be adaptable to the endovascular treatment of aneurisms. (20) the normally employed monitoring method is act, with guideline values > 200 s, most commonly between 250 and 300 seconds. (21) it is recommended to test the efficacy of the heparin regularly during the intervention. loading and continuous doses must be adapted to the patient’s weight to rapidly attain and maintain act objectives during the intervention, which may take several hours (3). preoperative oral anticoagulants are usually stopped 5 days before the intervention and replaced by heparin, which has the advantage of being easily antagonized in cases of intraoperative aneurism rupture. (3) protamine sulfate dose for dose in the last hour will rapidly terminate heparinization. some teams continue heparin infusion for 24–48 h, but the wfitn does not recommend pursuing anticoagulation postoperatively. (3) any rationale for postoperative use of heparin is unclear. indeed, no convincing clinical results have been published, and from a biological perspective it seems more pertinent to use antiplatelets. (3) on the other hand, there is insufficient evidence to support the use of either systemic or local thrombolysis in patients who have cerebral sinus venous thrombosis (cvst) according to european federation of neurologic societies guidelines. heparin use must be monitored. the effect of the heparin lasts for at least a few hours and patients usually need to be placed on antiplatelet therapy after the procedure. (15) in the resuscitation phase of any intracranial catastrophe, when the patient is receiving heparin, the presence of hemorrhage should elicit immediate heparin reversal (1 mg protamine for each 100 units of heparin given) and low normal mean arterial pressure. (19) there are reports regard the use of heparin as an adjunct to neurointerventional procedures that can result in rapidly progressive intracerebral hemorrhages; (2) abciximab, aspirin, thienopyridinederivates are also reported. careful management of coagulation is required to prevent thromboembolic complications during and after the neurointerventional procedure. (19) when a patient may be refractory to attempts to obtain adequate anticoagulation, (19) should be considered the switching from bovine to porcine heparin or vice versa. if antithrombin iii deficiency is suspected, administration of fresh frozen plasma may be necessary to allow heparin to have its desired anticoagulant effect. (19) thrombolytic therapy with recombinant tissue plasminogen activator (rt-pa) and secondary anticoagulation with heparin to prevent rethrombosis in acute stroke patients has been shown to be beneficial in large randomized trials, (22) but the major 372 zenteno et al use of heparin in neurointervention complication of this therapy is secondary postischemic symptomatic intracranial hemorrhage (sich), (23) which can be devastating. it is necessary to detect microbleeds (mbs) or hemorrhagic transformation (ht) early and accurately, and to institute rapid treatment decisionmaking according to neuroimaging findings to prevent development of a hemorrhageprone state and improve neurologic recovery. (24–26) other complications derived from the use of heparin, is the heparin-related ich, which is rare and data are sparse regarding appropriate treatment. one reasonable approach would be to reverse heparin with iv protamine sulfate at a dose of 1 mg to 1.5 mg per 100 units of heparin with a maximum dose of 50 mg. (27,28) heparin-induced thrombocytopenia (hit) is a rare but important adverse event for heparin anticoagulation. (19)the incidence of hit in neurological patients continues to increase with expansion of indication for neurointerventional procedures. the pathophysiology of hit is related to a hypersensitivity reaction against complex platelet factor 4. (29) the diagnosis is mostly clinical and is often confirmed by laboratory testing. (29) patients with hit have a higher rate of thromboembolic complications, both arterial and venous, and with worse neurological outcomes at the time of discharge. early diagnosis and heparin cessation are essential in the management of those patients. both immediate and prolonged alternative anticoagulation are necessary. understanding of the mechanism of action, indication and drug interaction of the alternative anticoagulants (direct thrombin inhibitors, fondaparinux and danaparoid) and warfarin is essential during management of these patients. (29) often, the thromboembolic risks in the endovascular treatment of aneurisms are lesser than those found in stenting or extracranial angioplasty (3). conclusion clearly, heparin is not an innocuous molecule; indications for its use should be clearly stated in individualized patients, assessing factors such as comorbidities, age, allergic states, time for use, and clinical evolution. however heparin may be useful only in cases where the patient has prothrombotic states. as stated previously, clinical studies had lead dosage to author’s criteria, thus there is not a widely assessed dosage for heparin, especially in patients with neurovascular conditions. it is needed more unification for indication, dosage and cessation criteria. prospective studies are needed to determine the effectiveness of heparin and avoid exposing patients to potential risks. disclosure the authors have no personal financial or institutional interest in any of the drugs, materials or device describe in this article. corresponding author: marco zenteno, md instituto nacional de neurologia y neurocirurgia “manuel velasco suarez”; 3877, méxico city, méxico; mazente@me.com, dr_angel_lee@yahoo.de references 1. kaufmann tj, huston j, mandrekar jn, schleck cd, thielen kr, kallmes df. complications of diagnostic cerebral angiography: evaluation of 19,826 consecutive patients. radiology 2007;243:812–9. romanian neurosurgery (2013) xx 4: 369 374 373 2. qureshi ai, saad m, zaidat oo, suarez ji, alexander mj, fareed m, suri k, ali z, hopkins ln. intracerebral hemorrhages associated with neurointerventional procedures using a combination of antithrombotic agents including abciximab. stroke 2002;33:1916–9. 3. bracard s, barbier c, derelle al, anxionnat r. endovascular treatment of aneurisms: pre, intra and post operative management. european journal of radiology n.d. 4. gao x, liang g, li z, wei x, cao p. a single-centre experience and follow-up of patients with endovascular coiling of large and giant intracranial aneurysms with parent artery preservation. journal of clinical neuroscience 2012;19:364–9. 5. cohen je, gomori jm, itshayek e, leker rr. adjuvant use of self-expanding stents in acute atherothrombotic vertebrobasilar occlusions. journal of clinical neuroscience 2013;20:597–601. 6. cohen je, itshayek e, moskovici s, gomori jm, fraifeld s, eichel r, leker rr. state-of-the-art reperfusion strategies for acute ischemic stroke. journal of clinical neuroscience 2011;18:319–23. 7. cruz culebras a, garcía-pastor a, reig g, fuentes b, simal p, méndez-cendón jc, caniego jl, castro e, frutos r, gil a, vivancos j, gil-núñez a, díeztejedor e, egido ja, alonso de leciñana m, masjuan j. neurovascular intervention in the acute phase of cerebral infarction. neurología (english edition) 2010;25:279–86. 8. dabus g, linfante i. the natural history of acute ischemic stroke due to intracranial large-vessel occlusion: what do we know? techniques in vascular and interventional radiology 2012;15:2–4. 9. perry jm, mccabe kk. recognition and initial management of acute ischemic stroke. emergency medicine clinics of north america 2012;30:637–57. 10. singh j, nguyen tn. endovascular and neurosurgical management of acute ischemic stroke. emergency medicine clinics of north america 2012;30:695–712. 11. titomanlio l, zanin a, sachs p, khaled j, elmaleh m, blanc r, piotin m. pediatric ischemic stroke: acute management and areas of research. the journal of pediatrics 2013;162:227–235.e1. 12. elijovich l, mainali s, doss v, arthur a, watridge c. medical management of free-floating carotid thrombus. clinical neurology and neurosurgery n.d. 13. guo x-b, fu z, song l-j, guan s. local thrombolysis for patients of severe cerebral venous sinus thrombosis during puerperium. eur j radiol 2013;82:165–8. 14. gordhan a, castillo r, reino w, jani j. primary stent revascularization for critical flow-limiting middle cerebral artery stenosis presenting with rapid neurologic decline. am j emerg med 2011;29:963.e5–8. 15. jahshan s, hopkins iii ln. if you want to learn new things, read old books: cutdown techniques are well described in the old literature. world neurosurgery 2012;77:83–4. 16. park h-k, horowitz m, jungreis c, genevro j, koebbe c, levy e, kassam a. periprocedural morbidity and mortality associated with endovascular treatment of intracranial aneurysms. ajnr am j neuroradiol 2005;26:506–14. 17. qureshi ai, luft ar, sharma m, guterman lr, hopkins ln. prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: part i-pathophysiological and pharmacological features. neurosurgery 2000;46:1344–59. 18. hussein hm, georgiadis al, qureshi ai. pointof-care testing for anticoagulation monitoring in neuroendovascular procedures. ajnr am j neuroradiol 2012;33:1211–20. 19. lee cz, young wl. anesthesia for endovascular neurosurgery and interventional neuroradiology. anesthesiology clinics 2012;30:127–47. 20. hirsh j, anand ss, halperin jl, fuster v. guide to anticoagulant therapy: heparin�: a statement for healthcare professionals from the american heart association. circulation 2001;103:2994–3018. 21. brott tg, halperin jl, abbara s, bacharach jm, barr jd, bush rl, cates cu, creager ma, fowler sb, friday g, hertzberg vs, mciff eb, moore ws, panagos pd, riles ts, rosenwasser rh, taylor aj. 2011 asa/accf/aha/aann/aans/acr/asnr/cns/sa ip/scai/sir/snis/svm/svs guideline on the management of patients with extracranial carotid and vertebral artery disease: a report of the american college of cardiology foundation/american heart association task f. journal of the american college of cardiology 2011;57:e16–e94. 22. hacke w, donnan g, fieschi c, kaste m, von kummer r, broderick jp, brott t, frankel m, grotta jc, haley ec, kwiatkowski t, levine sr, lewandowski c, lu m, lyden p, marler jr, patel s, tilley bc, albers g, bluhmki e, wilhelm m, hamilton s. association of outcome with early stroke treatment: pooled analysis of atlantis, ecass, and ninds rt-pa stroke trials. lancet 2004;363:768–74. 23. intracerebral hemorrhage after intravenous tpa therapy for ischemic stroke. the ninds t-pa stroke study group. stroke 1997;28:2109–18. 24. hjort n, butcher k, davis sm, kidwell cs, koroshetz wj, röther j, schellinger pd, warach s, østergaard l. magnetic resonance imaging criteria for thrombolysis in acute cerebral infarct. stroke 2005;36:388–97. 25. kang d-w, chalela ja, dunn w, warach s. mri 374 zenteno et al use of heparin in neurointervention screening before standard tissue plasminogen activator therapy is feasible and safe. stroke 2005;36:1939–43. 26. kidwell cs, saver jl, villablanca jp, duckwiler g, fredieu a, gough k, leary mc, starkman s, gobin yp, jahan r, vespa p, liebeskind ds, alger jr, vinuela f. magnetic resonance imaging detection of microbleeds before thrombolysis: an emerging application. stroke 2002;33:95–8. 27. gurol me, greenberg sm. management of intracerebral hemorrhage. curr atheroscler rep 2008;10:324–31. 28. caceres ja, goldstein jn. intracranial hemorrhage. emergency medicine clinics of north america 2012;30:771–94. 29. alaraj a, wallace a, tesoro e, ruland s, aminhanjani s, charbel ft, aletich v. heparin induced thrombocytopenia: diagnosis and management. j neurointerv surg 2010;2:371–8. microsoft word 7dumitrescudiagnostic.doc 64 romanian neurosurgery (2010) xvii 1: 64 72 diagnostic value of silver nitrate staining for nucleolar organizer regions in cerebral astrocytic tumors gabriela – florenta dumitrescu1, anca indrei2, i. poeata3, danisia haba4, elena adinisia agrigoroae1, fl. grămadă3, dana-mihaela turliuc3 1emergency clinical hospital “prof. dr. n. oblu” iaşi, department of pathology; 2university of medicine and pharmacy “gr. t. popa” iaşi, department of morphological sciences, discipline of anatomy; 3university of medicine and pharmacy “gr. t. popa” iaşi, department of surgery ii, discipline of neurosurgery; 4university of medicine and pharmacy “gr. t. popa” iaşi, department of oro-maxillo-facial surgery, discipline of general and dental radiology abstract aim: to compare the agnor's mean number with the histological type and grade of cerebral astrocytic tumors. 16 primary cerebral astrocytic tumors (4 diffuse astrocytomas, 4 anaplastic astrocytomas and 8 glioblastomas) stereotactic biopsied in the department of neurosurgery, clinical hospital „prof. dr. n. oblu” iaşi, and histopathologically conventional diagnosed in department of neuropathology of the same hospital, were retrospectively identified. tumor specimens were submitted to a combined staining technique: one – step silver nitrate method for agnor protein sites (modified after ploton et al, 1986) counterstained with periodic acidschiff staining for basement membrane of vascular components. the mean agnor values (magnor) for tumoral and vascular nuclei were determined. the average values of mean agnors/nucleus (magnor/nucleus) presented a linear increase with increasing grade of malignancy from 1.96 for diffuse astrocytoma (gii), 2.34 for anaplastic astrocytoma (giii), to 3.18 for glioblastoma multiforme (giv). magnor/tumoral nucleus also showed a linear correlation with the histological tumor grade: 2.27 for diffuse astrocytomas, 2.78 for anaplastic astrocytomas, and 3.35 for glioblastomas multiforme. a distinct difference between the mean values of agnors/vascular nucleus was expressed: 1.52 for diffuse astrocytoma (gii), 1.90 for anaplastic astrocytoma (giii), and 3.18 for glioblastoma multiforme (giv). there were some overlaps between giii and giv astrocytic tumors regarding the magnor/tumoral nucleus: maximum value in anaplastic astrocytomas (giii) was 2.91 and minimum value in small cells glioblastomas (giv) was 2.47. differentiation could be achieved with magnors/vascular nucleus as no extreme value overlapped: maximum value in anaplastic astrocytomas (giii) was 1.99 and minimum value in small cells glioblastomas (giv) was 2.54. the malignancy grade of an astrocytic tumor can accurately be establish both on histological features of the conventional stained sample and on the average number, the shape and the distribution of agnors within tumoral and vascular nuclei, as agnors determinations supplement the histological information in small biopsies. keywords: astrocytic tumor, nucleor organizer region, tumoral grade in the practice of neurooncology it is extremely important to know the histological grade of a brain tumor and particularly of an astrocytic neoplasia. objective tumor growth potential is achieved today by immunohistochemical gabriela – florenta dumitrescu et al diagnostic in cerebral astrocytic tumors 65 methods, but there are many other cell cycle-associated molecules that are potential targets for histochemistry assessment of cell proliferation. the metaphase nucleolar organizer regions (nors) are chromosomal segments or loops (rdna) containing ribosomal genes associated with proteins. these genes are clustered in 10 loci of the human acrocentric chromosomes 13, 14, 15, 21, and 22. the transcriptional activity of these intranuclear segments plays a pivotal role in the formation of nucleoli, directing the syntesis of both ribosomes and associated proteins [5]. nors associated protein [c23 (nucleolin) and b23 (nucleophosmin)] are selectively stained by silver impregnation technique in formalin-fixed paraffin-embedded tissues. after silver-staining, the nors can be easily identified as black dots exclusively localized throughout the nucleolar area, and are called “agnors”. the expression of agnor proteins was associated with several biological properties of neoplastic cells: metabolic activity, dna content, histological grade of differentiation and, especially, the rapidity of cellular proliferation [31, 7, 26, 25]. the specific significance of agnors is not well understood. agnor quantification was used in tumor pathology as a parameter to distinguish malignant cells from benign or normal cells [11, 10, 9]. in the latest 20 years more than 400 studies was done in order to determine the correlation of agnors' quantity and quality with tumor aggressivness and rapidity of proliferation, with variable success rates that depended on tumor type [5]. a large number of papers have shown a linear correlation between agnor count and growth fraction in various human malignancies: breast cancers [32, 18], urinary bladder carcinoma [6], colorectal carcinoma [23], bone tumors [10], utererine cancer [12], endocrine cancers [22], skin cancers [2], lung cancers [28], brain cancers [8, 20]. moreover, the method can be applied to small biopsies, can identify neoplastic clones with different proliferative activities and may stratify patients into different risk groups [25]. because assessment of agnors offers an alternative approach to measure the tumor growth fraction and because there are a small number of articles dealing with agnors expression in astrocytic tumors, in this article we analyze possible correlation between agnor's morphology and agnor’s number with histological tumor grade in order to establish a possible role for it as an objective indicator of tumor biological behavior, just after the resection of a cerebral astrocytic neoplasia. material and methods selection of cases 16 primary cerebral astrocytic tumors stereotactic biopsied in the department of neurosurgery, clinical hospital „prof. dr. n. oblu” iaşi, and histopathologically diagnosed in department of neuropathology of the same hospital, were retrospectively identified. in all cases, tumor samples were fixed in 10% buffered formalin, included in paraffin, and stained with h&e according to standard procedure. 66 romanian neurosurgery (2010) xvii 1: 64 72 table 1 histological subtypes and grade of malignancy of the 16 investigated astrocytomas histological subtypes with grade of malignancy no. of cases diffuse astrocytoma (grade ii) 4 anaplastic astrocytoma (grade iii) 4 glioblastoma multiforme (grade iv) with small cells with giant cells 8 4 4 all 16 cases were histopathological diagnosed and graded according to the who classification of brain tumors [19] and divided into groups (table 1). there were 4 cases of diffuse astrocytoma grade ii (gii), 4 cases of anaplastic astrocytoma grade iii (giii), and 8 cases of glioblastoma multiforme grade iv (giv). agnor staining technique five µm thick paraffin sections, obtained from paraffin blocks with the most representative tumoral areas, were selected and submitted to a combined staining technique: one – step silver nitrate method for agnor protein sites (modified after ploton et al, 1986) [27] counterstained with periodic acid-schiff staining for basement membrane of vascular components. briefly, slides were deparaffinized in xylene, and hydrated through descending concentrations of ethanol to double distilled, deionized water. the sections were stained with freshly prepared silver colloidal solution for 25 min in a thermostatically controlled environment (37oc). the working solution contained one volume of 2% gelatine in 1% aqueous formic acid and two volume of 50% aqueous silver nitrate solution. sections were counterstained with periodic acid schiff solution, dehydrated through ascending grades of ethanol, cleared in xylene, and mounted in canada balsam. quantification of the number of agnors histological sections, stained by the exposed method, were examined by eye, using in each case olympus microscope, magnification 1000x, an oil-immersion lens, and cedarwood oil. in all cases we focused the image throughout the section thickness using at least 10 different microscopic fields in order to determine the homogeneous agnor quantitation throughout the tumor. quantification of the agnor number has always been done in well preserved cells, excluding areas of tumoral necrosis, areas with staining artifacts or overlapping cells. we analysed the dense cellular areas and those with vessels that had maximal endothelial proliferation. using the average formula we determined the mean agnor values for tumoral and vascular cells, taken individually and then together, for every histological subtype and then for every grade of malignancy. mean number of agnors for each case was defined as the ratio between total number of black dots determinated in 100 individual tumor cells and the number of analysed cells. the same ratio was done for 100 individual vascular cells. at each determinated black dot were noted the size (subjective quantified in: small, medium and large), the appearance (granular or homogeneous), and any other morphological features encountered. gabriela – florenta dumitrescu et al diagnostic in cerebral astrocytic tumors 67 results the average values of mean agnors/nucleus (magnors/nucleus) for each investigated tumor and its correlation with malignancy grades were represented in table 2. taking into account both tumoral and vascular cells, the mean values of magnors/nucleus presented a linear increase with increasing grade of malignancy of cerebral astrocytomas from 1.96 for diffuse astrocytoma (gii), 2.34 for anaplastic astrocytoma (giii), to 3.18 for glioblastoma multiforme (giv). a distinct difference between the mean values of agnors/vascular nucleus was expressed: 1.52 for diffuse astrocytoma (gii), 1.90 for anaplastic astrocytoma (giii), and 3.18 for glioblastoma multiforme (giv). the correlation between magnors/tumoral nucleus and histological subtype of glioblastoma multiforme showed a distinct difference between small cells and giant cells variants, as giant cells glioblastoma expressed higher values (3.94) than small cells subtype (2.76). the differential diagnosis between anaplastic astrocytomas and small cells glioblastomas became very difficult to determine based only on magnors/tumoral nucleus because the mean values are almost identical (2.78 versus 2.76) as there were some overlaps of magnors/tumoral nucleus between these two grades of malignancy: maximum value in anaplastic astrocytomas (giii) was 2.91 and minimum value in small cells glioblastomas (giv) was 2.47. differentiation could be achieved by association of magnors/vascular nucleus as there was no overlap between any investigated astrocytic tumor: maximum value in anaplastic astrocytomas (giii) was 1.99 and minimum value in small cells glioblastomas (giv) was 2.54 (table 3). figure 1 diffuse astrocytoma (gii): 1 to 5 small black dots in tumoral nuclei (silver impregnation method, magnification x1000) figure 2 glioblastoma multiforme (giv): tumoral nuclei with 2 to 7 medium black dots scattered across nucleus area; one nucleus with bizarre great agnor dot (arrow) (silver impregnation method, magnification x1000) 68 romanian neurosurgery (2010) xvii 1: 64 72 table 2 mean values of agnors in tumoral and vascular nuclei of cerebral astrocytomas according to their histological subtypes and malignancy grades average number of agnors/nucleus tumoral cells vascular cells whole tumor malignancy grade range group mean range group mean range group mean±s d diffuse astrocytoma (g ii) 2.14 2.26 2.31 2.38 2.27 1.43 1.45 1.53 1.54 1.52 1.78 1.92 1.96 2.18 1.96 anaplastic astrocytoma (g iii) 2.63 2.74 2.85 2.91 2.78 1.82 1.82 1.98 1.99 1.90 2.28 2.30 2.36 2.42 2.34 glioblastoma multiforme (g iv) 2.47 2.68 2.79 3.12 3.76 3.83 4.02 4.15 3.35 2.54 2.72 2.72 3.60 2.77 2.86 3.04 4.00 3.03 2.50 2.75 2.92 3.14 3.34 3.59 3.39 3.88 3.18 table 3 differential diagnosis between glioblastoma multiforme and anaplastic astrocytoma based on magnor/tumoral nucleus and magnor/vascular nucleus histological subtype anaplastic astrocytoma small cells glioblastoma giant cell glioblastoma number of agnors/ nucleus range mean range mean range mean magnor/ tumoral nucleus 2.63 2.74 2.85 2.91 2.78 2.47 2.68 2.79 3.12 2.76 3.76 3.83 4.02 4.15 3.94 magnor/ vascular nucleus 1.82 1.82 1.98 1.99 1.90 2.54 2.72 2.72 3.60 2.895 2.77 2.86 3.04 4.00 3.167 gabriela – florenta dumitrescu et al diagnostic in cerebral astrocytic tumors 69 table 4 comparison between average values of agnors /nucleus in the literature and in the present study mean number of agnors/nucleus diffuse astrocytoma (gii) anaplastic astrocytoma (giii) glioblastoma multiforme (giv) author tumoral nucleus vascular nucleus nucleus tumoral nucleus vascular nucleus nucleus tumoral nucleus vascular nucleus nucleus dumitrescu g. (2009) 2,27 1,52 1,96 2,78 1,90 2,34 3,35 3,03 3,18 janczukowic z j. (2003) [17] 1.65 2.11 2.55 choi ym et al. (1997) [4] 1.2 ±0.26 1.90 ±0.64 1.96± 0.57 hara a. et al. (1991) [15] 1,52±0,07 1,80± 0,13 1,98± 0,23 2,87 ± 0,50 2,05 ± 0,29 3,13 ± 1,13 tokunaga y. et al. (1997) [30] 2.04± 0.54 2.40±0.7 7 2.71 ± 1.13 haberland c. et al. (1996) [14] 1,73 2,81 4,56 tokiyoshi k. et al. (1992) [29] 1.68±0.8 7 1,85±1.0 3 2,76±1.2 6 pedal w.p. et al. (1994) [24] 1,98 2,84 small cells gm: 3.33 giant cells gm: 4,24 discussion analysis of the agnors' mean number is a widely accepted method for diagnostic assessment of a wide range of tumors, both on histological and cytological preparations. in 1986, ploton et al. [27] have used and improved the silver impregnation method brought in histopathological practice by goodpasture and bloom in 1975 [13]. ploton et al. suggested that the number of agnors/cell correlates with cellular activity and may be an indicator of 70 romanian neurosurgery (2010) xvii 1: 64 72 malignancy, because a great number of agnors represents a more active proliferation, and thus a more malignant cell [27]. agnors have found to be markers of proliferation in brain astrocytomas because from 1990 onwards some articles showed linear correlations between the number of agnors, proliferating cell nuclear antigen (pcna), binding index of ki-67, or mitotic rate and the histological grade [20, 3, 21, 17, 4]. several studies have been conducted on the possibility of discrimination between astrocytomas with low malignancy and those with high malignancy, using only the mean number of agnor dots per nucleus (magnor/nucleus) [16]. the present study was designed to verify the usefulness of agnors determinations in discriminating histological malignancy grades of cerebral astrocytic tumors. we found a wide range of agnors values within each histological grade, probably reflecting that well known morphological heterogeneity and biological behaviour variations of cerebral astrocytic tumors. nevertheless there was a linear correlation between mean values of agnor/nucleus and histological grade. literature review on mean number of agnors in astrocytic tumors is summarized in table 5 and data are compared with the results of the present study. it must be noted that the average values of agnors obtained in our study are in agreement with previous reports. all the authors obtained a gradual increase spectrum of the average number of agnor from diffuse astrocytomas, anaplastic astrocytoma, to glioblastomas multiforme and concluded that the number of agnors reflect the grade of malignancy in these neoplasias [17, 4, 15, 30, 14, 29, 24]. janczukowicz (2003) found a statistically significant relationship between histological grade and expression of agnor in astrocytic tumors, but he stressed the presence of a small overlapping of extreme values between astrocytomas gii and giii and between giii and giv [17]. we also observed a remarkable overlapping of the extreme values of the average number of agnor/tumoral nucleus between anaplastic astrocytomas (giii) and small cells glioblastomas (giv) probably because some of the anaplastic astrocytomas considered samples were in fact infiltration areas of a glioblastoma, the sample was too small and had no visible vessel or necrosis. thus, agnor method may be particularly useful in small specimens or in biopsies from the infiltrating edge of an astrocytic tumor, where the usual histological features of malignancy may be absent. a further distinction between these two grades of malignancy could be made if magnor/vascular nucleus is taken into account because none of the obtained values overlapped when comparing anaplastic astrocytomas with glioblastomas multiforme. hara et al. (1991) calculated magnor/vascular nucleus of astrocytomas grade ii, iii and iv (1.80±0.13, 2.87±0.50, and 3.13±1.13) and found it significantly higher than that of vascular nucleus of normal brain gabriela – florenta dumitrescu et al diagnostic in cerebral astrocytic tumors 71 without neoplastic transformation (1.26 ± 0.05) [15]. it must be noted that in the present study we did not found such great values for magnor/vascular nucleus in anaplastic astrocytoma, probably because hara et al. used 1979 who histological typing of brain tumors and we used 2000 who brain classification, where no vascular proliferation is needed to establish grade iii of malignancy for these tumors. in the present study, the presence of increased average number of magnor/vascular nucleus in anaplastic astrocytomas (giii) and, especially, in glioblastomas multiforme (giv) suggested that proliferative processes of tumor cells and vascular cells are interconnected. all these results showed that proliferative activity, both in tumoral cells and in vascular tumoral cells of the cerebral astrocytomas, increased with increasing grade of malignancy and therefore quantification of agnors is a useful marker in assessing the malignancy of these tumors. conclusion a wide range of agnor values has been observed within each histological type and grade, probably reflecting variations in the biological behaviour. the number of agnors increased gradually from diffuse astrocytomas (gii) to anaplastic astrocytomas (giii) and glioblastomas multiforme (giv). some overlaps of magnor/tumoral nucleus have been detected between anaplastic astrocytomas (giii) and glioblastomas multiforme (giv) but the cause could be a wrong diagnostic of malignancy due to the small size of the stereotactic biopsies. the average number of magnors/vascular nucleus appeared to be a more precious indicator as there was no overlap between any investigated astrocytic tumors. agnor method proved to be a useful method for histological grading as it supplemented the information obtained with conventional histological assessment. references 1. bancroft jd, gamble m. theory and practice of histological techniques, churchill livingstone elsevier, 6th edition, 2007, p. 303. 2.barzilai a, goldberg i, yulash m, pavlotsky f, zuckerman a, trau h, azizi e, kopolovic j. silverstained nucleolar organizer regions (agnors) as a prognostic value in malignant melanoma am j dermathopathol 1998; 20:473-7 3.berny w, weiser a, markowska-woyciechowska a, jarmundowicz w, zub w, załuski r. analysis of pcna, ki67, agnor and p53 expression in brain glial tumors. neurol neurochir pol. 2004; 38(6):457-463 4.choi ym, kim ty, yoon kj, moon hb, kim jm. a comparative study on mib-1, agnors and pcna expressions in astrocytic tumors. j korean neurosurg soc 1997; 26(4):476-485 5.crocker j, murray pg (eds.), molecular biology in cellular pathology, 2003, wiley, england , 2nd ed., p. 147-8 6.cucer n, imamoglu n, tozak h, demirtas h, sarac f, atila tatlısen a, öztürk f. two-dimensional agnor evaluation as a prognostic variable in urinary bladder carcinoma: a different approach via total agnor area/nucleus area per cell. micron. 2007; 38(6):674-679 7.derenzini m, trerè d. silver-stained nucleolar organizer regions (agnor). pathologica. 2001; 93(2):99-105 8.ducrot p, joundi a, diebold md, pluot m. value of the nucleolar organizers (agnor) in brain gliomas. arch anat cytol pathol 1991; 39(3):88-93 9.elangovan t, mani nj, malathi n. argyrophilic nucleolar organizer regions in inflammatory, premalignant, and malignant oral lesions: a quantitative and qualitative assessment. indian j dent res 2008;19(2):141-148 10. eslami m, baghaee f, alaeddini m. diagnostic value of silver–stained nucleolar organizer regions in osteosarcoma, fibrous dyaplasia and ossifying fibroma of the jaws. acta medica iranica, 2005; 43(4):243-248 72 romanian neurosurgery (2010) xvii 1: 64 72 11.giuffrè g, barresi v, catalano a, cappiello a, stagno d'alcontres f, tuccari g. actinic keratosis associated with squamous and basal cell carcinomas: an evaluation of neoplastic progression by standardized agnor analysis, europ j histochem 2008; 52(1):53-60 12.giuffrè g, fulcheri e, gualco m, fedele f, tuccari g. standardized agnor analysis as a prognostic marker in endometrial carcinoma, endometrioid type. anal quant cytol histol 2001; 23(1):31-9 13. goodpasture c, bloom se. visualization of nucleolar organizer regions in mammalian chromosomes using silver staining. chromosoma 1975; 53(1):37-50. 14.haberland c, martin h, guski h, hufnagl p, vogel s. agnor analysis of astrocytoma in childhood. zentrallbl neurochir. 1996; 57(1):5-11 15. hara a, sakai n, yamada h, hirayama h, tanaka t, mori h. nucleolar organizer regions in vascular and neoplastic cells of human gliomas. neurosurg 1991; 29(2):211-5 16.hashmi iu, bukhari mh, tayyab m, qureshi irfan zia, naseer a chaudrhy, sabiha riaz. evaluation of nucleolar organizer region in normal brain tissues and astrocytic gliomas. biomedica 2006; 22(1):41-7 17.janczukowicz j. the prognostic role of proliferation activity in human cns tumors: the determination of agnor, pcna and ki-67 expression. part 1: agnor expression in cns tumors. folia neuropathol 2003; 41(2):97-101 18. kidogawa h, nanashima a, yano h, matsumoto m, yasutake t, nagayasu t. clinical significance of double staining of mib-1 and agnors in primary breast carcinoma anticancer res. 2005; 25(6b):3957-62 19.kleihues p, cavenee wk (eds.): world health organization classification of tumours. pathology and genetics of tumours of the nervous system. iarc press: lyon 2000 20.korkolopoulou p, christodoulou p, papanikolaou a, thomas-tsagli e. proliferating cell nuclear antigen and nucleolar organizer regions in cns tumors: correlation with histological type and tumor grade. am j surg pathol 1993; 17:912-9 21.koyuncuoğlu m, yücesoy k, cingöz s, canda mş, çabuk m, akta s. pronostic parameters in astrocytoma: p53 and c-erbb2 immunoreactivity, pcna, and agnor count. türkish neurosurgery 1999; 9: 85-91 22.lumachi f, ermani m, marino f, poletti a, basso smm, iacobone m, favia g. relationship of agnor counts and nuclear dna content to survival in patients with parathyroid carcinoma, endocr relat cancer 2004; 11:563-569 23.öfner d, riedmann b, maier h, hittmair a, rumer a, tötsch m, et al. standardized staining and analysis argirophilic nucleolar organizer region associated proteins (agnors) in radically resected colorectal adenocarcinoma – correlation with tumor stage and long-term survival. j pathol 1995; 175:427-441 24.pedal wp, warzok rw, hufnagl p, roth k. nucleolar organizer regions (agnors) in astrocytic tumors. zentralblatt pathol, 1994, 140(1): 89-94 25.pich a, chiusa l. margaria e, prognostic relevance of agnors in tumor pathology. micron. 2000; 31(2):133-41 26.pich a, margaria e, chiusa l. significance of the agnor in tumor pathology. pathologica 2002; 94(1):29 27.ploton d, visseaux – coletto b, canellas jc, bourzat c, adnet jj, lechki c, bonnet n. semiautomatic quantification of silver stained nucleolar organizer regions in tissue sections and cellular smears. anal quant cytol histol cytology 1992, 14(1):14-23 28.rodriguez or, antonangelo l, yagl n, minamoto h, schmidt af, capelozzi vl, goldenberg s, saldiva phn. prognostic significance of argyrophilic nucleolar organizer region (agnor) in resected non-small cell lung cancer (nsclc) jpn j clin oncol 1997; 27(5):298-304 29.tokiyoshi k, yoshimine t, maruno m, nokagawa h, iwata y, kuroda r, hayakawa t. the analysis of nuclear organizer regions of astrocytomas with various histologic malignancies, no to shinkei-brain and nerve, 1992, 44(12): 1083-1086 30.tokunaga y, khalid h, hiura t, shibata s. proliferation of human intracranial neoplasm assessed with ki-67 (mib-1) labeling index and argirophilic nucleolar organizer regions. acta med nagasaki 1997; 42:44-50 31.trerè d. agnor staining and quantification. micron 2000; 31(2):127-31 32.trerè d, ceccarelli c, montanaro l, tosti e, derenzini m. nucleolar size and activity are related to prb and p53 status in human breast cancer, j histochem cytochem 2004; 52:1601-1607 microsoft word 7iacobg_largeandgiant.doc romanian neurosurgery (2010) xvii 3: 305 – 312 305 large and giant vestibular schwannomas g. iacob, m. craciun clinic of neurosurgery, universitary hospital bucharest romania motto: “if any neurologic surgeon were asked to name the most difficult tumor to extirpate, his answer would doubtless to be the acustic tumor” dandy (1) abstract background: the main objective in treating large and giant vestibular schwannomas (vs) (large diameter exceeding 3.5 cm and giant diameter exceeding 4.5 cm) is their complete removal without significant morbidity. our experience on 7 cases (4 females, 3 males, mean age 42.5 years) with marked brainstem compression, operated between 2004-2009 focuses on factors influencing recurrence and morbidity, especially related to facial nerve function. these patients were included in a series of 32 consecutive vestibular schwannoma excisions. methods: this report is a retrospective analysis of the surgical outcome of 7 patients with large and giant vs using the retrosigmoid-transmeatal approach. several prognostic factors were evaluated: patient age, tumor size and consistency, extent of surgical removal, concurring hydrocephalus, hearing loss, facial nerve function, trigeminal nerve deficits, cranial nerve vi, ix and x palsy, tongue edema, ataxic gait and motor deficits. results: the mean age was 42.3 years, the mean tumor diameter was 51.8 mm. there were no deaths and the tumors were histologically benign. extensive microscopic tumor resection was performed in 5 cases related to solid tumor’s consistency. preoperatively hearing loss and high intracranial pressure were encountered in all patients. 4 patients had cerebellar ataxia. facial anatomical continuity was preserved in 6 cases with solid tumor consistency; 4 patients had a preoperative facial palsy, a good facial nerve function was achieved in 3 cases – housebrackmann grade i/ii. we have met other distinctive signs: cranial nerve v hypoesthesia, vi, ix and x palsy, tongue edema in 2 cases with slight contralateral motor deficit. all patients were clinical and mri monitored at 3, 6 and 12 months postoperatively. conclusion: total resection associated with a low morbidity rate is possible, avoiding recurrence, reintervention and severe scar tissue. in cases with subtotal resection, radiosurgery is recommended to improve outcome. keywords: large and giant vestibular schwannomas (vs), surgical approach, facial nerve function introduction the progress of neurosurgery as a specialty is related to the history of a vestibular schwannoma (vs) – the more accurate term of the classical acoustic 306 g. iacob, m. craciun large and giant vestibular schwannomas neuroma, suggesting the tumor origin from the superior (upper) division of the vestibular nerve, not from the cochlear (also known as the acoustic) nerve (2). microsurgical removal of large and giant vs is a daunting task to surgeons, presenting a greater challenge in the quest for total removal based on a clear surgical strategy, functional cranial nerve preservation and avoidance of any complications (3-8). for vs larger than 3 cm, associated with significant compression of the brainstem, gamma knife therapy cannot be used because of the need to program more than one isocenter for the radiation dose, exposing normal neural tissue to excess amounts of radiation (5)(9). we have made a retrospective analysis of the surgical outcome of 7 patients with large and giant vestibular schwannomas operated using the retrosigmoidtransmeatal approach. material and methods from 2004-2009, 32 consecutive vs resections were performed by the senior author (g.i.) using the retrosigmoidtransmeatal approach. inclusion criteria were all vs larger than 3 cm in size, corresponding to grade iv koos classification. we have identified in a review of the operations 7 cases with large or giant vs: 4 females, 3 males, mean age 42.5 years (ranging from 38-68 years). preoperative hearing loss the threshold retained for useful hearing was 60 decibel – norstadt classification for audiometric hearing (10) and high intracranial pressure with obstructive hydrocephalus were encountered in 2 patients. 4 patients (57.14%) had cerebellar ataxia; 5 patients (71.42%) had facial numbness, paresthesia; 4 (57.14%) patients had a preoperative facial palsy; 3 (42.8%) patients had swallowing difficulties and contralateral motor deficit was observed in 2 (28.57%) patients all patients underwent ct, mri t1 weighted imaging before and after gadolinium (gd ) administration and t2 – weighted imaging pre and postoperative; measurements were made on the largest diameter of the tumor excluding intracanalicular components. tumors classified as large presented a diameter above 3.5 cm, whereas the diameter of giant tumors exceeded 4.5 cm. there were 4 (57.14%) cases with giant tumors and 3 (42.85%) cases with large tumors (mean tumor diameter was 51.8 mm). the tumor’s consistency was classified as solid or cystic using t1 and t2 – weighted image with gd administration. we found that 28.5% of vs (2 cases) included in our study contained cystic elements. surgery was performed using the retrosigmoid – transmeatal approach in the lateral decubitus. in 2 cases a temporary shunt was placed intraoperatively to relieve hydrocephalus. a retrosigmoid suboccipital craniotomy of 4 cm diameter was made to expose the posterior part of the sigmoid sinus and the inferior part of the transverse sinus. we favor such an approach for the following arguments: a wider field of action, direct visualization of anterior inferior cerebellar artery (aica) and other brain stem vessels, dissection of all surfaces of the acoustic tumor always under direct vision, identification of the facial nerve in the lateral angle of the internal auditory canal, ready access to the facial nerve when either anastomosis or graft reconstruction may be necessary. the surgical technique was based on internal tumor debulking made in a romanian neurosurgery (2010) xvii 3: 305 – 312 307 systematic fashion. the ultimate goal of vs surgery being cranial nerves preservation, tumor removal is merely a byproduct. the surgical steps after dural opening tangent to sinuses are: -cisterna magna opening to allow cerebellar retraction, made by applying a single broad malleable blade from below upwards -identification of the double arachnoid membrane protecting the cerebellum, lower cranial nerves, anterior inferior cerebellar artery (aica) -the tumor capsule is separated from the cerebellum and the inferior tumor part is elevated from the lower cranial nerves and brain stem -centrifugal, rapid, tumor debulking, to shrink tumor using tumor forceps, dissector (cusa may perforate the arachnoid layer and damage the neural vasculature!); it’s better to leave a shelf of tumor “capsule” all around to avoid injury to all structures outside it -the tumor is further separated at the upper pole from the trigeminal nerve and pons -the meatus acusticus internum is exposed in two stages: drilling away the back wall, carrying out the remaining upper tumor; optional drilling the fundus. it is mandatory to avoid the semicircular canals (laterally) and the jugular bulb (inferiorly) whilst drilling; copious water irrigation whilst canal drilling to prevent thermal injury to vii & viii complex; stripping the dura from canal; waxing bone edges to keep the field bloodless; placement of muscle patch in iac after tumor removal to prevent csf leak -fine dissection close to nerves the remainder is separated from the facial nerve, brain stem, abducens nerve using a water-jet dissection. in our series, the facial nerve was displaced over the medial aspect of the tumor. dissection was made bidirectional from the medial and lateral direction meeting near the meatus acousticus internum where most adherences are to be seen. a small part of the capsule attached to the nerve should be leaved. several blood vessels should be preserved: internal auditory artery, aica and its branches – the most displaced vessel, sca, brain stem perforators; also the petrosal and mesencephalic veins. -dura is closed watertight using a wet fibrinoid-based collagen fleece (tachocomb), bone flap is refixed. -for extensive adherences of the tumor to the facial nerve and also to the brainstem in 2 (28.57%) cases a partial tumor removal was performed; no bipolar coagulation was used for hemostasis in this situation: applying a cottonoid, a gelfoam or surgicel is temporarily sufficient. trauma to arachnoidless brain stem surface can be predicted on pre-op ct/mri. possible postoperative complications could be induced by: forceful retraction of a densely adherent tumor, traction on the bridging vessels wich may lead to intra-pontine hemorrhage and coagulation of perforators that can induce brain stem infarction. to avoid such complications, tumor feeders should be coagulated and sectioned where they enter the tumor; also staying within the tumor arachnoid holds the key. functional outcome was measured using the karnofsky scale at 3, 6, 12 months postoperatively. several prognostic factors were evaluated: patient age, tumor size and consistency, extent of surgical removal, concurrent hydrocephalus, hearing loss, facial nerve function according to housebrackmann scale, trigeminal nerve deficits, 308 g. iacob, m. craciun large and giant vestibular schwannomas cranial nerve vi, ix and x palsy, tongue edema, ataxic gait, motor deficits. results extensive microscopic tumor resection was performed in 5 (71.42%) cases; diagnosis was confirmed by histopathology in all cases. there were no deaths and the tumors were histological benign (figure 1). partial tumor removal was performed for 2 cystic tumors were the arachnoidal plane was poorly defined, with severe adherences to brainstem and facial nerve, extensive bleeding and cerebellar edema. facial nerve anatomical continuity was preserved in 6 (85.71%) cases with solid tumor consistency and a good facial function was achieved in 3 (42.85%) cases house brackmann grade i/ii. for 4 (57.14%) patients with giant vs, the facial nerve deficit worsened postoperatively with respect to house-brackmann grading scale by iii grades, the face was rehabilitated with plastic surgery techniques. we have noticed a rapid tumor growth, short symptom duration and facial nerve involvement in 2 cystic tumors were a partial resection was performed. the karnofski score at discharge was superior to 80%. the major complications in this series were: 3 (42.85%) patients with cranial nerve v hypoesthesia, 5 (71.42%) patients with increased facial numbness, 4 (57.14%) patients with transient vi, ix and x palsy, tongue edema and 2 (28.57%) cases with contralateral motor deficit. these patients recovered well within 6 months after operation. in 2 cases with partially resected cystic tumors, at 12 months after the operation we have noticed on ct and mri the same dimensions of the tumor remnants. figure 1 preoperative cerebral ct showing giant vs (51 mm) with obstructive hydrocephalus (a-c); postoperative cerebral ct after 1 year follow-up showing complete resection (d, e); another case with giant vs (57 mm) showing pre and postoperative ct romanian neurosurgery (2010) xvii 3: 305 – 312 309 discussion vs are typically slow growing, benign skull base tumor of cerebellopontine angle, with natural unpredictable evolution and annual growth rate between 0.2-2 mm; they originate from the intracanalicular part of the vestibular nerve, in the region of the transition zone between central and peripheral myelin (2). while vs was first described by eduard sandifort in 1777, the first successful surgical removal was achieved by sir charles balance in 1894, cited by (2). several neurosurgical pioneers made major advancements in managing this usually benign skull base tumor: f. krause who introduced the retrosigmoid approach to the cerebellopontine angle and h. cushing who advocated for subtotal removal and was the first to reduce mortality from 50 to 7.7% cited by (11). w. dandy (1) recommended total excision with meticulous capsule dissection as goal of surgery in order to prevent recurrences, with an acceptable low mortality of 2.4%. in 1967 olivecrona (12) proposed to preserve the facial nerve, achieving this in 20% of his 304 patients with a total tumor removal in 217 patients and a mortality rate rising up to 23%. the translabyrinthine approach was adopted by panse in 1904 cited by (2) as a method to achieve tumor removal preserving the facial nerve. in 1964 house (13) introduced operating microscope for translabyrinthine approach and in 1965 rand and kurze cited by (2) were the first to introduce an operating microscope for the transmeatal posterior fossa approach. yasargil (14) improved the microsurgical technique, emphasizing the importance of the brain stem arterial supply and the need to optimize the preservation of facial nerve function. these technical advances have led to a 50% reduction in mortality, a rate of complete tumor removal reaching 85% and to a successful anatomical preservation of the facial nerve in 80% of the cases. the management of vs has evolved significantly with the advent of new radiological diagnostic procedures (high resolution ct, multiplanar mri) that allow early diagnosis of small and medium size vs; safe, modern anesthesia, development and refinements in the microsurgical techniques, neurophysiological intraoperative monitoring and working in multidisiplinary teams have led to a dramatic improvement in clinical outcome, with an operative mortality of around 1% and a rate of total tumor removal close to 95% (2-9)(15-24). in some expert hands: koos w. (18), rhoton al. (21), samii m. (2)(6), noren g., regis j., pellet w., cannoni m. – cited by (11), the preservation of useful hearing (gardner-robertson 1 or 2) has been achieved in selected small lesions with very good preoperative hearing and also the possibility of preserving normal facial motor function in many cases (housebrackman 1 or 2). although surgical procedures could be complex and difficult, even in large and giant vs compressing the brainstem, a complete tumor removal has become the rule in many cases, preserving all cranial nerves in exceeding numbers, without additional morbidity or mortality. in many cases the viith nerve may be so thin that it could be be confused with the arachnoid when very severely compressed. there are various anatomical relationships encountered during resection; nerve stimulator, electrophysiology may allow a gentle separation of vii nerve from tumor 310 g. iacob, m. craciun large and giant vestibular schwannomas by using micro dissector & sharp arachnoid dissection (6)(7)(18). brainstem compression, even brainstem dislocation, cerebellum and severe fourth ventricle compression can produce ventricular dilatation; the vii & viii complex, lower cranial nerves severely stretched occur in large or giant vs (10)(18). the most common clinical signs (5) are: cophosis, cerebellar ataxia, symptoms of raised intracranial pressure (headache, papilledema) and symptoms of normal pressure hydrocephalus in elderly (gait disturbance, dementia and incontinence). in our series a temporary shunt was placed intraoperatively to relieve hydrocephalus in 2 cases; generally the need of a preoperative shunt was as high as 66% in ancient series (14), others consider shunting rarely required because total surgical excision is sufficient (7). the approach is controversial: many surgeons prefer the retrosigmoid approach in the sitting, semi-sitting or lateral position (2-8)(15)(17-19)(21)(23). however sami (6) reported a high incidence of hematoma after retrosigmoid removal of cystic tumors in the semisitting position, as well as air embolism irrespective of anesthetic monitoring measures taken to prevent this complication. in the lateral position the peritumoral veins may generate intraoperative bleeding (5). the translabyrinthine approach is advocated by ent surgeons for good tumor exposure with minimal retraction of the cerebellum, early facial nerve identification and eases the repair of the facial nerve when it is transected (5)(13)(15)(16)(20)(24)(25). the disadvantages of the translabyrinthine approach (4) are: longer operating times, higher rates of postoperative facial paralysis and the risk of cerebrospinal fluid leak. in large vs, anderson (3) described a combined translabyrinthine-retrosigmoid approach especially for more lateral giant tumors that extend to the fundus of the iac. the rates of preserving good facial nerve function are similar among the retrosigmoid, translabyrinthine and middle fossa approaches in large vs: 42-52.6% with early identification of the root entry/exit zone and caution in tumor excision in the extrameatal region just outside the porus acusticus (5). only 18% of operated patients have excellent facial nerve function (house-brackmann grade i/ii) explained by the bad initial clinical status, the tumor size and the lack of systematic intraoperative facial monitoring (5)(8)(17)(19)(23). according to sami (6) facial nerve anatomical results (of 200 cases of grade t4 vs, total removal was achieved in 98% and anatomical facial nerve preservation was possible in 98,5%) were not correlated with functional results, while size was well correlated with facial function. even when the facial nerve is left anatomically intact, surgical interventions can have esthetic and functional consequences which greatly reduce the quality of life (4). removal of large and giant residual or recurrent vs is more difficult due to scar tissue and the absence of a clear arachnoid plane between tumor and brainstem, vessels, and nerves even for the most experienced surgeon (11,18). when excision is incomplete, the recurrence rate is usually high, depending of vs cellularity and vascularisation (7). recurrence rate reported was of 0-3.9% for gross total removal; 9.4-29% for near total resection as a result of surgical devascularization and 25-65% for subtotal resection, especially in romanian neurosurgery (2010) xvii 3: 305 – 312 311 the midcerebellopontine angle after the translabyrinthine approach (24). vestibular schwannomas can relapse 10-15 years postoperatively (10% of patients) even when surgeons have the impression that these have been completely removed (4). the growth rate of residual or recurrent vs is unpredictable: most authors reported a very low recurrence rate after complete tumor excision; however, a higher recurrence rate after subtotal removal has also been observed in 44-53% of patients (5). in cystic tumors (26) a rapid tumor growth with possible vascular compression led to a less favourable outcome than solid tumor, also some tumor remnants may not grow. also cystic vs demand careful dissection and may be subtotally resected for various reasons: the arachnoid plane is not easily preserved as it is densely adherent to the surrounding structures; the cranial nerves are displaced in a relatively uncertain position; cyst formation may predict a more intimate involvement of the neural tissue; high tendency to postoperative bleeding; dissection of the facial nerve from the tumor is more difficult (5)(6)(22). for subtotal tumor debulking confirmed by mri at 3 months, 6 months to 1 year postoperatively, the alternatives are (5)(6)(9)(17)(22)(26): -planned staged approaches – first tumor debulking via a retrosigmoid approach followed by a second stage translabyrinthine resection of the residual tumour -wait and see – in case a a small and stable residual tumor in elderly patients -subtotal tumor debulking followed by stereotactic radiotherapy which can offer excellent facial nerve function in 85.7% patients with house-brackmann grade i/ii (1) and tumor growth control. at the time of radiosurgery the tumor size is diminuished < 20 mm and radiosurgery could be made with a peripheral dose 11-13 gy and in the tumor centre the dose should be 22-26 gy. conclusion vs is a benign tumor in a malignant location (2). progressive improvement in the results of vs surgery was possible owing to: better clinical preoperative deficits evaluation, tumor size (the smaller the tumor, the better the outcome !), imaging innovations, intensive care, intraoperative monitoring, advent of microsurgery and of course increasing surgical experience (6-8)(18). complete vs removal at one stage while preserving neurological functions and the quality of life should be the optimal treatment, thus avoiding recurrency, reintervention and severe scar tissue. for large and giant vs the optimal treatment should be tried; however an alternative could be the combined staged therapy: subtotal intracapsular resection relieving mass effect and brainstem compression at the first stage, follow-up and stereotactic radiosurgery at a second stage for the residual tumor. references 1.dandy w.e. results of removal of acustic tumors by the unilateral approach, a.m.a. arch. surg. 1941, 42: 1026-1043 2.samii m. – vestibular schwannomas, sindou m. practical handbook of neurosurgery, springer wien new york, 2009, 333-345 3.anderson d.e., leonetti j., wind j.j. et al. – resection of large vestibular schwannomas: facial nerve preservation in the context of surgical approach and patient assessed outcome, j.neurosurg. 2005, 102 (4): 643-649 4.fuentes s., arkha y., et al. – management of large vestibular schwannomas by combined surgical resection and gamma knife radiosurgery, in regis j., 312 g. iacob, m. craciun large and giant vestibular schwannomas roche p.h. modern management of acustic neuroma, karger 2008, 79-82 5.laghmari m., ouahabi a. el., derraz s., khamlichi a. el. – treatment of large vestibular schwannomas: towards a compromise between recurrence and facial function preservation, pan arab journal of neurosurgery, 2009, vol.13, 1: 31-39 6.samii m., gerganov v., samii a. – improved preservation of hearing and facial nerve function in vestibular schwannoma surgery via the retrosigmoid approach in a series of 200 patients, j. neurosurg 2006, 105: 527-535 7.turel k.e. – surgical techniques & pitfalls in acustic neuroma, romanian neurosurgical congress, timisoara 2003. 8.yamakami i., uchino y.,kobayashi e. et al. – removal of large acoustic neurinomas (vestibular schwannomas) by the retrosigmoid approach with no mortality and minimal morbidity, j. neurol neurosurg psych 2004, 75: 453-458 9.lunsford l.d, niranjan a., flickinger j.c., maitz a., kondziolka d. – radiosurgery of vestibular schwannomas: summary of experience in 829 cases, j. neurosurg. 2005, 102 (suppl): 195-199 10.malis li – nuances in acoustic neuroma surgery, neurosurg. 2001, 49: 337-341 11.regis j. et al. introduction, in regis j., roche p.h. modern management of acustic neuroma, karger 2008, 1-5 12.olivecrona h. acustic tumors, j. neurosurg 1967, 26: 6-13 13.house w.f. translabyrinthine approach, in house w.f., luetje c.m. (eds) acustic tumors, baltimore, university park press 1979, 43-87 14.yasargil m.g. et al. microsurgical approach to acoustic neuromas, adv. tech. stand. neurosurg. 1977, 4, 93-129 15.briggs r.j., fabinyi g., kaye a.h. – current management of acustic neuromas: review of surgical approaches and outcomes, j.clin neurosci 2000, 7: 521-526 16.day j.d., chen d.a., arriaga m. – translabyrinthine approach for acoustic neuroma, neurosurgery 2004, 54: 391-395 17.iwai y., yamanaka k., ishiguro t. – surgery combined with radiosurgery of large acoustic neuromas, surg. neurol 2003, 59: 283-289; discussion: 289-291. 18.koos w.t., matula c., lang j. – color atlas of microneurosurgery of acustic neurinomas, thieme, 2002, 184-190. 19.jung s., kang s.s., kim t.s. et al. – current surgical results of retrosigmoid approach in extralarge vestibular schwannomas, surg. neurol 2000, 53: 370-377; discussion 377-378 20.mamikoglu b., wiet r.j., esquivel c.r. – translabyrinthine approach for the management of large and giant vestibular schwannomas, otol neurotol 2002, 23: 224-227 21.rhoton a.l. jr. – the cerebellopontine angle and posterior fossa cranial nerves by the retrosigmoid approach, neurosurgery 2000, 47: s93-s129 22.ricardo r., neto m.c. et al. treatment of large and giant residual and recurrent vestibular schwannomas, skull base 2007, 17(2): 109-117. 23.seol h.j., kim c.h.,park ck et al. – optimal extent of resection in vestibular schwannoma surgery: relationship to recurrence and facial nerve preservation, neurol med chir (tokyo) 2006, 46: 176-180; discussion 180-181 24.sluyter s., graamans k,tulleken c.a. et al. – analysis of the results obtained in 120 patients with large acoustic neuromas results obtained in 120 patients with large acoustic neuromas surgically treated via the translabyrinthine-transtentorial approach, j. neurosurg 2001, 94: 61-66 25.brackmann d.e., cullen r.d., fischer l.m. – facial nerve function after translabyrinthine vestibular schwannoma surgery. am otolaryngol head neck surg 2007, 136: 773-777 26.wandong s., meng l., xiangang l. et al. – cystic acoustic neuroma, j.clin neurosci 2005, 12: 253-255 microsoft word 6.breharfm_induction_f.docx romanian neurosurgery (2011) xviii 4: 425 433 425 induction of differentiation inhibits the tumorigenic potential of glioblastoma cancer stem cells f.m. brehar1, a.v. ciurea1, r.m. gorgan1, coralia bleotu2, a. tascu1, r.i. radulescu1, lilia matei2, otilia zarnescu3 1neurosurgical clinic, emergency clinical hospital “bagdasar-arseni” 2“stefan s nicolau” institute of virology, bucharest, romania 3faculty of biology, university of bucharest, bucharest, romania abstract the outcome of the patients with newly diagnosed glioblastoma remains dismal, despite the use of surgery, radiotherapy and adjuvant temozolomide and while new agents like anti-angiogenic agents seem to offer some promise, a new approach is needed. recent studies suggest that cancer stem cells (cscs) may play an important role in malignant gliomas invasion and proliferation. therefore, cscs became new therapeutical targets, and one of the main experimental therapies which could be used against cscs is the differentiation therapy. the purpose of this study was to characterize the cscs isolated from glioblastoma samples, to assess in vivo the tumorigenic potential of these cells and to induct the differentiation of the cscs. the changes in invasive markers (matrixmetalloproteases-mmps, cadherins and cathenins) expression were assessed. cscs exposed to differentiation inductor factors have been inoculated in nude mice and their tumorigenic potential has been evaluated. the stemness biological feature was correlated with increased of mmps, cadherins, catenin expression and with tumour contra-lateral invasion. the expression of mmps, cadherins and cadherins decreased after exposure of the cscs cultures to the differentiation inductor factors. in vivo experiments demonstrated the inhibition of tumorigenic potential of differentiated cscs cultures. in conclusion, differentiated cscs showed a decreased expression of invasive markers in vitro and lost their tumorigenic potential in vivo. keywords: glioblastoma, cancer stem cells, xenografts, differentiation therapy. introduction malignant brain tumors remain severe diseases with a dismal prognosis despite the modern multimodal therapeutically management (5). for example in glioblastoma, the mortality is 100% and the medium period survival is approximately 12 months (27). embryonic stem cells could suffer several genetic mutations during specific proliferation phase of ontogenesis (12). these genetic mutations could lead to early development of various types of cancer early during childhood (8). conversely, the adult stem cells could bear specific genetic mutation, and they can transform into cancer stem cells which secondary lead to oncogenesis (13). isolation and characterization of cancer stem cells (cscs) from human 426 f.m. brehar et al inhibition of tumorigenic potential in glioblastoma glioblastoma opened new opportunities in glioblastoma research and could offered alternative therapies for this severe disease (16; 14). the cancer stem cells theory proposes that transformed neural stem cells could be the origin of gliomas (10). in adult brain, neural stem cells are located mainly in two important regions: hippocampus and periventricular region. adult human subventricular zone of brain is composed of several important layers: deep subcortical white matter, a periventricular ribbon of cells that can function as neural stem cells, a dense layer of astrocytic processes and the ependymal lining. astrocytes from the subventricular zone exhibit a unique capacity for multipotency and self-renewal in vitro. the cancer stem cells theory proposed that tumoral transformation of the neural stem cells occurring at the periventricular zone, followed by migration of these transformed cells throughout brain parenchyma could be at the origins of gliomas (10). recent studies demonstrated that cscs represent a very important tumor cell population, responsible for chemotherapeutic and radiotherapeutic resistance, because these cells secrete multi drug resistance proteins (like breast cancer resistance protein-1 (bcrp1) (6). therefore cscs become now one of the main attractive therapeutically targets within the multimodal management of glioblastoma (1). according to vescovi et al., induction of differentiation of cscs, using bmp-4 molecule, is able to inhibit the tumorigenic potential of these cells (15). this strategy, called differentiation therapy, which has been initially used in malignant hemophaties (9; 11; 21) could represent in the future an important alternative therapy for glioblastoma. the purpose of this study was to assess in vitro the expression of invasive molecules like mmps and in vivo the tumorigenic potential of the cscs after exposing the cscs cultures to differentiation inductor factors. materials and methods cell cultures tumors from patients with confirmed glioblastoma multiforme (gbm) were mechanically and enzymatically dissociated and grown in neural stem cell expansion medium to generate neurospheres (dmem supplemented with 10-20ng/ml fgf; 10-20 ng /ml egf; 1x b27; 1xn2). u87 line was purchased from the european collection of animal cell cultures (ecacc no. 89081402). flow cytometry 5 x 105 cells were collected, washed twice in pbs, 0.1% bsa, and then cells were incubated for 1 h with monoclonal antibody cd133/2-pe, cd 45 (miltenyi biotec, germany), o4 and a2b5. the labeled cells were analyzed using a beckman coulter epics xl flow cytometer. ten thousand events were acquired and data were analyzed with flowjo software. positive cells were determined as percentages of gated cells. microarray experiments microarray analysis was performed using agilent technology according to one-color microarraybased gene expression analysis, version 5.5 / february 2007. we used microarray slides whole human genome oligo microarray with sureprint technology 4 x 44 k. the changes in the expression level of mmps, cadherins and cathenins have been assessed. induction of differentiation of cscs glioblastoma derived cscs cultures where exposed to dmem supplemented romanian neurosurgery (2011) xviii 4: 425 433 427 with fetal serum (10%) and several known differentiation inductor factors like bdnf, nt3 and all-trans retinoic acid (atra) which is known as a potent inductor of differentiation of cellular precursor in several malignant hemopathies (26), at different concentration levels. the effects of differentiation of cscs were assessed in vitro, by evaluating the morphology of cscs cultures and microarray expression of invasive markers. cscs exposed to the differentiation factors have been inoculated in nude mice and their tumorigenic potential has been assessed. in vivo tumor model three groups including 24 nude mice, 8–10-weeks-old (crl: cd-1-foxn1nu; charles river breeding laboratories, germany) were used in experiments. animals were anesthetized by intraperitoneal injection of xylazine and ketamine. mice were held in a stereotactic frame with ear bars (taxic-600, world precision instruments) and received stereotactically guided injections over 3 min into right forebrain. first group of eight animals received 5 x 105 cells of u87 culture in a volume of 3 μl pbs. the second group of eight animals received 2 x 105 cells of glioblastoma derived cscs culture in a volume of 3 μl pbs. the growth pattern of glioblastoma cscs xenografts were compared with u87 xenografts. in order to assess the effects of differentiation of cscs, glioblastoma derived cscs cultures exposed to fetal serum (10%) + differentiation inductor factors have been inoculated (2 x 105 cells) in the third group of 8 mice. all the surgical and experimental procedures involving animals were approved by the institutional animal care and use committee, in accordance with romanian governmental guidelines for ethics in animal experiments. histology mice bearing intracranial human glioblastoma xenografts were sacrificed at 21 and 28 days (first group) and at two months (second and third group) after cells implantation. brains were removed and were fixed in bouin solution or 4% paraformaldehide in pbs, dehydrated in ethanol, cleared in toluene and embedded in paraffin. about 6 �m-thick horizontal sections were used for hematoxylin and eosin (h&e) staining. the photomicrographs were taken by digital camera (axiocam mrc 5, carl zeiss) driven by software axio-vision 4.6 (carl zeiss). results in vitro results we initiated several primary cultures from glioblastoma samples using special medium for neural stem cells cultures. the medium was changed every 3 days. cells survived in cultures but the proliferation rate was low. the cells in the cultures organized in clusters similar to neurospheres, which are the morphological hallmarks of neural stem cells (figure 1 a, b). cells cultures obtained from malignant gliomas samples expressed stem cells and oligodendrocyte markers at different levels (table 1). however, all cultures expressed neural stem cells markers (especially cd133) at higher levels compared with u87 line (table 1, figure 2). in vivo results u87 developed intracranial xenografts with a specific growth pattern. the u87 xenografts were compact, round-shape, with no sign of infiltration of surrounding brain parenchyma (figure 3 a, b). the size of the xenografts was in accordance with literature data. 428 f.m. brehar et al inhibition of tumorigenic potential in glioblastoma at 28 days the u87 xenografts were voluminous, occupying more then a half of cerebral hemisphere (figure 3b), which appeared bulge and expanded at macroscopic examination. the detailed growth pattern of u87 xenografts has been described elsewhere by the authors (7, 24). a b figure 1 a, b neurospheres in glioblastoma derived cells cultures grown in special stem media: dmem: f12 supplemented with 10 ng/ml fgf, 20 ng/ml egf, n2, b27, at 370c (ob 20x) table 1 expression of neural stem cells markers (cd133, o4) and oligodendrocyte markers (a2b5, o4) in cells cultures culture cd133 o4 a2b5 u87 2,56 5,51 20,24 ston 39,57 2,09 13,97 faio 10 29,82 3,84 70,38 barb8 12,25 0,86 12,56 figure 2 expression of stem cells markers cd 133, cd 45 and o4 in cells cultures barb ston romanian neurosurgery (2011) xviii 4: 425 433 429 figure 3 u87 xenograft at 21 days (a) and 28 days alter inoculation. h&e staining the glioblastoma derived cscs induced xenografts with a different growth pattern. unlike u 87 xenograts, the cscs xenografts exhibits a more infiltrating pattern (figure 4). figure 4 cscs xenograft infiltrating the corpus callosum (arrow) in one specimen (a). voluminous cscs xenograft which infiltrates the opposite emisphere through the corpus callosum, in another specimen (b). h&e staining interestingly, migratory tumor cells were found at distance from the cscs xenografts, infiltrating surrounding brain parenchyma (figure 5 a) or even the white commissural fibers (figure 5 b). induction of differentiation of cscs – results important changes in cultures phenotype has been noticed at approximate 24-48 hours after exposure of the cells cultures to fetal serum and differentiation inductor factors. tumor cells lost their ability to form neurospheres and acquired a fibroblastic phenotype very similar to the morphology of standard glioblastoma lines (figure 6). the cscs cultures express mmps, cadherins and cathenins at higher level (up to ten times) compared with the fibroblastic aspect of the same cultures after exposure to the differentiation inductor factors (microarray studies) (figure 7). 430 f.m. brehar et al inhibition of tumorigenic potential in glioblastoma figure 5 tumor cells located near the cscs xenograft (arrows) infiltrating the hippocampus (a). migratory tumor cells (arrows) distant located from the cscs xenografts, in corpus callosum, migrating to the opposite hemisphere (b). h&e staining figure 6 the fibroblastic phenotype of the cscs after exposure of the cells cultures to the differentiation inductor factors figure 7 mmps (purple), cadherin (blue) and cathenins (red) expression in cscs cultures before and after exposure of the cell cultures to the differentiation inductor factors discussions initiation of cscs cultures we observed formation of cells clusters similar to neurospheres at approximately 14-21 days after initiation (figure 1 a, b). neurospheres could be passaged multiple times by mechanical dissociation of large spheres and reseeding in fresh proliferative medium every 2–3 weeks. some of the initiated cultures formed the free-floating structures generated by these cells in vitro, the "neurospheres", considered to be a characteristic feature of tumor neural stem cell, which were morphologically and functionally heterogeneous. the expression of neural stem cells markers (cd133, o4) were assessed by flow-cytometry analysis. all the newly initiated cultures expressed high level of neural stem cells markers compared with u87 cultures (table1, figure 2). among several markers considered to be specific for neural stem cell and cscs isolated from glioblastoma, cd 133 was the first and the most used (17, 23). despite of several published evidence that identified glioblastoma derived cscs population negative for cd 133 (3, 20), this marker remain one of the most used for identifying romanian neurosurgery (2011) xviii 4: 425 433 431 glioblastoma derived cscs. our glioblastoma derived cultures cells expressed high level of cd133 compared with u87, indicating the presence of a large population of cscs cells. the using of serum-free culture (neurosphere assay) allowed the selection of cscs containing subpopulation that were able to reproduce original tumor aspect in orthotropic xenografts. cscs xenografts cscs xenografts exhibit specific growth pattern, very different from the compact growth pattern of the u87 xenografts. at two months after inoculation, cscs induce usually smaller xenografts (figure 4 a) compared with 28 days u87 xenografts (figure 3 b), but with more extensive infiltrating pattern. however there were also cscs xenografts with a volume comparable with u87 xenografts (figure 4 b). u87 xenografts have a compact growth pattern with no obvious signs of brain infiltration. even if the xenografts reached considerable volume, tumor developed only in the ipsilateral cerebral hemisphere, at the inoculation area. in contrast with the u87 xenografts, cscs xenografts were highly infiltrating. the final behaviour was to infiltrate the opposite cerebral hemisphere, through the corpus callosum or dorsal hippocampal comissure (figure 4 a, b). this infiltrating growth pattern seems to be specific not only for glioblastoma but also for anaplastic astrocytoma derived cscs xenografts (4). when higher magnification was used, we could notice tumor cells with migratory features infiltrating not only the surrounding brain parenchyma, but also the white commissural tracts, explaining the infiltration of the tumor into the opposite hemisphere. these findings, which suggest that cscs could drive the invasive phenotype of malignant gliomas, are supported also by the in vitro results. cscs cultures expressed at higher levels (up to ten times) mmps and cadherins, compared with the differentiated cells cultures (figure 7). mmps and cadherins are important markers associated with cells invasion; therefore the high expression of these molecules could explain the infiltrating growth pattern of the cscs xenografts. according to beadler et al., the infiltrating glioblastoma cells and migratory precursor neural cells used the same molecular mechanisms (2). one of the main molecular mechanisms is the lis-1/dynein complex (18). this molecular mechanism could be used also by glioblastoma derived cscs. on the other hand, according to our previously reports, there are also other molecular markers potentially involved in cscs migration, like vcam-1, which could explain the high migratory feature of malignant gliomas cscs xenografts (25). induction of differentiation in order to see how the differentiation of cscs will influence the expression of invasive markers and their tumorigenic potential, cscs cultures were exposed to a combination of fetal serum (10%) and differentiation factors like bdnf, nt 3 and atra. the first change to be noticed was in the morphology of the cells. thus, the neurospheres become smaller and eventually disappeared in 24-48 hours, and the cells exhibited a fibroblastic phenotype and adhered to the bottom of the culture dish (figure 6). the expression of mmps, cadherins and cathenins, evaluated by microarray experiments, decreased after exposure of the cscs cultures to the differentiation inductor factors (figure 7). important to mention that in vitro changes was noticed only when the differentiation 432 f.m. brehar et al inhibition of tumorigenic potential in glioblastoma factors (bdnf, nt3 and atra) were used together with fetal serum. differentiated cscs with fibroblastic phenotype were not been able to induce the formation of tumor xenografts in mice brain. therefore in vivo experiments demonstrated the inhibition of tumorigenic potential of cscs cultures exposed to the differentiation factors. mmps and cadherins are key molecules involved in tumor invasion (19; 22). the marked decreased in the mmps and cadherins expression after exposure to the differentiation factors could explain the lost of tumorigenic potential of cells cultures. these findings suggest that differentiation therapy, which target cscs, could be successfully applied in glioblastoma. however, these are only preliminary results and further studies are needed in order to find the optimal combination of molecules able to induct a strong and irreversible differentiation of cscs and to block the proliferation and invasion of malignant gliomas cells. conclusions serum-free culture allowed the selection of a subpopulation containing cscs with increased tumorigenic potential. when exposed to a specific combination of differentiation inductor factors, cscs cultures showed a marked decrease of expression of invasive markers (mmps and cadherins) and lost their tumorigenic potential. our findings confirm the potential of differentiation therapy as a novel experimental therapy for infiltrative glioblastoma and further studies should be performed in order to assess the clinical potential of differentiation inductor molecules as a novel therapeutically agents in glioblastoma. abreviations atra: all trans retinoic acid cscs: cancer stem cells h&e: hematoxylin and eosin mmps: matrixmetalloproteases vcam-1: vascular cell adhesion molecule 1 correspondence author r. i. radulescu emergency clinical hospital “bagdasararseni”, berceni street 10-12, 041915 e-mail: radulescu_razvan01@yahoo.com bucharest, romania references 1. bao s, wu q, li z, sathornsumetee s, wang h, mclendon re, et al. targeting cancer stem cells through l1cam suppresses glioma growth. cancer res. 2008;68(15):6043-8. 2. beadle c, assanah mc, monzo p, vallee r, rosenfeld ss, canoll p. the role of myosin ii in glioma invasion of the brain. mol biol cell. 2008;19(8):335768. epub 2008 may 21 3. beier d., hau p., proescholdt m., lohmeier a., wischhusen j., oefner p.j., aigner l., brawanski a., bogdahn u., beier c.p., cd133+ and cd133– glioblastoma-derived cancer stem cells show differential growth characteristics and molecular profiles, cancer res., 2007, 67, 4010–4015 4. brehar fm, ciurea av, zarnescu o, bleotu c, gorgan rm, dragu d, matei l., infiltrating growing pattern xenografts induced by glioblastoma and anaplastic astrocytoma derived tumor stem cells, chirurgia (bucur). 2010 sep-oct;105(5):685-94 5. constantinovici a., ciurea a.v.: ghid practic de neurochirurgie, cap. 15,1997 6. fariba behbod and jeffrey m.rosen, will cancer stem cells provide new therapeutic targets?, carcinogenesis vol.26 no.4 pp.703--711, 2004 doi:10.1093/carcin/bgh293; 7. f. m. brehar, a.v. ciurea m.d, otilia zarnescu, mihaela chivu, denisa dragu, development of in vivo model for glioblastoma, romanian neurosurgery, 2008, xv(1) 19-26 8. frank s.a., nowak m.a., cell biology: developmental predisposition to cancer. nature, 2003, 422, 494. 9. kosugi h., towatari m., hatano s., kitamura k. et al histone deacetylase inhibitors are the potent inducer/enhancer of differentiation in acute myeloid romanian neurosurgery (2011) xviii 4: 425 433 433 leukemia : a new approach to anti-leukemia therapy, leukemia, 1999, 13(9) 1316-1324 ; 10. nader sanai, m.d., arturo alvarez-buylla, ph.d., and mitchel s. berger, m.d., neural stem cells and the origin of gliomas, n engl j med 2005;353:811-22; 11. ohno r., yoshida h., fukutani h., naoe t. et al; multi-institutional study of all-trans retinoic acid as a differentiation therapy of refractory acute promyelocytic leukemia leukemia, 1993; 7(11),1910-1920; 12. rafael h. stem cells.j neurosurg. 2008 apr;108(4):841-2. 13. reya t., morrison s.j., clarke m.f., weissman i.l., stem cells, cancer, and cancer stem cells. nature, 2001, 414, 105–111 14. rossella galli, elena binda, ugo orfanelli, barbara cipelletti, angela gritti, simona de vitis, roberta fiocco, chiara foroni, francesco dimeco, and angelo vescovi, isolation and characterization of tumorigenic, stem-like neural precursors from human glioblastoma, cancer research, 64, 7011–7021, october 1, 2004 15. s. g. m. piccirillo, b. a. reynolds, n. zanetti, g. lamorte, e. binda, g. broggi, h. brem, a. olivi, f. dimeco, a. l. vescovi, bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells, nature. 2006;444(7120):761-5. 16. sheila k. singh, cynthia hawkins, ian d. clarke, jeremy a. squire, jane bayani, takuichiro hide, r. mark henkelman, michael d. cusimano, peter b. dirks, identification of human brain tumour initiating cells, nature 432, 396-401, 2004 17. singh sk, clarke id, terasaki m, bonn ve, hawkins c, squire j, et al. identification of a cancer stem cell in human brain tumors. cancer res. 2003;63(18):5821-8 18. vallee rb, jin-wu tsai. the cellular roles of the lissencephaly gene lis and what they tell us about brain development. genes dev. 2006; 20:1384-93. 19. vanmeter te, rooprai hk, kibble mm, fillmore hl, broaddus wc, pilkington gj the role of matrix metalloproteinase genes in glioma invasion: codependent and interactive proteolysis, j neurooncol. 2001 jun;53(2):213-35; 20. wang j., sakariassen p., tsinkalovsky o., immervoll h., bøe s.o., svendsen a., prestegarden l., røsland g., thorsen f., stuhr l., molven a., bjerkvig r., enger p., cd133 negative glioma cells form tumors în nude rats and give rise to cd133 positive cells, int. j. cancer, 122, 4, 761 – 768, 2007. 21. waxman s., differentiation therapy in acute myelogenous leukemia (non-apl), leukemia, 2000; 14(3), 491-496. 22. wick w, platten m, weller m. glioma cell invasion: regulation of metalloproteinase activity by tgf-beta, j neurooncol. 2001 jun;53(2):177-85. 23. yuan xiangpeng, james curtin, yizhi xiong, gentao liu, sebastian hogiu, daniel l farka, keith l black and john s yu , isolation of cancer stem cells from adult glioblastoma multiforme, oncogene (2004) 23, 9392– 9400. doi:10.1038/sj.onc.1208311. 24. zarnescu otilia, felix mircea brehar, mihaela chivu, alexandru vladimir ciurea. immunohistochemical localization of caspase-3, caspase-9 and bax in u87 glioblastoma xenografts. j mol histol. 2008; 39(6):561-9. 25. zarnescu o, brehar fm, bleotu c, gorgan rm, co-localization of pcna, vcam-1 and caspase-3 with nestin in xenografts derived from human anaplastic astrocytoma and glioblastoma multiforme tumor spheres. micron. 2011 may 6. [epub ahead of print]. 26. zhen yi wang and laurent degos all trans retinoic acid in acute promyelocytic leukemia, leukemia,2001, 20 (49); 7140-7145. 27. zulch k.j., brain tumors. their biology and pathology. berlin: springer-verlag; 1986. 6checiug_thoracicspine 420 checiu et al thoracic spine type c injuries thoracic spine type c injuries: injury profile, management and outcome gheorghe checiu, cristian filip, daniel serban, niki adrian calina, marius podea, costica zamfir, florin exergian “bagdasar-arseni” clinical emergency hospital, spine surgery, bucharest in the last years we observed an increased number of patients with multiple lesions after high energy accidents. type c injuries of the thoracic spine are the most severe lesions, with the worse prognosis. the study analyzes the injury profile, management and outcome of all patients with thoracic spine, from t1to t10, type c injuries treated in the spinal surgery department of “bagdsararseni” emergency hospital, in the last 5 years. there were 26 patients admitted in the study, mostly male, 77%, with a mean age of 33.8 years. all of them were victims of high energy accidents, and all had spine injury associated with multiple lesions (head, thoracic, abdominal and limbs). we have chosen a posterior approach in all cases, with laminectomy or hemilaminectomy, permitting us to achieve all the major objectives of surgery, with the advantage of lower blood loss and a reduced operating time. the purpose of surgery was to achieve decompression of the spinal cord and stability of the thoracic spine. we treated 19 patient surgically and 4 patient conservative. thoracic spine type c fractures remain a challenge for the spinal surgeon. these lesions require a multidisciplinary team approach for the treatment of associated lesions. the main goal of surgery is to achieve stability of the fractured segments. the timing for surgery is indicated mainly by associated respiratory problems. key words: thoracic, fracture, type c, ao classification. introduction with an increasing number of car accident each year and a reorientation of the population’s recreational activities we observed an increased number of patients presenting with spine fractures resulting from high energy accidents. this study analyzes thoracic fractures type c, according to ao classification described by magerl and aebi in 1994. on the basis of this classification, type c lesions are the most severe fractures of thoracic and lumbar spine and, in the majority of cases are associated with neurologic disorders caused by spinal cord compression. the characteristics of this type of fracture are represented by anterior and posterior column romanian neurosurgery (2014) xxi 4: 420 – 430 421 injuries with associated rotation and translation of vertebral bodies, with rupture of all ligamentous structures including intervertebral discs, fractures of articular processes, transverse processes with costal dislocation or rib fractures affecting the proximal third of the rib. type c fractures are subdivided into 3 categories: c1, represented by type a fractures with rotational force associated, c2, type b fractures with rotational force associated and c3, represented by purely rotational injuries. (1, 2) the study included all patients that were admitted in the department of spine surgery of “bagdasar-arseni” emergency hospital with thoracic ,from t1 to t10 , type c fractures between january 2009 and august 2014. there were 26 patients admitted, with a mean age of 33.8 years, mostly male. all of these patients were victims of high energy accidents, mostly car and motorcicle accidents. because of the complexity of the ao classification its daily use is questionable, but, although there are newer classification methods, the ao classification is still used to determine the prognosis of patients and the choice of the most appropriate treatment. epidemiological data spine fractures represent approximately 6% of all fractures worldwide. the most affected segments of the spine are the thoracic and lumbar spine, with an incidence of 700000 cases per year. figure 1 characteristics of type c fractures according to ao classification. (magerl f, aebi m, gertzbein sd, harms j, nazarian s (1994) a comprehensive classification of thoracic and lumbar injuries) 422 checiu et al thoracic spine type c injuries approximately 50% of these fractures are situated at the thoracolumbar junction, 32% in the lumbar spine and 16% in the thoracic spine [1]. thoracic type c lesions represent 35.8% of all fractures situated in the thoracic spine [2]. there were 26 patients included with a mean age of 33.8 years. we observed a high incidence of type c thoracic fractures in young patients, 65% being between 20 and 40 years old. the main cause of injury was represented by car accidents in 46% of cases, followed by fall from heights in 38.5% of cases and motorcycle accidents in 11.5% of cases. comparing them to fractures of the lumbar spine or thoracolumbar junction which associate neurological impairment in 25.7% , respectively 23% of cases, thoracic spine fractures have a higher incidence of neurological disorders, 38.6% of patients presenting neurological impairment. thoracic type c fractures associate neurological deficits in 57.7% of cases, opposed to 16.6% in type a fractures and 35% in type b fractures. the highest percent of complete neurological lesions described in literature are also thoracic type c lesions, in 38.5% of cases [3]. the most common site of fracture in our study was t7-t8, in 23.3% of cases, followed by t9-t10, in 20% of cases and then t4-t5 and t5-t6 in 16.6% of cases each. figure 2 main cause of injury of patients with thoracic type c fractures table i site of fracture of patients with thoracic type c lesions fracture site percent of patients t1-t2 0% t2-t3 0% t3-t4 10% t4-t5 16.60% t5-t6 16.60% t6-t7 3.30% t7-t8 23.30% t8-t9 10% t9-t10 20% patients and methods the article represents a retrospective study that includes all patients treated in our department in the last 5 years. there were 20 males and 6 females, 65% of patients being between 20 and 40 years old. despite literature data, the majority of patients admitted presented complete neurologic lesions, graded frankel a. 21 out of 26 patients included were frankel a, 3 patients were frankel c and 2 patients were frankel d. the most frequent level of injury was t4, in 23% of cases, followed by t7 in 19.2% of cases and then t8 in 15.4% of cases. figure 3 neurologic status of admitted patients romanian neurosurgery (2014) xxi 4: 420 – 430 423 table ii neurologic level of injury of admitted patients neurologic level percent of patients t1 0% t2 0% t3 7.70% t4 23% t5 11.50% t6 11.50% t7 19.20% t8 15.40% t9 11.50% t10 0% one of the main problem of these patients is represented by associated complications, mainly pulmonary lesions. literature studies demonstrate a proportional relation between the type of spinal injury according to ao classification and associated lesions, 42% of patients with type a fractures presenting associated lesions, 62% in type b fractures and 66% in type c fractures (2). all patients included in the study presented with associated lesions, 100% of patients presented associated thoracoabdominal trauma, 88.5% traumatic brain injury and 42% presented with associated limb or pelvic fractures. out of the 26 patients, 69% associated mild traumatic brain injury, 8% moderate traumatic brain injury, 11.5% severe brain injury and 11.5% had no head injury. the main problem for this patients was represented by thoracoabdominal trauma, patients presenting in a severe state, the majority in respiratory insufficiency which delayed the moment of surgery until they were stable from a respiratory and cardiac point of view. thoracoabdominal trauma was associated in 100% of cases. 69% of patients presented with respiratory insufficiency which was caused by haemothorax, pneumothorax, rib fractures or pulmonary contusions. 92% of patients presented haemothorax, 15 patients with bilateral haemothorax and 9 patients with unilateral haemothorax. 23% of patients presented pneumothorax. out of this patients, a pleural drainage system was required in 69% of cases and was maintained for an average duration of 10 days. 50% of patients presented with rib fractures. thoracoabdominal associated trauma represented a major complication that dictated the moment of surgery. patients were scheduled for surgery when associated respiratory complications were resolved, meaning, patient could breathe on his own, without respiratory support, with an oxygen blood saturation over 90% and pulmonary xray or chest ct with little or no modifications. also 11.5% of patients associated spleen rupture which needed emergency surgical intervention. 11 patients presented limbs or pelvic fractures. 30.5% of admitted patients presented superior limbs fractures, 11.5% inferior limbs fractures and only 3.8% presented with pelvis fractures. the high percentage of patients with multiple lesions is a statement that sustains the severity of this lesions and the high energy accidents that produced them. also, it implies that the patient needs a multidisciplinary team approach. 424 checiu et al thoracic spine type c injuries table iii associated thoracoabdominal trauma associated thoracoabdominal trauma respiratory insufficiency 69% haemothorax 92% pneumothorax 23% rib fractures 50% spleen rupture 11.5% other rare complications included: decubitus lesions, pneumonia, pneumomediastine, superior digestive hemorrhage, pulmonary thromboembolism, urinary tract infections, diarrhea syndrome, transverse colon rupture, hepatic injury, azygos vein injury, burn injuries after electrocution, radial nerve palsy, brachial plexus elongation, stern fractures and amputated fingers. treatment there are two main types of treatment for spine fractures, surgical treatment and conservative treatment. the method of treatment is chosen on the following criteria: the instability grade of the fracture, neurological status and the impossibility of maintaining an external immobilization device for different reasons (5). in the vast majority of cases type c fractures of the thoracic spine are treated surgically because of their instability and associated neurological deficits. (1, 2, 3) out of the 26 patients admitted, 19 patients were operated, 4 were treated conservative, 2 patients died before surgical intervention an 1 patient was transferred to another clinic at will. conservative treatment we choose conservative treatment in 4 cases on the following criteria: 1) patients with complete neurological lesions, graded frankel a 2) fractures of the upper thoracic spine, a segment that need to sustain less axial pressure then the lower thoracic spine 3) multiple comorbidities associated 4) a high risk of surgical treatment the fractured vertebrae were t5-t6 for 2 patients, t4-t5 for one case and t8-t9 in another case. all patients presented complete or partial consolidation of the fracture at 2 months follow-up, and could sit in a wheel chair. there was no neurological improvement in any of these cases. surgical treatment 73% of patients underwent surgery for thoracic spine type c fractures. in all cases we chose a posterior approach with laminectomy in 63% of cases and hemilaminectomy in 37% of cases. there are different methods of approach described in literature, posterior, anterior or combined approaches. the most common approach is posterior, achieving all the major objectives of surgical treatment with lower blood loss and a smaller duration of surgery. operating time can extend up to 100% in combined approaches and up to 25% in anterior approaches. radiation exposure is also higher in case of a combined approach (3). the major objectives of surgical treatment were decompression of the spinal cord and spine fusion using metallic implants and bone graft fusion. it was observed that a reduction of the spinal canal increases the risk of romanian neurosurgery (2014) xxi 4: 420 – 430 425 neurological impairment 3.5 times comparing them with patient without reduction of the spinal canal. comparing with other segments of the spine, the thoracic spine has the highest rate of neurological impairment in case of spinal cord compression, 51.4% of patients presenting with neurological deficits, compared to 36.2% at the thoracolumbar junction and 30.6% in the lumbar spine. the reduction limit of the thoracic spinal canal before neurological deficits appear is 10%. all objectives of surgical treatment were achieved through a posterior approach. there was no need for an anterior or a combined approach. the timing of surgical treatment is an important problem for patients with thoracic type c fractures. normally, the prognosis is better if an early surgical intervention with decompression and fusion of the spine is done. unfortunately, early surgical treatment is not always possible, patients presenting with an altered general condition and multiple lesions associated (6) .literature articles sustain that white matter has a much higher resistance than grey matter, lesions of white matter being reversible even after 72 hours while grey matter lesions are instantly irreversible (7). animal studies returned good results for early decompression, in the first 8 hours after trauma (8, 9). this remains a controversial problem. burk, berryman (10) and hadley with associates (11) describe in a retrospective study that the moment of decompression for cervical spine lesions is more important for neurologic recovery than the method of decompression. on the other hand, vacaro and associates (12) published a prospective randomized study for cervical spine lesions and demonstrated that there is no neurological advantage associated with early decompression. another recent prospective study for lesions of the thoracic spine demonstrated an insignificant tendency of neurologic improvement associated with early decompression (13). weather early surgical intervention has an advantage on neurological improvement is unclear, although it is certain that surgical intervention in less than 72 hours reduces the average stay in icu, respiratory complications, morbidity and mortality (14, 15). in a revision of literature done by bellabarba and associates early surgical intervention is associated with a shorter icu stay and a shorter hospital stay (16). there are also studies sustaining that early fusion in this type of lesions associate reduced pulmonary complications, a reduced time of necessary mechanical ventilation hours and decreases the incidence of pneumonia. this favorable effects are clearer in case of thoracic spine fractures (17, 18, 19, 20, 21, 22, 23, 24). the obvious thought was that mortality is higher in case of early surgical intervention, but, a study on 871 patients who were split in 2 groups depending on the moment of surgery returned no differences (22). studies also revealed smaller costs associated with early surgical treatment (25, 17, 22). the timing of surgical treatment in our study was dictated primarily by pulmonary complications. the average time until surgery was 14 days, with a minimum time of 6 days and a maximum of 85 days. the average duration of surgery was 252 minutes and the average blood loss was 463 ml, with a 426 checiu et al thoracic spine type c injuries minimum value of 200 ml and a maximum of 1000 ml. one of the most important objectives of surgical treatment was to achieve stability of the spine. in the majority of cases stability was achieved through a metallic fusion, with transpedicular screws and rods associated with autologus bone graft fusion. metallic fusion was used in 84% of operated patients. giving the high degree of instability, all cases used bilateral fusion, with 6 screws and 2 rods in 37.5% of cases and 8 screws with 2 rods in 62.5% of cases. the metallic implants were also used to apply forces for reduction of fractured segments. bone graft fusion was used in 69% of cases. we evaluated all patients at 2 months after surgery and all cases showed complete consolidation of fractured segments. all cases used bone chips harvested from decompressive osteotomies and excision of mobile bone fragments. in the majority of cases the intervertebral discs were found ruptured. we proceeded with discectomy followed by interbody bone graft fusion. in some cases a posterolateral bone fusion was used. the advantage of bone graft fusion is that it offers long term stability after consolidation. the disadvantage of this method is that patients need at least 3 weeks of bed stay after surgery, increasing the risk of comorbidities associated with immobilization. to sum it all up, metallic fusion is used to achieve short term stability of the spine and to help in reduction of fractured segments. in our experience, we observed that this type of fusion is not enough for long term stability, as bone tissue suffers a resorption along the course of the screw. for best results in achieving long term stability bone graft fusion is the method to choose, although in comes with some disadvantages. fracture reduction was tempted in 16 cases, meaning 84.2% of operated patients. we managed to achieve reduction of the fractured segments in 14 cases, 73.5% and reduction was attempted but did not succeed in 2 cases, meaning 10.5%. reduction was not attempted in 3 cases, 16% of operated patients for different reasons. the main problem associated with fracture reduction was represented by late timing of surgery which led to a fibrous tissue that made reduction difficult or created adherents with large vessels risking a major bleeding. case presentation a 24 year old patient, male, that suffered a car accident with a thoracic spine fracture affecting the t8 vertebra with t7-t8 luxation, graded frankel a, with associated thoracic trauma and a mild traumatic brain injury. the patient was squedueled for surgery 13 days after presentation. we found the dura matter ruptured and complete destruction of the spinal cord. a metallic fusion was used with bilateral transpedicular screws t5, t6, t9 and t10 with 2 rods. we managed to reduce the fracture applying reduction forces on the screws. the t7-t8 disc was found ruptured, followed by t7 discectomy and t7-t8 interbody bone rgaft fusion. the patient was immobilized 6 weeks after surgery. at 2 months follow-up we observed complete consolidation of the interbody fusion. romanian neurosurgery (2014) xxi 4: 420 – 430 427 figure 4 24 year old patient with t7-t8 type c fracture before and after surgery another 21 year old patient, male, that suffered a car accident, with a type c thoracic fracture t7-t8, graded frankel a. intraoperative, the dura matter was not ruptured and we managed to decompress the spinal cord. a t6-t9 metallic fusion was performed, with 8 transpedicular screws and 2 rods. we managed to reduce the t7-t8 luxation. an intersomatic t7-t8 bone graft fusion was performed. the patient remained frankel a at 2 months follow-up but had no signs of clinical or radiological instability (figure 5). outcome the average hospital stay was 20 days, with a minimum of 3 days and a maximum of 74 days in 4 different admissions. the neurologic status over the course of hospital stay was stationary for 22 patients, 84.5%, all of these patients having a frankel a grade from admission. 4 patients, meaning 15.5% of all patients presented improved neurologic status over the course of hospital stay. 428 checiu et al thoracic spine type c injuries figure 5 21 year old patient with t7-t8 type c fracture before and after surgery complications the most frequent complications observed in patients with this type of fractures were represented by lesions of the thoracic cage, lungs or myocardium. 50% of patients associated rib fractures, 92% of patients haemothorax, 23% pneumothorax and 11.5% spleen rupture. literature studies described a lower incidence of associated lesions in patients with a reduced neurological impairment, only 20% associating multiple lesions (27). the most frequent postoperative complications observed in our study were csf fistula, in 3 cases, patients with worse neurological status in 1 case, pulmonary romanian neurosurgery (2014) xxi 4: 420 – 430 429 thrombembolism in 1 case and wound hematoma in 1 case. late complications included implant failure, observed in 2 cases, superficial wound infection in 2 cases and csf fistula in one case. csf fistula represents an important problem for this type of patients, almost half of them presenting dural rupture and csf leakage during surgical intervention. dural defect was found in 47% of operated cases and in 15.8% of operated cases patients presented radicular dilacerations. conclusions type c thoracic spinal fractures are the most severe lesions of the thoracic spine that occur secondary to high energy accidents and are frequently associated with multiple lesions, pulmonary lesions being the most severe associated complications which dictate the moment of surgery. patients require a multidisciplinary team approach. the spinal cord is affected in almost 100% of cases. surgical intervention through a posterior approach can resolve the main objectives of surgery represented by decompression of the spinal cord and spinal fusion. autologus bone graft fusion is very important for long term stability of the spine. references 1. harbrecht bg, djurasovic m: thoracolumbar spine trauma: diagnostic and therapeutic considerations for the general surgeon. am surg 75:191–196, 2009 2. magerl f, aebi m, gertzbein sd, harms j, nazarian s (1994) a comprehensive classification of thoracic and lumbar injuries. eur spine j 3(4):184–201 3. operative treatment of 733 patients with acute thoracolumbar spinal injuries: comprehensive results from the second, prospective, internet-based multicenter study of the spine study group of the german association of trauma surgery. m. reinhold • c. knop • r. beisse • l. audige´ • f. kandziora • a. pizanis • r. pranzl • e. gercek • m. schultheiss • a. weckbach • v. bu¨hren • m. blauth received: 11 november 2009 / revised: 7 march 2010 / accepted: 9 may 2010 / published online: 25 may 2010 springer-verlag 2010 4. schouten r, ory k, lee rs, street jt, boyd mc, paquette sj, et al: health-related quality-of-life outcomes after thoracic (t1-t10) fractures. spine j [epub ahead of print], 2013 5. wood kb, bohn d, mehbod a: anterior versus posterior treatment of stable thoracolumbar burst fractures without neurologic deficit: a prospective, randomized study. j spinal disord tech 18 (suppl):s15– s23, 2005 6. tator ch: review of treatment trials in human spinal cord injury: issues, difficulties, and recommendations. neurosurgery 59:957–987, 2006 7. harrop js, sharan a, ratliff j: central cord injury: pathophysiology, management, and outcomes. spine j 6 (6 suppl): 198s–206s, 2006 8. delamarter rb, sherman j, carr jb: pathophysiology of spinal cord injury. recovery after immediate and delayed decompression. j bone joint surg am 77:1042– 1049, 1995 9. fehlings mg, tator ch: an evidence-based review of decompressive surgery in acute spinal cord injury: rationale, indications and timing based on experimental and clinical studies. j neurosurg 91 (1 suppl):1–11, 1999 10. burke dc, berryman d: the place of closed manipulation in the management of flexion-rotation dislocations of the cervical spine. j bone joint surg br 53:165–182, 1971 11. hadley mn, fitzpatrick bc, sonntag vk, browner cm: facet fracture-dislocation injuries of the cervical spine. neurosurgery 30:661–666, 1992 12. vaccaro ar, daugherty rj, sheehan tp, dante sj, cotler jm, balderston ra, et al: neurologic outcome of early versus late surgery for cervical spinal cord injury. spine (phila pa 1976) 22:2609–2613, 1997 13. cengiz sl, kalkan e, bayir a, ilik k, basefer a: timing of thoracolomber spine stabilization in trauma patients; impact on neurological outcome and clinical course. a real prospective (rct) randomized controlled study. arch orthop traumasurg 128:959–966, 2008 430 checiu et al thoracic spine type c injuries 14. carreon ly, dimar jr: early versus late stabilization of spine injuries: a systematic review. spine (phila pa 1976) 36:e727–e733, 2011 15. xing d, chen y, ma jx, song dh, wang j, yang y, et al: a methodological systematic review of early versus late stabilization of thoracolumbar spine fractures. eur spine j 22: 2157–2166, 2013 16. bellabarba c, fisher c, chapman jr, dettori jr, norvell dc: does early fracture fixation of thoracolumbar spine fractures decrease morbidity or mortality? spine (phila pa 1976) 35 (9 suppl):s138–s145, 2010 17. croce ma, bee tk, pritchard e, miller pr, fabian tc: doesoptimal timing for spine fracture fixation exist? ann surg 233:851–858, 2001 18. delamarter rb, sherman j, carr jb: pathophysiology of spinal cord injury. recovery after immediate and delayed decompression. j bone joint surg am 77:1042– 1049, 1995 19. garfin sr, blair b, eismont fj, abitol jj: thoracic and upper lumbar spine injuries, in browner bd, jupiter jb, levine am, neurosurg focus / volume 37 / july 2014et al (eds): skeletal trauma: fractures, dislocations, ligamentous injuries, ed 2. philadelphia: wb saunders, 1998,vol 1, pp 947–1034 20. kerwin aj, frykberg er, schinco ma, griffen mm, arce ca, nguyen tq, et al: the effect of early surgical treatment of traumatic spine injuries on patient mortality. j trauma63:1308–1313, 2007 21. kerwin aj, frykberg er, schinco ma, griffen mm, murphy t, tepas jj: the effect of early spine fixation on non-neurologic outcome. j trauma 58:15–21, 2005 22. kerwin aj, griffen mm, tepas jj iii, schinco ma, devin t,frykberg er: best practice determination of timing of spinal fracture fixation as defined by analysis of the national trauma data bank. j trauma 65:824–831, 2008 23. krengel wf iii, anderson pa, henley mb: early stabilization and decompression for incomplete paraplegia due to a thoracic-level spinal cord injury. spine (phila pa 1976) 18: 2080–2087, 1993 24. schinkel c, frangen tm, kmetic a, andress hj, muhr g: timing of thoracic spine stabilization in trauma patients: impacton clinical course and outcome. j trauma 61:156–160, 2006 25. boakye m, arrigo rt, hayden gephart mg, zygourakis cc, lad s: retrospective, propensity scorematched cohort study examining timing of fracture fixation for traumatic thoracolumbar fractures. j neurotrauma 29:2220–2225, 2012 26. yurac r, marre´ b, urzu´a a et al (2006) residual mobility of instrumented and non-fused segments in thoracolumbar spine fractures. eur spine j 15:864–875 27. thoracic spine fractures: injury profile and outcomes of a surgically treated cohort bartolome´ marre´ • vicente ballesteros • celmira martı´nez • juan j. zamorano • francisco ilabaca • milan munjin • ratko yurac • alejandro urzu´a • miguel lecaros • jose´ fleiderman received: 21 june 2010 / revised: 4 december 2010 / accepted: 11 january 2011 / published online: 28 january 2011 springer-verlag 2011 romanian neurosurgery (2019) xxxiii (2): pp. 116-121 doi: 10.33962/roneuro-2019-023 www.journals.lapub.co.uk/index.php/roneurosurgery dual microcatheter technique for the treatment of a ruptured wide neck basilar tip aneurysm rares filep, dorin nicolae gherasim, septimiu popescu, botond tokes, lucian marginean * department of interventional radiology & department of neurosurgery, emergency county hospital, targu mures, romania abstract endovascular treatment is a safe and efficient therapy for intracranial aneurysms with lower complication and mortality rates compared to surgical clipping. wide-neck aneurysms still represent a challenge to complete and safe aneurysm occlusion in spite of techniques such as stent-assisted or balloon-assisted coiling, developed in order to achieve better occlusion rates. these techniques themselves may lead to further complications, so alternative methods such as the dual microcatheter technique were developed. this technique assumes that, via two microcatheters inserted into an aneurysm, simultaneous deployment of two coils achieves a stable coil frame without the use of adjunctive devices. the aim of this paper is to present a successfully treated basilar tip wide-neck aneurysm treated with the dual microcatheter technique. case report. a 46-year-old male patient with acute onset of severe headache presented in the emergency room with altered state of consciousness. nonenhanced ct scan showed subarachnoid and intraventricular haemorrhage. ct angiography revealed a wide-neck basilar tip aneurysm. digital subtraction angiography confirmed the presence of an aneurysm with a wide, 4.9 mm neck. dual microcatheter technique was chosen as the first treatment option, while a hypercompliant balloon was kept as backup. two microcatheters were placed inside de aneurysm and two coils were introduced in order to form a stable framing coil mass that served as a support for further coils deployed in an alternately manner through each microcatheter. no procedural complication occurred, and the patient’s evolution was uneventful with no neurological deficits at discharge. conclusion. the dual microcatheter technique is a safe and effective therapeutic option for wide-neck ruptured or unruptured intracranial aneurysms. periprocedural complication rates are similar to simple coiling or balloon-assisted coiling, but lower than for stent-assisted coiling. introduction endovascular treatment has become the therapy of choice for intracranial aneurysms owing to its lower complication and mortality rates, as compared to surgical clipping (5). however wide-neck aneurysms with a neck diameter greater than 4 mm or a dome-to-neck keywords subarachnoid haemorrhage, cerebral aneurysm, basilar artery, endovascular treatment corresponding author: dorin nicolae gherasim department of neurosurgery, emergency county hospital, targu mures, romania dorin.gherasim@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 117 dual microcatheter technique for the treatment of a ruptured wide neck basilar tip aneurysm ratio less than 2, still represent a procedural challenge attributable to the risk of intraprocedural coil herniation, a higher number of thromboembolic complications and higher rate of long-term recanalization (6). different techniques have been developed to assist wide-neck aneurysm coiling by covering the neck during coil deployment, thus allowing denser packing and better long-term occlusion rates. stents and balloons have been used for this purpose, but both techniques have their limitations. stent placement might be difficult in tortuous vessel anatomy and is associated with delayed thromboembolic events and in-stent stenosis. balloon-assisted coiling (bac) requires temporary flow arrest and may be associated with increased risk of vessel rupture and thromboembolic complications (7). one alternative to the above-mentioned procedures is a less used and under-reported method, the dual microcatheter technique (dmt), which requires simultaneous placement of two microcatheters in the aneurysm sac and deployment of coils through both of them with the aim of achieving a stable coil frame without the use of adjunctive devices (1). the aim of this paper is to present the case of a patient with a wide-neck basilar tip ruptured aneurysm, successfully treated using the dmt and to discuss its advantages and disadvantages compared to other techniques used for wide-neck aneurysm coiling. case report a 46-year-old male patient presented in the emergency department with abrupt-onset severe headache. clinical examination revealed a drowsy and confused patient (hunt-hess 3). non-enhanced ct and ct angiography of the head performed on 64channel machine (siemens, erlangen, germany) showed a subarachnoid and intraventricular hemorrhage (mfisher 4) and a wide-neck basilar tip aneurysm. (figure 1: a, b, c) figure 1. a. sagittal ncct image reveals a small amount of subarachnoid blood in the interpeduncular cistern and the 3rd ventricle (white arrows); b. axial ncct slice shows the blood clot in the 3rd ventricle (white arrow); c. coronal cta image reveals the basilar bifurcation aneurysm (white arrow) ncct = non-contrast computed tomography; cta = computed tomography angiography digital subtraction angiography (dsa) and 3d rotational angiogram obtained on a siemens biplane system (siemens, erlangen, germany) showed the basilar tip aneurysm measuring 7.1/5.1/5.4 mm (cc/ll/ap diameters) with a neck of 4.9 mm (dometo-neck ratio of 1.4), and a small secondary lobule along the left superior border of the aneurysm, thought to be the site of bleeding (figure 2: a, b). under general anesthesia the right common femoral artery was accessed with a 6f cordis sheath (cordis, freemont, california) and a 6f chaperon guiding catheter (terumo, tokyo, japan) was placed in the right vertebral artery (va). a headway 17 microcatheter (terumo, tokyo, japan) was then advanced into the aneurysm and a target 360 standard 5 mm x 15 cm coil (stryker, michigan, usa) a. b. c. 118 rares filep, dorin nicolae gherasim, septimiu popescu et al. was deployed. at this point an intravenous bolus of 2500 units of heparin was administered. the coil was quite stable in the aneurysm sac without impingement on the basilar artery. (figure 2: c.) we kept it attached to its introducer wire nevertheless, with the idea to keep it as support for further coils that will be inserted through a second microcatheter. a 5f cordis femoral sheath was inserted on the opposite side and a second headway 17 microcatheter was introduced into the aneurysm via a 5f navien support catheter (medtronic, minneapolis, usa) placed in the left va. a 3d axium prime 5 mm x 10 cm coil (medtronic, minneapolis, usa) was introduced through the second microcatheter, and by intertwining with the first coil, formed a secure, stable coil mass throughout the entire volume of the aneurysm. (figure 2: d, e) the second coil was detached, and an additional bolus of 2500 iu of heparin was administered. a third hydrocoil 3 mm x 8 cm coil (microvention, california, usa) was introduced through the second microcatheter, followed by the careful detachment of the very first coil. three further hydrogel-coated coils were introduced through both microcatheters, alternately, resulting in satisfactory occlusion of the aneurysm judged by the raymond-roy occlusion classification as 1 (figure 2: f). the patient had an uneventful postoperative course and was discharged 2 weeks later without neurological deficits, with a modified rankin scale 0. figure 2. a. ap dsa image from a right va injection shows a basilar tip aneurysm; b. 3d rotational angiographic reconstruction; c. ap unsubtracted image shows the first microcatheter and the first coil inside the aneurysm (white arrow); d. ap unsubtracted image a. b. c. d. e. f. 119 dual microcatheter technique for the treatment of a ruptured wide neck basilar tip aneurysm reveals the second microcatheter (white arrows) and a further coil inserted into the aneurysm; e. further coils are deployed simultaneous through both of the microcatheters; f. final control dsa angiogram shows the complete obliteration of the aneurysm. ap = anteroposterior, dsa = digital subtraction angiography discussions since its introduction in 1998 by baxter’s group (4), dmt has been used as an alternative to balloon or stent-assisted coiling (sac) for wide-neck intracranial aneurysms. it involves the use of two microcatheters inserted in the aneurysm sac followed by simultaneous or sequential deployment of coils. the general principle behind this technique is the stability obtained by the “entanglement” of the first two framing coils inserted simultaneously, thus creating a larger coil frame that prevents impingement on or herniation of the coil loops into the parent artery. one of the coils is usually detached at the end of the procedure thus conferring additional stability for further coils. the technique is aimed at wide-neck saccular aneurysms with a dome-to-neck ratio less than 2, irregular aneurysms with multiple daughter sacs and complex configurations and aneurysms with a vessel emerging from the neck (5). we considered dmt as the first therapeutic option for our case while a balloon was kept as back-up in case the coils were not stable inside the aneurysm. sac was excluded because the aneurysm was ruptured, and dual antiplatelet therapy was necessary. for a more detailed description of the technique we propose a step-by-step guide on how to approach aneurysms that are amenable to treatment with this procedure. 1. general procedural considerations endovascular treatment of intracranial aneurysms should be performed with the patient under general anesthesia. in our institution all catheters are continuously flushed with saline containing heparin (2500 iu heparin in 500 ml of saline). our protocol is to administer a bolus of 5000 iu heparin intravenously after the deployment of the first coil, although during this procedure, 2500 iu were administered after insertion of both guiding catheters in order to prevent thromboembolic events, and 2500 iu following the deployment of the first coil. 2. femoral artery access and guiding-catheter (gc) choice. unior bilateral access depends on how many gc’s are needed. generally, the dual microcatheter technique can be safely performed through one gc. in the majority of cases the internal carotid arteries (ica) or at least one of the vertebral arteries (va) can easily accommodate one larger device, although cases with small va’s may require the use of two gc’s in cases with posterior circulation aneurysms (4). advantages of using a unilateral approach are the smaller complication rates related to femoral artery puncture and large vessel access, like arterial spasm, dissection and embolic events. theoretically, using two gc’s can lead to a two-fold increase in such complications. the use of two gc’s can be avoided because the majority of 6 or 7 french (f) devices have a large enough lumen to contain both microcatheters. disadvantages of using only one device are the difficulty of obtaining quality roadmaps or control angiograms with two microcatheters that occupy a large luminal area of a 6f gc, although this can be overcome with the use of a 7f device. another disadvantage of two microcatheters inserted through the same gc is related to the risk of inadvertent forward/backward movement while manipulating them, which can lead to aneurysm perforation or dislodgement of the coil mass (4,3). due to the limited experience with this technique we felt safer with a bilateral approach in order to avoid inadvertent microcatheter movement and to have access with a hypercompliant balloon if the coils were not stable or if rupture of the aneurysm occurred. 3. aneurysm access the first option is to try coiling the aneurysm with one microcatheter. if this fails due to coil herniation or impingement on the parent artery, the second microcatheter is positioned as follows. to anticipate the deployment behavior of the coils it is useful to divide the aneurysm in two imaginary compartments, each one occupied by one of the first two coils, a simple example is to have a proximal and a distal compartment, and to position the tip of the two microcatheters in the corresponding compartment (3). 4. coil selection, deployment and detachment coil choice depends on the configuration of the aneurysm. for irregular aneurysms with multiple 120 rares filep, dorin nicolae gherasim, septimiu popescu et al. daughter sacs soft coils are recommended to avoid perforation. if this is not the case, standard, complex coils are preferred due to their larger radial force providing a better “anchoring” inside the aneurysm. the first coils should be longer, thus minimizing the number of subsequent coils necessary for a dense final packing. after achieving a stable frame with the first two coils, one of them is detached and further coils are inserted until complete obliteration is obtained, while the other is left attached to its pusher-wire. the decision which coil to detach first is usually based on its stability: the more stable looking coil is to be detached first, because it provides a better scaffold for further coils. another consideration to which coil should be detached first is the position of the microcatheter tip. it is safer to insert coils through the catheter sitting closer to the neck of the aneurysm than through the one positioned deeper inside due to the risk posed by the deep deposition of coils that might “push” the whole coil construct outside and into the parent vessel, consequently the one sitting deeper should be detached earlier (1,3,4). 5. microcatheter removal a potential risk of retrieving the microcatheters at the end of the procedure is the extraction of the coil mass outside the aneurysm. the best way to avoid this if the microcatheter’s tip is deep inside the aneurysm, is to push gently on the pusher-wire of the last coil until the tip protrudes outside, and only afterwards to detach the coil (6). dmt is a relatively under-used method for intracranial aneurysms compared to balloon or stent-assisted coiling, with only few case reports, series and retrospective studies published in the literature so far. the safety and efficiency of this approach has been assessed by durst et al in their retrospective analysis of 100 wide-necked aneurysms (2). they reported a morbidity and mortality of 1% and 2% respectively. intraprocedural rupture occurred in 3 patients (3%), 2 were successfully stopped immediately and 1 patient died due to massive hemorrhage and hydrocephalus. one other patient died as a consequence of the coils herniating in the parent vessel, obliterating the lumen and subsequent ischemic stroke. dmt was successfully carried out in 91 cases (91%). the remaining 9 failed due to the impossibility of stabilizing the coils inside the aneurysm. retreatment was necessary in 18% of cases after recanalization (2). the relatively low major complication rate of dmt (3%) is similar to that reported for simple coiling (0.65.1%) or bac (0.9-3.8%), but much lower than for stent-assisted coiling (sac) (9.4-12.2%) (7). two common downsides of bac and sac are the greater experience needed for device manipulation and the specific risks imparted by these devices on the procedure. balloons add the risk of intraprocedural vessel rupture while stents are permanent intraluminal devices prone to in-stent stenosis and thrombosis, requiring long-term antiplatelet therapy with an additional hemorrhagic risk. conversely, no special training is needed for dmt since the only devices used are those required for simple coiling, although special care is mandatory during aneurysm access, because two catheterization procedures mean an increased risk of wall perforation with either the guidewire or the microcatheters. one major issue of dmt is the retreatment rate of 18% (7), that compared to bac, between 5.7% and 15.6%, and sac, between 4.3% and 13.3% (8) is relatively high. this is especially important for young patients due to their longer life expectancy, therefore a judicious use of dmt is necessary in this patient population. conclusions the dual microcatheter technique is a safe and effective therapeutic option for wide-neck ruptured or unruptured intracranial aneurysms. periprocedural complication rates are similar to simple coiling or balloon-assisted coiling, but lower than for stent-assisted coiling. references 1. baxter bw, rosso d, lownie sp. double microcatheter technique for detachable coil treatment of large, widenecked intracranial aneurysms. ajnr am j neuroradiol. 1998 jun;19(6):1176–8. 2. durst cr, starke rm, gaughen jr, geraghty s, kreitel kd, medel r, et al. single-center experience with a dual microcatheter technique for the endovascular treatment of wide-necked aneurysms. j neurosurg. american association of neurological surgeons; 2014 nov. 121 (5): 1093–101. 3. horowitz m, gupta r, jovin t. the dual catheter technique for coiling of wide-necked cerebral aneurysms. an underreported method. interv neuroradiol. 2005 jun 30; 11 (2):155–60. 121 dual microcatheter technique for the treatment of a ruptured wide neck basilar tip aneurysm 4. kwon o-k, kim sh, kwon bj, kang h-s, kim jh, oh cw, et al. endovascular treatment of wide-necked aneurysms by using two microcatheters: techniques and outcomes in 25 patients. ajnr am j neuroradiol. 2005 apr;26(4):894–900. 5. molyneux aj, kerr rs, yu l-m, clarke m, sneade m, yarnold ja, et al. international subarachnoid aneurysm trial (isat) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. the lancet. 2005 sep;366(9488):809– 17. 6. pierot l, biondi a. endovascular techniques for the management of wide-neck intracranial bifurcation aneurysms: a critical review of the literature. journal of neuroradiology. elsevier masson sas; 2016 mar 11;:1–9. 7. piotin m, blanc r. balloons and stents in the endovascular treatment of cerebral aneurysms: vascular anatomy remodeled. front neurol. frontiers; 2014;5(suppl 3):41. 8. wang f, chen x, wang y., bai p, wang h-z, sun t, et al. stent-assisted coiling and balloon-assisted coiling in the management of intracranial aneurysms: a systematic review & meta-analysis. j neurol sci. 2016 may 15; 364: 160–6. microsoft word 5sanduaurelia_total 46 sandu and gorgan total resection in a giant left frontal arteriovenous malformation total resection in a giant left frontal arteriovenous malformation, grade v spetzler-martin case report aurelia mihaela sandu1, mircea radu gorgan2 1phd student in neurosurgery, “carol davila” university of medicine and pharmacy bucharest, faculty of medicine, department of neurosurgery clinic of neurosurgery, fourth department of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest 2“carol davila” university of medicine and pharmacy bucharest, faculty of medicine, department of neurosurgery head of clinic of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest abstract background: giant arteriovenous malformations (avms) are congenital lesions, with nidus sizing more than 6 cm. according to spetzler-martin scale, grade v avms have a nidus larger than 6 cm in diameter, profound venous drainage and are located in eloquent areas. method: we report a case of a 39 years old woman, with giant left frontal avm, grade v spetzler-martin, who was admitted for generalized seizures, with onset 32 years ago, refractory to full dose antiepileptic polytherapy, which severely impaired the patient’s quality of life. results: the patient underwent surgery and we performed total resection of the avm. we emphasize on surgical technique, intraoperative difficulties and outcome. conclusions: surgery is the therapy of choice in avms, because it provides cure of the lesion, and is the only treatment capable of preventing hemorrhage and controlling seizures. management in grade v avms is challenging, because of their large size, multiple dilated arterial feeders from anterior and posterior circulation and external carotid arteries, high blood flow, vascular steel from the surrounding brain, enlarged draining veins, profound venous drainage and location in eloquent area. giant avms with high flow nidus, causing a great degree of vascular steel in the surrounding brain, with hypoperfusion of normal parenchyma may develop early normal perfusion pressure breakthrough. total resection in grade v avms can be performed with minimal transient morbidity and favorable outcome. total resection permits control of intractable seizures with reduced dose of antiepileptic therapy. key words: arteriovenous malformation surgery, giant arteriovenous malformation, grade v spetzler-martin arteriovenous malformation background arteriovenous malformations (avms) contain a tangled cluster of vessels, called nidus, in which dysplastic arteries are directly connected through shunts with arterialized veins, with no existence of capillary bed. the nidus is usually compact, romanian neurosurgery (2013) xx 1: 46 – 56 47 without intervening brain parenchyma. dysplastic arteries lack muscularis layer and red draining veins are enlarged and carry oxygenated blood. avms are congenital lesions, which occur during the late somite stages of the fourth week of embryonic life. avms were first described by luschka and virchow in the mid 1800s, giordano performed the first surgical exposure of an avm in 1890, krause attempted surgical exclusion of an avm by ligating its feeding arteries in 1908 and olivecrona performed the first surgical excision of an avm in 1932. (1) the incidence of avms ranges between 0.15 and 3% (12; 19) and the prevalence is 0.14% (1; 6). avms accounts for approximately 6% of all intracranial lesions and 11% of all cerebrovascular malformations. (5) avms become clinically manifest in young people, the average age at diagnostic being 33 years, and about 64% of patients with avms are diagnosed before age 40. (5; 6; 14) the main clinical forms of presentation are rupture, with consequent hemorrhage and seizures. other symptoms are neurological deficits secondary to mass effect and intracranial hyperpressure, ischemia of the adjacent brain secondary to vascular steal and hydrocephalus due to venous hypertension. treatment of giant avms is challenging. according to spetzler-martin scale, grade v avms have a nidus bigger than 6 cm in diameter, profound venous drainage and are located in eloquent areas. surgery is the treatment of choice in avms, total resection offering cure of the lesion, eliminating the risk of rupture and improving seizure control. the morbidity and mortality rate in operated grade v avms is high. (5; 7; 11; 16) case presentation we report a case of a giant left frontal avm, grade v spetzler-martin, operated into the fourth department of neurosurgery, emergency clinical hospital bagdasar-arseni. we reviewed medical records, imaging, surgical treatment and follow-up. a 39 years old woman, right-handed was admitted in our department for headache, generalized seizures and postictal right hemiparesis and transient aphasia. the onset of seizures was at age 7, and they were refractory to antiepileptic drugs. the last antiepileptic scheme contained levetiracetam (keppra) 1000 mg/d, topiramat (topamax) 400 mg/d and valproic acid (depakine chrono) 1500 mg/d. reviewing the medical history, we found out that the patient was previous diagnosed, in another neurosurgical department, with left frontal avm, grade spetzler-martin vi, and therefore was refused for any curative treatment. on admission general physical exam was within normal limits. neurological exam found mild right hemiparesis and hyperactive deep tendon reflexes in the right hemibody. blood analysis (hg=13.6 g/dl), pulmonary x-ray and electrocardiography showed normal aspect. cerebral ct-scan showed giant left frontal avm, 7/6 cm in diameter, with multiple serpiginous vessels and left parasagittal parietal porencephalic cyst secondary to previous bleeding (figure 1). cerebral mri showed a giant left frontal avm, sizing 7/6.4/5 cm, with a tangle of multiple flow void sinuous vessels, with mass effect on the frontal horn of the left lateral ventricle and enlarged ventricles. part of the nidus was located into the left motor area. 48 sandu and gorgan total resection in a giant left frontal arteriovenous malformation figure 1 cerebral ct scan. giant left frontal avm, 7/6 cm, with mass effect on the frontal horn of the left lateral ventricle and enlarged ventricles, left parasagittal parietal porencephalic cyst middle cerebral arteries, anterior cerebral arteries and anterior communicating artery were enlarged due to increased flow. the left internal carotid artery was also enlarged and measured 7 mm in diameter. venous sinuses (predominantly sagittal and transverse sinus) were grossly enlarged, the sagittal sinus measuring 24 mm. in the left temporal lobe and left hippocampus there were multiple enlarged sinuous vessels. a porencephalic cavity measuring 41/27 mm was seen left parietal parasagittal. cerebral angio-mri showed complex, giant avm, containing a large left frontal nidus with feeding arteries from left anterior cerebral artery and anterior communicating artery. large veins drained into the superior sagittal sinus. the avm had mass effect, compressing the left lateral ventricle. six vessels angiography showed giant left frontal avm with feeding arteries from left middle cerebral artery, left anterior cerebral artery, anterior communicating artery, right anterior cerebral artery and left external romanian neurosurgery (2013) xx 1: 46 – 56 49 carotid artery. right a1 segment, left a1 segment and left middle cerebral artery were enlarged from increased flow. midline shift to the right of the cerebral vessels was seen. venous drainage was superficial into the superior sagittal sinus, through 3 sinuous and ectatic veins, and profound via straight sinus into the inferior sagittal sinus. the avm was also injected from the vertebrobasilar circulation via left posterior communicating artery and from arterial feeders from left posterior cerebral artery (figure 2). 50 sandu and gorgan total resection in a giant left frontal arteriovenous malformation figure 2 cerebral angiography. giant left frontal avm with feeding arteries from left middle cerebral artery, left anterior cerebral artery, anterior communicating artery, right anterior cerebral artery, left posterior communicating artery and left posterior cerebral artery. flow-related enlargement of right a1 segment, left a1 segment and left middle cerebral artery. superficial and profound venous drainage figure 3 intraoperatory aspect. corticalized giant left frontal avm, with feeding arteries coming from superficial branches from left middle cerebral artery the patient received dexamethasone 16 mg/d, mannitol 20% 250 ml/d, furosemid 40 mg/d, levetiracetam 1000 mg/d, topiramat 400 mg/d, valproic acid 1500 mg/d, analgesics, intravenous hydration and gastro-protective drugs. pre-anesthetic consult found a risk score asa iv. patient underwent surgery, under general anesthesia. the patient was placed in supine position and the head was turned 30° to the right. we performed a large left frontoparietal bone flap; dura mater was cut in a curvilinear fashion. after dural opening, the avm could be seen on the cortical surface on approximately 20 cm2. on the cortical surface, the avm presented multiple feeding arteries from superficial branches of left middle cerebral artery and a large draining vein entering the dura in closed vicinity with superior sagittal sinus (figure 3). we began to circumferentially dissect the nidus of the avm, progressively occluding feeding arteries from left middle cerebral artery. dissection followed the gliotic layer surrounding the avm. in the postero-superior part of the nidus we indentified and occluded a large feeding artery coming from the left posterior cerebral artery. dissection progresses towards the midline with occlusion of feeding arteries arising from right internal carotid artery. feeding arteries were sealed off using electrocoagulation or clipping; a total of 8 yasargil vascular titanium clips were used. after occluding all feeding arteries and fully circumferentially dissection of the nidus, 2 additional vascular clips were needed to occlude draining veins into the superior and inferior sagittal sinuses. careful hemostasis was done using electrocoagulation, abundant lavage with saline, h2o2, haemostatic agents and muscle. the hemostasis posed great difficulties due to brisk profuse bleeding secondary to early normal perfusion pressure breakthrough. closure and anchoring of dura mater, epidural external draining tube, and the bone flap was replaced back and fixed in place. the scalp romanian neurosurgery (2013) xx 1: 46 – 56 51 was closed with simple sutures in anatomical layers. operating time was 8 hours. during surgery the patient received 2 whole blood units, 9 fresh frozen plasma units, 16 packed red blood cells and 2 platelet concentrates. the patient was taken into intensive care unit, and was kept sedated 36 hours. postoperative outcome was favorable, patient was extubated after 36 hours, regained consciousness, obeyed commands, had no speech disturbances and presented right hemiparesis. the patient presented postoperative acute anemia, hg 6.08 g/dl, which was corrected using blood transfusions. during next days the neurological outcome was favorable, right hemiparesis improved. following operation the patient presented no seizure, under antiepileptic drugs. control cerebral ct scan showed minimal left frontal bleeding at the resection site, without mass effect (figure 4). control 4 vessels cerebral angiography revealed the absence of vascular nidus or abnormal vessels (figure 5). figure 4 postoperatory cerebral ct scan. minimal left frontal bleeding at the resection site, without mass effect 52 sandu and gorgan total resection in a giant left frontal arteriovenous malformation figure 5 postoperatory cerebral angiography. absence of vascular nidus or abnormal vessels the patient was discharge 26 days after surgery, neurologically improved, presenting only mild right hemiparesis and seizure free. at two month follow-up the patient regained full motor function, she presented no seizures under progressively reduced doses of antiepileptic therapy. discussions giant avms are lesions with nidus greater than 6 cm in diameter. most common forms of clinical presentation of avms are hemorrhage or seizures. our patient had imagistic history of previous bleeding, but intractable seizures were clinically significant. large avms are more likely to present with seizure, because their large size make them more likely to involve the brain tissue. (6) persistent, intractable seizures under full dose of antiepileptic drugs severely affect the quality of life. our patient presented incontrollable seizure for 32 years, in spite of full dose polytherapy anticonvulsivants, that severely impaired her quality of life. seizures may occur because the surrounding ischemic brain, secondary to vascular steal, has lower thresholds for seizures and higher susceptibility to epileptogenic activity, than normally perfused brain. (3; 18) the patient was diagnosed in another department with avm grade vi spetzlermartin. grade vi avms are considered untreatable lesion by any means: surgery, radiosurgery, embolization. if for grades i to v there are specific criteria and grade of the avm is easy calculated, by summing points assigned to three criteria (size, eloquence of the brain and pattern of venous drainage) classification as grade vi avm is subjective and the experience of the surgical team matters more. unlike grade romanian neurosurgery (2013) xx 1: 46 – 56 53 vi, grade v avms may be suitable for surgery. a study regarding large avms, grade iv and v, found a risk of hemorrhage of 10.4% per year in patients with residual nidus, compared with natural history of 1.5% per year rate of hemorrhage, and the authors concluded that surgery is indicated in such cases only if they are symptomatic and the avm impairs the quality of life. (7) surgery is the treatment of choice in avms, being the only one capable of preventing hemorrhage and controlling seizures, but it can only be perform in cases in which the lesion can be removed with acceptable morbidity and mortality risks. the aim of surgery is the complete removal of the nidus. surgical risk, concerning major neurological deficits and death, is directly proportionate with spetzler-martin grade of avms. (16) grade v spetzlermartin poses major surgical risks, due to large nidus measuring more than 6 cm in diameter, deep venous drainage and extension of a part of the nidus into motor area. besides this grading system a supplementary grading scale was propose in order to predict more accurate the outcome after surgery, that included also age, diffuseness of the nidus and hemorrhagic presentation. (10) taken into consideration this supplementary scale, our patients had a diffuse nidus and previous bleeding, seen as a parietal parasagittal porencephalic cavity. once surgery is chosen, one must considerate also arterial supply. giant avms presented complex arterial feeders arising from multiple main brain arteries, which enter the nidus in various sites. careful inspection of angiographic images helps to indentify all feeding arteries and draining veins. our patients had arterial feeders coming from left middle cerebral artery, left anterior cerebral artery, anterior communicating artery, right anterior cerebral artery, left posterior cerebral artery, left posterior communicating artery and left external carotid artery. angiography is also useful to reveal passage arteries, that only pass or skirt the nidus and pass through to supply normal brain and associated flowrelated aneurysm. we did not identify such arteries or flow related aneurysms. other difficulties posed by surgery are related to location of the avm in the dominant hemisphere and extension of the nidus to the motor area. surgery for avms must take into consideration several aspects. a large bone flap is needed, that fully circumscribes the nidus and offer access to vascular supply. bone flap must be larger than that performed for same size tumors, because unlike tumors avms cannot be debulked from inside, the nidus cannot be retracted and draining veins may restrict access. (9) if vascular supply from the left external carotid artery is present, the surgeon must expect an important bleeding during opening of the skull. dura mater must not be torn during bone flap removal, and cutting it must be done with great care, because draining veins can travel within the dura mater, and these veins must be preserved until the end of the operation. we found a draining vein that was entering the dura mater near the superior sagittal sinus. inspection of the brain revealed a corticalized avm and identified multiple arterial feeders and a superficial draining vein. when operating an avm, the surgeon must keep in mind that it is triangular in shape with the base towards the cortex and the apex towards the ventricle. as a golden rule, feeding arteries must be sealed off first and veins must be kept patent till the end, to prevent engorgement of the nidus and 54 sandu and gorgan total resection in a giant left frontal arteriovenous malformation rupture. (4; 6; 9; 11) we begun devascularization of the avm, we occluded first cortical feeders from superficial branches of left middle cerebral artery, than we started dissection by circumscribing the nidus. dissection progressed in the surrounding gliotic layer, further sealing off feeding arteries from left middle cerebral artery. dissection of the posterior part of the nidus was facilitated by the presence of a porencephalic cavity secondary to previous bleeding. the postero-superior part of the nidus was fed by a large artery coming from the left posterior cerebral artery. vascular supply of the medial part of the nidus came from branches from right internal carotid artery. the deep part of the nidus, which came up to the frontal horn of the lateral ventricle, was most challenging to dissect because here there were small high-pressure feeders arising from chroidal and ependymal arteries and fragile small veins, that are difficult to control and can retract into adjacent parenchyma, plus when reaching the deep part of the nidus occurs a vigorous attempt of recanalization the avm. (9; 11) the tip of the avm reaches the left lateral ventricle, therefore the surgeon must be prepared to enter into the ventricle. at the end of the operation draining veins were occluded. a total number of 10 yasargil vascular clips were used, 8 for sealing the arteries and 2 for veins. vascular clips were preferred instead of coagulation of the vessel, because of their big diameter, which made coagulation alone impossible or ineffective. a possible intraoperative difficulty may be premature occlusion of a major draining vein, which leads to nidus rupture and massive bleeding. this is the reason why before occluding a vessel, a temporary occlusion must be performed, and nidus changes must be observed. if the vessel is a vein the nidus will become tensed. in this case the temporary clip must be removed immediately and the vein must be preserved until the end of the operation. if the vessel is an artery, the nidus will not change turgor or it may shrink. care must be taken not to mistake a vein for an artery, because veins are red, containing oxygenated blood and enlarged. excessive intraoperative bleeding required massive blood and blood products transfusions. massive transfusions impair coagulation (15), making hemostasis more difficult. besides coagulation impairment, massive transfusions lead to acidosis, hypothermia, acid-base imbalances, electrolyte abnormalities (hypocalcemia, hypomagnesemia, hypokalemia, hyperkalemia), citrate toxicity and transfusion-associated acute lung injury. (15) even with all massive transfusions the patient presented acute postoperative anemia, which was aggressively corrected, to improve oxygen delivery to the brain tissue. normal perfusion pressure breakthrough occurs due to loss of autoregulation of cerebral vessels. (6; 17) a large amount of blood that was flowing through the nidus is redistributed to the adjacent brain after avm resection. vessels supplying normal brain present long-term vasodilatation due to prolong ischemia. in time, they lose the capacity of vasoregulation and when flow is redistribute these vessels, they are incapable of vasoconstriction, leading to brain swelling and hemorrhage. at the end of the operation an early normal perfusion pressure breakthrough occurred, that required prolong and careful hemostasis. this is due to large size of the avm, which romanian neurosurgery (2013) xx 1: 46 – 56 55 was stealing a large amount of blood, fact seen on cerebral angiography. right a1 segment, left a1 segment and left middle cerebral artery were enlarged from increased flow, and arteries supplying normal brain are barely visible, suggesting long-term ischemia. the presence of regional hypoperfusion due to vascular steal indicates a higher risk for normal perfusion pressure breakthrough occurrence. risk of developing normal perfusion pressure breakthrough is higher in large avms, with high flow, steal from vertebrobasilar system or controlateral circulation and feeders from external carotid artery. (11) the patient presented right hemiparesis, intensive kinesiotherapy program was initiated and motor deficit slowly improved, at discharge she presented mild to moderate right hemiparesis, predominantly brachial and on two month follow-up she regained full motor function. total resection of the avm permitted full seizures control with reduced dose of antiepileptic therapy. in giant avms multimodal treatment can also be applied. some authors recommend staged stereotactic surgery (4; 8), stereotactic radiation (2; 20) or embolization (11; 13; 21) in giant avms to convert them to surgery. conclusions surgery is the therapy of choice in avms, because it is the only curative treatment, capable of preventing hemorrhage and controlling seizures. management in grade v avms is challenging, because of their large size, multiple dilated arterial feeders from anterior and posterior circulation and external carotid arteries, high blood flow, vascular steel with prolong hypoperfusion of the surrounding brain, grossly enlarged draining veins, profound venous drainage and location in eloquent area. giant avms with high flow nidus, causing a great degree of vascular steel in the surrounding brain, with hypoperfusion of normal parenchyma may develop early normal perfusion pressure breakthrough. total resection in grade v avms can be performed with minimal transient morbidity and favorable outcome. total resection of the avm permitted control of intractable seizures with reduced dose of antiepileptic therapy. correspondence: aurelia mihaela sandu, address: emergency clinical hospital bagdasar-arseni, no. 10-12, berceni street, sector 4, bucharest; e-mail: aurasandu@gmail.com; tel. 0724.263.023 references 1. altschul d, smith ml, sinson gp. (2011). intracranial arteriovenous malformation. medscape emedicine[surgery/neurosurgery/vascular]. 2. andisheh b, brahme a, bitaraf ma, mavroidis p, lind bk. (2009). clinical and radiobiological advantages of single-dose stereotactic light-ion radiation therapy for large intracranial arteriovenous malformations. technical note. j neurosurg 111, 919926. 3. congar p, gaiarsa jl, popovici t, ben-ari y, crepel v. (2000). permanent reduction of seizure threshold in post-ischemic ca3 pyramidal neurons. j neurophysiol 83, 2040-2046. 4. deruty r, turjman f, pelissou-guyotat i. (2006). surgical managemnt of cerebral arteriovenous malformations. in schmidek hh, roberts dw (eds), operative neurosurgical techniques indications, methods, and results. philadelphia, saunders elsevier, pp 1263-1277. 5. gorgan rm: malformațiile arterio-venoase cerebrale. (2007). in popescu i (ed), tratat de chirurgie. bucurești, ed. academiei române, 2007, pp 323-335. 6. greenberg ms. (2010). vascular malformations. in greenberg ms (ed), handbook of neurosurgery. new york, thieme medical publisher, pp 1098-1142. 7. han pp, ponce fa, spetzler rf. (2003). intention to treat analysis of spetzler-martin grade iv and v avms: natural history and treatment paradigm. j neurosurg 56 sandu and gorgan total resection in a giant left frontal arteriovenous malformation 98, 3-7. 8. hanakita s, koga t, shin m, shojima m, igaki h, saito n. (2012). role of stereotactic radiosurgery in the treatment of high-grade cerebral arteriovenous malformation. neurol med chir (tokyo) 52, 845-851. 9. komotar rj, strake rm, otten ml. (2010). surgical treatment of cortical arteriovenous malformations. in connolly jr. es, mckhann ii gm, huang j, choudhri tf, komotar rj, mocco j (eds), fundamentals of operative techniques in neurosurgery. new york, thieme medical publishers, pp 138-143. 10. lawton mt, kim h, mcculloch ce, mikhak b, young wl. (2010). a supplementary grading scale for selected patients with brain artriovenous malformations for surgery. neurosurgery 66, 702-713. 11. marciano ff, vishteh ag, apostolides pj, spetzler rf. (2000). arteriovenous malformations – supratentorial. in kaye ah, black p (eds), operative neurosurgery. london, harcourt publishers limited, pp 1079-1091. 12. misra m, aletich v, charbel ft, debrun gm, ausman ji. (2000). multidisciplinary approach to arteriovenous malformations. in kaye ah, black pm (eds), operative neurosurgery. london, harcourt publishers limited, pp 1137-1151. 13. natarajan sk, ghodke b, britz gw, born de, sekhar ln. (2008). multimodality treatment of brain arteriovenous malformations with microsurgery after embolization with onyx: single-center experience and technical nuances. neurosurgery 62, 1213-1225. 14. ondra sl, troupp h, george ed, scawab k. (1990). the natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. j neurosurg 73, 387-391. 15. sihler kc, napolitano lm. (2010). complications of massive transfusion. chest 137, 209-220. 16. spetzler rf, martin na. (1986). a proposed grading system for arteriovenous malformations. j neurosurg 65, 476-483. 17. spetzler rf, wilson cb, weinstein p, mehdorn m, townsend j, telles d. (1978). normal perfusion pressure breakthrough theory. clin neurosurg 25, 651672. 18. srejic lr, valiante ta, aarts mm, hutchinson wd. (2013). high-frequency cortical activity associated with postischemic epileptiform discharges in an in vivo rat focal stroke model. j neurosurg published before print [published online february 15, 2013; doi: 10.3171/2013.1.jns121059.]. 19. stapf c, mast h, sciacca rr, berenstein a, nelson pk, gobin yp, pile-spellman j, mohr jp. (2003). the new york islands avm study: design, study progress, and initial results. stroke 34, e29-34. 20. xiao f, gorgulho aa, lin cs, chen ch, agazaryan n, vinuela f, selch mt, de salles aa. (2010). treatment of giant cerebral arteriovenous malformation: hypofractionated stereotactic radiation as the first stage. neurosurgery 67, 1253-1259. 21. xu f, ni w, liao y, gu y, xu b, leng b, song d. (2011). onyx embolization for the treatment of brain arteriovenous malformations. acta neurochir (wien) 153, 869-878. 8solomonadriana_pituitaryapoplexy 68 solomon et al pituitary apoplexy: clinical features, management and outcome pituitary apoplexy: clinical features, management and outcome. clinical study and review of the literature adriana elena solomon1,2*, ligia tataranu1,2, vasile ciubotaru1, mircea radu gorgan1,2 ¹neurosurgical clinic, “bagdasar-arseni” emergency clinical hospital, bucharest, romania ²“carol davila” university of medicine and pharmacy, bucharest, romania *student in neurosurgery abstract: background: pituitary apoplexy is a clinical syndrome secondary to rapid expansion of the content of the sella and extension to suprasellar region, cavernous sinus, sphenoid sinus secondary to a bleeding, ischemic or mixed episode taking place in a pituitary adenoma. this episode will determine a significant compression of the optic nerves, optic chiasm, cavernous sinus and hypothalamus, which translates clinically most often by headache, visual disturbances, deceased level of consciousness and ophthalmoplegia. material and methods: this paper presents a retrospective study over a period of five years, from january 2009 to december 2013 and includes 98 patients diagnosed with pituitary apoplexy and treated in the third department of neurosurgery, emergency clinical hospital bagdasar-arseni. of the 98 patients, 62 were females (63.3 %) and 36 were males (36.7 %) with a ratio of female to male of 1.7:1. the patients were aged between 17 and 75 years old, average age being approximately 50 years. follow-up period ranged from 2 months to 5 years. the main symptomsat presentation was sudden, intense headache, this symptom was encountered in 90 patients (91.83%), vomiting showed by 76 patients (77.55%), decreased visual acuity observed in 57 patients (58.16%), visual field deficits in 74 patients (75.51%), cranial nerves palsy (iii, iv, vi) observed in 14 patients (14.28 %). conclusions: pituitary apoplexy is a disease that can endanger patients' lives. the clinical presentation may vary from minor symptoms to major neurological deficits and even death so early diagnosis and treatment are vital. key words: apoplexy, pituitary adenoma. background and epidemiological considerations pituitary apoplexy is one of the major neurosurgical emergencies especially due to compression of the optic nerves and chiasm and associated hormonal imbalance. in this paper, we present a retrospective study conducted over a period of 5 years which includes patients diagnosed with pituitary romanian neurosurgery (2015) xxix (xxii) 1: 68 76 69 apoplexy and treated in the third department of neurosurgery from emergency clinical hospital bagdasar-arseni, bucharest. in this paper, we propose to draw attention to the importance of early diagnosis and treatment of these patients given the sometimes disastrous consequences of this condition on visual and endocrinefunction. also, we will make an analysis of the literature for a better understanding of this neurosurgical pathology. pituitary apoplexy is a clinical syndrome secondary to rapid expansion of the content of the sella and extension to suprasellar region, cavernous sinus, sphenoid sinus secondary to a bleeding episode, ischemic or mixed episode (ischemic and hemorrhagic) taking place in a pituitary adenoma. the hemorrhagic, ischemic or mixed episode will determine a significant compression of the optic nerves, optic chiasm, cavernous sinus and hypothalamus, which translates clinically most often by headache, visual disturbances, deceased level of consciousness and ophthalmoplegia. (1) the first subtemporal decompression for a pituitary adenoma was practiced by paul, a british neurosurgeon in 1892, in an acromegalic patient with intracranial hypertension. in 1898, baileydescribed the first case of pituitary adenoma associated with intratumoral hemorrhage. in 1906, hoursely reported a series of 10 patients with pituitary tumors treated by temporal and subfrontal approaches. a milestone in the treatment of these tumors was marked by schloffer, in 1907, when he approached sella turcica via an extensive lateral rhinotomy with resection of the septum and turbinates. in 1909, cushing used a variation of schloffler’s technique, he adopted sublabial incision, later described by halstead and kanavel. brougham et al, first described the signs and symptoms associated with hemorrhage in a pituitary tumor and named it pituitary apoplexy; the suffix "plexi" comes from greek term meaning to strike or to have a stroke. another important step in the treatment of this pathology is the transnasal transfenoidal approach, first described by hirsch in 1910. in 1960, hardy used operating microscope in a transnasal transsphenoidal approach of a microadenoma. from 1990, endoscopeis a tool widely used in surgical treatment of sellar tumors. (27) pituitary tumors represent about 10-15 % of all primary brain tumors, a much higher frequency, of 20-25%, is found for microadenomas discovered incidentally at autopsy. regarding pituitary apoplexy clinically evident, it has a frequency of 1-2%, maximum 10 % in some studies of total pituitary tumors, the frequency is about 28 % if we take intoconsideration clinically silent pituitary apoplexy when diagnosis is established in histopathological examination. (2) (27) approximately 50% of apoplectic events occur in patients who were not previously diagnosed with a pituitary tumor. the age range of affected patients is situated between first and eighth decades of life with the most cases in the fifth or sixth decade. most of the published studies demonstrated a higher frequency of pituitary apoplexy among male compared to female population. (24) 70 solomon et al pituitary apoplexy: clinical features, management and outcome material and methods this paper presents a retrospective study over a period of five years, from january 2009 to december 2013 and includes 98 patients diagnosed with pituitary apoplexy and treated in the third department of neurosurgery, emergency clinical hospital bagdasar-arseni. of the 98 patients, 62 were female (63.3%) and 36 were male (36.7%) with a ratio of female to male of 1.7:1. thus, we observe a slightly higher frequency in female population compared to studies published so far. the patients were aged between 17 and 75 years old, average age being approximately 50 years, this aspect is in line with studies published to date. follow-up period ranged from 2 months to 5 years. clinical presentation the main symptom at presentation was sudden, intense headache, this symptom was encountered in 90 patients (91.83%). other signs and symptoms were: vomiting showed by 76 patients (77.55%), decreased visual acuity observed in 57 patients (58.16%), visual field deficits in 74 patients (75.51%), cranial nerves palsy (iii, iv, vi) observed in 14 patients (14.28 %). none of the patients in our study did not show altered consciousness on admission (figure 1). figure 1 clinical status at admission. 0.00% 20.00% 40.00% 60.00% 80.00% 100.00% headache vomiting decreased visual acuity visual field deficits cranial nerve palsy 91.83% 58.16% 75.51% 14.28% 77.55 % romanian neurosurgery (2015) xxix (xxii) 1: 68 76 71 figure 2 endocrinological status at admission. endocrinological findings endocrinological evaluation was performed in all patients in the study, 64 patients had clinically nonfunctioning pituitary tumors (65.3%), 24 patients had prolactinomas (24.5%), 7 patients were known with gh secreting pituitary adenomas (7.1 %) and 3 patients had acth secreting pituitary adenomas (3.1%). pituitary apoplexy occurs with no predilection to a certain category of pituitary adenomas. a greater frequency of pituitary apoplexy in the studied population with clinically nonfunctioning pituitary tumors is due to higher overall frequency of this type of tumor than a certain predisposition (figure 2). imaging evaluation for imaging diagnosis of our patients we used ct scan and mri with and without gadolinium; we also used this investigations to evaluate the postoperative status of our patients. treatment in all cases included in our study, surgery treatment was practiced emergency. the time between diagnosis and surgery was of one to ten days. in all cases we used transnasal transsphenoidal approach. in cases with corticoid insufficiency, corticosteroid hormone replacement therapy was instituted. during surgery, and in the immediate postoperative period was performed monitoring of urine output and in patients with diabetes insipidus, treatment with desmopressin was made. patient outcomes in the immediate postoperative period the best recovery was observed for cranial nerve 65% 26% 7% 3% nonfunctional adenomas prolactinomas somatotroph adenomas adenoame corticotrofe 72 solomon et al pituitary apoplexy: clinical features, management and outcome palsy (nerves iii, iv and vi). as regards of visual function (decreased visual acuity or visual field deficits) recovery was partial after surgery. of the 57 patients with impaired preoperative visual acuity we observed its improvement after surgery in 46 patients (80.7%), from 74 patients with visual field deficits at admission, postoperative improvement was noted in 63 patients (85.1%). regarding paresis of cranial nerves iii, iv, vi, it was almost completely recovered after surgery, 12 of 14 patients with severe preoperative paresis (85.7%). our study shows that the recovery was better in cases where surgery was done in the first week after symptoms onset. this applies especially to recover deficits in visual acuity or visual field, in terms of recovery oculomotor nerve palsy, good results were obtained when surgery was made more than one week after the onset of the symptoms. of the 98 patients included in the study, 56 were operated during the first week after onset of the signs and symptoms and 42 patients were operated at less than a week. of the 56 patients operated in the first week, 54 had improvement of visual function (96.4%) while the percentage of recovery for patients operated more than a week is 50% (21 patients with improved visual function after surgery). postoperative endocrinological status of the 98 patients operated, all patients with hypopituitarism did not fully recover after surgery, so hormone replacement therapy on various axes was necessary in most patients. thus in our series of patients, 60 patients (61.2 %) required corticosteroid replacement therapy, 41 patients (41.8%) received thyroid hormone replacement, gonadotroph hormone replacement was necessary in 24 patients (25.5%) and desmopressin treatment in 7 patients (7.1%). discussion pituitary apoplexy is a clinical syndrome caused by the rapid expansion of a pituitary adenoma secondary to ischemia and /or intratumoral hemorrhage which causes compression of the cavernous sinus, chiasm and optic nerves. clinical syndrome is characterized by brutal installed headache, vomiting, vertigo, meningism, deceased level of consciousness, ophthalmoplegia, visual field deficits, and decreased visual acuity. (3-5) all types of pituitary tumors can develop intratumoral apoplexy. approximately 50% of apoplectic events occur in patients who had not been previously diagnosed with pituitary tumors, this leads to a delay in diagnosis. wakai et al noticed in their retrospective study that 16.6% of their patients with pituitary adenomas show bleeding or intratumoral hematoma but only 6.8% had a clinical apoplectic episode. deb and al observed intratumoral hemorrhage in 17.1% of patients, but only 5.4% had clinical signs and symptoms of pituitary apoplexy. (6, 7) the most common signs and symptoms present at admission were: headache (frontal or retroocular), visual field restriction, decreased visual acuity, ophthalmoplegia, nausea, vomiting, vertigo, meningism, deceased level of consciousness, facial pain or numbness, fever, hemiparesis, horner syndrome, seizures.(8) romanian neurosurgery (2015) xxix (xxii) 1: 68 76 73 hormonal status hormonal imbalance is often found in pituitary apoplexy. hypopituitarism is caused by increased intrasellar pressure, destruction of the pituitary gland by an existing adenoma or secondary to apoplectic event. vedhuis and hammond noted that after an episode of pituitary apoplexy, 88% of patients had growth hormone deficiency, 76% had inadequate secretion of luteinizing hormone, 67% had prolactin inappropriate secretion, 66% had inappropriate secretion of acth and 33 % had estradiol deficiency. (1, 26, 28) diabetes insipidus is rare and occurs in pituitary apoplexy secondary to tumor compression of the infundibulum made by edematous or hemorrhagic material so that it is prevented release of antidiuretic hormone fromhypothalamus. another possibility is the compression of the inferior hypophysial artery in the intracavernous portion by hemorrhagic material. baha and verrees found that diabetes insipidus occurs in only 2-3% of patients with pituitary apoplexy. (1) precipitating factors precipitating factors have been identified in about 50% of the cases diagnosed with pituitary apoplexy. the most common are: treatment with bromocriptine, estrogen therapy, anticoagulation, pregnancy, head trauma, bowel and other general surgery, diabetic ketoacidosis, cardiac bypass, radiotherapy, hypertension or hypotension, atherosclerosis. (1, 9, 10, 27) fluctuations in blood pressure associated to cardiac bypassand surgical interventions can lead to pituitary apoplexy. fragmentation of atherosclerotic plaques and engaging of particles within the pituitary vasculature may lead to gland infarction. infections, childbirth, and surgery may be associated with pituitary apoplexy secondary to increased gland activity in response to increased need for stress hormones in these circumstances. sneezing, coughing or ketoacidosis change blood flow and blood osmotic values precipitating pituitary apoplexy. (11, 12, 25) numerous studies have shown a higher rate of hemorrhage or ischemia in pituitary tumors due to large discrepancy between the development of local circulation and tumor size; however small tumors can also develop apoplexy events. (11, 12, 25) imaging studies ct scan has a detection rate of 21-46 % for pituitary apoplexy. the main detected issues are: hemorrhagic area, specific hyperdense, recent hemorrhage, mixed density when bleeding is associated with acute ischemic area. another aspect is subarachnoid hemorrhage, ct scan can detect invasion of the basal cisterns with blood, complication that can accompany a series of pituitary apoplexy. the ct scan bone window gives us important information about sella turcica and paranasal sinuses. (3, 13) (figure 3). figure 3 pituitary apoplexy – ct scan 74 solomon et al pituitary apoplexy: clinical features, management and outcome figure 4 pituitary apoplexy – mri images mri has a detection rate of 100 % for pituitary apoplexy. this imaging investigation has greater sensitivity and achieves better detection of the tissue. the issues detected in patients with pituitary apoplexy are specific heterogeneous density hemorrhage, edema and ischemia in the pituitary gland. (14) (figure 4). mri is the most effective imaging investigation for pituitary apoplexy. piotin et al wrote down that mri imaging for this condition can be very varied. (15) arita et al drew attention to parasellar dural changes. these changes are caused by changes in dural blood flow. he also noted about sphenoidal sinus mucosal thickening due to local venous obstruction. another cause could be sphenoid sinus mucosal inflammation induced by inflammatory substances produced by tumor necrotic tissue. (16, 17) differential diagnosis differential diagnosis of pituitary apoplexy can be done with subarachnoid hemorrhage secondary to aneurysm rupture, viral or bacterial meningitis, spontaneous bleeding (hypertension, amyloidosis, metastatic or primary pituitary tumor), cavernous sinus thrombosis, carotid-cavernous fistula, migraine, optic neuritis, diabetic oculomotor palsy, temporal arthritis, vertebrobasilar insufficiency, transtentorial herniation. (18) treatment the standard treatment for pituitary apoplexy includes high-dose of corticosteroid hormone which will lead to improvement of symptoms and surgical decompression using a transsphenoidal approach. pituitary gland is capable to secret suitable amounts of hormones even when only 10% of the gland remains functional. (19, 20) the treatment of choice for pituitary apoplexy is represent by surgical intervention which also decompress cavernous sinus and suprasellar structures; it is recommended especially when there is impairment of visual acuity or visual field, impaired consciousness or when there is progression of symptoms. transsphenoidal approach is safe and effective because it does not make a direct manipulation of the optic tract especially for pituitary apoplexy in the acute phase when there is an important compression of the optic pathway. (10, 21) transcranial approaches are recommended when there is an important hemispheric hemorrhage extension, presence of hemorrhage and/or necrosis that extends beyond the intact diaphragm or when there is a sphenoid sinus less aerated. the main transcranial approaches used are pterional, subfrontal, and subtemporal. (22, 23, 27) the main complications of transsphenoidal surgery are: damage to the hypothalamus, visual tract damage, vascular lesions, csf fistula, cavernous sinus injury (internal carotid artery, cranial nerves iii, iv, romanian neurosurgery (2015) xxix (xxii) 1: 68 76 75 vi), iatrogenic hypopituitarism, brainstem injury, and nasal complications (mucocele, sinusitis, fracture of hard palate or cribriform plate, nasal deformity). (22, 27) conclusions pituitary apoplexy is a disease that can endanger patients' lives. the clinical presentation may vary from minor symptoms to major neurological deficits and even death so early diagnosis and treatment are vital. abreviations ct – computerized tomography irm – magnetic resonance imaging acknowledgement this paper was co-financed from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 “excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields -excelis”, coordinator the bucharest university of economic studies. correspondence adriana elena solomon, address: emergency clinical hospital bagdasar-arseni, no. 10-12, berceni street, sector 4, bucharest; e-mail: adriana_ded@yahoo.com references 1.verrees m, arafah bm, selman wr. pituitary tumor apoplexy: characteristics, treatment, and outcomes. neurosurgical focus. 2004;16(4):e6. 2.lange m, woenckhaus m, segiet w, oeckler r. a rare fatal course of disease in a patient with spontaneous pituitary apoplexy. case report and literature review. neurosurgical review. 1999;22(2-3):163-9. 3.bills dc, meyer fb, laws er, jr., davis dh, ebersold mj, scheithauer bw, et al. a retrospective analysis of pituitary apoplexy. neurosurgery. 1993;33(4):602-8; discussion 8-9. 4.onesti st, wisniewski t, post kd. clinical versus subclinical pituitary apoplexy: presentation, surgical management, and outcome in 21 patients. neurosurgery. 1990;26(6):980-6. 5.randeva hs, schoebel j, byrne j, esiri m, adams cb, wass ja. classical pituitary apoplexy: clinical features, management and outcome. clinical endocrinology. 1999;51(2):181-8. 6.nelson pb, goodman ml, flickenger jc, richardson dw, robinson ag. endocrine function in patients with large pituitary tumors treated with operative decompression and radiation therapy. neurosurgery. 1989;24(3):398-400. 7.wakai s, fukushima t, teramoto a, sano k. pituitary apoplexy: its incidence and clinical significance. journal of neurosurgery. 1981;55(2):187-93. 8.inamasu j, hori s, sekine k, aikawa n. pituitary apoplexy without ocular/visual symptoms. the american journal of emergency medicine. 2001;19(1):88-90. 9.biousse v, newman nj, oyesiku nm. precipitating factors in pituitary apoplexy. journal of neurology, neurosurgery, and psychiatry. 2001;71(4):542-5. 10.arafah bm, taylor hc, salazar r, saadi h, selman wr. apoplexy of a pituitary adenoma after dynamic testing with gonadotropin-releasing hormone. the american journal of medicine. 1989;87(1):103-5. 11.peck v, lieberman a, pinto r, culliford a. pituitary apoplexy following open-heart surgery. new york state journal of medicine. 1980;80(4):641-3. 12.savage eb, gugino l, starr pa, black pm, cohn lh, aranki sf. pituitary apoplexy following cardiopulmonary bypass: considerations for a staged cardiac and neurosurgical procedure. european journal of cardiothoracic surgery : official journal of the european association for cardio-thoracic surgery. 1994;8(6):333-6. 13.nelson pb, robinson ag, hirsch w, jr. postoperative computed tomographic evaluation of patients with large pituitary tumors treated with operative decompression 76 solomon et al pituitary apoplexy: clinical features, management and outcome and radiation therapy. neurosurgery. 1991;28(2):238-40; discussion 40-1. 14.lundin p, pedersen f. volume of pituitary macroadenomas: assessment by mri. journal of computer assisted tomography. 1992;16(4):519-28. 15.piotin m, tampieri d, rufenacht da, mohr g, garant m, del carpio r, et al. the various mri patterns of pituitary apoplexy. european radiology. 1999;9(5):91823. 16.arita k, kurisu k, tominaga a, sugiyama k, ikawa f, yoshioka h, et al. thickening of sphenoid sinus mucosa during the acute stage of pituitary apoplexy. journal of neurosurgery. 2001;95(5):897-901. 17.liu jk, couldwell wt. pituitary apoplexy in the magnetic resonance imaging era: clinical significance of sphenoid sinus mucosal thickening. journal of neurosurgery. 2006;104(6):892-8. 18.glendenning p, pullan pt, knuckey nw. pituitary apoplexy: the importance of citing the differential diagnosis. the medical journal of australia. 2000;173(10):548-9. 19.kamiya y, jin-no y, tomita k, suzuki t, ban k, sugiyama n, et al. recurrence of cushing's disease after long-term remission due to pituitary apoplexy. endocrine journal. 2000;47(6):793-7. 20.de divitiis e, cappabianca p. microscopic and endoscopic transsphenoidal surgery. neurosurgery. 2002;51(6):1527-9; author reply 9-30. 21.cappabianca p, cavallo lm, colao a, del basso de caro m, esposito f, cirillo s, et al. endoscopic endonasal transsphenoidal approach: outcome analysis of 100 consecutive procedures. minimally invasive neurosurgery : min. 2002;45(4):193-200. 22.cappabianca p, cavallo lm, colao a, de divitiis e. surgical complications associated with the endoscopic endonasal transsphenoidal approach for pituitary adenomas. journal of neurosurgery. 2002;97(2):293-8. 23.de divitiis e, cappabianca p, cavallo lm. endoscopic transsphenoidal approach: adaptability of the procedure to different sellar lesions. neurosurgery. 2002;51(3):699705; discussion -7. 24. milazzo s, toussaint p, proust f, et al. (1996). ophthalmologic aspects of pituitary apoplexy. eur j ophthalmol 6:69–73. 25. da motta la, de mello pa, de lacerda cm, et al. (1999). pituitary apoplexy.clinical course, endocrine evaluations and treatment analysis. j neurosurg sci 43:25–36. 26. brucker-davis f, oldfield eh, skarulis mc, et al. (1999). thyrotropin-secreting pituitary tumors: diagnostic criteria, thyroid hormone sensitivity, and treatment outcome in 25 patients followed at the national institutes of health. j clin endocrin metab. 84:476. 27. youmans j.r. (2004). neurological surgery, 5th edition, h. richard winn, md, editor. saunders (elsevier), philadelphia. 28. veldhuis jd, hammond jm. (1980). endocrine function after spontaneous infarction of the human pituitary: report, review, and reappraisal. endocr rev 1:100–107. microsoft word ciureaav_tribute_f.docx romanian neurosurgery (2012) xix 1 tribute to professor constantin n. arseni (1912-1994) a.v. ciurea1, claudiu savu2, d. mohan3 1“carol davila” university school of medicine, the national center for excellency in neurosurgery bucharest, bagdasar-arseni teaching hospital 2euromedica clinic hospital, baia-mare 3university of oradea, faculty of medicine, dept. of neurosurgery, oradea county emergency hospital a big-hearted moldavian man, such as all the greatest surgeons ever born in romania, the one that would become one of the founding fathers of romanian neurosurgery, professor constantin arseni, was born in the county of suceava, in the small settlement of dolhasca, into a very poor family at the 3rd of february 1912. he leaves for cluj in 1929 where he graduates medical school 6 years later in 1935 and presents his phd thesis entitled “juxtaprotuberantial neurotomy for the treatment of intermittent trigeminal neuralgia” on the 30th of june 1936. a first such title for romania, as neurosurgery had never been before the subject of a phd thesis; the paper caught the attention of the professors examining it and received the highest score possible. committing his life to medicine, young arseni got his stripes quickly and entered the medical learning system as teaching assistant between the years 1937 and 1944 at the discipline of pathology which was led by professor i.t. niculescu. pursuing a career in surgery he worked for 3 years at the emergency hospital in bucharest where he honed his skills as a surgeon; soon after he will embark on a journey to help put the basis of the romanian school of neurosurgery. at only 34, the young doctor constantin arseni was appointed chief of the neurosurgical department at the central hospital for mental, nervous and endocrinological diseases, carrying on the legacy of professor d. bagdasar. he was appointed assistant professor in 1952 and professor of neurosurgery in 1963. in the year 1964 the clinic led by professor arseni had 220 beds. at the time it was the best outfitted neurosurgery department in the country. a true pillar of romanian medicine, professor arseni completes the titanic task to modernize the department and in the year 1975 the biggest neurosurgery clinic in europe is opened. the 550 available beds transformed the hospital into the confirmation of neurosurgery’s value among the medical specialties in romania. a.v. ciurea et al tribute to professor constantin n. arseni understanding the true necessity for a interdisciplinary approach of the patients, professor arseni reunites under the same roof all the neurosurgical specialties: craniocerebral trauma surgery, spinal trauma surgery, intracranial expansive process surgery, vascular neurosurgery, spinal tumor and degenerative disease surgery, pediatric neurosurgery, functional neurosurgery, neurorecovery and of course neurosurgical intensive care. at the same time the neurosurgical pathology department underwent a full development process. in this way the bagdasar-arseni hospital was born, the most modern and best equipped neurosurgery clinic in romania. an important element in prof. arseni’s activity was the real preoccupation for clinic and fundamental research. in this respect he created within the neurology, neuropsychiatry and neurosurgery institute a special research department which was outfitted at the standards of the period. not only research had to gain, but methods of investigation and treatment were updated as well. in the developing of the bucharest neurosurgery clinic, a tremendous achievement was the first usage of a computed tomography machine in 1982. this event immediately raised the value of diagnostics and follow-up for the neurosurgical pathology. under the careful and strict lead of professor arseni the scientific and publishing activities got a tremendous impulse. this explains the birth of 54 titles in neurosurgery, neurology, neurorecovery and neurosurgical intensive care. a few of these titles stand out. among them we mention • “vascular diseases of the brain and spinal cord”– c. arseni, i. petrovici, f. nash, v. cunescu – 1964 • “cranio-cerebral traumatology” – c. arseni, i. oprescu – 1972 • “neurosurgical semeiology” – c. arseni, a. constantinescu, m. maretsis – 1977 •“pathology of cns tumors” – c.arseni, n. carp 1978 • “treatise of neurology” (in 5 volumes) – c. arseni – 1979-1982 • “parasitic diseases of the central nervous system” – c.arseni, a.v. ciurea – 1981. • “epilepsy” – c. arseni, l popoviciu 1984 • “clinical atlas of electroencephalography” – c. arseni, i. roman 1986 a dedicated surgeon, prof. arseni practiced his job demanding from those around him nothing less than what he offered – the maximum. he committed himself to the patient publishing exceptional papers in the domain of pediatric neurosurgery. • “troubles in neurosurgical diagnostics in child patology” – c. arseni, l. horvath, a.v. ciurea 1978 • “neurosurgical pathology in infants” c. arseni, l. horvath, a.v. ciurea – 1981 romanian neurosurgery (2012) xix 1 his studies remained classical pieces in neurosurgery, especially in what regards parasitic diseases. his papers are quoted in this respect even in the year 2012. cerebral abcesses, cranial trauma surgery, classifications of traumatic comas, basal nuclei tumor approaches, pain pathology, neurosurgical semeiology, pathology of cns tumors or original classifications of craniostenoses are only a a.v. ciurea et al tribute to professor constantin n. arseni few of the topics he approached in his vast career. professor arseni was a teacher in the true meaning of the word. although criticized by some for his didactic extremism, he taught neurosurgery the hard way; most of the chiefs of the neurosurgery departments in romania today are his ex-students. as a token of gratitude for his contributions for the health of the romanian people, constantin arseni was appointed member of the romanian academy in the year 1980 and president of the romanian academy of medical sciences in 1982. he lifted romanian neurosurgery at high esteem in the world and left behind a legacy hard to match for those who followed him. there is no doubt that professor constantin arseni’s name will always be associated with the constant fight for perfection and with the absolute love a doctor has for his patients and fellow humans well being. refferences 1. greenblatt sh, dagi tf, epstein mh – a history of neurosurgery, thieme medical publishing, new york, 1997 2. ciurea av – istoria neurochirurgiei romane (l’histoire de la neurochirurgie roumaine), edit. viata medicala romaneasca, bucuresti 1995. 3. ciurea av – tratat de neurochirurgie, vol. 1, editura medicala, bucuresti, 2010. 4. arseni c. – prof. dr. d bagdasar – 30 de ani de la moarte. neurol. psihiat. neurochir. bucuresti. 1964 5. arseni c. aldea h. momente din istoria neurochirurgiei romanesti, ed. academiei, 1988 6. arseni c. ciurea a.v. – the history of romanian neurosurgery, ed. medicala, 1981 7. bagdasar d. arseni c. – traite de neurochirurgie, ed. academiei rsr, bucuresti 1951 8. bagdasar d. draganesco st. arseni c. – une nouvelle methode de traitement pour les craniostenoses. soc. med. hop. buc. 1941. 14agrawalamit_delayeddeterioration 120 agrawal et al delayed deterioration following the evacuation of posterior fossa extradural hematoma delayed deterioration following the evacuation of posterior fossa extradural hematoma amit agrawal1, s. satish kumar2, umamaheswara reddy v.3 1professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2associate professor of emergency medicine, department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 3assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract: a missed or delayed detection of intracranial injuries can lead to progressive neuronal damage and secondary brain damage. we present a case of 45 year female presented 8 after the road traffic accident and had a large posterior extradural hematoma on left side with mass effect. in addition there was a small speck of right frontal contusion with localized cerebral edema. the patient initially improved after evacuation of the hematoma. however on 3rd post-operative day she was complaining of headache and became progressively drowsy. a follow up ct scan showed increase in peri-lesional edema around the right frontal contusion with squashing of the lateral ventricles suggestive of diffuse cerebral edema. the patient was shifted back to intensive care unit and responded well to further conservative management. in our patient the events could be collaborated well with existing evidence (presence of contrecoup contusion and on clinical deterioration at day 3). key words: delayed deterioration, intracranial hematoma, clinical deterioration, epidural hematoma, posterior fossa. introduction posttraumatic posterior fossa extradural hematoma is complicates about 0.3% of all traumatic brain injuries and represents 4% to 12.9% of all extradural hematomas. (1-6) it is well known that a missed or delayed detection of intracranial injuries can lead to progressive neuronal damage and secondary brain damage that can have a negative impact on the clinical outcome. (7) we describe a case of delayed deterioration following evacuation a large posterior fossa extradural hematoma and discuss the possible underlying for this delayed deterioration. romanian neurosurgery (2015) xxix (xxii) 1: 120 123 121 case report a 45 year female presented 8 after the road traffic accident. she was in altered sensorium since the time of injury. she had multiple episodes of vomiting. there was no history of ent bleed or seizures. her general and systemic examination was unremarkable. she was in altered sensorium (gcs-e2, v2, and m5). pupils were bilateral equal and reacting to light. she was moving all four limbs equally. computed tomography (ct) scan brain plain showed a large posterior extradural hematoma on left side with mass effect and distortion of the 4th ventricle (figure 1). figure 1 pre-operative ct scan brain plain showing a large posterior fossa extradural hematoma with mass effect and small speck of right frontal contusion (please note the small size and distortion of the fourth ventricle) figure 2 follow up ct scan performed day 3 after surgery showing good evacuation of extradural hematoma, 4th ventricle is opened, however there is increase in peri-lesional edema around frontal contusion and squashing of the lateral ventricles suggesting increase in cerebral edema it also showed a small speck of right frontal contusion with localized cerebral edema. the patient was taken for emergency evacuation of the extradural hematoma. following surgery she became conscious by next day morning. her gcs was e4v5 and m6. there were no focal neurological deficits. in view of small speck of cerebral contusion she was started on anti-convulsants, however no anti-edema medications were given. she was apparently alright for two days after surgery and on day 3 she was complaining of headache and became progressively drowsy. there was no vomiting or fever. her gcs was e1, v1 and m3. pupils were bilateral equal and reacting. a follow ct 122 agrawal et al delayed deterioration following the evacuation of posterior fossa extradural hematoma scan performed day 3 after surgery showing good evacuation of extradural hematoma, 4th ventricle is opened, however there was increase in peri-lesional edema around the right frontal contusion with squashing of the lateral ventricles suggestive of diffuse cerebral edema (figure 2). the patient was shifted back to intensive care unit, in view of low gcs and respiratory distress endotracheal intubation was performed and she was kept on elective ventilation. she was started on anti-edema measures (injection mannitol 100 ml intravenous 8 hourly). she responded well to this conservative management, could be weaned off from ventilator and recovered without any neurological deficits. discussion it has been suggested that concurrent intracranial traumatic lesions which lead to increase in intracranial pressure provide a "protective mechanism" and as soon as this mechanism is withdrawn (either by the use of anti-edema measures or by evacuation of supratentorial mass lesions) it can result in delayed onset of edh. (8-10) in contrast to this in present case the patient developed increase in the size of supratentorial lesions and there was increase in cerebral edema which resulted in clinical deterioration. those patients who have associated intracranial injuries (i.e. a contrecoup injuries including subdural hemorrhage or traumatic subarachnoid hemorrhage) had a poor outcome. (11) formation of cerebral edema is recognized as one of the major factors which can lead to high mortality following traumatic brain injury. (12) it has been shown that delayed deterioration after edh can result from progressive cerebral edema and ischemia. (13) there is considerable evidence that brain water content is maximal at 2-3 days after traumatic brain injury and it is also the point at which intracranial pressure is also usually at peak. (12, 14) in our patient the events can collaborated well with existing evidence (presence of contrecoup contusion and on clinical deterioration at day 3). it can be recommended patients showing multiple lesions should be carefully observed until their condition is stabilized. (15) correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.garza-mercado r. extradural hematoma of the posterior cranial fossa. report of seven cases with survival. journal of neurosurgery 1983;59:664-672. 2.campbell e, whitfield rd, greenwood r. extradural hematomas of the posterior fossa. annals of surgery 1953;138:509-520. 3.ammirati m, tomita t. posterior fossa epidural hematoma during childhood. neurosurgery 1984;14:541544. 4.bozbuğa m, izgi n, polat g, gürel i. posterior fossa epidural hematomas: observations on a series of 73 cases. neurosurgical review 1999;22:34-40. 5.malik nk, makhdoomi r, indira b, shankar s, sastry k. posterior fossa extradural hematoma: our experience and review of the literature. surgical neurology 2007;68:155 romanian neurosurgery (2015) xxix (xxii) 1: 120 123 123 158; discussion 158. 6.neubauer uj. extradural haematoma of the posterior fossa. twelve years experiences with ct-scan. acta neurochirurgica 1987;87:105-111. 7.becker dp, miller jd, ward jd, greenberg rp, young hf, sakalas r. the outcome from severe head injury with early diagnosis and intensive management. journal of neurosurgery 1977;47:491-502. 8.riesgo p, piquer j, botella c, orozco m, navarro j, cabanes j. delayed extradural hematoma after mild head injury: report of three cases. surgical neurology 1997;48:226-231. 9.su t-m, lee t-h, chen w-f, lee t-c, cheng c-h. contralateral acute epidural hematoma after decompressive surgery of acute subdural hematoma: clinical features and outcome. the journal of trauma 2008;65:1298-1302. 10.thibodeau m, melanson d, ethier r. acute epidural hematoma following decompressive surgery of a subdural hematoma. canadian association of radiologists journal = journal l'association canadienne des radiologistes 1987;38:52-53. 11.jang jw, lee jk, seo br, kim sh. traumatic epidural haematoma of the posterior cranial fossa. british journal of neurosurgery 2011;25:55-61. 12.marmarou a. pathophysiology of traumatic brain edema: current concepts. acta neurochirurgica supplement 2003;86:7-10. 13.langfitt tw, gennarelli ta. can the out come from head injury be improved? journal of neurosurgery 1982;56:19-25. 14.stocchetti n, colombo a, ortolano f, et al. time course of intracranial hypertension after traumatic brain injury. journal of neurotrauma 2007;24:1339-1346. 15.takeuchi s, wada k, takasato y, et al. traumatic hematoma of the posterior fossa. acta neurochirurgica supplement 2013;118:135-138. microsoft word 13. report.doc romanian neurosurgery (2010) xvii 4: 509 – 510 509 the 7th national congress of the romanian society of neurosurgery with international participation 28 september 2 october, cluj napoca report prof. dr. ioan stefan florian the city of cluj-napoca, the cultural treasure of transylvania, had the honour to organize the 7th national congress of the romanian society of neurosurgery with international participation, held between 28th of september and 2nd of october and it was hosted by hotel napoca. the event gathered outsanding personalities of the neurosurgical field, among which prof. a.v. ciurea (romania), prof. bertrand devaux (france), prof. st.i. florian (romania), prof. m.r. gorgan (romania), prof. n. ianovici (romania), prof. ralf ketter (germany), dr. n. krayenbuhl (switzerland), dr. f.w. kreth (germany), prof. j.c. marchal (france), prof. i. nyary (hungary), prof. j. oertel (germany), prof. i. poeata (romania), prof. f.x. roux (france), prof. h.w.s. schoeder (germany), prof. w.i. steudel (germany), prof. l. steiner (usa), prof. m.s. tatagiba (germany), prof. p.p. varga (hungary), prof. k.r.h. von wild (germany), prof. g. zapuhlih (republic of moldova), and prof. m. zileli (turkey). unfortunately prof. j.m. derlon and prof. g. lena couldn’t attend this scientific event due to objective circumstances. the congress was preceded as every time by the french course of neurosurgery, organized by the french society of neurosurgery. the topics were varied covering approaches for craniostenosis, pituitary adenomas, pharmacoresistent epilepsy, and disembrioplazic and median line tumors at children. at the end of the day the social program offered an organ concert at the calvinist church and the official opening cocktail in the presence of the mayor, mr. sorin apostu at the opera plaza hotel. the first day of the congress, 30th october 2010, began with the opening ceremony in the presence of prof. dr. constantin ciuce, rector of the university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, prof. dr. a.v. ciurea, honorary president of rsn, prof. dr. n. ianovici, the president in charge of rsn, prof. dr. l. steiner, honorary member of rsn, prof. dr. dafin muresanu, president of ssnn and prof. dr. ioan stefan florian, president of the local organizing committee, in which the optimism of the organizers and guests had the desired echo during the whole congress. around 45 lectures were given, these being structured in six sessions of the congress: third ventricle and pineal region tumors, spinal metastasis, state of art in supratentorial malignant glioma, ssnn session, young neurosurgeon’s corner and varia. the conference not only offered the chance for presentation, but also for discussions and confrontations of ideas with daring questions and adequate answers. 510 report the 7th national congress of rsn the social program continued with a cocktail party which took place at the clujnapoca art museum, being accompanied by a spectacular string instruments concert and ended on the 1st of october by a visit to the salt mine of turda, a gorgeous establishment hosting the gala dinner. on the 1st within the general assembly of the romanian society of neurosurgery elections took place for the new board of the rsn for the next two years. prof. dr. ioan stefan florian was unanimously elected by open voting the new president of the society. prof. florian named the secretary of the society in the person of dr. alexandru lupsa and the treasurer of the society in the person of dr. virgil pasca. the vice-presidents were also elected by open voting and they are the following: prof. dr. ion poeata, prof. dr. radu mircea gorgan and dr. horia ples. dr. stefan mircea iencean is elected to remain the editor-in-chief of the romanian neurosurgery, and the elected members of the rsn board are the following: assoc. prof. mohan (oradea), dr. mitrica (military hospital bucharest) and dr. sora (petrosani) and dr. alin st. l. blaga as the representative of the residents. the young neurosurgeons’ corner and poster session were the closure of the congress, meanwhile emphasizing the existing potential among the resident and young neurosurgeons in romania. the closing ceremony was also optimistic, congratulations were addressed to the local organizing committee (prof. dr. i.st. florian, prof. dr. d.f. muresanu, dr. t. maior, dr. a. oslobanu, dr. i. szabo, dr. s. vidican) and to the event consulting, and also to the scientific committee (prof. dr. a.v. ciurea, prof. dr. n. ianovici, prof. dr. i. poeata, dr. st.m. iencean), to the guests and participants for the irreproachable organization of this high scientific level event. officially the next conference of the romanian society of neurosurgery in announced and its location, which would be targu mures and the invitation for the 1st regional conference of neurosurgery in the danube-carpathian region, 25th 27th may 2011, cluj-napoca is launched. 2alvismiranda_therapeutichypothermia romanian neurosurgery (2014) xxi 3: 259 268 259 therapeutic hypothermia in brain trauma injury: controversies hernando raphael alvis-miranda1, gabriel alcala-cerra2, andres m. rubiano3, omar ramirez4, luis rafael moscote-salazar2 1physician, universidad de cartagena, colombia 2neurosurgeon, universidad de cartagena, colombia 3neurosurgeon, southcolombian university, neurosurgery and critical care, neiva university hospital, huila, colombia, meditech foundation 4neurosurgeon, universidad el bosque, bogota, colombia abstract traumatic brain injury (tbi) is a common cause of death and disability in developed countries. it is a major cause of mortality in young patients worldwide. intracranial hypertension is the cause of death in more than 80% of patients with tbi. when secondary lesions occur, start a number of mechanisms that increase the metabolic injury to brain tissue. induction of hypothermia has been shown to alter the natural course of the disease process. the biological foundations suggest that hypothermia may have a potential benefit, although some publications have shown no improvement, it is clear that in a group of mostly young patients, early hypothermia may be beneficial. we present a practical review of the literature on this subject. key words: hypothermia, traumatic brain injury, intracranial hypertension. introduction morbidity and mortality from traumatic injuries are globally recognized as a severe health problem in constant development, these injuries are among the leading causes of death, occurs in all regions, affecting people of all ages and socioeconomic status. (1) traumatic brain injury (tbi) is a worldwide health problem, (2) according to predictions, the neurotrauma will remain representing a growing number of deaths worldwide by 2020. (3) among the tbi secondary lesions are increased intracranial pressure (ich), release of proinflammatory mediators and free radicals, decreased cerebral blood flow due to systemic hypotension and hypoxia, which are all recognized risk factors for poor outcome. (4–6) a potential therapy that improves outcomes in specific patient populations is therapeutic hypothermia (th). (7–11) hypothermia has been used therapeutically for centuries, (12,13) and has been studied extensively in tbi, (14–26) as a strategy to 260 alvis-miranda et al therapeutic hypothermia in brain trauma injury improve post-traumatic neurologic outcomes, (2) yet it is one of the few topics that has caused such debate and lack of consensus about its role in this type of injury. (27) although there is much information about the pathophysiology of tbi, (28,29) has not yet reached the successful handover of therapeutic interventions seen as promising in animal models to clinical practice. (30) ht is currently recommended by the american heart association (aha), as neuroprotective therapy in the post cardiac arrest care. (13,31) theoretically it is indicated for the treatment of complications associated with tbi such as ich (>20mm hg) and status epilepticus, (32) but is not considered as first-line treatment for tbi in usa, however, it is in use for tbi in 47% of neurotrauma centers in japan. (33) the aim of this paper is to briefly review some key aspects regarding therapeutic ht in the context of tbi. definition ht is a treatment modality conducted by the physician in order to reduce the core temperature. (13) hypothermia is defined as a body temperature below 35 ºc (95 °f). it can be classified by their intensity in five groups: (34) • mild: 32 a 34º c • moderate: 28 a 31.9º c • intense: 11 a 28º c. • deep: 6 – 10 °c • ultradeep: ≤5 °c history the use of ht was described by the ancient egyptians, greeks and romans. hippocrates advised covered with ice and snow in poorly healing wounds to reduce blood loss. galen also described some uses of ht. in the 50s, several studies on the physiological effects of ht in humans were conducted, until now no randomized clinical trial. in 1972, robert boyle and james curie and later william osler attempted to use ht in the treatment of typhoid fever, immersing the patient in icy sea water and brine. osler reported a 17% reduction in deaths of patients at johns hopkins hospital. (34) in 1814, napoleon bonaparte´s general surgeon, baron larrey, described the wounded soldiers were placed near the fires died first than those who were not reheated. (35) the first attempt was made in november 28, 1938. (36, 37) the potential beneficial effect of ht in the treatment of tbi has been reported since mid1940. (37) during world war ii, the nazis conducted studies on jewish men to simulate the conditions suffered by the army and the fallen pilots during wartime, with the objectives to determine the cause of death from hypothermia (cardiac or metabolic), to establish the exact temperature at which the death occurred, determine the best methods of resuscitation, and the most appropriate type of protective clothing. (38–40) posteriorly, with the works of bigelow, the intraoperative ht was used since 1950. (41) perhaps the most important lesson of the ht history is that it not only seeks to reduce metabolism, but also that mild ht is sufficient, that intensive care in these patients is always necessary, and that the implementation of strategies is needed. romanian neurosurgery (2014) xxi 3: 259 268 261 mechanism of action to facilitate the use of ht in specific tbi populations is important not only understanding the mechanisms of secondary damage in which the ht mediate, but also the potentially repair mechanisms that can be regulated by hypothermia. (42, 43) ht reduces histopathological damage resulting from the brain injury, to mediate multiple and specific mechanisms of secondary injury as consequence of tbi, such as ich, (10, 14, 32, 44–46) but the exact mechanisms by which ht has beneficial effects are unknown. before 1990 it was felt that the htmediated neuroprotection was due to reduced cerebral metabolism. (14) although such reduction does exist, there are other neuroprotective mechanisms. decreasing core temperature, so does the metabolic rate, and in turn the consumption of oxygen and glucose, also decreases the production of carbon dioxide, fact that by limiting oxygen delivery, may help to prevent or ameliorate injury. (47) electrolyte levels are affected due to tubular dysfunction or fluid movement between the intracellular and extracellular spaces. although the ht appears to block apoptotic pathways in early stages, there is a small therapeutic window through which the ht can affect this process. (48) ht also reduces or ameliorates the lesion produced by the excitatory neurotransmission. experimental evidence suggests that the ht decrease icp through modulation of inflammatory reactions, by reducing cerebral metabolic rate, epileptic discharges and the generation of reactive oxygen species. (49–52) unfortunately, such theoretical benefits remain as inconclusive in clinical studies. (2) metodology to implement hypothermia there are three commonly recognized phases in the implementation of hypothermia: induction, maintenance and overheating. the purpose of the induction phase is to lower the temperature as fast as possible. in tbi, clinical evidence indicates that the temperature range associated with better outcomes appears to be 32-35°c. (45) it is preferable to reach the maintenance phase quickly because the induction phase may be associated with immediate side effects such as electrolyte disorders, hyperglycemia, and tremor, (53) therefore continuous monitoring of ventilation, blood pressure, sedation, glucose and electrolytes is required. there are several methods for the induction of th: (53) • surface cooling with air: traditional methods such as skin exposure to air, which can be combined with sponge baths are effective, cooling blankets with airflow are also available. • surface cooling with fluids: here are included ice bags, pillows or blankets suits with cooling air circulation, also circulating water pads coated with hydrogel. • central cooling: here are used ice-cold fluid infusions. more invasive devices such as intravascular catheters with balloons full of cold saline. cold metal components and antipyretic drugs are also used. desired temperature is reached more quickly by combining methods. (53) 262 alvis-miranda et al therapeutic hypothermia in brain trauma injury in the maintenance phase, core temperature must be accurately controlled to maintain stability of the patient. once at this stage, precautionary measures against side effects of ht should be taken, such as nosocomial infections, or pressure ulcers, especially if therapy is for prolonged time. rewarming involves slow temperature increase to normal ranges, at a preferred rate of 0.25°c per hour. should be slow to: (54) • minimize electrolyte abnormalities as consequence of movement of fluid between the intra-and extracellular compartments. • reduce insulin sensitivity and the risk of hypoglycemia in the case of receiving insulin the patient. • prevent exacerbation of injury mechanisms in the injured brain as consequence of the rapid warming. • minimizing vasodilation heating degree in order to maintain blood pressure and cerebral perfusion pressure. hyperthermia occurs quite commonly after rewarming phase. normothermia must be maintained because fever is independently associated with adverse outcomes in various forms of brain injury. (53,55–57) energy crisis and phospholipid degradation occur very easily after tbi in the perilesional tissue. it has been demonstrated by microdialysis studies in patients with severe tbi that mild ht protects perilesional tissues better than to normal brain tissue, to reduce lactate/glucose, lactate/pyruvate ratios and glycerol levels in such areas. (58) apparently, a high temperature appears not to alter brain neurochemistry substrates and adequate oxygen delivery, (59) however, has been observed that in critically ill patients undergoing hypothermia have less glutamate and lactate/pyruvate ratios, indicating that hypothermia can also participate. in an animal model of mild tbi was observed that hyperthermia at 39 °c for 15 minutes before the occurrence of injury exacerbates the lesion, causing that mild tbi were vulnerable to cerebrovascular and metabolic processes, such as increased extracellular glutamate concentration, intracellular levels of calcium in the bloodbrain barrier and increased inflammation. (60) hypothermia reduces cerebral metabolism during stress, reduces the release of excitatory neurotransmitters, and reduces the permeability of the blood brain barrier. (61) complications hypothermia can lead to several complications, including increased risk of infections, electrolyte disturbances such as hypokalemia, hyperkalemia, increased bleeding time, thrombocytopenia, neutropenia, acute renal failure, sepsis, decreased pulse, decreased cardiac output, hypoventilation, cns depression, hyporeflexia or areflexia, bradycardia, atrial fibrillation, acute pulmonary edema, ventricular fibrillation and asystole. importantly, many of these complications occur only in cases of severe hypothermia, some have been documented in moderate hypothermia; therefore, the current recommendation is the use of mild hypothermia. romanian neurosurgery (2014) xxi 3: 259 268 263 evidence the neuroprotective effects of ht in isolated injuries, more often tbi or or spinal cord injury have yielded conflicting results (mortality and functional outcome) in clinical trials. (62, 63) a partial explanation for such conflicting results derived from the different methodological designs used in clinical trials, basically these studies can be divided into those in which the ht was used to treat ich or studies in which ht was intended to act as neuroprotective therapy to mediate the cease of biochemical and inflammatory cascade, so that comparisons between the studies end controversial. (63) specifically in tbi, harris et al., (64) in their meta-analysis about the role of ht in the management of severe tbi reported no benefit, indeed, clifton et al., (65) reported a negative effect on the outcome of patients with the same severity of tbi. polderman et al., (66) demonstrated the effectiveness of ht for the treatment of ich in patients with severe tbi. in their meta-analysis, peterson et al., (67) reported a statistically significant reduction in mortality and an increase in favorable neurological outcomes, the benefits were greater in ht maintained for more than 48 hours, however, the increased risk of developing pneumonia opaque favorable findings. hutchinson et al., (68) in its international multicenter study showed that in children with severe tbi, ht initiated within 8 hours after the offending event and that continued for 24 hours does not improve neurological outcome, and may even increase mortality. it has also been shown effective not selective cooling systems for achieving desired temperature gradients. (69) findings like these generate controversy, especially because there are compelling evidence showing benefits of ht in animal models, (14, 70) and human clinical studies have shown the beneficial impact of ht to reduce intracranial pressure, one of the cornerstones in the treatment of tbi. (27, 71, 72) georgiou et al., (73) in their meta-analysis on the effect of ht initiated immediately upon admission, mortality and neurologic outcomes in patients with tbi reported the association of ht with cerebrovascular disorders in rewarming, and did not identify benefits on mortality or neurologic morbidity. in a study of 37 patients with severe tbi admitted to icu, childs et al., (57) were monitored the behavior of the brain temperature regarding survival. the results support the widespread view that an early increase in temperature of patients with tbi may be associated with poor prognosis, but also suggest an increased risk of death when the temperature is consistently below the "normal" during the first 48h. the randomized clinical trial 'national acute brain injury study: hypothermia ii' (nabis ii trial) (42) showed no beneficial effect on the early use of ht in patients with tbi, however an interesting point to consider is the fact that overheating was induced very early, probably increasing the icp and then worsening outcomes. (23) currently studies are underway, as the european trial 'eurotherm' (isrctn34555414), (74) the prophylactic hypothermia trial to lessen traumatic brain injury (polar-rct; nct00987688). 264 alvis-miranda et al therapeutic hypothermia in brain trauma injury according to guidelines issued by the brain trauma foundation /american association of neurological surgeons, the optional and cautious use of ht in adults with tbi is a level iii recommendation. (5) conclusions most of the evidence for the neuroprotective effects of mild to moderate ht derived from animal research models, their clinical role is still undefined, so human studies are needed to clarify its real therapeutic effect. (62) correspondence dr. luis rafael moscote salazar, universidad de cartagena, cartagena de indias, colombia, southamerica e-mail: mineurocirujano@aol.com references 1. hyder aa, aggarwal a. the increasing burden of injuries in eastern europe and eurasia: making the case for safety investments. health policy (new york) [internet]. 2009 jan [cited 2013 jan 26];89(1):1–13. available from: http://www.ncbi.nlm.nih.gov/pubmed/18571277 2. bukur m, kurtovic s, berry c, tanios m, ley ej, salim a. pre-hospital hypothermia is not associated with increased survival after traumatic brain injury. j surg res [internet]. 2012 jun 1 [cited 2012 nov 27];175(1):24–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/21872881 3. murray cj, lopez ad. alternative projections of mortality and disability by cause 1990-2020: global burden of disease study. lancet [internet]. 1997 may 24 [cited 2012 nov 7];349(9064):1498–504. available from: http://www.ncbi.nlm.nih.gov/pubmed/9167458 4. enriquez p, bullock r. molecular and cellular mechanisms in the pathophysiology of severe head injury. curr pharm des [internet]. 2004 jan [cited 2013 jan 26];10(18):2131–43. available from: http://www.ncbi.nlm.nih.gov/pubmed/15281889 5. bratton sl, chestnut rm, ghajar j, mcconnell hammond ff, harris oa, hartl r, et al. guidelines for the management of severe traumatic brain injury. iii. prophylactic hypothermia. j neurotrauma [internet]. 2007 jan [cited 2013 jan 25];24 suppl 1:s21–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/17511540 6. sharma d, vavilala ms. perioperative management of adult traumatic brain injury. anesth clin [internet]. 2012 jun [cited 2012 nov 17];30(2):333–46. available from: http://www.ncbi.nlm.nih.gov/pubmed/22901613 7. bernard sa, gray tw, buist md, jones bm, silvester w, gutteridge g, et al. treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. n engl j med [internet]. 2002 feb 21 [cited 2012 nov 12];346(8):557–63. available from: http://www.ncbi.nlm.nih.gov/pubmed/11856794 8. eicher dj, wagner cl, katikaneni lp, hulsey tc, bass wt, kaufman da, et al. moderate hypothermia in neonatal encephalopathy: efficacy outcomes. pediatr neurol [internet]. 2005 jan [cited 2012 nov 13];32(1):11– 7. available from: http://www.ncbi.nlm.nih.gov/pubmed/15607598 9. holzer m, bernard sa, hachimi-idrissi s, roine ro, sterz f, müllner m. hypothermia for neuroprotection after cardiac arrest: systematic review and individual patient data meta-analysis. crit care med [internet]. 2005 feb [cited 2013 jan 21];33(2):414–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/15699847 10. marion d, bullock mr. current and future role of therapeutic hypothermia. j neurotrauma [internet]. 2009 mar [cited 2013 jan 26];26(3):455–67. available from: http://www.ncbi.nlm.nih.gov/pubmed/19292697 11. shankaran s, laptook ar, ehrenkranz ra, tyson je, mcdonald sa, donovan ef, et al. whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. n engl j med [internet]. 2005 oct 13 [cited 2012 nov 27];353(15):1574–84. available from: http://www.ncbi.nlm.nih.gov/pubmed/16221780 12. varon j, sternbach gl. cardiopulmonary resuscitation: lessons from the past. j emerg med [internet]. [cited 2013 jan 26];9(6):503–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/1787299 13. alzaga ag, cerdan m, varon j. therapeutic hypothermia. resuscitation [internet]. 2006 sep [cited 2012 oct 26];70(3):369–80. available from: http://www.ncbi.nlm.nih.gov/pubmed/16930801 romanian neurosurgery (2014) xxi 3: 259 268 265 14. polderman kh. induced hypothermia and fever control for prevention and treatment of neurological injuries. lancet [internet]. 2008 jun 7 [cited 2013 jan 27];371(9628):1955–69. available from: http://www.ncbi.nlm.nih.gov/pubmed/18539227 15. tokutomi t, morimoto k, miyagi t, yamaguchi s, ishikawa k, shigemori m. optimal temperature for the management of severe traumatic brain injury: effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism. neurosurgery [internet]. 2007 jul [cited 2013 jan 26];61(1 suppl):256–65; discussion 265–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/18813163 16. hachimi-idrissi s, huyghens l. therapeutic hypothermia after traumatic brain injury in children: to cool or not to cool? resuscitation [internet]. 2008 nov [cited 2012 nov 27];79(2):185–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/18951112 17. christian e, zada g, sung g, giannotta sl. a review of selective hypothermia in the management of traumatic brain injury. neurosurg focus [internet]. 2008 oct [cited 2012 oct 29];25(4):e9. available from: http://www.ncbi.nlm.nih.gov/pubmed/18828707 18. abate mg, cadore b, citerio g. hypothermia in adult neurocritical patients: a very hot’' strategy not to be hibernated yet! minerva anestesiol [internet]. 2008 [cited 2013 jan 26];74(7-8):425–30. available from: http://www.ncbi.nlm.nih.gov/pubmed/18356803 19. clifton gl. is keeping cool still hot? an update on hypothermia in brain injury. curr opin crit care [internet]. 2004 apr [cited 2013 jan 26];10(2):116–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/15075721 20. honeybul s, ho k, lind c, gillett g. hypothermia in patients with brain injury: the way forward? lancet neurol [internet]. 2011 may [cited 2013 jan 26];10(5):405–6; author reply 406–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/21511192 21. lee h-c, chuang h-c, cho d-y, cheng k-f, lin ph, chen c-c. applying cerebral hypothermia and brain oxygen monitoring in treating severe traumatic brain injury. world neurosurg [internet]. 2010 dec [cited 2012 nov 12];74(6):654–60. available from: http://www.ncbi.nlm.nih.gov/pubmed/21492636 22. nichol ad, trapani t, murray l, vallance s, cooper dj. hypothermia in patients with brain injury: the way forward? lancet neurol [internet]. 2011 may [cited 2013 jan 26];10(5):405; author reply 406–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/21511193 23. polderman kh, andrews pjd. hypothermia in patients with brain injury: the way forward? lancet neurol [internet]. 2011 may [cited 2012 dec 19];10(5):404–5; author reply 406–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/21511190 24. potapov a. applying cerebral hypothermia and brain oxygen monitoring in treating severe traumatic brain injury: a preliminary study. world neurosurg [internet]. 2010 [cited 2013 jan 26];74(2-3):259–60. available from: http://www.ncbi.nlm.nih.gov/pubmed/21492551 25. schibler a, humphreys s. increased brain tissue oxygen tension in children with traumatic brain injury using temperature-corrected guided ventilation during prophylactic hypothermia. crit care resusc [internet]. 2012 mar [cited 2013 jan 26];14(1):20–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/22404057 26. takeuchi s, nawashiro h, otani n. hypothermia in patients with brain injury: the way forward? lancet neurol [internet]. 2011 may [cited 2013 jan 26];10(5):404; author reply 406–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/21511191 27. rubiano am, sanchez ai, estebanez g, peitzman a, sperry j, puyana jc. the effect of admission spontaneous hypothermia on patients with severe traumatic brain injury. injury [internet]. 2012 dec 27 [cited 2013 jan 26]; available from: http://www.ncbi.nlm.nih.gov/pubmed/23273319 28. bigler ed, maxwell wl. neuroimaging and neuropathology of tbi. neurorehabilitation [internet]. 2011 jan [cited 2013 jan 26];28(2):63–74. available from: http://www.ncbi.nlm.nih.gov/pubmed/21447905 29. bramlett hm, dietrich wd. pathophysiology of cerebral ischemia and brain trauma: similarities and differences. j cereb blood flow metab [internet]. 2004 mar [cited 2012 nov 30];24(2):133–50. available from: http://www.ncbi.nlm.nih.gov/pubmed/14747740 30. maas air, roozenbeek b, manley gt. clinical trials in traumatic brain injury: past experience and current developments. neurotherapeutics [internet]. 2010 jan [cited 2013 jan 21];7(1):115–26. available from: http://www.ncbi.nlm.nih.gov/pubmed/20129503 31. part 7.5: postresuscitation support. circ [internet]. 2005 dec 13;112 (24 suppl ):iv–84–iv–88. available from: 266 alvis-miranda et al therapeutic hypothermia in brain trauma injury http://circ.ahajournals.org/content/112/24_suppl/iv84.short 32. jiang j-y, xu w, li w-p, gao g-y, bao y-h, liang ym, et al. effect of long-term mild hypothermia or shortterm mild hypothermia on outcome of patients with severe traumatic brain injury. j cereb blood flow metab [internet]. 2006 jun [cited 2012 nov 7];26(6):771–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/16306933 33. suehiro e, fujisawa h, koizumi h, yoneda h, ishihara h, nomura s, et al. survey of current neurotrauma treatment practice in japan. world neurosurg [internet]. [cited 2012 nov 21];75(3-4):563–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/21600513 34. osler w. the cold-bath treatment of typhoid fever. medical news philadelphia. 1892; 35. cushing j. memoirs of military surgery, and campaigns of the french armies, on the rhine, in corsica, catalonia, egypt, and syria; at boulogne, ulm, and austerlitz; in saxony, prussia, poland, spain, and austria. memoirs of military surgery and campaigns of the french armies. baltimore; 1814. p. 156–64. 36. fay t. observations on prolongued human refrigeration. n y st j med. 1940;40:1351–4. 37. fay t. observations on generalized refrigeration in cases of severe cerebral trauma. assoc res nerv ment dis proc. 1943;24:611–9. 38. tierney e. the nazi hypothermia experiments: forbidden data? anaesthesia [internet]. 2005 apr [cited 2013 jan 30];60(4):413. available from: http://www.ncbi.nlm.nih.gov/pubmed/15766350 39. post sg. the echo of nuremberg: nazi data and ethics. j med ethics [internet]. 1991 mar [cited 2013 jan 30];17(1):42–4. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=1375971&tool=pmcentrez&rendertype=abstract 40. pozos r. nazi hypothermia research: should the data be used? military medical ethics. p. 437–61. 41. bigelow wg, callaghan jc, hopps ja. general hypothermia for experimental intracardiac surgery; the use of electrophrenic respirations, an artificial pacemaker for cardiac standstill and radio-frequency rewarming in general hypothermia. ann surg [internet]. 1950 sep [cited 2013 jan 30];132(3):531–9. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=1616776&tool=pmcentrez&rendertype=abstract 42. clifton gl, valadka a, zygun d, coffey cs, drever p, fourwinds s, et al. very early hypothermia induction in patients with severe brain injury (the national acute brain injury study: hypothermia ii): a randomised trial. lancet neurol [internet]. 2011 feb [cited 2012 nov 5];10(2):131–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/21169065 43. dietrich wd, atkins cm, bramlett hm. protection in animal models of brain and spinal cord injury with mild to moderate hypothermia. j neurotrauma [internet]. 2009 mar [cited 2012 nov 27];26(3):301–12. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=2848835&tool=pmcentrez&rendertype=abstract 44. bratton sl, chestnut rm, ghajar j, mcconnell hammond ff, harris oa, hartl r, et al. guidelines for the management of severe traumatic brain injury. ii. hyperosmolar therapy. j neurotrauma [internet]. 2007 jan [cited 2012 oct 29];24 suppl 1:s14–20. available from: http://www.ncbi.nlm.nih.gov/pubmed/17511539 45. dietrich wd, bramlett hm. the evidence for hypothermia as a neuroprotectant in traumatic brain injury. neurotherapeutics [internet]. 2010 jan [cited 2012 dec 11];7(1):43–50. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=2819078&tool=pmcentrez&rendertype=abstract 46. qiu w, zhang y, sheng h, zhang j, wang w, liu w, et al. effects of therapeutic mild hypothermia on patients with severe traumatic brain injury after craniotomy. j crit care [internet]. 2007 sep [cited 2012 dec 11];22(3):229– 35. available from: http://www.ncbi.nlm.nih.gov/pubmed/17869973 47. polderman kh. mechanisms of action, physiological effects, and complications of hypothermia. crit care med [internet]. 2009 jul [cited 2013 jan 30];37(7 suppl):s186– 202. available from: http://www.ncbi.nlm.nih.gov/pubmed/19535947 48. moore em, nichol ad, bernard sa, bellomo r. therapeutic hypothermia: benefits, mechanisms and potential clinical applications in neurological, cardiac and kidney injury. injury [internet]. 2011 sep [cited 2012 nov 13];42(9):843–54. available from: http://www.ncbi.nlm.nih.gov/pubmed/21481385 49. wang gj, deng hy, maier cm, sun gh, yenari ma. mild hypothermia reduces icam-1 expression, neutrophil infiltration and microglia/monocyte accumulation following experimental stroke. romanian neurosurgery (2014) xxi 3: 259 268 267 neuroscience [internet]. 2002 jan [cited 2013 jan 26];114(4):1081–90. available from: http://www.ncbi.nlm.nih.gov/pubmed/12379261 50. jiang j-y, xu w, yang p-f, gao g-y, gao y-g, liang y-m, et al. marked protection by selective cerebral profound hypothermia after complete cerebral ischemia in primates. j neurotrauma [internet]. 2006 dec [cited 2013 jan 26];23(12):1847–56. available from: http://www.ncbi.nlm.nih.gov/pubmed/17184193 51. ehrlich mp, mccullough jn, zhang n, weisz dj, juvonen t, bodian ca, et al. effect of hypothermia on cerebral blood flow and metabolism in the pig. ann thorac surg [internet]. 2002 jan [cited 2013 jan 26];73(1):191–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/11834009 52. maier cm, sun gh, cheng d, yenari ma, chan ph, steinberg gk. effects of mild hypothermia on superoxide anion production, superoxide dismutase expression, and activity following transient focal cerebral ischemia. neurobiol dis [internet]. 2002 oct [cited 2013 jan 26];11(1):28–42. available from: http://www.ncbi.nlm.nih.gov/pubmed/12460544 53. polderman kh, herold i. therapeutic hypothermia and controlled normothermia in the intensive care unit: practical considerations, side effects, and cooling methods. crit care med [internet]. 2009 mar [cited 2012 oct 25];37(3):1101–20. available from: http://www.ncbi.nlm.nih.gov/pubmed/19237924 54. van den broek mph, groenendaal f, egberts acg, rademaker cma. effects of hypothermia on pharmacokinetics and pharmacodynamics: a systematic review of preclinical and clinical studies. clin pharmacokinet [internet]. 2010 may [cited 2013 jan 26];49(5):277–94. available from: http://www.ncbi.nlm.nih.gov/pubmed/20384391 55. busto r, dietrich wd, globus my, valdés i, scheinberg p, ginsberg md. small differences in intraischemic brain temperature critically determine the extent of ischemic neuronal injury. j cereb blood flow metab [internet]. 1987 dec [cited 2013 jan 29];7(6):729– 38. available from: http://www.ncbi.nlm.nih.gov/pubmed/3693428 56. dietrich wd, alonso o, halley m, busto r. delayed posttraumatic brain hyperthermia worsens outcome after fluid percussion brain injury: a light and electron microscopic study in rats. neurosurgery [internet]. 1996 mar [cited 2013 jan 29];38(3):533–41; discussion 541. available from: http://www.ncbi.nlm.nih.gov/pubmed/8837806 57. childs c, vail a, leach p, rainey t, protheroe r, king a. brain temperature and outcome after severe traumatic brain injury. neurocrit care [internet]. 2006 jan [cited 2013 jan 29];5(1):10–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/16960288 58. wang q, li a, zhi d, huang h. effect of mild hypothermia on glucose metabolism and glycerol of brain tissue in patients with severe traumatic brain injury. chin j traumatol [internet]. 2007 aug [cited 2013 jan 29];10(4):246–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/17651596 59. spiotta am, stiefel mf, heuer gg, bloom s, maloney-wilensky e, yang w, et al. brain hyperthermia after traumatic brain injury does not reduce brain oxygen. neurosurgery [internet]. 2008 apr [cited 2013 jan 29];62(4):864–72; discussion 872. available from: http://www.ncbi.nlm.nih.gov/pubmed/18414135 60. sakurai a, atkins cm, alonso of, bramlett hm, dietrich wd. mild hyperthermia worsens the neuropathological damage associated with mild traumatic brain injury in rats. j neurotrauma [internet]. 2012 jan 20 [cited 2013 jan 29];29(2):313–21. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3261791&tool=pmcentrez&rendertype=abstract 61. curry p, viernes d, sharma d. perioperative management of traumatic brain injury. int j crit illn inj sci [internet]. 2011 jan [cited 2012 nov 6];1(1):27–35. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3209993&tool=pmcentrez&rendertype=abstract 62. dietrich wd. therapeutic hypothermia for acute severe spinal cord injury: ready to start large clinical trials?. crit care med [internet]. 2012 mar [cited 2013 jan 29];40(2):691–2. available from: http://www.ncbi.nlm.nih.gov/pubmed/22249057 63. tomura s, de rivero vaccari jp, keane rw, bramlett hm, dietrich wd. effects of therapeutic hypothermia on inflammasome signaling after traumatic brain injury. j cereb blood flow metab [internet]. 2012 oct [cited 2013 jan 29];32(10):1939–47. available from: http://www.ncbi.nlm.nih.gov/pubmed/22781337 64. harris oa, colford jm, good mc, matz pg. the role of hypothermia in the management of severe brain injury: 268 alvis-miranda et al therapeutic hypothermia in brain trauma injury a meta-analysis. arch neurol [internet]. 2002 jul [cited 2013 jan 27];59(7):1077–83. available from: http://www.ncbi.nlm.nih.gov/pubmed/12117354 65. clifton gl, miller er, choi sc, levin hs, mccauley s, smith kr, et al. lack of effect of induction of hypothermia after acute brain injury. n engl j med [internet]. 2001 feb 22 [cited 2013 jan 26];344(8):556–63. available from: http://www.ncbi.nlm.nih.gov/pubmed/11207351 66. polderman kh. application of therapeutic hypothermia in the icu: opportunities and pitfalls of a promising treatment modality. part 1: indications and evidence. intensive care med [internet]. 2004 apr [cited 2012 oct 26];30(4):556–75. available from: http://www.ncbi.nlm.nih.gov/pubmed/14767591 67. peterson k, carson s, carney n. hypothermia treatment for traumatic brain injury: a systematic review and meta-analysis. j neurotrauma [internet]. 2008 jan [cited 2012 oct 28];25(1):62–71. available from: http://www.ncbi.nlm.nih.gov/pubmed/18355159 68. hutchison js, ward re, lacroix j, hébert pc, barnes ma, bohn dj, et al. hypothermia therapy after traumatic brain injury in children. n engl j med [internet]. 2008 jun 5 [cited 2013 jan 27];358(23):2447–56. available from: http://www.ncbi.nlm.nih.gov/pubmed/18525042 69. harris oa, muh cr, surles mc, pan y, rozycki g, macleod j, et al. discrete cerebral hypothermia in the management of traumatic brain injury: a randomized controlled trial. j neurosurg [internet]. 2009 jun [cited 2012 nov 29];110(6):1256–64. available from: http://www.ncbi.nlm.nih.gov/pubmed/19249933 70. sahuquillo j, vilalta a. cooling the injured brain: how does moderate hypothermia influence the pathophysiology of traumatic brain injury. curr pharm des [internet]. 2007 jan [cited 2013 jan 27];13(22):2310– 22. available from: http://www.ncbi.nlm.nih.gov/pubmed/17692002 71. gal r, cundrle i, zimova i, smrcka m. mild hypothermia therapy for patients with severe brain injury. clin neurol neurosurg [internet]. 2002 sep [cited 2013 jan 27];104(4):318–21. available from: http://www.ncbi.nlm.nih.gov/pubmed/12140097 72. lavinio a, timofeev i, nortje j, outtrim j, smielewski p, gupta a, et al. cerebrovascular reactivity during hypothermia and rewarming. br j anaesth [internet]. 2007 aug [cited 2012 nov 22];99(2):237–44. available from: http://www.ncbi.nlm.nih.gov/pubmed/17510046 73. georgiou ap, manara ar. role of therapeutic hypothermia in improving outcome after traumatic brain injury: a systematic review. br j anaesth [internet]. 2013 jan 25 [cited 2013 jan 29]; available from: http://www.ncbi.nlm.nih.gov/pubmed/23353036 74. andrews pjd, sinclair hl, battison cg, polderman kh, citerio g, mascia l, et al. european society of intensive care medicine study of therapeutic hypothermia (32-35 °c) for intracranial pressure reduction after traumatic brain injury (the eurotherm3235trial). trials [internet]. 2011 jan [cited 2013 jan 29];12:8. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3027122&tool=pmcentrez&rendertype=abstract 6moscotesalazar_osteoporoticvertebral 172 moscote-salazar et al osteoporotic vertebral fracture simulating a spinal tumor osteoporotic vertebral fracture simulating a spinal tumor: a case report luis rafael moscote-salazar1, gabriel alcala-cerra1, hernando raphael alvis-miranda2, carlos fernando lozano-tangua1, sandra milena castellar leones, maria jose merlano almanza universidad de cartagena, colombia 1neurosurgeon; 2physician abstract: vertebral fractures are a frequent entity, mainly in the thoracolumbar and lumbar spine. in some circumstances the differential diagnosis of vertebral injuries can confuse the physician, since the difference between an osteoporotic vertebral fracture and a fracture secondary to a tumor is not clear. we report the case of a patient with osteoporotic vertebral fracture simulating a spinal tumor, handled by our department of neurosurgery as illustrative experience to guide the approach in those cases, in which the definitive diagnosis is crucial for therapeutic decision making. key words: osteoporosis, spine, vertebral fracture. introduction vertebral fractures associated with osteoporosis are a common entity. (1) the consequences of this type of fragility fractures are diverse. osteoporosis is estimated to affect 30-40% of all postmenopausal women and 50% of people over 76 years. (2) occasionally, differentiate between an osteoporotic fracture and a tumoral lesion becomes a challenge. we report the case of a patient managed by the neurosurgical service of the university of cartagena. case report female patient, 60 years old, with a history of arterial hypertension diagnosed 10 years ago, handled regularly with hydrochlorothiazide in a controlled manner. she consults to the emergency department because of thoracolumbar pain that started 2 month ago, and increased in intensity until difficulty the gait, associated with appearance of sacral skin ulcer as result of being bedridden for several days. she denies history of recent trauma. admission physical examination of head and neck was normal, cardiopulmonary and abdomen without alterations, symmetrical romanian neurosurgery (2015) xxix 2: 172 175 173 limbs, skin ulcer in right sacral region with fetid serous discharge, pain on dorsolumbar movements, lower limbs flexion limited by pain, left lassegue sign positive, bragard, patrick and faber signs negative. neurologically conscious, oriented, no meningeal signs, sensitivity: not identified sensory level, proprioceptive function preserved (vibration and position) and estereoceptive (touch, pain and temperature); muscular strength: 5/5 in the upper limbs, with bilateral paraparesis 4/5 on lower limbs; left antalgic gait of few steps because of exquisite pain, tendon reflexes: +/++++ symmetrics, generalized; bilateral neutral plantar reflex; abdominal skin reflexes normal; digital rectal examination: eutonic sphincter, sphincter reflex present, preserved perianal sensitivity. laboratories on admission showed: leukocytosis with neutrophilia, increased acute phase reactants, normoglycemia, normal serum electrolytes, renal and hepatic profile unaltered, and normal coagulation tests. dorsal and lumbar spine radiographies were performed showing t12 fracture. the patient is evaluated by the neurosurgery service, which considered a spinal cord compression syndrome secondary to a t12 pathological fracture on study, it is considered to perform lumbar spine mri, reporting change in the shape of the t12 vertebral body with collapse and mixed images infiltrating periand sub-dural space with medullary parenchymal commitment and compression, suggesting metastatic etiology. concomitantly is valued by internal medicine who establishes management for the infectious process with oxacillin and ciprofloxacin, wound healing, antithrombotic therapy, proton pump inhibitors and general measures. likewise, general surgeries validates the patient, and consider to practice skin ulcer washing and sampling for culture, which reported acinetobacter baumani sensitive to clindamycin and imipenem, so the antibiotic is rotated. medical board was performed for suspected metastatic lesion, which decides scheduled for surgery to open spinal biopsy, after resolution of the infectious process in the sacral bedsore. during surgery, are dissected the spinous apophysis and left sheets of t11t12-l1; sheets looks gray-white unpolished. ligament is dissected and t12 hemilaminectomy is performed with kerrinson tweezers. samples are taken for histology. yellow ligament is repaired and cut with scalpel and kerrinson tweezers. free nerve root and dural sac are identified, which are not imprisoned. it is observed t12 vertebral body destruction and partial absence of the same, with reduced height. vertebral body samples were taken for histological study. intervertebral discs had fibrosed aspect. samples are taken from upper and lower disc and soft tissue. compressive or infiltrative lesion is not apparent in the canal. integrity of the root and dural sac is verified, with bipolar coagulation for hemostasis. muscle is approximated with poliglactina 910, muscle fascia is sutured with poliglactina 910 continuous points. subcutaneous fat is approximated with poliglactina 910and skin with nylon 3/0 suture with continuous crossed points. approximated bleeding volumen: 50 cc. 174 moscote-salazar et al osteoporotic vertebral fracture simulating a spinal tumor pathology report is consistent with osteoporotic fracture, medical management for osteoporosis is started, and then is performed posterior thoracolumbar fusion. postoperative course was satisfactory. patient continues in outpatient control with neurosurgery and internal medicine. figure 1 a, b ap and lateral lumbar spine radiograph evidencing t12 fracture by crushing (see arrow) figure 2 a, b mri of the thoracolumbar spine, sagittal reconstruction evidence vertebral collapse figure 3 a, b mri of the thoracolumbar spine, sagittal cut evidencing vertebral body infiltration discusion some imaginological characteristics have been defined on mri to help in the differentiating between osteoporotic and tumoral fractures. a. in metastatic fracture often can be identified a convex edge in the posterior wall (74%). (2, 3) b. in tumor fractures, the pedicles and posterior elements have abnormal signal intensity (85%). (4, 5) c. epidural lesions can be identified in pathological fractures (74%), the presence of paraspinal focal masses are not suggestive lesions to differentiate between osteoporotic from tumoral lesions. among injuries that must be taken in consideration is the plasmacytoma, this represents a subtype of b-cell lymphocytic tumor; it is located predominantly in the lumbar region and can cause pathological fractures; in these cases, often, is very difficult to define it preoperatively either by clinical features and / or imaging. (3, 6) common benign lesions are the hemangiomas, the edema of degenerative disease, osteoporotic fractures with edema and espondilodisquitis. atypical hemangiomas and excessive edema due to degenerative problems may be a problem in the differential diagnosis of malignancy. malign lesions are represented by malignant metastatic lesions, myeloma, malignant primary bone tumors and primary and secondary lymphoma. myeloproliferative diseases can also be found, including leukemia. (7, 8) romanian neurosurgery (2015) xxix 2: 172 175 175 conclusion this article shows that in patients with suspected tumoral fractures should be considered in the differential diagnosis the presence of osteoporotic fractures, sometimes the diagnosis becomes a neurosurgical challenge. correspondence luis rafael moscote salazar universidad de cartagena, cartagena de indias, colombia email: mineurocirujano@aol.com references 1. camins m, oppenheim j, perrin r. tumours of the vertebral axis: benign, primary malignant, and metastatic tumors. youman’s neurol surg. philadelphia: elsevier saunders; 2011. p. 3131–67. 2. cuénod ca, laredo jd, chevret s, hamze b, naouri jf, chapaux x, et al. acute vertebral collapse due to osteoporosis or malignancy: appearance on unenhanced and gadolinium-enhanced mr images. radiology [internet]. 1996 may [cited 2013 nov 13];199(2):541–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/8668809 3. tan sb, kozak ja, mawad me. the limitations of magnetic resonance imaging in the diagnosis of pathologic vertebral fractures. spine (phila pa 1976) [internet]. 1991 aug [cited 2013 nov 13];16(8):919–23. available from: http://www.ncbi.nlm.nih.gov/pubmed/1948377 4. mubarak f, akhtar w. acute vertebral compression fracture: differentiation of malignant and benign causes by diffusion weighted magnetic resonance imaging. j pak med assoc [internet]. 2011 jun [cited 2013 nov 13];61(6):555–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/22204209 5. wonglaksanapimon s, chawalparit o, khumpunnip s, tritrakarn s-o, chiewvit p, charnchaowanish p. vertebral body compression fracture: discriminating benign from malignant causes by diffusion-weighted mr imaging and apparent diffusion coefficient value. j med assoc thai [internet]. 2012 jan [cited 2013 nov 13];95(1):81–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/22379746 6. shih tt, huang km, li yw. solitary vertebral collapse: distinction between benign and malignant causes using mr patterns. j magn reson imaging [internet]. 1999 may [cited 2013 nov 13];9(5):635–42. available from: http://www.ncbi.nlm.nih.gov/pubmed/10331758 7. sugimura k, yamasaki k, kitagaki h, tanaka y, kono m. bone marrow diseases of the spine: differentiation with t1 and t2 relaxation times in mr imaging. radiology [internet]. 1987 nov [cited 2013 nov 13];165(2):541–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/3659380 8. baur-melnyk a. malignant versus benign vertebral collapse: are new imaging techniques useful? cancer imaging [internet]. 2009 jan [cited 2013 nov 13];9 spec no:s49–51. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=2797458&tool=pmcentrez&rendertype=abstract doi: 10.33962/roneuro-2022-010 planning neurosurgical interventions in patients with anticoagulant therapy quiñones-ossa g.a., angulo-mariño s.l., garcia-ballestas e., moscote-salazar l.r., agrawal amit, amrita ghosh, ranabir pal romanian neurosurgery (2022) xxxvi (1): pp. 52-61 doi: 10.33962/roneuro-2022-010 www.journals.lapub.co.uk/index.php/roneurosurgery planning neurosurgical interventions in patients with anticoagulant therapy quiñones-ossa g.a.1-3, angulo-mariño s.l.1, garcia-ballestas e.2,3, moscote-salazar l.r.2-4, agrawal amit5, amrita ghosh6, ranabir pal7 1 faculty of medicine, universidad el bosque.bogotá, colombia 2 faculty of medicine, universidad de cartagena. cartagena, colombia 3 consejo latinoamericano de neurointensivismoclani, colombia 4 neurosurgeon-critical care. center for biomedical research (cib). director of research line cartagena neurotrauma research group. faculty of medicine university of cartagena. cartagena de indias, bolivar. 5 department of neurosurgery, all india institute of medical sciences, saket nagar, bhopal 462020, madhya pradesh, india 6 department of biochemistry, medical college, 88, college street, kolkata, india 7 department of community medicine, mgm medical college & lsk hospital, kishanganj, bihar, india abstract clinical practice guideline on anticoagulation is intended to manage patients undergoing neurosurgical procedures for the best possible short and long-term outcomes. in the clinical office practice, anticoagulation is offered to prevent thromboembolism with warfarin, heparin, novel oral anticoagulants. the management approach starts with the mitigation plans from a reversal of preprocedural anticoagulants for impending neurosurgical procedures by estimating procedural bleeding risk on the patients. the haemorrhage criteria and the timing of procedures are best assessed by the proceduralist during and after the intervention, standing on ground situations. yet, intraand post-procedure anticoagulant therapy should induct a multidisciplinary consultation paradigm for the best outcome in any emergent scenario. further, each anticoagulation event should be monitored closely with competence in the optimum reversal process. different neurosurgical procedures also should be weighed for their inherent hazards along with the probabilities of the bleeding and thromboembolism. the treating team should also concur to suggest a resumption of the pre-procedure anticoagulant therapy which may have been in place for altogether different morbidities. regarding the anticoagulant agent, there are special conditions and recommendations to bear in mind in the daily medical practice for patient management. in the clinical practice guidelines for neurosurgical procedures, decisions about initiation and continuation of anticoagulants require experience and thorough internalization of the planned procedure, to avoid the risks of inherent risks of bleeding and thromboembolism. keywords traumatic brain injury, neurosurgery, neurosurgical procedure, neurological surgery, anticoagulant, anticoagulation agents corresponding author: amit agrawal mm institute of medical sciences & research, mullana (ambala), india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 53 planning neurosurgical interventions in patients with anticoagulant therapy introduction human brain has poor tolerance to constant bleeding and major hemorrhage of brain occurs from non-compressible locations. in er, the physicians are confronted with the challenging scenario of patients, requiring surgical treatments, under anticoagulant, antiplatelet or thrombolytic medications; these therapies interfere with operative hemostasis (pre-, intra-, or post-operative hemostasis). the anticoagulant therapy is the cornerstone of the standard clinical care practice to avoid of thromboembolic episodes caused by diseases viz. atrial fibrillation (af), pulmonary embolism (pe), heart disease or deep venous thrombosis (dvt) 1-7. intracranial hemorrhages and the higher bleeding risks, are higher incident to the emergency room (er) irrespective of the trauma characteristics (minor or high impact trauma) in those patients on anticoagulant (or over anticoagulated) 7. thus, anticoagulation in neurosurgical patients represents two major implications, firstly, healthcare cost, and secondly, safety as well as prognosis 6. rapid identification and optimum interventions of anticoagulated neurosurgical patients are related to less healthcare and system cost with improved outcomes and good prognosis 8. the purpose of this study was to review the current literature about anticoagulation therapy before, during and after the neurosurgical procedure, while considering the co-morbidities and patient current status. overview anticoagulant medications increased due to higher atherosclerosis prevalence among the elderly2, 9 8, 9 who are also at higher risk of traumatic brain injuries (tbi) and intracranial hemorrhage (ich) from falls or violence 10 causing huge burden of mortality, morbidity, and disability. devastating consequences and fatal sequel have been reported after these traumas, especially when they are under anticoagulant therapy 8, 11. so, before neurosurgical interventions, it is important to reverse or counteract the effect depending on the type of anticoagulant1, if the patient is under anticoagulation therapy. those who are under oral anticoagulants therapy, have worse outcomes as reversal agents for these drugs are largely not available 2. type of anticoagulant warfarin warfarin, inhibits vitamin k dependent coagulation factors viz. ii, vii, ix, and x 1, 3; takes 3 days to achieve complete inhibition of the factors in the order of vii, ix, x, and ii; effect reversion also takes 3days after stoppage of doses, and is not an option when the patient needs an urgent neurosurgical procedure 1 and is linked to hematoma expansion in the ich patient with consequent poor prognosis12. warfarin advice require strict monitoring of internationally standardized ratio (inr) and, has known drug interactions 8, 9. inr value reflects anticoagulant effect: <1.0= non-anticoagulant effect; 2-3 indicates active effect, >3= hemorrhage risk 1, 6, 7, 13-15, inr increase is exponential depending on the dose and individual patient response 16. clinico-social factors also affect these levels viz. female gender, advanced age, black race, heart diseases, substance use, psychiatric disorders, and frequent hospitalizations 16, 17. further, in presence of or with risk of intracranial bleeding, prothrombin time (pt) is strictly kept below 11, inr >1.2 provides poor outcomes as in ich or a tbi 1, 6; in neurosurgical patients a target minor of 1 to 1.5 (or 1.3) of the inr is recommended 6. heparin this parenteral anticoagulant act as prophylaxis of dvt, by binding with plasma proteins and affect molecular configuration 1. heparin antithrombin complex rapidly interacts with circulating thrombin to inhibit the coagulation enzymes and reduce platelet aggregation by the inhibition of the von willebrand factor 1. the efficacy of heparin is measured by the partial thromboplastin time (ptt) to be 1.5-2.0 times of the patients baseline value 1; reversal effect after stoppage of dosage administration takes up to 1 hour which is also huge time gap to start an emergency neurosurgical intervention 1; protamine is used reversal at the dose of 1 mg per 100 units of heparin when an urgent surgery is contemplated. novel oral anticoagulants (noacs) versus direct oral anticoagulants (doacs) these are of two types: a) direct factor xa inhibitors (endoxaban, apixaban, rivaroxaban) and b) direct thrombin inhibitors (dabigatran) 8; used as first-line therapy in atrial fibrillation. there is need to review 54 quiñones-ossa g.a., angulo-mariño s.l., garcia-ballestas e. et al. the clinical history in absence of clear information on anticoagulant intake16 as these increase the bleeding risk or the progression of the ich 8. research groups reported reduction of venous thromboembolic episodes of noacs used as chemoprophylactic anticoagulation therapy in tbi patients within 24 hours without computed tomography (ct)-scan changes 4. noacs are safer and simpler alternative compared with warfarin with shorter half/life with predictable therapeutic rapid onset effects and do not require continuing monitoring8, 9, change the dietary pattern, less drug interactions; issues with lack of specific antidotes 3 and reversal antidotes are still evolving 8. few studies reported worse prognosis than warfarin with higher progression rate of ich and mortality after tbi8, while others, noted lower risks against vitamin k antagonist 6,12. noac used with a low aspirin dosage was reported safer and more effective than warfarin by other researchers in preventing strokes and intracranial hemorrhage 9, 18. during use of dabigatran (direct thrombin inhibitor), the normal ranges of thrombin time (tt) or the dilute tt (dtt) is rider for associated anticoagulation effect 6; “safe-zone” for tt before surgical interventions is <30 ng/ml; in case of a higher values (> 30 ng/ml) or with heavy bleeding, the antidote must be administered 6. activated partial thromboplastin time (aptt) help approximate time since the last dose19 as prolongation result due to the anticoagulant effect3 and suggest risk of bleeding if the value is twice the normal ratio19; not done in lupus syndrome or clotting factors deficiency disorders due to the intrinsic prolonged effect of aptt that may mask the true effects3. reversal with idarucizumab depends on the available tests; in absent of testing facilities and with active bleeding doses have to be repeated 6. studies reported rapid hematoma expansion and bad prognosis in ich patients with noacs intake even with minor intracranial bleeding 8, 20, 21. for the x-factor inhibitor, anticoagulants activity evaluation involves anti-activated factor x (anti-xa) calibrated to lmwh or the corresponding “xaban” available on limited scale6. noacs usage has increased in a colossal way in the last years replacing conventional anticoagulants especially in patients with trauma in er8. patients with ich, regardless of the origin, under dabigatran require urgent reversal, should be treated with idarucizumab3; on factor xa inhibitors intake to be treated with pcc 3. noacs use may need observation 6in circumstances viz. normal cct-scan and gcs, an open head injury with injured scalp reflecting normal coagulation status and with unilateral chronic subdural hematoma without neurological deterioration or red flags or minimal neurological symptoms6. management approach in anticoagulated patients er personnel should assess clinical status, triage and neurosurgical intervention with review of clinical records for co-morbidities, medications and anticoagulant use in tbi cases or with ich suspects followed by cranial computed tomography (cct) as the anamnesis or neurological status in anticoagulated patients is usually attributed to vascular origin3. the latter has high sensitivity for extent of intracranial damage with acute onset of the hemorrhage 6; contrast enhanced ct helps to identify the risk of bleeding expansion within the hematoma (spot signs)3. the prognosis of ich varies on age, clinical status, volume of hematoma and degree of anticoagulant activity7. regardless of the type of bleeding and anticoagulant agent, every lifethreatening hemorrhage should be managed initially with basic abc resuscitation protocol3; no uniform recommendation in the primary ich exists for noacs,3; ich is 11times worst compared to extracranial with vka therapy 3. even with normal cct on anticoagulant medication, patients should be observed in-hospital for 24 hours to exclude delayed intracranial hemorrhage; repeat cct scan needed in neurological deterioration6; with intubation, sedation, neurological concomitant disease, followup to be made by cct-scan 6. there is need to optimize neurosurgical procedure, reversal agents, risk of thromboembolism versus anticoagulation and reinduction of anticoagulation after procedure 3; correct management of blood pressure is related to a less neurological damage, hematoma expansion and unfavorable outcomes including improvement in functional recovery3. total correction of vka is achieved with a pcc infusion (20 ui/kg) or a bolus of 25 iu/kg and a single dose of 5 mg of vitamin k in order to get a value from 1.2-1.5 with an approximate 6hours effect 16; neurosurgical procedures require inr <1.3 16. [table 1] the surgical procedures can be unscheduled invasive surgery or emergency surgery, semi-urgent, relative delayable surgery, urgent diagnosis procedures (e.g. lumbar 55 planning neurosurgical interventions in patients with anticoagulant therapy puncture) or scheduled invasive procedures than can present high or moderate risk of hemorrhage, each needs special recommendations (table 2.)16 table 1. major hemorrhage criteria16 • excessive/fatal bleeding • symptomatic hemorrhage with a critical organ compromise (intracranial, spinal, intraocular, pericardial, intramuscular hemorrhage with a compartment syndrome, retroperitoneal hemorrhage). • a drop in hemoglobin levels that requires transfusion of more than two units of packed red blood cells or whole blood compounds. • damaged organ or special location (intracranial, spinal, digestive, thorax, pericardium, abdominal cavity). • massive hemorrhage that cannot be managed with conventional procedures. • requirement of invasive treatment (surgery, interventional radiology or endoscopy). table 2. recommendations according the timing of the procedure (8) type of procedure recommendation emergency surgery administration of pcc is effective in the first 30 minutes after administration and could last for 5 hours. in this case, is important to measure the inr after 5 hours after the initial dose. in neurosurgical procedures recommended to achieve an inr <1.3. semi-urgent surgery if it is performed within 24 hours the recommended values are still under 1.3 of the inr, but because of the allowed delayed time a single dose of vitamin k (5 to 10 mg) might be effective to achieve the hemostatic safety threshold. invasive unscheduled procedure with a high risk of hemorrhage (e.g. lumbar puncture) thrombotic and hemorrhage risk should be considered, in these types of procedures, if the bleeding can be controlled with local pressure there is no need to revert the anticoagulation effect. scheduled invasive procedures with moderate/ high bleeding risk in these cases, is recommended to stop vka treatment 5 days before the procedure and monitorization the inr levels. minimal and high-risk procedures neurosurgical patients under anticoagulant therapy have inherently higher risk of hemorrhages (ich) 10 though the thromboembolic event also carry of 343% risk 22, 23 which should be kept in mind as 50-50 chance in order to assess the risk versus benefit 22, 23. neurosurgical procedures can be invasive and noninvasive, the emergency procedures with other types and sub-types 22. a. lumbar puncture lumbar puncture (lp) is useful for therapeutic and diagnostic use in daily medical practice to help analyze cerebrospinal fluid (csf) especially for suspected neuroinfection24, 25, biomarkers for tbi prognosis 11, 26-28, to diagnose elevated intracranial pressure (icp) (syn. intracranial hypertension) 24, 29. after lp multiple complications can occur viz. epidurals, subarachnoid or subdural hematomas (trivial or massive) as traumatic lumbar puncture (tlp) due to a direct puncture in the radicular vessels and the sliding of the arachnoid on the dura30-32. the diameter of needle and catheter add higher risk of bleeding, when the patients are under anticoagulant therapy 30, 33. the spinal hemorrhages can lead to irreversible complications like paraplegia or paraparesis of lower limb34, medullar or compressive radicular syndrome (due to exacerbated fibrinolytic property of the csf related to a higher red blood cells count after the tlp) 33. it is recommended to avoid anticoagulation therapy with enoxaparin 24 hours before lp and 48 hours if under noacs therapy 34. b. decompressive craniectomy decompressive craniectomy (dc) is commonest treatments in treatment of high icp since last century to maintain intracranial equilibrium35 in high icp from cerebral tumors, neuroinfections, tbi, ich (whether spontaneous or traumatic)36-39 to avoid neurological complications, secondary insults, brain herniation and unfavorable outcomes including death 40, 41. there is a high risk of dvt after dc that need antithrombotic measurements and imaging studies 22; patients under anticoagulation should have coagulation profile; if abnormal, suspend the therapy and/or restore the coagulation time within 48 hours1, 22 as damaged tissues and platelets produce excessive thromboplastin and vasoconstrictors that might produce acidosis status and ischemia 22. the preventive management are recommended to avoid hypercoagulation and thrombosis episodes, initiate mechanical 56 quiñones-ossa g.a., angulo-mariño s.l., garcia-ballestas e. et al. compressive; reinitiating of anticoagulant therapy done after 15 days if there is pulmonary embolism in the postoperative period 22, 42; anticoagulation therapy are also used by others within first 24 hours; yet there is no clear consensus of the timing of the anticoagulation therapy after the surgical procedure42, 43. in impending risk of cerebral venous thrombosis (cvt), neurological monitoring and imaging studies considered; risk of intracranial bleeding and hematoma expansion should be thought in patients under anticoagulant therapy8, 12, 43-45. c. craniotomy in tumor resection cerebral tumors have frequent post-operative complications due to high risk of dvt (27-45%) or prothrombotic status related to the tumor itself 22. tumors predispose to a venous stasis and atherosclerosis by the intimal dysfunction, disturbance of vessels and major procoagulant factors22, 44 add higher risk of thromboembolic events. the enoxaparin or noacs treatment lead to major ich; it is better to use mechanical measurements to prevent thrombosis to decrease post-surgical bleeding22, 46. chronic anticoagulant treatment has not been associated with a postsurgical hemorrhage recurrence within first 72 hours compared to non-anticoagulated patients46, 47. lmwh usage in the first 48 hours after the procedure as a prophylactic therapy is recommended to avoid the thrombotic complications46, 47. d. ventriculoperitoneal shunt and ventriculostomies ventriculoperitoneal shunt (vps) is used treat high icp especially in hydrocephalies48. external ventricular drainage system drains csf and reduces icp; the hemorrhage risk is 7% but a significant hemorrhage reported in minority (0.8%); heparin is recommended in vps 9, 49, 50 dose adjustment no clinical practice guideline can replace clinical acumen and judgment on ground situations though many standard office procedures are based on 2012 accp guidelines for antithrombotic therapy and discussions are needed regarding different qualitative and quantitative approaches 51. warfarin in warfarin over-anticoagulated patients with high inr, 5-10mg vitamin k (oral or intravenous) is administered; takes up to 24 hours to full reversal 1, 6. thus in er, vitamin k as antidote or reversal agent is not recommended in hemorrhagic tbi or urgent surgery; useful as an adjunct therapy6. prothrombin complex concentrate (pcc) dosage depends on initial inr value, has the advantage of immediate reversal effect, vitamin k can be used to maintain effect 6. plasma transfusion therapy require high volumes and can lead to circulatory overload, pulmonary edema, congestive heart failure and immune-suppression; also takes longer time compared to pcc to reverse and normalize inr6. warfarin use causes higher postoperative bleeding than noacs3. pre-operative and peri-operative thromboembolism vs. bleeding risk prediction at first, bleeding versus embolism risk stratification needed using cha2ds2-vasc and has-bled scores are user-friendly for rapid assessment of thrombotic and hemorrhagic risk respectively 3, 52, 53. additionally, we have to consider risk factors of ich viz. older age, hypoor hypertension, micro-bleeds on echomagnetic resonance imaging gradient, and ich in lobar location3. to reach at correct treatment strategy, every patient under anticoagulation treatment requires an evaluation and categorization on urgency of the invasive procedure with a special consideration of thrombotic and hemorrhagic risk 16; otherwise carry risk of thrombosis or pulmonary embolism (pe) in 25-60% 52. other researchers prefer initiation of thromboembolism prophylaxis after first 24 hours only in radiographically and neurological stable tbi 6; restart of antithrombotic prophylaxis within first 72 hours has lower incidence of dvt and pe 6. post-operative management – when to restart anticoagulation therapy? intracranial bleeding represents a special condition for resumption of anticoagulation as in hemispheric location of hemorrhage the vka therapy should be permanently discontinued16 resumption of anticoagulation regimen is a clinical dilemma in ich or any neurosurgical procedure3, 9; after hemostasis achieved and ich has stopped, the resumption of 57 planning neurosurgical interventions in patients with anticoagulant therapy anticoagulants can add risk of bleeding or a future re-bleeding in tbi 6. ich management guidelines indicates that therapeutic anticoagulation should be reinitiated after 2 weeks post-trauma with stable injury and high cerebral ischemia risk secondary to mechanical valve prosthesis or atrial fibrillation with a high a cha2ds2vasc score6, 54, 55; with low risks of thromboembolism, anticoagulation therapy are reinitiated after 8 weeks 6. literature reports that vka’s therapy might be initiated within 7 days and with heparin after 3 days in ich without re-bleeding complications56 but others recommend anticoagulation therapy after the first 2 weeks to avoid hemorrhagic complications57. restarting the anticoagulation with warfarin within 14 days is associated with an increased hemorrhagic complications, thus anticoagulation after 2weeks is recommended16; some studies reported as ideal time to reinitiate warfarin after a week of the procedure9, 58. strategies to reduce the thromboembolism risk and non-pharmacological treatment thrombosis and embolism episodes are global public health problem with increasing mortality with co-morbidities the risk and incidence is doubled59. risks of impending thromboembolism are well assessed by the treating physician though the multidisciplinary and integral paradigm of prevention and medical approach. adoption of healthy lifestyle with good dietary habit, reduction of alcohol and tobacco consumption, oral anticonceptives, hormone replacement therapy is recommended 60 with non-pharmacological therapy for the patients management viz. pneumatic intermittent compression, compression stockings and drugs52. the prevention may start even before the surgical intervention regardless the concomitant pathologies that predispose to dvt or pulmonary embolism 22, 59. graduated compression stocking compress the lower extremities, graduated from the bottom (more intense) to the top (less compressive) to increase blood-flow; advised to use them from early deambulation till 2 years postprocedure61, 62, the intermittent mechanical compression increases blood flow in the veins of the lower limbs and is superior to graduated compression stocking to significantly reduce dvt by 7.3% and pulmonary embolism 1.2-2.8%; recommended to use it jointly with pharmacological prophylaxis. 61, 62 current issues with the anticoagulant therapy in anticoagulated neurosurgical patients anticoagulants inhibits the coagulation factors metabolism to avoid thrombotic complications including that of post-neurosurgical interventions 63, 64. the bone of contention here is decision of precise moments of interruption or resumption of anticoagulantion after neurosurgery 62, 65, 66 where the risk-benefit analysis of the associated factors, choice of drugs, type of procedure and neurosurgeons criteria must be taken into account63, 67. regarding inr measurement to analyze the effect, thromboelastometry (viscoelastic analysis method that qualitatively assesses coagulation and fibrinolysis through rates of clot formation, resistance and degradation, and interaction of coagulation factors) is useful, yet, not established for neurosurgical use 23, 68-70. further, human inherent anticoagulation genetic factors with two allelic variants (2c9*2 and 2c9*3) of the cyp2c9 enzyme 71, 72 usually require a minor anticoagulant dosage. on the other hand, the variant of vitamin k epoxide reductase isoenzyme 1 (vkeri1) generates resistance to the vka agents requiring higher dosages o achieve the therapeutic effect 73, 74. non-genetic factors are associated to personal habits, adherence to therapy, preference for alternative treatments, dosage mistakes and comorbidities the confounding variables 17. among the complications previously mentioned, one of the most important is the intracranial bleeding 75, followed by thrombosis that increase 2.5 times daily in anticoagulated patients whose therapy is interrupted for neurosurgical intervention; in addition the risk of developing hypercoagulability increases due to the limitation in postoperative ambulation 76-78. several studies recommend to avoid resumption of anticoagulation before 24 hours due to the risk of reactivation of bleeding in the intervened area, yet early restart between 4-7 days is the ideal time, with lesser complications compared to 14-day late restart, which increases the risk of cardioembolic infarction and ischemic stroke 58, 76. heparin use may be recommended after intracranial surgery within 24 hours with the intention to reduce dvt and pe 79, 80. the considerations to restart anticoagulant therapy, it is important to recap type of medication, possibility of control or not with inr, cognitive deterioration or diseases associated with memory disorders, labile 58 quiñones-ossa g.a., angulo-mariño s.l., garcia-ballestas e. et al. inr, high risk of stroke79, 80, and risk of bleeding or thromboembolic disease associated with nonsurgical scores such as cha2ds2-vasc and hasbled 53, 81. in addition, certain precautions should be taken in patients suffering from ckd (chronic kidney disease), patients over the age of 65, on treatment with macrolides and the use of antifungals such as ketoconazole and itraconazole 80-82. conclusions there is a widespread concern on the outcome of neurosurgical procedures while the patient is on anticoagulant therapy. a multipronged approach is needed involving specialities and sub-specialities ranging from haematology, biochemistry, pathology, pharmacy services, internal medicine, emergency medicine, family medicine, anaesthesiology, nephrology, and pre-hospital consult services roped in for specific patients who need more complex continuum of care with dosing and monitoring of anticoagulant medications. there is urgent need to develop consensus guidelines for the health care professionals regarding management of anticoagulation which may be playing as double aged sword in both risk factor and outcome. basic rules should be, while a more specific reversal agent of anticoagulant is available and approved to be used in the medical practice, antiplatelet agents can be continued throughout the perioperative period. references 1. powner dj, hartwell ea, hoots wk. counteracting the effects of anticoagulants and antiplatelet agents during neurosurgical emergencies. neurosurgery 2005;57:823831; discussion 823-831. 2. batey m, hecht j, callahan c, wahl w. direct oral anticoagulants do not worsen traumatic brain injury after low-level falls in the elderly. surgery 2018;164:814-819. 3. raval an, cigarroa je, chung mk, et al. management of patients on non-vitamin k antagonist oral anticoagulants in the acute care and periprocedural setting: a scientific statement from the american heart association. circulation 2017;135:e604-e633. 4. raychaudhuri r, litofsky ns. which traumatic brain injury patients should be treated with anticoagulants and when? expert review of neurotherapeutics 2014;14:237239. 5. roark cd, haines s. pharmacological anticoagulation and mechanical compression versus mechanical compression alone for venous thromboembolism prophylaxis for post‐operative neurosurgical patients. cochrane database of systematic reviews 2009. 6. wiegele m, schöchl h, haushofer a, et al. diagnostic and therapeutic approach in adult patients with traumatic brain injury receiving oral anticoagulant therapy: an austrian interdisciplinary consensus statement. critical care (london, england) 2019;23:62. 7. auer c, wurm g. outcome after acute head trauma needing neurosurgical intervention in patients with oral anticoagulants or anti-thrombotic agents. j trauma treat 2012;1:2167-1222.1000132. 8. zeeshan m, jehan f, o'keeffe t, et al. the novel oral anticoagulants (noacs) have worse outcomes compared with warfarin in patients with intracranial hemorrhage after tbi. the journal of trauma and acute care surgery 2018;85:915-920. 9. passer jz, loftus cm. postoperative anticoagulation after neurologic surgery. neurosurgery clinics 2018;29:575583. 10. tator ch. concussions and their consequences: current diagnosis, management and prevention. cmaj 2013;185:975-979. 11. quiñones-ossa g, padilla-zambrano h, pal r, et al. biomarkers in acute brain trauma: a narrative review. journal of acute disease 2019;8:1. 12. adachi t, hoshino h, takagi m, fujioka s. volume and characteristics of intracerebral hemorrhage with direct oral anticoagulants in comparison with warfarin
cerebrovascular diseases extra 2017;7:62-71. 13. levine ar, laliberte b, lin h, et al. weight based heparin dosing for thromboembolic disease is associated with earlier anticoagulation in surgical patients. international journal of surgery (london, england) 2014;12:1416-1419. 14. lillemäe k, järviö ja, silvasti-lundell mk, antinheimo jj, hernesniemi ja, niemi tt. incidence of postoperative hematomas requiring surgical treatment in neurosurgery: a retrospective observational study. world neurosurgery 2017;108:491-497. 15. vakharia vn, tai d, marcus h, vakharia nn, nandi d. new oral anti-coagulants: implications for neurosurgery. british journal of neurosurgery 2015;29:182-188. 16. lapostolle f, siguret v, martin a-c, et al. vitamin k antagonists and emergencies. european journal of emergency medicine 2018;25:378-386. 17. anguita sánchez m, bertomeu martínez v, cequier fillat á. quality of vitamin k antagonist anticoagulation in spain: prevalence of poor control and associated factors. revista espanola de cardiologia (english ed) 2015;68:761-768. 18. bennaghmouch n, de veer a, bode k, et al. efficacy and safety of the use of non-vitamin k antagonist oral anticoagulants in patients with nonvalvular atrial fibrillation and concomitant aspirin therapy: a metaanalysis of randomized trials. circulation 2018;137:1117-1129. 19. kimpton g, dabbous b, leach p. new oral anticoagulant and antiplatelet agents for neurosurgeons. british journal of neurosurgery 2015;29:614-621. 59 planning neurosurgical interventions in patients with anticoagulant therapy 20. beynon c, potzy a, sakowitz ow, unterberg aw. rivaroxaban and intracranial haemorrhage after mild traumatic brain injury: a dangerous combination? clinical neurology and neurosurgery 2015;136:73-78. 21. pakraftar s, atencio d, english j, corcos a, altschuler em, stahlfeld k. dabigatran etixilate and traumatic brain injury: evolving anticoagulants require evolving care plans. world journal of clinical cases 2014;2:362-366. 22. schoihet s. prevención de enfermedad tromboembólica en pacientes neuroquirúrgicos y neurológicos. revista chilena de cirugía 2007;59:311-316. 23. maegele m, schöchl h, menovsky t, et al. coagulopathy and haemorrhagic progression in traumatic brain injury: advances in mechanisms, diagnosis, and management. the lancet neurology 2017;16:630-647. 24. jovel cae, ramos ml, moreno cm, et al. utilidad y rendimiento diagnóstico de la punción lumbar en el servicio de urgencias. acta neurol colomb 2015;31:3948. 25. tan il, smith br, von geldern g, mateen fj, mcarthur jc. hiv-associated opportunistic infections of the cns. the lancet neurology 2012;11:605-617. 26. mondello s, robicsek sa, gabrielli a, et al. αii-spectrin breakdown products (sbdps): diagnosis and outcome in severe traumatic brain injury patients. journal of neurotrauma 2010;27:1203-1213. 27. weiss es, wang kk, allen jg, et al. alpha ii-spectrin breakdown products serve as novel markers of brain injury severity in a canine model of hypothermic circulatory arrest. the annals of thoracic surgery 2009;88:543-550. 28. zetterberg h, smith dh, blennow k. biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood. nature reviews neurology 2013;9:201-210. 29. gu j, huang h, huang y, sun h, xu h. hypertonic saline or mannitol for treating elevated intracranial pressure in traumatic brain injury: a meta-analysis of randomized controlled trials. neurosurgical review 2019;42:499-509. 30. sánchez-menoyo j, ruiz-ojeda j, martínez-arroyo a, garcía-moncó j, paz a-d, vicente-olabarría i. complicación espinal hemorrágica secundaria a una punción lumbar diagnóstica. revista de neurología 2009;48:418-420. 31. brown mw, yilmaz ts, kasper em. iatrogenic spinal hematoma as a complication of lumbar puncture: what is the risk and best management plan? surgical neurology international 2016;7:s581-589. 32. park jh, kim jy. iatrogenic spinal subarachnoid hematoma after diagnostic lumbar puncture. korean journal of spine 2017;14:158-161. 33. ruff rl, dougherty jh, jr. complications of lumbar puncture followed by anticoagulation. stroke 1981;12:879-881. 34. avila a, rivarola s, oliveros k, et al. hematoma espinal secundario a punción lumbar en paciente anticoagulado con rivaroxabán. revista hematología 2019;23:93-96. 35. lang ss, kofke wa, stiefel mf. monitoring and intraoperative management of elevated intracranial pressure and decompressive craniectomy. anesthesiology clinics 2012;30:289-310. 36. durango-espinosa y, moscote-salazar l, keni r, deora h, agrawal a. the puzzle of spontaneous versus traumatic subarachnoid hemorrhage. apollo medicine 2019;16:141-141. 37. heit jj, iv m, wintermark m. imaging of intracranial hemorrhage. j stroke 2017;19:11-27. 38. kim jy, bae hj. spontaneous intracerebral hemorrhage: management. j stroke 2017;19:28-39. 39. parker d, jr., rhoney dh, liu-deryke x. management of spontaneous nontraumatic intracranial hemorrhage. journal of pharmacy practice 2010;23:398-407. 40. lacerda gallardo áj. craniectomía descompresiva en el tratamiento del traumatismo craneoencefálico grave. revista cubana de neurología y neurocirugía 2013;3. 41. lubillo s, blanco j, lópez p, et al. papel de la craniectomía descompresiva en el enfermo neurocrítico. medicina intensiva 2009;33:74-83. 42. pizzi ma, alejos da, siegel jl, kim by, miller da, freeman wd. cerebral venous thrombosis associated with intracranial hemorrhage and timing of anticoagulation after hemicraniectomy. journal of stroke and cerebrovascular diseases : the official journal of national stroke association 2016;25:2312-2316. 43. andrade-lópez a, lara-ortega r, narvaez-rojas a, padilla-zambrano hs, moscote-salazar lr. anticoagulación y trombosis venosa cerebral: el dilema de la craniectomía descompresiva. acta neurol colomb 2018:223-224. 44. gessler f, bruder m, duetzmann s, et al. risk factors governing the development of cerebral vein and dural sinus thrombosis after craniotomy in patients with intracranial tumors. journal of neurosurgery 2018;128:373-379. 45. wassef sn, abel tj, grossbach a, et al. traumatic intracranial hemorrhage in patients taking dabigatran: report of 3 cases and review of the literature. neurosurgery 2013;73:e368-373; discussion e373-364. 46. greuter l, ullmann m, mariani l, guzman r, soleman j. effect of preoperative antiplatelet or anticoagulation therapy on hemorrhagic complications in patients with traumatic brain injury undergoing craniotomy or craniectomy. neurosurgical focus 2019;47:e3. 47. lan m, dambrino rjt, youssef a, et al. repeat surgery after decompressive craniectomy for traumatic intracranial hemorrhage: outcomes and predictors. world neurosurgery 2020;133:e757-e766. 48. huertas gonzález n. características clínicas, manejo y pronóstico de las hemorragias cerebrales asociadas al tratamiento con anticoagulantes orales. 2014. 49. bruder m, schuss p, konczalla j, et al. ventriculostomyrelated hemorrhage after treatment of acutely ruptured aneurysms: the influence of anticoagulation 60 quiñones-ossa g.a., angulo-mariño s.l., garcia-ballestas e. et al. and antiplatelet treatment. world neurosurgery 2015;84:1653-1659. 50. scheller c, strauss c, prell j, simmermacher s, brandt s. increased rate of ventriculostomy-related hemorrhage following endovascular treatment of ruptured aneurysms compared to clipping. acta neurochirurgica 2018;160:545-550. 51. blostein m, kerzner r. practice guidelines for anticoagulation management [online]. available at: https://cdn.ciussscentreouest.ca/documents/hgj/hemat ology/jgh_aco_guidelines_final_06-292012.pdf?1541434879. accessed 26 apr. 52. borab zm, lanni ma, tecce mg, pannucci cj, fischer jp. use of computerized clinical decision support systems to prevent venous thromboembolism in surgical patients: a systematic review and meta-analysis. jama surg 2017;152:638-645. 53. stanton r, woo d, moomaw c, haverbusch m, flaherty m, kleindorfer d. abstract wp327: chadsvasc and hasbed scores in patients with intracerebral hemorrhage and atrial fibrillation. stroke 2018;49:awp327-awp327. 54. kernan wn, ovbiagele b, black hr, et al. guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the american heart association/american stroke association. stroke 2014;45:2160-2236. 55. sahai t, tavares mf, sweeney jd. rapid response to intravenous vitamin k may obviate the need to transfuse prothrombin complex concentrates. transfusion 2017;57:1885-1890. 56. halvorsen s, storey rf, rocca b, et al. management of antithrombotic therapy after bleeding in patients with coronary artery disease and/or atrial fibrillation: expert consensus paper of the european society of cardiology working group on thrombosis. european heart journal 2017;38:1455-1462. 57. kuramatsu jb, sembill ja, gerner st, et al. management of therapeutic anticoagulation in patients with intracerebral haemorrhage and mechanical heart valves. european heart journal 2018;39:1709-1723. 58. alkherayf f, xu y, gandara e, westwick h, moldovan id, wells ps. timing of vitamin k antagonist re-initiation following intracranial hemorrhage in mechanical heart valves: systematic review and meta-analysis. thrombosis research 2016;144:152-157. 59. huisman mv, barco s, cannegieter sc, et al. pulmonary embolism. nature reviews disease primers 2018;4:18028. 60. villar ab, iturriaga lar. tromboembolismo pulmonar. archivos de bronconeumología 2010;46:31-37. 61. figueroa g, labarca e, cornejo r, et al. recomendaciones de la sociedad chilena de medicina intensiva para la prevención del tromboembolismo venoso en pacientes críticos médico-quirúrgicos adultos. revista chilena de medicina intensiva [internet] 2016;31:162-174. 62. ubaldini j. consenso de enfermedad tromboembólica. consenso argentino sac. revista argentina de cardiología 2009;77:411-428. 63. lara ml, pérez ml, lucio av. eficacia del tratamiento anticoagulante oral e incidencia de complicaciones en clínica de anticoagulantes. revista de especialidades médico-quirúrgicas 2013;18:292-298. 64. mateo j. nuevos anticoagulantes orales y su papel en la práctica clínica. revista española de cardiología suplementos 2013;13:33-41. 65. dewald ta, washam jb, becker rc. anticoagulants: pharmacokinetics, mechanisms of action, and indications. neurosurgery clinics of north america 2018;29:503-515. 66. dornbos d, 3rd, nimjee sm. reversal of systemic anticoagulants and antiplatelet therapeutics. neurosurgery clinics of north america 2018;29:537-545. 67. dudley rr, aziz i, bonnici a, et al. early venous thromboembolic event prophylaxis in traumatic brain injury with low-molecular-weight heparin: risks and benefits. journal of neurotrauma 2010;27:2165-2172. 68. carrillo-esper r, meza-márquez jm. monitoreo de la coagulación en el perioperatorio. revista mexicana de anestesiología 2015;38:406-409. 69. hunt h, stanworth s, curry n, et al. thromboelastography (teg) and rotational thromboelastometry (rotem) for trauma induced coagulopathy in adult trauma patients with bleeding. the cochrane database of systematic reviews 2015;2015:cd010438. 70. schneck mj. prophylactic screening for venous thromboembolism in neurosurgical patients. anticoagulation and hemostasis in neurosurgery: springer, 2016: 317-325. 71. chen x, jin dy, stafford dw, tie jk. evaluation of oral anticoagulants with vitamin k epoxide reductase in its native milieu. blood 2018;132:1974-1984. 72. hodroge a, matagrin b, moreau c, et al. vkorc1 mutations detected in patients resistant to vitamin k antagonists are not all associated with a resistant vkor activity. journal of thrombosis and haemostasis : jth 2012;10:2535-2543. 73. benavides f, grossman n, poggi h, et al. efecto de las variantes de vkorc1 y cyp2c9 sobre la dosis de anticoagulantes orales en individuos chilenos. revista médica de chile 2015;143:1369-1376. 74. kamali f, wynne h. pharmacogenetics of warfarin. annual review of medicine 2010;61:63-75. 75. chatterjee s, sardar p, biondi-zoccai g, kumbhani dj. new oral anticoagulants and the risk of intracranial hemorrhage: traditional and bayesian meta-analysis and mixed treatment comparison of randomized trials of new oral anticoagulants in atrial fibrillation. jama neurology 2013;70:1486-1490. 76. mehta va, wang ty, sankey ew, et al. restarting therapeutic anticoagulation after elective craniotomy 61 planning neurosurgical interventions in patients with anticoagulant therapy for patients with chronic atrial fibrillation: a review of the literature. world neurosurgery 2020;137:130-136. 77. divito a, kerr k, wilkerson c, shepard s, choi a, kitagawa rs. use of anticoagulation agents after traumatic intracranial hemorrhage. world neurosurgery 2019;123:e25-e30. 78. sadighi a, wasko l, dicristina h, et al. long-term outcome of resuming anticoagulation after anticoagulation-associated intracerebral hemorrhage. eneurologicalsci 2020;18:100222. 79. nassiri f, hachem ld, wang jz, et al. reinitiation of anticoagulation after surgical evacuation of subdural hematomas. world neurosurgery 2020;135:e616-e622. 80. saraf k, morris pd, garg p, sheridan p, storey r. nonvitamin k antagonist oral anticoagulants (noacs): clinical evidence and therapeutic considerations. postgraduate medical journal 2014;90:520-528. 81. baber u, mastoris i, mehran r. balancing ischaemia and bleeding risks with novel oral anticoagulants. nature reviews cardiology 2014;11:693-703. 82. ebright j, mousa sa. oral anticoagulants and status of antidotes for the reversal of bleeding risk. clinical and applied thrombosis/hemostasis : official journal of the international academy of clinical and applied thrombosis/hemostasis 2015;21:105-114. microsoft word kumar_convexity_f kumar ashish et al convexity meningiomas posing difficult challenges convexity meningiomas posing difficult challenges for neurosurgeons: two case reports and literature review kumar ashish, pandey p.n., ghani arshad, jaiswal gaurav ln hospital, maulana azad medical college, new delhi departement of neurosurgery, ln hospital, maulana azad medical college, new delhi abstract meningiomas have been intriguing since the time of harvey cushing. although, most of them have been conquered by “today’s neurosurgeons”, still they can pose difficult challenges sometimes. convexity meningiomas are relatively easier to tackle especially if they are not too large and do not displace critical neurovascular structures. however, they can complicate matters at times and hence, extreme precautions need to be practised. we report two such cases of convexity meningiomas with unusual set of events where one had an unusual post operative complication and the other had an unusual mode of presentation. extradural hematomas (edh) are a common complication after intracranial surgeries. they are usually picked up in the early post-operative scans and are managed according to their size and mass effect. the first patient is a 60 year old female where delayed edh was detected after a sudden bout of hypertension after the initial scan after 48 hours of surgery was normal. intraoperatively, middle meningeal artery (mma) had re-bled due to this sudden rise in the blood pressure. second case is a 33 year old female who presented with an intracerebral bleed due to hemorrhage within a convexity meningioma. keywords: convexity meningioma, extradural hematoma, intracerebral hemorrhage introduction meningiomas pose a tough challenge for neurosurgeons across the world due to their so called benign nature and expected excellent outcome after complete excision. very thin margins of error make the convexity meningioma surgery even more interesting as usually simpson grade 0 excisions are expected more often. but sometimes, these convexity meningiomas may have varied presentations and can cause unusual complications. we report two such patients who presented in rather unusual manner and hence deserve to be noticed so that, awareness regarding such presentations/complications makes surgeons expectant and wary of them. case 1 a 60 year old female presented to us with occasional severe headaches. she had no other symptoms and her neurological examination was normal. magnetic resonance imaging (mri) had revealed a convexity meningioma in the left parietal region which was isointense on t1weighted image, hypointense on t2weighted image and was intensely contrast enhancing (figure 1). she was hypertensive since many years and was on anti romanian neurosurgery (2011) xviii 2 hypertensive medicines. her prothrombin time and platelet counts were within normal range and she was not on any antithrombotic drugs. she wished to undergo surgery and underwent left parietal craniotomy and excision of meningioma after a thorough pre-operative work up. the surgery was straightforward. a thick posterior branch of the middle meningeal artery (mma) on the surface of dura (coming in the line of the dural incision) was controlled well with bipolar cautery. the meningioma was removed (simpson grade 0 excision) and duraplasty was done in the region of involved dura. the post operative period was uneventful and the patient was planned for discharge. the post operative computed tomography (ct) scan after 48 hours of surgery showed no evidence of blood in the tumour bed and was satisfactory (figure 2). after 6 hours of this scan, she suddenly started complaining of severe headache. she was given analgesics and the blood pressure medications as the pressure shot up to 190/120 mm of hg (millimetres of mercury). she developed altered sensorium within minutes and had respiratory distress. the pupil on the left side was blown up (4mm, not reacting to light). she underwent a second ct scan in a span of 6 hours, which showed a large extradural hematoma (edh) at the operative site with mass effect and midline shift (figure 3). her repeat coagulation profile was normal. the patient was immediately taken for resurgery and the hematoma was evacuated. the same branch of mma was found to be ferociously bleeding. it was coagulated and ligated this time. the patient was shifted to the intensive care unit (icu). post operatively, she was electively ventilated for 24 hours and the blood pressure was being closely monitored. 24 hours later, she developed another bout of hypertension (190/110 mm of hg) and started having hematemesis. she later developed multiple organ dysfunctions and succumbed to it. figure 1 figure 2 kumar ashish et al convexity meningiomas posing difficult challenges figure 3 figure 4 figure 5 figure 6 case 2 a 33 year old female presented to us with sudden loss of consciousness 12 hours back. although she had occasional headaches, nothing major was noticed by the relatives. on examination, she had bradycardia and her blood pressure was 100/60 mm of hg (millimetres of mercury). she had a glasgow coma scale (gcs) of 4/15 and the pupil on the left was dilated (3mm; non-reacting to light). she was immediately intubated and was taken up for an emergency ct scan (figure 4) which showed large left sided intra-cerebral hematoma with mass effect and midline shift. although, a tumour bleed was suspected, nothing could be conclusively established without a contrast scan (which was not available for the emergency scan). the patient was deteriorating rapidly and hence was taken for decompression surgery and clot evacuation. evaluation for the etiology was planned as a second stage procedure once the patient was optimized. intra-operatively, the brain was tense and hence the hematoma was first evacuated by middle frontal gyrus approach while a dural based hemorrhagic lesion (suspected to be a convexity meningioma) was observed too (figure 5). it was excised (simpson grade 0 excision) and lax duraplasty was done (figure 6). the patient was electively ventilated post operatively. however, she succumbed after 24 hours of surgery due to other metabolic complications. the histopathology was fibroblastic meningioma. discussion convexity meningiomas in both the cases posed great difficulties for us. in the first case, delayed edh after 56 hours of surgery with a satisfactory post operative romanian neurosurgery (2011) xviii 2 ct scan was unusual in our experience. the probable reason would have been a reactionary haemorrhage due to mma clot dislodgement due to a bout of hypertension. lee et al studied surgeries of 153 meningiomas and found statistically significant relationship of post-operative hematomas in patients older than 70 years and having platelet counts less than 150 ×109/l (8). gerlach et al have also echoed similar findings (2). the other possible risk factors not validated yet, are: the preoperative use of anti-thrombotic medicines, location and histology of meningioma, invasion of venous sinus, arachnoid infiltration and the extent of removal (partial versus total). although hematomas are commonly found more often after meningioma surgery than any other intra-cranial tumour surgery (4,10), most likely it occurs in the tumour bed itself and early ct should pick it up under most circumstances. palmer et al also found the majority of postoperative hematomas intraparenchymal (43%) and frequently occurring after meningioma surgery (6.2%) (10). our patient had a normal coagulation profile, but we think that the delayed reactionary haemorrhage (>56 hours) occurred due to a hypertensive episode and hence, post operative monitoring of the same should have been more stringent. although, old age patients with hypertension are prone for post-operative bleeding, such rare catastrophe has never been reported in the literature. we did not find any similar case where an edh developed so late in the post-operative period. in the second case, presentation as intracerebral bleed was unusual. bosnjak et al determined the clinico-pathological features of patients with intracranial bleeding from unsuspected meningioma and found out that an increased bleeding tendency was seen in patients <30 years and >70 years, in “convexity” and intraventricular locations and “fibrous” meningiomas (1). all these features were present in our patient. they further noticed that 96.2% patients survived after their meningiomas spontaneously hemorrhaged. in patients who were unconscious before surgery (as in our case), overall mortality rate was 74.1%, and that in surgically treated cases was 46.2%. various authors have reported similar cases in the past and most of them have reported this complication with an angioblastic meningioma (3,5,6,7,9). various hypotheses have been proposed for such an occurrence. most common one is the rupture of abnormal vascular network of tumour or the invasion of thin vessels by the tumour cells. the other possible explanation is the rapid growth of lesion causing intratumoral necrosis and hemorrhage. the objective of this article is to highlight a rare presentation and complication associated with convexity meningiomas. we suggest that high risk patients should be closely observed for hemodynamic stability for a significantly longer post-operative period and also, intraoperatively, if any significant calibre mma branches are encountered in the line of durotomy, it should be both ligated and coagulated so as to remain doubly secure and hence prevent such mishaps accounting to high mortality and morbidity. patients with intracerebral hematomas should be first managed by hematoma evacuation. excision of the meningioma later will lead to improved outcomes once the intracranial pressure (icp) has been brought down. inspite of this, the prognosis remains grave which stresses on the role of screening in population for such tumours. kumar ashish et al convexity meningiomas posing difficult challenges corresponding author: dr ashish kumar, room number 21, pg men’s hostel, maulana azad medical college, new delhi-110002, phone: 9999622962, email: drashishmch@hotmail.com references 1. bosnjak r, derham c, popović m, ravnik j. spontaneous intracranial meningioma bleeding: clinicopathological features and outcome.j neurosurg. 2005 ;103:473-84. 2. gerlach r, raabe a, scharrer i, meixensberger j, seifert v: post-operative hematoma after surgery for intracranial meningiomas: causes, avoidable risk factors and clinical outcome. neurol res 26: 61-6,2004. 3. helle tl, conley fk. haemorrhage associated with meningioma: a case report and review of literature. journal of neurology, neurosurgery, and psychiatry, 1980;43: 725-29. 4. kalfas ih, little jr : postoperative hemorrhage : a survey of 4992 intracranial procedures. neurosurgery 23: 343-347, 1988. 5. kohli cl, crouch rl. meningioma with intracerebral hematoma. neurosurgery 1984;15: 23740. 6. kurokawa h, kikuchi k, kamisato n, miura s, ishida y. massive intracerebral hemorrhage due to a convexity meningioma. rinsho hoshasen 1989 ;34:7236. 7. lazaro rp, messer hd, brinker rp. intracranial hemorrhage associated with meningioma. neurosurgery 1981;8:96-101. 8. lee by, hong sk, chu wh, kang jk: risk factors of postoperative hematomas after surgery for intracranial meningiomas. j korean neurosurg soc 39:109-113,2006. 9. nakao s, sato s, ban s, inutsuka n, yamamoto t, ogata m: massive intracerebral hemorrhage caused by angioblastic meningioma. surg neurol 1977;7:245-48. 10.palmer jd, sparrow oc, fausto i : postoperative hematoma : a 5-year survey and identification of avoidable risk factors. neurosurgery 35:1061-64, 1994. 18kumar_intramedullarymature romanian neurosurgery (2014) xxi 3: 353 357 353 intramedullary mature teratoma of cervical spine in an infant: a rare case report rakesh kumar1, amit chanduka2, devendra purohit3, radhe shyam mittal4, ronyl kaushal5 sawai man singh medical college, jaipur, rajasthan, india 1registrar, department of neurosurgery 2senior registrar, department of neurosurgery 3professor, department of neurosurgery 4professor & head department of neurosurgery 5senior registrar, department of neurosurgery abstract spinal teratomas are rare tumor and cervical intramedullary location in infancy still rarer. only eleven cases of cervical intramedullary teratoma in pediatric patients is reported in available literature (1, 11).we are reporting a case of an infant presenting with cervical mature teratoma with associated dysraphism, adding the next in this rare case series. arising as a result of dysembryogenesis, these lesions by virtue of their content are difficult to diagnose preoperatively. heterogeneous intensities on mri produced by intralesional lipomatous and osseous elements are helpful but rarely enough to diagnose the tumor. histology is confirmatory. mature teratomas generally have good prognosis and a timely intervention can prevent further neurological deterioration. however a strict clinical and radiological follow up is recommended. key words: intramedullary, spinal tumour, teratoma. introduction teratomas involving the central nervous system are rare and account for approximately 0.1-0.5% of all spinal tumors (5, 10). pediatric intramedullary spinal teratomas are still rarer, excluding the sacro-coccygeal form often seen in neonates.the majority of these have been described in the literature as isolated case reports. (3, 13) by definition, they are tumors of pleuripotent cells derived from all 3 germ cell layers and recapitulate normal organogenesis. broadly, they are classified as mature, immature and malignant. these lesions are rare and their uncertain clinical behavior makes diagnosis and management a difficult task. as teratomas are rarely suspected preoperatively, the diagnosis of teratoma is usually made at the time of pathological assessment. radiology is helpful in ascertaining nature of the lesion but is not 354 kumar et al intramedullary mature teratoma of cervical spine in an infant diagnostic. histopathology is the gold standard for diagnosis. here we report a case of cervical intramedullary teratoma associated with spinal dysraphism in an infant. case report an 11 month old male child presented with swelling in cervical region, opposite c6-c7 vertebral level (figure 1). there was no history of delayed milestones or any history suggestive of urinary or faecal incontinence. general physical examination was unremarkable except a pedicled firm swelling in cervical region. no other cutaneous stigmata of spinal dysraphism seen along the spine. fontanellae were open and not bulging. neurological examination revealed no sensory-motor deficits and normal bowel bladder function for the age. on x-ray of cervical spine posterior arch elements of c6 and c7 vertebrae were deficient in midline. mri showed a solid cystic extra cutaneous lesion against c6-7 vertebral level pedicled to the dura at c6 level. two intradural cystic lesions and one heterogeneous intramedullary solid lesion were seen (figure 2). figure 1 photographs of patient showing pedicled swelling in cervical region figure 2 t2 weighted mri saggital image showing extracutaneous swelling with deficient posterior arch element at c6-7 (white arrow), with well defined hyperintense intradural cystic lesion and a heterogenous iso to hyperintense intramedullary sol (red arrow) figure 3 intraoperative image showing intradural extension of cutaneous lesion through a fibrous tract romanian neurosurgery (2014) xxi 3: 353 357 355 c6-c7 laminectomy with drainage of intradural cystic jelly like component with complete enucleation of intramedullary space occupying lesion containing lipomatous and osseous elements done (figure 3). histology was suggestive of mature teratoma. post operative recovery was uneventful. at 5 months follow up child is doing well, achieving normal milestones and no neurological deficit. discussion teratomas are composed of a mixture of cell types derived from three germ cell layers and can occur at many locations throughout the body. spinal teratomas are infrequent and very small proportion of cns teratomas occur in the spinal cord, constituting only 0.2– 0.5% of all spinal cord tumors (10). spinal teratomas have been reported throughout the spinal axis and the most common sites are lumbar, conus and dorso-lumbar regions. cervical location is rare. hamada et al (6) in their study of 18 intraspinal teratomas found conus medullaris as the most frequent location (70.6%). adults were more commonly affected than children. agrawal et al (1) in their study of 8 cases of spinal teratoma found cervical spine as common a location as lumbar spine (4/8, 50%). however involvement of cervical spine in pediatric age group was seen in 2 cases only. a similar study by sharma et al (14) with 27 cases revealed 62.9% occurrence in childhood with associated dysraphism in 77.7%. however no intramedullary pediatric cervical involvement was found. on searching literature, we could retrieve only eleven patients with cervical intramedullary teratoma in pediatric patients (1, 11). ours is a case of an infant presenting with cervical mature teratoma with associated dysraphism, adding the next in this rare case series. several hypotheses have been proposed with regard to the origin of spinal teratomas. the traditional view is that these lesions are neoplastic and arise from misplaced primordial germ cells into the dorsal midline during their normal migration from the primitive yolk sac to the gonadal ridges (2, 3, 7, 9, 15). an alternative hypothesis is that these lesions are not neoplastic and are the result of a dysembryogenic mechanism as many of them are associated with a dysraphic state (7). however, teratomas without associated dysraphic features are also reported. (14) for diagnosis of spinal teratomas, conventional x-rays and ct scans have very limited roles and primarily suggests associated bony anomaly, bony changes like vertebral erosions or increased interpedicular distance, associated diastometamyelia or tumors with calcification. mri is regarded as the gold standard diagnostic technique. radiologically mixed solid and cystic morphology, fat signal and areas of calcification are seen which appears on mri as heterogenous iso to hypointense on t1-weighted and heterogenous hyperintense on t2-weighted images. they are non-enhancing on contrast. mri has localizing value but is not definite for diagnosis. intramedullary component has been shown to be associated with meningomyelocele or split-cord malformation in few cases (14). malignant nature is suspected if the lesion is predominantly solid and/or contrast enhancing. 356 kumar et al intramedullary mature teratoma of cervical spine in an infant histopathologically, teratomas are composed of the remnants of all 3 germ cell layers (2, 4, 5, 7, 10, 12). they are classified into 3 types: mature, immature and malignant teratomas. mature teratomas contains mature elements of ecto, endo and mesodermal origin. on the other hand, immature teratomas are aggressive tumors, comprising primitive, undifferentiated components; these tumors tend to recur frequently. malignant teratomas are derived from the yolk sac or endoderm sinus, and especially, malignant teratomas, along with the high levels of serum αfetoprotein, are associated with a poor prognosis (2, 7). however, it is essential that elements of the 3 germ cell layers are identified for it to be diagnosed as a spinal teratoma. surgery is the treatment of choice, and radical removal of the tumor should be the aim of surgical intervention whenever possible. in children, extensive laminectomies may lead to spinal instability. so laminotomy and laminoplasty should be done. however, complete removal may not always be possible due to the location of tumor. even a benign tumor can recur due to incomplete removal. radiotherapy or chemotherapy should be reserved for teratomas which show an immature or malignant component8. prognosis is poor for teratocarcinomas and teratomas with malignant transformation. conclusion teratomas are rare cns tumor with rarer involvement of cervical intramedullary location in infants. preoperative diagnosis is difficult and most of the cases diagnosed intraoperatively or on histology. mature teratoma have good prognosis and timely intervention can prevent further neurological deterioration. correspondence dr. rakesh kumar 4kh-2, housing board, shastri nagar, jaipur, rajasthan, india, 302016. e-mail: rksingh2226@gmail.com. dr_mittal@hotmail.com references 1. agrawal m, uppin ms, patibandla mr, bhattacharjee s, panigrahi mk, saradhi v, rani jy,purohit ak, challa s. teratomas in central nervous system: a clinicmorphological study with review of literature.neurology india;58,6:841-846, 2010. 2. ak h, ulu mo, sar m, albayram s, aydin s, uzan m: adult intra-medullary mature teratoma of the spinal cord: review of the literature illustrated with an unusual example. acta neurochir (wien) 148: 663-669; discussion 669, 2006. 3. al-sarraj st, parmar d, dean af, phookun g, bridges lr clinico-pathological study of seven cases of spinal cord teratoma: spinal teratoma 251 a possible germ cell origin. histopathology 32:51–56,1998. 4. cavazzani p, ruelle a, michelozzi g, andrioli g: spinal dermoid cysts originating intracranial fat drop causing obstructive hydrocephalus: case report. surg neurol 43: 466-469; discussion 469-470, 1995 5. fernandez-cornejo vj, martinez-perez m, pologarcia la, martinezlage jf, et al: cystic mature teratoma of the filum terminale in an adult. case report and review of the literature. neurocirugia (astur) 15: 290293, 2004. 6. hamada h, kurimoto m, hayashi n, hirashimma y, matsumura n, endo s. intramedullary spinal teratoma with spina bifida. child nerv syst;17:109-11, 2001. 7. koen jl, mclendon re, george tm intradural spinal teratoma: evidence for a dysembryogenic origin. report of four cases. j neurosurg 89:844–851,1998. 8. ling yj, lai dm, tsu hc, lin sm. primary intracranial teratocarcinoma with extraneural metastasiscase report and review of literature. acta neurol sin;2:332-7. 1993. romanian neurosurgery (2014) xxi 3: 353 357 357 9. makary r, wolfson d, dasilva v, mohammadi a, shuja s: intramedullary mature teratoma of the cervical spinal cord at c1-2 associated with occult spinal dysraphism in an adult. j neurosurg spine 6: 579-584, 2007 10. nonomura y, miyamoto k, wada e, hosoe h, nishimoto h, ogura h, et al: intramedullary teratoma of the spine: report of two adult case. spinal cord 40: 40-43, 2002 11. paterakis kn, karantanas ah, barbanis s, hadjigeorgiou gm, karavelis a cervical spinal cord intramedullary teratoma. clin neurol neurosurg 108:514–517. 2006. 12. poeze m, herpers m, tjandra b, freling g, beuls e: intramedullary spinal teratoma presenting with urinary retension: case report and review of the literature. neurosurgery 45: 379-385,1999. 13. sharma mc, aggarwal m, ralte am et al clinicopathological study of spinal teratomas. a series of 10 cases. j neurosurg sci 47:95–100, 2003. 14. sharma mc, jain d, sarkar c, suri v, garg a, singh m, et al. spinal teratomas: a clinico-pathological study of 27 patients. acta neurochirurgica;151:245-52, 2009 15. stevens qe, kattner ka, chen yh, rahman ma: intradural extramedullary mature cystic teratoma, not only a childhood disease.j spinal disord tech 19: 213216, 2006. microsoft word 12.popescuroxana_theimportance_f.docx 476 roxana popescu et al ct imaging in orbital and facial foreign bodies the importance of ct imaging for detecting traumatic intraorbitar and maxillofacial foreign bodies roxana popescu1, b. dobrovăţ2, a. nemţoi2, oana lăduncă2, danisia haba3 1phd student, faculty of medicine, university of medicine and pharmacy “gr. t. popa” iaşi, resident in radiology and medical imaging 2phd studentdepartment of general and dental radiology, faculty of medicine, university of medicine and pharmacy “gr.t. popa” iaşi 3department of general and dental radiology, faculty of medicine, university of medicine and pharmacy “gr. t. popa” iaşi, emergency hospital “n. oblu” iasi abstract the study represents an evaluation of the ability of spiral and conventional computer tomography in the diagnoseof intraorbitar and intraocular foreign bodies. the study includes 19 patients, aged between 15 and 52 years, 10 men and 9 women, presenting intraocular or intraorbitar foreign bodies or as a result of an traumatic injuries, who addressed the emergency hospital n. oblu iasi, between september 2010 march 2011. the ct examination was the main imaging method of investigation in addition to conventional radiographs; it was conducted on a philips aura single-slice unit and a siemens somatom ar.c unit in the department of radiology and medical imaging in thehospital “n. oblu” iasi. one patient presents an ct image of carbonite iofb, 5 patients present metallic iofb, the images are obtained using used incremental ct (somatom arc, siemens). 2 patients present spiral ct image of a metallic penetrating intraocular foreign body, 11 patients present spiral ct image of a metallic penetrating intraocular and maxillofacial foreign body. the classical computer tomography and spiral ct are among the most effective methods of examination and management of intraocular foreign bodies, maxillofacial or intraorbital. the spiral ct realise a continuous scanning of a volume of the patients body during table movement and reduces examination time and radiation exposure. keywords: computertomography, iofb, orbit introduction intraorbital foreign bodies (iofbs) are a common occurrence worldwide and happen at a frequency of once in every six cases of orbital trauma. metallic foreign bodies are more frecqent than organic, carbonite or glass iofb (1, 2). imaging and management should be tailored individually. the intraorbital foreign bodies represent a medical emergency due to major problems caused by complete/ partial loss of vision. the importance results also from the high price of the tratement and of the difficult rehabilitation of the patients. the purpose of the study is the comparative evaluation of the results of romanian neurosurgery (2011) xviii 4: 476 482 477 incremental ct scan comparing to spiral ct. ct is generally considered to be the gold standard for iofbs. it is safe to use with metallic iofbs, excludes orbitocranial extension, and is also able to diagnose orbital wall fractures and orbital sepsis with high accuracy. abscess formation in the orbit, bone, and brain are other complications that ct may exclude. spiral ct reduces artifacts from metallic intraorbital foreign bodies, also reduces patients irradiation and the images obtained are higher quality than those from the conventional ct. ct is also accurate for the detection and localization of glass, metal, and stone foreign bodies, and the nature of the iofb may be deduced from the hounsfield numbers. metallic density is easily distinguished on ct, but size overestimation of metals on soft tissue window settings is a wellrecognized occurrence. the ct threshold size for the detection of metallic foreign bodies is 0.07 mm3 with thin slice ct, method is lower sensitivity in case of radiolucent foreign bodies, or where they are located near the sclera (1, 2, 3). ct is useful in case of complex orbital trauma, allowing visualization of soft tissue, bone structures and intraorbital foreign bodies. advantages of ct examination for are important for complex trauma, in case we have an association of a head injury and orbital, intraocular foreign bodies and the possibility exam the vascular using the contrast substances. material and method the study includes 19 patients, aged between 15 and 52 years, 10 men and 9 women, presenting intraocular or intraorbitar foreign bodies or as a result of an traumatic injuries, who addressed the radiology and ophthalmology departments of the hospital “n. oblu” iasi, between september 2010 march 2011. the ct examination was the main imaging method of investigation in addition to conventional radiographs; it was conducted on a philips aura single-slice unit and a siemens somatom ar.c unit in the department of radiology and medical imaging in the hospital “n. oblu” iasi. the examination protocol was different depending on the apparatus used: the device siemens have used sections with a thickness of 3 mm and reconstruction at 3 mm, and on the philips it could have spiral acquisitions, usually with 2 mm sections, pitch of 3 mm (1.5) and reconstruction at 1 mm. the examination was native, depending on clinical indications and the native exam results, contrast was sometimes given intravenously (iopamiro, bracco ewopharma, ultravist, schering, omnipaque, ge amersham). routine were performed 2d reconstruction (mpr "multiplanar reconstructions" or mip "maximum intensity projections") and sometimes 3d reconstruction (ssd "surface shaded display "dvr-" direct rendering volumes"). were usually performed section in the axial plane, but for the pathological lesions that affect the orbital floor or ceiling were made direct coronal sections. the opportunity to evaluate fast and very precise the bone and soft tissue damage (orbit, superficial, endocranial) made this method to be preferred for cranio-facial trauma patients, making often in the first line. 478 roxana popescu et al ct imaging in orbital and facial foreign bodies results one case revealed anincremental ct image of a carbonite intraocular and intraorbitar foreign body.in 5 cases we found out incremental ct images of a metalicintraorbitar foreign body. in 3 cases we havespiral ct images of glass intraorbitar foreign bodies. in 2 cases we discovered the spiral ct image of a metallic penetrating intraocular foreign body. the rest of the cases shows spiral ct image of a metallic penetrating intraocular and maxillofacial foreign body. figures 1, 2, 3 incremental ct image of a carboniteintraorbital and intraocular foreign romanian neurosurgery (2011) xviii 4: 476 482 479 figures 4, 5, 6 incremental ct image of an intraorbital foreign body figures 7, 8, 9 images of ct spiral philips aura glass intraorbital foreign body figures 10, 11, 12 spiral ct images of penetrant metallic intraocular foreign bodies 480 roxana popescu et al ct imaging in orbital and facial foreign bodies discussion computer tomography (ct) is an imaging technique that generates sectional images in the axial plan by scanning a beam of x-rays around the body to be examined. ct is based on the determination of attenuation coefficients ( linear absorption) in tissue – density – of an x-ray beam that passes through the body, the ct image is a "map" of the distribution of tissue densities in the volume of of the section examined (4, 5, 6). a collimate beam (narrow) x-ray beam passes through the patient body and the intensity is measured by an emergent crown of detectors, disposed diametrically opposite to the x-ray tube; for a given position of the radiogenic tube the measured value of the intensity of the emergent beam is called projection. imagine the object beam is reconstructed by computer through the mathematical analysis of its multiple projections (8). an orbital foreign body may lead to variety of signs, symptoms and clinical findings according to its size, location, velocity and composition. the patients in this study suffered mostly traumatic injuries. even if the study involved a small number of pacients, the results are similar with other studies on this theme, like the study of nasr am, haik bg, fleming jc, or study ofleal fam, silva e filho ap. the patients in this study are 12 aged between 25 45 years old, 3 aged between 15 -25 years old, 4 persons aged between 35 45 years old and 1 person in the interval between 45 -52 years old. we can conclude that the incidence of intraorbital and intraocular foreign bodies from traumatic injuries ( which represents 63,16% from our cases) is increased at persons aged nearly thirteen. we observe that in five cases we have pacients with metallic intraorbital bodies which are the result of small fireworks, petards which expoded in their faces. in three cases the iofb are made by glass as result of an traffic accidents. one case the iofb is carbonite in ancasnic accidents. the rest of our cases are also from traffic accidents and the iofb are metallic. we can see that 52,63% from iofb at our pacients are from car accidents. carbonite casnic accidents; 5,26% metallic petard, fireworks explosions; 26,32% glass car accidents; 15,79% metallic intraorbital, intraocular or intramaxillar car accidents; 52,63% 0,00% 10,00% 20,00% 30,00% 40,00% 50,00% 60,00% foreign body type related to generating source carbonite casnic accidents metallic petard, fireworks explosions glass car accidents metallic intraorbital, intraocular or intramaxillar car accidents romanian neurosurgery (2011) xviii 4: 476 482 481 intraorbital fbs can be associated with severe injuries leading to loss of vision or may lead to sight-threatening complications (8). a retained metallic intraorbital fb may cause a variety of signs, symptoms, and clinical findings, based on its size, location, and composition. loss of vision is usually due to the initial trauma and is generally not influenced by surgical intervention. the best management of retained metallic intraorbital fbs remains a controversial subject. the decision regarding surgical removal depends mainly on the location and type of intraorbital fb (7). however, the removal of foreign body from the orbit, which is crowded with delicate structures, is not safe. retained metallic iofbs are well tolerated and should be managed conservatively in the absence of specific indications for removal (12). when the foreign body is impinging on neurological structures or causing mechanical restriction to ocular movements, one should consider removal of the fb after detailed and precise localization to minimize damage to the adjacent ocular structures (13). conclusion the classical computer tomography and spiral ct are among the most effective methods of examination and management of intraocular foreign bodies, maxillofacial or intraorbital. the spiral ct realise a continuous scanning of a volume of the patients body during table movement (9, 10). the main advantages are related to the fact that there is no section "lost" due to uneven breathing of the patient from one section to another, it can be achieved quality reconstruction in different planes of space and last but not least we have reduced examination time and radiation dose to the patient that is exposed. ctexam is very important to establish the exact location of the foreign body, to see if the is also an asociated fracture of the 15-25 years; 10,53% 25-35 years; 63,16% 35-45 years; 21,05% 45-52 years; 5,26% 0,00% 10,00% 20,00% 30,00% 40,00% 50,00% 60,00% 70,00% patient age distribution (%) 15-25 years 25-35 years 35-45 years 45-52 years 482 roxana popescu et al ct imaging in orbital and facial foreign bodies bones of orbit or other bones of the face, and for decide the specific surgical intervention. references 1. adesania o, dawkins d. intraorbital wooden foreign body. emergradiolog 2007. 14: 45-49. 2. betharia sm, kumar h. orbital wooden foreign bodies-a case report. indian j ophthalmol. 1989; 37:146–7. 3. brock l, tanenbaum hl. retention of wooden foreign bodies in the orbit. can j ophthalmol. 1980;15(2):70-2. 4. bullock jd, warwar re, bartley gb, waller rr, henderson jw. unusual orbital foreign bodies. ophthalplastreconstr surg. 1999;15(1):44-51. 5. cartwright mj, kurumety ur, frueh br. intraorbital wood foreign body. ophthalplastreconstr surg. 1995;11(1):44-8. 6. cohen ma, boyes-varley g. penetrating injuries to the maxillofacial region. j oral maxillofac surg. 1986;44(3):197-202. 7. espaillat a, enzer i, stephren l. intraorbitalmaetallic foreign body. arch. ophthalmology 1998; 116:824. 8. figueira ec,francis ic,wilcsek ga. intraorbitalglassforeignbody missed onctimaging. ophthalplastreconstr surg.2007; 23(1): 80-2. 9. finkelstein m, legmann a, rubin pa. projectile metallic foreign bodies in the orbit; a retrospective study of epidemiologic factors, management, and outcomes. ophthalmology 1997; 104: 96 103. 10. fulcher tp, mcnab aa, sullivan tj. clinical features and management of intraorbital foreign bodies. ophthalmology 2002; 109: 494 500. 11. harris amp, wood re, nortjé cj, grotepass f. deliberately inflicted, penetrating injuries of the maxillofacial region (jael's syndrome). report of 4 cases. j craniomaxillofac surg. 1988; 16(2):60-3. 12. hudson da. impacted knife injuries of the face. br j plast surg. 1992;45(3):222-4. 13.kuckelkorn r, kottek a, schrage n, reim m. poor prognosis of severe chemical and thermal eye burns: the need for adequate emergency care and primary prevention. int arch occup environ health. 1995; 67:281–4. 14.leal fam, silva e filho ap, neiva dm, learth jcs, silveira db. trauma ocular ocupacionalporcorpoestranho superficial. arq bras oftalmol. 2003;66(1):57-60. 15.macrae ja. diagnosis and management of a wooden orbital foreign body: case report. br j ophthamol. 1979;63(12):845-51 16.mauriello m, lee h, nguyen l. ct of soft tissue injuries and orbital fractures. radiologic clinics of north america 1999. 17.motomura h, taniguchi t, harada t, muraoka m. a combined flap reconstruction for full-thickness defects of the medial canthal region. j plastreconstraesthet surg. 2006; 59:747–51. 18.nasr am, haik bg, fleming jc, al-hussain hm, karcioglu za. penetrating orbital injury with organic foreign bodies. ophthalmology 1999;106(3):523-32 19.paia c, pinsard l, bluestel c. intraorbital foreign body.journalfrancaisd’ophtalmology 2010; 33(9): 65766. 20.reim m, redbrake c, schrage chemical and thermal injuries of the eyes. surgical and medical treatment based on clinical and pathophysiological findings. arch socespoftalmol. 2001; 76:79–124. 21.singh v, kaur a, agrawal s. an unusual intraorbital foreign body. indian j ophthalmol. 2004;52:64–5. 22.shinohara eh, heringer l, de carvalho jp. impacted knife injuries in the maxillofacial region: report of 2 cases. j oral maxillofac surg. 2001;59(10):1221-3. 23.tian-lin x,nileshkumar m, zhi-han y, wei c, xiao-qiang l, zhen-quan z, ye-hui z. trochlear calcification and intraorbital foreign body in ocular trauma patients. chinese journal of traumatology 2009. 210 – 213. 24.tuppurainen k, mantyjarvi m, puranen m. wooden foreign particles in the orbit spontaneous recovery. actaophthamol scand. 1997;75(1):109-11. 25.zhu y, li zg, zhang yf. problems in diagnosis and treatment of orbital foreign body--an analysis of 24 cases. zhonguaya ken 2008. 44(8) 676-80. 01_paper romanian neurosurgery (2015) xxix 4: 381 384 381 doi: 10.1515/romneu-2015-0053 spontaneous regression of lumbar herniated disc case presentation a. chiriac, giorgiana ion*, z. faiyad*, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi “prof. dr. n. oblu” clinic emergency hospital, iasi abstract: intervertebral disc herniation is a common disease that usually requires surgical intervention. however, in some cases, neurological symptoms may improve with conservative treatment. in this article, we present a case with spontaneous regression of extruded lumbar herniated disc correlated with clinical improvement and documented with follow up mri studies. key words: intervertebral disc herniation, spontaneous regression introduction the intervertebral disc herniation of the lumbar spine is one of the most common muscle-skeletal diseases usually characterized by low back pain and nerve root radiculopathy. even if it passes more than 60 years from the first reported surgery for lumbar disc herniation some aspects concerning the most effective treatment are still in discussion. most of patients with extruded lumbar disc herniation require surgical intervention due to their clinical manifestation. also, there are many reports of total clinical symptoms remission after conservative treatment and imagistic spontaneous regression of intervertebral disc herniation. in this paper we present one case with spontaneous regression of extruded lumbar herniated disc documented on follow up mri studies, in which the clinical symptoms improved with time. a short review of literature and mechanisms, precipitating factors of spontaneous disc regression, and proper treatment are discussed. case presentation a 38-year-old man with a 6-months history of low back and right leg pain was admitted to our department on february 2014. the patient declares a history of intermittent low back pain over the previous 2 years. the neurological examination revealed a slight peripheral l5 radiculopathy and paresthesias predominantly at right big toe. straight leg raising test was positive on the right side. the patient was able to walk normally, but presented difficulty walking on their toes. he declares a treatment 382 chiriac et al spontaneous regression of lumbar herniated disc with anti-inflammatory and muscle relaxants medication. magnetic resonance imaging (t2weighted) of the lumbar spine performed shortly after his admission to our department had shown a large right-sided paracentral extruded disc fragment at the l4–l5 disk space, compressing the traversing l5 nerve root and the dural sac. the pathological mri image found corresponds with the patient’s clinical symptoms (figure 1a, c). even if we had offered an operative treatment, the patient preferred to follow a conservative treatment that included physical and medical therapy with bed rest. after the next six weeks at first clinical control, the patient no longer had leg pain or physical findings of nerve root tension. he did have residual left-sided grade 4 out of 5 weakness of his great toe extensor. the patient came 12 months later to our outpatient clinic for folow-up lumbar spine mri examination. this second magnetic resonance imaging study showed substantial regression of the extruded l4–l5 disc fragment without significantly reduction of height disc space compared to other levels (figure 1b, d). romanian neurosurgery (2015) xxix 4: 381 384 383 doi: 10.1515/romneu-2015-0053 figure 1 t2 weighted mri sagittal and axial sequences showing a, c l4/l5 herniated disc and b, d – spontaneous regression of l4/l5 herniated disc discussions the intervertebral disc disease is a very well documented disorder characterized by high work disability and healthcare costs. although the first reported case of spontaneous regression of herniated intervertebral disc was published by guinto et al in 1984, there still had remains particular aspects to be discussed. regression of herniated discs has been described not only in the lumbar region but also in the thoracic and cervical spine, and for different clinical presentation as radiculopathy or myelopathy [11]. the exact mechanism causing the spontaneous disc regression remains an important discussion in the present literature. we identified three possible mechanism of spontaneous disc regression stated in literature. the first mechanism assumes gradual dehydration and shrinkage of the herniated nucleus pulposus and its regression via tear in the annulus. the second mechanism states that the herniated nucleus pulposus and annulus retracts back into the intervertebral space in the flexed position of bed rest. this situation is typical to protrude or bulge disc, not for the situation of completely extruded or separated disc material. the last hypothesis is based on enzymatic degradation and phagocytic cellular resorptive mechanisms. thus, the exposure of the herniated material to the vascular environment of the epidural space favors the mechanisms triggering the above due to inflammatory reaction and neovascularization of disc herniation. the “vascular response” represented by local reaction around the disc fragment (proliferation of the blood vessels and migration of the phagocytosis of the disc material) plays an important role in disc resorption. also, production of matrix proteinases and increased cytokine levels are very strong implicated in the spontaneous c d 384 chiriac et al spontaneous regression of lumbar herniated disc regression process [1, 7]. some histological studies have shown that sequestrated discs are characterized by a faster resorption due to its higher potential of granulation tissue generation and heavier chronic inflammatory cell infiltration than other types of disc protrusion [1, 3, 7]. a number of studies have shown that mri imaging may play a role as predictability factor of herniated disc regression. thus, the presence of rim enhancement on gdenhanced mr around herniated mass showed a significant decreases or total disappearance in 75-100% of cases with herniated discs. rim enhancement on mr images represents accumulation of contrast material within the hipervascularized granulation tissue surrounding the avascular herniated disc. the hyperintense signal on t2 mri sequence around sequestrated discs represents high water content of the material disc or edema due to neovascularization and inflammatory reaction [1, 2, 3, 7]. usually, regression of the herniated disc coincided with the improvement of associated neurological symptoms. conclusions spontaneous regression of herniated disc is not a common condition, but conservative treatment may be considered in patients without neurological deficits and highlighting mri imaging signs suggestive for herniated disc regression. we considered that all three mechanisms described by literature for herniated disc regression may have been involved in this particular phenomenon. references 1. kim, s. g., yang, j. c., kim, t. w., & park, k. h. (2013). spontaneous regression of extruded lumbar disc herniation: three cases report. korean journal of spine, 10(2), 78-81; 2. macki, m., hernandez-hermann, m., bydon, m., gokaslan, a., mcgovern, k., & bydon, a. (2014). spontaneous regression of sequestrated lumbar disc herniations: literature review. clinical neurology and neurosurgery, 120, 136-141; 3. martínez-quiñones, j. v., aso-escario, j., consolini, f., & arregui-calvo, r. (2010) spontaneous regression from intervertebral disc herniation. propos of a series of 37 cases, neurocirugia (asturias, spain), 21(2), 108-117; 4. monument j.michael, salo t. paul (2011) spontaneous regression of a lumbar disk herniation, cmaj, april 19, 183(7):823; 5. orief t, orz y, attia w, almusrea k: (2012) spontaneous resorption of sequestrated intervertebral disc herniation. world neurosurg 77:146-152; 6. parag suresh mahajan, nawal m. al moosawi, and islam ali hasan (2014) a rare case of near complete regression of a large cervical disc herniation without any intervention demonstrated on mri,” case reports in radiology, vol. 2014, article id 832765, 4 pages; 7. sabuncuoğlu, h., ozdoğan, s., & timurkaynak, e. (2008). spontaneous regression of extruded lumbar disc herniation: report of two illustrative case and review of the literature. turkish neurosurgery, 18(4), 392; 8. slavin kv, raja a, thornton j, wagner fc jr: (2001) spontaneous regression of a large lumbar disc herniation: report of an illustrative case. surg neurol 56:333-336; 9. tarukado k, ikuta k, fukutoku y, tono o, doi t. (2013) spontaneous regression of posterior epidural migrated lumbar disc fragments: case series. spine j 13:981-988; 10. veli çitişli, muhammet i̇brahimoğlu (2015) spontaneous remission of a big subligamentous extruded disc herniation: case report and review of the literature, korean j spine. mar;12(1):19-21; 11. chun-wei chang, ping-hong lai, chi-man yip, shushong hsu (2009) spontaneous regression of lumbar herniated disc, chin med assoc , vol 72, 12:650-3. doi: 10.33962/roneuro -2020-043 post-traumatic arachnoid cyst without neurological sequels. a case report raphael oliveira ramos franco netto, joão italo fortaleza de melo, victor augusto ramos fernandes, juliana de almeida rodrigues franco netto, leonardo gattass ferreira, luiz dias dutra romanian neurosurgery (2020) xxxiv (1): pp. 294-297 doi: 10.33962/roneuro-2020-043 www.journals.lapub.co.uk/index.php/roneurosurgery post-traumatic arachnoid cyst without neurological sequels. a case report raphael oliveira ramos franco netto1, joão italo fortaleza de melo1, victor augusto ramos fernandes2, juliana de almeida rodrigues franco netto1, leonardo gattass ferreira1, luiz dias dutra1 1 radiology and diagnostic imaging centre cerdil, dourados – ms, brazil 2 laboratory of tissue morphology, faculty of medicine of jundiaífmj, jundiaí-sp, brazil abstract an eight-year-old male patient was admitted to the hospital with a history of left median paramedian frontal craniectomy due to car trauma at six months of age. axial computed tomography of the skull with reconstruction in three dimensions revealed an arachnoid cyst with slight herniation of the brain in the frontal lobe, leading to protrusion against the skullcap, causing dilation of the ex-vacuum of the anterior extension of the homolateral lateral ventricle. he presented asymmetrical lateral ventricles, a reduced base cistern, and a slightly ectatic iv centred ventricle. after the physical examination, no neurological deficit was found, despite the changes identified in the images. it is believed that such conditions may progressively worsen with the development and maturation of nervous tissue over the age of the assessed child. to confirm this, specialized monitoring is of fundamental importance. introduction the arachnoid cyst is a meningeal expansion, in the form of a bag, filled with liquid with characteristics identical to the liquor, and it can develop in any place where there is an arachnoid. they are congenital and are formed due to valve defects in the arachnoid membranes that facilitate the passage of the cerebrospinal fluid into the cyst and, in the same way, hinder the exit(1). although many may constitute incidental findings, others cause symptoms due to compression of the brain parenchyma or increased intracranial pressure (2). due to the complexity and rarity of the case, as it is a post-traumatic arachnoid cyst of the skull in the frontal lobe region in a young patient, aged eight, without any apparent neurological impairment, it was considered relevant for the scientific literature describing this case. keywords encephalocele, tomography, x-ray computed, craniocerebral trauma, diagnostic imaging corresponding author: raphael oliveira ramos franco netto radiology and diagnostic imaging centre cerdil, dourados – ms, brazil raphael_ fn@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 295 post-traumatic arachnoid cyst without neurological sequels case report male patient, eight years old, enters the surgical center with a history of left median paramedian frontal craniectomy due to car trauma at 6 months of age. a computed tomography scan of the skull was performed with 3d reconstruction, showing an arachnoid cyst in the frontal lobe protruding into the skull cap determining dilation of the ex-vacuum of the anterior extension of the homolateral lateral ventricle. it also has asymmetrical lateral ventricles, a reduced base cistern and a slightly ectatic centralized ventricle (figures 1,2 and 3). on physical examination, the patient did not show a neurological deficit. figure 1: sagittal (a) and coronal (b) skull computed tomography showing an arachnoid cyst in the frontal lobe protruding into the skullcap, reduced volume cistern and slightly ectasied centered ventricle. figure 2: sequence a of computed tomography of the skull, axial section showing an arachnoid cyst in the frontal lobe protruding 296 raphael oliveira ramos franco netto, joão italo fortaleza de melo, victor augusto ramos fernandes et al. in the skullcap. sequence b of computed tomography shows dilation of the ex-vacuum of the anterior extension of the homolateral lateral ventricle. asymmetric lateral ventricles are observed. figure 3: sequences a and b are computed tomography scans of the skull with 3d reconstruction showing the absence of bone fusion of the anterior fontanelle. discussion intracranial cysts represent 1% of lesions with a mass effect. most have a congenital origin and an intraarachnoid situation, presenting or not communicating with the subarachnoid space (1,2-6). the arachnoid cyst is a meningeal expansion, in the form of a bag, filled with fluid with characteristics identical to cerebrospinal fluid or csf, and maybe develop in any location where arachnoid exists. most have a congenital origin and an intra-arachnoid situation, with or without communication with the subarachnoid space (1,2-6). the development of the cyst can occur due to a primary malformation of the arachnoid, as a consequence of a duplication of the membrane, at an early stage of embryogenesis, however, some cysts originate from the rupture or fragility of the arachnoid membrane in the presence of trauma, tumor or infection (1). arachnoid cysts occur more frequently in children and young adults, most of them under the age of 20 years (3,5,6), the reasons for this fact are still not well understood. there is no direct relationship between the volume of the cyst and the clinical findings. large cysts may be accompanied by moderate symptoms and this may occur due to their location and the brain's adaptability. among the most frequent clinical manifestations are macrocephaly, headache, focal signs and seizures. conclusions the therapeutic strategies currently used are essentially surgical, depending on the symptoms, however, as the patient did not present clinical symptoms, the literature has reported the indication for performing craniotomy with membranectomy (1,5,6) or drainage utilizing cystoperitoneal shunt (79). references 1. grollmus jm,, wilson cb, newton th. paramesencephalic arachnoid cysts. neurology 1976;26:128-134. 2. koga h, mukawaa j, miyagi k, kinjo t, okuyama k. symptomatic intraventricular arachnoid cysts in an elderly man. acta neurochir (wien) 1995;137:113-117. 3. galassi e, tognetti f, gaist g, fagioli l, frank f, frank g. ct scan and metrizamide ct cisternography in arachnoid 297 post-traumatic arachnoid cyst without neurological sequels cysts of the middle cranial fossa:classification and pathophysiological aspects. neurology 1982;7:363-369. 4. handa j, okamoto k, sato m. arachnoid cyst of the middle cranial fossa: report of bilateral cysts in siblings. surg neurol 1981;16:127-130. 5. hayashi t, anegawa s, honda e, et al.. clinical analysis of arachnoid cysts in the middle fossa. neurochirurgia 1979;22:127-130. 6. jallo gi, woo hh, meshkii ch, epstein fj, wisoff jh. arachnoid cysts of the cerebellopontine angle: diagnosis and surgery. neurosurgery 1997;40:31-38. 7. schroeder hhws, gaab mr. endoscopic observation of a slit-valve mechanism in a suprasellar prepontine arachnoid cyst: case report. neurosurgery 1997;40:198200. 8. arai h, sato k, wachi a, okuda o, takeda n. arachnoid cysts of the middle cranial fossa: experience with 77 patients who were treated with cystoperitoneal shunting. neurosurgery 1996;39:1108-1113. [ links ] 9. borges g, fernandes yb, gallani nr. hemorragia do tronco cerebral após remoção cirúrgica de cisto aracnóide da fissura silviana. arq neuropsiquiatr 1995;53:825-830 11_ienceana_three-level romanian neurosurgery (2015) xxix 3: 305 311 305 three-level cervical disc herniation case report and review of the literature andrei st. iencean1,3, ion poeata2,3 1phd student, “grigore t. popa” university of medicine and pharmacy iasi 2“grigore t. popa” university of medicine and pharmacy iasi 3neurosurgery, “n. oblu” emergency hospital iasi abstract: multilevel cervical degenerative disc disease is well known in the cervical spine pathology, with radicular syndromes or cervical myelopathy. one or two level cervical herniated disc is common in adult and multilevel cervical degenerative disc herniation is common in the elderly, with spinal stenosis, and have the same cause: the gradual degeneration of the disc. we report the case of a patient with two level cervical disc herniation ( c4 – c5 and c5 – c6) treated by anterior cervical microdiscectomy both levels and fusion at c5 – c6; after five years the patient returned with left c7 radiculopathy and mri provided the image of a left c6 – c7 disc herniation, he underwent an anterior microsurgical discectomy with rapid relief of symptoms. three-level cervical herniated disc are rare in adults, and the anterior microdiscectomy with or without fusion solve this pathology. key words: anterior cervical microdiscectomy, cervical radiculopathy, surgery in different time points, three-level cervical disc herniation. introduction the most common cause of a cervical disc herniation is the degeneration of the cervical intervertebral disc, sometimes a cervical herniated disc can occur after a cervical trauma. usually the patients present isolated neck pain or arm pain or typically cervical radiculopathy, in rare cases a large cervical disc herniation can cause paraplegia, bladder incontinence and it is a surgical emergency. the multilevel cervical degenerative disc disease is accompanied by formation of bone spurs and osteophytes of the facet joints and hypertrophy of the ligamentum flavum with cervical stenosis or cervical myelopathy. medical exploring using cervical mri defines the diagnose of herniated disc or of spinal stenosis and neurologic compression. concerning the cervical herniated disc, the annual incidence is of 5.5/100,000 people, the most frequent level involved is c5-c6, followed by c4-c5 and c6-c7 and most patients are in the fifth decade of age. surgery remove the compression of the cervical nerve root with the relief of symptoms. surgical treatment can be anterior cervical microdiscectomy and/ without fusion or microscopic posterior cervical foraminotomy. the outcome is generally very good with rapid relief of symptoms and return to normal activities. we report the case of a patient with two level cervical herniated disc , c4 – c5 and c5 – c6, treated by anterior cervical microdiscectomy both levels and fusion at c5 – c6 and after five years he returned with left c7 radiculopathy and mri provided the image of a left c6 – c7 herniated disc and the surgical approach was an anterior microsurgical discectomy. 306 iencean, poeata three-level cervical disc herniation case report a 43-year-old man presented for neck pain radiating to his right arm and forearm, also numbness and tingling along with pain radiate to the thumb side of the right hand and weakness of his right hand. these symptoms occurred after a physical effort performed two months ago and he reported the pain and the weakness increase last three weeks. physical exam found a diminished right brachioradialis reflex. a magnetic resonance imaging (mri) scan showed two level cervical herniated disc herniation: right c4 – c5 herniated disc and median c5 – c6 disc herniation (figures 1, 2, 3). an anterior cervical approach was performed: microdiscectomy both levels and fusion at c5 – c6 with rapid relief of symptoms and the patient returned to work in a month. five years later, at age 48 years, the patient returns with neck pain, left arm pain and numbness in left middle finger appeared a week ago, and physical exam find a diminished left triceps reflex. a new magnetic resonance imaging (mri) scan showed a left c6 – c7 disc herniation (figures 4, 5). he underwent a new anterior cervical approach with microsurgical discectomy of left c6 – c7 disc herniation without fusion, without complications and with relief of symptoms. figure 1 mri scan: right c4 – c5 herniated disc romanian neurosurgery (2015) xxix 3: 305 311 307 figure 2 mri scan: right c4 – c5 herniated disc and median c5 – c6 disc herniation figure 3 mri scan: right c4 – c5 herniated disc and median c5 – c6 disc herniation 308 iencean, poeata three-level cervical disc herniation figure 4 mri scan: left c6 – c7 herniated disc figure 5 mri scan: left c6 – c7 herniated disc the patient had complete resolution of all the symptoms after 6 weeks and he was able to return to his work. discussion cervical disc herniation occurs when the nucleus pulpous herniates through the annulus fibrosus caused by overstress on the normal intervertebral disc or repeated excessive stress on the degenerate intervertebral disc. symptoms of cervical herniated disc may include neck pain, unilateral arm pain that radiates down to the hand or fingers, numbness or tingling in the arm or hand, unilateral weakness etc. magnetic resonance imaging romanian neurosurgery (2015) xxix 3: 305 311 309 (mri) examination of the cervical spine is performed and shows the disc herniation, the possible neural foraminal stenosis or central canal stenosis, also the cervical cord. treatment can be nonoperative (medications and rehabilitation) and surgery: anterior cervical discectomy with or without fusion, posterior foraminotomy or cervical total disc replacement, whose indications are controversial. our case presented symptomatic simultaneous three-level disc herniation in the cervical, which were operated on at two different timepoints: first two level cervical disc herniation (c4 – c5 and c5 – c6) treated by anterior cervical microdiscectomy both levels and fusion at c5 – c6 and after five years the patient underwent the second anterior microdiscectomy for a left c6 – c7 herniated disc. surgical attitude varies in literature from anterior cervical discectomy with or without fusion to posterior foraminotomy, laminoplasty or cervical total disc replacement. kawakami et al. presented one hundred thirty-six patients with two cervical surgical approaches: anterior decompression and fusion to treat patients with oneor two-level lesions without spinal canal stenosis and laminoplasty for patients with more than threelevel lesions or spinal canal stenosis. the authors found no differences in recovery rate for patients between two groups. fraser and härtl presented a metaanalysis of twenty-one papers including 2682 patients who underwent an anterior approach of the cervical spine: anterior cervical discectomy (acd), acd with interbody fusion (acdf), acdf with placement of an anterior plate system (acdfp) and corpectomy with plate. the study evaluates the fusion rates, but it can note that there are a large number of anterior cervical discectomy without fusion in this series of 2682 patients. klaiber, von ammon and sarioglu studied the anterior microsurgical approach for degenerative cervical disc disease on a series of one hundred-ninety-six patient operated by anterior microsurgical discectomy without graft. there were explored two-hundredeighty-eight levels: 124 one level, 54 two level, 17 three level and 2 four level. they did not find significant differences between their patients and other published series with intervertebral autologous bone graft after disc removal, therefore they recommend “the anterior microsurgical discectomy without fusion as the treatment of choice”. they had only 17 patients with three-level disc herniation in a group of approximately two hundred patients. we also usually used the anterior microdiscectomy for cervical herniated disc and anterior discectomy with fusion only in the cases with spinal instability. barbagallo et al. presented their series of twenty-four patients and they had seven patients with three-level anterior cervical discectomy for cervical degenerative disc disease. most cases of the literature are patients over 50 years and the cervical herniated discs occurred in the context of the cervical degenerative disc disease. the presented patient was of 43-year old at his first cervical approach for two level herniated disc and then he was of 48 years old at the second anterior cervical e discectomy; the first was right herniated disc and a median herniated disc and the second approach was for a left cervical herniated disc on the lower level. cervical mri did not show other cervical degenerative images and we can consider the cause of these disc herniation can be the overstresses of a quasi-normal intervertebral discs or of an incipient degenerate disc. for the c6 – c7 disc herniation we can consider also the block of the c5 – c6 level and the mobility reduction at this level can lead to the degeneration of adjacent level. 310 iencean, poeata three-level cervical disc herniation conclusion three-level cervical herniated disc are not common in adult without cervical degenerative disc disease and the overstresses of the intervertebral discs contributes to disc herniation. the diminution of the normal mobility on the adjacent level caused by the fusion can contribute to the degeneration of the intervertebral discs and then the third disc herniation at this patient. the anterior cervical microdiscectomy with or without fusion for multilevel cervical herniated disc can solve this pathology. correspondence andrei st. iencean e-mail: andrei.iencean@gmail.com references 1. baptiste dc, fehlings mg pathophysiology of cervical myelopathy. spine j 2006, 6:190-197. 2. barbagallo gm, assietti r, corbino l, olindo g, foti pv, russo v, albanese v. early results and review of the literature of a novel hybrid surgical technique combining cervical arthrodesis and disc arthroplasty for treating multilevel degenerative disc disease: opposite or complementary techniques? eur spine j. 2009 jun;18 suppl 1:29-39. 3. callaghan, j.p. and mcgill, s.m.. intervertebral disc herniation: studies on a porcine model exposed to highly repetitive fl exion/extension motion with compressive force. clin. biomech. (bristol., avon), 2001, 16(1):28– 37 4. fraser jf, härtl r. anterior approaches to fusion of the cervical spine: a metaanalysis of fusion rates. j neurosurg spine. 2007 apr;6(4):298-303. 5. hida k, iwasaki y, yano s, akino m, seki t. longterm follow-up results in patients with cervical disk disease treated by cervical anterior fusion using titanium cage implants. neurol med chir (tokyo). 2008 oct;48(10):440-6 6. kawakami m, tamaki t, iwasaki h, yoshida m, ando m, yamada h. a comparative study of surgical approaches for cervical compressive myelopathy. clin orthop relat res. 2000 dec;(381):129-36. 7. klaiber rd1, von ammon k, sarioglu ac. anterior microsurgical approach for degenerative cervical disc disease. acta neurochir (wien). 1992;114(1-2):36-42. 8. korovessis p, maraziotis t, stamatakis m, baikousis a. simultaneous three-level disc herniation in a patient with multiple sclerosis. eur spine j. 1996;5(4):278-80. 9. lee mj, dumonski m, phillips fm, voronov li, renner sm, carandang g, havey rm, patwardhan ag. disc replacement adjacent to cervical fusion: a biomechanical comparison of hybrid construct versus two-level fusion. spine (phila pa 1976). 2011 nov 1;36(23):1932-9. 10. sherry tsao, peter pidcoe the management of a patient with a cervical disc herniation: a case report. clinical medicine: case reports 2008:1 45–49 11. si w, zhang h, wang a, sun y, bai y. [clinical research of dynamic cervical implant and cage fusion in two-level cervical disc protrusion]. zhongguo xiu fu chong jian wai ke za zhi.[ journal] 2014 jan;28(1):603. 12. terai h, suzuki a, toyoda h, yasuda h, kaneda k, katsutani h, nakamura h. tandem keyhole foraminotomy in the treatment of cervical radiculopathy: retrospective review of 35 cases. j orthop surg res. 2014 may 16;9:38. 13. trahan j, abramova mv, richter eo, steck jc. feasibility of anterior cervical discectomy and fusion as an outpatient procedure. world neurosurg. 2011 jan;75(1):145-8 14. tu th, wu jc, huang wc, guo wy, wu cl, shih yh, cheng h. heterotopic ossification after cervical total disc replacement: determination by ct and effects on clinical outcomes. j neurosurg spine. 2011 apr;14(4):457-65 09_paper romanian neurosurgery (2015) xxix 4: 459 464 459 doi: 10.1515/romneu-2015-0061 cervical spine disc herniation at c2-c3 level: study of a clinical observation and literature review dominique n'dri oka1, fulbert kouakou2, yacouba haro3, souleymane sarki3 1associate neurosurgery professor, 2professor assistant (anatomist) 3neurosurgery resident physician department of medical sciences of abidjan, university félix houphouet boigny neurosurgery, university teaching hospital of yopougon (abidjan ivory coast) abstract: cervical c2-c3 herniated disc is rare. it is characterized by its clinical polymorphism. several surgical approaches have been described for the discectomy of a herniated disc. this work aims at discussing through personal observations and literature review clinical semiology and surgical treatment. key words: c2-c3 herniated disc/ clinical presentation / surgical treatment introduction the cervical herniated disc is common especially in the c5-c6 and c6-c7 lower segment; as for the c2-c3 segment, it occurs in the elderly and results in common clinical symptomatology. its diagnosis and management remain delicate. indeed, as it is difficult to perform the c2-c3 disc exposure, this makes it difficult to carry out exeresis, and leads to an obsession for surgeons. we are hereby reporting a case of c2-c3 herniated disc in a young patient. clinical presentation a 34-year-old patient complained of neck pain associated with distal weakness in upper limbs, located in fingers. this clinical history started a month ago with a neck pain (torticollis) felt when in sitting position for long periods. then, the patient found out about her hands being weak when making gestures and trying to grasp, predominantly on the right-hand side. no spine trauma history was found during history taking. clinical examination found a distal brachial paresis affecting c8 and t1 roots with a motor deficit on a side at 3/5 left and 2/5 right. deep tendon reflexes were normal in all limbs. there was no sign of a pyramidal syndrome. mri and ct scan of the spine revealed a posterior medial c2-c3 herniated disc lateralized to the right, compressing the cervical spinal cord and the thecal sac (figures 1 and 2). 460 n'dri oka et al cervical spine disc herniation at c2-c3 level a b figure 1 tdm axial section showing a posterior median c2-c3. and axial mri sequence showing the c2-c3 disc herniation a b figure 2 t2 sagittal mri sequence (a) showing c2c3 disk herniation and (b) post-operative control showing the freedom of the dural sheath and highlighting the cage in place within the disc space c2-c3 romanian neurosurgery (2015) xxix 4: 459 464 461 doi: 10.1515/romneu-2015-0061 a b figure 3 ct scan in front of view(a) and sagittal view after removing (a) c2-c3 disk herniation and (b) post-operative control highlighting the cage in place within the disc space c2-c3 figure 4 peroperative view surgical technique the incision primarily chosen was right anterolateral and pre-sternocleidomastoid. the procedure was performed under fluoroscopy and surgical microscope. under general anaesthesia and naso tracheal intubation, the patient was installed in the supine position, head on a headrest, hyperextension and turned to the left at 45°, a block under the shoulders, arms along the body. after rigorous asepsis, a c2c3 level fluoroscopy tracking, then the front edge of the sterno-mastoid muscle fluoroscopy tracking by palpation was performed. the incision was made from a curved line with dorsal concavity along the anterior edge of the right sterno-mastoid muscle towards the right mastoid. (figure 3) after separating the platysma muscle, we performed a gradual dissection to the upper 462 n'dri oka et al cervical spine disc herniation at c2-c3 level thyroid artery we ligated. installing spacers enabled reclination of the sternocleido mastoid, homo-hyoid muscles and nervous vascular package outside and inside aerodigestive tracts exposing the anterior longitudinal ligament. a c2-c3 discectomy was performed with an intersomatic cage set up. at the end of the operation a check through imaging was performed to verify whether the thecal sac was free and the mounting stable (figures 4, 5, 6 and 7). discussion the c2-c3 herniated disc is very rare [11, 16]. to our knowledge this case represents the thirtieth (30th) case published in the literature [1-12; 15-19] (table no. 1). its incidence is estimated at 0.45% [11]. the most frequently affected are c5-c6 and c6-c7 levels. indeed in the young patient, the cervical spine will recover its maximum mobility in lower segment undergoing more stress during a movement. as senescence occurs, bone remodelling (uncocervicarthrose) and discal remodelling (degeneration) takes place resulting in a fusion of the lower discs, which significantly reduces the mobility of the lower segment and increases the load distribution to the c2-c3 and c3-c4 disc [16]. therefore, the c2-c3 disc herniation is a condition for the elderly with a mean age of onset at 67 [5, 7] except for the strain, strenuous activity, repeated lifting of heavy loads [8], no other factor favouring has been incriminated in our patient. its late onset, usually in the context of degenerative damage, reflects the diversity of clinical signs, from simple sensory and / or motor radiculopathy to brown sequard syndrome or severe myelopathy [1, 3, 5, 11]. the distal brachial paresis noted would be the expression of an incipient myelopathy. in many cases imaging reveals an excluded hernia with retro odontoid migration leading to the issue of differential diagnosis with the masses among which there are metastases, meningiomas, neurolemmomes and synovial cysts [1, 4 ,5 -19]. the simple hernia without migration form is diagnosed early, justifying the brevity of the clinical history of the patient; (table 1). several surgical approaches have already been described but there is no consensus as regards the choice of the first one. this is the area around posterior trans dural [16] and epidural, of the trans oral odontoidectomy [2], and the anterolateral area. the major limitation of the posterior tract is the risk of neuro-aggressiveness and reduced stability due to non-economic resections of parts of posterior columns of denis [16, 17,19] the oral trans odontoidectomy is aggressive and requires occipital cervical fusion; it is indicated in cases of excluded hernia with retro dens migration. strict lateral approach is very rarely practiced and thus limited to the lateral foraminal hernia [14]. romanian neurosurgery (2015) xxix 4: 459 464 463 doi: 10.1515/romneu-2015-0061 table 1 review of cases published in literature acdf: anterior cervical discectomy + autograft fusion authors and year number of cases presentation location of the disc material surgical technique outcome espersen et al, 1984 1 c2-c3 level cloward’s technique jomin et al, 1986 2 c2-c3 level acdf rosemberg et al, 1991 2 myelopathy retro-odontoïd posterior transdural 1 improved, 1 stable nishizawa et al, 1996 1 myelopathy retro-odontoïd posterior transdural chen and luis, 1997 1 myelopathy retro-odontoïd transoral odontoidectomy+c1–c2 fusion improved nishizawa et al, 1999 3 myelopathy 2 retro-odontoïd 1 c2-c3 level posterior transdural all improved antich et al, 1999 1 myelopathy c2-c3level acdf improved campbell, 2000 1 myelopathy retro-odontoïd transoral odontoidectomy chen, 2000 8 myelopathy c2-c3 level acdf 6 improved 2 stable matsutano et al, 2004 1 myelopathy retro-odontoïd far lateral deshmukh et al, 2004 1 c2 radiculopathy retro-odontoïd posterior extradural improved türe et al, 2007 1 c3 radiculopathy c2-c3 level anterolateral extradural approach improved chan et al, 2009 1 myelopathy c2-c3 level c3 transcorporeal kotil et al, 2011 5 myelo-radiculopathy c2-c3 c2-c3 level discectomie antérieure + greffe 3 improved, 2 stable n'dri et al, 2014 1 myelo-radiculopathy c2-c3 level anterolateral extradural approach improved the choice of the anterolateral approach in our patient is supported by the initial seat of the compression and the effectiveness of past approaches in cases where the two approaches are possible [13,10]. indeed a retrospective study conducted in hospitals [7] has confirmed the efficacy of surgical treatment of cervicarthrosic myelopathy by anterior decompression in the event of pain and predominant and posterior brachialgia if patients are in bedridden or precarious condition. the deep location of c2-c3 disc, the control of the vertebral artery v2 segment and obesity makes it very difficult to expose the disc and makes its surgery a challenge [11, 13]. although its anatomy is not different from the other discs, practitioners avoid the introduction of osteosynthesis material at its level [10,16]. our gesture being limited to discectomy, the intersomatic cage was the best 464 n'dri oka et al cervical spine disc herniation at c2-c3 level anatomy restoration means compatible with spinal stability and satisfactory spinal mobility. conclusion the c2-c3 herniated disc is very rare and usually occurs in the elderly. when it occurs in young subjects its treatment offers the patient the preservation of mobility, reduction in the degeneration of adjacent segments and a significant clinical improvement. correspondence n’dri oka dominique e-mail: ndriokad@gmail.com 21 bp 632 abidjan21 mobile: 0022546261800 references 1.antich pa., sanjuan ac., girvent fm., simó jd. high cervical disc herniation and brown-séquard syndrome a case report and review of literature. journal of bone and joints surgery 1999;( 81-b, )3 2.campbell sf, tannenberg ae, mowat p: transoral resection of retroodontoid disc sequestration: case report and review of the literature. j clin neurosci 20007:325327 3. chen ty: the clinical presentation of uppermost cervical disc protrusion. spine 2000 25:439-442 4. chen ty, lui t: retrodental fibrocartilaginous mass. report of a case. spine 1997; 22:920-923 5. deshmukh vr, harold l. rekate, volker k. h. sonntag. high cervical disc herniation presenting with c2 radiculopathy case report and review of the literature j neurosurg (spine 3) 2004;100:303:306 6. espersen jo, buhl m, eriksen ef, et al: treatment of cervical disc disease using cloward’s technique. i. general results, effect of different operative methods and complications in 1,106 patients. acta neurochir (wien) 1984 8;70:97-114, 7.goubier j.n., benazet j.p., saillant g. décompression chirurgicale desmyélopathies cervicarthrosiques: comparaison des abords antérieur et postérieur. revue de chirurgie orthopédique 2002; 88: 591-600 8. haid rw the soft cervical disc: natural history and management. cooper pr (ed) degenerative disease of the cervical spine. aans publications, chicago1993 9 :113-124 9. tan j1, zheng y, gong l, liu x, li j, du w. anterior cervical discectomy and interbody fusion by endoscopic approach: a preliminary report. j neurosurg spine 8:17– 21, 2008 10. jomin m, lesoin f, lozes g, et al: herniated cervical discs: analysis of a series of 230 cases. acta neurochir (wien) 1986;79:107-111, 11. kotil kt, se sengoz a. the management in the c2-c3 disc herniations: a clinical study. turkish neurosurgery 2011, 21(1):, 15-21 12. matsutano a, nakashima m, murakami m, nagashima t . microsurgical excision of a retro odontoid disc hernia via a far-lateral approach: successful treatment of a rare cause of myelopathy: case report neurosurgery 2004; 54(4):1015-8. 13. mcafee pc, bohlman hh, riley lh jr, et al: the anterior retropharyngeal approach to the upper part of the cervical spine. j bone joint surg am 198769:13711383 14. murphey f, simmons jch, brunson b: surgical treatment of laterally ruptured cervical disc: review of 648 cases, 1939 to 1972. j neurosurg 1973 38:679-683, 15. nishizawa s, ryu h, yokohama t, uemura k: myelopathy caused by retro-odontoid disc hernia: case report. neurosurgery 1996;39: 1256-1259 16. nishizawa s, yokoyama t, yokota n, et al: high cervical disc lesions in elderly patients—presentation and surgical approach. acta neurochir199910141:119–126, 17.rosenberg ws, rosenberg ae, poletti ce: cervical disc herniation presenting as a mass lesion posterior to the odontoid process. report of two cases. j neurosurg1991 75:954–959 18.shim cs, jung t-g, lee s-h. transcorporeal approach for disc herniation at the c2-c3 level: a technical case report. spinal disord tech. (22) 6, 459462. 19. türe u, güçlü b, naderi s. anterolateral extradural approach for c2–c3 disc herniation: technical case report. neurosurg rev ,2008 3:117-121 doi: 10.33962/roneuro-2021-043 particular management strategy for intraprocedural coil migration during endovascular treatment of intracranial aneurysm a. chiriac, n. dobrin, georgiana ion, z. faiyad, i. poeata romanian neurosurgery (2021) xxxv (3): pp. 257-261 doi: 10.33962/roneuro-2021-043 www.journals.lapub.co.uk/index.php/roneurosurgery particular management strategy for intraprocedural coil migration during endovascular treatment of intracranial aneurysm a. chiriac, n. dobrin1, georgiana ion1, z. faiyad1, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi, romania 1 “prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract migration of coils represents one of the most challenging complications of endovascular management of cerebral aneurysms with a potentially catastrophic result. in this article, we present the successful management of a coil migration during the endovascular occlusion of an anterior communicating artery aneurysm. a stent fixation technique was used with good vascular repermeabilisation. the reported frequency, risk factors and management strategies are also discussed. introduction cerebral aneurysms occlusion by endovascular coiling is considered the main treatment in most neurosurgical centres in the world. with this evolution of treatment, numerous studies have reported coil migration as significant intraprocedural complication which can lead to catastrophic neurological consequences without proper management. the reported rates of coil migration that range from 2% to 6% have not significantly changed over time. however, the outcome of patients with this complication has been greatly improved as a result of development of different techniques and devices for retrieval or repositioning of the migrated coils. in this paper we present a particular management strategy for correction of a distal coil migration in a patient undergoing endovascular coil embolization of an anterior communicating artery aneurysm. we also summarize the current literature describing the management of intraprocedural coil migration [2,4]. case presentation a 44-year-old man addressed to emergency department from a local hospital for severe headache started in the same day. a head ct-scan investigation was performed immediately and showed a mild subarachnoid haemorrhage in the interhemispheric fissure and both keywords coil migration, stent fixation technique corresponding author: a. chiriac “gr. t. popa” university of medicine and pharmacy, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 258 a. chiriac, n. dobrin, georgiana ion et al. sylvian fissures. the ct angiography demonstrated an anterior communicating artery aneurysm as source of hemorrhage. the patient was immediately transferred to our hospital for further treatment. at admission he was confused and presented mild nuchal rigidity. his past medical history included hypertension with no regular treatment. the patient was scheduled for an endovascular aneurysm occlusion for the next day. a written informed consent was obtained prior to the treatment from the family. the intervention was performed on a biplane angiography system (infinix, toshiba, canon medical system) under general anesthesia by our neurosurgical team with many years of experience in neuroendovascular interventions. femoral artery access was established with a 6 f/11 cm sheath from merit medical. different angled cerebral angiography was performed to clarify the relationship of aneurysm / neck / arterial branches. the aneurism was injected from both carotid artery but with a better visualisation from the left side injection. a b c d 259 particular management strategy for intraprocedural coil migration fig. a. diagnostic head ct; b – brain angio-ct showing a coa aneurysm; c, d – dsa right and left ica demonstrating a coa aneurysm: e – partially coil migration to right a2; f, g – frontal and lateral view with attempt of coil retrieval; h – dsa image with distal coil migration and arterial occlusion; -i, j – microguide and microcatheter passing the coil; k – dsa image showing slightly right a2 repermeabilisation; -l dsa showing total right a2 repermebilization by coil fixation with a detachable intracranial stent; m, n frontal and lateral view demonstrating adequate coils occlusion of the aneurysm. a 6f chaperon guiding catheters (microvention) was carefully advanced over 0.035 glidewire up to the proximal segment of the left internal carotid artery. a prowler 10 microcatheter (codman j&j) was then very carefully advanced over a 0.014 transed microwire (boston scientific) and positioned into the aneurysm sac. one 4/8 mm galaxy g3™ xsft coils (cerenovus johnson&johnson) was then inserted and detached into aneurysm. at the beginning of the introduction of the second coil 3/4, the tip of the microcatheter descended to the aneurysm neck. as soon as it was detached, the flow carried a part of the coil from the aneurysm to a2 segment of the right anterior cerebral artery. the next contrast injection demonstrates thrombosis of the right a2 without flow distal to the migrated coil. the right a2 was then catheterized through the left a1 with an excelsior 10 microcatheter. the microcatheter was advanced proximal to the migrated coil, and 5 ml heparin solution was infused. the microcatheter was passed carefully distal to the coil, and a 3/30 mm atlas 2 stent (stryker) was deployed and successfully fixed and stabilized the migrated coil. the following injection demonstrates a good repermeabilisation of the right a2 segment. a new aneurysm microcatheterization with a prowler 10 microcatheter was obtained. a complete angiographic occlusion of the aneurysm was obtained after the safe insertion and detachment of other two coils (2/ 8 mm galaxy g3™ xsft and 1.5/ 4 mm galaxy g3 mini). the microcatheter is then carefully retracted and a dsa acquisition is performed to check the permeability of all vessels. finally, the entire guiding system is retracted with a compressive dressing of the femoral puncture site. the patient was placed into intensive care and received 75mg clopidogrel and 100mg aspirin daily. postoperatively the patient remains neurologically 260 a. chiriac, n. dobrin, georgiana ion et al. intact. a cerebral ct scan was performed 7 days postoperatively and showed the total sah resorption. the patient was discharged home after 17 days of hospitalisation in good neurological condition. discussion with the increasing use of spiral embolization techniques, the migration of these removable implants during endovascular embolization of intracranial aneurysms has become a potentially serious intraprocedural complication. the phenomenon of prominence and / or migration of a coil can most often manifest itself on the circulatory hemodynamics at the level of arterial vascularization by creating a thrombogenic nidus that can have an occlusive or embolic effect. occlusions of the major parent artery or distal vessels branches may result in a large territory infarct with sever neurological consequences. even if coil migration is not a common occurrence the incidence reported in the literature varied between 0.5–6% [1,2,3].one of the largest retrospective studies on 1811 patients demonstrated an incidence of coil migration phenomenon of 2,5% [2,3,4]. higher incidences of this phenomenon have been reported in early studies (casasco et al, 5.6%) compared to more recent studies (abdalkader et al, 0.3%). this discrepancy in reported rates it could be in part related to use of the term 'coil migration' in literature for different related situation like coil malpositioning, partial coil stretching, partial prolapse, and total displacement of coils from the aneurysmal cavity. on the other hand, the continuous development of coils and embolization techniques has led to a decrease in the complication rate due to the migration phenomenon[3,5]. coil migration could be classified depending on the time of detection in acute intraprocedural or delayed postprocedural migration (after completing the coiling procedure). a number of factors such as anatomical, flow and techniques have so far been described as being responsible for coil migration in the treatment of cerebral aneurysms. there have been reports that have shown a direct relationship between the increased risk of coil migration and the increased width of the aneurysm neck, the presence of vascular conditions and high flow conditions [2,3]. from a technical point of view the unstable configuration, the early detachment and the oversized/undersized use of the coils are the main factors for the migration of the coils. coil migration management can vary depending on the migration time (acute or delayed), the location of the migrated coil (proximal or distal) and the permeability of the target vessel and the eloquence of the vascular territory. thus, endovascular retrieval or fixation techniques, surgical extraction and conservative treatment have been described as management methods in coil migration. migrated coil retrieval methods should be considered when the migration occurs intraprocedurally and may include stent retrievers, snaring, alligator, and merci devices, aspiration and wire recanalization techniques. the fixation technique by deploying a stent across the migrated coil to restore the arterial flow may be applied in cases in which coil displacement occurs in tortuous and distal intracranial vessels or unsuccessful coil retrieval. the open surgical option must be carefully considered due to its complexity, extremely high risk of morbidity which usually outweighs the potential benefits. conservative medical management with antiplatelets and/or anticoagulation should be the first option when the migrated coil is too distal to safely pursue, or there is no associated vessel occlusion and as a possible option following unsuccessful attempts at recovery. conclusions coil migration during cerebral aneurism endovascular treatment it can have a devastating course in the absence of proper management. even if no “gold standard” method has been identified for retrieval or repositioning migrated coils, several techniques and devices have proven effective in managing this type of complication. the management of our case demonstrates that stent fixation of a distal migrated coil can be used successfully to rescue patients with this potentially devastating complication. references 1. abdalkader, m., piotin, m., chen, m., ortega-gutierrez, s., samaniego, e., weill, a., ... & nguyen, t. n. (2020). coil migration during or after endovascular coiling of cerebral 261 particular management strategy for intraprocedural coil migration aneurysms. journal of neurointerventional surgery, 12(5), 505-511. 2. ding, d., & liu, k. c. (2014). management strategies for intraprocedural coil migration during endovascular treatment of intracranial aneurysms. journal of neurointerventional surgery, 6(6), 428-431. 3. kung, d. k., abel, t. j., madhavan, k. h., dalyai, r. t., dlouhy, b. j., liu, w., jabbour, p. m., & hasan, d. m. (2012). treatment of endovascular coil and stent migration using the merci retriever: report of three cases. case reports in medicine, 2012, 242101. https://doi.org/10.1155/2012/ 242101; 4. lehmann, p., brun, g., & dory-lautrec, p. (2021). an unusual stroke etiology: delayed coil migration. case report. sn comprehensive clinical medicine, 3(1), 360362. 5. stanzani, r., yamada, y., kawase, t., devareddy, g., kadam, c., shukurov, f., ... & kato, y. (2020). acute coils migration causing significant m3 branch occlusion: a case report of rescue surgery with superficial temporal arterymiddle cerebral artery bypass. asian journal of neurosurgery, 15(2), 428. 15dumitrescub_pregnantwoman 482 dumitrescu et al pregnant woman with an intracranial meningioma pregnant woman with an intracranial meningioma – case report and review of the literature bogdan constantin dumitrescu1,2, ligia gabriela tataranu2,3, mircea radu gorgan2,3 1phd student, university of medicine and pharmacy “carol davila”, bucharest 2clinic of neurosurgery, emergency clinical hospital “bagdasar arseni”, bucharest 3university of medicine and pharmacy “carol davila”, bucharest abstract: it is about a 33-year-old female, with a 36 weeks uncomplicated pregnancy and with signs of increased intracranial pressure. hours after admission and an obstetric evaluation, uterine contraction started and the patient was taken to the delivery room, where she presented a partial motor seizure on the left side with secondary generalization and urine emission. a caesarean section was performed without fetal or maternal complications. the urgent mri gadolinium-enhanced brain scan revealed a 39/50/54 mm tumoral mass having an aspect of an anterior third falx cerebri meningioma. the patient was transferred to our neurosurgical department and afterwards surgery was performed with gross total removal of the tumoral mass. histological examination revealed atypical meningioma with direct invasion into the adjacent brain parenchyma. a week later she was discharged from the hospital in good condition. one month after surgery, a contrastenhanced magnetic resonance imaging of the brain did not reveal any signs of tumor recurrence or residual tumor. our recommendation is for postpartum surgery when is possible. urgent neurosurgical interventions should be made in case of patients with malignant tumors, active hydrocephalus or benign intracranial tumor such as meningioma associated with signs of impending herniation, progressive neurological deficits. introduction intracranial tumors in pregnant women are rare, with an estimated incidence of about seven cases per 125.000 pregnancies. the first case of a pregnant woman with a brain tumor was described by bernard in 1898. (1, 2, 3, 4, 5) the occurrence of a meningioma during pregnancy is also rare, comparable with that in non-pregnant women in the same age group. (1, 2, 3, 4) particular for meningiomas is the expression of hormone receptors. these tumors response to the increased level of serum progesterone during the second half of pregnancy by accelerating its growth. tumor romanian neurosurgery (2014) xxi 4: 482 – 489 483 enlarges by fluid retention, enhanced vascularity and therefore patients may become symptomatic. (1) the clinical presentation with signs and symptoms of elevated intracranial pressure, focal seizures, lateralising neurological deficits, abnormal funduscopic examination suggests the diagnosis of an intracranial mass and should not be confused with hyperemesis gravidarium, eclampsia or puerperal psychosis. (1, 5) magnetic resonance imaging of the brain is the method of choice for prompt diagnosis of meningioma during pregnancy. (1) the management strategy for intracranial tumors during pregnancy should be individualised and include mainly surgery. surgery during pregnancy associates a great risk for fetus and also for the mother. the general recommendation is for caesarean section as first surgery and then the neurosurgical intervention when the patient’s neurological status and the gestational age allow. (9) urgent neurosurgical interventions should be made in case of patients with malignant tumors, active hydrocephalus or benign intracranial tumor such as meningioma associated with signs of impending herniation, progressive neurological deficits. (5) radiotherapy and mifepristone are recommended for unresectable or recurrent meningioma. (4) case report a 33-year-old right-handed female, 36 weeks pregnant presented to her obstetrician with one month history of headache, 24 hours before admission she accused repeated vomiting. an obstetric evaluation revealed an uncomplicated pregnancy at 36 weeks. the ultrasound and the fetal monitoring was in normal ranges. four hours from admission uterine contraction started and the patient was taken to delivery room, here she presented a partial motor seizure on the left side with secondary generalization and urine emission. after seizure the patient was drowsy, her mental status depressed progressively. she was urgent transfer to operation room and caesarean section was performed under general endotracheal anesthesia. the caesarean section went well without fetal or maternal complications. after delivery the patient underwent imaging investigation. the urgent irm scan of the brain with gadolinium revealed a 39/50/54 mm tumoral mass with the same density, which captured intense and homogeneous contrast. the tumor was plated on the anterior 1/3 of the falx cerebri on the right side. midline was shifted to the left side by about 14 mm. the tumor was also accompanied by significant perilesional edema. (figure 1) in this stage the patient was transferred to our neurosurgical department. on admission the patient was afebrile with normal vital signs. the general examination was normal. the neurological exam revealed impaired consciousness, left-sided hemiparesis with a left-sided pronator drift. reflexes were diminished on the left side and the babinski sign was present on the left side. the funduscopic examination showed bilateral papillary edema. anticonvulsant and corticoid therapy was immediately started and the neurological status of the patient improved. 484 dumitrescu et al pregnant woman with an intracranial meningioma figure 1 preoperative mri. well-defined, contrast enhancing, extraaxial tumor, attached to the anterior third of falx cerebri, with mass effect and surrounding edema romanian neurosurgery (2014) xxi 4: 482 – 489 485 figure 2 postoperative mri. complete tumor resection, no tumor recurrence 486 dumitrescu et al pregnant woman with an intracranial meningioma after few days the neurosurgical operation was scheduled. under general anesthesia a right frontal craniotomy was performed. the tumor was easily identified as a hypervascular mass adherent to the anterior 1/3 of the falx. a peritumoral plane of dissection was developed and tumor was resected with coagulation of its falx adhesions. histological examination revealed atypical meningioma with direct invasion into the adjacent brain parenchyma. after surgery patient was conscious, with minimal left hemiparesis and no seizure. she was discharged from the hospital 7 days later, in good condition. approximately one month after surgery, a contrast-enhanced magnetic resonance imaging of the head was performed; it does not reveal any signs of tumor recurrence or residual tumor. (figure 2) discussion meningioma is the most common primary intracranial tumor in the adult population; it is a slow growing extra-axial brain neoplasm that arise from the arachnoid cells. this tumor accounts for 10-20% of all central nervous system neoplasms with an incidence among women of 3 in 100.000. the occurrence of a meningioma during pregnancy is rare because pregnant women tend to be young and healthy, so the general incidence of this pathology does not exceed that of nonpregnant women in the same age group. (1, 2, 3, 4) in 1898, bernard described the first case of a pregnant woman with a brain tumor. in 1937, hagedoorn presented a documented study about the effects of pregnancy on intracranial meningioma. (5, 6, 7). the relationship between pregnancy and the rapid increase of neurologic symptoms in women with meningioma was first described by cushing and eisenhardt. (8, 9) the predominance of meningiomas in women and accelerated growth during luteal phase of menstrual cycle and during pregnancy is determined by the expression of progesterone and estrogen receptors. swensen and kirsch noted in their study from 2002 that meningiomas express estrogen receptors in 13% of cases and progesterone receptors in 69 % of cases. (4, 10) meningiomas may also express hormone receptors not only for progesterone and estrogen but also for androgen, placenta growth factor andother exogenous hormones. (1, 11, 12, 13) these tumors response to increased level of serum progesterone in the second half of pregnancy by accelerated growth, so the tumor enlarges by fluid retention and enhanced vascularity. (1, 9, 14) the acceleration of meningioma growth in the second or third trimesters of pregnancy may be determined also by the absence of luteinising hormone and follicle-stimulating hormone and by the falling level of human chorionic gonadotropin in these stages of pregnancy. these observations were made in a vitro study on meningiomas by boyle-walesh, shenkin and white in their paper published in 1995. (15) the phenotypic profile of hormone receptor in meningioma has been classified into a high percentage of tumors displaying high level of progesterone receptor (pr); a smaller subgroup containing moderate concentrations of androgen receptor (ar); the level of estrogen receptor (er) has been equivocal, ranging from low to virtually romanian neurosurgery (2014) xxi 4: 482 – 489 487 undetectable by immunohistochemistry. (9, 16) in our days, positron emission tomography helps us to measure in vivo the receptor density and occupancy in this type of tumor. (17) the main signs and symptoms of intracranial meningioma are headache, vomiting and seizure, this clinical picture can be confused with hyperemesis gravidarium, puerperal psychosis in the first trimester of pregnancy or with eclampsia in late pregnancy. (1, 5) the presence of papillary edema, visual disturbances, focal seizure, and lateralizing neurological deficits should suggest an intracranial lesion. the appearance or aggravation of signs and symptoms during pregnancy is determined by one of the following mechanisms: maternal metabolic changes causing fluid retention, vascular engorgement, and increased edema or positive hormone receptors on tumor cells with dramatic growth of the meningioma. the presence of progesterone receptors on tumor cells is correlated with worsening symptoms of meningioma. (5, 18, 19) therefore, in women in late pregnancy presenting with symptoms of increased intracranial pressure and focal signs or presenting with progressive worsening of neurological symptoms, an intracranial pathology should be considered and further imagistic investigations should be made to establish correct diagnosis. magnetic resonance imaging of the brain is the method of choice for prompt diagnosis of meningioma during pregnancy. we must note its limitations due to the inability to use contrast agents during pregnancy. the ct scan is not recommended because carries the risk of radiation damage. (1) the management strategy for intracranial tumors during pregnancy should be made depending on patient’s physical status, localization of the tumor, gestational age and other concomitant factors. surgical excision is the treatment of choice for intracranial meningiomas but surgical intervention should be avoided during pregnancy when is possible because of the increased risk to both mother and fetus. postpartum surgery of meningioma is recommended by most authors in the literature, with non-surgical treatment of the increased intracranial pressure until fetal lung maturity is reached. (9, 18) others consider that non-invasive fetal monitoring such as fetal biophysical profit scoring system and umbilical artery doppler velocimetry, and neuroanesthesia and microsurgical techniques permit a safe neurosurgical treatment of intracranial tumors during pregnancy. (5) our recommendation is for postpartum surgery when is possible. urgent neurosurgical interventions should be made in case of patients with malignant tumors, active hydrocephalus or benign intracranial tumor such as meningioma associated with signs of impending herniation, progressive neurological deficits. (5) neurosurgery during pregnancy associates important risks for the mother. general endotracheal anesthesia is complicated by the upper airway mucosal edema, decreased functional residual capacity, venous engorgement, water retention, increased risk for reflux and aspiration, weight gain. in pregnancy the use of diuretics is not recommended so the neurosurgeon will confront with the lack of brain relaxation and that makes the operation more difficult. the surgery can also induce labor and it can be 488 dumitrescu et al pregnant woman with an intracranial meningioma associated with important blood loss. (1, 20, 21, 22) brain surgery can also harm the fetus, it can cause stillbirth, birth defects (in the early stage of pregnancy), premature labor, premature delivery or fetal asphyxia. (1, 23) from another perspective, if the neurosurgery is not made, the tumor may enlarge, and it can cause seizure or even herniation. (1, 21, 24) complete surgical resection is the only definitive cure for meningiomas. complete resection is determined by the tumor site. mirimanoff et al, consider that total excision depends on the accessibility of the tumor (28% for sphenoid wing and 96% for convexity meningiomas). high risk of recurrence is also associated with atypical or anaplastic meningioma and with a proliferative index greater than or equal to 20%. (25, 26, 27) medical treatment before and after surgery includes corticosteroids, the usual dose is 2-4 mg of dexamethasone every 6 hour. anticonvulsant medication is also needed, preferably monotherapy. the patients on anticonvulsant therapy should receive folic acid and supplemental vitamin-k1 three weeks before and during confinement to minimalize the risk of drug induced neural tube defects or blood dyscrasias. manitol should be administrated only for acute emergency because sudden decrease in plasma volume might compromise uteroplacentar perfusion and put the fetus to risk. (28, 29, 30) mifepristone, hidroxyurea as antiprogesterones, temozolomide or radiotherapy can be used for unresectable benign meningioma, recurrent or malignant meningioma. interferon as an angiostatic may also be considered. (31, 32, 33) conclusions the management of a pregnant woman with an intracranial meningioma should be individualized and the final decision must be made on the intracranial pathology, gestational age and not least to be taken into account the patient’s wishes. pregnant women with repeated vomiting, nausea and headache should be examined with care and an intracranial pathology should be considered. acknowledgement: this paper was co-financed from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 “excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis”, coordinator the bucharest university of economic studies. correspondence bogdan constantin dumitrescu, address: emergency clinical hospital bagdasar-arseni, no. 10-12, berceni street, sector 4, bucharest; e-mail: dumitrescu.bog@gmail.com; tel. 0745.696.966 references 1. kasper em, hess pe, silasi m, lim kh, gray j, reddy h, gilmore l, kasper b. a pregnant female with a large intracranial mass: reviewing the evidence to obtain management guidelines for intracranial meningiomas during pregnancy. surg neurol int. 2010 dec 25; 1:95 2. sahu s, lata i, gupta d.management of pregnant female with meningioma for craniotomy.j neurosci rural pract. 2010 jan;1(1):35-7 3. rohringer m, sutherland gr, louw df et al. incidenceand clinicopathological features of meningioma. j neurosurg 1989;71:665-72 4. lucy d, pratima m, puspa k, umakant s, niharika p. pregnancy with meningioma. j obstet gynecol india.2008 march/april; 58 (2): 156-158 romanian neurosurgery (2014) xxi 4: 482 – 489 489 5. kanaan i, jallu a, kanaan h. management strategy for meningioma in pregnancy: a clinical study. skull base. 2003 nov;13(4):197-203 6. bernard mh. sarcome cerebral à evolution rapide au cours de la grossesse et pendant les suites des couches. bull soc d'obst de paris 1898;1:296-298 7. hagedoorn a. the chiasmal syndrome and retrobulbar neuritis in pregnancy. am j ophthalmol 1937;20:690-699 8. cushing h, eisenhardt l. meningiomas. their classification, regional behaviour, life history, and surgical end result. springfield, illinois: 1938. 9. alluwimi i, al-anazi ar. meningioma in pregnancy. bahrain madical bulletin. 2004 june; 26 (2): 1-8. 10.gabos s, berkel j. meta-analysis of progestin and estrogen receptors in human meningiomas. neuroepidemiology 1992; 11:255-60. 11.carroll rs, zhang j, black pm. expression of estrogen receptors alpha and beta in human meningiomas. j neurooncol 1999; 42: 109-16. 12.donnini s, machein mr, pateu kh, weich ha. expression and localization of placenta growth factor and pigf receptors in human meningiomas. j pathol 1999; 189: 66-71. 13.claus eb, black pm, bondy ml, calvocoressi l, schidkraut jm, wiemels jl, et al. exogenous hormone use and meningioma risk: what do we tell our patients? cancer 2007; 110: 471-6. 14.hatiboglu ma, cosar m, iplikcioglu ac, ozcan d. sex steroid and epidermal growth factor profile of giant meningiomas associated with pregnancy. surg neurol 2008; 69: 356-62. 15.boyle-walesh e, shenkin a, white mc, et al. effect of gylcoprotein and protein on human meningioma cell proliferation in vitro. j endocrinol 1995;145:155-161. 16.konstantinidou ae, korkolopoulou p, mahera h, et al. hormone receptors in non-malignant meningiomas correlate with apoptosis, cell proliferation and recurrence-free survival. histopathology 2003;43:280-1. 17.moresco rm, scheithauer bw, lucignani g, et al. oestrogen receptors in meningiomas: a correlative pet and immunohistochemical study. nuclear medicine communications 1997; 18:606-15. 18.benzel ec, gelder fb. correlation between sex hormone binding and peritumoral edema in intracranial meningiomas. neurosurgery 1988;23:169-74. 19.balki m, manninen ph. craniotomy for suprasellar meningioma in a 28-week pregnant woman without fetal heart rate monitoring. can j anaesth. 2004; 51:573-6. 20.finfer sr. management of labour and delivery in patients with intracranial neoplasms. br j anaesth.1991;67:784-7. 21.wang lp, paech mj. neuroanesthesia for the pregnant woman. anesth analg 2008;107:193-200. 22.chang l, looi-lyons l, bartosik l, tindal s. anesthesia for cesarean section in two patients with brain tumours. can j anaesth 1999;46:61-5. 23.goldberg m, rappaport zh. neurosurgical, obstetric and endocrine aspects of meningioma during pregnancy. isr j med sci. 1987;23:825-8. 24.haas jf, janisch w, staneczek w. newly diagnosed primary intracranial neoplasms in pregnant women: a population-based assessment. j neurol neurosurg psychiatry. 1986;49:874-80. 25.mirimanoff ro, dosoretz de, longgood rm, et al. meningioma: analysis of recurrence and progression following neurosurgical resection. j neurosurg 1985;62:18-24. 26.jnskelninen j, haltia m, servo a. atypical and anaplastic meningiomas. radiology, surgery, radiotherapy and outcome. surg neurol 1986;25:233-42. 27.may pl, broome jc, lawry j, et al. the prediction of recurrence in meningiomas. a flow cytometric study of paraffin-embedded archival material. j neurosurg 1989;71:347-51. 28.douglas h. haemorrhage in the new-born. lancet 1966; 1:816-817 29.mountain kr, hirsch j, gallus as. neonatal coagulation defect due to anticonvulsant drug treatment in pregnancy. lancet 1970;1:265-268. 30.balki m, manninen ph. craniotomy for573 suprasellar meningioma in a 28-week pregnant woman without fetal heart rate monitoring. can j anesth 2004; 51:573-6. 31.grunberg sm, weiss mh, spitz im et al. treatment of unresectable meningiomas with the antiprogesterone agent mifepristone. j neurosurg 1991;74:861-6. 32.adams rd, victor m, ropper ah. principles ofneurology. 7th ed. new york: mc graw-hill; 2001. 33.indiyarty r. occipito-cervical meningioma in pregnancy. univ med 2008; 27: 143-9. 3abrudanc_assessment2014 romanian neurosurgery (2014) xxi 1: 18 29 19 assessment of temozolomide action encapsulated in chitosan and polymer nanostructures on glioblastoma cell lines c. abrudan1, i.s. florian1, a. baritchii1, o. soritau2, s. dreve3, c. tomuleasa2, b. petrushev2 1department of neurosurgery, clinical university emergency hospital, cluj napoca 2department of cancer immunology, ion chiricuta oncology institute, cluj napoca 3national institute for r&d of isotopic and molecular technologies, cluj-napoca abstract purpose: glioblastoma multiforme (gbm) remains one of the most devastating diseases known to mankind and affects more than 17,000 patients in the united states alone every year. this malignancy infiltrates the brain early in its course and makes complete neurosurgical resection almost impossible. recent years have brought significant advances in tumor biology. many cancers, including gliomas, appear to be supported by cells with stemlike properties. nanoparticles are excellent candidates to serve as delivery vectors of drugs or biologically active molecules because of their unique chemical and physical properties that result in specific transportation and deposition of such agents in specific organs and tissues.. in the current study we have investigated the in vitro action of nanostructural systems (temozolomide encapsulated in chitosan and polymer nanostructures) on high-grade gliomaderived cancer stem cells (cscs), with the intention of developing a new therapy to treat specific brain tumors with increased efficacy and minimal toxicity. in vitro cytotoxicity and apoptosis measurements indicated that the drug/vector combination facilitated the ability of the alkylating drug tmz to alter the resistance of these cancer stem cells, suggesting a new chemotherapy strategy even for patients diagnosed with inoperable or recurrent malignant gliomas methods: at the national institute for r & d of isotopic and molecular technologies form cluj napoca were synthesized three types of nanostructures chitosan-tmz, tmz-chitosan-peg (polyethylene glycol), tmz-chitosan-ppg (polypropylene glycol). three type of cell lines (glioma-derived stem, hfl and huvec) were treated with the 3 types of nanostructures and the survival rate of the cells was compare to standard therapy (tmz). results: the results showed a reduction in the rate of survival of the tumor cells. cell proliferation assays clearly demonstrate the differences between 20 abrudan et al temozolomide action encapsulated on glioblastoma cell lines conventional chemotherapy (tmz) and temozolomide encapsulated in chitosan and polymer nanostructures. conclusion: nanostructures like chitosan, peg, ppg are useful as vectors for drugs transport. despite combined therapy (surgery, radiotherapy, chemotherapy), currently median patient survival is reduced. the key to improving life expectancy could be an effective therapy targeted, customized for each case. an increasingly important role will be new methods of treatment such as immunotherapy, gene therapy or nanotherapy. key words: malignant gliomas, primary tumor cell culture, temozolomide. introduction malignant gliomas are responsible for the death of approximately 11,000 patients per year.[1] the standard care for patients diagnosed with high-grade central nervous systems (cns) gliomas include, postoperatively, temozolomide (tmz) concomitant and adjuvant to radiotherapy. this therapeutic strategy is, however, associated with high toxicity, limited efficiency and significant side effects. the median length of survival for patients with high-grade primary glial tumors ranges from 11 to 33 months after initial diagnosis and an average of 7 months following recurrence.[2,3] the failure of current approaches to the treatment of malignant gliomas has been attributed to the existence of a subpopulation of cancer cells malignant glioma cancer stem cells (cscs), which have the ability to withstand chemotherapeutics and ionizing radiation based on certain of their unique properties: high expression of anti-apoptotic proteins, high expression of abc pumps, and remarkable dna repair capability. [4-6] traditional therapies, such as dna alkylating or methylating drugs along with radiation oncology treatments, have low treatment efficacy for these cell types. more complex treatments capable of overcoming the cscs’ ability to eliminate anti-cancer drugs and perform other protective functions are therefore critically needed. for this reason, a combination of traditional treatments and nanotechnologybased approaches offers attractive possibilities. more efficient and less toxic therapeutics that can cross the cscs protective barriers are urgently needed. in this context, nanomaterials could play an important role based on their unique electronic, optical, magnetic, and structural properties that are found neither in bulk materials nor in single molecules and which are necessary to develop advanced cancer treatments. theoretical considerations of nanotherapy nanoparticles are biodegradable or bioresistence polymer matrix, with an average diameter of approx. 200 nm. nanoparticles are obtained by polymerization of monomers or directly from the processed polymer. the advantages of nanoparticles are: relatively simple preparation, they ensure protection of the active principles from romanian neurosurgery (2014) xxi 1: 18 29 21 chemical and enzymatic degradation (nanocapsules) limiting side effects of active substances and provide transportation and release to the target by the biodegradable matrix. disadvantages are the high costs of technology (equipment, raw materials) and toxicity of adjuvants [7]. a large area relative to their volume, increased bioavailability, provide controlled release of the active substance and support the intracellular and molecular vectors. due to the extremely small size, nanoparticles vectors easily cross biological barriers (blood-brain barrier in our case)[8]. theoretical considerations of nanotherapy in brain tumors molecular nanodiagnostic. nanoparticles increased sensitivity and specificity for high-resolution noninvasive medical imaging, at molecular and cellular level (ultrasound, ct, mri, oi. pet). (pegchitosan-clorotoxin-fluoroscopic agent nanoparticles may improve the resolution by 10 times)[9]. nanovaccines are useful for immunotherapy, nanoantibiotherapy offers a lower risk of developing resistance to antibiotics and some nanostructures can be used in neuronal nanoprotection [10]. transport nanosystems for gene therapy (to replace viruses as vectors) are less likely immunologic and allow the transfer of large quantities of genetic material. a polyglycerol dendrimer polymer has been shown to improve rna stability and accumulation in brain tumors in animals[7]. antitumoral nanotherapy peg dimethacrylate methyl ether methacrylate and iron oxide nanostructures can be used as a biomaterial for the thermal treatment of gbm. many types of nanoparticles such as biodegradable polymers (peg, ppg, pbca) lactic acid loaded with different type of chemotherapy agents increased tumor cytotoxicity and survival in laboratory animals with decreased side effects of cytostatic. use of nanoparticles can increase the effectiveness of radiotherapy with decrease of side effects [11]. methods at the national institute for r & d of isotopic and molecular technologies form cluj napoca were synthesized three types of nanostructures chitosan-tmz, tmzchitosan-peg (poly-ethylene glycol), tmzchitosan-ppg (polypropylene glycol). chitosan [poly(b-(10/4)-2-amino-2deoxy-dglucose)] is a natural cationic polysaccharide derived from chitin, which is copolymer, a glucosamine and an nacetyl glucosamine units, combined together [12]. chitosan is being widely used as a pharmaceutical excipient, comprising a series of polymers varying in their degree of deacylation, molecular weight, viscosity, pka etc. the presence of a number of amino groups permits cts to chemically react with anionic systems, thereby resulting in alteration of 22 abrudan et al temozolomide action encapsulated on glioblastoma cell lines physicochemical characteristics of reactants and developing new properties of such combinations [1]. temozolomide (brand names temodar and temodal and temcad) is an oral alkylating agent used for the standard treatment of grade iv astrocytoma. chitosan structural formula peg poly-ethylene-glycol ppg poly-propylene-glycol structural formula of temozolomide peg + chitosan + tz (micrometer structures of chitosan with poly-ethylene-glycol and temozolomide.. spheres of 5-15 microns) ppg + chitosan + tz (micrometer structures of chitosan poly-propylene glycol and temozolomide filaments with a length of 10-50 microns) chitosan + tz (structures of chitosan and temozolomide, sub-micrometer (nanometer) spheroids) chitosan (cts) from crab shells with 85% deacetylation degree, poly-ethyleneglycol, poly-propylene-glycol, were purchased from sigma aldrich. cts was dissolved in 1% (v/v) acetic acid aqueous solution stirring for 6 hours at 300c temperature, at final the solution being pale yellow, with a homogenous consistence and aspect. the cts solution was split in 5 equal volumes, 50 ml each, and to each cts sample was added 0,5 ml linking additive agent and 10 mg powder from temodal. calculations assured that each sample contains 10 mg tmz. we obtain a temozolomide concentration of 50 micromol/l . the solutions were further stirred for 30 min and then ultrasonically treated in an romanian neurosurgery (2014) xxi 1: 18 29 23 elmasonic e60h ultrasonic bath for 360 min. microspheres of cts-based polyelectrolyte complex containing tmz/linker were characterized by ftir electronic microscope connected to ftir jasco 6100 spectrometer. the malignant glioma cancer stem cells (cscs), used in this study were isolated from a glioblastoma multiforme biopsy. briefly, after mechanical dissociation of tumor tissue, the fragments were placed in 1 ml of fetal calf serum (fcs). after three hours, 3 ml of dmem/f-12 medium supplemented with 15% fcs was added to the dish. after reaching a subconfluent monolayer, cells were detached using trypsin/ edta and resuspended in a serum-free media: dmem/f12 (1:1) medium, supplemented with 15 ng/ml basic fibroblast growth factor (bfgf), 20 ng/ml epidermal growth factor (egf), 2mm/l l-glutamine, 4 u/l insulin growth factor-1 (igf-1) and b 27 supplement (1:50) (sigma aldrich). isolated and expanded cells revealed some stem-cell specific features, such as the expression of cellular markers (cd133, cd105, cd90, nanog, oct ¾ (immunocytochemistry) expression of specific genes, such as : cxcr4, nestin, glial fibrillary acidic protein (gfap), and neurofilament protein (nf) (reverse transcription-pcr). cells also displayed a high proliferative potential despite chemotherapy and irradiation and also had the ability to form spheroids in suspension. the three type of cell lines (gliomaderived stem, hfl-normal fibroblasts human isolated from lung and endothelial cell line huvec-human umbilical vein endothelial cell.) were treated with the 3 types of nanostructures and the survival rate of the cells was compare to standard therapy (tmz). we used three cell lines to study the difference between tumor cells and normal cell lines (fibroblasts and endothelial cells). the four compounds (peg + chitosan + tz, tz + ppg + chitosan, chitosan + tz and tz) after binding were filtered through a 220nm filter sterilized stem cells are in the exponential phase of cell growth they are detached by exposure for 5 min in 0.25% trypsin edta after 3 washes with pbs. trypsin is inactivated by the addition of culture medium with 10% fetal calf serum, and the cell suspension centrifuged 5 min at 1100 rpm. cell viability is checked by trypan blue 0.4%. the cells are counted with a thoma chamber. the 3 cell lines (gm 1, hfl and huvec) after being counted are seeded in 96-well plates each 7500 cells / well and suspended in 200 ml medium; after 24 h cells were subjected to treatment that joined us and after a further 24 hours mtt assay was performed mtt test. twenty-four hours after therapy culture medium was aspirated and the cells will be exposed to 100 ml solution of mtt 1mg/ml (tetrazolium bromide thyazolyl blue) for 1 hour at 37 ° c. mtt is a tetrazolium salt which is converted in 24 abrudan et al temozolomide action encapsulated on glioblastoma cell lines cellular mitochondria of viable cells into a formazan compound dark blue colored, insoluble in aqueous solutions. after the incubation period, mtt solution is aspirated from the wells and formazan crystals were dissolved with dmso 150µl/well (dimethyl sulfoxide) obtaining a color reaction. for measuring the optic density, boards are analyzed at 492 nm using a plate reader biotek synergy2. each determination shall be made in triplicate. statistical analysis statistical significance values were obtained using a one-way analysis of variance (anova), with 95% confidence (c.i.) level, using graphpad prism 5 statistics program (graphpad inc, san diego, ca, usa). bonferroni’s multiple comparison test was considered statistically significant at p <0.05. all experiments were performed in triplicate. results in our experiments,. there was an impotant difference between tmz alone (at the same concentration) and the control sample on the one hand and the three types of nanostructures studied (peg + chitosan + tz, tz + ppg + chitosan, chitosan + tz) on the other hand for each cell type (glioma-derived stem, hfl and huvec). figure 1 figure 1 survival chemotherapy graphics for the three type of cell lines (glioma-derived stem, hfl-normal fibroblasts human isolated from lung and endothelial cell line huvec-human umbilical vein endothelial cell.) treated with the 3 types of nanostructures and standard therapy (tmz). the vertical axis represents the optical density (remaining cell population) and the horizontal axis the various therapy options. hfl bonferroni's multiple comparison test mean diff. t significant? p < 0.05? summary 95% ci of diff ctrl vs peg+cts+tmz 0.3903 20.68 yes *** 0.3282 to 0.4523 ctrl vs ppg+cts+tmz 0.5728 30.35 yes *** 0.5107 to 0.6348 romanian neurosurgery (2014) xxi 1: 18 29 25 ctrl vs cts+tmz 0.3183 16.86 yes *** 0.2562 to 0.3803 ctrl vs tmz 0.04825 2.557 no ns -0.01376 to 0.1103 peg+cts+tmz vs ppg+cts+tmz 0.1825 9.671 yes *** 0.1205 to 0.2445 peg+cts+tmz vs cts+tmz -0.07200 3.815 yes * -0.1340 to -0.009987 peg+cts+tmz vs tmz -0.3420 18.12 yes *** -0.4040 to -0.2800 ppg+cts+tmz vs cts+tmz -0.2545 13.49 yes *** -0.3165 to -0.1925 ppg+cts+tmz vs tmz -0.5245 27.79 yes *** -0.5865 to -0.4625 cts+tmz vs tmz -0.2700 14.31 yes *** -0.3320 to -0.2080 gm1 bonferroni's multiple comparison test mean diff. t significant? p < 0.05? summary 95% ci of diff ctrl vs peg+cts+tmz 0.4933 10.53 yes *** 0.3394 to 0.6471 ctrl vs ppg+cts+tmz 0.6788 14.49 yes *** 0.5249 to 0.8326 ctrl vs cts+tmz 0.5603 11.96 yes *** 0.4064 to 0.7141 ctrl vs tmz 0.1325 2.829 no ns -0.02138 to 0.2864 peg+cts+tmz vs ppg+cts+tmz 0.1855 3.961 yes * 0.03162 to 0.3394 peg+cts+tmz vs cts+tmz 0.0670 1.431 no ns -0.08688 to 0.2209 peg+cts+tmz vs tmz -0.3608 7.704 yes *** -0.5146 to -0.2069 ppg+cts+tmz vs cts+tmz -0.1185 2.531 no ns -0.2724 to 0.03538 ppg+cts+tmz vs tmz -0.5463 11.66 yes *** -0.7001 to -0.3924 cts+tmz vs tmz -0.4278 9.134 yes *** -0.5816 to -0.2739 huvec bonferroni's multiple comparison test mean diff. t signific ant? p < 0.05? summar y 95% ci of diff ctrl vs peg+cts+tmz 0.06200 3.918 yes * 0.01001 to 0.1140 ctrl vs ppg+cts+tmz 0.1303 8.232 yes *** 0.07826 to 0.1822 ctrl vs cts+tmz -0.01775 1.122 no ns -0.06974 to 0.03424 ctrl vs tmz 0.02625 1.659 no ns -0.02574 to 0.07824 peg+cts+tmz vs ppg+cts+tmz 0.06825 4.313 yes ** 0.01626 to 0.1202 peg+cts+tmz vs cts+tmz -0.07975 5.040 yes ** -0.1317 to -0.02776 peg+cts+tmz vs tmz -0.03575 2.259 no ns -0.08774 to 0.01624 ppg+cts+tmz vs cts+tmz -0.1480 9.354 yes *** -0.2000 to -0.09601 ppg+cts+tmz vs tmz -0.1040 6.573 yes *** -0.1560 to -0.05201 cts+tmz vs tmz 0.04400 2.781 no ns -0.007993 to 0.09599 26 abrudan et al temozolomide action encapsulated on glioblastoma cell lines a b figure 2 (a) a typical pre-apoptotic cell after 24h incubation with chitosan+tmz (plasdic phase contrast, magnification 400x), and (b) in comparison with control (cells culture without chitosan+tmz),(white light microscopy, plasdic contrast phase, magnification 400x) after cell gm1 treatement with chitosan+tzm autophagic cells were observed. figure 3 autophagic cell gm1with intracytoplasmic vacuoles it was observed for chitosan+tzm nanoparticles. (phase contrast, magnification x400) discussion and conclusion long-term survival of patients diagnosed with high-grade gliomas remains poor, with population-based studies estimating that the 3-year survival rate is under 5%. [22-25]. conventional treatment for newly diagnosed malignant gliomas was traditionally consisted of initial surgical resection followed by fractionated external beam rt, with or without chemotherapy usually using regimens containing alkylating agents. until recently the benefit of chemotherapy in this setting remained controversial but tmz, an oral alkylating agent, has proven to be efficient, primarily in the recurrent setting. the failure of current approaches to the treatment of malignant gliomas has been attributed to the existence of a subpopulation of cancer cells malignant glioma cancer stem cells (cscs), which have the ability to withstand chemotherapeutics and ionizing radiation romanian neurosurgery (2014) xxi 1: 18 29 27 based on certain of their unique properties: high expression of anti-apoptotic proteins, high expression of abc pumps, and remarkable dna repair capability.[13-15] traditional therapies, such as dna alkylating or methylating drugs along with radiation oncology treatments, have low treatment efficacy for these cell types. more complex treatments capable of overcoming the cscs ability to eliminate anti-cancer drugs and perform other protective functions are therefore critically needed. for this reason, a combination of traditional treatments and nanotechnologybased approaches offers attractive possibilities. more efficient and less toxic therapeutics that can cross the cscs protective barriers are urgently needed. in this context, nanomaterials could play an important role based on their unique electronic, optical, magnetic, and structural properties that are found neither in bulk materials nor in single molecules and which are necessary to develop advanced cancer treatments. similarities between the self-renewal mechanisms of stem cells and cancer cells have led to the new concept of cancer stem cells (cscs). over the course of the past 10-15 years, there has been increasing evidence to support the cancer stem cell hypothesis, which postulates that cscs are responsible for tumor initiation, metastasis, and resistance to treatment. it is now generally believed that a tumor has its origin in cscs, which come either from transformed tissue stem cells or from transformed progenitor cells that have regained self-renewal activity.[16] these rare cscs could be crucial in controlling and curing cancer: through asymmetric division, cscs drive tumor growth and evade therapy with the help of traits shared with normal stem cells such as quiescence, self-renewal ability, and multidrug resistance pump activity.[17] these cells were first identified in hematologic cancers, but recently have been isolated from solid tumors. cscs are tumor initiating cells in immunocompromised mice and have the ability to generate heterogeneous cancer cell populations.[18] the gold standard assay to determine whether a stem cell is or not a csc involves serial transplantation in animal models. potential surface markers of cscs include the following: cd133, aldehyde dehydrogenase 1 (aldh1), cd44, and cd24. efflux of hoechst or rhodamine dyes, also referred to as side population (sp), have also been used to identify putative cscs. however, these markers have certain limitations in that they fail to identify all cscs and merely designate a subpopulation that is enriched for clonogenic and tumorigenic activity. also, not all cells with a csc marker phenotype behave as cscs. most markers for separating cscs were chosen due to their expression on normal stem cells of certain tissues, and, interestingly, there are a number of molecules that are commonly expressed in normal and cancer stem cells that lead to different phenomena depending on the local environment.[19] 28 abrudan et al temozolomide action encapsulated on glioblastoma cell lines using bonferroni’s multiple comparison test, we found statistically significant results (p<0.05) between the cscs (control) and the ctr+ peg+cts+tmz (95 ci of 0,3394 to 0,6471), ctr+ppg-cts-tmz (95% cl of 0,5249 to 0,83260), ctr+cts-tmz (95% of 0,4064 to 0,7141). when one or more initiating genetic changes appeared at the progenitor level, all of the downstream cells continued this change. in one particular case, it is possible that a daughter cell acquired not only the properties of the stem cell, but also the additional alterations that allow the glioma to progress to the next step and invade surrounding tissues. due to the small population of glioblastoma-derived stem cells, the malignant gliomas have a negative response to various conventional treatments.[20] the killing efficiency of the peg+cts+tmz, ppg-cts-tmz, cts-tmz nanostructures on glioblastomaderived stem cells is better compared with the drug temozolomide, alone. our proposed nanoscaled drug delivery system offers also a new chemotherapy strategy for patients diagnosed with unresectable or recurrent malignant gliomas. current therapies are not yet curative, as cscs may survive as a result of the increased efflux of chemotherapy agents due to abcg2 cell membrane proteins and increased dna repair.[21] cancer cells are very complex biological structures that perform functions ranging from invasion or metastasis to the elimination of anticancer drugs from the cell membrane. although the exact mechanisms need to be explored further, combining advances in fundamental oncology and nanotechnology offers the opportunity to significantly impact future diagnostics and therapeutics. we have shown that drug delivery vectors based on chitosan and polymers have the ability to deliver temozolomide (tmz), a cytostatic drug, to treat malignant gliomas. our studies have shown that a novel drug delivery has low toxicity and the ability to internalize tmz. malignant gliomas are highly infiltrative and lethal cancers of the central nervous system. the highly infiltrative nature of glioma cells often renders a complete surgical removal impossible and inevitably will lead to tumor recurrence. the attention of the scientific community is currently focused on nanoparticles, a novel vector for the delivery of anticancer drugs to target cancer cells. these particles have many advantages which recommend it over classically administered drugs. due to their submicroscopic size and modifiability, nanoparticles have an enhanced access to cancer cells, being able to maintain high concentrations of drugs in target tissues. because of their special distribution, drugloaded nanoparticles may even have a decreased risk of systemic adverse effects which normally occur at increased drug doses, while locally maintaining effective concentrations. nanoparticles loaded with various cytostatics may prove to have numerous additional advantages. the romanian neurosurgery (2014) xxi 1: 18 29 29 increased drug concentrations may also be explained by the facilitated penetration of the particles in the tumor through endocytosis, which has the advantage of bypassing the transportermediated drug internalization systems. moreover, the intracellular drug concentration increases in spite of tumor cell multidrug resistance protein activity, which may result in better tumor-level effect of the drug in spite of multidrug resistant tumor phenotype. another positive viewpoint of using nanoparticles is their capacity to cross the blood brain barrier, which shapes new directions for drug delivery into the brain. most drugs partially cross the blood brain barrier, but its incorporation into nanoparticles may enhance its passage and increase the relative amount of drug reaching brain tissue. therefore, the use of loaded nanoparticles could be of paramount importance for glioblastomas, aggressive tumors with a very dismal prognosis, for which temozolomide has been entitled “the most clinically relevant drug ever reported for targeting of gliomainitiating cells”.[25] nanostructures like chitosan, peg, ppg are useful as vectors for temozolomide transport. our study shows a net decrease of cell population by treating them with drugnanostructures. cell population decrease was more important in tumor cell cultures (gm1) compared with normal cells fibroblasts (hfl) or endothelial cells (huvec). the best response was obtained for chitosan-tz, considering that drug chemotherapy should be aggressive on tumor cells and less aggressive on normal cells. our study tries to find new drugs for the treatment of glioblastoma. results must be confirmed by in vivo studies. despite combined therapy (surgery, radiotherapy, chemotherapy), currently median patient survival is 10-12 months. the key to improving life expectancy could be an effective therapy targeted, customized for each case. an increasingly important role will be new methods of treatment such as immunotherapy, gene therapy or nanotherapy. references 1. behin a, hoang-xuan k, carpentier af, delattre jy. primary brain tumors in adults. lancet 2003; 361: 323331. 2. wen py, kesari s. malignant gliomas in adults. n engl j med 2008; 359: 492-507. 3. stupp r, hottinger af, van den bent mj et al. frequently asked questions in the medical management of high-grade gliomas: a short guide with practical answers. esmo educational book. ann oncol 2008; 19 (suppl 7): vii209-vii216. 4. stupp r, tonn jc, brada m, pentheroudakis g. high-grade malignant gliomas: esmoclinical practice guidelines for diagnosis, treatment and follow-up. ann oncol 2010; 21 (suppl 5): v190-v193. 5. stupp r, mason wp, van den bent mj et al. radiotherapy plus concomitant adjuvant temozolomide for glioblastoma. n engl j med 2005; 352: 987-996. 6. tomuleasa c, soritau o, rus-ciuca d et al. functional and molecular characterization of glioblastoma multiforme-derived cancer stem cells. j buon 2010; 15: 583-591. 7. jain kk: potential of nanobiotechnology in management of glioblastoma multiforme. in: glioblastoma: molecular mechanisms of pathogenesis and current therapeutic strategies. ray sk (ed.). springer, ny, usa, 399–419 (2010). 8. jain kk: potential of nanobiotechnology in 30 abrudan et al temozolomide action encapsulated on glioblastoma cell lines management of glioblastoma multiforme. in: glioblastoma: molecular mechanisms of pathogenesis and current therapeutic strategies. ray sk (ed.). springer, ny, usa, 399–419 (2010). 9. wang j, yong wh, sun y et al.: receptor-targeted quantum dots: fluorescent probes for brain tumor diagnosis. j. biomed. opt. 12, 044021 (2007). 10. jain kk: textbook of personalized medicine. springer, ny, usa (2009). 11. maier-hauff k, ulrich f, nestler d et al.: efficacy and safety of intratumoral thermotherapy using magnetic iron-oxide nanoparticles combined with external beam radiotherapy on patients 12. svirshchevskaya e.v. et al. european j. of medicinal chemistry 44 5 (2009) 2030-2037. 13. eyler ce, rich jn. survival of the fittest: cancer stem cells in therapeutic resistance and angiogenesis. j. clin. oncol. 26(issue number??), 2839–2845 (2008). 14. li x, lewis mt, huang j et al. intrinsic resistance of tumorigenic breast cancer cells to chemotherapy. j. natl. cancer inst. 100 (issue?), 672-67 (2008). 15. diehn m, cho rw, lobo na et al. association of reactive oxygen species levels and radioresistance in cancer stem cells. nature 458 (issue?), 780-783 (2009). 16. dittmar t, nagler c, schwitalla s, reith g, niggemann b, zänker ks. recurrence cancer stem cells-made by cell fusion? med hypotheses 73(4), 542-7 (2009). 17. fabian a, barok m, vereb g, szollosi j. die hard: are cancer stem cells the bruce willises of tumor biology? cytometry; part a 75a, 67-74 (2009). 18.keysar s b, jimeno a. more than markers: biological significance of cancer stem cell-defining molecules. mol cancer ther 9 (issue number?):2450-2457 (2010). 19. iwasaki h, suda t. cancer stem cells and their niche. cancer sci. 100(7), 1166-72 (2009) 20. florian is, tomuleasa c, soritau o et al. cancer stem cells and malignant gliomas. from pathophysiology to targeted molecular therapy. j buon. 16(1), 16-23 (2011). 21. frosina g. dna repair and resistance of gliomas to chemotherapy and radiotherapy. mol cancer res 7(7), 989-999 (2009). 22. nino lomadze, hans jorg schneider tetrahedron 61 36 (2005) 8694-8698. 23. o. soritau, c. tomuleasa, m. aldea et al. metformin plus temozolomide-based chemotherapy as adjuvant treatment for who grade iii and iv malignant gliomas journal of buon 16 (2011): 282-289, 24. gerster er, batchelor tt. imaging and response criteria in gliomas.curr opin oncol 2010; 22: 598-603. 25. grossman sa, ye x, piantadosi s et al. survival of patients with newly diagnosed glioblastoma treated with radiation and temozolomide in research studies in the united states. clin cancer res 2010; 16: 2443-2449. microsoft word 4iacob_atypical.doc romanian neurosurgery (2012) xix 3: 203 209 203 atypical meningioma g. iacob, m. craciun universitary hospital bucharest motto: “scientific observation is allways a polemic observation” gaston bachelard abstract objective: atypical meningioma are an intermediate group of meningiomas, exhibiting less favourable biological behavior than classic benign tumours, but a relatively more favourable biological behavior than definitive malignant meningiomas. subject of controversy, atypia in meningioma still generate discordance between accurate criteria defining malignancy and biological behavior, prediction of recurrence. methods: this retrospective study intend to evaluate diagnosis on clinical and pathological data, treatment trends and early outcomes for 6 cases with atypical meningiomas occuring in 63 patients operated for benign meningioma in the last 5 years in our clinic between 2006-2011. all patients were explored ct, mri, preoperative selective angiography and in all cases the who 2000 classification criteria were used to define atypical meningioma results: between 2006-2011 we operated 6 atypical meningioma of 63 benign meningiomas (9,52%). tumor sites in the patients were: parasagittal (3 cases), convexity (2 cases), spheno-cavernous (1 case). all patients were operated and dural graft was done to all cases. the extent of surgical resection was simpson’s grade 1 in 2 cases and simpson’s grade 2 in four cases, to which radiation was administered after the first surgery with a dose ranging from 52-62 gy. regrowth (enlargement of tumour after subtotal resection) was noticed in 2 irradiated cases: one case after 2 years after the first operation, the patient was again operated pathological diagnosis was malignant meningioma; in another case after 3 years, at operation it was the atypical meningioma. no chemotherapy was used in our cases. conclusions: atypical meningiomas are rare tumors, grow more rapidely, the diagnosis age ≥ 60 years, several histological criteria can define accurate identification to understand the biology of this group of tumors. heterogenous contrast enhancement with marked peritumoral edema in neuroimaging are important; cerebral edema has prognostic value and should encourage fundamental and farmacologic research using anti vegf and somatostatine analogs treatments. surgery (simpson grade 1) referring both tumor and dural implant area should be done de novo but also for recurrencies. radiotherapy still are controversial without proven benefit and chemotherapy without statistic argues to improve quality of life. key words: atypical meningioma, malignant meningioma introduction despite maningiomas are considered benign tumors, slow growing, very little multiplication of cells, very rarely invade 204 iacob, craciun atypical meningioma the brain tissue, less likely to recur; atypical meningioma remain a controversial topic because of the limited signs of histological anaplasia, lack of universally accepted criteria for grading histological malignancy few large series have been conducted to evaluate the problem of malignancy and because biological behavior, prediction of recurrence is still difficult to predict. our study present our experience with such tumors between 2006-2011, operated in our clinic. materials and methods 6 cases with atypical meningiomas occuring in 63 patients operated for benign meningioma in the last 5 years in our clinic between 2006-2011 were evaluated pre and postoperatory, also at 1 and 2 years after. all patients were explored ct, mri, preoperative selective angiography concerning topography, unique or multiple tumors, the presence of irregular margins and fringes, even prominent tumour pannus extending away from the globoid mass, the pattern of enhancement, the degree of peritumoral oedema, calcifications, brain invasion, spontaneous necrosis in the absence of embolization, vascularization. in all cases the who 2000 classification criteria were used to define atypical meningioma on pathological data. all patients were operated on once aiming for gross total resection of the tumour as well as its overlying dura. the extent of surgical resection was graded according to simpson’s classification. results in the last 5 years 63 meningiomas were operated on at neurosurgery clinic universitary hospital bucharest; of this 6 (9,52%) were atypical meningiomas. patient age were range 53-78, mean age 67; there was four males and two females; no signs of neurofibromatosis type 2 or another associated tumoral pathologies were noticed. at presentation all patients had intracranial hypertension syndrome: headache, papillary oedema, confusion 1 case; also slight hemiparesis or only limb paresis, focal seizures. tumor sites in our patients were: parasagittal (3 cases), convexity (2 cases), spheno-cavernous (1 case). cerebral mri an ct scans were done in all patients. the tumors were slighty hyperdense with no calcification. all tumours exhibited homogenous dense contrast enhancement, with marked or moderate peritumoral oedema, irregular tumor margins. angiography was performed in all cases with homogenous vascular blush, in two convexity meningiomas vascular feeders were seen from external carotid artery suited by embolization. (figure 1) a b c d romanian neurosurgery (2012) xix 3: 203 209 205 e f g h figure 1 a-c pre and postop ct scan in frontal atypical meningioma with important perilesional oedema; d-e pre-op ct scan and f-g mri of a spenocavernous atypical meningioma; h post-op ct scan all patients were operated and dural graft (autologous or synthetic) was done to all cases. the extent of surgical resection was simpson’s grade 1 in 2 cases and simpson’s grade 2 in four cases, to which radiation was administered after the first surgery with a dose ranging from 52-62 gy. pathological characteristics in all cases were based according to the who 2000 classification: at least 4 mitoses in 10 hpf or 3 of the following criteria: increased cellularity, high nuclear-to-cytoplasm ratios, prominent nucleoli, uninterrupted patternless or sheet-like growth or necrosis. (figure 2) the median follow-up was 26 months (range 12 48 months). all patients with atypical meningioma in our series survived. regrowth (enlargement of tumour after subtotal resection) was noticed in 2 irradiated cases: a b c d figure 2 atypical meningioma – pathological characteristics: a. necrosis (he x 20), b increased cellularity and sheet-like growth (he x 20), c prominent nucleoli (he x 40), cellular atypia (he x 40) one case after 2 years after the first operation, the patient was again operated pathological diagnosis was malignant meningioma; in another case after 3 years, at operation it was the atypical meningioma. no chemotherapy was used in our cases. discussion usually benign, recognized as a clinical entity for nearly 200 years, arising from arachnoidal cells of neural crest (1)(2)(3), meningiomas are the most common, primary, intracranial extraaxial brain tumours and comprise 13-20% of all primary intracranial neoplasms; they can invade dura and the skull by osseous hyperplasia (4). acordind to the who classification system 2000 (5)(6), meningiomas are regarded as a heterogeneous group of tumours and are 206 iacob, craciun atypical meningioma histologically categorized into 14 distinct subgroups with three grades of malignancy: benign (grade i – typical meningiomas) 90%: meningothelial, fibrous, transitional, psammomatous, microkystic, angioblastic (most aggressive), metaplasic; these tumours exhibit slow growth and very little multiplication of cells and very rarely invade the brain tissue. overall, benign meningiomas are less likely to recur than the atypical and malignant grades. atypical (grade iim2, atypical) 5%10%: atypical variants of their original histologic types: meningothelial, fibroblastic, transitional, including brain invasion, chordoid (foci of chordoid similar to a chordoma), clear cell (poligonal cells with clear cytoplasma by glicogen accumulation). it’s to be remarked that dura and adjacent bone invasion are not atypia signs. these tumours exhibit increased cellularity, cell abnormalities: prominent nucleoli, small cells, modified cell architecture, spontaneous necrosis in the absence of embolisation, a faster growth rate than benign meningiomas, some degree of brain invasion and a higher likelihood of recurrence than benign. anaplastic (grade iii – m3, malignant) 3-5% of all meningiomas: papillary, rhabdoid, anaplastic. these tumours show frequent mitoses, increased cellular abnormalities, high nuclear to cytoplasmic ratio, foci of necrosis; exibit a faster growth rate compared to benign and atypical meningiomas, recur and are the most likely to invade the brain and spread (metastasize) to other organs in the body. accordind to who 2000 classification (5) atypical meningiomas have at least: 3 of the 5 following criteria: increased cellularity, high nuclear to cytoplasm ratios, prominent nucleoli, uninterrupted patternless or sheet-like growth or necrosis; also 4 mitoses in 10 hpf (x400). the new who 2007 classification mentain the ancient classification, for atypical meningioma; brain invasion is not a criteria, but is recognised as an evolutivity criteria (7). although recognised as as pronostic factors of agresivity: brain invasion, elevated mib-1 labeling (8)(9) and ki67 proliferative cells are not criteria for atipic meningioma (10), despite recognized predisposition for tumor recurrence and overal survival (10) when these factors are noted. nagashima (11)(12) has noted cmyc expression level, the protooncogene and his protein proving positive correlation between c-myc expression level and the proliferative cell index by anti ki67 immunomarking. their etiology is uncertain, but typical meningiomas may undergo gene losses and gains, transforming them into atypical ones (13). radiation-induced meningiomas are also more likely to be atypical (14) atypical meningiomas are rare, more aggressive and invasive than typical meningiomas, grow more rapidely, become symptomatic at an earlier age, are predominant in adults (2)(10)(15-21). interesting especially the 4th and 5th decade, age egal or over 60 years are a negative prognostic facto in multivariants analisis. considering gender distribution, asa in our cases, the female prodominance of 2/1 seen in benign meningiomas are no more observed, there is a inversion tendency for men for meningioma progressing from atypical to malignant meningioma, even biochemical studies have shown that progesterone activity correlates inversely with atypical in meningiomas. clinical features are not specific, but as a romanian neurosurgery (2012) xix 3: 203 209 207 reflection of increased peritumoral oedema in atypical meningioma are more likely related with objective neurological deficits (22). more common atypical meningioma occur over cerebral convexities, parasagittal and falx;, few reports identify other locations as: infratentorially, supra and infratentorial extensions, intraventricularly (2). ct as mri could not be an indicative to differentiate benign from atypical meningiomas, also to predict aggressive potential. atypical meningiomas may be plaquelike in configuration and extend through the dura to the skull and scalp or can spread via the perivascular spaces (14) marked peritumoral oedema, heterogenous contrast enhancement in 5,4%, minimal or calcifications absence, irregular or indistinct margins, musjroomlike projections of the main tumor mass are the most important findings in atypical meningiomas. (2)(15)(20)(22-24). dwi (diffusion-weighted imaging) signal intensity of tumors classified as hypo-, iso or hyper-intense to grey matter and apparent diffusion coefficient (adc) measurements to differentiate benign from atypical/malignant meningiomas and among different sub-types do not seem reliable in grading meningiomas or identifying histological sub-types. hence, these parameters should not be recommended for surgical or treatment planning.(6) concerning cerebral oedema in atypical meningiomas several considerations could be stated: there is no correlation between peritumoral oedema and tumor grade in meningioma (25), a significant relation was statued between microvascular density, the value of the vascular endothelial growth factor expression (vegf) known also as a vascular permeability factor and some somatostatine receptors (sst2) (26). somatostatine by his receptors has an antiproliferative activity on several cells (27) for this reason these receptors offers new tendency for research in tumor recurrency treatment. in the absence of a prospective study concerning the surgery effect on meningioma (28) the best attitude still is the surgical approach with large dural implant base resection, to reduce recurrency and mortality.(2)(19)(29) using a univariate analysis palma (16) has proved that simpson 1 rezection versius 2-3 can improve global survival for atypical meningiomas (p<0,0071), especially when tumor is on convexity. to improve tumor resection several methods were used: neuronavigation, somatostatine analogs used intraoperatory for a better identification (30), specific imaging octreoscan, microsurgery (6). radiation therapy in the treatment of atypical meningioma still are controversial (2)(31). despite classical conception of meningioma radioresistance, radiotherapy was used indifferent of the extent of surgical resection, the mean dosis 53,57 gray +/_6,06 grays. on retrospective studies radiotherapy has doubtful results without consensus: some authors recommend radiotherapy after the first recurrency 60,5%, another authors proved that radiotherapy has no impact on general survival and even can deteriorate prognosis. radiotherapy should be proposed especially when tumor is passing from grade 2 to 3. radiotherapy did no prevent or retard the recurrence of tumours regardless of the extent of resection (31). no chemotherapy is usefull (6). despite gross total resection, approximately 29-40% of atypical meningiomas recur and survival of higher 208 iacob, craciun atypical meningioma grade tumours correlated with specific histological features have produce conflicting data (21). conclusions atypical meningiomas are rare tumors, with uncertain etiology, grow more rapidely, the diagnosis age ≥ 60 years, several histological criteria can define accurate identification to understand the biology of this group of tumors. heterogenous contrast enhancement with marked peritumoral edema in neuroimaging are important; cerebral edema has prognostic value and should encourage fundamental and farmacologic research using anti vegf and somatostatine analogs treatments. surgery (simpson grade 1) referring both tumor and dural implant area should be done de novo but also for recurrencies. radiotherapy still are controversial without proven benefit and chemotherapy without statistic argues to improve quality of life. references 1. claus e.b. et al. – epidemiology of intracranial meningioma, neurosurgery 2005, 57 (6), 1088-95; 2. sakr s.a., salem m. – atypical meningioma: clinicopathological analysis of a new classification, pan arab journal of neurosurgery 2011, 15, 1 36-41; 3. cushing h.w., eisenhardt l. meningiomas: their classification, regional behavior, life history and surgical end results, springfield, ill: charles c. thomas, 1938, 47-50; 4. maier h., öfner d., hittmair a., et al. classic, atypical, and anaplastic meningioma: three histopathological subtypes of clinical relevance, j neurosurg. 1992, 77:616-623; 5. louis d.n., et al. – meningiomas. world health organization classification of tumours, pathology and genetics. tumour of the nervous system 2000, 175-184; 6. durand anne – meningiomes de grade ii et de grade iii: etude des facteurs pronostiques, these 2007, universite de limoges; 7. louis d.n. et al. – who classification of tumours of the central nervous system, fourth edition, iarc who classification of tumours 2007, acta neuropathol 2007, 114: 97-109; 8. modha a., gutin p.h. – diagnosis and treatment of arypical and anaplastic meningiomas: a review, neurosurgery, 2005, 57(3), 538-550; discussion 538550; 9. schiffer d., ghimenti c., fiano v. – absence of histological signs of tumor progression in recurrences of completely resected meningiomas, j. neurooncol. 2005, 73(2), 125-130; 10. bruna j. et al. – ki-67 proliferative index predicts clinical outcome in patients with atypical or anaplastic meningioma, neuropathology 2007, 27(2), 114-120; 11. nagashima g., et al. – different distribution of cmyc and mib-1 positive cells in malignant meningiomas with reference to tgfs, pdgf and pgr expression, brain tumor pathol, 2001, 18(1), 1-5; 12. nagashima g., et al. – involvement of disregulated c-myc but not c-sis/pdgf in atypical and anaplastic meningiomas, clin neurol neurosurg. 2001, 103 (1),13-18; 13. wrobel g, et al. microarray-based gene expression profiling of benign, atypical and anaplastic meningiomas identifies novel genes associated with meningioma progression". int. j. cancer 2005, 114 (2): 249–256; 14. russ e., castello m. – atypical meningioma spreading via the perivascular spaces american journal of roentgenology, 2002, 178, 3, 768-769; 15. alvarez f., roda j.m., romero m.p et al. – malignant and atypical meningiomas: a reappraisal of clinical, histological and computed tomographic features, neurosurg. 1987, 20(5), 688-694; 16. palma l.et al. – long-term prognosis for atypical and malignant meningiomas: a study of 71 surgical cases, j.neurosurg. 1997,86(5), 793-800; 17. ko k.w. et al. – relationship between malignant subtypes of meningioma and clinical outcome, j.clin neurosci 2007, 14(8), 747-753; 18. joseph e., sandhyamani s. et al. atypical meningioma: a clinicopathological analysis, neurol india 2000; 48:338; 19. kepes jj: comment on mahmood a, caccamo dv, tomecek fj, et al. atypical and malignant meningiomas: a clinicopathological review, neurosurgery 1993, 33:963; 20. mahmood a., caccamo d.v., tomecek f.j., et al. atypical and malignant meningiomas: a clinicopathological review, neurosurgery 1993, 33:955963; 21. yang s.y. et al. atypical and anaplastic meningiomas: prognostic implications of clinicopathological features, j. neurol neurosurg psychiatry. 2008, 79(5): 574-80; 22. joseph e, et al. atypical meningioma: a clinicopathological analysis, neurol india 2000;48:338 romanian neurosurgery (2012) xix 3: 203 209 209 23. buetow m.p. et al. typical, atypical, and misleading features in meningioma, radiographics 1991, 11 (6): 1087–106; 24. jääskeläinen j, haltia m, servo a. atypical and anaplastic meningiomas: radiology, surgery, radiotherapy and outcome, surg neurol 1986, 25:233242; 25. lamszus k. – meningioma pathology, genetics and biology, j. neuropathol exp neurol 2004, 64 (4), 275286; 26. pistolesi s. et al. – the role of somatostatin in vasogenic meningioma associated brain edema, tumori 2003, 89(2), 136-140; 27. dutour a. et al. – expression of somatostatin receptor subtypes in human brain tumors, int.j.cancer 1998, 76(5), 620-627; 28. weber d.c. – adjuvant postoperative high-dose radiotherapy for atypical and malignant meningioma: a phase ii and observation study 2006; 29. delamonte s.m., flickinger j., linggood r.m. histopathological features predicting recurrence of meningiomas following subtotal resection, am j surg pathol 1986, 10:836-843; 30. gay e. et al. – intraoperative and postoperative gamma detection of somatostatin receptors in bone invasive en plaque meningiomas, neurosurgery 2005, 57 (1suppl), 107-113; discussion 107-113; 31. combs s.e. et al. treatment of patients with atypical meningiomas simpson grade 4 and 5 with a carbon ion boost in combination with postoperative photon radiotherapy: the marcie trial, bmc cancer 2010, 10:615 doi:10.1186/1471-2407-10-615. microsoft word 9ciureaavintracranian 68 a.v. ciurea et al intracranian arahnoid cysts in children (acs) intracranian arahnoid cysts in children (acs) a.v. ciurea1, a. tascu1, a. iliescu1, c. mihalache2, f. brehar1, c. palade1, a. spatariu1 1i-st neurosurgical clinic, clinic hospital “bagdasar-arseni” 2sf. andrei emergency county hosp. galati neurosurg departament, galati abstract intracranial arachnoid cysts (acs) represent an extremely common condition in pediatric pathology. with the development of ct scan and especially mri these cysts could be find more constantly. acs are congenital lesions with maximum frequency in middle cranial fossa, followed by supraselar aria , pontocerebelar angle and cranial posterior fossa. these cysts are often incidentally uncovered during a routine neuroimaging investigations for cranio-cerebral trauma or other diseases. the authors present a series of 317 cases in children with acs over a period of 10 years. the authors avocate over the mri evaluation of acs and refering to therapeutic approach it is recomanded only in compresive forms with focal neurologica sings or seizures. are rewiewed therapeutical procedures as: microsurgical fenestration with cystwall excision, endoscopic approach, stereotaxic suction, cyst shunting by cysto-peritoneal procedures. a number of cases remain under observation the surgical treatment beeing unnecesary. the surgical treatment must be carfuly chosen, there is non therapeutical priority. it remains that improved neuroendoscopic methods to improve operator prognosis in acs. keywords: intracranial arachnoid cyst, mri, microsurgical fenestration, endoscopic approach, cyst shunting, increased intracranial pressure, seizures introduction intracranial arachnoid cysts(acs) also known as leptomeningeal cysts, are congenital, benign, nonneoplasic, extraxial lesions. acs arise during development from splitting of arachnoid membrane, and are distinct from posttraumatic cysts and unrelated to infection. bright (1831) describe the intraarahnoidian origin of these lesion as “serous cysts forming in connection with the arachnoid and apparently lying between its layers.”, starkman et all (1958) proposed that the asociated temporal hypoplasia is secandary to cyst expansion and pressure on the temporal operculum. also robinson (1961) the primary source of the problem lay in a congenital failure of temporal lobe development. acording to di rocco et all(2010), acs are developmental defect, that occurs within the first three months of gestational life, in the duplication or splitting of the arachnoid layers, and are related to abnormalities of csf flow. this theory cover the whole development of intracranial arachnoidian cysts. acs are romanian neurosurgery (2011) xviii 1: 68 – 76 69 associeted with other developmental abnormalities of the brain, such as heterotopias. incidence of acs in 5 per 1000 in autopsy series and represent 1% of all intracranial masses. the male: female rate is 4:1, di rocco et all.( 2010). multiple or bilateral arachnoid cysts are unusual, and familial occurrence has been reported in only a few cases. location in 50% intracranian araschnoid cyst involve the sylvian fissure/middle cerebral fossa . rengachary&watanabe (1980) (table i). acording to gallasi et all. (1980) sylvian acs can be classified into three subgoups in connection with cysts dimensions and extensions. gallasi type i: small, biconvex, located in anterior temporal tip, no mass effect, communicates with subarachnoid space.(figure 1). in gallasi type ii: involves proximal and intermediate segments of sylvian fissure, completely open insula gives rectangular shape,partial communication with subarachnoidian space (figure 2). figure 1 mri-aspect of gallasi i left temporal arachnoid cyst in gallasi type iii: involves entire sylvian fissure, midline shift, bony expansion, minimal communication with the subarahnoidian space and surgical treatment usually does not result in efficient expansion of brain (figure 3). figure 2 mri – aspect of gallasi ii left temporoinsular arachnoid cyst figure 3 mri aspect of gallasi iii left cerebral hemisfere arachnoid cyst with middle line shift 70 a.v. ciurea et al intracranian arahnoid cysts in children (acs) other common locations are: cp angle, the quadrigeminal cistern, the retrocerebelar area and the sellar/supraselar region. less commonly acs can develope within the interhemisferic fissure and cerebral convexity (tabel i). clinical findings acs become symptomatic mainly during childhood and adolescence, depending on the location of the cyst not to it’s dimension. asymmetrical macrocranian or a focal bulging of the skull in the temporal region is the most common symptom, headaches, focal neurological symptoms, epilepsy and sings of increased intracranial pressure. in suprasellar acs endocrine disfunctions (60% of cases), hydrocephalus (40% of cases probably due to compression of the third ventricle) and visual impairment are the most common presenting symptoms. natural evolution occuring without sings of: inflammation, trauma or hemorrhage. may be associated with other congenital anomalies (agenesis of the corpus callosum). often do not expand and rarely may spontaneously regress or disappear terapeutical options observation many authors recommend not treating arachnoid cysts that do not cause mass effect or symptoms, regardless of their size and location. fatih e, burkan b, pinar o (2003) multimodal surgical treatment consisting of shunting the cyst into peritoneum, craniotomy (microsurgery) with fenestration and cystwall excision, endoscopic fenestration or stereotactic suction.ciurea et all.( 2010) nowadays endoscopic fenestration represent the main therapeutical option in arachnoid cyst for decompression and restoration of csf circulation. each procedures has advantages and disadvantages as described in table ii. tabel i localization of acs(rengachary&watanabe 1981) location % sylvian fissure 49% cpa 11% supracollicular 10% pineal aria 9% sellar & suprasellar 9% interhemispheric 5% cerebral convexity 4% clival 3% tabel ii surgical treatment options for arachnoid cysts (keyvan abtin and marion l 2010) procedure advantages disadvantages drainage by needle aspiration or bur hole evacuation • siple • quik • high rate of recurrence of cyst and neurologic deficit craniotomy, excising cyst wall and fenestrating into basal cistern • permits direct inspection of cyst • loculated cysts treated more effectively • avoid permanent shunt • allows visualization of bridging vessels • subsequent scarring may block fenestration allowing reaccumulation • signifiant morbidity and mortality romanian neurosurgery (2011) xviii 1: 68 – 76 71 endoscopic cyst fenestration • minimal invasive • avoid permanent shunt • no visualization of bridging vesseleshemoragic risk • fenestration may close shunting of cyst into peritoneum • low morbidity/mortality • low rate of recurrence • patient “shunt dependent” risk of shunt infection patients and methods the authors study 317 cases of arachnoid cysts, admited in 1st neurosurgical clinic, pediatric neurosurgical departament bagdasar-arseni hospital betweem january 2002-january 2010 (8 years). admission criteria was: age betwenn 0 to 16 years old and patients diagnosed, treated and fallowed in 1st neurosurgical clinic. there were excluded all patients over 16 years old or treated in other neurosurgical services. results localisation of acs: sylvian fissure 172 cases(54%), cp angle 38 cases(12%), sellar and suprasellar region 32 cases(10%), pineal area 28 cases(9%), retrocerebelar 28 cases (9%) and interhemisferic 19 cases(6%). (table iii) table iii location of intracranial acs current study location number of cases percentage % sylvian fissure 172 54 cpa 38 12 sellar & suprasellar area 32 10 pineal area 28 9 retrocerebelar 28 9 interhemisferic 19 6 total 317 100 the most common clinical finding was the focal bulging of the skull 62% (196 cases), irritability 51%(162 cases), epilepsy 32%(101 cases) minor focal neurological symptoms 18%(57 cases), cranial nerves palsy 11%(35 cases) and increased intracranial pressure syndrome in 13% (41cases) (tabel iv). table iv clinical findings in current study elected treatment was: (table v) table v elected treatment in current study type of intervention number of cases percentage % observation 40 12,6 unishunt cystoperitoneal dr. 162 51,4 low pressure valv cps 20 6,3 endoscopic procedure 31 9,7 mycrosurgery 64 20,1 total 317 100 72 a.v. ciurea et al intracranian arahnoid cysts in children (acs) observation in 40 de cases(12,6%) case presentation i a 16 years old girl presenting with migrenal syndrome . the mri investigation show a gallasi tip i cyst of the left middle fossa. the elected treatment was observation with mri reevaluation annually. figure 4 mri gallasi i left temporal pole acs observational treatment unishunt cysto-peritoneal drainage 162 cases (51,4%) & low pressure valv cysto-peritoneal shunt in 20 cases (6,3%). case presentation ii a 4 years old girl presenting with epileptic seizures. the preoperative investigation show a gallasi tip ii left middle fossa cyst. the elected treatment was a unishunt cysto-peritoneal shunt. figure 5 mri preoperative aspect of a gallasi ii left temporal acs figure 6 ct scan postoperative aspect of the same cyst as figure 5 after cysto-peritoneal shunting, and the pacient microsurgucal approach with cystwall excision and fenestration in 64 cases (20,1%). case presentation iii a 3 yers old boy presenting with seizures unresponsive to medical treatment. the mri evaluation show a gallasi iii arachnoidian cyst of left cerebral hemisphere. the elected treatment was mycrosurgical approach with cyst wall excision and fenestration. the outcome was a good recovery. romanian neurosurgery (2011) xviii 1: 68 – 76 73 figure 7 preoperative mri aspect of a gallasi iii left cerebral hemisphere acs microsurgucal approach with cystwall excision and fenestration is recommended as an initial approach to avoid shunting shunt independence an important surgical goal. keyvan abtin & marion l. walker (2007) endoscopic procedure in 31 cases (9,7%) figure 8 postoperative ct scan aspect of the same cyst as in figure7 after microneurosurgical treatment figure 9 preoperative mriaspect of a supracollicular giant acs case presentation iv a 1 year old girl presenting with hypotonic syndrome and psymotor retardation. the mri examination show a supracollicular giant acs, the elected treatment was endoscopic fenestration. 74 a.v. ciurea et al intracranian arahnoid cysts in children (acs) figure 10 postoperative ct scan aspect of the same cyst as in figure 9, after endoscopic fenestration, and the pacient discution intracranial arahnoid cysts are mentioned throughout the specialised literature. the discovery of such cysts in almost all cases is done when is made an ct scan or mri exam of the brain for other diseaze of nervous sistem. once the intracranial arachnoidian cyst is fount, one has to establish very careffuly the clinical findings, neuroimaging evaluation and after that we may proceed to a posible surgical treatment. there are 2 histological types of acs: 1. “simple arachnoid cysts”: arachnoid lining with cell that appear to be capable of active csf secretion. middle fossa cysts seem to be excusively of this type. 2. cysts with more complex lining which may also contain neuroglia, ependyma and other tissue types. mayr u. aicher f, bauer g et all (1982) many authors recommend observation and monitoring of these cysts on mri. the rarity of expanding arachnoid cysts makes frequent serial neuroimaging unnecessary and cost ineffective. the recommended follow-up neuroimaging is at one year. in case of a simptomatic cyst by neurologica focal deficit, epilepsy or reised icp the best surgical solution to release pressure on the cerebral structure has to be found. for a long time shunting mettods were prefered. but with the apperence of shunt complication this mettods where abandoned. microneurosurgycal approach of fenestration are very effective but they require latge opening of basal cistern. nowadays as miminaly invasic procedure the endoscopic procedures has become increasingly popular ”the procedure of choice” and has been used to decrease the number of shunts. hopf n j, perneczky a (1998) as effective and safe and less invasive but great care in needed to avoid bleeding -acs are associated with large bridging veins. f. di rocco et all (2010) intraoperative ultrasound or frameless romanian neurosurgery (2011) xviii 1: 68 – 76 75 stereotaxy, especially with intravenous contrast enhanced ct or mr imaging guidance, is helpful in choosing the trajectory of the bridging veins. main limitation is anatomical: due to the relation of the cyst with the basal cisterns and the temporal lobe displacement. c di rocco et all (2010) conclusions acs are very frequent congenital intracranial malformation. more than 80% of acs are incidental findings being completely asymptomatic. treatment is recommended only in symptomatic acs by focal neurological deficits, skull deformities, signs/symptoms related to increased icp and seizures not responsive to medical treatment. current series of 317 cases constitute a uniform cohort because cases are diagnosed, treated and followed in a single pediatric neurosurgical service. choice of treatment was performed very carefully to obtain the best clinical outcome and imaging properly, reducing the size of the cyst. ciurea at all (2010) all cases requiring follow predominantly by mri to monitor the possible expansion of the cerebrale structures.in a significant number of cases the expected expansion did not occur because of the cyst membranes were not enough fenestrated into basal cisterns and csf cisculatia not restored properly. in these cases depending on clinical aspects the therapeutical process can be repeated, minimally invasive by endoscopy. basically we can say that there is no “best treatment” in acs, and each case must be analyzed separately. ciurea et all (2010) abbreviations: acs intracranial arachnoid cysts csf cerebro spinal fluid cpa cerebro-pontine angle cpd cisto-peritoneal drenage mri magnetic resonance imaging ct computer tomography icp intracranian pressure references 1. anne g. osborn: arachnoid cyst, prymary nonneoplastic cysts. osborn (2010) 7: 6-9 2. barbara spacca, jothy kandasamy et all : endoscopic treatment of middle fossa arachnoid cysts: a series of 40 patient treated endoscopically in two centres. in childs nerv syst(2010) 26: 163-172 3. bright r: serous cysts of the arachnoid.report of medical cases vol 2, part 1, london: longmans (1831) 4. catala m, poirier j. arachnoid cysts: histologic, embryologic and physiopathologicreview. rev neurol paris (1998) 154:489–501. 5. ciurea a.v et all: treatment options in intracranial arachnoid cysts: 7th national congres of romanian society of neurosurgery, october 2010 cluj napoca romania pub in romanian neurosurgery (2010) 4 6. c. di rocco, l. d’angelo,l. massimi –arachnoid cysts in esential practice of neurosurgery access publishing co. ltd (2010) 1235-1244 7. concezio di rocco : sylvian fissure arachnoid cysts: we do operate on them but should it be done? in childs nerv syst (2010) 26: 163-172 8. fatih ersay deniz, burkan bilginer, pinar ozirik: araknoid kist he birlikte eozinofilik graniilom: vaka sunumu turkish neurosurgery (2003) 13: 118-121, 9. federico di rocco, syril r. james, thomas roujeau, stephanie puget, christian sainte-rose , michel zerah: limits of endoscopic treatment of sylvian arachnoid cysts in children. childs nerv syst (2010) 26: 155-162 10. gallasi e, tohnetti f, gaist g. et al,:ct scan and metrizamide ct cisternography in arachnoid cysts of the middle fossa: classification and pathophysiological aspects. suerg neurol. (1982) 17:363-369 11. hopf n j, perneczky a: endoscopic neurosurgery and endoscope assisted microneurosurgery for the treatmetn of intracranial cyst. neurosurgery (1998) 43 1330-7. 12. keyvan abtin and marion l. walker: congenital arachnoid cysts and dandy walker complex. in albright principles and practice of pediatric neurosurgery (2007) 7:125141 76 a.v. ciurea et al intracranian arahnoid cysts in children (acs) 13. rengachary ss, watanabe i. ultrastructure and pathogenesis of intracranial arachnoid cysts. j neuropathol exp neurol. (1981) 40:61-83. 14. pierre-kahn a, capelle l, brauner r, et al: presentation and management of suprasellar arachnoid cysts: rewiew of 20 cases. j neurosurg (1990) 73:355-9 15. mayr u. aicher f, bauer g et all: supratentorial extracerebral cyst of the middle cranial fossa: a report of 23 consecutive cases of so colled temporal lobe agenesis syndrome. neurochirurgia(1982) 25: 51-6. 16.rao g. et all expansion of arachnoid cysts in children report of two cases and review of the literature. j neurosurg (pediatrics 3) (2005)102:314– 317. 17. robinson r.g: congenital cysts of the brain: arachnoid malformations.prog neurol surg( 1971) 4:133–174. 18. robinson r. g: the temporal lobe agenesis syndrome. brain (1964) 88:87–106. 19. russon. et all: spontaneous reduction of intracranial arachnoid cysts: a complete review british journal of neurosurgery, october (2008), 22(5): 626–629 20. tamburrini g. et all: sylvian fissure arachnoid cysts: a survey on their diagnostic workout and practical management; childs nerv syst (2008) 24:593–604 21. w. n. al-halou, c.o. maher et all. the natural history of pineal cysts in children and young adults. in jurnal neurosurg pediatrics(2010) 5: 162-166 a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 438-442 doi: 10.33962/roneuro-2019-069 www.journals.lapub.co.uk/index.php/roneurosurgery extremely rare complication of granulomatosis with polyangiitis. aneurysmal subarachnoid haemorrhage oguz baran1, selçuk ozdogan1, nail demirel1, sevket evran1, hanife gulden duzkalir2, ayhan kocak1 1 department of neurosurgery, haseki research and training hospital, istanbul, turkey 2 department of neurosurgery, kartal dr. lutfi kirdar research and training hospital, istanbul, turkey 3 department of neurosurgery, istanbul research and training hospital, istanbul, turkey 4 department of radiology, istanbul research and training hospital, istanbul, turkey abstract the systemic vasculitis of the small-medium arteries, arterioles, venules and rarely large arteries that involves respiratory system and kidneys was defined as granulomatosis with polyangiitis (gpa) disease by wegener in 1936. intracranial aneurysms and subarachnoid haemorrhage (sah) are extremely rare complications of gpa and our case will be the 2nd case treated with clipping aneurysm and the 11th case with subarachnoid haemorrhage in the literature. a 43-year-old man presented to the emergency room with a severe headache and was admitted for further evaluation. he had gpa diagnosis 14 years ago with cytoplasmic anti-neutrophil cytoplasmic antibody (c-anca) and pr3-anca positive laboratory tests and kidney biopsy. sah was seen on cranial computed tomography (ct) images. then cerebral digital substraction angiography (dsa) performed and right middle cerebral artery aneurysm exposed. aneurysm was clipped without any complication. intracranial aneurysms and sah are extremely rare complications of gpa. gpa related aneurysmal sah is an exceptional condition in neurovascular pathology. monitoring patients with gpa for sah must be remembered and kept in mind as a diagnosis. introduction the systemic vasculitis of the small-medium arteries, arterioles, venules and rarely large arteries that involves respiratory system and kidneys was defined as granulomatosis with polyangiitis (gpa) disease by wegener in 1936 (1). wegener defined the disease with the findings that includes focal necrotizing glomerulonephritis, respiratory tracts' keywords granulomatosis with polyangiitis, complication, subarachnoid haemorrhage, aneurysm corresponding author: oguz baran department of neurosurgery haseki research and training hospital istanbul, turkey oguzbaran@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 439 extremely rare complication of granulomatosis with polyangiitis necrotizing granulomatous vasculitis and systemic vasculitis as a diagnostic triad (1). inflammatory and autoimmune mechanisms are discussed for the pathogenesis of gpa but it still remains controversial. the involvement of central nervous system (cns) has been reported in 7-11% whereas the cases with aneurysmal subarachnoid hemorrhage (sah) are excepted (2). clinical symptoms with positive proteinase 3 (pr-3) antineutrophil cytoplasmic antibody (anca) laboratory test shows both high sensitivity and specificity in diagnosis of gpa. intracranial aneurysms and subarachnoid hemorrhage are extremely rare complications of gpa. previously, only 10 cases of sah related to gpa have been reported in the literature. only 1 of them was treated with surgical aneurysm clipping. case report a 43 year old man presented to the emergency room with a severe headache. no pathological findings were detected in the neurological examination. he had no history of hypertension or a cardiac disease. cranial computed tomography (ct) was performed and the patient was diagnosed with subarachnoid hemorrhage (figure 1a). while the patient was preparing for cerebral digital substraction angiography (dsa), his neurological examination suddenly worsened. the patient was intubated and cranial ct performed again (figure 1b). cerebral dsa was performed to the patient who had bleeding again and right middle cerebral artery aneurysm exposed (figure 1c, d). fi̇gure 1 a. preoperative cranial ct image showing sah; b. intracerebral hemorrhage is seen after re-bleeding; c-d. preoperative dsa images showing right middle cerebral artery aneurysm. it was learned that the patient was followed up with the diagnosis of gpa. he applied to hospital with the symptoms of fever, coughing and hemopthisia in 2003. in his examination, bilateral arthritis on lower extremities, palpable purpura, episcleritis in the eyes were present. in thorax ct, consolidation areas and 10 cm cavitation were detected in the right lung. urine test showed proteinuria and kidney biopsy reported as gpa. laboratory tests revealed cytoplasmic anti-neutrophil cytoplasmic antibody (canca) and pr3-anca positivity. as a result of all tests, steroid and cyclophosphamide treatment was given to the patient. in 2015, the patient had a tonic-clonic seizure in the bathroom and was found unconscious. he had homonim hemianopsia, left facial paralysis and hemiparesia. there was no hemorrhage on cranial ct. the diffusion weighted magnetic resonance imaging (dw-mri) showed an acute ischemia in the right temporal-occipital and frontobasal areas. mriangiography had been found normal. fi̇gure 2 a-b. cranial ct axial sections in the early and late postoperative periods; c-d. postoperative dsa images showing severe vasospasm and right middle cerebral artery aneurysm clipped without remnant. 440 oguz baran, selçuk ozdogan, nail demirel et al. decompressive craniectomy was performed and right middle cerebral artery aneurysm was clipped without any complication. external ventricular drainage was placed due to hydrocephalus. cranial ct was performed in the early and late postoperative periods (figure 2a, b). postoperative dsa was performed to the patient. the aneurysm was clipped without remnant, but serious vasospasm was observed (figure 2c, d). chest x-ray and thorax ct showed noduler infiltrations (figure 3a, b). the patient died on the 26th postoperative day due to respiratory tract infection and severe vasospasm. fi̇gure 3 a. x-ray chest graphy and; b. thorax ct axial section showing noduler infiltrations in medial region. discussion gpa is typically diagnosed with by activated neutrophils accumulations, vasculitis, formation of microabscess, granulomas, glomerulonephritis and necrosis in pathological examination (3). wegener defined the disease with the findings that includes focal necrotizing glomerulonephritis, respiratory tracts' necrotizing granulomatous vasculitis and systemic vasculitis as a diagnostic triad (1). in 1990, the american college of rheumatology announced diagnostic criterias to classify gpa (4). classical diagnostic criterias were an abnormal sediment of urine, abnormal findings like cavities, nodules and infiltrations on a chest radiograph, oral or nasal mucosal ulcers; and biopsy concluded with granulomatous inflammation. minimum two of the four criterias requested for the diagnosis of gpa and hemoptysis is added to the traditional format so classification tree was defined (4). classification tree was reported more specific and sensitive than the traditional format (4). neurologic involvement is rarely seen in gpa and reported as ranging from 22% to 54% in the literatüre (5). drachman et al. have discussed three major mechanisms which could be summarized as vasculitis of cns, intracranial granuloma and extracranial granuloma invasions on causes of cns involvement in gpa (6). seror et al. reported cns involvement of gpa with six patients that three of them with pituitary involvement, two patients with pachymeningitis, and last patient with cerebral vasculitis (7). the cns involvements were attributed to gpa because they were diagnosed at disease onset or flare and also extracranial involvements, other cns disease etiologies had been excluded, and/or they had attributed to sustained immunosuppressive therapy. cns vasculitis was reported as the cause of intracranial hemorrhages, transient ischemic strokes, cerebral infarctions, venous or arterial thrombosis, encephalopathy, ischemic myelopathy, seizures, dementia, altered consciousness, cortical blindness, visual loss and cognitive impairment (3, 811). because of the rarity of cns involvements in gpa, no specific treatment suggestions exist for management of them except combining cyclophosphamide and corticosteroids as systemic gpa therapy (12, 13). subarachnoid hemorrhage in gpa has been rarely reported in the literature (table 1) (2, 6, 8, 1419). only two cases presented with subarachnoid hemorrhage and exposed the aneurysms with cerebral angiography. takei et al. confirmed an anterior choroid artery aneurysm and marnet et al. 441 extremely rare complication of granulomatosis with polyangiitis reported an anterior communicating artery aneurysm (2, 16). our case is 3rd as the middle cerebral artery aneurysm. takei et al. had clipped the aneurysm as a first case, but marnet et al. could not have clipped the aneurysm because of a vasculitis flare-up of disease (2, 16). so our case is the 2nd case of subarachnoid hemorrhage treated by clipping the aneurysm. onodera et al. reported an incidentally found carotis aneurysm without subarachnoid hemorrhage in gpa but they made baloon occlusion with endovascular procedure for treatment (5). survival rate is very low for the aneurysms of gpa but we can not evaluate the reason of it because the information about patients is limited due to fast deterioration (table 1). author age gender clinical presentation diagnosis treatment result tuhy et al. (14) 39 m fatigue, cough, arthralgias, weight loss lumbar puncture and autopsy: sah medical death drachman et al. (6) 30 m chronic rhinitis, persistent skin ulcers autopsy: sah n/a death venning et al. (15) 50 m epistaxis, nasal discharge, nasal polyp ct: sah medical recovery venning et al. (15) 36 m weight loss, hemoptysis, night sweats lumbar puncture: sah medical recovery cruz et al. (8) 71 m subarachnoid hemorrhage lumbar puncture and ct: sah medical recovery takei et al. (16) 34 m recurrent nasal obstruction ct and cerebral angiography: aneurysm clipping recovery nardone et al. (17) 78 f dyspnea, fever,hemopty sis ct: intracerebral hemorrhage and sah medical death fomin et al. (18) 17 m cough, fever ct&mri: sah and intravent. hemorrhage medical death miles et al. (19) 74 f paresthesias, diplopia, dizziness ct: sah and intraventricula r hemorrhage medical death marnet et al. (2) 63 f subarachnoid hemorrhage cerebral angiography: aneurysm medical follow-up table 1. cases of subarachnoid hemorrhage with gpa in the literature 442 oguz baran, selçuk ozdogan, nail demirel et al. takei et al. reported the possible mechanism for the aneurysmal bleeding with gpa may have involved the anca-cytokine sequence, with activated polymorphonuclear neutrophils adhering to the endothel of the aneurysm origin, and with polymorphonuclear neutrophils degranulation liberating pr-3 and human leukocyte elastase (hle) (16). then pr-3 caused apoptosis of arterial smooth muscle cells. the destruction of the internal elastic lamina may also attributed to aneurysm formation and rupture (16). conclusion intracranial aneurysms and subarachnoid hemorrhage are extremely rare complications of gpa. gpa related aneurysmal sah is an exceptional condition in neurovascular pathology. as inflammatory mechanisms are involved in the pathogenesis of aneurysm, the vasculitis flare-up could account for this sah. surgical clipping of aneurysm could be done for the treatment of aneurysmal subarachnoid hemorrhage in gpa patients. finally, monitoring patients with gpa for sah must be remembered and kept in mind as a diagnosis. references 1. wegener f. über generalisierte, septische gefässerkrankungen. verh dtsch ges pathol 1936;29:202– 9. 2. marnet d, ginguené c, marcos a, cahen r, mac gregor b, turjman f, vallée b. wegener granulomatosis and aneurysmal subarachnoid hemorrhage: an insignificant association? neurochirurgie 2010;56(4):331-6. 3. hoffman gs. wegener’s granulomatosis. curr opin rheumatol 1993;5:11–7. 4. leavitt ry, fauci as, bloch da, michel ba, hunder gg, arend wp, calabrese lh, fries f, lie jt, lightfoot rw. the american college of rheumatology 1990 criteria for the classification of wegener’s granulomatosis. arthritis rheum 1990;33(8):1101–7. 5. onodera h, hiramoto j, morishima h, tanaka y, hashimoto t. treatment of an unruptured fusiform aneurysm of the internal carotid artery associated with wegener's granulomatosis by endovascular balloon occlusion. case report. neurol med chir 2012;52(4):216-8. 6. drachman da. neurological complications of wegener’s granulomatosis. arch neurol 1963;8:45–55. 7. seror r, mahr a, ramanoelina j, pagnoux c, cohen p, guillevin l. central nervous system involvement in wegener granulomatosis. medicine (baltimore) 2006;85(1):54–65. 8. cruz dn, segal as. a patient with wegener’s granulomatosis presenting with a subarachnoid hemorrhage: case report and review of cns disease associated with wegener’s granulomatosis. am j nephrol 1997;17:181–6. 9. mattioli f, capra r, rovaris m, chiari s, codella m, miozzo a, gregorini g, filippi m. frequency and patterns of subclinical cognitive impairment in patients with anca-associated small vessel vasculitides. j neurol sci 2002;195:161–6. 10. reinhold-keller e, de groot k, holl-ulrich k, arlt ac, heller m, feller ac, gross wl. severe cns manifestations as the clinical hallmark in generalized wegener’s granulomatosis consistently negative for antineutrophil cytoplasmic antibodies (anca). a report of 3 cases and a review of the literature. clin exp rheumatol 2001;19:541–9. 11. sivakumar mr, chandrakantan a. a rare case of stroke in wegener’s granulomatosis. cerebrovasc dis 2002;13:143– 4. 12. fauci as, haynes bf, katz p, wolff sm. wegener’s granulomatosis: prospective clinical and therapeutic experience with 85 patients for 21 years. ann intern med 1983;98:76–85. 13. reinhold-keller e, beuge n, latza u, de groot k, rudert h, nolle b, heller m, gross wl. an interdisciplinary approach to the care of patients with wegener’s granulomatosis: long-term outcome in 155 patients. arthritis rheum 2000;43:1021–32. 14. tuhy je, maurice gl, niles nr. wegener’s granulomatosis. am j med 1958;25:638–46. 15. venning mc, burn dj, bashir sh, deopujari ce, mendelow ad. subarachnoid haemorrhage in wegener’s granulomatosis, with negative four vessel angiography. br j neurosurg 1991;5:195–8. 16. takei h, komaba y, kitamura h, hayama n, osawa h, furukawa t, hasegawa o, iino y, katayama y. aneurysmal subarachnoid hemorrhage in a patient with wegener’s granulomatosis. clin exp nephrol 2004;8(3):274–8. 17. nardone r, lochner p, tezzon f. wegener's granulomatosis presenting with intracerebral hemorrhages. cerebrovasc dis 2004;17(1):81-2. 18. fomin s, patel s, alcasid n, tang x, frank e. recurrent subarachnoid hemorrhage in a 17 year old with wegener granulomatosis. j clin rheumatol 2006;12(4):212-3. 19. miles jd, mcwilliams l, liu w, preston dc. subarachnoid hemorrhage in wegener granulomatosis: a case report and review of the literature. cns spectr 2011;16(5):121-6. microsoft word 1editorpage12011 editor’s page january – march 2011 st.m. iencean, editor clinical emergency hospital “prof. dr. nicolae oblu” iasi, romania e-mail: mirceasteffan@yahoo.com romanian neurosurgery 2011 this first issue of romanian neurosurgery for 2011 allows us to announce you that our journal has maintained for this year its b+ category given last year by national council for scientific research in higher education (cncsis); also from january our journal was included in directory of open access journals ( doaj ), an international database allowing increase the international visibility of romanian neurosurgery. (www.doaj.org/doaj?func=bytitle&hybrid=&query=r ) we have fulfilled our promise to publish some articles in advance: first online articles on our site (www.roneurosurgery.eu) before the printed issue and also this year we will continue the quarterly publication of romanian neurosurgery. this january march issue starts with an interesting case report of a patient operated in her childhood by professor dimitrie bagdasar, 72 years ago, allowing a brief historical overview of the one who was the pioneer of modern neurosurgery in romania. a comprehensive and extensive review of neuroprotection in traumatic brain injury is presented by g. onose et al. showing its importance for reductions in the extent of brain damage and consequent significant neurological recovery after traumatic brain injury. several important original articles are included on different topics. pendefunda presents a retrospective study about transcranial doppler exploration and vasodilators therapy in acute ischemic stroke of 328 patients and shows a highly significant correlation between the increased rate of risk factors for the early outcome of an ischaemic stroke and the pursuit of the reactivity index to prevent a major stroke. abrudan, florian et al. studied the surgery of high grade gliomas based on 433 cases of high grade cerebral glioma operated during 10 years at neurosurgery in cluj and this study confirms other results from literature that long term postoperative outcome after radical surgical resection are better than the results of either partial resection or simple biopsy. ciurea, tascu et al. have analyzed thirty one cases of colloid cysts operated and they concluded that the microsurgical approach is the best treatment for third ventricular colloid cysts because of the possibility of total resection of the cyst, good control of the bleeding source during the procedure and a better exposure of the anatomical landmarks compared with the endoscopic approach. an original article of gramada, dumitrescu et al. shows which are the steps to get the ethiological diagnosis of brain metastases whose origin is unknown and ciurea, tascu et al present a series of 317 cases in children with intracranial arachnoid cysts over a period of 10 years and conclude that there is no best treatment in intracranial arachnoid cysts, and each case must be analyzed separately. there are also two interesting case reports: a rare case of severe craniocerebral trauma with penetrating head injury (iordache et al.) and two case diagnosed with direct carotid-cavernous fistula and glaucoma (petraru et al). this issue ends with selected abstracts from the 3rd annual conference “ortho posturo gnosis” (rehabilitative medicine) taken place in iasi, december, 2010. the editorial office hope you enjoy reading the content of this first issue for 2011. romanian neurosurgery (2011), xviii, 1, 5 15chaurasiams_posttraumatic 124 chaurasia et al post traumatic glioma post traumatic glioma – an association questioned i.d. chaurasia, arpan chaudhary, nitin verma, ishant kumar chaurasia, mahim koshariya, m.c. songra department of surgery, gandhi medical college, bhopal, india abstract: post traumatic glioma has been a matter of debate. few reports favor its occurrence in previous head injury scar, subsequently developing into glioma. here we report a case of young patient presented with headache, seizures and gradual loss of vision. on investigation found to have brain tumor. patient had head injury occurred 3 yrs back. it fulfills all the criteria required to establish traumatic origin, further supporting the association. key words: post traumatic glioma, brain tumor, head injury introduction cns tumors occur due to various reasons, however causal association to previous head trauma has been questioned. recently many authors have reported occurrence of gliomas in scar of old brain injury patients [1,2]. here we are reporting one case of post traumatic glioma meeting all criteria, further supporting the association. case a 35 yrs old young healthy male patient presented neurosurgery opd with complaints of headache for 3 yrs, generalized seizures for 2 yrs, vomiting and gradual vision loss for 1 year. patient had history of rta with head injury 3 yrs back, loss of consciousness was present, for which he was hospitalized. at the time of admission patient was conscious, oriented and bilateral pupils reacting to light. vision was 12/6 in right eye and 9/6 in left eye with bilateral papilloedema present. left sided hemiparesis was found with muscle power 3/5. treatment patient was initially put on iv mannitol, steroid and anticonvulsant measures. ct head showed space occupying lesion involving right frontal lobe extending anteriomedially with surrounding edema and compression of anterior horn of lateral ventricle. there was a small area anteriolateral to sol suggestive of previous scar with glioma (figure 1). mri head revealed ill defined, complex soft tissue mass lesion showing cystic as well as solid component within right frontal lobe cortical and subcortical region with few hyperintense areas on t1 images. there was a thin layer of gliosis seen in anterior basal part of mass, along with diffuse cerebral edema (figure 2). romanian neurosurgery (2015) xxix (xxii) 1: 124 126 125 figure 1 ct head showing space occupying lesion involving right frontal region head with adjacent scar figure 2 mri head showing mass occupying right frontal lobe with solid and cystic component and a layer of gliosis over anteriobasal part representing an old scar right frontal craniotomy was done. tumor was found in frontal area, grayish in color, moderately vascular and soft suckable in consistency. excision of tumor was done. follow up postoperatively, mannitol, anticonvulsant and steroids were continued for 10 days and patient made quick recovery with vision started improving 4th day onwards and hemiparesis resolved gradually. headache and vomiting were also subsided. biopsy revealed diffuse fibrillary astrocytoma. patient referred to radiotherapy dept for further treatment. at 6 months of follow up, patient was doing well. discussion the relationship between the glioma and head injury has been debated for years. though there are few cases reported in literature which showed the association of development of glioma following head trauma. zulch described the following criteria for the acceptance of a causal relationship between trauma and the onset of cerebral tumors [3]: 1. the patient must have been in good health before suffering the head injury. 2. the blow must be severe enough to cause brain contusion and a secondary reparative process. 3. the location of the impact and the tumor should correspond exactly one to the other. 4. there should be a time interval between trauma and the appearance of the tumor of at least 1 year, a longer latent period increasing the likelihood of a causal relationship. 5. the presence of the tumor must be proved histologically. 6. trauma should consist of an external force. 126 chaurasia et al post traumatic glioma manuelidis in 1972 added three more criteria [4]: 1. the traumatized brain must also be proved histologically. 2. bleeding, scars and edema secondary to the presence of the tumor must be clearly differentiated from that caused by trauma. 3. tumor tissue should be in direct continuity with the traumatic scar, not merely in its vicinity or separated by a narrow zone of healthy or slightly altered brain tissue. the recent reports showed the ct scans at the time of the trauma demonstrating significant injury and the follow-up scans demonstrating tumor at the same site [5]. with the routine use of ct and mri, some of the pathologic criteria can be replaced or supplemented by imaging criteria. ct/mri, which elegantly reveal the severity and location of the traumatic brain injury and the subsequent formation of a neoplasm at the same site, can provide convincing evidence for the traumatic causation of a brain tumor [6]. pathogenesis of post-traumatic glioma is still obscure. regenerative and scarring processes following trauma have been thought play some role to stimulate neoplastic transformation. tumor should arise from old trauma scar for a causal relationship to establish [7]. if the tumor arises at different site of the old lesion, should be coincidence [8]. however prospective studies following head injury failed to establish a direct association. conclusion • an association between head trauma and brain tumor cannot be ruled out. • brain tumor can occur several years after head injury at the site of previous scar. • for accurate diagnosis, zulch’s and manuelidis criteria should meet along with space occupying lesion in ct or mri near old scar. • treatment requires surgical excision along with anticonvulsant and antiedema measures. • in a follow up case of head injury with additional neurological symptoms, possibility of tumor should be kept in mind. correspondence i.d. chaurasia chaurasiaid@gmail.com address: department of surgery gandhi medical college bhopal 462001 phone no. +91755-4224452 references 1. salvati m, caroli e, rocchi g, frati a, brogna c, orlando er: post traumatic glioma. report of four cases and review of the literature. tumori, 90: 416-419, 2004 2. anselmi e, vallisa d, berte r, et al. post-traumatic glioma: report of two cases. tumori. 2006; 92:175-7. 3. zulch kj. brain tumors: their biology and pathology, 2nd edition. new york, usa: springer verlag publisher; 1965: 51-58. 4. manuelidis eh. glioma in trauma. in: minckler j, ed. pathology of the nervous system. new york, usa: mcgraw hill publisher; 1972. 5. henry pt, rajshekhar v: post-traumatic malignant glioma: case report and review of the literature. br j neurosurgery. 2000; 14:64-7. 6. bo zhou, weiguo liu: post-traumatic glioma: report of one case and review of the literature. int. j. med. sci.2010, 7. 7. di trapani g, carnevale a, scerrati m, et al. post traumatic malignant glioma. report of a case. ital j neurol sci. 1996; 17:283-286. 8. hu xw, zhang yh, wang jj, et al. angiocentric glioma with rich blood supply. j clin neurosci. 2010; 17(7): 917-8. 2_iacobg_averyrare romanian neurosurgery (2015) xxix 3: 239 246 239 a very rare, petro-clival, neurothekeoma tumor. case report g. iacob1, silvia tene1, mariana iuga1, g. simion2 1neurosurgery clinic university hospital, bucharest, romania 2department of pathology – university hospital, bucharest, romania abstract: known as nerve sheath myxoma too, neurothekeoma are benign tumors, usually arise in the skin of the head, neck region and upper extremities, in young females. cerebral neurothekeoma are very rare, a few cases were already described in the parasellar area, in the middle cranial and posterior fossa. we present a petro-clival neurotekoma. a 78-year-old male was admitted for two years left fronto-temporal headache completed in the last 6 months with left trigeminal v1 neuralgia, left facial hypoesthesia, diplopia, swallowing disorders for liquid foods, balance disorders. from his medical records we noticed: stage 2 chronic kidney disease, hypertension, prostate adenoma, dyslipidemia hypercholesterolemia. the mri showed a macronodular petroclival mass in hiper t2, hipo t1, flair iso signal; normal cerebral angiography. the patient was operated on using a left retrosigmoid, retromastoidian approach. a 4/3/3 cm tumor, gray, encapsulated, soft consistency, partially cystic, less bleeding, attached to the dura, displacing the basilar artery and brain stem controlateral, encasing the trigeminal nerve. the tumor was totally removed with a good postop evolution. six months follow up he had no more facial pain, but only persistant left facial hypoesthesia. histologically the tumor had lobular appearance with spindle or stellate cells embedded in abundant myxoid background. the tumor cells were diffusely positive for s100, pgp9.5’, cd 34” positive in vessels, ki67’positive in 5%. cranial mri performed one month after surgery did not show any residual tumor. also known as nerve sheath myxomas, neurothekoma are rare benign tumors. for intracranial neurothekoma surgical indication is mandatory key words: intracranial neurothekoma, petro-clival tumor, nerve sheath myxoma. introduction neurothekeoma is a benign, predominantly cutaneous tumor, of probable nerve sheath origin (1-7), quite common, presented as a solitary nodule in the head (5), oral cavity (7), hypopharynx (8), tongue (9), maxilla (10), breast (11), neck shoulders or upper limbs (12), peripheral nerve median nerve (13), spinal intradural (6)(14)(15), even cervical intramedullary (14). the intracranial localization was reported in only few cases (16)(17): disposed in the pituitary area (18), medium (19) and posterior fossa (20)(21): cerebelopontine angle (22), pons (23). after our knowledge the current report is first in world literature with neurothekeoma located petro-clival. case report a 78-year-old male was admitted in our clinic for two years left fronto-temporal headache completed in the last 6 months with 240 iacob et al a very rare, petro-clival, neurothekeoma tumor left trigeminal v1 neuralgia (cvasi constant, without benefit from analgesics), left facial hypoesthesia, diplopia, swallowing disorders for liquid foods, balance disorders. from his medical records we noticed: stage 2 chronic kidney disease, hypertension, prostate adenoma, dyslipidemia, hypercholesterolemia. biochemical investigations showed too: a slight nitrate retention: urea 74 mg/dl, creatinina 1.7 mg/dl and slight hypopotasemia 3,4 mmol/l. axial, coronal, and sagittal mris of the head displayed: an extranevraxial petro-clival mass, well delineated, with heterogeneous tissue component with peripheral cystic component, hypointense on t1-weighted images, hyperintense on t2-weighted images with heterogeneous enhancement following contrast agent administration, measuring 33 mm transverse ø, 23 mm antero-posterior ø and 37 mm cranio – caudal ø, with distortion of the brain stem, left nerves vii, vi, iii; also the adjacent arteries: basilar trunk, superior left cerebellar artery and posterior cerebral artery (figure 1). important periventricular demyelinating lesions and cerebral atrophy associated, dilatation of ventricular system with periventricular lucency. a b c d figure 1 preoperatory mri: a-c axial, d coronal images showing the extranevraxial petro-clival tumor mass, with heterogeneous tissue component and peripheral cystic component, distorting the brain stem, left nerves vii, vi, iii, the adjacent arteries: basilar trunk, superior left cerebellar artery and posterior cerebral artery using a left retromastoidian, retrosigmoidian approach an encapsulated, gray tumor was discovered in the petro-clival area. this tumor has soft consistency, partially cystic, mixed with areas of fibrotic tissue, less bleeding, attached to the dura, encasing trigeminal nerve, displacing the basilar artery and brain stem controlateral. the tumor was totally removed. postoperatory evolution was uneventfull; six months follow up he had no more facial pain, but only persistant left facial hypoesthesia. histological and immunohistochemical staining was performed. histologically the tumor was encapsulated by a thin fibrous connective tissue and composed by fusiform and stellate cells, with loose, pale, myxoid stroma; arranged in ovoid lobules of varying sizes separated by fibrous septae; rare high cell density areas presenting cells with central monomorphic nuclei showing spindle-shaped extensions and clear peripheral cytoplasm were observed. no mitosis and mild nuclear pleomorphism was noted (figure 2). a b romanian neurosurgery (2015) xxix 3: 239 246 241 c d figure 2 a. col. h.e. 10 x 4 overview image: low density cells, arranged in lobules of varying sizes, separated from conjunctival vascular septa; fusiform and stellate monomorphic nuclei with schwanoid aspect b. col h.e. 10 x 10: tumor cells lobules arranged in a lax, pale, myxoid background, separated by conjunctival vascular septa with inflammatory elements c. col h.e. 10 x 20 : lax, mixoid, peripheric cellular tumoral areas and central tumoral area with antoni b schwannoma type appearance d.col h.e. 10 x 40 detail: “schwanoid” tumoral area on immunohistochemical studies diffuse positive staining of the cells with s-100 and vimentin was observed. glial fibrillary acidic protein (gfap), epithelial membrane antigen (ema), cytokeratin antibody (mnf116) and neurokinin 1 (nk1) were negative. cd34 was positive in vessels and ki67 was positive in 5% of cases. these histological and immunohistochemical findings are considered characteristic of neurothekeoma, with low relevant aggression proliferation (figure 3) after operation facial pain progressively diminuished; balance disorder and swallowing disorders for liquid foods disappear. a 5 day postop mri demonstrate important reduction of mass effect on brain stem, no parenchimal tumor mass anteriorly described (figure 4) six months follow up he had only persistent left facial hypoesthesia. no chemotherapy or radiation was used in this case. a b figure 3 immunohistochemichal stains: a. s100, 4 x 10: diffuse positivity in tumoral cells and negativity in vascular structures b. gfap, 4 x 10: negative, proving no glial origin a b figure 4 postoperatory mri: axial and sagital t1 showing important reduction of mass effect on brain stem, without tumoral remnants discussion neurothekeoma is a benign, predominantly cutaneous neoplasm of presumed neural sheath origin, usually arising in the skin of the scalp, nose, orbital region especially eyelids, cheeks, paranasal sinuses, oral mucosa hypopharynx, chin, neck, the upper trunk, breast also in spinal topography of children and young adults as a flesh-colored solitary nodules solitary nodule with overlying erythema on cutaneous examination. the lesions range in size from about 0.5 cm to most commonly less than 2 cm in diameter; mean age of 25 years – but may occur at any age, 242 iacob et al a very rare, petro-clival, neurothekeoma tumor with a female preponderance, the male to female ratio is approximately 1:4,3 (1)(3)(17). this tumor was initially described by harkin and reed (2) in 1969 by the name “nerve sheath myxoma”. in 1980, gallager and helwig (3) termed the lesion neurothekeoma (greek: theke, sheath) to connote the histologic nested appearance in order to reflect the presumed origin of the lesion from nerve sheath; cells are usually spindle-shaped and arranged in fascicular or whorled patterns (5)(17). epithelioid cells have been observed in these tumors. several names were used for this tumor: “bizarre cutaneous neurofibroma”, “plexiform myxoma”, “myxoma of nerve sheath”, “pacinian neurofibroma”, cutaneous lobular neuromyxoma, perineurial myxoma reflecting the uncertainty regarding their true “histogenesis” or precise line of differentiation (15)(16)(22). histologically neurothekoma on gross examination appear as dermal tumors commonly measuring 0.5 to 2 cm in dimension (2)(5). on microscopy (22)(24) neurothekomas could be: myxoid generally agreed of neural origin, displaing a lobulated, non-encapsulated but well-circumscribed proliferation of stellate, spindle-shaped and epithelioid cells – less commonly situated in multiple, closely spaced nodules of varying sizes, with abundant eosinophilic, finely granular cytoplasm, embedded within a myxoid stroma. due to the large amount of myxoid stroma separating the cells, the tumor cells are said to display a random growth pattern. cellular subtype: first described by barnhill in 1990 (26), contains little myxoid material, hypercellular nests and fascicles of epithelioid cells with vesicular nuclei containing scant myxoid stroma, also sclerotic collagen, poorly circumscribed, no immunoreactivity to the s-100 protein (5). the nodules of cellular neurothekeoma are smaller than those of the myxoid subtype. several variants of cellular neurothekoma are described: atypical or desmoplastic with low mitotic activity, with perineural and vascular invasion, osteoclastic giant cells in a minority of cases, neurothekoma mimicking nevomelanocytic tumors (2)(3)(5)(17)(26) are described. intermediate subtype demonstrate a whorled growth pattern with features of both cellular and myxoid variants the etiology of neurothekeoma arising in the parenchyma remains enigmatic (5)(25): by neural differentiation – see myxoid areas similar to classic myxoid neurothekeoma, by smooth muscle differentiation myofibroblastic or by the epithelioid variant of dermatofibroma represented by cellular neurothekeoma. since the time of their first description, it has been reported that the probable cell of origin could be the schwann cell innervating the blood vessels (2)(3)(17)(22). although they are similar in appearance and in behavior, neurothekeoma and nerve sheath myxoma are likely not of nerve sheath origin, as implied by the term and not related histogenetically. anothers possible origins could be: perineural cell of the nerves in the dura mater, around the blood vessels or by extreme differentiation of the precursor pluripotent cell resting inside the brain parenchyma under suitable conditions to the schwannian phenotype (31). neurothekeoma immunohistochemistry (24)(27)(28) demonstrates: -for myxoid subtype: diffuse s100 protein and glial fibrillary acidic protein (gfap) immunoreactivity, supporting its schwannian differentiation. the myxomatous type generates large amounts of myxoid matrix and is typically immunoreactive to the s-100 protein (27). -for cellular subtype: focal positivity for s100 protein in a minority cases (5), nk1/c3, an antibody that stains neuroectodermal tissue and pgp9.5, a broad marker for neuroectodermally derived tumors romanian neurosurgery (2015) xxix 3: 239 246 243 demonstrates positivity; but these two markers are not specific; smooth muscle actin (sma) & neuron-specific enolase (nse) have shown positivity. a very high sensitivity has s100 a6 is a member of the s100 protein family, but with low specificity. neurothekeomas can also show immunoreactivity to vimentin. the tumor in our case was encapsulated, composed by fusiform and stellate cells, with loose, pale, myxoid stroma; arranged in ovoid lobules of varying sizes separated by fibrous septae, no mitosis and mild nuclear pleomorphism was seen, rare high cell density areas presenting cells with central monomorphic nuclei showing spindle-shaped extensions and clear peripheral cytoplasm. the immunohistochemichal findings in our case shows: diffuse positive staining of the cells with s-100 and vimentin and negative glial fibrillary acidic protein (gfap), epithelial membrane antigen (ema), cytokeratin antibody (mnf116) and neurokinin 1 (nk1). cd34 was positive in vessels and ki67 was positive in 5% of cases. the histological and immunohistochemical findings are considered characteristic of neurothekeoma, with low relevant aggression proliferation (fig. 3). a rare variant of this neoplasm constitute the atypical cellular neurothekeoma (29) seen occasionally, starting from cellular and intermediate subtype. for this variant, large tumor size (up to 6 cm), atypical histologic features: cellular atypia (rounded or ovoid nucleus with abundant cytoplasm), few individual cell necroses, high mitotic rate ranged from 8 to 12 per 10 high-powered fields, marked cytologic pleomorphism correlates with local invasion: deep penetration extending into skeletal muscle and/or adipose infiltration, diffusely infiltrative borders, vascular invasion, possible recurrence if surgical excision of these lesions was incomplete, without metastases. there are few reports referring to neurothekeomas with an intracranial location (16)(30)(31): disposed in the pituitary area (17), middle cranial fossa (18) and posterior fossa (20)(21): cerebelopontine angle (22), pons (23). the most common type of intracranial neurothekeoma is myxoid; characterized by hypocellularity, with small spindle or stellate cells loosely arranged in abundant mucinous stroma. on immunohistochemical staining, the tumor cells are typically immunoreactive to the s100 protein (1-3,8), nerve growth factor receptor (p75ngfr), collagen type iv, cd34, glial fibrillary acidic protein, and cd. in our case, the neurothekeoma was hypointense in t1-weighted images and hyperintense in t2-weighted images using mri, similar to the mri findings of a previously published neurothekeoma cases, with heterogeneous enhancement following gadolinium administration, of the peripheral portions and nonhomogeneous uptake in the central areas, which corresponded histologically to the vascular capsule and the myxoid center (2)(16) in general surgery are beneficial, gross total resection is recommended and appears to be the definitive therapy (16)(31), without causing neurologic deficit for the patient; incomplete excision of neurothekeomas may lead to recurrence and local invasion (5)(17). even if the trigeminal nerve was encased in the tumor – see our case, the resection was easy, without causing neurologic deficit for the patient. because both myxoid and cellular types of neurothekeomas are benign; there are no reported cases of metastases and the lesion does not need postoperative radiotherapy (31) or adjuvant chemotherapy (21). follow-up for surveillance is necessary to detect recurrence in casese of incomplete intracerebral neurothekeomas excision (16)(22). differential diagnosis in neurothekeomas should be made with (16)(18)(20)(22)(31): 244 iacob et al a very rare, petro-clival, neurothekeoma tumor -epidermal inclusion cysts, intradermal spitz nevi, smooth muscle tumors, fibrohistiocytic tumors lipomas, pilomatrixomas, dermatofibromas, melanomas – sometimes difficult to be distinguish histologically from cellular neurothekeoma (melanocytic tumor are s100 positive, while cellular neurothekeoma are s100 negative), carcinomas -schwannomas well-circumscribed, sometimes cystic and often heterogeneously enhancing mass on mri, usually seen in the oculomotor and the ambient cistern (32). the myxoid type of neurothekeoma may resemble to schwannoma, but lacks verocay bodies and the antoni a, b arrangement seen in schwannoma. -meningiomas typically isointense, contrast-enhancing extraaxial tumor with “dural tail”, surrounding the dural perimeter of the mass on mri, -epidermoid hyperintense lesion. -gliomas, meningiomas, sarcomas showing myxoid degeneration also cardiac myxomas metastasizing to the brain and soft tissue myxomas penetrating the skull -spinal myxoid neurofibroma (6)(14) -perineuromas are rare tumours which appear myxomatous, but no lobulation is noted, composed exclusively of perineural cells (22) conclusion intracranial neurothekeoma is a a benign, rare tumor, similar to the cutaneous type, with a distinctive clinic and histopathologic entity, unlikely to recur if totally excised, even in a petro-clival topography. references 1.fetsch jf, laskin wb, et al. "neurothekeoma: an analysis of 178 tumors with detailed immunohistochemical data and long-term patient followup information". american journal of surgical pathology 2007, 31, 7, 1103–1114 2.harkin jc, reed rj tumors of the peripheral nervous system, in armed forces institute of pathology, ed: atlas of tumor pathology, 2nd series, fascicle 2, washington, d.c.: armed forces institute of pathology 1969:60-64 3.gallager rl, helwig eb "neurothekeoma-a benign cutaneous tumor of neural origin", american journal of clinical pathology 1980, 74, 6, 759–764 4.pulitzer dr, reed rj "nerve-sheath myxoma (perineurial myxoma)", american journal of dermatopathology 1985, 7, 5, 407–421 5.reed rj, pulitzer, dr tumors of neural tissue, chapter 35 in lever’s histopathology of the skin, 2008, ninth edition, elder, d, et al, eds, philadelphia: lippincott raven 6.lee d, suh yl, han j, kim es. spinal nerve sheath myxoma (neurothekeoma), pathol int. 2006, 56, 3, 144– 149 7.katsourakis m, kapranos n, et al.: nerve-sheath myxoma (neurothekeoma) of the oral cavity: a case report and review of the literature, j oral maxillofac surg. 1996, 54, 904–906 8.chow lt, ma tk, chow wh cellular neurothekeoma of the hypopharynx, histopathology 1997, 30, 192–194 9.makino t, utsunomiya t, kamino y, et al. nerve sheath myxoma of the tongue in a child, int j oral maxillofac surg. 2002, 31, 4, 451–454 10.cohen na, samadi ds, et al. cellular neurothekeoma of the maxilla, ann otol rhinol laryngol. 2004, 113, 5, 384–387 11.wee a, tan ce, raju gc: nerve sheath myxoma of the breast. a light and electron microscopic, histochemical and immunohistochemical study, virchows arch a pathol anat. histopathol 1989, 416, 163-167 12.fetsch jf, laskin wb, miettinen m. nerve sheath myxoma: a clinicopathologic and immunohistochemical analysis of 57 morphologically distinctive, s-100 proteinand gfap-positive, myxoid peripheral nerve sheath tumors with a predilection for the extremities and a high local recurrence rate. am j surg pathol 2005, 29:16151624 13.fanto sa, fanto e. neurothekeoma of the median nerve: case report, j hand surg am. 2012, 37, 6, 11841186 14.pasaoglu a, patiroglu te, et al. cervical spinal intramedullary myxoma in childhood, case report. j. neurosurg 1988, 69, 772-777 15.paulus w, jellinger k, perneczky g intraspinal neurothekeoma (nerve sheath myxoma), a report of two cases. am j clin pathol 1991, 95, 511–516 16.paulis w, warmuth-metz m, sörensen n. intracranial neurothekeoma (nerve sheath myxoma). case report. j. neurosurg 1993, 79:280-282 17.erdem y. , koktekir e. et al. characterization of an intracranial neurothekeoma: case report, turkish neurosurgery 2012, 22, 1, 109-112 18.nagatani m, et al. primary myxoma in the pituitary fossa: case report. neurosurgery 1987, 20, 329-331 romanian neurosurgery (2015) xxix 3: 239 246 245 19.pal l, bansal k, et al. intracranial neurothekeoma, a rare parenchymal nerve sheath myxoma of the middle cranial fossa, clin neuropathol 2002, 21, 47-51 20.klein mv, schwaighofer bw, et al. primary myxoma of the posterior fossa, neuroradiology 1990, 32, 250-251 21.alexandru d. et al. neurothekeoma in the posterior fossa: case report and literature review, perm j. 2012, 16(3): 63–64 22.vij m., jaiswal s. et al. nerve sheath myxoma (neurothekeoma) of cerebellopontine angle: case report of a rare tumor with brief review of literature, turkish neurosurgery 2013, 23, 1, 113-116 23.erdem y. , koktekir e. et al. characterization of an intracranial neurothekeoma: case report, turkish neurosurgery 2012, 22, 1, 109-112 24.hornick j.l., fletcher c.d. cellular neurothekeoma: detailed characterization in a series of 133 cases, am j surg pathol. 2007, 31(3), 329-340 25.webb jn. the histogenesis of nerve sheath myxoma: report of a case with electron microscopy. j pathol 1979, 127, 35-37 26.barnhill rl, mihm mc jr cellular neurothekeoma: a distinctive variant of neurothekeoma mimicking nevomelanocytic tumors. am j surg pathol 1990, 14, 113-120 27.husain s, silvers dn, et al. – histologic spectrum of neurothekeoma and the value of immunoperoxidase staining for s-100 protein in distinguishing it from melanoma. am j dermatopathol 16:496-503, 199 28.laskin wb, fetsch jf, miettinen m. the “neurothekeoma” : immunohistochemical analysis distinguishes the true nerve sheath myxoma from its mimics. hum pathol. 2000, 31(10),1230–1241 29.bhatia s, chu p, weinberg jm.atypical cellular neurothekeoma, dermatol surg. 2003, 29, 11, 1154-1157 30.paulus w, warmuth-metz m, sörensen n. intracranial neurothekeoma (nerve-sheath myxoma). case report. j neurosurg 1993, 79, 280-282 31.pal l, bansal k, et al. intracranial neurothekeoma a rare parenchymal nerve sheath myxoma of the middle cranial fossa. clin neuropathol 2002, 21, 47-51 32.tanriover n, kemerdere r, et al. oculomotor nerve schwannoma located in the oculomotor cistern. surg neurol 2007, 67(1), 83-88 19_sharmaanand_prevalence romanian neurosurgery (2015) xxix 3: 353 362 353 prevalence and determinants of depression and its association with quality of life in traumatic brain injury (tbi) patients anand sharma1, akhilesh jain2, achal sharma1, r.s. mittal1, i.d. gupta1 1sawai man singh medical college, jaipur, rajasthan, india 2esic model hospital, jaipur, rajasthan, india abstract: introduction: traumatic brain injury (tbi) is a major cause of disability. assessment and treatment of tbi typically focus on physical and cognitive impairments, yet psychological impairments represent significant causes of disability. depression may be the most common and disabling psychiatric condition in individuals with tbi. objective: this cross-sectional study was design to investigate prevalence and risk factors of depression in traumatic brain injury (tbi). material and method: the group studied consists of 204 patients of mild and moderate tbi between 14days to one-year post injury. demographic characteristics of the participants were assessed on a selfdesigned semi structured performa. interviews focused on assessment of severity of tbi, depression and quality of life (qol) using gcs, phq-9 and whobref-qol respectively. results: total 204 patients were included. 42.15% participants were found to have depression. none of the demographic variables were associated with depression except female sex, severity and time since injury. moderate tbi patient (55.80%) had significantly higher occurrence of depression than the mild cases (44.2%). patients with lesser duration (time since injury) of tbi had high incidence (50.2%) of depression compare to longer duration of tbi. depressed patients also had poor qol than those without depression in all domains except physical health domain. neuroanatomical localization was also correlated with depression. cerebral contusions were the most common (44.24%) lesions associated with depression. conclusion: depression is commonly associated, yet under diagnosed clinical entities in head injury and have tremendous impact in overall outcome measures. every patient of head injury warrants psychiatric evaluation and concomitant treatment if required to ensure the attainment of not only neuroanatomical intact but overall productive and qualitative life vindicating the holistic and multidisciplinary treatment approach. key words: traumatic brain injury, depression, quality of life introduction traumatic brain injury (tbi) is a major cause of death and disability (21). many patients face long-term disability. with regard to emotional functioning, depression is often a significant clinical concern. major depressive disorder (mdd) may be the most common and disabling psychiatric condition in individuals with tbi (24). depression after tbi is well documented in the literature. the frequency of depressive disorders has been reported to range between 16% and 60% (21), and mdd is the most commonly reported mood disorder after tbi, ranging from 24% to 35%. (21), (13). the 354 sharma et al depression and its association with quality of life tbi pacients frequency of mdd is particularly noteworthy when contrasted with base rates of 6% to 7% in community-based samples (12). although some persons who experience post-tbi depression have a history of mdd or other depressive disorders before their tbi, the frequency of depression after tbi far exceeds premorbid rates (11). post-tbi depression has been associated with numerous negative outcomes including sadness, irritability, loss of interest, fatigue, sleep disturbance, psychomotor retardation, greater sexual dysfunction, and lower ratings of health, poor subjective well-being, poorer qol, and increased rates of suicidal ideation (11)(18)(2). these negative consequences can hamper the person's reintegration into the community, adjustment after injury, and overall qol. despite researchers’ best efforts, the rates, predictors, and outcomes of mdd after tbi remain uncertain. incidence of depression has varied widely, ranging from 6-77%. (19). more elaborative studies may prove more informative and credible in recognition of this important secondary condition. the present study was designed to investigate the prevalence and determinants of depression in tbi and its correlation with quality of life. we have also implored the connection between neuroanatomical localization of tbi and depression. material and method study design the present study was a cross sectional study conducted at sms medical college and group of hospitals (smsh) over a period of six months from jan 2013 to june 2013. smsh is a tertiary care super specialty treatment centre. being the largest medical institute in the state of rajasthan, it caters the health needs of entire state as well as neighboring states. the institutional ethical committee approved the study protocol. participants the group studied consists of 204 patients of mild and moderate tbi between 14days to one-year post injury. sample was recruited through the follow up in neurosurgery opd and indoor of smsh. definition of mild traumatic brain injury was adopted as developed by the mild traumatic brain injury committee of the head injury (4). mild tbi was defined as “a person who has had a traumatically induced physiological disruption of brain function, as manifested by one or more of the following 1. any period of loss of consciousness for up to 30 minutes 2. any loss of memory for events immediately before or after the accident for as much as 24 hours, 3. any alteration of mental state at the time of the accident (e.g., feeling dazed, disoriented, or confused), 4. focal neurological deficit(s) that may or may not be transient”. moderate head injury was classified as if the lowest post resuscitation gcs score was 9±12 with or without evidence of lesion on ct. to be included in the study, participants had to be 18 years or older, and be able to comprehend or answer verbal or written questionnaires. participants with severe head injury and history of current or past psychosis, substance abuse disorder were excluded from the study as these factors can affect outcome independently. the nature and purpose of the study was explained to the participants and written informed consent was obtained. demographic characteristics of the participants were recorded on a self-designed semi structured per-forma by interviewing the participants by psychiatrist and exploring the medical records and neuro-radiological investigations. the interview was focused on assessment of severity of tbi, depression and quality of life (qol) measured on post injury gcs, phq-9 and whoqol-bref respectively. romanian neurosurgery (2015) xxix 3: 353 362 355 instruments severity of the tbi was assessed using the glasgow coma scale (gcs) (8). it is used for assessing the depth and duration of impaired consciousness and coma. according to this measurement, gcs scores between 13 and 15 defined mild head injury; between 9 and 12, moderate head injury; and between 3 and 8, severe head injury. these can be evaluated consistently by doctors and nurses and recorded on a simple chart, which has proved practical both in a neurosurgical unit and in a general hospital. depression was assessed by administering the nine-item phq-9, a self-report version of prime-md11 which assesses the presence of major depressive disorder using modified diagnostic and statistical manual, fourth edition (dsm-iv) criteria. there is good agreement reported between the phq diagnosis and those of independent psychiatry health professionals (for the diagnosis of any one or more phq disorder, kappa=0.65; overall accuracy, 85%; sensitivity, 75%; specificity, 90%) (15). in this study hindi version of phq-9 was used. it has been validated in indian population and is considered to be reliable tool for diagnosis of depression (16). for the diagnosis of depression, we defined clinical significant depression as: a phq-9 score of 10 or above. the whoqol-bref was developed by the world health organization quality of life group, in 15 international field centers (22). it is a self-report questionnaire that contains 26 items, and each item represents one facet. among the 26 items, 24 of them make up the 4 domains of physical health (7 items), psychological health (6 items), social relationships (3 items), and environment (8 items). the other 2 items measure overall quality of life and general health. in this study hindi version (20) was used. the scale has been shown to have good discriminant validity, sound content validity and good testretest reliability at several international whoqol centres. lesion locationassessment of lesion location was obtained via retrospective assessment of clinical record and post injury ct scan. for the purpose of this analysis, results were characterized as presence or absence of contusion, epidural bleed, subdural bleed in different brain regions grouped as frontal, temporal, parietal, occipital, subcortical, and/or cerebellar sites. statistical analyses data were analyzed using spss version 20, with a 2-tailed α level of 5%. statistical analyses were performed by correlation analyses (pearson and spearman), and independent t test analyses. the criterion for statistical significance was set at p_0.05, and for statistical trend at p_0.10. results participants and prevalence total 204 patients were included in study, mean age of patients were 33.34 (sd12.89) year. 77.9 percent were males (n=159) and 22.1 percent (n=45) were female. motor vehicle accidents were the most common cause (52.9%, n=108) of tbi, followed by falls and assaults each accounted for 19.6 %( n=40) and 21.1% (n=43) respectively. eightysix of the 204 participants (42.15%) were found to have depression as measured by phq9 with a cut off score of 10 and above. (table i) relationship between demographic variables, injury characteristics with depression depression was found in 37.33 % of male patients against 57.77 % females and this difference was statistically significant (p <0.016, df 1). other sociodemographic variables did not appear to have significant association with depression. amongst injury 356 sharma et al depression and its association with quality of life tbi pacients characteristics, time since injury and severity of tbi had significant association with depression. moderate tbi patients (55.8%) had significantly higher occurrence of depression than the mild cases (44.2%). (p=0.000, df 1). half (50.0%) of the patients with depression had lesser duration post injury (< 3-month) compare to longer duration since injury. this was found statistically significant (p<0.037). (table ii). distributions of ct finding in depressed individuals neuroanatomical localization was also correlated with depression. 44.2% of depressed patients had cerebral contusion followed by multiple lesion including contusions as well in 18.6% of the cases. other injury like edh, sdh, sah and even fracture were also found to be involved although in lesser frequency with depression. a very few patients with depression were also found to have normal cat brain (table ii). we further tried to explore the distribution of cerebral contusion in patients with depression and observed multiple contusions in most (36.8%) of the patients, though single lobe contusion were also associated with depression particularly in left frontal and left temporal region. (table iii) table i correlation of depression and no depression with demographic and injury-related factors no depression depression p valve n % n % sex r .168, p<.016, male 99 62.26 60 37.73 female 19 42.22 26 57.77 age (years) r .01, p< .882 18–24 28 23.7 26 30.2 25–34 44 37.3 23 26.7 35–44 25 21.2 18 20.9 45–54 8 6.8 11 12.8 55–64 12 10.2 5 5.8 65 or older 1 0.8 3 3.5 type of injury r -.016, p <. 882 rta 60 50.8 48 55.8 ffh 25 21.2 15 17.4 assault 27 22.9 16 18.6 other injury 6 5.1 7 8.1 gcs r .272, p<. 001 mild 84 71.2 38 44.2 moderate 34 28.8 48 55.8 duration of head injury r .130, p<. 005 less <3 month 79 66.9 43 50.0 3-6 month 23 19.5 29 33.7 >6 month 16 13.6 14 16.3 monthly income r -.024, p< .734 <50000 72 61.0 57 66.3 5000-10000 36 30.5 22 25.6 romanian neurosurgery (2015) xxix 3: 353 362 357 10000-20000 10 8.5 5 5.8 >200000 0 0 2 2.3 marital status r .068, p< .379 married 94 79.7 64 74.4 unmarried 24 20.3 22 25.6 table ii distribution of ct finding in depressed patients table 3 distribution of cerebral contusions in depressed patients table 4 quality of life in depressed and nondepressed patients domains non depressed (mean) sd depressed (mean) sd t test p value physical health 59.65 19.63 55.73 19.14 1.423 .156 psychological health 63.22 19.63 57.06 18.36 2.2 .024 social relationship 62.88 19.47 56.98 18.34 2.186 .030 environmental health 58.70 19.39 53.29 18.75 1.996 .047 assessment of qol in depressed and nondepressed individuals patients with depression scored lower than those without depression in all four domains of qol including physical health (55.73v/s 59.65,p=0.156), psychological health (57.06 v/s 63.22,p=0.024), social relationship (56.98 v/s 62.88,p=0.030) and environmental health (53.29 v/s 58.70,p=0.047). this finding was statistically significant in respect of all domains except physical health (table iv). discussion depression was found in 42.15% of study sample after mild and moderate head injury. the cumulative rate of depression in this study sample was almost 7 times higher than general population (42.15% in our cohort v/s 6.71 % in general population (12). this rate was virtually identical to that reported by jorge et al (11) who applied dsm criteria to establish prevalence rate and less than the 77% reported by varney et al (25) who used dsm-iii sn ct finding frequency percent 1. contusion 38 44.2 2. multiple lesion 16 18.60 3. sdh 11 12.79 4. edh 5 0.05 5. fracture 6 0.06 6. sah 2 0.02 7. nad 8 0.09 total 86 100 1 distribution of contusions frequency percent 2 multiple lobe contusions 14 36.8 3 right frontal lobe 4 10.5 4 left frontal lobe 6 15.8 5 right temporal lobe 3 7.9 6 left temporal lobe 10 26.3 7 left subcortical 1 2.6 8 right parietal lobe 0 9 left parietal lobe 0 10 right occipital 0 11 left occipital 0 12 right subcortical 0 13 cerebellum and brain stem 0 total 38 100 358 sharma et al depression and its association with quality of life tbi pacients criteria, conversely, it is considerably more than the 14% reported by deb et al (5) who relied on icd-10 diagnostic criteria. this variation in prevalence rates may have been caused by methodological issues including differences in depression assessment tools used in the research, the time course of depression assessment, and differences in injury severity of persons with tbi (mild vs. severe injuries). factors associated with depression were investigated in this study. none of the sociodemographic variables were associated with depression in tbi except gender variable. however, female gender has not been consistently associated with posttraumatic depression. fedoroff et al. (7) and blazer et al. (1) have reported that women are at twice the risk of developing depression than men while jorge et al. (11) on contrary have reported no significant differences in this regard between the patients with major depression and those who did not have depression. correlation between depression and injury characteristics were also assessed. severity of tbi was found strongly associated with higher proportion of depression, as depression was much higher in moderate tbi cases than the mild cases. controversy exists whether severity of tbi is directly correlated with increased prevalence of depression. dickmen et al. (6) showed an inverse relationship and holsinger et al. (9) noted increased prevalence with increasing severity of tbi. some researchers have postulated the reason for this counterintuitive finding lies in the fact that the people with severe brain injury likely underreport and those with milder injury are more aware of their problem and therefore more likely to report about depression. moderate tbi patients exhibited more severe injuries, had greater frequency of diffuse injury, which may have led them to develop mood symptoms. the study data also support the relationship between incidence of depression and duration of tbi post injury (time post injury). depression rate was high (50%) with lesser duration of tbi compare to longer duration post injury. several studies found that depression is common after years following injury (14) while other studies determined that depression rates decrease with time from injury within the tbi population (20). jorge et al. (11) found that 80% of persons were diagnosed with depression within the first 3 months post injury. at 1 year post-injury only 33% of persons were troubled by depression, which could either be due to decreased depression rates in the population or due to the natural recovery of symptoms over time. our data in this regard contradicts the theory that poor awareness of impairment precludes depressive reaction during the first six month of injury (10) and suggests a window of opportunity for early identification and treatment or prevention efforts. during the acute stage, depression of mood appears to be a function of the diffuse disruption of cerebral functioning in the wake of both direct physical damage to the brain and secondary neuropathological events. as brain functioning becomes re-organized and some degree of neurologic stabilityis re-established, mood symptoms could be expected to normalize. this study has also tried to explore the neuroanatomical localization of injury in respect of depression. cerebral contusion was the most commonly implicated lesion involving multiple lobes particularly left frontal and left temporal lobe, however single lobe involvement like right frontal and right temporal lobe and extradural injury was also associated with depression in few of the cases. jorge et al. (10,11) reported in two studies that major depression post-tbi is consistently associated with damage to the prefrontal cortex, basal ganglia, and the white matter tracts that connect these structures. brain injury (by an extradural, subdural or intraparenchymal hematoma or parenchyma romanian neurosurgery (2015) xxix 3: 353 362 359 contusion of cerebral hemispheres), can potentially compromise these fronto-striatalthalamic circuits. rao et al. (17) in his assessment of 17 brain injury patient suggest a possible role for frontal cortex, temporal lobe, and basal ganglia pathology in post-tbi depression, as well as reduced left occipital volume. we also tried to understand the association between injury severity and presence of depression with qol. depressed patients had poor quality of life than those without depression in all domains except physical health domain. charles hb et al. (3) described major depressive disorder within first year of tbi was associated with greater problems leading to poor health related quality of life (hrql). many other studies (23) in recent past have also reported significant association between depression and poor qol in tbi. this finding implies that long-term rehabilitation intervention programs for preventing the occurrence of depression and its deterioration are required. limitations of the study there are multiple limitations in the current investigation. patient complaints were based on self-reported questionnaire, which may have resulted in underreporting or over reporting of symptoms. it is recognized, however, that subjective depression experience provides only a partial, and sometimes inaccurate, portrayal of the nature and severity of objective depressive difficulties. patients with depression often report greater disruption than is evidenced by objective recordings. severe tbi cases were not included in our study owing to their inability to comprehend the directions, and hence present study does not give overall picture of tbi population. it is therefore important to consider objective depressive data in addition to subjective measures to understand post-tbi depression. this represents an important direction for further study. conclusion depression after tbi is highly prevalent and associated with adverse impact on qol. because depression after tbi is an invisible disorder within invisible injury, aggressive and scrupulous efforts are needed to educate the clinician about the importance of mood symptoms in this population to promote integrated system of detection and multidisciplinary care. correspondence dr. anand sharma, mch neurosurgery sms medical college, jaipur, india phone: +919873190047 dranandsharma100123@gmail.com references 1.blazer dr, kessler rc, mcgonagle ka, swartz ms. the prevalence and distribution of major depression in a national comorbidity sample: the national comorbidity survey. am j psychiatry.1994; 151:979-986. 2.bowen a, neumann v, conner m, tennant a, chamberlain ma. mood disorders following traumatic brain injury: identifying the extent of the problem and the people at risk. brain inj. 1998;12:177–190. 3.bombardier ch, fann jr, temkin nr, esselman pc, barber j, dikmen ss. rates of major depressive disorder and clinical outcomes following traumatic brain injury. jama. 2010; 19; 303(19): 1938-45. 4.definition of mild traumatic brain injury. developed by the mild traumatic brain injury committee of the head injury. interdisciplinary special interest group of the american congress of rehabilitation medicine. j head trauma rehabil 1993;8(3): 86-87. 5.deb s, lyons i, koutzoukis c, ali i, mccarthy g. rate of psychiatric illness 1 year after traumatic brain injury. am j psychiatry. 1999;156:374–378. 6.dikmen ss, bombardier ch, machamer j, fann jr, temkin nr. natural history of depression in traumatic brain injury. arch phys med rehabil.2004; 85:14571464. 7.fedoroff jp, starkstein se, forrester aw, geisler fh, jorge re, arndt sv, robinson, rg. depression in 360 sharma et al depression and its association with quality of life tbi pacients patients with acute traumatic brain injury.am j psychiatry.1992; 149,918-923. 8.graham teasdale, bryan jennett. assessment of coma and impaired consciousness: a practical scale .the lancet, 304, 7872,81-84. 9.holsinger t, steffens dc, phillips c, et al. head injury in early adulthood and the lifetime risk of depression. arch gen psychiatry. 2002;59:17–22. 10.jorge re, robinson rg, arndt sv, starkstein se, forrester aw, geisler f. depression following traumatic brain injury: a 1 year longitudinal study. j affect disord. 1993;27:233–243 11.jorge re, robinson rg, moser d, tateno a, crespofacorro b, arndt s. major depression following traumatic brain injury. arch gen psychiatry. 2004;61:42– 50. 12.kessler rc, chiu wt, demler o, merikangaskr ,walters ee. prevalence, severity, and comorbidity of 12month dsm-iv disorders in the national comorbidity survey replication. arch gen psychiatry. 2005; 62(6): 617-627. 13.koponen s, taiminen t, portin r, et al. axis i and ii psychiatric disorders after traumatic brain injury: a 30year follow-up study. am j psychiatry. 2002;159:1315– 1321. 14.kreutzer js, seel rt, gourley e. the prevalence and symptom rates of depression after traumatic brain injury: a comprehensive examination. brain inj. 2001;15:563– 576. 15.kroenke k, spitzer rl, williams jb. the phq-9: validity of a brief depression severity measure. j gen intern med. 2001; 16 : 606-13. 16.kochhar ph, rajadhyaksha ss, suvarna vr. translation and validation of brief patients health questionnaire against dsm iv as a tool to diagnose major depressive disorder in indian patients. j postgrad med 2007; 53 : 102-7. 17.rao v, munro ca. rosenberg p, ward j, bertrand m, degoankar m, horskaa ,pham d,yousem dm, barker. neuroanatomical correlates of depression in post traumatic brain injury: preliminary results of a pilot study.j neuropsychiatry clinneurosci. 2010 ;22(2):2315. 18.rapoport mj, mccullagh s, shammi p, feinsteinb a. cognitive impairment associated with major depression following mild and moderate traumatic brain injury. j neuropsychiatry clinneurosci. 2005;17:61–65. 19.rosenthal m, christensen bk, ross tp. depression following traumatic brain injury. arch phys med rehabil. 1998;79(1):90-103. 20.saxena s, chandramani k, bhargava r. whoqol hindi: a questionnaire for assessing quality of life in health care setting in india. natl med. j. india 1998; 11: 160–166. 21.seel rt, kreutzer js, rosenthal m, hammond fm, corrigan jd, black k. depression after traumatic brain injury: a national institute on disability and rehabilitation research model systems multicenter investigation. arch phys med rehabil. 2003; 84:177–184. 22.skevington sm, lotfy m, o'connell ka. the world health organization's whoqol-bref quality of life assessment: psychometric properties and results of the international field trial. a report from the whoqol group.qual life res. 2004;13:299-310. 23.steadman pare d, colaytonio a, ratcliff g, chase s, vernich l. factors associated with perceived quality of life many years after tbi. j head trauma rehabil.2001; 16:330-342. 24.trevena l, cameron i. traumatic brain injury-long term care of patients patients in general practice. aust fam physician.2011;40(12):956-61. 25.varney nr, martzke js, roberst rj. major depression in patients with closed head injury. neuropsychology.1987; 1:7-9. agrawalamit_giant 122 agrawal et al giant high occipital encephalocele giant high occipital encephalocele amit agrawal1, umamaheshwara reddy v.2, kishor v. hegde2, suneetha p.2, divya siddharth kolikipudi2 narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 1department of neurosurgery; 2department of radiology abstract: encephaloceles are rare embryological mesenchymal developmental anomalies resulting from inappropriate ossification in skull through with herniation of intracranial contents of the sac. encephaloceles are classified based on location of the osseous defect and contents of sac. convexity encephalocele with osseous defect in occipital bone is called occipital encephalocele. giant occipital encephaloceles can be sometimes larger than the size of baby skull itself and they pose a great surgical challenge. occipital encephaloceles (oe) are further classified as high oe when defect is only in occipital bone above the foramen magnum, low oe when involving occipital bone and foramen magnum and occipito-cervical when there involvement of occipital bone, foramen magnum and posterior upper neural arches. chiari iii malformation can be associated with high or low occipital encephaloceles. pre-operatively, it is essential to know the size of the sac, contents of the sac, relation to the adjacent structures, presence or absence of venous sinuses/vascular structures and osseous defect size. sometimes it becomes imperative to perform both ct and mri for the necessary information. volume rendered ct images can depict the relation of osseous defect to foramen magnum and provide information about upper neural arches which is necessary in classifying these lesions. key words: giant encephalocele, high occipital encephalocele, occipital encephalocele, meningocele, cephalocele, posterior encephalocele introduction encephaloceles are rare embryological mesenchymal developmental anomalies resulting from inappropriate ossification defect in skull through with herniation of intracranial contents. (1-4) nomenclature is mainly based on location and the contents of the herniated sac. when meninges alone are the content they are meningoceles, when brain tissue along with meninges is the content of herniation it is called meningoencephalocele or encephalocele and occasionally they may include a ventricle then they are called as hydroencephaloceles. (3, 4) dural sinuses as romanian neurosurgery (2016) xxx 1: 122 126 123 contents of encephalocele are also seen infrequently. (3, 4) atretic encephaloceles contain fibrous tissue within the sac and sometimes intracranial communication may not be present. (5) encephaloceles cause severe morbidity and mortality if untreated. occipital encephalocele (oe) is posterior encephalocele which is a result of herniation of intracranial contents through occipital bone defect with or without associated foramen magnum and upper cervical vertebral defects. (1, 2, 6-8) giant occipital encephaloceles (goe) because of their size they are a neurosurgical challenge. (1) herein we report a 40 day old female child who presented to us with giant high occipital encephalocele and imaging played a decisive role in providing preoperative information. case report a 40 days old female child was brought to pediatric outpatient department with complaints of swelling over back of head since birth. the mother due to her poor socioeconomic status did not have regular antenatal checkups and antenatal ultrasound. baby was delivered through caesarian section, as there was delay in head fixation after onset of labor pains. baby cried immediately after birth. large occipital swelling was noticed at birth and apgar score was 10. there was no h/o similar births in family. on examination, there was a single large gray colored round shaped 8 x 8 cm swelling at occipital region of head. skin over the swelling was normal. all the scalp veins were dilated. the swelling was compressible & baby cried on compression of the swelling. transillumination test was positive with dark areas showing reduced transillumination. child did not have any other associated abnormalities. routine investigations were normal except for persistent elevation of serum potassium levels (serum potassium6.2 meq/l, na-136 meq/l, cl: 94 meq/l, urea 14.8 mg/dl and creatinine: 0.56 mg/dl.). ct scan was advised which showed high occipital bony defect with herniation of meninges and posterior fossa contents (figures 1, 2). surface rendered and volume rendered images showed detail of giant occipital encephalocele, size of osseous defect, and relation to foramen magnum. (figure 3). mri showed details of total herniation of cerebellum, occipital horn of lateral ventricle and part of mid brain (figures 4, 5). there was no associated chiari malformation. diagnosis of high occipital encephalocele was made. the child underwent complete surgical excision and repair of the meningocoele and doing well at follow up. figure 1 axial ct scan images brain window (a) and soft tissue windowing (b) showing larger posterior fossa defect, with herniation of brain tissue and meninges 124 agrawal et al giant high occipital encephalocele figure 2 saggital reconstructed ct scan images showing herniation of posterior fossa structures through the defect figure 3 surface rendered images (a) showing the cyst size, volume rendered images of skull (b) showing the size of osseous defect (white arrows) in relation to foramen magnum (arrow heads) figure 4 t1 (a, b) and t2 weighted axial images (c) of mri showing dysmorphic cerebellar tissue, fourth ventriclular contents and meninges herniated through the defect, also note stretching of tectum figure 5 t1 (a) and t2 (b, c) weighted axial images showing the herniation of posterior fossa structures and beaking of the tectum discussion encephaloceles are identified and classified based on the location of the osseous skull defect. when defect is located in frontoethmoidal, nasofrontal, nasoethmoidal, naso-orbital, interfrontal regions it is called as sincipital encephalocele. (3) convexity encephaloceles have osseous defect located in parietal, occipital, occipital-cervical regions and finally basal encephaloceles have defect in the skull base. (3) incidence of encephaloceles is 0.8 3.0 per 10,000 live births and varies based on geological location and race. (3, 6) however with improvement of antenatal detection of these lesions, incidence has decreased significantly in recent times. (4) associated anomalies (microcephaly, chiari iii malformation, craniosynostosis, and syringomelia and neural tube defects are seen in approximately 20% of children. (3, 4) anterior encephaloceles are more common than posterior ones in asian continent. (3) oe are further classified as high oe when defect is only in occipital bone above the foramen magnum, low oe when involving occipital bone and foramen magnum and occipitocervical when there involvement of occipital bone, foramen magnum and posterior upper neural arches. chiari iii malformation can be associated with high or low occipital encephaloceles. (9) the size of occipital oe may vary from small to giant masses. (1, 6) giant encephaloceles can be some times larger than size of baby skull and because of their enormous size pose a great surgical challenge. (1) oe are normally covered by healthy skin or abnormal skin, sometimes only a thin romanian neurosurgery (2016) xxx 1: 122 126 125 meningeal membrane may be covering the oe. (10) contents within the herniated sac are variable. (1, 6) ultrasound and doppler are cheap readily available tools for knowing contents of sac; however mri may be required to know contents of sac in detail. ct is mainly used to assess the size of the osseous defect. (3, 4) conservative approach for encephalocele is not advised as many complications such as infection, trauma, and hydrocephalus can worsen the clinical scenario. (3, 6, 8) amount of viable brain tissue, size of the oe, skin covering and associated congenital anomalies should be considered in planning surgery. repair of oe without active csf leak or overlying skin necrosis should be an elective procedure and be done without delay. anaesthetic support is extremely important while operating oe, endotracheal intubation is real challenge in these patients and it should be done in right or left lateral position based on individual anaesthetist expertise. (11, 12) in general dysplastic brain tissue and meninges should be excised preserving the vascular structures. attempts should be made to preserve normal brain parenchyma and ventricles by expansion cranioplasty and ventricular reduction. reconstructive surgeries like skin flap rotation should be performed when there is inadequate skin for primary closure. (1-3, 6) great importance should be given for two-layered watertight closure. (6) osteogenic properties of dura can reduce the bony defect obviating the need for cranioplasty. titanium mesh closure of defect can also be tried. (3) surgical outcome is generally good independent of size depending upon amount of neural tissue. even giant oe with less neural tissue have excellent prognosis. (1, 4, 6, 8) however in giant oe due to the removal of abundant csf volume, electrolyte imbalances can occur which should be corrected peri-operatively. amount of normal viable brain tissue after surgery also is important in assessing the prognosis. conclusion giant high occipital encephaloceles are rare congenital lesions. diagnosis can be made soon after birth by clinical examination and because of their enormous size they pose a great surgical challenge. elective surgical repair can be performed as early as possible. pre-operatively it is essential to know the size of the sac, contents of the sac, relation to the adjacent structures, presence or absence of venous sinuses/vascular structures and osseous defect size. sometimes it becomes imperative to perform both ct and mri for the necessary information. volume rendered ct images can depict relation of osseous defect to foramen magnum and information about upper neural arches which is necessary in classifying these lesions. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email: dramitagrawal@gmail.com dramit_in@yahoo.com mobile: +91-8096410032 126 agrawal et al giant high occipital encephalocele references 1. agrawal a, lakhkar bb, lakhkar b, grover a. giant occipital encephalocele associated with microcephaly and micrognathia. pediatric neurosurgery 2008;44:515. 2. arora p, mody s, kalra vk, altaany d, bajaj m. occipital meningoencephalocele in a preterm neonate. bmj case reports 2012;2012:bcr2012006293. 3. munyi n, poenaru d, bransford r, albright l. encephalocele–a single institution african experience. east african medical journal 2009;86. 4. raja ra, qureshi aa, memon ar, ali h, dev v. pattern of encephaloceles: a case series. j ayub med coll abbottabad 2008;20:125-128. 5. hong ek, kim nh, lee jd. atretic encephalocele/myelocele: case reports with emphasis on pathogenesis. journal of korean medical science 1996;11:364-368. 6. walia b, bhargava p, sandhu k. giant occipital encephalocele. medical journal armed forces india 2005;61:293-294. 7. agrawal d, mahapatra a. giant occipital encephalocele with microcephaly and micrognathia. pediatric neurosurgery 2004;40:205-206. 8. kiymaz n, yilmaz n, demir i, keskin s. prognostic factors in patients with occipital encephalocele. pediatric neurosurgery 2009;46:6-11. 9. castillo m, quencer rm, dominguez r. chiari iii malformation: imaging features. ajnr american journal of neuroradiology 1992;13:107-113. 10. andarabi y, nejat f, el-khashab m. progressive skin necrosis of a huge occipital encephalocele. indian journal of plastic surgery: official publication of the association of plastic surgeons of india 2008;41:82. 11. özlü o, sorar m, sezer e, bayraktar n. anesthetic management in two infants with giant occipital encephalocele. pediatric anesthesia 2008;18:792-793. 12. vasudevan a, kundra p, priya g, nagalakshmi p. giant occipital encephalocele: a new paradigm. pediatric anesthesia 2012;22:586-588. 7chiriaca_acuteintracerebral 176 chiriac et al acute intracerebral haemorrhage complication after carotid artery stenting acute intracerebral haemorrhage complication after carotid artery stenting a. chiriac, georgiana ion*, n. dobrin*, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi *“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: intracranial hemorrhage following carotid artery stenting is a recognized rare complication but with potentially devastating evolution. reports of acute cerebral hemorrhage injury following internal carotid artery (ica) angioplasty are few, and usually were discussed in correlation with hyperperfusion syndrome. in this article we present a patient who experienced a fatal ipsilateral basal ganglia hemorrhage within 10 minutes after carotid angioplasty and stent placement. key words: carotid artery stent, cerebral hyperperfusion syndrome, acute intracranial hemorrhage. introduction improvements in endovascular techniques, especially in the emboli-prevention devices have significantly reduced the incidence of ischemic stroke following carotid artery stenting (cas). in this condition intracerebral haemorrhage become the major complication following endovascular carotid artery revascularization. this complication was attributed to so called cerebral hyperperfusion syndrome. the reported incidence of this phenomenon after endovascular carotid revascularization procedures remains questionable. however, first studies reported an incidence of 0.3–1.2% of cerebral hyperperfusion syndrome associated with intracerebral haemorrhage after carotid angioplasty and stent placement, while more recent studies showed a relatively higher rate of up to 5% [1, 2, 3]. in this article we report two case of fatal intracerebral haemorrhage subsequent to carotid artery stenting after a time of 10 minutes and 30 minutes respectively. cases description a 63-year-old man was referred for endovascular treatment after several transient ischemic attacks with left-side hemiparesis. the last episode occurred while the patient was undergoing medical treatment with 100mg acetylsalicylic acid and 75mg clopidogrel from 4 months. he had a long history of heavily smoke (3 packs / day) and romanian neurosurgery (2015) xxix 2: 176 181 177 alcohol abuse. the patient presented vascular risk factors including peripheral arterial occlusive disease, chronic heart failure class ii, obesity, hypertension and high blood cholesterol. when assessed in our hospital 2 months later, his blood pressure was 150/90 mm hg and he had mild left-side hemiparesis and vestibular syndrome. all haematological and biochemical tests were normal, with a normal platelet count and coagulation screen. figure 1 native cerebral ct scan showing old ischemic lesions a native cranial ct performed at admission demonstrated old ischemic microvascular lesions on right hemisphere, cortical and subcortical general atrophy and moderate leukoaraiosis (figure 1). the patient underwent bilateral carotid color doppler ultrasound that showed a severe stenosis of the right internal carotid artery (ica) (figure 2). figure 2 color doppler ultrasound showing a severe stenosis of the right ica the digital subtraction angiography performed next day via a femoral approach under local anesthesia confirmed 96% stenosis of right internal carotid artery (figure 3). the patient has received a right carotid stenting procedure three days later. the procedure was performed with the patient under local anesthesia via an 8 f introducer sheath on right femoral artery. the patient was given 5000iu heparin and 0.5 mg atropine iv. an 8f mach 1 guide catheter (boston scientific) was positioned into the right common carotid 178 chiriac et al acute intracerebral haemorrhage complication after carotid artery stenting artery and the stenosis was crossed with a 0.010 transend guidewire (boston scientific). the stenosis was predilated with a quantum maverick 2x20 mm balloon (boston scientific) and stented with a 7/9/40 mm xact abbott stent. after placement of the stent, the residual stenosis was dilated with the use of a maverick 5.5/20 mm balloon catheter (boston scientific). there were no procedural complications and blood pressure varied between 160/90 mm hg and 180/105 mm hg during the intervention. approximately 10 minutes after the intervention patient suddenly become very anxious and unexpressive. then he developed a left-sided hemiplegia and become comatose. blood pressure recorded was 200/110mmhg. emergency unenhanced cranial ct showed a large right-sided intracranial hematoma affecting the basal ganglia and the thalamus (figure 4). the patient was intubated and transferred to intensive care unit. neurologic examination performed at 24 hours showed an unresponsive patient with dilated pupils and no reaction to painful stimuli. the patient died 3 days later. romanian neurosurgery (2015) xxix 2: 176 181 179 figure 3 a, b, c: dsa – right ica angioplasty figure 4 a, b: native ct showing a large rightsided intracranial hematoma discussions despite the increasing use of extracranial carotid artery stenting there are only few reports of “hyperperfusion injury” following this treatment in the literature to date. over time three different entities of hyperperfusion syndrome were differentiated in the literature. thus, there were identified 2 early types and the so called “classic” delayed type. the “classic” hyperperfusion syndrome first described by sundt and collaborators typically developed 5 to 7 days after carotid artery revascularization, in which the typically clinical presentation consist in frontotemporal or retro-orbital headache, nausea, vomiting, seizures and other neurologic signs of elevated brain pressure. intracerebral hemorrhage is not an obligate component of this complication but can also occur [3]. the early types of hyperperfusion syndrome after carotid artery stenting were 180 chiriac et al acute intracerebral haemorrhage complication after carotid artery stenting first described by coutts et al. the 2 early entities consist in acute focal edema usually characterized by a favorable outcome and acute intracerebral hemorrhage with often fatal outcome. mccabe et al and chamorro et al showed that the presence of cerebral microvascular changes like cerebral microangiopathy and insufficient intracranial collateralization signs represents possible risk factors for hyperacute intracerebral hemorrhage in patients with carotid artery stenting. if in carotid endarterectomy occurrence of cerebral hyperperfusion injury were noted both in the presence of normal or elevated blood pressure, after carotid angioplasty these hemorrhagic complications has been usually associated with severe hypertension. most of the authors have reported increased velocity measurements on color doppler ultrasound in patent with stented internal carotid artery immediately after the procedure. one explanation of this phenomenon is that carotid sinus baroreceptors respond to the carotid blood flow by a corresponding decrease in systemic blood pressure. thus, the increased cerebral perfusion pressure exceeds capacity arteriolar vasoconstriction and can lead to intracerebral hemorrhage [4]. buhk and co-authors suggested that preinterventional highlighting of an acute infarct area is not necessarily a risk of hyperacute intracerebral hemorrhage after carotid angioplasty with stent. they have suggested that is a different cerebral hypoperfusion syndrome entity than described by sundt et al, with different pathophysiological mechanism that leads to hyperacute intracerebral hemorrhage [3]. nearly all literature reports on acute intracerebral haemorrhage after carotid angioplasty with stent have in common patients who had high-grade stenoses in the treated vessel or contralateral occlusion or subocclusion statements. buhk et al have proposed a more differentiated view on the term hyperperfusion syndrome. thus, the mechanism of parenchymal injury in patients with hyperacute intracerebral haemorrhage seems to be not hyperperfusion but rather blood pressure normalization [3]. conclusions acute intracerebral hemorrhage is a serious complication of carotid revascularization by stent angioplasty. even the pathological mechanism of this complication was usually attributed to impaired cerebral autoregulation or postoperatively elevated systemic blood pressure, the subject remain open to discussions. clinical studies have identified potential risk factors of hemorrhagic complication for subgroups of patients with carotid stent angioplasty indication. treatment strategies in these high-risk patients with severe vessel disease and highgrade stenosis must be directed towards regulation of blood pressure and limitation of rises in cerebral perfusion. references 1. yasuhiko kaku, shin-ichi yoshimura, and jouji kokuzawa (2004) factors predictive of cerebral romanian neurosurgery (2015) xxix 2: 176 181 181 hyperperfusion after carotid angioplasty and stent placement, am j neuroradiol 25:1403–1408; 2. solomon ra, loftus cm, quest do, correll jw. (1986) incidence and etiology of intracerebral hemorrhage following carotid endarterectomy. j neurosurg, 64:29–34; 3. j.-h. buhk, l. cepek, m. knauth (2006) hyperacute intracerebral hemorrhage complicating carotid stenting should be distinguished from hyperperfusion syndrome. am j neuroradiol 27:1508 –13; 4. djh. mccabe, m. brown, a. clifton (1999) fatal cerebral reperfusion hemorrhage after carotid stenting, stroke. 30:2483-2486; 5. choi bs, park jw, shin je, lu ph, kim jk, lee dh, et al. (2010) outcome evaluation of carotid stenting in high risk patients with symptomatic carotid near occlusion. interv neuroradiol, 16:309-16; 6. moulakakis kg, mylonas sn, sfyroeras gs, andrikopoulos v. (2009) hyperperfusion syndrome after carotid revascularization. j vasc surg. 49:1060-8; 7. goldberg jb, goodney pp, kumbhani sr, roth rm, powell rj, likosky ds. (2011) brain injury after carotid revascularisation: outcomes, mechanisms, and opportunities for improvement. ann vasc surg. 25:27086; 8. shindo a, kawai n, kawakita k, kawanishi m, tamiya t, nagao s. (2007) intracerebral hemorrhage after carotid artery stenting without evidence of hyperperfusion in positron emission tomography. interv neurorad. 13:191-9. 7prasadv_converting romanian neurosurgery (2014) xxi 4: 431 – 441 431 converting a paper proforma template to a user friendly electronic database to collect traumatic brain injury data m. veera prasad1, amit agrawal2, s. satish kumar3, b.v. subrahmanyan4, g. malleswara rao2 narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 1department of hospital administration 2professor of neurosurgery, department of neurosurgery 3associate professor of emergency medicine, department of emergency medicine 4professor of forensic medicine, department of forensic medicine abstract: a structured reporting system which is based on a uniform template will permit uniform data collection and future statistics and will facilitate and validate independent or comparative audit of performance and quality of care. the successful establishment of a multi-center registry depends on the development of a concise data entry form, data entry system and data analysis to continuously maintain the registry. in the first phase we introduced the paper data collection form, in second phase this data form was converted to an electronic interface. in this second phase of the study the paper proforma which was developed in the first phase was converted into an electronic database by using the filemaker pro 13 advanced®. the filemaker pro 13 advanced® is capable to store the data, provides user friendly interface to enter data and can be converted the standalone runtime program to install in any other computer system. the next step is to explore the possibility whether it would be feasible to use this as a multicenter traumatic brain injury registry. key words: registry, trauma, head injury, traumatic brain injury, filemaker pro 13 advanced®. introduction the successful establishment of a multicenter trauma registry depends on the development of a concise data entry form, data entry system and data analysis to continuously maintain the registry. (1) the use of the common trauma template has been shown feasible across international registries for the majority of the data variables. (2) based on the recommendation we have selected different data variables and we are making continuous efforts to identify the core variables versus optional data which can easily be used across many centers without compromising the quality of data. (3-5) in present article we describe our ongoing experience to convert an 432 prasad et al converting a paper proforma template to a user friendly electronic database existing paper based data collection system into an electronic form based data collection interface. material and methods the present study was conducted in the departments of hospital administration, neurosurgery and department of accident and emergency medicine of the narayana medical college and hospital (nmch) in nellore, india. after approval from the institutional ethical committee, all patients with the diagnosis of traumatic brain injury (as per the criteria laid by international classification of disease injury codes icd 10) presenting to the departments of neurosurgery and emergency medicine were included in the study. (6) it was the second phase of the ongoing project where core variables which were identified in the phase i were converted into an electronic database to maintain the uniformity and reproducibility. (7) in this second phase of the study the paper proforma which was developed in the first phase was converted into an electronic database by using the filemaker pro 13 advanced®. the filemaker pro 13 advanced® is capable to store the data, provides user friendly interface to enter data and can be converted the standalone runtime program to install in any other computer system. variables were identified as per the international norms and the data points were selected which included demographic details, pre-hospital characteristics, clinical details in emergency room, injury details, course during hospital stay, treatment, diagnosis, disposition and follow up. (8-10) glasgow coma scale score was used to classify severity of the traumatic brain injury (11) and acute injury severity scoring (ais) was used to grade the severity of the injury. (12) additional grading systems were used to classify the severity of diffuse axonal injury (13) and subarachnoid hemorrhage on ct scan. (14, 15) glasgow outcome scale (gos) will be used to assess the follow up and outcome. (16) statistical analysis data were presented as the mean and standard deviation for continuous variables and as a percentage for categorical variables. statistics were calculated using pspp statistical software. (17) results paper proforma (annexure i) which was used for data collection able to collect the patient information, clinical details, injury details, details regarding pre-hospital care, emergency room data, investigation detail (including details of ct scan), management offered, immediate outcome and details of short as well as long term follow up. electronic counterpart which was developed by using the filemaker pro 13 advanced® replicated all these details and had all the variables which were included on the paper proforma. all the variables were stored in a single table in the background. this similarity provided an opportunity to uniformly display the contents and ease of data entry. to facilitate data entry, data were separated into sub groups by tabs which included patient demographics, injury details, emergency evaluation, treatment, inhospital course, discharge details, diagnosis and follow up. the collected data can be exported into spreadsheet for further analysis by any statistical software program. interim romanian neurosurgery (2014) xxi 4: 431 – 441 433 analysis revealed that we were able to capture data for age, gender, education, brought by, date of admission, loss of consciousness, vomiting, nausea, ear bleed, nasal bleed, oral bleed, headache and seizures in all 100% instances (table 1). the most useful features of the program were similarity between paper and electronic interface (means easy to capture data and easy to enter data feature) (figure 1) and ability to export data in a format which can be easily utilized for data analysis. discussion many of the data registries are guided through the american college of surgeons guidelines for selection of data points. (18, 19) the amount of information captured may vary from a "minimal dataset" collected in emergency departments to a "comprehensive dataset" with information encompassing from pre-hospital care, management, follow up to rehabilitation. (19-22) the paucity of data, incomplete understanding of the problem and non-availability of definitive guidelines is a challenge to answer many important clinical questions and questions related to the management of traumatic brain injuries. (23) data collection particularly a registry database is considered indispensable (at the same time it must be as inexpensive as possible). (24) in our previous studies we have found that a welldesigned proforma based under supervision data collection in a relatively low volume trauma center and at regular intervals can be costeffective which can be managed by personnel with basic training. (7, 25-29) table i completeness of data details in the ongoing for the selected variables data variable total percent age 311 100% gender 311 100% education 311 100% brought by 311 100% date of admission 311 100% loss of consciousness 311 100% vomiting 311 100% nausea 311 100% ear bleed 311 100% nasal bleed 311 100% oral bleed 311 100% headache 311 100% seizures 311 100% arrival time in ed 288 92.6% left time from ed 285 91.6% time of admission 283 91.0% glasgow coma scale 270 86.8% best motor response 270 86.8% blood pressure systolic 267 85.9% blood pressure diastolic 266 85.5% best eye response 262 84.2% best verbal response 262 84.2% pulse rate 260 83.6% temperature 206 66.2% respiratory rate 196 63.0% hemoglobin 91 29.3% blood sugar random 78 25.1% date of discharge 70 22.5% total leucocyte count 68 21.9% time of injury 67 21.5% date of injury 58 18.6% 434 prasad et al converting a paper proforma template to a user friendly electronic database figure 1 screenshot demonstrate that the exactly similar appearance between paper proforma and screen appearance romanian neurosurgery (2014) xxi 4: 431 – 441 435 436 prasad et al converting a paper proforma template to a user friendly electronic database romanian neurosurgery (2014) xxi 4: 431 – 441 437 438 prasad et al converting a paper proforma template to a user friendly electronic database data variables before establishing a multi-center national data registry it is advisable to development a suitable and concise registry data entry form, database, secure electronic form, availability accessibility to a computer and internet connection, funded data entry personnel and experienced personnel in trauma injuries in order to continuously maintain and analyze the registry. (1) many studies have recommended that before starting the data registry it will be useful to define the data set well in advance as it will ensure standardization of variables and will ensure outcome comparison in terms of patient and injury characteristic across many international studies. (2, 19, 24, 30-32) however, the datasets of existing trauma registries frequently lack compatible definitions of common data variables. (33-37) the fundamental principle to develop a data collection form is to avoid a cumbersome forms and the data collection forms should be of simple digital, analogue and 'tick box' design as where possible. (3) it is import to understand that too little data would be having limited value, but too much data could be time-consuming and expensive to collect and administer. (38-42) database now a days relational databases are the becoming popular as these are simpler and reliable. 1 the database can be developed as a standalone system or as a web-based system which depend on the ultimate purpose of this database. 1 while converting a paper based data registry to computer based registry many technical considerations (include expert advice from information technologists) needs to be addressed which include selection of hardware, software, operating systems, memory support, and security. (30) it has been found that a simple standalone database is preferred to establish own data registry and a web-based model is preferred to establish a nationwide multi-center trauma registry then a web-based model is preferred. (1) in addition an attractive yet simple user interface will help to simplify the medical terminology and trauma score complexities. (1) to address the issue of an uninterrupted power supply (a condition unattainable in most developing countries) portable computer platforms can be the excellent solution. (43) data collection real-time data collection is the ideal but needs extensive funding, the continual presence of a dedicated data collector and almost unlikely to be practical in the prehospital phase (3) particularly in developing countries. a careful prospective planning for collecting data and full co-operation between pre-hospital and in-hospital personnel is mandatory to minimize the possibility of omission or duplication of data. (3) further data collection can be optimized and simplified if the baseline data can be imported from the hospital electronic medical record system. (19, 30, 44-46) data security can be ensured by providing username and password, encrypted data transfer which will give access to only authorized technicians and data managers. (1) challenges the main factors leading to the successful establishment of a multi-center trauma registry are the development of a concise data entry form, development of a user-friendly romanian neurosurgery (2014) xxi 4: 431 – 441 439 secure web-based database system, the availability of a computer and internet connection in each data collection center, funded data entry personnel well trained in extracting medical data from the medical record and entering it into the computer, and experienced personnel in trauma injuries and data analysis to continuously maintain and analyze the registry. (1, 30) data collection efforts can be hampered by several difficulties, particularly scarcity of funds and lack of adequately trained staff. (30) the cost can be a major determinant for the successful deployment of a data registry system; however as our previous experience has also revealed data trauma registries can be implemented in a cost-effective manner in developing countries. (7, 29, 30) further as has been described in the literature our study was conducted in a single tertiary-care academic institution with an electronic record keeping system, full-fledged trauma team and roundthe-clock availability of computed tomography (ct) and many other diagnostic modalities and these setting may not reflect the reality of many of the health care facilities in developing countries. (47) recommendations implementation of the paper trauma registry can be a useful adjunct before the planned implementation of the electronic data collection system. (9) it is evident that a structured reporting system which is based on a uniform template will permit uniform data collection and future statistics and will facilitate and validate independent or comparative audit of performance and quality of care. (48, 49) although different personnel take part at different stages of trauma care with requirements for data collection, yet there is a potential for the development of a single unifying model which can include a glossary of terms used in the pre-hospital and early hospital phase, and definitions, time points, and intervals. (3) we agree with the recommendations made in 1996, during the 9th itaccs symposium in london, where the working group suggested an urgent need for a common terminology and reporting template to facilitate the acquisition, processing, audit and analysis of data which will not only be compatible but comparable also. (3) conclusion we believe that the present data entry system has the potential to provide a clearer and user friendly descriptive data collection platform based on that a multicenter data entry template can be developed. in the first phase we introduced the paper data collection form, in second phase this data form was converted to an electronic interface. the data collection is continued in the paper form which is now entered into the electronic database for future reference. the next step is to explore the possibility whether it would be feasible to use this as a multi-center traumatic brain injury registry. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email dramitagrawal@gmail.com dramit_in@yahoo.com mobile +91-8096410032 440 prasad et al converting a paper proforma template to a user friendly electronic database references 1.shaban s, eid h, barka e, abu-zidan f. towards a national trauma registry for the united arab emirates. bmc research notes 2010;3:187. 2.ringdal kg, lossius hm, jones jm, et al. collecting core data in severely injured patients using a consensus trauma template: an international multicentre study. crit care 2011;15:r237. 3.dick wf, baskett pj. recommendations for uniform reporting of data following major trauma--the utstein style. a report of a working party of the international trauma anaesthesia and critical care society (itaccs). resuscitation 1999;42:81-100. 4.lossius hm, langhelle a, søreide e, et al. reporting data following major trauma and analysing factors associated with outcome using the new utstein style recommendations. resuscitation 2001;50:263-272. 5.who | injury surveillance guidelines [online]. available at: http://www.who.int/violence_injury_prevention/publica tions/surveillance/surveillance_guidelines/en/. 6.icd-10 version:2010 [online]. available at: http://apps.who.int/classifications/icd10/browse/2010/en. 7.agrawal a, prasad mv, kumar ss, subrahmanyan bv, harisha pn, rao gm. developing a traumatic brain injury registry: lessons learned from difficulties. romanian neurosurgery 2014;xxi:307-312. 8.tbi standards ninds common data elements [online]. available at: http://www.commondataelements.ninds.nih.gov/tbi.as px#tab=data_standards. 9.morris sc, manice n, nelp t, tenzin t. establishing a trauma registry in bhutan: needs and process. springerplus 2013;2:231. 10.burkhardt m, nienaber u, holstein jh, et al. trauma registry record linkage: methodological approach to benefit from complementary data using the example of the german pelvic injury register and the traumaregister dgu((r)). bmc medical research methodology 2013;13:30. 11.teasdale g, jennett b. assessment of coma and impaired consciousness. a practical scale. lancet 1974;2:81-84. 12.greenspan l, mclellan ba, greig h. abbreviated injury scale and injury severity score: a scoring chart. the journal of trauma 1985;25:60-64. 13.marshall lf, marshall sb, klauber mr, et al. a new classification of head injury based on computerized tomography. special supplements 1991;75:s14-s20. 14.fisher cm, kistler jp, davis jm. relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. neurosurgery 1980;6:1-9. 15.frontera ja, claassen j, schmidt jm, et al. prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified fisher scale. neurosurgery 2006;59:21-27; discussion 21-27. 16.jennett b, bond m. assessment of outcome after severe brain damage: a practical scale. the lancet 1975;305:480-484. 17.pspp gnu project free software foundation [online]. available at: http://www.gnu.org/software/pspp/. 18.report from the 1988 trauma registry workshop, including recommendations for hospital-based trauma registries. the journal of trauma 1989;29:827-834. 19.moore l, clark de. the value of trauma registries. injury 2008;39:686-695. 20.clark de, hahn dr. hospital trauma registries linked with population-based data. the journal of trauma 1999;47:448-454. 21.lucas ce, buechter kj, coscia rl, et al. the effect of trauma program registry on reported mortality rates. the journal of trauma 2001;51:1122-1126; discussion 1126. 22.williams jm, furbee pm, prescott je, paulson dj. the emergency department log as a simple injury-surveillance tool. annals of emergency medicine 1995;25:686-691. 23.agrawal a, joharapurkar sr, golhar kb, shahapurkar vv. early tracheostomy in severe head injuries at a rural center. j emerg trauma shock 2009;2:56. 24.rutledge r. the goals, development, and use of trauma registries and trauma data sources in decision making in injury. the surgical clinics of north america 1995;75:305-326. 25.agrawal a. injury surveillance or trauma registry: need of hour and time to start. the indian journal of neurotrauma 2011;8:37-39. 26.agrawal a. fatal road traffic cranio-cerebral injuries: time to act and need to study. the indian journal of neurotrauma 2012;9:156-157. 27.agrawal a. a critical appraisal of neurotrauma and neurocritical care perspectives of traumatic brain injuries in indian scenario. the indian journal of neurotrauma 2013;10:38-42. 28.agrawal a, galwankar s, kapil v, et al. epidemiology and clinical characteristics of traumatic brain injuries in a rural setting in maharashtra, india. 2007-2009. international journal of critical illness and injury science romanian neurosurgery (2014) xxi 4: 431 – 441 441 2012;2:167-171. 29.agrawal a, kakani a, baisakhiya n, galwankar s, dwivedi s, pal r. developing traumatic brain injury data bank: prospective study to understand the pattern of documentation and presentation. the indian journal of neurotrauma 2012;9:87-92. 30.nwomeh bc, lowell w, kable r, haley k, ameh ea. history and development of trauma registry: lessons from developed to developing countries. world journal of emergency surgery 2006;1:32. 31.nathens ab, brunet fp, maier rv. development of trauma systems and effect on outcomes after injury. lancet 2004;363:1794-1801. 32.ringdal kg, coats tj, lefering r, et al. the utstein template for uniform reporting of data following major trauma: a joint revision by scantem, tarn, dgu-tr and ritg. scandinavian journal of trauma, resuscitation and emergency medicine 2008;16:7. 33.edwards a, di bartolomeo s, chieregato a, et al. a comparison of european trauma registries. the first report from the eurotarn group. resuscitation 2007;75:286-297. 34.garthe e. overview of trauma registries in the united states. j ahima 1997;68:26, 28-32; quiz 33-24. 35.mann nc, guice k, cassidy l, wright d, koury j. are statewide trauma registries comparable? reaching for a national trauma dataset. academic emergency medicine 2006;13:946-953. 36.owen jl, bolenbaucher rm, moore ml. trauma registry databases: a comparison of data abstraction, interpretation, and entry at two level i trauma centers. the journal of trauma 1999;46:1100. 37.ringdal kg, lossius hm. feasibility of comparing core data from existing trauma registries in scandinavia. reaching for a scandinavian major trauma outcome study (mtos). scand j surg 2007;96:325-331. 38.cameron pa, finch cf, gabbe bj, collins lj, smith kl, mcneil jj. developing australia's first statewide trauma registry: what are the lessons? anz journal of surgery 2004;74:424-428. 39.zafar h, rehmani r, raja aj, ali a, ahmed m. registry based trauma outcome: perspective of a developing country. emergency medicine journal 2002;19:391-394. 40.podang j, singhasivanon p, podhipak a, santikarn c, sarol jn, ancheta ca. primary verification: is the triss appropriate for thailand? the southeast asian journal of tropical medicine and public health 2004;35:188-194. 41.onwudike m, olaloye oa, oni oo. teaching hospital perspective of the quality of trauma care in lagos, nigeria. world journal of surgery 2001;25:112-115. 42.talwar s, jain s, porwal r, laddha bl, prasad p. trauma scoring in a developing country. singapore medical journal 1999;40:386-388. 43.acosta ja, hatzigeorgiou c, smith ls. developing a trauma registry in a forward deployed military hospital: preliminary report. the journal of trauma 2006;61:256260. 44.schultz cr, ford hr, cassidy ld, et al. development of a hospital-based trauma registry in haiti: an approach for improving injury surveillance in developing and resource-poor settings. the journal of trauma 2007;63:1143-1154. 45.cameron pa, gabbe bj, cooper dj, walker t, judson r, mcneil j. a statewide system of trauma care in victoria: effect on patient survival. med j aust 2008;189:546-550. 46.probst c, paffrath t, krettek c, pape h. comparative update on documentation of trauma in seven national registries. european journal of trauma 2006;32:357-364. 47.mehmood a, razzak ja. trauma registry—needs and challenges in developing countries. j pak med assoc 2009;59:807-808. 48.cummins ro, chamberlain d, hazinski mf, et al. recommended guidelines for reviewing, reporting, and conducting research on in-hospital resuscitation: the inhospital 'utstein style'. a statement for healthcare professionals from the american heart association, the european resuscitation council, the heart and stroke foundation of canada, the australian resuscitation council, and the resuscitation councils of southern africa. resuscitation 1997;34:151-183. 49.spaite d, benoit r, brown d, et al. uniform prehospital data elements and definitions: a report from the uniform pre-hospital emergency medical services data conference. annals of emergency medicine 1995;25:525534. microsoft word danailaleon_long_f.docx romanian neurosurgery (2012) xix 1 long delay cerebral metastases leon danaila, mugurel radoi, roxana popa, florin stefanescu neurosurgery clinic of the national institute of neurology and neurovascular diseases, bucharest abstract in adults, cerebral metastases are the most common intracranial tumors, and their incidence has been rising in the last decades. the median interval between the diagnosis of the primary cancer and the detection of brain metastasis is relatively short, generally around one or two years. this study made a selection of six cases with a more than five years delay until the diagnosis of a cerebral metastases, from over 246 patients with brain metastases, admitted in our department, between 20062010. all six patients underwent surgery for their primary neoplasm, prior to neurosurgical diagnosis and treatment. we found 6 patients, having renal, breast or lung cancer, in which the delay between diagnosis of the primary tumor and that of the brain metastases started from 5 years and reached even 18 years. in all cases, this delay was longer than the median interval found in the most neurosurgical series. very probably the immune system plays a major role in controlling recurrences and new metastases in the nervous system keywords: cancer, cerebral metastases, long delay cerebral metastases, prognostic factors introduction brain metastases represent a significant source of morbidity and mortality in patients with systemic cancer. nowadays, cancer patients have a longer life expectancy because of the important advances in cancer diagnosis and therapy. the incidence of brain metastases is difficult to determine with precision. in earlier neurosurgical series the overall incidence of cerebral metastases was 20% 30% for all patients with systemic cancer (20). estimates based on more recent series and autopsy studies show a much higher incidence of brain metastases, with incidences varying between 8.3 to 11.1 per 100.000 individuals (12). approximately 40% of intracranial neoplasms are metastatic (10, 23). these estimates place brain metastases first in frequency among all intracranial tumors, before intracranial glioma and meningioma (18, 21, 27). the histological type of the primary tumor appears to be the major factor of the frequency and pattern of intracranial spread. multiple, large autopsies series suggest that, in order of decreasing frequency, lung, breast, melanoma, renal and colon cancer are the most common primary tumors that metastasize to brain (10, 12, 21, 27). primary lung tumors account for 30% to 60% of all brain metastasis cases (13, 15). breast cancer ranks second, contributing 10% to 30% (13, 15) of all brain metastases among women (21), and renal cancer has a frequency of 11% (2, 23). when the ability of a primary leon danaila et al long delay cerebral metastases tumor to spread to the brain is considered, melanoma ranks first followed by lung and breast cancers (1, 16, 19). the median interval between the diagnosis of the primary cancer and the detection of brain metastasis is relatively short, generally around one or two years (4, 24). this study made a selection of six cases with a more than five years delay. material and methods we made a retrospective study over 246 patients with brain metastases, which were admitted and operated in our department, the neurosurgery clinic of the institute of cerebrovascular diseases “prof. dr. v. voiculescu” – bucharest, between 20062010. in this series, we found 6 patients, having renal, breast or lung cancer, in which the delay between diagnosis of the primary tumor and that of the brain metastases was longer than the median interval found in the most neurosurgical series. the time interval was measured between the month recorded from the primary cancer surgery and that for the cerebral tumor surgery. all patients underwent surgery for their primary neoplasm, prior to the diagnosis of the intracranial tumor. we performed a radical surgical treatment with removal of the entire cerebral metastases, proved by postoperative contrast ct scans. ilustrative case patient c.l., female, 69 years old, was admitted in our clinic in october 2010. she complained of persistent headache and balance disorders. neurological examination revealed a right pyramidal syndrome and motor aphasia. contrast cerebral ct scan showed a large, relatively well-circumscribed tumor, located in the left frontal lobe, with nonhomogenous contrast enhancement and important peritumoral edema. from her previous pathological history we noted that in 1992 she underwent surgery for a left breast carcinoma when a left mastectomy was achieved. the histological exam showed an infiltrating ductal carcinoma. postoperatory, the patient underwent radiation therapy and followed a chemotherapy protocole. in 1998, she was operated for a right breast mastosis, when a pattey-type mastectomy was performed. the patient underwent surgery for her left frontal lobe tumor. we performed a frontal craniectomy, located on the lesion, and achieved a total gross removal of a 6 cm. in diameter tumor, with central necrosis. the histological exam revealed a metastasis from a breast ductal carcinoma. the patient followed postoperative radiation therapy with a total radiation dose of 60gy. the last clinical examination, performed 12 months after surgery, proved a good general and neurological health condition of the patient. control cerebral ct scan showed absence of any tumor recurrences. the interval of time between the diagnosis of the breast cancer and that of cerebral metastasis was18 years. results as we mentioned, our selection criteria was a long delay between the diagnosis of the cancer and the detection of the cerebral metastases. two patients with renal cancer had the same 7 years delay between the diagnosis of the cancer and that of cerebral metastasis. two patients, operated for a breast cancer, had a delay of 8, respectively 18 years. romanian neurosurgery (2012) xix 1 figure 1 a preoperative contrast cerebral ct scan showing a large left frontal tumor, with important peritumoral edema and shifting of the midline; b postoperative contrast ct scan (12 months after surgery) showing a total gross resection of the frontal metastases and lack of local recurrence. one patient with a laryngian neoplasm, than operated on for a lung metastasis, showed two cerebral tumors with a delay of 7 years from the diagnosis of his cancer. the last patient, operated for a lung cancer, presented a cerebral metastasis after 5 years from the diagnosis of his lung neoplasm. statistic dates case1 case 2 case 3 case 4 case 5 case 6 sex f m f f m m age 57 57 50 69 54 50 primary cancer (date of surgery) renal cancer (02. 2002) renal cancer (10.2002) breast cancer (12.2000) breast cancer (03.1992) laryngian cancer (06.2002) lung cancer (04.200 5) cerebral metastasis surgery 11.2009 10.2009 10.2008 10.2010 05.2009 07.2010 no. of cerebral metastases 1 1 1 1 2 1 length of time interval (years) 7 7 8 18 7 5 postoperative follow-up (months) 19 14 26 12 10 10 systemic metastases no yes (bone metastasis; 02.2007) no no yes (lung metastases; 09.2007) no postoperative cerebral radiotherapy/ systemic chemotherapy yes/yes yes/no no/no yes/no yes/yes yes/no discussion the histology of the primary tumor appears to be the major dictator of the frequency and pattern of intracranial extension. virtually any type of cancer has the ability to produce brain metastases. half of the patients with brain metastases in autopsy series had lung or breast cancer as the primary tumor (14, 22). the process of tumor metastasis is highly selective and consists of a series of sequential, interrelated steps. to produce clinically relevant lesions, metastatic cells must complete all steps of this process. more than a century ago, stephen paget questioned whether the organ distribution leon danaila et al long delay cerebral metastases of metastases produced by different human neoplasms was due to chance. he analyzed more than 1.000 autopsy records of women with breast cancer. his research documented a nonrandom pattern of metastasis, suggesting that the process was not due to chance but rather, that certain tumor cells (the "seed") had a specific affinity for the milieu of certain organs (the "soil"); metastases resulted only when the seed and soil were compatible (17). some 40 years later, j. ewing challenged paget's "seed and soil" theory and hypothesized that metastatic dissemination occurs by purely mechanical factors that are a result of the anatomical structure of the vascular system (7). these explanations have been evoked separately or together to explain the metastatic site preference of certain types of neoplasms. it is proved today, that only certain cancer cell lines (cell clones) could cover all the stages of the metastatic cascade process (8). also, the development of a metastasis in certain area of the central nervous system is specific to selected clone cells depending on the histology of the primary tumor (8, 9). in our study were reviewed brain metsteses from lung, breast and renal cancers. therefore, we selected few informations about these neoplasms. primary lung tumors account for 30% to 60% of all cases of brain metastasis (14, 16). lung cancer ranks second among all cancers in its tendency to invade the brain (5,14). of patients with lung cancer, 18% to 65% will develop brain metastases and the specific histology of the primary lung tumor is very important in determining metastatic frequency (5, 22). there are five histological subtypes of lung cancer: small cell lung cancer, squamous cell carcinoma, adenocarcinoma, large cell cancer and carcinoid tumor. indeed, more than 40% of patients with small cell lung cancer and lung adenocarcinoma have brain metastases in clinical series or at autopsy (5). it represents more than twice the rate of metastasis found with the other types of lung cancer such as squamous cell carcinoma (5,22). in a clinical series of patients with brain metastases from lung cancer in turkey (22), adenocarcinoma, epidermoid carcinoma, and small cell carcinoma gave rise to 84% of these metastatic lesions. in a clinical series of patients presenting with brain metastases as the first sign of their malignancy at the gustave-roussy institute, france, 44% had adenocarcinoma and 30% had undifferentiated or small cell lung carcinoma, compared with only 12% who had squamous cell lung carcinoma (12). the median interval between the diagnosis of lung cancer and the detection of brain metastasis falls between two and nine months and is shorter than is seen for other cancers (16, 22). in our study, the delay was a few times longer, 5 years for the lung tumor and respectively 7 years for the laryngian one. for the lung neoplasm the histological result was adenocarcinoma. primary breast cancer ranks second to lung cancer as the most frequently occurring primary tumor in patients with brain metastases. among women, breast cancer is the most common cause of brain metastasis, resulting in 5% to 30% of all brain metastases (25, 26). breast cancer ranks third, after lung cancer and melanoma, among primary cancers in its tendency to metastasize to the brain, and approximately 20% to 30% of patients with breast cancer will develop a brain metastasis (21, 26). romanian neurosurgery (2012) xix 1 brain metastases from breast cancer typically occur late in the course of the disease, between 2 and 3.3 years after diagnosis (16,22). in our study, both patients had a breast ductal adenocarcinoma metastasis, and had an 8 respectively 18 years delay. primary renal cancer frequently metastasizes to the brain. in an autopsy series, the frequency of brain metastases in renal adenocarcinoma patients was 11% (2, 23). in a clinical series by harada et al. 5.5% of 325 patients who had renal cell carcinoma that was treated at osaka university hospital from 1957 to 1993, developed brain metastases (11). the median interval between diagnosis of renal cancer and brain metastasis caused by it ranges from 1 year to 2.3 years (3, 11). in our study both patients showed a same 7 years time interval and had clear cell carcinoma metastases on histological exams. long delay between diagnosis of the primary tumor and the development of the brain metastasis represents, in most series, a favorable prognostic factor associated with a longer median survival (6, 19, 24). other favorable prognostic factors are: primary cancer under control, absence of extracranial metastases, karnofsky score > 70, age under 60, female gender and, of course, gross total resection of the metastasis. the median patient survival time after surgical excision of a single brain metastasis is 9 to 14 months, depending on such factors as the type of primary cancer, length of time between diagnosis of the primary tumor and diagnosis of brain metastasis, neurological performance status, and presence or absence of systemic disease (6, 19). contrary to classical teaching, recent reports demonstrated that surgery improves the survival of patients with multiple brain metastases, so long as all the lesions can be removed. these good results are achieved only in patients with two or three metastases and it must be emphasized that for resection to be beneficial, all the lesions must be resected (4). conclusions generally, the longest survival intervals were recorded in patients operated on for breast, renal and lung cerebral metastases, and the shortest intervals in patients with melanoma metastasis. all our six patients demonstrated at their last control registered in our clinic records, a good general and neurological performance status. none of them presented cerebral recurrences at the control ct scan examination. in all cases we performed a radical surgical treatment with removal of the entire tumoral mass. because a long interval between the diagnosis of the primary cancer and that of cerebral metastases plays an important role in obtaining a longer patient survival an aggressive surgical approach should be encouraged in these selected cases. in the articles that we had reviewed we did not find a clear explanation of this long delay in metastatic process. very probably the immune system plays a major role in controlling recurrences and new metastases also in the nervous system. conceivably in such cases (as, probably, in ours), some neoplastic nidi were kept dormant by an uncertain balance between the neoplastic aggressiveness and the defensive factors of the organism. as long as this balance operated, the metastases were prevented from developing enough to give rise to clinical symptoms and hence detection. leon danaila et al long delay cerebral metastases corresponding author dr. radoi mugurel e-mail: muguradoi@yahoo.com tel:0723527292 references 1. adam d. multiple melanoma metastasis. case report. chirurgia 2010 jul-aug; 105(4):563-9. 2. anderson rs, el-mahdi am, kuban da, et al: brain metastases from transitional cell carcinoma of urinary bladder. urology 39: 17-20,1992. 3. badalament ra, gluck r, wong gy, gnecco c, kreutzer e, herr hw, fair wr, galichi jh. surgical treatment of brain metastases from renal cell carcinoma. urology 1990; 36: 112-117. 4. bindal rk, sawaya r, leavens me et at: surgical treatment of multiple brain metastases. j neurosurg 1993; 79: 210-216 5. cox jd, barber-derus s, hartz aj, et al.: is adenocarcinoma/ large cell carcinoma the most radiocurable type of cancer of the lung? int j radiat oncol biol phys 1986;12: 1801-1805. 6. danaila l, adam d. sinteze neurochirurgicale. ed. ceres, buc., 2001; cap. tratamentul metastazelor cerebrale pg.512-524. 7. ewing j: neoplastic diseases. 6th ed. philadelphia, pa, w.b. saunders co, 1928. 8. fidler ij: critical factors in the biology of human cancer metastasis: twenty-eighth gha clowes memorial award lecture. cancer res 1990; 50:61306138. 9. fidler ij: molecular biology of cancer: invasion and metastasis. in devita vt, hellman s, rosenberg sa (eds): cancer: principles and practice of oncology. philadelphia, pa, lippincott-raven, 1997, pp. 135-152. 10. gorgan m., bucur n, neacsu a, pruna vm, craciunas s, et al. deontological issues – possible misdiagnosis of cerebral metastases. romanian neurosurgery 2011; 13:240-254. 11. harada y, nonomura n, kondo m, et al.: clinical study of brain metastasis of renal cell carcinoma. eur urol 1999; 36: 230-235. 12. kehrli p. epidemiologie des metastases cerebrales. neurochirurgie, 1999, 45, nr.5, 357-363. 13. lang ef, slater j: metastatic brain tumors: results of surgical and nonsurgical treatment. surg clin north am 44:865-872, 1964. 14. macgee ee: surgical treatment of cerebral metastases from lung cancer. the effect on quality and duration of survival. j neurosurg 1971; 35:416-420. 15. markesbery wr, brooks wh, gupta gd, et al: treatment for patients with cerebral metastases. arch neuro135:754-756,1978. 16. nussbaum es, djalilian hr, cho kh, hall wa. brain metastasis. histology, multiplicity, surgery and survival. cancer 1996; 78: 1781-1788. 17. paget s: the distribution of secondary growths in cancer of the breast. lancet 1889; 1: 571-573. 18. papacocea t, rosca t, badarau a, papacocea r, ciornei c, ion a.d. meningiom chistic – prezentare de caz. chirurgia 2009; vol.104 (1);pp 99-103. 19. patchell ra, tibbs pa, walsh jw et al. a randomized trial of surgery in the treat¬ment of single metastases to the brain. n engl med 1990; 322:494-500. 20. percy ak, elveback lr, okazaki h, et al: neoplasms of the central nervous system: epidemilogic considerations. neurology 22:40-48, 1972. 21. posner jb: neurologic complications of cancer. philadelphia, f. a. davis, 1995, pp. 3¬14; 77-110. 22. sen m, demiral as, cetingoz r, et al.: prognostic factors in lung cancer with brain meta¬stasis. radiother oncol 1998; 46: 33-38. 23. steinfeld ad, zelefsky m: brain metastases from carcinoma of bladder. urology 29:375-376, 1987. 24. sundaresan n, galicich jh. surgical treatment of brain metastases. clinical and computerized tomography evaluation of the results of treatment. cancer 1985;55:1382-1388. 25. tsukada y, fouad a, pickren jw, et al.: central nervous system metastasis from breast carcinoma. autopsy study. cancer 1983; 52: 2349-2354. 26. vieth rg, odom gl: intracranial metastases and their neurosurgical treatment. j neurosurg 1965; 23: 375-383. 27. wingo pa, tong t, bolden s: cancer statistcs, 1995. ca cancer j olin 45:8-30, 1995. microsoft word 6stefanescuflorin_cerebellar_ff romanian neurosurgery (2013) xx 1: 57 65 57 cerebral vasospasm – a serious obstacle in a successful aneurysm surgery florin stefanescu, stefanita dima, ram vakilnejad, mugurel radoi national institute of neurology and neurovascular diseases bucharest, neuropathological department abstract background: cerebral vasospasm that occurs after subarachnoid hemorrhage (sah) can be an important cause of mortality and morbidity for patients successfully operated for a cerebral aneurysm. methods: five cases of prompt diagnostic and surgical treatment of a cerebral aneurysm, with important sah on cerebral computed tomography (ct) at onset, are presented. all patients were admitted in a poor neurological state and developed severe vasospasm. both, the correct clipping of the aneurysm and the cerebral vasospasm were angiographic demonstrated in all cases. two patients showed complete obliteration of one carotid artery. results: postoperatory, four of the patients were treated with intrathecally administered nimodipine (10mg/50ml). in three cases, the procedure caused the reverse of the vasospasm and clinical improvement of the patients. their clinical outcomes were very good and were discharged with minimal neurological deficits. in one case, repeated intraarterial administration of nimodipine, showed no reduction of the vasospasm, and no improvement of patient’s clinical status. the patient was conscious, but presented focal neurological deficits (hemiplegia and aphasia). one patient did not benefit from this treatment and had a poor clinical outcome, remaining in a vegetative state. conclusions: cerebral vasoconstriction after sah could be an important obstacle in obtaining very good results in aneurysm surgery. intra-arterial administration of nimodipine is an important and useful treatment, but good results in reversal severe cerebral vasospasm are not always mandatory. key words: cerebral aneurysms, cerebral vasospasm, clipping of the aneurysm, postoperative results. introduction cerebral vasospasm is a known source of considerable morbidity and even mortality following subarachnoid hemorrhage (sah) (17, 20). it is a prolonged, sometimes severe, but ultimately reversible cerebral arterial narrowing that occurs days after subarachnoid space bleeding. angiographic vasospasm was first described by a neurosurgeon, ecker, along with a radiologist, riemenschneider, in syracuse, new york, in 1951 (5). a number of studies described the direct relationship between the location and amount of subarachnoid blood seen on admission computed tomography (ct) and the risk and distribution of angiographic vasospasm (3, 21). in 1980, fisher and co-workers provided a useful predictive grading scale 58 stefanescu et al cerebral vasospasm for vasospasm based on the location and thickness of the clot (10). first neurosurgical studies (12), which evaluated the impact of clinical and angiographic vasospasm over patients’ outcome, estimated that roughly one half of patients with sah developed angiographic vasospasm, one half of this group would become symptomatic and one half of these symptomatic patients would die of cerebral infarction. modern perioperative care of sah clearly improved this situation and the aggressive treatment of symptomatic vasospasm have reduced the combined risk of all morbidity and mortality due to vasospasm to between 10% and 15%, in more recent sah patient series (2, 8). the aim of this study is to present five cases with severe angiographic and clinical vasospasm, in which, despite an early surgery that had provided a correct clipping of the aneurysms, and allowed an aggressive perioperative medical treatment of vasospasm, we faced important morbidity due to clinical vasospasm. material and methods we reported the cases of five patients with important subarachnoid hemorrhage on ct scan at admission and who were diagnosed by four vessels digital subtraction angiography with cerebral aneurysms. in all cases, cerebral vasospasm implied the simultaneous presence of angiographic vasospasm and clinical vasospasm. in all cases, angiographic vasospasm was noted before surgery, at that time when the diagnostic cerebral arteriography was performed. admission glasgow coma scale was between 6 and 10 points. as a rule for treatment of anterior circulation aneurysms in our neurosurgical department, we performed surgical clipping of the aneurysms as soon as possible after its diagnosis. in all five patients, we performed early aneurysm clipping, which afforded us the opportunity to mechanically reduce the subarachnoid clot burden and reduced the vasospasm risk. interval between diagnostic and surgery ranged between 24 to 72 hours. both, the correct clipping of the aneurysm and the postoperative presence of arterial vasospasm were angiographic demonstrated in all cases. nimodipine administration started at admission in continuous intravenous perfusion (at a speed varying between 8-12 ml/h depending on blood pressure). in four cases, local intra-arterial nimodipine was infused during control arteriography. in one case, this procedure was repeated three times postoperatively. illustrative case 1 a 68 years female was admitted to our clinic, 8 days after the onset of symptoms, with the diagnostic of sah. at admission she was in a poor neurological state, with a gcs of 8 points, somnolence, third left cranial nerve palsy, right hemiparesis and motor aphasia. initial cerebral ct scan showed blood in the main subarachnoid cisterns and in most of the cortical sulci (figure 1a). cerebral angiography, performed in the next day after her admission, revealed a left posterior communicating artery aneurysm and an important cerebral vasospasm (figure 1b). she was operated within 24 hours after admission, and the clipping of the left posterior communicating aneurysm was performed. in the second day after surgery, we performed control cerebral angiography (figure 2b, c, d). it demonstrated the correct clipping of the aneurysm, but revealed a severe and diffuse cerebral romanian neurosurgery (2013) xx 1: 57 65 59 vasospasm which involved anterior cerebral artery (aca) andmiddle cerebral artery (acm). in the same session, using the intra-arterial micro-catheter, we administrated locally nimodipine, in the both aca and acm arteries. due to the severity of the vasospasm, the presence of symptomatic infarcts and the lack of the possibility to perform angioplasty, we repeated local administration of nimodipine by the mean of intra-arterial catheters two more times, in the 4th and, respectively, the 6th postoperative day. no signs of the resolving of the intensity of the vasospasm were demonstrated. cerebral ct scans showed diffuse area of infraction in the aca and acm supplying territories on both sides (figure 2a). continuous intravenous perfusion of nimodipine was maintained 14 days after surgery. despite a good evolution of her neurological status in the first postoperative week, meaning the improvement of the consciousness, right hemiparesis and aphasia, her neurological evolution became stationary in the second and third postoperative week and showed progressive worsening starting with the fourth week. after one month from surgery her gos score was 3. her evolution complicated with bronchopneumonia and died 48 days after surgery. illustrative case 2 a 45 years old male was admitted to our clinic, 3 days after the onset of symptoms, presenting severe headache, neck stiffness, photophobia, confusion and a slight left hemiparesis. initial cerebral ct scan (figure 3a) showed subarachnoid hemorrhage and a thick clot in the anterior interhemispheric fissure (grade 3 on fischer scale). cerebral angiography, performed within 48 hours of his admission, revealed an anterior communicating artery aneurysm and vasospasm on the proximal portion of the left aca (segment a1) and its distal branches (figure 3b). he was operated after three days of his admission, and the clipping of the anterior communicating artery aneurysm was performed. in the third postoperative day, he showed increasing of his left hemiparesis and became somnolent. a b figure 1. preoperative images: (a) native ct scan showing blood in the main subarachnoid cisterns and in most of the cortical sulci; fischer scale–2, (b) four vessels cerebral angiography showed a left posterior communicating artery aneurysm and an important and diffuse cerebral vasospasm 60 stefanescu et al cerebral vasospasm a b c d figure 2. postoperative images (48 hours after surgery): (a) – native ct scan showing ischemic hipodensities in the left aca and acm territories, (b, c, d) control cerebral angiography showed the correct clipping of the aneurysm and a severe and persistent vasospasm, which did not resolve after intra-arterial infusion of nimodipine a b figure 3. preoperative images: (a) native ct scan showing subarachnoid hemorrhage and a thick clot in the anterior interhemispheric fissure (grade 3 on fischer scale), (b) four vessels cerebral angiography showed an anterior communicating artery aneurysm and vasospasm on the proximal portion of the left aca (segment a1) and its distal branches romanian neurosurgery (2013) xx 1: 57 65 61 control angiography was performed four days after surgery, and demonstrated the correct clipping of the aneurysm (figure 4b, c, d). because of the increased vessels narrowing in the proximal and distal branches of the left aca, compared with the diagnostic angiography, we locally injected nimodipine, using the intra-arterial micro-catheter, in order to reduce vasospasm in those arteries. control ct scans showed the resolution of the initial frontal interhemispheric clot, and no other sign of focal ischemia (figure 4a). continuous intravenous perfusion of nimodipine was maintained 8 days after surgery, and it was continued orally. the medical treatment went successfully and the patient had no ischemic sequelae. he had a very good recovery and presented no permanent neurological deficits at 3 months follow-up (gos 15 points). a b c d figure 4. postoperative images (4 days after surgery): (a) – native ct scan showing resolution of the initial frontal interhemispheric clot, and no other sign of focal ischemia, (b, c, d) control cerebral angiography showed the correct clipping of the aneurysm and moderate vasospasm in the proximal and distal branches of the left aca results patient outcome was directly dependent on admission gcs, time interval between onset of symptoms and diagnostic/surgical treatment and intensity of vasospasm. it mainly affected the arterial branches of the anterior part of the circle of willis. unfortunately, two important means of reversing vasospasm were not used in our clinic: intra-arterial papaverine administration (lack of experience) and 62 stefanescu et al cerebral vasospasm percutaneous transluminal balloon angioplasty (lack of materials). only in one patient we noted the decreasing of vasospasm intensity at the control angiography. in two cases we encountered severe vasospasm, and, in the other three, the intensity was moderate. in one patient the aneurysm re-bleed before surgery, which delayed the clipping of aneurysm and led to development of hydrocephalus. the patients who presented a severe angiographic and clinical vasospasm, with signs of infarction on ct scan, had a poor outcome. one died of non-neurological complications (bronchopneumonia), and the other had permanent sequlae (gos 3). in the other three patients, the medical treatment successfully reversed ischemia and vasospasm, and the outcome at 3 months after surgery was good, with minimal neurological deficits. discussion a review of the literature found that the overall incidence of angiographic vasospasm after sah was roughly 50%, although the estimates ranged from 20% to nearly 100% (10). the variation appeared due to inconsistencies in the timing of cerebral angiography and definitions of vasospasm used (7). in a recent randomized trial, findlay and co-workers, assessing the amount of subarachnoid clot on the admission ct scan, showed that almost 60% of patients with thick clots developed moderate to severe angiographic vasospasm in at least one major cerebral artery (9). table 1 important clinical and imagistic parameters of a series of five patients with angiographic and symptomatic vasospasm case 1 case 2 case 3 case 4 case 5 sex m f f m m age 45 68 58 41 51 admission gcs 10 8 8 6 10 fischer scale 3 2 4 4 2 huntαhess 2 3 3 4 2 interval between onset/admission 3 days 8 days 5 days 4 days 5 days interval between diagnostic/surgery 48h 24h 72h (aneurysm re-rupture) 24h 24h vasospasm before surgery yes yes yes yes yes vasospasm after surgery increased increased increased decreased increased other sah related complications none hydrocephalus rerupture/hydroce phalus none none 1 months follow-up (outcome) good (gos5) poor (gos-3) poor (gos-3) good (gos-4) good (gos-5) 4 months follow-up (outcome) good (gos -5) death no dates good (gos-5) good (gos – 5) romanian neurosurgery (2013) xx 1: 57 65 63 related to this subject is the demonstration that reducing the subarachnoid clot amount by early surgery (within 48 hours of rupture) decreases the risk of severe angiographic vasospasm (9, 19). delayed-onset cerebral ischemia and infarction account for 15 to 20% of all unfavorable outcomes (22). risk factors for symptomatic vasospasm are: thick subarachnoid clots on cerebral ct, poor neurological condition on admission, age younger than 35 and older than 65, cigarette smoking, preexisting hypertension, incomplete circle of willis (19). the most important measure in preventing vasospastic ischemia was avoiding of post-sah hypovolemia, hypotension and raised intracranial pressure. because all our patients presented angiographic and clinical vasospasm, we increased fluid administration in order to maintained systemic blood pressure in a moderate hypertensive range (140 to 160 mmhg). deliberate hypervolemia has not been proven to reduce symptomatic ischemia and can precipitate cardiopulmonary decompensation in older patients (1). we did not use transcranial doppler in monitoring blood velocities, as a test to demonstrate the presence of angiographic vasospasm. nimodipine prevents intracellular calcium increases by blocking dihydropyridine-sensitive (l-type) calcium channels and in a series of randomized controlled trials has had a modest but statistically significant beneficial impact on clinical outcome after aneurysmal sah (13, 15). the largest and most compelling study was the british aneurysm nimodipine trial (brant) (16), which encompassed 554 patients of all grades, who received treatment within 4 days of hemorrhage, consisting of either placebo or nimodipine 60 mg every 4 hours for 21 days. results were as follow: cerebral infarction occurred in 22% of nimodipine-treated patients versus 33% of those who received placebo, and poor outcomes (severe disability, vegetative state and death) were significantly reduced in the nimodipine group, 20% versus 33% for placebo (16). in our series, nimodipine administration started at admission in continuous intravenous perfusion, at a speed varying from 8-12ml/h depending on blood pressure, and lasted for more than one week after surgery (range between 8 and 14 days). in all cases, parenteral administration of nimodipine was followed by oral uptaking for more than 7 days. in four cases, local cerebral intra-arterial nimodipine was infused during control angiography, and in one patient, the procedure was repeated three times after surgery, only for the mean to overcome the vasospasm. numerous treatments for cerebral arterial vasospasm have been evaluated. it is worth to be noted that vasospasm in humans does not respond to the large variety of drugs that reverse experimental vasospasm in animal models (11). some of the treatment options in post-sah vasospasm can only: (a) prevent, but not reduce vasospasm early surgery with removal of blood clots, avoidance of hypovolemia and anemia (b) protect the brain from ischemic injuries – calcium channel blockers, nmetil-d-aspartate (nmda) receptor antagonists, free radical scavengers (e.g tirilazad mesylate, nicaraven) (c) improve the rheologic properties of intravascular blood to enhance perfusion of ischemic zones (e.g plasma, albumin, low 64 stefanescu et al cerebral vasospasm molecular weight dextran) (11) the only vasospasm treatment options that have been proved by many studies, to reverses ischemia or vasospasm are presented in table 2 (7). table 2 management of vasospasm and cerebral ischemia after aneurysmal sah strategies for vasospasm and/or cerebral ischemia reversal after aneurysmal subarachnoid hemorrhage reverses ischemia 1. hypervolemia, hemodilution and hypertension reverses vasospasm 1. intra-arterial papaverine administration 2. percutaneous transluminal balloon angioplasty the presence of angiographic vasospasm within 48 hours of aneurysm rupture, as it was in our cases (at admission and detected on diagnostic angiography), although difficult to assess with certainty without a previous arteriography, has been correlated with a higher risk for later symptomatic vasospasm and a poor outcome (18). our available options, in treatment of angiographic and clinical vasospasm, were the following: (a) early surgery (b)direct pharmacological arterial dilatation using calcium channel blockers (nimodipine); using intra-arterial microcatheters, it was injected locally at the site of vasospasm, during control angiography (c) indirect intra-arterial dilatation utilizing triple h therapy (d) removal of potential vasospasmogenic agents (removal of blood clot and cerebrospinal fluid drainage) (e) administration of plasma, dextran or albumin to enhance perfusion of the ischemic zones. as we previously underlined, two very important vasospasm treatment options, angioplasty and direct intra-arterial administration of papaverine, which were proved by several studies (6, 14) in reversing vasospasm, were not use in our clinic. conclusion many treatment strategies for combated angiographic and clinical vasospasm after aneurysmal subarachnoid hemorrhage have been described. vasospasm remains an important clinical problem, a leading cause of preventable death and disability after sah, and one of the most important independent predictors of poor outcome when it occurs. intra-arterial administration of nimodipine is an important and useful treatment, but good results in reversal severe cerebral vasospasm are not always mandatory. in the future it is anticipated that better vasospasm prevention will be possible, likely through combined treatments, because vasospastic process is very complex. nowadays, rescue treatment with hypervolemia, hypertension, and angioplasty is proved to be effective in reversing ischemia and preventing vasospasm-related morbidity and mortality. corresponding author: mugurel petrinel radoi md, phd national institute of neurology and neurovascular diseases bucharest, neurosurgical department, postal adress: 10-12 berceni str., 041902 bucharest, romania e-mail address: muguradoi@yahoo.com phone: 0040723527292 romanian neurosurgery (2013) xx 1: 57 65 65 references 1. bailes je, spetzler jf, hadley mn, baldwin hz (1990). management and morbidity of poor-grade aneurysm patients. j neurosurg 72:559-566. 2. broderick jp, brott tg, duldner je, tomsick t, leach a (1994). initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage. stroke 25: 1342-1347. 3. davis jm, davis kr, crowell rm (1980). subarachnoid hemorrhage secondary to ruptured intracranial aneurysm: prognostic significance of cranial ct. ajnr am j neuroradiol 1:17-21. 4. dorsch nwc, king mt (1994). a review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage: i. incidence and effects. j clin neuroscience 1:19-26. 5. ecker a, riemenschneider pa (1951). arteriographic demonstration of spasm of the intracranial arteries: with special reference to saccular arterial aneurysm. j neurosurg 8:660-667, 1951. 6. eskridge jm, mcauliffe w, song jk, deliganis av, newell dw, lewis dh, mayberg mr, winn hr (1998). balloon angioplasty for the treatment of vasospasm: results of first 50 cases. neurosurgery 42:510-517. 7. findley j.m. (2004). cerebral vasospasm. in h. richard winn (eds). youmans neurological surgery fifth ed. (pp. 1839-1867). philadelphia, pennsylvania: saunders elsevier. isbn 0-7216-8291-x. 8.findlay jm, deagle jm (1998). causes of morbidity and mortality following intracranial aneurysm rupture. can j neurol sci 25:209-215. 9. findlay jm, kassell nf, weir bka, disney lb, grace mga (1995). a randomized trial of intraoperative, intracisternal tissue plasminogen activator for the prevention of vasospasm. neurosurgery 37:168-178. 10. fischer cm, kistler jp, davis jm (1980). relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. neurosurgery 6:1-9. 11. greenberg ms (2006). handbook of neurosurgery, sixth ed. lakeland, florida. thieme medical publishers new york, ny. 12. heros rc, zervas nt, varsos v (1983). cerebral vasospasm after subarachnoid hemorrhage: an update. ann neurol 14:599-608. 13. mee e, dorrance d, lowe d, neil-dwyer g (1988). controlled study of nimodipine in aneurysm patients treated early after subarachnoid hemorrhage. neurosurgery 22:484-491. 14. nakagomi t, kassell nf, hongo k, sasaki t (1990). pharmacological reversibility of experimental cerebral vasospasm. neurosurgery 27:582-586. 15. philippon j, grob r, dagreou f, guggiari m, rivierez m, viars p (1986). prevention of vasospasm in subarachnoid hemorrhage: a controlled study with nimodipine. acta neurochir 82:110-114. 16. pickard jd, murray gd, illingworth r, shaw md, teasdale gm, foy pm (1989). effect of oral nimodipine on cerebral infarction and outcome after subarachnoid hemorrhage: british aneurysm nimodipine trial. bmj 298:636-642. 17. qureshi ai, sung gy, razumovsky ay, lane k, straw rn, ulatowski ja (2000). early identification of patients at risk for symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. crit care med 28:948-990. 18. qureshi ai, sung gy, suri mak, straw rn, guterman lr, hopkins ln (1999). prognostic value and determinants of ultra-early angiographic vasospasm after aneurysmal subarachnoid hemorrhage. neurosurgery 44:967-974. 19. rabb ch, tang g, chin ls, giannotta sl (1994). a statistical analysis of factors related to symptomatic cerebral vasospasm. acta neurochir (wien) 127:27-31. 20. ropper ah, zervas nt (1984). outcome 1 year after sah from cerebral aneurysm. management morbidity, mortality and functional status in 112 consecutive good-risk patients. j neurosurg 60:909915. 21. sano h, kanno t, shinomya y. (1982). prospection of chronic vasospasm by ct findings. acta neurochir (wien) 63:23-30. 22. zambraski j.m., hamilton m.g (2000). cerebral vasospasm. in carter lp α spetzler rf (eds). neurovascular surgery (pp. 583-600). mcgraw-hill, inc. croitorucristina_myasthenia romanian neurosurgery (2016) xxx 1: 77 82 77 myasthenia gravis – a beginning with no end cristina georgiana croitoru1, dana mihaela turliuc1,2, florentina danciu1, a.i. cucu1, s. turliuc2, claudia florida costea1,2 1“prof. dr. n. oblu” emergency clinical hospital iasi, romania 2“grigore t. popa” university of medicine and pharmacy iasi, romania abstract: myasthenia gravis is one of the neurological diseases with a relatively recent history, full of mistakes, in which the british and german neurology schools have attempted to find answers when confronted with the unknown. the paper aims at making a historical account of the disease from its discovery in the 16th century, when the first case of myasthenia gravis was medically diagnosed, to the beginning of the 20th century, when the dawn of modern therapy started to show. key words: myasthenia gravis, history of medicine, neuromuscular disease disease is very old. nothing about it has changed. it is only we who change as we learn to perceive what was formerly imperceptible. jean martin charcot (1825-1893) introduction myasthenia gravis (mg) is a neuromuscular disease that may be congenital or not, immune-mediated or not, due to a presynaptic, synaptic or postsynaptic defect. the very etymology of the words myasthenia gravis reflect its definition, as it consists of the greek words mios (gr.) meaning muscle, asthenia (gr.) meaning weakness and gravis (lat.) meaning severe. mg history is relatively recent, full or errors and ambiguities, a history in which especially the german and british neurology schools have attempted, over time, to find answers when confronted with the unknown. writing is an art and good writings are expression of maturity (14), and various neurologists, psychiatrists, neurosurgeons, anatomists, pathologists and philosophers have tried to write its history throughout the centuries. initially called erb’s palsy, a term coined after the name of the german neurologist wilhelm erb (1840-1921) who achieved the first classical description of the illness, myasthenia gravis was included in the list of diseases under the name of the erb-goldflam 78 croitoru et al myasthenia gravis syndrome until 1895, when, at a medical conference in berlin, the german neurologist and psychiatrist friedrich jolly (1844-1904), showed to the audience two patients suffering from this disease, which he called myasthenia gravis pseudoparalytica (1, 12). the first case of mg mentioned in the history of medicine may be considered the case of an indian tribe chief, the native-american opechankanough (1554-1644) who, according to the historical records based on colonial correspondence, suffered from extreme muscle fatigue which made it impossible for him to walk and which was alleviated by rest. moreover, the historical records also described the fact that opechankanough suffered from bilateral palpebral ptosis, so that his eyelids were kept open by his servants (19). thomas willis (1621-1975) – the first description many researchers (1, 2, 12, 20) credit the famous english neurologist thomas willis (1621-1675) (figure 1) with the first description of the mg disease. he is especially known in neurology and neurosurgery for willis polygon, which he named circulus arteriosus cerebri and which he described very well in 1664, thus revolutionizing cerebral circulation physiology (79, 17). in 1672, professor willis notes in several of his patients the occurrence of a chronic condition characterized by muscle fatigue, with fluctuating progress, yet typically aggravated by physical effort and alleviated by rest. it is much later that his descriptions were connected with mg, namely in 1903, by the english pediatrist leonard george guthrie (1858-1918), who writes down his assumptions in the paper entitled myasthenia gravis in the seventeenth century published by the prestigious lancet journal (11). in one of his books written in latin, de anima brutorum, and then translated into english in 1688 by the english poet samuel pordage (1633-1691), thomas willis describes as spurious palsy the case of a woman exhibiting fluctuating muscle fatigue in the limbs and tongue (28). when he looks for an explanation for these bizarre manifestations, willis suggests the existence of a substance in the blood that would facilitate muscle contraction, and this type of palsy would be due to fluctuations in the blood concentration of this substance: it may be suspected, that not only de spirits themselves,...are in fault but...the impotency of local motion doth in some measure also depend upon the fault of the explosive copula, suffused everywhere from the blood, into the moving fibers (28). this assumption, too daring for the 17th century, cannot be recorded without the slightest shadow of a doubt, since pordage’s work could not be a very faithful translation of willis’ thoughts (13). therefore, there are scientists who challenged the accuracy of pordage’s description. sir samuel wilks (1824-1911) – the grand old man of british medicine two centuries had to elapse until the first modern description of mg was done by another english doctor, sir samuel wilks (1824-1911) (figure 1) rightfully called the grand old man of british medicine (24). of the four brilliant minds of the guy’s hospital in london, namely richard bright, thomas romanian neurosurgery (2016) xxx 1: 77 82 79 addison, thomas hodgkin and samuel wilks, only the last acknowledged the importance of pathological anatomy and promoted it in numerous works published in the guy’s hospital reports, which he edited between 1854 and 1865. in all his publications, wilks supported the performance of autopsy on every occasion in order to set correlations between clinical medicine and pathological anatomy. samuel wilks’ contributions changed medical thought both as concerns systemic diseases (lymphoma, intestinal inflammatory diseases, bacterial endocarditis, syphilis), and as regards neurological diseases (alcoholic neuropathy, epilepsy, migraine) (22). moreover, wilks was also the first scholar who claimed that in epilepsy, the seat of the condition was not in the spinal cord, but in the cerebral cortex (4, 18, 22, 23). in 1877 wilks described the case of a woman of uncertain age suffering from bulbar palsy, whose disease progressed in a fluctuant manner from the viewpoint of symptom strength and who eventually died. after an autopsy had been conducted, although he was familiar with the histopathological changes occurring in the brainstem nuclei in case of bulbar palsy and motor neuron disease, samuel wilks noted the absence of macroscopic and microscopic changes. at first, he tried to account for the specificity of his case by diagnosing hysteria, but his conclusions were: bulbar paralysis; fatal; no disease found (27). wilhelm erb (1840-1921) – the first classical description of the disease the first classical description of mg may be found in the first book dealing exclusively with this disease and it was made in 1878, by the german neurologist wilhelm erb (18401921) (figure 1). thus, in his work entitled on a new symptomatic complex, probably bulbar, erb described three cases with similar symptoms and concluded that diplopia, bilateral palpebral ptosis, dysphagia, facial palsy, neck muscle fatigue, all of them with fluctuating progress and numerous recurrences and relapses, were components of a new pathological entity, different from progressive bulbar palsy (6). erb was also the first scholar who attempted to treat the condition by applying galvanic current and by administering iron, potassium iodide or quinine. the condition of one of the three cases improved after galvanotherapy, the condition of the second patient worsened and that of the third patient improved after quinine had been administered (20). after 1878 many cases of mg were described in medical literature as particular forms of bulbar palsy, with fatal fluctuating progress. the doctors noted that all these conditions had in common the fact that the forensic examination revealed no pathological findings. among these cases, the german doctor eisenlohr published in 1886 the case of an 18-year-old boy who had died due to respiratory muscle paralysis (5), the german neurologist herman oppenheim (1858-1919) published the case of a 29-year-old woman in 1887 (21), while the english pathologist julius dreschfeld (1845-1907) published, in 1893, the case of a 36-year-old woman, which was very well documented from a pathological anatomy point of view (3). 80 croitoru et al myasthenia gravis herman hoppe (1867-1929) –elucidation of the characteristics of the disease starting with 1892 doctors from countries other than germany and england began to document such cases. the first one to do that was doctor herman hoppe (1867-1929), of the united states, who published a complex work dealing with the cases described by wilks, eisenlohr and oppenheim under the name of a single condition, despite their being distinct from a clinical, paraclinical and histopathological point of view. he emphasizes the characteristics of the disease: target muscle groups, no muscle atrophy, circadian fatigability variations (more prominent in the evening) and progress which included remissions and relapses. he also noted that the muscular response to electric stimulation did not have the typical denervation appearance, and the histopathological examination surprisingly revealed no neural mass loss (16). samuel goldflam (1852-1932) – distinction from progressive bulbar palsy a year later, i.e. in 1893, the polish neurologist samuel goldflam (1852-1932) (figure 1) revived erb’s theory and pointed out that muscle fatigue was the cardinal symptom and commented on the disease variants and severity, and suggests the idea of prognostic. in a review of wilks’, erb’s, eisenlohr’s, oppenheim’s and hoppe’s works, he reports three new cases and describes the disease as an apparently curable bulbar paralytic symptom complex (10). this description is considered by many scholars “in many ways the most important ever written in the history of the disease” (25). just like erb before him, goldflam groups the symptoms in a pathological entity which he clearly distinguishes from progressive bulbar palsy and hysteria, without however giving it a name. friedrich jolly (1844-1904) – myasthenia gravis pseudoparalytica in 1895, the german neurologist and psychiatrist friedrich jolly (1844-1904) (figure 1) calls this condition for the first time myasthenia gravis pseudoparalytica when he reports the cases of two 14 and 15-year-old boys. by using faradic current for the electric stimulation of different groups of muscles, jolly sets the electrophysiological pattern of mg. the test was known by the name of the jolly test, yet the doctor’s residents would call it the not-so-jolly test because of the pain it inflicted. jolly thus noted that fatigue also occurred in non-stimulated muscle groups, which virtually reiterated what thomas willis had suggested almost 250 years before, namely that mg physiopathology was due to a circulating factor causing muscle fatigue. moreover, jolly noticed that fatigability set in on indirect recurrent stimulation, through the nerve, and that muscle contraction stopped at some point. he concluded that mg seemed to be a neuromuscular plate condition (15). starting with the 20th century, the number of mg cases increases exponentially, and the following natural step in the medical world was the attempt to clarify disease etiopathogenesis in order to find efficient therapies. the first connection between thymus and mg was suggested in 1899 by the german doctor hermann oppenheim (1858-1919) who discovered incidentally, when performing an autopsy on a mg patient, a tumor the size romanian neurosurgery (2016) xxx 1: 77 82 81 of a tangerine (20). a few years later, i.e. in 1901, the german forensic doctor karl weigert (1845-1904) detected a tumor in the anterior mediastinum of a mg patient, which originated in the thymus. the 5-5-3 cm tumor was made of lymphocytes, the same cells that also occurred in the striated muscle fibers. weigert closed the case by concluding that it was a particular form of mg, complicated by a thymus lymphoma, which caused metastases in the deltoid and diaphragm muscles (26). conclusions mg has a complicated history, with a golden age in the absence of which scientists would have been unable to elucidate the condition and doctors would have been unable to treat it. although the beginnings were vague, with a description recorded by historians, as science and hence the man’s ability to understand things evolved, increasingly relevant proof was collected, which contributed to the current clearly outlined etiopathogenesis of mg and accurate therapeutic guidelines. the complexity of the disease still holds nowadays, as the medical world has been exploring it and placing an emphasis on the genes involved, on new autoantigens and on new therapies to be administered both during seizures and as background therapy. what lasted for almost 350 years may be summarized in a single sentence: the first description originated in england, as did the first modern description of it, then its symptoms and name were set in germany, whereas its therapy and immunopathological foundations were laid later, starting with 1930, in the united states. figure 1 contributors to the physiopathology of the myasthenia gravis disease 82 croitoru et al myasthenia gravis correspondence dana mihaela turliuc “prof. dr. n. oblu” emergency clinical hospital iasi, romania e-mail: turliuc_dana@yahoo.com references 1.afifi ak. myasthenia gravis from thomas willis to the present. neurosciences (riyadh). 2005; 10(1): 3-13. 2.cunha fm, scola rh, werneck lc. myasthenia gravis. historical aspects. arq neuropsiquiatr. 1999; 57(2b):531536. 3.dreschfeld j. on a case of polioencephalomyelitis without any anatomical lesions. brit med j. 1893; 2:176177. 4.eadie mj. samuel wilks (1824-1911): neurologist and generalist of the mid-victorian era. j med biogr. 2008; 16(4):215-220. 5.eisenlohr c. ein fall von opthalmoplegia externa progressive und finaler bulbarparalzse mit negative sections-befund. neurol centralblat. 1887; 6: 337-390. 6.erb wh. handbook of electrotherapeutics. new york: william woods, 1833. 7.eycleshymer ac. anatomical names. new york: w. wood, 1917. 8.finger s, boller f, tyler kl. history of neurology: handbook of clinical neurology. edinburg: elsevier, 2009. 9.fortuine r. the words of medicine: sources, meanings, and delights. springfield: charles c thomas publisher, 2001. 10.goldflam s. ueber einen scheinarheilbaren bulbarparalytischen symptomencomplex mit beheiligung der extremitaten. deutsch z. nervenheilk. 1893; 4: 312-352. 11.guthrie l. myasthenia gravis in the seventeenth century. lancet. 1903; 1: 330-331. 12.hughes t. the early history of myasthenia gravis. neuromuscul disord. 2005; 15(12):878-886. 13.hughes jt. thomas willis 1621-1675: his life and work. n engl j med. 1933; 328: 816-817. 14.iacob g. writing in neurosurgery. romanian neurosurgery. 2016; xxx 1. 15.jolly f. ūber myasthenia gravis pesudoparalytica. berl klin wochenschr. 1895; 32:1-7. 16.keesey j. the role of herman hope of cincinnati in the initial clinical recognition of myasthenia gravis. journal of the history of the neurosciences. 2003; 2: 167174. 17.koehler pj, bruyn gw, pearce jms. neurological eponyms. oxford: oxford university press, 2000. 18.magiorkinis e, diamantis a, sidiropoulou k, panteliadis c. highights in the history of epilepsy: the last 200 years. epilepsy res treat. 2014; 2014: 1-13. 19.marsteller hb. the first american case of myasthenia gravis. archives of neurology.1988; 45(2): 185-187. 20.mimenza-alvarado a, tellez-zenteno j, garciaramos g, estañol b. the history of myasthenia gravis. men and ideas. neurologia. 2007; in press. 21.oppenheim h. ueber ein fall von chronischer progressive bulbar paralyse ohne anatomischen befund. virch archiv path anat phys. 1887; 180: 522-530. 22.pearce jms. sir samuel wilks (1824-1911): the most philosophical of english physicians. eur neurol. 2009; 61:119-123. 23.pearce jms. sir samuel wilks (1824–1911): on epilepsy. eur neurol. 2009; 61:124–127. 24. stone mj. samuel wilks: the “grand old man” of british medicine. proc (bayl univ med cent). 2010; 23(3): 263–265. 25.viets hr. a historical review of myasthenia gravis from 1672 to 1900. jama. 1953; 153:1273-1280. 26.weigert c. pathologisch-anatomischer beiträg zur erb’schen krankheit (miashenia gravis). neurologisches centralblatt. 1901; 20:597-601. 27.wilks s. on cerebritis, hysteria and bulbar paralysis. guy’s hospital reports. 1877; 22:7-55. 28.willis t. pordage s. de anima brutorum. two discourses concerning the soul of brutes, which is that of the vital and sensitive of man. london: dring, 1683. doi: 10.33962/roneuro-2020-086 multilocular hydrocephalus harold vasquez, ezequiel garcía-ballestas, luis rafael moscote -salazar, sergio a serrato, william a florez, amit agrawal romanian neurosurgery (2020) xxxiv (4): pp. 509-511 doi: 10.33962/roneuro-2020-086 www.journals.lapub.co.uk/index.php/roneurosurgery multilocular hydrocephalus harold vasquez1,5, ezequiel garcía-ballestas2, luis rafael moscote-salazar3, sergio a serrato4, william a florez5, amit agrawal6 1 facultad de ciencias de la salud, universidad del sinu elias bechara zainum, cartagena de indias, colombia 2 center for biomedical research (cib). faculty of medicine university of cartagena, colombia 3 neurosurgeon. critical care. center for biomedical research (cib). director of research line cartagena neurotrauma research group. faculty of medicine university of cartagena, colombia 4 uros clinic, neiva, colombia 5 latin-american council of neurointensivism clani, cartagena, colombia 6 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india abstract multilocular hydrocephalus is an entity that occurs relatively frequently in neurosurgical practice. we are present an editorial letter with a mini-review of the pathophysiology, surgical, and medical treatment. multiloculated hydrocephalus (mh) has also been termed as a multiseptate hydrocephalus, polycystic hydrocephalus, interventricular septum and can be unilocular or multiloculated. 5,6,9 mh is characterized by the presence of septations or obstructions within the normal ventricular system, leading to cerebrospinal fluid (csf) accumulation due to a lack of communication between ventricles 4,6,8,10,11. although the etiology and pathogenesis not clearly known, the presence of septations has been considered to be caused by a fibrous adhesion within the ventricles or by inflammation leading to sub ependymal gliosis leading to glial bumps and septations leading to ventricular obstruction4,8,9 . many etiological factors have been shown to associate with multiloculated hydrocephalus such as many intracranial processes as infection, intracranial hemorrhage, bacterial or fungal meningitis, congenital malformations, birth trauma, tumors, intracranial surgery, among others 2, 6, 8,10,11 histologically, ventricular septum it is origins from a glial protrusion keywords multilocular hydrocephalus, hydrocephaly, endoscopic neurosurgery, operative approach corresponding author: william a florez latin-american council of neurointensivism clani, cartagena, colombia william-florez@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 510 harold vasquez, ezequiel garcía-ballestas, luis rafael moscote-salazar et al. in ventricles4. the clinical presentation is determined by the most frequent manifestations of complicated hydrocephalus, such as: enlargement of the head, convulsions, neurological impairment, sign of the setting sun (inability to look upwards, observed with higher frequency in infants), headache or mental retardation3,7. on the other hand, in the worst scenario, many patients may have the intracranial pressure (icp) increased, presented as a consequence of the expansion or enlargement of the ventricles (ventriculomegaly) 3,10. computed tomography (ct) and magnetic resonance imaging (mri) allow visualization of the multiple cavities with csf and irregular dilations with multiple septations (figure -1)2,4,9,10. the complications may be obtained by catheters and interventions to relief the symptoms caused by raised intracranial pressure, however, the primary goal is to establish communication between existing compartments and thereby achieve the diversion of the csf 8,10 treatment seeks to restore communication between isolated intraventricular compartments, in order to create a single cavity and implement a single bypass 11 .treatment options include placement of multiple bypass systems, endoscopic fenestration of localized compartments, septostomy, third endoscopic ventriculostomy, stereotactic aspiration, or craniotomy for the microsurgical fenestration of localized compartments or combination of several surgical principles.2,3,4,10 this mentioned open surgical and endoscopic approach effective at improving adequate function of csf derivation. furthermore, endoscopic techniques have the advantage in decrease time of surgery, need of transfusion and length hospital stay1.the craniotomy and open surgical approach show a better success rate in severity and/or refractory chases1,2 figure 1. ct scan (a-e), mri (f and g) and usg images showing characteristic imaging appearance of multiloculated hydrocephalus i.e., dilated ventricle and multiple septations. references 1. akbari sha, holekamp tf, murphy tm, mercer d, leonard jr, smyth md, et al. surgical management of complex multiloculated hydrocephalus in infants and children. child’s nerv syst. 2015;31(2):243–9. 2. andresen m, juhler m. multiloculated hydrocephalus: a review of current problems in classification and treatment. child's nervous system: chns : official journal of the international society for pediatric neurosurgery 2012;28:357-362. 3. chamilos c, sgouros s. intrauterine grade iv intraventricular hemorrhage in a full-term infant leading to hydrocephalus. child's nervous system: chns: official journal of the international society for pediatric neurosurgery 2013; 29:861-865. 4. el-ghandour nm. endoscopic cyst fenestration in the treatment of multiloculated hydrocephalus in children. 511 multilocular hydrocephalus journal of neurosurgery pediatrics 2008;1:217-222. 5. eshra ma. endoscopic management of septated, multiloculated hydrocephalus. alexandria journal of medicine 2014;50:123-126. 6. jamjoom ab, mohammed aa, al-boukai a, jamjoom za, rahman n, jamjoom ht. multiloculated hydrocephalus related to cerebrospinal fluid shunt infection. acta neurochirurgica 1996;138:714-719. 7. kirkpatrick m, engleman h, minns ra. symptoms and signs of progressive hydrocephalus. archives of disease in childhood 1989;64:124-128. 8. lee yh, kwon ys, yang kh. multiloculated hydrocephalus: open craniotomy or endoscopy? j korean neurosurg soc 2017;60:301-305. 9. lewis ai, keiper gl, jr., crone kr. endoscopic treatment of loculated hydrocephalus. journal of neurosurgery 1995;82:780-785. 10. sandberg di, mccomb jg, krieger md. craniotomy for fenestration of multiloculated hydrocephalus in pediatric patients. neurosurgery 2005;57:100-106; discussion 100-106. 11. zuccaro g, ramos jg. multiloculated hydrocephalus. child's nervous system : chns : official journal of the international society for pediatric neurosurgery 2011;27:1609-1619. 19kumar_posttraumaticchronic 358 kumar, mittal posttraumatic chronic ossified extradural hematoma posttraumatic chronic ossified extradural hematoma: a rare case report rakesh kumar1, radhe shyam mittal2 sawai man singh medical college, jaipur, rajasthan, india 1registrar, department of neurosurgery 2professor & head department of neurosurgery abstract posttraumatic chronic ossified extradural hematomas are rare entities. natural absorption of edh does not occurs due to calcification. chronic ossified edh is frequently present in paediatric age group. careful regular follow-up is mandatory in conservatively managed case of edh in children. we report a rare case of posttraumatic chronic ossified extradural hematomas in a 10-years old girl presenting six years after head injury with right temporal region swelling. key words: chronic extradural hematoma, ossification, head injury. introduction chronic ossified extradural hematomas are rare entities. most of the reported cases are in paediatric age group [6]. patients with good neurological state can be follow-up with computed tomography. in conservatively managed case of edh in children careful follow-up is mandatory [12]. the mechanism of calcification of edh is not well understood. we report a case of posttraumatic chronic ossified edh in child presented with progressively increasing swelling in right temporal region since one year, having past history of fall from tree six years back.. case report a 10 years old female patient presented with complain of gradual progressive painless swelling in right temporal region since one year. on examination patient was conscious oriented without any neurological deficient. patient vitals were stable. her complete blood count, coagulation profile, and serum biochemistry were in the normal range. she had past history of fall from tree six years back, following that she developed swelling in right temporal region. patient was treated by local doctor and as patient was conscious oriented, she was managed conservatively. no x-ray or ct scan head was done at that time. this swelling persisted in right temporal region without any symptom, so no medical advice was taken by patient. after increase in size of the swelling x-ray skull was done by local doctor which shows calcification in right temporal region (figure romanian neurosurgery (2014) xxi 3: 358 360 359 1). at our hospital ct scan head was done which revealed right temporal extradural heterogenous lesion with calcified walls (figure 2). craniectomy with excision of underlying bone and evacuation of hematoma was done. liquefied altered blood with thick hard calcified walls adherent to duramater was present. on histological examination of the specimen chronic ossified hematoma full of blood mixed fluid was confirmed. patient was discharged on seventh postoperative day. cranioplasty was done after six months by using bone cement. figure1 shows calcification in right temporal region (black arrow) discussion the incidence of post traumatic edh ranges from 2.7% to 4%. (4, 5, 6, 9, 10, 11). chronic edh accounts for 3-30% of all epidural hematomas. trauma being the most common cause, the other causes may be following neurosurgical procedures like shunt or posterior fossa surgery (1). chronic extradural hematoma calcification has been reported in literature as an isolated case report (4, 5, 6, 9, 10, 11). figure 2 shows right temporal extradural heterogenous lesion with calcified walls (black arrow) early calcification in traumatic edh is extremely rare. epidural hematoma may have various clinical presentation, mostly they present as neurosurgical emergencies requiring urgent surgical evacuation. initially they may be asymptomatic, and may also enlarge producing pressure symptoms later. the usual symptoms are headache, seizure or may be asymptomatic. in paediatric age group, due to relatively firm adherence of dura to inner table and suture line the occurrence of edh is unusual. in children, the edh is of venous origin which takes longer time for accumulation of blood upto an adequate volume to cause significant mass effect and symptoms (8).in a case reported by kawata et al, ossification of edh occurred 4 months and 12 days after head injury (7). erdogen et al reported a case of epidural hematoma ossification within 10 days of injury in a 8 year old child (5). chang et al reported ossification of edh 73 days after head injury with 360 kumar, mittal posttraumatic chronic ossified extradural hematoma emphasis on surgical importance even if the patient condition is stable (4).the precise mechanism of calcification or ossification is uncertain. it has been hypothesized that vascularised tissue damage such as bone and dura provokes inflammation and remodelling in tissues (2).the natural sequence of healing is more rapid in children than adult. meanwhile, edh expansion may result from repeated bleeding of inner table of skull (8) or due to oozing from dural surface veins (13). some authors presume that the ossification starts at junction between dura and hematoma capsule (6, 11). a characteristic intracranial, double outlined contour on plain skull x-ray and ct scan represents bone formation and calcification of hematoma capsule adjacent to dura (3). for calcified edh causing mass effect or neurological deterioration, surgical treatment in form of evacuation is recommended. conclusion we conclude that while conservative management of edh in children, regular follow up is mandatory. calcification of edh should be considered in children with persistent symptoms, seizures or neurological deterioration. urgent evacuation of edh should be considered for children with symptoms of mass effect or neurological deterioration. correspondence dr radhe shyam mittal (mch.) professor & head of department, department of neurosurgery, sawai man singh medical college, jaipur, rajasthan, india, 302004. e-mail: rksingh2226@gmail.com. dr_mittal@hotmail.com abbrebiations: edh: extradural hematoma references 1. bayri y, ulas a.k, aykan u, kaya a.h, dagcınar a: iatrogenic chronic calcified/ossified epidural hematoma: case report j nervous sys surgery 2009; 2(2):91-94 2. buckwalter ja, cruess rl. healing of the masculoskeletal tissues; in rockwood ca, green dp, bucholz rw (eds):fractures in adults, ed 3, philadelphia, lippincott 1991; vol1, pp 181-222. 3. cambria s, marra ga, di perri r, bramanti p. ossified epidural hematoma. report of a case with epilepsy. j neurosurg sci 1985;29:285-8.15. 4. chang jh, choi jy, chang jw, park yg, kim ts, chung ss.chronic epidural hematoma with rapid ossification.childs nerv syst 2002;18:712-6. 5. erdogan b, sen o, bal n, cekinmez m, altinors n. rapidly calcifying and ossifying epidural hematoma pediatr neurosurg 2003;39:208-11. 6. iwakuma t, brunngraber cv. extradural ossification following an extradural hematoma. j neurosurg 1974;41:104-6. 7. kawata y, kunimoto m, sako k, hashimoto m, suzuki n, ohgami s,et al. ossified epidural hematomas: report of two cases. no shinkei geka 1994;22:51‑4. 8. kaye em, cass pr, dooling e, rosman np. chronic epidural hematomas in childhood: increased recognition and non‑surgical management. pediatr neurol 1985;1:255‑9. 9. leclercq ta,rozycki t. chronic calcified epidural hematoma in a child ri med j 1979; 62, 97-9. 10. mathuriya sn, kak vk, banerjee ak. ossified epidural hematomas: report of two cases.clin neurol neurosurg 1989; 91:269-72. 11 nagane m, oyama h, shibui s, nomura k, nakanishi y,kamiya m. ossified &calcified epidural hematoma incidentally found 40 years after head injury: case report.surg neurol 1994; 42: 65-69.. 12. pang d, horton ja, herron jm, wilberger je jr, vries jk. nonsurgical management of extradural hematomas in children. j neurosurg 1983;59:958-71. 13. raimondi aj: trauma; in raimondi aj (eds): pediatric neurosurgery, new york, springer, 1987; pp 343-377. microsoft word dobrin_acquired_f n. dobrin et al acquired parietal intradiploic encephalocele acquired parietal intradiploic encephalocele. case report and review of the literature n. dobrin¹, mihaela bălinişteanu¹, b. costăchescu¹, cornelia tudorache², a. chiriac, i. poeată¹ “prof. dr. n. oblu” clinical emergency hospital, iaşi, romania ¹department of neurosurgery; ²department of radiology abstract very few cases of intradiploic encephalocele in adulthood have been reported in the literature. in our paper we describe a case of parietal intradiploic encephalocele, which presents with simple partial seizures. preoperative imaging (ct and mri) showed brain herniation within the intradiploic space. diagnosis was confirmed at surgery. postoperatively the patient recovered from his presenting symptoms. keywords: brain herniation, intradiploic encephalocele introduction parietal cephaloceles may develop spontaneously as congenital maldevelopments or may occur subsequently to acquired processes, such as infection, trauma, neoplasms, surgical procedures. an intradiploic location of these cephaloceles is extremely rare. in this communication, we report a case of symptomatic parietal intradiploic encephalocele and we debate upon its possible origin and review the pertinent literature. case report history and examination a 75-year-old man presented to our clinic with a 1-month history of partial seizures in the right inferior limb. his neurological examination revealed no focal abnormalities. nothing was found on the examination of his scalp. his medical history revealed type 2 diabetes, high blood pressure, coronary heart disease, hepatitis c, but no head trauma, febrile seizures, stroke, brain tumor, central nervous system infection. his family history was uneventful. neuroimaging the axial bone window ct image depicts a small defect of the inner table, widened diploic space, and thinned outer table in the left parietal parasagittal bone. the axial brain window ct image (semioval center section) reveals small brain herniation through the osseous defect (figure 1). figure 1 left: the axial bone window ct-onecentimeter inner table parietal calvarial defect is noted, with scalloped margins of the intradiploic calvarial lesion. thinning of the outer table of the calvarium is marked. right: the parietal osseous defect has marginal sclerosis and contains a small amount of herniated brain. romanian neurosurgery (2011) xviii 2 magnetic resonance (mr) imaging showed a lesion in the left parietal parasagittal intradiploic space continuous with the left parietal lobe appearing isointense with the normal brain on t1weighted (figure 2) and t2-weighted images (figure 3). coronal t2-weighted, sagittalt1weighted images (figure 4) show a defect in the left parietal bone, which contains csf and herniated cerebral tissue. the csf is continuous with the subarachnoid space. the underlying parietal lobe had similar signal intensity properties. the superior sagittal sinus is intact. t1-weighted mr imaging with gadolinium revealed no enhancement of the lesion. (figure 5) figure 2 axial t1w image shows intradiploic extension within the left parietal bone figure 3 axial t2w image shows a signal isointense to the csf in the left parietal bone figure 4 coronal t2w image (left) reveals the patency of the superior sagittal sinus and the dural discontinuity and brain herniation on sagittal t1w image (right) figure 5 coronal and sagittal t1w contrastenhanced mr image surgery after the endotracheal induction of general anesthesia, the patient was placed in a supine position, with the head slightly raised and turned to the right side. an arcuate skin incision was performed and the pericranium was preserved carefully. the exposed underlying paper-thin bone (1 cm diameter) was pulsatile. we performed a craniectomy around the margin of the bone lesion exposing a dural defect of approximately 1 cm in diameter in which a small amount of brain herniated. the superior sagittal sinus was intact. the margins of the dura were carefully dissected and the herniated tissue excised. dura was reconstructed afterwards with the aid of pericranium; following local hemostasis the skin incision was closed with separate sutures. pathological examination of the n. dobrin et al acquired parietal intradiploic encephalocele resected specimen revealed gliotic and normal cerebral cortex. postoperative course the patient received 600 mg carbamazepine per day for three months after surgery, and he remained seizure free on his 6-month follow-up. discussion and conclusions a cephalocele is defined as a protrusion of intracranial contents through a defect in the skull or dura. cephaloceles are classified by their contents (meningocele, meningoencephalocele, hydromeningoencephalocele) and by the location of the cranial defect through which the herniation occurs. the herniating neural tissue may include meninges, brain parenchyma, ventricles and vascular structures [4]. a cephalocele can result from various causes: infection, trauma, surgery, tumors. those which develop in absence of an evident cause are congenital or early postnatal maldevelopments termed spontaneous meningoencephaloceles. these spontaneous lesions usually occur at the site of a cranial suture, and most of them represent primary or secondary midline closure defects of the neural tube. the vault of the neurocranium is derived from the paraxial mesoderm. during the 8th week of development, the two parietal bones undergo membranous ossification from two primary centers for each bone, appearing on the parietal tuber. at 4 months, the fusion between these centers is complete. at birth the parietal bones are unilaminar and are separated by the sagittal suture. at the age of 4 there appears the differentiation between inner and outer table and the ossification of the sagittal suture begins at the same time for the two layers, but the outer tables could fuse slowerly and sometimes incompletely. a complete fusion takes place by the age of 20. defects in closure of the sagittal suture allow the herniation of the brain, but they involve both tables [3, 12, 13]. parietal cephaloceles are very rare (1% of all cerebrospinal malformations and 10% of cephaloceles [11]) and if they are congenital, they are usually associated with many anomalies such as corpus calosum agenesis, chiari ii, dandy-walker malformation. the intradiploic encephaloceles are also extremely rare, only few cases are mentioned in the literature. in their case report patil, et al. [9] presented a 64-yearold man with a posttraumatic intradiploic meningoencephalocele after a head trauma. he bumped his head on a garage door and 8 months post-trauma he came to the hospital with a lump on his head. the authors concluded that their case was a variation of an adult growing skull fracture due to the blunt trauma to the head, an intradiploic arachnoidal cyst containing csf and brain. lenthall, et al. [6], also presented a case of a growing skull fracture with the intradiploic extension within the occipital and parietal bone in a 6-month-old baby who sustained a head trauma after falling down the stairs, but, in this case, both inner and outer bone tables were eroded. a'teriitehau, et al. [1] described an intradiploic parietal encephalocele in a 73year-old woman with no history of significant head trauma, but they attributed the intradiploic defect to a minor trauma, without loss of consciousness, but strong enough to produce the destruction of the inner table and a dural tear. peters, et al. [11] came to the same conclusion with their patient who showed coordinative problems in his right leg, also without history of head trauma. martinez-lage, et romanian neurosurgery (2011) xviii 2 al. [8] reported a frontal intradiploic meningoencephalocele following a dural tear produced during surgery for craniosynostosis. this unusual lesion resembles the mechanism of the growing skull fracture. although the majority of reported intradiploic encephaloceles is of traumatic origin, four reports found no certain cause for these lesions [2, 5, 7, 14]. in all these cases, the lesion was at some distance from the midline and affected only the inner table. one patient [7] with an occult intradiploic encephalocele became symptomatic after a paroxysmal increase in the intracranial pressure. in another case [5], presenting generalized seizure and aphasia, the authors agreed to the congenital origin of the dural defect, through which the brain herniated. among the particularities of this case we can enumerate: the location of the lesion (close to the sagittal suture and superior sagittal sinus), the absence of significant head trauma, infection or neoplastic history, the integrity of the outer table. the differential diagnosis must be made between an acquired lesion and a congenital one. the location and the absence of an evident cause could suggest that the lesion in our patient was a congenital anomaly. however in a report conducted by patterson, et al. [10], in all cases of congenital parietal encephaloceles there was a global defect of both inner and outer table. also considering the embryologic development, a congenital lesion never involves just the inner table [3, 12, 13]. the absence of an associated malformation and the aspect of the bone defect led us to believe that the lesion was acquired, maybe due to an insignificant head trauma in early childhood. references 1. a'teriitehau c, adem c, levêque c, cordoliani ys.: intradiploic parietal meningoencephalocele. j radiol. 2004 may; 85 (5 pt 1): 646-8. 2. froelich s, botelho c, abu eid m, kehrli p, dietemann jl, maitrot d.: intradiploic encephalocele in an adult. a case report and review of the literature. neurochirurgie, 2006 dec; 52(6): 551-4. 3. gilbert-barness e, debich-spicer d: embryo and fetal pathology: color atlas with ultrasound correlation, cambridge university press, cambridge, 2004, pp 335366 4. ketonen l, hiwatashi a, sidhu r. pediatric brain and spine, an atlas of mri and spectroscopy. springerverlag berlin heidelberg , 2005, pp 28-33. 5. kosnik ej, meagher jn, quenemoen lr.: parietal intradiploic encephalocele. case report. j neurosurg, 1976 may; 44(5): 617-9. 6. lenthall r, penney c.: growing skull fracture extending posteriorly to the superior sagittal sinus with intradiploic extension. br j radiol. 1999 jul; 72 (859): 714-6. 7. loumiotis i, jones l, diehn f, lanzino g.: symptomatic left intradiploic encephalocele. neurology, 2010 sep 14; 75 (11): 1027. 8. martínez-lage jf, lópez f, piqueras c, poza m.: iatrogenic intradiploic meningoencephalocele. case report. j neurosurg. 1997 sep; 87 (3): 468-71. 9. patil aa, etemadrezaie h.: posttraumatic intradiploic meningoencephalocele. j neurosurg. 1996 feb; 84 (2): 284-7. 10. patterson rj, egelhoff jc, crone kr, ball ws jr.: atretic parietal cephaloceles revisited: an enlarging clinical and imaging spectrum? ajnr am j neuroradiol 1998 april; 19: 791-795. 11. peters j, raab p, marquardt g, zanella fe.: intradiploic meningoencephalocele. eur radiol. 2002 dec; 12 suppl 3:s25-7. epub 2002 apr 26. 12. sadler tw: langman’s medical embryology. 10th ed, lippincott williams &wilkins, baltimore, 2006, pp 126-143, 286-317 13. sperber gh, gutterman gd, sperber sm: craniofacial development, hamilton (on): bc decker inc, 2001, pp 81-88 14. tsuboi y, hayashi n, noguchi k, kurimoto m, nagai s, endo s.: parietal intradiploic encephalocelecase report. neurol med chir (tokyo), 2007 may; 47(5): 240-1. calinanikiadrian_chordomas romanian neurosurgery (2016) xxx 1: 15 27 15 chordomas, malignant spinal tumors: a 15-year experience niki adrian calina, cristian filip, daniel serban, marius podea, costica zamfir, gheorghe checiu, morosanu eduard, florin exergian “bagdasar-arseni” clinical emergency hospital, spine surgery, bucharest abstract: objective: spinal chordomas are rare, locally invasive, malignant neoplasm, representing 5% of all malignant tumors of the skeleton. in the majority of cases the segment involved is the sacrum. this study reviews our experience during the last 15 years at the spinal surgery department of “bagdasar-arseni” clinical hospital, to determine the effects of various treatment methods on the overall course of this disease process. methods: a retrospective study was performed, from 2000 to 2015, in which, 31 patients with spinal chordomas were evaluated at our institution. results: two thirds of patients were male, with a mean age of 57 years. patients presented with local pain, radiculopathy and bladder-bowel dysfunction at hospital admission. there were 24 patients with sacral chordomas, 4 with cervical chordomas, 2 with thoracic and one with lumbar chordoma. all patients underwent at least one surgical procedure. the main goal of surgery was to achieve total resection of the tumor. conclusion: our study suggests that spinal chordomas are rare tumors with a high risk of tumor recurrence. if total resection is achieved, the risk of recurrence diminishes. if the tumor resection is subtotal, than recurrence appears in all cases. after tumor resection, the surgeon faces the problem of spinal instability that needs solving. based on these findings, we think that, whenever possible, radical resection should be the treatment of choice for spinal chordomas. key words: chordomas, spine, tumor introduction chordomas are rare tumors, representing almost 5% af all malignant spinal tumors of the skeleton. they are regarded as slow growing tumors originated from the notochord which is implicated in the development of the axial skeleton. the superior portion of the notochord approaches the future sphenoid bone and develops into the occipital bone and the inferior portions develops into the sacrum and the coccyx. so chordomas can be located all the way from the spheno-occipital region to 16 calina et al chordomas: a 15-year experience the sacrococcygeal region. the main affected segment is the sacrum, followed by the spheno-occipital region and only in rare cases the mobile spine. (1) despite their slow growth treating spinal chordomas remains a challenge for neurosurgeons as tumor recurrence is very often. radiation therapy has been used for the treatment of spinal chordomas in association with surgical treatment. (2, 3, 4) patients that present with sacrococcygeal chordomas are in the majority of cases between 50 an 70 years old, and, usually, patients with tumors located in the sphenooccipital region are one decade younger. the reason for this is probably less space for spheno-occipital chordomas before causing clinical symptoms. (5) metastases are mainly located in the lungs, liver and lymph nodes and occur in 3-48% of patients. (8-10) local recurrence is the main problem in spinal chordomas and the main adverse prognostic factor. they are often insensitive to chemotherapy and radiotherapy. epidemiological data chordomas are malignant tumors with a very aggressive local invasion. the incidence is 0.08 per 100.000 people and make up for almost 5% of all malignant primary tumors of the skeleton. (6) the main category affected by this disease is represented by people above 50 years. the presence of chordomas is very rare in people younger than 40 years. the median survival period is 6.29 years with a 10 year survival of 39.9% (7). we included 31 patients with spinal chordomas, that were treated between 2000 and 2014 with a mean age of 57 years old. the youngest patient treated was 6 years old and the oldest patient was 81 years old. we observed that 80% of patients were older than 50 years and also noted a male predominance, the sex ratio male / female being 2/1 . 67.7% of patients were male and 32.3% female. figure 1 sex distribution in patients with spinal chordomas the study did not include patients with chordomas of the spheno-occipital region, only patients with spinal chordomas being admitted. in the majority of cases, 24 patients, the tumor was located in the sacral segment of the spine. there were 7 patients with chordomas of the mobile spine, 4 in the cervical region, 2 in the thoracic region and 1 in the lumbar region of the spine. although we observed a higher prevalence for the thoracic spine the limited number of patients did not allow us to determine the most frequent vertebral level affected in the mobile spine. in the majority of cases with sacral chordomas, 21 cases, the tumor involved only the inferior part of the sacrum. we observed a very low percentage of tumors located at the sacro-lumbar junction. romanian neurosurgery (2016) xxx 1: 15 27 17 figure 2 most frequent location of spinal chordomas figure 3 most frequent location of mobile spine chordomas figure 4 admission symptoms of patients with spinal chordomas patients and methods the article represents a retrospective study that includes all patients with spinal chordomas treated in our department in the last 15 years. there were 31 patients included, 21 male and 10 female. the majority of patients admitted presented for local pain and only in rare cases, patients presented for radiculopathy or bladder and bowel dysfunctions. local pain was present in 28 cases, radiculopathy in 4 cases, bladder or bowel dysfunctions in 4 cases and mielopathy in only one case. in evolution, the first symptom that occurred was local pain, which, if left untreated, lead to radiculopathy and in late stages to bladder and bowel dysfunctions. the mean duration of symptoms was 16 months, 12 months for men and 20 months for female. symptoms presented a slow progression from initial appearance to the moment of surgery. clinical symptoms are not specific for these lesions and progression is slow causing late hospital presentation and late diagnosis, in advanced stages with large tumor extension. diagnostic procedures the first diagnostic procedure is represented by plain x-ray demonstrating a lytic lesion or osteosclerosis in rare cases. (12, 13, 14, 15, 16, 17) the most frequent radiological finding is considered to be destruction of spine segments with soft-tissue extension. chordomas localized in the mobile spine originate in a single vertebral body usually. the intervertebral discs are spared by tumor extension. (18, 19, 20) 18 calina et al chordomas: a 15-year experience computerized tomography scanning is very important in establishing the grade of tumor extent. (12) the main tumor extension is usually anterior to the vertebral body displacing the major vessels or the ureters depending on the vertebral segment implied. ct scan is very useful for demonstrating the full extent of the tumor. (21) chordomas present low-intensity signal on t1weighted mri and high-intensity signal on t2weighted mri. mri offers the best possibility of diagnosis in spinal chordomas being very valuable in preoperative assessment, accurately depicting the tumor extent. (22, 23, 24, 25, 26, 27, 28) in our study we observed the presence of osteolytic processes in 100% of cases, being the major imagistic characteristic for spinal chordomas. we also observed the presence of soft tissue extension in 93% of cases. there were also 6% of cases that presented intratumoral calcifications. another imagistic characteristic observed in the study was reduced uptake on bone scintigraphy. table 1 imagistic characteristics imagistic characteristics of spinal chordoma osteolytic process 100% soft tissue extension 93% intratumoral calcifications 6% treatment there are two main types of treatment for spinal chordomas, surgical treatment and radiotherapy. surgery is the treatment of choice, offering the best an only change of cure. (29, 30, 31) surgical treatment the main goal of surgical treatment is complete tumor resection, spinal decompression (if needed), and, after tumor resection, spinal reconstruction. any surgical procedure without complete tumor resection will lead to tumor recurrence, usually with a more aggressive behavior and with a very low chance of complete resection leading inevitable to death. (23, 32) complete tumor resection should be done with wide resection margins. often, wide excision is difficult to achieve, but, the surgeon should have in mind that complete tumor resection is the only hope of total cure. in order to achieve complete resection careful preoperative case assessment is imperative. (23, 32, 33, 34, 24, 35) surgical treatment was applied in all cases the main goal being complete tumor resection and spinal decompression without neurologic impairment for the patient. we managed to achieve complete macroscopic tumor resection in 77% percent of cases and incomplete tumor resection in 33% of cases. none of the patients included in the study underwent spinal biopsies. the main factor that influenced tumor resection was the vertebral level implied. out of the 24 patients with sacral chordoma, complete tumor resection was achieved in 21 cases. there were 4 patients with cervical chordoma, 2 with complete tumor resection and 2 with incomplete resection, 2 patients with thoracic chordoma, both with incomplete tumor resection and one patient with lumbar romanian neurosurgery (2016) xxx 1: 15 27 19 chordoma with incomplete tumor resection. the type of resection was evaluated macroscopic and under magnification. table 2 resection type depending on tumor location region complete resection incomplete resection cervical 2 2 thoracic 0 2 lumbar 0 1 sacral 21 3 a throw preoperative evaluation of each case is needed, each case being particular. we used a multidisciplinary team approach in 8 cases associating a thoraco-abdominal surgeon and sometimes even a plastic surgeon. only 5 cases out of the 31 patients required spinal reconstruction using autologus bone grafts, screws, rods, and intervertebral implants. the reduced number of cases with spinal reconstruction is justified by the large number of tumors located in the inferior part of the sacrum where there is no need for spinal reconstruction. in all of the cases with spinal reconstruction the tumor was located in the mobile spine, 4 in the cervical spine and one in the thoracic spine. complete tumor resection was achieved in 2 out of this 5 cases. surgical treatment in sacral chordoma the sacrum represents the main location for sacral chordomas. 77% of patients (24 cases) presented sacral chordomas. surgical treatment was applied in all cases. in 21 cases we have chosen a posterior approach and, in 3 cases, a combined approach. we managed to achieve complete tumor resection in 21 cases and incomplete resection in 3 cases. in these 3 cases patients presented in a very late stage of tumor evolution with large tissue invasion. in these cases the tumor presented anterior extension surpassing the retrorectal fat tissue invading the rectum. a mixed operatory team was necessary and a combined approach, anterior and posterior was used. all 3 cases required rectal excision and colostomy. despite extensive surgical interventions, complete tumor resection was not possible. figure 5 number of surgical procedures per patient with sacral chordoma in 17 cases with sacral chordoma, only one surgical procedure was needed. it should be noted that the best chance of achieving complete tumor resection is in the first surgical procedure. reintervention for tumor recurrence has a higher degree of difficulty and the chances of complete resection are slim. 5 patients required 2 surgical procedures and one patient required three surgical procedures. as we reminded earlier, complete tumor resection is the main objective in treating chordomas. we observed that the tumor recurrence rate in patients with incomplete tumor resection was 100%, and only 14% in 20 calina et al chordomas: a 15-year experience patients with complete macroscopic tumor resection. the disease free interval was also very different between the 2 groups, 27 months in patients with complete resection opposed to only 8 months in patients with incomplete tumor resection. although we classified it as complete tumor resection after macroscopic and magnification evaluation, 14% of patients presented tumor recurrence. figure 6 disease free interval in patients with sacral chordoma another challenge for the surgeon is the embedding of sacral nerve roots in the tumor mass. in the majority of cases the sacral nerves were embedded in the tumor or very adherent to the tumor mass. in 87% of cases at least one sacral nerve had to be sacrificed. from 24 patients with sacral chordoma, 4 patients presented tumors with large extend, involving bilateral sacral nerves. all 4 patients presented with bladder and bowel dysfunction from admission. aggressive tumor resection required sacral nerve sacrifice because dissection and decompression were not possible. the tumor embedded the sacral nerves from s1 to s5. patients remained with permanent urinary catheter after surgical procedure. in 17 cases the sacrifice was limited to 1 or two nerves, unilateral and below s2 sacral nerve. we observed that preserving at least one s2 sacral nerve preserved the patient bladder function. as a general rule, if sacral nerve resection is needed in order to achieve total tumor resection, sacral nerves can be sacrificed safely, unilateral or bilateral, by preserving s1 and s2 sacral nerve roots. in cases with tumors that involved s1 and s2 nerves, preserving these nerves was impossible in order to achieve large tumor resection. postoperative complications were mainly represented by bladder and bowel dysfunctions. although it was included in the preoperative planning and not considered a complication, it should be noted that rectal resection and permanent colostomy was needed in 3 cases. 29% of patient presented bowel dysfunction after the surgical procedure which varies from minor emptying difficulties to incontinence. we observer that preserving s2 and s3 sacral nerve roots preserves bowel function and, sacrificing s3 nerve roots causes a large array of bowel dysfunctions. 50% of patients presented bladder dysfunction after surgical procedure, 33% without the need for a urinary catheter and 17% requiring permanent urinary catheter. patients with intact s2 sacral nerves presented minor or no bladder dysfunctions. romanian neurosurgery (2016) xxx 1: 15 27 21 figure 7 postoperative complications in patients with sacral chordoma we could not establish a standard approach for the treatment of spinal chordomas. each case requires preoperative planning and cautious evaluation in order to achieve the maximal resection possible. the approach was influenced by tumor location, tumor size and adjacent tissue extension. tumors that involve the s1 segment of the sacrum with downwards extension required complete sacrectomy, raising the problem of sacro-pelvic reconstruction. the indications for sacral reconstruction were: sacral resection above s2 vertebra, total sacral resection in which the whole sacroiliac joint is removed or partial sacral resection involving more than 50% of sacroiliac joint on each side. the surgical procedure is very complex, requiring the participation of specialists from several areas including neurosurgery, general surgery and plastic surgery. a variety of instrumentations has been used previously for reconstruction after total sacrectomy. from a biomechanical standpoint these devices progress in their level of sophistication as follows: the use of sacral bars spanning the ilia and connected to the spine with harrington rods and hooks (8), the use of the more advanced cotrel–dubousset rods and hooks with the sacral bars (or ao plates) (37, 38), the use of transpedicular screws (and an internal spinal fixator) with iliac screws connected by plates (39) and the use of vertical galveston rods attached to cross connecting spinal rods, plus a threaded transiliac rod. reviewing the literature, a variety of techniques for sacro-pelvic reconstruction are described: sacro-iliac joint screw fixation, iliac-sacral screw fixation, posterior ilio-sacral plating and screw fixation, custom-made prosthesis, galveston rod fixation with iliac screws and trans-iliac rods. in the majority of cases, 21 patients, we used a posterior approach. a combined approach was used in only 3 cases. a posterior approach is suitable for the majority of patients with sacral chordomas because it provides good visibility of the sacral nerves and the rectum, allows good visibility and resection of paravertebral tissue invasion which in believed to be involved in tumor recurrence and it facilitates a complete resection using the retrorectal fat tissue as cleavage plan. it is also a more common approach because of the familiarity with sacral anatomy for neurosurgeons. the approach strategy needs to be cautiously evaluated before the surgery. al 21 patients operated through a posterior 22 calina et al chordomas: a 15-year experience approach alone presented with sacral chordomas that didn’t extend beyond the retrorectal fat tissue invading the rectum. al 3 cases with rectal invasion were operated using a mixed operatory team through a combined approach, anterior and posterior. all cases associated rectal resection and permanent colostomy. as a general rule, posterior approach alone is not recommended in patients with sacral chordomas with rectal invasion. surgical treatment in cervical chordoma in the studied interval 4 patients with cervical chordomas where admitted in our department. the vertebral levels affected were c5 in one case, c5 and c6 in one case, c3 and c4 in one case and c4, c5, c6 in one case.. surgical treatment was applied in all cases, with spinal cord decompression, tumor resection and reconstruction. en block resection was not possible, piecemeal tumor resection being used in all cases. anterior approach was used in 2 cases and a combined, anterior and posterior approach in the other 2 cases. all 4 cases required anterior reconstruction using bone graft fusion harvested from the iliac crest or from the fibula associated with anterior metallic fusion. patients that were treated through a combined approach benefited also from posterior fusion using transarticular screws and rods. total tumor resection was achieved in 2 cases using a combined approach. in the other 2 cases treated through an anterior approach only incomplete tumor resection was possible associated with spinal cord decompression. in one case, the tumor invaded the cervical nerves from c4 to c6, and in the other case both vertebral arteries were involved in the tumor mass. the tumor was very adherent to the adjacent tissues and we could not find a cleavage plan to separate these structures from the tumor mass. as complete tumor resection was never an option in these cases only palliative surgery was used with spinal cord decompression and anterior spinal reconstruction without a secondary posterior approach. the only complication observed was transitory dysphonia in 2 cases. radiotherapy for spinal chordomas radiotherapy was recommended in all cases treated in our department. the value of radiotherapy in chordomas is long debated. radiation doses of 30 to 50 gy are indicated as palliative treatment with minimal risks. there are studies that report no difference in survival, duration of symptoms and progression in a heterogeneous group of patients that underwent radiotherapy with 50 to 60 gy compared with conventional fractions of less than 50 gy. (40) higher doses of 60 to 70 gy are required for potentially curative intent. (41) to achieve this high doses the technique implies the association of conventional radiotherapy and proton-beam irradiation. although the biological properties of proton beam are not significantly different from x-ray beams, their physical characteristics exhibited by a finite range of energy deposition with only minimal exit dose beyond the target region are significantly advantageous. these advantages are particularly important in achieving high-dose delivery to sacral chordomas. using this romanian neurosurgery (2016) xxx 1: 15 27 23 approach of x-ray and proton beam therapy combined with optimal surgery, improved local control was achieved at doses greater than 77 cge. (42) all patients admitted in the study were treated after surgery with conventional radiotherapy. unfortunately, proton beam therapy was not available. the results were disappointing. although treated with radiotherapy patients developed tumor recurrence in all cases with incomplete resection and in 14% of cases with radical tumor resection. case presentation a 65 year old woman presents to our department for local pain localized in the thoraco-lumbar junction, and neurologic deficit, graded frankel d below t11, and radicular pain in t12 and l1 dermatomes on the right side. plain x-rays were not helpful for diagnosis. after spinal mri, we revealed a tumor with extension into the spinal canal, very adherent to the dura mater and severe cord compression with massive paravertebral extension and anterior extension to the limit of the retroperitoneal space, coming in close contact with the right kidney without invading it. . we used a posterior approach through l1 complete laminectomy and partial t12, l2 laminecomty. almost all structures of l1 vertebra were destroyed by the tumor mass. an l1 corpectomy was necessary with t12 and l1 discectomy. for spinal reconstruction we used an expandable cage, pmma and posterior metallic fusion with transpedicular t12 and l2 screws. we managed to achieve complete tumor resection under optic magnification. the pacient was released from the hospital without with minimal neurologic deficit, and was without neurologic deficit at the 2 months follow-up. figure 8 initial mri image of l1 spinal chordoma 24 calina et al chordomas: a 15-year experience after 1 year, she presented with frankel d paraplegia, and radicular pain in l1 and l2 dermatomes on the left side. spinal mri shows tumor recurrence situated on the left side with spinal cord compression. a second surgical procedure was necessary focused on the left side this time with disection and in-block resection of the tumor mass. the intersomatic cage was left in place and we used reconstruction with pmma also in t12 and l2 for better stability. complete tumor resection under optic magnification was achieved. the patient was released with no neurologic deficit and no symptoms of spinal instability. at the 5 year follow-up patient presented without tumor recurrence. figure 9 mri image showing tumor recurrence after 1 year and postoperative control image after second surgical intervention prognosis factors because of the low incidence, only 0.5 cases per million people, there are few centers with large experience in treating this type of tumors, the majority of studies presenting very small series of patients or case presentations. (43, 44) the majority of earlier studies reported a very high rate of local recurrence and metastasis in up to 60% of sacral chordomas. (10, 24) the reported rates of local recurrence and metastasis depend on the quality of the initial surgery, the length of follow-up, and the autopsy rate. (44, 45) tumor control in spinal chordomas improved significantly with more aggressive surgery. local recurrence was almost a rule in the past, but, in our last 15 years we observed a tumor recurrence rate of 32%. based on the type of tumor resection, the recurrence rate was 14% in cases considered with complete tumor resection and 100% in cases with incomplete tumor resection. the resection margins appear to be a critical factor in the final outcome of patients. romanian neurosurgery (2016) xxx 1: 15 27 25 based on our study we concluded that the main adverse prognosis factors in the treatment of spinal chordomas are: • incomplete resection of the tumor with inadequate surgical margins • large tumor size • surgical procedures for tumor recurrence • presence of metastases • presence of microscopic tumor necrosis we noted some differences observed in 15 years of treating spinal chordomas. the incidence increased over time, which we believe is mainly associated with an increased accessibility for ct and mri imaging over the years. we also observed that postoperative neurologic impairment after surgery decreased in time. although the percentage of patients with total tumor resection increased, the surgical procedures that were used were less invasive over time. another thing that benefits complete tumor resection even if that means complete corpectomy or vertebrectomy is the evolution of spinal implants, restoring stability after complete tumor resection being no longer a problem. conclusions chordomas are rare tumors, affecting mainly the sacral segment of the spine. patients present with unspecific clinical symptoms causing late hospital presentation and late diagnosis. the biggest concern is represented by tumor recurrence and local invasion if gross total resection is not achieved. the treatment of chordomas requires both aggressive resection and caution in achieving marginal tumor resection. if total resection is not achieved, tumor recurrence is a rule. extensive tumor resection above s2 vertebra raises the problem of sacral reconstruction. from a histopathological point of view, chordomas are considered benign tumors, but, thanks to their aggressive recurrence they are classified as malignant tumors. metastasis are rare but can occur, mainly in the lungs, liver and lymph nodes. adjuvant therapy is controversial but known to contribute to longterm disease control and survival. acknowledgements this paper is supported by the sectoral operational programme human resources development (sop hrd), financed from the european social fund and by the romanian government under the contract number posdru/187/1.5/s/156040/ references 1. willis ra: pathology of turnouts, ed4. london: butterworths, 1967, p 937 2. murad tm, murthy msn: ultrastructure of a chordoma.cancer 25:1204-1215, 1970 3. ribbert h: ueber die ecchondrosisphysalifora sphenooccipitalis. zallg path pathanat 5:457-461, 1894 4. windeyer bw: chordoma. president's address. proc r. soc med 52:1088-1100, 1959 5. papagelopoulos pj, mavrogenis af, galanis ec, et al.chordoma of the spine: clinicopathological features, diagnosis and treatment. orthopedics 2004;27:1256–63. 6. volpe r, mazabraud a. a clinicopathologic review of 25 cases of chordoma (apleomorphic and metastasizing neoplasm). am j surgpathol1983;7:161–70. 7. mcmaster ml, goldstein am, bromley cm, ishibe n, parry dm. chordoma: inci-dence and survival patterns in the united states, 1973–1995. cancer causescontrol2001;12:1–11. 8. mcpherson cm, suki d, mccutcheon ie, gokaslan zl, rhines ld, mendel e.metastatic disease from spinal 26 calina et al chordomas: a 15-year experience chordoma: a 10-year experience. j neurosurgspine2006;5(4):277–80, http://dx.doi.org/10.3171/spi.2006.5.4.277. 9.vergara g, belinchón b, valcárcel f, veiras m, zapata i, de la torre a.metastatic disease from chordoma. clintransloncol2008;10(8):517–21, http://dx.doi.org/10.1007/s12094-008-0243-4. 10. chambers pw, schwinn cp. chordoma. a clinicopathologic study of metastasis.am j clinpathol1979;72:765–76. 11. bergh p, kindblom lg, gunterberg b, remotti f, ryd w, meis-kindblomjm.prognostic factors in chordoma of the sacrum and mobile spine: a study of 39patients. cancer 2000;88(9):2122–34. 12. edwards cc: spinal tumors, in donovan post mj (ed): computed tomography of the spine. baltimore: williams & wilkins,1984, p 705 13. macnab i, mcculloch j: backache, ed 2. baltimore: williams & wilkins, 1990, pp 72–74 14. utne jr, pugh dg: the roentgenologic aspects of chordoma. ajr 74:593–608, 1955 15. ducou-le pointe h, brugières p, chevalier x, et al: imaging of chordomas of the mobile spine. j neuroradiol 18:267–276,1991 16. roddie m, adam a, lambert h, et al: case report 516: lumbar vertebral chordoma causing sclerosis of affected vertebra (3rdlumbar vertebra). skeletal radiol 17:611– 613, 1989 17. wellinger c: [spinal chordoma. ii. review of the literature since 1960.] rev rhum mal osteoartic 42:195– 204, 1975 (fr) 18. sennet e j: chordoma: its roentgen diagnostic aspectsand its response to roentgen therapy. am j roentgenol69:613-622, 1953 19. utne jr, pugh dg: the roentgenologic aspects ofchordoma. am j roentgenol 74:593-608, 1955 20. wood eh jr, himadi gm: chordomas: a roentgenologic study of sixteen cases previously unreported. radiology 54:706-716, 1950 21. spinal chordomasnarayan sundaresan, m.d., joseph galicich, m.d., florence, c chu, m.d.,and andrew g. huvos, m.d., j neurosurg 50:312-319, 1979 22. bas t, bas p, prieto m, et al: a lumbar chordoma treated with a wide resection. eur spine j 3:115–117, 1994 23. benoit j, videcoq p, hardy p, et al: [spinal chordoma. a case report on chordoma of the l3 vertebra.] rev rhum mal osteoartic57:557–561, 1990 (fr) 24. chevalier x, voisin mc, brugières p, et al: [chordoma of the mobile spine. report of 9 cases. review of the literature.] revrhum mal osteoartic 57:767–778, 1990 (fr) 25. ducou-le pointe h, brugières p, chevalier x, et al: imaging of chordomas of the mobile spine. j neuroradiol 18:267–276, 1991 26. findlay gfg: tumors of the lumbar spine, in jayson miv (ed): the lumbar spine and back pain, ed 4. edinburgh: churchill livingstone, 1992, pp 355–369 27. stephens gc, schwartz hs: lumbosacral chordoma resection: image integration and surgical planning. j surgoncol 54: 226–232, 1993 28. yuh wt, flickinger fw, barloon tj, et al: mr imaging of unusual chordomas. j comput assist tomogr 12:30–35, 1988 29. higinbotham nl, phillips rf, farr hw, et al: chordoma.thirty-five-year study at memorial hospital. cancer 20: 1841–1850, 1967 30. rich ta, schiller a, suit hd, et al: clinical and pathologic review of 48 cases of chordoma. cancer 56:182–187,1985 31. sundaresan n, galicich jh, chu fc, et al: spinal chordomas. j neurosurg 50:312–319, 1979 32. sundaresan n: chordomas. clinorthop 204:135–142, 1986 33. stener b: complete removal of vertebrae for extirpation oftumors. a 20-year experience. clinorthop 245:72–82, 1989 34. stephens gc, schwartz hs: lumbosacral chordoma resection: image integration and surgical planning. j surgoncol 54:226–232, 1993 35. hartofilakidis-garofalidi sg, papathanassiou bt, kamabouroglou g: chordoma of the lumbar spine. intsurg 50:566–570,1968 36. shikata j, yamamuro t, kotoura y, et al: total sacrectomy and reconstruction for primary tumors. j bone joint surg (am)70:122–125, 1988 37. santi md, mitsunaga mm, lockett jl: total sacrectomy for a giant sacral schwannoma. a case report. clinorthop 284: 285–289, 1993 38. tomita k, tsuchiya h: total sacrectomy and reconstruction for huge sacral tumors. spine 15:1223– 1227, 1990 39. blatter g, ward egh, ruflin g, et al: the problem of stabilizationafter sacrectomy. arch orthop trauma surg romanian neurosurgery (2016) xxx 1: 15 27 27 114: 40–42, 1994 40. cummings bj, hobson di, bush rs: chordoma: the results of megavoltage radiation therapy. int j radiatoncolbiolphys9:633–642, 1983 41. aprin h: primary malignant tumors of the spine, in akbarniaba (ed): spine: state of the art reviews. philadelphia: hanley&belfus, 1988, vol 2, pp 289–299 42. hug eb, fitzek mm, liebsch nj, et al: locally challenging osteoand chondrogenic tumors of the axial skeleton: results of combined proton and photon radiation therapy using threedimensionaltreatment planning. int j radiatoncolbiolphys31:467–476, 1995 43. eriksson b, gunterberg b, kindblom lg. chordoma. a clinicopathologicand prognostic study of a swedish nationalseries.actaorthopscand1981;52:49 –58. 44. gunterberg b, norlen l, stener b, sundin t. neurourologicevaluation after resection of the sacrum. invest urol1975; 13:183–8. 45. chambers pw, schwinn cp. chordoma. a clinicopathologicstudy of metastasis.am j clinpathol1979;72:765–76. 3stefanescuf_surgicaltreatment romanian neurosurgery (2014) xxi 3: 269 273 269 surgical treatment of a dissecting aneurysm of the superior cerebellar artery: case report florin stefanescu1, stefanita dima2, mugurel petrinel radoi1 national institute of neurology and neurovascular diseases – bucharest 1neurosurgical department 2neuroradiological department abstract dissecting aneurysm located in the peripheral region of the superior cerebellar artery is very rare. there is little experience regarding their surgical or endovascular treatment. we present the case of a peripheral dissecting superior cerebellar artery aneurysm treated by surgical clipping. key words: dissecting peripheral aneurysm, superior cerebellar artery, surgical treatment. introduction aneurysms located on the superior cerebellar artery (sca) are uncommon, accounting for only 0.2% of all intracranial aneurysms (11, 12, 17). few cases of dissecting aneurysms involving the distal portion of the sca have been previously described (14, 18). due to the rarity of these aneurysms, there is little consensus in the literature about their assessment, treatment and prognosis. owing the proximity to the vital structures and to the frequent inability to preserve the involved parent artery, surgery of these lesions is challenging. endovascular therapeutic approach becomes an alternative method of treatment (3, 4). along with a review of the existing literature on this matter, we described our experience with a case of peripheral sca dissecting aneurysm treated by microsurgical clipping. case report a 28-year-old woman was admitted to hospital presenting with a 4-day history of headache, dizziness, vomiting and diplopia. she had no relevant medical history. neurological examination revealed only a right-sided fourth cranial nerve palsy, slight right dismetria and mild nuchal rigidity. initial unenhanced cerebral computed tomography (ct) scan showed perimesencephalic and right cerebellopontine angle (cpa) subarachnoid hemorrhage (sah). four vessels cerebral angiogram revealed an irregular aneurysm, 3 mm. in diameter, on the right sca, distal located of the basilar artery, in its cerebellomesencephalic (quadrigeminal) segment (figure a). 270 stefanescu et al surgical treatment of a dissecting aneurysm of the superior cerebellar artery figure a initial cerebral angiographic images showed a 3 mm. irregular aneurysm (black arrow), distally developed on the right sca (white arrow), in its quadrigeminal segment; figure b second preoperative cerebral angiography, performed 28 days later, revealed a dissecting, partially thrombosed aneurysm (black arrow), with important changes of the aneurysm’s sac, which triple its size (10 mm.); figure c postoperative angiographic images demonstrate complete obliteration of the aneurysm with flow preservation in the parent artery (white arrow); figure d postoperative native ct scan, performed 2 months after surgery, showed clips artefacts in the right cerebellopontine angle. initially, we considered this lesion as a mycotic peripheral aneurysm and the patient received antifungal therapy (fluconazole, 200 mg once daily). her condition did not improve continuing to present headache, vomiting and two episodes of loss of consciousness. rightsided cranial nerve palsy, right dismetria and slurred speech were still present at 4 weeks after the onset of the symptoms. a follow-up cerebral angiogram, performed 28 days after the first one, revealed an important growth of the aneurysms sac, which triple its size measuring 10 mm. in diameter (figure b). we romanian neurosurgery (2014) xxi 3: 269 273 271 considered it as a dissecting aneurysm and proposed surgery as method of treatment. we approached the aneurysm through a right lateral suboccipital craniotomy. the aneurysm was located distally on the sca, 25 mm from basilar artery, behind the brainstem perforating arteries. it was exposed on the lateral aspect of the brainstem along with the parent artery. after aneurysm reconstruction and without intra-operative complications, two curved aneurysm clips were applied to the neck in parallel to the sca main trunk, preserving its patency. postoperative angiography showed complete exclusion of the aneurysm with flow preservation in the distal right sca (figure c) postoperative period was uneventful and no additional deficits were noted. the patient was discharged complaining only of mild diplopia, blurred vision and dizziness. six months after surgery the patient was in good general condition, without neurologic motor deficits and complete improvement of diplopia and blurred vision. non-contrast ct scan showed a normal postoperative aspect with clips artefacts in the right cerebellopontine angle (figure d). discussion the overall incidence of peripherally located aneurysms in the anterior cerebral artery distribution is between 7% and 9%, followed by 2%-7% for the middle cerebral artery location, and only 5% for the posterior circulation (8, 15). usually, superior cerebellar artery aneurysms manifest with subarachnoid hemorrhage (sah). a peripheral ruptured aneurysm of the superior cerebellar artery (sca) should be considered when sah predominates in perimesencephalic and superior cerebellar cisterns (6). although many of these lesions are saccular, fusiform and dissecting aneurysms are not unusual (1, 9, 13, 17). despite being a distal lesion, a mycotic origin has seldom been proven in sca aneurysm (9, 13). when presenting with sah, the diagnosis of a dissecting aneurysm of the sca can be difficult, as in our case, requiring serial angiograms to demonstrate progressive change in affected vascular segments. distal sca aneurysms may have distinctive clinical features in accordance with their location. the trochlear nerve, located beneath the tentorium, is vulnerable to injuries related to aneurysms involving the nearby posterior cerebral artery (p2 and p3 segments) or to sca (4, 5, 17). according to a general consensus on sca aneurysms, the presence of important perforating arteries and adjacent cranial nerves makes clipping of the sca aneurysms a very challenging surgery. many complications are related to lower cranial nerve dysfunction because of the intimate relationship between these aneurysms and cranial nerves (10, 14). in the case of dissecting sca aneurysms surgical options include proximal occlusion, trapping, clip reconstruction and distal outflow occlusion (14, 15). in any event, care should be taken to preserve the parent artery and ventral brainstem perforating branches, and to mitigate the risk of brainstem infarction. when proximal occlusion or trapping are used, it is advisable to use combined distal revascularization techniques to prevent permanent ischemic damage to the brainstem 272 stefanescu et al surgical treatment of a dissecting aneurysm of the superior cerebellar artery and cerebellar hemisphere due to unpredictable collateral supply (14, 15, 16). the surgical approach depends on the site of the aneurysm. aneurysm of the cisternal segments may be treated by the pterional transsylvian, subtemporal transtentorial or occipital transtentorial approach, whereas aneurysms of the cortical segments are usually clipped through suboccipital approach for the marginal branch, infratentorial supracerebellar or occipital transtentorial approach for the hemispheric branch, and suboccipital, infratentorial supracerebellar or occipital transtentorial approach for the vermian branch (18, 19). in our case, we preferred the lateral suboccipital approach because angiographic findings suggested that the aneurysm was partially trombosed indicating a larger lesion and it was located more distally. dissection was carried out over the cerebellar hemisphere and the relationship between the brainstem and aneurysm was considered without difficulty. the endovascular therapy may be a good alternative for the treatment of sca aneurysms. endovascular occlusion with detachable coils is feasible with good angiographic and clinical results and with low morbidity (3, 7). endovascular option includes coil embolization of narrow, mostly saccular aneurysms and stent-supported coil placement for wider, fusiform aneurysms (2). conclusions peripheral, dissecting aneurysms of the sca are rare and there is little consensus over their surgical or endovascular management. when endovascular occlusion of the parent artery is performed the risk of the ischemic injury should always be considered. we presented the case of a peripheral sca aneurysms which had radiological features suggestive of dissecting lesions, and considered that an experienced neurovascular surgeon team could clip the aneurysm with parent artery preservation. correspondence mugurel petrinel radoi md, phd affiliation: national institute of neurology and neurovascular diseases bucharest, neurosurgical department, postal address: national institute of neurology and neurovascular diseases bucharest, neurosurgical department, 10-12 berceni str., 041902 bucharest, romania e-mail address: muguradoi@yahoo.com telephone: 0040723527292 references 1. atalay b, altinors n, yilmaz c, caner h, ozger o. fusiform aneurysm of the superior cerebellar artery: short review article. acta neurochir (wien) 149: 291-294, 2007. 2. cardoso ca, almeida lima el, barbosa tm. dissecting aneurysm of the distal superior cerebellar artery – case report and assessment of endovascular treatment. arq bras neurocir 32(2):118-21, 2013. 3. chaloupka jc, putman cm, awad ia. endovascular therapeutic approach to peripheral aneurysms of the cerebellar artery. ajnr am j neuroradiol. 1996; 17(7):1338-42. 4. danet m, raymond j, roy d. distall superior cerebellar artery aneurysm presenting with cerebellar infarction: report of two cases. ajnr am j neuroradiol 22:717-720, 2001. 5. drake cg. the treatment of aneurysms of the posterior circulation. clin neurosurg 26:96-144, 1979 6. gacs g, vinuela f, fox aj, drake cg. peripheral aneurysms of the cerebellar arteries. j neurosurg 1983;58:63-8. romanian neurosurgery (2014) xxi 3: 269 273 273 7. haw c, willinsky r, agid r, terbrugge k. the endovascular management of superior cerebellar artery aneurysms. can j neurol sci. 31(1):53-7, 2004. 8. kubota s, ohmori s, tatara n, nagashima c. a ruptured peripheral, superior cerebellar artery aneurysm: a case report and a review of the literature as to surgical approaches. no shinkei geka 1994;22:279-83. 9. kurosu a, fujii t, ono g. distal superior cerebellar artery aneurysm. br j neurosurg 14:244-246, 2000. 10. lubicz b, leclerc x, gauvrit jy, lejeune jp, pruvo jp. endovascular treatment of peripheral cerebellar artery aneurysms. ajnr am j neuroradiol 24(6): 1208-1213, 2003. 11. matricalli b, seminara p. aneurysm arising from the medial branch of the superior cerebellar artery. neurosurgery. 1986;18 (3):350-2. 12. murtagh f, balis ga. ct localization of posterior fossa bleeding sites in subarachnoid hemorrhage. surg neurol. 1981; 16:211-7. 13. nakai y, hyodo a, yanaka k, akutsu h, nose t. distal superior cerebellar artery aneurysm in a patient with systemic lupus erythematosus: case report. surg neurol 54:73-76, 2000. 14. nussbaum es, defilloa, zelensky a, stoller r, nussbaum l. dissecting peripheral superior cerebellar aneurysms: report of two cases and review of the literature. surg neurol int. 2011; 2:69. 15. nussbaum es, madison mt, goddard jk, lassig jp, nussbaum la. peripheral intracranial aneurysms: management challenges in 60 consecutive cases. j neurosurg 2008;109:23-7. 16. nussbaum es, madison mt, myers me, goddard jk, janjua tm. dissecting aneurysms of the posterior inferior cerebellar artery: retrospective evaluation of management and extended follow-up review in 6 patients. j neurosurg 2008; 109:23-7. 17. peluso jip, van rooij wj, sluzewsky m, beute gn. distal aneurysms of cerebellar arteries: incidence, clinical, presentation, and outcome of endovascular parent vessel occlusion. ajnr am j neuroradiol 28:1573-1578, 2007. 18. sato m, kodama n, sasaki t, watanabe z. aneurysms arising from the cortical segment of the superior cerebellar artery – two case reports. neurol med chir (tokyo). 39:858-862, 1999. 19. yasargil mg (ed). distal superior cerebellar aneurysms, in: microneurosurgery ii, new york: thieme 1984: 279-280. 9hawisabdul_general romanian neurosurgery (2015) xxix (xxii) 1: 77 84 77 for residents general considerations in lumbar spinal stenosis hawis abdul salam abdul rahman1, gabriel iacob2 1syria, 2neurosurgery clinic bucharest romania “the secret of being a bore is to tell everything” voltaire sept discours en vers sur l'homme, 1738 definition lumbar spinal stenosis (lss) is a common and often disabling, well-recognized spinal disorder that generally occurs in the sixth or seventh decade of life, although it can uncommonly occur in younger individuals, congenital or acquired, focal or diffuse (multilevel), defining a osteo-ligamentous narrowing (congenital) or shrink (secondary – acquired) of the lumbar spinal canal, a conflict between the lumbar spinal canal with vertebral body osteophytes, hypertrophy of the ligamentum flavum, zygapophyseal joint, lumbar disc hernia or a combination of these and the content represented by the cauda quina roots, lumbar spinal roots and ganglia, generating a complex set of symptoms of which the hallmark is neurogenic claudication, physical findings and radiological abnormalities. lumbar spinal stenosis or “loss of epidural reserve” could affect the central lumbar spinal canal ± lateral recess ± the neuroforamen or any combination of these, causing nervous impingement and vascular structures compression (1-4). it can coexist with cervical stenosis too. it’s important to underline that diagnosis of lss should be defined by symptoms and clinical findings that must be supported by neuroimagistic evidences. computed tomography and magnetic resonance imaging are often nonspecific and there may be discrepancies between clinical symptoms and imaging findings in cases of lss. example: for central stenosis according to the sagittal diameter of the lumbar spinal canal there are absolute lumbar spinal stenosis <10 mm and relative lumbar spinal stenosis 10 to 14 mm (5-7). spinal stenosis was first described only sixty five years ago by verbiest (8): “it is characterized by narrowing of the spinal canal, the nerve root canals or the neural foramina and can produce a debilitating condition in older adults” history (1-3) (9-18) 1803 – the first medical report of spinal stenosis: portal in france postulated that back and leg pain could be caused by bone impingement on the nerves (1-3) (9-11). 78 rahman, iacob general considerations in lumbar spinal stenosis 1893 – first decompressive laminectomy: lane in england did a to relieve a woman of cauda equina syndrome caused by spinal stenosis (1-3) (9-11) 1900 connexion between lumbosciatalgic pain and nerve compression was first remarked by sachs b and fraenkel j. (12) 1945 sarpyener m.a. reveal congenital stricture of the spinal canal (14) 1948 van gelderen c. suggest that ligamentum flavum hypertrophy could be a possible cause of lumbar spinal stenosis reffering to two clinical observations. (1-3) (10-11) 1954 –verbiest h.a. a. – a holland surgeon, defined first the clinical syndrome of lumbar stenosisin seven patients who had bilateral radicular pain and motor and sensory disturbances in the legs, caused by standing and walking and made first the difference between “narrow” and “shrink”.(15). he also remarked clinical signs in congenital lumbar spinal stenosis justified by mechanical nerve compression at saccoradiculography (16). (16)(115)(16) 1955 schlesinger (cited by 11) and 1972 epstein et al. (17) reported some cases and described the clinical and radiographic findings of facet syndrome. they pointed out the importance of the height of the intervertebral foramen on plain radiographs in narrow lateral recess cases. since then several authors recognized and described lateral recess stenosis and lateral entrapment syndrome (18-20). in the 1960s and 1970s spinal stenosis began to be recognized as an impairing condition, also during the 1970s and 1980s, many case reports showed successful surgical treatment rates, but these were based on subjective assessment by surgeons. 1974 kirkaldy-willis p. paine k, cauchoix j, et al. precise the anathomo-pathological aspects in lss and made correlation with clinical signs (21). 1978 porter and colleagues discovered that individuals who experience back pain and other symptoms are likely to have smaller spinal canals than those who are asymptomatic (22) 1982 rothman reported that a normal sized lumbar canal is rarely encountered in persons with either disc disease or those requiring a de-roofing (laminectomy) procedure (23). 1992, johnsson, rosén and udén described the natural history of lss (24) and concluded that a reasonable treatment optionfor lumbar stenosis is observation. another investigators appreciate that significant neurologic deterioration is rare: 70% of patients reported no significant change in symptoms, 15% showed significant improvement, whereas 15% showed some deterioration (25)(26). frequency lss are frequent, the incidence of this condition has been reported to be 8–11% of population, generally occurs in the sixth or seventh decade of life, except congenital; in the 4th decade to men in central lumbar stenosis, in the 5-6 th decades to women in lateral stenosis. lss is more frequent to woman: ratio woman/men: 3/1 to 5/1400,000 (30). 400,000 americans are estimated to have spinal stenosis with increased incidence with the expansion of life-expectancy (3). romanian neurosurgery (2015) xxix (xxii) 1: 77 84 79 for residents generally lss are 5 times less frequent as lumbar disc hernia. no clear correlation exists between the symptoms of stenosis and race, occupation, sex or body type; the anvergure of the degenerative process which cannot be prevented by diet, exercise or lifestyle (1-3). the anvergure of the problem is expanding: americans are estimated to have spinal stenosis with increased incidence with the expansion of life-expectancy, especially by increasing place of neuroimagistic procedures; prevalence 1 case at 1000 persons (27). ubiquitous degeneration associated with aging may lead to stenosis of the spinal canal, especially along the lumbar spine. as a result of the changing societal age structure, the incidence of symptomatic lumbar spinal stenosis is increasing exponentially. inpatients older than 60, lumbar spinal stenosis is found on magnetic resonance imaging in more than 20% of cases (28). older patients’ desires for mobility and functionality, combined with improved perioperative management, have resulted in a situation where surgical intervention is being increasingly considered. in the united states, the incidence of surgery has increased eight-fold from 1979 to 1992 (29) and in 2007 37,598 people were treated surgically for lumbar stenosis in the us, totally a bill of 1.65 billion dollars (25) (26). lss classifications anatomical classification (1-3) (31-33): lss are defined by the anterior-posterior diameter less than 15 mm (normal value 15-25 mm) and lateral recess less than 3 mm. it’s to be remarked that adult cross section lumbar spinal area (av. 194 sq mm) are similar to those seen of 4 years old. lss could be (figure 1): segmentary (2 levels 45%, 1 level 37%, 3 levels 17%) or diffuse; central, 10% due to hypertrophic spurring, bony projection or ligamentum flavum/laminar thickening clover leaf (“fleur de lis”): laminar thickening with subsequent postero-lateral bulging medial secondary to iap hypertrophy lateral recess and foraminal stenosis 45%, secondary to sap hypertrophy mixed 45% a b c d e 80 rahman, iacob general considerations in lumbar spinal stenosis f g figure 1 lss modified after (1)(32): a normal aspect, b short pedicles reducing the antero-posterior diameter, c central stenosis, articular process are disposed in sagittal plane, d clover leaf central stenosis, e severe stenosis macroscopic aspect, f different shapes of spinal canal in spinal stenosis, g didactic schema in central stenosis aetiological classification (1-3) (10) (11) (21) (22) (30) 1. congenital stenosis (narrowed lumbar channel) – described by sarpyener at childrens (14), verbiest in adults (8), are rare, occurring in only 5-9 % of cases. congenital lumbar stenosis could be idiopathic or concomitent with anatomical variants: partial or total lss; unilateral asymmetric, with discontinuity in stenosis; normal lumbar segment between 2 stenotic segments; normal central lumbar canal with lateral recess stenosis or associated with sacral stenosis. anatomically lumbar constitutional stenosis are related to short pedicles, and short, thick, vertical lamae; sometimes medial articular part are in contact with spinous process, short interspinous and interlamae spaces, the antero-posterior diameteris ≤ 15 mm and interpedicular diameter has cvasinormal dimmension or < of 25 mm. generally congenital stenosis are insufficient to generate clinical symptoms, but able to decompensate by secondary lesions (35) (36): dysplastic lesions: achondroplasic, acromesomelic, arterio-hepatic, diastrophic, osteo glophonic nanism, hypochondroplasic, thanatophoric, smith-mccort syndrome, weill-marchesani syndrome, gordon syndrome – all spinal canal could be stenotic dysostotic lesions: cheiro-lumbar, gorlin baso celullar naevomatose, wyers & thier syndrome, acrodysostose a rare cause of lumbar canal stenosis are idiopathic lumbar epidural lipomatosis (37). 2. secondary (acquired) stenosis (shrink lumbar channel): nonspecific: degenerative changes more frequent in aged persons related to hypertrophic frequent asymmetric articular process; include central canal and lateral recess stenosis from posterior disc protrusion, zygapophyseal joint and ligamentum flavum hypertrophy/calcification, degenerative spondylolisthesis – characterized by forward displacement of a vertebra due to disc and facet degeneration (38), synovial cysts, lumbar epidural varices (39), lumbo-sacral transitional vertebra; degenerative process stages responsible for dysfunction, instability specific: -traumatic romanian neurosurgery (2015) xxix (xxii) 1: 77 84 81 for residents systemic processes include: paget disease, fluorosis, acromegaly, ankylosing spondylitis, renal osteodystrophy, neoplastic, infectious, lipomatous epiduritis of cushing disease, tabetic arteriopaty iatrogenic changes result following surgical procedures such as laminectomy, fusion, discectomy, malpositioned osseous grafts used for osteosynthesis 3. combined congenital and degenerative in several cases generally degenerative stages made symptomatic a constitutional lumbar stenosis. pathophysiology of lss lss is a slow, fluctuent progression disease, occur in all affected individuals. lss is more frequent on l3-l4 and l4-l5, segments; several patho-physiological mechanisms could be related to this condition. no clear correlation exists between the symptoms of stenosis and race, occupation, sex, body type. the degenerative process cannot be prevented by diet, exercise or lifestyle. acute cauda equina syndrome is rare. degenerative process stages in lss are: dysfunction, instability, stabilization and three main factors are responsiblefor the development of ths spinal disorder (1-3) (40): 1. disk protrusion as a a consequence of disk degeneration of a motion segment leed to height segment loss, lateral recess, neural foramen and central canal narrowing. as a consequence it effects ligamentous laxity with increased segmental mobility, with additional strain especially on the facet joints. this subclinical instability of the segment generate osseous hypertrophy, especially the facet joints, fibrotic hypertrophy of the ligamentum flavum, in addition to folding inwards subsequent to height loss. if these reactive processes do not succeed in stabilizing the segment, disk degeneration, laxity of capsules and ligaments may result in the manifest instability of spondylolisthesis. 2. the position of the spine may generate nerve root compression: the strain imposed by standing is in itself sufficient to result in hyperlordosis of the affected segment, with further protrusion of the ligamentum flavum into the spinal canal. 3. both arterial ischemia as well as venous factors are implied in mechanical nervous roots compressions. experimental studies have been made looking on lombar roots during walking, on normal asymptomatic patients and to those patients with claudication by lss, using microendoscopic techniques, under local anesthesia (41). during walking oxygen roots needs are demanding a supplementary arterial supply. the strain and weight imposed by walking results in decompensation of the vascular flow to the spinal nerves, which is mostly sufficient during rest. if patient is bending anteriorly (figure 2), both the canal diameter and arterial supply is bigger. if that is not enough the patient need to sit down to restablish the normal metabolic situation. also mechanical pressure on cauda equine is generating venous stasis affecting nervous influx by local demielination and axonal degenerescence. 82 rahman, iacob general considerations in lumbar spinal stenosis in extension or walking, narrowing occurs in flexion, the size of the spinal canal increases figure 2 lss – modified after (1) (32): patients walk in flexion and prefer to sit and lean forward in synthesis, in lss the mechanisms explaining simptomatology are neural compression: anterior: disk protrusion or herniation osteotic overgrowth: osteophytes posterior: lamar& ligamentous hypertrophy (the role of tgf-β1, timp-1 and timp-2 on hypertrophy of the ligamentumflavum in spinal stenosis patients is a local phenomenon, not systemic)(42) facet hypertrophy, synovial cyst spinal lipomatosis, etc pain mechanisms may be due to: mechanical: chronic compression of the nerve root in lss causes compromise of blood flow leading to venous congestion, ischaemia, +/-microcirculation anomalies, intraneural edema. this then leads to the development of periradicular fibrosis. neurogenic claudication likely arises from increased metabolic demands of the nerve root in the presence of vascular compromise and traction on the adhesed nerve root when lower extremity movement occurs during walking instability biochemical component especially by cytochines when disc is involved nucleus pulposus inflammatory–arthritis instability: defined by white and panjabi (43): “the loss of the spine’s ability to maintain its romanian neurosurgery (2015) xxix (xxii) 1: 77 84 83 for residents patterns of displacement, under physiologic loads so there is no initial or additional neurologic deficit, no major deformity and no incapacitating pain” mechanical instability without clinical signs symptomatic instability: intermitent pain + clinical signs of lss instability mechanisms are leading and responsible for spondylolisthesis and scoliosis may be due to: loss of discal integrity loss of ligamentous integrity loss of facetal integrity loss of supportive integrity: paraspinal and abdominal muscle tone and power conclusion pathologic determinants that result in a stenotic canal are protruding discs, ligamentum flavum, facet and lamina hypertrophy, lysthesis, degenerative scoliosis and rotational deformities. references 1.iacob g. craciun m lumbar spinal stenosis (lss): indications and operative treatment – the “bucharest wiew”, german-romanian course cluj-napoca 24-25 may 2011 2.iacob g. craciun m personal experience in lumbar spinal stenosis (lss), romanian neurosurgery 2011, xviii, 4, 400-411 3.iacob g. neurochirurgia in managementul coloanei dureroase, congresul asociatiei romane pentru studiul durerii, “managementul durerii acute pentru medicii din ambulator” howard-johnson grand plaza, bucuresti, 1415. 10. 2011 4.awmf-leitlinie: leitlinien der deutschen gesellschaft für neurochirurgie„lumbale spinal kanal stenose“ 2005, http://www.uni-duesseldorf.de/awmf/ll-na/008-022.htm 5.degraaf i, prak a, et al. diagnosis of lumbar spinal stenosis: a systematic review ofthe accuracy of diagnostic tests. spine 2006, 31, 1168-1176 6.beattie pf, meyers sp, et al. associations between patient report of symptoms and anatomic impairment visible on lumbar magnetic resonance imaging. spine 2000, 25, 819-828 7.amundsen t, weber h, et al. lumbar spinal stenosis. clinical and radiologic features, spine 1995, 20, 11781186 8.verbiest h. primary stenosis of the lumbar spinal canal in adults, a new syndrome, ned tijdschr geneeskd.1950, 94, 2415-33 9.spivak j. degenerative spinal stenosis, j bone joint surg 1998, 80, 1053–1066 10.katz j, dalgas m, et al. diagnosis of lumbar canal stenosis, rheum dis clin north am 1994, 20, 471–483 11.garfin s, et al. spinal stenosis, aaos instructional course lectures 2000, 49, 361–374 12.arbit e, pannulo s. lumbar stenosis-a clinical review, clinorthop 2001, 384, 137–143 13.sachs b, frankel v. progressive and kyphotic rigidity of the spine, j nervment dis 1900, 27, 1–15 14.sarpyener ma. congenital stricture of the spinal canal, j bone joint surg 1945, 27,70-9 15.verbiest h. a radicular syndrome from developmental narrowing of the lumbar vertebral canal. j bone joint surg br 1954, 36(2), 230-237 16.verbiest h. further experiences on the pathological influence of a developmental narrowness of the bony lumbar vertebral canal. j bone joint surg br 1955, 37(4):576-583 17.epstein ja, epstein bs, et al.sciatica caused by nerve root entrapment in the lateral recess: the superior facet syndrome. j neurosurg1972, 36(5), 584–589 18.shenouda ef, gill ss laminal fenestration for the treatment of lumbar nerve root foraminal stenosis. br j neurosurg2002, 16(5), 494–497 19.ciric i, mikhael ma, tarkington ja, vick na the lateral recess syndrome: a variant of spinal stenosis. j neurosurg1980, 53, 433–443 84 rahman, iacob general considerations in lumbar spinal stenosis 20.lee ck, raushning w, glenn w lateral lumbar spinal canal stenosis: classification, pathologic anatomy and surgical decompression. spine 1988, 13(3), 313–320 21.kirkaldy-willis wh, paine kwe,et al.: lumbar spinal stenosis. clinorthop. 1974, 99, 30-50 1974 22.porter rw, et al. the spinal canal in symptomatic lumbar disc lesions, j bone joint surg br 1978, 60–b (4), 485–487 23.rothman rh.,semeone fa, the spine. philadelphia: saunders. 1982,. 518. isbn 0-7216-7718-5 24.johnsson ke, rosén i, udén a the natural course of lumbar spinal stenosis", clin. orthop. relat. res.1992, (279), 82–86 25.djurasovic m, glassman sd, et al. contemporary management of symptomatic lumbar spinal stenosis, orthop. clin. north am. 2010, 41 (2), 183–191 26.genevay s, atlas sj. lumbar spinal stenosis, best pract res clinrheumatol 2010, 24 (2), 253–65 27.lurie j.d. – lss, spine 2003, 28, 616-620 28.boden sd, davis do, et al. abnormal magneticresonance scans of the lumbar spine in asymptomatic subjects. a prospective investigation. j bone joint surg am 1990, 72, 403-408 29.ciol ma, deyo ra, et al. an assessment of surgery for spinal stenosis: time trends, geographic variations, complications and reoperations. j am geriatrsoc 1996, 44, 285–290 30.bridwell k. lumbar spinal stenosis. diagnosis, management and treatment. clingeriatr med 1994, 10, 677–701 31.keim ha, hajdu m, et al. lss, spine 1985 may, 10(4), 338-344 32.iqbal j. surgery for lumbar canal stenosis: micro or macro? 9th dubai spine conferencemay 14th-15th, 2008 33.mohamed el-fiki -spinal stenosis; is there a place for limited procedures? 9th dubai spine conference, may 14th-15th, 2008 34.arnoldi c, brodsky a, et al. definition and classification of lumbar spinal stenosis and nerve root entrapment syndromes, clinorthop 1976, 115, 4–5 35.garfin sr, rauschning w. spinal stenosis, instr course lect. 2001, 50, 145-52 36.resnick d. degenerative disease of the spine, in: resnick d(ed): diagnosis of bone and joint disorders (4th ed). philadelphia:w.b. saunders 2002, 1382-1475 37.thiagarajan g., dhandapani s. idiopathic lumbar epidural lipomatosis: a rare cause of lumbar canal stenosis, pan arab journal of neurosurgery 2010, 14, 2, 117-118 38.herkowitz h. degenerative lumbar spondylolisthesis spine 1995, 20, 1084–1090 39.farrokhi m.r., niknam h. lumbar radicular pain caused by epidural varices, pan arab journal of neurosurgery 2010, 14, 2, 115-116 40.porter r.w. spinal stenosis and neurogenic claudication, spine 1996, 21: 2046–2052 41.yong-hing k, kirkaldy-willis w.h the pathophysiology of surgery for diseases of the lumbar spine. orthopclin north am 1983, 14, 491-504 42.kim h.j. et al. – serum levels of tgf-ß1, timp-1 and timp-2 in patients with lumbar spinal stenosis and disc herniation, asian spine journal 2007, 1, 1, 8-11 43.white a.a., panjabi m.m. clinical biomechanics of the spine, 2nd ed, lippincott, philadelphia, pa, 1990 microsoft word 2anuntneurooftalmo 6 novelties in neuro-ophthalmology novelties in neuro-ophthalmology the second conference entitled topical issues in neuro-ophthalmology will be held in iasi, at the bucium motel, during the period 07-09 april 2011. the conference will also include a lecture addressed to residents and young specialists. every year, the lecture will have a different topic, focusing on a different field of ophthalmology. the conference and the lecture will be organized under the auspices of: “gr.t. popa” university of medicine and pharmacy of iasi, the romanian society of neuro-ophtalmology, the college of physicians, ophtalmology clinic no. 2 of iasi. it is open to senior mds, consultants and residents: ophthalmologists, neurologists, neurosurgeons, cardiologists/internal medicine specialists, general practitioners. at the end of the conference the registered participants will be awarded a diploma accredited by the college of physicians. each participant will be able to register, free of charge, his/her clinic/cabinet, on the www.informatiamedicala.ro site (the normal rate is of 50 euro + vat) topics • ischemia, inflammation, oxidative stress and light stress: determinant risk factors in the evolution of neuroophthalmologic diseases • neuro-ophthalmologic emergencies • varia • lecture for young specialists and residents • cataract surgery: first steps in phacoemulsification • demonstrative operative program • clinical cases professor d. costin “gr.t. popa” university of medicine and pharmacy of iasi microsoft word 13.iliescub_therole_f.docx romanian neurosurgery (2011) xviii 4: 483 490 483 the role of mr tractography in pre-surgical planning – personal series of 25 cases and a review of the literature bogdan iliescu, anca dabija1, ziyad faiyad, sergiu gavas, ion poeată department of neurosurgery, “prof. dr. n. oblu” clinical emergency hospital, “gr. t. popa” university of medicine and pharmacy, iasi 1department of mr imaging, supermeditest, iasi abstract diffusion tensor imaging (dti) contains a wealth of information on molecular diffusion in biological tissues [1,2]. visualizing the white-matter tracts using diffusion anisotropy maps represents one of the applications with a major impact on neurosurgical case management [3]. knowledge of the topography, integrity, and involvement by the pathological process of the white matter tracts is an important factor in pre-surgical planning for patients with brain lesions. we have evaluated the clinical utility of a magnetic resonance tractography technique based on dti. we studied, in a prospective manner, 25 cases with lesions involving salient intracerebral and medullary tumors (22 and 3 cases respectively). all cases followed a preoperative imaging protocol that included dti on top of the usual mr imaging protocol. we analyzed the dti findings preoperatively and looked at the significant information that influences the surgical plan: position of the significant white matter tracts, the degree of their involvement in the pathological process and anatomical integrity, relationships with important anatomical landmarks and with the major surgical approach paths. we present the postoperative results and some of the most illustrative cases in the series and compare our results with the similar studies in the literature. our experience, based on the results of the present study strongly suggests that in depth knowledge of the white matter tracts involvement in an intracerebral or intramedullary pathological process improves significantly the surgical planning in terms of surgical procedure safety and functional outcome. introduction planning the adequate surgical procedure for removal of a pathological process within the brain or the spinal cord requires a thorough knowledge of the particular relevant anatomy preoperatively. the goal of maximal safe resection is difficult to achieve without detailed information of functional areas and structures and their relationship with the pathology. the advent of diffusion tensor imaging has revolutionized the study of white matter tracts in the living human brain. tractography has made it possible to study the detailed anatomy of white matter tracts and to depict important information for neurosurgical planning. arguably correct pre-operative identification of white matter tracts is at least as important as the identification of 484 bogdan iliescu et al mr tractography in pre-surgical planning eloquent cortices, such as the motor cortex. first, the precentral gyrus (the location of the motor cortex) can usually be identified by the operating neurosurgeon by visual inspection. second, direct intraoperative white matter stimulation is much less reliable than cortical stimulation. on the other hand, it is essentially impossible to identify separate white matter tracts, such as the cortico-spinal tract (cst the main motor tract) or the thalomo-cortical tract (the main sensory tract) by visual inspection as they traverse the corona radiata. in the present study we have investigated the role of mr tractography in pre-surgical planning for pathological processes affecting both the brain and the spinal cord. all patients underwent neurological evaluation, including assessment of motor and language functions preoperatively and at two points postoperatively. the imaging and clinical data was retrospectively analyzed to assess the factors that help predict the postoperative outcome and the contribution of white matter tracts involvement in the pathological process as an outcome prognostic factor. a special emphasis was given to the tailoring of surgical approach when tract information (direction of displacement, relationship with the tumor) is included in the surgical algorithm. materials and method 25 patients with expansive processes of functional areas were introduced in the study. the age of patients was between 20 and 66 years (median 48 years). all patients, 14 men and 11 women underwent a magnetic resonance investigation protocol which included standard sections (t1, enhanced t1, t2, flair, tof) supplemented with diffusion tensor imaging. magnetic resonance imaging studies were performed on a 1.5 t scanner standard rm (siemens avanto) using a standard rectangular cage. dti studies were performed as part of a preoperative imaging protocol. component of an institutional protocol, informed consent was obtained for each patient to participate in the dti study, prior to investigation. the color-coded maps obtained from the dti scan were analyzed. in each case the tumors were confined to just one hemisphere which favored a direct, within subject comparison of the affected white matter tracts in the tumor baring hemisphere with the contralateral, control hemisphere. the white matter tracts were characterized as follows: displaced, if they maintained normal anisotropy relative to corresponding contralateral tract but was located in an abnormal location or abnormal orientation according to the standard color code, edematous, if they maintained normal anisotropy and orientation but showed obvious increase in intensity on t2 images, infiltrated if they were characterized by reduced anisotropy yet remained visible on the orientation maps and degenerated if the anisotropy was significantly reduced as such there was no identifiable tract on the orientation maps. for tracts characterized as infiltrated we did not try to determine whether anisotropy was reduced as a result of vasogenic edema, tumor infiltration or a combination of these factors. such a distinction is extremely difficult if not impossible only by dt imaging. patients with lesions that involved the speech areas underwent awake surgery as a method to monitor the specific neurologic function intraoperatively. these patients received local anesthesia so that the basic romanian neurosurgery (2011) xviii 4: 483 490 485 functions of motor speech could be evaluated. patients were not intubated in order to be able to respond coherently to the tests performed during surgery. in the first stage, cortical mapping was performed by identifying tumor and sulci and giri using macroscopic anatomical landmarks and intraoperative ultrasound. the same mapping was repeated before resection, to avoid any damage to the eloquent area. the patient was asked to perform various counting exercises (repeat counting several times from 1 to 10) and the image naming tests. for the naming task, we used the do 80, which consists of 80 black and white pictures selected according to variables such as frequency, familiarity, age of acquisition and level of education. [13] results for the 25 patients that were included in the present study the location of the pathological process was temporal lobe in two cases, frontal lobe, two cases, insula, five cases and parietal region in three cases. dominant neurological symptoms on admission, except for headache with or without intracranial hypertension syndrome (present in 18 cases), were motor deficits and motor aphasia (11 and 9 cases respectively), and seizures (9 cases), accompanied by a severe confusional syndrome in 3 cases. intracranial hypertension was manifested in three patients enrolled in the study (figure 1). pathological examination of the resection specimens documented glioblastoma in twelve cases, grade one astrocytomas in five cases and grade two in one case, meningioma in five cases, mature teratoma and avm in one case respectively. we managed to identify the degree of involvement of white matter tracts in all cases using dt imaging 2d maps and 3d reconstructions. normal white matter tracts were highlighted in the controlateral hemisphere in all patients. changes in tracts structure and position were characterized for each patient. white matter involvement by the expansive replacement space was classified according to criteria: displacement, infiltration, degeneration and edema in relation to contralateral correspondents (figure 2). upper longitudinal beam was deflected in the axial direction or lateral median in twelve cases. corticospinal tract was diverted in fifteen cases. locating individual displacement was a variation depending on where the tumor lesion. deviation has been emphasized in the corona radiate (figure 3). white matter tract edema was documented in three cases. reconstruction of dti showed reduced anisotropy without displacement of white matter architecture, which is suggestive of tumor invasion. diffusion tensor imaging documented the destruction of white matter tracts in seven cases (figure 4). lower anterior longitudinal component of the beam in the temporal lobe was engulfed by glioblastoma. in the second case, another massive temporo-insular glioblastoma produced distruction of antero-posterior oriented fibers and projections, especially cortico-spinal tract and previous thalamic radiation, the more evident when compared with fibers intact controlateral hemisphere. in one case it revealed diffuse swelling along the outer edges of the tumor. in one case with glioblastoma temporal lobe edema on the outskirts of optical radiation involved parietal and temporal regions. edema affecting optic radiation white tracts was demonstrated on t2 images of conventional mri. 486 bogdan iliescu et al mr tractography in pre-surgical planning a b c d figure 1 a sex distribution of the cases in our series. b major location of cerebral lesions in all cases. c age distribution; d symptoms at presentation figure 2 the type of white matter tract involvement by the pathological process a romanian neurosurgery (2011) xviii 4: 483 490 487 b c figure 3 illustrative case for the imagistic work-up in our series. a t2-weighted and mri angio of the primary lesion. b 2d and 3d tractography showing displacement of the longitudinal temporal white matter tracts and compression on the pyramidal tract. c postoperative control ct with the artefacted image of a vascular clip a b figure 4 illustrative case for a spinal cord tumor in our series. a t1-weighted sagittal (left) and axial (right) mr image showing compression at the level of d6. b 3d tractography (whole – left and detail – right) showing almost complete distruction of the descendent white matter tracts in the spinal cord using a preoperative planning that takes into account important functional mapping elements directly or indirectly involved in the intracranial expansive process as well as an appropriate selection of cases for intraoperative monitoring of motor and 488 bogdan iliescu et al mr tractography in pre-surgical planning language functions, postoperative results allowed for good postoperative results. thus, all patients included in this study showed postoperatively similar or improved neurologic status (no iatrogenic neurological deficit). evaluation of preand postoperative karnofsky performance scale (karnofsky performance scale kps) is detailed in figure 5. a b c figure 5 karnofsky performance scale values pre and postoperatively (a and b, respectively) and the tendency in the kps in the whole group. full bars indicate a negative tendency while the empty bars show positive tendency discussion brain tumors can affect both functional cortical gray matter and white matter tracts. a good neurological outcome following the resection of intracerebral pathological processes requires a detailed preoperative understanding of their anatomical relationships with functional areas and of adjacent cortical white matter tracts. this is of paramount importance when the tumor develops in or near a functional cortical area in the dominant hemisphere, be it motor, sensory, or cognitive. understanding the location of the lesion in relation to surrounding functional tissue is a vital element in developing an efficient surgical plan. the purpose of using various techniques of mapping is to delineate functional areas so they can be preserved during surgery. maximal tumor resection was shown to be an element closely related to patient survival and improved clinical status of patients on long-term, indicating a main predictor of clinical course. the present data show that tumors that invade massively the functional cortex areas of maintain still intact white matter tracts in the mass of the pathological tissue. diffusion tensor imaging provides valuable information for identifying tracts when they are displaced by the tumor. twenty-five cases were analyzed in our study to demonstrate how diffusion tensor imaging contributes important additional information that may help elucidate the complex relationship between a tumor and surrounding brain tissue. imaging evidence of the existence of intact white matter tracts n o of c as es n o of c as es n o of c as es p < 0.0001 (wilcoxon si mann-whitney test) romanian neurosurgery (2011) xviii 4: 483 490 489 in the areas of tumor invasion were obtained in four patients. other patients showed tracts displacement from their normal anatomy position. in one case with glioblastoma located centrally in the left hemisphere, corticospinal tract lesion in the corona radiata moved medially and superiorly. the information on the displacement of the tracts helped surgical planning by providing information about localization and adaptation of new surgical corridor so as to avoid intraoperative destruction of intact tracts. in this case the tumor was approached from a posterior temporal direction, allowing for aggressive resection of the tumor while avoiding motor fibers previously diverted. in our study we found that the use of an operator plan which aims at maintaining an intact neurological function is checked by favorable postoperative results. we mention that new neurological deficits occurred in only 12.5% of patients and have largely improved in the first month postoperatively. these results indicate that although they minimize the risk of injury of the functional cortex or tracts adjacent or involved in the pathological process, the methods used do not guarantee the absence of postoperative dysfunction. these deficits were caused probably by touching the subcortical areas, retraction, edema or ischemia. however, based on the results of this study, the risk of harming a previously intact patient during awake craniotomy remains low. this information about the risks of surgery is useful and should be communicated by the surgeon to the patients and their families. conclusions in agreement with the existing prospective studies, our study suggests that preoperative planning based on functional criteria and the use of awake craniotomy offers clear advantages for the resection of intraxial and spinal pathological processes. this allows for intraoperative brain mapping that helps identify (and by consequence, protect) eloquent functional cortex, and is an effective surgery for lesions of different histological types that occur in various locations in the brain. awake craniotomy to avoid complications of general anesthesia, based on the data of this study and others, is associated with reduced complications and mortality rates and reduced use of resources. as a general principle, we suggest that the awake craniotomy provides an excellent alternative to traditional surgery for supratentorial brain lesions. the effect of brain tumors on white matter tracts is clearly demonstrated by means of standard diagnostic imaging. diffusion tensor imaging allowed identification of several viable tracts within a cerebral hemisphere invaded by a tumor. in our series, information provided by dt imaging allowed precise definition of relationships between cortical structures and subcortical white matter and brain tumors. involvement of white matter tracts is important information in planning the surgical approach in assessing the extent of tumor resection to keep it within safe limits. references 1. ammirati m, vick n, liao yl, et al: effect of the extent of surgical resection on survival and quality of life in patients with supratentorial glioblastomas and anaplastic astrocytomas. neurosurgery 21:201–206, 1987 2. atlas sw, howard rs ii, maldjian j, et al: functional magnetic resonance imaging of regional brain activity in patients with intracerebral gliomas: findings and 490 bogdan iliescu et al mr tractography in pre-surgical planning implications for clinical management. neurosurgery 38:329–338, 1996 3. bittar rg, olivier a, sadikot af, et al: cortical motor and somatosensory representation: effect of cerebral lesions. j neurosurg 92:242–248, 2000 4. cosgrove gr, buchbinder br, jiang h: functional magnetic resonance imaging for intracranial navigation. neurosurg clin n am 7:313–322, 1996 5. doran m, hajnal jv, van bruggen n, et al: normal and abnormal white matter tracts shown by mr imaging using directional diffusion weighted sequences. j comput assist tomogr 14:865–873, 1990 6. giese a., westphal m. glioma invasion in the central nervous system. neurosurgery 39:235–252, 1996 7. grafton st, woods rp, mazziotta jc, et al: somatotopic mapping of the primary motor cortex in humans: activation studies with cerebral blood flow and positron emission tomography. j neurophysiol 66:735– 743, 1991 8. handler t, et. al. delineating gray and white matter involvement in brain lesions: three-dimensional alignment of functional magnetic resonance and diffusion-tensor imaging. j neurosurg 99:1018–1027, 2003. 9. krings t, reinges mht, thiex r, gilsbach jm, thron m. functional and diffusion-weighted magnetic resonance images of space-occupying lesions affecting the motor system: imaging the motor cortex and pyramidal tracts. j neurosurg 95:816–824, 2001. 10.lehericy s, duffau h, cornu p, et al: correspondence between functional magnetic resonance imaging somatotopy and individual brain anatomy of the central region: comparison with intraoperative stimulation in patients with brain tumors. j neurosurg 92:589–598, 2000 11.mcdonald jd, chong bw, lewine jd, et al: integration of preoperative and intraoperative functional brain mapping in a frameless stereotactic environment for lesions near eloquent cortex. technical note. j neurosurg 90:591–598, 1999 12.mcgirt m.j., chaichana k.l., gathinji m., attenell f.j., than k., olivi a., weingart j.d., brem h., quiñones-hinojosa a. independent association of extent of resection with survival in patients with malignant brain astrocytoma. j neurosurg 110:156–162, 2009 13.metz-lutz m, kremin h, deloche g, et al. standardisation d’un test de dénomination orale: controle des effets de l’age, du sexe et du niveau de scolarité chez les sujets adultes normaux. rev neuropsychol 1991;1 :73-95. 14.mueller wm, yetkin fz, hammeke ta, et al: functional magnetic resonance imaging mapping of the motor cortex in patients with cerebral tumors. neurosurgery 39:515–521, 1996 15.nagano n, sasaki h, aoyagi m, hirakawa k: invasion of experimental rat brain tumor: early morphological changes following microinjection of c6 glioma cells. acta neuropathol 86:117–125, 1993 16.pajevic s, pierpaoli c: color schemes to represent the orientation of anisotropic tissues from diffusion tensor data: application to white matter fiber tract mapping in the human brain. magn reson med 42:526–540, 1999 17.pierpaoli c, jezzard p, basser pj, et al: diffusion tensor mr imaging of the human brain. radiology 201:637–648, 1996 18.roux fe, boulanouar k, ranjeva jp, et al: cortical intraoperative stimulation in brain tumors as a tool to evaluate spatial data from motor functional mri. invest radiol 34:225–229, 1999 19.wieshmann uc, symms mr, parker gj, et al: diffusion tensor imaging demonstrates deviation of fibers in normal appearing white matter adjacent to a brain tumor. j neurol neurosurg psychiatry 68:501– 503, 2000 16manishjaiswal_rarecase 490 jaiswal et al post traumatic bilateral abducens nerve palsy a rare case of post traumatic isolated bilateral abducens nerve palsy manish jaiswal1, saurabh jain1, ashok gandhi1, achal sharma2, r.s. mittal1 1department of neurosurgery, sms medical college and hospital 2jln marg, jaipur (302004), rajasthan, india abstract: although unilateral abducens nerve palsy has been reported to be as high as 1% to 2.7% of traumatic brain injury, bilateral abducens nerve palsy following injury is extremely rare. in this report, we present the case of a patient who developed isolated bilateral abducens nerve palsy following minor head injury. he had a glasgow coma score (gcs) of 15 points. computed tomography (ct) images & magnetic resonance imaging (mri) brain demonstrated no intracranial lesion. herein, we discuss the possible mechanisms of bilateral abducens nerve palsy and its management. key words: abducens nerve palsy, sixth nerve palsy, false localizing sign. introduction the abducens nerve is the most vulnerable nerves due to its extremely long extracerebral intracranial course. it usually presents as false localizing sign in various intracranial disorders like brain tumour & idiopathic intracranial hypertension. it is usually unilateral & associated with major head injury with brain stem injury and associated neurological findings due to compression near petrous apex and narrowed bony canal (dorello’s canal). isoleted bilateral involvement of abducens nerve is uncommon in head injury & extremely rare in minor head injury. here we are discussing an unusual case of minor head injury where the patient presented with bilateral sixth nerve palsy without any other neurological deficit & all investigations failed to find cause. case report a 40 year old male was admitted with the history double vision after an episode of minor head injury (glasgow coma scale 15/15). the injury was sustained due to head on collision of his bike with a moving car coming from opposite direction on a local road at very low speed. immediately following the accident, the patient had transient loss of consciousness but regained consciousness after about five minutes. as seen by nearby relative there is no history of vomiting, seizure or bleeding from ear nose or mouth. patient was brought to our romanian neurosurgery (2014) xxi 4: 492 – 492 491 hospital where he was given primary care. on examination bilateral lateral rectus palsy was present (figure 1). no other positive finding recorded in general physical, neurological and ophthalmological examination. computed tomography head (ct head) (figure 2) and magnatic resonance imaging (mri) of brain (figure 3) were failed to reveal any significant finding explaining this condition. a formal diagnosis of post traumatic isolated bilateral abducens palsy was made. patient was managed conservatively with oral steroids (prednisolone 1mg/kg per day dose) for ten days followed by alternate day regime for next three weeks and tapering regimen along with oral methylcobalamine. the abducens palsy improved with time and resolved partially in six months. figure 1 isolated bilateral lateral rectus (abducens nerves) palsy in minor head injury patient figure 2 computed tomographic scan head showing no intracranial lesion or fracture figure 3 magnatic resonance imaging brain showing no patology justifying to abducens nerve palsy discussion abducens nerve originates from the brain stem and course up to the lateral rectus muscle. initially this nerve runs up to petrous ridge and changes direction approximately 120° forward. the further path of this delicate nerve is traversed in a very narrow bony tunnel known as dorello’s canal. after passing through dorello's canal, the nerve passes through the cavernous sinus and the superior orbital fissure and innervates the lateral rectus muscle (1, 2, 3, 5). two possibilities are theorized for damage of abducens nerve. one is an angle near the petrous apex and another is passage through the bony canal (dorello’s canal). bilateral abducens nerve palsy following trivial trauma is a relatively rare occurrence. berlit et al evaluated 165 patients suffering from abducens nerve palsy as the main presenting symptom (6). a vascular origin (29.7%), inflammatory diseases (19.4%) and tumours (10.9%) were the most common causes while traumatic abducens paresis (3.1%) was rare out of which only 10% of the 492 jaiswal et al post traumatic bilateral abducens nerve palsy patients were presented with bilateral palsy. posttraumatic bilateral abducens palsy has been reported mainly in various case reports thus emphasising its relative rarity. holmes et al in his study concluded that non-recovery from acute traumatic sixth nerve palsy was associated with complete palsy and/or a bilateral palsy (7). treatment of post traumatic bilateral abducens nerve palsy is usually conservative though kao et al showed that such patients treated with subtenon injection of botulinum toxin showed higher recovery rates than patients treated conservatively (8). mutyala et al reported a spontaneous improvement rate of 27% in unilateral traumatic sixth-nerve palsy and 12% in bilateral traumatic sixth-nerve palsy (9). however, holmes et al reported an overall spontaneous recovery rate of 73% (7). spontaneous recovery was more frequent in unilateral cases (84%) than in bilateral cases (38%) (7). our patient was managed conservatively with oral steroids and showed partial improvement after six months follow up. conclusion in conclusion bilateral isolated sixth nerve palsy is an extremely rare occurrence in minor head injury and very few cases have been reported in available literature. this case highlights the occurrence and management of posttraumatic bilateral sixth nerve palsy. full or partial recovery is the natural history in the majority of traumatic abducens nerve palsies, and this is an important consideration when counselling patients with such injuries. correspondence manish jaiswal a 33/48 a 2, omkareshwar, varanasi, 221001, uttar pradesh, india phone – 091-8933816028, e mail – manishmlnmc@gmail.com references 1. arias mj. bilateral traumatic abducens nerve palsy without skull fracture and with cervical spine fracture: case report and review of the literature. neurosurgery. 1985;16:232-234. 2. marconi f, parenti g, dobran m. bilateral traumatic abducens nerve palsy: case report. j neurosurg sci. 1994;38:177-180. 3. limnaios ee, papageorgiou ct. bilateral abducens nerve palsy. ophthalmologica. 1980;181:326-329. 4. uzan m, hanci m, sarioglu ac, et al. bilateral traumatic abducens nerve paralysis with cervical spine flexion injury. eur spine j. 1996;5:275-277. 5. baker rs, epstein ad. ocular motor abnormalities from head trauma. surv ophthalmol. 1991;35:245-267. 6. berlit p, reinhardt-eckstein j, krause kh. isolated abducens paralysis-a retrospective study of 165 patients. [article in german] fortschr neurol psychiatr 1989;57:32-40. 7. holmes jm, beck rw, kip ke, droste pj, leske da. predictors of non recovery in acute traumatic sixth nerve palsy and paresis. ophthalmology 2001;108:1457-60. 8. kao ly, chao an. subtenon injection of botulinum toxin for treatment of traumatic sixth nerve palsy. j pediatr ophthalmol strabismus 2003;40:27-30. 9. mutyala s, holmes jm, hodge do, younge br. spontaneous recovery rate in traumatic sixth-nerve palsy. am j ophthalmol 1996;122:898-9. microsoft word 10iordacheaararecase romanian neurosurgery (2011) xviii 1: 77 – 81 77 a rare case of severe craniocerebral trauma with penetrating head injury a. iordache1, j.m. kaya2, j.r. alliez2, b. alliez2 1md, phd student in neurosurgery, “gr.t. popa” university of medicine and pharmacy, iasi 2service de neurochirurgie, hopital nord, marseille abstract penetrating head injury remains an important issue even in modern neurosurgery. less frequent than other neurosurgical diseases, they may still pose some management problems. the authors present one extremely rare case of suicide attempt by penetrating head injury with harpoon at a male middle aged patient associated with iatrogenous pneumothorax. operated with a simple occipital craniectomy, the patient had a pretty good recovery with minimal neurological deficit (facial paresis). keywords: harpoon, penetrating head injury head injuries represent only a small percentage of cranio-cerebral traumas; however, they come into prominence through their clinical gravity and often through the atypical therapeutic strategies they require. out of the total head injuries, the number of autolytic attempts is relatively small, most of them being represented by aggressions or road accidents. next, we are going to present the case of a patient aged 58, c.i., who was taken from home with a gcs (glasgow coma scale) of 7; the clinical examination presents a harpoon (approximately 1.5 meters long) which penetrates the skull base through the oral cavity. the patient has a history of chronic alcoholism, depression and multiple antolytic attempts by drug intoxication, also being under specific psychiatric treatment. according to therapeutic protocol, the ambulance doctor tried during the transportation to intubate the patient without any success. on admission to the intensive care unit, the patient has a gcs of 6 and a reduction in bilateral vesical murmur with a sao2 of 65%. the patient undergoes a tracheostomy. case presentation the patient had a full-body scan and a cerebral angiography. both the clinical examination and the ct exam, together with the ultrasound examination show a traumatic pneumothorax, and the cerebral angiography shows the presence of a metallic foreign body (the patient had no cerebrovascular lesions). the drainage of pneumothorax had been done in emergency and after that it could be seen an improvement in the o2 saturation level (96%). after that, it has been decided on the emergency neurosurgical intervention. 78 a. iordache et al a rare case of severe craniocerebral trauma figure 1 harpoon penetrating the oral cavity figure 2 bilateral traumatic pneumothorax a b figure 3 metallic object with upward, posterior trajectory, situated left paramedian, which crosses the pharynx, the clivus and the occiput – numerous artefacts the surgical intervention could be undergone only after cutting off another 2 cm from the harpoon which protrudes at the oral cavity level. it was chosen a left paramedian approach to allow both a supra and subtentorial approach. it was practiced a paramedian semicircular cutaneous flap (figure 4a). a minimum fracture site is identified on the left occipital. it was practiced the drilling to the occipital bone (figure 4b) near the harpoon tip and afterwards the end of the harpoon was released. what follows next is the axis traction in one direction in order to prevent further brain injuries caused by the harpoon’s socket piece (figure 4c). the postoperative evolution is marked by the presence of a cerebellar syndrome marked by ataxia and dysarthria (possibly due to the interception of superior cerebellar peduncle) but also by the presence of facial nerve paralysis on the left side. romanian neurosurgery (2011) xviii 1: 77 – 81 79 afterwards, the cerebellar disorders present a significant improvement; however, the patient still had central facial paralysis after 6 months. a b c d figure 4 left paramedian approach a b figure 5 a craniocerebral ct after 2 weeks; b brain mri after 4 months 80 a. iordache et al a rare case of severe craniocerebral trauma ct and mri exams after 2 weeks and 4 months respectively show disabling injuries and left paramedian scars without vascular lesions or blood collections on the foreign body trajectory. cranio-cerebral injuries by a harpoon lance are very serious most of the time. they are most of the time the result of accidental injuries – especially fishing. the case we have presented so far – transfixiant wound occipital bone clivus by a harpoon lance for suicidal purpose represents an extremely rare case (after a long bibliographical research in the field), if not a unique case. the patient showed no vascular or infectious complications as a result of the injury. the patient demonstrated good evolution in the surgical context but the prognosis remains questionable due to his mental illness and suicidal history, even in conditions where the patient would remain under psychiatric supervision for a long time. in such case, similar to gunshot wounds, the essential of the management is to remove the foreign object with minimum of injury, associated with the excision of the necrotic brain tissue surrounding the trajectory of the foreign body and eventually the blood clots. good haemostasis is compulsory and watertight suture of the duramater is necessary eventually with duraplasty in order to avoid secondary dural fistula – a common complication of the lesions in the posterior fossa. in the presented case there was no need for duraplasty because of the minimal laceration of the dura(only the tip of the harpoon was penetrating the dura) and was no need to remove bone fragments because there was only a minimal extrusive fracture of the occipital bone. in this case anterior csf fistula was prevented by the early intubation with pharyngeal tenting, immediately after the removal of the foreign body. these kind of penetrating head injuries are quite rare though we had another case at a paediatric patient, with a less good result at long term. in the paediatric patient the mechanism was also trans pharyngeal penetration, but accidental. a b figure 6 transpharyngeal intracranial penetrating harpoon in a paediatric patient romanian neurosurgery (2011) xviii 1: 77 – 81 81 references 1. camperon f., borne g., graille r., cristau p. orbito-cranio-cerebral injury by an underwater harpoon lance presse med. 1967;75(48):2465-6 2. fernandez-melo r., moran a.f., lopez-flores g., bouza-molina w., garcia-maeso i., benavidesbarbosas j. penetrating head injury from harpoon. case report; neurocirugia (astur). 2002;13(5):397-400. 3. gutierez a., gil l., sahuquillo j., rubio e. unusual penetrating craniocerebral injury surg neurol. 1983; 19(6):541-3. 4. hefer t., joachims h.z., loberman z., gdal-on m., progas y.; harefuah facial injury by fishing harpoons harefuah. 1994;127(9):295-8, 360 5. janeke s. an unusual craniofacial injury. a case report afr med j. 1984 4;66(5):190; 6. lopez f., martinez-lage j.f., herrera a., sanchezsolis m., torres p., palacios m.i., poza m. penetrating craniocerebral injury from an underwater fishing harpoon childs nerv syst. 2000;16(2):117-9; 7. roman f., salgado-pineda p., bartres-faz d., sanchez-navarro j.p., martinez-lage j., lopezhernandez f., bargallo n., junque c. orbito-craniocerebral injury by an underwater harpoon lance presse med. 1967, 18;75(48):2465-6. 8. rocca a., casu g., sechi c.s. penetrating craniocerebral injuries. report of two unusual cases j neurosurg sci. 1987;31(1):19-21; 9. windle-taylor p.c. transorbital injury from a harpoon involving the paranasal sinuses j otorhinolaryngol relat spec. 1978;40(5):278-84 12_kumara_demographic 312 kumar et al demographic pattern, clinical profile and outcome of traumatic spinal cord injuries demographic pattern, clinical profile and outcome of traumatic spinal cord injuries at a tertiary care hospital k. aswani kumar1, b.v. subrahmanyam2, s.v. phanidra2, s. satish kumar3, p.n. harish4, p. ramamohan5, amit agrawal6 narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 1resident forensic medicine, department of forensic medicine 2professor of forensic medicine, department of forensic medicine 3associate professor of emergency medicine, department of emergency medicine 4associate professor of neurosurgery, department of neurosurgery 5associate professor of pharmacology, department of forensic pharmacology 6professor of neurosurgery, department of neurosurgery abstract: background: traumatic spinal cord injury (sci) is recognized as a serious public health problem resulting in significant morbidity, mortality and permanent disability. the present study is aimed to describe the epidemiological characteristics and outcome of patients with traumatic spinal cord injury in rural tertiary referral care center form south india. material and methods: the present study was conducted at narayana medical college and hospital, nellore. all patients admitted and managed for traumatic spinal cord injury were retrieved and data collected in a pre-designed proforma. patient characteristics, details of etiology, mechanism of injury, level of injury, extent of neurological deficits, details of investigations, details of management and immediate outcome were recorded. results: a total 152 patients were included in the present study. the mean age was 38.45 years and majority the patients were young adult males. the mean hospital stay was 19.12 days. 71.7% percent patients were non-agriculture workers (mainly involved in construction work) and 28.3% patients were farmers. 61.2% of the patients sustained injuries due to fall from height and 34.2% patients sustained injuries due road traffic accidents. cervical spine injuries were most common (44.1%), followed by thoraco-lumbar region (36.8%) and dorsal spinal region (19.1%). 9 patients expired in post-injury during hospital stay and all of them had complete cervical spinal cord injury. all patients received aggressive rehabilitation care. conclusion: in accordance with the literature our results reflect that traumatic spinal cord injuries affect young population and can leave these persons with significant functional and physical morbidity. the major limitation of the study is that it is a single institution based and may not reflect the true spectrum of traumatic spinal cord injuries in the population. key words: spinal cord injury, spinal injuries, spinal trauma introduction traumatic spinal cord injury (sci) is recognized as a serious public health problem that can result in significant morbidity, mortality and permanent disability (leading to emotional and financial hardships). (1-3) only few studies report the epidemiological characteristics of traumatic sci in developing countries and describe their etiology, demographic and clinical characterizes and management option. (4, 5) the present study is aimed to describe the epidemiological characteristics and outcome of patients with traumatic spinal cord injury in rural tertiary referral care center form south india. romanian neurosurgery (2015) xxix 3: 312 317 313 material and methods the present study was conducted at narayana medical college and hospital, nellore. after approval from the institutional ethical committee, the medical records of all patients admitted and managed for traumatic spinal cord injury were retrieved and data collected in a pre-designed proforma. patient characteristics including age, gender, occupation were noted. details of etiology, mechanism of injury, level of injury, extent of neurological deficits, details of investigations, details of management and immediate outcome were recorded. the details of motor and sensory functions were recorded by using the american spinal injury association (asia) scale and the severity was classified as complete or incomplete injury. (6) the data were analyzed on epiinfo ® version 7. the descriptive statistics were used to calculate mean and frequencies of data. results a total of 152 patients were included in the present study. the mean age was 38.45 years (range 6-72 years sd±14.566 years). in present study majority of the patients were young adult males (figure 1). the mean hospital stay was 19.12 days (range 4-59 days sd±10.699 days). 71.7% percent patients were non-agriculture workers (mainly involved in construction work) and 28.3% patients were farmers. 61.2% of the patients sustained injuries due to fall from height and 34.2% patients sustained injuries due road traffic accidents. cervical spine injuries were most common (44.1%), followed by thoracolumbar region (36.8%) and dorsal spinal region (19.1%). in our series majority of the patients had incomplete spinal cord injury. 18 patients had associated traumatic brain injury and had low glasgow coma score at the time of presentation. ct scan was performed for all these patients and two patients had lesions (one patient extradural hematoma and one patient acute subdural hematoma) those required neurosurgical intervention. twenty two patients were managed conservatively and 130 patients underwent spinal fusion and fixation. elective mechanical ventilation was required in 19 cases (all cases were of cervical spine injuries). 9 patients expired post-injury during hospital stay and all of them had complete cervical spinal cord injury. all patients received aggressive rehabilitation care (chest physiotherapy, bowel, bladder and back care). 314 kumar et al demographic pattern, clinical profile and outcome of traumatic spinal cord injuries figure 1 age and gender distribution (n=152) figure 2 distribution of the patients according to the month of the year discussion as we observed and many studies have reported in the past, traumatic spinal cord 0 5 10 15 20 25 30 35 0-10 11-20 21-30 31-40 41-50 51-60 > 61 male female 0 2 4 6 8 10 12 14 16 18 20 patients romanian neurosurgery (2015) xxix 3: 312 317 315 injury young adult males in their productive years. (7-9) (1, 9-13) as reported in many, fall from height was the leading cause of spinal cord injuries in our series (mainly in nonagricultural workers followed by agricultural workers). (14-19) in contrary to this many other studies have reported where the authors found agricultural workers (9, 20) and road traffic injuries (21-23) as the commonest causes of traumatic spinal cord injuries respectively. we found incomplete injuries more than the complete injuries and cervical spine injuries were being the most common (44.1%), followed by thoraco-lumbar injuries (36.8%) and dorsal spinal injuries (19.1%). in literature the distribution of incomplete and complete injuries varies as per the anatomical involvement, location and mechanism of the injuries. (1, 9, 20, 24-26) most of the traumatic spinal injuries are managed by neurosurgeons, spinal surgeons and by orthopedic surgeons (followed by intensive rehabilitation) and the management of spinal cord injury patients is determined by their neurological status, instability of the spine and ability to tolerate neurosurgical intervention. (4, 27, 28) as described in the literature, in majority of our patients surgical interventions were performed for different indication to stabilize the spine and/or to decompress the spinal cord. (29-32) depending on the severity of level of the spinal cord injury, the duration of the hospital stay varies. in present study we noted that tthe mean hospital stay was 19.12 days (range 4-59 days sd±10.699 days). lan et al reported that the average hospital stay for paraparetic was 62 days, for paraplegics 118 days, for tetraparetics 102 days and for tetraplegics 132 days. (24) in another study the authors reported that the mean hospital stay for paraparetic was 44 days, for paraplegics, for tetrapareties 90 days and for tetraplegics patients it was 100 days. (1) in present study we found the mortality rate of 5.9%. chen et al (1) reported a mortality rate of 6.0% and lan et al (24) reported a mortality rate of 10.1%. respiratory failure (particularly in tetraplegic) was the leading cause of mortality. (1, 24) other causes those can influence the outcome include sepsis (from pressure ulcers), renal failure and other associated systemic injuries (abdominal/chest injuries, head injury). (1, 24) in present study we did not collect data regarding financial implications of spinal cord injuries. however because of the difficult to cure and their potential to give rise to much human stress traumatic spinal cord injury can cause great loss not only to the individuals but also to the society. (33) the lifetime cost of the traumatic spinal cord injuries has been shown to be directly attributed to the age at the time of injury and the severity of injury. (30) it has been estimated that the lifetime costs for an incomplete motor lesion at age 50 years at any level range from $300,000 to $1.7 million for a person who sustain higher injuries (tetraplegia) at the age of 25 years. (34) type of transportation depends on locations of treating facilities and availabilities of prehospital care. in major cities there is greater availability of ambulance networks equipped with trained and semi-trained personnel’s, in contrary to this in rural areas these patients are transferred by untrained personnel’s with different means. (35, 36) conclusion in spite of much advancement for the management of spinal cord injury patients, there is no definitive treatment modality which can help to recover the neurological functions. hence the preventive programs have been promoted to prevent spinal cord injuries. (17, 20) preventive strategies and policies needs to be focused on subjects with high risk activities: sports activities (diving and motorcycles accidents) for young people; road traffic acci¬dents for adults; injuries due to fall in elderly population. (37) the major limitation of the study is that it is a single institution based and may not reflect the true 316 kumar et al demographic pattern, clinical profile and outcome of traumatic spinal cord injuries spectrum of traumatic spinal cord injuries in the population. however in accordance with the literature our results reflect that traumatic spinal cord injuries affect young population and can leave these persons with significant functional and physical morbidity. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.chen cf, lien in. spinal cord injuries in taipei, taiwan, 1978-1981. paraplegia. 1985;23(6):364-70. 2.mcdonald jw, sadowsky c. spinal-cord injury. lancet. 2002;359(9304):417-25. 3.tascu a, exergian f, daniel s, iliescu a, pascal c, popescu g, et al. traumatic spine injuries in children. experience on 434 cases and therapeutic perspectives. romanian neurosurgery. 2015;xxix(2):135-40. 4.rathore mfa, hanif s, farooq f, ahmad n, mansoor sn. traumatic spinal cord injuries at a tertiary care rehabilitation institute in pakistan. jpma. 2008;58(2):537. 5.rahimi-movaghar v, sayyah mk, akbari h, khorramirouz r, rasouli mr, moradi-lakeh m, et al. epidemiology of traumatic spinal cord injury in developing countries: a systematic review. neuroepidemiology. 2013;41(2):65-85. 6.american spinal injury association. international standards for neurological classification of spinal cord injury revised chicago asia. 2002. 7.girard r, boisson d, depassio j, boucand m, eyssette m. the female paraplegic: a statistical survey. spinal cord. 1983;21(3):149-53. 8.girard r, minaire p, castanier m, berard e, perrineriche b. spinal cord injury by falls: comparison between suicidal and accidental cases. paraplegia. 1980;18(6):381. 9.minaire p, castanier m, girard r, berard e, deidier c, bourret j. epidemiology of spinal cord injury in the rhône-alpes region, france, 1970-75. paraplegia. 1978;16(1):76-87. 10.burke dc, toscano j. incidence and distribution of spinal cord injury. menzies foundation technical report. 1987;1 13-47. 11.gjone r, nordlie l. incidence of traumatic paraplegia and tetraplegia in norway: a statistical survey of the years 1974 and 1975. paraplegia. 1978;16(1):88-93. 12.stover sl, fine pr. the epidemiology and economics of spinal cord injury. paraplegia. 1987;25(3):225-8. 13.chacko v, joseph b, mohanty sp, jacob t. management of spinal cord injury in a general hospital in rural india. paraplegia. 1986;24(5):330-5. 14.dryden dm, saunders ld, rowe bh, may la, yiannakoulias n, svenson lw, et al. the epidemiology of traumatic spinal cord injury in alberta, canada. the canadian journal of neurological sciences. 2003;30(2):113-21. 15.pickett ge, campos-benitez m, keller jl, duggal n. epidemiology of traumatic spinal cord injury in canada. spine. 2006;31(7):799-805. 16.pickett w, simpson k, walker j, brison rj. traumatic spinal cord injury in ontario, canada. the journal of trauma. 2003;55(6):1070-6. 17.shingu h, ohama m, ikata t, katoh s, akatsu t. a nationwide epidemiological survey of spinal cord injuries in japan from january 1990 to december 1992. paraplegia. 1995;33(4):183-8. 18.kannus p, palvanen m, niemi s, parkkari j. alarming rise in the number and incidence of fall-induced cervical spine injuries among older adults. the journals of gerontology series a, biological sciences and medical sciences. 2007;62(2):180-3. 19.nobunaga ai, go bk, karunas rb. recent demographic and injury trends in people served by the model spinal cord injury care systems. archives of physical medicine and rehabilitation. 1999;80(11):137282. 20.dincer f, oflazer a, beyazova m, celiker r, basgöze o, altioklar k. traumatic spinal cord injuries in turkey. paraplegia. 1992;30(9):641-6. 21.hung cc, chiu wt, tsai jc, laporte re, shih cj. [an epidemiological study of head injury in hualien county, taiwan]. journal of the formosan medical association. 1991;90(12):1227-33. 22.thurman dj, burnett cl, beaudoin de, jeppson l, sniezek je. risk factors and mechanisms of occurrence in motor vehicle-related spinal cord injuries: utah. accident analysis & prevention. 1995;27(3):411-5. 23.thurman dj, burnett cl, jeppson l, beaudoin de, sniezek je. surveillance of spinal cord injuries in utah, usa. paraplegia. 1994;32(10):665-9. 24.lan c, lai js, chang kh, jean yc, lien in. traumatic spinal cord injuries in the rural region of taiwan: an epidemiological study in hualien county, 1986-1990. paraplegia. 1993 jun;31(6):398-403. pubmed pmid: 8337004. epub 1993/06/01. eng. romanian neurosurgery (2015) xxix 3: 312 317 317 25.richardson rr, meyer pr. prevalence and incidence of pressure sores in acute spinal cord injuries. paraplegia. 1981;19(4):235-47. 26.tator ch, fehlings mg. review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. journal of neurosurgery. 1991;75(1):15-26. 27.scivoletto g, morganti b, molinari m. early versus delayed inpatient spinal cord injury rehabilitation: an italian study. archives of physical medicine and rehabilitation. 2005;86(3):512-6. 28.guttmann l. new hope for spinal sufferers: ludwig guttmann. reproduced from medical times, november 1945. paraplegia. 1979;17(1):6-15. 29.esce, haines. acute treatment of spinal cord injury. current treatment options in neurology. 2000;2(6):51724. 30.becker d, sadowsky cl, mcdonald jw. restoring function after spinal cord injury. the neurologist. 2003;9(1):1-15. 31.chen ty, dickman ca, eleraky m, sonntag vk. the role of decompression for acute incomplete cervical spinal cord injury in cervical spondylosis. spine. 1998;23(22):2398-403. 32.mirza sk, krengel wf, chapman jr, anderson pa, bailey jc, grady ms, et al. early versus delayed surgery for acute cervical spinal cord injury. clinical orthopaedics and related research. 1999 (359):104-14. 33.shingu h, ikata t, katoh s, akatsu t. spinal cord injuries in japan: a nationwide epidemiological survey in 1990. paraplegia. 1994;32(1):3-8. 34.westergren h, farooque m, olsson y, holtz a. spinal cord blood flow changes following systemic hypothermia and spinal cord compression injury: an experimental study in the rat using laser-doppler flowmetry. spinal cord. 2001;39(2):74-84. 35.srinivasan u. acute spinal cord injury: managing at the site of impact and addressing reality gap. japi 2012;60:7-9. 36.singh r, sharma sc, mittal r, sharma a. traumatic spinal cord injuries in haryana: an epidemiological study. indian j community med. 2003;28(4):184-86. 37.kiwerski j. the causes, sequelae and attempts at prevention of cervical spine injuries in poland. spinal cord. 1993;31(8):527-33. microsoft word 5iencean_traumatic.doc 210 iencean et al traumatic spinal cord injuries traumatic spinal cord injuries: neuroprotection and recent outcomes st.m. iencean, i. poeata, didona ungureanu, d. cuciureanu, b. costachescu, al. chiriac “grigore t. popa” university of medicine and pharmacy iasi, romania *clinic of neurosurgery, “prof. dr. nicolae oblu” hospital iasi, romania abstract traumatic spinal cord injury has major effects on the injured person. in case of acute complete traumatic spinal cord injury methylprednisolone is a standard treatment option and surgery is often necessary, but these are not a cure for a complete spinal cord injury. this paper analyses the treatment outcomes in 37 cases of complete traumatic spinal cord injuries of which some patients received usual treatment and some patients received cerebrolysin, as neuroprotection and a protocol of intravenous fluids to ensure the spinal cord perfusion pressure augmentation, and standard surgical treatment. key words: neuroprotection, paraplegia, spinal cord injury. introduction spinal cord injury can occur at any age, can lead to paraplegia or quadriplegia and many young people are affected. when a spinal trauma occurs there are two types of lesions associated with a spinal cord injury: a complete spinal cord injury and an incomplete spinal cord injury. in complete spinal cord injury the normal human spinal cord is disrupted. sandrine thuret et al showed that spinal cord injury can result from contusion, compression, penetration or maceration of the spinal cord. spinal cord lesion consists of injury of the neurons, blood vessels injury, bleeding in the central grey matter, spinal cord edema and hypoperfusion of the spinal cord and the dura mater injury. after the acute spinal cord injury, damage to nerve cells and fibers and to supporting cells within the spinal cord continues to progress for several days, perhaps even weeks and it is the secondary damage. spinal cord injury leads to the death of nervous cells and the interruption of the descending and ascending axonal tracts. spinal cord injury culminates in glial scarring and the scar is often oriented perpendicular to the neuraxis and appears impenetrable. the scar contains secreted molecular inhibitors of axon growth. the immediate surgical treatment must remove the tissues causing spinal cord compression, must correct a gross misalignment and must stabilize the spine. during the delayed secondary spinal cord injury the early treatment may reduce the extent of disability. the secondary spinal cord injury is the damage that continues in the hours following trauma and consists of reduction in blood flow at the level of injury, excessive release of neurotransmitters (glutamate), inflamatory response, free radicals attack neurons and romanian neurosurgery (2012) xix 3: 210 216 211 neuronal apoptosis. during this delayed secondary spinal cord injury the treatment may reduce the extent of disability, eg. methylprednisolone given within 8 hours of the injury occuring significantly improves recovery in humans (nascis trials i, ii and iii). after a complete spinal cord injury there are two types of lesions: complete disruption of the spinal cord or different types of scars. the aim of the present study was to assess clinical outcome in a recent serie of patients, to analyse whether there is a difference in outcome with regard to the standard treatment including methylprednisolone versus the same type of surgical treatment and nonsteroidal antiinflammatory drugs and to compare the results. methods thirty-seven patients of complete traumatic spinal cord injuries were enrolled in this study. this study included patients with complete acute traumatic spinal cord injury admitted within 24 hours of injury with a complete neurological evaluations and with ct and /or magnetic resonance imaging before surgery. in a period of 9 months from a total of 262 patients with traumatic spinal cord injuries were 37 patients with complete traumatic spinal cord injuries: a and b score on asia scale. there were nine patients with complete cervical injuries with tetraplegia, three patients with dorsal (d5-d7) spinal cord injuries with paraplegia and 25 patients with dorsolumbar (d11-l1) spinal cord injuries with paraplegia. thirty-two patients received usual treatment: methylprednisolone and surgery for decompression, to realign and to stabilize the spine and five patients (only a score on asia scale) received cerebrolysin and a protocol of intravenous fluids to ensure the spinal cord perfusion pressure augmentation. the five patients group consisted of: two cervical spinal cord injuries, one of medium dorsal spinal cord injury and two patients with dorso-lumbar spinal cord injuries. surgical procedure consisted of spinal cord decompression and then to realign and to stabilize the spine. results concerning the thirty-two patients with complete chronic spinal cord injury no significant motor or sensory improvements were observed immediate and three to six months afterwards. the five patients group receiving additional therapy presented in evolution a sensory improvements, but no significant motor improvements. three patients in this group of five patients: one with thoracal and two dorso-lumbar complete spinal cord injuries received cerebrolysin one to three months postoperatively and the results for these three patient were the partial sensory recovery including the sensations of touch, pressure, vibration and pain: from a tob score on asia scale. 212 iencean et al traumatic spinal cord injuries a b romanian neurosurgery (2012) xix 3: 210 216 213 c figure 1 a, b, c fracture and dislocation of lower cervical spine ( c6-c7) with spinal cord injury ( cervical spine mri) discussion patients with acute traumatic complete spinal cord injuries with paraplegia or tetraplegia have a complete disruption of the spinal cord, an extensive contusion or an extensive hematoma with secondary spinal cord injury and late maceration of the spinal cord. patients with a complete spinal cord injury have an infinitesimal chance of recovery. the surgical treatment (ideally within eight hours of the injury occuring) must remove the tissues causing spinal cord compression, must correct a gross misalignment and must stabilize the spine. therefore immediate surgery for spinal cord decompression including the duraplasty, is of high importance for the prognosis and evolution of spinal cord injury. various therapies have been applied that may be neuroprotective when administered soon after injury. some of these therapies are approaches used for other health purposes but have also shown potential in animals with experimental sci. niklas marklund in an excellent recent material about the spinal cord regeneration said that “the current treatment options for patients with sci are limited and the neurosurgeon is crucial in the initial management, including the medical stabilization and the timing of the surgical treatment.”also he showed that „initial prehospital management of sci should follow the atls principles including stabilization, airway management and blood pressure control. 214 iencean et al traumatic spinal cord injuries a b figure 2 a, b c5 cervical spina fracture with traumatic acute spinal cord hemorrhage, tetraplegia romanian neurosurgery (2012) xix 3: 210 216 215 improved patient management and lower morbidity and mortality following acute sci in specialized centers has repeatedly been demonstrated and it is plausible that the same holds true for intensive care unit monitoring and aggressive medical management of secondary insults.” “methylprednisolone is not standard of care anymore, öptional”at best, although could still be considered in view of the lack of other treatment options”. the current recommendation is to treat all patients with sci according to the local protocol. if steroids are recommended, they should be initiated within 8 hours of injury with the following steroid protocol: methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the bolus. other drugs with therapeutic potential in acute spinal cord injury are: gm-1 ganglioside (sygen ) decreases injury-induced, over-release of damageperpetuating excitatory substances. erytropoietin has neuroprotective effects and contributes to neurons regeneration neotrofin stimulates growth-factor production, enhances proliferation of cns stem cells, and protects neurons from the release of excitatory substances. minocycline promotes functional recovery, enhances axonal survival, and reduces injury-site lesion size etc. after passage of acute and subacute stages the patient has a chronic traumatic spinal cord injury with complete paraplegia or complete tetraplegia; he has one of two types of lesions: complete disruption of the spinal cord or different types of scars. the complete disruption of the spinal cord is the interrupting of the continuity of spinal cord without of therapy until now. the scar of the spinal cord can be: a complete and impenetrable glial scar on the site of spinal cord injury, an incomplete scar and a posttraumatic syringomyelia or cysts on the site of sci a filiform connective scar of the two segments of damaged spinal cord. the glial scar is a major impediment to axonal regeneration following injury there is an inability to repair spinal cord damage. therefore the first steps in the management of sci can assure an efficient treatment in order to minimize the direct traumatic effects on the spinal cord and to block the evolution and progression of the secondary spinal cord injury. in addition of the standard surgical treatment and with or without methylprednisolone, we tryed to give for some patients: cerebrolysin and a protocol of intravenous fluids to ensure the spinal cord perfusion pressure augmentation. the group of thirty-two patients with complete chronic spinal cord injury had no significant motor or sensory improvements immediate and three to six months afterwards. the five patients group receiving additional therapy presented in evolution a sensory improvements, but no significant motor improvements: from a to b score on asia scale. this is a preliminary study of a combination of cerebrolysin and of intravenous fluids to ensure the spinal cord perfusion pressure augmentation in complete traumatic acute spinal cord injury and there are few cases with modest results but promising, compared to the lack of any effective therapeutic alternative. 216 iencean et al traumatic spinal cord injuries conclusion initial prehospital management of traumatic acute spinal cord injury is crucial for the morbidity and mortality following acute sci. this study show that cerebrolysin as immediate neuroprotective therapy and ensuring the spinal cord perfusion pressure augmentation has no complications and the results are promising, but much follow-up work is needed to document the long-term benefits. this study about treatments in acute traumatic spinal cord injury is the subject of the grant: “immediate neuroprotective therapy in acute traumatic spinal cord injury”, that won the 2011 national competition of national research council (cncs), ideas, grant number: pn-ii-idpce-2011-3-0569, funded by cncs – uefiscdi romania. corresponding author a.st. iencean neurosurgery, “prof. dr. nicolae oblu” hospital iasi, andrei_steffan@yahoo.com references 1. bunge mb. novel combination strategies to repair the injured mammalian spinal cord. j spinal cord med. 2008;31(3):262-9; 2. dallo jg, reichert bv, valladão júnior jb et all. differential astroglial responses in the spinal cord of rats submitted to a sciatic nerve double crush treated with local injection of cultured schwann cell suspension or lesioned spinal cord extract: implications on cell therapy for nerve repair. acta cir bras. 2007 ;22(6):485-94; 3. fernandez e, pallini r. connective tissue scarring in experimental spinal cord lesions: significance of dural continuity and role of epidural tissues.acta neurochir (wien).1985; 76 (3-4):145-8; 4. haninec p, houst'ava l, stejskal l, dubový p. rescue of rat spinal motoneurons from avulsioninduced cell death by intrathecal administration of igfi and cerebrolysin. ann anat. 2003 ;185(3):233-8; 5. haninec p, dubový p, sámal f et al reinnervation of the rat musculocutaneous nerve stump after its direct reconnection with the c5 spinal cord segment by the nerve graft following avulsion of the ventral spinal roots: a comparison of intrathecal administration of brain-derived neurotrophic factor and cerebrolysin. exp brain res. 2004 ;159(4):425-32; 6. iannotti c, zhang yp, shields lb, han y et all.. dural repair reduces connective tissue scar invasion and cystic cavity formation after acute spinal cord laceration injury in adult rats. j neurotrauma. 2006,23(6):853-65; 7. şt.m. iencean, i. poeată, gh. solcan, dana turliuc, e.c. popescu, b. costăchescu, a.şt. iencean: news and views of neuroprotection in complete traumatic spinal cord injuries, romanian neurosurgery, 2011, vol xviii, 4; 8. kwon bk, fisher cg, dvorak mf, tetzlaff w. strategies to promote neural repair and regeneration after spinal cord injury. spine. 2005 1;30(17 suppl):s313; 9. lim pac, adela m tow recovery and regeneration after spinal cord injury: a review and summary of recent literature. ann acad med singapore 2007;36:49-57; 10. lima c et al., olfactory mucosa autografts in human spinal cord injury: a pilot clinical study, journal of spinal cord medicine 2006, 29, 191-203; 11. marklund niklas: spinal cord regeneration – current and future treatment options for traumatic spinal cord injury, eans training courseleeds, 26 – 30 august 2012; 12. popovich pg, guan z, wei p, huitinga i, van rooijen n, stokes bt. depletion of hematogenous macrophages promotes partial hindlimb recovery and neuroanatomical repair after experimental spinal cord injury. exp neurol. 1999 ;158(2):351-65; 13. ratan rr, noble m. novel multi-modal strategies to promote brain and spinal cord injury recovery. stroke. 2009 ;40(3 suppl):s130-2; 14. sharma hs. new perspectives for the treatment options in spinal cord injury. expert opin pharmacother. 2008;9(16):2773-800; 15. tsai ec, tator ch. neuroprotection and regeneration strategies for spinal cord repair. curr pharm des. 2005;11(10):1211-22. kakucsc_drotaverinum romanian neurosurgery (2016) xxx 2: 177-183 | 177 drotaverinum – a new modality of prevention and treatment in cerebral vasospasm after subarachoidian hemorrhage? c. kakucs1,2, c. berce3, a. tamas-szora4, g. ungureanu2, i.st. florian2,5 1phd student, university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania, neurosurgical department; 2cluj county clinical emergency hospital, neurosurgical department; 3university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania, laboratory animal facility; 4university of medicine and pharmacy “iuliu hatieganu” clujnapoca, romania, human anatomy and embriology department; 5university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania, neurosurgical department abstract: aim: this study want to demonstrate the efficaciousness of drotaverinum as a replacer of papaverine in the prevention and treatment of vasospasm. material and method: in this study were used 20 albino wistar male rats. rats were divided in two groups and vasospasm was induced to the both femoral artery and after that irrigation of the femoral arteries with drotaverinum was performed to demonstrate the vasodilatation that can appear (group a). in the group b after the obtaining of vasospasm irrigation of the femoral arteries with saline solution was performed and this group was used as witness. the length of the vessels was measured when was achieved the vasospasm and also before and after the administration of the solutions. pictures were taken at every step of dissection and solutions administration to can measure the length of arteries before and after the administration of drotaverinum and the saline solution. results: in all rats was obtained vasospasm at the femoral artery after clipping the artery and after we irrigate with adrenaline. in the group with drotaverinum we obtained the vasodilatation and in the witness group the caliber of the vessels remain the same. the statistical analysis of the data demonstrate a significant differences between the group were was used drotaverinum and the witness group were was used the saline solution (p<0,001). conclusions: drotaverinum has a good vasodilatative effect on arteries and he can prevent the apparition of vasospasm and it can even treat vasospasm if occur by producing local vasodilatation and a good circulation in the area where is administrated. this study showed quantitatively that drotaverinum can treat the experimental peripheral vasospasm in rats. key words: vasospasm, drotaverinum, experimental study 178 | kakucs et al drotaverinum – prevention and treatment in cerebral vasospasm introduction cerebral vasospasm can occur after subarachnoidian hemorrhage and is one of the leading causes of morbidity and mortality in this type of pathology (1-3). subarachnoidian hemorrhage represent the bleeding in the subarachnoidian space and the most frequent pathology that can determine that bleeding are the ruptured aneurysms (4). cerebral vasospasm after subarachnoidian hemorrhage represent a challenge problem from the prevention and treatment point of view and contributes to the most devastating injury: delayed cerebral ischemia (2, 5, 6). when delayed cerebral ischemia occur the patient outcome is poor and this can lead even to death (6). the objective of our study was to demonstrate on rats models the benefits of drotaverinum when is applied on a spastic artery and to demonstrate the efficacy instead of papaverine. also intraoperatory cisternal irrigation with drotaverinum of the arteries after the aneurysm is clipped is performed to prevent the apparition of the vasospasm or even to treat this if already has developed. in our statistics the incidence of cerebral vasospasm is lower than the data from the literature and we thought that is happening because of the use of drotaverinum. in the literature are studies about cisternal irrigation after clipping the aneurysm but with papaverine not with drotaverine (7). in literature are studies about the resistance against intra-arterial papaverine in cerebral vasospasm or about the efficacy of papaverine in this type of pathology but about drotaverinum there’s no study to see if is a good option to use it instead of papaverine (8, 9). materials and methods animals and housing twenty (n=20) male hsdola:wi rats weighing between 300 and 350 grams were used in the present study. the animals were housed in polysulfone type iii open-top cages (tecniplast, italy) and had access to filtered tap water in bottles and peletted feed (nutret combinat granulat, cantacuzino institute, romania) ad libitum. the rats were kept in the laboratory animal facility of the „iuliu hatieganu” university of medicine and pharmacy at a standard temperature of 24 ± 2 °c, a relative humidity of 55 ± 10%, 12:12-h light:dark cycle (lights on, 0700 to 1900). all experimental protocols were approved by the ethics comittee of the university (no. 301/29.05.2015 ) and were conducted in accordance the eu directive 63/2010, as per which, the experimental procedure severity was classified as moderate, as the animals fully recovered and were not sacrificed after the procedure. experimental procedure the animals were randomly assigned into two (n=2) groups of ten (n=10) individuals per group. group a was used to assess the efficiency of drotaverinum for preventing the occurrence of vasospasm, while group b was used as a control group. the rats were anesthetized by a intramuscular injection of a xylazine:ketamine cocktail in a dosage of 8 mg/kg xylazine to 80 mg/kg ketamine. after romanian neurosurgery (2016) xxx 2: 177-183 | 179 anesthesia, the animals were positioned in a dorsal decubitus. after positioning the rats was performed shaving the medial part of the posterior legs and was make a skin incision about 2 cm and dissect the anatomical structures till was discovered the femoral artery and of course the femoral vein and sciatic nerve in the medial and respectively lateral side of artery. the dissection was continued till the femoral artery was isolated (figure 1). after the preparation of the femoral artery a vascular clip was put (figure 2) and maintained it for 2 minutes and at the same time the artery was irrigated with adrenaline (0,1 ml with concentration of 1/1000). after 2 minutes the clip was removed and the narrowing of the lumens artery was obtained (figure 3). when the experimental vasospasm was obtained the irrigation of the femoral artery with drotaverinum (0,1 ml) was performed and after another 2 minutes the vessel was dilated (figure 4). this protocol was applied for all the 10 animal models from the group a and the experiment was made on the both posterior legs. in the witness group was used the same protocol as was mentioned above with the exception that the irrigation of the femoral artery, after the experimental vasospasm, was made with saline solution not with drotaverinum. in this group was observed that the saline solution does not produce vasodilatation and the vessels remains narrowed were was put the vascular clip. the dissections were performed with microsurgical instruments under the microscope (leika). each step of the study protocol with the femoral artery was photographed. after finishing the study measurements on arteries after clipping, after tamponing with drotaverinum and with saline solution was achieved. the measurements were performed with a special soft of morphometry (axiovision rel 4.6.) (figures 5 and 6). after the experimental study the animal models were observed till 7 days to see if they develop some complications after the vasospasm that was induced. in group a doesn’t occur any complication due to vasospasm, but in the group b occurred 2 posterior limb ischemia that maybe was produced by the narrowing of the femural artery. the statistical analysis was performed using medcalc soft. the statistical tests which were applied were t-test and correlation coefficient that will be shown in the results. figure 1 femoral artery of the right posterior limb and its relationship with the sciatic and femoral vein 180 | kakucs et al drotaverinum – prevention and treatment in cerebral vasospasm figure 2 the vascular clip on the femoral artery figure 3 we can observe the experimental vasospasm obtained on femoral artery that appeared after clipping and irrigate the artery with adrenaline figure 4 the dilated artery after the irrigation with drotaverinum figure 5 measurement of the femoral artery after clipping and irrigation with adrenaline romanian neurosurgery (2016) xxx 2: 177-183 | 181 figure 6 measurement of the femoral artery after irrigation with drotaverinum graph no.1 the diameter of the vessel is depicted before and after the irrigation of the arteries with drotaverinum figure 7 data platted for group a and b. error bars drown at the 95% confidence interval. red points representing the means results after the dissections and the measurements that were performed on the femoral arteries we analyzed all the data using medcalc soft. the first statistical tests was applied to see if there is a significant difference between group a were was used the drotaverinum and the group b were was not administrated the drotaverinum. after the statistical analysis we obtained a significant difference between the 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 ratio post inainte toate nospa ratio post inainte toate martor 182 | kakucs et al drotaverinum – prevention and treatment in cerebral vasospasm two groups with p<0,0001 and that suggest the benefits of the irrigation with drotaverinum when vasospasm is occurred. in graph no.1 the diameter of the vessel is depicted before and after the irrigation of the arteries with drotaverinum. the mean of the vessels before irrigation with drotaverinum was 37,66 and after the administration of drotaverinum the mean was 56,97. the statistical analysis depicted a significant difference between the two means (p<0,05). statistical tests in the group b were applied before and after the irrigation with saline solution. the mean before irrigation was 45,44 and after irrigation with saline solution the mean was 44,23. in this group we observe the saline solution has no effect on the vessels. between the two groups there was no differences in the diameter of the vessels before the irrigation with drotaverinum or with the saline solution and the standard deviation was 7,83±1,75. after the irrigation with drotaverinum in the group a and the irrigation with saline solution the group b the mean of the vessels diameter in the first group was 52,02 and in the group b the mean was 44,23. the statistical analysis depicted a significant difference between the two means (p<0,001). all the data were analyzed and we obtained a statistically significant difference between the two groups after the irrigation with drotaverinum (p<0,001) with a standard deviation 13,76±3,07. in figure 7 we can see the data platted for group a and b. the red points represent the means. p<0.001. discussion cerebral vasospasm is a difficult pathological entity to treat or to deal with it and also in the literature are a lot of studies and trials about the controversies concerning the prevention and the treatment of the cerebral vasospasm that can occur after subarachnoidian hemorrhage (10-13). cerebral vasospasm after subarahnoidian hemorrhage produced by ruptured aneurysms remains still a very controversial topic (14). cerebral vasospasm represent the leading cause of mortality and morbidity in subarachnoidian hemorrhage and can lead to delayed cerebral ischemia (1, 2). in the treatment of cerebral vasospasm the only medication that was proven to reduce delayed cerebral ischemia is the nimodinipine (1, 15-17). about 30% of patients who suffered nontraumatic subarachnoidian hemorrhage develop cerebral vasospasm and secondary to this they develop ischemia (10). cerebral vasospasm occur often in the third day after the hemorrhage and in the day 5 to 7 riches the maximum (11). in the treatment of cerebral vasospasm are included the triple h therapy (hypertension, hypervolemia, hemodilution), balloon angioplasty, intra-arterial vasodilatators, administration of substances like statins, endothelina-1 antagonists and magnesium sulfate (2, 5, 11). conclusions our study demonstrate the importance of using the drotaverinum after the vasospasm occurrence and is very important to perform romanian neurosurgery (2016) xxx 2: 177-183 | 183 irrigation with drotaverinum on the cerebral arteries after clipping the aneurysm because this will prevent the occurrence of vasospasm or will treat it if occurred. drotaverinum has no complication if we use it to irrigate the cerebral arteries and the vasodilatation that appears after using drotaverinum is useful because is achieved a better blood circulation in the area and prevent the ischemia occurrence. in our opinion after the aneurysm is clipped the irrigation of the vessels, surrounding the aneurysm, with drotaverinum can decrease the incidence of vasospasm. also if, intraoperative, we find a visible vasospasm the irrigation of the arteries with drotaverinum will help the vessel to dilate and to return to optimal caliber for the blood flow. references 1.keyrouz sg, diringer mn. clinical review: prevention and therapy of vasospasm in subarachnoid hemorrhage. critical care. 2007;11(4):220. 2.athar mk, levine jm. treatment options for cerebral vasospasm in aneurysmal subarachnoid hemorrhage. neurotherapeutics: the journal of the american society for experimental neurotherapeutics. 2012;9(1):37-43. 3.ladner tr, zuckerman sl, mocco j. genetics of cerebral vasospasm. neurology research international. 2013;2013:291895. 4.odom mj, zuckerman sl, mocco j. the role of magnesium in the management of cerebral vasospasm. neurology research international. 2013;2013:943914. 5.diringer mn. management of aneurysmal subarachnoid hemorrhage. critical care medicine. 2009;37(2):432-40. 6.kistka h, dewan mc, mocco j. evidence-based cerebral vasospasm surveillance. neurology research international. 2013;2013:256713. 7.kim jh, yi hj, ko y, kim ys, kim dw, kim jm. effectiveness of papaverine cisternal irrigation for cerebral vasospasm after aneurysmal subarachnoid hemorrhage and measurement of biomarkers. neurological sciences: official journal of the italian neurological society and of the italian society of clinical neurophysiology. 2014;35(5):715-22. 8.jabbarli r, glasker s, weber j, taschner c, olschewski m, van velthoven v. predictors of severity of cerebral vasospasm caused by aneurysmal subarachnoid hemorrhage. journal of stroke and cerebrovascular diseases: the official journal of national stroke association. 2013;22(8):1332-9. 9.kerz t, boor s, beyer c, welschehold s, schuessler a, oertel j. effect of intraarterial papaverine or nimodipine on vessel diameter in patients with cerebral vasospasm after subarachnoid hemorrhage. british journal of neurosurgery. 2012;26(4):517-24. 10.lee y, zuckerman sl, mocco j. current controversies in the prediction, diagnosis, and management of cerebral vasospasm: where do we stand? neurology research international. 2013;2013:373458. 11.siasios i, kapsalaki ez, fountas kn. cerebral vasospasm pharmacological treatment: an update. neurology research international. 2013;2013:571328. 12.reddy d, fallah a, petropoulos ja, farrokhyar f, macdonald rl, jichici d. prophylactic magnesium sulfate for aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. neurocritical care. 2014;21(2):356-64. 13.cossu g, messerer m, oddo m, daniel rt. to look beyond vasospasm in aneurysmal subarachnoid haemorrhage. biomed research international. 2014;2014:628597. 14.aydin he, ozbek z, aydin n, bolluk o, vural m, arslantas a, et al. application of lumbar drainage in vasospasm after spontaneous subarachnoid hemorrhage and prevention of late cerebral infarction. acta neurochirurgica supplement. 2015;120:255-8. 15.macdonald rl, diringer mn, citerio g. understanding the disease: aneurysmal subarachnoid hemorrhage. intensive care medicine. 2014;40(12):1940-3. 16.raya ak, diringer mn. treatment of subarachnoid hemorrhage. critical care clinics. 2014;30(4):719-33. 17.heffren j, mcintosh am, reiter pd. nimodipine for the prevention of cerebral vasospasm after subarachnoid hemorrhage in 12 children. pediatric neurology. 2015;52(3):356-60. 10_paper romanian neurosurgery (2015) xxix 4: 465 475 465 doi: 10.1515/romneu-2015-0062 evaluation of the clinical efficiency of transforaminal epidural steroid injection in the treatment of sciatica zafer gündoğdu1, i̇brahim burak atcı2, serdal albayrak2, hakan yılmaz3, aykut urfalıoğlu4 1elazig education and research hospital, department of anesthesiology and pain medicine, elazig, turkey 2elazig education and research hospital, department of neurosurgery, elazig, turkey 3duzce state hospital, department of neurosurgery, duzce, turkey 4kahramanmaras sutcu imam university, department of anesthesiology and pain medicine, kahramanmaras, turkey abstract: objective: evaluation of clinical efficiancy of fluoroscopy-accompanied transforaminal epidural steroid injection in patients with symptomatic lumbar foraminal intervertebral disc herniation and foraminal stenosis. methods: fifty patients, who underwent fluoroscopic-guided epidural steroid injection between 19.12.2013 28.02.2014, were evaluated retrospectively. pain levels of patients before the procedure, after 3 weeks and after 6 months were compared using visuel analog scale (vas). fifty percent or more decrease, less than 50% decrease and no change in vas were evaluated as sufficient response, insufficient response and unresponsiveness, respectively. the patients were asked whether they would undergo this process again and “yes”, “maybe” and “no” answers were evaluated for patient satisfaction score. results: in 50 patients (32 female, 18 male), average pain levels were found to be 8.4 (vas 7-9), 4.3 (vas 1-9) and 4.4 (vas 0-9) before the procedure, 3 weeks after the procedure and 6 months after the procedure, respectively. while thirty-seven (74%) of the patients were found to have sufficient response to treatment 3 weeks after the procedure, 10 (20%) patients were found to have insufficient response. there was no response to treatment in 3 (6%) patients. while thirty-five (70%) of the patients were found to have sufficient response to treatment 6 months after the procedure, 10 (20%) patients were found to have insufficient response. six months after the procedure, there was no response to treatment in 5 patients (%10). statistically significant improvement was observed when the pre and post-procedure vas scores were compared. forty (80%) patients gave the answer “yes” to the question whether they would undergo this procedure again. conclusion: we found that fluoroscopic guided transforaminal epidural steroid injection is effective in pain relief in patients with lumbar foraminal intervertebral disc herniation and foraminal 466 gündoğdu et al transforaminal epidural steroid injection in the treatment of sciatica stenosis that are resistant to pharmacological and physical therapy and have no absolute indication for surgery. key words: epidural steroid injection, lumbar disc herniation, transforaminal epidural steroid introduction nowadays, lumbar pain accompanied by radicular symptomsis one of the most serious medical and socio-economic problems. lumbar intervertebral disc herniation and spinal stenosis are two leading frequent reasons of this condition, which causes serious limitations in the social life. lumbar pain is a health problem that is experienced by 80% of the individuals in the society at least once during their lives [1,12]. most of the patients have acute pain and their pains are mostly relieved by rest and medical treatment. in approximately 10% of the cases, the pain lasts more than 4-6 weeks and becomes chronic. lumbosacral radiculopathy improves mostly with conservative treatment procedures (life style change, bed rest, exercise, antiinflammatory drugs, muscle relaxants and opioids). transforaminal epidural steroid injection is a frequently used, low-risk treatment option that is used in patients with no response to aforementioned treatment options and no surgical indication [1, 7, 12, 14]. in this retrospective study, we aimed to present the effectiveness of transforaminal epidural steroid injection (tfesi) under carm fluoroscopy guidance in patients with complaints of lumbar and leg pain that were due to lumbar foraminal intervertebral disc herniation and spinal foraminal stenosis and were unresponsive to conservative treatment options. material and method this study was performed by retrospectively investigating the records of the tfesi procedures that were implemented in the operation room through the guidance of c-arm fluoroscopy to patients, who applied to the algology clinic due to radiculopathy and lumbalgia related to lumbar foraminal intervertebral disc herniation and spinal foraminal stenosis and whose complaints did not reveal with conservative treatment and who did not have an indication for surgery. the data of the study were obtained from the file data of 50 patients, who had undergone tfesi treatment for a period of 3 months, covering the dates 19.12.2013-28.02.2014. the patients were within the age range of 28-79 years old. local ethics committee approval was obtained. all of the patients were informed verbally and in written about the procedure and their approvals were obtained. the degree of epidural injection was determined following physical examination findings and the magnetic resonance imaging (mri) or computed tomography (ct) images of the patients. in 50 patients, transforaminal epidural injection was performed between lumbar 3–sacral 1 vertebrae, starting from the level at which lumbar foraminal intervertebral disc herniation or spinal foraminal stenosis was observed. the age, gender, occupation, severity of the pain and radiological findings of romanian neurosurgery (2015) xxix 4: 465 475 467 doi: 10.1515/romneu-2015-0062 the patients were evaluated. the visual analog scale (vas) was used for scoring the pain between 0-10. the vas scores of patients were recorded before the intervention, 3 weeks after the intervention and 6 months after the intervention. fifty percent or more decrease, less than 50% decrease and no change in vas were evaluated as sufficient response, insufficient response and unresponsiveness, respectively. the patients were asked whether they would undergo this process again and “yes”, “maybe” and “no” answers were evaluated for patient satisfaction score. patients with spinal instability, local or generalized infection, bleeding diathesis, psychological problems and who did not consent were excluded. all the patients had no history of previous lumbar surgery. chisquare test was used for statistical analysis of the data. tfesi implementation electrocardiography, pulse oximeter and arterial blood pressure monitoring following peripheral vascular access and isotonic sodium chloride infusion were performed. the patients were prone positioned in the operating room and a pillow was placed under the abdomen for flattening the lumbar curvature. two lt/min. oxygen, 2-3 mg midazolam and 50 microgram fentanyl were administered and sedoanalgesia was provided in order to decrease the anxiety and pain of the patients. the lumbar region was cleaned according to the rules of asepsis – antisepsis and was covered with sterile drapes. a 1mg/kg dose of lidocaine was applied as a local anesthetic into subcutaneous and deep tissues. the nerve stimulator needle was advanced 1015 cm to the implementation level through the guidance of c arm fluoroscopy after the local anesthesia. target vertebral foramen level was reached with 1.0-milliampere (ma) stimulator via safe triangle method (subpedicular approach). in the subpedicular approach, the agents are injected at the exit zone as the distal site of the nerve root. in this approach, gauge spine needle is progressed toward the subjacent pedicle and inferolateral to the pars interarticularis (safe triangle) for the superior intervertebral foramen. when the tip of the needle reached the inferolateral border, the carm was rotated for lateral view; and the needle was gradually advanced towards the anterior and superior aspects of the intervertebral foramen. the current was then decreased to 0.3 ma when muscle contraction was seen. then the needle was retracted 1 mm and its position was verified by visualizing the spread of the contrast agent (iohexol 14 mg/ml) to the nerve root and the anterior epidural area (figure 1, figure 2). in case of a vascular leakage, the needle was retracted and positioned again. afterwards, a 2-5 cc mixture of 80 mg triamcinolone, 40 mg lidocaine and 2 ml saline was injected to the foramen. after the procedure, the patients were monitored in the algology clinic service for 3-4 hours for probable complications. a bed rest of approximately one week and a salt-free diet were recommended to the patients. the patients were discharged after being asked for a three-week and six-month follow-up controls. 468 gündoğdu et al transforaminal epidural steroid injection in the treatment of sciatica figure 1 advancing the peripheral nerve stimulator needle to the l4-l5 level through the guidance of c arm fluoroscopy for right foraminal stenosis figure 2 visualizing the spread of the contrast agent to the s1 nerve root and the anterior epidural area results the patients had diagnoses of lumbar intervertebral disc herniation and spinal stenosis. the mean age of the patients was 51.36 years, ranging between 28 and 79. there were 32 female and 18 male patients, with a f/m ratio of 1.76. the mean age of female patients was 51 years and the mean duration of complaint was 37 months. the mean age of male patients was 52 years and the mean duration of complaint was 36 months. all female patients (96.9%), except 1 (3.1%), were housewives. of the male patients, 8 (44.4%) were workers and the remaining (55.6%) was retired or was not working. a total of 60 transforaminal epidural steroid injections were performed. injections were made between l3s1 vertebrae. forty patients had single level injection, whereas 10 patients had multiple level injections during the same session. the patients who underwent multiple level injections were the ones with lumbar intervertebral disc herniation and spinal stenosis at more than one level. all the patients had lumbar mri or ct scans before the procedure. of all 50 patients, levels of foraminal intervertebral disc herniation and foraminal stenosis were as follows; 7 at l3 – 4 levels, 18 at l4 – 5 levels, 15 at l5 s1 levels, 5 at l4 – 5 + l5 s1 levels, 3 at l3 – 4 + l4 – 5 levels and 2 at l3 – 4 + l5 s1 levels. the procedure levels were l4 – 5 for 26 (43.3%) patients, l5 s1 for 22 (36.6%) patients and l3 – 4 for 12 (20%) patients (table 1). the levels of pain of the patients were measured before, 3 weeks and 6 months after the procedure and were compared using visual analog scale (vas). the mean pain score of patients was found to be 8.4 (vas range 7-9) before the injection, 4.3 (vas range 1-9) 3 weeks after the injection and 4.4 (vas range 09) 6 months after the injection (graph 1). fifty percent or more decrease, less than 50% romanian neurosurgery (2015) xxix 4: 465 475 469 doi: 10.1515/romneu-2015-0062 decrease and no change in vas were evaluated as sufficient response, insufficient response and unresponsiveness, respectively. while thirty-seven (74%) of the patients were found to have sufficient response to treatment 3 weeks after the procedure, 10 (20%) patients were found to have insufficient response. there was no response to treatment in 3 (6%) patients (graph 2). while thirty-five (70%) of the patients were found to have sufficient response to treatment 6 months after the procedure, 10 (20%) patients were found to have insufficient response. six months after the procedure, there was no response to treatment in 5 patients (%10) (graph 3). statistically significant improvement was observed when pre and post-procedure (3week and 6-month) vas scores were compared (p<0.05). when post-procedure 3week and 6-month vas scores were compared, even though there was an increase in vas scores, the difference between these values was considered as statistically insignificant (p> 0.05). table 1 the levels of transforaminal epidural steroid injection injection levels the number of patients l4-5 26 l5-s1 22 l3-4 12 table 2 the vas scores of patients before, 3 weeks and 6 months after the intervention patient number vasbefore intervention vas3 weeks after intervention vas6 months after intervention 1 9 2 0 2 8 8 8 3 9 9 9 4 8 3 4 5 9 4 5 6 8 7 8 7 9 2 8 8 9 8 3 9 8 1 3 10 9 2 2 11 7 1 3 12 8 3 2 13 9 3 3 14 8 3 3 15 9 3 4 16 7 3 3 470 gündoğdu et al transforaminal epidural steroid injection in the treatment of sciatica 17 8 4 4 18 9 4 4 19 8 4 4 20 9 4 3 21 8 4 4 22 7 3 5 23 9 8 8 24 8 6 4 25 9 6 4 26 8 4 4 27 8 3 3 28 8 6 1 29 8 3 3 30 9 4 4 31 8 3 4 32 9 3 4 33 9 4 4 34 8 4 4 35 9 4 6 36 8 4 1 37 8 4 4 38 9 4 8 39 8 4 4 40 9 7 4 41 8 4 4 42 9 6 7 43 9 7 2 44 9 3 3 45 9 4 8 46 8 4 4 47 9 4 7 48 8 8 8 49 8 7 8 50 9 4 7 romanian neurosurgery (2015) xxix 4: 465 475 471 doi: 10.1515/romneu-2015-0062 graph 1 mean pain scores of patients before the injection, 3 weeks after the injection and 6 months after the injection graph 2 the response to epidural steroid injection at 3 weeks 0.00 1.00 2.00 3.00 4.00 5.00 6.00 7.00 8.00 9.00 vas(0-10) before the intervention 3 weeks after intervention 6 months after intervention sufficient 74% insufficient 20% unresponsiveness 6% the response to epidural steroid injection at 3 weeks 472 gündoğdu et al transforaminal epidural steroid injection in the treatment of sciatica graph 3 the response to epidural steroid injection at 6 months the patients were asked whether they would undergo this process again and “yes”, “maybe” and “no” answers were evaluated for patient satisfaction score. forty patients (80%) gave the answer ‘‘yes’’ to the question, 5 (10%) patients gave the answer ‘‘no’’ and 5 (10%) patients gave the answer ‘‘maybe’’. in 4 of 10 patients with insufficient response at the end of 6 months and in 3 of 5 patients with no response to treatment at the end of 6 months, control mri revealed indication for surgery, so surgery was planned for those patients. technical success was achieved in all of the injections evaluated in the study and no complication such as dural puncture, epidural hematoma and intra-arterial injection was seen. discussion in the treatment of lumbar disc herniation and spinal stenosis, epidural steroid injection is an alternative treatment method that is implemented increasingly [4, 6]. the effectiveness of the corticosteroids in the treatment of pain is by decreasing the inflammation, which is related to mechanical compression, ischemia and chemical irritation of the nerve root. the corticosteroids damages pla2 cascade and decrease formation of arachidonic acid metabolites, prostaglandins and leukotrienes that ease pain formation [6]. these inflammatory mediators cause intraneural edema and venous congestion. since the corticosteroids directly affect the mesodermal elements, the arachnoid tissue and the fibrous tissue, local injection is more effective than the systemic injection. because sufficient 70% insufficient 20% unresponsiveness 10% the response to epidural steroid injection at 6 months romanian neurosurgery (2015) xxix 4: 465 475 473 doi: 10.1515/romneu-2015-0062 the corticosteroids have the membrane stabilization effect on the nerve, they may obstruct the ectopic discharge. the corticosteroids slow down the conduction in the c fibers. besides, they also have local anesthetic effects. the epidural steroid injection can be performed through caudal, interlaminar and transforaminal routes [4, 6]. in fact, the history of transforaminal epidural block is not new. in 1952, robecchi and capra implemented s1 sacral transforaminal steroid injection for lumbar pain. lievre implemented sacral transforaminal injection in 1953 as well. in 1971, macnab has published the diagnostic value of selective nerve infiltration in radiculopathy in usa. lumbar transforaminal injection has been commonly implemented since that time [1, 3]. it is thought that the radicular symptoms are caused by mechanical irritation of the nerve root by the disc material rather than a mechanical pressure to the nerve root. regarding this, the local implementation of corticosteroids to compressed and inflamed nerve root seems to be the most appropriate method for the treatment of radiculopathy [8]. the aim of the lumbar transforaminal epidural block is to directly reach to the nerve root. it is believed that the selective effectiveness of the drug is increased by applying steroid in high concentration to the region of the pain. contrary to the traditional methods, a much higher tissue concentration is provided with much lesser steroid with the transforaminal approach. however, there are some disadvantages such as intravascular injection, intraneural injection and nerve injury [10, 13, 15]. in our study, we applied a mixture of 3-5 cc mixture of 80 mg triamcinolone, 40 mg lidocaine and 2 ml saline to the target area. the lumbar transforaminal epidural bloc must certainly be implemented under the guidance of fluoroscopy. this fact provides the safety of the transforaminal epidural steroid injection. even though the lumbar transforaminal epidural steroid injection seems to be easily implemented, the anatomical properties of the region should be well known for a successful implementation and the operation should be done by following the rules [1, 12]. in the study by rosenberg et al., it was determined that the lumbar pain is seen mostly around the age of 60 and more in women than in men [11]. similarly, the mean age of female patients was 51 and the mean age of male patients was 52 in our study, and female/male ratio was 1.77. in a study by bottwin et al., the most affected levels were l5-s1, l4-5 and l34, respectively. in our study, mostly involved levels were as follows; l4-5, l5-s1 and l3-4 [5]. manchikanti et al., compared three methods of epidural steroid injection in patients having lumbar pain [9]. in this retrospective study on 225 people, even though it was demonstrated that all of the three methods are effective in providing pain control, they obtained more effective results for a longer period in caudal and transforaminal routes. in a study by joon woo lee at al., fluoroscopy-guided transforaminal injection was applied to 248 patients, who were diagnosed having single level nerve root 474 gündoğdu et al transforaminal epidural steroid injection in the treatment of sciatica pressure related to lumbar disc herniation or spinal stenosis [8]. the pain levels before the injection and 2 week after the injection were compared. a decrease of 50% or more in the pain score was considered as a successful response and a successful response was achieved in 76.8% of the patients. in a study by abdulkadir et al., 37 patients were examined retrospectively and the vas scores of the patients at the 3rd week and at the 6th month were evaluated [2]. of the patients, 84.6% were found to have successful response at the 3rd week and 78% were found to have successful response at the 6th month. in our study, a sufficient response was obtained in 37 patients (74%) and an insufficient response was obtained in 10 patients (20%) at the 3rd week. no response was seen in 3 (6%) patients. while 35 (70%) patients had a sufficient response, 10 patients (20%) had insufficient response at 6th month after the injection. no response was seen in 5 (10%) patients at 6th month after the injection. in a study by vad et al., 48 patients from two separate treatment groups were monitored during 16 months [15]. the success rate was found to be 84% in the transforaminal anterior epidural steroid injection group, whereas it was 48% in the placebo group. in a study by botwin et al., on patients who underwent fluoroscopy-guided transforaminal anterior epidural steroid injection, they found that there was at least a 50% decrease in vas scores of 75% of the patients during a 6-week follow up period [5]. conclusion in this study, we aimed to present the effectiveness of fluoroscopy-guided transforaminal epidural steroid injection (tfesi) in patients with symptomatic lumbar foraminal intervertebral disc herniation and foraminal stenosis. we found that fluoroscopic guided transforaminal epidural steroid injection is effective in pain relief in patients with lumbar foraminal intervertebral disc herniation and foraminal stenosis that are resistant to pharmacological and physical therapy and have no absolute indication for surgery. competing interests the authors declare that they have no competing interests. correspondence hakan yilmaz department of neurosurgery, duzce state hospital, duzce, turkey. phone: 0506 621 18 29 e-mail: dr_hakanyilmaz@hotmail.com references 1. abdi s, datta s, trescot am, schultz dm, adlaka r, atluri sl, et al. epidural steroids in the management of chronic spinal pain: a systematic review. pain physician 2007; 10:185-212. 2. abdulkadir a, suleyman d, oguz k, mehmet o, tarik p, ercan k. assessment of the effectiveness of lumbar transforaminal epidural steroid injection for low back pain. agri 2011; 23(3):114-118. 3. bosscher ha, gitlin mg, kaye ad. epidural steroids. in: raj pp, editor. textbook of regional anesthesia. philadelphia: churchill livingstone; 2002.p.687-702. 4. boswell mv, hansen hc, trescot am, hirsch ja. epidural steroids in the management of chronic spinal pain and radiculopathy. pain physician 2003; 6(3):319-34. romanian neurosurgery (2015) xxix 4: 465 475 475 doi: 10.1515/romneu-2015-0062 5. botwin kp, gruber rd, bouchias cg, torres-romas fm, sanelli jt, freeman ed, et al. fluoroscopically guided lumbar transforaminal epidural steroid injections in degenerative lumbar stenosis: an outcome study. am j phys med rehabil 2002; 81:898-905. 6. buenaventura rm, datta s, abdi s, smith hs. systematic review of therapeutic lumbar transforaminal epidural steroid injections. pain physician 2009; 12:23351. 7. karaeminogullari o, aydinli u. degenerative lomber spinal stenosis. journal of turkish association of orthopaedics and traumatology 2004; 3:3-4. 8. lee jw, kim sh, lee is, choi ja. therapeutic effect and outcome predictors of sciatica treated using transforaminal epidural steroid injection. ajr 2006; 187:1427-31. 9. manchikanti l, pakanati rr, pampati v. comparison of three routes of epidural steroid injections in low back pain. pain digest 1999; 9:277-85. 10. manchikanti l. transforaminal lumbar epidural steroid injections. pain physician 2000; 3(4):374-98. 11. rosenberg sk, grabinsky a, kooser c, boswellmv. effectiveness of transforaminal epidural steroid injections low back pain: a one year experience. pain physician 2002; 5(3):266-70. 12. schaufele mk, hatch l, jones w. interlaminar versus transforaminal epidural injections for the treatment of symtomatic lumbar intervertabral disc herniations. pain physician 2006; 9:361-366. 13. smuck m, fuller bj, yoder b, huerta j. incidence of simultaneous epidural and vascular injection during lumbosacral transforaminal epidural injections. spine j 2007; 7(1):79-82. 14. suslu h, atar e, arslan g, alatli i, altun m, abraz s. efficiency of the transforaminal epidural steroid treatment in chronic low back pain. the journal of kartal training and research hospital 2008; 19(2): 67-72. 15. vad vb, bhat al, lutz ge, cammisa f. transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. spine 2002; 27:11-16. 4ienceana_cerebrospinalfluid 274 iencean et al cerebrospinal fluid phosphorylated neurofilament subunit nf-h cerebrospinal fluid phosphorylated neurofislament subunit nf-h (pnf-h) is specific predictive biomarker in spinal cord injury a.şt. iencean1,2, didona ungureanu3, al. tascu4, şt.m. iencean3 1ph student “grigore t. popa” university of medicine and pharmacy iasi 2neurosurgery, emergency hospital “prof. dr. n. oblu” iasi 3“grigore t. popa” university of medicine and pharmacy iasi 4“carol davila” university of medicine and pharmacy bucharest doi: 10.33962/roneuro-2022-011 acute phase of traumatic brain injury. overview of neuroimaging tools and significant findings maria paz bolaño-romero, gustavo gaitan-herrera, daniel galarza-garrido, diana carolina caicedo-posso, n. carolina ordóñez-veloza, cristian javier guerrero -eraso, jesús david hidalgo-pasaje, jesús david castillo-martínez, sebastian pinzon-vargas, michael gregorio ortega-sierra romanian neurosurgery (2022) xxxvi (1): pp. 62-69 doi: 10.33962/roneuro-2022-011 www.journals.lapub.co.uk/index.php/roneurosurgery acute phase of traumatic brain injury. overview of neuroimaging tools and significant findings maria paz bolaño-romero1,2, gustavo gaitan-herrera2, daniel galarza-garrido2, diana carolina caicedo-posso3, nathalia carolina ordóñez-veloza4, cristian javier guerrero-eraso5, jesús david hidalgopasaje6, jesús david castillo-martínez7, sebastian pinzon-vargas8, michael gregorio ortega-sierra2 1 grupo prometheus y biomedicina aplicada a las ciencias clínicas, school of medicine, universidad de cartagena, cartagena, colombia 2 medical and surgical research center, st mary’s medical group, cartagena, colombia 3 school of medicine, universidad icesi, cali, colombia 4 school of medicine, universidad de manizales, manizales, colombia 5 school of medicine, fundación universitaria san martín, bogotá, colombia 6 school of medicine, universidad de antioquia, medellín, colombia 7 school of medicine, universidad nacional, bogotá, colombia 8 school of medicine, universidad de santander, bucaramanga, colombia abstract in neurotrauma, diagnostic imaging plays a fundamental role in the early detection of treatable injuries or the mitigation of secondary injuries. currently, the routine imaging techniques used in the setting of a head trauma patient include non-contrast computed tomography (ct), computed tomography angiography (cta), conventional magnetic resonance imaging (mri) with t1, t2 or diffusion imaging. of the above mentioned, ct is superior to mri in terms of speed of examination, due to the greater access to portable equipment in the patient's environment, which reduces the risk of secondary complications at the time of transfer to the radiology department. nevertheless, mri provides a much higher quality of images than ct. mri is not indicated for the diagnosis of acute brain injury, but if the results of ct without contrast are normal, and neurological manifestations are present, it is indicated. as a result, ct should be the first study requested to the imaging service by the medical team in charge of the patient during the acute phase of the traumatic brain injury. the main objective of this review is to present some of the advantages and disadvantages offered by the different diagnostic imaging methods when approaching and managing brain-injured patients, with emphasis on the acute phase of trauma. keywords brain injuries, neurotrauma, cerebral haemorrhage, skull fractures, tomography, traumatic brain injury corresponding author: michael gregorio ortega-sierra medical and surgical research center, st mary’s medical group, cartagena, colombia mortegas2021@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 63 acute phase of traumatic brain injury introduction the improvements in the technology have provoked a modern advent of the image analysis to establish clinical variables at different scales, so that the interpretation of these can create a very powerful diagnostic approach [1]. diagnostic images play an important role in the detection of treatable lesions and prevention or mitigation of secondary injuries [2]. currently, imaging techniques routinely used in the context of neurotrauma include computed tomography (ct) without contrast, computed tomography angiography (cta) and conventional magnetic resonance imaging (mri) with t1, t2, susceptibility or weighting diffusion [3]. other studies exist but have minimal impact. neuroimaging may allow for better characterization of patients for both treatment decisions, and the improved selection for clinical trials [4]. despite its limitations, the glasgow coma scale (gcs) is a practical, reliable and objective method to assess the level of consciousness. patients are scored according to their best response in three categories (eye opening, verbal responses and motor score), and classified as mild, moderate and severe [5]. gcs is one of the most frequently used methods to identify patients that benefit from imaging studies [5]. in 2007 the traumatic head injury guide produced by nice, replaced the head plain x-ray as the primary imaging modality for traumatic brain injury (tbi) by computerized axial tomography, which at first caused an increase in the cost of attention to the destabilization of the system; therefore, with the intention of balancing clinical benefit with costs, as well as exposure to radiation, strict criteria have been established for its realization [6]. the following are the imaging investigations used for the management of patients with tbi, their indications and relevant findings. methods a bibliographic search was carried out in the databases pubmed and science direct and in the google scholar search engine using the following terms: brain injuries, neurotrauma, cerebral hemorrhage, skull fractures, tomography, traumatic brain injury. articles in english language were included, emphasizing the importance of neuroimaging for a correct approach to the patient with acute brain injury, through different studies where ct stands out as the main imaging method that allows to cover a wide range of pathologies that may go unnoticed or not be identified by other types of imaging during the acute phase. a total of 185 articles were identified, including original articles, subject reviews, systematic reviews, letters to the editor, case reports and case series. 43 articles were selected that matched the aim of the article. results plane x-rays plane x-ray (sr) of the head (skull) has no indication for the initial evaluation of the patient with traumatic brain injury. even tough skull fractures are associated to brain injuries, its sensitivity is quite low and, in many instances, increase the chances of diagnostic failure. thus, both the centers for disease control and prevention (cdc) and the practice guidelines of the american college of emergency physicians (acep) no longer recommend the use of plain head x-rays for acute traumatic injuries [3]. hitesh et al. studied the effectiveness of plain xrays for the identification of skull fractures and compared to ct scan, autopsies and sr and tac. the sr eluded skull fractures by 19% and ct by 11.9%. thus, the sr has no advantage and little benefit with respect to the ct, leads to the delay in the diagnosis of the injury and exposes the patient to unnecessary and harmful radiation [7]. computed tomography ct is the neuroimaging that is requested in the first instance in cases of tbi [8,9] (figures 1-2). it is superior to the mri in terms of the speed of the examination, due to the greater accessibility to portable equipment that can be located around the patient, reducing the risk of complications secondary to transfer to radiology services. in addition, most institutions have tomographic equipment and to a lesser extent have resonators, so the initial examination is the ct scan. however, the resolution quality of the images is lower than the data offered by the mri [8]. computed tomography provides important prognostic predictors of severe head injury in children too [10]. at present, the head fixation frame of most ct scanners has certain limitations. the width cannot be effectively adjusted and texture is hard, so the head cannot be effectively fixed. the patient's intentional and unintentional movements cause head movements. furthermore, the noise during ct operation also causes the test 64 maria paz bolaño-romero, gustavo gaitan-herrera, daniel galarza-garrido et al. subject to be agitated to a certain extent. once the head movement coefficient is too large, it will significantly affect the image data quality. this has forced medical workers to repeat ct scanning, which could expose patients to increased radiation doses and increase the workloads of medical and paramedical staff and machines, leading to increased costs and less efficient emergency service [11]. current organization-specific practice involves placing the patient for observation and obtaining a repeat ct scan within 24 hours of initial imaging. this requires increased utilization of health care resources with increasing costs and potentially an increase in hospital-related adverse events and may also place a burden on patients and their families. we hypothesize that the vast majority of patients with low-mechanism closed head trauma who receive direct oral anticoagulant without abnormal initial cephalic ct findings will not have a late intracranial rebleed and, in fact, will not benefit from a prolonged hospital stay or repeat imaging [12]. figure 1. a, b. computed tomography image showing skull fracture of the frontal bone indications: some guidelines state that simple ct should be performed in patients with moderate or severe trauma (gsc <13) due to the higher incidence of acute intracranial hemorrhage, however different studies have shown that from 16% to 21% of patients with gcs 13 to 15 have acute intracranial hemorrhage so the ct scan should be performed [13]. figure 2. computed tomography image showing skull fracture secondary to a firearm most relevant findings: skull fractures, hemorrhages, bruises, or cerebral edema, commonly determine the impact of the lesions on adjacent brain tissue (the mass effect, the compressed ventricle), as well as the extent and location of the injuries [6]. the main objective for the ct scan is to identify lesions can be treated by surgery, but also to monitor the patients to prevent or early identify the appearance of phenomena compatible with injuries secondary to trauma [3,7]. skull fractures ct linear fractures, such as those of the groove of the middle meningeal artery, may be associated with epidural hematoma while temporal bone fractures, due to the bone lesser stiffness and the intracranial venous sinuses. depressed skull fractures are defined by the concavity of the affected bone, and is associated with severe complications such as hemorrhages, seizures and neuroinfection [14]. when penetrating fractures are detected, the presence of factors related to a complex prognosis should be ruled out. basilar fractures may be missed by the ct scan, and should be suspected when facial bones fractures such as 65 acute phase of traumatic brain injury ethmoid, sphenoid, lamina cribrosa, occipital or petrous area of the temporal fractures are identified [15]. the detection of skull fracture on ct can be interpreted not only as an objective indicator of primary injury but also as a factor causing secondary damage, including the release of neuroinflammatory cytokines and coagulopathy [16]. while computed tomography plays an essential role in the management of these particular patients, there is currently no support in the literature to suggest rapid repeat imaging in this population. there are several risk factors that may be associated with worse outcomes in the setting of depressed skull fractures. these predictors include the gcs score at presentation, fracture site, and fracture type. fractures involving more than one area and those associated with other intracranial injuries have also been shown to worsen outcome and increase the need for surgical intervention [17]. intracerebral hemorrhage ct can also show us the existence or not of bruising. brain contusions are also detected by ct. the imaging characteristics are related to the time of establishment of the lesion and the presence or absence of bleeding. they are usually located in the frontal and temporal lobes [1,8]. acute intracranial hemorrhage appears on ct as a region of increased density owing to the linear relationship between attenuation and hematocrit, predominately owing to hemoglobin concentration [18]. with the widely used of the ct, clinicians and researchers are able to qualitatively and quantitatively describe the characteristics of a hemorrhage to guide interventions and treatments. among these characteristics, the volume of intracranial hemorrhage is an important diagnostic indicator of stroke severity, long-term functional outcome, and mortality [19]. extra axial hemorrhage the epidural hematoma classically is characterized by a biconvex morphology, with location outside the axial plane and hyperdensity in the images [1,8]. the majority of patients with acute subdural hematomas have concomitant parenchymal brain injuries. the acute subdural and epidural hematomas are adequately diagnosed with ct and almost never reach the mri room [20]. while the subdural hematomas have a semilunar appearance. traumatic subarachnoid hemorrhages are usually located in convex areas such as cisterns [8]. the subarachnoid hemorrhage (sah) occurs in the space between the arachnoid membrane and the pia. the most common cause of sah is trauma. in 85% of non-traumatic cases, sah is caused by ruptured aneurysms, while 10% fit the pattern of so-called non-aneurysmal perimesencephalic hemorrhage. the remaining 5% is due to various rare diseases, such as cocaine abuse [21]. sources of sah in trauma include tearing of pial vessels, extra-axial extension of a hemorrhagic contusion, and redistribution of intraventricular hemorrhage caused by damage to subependymal veins. often the highest concentration of sah occurs contralateral to the side of direct impact [22]. the quantitative evaluation of the data provided by the ct has not been widely studied, however, the implementation of computer-aided diagnosis technology in the measurement of injuries seems to be very promising. some studies have shown that the quantification of midline displacement from the day of injury and the volume of bleeding correlate significantly with morbidity and mortality in severe tbi [9]. other findings pathological findings in ct with poor prognosis [9]: ▪ herniation ▪ injury affecting several lobes ▪ intraventricular or subarachnoid hemorrhage ▪ injury that compromises the entire brain there is convincing evidence that tbi increases the incidence of stroke and some epidemiological evidence that stroke outcomes are worse in patients with a history of tbi. given the very large number of tbi that occur annually it is critically important that we determine why this population is at a greater risk for both more strokes and worse outcomes [23]. intraventricular hemorrhage on early ct independently predicts poorer shortand long-term outcome in tbi. these findings may help guide intervention, and prognosis when intraventricular hemorrhage (ivh) is present on acute ct imaging. evidence suggesting that ivh observed on ct may be a surrogate marker for white matter injury warrants further study with mri imaging [24]. 66 maria paz bolaño-romero, gustavo gaitan-herrera, daniel galarza-garrido et al. magnetic resonance imaging beyond ct and mri has proven particularly effective in identifying brain regions involved with tbi. in addition, diffusion imaging of white matter (wm) fiber pathways in blast-exposed military veterans who show no visible symptoms of injury sequelae has proven to be a useful diagnostic tool [25]. in complicated mild tbi, magnetic resonance is superior to computed tomography without contrast in diagnosing subarachnoid hemorrhages, contusions and axonal lesions. the sequences used for the tbi are t1, t2, t2-flair, t2-gre and image by diffusion [26]. recent contributions to the body of knowledge on tbi favor the view that multimodal neuroimaging using structural and functional magnetic resonance imaging (mri and fmri, respectively) as well as diffusion tensor imaging (dti) has excellent potential to identify new biomarkers and predictors of tbi outcome (27). mri is the study of choice to further characterize intracranial hemorrhage, offering greater sensitivity in the detection of hemorrhage during all stages of hematoma evolution as well as the ability to more accurately assess the temporal evolution of hemorrhage. mri also allows more specific investigation of the etiology of intracranial hemorrhage [18]. indications: mri is not indicated during the initial management of acute mild tbi. it is indicated when the results of the computed tomography without contrast are normal, and there is persistence of neurological manifestations [28]. mri can diagnose subcortical lesions that are missed by other imaging techniques [14]. main findings: diffuse axonal injury (dai) is present in a high proportion of patients with severe tbi. mri has a greater sensitivity/specificity than ct scan for identifying dai [1,21]. in a study by cicuendez et al. comparing conventional mr and the diagnosis of dai, found that the t2, flair, and t2-gre sequences provide the best visualization in more than 80% of the cases. in addition, with the flair sequence, the hemispheric dai was better evidenced at the subcortical level while the t2-gre distinguished hemorrhagic dai. therefore, they recommend carrying out mri in the subacute period of a severe tbi for the accurate diagnosis of dai, using the sequences t2, flair and gradient echo [29]. other radiological findings, such as a midline shift, epidural hemorrhage, subarachnoid hemorrhage, and the volume of the hematoma could be additional variables to account for in predicting dai prognosis [30]. mri allows the precise quantification, of the size of the lesions as well as, clinically useful prognostic information [28]. the disadvantages of magnetic resonance include prolonged time being a long test and the lower probability of diagnosing fractures [29]. for subacute to chronic tbi, magnetic resonance is the test of choice due to its high sensitivity for the detection of cerebral atrophy [28]. actually, the modified ultrafast mri protocol for brain imaging demonstrates clinically acceptable image quality in four out of five sequences and has high accuracy in diagnosing normal and clinically significant abnormalities when compared against the standard mri protocol for brain imaging. it could potentially benefit a select group of pediatric patients who require neuroimaging [31] routine clinical use of synthetic mri can be feasible for neuroimaging in daily practice because the overall image quality and conspicuity of anatomical details were acceptable. in addition, the two attending neuroradiologists had no significant challenge during radiologic assessment of all synthetic images. in previous clinical studies using synthetic mri, the synthetic images had a similar diagnostic utility with sufficient or better image quality when compared to conventional mri scans [32]. also, mri and ct brain imaging may be equally accurate for detecting acute brain hemorrhages in people with acute focal stroke symptoms. however, mri may be more accurate than ct imaging for detecting chronic brain hemorrhages [33]. functional neuroimaging: a variant deserving mention is proton mri spectroscopy, which evaluates metabolic and biochemical alterations in patients with tbi. the detection of different metabolites allows the diagnosis of anomalous neurometabolic profiles such as the reduction in the levels of n-acetylaspartate (naa), naa/choline and naa/creatinine. the metabolite reduction persists for weeks to months and is evident both in apparently healthy white matter tissue and in perilesional areas, even though conventional mri does not show such structural alterations. biochemical alterations due to neural structural 67 acute phase of traumatic brain injury deformation caused by tbi imbalances neurotransmitters release that can affect the cellular sodium–potassium (na+-k+) pump and results in distribution of membrane homeostasis [34]. the advantage of this imaging tool is to allow correlation with the functional outcome by 6 months after tbi [13]. recent meta-analysis showed that significant changes in the ratios naa / creatinine and choline / creatinine and in the absolute values of naa are associated with clinical outcome in tbi [35]. future perspectives progress in the advancement of strategies and models to improve sensitivity and specificity in the use of neuroimaging is one of the fields of radiology, neurology and neurosurgery studies with the greatest impact today [36-38]. the investment in robotic neurosurgery and the deepening of neurosurgical education during undergraduate, are objectives to be reinforced in lowand middleincome countries, in order to promote in-hospital care of patients with neurosurgical pathology and, in particular, patients with neurotrauma [39-41]. translational research in neurosurgery, through the search for biomarkers and gene expression (currently known as neurogenomics and neuroimaging genomics), can substantially improve the diagnosis, management and prognosis of this type of patients, by improving the diagnostic accuracy and management of intervention times [4143]. it is necessary to continue working from the global neurosurgery, to the approach of strategies that help the technological and academic development of neurosurgery in third world countries [37]. conclusion tc scan is the imaging test of choice for the early evaluation of tbi patients. the primary objective is to diagnose injuries amenable to surgery, and have been shown to reduce mortality. plane head x-rays are no longer indicated. for patients suspected of harboring vascular injuries, computed tomography angiography or magnetic resonance angiography are indicated. mri is used at a later phase of managing tbi patients and most often for the diagnosis of a diffuse axonal lesion and prognosis determination. references 1. su e, bell m. diffuse axonal injury. in: laskowitz d, grant g, editors. translational research in traumatic brain injury. boca raton (fl): crc press/taylor and francis group; 2016. chapter 3. available from: https://www.ncbi.nlm.nih.gov/books/nbk326722/ 2. chang wt, badjatia n. neurotrauma. emerg med clin north am. 2014; 32(4):889-905. 3. shin ss, bales jw, edward dixon c, hwang m. structural imaging of mild traumatic brain injury may not be enough: overview of functional and metabolic imaging of mild traumatic brain injury. brain imaging behav. 2017; 11(2):591-610. 4. newcombe v. neuroimaging of tbi, moving towards ‘big data’ and precision management. journal of the neurological sciences. 2019: 405:39-40. 5. murray gd, brennan pm, teasdale gm. simplifying the use of prognostic information in traumatic brain injury. part 2: graphical presentation of probabilities. j neurosurg. 2018; 128(6):1621-1634. 6. hodgkinson s, pollit v, sharpin c, lecky f; national institute for health and care excellence (nice) guideline development group. early management of head injury: summary of updated nice guidance. bmj. 2014; 348:g104. 7. chawla h, malhotra r, yadav rk, griwan ms, paliwal pk, aggarwal ad. diagnostic utility of conventional radiography in head injury. j clin diagn res. 2015; 9(6):tc13-5. 8. williamson c, morgan l, klein jp, care n. imaging in neurocritical care practice. 2017; 1(212):840–51. 9. pervez m, kitagawa rs, chang tr. definition of traumatic brain injury, neurosurgery, trauma orthopedics, neuroimaging, psychology, and psychiatry in mild traumatic brain injury. neuroimaging clin n am. 2018; 28(1):1–13. 10. ortega rodríguez j, costa clar jm, caritg bosch j, martín rodrigo jm, et al, severe head injury among children: computerised tomography evaluation and intracranial pressure monitoring as prognostic factors. medicina intensiva. 2001; 25(1):8-13. 11. wang h, dong l, xia b, li y, pei y, zhang j. letter to the editor regarding “what is the best timing of repeated ct scan in mild head trauma with an initially positive ct scan?”. world neurosurgery. 2020; 141:552. 12. mourad m, senay a, kharbutli b. the utility of a second head ct scan after a negative initial ct scan in head trauma patients on new direct oral anticoagulants (doacs). injury. 2021; 52(9):2571-2575. 13. cook nf. the glasgow coma scale: a european and global perspective on enhancing practice. critical care nursing clinics of north america. 2021; 33(1):89-99. 14. vespa pm. imaging and decision-making in neurocritical care. neurol clin. 2014; 32(1):211–24. 15. al-sarraj s. the pathology of traumatic brain injury (tbi): a practical approach. diagnostic histopathology. 2016; 22(9):318-326. 68 maria paz bolaño-romero, gustavo gaitan-herrera, daniel galarza-garrido et al. 16. fujiwara g, okada y, ishii w, iizuka r, murakami m, sakakibara t, et al. association of skull fracture with inhospital mortality in severe traumatic brain injury patients. am j emerg med. 2021; 46:78-83. 17. berg a, voigt b, kaul s. delayed evolving epidural hematoma in the setting of a depressed skull fracture: a case report and review of the literature. trauma case rep. 2019; 22:100193. 18. saad af, chaudhari r, fischbein nj, wintermark m. intracranial hemorrhage imaging. semin ultrasound ct mr. 2018; 39(5):441-456. 19. kuang z, deng x, yu l, wang h, li t, wang s. ψ-net: focusing on the border areas of intracerebral hemorrhage on ct images. comput methods programs biomed. 2020; 194:105546. 20. karantanas ah, komnos a, paterakis k, hadjigeorgiou g. differences between ct and mr imaging in acute closed head injuries. cmig extra: cases. 2005: 29(1):1-8. 21. vermeulen l, goethem av, van den hauwe l, beuls e, parizel pm, jacobs w. pseudo-subarachnoid hemorrhage: a tricky ct finding with serious medicolegal implications. forensic imaging. 2021; 24:200427. 22. hijaz ta, cento ea, walker mt. imaging of head trauma. radiologic clinics of north america. 2011; 49(1):81-103. 23. anderst j, carpenter s, frazier t, appavu b, noetzel m, beslow la, et al. subdural hemorrhage in a cohort with cerebral sinovenous thrombosis: application to abusive head trauma. child abuse negl. 2021; 117:105119. 24. atzema c, mower wr, hoffman jr, holmes jf, killian aj, wolfson ab, et al. prevalence and prognosis of traumatic intraventricular hemorrhage in patients with blunt head trauma. j trauma. 2006; 60(5):1010-7. 25. bhattrai a, irimia a, van horn jd. neuroimaging of traumatic brain injury in military personnel: an overview. j clin neurosci. 2019; 70:1-10. 26. enríquez o. imaging in trauma. rev médica clínica las condes. 2013; 24(1):68–77. 27. irimia a, wang b, aylward sr, prastawa mw, pace df, gerig g, et al. neuroimaging of structural pathology and connectomics in traumatic brain injury: toward personalized outcome prediction. neuroimage clin. 2012; 1(1):1-17. 28. wintermark m, sanelli pc, anzai y, tsiouris aj, whitlow ct. imaging evidence and recommendations for traumatic brain injury: conventional neuroimaging techniques. j am coll radiol. 2015; 12(2):e1–14. 29. lozada martinez id, ortega-sierra mg, zambrano-arenas mdp, páez-escallón n, perea-martinez dg, calderaarrautt ys, et al. essentials of cerebral fat embolism syndrome: a hidden enemy in trauma. roneuro. 2021; 35(3):316-20. 30. cicuendez m, castaño-león a, ramos a, hilario a, gómez pa, lagares a. magnetic resonance in traumatic brain injury: a comparative study of the different conventional magnetic resonance imaging sequences and their diagnostic value in diffuse axonal injury. neurocirugia. 2017; 28(6):266–75. 31. guarnizo a, chung hs, chakraborty s. subcallosal haemorrhage as a sign of diffuse axonal injury in patients with traumatic brain injury. clin radiol. 2021 ;76(3):237.e15-237.e21. 32. ahamed sh, lee kj, tang ph. role of a modified ultrafast mri brain protocol in clinical paediatric neuroimaging. clin radiol. 2020; 75(12):914-920. 33. ryu kh, baek hj, moon ji, choi bh, park se, ha jy, et al. initial clinical experience of synthetic mri as a routine neuroimaging protocol in daily practice: a single-center study. j neuroradiol. 2020; 47(2):151-160. 34. kidwell cs, chalela ja, saver jl, starkman s, hill md, demchuk am, et al. comparison of mri and ct for detection of acute intracerebral hemorrhage. jama. 2004; 292(15):1823-30. 35. rakib f, al-saad k, ahmed t, ullah e, barreto ge, md ashraf g, et al. biomolecular alterations in acute traumatic brain injury (tbi) using fourier transform infrared (ftir) imaging spectroscopy. spectrochim acta a mol biomol spectrosc. 2021; 248:119189. 36. brown m, baradaran h, christos pj, wright d, gupta a, tsiouris aj. magnetic resonance spectroscopy abnormalities in traumatic brain injury: a meta-analysis. j neuroradiol. 2018; 45(2):123–9. 37. acevedo-aguilar l, gaitán-herrera g, reina-rivero r, lozada-martínez id, bohorquez-caballero a, paézescallón n, et al. pulmonary injury as a predictor of cerebral hypoxia in traumatic brain injury: from physiology to physiopathology. j neurosurg sci. 2021 nov 11. 38. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. 39. ortega-sierra mg, durán-daza rm, carrera-patiño sa, rojas-nuñez ax, charry-caicedo ji, lozada-martínez id. neuroeducation and neurorehabilitation in the neurosurgical patient: programs to be developed in latin america and the caribbean. j neurosurg sci. 2021. 40. miranda-pacheco ja, de santis-tamara sa, parra-pinzón sl, gonzález-monterroza jj, lozada-martínez id. medical interest groups and work policies as emerging determinants of a successful career: a student perspective correspondence. int j surg. 2021; 92:106020. 41. ortega-sierra mg, prado-grajales v, martinez-imbett r, unás-perea k, lozada martinez id. research career in neurosurgery: a challenge for future neurosurgeons. j neurosurg sci. 2021 aug 3. 42. blanco-teherán c, quintana-pájaro l, narvaez-rojas a, martínez-pérez r, garcía-ballestas e, moscote salazar l, et al. evidence-based medicine in neurosurgery: why and how? j neurosurg sci. 2021 aug 3. 43. herrera-martinez mp, garcía-ballestas e, lozadamartinez i, torres-llinás d, moscote-salazar l. letter to the editor. creating the conditions for gender equality to 69 acute phase of traumatic brain injury end sexual harassment in neurosurgery. j neurosurg. 2021 feb 5:1-2. 44. lozada-martínez i, bolaño-romero m, moscote-salazar l, torres-llinas d. letter to the editor: 'medical education in times of covid-19: what's new in neurosurgery?'. world neurosurg. 2020; 143:603. 11alvismiranda_glycemia romanian neurosurgery (2014) xxi 3: 313 324 313 glycemia in spontaneous intracerebral hemorrhage: clinical implications hernando alvis-miranda1, gabriel alcala-cerra2, luis rafael moscote-salazar2 universidad cartagena, colombia 1cartagena de indias; 2neurosurgeon abstract spontaneous cerebral hemorrhage or intracranial hemorrhage accounts for 10-15% of all strokes. intracranial hemorrhage is much less common than ischemic stroke, but has higher mortality and morbidity, one of the leading causes of severe disability. various alterations, among these the endocrine were identified when an intracerebral hemorrhage, these stress-mediated mechanisms exacerbate secondary injury. deep knowledge of the injuries which are directly involved alterations of glucose, offers insight as cytotoxicity, neuronal death and metabolic dysregulations alter the prognosis of patients with spontaneous intracerebral hemorrhage. key words: intracranial hemorrhage, glycemia, stroke, neurosurgery introduction spontaneous intracerebral hemorrhage (sich) is a devastating and disabling disease (1, 2). is the second most common form of stroke, representing 10-30% of first-ever strokes (3). overall incidence sich worldwide is 24.6 per 100,000 person-years with approximately 40,000 to 67,000 cases per year in the united states (4-7), approximately half of this mortality occurs within the first 24 hours, highlighting the critical importance of early and effective treatment in eds (8). deleterious effect of metabolic derangements like hyperglycemia has been studied since claude bernard described the relationship between hyperglycemia and cerebral injury (9). the occurrence of hyperglycemia is a known phenomenon in various types of acute cerebral injury. when measured at arrival to ed, hyperglycemia is associated with worse outcome in both diabetic and nondiabetic patients (10-13). a high proportion of patients (about 60%) might develop hyperglycemia even in the absence of a previous history of diabetes after sich (14). increased blood glucose in the acute setting of sich is probably a response to stress and severity of sich (15) and can persist for up to 72 h after sich (14). declining glucose values after sich are associated with a decreased risk of hematoma expansion and poor outcome, suggesting that early glucose 314 alvis-miranda et al glycemia in spontaneous intracerebral hemorrhage control may improve outcomes (16). many studies have shown that increased serum glucose on admission is associated with larger haematoma size, expantion, perihematomal oedema, cell death, intraventricular extention (17), and increased risk of poor outcome (10, 11, 14, 18, 19), furthermore is a potent predictor of 30 day mortality in both diabetic and non-diabetic patients with sich as well as an independent predictor of early mortality and worse functional outcome in non-diabetic patients with sich (11, 19, 20). glucose and brain physiology (21-48) the brain is an expensive energy organ. brain function requires the 15% of the cardiac output, consumes 20% of the oxygen and the 25% of the total organism glucose; has a high tolerance to the temporal fuel deficit, because it only consumes approximately 33% of the available oxygen and a 10% of the total glucose. the cerebral blood flow (cbf) is the supply of energetic sources, in a mean of 50ml/100g/min, with a brain oxygen consumption of 50cm3/min, and a similar carbon dioxide production, with a respiratory quotient near to 1, indicating that carbohydrates are the main substrates for the brain oxidative metabolism (49). all the different cells types in the central nervous system (i.e., neurons, glia and vascular cells) show a different metabolic glucose consumption rate. virtually, the only metabolic fuel of the brain is glucose; under aerobic conditions this molecule undergoes glycolysis to adenosine triphosphate (atp) and pyruvate. pyruvate is converted to acetylcoa via the kreb’s cycle to generate atp and reducing equivalents, this is the aerobic way, renders 30 moles of atp; exists another way to convert glucose to atp, the anaerobic way, but it is inefficient, just renders 2 moles of atp through production of lactic acid. glucose entre to the brain through glut family of hexose transportes; astrocytes express glut1, glut2, and glut4, neurons express glut3, glut4, and glut8 (50). if neurons, preferentially access to glucose directly from the brain interstitial fluid or if the metabolism of glucose to lactate by astrocytes is a required step, is still in debate (51, 52). brain needs glucose, but also controls the glucose levels when integrating information from peripheral receptors (53). has been established that brain insulin plays a crucial role in the regulation of the metabolism, enhancing glucose uptake by astrocytes (54). studies using spect technology have suggested that glucose transport and metabolism in human brain are dependent of blood supply. has been demonstrated insulinmediated increases in mean global rate of brain glucose utilization, suggesting that insulin may play some role in the regulation of cerebral glucose, especially in the cortex (55). alterations of the insulin actions in the brain are involved in metabolic diseases. the mechanisms by which glucose sensitive neurons detect changes in glycemia and alter their firing pattern are still being investigated. in the glucose sensing process participate the same proteins that control glucose signaling in pancreatic beta-cells (56), i.e., the glut2, the enzyme glucokinase and the atp sensitive potassium channel. in the response to romanian neurosurgery (2014) xxi 3: 313 324 315 hypoglycemia participate the amp-activated protein kinase (57). when an injury impaired the oxidative phosphorylation, either lower arterial oxygen tension, mitochondrial dysfunction or brain lesions, the glycolysis is deviated to the anaerobic way, producing lactic acid and hydrogen ions, generating tissue acidosis and reactive species of oxygen, respectively. when this takes place, trigger deleterious effects in the neuronal cells, product of the activation of calcium entry to the cells, the release of cytotoxic free fatty acids and excitotoxic neurotransmitters like glutamate. although the intermediate metabolites of glucose breakdown, pyruvate and lactate, in some circumstances can sustain the energy demand of the neuronal activity, both lack the ability to cross the blood-brain barrier. in pathological states, also are used as metabolic substrates the ketonic bodies. brain glycogen is primarily located in the astrocytes (58). and its stores finishes in about 5 minutes, when needed. in an animal model of type 2 diabetes mellitus, glycogen metabolism has been demonstrated to be important for supporting glutamatergic and gabaergic homeostasis, maintaining a proper ratio between excitatory and inhibitory neurotransmitters (59). different animal and human studies evidence a significantly compromised altered glucose metabolism in the setting of traumatic brain injury, cerebral ischemia and hemorrhages. due to the mitochondrial membrane dysfunction during hypoxic and hyperglycemic insults, the cells in the perihemorrhagic area are unable to metabolise the excess of glucose, this happens specifically in intracerebral hemorrhage, and are the main phenomena to comprehend why hypo/hyperglycemia are so deleterious in the setting of an acute brain lesion. hyperglycemia and the sich the hyperglycemic state results from metabolic derangements in the glucose metabolism (60). in the acute phase of sich develops an unspecific, programmed and adaptive response to the stress that induce activation of the hypothalamic-hypophysisadrenal axis and the subsequent releasing of hyperglycemic hormones (61-64), activation of the autonomous nervous system and changes in the behavior, everything as a part of the well described metabolic–hormonal response to stress and to the systemic inflammatory response syndrome (sirs). in the context of a lesion, irrespective of the nature, the mechanism that drives to a stress hyperglycemia are the increased gluconeogenesis and insulin resistance, the later, may be result from impaired insulin receptor binding and signal transduction, increased hepatic glucose production, and decreased peripheral glucose uptake (65). the big final effect, a stress-induced hyperglycemic state, constitutes an aggravating factor of the lesion. also has been demonstrated an independent relationship between the kind and the severity of the neurologic injury (66, 67). the surgical procedures also contribute to activate a neuroendocrine response that predispose the patient to develop hyperglycemia and ketoacidosis because its antagonizing action on the insulin activity (60, 63). other well documented effects of stress-induced 316 alvis-miranda et al glycemia in spontaneous intracerebral hemorrhage hyperglycemia are the endothelial cell dysfunction, increased oxidative stress, cardiovascular effects and lesion in other specific brain areas (68-70). when the hyperglycemic state is stablished, it plays a range of deleterious mechanisms on the injured brain, through the increase of oxidative stress, inflammatory cytokines, induction of excitotoxicity [e.g., stimulation of the n-methyl-daspartate (nmda) receptor] potentiating the calcium entry to the cells, alters the brain metabolism and therefore the perfusion (71-73). due to the above, glucose neurotoxicity the excessive glucose concentration in the lesions microenvironment induces lipid peroxidation, protein carbonilation, and dna damage. as the superoxyde is been neutralizing the nitric oxide, the vasodilation is impaired (74, 75). as result of the productions of reactive species of oxygen (rso), then is activated an inflammatory response that leads to immune cells attraction, and then increasing the production of eros. lactic acid is also concentrated, so is an easy way to turn acidotic the neuron cells, this acidosis alters mitochondrial function (76, 77). in rat models of intracerebral hemorrhage (78-80) have been demonstrated the mentioned physiopathological events, and higher size of hemorrhage in the hyperglycemic rat groups. in a recent experiment was observed that in response to the intracerebral hemorrhage lesion, significant increase of albumin was ubiquitously observed in the brains of normoglycemic rats but not in the brains of hyperglycemic rats. in the last group, more significant neuronal apoptosis were found in the perihematomal regions of hyperglycemic rats, suggesting a protection role of albumin in acute stage of intracerebral hemorrhage, which may be dependent on different blood sugar levels (81). hypoglucemia and the schi defined as glucose plasma level <50mg/dl (<2.8mmol/l) with/without symptoms (49). currently, there is a paucity of data on cerebral glucose metabolism in human subjects with spontaneous intracerebral hemorrhage, but have been demonstrated that hypoglycemia, the other side of the coin, also worsens the outcome of patients with critical illness. in the acute injured brain, hypoglycemia could be particularly harmful. the “neurological injury glucose threshold” varies with some patient’s factors, i.e., history of diabetes mellitus, the speed of the glucose level drop, the duration of the hypoglycemia event and the cerebral blood flow, etc. in patients with poor-grade subarachnoid hemorrhage the acute reductions in serum glucose, even to levels within the normal range, could generate brain energy metabolic crisis and lactate/pyruvate ratio elevation (82). when the brain’s metabolism autoregulation is altered, there ares parts of them specially more susceptible than others (83-86), when could be thoughtful glucose level as “sufficient” in a patient whith acute brain lesion this might be insuffient and even deleterious. the brain’s compensation systems (release of conter-regulatory hormones, increase the cerebral blood flow, use of the glycogen storages) to the glycopenia are limited (87-89). the big problem with a romanian neurosurgery (2014) xxi 3: 313 324 317 hypoglycemia state is that is associated with aberrant depolarization in the perilesional tissue that drives to a perpetuating glucose depletion, as has been demonstrated in traumatic brain injury (32, 90) mortality and other outcomes as stated in other items of this review, the hyperglycemia measured in peripheral blood is both a marker of injury severity and of poor outcome, a relationship that has captured the attention of clinicians over the past few years. studies evaluating the association of glycemia derangements and sich are scarce (10, 14), in comparison with other types of stroke, where later researches utilize multimodal neuromonitoring with intracerebral microdialysis catheters, brain oxygen monitors and measurements of both, peripheral and cerebral blood glucose. kimura and colleagues with a prospective observational study design and 100 patients with acute supratentorial intracerebral hemorrhage, assessing clinical characteristics and plasma glucose. ich volume was measured on admission ct (b24 h) and follow-up ct (b48 h) scans. patients were divided into two groups: the death group, who died within 14 days of onset, and the survival group. using receiver operating characteristic (roc) curve, founded that cut-off values that predicted early death were 150 mg/dl for the glucose level and n20 ml for the initial ivh volume, they conclude that admission hyperglycemia may independently increase the risk of early death in acute spontaneous intracerebral hemorrhage (10). godoy and collegues in a prospective study with 250 patients with a well-defined diagnosis of sich admitted into 24 h in three primary referred centers. patients had extensive monitoring of bg values and those with bg values >8.29 mmol/l (150 mg/dl) received a variable intravenous insulin dose to maintain bg concentrations during the first 72 h after sich between 3.32 and8.29 mmol/l (60–150 mg/dl) using pre-specified insulin dosing schedule protocol, and using a cutoff value of >164mg/dl, they conclude that hyperglycemia is a common condition after sich that could worsen prognosis and the very early insulin therapy does not improve prognosis, also show an increased risk of poor outcomes and death. stress hyperglycaemia is a common finding in patients presenting with intracerebral haemorrhage. it is a marker of poor outcomes and higher mortality, more so in patients with no known history of diabetes (91). over the years ich has been reported to have a mortality rate between 35–52% and poor functional outcome of survivors, with only 10– 20% living independently at 30 days (92-96) literature has reported glasgow coma scale (gcs) on arrival, blood pressure on presentation, volume of hemorrhage, concomitant intraventricular hemorrhage, previous ischemic stroke, and national institutes of health stroke scale (nihss) score as predictors of early mortality in patients with ich (11). for evaluating glycaemia derangements in unspecific medical conditions but in critically ill patients a study look for evaluate the compared risk adjusted mortality when those patients were admitted to a surgical intensive care over 4 years. patients were divided into glycemic groups: hyper (≥1 episode > 180 318 alvis-miranda et al glycemia in spontaneous intracerebral hemorrhage mg/dl, any <60), hypo (≥1 episode < 60 mg/dl, any >180), both (≥1 episode < 60 and ≥1 episode > 180 mg/dl), normo (all episodes 60-180 mg/dl), hyper-only (≥1 episode > 180, none <60 mg/dl), and hypoonly (≥ episode < 60, none >180 mg/dl). the mortality ratios (o/e) were studied using the expected acute physiology and chronic health evaluation (apache) iii. number of adverse glycemic events was compared with mortality. hypoglycemia and hyperglycemia occurred in 18 per cent and 50 per cent of patients. mortality was 12.4 per cent (o/e = 0.88). both had the highest o/e ratio (1.43) with hypo the second highest (1.30). groups excluding hypoglycemia (normo and hyper-only) had the lowest o/e ratios: 0.56 and 0.88. increasing number of hypoglycemic events were associated with increasing o/e ratio: 0.69 o/e for no events, 1.19 for 1-3 events, 1.35 for 4-6 events, 1.9 for 7-9 events, and 3.13 for >/= 10 events. as result was observed that, ten or more hyperglycemic events were needed to significantly associate with worse mortality (o/e 1.53); and hyper/hypoglycemia increase mortality compared with apache iii expected mortality, with highest mortality risk if both are present. in this study hypoglycemia was associated with worse risk, so the authors recommend that glucose control may need to be loosened to prevent hypoglycemia and reduce glucose variability (97). in a study evaluating the prognosis and outcome of acute stroke in an universitary hospital in nigeria, founded that age above 39 years, male gender, systemic hypertension, early onset of coma after stroke, and presence of co-morbidities were associated with poor stroke outcome, the 78.8% of all stroke subtypes corresponded to intracerebral hemorrhage (98). the effects of parameters as elevation of white blood cell count (wbc), c-reactive protein (crp), and blood glucose (bg) concentration at presentation prognosticate poor outcome in sich patients were investigated for di napoli and colleagues conclude that higher wbc, crp, and bg are associated with increased mortality in sich patients, and also founded that only crp elevation portends higher risk of death independently of other indicators of sich severity (99). in the acute brain bleeding analysis study, a korean study for evaluate the effects of glucose level on early and long-term mortality after intracerebral haemorrhage was observed a long-term mortality rate of 21.1% after a mean follow-up of 434.3 +/223.2 days and was found to increase significantly with glucose quartile (p < 0.001). the admission glucose level was an independent risk factor for early mortality (adjusted hr 1.10 [95% ci 1.01-1.19]), but not for long-term mortality. moreover, when analysis was restricted to patients without diabetes, glucose level was found to be an independent risk factor for post-ich mortality (n = 1,119; adjusted hr 1.10 [95% ci 1.03-1.17]) and had marginal significance for early (p = 0.053) and longterm mortality (p = 0.09). from the above is conclusive that admission glucose levels are associated with early mortality after intracerebral hemorrhage. in patients without diabetes, admission glucose levels were romanian neurosurgery (2014) xxi 3: 313 324 319 associated with long-term mortality (19). kimura and colleagues have founded an association between hyperglycemia at admission to eds and an increased risk of early death (10). other worry about the assessment of mortality in sich is that in comparison with other cerebrovascular diseases, there are no grading prognostic scales routinely used in sich around the world. correspondence dr. luis rafael moscote-salazar, universidad de cartagena, cartagena de indias, colombia. e-mail: mineurocirujano@aol.com references 1.qureshi ai, tuhrim s, broderick jp, batjer hh, hondo h, hanley df. spontaneous intracerebral hemorrhage. the new england journal of medicine. 2001 may 10;344(19):1450-60. pubmed pmid: 11346811. epub 2001/05/11. eng. 2.flaherty ml, haverbusch m, sekar p, kissela b, kleindorfer d, moomaw cj, et al. long-term mortality after intracerebral hemorrhage. neurology. 2006 apr 25;66(8):1182-6. pubmed pmid: 16636234. epub 2006/04/26. eng. 3.balami js, buchan am. complications of intracerebral haemorrhage. the lancet neurology. 2012;11(1):101-18. 4.aguilar mi, freeman wd. spontaneous intracerebral hemorrhage. seminars in neurology. 2010 nov;30(5):55564. pubmed pmid: 21207348. epub 2011/01/06. eng. 5.broderick j, connolly s, feldmann e, hanley d, kase c, krieger d, et al. guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the american heart association/american stroke association stroke council, high blood pressure research council, and the quality of care and outcomes in research interdisciplinary working group. circulation. 2007 oct 16;116(16):e391-413. pubmed pmid: 17938297. epub 2007/10/17. eng. 6.broderick jp, brott t, tomsick t, miller r, huster g. intracerebral hemorrhage more than twice as common as subarachnoid hemorrhage. journal of neurosurgery. 1993 feb;78(2):188-91. pubmed pmid: 8421201. epub 1993/02/01. eng. 7.van asch cj, luitse mj, rinkel gj, van der tweel i, algra a, klijn cj. incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. lancet neurology. 2010 feb;9(2):167-76. pubmed pmid: 20056489. epub 2010/01/09. eng. 8.elliott j, smith m. the acute management of intracerebral hemorrhage: a clinical review. anesthesia and analgesia. 2010 may 1;110(5):1419-27. pubmed pmid: 20332192. epub 2010/03/25. eng. 9.berard c. chives rendus diabétiques. cr soc bilo (paris). 1849;1:10. 10.kimura k, iguchi y, inoue t, shibazaki k, matsumoto n, kobayashi k, et al. hyperglycemia independently increases the risk of early death in acute spontaneous intracerebral hemorrhage. journal of the neurological sciences. 2007 apr 15;255(1-2):90-4. pubmed pmid: 17350046. 11.stead lg, jain a, bellolio mf, odufuye a, gilmore rm, rabinstein a, et al. emergency department hyperglycemia as a predictor of early mortality and worse functional outcome after intracerebral hemorrhage. neurocritical care. 2010 aug;13(1):67-74. pubmed pmid: 20390379. epub 2010/04/15. eng. 12.alberti o, becker r, benes l, wallenfang t, bertalanffy h. initial hyperglycemia as an indicator of severity of the ictus in poor-grade patients with spontaneous subarachnoid hemorrhage. clinical neurology and neurosurgery. 2000 jun;102(2):78-83. pubmed pmid: 10817893. epub 2000/05/19. eng. 13.passero s, ciacci g, ulivelli m. the influence of diabetes and hyperglycemia on clinical course after intracerebral hemorrhage. neurology. 2003 nov 25;61(10):1351-6. pubmed pmid: 14638954. epub 2003/11/26. eng. 14.godoy da, pinero gr, svampa s, papa f, di napoli m. hyperglycemia and short-term outcome in patients with spontaneous intracerebral hemorrhage. neurocritical care. 2008;9(2):217-29. pubmed pmid: 18300001. 15.fogelholm r, murros k, rissanen a, avikainen s. admission blood glucose and short term survival in primary intracerebral haemorrhage: a population based 320 alvis-miranda et al glycemia in spontaneous intracerebral hemorrhage study. journal of neurology, neurosurgery, and psychiatry. 2005 mar;76(3):349-53. pubmed pmid: 15716524. pubmed central pmcid: pmc1739544. epub 2005/02/18. eng. 16.anderson cs, huang y, arima h, heeley e, skulina c, parsons mw, et al. effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: the intensive blood pressure reduction in acute cerebral haemorrhage trial (interact). stroke; a journal of cerebral circulation. 2010 feb;41(2):307-12. pubmed pmid: 20044534. epub 2010/01/02. eng. 17.appelboom g, piazza ma, hwang by, carpenter a, bruce ss, mayer s, et al. severity of intraventricular extension correlates with level of admission glucose after intracerebral hemorrhage. stroke; a journal of cerebral circulation. 2011 jul;42(7):1883-8. pubmed pmid: 21636822. epub 2011/06/04. eng. 18.broderick jp, diringer mn, hill md, brun nc, mayer sa, steiner t, et al. determinants of intracerebral hemorrhage growth: an exploratory analysis. stroke; a journal of cerebral circulation. 2007 mar;38(3):1072-5. pubmed pmid: 17290026. epub 2007/02/10. eng. 19.lee sh, kim bj, bae hj, lee js, lee j, park bj, et al. effects of glucose level on early and long-term mortality after intracerebral haemorrhage: the acute brain bleeding analysis study. diabetologia. 2010 mar;53(3):429-34. pubmed pmid: 20091021. epub 2010/01/22. eng. 20.bejot y, aboa-eboule c, hervieu m, jacquin a, osseby gv, rouaud o, et al. the deleterious effect of admission hyperglycemia on survival and functional outcome in patients with intracerebral hemorrhage. stroke; a journal of cerebral circulation. 2012 jan;43(1):243-5. pubmed pmid: 21940959. epub 2011/09/24. eng. 21.bullock r, zauner a, woodward jj, myseros j, choi sc, ward jd, et al. factors affecting excitatory amino acid release following severe human head injury. journal of neurosurgery. 1998 oct;89(4):507-18. pubmed pmid: 9761042. epub 1998/10/07. eng. 22.de salles aa, muizelaar jp, young hf. hyperglycemia, cerebrospinal fluid lactic acidosis, and cerebral blood flow in severely head-injured patients. neurosurgery. 1987 jul;21(1):45-50. pubmed pmid: 3614603. epub 1987/07/01. eng. 23.frykholm p, andersson jl, langstrom b, persson l, enblad p. haemodynamic and metabolic disturbances in the acute stage of subarachnoid haemorrhage demonstrated by pet. acta neurologica scandinavica. 2004 jan;109(1):25-32. pubmed pmid: 14653847. 24.harris jj, attwell d. the energetics of cns white matter. the journal of neuroscience : the official journal of the society for neuroscience. 2012 jan 4;32(1):356-71. pubmed pmid: 22219296. pubmed central pmcid: 3272449. 25.he y, liu w, koch lg, britton sl, keep rf, xi g, et al. susceptibility to intracerebral hemorrhage-induced brain injury segregates with low aerobic capacity in rats. neurobiology of disease. 2012 aug 24;49c:22-8. pubmed pmid: 22939993. 26.hertz l. bioenergetics of cerebral ischemia: a cellular perspective. neuropharmacology. 2008 sep;55(3):289309. pubmed pmid: 18639906. 27.illanes s, liesz a, sun l, dalpke a, zorn m, veltkamp r. hematoma size as major modulator of the cellular immune system after experimental intracerebral hemorrhage. neuroscience letters. 2011 mar 3;490(3):170-4. pubmed pmid: 21130839. 28.kawamura s, sayama i, yasui n, uemura k. sequential changes in cerebral blood flow and metabolism in patients with subarachnoid haemorrhage. acta neurochirurgica. 1992;114(1-2):12-5. pubmed pmid: 1561932. 29.kinoshita k, moriya t, utagawa a, sakurai a, mukoyama t, furukawa m, et al. change in brain glucose after enteral nutrition in subarachnoid hemorrhage. the journal of surgical research. 2010 aug;162(2):221-4. pubmed pmid: 19815233. 30.marsh wr, anderson re, sundt tm, jr. effect of hyperglycemia on brain ph levels in areas of focal incomplete cerebral ischemia in monkeys. journal of neurosurgery. 1986 nov;65(5):693-6. pubmed pmid: 3772458. epub 1986/11/01. eng. 31.oertel mf, schwedler m, stein m, wachter d, scharbrodt w, schmidinger a, et al. cerebral energy failure after subarachnoid hemorrhage: the role of relative hyperglycolysis. journal of clinical neuroscience : official journal of the neurosurgical society of australasia. 2007 oct;14(10):948-54. pubmed pmid: 17669657. 32.parkin m, hopwood s, jones da, hashemi p, landolt h, fabricius m, et al. dynamic changes in brain glucose and lactate in pericontusional areas of the human cerebral romanian neurosurgery (2014) xxi 3: 313 324 321 cortex, monitored with rapid sampling on-line microdialysis: relationship with depolarisation-like events. journal of cerebral blood flow and metabolism : official journal of the international society of cerebral blood flow and metabolism. 2005 mar;25(3):402-13. pubmed pmid: 15703701. 33.rehncrona s, hauge hn, siesjo bk. enhancement of iron-catalyzed free radical formation by acidosis in brain homogenates: differences in effect by lactic acid and co2. journal of cerebral blood flow and metabolism : official journal of the international society of cerebral blood flow and metabolism. 1989 feb;9(1):65-70. pubmed pmid: 2492027. epub 1989/02/01. eng. 34.siesjo bk, wieloch t. cerebral metabolism in ischaemia: neurochemical basis for therapy. british journal of anaesthesia. 1985 jan;57(1):47-62. pubmed pmid: 3917676. epub 1985/01/01. eng. 35.smith ml, von hanwehr r, siesjo bk. changes in extraand intracellular ph in the brain during and following ischemia in hyperglycemic and in moderately hypoglycemic rats. journal of cerebral blood flow and metabolism : official journal of the international society of cerebral blood flow and metabolism. 1986 oct;6(5):574-83. pubmed pmid: 3760041. epub 1986/10/01. eng. 36.statler kd, janesko kl, melick ja, clark rsb, jenkins lw, kochanek pm. hyperglycolysis is exacerbated after traumatic brain injury with fentanyl vs. isoflurane anesthesia in rats. brain research. 2003;994(1):37-43. 37.antonow-schlorke i, ebert m, muller t, schubert h, gschanes a, witte ow, et al. glucose transporter proteins glut1 and glut3 like immunoreactivities in the fetal sheep brain are not reduced by maternal betamethasone treatment. neuroscience letters. 2006 aug 7;403(3):261-5. pubmed pmid: 16782269. 38.nehlig a, rudolf g, leroy c, rigoulot ma, simpson ia, vannucci sj. pentylenetetrazol-induced status epilepticus up-regulates the expression of glucose transporter mrnas but not proteins in the immature rat brain. brain research. 2006 apr 12;1082(1):32-42. pubmed pmid: 16516869. 39.vorbrodt aw, dobrogowska dh, tarnawski m. immunogold study of interendothelial junctionassociated and glucose transporter proteins during postnatal maturation of the mouse blood-brain barrier. journal of neurocytology. 2001 aug;30(8):705-16. pubmed pmid: 12118158. 40.tsukamoto h, hamada y, wu d, boado rj, pardridge wm. glut1 glucose transporter: differential gene transcription and mrna binding to cytosolic and polysome proteins in brain and peripheral tissues. brain research molecular brain research. 1998 jul 15;58(12):170-7. pubmed pmid: 9685631. 41.vannucci sj, maher f, simpson ia. glucose transporter proteins in brain: delivery of glucose to neurons and glia. glia. 1997 sep;21(1):2-21. pubmed pmid: 9298843. 42.vannucci sj, seaman lb, brucklacher rm, vannucci rc. glucose transport in developing rat brain: glucose transporter proteins, rate constants and cerebral glucose utilization. molecular and cellular biochemistry. 1994 nov 23;140(2):177-84. pubmed pmid: 7898489. 43.maher f, vannucci sj, simpson ia. glucose transporter proteins in brain. faseb journal : official publication of the federation of american societies for experimental biology. 1994 oct;8(13):1003-11. pubmed pmid: 7926364. 44.goodman jr, gamble d, kay mm. distribution and function of multiple anion transporter proteins in brain tumor cell lines in relation to glucose transport. brain research bulletin. 1994;33(4):411-7. pubmed pmid: 8124579. 45.kainulainen h, schurmann a, vilja p, joost hg. invivo glucose uptake and glucose transporter proteins glut1 and glut3 in brain tissue from streptozotocindiabetic rats. acta physiologica scandinavica. 1993 oct;149(2):221-5. pubmed pmid: 8266811. 46.maher f, simpson ia, vannucci sj. alterations in brain glucose transporter proteins, glut1 and glut3, in streptozotocin diabetic rats. advances in experimental medicine and biology. 1993;331:9-12. pubmed pmid: 8333352. 47.maher f, vannucci s, takeda j, simpson ia. expression of mouse-glut3 and human-glut3 glucose transporter proteins in brain. biochemical and biophysical research communications. 1992 jan 31;182(2):703-11. pubmed pmid: 1734877. 48.huang y, lei l, liu d, jovin i, russell r, johnson rs, et al. normal glucose uptake in the brain and heart requires an endothelial cell-specific hif-1alphadependent function. proceedings of the national academy of sciences of the united states of america. 2012 oct 23;109(43):17478-83. pubmed pmid: 23047702. pubmed central pmcid: 3491491. 322 alvis-miranda et al glycemia in spontaneous intracerebral hemorrhage 49.godoy da, rabinstein a, videtta w, murillo-cabezas f. manejo óptimo de la glucemia en el paciente neurocrítico. revista de neurologia. 2010;51:745-56. 50.qutub aa, hunt ca. glucose transport to the brain: a systems model. brain research brain research reviews. 2005 nov;49(3):595-617. pubmed pmid: 16269321. 51.chih cp, roberts jr el. energy substrates for neurons during neural activity: a critical review of the astrocyteneuron lactate shuttle hypothesis. journal of cerebral blood flow and metabolism : official journal of the international society of cerebral blood flow and metabolism. 2003 nov;23(11):1263-81. pubmed pmid: 14600433. epub 2003/11/06. eng. 52.forsyth r, fray a, boutelle m, fillenz m, middleditch c, burchell a. a role for astrocytes in glucose delivery to neurons? developmental neuroscience. 1996;18(56):360-70. pubmed pmid: 8940607. epub 1996/01/01. eng. 53.yarkov a, montero s, lemus m, roces de alvarezbuylla e, alvarez-buylla r. arginine-vasopressin in nucleus of the tractus solitarius induces hyperglycemia and brain glucose retention. brain research. 2001 jun 1;902(2):212-22. pubmed pmid: 11384615. 54.kum w, zhu sq, ho sk, young jd, cockram cs. effect of insulin on glucose and glycogen metabolism and leucine incorporation into protein in cultured mouse astrocytes. glia. 1992;6(4):264-8. pubmed pmid: 1464458. 55.bingham em, hopkins d, smith d, pernet a, hallett w, reed l, et al. the role of insulin in human brain glucose metabolism: an 18fluoro-deoxyglucose positron emission tomography study. diabetes. 2002 dec;51(12):3384-90. pubmed pmid: 12453890. 56.marty n, dallaporta m, thorens b. brain glucose sensing, counterregulation, and energy homeostasis. physiology (bethesda, md). 2007 aug;22:241-51. pubmed pmid: 17699877. epub 2007/08/19. eng. 57.minokoshi y, alquier t, furukawa n, kim yb, lee a, xue b, et al. amp-kinase regulates food intake by responding to hormonal and nutrient signals in the hypothalamus. nature. 2004 apr 1;428(6982):569-74. pubmed pmid: 15058305. epub 2004/04/03. eng. 58.cataldo am, broadwell rd. cytochemical identification of cerebral glycogen and glucose-6phosphatase activity under normal and experimental conditions. ii. choroid plexus and ependymal epithelia, endothelia and pericytes. journal of neurocytology. 1986 aug;15(4):511-24. pubmed pmid: 3018177. 59.sickmann hm, waagepetersen hs, schousboe a, benie aj, bouman sd. brain glycogen and its role in supporting glutamate and gaba homeostasis in a type 2 diabetes rat model. neurochemistry international. 2012 feb;60(3):267-75. pubmed pmid: 22244844. 60.godoy da, di napoli m, biestro a, lenhardt r. perioperative glucose control in neurosurgical patients. anesthesiology research and practice. 2012;2012:690362. pubmed pmid: 22400022. pubmed central pmcid: 3286889. 61.godoy da, di napoli m, rabinstein aa. treating hyperglycemia in neurocritical patients: benefits and perils. neurocritical care. 2010 dec;13(3):425-38. pubmed pmid: 20652767. 62.nylen es, muller b. endocrine changes in critical illness. journal of intensive care medicine. 2004 marapr;19(2):67-82. pubmed pmid: 15070518. epub 2004/04/09. eng. 63.mccowen kc, malhotra a, bistrian br. stressinduced hyperglycemia. critical care clinics. 2001 jan;17(1):107-24. pubmed pmid: 11219223. epub 2001/02/24. eng. 64.gearhart mm, parbhoo sk. hyperglycemia in the critically ill patient. aacn clinical issues. 2006 janmar;17(1):50-5. pubmed pmid: 16462409. 65.robinson le, van soeren mh. insulin resistance and hyperglycemia in critical illness: role of insulin in glycemic control. aacn clinical issues. 2004 janmar;15(1):45-62. pubmed pmid: 14767364. epub 2004/02/10. eng. 66.garg r, chaudhuri a, munschauer f, dandona p. hyperglycemia, insulin, and acute ischemic stroke: a mechanistic justification for a trial of insulin infusion therapy. stroke; a journal of cerebral circulation. 2006 jan;37(1):267-73. pubmed pmid: 16306459. epub 2005/11/25. eng. 67.mccormick mt, muir kw, gray cs, walters mr. management of hyperglycemia in acute stroke: how, when, and for whom? stroke; a journal of cerebral circulation. 2008 jul;39(7):2177-85. pubmed pmid: 18436889. epub 2008/04/26. eng. 68.harada s, fujita-hamabe w, tokuyama s. effect of orexin-a on post-ischemic glucose intolerance and neuronal damage. journal of pharmacological sciences. romanian neurosurgery (2014) xxi 3: 313 324 323 2011;115(2):155-63. pubmed pmid: 21258173. epub 2011/01/25. eng. 69.allport le, butcher ks, baird ta, macgregor l, desmond pm, tress bm, et al. insular cortical ischemia is independently associated with acute stress hyperglycemia. stroke; a journal of cerebral circulation. 2004 aug;35(8):1886-91. pubmed pmid: 15192241. epub 2004/06/12. eng. 70.simpson ia, appel nm, hokari m, oki j, holman gd, maher f, et al. blood-brain barrier glucose transporter: effects of hypoand hyperglycemia revisited. journal of neurochemistry. 1999 jan;72(1):238-47. pubmed pmid: 9886075. epub 1999/01/14. eng. 71.tomlinson dr, gardiner nj. glucose neurotoxicity. nature reviews neuroscience. 2008 jan;9(1):36-45. pubmed pmid: 18094705. 72.molz s, decker h, oliveira ij, souza do, tasca ci. neurotoxicity induced by glutamate in glucose-deprived rat hippocampal slices is prevented by gmp. neurochemical research. 2005 jan;30(1):83-9. pubmed pmid: 15756936. 73.annetta mg, ciancia m, soave m, proietti r. diabetic and nondiabetic hyperglycemia in the icu. current anaesthesia & critical care. 2006;17(6):385-90. 74.shah gn, price to, banks wa, morofuji y, kovac a, ercal n, et al. pharmacological inhibition of mitochondrial carbonic anhydrases protects mouse cerebral pericytes from high glucose-induced oxidative stress and apoptosis. the journal of pharmacology and experimental therapeutics. 2012 dec 17. pubmed pmid: 23249625. epub 2012/12/20. eng. 75.higashi y, noma k, yoshizumi m, kihara y. endothelial function and oxidative stress in cardiovascular diseases. circulation journal : official journal of the japanese circulation society. 2009 mar;73(3):411-8. pubmed pmid: 19194043. 76.anderson re, tan wk, martin hs, meyer fb. effects of glucose and pao2 modulation on cortical intracellular acidosis, nadh redox state, and infarction in the ischemic penumbra. stroke; a journal of cerebral circulation. 1999 jan;30(1):160-70. pubmed pmid: 9880405. 77.wang jw, liu jy, yan ph, wang j, wang h. [effects of lactate on cell injury in primary cultures of rat cortical neurons during hypoxia/reoxygenation]. zhongguo ying yong sheng li xue za zhi = zhongguo yingyong shenglixue zazhi = chinese journal of applied physiology. 2008 nov;24(4):434-8. pubmed pmid: 21158145. epub 2008/11/01. chi. 78.wu g, bao x, xi g, keep rf, thompson bg, hua y. brain injury after intracerebral hemorrhage in spontaneously hypertensive rats. journal of neurosurgery. 2011 jun;114(6):1805-11. pubmed pmid: 21294617. pubmed central pmcid: pmc3107381. epub 2011/02/08. eng. 79.krafft pr, bailey el, lekic t, rolland wb, altay o, tang j, et al. etiology of stroke and choice of models. international journal of stroke : official journal of the international stroke society. 2012 jul;7(5):398-406. pubmed pmid: 22712741. epub 2012/06/21. eng. 80.keep rf, hua y, xi g. intracerebral haemorrhage: mechanisms of injury and therapeutic targets. the lancet neurology. 2012 8//;11(8):720-31. 81.chiu cd, chen ty, chin lt, shen cc, huo j, ma sy, et al. investigation of the effect of hyperglycemia on intracerebral hemorrhage by proteomic approaches. proteomics. 2012 jan;12(1):113-23. pubmed pmid: 22065606. epub 2011/11/09. eng. 82.helbok r, schmidt jm, kurtz p, hanafy ka, fernandez l, stuart rm, et al. systemic glucose and brain energy metabolism after subarachnoid hemorrhage. neurocritical care. 2010 jun;12(3):317-23. pubmed pmid: 20135362. epub 2010/02/06. eng. 83.perantie dc, wu j, koller jm, lim a, warren sl, black kj, et al. regional brain volume differences associated with hyperglycemia and severe hypoglycemia in youth with type 1 diabetes. diabetes care. 2007 sep;30(9):2331-7. pubmed pmid: 17575089. epub 2007/06/19. eng. 84.bingham em, dunn jt, smith d, sutcliffe-goulden j, reed lj, marsden pk, et al. differential changes in brain glucose metabolism during hypoglycaemia accompany loss of hypoglycaemia awareness in men with type 1 diabetes mellitus. an [11c]-3-o-methyl-d-glucose pet study. diabetologia. 2005 oct;48(10):2080-9. pubmed pmid: 16143864. epub 2005/09/07. eng. 85.berbel-garcia a, porta-etessam j, martinez-salio a, ballesta f, saiz-diaz ra, perez-martinez da, et al. [transient cerebral oedema associated to hypoglycaemia]. revista de neurologia. 2004 dec 115;39(11):1030-3. pubmed pmid: 15597265. epub 2004/12/15. edema cerebral transitorio asociado a hipoglucemia. spa. 324 alvis-miranda et al glycemia in spontaneous intracerebral hemorrhage 86.macleod km, gold ae, ebmeier kp, hepburn da, deary ij, goodwin gm, et al. the effects of acute hypoglycemia on relative cerebral blood flow distribution in patients with type i (insulin-dependent) diabetes and impaired hypoglycemia awareness. metabolism: clinical and experimental. 1996 aug;45(8):974-80. pubmed pmid: 8769355. epub 1996/08/01. eng. 87.choi iy, seaquist er, gruetter r. effect of hypoglycemia on brain glycogen metabolism in vivo. journal of neuroscience research. 2003 apr 1;72(1):25-32. pubmed pmid: 12645076. pubmed central pmcid: pmc1471897. epub 2003/03/20. eng. 88.oz g, kumar a, rao jp, kodl ct, chow l, eberly le, et al. human brain glycogen metabolism during and after hypoglycemia. diabetes. 2009 sep;58(9):1978-85. pubmed pmid: 19502412. pubmed central pmcid: pmc2731528. epub 2009/06/09. eng. 89.oz g, henry pg, seaquist er, gruetter r. direct, noninvasive measurement of brain glycogen metabolism in humans. neurochemistry international. 2003 sepoct;43(4-5):323-9. pubmed pmid: 12742076. epub 2003/05/14. eng. 90.feuerstein d, manning a, hashemi p, bhatia r, fabricius m, tolias c, et al. dynamic metabolic response to multiple spreading depolarizations in patients with acute brain injury: an online microdialysis study. journal of cerebral blood flow and metabolism : official journal of the international society of cerebral blood flow and metabolism. 2010 jul;30(7):1343-55. pubmed pmid: 20145653. pubmed central pmcid: 2949215. 91.samiullah s, qasim r, imran s, mukhtair j. frequency of stress hyperglycaemia and its' influence on the outcome of patients with spontaneous intracerebral haemorrhage. jpma the journal of the pakistan medical association. 2010 aug;60(8):660-3. pubmed pmid: 20726199. epub 2010/08/24. eng. 92.bamford j, sandercock p, dennis m, burn j, warlow c. a prospective study of acute cerebrovascular disease in the community: the oxfordshire community stroke project--1981-86. 2. incidence, case fatality rates and overall outcome at one year of cerebral infarction, primary intracerebral and subarachnoid haemorrhage. journal of neurology, neurosurgery, and psychiatry. 1990 jan;53(1):16-22. pubmed pmid: 2303826. pubmed central pmcid: pmc1014091. epub 1990/01/01. eng. 93.bamford j, sandercock p, dennis m, warlow c, jones l, mcpherson k, et al. a prospective study of acute cerebrovascular disease in the community: the oxfordshire community stroke project 1981-86. 1. methodology, demography and incident cases of firstever stroke. journal of neurology, neurosurgery, and psychiatry. 1988 nov;51(11):1373-80. pubmed pmid: 3266234. pubmed central pmcid: pmc1032805. epub 1988/11/01. eng. 94.douglas ma, haerer af. long-term prognosis of hypertensive intracerebral hemorrhage. stroke; a journal of cerebral circulation. 1982 jul-aug;13(4):488-91. pubmed pmid: 7101349. 95.helweg-larsen s, sommer w, strange p, lester j, boysen g. prognosis for patients treated conservatively for spontaneous intracerebral hematomas. stroke; a journal of cerebral circulation. 1984 nov-dec;15(6):10458. pubmed pmid: 6506116. 96.kojima s, omura t, wakamatsu w, kishi m, yamazaki t, iida m, et al. prognosis and disability of stroke patients after 5 years in akita, japan. stroke; a journal of cerebral circulation. 1990 jan;21(1):72-7. pubmed pmid: 2300993. epub 1990/01/01. eng. 97.chi a, lissauer me, kirchoffner j, scalea tm, johnson sb. effect of glycemic state on hospital mortality in critically ill surgical patients. the american surgeon. 2011 nov;77(11):1483-9. pubmed pmid: 22196662. epub 2011/12/27. eng. 98.obiako or, oparah sk, ogunniyi a. prognosis and outcome of acute stroke in the university college hospital ibadan, nigeria. nigerian journal of clinical practice. 2011 jul-sep;14(3):359-62. pubmed pmid: 22037085. epub 2011/11/01. eng. 99.di napoli m, godoy da, campi v, del valle m, pinero g, mirofsky m, et al. c-reactive protein level measurement improves mortality prediction when added to the spontaneous intracerebral hemorrhage score. stroke; a journal of cerebral circulation. 2011 may;42(5):1230-6. pubmed pmid: 21474813. epub 2011/04/09. eng. 20manishjaiswal_panda romanian neurosurgery (2014) xxi 3: 361 363 361 “panda smiled again credit goes to repeated early stage computed tomography scan: an interesting case report” manish jaiswal, ashok gandhi, devendra purohit, r.s. mittal department of neurosurgery, sms medical college and hospital jln marg, jaipur (302004), rajasthan, india abstract extradural hematoma (edh) is considered to be a rare in head trauma associated with arrested hydrocephalus, and represents a serious pathology from which complete recovery can be expected if urgent intervention done in time. in this case report, the authors present an arrested hydrocephalus patient who was apparently asymptomatic at the time of hospital admission with a mild head injury and developed rapidly increasing size of edh. the value of repeated early computed tomography (ct) scan and the pathogenesis of rapidly increasing size of edh in arrested hydrocephalic patient are discussed. key words: edh; arrested hydrocephalus; repeated early stage ct scan. introduction extradural hematoma (edh) is considered to be a rare in head trauma associated with arrested hydrocephalus, and represents a serious pathology from which complete recovery can be expected if urgent intervention done in time. in this case report, the authors present an arrested hydrocephalus patient who was apparently asymptomatic at the time of hospital admission with a mild head injury and developed rapidly increasing size of edh. the value of repeated early computed tomography (ct) scan and the pathogenesis of rapidly increasing size of edh in arrested hydrocephalic patient are discussed. case report a 38 year old man was admitted after road traffic accident. he was conscious but had mild symptom of giddiness but glassgow coma scale (gcs) was 15. ct head was performed, which revealed arrested hydrocephalus with left temporo-parietal thin extradural haematoma (edh), an interesting finding was smiling panda face appearance in ct head due to dilated lateral ventricle (figure 1). urgent repeat early stage ct head was done, revealing increased size of edh causing distortion of the previous panda face giving punched panda face appearance (figure 2) with midline shift. urgent surgical intervention done and patient regained consciousness. next day post-operative ct head shown again smiling face of panda 362 manish jaiswal et al traumatic extradural hematoma in arrested hydrocephalus (figure 3) and no mid line shift. patient was conscious and no neurological deficit at the time of discharge 5th day post operatively. figure 1 “smiling panda face appearance” at the time of admission in ct scan figure 2 “punched panda face appearance: 6 hours after admission in ct scan figure 3 post operative ct scan showing “smiling face” again discussion extradural haematoma occurs in approximately 2% of all patients with head injuries and 5-15% of patients with fatal head injuries. edh is considered to be one of the most serious complications of head injury, requiring immediate diagnosis and surgical intervention. incidence of deleyed extradural haematoma is reported in 10-30% (1). the risk factors for increasing edh size include lowering of intracranial pressure medically and /or surgically, thus reducing the temponading effect, rapid correction haemodyanamic shock and coagulopathies (2). but in our patient there was incidental finding of dialeted ventricles along with left temporoparietal bone fracture and thin edh. because there was no sign and symptom of raised intracranial pressure so it was assumed the case of arrested hydrocephalus and so romanian neurosurgery (2014) xxi 3: 361 363 363 there was no tamponading effect over dura to prevent further increase in size of edh, which result in rapid evolution of edh causing finally mass effect and manifesting as rapid neurological deterioration of patient. broader indications for computed tomographic (ct) scanning allow the early detection and treatment of an extradural hematoma (3). importance of follow-up ct scans at an early stage in cases which showed rapid deterioration within a few hours after head injury has been studied (4, 5, 6) and proven worthy in term of saving life as in our case. conclusion take home message is that “always perform repeat early stage ct scan head in case of head injury associated with arrested hydrocephalus even there is no neurological deterioration and thus may be of value in detecting changes at an early stage to save life.” correspondence manish jaiswal a 33/48 a 2, omkareshwar, varanasi, 221001, uttar pradesh, india phone – 091-9799980494, email – manishmlnmc@gmail.com references 1. borovich b, braun j, guilburd jn, et al. delayed onset of traumatic extradural haematoma. j neurosurg. 1985;63:30-4 2. chandra ps, jaiswal a, mahapatra ak. bifrontal epidural haematomas following surgery for occipital falcine meningioma:an unusual complication of surgery in the prone position. j clin neurosci. 2002;9:582-4 3. bor seng shu e, de almeida leme rj, aguiar ph, de andrade af, teixeira mj, plese jp.traumatic acute giant epidural hematoma in a hydrocephalic shunted child. pediatr neurosurg. 2000 apr;32(4):176-9. 4. servadei f, staffa g, morichetti a, burzi m, piazza g.asymptomatic acute bilateral epidural hematoma: results of broader indications for computed tomographic scanning of patients with minor head injuries. neurosurgery. 1988 jul;23(1):41-3. 5. lesoin f, viaud c, giraldon jm, clarisse j, jomin m. delayed traumatic intracranial hematomas. value of computer tomography. neurochirurgie. 1982;28(6):3738. 6. yoshimizu n, hiramoto m, notani m.study of those cases which showed rapid deterioration within a few hours after head injury--importance of follow-up ct scans at an early stage. neurosurg rev. 1989;12 suppl 1:175-7. balasad_traumatic romanian neurosurgery (2016) xxx 2: 237-240 | 237 traumatic extradural lumbar haematoma due to a pathological metastatic vertebral body fracture l3. case report and review of the literature daniel balasa1, gabriela butoi2, radu baz3, anca hancu4 1department of neurosurgery, clinical county hospital, constanta 2medimar, private radiological clinic, constanta 3pozimed, private radiological clinic, constanta 4department of neurology, clinical county hospital, constanta abstract: spinal epidural haematoma (seh) is a rare entity. we present the case of a 45 years old patient with lumbar epidural hematoma produced by a l3 vertebral tumoral (metastatic) fracture. neurological status: cauda equina syndrome with sphincterian deficits, incomplete paraplegia (frankel c), with neurological level l1. emergency surgery was performed (l3-l2-bilateral laminectomy, l1 left laminectomy, posterior stabilization l2-l4 by titan screws) offering the possibility to progressive motor, sensitive and sphincterian deficites recovery. abbreviations: computer tomography -ct, magnetic resonance imaging-mri, spinal epidural haematoma-seh, visual analogue scale of pain-vas. conclusion: we present a patient with a compressive subacute extradural haematoma, due to a traumatic fracture on a vertebral metastatic tumor who produced cauda equina syndrome. surgical emergency intervention was mandatory for a good neurological outcome. key words: spinal extradural haematoma, pathological vertebral fracture introduction spinal extradural haematoma (seh) is a rare pathology and represents an important cause of neural (spinal cord or cauda equina) compresion (2). seh could be produced spontaneously, by spine trauma, iatrogenic (postoperative, by lumbar puncture, epidural anestesia), spinal epidural malformation, pregnancy, coagulation abnormalities (2), spinal tumors. seh is very rare and represents near 1% from the complication of spine injuries (2) and between 0,3-0,9% of all space-ocuppying lesions of the spinal canal(12). seh is complicate with serious morbidity, if the surgical treatment is delayed. 238 | balasa et al traumatic extradural lumbar haematoma case report a 45 years old male patient suffered a car accident with direct spinal lumbar impact. immediately after the accident he started feeling vertebral pain of high intensity (vas 9/10) which improved after the use of painkiller drugs and few days of bed rest. two weeks after, while the patient was having a sexual intercourse he reported sudden paresthesia, incomplete paraplegia (score frankel c), progressive loss of sphincter control. radiography and mri scan of the spine revealed an extradural subacute anterior haematoma l1, l2, l4, compressive on the cauda equina, cominutive fracture of a pathological (tumoral) vertebral body of l3. tumoral lesions where also detected (few mm) within the vertebral bodies of t9, t10, t11, t12, l1, l5 and the first rib, sacrum and iliac wing. the tumors had the aspect of hematogenous metastasis. the patient did not previously use anticoagulant drugs. figure 1 mri scan , t2 , sagital view: 2 vertebral lesions relevant for hematogenous metastasis, in l3 and t11. heterogenous hyperintensity of the vertebral body l3 (small white arrows), anterior extradural collection l1-l2-l3 with aspect of a subacute haematoma, compressive on the cauda equina white-red arrow figure 2 mri scan, t1 with gadolinium, sagital view: heterogeous hypointensity of the vertebral body l3 (white arrow), anterior extradural collection l1-l2-l3 with aspect of a subacute haematoma, compressive on the cauda equina – white-red arrow figure 3. mri scan , t2 , axial view: l1 extradural anterior heterogenous hyperdense lesion (subacute haematoma) white arrow emergency surgery was performed (l3, l2 bilateral laminectomy, -l1 left laminectomy, removal of haematoma, vertebral bilateral posterior fusion l2l4, transpedicular with titanium screws) romanian neurosurgery (2016) xxx 2: 237-240 | 239 figure 4 posterior transpedicular bilateral rahisinthesys l4-l2. pathological aspects can be seen on vertebral body of l3 and the pedicle of l3 (heterogenous aspect hypertransparecies with lythical aspect, cuneiforme fracture of the body l3) white arrows postoperative evolution was favorable. the pacient showed progressive motor improvement with normalisation of crural strenght within 2-3 days, paresthesias decreased significantly within the following 6 days. sphincter control was regained partially, but slower than the motor and sensitive functions. the patient chose to treat the remaining tumoral pathology in his native country (usa). discussion the causes of seh are vertebral fractures, iatrogenic (lumbarpuncture, surgical procedures, epidural anesthesia), bullet injuries, obstetric birth trauma, spinal epidural malformation, spinal tumors. in this case the etiology was spine trauma and spine tumor of the vertebral body of l3 (4). spinal edh can occur throughout the spine but is most common in the cervicothoracic region, usually posterior to the thecal sac over 2-4 vertebral levels (1, 4). according to klekamp and samii (10) 80% of metastasis are located in the vertebral bodies with spinal cord compression from anterior. the spinal cord compression may be increased from vertebral fracture (10) and haematoma as in this case. anterior extradural lumbar subacute haematoma secondary to a cominuted pathological (metastatic) vertebral body fracture is an extremely rare case. i didn’t find another case in international literature. mri is the golden standard for diagnosing the seh. according to boukobza (1) the specific signals are isointense in t1 and hyperintense in t2. the cause of seh may be considered bleeding from valve less venous plexus in the epidural space, produced by blunt vertebral lumbar trauma (3), in a patient with a comminutive vertebral fracture, with multiple bony vertebral metastasis. the patient presented in this case report accused intense pain in the vertebral area, 240 | balasa et al traumatic extradural lumbar haematoma followed in few hours by a cauda equina syndrome. the golden standard for the patients with symptomatic seh is rapid decompression, laminectomy 11) and for asymptomatic seh is corticosteroids and close observation (6, 9) in this case the emergency was cauda equina syndrome produced by the seh which imposed emergent decompression (laminectomy) and, due to the associated comminuted fracture metastatic l3, the transpedicular stabilization. postoperative outcome is generally favorable with a great percentage of improvement. according to lawton and co. (12) the percentage of improvement of 30 patients with seh was 87%. according to hosono and co. (8), there was a 94% postoperative pain relief, and 81% motor improvement. in this case the patient had a fast improvement in sensibility and motor strenght. the sphincter control improved slower than motility and sensibility. correspondence daniel balasa daniel_balasa@hotmail.com references 1. boukobza m, guichard jp, boissonet m, george b, reizine d, gelbert f, et al. spinal epidural haematoma: report of 11 cases and review of the literature. neuroradiology. 1994;36(6):456-9 2. cuenca pj, tulley eb, devita d, stone a. delayed traumatic spinal epidural hematoma with spontaneous resolution symptoms. j emerg med. 2004;27(1):37-41. 3. foo d, rossier ab. preoperative neurological status in predicting surgical outcome of spinal epidural hematomas. surg neurol. 1981;15(5):389-401. 4. foo d, rossier ab. post-traumatic spinal epidural hematoma. neurosurgery. 1982;11(1 pt 1):25-32. 5. fukui mb, swarnkar as, williams rl. ajnr am j neuroradiol. 1999;20 (7): 1365-72., acute spontaneous spinal epidural hematomas. 6. hentschel s, woolfenden ar, fairholm dj. resolution of spontaneous spinal epidural hematoma without surgery: report of two cases. spine. 2001;26(22):e525-7 7. hsieh ct1, chiang yh, tang ct, sun jm, ju dt., am j emerg med. 2007 jan;25(1):69-71., delayed traumatic thoracic spinal epidural hematoma: a case report and literature review 8. hosono n, yonenobu k, fuji t, ebara s, yamashita k, ono k (1995) vertebral body replacement with a ceramic prosthesis for metastatic spinal tumors. spine 20:2454– 2462 9. jamjoom za. acute spontaneous spinal epidural hematoma: the influence of magnetic resonance imaging on diagnosis and treatment. surg neurol. 1996;46(4):3459 10. klekamp j, samii m., surgery of spinal tumors, 2007, 450-481 11.luciano miller, reis rodrigues, felipe abreu, edison noboru fujiki, carlo milani, einstein (são paulo) vol.8 no.4 são paulo oct./dec. 2010, delayed traumatic spinal epidural hematoma with neurological deficits 12. lawton mt, porter rw, heiserman je, jacobowitz r, sonntag vk, dickman ca. surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome. j neurosurg. 1995;83(1):1-7. 13. robert z. tashjian, md, michael p. bradley, md, phillip r. lucas, md, brown medical school, rhode island hospital, department of orthopaedic surgery, 2 dudley street, providence, ri 02905, usa, spinal epidural hematoma after a pathologic compression fracture: an unusual presentation of multiple myeloma kankanekumar_large romanian neurosurgery (2016) xxx 1: 127 131 127 large tentorium meningioma causing chiari malformation type-1 with syringomalia with complete resolution of syrinx and chiari after surgical excision: rare case report with review of literature vivek kumar kankane, gaurav jaiswal, tarun kumar gupta department of neurosurgery, r.n.t. medical college & m.b. hospital, udaipur, rajasthan, india abstract: a 35-year-old female was admitted with a 3-year history of headache, gait disturbance and vertigo on & off and one year history of nasal regurgitation. magnetic resonance imaging demonstrated a large tentorium meningioma left sided and syringomyelia in the upper cervical cord associated with caudal displacement of the cerebellar tonsil (chiari type -1 malformation). herniation of the cerebellar tonsil and distortion of the brain stem had probably caused disturbance of cerebrospinal fluid flow which combined with obstruction of the spinal canal, caused the syrinx. complete excision of the tumor resulted in symptomatic improvement of these symptoms with complete resolution of syrinx & chiari. key words: syringomyelia, posterior fossa, brain tumor, meningioma, chiari malformation introduction chiari & syringomyelia is well-known to be associated with anomalies in the craniocervical junction. the combination of chiari type-1 with syringomyelia and posterior fossa tumor is rare. we describe a case of syringomyelia with chiari malformation (cm) type -1 associated with tentorial meningioma and discuss the pathogenesis based on neuroimaging findings. case report a 36-year-old female was admitted with complaints of suboccipital headache, vertigo on & off and gait difficulty persisting for the last 3 years and nasal regurgitation for last 1 year. neurological examination revealed left cerebellar sign present with nystagmoid ocular movement and hypertonia in both lower limb and power all four limbs 5/5 except both hand grip 80%. all deep tendon reflexes exaggerated with bilateral knee clonus present. magnetic resonance (mr) imaging with gadolinium-diethylenetriaminepenta-acetic acid also demonstrated a homogeneously enhanced extra axial lesion in the left 128 kankane et al large tentorium meningioma causing chiari malformation type-1 tentorium causing mass effect on left cerebellar hemisphere with effacement of fourth ventricle resulting dilatation of supra tentorial ventricle with tonsilar herniation. sagittal mr imaging indicated a peg-like deformity of the cerebellar tonsil and descend up to c2 with syringomyelia of the upper cervical region of spinal cord (figures 1, 2). midline suboccipital craniectomy with extending left suboccipital craniectomy with foramen magnum decompression with simpson grade ii excision of meningioma was done. histological examination showed transitional meningioma. the postoperative course was uneventful. mr imaging done 6 months after the surgery does not show any caudal displacement of tonsil and complete resolution of syringomyelia (figure 3). patient is completely asymptomatic at present. a b figure 1 a&b t1 & t2 weighted sagittal mr image showed a descent and plugging of the cerebellar tonsils up to c2 with presence of a syringomyelia extending from the cervicomedullary junction till c4 segment. however, some signal changes probably suggestive of myelomalacia a b figure 2a t1 weighted axial mri brain with contrast revealed extra axial mass lesion in left cerebellar hemisphere along tentorium with effacement of forth ventricle figure 2b t1 weighted sagittal mri brain with contrast revealed extra axial mass lesion along left tentorium with cerebellar tonsil herniation up to c2 romanian neurosurgery (2016) xxx 1: 127 131 129 figure 3 t2 & t1 weighted sagittal mri brain with spine revealed complete resolution of syrinx and tonsilar herniation discussion posterior fossa tumors associated with syringomyelia include brainstem glioma, (20) meningioma, (9, 12, and 16, 10, 7, 2) cerebellar astrocytoma, (13) cerebellar hemangioblastoma, (6) and fourth ventricular epidermoid tumor (11). there are several theories to explain the pathophysiology of syringomyelia. gardner’s (8) suggested that a congenital imperforate of magendie's foramen disturbs the cerebrospinal fluid flow out of the cisterna magna and an intracranial arterial pulse produces a water-hammer effect on the central canal, leading to enlargement of the syrinx. williams and timperley (20) stressed the importance of craniospinal pressure dissociation, with the venous pressure change occurring soon after coughing evacuating the central canal with syrinx extension. the check valve effect associated with foramen magnum obstructive lesions may enhance syringomyelia, (19) a theory accepted by many clinicians. ball and dayan (4) found that cerebrospinal fluid leaking into the spinal cord along virchow-robin spaces may cause syringomyelia. aubin et al. (3) observed the transneural passage of cerebrospinal fluid into the spinal cord by comparison of the ct density of the subarachnoid space, spinal cord, and syringomyelic cavity. barnett et al. (5) classed syringomyelia into communicating and non-communicating types. communicating syringomyelia is consistent with gardner's hydrodynamic theory, with communication between the syrinx and fourth ventricle. non-communicating syringomyelia is secondary to intramedullary tumors or spinal injury, with no communication between the syrinx and fourth ventricle. various pathogeneses for syringomyelia with posterior fossa tumor have been identified. de reucket al. (6) reported syringomyelia with cerebellar hemangioblastoma and concluded that faulty closure of the dorsal raphe with glial inclusion caused the syrinx. williams and timperley (20) reported three cases of syringomyelia with brainstem glioma and emphasized the importance of craniospinal pressure dissociation and evacuation of the central canal. neuroimaging of the present case revealed caudal displacement of the lower cerebellar tonsil with the same configuration as that of chiari type i malformation. however, removal of the tumor resulting the cerebellar tonsil to return to its normal position. this observation suggests that the cause of syringomyelia must be an anatomical change around the craniocervical junction. several theories have been proposed to explain the development of syringomyelia. failure of the foramina of the 130 kankane et al large tentorium meningioma causing chiari malformation type-1 fourth ventricle to open with continuing communication between the fourth ventricle and the cystic space within the spinal cord via the obex may allow increased pressure within the ventricles to be transmitted to the central canal (8). csf pressure waves can cause forced flow of the csf into the syrinx along the virchow-robin spaces (4). partial blockage of the subarachnoid space in the region of the cisterna magna may direct csf into the communication, providing an intermittent distending force which may be active for many years (18). obstruction at the cisterna magna associated with a high venous pressure can lead to transmedullary passage of csf which could create a syrinx cavity (1). excessive absorption of csf from the spinal cord might cause chiari type i malformation, leading to a foraminal obstruction and ultimately producing a syrinx (17). recently, a detailed analysis of the configuration of the central canal in the normal population as well as in syringomyelia patients showed that a large portion of the normal group has an obstructed central canal except in their early stages of life. the spinal cord with syrinx shows three patterns of communication with the fourth ventricle and central canal: central canal syrinx (communicating), central canal syrinx (noncommunicating), and extracanalicular syrinx. central canal syrinx (communicating) is observed predominantly in children with hydrocephalus. central canal syrinx (noncommunicating) has a cavity consisting of a focal dilation of central canal that is separated from the fourth ventricle by a syrinx-free segment of spinal cord and occurs predominantly in adult patients with various diseases which cause csf circulatory disturbance around the cervicomedullary junction. extracanalicular syrinx is seen as a result of spinal cord injury. mr images of patients with brain tumors which demonstrate syrinx may suggest that the central canal has already been occluded in some locations. phase-contrast/cine mr imaging indicates that a disturbance of csf circulation in the spinal subarachnoid space may cause fluid to be forced into the central canal through the interstitial space of the spinal cord in such cases (14). syringomyelia may occur secondary to the brain tumor within the posterior fossa but without symptoms suggestive of syringomyelia. (2, 7, 9, 10, 12, 13, 15, 16, 20) sagittal mr imaging of our case showed a large and slow-growing brain tumor, which had resulted in elimination of csf from the posterior fossa and herniation of the cerebellar tonsil through the foramen magnum. herniation of the cerebellar tonsil and distortion of the lower brain stem may have disturbed csf circulation in the spinal subarachnoid space, and resulted in transmedullary passage of csf. furthermore, the obstructed central canal may also have prevented free passage of csf outside the central canal. consequently, these pathological csf flows and accumulations caused a compartment of the central canal force to dilate. the symptoms of brain tumor in the posterior fossa, as with all cases with tonsilar herniation, are too severe to remain untreated. syringomyelia with cm type-1 associated with various intracranial diseases can be diagnosed by neurological imaging. an early diagnosis is essential for a good prognosis. romanian neurosurgery (2016) xxx 1: 127 131 131 conclusion extra-axial tumor of posterior fossa is rarely associated with syringomalia & chiarimalformation. surgical excision of the primary lesion (tumor) resulting complete resolution of syrinx & chiari. correspondence vivek kumar kankane, m.ch. neurosurgery resident, r.n.t. medical college & m.b. hospital, udaipur, rajasthan, india. email: vivekkankane9@gmail.com address: c/o dr. khamesara 59 sardarpura, udaipur, rajasthan, india, pincode 313001 mobile no. 8955337812 references 1. aboulker j: la syringomy & eacute;leiet les liquides intrachidiens. neurochirurgie1979; 25 (suppl 1): 1144. 2. anegawa s, hayashi t, torigoe r, iwaisako k, higashioka h.cerebellopontine angle meningioma causing asymptomatic syringomyelia--case report. neurol med chir(tokyo)1997 aug;37(8):624-626 3. aubin ml, vignad j, jardin c, bar d: computed tomography in 75 clinical cases of syringomyelia. ajnr1981; 2: 199-204. 4. ball mj, dayan ad: pathogenesis of syringomyelia. lancet1972; 2: 799-801. 5. barnett hjm, foster jb, hudgson p (eds): syringomyelia. major problems in neurology, vol 1. london, wb saunders, 1973, pp 295-296 6. de reuck j, alva j, roels h, vander eecken h: relation between syringomyelia and von hippel-lindau's disease. eur neurol 1974; 12: 116-127. 7.fukui k, kito a, iguchi i: asymptomatic syringomyelia associated with cerebellopontine angle meningioma. case report. neurol med chir (tokyo)1993; 33: 833-835. 8. gardner wj: hydrodynamic mechanism of syringomyelia: its relationship to myelocele. j neurol neurosurg psychiat1965; 28: 247-259. 9. hirata y, matsukado y, kaku m: syringomyelia associated with a foramen magnum meningioma. surg neurol1985; 23: 291-294. 10. jaiswal ak, chandra ps. cerebellopontine angle meningioma with acquired chiari and syringomyelia: neuroimage. neurol india. 2001 sep;49(3):323 11. kan s, fox aj, vinuela f, barnett hjm, peerless sj: delayed ct metrizamide enhancement of syrin gomyelia secondary to tumor. ajnr1983; 4: 73-78. 12. kosary iz, braham j, shaked i, tadmor r: cervical syringomyelia associated with occipital meningioma. neurology (minneap)1969; 19: 1127-1130. 13. kumar c, panagapoulos k, kalbag rm, mcallister v: cerebellar astrocytoma presenting as a syringomyelic syndrome. surg neurol 1987; 27: 187-190 14. milhorat th, kotzen rm, anzil ap: stenosis of central canal of spinal cord in man: incidence and pathological findings in 232 autopsy cases. j neurosurg 1994;80: 716-722. 15. oldfield eh, muraszko k, shawker th, patronas nj:pathophysiology of syringomyelia associated with chiari i malformation of the cerebellar tonsils. implications for diagnosis and treatment. j neurosurg1994; 80:3-15. 16. urasaki e, soejima t, yokota a, matsuoka s:association of asymptomatic syringomyelia with tentorial meningioma. no shinkei geka1989; 17: 985989. 17. welch k, shillito j, strand r, fisher eg, winston kr: chiari i & ldquo;malformations & rdqaucqou ;& irmedd asdhi;saonr der? jneurosurg1981; 55: 604-609 18. williams b: a critical appraisal of posterior fossa surgery for communicating syringomyelia. brain1978; 101: 223-250 19. williams b: on the pathogenesis of syringomyelia: a review. j r soc med 1980;73: 798-806. 20. williams b, timperley wr: three cases of communicating syringomyelia secondary to midbrain gliomas. j neurol neurosurg psychiatry1977; 40: 80-88 02_paper romanian neurosurgery (2015) xxix 4: 385 396 385 doi: 10.1515/romneu-2015-0054 idiopathic intracranial hypertension: case report g. iacob1, andreea marinescu2 1neurosurgery clinic university hospital, bucharest, romania 2radiology clinic university hospital, bucharest, romania abstract: idiopathic intracranial hypertension – iih (synonymous old terms: benign intracranial hypertension bih, pseudotumor-cerebri ptc) it’s a syndrome, related to elevated intracranial pressure, of unknown cause, sometimes cerebral emergency, occuring in all age groups, especially in children and young obese womans, in the absence of an underlying expansive intracranial lesion, despite extensive investigations. although initial symptoms can resolve, iih displays a high risk of recurrence several months or years later, even if initial symptoms resolved. results: a 20-year-old male, obese since two years (body mass index 30, 9), was admitted for three months intense headache, vomiting, diplopia, progressive visual acuity loss. neurologic examination confirmed diplopia by left abducens nerve palsy, papilledema right > left. at admission, cerebral ct scan and cerebral mri with angio mri 3dtof and 2d venous tof was normal. despite treatment with acetazolamide (diamox), corticosteroid, antidepressants (amitriptyline), anticonvulsivants (topiramate) three weeks later headache, diplopia persist and vision become worse, confirmed by visual field assessment, visual evoked potential (vep). a cerebral arteriography demonstrate filling defect of the superior sagittal sinus in the 1/3 proximal part and very week filling of the transverse right sinus on venous time. trombophylic profile has revealed a heterozygote v factor leyden mutation, a homozygote mthfr and pai mutation justifying an anticoagulant treatment initiated to the patient. the mri showed a superior sagittal sinus, right transverse and sigmoid sinus thrombosis, dilatation and buckling of the optic nerve sheaths with increased perineural fluid especially retrobulbar, discrete flattening of the posterior segment of the eyeballs, spinal mri showed posterior epidural space with dilated venous branches, with mass effect on the spinal cord, that occurs pushed anterior on sagittal t1/t2 sequences cervical and thoracic. the opening pression of lumbar puncture, done with the patient in the lateral decubitus position, was 60 cm h2o, the cytochemical csf study were normal. the patient was operated: a lombo-peritoneal with a variable pressure valve was inserted. two months after the patient general condition improved: he was without headache, abducens palsy and the visual field assessment, ocular motility examination, ophthalmoscopy were normal. conclusion: ihh is rare, variable in evolution, and in many cases it disappears on its own within 6 months without affecting life expectancy. 386 iacob, marinescu idiopathic intracranial hypertension weight loss, fluid or salt restriction, in conjunction with medical treatment, angioplasty and venous stenting across the sinus stenosis under general anesthesia and surgical treatment (shunting, optic nerve sheath decompression and fenestration, gastric by-pass surgery) are treatment alternatives. such disorder should be closed monitored because 10 to 25% of cases could be affected by recurrencies or by permanent vision loss to those patients with resistant papilledema despite treatment. key words: idiopathic intracranial hypertension-iih, benign intracranial hypertension bih, pseudotumor-cerebri – ptc, superior sagittal and transverse sinus thrombosis, intracranial pressure, visual evoked potential (vep) introduction idiopathic intracranial hypertension – iih (synonymous old terms: benign intracranial hypertension bih, pseudotumor-cerebri ptc) it’s a syndrome, related to elevated intracranial pressure of unknown cause, sometimes cerebral emergency, occurring in all age groups, especially in children and young obese womans, with several symptoms includind visual loss; without underlying expansive intracranial lesion, hydrocephalus, dural sinus thrombosis; with a recurrency potential months or even years later, even if initial symptoms resolved. (1-12) case report a 20-year-old male, obese since two years (body mass index 30,9), was admitted june 2015 in a neurology department for three months intense headache, vomiting, diplopia, progressive visual acuity loss. from his medical records we noticed: left otomastoiditis since childhood, a car accident with craniocerebral trauma in 2007 with a 3 mm nonoperated left subdural haematoma and epicranian haematoma. clinical examination revealed good clinical condition, without motor or sensitive deficits, orientated, no ataxy, ocular motility examination diplopia by left abducens nerve palsy, visual function tests: both eyes 2/3 without corrections, visual field assessment is normal with light colour desaturation for red and green, ophthalmoscopy: papilledema right > left, with peripapillary flame hemorrhages, venous engorgement. angiofluoroscopy: arteriolar filling at 11 seconds, papillar leakage of contrast substance, both papilla becomes hyperflorescent on late exposures, dilated vessels. the study of visual evoked potentials (vep) has shown on the right eye latency of p100 wave 145 ms (normal value = 110 ms) and amplitude of 71mv (normal value > 5μv). to the left eye, the latency of p100 wave was 121 ms, amplitude of 58 mv. an immunologic screening demonstrate crp positive, ana positive, ac anti dna dc, ac anti sm, ac anti ro, ac anti la, canca,panca, ac anti u1rnp, ac anti gp1beta. an infectious screening was negative for ac anti hiv, ac anti hcv, ag hbs, ac anti cmv, ac anti ebv, ac anti hsv, ac anti romanian neurosurgery (2015) xxix 4: 385 396 387 doi: 10.1515/romneu-2015-0054 borrelia, ac anti mycoplasma, ac anti chlamydia, ac anti toxoplasma. theriascreening for tsh, fsh, lh, prl and gh found normal levels. at admission, cerebral ct scan was nomal (figure 1). cerebral mri with angio mri 3dtof and 2d venous tof showed: supra and infratentorial structures with normal morphology and normal mri signal, no acute cerebral lesions visible in diffusion. on t2 eg sequence no hemorrhages supra or infratentorial, ventricular system with normal dimensions, shapes, topography. selar and paraselar region, orbital region and optic nerves with normal mri signal, no vascular malformations, nomal dural sinuses. a b figure 1 normal cerebral ct scan at admission: a axial section, b sagittal section the patient was put on a low calories diet, corticosteroid therapy was initiated and consisted of a bolus methypredisolone 1g/d for 5 days, followed by an oral corticosteroid dose decreasing over three weeks), associated with acetazolamide (diamox 1g/d), antidepressant (amitriptyline), anticonvulsivant (topiramate). three weeks later headache, diplopia persist and vision become worse (1/10 on the right side and 3/10 on the leftside). a cerebral arteriography demonstrate normal arteriography on right side arterial time; filling defect of the superior sagittal sinus in the 1/3 proximal part and very week filling of the transverse right sinus on venous time. on the left side cerebral angiography was normal (figure 2) the opening pression of lumbar puncture, done with the patient in the lateral decubitus position, was 60 cm h2o, the cytochemical csf study were normal (protein concentration: 0.23 g/ l, csf glucose: 0.42 g/ l and 3 white cell /mm³). a 388 iacob, marinescu idiopathic intracranial hypertension b c figure 2 cerebral arteriography revealing venous filling defect of the superior sagittal sinus in the 1/3 proximal part (a&b sagittal view, c coronal view) trombophylic profile has revealed a heterozygote v factor leyden mutation, a homozygote mthfr and pai mutation justifying an anticoagulant treatment initiated to the patient. a new cerebral and spinal mri revealed (figure 3): a b c d figure 3 cerebral mri a coronal cerebral mri (flair): venous sinuses with gracile lumen b&c detail: cerebral mri (axial stir): dilatation and buckling of the optic nerve sheaths with increased romanian neurosurgery (2015) xxix 4: 385 396 389 doi: 10.1515/romneu-2015-0054 perineural fluid especially retrobulbar, discrete flattening of the posterior segment of the eyeballs d: cerebral mri (tof sequence) confirming filling defect of the 1/3 anterior part of the superior sagittal sinus (sss) e f g h figure 3 spinal mri efgh: spinal mri showed posterior epidural space with dilated venous branches, with mass effect on the spinal cord, that occurs pushed anterior on sagittal t1/t2 sequences cervico-thoracal and thoracic (arrows) a week after, headache increased and the patient was transferred and operated to the neurosurgery department. a lomboperitoneal shunt with a variable pressure medtronic valve was performed. at operation the opening pression of lumbar puncture, done with the patient in the lateral decubitus position was 85 cm h2o. two months after, the patient general condition improved: he was without headache, abducens palsy and the visual field assessment, ocular motility examination, ophthalmoscopy, visual evoked potentials were normal. the peculiarity of this case lies in the progressive emergence of a severe idiopathic intracranial hypertension syndrome at a young male, age of 20 years, obese recently instaled, not leated to a endocranial cause, with normal hormonal tests, to which trombophylic profile has revealed a heterozygote v factor leyden mutation, a homozygote mthfr and pai mutation; also the opening pression of lumbar puncture, done with the patient in the lateral decubitus position, was initial 60 cm h2o and at operation 85 cm h2o. the medical treatment failed, but lombo-peritoneal shunt with a variable pressure medtronic valve was beneficial. discussion idiopathic intracranial hypertension – iih occurs in about 1-2 per 100,000 people, each year, with severe visual loss in 10-30% of patients, at a median age of 20-45 years and affects women four to nine times more frequent than men (6, 12, 13). in young obese women, the incidence of iih has been shown 390 iacob, marinescu idiopathic intracranial hypertension to reach 20 cases per 100,000 (1, 2, 13, 14). although this condition has no genetic or ethnic predilection, studies have shown a higher prevalence of iih in overweight and obese people (1, 2, 15). historical considerations (10, 11, 16, 17) 1893 quincke heinrich (18) is credited with the first report of iih, wrong referring to serous meningitis 1904 nonne max (19) introduced the term "pseudo-tumor-cerebri" to define those patients in whom no tumour was found, but a disease mimicking a brain tumor was described 1937 dandy walter (20) identified the diagnostic criteria for iih and introduced subtemporal decompressive surgery in the treatment of this disease 1949 ventriculo-peritoneal shunts were first used and were later replaced in 1971 by lombo-peritoneal shunts, with better results 1954 sir charles symonds (21) suggested middle ear infection as a cause of venous sinus thrombosis and otitic hydrocephalus 1955 same condition was renamed "benign intracranial hypertension" by foley, cited by (11) 1969 buchheit, cited by (16), introduced the term idiopathic intracranial hypertension, replacing the term ‘benign intracranial hypertension’, abandoned due to visual disturbances. 1989 the terminology of this disease was revised to "idiopathic (of no identifiable cause) intracranial hypertension" 1988-1993 optic nerve fenestrations – first described in 1871 were made after negative reports on shunting in the 1980s several conditions have been associated with iih (2, 3, 5, 10, 11, 15, 22) obesity: obese women of childbearing age are more likely to the disorder due to elevate intraabdominal pressure, venous and even intracranial venous pressure. in our case obesity was recently instaled, not leated to a endocranial cause, with normal hormonal tests. onset of menstruation (menarche) pregnancy at any stage medications (no fully clarified causal relation with this disorder) including: highdose vitamin a > 100,000 u/day see isotretinoin for acne, long-term antibiotherapy with penicillin, cyclosporine, minocycline, tetracycline, nalidixic acid, nitrofurantoin, carbidopa, levodopa, indomethacin, ketoprofen, corticosteroids topical and systemic, phenytoin, growth hormone, oral contraceptives, tamoxifen, lithium and anabolic steroids diseases such as: addison, cushing’s, behcet's (23), polycystic ovary syndrome, systemic lupus erythematosus, multiple sclerosis, herpetic encephalitis, reye syndrome, sleep apnea, chronic kidney disease, chronic respiratory insufficiency, familial mediterranean fever or others disorders, such as iron deficiency, anemia, uremia, thrombocytopenic purpura, hypothyroidism, hypoparathyroidism, psittacosis, metabolic, toxic causes disorders of cerebral venous drainage: secondary thrombosis due to coagulopathy, relative stenosis due to a venous flow anomaly or even extravascular tumors that may impare due absorption of csf; increased venous red romanian neurosurgery (2015) xxix 4: 385 396 391 doi: 10.1515/romneu-2015-0054 blood cell (rbc) aggregation and relatively elevated fibrinogen concentrations. to explain the pathogenesis of iih, starting from 4 evidences: a high rate of occurrence in obese women during the childbearing years, csf outflow has reduced conductance, normal ventricular size, no hydrocephalus and no histologic evidence of cerebral edema, several theories have been advanced, generating pathological conditions acting simultaneously as follows: (1-3, 11, 13, 24-26) the increased production of cerebrospinal fluid was the first hypothesis to be proposed, but later dismissed following experimental data (27) the increased resistance to cerebrospinal fluid absorption (13, 24) the increased blood flow to the brain or cerebral tissue was suggested using phase contrast mra studies and biopsy samples. iih is only an incomplete intracranial hypertension syndrome initial: increased intracranial pressure is very important, up to 60–80 mmhg, but the brain vascular auto regulation compensates the increase in intracranial pressure and maintains cerebral blood flow (24) restricted venous drainage, by narrowing or stenosis of two large sinuses in the brain low grade stenosis of the sss and transverse sinus a condition which could be an effect or a cause of iih: raised intracranial pressure causes venous narrowing in the transverse sinuses, resulting in venous hypertension (raised venous pressure), with decreased cerebrospinal fluid resorption via arachnoid granulations and further lead to a rise of intracranial pressure and cerebral oedema (4, 17, 28-33) obesity increases intra-abdominal pressure, raises cardiac filling pressures and impedes venous return from the brain due to the valveless venous system that exists from the brain to the heart, with a subsequent elevation in intracranial venous pressure, chronic interruption of the axoplasmic flow of the optic nerves and ensuing papilledema as a consequence of this pressure, leading to irreversible optic neuropathy (2) iih diagnosis (1, 3), is based on the criteria devised by dandy in 1937 (20) and subsequently modified by: smith 1985 (34) replaced ventriculography with ct scan digre and corbett 2001 (3) added the requirement that the patient is awake and alert, no other cause for the raised icp is found, including exclusion of venous sinus thrombosis as an underlying cause friedman and jacobson 2002 (35) mr venography is only required in atypical cases: men and woman with normal weight age over 44 years, prepubertal children. the lumbar puncture should be performed with patient lying sideways current diagnostic iih criteria (1-3, 5, 15, 29, 35, 36) require the following: 1. signs and symptoms of intracranial hypertension syndrome moderate to severe headaches in 92–94% of cases, revealing, progressive, starting retroorbital, worsening with eye movement, generalized in character and throbbing in nature, especially in the morning or during 392 iacob, marinescu idiopathic intracranial hypertension physical activity; exacerbated by coughing and sneezing radicular pain uncommon symptom, usually in the neck and shoulders nausea, vomiting dizziness pulsatile tinnitus in one or both ears (64– 87%), synchronous with the pulse (37) visual disturbances (80 % of cases): blurred or distortion (metamorphopsia) of central vision caused by macular wrinkling and subretinal fluid spreading from the swollen optic disc, often predominantly orthostatic, initially in the periphery, in the nasal inferior quadrant but progressively towards the center of vision; loss of color vision; visual obscurations affecting one or both eye – seconds lasting episodes or blindness in 30% of cases; photopsia light flashes; sudden visual loss in 91% of cases due to ischemic optic neuropathy or a retinal vascular occlusion associated with the papilledema; diplopia by abducens paly uni or bilateral. rarely, patients presenting with increased icp with related optic nerve edema may be asymptomatic. visual acuity is usually normal until significant peripheral visual field loss with progressive postpapilledema by optic atrophy has occurred (23). in children, numerous nonspecific signs and symptoms may be present: numbness of the extremities, generalized weakness, loss of smell and coordination; rarely third, fourth or even facial nerve nerve palsy uni or bilateral may appear (15, 35), papilledema in addition to subretinal hemorrhages are poor visual prognostic signs. uncontrolled papilledema results in progressive peripheral visual field constriction or nerve fiber bundle defects (11). 2. normal neurological examination excepting diplopia by abducens palsy, uni or bilateral 3. the patient is awake and alert 4. normal cranio-cerebral and spinal investigations (1-3, 36, 38-42) ct with and without contrast, angio-ct venous time emmergency mri including the following sections: native in sagittal t1, axial: t2 flair, diffusion t2*;with contrast (gadolinium)t1 fat sat on orbits, axial cuts t1 on the brain; using axial and coronal sections 2 mm thick centered on orbits fse t2 mr venography, a cerebral angio mrv with gadolinium and manometry to exclude the possibility of an intracranial mass, a cerebral venous sinus thrombosis, venous sinus stenosis/obstruction or a dural fistula, to explain physiopathology or even for therapeutic interest to implant a stent (4, 5, 15, 32, 35). iih commonly presents with: normal or small (slit-like) and symmetric lateral ventricles, tortuous optic nerves, dilatation and buckling of the optic nerve sheaths with increased perineural fluid (42), minimal flattening of the posterior segment of the eyeballs, bulging optic discs, possible moderate to severe smooth-walled venous stenosis affecting the longitudinal or transverse sinus; "empty sella sign" (flattening of the pituitary gland due to increased pressure) and enlargement of meckel's caves (41). occasionally: t2 signal intensity of the optic nerve, discreet ptosis of cerebellar tonsils romanian neurosurgery (2015) xxix 4: 385 396 393 doi: 10.1515/romneu-2015-0054 (40). follow-up mri or ct scans may be needed to rule out hidden cancer. 5. increased opening pression of lumbar puncture, performed with the patient in the lateral decubitus position, csf pressure > 25 cmh2o with normal biochemical and cytological composition of csf 6. no other explanation for the raised intracranial pressure as metabolic, toxic or hormonal in addition to iih diagnostic criteria the following investigations should be performed (1-3, 11, 15): visual function tests, visual field assessment, ocular motility examination, ophthalmoscopy (funduscopy) are mandatory to diagnose and monitories patients with iih. at ophthalmoscopy: papilledema is seen in 95% of cases, without correlation with visual impairment severity, absent or unilateral especially in young children, sometimes bilateral, asymmetric; peripapillary flame hemorrhages, venous engorgement, hard exudates, telangiectatic vessels on the disc surface, optociliary shunt veins. chronic papilledema is associated with optic disc pallor, paton lines (arc-shaped retinal wrinkles concentric with disc margin) along the temporal side of inferior pole of disc. late chronic optic atrophy can also be seen: decreased visual acuity with significant peripheral visual field loss especially in the inferior nasal quadrant of the visual field, diffuse pallor of disc and absence of small arterial vessels on surface are noted, with very little disc elevation. disc margin in the upper and lower poles and nasal margin is obscured by some residual edema in nerve fiber layer and gliosis that often persists even after all edema has resolved. in general the impact of idiopathic hic on visual function is usually appreciated by repeated studies of the visual field, also by altered visual evoked potential (vep) see our case too (41). blood tests to patients with iih (1, 2, 5) are necessary for ruling out systemic lupus erythematosus, collagen-vascular diseases, to identify the procoagulant profile, etcetera. they include: complete blood count, erythrocyte sedimentation rate, serum iron, iron-binding capacity, full procoagulant profile regardless to those patients of previous history of thrombosis or mri including protein s, protein c, homocysteine levels, antithrombin iii, factor v leiden variant, antiphospholipid/anticardiolipin antibodies, lupus anticoagulant and platelet aggregation studies; also antinuclear antigen (ana) profile (eg, anti-dsdna and anti-ssdna), lyme screening test enzyme-linked immunosorbent assay elisa to those patients who have a history of exposure to lyme in areas of endemic disease. cerebrospinal fluid studies (2, 11) include the following: opening pressure, white blood cell and differential counts, red blood cell count, total protein, quantitative protein electrophoresis, glucose, bacterial culture and sensitivity, cryptococcal antigen especially in patients with hiv, syphilis markers eg, rapid plasma reaginrpr, tumor markers and cytology (in patients with a history of cancer or with clinical features suggesting occult malignancy) ihh treatment goals are (2, 3, 15, 23, 31, 39, 43, 44): the prevention of visual loss and 394 iacob, marinescu idiopathic intracranial hypertension blindness, symptom control, weight loss, fluid or salt restriction. medical treatment (1-3, 7, 43, 44) is based on: acetazolamide (diamox) for six months in conjunction with a low-sodium weightreduction diet modestly improved vision, reduced intracranial pressure, improved quality of life and reduced papilledema; furosemide; digoxin (reduces csf production by as much as 78% in humans, probably by inhibiting the na-k-atpase pump); analgesics: primary headache prophylaxis with antidepressants (amitriptyline), anticonvulsivants (topiramate); corticosteroids – as in our case is usefull especially in patients with papilledema (reducing csf production by as much as 78% in humans, probably by inhibiting the na-katpase pump binder). repeated lumbar punctions to control icp should be abandoned due to questionable results and infectious risks (11). for patients with raised icp due to severe transverse sinus stenosis, angioplasty and venous stenting across the stenosis, under general anesthesia, may improve csf resorbtion, decrease and even cure iih symptoms as well as papilloedema (28, 38, 45, 46). surgical treatment of iih (1-3, 43) is recommended if: medical therapy proves unsuccessful or is not tolerated, vision deteriorate; as in our case. in the absence of randomized controlled trials, surgical treatment include: shunting – lomboperitoneal or ventriculo-peritoneal with ventricular cateter inserted stereotactically preferably with a variable pressure valve (42, 47-51), optic nerve sheath decompression and fenestration (52, 53), gastric bypass surgery for obese patients (5). iih may resolve after initial treatment, may go into spontaneous remission (although it can still relapse at a later stage) or may continue chronically (5, 35). conclusion ihh is rare, variable in evolution, and in many cases it disappears on its own within 6 months without affecting life expectancy (2). weight loss, fluid or salt restriction, in conjunction with medical treatment, angioplasty and venous stenting across the sinus stenosis under general anesthesia and surgical treatment (shunting, optic nerve sheath decompression and fenestration, gastric by-pass surgery) are treatment alternatives. therefore a long term follow up of these patients is essential to improve the prognosis, because 10 to 25% of cases (5, 23) could be affected by recurrencies or by permanent vision loss to those patients with resistant papilledema despite treatment. references 1.bandyopadhyay s "pseudotumorcerebri". archives of neurology, 2001, 58 (10), 1699–701 2.gans m.s. idiopathic intracranial hypertension, emedicine, medscape, overview, 2014, 02.05 3.digre k.b., corbett j.j. "idiopathic intracranial hypertension (pseudotumorcerebri): a reappraisal", neurologist 2001, 7, 2–67 4.farb r.i, vanek i., et al. idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis, neurology. 2003, 60, 1418–1424 5.binder d.k., horton j.c., et al. "idiopathic intracranial hypertension", neurosurgery 2004, 54 (3), 538–51; discussion 551–552 6.iencean s.m., ciurea a.v. intracranial hypertension: romanian neurosurgery (2015) xxix 4: 385 396 395 doi: 10.1515/romneu-2015-0054 classification and patterns of evolution, j.med life 2008, 15, 1(2), 101-107 7.dhellemmes p., defoort s., vinchon m, hypertension intracrâniennebenigne: place du traitement medical, neurochirurgie 2008, 54, 717-720 8.klein o. – hypertension intracrânienne benign – pseudotumorcerebri préambule, neurochirur-gie 2008, 54, 703 9.lesler a., fattal-valevski a. – idiopathic intracranial hypertension in the pediatric population, j. child neurol 2002, 17, 745-758 10.pearce j.m. – from pseudotumourcerebri to idiopathic, intracranial hypertension, pract. neurol. 2009, 9, 353-356 11.wall m. idiopathic intracranial hypertension, neurolclin, 2010, 28(3), 593–617 12.george d. idiopathic intracranial hypertension. a prospective study of 50 patients, brain 1991, 114, 155–180 13.iencean, s.m. idiopathic intracranial hypertension and idiopathic normal pressure hydrocephalus: diseases with opposite pathogenesis?, medical hypotheses 2003, 61, 5-6, 526-528 14.radhakrishan k, ashlskog f, et al. idiopathicintracranial hypertension: subject review, mayo clin proc 1994, 69, 169-180 15.soler d, cox t, et al. "diagnosis and management of benign intracranial hypertension". archives of disease in childhood 1998, 78 (1), 89–94 16.johnston i. "the historical development of the pseudotumor concept". neurosurgical focus 2001, 11 (2), 1 17.mihorat t.h.. classification of the cerebral edemas with reference to hydrocephalus and pseudotumorcerebri, childs nerv syst. 1992, 8, 301–306 18.quincke h.i. "meningitis serosa", sammlungklinischervorträge 1893, 67, 655 19.nonne m. "uber falle vom symptom komplex "tumor cerebri" mitausgang in heilung (pseudotumorcerebri)", deutsche zeitschrift für nervenheilkunde 1904, 27, (3-4), 169–216 20.dandy w.e. "intracranial pressure without brain tumor diagnosis and treatment", annals of surgery 1937, 106 (4), 492–513 21.symonds c.p. "otitic hydrocephalus", brain 1931, 54 (3705), 55–71 22.horton jc, lawton mt, mcdermott mw "idiopathic intracranial hypertension", neurosurgery 2004, 54 (3), 538–51; discussion 551–2 23.acheson jf "idiopathic intracranial hypertension and visual function", british medical bulletin 2006, 79-80 (1), 233–44 24.iencean s.m. idiopathic intracranial hypertension. review and hypothesis of the pathogenesis, res j med and medical sciences, 2006, 1, 104–108 25.cognard c, casasco a, et al. dural arterio-venous fistulas as a cause of intracranial hypertension due to impairment of cranial venous outflow, j neurol.neurosurg.psychiatry 1998, 65, 308-316 26.bloomfield g.l, ridings p.c, et al. a proposed relation ship between raised intra-abdominal, intrathoracic, and intracranial pressure, crit care med 1997, 25, 496-503 27.binder dk, horton jc, et al. "idiopathic intracranial hypertension", neurosurgery 2004, 54 (3), 538–551, discussion 551–552 28.ahmed r.m., wilkinson m., et al "transverse sinus stenting for idiopathic intracranial hypertension: a review of 52 patients and of model predictions", american journal of neuroradiology 2011, 32 (8), 1408–14 29.biousse v., ameri a., bousser m.g. isolated intracranial hypertension as the only sign of cerebral venous thrombosis, neurology 1999, 53, 1537–1542 30.stevens s.a., stimpson j. a model for idiopathic intracranial hypertension and associated pathological icp wave–forms, ieee trans biomed eng. 2008, 55, 388–398 31.corbett j.j., digre k. – idiopathic intracranial hypertension: an answer to, “the chikenor the egg?, neurology 2002, 58, 5-6 32.king j.o, mitchell p.j, et al. cerebral venography and manometry in idiopathic intracranial hypertension. neurology 1995, 45, 2224-2228 33.karahalios d.g, rakate h.l, et al. – elevated intracranial venous pressure as a universal mechanism in pseudotumorcerebri of varying etiologies, neurology 1996, 46, 198-202 34.smith jl "whence pseudotumorcerebri?", journal of clinical neuroophthalmology 1985, 5 (1), 55–56 35.friedman di, jacobson dm "diagnostic criteria for idiopathic intracranial hypertension", neurology 2002, 59 (10), 1492–1495 36.degnan a., levy l. – pseudotumorcerebri; brief review of clinical syndrome and imaging findings, ajnr 2011, 18 37.sismanis a. "pulsatile tinnitus. a 15-year experience". american journal of otology 1998, 19 (4), 472–7 38.bracard s., schmitt e. et al. hypertension intracrânienne “bénigne”: imagerie et thérapeutiques 396 iacob, marinescu idiopathic intracranial hypertension endovasculaires, neurochirurgie 2008, 54, 6, 721-723 39.klein o., joud a., marchal j.c. – prise en charge de l’hypertension intracrânienne bénigne: analyse de la série nancéenne, neurochirurgie 2008, 54, 710-713 40.jirari m., behr j. et al. – aspects irm de l’hypertension intracrânienne idiopatique, http://pe.sfrnet.org/data/moduleconsultationposter/pdf/ 2011 41.makri s., abdellaoui w., et al. “hypertension intracrânienne idiopathique avec selle turcique vide : a propos de deux observations”, rmnsci.net 2009, 4 http://www.rmnsci.info/document.php?id=721. 42.peter p, philip n, singh y. reversal of mri findings following csf drainage in idiopathic intracranial hypertension, neurol. india 2012; 60, 267-268 43.corbett j.j., thompson hs. the rational management of idiopathic intracranial hypertension, archneurol 1998, 46, 1049-1051 44.johnson l.n, krohel g.b, et al. the role of weight loss and acetazolamine in the treatment of idiopathic intracranial hypertension, ophthalmology 1998, 105, 23132317 45.teleb m.s., cziep m.e. et al. "idiopathic intracranial hypertension. a systematic analysis of transverse sinus stenting", interventional neurology 2013, 2 (3), 132–143 46.rajpal s., niemann d.b., turk a.s. – transverse venous sinus stent placement as treatment for beningn intracranial hypertension in a young male: case report and review of the literature, j. neurosurg. 2005, 102, 342-346 47.curry w.t., butler w.e, barker f.g. "rapidly rising incidence of cerebrospinal fluid shunting procedures for idiopathic intracranial hypertension in the united states, 1988-2002", neurosurgery 2005, 57 (1), 97–108; discussion 97–108 48.yadav y.r. parihar v. sinha m. "lumbar peritoneal shunt", neurology india, 2010, 58 (2), 179–184 49.garton h.j. – cerebral fluid diversion procedures, j neuro ophthalmol. 2004, 24, 146-155 50.rosenberg m.l, corbett j.j., et al. – cerebrospinal fluid diversion procedures in pseudotumorcerebri, neurology 1993, 43, 1071-1072 51.eggenberger e.r, miller n.r, vitale s. lumboperitoneal shunt for the treatment of pseudotumorcerebri, neurology 1996, 46,1524-1530 52.keltner j.l. optic nerve shealth decompression. how does it work? has its time come? archophthamol 1988, 106, 1365-1369 53.maalouf t., george j.l. – traitement chirurgical de l’hypertension intracrânienne bénigne: fenestration des gaines du nerfoptique, neurochirurgie 2008, 54, 714-716. 16agrawalamit_delayedneurological romanian neurosurgery (2015) xxix (xxii) 1: 127 130 127 delayed neurological deterioration due to progressive pneumocephalus amit agrawal1, s. satish kumar2, umamaheswara reddy v.3 1professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2associate professor of emergency medicine, department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 3assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract: pneumocephalus can develop immediately following head trauma or clinical presentation may be delayed for days. we report a case of 35 year male whose initial ct scan brain plain small specks of pneumocephalus in left para-sellar region. however the next day he was complaining of severe headache and had multiple episodes of vomiting. repeat ct scan showed increase in the size of pneumocephalus including appearance of intraventricular air with mild cerebral edema. the patient recovered well with conservative management. the present case is a gentle reminder that in a subgroup of head injury patients, intracranial air can produce significant mass effect leading to tension pneumocephalus which can can behave like other intracranial mass lesions and causes worsening of the neurological status of these patients. key words: pneumocephalus, traumatic pneumocephalus, traumatic brain injury, basal skull fracture. introduction pneumocephalus or intracranial aerocele is collection of air in the intracranial cavity and is an uncommon complication of head injury. 1 pneumocephalus can develop immediately following head trauma or may be delayed for days before patients become clinically symptomatic. (2) in majority of the patients the size of pneumocephalus is small, behave benign and can be managed conservatively. (3) however in some cases there can be a significant amount of air collection which can lead to tension pneumocephalus behaving like an intracranial space occupying lesion and causing increase in intracranial pressure with subsequent neurological deterioration. (1, 3, 4) case report a 35 year male presented with the history of fall from motor cycle. he had transient loss 128 agrawal et al delayed neurological deterioration due to progressive pneumocephalus of consciousness for 15 minutes and multiple episodes of vomiting. there was history of nasal bleeding. there was no history of seizures. his general and systemic examination was unremarkable. at the time of examination in emergency room he was opening eyes to all, obeying commands and well oriented. motor and sensory examination was normal. there was evidence of nasal bleed. the patient underwent ct scan brain plain and it showed fracture of left temporal bone with small specks of pneumocephalus in left para-sellar region (figure 1). the patient was admitted for observation. next day morning he was complaining of severe headache and had multiple episodes of vomiting. the ct scan was repeated and it showed increase in the size of pneumocephalus including appearance of intraventricular air with mild cerebral edema (figures 2 and 3). there was no watery discharge through nose and there was no fever and meningeal signs. the patient was started on 100% oxygen and anticonvulsants. with conservative treatment he recovered completely and is doing well at follow up. figure 1 ct scan brain plain showing depressed fracture of squamous part of left temporal bone with small hemorrhagic contusion in left temporal pole and air specks in left para-sellar region and temporal region suggestive of pneumocephalus figure 2 follow up ct scan images showing significant increase in pneumocephalus; extending into subarachnoid spaces (right sylvian cistern, suprasellar cisterns, basal cisterns) and ventricles with mild cerebral edema figure 3 axial plain ct scan image bone window showing depressed fracture of squamous part of left temporal bone discussion pneumocephalus can be acute (<72 hours) or delayed (>72 hours) and occur in 3.9-9.7% of the cases of head injury. (4-6) two theories have been postulated to explain the underlying mechanism by which pneumocephalus develop after injury i.e. ball valve mechanism by dandy (a uni-directional air movement from the outside into the cranial cavity which then gets trapped) (7) and the soda bottle theory (drainage of csf leading to a negative intracranial pressure gradient which is relieved by the influx of air). (8) the air may be located in the extradural, subdural, subarachnoid, intraventricular, and intracerebral spaces (intracerebral and intraventricular pneumocephalus suggest breach in the dural and arachnoid layers). (2) the amount of pneumocephalus is usually independent of the romanian neurosurgery (2015) xxix (xxii) 1: 127 130 129 size of the defect and smaller defects are sealed easily by blood clots or granulation. (9) however a large collection of intracranial air can produce the mass-effect intracranial hypertension (tension pneumocephalus) and neurological deterioration. (3, 6) in presence of head injury, the diagnosis of tension pneumocephalus can be difficult as the symptoms and mechanism of injury may mimic other intracranial lesion (i.e. hemorrhage). (2) usual clinical features of tension pnemocephalus include headache, nausea and vomiting, seizures, dizziness, altered sensorium (2, 3, 10-12) and csf rhinorrhoea or otorrhoea. (2) plain radiographs can show the presence of pneumocephalus. ct scan of the brain is a golden standard to diagnose pneumocephalus. (2, 3, 13, 14) ct scan will allow determining the precise location of the air collection, amount of mass effect on the brain and its relationship to the basal skull fracture site or air sinuses. (2, 13, 15) depending on the site and extent of air distribution various signs have been described to identify the tension pneumocephalus (“mount fuji sign” significant quantities of air over the frontal convexities and “air bubble sign” producing characteristic multiple small air bubbles scattered through several cisterns). (2, 13, 16, 17) majority of the cases of traumatic pneumocephalus respond well to conservative management (bed rest, 100% supplemental o2, head end elevation, avoidance of positive pressure, and pain control). (2, 3, 9, 11, 18, 19) surgical intervention can be needed in patients with recurrent pneumocephalus & in patients with significant tension pneumocephalus with signs of increasing intracranial pressure. (2, 3, 6, 9, 20) surgery is aimed to remove mass effect as in cases of tension pneumocephalus and for adequate skull base defects closure (particularly large defects). (2, 6) conclusion in summary in a subgroup of head injury patients, intracranial air can produce significant mass effect leading to tension pneumocephalus. this can behave like other intracranial mass lesions and causes worsening of the neurological status of these patients. it is important to have a high index of suspicion to make the correct diagnosis as appropriate intervention will prevent morbidity and mortality in these patients. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.lee sh, koh js, bang js, kim mc. extensive tension pneumocephalus caused by spinal tapping in a patient with basal skull fracture and pneumothorax. journal of korean neurosurgical society 2009;45:318-321. 2.leong km, vijayananthan a, sia sf, waran v. pneumocephalus: an uncommon finding in trauma. the medical journal of malaysia 2008;63:256-258. 3.schirmer cm, heilman cb, bhardwaj a. pneumocephalus: case illustrations and review. 130 agrawal et al delayed neurological deterioration due to progressive pneumocephalus neurocritical care 2010;13:152-158. 4.komolafe e, faniran e. tension pneumocephalus-a rare but treatable cause of rapid neurological deterioration in traumatic brain injury. a case report. african journal of neurological sciences 2010;29:88-91. 5.kon t, hondo h, kohno m, kasahara k. severe tension pneumocephalus caused by opening of the frontal sinus by head injury 7 years after initial craniotomy--case report. neurologia medico-chirurgica 2003;43:242-245. 6.solomiichuk vo, lebed vo, drizhdov ki. posttraumatic delayed subdural tension pneumocephalus. surgical neurology international 2013;4:37. 7.dandy we. pneumocephalus (intracranial penumatocele or aerocele). archives of surgery 1926;12:949-982. 8.horowitz m. intracranial pneumocoele. an unusual complication following mastoid surgery. the journal of laryngology and otology 1964;78:128-134. 9.delgaudio jm, ingley ap. treatment of pneumocephalus after endoscopic sinus and microscopic skull base surgery. american journal of otolaryngology 2010;31:226-230. 10.markham jw. the clinical features of pneumocephalus based upon a survey of 284 cases with report of 11 additional cases. acta neurochirurgica 1967;16:1-78. 11.standefer m, bay jw, trusso r. the sitting position in neurosurgery: a retrospective analysis of 488 cases. neurosurgery 1984;14:649-658. 12.stavas j, mcgeachie re, turner da, nelson mj. symptomatic intracranial pneumatocele from mastoid sinus of spontaneous origin. case report. journal of neurosurgery 1987;67:773-775. 13.agrawal a, singh br. mount fuji sign with concavoconvex appearance of epidural haematoma in a patient with tension pneumocephalus. journal of radiology case reports 2009;3:10-12. 14.osborne h, höllt v, herz a. potassium-induced release of enkephalins from rat striatal slices. european journal of pharmacology 1978;48:219-221. 15.keskil s, baykaner k, ceviker n, işik s, cengel m, orbay t. clinical significance of acute traumatic intracranial pneumocephalus. neurosurgical review 1998;21:10-13. 16.ishiwata y, fujitsu k, sekino t, et al. subdural tension pneumocephalus following surgery for chronic subdural hematoma. journal of neurosurgery 1988;68:58-61. 17.michel sj. the mount fuji sign. radiology 2004;232:449-450. 18.dexter f, reasoner dk. theoretical assessment of normobaric oxygen therapy to treat pneumocephalus. anesthesiology 1996;84:442-447. 19.gore pa, maan h, chang s, pitt am, spetzler rf, nakaji p. normobaric oxygen therapy strategies in the treatment of postcraniotomy pneumocephalus. journal of neurosurgery 2008;108:926-929. 20.cho c-h, jung g-h, song k-s. tension suture fixation using 2 washers for proximal humeral fractures. orthopedics 2012;35:202-205. saban_fusion of axis 284 | saba et al fusion of axis with third cervical vertebra fusion of axis with third cervical vertebra: a case report n. saba1, a. rani1, g. sehgal1, rk verma1, ak srivastava1, m. faheem2 1department of anatomy, king george’s medical university, lucknow-226003, uttar pradesh, india 2department of neurosurgery, king george’s medical university, lucknow-226003, uttar pradesh, india abstract: introduction: fusion of one or more contiguous vertebral segments is usually the result of embryological failure of normal spinal segmentation. it may be associated with syndromes such as klippel-feil. fused cervical vertebrae (fcv) may also be acquired or pathologic. fcv is generally associated with disease like tuberculosis, other infections, juvenile rheumatoid arthritis and trauma. the commonest site of involvement is c2-c3. in condition of fusion the two vertebrae appear not only structurally as one but also function as one. this anomaly may be asymptomatic; however, it may also manifest in the form of serious clinical features such as myelopathy, limitation of the neck movement, muscular weakness, atrophy or neurological sensory loss. case report: we observed the fusion of axis with 3rd cervical vertebra. body, laminae and spines of c2 and c3 were completely fused on both anterior and posterior aspects, whereas the pedicles and transverse processes were not fused. foramen transversarium was present on both the vertebrae bilaterally. conclusion: this variation is noteworthy to neurosurgeons and radiologists in studying computed tomography (ct) and magnetic resonance imaging (mri) scans. key words: axis, 3rd cervical vertebra, fusion, block vertebra, foramen transversarium, variation introduction cervical vertebrae are seven in number of which c3-6 are typical, sharing similar features whereas c1 (atlas), c2 (axis), and c7 (vertebrae prominence) are atypical having different characteristic features. (1) vertebrae and intervertebral discs are one of the main manifestations of body segmentation or metamerism. (2) developmental and ossification process of c2 vertebra is the most complex among all the vertebrae. (3)fusion of one or more contiguous vertebral segments results from the embryological failure of normal spinal segmentation. the incidence is 0.4% to 0.7% with no sex predilection. (4) recent studies have documented associations between fusion of the cervical vertebral column and craniofacial morphology, romanian neurosurgery (2016) xxx 2: 284-288 | 285 including head posture in patients with severe skeletal malocclusions. this finding is expected to have importance for diagnostics and elucidation of etiology and thereby for optimal treatment. (5) skeletal abnormalities of cervical region or in cranio-cervical region are of interest to the anatomists, neurosurgeons radiologists and even orthodontists. (6) block vertebrae, formed after fusion of adjacent vertebrae is a condition which has embryological importance and clinical implications. since the fusion of cervical vertebrae 2nd with 3rd has a clinical importance, we need to emphasize the importance of multidisciplinary approach to help establish the precise occurrence of this congenital anomaly for preventing any serious damage such as osteoarthritis by early diagnosis and treatment. case report during routine survey of bones in the department of anatomy, king george’s medical university, lucknow, uttar pradesh, india, it was observed that the axis was fused with 3rd cervical vertebra. features of this block vertebra were analyzed and the specimen was photographed from different aspects. body, laminae and spines of c2 and c3 were completely fused on both anterior and posterior aspects. a ridge was noted on the dorsal surface of fused arches. joints between the inferior articular facet of c2 and superior articular facet of c3 displayed synostosis bilaterally (figures 1 and 2). diameters of foramen transversaria were measured from supero-lateral aspect of c2 and inferior aspect of c3. the diameters of foramen transversarium of c2 on right and left side were 5.5 mm and 5.0 mm respectively while of c3 vertebra was 6.0 mm on right side and 6.5 mm on left side. the pedicles and transverse processes were not fused (figure 3). figure 1 photograph showing complete fusion of body of c2 and c3 from anterior aspect figure 2 photograph showing complete fusion of laminae and spines of c2 and c3 from posterior aspect, presence of ridge on dorsal surface of fused arches (arrow 1), bilateralsynostosis between inferior articular facet of c2 and superior articular facet of c3 (arrow 2), foramen transversarium is seen in c2 vertebra superolaterally (arrow 3). 286 | saba et al fusion of axis with third cervical vertebra figure 3 photograph showing non-fusion of pedicles and transverse processes of c2 and c3 in left lateral aspect discussion in condition of the fusion of cervical vertebrae, two vertebrae appear not only structurally as one but also function as one. (7) it is important to identify the cause of fcv i.e. congenital, acquired or pathologic. embryologically, c2-c3 fusion was explained as improper separation of adjacent somites or their associated mesenchyme. (8) also it was found to be due to non-segmentation of primitive sclerotome.(9) in a condition known as chorda dorsalis, congenital fused cervical vertebra is one of the primary malformations believed to be due to defects during the development of the occipital and cervical somites. between 3rd to 8th weeks of embryonic life, cartilaginous framework of a vertebra is formed from paraxial mesoderm. (10) congenital fusion of two or more cervical vertebrae as seen in klippel-feil syndrome was believed to result from faulty segmentation along the embryos developing axis during weeks 3-8 of gestation. (11) cause of this anomaly is often a combination of environment and genetics which occurs during the third week post-conception. it has been described as an autosomal dominant condition. mutation in pax gene and notch signaling pathway and a chromosomal inversion inv (8) (q22.2q23.3) causes familial klippel-feil syndrome. (9) this syndrome was also hypothesized to result from embryological subclavian artery supply disruption sequence. (12) it was suggested that decreased local blood supply during third to eighth week of development may be a causative factor4. absence of the joints between articular facets in the fused vertebrae suggests failure of normal development and differentiation of vertebrae (i.e. fusion at the pre-cartilaginous stage of vertebral development). independent pedicle, transverse process and ridge on dorsal surface of fused arches suggest normal initial development followed by fusion. acquired fcv is generally associated with diseases like tuberculosis, other infections, juvenile rheumatoid arthritis and trauma. cause of these abnormalities may be multifactorial which also includes the role of certain drugs like thalidomide, lovastatin and progestin/estrogen on the developing fetus. the present case is very much similar to some previous studies in which the body, laminae and pedicles of c2 and c3 were completely fused on both anterior and posterior aspects. (1, 6) but in our case the pedicles were not fused while spines of the two vertebrae were fused on both anterior and posterior aspects. this anomaly may be romanian neurosurgery (2016) xxx 2: 284-288 | 287 asymptomatic, may appear with manifestations of serious clinical features such as myelopathy, muscular weakness, atrophy and neurological sensory loss or may be associated with syndromes such as klippelfeil in the form of limitation of neck movement. (7) the orthodontist may be the first person to detect cervical spine abnormalities as they are asymptomatic until adolescence or young adulthood and early diagnosis is based on incidental radiographic findings. symptoms vary according to the extent of pathology and may result in severe neck pain, decreased neck mobility, muscular weakness or sensory deficits of both upper limbs and sudden unexpected death. (6) normally aligned congenital synostosis of c23 is rarely associated with a junctional problem, whereas a kyphoticsynostosis is associated with a caudal junctional problem.(13) persons with klippel-feil syndrome and cervical stenosis may be at increased risk for spinal cord injury after minor trauma as a result of hypermobility of the various cervical segments. cervical spondylosis, disc herniation and secondary degenerative changes are more at levels adjacent to fused vertebra. there is increased incidence of osteophyte formation in the adjacent levels in cervical fusion. neurological signs and symptoms are variable, depending on the degree of pathology. another syndrome associated with this anomaly is wildervanck syndrome, characterized by klippel–feil (kf) deformity of the cervical spine in association with abducens palsy with retracted bulbi and hearing loss. the main clinical consideration of this deformity is a difficult airway due to the short, thick and immobile neck secondary to fused cervical segments, which compromises bag and mask ventilation if airway management is required. (14) persons with klippel-feil syndrome may be at high risk for developing a transient neurolgoic deficit due to cervical spinal cord injury following minor trauma, as these subjects are particularly prone to hyperextension trauma. conclusion fusion of axis and third cervical vertebrae is a rare and unusual finding which is clinically significant. this variation is noteworthy to neurosurgeons and radiologists in studying computed tomography (ct) and magnetic resonance imaging (mri) scans. it is of equal significance to the anaesthetists doing endotracheal intubation as in persons with block vertebra in cervical region hyperextension may precipitate disc prolapse. if cisternal puncture or lumbar puncture is to be done, we should look for possibility of block vertebrae in cervical and lumbar regions respectively. acknowledgement i would like to thank the faculty of the department of anatomy, king george’s medical university, uttar pradesh, lucknow, india and my husband for providing necessary help and valuable suggestions. correspondence dr. noor us saba department of anatomy, king george’s medical university, lucknow-226003, uttar pradesh, india e-mail: noorussaba83@gmail.com phone (mobile): 91-9368480101 288 | saba et al fusion of axis with third cervical vertebra references 1.wazir s, mahajan a. fusion of axis with third cervical vertebraea case report. indian journal of fundamental and applied life sciences. 2011; 1(4): 164-166. 2.standring s. gray’s anatomythe anatomical basis of clinical practice. 40thed. churchill livingstone; 2008.p 720-721. 3.pate d. normal radiographic differences between the adult and pediatric cervical spine.dynamic chiropractic.2012; 30(4). 4.solan s. fused axis vertebrae with a third cervical hemivertebrae a rare case report.iosr journal of dental and medical sciences. 2013; 10(4): 83-85. 5.sonnesen l.associations between the cervical vertebral column and craniofacial morphology.international journal of dentistry.2010; 2010. 6.yadav y, goswami p, bharihoke v. cervical vertebra synostosis (c2-c3) a case report, american journal of medical case reports. 2014; 2(6): 120-122. 7.erdil h, yildiz n, cimen m. congenital fusion of cervical vertebrae and its clinical significance.j anat. soc. india. 2003; 52(2): 125-127. 8.kaplan km, spivak jm, bendo ja. embryology of the spine and associated congenital abnormalities: review article. the spine journal.2005; 5: 564-576. 9.kulkarni v, ramesh br. a spectrum of vertebral synostosis. international journal of basic and applied medical sciences. 2012; 2(2): 71-77. 10.moore kl, persaud tvn, torchia mg. the developing human: clinically oriented embryology in skeletal system. 9th ed. elsevier.new delhi; 2013.p348350. 11.vaidyanathan s, hughes pl, soni bm, singh g, sett p. klippel-feil syndrome – the risk of cervical spinal cord injury: a case report. bmc fampract.2002; 3: 6. 12.tiwari a, chandra n, naresh m, pandey a, tiwari k. congenital abnormal cervical vertebrae–a case report.j anat. soc. india. 2002; 51(1): 68-69. 13.moon ms, kim ss, lee bj, moon jl, lin jf, moon yw. radiographic assessment of congenital c2-3 synostosis. journal of orthopaedic surgery. 2010; 18(2): 143-7. 14.schisler t, huttunen h, tang r,vaghadia h. ultrasound-assisted spinal anaesthesia in a patient with wildervanck syndrome and congenital abnormalities of the lumbar spine. british journal of anaesthesia.2012; 109(2): 290-291. 20_jagadalerr_dumbell romanian neurosurgery (2015) xxix 3: 363 367 363 dumbell hydatid disease of spine with posterior paraspinal muscle involvement ranjeet ramesh jagadale1, kanicka yashi2, umamaheswara reddy v.3, amit agrawal4 1consultant radiologist at max superspeciality hospital, maharastra, india 2kasturba medical college hospital, manipal, karnataka, india 3assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 4professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: spinal hydatid disease is a rare form of hydatid disease caused by the larval form of echinococcus granulosus (e. granulosus). dogs are primarily the definitive hosts of e. granulosus with man and sheep serving as intermediate hosts. spinal hd contributes to approximately 45 % of all skeletal hydatid disease cases. spinal hd is perhaps the worst form of parasitic infestations associated with morbidity requiring surgical correction. braithwaite and lees have classified spinal hydatids into five types (1) intramedullary (2) intradural extramedullary (3) extradural intraspinal disease (4) vertebral hydatid (5) paravertebral hydatid. when hydatid disease from spinal canal extends into retroperitoneal space through the neural foramen, it gives dumbell formation (similar to nerve sheath tumors). symptoms of hydatid are mainly due to compressive effects of the cyst, low back pain accompanying motor weakness, sensory disturbances, bowel and bladder disturbances and cauda equina syndrome. extensive vertebral hydatidosis can cause fractures of vertebrae. serology tests are used in diagnosing suspected cases of hydatid disease. mri with soft tissue detail is more preferable than other modalities in diagnosing spinal hydatid. successful treatment of spinal hydatid disease necessitates adequate neuroimaging evaluation, careful surgical removal without spillage of cystic components and adding adjuvant chemotherapy in few cases is the mainstay of treatment. sometimes when it is difficult to retrieve all the cysts in toto, debulking is advised. key words: spinal hydatid, dumbell hydatid, echinococcosis. introduction spinal hydatid disease is a rare form of hydatid disease caused by the larval form of echinococcus granulosus (e. granulosus). (14) dogs are primarily the definitive hosts of e. granulosus with man and sheep serving as intermediate hosts. hence, the disease is prevalent in sheep-rearing communities. (1-4) hydatid disease in man begins with ingestion of ova-contaminated water or food. the egg hatches in the intestines and the larvae migrate into the lungs and liver via the portal venous system. hydatid commonly affects liver followed by lung, cns and spine. osseous hydatid accounts for approximately 0.5 4 % 364 jagadale et al dumbell hydatid disease of spine with posterior paraspinal muscle involvement of all cases. (4) spinal hd contributes to approximately 45 % of all skeletal hydatid disease cases. (5) thoracic region is commonly affected in hydatid disease followed by cervical and lumbar regions. (3, 5, 6) we report a case of dumbell spinal hd of the lumbar region which had paraspinal cystic component and was effectively managed by laminectomy and facetectomy. case report a 64-year-old diabetic man presented with complaints of painful swallowing for three days, epigastric pain radiating to back, abdominal pain accompanied by bilious vomitus and urinary retention. abdomen was soft on palpation. however, there was severe tenderness in epigastric region and a palpable swelling was noticed in the back which was soft in consistency. neurological assessment of the lower extremities revealed 4/5 power in bilateral lower limbs, bilateral +1 knee reflexes, areflexia of bilateral ankle joints and bilateral babinski sign positive. additionally, sensory system was intact in both limbs and there were no cerebellar signs. laboratory investigations revealed hyponatremia, raised erythrocyte sedimentation rate, leukocytosis and elevated amylase and lipase. chest x-ray showed minimal left pleural effusion with basal consolidation. abdominal usg showed bulky pancreas with increased echogenicity of the surrounding fat, no necrosis, no fluid collections and a retroperitoneal cystic lesion. ultrasound of back revealed a cystic lesion (figure 1). magnetic resonance imaging of the lumbar spine revealed hydatid disease of the retroperitoneum, spinal canal and paraspinal muscles and a diagnosis of acute pancreatitis, dumbell hydatid cyst with paraspinal component was made (figure 2 and 3). the patient was initially managed symptomatically with intravenous normal saline, oral nystatin drops and antibiotics. besides, patient was catheterized to relieve urinary retention. posterior paraspinal exploration of the swelling with laminectomy and facetectomy was done and cysts were extracted carefully (figure 4). the procedure was successful and a sample was taken for histopathology to confirm diagnosis (figure 5). post operative period was uneventful. surgery for retroperitoneal component was planned on a later date. the patient was discharged on mebendazole 1gram daily for 3 months. on follow up, patient showed improvement in power and reflexes of bilateral lower limbs. figure 1 ultrasound image of paraspinal region showing numerous round cystic lesions (daughter cysts) figure 2 axial t1 and t2 (a,b,c) images showing daughter cysts in intradural space displacing the nerve roots which are seen to extend through neural foramina to paravertebral space. numerous daughter cysts are also seen in the paraspinal muscles to the left. axial t1w contrast image showing peripheral enhancement of the cysts and enhancement of adjacent muscles romanian neurosurgery (2015) xxix 3: 363 367 365 figure 3 sagittal and coronal t2w weighted images showing crumpled membranes and daughter cysts figure 4 intraoperative picture showing removal of rounded glistening transparent daughter cysts figure 5 histopathology (a, b, c) showing cyst wall and multiple daughter cysts discussion spinal hd is perhaps the worst form of parasitic infestations associated with morbidity requiring surgical treatment. (5) because of its aggressive nature it is compared with locally aggressive neoplasms and the mortality is approximately 50% after onset of symptoms. (2, 4-6) braithwaite and lees have classified hydatids into five types (1) intramedullary (2) intradural extramedullary (3) extradural intraspinal disease (4) vertebral hydatid (5) paravertebral hydatid. when hydatid disease from spinal canal extends into retroperitoneal space through the neural foramen, it gives dumbell configuration, (similar to nerve sheath tumors). (7) symptoms of hydatid are mainly due to compressive effects of the cyst, low back pain accompanying motor weakness, sensory disturbances, bowel and bladder disturbances and caudaequina syndrome. (1, 2, 8-11) extensive vertebral hydatidosis can cause fractures of vertebrae. (3, 4) serology tests are used in diagnosing suspected cases of hydatid disease. identifying antibody to echinococcal polypeptide antigen has the highest specificity. elisa, complement fixation tests and indirect hemagglutination (iha) are other specific tests for diagnosing hydatid disease with specificity ranging from 80% to 100%. (12) imaging is more sensitive than serodiagnosis in spinal hydatid disease. to confirm elisa and iha immunoblotting (antigen 5 precipitation: arc-5) techniques can be used. however it is important to note sensitivity and specificity of this test for extrahepatic hydatid diseases is very low. spinal hydatid can be evaluated by ultrasound, computed tomography and mri, sometimes combination of all the modalities is required for achieving diagnosis and treatment. (2, 3, 6-8, 13) mri with soft tissue detail is more preferable than other modalities in diagnosing spinal hydatid. when presented with paraspinal cystic component numerous differentials like epidermoid, teratoma, dermoid, cystic hamartoma (tail gut cyst), tarlov cyst and neurenteric cysts can be considered. (5) when hydatid is involving the bone along with other tissues, common differentials to be thought are chordoma and aneurysmal bone cyst. (5) successful treatment of spinal hydatid disease necessitates adequate neuroimaging 366 jagadale et al dumbell hydatid disease of spine with posterior paraspinal muscle involvement evaluation, careful surgical removal without spillage of cystic components and adding adjuvant chemotherapy in few cases is the mainstay of treatment. (1, 3, 5, 6) sometimes when it is difficult to retrieve all the cysts, in toto debulking is advised. however it is important to note that recurrences are high in case of spinal hydatids (40-50%). follow up imaging should be performed frequently to detect the recurrences as early as possible. (1, 3, 5, 6) correspondence dr. umamaheswara reddy. v (md) assistant professor, department of radiology narayana medical college hospital chinthareddypalem. nellore-524003 andhra pradesh (india) emailmahesh.rd2112@gmail.com mobile+91 9959632228 references 1. emara km, abd elhameed d. hydatid disease of the lumbar spine: combined surgical and medical treatment– a case report. am j orthop (belle mead nj) 2007;36:e12-14. 2. joshi k, jagannath a, varma r. dumbbell shaped spinal hydatidosis. neurology india 2014;62:113. 3. neumayr a, tamarozzi f, goblirsch s, blum j, brunetti e. spinal cystic echinococcosis–a systematic analysis and review of the literature: part 2. treatment, follow-up and outcome. plos neglected tropical diseases 2013;7:e2458. 4. prabhakar mm, acharya aj, modi dr, jadav b. spinal hydatid disease: a case series. the journal of spinal cord medicine 2005;28:426. 5. bhake a, agrawal a. hydatid disease of the spine. journal of neurosciences in rural practice 2010;1:61. 6. vujović r, živković n, stanić m. spinal echinococcosis: review of the literature. materia medica 2012;28:777-779. 7. braithwaite pa, lees rf. vertebral hydatid disease: radiological assessment. radiology 1981;140:763-766. 8. berk c, ciftci e, erdoğan a. mri in primary intraspinal extradural hydatid disease: case report. neuroradiology 1998;40:390-392. 9. karadereler s, orakdögen m, kiliç k, özdogan c. primary spinal extradural hydatid cyst in a child: case report and review of the literature. european spine journal 2002;11:500-503. 10. karakasli a, yilmaz m, mucuoglu ao, yurt a. a large primary dumbbell hydatid cyst causing neural foraminal widening of the thoracic spine: a case report and literature review. international journal of surgery case reports 2015. 11. tekkök ih, benli k. primary spinal extradural hydatid disease: report of a case with magnetic resonance characteristics and pathological correlation. neurosurgery 1993;33:320-323. 12. babba h, messedi a, masmoudi s, et al. diagnosis of human hydatidosis: comparison between imagery and six serologic techniques. the american journal of tropical medicine and hygiene 1994;50:64-68. 13. doganay s, kantarci m. role of conventional and diffusion-weighted magnetic resonance imaging of spinal treatment protocol for hydatid disease. the journal of spinal cord medicine 2009;32:574. microsoft word 9.selectedabstracts.doc romanian neurosurgery (2012) xix 4: 309 – 355 309 selected abstracts the 8th international congress of the romanian society of neurosurgery 26 29 september 2012, bucharest current surgical strategies in intramedullary spinal cord ependymomas prof. jacques brotchi, m.d., ph.d. (belgium) introduction: it is well known that the gold standard treatment for low grade intramedullary spinal cord ependymomas (isce) is complete surgical removal. that should be the ultimate goal. results: our experience is based on 188 isce among 480 operated intramedullary tumors. in all cases, the surgical approach was done through the posterior midline. debulking with the cusa and gently separation of the tumor from spinal cord under magnification were the rule. complete removal has been achieved with success in 166 cases (89%) with only two recurrences. subtotal or partial removal happened in 22 (11%), most of them being patients operating first elsewhere, sometimes with complementary radiation therapy which is a nonsense and coming to us with a recurrence. in those cases, we have been faced with a lack of a clear cleavage plane. motor evoked potentials (meps) have been of great help to keep a good quality of life after surgery in patients where there was not a clear limit between the tumor and spinal cord. but when a clear plane was present between the ependymoma and spinal cord, we did not stop surgery even when meps were lost, without facing neurological motor deficit postoperatively. it means that meps are not an absolute criteria but an alarm to take in consideration. in partial removal, we had to operate again several years later, sometimes in succeeding to perform a complete removal (8 cases) but in 10 patients, we failed and they regularly have to be operated again. in two patients, the remaining bud stays stable on yearly follow-up mris. two patients have been operated recently. our follow-up runs from several months to 24 years. in 128 patients, we have a follow-up longer than 5 years. in all, we recommend a yearly mri since in two cases, even after complete removal and clean mri at 5 years, we observed a recurrence after 18 and 19 years respectively. conclusion: we should keep in mind that even after complete removal, isce may recur many years after a successful surgery. mri follow-up of those patients should never stop. in 89% isce have been totally removed. but in 11% no clear plane of delineation has tempered our surgical aggressivity to keep a good quality of life post-operatively. surgery again in recommended when those tumors regrow. 310 selected abstracts the 8th international congress of the rsn there is no indication for radiation therapy either after surgery or in recurrent isce. spinal cord hemangioblastomas. classification and surgical treatment prof. jacques brotchi, m.d., ph.d. (belgium) complete removal of spinal cord hemangioblastomas (sch) must be neurosurgeons’ ultimate goal. we have tried to draw up a simple topographic classification in order to achieve this goal with respect to patients’ post-operative neurological status. we have classified the lesions in three topographical categories based on our experience on 56 cases: a. pure intramedullary sch (n=4) b. subpial posterior and postero-lateral sch (n=40) c. small subpial lateral or anteriorsided sch (n=12--10 lateral and 2 anterior) different surgical approaches related to topographic classification were used: class a. when the hemangioblastoma was not visible we opened the posterior sulcus along the midline using the same procedure as for any other intramedullary spinal cord tumor. class b. classical “en-bloc” resection with careful dissection of the lesion from spinal cord. class c. in all the cases a tense syringomyelic cyst was present and aspirated with a 22g needle to deflate spinal cord and give an easy access to the solid nodular tumor after division of the dentate ligament and gentle rotation of spinal cord. cusa was never used, nor debulking of the tumor. surgical technique started by cutting pia all around the tumor with coagulation and division of all vessels on the way in order to perform “en bloc” resection. complete removal was achieved in all cases except in one previously operated upon twice and irradiated in another institution. improvement was observed in 29, stabilization in 25 and worsening in 2 patients. the results were closely related to the pre-operative status. patients with a good pre-operative neurological status or harboring a large cystic cavity had a better prognosis than others. radiation therapy has no place in sch. evolution of transsphenoidal surgery from microsurgery to endoscopy; the foch hospital experience prof. stephane gaillard, m.d., ph.d. (france) there is an old tradition for pituitary and skull base surgery in our department, at first by microscopic approach and since few years by endoscopic endonasal approach. since 2006, we have gone through a transition from microscope to endoscopic endonasal approach for pituitary disease and skull base tumor surgery. we submit some remarks on this transition from microscope to endoscope based on our experience about more than one thousand endoscopic endonasal procedures. from 2006 to 2011, more than 1000 endoscopic endonasal approaches for pituitary disease and skull base tumors have been performed in our department by the same senior neurosurgeon (sg). we had used a simple transsellar approach for the majority of pituitary romanian neurosurgery (2012) xix 4: 309 – 355 311 adenomas, and an extended endonasal endoscopic approach for other tumors or skull base surgery (craniopharyngiomas, meningiomas, odontoid resection…..). the endonasal endoscopic approach for pituitary adenoma surgery decrease rhinologic complications, increase the patient’s comfort by avoiding post operative nasal packing, get a better view of the intra sellar and supra sellar aeras, reach the same endocrinological results, get a better control of the invasion of the cavernous sinus, and in some cases to allow their removal. we believe it is very important to separate the two various approaches: the endoscopic endonasal trans sellar approach and the endoscopic endonasal extended approaches, and to avoid at the needless extended approaches. for the lesions localized between tuberculum sellae and the odontoid, we found an important added value to the use of an endoscopic endonasal approach. but for the lesions localized in the front of the tuberculum sellae the added value of endoscopic endonasal approaches is not evident and must be evaluated in the future in comparison with mini invasive intracranial approaches. surgical management anterior skull base and sellar meningiomas prof. madjid samii, m.d., ph.d. (germany) the complex structure of the anterior skull base and the sellar region determine the risks, associated with surgery in those areas. meningiomas are the most common tumors, involving these areas. the operative strategy and surgical approach chosen should be selected according to the precise location of the tumor and the neurological condition of the patient. the approach in itself should not be related to significant approach-related morbidity, but rather should increase the extent and safety of resection. we favour the frontolateral as the most suited approach to these region of the skull base. in the presentation we will present and discuss our experience with surgery of the anterior skull base and the sellar meningiomas and discuss our treatment strategy. surgical strategies for craniovertebral junction pathology prof. madjid samii, m.d., ph.d. (germany) the common pathological entities in the region of the craniocervical junction include congenital, developmental, inflammatory, and neoplastic abnormalities. in our series most frequent were the neoplastic lesions, both intra-and extraaxial. surgery in the region of the craniovertebral junction is related to significant risk of morbidity and even mortality. besides removal of the lesion and decompression of the lower brain stem and cervical spinal cord, surgery should avoid or treat any existing instability. all these issues will be discussed in our presentation based on our extensive experience. management of lesions in the brainstem prof. ladislau steiner, m.d., ph.d. (germany) background: the fact that the brainstem is packed with neural cell bodies and fiber 312 selected abstracts the 8th international congress of the rsn tracts, any trial to extirpate lesions at this level may result in significant deficits. objective: in the present report the imaging and clinical outcome in low grade astrocytomas, metastatic tumors, as well avms following gamma surgery (gs) has been compared with the published results obtained after microsurgery or endovascular procedure. methods: retrospective analysis of 21 astrocytomas, 53 metastatic lesions as well 85 avms located in brainstem which has been treated with gs. of 21 astrocytomas the tissue diagnosis was established only in 10 cases before gs. the tumors had been located in midbrain in 16 patients, 4 were in the pons, and 1 in medulla oblongata. the mean tumor volume was 2.5 cm³ and the mean prescription dose was 15 gy (range, 10-18). the mean volume of the metastatic lesions was 2.8 cm³ (range, 0.5-21) and have been treated with a mean prescription dose of 17.6 gy (range, 9-25). mean volume was 1.9 cm³ (range, 0.18.9) in avms and the prescription dose was 19.9 gy (range, 5-32). the mean follow up time with mri was 83.3 months (range, 24-252). results: after treatment with gs, in patients with astrocytoma, tumor disappeared in 4 (20%), shrank in 12 (60%), and progressed in 4 (20%). in metastatic cases the lesion disappeared in 7 shrank in 22, remained unchanged in 3, and grew in 5. the angiographically obliteration in brainstem avms was achieved in 50 patients (59%) and radiation induced changes were observed within 34 patients (40%). conclusion: when the risks of surgery or embolization for lesions located in the brainstem are high or there are residuals left, gs can be a treatment option especially for nidi within the brainstem parenchyma. functional preoperative planning for brain tumor surgery in critical areas francesco tomasello, md department of neurosurgery, aou policlinico “g. martino”, university of messina, italy preoperative cortical mapping is increasingly recognized as a fundamental procedure for better planning the surgical treatment of brain tumors in critical areas. different technologies are currently available to perform a pre-operative identification of functional brain areas. functional magnetic resonance imaging (fmri) is probably the most commonly used technique. fmri has a good spatial resolution, but a low temporal resolution and brain tumors may cause metabolic changes that may blur the identification of functional hypermetabolic areas. transcranial magnetic stimulation (tms) is an electrophysiological technique developed for the investigation of human cortical functions. navigated brain stimulation (nbs) is a combination of tms with 3-d mri and computer analysis using a neuronavigation system, to provide feedback on the exact position of maximal stimulation. nbs offers different advantages for brain mapping over conventional technologies including the fact that it does not passively record brain activity during voluntary patient movements. instead, nbs actively stimulates the patient’s motor cortex recording emg changes. few clinical studies have shown that preoperative nbs mapping of the motor cortex in brain tumor patients is more reliable than preoperative fmri mapping and agreed well with the gold standard intraoperative direct cortical stimulation romanian neurosurgery (2012) xix 4: 309 – 355 313 (dcs). here we reviewed our experience in pre-operative brain mapping using nbs and nbs combined with subcortical tractography and direct cortical and subcortical stimulation in patients with brain tumors including gliomas and metastases. our preliminary data, based on surgical and clinical results in a consecutive series, showed that the nbs had a clear impact on the planning and surgery by changing the indications, the approach and the possibilities of tumor resection. nbs allowed a precise mapping of the motor cortex and the visualization of its spatial relationship with the tumor. finally, comparison with dcs confirmed the spatial reliability of the pre-surgical brain mapping achieved by nbs. telovelar microsurgical approach to fourth ventricle tumors francesco tomasello, md department of neurosurgery, aou policlinico “g. martino”, university of messina, italy fourth ventricle tumors are rare lesions and represent still today a neurosurgical challenge according to the relationships with vital neural structures and tumor histotype. this presentation deals with a series of 42 patients, 27 males and 15 females with mean age of 22.5 years (range 166), harboring iv ventricle tumors both secondarily invading the ventricle and primarily growing into the cavity. in all these cases a telo-velar approach was used to enter the ventricle and to remove the tumor. the most frequent histotypes were gliomas and medulloblastomas. according to post-operative neuroradiological examination, the extent of removal was complete in 38 patients (90.5%) and subtotal in 4 (9.5%). one patient harboring a iv ventricle metastatic lesion died post-operatively. one patient developed post/operative transient vi c.n. palsy (completely recovered at 3 months follow-up). 2 patients (4.8%) had postoperative csf leakage requiring a permanent vp shunt. no significant damage of cerebellar tonsils and uvula was produced as demonstrated by intraoperative view and post-operative neuroradiological imaging. the approach allowed adequate control of lateral recesses and the rostral portion of the cavity up to the sylvian acqueduct . opening of the arachnoidal planes of the tela and inferior medullary velum and dissection of the tumor from the floor of the fourth ventricle are illustrated. tips and tricks are suggested on the basis of the author personal experience. csf pathway patency is a significant advantage of the telo-velar approach, as demonstrated by the low incidence of post-operative hydrocephalus requiring vp shunt or third ventriculostomy. since few years after its original description, telo-velar approach represents the gold standard. this series suggests that the transvermian route has no further role in the surgical strategy for these tumors. surgical strategy for the treatment of giant and complex intracranial aneurysm yong-kwang tu, m.d., ph.d department of neurosurgery, college of medicine and hospitals national taiwan university, taipei, taiwan 314 selected abstracts the 8th international congress of the rsn since the advent of many hightechnology devices in endovascular therapy for cerebrovascular diseases, the role of microsurgical clipping of intracranial aneurysm is gradually replaced by endovascular means. for instance, a wide neck aneurysm was considered as not to be a good candidate for coiling, however, nowa-days the combination of coiling and stenting technique can easily solve this problem. however, due to the high occurrence rate of compaction phenomenon, microsurgical clipping is still the treatment of choice for giant aneurysm. in some giant aneurysm with the complexity of its configuration or its surrounding anatomy, neither clipping nor coiling modality can accomplish a satisfactory treatment, then various bypass procedure with trapping of the aneurysm may be needed as the ultimate method of treatment. in the past 12 years, a total of 63 ec-ic bypass operations were done for 61 patients. one patient with a stag horn shape aneurysm at the ica bifurcation underwent two bypasses; one radial arterial graft bypass from the cervical eca to the mca and a side-to-side anastomosis of both acas at the a3 segments. another patient has multiple aneurysms of the anterior and posterior circulation underwent two ec-ic bypasses to the mca and pca. two more patients had their sta-mca bypasses failed initially underwent the second operation for graft bypass. of the 31 patients with cavernous ica aneurysm all patient has a good patent of their graft bypass and one patient experience a transient ischemic attack after the bypass surgery. of the 14 patients with their aneurysm at the supraclinoidal segment of the ica, 10 patients underwent graft bypass and 4 underwent sta-mca bypass. one patient with graft bypass has her graft occlude and two patients with sta-mca bypass had their anastomosis occlude. a second graft bypass was performed on each of these two patients with occluded sta-mca anastomosis. in this group of patients, there is no postoperative morbidity. for the patients with giant mca aneurysm, two underwent interpositional short graft bypass for the main trunk of mca, two underwent reimplantation of one of the major branch to the mca main trunk, the other one had a graft bypass. one of the two patients with interpositional graft bypass developed major stroke after the surgery and eventually died at two months after the surgery. for the posterior circulation, one patient underwent sta-mca bypass for va aneurysm and the other patient underwent occipital artery to pica anastomosis had their anastomosis occluded. the later patient has his aneurysm trapped during the surgery developed lateral medullary syndrome after the surgery whereas the former did not have his main artery trapped had no postoperative neurological deficit and is waiting for the second surgery. in this series of patients, the overall bypass patent rate is 93%. there is no mortality and four mordibity (5.1%) after the bypass surgery and trapping of the aneurysm.. in conclusion, we still need to train neurosurgeons for mastering various clipping technique in microsurgical treatment of complex aneurysm. however, with the decreasing patient volume for microsurgery, the training of a good microvascular neurosurgeon will be a dilemma. on the other hand microvascular anastomosis technique as neglected by the romanian neurosurgery (2012) xix 4: 309 – 355 315 majority of neurosurgeons will be a pertinent skill for microvascular neurosurgeons in the future. surgical treatment of the third ventricle tumors grigore zapuhlih, serghei borodin, radu safta objective: tumors of the third ventricle are among the lesions that are most difficult to treat. they pose great technical challenges, given their intimate relationships with the neural and vascular structures of the base of the brain, as well as with the hypothalamo-pituitary axis. we are going to share our experience with the treatment of this particular type of tumors. design: we report the technique, outcome and complications seen in 63 cases of third ventricle tumors operated by our neurosurgical team, in the institute of neurology and neurosurgery, from chisinau, moldova. patients/materials and methods: sixty-three patients with third ventricle tumors, including 47 tumors of the anterior third ventricle and 16 tumors of the posterior third ventricle, were operated in our institution during the period from april 2006 to may 2011. the most common types were craniopharyngiomas (21 cases), colloid cysts (16 cases) and gliomas (8 cases). for the anterior third ventricle the most usually used routes were the interhemispheric transcallosal transforaminal approach, pterional or fronto-lateral approach, and the lamina terminalis approach. most of the colloid cysts (11 cases) were removed using the fully endoscopic technique. the tumors of the posterior third ventricle, represented by the tumors of the pineal region, were approached by infratentorial supracerebellar route in 13 cases, combined suprainfratentorial approach in 2 cases, and through the third ventricle, fully endoscopically, in 1 case. results: good and excellent results were obtained in the majority of the colloid cyst cases. a zero mortality rate was obtained in this group of patients. in 14 cases the colloid content and the cyst walls were completely removed. the results were totally different in the craniopharyngioma series, where a high mortality (4 cases) and morbidity rate was observed. total excision was obtained in 12 cases of craniopharyngioma, subtotal in 7 cases and partial removal in 2 cases. all the patients received post-resection radiation therapy. five patients where reoperated because of tumor recurrence. the most devastating complications included acute hypothalamic-pituitary dysfunction, diabetes insipidus and formation of a hematoma into the tumor bed. conclusions: the tumors of the third ventricle are often histologically benign and the main goal of the surgery is safe and total removal. knowledge of the surgical anatomy of the third ventricle, high quality image diagnostic techniques, use of microsurgical techniques and neuronavigation favors the treatment of this type of tumors with good results. first experience of using ultrasound integrated neuronavigation in moldova grigore zapuhlih, andrei peciul, constanta dogaru-peciul state medical and pharmaceutical university “n. testemitanu”, neurosurgery department 316 selected abstracts the 8th international congress of the rsn objective: reliable intraoperative orientation in neurosurgery remains paramount. anatomical topographic landmarks, frame based and frameless neuronavigation, intraoperative ultrasound (ius) allow the neurosurgeon to localize the lesion and surrounding structures, to aid in optimizing the approach and achieve safe maximal resection. patients/materials and methods: recent advances in probe technology, image fusion, 3d techniques have provided significant improvements to image quality. by integrating neuronavigation and 2d ultrasound it is possible to create 3d us volumes and to navigate directly based on 3d us data. we have used a system (sonowand invite) where the 3d us volume is reconstructed from 100–200 2d images, created by making a move or tilt over the area of interest with a precalibrated and tracked us probe. the optical tracking system reads the position of the patient reference frame and the us probe. in addition to tissue images it is also possible to make images of vessels (us angiography) based on recordings of the power doppler signals from the blood stream. in our practice the main applications of intraoperative ultrasound (ius) were: neurooncology (tumour localization, tumour resection control corpus callosum glioblastoma, third ventricular craniopharyngioma, occipital anaplastic astrocytoma, recidivant vestibular schwannoma); vascular (acoa aneurysm, avm spetzler-martin grade 4), spontaneous intracerebral hemorrhages. lesion localization and planning of optimal approach: once the craniotomy has been performed, the ius can be used to localize the lesion and neuroanatomical structures such as the ventricle, falx, main vessels and to assess the brain shift (responsible factors gravity, brain swelling, loss of csf, tumour debulking). at the end of the procedure, once the dura is closed but before bone replacement, a quick ius scan facilitates assessment of early haemorrhage or hydrocephalus. resection control: in lesions with clear margins before excision, ius can be used to check if the exeresis is complete. vascular structures: power angio provides information on blood flow and vasospasm in avm and aneurysm surgery. this allows real time evidence of vessel patency or flow disruption following clipping, and facilitates identification of an aneurysm within a haematoma. results: using neuronavigation system with integrated us in our practice helps us to optimize neurosurgical treatment of the: supraand infratentorial tumours, avm, aneurisms, spontaneous intracerebral hemorrhages. conclusions: ius provides low cost real time imaging that is easy to use and has a rapid learning curve. with the future development of ultrasound technology intra-operative 3d us will be used on a daily basis in most neurosurgical departments. management of difficult tumors of spine prof. mehmet zileli, m.d., ph.d. (turkey) spine surgery has evolved in the last decades. new techniques by application of detailed knowledge of anatomy and new implants for fixation, diifcult tumors of the spine could be removed radically. especially primary tumors and solitary metastasis are amenable to extramarginal resections. romanian neurosurgery (2012) xix 4: 309 – 355 317 in this paper, the author will present his experience on spine tumors, especially primary tumor in difficult areas such as craniocervical junction and sacrum. the technical pitfalls and complications will be discussed. surgery for kyphosis prof. mehmet zileli, m.d., ph.d. (turkey) kyphosis is a difficult topic of spinal surgery and its management contains many controversies. surgical management needs consideration of different aspects of the kyphotic deformity such as neurological status, the presence of spinal cord compression, angle of the kyphosis, the quality of bone and accompanying diseases. in case of significant cord compression and neurological compromise, anterior surgery should have the priority. however, in smooth angled kyphosis and ankylosing spondylitis patients, deformity can easily be reduced by a posterior only approach. since they have no nerological deficits, and large spinal canals, most suitable patients for pedicle subtraction osteotomy are the patients with ankylosing sponylitis in lumbar kyphosis one level pedicle subtraction osteotomy (especially at l2 or l3 levels), in thoracic kyphosis multilevel osteotomies, in cervicothoracic kyphosis an osteotomy at c7-t1 level should be preferred. pedicle subtraction osteotomy is a technically demanding procedure that requires surgeons to perform meticulous technique and consider biomechanical issues to achieve satisfactory results and avoid complications. an attempt to correct the rigid fixed spinal deformity is a diffcult task and requires the capability of a highly experienced spine surgeon. although the physical outcome and patient satisfaction of surgical treatment is quite good, risks and complications shoould always be considered by both the physician and patient. sellar and parasellar meningiomas how to approach i.s. florian*, g. ungureanu*, bianca pintea**, zorinela andrasoni** *university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery cluj-napoca romania ** county emergency hospital, department of neurosurgery cluj-napoca romania objective: suprasellar meningiomas originating from the tuberculum sellae, diaphragma sellae and planum sphenoidale are uncommon. tuberculum sella meningiomas characteristically lie in a suprasellar subchiasmal midline position. occasionally meningiomas have no attachment to the tuberculum and appear to arise from the diaphragma sella; these are called diaphragmatic meningiomas. we aimed to determine relevant, clinical, imagistic, surgical and histological particularities, correlating these case specifics to the postoperative results. this study was done to evaluate the importance of the size of the lesions and early identification of the symptoms and their effect on the outcome in patients with sellar meningiomas. design: we emphasize our surgical techniques for resection of these tumors and we discuss the advantages of different approaches, depending on the size of tumor and the relationship of the tumor to the optic nerves. 318 selected abstracts the 8th international congress of the rsn patients/ materials and methods: we retrospectively analyzed our series of 78 consecutive patients, who were admitted and operated for a tuberculum sella or a diaphragma sella meningioma between 01.01.2000 and 01.07.2012 at the department of neurosurgery of county emergency hospital clujnapoca. all patients were evaluated by mri and ct scans before surgery, and tumor location, size and relation to neighboring anatomical structures were determined. we discussed the tumor’s characteristics that could influence the treatment decision and the choice of the most reliable approach. results: we encounterd 78 cases of sellar meningiomas; with dural insertion at the tuberculum sellae (40 cases), sellar diaphragm (26 cases) and planum sphenoidale (12 cases).we noted a sex ratio f: m, about 1.8, with female predominance in all age groups. the age of the patients ranged from 24 to 70 years (average 53 years), with the highest number of patients in their 50s. all our cases underwent surgery by transcranial approach; standard fronto-temporal approach was performed in 74 of cases, while in 4 of the cases a bifrontal osteotomy was preferred. the most common ophthalmic presentation was blurred vision, in 90% of cases. headache, the second most common presentation, was presented in 68% of cases. in 70 patients (90%) complete tumor removal was achieved graded as simpson 1 and 2. shortterm postoperative complications consisted in: wound infections (2 cases), hematomas (3 cases), hydrocephalus (4 cases), and transient visual alteration (6 cases). during the short follow-up period of our patients, no such recurrence was detected in any of our patients. the mortality rate was 1%. conclusions: most suprasellar meningiomas can be removed completely and safely. the most used surgical approach is the standard fronto-temporal approach, with preservation and even improvement of visual function after surgery. the pterional approach is a well-known pathway, and the direct verification of the optical nerves, the carotid arteries, the pituitary stalk, the meningioma and its relationship with the suprasellar structures represents a safer surgical decision. surgical management of sellar and parasellar menigiomas r. chinezu, a. balasa county emergency hospital, department of neurosurgery tg. mures, romania objective: sellar and paraselar meningiomas represent 4 – 10 % of all intracranial meningiomas. due to their close proximity to the arteries of the anterior circulation, anterior visual pathways, hypothalamus and pituitary stalk the have always been regarded as challenging cases. traditionally these cases have been operated via intracranial approaches (subfrontal, frontopterional, supraorbital) but advances hardware and technique have included this pathology in the indications of transsphenoidal endoscopic operations. material and method: patients operated in the past 5 years at the neurosurgery department of the targu mures clinical emergency hospital. results: a number of 30 cases have been operated for sellar and parasellar meningiomas: 13 meningiomas of the 1/3 inner sphenoid wing and anterior clinoid, 12 tuberculum sellae meningiomas, 5 romanian neurosurgery (2012) xix 4: 309 – 355 319 planum sphenoidale meningiomas. all cases have been operated by cranial approach ( subfrontal , frontopterional) the mean age of the group is 51+/17 years, sex ratio f/m is 23/7. primary symptoms were visual disturbances (loss of sight or visual impairment, diplopia), followed by convulsive seizures and personality changes. 22 cases presented increase in visual acuity, in 5 cases preservation of sight has been achieved while in 3 case patients postoperatively presented decreased visual acuity. we had 1 scalp infection that required surgical removal of the bone and later cranioplasty. in one case there was a severe thrombosis of the intracavernous carotid that resulted in the death of the patient. conclusion: microscopic intracranial approaches are a safe technique and widely used technique. endoscopic approaches have been proven to be effective in selected cases, but further studies are required. operative treatment of tuberculum sellae meningiomas ligia tătăranu*, v. ciubotaru**, d. păunescu**, adriana dediu, m. r. gorgan*, anica dricu*** *“carol davila” university of medicine and pharmacy, neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania **neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania ***university of medicine and pharmacy, craiova, romania objective: tuberculum sellae meningiomas have a close relationship with the arteries of the anterior circulation, anterior visual pathways and the hypothalamus. the authors report on a series of tuberculum sellae meningiomas, resection being achieved by different surgical approaches. methods and results: a retrospective analysis was conducted on 24 consecutive patients with tuberculum sellae meningiomas, operated on at the 3rd neurosurgical clinic, “bagdasar – arseni” clinical hospital bucharest, between january 2002 and july 2012. the mean age of the 19 women and 5 men enrolled in the study was 51 years (range 21 – 75 years). the presenting symptom was visual compromise in 83.3 % of the patients (20 cases). in addition, 25 % of the patients (6 cases) had preoperative hormonal abnormalities. the radiological evaluation was made predominantly by mri and angio mri. a frontolateral approach was used in 21 patients (87.5 %) and an endoscopic endonasal extended transsphenoidal approach was used in 3 patients (12.5 %). these approaches allowed quick access to the tumor and were minimally invasive with less brain exposure, while keeping the complications to a minimum. radical tumor removal was possible in all but 2 patients (91.7 %). postoperatively, vision improved in 19 patients (79.2 %), did not change in 4 patients (16.7 %) and worsened in one patient (4.2 %). there was no perioperative mortality. the follow-up period ranged from 3 to 85 months (median: 46 months). conclusion: in the majority of patients with tuberculum sellae meningiomas, total resection is the goal of treatment and can usually be accomplished safely, with minimal postoperative complications and morbidity. the extent and duration of visual symptoms, encasement of the anterior cerebral artery complex and size of the tumor are the important factors that influence the treatment strategies. 320 selected abstracts the 8th international congress of the rsn unilateral versus bilateral surgical approach in anterior cranial fossa meningiomas f. stefanescu, m. radoi, r. olteanu national institute of neurology and neurovascular diseases, bucharest, romania introduction: large anterior cranial fossa meningiomas arise at the cribriform plate of the ethmoid bone and the area of the suture adjoining the planum sphenoidale. these meningiomas, which are predominantely represented by olfactory groove meningiomas, cover the entire crista gali to the posterior part of the planum sphenoidale, and grow simetrically to the anterior sagittal sinus and falx or mainly to one side. material and methods: we conducted a retrospective study of 56 patients with large anterior cranial fossa meningiomas, which were evaluated and operated in the neurosurgical department of the national institute of neurology and neurovascular diseases between 2000 – april 2012. the diameter of the meningioma varied between 4.7 – 10 cm. tumors were operated on through the unilateral frontolateral (42 patients) and bifrontal approaches (14 patients). the extent of the tumor resection was classified according to the simpson classification. all the 56 patients were followed-up with annual ct or mri scans and neurologically evaluated in our clinic. the follow-up period ranged widely from 4 to 324 months (mean, 98 months). results: total tumor removal (simpson grade 1 or 2) was achieved in most of the cases, 51 patients (91%).). meningiomas operated through the bifrontal approach were entirely resected in 12 (85.71%) out of 14 cases. in patients operated through the frontolateral approach (42 patients), total tumor removal was achieved in 39 cases (92.85%). as postoperative complications, were encountered: subdural hygroma, postoperative hemorrhage, cerebrospinal fluid (csf) leak, postoperative seizures, diffuse cerebral edema and local infection. postoperative mortality was 7.14% (4 patients). in our series, tumor recurrence occurred in 4 patients (7.14%). all of them required surgery. the recurrence rate was higher in patients with tumors having paranasal extension and which were mainly operated through bifrontal approach. none of the patient underwent postoperative radiation or radiosurgery. conclusions: for the removal of large anterior cranial fossa meningiomas we used two different surgical approaches: unilateral frontolateral approach and bifrontal approach. the use of microsurgical techniques allowed total removal of the large meningiomas, with low rates of mortality and mortality. considering the operative morbidity and mortality encountered in the resection of large anterior cranial fossa meningiomas, we could conclude that, the frontolateral approach provided an important improvement compared with the bifrontal one. romanian neurosurgery (2012) xix 4: 309 – 355 321 parasagital and falx meningiomas a five years experience in bagdasar arseni hospital, neurosurgical clinic m.r. gorgan*, a.v. ciurea*, v. ciubotaru*, v. munteanu**, ligia tătăranu*, al. tascu*, a. buliman**, nicoleta diaconu**, b. ghinguleac**, v. prună** *“carol davila” university of medicine and pharmacy, **neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania our work is based on 1084 cases of meningiomas treated between 2007-2012. 151 of this cases where parasagital and falx meningioma. meningiomas are slow-growing, extra axial tumors with arachnoid cap-cell origin. there are curable intracranial tumors, only if they are completely removed,which is not always possible. most commonly located are along falx, convexity and sphenoid bone they account for 14-19% of primary intracranial tumors. the peak incidence is around 45 years of age with a sex ratio 1,8/1 for women. 1,7% of this are hystologicaly malignant. they evolve for long time asymptomatically. all these cases were initially investigated using ct scan with i.v. contrast and mri. in approximately 95% of cases we had an angio-mri. in all cases we performed an angiography, especially to see the sagittal sinus patency, but also the external carotid vascularization with the characteristic tumor blush. in more than 85 percent of cases we performed a total removal of the tumor and in the other 15% a grade ii resection on the simson scale was performed (due to large falx insertion). all patients have been cured of the prior existing seizures linked to the mass effect lesion. in 18% of cases after surgery we observed an increase of a prior existing deficit or a new one occurred. in these cases, 15% of the patients had a deficit 4 out of 5 on the asia scale after a six months period.3% of the cases had a persisting disabling deficit which required help day by day. we have records of 6 patients who died after 8 and 10 months, one of pulmonary oedema and one after myocardic infarction. conclusion: we consider for this pathology, that surgery is the best treatment followed by gamma knife terapy where required. the role of cortical mapping on surgical morbidity in rolandic area meningioma treatment planning j. ciurea, coman teodora camelia, b. bălănescu, g. grigore, a. rasina clinic hospital bagdasar-arseni, bucharest, romania objective: this study relives the role of transcranial magnetic stimulation (tms) in neurosurgical planning for meningiomas located in rolandic area of the brain. patients and method: the study included 9 cases of meningiomas in eloquent areas which were operated during the last year. there were 8 females and 1 male with age between 30-70 year old. preoperative tms was performed in all cases to give us a brain map of the rolandic area in order to improve the surgical outcome in this type of tumor. from all the 9 cases, 6 were located on the right side and 3 on the left side. in 7 cases the rolandic area was found to be displaced because of meningioma shift in comparison with the opposite side. in all cases total removal (simpson 1 and 2) was 322 selected abstracts the 8th international congress of the rsn performed. the tumor resections begin with tumor debulking in cases with rolandic area displacement in order to avoid postoperative morbidity caused by brain edema, microthrombosis, etc. in the other 2 cases the meningioma resection was performed “en bloc”. in all cases the ultrasonic aspiration (cusa) was used for tumor resection under microscopic magnification. results: from histological point of view, 5 cases were meningothelial, 2 cases transitional and 2 cases atipic meningiomas. postoperative morbidity consists in transitory controlateral hemiparesis in 3 cases and transitory aphasia in 2 cases. none of cases in which the rolandic area was not displaced presents postoperative morbidity. all 9 cases presents without neurological deficits 3 months postoperatively. conclusions: tms can be considered an alternative to the intraoperative direct cortical electrical stimulation without adverse effects and with similar results. the advantage of the tms consists in: noninvasive method, useful in preoperative planning, and an accurate preoperative evaluation of the displacement of functional areas or compression. in our opinion the tms is useful in neurosurgical planning for meningiomas located in rolandic area. the type of surgical approach depends on the rolandic area shift relived preoperatively by tms. this method avoid postoperative morbidity after total removal of the tumor. posterior cranial fossa meningiomas 5 years experience and results clinic emergency hospital “bagdasar-arseni” bucharest m.r. gorgan*, bucur narcisa**, neacsu angela**, v. pruna**, f.m. brehar*, sandu aurelia mihaela**, v. ciubotaru**, tataranu ligia gabriela*, d. paunescu**, a. tascu*, a.v. ciurea*, c. pascal**, j. ciurea**, catioara fanica cristescu**, a. buliman** *“carol davila” university of medicine and pharmacy, neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania **neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania authors presents a retrospective study based on 103 case series of posterior fossa meningiomas treated in clinic emergency hospital “bagdasar-arseni” between june 2007june 2012, in four neurosurgery departments, sharing the same methods and principles of treatment. our center in a national reference university hospital deserving about 6 million people. data was collected and analyzed from electronic data base and hospital registry. they were 20 man and 83 women with a median age of 54.5 years old. main methods of treatment consisted in: observation, open surgery, gamma-knife surgery and combined methods. 13 patients were observed for one year, and then they decided for: open surgery, 8cases, and gamma-knife surgery, 5 cases. 39 cases were treated only by gammaknife surgery and followed up after treatment for a medium interval of 43 months. 57 patients supported open surgery in one or more stages, depending on tumor size and location, 26 of them benefited too from a ventriculoperitoneal shunt, 4 in an romanian neurosurgery (2012) xix 4: 309 – 355 323 acute phase. tumor size was between 3-5 cm in 33 cases, and over 5 cm in 21 cases. 2 of this category of patients supported 2 and respectively 3 stages of resection. according to simpson scale, total resection was achieved in 20.34%, grade ii in 11.86 %, grade iii in 35.9 %, and grade iv in 28.81%. the most frequent location was petroclival area (37.86%) followed by cerebellar convexity (27.18%) and pontocerebellar angle (24.27%). most frequent pathological samples showed transitional meningioma (33.9%) followed by meningothelial (15.09%) and fibrous type (13.21%). they were 10 cases with atypical and anaplastic meningiomas (19%). in 95.15 % of cased the postoperative neurological status remained the same or improved. 5 cases (4.85%) presented neurological deterioration, 3 reversed on the follow-up period, and 2 remained permanent. one case with a giant hemifossa tumor deceased by complications related to brain stem decompression. they were 2 csf postoperative fistulas, one postoperative wound infection, two postoperative cerebellar hematomas, and 17 patients presented decompensations of previous illnesses (heart and lung). they were recorded 5 tumor re-growth in malignant meningiomas, and 4 in the non-malignant group. all cases benefited of treatment: 6 casesgamma-knife and 3 cases-open surgery. mean general follow up period was 32 months. conclusion: general results of the treatment of posterior fossa meningioma are very good in our clinic, due to homogenous neurosurgical attitude, experienced teams and adequate perioperative treatment. rate of total resection is significant affected by lesions over 5 cm diameter, and lesions located in petroclival area. modern management strategies in posterior fossa meningioma treatment b. iliescu*, s. gaivas*, ziyad faiyad*, i. poeată** *“prof. dr. nicolae oblu” clinical emergency hospital, iasi, romania **university of medicine and pharmacy “gr t popa” iasi, romania introduction: posterior fossa meningioma is the second most common tumor in the cerebellopontine angle, accounting for 10% to 15% of neoplasms in this area. unlike acoustic neuroma, posterior fossa meningioma presents a real surgical challenge. the variable location of these tumors, their usually large size at diagnosis, their frequent encroachment on neural and vascular structures, and their potentially invasive behavior are some of the criteria that make the resection of these lesions a difficult task. material and methods: 29 posterior fossa meningioma patients managed in our department in the last three years were reviewed. 24 patients underwent surgery with 26 surgical procedures. the approaches used were retrosigmoid in 16 cases, far lateral in 2 cases, subtemporal transtentorial in 3 cases, suboccipital in 2 cases and combined suboccipital supracerebellar in one case. results: gross total removal was achieved in 17 cases, with partial resection in the rest of 7 cases. in 2 cases the complete removal was possible just after a second surgical procedure. in 3 cases the subtotal removal was the planned surgical strategy due to 324 selected abstracts the 8th international congress of the rsn obvious imagistic restrains and the availability of gamma-knife adjuvant therapy. facial nerve was preserved in 79% of the cases with various degrees of dysfunction in the rest. 2 cases presented with significant cranial nerve (other than facial) dysfunction. there were only two cases of perioperative deaths and 2 cases showed radiological recurrence so far. the cases that were not operated were sent directly to gk (3 cases) and observed (2 cases). conclusion: radical extirpation of posterior fossa meningioma with the least possible morbidity requires the flexible utilization of different approaches, the choice of which should be adapted to each individual case. surgical removal was the treatment of choice of posterior fossa meningioma. however, in selected cases it was felt prudent to delay surgery. the availability of non-invasive radiosurgery brings a salutary therapeutic option for selected cases be it as a first intention treatment or as adjuvant therapy, improving the overall outcome of posterior fossa meningioma patients. upper cervical spine tumor pathology c1-c2 therapeutic attitude d. serban, n.a. calina, f. exergian, m. podea, c. zamfir spinal surgery department, i neurosurgical clinic, emergency hospital “bagdasar-arseni”, bucharest, romania surgical treatment of upper cervical spine tumors, whether they are vertebral, epidural, subdural or intramedullary, raises technical and decisional difficulties regarding the approach of the region as well as in maintaining its stability. the authors performed a retrospective study on c1, c2 spinal tumor pathology, managed surgically in the spinal surgery department of ”bagdasar arseni” clinical hospital, between january 2007 and december 2011. we included in the study 44 patients, operated for c1, c2 cervical spine tumors, 23 men and 21 women with ages between 13 and 71 years. the pathology included 24 c1-c2 vertebral tumors, 11 subdural tumors, 2 epidural tumors and 7 intramedullary tumors. presenting symptoms were cervical pain, occipital neuralgia, medullary compression syndrome, and/or cranio-spinal junction instability. the purpose of surgery was to establish a histopathologic diagnosis and to decompress the neural elements by attempting a total tumor removal as well as to stabilize the craniocervical junction in order to improve the patient’s quality of life. the approach was chosen based on tumor location, prognosis and the need for fixation. for 6 patients an anterior approach was used, for 31 pacients we used a posterior approach and 7 patients required a combined anterior and posterior approach. neurological improvement was observed in 17 patients, with a mean increase of 8 points on asia scale, 7 patients worsened immediately postoperatively with a mean decrease of 10 points on asia scale and 20 patients without neurological deficits preoperatively remained unchanged. in all cases where the craniospinal junction instability was the cause of occipito-cervical pain we noted the disappearance of pain after surgery. the development of new surgical techniques and fixation systems paved the way to a successful treatment for these romanian neurosurgery (2012) xix 4: 309 – 355 325 difficult tumors, some of them considered inoperable in the past. cranio-spinal junction tumors: a series of 24 cases a.s. iencean m.d.***, faiyad ziyad*, m. ivanov**, s. gaivas*, b. iliescu*, al. chiriac*, s.m. iencean***, i. poeata*** *“prof. dr. nicolae oblu” clinical emergency hospital, 3rd department of neurosurgery, iasi, romania **plymouth hospitals nhs trust, derriford hospital plymouth, great britan ***university of medicine and pharmacy “gr.t.popa”/“prof. dr. nicolae oblu” clinical emergency hospital, iasi, romania objective: we present our surgical experience in the treatment of 24 patients with tumors of the cranio-spinal junction that were warded between 2007-2012 in our department. design: the pathology of the craniospinal junction is complex and the tumors of this region may present diagnostic and management problems. methods: in six years we treated twentyfour patients with tumors of the craniospinal junction: eight foramen magnum meningiomas, six vertebral tumors c1/c2, four jugular foramen tumors, four cases of lower brainstem tumors and two occipital condyle tumors. all patients were explored preoperatively by mri or ct. results: the suboccipital (midline and paramedian) approach was performed in nine cases, seven of them required additional resection of the posterior arch of c1/c2. in six patients the surgical approach implied only the resection of posterior arch of c1/c2; the far-lateral approach was used in eight patients and in one case we used the transoral approach. all patients benefited by a microsurgical approach; gross total removal was achieved in 10 out of 24 cases. conclusions: the preoperative diagnosis and the operative planning are very important for the surgical handling of cranio-spinal junction tumors. the microsurgical approaches provide the best operative results. surgical approaches for the cranio-cervical junction tumours i.s. florian,* t. maior*, c. abrudan**, zorinela andrasoni** *university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery, cluj-napoca, romania **cluj county emergency hospital, department of neurosurgery cluj-napoca, romania choosing the most adequate surgical approach it is an intriguing topic not because it is a difficult region to deal with, but also because there is a place where along neurosurgeons there are other specialties that are disputing the priorities and arguing the best management to perform surgery like ent surgeons, spinal surgeons or those specialized in craniofacial surgery. the great difficulty of approaching this region consists not only in the osteomuscula ligament complex that permits stability and complex movement of the head, but also in the great number of vital neurovascular structures and their great anatomical variability. when dealing with a tumor of the cvj the selection of a certain approach is depending on several factors like tumor location, type and size, neurological and general status of the patient, and the 326 selected abstracts the 8th international congress of the rsn relation to the dura, namely if the tumor is epi or intra dural. nevertheless the surgeon’s preference and confidence for a certain approach is a factor that is less discussed, but in fact it is a decisive one. in the present thanks to the progresses in the surgical techniques, a tumor located in this region can be circumferentially approached, from anterior, antero-lateral, lateral postero-lateral and median posterior. the idea is to approach the tumor on the shortest distance, and to intersect less neurovascular structures. the different kind of approaches are presented based on the procedure, extent of exposure, common pathology, advantages offered, limitations, and risk and long-term side effects. the data presented is well illustrated by cases from the authors’ personal experience. our experience in two cases of dural arteriovenous fistulas at the craniocervical junction al. chiriac,* i. poeată**, faiyad ziyad*, n. dobrin*, a.s. iencean* *university of medicine and pharmacy “gr t popa” iasi, romania **clinical emergency hospital “prof. dr. n.oblu” iasi, romania background: dural arteriovenous fistulas (davf) at the craniocervical junction are uncommon lesions that may result in various neurological presentations. these lesions are a rare cause of intracranial subarachnoid hemorrhage (sah). methods: we performed a retrospective study on two patients with craniocervical junction davf. the clinical and imagistic dates with surgical video recordings were reviewed by the authors. the follow-up six month dates were also analyzed. results: one patient presented with meningeal symptoms due to a subarachnoid hemorrhage, and the other one had a slowly progressive cervical myelopathy (with progressive quadriparesis) associated with a single episode of lost of consciences. this last patient had a c4 – c6 davf with single or main ascending venous route into the intracranial vein. both cases were treated by surgical interventions technique. the overall clinical outcomes were good during an average follow-up period of 10 months. in particular, follow-up angiographs performed one months later revealed the complete disappearance of davf in both patients. conclusions: davf of the craniocervical junction are unusual condition characterized by important severe neurological deficits referable to this region. our experience showed that microsurgical approach of these lesions a clinical cure of the patients with their clinical improvement. our experience in chiari malformations surgical treatment a. bălasa, d. n. gherasim county emergency hospital, department of neurosurgery tg. mures romania introduction: “as described and classified over a century ago, herniation of the cerebellar tonsils more than 5 mm into the cervical spinal canal with obliteration of the cerebellomedullary cistern and obstruction of foramen magnum is the primary feature of chiari i malformation.” pathophysiology: the chiari malformation constitutes an heterogeneous and multifactorial entity, in which congenital romanian neurosurgery (2012) xix 4: 309 – 355 327 forms of isolated presentation or with a genetic background and forms of acquired etiology exist. no unitary clasification exists to this date. clinic and symptoms: one estimate based on extrapolations from a previous study suggested a prevalence of tonsillar ectopia inthe general population of approximately 3.5%. the proportion of these individuals who go on to develop symptoms is unknown. nevertheless, the disorder can be associated with significant symptomatology, risk of secondary injury due to trauma and the risk of progression and damage of the spinal cord due to associated syringomyelia. surgical treatment: the goal of surgery is to relieve cord compression and to reestablish adequate csf flow. there have been no prospective studies in which one treatment form is directly compared with another. conclusions: in light of the many theories of pathophysiology, broad clinical presentations, and multitude of surgical interventions with variable outcomes, it is no wonder that a single surgical approach does not exist. we recommend tailoring the surgical approach to treat the dominant clinical problem. early diagnosis and treatment is critical in obtaining the best outcome for the patient. the presence of syringomyelia is a sign of advanced structural abnormality, as it is associated with the presence of sensory and motor deficits, as well as with the presence of spinal deformity. the preoperative presence of deficit is a predictor of poorer neurological outcome, making a strong case for early surgical intervention. minimally invasive spine surgery: the way of the future g. tender louisiana state university, new orleans, us minimally invasive spine surgery involves surgical techniques that require smaller incisions, result in less soft tissue disruption, and involve limited surgical corridors. they are typically associated with decreased blood loss, decreased infection rates, and decreased hospital stay. historically, prof. yasargil used the operative microscope for the first time in 1976 to perform a lumbar discectomy. in the early ‘90’s, laparoscopic cholecystectomy became the method of choice for removing the diseased gall bladder. after 2000, minimally invasive spine techniques became increasingly popular. the initial operations involved simple spinal decompressions. through a skin incision of less than 2 cm in length, a system of tubular dilators was used to split the muscle fibers and allow for placement of an 18mm-diameter tubular retractor that rested on the lamina or facet of the diseased segment. the most common operation was the lumbar microdiscectomy, but other pathology, such as segmental spinal stenosis, lateral soft cervical disc herniations, or gunshot wounds to the spine with retained bullet fragments, was also addressed via this tubular retractor. later, technological advancements like better instrumentation, illumination and magnification, as well as a better understanding of the anatomical approaches, allowed for more complex operations to be performed using the minimally invasive techniques. lumbar 328 selected abstracts the 8th international congress of the rsn fusion patients were by far the main beneficiaries of these techniques. the posterior and transforaminal lumbar interbody fusions (plif or tlif) have become in recent years the preferred method in cities with advanced surgical care like new york and los angeles. other surgical techniques take advantage of new pathways to the lumbar spine. the extreme lateral interbody fusion (xlif), used at or above the l4-5 level, is indicated in patients with previous midline approaches as well as patients with segmental deformity. the presacral approach (axialif) provides similar advantages at the l5-s1 segment and has the lowest complication rate of all fusion procedures. more advanced surgical interventions, like thoracic or high lumbar corpectomies for trauma, infection, or tumor, can also be currently treated with small skin incisions and reduced postoperative morbidity. the minimally invasive spine surgery techniques are currently the fastest growing trend in the us and are employed by about 80% of the spine surgeons in the large cities with highly educated patients. it is probable that miss will become the treatment of choice for elective spine patients all across us in the near future. traumatic pathology of the thoracic and lumbar spine our perspective tiberiu maior department of neurosurgery, cluj county emergency hospital, romania objective & design: the paper presents the surgical treatment protocol in trauma pathology located in dorsal and lumbar spine area. aspects related to vertebral body surgery, lengths and type of instrumentation, reason of treatment, and pitfalls in trauma surgery are discussed. material and methods: 180 of cases were studied with at least one year post-op follow-up, operated according to the same criteria. the treatment algorithms area presented, including some representative cases of posterior approaches, and of combined (anterior and posterior) approaches. all presented cases are from the author’s personal archive and underwent surgery using the same system of stabilization and the same technique. results & conclusions: obvious advantages of the transpedicualr stabilization, ligamentotaxis and the reconstruction of the vertebral body. images of illustrated cases are presented. the advantages of the anterior approach in the tumor pathology of the spine tiberiu maior department of neurosurgery, cluj county emergency hospital, romania objective & design: this paper proposes to highlight the necessity, the advantages of the anterior approaches in spine tumor pathology. the current tendency in this field is total removal of the tumor; in this respect the “en block” resections become the gold standard, especially in primary spine tumors. as a result of the outstanding progresses in the oncological field total removal (ideal “en block) became also a standard in spine metastasis, even in multiple spine metastases. material and methods: the paper analyzes 55 complex surgeries of spinal pathology, which had as a result the total removal of romanian neurosurgery (2012) xix 4: 309 – 355 329 the tumors using combined approaches: anterior and posterior. all presented cases are from the author’s personal archive and they are representative for all regions of the spine, with special emphasize on the transition areas. results & conclusions: the present paper underlines the mandatory aspect of the anterior approaches in order to obtain a total tumor resection. meanwhile practical aspects are presented among which pitfalls, tricks and tips are considered by the author essential in performing these types of surgeries. management of brainstem lesions i.st. florian*, attila kiss**, zorinela andrasoni** *university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery, cluj-napoca, romania **cluj county emergency hospital, department of neurosurgery, cluj-napoca romania objective & design: the surgical approach of the brainstem lesions is very difficult because of high density of vital areas at this level of the central nervous system. our aim is to share the experience that we achieved in diagnosis, therapeutical protocol, and the neurosurgical approaches of brainstem lesions in the past fourteen years. materials and methods: this study consists in a retrospective analysis of 76 cases of patients diagnosed with brainstem lesions and surgically treated in our department between january 1998 and december 2011. we studied epidemiological aspects, pathological findings, clinical features, diagnosis methods, surgical approaches, and outcomes of our case series. results: from all brainstem lesions, 62 cases were tumors and 14 cavernomas. brainstem tumors represent almost 15 % of posterior fossa tumors operated in our department. our peak incidence is in the first four decades of life. gender distribution shows a slightly male predominance (35 cases). signs of intracranial hypertension, motor deficiencies and cranial nerve palsies were the main clinical findings. in each case cerebral mri was performed, with or without cranial ct scan. fourty nine patients were operated by open surgery. in all cases suboccipital craniectomy in sitting position was preferred, except in two cases of diencephalo – mezencephalic tumor the subtemporal approach was chosen. using the sitting position, in combination with a meticulous microsurgical technique, ecg, blood pressure, central venous line, endtidal carbon dioxide, and oxygen pressure monitoring, no clinical evidence of air embolism was detected. total resection was possible in 20 cases versus subtotal resection in 29 cases of brainstem tumors and we performed only drainage of hydrocephalus in 13 cases, without tumor resection. histological finding shows that the most common tumors are low grade gliomas. brainstem cavernomas represent 25 % of al cavernomas treated surgically in our department. complete surgical removal of cavernoma was successfully performed in all cases using the same sitting position. conclusions: despite of their location, many of brainstem lesions can be totally removed surgically due to their benign nature. in this case the neurosurgical treatment can have healing effect. in the presence of malignancy signs, the possibly maximum tumor resection with or without drainage of hydrocephalus can improve 330 selected abstracts the 8th international congress of the rsn rapidly the patient clinical status and it creates good conditions for the adjuvant therapy. our experience in image guided stereotactic biopsy for infiltrative cerebral gliomas f.m. brehar,* aura sandu**, m. lisievici**, m.r. gorgan** *“carol davila” university of medicine and pharmacy bucharest, faculty of medicine, department of neurosurgery, bucharest, romania **“bagdasar-arseni” emergency clinic hospital, department of pathology bucharest, romania objective: minimally invasive approaches, like stereotactic biopsy, are frequently required in many cases of infiltrative cerebral gliomas, because the invasive growth pattern precludes the gross total resection of these types of lesions. the authors present their experience in 85 cases of stereotactic biopsies performed for infiltrative cerebral gliomas. materials and methods: eighty-five patients with infiltrative, multicentric and deepseated gliomas have been included in this study. all patients underwent the stereotactic biopsy according to the standard protocols. stereotactic and neuroimagistic tools used for these procedures included the leksell stereotactic system and the software: stereotactic planning system (sps), ntps 8.2. results: the histopatological results (according to world health organization (who) classification) were: 51 cases of glioblastomas (grade iv) (60%), 7 cases of anaplastic astrocytomas (grade iii) (8,2%), 13 cases of grade ii diffuse astrocytomas (15,3%), 6 cases of grade i astrocytomas (7,1%), one case of grade ii oligodendroglioma (1,2%), 3 cases of anaplastic oligodendrogliomas (grade iii) (3,5%), one case of grade i ganglioglioma (1,2%), one case of anaplastic ganglioglioma (grade iii) (1,2%), and 2 cases of anaplastic ependymomas (grade iii) (2,3%). in 21 cases (24,7%) the immunohistochemistry has been performed in order to obtain an accurate histopathological result. in this series, the early postoperative mortality was 0%, with no cases of clinically significant hemorrhages after biopsy procedures. temporary increase of neurological deficits has been noticed in 7 patients (8,2%). conclusions in conclusion, image-guided stereotactic biopsy represents now a safe and accurate diagnostic method for infiltrative, multicentric and deep-seated cerebral gliomas. the experience of the surgical management of the intracranial vascular malformations i.st. florian*, s. trifoi**, andreea mogyoros**, zorinela andrasoni** *university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery cluj-napoca, romania **cluj county emergency hospital, department of neurosurgery, cluj-napoca, romania objectives & design: nowadays, the multimodal treatment (microsurgery, radiosurgery, interventional neuroradiology) is used to provide a more effective and less morbid therapy for the arteriovenous malformations. the purpose of this paper is to describe our surgical experience and current management of these vascular disorders, which lead to successful surgical removal in the absence romanian neurosurgery (2012) xix 4: 309 – 355 331 of endovascular preoperative embolisation, neuronavigation or intraoperative monitoring opportunities. material and methods: we report a retrospective analysis of 184 intracranial vascular malformations treated by surgical excision in our medical center between june 1996 and december 2011. from these 67% were diagnosed as avms and 33% as cavernomas. the preoperative evaluation consisted of clinical exam, ct, mri and angiography. clinical data analysis found the peak incidence in the 5th decade and a slight male preponderance was observed (55%). results: in our series the major clinical findings were hemorrhage, seizures, progressive neurological deficits, and headache and according to spetzlermarting grading system the majority of the cases were grade ii and grade iii (64%) postoperative morbidity consisted of transient neurological deficits (12%), hydrocephalus and re-bleeding. we obtained gos score of 4 and 5 in 88% of the patients. the association of intranidal aneurysms was observed in 12% of avms, and they were addressed in the same operative session. first of all the decision for the surgical treatment should take into consideration the sum of the risks of all the interventions and should be compared to the natural history of the lesions. the nonsurgical treatment has a significant impact on the patients suffering from these cerebrovascular lesions, but still has some unsolved problems. conclusion: due to the shortage of endovascular/radiosurgery facilities in our department, surgery remains the single treatment strategy to cure these lesions. even though many of the cases were admitted with a severe neurological status, a successful surgical treatment requires besides microsurgical techniques, microsurgical gestures too. our first experience in stent and stent-assisted coil embolization of intracranial aneurysms al. chiriac*, n. dobrin**, a.st. iencean**, i. poeata*** *university of medicine and pharmacy, iasi, romania **clinical emergency hospital “prof. dr. n.oblu”, iasi, romania ***„gr. t. popa” university of medicine and pharmacy, iasi, romania background and purpose: the endovascular detachable coil embolization for cerebral aneurysms treatment has become an important method witch poses a significant technical challenges, particularly in widenecked aneurysms. we present the results of our initial experiences in using a selfexpanding neurovascular stent and detachable coils in the management of wide-necked intracranial aneurysms. methods: two consecutive patients with a wide-necked intracranial aneurysm were treated by neuroform stent deploying as flow-diverting embolization and neuroform stent-assisted coil embolization. we assessed patients’ history, aneurysm morphology, indications for stenting technique, and technical feasibility and efficacy of the procedures, complications and midterm follow-up data. results: in all patients, the stent placement in the desired position with complete or nearly complete embolic efect of the aneurysms was achieved. both patients had followed a strong anticoagulation regimen immediately after procedure. in one patient, some urologic 332 selected abstracts the 8th international congress of the rsn complication had occurred with necessitate transfer to a specialized clinic. six-month follow-up demonstrated no focal neurologic sequelae in any of the patients, except slight memory dysfunction in the patient with vertebro-basilar junction aneurysm. conclusion: these preliminary data results indicate that stent-assisted coil embolization can be an easily, safely and effective technique in the treatment of intracranial wide-necked aneurysms. further studies by long-term angiographic and clinical follow-up are needed to evaluate the permanent vessel patency and long-term durability of stent-assisted aneurysm occlusion. aneurysms in children – particularities an experience of 40 cases a.v. ciurea*, a. tascu*, a. iliescu**, d. talianu**, f. brehar*, a. giovani** *carol davila university school of medicine, bagdasararseni teaching hospital, 1st neurosurgical unit, the national center for excellency in neurosurgery, bucharest, romania **bagdasar-arseni teaching hospital, 1st neurosurgical unit, the national center for excellency in neurosurgery, bucharest, romania introduction: intracranial aneurysms in children are a very rare pathology which generally appears in the literature in limited series of 15-30 cases. most cases of intracranial aneurysms in children are preponderantly congenital and often associated with other malformations such as polycystic kidney disease, aortic coarctation, ehlersdanlos syndrome, thalassemia, etc. a limited number of cases are with familial incidence. aneurysmal rupture is extremely rare in the first decade of life. the incidence gradually increases each decade and peaks in the fourth decade of life. material & method: the authors present 40 cases of children with intracranial aneurysms (0-16 y.o.), which represent 6.1% of all cases (648 cases) of intracranial aneurysms operated by the authors between january 1997 and december 2011 15 years. the mean age was 14,3 years in all literature data the median age was between 14-18 y.o. there were more boys (24 cases, 59%) than girls, like in all official data. the clinical features are dominated by headache (98%), neck stiffness (94%), vomiting (92%), focal neurological deficit (81%), an altered level of consciousness (67 %), seizures (46 %), fever (36%). the majority of patients has hunt & hess scale grade ii at admittance (21 cases, 53%). all neuroimagistic investigations were done in the first 48 hours. the anterior communicating artery aneurysm (14 cases, 35,3%), followed by middle cerebral artery aneurysms (11 cases, 26,5%) and carotid artery bifurcation aneurysms (8 cases, 20,5%) were preponderant. there was one case concerning multiple aneurysms. many aneurysms are large and giant (14 cases, 35,2%). the particularities of the microsurgical approach are: easy aneurismal dissection, no ateromatous plaques in the cerebral vessels and an easy management of brain edema via versatile anesthetic control. in these conditions the surgical timing is essential. all aneurysms were clipped directly, with non-important complications in the pediatric intensive care unit (p.i.c.u.). there was one case of preoperative mortality in our data. all cases received a romanian neurosurgery (2012) xix 4: 309 – 355 333 perfect neuro-rehabilitation therapy. in our data no embolization was performed. conclusions: intracranial aneurysms in children are very rare and were discovered and treated in neurosurgical pediatric departments. early microsurgical approach is mandatory and has excellent results (good recovery). aneurysms represent an important challenge for all neurosurgeons. quality of life and global outcome in intracranial cavernous angiomas a.v. ciurea*, a. tascu*, a. iliescu**, f. brehar*, f. stoica**, r. rizea*, h. moisa*** *carol davila university school of medicine, bagdasararseni teaching hospital, 1st neurosurgical unit, the national center for excellency in neurosurgery, bucharest, romania **bagdasar-arseni teaching hospital, 1st neurosurgical unit, the national center for excellency in neurosurgery, bucharest, romania ***carol davila university school of medicine, romania introduction: intracranial cavernomas (ic) count of 0.02 0.53% of all intracranial lesions and 8-15% of all avms. the association with avm is found in 10-30% cases. the lesions become symptomatic when the size of the lesion is bigger than 1 cm. these vascular malformations have started to be easily diagnosed with the introduction of routine mri scans. material and method: the cohort of 109 consecutive operated cases of intracranial cavernomas were admitted in the 1st department of neurosurgery of the bagdasar-arseni hospital in the period of time between january 1998january 2012 (14 years). all cases received a complex neuroimagistic diagnosis based on ct, mri & dsa angiography. the cases were operated and followed up in the bagdasararseni hospital in bucharest for a period ranging from 6 months to 9 years. the sex distribution was 55 males and 54 females aged between 1156 years old with a peak of incidence in 31 year olds. the cavernomas localization was as follows: supratentorial in 75 cases (68,8%), infratentorial in 24 cases (22,0%), deep, basal ganglia & multiple 10 cases (9.1%). the lesions were located: frontal lobe 34 cases (31.2%), parietal lobe 15 cases (13.7%), temporal lobe 23 cases (21.1%), occipital lobe 3 cases (2.7%). multiple 3 cases (2.7%), deep and basal ganglia 7 cases (6.4%) brainstem 19 cases (17.4%), and cerebellum 5 cases (4.5%). in what concerns multiple cavernomas, we proceeded with surgery only for those either manifesting mass effect or presenting with hemorrhagic attack. the clinical symptoms were characterized by seizures 70 cases (64.2%), neurological deficits 16 cases (14.6%) hemorrhage 23 cases (21.1%). a special chapter of the study was dedicated to non-operated cases. they were: 7 cases multiple lesions, 9 asymptomatic and 5 lesions deep situated. in 2 cases of deep situated lesions, the therapy with gamma-knife surgery was applied. results: in this series of 109 operated patients, the global outcome scale (gos) at 6 months was: good recovery 82 cases (75.2%), moderate disability 18 cases (16.5%), severe disability 9 cases (8.2%), vegetative state 0 cases (0%) and death 0 cases (0%). the severe disability appears especially in brainstem cavernomas, but, in time, the cases improved exponentially. 334 selected abstracts the 8th international congress of the rsn the follow-up period was between 6 months and 9 years, with a mean range of 7,6 years. out of the 70 cases exhibiting seizures, all cases were operated: in 52 cases (74,2%) we performed a lesionectomy with perifocal gliosis excision and in 18 cases (25,7%) only lesionectomy. conclusions: intracranial cavernous angiomas (cavernomas) are rare lesions characterized by epilepsy in the majority of cases or intracerebral hemorrhagic onset. when the main symptoms are seizures, the best prognosis results after the excision of the lesion and the perilesional gliosis. the neuronavigator-guided approach achieved in all cases the removal of the lesions with a good accuracy in the “target”, avoiding the post-operative deficits and improving the clinical outcome. furthermore, it avoids the discomfort of the stereotactic frame. in multiple lesions, the hemorrhagic or mass effect lesion must be managed. the option of gamma-knife surgery (gks) in cavernomas is disputed. in asymptomatic cavernomas, the best management is clinical follow-up and mri observation. twenty years of lumbar disk surgery s.m. iencean grigore t. popa university of medicine and pharmacy, iasi, romania objective: the objective of the study was to determine the 20 -year clinical outcomes of discectomy for the treatment of lumbar disc herniation. design: this report retrospectively evaluates 1500 cases of surgical lumbar discectomy performed by one neurosurgeon to evaluate the indications and efficacy of lumbar discectomy. materials and methods: only 1500 patients who underwent lumbar discectomy, based on specific objective criteria, were reviewed. diagnosis and localization of the root compression were determined preoperatively by the lumbar myelogram during the years 1989 – 1994, by lumbar computed tomographic myelography during the years 1995 – 2002 and spinal mri during the years 2003 – 2010. results: 81% patients were rated as excellent, 16% as good, 2 % as fair, and 1 % as poor. only 2,5 % patients required additional surgery due to a recurrence of herniation. 72% of the patients were able to maintain their primary occupations. conclusions: the 20-year follow-up study showed that the clinical outcomes of of surgical lumbar discectomy are very good and satisfacatory. percutaneous nucleoplasty versus open discectomy in patients with lumbar disc protrusions d. adam “carol davila” medicine and pharmacy university, “victor babes” clinic, bucharest, romania introduction: degenerative disc disease can be treated conservative or operative by many approaches. nucleoplasty by coblation is a minimally invasive procedure increasingly applied for treatment of lumbar disc herniations. material and method: during 1 year period (september 2009-september 2010) two cohorts of 80 patients each were operated by nucleoplasty and open discectomy respectively. there were not significant differences regarding sex distribution, age, or level of disease. inclusion criteria are different: mri evidence of contained disc romanian neurosurgery (2012) xix 4: 309 – 355 335 herniation £ 6 mm for nucleoplasty, > 6 mm for open discectomy. common criteria were radicular pain resistant to conservative treatment for a period of at least 6 weeks, one level protrusion, and virgin spine at the level of interest. nucleoplasty was performed in an outpatient setting, with the patient in lateral decubitus. the entry point was situated at 10-12 cm from midline. with a bipolar rf probe six channels were created in the nucleus by advancing the rf probe in ablation mode and withdrawing it in coagulation mode using coblation energy which dissolve nuclear material through normothermic molecular dissociation. open discectomy was performed in a standard fashion by interlaminar approach with foraminotomy. results: vas score was reduced at 3 months follow-up with 40% and 60% for nucleoplasty and open discectomy respectivelly, and at 1 year follow-up 60% and 78% respectivelly. all patients with coblation return to work 3 days later. most of discectomy patients remain work-off for 3 months followed by temporary retirement. results of roland-morris questionnaire show an improvement at 12 months of 60% in nucleoplasty group, and 78% in discectomy group. patients satisfaction after nucleoplasty was 73%. conclusions: nucleoplasty is a relative new technique, situated at middle way between conservative and open surgical treatment of patients with degenerative disc disease and lumbar disc protrusion. nucleoplasty is efficacy and safe procedure. dorsal rhizotomy in children with spastic paraplegia: a new simplified surgical technique j. ciurea, a. rasina, b. bălănescu, teodora coman the 5-th dept. of functional neurosurgery, clinical emergency hospital bagdasar-arseni, bucharest introduction: over a hundred years the lumbosacral dorsal rhizotomy is the neurosurgical indication in spastic children with cerebral palsy. objective: analysis of clinical and functional results obtained with a new simplified surgical technique, quintessence of the two technical principles that govern dorsal rhizotomy: anatomical approach and selective functional approach. method: we illustrated eight cases of spastic paraplegia children: five ambulatory spastic subjects operated at l5-s1 spinal root level and three non-ambulatory cases with more severe functional spastic paraplegia, clinically presented as quadriped crawlers or bunny hoppers, operated at l4s1 spinal root level. statistical analysis using the wilcoxon test (spss program) shows both a clinical improvement on ashworth, tardieu and penn scales and an improvement on main functional scales as gillette, test get-up and go or physician rating score. discussions: our anatomical and electrophysiological intraoperative observations are the basis for a new technical approach that respects both the classical selective sectoral surgical direction promoted by gros and sindou, the partial limited one of lazareff and the partial limited one promoted by peacock, steinbok and mittal. 336 selected abstracts the 8th international congress of the rsn conclusion: postoperative clinical and functional improvement allows presentation of the main advantages of our surgical technique: nerve root ablation standardization and reduction of operative time. cerebrolysine: an important factor for the improvement of the limits of the brain a.v. ciurea*, r.m. gorgan*, n. ianovici**, c. mihalache***, h. moisa* *“bagdasar-arseni” clinic hospital, 1st neurosurgical unit & the national center for excellency in neurosurgery, bucharest, romania; carol davila university school of medicine, department of neurosurgery **grigore t. popa university school of medicine, iasi, romania ***dpt. of neurosurgery, sf. andrei clinic hospital – galati, romania the development of the human bypedal posture has led to major modifications in the structure of the cns and especially that of the cerebral cortex. the cerebral cortex or pallium (shell) is a structure 2-4 mm thick being made out of aprox. 50 billion neurons, about 500 billion neuroglial cells and a dense capillary bed. microscopy reveals the cortex to have both a laminar and a columnar structre. the general cytoarchitecture varies in detail from one region to another, permiting the cortex to be mapped into dozens of histologically different areas, each with its own functionality – the so called areas of brodman. the normal human brain contains about 100 billion (1014) neurons which give birth to a very complex network containing from 60 trillion synapses, (6x1018) up to 240 trillion synapses (24x1019)the literature data states that a number of 85.000 neurons die each day (aprox. 1 per second). in these circumstances a human being could live up to the age of 300 years. furthermore, each living cells end it’s life cycle with the phenomenon of apoptosis. there are a series of factors that increase the rate of occurrence for apoptosis in neurons.these include the neuronal refractary period, vascularization, nutritional needs, lesions, blood brain barrier modifications, endogenous and exogenous toxicity, vascular dementia, neuronal flux variations, stress, structural damage, narcotics and last but not least drugs. to limit the effects of the factors mentioned above we feel that a physiological nutritional balance has to be installed, social interactive factors have to be as well taken into account. the balance between activity and rest, the importance of pauses and food, the prevention of head injuries, the reduction of stress factors, the decrease of exposure to radiations, and the restriction of alcohol consume, avoiding smoking and drugs and cell phone use. furthermore, the work of dr. masaru emoto has proven that the human consciousness and emotions have an important effect on the molecular structure of the water. the effect is very important given the fact that the human brain is 7778% composed of water. cerebrolysine brings a significant improvement in cerebral function. a mixture of low molecular polypeptide, extracted from pig brain, the drug, increases motor function, enhances cognitive performances, increases memory & attention and improves the bioelectrical activity in the brain. in the literature there are more than 500 substances studied for neuroprotective properties but romanian neurosurgery (2012) xix 4: 309 – 355 337 cerebrolysine with its low molecular weight passes easily through the bbb. the effect of cerebrolysin for neuroprotection consist in activation of calpaine system. the important additional cerebrolysin effects are: cerebral excitability and hypoxia, improving eeg signal and motor activity after mild brain ischemia and also antioxidative properties. in conclusion, after presenting various data regarding the anatomy and physiology of the brain, the authors militate for what would be referred as a cerebral hygiene – just as bodily hygiene. cerebral hygiene would lengthen the functional period of the human nervous system in the conditions of the improvement of average lifespan and it’s quality. all the substances with neuroprotective effects (like cerebrolysine) are very efficient in improving the cerebral function. last but not least we advocate that cerebrolysine is proven clinically as a protector factor in tbi and ischemic brain lesions. traumatic diffuse axonal injuries i.st. florian, dana racasan, d.f. muresanu, s. horatiu department of neurosurgery, university of medicine and pharmacy “ iuliu hatieganu”, cluj-napoca, romania background: traumatic brain injury (tbi) is a common cause of morbidity and mortality emphasized by the fact that it affects all age groups. diffuse axonal injuries (dai) associated with tbi are a great challenge to physicians due to the difficulty of early diagnosis and effective treatment. no efficient criteria for prognosis of the disease have been developed so far, due to the lack of efficient imaging and other diagnostic techniques. the purpose of this study is to evaluate prognostic criteria for mortality, functional and neurocognitive outcome. material and method: a systematic review of literature was performed, using the pubmed, mbase, the cochrane library, willey online library, scopus, science direct medical databases between january 1990 and july 2011. 11.398 articles were found using the keywords “diffuse axonal lesions/injury ,”traumatic brain injury”, “treatment of traumatic brain injury”, “treatment of diffuse axonal injury”, “prognosis of tbi/dai”, ”outcome after tbi/ dai”,”neurocognitive impairment after tbi/dai|”, “patient perspective after tbi/dai”. the analyzed articles were indexed according efns criteria. article abstracts reporting original research and reviews were consulted. 77 articles were finally selected for inclusion. results: dai is a predisposing factor for memory, executive and behavioral dysfunction. a reduced score on gcs scale, older age, pupillary reflex abnormalities and corpus callosum lesions are associated with a poor outcome. younger age is associated with dysautonomia, being correlated with a poorer outcome. mri is more accurate than ct for diagnosis and prognosis of dai. dwi and dti have prognostic value in evaluating functional outcome, with dti being an efficient biomarker for microstructural changes and neurocognitive impairment. no efficient biomarkers for dai were highlighted until now. conclusions: clinical case history and advanced imaging techniques can improve our ability to diagnose dai and have the potential to become valuable instruments in establishing prognosis for this condition. 338 selected abstracts the 8th international congress of the rsn cerebrolysin treatment in traumatic brain injury – a retrospective, multicentric cohort study r. m. gorgan*, f. m. brehar,*a.v. ciurea*, eva gheorghita*, narcisa bucur,* f. stefan**, n. ianovici***, st.m. iencean***, d. b. davidescu****, c. mihalache,***** v. prună*, b.o. popescu,** d. f. muresanu** *emergency clinical hospital “bagdasar-arseni”, bucharest, romania **university of medicine and pharmacy “iuliu hatieganu”, cluj-napoca, romania ***emergency clinical hospital “sf. treime”, iasi, romania ****emergency clinical hospital constanta, romania *****emergency county hospital galati, romania introduction: traumatic brain injury (tbi) represents a leading cause of death and disability and mainly affect the young adults. neuroprotection remains an important strategy for tbi, targeting deleterious pathophysiological processes which lead to secondary tissue damage and related functional deficits. cerebrolysin is the only clinically available drug that contains active fragments of different neurotrophic factors with low molecular weight that are able to pass the blood-brain barrier. the primary objective of this study was to test the outcome in cerebrolysin treated patients compared to the control group, at 10 and 30 days post-tbi, and the secondary objective to evaluate the safety of cerebrolysin for tbi patients. material and method: in this study were included 7769 adult patients with traumatic brain injury (tbi), admitted in 10 departments of neurosurgery in romania, between 2005 -2010. from the medical records, general data were collected at admission (gender, age, etiology, medical history, concomitant medication, glasgow coma scale score, clinical neurological examination, ct result, whether a surgical intervention was performed). at days 10 and 30 posttbi patients were ranked on glasgow outcome scale (gos) and modified rankin disability score (rds). 1618 patients received cerebrolysin and 6151 patients were in the control group. results: in mild tbi, treatment with cerebrolysin, both 20 ml and 30 ml/day regimens, significantly improves gos and rds scores at 10 days as compared to control patients. treatment with cerebrolysin in medium tbi, both 20 ml and 30 ml/day regimens, significantly improves gos and rds scores at 10 and 30 days as compared to control patients. moreover, a significant dose dependent effect is seen for cerebrolysin on gos score at 10 and 30 days. treatment with cerebrolysin, both 20 ml and 30 ml/day regimens, significantly improves gos and rds scores at 10 and 30 days as compared to control patients in severe tbi. moreover, a significant dose dependent effect is seen for cerebrolysin on gos score at 10 and 30 days. the frequency of usual adverse events is similar between the control group and cerebrolysin groups. no severe adverse events were noticed in cerebrolysin groups. conclusions: this large retrospective study shows significant beneficial effects on outcome of early cerebrolysin treatment in tbi and supports the basis for a large cerebrolysin prospective study in tbi. romanian neurosurgery (2012) xix 4: 309 – 355 339 need of immediate neuroprotection in traumatic spinal cord injuries st.m. iencean*, i. poeata*, d. cuciureanu*, b. costachescu*, al. chiriac*, a. st. iencean** *“grigore t popa” university of medicine and pharmacy, iasi, romania **a. st. iencean m.d., **clinic of neurosurgery, “prof. dr. nicolae oblu” hospital, iasi, romania objective: analysis of current status and effectiveness of immediate neuroprotection in traumatic spinal cord injuries. design: traumatic spinal cord injury (sci) has major effects and these patients have not any treatment. in acute complete traumatic sci, methylprednisolone as a standard treatment option is insufficient and it is necessary to add new immediate procedures at the standard treatment performed today. materials and methods: the study included analysis of two groups of 50 patients with cervical and thoracal traumatic sci who received (a) surgery for decompression, to realign and to stabilize the spine and ( b) standard methylprednisolone treatment and surgery and (c) 5 cases of traumatic sci with standard methylprednisolone and surgery treatment and also adenosine triphosphate (atp) to improve blood flow at the site of injury and indomethacine as local anti inflammatory. results: no significant differences were found between groups a and b at 6 months and 18 months postinjury; the 5 patients in group c had a more rapid stabilization of spinal injury. conclusions: although the number of cases is small and further study is needed it can be estimated as immediate use of neuroprotection, even at the scene of spinal injury, may improve prognosis of these patients. imagistic diagnostic traps multiple faces of meningioma b. iliescu, s. gaivas*, z. faiyad*, i. poeata*, c. apetrei*, anca dabija** *clinic of neurosurgery, “prof. dr. nicolae oblu” hospital, iasi, romania **supermeditest, iasi, romania introduction: an accurate and reliable imagistic diagnosis represents a key element in the surgical planning. numerous aspects of the surgical setup and strategy are based on the possible behavior of a certain intracranial mass occupying lesion. the progress of mr technique and the various algorithms that help a differential diagnosis between various intracranial pathologies brought a significant improvement in our ability to formulate a more accurate preoperative imagistic diagnosis. however, the variability in intracranial tumor development allows for a good probability of misdiagnosis. material and methods: we analyze the meningioma cases that presented with imaging aspects that were far from the classic appearance of this tumor over a period of 3 years. the selected cases are discussed in terms of imaging characteristics, preoperative assessment, and discuss the potential places of misjudgment and possible strategies to improve the preoperative imagistic diagnostic. results: the controversial imagistic cases represented 7% of the total meningioma cases newly diagnosed and operated in our department over a period of 3 years (2010 340 selected abstracts the 8th international congress of the rsn 2012). the error generators were represented by extensive cystic components that disrupted the homogenous structure typically associated with meningioma, excessive necrosis and intratumoral bleeding, or a combination of atypical imagistic composition with less frequent localization. conclusion: although a lesion with a typical imagistic appearance and clear diagnostic features especially on mr images, meningiomas present in specific cases a very unusual imagistic anatomy that can mimic cerebral or bony malignancies. in these cases the correct diagnosis is usually an intraoperative surprise. careful analysis of the preoperative imaging data and a cautious preoperative planning allow for a good diagnosis and a successful surgery. intraorbital meningiomas real neurosurgical controversies i. szabo, bataneant lucy department of neurosurgery, cluj county emergency hospital, romania objective & design: primary intraorbital meningiomas are tumors developed from the optic nerve dural sheath, ectopic arachnoid cells within the orbit or from the arachnoid cells around the superior orbital fissure. secondary intraorbital meningiomas are extended from the surrounding intracranial regions into the orbit. material and methods: we present our personal cases, the medical records of all patients with intraorbital menigiomas admitted in the neurosugical department of the cluj county emergency hospital between 1969 2012. in this period of time, 858 cases of orbital masses were admited, 68 cases were intraorbital meningiomas (7.9%) clinical data, neuroimagistical aspects, treatment and postoperative course of the desease and the quality of life are discussed. results: primary intraorbital meningiomas are rare, 11 cases (12.7%). the most important primary intraorbital meningiomas were optic sheath meningiomas (6 cases – 6.9%) and intraorbital ectopic meningiomas ( 5 cases 5,8). secondary intraorbital meningiomas were more frequently found in neurosurgical practice, 57 cases (87.3%): internal sphenoid wing meningioams with intraorbital extension, 26 cases (30,2%), cavenous sinus meningiomas with intraorbital extension, 9 cases (10.4%), multiple meningiomatosis with intraorbital extension, 6 cases (6.9%), olfactory grove meningiomas with intraorbital extension, 5 cases (5.8%), clinoid meningiomas with intraorbital extension, 3 cases (3.4%), orbital roof meningiomas with intraorbital extension, 3 cases (3.4%). in 2 cases, secondary intraorbital meningiomas were associated with nf type1. recurrent intraorbital meningiomas 1 recurrency in 8 cases, 2 recurrecies in 6 cases 3 or more recurrecies in 3 cases. the treatment is individually recommended in each case, depending on the location, dimensions and growth rate of the tumor, consists of on decompression, tumor biopsy, partial or total removal of the tumor, according to the balance of risk and benefits after surgery. conclusions: in the intraorbital meningioma cases, not only the treatment, but even some diagnostic and neuroimagistical data are controversial. in primary optic sheath meningiomas radical romanian neurosurgery (2012) xix 4: 309 – 355 341 surgery always lead to visual loss, in deep apically located meningiomas, postoperative sequelae are hardly acceptable. in this cases, late surgical treament is recommended. secondary intraorbital extensions of the intracranial meningiomas present the better postoperative outcome after total removal. in some cases, subtotal extension and radiotherapy is the best choice. in vitro influence of 2methoxyestradiol on glioblastoma stem cells g.ungureanu*, c. berce**, o. soritau***, i. iancu*, i.s. florian* *department of neurosurgery, cluj county emergency hospital, romania **university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania ***“prof ion chiricuta” oncology institute clujnapoca, romania objectives and design: glioblastomas (gbm) are the most frequent type of glial tumors. although extensive research has been done in search for a curative treatment, the actual multimodal treatment still offers only poor prognosis. 2methoxyestradiol (2-me) is a natural steroid hormone, formed by hydroxylation and o-methylation of the estradiol molecule. our purpose was to investigate the effect of 2-me on the proliferation of glioblastoma stem cells and if it influenced the effect of other consecutive therapies. material and method: cultures of glial tumor stem cells-isolated from the gbm of a 55 year old female patient, characterised by a very high proliferation rate, were treated with increasing doses of of 2, 10, 25 and 50 μm 2-me and 10 μm 2-me and 100 mg of temozolomide. cells were then kept either in normal or hypoxic conditions for 48 h. radiation therapy consisting of a unique dose of 6 gy was then applied to some of the cultures. proliferation rate was measured at 72 h using the mtt protocol. results: hypoxia didn’t exert any significant influence over proliferation. the 25 μm 2-me dose inhibited proliferation both in hypoxic and normal conditions (p<0.05, 95% ci of 0.225-0.039, 0.110.0734 respectively). the 50 μm 2-me dose had the same inhibitory effect (p<0.05, 95% ci of 0.235-o.047, 0.130.0632 respectively. this effect was visible both in irradiated and non-irradiated cells. the combination of 2-me and temozolomide had the same inhibitoty effect both in irradiated and non-irradiated cultures. conclusions: we conclude that 2-me could be a viable part in the multimodal therapy of glioblastoma. the effect of 2-me is not dose dependent. also the inhibitory effect on proliferation of gbm stem cells is independent of consecutive applied radiation or other chemotherapy. cervical spinal cord herniation at seven years after surgery for cervical ependimoma a.st. iencean*, s. gaivas,* z. faiyad*, b. chirita*, st.m. iencean**, i. poeata** *“prof. dr. nicolae oblu” clinical emergency hospital, 3rd department of neurosurgery, iasi, romania **university of medicine and pharmacy “gr.t.popa”/“prof. dr. nicolae oblu” clinical emergency hospital, iasi, romania objective: we describe the case of a man, 50 years old, who was operated for a cervical ependimoma 7 years ago. he presented with a 2-year hystory of 342 selected abstracts the 8th international congress of the rsn progressive tetraparesis and the imaging studies showed a postoperative cervical spinal cord herniation. design: herniation of the spinal cord is a relative rare pathology and can be spontaneous, iatrogenic and posttraumatic. materials and methods: a 50-year-old male patient presented with progressive tetraparesis that began 2 years ago; he had surgery 7 years ago for a cervical ependimoma, that was removed totally. imaging studies showed a spinal cord herniation at c2-c3 level through a posterior dural defect. the surgery was the resection of the dural scar around the spinal cord herniation and reconstruction of dura with a musculo-adipose patch. results: postoperatively, the patient made significant neurological improvements, and mri showed the resolution of spinal cord compression. conclusions: spinal cord herniation is a reversible cause of medullary dysfunction. the treatment of choice, particulary if there is associated a neurological deficit, is the surgical repair of the dural defect. because this condition is rare and relatively unknown, there is often a delay in the diagnosis and surgical treatment. this pathology must be recalled when addressing a patient with progressive neurologic disturbance, especially if the patient has a clinical record of surgery involving the spinal cord. posters percutaneous interspinous device for lumbar spinal stenosis d. adam*, e. pevzner** *“carol davila” medicine and pharmacy university, “victor babes” clinic, bucharest, romania **sapir medical center, meir general hospital kfar sava, il introduction: the percutaneous interspinous distraction devices are an alternative to conventional open surgical procedures in the treatment of symptomatic degenerative lumbar spinal stenosis. a new interspinous process implant, superion, is used under local or general anesthesia, to treat patients with lumbar spinal stenosis. material and method: a cohort of 103 patients were operated between july 2007 july 2008. all patients had back pain, neurogenic claudication with relief in flexion. mri of the lumbar spine showed moderate foraminal or canal stenosis. in 18 patients superion was implanted at 2 levels. in 85 patients it was implanted at 1 level: l4/5 (n=45), l3/4 (n=40). the mean follow-up was 35 months. results: vas, sf-12 and odi were improved in all but 15 patients. in 2 patients the implants were collapsed after 1 and 2 months. two other patients underwent formal laminectomy with fusion. conclusion: implantation of superion is a minimally invasive alternative to traditional spinal surgery, a safe and effective treatment for patients with moderate lumbar stenosis. romanian neurosurgery (2012) xix 4: 309 – 355 343 lumbar epidural lipomatosis in a patient with hodgkin lymphoma m. dabija, d. andronic, c. ghiorghita “prof. dr. nicolae oblu” clinical emergency hospital, 3rd department of neurosurgery, iasi, romania background/objectives: spinal epidural lipomatosis (sel) is a pathological condition in which fat tissue is deposed in the spinal canal around the thecal sac in excess, causing neurological symptomatology (7, 9, 12). fat tissue is present in our body almost everywhere. when the normal quantity is exceeded is created a pathological situation. case presentation: we present a 33 old man case with fat tissue excess deposited in lumbar spine canal. the pathological history of our patient includes a nodular form of stage ia hodgkin lymphoma diagnosed in 2011 for what he went combined radio-chemotherapy. he also has ben diagnosed with grad i obesity. in last month he presented with rapidly progressive symptoms like lower back pain, parparesis and sphincters dysfunctions. findings: thoracic magnetic resonance imaging (mri) establishes a lumbar lipomatosis located in l3-s5 spinal canal. pathology results confirm the imagistic diagnostic. under surgery was performed a median laminectomy with fat tissue excision with good results in patient symptomatology. conclusion: cortisone chronic therapy may lead to sel. however in our case, hodgkin lymphoma therapy led to cortisone complications. neurological symptomatically patients should be treated surgically. dorsal rhizotomy in children with spastic paraplegia: a new simplified surgical technique j. ciurea, a. rasina, b. balanescu, teodora coman the 5-th dept. of functional neurosurgery, clinical emergency hospital bagdasar-arseni, bucharest, romania introduction: over a hundred years the lumbosacral dorsal rhizotomy is the neurosurgical indication in spastic children with cerebral palsy. objective: analysis of clinical and functional results obtained with a new simplified surgical technique, quintessence of the two technical principles that govern dorsal rhizotomy: anatomical approach and selective functional approach. method: we illustrated eight cases of spastic paraplegia children: five ambulatory spastic subjects operated at l5-s1 spinal root level and three non-ambulatory cases with more severe functional spastic paraplegia, clinically presented as quadriped crawlers or bunny hoppers, operated at l4s1 spinal root level. statistical analysis using the wilcoxon test (spss program) shows both a clinical improvement on ashworth, tardieu and penn scales and an improvement on main functional scales as gillette, test get-up and go or physician rating score. discussions: our anatomical and electrophysiological intraoperative observations are the basis for a new technical approach that respects both the classical selective sectoral surgical direction promoted by gros and sindou, the partial limited one of lazareff and the partial limited one promoted by peacock, steinbok and mittal. 344 selected abstracts the 8th international congress of the rsn conclusion: postoperative clinical and functional improvement allows presentation of the main advantages of our surgical technique: nerve root ablation standardization and reduction of operative time. is “metabolic coupling” across primary motor areas and cerebellum altered in cervical myelopathy? s.c. craciunas*, m.r. gorgan*, ali baniahmed**, carmen m. cirstea** *bagdasar-arseni hospital bucharest, romania **kansas university medical center kansas city, us introduction: in patients with cervical spondylotic myelopathy (csm), proton magnetic resonance spectroscopy (1hmrs) studies reported abnormal cerebral metabolites concentrations within radiologically normal-appearing motorrelated brain areas. recently, we found significantly higher choline, a marker of cell membrane integrity, in primary motor cortices (m1), and generally lower nacetylaspartate, a marker of neuronal integrity, and higher myo-inositol, a putative marker of glial cells, in m1 and cerebellum1. in some instances, choline levels relate to clinical severity1. although brain metabolic demands might be accomplished through pathways that link metabolites across multiple areas, how altered metabolite concentrations within one area are related to metabolite changes within another in cervical myelopathy is yet to be determined. thus, our goal was to identify whether correlations among metabolites or “metabolic coupling” between m1 and cerebellum was altered in csm patients. methods: in moderately impaired csm patients, n-acetylaspartate, myo-inositol, and choline were quantified (lcmodel) in left and right m1 and cerebellum using press at 1.5 tesla (te=30ms, tr=1500ms, flip angle=90, spectral width=1000hz, 15x15x15mm in m1, 20x20x20mm in vermis). thirteen csm patients (confirmed by t2-weighted mri) were studied before surgery. spearman rank order correlation was used to determine the putative relationships between metabolites within (intra-regional) and across (inter-regional) our regions of interest. the mean metabolite correlation between these specific regions was compared between csm patients and 14 ageand sex-matched healthy controls (mann-whitney u-test). results: intra-regional correlations: generally lower mean correlations between all metabolites were found in left m1 (0.02±0.27 vs. 0.35±0.08, p=0.08) and cerebellum (0.33±0.30 vs. 0.57±0.14, p=0.2). myo-inositol-choline correlation was the most altered (0.15 vs. 0.42 in left m1, 0.09 vs. 0.59 in cerebellum). interregional correlations: significant weaker metabolite correlations between right m1 and cerebellum were found (-0.12±0.36 vs. 0.16±0.10, p=0.03). a trend to weaker correlations was also found between right m1 and cerebellum (0.04±0.38 vs. 0.21±0.20, p=0.2). cerebral myo-inositolcerebellar choline and cerebral nacetylaspartate-cerebellar n-acetylaspartate correlations were significantly decreased in csm patients (left m1-cerebellum: -0.68 vs. 0.12, 0.07 vs. 0.67 respectively; right m1-cerebellum: -0.62 vs. 0.10, -0.17 vs. 0.33 respectively). conclusions: these preliminary results are the first evidence for the presence of weaker “metabolic coupling” (as measured romanian neurosurgery (2012) xix 4: 309 – 355 345 by correlation coefficients) within and between m1 and cerebellum in patients with cervical myelopathy, suggesting an alteration of neuron-glial interactions and consequently perturbed neuronal function. by moving beyond analysis of change in metabolite concentration within individual brain region, these results can increase our understanding of how 1h-mrs markers of metabolic processes are related in patients with cervical myelopathy. aknowledgments: this study was supported by aospine international (grant hjw2011-su20). ablation of deep brain cerebral tumors using stereotactically guide p. patrascu, a. iliescu, s. gheorghe, c. tudor bucharest emergency university hospital, bucharest, romania “by using the stereotactic guide in deep brain ablation lesions, huge advantages are conferred, approach to the lesion being done with minimal damage to the brain parenchyma and avoid areas elocventel. in neurosurgery clinic i of bucharest emergency university hospital there have been few cases of deep brain lesions operated using stereotactic guide. we present the case of a 34 years old man operated for deep temporal lesion. the surgery was a success using stereotactic guide and patient was discharged without neurological deficits. ruptured aneurysm of aberrant frontopolar artery emerging from anterior communicating artery: a case report diana iordache*, andreea rusu*, z. faiyad**, a. chiriac,** b. iliescu**, i. poeata* *university of medicine and pharmacy “gr.t.popa”/“prof. dr. nicolae oblu” clinical emergency hospital, iasi, romania **“prof. dr. nicolae oblu” clinical emergency hospital, iasi, romania introduction: aneurysms are often associated with anomalies of cerebral arteries and they should be identified pre and intra-operatory. a large number of studies focused on the anatomical variations of the anterior cerebral – anterior communicating artery (aca – acoa) vascular complex. in this region we are interested in the frontopolar (fpa) which normaly branches off aca distal to acoa (a2 segment). literature reports of the aberrant origin of the frontopolar artery, refer only to its anomalous origin from the a1 segment of aca, from a common vascular trunk with orbitofrontal artery and from calosomarginal artery, but no reference mentions its origin from the acoa. aneurysms of the aca branches are very rare and they are frequently saccular and rather small. case presentation: we present a case of a ruptured, fusiform aneurysm located on an aberrant fpa originating in the acoa. a 19 year old man presented with severe headache, nausea and photophobia. computer tomography (ct) showed focal subarachnoid hemorrhage in the interhemispheric fissure while cerebral angiography (seldinger) revealed a prominent aneurysm emerging from an artery with the origin in the acoa. intraoperative diagnosis was that of voluminous, fusiform aneurysm stemming from the left fpa that arises from the left side of the anterior communicating artery. 346 selected abstracts the 8th international congress of the rsn the aneurysm was successfully clipped via pterional approach. the postoperative outcome was favorable and the patient had no neurological deficit. conclusion: our review of the literature revealed no reports on the aberrant origin of the fpa from the acoa nor an aneurysm related to this anomaly. this may be because injuries of the fpa have little clinical impact and this particulary origin of fpa from acoa is extremely rare. the particularity of the presented case consists also in the unusual shape and the considerable size of the aneurysm that led to clinically significant complications. so we call attention to another rare anomaly of the aca branches. all these points emphasize how important is for neurosurgeons to recognize the anatomical variations of the cerebral arteries in order to reduce poor postoperative outcome. emergency decompressive craniotomy for incidental migration of coils inside ica-case report bucur narcisa*, neacsu angela*, v. pruna*, sandu aurelia mihaela*, a. chefneaux**, cristescu catioara fănica ***, m.r. gorgan* *clinic emergency hospital ‘bagdasar-arseni’ bucharest, fourth neurosurgical department, romania **interventional neuroradiology department, clinic emergency hospital ‘bagdasar-arseni’ bucharest, romania ***anesthesiology and icu department, clinic emergency hospital ‘bagdasar-arseni’ bucharest, romania the team presents the case of a 30 years old woman admitted to our department for sah predominat in the anterior basal cisterns, in a good neurological condition (wfns 1, gcs 15, fisher 1). dsa angiography revealed an left ica sacular aneurysm located on the c6 segment, 3.2 mm distal of the origin of ophtalmic artery and 2.4 mm proximally of the left p com artery. the maximum size was 16.01 mm /4.51 mm. the patient solicited endovascular embolisation. the procedure was performed according with standards. at starting the neuroradiologist remarqued vasospasm and injected 20 ml nimotop iv in 20 minutes. he introduced safely the microcatheter and the coil (standard 11/30) inside the aneurysm. after coil detachment the coil was displaced and a new microcatheter was introduced in order to correct the position. a new control angiography in the next 15 minutes, revealed the irreducible displacement of an important part of coil inside the left carotid artery with complete occlusion. the circulation was partially compensated by vertebral arteries and controlateral ica. a rapid decompressive craniotomy was decided in combination with iv anticoagulant, taking into consideration the next factors: dominat hemisphere, good neurological status pre-embolisation, young age, possible circulatory compensation through an efficient willis polygone. the patient was immediately operated and after 24 hours she was weaned from advanced life support with a mild right hemiparesis and drowsiness. she recovered completely in 6 days and cranioplasty was performed after 3 weeks. two months after, the patient returned to her previous life. conclusion: emergency decompressive craniotomy in acute incidental ica occlusion is a life saving procedure. when willis polygone is efficient for circulatory compensation the postoperative quality of life might be the normal one. romanian neurosurgery (2012) xix 4: 309 – 355 347 operative strategies in ruptured posterior inferior cerebellar artery aneurysms v. pruna, bucur narcisa, angela neacsu, f.m. brehar, r.m. gorgan clinic emergency hospital ‘bagdasar-arseni’ bucharest, fourth neurosurgical department, romania introduction: posterior inferior cerebellar artery (pica) aneurysms represent approximately 3% of all intracranian aneurysms. the most frequent location is on the vertebral artery-pica bifurcation. the distal locations are less frequent but these aneurysms have a more fragile aneurysm wall and are more prone to rebleeding. materials and methods: the authors of this study present their experience in four patients with ruptured pica aneurysms admitted and operated in our clinic between 2004 and 2012. all patients have been investigated by ct scan, 3d ctangiography or 3d dsa and have been operated using operative strategies according to the location of aneurysm on pica segments. in three patients the aneurysm was clipped using a yasargil vascular clip and in one case a wrapping has been performed. the follow-up period was between 4 months and 7 years (mean 3, 5 years). results: in our series there was one death at three days postoperatively secondary to a pulmonary embolism. the other three patients had a good outcome with no neurological deficits postoperatively. all three patients required ventriculoperitoneal shunts during the follow-up period, between 5 and 31 days after the operation. conclusions: the pica aneurysms remain a neurosurgical challenge even for the most experienced neurosurgeons. the operative strategies must be adapted to the location of the aneurysm on the pica segments and to the size and the configuration of the aneurysm. far lateral approach for a giant dumbbell-shaped c2 cervical schwannoma case report m. catană, v. prună, m.r. gorgan clinic emergency hospital ‘bagdasar-arseni’ bucharest, fourth neurosurgical department, romania introduction: schwannomas are some of the most common extramedullary tumors, whose location at the cranio-vertebral junction is very rare. giant tumors appear as dumbbell-shaped tumors and they develop mainly extradural with a huge extension outside the spine. the intradural position followed by penetration of the dural sac is very rare, especially when it is in front of the spinal cord. the far-lateral approach allows adequate exposure of the lesion to prevent manipulation of neural and vascular structures. case presentation: we report a case of 63 years old man, admitted in our clinic for neck pain and left body dysesthesia. cervical mri highlights a giant left c2 dumbbell-shaped intradural extradural tumor (4/3 cm) which shifts spinal cord to the right side. surgery was performed by a far-lateral approach with total resection of the posterior arc c1, left hemilaminectomy c2 and left suboccipital craniectomy. complete resection of paravertebral component of the tumor was done, with left c2 nerve root section. after incision of the dura mater, the intradural component is 348 selected abstracts the 8th international congress of the rsn distinguished, which ascend in the posterior cranial fossa in front of the spinal cord and the bulbo-medullary jonction. the left xi nerve was preserved and the dentate ligament was sectioned. after tumor debulking, the total resection was completed. outcome was favorable with improvement of preoperative symptoms. the pathological diagnosis was schwannoma. conclusion: far – lateral approach is one of the best ways for surgical resection of these tumors and provides optimal visualization, without spinal cord manipulation. brain abscess in 95 patients: factors influencing outcome and mortality m.r. gorgan, angela neacsu, narcisa bucur, v. pruna, catalina lipan, aurelia mihaela sandu, catioara fanica cristescu clinic emergency hospital ‘bagdasar-arseni’ bucharest, fourth neurosurgical department, romania objective: to analyze the management and variables determining morbidity, mortality and outcome in 84 subjects with brain abscesses treated over a 12-year period. methods: a retrospective study was performed on a series of 84 patients with brain abscesses surgically treated with open craniotomy excision between january 2000 – december 2011, in the fourth neurosurgical department by the same team. such variables as age, gender, clinical presentation, number of days to diagnosis, location, number of lesions, predisposing factors, mechanism of infection, etiological agent and therapy were analyzed independently. results: in our series, the average age was 42.96 years (range: 11-75), 72.62% (n=61) were males and 27.38% (n=23) females. the median number of days to diagnosis was nine (range: 2-45 days). majority of cases (76.19% 64 cases) presented a supposed medical condition favoring dissemination of a previous most frequent clinical presentation included headache (40.47%, n=34), fever (35.71%, n=30), focal neurologic deficits (29.76%, n=25), increased intracranial pressure (28.57%, n=24) and seizures (11.90%, n=10). mechanism of infection was hematogenous spread (35.71%, n=30), contiguous spread (33.33%, n=28), post-neurosurgical procedures (13.09%, n=11), and open head injury (5.95%, n=5). the route of transmission was unknown for 23.8% of the patients (n=20). according to our treatment policy all cases except two, (treated by burr-hole and aspiration) benefited of open surgery and removal of the lesions by craniotomy with resection of the capsule, without local recurrence. outcome was favorable in 82.14% (n=69) of the subjects. six cases remained with permanent motor deficit (7.14%), only one patients had new neurological deficits postoperatively. four patients (4.76%) remained with controllable seizures. general morbidity was 26.19% (n=22), and mortality stood at 7.14% (n=6). out of a total 33.33% (n=28) of complications, 64.28% were secondary to medical causes (66.66%, n=4, of deaths were due to medical causes not directly related to surgery) . age was related to favorable postoperative outcome. the mean age of patients with good outcome was 40.57±16.25 years, and 55.48±20.34 years in the case of subjects with poor gos romanian neurosurgery (2012) xix 4: 309 – 355 349 scores. compared with other mechanisms of infections, hematogenous spread correlated with unfavorable outcome. conclusions: co-morbidities, advances age and hematogenous spread were predictors of poor prognosis. most of the complications following brain abscess management were not directly related to surgery. anterior clinoidal meningiomas: microsurgical management and outcome in a consecutive series of 38 patients ligia tătăranu*, v. ciubotaru**, adriana dediu**, d. păunescu**, anica dricu*** *“carol davila” university of medicine and pharmacy, bucharest, romania **neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania ***university of medicine and pharmacy, craiova, romania objective: anterior clinoidal meningiomas are difficult and challenging to remove completely and safely especially when they compress, or displace the adjacent critical neurovascular structures. the purpose of this paper is to delineate the advantages of the surgical techniques in achieving an improved extent of tumor excision and enhancing the patients’ overall outcome. methods and results: a retrospective analysis was performed on 38 consecutive patients with anterior clinoidal meningiomas who underwent surgical resection at the “bagdasar – arseni” clinical hospital between january 2007 and december 2011. the patients’ age ranged from 18 to 75 years old with an average age of 47 years old. there were 25 females (66%) and 13 males (34%). the presenting symptoms were mostly visual impairment; others symptoms were also encountered, such ad raised intracranial pressure syndrome, cranial nerve palsies, seizures, mental changes, hemiparesis. the diagnosis was made predominantly by the mri and angio mri. angiography was still useful to show relationship between the tumor and arteries. all patients had preoperative and postoperative ophthalmological evaluations. a fronto-temporal approach was used in 29 patients (76.3 %) and cranio-orbital approach with resection of the zygomatic arch was used in 9 (23.7 %). in 8 cases (21 %), according to the grading scale of almefty, the masses were group i, having originated from the lower part of the clinoid; in 27 cases (71 %) the masses were group ii, having originated from the upper or lateral part of the clinoid process; and in 3 cases (8 %) the masses were group iii since they arose from the optic foramen. the complete removal was obtained in 26 cases (68.4 %). postoperatively, 18 patients showed an improvement (47.4 %), 11 were unchanged (28.9 %) and 9 presented further deficits (23.7 %). three patients (7.9 %) died after surgery: one from pulmonary thrombembolism, one from cerebral ischemia after severe vasospasm of the internal carotid artery (unresponsive to treatment) and one from acute renal failure. the mean follow-up was 26.4 months. during this period, there were three recurrences and one patient underwent resection again. adjuvant radiotherapy was not performed. conclusion: although the use of modern microsurgical technique has clearly improved the outcome of clinoidal meningiomas, the chance for surgical cure remains problematic, especially in cases 350 selected abstracts the 8th international congress of the rsn with adherences to the internal carotid artery and its branches, involvement of the cavernous sinus and orbital structures. outcome of transsphenoidal surgery for clival chordomas ligia tătăranu*, v. ciubotaru**, adriana dediu**, d. păunescu** *“carol davila” university of medicine and pharmacy, bucharest, romania **neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania objectives: chordomas are uncommon tumors, arising from remnants of the primitive notochord and frequently located within the clivus. the location of the tumor determines the path of its growth and the surgical approach. the authors describe their experience with surgical access to the clivus via an extended endonasal transsphenoidal approach and discuss the utility of incorporating an endoscope into an open surgical procedure. material and methods: between january 2001 and december 2011, 21 patients underwent extended endonasal transsphenoidal surgery for clival chordomas (13 males and 8 females, mean age – 47 years). in one case, an additional suboccipital approach was necessary to accomplish resection of an intradural extension of tumor. patients were followed up from 6 months to 11 years. 27 endonasal transsphenoidal approaches were performed in 21 patients (two patients had second surgery and two patients had two additional surgeries). in 15 cases, the approach was endoscopically assisted. results: postoperative mris after the initial operation showed gross total resection in 8 cases (38.09 %). near total removal (> 90%) was achieved in 7 cases (33.33 %). subtotal resection was noted in 6 cases (28.57 %). tumor regrowth imposed additional surgery in 4 cases (19.04 %). use of the endoscope was associated with gross total or near-total removal. gamma-knife radiosurgery was used in 4 cases (19.04 %). conclusions: the extended endonasal microscopic transsphenoidal approach yields excellent access to the clivus, medial cavernous sinus and intradural space anterior to the brainstem. the addition of the endoscope allows for a more panoramic view and permits widening of the approach in all directions. results after surgery for non-functioning pituitary adenomas v. ciubotaru**, ligia tătăranu*, d. păunescu**, violeta ioana pruna*** *“carol davila” university of medicine and pharmacy, bucharest, romania **neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania ***clinica oftapro, bucharest, romania aims: clinically non-functioning pituitary adenomas range from being asymptomatic to causing significant hypothalamic and pituitary dysfunction and visual field defects. the object of this study was to evaluate the efficacy and safety of surgery in our cases of non-functioning pituitary adenomas. methods: the authors performed a retrospective analysis of 154 patients who underwent resection of non-functioning pituitary adenomas from january 2009 through may 2011. there was 87 male and 67 female (mean age = 52.3 years; followup = 6 28 months). romanian neurosurgery (2012) xix 4: 309 – 355 351 results: tumors where usually large at the time of diagnosis, commonly presenting with headache (109 cases – 70.7 %), visual field defects (56 cases – 36.3 %) and hypopituitarism (80 cases – 51.8 %). pituitary apoplexy was the presenting symptom in 33 cases (21.4 %). transsphenoidal surgery was the primary treatment for adenomas, whereas transcranial surgery was reserved for the cases in which the sphenoid sinus was not pneumatised or when the tumour was mainly extrasellar. gross total removal was achieved in 95 out of 154 patients (61.7 %). residual tumours or tumour regrowth imposed additional surgery in 34 cases (22.0 %). the improvement of vision was achieved in 85.7 % of cases. postoperatively, patients showed varying improvement of pituitary function. there were no serious operative complications. stereotactic radiosurgery was used for control of residual tumours. conclusions: transsphenoidal surgery remains the treatment of choice for rapid decompression of neighbouring structures in non-functioning pituitary adenomas, often bringing to normalisation or improvement of visual and pituitary function. endoscopic endonasal transsphenoidal surgery for pituitary adenomas ligia tătăranu*, v. ciubotaru**, adriana dediu**, violeta ioana pruna*** *“carol davila” university of medicine and pharmacy, bucharest, romania **neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania ***clinica oftapro, bucharest, romania aim: to assess the effectiveness of the endoscopic endonasal transsphenoidal approach in the management of pituitary adenomas. methods: we retrospectively analyzed 152 patients with pituitary adenomas who was operated on between january 2003 and december 2011 (85 women and 67 men; mean age = 43 years; follow-up = 6 months 9 years). the series consisted of 49 gh-secreting adenomas, 20 prlproducing adenomas, 21 mixed gh&prlproducing adenomas, 8 corticotroph adenomas, one case of thyrotroph adenoma and 53 non-functioning pituitary adenomas. results: among the 20 patients with prolactinomas, 14 patients exhibited normalized prolactin levels postoperatively. in the acromegalic patients, there were 12 macroadenomas and 58 microadenomas. among the macroadenomas, endocrinologic remission was observed in 4 cases, minimal improvement in 2 cases and no changes in 6 cases. among the microadenomas, endocrinologic remission was observed in 34 cases, improvement in 10 cases, minimal improvement in 4 cases and no changes in 10 cases. when a residual tumor in the cavernous sinus was identified, gamma-knife surgery was used. the 8 patients with cushing’s disease had resolution of hypercortisolism clinically and chemically. the surgery was curative also in the case of thyrotroph adenoma. postoperative morbidities included cerebrospinal fluid leak in 4 cases (2.63%), temporary diabetes insipidus in 8 cases (5.26%) and sinusitis in 2 cases (1.31%). conclusions: the endoscopic endonasal transsphenoidal approach is an effective surgical option for pituitary adenomas. a low incidence of complications has been observed, likely because of the improved visualization of the anatomy and the decreased surgical trauma. 352 selected abstracts the 8th international congress of the rsn 1001 lumbar disc hernia microscopic aproach – results a 5 year experience v. munteanu, nicoleta diaconu, r. stanescu, g. grigore, a. spatariu neurosurgery, “bagdasar – arseni” clinical hospital, bucharest, romania removal of a herniated disc with the use of the operative microscope was first performed by yasargil in 1977. however, it began to be used more and more only in the late 1980s. the merits of this technique are that it allows every type of disc herniation to be excised through a short approach to skin, fascia and muscles as well as a limited laminoarthrectomy. for these reasons, it has been, and still is, considered the “gold standard” of surgical treatment for lumbar disc herniation, and the method used by the vast majority of spinal surgeons. the series that we present here was selected as only lumbar disc hernia without any other associated pathology (lumbar stenosis, spondylolisstesys, etc). all cases have been treated by microdiscectomy technique. we use zeiss vario opmi+ s88 microscope. in all caseses the intersomatic control have been achieved by seing at the and of the surgery the anterior longitudinal ligament, all fragments being taken away, the root being left mobile and free beyond the ganglia and the conjunction foramina being controlled and left mobile and free by any disc fragments. after removal of the disc the space was washed with bethadine solution.the suture has been carried on with vicryl 2-0 in a continuous way, as well as the subcutaneous tissue. skin closure with 3-0 silk, continuously. no infections after 5 years we encountered, and for five patients we do perform another surgery at the same level, two of them after mild lumbar trauma. the other patients went well with kinetotherapy, and from 32% of cases with mild to severe deficits before surgery, more than 90% recovery was very good (4+ out of 5 motor scale). multiple little intracranian aneurysms with familial inheritance v. munteanu*, m.r. gorgan**, n. diaconu*** *student in neurosurgery, “carol davila” university of medicine an pharmacy bucharest, faculty of medicine, departament of neurosurgery, romania **”carol davila” university of medecine an pharmacy bucharest arseni – bagdasar hospital, romania ***neurosurgery, “bagdasar – arseni” clinical hospital, bucharest, romania in this particular case, the authors have studied a family in wich two of the members on the same genetic line-mother and daughter have suffered intracranial bleeding from ruptured aneurysm. the congenital nature and the patterns of inheritance of the disease are discussed. the indications for elective investigation of the asymptomatic relatives and surgical prophylaxis on asymptomatic aneurysms are also discussed. material and method: two cases, same hereditary line, same nosocomial pattern, rare case of multiple intracranial aneurysms. surgical treatment of ruptured and unruptured aneurysm, same part, same time. results: operated patient done well without neurological deficits after one year. conclusions: making good judgment based on complete investigations lead to a good outcome. further investigations on family hereditary aneurysm small lesions should be perform. familial intracranial romanian neurosurgery (2012) xix 4: 309 – 355 353 aneurysms are uncommon. multiple familial intracranial aneurysms are much more uncommon. according to our review of the literature, only few families are known to have more than one of their members with multiple aneurysms. our report describes a family in which mother and daughter had multiple intracranial aneurysms. role of neuronavigation in eloquent area lesions v. munteanu, nicoleta diaconu, g. grigore, a. spatariu neurosurgery, “bagdasar – arseni” clinical hospital, bucharest, romania this work is ment to present the important role of neuronavigation either in localizing small lesion especially in eloquent areas but as well the help during surgery in modifying the technic and simplifying the judgment during surgery. we have now 17 cases of cerebral lesions in a 6 year period, (5 cavernomas, 5 meningiomas, 4 metastasis, 3 gliomas). in all cases we perform an contrast cerebral irm and angio-irm, and planned the surgery according with the calculations made on the console. the shortest route has been choosed, the as possible fine dissection has been carried on, and in 8 patients we have an improved neurological deficit after the surgery, 6 cases with seizures free postoperative course, 2 cases with hemorrhage in tumoral bad witch necessitate evacuation and one with melanotic metastasis with a 46 days free of symptoms with good radiologic control, and after with a smaller recurrence in the same place. we do learn after using the neuronavigation system that even the work is more time consuming in planning the surgery the satisfaction by easing the surgery itself worth using. pituicytoma mr imaging, clinical simptoms and outcome v. munteanu, nicoleta diaconu neurosurgery, “bagdasar – arseni” clinical hospital, bucharest, romania we report a case of pituicytoma, a rare primary tumor of the neurohypophysis. a 48-year-old woman presented with progressive visual complaints, bitemporal hemianopsia, and headache with vomiting. in the past year the pacient have been hospitalise in psihiatric departement for acute depressive state, during the last being scanned on ct wich disclosed a large suprachiasmatic multicistic mass lesion and had been refferd to us. imaging studies revealed distinctive features of a mass lesion that thickened the pituitary stalk with a multicistic protrusion extending into the hypothalamus, temporal lobe, mesencefalon and cavernous sinus. pituicytomas are very rare primary tumors of the adult neurohypophysis, and only a few case reports of true pituicytomas exist in the literature. pituicytes are glial cells of the neurohypophysis that support the large axons of vasopressin and oxytocinproducing hypothalamic neurons. pituicytomas are considered low-grade astrocytomas of the neurohypophysis, distinct from intracranial granular cell tumors (gct) and pilocytic astrocytomas. they are histologically benign, but their hypervascular nature makes surgical resection difficult.in the literature local recurrence after subtotal resection is 354 selected abstracts the 8th international congress of the rsn common. the imaging characteristics of pituicytomas are nonspecific, but mr imaging are essential for surgical planning and can reveal details about the extension and structures being compressed by the tumor. sacral arachnoidian cyst – case report, surgical tehnical method v. munteanu, nicoleta diaconu, g. grigore, a. spatariu neurosurgery, “bagdasar – arseni” clinical hospital, bucharest, romania we present a case of a young woman, 39 years old, medical nurse, who came first time in our hospital with moderate nuchal pain, easily reliefed by common antalgic treatment. she has been investigated with cervical spine mri which show moderate modifications of cervical discs. two weeks after his first presentation, suddenly present slowly growing pain in the lumbar region, from light pain to unbearable pain and has been address in emergency to another hospital for emergency treatment. the day after we admitted the patient and perform an lumbo-sacral mri which show multiple sacral s2-s3 cysts of 5 cm in contact, with pressure on the sacral anterior wall and bone destruction both anteriorly and posteriorly, the pressure effect making the maximum thickness of the bone around 1 mm. any treatment ot all could this time kill the pain so we propose surgery and the patient accepted willingly. a linear midline lumbosacral incision and we found a translucid bone under 1mm thickness that we removed under the microscope. the cyst on the left side appear immediately and we made a linear incision, drain the fluid and observe the rooth inside floating free. a reshape of the cyst wall was performed by cutting free 1 cm on both side of the incision edge, superposed the margins on another 1cm common soil and making a noninterrupted, nonresorbable 50 suture. the pain disappears the day after the surgery, no deficits, no urinary disturbances. ten days a small leakage at the incision site appears of csf witch has been solved with bad rest and local pressure. eight month after the surgery the patient is back on her job. anterior circulation intracranial aneurysms personal series c. toader*, m. stroi** *”carol davila” university of medecine an pharmacy bucharest arseni – bagdasar hospital, romania **national institute of neurology and neurovascular diseases, bucharest, romania cerebral aneurysms represents the most common cause of nontraumatic subarachnoidian hemorrhage.overall, about half the patients die within the first month of their hemorrhage.they represents major cerebrovascular emergencies, whose management requires a tight collaboration between neurologist, neurosurgeon and neuroradiologist.the treatment modalities are numerous, but surgical clipping remains the most effective and safe method of management.surgical clipping of the neck of the aneurysms and flow preservation in all the efferent vessels remains the gold standard of intracranial aneurysms therapy.intracranial aneurysms may pose formidable surgical problems, even to the most experienced romanian neurosurgery (2012) xix 4: 309 – 355 355 neurosurgeons.surgical approaches must be large, with minimal retraction and maximal surgical exposure. we present a series of 48 intracranial anterior circulation aneurysms in 42 consecutive patients admitted to the neurosurgical departament of the national institute of neurology and neurovascular disease, between september 2010-september 2012, and whose management consisted in surgical clipping in 91,8%. surgical nuances in distal anterior circulation intracranial aneurysms c. toader*, m. stroi** *”carol davila” university of medecine an pharmacy bucharest arseni – bagdasar hospital, romania **national institute of neurology and neurovascular diseases, bucharest, romania distal anterior cerebral artery(daca) aneurysms, also called the pericallosal artery aneurysms are rare, being encountered in about 6% of all intracranial aneurysms and are located distally to the anterior communicating artery (acoa) on the a2– a5 segments of the aca, the most common at the a3 segment, anterior to the genu of the corpus callosum. daca aneurysms are small, and often with wide necks and presents more often with intracerebral hematomas than ruptured aneurysms in general and are associated with anomalies of the aca. surgical clipping is a safe and effective treatment method, which requires detailed knowledge of the microanatomy of the anterior cerebral artery and the surrounding structures.the challenge is to select the appropriate approach,locate the aneurysm deep inside the interhemispheric fissure, and to clip the neck adequately without obstructing the branching arteries. we present a personal series of four cases who underwent surgical clipping between february and august 2012 in the neurosurgical department of the national institute of neurology and neurovascular diseases. 3_oslobanua_biomarker romanian neurosurgery (2015) xxix 3: 247 253 247 is ykl-40 (chi3-l1) a new possible biomarker prognosticator in high grade glioma? a. oslobanu1, st.i. florian2 university of medicine and pharmacy, “iuliu hatieganu” cluj-napoca 1assistant professor in neurosurgery, 2professor in neurosurgery abstract: a biomarker is “a naturally occurring molecule, gene, or characteristic by which a particular pathological or physiological process, disease, etc. can be identified” and it could be used a measurable indicator for the presence or severity of disease state. ykl-40 is a secreted glycoprotein associated with extracellular matrix, a member of the mammalian chitinase-like proteins that is expressed in a several types of solid tumors. although the implication of this biomarker in tissue remodeling processes or the role in cancer cell proliferation, invasiveness, angiogenesis, and remodeling of the extracellular matrix is going to be well recognized, the regulation and role in glioblastoma multiforme (gbm) progression remains unknown. using the serum level of ykl-40 as a single screening test in cancer cannot be used, but in association with other tumoral biomarkers and imaging techniques can be a useful tool as a “prognosticator.” moreover, elucidation of the ykl-40 functions could be an attractive target for antitumor therapy. key words: biomarkers, high grade glioma, ykl-40. introduction in the last 10 years great efforts were made to find new biological markers in human pathology, and special attention was done to discover new tumoral markers that could help in defining new treatment possibilities, and to offer a better way to perform a prognosis with a high accuracy. high grade glioma represent an important group of human brain tumors, and in this respect finding new characteristics in their biology could open new ways in what represent challenges in therapy for this highly malignant with rapid evolution, and a dismal prognosis. the majority of the primary tumors of the central nervous system are represented by gliomas, and they are classified according to who into four different classes with the grade iv or glioblastoma multiforme (gbm) exhibiting the highest level of malignancy in terms of invasion, proliferation, angiogenesis, and necrosis. gbm is one of the most common primary brain tumor, and the most fatal in terms of survival, meaning that the survival time is 10 to 14 months with the current standard of care, including surgical removal, radiotherapy, and chemotherapeutic agent temozolomide. the gbm cells aggressively infiltrates the surrounding brain tissue, and this is the cause of his very high recurrence rate.[1] the complex nature of these tumors lead to classified gbm in subtypes, just in an attempt to guide research to develop new targeted therapies, listed in the best prognostic order as neural, pro-neural, classical, and mesenchymal. the neural and pro-neural resembles normal brain cells, in contrast with classical and mesenchymal subtypes that are much less differentiated and have a much worse prognosis.[2] one of the most overexpressed proteins by gbm cells is ykl-40. is a glycoprotein that 248 oslobanu, florian is ykl-40 (chi3-l1) a new possible biomarker prognosticator in high grade glioma? play a major role in the maturation of some cells of the immune system and it’s implications in inflammatory diseases and in some forms of solid tumors is growing. but, the exact mechanisms of ykl-40 in gbm remain unknown, and to validate it as a biomarker needs more work to be done. chi3-l1/ykl-40 in the last years a secreted glycoprotein associated with extracellular matrix, ykl-40, was identified to be the most highly upregulated protein, and even more the microarray analysis offer the information that ykl-40 could be one of the most overexpressed genes compare to normal brain tissue, but the role in progression of gbm remains elusive.[1] this glycoprotein in the light of the last years could represent a possible biomarker used in situation of patients with high grade gliomas (hgg), but according to the tumor marker utility grading system, a number of requirements must fulfilled before considering to have reached level of evidence i (loe i) to be clinical implementation feasible. in the most situations, including ykl-40, the studies of biomarkers are at the level loe iii, defined as retrospective studies. the loe ii, an intermediate level, is defined as studies with prospectively collected specimens.[3] the 18 glycosyl hydrolase family of chitinases is widely expressed from prokaryotes to eukaryotes, including mammals, despite the absence of endogenous chitin. acidic mammalian chitinase (amcase) play a multiple roles including inhibiting chitin-induced innate inflammation; augments chitin-free, allergen-induces th2 inflammation; and mediates effector functions of il-13. the ykl-40/chitinase-like proteins brp-39 plays important roles in inhibiting oxidant-induced lung injury, augments adaptive th2 immunity, regulates apoptosis, stimulates alternative macrophage activation, and contributes to fibrosis and wound healing.[4] ykl-40 was first discovered in human osteosarcoma cell line, mg-63, and is a 40 kda protein, and its first three aminoacids tyrosine, lysine, and leucine giving his name. even ykl-40 can bind to chitin directly, but the glycosyl hydrolase activity to break down chitin is absent. the ykl-40 is expressed by activated neutrophils, macrophages, vascular smooth cells, and chondrocytes and play an important role in extracellular matrix remodeling, macrophage induced inflammation, and t-cell function. that’s why the ykl-40, implicated in maturation of some cells of the immune system, especially macrophages, may act as a prognostic marker for inflammatory diseases and cancer, but the role of ykl-40 in relation to tumors development and progression still remains unknown, and more work must be done to validate it as a tumoral marker. the location of gene encoding the ykl-40 is on chromosome 1q32.1, and chitinases (including ykl-40) are endo-�-1,4nacetylglucosamides are part of the innate immune response being involved in the host defense against organisms that contain chitin, which is found in the cell walls of many bacteria and fungi.[1] ykl-40 serum level in patients with tumors the serum level of the ykl-40 is found elevated in patients with different types of solid tumors, including adenocarcinomas, small cell lung carcinoma, glioblastoma, and melanoma, with the highest level in patients with advanced cancer and the poorest prognosis, and in many cases could provides independent information of survival, but at this time he cannot be used as a single screening test for cancer.[3] romanian neurosurgery (2015) xxix 3: 247 253 249 in vitro, ykl-40 is secreted by a number of cell lines, including the glioblastoma cell line u87 and the glioma cell lines u1242mg, u343mg and u1231mg. microarray gene analyses in glioblastomas and astrocytomas showed that ykl-40 is overexpressed compared to normal tissue, and it’s expression increases with glioma grade, being higher in glioblastoma than in astrocytic or oligodendroglial tumors. this high expression of ykl-40 was associated with a poor response to radiotherapy and a short time to disease progression and death. for adult patients operated for hgg, plasma level of ykl-40 during follow-up was lower in cases with no radiographic evidence of recurrences compared to patients with signs of disease and was associated with short survival, but in pediatric hgg overexpression of ykl-49 is less frequent and is not correlated with survival.[5] the results show that ykl-40 plays a pivotal role in proliferation of glioma cells through activation of the mapk and akt pathways [6], and suppression by shrna reduced glioma cell invasion, anchorageindependent growth and increase cell death triggered by chemotherapy (e.g. cisplatin, etoposide and doxorubicin).[7] ykl-40 and angiogenesis tumor cell invasion and metastasis can be influenced by inhibition of angiogenesis, and blockading vascular endothelial growth factor receptor-2 (vegfr-2) with monoclonal antibody dc101 inhibit gbm cell growth, but can increase tumor cell invasion using the preexistent vasculature. this increased invasion of the gbm cell can be inhibited by simultaneous blockade of epidermal growth factor receptor (egfr).[8] clinical trials in recurrent gbm testing an anti-vegf antibody show minimal benefit in terms of survival. moreover, a knockdown of the vegf gene in the u87 gbm cell line will up-regulate ykl-40 levels, and remains to be determined the regulatory relationship between ykl-40 and vegf, but both act as potent angiogenic factors in a synergistic effects on angiogenesis.[1] the ykl-40 is not regulated by vegf, and a long-term blockade of vegf will have an angiogenic compensative activity of gbm cells by inducing ykl-40. the phenomenon of promoting vascular development observed in tumor models treated chronically with a single anti-angiogenic drug is known as angiogenic rebound.[9][10] studies demonstrated that ykl-40 could enhance angiogenesis, radioresistance, and progression of gbm cells, and in the end ykl-40 can drove gbm cells into mesenchymal phenotype, where the tumor cells act as mural-like cells.[2] the receptors for ykl-40 still remains unknown, but ykl-40 induces interactions between integrin ���3 and sindecan-1 in endothelial cells, though sindecan-1 don’t mediate migration and invasion of gbm cells induced by ykl-40. other studies indicated that extracellular matrix is important for migration and invasion of the glioma cells, and ykl-40 can bind the heparin binding domain of syndecan-1, a transmembrane heparin sulfate proteoglycan in endothelial cells. however, syndecan-4 is at high levels in all glioma cells, and his down-regulation will reduced ykl-40-induced u373 cells migration.[1] ykl-40 in clinical practice recently, ykl-40 was introduced into clinical practice, but its application remains restricted.[11] the serum level of ykl-40 and mmp-9 can be monitored to help confirm the absence of active disease in gbm and ykl40 in anaplastic glioma patients.[12] in a study made for ykl-40 expression in 36 patients with glial tumors and 33 age 250 oslobanu, florian is ykl-40 (chi3-l1) a new possible biomarker prognosticator in high grade glioma? matched healthy persons, expression of ykl40 was measured by gene analysis, immunohistochemistry and elisa. in patients with hgg the ykl-40 serum levels was significantly increased compare to healthy subjects, and serum concentrations increased with tumor grade and correlated positively with transcript rate.[13] a prospective longitudinal study made a correlation between the serum levels of ykl40 and mri findings in 197 patients with gbm. in patients with no radiographic evidence of disease the serum levels of ykl40 was significantly lower compared to patients with radiographic evidence of tumor. furthermore, a smaller study was made in 60 patients with gbm who underwent gross total resection or subtotal resection, and showed that in patients who had more extensive tumor resection the levels of ykl-40 dropped postoperatively. in a study of 105 patients, the most important prognostic factors in patients with primary gbm were the extent of resection, mgmt promoter methylation status and ykl-40 expression by immunohistochemistry.[14] also, longitudinal increases in serum level of ykl-40 is associated with increased risk of death in patients with gbm or anaplastic gliomas.[15] glial fibrillary acidic protein is the current standard immunohistochemical marker used to differentiate between different types of gliomas, but in one study ykl-40 staining offer a better distinction of gbm versus anaplastic oligodendroglioma, and a combination of those two staining’s offer even a greater diagnostic accuracy.[16] despite identical histological features, the biology of hgg in children differs from that in adults.[17] does therapy influence ykl-40 serum level? in a study of 60 patients who underwent a standard treatment (surgery, radiotherapy and chemotherapy) and standard radiological monitoring (mri at pre-defined stages) the ykl-40 serum level was evaluated. patients were divided in two groups based on the extent of resection (total or subtotal) in accordance with mri results after 48 hours following surgery. at multivariate analysis a significant hazards ratio of 1.97 was found, and a significant association with shorter outcome in patients whose postoperative ykl-40 concentration increases higher than 100%; a negative prognostic index is still considered for a 50% increase. as a conclusion, biomarker ykl-40 could provide earlier and additional information and is a further aid in establishing the prognosis of gbm patients who undergone surgery.[18] in another study, poorer radiation response, shorter time to progression and shorter overall survival was associated with higher ykl-40 expression in the subtotal resection group and it was validated in the gross-total resection group by association with higher ykl-40 expression. the ykl-40 was an independent predictor of survival, after adjusting for patient age, performance status, and extent of resection.[19] a combination of preoperative profile igfbp-2, gfap, and ykl-40 plasma levels could serve as an additional tools for patients with inoperable brain lesions suggestive of gbm.[20] the most important factor who influence the os of patients with gbm is the extent of removal, and is an independent prognostic factor that predicts os better than mgmt status.[21] a mouse monoclonal anti-ykl-40 antibody (may) bind specifically with recombinant ykl-40 and with ykl-40 secreted from osteoblastoma cells mg-63 and brain tumor cells and thus inhibit tube formation of microvascular endothelial cells; romanian neurosurgery (2015) xxix 3: 247 253 251 also abolish activation of the membrane receptor vegf receptor 2 and intracellular signaling mitogen-activated protein kinase extracellular signal-regulated kinase (erk) 1 and erk 2; enhance cell death response of u87 line to γ-irradiation.[22] thus the conjunction therapy with may and radiotherapy synergistically inhibit vascularization and progression in tumor.[23] ykl-40 can be used as predictor of survival in patients with hgg, and longitudinal studies with a larger patient population are needed to confirm these findings.[12] 252 oslobanu, florian is ykl-40 (chi3-l1) a new possible biomarker prognosticator in high grade glioma? conclusion can we use ykl-40 as a biomarker in gbm? ykl-40, this 40kda glycoprotein belonging to the chitinase family but without chitin hydrolase activity is a new possible biomarker in gbm. it acts as an antiapoptoic protein, but the exact mechanism in gbm progression, invasiveness and angiogenesis remains elusive. according to werner et al. there are six different clinical criteria to assess the value of tumor markers in clinical practice, such as biochemical characteristics, organ specificity, or clinical usefulness.[24] ykl-40 is neither organnor tumor-specific, and in the “tumor marker utility grading system” introduced by hayes and colleagues is on the “utility scale +” and “utility scale +/-”, indicate that serum level of ykl-40 may have a role in screening and monitoring of patients with cancer.[25] the importance of ykl-40 in screening and monitoring of the patients with gbm needs to be proved by appropriate prospective study in which is assessed the benefit of using serum levels of ykl-40 in clinical decision-making process. references [17] antonelli m, buttarelli fr, arcella a, nobusawa s, donofrio v, oghaki h, giangaspero f. prognostic significance of histological grading, p53 status, ykl-40 expression, and idh1 mutations in pediatric high-grade gliomas. j neurooncol. 2010 sep;99(2):209-15. doi: 10.1007/s11060-010-0129-5. epub 2010 feb 21 [18] bernardi d, padoan a, ballin a, sartori m, manara r, scienza r, plebani m, della puppa a. serum ykl-40 following resection for cerebral glioblastoma. j neurooncol. 2012 apr;107(2):299-305. doi: 10.1007/s11060-011-0762-7. epub 2011 nov 19 [4] chun geun lee, carla a. da silva, charles s. dela cruz, farida ahangari, bing ma, min-jong kang, chuanhua he, seyedtaghi takyar, and jack a. elias. role of chitin and chitinase/chitinase-like proteins in inflammation, tissue remodeling, and injury; annu rev physiol. 2011; 73: 10.1146/annurev-physiol-012110142250.doi: 10.1146/annurev-physiol-012110-142250 [22] faibish m, francescone r, bentley b, yan w, shao r. a ykl-40-neutralizing antibody blocks tumor angiogenesis and progression: a potential therapeutic agent in cancers. mol cancer ther. 2011 may;10(5):74251. doi: 10.1158/1535-7163.mct-10-0868. epub 2011 feb 25 [2] francescone, ralph anthony, "the role of ykl-40 in the progression of glioblastoma" (2013). dissertations. paper 793 [20] gállego pérez-larraya j, paris s, idbaih a, dehais c, laigle-donadey f, navarro s, capelle l, mokhtari k, marie y, sanson m, hoang-xuan k, delattre jy, mallet a. diagnostic and prognostic value of preoperative combined gfap, igfbp-2, and ykl-40 plasma levels in patients with glioblastoma. cancer. 2014 dec 15;120(24):3972-80. doi: 10.1002/cncr.28949. epub 2014 aug 19 [25] hayes df, bast rc, desch ce, et al. tumor marker utility grading system: a framework to evaluate clinical utility of tumor markers. j natl cancer inst 1996;88:1456-66 [12] hormigo a; gu b; karimi s; riedel e; panageas ks; edgar ma; tanwar mk; rao js; fleisher m; deangelis lm; holland ec. ykl-40 and matrix metalloproteinase9 as potential serum biomarkers for patients with highgrade gliomas. clin cancer res. 2006; 12(19):5698-704 (issn: 1078-0432) [14] iwamoto fabio m, hormigo adilia. unveiling ykl40, from serum marker to target therapy in glioblastoma. front. oncol., 28 april 2014;http://dx.doi.org/10.3389/fonc.2014.00090 [15] iwamoto fm; hottinger af; karimi s; riedel e; dantis j; jahdi m; panageas ks; lassman ab; abrey le; fleisher m; deangelis lm; holland ec; hormigo a. serum ykl-40 is a marker of prognosis and disease status in high-grade gliomas.; neuro oncol. 2011; 13(11):1244-51 (issn: 1523-5866) [3] julia s. johansen, benny vittrup jensen, anne roslind, dorte nielsen and paul a. price. serum ykl40, a new prognostic biomarker in cancer patients?, cancer epidemiol biomarkers prev 2006;15(2):194–202 [11] kazakova mh, sarafian vs. ykl-40--a novel biomarker in clinical practice?; folia med (plovdiv). 2009 jan-mar;51(1):5-14 [13] kazakova mh, staneva dn, koev ig, staikov dg, mateva n, timonov pt, miloshev ga, sarafian vs. protein and mrna levels of ykl-40 in high-grade glioma. folia biol (praha). 2014;60(6):261-7. (issn: 0015-5500) [7] ku bm, lee yk, ryu j, jeong jy, choi j, eun km, shin hy, kim dg, hwang em, yoo jc, park jy, roh gs, kim hj, cho gj, choi ws, paek sh, kang ss. chi3l1 (ykl-40) is expressed in human gliomas and regulates the invasion, growth and survival of glioma cells. int j cancer. 2011 mar 15;128(6):1316-26. doi: 10.1002/ijc.25466 romanian neurosurgery (2015) xxix 3: 247 253 253 [8] lamszus k, brockmann ma, eckerich c, bohlen p, may c, mangold u, fillbrandt r, westphal m. inhibition of glioblastoma angiogenesis and invasion by combined treatments directed against vascular endothelial growth factor receptor-2, epidermal growth factor receptor, and vascular endothelial-cadherin. clin cancer res. 2005 jul 1;11(13):4934-40 [5] nicolai a. schultz and julia s. johansen. ykl-40— a protein in the field of translational medicine: a role as a biomarker in cancer patients?; cancers 2010, 2(3), 1453-1491; doi:10.3390/cancers2031453 [16] nutt cl, betensky ra, brower ma, batchelor tt, louis dn, stemmer-rachamimov ao. ykl-40 is a differential diagnostic marker for histologic subtypes of high-grade gliomas. clin cancer res. 2005 mar 15;11(6):2258-64 [1] osrah, bahiya, "analysis of the mechanism by which ykl-40 promotes glioma cell migration" (2011). vcu theses and dissertations. paper 2456 [19] pelloski ce, mahajan a, maor m, chang el, woo s, gilbert m, colman h, yang h, ledoux a, blair h, passe s, jenkins rb, aldape kd. ykl-40 expression is associated with poorer response to radiation and shorter overall survival in glioblastoma. clin cancer res. 2005 may 1;11(9):3326-34 [9] rong shao. ykl-40 acts as an angiogenic factor to promote tumor angiogenesis; front. physiol., 28 may 2013;http://dx.doi.org/10.3389/fphys.2013.00122 [21] salvati m, pichierri a, piccirilli m, floriana brunetto gm, d'elia a, artizzu s, santoro f, arcella a, giangaspero f, frati a, simione l, santoro a. extent of tumor removal and molecular markers in cerebral glioblastoma: a combined prognostic factors study in a surgical series of 105 patients. j neurosurg. 2012 aug;117(2):204-11. doi: 10.3171/2012.4.jns101702. epub 2012 jun 1 [10] saidi a, javerzat s, bellahcène a, de vos j, bello l, castronovo v, deprez m, loiseau h, bikfalvi a, hagedorn m. experimental anti-angiogenesis causes upregulation of genes associated with poor survival in glioblastoma. int j cancer. 2008 may 15;122(10):218798 [23] shao r, francescone r, ngernyuang n, bentley b, taylor sl, moral l, yan w. anti-ykl-40 antibody and ionizing irradiation synergistically inhibit tumor vascularization and malignancy in glioblastoma. carcinogenesis. 2014 feb;35(2):373-82. doi: 10.1093/carcin/bgt380. epub 2013 nov 26 [24] werner m, faser c, silverberg m. clinical utility and validation of emerging biochemical markers for mammary adenocarcinoma. clin chem 1993;39:2386-96 [6] zhang w, kawanishi m, miyake k, kagawa m, kawai n, murao k, nishiyama a, fei z, zhang x, tamiya t. association between ykl-40 and adult primary astrocytoma. cancer. 2010 jun 1;116(11):268897. doi: 10.1002/cncr.25084 gorganrm_surgicalmanagement 28 gorgan et al intracerebral and intramedullar multiple cavernomas surgical management of symptomatic spinal cord and intracerebral cavernomas in a multiple cavernomas case r.m. gorgan, f. brehar, m. catana, v. pruna, ana gheorghiu, g. popescu, catioara cristescu, a. giovani clinic of neurosurgery, “bagdasar – arseni” emergency clinical hospital, “carol davila” university of medicine and pharmacy, bucharest abstract: multiple cavernous malformations are associated with familial cases and are present in 10-20% of all cavernoma cases. 5% of cavernomas are located intramedullary and of these only 10% present multiple cavernomas. with the availability of echo gradient mri the cases of multiple cavernomas are diagnosed earlier and it is not rare that it uncovers multiple cavernomas in cases where only a single lesion can be identified on regular mri sequences. we present the case of a 55 years old woman presented with a two years history of mild backache, followed by progressive lower legs motor deficit and urinary retention. the spine mri showed an intramedullary t2/3 lesion and the cerebral mri established the diagnosis of multiple cavernomas. one year after the intramedullary cavernoma was operated with success, she developed generalized seizures and a new cerebral mri showed bleeding and volume growth of one right temporal pole cavernoma. the cerebral lesion was resected successfully and the patient was discharged free of seizures. this familial type multiple cavernomas cases should be screened and followed with repeated brain and spine mri’s every year. key words: multiple cavernous malformations, spinal cord, seizures, motor deficit introduction multiple cavernous malformations are associated with familial cases and are present in 10-20% of all cavernoma cases. 5% of cavernomas are located intramedullary and of these only 10% present multiple cavernomas. reports of multiple cavernomas are yet rare in literature and they usualy focus on intracranian lesions. after the mri was introduced in clinical practice the study of cavernous malformations shifted from a few anecdotal case reports to large series, some of them larger than 300 cases. with the availability of echo gradient mri the cases of multiple cavernomas are diagnosed earlier and it is not rare that it uncovers multiple cavernomas in cases where only a single lesion can be identified on regular mri sequences (1, 6, 9). spinal intramedullary cavernomas are at times difficult to differentiate from other romanian neurosurgery (2016) xxx 1: 28 34 29 intramedullary tumors but a few mri characteristics like the hypointense hemosiderin ring surrounding the lesion should orient the diagnosis. compared to intracranian lesions the compactness of white matter long tracts and grey matter nuclei intramedullary makes dangerous lesions of the cavrnomas in this location. this is the reason why most of the patients with both spinal and intracranian cm have the intramedullary lesion removed first. (3, 16, 17) we present a young woman’s case of multiple cavernomas located both at spinal level and intracranian levels, with emphasis on the surgical technique for removal of two intramedullary and temporal lesions. case presentation a 55 years old woman presented with a two years history of mild backache. a few months before admission she noted mild lower legs motor deficit progressing to difficulty ambulating without help and urinary retention. the patient had previous surgery for a thyroid tumor and hysterectomy and she received medication for mild arterial hypertension. on admission she showed 3/5 motor weakness and mild sensory deficit in both lower limb. her ankle and knee reflexes were diminished and she had difficulty urinating. the mri scan showed an enlarged spinal cord at the t3-t4 level with an inhomogeneous central signal and a peripheral hyperintensity prolonged from t2 to t4 disk. an area corresponding to t3 disk abnormal serpentine vessels were observed. no angiography was performed because the brain mri confirmed the diagnosis of multiple cavernomas. figure 1 t2-t3 intramedullary lesion, a hypointense signal in t2 indicates old bleeding first surgery the patient was placed prone on the operating table with the head resting in horseshoe. a midline incision over the involved level and a laminectomy centered on and continued one level above and one level below the lesion were performed. the operative microscope was used. the spine was 30 gorgan et al intracerebral and intramedullar multiple cavernomas not considered instable as the articulars were left intact at all levels. after opening the sura in the midline the arachnoid was incised and suspended to the dura from t2 to t4 and then the pia was opened and stitched laterally to the dura in a few suture points. with gentle moves of the baionet the medulla was split uncovering a hemosiderin rich gliosis tissue. deep to this tissue a tangled vessels reddish blue tumor was identified and gently dissected circumferential from the surrounding gliosis. an afferent vessel coming from the anterior spinal artery was coagulated and cut before complete resection. the pia was approximated with a few interrupted sutures and the arachnoid was closed with continuous 6.0 and the dura was tightly closed with 4.0 surjet. the patient’s deficit persisted postoperatively. it took 6 months of motor recovery for the patient to be able to ambulante with a cane and to completely recover the bladder function. as none of the cerebral lesions were symptomatic the patient was treated conservatively for 1.4 years. as she suffered a few temporal seizures she was readmitted and a new mri was performed. the echo gradient sequence showed a big 2/3 cm hypointense lesion in the right temporal pole and many infracentimetric lesions distributed both infratentorial and supratentorial bilateral, the biggest of the infratentorial lesions was located at the left posterior medulla level, pand of the supratentorial lesions, in the inferior parietal lobule. the patient was operated for resection of the right temporal pole cavernoma that increased in size due to rebleeding and manifested with seizures. figure 2 after the dura has been opened over the tumor, the pia is retracted by interrupting sutures figure 3 the strawberry like lesion is found surrounded by a yellow, hemosiderin gliosis tissue figure 4 complete removal of the tumor using extracapsular dissection figure 5 the pia is sutured after hemostasis was achieved romanian neurosurgery (2016) xxx 1: 28 34 31 figure 6 echo gradient mri sequence showing multiple cavernomas the biggest of the in the right temporal pole. many small cavernomas are located in the brain stem second surgery after elevating the right shoulder the head was rotated 45 degrees to the left and fixed with tape to the horseshoe. a curved incision starting 2 cm in front of the tragus and continued inside the hairline towards the midline was performed to allow the execution of a frontotemporal craniotomy. the scalp and the temporalis muscle were dissected with care in separate plans to avoid injury to the superficial temporal artery of to the facials nerve. a small craniectomy was performed using a perforator and gigli saw and after removing the bone the sphenoid wing was drilled flat with the middle fossa floor. the dura was incised with superior pedicle and a subtemporal route was choosen to open the basal cysterns. when a good brain relaxation was obtained, an approach through the sylvian fissure was used to see the discoloration area the cavernoma created in the inferior temporal girus. using the hemosiderin as landmark the cavernous malformation was approached and dissected circumferentialy using suction and cottonoids. after coagulating the feeder coming from an m3 branch the lesion was removed as a single piece with the surrounding hemosiderin ring attached. the lesion bed was inspected for a good hemosthasis and the dura was tightly sutured and suspended. an epidural drain was left in place under the bone flap and the scalp was sutured. 32 gorgan et al intracerebral and intramedullar multiple cavernomas figure 7 using a sylvian fissure corridor and a small corticotomy in t 1 the cavernoma is identified and circumferentially disected along with the hemosiderin rich gliosis ring figure 8 using cottonoids to create a plane between the lesion and the parenchima, the cavernoma is resected in one piece figure 9 the cavernoma bed after resection and hemostasis romanian neurosurgery (2016) xxx 1: 28 34 33 figure 10 postoperative ct scan, showing total resection of the cavernoma the postoperative course was uneventful with no deficits or seizures. the patient was discharged in good health one week after the surgery. discussion intramedullary cavernous malformations are rare lesions with only few cases reported in literature yet the association between intramedullary location and the presence of multiple cavernomas is extremely rare. (2, 4, 7) the most common site for intramedullary lesions is the thoracic cord, but they have been described at cervical level and cauda equina. (5, 8, 12) in most of the cases the slowly progressive myelopathy is the usual presentation a fact that is characteristic for low flow vascular malformations with tendency to repeated bleeding episodes, such as these. in the case of supratentorial location the most common presentation are partial or generalized seizures preceded by a few years history of headache. (11, 13) the cavernomas present as mixed signal intensity masses surrounded by a decreased signal intensity rim yet this was not the case here as both the spinal and the temporal lesions had bled recently. given the high density of eloquent areas intramedullary these lesions are better observed if asymptomatic. (14, 15) cases like this with multiple cavernomas will unfortunately never be cured of the disease and will come to the attention of the neurosurgeon every time one small lesion will encounter acute growth following a bleeding episode. conclusion multiple cavernoma cases present difficulties in the strategic long term management and surgery as the only curative option should remain the ultimate alternative when the new neurological deficits arise. this reported case is illustrative for the need to perform both cerebral and spinal mris in patients suspected for multiple cavernomas and these patient’s family members should be investigated to rule out this pathology. references 1.abdulrauf si, kaynar my, awad ia: a comparison of the clinical profile of cavernous malformations with and without associated venous malformations. neurosurgery 44:41–47,1999 crossref, medline 2.aiba t, tanaka r, koike t, kameyama s, takeda n, komata t: natural history of intracranial cavernous malformations. j neurosurg 83:56–59, 1995 link 3.sergio canavero. (1993) intramedullary cavernous 34 gorgan et al intracerebral and intramedullar multiple cavernomas angiomas of the spinal cord.neurosurgery 32, 693-694. . online publication date: 1-apr-1993. [crossref] 4.pierpaolo lunardi, michele acqui, luigi ferrante, aldo fortuna. (1994) the role of intraoperative ultrasound imaging in the surgical removal of intramedullary cavernous angiomas. neurosurgery 34, 520-523. 5.joseph m. zabramski, m.d., thomas m. wascher, m.d., robert f. spetzler, m.d., blakejohnson, m.d., john golfinos, m.d., burton p. drayer, m.d., ben brown, m.d., danielrigamonti, m.d., and geraldine brown, r.n., m.s.. (1994) the natural history of familial cavernous malformations: results of an ongoing study 6.p. drigo, i. mammi, p. a. battistella, g. ricchieri, c. carollo. (1994) familial cerebral, hepatic, and retinal cavernous angiomas: a new syndrome. child's nervous system 10, 205-209 7.a gil-nagel. (1995) familial cerebral cavernous angioma: clinical analysis of a family and phenotypic classification. epilepsy research 21, 27-36. online publication date: 1-may-1995 8.douglas kondziolka, m.d., m.sc., f.r.c.s.(c), l. dade lunsford, m.d., and john r. w.kestle, m.d., m.sc., f.r.c.s.(c). (1995) the natural history of cerebral cavernous malformations. journal of neurosurgery 83:5, 820-824. . online publication date: 1-nov-1995 9.issam awad, m.d., and pascal jabbour, m.d.. (2006) cerebral cavernous malformations and epilepsy. neurosurgical focus 21:1, 1-9. . online publication date: 1-jul-2006 10.filiz koc, deniz yerdelen, zafer koc. (2008) multiple supratentorial and infratentorial cavernous malformations. neurosurgery quarterly 18, 141-143. online publication date: 1-jun-2008. 11.filiz koc, deniz yerdelen, zafer koc. (2008) multiple supratentorial and infratentorial cavernous malformations. neurosurgery quarterly 18, 141-143. . online publication date: 1-jun-2008. 12.shigeru miyake, yoshito uchihashi, yoshiaki takaishi, yoshio sakagami, eijikohmura. (2007) multiple cavernous angiomas of the cauda equina-case report-.neurologia medico-chirurgica 13.nundia louis, robert marsh. (2016) simultaneous and sequential hemorrhage of multiple cerebral cavernous malformations: a case report. journal of medical case reports 10. . online publication date: 1dec-2016. 14.juri kivelev, mika niemelä, riku kivisaari, reza dashti, aki laakso, juha hernesniemi. (2009) longterm outcome of patients with multiple cerebral cavernous malformations. neurosurgery 65, 450-455 15.juri kivelev, mika niemelä, riku kivisaari, reza dashti, aki laakso, juha hernesniemi. (2009) longterm outcome of patients with multiple cerebral cavernous malformations. neurosurgery 65, 450-455. . online publication date: 1sep-2009. 16.bradley a. gross, m.d., rose du, m.d., ph.d., a. john popp, m.d., and arthur l. day, m.d. intramedullary spinal cord cavernous malformations, neurosurgical focus sep 2010 / vol. 29 / no. 3 / page e14 17.john a. anson, m.d., and robert f. spetzler, m.d. surgical resection of intramedullary spinal cord cavernous malformations ; journal of neurosurgery mar 1993 / vol. 78 / no. 3, pages 446-451 doi: 10.33962/roneuro-2021-044 talk and die syndrome. a comprehensive review ivan david lozada-martínez, alexandra galeano-buelvas, a.c. pearson-arrieta, oscar javier diaz-castillo, michael gregorio ortega-sierra, j.s. robledo-arias, j.s. serna-trejos, julio césar mantilla-pardo, d.a. betancourt-cundar, randy eliecer frias-bechara, harold yesid mendez -martinez, luis rafael moscote -salazar romanian neurosurgery (2021) xxxv (3): pp. 262-269 doi: 10.33962/roneuro-2021-044 www.journals.lapub.co.uk/index.php/roneurosurgery talk and die syndrome. a comprehensive review i.d. lozada-martínez1,2,3, a. galeano-buelvas1, a.c. pearson-arrieta4, o.j. diaz-castillo4, m.g. ortega-sierra5, j.s. robledo-arias6, juan santiago serna-trejos7, julio césar mantilla-pardo8, d.a. betancourtcundar9, randy eliecer frias-bechara5, harold yesid mendez-martinez10, luis rafael moscotesalazar1,2 1 medical and surgical research centre, university of cartagena, cartagena, colombia 2 colombian clinical research group in neurocritical care, university of cartagena, cartagena, colombia 3 global neurosurgery committee, world federation of neurosurgical societies, latin american chapter, colombia 4 school of medicine, universidad del sinú, cartagena, colombia 5 school of medicine, corporación universitaria rafael nuñez, cartagena, colombia 6 school of medicine, universidad del quindío, armenia, colombia 7 school of medicine, universidad libre, cali, colombia 8 school of medicine, universidad icesi, cali, colombia 9 school of medicine, universidad de antioquia, medellín, colombia 10 school of medicine, universidad de sucre, sincelejo, colombia abstract the "talk and die" syndrome is described as the clinical deterioration following a mild to moderate traumatic brain injury. in the face of this event, individuals are able to articulate recognizable words and then deteriorate within 48 hours of the injury. this syndrome represents a major public health challenge due to its high morbidity and mortality rate; it develops from an intracranial haemorrhage causing an increase in intracranial pressure and leading the person to a neurological crisis with focal signs, coma and later death. introduction the talk and die syndrome represents a major public health challenge because of its high mortality and disability rate, it can occur at any age, but the risk is significantly higher as the age increases [1]. people who keywords talk and die syndrome, traumatic brain injury, neurocritical care, neurosurgery, narrative review corresponding author: ivan david lozada-martinez medical and surgical research center, university of cartagena, cartagena, colombia ivandavidloma@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 263 talk and die syndrome "talk and die" after a head injury may suffer late complications that may be highly preventable if detected early [1,2]. intracranial hematoma is the main reason why a patient whose injury does not appear serious at first, subsequently dies [1,2]. [3]. the high risk of death following this event is that the victim initially appears stable after receiving an apparently minor head trauma, while intracranial hemorrhage either inside or outside the brain is ongoing. major warning signs include loss of consciousness on impact and severe headaches. if the hemorrhage progresses without being treated in time, the affected person may fall into a coma and even die [4]. the epidemiological study by dylan dean et al. found that patients who talk and died were older (median age, 81 years; interquartile range, 67-87 years), normotensive (median systolic blood pressure, 138 mm hg; interquartile range, 116-160 mm hg), commonly fall-injured (71.3%), and often (52.4%) died in non-trauma hospitals [5]. the prognosis is related to the amount of hemorrhage found at the time of diagnosis, so it is essential to take early action regarding the management and follow-up of these individuals, especially if they are high-risk groups such as elderly adults [6]. based on the above, the objective of this review is to provide information that favors the detection and timely treatment of this syndrome, thus having an impact on the reduction of deaths due to this cause. definition "talk and die" represents a small number of patients with mild head trauma who, due to intracranial causes, deteriorate and die [7]. really et al in 1987 first introduced the term "talk and die," used to describe a group of patients with potentially recoverable head injuries in whom the primary injury was not severe enough to destroy higher cognitive function. their ultimate demise was thought to represent a combination of secondary brain injury as well as other potentially preventable factors. for this reason, patients who talk and die have been the focus of multiple studies, most of which were relatively small with limited ability to identify associated factors [1]. the main cause leading to this syndrome is penetrating trauma [8]. in lower frequency are also found falls (28%), traffic accidents (20%), road traffic accidents (19%), assaults (11%), unknown cause (9%), bicycle (3%) and suicide (1%) [9]. injury severity is associated with risk factors such as older age, lower glasgow scale score on admission, higher injury severity score (iss), hypotension on arrival and comorbidities such as congestive heart failure, chronic kidney disease, liver cirrhosis and hematological disorders, subdural hemorrhage, contusion and vault fracture) [10]. therefore, it is essential to perform a multifocal approach in these individuals in terms of the etiology of the injury, pre-hospital care, initial treatment including the neurocritical care unit and surgical treatment in order to avoid progressive deterioration and multi-organ failure leading to death during the postoperative period [11,12]. mechanism of injury the magnitude of the brain injury and the time of duration depends on the severity of the resulting concussion, which is defined as a transient interruption of brain functions caused by a mechanical force. memory, consciousness, motor control or brainstem functions may be temporarily disrupted or impaired during this phenomenon. the mechanical deformation of brain tissue in a concussion injury is sufficient to interfere with both the functions of polarized neuronal membranes and synapses and render numerous brain neurons temporarily dysfunctional. a concussion is usually not sufficient to cause structural damage, but may result in abnormal brain metabolism for weeks after the initial injury [13]. the basic physiological sequelae that constitute the state of vulnerability induced by traumatic brain injury appear to be due to cellular ionic and metabolic alterations [14]. these pathological changes in the aging brain may trigger secondary brain injury contributing to more severe and irreversible damage in middle-aged and elderly patients, which explains why age plays an important role in the prognosis of those affected [15]. in the growing attempt to understand the pathophysiology of fatal non-projectile head injuries, three grades of diffuse axonal injury have been identified. in grade 1, histologically, axonal injury is seen in the white matter of the cerebral hemispheres, corpus callosum, brainstem and, less frequently, the cerebellum; in grade 2, there is also a focal lesion in the corpus callosum; and in grade 3, 264 i.d. lozada-martínez, a. galeano-buelvas, a.c. pearson-arrieta et al. there is also a focal lesion in the dorsolateral quadrant(s) of the rostral brainstem. it is worth mentioning that focal lesions can only be identified microscopically in most cases [16]. intracranial hematomas are the most frequent cause of deterioration in head trauma patients, so rapid diagnosis and decompression are the most important factors in saving these patients. [17]. the above is due to the increasing volume of accumulated blood which causes a progressive increase in intracranial pressure that can even force the brain down through the foramen magnum causing a brain herniation. this compresses the brain stem with such force that the centers controlling consciousness, respiration, heart rate and blood pressure cease to function, resulting in coma and death [4]. the area in which the intracranial hemorrhage occurs will be a determining factor in its pathophysiology. intra-axial hemorrhages occur directly in the substance of the brain due to the rupture of blood vessels caused by impact [4]. as for traumatic intraventricular hemorrhages, regardless of the presence or absence of neurological deficits should have close follow-up by emergency physicians because of the possibility of acute obstructive hydrocephalus requiring prompt surgical evacuation before unexpected but avoidable deterioration occurs [12]. on the other hand, among extra-axial hemorrhages, there are epidural, subdural and subarachnoid types of hemorrhage; the latter, for example, its mechanism is that blood leaks into the subarachnoid space, filled with cerebrospinal fluid and reaches the ventricles, causing severe headache, nausea and vomiting. meanwhile, in subdural hematoma, the bridging veins that drain the surface of the brain into the venous sinuses are torn generating a low-pressure venous hemorrhage. among the adverse consequences of hemorrhage is hydrocephalus, which, if uncontrolled, can lead to coma and death. another complication is an intense vasospasm, which can be so marked that it restricts blood flow to that region of the brain, leading to ischemic stroke [4]. vasospasm is proposed as the cause of secondary ischemic hypoxia associated with a high incidence of acute subdural hematomas and brain swelling. suggestions for further testing this hypothesis and implications for preventive management are discussed [13]. it is recognized that an apparently minor head injury can cause diffuse cerebral edema with serious consequences. among the two possible mechanisms described by mccrory are, first, cerebral hyperemia and increased blood volume as a result of disordered cerebrovascular autoregulation, commonly known as "malignant cerebral edema". the second is due to true cerebral edema [18]. the distinction between cerebral swelling and cerebral edema was made by klazko, who observed that cerebral edema could be cytotoxic or vasogenic and that both could occur after craniocerebral trauma. therefore, the mechanism of death would be a transtentorial herniation of the brain stem as a consequence of elevated intracranial pressure, which would affect the cardiorespiratory centers of the brain stem [18]. findings from diffusion mri and apparent diffusion coefficient (adc) mapping suggest that cellular swelling is predominant in the peripheral area for a period of 24 to 72 hours while cells in the central area of the contusion undergo shrinkage, disintegration and homogenization [19]. clinical manifestations the fact that the patient is talking implies a less severe primary brain injury, but does not necessarily place the patient in the mild head injury category (gcs 13-15) as there are cases with an eye-opening score of 2 or 3, a verbal score of 3 and a motor score of 5 or 6 (gcs of 10-12), which gives a gcs between 9 12, placing the patient in the moderate injury group, which of course is associated with a worse prognosis [20]. in addition, in children admitted with head trauma caused primarily by motor vehicle accidents or falls, they had initial glasgow coma scale scores equal to or greater than 9 and demonstrated irritability and restlessness just prior to deterioration [21]. the main primary clinical manifestation is a severe headache followed by problems with speech, vision and even coma. it should be noted that at the beginning people usually do not present any symptoms, but in the course of time may manifest severe headaches, weakness and confusion resulting from lesions of intracranial masses and increased intracranial pressure (icp) that were progressively established [22]. the mean age, the degree of midline shift observed on computed tomography (ct) and the presence of subdural hematoma are the main factors influencing the 265 talk and die syndrome evolution (recovery or death) of patients who talk [23]. the difference between those with and without a lucid period is related to the degree of primary lesion by diffuse white matter impingement and the presence of ventriculomegaly with large sulci rarely found in lucid patients [24]. in the study by kim et al. it was observed that the median age of patients who died due to hematomas was 82.5 years, compared to 54.0 years for patients who died from refractory icp elevations (p = 0.003). hyponatremia occurred during the first 7 days in 38.9% of patients who died due to hematomas and in only 14.3% of patients in the icp group (p = 0.236). no seizures were observed in any of the patients in either group. skull fractures were present in four of the 18 (22.2%) patients who died of hematomas, in contrast to four of the seven (57.1%) patients who died of refractory icp [25]. the presence of a fracture line proved to be significant, as it was accompanied by approximately 38% intracranial abnormalities versus 6% in nonfractured cases. in addition, high-volume hematomas are associated with more brain injury after a worse clinical course of the patient prior to evacuation, but evacuation does not improve executive functioning in these individuals. early detection of any asymptomatic intracranial pathology allowed immediate transfer of patients to the neurosurgical center, where surgical treatment was performed, when indicated, without mortality or morbidity [26,27]. in 2 cases of severe traumatic brain injury (tbi) with acute subdural hematoma in which cerebral blood flow (cbf) and cerebral blood volume (cbv) measurements were obtained before evacuation of the subdural hematoma and immediately after removal. the younger patient had the highest preoperative cbf. thus, it is possible that the cerebral circulation is more easily compromised in older patients; however, it is also possible that the brains of younger patients are more tolerant to similar low levels of cbv [22]. likewise, patients whose cbf returns to normal 2-3 weeks after severe traumatic brain injury after being abnormally low in the acute phase of the injury can be expected to achieve a good neurological outcome [28]. diagnosis to diagnose an intracranial hemorrhage we can detect as warning signs: loss of consciousness at the moment of impact, nausea, vomiting, severe headache, focal neurological deficits, confusion, lethargy, any change in neurological status, seizures, use of antiplatelet drugs, anticoagulants and individuals with coagulopathies that result in poor clotting ability [4]. despite the above, diagnosis is often slowed down by the lack of knowledge of these signs on the part of medical personnel and by the existence of underestimation predictors such as the characteristics of the lesions (severe cranial and pelvic lesions), the characteristics of the patients (middle-aged and conscious) and the time of day (nocturnal) [29]. generally, the level and duration of consciousness is related to the prognosis of those affected, for this reason, it is common to assume that the individual is stable after he/she speaks after having suffered a brain injury, however, this is the trigger for these patients to have a high mortality rate despite the fact that they may be potentially survivable [30]. although talking indicates a nonlethal impact brain injury, deterioration is a marker of poor prognosis. thus, outcome depends on early recognition of deterioration and rapid removal of mass lesions. the challenge for emergency physicians is to distinguish patients at risk for deterioration from the many patients evaluated after traumatic brain injury [31]. the following are independent predictors of outcome (in order of importance): glasgow coma scale score after deterioration into coma, highest intracranial pressure during the patient's evolution, degree of midline shift, type of intracranial injury, and patient age. in contrast, the mechanism of injury, the glasgow coma scale verbal score during the lucid interval, and the time to deterioration or to surgical intervention did not influence the final outcome [32]. the diagnostic value of gcs ≤8 for severe tbi in patients with multiple injuries has low sensitivity (56.1%) but higher specificity (82.2%). because of the low sensitivity of gcs, we suggest the use of the anatomic scoring system with ais head ≥3 to define severe tbi in patients with multiple lesions [33]. computed tomography (ct) constitutes a gold standard in the evaluation of patients after tbi. none of the available guidelines address the role of repeat ct as a follow-up procedure after head injury in pediatric patients. experience suggests that a repeat ct scan should be a routine component of 266 i.d. lozada-martínez, a. galeano-buelvas, a.c. pearson-arrieta et al. postoperative management, especially in pediatric patients after neurosurgery or in a barbiturate coma [34]. age, type of injury, loss of consciousness, posttraumatic seizures, otorhinolaryngologic bleeding, vomiting, scalp injury, and polytrauma were not found to be predictors of a positive ct scan. gcs score on admission, focal neurologic deficits, and fractures detected by skull radiography were found to be statistically significant predictors of positive ct findings [35]. studies have found considerable variation among institutions and individual physicians in ordering ct scans for patients with minor head injuries. although emergency physicians were selective in ordering ct, the yield of radiography was very low across hospitals. these findings suggest great potential for a more standardized and efficient use of ct of the head, possibly through the use of a clinical decision rule [36]. increased pulsatility index after mild to moderate tbi is cause for concern about the possibility of further neurological deterioration so ct and doppler measurements could be combined to detect on admission patients at risk of secondary neurological deterioration in order to improve their initial disposition [37]. forensic autopsy is important in patients with "talk and die" to clarify the causal relationship with the head injury in relation to any other forensic disputes. the deaths of these patients raise medicolegal questions, about the precise causes of death and the possible correlation of death with the head injury, especially when such deaths occur after a prolonged period of time following the event [30]. in an investigation of 13 autopsies with examination of the brain, it was found that 5 patients died with severe brain injuries not complicated by iatrogenic factors and 4 patients died with associated severe injuries. iatrogenic factors significantly complicated the death of 40% of the patients, a considerable alarming figure [12]. using a decision tree analysis, studies have found hypotension and low cerebral perfusion pressure (cpp) to be the best predictors of death [38]. other parameters are also found to be predictors of mortality such as (in order of importance): glasgow coma scale score after deterioration into coma, the highest intracranial pressure score during the patient's evolution, the degree of midline shift, the type of intracranial injury, and the patient's age. in contrast, the mechanism of injury, the glasgow coma scale verbal score during the time interval between lucidity and clinical deterioration or until the patient underwent surgery, did not prove to influence the final outcome [32]. evidence suggests that 92% of patients with icp plasma levels greater than 15 µg/ml or d-dimer levels greater than 5 µg/ml died regardless of their level of consciousness on admission, whereas all patients recovered well when their icp levels were less than 2 µg/ml or d-dimer levels were less than 1 µg/ml. thus, it was revealed that plasma icp and ddimer levels on admission are reliable prognostic markers of head injury. using these markers, patients with unfavorable outcomes (progressive brain injury), such as the talk anddeteriorate type, could be easily identified on admission [39]. the ddimer value was significantly higher in the talk and die group at any time and was considered the best coagulation/fibrinolytic parameter to monitor from the early stage of injury predicting outcome [40,41]. treatment the most important factors in saving these patients are prompt diagnosis and immediate surgical decompression before irreversible brain damage occurs [42]. in 1983, a uniform protocol for the initial treatment of patients with head injuries was introduced, based on knowledge of the epidemiology of head injuries, the importance and frequency of preventable factors in the region, and also adjusted to the specific geographic conditions. this protocol is guided by the level of consciousness prior to arrival at the hospital, the initial assessment of the level of consciousness and neurological status on arrival at the hospital and, finally, subsequent changes in the level of consciousness and neurological status [43]. most people admitted to the emergency department for traumatic brain injury are discharged after one or two days [3]. the study by eric cecala peterson et al. found that all patients were managed with observation in the intensive care unit and hyperosmolar therapy to maintain serum osmolarity at 300. overall, 7 of 13 (54%) suffered clinical deterioration with a mean of 4.5 days after the injury. of those injured with immediate surgical decompression, all had good results and returned to work. there was no difference in contusion or edema volumes between patients with and without clinical deterioration. based on this series and experience in 267 talk and die syndrome other tbi patients, prophylactic hypertonic saline (hts) infusions are no longer used in the setting of head trauma. management of these patients with intensive care unit, admission and early intracranial pressure monitoring is recommended. if they deteriorate despite these measures, rapid bifrontal decompression may lead to good functional outcomes [44]. potential adverse events that have been associated with hts include renal failure, central pontine myelinolysis rebound icp elevation [45]. for individual therapeutic management there is currently the use of transcranial doppler (measuring mean cerebral artery systolic, diastolic and mean cerebral artery (mca) flow velocities and a derived value, pulsatility index, jugular venous oxygen measurement, intracranial pressure waveform analysis and near infrared spectroscopy. in addition, it has been suggested that the complexity of the lesion may necessitate the administration of combinations of neuroprotective agents acting at various steps in secondary self-destructive injury cascades. each cascade may have its own critical window for treatment, so sequential or concurrent combinations of therapeutic agents may be necessary. for example, administration of a single intravenous bolus of mg salts for up to 12 h after injury has demonstrated improvement in neurological recovery after injury in rats [46]. studies by the adelaide head injury group suggest that the beneficial effects of mg may be related to the positive mrna regulation of betaamyloid precursor protein (app), which is a normal component of neurons and there is evidence of its role in the repair and regeneration of these cells. on the other hand, the apoe genotype, specifically the apolipoprotein 4 allele, has been associated with increased odds of having a poor outcome at 6 months, increased odds of having plaques of amyloid protein deposits, and have a 10-fold increased risk of alzheimer's disease [46]. controversy exists regarding prehospital intubations in patients with severe and moderate head injuries. it is unclear whether field intubations actually improve neurologic outcome or survival. failed attempts at field intubations may increase outof-hospital time and increase the risk of aspiration or hypoxia. hypoxia and hypotension have been found to worsen outcome in head trauma [47]. with respect to surgical procedures, all strategies of craniotomy, decompressive craniectomy, and initial trepanation appear to be effective, but the superiority of each procedure has not yet been established. since glasgow coma scale (gcs) scores, age, papillary reaction, and computed tomography findings are strongly correlated with outcome, each factor has been investigated as an indicator of resiliency [48]. individuals with ct-proven anisocoria, trephination of the skull prior to transfer resulted in uniformly good results without complications. time to relief of intracranial pressure was significantly shorter with trephination and neurological outcomes were not different [49]. as for craniotomy for evacuation of hematomas and/or intracranial contusions, it was the most common treatment recorded (performed in 30% of all cases), followed by treatment of barbiturate coma (8%) and decompressive craniectomy (6%) [50]. repeated use of ct should be a routine component of postoperative management, especially in pediatric patients after neurosurgery or in a barbiturate coma, because it prevents such revelations as a case of a previously undetected acute epidural hematoma in the right frontoparietal region with mass effect that displaced contiguous brain tissue to the contralateral side and, following this finding, the hematoma can be evacuated and bleeding from the ruptured middle meningeal artery can be stopped without any problems [34]. preventing secondary insults will remain the primary goal of treatment, but the next major advances in the treatment of head injury are likely to be through cell biology, with therapy. targeting specific intracellular targets and perhaps promoting genes that lead to repair and regeneration [46]. conclusions in order to reduce the morbimortality rate of the talk and die syndrome, it is essential to educate the population about the risks of suffering apparently mild or moderate cranioencephalic traumas that are not monitored by a health professional. in turn, in the medical field, specifically in the area of emergency and traumatology, health personnel should be educated about this syndrome in order to increase clinical suspicion and with it, the strict and constant monitoring of the vital functions of these patients, in order to be able to detect in time possible warning signs that can prevent serious sequelae and 268 i.d. lozada-martínez, a. galeano-buelvas, a.c. pearson-arrieta et al. even death of those affected. it should be noted that this syndrome can affect any age group; however, greater emphasis should be placed on high-risk populations such as older adults and individuals who use anticoagulants or antiplatelet drugs. references 1. davis dp, kene m, vilke gm, sise mj, kennedy f, eastman ab, et al. head-injured patients who “talk and die”: the san diego perspective. j trauma. 2007;62(2):277–81. 2. dunn lt, fitzpatrick mo, beard d, henry jm. patients with a head injury who “talk and die” in the 1990s. j trauma. 2003;54(3):497–502. 3. reilly p, graham d, hume adams j, jennett b. patients with head injury who talk and die. lancet. 1975;306(7931):375–7. 4. hodge sd jr, hubbard je. “talk and die syndrome” – the medical and legal consequence of an intracranial hemorrhage. depaul j health care law. 2018;19(1):1. 5. dean d, wetzel b, white n, kuppermann n, wang ne, haukoos js, et al. from 9-1-1 call to death: evaluating traumatic deaths in seven regions for early recognition of high-risk patients. j trauma acute care surg. 2014;76(3):846–53. 6. tan je, ng i, lim j, wong hb, yeo tt. patients who talk and deteriorate: a new look at an old problem. ann acad med singapore. 2004;33(4):489–93. 7. goldschlager t, rosenfeld jv, winter cd. “talk and die” patients presenting to a major trauma centre over a 10 year period: a critical review. j clin neurosci. 2007;14(7):618–23; discussion 624. 8. mandavia dp, greenspan j, pritchard bj. sudden death following injury: analysis of the “talk and die” scenario. ann emerg med. 1999;34(4):s101 9. stanly s, tejasree t, nandini vld, ponnusankar s. talk and die syndrome: an unending mystery. ind j pharm pr. 2018;10(4):248–50. 10. shibahashi k, sugiyama k, okura y, hoda h, hamabe y. multicenter retrospective cohort study of “talk and die” after traumatic brain injury. world neurosurg. 2017;107:82–6. 11. cagetti b, cossu m, pau a, rivano c, viale g. the outcome from acute subdural and epidural intracranial haematomas in very elderly patients. br j neurosurg. 1992;6(3):227–31. 12. inamasu j, hori s, aikawa n. traumatic intraventricular hemorrhage causing talk and deteriorate syndrome. am j emerg med. 2001;19(2):167–8. 13. veevers ae, lawler w, rutty gn. walk and die: an unusual presentation of head injury. j forensic sci. 2009;54(6):1466–9. 14. doberstein ce, hovda da, becker dp. clinical considerations in the reduction of secondary brain injury. ann emerg med. 1993;22(6):993–7. 15. tokutomi t, miyagi t, ogawa t, ono j-i, kawamata t, sakamoto t, et al. age-associated increases in poor outcomes after traumatic brain injury: a report from the japan neurotrauma data bank. j neurotrauma. 2008;25(12):1407–14. 16. adams jh, doyle d, ford i, gennarelli ta, graham di, mclellan dr. diffuse axonal injury in head injury: definition, diagnosis and grading. histopathology. 1989;15(1):49–59. 17. rockswold gl, leonard pr, nagib mg. analysis of management in thirty-three closed head injury patients who “talked and deteriorated.” neurosurgery. 1987;21(1):51–5. 18. katayama y, kawamata t. edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of cerebral contusion in head trauma patients. acta neurochir suppl. 2003; 86:323–7. 19. humphreys rp, hendrick eb, hoffman hj. the headinjured child who ?talks and dies?: a report of 4 cases. childs nerv syst. 1990;6(3):139–42. 20. brett bl, gardner rc, godbout j, dams-o'connor k, keene cd. traumatic brain injury and risk of neurodegenerative disorder. biol psychiatry. 2021: s0006-3223(21)01359-7. 21. stanly s, tejasree t, nandini vld, ponnusankar s. talk and die syndrome: an unending mystery. ind j pharm pr. 2018;10(4):248–50. 22. schröder ml, muizelaar jp, kuta aj. documented reversal of global ischemia immediately after removal of an acute subdural hematoma. report of two cases: report of two cases. j neurosurg. 1994;80(2):324–7. 23. marshall lf, toole bm, bowers sa. the national traumatic coma data bank. part 2: patients who talk and deteriorate: implications for treatment: part 2: patients who talk and deteriorate: implications for treatment. j neurosurg. 1983;59(2):285–8. 24. bruce da, alavi a, bilaniuk l, dolinskas c, obrist w, uzzell b. diffuse cerebral swelling following head injuries in children: the syndrome of “malignant brain edema.” j neurosurg. 1981;54(2):170–8. 25. kim j, kemp s, kullas k, hitos k, dexter ma. injury patterns in patients who “talk and die”. j clin neurosci. 2013;20(12):1697–701. 26. león-carrión j, alarcón jc, revuelta m, murillo-cabezas f, domínguez-roldán jm, domínguez-morales mr, et al. executive functioning as outcome in patients after traumatic brain injury. int j neurosci. 1998;94(1–2):75–83. 27. servadei f, ciucci g, morichetti a, pagano f, burzi m, staffa g, et al. skull fracture as a factor of increased risk in minor head injuries. indication for a broader use of cerebral computed tomography scanning. surg neurol. 1988;30(5):364–9. 28. inoue y, shiozaki t, tasaki o, hayakata t, ikegawa h, yoshiya k, et al. changes in cerebral blood flow from the acute to the chronic phase of severe head injury. j neurotrauma. 2005;22(12):1411–8. 29. nakahara s, matsuoka t, ueno m, mizushima y, ichikawa m, yokota j, et al. predictive factors for undertriage 269 talk and die syndrome among severe blunt trauma patients: what enables them to slip through an established trauma triage protocol? j trauma. 2010;68(5):1044–51. 30. kibayashi k, ng’walali pm, hamada k, honjyo k, tsunenari s. discrepancy of clinical symptoms and prognosis of a patient — forensic significance of “talk and die” head injury. leg med (tokyo). 2000;2(3):175–80. 31. rockswold gl, pheley pj. patients who talk and deteriorate. ann emerg med. 1993;22(6):1004–7. 32. lobato rd, rivas jj, gomez pa, castañeda m, cañizal jm, sarabia r, et al. head-injured patients who talk and deteriorate into coma. analysis of 211 cases studied with computerized tomography: analysis of 211 cases studied with computerized tomography. j neurosurg. 1991;75(2):256–61. 33. grote s, böcker w, mutschler w, bouillon b, lefering r. diagnostic value of the glasgow coma scale for traumatic brain injury in 18,002 patients with severe multiple injuries. j neurotrauma. 2011;28(4):527–34. 34. zapolska g, komarowska m, turek g, hermanowicz a, matuszczak e, zielinska-turek j, et al. “talk and deteriorate” syndrome and the role of an immediate follow-up computed tomography of the head in children. pediatr pol. 2016;91(2):155–60. 35. thiruppathy sp, muthukumar n. mild head injury: revisited. acta neurochir (wien). 2004;146(10):1075–82; discussion 1082-3. 36. stiell ig, wells ga, vandemheen k, laupacis a, brison r, eisenhauer ma, et al. variation in ed use of computed tomography for patients with minor head injury. ann emerg med. 1997;30(1):14–22. 37. jaffres p, brun j, declety p, bosson j-l, fauvage b, schleiermacher a, et al. transcranial doppler to detect on admission patients at risk for neurological deterioration following mild and moderate brain trauma. intensive care med. 2005;31(6):785–90. 38. andrews pjd, sleeman dh, statham pfx, mcquatt a, corruble v, jones pa, et al. predicting recovery in patients suffering from traumatic brain injury by using admission variables and physiological data: a comparison between decision tree analysis and logistic regression. j neurosurg. 2002;97(2):326–36. 39. takahashi h, urano t, takada y, nagai n, takada a. fibrinolytic parameters as an admission prognostic marker of head injury in patients who talk and deteriorate. j neurosurg. 1997;86(5):768–72. 40. nakae r, takayama y, ogawa f, naoe y, yokota h. ddimer as a prognostic marker for head injury patients who talk and deteriorate. nihon kyukyu igakukai zasshi. 2014;25(6):247–53. 41. nakae r, takayama y, kuwamoto k, naoe y, sato h, yokota h. time course of coagulation and fibrinolytic parameters in patients with traumatic brain injury. j neurotrauma. 2016;33(7):688–95. 42. shively sb, priemer ds, stein mb, perl dp. pathophysiology of traumatic brain injury, chronic traumatic encephalopathy, and neuropsychiatric clinical expression. psychiatr clin north am. 2021; 44(3):443-458. 43. nordström ch, messeter k, sundbärg g, wåhlander s. severe traumatic brain lesions in sweden. part i: aspects of management in non-neurosurgical clinics. brain inj. 1989;3(3):247–65. 44. peterson ec, chesnut rm. talk and die revisited: bifrontal contusions and late deterioration. j trauma. 2011;71(6):1588–92. 45. heegaard w, biros m. traumatic brain injury. emerg med clin north am. 2007;25(3):655–78, viii. 46. reilly pl. brain injury: the pathophysiology of the first hours.’talk and die revisited’. j clin neurosci. 2001;8(5):398–403. 47. servadei f. prognostic factors in severely head injured adult patients with acute subdural haematoma’s. acta neurochir (wien). 1997;139(4):279–85. 48. karibe h, hayashi t, hirano t, kameyama m, nakagawa a, tominaga t. surgical management of traumatic acute subdural hematoma in adults: a review. neurol med chir (tokyo). 2014;54(11):887–94. 49. smith sw, clark m, nelson j, heegaard w, lufkin kc, ruiz e. emergency department skull trephination for epidural hematoma in patients who are awake but deteriorate rapidly. j emerg med. 2010;39(3):377–83. 50. nyholm l, howells t, enblad p, lewén a. introduction of the uppsala traumatic brain injury register for regular surveillance of patient characteristics and neurointensive care management including secondary insult quantification and clinical outcome. ups j med sci. 2013;118(3):169–80. 8gorganmr_partially 442 gorgan et al partially trombosed glomus type spinal arteriovenous malformation partially trombosed glomus type spinal arteriovenous malformation – case presentation m.r. gorgan, narcisa bucur, catioara cristescu, a. giovani abstract: spinal avm are very rare vascular lesions and most o the studies give reports on only a few cases. given their localization between the spinal tracts and the gray matter core of the medulla and their multiple feeders from posterior and anterior spinal arteries they are amongst the most difficult surgical pathology in the nervous sistem. we present the case of a 60 years old male with a glomus type t10-l2 spinal avm that presented with motor deficit in the lower limbs and urinary incontinence. the partially thrombosed lesion was completely resected without previous embolisation, and the patient was walking with assistance at discharge. this is a rare case that presented with progressive neurological deterioration consistent with an ischemic rather than a hemorrhagic event. microsurgery is a better option than conservative treatment in these rare cases of spontaneous occlusion of intramedullary arteriovenous malformations. key words: arteriovenous malformation, spinal cord ischemia. introduction only 4% of primary intraspinal masses are avm’s, and most of the publications include reports on a small number of cases. lawton et al. analised one of the most comrehensive series of 304 pacients trated with avm resection over a period of 7, 8 years and concluded that 25% of the patients presented diffuse niduses and 18% had deep perforating artery supply. these lesions are most common in the adult age. (15, 23) eighty-five percent of spinal avms involve progressive neurological symptoms over months to years, especially back pain associated with progressive sensory loss and lower extremity weakness. ten percent to 20 percent involve a sudden onset of weakness, numbness, difficulty urinating, urinary incontinence, fecal incontinence, or paralysis (usually in patients younger than 30) as a result of hemorrhage. (20, 21, 24) many classifications have been proposed for arteriovenous fistulas and arteriovenous malformation. spetzler et all proposed the most complete classification for spinal arteriovenous lesions recognizing 3 types of arteriovenous fistulas namely dorsal intradural, ventral intradural and extradural and 3 types of arteriovenous malformations namely intramedullary, extra-intradural, and conus. intramedullary avm’s are also called romanian neurosurgery (2014) xxi 4: 442 – 447 443 type ii spinal avm’s, glomus type lesions or angioma racemosum arteriovenosum. (26, 27) as most of these lesions are treated either by embolisation or microsurgery when they are discovered, there is little data available on the natural history of these avm’s. (2, 5) usually this high flow lesions are supplied from a few arterial sources from anterior and posterior spinal arteries and drain into the coronal venous plexus. the veins are in most cases tortuous and dilated. (12, 13, 25) the neurological deficit that brings the patient to the hospital can be caused either by hemorrhage resulting from the avm rupture mass effect vascular steal or ischemia related to venous thrombosis of the malformation. we present a rare case of spontaneously occluded intramedullary avm. case presentation a 60 years old man presented with a slowly progressive neurological deficit over several months. the neurological exam showed grade 2/5 motor deficit in the right lower limb and 3/5 motor deficit in the left lower limb and urinary incontinence. he was known with hepatitis b virus infection and an l1 fracture with anterior l1/l2 dislocation after a vertebral trauma 24 years before. at that time (1989) the dislocation was reduced and anteriorly fixated. spinal mr imaging showed a t11-l1 intramedullary lesion suggestive for arteriovenous malformation. there was no evidence of spinal cord hemorrhage. unfortunately the angiography was not available. the surgery was performed via a posterior approach, using multilevel laminectomies extending one level above and one level below the avm nidus. figure 1 t1 and t2 sagital mr image of a intramedullary lesion 444 gorgan et al partially trombosed glomus type spinal arteriovenous malformation figure 2 axial mri through the intramedullary lesion showing the tangled thrombosed vessels the dura was opened through a midline incision from t10 to l2 given the posterior location of the lesion and suspended to the musculature. two large nests of tangled draining veins, one at t11 and one at l1, connected by a large tortuous vein were observed on the surface of the medulla. by carefully inspecting the lesion we observed that the nidus extended from the parenchyma into the extrapial space. using an intrapial technique we mobilized the tortuous veins and we observed no change in the colour of the veins by sqeezing them berween the bipolar forceps, this being the test of them being thrombosed. than the nidus was shrinked using the bipolar at the lowest and the extrapial portion of the avm was completely resected. even the intraparenchymal portion of the nidus was left intact in order to avoid supplementary lesions to the medulla as the avm has been devascularised. an arterial source from the adamkiewicz artery is clipped and coagulated, leaving the artery pulsatile. before closure of the dura, the pale medulla regains a normal vascular design. in the first few days postoperative, the neurological deficit improved to a motor deficit of 3/5 in the right leg and 4/5 in the left leg. the pacient was discharged one week after surgery when he was able to walk with support. figure 3 a – superior nest of extrapial nidus figure 3 b – superior and inferior parts of the extrapial nidus united by a dilated vein on the right side of the medulla (arrow) romanian neurosurgery (2014) xxi 4: 442 – 447 445 figure 3 c – after resection of the superior portion of the nidus figure 3 d – the dissector is pointing to the artery feeding the nidus figure 3 e – length of the inferior portion of the nidus figure 3 f – clip on the vein of the avm that goes to the intrapial nidus figure 3 g – final aspect after coagulation of the venous drainage discussion the progressive exacerbation-remission neurological deficit suggests an ischemic rather than a hemorrhagic sufferance of the medulla. as the blood supply of the spinal cord comes from radicular arteries, two watershed areas can be defined, one between cervicothoracic and midthoracic area and one between midthoracic and thoracolumbar area that are devoid of radicular arteries. this anatomical fact predisposes these regions to ischemic injury. as hypoxia leads to the release of several cytokines that affect the local angioarchitecture it is easy to suppose that an avm present at birth goes through a series of vascular remodeling and in time the venous drainage becomes impaired. from the vascular rearrangement standpoint the fate of any spinal avm is either thrombosis or bleeding secondarily to proteolitic wall dissection. (3, 4) the blood flow in this high flux lesions has two direct consequences leading to hipoxia, first of all the vascular steal, preventing arterialized blood to reach the capillaries and the turbulence that is recognized as a prothrombotic factor. both of these promote venous outflow obstruction, leading to stasis and thrombosis. (17, 18, 19) 446 gorgan et al partially trombosed glomus type spinal arteriovenous malformation two approaches have been used to resect intramedullary avm’s , one is going for the arterial supply first and sacrificing the draining veins as the final act of the resection, as described by spetzler as the pial resection technique and the other preferred by most of the other authors goes to resecting the venous elements at the beginning. we only completed the resection of the extrapial nidus after coagulating the main arterial afferent coming from the adamkiewicz artery. (6, 7) we found only three cases of spontaneous occlusion of an intramedullary avm in the literature, demonstrated on angiography but none of them was microsurgically explored. (1) even if there is no direct relationship between the vertebral trauma the patient suffered 24 years earlier and his intramedullary malformation, we can speculate that the trauma, by modifying the local blood flow and inducing a grade of hypoxia, stimulated remodeling of the malformation’s venous system and contributed to the growth of the nidus as to aquire this three metameres length and ultimately to the venous thrombosis. (8, 9, 10) conclusion spinal avm’s are very complex vascular lesions and the first line of treatment is endovascular. there are cases where endovascular treatment cannot be employed and microsurgery comes into play. it is not advisable though to go for a complete occlusion given the high risk of disastrous consequences. considering the good outcome of the surgery it appears that microsurgery is a better option than conservative treatment in these rare cases of spontaneous occlusion of intramedullary arteriovenous malformations. correspondence giovani andrei giovani.andrei@gmail.com references 1. chun jy, gulati m, halbach v, lawton mt: thrombosis of a spinal arteriovenous malformation after hemorrhage: case report. surg neurol 61:92–94, 2004 2. connolly es jr, zubay gp, mccormick pc, stein bm: the posterior approach to a series of glomus (type ii) intramedullary spinal cord arteriovenous malformations. neurosurgery 42:774–776, 1998 3. corkill ra, mitsos ap, molyneux aj: embolization of spinal intramedullary arteriovenous malformations using the liquid embolic agent, onyx: a single-center experience in a series of 17 patients. j neurosurg spine 7:478–485, 2007 4. djindjian r, cophignon j, rey a, theron j, merland jj, houdart r: superselective arteriographic embolization by the femoral route in neuroradiology. study of 50 cases. ii. embolization in vertebromedullary pathology. neuroradiology 6: 132–142, 1973 5. doppman jl, di chiro g, dwyer aj, frank jl, oldfield eh: magnetic resonance imaging of spinal arteriovenous malformations. j neurosurg 66:830–834, 1987 6. felner ei, goto cs: acute flank pain: an unusual presentation of a spinal avm. am j emerg med 17:382– 384, 1999 7. ferch rd, morgan mk, sears wr: spinal arteriovenous malformations: a review with case illustrations. j clin neurosci 8:299–304, 2001 8. frisbie jh: spinal cord lesions caused by arteriovenous malformation: clinical course and risk of cancer. j spinal cord med 25:284–288, 2002 9. gilsbach jm: treatment options in spinal nidus-type plexiform avms. surgery. riv neuroradiol 17:383–388, 2004 10. hida k, shirato h, isu t, seki t, onimaru r, aoyama h, et al: focal fractionated radiotherapy for intramedullary spinal arteriovenous malformations: 10year experience. j neurosurg 99:34–38, 2003 11. horton ja, latchaw re, gold lh, pang d: embolization of intramedullary arteriovenous malformations of the spinal cord. ajnr am j neuroradiol 7:113–118, 1986 12. ito m, yamamoto t, mishina h, sonokawa t, sato k: romanian neurosurgery (2014) xxi 4: 442 – 447 447 arteriovenous malformation of the medulla oblongata supplied by the anterior spinal artery in a child: treatment by microsurgical obliteration of the feeding artery. pediatr neurosurg 33:293–297, 2000 13. kuga t, esato k, zempo n, fujioka k, harada m, furutani a, et al: successful management of a giant spinal arteriovenous malformation with multiple communications between primitive arterial and venous structures by embolization: report of a case. surg today 26:756–759, 1996 14. lasjaunias p, rodesch g, alvarez h: treatment options in spinal avms. endovascular approach with nbca. riv neuroradiol 17:375–376, 2004 15. lundqvist c, andersen o, blomstrand c, svendsen p, sullivan m: spinal arteriovenous malformations. healthrelated quality of life after embolization. acta neurol scand 90:337–344, 1994 16. mccormick pc, torres r, post kd, stein bm: intramedullary ependymoma of the spinal cord. j neurosurg 72:523–532, 1990 17. meisel hj, lasjaunias p, brock m: modern management of spinal and spinal cord vascular lesions. minim invasive neurosurg 38:138–145, 1995 18. menku a, akdemir h, durak ac, oktem is: successful surgical excision of juvenile-type spinal arteriovenous malformation in two stages following partial embolization. miniminvasive neurosurg 48:57– 62, 2005 19. morgan mk: outcome from treatment for spinal arteriovenous malformation. neurosurg clin n am 10:113–119, 1999 20. newton th, adams je: angiographic demonstration and nonsurgical embolization of spinal cord angioma. radiology 91:873–876, passim, 1968 21. niimi y, berenstein a, setton a, neophytides a: embolization of spinal dural arteriovenous fistulae: results and followup. neurosurgery 40:675–683, 1997 22. ohata k, takami t, gotou t, el-bahy k, morino m, maeda m, et al: surgical outcome of intramedullary spinal cord ependymoma. acta neurochir (wien) 141:341 347, 1999 23. rosenblum b, oldfield eh, doppman jl, di chiro g: spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural avm's in 81 patients. j neurosurg 67:795–802, 1987 24. schievink wi, vishteh ag, mcdougall cg, spetzler rf: intraoperative spinal angiography. j neurosurg 90:48–51, 1999 25. sinclair j, chang sd, gibbs ic, adler jr jr: multisession cyberknife radiosurgery for intramedullary spinal cord arteriovenous malformations. neurosurgery 58:1081–1089, 2006 26. spetzler rf, detwiler pw, riina ha, porter rw: modified classification of spinal cord vascular lesions. j neurosurg 96:145–156, 2002 27. spetzler rf, zabramski jm, flom ra: management of juvenile spinal avm's by embolization and operative excision. case report. j neurosurg 70:628–632, 1989 8satyartheeguru_liponeurocytoma 182 satyarthee et al liponeurocytoma liponeurocytoma of cerebellum: rare entity, case based study guru dutta satyarthee1, a.k. mahapatra2 department of neurosurgery 1all india institute of medical sciences, new delhi, india, new delhi 2all india institute of medical sciences, bhuwneshwar, orissa, india abstract: cerebellar liponeurocytoma (lnc) is a very rare neuroepithelial tumor. about thirty eight cases have been reported, in literature till date, mostly in the form of isolated case reports due to rarity of the occurrence. authors report interesting case in 27-year old male presented with headache and cerebellar signs. mri imaging revealed posterior fossa mass. he underwent sub occipital ctraniectomy with gross total resection of lesion. histopathological report of specimen was consistent with liponeurocytoma with range of mib index less than three. he is under regular follow-up. however he was not advised any adjuvant therapy. diagnosis of lnc requires high index of suspicion and neuroimaging with typical mri findings may be help to confirm the diagnosis. the tumor needs to be differentiated from medulloblastoma, which is far more common and aggressive and requires post-operative chemo-radiation and carries poor prognosis management and pertinent literature will be reviewed. key words: liponeurocytoma, imaging, surgical management introduction liponeurocytoma is a rare neuroepithelial neoplasm involving cerebellum usually seen in adult population. these tumors are slowgrowing, runs indolent course. anatomically cerebellar hemispheres are commonly involved, but may have epicentre in the paramedian region or even vermis (1). it is typically well circumscribed and does not infiltrate surrounding neural tissue, however, may show pressure effect on adjoining anatomical structure, with progress in the size of lesion cause pressure and distortion over fourth ventricle leading to blockage of csf pathway with development of obstructive hydrocephalus. the patient initially presents with cerebellar signs and as lesion progresses features of raised intracranial pressure also appears. it runs favourable course and surgical management is treatment of choice. it needs to be differentiated from medulloblastoma, where surgical treatments followed by adjuvant chemotherapy constitute an integral part of management due to aggressive romanian neurosurgery (2015) xxix 2: 182 186 183 biological behaviour. microscopically it consists of neurocytic cells with focal areas of differentiated cells resembling mature adipose tissue (2). case report a 27-year old male presented with complaints progressive continuous headache associated intermittent vomiting for four months. he also noticed imbalance while walking two months back prior to admission. for 3 months and gait imbalance for 2 months. patient did not give any history of systemic complaints on examination. there was no history of any co-morbidity. visual acuity was normal funfi examination showed bilateral papilloedema, had bilateral cerebellar signs more prominent on left side, and rest of the neurological examination were within normal limit. routine hematological and biochemical investigations were within normal limits. non contrast computed tomogram (ncct) scan of head revealed hypodense lesion in midline posteror to fourth ventricle with obstructive hydrocephalus (figure 1). magnetic resonance imaging (mri) of brain revealed heterogeneous space-occupying lesion without perilesional edema in vermis and adjoining cerebellar hemisphere more towards left side, with a dimension of 4.4 x 4.3 x 3.9 cm sized causing compression of fourth ventricle. which was hyperintense on t1w i (fig2a), hypointense on t2w images (figures 2b&2c) and showed mild patchy enhancement after injection of intravenous gadolinium (figure 3). in view of feature of raised intracranial pressure and cerebellar signs and atypical radiological findings, patient was planned for surgery. he underwent midline sub occipital ctraniectomy in the prone position, posterior arch of c1 removed. after dural opening, csf was released. the tumor was a grayish-yellow, soft, intra-axial lesion, arising from the vermis. it was encapsulated and moderately vascular and cusa suckable, after securing hemostasis dura was closed primarily and wounds closed in layers. gross total excision of the tumor was done. the frozen section showed features suggestive of liponeurocytoma. he had an uneventful postoperative course and was discharged on fifth postoperative day. post-op stay in the hospital was uneventful and his headache and vomiting subsided. postoperative computerized tomography (ct) brain did not show any evidence of residual tumor. (figure 4) patient was not advised postoperative chemotherapy and radiotherapy and was doing well at last follow-up visit six months after surgery. histopathological examination of the excised specimen showed a cellular lesion with extensive areas of lipomatous differentiation. the tumor was composed of round to polygonal cells with distinct cellular outline and moderate amount o cytoplasm. no mitosis, necrosis or endothelial proliferation was seen. the tumor cells were immunopositive for synaptophysin, nse, map, and negative for p53. the mib i labeling index was approximately 3%. the final impression was liponeurocytoma of who grade ii. 184 satyarthee et al liponeurocytoma figure 1 non-contrast computed tomography head showing hypodense lesion in midline in the posterior fossa causing obstructive hydrocephalus 2a 2b 2c figure 2 magnetic resonance images showing posterior fossa mass, 2a: t1-weighted axial scan axial section showing hyperintense, 2b. t2-weighted axial scan and 2c. t2-weighted coronal scan showing hyperintense mass figure 3 contrast-enhanced magnetic resonance images showing mass in the posterior fossa with heterogeneous contrast enhancement figure 4 post-operative computed tomography scan showing complete excision of lesion discussion cerebellar liponeurocytoma is an uncommon tumor occurring in adult age group in the cerebellum; it was first described in 1978 by bechtel (3). it was recognize as a distinct clinical entity and placed as grade ii tumor in year 2000, revised who classification of cns tumors in (10). it is a rare tumor occurring in the posteror fossa usually involving cerebellar hemisphere. in a review carried out by de araújo et al in 2011 reported a total of 32 cases including his one case report (6). different synonyms has been used in the romanian neurosurgery (2015) xxix 2: 182 186 185 literature to denote such tumor lipomatous medulloblastoma(4, 9), loipidized medulloblastoma (5), and others include medullocytoma, lipomatous glioneurocytoma (2 ) to emphasize similarity to central neurocytoma and differentiate the prognosis from medulloblastoma. these tumors mostly affect adult population (5) and there is no gender predisposition (2). patients usually presents with feature of cerebellar signs with raised intracranial pressure as pressure on fourth ventricle lead to obstructive hydrocephalus. clinical symptoms may range s few months. neurological evaluations usually show presence of cerebellar symptoms. pathoanatomically commonly occurs in the cerebellar hemispheres but may have epicentre in the paramedian region or even vermis (1). it is typically well circumscribed but may show pressure effect on adjoining anatomical structure. with advent of blockage of csf pathway can have obstructive hydrocephalus. on computed tomography imaging, it may appear heterogeneous isodense or hypodense with respect to brain parenchyma with focal areas of marked hypodensity like to fatty tissue (5). mri is investigation of choice and appearance is heterogeneous caused by distribution and proportion of loipidized content, which may vary from case to case and even in the same lesion on t1-weighted image is usually heterogeneous iso to hyperintense (1, 5). on contrast administration, it shows usually irregular and heterogeneous minimal enhancement. on t2weighted slightly hyperintense to the surrounding brain, with focal areas of more pronounced hyperintensity. peritumoral oedema is may be typically absent or minimal (1, 5). the optimum mode of treatment of these lesions is gross total surgical excision to aid in diagnosis of lesion and ameliorating feature of raised intracranial pressure. as surgery provides immediate relief in headache and vomiting, however, controversies prevail regarding the ideal adjuvant therapy. lnc is a neuroectodermal tumor and consists of both glial and neural components. immunohistochemistry for gfap, synaptophysin and nse are usually positive showing origin of mixed glial and neuronal elements. microscopically, the tumor consists of small, ovoid cells with areas of mature adipocytes4 resembling loipidized cells (2). mitotic activity is usually absent and mib-1 labeling index usually lies in the range of 1%3%. most of the available pertinent literature shows case reports only and there is no consensus yet on the optimum line of management of this rare entity (1, 2). lnc has a relatively benign clinical course following surgery (7, 11). usually surgery is the treatment of choice and radiotherapy or chemotherapy is usually not advocated, when gross total excision has been carried out during primary surgery. in the literature 5 year survival has been reported to be 81%; however recurrence were encountered in 2032% patients on an average follow-up of 10 years following surgical treatment (11). however, jenkinson et al reported case which recurred 12 months following subtotal resection with atypical highly aggressive course unresponsive to radiation (8). 186 satyarthee et al liponeurocytoma kleihues advocated avoidance of adjuvant therapy is if the mib-1 index is within the range of 1% to 3% and no residual lesion following surgical decompression and such case carry favorable prognosis (9). there is no report of spinal drop metastasis and hence spinal radiation is not advisable (2). diagnosis of lnc requires high index of suspicion and neuroimaging with typical mri findings may be help to confirm the diagnosis. the tumor needs to be differentiated from medulloblastoma, which is far more common and aggressive and requires postoperative chemo-radiation and carries poor prognosis (6). conclusion cerebellar neurocytoma is a newly acknowledged clinicopathological entity, very rare tumor. usually surgical excision is the initial mode of treatment. in view of favourable prognosis with probable benign nature of the lesion mandates follow up without any adjuvant chemotherapy or radiotherapy following gross total surgical excision and, post operative scan showing no residual lesion and the mib-labeling index is less than three percent. preoperative awareness on basis of neuroimaging can lead to total excision and can obviate need for chemo-radiation adjuvant therapy. neuroscientist should differentiate it from medulloblastoma, which is far more common in occurrence, runs much aggressive clinical course with repeated recurrence even after post-operative chemo-radiation adjuvant therapy following micro-neurosurgical excision. correspondence dr. guru dutta satyrathee, associate professor, department of neurosurgery all india institute of medical sciences, new delhi, india, new delhi -110029 email: duttaguru2002@yahoo.com references 1.alkahdi h, keller m, brandner s, yonekawa y, kollias ss. neuroimaging of cerebellar liponeurocytoma: case report. j neurosurg 95 (2):324–331, 2001. 2.bayar ma, pulat h, celik h, erdem y, gokeck c, edebali n, yasitli u, teknier a, kilic c: cerebellar liponeurocytoma – a case report. turkish neurosurg 16: 150-153, 2006. 3.bechtel jt, patton jm, takei y: mixed mesenchymal and neuroectodermal tumor of the cerebellum. acta neuropathol 41: 261-263, 1978 4.budka h, chimeli l. lipomatous medulloblastoma in adults; a new tumor type with possible favorable prognosis. human pathol 25: 730-731, 1994 5.davis dg, wilson d, schmitz m, markesbery wr: lipidized medulloblastoma in adults. human pathol 24: 990-994, 1993 6.de araújo a s jr, de aguiar p h pires, maldaun, m v, panagopoulos a, melgar m, rosemberg s. cerebellar liponeurocytoma: a literature review and case report. neurosurgery quarterly: 21: 39–41. 2011 7.jackson tr regine wf, wilson d, davis dg: cerebellar liponeurocytoma – case report and review of literature. j neurosurg. 95:700-703, 2001 8.jenkinson md, bosma jjd, du plesis d, ohgaki h, kleihues p, warnk p, rainou ng. cerebellar liponeurocytoma with unusually aggressive course: case report. neurosurg 53:1425-1428, 2003 9.kleihues p, egnaczyk g. f. “lipomatous medulloblastoma,” in: p. kleihues and w. k. cavenee, eds., pathology and genetics of tumors of the nervous system, pp. 107-109, 1997 10.kleihues p, louis dn, scheitauer bw, rorke lb, reifenberger g, burger pc, cavenee wk: the who classification of tumors of the nervous system. j neuropathol exp neurol 61:215-225, 2002 11.montagna n, moreira d, vaz lc, reis m: cerebellar liponeurocytoma – a newly recognized clinicalpatological entity. arq neuropsiquiatr, 60:725-729, 2002 flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 329 333 | 329 giant posterior fossa mature teratoma with adjacent subacute haematoma, compressive on the brainstem, with acute hydrocephalus. case report d. balasa1, o. carp1, l. mocanu2, g. butoi3, v. taran3 1department of neurosurgery, “sfantul andrei” hospital, constanta, romania 2department of anatomy, “sfantul andrei” hospital, constanta, romania 3department of radiology, medimar, constanta, romania abstract: mature teratoma of the vermis is a rare entity in neurosurgical adulthood pathology. we present the case of a 65 years old patient, admited as an emergency for intense headache (vas 8/10), nausea, vomiting, gait ataxia, orizontal nistagmus, dismetria, disdiadocokinezia, predominant on the left side, long tracts signs, predominant on the left side. native and contrast ct and mri scan of the head revealed a tumoral lesion, in the vermian, paravermian and in the fourth ventricle, with the aspect of a teratoma with intratumoral subacute haemorrhage including a giant lesion 5,5/5/4,5 cm, compressive on mesencephalon, and with suprajacent acute internal hidrocephalus. emergency neurosurgery was performed (occipital infratentorial craniectomy, microneurosurgical total tumoral resection and haematoma evacuation). postoperative, the patient recovered progressivelly , subtotal neo and arhicerebellar symptoms. the motor long tract signs recovered slower and persisted incomplete. abbreviations: visual autologus pais scale vas, scor karnofskysk, computer tomografct, magnetic resonance imagingmri, cerebrospinal liquid-lcr, ceacarcino embrionar antigen key words: giant tumor, posterior fossa, mature teratoma introduction introduction: mature teratomas are germ cell tumors differentiated into all three germ layers with very low incidence (0,2%)1. posterior fossae teratoma is a lesion with high morbidity (by neo and arhicerebellar syndrome) and mortality (by direct compression on mesencephalon and/or pons, by compression on the fourth ventricle with acute internal hydrocephalus and acute intracranial hypertension). we present the case of a patient admitted in our clinic for a posterior fossa and fourth ventricular tumor with intratumoral haemorrage compressive on 330 | balasa et al giant posterior fossa mature teratoma mesencephalon and acute internal hydrocephalus. the surgical intervention is urgent and mandatory because of the severity of this tumor and in this particular area. case report: a 65 years old patient was admitted in our hospital as an emergency, presenting headache for a few months, suddenly increased within the previous seven days, which became intense (vas 8/10), drowsiness, frequent vomiting, gait ataxia with large base, left 6th nerve incomplete paralisya, left disdiadocokinesia, left long tact signs, predominant motor, sk 70. ct scan of the head revealed a giant posterior fossa 5,5/5/4,5 cm tumor, vermian and left paravermian, with gadolinofil mural nodule 21/23 mm with calcified nodules, with hyperdense lesion adjacent with significance of subacute intratumoral haemorhage compressive on mesencephalon, with supraiacent internal hydrocehalus, suggestive for a teratoma with subacute intumoral haemorhage. figure 1 preoperative aspect: cranial ct scan with contrast substance: vermian posterior, left paravermian and in the fourth ventricle tumoral lesion, moderate heterogeneous with a hypodense part having 3 calcified microopacities (white arrow). anterior vermian and left paravermian haemorrhage (black arrow). the 2 lesions together were compressive on the mesencephalon and on the adiacent cerebellar hemispheres figure 2 preoperative aspect. cerebral mri, t1 with gadolinium coronal incidence: central vermian and left paravermian heterogeneous lesion, with a posterior and central part of about 2,2/1,5 cm hypointensity, having inside small hyperintense areas (white arrow). adiacent, superior vermian and left paravermian subacute haematoma (white and blue arrow) romanian neurosurgery (2016) xxx 3: 329 333 | 331 figure 3 preoperative aspect. cerebral mri, t1 with gadolinium enhancement sagital view: giant tumoral and hemorrhagic lesion described in figure 2 in the vermis and the fourth ventricle (5,5/5/4,5 cm), severelly compressive on the ponto-mesencephalic junction with supraiacent acute internal hydrocephalus (white arrow) ophtalmological examination revealed bilateral papilarry edema. corticosteroids were administered 24 hours preoperative, which diminished the drowsiness. emergency neurosurgery was performed, consisting of occipital infratentorial craniectomy,total microsurgical tumoral and haematoma evacuation. postoperative native and contrast cranial ct scan revealed total resection of the tumor and total evacuation of the haematoma, with subsequent slight reduction of the internal hydrocephalus. postoperative, the patient developed chemical meningitis which was treated with corticotherapy and multiple serial lumbar punctures. after 2 weeks the chemical meningitis ceased, and the patient underwent progressive recovery of the arhi and neocerbellar symptoms. long tract signs and the left sixth nerve paresis recovered slowly. papilarry edema disapeared also. the patient was clinically, radiologically and ophtalmologically followed within the following 11 months. figure 4 postoperative control. cranial ct scan with contrast: total resection of the tumor and evacuation of the haematoma (white arrow) anatomopatologic exam revealed: figure 5 squamous stratified epithelium (red-white arrow) and the content of the clusters (cholesterol, hystiocytes-red arrows) 332 | balasa et al giant posterior fossa mature teratoma figure 6 unistratified cubic epithelium which is lining the internal surface of the cystic tumor confirming the endodermal origin of the teratoma (red arrow) figure 7 pilar keratin in the content of the cyst(red arrow). the ectodermal origin of the teratoma cyst was confirmed (blue–white arrows) discussion according to sanyal (1), teratomas are nonseminomatous germ cell tumors differentiating into all three germ layers. intracranial mature teratomas are tumors with a very low incidence (0.2%), having a clear male predominance (5: 1). a posterior fossa teratoma is a rare occurrence (2, 5, 6). according to coulibaly (3), intracranial teratomas are congenital neoplasms most diagnosed in pediatric hood. teratomas which involve the posterior fossa represent less than 0,5% of all intracranial tumors3. according to bohara (4), standard histopathological examination for a mature teratoma showed a tumor with components of all the three germ layers. the histopathological differentiation between teratoma and dermoid cyst is very valuable for ruling out the presence of immature/malignant or germinomatous components that would require further adjuvant therapies (4). according to desai and goel (6), the outcome of teratoma is very poor6. according to kondziolka (7) the mechanism which explains the hemorrhage into the tumor are the pathological deficits within the walls of the tumoral blood vessels such as hyalinization, necrosis or degeneration. in the above described patient certain intratumoral haemorhage aggravated the evolution of the tumor by direct compression on the brain stem, acute internal hydrocephalus and increased intracranial pressure. emergency neurosurgery was performed (occipital infratentorial craniectomy, total microsurgical tumoral resection and haematoma evacuation). ventricular drainage was not compulsory. multiple drainage lumbar punctures performed for the treatment of postoperative chemical meningitis accomplished well the treatment of internal hydrocephalus. papilar edema ceased progressive postoperative. postoperative cranial ct revealed total microscopic resection of the tumor and hematoma evacuation. the patient was romanian neurosurgery (2016) xxx 3: 329 333 | 333 clinically and radiologically followed for the next 11 months after surgery. according to my personal research, this is the first description of a giant mature teratoma in posterior fossa and the fourth ventricule with intratumoral haemorrage in an adult patient in romanian neurosurgical literature. conclusion giant mature teratoma of the posterior fossa and fourth ventricle is a rare tumor in adults with high morbidity and mortality. emergency neurosurgery (craniectomy, tumor resection and haematoma evacuation) was mandatory because of the vital risk and also for the reduction of morbidities induced by the presence of the tumor. correspondence daniel balasa bulevardul 1 mai, 50 bis, bloc i2, apartament 19, constanta, phone 0744682613, e-mail: daniel_balasa@hotmail.com references 1.parikshit sanyal, sanghita barui, smriti mathur, utpal basak a case of mature cystic teratoma arising from the fourth ventricle, case reports in pathology volume 2013 (2013), article id 702424, 3 pages 2.algahtani ha, al-rabia mw, al-maghrabi hq, kutub hy. posterior fossa teratoma. neurosciences (riyadh). 2013 oct;18(4):371-4. 3. o. coulibaly, , , el kacemi, n. fatemi, r. gana, a. saïdi, r. maaqili, m. jiddane, f. bellakhdara. mature posterior fossa teratoma mimicking infratentorial meningioma: a case report. neurochirurgie volume 58, issue 1, february 2012, pages 40–43 4.bohara m, yonezawa h, karki p, bakhtiar y, hirano h, kitazono i, matsuyama n, arita k. mature posterior fossa teratoma mimicking dermoid cyst brain tumor pathol. 2013 oct;30(4):262-5. doi: 10.1007/s10014-012-0129-6. epub 2012 dec 23. 5.daugherty c. ngo t. drehner d. maugans t. mature teratoma confined to the posterior fossa. pediatr neurosurg 2016;51:93-98 (doi:10.1159/000442178) 6.desai k, nadkarni t, muzumdar d, goel a. midline posterior fossa teratoma--case report. neurol med chir (tokyo). 2001 feb;41(2):94-6. 7. kondziolka d, bernstein m, resch l, tator ch, fleming jf. et al. significance of hemorrhage into brain tumors: clinicopathological study. j neurosurg. 1987;67(6):852-856 5pintea_craniopharyngioma2014 romanian neurosurgery (2014) xxi 1: 37 49 37 craniopharyngioma: how to deal with? bianca st. pintea, zorinela andrasoni, i.st. florian cluj county emergency hospital, department of neurosurgery abstract craniopharyngiomas are rare, highly complex tumors with bimodal incidence in the pediatric and adult age groups. in our opinion, depending on the means possible, total microscopic ablation offers the best chance of healing, or at least prolongs the time interval of recurrences. objective: the purpose of this paper is to add our surgical experience to in the last 11 years, in the context of the large debate from literature regarding the best therapeutically option concerning craniopharyngioma treatments. materials and methods: we performed a retrospective analysis of 42 consecutive patients with craniopharyngioma who underwent surgical resection by one surgeon at the neurosurgical department of cluj-napoca county emergency hospital between january 2002 and december 2012. we perform a systematic review of the published review on goals and techniques associated with selected surgical strategies for the treatment of cph. results: during this period a total of 42 patients with craniopharyngioma were treated in our institution by a single neurosurgeon, representing 12% from all cases of sellar and parasellar tumors respectively operated in last 11 years. there is a significant male preponderance. nine patients were less than 18 years of age at admission. the patient age distribution showed a peak incidence between 10 and 15 years and another between 45 and 50 years. considering the pediatric and adult populations together, the most common presenting symptom was visual disturbances with 60% of patients presenting in this manner, followed by severe headache in more than 50% of cases. obstructive hydrocephalus occurred in 31% of cases. calcifications were seen in 45% of cases, more frequently in children. all our cases underwent surgery by transcranial approach; extended frontotemporal, as the first choice, in 57% of cases. gross total removal was achieved in over half of cases and near total resection was achieved in 40% of cases. the most frequent postoperative complications: diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion. no visual impairment was observed after surgery in the patients with 38 pintea et al craniopharyngioma: how to deal with? normal visions at presentation. only 3 of cases primarily operated by us recurred, in an interval of one to five years. the mortality rate in our cases treated by transcranial surgery was 2% in primary cases and 7% in cases of tumor recurrence. conclusions: radical surgery offers the best chance for cure. radical surgery is also associated with a higher risk of postoperative morbidity, being the reason for why many neurosurgeons recommend a subtotal resection followed by radiotherapy. in our opinion radical surgery is possible in large majority of the cases, fronto-temporal approach offering the most appropriate way to reach this objective. every case must be judged with maximal attention based on preoperative neuroimagistic data but decisively, on intraoperative findings. introduction craniopharyngiomas are rare, highly complex tumors with bimodal incidence in the pediatric and adult age groups. these dysontogenic tumors are benign histology but with malignant behavior by infiltrative tendency into critical parasellar neurovascular structures, and by tendency to recurrence despite the impression that they were completed resected. [26] craniopharyngioma, described by cushing as “one of the most baffling problems which confront the neurosurgeon”, account for less than 3% of all intracranial tumors at adults and 67% from all brain tumors in children. [24, 44] in recent years there is a large difference of opinion in regards to multimodal treatment of cph, from intracranial approaches with total tumor resection or subtotal resection followed by radiotherapy, to an endoscopic approach, or a combination of both. in regards to residual tumors of small dimensions, the recent trend is to use of 3-dimensional conformal radiation treatment (3d crt), stereotactic radiosurgery (srs), stereotactic radiotherapy (srt), and intensitymodulated radiation therapy (imrt). [42] in our opinion, depending on the means possible, total microscopic ablation offers the best chance of healing, or at least prolongs the time interval of recurrences. objective the purpose of this paper is to add our surgical experience to in the last 11 years, in the context of the large debate from literature regarding the best therapeutically option concerning craniopharyngioma treatments. materials and methods we performed a retrospective analysis of 42 consecutive patients with craniopharyngioma who underwent surgical resection by one surgeon at the neurosurgical department of cluj-napoca county emergency hospital between january 2002 and december 2012. we discussed the tumor’s characteristics that could influence the treatment decision and the choice of the most reliable approach. the postoperative follow-up was done at one and three month when first control romanian neurosurgery (2014) xxi 1: 37 49 39 mri is also performed. all the patients were followed up every 3 to 6 months in the first year after discharge from the hospital, and mail correspondence and/or telephone interviews were used after one year. we perform a systematic review of the published review on goals and techniques associated with selected surgical strategies for the treatment of cph. results from january 2000 to december 2012 a total of 42 patients with craniopharyngioma were treated in our institution by a single neurosurgeon, representing 12% from all cases of sellar and parasellar tumors respectively 1, 39% of all tumors (3006 cases) operated in this period. at pediatric age we found that approximately half of all suprasellar tumors are craniopharyngioma, compared with only about 10% in adults. figure 1 a preoperative sagittal contrastenhanced t1 weighted mri showed a case of suprasellar solid craniopharyngioma extending from the infudibular area into the third ventricle figure 1 b postoperative t1 weighted mri shows a total removal of the craniopharyngioma by frontotemporal approach figure 2 a, b, c, d preoperative axial (a), coronal (b) and sagittal (c) t1-weighted mri showed a giant suprasellar craniopharyngioma with a cystic portion extending into the third ventricle and left lateral ventricle. three weeks after operation post-contrast ct scan (d) showed a small calcified nodule residual 40 pintea et al craniopharyngioma: how to deal with? figure 3 a, b preoperative sagittal and coronal contrast-enhanced t1 weighted mri demonstrating a suprasellar tumor with inhomogeneously enhancing solid tumor part figure 3 c, d ct scan at 48 hours after modified right frontotemporal approach. a gross total tumor resection was achieved. figure 4 a, b, c preoperative coronal, axial and sagittal contrastenhanced t1 weighted mri demonstrating a giant suprasellar tumor with a large cyst extending in the third ventricle and left lateral ventricle with areas of calcifications and the presence of the ommaya reservoir. figure 4 d, e, f ct scan at 48 hours after modified right bifrontotemporal approach. a gross total tumor resection was achieved. there is a significant male preponderance. of the 42 patients, 24 were males and 18 were females, with a mean age of 27 years (range 4 to 70 years). nine patients (22%) were less than 18 years of age at admission. the patient age distribution showed a peak incidence between 10 and 15 years. another peak was found between 45 and 50 years. in 17% of the cases, the histological characteristics of the craniopharyngiomas were of the papillary type and in 83% of the adamantinomatous type. overall the clinical disorders were nonspecific and have included visual deficits, endocrine and behavioral impairments. considering the pediatric and adult populations together, the most common presenting symptom was visual romanian neurosurgery (2014) xxi 1: 37 49 41 disturbances (visual field defects, decreased visual acuity or visual deterioration), with 60% of patients presenting in this manner, followed immediately by severe headache in more than 50% of cases. neurological symptoms were relatively uncommon. symptoms related to hydrocephalus, headaches, nausea and vomiting occurred more frequently in children than in adults. in children, the most common presentation was that of growth failure. in adults, hypogonadism was the most common presentation followed by visual deficits and symptoms of raised intracranial pressure. other less common features include seizures, motor disorders, emotional lability, hallucinations, and precocious puberty, polyuria/polydipsia and weight disorders. preoperative work-up tests included computerized tomography (ct) scanning and magnetic resonance imaging (mri). obstructive hydrocephalus occurred in 13 (31%) of cases. calcifications were seen in 19 (45%) of cases, more frequently in childhood populations. predominantly cystic mass was detected in 24 % of cases, partially cystic tumor and solid tumor in the rest of 76% cases. all our cases underwent surgery by transcranial approach, extended frontotemporal, as the first choice, in 24 of cases (57%); we have choose transcallosal interemispheric route or subfrontal interemispheric route by bifrontal approach in 8 of cases (19%); bifrontopterional craniotomy and combined routes were reserved for multidirectional approach of giant tumors, in 24% of cases. four patients (10%) had undergone previous surgery in other centers. in one case we have inserted an ommaya reservoir and we operated the case after 11 years, because of refuse of parents to accept radical intervention. in this particular case we obtain a gross total removal in a single surgical stage, despite the huge dimensions of the tumor. our intention was gross total resection in all cases and we succeed this in over half of the patients. near total resection, meaning that a small remnant of tumor capsule or calcified portion of the tumor was left in place because of was a firm adherence to hypothalamus, major calcifications, very thin capsule and adherence to perforating vessels or greater vessels from the polygon of willis, was achieved in 40% of our cases. of all the survival patients the most frequent postoperative complications was diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion, despite de fact that the preservation of pituitary stalk is one of our goals during the surgery. one of the most difficult problems in the postoperative period was the treatment of hydroelectrolithic disturbances encountered especially in very large tumors. postoperative endocrine abnormalities were treated by corticosteroids and thyroid hormone replacement. treatment of long-term hormone deficits varies based on the type of deficiency and it’s made by endocrinologist. visual acuity and visual 42 pintea et al craniopharyngioma: how to deal with? field defects were found in 25 of patients before surgery; in two of them the symptoms was transient aggravated after the operation, while in 12 (48%) patients there was an improvement of vision at 1 month after surgery. no visual impairment was observed after surgery in the patients with normal visions at presentation. two patients had oculomotor paralysis after the operation, one of them recovered significantly. among the long-term complications found in our series, we mention: diabetes insipidus with impaired sense of thirst, hypothalamic disturbances with hyperphagia and obesity, the deterioration of cognitive function and excessive daytime sleepiness. only three of cases primarily operated by us recurred, in an interval of one to five years. treatment of recurrences is difficult and perioperative morbidity is significantly increased compared to treatment of primary tumor. the operative mortality rate in our cases treated by transcranial surgery was 2% in primary cases and 7% in cases of tumor recurrence. discussion there is no agreement in regards to the optimal management of craniopharyngiomas; there are proponents to aggressive total surgical resection, when others are in favor of partial resection followed by radiotherapy. the natural history of these lesions is not fully known yet. surgical resection is the mainstay of definitive treatment and it is the most effective in order to prevent recurrences. skull base approaches described for the excision of craniopharyngiomas can be simplified into: anterior midline (subfrontal, transsphenoidal); anterolateral (pterional, orbitozygomatic); and intraventricular (transcallosal–transventricu-lar, transcortical–transventricular, translamina terminalis) approaches. [2, 10, 21] since such a variety of surgical approaches exists in the management of these tumors, the experience of the surgical team is extremly important. from a topographical standpoint, there are two types of craniopharyngiomas: intrasellar, localized in the anterior pituitary gland with extension sometimes even before the optic chiasma, and infundibulotuberian, whose anterior extension to the chiasma is rare; also describing cph which develop especially on the floor of the third ventricle. [26, 44] histologically, there are two types of cph: classic adamantin type, heterogenic, in the most part solid, which is most likely found in children; and a papillary type (scuamos papillary and adamantinomatous). scuamous papillary is predominantly cystic, found almost exclusively in adults, and seems to have a better prognosis than the adamantin. criteria for choosing a surgical approach depends on the origin of the tumor with relation to the diaphragma sellae, enlargement of the sella turcica, the extension of intratumoral cysts, shape and size of the cph, as well as extension under the pia mater. romanian neurosurgery (2014) xxi 1: 37 49 43 intraoperative mris have proven useful in detecting residual tumor and in obtaining a more radical resection. although, they can produce false images due to blood which may accumulate intraoperatively, making it difficult to differentiate between intracapsular hemorrhage and residual tumor. [40]. in hoffman's 1998 opinion [21], which advocated total excision whenever possible and achieve gross total resection in the majority of cases in their series of suprasellar tumors, transcranial surgical approaches indicated for cph resection can be classified by: 1. pterional transsylvian approach: small suprasellar tumors, as well as large intrasellar tumors with suprasellar extension; translaminaterminalis pterional approach for intraventricular tumors. 2. combined pterional-transcallosal anterior-transventricular approach: large suprasellar tumors with 3rd ventricle extension. 3. transcallosal-transventricular approach: tumors exclusively intraventricular our experience is in agreement with the report of yasargil et al. [56] they point out the crucial role of complete tumor removal rather than risking repeated surgical procedures and/or radiation therapy for tumor recurrences. according to them [56 ]the pterional (aka frontotemporal) approach is the workhorse for the surgical resection of craniopharyngiomas involving primarily the suprasellar cistern.[56] this exposure is suitable for removing craniopharyngiomas involving the intrasellar, suprasellar, prechiasmatic, and retrochiasmatic regions. this is also the preferred method in patients with a prefixed chiasm, because the tumor can be resected beneath the chiasm. a disadvantage of the pterional approach is the limited view of the contralateral opticocarotid triangle and the contralateral retrocarotid space. [10] baskin ds et al studied on 74 patients retrospectively with craniopharyngiomas treated during a 15 year period. they reviewed the radiological appearances, presenting symptoms before and after treatment initiation, surgical approaches and the degree of tumoral resection. based on this data they concluded that radical subtotal removal followed by radiotherapy is an acceptable treatment for craniopharyngioma. [3] broggi believes that the standard pterional approach is still indicated for middle fossa extension of tumors even though the use of the pterional approach decreased in the last decade in favor of less invasive approaches. in case of cystic craniopharyngiomas cystoventriculostomy/cystocysternostomy may be used. [5] in chakrabarti et al 2005’s opinion, [9,11] the scope of surgical intervention consists of resecting as much as possible of the tumor from the first intervention, any residual tumor being controlled by radiosurgery, considering that it is easier to accept a subtotal resection than a severe complication. n.gupta et al suggests that 44 pintea et al craniopharyngioma: how to deal with? in case of pediatric craniopharyngiomas gross total removal is associated with increased rates of endocrinopathies compared with subtotal removal and radiotherapy. [1, 19] on the contrary, fahlbush, [14] in a study of 168 consecutive patients, treated between january 1983 and april 1997, concludes that total tumor removal with condition of avoiding intraoperative hazardous gestures offers favorable results immediately postoperative and a longer time frame until recurrence. total tumor resection was obtained in 50% of cases with transcranial approaches and in 85% by transsphenoidal approaches. the most frequent surgical approach used in his study was a pterional approach in 39% of cases, followed by transsphenoidal in 23% of cases, bifrontal interemispherical approach being reserved for large retrochiasmatic craniopharyngiomas. so authors recommended the pterional transsylvian approach in all situations where the optic chiasm is postfixed but, if required, the these approach also allows access to the inferior anterior third ventricle through the lamina terminalis. in a large study of 284 patients with cph which were treated exclusively by transcranial approaches by shi xang et al, [48] the pterional approach was chosen in 191 cases, due to the inferior or superior location of the tumor in relation to the floor of third ventricle. they consider that preserving the integrity of the hypothalamic structures, the perforating artery of the the pituitary gland being possible by choosing an optimal approach based on the relation of the tumor to the floor of the 3rd ventricle. in the period from 2001-2011, 66 patients with giant craniopharyngiomas were operated on at the international neuroscience institute in hannover, via the frontolateral approach. the resection was confirmed using intraoperative mri or early postoperative mri in some cases. the authors conclude that frontolateral approach allows safe and radical removal even of giant or extensive craniopharyngiomas; hidden parts can be examined with an angled endoscope. [18] on the contrary, j. c. fernandezmiranda, e. w. wang et al [30] studied on 55 patients retrospectively with craniopharyngiomas admitted at neurosurgery department of pittsburgh medical center (42 with primary craniopharyngiomas and 13 with recurrent). they present that total or near total (>95% of tumor) resection was achieved in 66.6% of cases by endoscopic endonasal surgery. recurrence occurred in 18 patients (32.7%), and they were treated with repeat surgery or radiosurgery. based on this data they concluded that this approach provides good results comparable with traditional approaches. [30] in case of pediatric craniophryngiomas opinions varies depending on patients age. at center for endoscopic skull base surgery, bologna, italy, endoscopic endonasal surgery has become the approach of choice for midline pediatric craniopharyngiomas, in patients older than romanian neurosurgery (2014) xxi 1: 37 49 45 13 years with gross total removal in majority of cases and without signs of hypothalamic compromising. [16] michael l.levy, in his study on 54 cases of pediatric craniopharyngiomas concludes that the best approach is the one who provides optimum exposure to maximize the chances for total resection, even combined surgical approaches. besides classic frontopterional approaches, neuroendoscopic procedures are becoming more popular in the neurosurgical treatment of craniopharyngioma. typically, transsphenoidal approaches were reserved for sellar tumors and for those with suprasellar extension if the sella turcica appears enlarged, but even in “hourglass” tumors, more so if suprasellar extension is round and symmetrical. [11, 14] presently, the indications of this approach have expanded including suprasellar tumors with normal dimensions, introducing another two types of transsphenoidal approaches: transsellar-transdiaphragmatic and presellar-tubercular. [27, 29] in 1990, yasargil used this approach in 9.7% of 144 cases studied, van effentere in just 8%, and maira in his 2004 study declares 63% of cases confirmed a complete cph resection by a transsphenoidal approach. [35, 53, 56] in fahlbush opinion [14] transsphenoidal surgery has the great advantage of not disturbing hypothalamic function. in a study conducted by shozo y.et al [49] 90 patients with craniopharyngiomas were evaluated prospectively at department of the hypothalamic and pituitary surgery tokyo and treated by transsphenoidal surgery or extended transsphenoidal surgery; total removal was achieved in 77,8% of cases, including supradiaphragmatic type, with a good outcome. according to the authors dural fascia graft is a very effective technique to prevent csf leaks in this cases. [49] regarding the management of intradural bleeding during the extended transsphenoidal surgery cappabianca’s opinion is that the thrombingelatin topical haemostatic could be a valuable tool when other strategies to stops bleeding, at the level of superior intercavernous sinus are ineffective, even the ones with highflow. [7] craniopharyngiomas have a tendency to recur even after apparent total resection and radiation therapy. [54] literature reports between 0 to 50%. recurrence rates of craniopharyngiomas even after aggressive surgical resection reported by yasargil in his study was of 7%; [56] backland in his 1994 study regarding recurrence rates in a large time interval came to the conclusion that it can reach 50%. [2] there are also some cases reported of ectopic recurrences, at a distance of the tumor location as well as the surgical path. [34]. treatment options for recurrent craniopharyngioma include repeat surgery, radiotherapy and intracystic bleomycin therapy. the most consistently reported feature predictive for recurrence of craniopharyngioma is the extent of 46 pintea et al craniopharyngioma: how to deal with? resection at initial surgery as well the tumor diameter greater than 4 cm to 5 cm; extrasellar extension; extension into the third ventricle; the degree of tumor adhesion; hydrocephalus and tumors with greater than 10% calcification.[ 12, 13, 19, 24, 48, 56]. matson and crigler, in 1969, postulated that “total excision must be attempted at the first operation” [37] radiation therapy is a reference point in the therapeutic management of craniopharyngioma. today less radical surgery in combination with radiation therapy is favored achieving a progressionfree survival between 70 and 90%. [14, 52] the major advantage of proton therapy is the high degree of dose conformity to the target. beltran et al, [4] retrospectively evaluated proton treatment plans with imrt plan. he concluded that compared with photon imrt proton therapy has the potential to significantly reduce whole brain and body irradiation. retrospective evaluation of outcomes in 15 patients with craniopharyngioma treated with a mix of photon and protons by fitzek et al. reveals that the tumor control rates at 5 and 10 years were 93 and 85%, respectively. [15] stereotactic instillations of radioisotopes represent in the last period an alternative therapeutic option, for monocystic craniopharyngioma recurrences. though, this treatment method is restricted to cystic childhood craniopharyngioma and should be considered only for postoperative recurrences and after percutaneous irradiation. [25, 50] in opinion of voges and hasegawa [20, 55], response rates and cyst controls can be achieved in more than 80% case of cystic craniopharyngiomas after intracavitary application of different isotopes such as rhenium186, yttrium90, or phosporus32. researchers are studying several theories about the radiosurgery and conclude that tumor control is inferior to fractionated treatments and might carry the risk for optic neuropathies unless only smaller lesions are treated away from the optic apparatus. [39, 51] bleomycin, an antineoplastic antibiotic that interferes with dna production, was first introduced in cystic cph treatment by takahasi in 1985. intracystic administration by stereotactic techniques determines a decrease in intracystic fluid secretion and favors tumor cell degeneration. in recent years the routine use of bleomycin has been decreased due to a series of complications reported such as occlusive vasculopathy, pulmonary fibrosis, bilateral hypoacusis, hypersomnia, thermal disfunction. [45,46]. recent reports on the effect and tolerability of intracystic instillation of interferon α are promising [23] according to cavalhero et al in their 1996 study, the implantation of an intracystic catheter with a subcutaneous reservoir and instillation of sclerosing substances represent a useful therapeutic method for cystic recurrent tumors whose anatomical configuration and localization make them difficult to resect. [8, 47] romanian neurosurgery (2014) xxi 1: 37 49 47 in a study published in 2004, bricolo and collaborators present therapeutic efficiency of a multimodality stereotactic approach to regrowing/recurrent cystic craniopharyngiomas: neuroendoscopy, intracavitary bleomycin and gamma knife (gk) radiosurgery. [32, 39] ohata k. et al [41] conclude that “the use of radiosurgery for craniopharyngioma is still a matter of discussion”. conclusions radical surgery offers the best chance for cure. radical surgery is also associated with a higher risk of postoperative morbidity, being the reason for why many neurosurgeons recommend a subtotal resection followed by radiotherapy. in our opinion radical surgery is possible in large majority of the cases, fronto-temporal approach offering the most appropriate way to reach this objective. every case must be judged with maximal attention based on preoperative neuroimagistic data but decisively, on intraoperative findings. radical surgery could be an objective, but this must not be an objective with every cost, because the cost could be too high. despite advances in neuroimaging, microsurgical techniques and hormone replacement multimodal treatment, the overall prognosis remains reserved on long term follow-up. references 1.aaron j. clark, m.d., ph.d., tene a. cage, m.d., derick aranda, m.d., nalin gupta, m.d., ph.d, treatment-related morbidity and the management of pediatric craniopharyngioma. a systematic review. journal of neurosurgery: pediatrics: oct 2012 / vol. 10 / no. 4 / pages 293-301 2. backlund eo: treatment of craniopharyngiomas: the multimodality approach. pediatr neurosurg 1994, 21: 8289 3.baskin ds, wilson cb. surgical management of craniopharyngiomas. a review of 74 cases. j neurosurg. 1986 jul; 65(1):22-7. 4.beltran, c., roca, m., and merchant, t. e. (2011). on the benefits and risks of proton therapy in pediatric craniopharyngioma. int. j. radiat. oncol. biol. phys. 5.broggi m., castiglione, m., schiariti, m.; acerbi, f.; tringali, g.; broggi, g.: twenty years experience of craniopharyngioma surgery in 111 cases: the evolution toward minimally invasive surgery: journal of neurological surgery part b: skull base; issue s 02, 2012 6.caldarelli m, di rocco c, papacci f, colosimo c jr: management of recurrent craniopharyngioma. acta neurochir (wien) 140:447–454, 1998 7.cappabianca p, esposito f, esposito i, et al: use of thrombingelatin haemostatic matrix in endoscopic endonasal extended approaches: technical note. acta neurochir 151: 6977, 2009 8.cavalheiro s, sparapani fv, franco jo, da silva mc, braga fm use of bleomycin in intratumoral chemotherapy for cystic craniopharyngioma. j neurosurg 84:124–126,1996 9.chakrabarti i, amar a, couldwell w, et al: long term neurological visual and endocrine outcomes following transnasal resection of craniopharyngiomas. j.neurosurg 102: 650657, 2005 10.choux m, lena g: craniopharyngioma, in apuzzo mlj (ed): surgery of the third ventricle, ed 2. baltimore: williams & wilkins, 1998, pp 1143–1181 11.couldwell wt, weiss mh, rabb c, et al: variations on the standard transsphenoidal approach to the sellar region, with emphasis on the extended approaches and parasellar approaches: surgical experience in 105 cases. neurosurgery 55:539–550, 2004 12.di rocco c, caldarelli m, tamburrini g, massimi l: surgical management of craniopharyngiomas— experience with a pediatric series. j pediatr endocrinol metab 19:355–366, 2006 13. duff j, meyer f, et al. long-term outcomes for surgically resected craniopharyngiomas neurosurgery, 46 (2000), pp. 291–302 [discussion 302–5] 14.fahlbusch, r., honegger, j., paulus, w., huk, w., and buchfelder, m. surgical treatment of 48 pintea et al craniopharyngioma: how to deal with? craniopharyngiomas: experience with 168 patients. j. neurosurg. 90, 237–250, 1999 15.fitzek, m. m., linggood, r. m., adams, j., and munzenrider, j. e. combined proton and photon irradiation for craniopharyngioma: long-term results of the early cohort of patients treated at harvard cyclotron laboratory and massachusetts general hospital. int. j. radiat. oncol. biol. phys. 64, 1348–1354, 2006 16.frank, g.; mazzatenta, d.; zoli, m.; faustini-fustini, m.; pasquini, e.endoscopic endonasal surgery in pediatric craniopharyngiomas with suprasellar extension journal of neurological surgery part b: skull base; issue s 02, 2012 17.garnett mr, puget s, grill j, sainte-rose c: craniopharyngioma. orphanet j rare dis 2:18, 2007 18.gerganov, v.; metwalli, h.; fahlbusch, r.; samii, a.; samii, m.: surgical removal of giant craniopharyngiomas via the frontolateral approach: operative technique and analysis of the outcomejournal of neurological surgery part b: skull base; issue s 02, 2012 19.gupta d.k. , ojha b.k, sarkar c. et al. recurrence in craniopharyngiomas: analysis of clinical and histological features j clin neurosci, 13 (2006), pp. 438–442 20.hasegawa, t., kondziolka, d., hadjipanayis, c. g., and lunsford, l. d. (2004). management of cystic craniopharyngiomas with phosphorus-32 intracavitary irradiation. neurosurgery 54, 813–822. 21.hoffman h: surgical management of craniopharyngiomas. in setti s. rengachary@ robert h. wilkins(eds), neurosurgical operative atlas, aans 7> 173/ 181, 1999. 22.hukin j, steinbok p, lafay-cousin l et al: intracystic bleomycin therapy for craniopharyngioma in children. cancer 109:2124–2131, 2007 23.ierardi df, fernandes mj, silva ir, thomazinigouveia j, dastoli p,cavalheiro s 2007 apoptosis in α interferon (ifn-α) intratumoral chemotherapy for cystic craniopharyngiomas. childs nerv syst 23:1041– 104 24.isaac ma, hahn ss, kim ja et al. management of craniopharyngioma cancer j, 7 (2001), pp. 516–520 25.julow j, backlund eo, lányi f, hajda m, nyáry i, 2007 long-term results and late complications after intracavitary yttrium-90 colloid irradiation of recurrent cystic craniopharyngiomas. neurosurgery 61:288–295; discussion 295–296 26.karavitaki n, cudlip s, et al.: craniopharyngiomas. endocr rev 27. 371-397.2006 27.kato t, sawamura y, abe h, et al: transsphenoidaltranstuberculum sellae approach for supradiaphragmatic tumors: technical note. acta neurochir 140:715–719, 1998 28.kobayashi t, kida y, mori y, hasegawa t: longterm results of gamma knife surgery for the treatment of craniopharyngioma in 98 consecutive cases. j neurosurg 103 (6 suppl):482–488, 2005 29.kouri jg, chen my, watson jc, et al: resection of suprasellar tumors by using a modified transsphenoidal approach. report of four cases. j neurosurg 92:1028– 1035, 2000 30.koutourousiou, m.; paluzzi, a.; tormenti, m. j..; fernandez-miranda, j. c.; wang, e. w. et al. endoscopic endonasal surgery for craniopharyngiomas, journal of neurological surgery part b: skull base; issue s 02, 2012 31.landolt a m. history of pituitary surgery from the technical aspect. neurosurg clin n am. 2001; 12:37– 44. 32.lee, m., kalani, m. y., cheshier, s., gibbs, i. c., adler, j. r., and chang, s. d. (2008). radiation therapy and cyberknife radiosurgery in the management of craniopharyngiomas. neurosurg. focus 24, e4. 33.liu jk, weiss mh, couldwell wt: surgical approaches to pituitary tumors. neurosurg clin n am 14:93–107, 2003 34.liu jm, garonzic im, eberhart cg, et al: ectopic recurrence of craniopharyngioma after an interhemispheric transcallosal approach: case report. neurosurgery 50: 639645, 2002 35.maira g, anite c, albanese a, et al: the role of transsphenoidal surgery in the treatment of craniopharyngiomas. j neurosurg 100: 445451, 2004 36.maira g, anite c, colosimo c, et al: craniopharyngiomas of the third ventricle: translamina terminalis approach. neurosurgery 47: 857865, 2000 37.matson d., crigler j.: management of craniopharyngioma in childhood. j neurosurg 30. 377390.1969 38.merchant te, kiehna en, kun le, mulhern rk, sanford ra 2006 phase ii trial of conformal radiation therapy for pediatric patients with craniopharyngioma and correlation of surgical factors and radiation dosimetry with change in cognitive function. j neurosurg 104(2 suppl):94–102 39.minniti, g., esposito, v., amichetti, m., and enrici, r. m. the role of fractionated radiotherapy and romanian neurosurgery (2014) xxi 1: 37 49 49 radiosurgery in the management of patients with craniopharyngioma. neurosurg. rev. 32, 125–132, 2009 40.nimsky c, ganslandt o, hofmann b, fahlbusch r: limited benefit of intraoperative low-field magnetic resonance imaging in craniopharyngioma surgerz. neurosurg 53: 7281, 2003 41.ohata k, kunihieo n, goto t et al .role of skull base surgery for radical resection of craniopharyngioma in the era of radiosurgeryjournal of neurological surgery part b: skull base; issue s 02, 2012 42.puget s, garnett m, wray a, grill j, habrand jl, bodaert n, sainte-rose c 2007 pediatric craniopharyngiomas: classification and treatment according to the degree of hypothalamic involvement. j neurosurg 106(1 suppl):3–12 43.rajan b, ashley s, gorma c, et al: craniopharyngiomas-long term results following limited surgery and radiotherapy. radiother oncol 26:1-10, 1993. 44.rushing e, giangaspero f, paulus w et al. craniopharyngioma d. louis, h. ohgaki, o. wiestler, w.k. cavenee (eds.), who classification of tumours of the central nervous system, who press, geneva (2007), pp. 238–240 45.sajoh m, murakami h, hirase y, et al: occlusive cerebrovasculopathy after internal radiation and bleomicin therapy for a craniopharyngioma: case report. neurol med chir (tokyo) 37: 920923, 1997 46.savas a, erdem a, tun k, et al: fatal toxic effect of bleomycin in brain tissue after intracystic chemotherapy for a craniopharyngioma: case report. neurosurgery 46: 213217, 2000 47.schubert t, trippel m, tacke u, van velthoven v, gumpp v, bartelt s, et al: neurosurgical treatment strategies in childhood craniopharyngiomas: is less more? childs nerv syst 25:1419–1427, 2009 48.shi xe, wu b, zhou zq, fan t, zhang yl: microsurgical treatment of craniopharyngiomas: report of 284 patients.chin med j (engl) 119:1653–1663, 2006 49.shozo yamadaemail, noriaki fukuhara, kenichi oyama, et al: surgical outcome in 90 patients with craniopharyngioma: an evaluation of transsphenoidal surgery. world neurosurgery volume 74, issue 2, pages 320-330, 2010 50.szeifert gt, bálint k, sipos l, sarker mh, julow j 2007 pathological findings in cystic craniopharyngiomas after stereotactic intracavitary irradiation with yttrium90 isotope. prog neurol surg 20:297–302 51.tishler, r. b., loeffler, j. s., lunsford, l. d., duma, c., alexander, e. iii, kooy, h. m., and flickinger, j. c. (1993). tolerance of cranial nerves of the cavernous sinus to radiosurgery. int. j. radiat. oncol. biol. phys. 27, 215–221. 52.tomita, t., and bowman, r. m. (2005). craniopharyngiomas in children: surgical experience at children’s memorial hospital. childs nerv. syst. 21, 729–746. 53.van effenterre r, boch al: craniopharyngioma in adults and children; a study of 122 surgical cases. j neurosurg 97:311, 2002 54.veeravagu a, lee m, jiang bv et al. the role of radiosurgery in the treatment of craniopharyngiomas neurosurg focus, 28 (2010), p. e11 55.voges j, sturm v, lehrke r, treuer, et al. cystic craniopharyngioma: long-term results after intracavitary irradiation with stereotactically applied colloidal betaemitting radioactive sources. neurosurgery 40, 263–270. 1997 56.yaşargil mg, curcic m, kis m, siegenthaler g, teddy pj, roth p: total removal of craniopharyngiomas. approaches and long-term results in 144 patients. j neurosurg 73:3–11, 1990. 10atascua_spontaneousintracranial romanian neurosurgery (2015) xxix (xxii) 1: 85 92 85 spontaneous intracranial hemorrhage in children – ruptured lobar arteriovenous malformations: report of two cases a. tascu1, c. pascal2, s.m. florea2, st.m. iencean3 1“carol davila” university of medicine and pharmacy, bucharest 2first neurosurgical clinic, “bagdasar-arsen” clinical hospital, bucharest 3“grigore t. popa” university of medicine and pharmacy iasi abstract: brain arteriovenous malformations (avms) are lesions thought to be primarily congenital in origin, consisting of fistulous connections of abnormal arteries and veins, without normal intervening capillary beds and no cerebral parenchyma between vessels. in the pediatric population, avms represent the most common cause of spontaneous intracranial hemorrhage (ich), with a high recurrent bleeding risk. the aim of this paper is to report 2 cases of ruptured lobar avms in children, presenting with spontaneous ich. due to the patients’ neurological status, the only imaging examination performed preoperatively was a ct scan, showing intraparenchymal hemorrhage. thus, there was no mri/angiographic examination to prove the existence of a brain avm prior to the surgical interventions. also, the cerebral angiography performed after the surgery showed, in both patients, no signs of residual vascular malformations. therefore, the diagnosis of avm was certified by macroscopic and microscopic pathological findings, with no brain imaging suggestive of a vascular malformation. key words: brain avm, pediatric, intracranial hemorrhage introduction arteriovenous malformations (avms) are vascular lesions constituted by abnormal intracranial vessels, both arteries and veins, connected between them, with no capillary bed interposed (1, 2). there are 3 typical morphological structures composing an avm: feeding arteries, draining veins and a vascular nidus formed by a tangle of numerous av shunts with no brain tissue included (1, 36). avms are considered to have congenital origins, but reports of de novo cases were also recorded in the neurosurgical literature (1-2, 7-9). although the most common age at diagnostic for patients is 20 to 40 years old (12, 12-14), 3 to 20% of patients with avms are children and this pathology causes 30 to 50% of intracranial spontaneous hemorrhage in the 86 tascu et al spontaneous intracranial hemorrhage in children pediatric population (9-11, 15). the main imaging diagnostic techniques in avms are computed tomography (ct), magnetic resonance imaging (mri) and catheter angiography, from which the most useful in ruptured malformations is ct scan, as it offers information on the mass effect and displacement of cerebral structures caused by the blood clot (1, 2, 15). arteriovenous malformations are classified, according to the martin-spetzler scale (table 1) in v grades, based on size, location and pattern of venous drainage, and it has been widely adopted as it has proven to be a good predictor of surgical morbidity risk (15, 19, 20). there are 5 main options to treat avms, proposed by drake in 1979 and still present in the brainsurgeons treatment planning: expectant behavior, surgery, endovascular treatment, radiotherapy or a combination of preceding options (2, 21). the last of the five points appear to increase chances of obliteration and decrease risk of bleeding (2, 15, 22). table 1 martin spetzler grading scale for avms characteristic points avms size ◦ small (<3cm) ◦ medium (3-6cm) ◦ large (>6cm) 1 2 3 location ◦ non-eloquent site ◦ eloquent site* 0 1 pattern of venous drainage ◦ superficial ◦ deep drainage component 0 1 *sensorimotor, language, visual cortex, hypothalamus, thalamus, internal capsule, brain stem, cerebellar peduncles, cerebellar nuclei case 1 history and examination: an 11 year old girl presented at the emergency department with headache, nausea/vomiting, that started during the morning, followed by grand mal seizures and coma – glasgow coma scale of 5 points. the neurological examination showed left hemiplegia and no pupillary reflexes. due to acute respiratory failure, the girl needed orotracheal intubation and mechanical ventilation. patient’s parents reported no trauma history. imaging: we performed an emergency computed tomography (figure 1) that revealed the presence of a large right frontal hematoma that exerted a significant mass effect over the midline structures, accompanied by intraventricular bleeding. operation: considering the patients’ neurological status and the ct scan aspect, we opted for life saving clot evacuation surgery. during the procedure, there were no anatomical signs of an arteriovenous malformation. patient’s neurological status improved postoperatively, reaching a glasgow coma scale of 8 points 24 hours after the intervention. she was also able to breathe on her own, through the intubation tube. a control ct scan (figure 2) showed a new bleeding, and a new surgical intervention had to be performed. after the blood clot evacuation, the surgical team was able to see a drainage vein with arterialized blood, arterial vessels and a nidus of aprox 1,5 cm, aspect consisting with an arteriovenous malformation. the avm was dissected, excised and then sent for histopathological analysis. the histological examination confirmed the presence of an avm. romanian neurosurgery (2015) xxix (xxii) 1: 85 92 87 figure 1 ct scan at admission, showing a large right frontal hematoma and intraventricular hemorrhage, with significant midline shifting postoperative course: the patient’s neurological status improved after the second surgical intervention and the control ct scan performed 2 days after the operation (figure 3) showed complete evacuation of the hematoma and no signs of an arteriovenous malformation. at discharge, the patient presented no neurological deficits. figure 2 ct scan 24 hours postoperatively revealed a new blood clot that needed surgical intervention follow-up: at the 1 month postoperatively the catheter cerebral angiography showed no signs of a residual avm (figure 4). 88 tascu et al spontaneous intracranial hemorrhage in children figure 3 ct scan aspect 2 days after the second intervention figure 4 angiography performed 1 month after the acute episode case 2 history and examination: a 9 year old girl presented with symptoms of increased intracranial pressure that started with headache, 2 days before admission, followed by nausea and vomiting. the patient’s level of consciousness was decreased at 10 points on the glasgow coma scale. the neurological examination showed slow reactive pupils, bilateral babinski sign and globally increased osteotendinous reflexes. family reported no traumatic events. imaging: ct scan at admission (figure 5) showed a right parietal-occipital hematoma, with midline shifting to the left side. operation: emergency surgical intervention to evacuate the hematoma was requested. at first, there were no signs of an avm, but after the blood clot was evacuated, during hemostasis, as the clot’s mass effect decreased, we discovered an arterialised vein, further dissection revealing an arteriovenous malformation that was completely excised, with no incidents. the piece was sent for histological examination that confirmed the presence of a racemous hemangioma. romanian neurosurgery (2015) xxix (xxii) 1: 85 92 89 figure 5 ct scan at admission showing a blood clot with mass effect on the surrounding structures postoperative course: the patient’s postoperative course was uneventful, and his symptoms completely resolved after surgery. postoperative ct scan (figure 6) showed the complete evacuation of the blood clot. follow-up: the patient presented at the 1 month follow-up with no neurological deficits. we performed a catheter angiography that showed no signs of residual vascular malformation (figure 7) figure 6 postoperative control ct scan 90 tascu et al spontaneous intracranial hemorrhage in children figure 7 angiographic control, 1 month after the neurosurgical intervention discussions the most common form of clinical presentation in children with avms is intracerebral hemorrhage, followed by first time seizure (less common), intracranial hypertension or focal neurological symptoms (1, 2, 15, 16). in young children (<2 years old), large avms may clinically present as highoutput heart failure (1-2, 15, 17, 18). spontaneous ich in children must be considered a ruptured vascular malformation until proven otherwise. we reported 2 clinical cases of children presenting with altered neurological status and symptoms of increased intracranial pressure due to intracerebral hemorrhage, with no recent traumatic events. intraoperative findings proved that the bleeding source was a ruptured arteriovenous malformation, the only evidence sustaining this diagnosis being the histological examinations. there are multiple imaging techniques to diagnose an avm. on ct scan, avms appear as serpiginous iso/hyperintense vessels that enhance contrast strongly. ct scan is mostly useful for showing acute hemorrhage, a mass effect or displacement of normal structures. magnetic resonance imaging (mri) is superior in sensitivity and specificity to the ct scan, showing size, location, previous symptomatic /asymptomatic hemorrhage, as well as changes like mass effect, edema or ischemia of the surrounding tissue. cerebral angiography, in addition to details offered by ct/mri, allows the identification of feeding and draining vessels, along with other associated vascular abnormalities. however, it may be negative after an acute hemorrhage or spontaneous avm thrombosis. another usefull imaging tool could be computed tomography angiography (cta), that can guide the surgeon in emergency surgery performed on patients with ruptured vascular malformations. still, it is not as detailed as mri or catheter angiograpy and it can also be a source of false negatives, especially in important bold clots with significant mass effect (1, 2, 15). due to the altered general and neurological status in the 2 cases presented, the surgical intervention for decompression of the hematoma had to be performed in emergency, with no time for further imaging investigations that could come useful for the surgical team. the particularity of these cases was the lack of anatomical evidence of an avm at first, followed by the ulterior identification of the vascular malformation. local anatomical and pressional changes, induced by the presence of the blood clot, may alter the blood circulation romanian neurosurgery (2015) xxix (xxii) 1: 85 92 91 inside the arteriovenous malformation and ‚hide’ it from the surgeons view. also, after the malformation ruptures, small blood clots that obliterate the av shunts may form within the malformation, and temporary interrupt the blood flow inside, making it difficult to be identified. the fact that, in both cases, the malformation became visible after the hematoma evacuation, together with the premise that all spontaneous intracerebral hemorrhages are arteriovenous malformations until proven otherwise, suggests the importance of continuously inspecting the operating wound after the clot removal. complete excision of the malformation is the key to completely cure it, especially since the postoperatove patient’s complications (such as rebleeding, seizures, edema, stroke or vascular thormbosis) depend almost entirely on the extent of resection (15, 23, 24). in both cases, hematoma evacuation and complete excision of the malformation lead to patient’s full recovery, despite the severely altered consciousness state and neurological deficits at admission. another factor to be taken into consideration when operating on children with ruptured avms, is the functional outcome, as the pediatric population has a better capacity to completely/mostly recover postoperatively, compared to adults15, 25-27. if the surgical intervention fails to completely remove the vascular lesion, multimodality treatment should be taken into consideration, since it appears to improve obliteration and decrease rebleeding rate (1, 2, 15, 22). an angiographic control should be obtained during follow-up, to certify the complete obliteration of the vascular malformation. conclusions whenever a brain surgeon faces spontaneous intracerebral hemorrhage in children the first thought should be a ruptured vascular malformation. during hemostasis, even if there are no signs of a patent avm while evacuating the hematoma, we should look for anatomical features suggestive of an avm, since the local alterations caused by the blood clot could have temporarily obliterated the malformation and ‘hide’ it from surgeon’s view. references 1. youmans neurological surgery, 6th ed., elsevier saunders, pa, 2011. 2. schmidek & sweet operative neurosurgical techniques: indications, methods and results, 6th ed., vol. 2, elsevier saunders, pa, 2012. 3. awad ia, robinson jr jr, mohanty s, et al. mixed vascular malformations of the brain: clinical and pathogenetic considerations, neurosurgery, 1993; 33:179-188. 4. gao e, young wl, ornstein e, et al. a theoretical model of cerebral hemodynamics: application to the study of arteriovenous malformation. j cereb blood flow metab. 1977; 17:905-918. 5. gault j, sarin h, et al. pathobiology of human cerebrovascular malformations: basic mechanisms and clinical relevance. neurosurgery. 2004; 55:1-17. 6. kader a, young wl, pile-spellman j, et al. the influence of hemodynamic and anatomic factors on hemorrhage from cerebral arteriovenous malformations. neurosurgery. 1994; 34:801-808. 7. gonzalez lf, bristol re, porter rw, spetzler rf. de novo presentation of an arteriovenous malformation. case report and review of literature. j of neurosurgery 2005; 102:726-729. 92 tascu et al spontaneous intracranial hemorrhage in children 8. minakawa t, tanaka r, koike t, takeuchi s, sasaki o. angiographic follow-up study of cerebral arteriovenous malformations with reference to their enlargment and regression. neursurgery 1989; 24: 68-74. 9. bristol rh, albuquerque fc, spetzler rf, rekate hl, mcougall cg. surgical management of arteriovenous malformations in children. j of neurosurgery 105:88-93, 2006 10. celli p, ferrante l, palma l, cavedon g. cerebral arteriovenous malformations in children and in adults. surg neurol 22:43-49, 1984 11. smith er, butler we, ogilvy cs. surgical approaches to vascular anomalies of the child’s brain. curr opin neurol 15:165-171, 2002 12. humphreys rp, hoffman hj, drake jm, ruthka jt. choices in the 1990s for the management of the pediatric cerebral arteriovenous malformations. pediatr neurosurg 1996; 25:277-285. 13. kiris t, sencer a, sahinbas m, sencer s, imer m, izgi n. surgical results in pediatric spetzler-martin grades iiii intracranial arteriovenous malformations. childs nerv syst 2005; 21:69-74. 14. mori k, murata t, hashimoto n, handa h. clinical analysis of arteriovenous malformations in children. childs brain 1980; 6:13-25. 15. intracranial arteriovenous malformations: stieg pe, batjer hh, samson d, informa healthcare usa inc, ny, 2007 16. fullerton hj, achrol as, et al. long term hemorrhage risk in children versus adults with brain arteriovenous malformations. stroke 2005; 36:2099-2104. 17. hofmeister c, stapf c, hartmann a et al. demographic, morphological and clinical characteristics of 1289 patients with brain arteriovenous malformations . stroke 2000; 31:1307-1310. 18. celli p, ferrante l, palma l, cavedon g. cerebral arteriovenous malformations in children. acta neurochir (wein) 1984; 142:145-158. 19. hamilton mg, spetzler rf. the prospective application of a grading system for arteriovenous malformations. neurosurgery 1994; 34:2-7. 20. spetzler rf, martin na. a proposed grading system of arteriovenous malformations. j neurosurg 1986; 65:476-483. 21. drake c. brain arteriovenous malformations. considerations for and experience with surgical treatment in 166 cases. clin neurosurg. 1979; 26:145-208 22. darsaut te, guzman r, marcellus ml, et al. management of pediatric intracranial arteriovenous malformations: experience with multimodality therapy. neurosurg. 2011; 69:540-556 23. heros rc, korosue k, diebold ps. surgical excision of cerebral arteriovenous malformations; late results. neurosurg 1990; 26;570-578. 24. yes hs, tew jm, gartner m. seisure control after surgery on cerebral arteriovenous malformations. j neurosurg 1993; 78:12-18. 25. sanchez-mejia ro, chennupati sk, gupta n et al. superior outcomes in children compared with adults after microsurgical resection of braio=n arteriovenous malformations. j neurosurg 2006; 105:82-87. 26. dirocco c, tamburrini g, roolo m. cerebral arteriovenous malformations in children. acta neurochir (wein) 2000; 142:145-158. 27. meyer pg, orliaguet ga, zerah m, et al. emergent management of deeply comatose children with acute rupture of cerebral arteriovenous malformations. cn j anaesth 2000; 47:758-766. ghodsali_carotid romanian neurosurgery (2016) xxx 1: 83 91 83 carotid-ophthalmic aneurysms – protective features making them a rare cause of subarachnoid hemorrhage ali ghods, david straus department of neurosurgery, rush university medical center, chicago, il, usa abstract: objective: to review the rate of carotid-ophthalmic aneurysm (coa) rupture and to identify protective features that may contribute to their low rupture rate. methods: we reviewed the records of 790 patients with 773 aneurysms greater than 2 mm treated by endovascular routes between 2002 and 2012 at our institution. seventy five carotidophthalmic aneurysms were identified in 72 patients. three injected human cadaver heads were studied to evaluate the perianeurysmal environment of the carotidophthalmic region. results: only 2 (2.8%) of these 72 patients presented with acute sah due to a ruptured carotid-ophthalmic aneurysm. the average size of ruptured coa was 11.3 mm versus 7 mm for unruptured aneurysms. most of the aneurysms were discovered in patients who were asymptomatic. the most common presenting symptom was headache. in this study, we also provide cadaveric anatomic illustrations of the perianeurysmal environment in order to investigate the low rate of coa rupture. additionally, we highlight the existence of a double arachnoid layer consisting of the arachnoid on the inferior aspect of the optic nerve and surrounding the internal carotid artery (ica), which could further contribute to the low rupture rate of these aneurysms. conclusions: carotid-ophthalmic aneurysms are uncommon sources of subarachnoid hemorrhage. the perianeurysmal environment surrounding these aneurysms may provide protection, lending these aneurysms to a relatively benign natural history. key words: internal carotid artery, intracranial aneurysm, ophthalmic artery, subarachnoid hemorrhage, optic cistern, optic membrane introduction asymptomatic, unruptured intracranial aneurysms have been detected in 3 to 6% of the general population. however, aneurysmal subarachnoid hemorrhage (sah) occurs in 6 to 8 per 100,000 people per year. (8, 23, 24) the prognosis of ruptured aneurysms remains poor, with mortality nearing 50% and severe disability occurring in approximately 20% of patients. with the increase use of computed tomography (ct) and magnetic resonance 84 ghods, straus carotid-ophthalmic aneurysms imaging (mri), incidental aneurysms are being identified and treated more frequently. whether or not to treat incidental aneurysms has been a subject of much debate, as there still remains much conflict in the literature surrounding the natural history, risk of aneurysm rupture, and morbidity of microsurgical and endovascular interventions. risk factors for aneurysm rupture and subsequent sah include smoking, hypertension, atherosclerosis, and alcohol consumption. (12) some authors also have proposed other independent risk factors, including aneurysm size, irregularity in the shape of the aneurysm, and location. (9, 12) overall, aneurysms of the posterior communicating artery (pcoa) and anterior communicating artery (acoa) more often present with sah compared to those located at other regions, such as the paraclinoid region of the internal carotid artery (ica). (5, 7, 14, 25) this disparity may be due to differences in the perianeurysmal environment (pae), including certain anatomical constraints. surrounding bone, dura, nerves, and brain parenchyma may be encountered by aneurysms as they grow, affecting their propensity to rupture. (19, 20) such constraints may also alter wall shear stress (wss), a concept has been shown to play a prominent role in aneurysm formation, propagation, and rupture. (1, 9, 21) indeed, seshaiyor et al demonstrated that contact of the aneurysm with surrounding structures may decrease the stress at the fundus of a saccular aneurysm, thereby providing a protective effect and hindering aneurysm rupture. (20) a limited number of studies have investigated the potential constraints of the perianeurysmal environment and the effect they may have on the risk of aneurysm rupture. (need references for these studies) these studies suggest that the anatomical constraints of the pae may prevent aneurysm rupture. it is also conceivable that, in these cases, the components of the pae may provide a protective barrier when aneurysm rupture occurs, resulting in a more contained hemorrhage and benign clinical course. in this study, we retrospectively reviewed the rupture rate, presenting symptoms, and perioperative morbidity of 75 endovascularly treated carotid-ophthalmic aneurysms (coa’s) treated in 72 patients at our institution. we also evaluated the pae of coa’s to investigate possible explanations for the low rate of rupture of these aneurysms. materials and methods this study was approved by the institutional review board of rush university medical center. we conducted a retrospective chart review of 790 patients with 773 intracranial aneurysms larger than 2 mm treated by endovascular embolization between 2002 and 2012. these aneurysms were treated by three physicians (dkl, rm, mc). of these 773 aneurysms, 75 (9.7%) occurred at the carotid-ophthalmic junction. admission data, operative reports and imaging studies were reviewed to collect information on patient’s age, gender, aneurysm location, size and aneurysm rupture status. we also performed dissection of the carotid-ophthalmic region in three formaline romanian neurosurgery (2016) xxx 1: 83 91 85 fixed human cadaver heads to describe the pae of the ophthalmic carotid region from which aneurysms arise. on each cadaver head, a standard pterional craniotomy was performed followed by extradural drilling of the lesser wing of the sphenoid. this was followed by opening of the dura and proximal sylvian fissure dissection under 20x microscope magnification. the carotid artery medial to the anterior clinoid was identified in each head. anterior clinoidectomy was performed and the ophthalmic artery was identified. subsequently the region lateral, medial, and superior to the ophthalmic artery was identified and examined. results 75 endovascularly treated carotidophthalmic aneurysms: of 773 endovascularly treated aneurysms at our institution, 75 were found to be located at the carotid-ophthalmic junction. these 75 coa’s occurred in 72 patients. data surrounding these coa’s is presented in table 1. the presenting symptoms of the 72 patients with coa’s is presented in table 2. most of the aneurysms were discovered in patients who were asymptomatic. the most common presenting symptom was headache. other presenting symptoms included visual disturbance, dizziness and syncope. all the aneurysms in this series were treated via endovascular methods. specific treatment methods are listed in table 1. six patients (8.3%) presented with acute subarachnoid hemorrhage. however, in four of these patients the source of the hemorrhage was very clearly defined to be an aneurysm other than the one in the carotid-ophthalmic region. only 2 (2.8%) patients presented with acute sah due to ruptured coa’s. one of these patients had bilateral coa’s. one presented as hunt and hess grade 1, while the other patient presented as hunt and hess grade 3. one patient had a modified fisher grade 1 sah and one patient had a modified fisher grade 2 sah. no patient presenting with a ruptured coa required permanent cerebrospinal fluid (csf) diversion. the mean size of unruptured coa’s was 7.0 x 6.4 mm, while the mean size of ruptured aneurysms was 11.3 x 9.3 mm. complications occurred in 9 of the 72 (12.5%) treatment procedures (table 3). the most common complication was procedurerelated infarction, which occurred in 4 patients (5.5%). groin-related complications occurred following 2 (2.8%) procedures. one of these was a femoral artery pseudoaneurysm requiring thrombin injection, while the other was a superficial groin hematoma that spontaneously resolved. acute intraprocedural, in-stent thrombosis occurred in 1 patient. angioplasty was performed immediately and the patient was placed on a heparin drip post-operatively. there were no clinical sequelae. evaluation of the pae in cadaveric models: we evaluated the carotid-ophthalmic junction in three human cadaver models and found that coa’s may be situated in a unique environment (figures 1-6). the ophthalmic segment of the internal carotid artery (ica) is located between the origin of the ophthalmic artery (oa) and the origin of the pcoa. (4) 86 ghods, straus carotid-ophthalmic aneurysms table 1 characteristics of 75 endovascularly treated carotid-ophthalmic aneurysms treated in 72 patients mean age, yrs (sd) 55.0 (14.5) male, n (%) 9.0 (12.5) mean height, mm (sd) 9.1 (5.5) mean width, mm (sd) 6.5 (4.6) ruptured*, n (%) 2.0 (2.8) treatment, n (%): neuroform stent + coiling 34 (45.3) pipeline embolization device 17 (22.7) enterprise stent + coiling 10 (13.3) pipeline embolization device + coiling 4 (5.3) coiling alone 5 (7.3) other 5 (7.3) *six patients presented with acute subarachnoid hemorrhage. in 4 of these patients the source of subarachnoid hemorrhage was determined not to be the carotid-ophthalmic aneurysm. table 2 presenting symptoms of 72 patients with co aneurysms symptom n % asymptomatic 35 48.6 headache 16 22.2 acute sah 6 8.3 visual disturbance 7 9.7 dizziness 3 4.2 syncope 2 2.8 other 2 2.8 table 3 complications occurring in 72 endovascular procedures complication n % infarct causing hemiparesis 4 5.6 retroperitoneal hematoma 2 2.8 groin complications: femoral artery pseudoaneurysm 1 1.4 groin hematoma 1 1.4 acute in-stent thrombosis 1 1.4 figure 1 view of the supracliniod internal carotid artery (ica) from a left sided approach. a) ophthalmic segment of internal carotid artery; b) optic nerve; c) oculomotor nerve; d) posterior clinoid; f) falciform ligament romanian neurosurgery (2016) xxx 1: 83 91 87 figure 2 view of the supraclinoid ica from the left side. the left temporal lobe has been resected to better view the region of interest. a) ophthalmic segment of ica; b) optic nerve; c) oculomotor nerve; d) anterior clinoid process; e) roof of optic canal (anterior root of lesser wing of the sphenoid bone); f) falciform ligament; g) planum sphenoidale; h) reflected dura figure 3 -view of the supraclinoid ica from the left side through a trans-sylvian approach. a) optic nerve (cut and reflected superiorly); b) entrance to carotid cave; c) ica; d) oculomotor nerve; *) double arachnoid layer of the carotid artey and the inferior aspect of the optic nerve ; �) superior hypophyseal arteries figure 4 a) optic nerve; �) double arachnoid layer consisting of the arachnoid layer on the inferior aspect of the optic nerve and surrounding the ica; b) lateral edge of falciform ligament after sectioning; *) ophthalmic artery origin; c) ica; d) superior hypophyseal arteries figure 5 left sided approach after anterior clinoidectomy with the left temporal lobe removed. a) optic nerve; b) ophthalmic artery; c) distal dural fold; d) ica; f) superior hypophyseal arteries 88 ghods, straus carotid-ophthalmic aneurysms figure 6 left sided vew of the carotid ophthalmic region through a trans-sylvian approach. a) optic nerve; �) the double arachnoid layer of the carotid artery and optic nerve in the area of ophthalmic artery was identified in every caver head; b) ophthalmic artery; c) distal dural fold; d) carotid cave; e) ica; f) superior hypophyseal artery the origin of the oa, and thus the proximal limit of the ophthalmic segment, is typically (85%) located distal to the distal carotid dural ring and, therefore, within the subarachnoid space. (6) the ophthalmic artery arises from the dorsal or dorsomedial portion of the ica underneath the optic nerve. (4) aneurysms of the carotid-ophthalmic junction arise from the superior wall of the ica, just distal to the oa origin, and extend superiorly towards the overlying optic nerve. the falciform ligament, connecting the dura of the anterior clinoid process (acp) and the planum sphenoidale, covers the optic nerve in the region of the oa origin. in its ophthalmic segment, the ica is surrounded by the acp laterally, the optic nerve, falciform ligament and roof of the optic canal superiorly, the tuberculum sella medially and the middle clinoid and interclinoid dural folds inferiorly. these bony and dural structures provide biomechanical rigidity to the ophthalmic segment of the ica. moreover, in our cadaveric dissection, we consistently identified a double arachnoid layer formed by the arachnoid of the inferior aspect of the optic nerve and the arachnoid surrounding the ica. this double arachnoid layer potentially could give the dome of the formed coa more protection and contribute to a decreased risk of rupture. furthermore, if the rupture takes place, this double arachnoid layer could limit the degree of dissemination of the subarachnoid hemorrhage. discussion unruptured intracranial aneurysms have been detected in up to 6% of the general population, yet aneurysmal subarachnoid hemorrhage occurs in only 6 to 8 per 100,000 people per year. according to the isuia study, the annual risk of rupture of anterior circulation aneurysms less than 7 mm is quite low (0-1.5%) compared to larger ones (6.440%). (25) given the poor prognosis and significant morbidity associated with sah, treatment of aneurysms less than 7 mm incidentally found has been advocated by many. aneurysms of the carotid-ophthalmic junction are rare. prior studies have reported particularly low rates of rupture among aneurysms occurring at the carotidophthalmic junction.16,17 the rupture rate of coa’s in our series (2.8%) is similar to that reported previously in the literature. the isat investigators found coa’s to be romanian neurosurgery (2016) xxx 1: 83 91 89 responsible for only 1.4% of sah.14 similarly, fukerson et al reported a rupture rate of 1.5%, while henkes et al reported a rupture rate of 2% for co aneurysms.3,5 these studies, as well as ours, demonstrate that the rate of rupture of aneurysms at the co segment is low. given the particularly low rate of coa rupture, the decision to treat unruptured, incidental coa’s less than 7 mm should be approached with caution. a coa of 7 mm might not behave the same as a 7 mm acoa or pcoa aneurysm due to its surrounding anatomic environment. studies evaluating the endovascular treatment of coa’s specifically have reported similar complication rates to ours. fukerson et al reported a morbidity of 7.1% in coa’s treated by endovascular methods.3 similarly, sherif et al and loumiotis et al reported morbidities of 5.3% and 18% and mortality rates of 2.6% and 3%, respectively.13,22 in our series, we experienced a morbidity of 12.5% (n=9). it should be noted that all complications except one were self-resolving or of minimal clinical significance. one patient in our series had a long-term dense hemiparesis that significantly affected her quality of life. we experienced no procedurerelated mortality. in our series the ruptured coa’s were larger than the unruptured aneurysms. one explanation for this finding could be that once the aneurysm grows to a larger size, it expands beyond the aforementioned protective barriers of the carotid-ophthalmic region. we were unable to identify a particular threshold, above which the aneurysm’s size no longer permits protection by the pae. this may be a function of differences in this region amongst individuals. while the exact reason for the low rate of rupture of co aneurysms is unknown, it may be due to a disparity in the aneurysm size, morphology, or wall shear stress. these features, at least in part, may be determined by the anatomical constraints of the perianeurysmal environment at this location.4,6 the anatomic features of the ophthalmic segment of the carotid artery, as described above, may have important implications for the risk of aneurysm rupture and the extent of subarachnoid hemorrhage that occurs when co aneurysms rupture. the rigid surroundings of the oa origin and the superior orientation of the aneurysmal axis results in a physically constraining pae. structures such as the falciform ligament, optic nerve, anterior clinoid and the distal dural ring may serve to reduce the transmural pressure of the aneurysm. furthermore, the double arachnoid layer described in this study also could contribute to decreasing the transmural pressure. this membrane may lead to the stability of these aneurysms, decreasing their rate of rupture and possibly limiting the extent of hemorrhage. conclusion: traditionally, in unruptured aneurysms, size and location have been a main determinant in the decision of whether or not to treat. however, anatomic features associated with aneurysm location may play an important role in their natural history and risk of rupture. here, we demonstrated that coa’s have an exceptionally low risk of rupture. we evaluated the pae surrounding these 90 ghods, straus carotid-ophthalmic aneurysms aneurysms and found that coa’s may be protected by the imposed anatomical constraints of surrounding structures. we propose that this unique environment may play an important protective role in the low incidence of coa formation and rupture. treatment of incidentally small coa’s should be considered with caution. correspondence david straus rush university medical center department of neurosurgery 1725 w. harrison, suite 855 chicago, il 60612 davidstraus@gmail.com telephone: 312-942-1854 references 1.beck j, rohde s, el beltagy m, zimmermann m, berkefeld j, seifert v, et al: difference in configuration of ruptured and unruptured intracranial aneurysms determined by biplanar digital subtraction angiography. acta neurochirurgica 145:861-865; discussion 865, 2003 2.brilstra eh, rinkel gj, van der graaf y, van rooij wj, algra a: treatment of intracranial aneurysms by embolization with coils: a systematic review. stroke; a journal of cerebral circulation 30:470-476, 1999 3.fulkerson dh, horner tg, payner td, leipzig tj, scott ja, denardo aj, et al: results, outcomes, and follow-up of remnants in the treatment of ophthalmic aneurysms: a 16-year experience of a combined neurosurgical and endovascular team. neurosurgery 64:218-229; discussion 229-230, 2009 4.gibo h, lenkey c, rhoton al, jr.: microsurgical anatomy of the supraclinoid portion of the internal carotid artery. journal of neurosurgery 55:560-574, 1981 5.henkes h, fischer s, weber w, miloslavski e, felber s, brew s, et al: endovascular coil occlusion of 1811 intracranial aneurysms: early angiographic and clinical results. neurosurgery 54:268-280; discussion 280-265, 2004 6.horiuchi t, tanaka y, kusano y, yako t, sasaki t, hongo k: relationship between the ophthalmic artery and the dural ring of the internal carotid artery. clinical article. journal of neurosurgery 111:119-123, 2009 7.im sh, han mh, kwon ok, kwon bj, kim sh, kim je, et al: endovascular coil embolization of 435 small asymptomatic unruptured intracranial aneurysms: procedural morbidity and patient outcome. ajnr. american journal of neuroradiology 30:79-84, 2009 8.inagawa t, hirano a: autopsy study of unruptured incidental intracranial aneurysms. surgical neurology 34:361-365, 1990 9.kondo s, hashimoto n, kikuchi h, hazama f, nagata i, kataoka h: cerebral aneurysms arising at nonbranching sites. an experimental study. stroke; a journal of cerebral circulation 28:398-403; discussion 403-394, 1997 10.lanterna la, tredici g, dimitrov bd, biroli f: treatment of unruptured cerebral aneurysms by embolization with guglielmi detachable coils: casefatality, morbidity, and effectiveness in preventing bleeding--a systematic review of the literature. neurosurgery 55:767-775; discussion 775-768, 2004 11.levy e, koebbe cj, horowitz mb, jungreis ca, pride gl, dutton k, et al: rupture of intracranial aneurysms during endovascular coiling: management and outcomes. neurosurgery 49:807-811; discussion 811-803, 2001 12.longstreth wt, jr., koepsell td, yerby ms, van belle g: risk factors for subarachnoid hemorrhage. stroke; a journal of cerebral circulation 16:377-385, 1985 13.loumiotis i, d'urso pi, tawk r, cloft hj, kallmes df, kairouz v, et al: endovascular treatment of ruptured paraclinoid aneurysms: results, complications, and follow-up. ajnr. american journal of neuroradiology 33:632-637, 2012 14.molyneux a, kerr r, stratton i, sandercock p, clarke m, shrimpton j, et al: international subarachnoid aneurysm trial (isat) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. lancet 360:1267-1274, 2002 15.naggara on, white pm, guilbert f, roy d, weill a, raymond j: endovascular treatment of intracranial unruptured aneurysms: systematic review and metaanalysis of the literature on safety and efficacy. radiology 256:887-897, 2010 romanian neurosurgery (2016) xxx 1: 83 91 91 16.nguyen tn, raymond j, guilbert f, roy d, berube md, mahmoud m, et al: association of endovascular therapy of very small ruptured aneurysms with higher rates of procedure-related rupture. journal of neurosurgery 108:1088-1092, 2008 17.park hk, horowitz m, jungreis c, kassam a, koebbe c, genevro j, et al: endovascular treatment of paraclinoid aneurysms: experience with 73 patients. neurosurgery 53:14-23; discussion 24, 2003 18.qureshi ai, luft ar, sharma m, guterman lr, hopkins ln: prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: part i--pathophysiological and pharmacological features. neurosurgery 46:13441359, 2000 19.san millan ruiz d, yilmaz h, dehdashti ar, alimenti a, de tribolet n, rufenacht da: the perianeurysmal environment: influence on saccular aneurysm shape and rupture. ajnr. american journal of neuroradiology 27:504-512, 2006 20.seshaiyer p, humphrey jd: on the potentially protective role of contact constraints on saccular aneurysms. journal of biomechanics 34:607-612, 2001 21.sforza dm, putman cm, cebral jr: hemodynamics of cerebral aneurysms. annual review of fluid mechanics 41:91-107, 2009 22.sherif c, gruber a, dorfer c, bavinzski g, standhardt h, knosp e: ruptured carotid artery aneurysms of the ophthalmic (c6) segment: clinical and angiographic long term follow-up of a multidisciplinary management strategy. journal of neurology, neurosurgery, and psychiatry 80:1261-1267, 2009 23.vernooij mw, ikram ma, tanghe hl, vincent aj, hofman a, krestin gp, et al: incidental findings on brain mri in the general population. the new england journal of medicine 357:1821-1828, 2007 24.wardlaw jm, white pm: the detection and management of unruptured intracranial aneurysms. brain : a journal of neurology 123 ( pt 2):205-221, 2000 25.wiebers do, whisnant jp, huston j, 3rd, meissner i, brown rd, jr., piepgras dg, et al: unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. lancet 362:103-110, 2003 doi: 10.33962/roneuro-2022-014 osteochondroma of axis vertebra treated with en bloc resection and arthrodesis. a case report and review of literature deepak kumar singh, diwakar shankar, vipin chand, mohammad kaif romanian neurosurgery (2022) xxxvi (1): pp. 84-87 doi: 10.33962/roneuro-2022-014 www.journals.lapub.co.uk/index.php/roneurosurgery osteochondroma of axis vertebra treated with en bloc resection and arthrodesis. a case report and review of literature deepak kumar singh, diwakar shankar, vipin chand, mohammad kaif dr. ram manohar lohia institute of medical sciences, lucknow, india abstract osteochondromas are capped benign bony neoplasm that forms on the outer surface of the bone. they are most commonly found in appendicular skeletal but rare in the spine. the cervical spine is commonly involved in spinal osteochondromas. here we discuss a case of a 24-year-old male with osteochondroma arising from the posterior arch of c2 (axis) vertebra presenting with myelopathy. most of the cases are asymptomatic needing only observation. surgery is needed in case of progressive neurologic deficit. it is recommended to do an en bloc resection of the lesion along with cartilage cap to prevent recurrence and spinal stabilization with arthrodesis to avoid postoperative kyphosis. introduction osteochondromas are the most common benign primary tumor of bone constituting 20-50% of all benign bone tumors and 10-15% of all bone tumors [5]. according to world health organization (who), osteochondromas are capped benign bony neoplasm that forms on the outer surface of the bone. tumor originates from the ends of the bone near the growth plate where metaplastic cartilage undergoes endochondral ossification with subsequent proliferation. it is most commonly found in the appendicular skeleton but rare in the spine [6]. more than 50% of spinal osteochondromas are found in the cervical region [4]. here we discuss a case of a 24-year-old male with osteochondroma arising from the posterior arch of axis vertebra presenting with myelopathy. case report a 24-year-old male patient presented with complaints of progressively increasing difficulty in walking with weakness in the right upper and lower limbs for the last year. there was no history of trauma. there was no family history of mhe. his neurological examination revealed weakness (medical research council, mrc muscle power grading 4/5) of the right upper and lower limbs. deep tendon reflexes across major keywords osteochondroma, c2 osteochondroma, axis osteochondroma, spinal tumour, posterior arch osteochondroma corresponding author: diwakar shankar dr. ram manohar lohia institute of medical sciences, lucknow, india dev123diwakar@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 85 osteochondroma of axis vertebra treated with en bloc resection and arthrodesis joints were brisk. bilateral plantars reflex were extensor. bilateral hoffmann signs were positive. no involvement of bladder and bowel was seen. sensory modalities were intact. the breath-holding time was 42s. the modified japanese orthopedic association (mjoas) score was 16/18. plain radiographs and computer tomography (ct) cervical spine revealed lobulated circumscribed bony growth along inner margin of right lamina of the axis (c2) vertebra with extension anteriorly into the spinal canal and producing marked canal stenosis (figure 1). mri cervical spine showed a large extradural mass lesion arising from axis vertebral lamina causing major compression at c2 vertebral level with myelopathic changes in the cord which was corelated to the clinical complaints and examination of the patient (figure 2). the patient was taken for surgery. preoperative positioning was as per standard guidelines. fluoroscopic guidance was used for surgery. intraoperative en bloc resection of the lesion along with bilateral c2 vertebral lamina was done (figure 3). bilateral c1 and c3 vertebra lateral masses were fixed with titanium screws and rods system. onlay autologous bone grafts were placed between c1 and c3 lamina. the postoperative ct cervical spine showed complete removal of the lesion with an increased effective canal diameter at the level of the c2 vertebral body (figure 4). pathologic examination was consistent with osteochondroma. the patient had significant improvement in his symptoms and was discharged with a hard cervical collar for three months. in six months, follow-up patient was improved. figure 1. preoperative computer tomography (ct) images with the 3d reconstruction of the cervical spine showing pedunculated circumscribed bony growth along the inner margin of the right lamina of axis (c2) vertebra with extension anteriorly into the spinal canal and producing marked canal stenosis. figure 2. preoperative magnetic resonance imaging (mri) of the cervical spine showed a large extradural mass lesion arising from the right c2 vertebral lamina causing major compression at c2 vertebral level with myelopathic changes in the cord. figure 3. intraoperative image showing en bloc resection specimen of the osteochondroma along with c2 (axis) vertebral lamina. figure 4. the post-operative computer tomography (ct) of the cervical spine showed complete removal of the lesion with an 86 deepak kumar singh, diwakar shankar, vipin chand, mohammad kaif increased effective canal diameter at the level of the c2 vertebral body. discussion osteochondromas are the most common benign primary tumor of bone constituting 20-50% of all benign bone tumors and 10-15% of all bone tumors [5]. it is twice more common in females. the usual age of presentation is 20-30 years. according to world health organization (who), osteochondromas are capped benign bony neoplasm that forms on the outer surface of the bone. it arises from epiphyseal growth plate where microtrauma can lead to fibroblastic proliferation and the formation of new bone. osteochondromas can present in two forms, solitary exostosis (se) and multiple hereditary exostosis (mhe). solitary exostosis is the sporadic form of the disease and constitutes 85% whereas mhe occurs as autosomal dominant syndrome which constitutes 15% of all osteochondromas. osteochondromas can be sessile or pedunculated. our patient had a solitary pedunculated lesion over the right lamina of the axis vertebra. it is most commonly found in the appendicular skeleton including femur, proximal tibia and humerus, and pelvis but rare in the spine[1]. spinal osteochondromas constitute 1-9% of all cases[4]. more than 50% of spinal osteochondromas are found in the cervical region[4]. this is due to increased mobility leading to the displacement of cartilage and resulting exostosis. osteochondromas most commonly originate from the posterior element where ossification centers are present. the axis vertebra is the most common site of osteochondroma in the spine as was in our case followed by the c3 and c6 vertebra [2]. most of the cervical osteochondromas are asymptomatic as they commonly grow outwards away from the spinal cord. inward growth causes myelopathy and radiculopathy which is seen in 0.51% cases[1]. other symptoms include pain, weakness, numbness, neck mass, etc. as osteochondroma grows slowly, the patient may develop progressive symptoms. sometimes it may present early after a trauma leading to compression of the spinal cord. plain skiagram and ct scan can be used for establishing the diagnosis. ct is the imaging modality of choice[9]. on ct scan there is a direct continuity of lesion with the cortical and medullary cavity of the underlying bone. magnetic resonance imaging (mri) is useful in assessing the degree of spinal cord compression as well as malignant transformation. the most common treatment modality for asymptomatic cases is observation. symptomatic patients with pain or progressive neurological deficit require surgery. also, surgical excision may be done to establish the diagnosis[3]. previously surgical decompression without fusion was popular but it was associated with postoperative kyphotic deformity, cervical instability, late neurological deficit. hence, a shift towards en bloc resection with arthrodesis has been seen in recent times. complete surgical excision of the cartilaginous cap is critical to prevent recurrence[4]. sclubba et al in their study found that the recurrence rate increased from 11% after en bloc resection to 33% after intralesional resection. there is no role of neoadjuvant or adjuvant radiotherapy or chemotherapy. recurrence is seen in 2-11% of postoperative cases[4,8]. malignant transformation, mostly into chondrosarcoma, is seen in 1% of se and 3-15% of mhe cases. features of malignant transformation are rapid growth, growth after skeletal maturity, cartilage cap thickness >3mm, recurrence after complete resection[7]. in our case, complete resection with arthrodesis was done which is found to be more effective than resection alone. conclusion osteochondromas are the most common benign primary tumor of bone. most of them are found in the appendicular skeletal but rare in the spine. c2 vertebra is the most commonly affected vertebra. most of the cases are asymptomatic needing only observation. surgery is needed in case of progressive neurologic deficit. it is recommended to do an en bloc resection of the lesion along with cartilage cap to prevent recurrence and spinal stabilization with arthrodesis to avoid postoperative kyphosis. references 1. brastianos p, pradilla g, mccarthy e, gokaslan z. solitary thoracic osteochondroma case report and review of the literature. neurosurgery 2005; 56: e1379. 2. chatzidakis e, lypiridis s, kazdaglis g, chatzikonstadinou k, papatheodorou g. a rare case of solitary osteochondroma of the dens of the c2 vertebra. acta neurochir (wien) 2007;149(6):637–8. 87 osteochondroma of axis vertebra treated with en bloc resection and arthrodesis 3. gul rkanlar d, acıduman a, gul naydın a, kocak h, clelik n. solitary intraspinal lumbar vertebral osteochondroma: a case report. j clin neurosci 2004; 11:911–913. 4. lotfinia i, vahedi a, stefanaki k, tubbs rs, vahedi p. cervical osteochondroma with neurological symptoms: literature review and a case report. spinal cord ser cases. 2017;3:16038. 5. murphey m, choi j, mark j, kransdorf m, flemming d, gannon f. imaging of osteochondroma: variants and complications with radiologic pathologic correlation. radiographics 2000; 20: 1407–1434. 6. quirini g, meyer j, herman m, russell e. osteochondroma of the thoracic spine: an unusual cause of spinal cord compression. ajnr 1996; 17: 961–964. 7. srikantha u, bhagavatula id, satyanarayana s, somanna s, chandramouli ba. spinal osteochondroma: spectrum of a rare disease. j neurosurg spine. 2008;8:561–6. 8. veeravagu a, li a, shuer lm, desai am. cervical osteochondroma causing myelopathy in adults: management considerations and literature review. world neurosurg. 2017;97,752.e755-752.e753. 9. victory f, ali k. solitary, asymptomatic, posterior, vertebral, intracanal, cervical spine osteochondroma. radiology case reports. 2011;6:572. microsoft word 7.selectedabstracts_f_emn.doc 124 abstracts 17th annual emn congress cluj-napoca, romania 17th annual emn congress cluj-napoca, romania 27th – 28th of april, 2012 the scientific program of emn 2012 offered lectures and discussions with renowned experts and focus on: a) craniovertebral pathologies b) assessment of quality of life c) neuroprotection acute and chronic d) advances in neurotrauma e) new methods in motor and competitive rehabilitation f) free papers prof. dr. ioan stefan florian was the congress president of 17th annual emn congress, cluj-napoca, romania, april, 27-28, 2012. the congress was attended by numerous foreign guests and romanian neurosurgeons, including the presence of emn president, prof. dr. wolf-ingo steudel, ceo saarland university medical center homburg, germany. abstracts posttraumatic syringomyelia – about cause and treatment gregor freude, ulrich kunz, uwe max mauer department of neurosurgery, military hosptal of ulm, ulm, germany introduction: syringomyelia is caused by a disturbance of cerebral spinal fluid (csf) flow. causal treatment requires that the exact location of this disturbance be identified by imaging. cardiac-gated phasecontrast magnetic resonance imaging (mri) is an effective tool for this purpose. a traumatic lesion of the arachnoid does not nessitate a spinal cord injury. we investigated the question of whether every cause of posttraumatic syringomyelia requires surgery. material and methods: from 2001 to 2009, cardiac-gated phase-contrast mri of the skull and the whole spine was used to detect the site of csf obstruction in 693 patients with syringomyelia (417 women, 276 men; mean age: 38.5 years, range: 1–79 years). csf flow is demonstrated in the craniocaudal direction in a strictly median sagittal plane. results: 34 patients (7 women, 27 men) had a posttraumatic syringomyelia. 6 patients had after the trauma no neurological deficit. time between injury and diagnostic was in mean 8 years (0.5 to 29 years). there is no correlation between level of the spinal cord injury and the extension of the syringomyelia. with csf pulsation imaging the adhesions are romanian neurosurgery (2012) xix 2: 124 – 144 125 identified. chiari malformation was the most common cause of syrinx formation (154 patients). a total of 93% of the patients with chiari i malformation underwent surgery. conclusions: the level of the adhesion which causes the syringomyelia cannot be identified without cardiac-gated phasecontrast mri. in these cases, causal treatment cannot be given without cardiacgated phase-contrast mri if surgery is needed. not all patients with posttraumatic syringomyelia require surgery. do the calpain inhibitors and hepatocyte growth factor have an effect in spinal cord injury? ioan stefan florian1, adriana baritchii1, ioan groza2, cornel cătoi2, anca buzoianu1 1university of medicine and pharmacy “iuliu hațieganu”, cluj-napoca 2university of agricultural science and veterinary medicine, cluj-napoca objectives: the pharmacological effects of calpaine inhibitors and hepatocyte growth factor (hgf) have been extensively described but from our knowledge there are no studies to evaluate the association of these two drugs in spinal cord injury (sci). methods: fifty albino wistar rats were used for the study. the animals were divided into five groups: in group i (sham operated group) only laminectomy was performed; the rats from group ii-v underwent traumatic sci by using clipcompression model and they received the following substances: group ii received calpain inhibitor vi, group iii received hepatocyte growth factor (hgf), group iv received a combination of calpain inhibitor vi and hgf; the control group (vi) received dimethyl sulfoxide (dmso) only. the motor recovery of the animals was evaluated using the ferguson et al. modification of the bbb scale. after seven days the rats were sacrificed. results: we found no statistically significant differences between the control group and the groups that received the two substances, alone or in combination regarding the motor recovery (p> 0.05). conclusion: there are no drugs capable of targeting directly the nervous tissue after the spinal cord injury. the treatment with methylprednisolone has improved the long term recovery as shown in different studies, but the results remain modest. from our experience the calpain inhibitor and hgf had no clinical benefits. more studies are mandatory to ascertain the benefits of the drugs for both acute and chronic sci. keywords: spinal cord injury, calpain inhibitors, hepatocyte growth factor. prehospital and early inhospital treatment of tbi – study from austria alexandra brazinova1,2, walter mauritz1, veronika rehorcikova2 1international neurotrauma research organization, vienna, austria 2faculty of health and social work, trnava university, bratislava, slovak republic introduction: international neurotrauma research organization has 12 years of experience in quality of care, patient outcome and comparative effectiveness research in the area of brain trauma. aims of study: we investigated early management of patients after tbi in 126 abstracts 17th annual emn congress cluj-napoca, romania austria. methods: between 4/2009 und 4/2010 we have enrolled 16 austria centers into an observational study of prehospital and early in-hospital care of tbi and collected data on 446 patients. the study was funded by the ministry of health and the auva (austrian trauma insurance). for each patient we have collected data on prehospital status & treatment, status & treatment in trauma room, times of trauma, ambulance pick up, hospital/ icu admission and discharge/death, icu treatment summary, hospital & 6-months outcome. for each patient we have calculated intervals (ems-hosp; arrivalct, ct-or, etc.), probability of mortality and probability of poor outcome. the study is a part of a 5 year project (2008-2012), with interim analysis at halftime, described in this presentation. results: severe tbi had 2/3 of patients. overall hospital mortality was 31.8%. factors associated with significantly increased mortality were age > 50 years, poor neurological status, higher trauma severity, pre-existing illness and use of antithrombotic medication. conclusion: in prehospital setting, use of capnography and pulse oximetry and use of hypertonic saline were associated with lower o/e ratios. in in-hospital setting, administration of ct scan within 10 minutes of hospital admission, start of neurosurgery within 30 minutes of hospital admission and use of optimizing coagulation were factors associated with lower o/e ratios. experiences using mobile near-infrered-spectroscopy systems for noninvasive detection of intracranial hematoma lars kläbe, chris schulz, uwe max mauer, ulrich kunz department of neurosurgery, military hosptal of ulm, ulm, germany objectives: early recognition of intracranial hematoma strongly influences the sequelae of patients after traumatic brain injury. three different mobile laseroptic systems for quick diagnosis were testet for the ability to detect traumatic intracranial hematoma. method: patients after traumatic brain injury were examined using one of the near –infrared spectroscopy systems (crainscan; infrascanner 1000 or infrascanner 2000) and the results were compared to the corresponding ct or mri imaging. results: intracranial hematoma were detectable in 67% of the cases. the absence of any hematoma was correctly shown in 69% of the patients. conclusions: unilateral hematomas underlaying the calvarian bone are detectable in a safe manner if artificial factors are absent. the positive predictive value is low in patients with severe skull injury. bilateral bleeding is not detectable. the system is helpful in continuous monitoring of patients with mild to moderate skull trauma, especially of those without relevant soft tissue damage. the computed tomography can not be replaced by nearinfrared-spectroscopysystems. romanian neurosurgery (2012) xix 2: 124 – 144 127 infrascanner in the diagnosis of intracranial damage in children with traumatic brain injuries a. v. marshintsev, j. b. semenova, a. v. melnikov, s. v. meshcheryakov, a. r. adayev, v. i. lukyanov neurosurgical department, clinical and research institute of emergency children’s surgery and trauma, moscow, russian federation the aim: to estimate the efficiency of using the infrascanner model 1000 scanner during the diagnosis of intracranial hemorrhages among children with mild traumatic brain injuries. materials and methods: the basis for this study consisted of 95 patients with mild traumatic brain injuries. all the patients underwent a standard examination under the conditions in place in the emergency department which included a checkup by a neurosurgeon and cranial radiographs. computed tomography was performed on 43 patients (45%), while 52 patients (55%) with a low risk of intracranial damage were placed under dynamic observation. the neurosurgeon on duty performed a near infrared scan using the infrascanner. result: one of the most significant conclusions arising from our work concerns the high sensitivity and specificity of the infrascanner during the determination of hemorrhagic foci. the instrument’s specificity reaches 0.91, while its sensitivity reaches 1.00 (0.89; 1.00). the experience acquired during our work made it possible to define the infrascanner’s capabilities for this category of injured persons. it is obvious that such an examination was not very effective among children up to 2 years of age. this still leaves the problem of the damage (contusions) of the soft tissues of the skull cap that also accompany traumatic brain injuries. the infrascanner’s high sensitivity and specificity relative to the occurrence of an extravasal accumulation of blood when even small lesions are present in the soft tissues frequently constitute the reason for what is called a false-positive response. furthermore, taking the high specificity and sensitivity of the technique into account, together with the simplicity of its use, the result obtained makes it possible to view the infrascanner as a screening technique for the diagnosis of intra-cranial hemorrhages during initial specialized medical care. the evacuation of a neurosurgical ward in the terroristic menance – point of view of a neurosurgical resident gregor freude, uwe max mauer, ulrich kunz department of neurosurgery, military hosptal of ulm, ulm, germany introduction: the 16 th of july 2007 at 1 p.m. the editorial office of the neu-ulmer zeitung received a message by telephone, that at 3 p.m. seven bombs will explose in the military hospial of ulm. this message was classified by the police as serious. therefore we decided to evacuate the entire hospital. result: in our departement we we had to evacuate 31 patients (3 in the operation theatre, 22 who could walk, 1 lying in bed, 4 in wheelchair). within 55 mins we had 10 persons (4 doctors, 5 nurses, 1 secretaire) to 128 abstracts 17th annual emn congress cluj-napoca, romania evacuate all the patients from the 6th floor to the ground level. we transfered the patients to different reception centers. that day we had very good weather conditions. the transport back to the hospital started 8 hours later. conclusion: the evacuation of a hospital in the terrostic menance is a very difficult situation for the patients and the coworkers. this catastrophic situation can not be planned or calculated. the succes of this evacuation was realized by the improvisation, the very high motivation and the flexibility by all coworkers. the very good cooperation in the hospital, the hospitals around, the firemen, the police, the soldiers and the emergency medical services was the fundamental base of the fast evacuation. operative decision and follow-up using phasecontrast mri imagery in cranial and spinal pathologies affecting csf flow paul c. flore, horia pleş, gabriela cătău department of neurosurgery, county hospital, timişoara, românia modern-day neurosurgical practice benefits consistently from new and remarkable neuroimaging tools, especially by magnetic resonance. nevertheless, most of those fail to assess some essential physiological central nervous system processes like the cerebrospinal fluid circulation. the pathological loop of initial structural anomaly affecting the csf dynamics which further enhance the parenchymal damages is well documented in the literature. cine phase-contrast mri is a reliable and non-invasive method that allows the visualization and measurement of cerebrospinal fluid flow throughout the intracranial and spinal compartments. it has become available in our neurosurgical center since 2007. we found it successfully applicable in a wide range of neurosurgical pathologies which at some point interfere with the normal flow dynamics. in this work we show how carefully conceived cine phase-contrast studies can prove to be not only a valuable complement, but a decisive component in some problematic or equivocal clinical situations where other neuroimaging methods are inconclusive. principles of treatment severe traumatic brain injury in children j.b. semenova, l.m. roshal, o.v. karaseva, a.v. melnikov, s.v. mescheryakov, v.i. lukyanov neurosurgical department, clinical and research institute of emergency children’s surgery and trauma, moscow, russian federation since 2003 in our institute the basic principles of treatment stbi strategies were formulated according contemporary recommendations. the aim of our research is to evaluate the efficiency of treatment for children with combined and isolated stbi. we studied 129 children with stbi (gcs ≤ 8). 58% of them had combined trauma. statistical analysis of 230 parameters revealed significant factors for prognosis of severe tbi outcomes. there are: 1) mydriasis (p = 0.0019), 2) gcs level (p <0.05), 3) hypoxia (po2 <60mmhg) (p <0.05), romanian neurosurgery (2012) xix 2: 124 – 144 129 4) hypotension (cystolic bp<90) (p <0.05), 5) intracranial pressure> 26 mm hg. for more than 30 minutes, 6) marshal scale 3, 4 and 6 (p <0.05), 7) iss 45 ± 4 in groups with gcs = 6-8 score. there was not significant influence of iss on outcomes in the groups of combined injuries with gcs = 3-5 score. prospects for improving outcomes for children with severe combined or isolated tbi we associate with early restoration and maintenance of vital functions, early identification and elimination of damage which complicate general vital functions, followed by early restoration of anatomical arrangements. under these conditions, the fundamental importance is the maintenance of “physiological corridor” (vital functions) under the multi-modal monitoring control. the monitoring of intracranial pressure must be used as a important criterion for determining for the method of treatment. non-invasive icp monitoring? ulrich kunz, uwe max mauer, eduard stettin, chris schulz neurosurgical department, armed forces military hospital, ulm, germany introduction / objective / objectives: icp registration is a valuable but invasive tool for observation of the intracranial situation after traumatic brain injury. together we developed several methods for non-invasive observation of the pressure curve. this gives a signal curve like icp by the electrical signal change on lateral electrodes at the skull by the change of the relation between blood, brain and csf during the cardiac cycle. patient and methods / material and methods / methods / purpose now we used within the closed external meatus acusticus a pressure registration which gives the transmitted information of intracranial pressure through the aqueductus cochlea. 22 patients (17 nph, 2 sab, 1 icb, 2 intraventricular hemorrhage) were observed during invasive (17 epidural, 5 intraventricular) icp registration, 17 of them had a lumbar infusion test to determine a normal pressure hydrocephalus. the 14 volunteers were observed in different positions on a tilting table. results / result: in 73% of the patients and 94% of the volunteers the icp change was recognizably. the highest curve peac was earlier in enlarged icp. the curve shape give some information about the icp level conslusion / conslusions: reported by wloydka 1978 it may be that after the age of 40 years the aqueductus cochlea occluded in 50%. and no measurement is possible by this method. like in other experience a high sensitivity to patient movement causes a lot of artifacts. the primary curve and situation has a high interindividual change. the method allows no zero point estimation and therefore there is a loss of objective value of the registration which may be excluded by fuzzy logic. although these methods allow an orientation of intracranial pressure course. 130 abstracts 17th annual emn congress cluj-napoca, romania fiberendoscopic airway management does not compromise haemodynamic stability or gas exchange jan-peter jantzen dept. of anaesthesiology, intensive care medicine and pain management, academic teaching hospital nordstadt, hannover, germany securing the airway of patients with cervical spine injury requires a technique compatible with the tenet primum nihil nocere. laryngoscopical endotracheal intubation may jeopardize integrity of the cervical spine, which cannot be prevented by stabilizing collars reliably [1]. nasotracheal fiberoptic intubation under local anaesthesia obviates the need for direct laryngoscopy and was proven safe for the neurosurgical patient [2]. waiving mask ventilation and general anaesthesia may, however result in hypoxia, hypercapnia or hypertension, particularly undesirable in patients with associated tbi. we have assessed effects of airway management techniques on heart rate, blood pressure and blood gases in patients presenting for elective craniotomy. methods: informed consent was obtained from100 consecutive patients undergoing intracranial procedures. 50 patients each were randomly allocated to one of two groups. patients in group one received laryngoscopical orotracheal intubation following denitrogenation and induction of general anaesthesia (ga), patients in group two were intubated nasotracheally with a flexible fiberbronchoscope under local anaesthesia (“spray-as-you-go”) and oxygen insufflation (3 l/min via nasal prong) (la). patients in both groups received midazolam 3,75-7,5 mg/kg per os prior to transfer to the theatre and 20 ml of sodium citrate before induction. instrumentation included central venous line and arterial cannula. anaesthesia was induced / maintained with propofol (1-2 mg*kg-1/ 6 mg*kg-1*h-1) and sufentanil (0,01 mg / 0,5 μg*kg-1*h-1). in the ga-group, intubation of the trachea was facilitated with atracurium, 0,5 mg*kg1. in the la-group, patients received an initial dose of 0,01 mg sufentanil, i.v.; the nasopharyngeal passage was prepared with a nasal decongestant (oxymetazoline 0,01%) and local anaesthetic gel (lidocaine 2%). following endoscopical visualization of the larynx, lidocaine 2% was sprayed on the vocal chords through the biopsy channel 2 ml each on the upper and lower aspects, allowing 2 minutes to take effect. data collected for analysis included heart rate (hr), arterial blood pressure (sap / dap) and saturation (so2); arterial blood samples were analysed for ph, po2 and pco2. data were documented at five time intervals: t1 = after instrumentation, t2 = during denitrogenation, t3 = after sufentanil, t4 = during direct or indirect laryngoscopy, t5 = after completion of tracheal intubation. statistical analysis relied upon t-tests and wilcoxon-tests; significance was assumed at p<0,05. results: demographic data revealed no differences among groups; tracheal intubations were carried out without complications. in the la-group, hr (80 -> 73), sap (155 -> 136), dap (73 -> 69), so2 (99 -> 98), po2 (185 -> 147) and ph (7,42 -> 7,39) decreased from t4 to t5; pco2 (36,2 -> 41,8) increased from t4 to t5 (p<0,05). in the ga-group results for so2, po2, ph and pco2 were similar; haemodynamic variables (hr, sap and dap) were found increased at t5 (p<0,05). conclusion: awake fiberoptic romanian neurosurgery (2012) xix 2: 124 – 144 131 nasotracheal intubation .does not cause clinically significant perturbations of physiological variables; in particular, it does not result in hypercapnia or hypoxia. we conclude that awake fiberendoscopic nasotracheal intubation under local anaesthesia is a safe means of primary airway management, in particular when direct laryngoscopy shall be avoided. references: [1] mccabe jb, nolan dj (1986) comparison of the effectiveness of different cervical immobilization collars. ann emerg med 15:50-53 [2] wangemann bu, jantzen j-p (1993) fiber-optically guided endotracheal intubation in neurosurgical patients. neurochirurgia 36:117-122. telemetric monitoring of icp profile before and after hydrocephalus therapy sebastian antes, melanie schmitt, regina eymann, michael kiefer, wolf-ingo steudel, joachim oertel department of neurosurgery, saarland university, homburg, germany background: neurosurgical treatment in hydrocephalus therapy generally tends on normalization of intracranial pressure (icp). as pretherapeutic intracranial conditions are often known due to appropriate diagnostics, changes in icp after therapy usually remain unidentified. therefore, the implantation of a telemetric intraparenchymal measurement device offers the unique opportunity to analyze the influence of different neurosurgical procedures on icp profile. methods: telemetric icp measurement devices were implanted into the frontal brain parenchyma of 21 patients who suffered from chronic hydrocephalus. definitive surgical treatment consisted of first-time shunt implantation (n=6), endoscopic third ventriculostomy (n=7) and gravitational valve augmentation of an overdraining shunt system (n=8). each patient was pre-and postoperatively measured; gathered icp data were analyzed (mean, minimal and maximal values) and finally compared to reveal therapy-related changes. results: first-time shunt implantation could be proven to be an effective method both to immediately reduce mean icp and to intercept icp peaks. gravitational valve insertion could successfully counteract csf overdrainage by increasing minimal and mean icp values. interestingly, measurements within the first postoperative days after endoscopic third ventriculostomy revealed icp increases in most cases. conclusion: telemetric technique allows – for the first time – to exactly demonstrate influences of different neurosurgical measures on icp in hydrocephalus therapy. indications of computed tomography in craniocerebral traumatic lesions a.v. ciurea, r.m. gorgan, h. moisa “bagdasar-arseni” clinic hospital, 1st neurosurgical unit & the national center for excellency in neurosurgery, bucharest, romania; carol davila university school of medicine, department of neurosurgery background: the appearance of modern medical imaging technologies has shaped completely the diagnosis in neurosurgical pathology. the main investigative methods in use today are computed tomography with its derivatives (native, with contrast 132 abstracts 17th annual emn congress cluj-napoca, romania substance, bone window, 3d reconstructive ct, angio-ct) and magnetic resonance imaging (mri), native, with contrast substance and angio-mri. materials and methods: for the traumatic craniocerebral pathology, the emergency investigative method which grants a maximum of efficiency at patient admission is the native ct-scan. if skull fractures are suspected the next option is 3d reconstructive ct-scan and if the lesions are more severe and intracerebral traumas are suspected another scanning option presents itself through ct-scanning with contrast substance. any county hospital should have the logistics to provide its patients a ct-scan at admission for diagnostic and forensic reasons. to determine the extent of the lesions it is important that the ct-scan should be repeated at 6, 12 or 24 hours after admission. any patient with a head trauma must have a discharge ct-scan for control. the results of the ct-scan must be correlated with the patient’s glasgow score, conscience status and eventual existing injuries. in children, the abusive usage of ctscans can lead to modifications of the eye lens. in these conditions a repeated clinical examination and a follow-up of all diagnostic elements might avoid a repeated ct-scan. last but not least, the marshall scale must also be taken into account as it distinguishes focal and diffuse intracranial lesions while correlating them to the patient’s status. the second greatest indication of computed tomography is subarachnoid hemorrhage which raises the suspicion of a burst vascular aneurismal malformation and imposes the necessity of several other investigations to confirm the diagnosis. in the intracranial tumoral pathology computed tomography has only an orientative part. the elective investigation is magnetic resonance imaging. this allows for a definitive diagnosis and therapeutical attitude. in such a situation computed tomography is used only for post-op follow up of hemorrhage in the tumoral bed, ischemia or edema. conclusions: we consider that computed tomography has clear indications in the traumatic pathology, but this method must not be used abusively in non-traumatic lesions. keywords: computed tomography (ctscan), magnetic resonance imaging (mri), 3d reconstruction ct, head trauma, craniocerebral injury. prognostic factors in traumatic diffuse axonal injuries dana răcășan, dafin fior muresanu, horatiu stan, ioan stefan florian department of neuroscienes, university of medicine and pharmacy “iuliu hațieganu:, cluj-napoca, românia background: traumatic brain injury (tbi) is a common cause of morbidity and mortality emphasized by the fact that it affects all age groups. diffuse axonal injuries (dai) associated with tbi are a great challenge to physicians due to the difficulty of early diagnosis and effective treatment. no efficient criteria for prognosis of the disease have been developed so far, due to the lack of efficient imaging and other diagnostic techniques. the purpose of this study is to evaluate prognostic criteria for mortality, functional and neurocognitive outcome. romanian neurosurgery (2012) xix 2: 124 – 144 133 material and method: a systematic review of literature was performed, using the pubmed, mbase, the cochrane library, willey online library, scopus, science direct medical databases between january 1990 and july 2011. 11.398 articles were found using the keywords “diffuse axonal lesions/injury”, “traumatic brain injury”, “treatment of traumatic brain injury”, “treatment of diffuse axonal injury”, “prognosis of tbi/dai”, “outcome after tbi/ dai”,”neurocognitive impairment after tbi/dai|”, “patient perspective after tbi/dai”. the analyzed articles were indexed according efns criteria. article abstracts reporting original research and reviews were consulted. 77 articles were finally selected for inclusion. results: dai is a predisposing factor for memory, executive and behavioral dysfunction. a reduced score on gcs scale, older age, pupillary reflex abnormalities and corpus callosum lesions are associated with a poor outcome. younger age is associated with dysautonomia, being correlated with a poorer outcome. mri is more accurate than ct for diagnosis and prognosis of dai. dwi and dti have prognostic value in evaluating functional outcome, with dti being an efficient biomarker for microstructural changes and neurocognitive impairment. no efficient biomarkers for dai were highlighted until now. conclusions: clinical case history and advanced imaging techniques can improve our ability to diagnose dai and have the potential to become valuable instruments in establishing prognosis for this condition. keywords: traumatic brain injury, diffuse axonal injury, neurological deficit, dysautonomia, neurocognitive outcome. update in decompressive craniectomy in tbi including own experiences zbigniew czernicki department of neurosurgery, 2nd faculty of medicine, medical university of warsaw, warsaw, poland the role of decompressive craniectomy (dc) in previous treatment protocols of tbi was limited because of an invasive character of the procedure. however the often poor prognosis in tbi treatment justifies nevertheless more and more wilder acceptance of the dc treatment. the dc has to be performed early enough and big enough. according to own studies depending on craniectomy diameter the patients can gain ca 100 ml of an extra space. especially promising results can be achieved when patients are blow 50 y.o. in my opinion the sufficient dc plays an important role in the treatment of tbi. effects of decompressive surgery in patients with severe traumatic brain injury and bilateral non reactive dilated pupils ethem göksu1, tanju uçar1, mahmut akyüz1, murat yılmaz2, saim kazan1 1department of neurosurgery, 2department of anaesthesiology and intensive care; akdeniz university school of me dicine, antalya, turkey background: we investigated glasgow coma scale (gcs) scores, intracranial pressure (icp), cerebral perfusion pressure (cpp) changes and long-term clinical outcomes in patients with severe traumatic brain injury (stbi) associated with bilateral non-reactive dilated pupils (bndp) who underwent decompressive surgery (ds). 134 abstracts 17th annual emn congress cluj-napoca, romania methods: the study group consisted of 28 patients with bndp from among 147 patients underwent ds due to stbi in our department. results: the mean gcs score was 4.96 ± 1.20 at admission and 4.0 ± 0.00 at preoperatively. mean icp in non surviving patients after ds was higher (p < 0.05). icp decreases after ds, in surviving patients were also higher than in non surviving patients (p < 0.05). the overall mortality rate was 61.02 %. the higher score of than 2 of motor score of gcs at admission was associated with lower mortality (p < 0.05). four of surviving patients (14.28 %) had a functional outcome (glasgow outcome score: 4 and 5) at one year after hospital discharge. conclusion: outcome in patients with bndp after stbi may not be always fatal or poor. rapid ds may have increased the chance of functional survival especially in patients with admission gcs score of 6, 7. decompressive craniectomy in the treatment of severe traumatic brain injury: optional or recommended lászló fügedi, andrás csókay department of neurosurgery, borsod county university teaching hospital, miskolc, hungary severe traumatic brain injury with refractory intracranial hypertension is a multifactorial lifethreatening disease, especially in the polytraumatized patients. nowadays decompressive craniectomy became a very important part in the treatment of stbi. on the basis of evidence based medicine’s rules many prospetcive, randomized trials were created to find the exact indication and timing of the decompressive craniectomy, but the results are controversial like in the decra study. in our opinion considering the principles of bioethics good clinical experiences with decompressive craniectomy are enough to recommend this procedure in the treatment of stbi. method and results: in the past 10 years we published more articles about new technical innovations wich can prove the outcome after decompressive craniectomy.these processes are used in many neurotruma centers , but in the guidelines of stbi we could’t reach the adequate part oh this procedure. conclusion: it is questionable, that we could agree on the rule of decomressive craiectomyin the treatment of stbi patients, but we hope, that the good results and outcomes will help in this field. effects of selective brain hypothermia and decompressive craniectomy on neurological and radiological sequelae of closed head injury in mice jacek szczygielski1, angelika e. mautes1, andreas müller2, christoph sippl1, cosmin glameanu1, karsten schwerdtfeger1, wolf-ingo steudel1, joachim oertel1 1department of neurosurgery, 2department of radiology; saarland university hospital, homburg / saar, germany objective: both hypothermia and decompressive craniectomy have been proposed as treatment of severe traumatic brain injury. the goal of our experiment was to determine whether the selective brain hypothermia could impact the effect of craniectomy after brain trauma. romanian neurosurgery (2012) xix 2: 124 – 144 135 methods: male cd-1 mice where randomly assigned into the following groups (n=8 each): sham, decompressive craniectomy(dc), closed head injury(chi), chi followed by craniectomy(chi+dc) and chi and dc followed by focal hypothermia(chi+dc+h). at 24h posttrauma animals were subjected to neurological severity score (nss) test and beam balance score (bbs) test. the neurological outcome was specified as impairment score for nss (0-10 points) and bbs (0-5 points). in 5 animals of each group (n=5) mrimaging using a 9.4 tesla mri scanner was performed. a volumetric evaluation of apparent diffusion coefficient (adc) calculated from diffusion weighted imaging (dwi) sequence and rapid acquisition with refocused echoes (rare) images was used to assess edema and contusion, respectively. one-way anova was used for statistical analysis. results: the animals subjected to both trauma and craniectomy performed significantly worse(chi+dc:6.84±2.1,p<0.001) than animals with craniectomy alone(dc:2.71±1.51). this deleterious effect disappeared if additional hypothermia was applied (chi+dc+ h:4.41±1.8,ns). bbs was significantly worse in chi group(2.33±1.35,p<0.05) and in chi+dc group (2.63±1.53,p<0.05) but not in chi+dc+h group(1.5±1.41,ns) when compared to the sham group(0.67±0.47). both edema and contusion volume was significantly increased in trauma and craniectomy group (chi+dc: edema:54.4mm3±23.4,p<0.05; contusion: 61.5mm3±21.7, p<0.01) but again not in hypothermia group (chi+dc+ h:edema:33.9mm3±14.7,ns; contusion: 34.1mm3±14.2,ns) compared to craniectomy alone (dc:edema: 17mm3 ±12.8; contusion:17.1mm3±13.9). conclusions: there was synergistic deleterious effect of mechanical and surgical trauma. selective brain cooling applied after trauma and craniectomy effaced the negative effect of additional surgical trauma on neurological function and radiological sequelae of brain injury. therefore the local hypothermia may be a very promising alternative to complication-burdened systemic hypothermia. the potential of this treatment option should be explored in clinical feasibility study. early dc to avoid the sudden increase of icp in children after brain injury csókay andrás, l. fügedi, t. pentelényi dept. of neurosurgery, miskolc, hungary the purpose of the retrospective study of 8 consecutive patients is to call our attention to the optimal timing of the decompressive craniectomy (dc) in children. method: we report the outcomes of 8 children under the age of 12 with severe head injuries. dc was performed at different intracranial pressure (icp) (20 and 25 mmhg) levels. results: our results suggest that above 20 mmhg, very fast progression of icp (within15min.) can be occured, which may limit the time available to plan and perform dc with a successful patient outcome. conclusion: considering the anamnestic data it could be useful to perform dc at 20-22 mmhg icp in young patients in 136 abstracts 17th annual emn congress cluj-napoca, romania order to prevent the potential of very fast brain swelling if there is no possibility to perform durotomy within 20min after the onset of raising the icp. it is especially considerable in poor countries where the emergency route could be less organized because of locations of building and extreme load of the staff. prospective randomized trials are not necessary to evaluate the indication and standardization in lifethreatening illness as the rule of bioethics states. scientific rationale enough to accept a consideration. in vitro and in vivo evidence to clarify the effectiveness of the vascular tunnel technique in the course of dc csókay andrás, l. fügedi, t. pentelényi dept. of neurosurgery, miskolc, hungary introduction: to prove the evidence of the stability of vascular tunnels which protect the bridging veins during decompressive craniectomy (dc). method: the observation was carried out in vitro (cadaver) and in vivo (surgery and mri) in order to verify the durability of the vascular tunnel. results: in vivo observation proved the durability of vascular tunnel even 2 months later. conclusion: it has been concluded that vascular tunnel guarantees the efficacy of dc even at a high level of icp. on the other hand surgical intervention could be dangerous without a vascular tunnel even at an acceptable level of icp, because of possible occlusion of bridging veins. prospective randomized trials are not necessary to evaluate the indication and standardization in life threatening illness as the rule of bioethics states. scientific rationale enough to accept a consideration. craniotomy or decompressive craniectomy for evacuation of acute subdural haematomas: proposal for a multicentre randomised trial angelos g. kolias1, a. david mendelow2, antonio belli3,4, b. anthony bell5, andrew t. king6, diederik o. bulters4, marios c. papadopoulos5, lucia m. li1, ivan timofeev1, elizabeth a. corteen1, sian c. ingham1, thomas santarius1, john d. pickard1, david k. menon7, peter j. kirkpatrick1, peter j. hutchinson1 1division of neurosurgery, addenbrooke’s hospital & university of cambridge, cambridge, uk 2division of neurosurgery, royal victoria infirmary & newcastle university, newcastle, uk 3nihr centre for surgical reconstruction and microbiology, queen elizabeth hospital & university of birmingham, birmingham, uk 4wessex neurological centre, southampton general hospital, southampton, uk 5academic neurosurgery unit, st. george’s, university of london, london, uk 6department of neurosurgery, salford royal hospital & university of manchester, manchester, uk 7division of anaesthesia, addenbrooke’s hospital & university of cambridge, cambridge, uk background: acute subdural haematomas (asdh) in addition to exerting mass effect are often associated with underlying parenchymal injury and significant brain swelling. in some patients evacuation of the asdh via a craniotomy with bone flap replacement may not adequately control raised icp despite post-operative management in icu. the btf guidelines romanian neurosurgery (2012) xix 2: 124 – 144 137 published in 2005 identified the role of decompressive craniectomy (dc) versus craniotomy as the top key issue for future investigation likely to improve the care of patients with asdh. design: we propose a multicentre randomised parallel group trial comparing dc with craniotomy for evacuation of asdh. subjects: eligible patients will be identified taking into account the following inclusion and exclusion criteria. inclusion criteria: clear history of trauma, initial gcs ≤13, asdh evident on ct scan, the admitting neurosurgeon feels that the haematoma needs to be evacuated, lower age cut-off 5 or 10 years, upper age cut-off 65 or 75 years. exclusion criteria: intra-operative brain swelling such that the bone flap cannot be replaced, patient is obeying commands immediately pre-operatively, bilateral fixed and dilated pupils, devastating extra-cranial injuries with survival >24 hours being unlikely, brainstem injuries on ct. outcome measures: the primary outcome measure will be the egos at 6 months after injury. secondary endpoints include: egos at 1 and 2 years after injury, quality of life (sf-36 at 1 and 2 years after injury), gcs on discharge from icu and from hospital, length of stay in icu and neurosurgical unit, major adverse events, health economic analysis, early return to operating theatre, incidence of hydrocephalus. sample size: retrospective studies have shown a favourable outcome in about 35% of patients undergoing evacuation of asdh. based on impact recommendations, statistical analysis will use an ordinal approach, based on proportional odds methodology. the estimated sample size is 800 patients (400 in each arm) to detect a 7% absolute difference in favourable outcome [power 80% and significance 5% (35% vs 42%)]. conclusions: if such a trial is also accompanied by prospective data collection for nonrandomised, eligible patients, then it is likely that clinicians in the future will be better guided when making decisions regarding the management of patients with asdh. traumatic brain injury: medico-legal expertise in france jean-luc truelle, pierre north, michèle montreuil department of neurorehabilitation, university hospital, garches, paris, france objective: to report the french current practice of medico-legal expertise for persons with traumatic brain injury (tbi). methods: up to date analysis of the expert appraisal dedicated to tbi persons, in the light of recent rules and improvements to do with the procedure, the examination, the ways of assessment and of compensation. results: 1. procedure: the specificities of the handicap require a specialized expert, a specific mission, a stage by stage expertise. there are 2 expertise types: “amicable” and judicial: both need to be contradictory. 2. examination: it requests the family witness, a thorough neuropsychological examination, taking into account the behavior, the assessment of autonomy, participation and quality of life and a mri. 3. evaluation and compensation need specific tools and argumentation. the most important domains to evaluate are the pretraumatic state, the functional deficit, the 138 abstracts 17th annual emn congress cluj-napoca, romania help needed, the vocational consequences and the limitation to build a couple and to raise children. conclusion: the tbi long-term and often hidden handicap needs specific means to perform an assessment adapted to mild and severe tbi as well. traumatic brain injury: the role of mediation in community integration jean-luc truelle, michèle montreuil department of neurorehabilitation, university hospital, garches, paris, france objective: to report the role of mediation in traumatic brain injury (tbi) re-entry. methods: mediation is a non-violent answer in conflict-solving between brain injured people, families and professionnals. therefore it could avoid a lawsuit, a destabilisation of the person in the rehabilitation process. how such an approach could apply to tbi? results: 1. the success factors: each protagonist’s will to solve their conflict in a peaceful way; the time dedicated to conflict-solving. 2. the very process of mediation: be able to express their pains and their needs… before starting off a dialogue or seeking an agreement; watch when a « swing » towards a harmonization of views is on the way to let both sides develop a solution. 3. the mediator himself: licensed in mediation; skilled in the subject matter; not an arbitrator, help both parties to meet halfway; «be confused», remain open, without being prejudiced. 4. deal with tbi specificities: an inferior position due to mental disorders, in relation to interlocutors with full capacities; this asymmetry can be compensated by family, lawyer and by previous one-to-one; reformulate, identify fatigue and tension, more short interviews rather than long ones. an example is presented. conclusion: « an existence which, on a human scale, seemed to be heading towards a blind alley, actually became a passage » (k. wojtyla, 1998). returning home following s evere cerebal injury and disease paul-jürgen hülser neurologische klinik, fachkliniken wangen, wangen, baden-württemberg, germany besides vital threat severe damage to the brain causes loss of communication, cognitive functions, control of body functions and mobility. early neurological rehabilitation is reserved to patients with the most severe injury impact and is characterized by the combination of acute medical care and rehabilitative procedures. returning home of survivers from severe cerebral injury and disease gives an overall measurement of the quality of medical and rehabilitational performance. the neurological clinic in wangen provides 20 hospital beds for early rehabilitation. over a period af 10 years 1133 patients have been treated. about one third was suffering from severe traumatic brain injury, another third ischemic or hemorrhagic brain infarction, 15 % subarachnoid hemorrhage, 10 % cerebral hypoxia, 8 % other etiologies (encephalitis, surgical interventions for cerebral abscess or neoplasm). usually, returning home requires relevant improvement in cognition, communication, mobility and romanian neurosurgery (2012) xix 2: 124 – 144 139 self care. our rehabilitation concepts preferentially cover these domains. in addition in appropriate cases the relatives were instructed how to manage remaining problems. the in-hospital mortality was 3 %. 15 % of our patients had to be transferred to another hospital, partly due to lifethreatening complications, partly due to intended treatment of concomitant medical problems as fractures. 10 % did not achieve a state of at least partial independency in daily life and went to a special-care home. 10 % remained completely dependant as well but were cared for by their relatives at home. early rehabilitation is followed by an intermediate rehabilitation in patients who exhibit a favourable course. these persons, 42 % of 1133 in our collective, showed partial or complete independency at the end of the in-hospital rehabilitation and could live at home without any (about one half) or with little assistance. this result justifies intensive efforts. the psychotherapy’s importance in neurorecovery of neurosurgical patients virginia rotărescu2, a. v. ciurea1 1academy professor, phd., m.d., msc, clinical emergency hospital “bagdasar-arseni” 2senior clinical psychologist, phd, clinical emergency hospital “bagdasararseni” the existence of reciprocal psyche-soma influence requires a double relationship, medical and psychological; the consequences of poor communication include noncompliance to treatment and malpractice legal actions. this paper provides explanations which necessarily require psychosomatic approach of each patient, the patient reacting massively in psychological plan. various studies revealed the fact that psychological intervention enhances not only the patient’s comfort but also his/her life quality itself and that it can help him leave longer. the results of these studies clearly indicate the fact that psychotherapy has positive effects on emotional adaptability, functional adaptability and on symptoms related to the illness and treatment in the case of patients with neurosurgical pathologies. delimitation of competence of various specialties is only for the benefit of the patient, who will be investigated and treated according to custom issues (“there are no diseases, only ill people”), imposing thus the integration of the psychologist in the therapeutic team. keywords: neurosurgical, psychotherapy, patient, quality of life, team, multidisciplinary. decompressive craniectomy in the treatment of severe traumatic brain injury: optional or recommended caterina pistarini, s.maugeri foundation institute, pavia, italy in the field of neurorehabilitation there is an increasing awareness about the importance of translation from basic scientific findings into practical application while most of the therapeutic interventions have encountered barriers during exploration of evidencebased effectiveness. appropriate research programs are thus essential to develop highquality research methods supporting specific treatment models in nrb practice. evidence based 140 abstracts 17th annual emn congress cluj-napoca, romania medicine model has been adopted in nrb clinical research to face many methodological challenges affecting the bench-to-bedside process. no longer based on subjectivity ebm model has shown to enhance appropriateness of rehabilitation actions in several neurological settings, such as multiple sclerosis, parkinson’s disease, children with cerebral palsy and stroke through a critical use of the best scientific evidences. nonetheless a dissonance when trying to apply research findings to the clinical encounter still exists because of the complexity of socio-cultural setting where physician and patient co-operate. a tempt to provide a way for examining these individual and contextual factors is represented by narrative based medicine, a model based on patients’ story of illness which restores the role of emotional experience within the relational context of care. starting from ebm and nbm a new integrated and bio-psycho-social oriented model could meaningfully fill the gap between research and clinical practice in nrb both theoretically and practically. evidence based medicine: what it is and what it isn’t. 1996. sackett dl, rosenberg wm, gray ja, haynes rb, richardson ws. clin orthop relat res. 2007 feb;455:3-5. narrative evidence based medicine. charon r, wyer p; nebm working group. lancet. 2008 jan 26;371(9609):296-7. what quality of life after traumatic brain injury? a novel instrument, qolibri jean-luc truelle, klaus von wild, michel onillon, michèle montreuil department of neurorehabilitation, university hospital, garches, paris, france objective: to report the clinical use of the qolibri, a disease-specific measure of health-related quality-of-life after traumatic brain injury (tbi). methods: the qolibri, with 37 items in six scales (cognition, self, daily life and autonomy, social relationships, emotions and physical problems) was completed in seven languages (finnish, german, italian, french, english, dutch, portuguese). qolibri scores were examined by variables likely to be influenced by rehabilitation interventions and included socio-demographic, functional outcome (gose), health status (sf-36) and mental health variables (hads). results: the qolibri was selfcompleted except for severe tbi who completed it in interview. it was sensitive to areas of life amenable to intervention, such as accommodation, work participation, health status (including mental health) and functional outcome. conclusion: the qolibri provides information about patient’s subjective perception of his/her hrqol which supplements clinical measures and measures of functional outcome. it can be applied across different populations and cultures. it allows the identification of personal needs, the prioritization of therapeutic goals and the evaluation of individual progress. it may also be useful in clinical trials and in longitudinal studies of tbi recovery. pharmacological and nonpharmacological strategies in brain protection and recovery dafin fior mureșanu romanian neurosurgery (2012) xix 2: 124 – 144 141 department of neurosciences, university of medicine and pharmacy “iuliu hațieganu”, cluj -napoca, romania the old concept that neuroprotection means suppressing pathophysiological processes, the idea that a single mechanism molecule might be effective in clinical practice are obsolete today, and represents the root cause of failure. the effects of etiological agents on the brain traditionally are conceived as a linear sum of independent pathophysiological processed (excitotoxicity, inflammation, apoptosislike, oxidative stress, etc) generating the pathways of pathological cascades (ischemic, traumatic, neurodegenerative). the pathway approach has produced a very detailed understanding of molecular changes in the postlesional brain but it possesses blind spots that are critically related to the failure of neuroprotection. this has influenced the simplistic way of understanding the concepts and as well, all attempts at clinical neuroprotection. the idea that a system is a linear sum of its component parts is called “superposition”, and the associated approach is called “reductionism”. the failure of clinical neuroprotection, recovery and modifying disease therapies in many chronic conditions, is measuring the failure of the reductionistic approach to the problem. the pathways can and do interact in a variety of fashions, via cross-talk, positive and negative feedback, etc, but the pathway heuristic itself offers no formal means of understanding such interactions. the expectation of discovering the magic cell death pathway x has affected experimental designs of neuroprotection studies. the causality demonstrated by the application of the plus/minus strategy is ultimately an illusion. to overcome the limits of the pathway view of cell function, a different approach is needed. such an approach is provided by network concepts applied to complex systems. the bistable model based on these assumptions seems to be a better instrument for a successful translational approach in brain lesion and recovery. unresponsive wakefulness syndrome (uws) why we need a new name for the apallic syndrome or vegetative state klaus von wild professor of neurosurgery, medical faculty westphalia wilhelm’suniversity münster; professor of neurorehabilitation and reengineering of brain and spinal cord lesions, international neuroscience institute, ini, hannover, d; professor h.c. for neurosurgical rehabilitation, med. faculty, al-azhar university, cairo, eg objective: some patients awaken from coma but remain unresponsive without response to command. this syndrome is known as apallic syndrome, coma vigile, and vegetative state. based on the results of modern neuroelectrophysiological investigations and functional brain imaging we here would like to introduced in the german speaking countries a new name for this syndrome of severest brain functional disturbances which we called in english unresponsive wakefulness syndrom (abbreviated uws) in 2010 (see http://www.biomedcentral.com/1741 142 abstracts 17th annual emn congress cluj-napoca, romania 7015/8/68; www.aerzteblatt.de/grundsaetze) patients and method: in europe, this clinical syndrome was initially termed apallic syndrome by 1940 kretschmer (1949), coma vigil by calvet and coll (1959), but it is currently known in the medical community and media as persistent vegetative state (pvs), jennet and plum (1972). it’s characterized by the clinical feature when patients awaken from coma but remain unresponsive without response to command. results: the prevalence of vs/as in hospital settings in europe is 0.5–2/100.000 population / year; one-third following acute traumatic brain damage. functional neuroimaging and cognitive evoked potential studies demonstrated that physicians should be cautious to make strong claims about awareness in some patients without behavioral responses to command. given these concerns regarding the negative associations intrinsic to the term vegetative state/apallic syndrome as well as the diagnostic errors the european task force on disorders of consciousness claim for a new term. discussion: many clinicians feel uncomfortable when referring to patients as vegetative. indeed, to most of the lay public and media vegetative state has a pejorative connotation and seems inappropriately to refer to these patients as being vegetablelike”. politicians and religious groups have hence felt the need to emphasize these vulnerable patients’ rights as human beings. conclusion: to offer physicians the possibility to refer to the diagnose of an unresponsive wakefulness syndrome equivalent to full stage as/vs, abbreviation uws. since this neutral descriptive term indicates patients showing a number of clinical signs (hence syndrome) of unresponsiveness in the presence of wakefulness. this new term respects the dignity and rights of the patient and the beloved. robot-assisted assessment of the arm in neurorehabilitation verena klamroth-marganska, urs keller alexander duschau-wicke, sabine schölch, robert riener sensory motor systems lab, department of health sciences and technologies, eth zurich, switzerland one major limitation in neurorehabilitation is the lack of repeatable and objective assessment of performance and progress of the patient. we developed a robot-assisted assessment tool for objective and quantitative assessment of the arm in patients with neurological deficits, e.g. after spinal cord injury (sci). the robot-assisted assessment tool is integrated in the arm therapy robot armin which has been developed by the groups of r. riener, v. dietz and a. curt at eth zurich and university hospital balgrist (university of zurich). armin is an exoskeletal robot with seven degress of freedom. the assessment tool consists of software and a visual display and includes tests for passive and active range of motion (a-rom), workspace and speed of movement (amove), maximum voluntary force (aforce), distance to path ratio and deviation from target (a-goal), and stiffness (a-stiff). we present the results of robot-assisted assessments in four patients after sci and the correlation with clinical tests (range of motion with goniometer, ashworth scale, tardieu scale, van lieshout test, grassp, romanian neurosurgery (2012) xix 2: 124 – 144 143 scim, mmt of the upper limb). the results of the study are promising. the assessments correlate with clinical scores; they reflect an improvement of function over time and detect even small changes in the quality of movements which cannot be measured in clinical testing. should lobar intracerebral haematomas due to cerebral amyloid angiopathy be excluded from the stich ii trial: a neuropathological study? jacques de reuck department of neuropathology, université lille nord de france, lille, france background: stich ii is a multicentre randomized trial comparing early craniotomy to evacuate the lobar haematoma with an initial conservative treatment. lobar haematomas in elderly patients are frequently due to cerebral amyloid angiopathy (caa). caa is a generalized cerebrovascular disease with bad outcome and frequently associated to alzheimer dementia (ad). purpose: the present post-mortem study aims to compare the incidence of cerebrovascular lesions in elderly demented patients, with and without caa, and in age-matched controls. patients and methods: thirty brains of ad patients with caa were compared to thirty ad brains without caa, twenty brains with lewy body dementia (lbd) and fifteen controls. prevalence and severity of ischaemic as well as of haemorrhagic lesions were compared. results: sixteen out of the thirty brains with caa had an intracerebral haemorrhage with a total number of twenty haematomas: eighteen had a lobar, one a thalamic and one a cerebellar location. multiple haematomas of different age were observed in three brains. lobar haematomas, white matter changes, cortical microbleeds and subarachnoid haemorrhages prevailed and were more severe in the caa group compared to the ad without caa, lbd and control groups. conclusions: on gross brain examination one should suspect caa in elderly patients with mainly recurrent lobar and subarachnoid haemorrhages, severe white matter changes and microbleeds. the in vivo suspicion of caa can only be made by using flair, t2 and t2* mri sequences. inclusion of patients with lobar intracerebral haematomas due to caa could weaken the results of the stich ii trial. traumatic ich: characteristics of patients in the ongoing stitch(trauma) trial elise rowan, richard francis, barbara gregson, patrick mitchell, a.d. mendelow neurosurgical trials unit, newcastle university, newcastle upon tyne, uk introduction/objective: stitch (trauma) is the first international randomised controlled trial of early surgery versus initial conservative treatment for patients with traumatic ich (tich). although there have been previous trials for patients with spontaneous ich (sich), we cannot assume that the pathogenesis of tich and sich are the same and that the patients affected by these conditions will respond identically to current treatments. here we describe the characteristics of stitch(trauma) patients and compare them to lobar sich patients in stich ii. methods: adult head injury patients are 144 abstracts 17th annual emn congress cluj-napoca, romania eligible for stitch(trauma) if they: have ct evidence of 1 or 2 tichs/contusions: each with a volume > 10ml. are within 48 hours of head injury. demonstrate clinical equipoise in the opinion of their neurosurgeon. patients randomised to early surgery undergo surgery as soon as possible. the appropriate surgical technique is at the discretion of the treating surgeon. outcome is measured by postal questionnaire. results: on 31 dec 2011, 120 patients were recruited into stitch(trauma) and 521 into stich ii. stitch(trauma) patients had a median age of 51 years, randomisation gcs of 12 and primary haematoma volume of 23 ml. stich ii patients had a median age of 65 years, randomisation gcs of 13 and haematoma volume of 36ml. conclusion: stitch(trauma) patients do differ: they are are younger and have smaller primary haematomas than stich ii patients. whilst stich ii will finish this year, recruitment into stitch(trauma) will continue so that we can precisely define the indications for surgical intervention for tich in future. should we measure outcome at 12 months as well as 6 months for acute brain injury trials: evidence from [stitch(trauma)]? barbara a. gregson, elise n. rowan, richard francis, a. david mendelow neurosurgical trials unit, newcastle university, newcastle upon tyne, uk introduction: the ongoing stitch (trauma) study aims to determine whether a policy of early surgery in patients with traumatic ich improves outcome compared to a policy of initial conservative treatment. in study design, identification of the most appropriate outcome measure is vital. the six-month time point is commonly used but would 12 months provide better information on recovery from the intervention? methods: this international randomised controlled trial had recruited 128 patients by the end of january 2012. this analysis examines the relationship between outcome at 6 and 12 months and between baseline variables and outcome. results: of the 40 patients who had reached 12 month follow-up, outcome was available for 38: 10 had died (all before 6 months), 14 were good recovery, 8 moderate disability and 6 severe disability. of the surviving patients 61% had maintained the same level as at 6 months, 29% improved and 11% deteriorated. examination of the rankin in survivors shows a similar picture with the majority of patients being grade 0 or 1. outcome at 12 months was significantly related to admission gcs (p=0.001) and patient’s age (p=0.038). at six months outcome for the same patients was significantly related to admission gcs (p=0.015) and time to randomisation (p=0.044). conclusions: this analysis, although conducted on a small number of patients, suggests that for an acute intervention primary outcome measurement should be conducted at 6 months. although patients do go onto improve beyond this point they are also likely to suffer from other problems that affect their outcome. 17umamaheswara_massive romanian neurosurgery (2014) xxi 4: 493 – 497 493 massive infarction and cavernous sinus thrombosis: an uncommon complication of tooth extraction umamaheswara reddy v.1, amit agrawal2, kishor v. hegde3, srikanth v.4, sahith reddy k.4 narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 1assistant professor of radiology, department of radiology 2professor of neurosurgery, department of neurosurgery 3professor of radiology, department of radiology 4resident of radiology, department of radiology abstract: cavernous sinus thrombosis (cast) is a rare and potentially fatal complication following tooth extraction. in present case of a 55 year old male known case of diabetes mellitus underwent tooth extraction. after 5 days, he noticed swelling around the cheek, high grade fever, and frontal headaches. diagnosis of alveolar abscess after inspection was made, for which incision and drainage was done. next morning, he noticed that the cheek swelling progressed to left eye and there was ct brain was performed which showed hyperdense areas in cavernous sinus on left side and left sylvian fissure with hemorrhagic venous infarct in left temporal and frontal lobes. more caudal sections revealed mucosal thickness in left maxillary and ethmoidal sinuses, edema over cheek, preseptal orbital swelling, retro-orbital fat stranding and axial proptosis. a diagnosis of rhino-orbital infection from dental source with cavernous sinus extension causing left temporo-frontal hemorrhagic venous infarction was made emergency surgery for decompression was performed but the patient did not responded to the treatment and succumbed to the infection. this case is a reminder that in patients with uncontrolled diabetes, undergoing dental procedures should be carefully dealt with appropriate antibiotic cover. early signs like unilateral facial edema, orbital chemosis, edema, and proptosis should raise high index suspicion of cavernous sinus thrombosis. key words: cavernous sinus thrombosis, venous infarction, diabetes mellitus, dental infection. introduction cavernous sinus thrombosis (cast) is a rare and potentially fatal complication following tooth extraction. (1-4) in present case we report a rare complication of tooth extraction where patient developed cavernous sinus thrombosis with resultant fatal outcome. 494 umamaheswara reddy et al massive infarction and cavernous sinus thrombosis case report a 55 year old male known case of diabetes mellitus went to the dental opd in rural hospital with left sided tooth ache. he was diagnosed to have cavity in the left second upper premolar: 25 which was extracted. he was prescribed oral analgesics and antibiotics (ampicillin -500 mg twice daily). after 5 days, he reported to the dentist for swelling around the cheek, high grade fever, frontal headaches. diagnosis of alveolar abscess after inspection was made, for which incision and drainage was done. patient was referred to diabetologist for his high blood sugar of 369 mg/ dl. patient postponed the meet with doctor as he got some symptomatic relief with the analgesics. next morning, he noticed that the cheek swelling progressed to left eye and there was purulent discharge from left eye. while patients’ relatives were making necessary arrangements to shift him to tertiary care center, he developed right side hemiparesis. during the transportation, condition of the patient rapidly deteriorated and patient was brought to our hospital with poor gcs – 5. on examination, he had swelling of left cheek, eyelid necrosis and his neurological examination revealed decreased tone on right side. vital parameters at the time of arrival were pulse -114bpm, blood pressure-70/30 mmhg, rbs409 gm/dl, rr-30 cpm, spo2 85%. tone and reflexes were decreased on the right side. routine investigations showed ketonuria, wbc-20000/mm3 (neutrophil75%, lymphocytes-23%, monocytes-2%), plts-1.5 lacs. ct brain was performed which showed hyperdense areas in cavernous sinus on left side and left sylvian fissure with hemorrhagic venous infarct in left temporal and frontal lobes. more caudal sections revealed mucosal thickness in left maxillary and ethmoidal sinuses, edema over cheek, preseptal orbital swelling, retro-orbital fat stranding and axial proptosis. a diagnosis of rhino-orbital infection from dental source with cavernous sinus extension causing left temporo-frontal hemorrhagic venous infarction was made. in view of extensive mass effect and compression on ipsilateral cerebral peduncle. emergency surgery for decompression was performed. however there was no improvement of gcs after the surgery and patient succumbed to death. discussion intracranial infection from odontogenic source resulting in cast is rare and contributes only upto 10% cases of cast. (1, 3) spread of extracranial infection to cavernous sinus can occur from paranasal sinuses, orbits, teeth, periodontal tissues, skin over face and cheek is facilitated by network of valve less venous plexus in which blood flow is pressure gradient dependent. (5) dental pathogens and septic emboli can spread into cavernous sinus through pterygoid venous plexus. (3) numerous bacterial (aerobic and an-aerobic) and fungal pathogens can cause cavernous sinus thrombosis. staphylococcus is most common organism causing cavernous sinus thrombosis. (4, 6) romanian neurosurgery (2014) xxi 4: 493 – 497 495 figure 1 axial ct images (a, b) showing hyperdense material within the left cavernous sinus, cavernous sinus is showing convex borders and axial orbital proptosis. axial ct images (c, d) showing blood within the sylvian fissure. large variegated intraparenchymal hemorrhage is seen in left temporo-frontal lobes causing midline shift (e, f) occurrence of cast multiplies by many folds in immunocompromised patients, as normal flora in otherwise healthy individuals become pathogenic due to ineffective defense mechanisms. (7) even minor infections in head and neck region in these patients should be judiciously treated to prevent this life threatening complications. (5) high index suspicion is required to have a diagnosis of cast: unilateral facial swelling, chemosis and acute onset of proptosis are warning signs which should raise the suspicion. (5) contrast ct scan or contrast mri is mainstay in diagnosing this condition. (4) filling defects within the cavernous sinus, convex bulge of the cavernous sinus, dilated ophthalmic vein are typical imaging signs. imaging should also be targeted to look for later consequences of cast like meningitis, empyemas, infarctions, aneurysms of cavernous sinus, fistulas etc. (4, 5) once diagnosis of cavernous sinus thrombosis is established, broad spectrum antibiotics should be empirically started as any delay in due process can result in devastating complications. however, antibiotics should be tailored later according to the culture reports. (3) role of anti-coagulants in treatment is controversial. (8) mortality and morbidity after effective treatment is still high. 496 umamaheswara reddy et al massive infarction and cavernous sinus thrombosis figure 2 coronal reconstructed ct scan images (a, c, d) showing iso-hyperdense material within the left maxillary sinus and left retro orbital inflammation suggestive of cellulitis. cranio-caudal extensions of intraparenchymal hemorrhage and midline shift are better appreciated on image (b) this case is a reminder that in patients with uncontrolled diabetes, undergoing dental procedures should be carefully dealt with appropriate antibiotic cover. early signs like unilateral facial edema, orbital chemosis, edema, and proptosis should raise high index suspicion of cavernous sinus thrombosis. time is most important while dealing these cases as the initial manifestations may be subtle but there may be rapid clinical deterioration which can occur within hours of onset. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) email dramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1. ogundiya da, keith da, mirowski j. cavernous sinus thrombosis and blindness as complications of an odontogenic infection: report of a case and review of literature. journal of oral and maxillofacial surgery: official journal of the american association of oral and maxillofacial surgeons 1989;47:1317-1321. romanian neurosurgery (2014) xxi 4: 493 – 497 497 2. okamoto h, ogata a, kosugi m, takashima h, sakata s, matsushima t. cavernous sinus thrombophlebitis related to dental infection--two case reports. neurologia medico-chirurgica 2012;52:757-760. 3. verma r, junewar v, singh rk, ram h, pal us. bilateral cavernous sinus thrombosis and facial palsy as complications of dental abscess. national journal of maxillofacial surgery 2013;4:252. 4. ebright jr, pace mt, niazi af. septic thrombosis of the cavernous sinuses. archives of internal medicine 2001;161:2671-2676. 5. jones rg, arnold b. sudden onset proptosis secondary to cavernous sinus thrombosis from underlying mandibular dental infection. bmj case reports 2009;2009:bcr0320091671. 6. kamouchi m, wakugawa y, okada y, et al. venous infarction secondary to septic cavernous sinus thrombosis. internal medicine (tokyo, japan) 2005;45:25-27. 7. fehrenbach mj, herring sw. spread of dental infection. practical hygiene 1997;6:13-19. 8. bhatia k, jones n. septic cavernous sinus thrombosis secondary to sinusitis: are anticoagulants indicated? a review of the literature. the journal of laryngology & otology 2002;116:667-676. 1grigoreflorina_currentperspectives romanian neurosurgery (2015) xxix (xxii) 1: 3 19 3 current perspectives concerning the multimodal therapy in glioblastoma florina grigore1, felix mircea brehar1,2, mircea radu gorgan1,2 1emergency clinical hospital “bagdasar-arseni”, bucharest, romania 2"carol davila" university of medicine and pharmacy, bucharest abstract: gbm (glioblastoma) is the most common, malignant type of primary brain tumor. it has a dismal prognosis, with an average life expectancy of less than 15 months. a better understanding of the tumor biology of gbm has been achieved in the past decade and set up new directions in the multimodal therapy by targeting the molecular paths involved in tumor initiation and progression. invasion is a hallmark of gbm, and targeting the complex invasive mechanism of the tumor is mandatory in order to achieve a satisfactory result in gbm therapy. the goal of this review is to describe the tumor biology and key features of gbm and to provide an up-to-date overview of the current identified molecular alterations involved both in tumorigenesis and tumor progression. key words: glioblastoma, molecular pathways, invasion, targeted therapy. introduction malignancies involving the central nervous system (cns) are undoubtedly a diagnostic and therapeutic challenge. among them, high-grade gliomas, are by far the most challenging issue for neurosurgeons and neuro oncologists. glioblastoma is the highest-grade glioma tumor (who grade iv) [65], the most common type of primary malignant brain tumor in humans [43, 15], and one of the deadliest cancers. despite extensive efforts to streamline the methods of diagnosis and treatment, gbm remains the neurosurgeon’s eternal hydra [84] and an invariably lethal tumor with a median survival of 15-17 months [101], despite maximal therapy. the standard of care [11] for patients with newly diagnosed gbm encompasses maximal safe surgical resection, if feasible, or stereotactic/open biopsy if tumor resection is not an option, followed by radiation therapy plus concomitant and adjuvant chemotherapy with temozolomide. unfortunately the standard treatment for patients with gbm remains palliative; it is virtually impossible to "cure" gbm, as complete resection is possible in only few cases and recurrence is diagnosed in as much as 83% of the patients [9]. the failure of standard therapy in gbm is reflected by the recurrence rates, a highly aggressive tumor behavior in relapses and the poor overall 4 grigore et al current perspectives concerning the multimodal therapy in glioblastoma patient prognosis. if we had to choose one word to describe gbm it would likely be heterogeneity that is reflected not only from a clinical, gross-morphological or histopathological perspective but also in terms of genetic, molecular and newer, proteomic, perspectives [76, 58]. genotyping of brain tumors may have applications in stratifying patients for clinical trials of various novel therapies [94]. cytogenetic and molecular analysis of the tumor along with robust animal models [1] set a new direction in understanding tumor pathogenesis and in developing a complex multimodal therapeutic sequence. in 2008 the cancer genome atlas research team (tcga) which aims at establishing a database of high-resolution expression profiles in tumors, choose gbm as the path breaker tumor [67]. a future genetic classification of brain tumors, derived from the technical tour de force of gene microarrays will provide a useful database and the path to improve results in cancer therapy [54]. a thorough understanding of the tumor biology and especially of the complex invasive and migratory mechanism of gbm is mandatory in order to develop a new generation of targeted, highly specific therapies and to fight "the terminator ", as gbm is often called [41]. epidemiology, clinical features and imaging gbm is the most frequent type of primary brain malignancy, with an overall incidence rate of 3.19 per 100,000 person-years in usa [15] and 3.32 (ci, 2.69–4.09) for male cases and 2.24 (ci, 1.56–3.22) for female cases, ageadjusted to the world standard population as showed by a population-based study on glioblastoma in the canton of zurich, switzerland [75]. the highest incidence rates of gbm are found in the 6th and 7th decades of life. primary and secondary glioblastoma constitute distinct disease subtypesthe majority of cases (>90%) are primary glioblastomas that develop rapidly -de novo, while secondary glioblastomas develop through progression from low-grade, diffuse astrocytoma or anaplastic astrocytoma, manifest in younger patients, and have different genetic pathways [76] and prognosis [27]. data suggest that older age, male gender and higher socio economic status, increase the risk for gbm [16]. in the majority of cases, the clinical presentation of glioblastoma is superposable on that of all intracranial expansive processes, expressing the progressively increased intracranial pressure against the incompressible compartment of the skull, as stated by the monroe kellie doctrine [70]. common findings include: persistent headache, papilledema, incoercible vomiting, ocular palsies, altered level of consciousness. the clinical elements of glioblastoma can be summarized in general and focal signs (hemiparesis, sensory loss, visual loss, aphasia). of the clinical elements is distinguished by frequency: headaches, as a constant finding [31], neurocognitive impairments and seizures. there are however a number of issues suggestive for an underlying gbm: the most remarkable aspect is the galloping pace of progression and worsening of symptoms (clinical manifestations in primary glioblastoma have a duration of <3 months to >50% of patients at the time of diagnosis [12], and the mean romanian neurosurgery (2015) xxix (xxii) 1: 3 19 5 period from first symptoms to histological diagnosis is around 6 months. the clinical picture of gbm depends on several aspects: the location of the tumor and adjacent structures involved in tumor expansion, the rhythm of tumor progression, the marked invasive behavior, a hallmark for gbm, bleeding either within the tumor (glioblastomas are strongly vascularized tumors, with an impressive potential of neoangiogenesis), or bleeding in other vascular structures secondarily involved in the extending infiltrative lesion, the existence of multifocal lesions, patient age and comorbidities. there have been reported cases with atypical clinical features such as ulnar neuropathy, syncopal events [93], or even sudden unexpected death [88]. the progress of medical imaging tools, today owning a remarkable degree of accuracy in describing different types of lesions, decreased the importance of a thorough clinical approach in order to establish the topography of the tumor. however, we always must pay attention to the "warning signs" that alert on the possibility of an evolving tumor process: 1) any signs or symptoms that suggest a progressively increased icp; 2) any evolving neurological deficit; 3) occurrence of epilepsy in adult life[109]; and mostly an accelerated worsening in any above suggestive for an underlying gbm . gbm is a "colorful but deadly tumor" [80], with pleomorphic aspects in imaging tools findings. usually ct-scan is the first step in the imaging investigations. it usually describes an iso/hypo dense lesion with irregular boundries and a central hypodense area that reflects the necrosis [79]. peritumoral edema and bleeding areas within the lesion are also constant findings. despite important improvements in ct-scan technique [21], mri is the best choice [26] to describe the morphology of the tumor, as ct-scan can miss posterior fossa lesions-despite it's not a common topography for gbm, it can also overpass small tumors that fail to capture the contrast agent. the preoperative imaging modality of choice is gadolinium-enhanced magnetic resonance imaging (mri) [35]. other imaging modalities, such as positron emission tomography with (18f)-fluorodeoxy-d-glucose or spect-mri, may also be considered in selected cases [24]. however the standard mri-approach has its limits: viable tumor areas extend beyond the region signal switch, therefore the magnitude of tumor extension and infiltration cannot be assessed accurately by mri studies. the indefinable borders of glioblastoma cell infiltration into the surrounding healthy tissue prevent complete surgical removal. another drawback of mri studies is that sometimes fail to distinguish post-treatment radiographic imaging changes [113] the so called "pseudoprogression” from true tumor progression [103]-underlying once more the need for improvement in the tumor imaging field. from stem to gbm over time there have been questioned some ethiopathogenic hypotheses about gbm, each having a number of arguments more or less sustainable with scientific evidence. initially it was thought that glioblastoma tumor cells derive from embryonic primitive 6 grigore et al current perspectives concerning the multimodal therapy in glioblastoma cells the embrional remains theory of bailey and cushing (1926), which dominated the tumor pathogenesis for many years [4] and encompasses the general concept that cancers arose from embryo-like cells, which remained in a tissue. subsequently came the astrocyte origin-theory, a prominent theory that encompasses the idea that this tumors arise from neoplastic transformation of mature adult cells (dedifferentiation)-brought into perspective by kernohan, suggesting that a normal astrocyte is transformed into a neoplastic cell by "escaping" certain points in the cell cycle and gaining resistance to apoptosis by blocking apoptotic pathways in cells-becoming malignant cells. as it multiplies, the daughter cells become variably anaplastic [91]. however, it is currently thought that highgrade gliomas arise from more primitive elements, specifically stem cells, and it may be that the ostensible dedifferentiation is an artifact of the histologic appearance of tumors. the characterization of a fraction of tumor cells in many types of cancer (colon, breast, blood, brain) opened a new chapter in cancer research, providing a new, hierarchic model of malignancy for gbm. cancer stem cell can become specific targets that can be incorporated into the development of multimodal therapeutic strategies. cancer stem cells have been identified in gbm and some pediatric brain tumors especially medulloblastoma [29, 111]. this fraction of cells is different from the bulk tumor cells by several aspects: they own an abnormal expression of cellular pathways such as notch or stat3 and they are somehow resistant to classic therapychemo-resistant and resistant to radiation therapy. stem cells theory in gliomagenesis [92] practically revolutionized the concept of gbm tumor ontogeny. the idea that states the absence of neural regenerative potential may be considered invalid by the results of recent research [98, 59]. on top of this pyramid is a cell group possessing a distinctive behavior-neural stem cells. this cell population permits the tumor survival, but the cells are also involved in the highly invasive nature characteristic of this type of tumor. neural stem cells population provides the "fuel" for the invasive behavior of the tumor. it raises naturally the question about the origin of these stem cells and the extent to which these cell populations normally reside in certain areas of the cns, and the event that triggers malignant transformation of stem cells. in certain types of malignancies that develop in this stem-model (the so called "stem cells disease") such as chronic myeloid leukemia [8] it is clear that these malignant stem cells arise from normal hematopoietic stem cells that undergo a series of genetic mutations and epigenetic changes. the major attribute of these cells is the ability to selfrenewal [110], but first we have to find out what is "self" in terms of stem cells. however, the actual existence and features [93] of stem cells not only neural stem cells but also stem cells that reside in other parts of the body is subject of controversy as "seeing is believing" and no one yet succeeded to "catch " a stem cell under the microscope. what we have is a functional pattern for a stem cell, based on several phenotypic markers, the self-renewal ability being by far the most important aspect romanian neurosurgery (2015) xxix (xxii) 1: 3 19 7 that brings into perspective a possible stem cell emergence for gbm. underlying genetic alterations in tumor initiation malignant astrocytomas, and particularly glioblastoma, have a number of common characteristics with the rest of malignancies, features that generally define the hallmarks of cancer [37]: (1) the ability of cancer cells to stimulate their own growth; (2) the capacity to resist inhibitory signals that might otherwise stop their growth; (3) they resist their own programmed cell death (apoptosis); (4) they stimulate the growth of blood vessels to supply nutrients to tumors (angiogenesis); (5) they can multiply forever-potential immortalization with telomerase activation and (6) they invade local tissue and spread to distant sites (metastasis). gbm is a unique type of tumor, owing a very heterogeneous cell population, genetic and molecular pathways. in addition, another 4 cardinal aspects must be taken into account in understanding possible gliomagenesis: 1) abnormal metabolic pathways; (2) evading the immune system; (3) chromosome abnormalities and unstable dna; and (4) inflammation. following we try to present an integrated, evidence based view, on what we know about gbm pathways, tailored on what we recognize as oncogenic events in general. one of the main features of cancer ontogeny is genomic instability [63]. this feature can take many forms: aneuploidy or intimate changes in chromosomal structure are equally frequent. one of the most common chromosomal abnormality in gbm is the loss of heterozygosity [85]. the most frequent involved regions, as shown by hybridization studies, are: p, 6q, 9p, 10p, 10q, 13q, 14q, 15q, 17p, 18q, 19q, 22q, and y [53] .by far the most common finding is the loss of heterozygosity at 10 q level, ocuuring in 6080 % of the cases. loss of the heterozygous nature turns the hemizygotysm area in a vulnerable area. extensive studies found at least three distinct loci to be deleted at 10q level (e.g., 10p14–p15, 10q23–24, distal to 10q25) while some samples show a complete loss of a copy of chromosome 10 underlying once more the pleomorphic nature of gbm. integrating the main features of a malignant behavior and the findings that show this type of aneuploidy (as pten mutation is almost exclusively find in cases with loh) we can strongly suggest the possibility of tumor suppressor genes residing in this loci, and mark the genomic instability as the first hot spot gliomagenesis. the cell cycle encompasses a fine regulated sequence of biochemical processes, which is supervised by a very accurate structure the so called "cell cycle control system" [3]. rb pathway and p53, among others, are the "guardians" of the cell cyclethe key players in tumor suppressing activity. disturbances in cell cycle are the background of enhanced, uncontrolled cell proliferation. the tumor suppressing genes involved in rb (retinoblastoma) or p53 pathway [33], are either inactivated or encounter mutational defects [28, 95, 19] in gbm cases (loss of chromosome 9 which contains cdkn2a, cdkn2b, and ptprd genes involved in p53 and rb pathways is also identified in some cases). there is also strong evidence that genetic alterations in the pten tumor 8 grigore et al current perspectives concerning the multimodal therapy in glioblastoma suppressor gene on 10q23 become involved in this "mutational gained tumor independence". some data suggest even fine interactions between pten, p53, and rb pathways contributory to this anarchic proliferation as a result of a damaged suppressing activity [28]. summarizing, we can argue the existence of a second hot spot in tumor biology at the cell cycle control level with the respective complex mechanisms involved. any cellular structure whose volume exhibits 2-3 cm3 cannot virtually survive without a proper vascular backup. the processes of neo-angiogenesis [13] is a cancer hallmark and is highly accelerated in gbm adjusted to the speeding rhythm of growth and is mediated by fine mechanism that involve growth factors, and other local mechanism [44]. amplification of the epidermal growth factor receptor (egfr) gene on chromosome 7 is also a habitual finding in gbm. egfr gene amplification or mutation and subsequent activation of the pi3k/akt pathways is found in 30-40 % of primary gbm. egfr is a cell membrane receptor that is normally found in many cells. egfr and its ligands are expressed in variable proportions even during embryogenesis in the neural tissue and persists in postnatal and mature brain. abnormal expression or altered signaling of growth factors and their respective pathways is a common theme in gbm. altered function of egfr, vegf, pdgr, and tgf have all been implicated in gbm. moreover, up regulation of egfr was identified in a number of other cancers [74] (lung cancer, breast cancer, colon cancer), all above reputed in terms of malignancy. a majority of egfr amplifications in glioblastoma contain a mutant variant of egfr, that is egfrviii [25, 34] and is linked to a dismal prognosis [39]. murine glioma models confirmed the involvement of egfr in gliomagenesis. also deletion of nfkbia [89] (an egfr signaling inhibitor) [10] is related to a poor prognosis. as an important aspect, egfr amplifications and mutation scarcely occur in secondary gbm, suggesting different mechanism involved in the two types of gbm [106]. all above bring forward a third hot spot at the growth factor paths level. new data suggest that gbm de novo and secondary gbm can be regarded as completely different tumors each having an individual path of progression with just discreet overlap sequences [76]. idh1 encodes isocitrate dehydrogenase 1 and is involved in energy metabolism. idh1 mutations have been predominantly identified in secondary glioblastoma and low-grade gliomas [46], with mutations in more than 70% of cases and they are found only sporadically in primary glioblastoma [107]. therefore, idh1 could be used to differentiate primary from secondary glioblastoma, and moreover highlights abnormal cellular metabolic pathways as a fourth hot spot in tumor activity. current research data provide a multitude of presumed hot spots in gbm tumor initiation and progression that put into perspective possible new therapies [105] for this unique type of tumor. studies by the cancer genome atlas (tcga) have incorporated genomic alterations within expression analysis, and set molecular romanian neurosurgery (2015) xxix (xxii) 1: 3 19 9 subclasses in high-grade glioma, delineating a pattern of disease progression that resembles stages in neurogenesis, and have been used to classify glioblastoma into: proneural, neural, classic, and mesenchymal subtypes [82]. different subtypes of glioblastoma have been shown to behave differently in response to treatment [9]. gbm invasion one direction several molecular "vehicles" gbm is highly invasive by nature, it can be regarded as a referential model of malignancy. first, the tumor has an important local extension [51], the rapid, diffuse, infiltration of adjacent structures, and secondly there is a metastatic potential [62, 66] though not a common situation for gbm occurring especially in patients undergoing surgical procedures [42], which create favorable local conditions for dissemination and not least there are situations of multifocal tumors [2] in patients diagnosed with gbm situations that beyond the radiological diagnosis and coarse morphological description, question the possible existence of synchronous, methachronous tumors or the expression of complex mechanisms of invasion within the brain [5] still unsolvedso that the multifocal appearance could be a particular model of invasion [72]. in the local extension of gbm, there have been observed “selective routes" primarily it is known that the extension is elective in the brain parenchyma in different white matter structures depending on the specific topography of the primary tumor. the majority of supratentorial glioblastoma are localized in the cerebral hemispheres with epicenter in full white matter [1]. elective extension in the white matter [14] is argued by the fact that despite the highly invasive profile of the tumor, subarachnoid extension is rarely seen in glioblastomametastasis through the cerebrospinal fluid is exceptional. migrating glioma cells tend to move along the vessels, dendrites, and fibers in white matter. a preferred extension route used by gbm is the corpus callosum the tumor extends into the contralateral hemisphere generating a spectacular morphology, a symmetric bilateral transcallosal lesion described as "butterfly glioma". cerebral white matter myelin structure and the elective white matter-routes (internal capsule, fornix, etc.) in gbm local extension opens the hypothesis of alterations at the cohabitation mechanisms level between glial cells and the myelin sheet. normally, besides structural proteins, in myelin structure there are a number of proteins with highly specific functions, called neurite growth inhibitors ni35/250that inhibit the abnormal axonal regeneration, growth and proliferation of astrocytes and fibroblasts. blocking the abovementioned with monoclonal antibodies led to a "leak" at the white matter level as in vitro and in vivo studies show [14]. these white matter findings may be suggestive for the existence of an alteration in the mechanism of ni35/250 dampening in determining the invasive behavior of tumor cells particularly in the white matter. these characteristics suggest that gbm possesses specific biological mechanisms that mediate its invasive nature [57]. a sequential approach was proposed as a model of invasion [64]: 1) detachment of cells with invasive potential from the main tumor 10 grigore et al current perspectives concerning the multimodal therapy in glioblastoma mass 2) adhesion to extracellular matrix 3) degradation of the extracellular matrix 4) cell motility and contractility to integrate the infiltrated territory and further migration. in this sequence, there have been identified several "key-molecules". some presumed signaling pathways to invasion are linked to constitutive cell-membrane proteins such as: rtk (egfr, pdgfr), integrins [87, 104] and cd44 [112, 77]. overexpression of these membrane proteins, among other molecules is linked to gbm invasion. the primary event the detachment of cells from the primary tumor involves a series of events that lead in a first phase to an unstable status of the cell in the tumor microenvironment. this event was blamed on the links provided by cadherin disintegration [20]. cadherin provide a ca2 +-dependent transmembrane protein involved in cell adhesion, which contributes to the stabilization of the tissue cells. abnormal high expression of cadherin 11 was identified in gbm, especially near vascular structures [50, 81]. the pivotal cell or cells so destablished from the bulk tumor, can initiate the invasive path. continuing the invasive trajectory of the detached cells involves metalloproteinase activity (mmp) respectively mmp-2 and mmp-9 proteolytic activity which "destroy" barriers in the path of matrix invasion, while adaptive integration in microclimate is ongoing [30], as mmp are considered to be key regulators of the microclimate [52]. moreover, levels of mmp-2 and mmp-9 are considered the strongest predictors of glioblastic invasive potential [108]. however, it also raises the question of the selective high activity of these endopeptydase and orientation of the migratory route preferential toward areas discussed, as we still don't have a referential pattern of normal mmp in neural tissue, so that we can't shape an explanation of this "polarization" of the cell invasive route. the cell that migrates from the bulk tumor in the invasive gbm model, must have two fundamental characteristics: contractility and motility. myosin 2 is the substrate supposed to accomplish these 2 features. the migratory cell must adapt his diameter to fit in spaces even smaller than its nuclear diameter [6]. isoforms a and b of myosin 2 are those which allow performing these narrow areas. involvement of myosin 2 expression in invasive type behavior has been proved by the positive results of direct blocking of myosin 2 in counteracting gbm invasion [47]. figure 1 the modern diagnostic sequencing for gbm going deeper into the tumor cell biology we can refer to transcription factors involved in abnormal pathways. as next-generation romanian neurosurgery (2015) xxix (xxii) 1: 3 19 11 sequencing technologies are emerging, transcriptome description brings into perspective new key-molecules in gbm invasion. a transcription factor is a structure that binds to a specific dna region and controls the activity of selected genes. transcription factors are overactive in cancer cells [23] and they are strong candidates as targets for future specific molecular therapies in cancer [102]: (1) the nf-kappab and ap-1 families of transcription factors, 2) the stat family members and 3) the steroids receptors are just some examples [60]. transcription factor olig2 is often expressed in oligodendroglia and in “transit-amplifying cells” of the subventricular zone, the presumed site of most adult neural stem/progenitor cells. olig2 is frequently found in ng2-positive glia and is required for development of these cells. ng2 is a chondroitin sulfate proteoglycan that is thought to be another marker of oligodendrocyte progenitor cells. olig2 promotes the proliferation of both neural progenitors and gbm stem cells by repressing the p21 tumor suppressor [61]. twist is another transcription factor whose abnormal activity is related with gbm invasion underlying a mesenchymal change in promoting invasion [18] by a process called epithelial to mesenchymal transition [69]. this would help the cells detached from the primary lesion to survive and further infiltrate the trajectory. twist1 is also a strong candidate as a target molecule for future therapies. table 1 key molecules involved in gbm invasion and the underlying mechanism molecule cd44 function mediates ecm adhesion rhamm mediates ecm adhesion mmp9 cd44 cleavage=> ecm adhesion; degradation of ecm adam proteases cd44 cleavage=>ecm adhesion integrins avb3 and avb5 ecm adhesion and cytoscheletal rearrangement fak and pyk 2 cytoplasmic mediators for integrins=> ecm adhesion mmp2 degradation of ecm cadherin 11 detachment of the cells from the tumor egfr increases mmp1 expression=>degradation of ecm pten/pi3k/akt pathway regulation of mmp activity=>ecm adhesion and rearrangement, pten mutation is linked to an invasive phenotype myosin ii cell contractility and motility tf olig2 and twist cell integration in the migration path 12 grigore et al current perspectives concerning the multimodal therapy in glioblastoma this sequential model has a number of evidence-based arguments, and brings into the line a number of issues regarding gbm complex invasive mechanism, and further puts into perspective molecular therapeutic directions. but there are some obscure issues that remain to be elucidated as for example the probability of micro-regional heterogeneity in the extracellular matrix, the importance of coexpression and co-activation of surface receptors with consequent activation of cellular signaling mechanisms to initiate an invasive type of behavior, the exact order of any phase of the invasion and to what extent there is an overlap sequence in all above. state of the art in the treatment of gbm genetic mutations, epigenetic modifications and micro-environmental heterogeneity cause resistance to radioand chemotherapy altogether resulting in a hardly to overcome therapeutic scenario. multiple challenges remain in high-grade gliomas management [83]. upon initial diagnosis of glioblastoma, standard treatment consists of maximal surgical resection, radiotherapy, and concomitant and adjuvant chemotherapy with temozolomide [11, 35] (in selected cases less aggressive therapy is employed-patients older than 70 years undergo radiation therapy or temozolomide alone). patients should be evaluated by a specialized multidisciplinary team: antiepiletic drugs are prescribed for seizures; steroidtherapy, with glucose level monitoring; a careful assessment of the patients's ability to perform activity of daily living or to undergo therapy karnofsky performance status scale can be used, all above are important therapeutic aspectsmaintenance of quality of life should be the key end-point of the therapy [40]. surgery is an integral part of gbm treatment [90]. surgical removal of the glioblastoma by craniotomy can be beneficial for some people, both to alleviate symptoms associated with the tumor and to extend survival following radical removal. also the only accurate diagnosis of gbm relies on biopsy sample. the only way to be sure that a brain tumor is a glioblastoma is by looking directly at the tumor tissue-either by performing an open surgery procedure or by stereotactic means. fluorescence guidance in resection of malignant glioma has been shown to improve extent of resection and 6-month progression-free survival in a prospective, multi-institutional clinical and preliminary experience in the united states has confirmed the high correlation of this fluorescence with imaging and histologic features [99]. of course that the outcome of surgical treatment in patients with gbm is highly influenced by tumor topography [97], extension [10] and the actual extent of the surgical resection [78]. moreover, the extent of surgical resection is an independent prognostic factor-an analysis of 28 studies found a mean duration of survival advantage of total over subtotal resection for glioblastoma (14 vs. 11 month) [48]. the pivotal study of stupp [101] in nejm marked the split between pre and post temozolomide era in the treatment of gbm. we can analyze the difference between the two periods in terms of survival [49, 22]: the median survival of patients treated with surgery and a regimen of radiation therapy was romanian neurosurgery (2015) xxix (xxii) 1: 3 19 13 12.0 months while patients who underwent surgical procedures, radiation therapy plus temozolomide was 31.9 months. before temozolomide, glioblastoma has been viewed as a chemo-resistant tumor. temozolomide is currently used in the majority protocolos for gbm treatment [17]. adjuvant external-beam rt is well established in the postoperative treatment [56, 68].the addition of radiotherapy to surgery has been shown to increase survival from 3-4 months to 7-12 months [100].the responsiveness of glioblastoma to radiotherapy is highly variable. in many instances, radiotherapy can induce tumor remission, often marked with stability or regression of neurologic deficits as well as diminution in the size of the contrastenhancing mass, but the period of response is short-lived because the tumor typically recurs within 1 year, resulting in further clinical deterioration and the appearance of an expansive region of contrast enhancement [45]. alternative forms of fractionation have been investigated. several studies have reported no improvements in terms of survival, but also no increased toxicity was found. escalating doses beyond 60 gy has not been shown to be of value. in may 2009 fda approved bevacizumab for the treatment of glioblastoma, as a single agent for patients with progressive disease following prior therapy. bevacizumab is a vascular endothelial growth factor-specific angiogenesis inhibitor. the reasoning for using it in gbm resides in tumor pathogenesis, as mentioned before, one of the defining characteristics of gbm is an abundant and aberrant vasculature [38]. in a simple approach we try "to starve" the tumor by attacking his vascular backup. since 2009, several phase 2 studies and retrospective series have demonstrated that bevacizumab significantly increased six-month progressionfree survival [55] in patients with recurrent gbm and may do so in new-onset gbm [36]. bevacizumab can be used as a single-agent therapy and in combination therapy with cytotoxic agents, specifically irinotecan with no clear superiority among either regimen [71]. but despite general enthusiasm regarding bevacizumab, in 2013 a phase iii, international study showed that it failed to increase overall survival (os) or statistically significant progression-free survival (pfs) for glioblastoma patients in the frontline setting. the randomized, double-blind, placebocontrolled study enrolled 637 patients all of whom were newly diagnosed with glioblastoma. participants underwent surgery to resect some or most of the tumor, received the standard of care of chemo-radiation with temozolomide, and were randomized to receive either bevacizumab or placebo. the study was designed with two primary endpoints: pfs and os [32]. so that the real benefit of bevacizumab for patients with newly diagnosed gbm is still unclear [73]. conclusion new approaches for the management of gbm are necessary. a further understanding of the tumor pathways and enrollment of patients into clinical trials will generate new information regarding investigational therapies. all efforts should be directed to achieve not only a better overall prognosis, but 14 grigore et al current perspectives concerning the multimodal therapy in glioblastoma to get quality years of life for glioblastoma patients. correspondence florina grigore emergency clinical hospital “bagdasar-arseni” berceni street 10-12, bucharest, romania e-mail: florina.grigore@icloud.com references 1.agnihotri, s., burrell, k. e., wolf, a., jalali, s., hawkins, c., rutka, j. t., & zadeh, g. (2013). glioblastoma, a brief review of history, molecular genetics, animal models and novel therapeutic strategies. archivum immunologiae et therapiae experimentalis, 61, 25–41. doi:10.1007/s00005012-0203-0 2.agrawal, a., makannavar, j. h., shetty, j. p., shetty, l., & varkey, b. (2012). multifocal glioblastoma multiforme. european journal of general medicine, 9, 289–291. doi:citeulike-article-id:12139877 3.alberts, b., johnson, a., lewis, j., raff, m., roberts, k., & and walter, p. (2008). molecular biology of the cell. amino acids (vol. 54, p. 1725). retrieved from http://discovery.ucl.ac.uk/109973/ 4.bailey, p., & cushing, h. (1926). a classification of the tumors of the glioma group on a histogenetic basis with a correlated study of prognosis. jama : the journal of the american medical association, 87(4), 268. 5.barnard, r. o., & geddes, j. f. (1987). the incidence of multifocal cerebral gliomas. a histologic study of large hemisphere sections. cancer. 6.beadle, c., assanah, m. c., monzo, p., vallee, r., rosenfeld, s. s., & canoll, p. (2008). the role of myosin ii in glioma invasion of the brain. molecular biology of the cell, 19, 3357–3368. doi:10.1091/mbc.e08-03-0319 7.bleeker, f. e., molenaar, r. j., & leenstra, s. (2012). recent advances in the molecular understanding of glioblastoma. journal of neuro-oncology. doi:10.1007/s11060-011-0793-0 8.bonnet, d., & dick, j. e. (1997). human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. nature medicine, 3, 730– 737. doi:10.1038/nm0797-730 9.brandes, a. a., tosoni, a., franceschi, e., sotti, g., frezza, g., amistà, p., … ermani, m. (2009). recurrence pattern after temozolomide concomitant with and adjuvant to radiotherapy in newly diagnosed patients with glioblastoma: correlation with mgmt promoter methylation status. journal of clinical oncology : official journal of the american society of clinical oncology, 27, 1275–1279. doi:10.1200/jco.2008.19.4969 10.bredel, m., scholtens, d. m., yadav, a. k., alvarez, a. a., renfrow, j. j., chandler, j. p., … harsh, g. r. (2011). nfkbia deletion in glioblastomas. the new england journal of medicine, 364, 627–637. doi:10.1056/nejmoa1006312 11.brem, s. s., bierman, p. j., black, p., blumenthal, d. t., brem, h., chamberlain, m. c., … vrionis, f. d. (2005). central nervous system cancers: clinical practice guidelines in oncology. journal of the national comprehensive cancer network : jnccn, 3, 644–690. 12.bruce, j. n. (n.d.). glioblastoma multiforme clinical presentation. retrieved from http://emedicine.medscape.com/article/283252-clinical 13.carmeliet, p., & jain, r. k. (2000). angiogenesis in cancer and other diseases. nature, 407, 249–257. doi:10.1038/35025220 14.caroni, p., & schwab, m. e. (1988). antibody against myelin-associated inhibitor of neurite growth neutralizes nonpermissive substrate properties of cns white matter. neuron, 1, 85–96. doi:10.1016/0896-6273(88)90212-7 15.cbtrus; central brain tumor registry of the usa hisdale. (2011). cbtrus statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2004-2007. cbtrus statistical report. retrieved from http://www.cbtrus.org/2011npcr-seer/web-0407-report-3-3-2011.pdf 16.chakrabarti, i., cockburn, m., cozen, w., wang, y.p., & preston-martin, s. (2005). a population-based description of glioblastoma multiforme in los angeles county, 1974-1999. cancer, 104, 2798–2806. doi:10.1002/cncr.21539 17.chang, s. m., parney, i. f., huang, w., anderson, f. a., asher, a. l., bernstein, m., … laws, e. r. (2005). patterns of care for adults with newly diagnosed malignant glioma. jama : the journal of the american medical association, 293, 557–564. doi:10.1001/jama.293.5.557 18.childs, g., & segall, j. e. (2012). twists and turns of invasion. nature cell biology. doi:10.1038/ncb2477 19.chow, l. m. l., endersby, r., zhu, x., rankin, s., qu, c., zhang, j., … baker, s. j. (2011). cooperativity within romanian neurosurgery (2015) xxix (xxii) 1: 3 19 15 and among pten, p53, and rb pathways induces highgrade astrocytoma in adult brain. cancer cell, 19, 305– 316. doi:10.1016/j.ccr.2011.01.039 20.cifarelli, c. p. (2009). cadherin-dependent adhesion of human glioblastoma cells promotes neurite outgrowth and increased migratory capacity. neuro-oncology, 11, 572. retrieved from http://www.embase.com/search/results?subaction=viewr ecord&from=export&id=l70028680\nhttp://neurooncol ogy.dukejournals.org/cgi/reprint/11/5/563\nhttp://dx.do i.org/10.1215/15228517-2009-034 21.colonnese, c., & romanelli, p. (2012). advanced neuroimaging techniques in the management of glioblastoma multiforme. curr radiopharm. 22.darefsky, a. s., king, j. t., & dubrow, r. (2012). adult glioblastoma multiforme survival in the temozolomide era: a population-based analysis of surveillance, epidemiology, and end results registries. cancer, 118, 2163–2172. doi:10.1002/cncr.26494 23.darnell, j. e. (2002). transcription factors as targets for cancer therapy. nature reviews. cancer, 2, 740–749. doi:10.1038/nrc906 24.de witte, o., levivier, m., violon, p., salmon, i., damhaut, p., wikler, d., … goldman, s. (1996). prognostic value positron emission tomography with [18f]fluoro-2-deoxy-d-glucose in the low-grade glioma. neurosurgery, 39, 470–476; discussion 476–477. 25.del vecchio, c. a., giacomini, c. p., vogel, h., jensen, k. c., florio, t., merlo, a., … wong, a. j. (2012). egfrviii gene rearrangement is an early event in glioblastoma tumorigenesis and expression defines a hierarchy modulated by epigenetic mechanisms. oncogene. doi:10.1038/onc.2012.280 26.doblas, s., he, t., saunders, d., pearson, j., hoyle, j., smith, n., … towner, r. a. (2010). glioma morphology and tumor-induced vascular alterations revealed in seven rodent glioma models by in vivo magnetic resonance imaging and angiography. journal of magnetic resonance imaging : jmri, 32, 267–275. doi:10.1002/jmri.22263 27.dropcho, e. j., & soong, s. j. (1996). the prognostic impact of prior low grade histology in patients with anaplastic gliomas: a case-control study. neurology, 47, 684–690. doi:10.1212/wnl.47.3.684 28.england, b., huang, t., & karsy, m. (2013). current understanding of the role and targeting of tumor suppressor p53 in glioblastoma multiforme. tumour biology : the journal of the international society for oncodevelopmental biology and medicine, 34, 2063–74. doi:10.1007/s13277-013-0871-3 29.fan, x., & eberhart, c. g. (2008). medulloblastoma stem cells. journal of clinical oncology : official journal of the american society of clinical oncology, 26, 2821– 2827. doi:10.1200/jco.2007.15.2264 30.fillmore, h. l., vanmeter, t. e., & broaddus, w. c. (2001). membrane-type matrix metalloproteinases (mtmmps): expression and function during glioma invasion. journal of neuro-oncology, 53, 187–202. doi:10.1023/a:1012213604731 31.forsyth, p. a., & posner, j. b. (1993). headaches in patients with brain tumors: a study of 111 patients. neurology, 43, 1678–1683. doi:10.1212/wnl.43.9.1678 32.friedman, h. s., prados, m. d., wen, p. y., mikkelsen, t., schiff, d., abrey, l. e., … cloughesy, t. (2009). bevacizumab alone and in combination with irinotecan in recurrent glioblastoma. journal of clinical oncology : official journal of the american society of clinical oncology (vol. 27, pp. 4733–4740). doi:10.1200/jco.2008.19.8721 33.fulci, g., labuhn, m., maier, d., lachat, y., hausmann, o., hegi, m. e., … van meir, e. g. (2000). p53 gene mutation and ink4a-arf deletion appear to be two mutually exclusive events in human glioblastoma. oncogene, 19, 3816–3822. doi:10.1038/sj.onc.1203700 34.gan, h. k., kaye, a. h., & luwor, r. b. (2009). the egfrviii variant in glioblastoma multiforme. journal of clinical neuroscience : official journal of the neurosurgical society of australasia, 16, 748–754. doi:10.1016/j.jocn.2008.12.005 35.ghose, a., lim, g., & husain, s. (2010). treatment for glioblastoma multiforme: current guidelines and canadian practice. current oncology (toronto, ont.), 17, 52–58. doi:10.3747/co.v17i6.574 36.gil-gil, m. j., mesia, c., rey, m., & bruna, j. (2013). bevacizumab for the treatment of glioblastoma. clinical medicine insights. oncology, 7, 123–35. doi:10.4137/cmo.s8503 37.hanahan, d., & weinberg, r. a. (2011). hallmarks of cancer: the next generation. cell, 144(5), 646–674. doi:10.1016/j.yane.2012.02.046 38.hardee, m. e., & zagzag, d. (2012). mechanisms of glioma-associated neovascularization. the american journal of pathology. doi:10.1016/j.ajpath.2012.06.030 39.heimberger, a. b., hlatky, r., suki, d., yang, d., weinberg, j., gilbert, m., … aldape, k. (2005). 16 grigore et al current perspectives concerning the multimodal therapy in glioblastoma prognostic effect of epidermal growth factor receptor and egfrviii in glioblastoma multiforme patients. clinical cancer research : an official journal of the american association for cancer research, 11, 1462–1466. doi:10.1158/1078-0432.ccr-04-1737 40.henriksson, r., asklund, t., & poulsen, h. s. (2011). impact of therapy on quality of life, neurocognitive function and their correlates in glioblastoma multiforme: a review. journal of neuro-oncology, 104, 639–646. doi:10.1007/s11060-011-0565-x 41.holland, e. c. (2000). glioblastoma multiforme: the terminator. proceedings of the national academy of sciences of the united states of america, 97, 6242–6244. doi:10.1073/pnas.97.12.6242 42.houston, s. c., crocker, i. r., brat, d. j., & olson, j. j. (2000). extraneural metastatic glioblastoma after interstitial brachytherapy. international journal of radiation oncology, biology, physics. doi:10.1016/s03603016(00)00662-3 43.howlader, n., noone, a. m., krapcho, m., neyman, n., aminou, r., & waldron, w. (2011). seer cancer statistics review, 1975–2010, national cancer institute. bethesda, md, based on november 2012 seer data submission, posted to the seer web site, 2013. http://seer.cancer.gov/csr/1975_2010 (accessed on june 08, 2013). 44.huang, p. h., xu, a. m., & white, f. m. (2009). oncogenic egfr signaling networks in glioma. science signaling, 2, re6. doi:10.1126/scisignal.287re6 45.hulshof, m. c., schimmel, e. c., andries bosch, d., & gonzález gonzález, d. (2000). hypofractionation in glioblastoma multiforme. radiotherapy and oncology : journal of the european society for therapeutic radiology and oncology (vol. 54, pp. 143–148). doi:10.1016/s0167-8140(99)00183-8 46.ichimura, k., pearson, d. m., kocialkowski, s., bäcklund, l. m., chan, r., jones, d. t. w., & collins, v. p. (2009). idh1 mutations are present in the majority of common adult gliomas but rare in primary glioblastomas. neuro-oncology, 11, 341–347. doi:10.1215/152285172009-025 47.ivkovic, s., beadle, c., noticewala, s., massey, s. c., swanson, k. r., toro, l. n., … rosenfeld, s. s. (2012). direct inhibition of myosin ii effectively blocks glioma invasion in the presence of multiple motogens. molecular biology of the cell. doi:10.1091/mbc.e11-01-0039 48.jeremic, b., grujicic, d., antunovic, v., djuric, l., stojanovic, m., & shibamoto, y. (1994). influence of extent of surgery and tumor location on treatment outcome of patients with glioblastoma multiforme treated with combined modality approach. journal of neuro-oncology, 21, 177–185. doi:10.1007/bf01052902 49.johnson, d. r., & o’neill, b. p. (2012). glioblastoma survival in the united states before and during the temozolomide era. journal of neuro-oncology. doi:10.1007/s11060-011-0749-4 50.h., phillips-mason, p. j., burden-gulley, s. m., kerstetter-fogle, a. e., basilion, j. p., sloan, a. e., & brady-kalnay, s. m. (2012). cadherin-11, a marker of the mesenchymal phenotype, regulates glioblastoma cell migration and survival in vivo. molecular cancer research. doi:10.1158/1541-7786.mcr-11-0457 51.kaye, a. h. . m. b. m. f. ), & laws, edward r ( md, p. (n.d.). brain tumors: an encyclopedic approach. 52.kessenbrock, k., plaks, v., & werb, z. (2010). matrix metalloproteinases: regulators of the tumor microenvironment. cell, 141, 52–67. doi:10.1016/j.cell.2010.03.015 53.kim, d. (1995). chromosomal abnormalities in glioblastoma multiforme tumors and glioma cell lines detected by comparative genomic hybridization, 60(6), 812–9. 54.kong, j., cooper, l. a. d., wang, f., gutman, d. a., gao, j., chisolm, c., … brat, d. j. (2011). integrative, multimodal analysis of glioblastoma using tcga molecular data, pathology images, and clinical outcomes. ieee transactions on biomedical engineering, 58, 3469–3474. doi:10.1109/tbme.2011.2169256 55.lamborn, k. r., yung, w. k. a., chang, s. m., wen, p. y., cloughesy, t. f., deangelis, l. m., … prados, m. d. (2008). progression-free survival: an important end point in evaluating therapy for recurrent high-grade gliomas. neuro-oncology, 10, 162–170. doi:10.1215/152285172007-062 56.laperriere, n., zuraw, l., cairncross, g., cancer, t., & ontario, c. (2002). radiotherapy for newly diagnosed malignant glioma in adults: a systematic review. radiotherapy and oncology : journal of the european society for therapeutic radiology and oncology, 64, 259–73. retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12242114 romanian neurosurgery (2015) xxix (xxii) 1: 3 19 17 57.lefranc, f., brotchi, j., & kiss, r. (2005). possible future issues in the treatment of glioblastomas: special emphasis on cell migration and the resistance of migrating glioblastoma cells to apoptosis. journal of clinical oncology : official journal of the american society of clinical oncology, 23, 2411–2422. doi:10.1200/jco.2005.03.089 58.lemée, j.-m., com, e., clavreul, a., avril, t., quillien, v., de tayrac, m., … menei, p. (2013). proteomic analysis of glioblastomas: what is the best brain control sample? journal of proteomics, 85, 165–73. doi:10.1016/j.jprot.2013.04.031 59.levy, m. l., ho, a. l., hughes, s., menon, j., & jandial, r. (2008). stem cells and the origin of gliomas : a historical reappraisal with molecular advancements. stem cells and cloning: advances and applications, 1, 41–48. doi:http://dx.doi.org/10.2147/sccaas3851 60.libermann, t. a., & zerbini, l. f. (2006). targeting transcription factors for cancer gene therapy. current gene therapy, 6, 17–33. doi:10.2174/156652306775515501 61.ligon, k. l., huillard, e., mehta, s., kesari, s., liu, h., alberta, j. a., … rowitch, d. h. (2007). olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma. neuron, 53, 503–517. doi:10.1016/j.neuron.2007.01.009 62.liwnicz, b. h., & rubinstein, l. j. (1979). the pathways of extraneural spread in metastasizing gliomas: a report of three cases and critical review of the literature. human pathology. 63.lo, k. c., bailey, d., burkhardt, t., gardina, p., turpaz, y., & cowell, j. k. (2008). comprehensive analysis of loss of heterozygosity events in glioblastoma using the 100k snp mapping arrays and comparison with copy number abnormalities defined by bac array comparative genomic hybridization. genes, chromosomes & cancer, 47, 221–237. doi:10.1002/gcc.20524 64.lois, c., garcía-verdugo, j. m., & alvarez-buylla, a. (1996). chain migration of neuronal precursors. science (new york, n.y.), 271, 978–981. doi:10.1126/science.271.5251.978 65.louis, d. n., ohgaki, h., wiestler, o. d., cavenee, w. k., burger, p. c., jouvet, a., … kleihues, p. (2007). the 2007 who classification of tumours of the central nervous system. acta neuropathologica, 114, 97–109. doi:10.1007/s00401-007-0243-4 66.lun, m., lok, e., gautam, s., wu, e., & wong, e. t. (2011). the natural history of extracranial metastasis from glioblastoma multiforme. journal of neurooncology. doi:10.1007/s11060-011-0575-8 67.mclendon, r., friedman, a., bigner, d., van meir, e. g., brat, d. j., m. mastrogianakis, g., … aldape, k. (2008). comprehensive genomic characterization defines human glioblastoma genes and core pathways. nature. doi:10.1038/nature07385 68.mehta, m. p., tomé, w. a., & olivera, g. h. (2000). radiotherapy for brain tumors. current oncology reports, 2, 438–444. doi:10.1007/s11912-000-0064-2 69.mikheeva, s. a., mikheev, a. m., petit, a., beyer, r., oxford, r. g., khorasani, l., … rostomily, r. c. (2010). twist1 promotes invasion through mesenchymal change in human glioblastoma. molecular cancer, 9, 194. doi:10.1186/1476-4598-9-194 70.mokri, b. (2001). the monro-kellie hypothesis: applications in csf volume depletion. neurology, 56, 1746–1748. doi:10.1212/wnl.56.12.1746 71.moustakas, a., & kreisl, t. n. (2010). new treatment options in the management of glioblastoma multiforme: a focus on bevacizumab. oncotargets and therapy, 3, 27– 38. doi:10.2147/ott.s5307 72.nakada, m., kita, d., watanabe, t., hayashi, y., teng, l., pyko, i. v., & hamada, j.-i. (2011). aberrant signaling pathways in glioma. cancers. doi:10.3390/cancers3033242 73.narayana, a., gruber, d., kunnakkat, s., golfinos, j. g., parker, e., raza, s., … gruber, m. l. (2012). a clinical trial of bevacizumab, temozolomide, and radiation for newly diagnosed glioblastoma. journal of neurosurgery. doi:10.3171/2011.9.jns11656 74.normanno, n., de luca, a., bianco, c., strizzi, l., mancino, m., maiello, m. r., … salomon, d. s. (2006). epidermal growth factor receptor (egfr) signaling in cancer. gene, 366, 2–16. doi:10.1016/j.gene.2005.10.018 75.ohgaki, h., dessen, p., jourde, b., horstmann, s., nishikawa, t., di patre, p.-l., … kleihues, p. (2004). genetic pathways to glioblastoma: a population-based study. cancer research, 64, 6892–6899. doi:10.1158/00085472.can-04-1337 76.ohgaki, h., & kleihues, p. (2007). genetic pathways to primary and secondary glioblastoma. the american journal of pathology, 170, 1445–1453. doi:10.2353/ajpath.2007.070011 18 grigore et al current perspectives concerning the multimodal therapy in glioblastoma 77.okada, h., yoshida, j., sokabe, m., wakabayashi, t., & hagiwara, m. (1996). suppression of cd44 expression decreases migration and invasion of human glioma cells. international journal of cancer. journal international du cancer, 66, 255–260. doi:10.1002/(sici)10970215(19960410)66:2<255::aid-ijc20>3.0.co;2-a 78.orringer, d., lau, d., khatri, s., zamora-berridi, g. j., zhang, k., wu, c., … sagher, o. (2012). extent of resection in patients with glioblastoma: limiting factors, perception of resectability, and effect on survival. journal of neurosurgery. doi:10.3171/2012.8.jns12234 79.osborn, a. (n.d.). osborn’s brain: imaging, pathology, and anatomy (1 har/psc., p. 1200). 80.pappas, s., & (livescience). (n.d.). no title. retrieved february 11, 2014, from http://www.livescience.com/24098-colorful-but-deadlyimages-of-brain-cancer.html 81.perego, c., vanoni, c., massari, s., raimondi, a., pola, s., cattaneo, m. g., … pietrini, g. (2002). invasive behaviour of glioblastoma cell lines is associated with altered organisation of the cadherin-catenin adhesion system. journal of cell science, 115, 3331–3340. 82.phillips, h. s., kharbanda, s., chen, r., forrest, w. f., soriano, r. h., wu, t. d., … aldape, k. (2006). molecular subclasses of high-grade glioma predict prognosis, delineate a pattern of disease progression, and resemble stages in neurogenesis. cancer cell, 9, 157–173. doi:10.1016/j.ccr.2006.02.019 83.preusser, m., de ribaupierre, s., wöhrer, a., erridge, s. c., hegi, m., weller, m., & stupp, r. (2011). current concepts and management of glioblastoma. annals of neurology, 70, 9–21. doi:10.1002/ana.22425 84.quiñones-hinojosa, a. (2012). schmidek and sweet: operative neurosurgical techniques. indications, methods and results (expert consult online and print) (p. 2592). doi:10.1016/b978-1-4160-6839-6.10159-5 85.rasheed, b. k., mclendon, r. e., friedman, h. s., friedman, a. h., fuchs, h. e., bigner, d. d., & bigner, s. h. (1995). chromosome 10 deletion mapping in human gliomas: a common deletion region in 10q25. oncogene, 10, 2243–2246. 86.reya, t., morrison, s. j., clarke, m. f., & weissman, i. l. (2001). stem cells, cancer, and cancer stem cells. nature, 414, 105–11. doi:10.1038/35102167 87.riemenschneider, m. j., mueller, w., betensky, r. a., mohapatra, g., & louis, d. n. (2005). in situ analysis of integrin and growth factor receptor signaling pathways in human glioblastomas suggests overlapping relationships with focal adhesion kinase activation. the american journal of pathology, 167, 1379–1387. doi:10.1016/s00029440(10)61225-4 88.riezzo, i., zamparese, r., neri, m., de stefano, f., parente, r., pomara, c., … fineschi, v. (2013). sudden, unexpected death due to glioblastoma: report of three fatal cases and review of the literature. diagnostic pathology, 8, 73. doi:10.1186/1746-1596-8-73 89.rinkenbaugh, a. l., & baldwin, a. s. (2011). monoallelic deletion of nfkbia in glioblastoma: when less is more. cancer cell, 19, 163–165. doi:10.1016/j.ccr.2011.01.045 90.roberts, d. w., valdés, p. a., harris, b. t., hartov, a., fan, x., ji, s., … paulsen, k. d. (2012). glioblastoma multiforme treatment with clinical trials for surgical resection (aminolevulinic acid). neurosurgery clinics of north america. doi:10.1016/j.nec.2012.04.001 91.ropper, a. h., & samuels, m. a. (2009). adams and victor’s principles of neurology, ninth edition. mcgrawhill. 92.sanai, n., alvarez-buylla, a., & berger, m. s. (2005). neural stem cells and the origin of gliomas. the new england journal of medicine, 353, 811–822. doi:10.1056/nejmra043666 93.sanli, a. m., turkoglu, e., dolgun, h., & sekerci, z. (2010). unusual manifestations of primary glioblastoma multiforme: a report of three cases. surgical neurology international, 1, 87. doi:10.4103/2152-7806.74146 94.schmidt, m. c., antweiler, s., urban, n., mueller, w., kuklik, a., meyer-puttlitz, b., … von deimling, a. (2002). impact of genotype and morphology on the prognosis of glioblastoma. journal of neuropathology and experimental neurology, 61, 321–328. 95.sherr, c. j., & mccormick, f. (2002). the rb and p53 pathways in cancer. cancer cell, 2, 103–112. doi:10.1016/s1535-6108(02)00102-2 96.showalter, t. n., andrel, j., andrews, d. w., curran, w. j., daskalakis, c., & werner-wasik, m. (2007). multifocal glioblastoma multiforme: prognostic factors and patterns of progression. international journal of radiation oncology, biology, physics, 69, 820–824. doi:10.1016/j.ijrobp.2007.03.045 97.simpson, j. r., horton, j., scott, c., curran, w. j., rubin, p., fischbach, j., … nelson, j. s. (1993). influence of location and extent of surgical resection on survival of patients with glioblastoma multiforme: results of three romanian neurosurgery (2015) xxix (xxii) 1: 3 19 19 consecutive radiation therapy oncology group (rtog) clinical trials. international journal of radiation oncology, biology, physics (vol. 26, pp. 239–244). doi:10.1016/0360-3016(93)90203-8 98.slack, j. m. w. (2008). origin of stem cells in organogenesis. science (new york, n.y.), 322, 1498– 1501. doi:10.1126/science.1162782 99.stummer, w., pichlmeier, u., meinel, t., wiestler, o. d., zanella, f., & reulen, h.-j. (2006). fluorescenceguided surgery with 5-aminolevulinic acid for resection of malignant glioma: a randomised controlled multicentre phase iii trial. the lancet oncology (vol. 7, pp. 392–401). doi:10.1016/s1470-2045(06)70665-9 100.stupp, r., hegi, m. e., gilbert, m. r., & chakravarti, a. (2007). chemoradiotherapy in malignant glioma: standard of care and future directions. journal of clinical oncology : official journal of the american society of clinical oncology, 25, 4127–4136. doi:10.1200/jco.2007.11.8554 101.stupp, r., hegi, m. e., mason, w. p., van den bent, m. j., taphoorn, m. j. b., janzer, r. c., … mirimanoff, r.o. (2009). effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase iii study: 5-year analysis of the eortc-ncic trial. the lancet oncology (vol. 10, pp. 459–466). doi:10.1016/s14702045(09)70025-7 102.thorne, j. l., campbell, m. j., & turner, b. m. (2009). transcription factors, chromatin and cancer. the international journal of biochemistry & cell biology, 41, 164–175. doi:10.1016/j.biocel.2008.08.029 103.tran, d. k. t., & jensen, r. l. (2013). treatmentrelated brain tumor imaging changes: so-called “pseudoprogression” vs. tumor progression: review and future research opportunities. surgical neurology international, 4, s129–35. doi:10.4103/2152-7806.110661 104.uhm, j. h., gladson, c. l., & rao, j. s. (1999). the role of integrins in the malignant phenotype of gliomas. frontiers in bioscience : a journal and virtual library, 4, d188–d199. doi:10.2741/uhm 105.wang, y., & jiang, t. (2013). understanding high grade glioma: molecular mechanism, therapy and comprehensive management. cancer letters, 331, 139–46. doi:10.1016/j.canlet.2012.12.024 106.watanabe, k., tachibana, o., sata, k., yonekawa, y., kleihues, p., & ohgaki, h. (1996). overexpression of the egf receptor and p53 mutations are mutually exclusive in the evolution of primary and secondary glioblastomas. brain pathology (zurich, switzerland), 6, 217–223; discussion 23–24. doi:10.1097/00005072-19960500000017 107.watanabe, t., nobusawa, s., kleihues, p., & ohgaki, h. (2009). idh1 mutations are early events in the development of astrocytomas and oligodendrogliomas. the american journal of pathology, 174, 1149–1153. doi:10.2353/ajpath.2009.080958 108.wild-bode, c., weller, m., & wick, w. (2001). molecular determinants of glioma cell migration and invasion. journal of neurosurgery, 94, 978–984. doi:10.3171/jns.2001.94.6.0978 109.wilkinson, i., & lennox, g. (2005). essential neurology (4th ed., p. 288). wiley-blackwell. 110.wu, x.-z. (2008). origin of cancer stem cells: the role of self-renewal and differentiation. annals of surgical oncology, 15, 407–414. doi:10.1245/s10434-007-9695-y 111.yang, z.-j., ellis, t., markant, s. l., read, t.-a., kessler, j. d., bourboulas, m., … wechsler-reya, r. j. (2008). medulloblastoma can be initiated by deletion of patched in lineage-restricted progenitors or stem cells. cancer cell, 14, 135–145. doi:10.1016/j.ccr.2008.07.003 112.yoshida, t., matsuda, y., naito, z., & ishiwata, t. (2012). cd44 in human glioma correlates with histopathological grade and cell migration. pathology international, 62, 463–70. doi:10.1111/j.14401827.2012.02823.x 113.zhou, j., tryggestad, e., wen, z., lal, b., zhou, t., grossman, r., … van zijl, p. c. m. (2011). differentiation between glioma and radiation necrosis using molecular magnetic resonance imaging of endogenous proteins and peptides. nature medicine, 17, 130–134. doi:10.1038/nm.2268 microsoft word 8_selectedabstracts 180 abstracts 3rd national conference of neuro-oncology (ncno 2013) 3rd national conference of neuro-oncology (ncno 2013) with international participation 16th 20th april 2013 abstracts intramedullary mass lesions – function directed surgery vladimír beneš, svatopluk ostrý dept. neurosurgery, charles univ, prague recent advances of electrophysiological monitoring allow for safe surgery within the spinal cord. we have evaluated our series over the past 8 years to determine the effects of monitoring and to establish in how many cases the surgery was altered and directed by the electophysiological findings. in a period 2005-2012 total of 77 patients with various intramedullary pathologies were operated. the dominant lesions were ependymomas followed by astrocytomas and cavernomas. this series was compared to earlier series of 29 patients in whom electrophysiological monitoring was not used. the radicalism of surgery increased from 30 to 70%. in general clinically the patients remained the same as preoperativelly in both groups. in 29 patients the steps and techniques of surgery was changed according to mep and d wave findings during the procedure. conclusions: thanks to meps and d wave are highly sensitive and specific in outcome prediction. the better the preop neurological findings the better the outcome. monitorability depends on preop findings. the outcome depends on intraop monitoring. the surgeon must be able to change the surgical strategy whenever the warning is announced by the electrophysiologist. any surgery of the spinal cord should be performed with intraop monitoring posterior fossa meningiomas vladimír beneš dept. neurosurgery, charles univ, prague posterior fossa meningiomas are deemed to be difficult lesions. however, this seems to be true for certain tumors only. series of 123 posterior fossa meningiomas operated in a period 19982011 was reviewed and divided into various location groups and related to the extent of surgery and neurological outcome. overall mm rate was 5,7% and overall s1 and 2 resection was 73%. the tumours were finally divided into two groups only – a. anterior to the cranial nerves (n=63) and b. posterior to the nerves (n=60). mm rate in group a was 9,5% with some minor morbidity in another 23,6%. in the group b mm rate was 1,7% with zero minor morbidity. s1 and 2 resection was achieved in 73% of patients in group a and in 95% of patients in group b. romanian neurosurgery (2013) xx 2: 180 – 213 181 in conclusion surgery should be offered to all patients with tumors located posterior to the cranial nerves. in patients with tumors located anterior to the nerves other treatment modalities should be considered. anterior fossa midline skull base meningiomas – preservation of n.i function vladimír beneš, václav masopust dept. neurosurgery, charles univ, prague using a standard anterior skull base approach for olfactory groove meningioms does not allow preserving the function of the first cranial nerves. series of 67 meningiomas located in the midline skull base of anterior fossa was reviewed. the tumours growing from posterior (sellar) or from the side (sphenoid wing, clinoid) and reaching the cribriform plate were excluded. in the years 1998-2002 total of 21 such cases were treated. all the tumours were approached via anterior midline and in neither case the first nerve has been preserved. there was 0 mortality and 9% minor morbidity. anosmia was present in all patients. since 2003 we have preferred pterional approach to these tumors. in a period 2003 2011 we have treated 46 patients. the overall mortality was 4% and minor morbidity 4%. in 17 surgeries anterior midline cranitomy was introduced, in 3 endoscopic endonasal route was used, and in 26 pterinal approach was introduced. we were able to preserve at least some smell in 19 patients (41%). the best results were achieved in pterional craniotomy group – 50% smell preservation and 85% simpson 1 and 2 resections. the major advantage of pterional approach, apart from potential contralateral n.i preservation, is early exposure of important structures in the sellar region and early csf drainage. the potential of endonasal endoscopic approach is yet to be established. anterior subfrontal approach is reserved for the tumours reaching the most anterior parts of the anterior fossa and for the extra large tumours. the role of stereotactic biopsy in the management of infiltrative and multicentric cerebral gliomas felix brehar, mircea gorgan, alexandru tascu “carol davila” university of medicine and pharmacy bucharest, faculty of medicine, department of neurosurgery bucharest, romania diffuse and multi-centric growthpattern of glioma precludes the gross-total resection of these tumors and represents the main cause of the poor outcome of the patients. therefore, stereotactic biopsy is an alternative option for the management of these types of tumors. the authors present their experience in 102 cases of stereotactic biopsies performed for infiltrative, multicentric and deep-seated cerebral gliomas. one hundred and two patients with infiltrative, multicentric and deep-seated cerebral gliomas admitted in our clinic between november 2008 and february 2013 were included in this study. all patients underwent the stereotactic biopsy according to the standard protocols. stereotactic and neuroimagistic tools used for these procedures included the leksell stereotactic system and the software: stereotactic planning system (sps), ntps 8.2. the histopatological results (according to world health organization (who) 182 abstracts 3rd national conference of neuro-oncology (ncno 2013) classification) were: 66 cases of glioblastomas (grade iv) (64,7%), 7 cases of anaplastic astrocytomas (grade iii) (6,9%), 14 cases of grade ii diffuse astrocytomas (13,7%), 7 cases of grade i astrocytomas (6,9%), one case of grade ii oligodendroglioma (0,09%), 3 cases of anaplastic oligodendrogliomas (grade iii) (2,9%), one case of grade i ganglioglioma (0,09%), one case of anaplastic ganglioglioma (grade iii) (0,09%), and 2 cases of anaplastic ependymomas (grade iii) (1,9%). in 32 cases (31,4%) the immunohistochemistry has been performed in order to obtain an accurate histopathological result. in this series, the early postoperative mortality was 0%, with no cases of clinically significant hemorrhages after biopsy procedures. temporary increase of neurological deficits has been noticed in 9 patients (8,8%). in conclusion, image-guided stereotactic biopsy represents now a safe and accurate diagnostic method for infiltrative and deepseated cerebral gliomas, which can favorably infl uence the therapeutic management of the patients. key words: stereotactic biopsy, infiltrative gliomas, immunohistochemistry. new trends in treatment of elderly patients with high-grade glioma dana cernea1, stefan florian2, paula pruteanu1, cristina cercea1, diana sabau1, andrei stoian1, raluca stahiescu1, silviu halasag1, nicolae todor1 1oncology institute “prof. ion chiricuta” cluj-napoca, romania; 2neurosurgery county hospital clujnapoca, romania background: optimal treatment for elderly patients with high-grade glioma is not well defined. they are often excluded from multimodal approach due to concerns of increased morbidity due to poor performance index and associated diseases. we present our results in treatment of patients over 65 years with different type of high grade gliomas. the primary end point was overall survival. some data of recent clinical studies that will perhaps change the treatment decision for these patients will be presented. patients and methods: 65 patients, with a median age of 69 years, have been treated between 2005 and 2010 in our institution. female/male ratio was 37/28. histological type was: glioblastoma multiforme (gbm) 44 patients ( 66.6 %), anaplastic astrocitoma 7 patients (10.61 %), oligoastrocitoma grade 3 in one patient (1.54%). other histological types were less frequent representing 13, 86%. surgery was performed in all patients: complete resection in 50 patients (76.9%), subtotal resection in 13 patients (20%), and 2 biopsies (3.1%). postoperative 3d conformal radiotherapy was performed with two different type of fractionation: a) standard fractionation: td= 40-60 gy, mean dose 56 gy; and 2) hypofractionation: td= 3-45 gy, mean dose 32 gy. concomitant and adjuvant chemotherapy with temozolomide was done in 33.33% of patients, concomitant radiochemotherapy only in 22.75 % of patients and 37.88% of patients performed radiotherapy alone. at the beginning of postoperative treatment 58.4% of patients had karnofski index (ki) > 70. main associated diseases were high blood pressure, cardiovascular diseases, diabetes. results: overall survival at 36 month was 13% (ci: 7%-25%) with the worst survival for patients with gbm ( 8%). toxicity during radiotherapy was measured after romanian neurosurgery (2013) xx 2: 180 – 213 183 rtog scale and generally was 0-1 (6.07% of patients) with no significant difference between the two type of fractionation. conclusions: the number of patients in our study was small, but study show that elderly patients could be treated with radiochemotherapy without major toxicity. hypofractionated radiotherapy was well tolerated and could be a good option in order to shortening the treatment time for these patients. important decision factors for treatment type must be ki and the status of associated diseases. supratentorial low grade glomas latest developments in diagnosis and treatment a.v. ciurea1, d.a. nica2, i. ogrezeanu3, a. mohan4, h. moisa1 1carol davila university school of medicine, sanador medical center, department of neurosurgery, bucharest, romania; 2st. pantelimon teaching hospital, department of neurosurgery, bucharest, romania; 3bagdasar-arseni teaching hospital, department of neurosurgery, bucharest, romania; 4oradea county teaching hospital, department of neurosurgery, bihor county, romania introduction: low grade gliomas (lgg) are slow growing tumors. the aim of the treatment is to simultaneously combine an optimal resection by preservation of functional integrity with correct grading of tumor malignancy and the adequate adjuvant therapies in order to achieve a long survival, with a good postoperative quality of life. there are some important questions regarding lgg: what is the delimitation of lgg? what are the therapeutical decisions: observation, surgical removal or biopsy? does surgical removal alone ever cure lgg? if recurrences appear, is another surgery recommended? what is the efficiency of radiotherapy and chemotherapy in lgg recurrences? what are the indications of gamma knife surgery (g.k.s.)? material and methods: our experience in a series of 160 adult patients with supratentorial lgg, operated over a period of 11 years (january 2002december 2012) is presented, focusing on the newest achievements in the diagnostic of gliomas (neuroimaging, immunohistochemical analysis of tumor specimens), surgical treatment (intraoperative electrophysiology) and adjuvant therapies (oncological protocols). the preoperative diagnosis was based on 1t mri images. microsurgical resection was performed in all cases: total removal 79 cases (49,3 %), partial removal 81 cases (50,6 %), with no perioperative mortality. the outcome at 6 months (gos) showed: good recovery in 135 cases (84,3%), moderate disability in 21 cases (13,1%), severe disability in 4 cases (2,5%). the follow-up period ranged between 12 months and 9 years with a medium range of 4,5 years. the histological grading was assessed by classical pathologic examination and showed: fibrilary astrocytomas in 102 cases, oligodendriogliomas in 26 cases, oligoastrocytomas in 21 cases, dysembryoplastic neuroepithelial tumor in 5 cases, protoplasmic astrocytoma in 4 cases, ganglioglioma in 2 cases. in our data at 5 years postoperative we find: 11 lost patients, recurrences to grade iii-iv in 49 cases, regrowth grade ii-iii in 53 cases, 47 cases remain in evidence (grade ii). the total number of regrowthrecurrences is 102 (63,8%). it’s very important to perform a check-up mri every 6 months. 184 abstracts 3rd national conference of neuro-oncology (ncno 2013) lgg causing long-standing and medically refractory epilepsy are more likely to be associated with multiple epileptogenic foci, therefore intraoperative electrocorticography was used for tailoring the resection, together with intraoperative localization of central sulcus using somatosensory evoked potentials in tumors localized around the central area. intraoperative electrophysiological monitoring was performed in 31 cases. because actually, the final diagnosis requires immunohistochemistry and also, study of the molecular biology of these tumors is an important step for understanding the genesis and biological behavior of these diseases, in the last years of the study we have performed also immunohistochemical analysis of the tumor specimens. we have studied in order to identify, quantify and compare, in a series of 37 cases of glioma surgical specimens (low grade and high grade gliomas), previously classified concerning their histological grade (who), the following immunohistochemical markers: ki-67 proteins and pcna (markers of the cellular proliferation), p53 (product of the tumor suppressor gene tp53), cd 34, vegf, vegfr2, bfgf (markers for angiogenesis). surgical specimens were immunostained for p53 (clona do-7, biogenex usa); ki67 (mib-1; 1:50, dakoglostrup, denmark) and proliferating cell nuclear antigen (pcna; 1:10, pc10 dakote). proliferative activity (nuclear immunostain) was measured. p53 immunoreactivity was positive in all grade iii and iv gliomas, and in 50% of low grade gliomas. with a median of 12% and 24% for mib-1 and pcna respectively, for all neoplasms in the study, the mean percentage positive nuclear area for mib-1 and pcna was 3.06% and 13.11% in lowgrade (ii) astrocytomas, 14.34% and 29.68% in highgrade (iii) astrocytomas, and 18.77% and 44.11% in glioblastoma multiforme (grade iv). one-way analysis of variance showed a significant correlation between the histological grade and mib-1 and between the histological grade and pcna. isolated cases of low grade gliomas with high mib and pcna percentage were noticed. cd34, vegf, vegfr2 and bfgf expression were determined by immunohistochemistry (cd34, clone q band, immunotech; vegf, sc-152, santa cruz bioth.; vegfr2, sc-7269, santa cruz bioth; bfgf, bfgf88, biogenex). immunoreactivity for cd34 was positive in all types of the tumors. immunoreactivity for vegf, vegfr2 and bfgf was seen in both endothelial cells and tumor cells, with increased levels in more aggressive tumors, comparing with normal tissue where immunoreactivity was present only in endothelial cells. conclusions: lgg could be treated only surgically. we advocate the idea, that patients with lgg and medically refractory epilepsy, may undergo tailored resections. incompletely resected tumors may be managed with irradiation in the tumor bed, or by observation alone. proliferation in gliomas, measured as mib-1 and pcna, correlates significantly with histological grade, providing useful additional information for diagnosis evaluation of the tumor recurrence susceptibility. angiogenesis markers could indicate the invasiveness tendency of the tumor. correlated with the proliferation markers, they express the agressive tendency of the tumor and consequently, the prognosis. as romanian neurosurgery (2013) xx 2: 180 – 213 185 a result, the correct treatment and prognosis of the case could be evaluated, especially in lgg where the indication of radiotherapy is debatable. despite the optimism associated with prognostic in lgg, these tumors usually recur, having a higher grade of malignancy. we consider that new, even more aggressive treatment protocols are needed for their management. key words: low grade gliomas, supratentorial, microsurgery, intraperative electrophysiology, immunohistochemistry, neuro-oncology, gamma knife surgery (g.k.s.) treatment of brain metastases with cyberknife robotic radiosurgery alfredo conti1, g. iata1, a. pontoriero1, g. marino1, l. frosina1, f. midili2, c. siragusa2, a. brogna2, s. pergolizzi1, c. de renzis1, f. tomasello3 1department of radiation oncology; 2department of medical physics; 3department of neurosurgery university of messina, messina, italy objectives: cyberknife robotic radiosurgery is a potentially effective treatment strategy for brain metastases, including large or multiple lesions. aims of study: to evaluate efficacy and toxicity of cyberknife robotic stereotactic radiosurgery (srs) alone or in combination with whole brain radiotherapy (wbrt) in the treatment of metastatic brain lesions. case report: we retrospectively reviewed data of patients with brain metastases who underwent cyberknife srs at the university of messina, italy between july 2007 and february 2013 material and methods: in the study, we included 252 patients with 343 lesions with >18 months follow up. recursive partitioning analysis (rpa) was used to categorize clinical status of patients. treatment planning was obtained on ct and contrast-enhanced mri. the clinical target volume (ctv) adopted was the gross tumor volume (gtv) plus an isometric margin of 1-2 mm. follow up examinations were carried out 2-6-12 months after srs, then yearly. results: follow-up ranged 18-50 months. all patients were treated in single fraction, median tumor volume was 1.9 cc (range 0.06-22.9 cc), median dose was 20 gy (range 11-24 gy), median isodose 80% (range 60-90%). 55/252 patients were lost to follow up. median survival at 1 and 2 years were 63% and 55% respectively. one and two years local disease control were 84% and 62% respectively. median survival was 14, 7.6 and 4.8 months for rpa class 1, 2 and 3 respectively. 80% of the patients treated with srs only were alive at 40 months versus 43% of the patients treated with srs plus wbrt. patients who had been treated for lesions ≠2.5 cm who survived at 24 months were 78%versus 43% of the patients with lesions > 2.5 cm. early and late neurological effects were recorded in 17% of patients located in eloquent brain areas. conclusions: our results confirm the efficacy of cyberknife stereotactic radiosurgery in the treatment of brain metastases. best results were obtained in patients in rpa class 1, with lesions of ≠2.5 cm and in patients without or with controlled extracranial disease. furthermore, the preliminary data of this study suggest that the combination srs with wbrt adds no benefit over srs alone for oligo-metastatic patients. 186 abstracts 3rd national conference of neuro-oncology (ncno 2013) brain tumor related seizures lacramioara perju dumbrava neurology i, university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neuroscience cluj napoca cluj, romania approximately 4% of all seizures are secondary to brain tumors. seizures are the onset symptom in about 20-40 % of patients with a brain tumor diagnostic and about 20-45% of these patients will present a type of seizure during the course of the disease. objectives: the objective of our study was to analyse all cases of patients with a brain tumor diagnostic during a thirty nine month period, observing the incidence of seizures, seizure type, the relation of the seizure with the tumor type, the moment of the diagnostic and the treatment applied. aims of study: we were interested to create a clear picture of the relation between brain tumor and seizures in our neurological unit from emergency county hospital cluj. case report: the study has a retrospective design, including a number of 112 patients with a brain tumor, admitted from january 2010 to march 2013. material and methods: we analyzed brain tumor patients, grouping them according to demographical date, onset of seizure in relation with the moment of diagnostic, seizure type, tumor type and the antiepileptic treatment applied. results: from the 112 brain tumor patients included in this study, 76 patients (64.3%) never developed a seizure, 26 patients (23.2%) presented a seizure before the diagnostic and 21 patients (18.75%) developed seizures after the diagnostic was established. most of the cases were meningiomas (27.67%) and astrocitomas (24.1%). 56% of the pacients suffered from primary generalized seizures and 31.3% suffered from partial motor seizures. 41 pacients were submitted to monotherapy and 7 patients received dual aed therapy. conclusions: our results demonstrated once more that seizures are a major complication of brain tumors, the management of these patients being particularly difficult. angiogenesis in gliomas and plasma levels of vascular endothelial growth factor (vegf) and basic fibroblast growth factor (bfgf) yavor enchev1, d. handziev1, t. avramov1, b. iliev1, t. kondev1, g. kiuchukov2 department of neurosurgery 1university hospital “sv. marina” varna, bulgaria; 2university hospital “sv. anna”, medical university of varna, varna, bulgaria objectives: glioma progression and patient’s survival is strongly dependent on the development of a new vascular network that occurs primarily by angiogenesis. the knowledge of the plasma detectability of distinct angiogenic factors in patients with brain tumours is very limited. aims of study: the purpose of the study was to evaluate the plasma levels of the angiogenic factors vascular endothelial growth factor (vegf), and basic fibroblast growth factor (bfgf) in patients with brain tumours. material and methods: plasma samples of 25 patients with histologically confirmed intracranial tumours, divided in 2 groups group i (gliomasglioblastoma multiforme, who grade iv, n=6; astrocytoma, who grade ii-iii, n=4; romanian neurosurgery (2013) xx 2: 180 – 213 187 astrocytoma, who grade i, n=4) and group ii (meningiomas, n=11), were analyzed. group iii (the control group) included 10 clinically healthy patients. the plasma concentrations of the examined angiogenic factors were evaluated by highly specific enzyme-linked immuno sorbent assays (elisas). results: median levels of vegf and bfgf in plasma were significantly higher in patients with high-grade gliomas as compared with patients with low-grade gliomas or meningiomas. the serum levels of the investigated angiogenic factors demonstrated correlation to tumour grade and vascularity. conclusions: despite the limited number of patients, our data suggest that the plasma levels of vegf and bfgf correlate with the tumour type and grade. the levels of the angiogenic factors in the plasma correlate with the degree of tumour vascularity. the plasma detectability of the individual angiogenic factors seems to depend at least partly on the tumour type as well as on tumour progression. the value of microrna as a prognostic factor in high grade gliomas yavor enchev, d. handziev, t. avramov, b. iliev, t. kondev, a. tonchev department of neurosurgery university hospital “sv. anna”, medical university of varna, varna, bulgaria objectives: microrna (mirna) is a class of highly conserved, single-stranded, noncoding small rnas. after maturation, they entry into the rna interference pathway and regulate gene expression on the post-transcriptional level by inhibiting the translation of protein from mrna or by promoting the degradation of mrna. many studies have shown that mirnas control cell proliferation, differentiation, and apoptosis in different types of cells. aims of study: the purpose of the study was to evaluate the expression of a mir cluster in high grade glial tumours. material and methods: tumour samples (n=20) of high grade gliomas neurosurgically treated in our clinic were simultaneously fixed in formalin for histological analysis and refrigerated to 80oc in rnalater(ambion). after the isolation of pure and intact total rna from the samples, the expression of the mir cluster was investigated by rt-pcr. results: the histological examination confirmed the glial character of the tumours and demonstrated their highgrades according to the who classification. the molecularbiological analysis validated the existence of the examined mir cluster. conclusions: the mir cluster was expressed in high grade gliomas. the correlation between the expression levels and the histological grade and patients’ survival could be valuable for identifying new biomarkers predicting the behavior of theses tumours. micrornas may be clinically useful as prognostic biomarkers. intracranial meningiomas-an overview ioan ştefan florian1,2, pintea bianca1,2, ungureanu g.2, leat f.2, ilyes a.1, morosanu c.o.1, cosma g.m.1, florian i.a.1 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca; 2cluj county emergency hospital, department of neurosurgery introducere: intracranial meningiomas represent the second most frequent type of cerebral tumors encountered in 188 abstracts 3rd national conference of neuro-oncology (ncno 2013) neurosurgical practice. despite being characterized as benign tumors, the risks of recurrence or malignant transformation last for a lifetime. based on our surgical experiences, we wish to illustrate that, aside from the histopathological type or subtype, two other factors independently infl uence the risk of recurrence of these tumors: the tumor resection ratio and its location. material and methods: our retrospective study is based on the experience of the main author, encompassing 688 locations of intracranial meningiomas encountered in 657 patients (some patients with multiple meningiomas) requiring 817 surgical interventions (including recurrences). in our practice, intracranial meningiomas accounted for 22,9% out of the total of 3004 cerebral tumors surgically treated by the same author between 01.01.2000 and 31.12.2012. we present some surgical key point for different location and analyze the recurrence rate of meningiomas in relation to tumor location, world health organization (who) grading and gender and tested the statistical significance by using the chi square test. results: 597 cases with documented total macroscopic ablation met the inclusion criteria for statistical analysis. out of these, 83 cases were recurrences (13.9%), which had a median recurrence period of 3 years. 65% of the recurrences had a non skull base location, the most frequent cases being parasagittal and falcine meningiomas (35%), followed by convexital recurrences (30%). when analyzing the risk of recurrence in the case of parasagittal and falcine meningiomas, we found an odds ratio (or) of 1.92 (ci [1.17, 3.17]), p=0.008) compared to other locations. the risk of having a skull base meningioma recurrence was 1.41 (ci [0.85, 2.29], p=0.15). the or for recurrences in who grade ii-iii meningiomas was 3.3 (ci [1.73, 6.29], p=0.0001). we also found an or of 1.31 (ci [0.82, 2.1], p=0.24) for tumor recurrence in male patients. conclusion: considering that total ablation was noted in all of the tumors taken into calculation (gross total removal gtr, simpson grades i and ii), we clearly demonstrated that falcine and parasagittal meningiomas tend to recur, the risk of recurrence being almost twice greater compared to other locations. in addition, our study shows that there is a significant association between who grade ii-iii meningiomas and recurrences, the risk of recurrence being 3 times greater when harboring aggressive types of meningiomas. key words: intracranial meningiomas, surgery, recurrences, locations. cerebral gliomas-resuming a surgical experience ioan ştefan florian1,2, abrudan c.1,2, baritchii a.2, cheptea m.3, zoican a.1, durutya al.1, aldea c.1, florian i.a.1 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca; 2cluj county emergency hospital, department of neurosurgery 3“prof. dr. ion chiricuta” oncology institute introduction: the cerebral glioma category includes numerous histopathological types with varying peculiarities considering evolution, diagnosis, imaging and treatment. therefore, encompassing them within a single presentation might prove hazardous. in spite of their differences, all these tumors share, apart from their ultrastructural origin, two major similarities: their fatal evolution in large romanian neurosurgery (2013) xx 2: 180 – 213 189 majority of the cases and the principles of surgical treatment. this is why we are attempting to highlight some of the elements concerning the role of neurosurgery in the treatment of cerebral gliomas, with particularities regarding histopathological types, location, surgical strategy and results. material and methods: the presented retrospective study is based on the experience of the first author (prof. dr. florian) of 997 gliomas operated between 01.01.2000 and 31.12.2012, accounting for 33,18% out of the total of 3004 tumors operated within the same interval. 311 cases of hgg and 224 cases of lgg met the inclusion criteria for multivariate statistical analysis in order to define the role of radical surgery in multimodal glioma treatment. results: high-grade gliomas (hgg) represent 59,87% (597 cases) of all cerebral gliomas: anaplastic astrocitomas (25.7%), glioblastoma multiforme (65.5%), highgrade oligodendrogliomas (5.8%) and highgrade ependimomas (3%). from a total of 400 lgg cases (41,13% of all gliomas) pilocytic astrocitoma represent 23,5% (94 cases), grade ii gliomas (astrocitomas, mixed glioams) represent 44,5% (178 cases), oligodendrogliomas 10,7% (43 cases) and ependimomas (grade i and ii) 15,25% (61 cases). 121 of all glioma operated cases (12,13%) where at the pediatric age, the majority being represented by lgg (83,47 %). gross total removal (gtr) was achieved in 86% of hgg and in 88% of lgg. in hgg, at 24 months follow-up, the median survival was 12 months with gtr and only 6 months with str. the improvement of the kps scale is significantly higher (p< 0,05) in patients with lgg in whom gross total removal of the tumor was achieved. conclusions: the age and type of surgery were prognostic factors that had significantly infl uenced the survival rate at 12, 18 and 24 months for patients with hgg. in lgg extent of removal independently infl uences the outcome, but no correlation with malignant transformation could be established. radical surgery must be the goal in multimodal treatment of cerebral gliomas. risk versus benefit criteria of the microsurgical treatment for recurrent glioblastomas mircea gorgan, felix brehar “carol davila” university of medicine and pharmacy bucharest, faculty of medicine, department of neurosurgery; “clinic emergency hospital bagdasar arseni bucharest, first neurosurgical clinic glioblastoma is the most common primary intra-axial tumor of the central nervous system with a poor outcome, despite the multidisciplinary approach which consists in surgery, radioand chemotherapy. the rule is recurrence, which usually occurs between 6 and 12 months after primary treatment. there are divergent opinions regarding the management of the glioblastoma recurrence. while some authors support the surgical resection of tumor recurrences, others prefer the palliative oncological treatment. the authors of this study present a case series of glioblastoma recurrences – 185 cases (143 patients), operated in our clinic between 1998 and 2012 by the senior author. the majority of patients (119 cases) underwent one operation for recurrences, 18 patients have been operated for two times, 6 patients for three times and 3 190 abstracts 3rd national conference of neuro-oncology (ncno 2013) patients for four times. the surgical mortality in this series was 1,1 % (2 cases) and morbidity (new neurological deficits postoperatively) was 9,7% (18 cases). the medium survival time for recurrent glioblastoma was 6.5 months. the authors analyzed the risks and potential benefits of the microsurgical treatment for glioblastoma recurrences and tried to identify some preoperative criteria which predict a better postoperative outcome. therefore, the authors correlated the postoperative results (mortality, morbidity and the medium survival time) with the following preoperative parameters: age, tumor location (dominant or nondominat hemisphere), tumor volume and extension (lobar, multilobar, and bilateral), mass effect with midline shift, karnofsky preoperative score and associated diseases. authors identify several preoperative criteria which were predictive for a better outcome in the microsurgical treatment of glioblastoma recurrence: age<70 years, location in non-dominant hemispheres, extension in one lobe, karnofsky preoperative score>70. in conclusion, tumor resection should be considered for the majority of the patients with glioblastoma recurrences especially in those cases with age<70 years, tumor location in non-dominant hemispheres, non-infiltrative growth pattern of reoccurrence and symptoms related to tumor mass-effect. the goals of surgery for glioblastoma recurrences are tumor debulking, prolonging survival and family and social reinsertion. careful selection of the patients, based on analysis of several specific preoperative criteria (age, location, mass-effect, karnofsky score), is important in order to obtain a better outcome and a good quality of life. key words: recurrent glioblastoma, prognostic criteria, mortality, morbidity paraneoplastic sensory neuronopathy – and the cochrane study results wolfgang grisold, bruno giometto, roberta vitaliani department of neurology kfj hospital, vienna, austria neurologic department treviso, italy the classic paraneoplastic neuropathy is subacute sensory neuropathy (ssn). other types of peripheral neuropathy in cancer occur but are less well characterized this review is based on cancer related pns, and deliberately omits paraproteinemic neuropathies, as they are conventionally discussed as a separate entity. a cochrane review discussed the therapeutic options in paraneoplastic neuropathy (cochrane reviews:treatment for paraneoplastic neuropathies 2012) and came to the conclusion that presently no convincing therapies are available. objectives: paraneoplastic neuropathies occur in different types and tumor associations. the most characteristic syndrome is subacute sensory neuronopathy, which is usually a sensory ataxic neuropathy. motor involvement is discussed , and has been found in about 30 % in the europns study. other types of neuropathies as sensory neuropathy, sensorimotor neuropathy, infl ammatory neuropathies have been reported in singular cases, but have not been consistently reported. aims of study: the aim of the cochrane review was the effect of tumor treatment or therapy of paraneoplastic neuropathy. case report: the cochrane neuromuscular disease group specialized romanian neurosurgery (2013) xx 2: 180 – 213 191 register, central (2012, issue 1), medline january 1966-2013), embase (january 19802013) and liliacs (january 19822013) was searched for „paraneoplastic neuropathy“ and “treatment”. the following key words were used in conjunction with “treatment” and “therapy”: paraneoplastic neuropathy, paraneoplastic subacute sensory neuronopathy, paraneoplastic sensory ganglionopathy, paraneoplastic sensory neuropathy, paraneoplastic sensory motor neuropathy, paraneoplastic motor neuropathy, paraneoplastic immunemediated neuropathy, paraneoplastic polyradiculoneuropathy, paraneoplastic multiplex mononeuropathy, paraneoplastic autonomic neuropathies. studies were accepted when other causes of cancer associated neuropathy had been ruled out and the diagnosis was based on symptoms, signs and ncv studies. all types of interventions as surgery, radiotherapy, chemotherapy, immunemodulating (corticosteroids, ivig, plasmapheresis, immunosuppressants), supportive care and physiotherapy were considered. the treatments could be use alone or in combination. we evaluated stabilization or improvement versus worsening of disability after treatment. the data were analyzed according to two categories of treatments: tumor and immunemodulating treatment. results: paraneoplastic neuropathies are rare and for this reason quality controlled studies on their treatment are diffcult to conduct. most of the evidences is based on uncontrolled studies, case reports or expert opinion. in our search we found suffcient information on treatment of paraneoplastic neuropathy in 70 case reports, 12 case series (defined as a study with more than 3 patients), and 17 papers based on expert opinion. two categories of treatment were distinguished: tumor treatment and immunemodulatory treatment. tumor treatment: in the case series a total number of 315 patients with peripheral neuropathies were reported. the total number of treated patients is not known, but we found that 26 patients improved with tumor therapy among eight of whom also received immunotherapy. from the analysis of cases reports we found that 49 out of 70 patients received cancer treatment and 36 patients improved of whom 6 had also immunomodulatory treatment. in the case reports patients who improved after tumor treatment had heterogeneous tumors and neuropathy. the types neuropathies were: subacute sensory neuropathy (ssn), sensory motor neuropathy, sensory neuropathy, infl ammatory demyelinating neuropathy, and other entities in single cases. ivig: from the analysis of the studies, cases series and case reports we identified 43 patients who improved or stabilized with ivig. this hast to be considered with care as the duration of the ivig treatment, the ranking of improvement and detailed information on concomitant tumor treatment was soften missing. plasmapheresis (pe): directly removes antineuronal antibodies of other factors from the circulation. concerns in the use of pe in cancer patients involves the possibility that it will increase chemotherapeutic drugs clearance, once tumor treatment has been initiated. pe is not often used as a therapeutic approach for paraneoplastic neuropathy. we found 8 patients with paraneoplastic neuropathy which seemed to be responsive to pe treatment. 192 abstracts 3rd national conference of neuro-oncology (ncno 2013) steroids: are generally recommended for their effects on immune mediated disorders. we found 18 patients which had improved or stabilized after steroids. limitations in understanding their efficacy comes from the fact that steroids were given at different dosage and schedules. immunosuppressants: there is concern that the use of immunosuppressants in cancer patients favors tumor growth or enhances toxicity of cancer therapies. to date, however, this hypothetical concern has not been properly evaluated. cyclophosphamide, azothiaprine, often in combination with steroids have been used, but no recommendations can be given based on our analysis. conclusions: in conclusion the most promising treatment option is the identification and treatment oft he underlying tumor. the impact of the immunotherapy on paraneoplastic peripheral neuropathy is still unclear the reasons are the low number of patients treated, the combination of several interventions, and the concomitant cancer treatment. moreover treatment experience is based mainly on case report, small case series or open labeled studies while randomized prospective studies are missing. cancer around the brain wolfgang grisold department of neurology kfj hospital, vienna, austria objectives: neurooncology is concerned with direct and indirect effects of cancer on the nervous system. the main clinical focus is intraparenchymatose diseases as primary brain tumors and brain metastasis. in addition meningeal involvement by cancer and extraparenchymatous tumors as meningioma. in addition to metastasis also toxic, metabolic, infectious and paraneoplastic have to be considered. types of tumor spread: cancer can metastasize into the cavernous sinus, dura, calvaria, the base of the skull, cavities as nasal sinus, orbit and also into tissues as the skin, and the soft tissue of the neck, where nerves can be affected by compression, invasion and rarely solid nerve metastasis. the complications of cancer in and around the skull are more heterogeneous then the well defined intraparenchymatouse metastasis and are usually a diagnostic, as well as a therapeutic challenge. aims of study: the aim of this review is to define the mechanisms, sites and treatment of cancer metastasis occurring in the adjacent structures of the skull, and neck. material and methods: the review is based on a selected literature research aiming at the key words of the surrounding structures of the brain, skull , in particular the base of the skull and neck. own experience, based on observations and practical experience is added. mechanisms: nerves are can be damaged by cancer via compression, invasion and also by effects of treatment as surgery and radiotherapy. the particular mechanisms of nerve invasion have been classified into invasion, intranerval metastasis and antero and retrograde spread. in solid tumors, the invasion of peritumoral nerves is considered as a bad prognostic factor. results: primary brain tumors: usually primary brain tumors as glioma do not metastasize outside of the brain. the observations in the past years have shown, that metastasis, either to the lung or spinal seeding may be more often than previously expected. the invasion of adjacent structures as the meninges, the cavernous romanian neurosurgery (2013) xx 2: 180 – 213 193 sinus and the cranial nerves have been observed. interventions as biopsies can seed the tumor and induce skin metastases. brain metastases: several studies are ongoing to identify the best treatment of intracerebral metastasis. recent years have shown, that due to improved systemic tumor treatment also cerebral metastases occur in cancer types as prostate or intestinal cancers, which previously had been considered unlikely. meningeal involvement as meningeal carcinomatosis occurs in several cancer types and several studies have elaborated treatment, depending on the tumor type. the invasion or isolated metastasis into the dura, with or without osseous involvement occurs in several cancer types. although meningioma is often considered as typical in neuroimaging, rarely also metastasis can appear as a meningioma mimick. local extracerebral tumors can also compress the venous sinus. the base of skull metastasis can appear at several sites, and are usually classified according to the topography into orbital, parasellar, middle fossa, jugular foramen and occipital. they can be local or infiltrating invasive. local pain, often in combination with cranial nerve involvement are the typical presentations. within the skull not only the cavities as the orbits and sinus can be the side of cancer, but also mucous membranes and the skin. propagation of cancer via retrograde spread has been demonstrated. the spread of cancer outside of the skull, in particular of ent tumors, or metastasis can present with local pain syndromes, often projecting to the skull, cranial nerve lesions, and also compression and invasion of blood vessels. conslusion: the spread of cancer in structures around the brain, in the skull and neck is important in clinical neurooncology and usually no standardized treatment schedule is available. the lesion of nerves and nerve plexus is often associated by a combination of local pain and peripheral nerve damage. although the morphological patterns of nerve invasion have been described the pathophysiologic mechanisms need to be further elucidated. molecular targeting of glioblastoma: new experimental perspectives marc-eric halatsch, georg karpel-massler neurosurgery, university of ulm school of medicine, ulm, bw, germany several candidate genes for resistance of human glioblastoma cell lines towards erlotinib, an epidermal growth factor receptor tyrosine kinase inhibitor, have recently been proposed. in the current study, we sought to examine the antiproliferative effect of additionally inhibiting two of these candidate resistance gene products, i.e., rac1 and smo, on glioblastoma cell lines with erlotinibsensitive, somewhat responsive and resistant phenotypes. glioblastoma cell lines selected to represent the erlotinibsensitive, somewhat responsive and resistant phenotypes, respectively, were grown in 96-well plates and exposed to erlotinib, hhantag (an inhibitor of smo) and nsc23766 (an inhibitor of rac1) in various combinations and concentrations. after 10 days of continuous exposure, inhibitory concentration 50 (ic50) values were determined using a cytotoxicity assay, and drug combination effects (i.e., synergism, additivity, or antagonism) were calculated using the bliss equation. 194 abstracts 3rd national conference of neuro-oncology (ncno 2013) antiproliferative synergism among erlotinib, hhantag and nsc23766 was observed for the combination of erlotinib with either hhantag or nsc23766 as well as for the combination of all three agents in both the erlotinb-sensitive and – to a lesser extent – in the somewhat responsive cell line. importantly, in the erlotinib-resistant cell line, combinations of erlotinib plus hhantag or nsc23766 or both acted antagonistically. in a system of human glioblastoma cell lines with sensitive, somewhat responsive and resistant phenotypes, this study is the first to identify erlotinib combined with inhibitors of rac1 and smo to synergistically inhibit proliferation in a priori erlotinib-sensitive and somewhat responsive cell lines. these results strengthen the role of multitargeting approaches in the development of more effective therapies for glioblastoma. the antagonistic action of erlotinib, hhantag and nsc23766 in the erlotinibresistant cell line is counterintuitive and requires further clarification. taken together, combinations of targeted agents may act differentially depending on the glioblastoma cell phenotype. cerebral metastases bogdan iliescu, ziyad faiyad, sergiu gaivas, daniel rotariu, ion poeata 3rd neurosurgery “prof. dr. n. oblu“ clinical emergency hospital, iasi, romania objectives: brain metastases are common, occurring in 20-40% of cancer patients and contributing to 20% of annual cancer deaths. brain metastases are particularly common among patients with non-small cell lung cancer (nsclc), even at the time of diagnosis, accounting for approximately 18-64% of all brain metastasis diagnoses. overall prognosis of patients with brain metastases is limited, but has been shown to vary significantly, based on factors such as tumor histology, number of lesions, patient age and performance status. material and methods: we present our experience in brain metastases treatment. we analyzed retrospectively a series of 70 patients with cerebral metastatic involvement admitted to our department during 2011-2012. we present the particularities of our series in terms of demographics, attitude at admission, therapeutic options, surgical results, and subsequent management. results: 32 patients underwent surgery, the rest being submitted to oncology for systemic treatment. reasons for surgery included: solitary lesion with good general status, diagnosis, lesions that posed a vital risk. we discuss particular cases with rare localization or with atypical presentation and pathology findings conslusion: our review of the recent experience in the management of cerebral metastasis suggests, in accordance with the other published reports, that patients with neurometastatic disease represent a very polymorphic group. the decision making process has to be highly individualized for each case and should be a team effort, including neuroradiologists and oncologists. romanian neurosurgery (2013) xx 2: 180 – 213 195 gliadel and mgmt methylation: is there a correlation with patient’s prognosis? ralf ketter1, joachim oertel1, christoph tschan1, kai kammers2, steffi urbschat1 1department of neurosurgery, saarland university, homburg/ saar, germany; 2faculty of statistics, tu dortmund university, dortmund, germany clinical protocols combining local chemotherapy and concomitant radiochemotherapy have shown improvement of survival for patients with newly diagnosed malignant glioma. histomorphological diagnosis is the most valuable tool for the classification of human tumors, but provides insufficient information concerning of therapy response. on the other hand, genetic data becomes more and more important. our aim is to determine chromosomal alterations as well as the methylation status of mgmt, p15 (cdkn2b) and p16 (cdkn2a) in order to analyse their infl uence on survival time, radioand chemotherapy response. in our trail 72 glioblastoma patients were included, divided in two treatment groups: group a (36 patients) treated according the eortc-study and group b (36 patients) treated also according the eortc-study but receive additional local chemotherapy with gliadel. promoter hypermethylation of mgmt, p15 and p16 and cgh analysis were performed as described in standard protocols. univariate cox regression showed prolonged survival time of patients with tumors harbouring deletions on chromosome 9p and 10q under chemotherapy treatment (p=0.0042). no significant effect was observed for gains on chromosome 7p. promotor methylation mgmt in tumor tissue was not associated with prolonged overall survival (p=0.46). promotor hypermethylation of p16 was also not correlated with prolonged overall survival (p=0.821), whereas p15 showed significant differences between both groups (p=0.0684). although these results needs to be confirmed in larger series and under different treatment conditions, our retrospective study underlines that the tumor suppressor gene p15, involved in cell cycle control, can act as an attractive candidate for therapeutic approaches in glioblastomas. prognosis of meningiomas in the 1970s and today stefan linsler, jörg rahnenführer, urbschat steffi, ketter ralf, oertel joachim neurosurgery saarland university homburg gemany objectives: the benefit of the current strategy for diagnosis (computer tomography and magnetic resonance imagine) and treatment (microsurgery, microscope, endoscope) of meningiomas, in contrast to the standard treatment in use before ctand mr-imaging and the microsurgical era, has not yet been determined. aims of study: our new planning/navigation system has been designed with practical necessity for easy modification with minimum cost. accordingly, the support for new ideas from surgical side is possible with a simple but accurate realization. material and methods: a retrospective 196 abstracts 3rd national conference of neuro-oncology (ncno 2013) statistical analysis was performed for 1349 patients with meningiomas who underwent surgery at the neurosurgical department of the saarland university between 1965 and 2011. results: there were no major differences in symptomatology, tumor localization, and number of surgical procedures. the mean time until tumor diagnosis was significantly shorter after 1985. a significant better prognosis for patients operated after 1980 with regard to the postoperative duration of recurrence free survival could be revealed. conslusion: based on the results of this study, the time from diagnosis to treatment have been remarkably reduced within the last 30 years. also the overall prognosis for patients with meningiomas has changed from the 1960s until today. thus, the introduction of modern diagnostic modalities and surgical procedures has improved the outcome in patients with meningiomas signicifantly. management of neurologic manifestations of primary brain tumors: the role of the neurologist ioan marginean neurological clinic ii university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania the comprehensive care of patients with brain tumors involves a multidisciplinary team of specialists. neurologists serve as valuable members of this team and bring a unique perspective to this approach.complications in patients with brain tumors can result from the tumor itself (e.g., seizures), from treatment directed at controlling tumor growth (e.g., fatigue), or from treatments directed at controlling symptoms (e.g., corticosteroids). seizures are the presenting sign in roughly 15-50% of patients diagnosed with gliomas. levetiracetam is beneficial in patients with brain tumors with >50% reduction in seizure number in 20/25 brain tumor patients, but there is no role for seizure prophylaxis in patients with newly diagnosed brain tumors. the risk of deep venous thrombosis (vte) and pulmonary embolus is high for patients with brain tumors, especially gliomas. in general, pharmacologic anti-coagulation after the peri-operative period has not been recommended for cancer patients. therapeutic anticoagulation for patients with vte is widely accepted for at least 3 months after first thrombosis, and can be considered for longer periods in patients who are good medical candidates.thrombolytic therapy for vte, is contraindicated in patients with intracranial malignancies. improvements in mri over the past two decades have increased awareness of spontaneous intratumoral hemorrhage within malignant gliomas. the risk of symptomatic intracranial hemorrhage during treatment has become an area of interest as antiangiogenic treatments have become available. glucocorticoids are a mainstay of therapy for the cerebral edema associated with brain tumors. decadron is the preferred glucocorticoid due to its long half-life and low mineralocorticoid activity, but other corticosteroids may also be used. although these drugs are often required to treat increased intracranial pressure in patients with brain tumors, these drugs should be weaned as soon as possible to minimize side events. hydrocephalus can develop as a late complication of treatment. the development of new headaches or a significant worsening of baseline headaches romanian neurosurgery (2013) xx 2: 180 – 213 197 should prompt an evaluation for hydrocephalus. diversion of csf is the standard treatment for hydrocephalus. while some superficial infections can be treated with antibiotics alone, many will require surgical drainage with intensive post-operative antibiotics. pneumocystic jiroveci (pcp) pneumonia is a wellrecognized complication of patients with brain tumors. prophylactic bactrim is safe and effective; alternatively dapsone or pentamidine. fatigue directly affects quality of life by diminishing a patient’s ability to fully participate in personal, social, educational, and work related activities. exercise remains the most reliable treatment for this common problem. cognitive decline predicts tumor progression and may precede tumor progression by months.behavioral interventions, such as cognitive behavioral therapy and compensatory strategies (e.g., keeping lists), are important tools . in addition, stimulants such as methylphenidate may improve cognitive dysfunction related to subcortical white matter changes. palliative care focuses on supporting the patient’s physical, psychological, and social needs and is aimed at maximizing quality of life for patient’s and their families. spinal ependymoma up to date roxana mittler-matica neurosurgery department klinikum braunschweig braunschweig lower saxony germany ependymomas are lesions with a moderate cell density, originating from the ependymal lining of the central canal of the spinal cord, ependymal cell clusters in the terminal filum, or from ependymal rests left during embryonic development. the pathophysiologycal mechanism it is traditionally thought to be an oncogenetic event that transforms the ependymal cells phenotype. there are studies that suggest that epigenetic silencing of tumor suppressor genes, through dna methylation, is an important mechanism in the pathogenesis of ependymomas. the benign pathological nature of these tumours poses great difficulty in their early diagnoses and management. however, their compressive rather than infiltrative nature makes them amenable to surgical resection and the role of adjuvant radiotherapy and chemotherapy is still debated. despite previous research, prognostic factors for ependymoma remain relatively controversial. given the variety of localisation for this rare disease, the establishment of protocols for diagnostic or management is still a challenge. this paper proposes an updated overview regarding this challenging pathological entity. introduction / objective / objectives: ependymoma represent a relatively broad group of glial tumours which share a common origin from differentiated ependymal cells lining the ventricles of the brain or the central canal of the spinal cord. there are only about 230 spinal ependymomas diagnosed each year in the united states, yet they constitute the most common type of primary spinal cord tumors. owing to the rarity of the disease, the literature regarding ependymomas in adults is scarce and limited to retrospective series. thus, the level of evidence regarding therapeutic strategies is low and universally accepted guidelines are lacking. this broad group of glial tumors pose special problems regarding diagnostic and in many cases diagnostic is delayed. the patients with 198 abstracts 3rd national conference of neuro-oncology (ncno 2013) ependymoma of the filum terminale due to the difficulty of diagnosis are occasionally wrong labeled as psychosomatic or hypochondriac. given the rarity of the disease there are no generally established management protocols, for operative treatment the general principles of surgery of the spinal cord tumors apply. after operative management 50% of patients with ependymomas experience immediate postop worsening in terms of sensory disturbances due to posterior column retraction. the benign pathological nature of these tumours poses great difficulty in their early diagnoses and management. however, their compressive rather than infiltrative nature makes them amenable to surgical resection and the role of adjuvant radiotherapy and chemotherapy is still debated. despite previous research, prognostic factors for ependymoma remain relatively controversial. aim / aims / aims of study: the objectives of this paper are to present the actual knowledge level about the subject, offer an integrative update based on the newest studies, draw common lines for possible future protocols and identify new research directions. case report / design / background and aims: ependymomas are classified based on the morphologic phenotype (cellular, papillary, tanycytic, clear cell, pigmented and epithelioid, giant cell ependymoma) or on the who tumour grading as it follows: low grade (grade 1 or 2), or high grade (grade 3 or anaplastic). compared with intracranial ependymomas, spinal ependymomas are less prevalent, occur in a younger population, and exhibit a better prognosis. the fourth decade of age seems at most risk and the sex distribution is equal although some studies report a slight male prevalence. in the lumbosacral region, ependymomas are most commonly associated with the conus medullaris and cauda equina, but can also occur extradurally in the sacrum, presacral tissues, or subcutaneous tissues over the sacrum, extradural epedymomas are extremely rare entities. the clinical presentation can broadly vary according to location. diffuse dull pain constantly increasing due regional impediment of venous outfl ow is worse at night or upon awakening. when contact with nerve roots the pain becomes of a burning or fulgurant character and may irradiate radicularly. tactile and pain sensation are usually affected first because of the central topography of these tumors. motor deficits and pathological refl exes are also depending on the tumor location. mri is the radiological exam of choice, either for surgical planning or to rule out differential diagnosis. current efforts being made to identify the pathophysiology of this disease suggest that epigenetic silencing of tumor suppressor genes, through dna methylation, is an important mechanism in the pathogenesis of supratentorial and spinal ependymomas. there appears to be a consensus for radiation therapy in cases of subtotal resections of intradural tumors although the role of adjuvant therapy in subtotal resection is controversial. patient and methods / material and methods / methods / purpose: this paper is based on the review of relevant literature on spinal ependymoma. the latest studies converge to some key points usefull in helping the clinician to establish the best therapy option for each case. results / result: one interesting aspect of ependymoma is the pathophysiological mechanism; one theory assumes that ependymal cell rests arise from the romanian neurosurgery (2013) xx 2: 180 – 213 199 coccygeal medullary vestige, a remnant of the dural part of the terminal filum that involutes during embryonic development. others authors assume that these ependymal rests occur as a result of incomplete closure of the neural arch. ependymoma has been characterized at the dna copy number and mrna expression levels and was associated with an increase in expression of genes encoding for proteins involved in methylating dna. genes involved in the control of cell growth and death and the immune system including members of the jnk pathway seem to play an important role. genetic and transcriptional differences between tumors arising in different locations have been described. studies report that members of the c-jun n-terminal kinase (jnk) signaling pathway; mapk10 and map3k1 display hypermethylation in spinal ependymoma but they are not specific. cd99 monoclonal antibody could differentiate between ependymomas and nonependymal tumors, and so act as a marker but was of no consequence in determining the variant type or degree of histologic aggressiveness. in some studies is reported that over two thirds of the patients had experienced symptoms for more than 6 months before diagnosis. also patients who had tumors involving the spine had symptoms for a significantly longer time than patients who had ependymomas involving the brain. dissemination evidence of ependymoma cells into the cerebrospinal fl uid csf fl uid examination is a key factor in staging, prognosis, and treatment and allthough intradural ependymomas can spread throughout the cns they are not likely to metastasize outside it. a neuro-axis mrt study is recommended to rule out tumor dissemination. the optimal treatment for intramedullary spinal tumors is controversial. current therapeutic options include surgery, radiation therapy, chemotherapy, or a combination of these modalities. stereotactic radiosurgery for intramedullary spinal tumors is feasible and safe in selected cases. resection and conventional radiation therapy are associated with potential morbidity and so there is no optimal treatment established. some studies suggest that radiation therapy among adults might be somewhat deleterious to survival. age at diagnosis appears to be a strong predictor of the outcome of those patients according to some authors, tumor histology was more infl uential in adults than children, and complete resection was the most effective treatment option, regardless of age. conclusion / conclusions: multicentric studies could be a solution for getting a better insight on the spinal ependymoma complex problematic. for small tumors with no or little neurological deficit there is a tendency for conservative management with multiple follow up imaging studies. even if the diagnostic is not histologically established the conservative strategy is more often adopted in clinical practice due to the high risks correlated with the operation. for high cervical lesions the indication for surgery is even more difficult given the possible complications of spinal injury caused by the operation. adequate knowledge of anatomy and the correct use of microsurgical techniques allow total resection of some tumors with minimal morbidity and maximum functional recovery. there are no studies focused on fl uorescence assisted microsurgical extirpation for spinal ependymoma. cranial ependymomas are often being 200 abstracts 3rd national conference of neuro-oncology (ncno 2013) administrated a fl uorescent substance preceding the operation in order to allow a better demarcation of the tumor intraoperatively. a possible practical study direction can be establishing if fl uorescence is an efficient means to improve postoperative outcome for extended intraspinal ependymomas. clinical behavior and outcome of optic pathway gliomas in children emilia mihut, rodica cosnarovici, stefania neamtu, popita v., anca dumitrovici, dana cernea oncological institute “prof. dr. i.chiricuta” clujnapoca, romania background: tumorsof the optic pathways comprise 4-6% of pediatric intracranial tumors and may have a more aggressive course in younger children. methods: in the present study we retrospectively reviewed the clinical characteristics, treatment and outcomes of 15 children diagnosed with optic pathway gliomas (opg) between 2000 and 2010. results: the age range of the children at diagnosis was 11 months to 17 years (mean 8.1 years). the male/female ratio was 8/7. presentation included: decline in visual acuity (53%), headache (27%), proptosis (13%) and seizures (7%).forty per cent of the children with opg had neurofibromatosis type 1 (nf1). treatments included various combinations of surgery, chemotherapy and radiation. biopsy was not performed in two cases. five children were treated with chemotherapy alone, three with radiotherapy, threewith combined treatment, while four children were observed. after a median follow-up of 6 years, 12 patients are alive with stable disease. conslusion: despite the benign histology of optic pathway gliomas, its biological behavior is unpredictable. because of difficulties in defining progression and generally variable natural history the most favorable management of optical pathway gliomas is still controversial. association of nf1 is a favorable prognostic factor, these tumors tended to be less aggressive in nf1 patients. aspects of microsurgical treatment of craniospinal, cervico-medullary and cervical intramedullary tumors istván nyáry, péter banczerowski semmelweis university medical school, department of neurosurgery budapest, hungary surgical removal of intrinsic medullary tumors still make a challenge at any level of the spinal cord including the cauda equina, because of the risk inherent with surgical manipulation. this risk is even more enhanced within the cervical, cervicomedullary region. patient material: in the period between 1985 – 2005 we operated 216 cases of intramedullary lesion with different pathologies (108 ependymomas, 58 astrocytomas, 14 hemangioblastomas, 15 cavernomas, the others less frequently occurring pathologies), and 50%, 108 affected the cervical spinal cord, as well. within the cervical group two subgroups could be differentiated: cervico-medullary and high cervical, and low cervical, cervicothoracic group, roughly in two third-one third proportion, considering the frequency of occurrence. surgical strategy and techniques: only well romanian neurosurgery (2013) xx 2: 180 – 213 201 delineated, circumscribed tumors could be operated radically, and with good success. contrast enhanced mri was the most important factor in predicting operability. radical removal was avoided in cases of diffuse, infiltrative tumors, instead decompression, biopsy, and radiotherapy was done. at surgery bony exposure was kept at minimum, using a wide spectrum of minimally invasive approaches and standard microsurgical techniques were applied. in the high cervical group special postoperative intensive care was needed due to respiratory and lower cranial nerve problems. rehabilitation was also necessary in most of the cases. results: outcomes were measured according to the mccormick classification. according to our follow-up survey, most of our patients are still alive, if the underlying pathology permitted. the longest survival is 20 years, 18 had died on various reasons. conclusion: surgery should be done as soon as possible, in spite of the risks, since quality of life depends on the preoperative state. therefore, we adopted an aggressive surgical strategy, and gros total removal was the goal to be achieved. radiotherapy was applied depending on histology, and rehabilitation was followed after radical surgery. the brain tumour patient and caregiver: what is important for the journey? kathy oliver international brain tumour alliance (ibta) tadworth, surrey united kingdom brain tumours are one of the most devastating of diagnoses. whether benign or malignant, primary or secondary, they strike at the very core of who a person is, affecting not only physical abilities, but an individual’s cognitive and psychosocial aspects as well. one of the most notable things about brain tumours is that they intersect three major disease areas: cancer, neurological disease and rare disease. brain tumours are no respecter of race, religion, sex, age or geography. they strike people around the globe indiscriminately, and present a formidable enemy in any language. brain tumour patients and their caregivers face many medical, social and psychological challenges. but there are also other challenges for brain tumour patients and their caregivers beyond the medical ramifications – political and financial challenges which impact on each and every person on this journey. this presentation will include a discussion of these challenges as well as observations from the “coalface” as the speaker brings to the topic her own personal experiences as a caregiver to her young adult son colin who was diagnosed with a grade two astrocytoma in 2004 at age 24 and passed away seven years later, in 2011, at age 32 from a glioblastoma multiforme. this presentation will also focus on the role of brain tumour patient support organisations and the brain tumour caregiver. intracranial hemangiopericytomas lack typical cytogenetic and epigenetic features of meningiomas and gliomas samuel ige orie, dennis kraemer, ralf ketter, joachim oertel, steffi urbschat department of neurosurgery, saarland university, homburg/ saar, germany 202 abstracts 3rd national conference of neuro-oncology (ncno 2013) objective: intracranial hemangiopericytomas (chpc) are rare tumors of mesenchymal origin with a high proclivity towards recurrence and extraneural metastasis. total tumor resection is the main treatment of choice due to its radiochemical resistant nature. considering the paucity of reports dealing with the tumor genetics and epigenetics of chpc and the still ongoing debate over their histological standing, we examined a series of 9 chpc for known important meningioma and glioma specific cytogenetic and epigenetic aberrations. methods: in a total of nine histopathologically confirmed chpc, this study evaluated the promoter methylation status of mgmt, p15(cdkn2b), p16ink4a, timp3 and ndrg2 genes which have been shown to be epigenetically altered in gliomas and meningiomas, respectively. typical numerical chromosomal aberrations reported in gliomas and meningiomas were investigated using two-color fl uorescent in situ hybridization (fish) on touchpreparations with locus specific probe pairs detecting 1p36/22q11, 14q24/18q21, and 9p21/10q23. additionally, conventional comparative genomic hybridization (cgh) was performed to access genomic imbalances. results: all studied cases presented with an unmethylated status of the mgmt, p15 and timp3 promoters. one specimen was encountered with positive methylation signal for p16 in methylation specific pcr analysis. direct bisulfite sequencing for ndrg2 revealed only in 1 of 6 cases a moderately elevated average methylation degree. in fish analyses, disomy for all targeted chromosomal regions was found in 5 of 9 studied chpc specimens; in two tumors an oligocellular clone with hemizygous loss of 10q23 was detected. in one other specimen, virtually all nuclei harbored a hemizygous deletion of 9p21. one further cranial hemangiopericytoma was characterized by a tetraploid mainline with slight sidelines that contained trisomies of 9p21 and 10q23. cgh analysis showed a chromosomal imbalance in all nine specimens involving loss and or gains of partial or complete chromosome segments. the one chpc specimen that presented with positive methylation for p16 harbored the hemizygous deletion of 9p21 with corresponding loss of chromosome 9p in cgh. conclusions: this work shows that chpc obviously lack glioma and meningioma specific epigenetic and molecular cytogenetic lesions, further providing evidence that chpc represent a distinct tumor entity with different genetic features. these present findings prompt one to speculate on the possible role of the inactivation of p16ink4a, and deletions on chromosome 9p in the underlying tumorigenesis of a subgroup of cranial hemangiopericytomas. controversies in pathological bone fracture of the spine stanca ples neurosurgery department county hospital timisoara romania new imaging technologies offer for neurosurgeons important preoperative and postoperative data for spinal fractures. it is possible now to make the differential diagnosis for pathological bone fracture, to distinguish the tumoral from osteoporotic fractures. the new mri techniques we romanian neurosurgery (2013) xx 2: 180 – 213 203 currently use in neurosurgical clinic, county hospital timisoara are: diffusion weighted image(dwi) and spectroscopy (h-mrs) mri spectroscopy – can evaluate intra-lesional components (metabolites). offers the opportunity for establishing differential diagnosis (infl ammatory, tumoral, osteoporosis) diffusion weighted imaging (dwi)-is using the water diffusivity properties; the adc coeffcient is very different in osteoporotic comparing with tumoral fractures, helping in differential diagnosis. acquisitions are made with 1,5 t mri, siemens, avanto. we have examined 15 pacients with pathological bone fracture of spine: 10 osteoporotic and 5 neoplasic fractures. 13 pacient needed surgery and we have anatomo-pathological examination for this patients.. conclusions: using new imaging technologies we can , with 86% sensitivity of this methods, to establish the metabolic lesional components. our study make the differential diagnosis in pathological bone fractures using diffusion and mr spectroscopy. introduction: new imaging technologies offer for neurosurgeons important preoperative and postoperative data for spinal fractures. it is possible now to make the differential diagnosis for pathological bone fracture, to distinguish the tumoral from osteoporotic fractures. the new mri techniques we currently use in neurosurgical clinic, county hospital timisoara are: diffusion weighted image(dwi) and spectroscopy (h-mrs) aim: to evaluate if it is possible now to make the differential diagnosis for pathological bone fracture, to distinguish the tumoral from osteoporotic fractures. case report: we have examined 15 patients with pathological bone fracture of spine: 10 osteoporotic and 5 neoplasic fractures. 13 patient needed surgery and we have anatomo-pathological examination for this patients. material and methods: mri spectroscopy – can evaluate intralesional components (metabolites). offers the opportunity for establishing differential diagnosis (infl ammatory, tumoral, osteoporosis) diffusion weighted imaging (dwi)-is using the water diffusivity properties; the adc coefficient is very different as value in osteoporotic comparing with tumoral fractures, helping in differential diagnosis. results: using new imaging technologies we can, with 86% sensitivity of this methods, to establish the metabolic lesional components of bone fractures of spine. conclusion: our study succeed to make the differential diagnosis in pathological bone fractures using diffusion (dwi) and mr spectroscopy mr techniques. cerebral metastases-preoperative diagnostic, possible or not? stanca ples neurosurgery department county hospital timisoara romania new development in imaging technologies brings for neurosurgeons important preoperative and postoperative prospects for intracranial lesions and especially for cerebral metastatic disease evaluation. the new mri techniques we currently use in neurosurgical clinic, county hospital timisoara are: dti (diffusion tensor imaging), dwi(diffusion weighted imaging ), cerebral spectroscopy, swi (susceptibility weighted imaging), 204 abstracts 3rd national conference of neuro-oncology (ncno 2013) cerebral perfusion(pwi) dti (diffusion tensor imaging)mri techniqueapplication is useful for localizing white mater tracts in relation with intracranial lesions, mri spectroscopy – can evaluate intralesional components (metabolites). offers the opportunity for establishing differential diagnosis (ischemic, infl ammatory, tumoral). in tumor pathology it is used to establish tumoral grading, and to differentiate the metastatic from primary cerebral tumors. swi (susceptibility weighted imaging) a very new sequence in mri which evaluates magnetic properties of blood, iron and other structures. now it is used for diffuse axonal injuries, micro bleeds, angiogenesis in tumors, venous angiomas (slow fl ow vessels). acquisitions are made with 1,5 t mri, avanto in â€oeneuromed â€oe diagnostic image center timisoara. conclusions: using new imaging technologies we can , with 95% sensitivity and 91% sensibility of this methods, to establish the metabolic lesional components. our study tries to make the difference in cerebral lesional evaluation of primary cerebral tumors from metastatic cerebral lesions. introduction: new development in imaging technologies brings for neurosurgeons important preoperative and postoperative prospects for intracranial lesions and especially for cerebral metastatic disease evaluation. the new mri techniques we currently use in neurosurgical clinic, county hospital timisoara are: dti (diffusion tensor imaging), dwi (diffusion weighted imaging), cerebral spectroscopy, swi (susceptibility weighted imaging), cerebral perfusion (pwi). aim: our study tries to make the difference in cerebral lesional evaluation of primary cerebral tumors from metastatic cerebral lesions. case report: our study is made for 30 patients with secondary cerebral tumors. material and methods: acquisition is made with 1,5 t mri in â€oeneuromed â€oe diagnostic image center timisoara. used mri techniques are: dti (diffusion tensor imaging) mri technique-application is useful for localizing white mater tracts in relation with intracranial lesions, mri spectroscopy – can evaluate intralesional components (metabolites). offers the opportunity for establishing differential diagnosis (ischemic, infl ammatory, tumoral). in tumor pathology it is used to establish tumoral grading, and to differentiate the metastatic from primary cerebral tumors. swi (susceptibility weighted imaging ) a very new sequence in mri which evaluates magnetic properties of blood, iron and other structures. now it is used for diffuse axonal injuries, micro bleeds, angiogenesis in tumors, venous angiomas (slow flow vessels). results: using new imaging technologies we can, with 95% sensitivity and 81% specificity of this methods, to establish the metabolic lesional components. conclusion: using new imaging technologies we can, with 95% sensitivity and 81% specificity of this methods, to establish the metabolic lesional components. our study tries to make the difference in cerebral lesional evaluation of primary cerebral tumors from metastatic cerebral lesions. romanian neurosurgery (2013) xx 2: 180 – 213 205 follow-up in operated and nonoperated low grade gliomas stanca ples neurosurgery department county hospital timisoara, romania the follow-up in low grade gliomas can be accomplished in very good condition establishing protocols for each category of cases: operated and non -operated patients. in our clinic we have a 5 years followed -up 150 low grade gliomas: 85 operated, 65 non -operated. the protocol in this moment is :in first year, every 3 months conventional cerebral mr, in 2-nd and 3-d year every 6 month conventional mr, after that every year conventional cerebral mr. in every year we have a imaging neurodiagnose mri made with spectroscopy, diffusion, perfusion and swi. those protocols brings better results in this low grade gliomas follow-up. we can appreciate that by following this protocol. we can see the moment when this gliomas turn into high grade and we appreciate the moment of recurrence in post surgical cases. introduction: the follow-up in low grade gliomas can be accomplished in very good condition establishing protocols for each category of cases: operated and non operated patients. aim: the aim of our study was to share our experience in this diffcult follow -up of low grade gliomas. case report: in our clinic we have in 5 years followed-up 150 low grade gliomas: 85 operated, 65 non-operated. the protocol in this moment is: in first year, every 3 months conventional cerebral mr, in 2-nd and 3-rd year every 6 month conventional mr, after that every year conventional cerebral mr. material and methods: in every year we have a neurodiagnostic imaging mri made with spectroscopy, diffusion, perfusion and swi. results: our results were good, better than before this period of non protocoled follow up in low grade gliomas. conclusion: we can appreciate that following this protocol we can see the moment when this gliomas turn in high grade, and to appreciate the moment of recurrence in post surgical cases. common igs planning support for frame-based stereotaxy and frameless navigation ferenc pongracz, istvan valalik department of neurosurgery st. johnas hospital, budapest hungary our vister3d system is a new prototype of planning platform for frame-based and frameless stereotactic interventions which integrates most important elements of image guided navigation. according to general opinion, the frame-based systems have the advantage of proven clinical utility and instrument carriage with a high degree of mechanical stability and accuracy. frameless methods are more complex, but also very fl exible, and have already many applications in general neurosurgery. in general, comparisons until now have been limited between different planning platforms and different surgical sessions, utilizing commercial neuronavigation systems. vister3d planning platform integrates calculations for arc-based stereotactic frames (riechert-mundinger and mht, freiburg, germany) into frameless neuronavigation environments. the system communicates with polaris 206 abstracts 3rd national conference of neuro-oncology (ncno 2013) type cameras (northern digital inc, canada); registers surgical space to diagnostic images and visualizes tracked devices in volumetric and surface views. during frame-based stereotaxy, rigid reference system (marker plates) with recognizable landmarks in images, are used to align stereotactic space with imaging volume. the integrated platform is supported by detailed data parsing (for dicom and nifti images, as well as archive studies), ct-mr fusion algorithm (with subvolume targeting) and different 3d visualizations. the system is designed to determine the geometrical overlap of targeting, carried out, either in stereotactic space of the arc-based frame, or in moving reference space of the navigation platform. the main challenge in comparison is to have computations of identical rules for both environments. therefore, vister3d uses strictly 3d-based algorithms to get projection transform between any two coordinate spaces, that guarantees full transparency between frame-based and frameless techniques. objectives: the main motivation of this work is to develop a common igs (imageguided surgical) platform which is suitable for sharing surgical planning data in framebased stereotaxy and frameless, navigated brain surgery. the comparison until now has been based on planning with different platforms and review of associated variables of both techniques. in biopsy the final outcomes are compared by pathology diagnostic accuracy and (in electrode placement as well) immediate postoperative ct imaging. the eligibility of frameless technique depends on target size, anatomical location, with an ongoing debate on un-quantifiable variables which ultimately infl uence technique selection (anesthesia, size of craniostomy, diagnostic yield, etc). aims of study: our new planning/navigation system has been designed with practical necessity for easy modification with minimum cost. accordingly, the support for new ideas from surgical side is possible with a simple but accurate realization. case report: vister3d is usable for planning target and entry positions for dbs electrodes and sampling parameters along the path of biopsy needle. after graphical planning the surgeon can proceed with frame-based stereotaxial intervention or frameless navigation technique. the frameless method can be turned into different tracking modes supporting diagnostic needs during surgeries (tumor resection support, 3d localization of features, etc). material and methods: in our approach, common igs platform integrates fusioned ct and mr images and standard 3d planning tools for target trajectory. the electrode placement or biopsy techniques include riechert-mundinger or mht (freiburg, germany) stereotactic frames. the igs platform is able to calculate parameter settings for these frames with a newly developed algorithm providing for 3d transforms between diagnostic space, stereotactic space and patient local reference (ac-pc). moreover, the platform communicates with polaris spectra and vicra optical tracking devices (northern digital, inc.) and registers surgical space to diagnostic data. alignment tests of framebased and frameless geometries are possible: 1/ static: calibration procedures have been used to find the origin and axes direction of the arc-based system within the frameless reference. by collecting samples romanian neurosurgery (2013) xx 2: 180 – 213 207 from the frame geometry (with the pointer of navigation system), statistical calculation gives an estimate for location/orientation of stereotactic space within the frameless environments. 2/ dynamic: display/refresh polar coordinates for actual position of navigated device. the actual navigated position has been registered in ct volume and projected into stereotactic space using the registration transform of stereotactic space. after it, if the tracked device crossed distance of planned entry from the arc-surface, the device tip has been set as target position, and the cross point used as entry point and the polar settings continuously updated with these points. results: vister3d now is routinely used in planning trajectories for dbs electrode placement and biopsy sampling. number of frame-based stereotactic surgeries performed by the system now is close to 50. the planning procedure is very straightforward and easy to follow, thanks to the hierarchical workfl ow implemented in the system. the subvolume-targeted ct-mr fusion is found usable in finding the most accurate mr registration when compared to fusion with the whole volumes. stereotactic planning of target trajectory can follow steps known in the frame-based technique (finding the polar settings for dbs electrode or biopsy needle in frame reference), or can use the interface for frameless neuronavigation system. these results have been compared, and in some cases the electrode movement was detected by optical tracker and displayed with frame-based, planned data. in this tracking mode, the system converted the actual location/orientation of device into polar coordinates and, in parallel, visualized the model in ct volume. the difference between the planned and actual polar settings was tested. this difference proved to be very sensitive to the device calibration accuracy (i.e. the transform from tool sensor space to device coordinate space). conclusions: novel 3d algorithm has been implemented for frame-based stereotactic planning, which follows the rules known in frameless neuronavigation. this approach could help in a unified treatment of both techniques and can make the interpretations (at least) computationally transparent. direct comparison of surgeries using frame-based stereotaxy with sensor tracking approach is possible with this development. critical issue is the device calibration i.e. the accuracy of transform between the dbs electrode or biopsy needle geometry and the attached sensor’s space. further work is needed to explore more meaningful applications of the system. cauda equina cavernoma:clinical case prezentation and rewieu of the genetic findings george popescu1, popescu mihai2, grigorean v.t.1, strambu v.4, popescu irina6, miclea gabriela5, mihalache george2, popescu georgeta maria6 1spitalul clinic de urgenta “d. bagdasar-arseni”, bucuresti; 2spitalul judetean de urgenta pitesti; 3spitalul clinic de urgenta “sf. pantelimon”; 4spitalul clinic “carol davila”; 5spitalul orasenesc campeni; 6spitalul clinic de urgenta “sf. ioan” objectives: to present an rarely encountered case, diagnosed and operated in the neurosurgery department of pitesti of a patients with cauda equina cavernoma, which is the 15th worldwide case cited in the literature. material and methods: we present differential diagnosis in terms of clinical 208 abstracts 3rd national conference of neuro-oncology (ncno 2013) and imaging, and surgical technique approached and post-operative results. it is about 60 years old patient hospitalized for it atrocious lumbar pain, paravertebral muscle contraction associated with bilateral lombosciatica, relatively poorly systematized, installed after a heavy lifting exercise. simple x-ray orients us toward disc pain,highlighting a pinched l5-s1 disc space and posterior osteophytes at this level. we performed a lumbar spine ct highlighting an area of spontaneous hiperdensitay apparently intradural, at l4, followed by mri showing a well defined formation in t1 hipersemnal with areas of hemosideria located at the cauda equina level. we intervened surgically, ablation being performed entirely under the operator microscope of a purplish tumor, well defined, with diameter about 1.5 cm, developed between ponytail roots at l4 level complete clinical remission after surgery. it is a benign hamatom with vascular origin, occurring forms involving sporadic or familial forms of vascular malformations with autosomal – dominant transmission. etiology is unknown.in sporadic forms that implies a solitary cavernoma a contributinf factor that could induce cavernomas is radiotherapy. family forms involving two or more cavernoame occur in 50% of hispanic patients and 10-20% in the caucasian population. we identified mutations in 3 genes, with diferent loci 15: 1. ccm 1 on chromosome 7q 21.2, kriti-1 gene increases endothelial proliferation; 2. ccm2-15-p13 on chromosome 7p, mgc 4607 gene-role in the cellular response to osmolar insults. togheter with gene located on p 38 mapks give signals for modeling and vascular maturation; 3. ccm3 on chromosome 3q25.2-q27, the gene that encodes 212 amino acids 10 pdcd with role in apoptosis (a small muscle cells). in our case we didnt had the possibility to perform genetic studies. conclusions: cavernoimas found at the cauda equina lelvel is exceptional, this beeing only the 15th case publied in literature clinical symptoms include sphincter disturbances, motor and sensitivity acusses, our case having a totally atypical symptomatology. in our opinion, acute symptoms of the disease were caused by intratumoral bleeding, confirmed by histopathological examination. in terms of surgery our approach is through 2-level laminectomy, opening dura mater and cavernoma dissection grom cauda equina roots. treatment of peripheral nerve tumors multidisciplinary approach lukas g. rasulik, miroslav m. samardzic, vladimir lj. bascarevic, mirko v. micovic, irena s. cvrkota, jelena d. zivanovic, bojana m. zivkovic department for peripheral nerve surgery, functional neurosurgery and pain management surgery neurosurgical clinic, clinical centre of serbia belgrade, serbia objectives: peripheral nerve tumors are relatively rare lesions. most of these tumors are benign lesions built from the neural sheath cells: schwann cells, perineurial cells and fibroblasts. aims of study: aim of this paper is to present and analyze results of treatment of peripheral nerve tumors of all patients treated in our clinic during last ten years. case study: in this study, we included all patients treated in our clinic, during last romanian neurosurgery (2013) xx 2: 180 – 213 209 ten years, who have been admitted for surgical treatment of peripheral nerve tumor. relevant data about every patient, diagnostic procedures, course of treatment and outcome, has been collected through detailed analysis of 39 patient histories. material and methods: we analyzed demographic data, clinical presentation (occurrence of pain and paresthesia as symptoms, neurological deficit – quantified in six-grade system (m0-m5 and s0-s5 respectably), localization, size of the lesion, used diagnostic procedures, pathohystological type of tumor, and finally, treatment of choice for each case. results: analysis showed that there was slight gender predominance (53.8% female, and 46.2% male). over half of all patients (61.6%) were treated in six months to one year after first symptom occurred. most common tumor of peripheral nerves is schwannoma (66.7%). method of choice was microsurgical resection. in about 80% of all threated patients, after surgery, baseline function was preserved or improved. conclusions: clinical presentation, diagnosis, indication for specific type of treatment for peripheral nerve tumors are still actual debate topic. however, all collected data show that individual and multidisciplinary approach is necessary in treatment of these tumors. low grade gliomas – how to deal with daniel rotariu, bogdan iliescu, ziyad fayad, bogdan secara, ion poeata 3rd neurosurgical department clinical emergency hospital “prof. dr. n. oblu”, iasi, romania introduction: low grade gliomas represent a relative frequent part of the tumoral pathology of the cns, with a highly potential to recurrence and progression. we wanted to determine the prognostic factors associated with these two possibilities of evolution. material and methods: we have retrospectively analyzed the cases of low grade gliomas from the 3rd neurosurgical department at clinical emergency hospital “prof. dr. n. oblu” iasi from the last 5 years, 2008 -2012 results: low grade gliomas represent 15 to 20 % of cns tumors and aff ects mostly the young adults, 50% of our patients having ages between 20 and 40 years, with a slightly male predominance m:f ration 1,31:1. the most common presenting symptom was represented by seizures 70% of cases, the most frequent cerebral lobes were the frontal 46% and insular lobes 31%. 3 or more lobes were involved in only 17% od cases. contrast enhancement was observed in half of the cases comprised in our series and 31% presented a mixt structure of the tumor, solid and cystic component or solid with calcifications. 97% of the cases underwent surgical resection as a first line treatment with a rate of gross total resection of 41%. adjuvant treatment after surgery was used in 8 cases, with equal distribution between combined rxt+cht and rxt alone. the median follow up period was, and during this period we had 27% recurrences 11 cases from which 7 cases presented malignant transformation. the treatment of recurrences was represented by in 63% and rxt in 27% of the cases. conclusions: lgg represent a relative frequent pathology, with a better prognostic compared with their counterparts (high grade gliomas), but with a real potential of recurrence and progression (gross total 210 abstracts 3rd national conference of neuro-oncology (ncno 2013) resection being often difficult to achieve) facts that emphases the need for a close and rigorous follow up which sometimes can be difficult and which sometimes puts the neurosurgeon in a difficult position with regard to further treatment decisions. gamma-knife radiosurgery in brain metastases fery stoica savu, nicolae mircea, perin radu, rodica stempurszki gamma-knife department, “bagdasar-arseni” clinical hospital bucharest romania introduction: at least 12-13% of cancer patients develop symptomatic brain metastases and this figure is likely to rise as diagnostic technologies improve, allowing additional occurrences to be identified. with no treatment, patients with symptomatic brain metastases usually die within two months of diagnosis. however, early diagnosis and vigorous treatment, while rarely curative, may lead to a useful remission of neurological symptoms and enhance the quality of a patient’s life, as well as, prolong survival. given the number of cases, the question arises, how many of these cases are appropriate for gammaknife radiosurgery? material and methods: indications for gamma-knife radiosurgery in brain metastases are presented in relation with their location (deep seated or in eloquent areas) and their pathology. comparisons to alternative treatments (radiosurgery versus surgical resection, radiosurgery versus whole brain radiotherapy) and various combined indications (surgery, whole brain radiotherapy and radiosurgery) are reviewed using well established predictive factors regarding the clinical benefit for the patients with brain metastases, as part of an evidence-based clinical practice guideline. results: brain metastases are excellent targets for gamma-knife radiosurgery. this treatment has an important role in the management of patients with metastatic brain tumors. the authors present their experience, as well as studies from across the world, which have shown its eff ectiveness in treatment of brain metastases. local control provided by radiosurgery for the management of metastatic brain tumors in any brain location exceeds 85% on average. there is also a cost-effectiveness analysis of the economic impact of stereotactic radiosurgery for patients harboring brain metastases and improvement of the quality of life for these patients. conclusions: brain metastases constitute a significant disease burden and have major impact on morbidity and mortality. this presentation reveals the relative merits of stereotactic radiosurgery, whole brain radiotherapy and open surgery, which have to be used alone or in combination for the treatment of patients with brain metastases. treatment aims to provide disease control with a good quality of life, although prolonged survival may not be always be achieved. the effect of ferite nanoparticles on brain tumours in vitro ligia tataranu neurosurgical dept., “bagdasar-arseni” clinical hospital bucharest, romania one factor contributing to the poor response to the therapy of brain tumour romanian neurosurgery (2013) xx 2: 180 – 213 211 patients is the limitation of conventional drug delivery systems. recently, magnetic nanoparticles received enormous attention as new tools for drug delivery in cancer treatment. the aim of this study was to analyse the toxic effect of ferite nanoparticles in vitro, in order to evaluate their biological compatibility as drug support in brain tumour tratment. for this reason, we used two brain tumour primary cell cultutes: glioblastoma gb3b cells and astrocytoma ac1b cells. as a normal control, we used human fibroblast hdf cells. the cells were exposed to 0,25 ug/ml, 0,5aμg/ml 1 ug/ml ferrite nanoparticles and the proliferation rates were evaluated 24, 48 and 72 hours, after the treatment. statistical analysis revealed that no significant effect of ferrite nanoparticles treatment was induced on malignant or normal cell lines used in this study (p0,05). in conclussion, our results showed that ferite nanoparticles, did not cause significant cytotoxicity in brain tumour cells and encourage the use of these compound as drug carrier in brain cancer treatment grant support: 134/2011 uefiscdi romania multiple functional image-guided resection of cerebral low grade glioma francesco tomasello department of neurosurgery university of messina messina, italy objectives: early and extensive resection of low-grade gliomas (lggs) may lead to better patients survival. nevertheless, resection of lggs is often limited by extensive involvement of functional brain areas. we describe the surgical management of patients with tumors at risk due to their diffuse nature and relationships with functional neural tissue. material and methods: the use of multimodal neuroimaging, including routine mri for intraoperative neuronavigation, functional mri with speech and motor mapping, diffusion tensor imaging and tractography, and ct/mr perfusion, is described in preoperative evaluation of lggs. navigated transcranial magnetic stimulation (ntms) was performed to map the motor cortex. intraoperative motor mapping and monitoring were performed in a consecutive series of patients. tumor removal was performed through a transsylvian approach for insular lesions, and through a trans-sulcal approach in stimulation-confirmed noneloquent areas for all other lesions. resection was continued until neuronavigation-evidenced normal white matter or cortical or subcortical stimulation revealed functional areas. results: gross-total resection was achieved in 78% of cases, as assessed by postoperative mri. over the average follow-up duration of 24 months, no patient experienced tumor progression or recurrence. no patient experienced new deficits at the long-term follow up. intraoperative mapping and clinical results demonstrated that pre-operative planning using multimodal neuroimaging and ntms reliably identifies distribution of tumor, eloquent brain structures and their relationships. conclusions: significant resection of diff use lggs is possible, even in presumed eloquent neural tissue, without necessarily causing permanent neurological deficits. individualized preoperative neuroimaging evaluation, with preand intraoperative speech and motor mapping, is an essential tool in achieving a good outcome. 212 abstracts 3rd national conference of neuro-oncology (ncno 2013) genetic heterogeneity in gliomas steffi urbschat, ralf ketter, joachim oertel department of neurosurgery, saarland university, homburg/ saar, germany gliomas display a wide range of histopathological features and biological behavior, and an inherent tendency to progress to a highly malignant phenotype. molecularand cytogenetic studies revealed that different grades of gliomas correlate with specific genetic alterations. glioblastomas, the most malignant form of gliomas, may develop de novo (primary glioblastomas) or through progression from low-grade or anaplastic astrocytomas (secondary glioblastomas). to analyze the genetic heterogeneity, we performed different cytogenetic methods considering their methodic limitations. cell culture analysis may be biased by clonal selection artifacts. homogenized tissue lacks control over the tissue composition and permits contamination of the tumor specimen with preexisting and reactive nonneoplastic tissue. moreover, gliomas exhibit a diffuse infiltrating growth pattern into normal brain so that no tumor area contains a uniform cellular composition. in order to evaluate an intratumoral genetic heterogeneity we performed fish investigations and microdissection analysis in paraffin-embedded glioma tissue and correlated the cytogenetic data with the histomorphology of the given tumor areas. low-grade astrocytomas most often showed normal karyotypes, by conventional cytogenetic methods. however, we were able to identify numerous alterations in low-grade astrocytomas, especially in areas with a gemistocytic appearance. primary glioblastomas and secondary glioblastomas showed consistant as well as different genetic findings, which correlate partial with the histomorphological features of the investigated areas. our results provide clear evidence of interand intratumoral genetic heterogeneity in gliomas independent of the applied method. in order to develop genetic prognostic criteria, the distinct genetic heterogeneity of these tumors has to be considered. preoperative surgical planning with probabilistic fibre tractography istvan valalik, peter szloboda, gyorgy szekely department of neurosurgery st. johnas hospital, budapest hungary deterministic tractography are primarily based upon streamline algorithms where the local tract direction is defined by the major eigenvector of the diffusion tensor (white matter tractography). on the other hand the probabilistic tractrography uses the anisotropy of water to generate probabilistic maps of connectivity between brain regions and it may draw fibers into the grey matter. in the last decade numerous software was made to process diffusion tensor mri data and the application of tractrography has become more and more widespread in the neurosurgery. in this paper, we present our experiences and future opportunities of preoperative planning of brain surgery with the aid of probabilistic fibre tractography. in the course of our work we used 3t 32 directions diff usion-weighting and high resolution t1 mr images, fmrib software library (fsl 5.0) and 3d slicer software. at the surgical planning of the brain tumours in the delicate regions we visualized eloquent intact tracts in vivo to avoid them. this method is widely used for visualization of corticospinal tract pathway in the surgery of central region tumours. in romanian neurosurgery (2013) xx 2: 180 – 213 213 addition, we used tractography maps for surgery of tumours in the vicinity of language-related regions and improving the stereotactic targets of deep brain stimulations in movement disorders. the fibre tractography help to understand for the neurosurgeons the advantages and disadvantages of approaches in order to most benefit from pre-surgical mapping. objectives: deterministic tractography are primarily based upon streamline algorithms where the local tract direction is defined by the major eigenvector of the diffusion tensor (white matter tractography). on the other hand the probabilistic tractrography uses the anisotropy of water to generate probabilistic maps of connectivity between brain regions and it may draw fibers into the grey matter. in the last decade numerous software was made to process diffusion tensor mri data and the application of tractrography has become more and more widespread in the neurosurgery. aims of study: in this paper, we present our experiences and future opportunities of preoperative planning of brain surgery with the aid of probabilistic fibre tractography. material and methods: in the course of our work we used 3t 32 directions diffusionweighting and high resolution t1 mr images, fmrib software library (fsl 5.0) and 3d slicer software. results: at the surgical planning of the brain tumours in the delicate regions we visualized eloquent intact tracts in vivo to avoid them. this method is widely used for visualization of corticospinal tract pathway in the surgery of central region tumours. in addition, we used tractography maps for surgery of tumours in the vicinity of language-related regions and improving the stereotactic targets of deep brain stimulations in movement disorders. conclusions: the fibre tractography help to understand for the neurosurgeons the advantages and disadvantages of approaches in order to most benefit from pre-surgical mapping. doi: 10.33962/roneuro-2020-087 safety of metoclopramide in traumatic brain injury patients. a systematic review of literature said al jaadi, yahya al kindi, tariq al-saadi romanian neurosurgery (2020) xxxiv (4): pp. 512-517 doi: 10.33962/roneuro-2020-087 www.journals.lapub.co.uk/index.php/roneurosurgery safety of metoclopramide in traumatic brain injury patients. a systematic review of literature said al jaadi1, yahya al kindi1, tariq al-saadi1,2 1 college of medicine and health sciences, sultan qaboos university, oman 2 neurosurgeon. canada abstract background: one in every three related-injury deaths in united state are linked directly to traumatic brain injury (tbi), for which it is considered as a leading cause of death. traumatic brain injury took place due to severe head assault to a hard object, with headache and vomiting being amongst the most common presenting symptoms. metoclopramide is an old antiemetic agent that has been used widely for nausea and vomiting in tbi patients. aim: a systematic review of the literature to investigate the safety of metoclopramide in treating traumatic brain injury patients. methods: a literature review was conducted in 6 databases, we determine the pertinence of a study to the inclusion criteria by assessing the title, keywords, and abstracts. five studies were found to be relevant. data were extracted using multiple variables that were formulated incongruent with the study aim and then further analyzed. results: the collective sample size was 93 patients with an average of age 38.5 years. 51.6 % were male and 48.6% were females. most patients received 10 mg metoclopramide iv with a percentage of 77.4%. while only 22.5% received 20 mg iv metoclopramide. seventy-one patients received metoclopramide alone and 22 received combination therapy. headache was the most common reported side effect (46.2 %), followed by anxiety and drowsiness with (39.7%) and (27.9 %); respectively. fatigue reported in (24.7%), while dystonia was the least common and developed only in 5.3%. conclusion: metoclopramide is a common medication used to treat tbi patients in the emergency department. however, the review demonstrated that the central nervous system (cns) side effect is excepted. alternative options with lower cns side effects may be better tried. background one in every three related-injury deaths in the us are linked directly to tbi, for which it is considered as a leading cause of death (1). as for paediatric cases the prevalence across countries varies from 47 and 280 per 100,000 children, more than 80% of which are minor head injuries with gcs of 14-15(2). traumatic brain injury took place due to keywords traumatic head injury, metoclopramide, safety, side effect, headache, vomiting corresponding author: tariq al-saadi neurosurgeon. canada tariq.dh.95@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 513 safety of metoclopramide in traumatic brain injury patients severe head assault to a hard object, which then can be classified into mild, moderate, and sever using gcs (3). moreover, the main causes of tbi are road traffic accidents (rta), falling, physical violence, exercise-related head injuries among others (1,3). patients with tbi usually present to the emergency room (er) with headache, nausea, and vomiting (4). other common presentations are dizziness, blurred vision, loss of consciousness, amnesia, and disturbance in concentration (1,2,4). as for headache, 1 in every 4 patients reported persistent headache syndrome (4). tbi patients were treated with antiemetic agents for their symptoms. metoclopramide (4-amino-5-chloro-2-methoxy-n(2 dimethylamino methyl benzamide) is an old antiemetic agent that has been used widely for nausea and vomiting as well as other gastrointestinal disorders (2). it is an antidopaminergic agent, centrally and peripherally acting, in order to enhance upper gastrointestinal motility without affecting its secretion (3). metoclopramide administration through po takes about 1-2 hours for maximum plasma concentration while it takes only 15min on an iv root (2,3). it is metabolized by the hepatic cytochrome p450 cyp2d6 enzyme (2). the drug has multiple side effects such as; dystonia, restlessness or anxiety, fatigue, drowsiness, confusion, insomnia, and flushing (2,3). our main aim is to study the safety of metoclopramide in treating tbi cases by reviewing the literature. methodology literature search and formulating selection criteria this study is a literature review with the main aim being to study the safety of metoclopramide in treating tbi cases. we searched pubmed, ebsco, proquest, sciencedirect, wiley online, and springer for pertinent studies. moreover, we determined the pertinence of a study to the inclusion criteria by assessing the title, keywords, and abstracts. the keywords we used were; traumatic head injury, head injury, brain injury, subdural injury, epidural injury, metoclopramide, safety of metoclopramide, and metoclopramide side effect. furthermore, the inclusion criteria were; all english literature and articles about tbi that used metoclopramide and reported drug side effects while we excluded any articles that are non-completed, repeated, or did not meet any of the aforementioned criteria. data extraction data were extracted using multiple variables that were formulated incongruent with the study aim. the variables are; article type and author’s name, number of patients, the average age, gender, the dose of metoclopramide, drug combination, drug side effects, mechanism of injury, gcs, and duration of follow up. all of which were gathered in a table and were set for analysis. figure 1. prisma flow diagram show methodology characteristic of included study figure 1 represents flow chart depicting the study selection process. of 21 relevant studies, one of them was found to be a repetition, 14 were not eligible and one was irrelevant to the research aim. 5 pertinent literature were studied thoroughly for data extraction. data analysis data were collected in an excel sheet, formula builder was used to calculating simple mathematic, including the total number of patients, the number of females and males, and the percentage of each, total number of side effects reported. spss has been used to calculate the mean of age and the days of follow up using a bar of weight cases. result our study included 5 articles, as shown in table 1. two studies were randomized controlled, one was 514 said al jaadi, yahya al kindi, tariq al-saadi prospective, and two case reports. there were variations in the drug side effects reported in each study. two studies used diphenhydramine 25mg and cisapride as a combination thereby, while the remained used metoclopramide alone. all the studies used 10 mg iv metoclopramide except one study used 20 mg iv. headache was the most common reported side effect by 2 studies. there was some missing data especially on the mechanism of injury. our sample size was 93 patients with an average of age 38.5 years. 51.6 % were male and 48.6% were female (table 2). most patients received 10 mg metoclopramide iv with a percentage of 77.4%. while only 22.5% received 20 mg iv metoclopramide. seventy-one patients received metoclopramide alone and 22 received combination therapy. headache was the most common reported side effect (46.2 %), followed by anxiety and drowsiness with (39.7%) and (27.9 %); respectively. fatigue reported in (24.7%). while dystonia was the least common and developed only in 5.3%. discussion this is the first systemic review study of metoclopramide side effects on patients with tbi. there is a lack of clinical trial which study the side effect of metoclopramide in patients with tbi. our study identified 93 patients who received metoclopramide after tbi. the average age of patients was 6.9 years (4-69). male was relatively higher than female in our sample size as 51.6% of our sample size were male compared to 48.4% female. comparing done to identify the incidence and management of moderate to a severe head injury which showed that male to female ratio is 2:1(5). this might be due to the type of our research as it is a systemic review and most of our data were collected from prospective and clinical trial research. a previous study on the identification of the efficacy of metoclopramide in tbi, showed that the leading causes of tbi were rta, followed by fall (6). in comparison to our study fall and trip were the highest. in our review, 77.4% received 10 mg metoclopramide intravenously, and 22.5% received 20 mg intravenously. this dose was supported by the recommendation of the european medicines agency that the maximum daily dose of metoclopramide is between 10 mg to 30 mg in order to decrease the risk of neurological and other adverse effect (7). metoclopramide is a prokinetic agent that have been widely used in critically ill patient to improve gastric motility and the symptoms of head concussion, nausea, and vomiting (8). however, the concerns of metoclopramide’s safety have been raised (9). one of the studies included in our review showed that the effectiveness of metoclopramide and ondansetron was similar. however, because of the incidence of the complications in patients treated with metoclopramide were higher than ondansetron, they concluded with the suggestion to use ondansetron instead of metoclopramide inpatient with tbi (10). in tbi patient with an enteral feeding problem, the use of erythromycin instead of metoclopramide in some situation has been studied which show there is a significant decrease in high gastric aspirate volume with the use of erythromycin compared to metoclopramide (11). in the current systemic review, the most common symptom was the headache as it is presented in 45.2% of the sample size (10,12). in contrast to a survey study done by hale.t which showed that among 32 participants in the study, 1-7% of participants complained of some central side effects ranging from dizziness and headache. we can see that patients with tbi are more susceptible to develop a headache and other neurological side effects, including extrapyramidal side effects, from metoclopramide compared to others (13). in our review, the incidence of anxiety and drowsiness were 37 patients (29.0%) and 26 patients (27.9%), respectively. fatigue was only represented in 23 patients (24.7%)(10)(12). while another systemic review study done to study the use of metoclopramide in diabetic gastroparesis, showed that fatigue, drowsiness and lethargy were presented in 10% of patients (14). dystonia was represented in 5 patients (5.3%). the incidence of dystonia in the previous systemic review was in an approximately 0.2–6% of patients who received metoclopramide (14). these side effects may explain by the ability of metoclopramide to cross the bloodbrain barrier easily (15). the early signs of an increased icp are headache, vomiting or nausea, ocular palsies, and altered level of consciousness. side effects of metoclopramide overlap with raised icp symptoms, since it is subtle it is difficult to recognize a rise in icp unless you investigate it. in our literature review, a case report 515 safety of metoclopramide in traumatic brain injury patients identifies an increased in icp from baseline of 15 20mmhg to 36mmhg following a 10mg intravenous metoclopramide and the same dose in the following day reports another increases to 34 mmhg (16). such side effects raise a question of the safety of the metoclopramide in patients with tbi. inconsistent with our results that found an increased susceptibility for neurological side effects after metoclopramide administration in tbi patients. a controlled randomized clinical trial is recommended to exploit the relationship between raised icp and metoclopramide. limitations: the limitation of the study includes the lack of high evidence studies as there were only two randomized controlled trials and one prospective study. publication bias was not done because of the same reason. in addition, the lack of long term follows up was also noticed. in addition, in 75.2% of cases, the mechanism of injury was not mentioned. conclusion metoclopramide is a common medication used to treat tbi patients in the emergency department. however, the review demonstrated that the cns side effects are excepted. alternative options with lower cns side effects may be better tried. table 1. summary of metoclopramide and tbi studies article type author year of publication no. of patie nts age gender dose of metoclo pramide combin ation side effect mechanism of injury gcs duration of follow up controlled, randomize, double blind clinical trial majid zamani et al. 2015 60 36.1 m 33 10 mg, iv na headache 30/60(30%) drowsiness 26/60(43.3%) fatigue 23/60(38.3%) anxiety 37/60(61.7%) dystonia 5/60 (8.3%) na 1415 na f 27 prospective, randomize, controlled, doubleblind tarik zafer nursal 2007 10 43 m 8 10 mg, iv na 5/10 develop complication * tbi not defined 11-6 5 days f 2 prospective benjamin w 2018 21 45 m 5 20 mg, iv diphen hydra mine 25mg headache 12/19 (63%) trip/fall 9 impacted stationary object 4. projectile 4 assault 3 rta 1 na 5 days f 16 case report simon deehan 2002 1 22 m 1 10 mg, iv na increase icp raised map rta 3 4 days case report thomas altmayer, 1996 1 22 m 1 10mg, iv cisapri de none rta 9 69 days gcs: glasco coma scale rta: road traffic accident *not defined but none of which were extrapyramidal symptoms 516 said al jaadi, yahya al kindi, tariq al-saadi table 2. summary of metoclopramide and tbi studies finings number of patients 93 average of age 38.5 gender male 48(51.6%) female 45(48.4%) treatment metoclopramide only 71(76.3%) metoclopramide and diphenhydramine 21(22.5%) metoclopramide and cisapride 1(1.1%) dose of metoclopramide 10 mg, iv 72(77.4%) 20 mg, iv 21(22.5%) side effect headache 42(45.2%) drowsiness 26(27.9%) fatigue 23(24.7%) anxiety 37(29.0%) dystonia 5(5.3%) increase icp increase map 1(1.1%) mechanism of injury not defined 70(75.2%) rta 3(3.2%) trip/fall 9(9.7%) impacted stationary object, assault 7(7.5%) projectile 4(4.3%) undefined complication 5(5.3%) average of the follow up 6.9(4-69) abbreviation tbi: traumatic brain injury icp: intracranial pressure cns: central nervous system gcs: glasgow coma scale er: emergency room rta: road traffic accident map: mean arterial pressure references 1. report mw. surveillance for traumatic brain injury – related deaths — united states, 1997 – 2007. cdc. 2011;60(5):1997–2007. 2. moezzi m, delirrooyfard a, motamed h, mortazavi mk, specialist em. antiemetic effects of metoclopramide with and without dexamethasone in children with minor head trauma: a single blind randomized clinical trial. 2018;188(december):7307–13. 3. majid zamani, behnam namdar, reza azizkhani, omid ahmadi med. comparing the antiemetic effects of ondansetron and metoclopramide in patients with minor head trauma. in 2015. p. 137–40. 4. friedman bw, babbush k, irizarry e, gallagher ej, health m. an exploratory study of iv metoclopramide + diphenhydramine for acute post-traumatic headache. 2019;36(2):285–9. 5. maegele m, lefering r, sakowitz o, kopp ma, schwab jm, steudel wi, et al. inzidenz und versorgung des mittelschweren bis schweren schädel-hirn-traumas. dtsch arztebl int. 2019 mar 8;116(10):167–73. 6. dickerson rn, mitchell jn, morgan lm, maish go, croce ma, minard g, et al. disparate response to metoclopramide therapy for gastric feeding intolerance in trauma patients with and without traumatic brain injury. j parenter enter nutr. 2009 nov;33(6):646–55. 7. medical science news: fda requires boxed warning and risk mitigation strategy for metoclopramidecontaining drugs [internet]. [cited 2020 apr 20]. available from: https://elbiruniblogspotcom.blogspot .com/2009/02/fda-requires-boxed-warning-andrisk.html 8. nursal tz, erdogan b, noyan t, cekinmez m, atalay b, bilgin n. the effect of metoclopramide on gastric emptying in traumatic brain injury. j clin neurosci. 2007 apr;14(4):344–8. 517 safety of metoclopramide in traumatic brain injury patients 9. van der meer yg, venhuizen wa, heyland dk, van zanten arh. should we stop prescribing metoclopramide as a prokinetic drug in critically ill patients? crit care. 2014 sep 23;18(5). 10. zamani m, namdar b, azizkhani r, ahmadi o, esmailian m. comparing the antiemetic effects of ondansetron and metoclopramide in patients with minor head trauma. emerg (tehran, iran) [internet]. 2015 [cited 2020 apr 20];3(4):137–40. available from: http://www.ncbi.nlm.nih.gov/pubmed/26495402 11. makkar jk, gauli b, jain k, jain d, batra yk. comparison of erythromycin versus metoclopramide for gastric feeding intolerance in patients with traumatic brain injury: a randomized double-blind study. saudi j anaesth. 2016 jul 1;10(3):308–13. 12. friedman bw, babbush k, irizarry e, white d, john gallagher e. an exploratory study of iv metoclopramide + diphenhydramine for acute post-traumatic headache. am j emerg med. 2018 feb 1;36(2):285–9. 13. hale tw, kendall-tackett k, cong z. domperidone versus metoclopramide: self-reported side effects in a large sample of breastfeeding mothers who used these medications to increase milk production. clin lact. 2018;9(1):10–7. 14. shakhatreh m, jehangir a, malik z, parkman hp. metoclopramide for the treatment of diabetic gastroparesis. expert rev gastroenterol hepatol. 2019 aug 3;13(8):711–21. 15. jolliet p, nion s, allain-veyrac g, tilloy-fenart l, vanuxeem d, berezowski v, et al. evidence of lowest brain penetration of an antiemetic drug, metopimazine, compared to domperidone, metoclopramide and chlorpromazine, using an in vitro model of the bloodbrain barrier. pharmacol res. 2007 jul;56(1):11–7. 16. deehan s, dobb gj. metoclopramide-induced raised intracranial pressure after head injury. j neurosurg anesthesiol. 2002;14(2):157–60. 13_satyartheeguru_transientinternuclear__ 318 satyarthee et al ino associated with mutism following posterior fossa mass surgery transient internuclear ophthalmoparesis associated with mutism following midline cerebellar tumour surgery in an 8-year boy guru dutta satyarthee1, a.k. mahapatra2 1associate professor, department of neurosurgery, neurosciences centre, aiims new delhi 2professor, department of neurosurgery, aiims, bhuwneshwar, india abstract: mutism and neurobehaviour symptoms are well known features, which may occur following surgical excision of mass lesion of various histopathologies in the posterior cranial fossa, during the postoperative period. mutism may be rarely associated with ataxia of eyelid closure and paresis of external ocular muscles. however, internuclear ophthalmoparesis is not reported in association with mutism following posterior cranial fossa surgery. we report an 8-year–boy, who developed internuclear ophthalmoparesis following suboccipital craniectomy for decompression of vermian medulloblastoma. the clinical features, aetiopathogenesis, management of transient internuclear ophthalmoparesis associated with mutism and pertinent literature is reviewed in short. key words: posterior fossa, internuclear ophthalmoparesis, medulloblastoma surgery, mutism introduction internuclear ophthalmoparesis (ino) is one of the most localizing brainstem syndromes, which is caused by a lesion involving medial longitudinal fascicules in dorsomedial brain stem tegmentum of either the pons or the midbrain [1,2]. ino is an occulomotor syndrome characterized by ocular dysconjuancy during horizontal saccades, with slowing of adducting eye movements, with or without ocular limitation, and abduction nystagmus in the other abducting eye. internuclear ophthalmoparesis is rare occurrence following intracranial surgery. we report an 8-year -old –boy developed ino, in the immediate postoperative period following decompression of vermian medulloblastoma. the development of mutism and associated neuropsychiatric symptoms subsequently many reports have emphasized the importance of impaired eye openings, pseudo bulbar symptomatology. however, ino was not highlighted in any case report, except as associated signs in association of cerebellar mutism. however, no emphasis was put regarding the onset, course, and neuroimaging in a series of 12 cases reported by pollack et al [7]. case report patient presented with a six week history of progressive headache and ataxia. one week prior to admission ataxia markedly worsened, with head tilt and diplopia, on admission, he was conscious, irritable, and stable aerodynamically. fundi examination revealed bilateral papilloedema. left sixth cranial romanian neurosurgery (2015) xxix 3: 318 323 319 paresis was present. he power was normal in all limbs. he had marked ataxia, making walking difficult. he had bilateral cerebellar signs. neck rigidity was present. routine haematological, biochemical and coagulation profiles were normal. computerized tomography of brain revealed hypodense mass lesion involving vermis; it was 4 cmx4.5 cm in diameter, causing obstructive hydrocephalus. (figures 1-3) on contrast administration showed uniform enhancement. radiologically a diagnosis of vermian, mass with obstructive hydrocephalus was made. he underwent csf diversion procedure of ventriculoperitoneal shunt. two days following ventriculoperitoneal shunt surgery, he underwent elective suboccipital craniectomy in the sitting position. tumour was exposed and resected via an inferior transventricular approach. the tumour was completely excised using with help of internal decompression of cusa and haemostasis was achieved with bipolar cattery. the floor of fourth ventricle was not invaded or infiltrated by tumor. csf was freely flowing through the aqueduct. the content of posterior fossa was lax and pulsating. a histopathological examination confirmed the diagnosis of medulloblastoma. figure 1 mri brain, t1w1 axial section image of brain showing hyperintense mass lesion located in the midline involving vermis occupying and causing expansion of the fourth ventricle causing obstructive hydrocephalus with dilation of lateral ventricles figure 2 mri brain, t2wi axial section of brain of 8-year boy, mass lesion showing hyperintense signal intensity, with associate hydrocephalus figure 3 contrast enhanced mri brain (cemri brain), coronal section depicting heterogeneously enhancing mass lesion 320 satyarthee et al ino associated with mutism following posterior fossa mass surgery figure 4 postoperative ncct head axial section showing excision of medulloblastoma figure 5 clinical photograph of 8-year boy having mutism sixth postoperative days after reversal of anaesthesia, he was awake with intact neurologically, except left sided sixth nerve paresis and cerebellar ataxia. he was well for forty eight hours, and then developed mutism. he was lying curled –up in the bed with eyes closed. he was not obeying commands. he refused oral intake of solid and liquid fluid. (figure 4) nc ct scan head was done to evaluate for the deterioration in the neurological status revealed oedema around the resected cavity, however no haematoma was encountered in the tumour bed. (figure 5) magnetic resonance imaging could not be done in view of economic constrains. after 5 days, he showed progressive improvement in the neurological status and started accepting oral feed; personality carnages also improved .he becomes more cooperative. ocular muscle examination showed features consistent with the diagnosis of internuclear ophathalmoplegia. his speech also improved gradually. however feature of ophthalmoparesis did show improvement up to six weeks after surgery, but resolved completely, when seen at 8 weeks of follow up after surgery. the cranial ct scan with contrast-enhanced scan had revealed residual lesion, he received craniospinal irradiation. discussion common features of cerebellar mutism syndrome include a decreased speech output or mutism, transient irritability or apathy. although other features transient eye closure, difficulty with feeding, associated with incontinence of bladder and bowel is reported. siffert et al analyzed 16 cases of cerebellar mutism syndrome and defined more comprehensive neurological dysfunction in the cerebellar mutism syndrome [9]. a severe global cerbellar dysfunction, a communication impairment affecting receptive and expressive languages, severe inattention, apathy, hypokinesis, mood liability, irritability, apathy, hemiparesis, or motor apraxia, transient difficulty with eye opening and lack of control of bowel and balder. the causes and anatomical basis of cerebellar mutism syndrome in children with posterior fossa surgery is still controversial. cerebellum has been implicated for cerebellar mutism syndrome [4]. the mutism occur romanian neurosurgery (2015) xxix 3: 318 323 321 exclusively with midline cerebellar mass lesion, being resected via inferior vermian incision was suggested as bilateral injury to inferior vermian region is crucial for development [9]. although dailey et al. had suggested the splitting of the inferior vermis during a tumour resection, but less than 25 % of children undergoing similar procedure develops signs of cerebellar mutism syndrome. however several points indicate that anatomical location may not exactly in the inferior vermis, but localized to the adjacent structures. however, many cases of pollack et al where tumour was located in the superior vermis and inferior vermis was not violated also developed and this anatomical center may not be vermis but instead more laterally located [7]. the onset and recovery is usually delayed hours to days following surgical procedure. indicating it is caused by intraoperative injury or infarction [7]. pollack et al also observed postsurgical oedema has been implicated but clinical course often outlast the resolution of oedema. other mechanism as alteration in neurotransmitter levels and synaptic or transsynaptic degeneration of connecting structure may be responsible, which mighty correlate well with time lag between the time of actual surgical injury until the onset of symptoms. the recovery mechanisms also remain still unclear. after a several week of plateau, children usually notice a fast recovery of speech. however cerebellar ataxia may persist in the majority of cases, so some aspect of clinical recovery may not depend on cerebellar injury [4]. these may reflect the sequel of injury to the afferent or efferent pathway to dentate nuclei, which are involved in the initiation of violation movement [4, 7]. bilateral impairment of paramedian cerebellar dentate nuclei, its efferent or afferent connection or a combination of factors may be involved [7]. the delayed onset of speech impairment probably related interval of time required for oedema resulted due to surgical manipulation in the surgical field has reached the structure [7]. this symptom complex may be associated with a varied duration of speech impairment and spectrum of neurological and neurobehavioral abnormality can vary. in the simple form of spectrum, only impairment of in co-ordinating the complex bilateral integrated movement necessary for speech production. in relatively more severe cases may have additional impairment of incordination of oropharyngeal muscles movement involved in chewing or swallowing movement. however in more severe cases, may have broad spectrum of volitional movement impairment including eye opening and voiding. this more global impairment has also been substantiated on neuropsychiatry evaluation. accordingly, focal bilateral lesion to dentate nucleus and its connection to while more complex involves paravermian region or its connection. during recovery, which may occur days to weeks following onset, global akinesia, and urinary retention recovery is followed by eating and finally speech improvement may occur with a dysarthria or bizarre vocal quality and finally regaining of almost normal speech. wisoff et al described psseudobulbar syndrome after posterior fossa surgery in children, often associated with oedema of bilateral cerebellar peduncle and brainstem, may reflect dysfunction of brainstem [10]. however, unusual personality changes as also observed in mutism syndrome are well described and manifestation of primary brainstem lesion glioma of brainstem and vascular insufficiency from proximal basilar artery ischemia [6, 1]. these psseudobulbar manifestation may also be caused by bacterial meningitis. however, in our case also the ino also improved after four months. ino syndrome is caused by damage to these structures including medial longitudinal fasciculus, paramedian pontine reticular formation, or the ipsilateral sixth nerve 322 satyarthee et al ino associated with mutism following posterior fossa mass surgery nucleus. commonest causes of ino is multiple sclerosis and infarction of brain stem, however, lesser commoner are tumors of the brain stem and cerebellum and extremely rarely, can be detected in the postoperative period following of the posterior fossa tumors removal [2]. pollack et al. reported a case, had vermian lesion with metastasis in the both hemisphere with fourth ventricle invasion had medulloblastoma developed, mutism 72 hours after surgery, was lying curled in the bed and poor oral intake, improvement started on 18 th day and almost complete recovered by 4 weeks. however, no detail of onset or progress or remission of ino was provided. he also developed ino, left arm ataxia after 18 days of surgery and these improved over four weeks, however ataxia persisted [7]. correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: duttaguru2002@yahoo.com references 1.caplan lr. “top of basilar” syndrome. neurology. 80: 70-72, 1980 2.chern jj , relyea k, edmond jc, whitehead we, curry dj, luerssen tg, jea a. transient selective downward gaze paralysis complicating posterior fossa tumor resection in children. report of 2 cases. j neurosurg pediatr. 3(6): 467-71, 2009 3.frohman em, frohman tc, o’sulleabhain ps, zhang h, et al. quantitative oculographic characterisation of internuclear ophthalmoparesis in multiple sclerosis: the versional dysconjuancy index z score. j neurology neurosurg psychiat 73: 5-55, 2002 4. hirsch jf, reinier d, czernichow p, benveniste l, pierrekahn a. medullobalstoma in childhood: survival and functional results. acta neurochir (wien) 48: 1-15, 1979 5.newton hb, miner me" one-and-a-half" syndrome after a resection of a midline cerebellar astrocytoma: case report and discussion of the literature. neurosurg 29(5):768-72, 1991 6.petrino ja, edwards mob. management of brainstem tumors in children. contem neurosurg 11:1-6,1989 7.pollack if, albright al, towbin r, fitz c. mutism and psseudobulbar symptoms after resection of posterior fossa tumours in children: incidence and pathology. neurosurg 37: 885-893,1995 8.sakai h, sekino h, nakamura n. three cases of “cerebellar mutism “. shinkeinaika 12: 302-304, 1980 9.siffert j, poussaint ty, goumnerova lc, scott rm, la valley b, tarbell nj, pomeroy sl. neurological dysfunction associated with postoperataive cerebellar mutism. j neuro-oncol 48: 75-81, 2002 10.wisoff jh, epstein fj. pseudobulbar palsy after posterior fossa operation in children. neurosurg 15: 707707,1984. 5kakucsc_multiple romanian neurosurgery (2014) xxi 3: 279 282 279 multiple cerebral aneurysm – case report c. kakucs1,3, i.st. florian1,2 1cluj county clinical emergency hospital, neurosurgical department 2university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania, neurosurgical department 3phd student, university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania, neurosurgical department abstract this 41-years-old female presented with somnolence, confusion and nuchal rigidity. preoperative angio-ct scan showed two aneurysm located on both internal carotid artery (ica) at the site of posterior communicating artery (pcoma). during surgery we discovered another dilatation on the origin of left ophtalmic artery that proves to be an infundibullum. we clipped the two communicating posterior aneurysm from the left side and the ophtalmic infundibullum was wrapped. seven days after surgery the neurological status was improved and she was transferred to the neurological department. key words: multiple cerebral aneurysm, subarachnoidian hemorrhage, internal carotid artery, posterior communicating artery. introduction aneurysms are acquired lesions and the rupture of this lesions lead to subarachnoid hemorrhage (3). the incidence of multiple cerebral aneurysm is within 8% to 44% (5). the most common localization site of multiple aneurysm are on the middle cerebral artery (mca), ica and on the anterior communicating artery (acoma) (4). in our series the most frequent combination was between acoma-mca and acomapcoma. in almost all cases the rupture occurred on acoa aneurysm. a special group of multiple cerebral aneurysm are represented by the mirror-like aneurysm with an incidence between 5-36% (1). like in other studies, in our series too, the female represent the majority from the sex ratio point of view (2, 6, 7). the maximum incidence of aneurysmal rupture was reported in the fifth decade. the majority of multiple aneurysm were situated on the middle cerebral artery and the internal carotid artery (4). concerning the approach, we prefer to use unilateral approach for multiple cerebral aneurysm ("single stage – single opening"). this type of approach ("single stage – single opening") we perform after 3-4 days from the rupture because at that moment we will have a good brain relaxation, clinical and metabolically stability. 280 kakucs, florian multiple cerebral aneurysm figure 1 preoperative ct scan. intraventricular hemorrhage in the fourth and third ventricle. subarachnoidian hemorrhage in the basal cisterns and in the left sylvian fissure. fischer scale 4 grade figure 2 preoperative angio-ct scan. two aneurysm on the left and right ica. the aneurysm on the left side is bigger than the oposite side aneurysm case report a 41-years-old female patient who was admitted in our service from the neurology department with a 24 hours history of headache, somnolence and focal motor seizures in the right superior limb. at the neurological examination the patient presented a gcs of 13 points, nuchal rigidity, somnolence, confusion and she was without any motor deficits. we performed a ct scan that show as subarachoidian hemorrhage in the basal cistern and in the left sylvian fissure. the patient also presented intraventricular hemorrhage in the fourth and third ventricle (figure 1). romanian neurosurgery (2014) xxi 3: 279 282 281 figure 3 intraoperative image. left ica with the aneurysm situatted on the ophtalmic segment and the posterior communicating artery aneurysm figure 4 postoperator ct scan figure 5 postoperator ct scan – bone window. we performed a single opening after that we performed an angio-ct and that showed two aneurysms on the left and right ica at the site of pcoma (figure 2). the operation was performed in the second day after admission. after the endotracheal induction of general anesthesia, the patient was placed in a supine position, with the head slightly raised and turned to the right side. a left frontotemporal craniotomy was the chosen approach. dural opening was parallel with the skull base. after the dissection of the left sylvian fissure, the left optic nerve and the supraclinoidal segment of ica we observed a dilatation on the ophtalmic part of ica that proved to be an infundibullum (figure 3). the left anterior clinoid process was resected intraduraly in order to better define the neck of the aneurysm, than the definitive clip was placed on the left pcoma, along with wrapping of the left ophthalmic infundibullum. after the dissection of the arachnoid over the optic nerves and chiasm, the lamina terminallis was opened in order to have a better brain relaxation. the dissection was continued on the opposite side, above and beyond the contralateral optic nerve and ica. the dissection of the aneurismal neck was uneventful, and a curved definitive clip was placed on it, with a complete occlusion of the aneurysm. a standard wound closure with watertight duroplasty with autolog pericranium was performed. a follow-up ct –angio was performed at 48 hours postoperative period, demonstrating complete occlusion of the aneurisms with a normal caliber of both icas, with no additional brain lesions due to surgery (figures 4, 5 and 6). the postoperative course was uneventful, with a progressive improvement of neurological status. after seven days of hospitalization the patient, at a gos (glasgow outcame score) of four was transferred to the neurological department to continue the medical treatment. 282 kakucs, florian multiple cerebral aneurysm figure 6 postoperator angio ct scan. we can see the vessels are permeable and there are no aneurysms left discussion when we have multiple aneurysms we prefer to delay surgery for 3-4 days to have a good brain relaxation and clinical and metabolically stability. in multiple aneurysms we try to clip all aneurysms in a single stage, using the same unilateral approach. "single stage single opening" is a good option for multiple aneurysms with paramedian location. from our point of view we consider is better to make only one opening because is the less invasive technique to manage multiple aneurysms and in our series we had good results. in our series the mortality of patients with h&h third grade was 10%. also, in our series, 64% of patients with h&h third grade were discharged with a glasgow outcome scale of 4 or 5. acknowledgements: the study was funded by posdru grant no. 159/1.5/s/138776 grant with title: "model colaborativ instituțional pentru translaterea cercetării științifice biomedicale în practica clinică transcent". references 1.baccin ce, krings t, alvarez h, ozanne a, lasjaunas p: multiple mirror-like intracranial aneurysms. report of the case and review of the literature. acta neurochir 148: 1091-1096, 2006 2.baumann f, khan n, yonekawa y. patient and aneurysm characteristics in multiple intracranial aneurysms. acta neurochir suppl. 2008;103:19-28 3.caranci f, briganti f, cirillo l, leonardi m, muto m. epidemiology and genetics of intracranial aneurysms eur j radiol. 2013 oct;82(10):1598-605. 4.florian i șt, opțiuni terapeutice în accidentele vasculare cerebrale hemoragice. editura medicală universitară "iuliu-hațieganu" cluj-napoca, 2007, pp. 300-303. 5.heiskanen o, porras m, surgical management of unruptured cerebral aneurysms [chapter 80]; in schmidek and sweet: operatine neurosurgical techniques – indications, methods and results, fourth edition, wb saunders company, 2000. 6.inagawa t. incidence and risk factors for multiple intracranial saccular aneurysms in patients with subarachnoid hemorrhage in izumo city, japan. acta neurochir (wien). 2009 dec;151(12):1623-30. 7.lai hp, cheng km, yu sc, au yeung km, cheung yl, chan cm, poon ws, lui wm. size, location, and multiplicity of ruptured intracranial aneurysms in the hong kong chinese population with subarachnoid hemorrhage. hong kong med j. 2009 aug;15(4):262-6. 12agrawal_smallsupracilliary romanian neurosurgery (2014) xxi 3: 325 328 325 small supracilliary incision for the management of fracture of supraorbital rim and anterior wall of frontal sinus amit agrawal professor of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract with the development of biomedical materials and new techniques in craniofacial sinus surgery, the management of frontal sinus fractures is advanced considerably. we discuss a case of fracture of anterior wall of frontal sinus that was also associated with fracture of the supra-orbital rim and describe supracilliary approach through a small incision (approximately 3 cm) used for the management in this case. with this approach we could successfully expose and reduce the fracture fragments without the need for coronal incision, endoscope or intra-operative imaging. key words: fractures, bone, orbit, frontal, frontal bone, frontal sinus. introduction an estimated 1% to 9% of facial fractures can involve the supraorbital rim and the anterior table of the frontal sinus (1, 2, 3) resulting in significant ophthalmologic and cosmetic morbidity. (4, 5) with the development of biomedical materials and new techniques in craniofacial sinus surgery the management of frontal sinus fractures is advanced considerably. (4-8) we discuss a case of fracture of anterior wall of frontal sinus associated with fracture of supra-orbital rim and describe supracilliary approach through a small incision (approximately 3 cm) used for the management in this case. case report 24 year gentleman presented with approximately 6 hours after the road traffic accident. he had transient loss of consciousness and nasal bleeding. there was no history of vomiting or seizures. his general and systemic examination was normal. there were no neurological deficits. on local examination he had depression on the mid forehead and of the left supra-orbital rim. extra-ocular movements were full in all directions. computerized tomography (ct) scan showed depressed fracture of anterior wall of frontal sinus and associated fracture of left supra-orbital rim. there was no evidence of intra-cranial injury, the posterior wall of frontal sinus was intact and there was no blood 326 agrawal small supracilliary incision for the management of fracture of supraorbital rim in the sinus (figure 1). the fractured frontal sinus wall was exposed through a 3 cm left supracilliary incision (figures 2a and 2b). the edge of the frontal bone lateral to the fractured fragments on left side was drilled to make space to introduce the penfield’s dissector (figure 2c horizontal arrow). the dissector was introduced through the gap and fractured fragments could be elevated with ease with good alignment (figure 2c vertical arrow). patient is doing well at follow up with good cosmetics (figure 3). figure 1 ct scan showing isolated fracture of anterior table of frontal sinus figure 2 3 cm supracilliary incision (a), exposure of fractured fragments (b), edge lateral to the fracture was drilled (c, horizontal arrow) and fractured fragments were elevated figure 3 post-operative image showing good cosmetic result with least visible scar discussion the use of high-resolution ct is used for the evaluation of the frontal sinus and it also helps to rule out the damage to the posterior table of the frontal sinus, any associated romanian neurosurgery (2014) xxi 3: 325 328 327 intracranial or facial skeleton injuries. (4) before planning for surgical intervention through small corridor the patency of the frontonasal duct needs to be determined so to avoid delayed but serious infectious complications. (9, 10) the treatment of supraorbital rim fractures is indicated for functional and esthetic reasons and it ranges from conservative observation to open reduction and internal fixation of the fracture fragments. (4) a non-displaced supraorbital rim fracture generally requires no surgical intervention and treatment of concomitant neurological or soft tissue injuries may be the only management that is needed. (9) however, as in present case when the fracture segments are displaced, surgical exploration, reduction and stabilization is indicated. (4) classically, open reduction of isolated anterior table fractures require a bicoronal incision for exposure, reduction, and rigid fixation. (4, 11) while the success rates with a coronal incision are very high, the procedure can result in postsurgical stigmata including a large scar, possible alopecia, parasthesias, and, rarely, facial nerve injury. (11) the recent development of instrumentation and techniques for endoscopic brow-lifting has allowed access to anterior table frontal sinus fractures, without the need for a coronal incision. (7, 8, 11) the potential endoscopic treatment options for anterior table fractures include closed reduction without internal fixation, closed reduction with internal fixation, and fracture camouflage with bone cement. 11 or implant. (8) it is anticipated that the use of endoscopic technique will reduce operating time, surgical morbidity, and cost. (8) however, the endoscopy is challenging, success rates vary depending on fracture comminution and also it can only be used for moderately displaced fractures (1-5 mm). (11) recently a case is described where isolated depressed anterior wall fracture of the frontal sinus was treated by closed reduction to avoid coronal incision. (6) though the method was a less-invasive technique and could be performed without problem in selected cases, however may not be suitable for complex fractures of the frontal sinus. (6) in present case we used approximately 3 cm incision to expose and reduce the fracture fragments successfully without the need of coronal incision, endoscope or intra-operative imaging. it has been described in the literature that the reduction is often stable once the fragments have been levered into position because of the absence of muscular displacing forces. (12) we used this principle in our case and did not use the internal fixation as the fractured fragments were stable after reduction. supraorbital rim fractures, although uncommon, must be recognized promptly and can be best managed by an oral and maxillofacial surgeon or other specialist skilled in the management of facial bone fractures. (4) correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com 328 agrawal small supracilliary incision for the management of fracture of supraorbital rim dramit_in@yahoo.com mobile+91-8096410032 references 1.haug rh. management of the trochlea of the superior oblique muscle in the repair of orbital roof trauma. j oral maxillofac surg 2000; 58(6):602–6. 2.penfold cn, lang d, evans bt. the management of orbital roof fractures. br j oral maxillofac surg 1992; 30(2):97–103. 3.sullivan wg. displaced orbital roof fractures: presentation and treatment. plast reconstr surg 1991; 87(4):657–61. 4.mcguire tp, gomes pp, clokie cml, sándor gkb.. fractures of the supraorbital rim: principles and management. j can dent assoc2006; 72(6):537–40. 5.lakhani rs, shibuya ty, mathog rh, marks sc, burgio dl, yoo gh. titanium mesh repair of the severely comminuted frontal sinus fracture. arch otolaryngol head neck surg. 2001;127:665-669 6.mavili me, canter hi. closed treatment of frontal sinus fracture with percutaneous screw reduction. j craniofac surg. 2007;18(2):415-9. 7.manolidis s, hollier lh jr. management of frontal sinus fractures. plast reconstr surg. 2007;120(7 suppl 2):32s48s. 8.kim kk, mueller r, huang f, strong eb. endoscopic repair of anterior table: frontal sinus fractures with a medpor implant. otolaryngol head neck surg. 2007;136(4):568-72. 9.hirano a, tsuneda k, nisimura g. unusual frontoorbital fractures in chil¬dren. j craniomaxillofac surg 1991; 19(2):81–6. 10.stanley rb jr, becker ts. injuries of the nasofrontal orifices in frontal sinus fractures. laryngoscope 1987; 97(6):728–31. 11.strong eb, buchalter gm, moulthrop thm. endoscopic repair of isolated anterior table frontal sinus fractures. arch facial plast surg. 2003;5:514-521 12.lanigan dt, stoelinga pj. fractures of the supraorbital rim. j oral surg 1980; 38(10):764–70. doi: 10.33962/roneuro-2021-070 the importance of nuclear magnetic resonance (mri) in the diagnosis of cerebral cavernomas. case presentation dan bentia, andrei alexandru marinescu, florin papagheorghe, georgeta popa, alexandru vlad ciurea romanian neurosurgery (2021) xxxv (4): pp. 412-416 doi: 10.33962/roneuro-2021-070 www.journals.lapub.co.uk/index.php/roneurosurgery the importance of nuclear magnetic resonance (mri) in the diagnosis of cerebral cavernomas. case presentation dan bentia1, andrei alexandru marinescu2, florin papagheorghe3, georgeta popa4, alexandru vlad ciurea5,6 1 department of neurosurgery, sanador clinical hospital, bucharest, romania 2 department of neurosurgery, national institute of neurology and neurovascular diseases, bucharest, romania 3 department of neurosurgery, bucharest emergency university hospital, bucharest, romania 4 department of radiology and medical imaging, sanador clinical hospital, bucharest, romania 5 department of neurosurgery sanador clinical hospital, bucharest, romania 6 “carol davila” university of medicine and pharmacy, bucharest, romania abstract introduction: cavernomas are one of the four types of vascular malformations which develop in the central nervous system. from an imaging point of view, they are low flow small vessel malformations that cannot be seen on conventional angiography and are rarely visible on ct. they can be seen on mri because of the para-magnetic haemoglobin break-down products within them. case presentation: a 35 years old male presented at the emergency room following a tonic-clonic seizure, without urine emission. after a clinical exam, it was decided to perform a cerebral mri with contrast substance and angiographic sequence. clinical and imagistic results showed a superficial left temporal cavernoma, which showed signs of recent bleeding. after the surgery, the patient has no neurological deficits and is discharged afebrile and without any other symptoms. at 6 weeks after the surgery, the patients returned for neurosurgical reevaluation in perfect neurological condition, without motor deficit or intracranial hypertension. conclusions: cavernomas are angiographic cryptic vascular lesions that need an mri investigation in order to appreciate them correctly. introduction cavernomas are one of the five types of vascular malformations which develop in the central nervous system, representing about 5-15% in keywords cavernomas, gks, neurosurgery corresponding author: alexandru vlad ciurea professor. “carol davila” university of medicine and pharmacy, bucharest, romania prof.avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 413 the importance of nuclear magnetic resonance (mri) in the diagnosis of cerebral cavernomas. total. cerebral cavernomas are cryptic angiographic lesions, classically defined as dilated vascular structures, with thin walls, located in the cns (central nervous system), without any cerebral parenchyma interposed. [1,2] in 1984, mccormick presented a study in which out of 5734 autopsies, only 19 cavernomas were discovered. this results in an incidence of 0.34%. a few years later, otten et al report 131 cases of cavernomas out of a group of 24,535 autopsies. thus, the incidence was 0.53%. [3] according to mccormick's 1966 classification, neurovascular malformations can be divided into 5 large categories: [4] • telangiectasias • varicose veins • cavernous malformations • arteriovenous malformations (avm) • venous angiomas this classification was later modified: varicose veins were combined with venous malformations/venous angiomas and were put together in the category of venous developmental abnormalities (adv). several pathological classification criteria for each malformation have been suggested in the literature, but their nomenclature and structuring criteria are ambiguous and variable. in addition, cases of mixed forms and transitions from one form to another have been reported. also, in the literature there are cases of coexistence of these malformations. the most common malformation associated with cavernomas is adv. another common combination is capillary telangiectasia. a few similarities such as pontin damage, the presence of a family form and multiplicity are reasons to consider telangiectasias a precursor to cavernomas. [3] the term “cavernoma” was used for the first time by rokitansky in 1846 and it was referring to a vascular lesion located in the brain. later, in 1956 rudolf virchow made for the first time a histopathological description of these lesions. in 1956, crawford and russel introduced the term cryptic, to describe an arterio-venous pathology or venous hamartomas located in the encephalon and which often led to hemorrhage. later, this term was used for the cerebrovascular lesions which couldn’t be observed on angiography, along with the term „angiographically occult vascular malformation”. the current nomenclature includes the following terms: cavernoma, cavernous angioma, cavernous hemangioma or cavernous malformations.[5] the use of mri leads to the diagnosis of cavernomas even before the histopathological diagnosis. the right treatment of these lesions requires a good knowledge of epidemiology, histopathological characteristics and of their natural evolution. the clinical picture of cavernous angiomas varies significantly, by including asymptomatic forms which are discovered on ct or mri examination (performed for a headache syndrome or after a traumatic event), but also forms discovered during autopsy after a fatal intracranial hemorrhage. neuroimaging diagnosis today, the advances in neuroimaging allow the diagnosis of cavernomas even before the histopathological exam. the ct examination shows a spontaneously hyperdense lesion, given the inhomogeneous hemosiderin impregnation, with a round welldefined contour or irregular shape. after administering the contrast substance, cavernomas have different behaviors, in some cases appearing filled with contrast substance, especially if the examination is performed tardy. it is worth noting that these lesions are characterized by a slow flow and that in some cases, calcifications can be seen at this level. the mri examination represents the „gold standard” for the diagnosis in most cases. the typical image for a cavernoma is a well-circumscribed lesion, with an inhomogeneous “popcorn” appearance and an hypointense ring on the outside which represents the hemosiderin impregnation. traces of older or more recent microhemorrhages can be seen in the lesion or in the adjacent areas. rarely, a draining vein can be seen. in the t2 sequence of mri we can see a hypointense area at the periphery of the lesion due to the edema of the parenchyma. (figure 1) figure 1. cerebral mri: left infratentorial cerebellar 414 dan bentia, andrei alexandru marinescu, florin papagheorghe et al. cavernoma. (from the personal collection of prof. alexandru vlad ciurea, md. phd.) cerebral angiography is negative in most of the cases, cavernomas representing most of the occult vascular malformations. rarely, it can show an avascular area or a capillary cluster. usually, it is not indicated for cavernomas diagnosis unless it is necessary to obtain information regarding the vascular anatomy of the region or if an association with another vascular malformation is suspected. therapeutic attitude cavernomas, being by their nature well-defined lesions, with feeding vessels with a reduced blood flow, offer the premises for a total surgical resection. currently, there is a general attitude of extending the surgical indications even in young patients, with minor symptoms, thus removing the risk of hemorrhage and its consequences. this therapeutical attitude is possible thanks to the advances in neuroimaging and the introduction of neuronavigation, it is worth noting that complications may occur in lesions with critical locations: cortical or subcortical cavernomas of eloquent areas or deep regions, such as the basal nuclei, thalamus, corpus callosum, paraventricular or brainstem. case presentation male patient, 35 years old, with no neurological pathology associated, came in the emergency room of sanador clinical hospital following a tonic-clonic seizure, without urine emission. following the neurological and neurosurgical consult, it was decided to perform a cerebral mri with contrast substance and angiographic sequence. (figure 2) figure 2. cerebral mri with contrast substance which shows a left temporal cavernoma, with recent haemorrhage. clinical and imagistic evaluation of the patient showed a superficial left temporal cavernoma, which showed signs of recent bleeding. together with the neurosurgical team from sanador clinical hospital, it is decided to perform the total ablation of the cavernoma using kinevo 900 operating microscope and neuronavigation. after the surgery, the patient has no neurological deficits and is discharged afebrile and without any other symptoms. at 6 weeks after the surgery, the patients returned for neurosurgical reevaluation in perfect neurological condition, without motor deficit or intracranial hypertension. this is confirmed by the postoperative mri with contrast substance. (figure 3) figure 3. postoperative cerebral mri with contrast substance which shows total ablation of the left temporal cavernoma. discussions cavernomas are low flow small vessel malformations that cannot be seen on conventional angiography and are rarely visible on ct, so if we want to be certain of the diagnosis, we must perform an mri. this type of imaging can show us the cavernous malformations because of the paramagnetic hemoglobin break-down products within them. over time, it has been debated what is the best treatment for cavernomas, between surgical approach, radiotherapy (gks) and conservative treatment. according to the literature, the best approach is the neurosurgical one in the case of symptomatic, superficial lesions that are not located in the eloquent area. for the other cavernomas (asymptomatic, multiple, located in eloquent or deep areas) the risk-benefit ratio must be balanced. so, it will be decided together with the patient, between the surgical approach and the conservative treatment. h. bertalanffy et al. (2001) presented an analysis that consist 72 patients operated in 5 years, of which 24 had the lesion located within the brainstem, 18 415 the importance of nuclear magnetic resonance (mri) in the diagnosis of cerebral cavernomas. within the deep white matter of the hemispheres, 12 in the basal ganglia or thalamus, 11 in superficial areas of the hemispheres and seven within the cerebellum. they reinforce the fact that angiography was the first imaging study used to see cerebrovascular malformations, but it shows no pathological changes. in the mid-1970s, the computed tomography (ct) became available and the detection of symptomatic cavernomas increased significantly, but this kind of imaging study has poor specificity. the most important and with the highest accuracy imaging study is mri.[6] rigamonti et al., being one of the firsts to describe the mri features of cavernomas, are recalled in this study for their article in which they presented the differences between ct scan and mri. from 10 patients, ct scans detected 14 lesions, while mri detected 27 distinct lesions, so it can be seen how specific is mri besides ct scan for the cavernous malformations diagnosis.[7] d. cavalcanti et al. (2011) described that genetics have an important part in cavernous malformations. cavernomas can be both sporadic and familial. according to them, “half of ccms are familial, and they inherited in an autosomal dominant fashion with variable penetrance”. the most of familial ccms are identified on mri as multiple lesions. this multiplicity of lesions is characteristic in up to 84% of familial cases, whereas it is reported in 10%-33% of supposed sporadic cases. annually, up to 6.4% of familial cavernomas can bleed and become symptomatic. to date, 3 distinct loci have been mapped in different families, ccm1, ccm2 and ccm3. these 3 loci account for 70%-80% of all cases of familial ccms. multilocus linkage analysis showed 40% of inherited cases that ccm1 account, 20% for ccm2 and 40% for ccm3.[8] the radiotherapeutic approach for cavernomas has been in constant debate since the invention of gamma knife surgery. still, this controversy reached a conclusion when one of the founders of gks, ladislau steiner published his comprehensive comparative study on this subject. l. steiner et al. (2010) came to the conclusion that gks it is not an effective approach for cavernous malformations and the surgical approach remains the best choice in treating this pathology.[9] j. k. liu et al. (2010) found in their article about cavernous malformations that the ct scans showed the oph cms as suprasellar hyperdense masses. cerebral angiography did not reveal any arterial feeding vessels. mri was performed at 88% of cases and the cavernomas could be seen as heterogenous with mixed signal intensities suggestive of different ages of blood, this appearance often described as a “popcorn-like” lesion.[10] in another case presentations similar to ours, p. feizi et al. (2020) described that a 50 years old woman has presented to the emergency room following new onset seizures and express her symptoms as right arm jerking, drooling, and encephalopathy. ct scans without contrast were effectuated and the results were multiple supratentorial and infratentorial hyperdensities measuring up to 8 mm, which were concerning for possible hemorrhagic metastases in the setting of history of malignancy. [11] an mri was performed too, with and without contrast, and was demonstrated that some of the lesions had peripheral vasogenic edema, and internal hyperperfusion. based on those imaging and clinical data and the patient`s known history of thyroid carcinoma, the first diagnosis was “possible multiple hemorrhagic brain metastases”. threemonth follow-up mri of the brain demonstrated vasogenic edema and left parietal lesion with a surrounding hemosiderin ring and heterogeneous internal signal now able to be visualized. so, the diagnosis of cavernous malformations became evident.[11] figure 4. (a) ct scan; (b) mri with swi sequence; (c) t1 mri image source: feizi p, lakhani da, kataria s, et al. multiple cerebral cavernous haemangiomas masquerading as haemorrhagic brain metastases. radiol case rep. 2020 aug 20;15(10):1973-1977. licensed under cc by-nc-nd 4.0; © 2020 the authors conclusions cavernomas are angiographic cryptic vascular lesions which need an mri investigation in order to appreciate them correctly. in the case of small cavernomas, such as the one presented, the ct examination does not reveal the lesion. thus, mri is a valuable investigation for neurosurgical 416 dan bentia, andrei alexandru marinescu, florin papagheorghe et al. emergencies, especially if the patient has a new comitial seizure, is young and does not have other neurological pathologies associated. references 1. gross ba, du r. diagnosis and treatment of vascular malformations of the brain. current treatment options in neurology. 2014;16(1). 2. mccormick wf, nofzinger jd. “cryptic” vascular malformations of the central nervous system. journal of neurosurgery. 1966;24(5):865-875. 3. kivelev j. brain and spinal cavernomas – helsinki experience. phd thesis. institute of clinical medicine, faculty of medicine, helsinki: university of helsinki; 2010 4. florian is, abrudan c, horațiu i. cavernoamele cerebrale in ciurea av. (coord), tratat de neurochirurgie, vol. 2. editura medicala; 2011; 159-170 5. kivelev j, niemelä m, hernesniemi j. treatment strategies in cavernomas of the brain and spine. journal of clinical neuroscience. 2012;19(4):491-497. 6. bertalanffy h, benes l, miyazawa t, alberti o, siegel am, sure u. cerebral cavernomas in the adult. review of the literature and analysis of 72 surgically treated patients. neurosurg rev. 2002; 25(1-2):1-53; discussion 54-5. 7. rigamonti d, drayer bp, johnson pc, hadley mn, zabramski j, spetzler rf. the mri appearance of cavernous malformations (angiomas). j neurosurg. 1987; 67(4):518-24. 8. cavalcanti dd, kalani my, martirosyan nl, eales j, spetzler rf, preul mc. cerebral cavernous malformations: from genes to proteins to disease. j neurosurg. 2012; 116(1):122-32. 9. steiner l, karlsson b, yen cp, torner jc, lindquist c, schlesinger d. radiosurgery in cavernous malformations: anatomy of a controversy. j neurosurg. 2010; 113(1):1621; discussion 21-2. 10. liu jk, lu y, raslan am, gultekin sh, delashaw jb jr. cavernous malformations of the optic pathway and hypothalamus: analysis of 65 cases in the literature. neurosurg focus. 2010; 29(3): e17. 11. feizi p, lakhani da, kataria s, srivastava s, tarabishy ar, deib g, sriwastava s. multiple cerebral cavernous hemangiomas masquerading as hemorrhagic brain metastases. radiol case rep. 2020; 15(10):1973-1977. maniram_moyamoyadisease 132 maniram et al moyamoya disease presenting as acute onset cortical blindness moyamoya disease presenting as acute onset cortical blindness: a case report dudi maniram1, bansal rajeev1, srivastava trilochan2, sardana r.v.3 sms medical college and hospitals jaipur, india 1neurosurgery; 2department of neurology; 3department of neurosurgery abstract: we report a case where acute onset cortical blindness is the mode of presentation in moyamoya disease. cortical blindness is very rare presenting symptom of moyamoya disease. progressive visual loss and homonymous anopsia has been described previously, but this case had acute visual loss. key words: moyamoya disease, cortical blindness, angiography introduction moyamoya disease is a rare progressive vasoocclusive disorder of an unknown etiology. it is characterized by progressive stenosis of terminal portions of internal carotid arteries bilaterally, and the main trunks of anterior and middle cerebral artery, and is associated with collateral vessels at the base of the brain ('moyamoya' vessels). the term moyamoya is a japanese word which means “a puff of smoke”. it was coined by suzuki and takaku in 1969 to describe the angiographic appearance of the collateral vessels at the base of brain in a group of 21 patients with internal carotid arterial occlusion. (16) the histopathology of the affected arteries demonstrate a fibrocellular thickening of the intima, proliferated smooth muscle cells, prominently tortuous and often duplicates internal elastic lamina, with no inflammatory or atheromatous involvement. (18) moyamoya disease can present as progressive visual loss and homonymous anopsia which has been described previously. (14, 15) case report a 12 year old girl admitted to our department had history of loss of vision in both eyes within 3 hours. the vision improved slightly after 10 days with perception of hand movements at 1 foot. brain ct showed small multiple infarcts and large bilateral parietooccipital lobe infarcts (figure 1a) and brain t2w mri showed flow voids around midbrain (1b). cerebral digital substraction angiography revealed occlusion of both supraclinoid internal carotid artery (figures 2a and 2b) with collateral circulation from multiple enlarged lenticulostriate (figure 2c) and thalamoperforating arteries (figure 2d) romanian neurosurgery (2016) xxx 1: 132 135 133 suggestive of moyamoya disease. the detailed laboratory workup did not reveal any cause of progressive arteriopathy. cortical blindness is very rare presenting symptom of moyamoya disease. moyamoya disease can present as progressive visual loss and homonymous anopsia which has been described previously, but this case had acute visual loss. figure 1 brain ct shows bilateral parieto-occipital lobe infarcts (1a). brain mri shows flow voids around midbrain (1b) figure 2 cerebral digital substraction angiography revealed occlusion of both supraclinoid internal carotid artery (2a & 2b) with collateral circulation from multiple enlarged lenticulostriate (2c) and thalamoperforating arteries (2d) suggestive of moyamoya disease discussion moyamoya disease, first described by takeuchi and shimizu, is a rare cerebrovascular condition characterized by progressive stenosis of bilateral internal carotid arteries with compensatory formation of extensive collateral circulation by the dural, leptomeningeal and other perforating blood vessels giving rise to the typical “a puff of smoke” appearance in angiogram (17). moyamoya disease is reported to primarily present at an early age, typically less than 10 years, and is more common in females (m:f 1:1.8). however, a second peak in the fourth decade has also been described in the literature. (10) etiology of moyamoya disease is controversial. even though several linkage studies have shown promising relations with gene loci (7, 8), no specific locus has yet been identified. however, these linkage studies, along with the familial occurrence of moyamoya, point towards a probable genetic basis underlying its etiology. investigations into understanding the pathogenesis of moyamoya disease have shown involvement of the csf basic fibroblast growth factor with receptor up regulation, and tgf beta 1 in altering the cerebral vasculature (2, 4, 12). intimal thickening has also been postulated resulting from altered permeability owing to enhanced prostaglandin release from the arterial smooth muscle. (19) the clinical features of patients with 134 maniram et al moyamoya disease presenting as acute onset cortical blindness moyamoya disease reflect the anatomic territory of the brain affected by the diseased vessel. yamaguchi et al. in the annual report for the special working group of welfare ministry for moyamoya in 1979 described four major types of moyamoya disease according to clinical manifestations; the hemorrhagic type, the infarction type, tia type, and epileptic type; with the first two types being the most common. (11) despite the reported risks associated with conventional angiography (5), it is still considered the gold standard for diagnosing moyamoya disease. mr angiography proved to be a helpful diagnostic tool identifying sites of stenosis and demonstrating the collateral vessels at the base of the brain. as a noninvasive procedure, it has been described in the literature as a promising alternative to classical angiography for this arterial disease (16). irrespective of the radiological method used for diagnosis, conditions like von recklinghausen's disease, down's syndrome, autoimmune vasculitis, head trauma, meningitis and brain tumors may have a similar angiographic picture and hence can possibly confuse the diagnosis. also, postpartum cerebral angiopathy and inflammatory angiopathy are two important differential diagnoses that may present with cerebral ischemia and imaging consistent with intracranial vasculopathy mimicking moyamoya disease. (9, 13) four types of surgical procedures have been described indirect procedures including encephaloduroarteriomyosynangiosis, direct revascularization via the superficial temporal artery and the middle cerebral artery bypass, combined approaches and rarely, denervation of cerebral vasculature. in general, pediatric cases benefit from indirect revascularization procedures and the direct bypass is useful in most of adult cases. (6) correspondence dr. rajeev bansal mch neurosurgery resident sms medical college and hospitals jaipur, india +91-9680310331 rajeev_bansal234@yahoo.co.in references 1. battistella pa, carollo c, pellegrino pa, soriani s, scarpa p: magnetic resonance angiography in moyamoya disease. childs nerv syst 1995, 11(6):329334. 2. fukui m: current state of study on moyamoya disease in japan.surgical neurology 1997, 47(2):138143. 3. goto y, yonekawa y: worldwide distribution of moyamoya disease. neurologia medicochirurgica 1992, 32(12):883886. 4. gosalakkal ja: moyamoya disease: a review. neurology india 2002, 50(1):610. 5. hankey gj, warlow cp, sellar rj: cerebral angiographic risk in mild cerebrovascular disease. stroke; a journal of cerebral circulation 1990, 21(2):209222. 6. houkin k, kuroda s, ishikawa t, abe h: neovascularization (angiogenesis) after revascularization in moyamoya disease. which technique is most useful for moyamoya disease? acta neurochirurgica 2000, 142(3):269276. 7. ikeda h, sasaki t, yoshimoto t, fukui m, arinami t: mapping of a familial moyamoya disease gene to chromosome 3p24.2p26. american journal of human genetics 1999, 64(2):533537. 8. inoue tk, ikezaki k, sasazuki t, matsushima t, fukui m: linkage analysis of moyamoya disease on chromosome 6. journal of child neurology 2000, 15(3):179182. 9. ishimori ml, cohen sn, hallegua ds, moser fg, weisman mh: ischemic stroke in a postpartum patient: romanian neurosurgery (2016) xxx 1: 132 135 135 understanding the epidemiology, pathogenesis, and outcome of moyamoya disease. 10. junichi m, jun o, takenori y: moyamoya disease. in stroke: pathophysiology, diagnosis and management. 3rd edition. edited by barnett h, mohr j, bernett m.edinburgh: churchill livingstone; 1998:815831. 11. maki y, enomoto t: moyamoya disease. volume 4. springer; 1988::204212. 12. malek am, connors s, robertson rl, folkman j, scott rm: elevation of cerebrospinal fluid levels of basic fibroblast growth factor in moyamoya and central nervous system disorders. pediatric neurosurgery 1997, 27(4):182189. 13. okamoto y, yamamoto t: postpartum angiopathy associated with reversible borderzone ischemia. internal medicine (tokyo, japan) 2008, 47(4):309312. 14. provost tt, moses h, morris el, altman j, harley jb, alexndor e, reichlin m. cerebral vasculopathy associated with collateralization resembling moyamoya phenomenon and with antiro/ss-a and antila/ss-b antibodies. arthritis rheum. 1991;34:1052-1055. 15. revascularization of calcarine artery in moyamoya disease: oa – cortical pca anastomosiscase report. neurol med chir (tokyo) 1991;31: 658-661. 16. suzuki j, takaku a: cerebrovascular "moyamoya" disease. disease showing abnormal net like vessels in base of brain.archives of neurology 1969, 20(3):288299. 17. takeuchi k, shimizu k . hypogenesis of bilateral internal carotid arteries. no ta shinkai 1957; 9: 37-43 18. yamashita m, oka k, tanaka k. histopathology of the vascular network in moyamoya disease. stroke 1983: 14: 50-8 19. yamamoto m, aoyagi m, fukai n, matsushima y, yamamoto k: increase in prostaglandin e(2) production by interleukin1beta in arterial smooth muscle cells derived from patients with moyamoya disease. circulation research 1999, 85(10):912918. doi: 10.33962/roneuro-2021-061 a case of sellar epidermoid tumour with haemorrhage ajaya kumar a., geetha gopal k. romanian neurosurgery (2021) xxxv (3): pp. 361-364 doi: 10.33962/roneuro-2021-061 www.journals.lapub.co.uk/index.php/roneurosurgery a case of sellar epidermoid tumour with haemorrhage ajaya kumar a., geetha gopal k. muthoot hospital, kozhencherry, pathanamthitta, india abstract introduction: intracranial epidermoid cysts are congenital inclusion tumours. cerebellopontine angle and parasellar locations are the common locations. this is a report of an intrasellar epidermoid cyst with haemorrhage, which is rare. case report: a 70-year-old female presented with bifrontal headache, vertigo, and nasal discharge. contrast-enhanced magnetic resonance imaging [mri] showed heterogeneously enhancing lesion in sella turcica. internal hemorrhagic foci were seen. computed tomography [ct] scan showed a slightly hyperdense tumour of sella. transnasal transsphenoidal excision was done. hemorrhagic and colloid material came out. histopathological examination showed cyst lined by stratified squamous epithelium with keratohyalin granules and keratin flakes, suggestive of an epidermoid cyst. discussion: usually epidermoid cyst is hypodense in ct scan. but hyperdensity can occur due to calcification of keratinized debris, increased protein content, and recurrent haemorrhage. enhancement with gadolinium in mri is mild and in cyst wall. haemorrhage and enhancement are probably due to foreign body granulation tissue developing from leakage. introduction intracranial epidermoid cysts are congenital inclusion tumors arising from the remnants of epithelial tissue during the closure of neural tube [1,2]. they constitute 0.8-1.2% of intracranial tumors. cerebellopontine angle is the most common location. but they can be seen in parasellar, suprasellar, middle fossa, and diploic locations. intrasellar location is rare. maccarty et al. reported four cases of sellar epidermoid with suprasellar or parasellar extension [3]. case report a 70-year-old female presented with bifrontal headache, vertigo, and nasal discharge. she had systemic hypertension, diabetes mellitus, and dyslipidemia. neurological examination was noncontributory. visual fields were normal. pupillary reaction was normal. there was mild ataxia on walking. contrast enhanced magnetic resonance imaging [mri] showed heterogenously enhancing lesion in sella turcica [fig.1]. coronal image showed capsular enhancement and thin sellar floor . internal keywords sella turcica, epidermoid cyst, haemorrhage, microsurgery, endoscopy corresponding author: ajaya kumar ayyappan unnithan muthoot hospital, kozhencherry, pathanamthitta, india drajayakumara@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 362 ajaya kumar a., geetha gopal k. hemorrhagic foci were seen. there was no compression on optic chiasm. computed tomography [ct] scan showed slightly hyperdense tumor of sella [fig. 2]. septation was seen in right half of sphenoid sinus. figure 1. mri coronalimage showing heterogeneous tumor with capsular enhancement and thin sellarfloor figure 2. ct scan showing hyperdense tumor of sella figure 3. cyst linedby stratified squamous epithelium and hemorrhage with inflammatory cells figure 4. high powerview of keratin flakes transnasal transsphenoidal excision was done. left side was chosen because of sphenoid septation on right side. left sphenoidal ostium was found following middle turbinate. ostium was enlarged. dura was opened and piecemeal decompression was done. hemorrhagic and colloid material came out. decompression was done till increased urine output was noticed. fat pad was used for closing the sphenoid. she recovered clinically. hourly urine output was in normal range. hormonal levels such as thyroid function tests, cortisol, and prolactin were within normal limits. postoperative ct scan showed gross total removal. initial squash cytology showed fibrocollagenous fragments, cells with round nuclei and eosinophilic cytoplasm, and red blood cells. this was suggestive of inflammatory tissue with hemorrhage. histopathological examination showed cyst lined by stratified squamous epithelium with 363 a case of sellar epidermoid tumour with haemorrhage keratohyaline granules and keratin flakes [fig. 3, and 4]. immunohistochemistry was positive for p63, suggestive of squamous differentiation. the features are of an epidermoid cyst. discussion the clinical presentations of sellar epidermoid tumors are frontal headache, bitemporal hemianopia, visual loss, diplopia, amenorrhea, galactorrhea, diabetes insipidus, failure of sexual development, and endocrine disturbances [2,3,4,5]. presentation with features of pituitary apoplexy also is reported6. the usual finding in ct scan is a hypodense lesion, due to lipid and cholesterol content [1,2]. but hyperdensity can occur due to calcification of keratinized debris, increased protein content, and recurrent hemorrhage. epidermoid tumor appears hypo-, isoor hyper-intense on t1-weighted mri7. on t2-weighted imaging, it appears hyper-intense. heterogeneous appearance also is described. diffusion weighted imaging of mri shows a restricted pattern as hyperintensity. the cyst appears insinuating into nearby structures. enhancement with gadolinium is mild and in cyst wall. differential diagnoses are pituitary adenoma, craniopharyngioma, arachnoid cyst, rathke’s cleft cyst, and dermoid cyst. pituitary adenomas are usually solid and has homogeneous enhancement8. craniopharyngioma has calcifications in ct and mixed solid and cystic appearances in mri7. arachnoid cyst is isointense to cerebrospinal fluid(csf) in all sequences. dermoid cyst resembles fat and appear hyperintense in t1-weighted image. because of avascular nature, hemorrhage is rare in epidermoid cyst9. hemorrhage and enhancement are probably due to foreign body granulation tissue developing from leakage. surgery is by endonasal transsphenoidal microsurgery or by endoscopic endonasal transsphenoidal approach [2,3,5,6]. often, the adherence of capsule with neurovascular structures prevented complete removal of the cyst wall. modification of endoscopic endonasal approach according to the extent of the tumor, can help in gross total removal2. total removal prevents recurrence with malignant change in future. on histopathological examination, epidermoid cyst is lined by keratinizing stratified squamous epithelium10. keratohyaline granules are basophilic granules in the cytoplasm of granular cells. keratin flakes also can be seen. the cyst is filled with keratin debris, lipid, and water. immunohistochemical positivity for p63 is useful in confirming squamous differentiation [11]. dermoid cyst is lined by simple stratified squamous epithelium1. rathke’s cleft cyst is lined by simple cuboidal or columnar epithelium with goblet cells. carcinoma in situ can occur in residual epidermoid cyst as a sequelae of inflammatory response to recurrent rupture and foreign body reaction [1,2]. the sellar tumors which were reported to present with hemorrhage are pituitary adenomas, craniopharyngiomas, epidermoid cyst, undifferentiated sarcoma, tuberculoma, atypical teratoid/rhabdoid tumor, and primary melanocytic tumor [12,13,14,15,16]. so these differential diagnoses also should be considered in case of a hemorrhagic sellar tumor. conclusion this is a report of an intrasellar epidermoid cyst with hemorrhage, which is rare. ct scan showed hyperdensity due to hemorrhage. there was enhancement with contrast in mri. hemorrhage and enhancement occur due to inflammatory tissue. transsphenoidal microsurgery and endoscopic endonasal approach are the preferred surgical methods. total resection is necessary to prevent malignant transformation. references 1. reddy mp, jiacheng s, xunning h, zhanlong m: intracranial epidermoid cyst: characteristics, appearance, diagnosis, treatment and prognosis. 2015 jun; sci lett 3:102–110. 2. nakassa aci, chabot jd, snyderman ch, wang ew, gardner pa, fernandez-miranda jc. complete endoscopic resection of a pituitary stalk epidermoid cyst using a combined infrasellar interpituitary and suprasellar endonasal approach: case report. j neurosurg. 2018 feb;128(2):437-443. 3. boggan je, davis rl, zorman g, wilson cb. intrasellar epidermoid cyst. case report. j neurosurg. 1983 mar;58(3):411-5. 4. fawcitt ra, isherwood i. radiodiagnosis of intracranial pearly tumours with particular reference to the value of computer tomography. neuroradiology. 1976 sep 21;11(5):235-42. 5. costa f, felisati g, maccari a, bauer d, lasio g: epidermoid cyst of the pituitary stalk: case report and 364 ajaya kumar a., geetha gopal k. review of the literature. neurosurg q. 2013 may; 23:108– 111. 6. tuna h, torun f, torun an, erdogan a. intrasellar epidermoid cyst presenting as pituitary apoplexy. j clin neurosci. 2008 oct;15(10):1154-6. 7. huo cw, caputo c, wang yy. suprasellar keratinous cyst: a case report and review on its radiological features and treatment outcome. surg neurol int. 2018 jan;9:15. 8. choi sh, kwon bj, na dg, kim jh, han mh, chang kh. pituitary adenoma, craniopharyngioma, and rathke cleft cyst involving both intrasellar and suprasellar regions: differentiation using mri. clin radiol. 2007;62(5):453-462. 9. chen cy, wong js, hsieh sc, chu js, chan wp. intracranial epidermoid cyst with hemorrhage: mr imaging findings. ajnr am j neuroradiol. 2006 feb;27(2):427-9. 10. mccormack ep, cappuzzo jm, litvack z, almira-suarez mi, sherman js. suprasellar epidermoid cyst originating from the infundibulum: case report and literature review. cureus. 2018 aug 29;10(8):e3226. 11. compton la, murphy gf, lian cg. diagnostic immunohistochemistry in cutaneous neoplasia: an update. dermatopathology (basel). 2015 apr 8;2(1):1542. 12. yousem dm, arrington ja, kumar aj, bryan rn. bright lesions on sellar/parasellar t1-weighted scans. clin imaging. 1990;14(2):99-105. 13. ganaha t, inamasu j, oheda m, hasegawa m, hirose y, abe m. subarachnoid hemorrhage caused by an undifferentiated sarcoma of the sellar region. surg neurol int. 2016;7(suppl 16):s459-s462. published 2016 jul 7. 14. mittal p, dua s, saggar k, gupta k. magnetic resonance findings in sellar and suprasellar tuberculoma with hemorrhage. surg neurol int. 2010;1:73. published 2010 nov 20. doi:10.4103/2152-7806.72624. 15. siddiqui m, thoms d, samples d, caron j. atypical teratoid/rhabdoid tumor presenting with subarachnoid and intraventricular hemorrhage. surg neurol int. 2019;10:139. published 2019 jul 5. doi:10.25259/sni-592019. 16. zhou hj, zhan ry, ma yh, cao f, zheng xj. primary sellar melanocytic tumor mimicking hemorrhagic pituitary macroadenoma: case report and literature review. br j neurosurg. 2015;29(2):298-302. doi:10.3109/02688697.2 014.967752. 21_sharmaanand_intraoperativecontralateral 368 sharma et al intraoperative contralateral extradural hematoma intraoperative contralateral extradural hematoma during evacuation of traumatic acute extradural hematoma anand sharma1, arti sharma2, yashbir dewan1 1artemis health institute, gurgaon, india 2nscb medical college, jabalpur, india abstract: introduction: extradural hematomas (edhs) accounts for approximately 2% of patients following head trauma and 5-15% of patients with fatal head injuries. when indicated, the standard surgical management consists of evacuation of the hematoma via craniotomy. intraoperative development of acute extradural hematoma (aedh) on the contralateral side following evacuation of acute extradural hematoma is uncommon and very few cases have been reported. case report: we report a case of 28 year-old-male who suffered from a severe head injury following assault and diagnosed as acute extradural hematoma over right fronto-parietal region with midline shift towards left. patient underwent emergency craniotomy with acute edh evacuation. following evacuation of acute edh the duramater was tense which was unusual finding. with anticipation of underling acute sdh small durotomy was done, but there were no sub dural hematoma. bone flap were repositioned and closure were done. patient was shifted for ncct head from ot, which revealed 2.7cm acute edh over left frantoparietal region. patient was again shifted back to ot and left frontoparietal craniotomy with evacuation of hematoma was done. postoperative ncct head was satisfactory. however, the patient remained severely disabled. conclusion: formation of contralateral edh after aedh surgery is a rare but potentially dangerous complication. a high degree of suspicion should be kept for contralateral extradural hematoma if during surgery there is tense duramater following aedh evacuation. we would advise urgent ncct head especially if a fracture is demonstrated on the preoperative ct scan on contralateral side. this would save some invaluable time, which may help in changing the outcome in some of the patients. key words: traumatic acute extradural hematoma, skull fracture, tense duramater, head injury introduction extradural hematomas
(edhs) accounts for approximately 2% of patients following head trauma and 5-15% of patients with fatal head injuries (8). an associated skull fracture is present in ~75% of cases. intracranial acute epidural hematoma is considered to be the most serious complication of head injury, requiring immediate diagnosis and surgical intervention. when indicated, the standard surgical management consists of evacuation of the hematoma via craniotomy. delayed romanian neurosurgery (2015) xxix 3: 368 372 369 formation of extradural hematoma (edh) on the contralateral side is a known entity (1) but intraoperative development of edh on the contralateral side following evacuation of aedh is uncommon. if unrecognized, this condition can cause devastating consequences. in this report, we presented our experience of a young male who developed a contralateral edh during the removal of a traumatic acute extradural hematoma with short review of literature. case report a 28-year male suffered from a severe head injury following assault. he arrived after 6hours of injury, on arrival at the emergency room; he was unconscious with labored breathing and a scalp hematoma over right frontoparietal area. his gcs was e1v1m2 with bilateral 5mm, nonrecting pupils. he was managed in emergency room with intubation, general care and antiepileptics. ncct head revealed right fronto-parietal 2.6 cm acute edh (figure 1a, 1b) with left sided midline shift of 6mm with left temporal contusion. a right-sided craniotomy was immediately performed to evacuate the hematoma. bleeding source was a tear in anterior branch of middle meningeal artery at the level of skull fracture. following evacuation of acute edh the duramater was tense which was unusual finding. with anticipation of underling acute sdh small durotomy was done, but there were no hematoma. bone flap were repositioned and closure were done. patient was shifted for ncct head from ot. his ncct head revealed 2.7 cm acute edh over left frantoparietal region (figure 2); patient was again shifted back to ot and left frontoparietal craniotomy with evacuation of hematoma was done. again bleeding source was a tear in anterior branch of middle meningeal artery at the level of skull fracture. following evacuation duramater become lax. postoperative ncct head was satisfactory (figure 3). however, the patient remained severely disabled. figure 1 – a – ncct head: right fronto-parietal acute extradural hematoma with midline shift towards left. b – bony window revealed linear fracture at left frontotemporal region 370 sharma et al intraoperative contralateral extradural hematoma figure 2 – immediate postoperative ncct head, revealed acute extradural hematoma over left frontoparietal region with midline shift towards right figure 3 – ncct head (postoperative) discussion “intraoperative hematoma”(9) is defined as a hematoma, not present on initial ct scan, but one that develops on the contralateral side during the process of evacuation of an acute traumatic hematoma. in contrast, “delayed epidural hematoma” (9) is any edh developing after an initial ct scan had revealed no hematoma. however, delayed edh can develop at any time after the initial ct scan, especially if the initial ct scan is done early (within first few hours following injury), our case represents a type of intraoperative extra dural hematoma. pathophysiology for development of intraoperative edh is primarily related to rapid loss of tamponade effect on dura and skull during a craniotomy (9, 5, 7) and the possible sources of bleeding include a ruptured meningeal arterial branch (tamponade because of edema, clot), venous lacerations, causing low tension bleeding, or a skull fracture the possible cause of the edh in our case could be due to rapid evacuation of the aedh resulting in shifting of the brain towards the operated site with separation of the dura on opposite side. evacuation of hematoma might have caused the loss of tamponade effect and bleeding from middle meningeal artery. intraoperative edh manifests as tense duramater (6) (10) and after durotomy there is massive brain bulge from durotomy site due to severe brain shift. other causes of massive brain bulge include acute cerebral vascular engorgement due to loss of cerebral vasomotor tone, intracerebral hematoma, expansion of other contusions in the same or opposite hemisphere and acute subdural hematoma (9, 5). the diagnostic approach to possible contralateral intraoperative edhs is challenging. some authors have proposed intraoperative brain swelling, postoperative neurologic deterioration, papillary dilation contralateral to the operative side, seizures, and intractable raised intracranial pressure (icp) as some indicator for the detection of such pathology (3). on presentation of these sign, immediate ct scan of the head and treatment of the cause is essential to the survival of the patient (9, 5, 3, 2). mahindra et al recommends routine postoperative ct immediately after cranial surgery for head trauma, which would help in timely detection and treatment of such a complication (7). in our case we did immediate ncct head after the surgery with immediate evacuation of contralateral hematoma. a careful review of reported cases (9, 5, 3) of this disorder suggest that the outcome is better in those patients in whom the edh was responsible for the worsening neurologic status rather than the underlying brain injury, romanian neurosurgery (2015) xxix 3: 368 372 371 and in whom the recognition and treatment of the first and the contralateral hematoma was promptly undertaken. patients with diffuse parenchymal injury and delay in treatment evidenced by poor neurologic status from the instant of trauma did poorly. our report is compatible with this finding. however, we think that edh evacuation still has potential value in improving the prognosis in these patients with severe head injury unless they have expressed the signs of brainstem failure. so we should evacuate the edh promptly if it causes significant mass effect. our case represents a therapeutic challenge with development of contralateral acute extradural hematoma. a high degree of suspicion should be kept for contralateral extradural hematoma if during surgery there is tense duramater following aedh evacuation. we would advise urgent ncct head especially if a fracture is demonstrated on the preoperative ct scan on contralateral side. this would save some invaluable time, which may help in changing the outcome in some of the patients. correspondence dr. anand sharma mch neurosurgery, associate consultant, neurosurgery, artemis health sciences, gurgaon, 122003(india), ph: +91-9873190047 email: dranandsharma100123@gmail.com references 1.alappat jp, baiju, praveen , jaya kumar k, sanalkumar p. delayed extradural hematoma : a case report.
neurol india 2002; 50:313-5. 2.borovich b, braun j, guilburd jn, zaaroor m, michich m, levy l, lemberger a, grushkiewicz i, feinsod m. delayed onset of traumatic extradural hematoma. j neurosurg.1985;63:30-4. 3.borah n, dutta d, baishya bk, hussain z. contralateral extradural hematoma formation following evacuation of chronic subdural hematomaa case report and review of literature. indian journal of neurotrauma. 2015;i-3. 4.eftekhar b, ketabchi e, ghodsi m, esmaeeli b. bilateral asynchronous acute epidural hematoma: a case report. bmc emerg med. 2003 dec 30;3(1):1. 5.feuerman t, wackym pa, gade gf, lanman t. becker d. intraoperative development of contralateral epidural hematoma during evacuation of traumatic extraaxial hematoma. neurosurgery 1988; 23: 480-4. 6.matsuno a, katayama h, wada h, et al. significance of consecutive bilateral surgeries for patients with acute subdural hematoma who develop contralateral acute epi or subdural hematoma. surg neurol 2003; 60:23-30. 7.mohindra s, mukherjee kk, gupta r, et al. decompressive surgery for acute subdural haematoma leading to contralateral extradural haematoma: a report of two cases and review of literature. br j neurosurg 2005;19:490–4. 8.rajput dk, kamboj r, srivastav ak, kaval p, kumar r. is management of spontaneous intracranial extradural hematoma in chronic renal failure is different with traumatic extradural hematoma case report and review of literature: indian journal of neurotrauma. 2010; 7:8184. 9.singh m, ahmad f u, mahapatra ak. intraoperative development of contralateral extradural hematoma during evacuation of traumatic acute subdural hematoma: a rare cause of malignant brain bulge during surgery. indian journal of neurotrauma 2005; 2:139-140. 10.wani aa, dhar a, laherwal m, ramzan au, malik nk, nizami fa, wani ma. bilateral sequential developed asynchronous extradural haematomas. indian journal of neurotrauma 2010,7,79-80. 11_paper romanian neurosurgery (2015) xxix 4: 477 480 477 doi: 10.1515/romneu-2015-0063 non traumatic fractures of the lumbar spine and seizures: case report luis rafael moscote-salazar1, andres m. rubiano2, hernando raphael alvis-miranda3, gabriel alcala-cerra1 1neurosurgeon, universidad de cartagena, cisneuro research group-colombia 2neurosurgeon, universidad el bosque, bogota, colombia 3resident of neurosurgery, universidad de cartagena, cisneuro research group-colombia abstract: injury-induced seizures may appear clinically asymptomatic and can be easily monitored by the absence of trauma and post-ictal impairment of consciousness. patients with epilepsy have a higher risk of compression fractures, leading to serious musculoskeletal injuries, this type of non-traumatic compression fractures of the spine secondary to seizures are rare lesions, and is produced by the severe contraction of the paraspinal muscles that can achieve the thoracic spine fracture. seizures induced lesions may appear clinically asymptomatic and can be easily monitored by the absence of trauma and post-ictal impairment of consciousness. we present a case report. key words: injury-induced seizures, spine fractures introduction the spine may present a risk of fracture during seizures. basically two factors may increase the risk, first, frequent crises and second, altered bone metabolism by anticonvulsant drugs. we report here a case of this rare condition. this type of non-traumatic compression fractures of the spine secondary to seizures are unusual lesions and are generated by a severe contraction of the paravertebral muscles that can achieve spinal fracture in different segments. these lesions may be asymptomatic in the absence of trauma. case report male 46 years old with a history of seizures and back pain of two days, was referred to our neurosurgery department. on admission blood pressure was 140/80, heart rate 100/min and oxygen saturation 95%. past medical history neither an even of fall nor an accident. at presentation the neurological examination of upper and lower limbs was normal. he complained of pain in the lumbar area. lumbar spine ct revealed l2 fracture. (figure 1 and 2). the patient was treated with posterior fusion. 3 months after at the latest follow up visit, the patient had no problem and returned to his previous activity. 478 moscote-salazar et al non traumatic fractures of the lumbar spine and seizures figure 1 ct scan of lumbar spine showed a fracture of l2 figure 2 three-dimensional ct reconstruction of l2 fracture discussion it is usual that forces generated during a seizure can cause severe pain and walking impairment, basically due to the repeated contraction, relaxation and trembling of one or more muscles abruptly, being violent forces generated during seizure activity. (3, 4) it is recognized that forces generated during tonic-clonic seizure can cause axial skeletal trauma, including thoracic and lumbar fractures. clinical signs of unstable fractures can be subtle. manifestations can be similar to those exhibiting stable fractures with anterior edge depression, affecting only the anterior column, leaving intact the middle and posterior column. these fractures are termed wedge fractures. this type of fracture occurs when there is comminution of the posterior part of the vertebral body plus subluxations or dislocations associated with the interapophyseal joints. these are referred to as comminuted fractures. they can also split the spinal fractures with or without neurological injury irrespective of stability or instability. trauma to the spine especially fractures present with pain, functional disability, deformation, increased volume, bruising and crepitus in some cases associated with fracture of the vertebral body may be associated with damage to the posterior arch. a high index of clinical suspicion is guaranteed to patients suffering from tonic-clonic seizures with associated risk factors. (4) vigorous muscle contractions during a seizure can result in vertebral compression fracture, especially in the middle thoracic region, the production mechanism of spinal fractures is hyperextension. a complaint of back pain after isoniazid -induced seizures in patients raises a strong suspicion of vertebral fracture and should be evaluated radiologically. (7) despite the relative romanian neurosurgery (2015) xxix 4: 477 480 479 doi: 10.1515/romneu-2015-0063 frequency of vertebral compression fractures as a complication of seizures, burst fractures are rare. health professionals who care for patients in postictal state should maintain a high index of suspicion for secondary injury and a detailed clinical examination. if there is any doubt about the diagnosis, appropriate imaging should be employed. (5) patients with epilepsy taking antiepileptic drugs tend to have an increased risk of fractures. (6) vestergaard et al., in their meta-analysis studied the effects of epilepsy in the risk of fractures and changes in bone mineral density (bmd) in patients with epilepsy. a weighted estimate of the relative risk of fractures and changes in bmd (z-score) was calculated. a total of 11 studies on the risk of fracture and 12 studies on bmd were recovered. the relative risk of any fracture increased (2.2, 95% ci 1.9 to 2.5, five studies), and spine fractures (6.2, 2.5 to 15.5, three studies). a high proportion of fractures (35%) seemed related to seizures. spine (mean +/sem: -0.38 +/0.06) and hip (-0.56 +/0.06) bmd z -score was significantly reduced hip over the spine (2p <0.05). projected increases in the relative risk of any fracture bmd z scores were 1.2 to 1.3, and significantly lower than that observed (2p < 0.05). the deficit in bmd in patients with epilepsy is too small to explain the observed increase in fracture risk. the remaining increase in the risk of fracture may be associated with seizures. (8) diagnosis is made by a good history (if possible), neurological examination together with clinical manifestations ranging from a totally asymptomatic patient to tetraplegia, lesions to the cervical plexus, brachial, partial or complete spinal cord injury. hence the importance of evaluating the mechanism of injury and the status of the same order to progress in clinical diagnosis, determine the degree of neurological compromise, instability, and determine proper handling. imaging resources combined with the clinical findings confirm the diagnosis. the former include the simple rx as a timely measure of first instance, ct, mri, according to the patient's needs and myelography as the last option to discard movements that compress the spinal cord. conclusions column fractures secondary to a seizure are rare entities; however in the context of the forces generated violently during neuronal hyperexcitability motor reactions generated contractility and overextension. clinical and neurosurgeon should be aware of the possibility of skeletal muscle damage after a seizure. correspondence luis rafael moscote-salazar universidad de cartagena, cartagena de indias, colombia e-mail: mineurocirujano@aol.com references 1. mehlhorn at, strohm pc, hausschildt o, schmal h, südkamp np. seizure-induced muscle force can caused lumbar spine fracture. acta chir orthop traumatol cech [internet]. 2007 jun [cited 2014 apr 25];74(3):202–5. 2. gnanalingham k, macanovic m, joshi s, afshar f, yeh j. non-traumatic compression fractures of the thoracic spine following a seizure -treatment by percutaneous 480 moscote-salazar et al non traumatic fractures of the lumbar spine and seizures kyphoplasty. minim invasive neurosurg [internet]. 2004 aug [cited 2014 apr 24];47(4):256–7. 3. harrison principios de medicina interna. convulsiones y epilepsia en español. 16a edición. cap. 363. harrison online en español. mcgraw-hill. 2006 4. youssef ja, mccullen gm, brown cc. seizureinduced lumbar burst fracture. spine (phila pa 1976) [internet]. 1995 jun 1 [cited 2014 apr 25];20(11):1301–3. 5. napier rj, nolan pc. diagnosis of vertebral fractures in post-ictal patients. emerg med j [internet]. 2011 feb [cited 2014 apr 24];28(2):169–70. available from: http://www.ncbi.nlm.nih.gov/pubmed/20935331 6. shiek ahmad b, hill kd, o’brien tj, gorelik a, habib n, wark jd. falls and fractures in patients chronically treated with antiepileptic drugs. neurology [internet]. 2012 jul 10 [cited 2014 apr 16];79(2):145–51. 7. kalaci a, duru m, karazincir s, sevinç tt, kuvandik g, balci a. thoracic spine compression fracture during isoniazid-induced seizures: case report. pediatr emerg care [internet]. 2008 dec [cited 2014 apr 25];24(12):842–4. 8. vestergaard p. epilepsy, osteoporosis and fracture risk a meta-analysis. acta neurol scand [internet]. 2005 nov [cited 2014 apr 25];112(5):277–86. 1tascua_traumaticspine romanian neurosurgery (2015) xxix 2: 135 140 135 traumatic spine injuries in children. experience on 434 cases and therapeutic perspectives a. tascu1, fl. exergian2, s. daniel2, a. iliescu1, c. pascal1, g. popescu1, st.m. iencean3 1pediatric neurosurgical department, “bagdasar-arseni”clinical hospital, bucharest, romania 2spine surgery department, “bagdasar-arseni”clinical hospital, bucharest, romania 3“gr. t. popa” university of medicine and pharmacy, iassy, romania abstract: traumatic spine injuries in pediatric patients have a low incidence, mainly due to a more flexible spine and is a specific matter in comparison to spinal injury in adults. pediatric spine fractures constitute 1 to 3% of all pediatric fractures. between 20 % and 60% of the fractures occur in the lumbar and thoracic spine. these spine injury appeared most frequently in sport events, followed by traffic events and accidental falling. the vast majority of the children with spinal trauma had grade d and e lesions on frankel scale and had a good recovery in 1 to 3 months after the event. prognosis and outcome is better in children with spine trauma, reducing toward adolescence and in young adults and the death rate was extremely low compared to the adult population. key words: pediatric spine fractures, spinal cord injuries. introduction traumatic injury of the spine in children is a specific matter in comparison to spinal injury in adults. in young children, there is a larger head relative to the cervical spine and supporting structures, there is a higher elasticity (eight times) of the spine compared to the spinal cord. also, there is a greater mobility of the pediatric bones and ligaments. by 15 years of age, the spine undergoes progressive anatomical and biochemical changes. spinal stiffness increases gradually together with the growth of the ossification centers and the spinal synchondrosis fusion. thus, injuries of the spine in children result in age specific traumatic patterns. taking into account the child’s age at the time of injury, neonatal and infant spine injury is related to the obstetrical trauma, where the upper cervical spine is mostly involved, atlanto-occipital dislocation occurring with high frequency. spinal injuries also occur in abused children. for children under three years old, injuries of the upper cervical spine involving the spinal cord occur in 47% of cases, and vertebral injuries occur in 53% of cases. for the lower cervical spine, injuries implying the spinal 136 tascu et al traumatic spine injuries in children cord occur in 53% and injuries affecting the vertebrae in 47% of the patients. in children under 8 years old, the cervical spine is more often affected (70 to 87%), atlanto-oocipital dislocation being most frequently encountered, presenting a high mortality rate (70 to 100%). spinal trauma in children over 8 years old also affects the other levels of the spine and the trauma patterns start to be more similar to the adult population. in pediatric spine injuries, the standard techniques of immobilization and transport may induce secondary lesions in the case of an unstable spine. of great importance are the indirect signs of spinal injury in noncooperative children: chin and facial abrasions or posterior ligament defects on spinal clinical examination. imaging is very important but should be carefully assessed. pediatric spine fractures constitute 1 to 3% of all pediatric fractures. between 20 % and 60% of the fractures occur in the lumbar and thoracic spine. the incidence is higher in the lumbar spine in older children. material and methods our study includes 434 pediatric patients presenting with traumatic spine injuries, admitted in the spinal surgery and pediatric neurosurgery departments of the bagdasar arseni clinical hospital, from 2003 to 2013. the diagnosis was made by clinical and imaging exams. the patients were identified in the hospital’s data base, using the terms vertebral/spinal cord trauma, and the patients’ medical records were taken from the hospital archive. the study group was divided into 4 age-related subgroups (0 to 3 years old, 4 to 7 years old, 8 to 14 years old and 15 to 18 years old) taking into account the age related risk factors. the degree of neurological deficits was established using the frankel classification grading system. figure 1 classification by trauma mechanism results our study concluded that spine injury appeared most frequently in sport events, followed by traffic events and accidental falling (fig.1). other accidents resulted in spine injury in 17% of patients. more than half of the injuries occurred in boys and the sex ratio was 1.48:1. the majority of the cases didn’t require surgical intervention. still, 152 patients were surgically treated. conservative treatment included all therapeutical options from pain killers to cervical collars. based on the information extracted from the medical files, we could establish distinct injury profiles, explained by anatomical and biomechanical features, which differentiates the young patient with an immature spine from the adolescent with an adult-like spine. still, missed diagnosis at first evaluation romanian neurosurgery (2015) xxix 2: 135 140 137 was found in 24% of the children younger than 8 years old and in 15% patients over 9 years old, mostly cervical lesions. boys are more prone to spinal trauma. the cervical spine was the most frequent spine level involved, due to specific anatomical and functional features of children (learning to walk, run, climb). the cervical lesions appeared in 56,5% of cases (245 cases), thoracic lesions in 18% of the cases (78 cases) and lumbar lesions in 25.5% of the cases (111 cases). sport and falling accidents were the main cause, encountered in 53% of the patients. it is important to emphasize that spine concussions are almost equal in proportion with the rest of the other lesions (210 cases versus 234 cases) (figure 2). the vast majority of the children with spinal trauma had grade d and e lesions on frankel scale (table 1) and had a good recovery in 1 to 3 months after the event. in 66% of the cases the treatment was conservative (figure 3). figure 2 distribution by type of lesion table i frankel scale classification in our study group nr. crt. neurological injury number of cases % of cases 1 frankel a 57 13,1% 2 frankel b 25 5,7% 3 frankel c 47 10,8% 4 frankel d 142 32,7% 5 frankel e 163 37,5% figure 3 type of treatment case reports case presentation 1 an 11 year old boy who suffered an electrocution accident was admitted to the pediatric neurosurgical department with a frankel c neurological lesion by a c1/c2 dislocation. conservative treatment was decided by hallo west immobilization, resulting in slow recovery of the neurological deficits presented at admission, in cca. 5 months (figure 4). case presentation 2 a 16 year old girl had fallen from a height, followed by vertebral and spinal cord trauma, 138 tascu et al traumatic spine injuries in children with a frankel c neurological lesion produced by a t10 fracture. she was operated on and full recovery was obtained 4 months after surgery (figure 5). case presentation 3 this case relates to a 12 years old girl who was involved in a traffic accident and had a l5 fracture. the treatment was conservative (figure 6). figure 4a ct scan reconstruction showing c1/c2 dislocation figure 4b cervical spine mri, sagittal view figure 5a ct scan – sagittal (upper) and axial (lower) sections figure 5b postoperative radiographic aspect romanian neurosurgery (2015) xxix 2: 135 140 139 figure 6a mri sagittal view figure 6b coronal view discussions traumatic spine injuries in pediatric patients have a low incidence, mainly due to a more flexible spine. the anatomical characteristics of children allow a better applicability of the conservative treatment. if we compare pediatric and adult spine injury we can conclude that identical situations lead to different neurological deficits. the nexus criteria for c-spine imaging in adult population takes into consideration the presence of focal neurological deficit, of midline spinal tenderness, of altered level of consciousness, of intoxication and of distracting injury. if none of these is present, the patient can be cleared. the clearance of the paediatric patients is more difficult than in adult patients therefore the nexus criteria of imagery were accordingly modified. particularly, for children between 0 and 3 years old who sustained a cervical spine trauma, assessment is hindered by the poor cooperation of a scared child. anderson and al. (2010) tried to coin a management algorithm for children less than 3 years old. the children with a cervical collar with positive imagery (xray or ct-scan if the x-ray is inconclusive) are sent to neurosurgery, the others are clinically evaluated as to whether there is spinal cord injury or a high-speed injury, cervical mri with stir or t2 fat suppression. if there is no lesion then the spine is clear, if there is a lesion the patient will be referred to the neurosurgeon. if inconclusive, fluoroscopy in flexion and extension should be done. the intubated patient should wait till they become fully awake then the mri should be performed. new therapeutic perspectives are opened by the studies on the predictive biomarkers for traumatic sci. in acute traumatic spinal cord injury the phosphorylated form of the high-molecular-weight neurofilament subunit (pnf-h) in csf can be a predictive biomarker because of its values pattern can show the reducing of the secondary lesion. studies have shown the complete sci cases with a favorable evolution had a specific pattern of daily values of pnf-h: a sudden increase up to a maximum value then a progressive decrease until normal. the cases with unfavorable outcome or 140 tascu et al traumatic spine injuries in children neurological stationary had two patterns: an increase to a plateau of pnf-h values or a progressive increase up to a peak and then it was followed by a progressive decrease to normal values. after decompression and stabilization during the first 24 hours we can use the predictive pattern of daily values of pnf-h in cases with unfavorable pattern. the second microneurosurgery in sci site can create favorable conditions for functional recovery of the remaining spinal cord. conclusions prognosis and outcome is better in children with spine trauma, reducing toward adolescence and in young adults. the prognosis depends on the severity of spinal cord injuries, with good neurofunctional recovery, noticeably increased in the pediatric population compared to the adult population. the death rate was extremely low compared to the adult population, with only 6 deceased patients out of 434 cases. acknowledgments this work is part of the grant: “immediate neuroprotective therapy in acute traumatic spinal cord injury”, grant number: pn-iiidpce-2011-3-0569, and was funded by the cncs– uefiscdi romania. references 1. benzel ec: the cervical spine, lippincott williams&wilkins, pennsylvania, 2012 2. benzel ec: spine surgey, 3rd ed., elesevier sunders, pa, 2012 3. bridwell kh, dewald rl: the textbook of spinal surgery, lippincott williams&wilkins, pennsylvania, 2011 4. exergian fe: tratat de patologie spinala traumatisme vertebro-medulare, bucuresti, 2004 5. exergian fe, craciunas s: epidemiology of spine and spinal cord injuries in romania, romanian neurosurgery, 9(2): 12-17, 2001 6. exergian fe, craciunas s, podea m: thoraco-lumbar spinaltrauma, romanian neurosurgery, 2(12): 34-41, 2007 7. fessler rg, sekhar ln: atlas of neurosurgical techniques: spine and peripheral nerves, thieme, ny, 2006 8. iencean stm. double noncontiguous cervical spinal injuries. acta neurochir (wien). 2002;144(7):695-70 9. iencean stm. classification of spinal injuries based on the essential traumatic spinal mechanisms. spinal cord. 2003;41(7):385-96. 10. didona ungureanu, şt m iencean, cristina dimitriu, a şt iencean, al tascu. determination of the phosphorylated neurofilament subunit nf-h (pnf-h) in cerebro-spinal fluid as biomarker in acute traumatic spinal cord injuries. romanian review of laboratory medicine. 2014; 22(3):377–386. 11. kim dh, vaccaro ar, dickman ca, cho d, lee s, kim i: surgical anatomy and techniques to the spine, 2nd ed, elsevier saunders, pa, 2013 12. schwartz e, flanders ae: spinal trauma: imaging diagnosis and management, lippincott williams&wilkins, pennsylvania, 2007 13. vaccaro ar: fractures of the cervical, thoracic and lumbar spine, mercel dekker, ny, 2002 14. van croethem j, van den hauwe l, parizel pm: spinal imaging-diagnostic imaging of the spine and spinal cord, springer, ny, 2007 15. winn hr: youmans neurological surgery, 6th ed., elesevier sunders, pa, 2011 popescug_5years 184 | popescu et al 5 years experience in epidermoid and dermoid cysts 5 years experience in epidermoid and dermoid cysts: case presentation and literature review g. popescu, a. giovani, n. bucur, a. neacsu, a. gheorghiu, s. mara, r.m. gorgan “bagdasar arseni” clinical emergency hospital, 4th neurosurgical department abstract: introduction: intracranial epidermoid and dermoid cysts are the result of an embryogenesis dysfunction leading to an abnormal migration of ectodermal cells characterised by a slow and benign rate of growth which is associated with minimal neurological symptoms in large or giant tumors. materials and methods: we retrospectively reviewed the case files of 17 patients with epidermoid and dermoid cysts operated using the operative microscope and neuronavigation in our department between january 2011 and december 2015. results: reviewing the case files we selected fourteen patients with epidermoid cysts and 3 patients with dermoid cysts who underwent surgical resection. most of the cysts were located infratentorial (64%) with a propensity for the cp angle (81%). total resection was attempted in all cases but was possible in only 13 cases. all cases with subtotal resection were infratentorially located in close relation to the brainstem or cranial nerves. conclusion: when the tumor extension reaches beyond the limits of the surgical approach used, the tumor remnant should be addressed in a second surgery. using the cysternal anatomy and the vessels dissection technique the risks aseptic meningitis and of injuring the cranial nerves are diminished. introduction dermoid cysts, also known as dermoid tumors or ectodermic inclusion cysts, are benign congenital inclusion cysts, representing one of the rarest forms of benign intracranial lesion, their frequency ranging from 0.04% to 0.6% of all intracranial tumors. they are usually sporadic rather than familial, but up to half of all patients with dermoid cysts have additional congenital abnormalities. because of a common congenital origin they have frequently been confused with epidermoid cysts, although intradural dermoid cysts are four to nine times less common than epidermoid lesions. as many as one third of dermoid cysts are associated with dermal sinus tracts. dermoid and epidermoid cysts are both thought to arise from defects in the separation of the neuroectodermic plate during the formation of the neural tube, leading to sequestration of romanian neurosurgery (2016) xxx 2: 184-194 | 185 ectodermic remnants. epidermoid cysts are more common and are not usually located in the midline, which is the location of most dermoid cysts. many reports indicate that the midline below the tentorium is the preferential location site of intradural dermoid cysts, often associated with the occipital dermal sinus. more recent series show a higher frequency of supratentorial than infratentorial dermoid cysts. intracranial dermoid cysts are well circumscribed and most often occur in the parasellar region, sylvian fissure, cerebellopontine angle, posterior fossa, and fourth ventricle. patients with dermoid cysts usually present with symptoms related to a focal mass effect, seizures, or recurrent meningitis. on ct scans, dermoid cysts usually appear as nonenhancing, hypodense lesions, and on mr images they demonstrate increased t1 and variable t2-weighted signal. less frequently, the cyst contents can be hyperdense mimicking a hemorrhage. it is important to recognize the unusual imaging characteristics of some dermoid cysts because they are managed differently from posterior fossa hemorrhage. materials and methods we retrospectively reviewed the case files of 14 patients with epidermoid and dermoid cysts operated in our department between january 2011 and december 2015. the microneurosurgical technique performed under the operative microscope was used in most of the cases. neuronavigation was also used in cases where we considered it was useful. in all the cases the diagnosis of epidermoid/dermoid cyst was suspected on the mri. the clinical setting, the preoperative and postoperative ct-scans and mri’s were reviewed and where available the entire operative video was analyzed in order to provide details associated with the impossible total resection. results fourteen patients with epidermoid cysts and 3 patients with dermoid cysts underwent surgical resection in our department during january 2011 and december 2015. the mean age at presentation was 32.4 years old, with a slight male predominance 10:7. most of the patients had a long symptoms history before surgery with an average of 6.7 years. the most common symptoms in patients with supratentorial cysts were headache and seizures while imbalance, headache and cranial nerve deficits (especially trigeminal and vestibulocochlear) predominate in the infratentorial location. most of the tumors (64.7%) were located infratentorially and most of these were located in the cerebellopontine angle (81.8%) and one was located predominantly inside the ivth ventricle and one in the prepontine cistern. pathological based distribution 186 | popescu et al 5 years experience in epidermoid and dermoid cysts location based case distribution main neurologic symptoms supratentorial -seizures -headache infratentorial -imbalance -cranial nerve deficit -headache all the tumors in this series were resected using the microdissection of the arachnoid space in order to free the vessels and nerves involved by the tumor. we achieved gross total resection in all supratentorial cysts and subtotal resection in 4 infratentorial tumors, one with interpeduncular extension and 3 with infra/supratentorial extension. all these 4 patients with incomplete removal of posterior fossa epidermoids lately presented with symptoms of hydrocephalus and required ventriculoperitoneal shunting. operative technique minimal brain retraction and minimal cortical damage was the key point we followed in choosing the surgical approach to the tumor. that is why we used skull base approaches or for the supratentorial location, where possible, natural corridors like fissures or large sulci to approach the tumor. the shortest way to the tumor was used in any case, and the neuronavigation was an advantage in reaching this purpose. once the tumor is reached, its capsule was entered with a scalpel followed by internal debulking with aspiration in order to avoid spilling the contents in the surgical corridor. after enough debulking has been achieved the capsule dissection is started and the vessels and nerves are carefully freed from the adherences to the capsule. traction on the tumor before the entire capsule has been freed should be avoided. we noticed a surgical difference between epidermoid and dermoid cysts in that the latter are more adherent to the arachnoid and even the pia mater. given the pattern of growth inside the cisterns we even achieved a total resection using a retrosygmoidian approach in a few cases with supratentorial parasellar extension. the most common complications encountered were hydrocephalus in 4 cases, aseptic meningitis in 3 cases. 3 patients with cp angle located tumors presented with new transient cranial nerve palsies. two patients presented with postoperative seizures that were controlled with medication. the mean follow up of the patients was of 2,4 years. there was no evidence of tumor recurrence in this follow up interval. case 1 the patient was accepted in our service with bilateral temporal headache and left facial parestesia. the neurological examination showed left facial paresis, without focal motor deficit, or epileptic seizures. romanian neurosurgery (2016) xxx 2: 184-194 | 187 imaging work-up showed a well-defined left paresellar tumor, with lipid and solid components, without enhancement after gadolinium injection, 3/3,5/5 cm in diameter showing homogenous hypointensity in t1 and hyperintensity in t2. angio mri was within normal limits making the differential diagnosis with a middle fossa meningioma. gross total resection was achieved through a fronto-temporal craniotomy, with opening of the carotid-optic cistern. the large tumor, was located in the temporal lodge to the sfenoidal sinus, was well defined, white and made of tissue, hair and fat. the histopathological examination revealed a dermoid cyst with didermic mature teratoma areas. 188 | popescu et al 5 years experience in epidermoid and dermoid cysts figure 1 left middle fossa dermoid compressing the cavernous sinus and displacing the left mca (a, b). hair is encountered during tumor debulking (c). part of the cyst capsule is resected to allow better extracapsular dissection (d). the left optic nerve and carotid are identified and followed distally in order to disect the tumor capsule from the middle cerebral artery (f). middle fossa dura after total resection and haemosthasis was achieved.postop ct scan showing total resection (g). https://www.youtube.com/watch?v=o4re9rpbtli case 2 a 32 yo male patient, was admitted in our clinic for history of headache, right hearing loss, dizziness for more than 1 month. the neurological examination revealed nonsystematic balance disorder; and sensitivity disorders: headache, dizziness. as well right hearing loss with uncertain debut was reported. the mri scan showed a pontocerebellar angle extranevraxial expansive lesion, that develops in the cerebellopontine angle cistern and extends inside the internal auditory canal (which appears enlarged) with mass effect on the acustico-vestibular nerves (that is compressed antero-superiorly) without infiltrating it and on the brainstem, mid cerebellar peduncle and the fourt ventricle (without hydrocephalus). the described cisternal mass has lobulated contour, romanian neurosurgery (2016) xxx 2: 184-194 | 189 heterogeneous structure, without gadolinium enhancement and 4,1/2,7 cm in diameter. the tumor was completely resected using a retrosigmoid approach and a microsurgical technique to dissect it from the cranian nerves, aica and sca. figure 2 left cp angle epidermoid cyst compressing the vth, vii and viiith nerves. internal tumor debulking. total removal after the cranial nerves were freed from the tumor capsule. 24h postoperative ct scan, showing the resection cavity. https://www.youtube.com/watch?v=3e39shadqzy case 3 a 39 yo male patient, was admitted for headache and epileptic seizures lasting for 190 | popescu et al 5 years experience in epidermoid and dermoid cysts more than 6 months. the ct scan showed a well-defined, left frontal intracranial expansive process, partially calcified, without edema and a normal midline ventricular system. the mri showed a left frontal extraaxial well-circumscribed mass, extending in the left ethmoidal cells. gross total resection of the described tumor was achieved using a subfrontal approach. the histopathological examination was suggestive for dermoid cyst (cholesteatoma). romanian neurosurgery (2016) xxx 2: 184-194 | 191 figure 3 frontoetmoidal giant epidermoid cyst displacing the left ophtalmic and optic nerves. intraoperative aspect after incising the cyst. the cyst wall seen from the inside during internal debulking. a view along the falx during the final hemosthasis after total removal was achieved. https://www.youtube.com/watch?v=zysc4oouk9o discussions since yasargil et al presented their series of 43 patients with epidermoid and dermoid cysts operated in 22 years there were many reports on this focus with a special interest in cp angle tumors with intraventricular or supratentorial extension. hitoshi et al. presented a series of 30 cp angle epidermoids operated in a time span of 14 years presenting with cranial nerves hyperactive dysfunction especially trigeminal neuralgia. in this series the patients with trigeminal neuralgia following direct trigeminal nerve irritation were significantly younger than those with symptoms caused by vascular compression. in 2008 liu et al. presented their results with 5 cases of ruptured intracranial dermoid cysts discussing clinical, diagnostic and therapeutic aspects. most of the patients have their epidermoid cysts discovered in the 2nd decade, yet some authors have reported series of patients commonly diagnosed in the 3rd or 4th decades of life. patients with posterior fossa dermoid cysts typically present with neurological symptoms when the cyst is larger than 3 cm. most cases are characterized by a chronic and progressive course rather than an acute clinical decline. neurological deficit, recurrent meningitis, seizures, and chronic headaches are the most common symptoms. the current theory is that the dermoid cyst develops from a tuck of skin which may be retained when the dura mater invaginates to form the tentorium, the high incidence of associated dermal sinuses confirms the dysembryogenetic theory. in all likelihood, supratentorial dermoid cysts arise due to misplacement of embryonic inclusions in the vicinity of the developing neural tube up to the 3rd week of life, during carnegie stages 8 to 10, when the neural groove begins to close. cranial abnormalities such as bone defects, dermal sinuses, or meningoencephaloceles are not associated with this development. because epidermoid/dermoid cysts have a 192 | popescu et al 5 years experience in epidermoid and dermoid cysts soft consistency they can grow to impressive dimensions spanning more than one cystern in some of the cases extending from one skull base fossa to another. because this tumors are well encapsuled and the capsule is not adherent to the vasculo-nervous elements it compresses, as well as because its contents are easily aspirable the approach to these tumors should focus not on the tumor itself but on the important structures related to the tumor that should be avoided during the approach. most of the epidermoid cysts in the posterior fossa (60%) are located in the cerebellopontine angle, where they are the 3rd most common tumor after vestibular schwannomas, and meningiomas. following the cp angle, the most common location for epidermoids is the iv’th ventricle. other rare locations can require a difficult surgical approaches like those for the petroclival, prepontine or pineal region. many classifications have been used for posterior fossa epidermoids given the unusual growth patterns of these tumors including those of yasargil and samii. bricolo et al. clasifies the posterior fossa epidermoids in cpa lesions with suprasellar/chiasmatic, parasellar/ temporobasal or mesencephalic/pineal extension, posterior fossa basal lesions with the same 3 possible extensions or 4th ventricle lesions. with permission from tallachi et al assessment and surgical management of posterior fossa epidermoid tumors: report of 28 cases, neurosurgery. 42(2):242-251, february 1998 most of the tumors located in the cp angle determine irritative symptoms usually in one of the involved cranial nerves either trigeminal, facial or acoustic. intracranial hypertension signs are rarely a complaint in posterior fossa epidermoids. the mri is the investigation of choice both because it differentiates the cyst from the adjacent cysterns and it makes a differential diagnosis between these cysts and the arachnoid cysts. the lack of peritumoral edema indicates that the blood brain barrier has not been disrupted by the slow growing tumor. one should always keep in mind during the surgery that all the tumors initiate their growth in the cisterns and develop where they find a cisternal enlargement or an intraventricular cavity even if their developement in the third and lateral ventricles is quite a rare manifestation. in large middle fossa extensions of posterior fossa epidermoids, the usual retrosigmoid approach should be combined with a presigmoid approach in order to attempt a total resection. romanian neurosurgery (2016) xxx 2: 184-194 | 193 figure 4 differential diagnosis between an arachnoid cyst (a) and an epidermoid cyst (b) – note that in t2 the images look alike yet a fine capsule can be distinguished surrounding the epidermoid, and also its content is less homogenous than the arachnoid cyst another important clue to a definitive cure of an epidermoid tumor is to avoid spilling the tumor into adiacent cysterns or anywhere in the surgical corridor as this may be the cause of distant spreading of the tumor or of aseptic meningitis. most authors report total removal in less than 60% of cases precisely because the tumor extension cannot beremoved through a single approach without causing collateral damage. conclusion all efforts should be made to achieve a total resection of epidermoid and dermoid cysts, using a clean technique that avoids spilling the cyst contents and diminishes the risk of distant recidives and aseptic meningitis. when the tumor extension reaches beyond the limits of the surgical approach used, the tumor remnant should be addressed in a second surgery. using the cysternal anatomy and the vessels dissection technique the risks aseptic meningitis and of injuring the cranial nerves are diminished. references 1. abramson rc, morawetz rb, schlitt m: multiple complications from an intracranial epidermoid cyst: case report and literature review. neurosurgery 24:574–578, 1989. 2. arseni c, danaila l, constantinescu ai, carp n, decu p: cerebral dermoid tumours. neurochirurgia (stuttg) 19:104–114, 1976. 3. berger ms, wilson cb: epidermoid cysts of the posterior fossa. j neurosurg 62:214–219, 1985. 4. carvalho ga, cervio a, matthies c, samii m: subarachnoid fat dissemination after resection of a cerebellopontine angle dysontogenic cyst: case report and review of the literature. neurosurgery 47:760–764, 2000. 5. lunardi p, missori p: supratentorial dermoid cysts. j neurosurg 75:262–266,1991. 194 | popescu et al 5 years experience in epidermoid and dermoid cysts 6. yasargil mg, abernathey cd, sarioglu ac: microneurosurgical treatment of intracranial dermoid and epidermoid tumors. neurosurgery 24:561–567,1989. 7. vinchon m, pertuzon b, lejeune jp, assaker r, pruvo jp, christiaens jl: intradural epidermoid cysts of the cerebellopontine angle: diagnosis and surgery. neurosurgery 36:52-57, 1995. 8. vion-dury j, vincentelli f, jiddane m, van bunnen y, rumeau c, grisoli f, salamon g: mr imaging of epidermoid cysts.neuroradiology 29:333-338, 1987. 9. lunardi p, fortuna a, cantore g, missori p: long term evaluation of asymptomatic patients operated on for intracranial epidermoid cyst: comparison of the diagnostic value of magnetic resonance imaging and computed-assisted cisternography for detection of cholesterin fragments.acta neurochir (wien) 128:122125, 1994. 10. alvord ec jr: growth rates of epidermoid tumors.ann neurol 2:367-370, 1977. 5tascua_cerebellopontine romanian neurosurgery (2016) xxx 1: 35 40 35 cerebellopontine angle subdural empyema in a 2-years old patient with bilateral mastoiditis a life-threatening condition. case presentation and review of literature a. tascu1,2, a. spatariu1, c. pascal1, st.m. iencean3 1“bagdasar-arseni” emergency hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania 3“grigore t. popa” university of medicine and pharmacy, iasi, romania abstract: infratentorial subdural empyema is a life-threatening condition, the common source being an ear infection. we present a 2-year old boy treated for bilateral mastoiditis, with infratentorialleft cerebellopontine angle subdural empyema. clinical presentation encompassed a systemic febrile illness, headaches, and a stiff neck. empyema was diagnosed with computed tomography and magnetic resonance imaging. the patient was successfully treated with surgery and appropriate antibiotics. empyema should be considered in patients with ent infection associated with neurological signs that suggest a posterior fossa lesion. key words: infratentorial subdural empyema, pediatric neurosurgery, outcome introduction subdural empyema is a rare infection of the central nervous system and most often is a secondary process to paranasal sinus infection, otitis or cranio cerebral trauma (4, 6, 8) it is a neurosurgical emergency and urgent surgical treatment is necessary in most cases. location in the posterior cranial fossa in general and cerebellopontine angle is unusual. in this paper we present the case of a child aged 2 years with subdural empyema of left cerebellopontine angle, secondary to bilateral otomastoiditis. the patient was successfully treated by neurosurgical intervention and targeted antibiotic therapy. although rare lesion empyema should be considered in patients presenting infection signs with ent and neurological symptoms. case presentation a 2-year old child is admitted with history of bilateral otitis, fever and occurrence of a left retro auricular pseudotumoral formation accompanied by celsian signs. this feverish patient is hospitalized with slightly weight deficit, neck stiffness increased intracranial pressure syndrome and balance disorders. in the service of infectious diseases where he was admitted previously, the patient received antibiotic treatment with meronem 1.5 g / day, vancomicin 600mg / day and 200mg ciprofloxacin / day treatment continued 36 tascu et al cerebellopontine angle subdural empyema in children during the current hospitalization. ct scanning reveals bilateral otomastoiditis with parafluid retention in otomastoid cavities. left cerebellar hemisphere heterogeneous densities adjacent to the temporal cliff and raise suspicion of left transverse sinus thrombosis. mri examination performed shows osteomyelitis and left cerebellar hemisphere abscess with hyper t2 and important perilesional edema. the transverse and sigmoid sinus were thrombosed to the side in the jugular bulb. the analysis shows a slight blood neutrophils and increased esr with leukopenia. fundus examination was normal. surgery is performed by wide a left posterior cranial hemifosa craniectomy and an empyema of left cerebellopontine angle with multiple adhesion to the cerebellar hemisphere is drained. the thrombosis of and transverse and sigmoid sinus are confirm on the left. pus is send for antibiogram analysis. postoperatively the patient's evolution is favorable, it shows minor csf leak which was treated by compression bandage. antibiotic therapy was continued postoperatively. no pathogen was found. the patient was referred to the ent service for mastoidectomy surgery. at 6 months postoperative the patient was fully recovered with no neurologica sign and the ct exam shows no relapse of infectious process. romanian neurosurgery (2016) xxx 1: 35 40 37 38 tascu et al cerebellopontine angle subdural empyema in children figure 1 preoperative images: brain ct and brain mri of the; cerebellopontine angle subdural empyema romanian neurosurgery (2016) xxx 1: 35 40 39 figure 2 postoperative images after craniectomy and drainage of empyema discussion the location of empyema in the posterior cranial fossa is rare (1, 2, 12) and are due in most cases of inappropriately treated recurrent otitis. subdural empyema is according to data from the literature (5, 9) between 10 and 41% of all cases of intracerebral pus collections and infratentorial cases represent approximately 0.6% of all intracranial abscesses. (7) pediatric cases of infratentorial subdural empyema sde are rare and are associated with increased morbidity and mortality. subdural empyema is a neurosurgical emergency requiring emergency evacuation of pus collections. infratentorial sde cases are briefly mentioned and represents a small number of cases (33 cases described in the literature). (3, 10) in infratentorial subdural empyema patient's condition deteriorates rapidly and often irreversible, so early diagnosis and prompt treatment are necessary. the most common clinical symptoms are headache, fever, vomiting, meningism and otorrhea. the cerebellar symptoms or cranial nerve deficits are most often absent. only approximately 21% of patients are presenting cranial nerve or cerebellar signs (1), that shows the importance of maintaining a high rate of suspicion of infratentorial subdural empyema in these patients, the diagnosis is not suggested by the clinical presentation in most cases. subdural empyema associated with hydrocephalus incidence is reported between 77 and 93% in large series. hydrocephalus benefit from external ventricular drainage in most cases, about 20% requiring a permanent drainage system. (8.12) patient condition can rapidly deteriorate and duration of symptomatology is shorter than in supratentorial empyema. brain mri investigation remains preferentially in identifying and localization of subtentorial empyema due to lack of bones artefacts that can make detection difficult in ct scan examinations. surgery is the primary treatment, we found only two cases in the literature that were treated exclusively antibiotic. we believe that antibiotics can only be an option in highly selected, special cases, due to the long treatment, the possibility of neurologic worsening and increased possibility of recurrence. ideal is to perform mastoidectomy in the same time with de empyema evacuation, thereby eliminating the 40 tascu et al cerebellopontine angle subdural empyema in children source of infection and preventing recurrence. maharaj & singh (11) in their study on 268 patients with intracranial complications of media otitis concludes that radical mastoidectomy is required only in those patients presenting with coleastoma, for the rest partial mastoidectomy allowing hearing preservation is feasible. conclusions infratentorial subdural empyema should be taken in consideration in patients with bacterial meningitis or otogenic infections. common clinical presentation includes fever, headache, increased intracranial pressure syndrome, meningism and otorrhea. in most cases there is a causal relationship with a chronic infection of the middle ear. surgical evacuation with targeted antibiotics is the main line to follow. although rare, infratentorial subdural empyema shows a high morbidity and mortality that can be lowered by access to neuroimaging investigations, specialized medical institutions and prompt surgical intervention. if prompt intervention and proper management of possible complications are performed good prognosis and outcome are expected. references 1.bakker s, kluytmans j, den hollander jc, lie st: subdural empyema caused by escherichia coli: hematogenous dissemination to a preexisting chronic subdural hematoma. clin infect dis 21: 458-459,1995 2.borovich b, jonston e, spagnuolo e: infratentorial subdural empyema: clinical and computerized tomography findings. report of three cases. j neurosurg 78: 299-301,1990 3.brahdari ys, sarkari nbs: subdural empyema. a review of 37 cases. j neurosurg 32: 35-39. 1970 4. dill sr, cobbs cg, mcdonald ck: subdural empyema: analysis of 32 cases and review. clin infect dis 20: 372386,1995 5.halvin ml, ratcheson ra: subdural empyema in kaye ah, black pm(eds): operative neurosurgery. london: harcourt 2000, vol 2, pp 1667-1678 6.miller es, dias ps, uttley d: management of subdural empyema: a series of 24 cases. j neurol neurosurg psychiatry 50: 1415-1418,1987 7.nathoo n, nadvi ss, van dellen jr: infratentorial empyema: analysis of 22 cases. neurosurgery 41: 12631269,1997 8. nathoo n, nadvi ss, van dellen jr, gouws e: intracranian subdural empyemas in era of computer tomography: a review of 699 cases. neurosurgery 44: 529536, 1999 9.nathoo n, nadvi ss, gouws e ,van dellen jr: craniectomy improves outcomes for cranial subdural empyemas: cumputed tomography era experience with 699 patients. neurosurgery 49. 872-878,2001 10. pathak a, sharma bs, mathuriya sn, khosla vk, khandelwal n, kak vk: controversies in the management of subdural empyemas: a study of 11 cases with review af the literature. acta neurochir(wien) 102: 25-32.1990 11.singh b, maharaj tj: radical mastoidectomy: its place in otitic intracranial complication. j laryngol otol 12: 1113-1118. 1993 12. vankatesh ms, pandey p, devi bi, khanapure k, satish s, sampath s: pediatric infratentorial subdural empyema: analysis of 14 cases. j neurosurg 105: 37-377, 2006 microsoft word 15.sanduaurelia_gorgan_multimodal_f.docx romanian neurosurgery (2011) xviii 4: 499 510 499 multimodal treatment for temporobasal arteriovenous malformation case report aurelia mihaela sandu1, mircea radu gorgan2 1phd student in neurosurgery, umph “carol davila” bucharest faculty of medicine, department of neurosurgery; clinic of neurosurgery, forth department of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest 2professor in neurosurgery, umph “carol davila” bucharest faculty of medicine, department of neurosurgery clinic of neurosurgery, forth department of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest abstract background: arteriovenous malformations (avms) are congenital lesions requiring multimodal approach. method: we report a case of a 25 years old woman, with ruptured temporobasal avm, who required multimodal treatment, emphasizing on treatment options, advantages and disadvantages of each treatment chosen, encountered difficulties, technical considerations and outcome. results: the patient, admitted for the first time in comatose state, underwent emergent surgery with evacuation of an intraparenchymatal hematoma and decompressive craniectomy. after neurological recovery, the patient was thoroughly investigated and positive diagnosis of left temporobasal avm was established. the patient underwent surgery with subtotal resection of the avm, followed by gamma knife stereotactic radiosurgery of the residual nidus. the outcome was favorable. conclusions: avms need complex treatment performed in a multidisciplinary team. surgery is the treatment of choice in management of the avms. gamma knife stereotactic surgery is required if a residual nidus is left in place following surgery. definitive treatment in avms is mandatory because of the high risks of hemorrhage with high morbidity and mortality. keywords: arteriovenous malformation, avm surgery, residual nidus, stereotactic radiosurgery introduction arteriovenous malformations (avms) are congenital lesions composed of a complex tangle of dysplasic arteries and arterialized veins connected by shunts. within the abnormal conglomerate of vessels, called nidus, blood is drained through feeding arteries directly into draining veins, without any capillary bed. arteries have a deficient muscularis layer and red draining veins are dilated and contain high flow oxygenated blood. avms were described for the first time by luschka and virchow in the mid 1800s and olivecrona performed the first surgical excision of an avm in 1932. (1) it is difficult to estimate the real incidence of avms, it usually ranges between 0.15 and 3%. (18, 26) prevalence is 500 aurelia mihaela sandu and m.r. gorgan treatment for temporobasal avm 0.14%. (1, 9) avms represent 6% of intracranial lesions. the average age at diagnostic is 33 years, and 64% of avms are diagnosed before age 40. (9, 20) avms are the main cause of hemorrhagic strokes in young patients. (8) the two main clinical presentation forms are rupture of the avm with consequent hemorrhage (intraparenchymatal, intraventricular or subarachnoidian bleeding) and seizures. other clinical manifestations are progressive neurological deficit secondary to the vascular steal phenomenon from de adjacent brain, hydrocephalus due to venous hypertension in the draining veins, neurological deficits secondary to mass effect of an enlarging avm and increased intracranial pressure. treatment options of avms consist of surgery, endovascular embolization, stereotactic surgery or multimodal approach. treatment must be individualized according to neurologic state at admission, general state, co-morbidities, age, characteristics of the avm and therapies available in the hospital of admission. method we report a case of a left temporobasal avm treated into the forth department of neurosurgery. we reviewed medical records, imaging, treatment and follow-up. patient bs, woman, 25 years old, with no significant previous history prior current episode, was transferred from another department on the 29th of october 2009 with the following diagnostic: ruptured profound left temporal avm. history: sudden onset 8 days before admission in our department, with headache, vomiting and impaired consciousness. patient was admitted in emergency in another department of neurosurgery with comatose state, gcs 6 points and right hemiparesis. emergency ct scan showed a left frontotemporoparietal intraparenchymatal hematoma. patient underwent emergent surgery, hematoma was evacuated and decompressive craniectomy was performed. two days after surgery a 4 vessel angiography was performed which revealed a profound left temporobasal avm. patient was redirected to our department for further treatment. on admission the patient presented impaired consciousness, gcs 9 points (m5, v2, o2), had right hemiparesis, hyperactive deep tendon reflexes right > left and bilateral babinski sign. the cerebral ct scan revealed postoperatory left temporal hipodensity, intraventricular hemorrhage (within both lateral ventricles) and decompressive craniectomy (figure 1). cerebral irm showed a left temporohippocampal avm, with consequent involvement of left internal capsule and thalamus, with feeding arteries from left middle cerebral artery and left posterior cerebral artery and venous drainage into left transverse sinus (figure 2). four vessels cerebral dsa (digital subtraction angiography) showed a left capsulothalamic avm grade iii spetzlermartin, with nidus measuring 3 cm in diameter, with feeding arteries from talamostriate arteries from left posterior communicating artery and left posterior cerebral artery, anterior choroidal artery and perforating branches from left segment m1 of the middle cerebral artery (figure 3). pulmonary x-ray and electrocardiography were normal. romanian neurosurgery (2011) xviii 4: 499 510 501 figure 1 cerebral ct scan, left temporal hipodensity, intraventricular hemorrhage, decompressive craniectomy 502 aurelia mihaela sandu and m.r. gorgan treatment for temporobasal avm figure 2 cerebral irm t2, left temporohippocampal avm involving left internal capsule with feeding arteries from left middle cerebral artery and left posterior cerebral artery figure 3 four vessels dsa, left internal corotid artery, left capsulothalamic avm with nidus measuring 3 cm in diameter, with feeding arteries from talamostriate arteries from left posterior communicating artery and left posterior cerebral artery, anterior choroidal artery and perforating branches from left segment m1 of the middle cerebral artery romanian neurosurgery (2011) xviii 4: 499 510 503 results she received dexamethasone 16 mg/d, mannitol 20% 250 ml/d, furosemid 40 mg/d, antiepileptic drugs, analgesics and intravenous hydration. neurological outcome was favorable, the patient regained consciousness, gcs 14 points, had severe right hemiparesis and dysphasia. in order to determine whether intraarterial embolization was a valid option we asked for an interventional neuroradiology consult which contraindicated embolization because the avm had no pedicles that can be catheterized with microcathethers of the equipment. gamma knife stereotactic radiosurgery was also contraindicated because the nidus includes the middle cerebral artery and comes into contact with left optic radiations. pre-anesthetic consult found a risk score asa iv and anemia (hg=8.6 g/dl). on the 9th of november 2009 the patient underwent surgery. the patient was position supine, with roll under her left shoulder. the head was turned 45° to the right. we reopened the wound on the previous skin incision for left temporal bone flap and we incised the neodura mater in a stellate fashion. we performed opening of the left sylvian fissure, with visualization of the left middle cerebral artery and sylvian artery trifurcation. a tangle of vessels (nidus) was discovered in close vicinity with middle cerebral artery, surrounding it. the nidus was dissected free from the middle cerebral artery, which was left intact. left internal carotid artery and left anterior choroidal artery were found and spared. a vascular clip was put on the feeding artery arising from left posterior cerebral artery. subtotal removal of the avm was performed, the part situated in the vicinity of the left middle cerebral artery. we copious irrigated the operative field with normal saline and performed carefully hemostasis. at the end of the operation normal brain pulsation were noticed. we performed wound closure with watertight duraplasty with pericranium and anchoring of dura mater, epidural drain, replacement and fixation of the bone flap conserved from previous surgery and skin suture. the patient was extubated and awaked in the operating room. immediate postoperatory examination revealed: efficient spontaneous breathing, right hemiparesis and dyphasia. the patient was taken to intensive care unit. the epidural drain was pulled out after 48 hours. during the following days dysphasia slowly recovered. postoperatory outcome was favorable, the patient regained consciousness, gcs 15 points, she had right hemiparesis and presented no aphasia. histopathological exam confirmed the diagnosis of racemous hemangioma (arteriovenous malformation). postoperatory ct scan was normal (figure 4). postoperatory 4 vessels dsa showed the residual nidus (figure 5). on 2nd of march 2010 (5 months after surgery) the patient was admitted for stereotactic irradiation of the residual nidus. gamma knife stereotactic radiosurgery was performed, using a marginal dose of 18.5 gy at the 60% isodose line, on a target volume of 1.4 cm3. total irradiation dose was 0.7 gy (1.3 j). postirradiation outcome was favorable. four vessels dsa performed in june 2011, 16 months after stereotactic 504 aurelia mihaela sandu and m.r. gorgan treatment for temporobasal avm radiosurgery, revealed complete obliteration of the residual nidus (figure 6). long term follow-up ct scan showed a normal postoperatory aspect (figure 7). neurological examination found right hemiparesis and no aphasia. the patient presented no seizure under fenobarbital 100 mg/d. she was included in a kinetotherapy intensive program. figure 4 cerebral ct scan, normal postoperatory aspect figure 5 four vessel dsa, left internal corotid artery, residual nidus romanian neurosurgery (2011) xviii 4: 499 510 505 figure 6 four vessel dsa, left internal corotid artery, residual nidus obliteration figure 7 cerebral ct scan, long term follow-up, normal postoperatory aspect discussions the patient had a typical sudden onset of ruptured avm. hemorrhage is the most common form of presentation, 50-70% of patients harboring such malformations present with bleeding. (9, 12, 24) bleeding occur most commonly intraparenchymatal, intraventricular, usually concomitant with intracerebral hematoma as a result of rupture into ventricles or pure intraventricular or rarely subarachnoid or subdural. (9) the patient had no history of seizure. usually patients having seizure are investigated and the avm is diagnosed before rupture. increasing age, initial rupture of the avm, deep brain location and exclusive deep venous drainage are independent predictors of subsequent hemorrhage. annual hemorrhage rates on follow-up ranged from 0.9% for patients without bleeding to 34.4% in people with ruptured and deep avms and with deep venous drainage. (6, 7, 27) hemorrhage carries a 10% mortality and 30-50% morbidity rates with each bleed. (9) the patient was admitted in emergency in another neurosurgical department. the first surgery was performed in order to save her life, this is why only evacuation of the intraparenchymatal hematoma and decompressive craniectomy for brain swelling were performed. although the postoperatory outcome was favorable, and the patient had no further vital risk, an ethiopathogenic treatment was mandatory. (6) she was transferred in our department for definitive treatment. the need for an ethiopathogenic treatment is sustained by risks of further rupture. the risk of hemorrhage from an avm is 2-4% per year, therefore the risk of bleeding over the entire life is very high. (9) the risk 506 aurelia mihaela sandu and m.r. gorgan treatment for temporobasal avm of bleeding is calculated with the following formula: risk of bleeding (at least once) = 1 – (annual risk of not bleeding)expected years of remaining life the annual risk of not bleeding is 1 annual risk of bleeding. in our patient aged 25, with expected 52 tears to live, for an average risk of hemorrhage of 3% per year, the total risk of bleeding at least once is 79%. (9) more, the risk of bleeding during the first year after primary rupture is 6%. (16) the risk deceases over the next years, but remains significant for decades. risk of bleeding is higher in avms with previous rupture, deep and infratentorial locations. (12, 19) at admission in our department the situation is different, because her life is not in danger and she could be thoroughly investigated prior definitive treatment. treatment options of avms, all available in our department, consist of surgery, endovascular embolization, stereotactic radiosurgery and multimodal treatment. (6) in 1986 spetzler and martin proposed a grading system of avms, based on size of avm, eloquence of adjacent brain and pattern of venous drainage. (25) spetzlermartin grading system is helpful in predicting surgical risk. (9, 16, 29) while in patients harboring grade i and ii surgical risk is low, patients with grade iii avms represent a more challenging decisionmaking dilemmas, because they carry a significant higher surgical risk. (16) in the algorithm of decision-making we must take into account other factors such as ruptured vs. nonruptured avm, clinical presentation, patient’s age and co-morbidities. embolization can be used as single treatment or as neoadjuvant for surgery or stereotactic surgery. in order to be done it requires an interventional neuroradiology department with trained personnel. embolization is a minimally invasive procedure and when used as a neoadjuvant technique it facilitates surgery, by reducing the volume of the malformation, decreasing the intraoperative bleeding, occluding deep or difficult to reach feeding arteries and associated aneurysms outside the operative field. (10, 28) using embolization alone the rate of complete occlusion is only 10%, and even in completed occluded avms the recanalization reaches 50%, but endovascular techniques reduce the volume of the malformation with 75%. (10) surgery must be performed within 3-30 days after embolization. if patient becomes symptomatic and he has no intracranial lesion requiring emergent surgery, the operation is postponed until he recovers. (9) morbidity and mortality rates following embolization are low. (5, 11, 13, 14) mortality is 1% and morbidity is 3.9%. (5, 11, 22) long-term permanent neurologic deficits are encountered in 8.6% of patients. (14) immediately following procedure, significant neurological complications occurred in 2.7-7.1%, yet a majority of deficits improve or resolve over time. (22, 28) embolization carries a procedural risk related to avm’s grade and number of occluded branches. (14) unfortunately microcathethers of the equipment were unable to catheterize the feeding pedicles. the avm had feeding arteries from talamostriate arteries arising from left posterior communicating artery and left posterior cerebral artery, anterior choroidal artery and perforating branches from left segment m1 of the middle cerebral artery. catheterization of such small branches requires very small catheters romanian neurosurgery (2011) xviii 4: 499 510 507 and carries a significant risk of improper embolization of the parental artery with post procedural morbidity. the answer to this problem is acquisition of smaller catheters. stereotactic radiosurgery is used in small avms, with nidus measuring 2.5-3 cm. stereotactic radiosurgery include gamma knife radiosurgery, proton beam radiosurgery, and linear accelerators (linac). advantages of stereotactic radiosurgery are: it is a non invasive procedure and it can be done in an ambulatory patient. principle of radiosurgery consists of directing radiation with narrow beam particles, consisting of 201 converged sources, given in a single session, to a predetermined target volume, with minimum risk of damage to surrounding brain. stereotactic radiosurgery causes gradual obliteration of the nidus. radiation of vessels causes proliferation of smoothmuscle cells and increases extracellular type iv collagen producing, which leads to progressive stenosis and obliteration of the nidus and, in the end, to cellular degeneration and hyaline transformation. (4, 23) because of the delayed obliteration of avms after radiosurgery, comprehensive long-term management and observational strategies are necessary. the risks associated with avms, including the risk of bleeding, persist during this period of time, therefore until obliteration the lesion cannot be considered cured. obliteration of the avms following stereotactic radiosurgery occurs late, after 1-3 years following initial procedure. (4, 9) imaging follow-up are recommended at six month intervals for the first three years to assess the effect of radiosurgery on avm. another disadvantage of stereotactic irradiation is the fact that it is limited to lesions measuring maximum 3 cm in diameter. if obliteration does not occur after 3 years, the irradiation can be safely repeated. (15) dose planning is based on location and volume of the avm and relation with the surrounding structures. marginal doses typically range from 16 to 25 gy in a single fraction. although the nidus measured 3 cm in diameter gamma knife stereotactic surgery was contraindicated because of the relation of the nidus with the middle cerebral artery and left optic radiation. inclusion of the middle cerebral artery into the target volume can lead to radiation artery wall lesions with stenosis and occlusion. also vicinity of optic radiations limits using stereotactic surgery. tolerable dose to the optic radiation is 8 gy, a dose similar to anterior optic pathways. (17) surgery is the treatment of choice, because if complete resection can be performed provides cure of the malformation. (7) total resection cannot be always done. causes that can prevent total excision are: anesthetic problems during surgery (patients develop cardiocirculatory instability, e.g. bradycadia, hypotension), high grade spetzler-martin avms (staged surgery is a solution for these cases), portion of the nidus located in eloquent areas, deep nidus with deep feeding arteries that cannot be approached, preoperative rupture of the avm (hematoma can compress the lesion, angiography is occult or it does not show all malformation, and after hematoma removal or clot dissolution the avm reopens), intraoperative rupture (due to accidental early vein occlusion with severe life-threatening bleeding), difficult anatomy with passage vessels supplying 508 aurelia mihaela sandu and m.r. gorgan treatment for temporobasal avm normal brain, which must be spared, included into a complex avm. surgery for avms must follow several principles. always perform a large bone flap, providing a wide exposure, completely circumscribing the avm and vessels. feeding arteries must be occluded first to hinder blood flow into the malformation. before occlusion arteries must be carefully inspected. passage arteries must be spared, because they supply normal brain, and improper sacrifice causes ischemia and postoperative neurological deficits. identification of passage arteries can be done by dissecting the nidus controlateral to vascular supply, and arteries emerging from the avm are followed back to the nidus. draining red veins, containing arterialized blood should be sacrificed last. if a vein must be occluded in order to proceed with removal, it should be temporary clipped first and malformation observed. if swallowing of the avm occurs the clip must be removed and vein must be kept until malformation is completed devascularized. small vessels are occluded using bipolar electrocautery, but larger ones necessities vascular clipping. dissection of the avm must be done into the gliotic plane circumscribing the nidus. previous rupture facilitates dissection because it creates a plane between malformation and adjacent brain. avm have a conic form. the deep part of the nidus is most difficult to remove because it contains small highpressure vessels. when the deep part is approached an attempt to recanalization of the avm occurs. (16) after nidus removal is done, carefully hemostasis is achieved at a postoperatory estimated blood pressure. difficulties of the present case are represented by passing middle cerebral artery. the sylvian fissure was split, middle cerebral artery trifurcation was identified, and the main truck was followed back to the nidus. location of the avm into the left temporal lobe poses a risk for worsening language function. avoidance of language area can be done using functional mri, electrocortical stimulation mapping and optical imaging of intrinsic signals. (2, 3, 21) in patients with high risk of language deterioration awake craniotomy with intraoperatory language monitoring can be done. (3) our patient presented dysphasia as a result of rupture of the avm. she presented aphasia immediately after surgery due to postoperative edema, but she fully recovered language function. this particular location is prone for developing right inferior homonymous quadrantanopsia because the avm comes in close vicinity with optic radiations. our patient had no preoperatory or postoperatory visual field deficits. right hemiparesis, in this particular location, can occur because the avm is in close relation with the left internal capsule and during resection of the deep portion the capsule can be damaged or secondary to arterial occlusion. the avm has feeding arteries from talamostriate arteries from left posterior communicating artery and left posterior cerebral artery, anterior choroidal artery and perforating branches from left segment m1 of the middle cerebral artery. improper occlusion of passage arteries supplying normal brain results in motor deficit. in our case although all arteries of passage were spared, the motor deficit was a prior sequel from the first rupture of the malformation with intraparenchymatal capsule-lenticulo-thalamic hematoma. internal capsule damage explains why the patient did not improve after hematoma removal. other complications following romanian neurosurgery (2011) xviii 4: 499 510 509 surgery such as rebleeding from residual nidus, normal perfusion pressure breakthrough, retrograde venous occlusion, ischemia, vasospasm, seizures or hydrocephalus did not occur in our patient. because total removal of the avm was not achieved with surgery we reconsidered adjuvant therapy. further treatment is still necessary after subtotal removal because the risk of hemorrhage form residual nidus remains. by removing the part of the avm circumscribing the middle cerebral artery gamma knife stereotactic surgery became a valid therapeutic option. resection of the part close to middle cerebral artery made it possible to exclude it from the target volume. the particularity of the presented case is presence of residual nidus after surgery, needing adjuvant gamma knife stereotactic surgery. conclusions avms need complex treatment performed in a multidisciplinary team, including neurosurgeon, interventional neuroradiologist and stereotactic neurosurgeon. avms should be addressed to specialized neurosurgical centers, where all treatment modalities are available and multimodal approach can be done for optimal results. surgery is the treatment of choice in management of the avms. reconsideration of treatment options for residual nidus after surgery is recommended. gamma knife stereotactic surgery is required if a residual nidus is left in place following surgery. definitive treatment in avms is mandatory because of the high risks of hemorrhage with high morbidity and mortality. abreviations avm arteriovenous malformation dsa digital subtraction angiography gcs glasglow coma scale correspondence and correction to aurelia mihaela sandu emergency clinical hospital bagdasar-arseni, no. 10-12, berceni street, sector 4, bucharest; e-mail: aurasandu@gmail.com; tel. 0724.263.023 references 1. altschul d, smith ml, sinson gp. intracranial arteriovenous malformation. medscape emedicine[surgery/neurosurgery/vascular]. 2011. 2. bookheimer s. pre-surgical language mapping with functional magnetic resonance imaging. neuropychol rev 17, 145-155. 2007. 3. cannestra af, pouratian n, forage j, bookheimer sy, martin na, toga aw. functional magnetic resonance imaging and optical imaging for dominanthemisphere perisylvian arteriovenous malformations. neurosurgery 55, 804-812. 2004. 4. fridman wa, bova fj. radiosurgery for arteriovenous malformations. neurol res 33, 803-819. 2011. 5. frizzel rt, fisher ws 3rd. cure, morbidity, and mortality associated with embolization of brain arteriovenous malformations: a review of 1246 patients in 32 series over a 35-year period. neurosurgery 37, 1031-1039. 1995. 6. gorgan rm: malformatiile arterio-venoase cerebrale, in popescu i (ed): tratat de chirurgie neurochirurgie. bucharest, ed. academiei romane, 2007, pp 323-335. 7. gorgan rm, neacsu a, bucur n, calina na, pruna vm, martin d. significance of factors contributing to progres after elective surgery of cerebral arteriovenous malformations. ro j stroke 10, 220-223. 2007. 8. greenberg ms: intracerebral hemorrhage, in greenberg ms (ed): handbook of neurosurgery. new york, thieme medical publishers, 2010, pp 1118-1142. 9. greenberg ms: vascular malformation, in greenberg ms (ed): handbook of neurosurgery. new york, thieme medical pulblication, 2010, pp 1098-1117. 10. hauck ef, welch bg, white ja, purdy pd, pride lg, samson d. preoperative embolization of cerebral arteriovenous malformations with onyx. ajnr 30, 492495. 2009. 11. haw cs, terbrugge k, willinsky r, tomlinson g. complications of embolization of arteriovenous malformations of the brain. j neurosurg 104, 226-232. 2006. 510 aurelia mihaela sandu and m.r. gorgan treatment for temporobasal avm 12. hernesniemi ja, dashti r, juvela s, vaart k, niemela m, laakso a. natural history of brain arteriovenous malformations: a long-term follow-up study of risk of hemorrhage in 238 patients. neurosurgery 63, 823-829. 2008. 13. jayaraman mv, marcellus ml, hamilton s, do hm, campbell d. neurologic complications of arteriovenous malformation embolization using liquid embolic agents. ajnr am j neuroradiol 29, 242-246. 2008. 14. kim lj, albuquerque fc, spetzler rf, mcdougall cg. postembolization neurological deficits in cerebral arteriovenous malformations: stratification by arteriovenous malformation grade. neurosurgery 59, 53-59. 2006. 15. liscak r, vladyka v, simonova g, urgosik d, novotny j jr, janouskoya l, vymazal j. arteriovenous malformations after leksell gamma knife radiosurgery: rate of obliteration and complications. neurosurgery 60, 1015-1016. 2007. 16. marciano fk, vishteh ag, apostolides pj, spetzler rf: arteriovenous malformations supratentorial, in kaye ah, black pm (eds): operative neurosurgery. london, harcourt publishers limited, 2000, pp 10791091. 17. maruyama k, kamada k, shin m, itoh d, masutani y, ino k, saito n. optic radiation tractography integrated into simulated treatment planning for gamma knife surgery. j neurosurg 107, 721-726. 2007. 18. misra m, aletich v, charbel ft, debrun gm, ausman ji: multidisciplinary approach to arteriovenous malformations, in kaye ah, black pm (eds): operative neurosurgery. london, harcourt publishers limited, 2000, pp 1137-1151. 19. neacsu a, gorgan rm, bucur n, sandu a, pruna mv. posterior fosa arteriovenous malformations case report. ro neurosurgery 16. 2009. 20. ondra sl, troupp h, george ed, schwab k. the natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. j neurosurg 73, 387-391. 1990. 21. prakash n, uhlemann f, sheth sa, bookheimer s, martin n, toga aw. current trends in intraoperative optical imaging for functional brain mapping and delineation of lesions of language cortex. neuroimag 47, t116-126. 2009. 22. saatchi i, geyik s, yavuz k, cekirge hs. endovascular treatment of brain arteriovenous malformations with prolonged intranidal onyx injection technique: long-term results in 350 consecutive patients with completed endovascular treatment course. j neurosurg 115, 78-88. 2011. 23. schneider bf, eberhand da, steiner le. histopathology of arteriovenous malformations after gamma knife radiosurgery. j neurosurg 87, 352-357. 1997. 24. sen s, webb sw, selph j, hogan el, talavera f, kirshner hs, lutsep hl. arteriovenous malformations. medscape surgery/neurosurgery/vascular. 2010. 25. spetzler rf and martin na. a proposed grading system for arteriovenous malformations. j neurosurg 65, 476-483. 1986. 26. stapf c, mast h, sciacca rr, berenstein a, nelson pk, gobin yp, pile-spellman j, mohr jp. the new york islands avm study: design, study progress, and initial results. stroke 34, e29-34. 2003. 27. stapf c, mast h, sciacca rr, choi jh, khaw av, connolly es, pile-spellman j, mohr jp. predictors of hemorrhage in patients with untreated brain arteriovenous malformation. neurology 66, 1350-1355. 2006. 28. starke rm, komotor rj, otten ml, hahn dk, fischer le, hwang by, garrett mc, sciacca rr, sisti mb, soloman ra, lavine sd, connolly es, meyers pm. adjuvant embolization with n-butyl cyanoacrylate in the treatment of cerebral arteriovenous malformations: outcomes, complications, and predictors of neurologic deficits. stroke 40, 2783-2790. 2009. 29. zhao j, wang s, li j, qi w, siu d, zhao y. clinical characteristics and surgical results of patients with cerebral arteriovenous malformations. surg neurol 63, 156-161. 2005. 5_chiriaca_extracranial internal romanian neurosurgery (2015) xxix 3: 263 268 263 extracranial internal carotid artery aneurysm treated by combined endovascular microsurgical techniques a. chiriac, georgiana ion*, n. dobrin*, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi *“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: extracranial internal carotid artery aneurysms are rare lesions that still represent a challenge from diagnosis and treatment point of view. giant complex aneurysms of extracranial internal carotid artery are usually completely excluded by surgical approaches. we present a case of a patient with an extracranial internal carotid artery aneurysm treated by a combined treatment, along with a short review of this pathology. key words: extracranial internal carotid artery aneurysms, combined treatment. introduction extracranial internal carotid artery aneurysms are very rare documented lesions. even if the spontaneous rupture is uncommon manifestation, they can cause life threatening complications especially represented by thromboembolic. these vascular lesions are characterized by different etiologies, multiple neurological disturbances and varying diagnostic and therapeutic approaches. open surgery is the first mode of treatment with satisfactory in long term. the endovascular approach is also a viable alternative especially when open access to the distal extent of the aneurysm is difficult. in this report we describe a case of giant extracranial carotid aneurysm with fulminant evolution treated by a combined endovascular and surgical technique. etiology and epidemiology most common etiological factors for extracranial internal carotid artery aneurysms include congenital factors, trauma (pseudoaneurysms), athero-sclerosis, infective and fibromuscular dysplasia (3). in the recent studies there has been a change of the etiological profile of extracranial internal carotid artery aneurysms with an increase incidence in atherosclerotic (42% to 70%) and dysplastic (20%) aneurysms and a decrease in infective and posttraumatic aneurysms [9]. extracranial internal carotid artery aneurysm could be characterized like a dilation of ica more than 50% of its normal diameter (0.55±0.66 cm in male and 0.49±0.07 cm in female) [8,9]. for the younger patients the common cause is represented by posttraumatic and infectious factors with possible associated diagnoses of tuberculosis, hiv or takayasu arteritis. salmonella and syphilis is known as main causes of so called mycotic aneurysms. in patients aged over 50 years, atherosclerosis is known as the main cause of these lesions, even if it serves for a secondary finding rather than a primary cause. fibromuscular dysplasia, collagen tissue disorders and irradiation are among the rare etiologies. in terms of location, they can be positioned proximal and distal to the blaisdell line. the proximal types are usually fusiform involving the common carotid artery, the carotid bifurcation and the first part of internal carotid 264 chiriac et al extracranial internal carotid artery aneurysm artery. the distal are usually saccular in shape and located near the angle of the jaw [3]. clinical symptoms the clinical symptoms of the patients with eca aneurysms vary from asymptomatic neck mass or with aerodigestive tract compression, to neurological deficits and aneurysm rupture. the mass effect can cause direct compression of the vagus, hypoglossal or glossopharyngeal nerves or dysphagia due to pressure on pharyngeal constrictor muscles, pharyngeal dysfunction due to pressure on mucous membranes and ear pain radiating to occipital area. horner’s syndrome can be developed due to the affected cervical sympathetic nerves and hoarseness can be seen as a result of vagus nerve compression. most of the patients addresses on admission for painful pulsatile mass at neck region. however, some patients may develop transient ischemic attack or stroke due to a thrombotic or embolic event from the aneurysmal contents. spontaneous rupture or bleeding are very rare but sometimes sever complication can be seen. among the patients of published literature, 60% experienced transient ischemic attack (33% amaurousis, 21% hemispheric) or obvious stroke (8%) [9]. the risk of rupture was documented to be higher in mycotic carotid aneurysms whereas traumatic ones tend to stabilize and show regression in time. imaging diagnosis early diagnosis and anatomical characterization of these lesions are very important in terms of both endovascular and surgical treatments. the diagnosis may be established by doppler ultrasound witch ensure determination of the size and extension of the aneurysm. doppler examination is sufficient to characterize vascular and pulsatile structure of these lesions, but without being able to give enough information concerning the thrombosed part and relation with its neighboring structures. conventional digital subtraction angiography remains the “gold standard” imaging investigation for the aneurysms diagnosis. even so, it has the disadvantage of offering incomplete information, only about their patent lumen. current angiographic explo-rations represented by angio-ct and angio-mri provide a complete diagnostic imaging and highlighting information on the vascular lumen, thrombosed portions and existing calcifications. treatment the treatment options are represented by surgical excision, endovascular interventions or conservative management. surgery remains the gold standard and the different procedures consisted in simply ligation of the internal carotid artery and aneurismal sac resection with wall reconstruction, end to end anastomosis, graft interposition of saphenous vein, ptfe or dacron or eca to ica by-pass. the aim of surgery is to remove the risk of thromboembolic events or rupture of the aneurysm. the end to end anastomosis procedure is indicated in case of presence of artery tortuosity especially in elderly patients. the main risks of surgical interventions are represented by transient ischemic attacks (8%), cerebrovascular accidents (4–4.5%), cranial nerve injury (glossopharyngeal, vagus and hypoglossal, 20.8–44%) and death [0% in elective cases, 50% in emergency cases] [8]. the endovascular techniques are indicated especially in poor surgical candidates or who refuse surgery and consisted in ica occlusion with detachable balloons, aneurysm coil embolization and stent graft reconstruction. case presentation romanian neurosurgery (2015) xxix 3: 263 268 265 a 62-year old man was referred to our neurosurgey department with a two-week history of an enlarging right neck mass. the patient declares a cranio-cervical trauma in last month by accidental dropping with laterocervical impact of a hard object. the physical examination revealed a pulsatil semi-solid cervical mass located anterior to the sternocleidomastoid muscle (figure 1). there was an associated pain and compressive symptoms with hoarseness, odynophagia or dysphagia for the last three days. he had no symptoms suggestive of cranial or peripheral neurologic deficits. figure 1 patient with latero-cervical mass imaging investigations started with an ultrasound doppler performed at admission, which revealed the “mass” to be a giant aneurysm of the right internal carotid artery (ica). the distal end of the internal carotid artery could not be highlight on ultrasound. the digital subtraction angiography performed revealed a giant dysplastic aneurysm at the right common carotid artery bifurcation with atherosclerotic partially calcified walls. the left common carotid artery bifurcation presents a partially calcified atherosclerotic plaque with extension in to internal carotid artery and without significant stenosis effect. both vertebral arteries are patent and no evidence of atheroma. 266 chiriac et al extracranial internal carotid artery aneurysm figure 2 dsa image of a giant right extracranial ica aneurysm figure 3 dsa image of an athermatous left ica bifurcation after discussing the options with the vascular team we decided to treat the patient by a combined approach, endovascular carotid occlusion and surgical aneurysm resection. a temporary balloon occlusion testing under fluoroscopic guidance was performed for 10 minutes. the procedure showed a good arterial compensation of the right internal carotid artery territory by left internal carotid injection via anterior communicating artery. the right vertebral artery injection with right carotid temporary balloon occlusion showed a partial posterior communicating artery contrast filling (figure 4). after occlusion testing a permanent obstruction of the right common carotid artery was performed by placing two latex detachable balloons (goldballoon 3) at the proximal part of the vessel (figure 5). romanian neurosurgery (2015) xxix 3: 263 268 267 figure 4 dsa images showing right ica test occlusion and good supplying of right ica territory by left ica injection figure 5 dsa images showing right ica occlusion with no contrast filling of the aneurysm the next day the patient was referred to the vascular surgery clinic for complete resection of the aneurysm. the procedure was performed under general anesthesia continuously systemic anticoagulation. the lesion was achieved through a standard approach along the anterior border of the sternocleidomastoid muscle. the aneurysm was exposed with carefully preservation of vii, x, xii cranial nerves. a total resection of the aneurysm was performed by vascular permanent clip placement above (ica, eca) and below (cca) the lesion. the postoperative course was very good and the patient was discharged on post-operative day 5. conclusions the possibility of an aneurysm at extracranial internal carotid artery should always be considered in patients with increasing volume mass in the neck. the good results obtained by both endovascular and surgical techniques are an important indicator for an urgent treatment in such patients with these particular vascular lesions. correspondence stefan m. iencean “gr. t. popa” university of medicine and pharmacy, iasi references 1. ak, k., i̇sbir, s., bayramiçli, m., tekeli, a., bozkurt, s., & arsan, s. (2009). aneurysm of extracranial internal carotid artery: a case report. http://hdl.handle.net/11424/2199. 2. blanco, e., serrano, f. j., reina, r., martín, a., moñux, g., ponce, a., & morata, c. (2008). saccular aneurysms of the extracranial internal carotid artery. experience and review of the literature. journal of cardiovascular surgery, 49(1), 73. 3. castelli, p., scamoni, c., caronno, r., piffaretti, g., tozzi, m., carnini, m., & canziani, m. (2005). giant aneurysm of the extracranial carotid artery: case report. ejves extra, 9(4), 84-86. 4. kakisis, j. d., giannakopoulos, t. g., moulakakis, k., & liapis, c. d. (2014). extracranial internal carotid artery aneurysm. journal of vascular surgery, 5(60), 1358. 5. lim, y. m., lee, s. a., kim, d. k., & kim, g. e. (2002). aneurysm of the extracranial internal carotid artery presenting as the syndrome of glossopharyngeal pain and syncope. journal of neurology, neurosurgery & psychiatry, 73(1), 87-88. 6. perrin, j. m., turowski, b., steiger, h. j., & hänggi, d. (2012). double-barrel extracranial–intracranial bypass 268 chiriac et al extracranial internal carotid artery aneurysm surgery followed by endovascular carotid artery occlusion in a patient with an extracranial giant internal carotid artery aneurysm due to ehlers–danlos syndrome. journal of neurointerventional surgery, neurintsurg-2012. 7. robijn, s. m., welleweerd, j. c., lo, r. t., moll, f. l., & de borst, g. j. (2015). treatment of an extracranial internal carotid artery aneurysm with a flow-diverting stent. journal of vascular surgery cases, 1(2), 191-193. 8. smith m., johnson p. (2013) spontaneous extracranial internal carotid artery aneurysm. a case report. westindianmedj2013;62(7):667. 9. yetkin, u., yürekli, i̇., & gürbüz, a. (2006). extracranial internal carotid artery aneurysms. internet j thorac cardiovasc surg, 10(2). 10. wu, j., chen, y., qu, l., he, y., zhi, k., bai, j., ... & wu, y. (2015). using ptfe covered stent-artery anastomosis in a new hybrid operation for giant juxtaskull internal carotid aneurysm with tortuous internal carotid artery. international journal of cardiology, (185), 25-28. microsoft word 6florestean_modern.doc romanian neurosurgery (2012) xix 3: 217 225 217 modern methods of endovascular approach to cerebral arteriovenous malformations n.c. florestean1, a.v. ciurea2 1phd. student umf “carol davila” , bucharest, emergency department, “bagdasar arseni” clinical emergency hospital; 2neurosurgical clinic, “bagdasar arseni” clinical emergency hospital, bucharest, romania abstract the article is a review of major historical events in the development of the methods of endovascular approach of arteriovenous malformations (avm) starting with the first cerebral angiography performed on a dog in 1926, serbinenko’s embolization techniques of cerebral vascular lesions using detachable balloons in 1974, ending with january 1991 when the first embolization with gdc (guglielmi detachable coils) was done on a brain aneurysm. it’s considered that there are approximately 1,100 patients diagnosed with cerebral arteriovenous malformation treated with gdc each month. key words: endovascular, embolization, arteriovenous malformations, detachable coils. immediately after the discovery of x rays in 1895, in vienna, hascheck and lindenthal visualized blood vessels by injecting an opaque substance into dead bodies (1). in 1926, moniz (2) performed the first angiography in dogs by injecting a solution of lithium bromide and strontium obtaining the first image of cerebral circulation. the first electrothermic thrombosis of a cerebral aneurysm was achieved by a transorbital insertion of a silver wire introduced through a special needle, the wire was heated to 80 ° c for 40 seconds. in 1960, mullan and his colleagues (3) studied different methods to induce aneurism thrombosis. in a preliminary study, they achieved a complete thrombosis in dogs by inserting small electrodes directly into the vessel wall and applying an electric current. subsequently, these authors have reported the treatment of 10 cerebral aneurysms by producing electro thrombosis. under fluoroscopic guidance, thrombosis was initiated by passing an electric current through a needle electrode inserted into the aneurysm. gallagher described his method called 'pilojection' which consists in introducing horse and dog hair in the aneurysmal sac (4). luessenhop and velasques, in the early 1960s, showed that navigation and catheterization through the cerebral vessels would be easier and without complications if there were used approximately equal pressures to the systolic blood pressure (5). in 1966, for navigation in cerebral arteries frei (6) used special catheters which had micro magnets inserted at their tip and which could be guided by an external magnetic field. 218 florestean, ciurea endovascular approach to cerebral arteriovenous malformations yasargil, who had experience both in cerebral angiography and in stereotactic therapy tried to inject iron particles in the cerebral vessels and to guide them towards by using stereotactic magnets. this attempt failed due to technical reasons. a student of yasargil, john alksne, used both iron particles and a combination of acrylic mixture and micro particles of iron (7). hilal in 1974 also used the magnetic directed catheters (8). the first stage of endovascular treatment of cerebral avm was to occlude the feeder vessel to the cerebral avm (figure 1). this treatment was successful in some cases (in the occlusion of internal carotid arteryicawith detachable balloons just proximal to the avm or by occlusion of both vertebral arteries (va) in post cranial fossa avms). these occlusions are preceded by vascular occlusion tests. cerebral artery occlusion test with non detachable balloons aims to assess the tolerance of these vessels to that occlusion. the goal is to treat huge avms-c that can not be selectively obliterated. it also evaluates the arterial supplantation provided by willis polygon (ica test occlusion). an intravenous heparin bolus injection of 5000 iu is administered at the beginning of the test. two arterial ways are used: either the femoral way or the carotid way of the avm-c side and a femoral way to study the supplantations (figure 2). hemispheric cerebral blood flow on each side is measured by the ica injection of isotope (xenon 133). middle cerebral artery (mca) blood flow velocity is also measured bilaterally with a transcranial doppler. these data once obtained, the balloon is inserted in the intracavernous segment of ica. then the balloon is inflated in order to obtain ica occlusion. this procedure should not exceed 30 minutes. figure 1 avm-c occipital (a, b), partial embolization (c) control after two months (d) (15) figure 2 the femoral approach romanian neurosurgery (2012) xix 3: 217 225 219 during occlusion the following parameters should be observed: • clinical tolerance (sensory, kinaesthetic and superior functions); • doppler examination (figure 3) is performed for three or four times within 30 minutes (a bigger asymmetry than 25% between the two hemispheres in mca blood flow velocity is not allowed); • blood flow is measured at 2, 10 and 20 minutes by xenon 133 injection in controlateral ica occlusion; • the study of arterial supplantations through angiography. if the mentioned criteria are not fulfilled, the test is rendered negative. the balloon is deflated and a temporo-sylvian anastomosis is performed. the interval between test repeating and performing temporo-sylviene anastomosis is between 15 days and 1 month. the test with diamox (acetazolamide) can be used in order to study the cerebral circulation, and especially the collateral circulation. the acetazolamide is a carbonic anhydrase inhibitor that inhibits the conversion of carbonic acid to co2 and h2o in the brain causing acidosis and decreased ph. these transformations lead to vasodilatation, but the acetazolamide does not cause low general blood pressure. figure 3 carotid dopplerecho the test was initially used to assess cerebral circulation in patients with carotid stenosis for revascularization procedures. tomography with 133 xe is performed in order to obtain the basic cerebral blood flow (cbf). then 1 mg of diamox is injected intravenously and tomography is repeated after 15-20 minutes. the two ct scans are compared. response to diamox varies from one patient to another. patients with normal collateral circulation have a normal response to acetazolamide without blood redistribution. this test can be used to study the brain areas surrounding the avm-c. (15) allock maneuver is also performed. it consists of injecting the va while ica is being occluded in turn; the size of posterior communicating artery is observed (if it is > 1mm in diameter; bilateral va occlusion is possible ). a study by fox in 1987 (9) performed in 68 patients, showed that only 13.2% had transient ischemic attacks and there was only a case of stroke. the second stage of development in endovascular treatment of cerebral vascular lesions is the selective occlusion of cerebral avms. in 1974, serbinenko (10) published in the journal of neurosurgery the endovascular treatment method with detachable balloons. the idea of using balloons in endovascular treatment came after observing children who were holding helium-filled balloons in the red square in moscow during the may 1 demonstration. serbinenko used latex balloons which were obtained by melting rubber bands (11). during this period, endovascular treatment method for cerebral vascular lesions with detachable balloons has become the standard method. in time, the main disadvantages of this method became apparent. thus, hyper selective 220 florestean, ciurea endovascular approach to cerebral arteriovenous malformations catheterization of cerebral vessels is difficult due to the impossibility of using guide wire. the balloon can not take the irregular shape of an ordinary aneurysmal sac. by using detachable balloons for occlusion of cerebral aneurysms there occur very often complications consisting of aneurysmal rupture and their recanalization (waterhammer effect). detachable balloons are currently used in the occlusion of vessels with giant, fusiform aneurysms. hilal and solomon (12) introduced pushable platinum coils in avm-c (pushthem-out-the-end). the big disadvantage of these coils is that they can not be retrieved. while introducing electric current through an electrode in an experimental aneurysm in 1980, guido guglielmi observed its accidental detachment. together with ivan sepetka, engineer for target therapeutics, they built gdc (guglielmi detachable coils). in march 1990, at ucla (university of columbia los angeles), after the failure of a detachable balloon occlusion of a carotidcavernous fistula caused by a ruptured cavernous sinus aneurysm, two venous gdc were used for the first time, which led to permanent occlusion of the fistula. in the same place, at ucla, in january 1991 (13) the first gdc embolization of cerebral aneurysm was performed, and in 1995 united states food and drug administration approved the use of gdc. by 2000, over 60,000 worldwide patients with cerebral aneurysms and cerebral arteriovenous malformations were treated with gdc and it is assumed that approximately 1,100 patients are treated with gdc every month (figure 4). future development of endovascular treatment of cerebral avm will probably know two ways of evolution. the first way would be to develop imaging techniques, especially the endoluminal ones (endoscopy, angiography) with real-time streaming. the second way of development would be to find an ideal embolization agent (14) with the following qualities: it must adjust itself to avm-c shape, not affect the nutritional vessel, absorb the energy transmitted to avm-c walls through pulses and prevent the further growth of avm-c (figure 5). study in the period january 1, 2000 december 31, 2009 a total of 426 patients with cerebral arteriovenous malformations [avm] were hospitalized in the neurosurgery i clinic of the "bagdasar arseni" emergency hospital. all the cases were investigated in the clinic with a view to setting up a good quality positive diagnosis by brain ct scan with contrast substance or mri with brain angio-mri. figure 4 embolization with gdc (14) romanian neurosurgery (2012) xix 3: 217 225 221 figure 5 left parietal avm-c multistage cyanoacrylate embolization (16) in order to evaluate the angioarchitecture and the hemodynamics of the nidus, and to determine the opportunity of the surgical, endovascular treatment indication by embolization or gammaknife radiosurgery of the avms, all the patients were investigated by carotid bilateral and vertebral digital sustraction angiography (dsa) (the so-called "four vessels angiography"). the patients diagnosed with cavernous vascular malformation following ct investigation and brain mri, undertook cerebral angiography only in the case of suspected association of cavernoma with a vascular malformation. we excluded from the study the cases with super-acute evolution (massive intraparenchimatous brain hemorrhages, intraventricular hemorrhages or massive hemorrhages of the brain trunk) in which the time elapsed from admission to the death only allowed for urgent resuscitation and hemodynamic stabilization to be applied, and did not allowed one of the therapy methods specific for vascular malformation to be applied. because one of the declared purposes of the study is to establish the therapeutic behavior and to determine the efficiency of the multimodal treatment of cerebral arterio venous malformation, we only kept in the study group the patients in whom at least one of the established active treatment methods were applied: microsurgery treatment, endovascular treatment or gamma-knife or the more reserved attitude of observation and surveillance of the lesions in asymptomatic or oligosymptomatic selected cases. thus, the criteria of inclusion and the exclusion in the study were established: inclusion criteria: clinical and paraclinical diagnosis (ct and/or brain mri) of cerebral arteriovenous malformation; assessment of angioarchitecture and hemodynamics by carotid bilateral and vertebral digital sustraction angiography (dsa); hospitalization in the period 01.01.2000 – 31.12.2009. exclusion criteria: the patients in whom, irrespective of the reasons (death in short time of admission, discharge upon demand or refusal of the treatment etc.), none of the active treatment methods was applied: micro-surgery treatment, endovascular treatment or gamma-knife treatment, or passive treatment: observation; the patients in whom the postprocedural follow-up period was less than 6 months; the patients who never appeared in the post-procedural control. 222 florestean, ciurea endovascular approach to cerebral arteriovenous malformations following the application of the above criteria, a group of 375 patients who meet all the six inclusion and exclusion criteria resulted. out of the 375 patients, in comparison to the 246 patients who undertook surgery, the remaining 129 patients benefited of multimodal treatment or other alternative therapy as follows: 46 patients (35.66%) benefited of stereotactic radiosurgery; 53 patients (41.08%) benefited of embolization; 19 patients (14.73%) were followed up clinically and paraclinically; 11 patients (8.53%) benefited of multimodal treatment, out of which • 4 patients (3.1%) received surgery and then radiotherapy by gamma-knife for the residual nidus; • 5 patients (3.8%) were treated by embolization in the first phase and then they were irradiated by stereotactic method; • 2 patients (1.5%) needed a complex, sequential treatment: embolization surgery gamma-knife or surgery embolization gamma-knife. (figure 6) we divided the study period in two: the patients treated with complementary therapies before putting into operation of the centre of excellence in neurosurgery of "bagdasar arseni" emergency hospital and the afterward period. thus, we have obtained excellent results for the patients treated before and after the opening of the center as follows: out of all the 57 cases treated by stereotactic radiosurgery 5 patients benefited in the period january 2000 october 2004 (in clinics abroad), and the remaining 52 patients were treated in our hospital; out of the 60 patients treated by embolization, in the neurosurgery i clinic, there were sent to clinics abroad 9 cases, and the remaining 51 patients were treated by embolization with coils or particles with glubran within the center of excellence in neurosurgery within our hospital. 246 46 53 4 52 19 distribuţia pacienţilor în funcţie de metoda terapeutică tratament chirurgical tratament gamma-knife embolizare chirurgie + radiochirurgie embolizare + gamma-knife embolizare + chirurgie + gammaknife observatie clinica si paraclinica figure 6 romanian neurosurgery (2012) xix 3: 217 225 223 so that we have a rate of 8.77% of patients who were treated by stereotactic radiosurgery method were sent to for treatment to clinics abroad, in the first period of 58 months, and 91.23% of the patients treated in the center of neurosurgery within our hospital in 62 months, in the second period. from among the patients treated in the neurosurgery clinic i of the hospital by the method of embolization of the arteries that nourish the cerebral arteriovenous malformations we notice that about 15% of patients were treated abroad, as compared with the remaining 85% of the cases treated in our hospital, in the same periods of time. we have a mortality of 5.84% with a morbidity of 41.6% in the first phase of the study (january 2000 october 2004) and in the second phase (november 2004 december 2009) we have a mortality 3.9% with a mortality of 21.8%. clinical case the patient d.c., aged 21 years, appeared in 2003 in our clinic with headache and commemorative crises of loss of conscience with onset about six months ago, for additional specialty investigations. brain ct scan reveals paraventricular space replacement process in the left occiptal horn that comes to contrast upon administration, without other cerebroventricular tomodensitometric changes that raises the suspicion of a vascular malformation (figure 7). decision is made to perform a "4 vessels" cerebral angiography, which shows a left parietal arterio-venous malformation with nidus of about 5 cm with multiple artery afferences from the left pericallous artery (which shows increased caliber due to flow rate arteriopathy), left posterior cerebral artery (also this with an increased caliber), left parietal-occipital artery, without other intranidal changes. the superficial venous drainage is made in the parietal portion of the sss by a main pedicle represented by a cortical sinuous and tortuous dilated vein and by 2-3 secondary pedicles represented by 2-3 cortical veins with normal caliber, and the deep venous drainage is made in the right sinus via galen’s ampoule through a very dilated sinuous and tortuous vein. the malformation also injects itself from right ica through a pedicle from the right anterior communicating artery and it shows a minimum displacement to the right of the median axis of the vascular tree (figure 8). figure 7 tomographic aspect of a left parietaloccipital cerebral arteriovenous malformation figure 8 angiographic aspect of left parietaloccipital cerebral avm 224 florestean, ciurea endovascular approach to cerebral arteriovenous malformations the diagnosis of martin-spetzler left parietal-occipital arterial-venous malformation grade iv is put, due to its location in an eloquent area, the size of the nidus and due to the superficial and deep complex drainage. due to the major risks presented by the neurosurgical intervention, the assessment of the malformation is decided, with a view to embolizing it. in february 2004 the first embolization is practiced with bioactive coils in a clinic abroad (interballcan medical center in salonioc-greece) (figure 9). in february, may and november 2005 the multi-stadialization of the embolization with glubran particles is continued in the center of excellence in neurosurgery of the "bagdasar arseni" emergency hospital (figure 10). unfortunately, after all the four embolization, a rest of the nidus of the arteriovenous malformation of about 1.5 cm remains, as revealed on brain mri (figure 11), so it is decided irradiation by gamma-knife in july 2008. the patient is neurologically improved under anticonvulsant therapy. a b c figure 9 a. preembolization; b. postembolization: c. intraembolization figure 10 succesive images after the three embolizations figure 11 mri image of the nidal rest of parietooccipital brain avm conclusions we notice a marked increase in the addressability to modern techniques of treatment by embolization and stereotactic radiosurgery gamma-knife, after the opening of the center of excellence in neurosurgery equipped according to the european standards, it being the sole center of this kind in this country, with significant decrease in the morbidity and mortality. the analysis of the presented study, related to the cerebral arteriovenous malformations, the casuistry of neurosurgery clinic i, reflects the current romanian neurosurgery (2012) xix 3: 217 225 225 situation in the romanian health system and in the romanian neurosurgery in the treatment of cerebral arteriovenous malformations, the "bagdasar-arseni" emergency hospital being the only center in this country where there are met all the conditions for application of the three active therapies currently practiced anywhere in the world, in mav-c treatment: microsurgical treatment, endovascular therapy and the gamma-knife stereotactic radiosurgery, as monotherapy or as multimodal approach. references 1. alksne, j.f., stereotactic thrombosis of intracranial aneurysms. n engl j med, 1971. 284(4): p. 171-4. 2. constantinovici, a., ciurea, av., tratamentul malformatiilor arterio-venoase ale snc. ghid practic de neurochirurgie. 1998 3. fox, p.l., g.m. chisolm, and p.e. dicorleto, lipoprotein-mediated inhibition of endothelial cell production of platelet-derived growth factor-like protein depends on free radical lipid peroxidation. j biol chem, 1987. 262(13): p. 6046-54. 4. frei, e.h., et al., the pod and its applications. med res eng, 1966. 5(4): p. 11-8. 5. gallagher, j.p., obliteration of intracranial aneurysms by pilojection. jama, 1963. 183: p. 231-6. 6. guglielmi, g., et al., electrothrombosis of saccular aneurysms via endovascular approach. part 2: preliminary clinical experience. j neurosurg, 1991. 75(1): p. 8-14. 7. haschek, e., lidenthal, ot., ein beitrag zur praktischen verwerthung der photographie nach rontgen. wien klin. wschr., 1896. 9: p. 63-64. 8. hilal, s.k., et al., magnetically guided devices for vascular exploration and treatment. radiology, 1974. 113(3): p. 529-40. 9. hilal, s.k. and r.a. solomon, endovascular treatment of aneurysms with coils. j neurosurg, 1992. 76(2): p. 337-9. 10. luessenhop, a.j. and a.c. velasquez, observations on the tolerance of the intracranial arteries to catheterization. j neurosurg, 1964. 21: p. 85-91. 11. moniz, e., l'encephalographie arterielle: son importance dans la localisation des tumeurs cerebrales. rev neurol (paris), 1927. 2: p. 72-89. 12. mullan, s., p.v. harper, and y. gerol, an experimental study in the use of a rapidly decaying beta source (pd109) in the production of deep cerebral lesions. am j roentgenol radium ther nucl med, 1960. 84: p. 108-12. 13. purdy, p.d., et al., arteriovenous malformations of the brain: choosing embolic materials to enhance safety and ease of excision. j neurosurg, 1992. 77(2): p. 21722. 14. serbinenko, f.a., balloon catheterization and occlusion of major cerebral vessels. j neurosurg, 1974. 41(2): p. 125-45. 15. serbinenko, f.a., [balloon occlusion of saccular aneurysms of the cerebral arteries]. vopr neirokhir, 1974(4): p. 8-15. 9breharf_severetbi 448 brehar et al severe tbi followed by cranioorbitar reconstruction severe tbi with complex craniofacial fractures followed by cranioorbitar reconstruction f. brehar, a. giovani, l. munteanu, r.m. gorgan abstract: young age is associated with better outcome in patients with severe traumatic brain injury (tbi). still the reported mortality rate in patients that present in profound coma glasgow coma scale (gcs) -3 pts is very high, even approaching 100% in the presence of fixed and dilated pupils in some series. we report a case of a 25 years old patient with a severe tbi in a car crush and presented in severe coma with a bilateral frontal and right temporal brain laceration with extended posttraumatic subarachnoid hemorrhage and a complex cominutive right frontal, maxillary and zygomatic fracture corresponding to le fort iii fracture. after a difficult postoperative course with complications of tracheostomy like candidosis and bronchopneumony, then after a slowly progressive recovery, the patient was hemiparetic and with a persistent right 3rd nerve paresis at 6 weeks after the traumatic event, but was able to speak and to ambulate with assistance. given the large bony defect that remained, a frontal and facial bony reconstruction was made by an interdisciplinary team using titanium plates and screws. considering the excellent results in this case we advocate that young patients who suffered severe tbi even if they present in a very bad neurological shape should be given access to the best treatment. key words: le fort iii fracture, severe brain injury, cranio-orbitar reconstruction. introduction data from the collaborative european neurotrauma effectiveness research in tbi (center-tbi) show that 2.5 million people will suffer from some form of traumatic brain injury (tbi) in europe every year, 1 million will be admitted to the hospital and 75000 will dye. in us the annual cost of tbi is over 75 billion usd. the last 3 decades showed important improvement in the surgical and medical treatment and in the outcome of severe tbi expressed in lower morbidity and mortality. (3, 4) the surgical treatment should be prompt and include evacuation of the contusions, hematomas or lacerations using large craniotomies and dural reconstruction with fascia to decrease the cerebral pressure. (5) every lesion which determines midline shift presents with a gcs<8 and has more than 2 romanian neurosurgery (2014) xxi 4: 448 – 453 449 cm diameter should be addressed surgically. the importance of the neurosurgical intensive care unit must be stressed but the neurosurgeon should direct the postoperative care of the patient as well. (2) the tracheostomy may be used only in situations when there is no other alternative. more and more departments use the monitorization of brain metabolism through jugular vein oxygen saturation. (6, 7) the secondary brain damage through seizures has to be avoided using anticritic medication and eeg monitoring to detect the seizure. while surgery aims survival the popstoperative recovery is of great help in lowering the morbidity. case presentation the 25 years old patient was driving a car that crushed frontally at more than 200km/h into a concrete wall. when he was brought by helicopter in the emergency department the only neurological response elicited was extension to nociception (gcs-4 pts.). a large frontal scalp laceration was visible, multiple bone fragments were palpable underneath with cerebral tissue extruded through the laceration. a ct scan with bone window and bone reconstruction was immediately obtained which showed bilateral frontal and right temporal brain laceration with extended posttraumatic subarachnoid hemorrhage. also bilateral frontoorbitar complex fractures and right temporal complex fracture. also the right maxilar and zigomatic bone presented cominution fractures and bilateral hemosinus was observed. 450 brehar et al severe tbi followed by cranioorbitar reconstruction figure 1 a ct scan with bone reconstruction at presentation: bilateral frontal and right temporal brain laceration and bilateral frontoorbitar complex fractures and right temporal complex fracture; right maxilar and zigomatic bone presented cominution fractures and bilateral hemosinus. b 1 month postop ct – note ischemia and bone defect the patient presented gross edema of soft tissue, bilateral circumorbital ecchymosis with bilateral subconjunctival hemorrhage, epistaxis, csf rhinorrhoea, enophtalmia, and left face deformity coresponding to lefort iii fracture. after other serious life threatening lesions were excluded the patient went directly to surgery. both the frontal brain lacerations were cured and hemostasis was achieved with difficulty. the bone fragments in the superior and lateral right orbital wall were removed then fragments from the right temporal bone. dura was reconstructed with fascia and gelaspon was applied on the defects. the patient neurological status does not improve after surgery and after 3 days a tracheostomy is needed. on day 10 post surgery the patient is febrile. a csf sample is sent for analysis and the result was candida infection. the antimicotic therapy is started. two weeks later the neurological status improves the pacient is extubated, spontaneously opens the eyes, and correctly executes verbal comands, but he has severe left sided hemiparesis. during the third postop week the neurological status is worsening and the patient needs to be reintubated (gcs 5 pts). the ct scan on this occasion shows a right frontal brain haemorrhagic laceration. emergency surgery is performed and the hematoma evacuated and the laceration is resected with aspiration and coagulation. figure 2 3 weeks postop – haemorrhagic transformation of right frontal brain laceration, with reintervention .and 6 weeks follow up ct scan romanian neurosurgery (2014) xxi 4: 448 – 453 451 after this second surgery the evolution is slowly favourable and the patient regains counsciousness. the patient is febrile again and staphilococcus and candida are found in the csf. the antibiotic treatment is adjusted according to the antibiogram. a lumbar drainage is required for 5 days draining about 150ml/24 h csf. after a slowly progressive neurological amelioration the patient is discharged from the icu to the ward, 6 weeks after admission, with severe left hemiparesis, and right 3rd nerve palsy. following 5 months of intensive neurorheabilitation, the patient shows an impressive recovery being able to ambulate with assistence and to entertain a normal conversation though with minimal recovery of the 3rd nerve paresis. given the bone defect that remained after these operations (figure 1) a third cranioplasty surgery was staged to reconstruct the frontotemporal defect and the roof and lateral wall of the orbita with perforated titanium plates. the surgery was performed by an interdisciplinary team including a maxilofacial surgeon. we used a large twisted sheet of titanium plate to reconstruct the superior orbital rim and the roof of the orbita. another titanium plate was used to reconstruct the temporal bone defect. discussion as tbi is considered “the most complex disease in our most complex organ.” there are many variables on which the outcome depends so it is difficult to be predicted. (1) tbi triggers a chain of chronic process, with progressive injury over hours, days, weeks, months, and even years. following severe tbi the survivors may develop various cognitive impairment and emotional disturbances thus impairing their normal function in society. (8, 11) this case report shows that a good outcome can be achieved after severe tbi that brings the patient to the hospital in profound coma. the sooner the time from the accident to the surgery the better the chance of survival, in this case with a good recovery. (12, 13) the complex frontoorbital fracture in this case may have reduced the mass effect and the imminence of brain herniation consecutive to such extensive brain lesions as the patient presented. even under a severe metabolic disturbance that followed the bronchopneumony associated with the intubation and the candida infection, the age of the patient may have been the decisive factor in the course he followed towards recovery. (9, 14) as long as there is no clear guideline in treating these patients and we cannot predict the outcomes of such severe tbi we believe these cases should not be abandoned and they should benefit from the best surgical and medical treatment. 452 brehar et al severe tbi followed by cranioorbitar reconstruction figure 3 right frontoorbitar reconstruction, 6 months after the first surgery correspondence giovani andrei giovani.andrei@gmail.com references 1. chesnut rm, marshall lf, klauber mr, blunt ba, baldwin n, eisenberg hm, et al: the role of secondary brain injury in determining outcome from severe head injury. j trauma 34:216–222, 1993 2. demetriades d, kuncir e, velmahos gc, rhee p, alo k, chan ls: outcome and prognostic factors in head injuries with an admission glasgow coma scale score of 3. arch surg 139:1066–1068, 2004 3. eisenberg hm, gary he jr, aldrich ef, saydjari c, turner b, foulkes ma, et al: initial ct findings in 753 patients with severe head injury. a report from the nih traumatic coma data bank. j neurosurg 73:688–698, 1990 4. fearnside mr, cook rj, mcdougall p, mcneil rj: the romanian neurosurgery (2014) xxi 4: 448 – 453 453 westmead head injury project outcome in severe head injury. a comparative analysis of pre-hospital, clinical and ct variables. br j neurosurg 7:267–279, 1993 5. gennarelli ta, champion hr, copes ws, sacco wj: comparison of mortality, morbidity, and severity of 59,713 head injured patients with 114,447 patients with extracranial injuries. j trauma 37:962–968, 1994 6. goebert hw jr: head injury associated with a dilated pupil. surg clin north am 50:427–432, 1970 7. kotwica z, jakubowski jk: head-injured adult patients with gcs of 3 on admission—who have a chance to survive? acta neurochir (wien) 133:56–59, 1995 8. lieberman jd, pasquale md, garcia r, cipolle md, mark li p, wasser te: use of admission glasgow coma score, pupil size, and pupil reactivity to determine outcome for trauma patients. j trauma 55:437–442, 2003 9. phuenpathom n, choomuang m, ratanalert s: outcome and outcome prediction in acute subdural hematoma. surg neurol 40:22–25, 1993 10. pickett w, ardern c, brison rj: a population-based study of potential brain injuries requiring emergency care. cmaj 165:288–292, 2001 11. signorini df, andrews pj, jones pa, wardlaw jm, miller jd: predicting survival using simple clinical variables: a case study in traumatic brain injury. j neurol neurosurg psychiatry 66:20–25, 1999 12. tien hc, cunha jr, wu sn, chughtai t, tremblay ln, brenneman fd, et al: do trauma patients with a glasgow coma scale score of 3 and bilateral fixed and dilated pupils have any chance of survival? j trauma 60:274–278, 2006 13. valadka ab: injury to the cranium, in mattox kl, feliciano dv, moore ee (eds): trauma (ed 4). new york: mcgrawhill, 2000, pp 377–399 14. waxman k, sundine mj, young rf: is early prediction of outcome in severe head injury possible? arch surg 126:1237– 1242, 1991 9chiriaca_combinedtreatment romanian neurosurgery (2015) xxix 2: 187 191 187 combined treatment for complex intracranial aneurysm a. chiriac1,*, georgiana ion*, n. dobrin*, st.m. iencean1, i. poeata1,* 1“gr. t. popa” university of medicine and pharmacy, iasi *“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: complex aneurysms often cannot be completely excluded by a single approaches. today successful treatment of these lesions requires a combination between microsurgical and endovascular techniques. planning of combined treatment require a very good understanding of aneurysm anatomy and a close collaboration between neurosurgeon and neuroendovascular interventionist. endovascular coiling can usually be used as early treatment for a partially aneurysm occlusion including the ruptured area and followed by definitive clipping. on the other hand microsurgical clipping also can be used as first treatment for complex aneurysm neck reconstruction, allowing successful secondary placement of coils inside the remnant aneurysm sac. key words: complex intracranian aneurysms, combined treatment. introduction the aim of treatment in patient with cerebral aneurysms is the permanently exclusion of the entire vascular lesion from the arterial circulation by a complete obliteration of their lumen. both surgical and endovascular treatments may offer a stable and totally occlusion of the cerebral aneurysm with long-term outcome. however, aneurysm remnants after microsurgical clipping were documented in 4% to 8% of the patients who undergo angiographycal evaluation postoperatively. these remnants are usually associated with a persistent risk of rebleeding with potentially sever or even fatal consequences. the rebleeding events were reported even short or long time after surgery. microsurgical reintervention is usually advocated in patients with incomplete aneurysm clipping. however, these procedures are often technically difficult due to a difficult brain scar microdisection around the clip or an instable medical condition after a second rebleeding. endovascular embolisation has been reported as successfully alternative for these postoperative aneurysm remnants and sometime may represents a good alternative for these special situations. we report a case with a rapid remnant aneurysm rebleeding after incomplete clipping who was successfully obliterated by endovascular coil occlusion. 188 chiriac et al combined treatment for complex intracranial aneurysm case report the female patient aged 54 years, was admitted to our emergency room in coma grade iii and blood pressure values of 80 mmhg under administration of dopamine. the family declares beginning of the symptoms in the morning with strong headache followed by vomiting and loss of consciousness. the emergency brain ct scan revealed a subarachnoid hemorrhage into both sylvian fissure, the basal cisterns and forth ventricle (figure 1). ct-angiography showed a complex left side posterior communicating artery aneurysm with large neck as source of bleeding. also, a small associated left anterior choroidal artery (acha) aneurysm was revealed (figure 2). the first decision was to stabilize the general conditions of the patient. during 48 hours hospitalization in to icu patient's condition improves at gcs = 14. the blood pressure values become stable at 120 mmhg without supportive treatment. in this condition a surgical closure of the aneurysms was decided. a left pterional approach was performed with micro dissection of carotid cistern and proximal part of sylvian fissure and aneurysms exposure. a total clip occlusion of the small left anterior choroidal artery aneurysm was obtained. the complex anatomical configuration of the ruptured pcoma aneurysm due to large aneurysmal neck with extension under anterior clinoid process and presence at the neck level of some perforating arteries led to the adoption of a strategy of neck reconstruction by partial clipping followed by coil endovascular occlusion. figure 1 brain ct scan showing a subarachnoid hemorrhage figure 2 angio ct scan aantero-posterior and b – profile showing a complex pcoma aneurysm and a small acha aneurysm romanian neurosurgery (2015) xxix 2: 187 191 189 figure 3 dsa a showing the aneurysm neck clip reconstruction and remnant aneurysm; b – showing the complete coil occlusion of the aneurysm coil embolization was performed under general anesthesia five days later after clipping. using seldinger technique, 6f arterial sheaths were placed in the right femoral arterie. a 6f guiding catheter was placed in the internal carotid artery or dominant vertebral artery providing arterial supply to the aneurysm remnant. multiple biplane dsa series were performed in different degrees of obliquity for a clearly exposure of aneurysmal neck after reconstruction by clipping. once an appropriate angle was obtained that optimally demonstrated the reconstructed neck of the aneurysm and its relationship to the parent vessel, a road-mapping acquisition was performed. an excelsior sl-10 microcatheter was then advanced over a transend 0.014 microguidewire under road-mapping guidance into the aneurysm remnant. successive gdcs were then advanced and detached in the aneurysm remnant until it was totally angiographic occluded. a 1000 u of heparin was administered after first coil detachment. once the aneurysm remnant was considered satisfactorily occluded, all catheters were removed through the femoral sheaths. the femoral sheaths were then removed from the femoral arteries and hemostasis was obtained by manual compression. anticoagulation was continued 5 days with 0.6 ml daily. control brain ct scan was achieved ct the day after the procedure. discussions endovascular embolization with coils for treatment of cerebral aneurysm remnant after incomplete surgical clipping is generally followed by a favorable clinical outcome. a poor outcome is usually associated with a significant subarachnoid hemorrhage rebleeding and a short interval between clipping and endovascular coil occlusion. one explanation of this unfavorable outcome could be a sever medical condition of these patients 190 chiriac et al combined treatment for complex intracranial aneurysm who require an urgent secondary treatment. the aneurysm remnant after microsurgical clipping could have a technical or “anatomical” origin. the technical problems consisted in anatomical difficulties of complete neck clipping at the time of surgery or in slippage of a correct placed clip due to its manufacturing or sterilization problems. the “anatomical” origin could be explained by the regrowth of a new aneurism lobe or initial aneurysm sac from a dysplastic or incomplete excluded neck. clearly highlighting these residues aneurysm can be achieved by postoperative angiographic exploration. this type of followup imaging is not the most common in specialized clinics. thus, most often, aneurysm remnants are angiographic highlighted immediately postoperative following a suspicion during surgery or a new rupture shortly after clipping. also, in other cases, highlighting an aneurismal remnant is an unexpected thing in a current angiographic exploration after an initial clipping considered successful. given the above, we believe that postoperative angiographic imaging is indicated from time to time in case of suspected residual aneurysm, incomplete clipping of aneurismal neck or in multiple aneurysms. the aneurysm remnants after incompletely clipped aneurysm was a subject discussed extensively in the literature due to due to their catastrophic potential on patient quality of life. table i summarized some literature reports concerning the recurrent hemorrhage after initial aneurysm surgery failure. table i literature reports concerning the recurrent hemorrhage after initial aneurysm surgery failure author, year total number of treated aneurysm number of aneurysm with recurrent hemorrhage time interval drake et all, 1984 115 24 2 wks – 10yrs feuerberg et al, 1987 715 2 4yrs – 13 yrs yamakawa et all, 1997 1436 27 4wks – 20yrs tsutsumi et all, 1998 220 6 3yrs – 17yrs wermer et all, 2005 752 18 10wks – 17yrs chung et all, 2014 312 4 2wks – 17 yrs the endovascular coil occlusion is considered today in many neurosurgical centers as the first intended technique in the management of cerebral aneurysm. some recent articles presented this technique as secondary treatment for complete occlusion of complex cerebral aneurysm. the main factors mentioned in the literature as favoring the incomplete aneurysm occlusion are represented by a large neck, a large-giant sac, suboptimal aneurysm exposure (due to thrombosis or other anatomical particularities), a large infundibular collateral artery originating from aneurysm neck or sac. romanian neurosurgery (2015) xxix 2: 187 191 191 concerning the most frequently location of aneurysm with difficult occlusion the literature reports the deep midline aneurysm of the posterior circulation, anterior communicanting artery and juxtaclinoid aneurysms (8.2% vs 0.6% other location). [2]. both, microsurgical clipping and endovascular coil occlusion can be viewed within a single therapeutic strategy of combined approach. their order of application will depend on a number of specific features of each case. thus, microsurgical clipping can be also applied in case of an incomplete endovascular aneurysm occlusion with coils. conclusions failure of aneurysm treatment failure represented by this remnant aneurysm can occur immediately postprocedural or after longer period of time especially for so-called complex aneurysms. assuming a therapeutic strategy that integrates both interventional methods of microsurgical clipping and endovascular coils occlusion represent the optimal solution to prevent further complications and successful resolution of these cases. correspondence stefan m. iencean “gr. t. popa” university of medicine and pharmacy, iasi mirceasteffan@yahoo.com references 1. forsting m1, albert fk, jansen o, von kummer r, aschoff a, kunze s, sartor k. (1996) coil placement after clipping: endovascular treatment of incompletely clipped cerebral aneurysms. report of two cases. j neurosurg. nov;85(5):966-9; 2. mangiafico s., cellerini m., villa g., ammannati f., paoli l., mennonna p. (2005) endovascular coiling of aneurysm remnants after clipping in patients with follow-up a single center experience, interventional neuroradiology 11: 41-48; 3. choudhri, o., mukerji, n., & steinberg, g. k. (2013). combined endovascular and microsurgical management of complex cerebral aneurysms. frontiers in neurology, 4:1-11; 4. michael t lawton, alfredo quinones-hinojosa, nader sanai, junaid y malek, christopher f dowd (2003) combined microsurgical and endovascular management of complex intracranial aneurysms. neurosurgery 52(2):263-275; 5. sung-chul jin, do hoon kwon, young song, hyun jung kim, jae seung ahn, byung-duk kwun (2008) multimodal treatment for complex intracranial aneurysms : clinical research, j korean neurosurg soc 44 : 314-319. costeaclaudia_krause romanian neurosurgery (2016) xxx 2: 241-247 | 241 fedor krause (1857-1937): the father of german neurosurgery claudia florida costea1,2, dana mihaela turliuc1,2, anca sava1,2, gabriela florența dumitrescu1, a.i. cucu1, emilia patrașcanu2,3, daniela trandafir2,4, ș.turliuc2 1“prof. dr. n. oblu” emergency clinical hospital iași, romania 2“grigore t. popa” university of medicine and pharmacy iași, romania 3regional institute of oncology iași, romania 4“sf. spiridon” emergency clinical hospital iași, romania abstract: rightfully regarded as the father of german neurosurgery, fedor krause made a major contribution not only in world neurosurgery, but also in medicine. the aim of this paper is to highlight once more the significance and importance of fedor krause’s work and exceptional human quality. key words: fedor krause, history of german neurosurgery, ophthalmology birth and youth of fedor krause the one who would one day become the father of german neurosurgery, fedor krause (1857-1937), was born on 10 march 1857 in friedland, a silesian town from germany. his father was a public servant in the district of waldenburg and died when fedor was still young (6). when he was nine years old, his mother decided to move the family to berlin, where it led an extremely modest life, at times bordering on poverty. this did not prevent fedor from studying at “sophien gymnasium” in berlin, where he became known for his talent (6), studying piano and violin and winning many awards (28, 30). fortunately, due to financial support from a private sponsor, the young fedor was able to continue his studies at post-graduate level, choosing medicine (30). he thus began his medical studies in 1875 and wrote his doctoral thesis in 1879, passing his final examinations in march 1880. after graduating from the medical school of berlin, krause worked for two years as an ophthalmologist in prestigious ophthalmology clinic of professor julius hirschberg’s (1843-1925). in this early period, krause also worked with famous bacteriologists of the time, the likes of robert koch (1843-1910) and karl friedländer (18471887), the pathologist karl weigart (18451904) and the surgeon bernhard von 242 | costea et al fedor krause (1857-1937) langenbeck (1810-1887), who left their mark on the young physician and motivated him to study bacteriology and histopathology. in his later works fedor would approach various unexplored topics in these medical fields. he worked with the renowned bacteriologist robert koch at the “imperial board of health” (23) and he aroused his interest to study the systemic manifestations of tuberculosis, especially bone tuberculosis (24). krause published many articles and papers as a result, the most important of which was “die tuberkulose der knochen unde gelenke” (tuberculosis of the bones and joints, 1891) (16). the beginnings of neurosurgery. the collaboration with professor richard von volkmann passionate by neuro-ophthalmology and visual pathways, krause became more and more interested in neurosurgery. thus, in 1883, he moved to halle, where he worked until 1892 as a resident surgeon in the famous surgery clinic of richard von volkmann (1830-1889), a renowned professor who was also chairman at the university of halle at that time (3, 15). volkmann was an important name in german surgery, one of the first listerians, and the one who introduced the practice of antisepsis in germany, in the period of the franco-prussian war (12). while he lived in halle, krause had a beautiful and sincere collaboration and friendship with professor volkmann (4). the city of halle was a heavily industrialized city and work accidents resulting in head injuries were frequent. thus, in 1885, together with volkmann, krause reported 36 surgical interventions for posttraumatic extradural and subdural hematomas, with no postoperative deaths (4). after spending four years in the “surgical hospital” in halle, krause defended his habilitation thesis entitled “malignant neuromas and their nerve fiber content”, in 1887, which, despite being regarded as inadequate for the profession of general surgeon, it was eventually accepted, with volkmann’s help. in 1889, after professor volkmann died of pneumonia, krause became the deputy chief of surgery for one year, after which he was replaced by the german surgeon friedrich gustav von bramann (1854-1913). afterwards, krause moved to hamburg where he became employed as an “oberarzt” at “altona municipal hospital”. in 1990 returned to berlin where he was appointed honorary professor in the friedrich-wilhelms university (e.g. humboldt university of berlin) and chief of surgery at “augusta hospital” (30). throughout his life, fedor krause venerated his mentor, and remained loyal to him even after he passed away. his disciples said that krause always spoke fondly of him, even while scrubbing with his assistants (32). moreover, krause also wrote memoires about him and even dedicated a book to him, entitle “zur erringerung an richard von volkmann” (in richard von volkmann’s memory), published one year after the professor’s death (6). in berlin, krause began collaboration with the neurologist hermann oppenheim (1858 romanian neurosurgery (2016) xxx 2: 241-247 | 243 1919) together with whom he studied neuroanatomy, neurophysiology and neurosurgery. krause regarded this collaboration and friendship very highly as well. later on, in the foreword to his book “chirurgie des gehirns und rückenmarks nach eigenem erfahrungen” (sugery of the brain and spinal cord – based on personal experiences), krause wrote: “i am most grateful to hermann oppenheim. hardly a week, frequently not a day, passed in which we did not consult at the bedside or in the operating-room. this invaluable and lasting connection, and the constant harmonious collaboration, bore in time fruit that we are now proud of in our operative therapy, despite the numerous and discouraging experiences” (12, 19). krause’s contributions in epileptology and functional neurosurgery influenced by the classical cortical stimulation work of fritsch and hitzig, ferrier and sherrington, krause thought that he could use electricity in neurosurgery and neurology as well. through this discovery, krause was considered to be the first surgeon who performed the first intraoperative electrical stimulation on the cerebral cortex (35). throughout his life, krause operated on 400 epileptic patients, which was by far the highest number of patients at that time (13). he was also the one who performed the first detailed motor map of the human cortex (25), and who used faradic stimulation to differentiate between the facial from the audiovestibular nerve in a patient with tinnitus, when he made a section of eighth cranial nerve (25, 32). it is important to note that krause was not only the first to describe the locating of a cranial nerve through electric stimulation, but also the first to record the spread of the current artifacts products (8). krause’s operative neurosurgical techniques during the first world war, krause was a surgical consultant (“generalarzt”) for the german army, gaining experience in treating head injuries. after the war, he went to central and south america, in countries such as brazil and argentina, in 1920 and 1911, lecturing and performing brain surgery (5). in 1893, krause described the subtemporal extradural approach to the trigeminal nerve roots and gasserian ganglion (gasserian ganglionectomy) (17, 25). despite the proximity of the gasserian ganglion to the internal carotid artery, krause wrote that, in 70 cases of gasserian ganglionectomy, he never injuried the carotid artery, which attests to his outstanding surgical skills (12). seven years later, krause removed a bullet from the clinoid process and optic foramen region of a young man who attempted to commit suicide out of love, through a frontal approach to the sella. krause noticed that he had a very good view of the sellar region. still in 1900, before the “berlin medical association”, he performed surgery on a cadaver (20) and proposed this type of approach for tumors in this region. four years later he attempted an unsuccessful resection of tuberculum sella meningioma and in 1908 a pituitary adenoma in an acromegalic patient, which was followed by improvement (12). 244 | costea et al fedor krause (1857-1937) in 1903 he described the cerebellopontine angle approach, which he performed through an unilateral suboccipital osteoplastic flap (18). nowadays, this approach is considered to be the predecessor of the retrosigmoid approach (14). it was performed for a vestibular schwannoma and krause concluded that tumors located in the cerebellopontine angle can be now safely resected. nonetheless, he considered them to be the most difficult and problematic of all brain tumors (31). four years later, krause resected a cerebellar tumor of the upper vermis, being regarded as the first surgeon who was successful in approaching the fourth ventricle (13). twenty-six years later, at his funeral, the otologist güttich wrote in his orbituary: “krause was the first person who looked into the fourth ventricle of a living human being” (28). in 1913 he conducted a resection of a pineal tumor through an infratentorial supracerebellar approach which he patented in neurosurgery and which would bear his name (2, 27, 29). krause also had a contribution in vascular neurosurgery, being the first neurosurgeon who operated cerebral angiomas. he attempted also to ligatures the feeding vessels (33). he also excelled in spinal cord neurosurgery and, together with the german neurologist heinrich oppenheim, in “augusta hospital” in berlin, he performed the first discectomy and laminectomy in a patient who had been suffering from severe sciatic pain for several years and who developed an acute cauda equina syndrome. the surgery consisted in laminectomy l2-l4, splitting the dura, mobilization the cauda equina by a retractor, exploring the operation field and removing a small fibrocartilage mass, which they later considered to be an enchondroma (26). his work (table no.1) is overwhelming and groundbreaking in the field of neurosurgery in germany and in europe at the beginning of the 19th century. one of the most important books he wrote is “chirurgie des gehirns und rückenmarks nach eigenem erfahrungen” (sugery of the brain and spinal cord – based on personal experiences) (20). the first volume was published in 1909, comprising the detailed and didactic writings of over 300 craniotomies with hand-drawn coloured illustrations of surgical procedures. several years later, in 1911 and 1912, the second and third volumes were published. even though his books were initially written in german, they became famous throughout europe, in spite of the fact that they were translated into english later on (4). his didactic work represented true atlases and textbooks, comprising at the same time many surgical techniques, described in great detail, and examples of cases from krause’s personal experience (32). another important work was his monograph “trigeminal neuralgia: including the anatomy and physiology of nerves” in which krause described his experience with 14 patients suffering from trigeminal neuralgia, and reviewed the entire literature on the subject. his knowledge of ophthalmology allowed him to avoid keratitis, a common complication of the denervation of the cornea by sectioning the first branch of the trigeminal nerve (12). romanian neurosurgery (2016) xxx 2: 241-247 | 245 table i chronology of krause’s contributions (11, 12) krause’s contributions on the surgical branches of medicine apart from his monograph on neurosurgery, krause also published a series of surgical monographs in which he studied various pathologies or described his innovations in: general surgery, plastic surgery (free transplantation of skin flaps (1) ), orthopedics (bone and joint tuberculosis, application of waking casts), urology (total cystectomy, bilateral ureterosigmoidostomy, reimplantation of the ureter into the bladder (1)), endocrine surgery (adrenotomy, transplantation of endocrinous tissue (22)), ent surgery (sympathectomy, carotid artery ligation (22)), and so on. moreover, in the field of anesthesiology, krause highlighted the risk of cerebral oedema caused by ether and chloroform. despite the fact that, while working with professor volkman, krause used this combination of morphine and chloroform, he was not convinced that this formula was beneficial for neurosurgical interventions. this motivated krause to continue his research in the field of neuroanesthesiology (10). krause the man krause was a shy, sensible and nobly modest man (figure 1). he did not like to attend large international meetings in order to present his techniques, preferring smaller conferences instead. what is more, when he was asked about how he would like people to remember him, he responded rather like a classical pianist than a neurosurgeon (9). figure 1 fedor krause (1857-1937), the father of german neurosurgery year pathology approach/technique discovered 1893 trigeminal neuralgia subtemporal extradural approach (gasserian ganglionectomy) 1897 tinnitus cerebellopontine angle approach (section of eight cranial nerve) 1904 tuberculum sella meningioma frontal transcranial approach to the sella 1908 herniated lumbar disc (“enchondroma”) discectomy, laminectomy 1908 arteriovenous malformation of the brain ligation of a feeding artery 1909 pituitary adenoma sphenoid ridge approach to sella 1913 pineal tumor supracerebellar infratentorial approach 246 | costea et al fedor krause (1857-1937) krause was described as a man with big hands, more suitable for manual labor than for brain surgery (34). nonetheless, he had a sensitive and artistic nature, having difficulty in choosing, in his youth, between a career as a pianist or as a physician. in a letter from 1889, one year before his death, professor volkmann wrote that his assistant, fedor krause, “had developed into a surgeon capable of performing all types of surgeries, that he led lectures and scientific work, and that he was endowed with an unusual clinical experience, with great talent and humane attitude” (32). krause’s retirement after his official retirement, he withdrew to rome, in 1930, together with his daughter, devoting the rest of his life to arts and music. krause held a series of private concerts (6), for which he was praised and appreciated by italian critics (11). upon his 80th birthday, while he was being celebrated in berlin, in 1937, the german surgeon ferdinand sauerbach said: “you can look back on your work with pride, and rejoice in its future progress and prosperity. even the notable progress in surgery of the central nervous system in other countries rests to a large extent on your basic work” (32). krause passed away during the same year, in badgaatstein, forever remaining the father of german neurosurgery in the consciousness of the german people. emil heymann (1878-1936), karl max behrend (1895-1963) and george merrem (1908-1971) continued on their father’s path, contributing to the development of neurosurgery in germany. they became great professors and modest men, like their mentor (1). george merrem was trained by emil heymann (1878-1936), krause’s successor in berlin, who perpetuated krause’s neurosurgical school (7) and developed neurosurgery in the german democratic republic after the second world war. the faculty of medicine of berlin awarded krause in 1915 with the highest academic position, “ordentlichen honorarprofessor” (21), and nowadays the german neurosurgical society awards the great neursurgeons with the "fedor krause medal" for outstanding work in the field of neurosurgery, which is the highest honor in neurosurgery. conclusions fedor krause is the father of german neurosurgery who has remained in the memory of the german people for his contribution not only in neurosurgery, but also in other branches of medicine. his main concern, however, for which he fought his entire life, was with finding safe approaches to inaccessible anatomical areas of the brain, which he actually succeeded. through his entire activity, krause is not only a pioneer in german neurosurgery, but a pioneer in world neurosurgery. correspondence dana mihaela turliuc “grigore t. popa” university of medicine and pharmacy, iași, romania e-mail: turliuc_dana@yahoo.com romanian neurosurgery (2016) xxx 2: 241-247 | 247 references 1.albert-niedler u, arnold u. gain and loss of the ability to complete some aspects of german neurosurgery up to the 1939. acta neurochir 1994; 126: 4-10. 2.behari s, garg p, jaiswal s, nair a, naval r, jaiswal ak, major surgical approaches to the posterior third ventricular region: a pictorial review. j pediatr neurosci. 2010; 5(2): 97-101. 3.behrend cm. fedor krause und die anfänge der neurochirurgie in deutschland. dtsch med wochenschrift. 1957; 82(15): 519-520. 4.behrend c. fedore krause un die neurochirurgie. zentralbl neurochir 1968; 3:122-126. 5.buchfelder m. from trephination to tailored resection: neurosurgery in germany before world war ii. neurosurgery. 2005; 56(3):605-613. 6.carmel pw, buchfelder m. 100 years ago in neurosurgery: description of the intracranial extradural approach to the gasserian ganglion--the hartley-krause operation. neurosurgery. 1993; 2(5):828-832. 7.collmann h, vitzthum he. historical perspective on neurosurgery in germany after world war ii. neurosurgery. 2008; 63(5):989-999. 8.eisner w, fiegele t. neuromonitoring in central skull base surgery. in dolenc vv, rogers l (eds): cavernous sinus: developments and future perspectives. wien: springer science & business media, 2009, pp 90. 9.ellenbogen rg, abdulrauf si, sekhar ln. principles of neurological surgery. philadelphia: elsevier health sciences, 2012, pp 29. 10.frost eam. clinical anesthesia in neurosurgery. stoneham: butterworth-heinemann, 1991, pp 11. 11.frowein r a, brock m, klinger m, head injuries: prognosis evoked potentials microsurgery brain death. berlin: springer verlag, 1989. 12.horwitz nh. fedor krause (1857-1937). neurosurgery. 1996; 38(4):844-848. 13.horwitz n: library: historical perspective, neurosurgery 1996, 38(2):416-419 14.iacob g, craciun m. large and giant vestibular schwannomas. romanian neurosurgery. 2010; xvii 3: 305-312. 15.jefferson g. fedor krause und die neurologische chirurgie: fedor krause gedächtnisvorlesung. acta neurochir. 1960; 9(1): 661-664. 16.krause f, von volkmann r. die tuberkulose der knochen und gelenke. leipzig: f.c.w. vogel, 1891. 17.krause f. resection des trigeminus innerhalb der schadelhohle. arch klin chir. 1892; 44:821–832. 18.krause f. zur freilegung der hinteren felsenbeinflache und des kleinhirns. beitr klin chir. 1903; 37:728-764. 19.krause f. surgery of the brain and spinal cord-based on personal experiences, vol iii (english translation).new york: rebman company, 1912. 20.krause f. surgery of the brain and spinal cord based on personal experiences. translated by haubold h, thorek m. (3 vols). new york: rebman co, 1910-1912. 21.kreuter a. deutschsprachige neurologen und psychiater: ein biographisch-bibliographisches lexikon von den vorläufern bis zur mitte des 20. jahrhunderts. berlin: walter de gruyter, 1995, pp 780. 22.lüders ho. textbook of epilepsy surgery. london: crc press, 2008, pp 38. 23.mcdowell f. the source book of plastic surgery. baltimore: williams & wilkins, 1977, pp 35. 24.oehlecker f. tuberkulose der knochen und gelenke. berlin: urban & schwarzenberg, 1924, pp 3. 25.olivier a, boling ww, tanriverdi t. techniques in epilepsy surgery: the mni approach. cambridge: cambridge university press, 2012, pp 2. 26.oppenheim h, krause f. über einklemmung bzw. strangulation der cauda equina. dtsch med wochenschr. 1909; 35: 697-700. 27.oppenheim h, krause f. operative erfloge bei geschwulsten der sehh ugel-und vierhugelgeggend. berl klin wochenschr. 1913; 50:2316–2322. 28.piscol k, klinger m, brock m. neurosurgical standards, cerebral aneurysms, malignant gliomas. berlin: springer science & business media, 1992, pp 17. 29.radoi m, danaila l, stefanescu f, vakilnejad r, popa r. meningioma of the pineal region. romanian neurosurgery. 2012; xix 2: 103-109. 30.rainov n, gantchev l, burkert w. back to the roots of modern neursurgery: neurosurgical pioneers in halle an der salle. surg neurol. 1996; 46:161-168. 31.reidel c, post kd. complications in the treatment of acoustic neuromas. in: post kd, friedman e, mccormick p (eds). postoperative complications in intracranial neurosurgery. new york: thieme, 1993, pp 91-110. 32.rosegay h. the krause operations. j neurosurg. 1992; 76(6):1032-1036. 33.sandu am, gorgan mr. total resection in a giant left frontal arteriovenous malformation, grade v spetzler-martin case report. romanian neurosurgery. 2013; xx 1: 46-56. 34.shucart w. fedor krause, 1856-1937. surg neurol. 1975; 3: 115-117. 35.wolf p. history of epilepsy surgery in europe. in: lüders h (ed). epilepsy surgery. new york: raven press, 1992, pp 9-17 satyarthee_pituitaryapoplexy romanian neurosurgery (2016) xxx 2: 289-295 | 289 pituitary apoplexy in residual pituitary adenoma following surgical treatment in the follow-up period: management strategy g.d. satyarthee, a.k. mahapatra the department of neurosurgery, all india institute of medical sciences, new delhi, postal code -110029, india abstract: pituitary apoplexy is a rare clinical event, used to occur spontaneously. although, some predisposing factors for pituitary apoplexy is reported ie. head injury, digital cerebral angiography, bromocriptine therapy, coughing, lumbar puncture for csf drainage, pneumoventriculography, even during surgery, in the immediate postoperative period and raised intracranial tension. although pituitary apoplexy occurring following radiotherapy as primary treatment modality is reported, however, apoplexy occurring in residual adenoma following surgery, receiving adjuvant radiation therapy for residual adenoma is not reported in the literature. authors reports two-cases of pituitary apoplexy, which occurred in the residual pituitary adenoma after a varying period in the follow-up period. these patients were previously operated by transcranial approach for decompression of the pituitary adenoma. the pituitary apoplexy occurred in one case after an interval of one and half years following surgical intervention for pituitary adenoma decompression and next case developed after five years. both the cases had also received radiotherapy in the postoperative period for residual pituitary adenoma. key words: pituitary apoplexy, residual pituitary adenoma, transsphenoidal surgery introduction pituitary apoplexy is clinical syndrome characterized by sudden onset of headache, commonly associated with vomiting, meningeal irritability, and often ophthalmoplegia or visual deterioration (13, 17-19). apoplexy mostly occurs spontaneously, although in some cases may have predisposing factors including head endocrine manipulation, trauma, cerebral angiography, bromocriptine therapy, radiation therapy of pituitary adenoma lumbar puncture, and in the immediate postoperative period. (5, 6, 7, 8, 11) we are reporting two cases of pituitary apoplexy, which was encountered in patients, who were operated 290 | satyarthee et al pituitary apoplexy in residual pituitary adenoma for pituitary adenoma and also received radiation therapy for residual many years prior to current occurrence of apoplexy. illustrated case i a 42yearold male presented to our neurosurgical services with a history of sudden onset headache, vomiting and rapidly progressive decline in the visual acuity for the last 15 days. he was operated for a pituitary adenoma four year back by transsphenoidal approach. (figures 1, 2, 3) the histopathology revealed chromophobe pituitary adenoma. he also received radiotherapy in, for residual adenoma. general examination was normal, with stable vitals. neurological examination revealed visual acuity of 6/9 and 6/24 respectively in the right and the left eye. he had bitemporal field defect. fundi revealed bilateral primary optic atrophy. he also had right seventh cranial nerve upper motorneuron paresis. the rest of the neurological examination was normal. the haematological and biochemical profiles were normal. however, urinary specific gravity ranged from 1008-1014. hormonal profile showed growth hormone 2 (normal upto-5ng/ml), serum cortisol (8 am) 0.8 µ g / dl (normal 5 -18), serum prolactin 12 ng /ml (normal 1.3-24), tsh2.8 µ iu /dl (normal 0.44.6), free t31.4 pg/ml (2.25) and, free t40.3 ng /dl (0.71.8). x-ray chest was normal. cranial ct scan revealed a pituitary macro-adenoma, showing fair enhancement with contrast agent. mri sagittal view showed large sellar mass with suprasellar extension having heterogeneous hyperintense signal on t1 weighted image (figure 4), and coronal t1 weighted image (figures 5, 6) suggestive of apoplectic bleed in the residual pituitary adenoma with further decent into sphenoid sinus due to deficient sellar floor, caused by previous surgery. there was associated mild hydrocephalus. he underwent decompression of pituitary adenoma through sub-labaial transsphenoidal approach. intra-operatively a large cyst containing fluid with evidence of old hemorrhage was encountered. histopathology revealed chromophobe pituitary adenoma with evidence of haemorrhage. immunohistochemistry morphological workup was negative prolactin and growth hormones. he showed unremarkable recovery in the postoperative period. his vision was 6/9and 6/12 in the right and left eye respectively at the time of discharge from hospital on fourth postoperative day. he was kept on cortisol and thyroxin as maintenance therapy. he was well at last follow-up 3 year after second surgery and follow-up ct scan revealed no residual. figure 1 contrast enhanced cranial ct, coronal view showing large enhancing sellar suprasellar mass with a right parasellar extension (preop) romanian neurosurgery (2016) xxx 2: 289-295 | 291 figure 2 mri brain, t!wi mage sowing homogeneous hyperintense mass (preop) figure 3 mri brain, contrast enhanced, image sowing homogeneous hyperintense mass in sell causing encasement of bilateral internal carotid artery (pre-op) figure 4 mri brain, t2wi , showing heterogeneous lesion in sella with areas of csf like intensity suggestive of apoplexy in residual pituitary adenoma ( follow-up scan after 5 -year of surgery ) figure 5 mri brain, t1w image, coronal section image, showing descent of suprasellar part with recurrent adenoma with apoplexy (follow-up scan after 5 -year of surgery) 292 | satyarthee et al pituitary apoplexy in residual pituitary adenoma figure 6 mri brain, sagittal section image, showing descent of suprasellar part with recurrent adenoma into sella due to deficient sellar floor due to past surgery, with apoplexy illustrated case ii a 27 year-old male presented with headache and sudden onset complete vision loss involving both eyes since three days prior to admission. he was operated pituitary macroadenoma by subfrontal route in 1997. he also received radiotherapy for residual pituitary adenoma. on admission his vitals were stable. neurological examination revealed, visual acuity in the right eye was just positive for perception of light and the left was negative for perception of light. fundi revealed bilateral primary optic atrophy. the routine haematological and biochemistry parameters were normal. endocrinological evaluation showed serum cortisol 14 µ g / dl (normal 5 18), serum prolactin 8 ng /ml (normal 1.3-24), tsh5 µ iu /dl (normal 0.44.6), free t3-1.2 pg/ml (2.25) and, free t40.4 ng /dl (0.7-1.8). growth hormone-4 (upto-5ng/ml). contrast ct scan of cranium revealed sellar-suprasellar mass with fluid level. a transnasal transsphenoidal radical decompression of tumour was carried out as an emergency procedure. at surgery altered dark blood with grayish tumor which was evacuated. morphological work-up on immunehistochemistry was negative growth and prolactin hormones. he showed remarkable improvement in the vision in postoperative period, 6/36 in the right eye and 6/18 in the left eye. he was continued on cortisol and thyroxin replacement therapy. contrast enhanced mri done at six months after second surgery revealed small residual in suprasellar region only which was not abutting the optic chiasma. gamma knife therapy was given for residual adenoma. he was well at last follow-up one year after gamma knife therapy. discussion pituitary apoplexy is common clinical syndrome (1-4, 6-8, 15-19). pituitary adenoma possesses comparatively bleeding frequency of 5.4 times higher than any primary intracranial neoplasm. (1) the incidence of pituitary adenoma with apoplectic presentation varies in literature between 1.5 27.7 %. (2, 3, 12) it is considered as complex clinical events, occurring following fulminate expansion of a pituitary tumor by haemorrhage, infarction, or combination of two, which involves adenoma and adjoining and surrounding pituitary gland. (4) clinically it may have wide spectrum of presentation; which may vary from subclinical infarction which could only be noticed during the surgery or on preoperative imaging to full blown apoplexy that mimics romanian neurosurgery (2016) xxx 2: 289-295 | 293 subarachnoid haemorrhage. (3) although most cases are reported to occur spontaneously. although, some predisposing factors are reported ie. head trauma, (6) cerebral angiography, (7) endocrine manipulation, (8) bromocriptine therapy, (5) coughing and sneezing, (9) radiotherapy of pituitary tumours (10, 11) lumbar puncture, (13) pneumoencephalography (13), and raised intracranial pressure, (13) weisberg et al (11) reported a series of 14 cases of pituitary apoplexy, out of which eight cases were associated with radiation therapy. these patients were treated with radiotherapy as primary mode of treatment without any prior surgery for pituitary adenoma. pituitary apoplexy occurred in five cases, which were receiving radiation therapy. it occurred in three cases during the first week of initiation of radiotherapy, one in third weeks and another one towards completion stage of radiotherapy treatment. in rest of cases, the onset of pituitary apoplexy were noted three to four years after completion of radiation therapy. however, surgery was required in these cases after pituitary apoplexy during the course of radiation therapy. in the present study, our both cases were subjected to transcranial decompression of pituitary adenoma along with radiotherapy for the residual tumour and after a varying period of follow-up developed apoplectic manifestation. various hypothesis put forward for pituitary apoplexy occurrence in post radiated pituitary adenoma, his rapid enlargement of cyst, which can cause compression over solid portion, resulting in ischemia and hypoxic necrosis. this leads to less radioresponsiveness and more likely to undergo hemorrhagic necrosis with initiation of radiotherapy. even radiotherapy can cause vascular damage to endothelium of fine blood vessel and damage neovascularity of tumour leading to hemorrhagic necrosis. goel et al (14) reported pituitary apoplexy in the residual tumour after partial decompression following transcranial surgical approach in two cases. however, re-exploration was required within 45 minutes in one case, while 12 hours after in the second case. rovit et al (4) reported higher incidence of apoplexy in patients in acromegalic or acth producing adenoma. weisberg et al (11) also noticed higher incidence in acromegalic after radiotherapy. however, our cases were with chromophobe pituitary adenoma. goel et al (14) reported sudden release of feeding tumour vessel from internal carotid artery, compromise of venous drainage, tumour manipulation, swelling and compression of hypophyseal artery at diaphragma sella resulting in ischemia and secondary tumour necrosis after partial decompression of pituitary adenoma. they further observed that attempt should be made to excise these tumours as radically as possible. similarly both of our patients underwent transsphenoidal decompression of pituitary adenoma and had uneventful postoperative period. a group of patients with residual pituitary adenoma following radiotherapy show re-growth, continuing vascular damage to blood vessel endothelium, and adenoma growth may outstrip the vascular requirement for adenoma leading to apoplexy, years after of surgery and radiotherapy. damage to 294 | satyarthee et al pituitary apoplexy in residual pituitary adenoma neovascularity of tumour can lead to hemorrhagic necrosis. the mechanism of pituitary apoplexy is not clear. ischemic necrosis of adenomatous tissue, compression of superior hypophyseal arteries against diaphgrama sellae and intrinsic vasculopathy of pituitary tumour has been suggested. further effect of apoplexy on pituitary function was assessed by marouf et al, who analyzed a total of 19 cases of pituitary apoplexy, who underwent surgery for pituitary apoplexy. (21) authors assessed the function of residual pituitary gland function in the postoperative phase, only five cases retained normal pituitary function, while eight cases developed pan-hypopituitarism, and the rest six with partial hypopituitarism. the mri study in the post-operative follow-up period demonstrated residual pituitary gland in 13 patients, out of which four had normal functional pituitary gland. (21) conclusion every case of pituitary adenoma with past history of surgical intervention or radiotherapy, showing clinical feature of apoplexy, should be investigated with imaging and if needed urgent surgical opportunity may be given to preserve good neurological outcome. the tumour decompression should be carried out as emergency procedure. during the first surgery itself, the aim should be radical decompression of adenoma to avoid residual adenoma, which carries a potential risk for apoplexy. correspondence g.d. satyarthee associate professor, department of neurosurgery all india institute of medical science new delhi – 110029, india. fax: 0091-11-6862663 e-mail: duttaguru2002@yahoo.com references 1.wakai s, yamakawa k, manaka s, et al. spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance. neurosurg 1982; 10: 437444. 2.cardoso er, peterson ew. pituitary apoplexy –a review. neurosurg 1984; 14: 363-373. 3.anderson jr, anton n, burnet n, et al. neurology of the pituitary gland. j neurol neurosurg psychiatry 1999; 66: 703-721. 4.rovit rl, fien jm. pituitary apoplexy: a review and reappraisal. j neurosurg 1972; 37: 280-288. 5.mc gregor am, scalon mf, hall k, et al. reduction in size of tumor by bromocriptine therapy. n england j med 1979; 300: 291-193. 6.lopez ia. pituitary apoplexy. j oslo city hospital 1970 ; 20: 17-27. 7.stiemle r, royeer j, opperman a, et al. hematome post-angiographique dans un adenoma de i’hypophyse: cecite et troubles oculomoteurs regressant après intervention d’urgence neurochirurgie 1974; 20: 599-608. 8.masago a, ueda y, kanai h, nagai et al. pituitary apoplexy after pituitary function test: a report of two cases and review of the literature. surg neurol 1995; 43:158-165. 9.dawson bh, kothandram p. acute massive infarction of pituitary adenomas. a study of five patients. j neurosurg 1972; 37: 275 -279. 10.onseti st, wisniewski t, post kd. clinical versus sub clinical pituitary apoplexy: presentation, surgical management, and outcome in 21 patients. neurosurg 1990; 26: 980-986. 11.weisberg la. pituitary apoplexy: association of degenerative changes in pituitary adenoma with radiotherapy and detection by cerebral computed tomography. ame j med 1977; 63:109-115. romanian neurosurgery (2016) xxx 2: 289-295 | 295 12.motta lacr, mello pa, lacerda cm, et al. pituitary apoplexy: clinical course, endocrine evaluations and treatment analysis. j of neurosci 1999; 43:25-36. 13.david nj, gargano fp, glaser js. pituitary apoplexy in clinical perspective. neuroophthalmol 1975; 8: 140-165. 14.goel a, deogaonkar m, desai k. fatal postoperative pituitary apoplexy: its causes and management brit j neurosurg 1995; 9:37-40. 15.powell m. recovery of vision following transsphenoidal surgery for pituitary adenomas. brit j neurosurg 1995; 9:367-373. 16.bills dc, meyer fb, laws jr er, et al. a retrospective analysis of pituitary apoplexy. neurosurgery, 1993; 33:602-609. 17. sugita s, hirohaya m, tokutomi t, et al. case of pituitary apoplexy in a child. surg neurol 1995; 4:154157. 18.mohr g, hardy j. hemorrhage, necrosis and apoplexy in pituitary adenoma. surg neurol 1982; 18 :181-189. 19.ebersold mj, laws er, scheithauer bw, et al. apoplexy treated by transsphenoidal surgery, a clinicopathological and immunohistocytochemical study. j neurosurg. 1983; 58: 315-320. 20. marouf r1, mohr g, assimakopoulos p, glikstein r. [apoplectic macroadenomas: the outcome of the residual pituitary gland]. neurochirurgie. 2010 ;56(4):324-30. [article in french] 18calderon-miranda_bilateral 498 calderon-miranda et al bilateral traumatic paralysis of abducent nerves bilateral traumatic paralysis of abducent nerves and clivus fracture: case report willen guillermo calderon-miranda1, hernando raphael alvismiranda1, gabriel alcala-cerra2, luis rafael moscote-salazar2 university of magdalena, colombia 1physician, 2neurosurgeon clivus fractures are a rare pathology, frecuently associated tohigh power trauma. such injuries may be associated with vascular and cranial nerves lesions. the abducens nerve is particularly vulnerable to traumatic injuries due to its long intracranial course, since their real origin until the lateral rectus muscle. the unilateral abducens nerve palsy of 12-7% occurs in patients with cranial trauma, bilateral paralysis is rare. we report a patient who presented bilateral abducens nerve palsy associated with a clivus fracture. key words: cranial fossa, posterior, skull fracture, neurotrauma, clivus introduction fractures of the clivus are uncommon lesions, occurring in 0.55% of patients with traumatic cranial injuries. they are classified as longitudinal, transverse and oblique. because of its medial location at the base of the skull, sometimes the diagnosis is not easy. mortality of longitudinal fractures ranges from 67-80% and is considered to have the potential to lead to the entrapment of the vertebrobasilar vessels and direct contusion of the brain stem. this type of injury is associated with high energy trauma. the longitudinal type has a high mortality rate, varying between 67-80%, because of the occlusion of the basilar artery and/or direct trauma to the brain stem. so far there are only 12 cases reported (7 in autopsies). the abducens nerve is particularly vulnerable to traumatic injuries due to its long intracranial course, from its real origin until reach the lateral rectus muscle. the unilateral abducens nerve palsy occurs in 1-7% of patients with head trauma, bilateral paralysis is rare. we present a case of a patient developing bilateral paralysis of the sixth cranial nerve, bilaterally, associated with clivus fracture. case report male patient, 50 years old, right-handed, sent to our institution from a local hospital, because of moderate traumatic brain injury, due to a fall from their own height. no history records of importance. on general physical romanian neurosurgery (2014) xxi 4: 498 – 500 499 examination we found a hemodynamically stable man in whom, neurological examination evidenced bilateral sixth cranial nerve palsy. brain ct scan showed a longitudinal fracture of the clivus (figure 1). the patient is admitted to the intensive care unit with general measures and ventilatory support; in the six day, his body temperature was 39.1 c and csf examination was compatible with bacterial meningitis. the patient was managed with third generstion cephalosporins. the patient’s antibiotic was used for 4 weeks. is extubated in the tenth day, no complications. no commitment of the posterior circulation or alteration of the cranial nerves was documented, on ambulatory monitoring. figure 1 brain ct scan obtained on admission showing a longitudinal fracture in the clivus (arrow) the clivus is considered the strongest bone, embryologically originates from the fusion of the sphenoid body to basiocciput, remaining separate up to 12 years through the sphenooccipital synchondrosis. (1, 2) the irrigation of the clivus is given by the meningohipophyseal trunk and caudally for the posterior meningeal artery, which anastomoses with the lateral clival artery. biomechanics of clivus fractures is controversial, it has been proposed the participation of vertical, lateral and anteroposterior forces. (3, 4, 5) the corradino’s classification divides clivus lesions in longitudinal, transverse and oblique. longitudinal fractures are associated with increased mortality, about 67-80%. high speed traumas, especially for car accidents, are related to these injuries. (6, 7, 8, 9) the risk of neurological injury is high, mainly by the proximity to brain stem structures, including the vertebrobasilar artery and cranial nerves. the longitudinal fracture type also are linked to the basilar artery entrapment and ischemia of the brain stem. due to its unique location in the center of the skull clivus fractures are difficult to diagnose. with standard radiography, is believed to clivus fractures are underdiagnosed, which has been overtaken by the studies of ct scan with bone window. mechanical forces believed to be responsible for basilar fractures involving the clivus are the sum of the outbending forces located far from the local impact that exceeds the elastic capacity of the skull and result in a fracture line that crosses the clivus. the subsequent bilateral sixth cranial nerve palsy to a clivus fracture can be explained for the relaxation of the grüber ligament that exerts mechanical effect on the mentioned neural structures. (10, 11, 12, 13, 14, 15, 16) 500 calderon-miranda et al bilateral traumatic paralysis of abducent nerves correspondence dr. luis rafael moscote-salazar, cisneuro research group, university of cartagena, cartagena de indias, colombia e-mail: mineurocirujano@aol.com references 1. hofmann e, prescher a. the clivus: anatomy, normal variants and imaging pathology.clin neuroradiol. 2012 jun;22(2):123-39 2. ochalski pg, adamo ma, adelson pd, okonkwo do, pollack if.fractures of the clivus and traumatic diastasis of the central skull base in the pediatric population.j neurosurg pediatr. 2011 mar;7(3):261-7 3. evers jj, vieth vv, hartensuer rr, raschke mm, vordemvenne tt management of an extended clivus fracture: a case report. bmc res notes. 2013 dec 23;6:554 4. ochalski pg, spiro rm, fabio a, kassam ab, okonkwo do.fractures of the clivus: a contemporary series in the computed tomography era. neurosurgery. 2009 dec;65(6):1063-9 5. dashti r, ulu mo, albayram s, aydin s, ulusoy l, hanci m. concomitant fracture of bilateral occipital condyle and inferior clivus: what is the mechanism of injury? eur spine j. 2007 dec;16 suppl 3:261-4. 6. yavuz c, sencer a, kabata? s, imer m, kiri? t, unal f. [longitudinal clival fractures: a report of three cases]. ulus travma acil cerrahi derg. 2006 oct;12(4):321-5. 7. menkü a, koç rk, tucer b, durak ac, akdemir h. clivus fractures: clinical presentations and courses. neurosurg rev. 2004 jul;27(3):194-8. 8. de melo pm, kadri pa, de oliveira jg, suriano ic, cavalheiro s, braga fm. cervical epidural haematoma with clivus fracture: case report. arq neuropsiquiatr. 2003 jun;61(2b):499-502. 9. sato s, iida h, hirayama h, endo m, ohwada t, fujii k. traumatic basilar artery occlusion caused by a fracture of the clivus--case report. neurol med chir (tokyo). 2001 nov;41(11):541-4 10.ogungbo b, sengupta r. traumatic fracture of the clivus and vermian contusion in a child. br j neurosurg. 2001 apr;15(2):159-61. 11.fuentes s, bouillot p, dufour h, grisoli f.occipital condyle fractures and clivus epidural hematoma. case report. neurochirurgie. 2000 dec;46(6):563-567. 12.khan n, zumstein b. transverse clivus fracture: case presentation and significance of clinico-anatomic correlations. surg neurol. 2000 aug;54(2):171-7. 13.corradino g, wolf al, mirvis s, joslyn j. fractures of the clivus: classification and clinical features. neurosurgery. 1990 oct;27(4):592-6. 14.joslyn jn, mirvis se, markowitz b. complex fractures of the clivus: diagnosis with ct and clinical outcome in 11 patients. radiology. 1988 mar;166(3):817-21 15.kapila a, chakeres dw. clivus fracture: ct demonstration. j comput assist tomogr. 1985 novdec;9(6):1142-4. 16.sights wp. incarceration of a vertebral artery in a fracture of the clivus. j neurosurg. 1968;28:588-591. doi: 10.33962/roneuro-2020-076 global warming, neurosurgery and neurocritical care ezequiel garcía-ballestas, luis rafael moscote-salazar, andrei joaquim, amit agrawal romanian neurosurgery (2020) xxxiv (1): pp. 463-464 doi: 10.33962/roneuro-2020-076 www.journals.lapub.co.uk/index.php/roneurosurgery global warming, neurosurgery and neurocritical care ezequiel garcía-ballestas1, luis rafael moscote-salazar2, andrei joaquim3, amit agrawal4 1 medical student. center for biomedical research (cib), faculty of medicine, university of cartagena, colombia 2 neurosurgeon. critical care, center for biomedical research (cib). director of research, line cartagena neurotrauma research group. faculty of medicine, university of cartagena, colombia 3 prof. of neurosurgery. university of campinas (unicamp), campinas-sp, brazil 4 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india abstract the changing temperatures are making an impact on health-related mortality outcomes with many studies on the role of temperature and mortality risks in cardiovascular and respiratory illnesses. global warming a real phenomenon, progressing rapidly and producing changes in the ecosystem and have economic, social and public health implications. the changing temperatures are making an impact on health-related mortality outcomes with many studies the role of temperature and mortality risks in cardiovascular and respiratory illnesses. 1 global warming a real phenomenon, progressing rapidly and producing changes in the ecosystem and have economic, social and public health implications. climate change is causing warmer and more variable temperatures as well as a physical flux in natural populations, will affect the ecology and evolution of infectious disease epidemics. the greenhouse effect has increased the temperature by more than 0.5 ° c and it is estimated that there will be another increase of 0.5 ° c in the next coming decades. 2, 3 despite the alarming rise we have turned a blind eye to these problems and now we may face the consequences of this phenomenon in every field. ali et al 4 analyzed 111 patients to assess the impact of the lunar cycle and season on the incidence of aneurysmal subarachnoid hemorrhage and noted incidence peak for aneurysm rupture was observed during the phase of new moon, which was statistically significant, however no seasonal variation in the keywords global warming, traumatic brain injury, cerebral stroke, subarachnoid haemorrhage, prevention corresponding author: luis rafael moscote-salazar center for biomedical research (cib). faculty of medicine university of cartagena, cartagena, colombia rafaelmoscote21@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 464 ezequiel garcía-ballestas, luis rafael moscote-salazar, andrei joaquim et al. incidence of overall total subarachnoid hemorrhage caused by various etiology was observed. authors concluded lunar cycle affect the incidence of intracranial aneurysm rupture, with the new moon being associated with an increased risk of aneurysmal subarachnoid hemorrhage. 4 chyatte et al. 5 analyzed 1487 patients with a primary diagnosis of aneurysmal subarachnoid hemorrhage. men showed a single large peak in late fall, and late spring in women changing climatic conditions precede aneurysm rupture in men but not in women, which suggests that weather is causally related to aneurysm rupture in men and that factors that lead to aneurysm rupture in women may be different from those in men. these data do not explain why weather fronts or gradients are associated with aneurysm rupture in men. 5 li et al 6 estimated temperature-related mortality projection for acute ischemic heart disease and ischemic and hemorrhagic stroke with concomitant climate warming. the median number of projected annual temperature-related deaths for hemorrhagic stroke had virtually no change compared with the 1980s, and for acute ischemic heart disease authors projected temperature-related mortality associated with ischemic stroke can increase dramatically as an effect of climate warming. however, projected temperature-related mortality pertaining to acute ischemic heart disease and hemorrhagic stroke should remain relatively stable over time. 6 it is anticipated that the incidence of traumatic brain injury is likely to rise as level of industrialization will continue to increase. increases number of natural disasters like cyclones and floods will lead to greater load of trauma. many centers now have fully functional round-the-clock operation theaters and cooling them needs large amounts of power. again, most of the computed tomography machines and magnetic resonance imaging machines need supercooled magnets which against needs electricity. thus, global warming will lead to greater health care expenditures which will trans late to increased health care costs and thus non-affordability will rear its ugly head again. changes made before the problem becomes unreversible is the only solution. 7 the global warming and ecological changes may produce myriad of health hazard including cerebral stroke, aneurysmal subarachnoid hemorrhage. the real inconvenience shall be in the mangement of diseases that will arise dur to this and will push us back in terms of our advancement adn health care delivery. it is best to control global climate changes and warming with the help of international cooperation further health hazard. references 1. chan eyy, ho jy, hung hhy, liu s, lam hcy. health impact of climate change in cities of middle-income countries: the case of china. british medical bulletin 2019;130:5-24. 2. epstein pr. is global warming harmful to health? scientific american 2000;283:50-57. 3. lemonick md, bjerklie d, boyle rh. life in the greenhouse. time 2001;157:24-29. 4. ali y, rahme r, matar n, et al. impact of the lunar cycle on the incidence of intracranial aneurysm rupture: myth or reality? clinical neurology and neurosurgery 2008;110:462-465. 5. chyatte d, chen tl, bronstein k, brass lm. seasonal fluctuation in the incidence of intracranial aneurysm rupture and its relationship to changing climatic conditions. journal of neurosurgery 1994;81:525-530. 6. li t, horton rm, bader da, liu f, sun q, kinney pl. longterm projections of temperature-related mortality risks for ischemic stroke, hemorrhagic stroke, and acute ischemic heart disease under changing climate in beijing, china. environment international 2018;112:1-9. 7. deora h, tripathi m, yagnick ns, deora s, mohindra s, batish a. changing hands: why being ambidextrous is a trait that needs to be acquired and nurtured in neurosurgery. world neurosurgery 2019;122:487-490. moscote-salazarluis_post 92 moscote-salazar et al post-traumatic cerebellar infarction post-traumatic cerebellar infarction due to vertebral artery foramina fracture: case report luis rafael moscote-salazar1, andres m. rubiano2, willem guillermo calderon-miranda3, amit agrawal4 1neurosurgery-critical care, red latino. latin american trauma & intensive neuro-care organization, bogota, colombia 2neurosurgery, red latino. latin american trauma & intensive neuro-care organization, meditech foundation, universidad el bosque, bogotá, colombia 3radiology, unam-national autonomous university of mexico, mexico d.f. mexico 4department of neurosurgery, narayna medical college hospital chinthareddypalem nellore, andhra pradesh, india abstract: posttraumatic cerebral infarction is an uncommon cause of morbidity and mortality and many studies have highlighted that trauma needs to considered as causative factor for cerebellar infarction. we present a case of cerebellar infarction in a 35 year old young patient secondary to vertebral fracture involving the vertebral foramen and vertebral artery injury. ct scan cervical spine showed c2-3 fracture on left side with fracture extending into the left vertebral foramen. a ct scan angiogram could not be performed because of poor neurological status. possibly the infarction was due to left vertebral artery injury. without surgical intervention prognosis of these patients remain poor. prognosis of patients with traumatic cerebellar infarction depends on the neurological status of the patient, intrinsic parenchymal damage and more importantly extrinsic compression of the brainstem by the edematous cerebellar hemispheres. key words: cerebellar infarction, traumatic brain injury, cervical spine injury, vertebral artery injury introduction posttraumatic cerebral infarction is an uncommon cause of morbidity and mortality in patients with traumatic brain injury. (1-5) many studies have highlighted that trauma needs to considered as causative factor for cerebellar infarction particularly in young patients. (2, 4-7) we present a case of cerebellar infarction in a young patient secondary to vertebral fracture involving the vertebral foramen and vertebral artery injury. case report a 35 year old gentleman met a road traffic accident while he was trying to overtake another vehicle and driver lost the control and romanian neurosurgery (2016) xxx 1: 92 97 93 collided with the vehicle. drive died on the spot. details of pre-hospital care were not available. he was brought to the emergency department 25 hours after the accident. the patient was put on cervical collar. his gcs was e1vtm4. pupils were bilateral 3 mm and nonreactive to light. ct scan brain showed thin left fronto-temporo-parietal acute subdural hematoma with minimal mass effect and midline shift. ct scan also showed left cerebellar infarction. with mass effect and diffuse deep cerebral edema. in addition ct scan cervical spine showed c2-3 fracture on left side with fracture extending into the left vertebral foramen. a ct scan angiogram could not be performed because of poor neurological status. possibly the infarction was due to left vertebral artery injury. in view of poor neurological status the patient relatives opted for conservative management. poor prognosis was explained and in spite of all measures the patient could not be revived. figure 1 (a) ct scan showing right cerebellar infarction, (b) follow-up ct scan showing infarction, and (c) postoperative scan showing the opened up ventricle ct scanning reveals large bilateral cerebellar and occipital infarct in the territory of pcas, scas and aicas with acute hydrocephalus 94 moscote-salazar et al post-traumatic cerebellar infarction figure 2 figure 3 romanian neurosurgery (2016) xxx 1: 92 97 95 discussion a number of mechanisms have been described to explain the cerebellar infarction following head injury. these include dissections (with progressive thrombosis and vascular occlusion) or vertebrobasilar spasm, embolization, and systemic hypoperfusion compromising the vascular supply to the cerebellum, (2, 5, 8-10) local trauma severe enough to deform the overlying occipital bone and causing injury to the cerebellar cortical artery thus leading to the cerebellar infarction. (2, 4) once the infarcts sets in than it leads to cerebellar edema and compression of the fourth ventricle and brain stem responsible for neurological deterioration and if not intervened early than this can be fatal. (11) clinical features of the cerebellar infarction are similar to the intrinsic cerebellar lesions and depend on the size of the lesions, any associated compression of the fourth ventricle and brain stem and extent of other associated intracranial lesions. (12-16) in early stages there may be headache, dizziness, nausea, vomiting, loss of balance, signs of truncal and appendicular ataxia, nystagmus, and dysarthria. (12-14) however, if the lesion is large enough there may altered level of consciousness, ataxic respirations, extensor plantar responses, posturing, or flaccidity, impaired oculocephalic responses, decreased or absent corneal responses, and impaired or absent pupillary responses. (12, 14-17) in majority of the cases of traumatic brain injury ct scan brain with bone window is the investigations of choice and can show cerebellar infarction as a focal hypodense area (with or without evidence of fourth ventricular compression) (18); however we need to remember that in early stages ischemic changes and presence of cerebellar infarction can be missed. (1, 5) where there is high index of suspicion an mri of the brain shall provide greater details of cerebellar infarction, details of brain stem compression and presence of any associated hydrocephalus. (16, 18, 19) conventional digital subtraction angiography is the gold standard to diagnose injury to the neck vessels but may not be feasible in emergency situation. (1) same holds true for magnetic resonance imaging and magnetic resonance angiography, it can demonstrate the vascular pathology but will be difficult to perform in emergency situation like head injury. (10) to detect the injury to the neck vessels doppler can be used as a screening investigations, however it will be difficult to interpret the vertebra-basilar system. (20) in a patient with head injury now a day’s computed tomography angiography (cta) is recommended a noninvasive, highly specific, and sensitive imaging modality to rule out vascular injuries. (21) the management of post-traumatic cerebellar infarction is controversial and it is directed to reduce the intracranial pressure i.e. diversion of csf (external ventricular drain) to control hydrocephalus and/or decompression of the posterior fossa to reduce the mass effect on brain stem. (1, 5, 13, 14, 17, 22) many authors advocate that surgical decompression should be performed first to reduce the mass effect and if the clinical features continue to persist or there is deterioration in neurological status a csf 96 moscote-salazar et al post-traumatic cerebellar infarction diversion procedure can be performed. (5, 11, 23-27) management of the hydrocephalus with external ventricular drainage alone without posterior fossa decompression will not help to reduce the mass effect from the brain stem and shall be carrying the inherent risk of upward herniation. (2) there is a need to emphasize here that medical management (steroids, mannitol and hyperventilation) to reduce the intracranial pressure are usually ineffective in these cases. (22, 28) conclusion prognosis of patients with traumatic cerebellar infarction depends on the neurological status of the patient, intrinsic parenchymal damage and more importantly extrinsic compression of the brainstem by the edematous cerebellar hemispheres. (13, 22, 27) for traumatic cerebellar infarction, surgical intervention is the mainstay of treatment. (13, 14, 18, 29) without surgical intervention prognosis of these patients remain poor. (1, 13) correspondence luis rafael moscote-salazar, neurosurgeon, colombia, southamerica e-mail: mineurocirujano@aol.com references 1.behzadnia h, emamhadi m-r, yousefzadeh-chabok s, alijani b. posttraumatic cerebellar infarction in a 2-yearold child. caspian journal of neurological sciences 2015;1:49-54. 2.agrawal a, kakani a. cerebellar infarction after head injury. journal of emergencies, trauma, and shock 2010;3:207-209. 3.nichelli p, gibertoni m, guerzoni c. delayed cerebellar infarction following a car accident. stroke; a journal of cerebral circulation 1983;14:617-619. 4.taniura s, okamoto h. traumatic cerebellar infarction. the journal of trauma 2008;64:1674. 5.tyagi ak, kirollos rw, marks pv. posttraumatic cerebellar infarction. british journal of neurosurgery 1995;9:683-686. 6.barinagarrementeria f, amaya le, cantú c. causes and mechanisms of cerebellar infarction in young patients. stroke; a journal of cerebral circulation 1997;28:2400-2404. 7.cano lm, cardona p, quesada h, mora p, rubio f. [cerebellar infarction: prognosis and complications of vascular territories]. neurologia (barcelona, spain) 2012;27:330-335. 8.guyot ll, kazmierczak cd, diaz fg. vascular injury in neurotrauma. neurological research 2001;23:291-296. 9.byrd lr, vogel hl. ischemic cerebellar infarct in a 5year-old boy: sequela to minor back trauma. the journal of the american osteopathic association 1996;96:245249. 10.duval el, van coster r, verstraeten k. acute traumatic stroke: a case of bow hunter's stroke in a child. european journal of emergency medicine : official journal of the european society for emergency medicine 1998;5:259-263. 11.mostofi k. neurosurgical management of massive cerebellar infarct outcome in 53 patients. surgical neurology international 2013;4:28. 12.george b, cophignon j, george c, lougnon j. [surgical aspects of cerebellar infarctions based upon a series of 79 cases (author's transl)]. neuro-chirurgie 1978;24:83-88. 13.heros rc. cerebellar hemorrhage and infarction. stroke; a journal of cerebral circulation 1982;13:106-109. 14.norris jw, eisen aa, branch cl. problems in cerebellar hemorrhage and infarction. neurology 1969;19:1043-1050. 15.neugebauer h, witsch j, zweckberger k, jüttler e. space-occupying cerebellar infarction: complications, treatment, and outcome. neurosurgical focus 2013;34:e8. 16.savitz si, caplan lr, edlow ja. pitfalls in the diagnosis of cerebellar infarction. academic emergency medicine : official journal of the society for academic emergency medicine 2007;14:63-68. 17.lehrich jr, winkler gf, ojemann rg. cerebellar infarction with brain stem compression. diagnosis and surgical treatment. archives of neurology 1970;22:490498. romanian neurosurgery (2016) xxx 1: 92 97 97 18.amarenco p. the spectrum of cerebellar infarctions. neurology 1991;41:973-979. 19.edlow ja, newman-toker de, savitz si. diagnosis and initial management of cerebellar infarction. the lancet neurology 2008;7:951-964. 20.rommel o, niedeggen a, tegenthoff m, kiwitt p, bötel u, malin j. carotid and vertebral artery injury following severe head or cervical spine trauma. cerebrovascular diseases (basel, switzerland) 1999;9:202209. 21.pugliese f, crusco f, cardaioli g, et al. ct angiography versus colour-doppler us in acute dissection of the vertebral artery. la radiologia medica 2007;112:435-443. 22.heros rc. surgical treatment of cerebellar infarction. stroke; a journal of cerebral circulation 1992;23:937-938. 23.amar ap. controversies in the neurosurgical management of cerebellar hemorrhage and infarction. neurosurgical focus 2012;32:e1. 24.raco a, caroli e, isidori a, salvati m. management of acute cerebellar infarction: one institution's experience. neurosurgery 2003;53:1061-1065; discussion 1065. 25.tsitsopoulos pp, tobieson l, enblad p, marklund n. clinical outcome following surgical treatment for bilateral cerebellar infarction. acta neurologica scandinavica 2011;123:345-351. 26.mendelow ad, gregson ba, fernandes hm, et al. early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the international surgical trial in intracerebral haemorrhage (stich): a randomised trial. lancet (london, england) 2005;365:387-397. 27.heros rc. cerebellar infarction resulting from traumatic occlusion of a vertebral artery. case report. journal of neurosurgery 1979;51:111-113. 28.chen hj, lee tc, wei cp. treatment of cerebellar infarction by decompressive suboccipital craniectomy. stroke; a journal of cerebral circulation 1992;23:957-961. 29.kase cs, wolf pa. cerebellar infarction: upward transtentorial herniation after ventriculostomy. stroke; a journal of cerebral circulation 1993;24:1096-1098. 10paunescud_rarelocation romanian neurosurgery (2015) xxix (xxii) 1: 93 99 93 rare location of a colloid cyst case presentation d. păunescu*, m. gorgan, v. ciubotaru, ligia tătăranu “bagdasar-arseni” clinic emergency hospital, bucharest, romania *phd student in neurosurgery, "carol davila" university of medicine and pharmacy bucharest, faculty of medicine, department of neurosurgery abstract: not only pituitary adenomas, but also a number of tumors may arise from within the sella presenting a diagnostic and therapeutic challenge at a multidisciplinary specialist level. this article presents a case of a colloid cyst located in sellar region, with overlapping symptoms of a nonfunctioning pituitary adenoma. key words: colloid cyst, transsphenoidal approach case presentation a 67-year-old woman presented to the endocrinology department with a 3-months history of frontal and retroocular persistent headache. her past medical history was: type 2 diabetes mellitus treated with metformin and acarbose, hypertension and ischemic heart disease treated with simvastatin, carvedilol, trimetazidine and acetylsalicylic acid. she also has glaucoma, cataract and multinodular goiter. on presentation his vital signs were: blood pressure 120/70 mm hg, heart rate 88 beats/min. general examination revealed that the patient was awake, and cooperative. endocrinological examination revealed obesity (bmi= 31.25 kg/m2), no signs of galactorrhea and a micronodular normal-sized thyroid. no focal neurological deficits and no signs of intracranial hypertension were present. hormonal biomarkers were in normal range: cortisol 391.8 nmol / l (normal range : 710 a.m. 171-536 nmol / l, 4-8 pm 64340 nmol / l); fsh 31.5 miu / ml (normal range menopause: 25.8 134.8 miu); prolactin 137 uiu / ml (normal range: 72511 uiu / ml); ft4 16.1 pmol / l (normal range: 12-22 pmol / l); tsh 1.69 miu / ml (normal range: 0.274.2 miu / ml); igf-1: 79 ng / ml (normal range: 69-200 ng / ml). the functional evaluation of the posterior pituitary gland was carried out by means of tests for diabetes insipidus. 94 păunescu et al rare location of a colloid cyst figure 1 ct scan: tumoral mass located in the sellar region with suprasellar extension cranial computer tomography scan (ct) demonstrated an 11 mm hyperdense tumoral mass, without contrast enhancement, located in the sellar region with suprasellar extension, without other pathological changes. chest x-ray showed pulmonary emphysema, chronic bronchitis and basal bronchiectasis. turkish radiography: enlarged sella. magnetic resonance imaging (mri) of the brain: sellar mass measuring 1.15/1.11/1.35 cm with relatively homogeneous structure, developed mainly in the left half. tumor extended superiorly into the suprasellar cistern and impinge on the optic chiasm and homogeneously enhancing after contrast administration. romanian neurosurgery (2015) xxix (xxii) 1: 93 99 95 figure 2 preoperative mri. colloid cyst of sellar region that extend up to the optic chyasma ent (otolaryngology) examination was within normal limits. cardiac exam revealed: stable angina pectoris, stage iii hypertension and type 2 diabetes mellitus. visual field examination shows optochiasmatic syndrome: figure 3 visual field examination given the nature of non-secreting tumor and the presence of optochiasmatic syndrome we have chosen the transsphenoidal approach. 96 păunescu et al rare location of a colloid cyst surgical technique we performed endonasal surgery. after induction of general anesthesia, patient was placed in the supine position. we chose right nostril for the approach and the entire procedure was performed with an operating microscope. a handheld nasal speculum was inserted into the nostril in a trajectory along the middle turbinate, which reliably led to the sella turcica. in the posterior nasal cavity we made a vertical mucosal incision. the septum, with its mucosa intact, was then pushed off from the midline by the medial blade of the handheld speculum. bilateral mucosal flaps were elevated over the keel of the sphenoid bone and laterally reflected. the sphenoid ostia were identified. the hand-held speculum was then replaced by a hardy speculum. rongeurs were used to make a large opening into the sphenoid sinus to provide adequate sellar exposure. the osseous sellar floor was widely opened and the sellar dura mater was incised. tumor removal proceeded in a standard way using bayoneted ring curettes, irrigation, and suction. after removal of the speculum, the nasal septum was returned to the midline and the ipsilateral out-fractured middle turbinate was moved toward the midline. nasal packing was placed for 48 hours. (swearingen & biller, 2008) for the next two days, patient was held under observation in order to detect diabetes insipidus and hyponatremia, and to monitor anterior pituitary function. patient was discharged home on postoperative day 3. pathologic examination confirmed the diagnosis of colloid cyst. figure 4 postoperative mri images. complete removal of sellar colloid cyst romanian neurosurgery (2015) xxix (xxii) 1: 93 99 97 at the 3rd month follow-up visit the patient did not show any endocrinological or focal neurological deficits. mri brain images revealed total resection of colloid cyst and no compression on optic chiasma (figure 4). discussion pituitary adenomas comprise more than 90% of sellar masses. the remaining 10% include pituitary-origin tumours (rathke’s cleft cysts, craniopharyngiomas, pituitary carcinomas and astrocytomas) and nonpituitary origin tumours (meningiomas, germ cell tumours, chondrosarcomas/chordomas, giant cell tumours, epidermoid cysts, aneurysms, metastatic lesions and colloid cyst). owing to their common location, nonadenomatous sellar lesions frequently mimic pituitary macroadenomas on magnetic resonance imaging and computed tomography, resulting in a diagnostic challenge. macroadenomas are typically isointense on t1-weighted mri sequences, variable on t2, and show homogeneous enhancement1. they almost invariably expand the sella turcica, which can be a helpful clue to a non-adenomatous lesion when this feature is absent. while most macroadenomas can be resected via a transsphenoidal neurosurgical approach, non-adenomatous lesions may require a transcranial approach. thus, preoperative diagnosis of a nonadenomatous pituitary tumour is difficult in directing therapy and preventing complications in case of an inadvertent transsphenoidal approach, such as: incomplete tumor resection, cerebrospinal fluid (csf) leak or meningitis. but the absolute differentiation of macroadenomas from nonadenomatous pituitary tumors is not always possible prior to surgery (2). colloid cysts represents 0.2 2% of brain tumors and less than 1% of symptomatic brain tumors (3). although these tumors are considered congenital, their diagnosis during childhood is rare. they are slow growing and the initial onset of symptoms is usually between 20 and 50 years of age, although the youngest reported patient was 2 months old and the oldest was 82 years old (4). colloid cysts are found throughout the neuroaxis, but over 99% of them develop in the third ventricle, in most cases in the anterior roof5. sometimes these tumors develop in sellar region, in the fourth ventricle (6, 7), velum interpositum (8, 9), intrapontomesencephalic (10), premedullary/pontine cistern (11), cerebellum (12), the region of the optic chiasma (13) or frontal lobe (14). colloid cysts of the pituitary gland are very rare pathological lesions occurring in sellar region. their pathogenesis is not clear but is believed to be of endodermal origin from a vestigial ventricular structure (the paraphysis). they are located between the anterior and posterior lobe of the pituitary. colloid cysts of the pituitary gland are space occupying lesions and could induce hypopituitarism, diabetes insipidus or visual disturbances. magnetic resonance imaging is the preferred neurodiagnostic method in evaluating these lesions (15). diagnostic imaging of colloid cysts includes both mri and ct examinations. these tumors are filled with mucus that on ct may be either hyperdense in comparison to the 98 păunescu et al rare location of a colloid cyst grey matter (two thirds) or hypodense/ isodense (one third). there are no calcifications and there is usually enhancement of the cyst wall after contrast administration. these are mainly oval or round structures. on mri, colloid cysts may produce diverse signal intensity. some lesions are heterogeneous. a marked shortening of the t2 relaxation time is often noticed in the central part of the cyst (16). approximately 50% of these pathological lesions are hyperintense in t1-weighted images. the rest may be isoor hypointense as compared to the gray matter. in t2-weighted images, most of the colloid cysts show decreased signal intensity, while flair sequences reveal increased signal intensity. in dwi sequences, those cysts are shown to form areas of decreased signal intensity. colloid cysts of the pituitary gland reveal some typical mri features which can be helpful in establishing the appropriate diagnosis. due to the location of the colloid cyst in pars intermedia of the pituitary gland, in sagittal sections the lesion is placed between the anterior and the posterior lobe of the pituitary gland (17). according to laboratory studies of multiple cases, hyperprolactinaemia is found in as much as 72% of patients (3). in our case, the colloid cyst manifested only by persistent headaches and visual disturbances (mri and visual field examination showed optic chiasm compression). all hormonal biomarkers were in normal range before and after the surgical intervention. in the case of symptomatic sellar colloid cysts (causing endocrinological or neurological disturbances) transphenoidal resection remains the treatment of choice. conclusions apart from pituitary adenomas, a number of tumors may arise from within the sella presenting a diagnostic and therapeutic challenge at a multidisciplinary specialist level. the absolute differentiation is often not possible prior to invasive therapeutic or diagnostic procedures but subtle ct and mri clues can indicate the possibility of a nonadenomatous lesion. this information is guiding the surgeon to the best operative approach and preventing the undue complications of an unnecessary or incomplete trans-sphenoidal resection. acknowledgement this paper was co-financed from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 “excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis”, coordinator the bucharest university of economic studies. references 1.johnsen de, woodruff ww, allen is, cera pj, funkhouser gr, coleman ll. mr imaging of the sellar and juxtasellar regions. radiographics 1991;11:727-58. 2.abele ta, yetkin zf, raisanen jm, mickey be, mendelsohn db. non-pituitary origin sellar tumours mimicking pituitary macroadenomas. clinical radiology 2012;67:821-7. 3.nomikos p, buchfelder m, fahlbusch r. intraand suprasellar colloid cysts. pituitary 1999;2:123-6. romanian neurosurgery (2015) xxix (xxii) 1: 93 99 99 4.hwang dh, townsend jc, ilsen pf, bright dc. colloid cyst of the third ventricle. journal of the american optometric association 1996;67:227-34. 5.kornienko vn, pronin in. diagnostic neuroradiology; 2009. 6.parkinson d, childe ae. colloid cyst of the fourth ventricle; report of a case of two colloid cysts of the fourth ventricle. journal of neurosurgery 1952;9:404-9. 7.jan m, ba zeze v, velut s. colloid cyst of the fourth ventricle: diagnostic problems and pathogenic considerations. neurosurgery 1989;24:939-42. 8.hingwala dr, sanghvi da, shenoy as, dange nn, goel ah. colloid cyst of the velum interpositum: a common lesion at an uncommon site. surgical neurology 2009;72:182-4. 9.morris tc, santoreneos s. colloid cyst of velum interpositum: a rare finding. journal of neurosurgery pediatrics 2012;9:206-8. 10.inci s, al-rousan n, soylemezoglu f, gurcay o. intrapontomesencephalic colloid cyst: an unusual location. case report. journal of neurosurgery 2001;94:118-21. 11.goel a, muzumdar d, chagla a. endodermal cyst anterior and anterolateral to the brainstem: a report of an experience with seven cases. british journal of neurosurgery 2005;19:163-6. 12.muller a, buttner a, weis s. rare occurrence of intracerebellar colloid cyst. case report. journal of neurosurgery 1999;91:128-31. 13.killer he, flammer j, wicki b, laeng rh. acute asymmetric upper nasal quandrantanopsia caused by a chiasmal colloid cyst in a patient with multiple sclerosis and bilateral retrobulbar neuritis. american journal of ophthalmology 2001;132:286-8. 14.tanei t, fukui k, kato t, wakabayashi k, inoue n, watanabe m. colloid (enterogenous) cyst in the frontal lobe. neurologia medico-chirurgica 2006;46:401-4. 15.zielinski g, podgorski jk, siwik j, warczynska a, zgliczynski w. [colloid cysts of the pituitary gland]. neurologia i neurochirurgia polska 2002;36:293-306. 16.maeder pp, holtas sl, basibuyuk ln, salford lg, tapper ua, brun a. colloid cysts of the third ventricle: correlation of mr and ct findings with histology and chemical analysis. ajr am j roentgenol 1990;155:13541. 17.bladowska j, bednarek-tupikowska g, biel a, sasiadek m. colloid cyst of the pituitary gland: case report and literature review. polish journal of radiology / polish medical society of radiology 2010;75:88-93. 14_govindmangal 324 govind et al primary intracranial extraosseus myxoid chondrosarcoma of dominant frontal lobe primary intracranial extraosseus myxoid chondrosarcoma of dominant frontal lobe mangal govind1, mittal radheyshyam2, sharma achal3, gandhi ashok4 sms medical college and hospitals jaipur, india 1mch resident in neurosurgery; 2professor and head of department, department of neurosurgery; 3professor and faculty, department of neurosurgery; 4associate professor and faculty, department of neurosurgery introduction primary intracranial extraosseus myxoid chondrosarcoma are an extremely rare neoplasm. till date there are only nine cases of this entity has been reported. the authors present a case of primary intracranial extraosseus myxoid chondrosarcoma of the dominant frontal lobe. case report a 40 years old male was admitted to our department with complaints of headache on and off and recurrent seizures for last five years. patient was on antiepileptic drugs as advised by his treating physician and he responded well earlier but for last one year seizures were not in control hence he was investigated. on imaging, ncct brain shows an ill-defined heterogenous mass in left frontal region with focal areas of calcification. mri brain shows a well circumscribed intra-axial heterogeneously hypointense mass on t1w and hyperintense on t2w and flair mri sequence. there was minimal perilesional edema. no restriction of diffusion seen on dwi and diffusion coefficient was increased on adc sequence. faint patchy enhancement seen on contrast images. left frontotemporoparietal craniotomy with complete excision of mass done. tumor was well circumscribed greyish white in colour, firm to hard in consistency, relatively avascular, loosely adherent to surrounding brain parenchyma. a plane of cleavage was present at the lesion brain interface. on histopathology, sections shows circumscribed lobulated growth pattern with areas having hyaline cartilage. the lobules are variable in size. the capsule is moderately thickened and is showing mild lymphocytic infiltrate. the tumor has low to moderate cellularity and nuclear pleomorphism. predominantly the lacunae are mononucleated however binucleated and multinucleated lacunae are also seen. focal areas of calcification and fibromyxoid changes are also seen. overall morphology is in favour of chondrosarcoma/chondroma grade -1. on immunohistochemistry tumor cells are strongly positive for vimentin. 50-75 percent cells shows bcl-2 expression. cd99, p-53, ecadherine, ema, ck8/18 and ck pan (ae1ae3) are negative in the tumor cells. postoperative period was uneventful and patient was discharged on fifth postoperative day without any neurologic deficit. antiepileptics were initially prescribed for one month and then tapered gradually over fifteen days. on follow up of six months patient had no complaints and seizures were under control on phenytoin 300mg per day. romanian neurosurgery (2015) xxix 3: 324 328 325 figure 1 ncct brain shows an ill defined heterogenous mass in left frontal region with focal areas of calcification figure 2 mri brain shows a well circumscribed intra-axial heterogeneously hyperintense on t2w imaging figure 3 tumor was well circumscribed greyish white in colour, firm to hard in consistency, relatively avascular figure 4 postoperative ncct brain suggestive of left frontotemporoparietal craniotomy with complete excision of mass 326 govind et al primary intracranial extraosseus myxoid chondrosarcoma of dominant frontal lobe figure 5 showing cells are bcl-2 positive figure 6 showing cells are s-100 positive (high power) figure 7 there is blue myxoid matrix located in lacunae. tumor cells are lobulated and double nucleated cells are presentwith foci of calcification discussion since enziner and shiraki first described myxoid chondrosarcoma in 1972 as a deep soft tissue tumor of the extremities only nine cases of primary intracranial extraosseus myxoid chondrosarcoma have been reported as per authors’ knowledge. (2, 4, 5, 9, 10, 13, 15, 16, 17). intracranial myxoid chondrosarcoma is extremely rare and is thought to arise from the choroid plexus, dura or in rare instances the pineal region. (1, 3, 6, 9, 14, 17). histologically only three subtypes of intracranial chondrosarcomas have been described: classic chondrosarcoma, mesenchymal chondrosarcoma and myxoid chondrosarcoma. (5, 8, 11). most of the primary intracranial extraosseus chondrosarcoma show a dural involvement. however those within the brain parenchyma without any attachment to the cranium or the meninges are very rare. the case of author is of myxoid chondrosarcoma having no dural involvement. the classic cranial and intracranial chondrosarcoma usually arise at the skull base and most frequently affect adults. (8, 15). the classic subtype has a better prognosis than the mesenchymal subtype. (15). mesenchymal type usually occurs in the frontoparietal region and is highly vascular (15) it is the most aggressive subtype with a tendency for recurrence and metastasis. (8, 15). calcification was more common in cranial myxoid chondrosarcoma and it lacks hyaline. the optimal treatment for intracranial myxoid chondrosarcoma is radical excision, and total removal of the tumor is critical. (5, 8, 12, 14, 15). adjuvant therapies, including radiotherapy, brachytherapy, and proton beam treatment, have been found to improve patient outcomes for this rare cancer. (5, 11, 15). however there have been no reports on the advantages of adjuvant chemotherapy for patients with intracranial extraskeletal myxoid chondrosarcomas till date. in addition, intracranial myxoid chondrosarcomas are not associated with a good prognosis after treatment. romanian neurosurgery (2015) xxix 3: 324 328 327 correspondence dr. govind mangal mch neurosurgery resident sms medical college and hospitals jaipur, india +91-9414728062 dr.govindmangal@gmail.com references 1.bourgouin pm, tampieri d, robitaille y, robert f, bergeron d, del carpio r, et al.: j comput assist tomogr 16: 268-273, 1992.10 2.chaskis c, michotte a, goossens a, stadnik t, koerts g, d’haens j: primary intracerebral myxoid chondrosarcoma. case illustration. j neurosurg 97: 228, 2002.2 3.cummings tj, bridge ja, fukushima t: extraskeletal myxoid chondrosarcoma of the jugular foramen. clin neuropathol 23: 232-237, 2004 . 11 4.enzinger fm, shiraki m: extraskeletal myxoid chondrosarcoma. an analysis of 34 cases. hum pathol 3: 421-435, 1972 . 1 5.gonzález-lois c, cuevas c, abdullah o, ricoy jr: intracranial extraskeletal myxoid chondrosarcoma: case report and review of the literature. acta neurochir (wien) 144: 735-740, 2002 .3 6.grossman ri, davis kr: cranial computed tomographic appearance of chondrosarcoma of the base of the skull. radiology 141: 403-408, 1981.12 7.harsh gr iv, wilson cb. central nervous system mesenchymal chondrosarcoma: case report. j neurosurg 1984; 61:375-81.16 8.hassounah m, al-mefty o, akhtar m, jinkins jr, fox jl: primary cranial and intracranial chondrosarcoma. a survey. acta neurochir (wien) 78: 123-132, 1985 .14 9.im sh, kim dg, park ia, chi jg: primary intracranial myxoid chondrosarcoma: report of a case and review of the literature. j korean med sci 18: 301-307, 2003.4 10.jin hoon park, mi-jung kim, chang jin kim, jeong hoon kim, j korean neurosurg soc 52: 246-249, 2012.8 11.korten ag, ter berg hj, spincemaille gh, van der laan rt, van de wel am: intracranial chondrosarcoma: review of the literature and report of 15 cases. j neurol neurosurg psychiatry 65: 88-92, 1998 .15 12.o’brien j, thornton j, cawley d, farrell m, keohane k, kaar g, et al.: extraskeletal myxoid chondrosarcoma of the cerebellopontine angle presenting during pregnancy. br j neurosurg 22: 429-432, 2008 .17 13.peker, betül c. md*; saral, hatice d. md*; baloğlu, murat md†; ataizi, serdar md†yurdasiper, alper md‡ neurosurgery quarterly:august 2013 volume 23 issue 3 p 153–155.9 14.sala f, talacchi a, beltramello a, iuzzolino p, bricolo a: intracranial myxoid chondrosarcoma with early intradural growth. j neurosurg sci 42: 159-163, 1998.13 15.salcman m, scholtz h, kristt d, numaguchi y: extraskeletal myxoid chondrosarcoma of the falx. neurosurgery 31: 344-348, 1992 .5 16.scott rm, dickersin r, wolpert sm, twitchell t: myxochondrosarcoma of the fourth ventricle. case report. j neurosurg 44: 386-389, 1976.6 17.sorimachi t, sasaki o, nakazato s, koike t, shibuya h: myxoid chondrosarcoma in the pineal region. j neurosurg 109: 904-907, 2008.7 doi: 10.33962/roneuro-2020-031 presentation, management and outcomes of pituitary adenomas. a 10year experience from a single tertiary neurosurgery centre bogdan ionut david, ligia gabriela tataranu, vasile gheorghe ciubotaru, aurelia mihaela sandu, radu mircea gorgan romanian neurosurgery (2020) xxxiv (1): pp. 195-200 doi: 10.33962/roneuro-2020-031 www.journals.lapub.co.uk/index.php/roneurosurgery presentation, management and outcomes of pituitary adenomas. a 10-year experience from a single tertiary neurosurgery centre bogdan ionut david1,3, ligia gabriela tataranu2,3, vasile gheorghe ciubotaru3, aurelia mihaela sandu3, radu mircea gorgan2,3 1 phd student. university of medicine and pharmacy “carol davila”, bucharest, romania 2 university of medicine and pharmacy “carol davilaˮ, bucharest, romania 3 department of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest, romania abstract introduction: one of the most frequently encountered intracranial tumours are the pituitary adenomas, these accounting for 5% to 20%. therapeutic strategies vary largely, from medical therapy to complex neurosurgical procedures. the transsphenoidal approach can solve most of the lesions of the pituitary area, as long as the invasion of the adjacent structures is not significant. the transcranial approach is indicated in tumours with extensive invasion materials and methods: we performed a retrospective study in the bagdasar-arseni emergency hospital neurosurgery that aimed to analyze the demographics, signs and symptoms, therapeutic strategy, surgical approach, complications, and histopathology, from 2010 to 2019. results: the total number of hospitalization records, including the follow-up hospitalization and/or second surgery hospitalization, was of 1107. furthermore, there were 704 unique patients. the most common signs and symptoms encountered for the first admission were headache (245 – 34.56%), optic chiasm deficits (153 – 21.58%), acromegaly (85 – 11.99%). however, the majority of patients (507 – 71.51%) presented with some sort of hormonal imbalance or diabetes insipidus. on the one hand, a number of 325 (45.84%) patients had non-surgical treatment. on the other hand, a total of 384 (54.16%) surgeries for pituitary tumours were performed in this period. discussion: in our study, the patients who underwent surgery benefited from either microsurgical transsphenoidal or transcranial surgeries. even if the transsphenoidal approach was used far more, there was a greater relapse proportion in these patients. transcranial surgery, even if followed by a far less proportion of relapse surgery, carried with it the burden of more days spent in hospital (most of the time twice as much as for the transsphenoidal patients). keywords pituitary adenoma, transcranial approach, transsphenoidal approach corresponding author: bogdan ionut david university of medicine and pharmacy “carol davilaˮ, bucharest, romania david.bogdan.med@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 196 bogdan ionut david, ligia gabriela tataranu, vasile gheorghe ciubotaru et al. conclusion: both transsphenoidal and transcranial approaches have advantages and disadvantages, thus the best strategy would be to tailor each surgery to each patient, keeping an open mind to all available approaches introduction one of the most frequently encountered intracranial tumors are the pituitary adenomas, these accounting for 5% to 20% of all tumor lesions at this level. most of the developing countries of the world estimate an incidence of about 20 cases per 100.000 population (1), while european developed countries agree on 3,9-4 new cases per 100.000 people each year, the prevalence hovering between 78 and 94 cases per 100.000 people. while most of the tumors that originate in the pituitary gland are usually benign, the behavior of these lesions can be unpredictable. thus, one can encounter anything from clinically silent, indolent tumors, all the way to extremely aggressive malignancies. therefore, a meticulous understanding of the anatomy of the area and also of the specific physiology of the hypothalamopituitary complex is mandatory. (2) the therapeutic strategies vary largely, from medical therapy to complex neurosurgical procedures, depending on the aforementioned characteristics of the lesions. as far as signs and symptoms are concerned, these again vary according to the nature of the tumor and the local extension. the clinician has to look for hormonal dysfunction, visual field deficits, decreased visual acuity, anterior pituitary dysfunction and headache. (3) the usual therapeutic strategy is to try to medically manage any case. if this is not enough or neurological/hormonal deficits occur, the obvious step is taken towards surgical management. at this stage, the neurosurgeon has to decide which surgical approach and technique best tailors every case: transcranial, transsphenoidal microsurgical or transsphenoidal endoscopic, as well as any combined approach that he or she might find adequate. regarding surgical approach used, one must look back to the era of schloffer (1907), hirsch (1910s) and cushing (1920s). they were the ones who paved the road for the transsphenoidal approach for pituitary lesions. however, in the first half of the 20th century, due to lack of antibiotic therapy, the results were dismal. hence, cushing abandoned the technique and favored the transcranial approach. however, with introduction of the operating microscope, endoscope and development of powerful antibiotics, the transsphenoidal approach soon regained attention. nowadays, there is a general consensus that the transsphenoidal approach can solve most of the lesions of the pituitary area, as long as the invasion of the adjacent structures is not significant. furthermore, an experienced neurosurgeon, more familiar with the transcranial approach, will usually have similar results by using this method. therefore, as long as the lesion permits both surgical strategies, it usually comes down to surgeon preferences and experience. non the less, the more complex the lesion, the more surgeons prefer the transcranial approach. (3). materials and methods this is a retrospective study conducted in the bagdasar arseni emergency hospital neurosurgery departments 3 and 4 that aims to analyze the demographics, signs and symptoms, therapeutic strategy, surgery approach used, complications associated with these approaches, histopathology of pituitary tumors, over the course of 10 years, from january 2010 to december 2019. to keep in line with confidentiality agreements and laws, each patient was coded and the original identification was removed. data was collected directly from the electronic patient charts by the primary author. data included in the study were age, gender, number of days of hospitalization, number of hospitalizations for each patient, signs, symptoms, type of surgery (approach used), perioperative complications (csf leak, hematoma, neurological deficits) and also death within period of hospitalization. in order to be included in the study, the patients had to have diagnosis of pituitary tumor, be of either gender, with no limit in regard to age. the patient had to had been inbound in one of either neurosurgery 3 or 4 department and have an outgoing diagnosis of pituitary adenoma. all patients presenting with other sellar or parasellar masses were excluded (such as craniopharyngioma, epidermoid cyst, anterior circulation aneurysm). results the study included all patients presenting with pituitary tumors between january 2010 and 197 presentation, management and outcomes of pituitary adenomas december 2019 on either of department 3 or 4 of neurosurgery in bagdasar arseni hospital, bucharest. thus, 1107 hospitalization records were taken into account, including the follow-up hospitalization and/or second surgery hospitalization. furthermore, there were 704 unique patients (personal identification numbers were analyzed). the gender distribution was 243 (34.27%) women and 466 (65.73%) men (figure 1), minimum age was 14 and maximum was 84, with a mean age of 56.24 (62.77 years old for women and 52.77 years old for men) (figure 2). figure 1. figure 2. the most common signs and symptoms encountered for the first admission were headache (245 – 34.56%), optic chiasm deficits (153 – 21.58%), acromegaly (85 – 11.99%). however, the majority of patients (507 – 71.51%) presented with some sort of hormonal imbalance or diabetes insipidus (figure 3). on the one hand, a number of 325 (45.84%) patients had non-surgical treatment: they were either referred to an endocrinology department to begin conservative treatment, or a "watchful waiting" ensued after the first radiological evaluation (figure 4). figure 3. figure 4. on the other hand, a total of 384 (54.16%) surgeries for pituitary tumors were performed in this period as follows: 243 primary transsphenoidal surgeries, 36 primary transcranial surgeries, 62 transsphenoidal reinterventions, 18 transcranial interventions for relapse after transsphenoidal surgeries, 6 transsphenoidal surgeries after failed gamma-knife therapy, 8 combined approach surgeries (both transsphenoidal and transcranial) and 2 transcranial approaches after transcranial relapse (figure 5). figure 5. 243 34% 466 66% gender distribution of patients women men 507 245 153 85 0 100 200 300 400 500 600 signs/symptoms 384 54% 325 46% treatment strategy surgical non-surgical 243 36 62 18 6 82 surgery strategy primary transsphenoidal primary transcranian 198 bogdan ionut david, ligia gabriela tataranu, vasile gheorghe ciubotaru et al. out of the patients who underwent surgery, 122 (31.77%) were macroadenomas, with extension ranging from only suprasellar, to one or both cavernous sinuses, anterior cranial fossa or third ventricle. the histopathology examination revealed 95 gh secreting tumors (24.74%), 21 acth secreting tumors (5.46%), 18 prolactinomas (4.68%), 11 gonadotropin secreting hormones (2.86%). the rest were non secreting tumors (62.26%) (figure 6). figure 6. the mean number of days of hospitalization was of 7.5 for the entire group, with an average of 7 days for the transsphenoidal approach and an average of 13 days for the transcranial approach (figure 7). figure 7. the most common surgical complication encountered was pituitary insufficiency reported in 23 cases, while csf leakage was observed in 17 cases. for the total number of hospitalizations, 4 deaths were recorded: one after transsphenoidal surgery of a patient with a macroadenoma invading both cavernous sinuses, two patients who presented with acute hydrocephalus at admission and gcs less than 6, and one patient died of cardiac arrest in his sleep prior to surgery. no deaths were recorded for the transcranial group. discussions hypothalamic/pituitary disorders represent a multifaceted pathology and, due to advancement of treatments, technology and understanding of physiopathology of the region, lately, not one type of strategy gets to be the gold standard. (2) thus, recent understanding of complex mechanisms concerning cellular and molecular biology has brought medical treatment very high up in the list of strategies of treatment for pituitary tumors. hence, almost half the patients who were admitted to our neurosurgical clinic benefited from a conservative treatment. on the other hand, even though there is no consensus on the world stage of neurosurgery regarding the gold standard treatment in case of incidental discovered pituitary tumors, there is a different story when it comes to tumors which provoke neurological deficits of any sort, endocrine dysfunction beyond the drugs' capacity of compensating, or even pose an immediate threat to the patient's life. most recent articles (4), (5) suggest a surgical strategy as first option in these cases, but this is where the consensus stops. there are mainly three types of surgical approaches: transcranial, microsurgical transsphenoidal and endoscopic transsphenoidal, each with its own advantages and disadvantages. in our study, the patients who underwent surgery benefited from either microsurgical transsphenoidal or transcranial surgeries. even if the transsphenoidal approach was used far more, there was a greater relapse proportion in these patients (figure 8). furthermore, there were patients who underwent as many as 10 consecutive transsphenoidal surgeries in the course of the 10 years analyzed. moreover, there were a number of patients who needed transcranial reintervention after the transsphenoidal approach did not offer the desired result. only two patients underwent reintervention after transcranial approach, both of them with no relapse after the second surgery. non secreti ng tumors gh secreti ng tumors acth secreti ng tumors prolact inomas gonad otropi nomas series1 239 95 21 18 11 0 50 100 150 200 250 300 hystology of tumor 199 presentation, management and outcomes of pituitary adenomas figure 8. on the other hand, transcranial surgeries, even if followed by a far less proportion of relapse surgery, carried with it the burden of more days spent in hospital (most of the time twice as much as for the transsphenoidal patients). moreover, there were cases in which the transcranial approach was not enough for the tumor to be completely removed, in which case, a second transsphenoidal approach was used during the same hospitalization (the combined approach cases – 8 patients). we also found a number of cases in which the first treatment option was gamma-knife therapy that proved not sufficient and a transsphenoidal approach was used in these cases. in accordance with most of the studies published, our patient data base revealed a clear dominance of male over female patients and also a younger age of debut for the disease (or diagnosis) for men as opposed to women. furthermore, due to the relative early diagnosis in the natural evolution of the disease, only 122 cases out of 384 operated patients presented with macroadenommas. moreover, all of the patients who underwent transcranial approach presented with macroadenomas. the most common symptoms that brought patients to the doctor were headache, optic chiasm deficits and body modification specific to gh hypersecretion. however, there was quite a large proportion of patients (mostly microadenomas) who were diagnosed with a brain tumor after the hormonal imbalances were discovered or patients who underwent a ct scan for another pathology (for example: post-traumatic ct scans performed after car crashes that reveal pituitary tumors). the most notable complications were csf fistulae and pituitary insufficiency. these appeared in a total of less than 1% of all hospitalizations and less than 7% out of the patients who underwent surgery (17 fistulae, 23 pituitary insufficiency). furthermore, all of the patients with csf fistulae were part of the trassphenoidal approach group, none of the transcranial approach group presenting this complication. out of the total number of hospitalizations (1107), 4 deaths were reported, out of which only one directly related to the treatment optiontranssphenoidal surgery, thus a death rate of less than 0.72 for the entire group. conclusions even with the advancements in molecular and cellular biology, surgery remains one of the most important aspects of pituitary tumors treatment. even if there is still no general consensus on what the ideal approach should be, our study reveals that both transsphenoidal and transcranial approaches have advantages and disadvantages, thus the best strategy would be to tailor each surgery to each patient, keeping an open mind to all available approaches. conflicts of interest the authors declare no conflict of interests funding: none. references 1. presentation, management, and outcomes of nonfunctioning pituitary adenomas: an experience from a developing country. das b, batool s, khoja a, et al. e5759, s.l.: cureus 11(9), september 25, 2019. doi: 10.7759/cureus.5759. 2. a survey on pituitary surgery in italy. domenico solari, paolo cappabianca et al. e1-e10, s.l. : world neurosurgery, 2018. https://doi.org/10.1016/j.wneu.2 018.11.186. 3. complications associated with microscopic and endoscopic transsphenoidal pituitary surgery: experience of1153 consecutive cases treated at a single transs pheno idal transc ranian primary intervention 243 36 relapse intervention 80 2 0 50 100 150 200 250 300 350 number of relapse surgeries primary intervention relapse intervention 200 bogdan ionut david, ligia gabriela tataranu, vasile gheorghe ciubotaru et al. tertiary pituitary center. matthew s agam, bs, gabriel zada, md et al. june 1, los angeles, california : journal of neurosurgery, published online june 1, 2018. doi: 10.3171/2017.12.jns172318.. 4. endoscopic versus microscopic pituitary adenoma surgery: a single-center study. ajler pablo, beltrame sofia, toscano maximiliano, fainstein day patricia, campero alvaro, yampolsky claudio, carizzo antonio. 4, s.l. : neeurology india, 2019, vol. 67. doi: 10.4103/00283886.266241. 5. comparison of endoscopic versus microsurgical resection of pituitary adenomas with parasellar extension and evaluation of the predictive value of a simple 4-quadrant radiologic classification. gianluca trevisi, vera vigo, maria grazia morena, domenico luca grieco, mario rigante, carmelo anile, annunziato mangiola. e1-e6, s.l. : world neurosurg., 2018. https://doi.org/10.1016/j.wneu.2018.09.215. . 2tascua_aggressive 384 tascu et al aggressive or conservative management in extradural hematomas in children aggressive or conservative management in extradural hematomas in children – a challenging neurosurgical choice a. tascu1, c. pascal2, st.m. iencean3, m.r. gorgan1 1“carol davila” university of medicine and pharmacy bucharest 2neurosurgery, “bagdasar arseni” hospital, bucharest 3“grigore t. popa” university of medicine and pharmacy iasi abstract: epidural hematomas (edh) in children appear as a consequence of head trauma. although emergency surgical intervention was the classical neurosurgical treatment for edh, lately there has been observed a tendency to replace operation by conservative management, whenever the neurological status and imaging appearance allows it. the aim of this article is to present our experience in treating edh in children 0-3 years old and to establish a management protocol for edh in infants, by evaluating the clinical and neuroimaging status, of both surgically and conservatively treated patients, from hospital admission to discharge. retrospective study includes 52 patients diagnosed with an extradural hematoma, admitted in the first neurosurgery department of the clinical hospital ‘bagdasar-arseni’ in bucharest, from january 2004 to december 2013. the patients were identified by diagnosis from the clinic’s database; clinical and imaging data was extracted from the patient’s individual records and crosschecked with the operating protocols. cerebral ct scan was the preferred imaging investigation for diagnosis. our study includes 52 patients (26 boys and 26 girls), with a mean age of 14.5 months (range 6 weeks – 3 years old). 25 patients were surgically treated, while the other 27 received symptomatic medication and were monitored clinically and by imaging exams. the most frequent clinical manifestations were intracranial hypertension (21 patients) and psychomotor agitation (19 patients). the traumatic mechanisms were: accidental falling (38 patients), blunt head trauma (3 patients), road accident (2 patients), unspecified (8 patients) other causes (1 patient). based on the glasgow coma scale classification of tbi, 39 patients suffered a mild tbi, 7 a moderate tbi and 6 patients suffered a severe tbi. most of the patients had a good recovery; there was a total of two deaths. the most common location for the edhs was parietal (20 patients) and temporal-parietal (11 patients). both surgical treatment and conservative management of edh have a good clinical outcome. clinical and neuroimaging evaluation at admission/reevaluation plays an imperative role in deciding the appropriate therapeutic attitude for each patient. key words: conservative therapy, extradural hematomas in children, surgical therapy. romanian neurosurgery (2014) xxi 4: 384 – 393 385 introduction an extradural hematoma (edh) is a blood clot that develops between the dura mater and the skull, it usually has a biconvex shape and it is found in 2.5% to 5% of head injured patients(1). head trauma in children 0-3 years old is completely different compared with adults – ‘children are not young adults’ (2). edhs are not a common finding in children presenting with head trauma, being diagnosed in only 1-3% of these patients (3-5). the most frequent mechanisms for head trauma in children are either accidental falling of blunt head trauma (7-9). in 73% of the edh the bleeding source is the middle meningeal artery or vein, usually associated to a temporal bone fracture (10). edhs may also be of venous origin as the result of tearing of venous dural sinuses, emissary veins, or venous lakes within the dura mater. most traumatic venous edhs occur in children, and most are not associated with a skull fracture (10). edhs are often located temporal-parietal, due to the easily detachment of the dura from the bone structure – dural detachment areas of gerardmarchand. the specific management of epidural hematomas was not thoroughly established and proposed in class i or ii evidence-based guidelines, and their treatment is based on clinical and brain imaging criteria such as gcs score, pupillary anomalies, volume, thickness and mass effect detected on ct scan, as well as the neurosurgeon’s personal experience. our study describes the results on 52 pediatric patients (age 0-3 yo) treated surgically or conservative. methods inclusion and exclusion criteria. the study includes 52 patients diagnosed with an extradural hematoma, admitted in the first neurosurgery department of the clinical hospital ‘bagdasar-arseni’ in bucharest, from january 2004 to december 2013. there were 72 patients admitted with a diagnosis of epidural hematoma, but 20 patients were not included in the study due to the incomplete data in the patients files. study design and database. the present study is a retrospective analysis of 52 patients aged 0-3 years old, treated in our department during the period from january 2004 to december 2013 for a edh. the patients were identified by diagnosis (icd 10 s06.4: epidural hemorrhage) from the clinic’s computerized database; clinical and imaging data was extracted from the patient’s individual records and crosschecked with the operating protocols. the following data was analyzed: demographic data – age, sex; case history data regarding the mechanism of the tbi and the patients clinical symptoms immediately after the head trauma (e.g. loss of conscience); clinical findings (mainly neurological status); imaging aspect (head ct scan). patients. we included 52 patients, 26 boys and 26 girls (sex ratio 1:1) diagnosed with epidural hematoma in our department on a 10 year period. the patients mean age was 14.5 months, ranging from 6 weeks to 3 years old. most of the patients were 0-1 yo – 26 (50%) patients, 12 (23%) were 1-2 yo and 14 (27%) aged 2-3. 386 tascu et al aggressive or conservative management in extradural hematomas in children radiological assessments. every patient was examined at admission by ct scan or, sometimes, mri. the neuroimaging examinations offer data regarding to the edh location, associated brain lesions, associated skull lesions and their evolution in time (figure 1 a, b). figure 1 a acute subdural hematoma in a 3 yo child that suffered a moderate tbi by accidental falling from a different level. clinical status: signs of intracranian hypertension, gcs=9points figure 1 b postoperative aspect romanian neurosurgery (2014) xxi 4: 384 – 393 387 treatment. 25 (48%) patients were operated, while the other 27 were treated with symptomatic drugs and were carefully monitored clinically and by cerebral imaging. the surgical technique for edh evacuation consisted in craniotomy based over the hematoma; it is imperious to obtain an adequate exposure of the hematoma, in order to control the bleeding source. after we lifted the bone flap, we removed the epidural hematoma by cup forceps, suction and irrigation, followed by the coagulation of the bleeding source. we’ve also incised the dura, to make sure there is no subdural bleeding subjacent to the epidural hematoma. the dura mater was then suspended to the perimeter of the craniotomy by several ‘sleep stitches’ and the bone flap was repositioned. for the posterior cranial fossa edh, the incision was performed on the midline, then we practiced a suboccipital bilateral craniotomy, followed by the evacuation of the hematoma and the tacking of the dura to the bone margins. we always placed a subgaleal drain tube maintained for 24 hours postoperatively. outcome evaluation. the clinical status was evaluated by pediatric glasgow coma scale at admission, neurological status during hospitalization and glasgow outcome scale at discharge. table 1 pediatric glasgow coma scale and glasgow outcome scale pediatric glasgow coma scale glasgow outcome scale eye opening d = dead spontaneous 4 pvs=persistent vegetative state to speech 3 sd=severe disability to pain 2 md-moderate disability no response 1 gr=good recovery verbal response smiles, oriented to sounds, follows objects, interacts 5 cries but consolable, inappropriate interactions 4 inconsistently inconsolable, moaning 3 inconsolable, agitated 2 no response 1 motor response moves spontaneously or purposefully 6 withdraws from touch 5 withdraws from pain 4 abnormal flexion to pain for an infant (decorticate response) 3 extension to pain (decerebrate response) 2 no motor response 1 388 tascu et al aggressive or conservative management in extradural hematomas in children results the most frequent cause for edh was accidental falling, encountered in 38 (73.07%) patients, 8 (15.38%) patients couldn’t specify the cause, 3 (5.77%) patients suffered a blunt head trauma and 2 (3.84%) patients were victims of road accidents (table 2). we classified the tbi based on the glasgow coma scale, considering as mild tbi the patients with a gcs=13-15pts, moderate tbi at gcs=12-9pts and severe tbi patients with gcs=8 or less. 39 (75%) patients suffered a mild tbi, 7 (13.46%) a moderate tbi and 6 (11.54%) patients had a severe tbi. the predominant clinical manifestations (table 3) were those of intracranial hypertension such as headache, nausea/vomiting and drowsiness – 21 (40.30%) patients and psychomotor agitation – 19 (36.53%) patients. 8 (15.38%) patients presented with drowsiness/decreased level of consciousness, 5 (9.61%) had pupillary anomalies and 3 (5.77%) patients presented with controlateral hemiparesis. the classical scenario with initial loss of consciousness followed by a lucid period and ulterior clinical manifestations was seen in 5 (9.61%) patients. table 2 head trauma mechanisms in our patients traumatic mechanism no. of patients (n) ratio (%) accidental falling 38 73.07 blunt head trauma 3 5.77 road accident 2 3.84 unspecified 8 15.38 other 1 1.92 5 (9.61%) patients were comatose on admission. in 34 patients we found an epicranial hematoma and in 10 patients we had to evacuate the hematomas by puncturing. only 2 patients had a posterior fossa hematoma (figure 2 a, b), the other 50 patients presented with a supratentorial epidural blod clot. the most frequent localizations for of the epidural hematoma were parietal – 20 patients and temporalparietal – 11 patients. a total of 37 patients presented a skull fracture subjacent to the epidural hematoma and in 34 patients we found an epicranial hematoma above. in 14 patients we had to evacuate the epicranial hematoma by puncturing. other associated lesions were cerebral edema, subdural hematoma, subarachnoid hemorrhage and contusions (table 4). table 3 clinical manifestations symptom no. of patients (n) ratio (%) intracranial hypertension 21 40.38 psychomotor agitation 19 36.53 drowsiness/decreased level of counsciousness 8 15.38 coma (gcs<9pts) 5 9.61 nausea/vomiting 5 9.61 loss of counsciousness 5 9.61 pupilary anomalies 4 7.7 contralateral hemiparesis 3 5.77 headache 3 5.77 seizure 1 1.92 romanian neurosurgery (2014) xxi 4: 384 – 393 389 figure 2 a posterior fossa edh in a 2 yo child figure 2 b postoperative aspect of the posterior cranian fossa edh figure 3 a temporal-parietal epidural hematoma in a 5 months baby that suffered a tbi caused by accidental falling from approximately 1 meter. gcs=9pts figure 3 b postoperative aspect table 4 associated lesions lesion type no. of patients (n) ratio (%) skull fracture 37 71.15 epicranian hematoma 34 65.38 diffuse cerebral edema 20 38.46 subarachnoid hemorrhage 13 25 subdural hematoma 6 11.54 hemorrhagic contusion 4 7.7 390 tascu et al aggressive or conservative management in extradural hematomas in children 25 (48%) patients were operated, while the other 27 were treated with symptomatic drugs and were carefully monitored clinically and by cerebral imaging. in the nonoperated group, all the patients had a mild tbi, while in the surgically treated group of patients, 12 had a minor tbi, 7 a moderate tbi and 6 patients suffered a severe tbi. clinically, the decision to surgically evacuate the hematoma was considered in case of over 2 points loss on glasgow coma scale or the presence of pupillary changes. the imaging criteria for surgical treatment were: hematoma volume of minimum 25 cm3, epidural hyper density with a thickness larger than 10 mm and a mid-line shift (mls) over 5 mm (figure 3 a, b). 19 (36.53%) of the operated patients presented postoperative complications, such as acute post-hemorrhagic anemia, pneumocephalus, headache or hematoma recurrence. 20 patients in the operated group were gos/gr at discharge, 3 patients remained with neurological deficits postoperatively and 2 patients died; thus, the mortality rate in our study group was 3.84%. both deceased patients had severe associated traumatic injuries such as subdural hematomas, cerebral lacerations/contusions or moderate to severe thoracic/abdominal trauma, and the traumatic mechanism was road accidents. all the nonoperated patients had a good clinical outcome, with the remission of the acute neurological symptoms (gos/gr) at discharge. in 5 of the conservative treated patients the hematoma had a volume of over 25 cm3 and a midline shift of over 4 mm, but the decision to not operate on them was based on the good neurological status (figure 4 a, b). figure 4 a edh in a 5 month girl, gcs=15pts figure 4 b control ct scan 2 weeks after the tbi the medium number of hospitalization days was 9 for the operated patients (range 530 days) and 4 in the conservative treated patients. discussions our clinic is the most important pediatric neurosurgery center in the country, approaching a various cerebral pathology, mostly represented by traumatic head injuries. our study includes all the patients diagnosed with an epidural hematoma, certified by cerebral ct scans, regardless the mechanism. cerebral ct scan is an essential diagnosis and monitoring element in neurosurgery, especially head trauma; it represents the imaging investigation of choice to diagnose intracerebral hematomas, and it offers details regarding the location of the hematoma, clot volume and thickness and the effect it has on the midline structures, ventricular system and basal cisterns. therefore, a ct scan must be performed without delay (11, 12). all the romanian neurosurgery (2014) xxi 4: 384 – 393 391 patients included in our study were diagnosed and monitored by ct scan, and the imaging findings played an essential role in determining the type of treatment for each child. epidural hematomas were considered a neurosurgical emergency that can quickly lead to death of the patient if left untreated. lately, the conservative treatment and careful monitoring of the clinical status and the neuroimaging aspect is considered a valid approach, on the condition that the patients neurological and imaging status allows it (10, 13). our study comes to reinforce this concept that patients should not be treated surgically unless some well-defined clinical and imaging criteria are present. the criteria to decide in favor of surgical treatment considered were described, for adult population, by bullock and colab. (11): hematoma volume larger than 30 cm3, midline shift of over 5 mm and clot thickness over 15 mm on cerebral ct scan (figure 5 a, b, c, d). also, bullock and colab. (11) recommend that all comatose patients (gcs<9pct) and pupillary asymmetry with an epidural hematoma should be operated in emergency to evacuate the blood clot. figure 5 a acute edh in a 4 month child, presenting with pupilarry anomalies, coma (gcs=5pct) figure 5 b recurrence of the edh 392 tascu et al aggressive or conservative management in extradural hematomas in children figure 5 c postoperatively aspect figure 5 d ct aspect 2 months postoperatively the surgical treatment indications consider clinical status and imaging findings in each individual; patients included in our study were operated according to the following criteria, published in an earlier study (11, 14): • comatose patient, pupillary anomalies and confirmation of diagnosis on ct scan require urgent surgery • coma and worsening of neurological state in case of edh’s volume > 25 ml • edh’s volume > 30 ml, even in the absence of clinical signs • edh’s > 25 ml, if edh is located within the posterior fossa or temporal region • midline shift > 4 mm, with worsening of clinical status • edh volume increase observed on neuroimaging monitoring. children that suffered head trauma but have no focal neurological deficits, with a ct scan appearance of an acute edh having a volume <25 ml, less than 10 mm thickness and mls <4mm can receive conservative treatment, but with careful monitoring the romanian neurosurgery (2014) xxi 4: 384 – 393 393 clinical and neuroimaging status. these patients have to be admitted in a specialized clinic where they can quickly be operated in case of neurological worsening (14, 15). rivas and all. found that hematoma volume and severity of mls were related to preoperative coma in patients with edh(16). in comatose patients, a hematoma volume greater than 150cm3 and an mls greater than 12 mm were associated with increased mortality. location of the lesion did not influence outcome. selig et al. did not find a relationship between location of blood clot, mls and outcome in 51 comatose patients undergoing surgery for edh (17). conclussions both surgical treatment and conservative management of edh have a good clinical outcome. clinical and neuroimaging evaluation at admission/reevaluation plays an imperative role in deciding the appropriate therapeutic attitude for each patient. conservative treatment should be applied in specialized centers that can assure quick measurements if the patients’ neurological status worsens. correspondence st.m. iencean “grigore t. popa” university of medicine and pharmacy iasi e-mail: mirceasteffan@yahoo.com references 1. schmidek & sweet operative neurosurgical techniques: indications, methods and results, 6th ed., vol. 2, elsevier saunders, pa, 2012 2. choux m, lena g, genitori l. intracranial hematomas. in: head injuries in the newborn and infant, raimondi a, choux m, dirocco c. (eds), springer-verlag inc, new york 1986. p.204. 3. kim ka, wang my, griffith pm, et al. analysis of pediatric head injury from falls. neurosurg focus 2000; 8:e3. 4. obana wg, pitts lh. management of head injury. extracerebral lesions. neurosurg clin n am 1991; 2:351. 5. rocchi g, caroli e, raco a, et al. traumatic epidural hematoma in children. j child neurol 2005; 20:569. 6. aronyk ke. post-traumatic hematomas. in: pediatric neurosurgery: surgery of the developing nervous system, cheek wr, marlin ae, mclone dg, et al. (eds), wb mason, philadelphia 1994. p.279. 7. ciurea av, kapsalaki ez, coman tc, et al. supratentorial epidural hematoma of traumatic etiology in infants. childs nerv syst 2007; 23:335. 8. schutzman sa, barnes pd, mantello m, scott rm. epidural hematomas in children. ann emerg med 1993; 22:535. 9. bullock et all, guidelines for the surgical management of traumatic brain injury, neurosurgery march 2006, 3:58 10. shu ebs, leme rja, aguilar ph, andrade af, teixeira mj, plese jpp. traumatic acute giant epidural hematoma in a hydrocephalic shunted child. pediatr neurosurg 2000; 32: 176-179 11. dachling pang, m.d., f.r.c.s.(c), joseph a. horton, m.d., john m. herron, ph.d., james e. wilberger, jr., m.d., john k. vries, m.d. nonsurgical management of extradural hematomas in children j neurosurg 59:958971, 1983 12. ciurea av, gorgan mr, tascu a, sandu am, rizea re, traumatic brain injury in infants and toddlers, 0-3 years old, j med life vol 4, is 3,july‐september 2011 13. balmer b, boltshauser e, altermatt s, gobet r. conservative management of significant epidural haematomas in children. childs nerv syst 2006; 22: 363367 14. rivas jj, lobato rd, sarabia r, cordobés f, cabrera a, gomez p extradural hematoma: analysis of factors influencing the courses of 161 patients. neurosurgery. 1988 jul;23(1):44-51. 15. seelig jm, marshall lf, toutant sm, toole bm, klauber mr, bowers sa, varnell ja. traumatic acute epidural hematoma: unrecognized high lethality in comatose patients flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 334 | turliuc et al neurovascular conflict in the trigeminal neuralgia to be or not to be a neurovascular conflict: importance of the preoperative identification of the neurovascular conflict in the trigeminal neuralgia dana mihaela turliuc1,2, b. dobrovăţ1,2, a.i. cucu2 , ş. turliuc1, daniela trandafir1,3, claudia florida costea1,2 1“grigore t. popa” university of medicine and pharmacy iași, romania 2“prof. dr. n. oblu” emergency clinical hospital iași, romania 3“sf. spiridon” emergency clinical hospital iași, romania abstract: the trigeminal neuralgia caused by neurovascular compression is a neurosurgical pathology requiring the preoperative identification as exact as possible of the neurovascular conflict. in this case, neuroimaging is very useful, as it allows not only the determination of the neurovascular conflict of the trigeminal nerve, but also the correct indication of an adequate surgical approach. key words: trigeminal neuralgia, neurovascular compression syndrome, trigeminal nerve introduction described since the second century a.d. in the writings of aretaeus of cappadocia (18), the trigeminal neuralgia (tn) is the “worst pain humans have been afflicted with” (15), known as “suicide disease” because of the significant numbers of people taking their own lives before effective treatments were discovered. in 1994, the association for the study of pain describes the trigeminal neuralgia as “a sudden, usually unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve” (36). the most frequent cause of the tn is the focal compression of the trigeminal nerve root at the place of entry into the pons (root entry zone) produced by an artery, most of the times, or by a vein (31). the concept of neurovascular compression and the cause of the tn have been proposed for the first time in 1934 by walter dandy (16), his hypothesis being supported in 1962 by james w. gardner (20). only 5 years later, in 1967, the american neurosurgeon peter joseph jannetta confirmed this hypothesis and promoted in neurosurgery the microvascular decompression as a treatment method of the tn due to neurovascular compression (23). pathogenesis in the tn, the prevailing model is the neurovascular compression theory, where a redundant or aberrant looping of intracranial vessels results in neurovascular conflict (41). even though any intracranial anatomic (artery, vein, etc) or subsequently developed romanian neurosurgery (2016) xxx 3: 334 341 | 335 (tumor) structure can compress the trigeminal nerve (v nerve) at its exit from the brainstem, the studies show that the superior cerebellar artery and the anterior inferior cerebellar artery are the most frequently involved (1, 31, 52, 53) (figure 1, figure 2). the most frequently, the compression is at the level of the transition zone of the v nerve, which represents a point of transition from the central myelin (derived from the oligodendroglia) to the peripheral myelin (derived from schwann cells) (31, 33). diagnostic clinically, the tn is characterized as a facial pain syndrome with intense lancinating pain episodes, located within the sensory area of the v nerve. the nature of the pain in the tn is typical: paroxysmal, lancinating, electric-like, unilateral, extremely severe, episodic, lasting a few seconds with remissions and recurrences, often exacerbated by cutaneous stimuli such as cold air, shaving, tooth brushing, chewing or the simple tactile touch (37). the neurological examination is usually normal and one can rarely detect a subtle trigeminal sensory deficit (13). usually, up to the imaging identification of a neurovascular conflict at the level of the v nerve, the patients are treated with carbamazepine or gabapentin, which diminish pain, but for short periods. imaging the election imaging examination in the neurovascular compression syndrome (nvcs) is represented by the high-spatial resolution magnetic resonance (mr) (33) which is performed so as to detect first of all the neurovascular contact (figure 1) and secondly so as to exclude other causes of tn, such as the posterior fossa tumors or the multiple sclerosis lesions (32, 39). among the mr sequences, the most important are the high-spatial-resolution performed with t2-weighted sequences (3d tof, 3d fiesta) and, of course, the mr angiography so as to visualize the artery which compresses the v nerve (17, 30, 56). imagistically (mr), the neurovascular conflict can be classified in three grades: grade i: simple contact between the nerve and the vessel, grade ii: artery distorting/displacing the nerve and grade iii: artery indents the nerve root, producing the thinning of the nerve (21) (figure 2). one of the mr limits is that the neurovascular contacts can also be found in asymptomatic persons and, as a consequence, this imaging method is not very specific for the nvcs (1, 33). moreover, in the mr imaging, in a study, 30% of the healthy subjects had neurovascular contact grade i and 2% grade ii, so that the imaging diagnostic must be very well judged in the clinical context (21). precisely in order to try an approximation as good as possible of the diagnostic, it is recommended to perform three highresolution sequences, in association, because of their complementariness (29, 50): 1. 3d t2 high-resolution sequences: allow the visualization of the nerve root, its trajectory, its diameter and indentations. moreover, these sequences allow the visualization of the cerbellopontine angle and the cerebrospinal fluid cisterns. a limitation of this exploration would be the absence of the differentiation between nerves and vessels. 2. 3d tof mra: visualizes only the highflow vessels (arteries). 336 | turliuc et al neurovascular conflict in the trigeminal neuralgia 3. 3d t1 sequence with gadolinium: visualizes all vessels, both arteries and veins. more recently, among the mr sequences, the diffusion-tensor imaging with tractography can allow the analysis of white matter integrity from the v nerve by measuring in vivo the molecular diffusivity (9, 22, 28, 33). this sequence practically assesses the damage and degeneration of white matter tracts appearing as a consequence of the loss of myelin and axonal membranes at the level of the neurons composing the v nerve (7, 38). another imaging exploration which must be carried out in the tn, but rather for the differential diagnosis is the computertomography which can evaluate the bony anatomy of the posterior cranial fossa and the bone lesions which may cause bone destruction (skull base osteomyelitis, external otitis, langerhans’ cell histiocytosis), proliferation (fibrous dysplasia, chondrosarcoma) or remodeling (meningiomas, schwannomas) (8, 43). in other words, the preoperative imaging is very important in recognizing the neurovascular conflict and in establishing a correct surgical approach. for instance, in case of the tn compression by a transverse pontine vein, a conventional sub occipital approach can be insufficient in the visualization (21), a lateral suboccipital approach being preferable so as to visualize meckel’s cave (49). treatment from the initial description in 1932 of the nvcs by walter dandy and to date, several treatment methods in the tn have been proposed: the medical therapy, the stereotactic radiosurgery, the glycerol rhizotomy, the radiofrequency thermal rhizotomy and the balloon microcompression (5). unfortunately, these alternative treatments are associated with poorer long-term pain control and higher incidence of recurrences varying between 1746% (44, 45, 57). even though the initial treatment is the medical one, with antiepileptic drugs, the neurovascular decompression represents the election treatment in the nvcs, being the most efficient treatment to achieve initial and long-term pain control for tn (2, 25, 55), with a success rate of 63%-94% (3, 5, 11, 26, 35, 51) and a complications rate of almost 1-5% (3, 5, 6). moreover, in 91-97% of the cases, pain relief appears immediately after the surgery (19). the surgical treatment (microvascular decompression) is indicated in the patients with debilitating pain refractory in at least three medicines, including carbamazepine (14). the surgery indication must be correctly made, because in the reported cases, the absence of the intraoperative neurovascular compression varied between 4 and 89%, with an average of 7.5% (27). even in the cases where inntraoperative there was no vascular compression, certain studies suggest that the manipulation with minimal trauma had a favorable therapeutic effect in the patients with tn (4, 34, 57), even though in these cases, most of the operators prefer a partial sensory rhizotomy when they are not persuaded of the existence of the neurovascular conflict (45). the surgery consists in microvascular decompression of the v nerve and the positioning of teflon pledgets to separates offending vessels from the v nerve. teflon is the most popular material used in nvcs even romanian neurosurgery (2016) xxx 3: 334 341 | 337 though it also presents complications, of which the most frequent is the inflammatory foreign body reaction, with an incidence of 5% (12, 42). chen et al have issued in their study a hypothesis according to which teflon induces an inflammatory giant-cell foreign body reaction when it comes into contact with the dura mater or with the tentorium (12). pain prognostic factors the most important prognostic factors are: the immediately postoperative pain relief (54), the age of the patient, the medical comorbidities (15) and the nature of the compressive vessel (venous compression representing a poor prognostic factor) (27). among them, the most important prognostic factor is pain relief (54). complications the most frequent complications are represented by: 1. cerebrospinal fluid leak, the most frequent complication of the nvcs with an incidence of 0.9-12% (40) 2. meningitis 3. cerebellar injury. this complication type can be avoided by realizing an optimized petrotentorial corridor, by the retraction of the cerebellum in a direction that is infero-lateral rather than directly lateral (tangential to the course of the viii nerve) (10) 4. post-operative hemorrhage, including the subdural hematoma (15) 5. cranial nerve palsies: facial palsy by the injury of the vii nerve and hearing loss by the injury of the viii nerve which appears as a consequence of the excessive retraction of the cerebellum while trying to expose the trigeminal cistern, direct trauma on the nerve or its vascular supply. once with the intraoperative introduction of the brain stem auditory evoked potential monitoring, this complication was reduced from 19 to 2% (11, 55). 6. trigemino-cardiac reflex is a complication which may occur because of the stimulation of any of the sensory branches of the v nerve (47). the physiopathological mechanism consists in the decrease of the mean arterial blood pressure and heart rate by more than 20% and appears once with v nerve manipulation. this reflex is characterized by arterial hypotension, bradycardia, apnea and gastric hypermotility (46, 47, 48). after the cessation of the surgical manipulation, the mean arterial blood pressure and heart rate come back to normal and because of that is very important to perform the gentle manipulation of the vascular-nervous structures during the surgery. 7. anesthesia “dolorosa” is a continuous, dysesthetic pain, with burning character, which appears because of the trigeminal deafferentation (13) 8. recurrence. the factors which proved to be predictable in the recurrence are: symptomatology lasting for more than eight years, v nerve compression by a vein, absence of the immediate postoperative pain relief, female gender, minimizing nerve trauma by careful manipulation (6, 25), age younger than 53 years, symptoms duration of more than 10 years and pain localization on the left in men (55) 9. death: the mortality associated with this intervention is of 0.1% in jannetta series (24). conclusions the tn caused by the neurovascular conflict represents a neurosurgical pathology which can be safely solved in the current 338 | turliuc et al neurovascular conflict in the trigeminal neuralgia context. so as to issue a correct surgical indication in case of a nvcs, the neuroimaging is very important because it establishes the neurovascular contact, the surgical approach, but also the exclusion of other causes of the tn. figure 1 mri 3dt1 axial (a) and sagital (b) sections showing left trigeminal nerve, compressed by an aberrant loop of anterior inferior cerebellar artery (aica); the right trigeminal nerve is normal (dr. b. dobrovat’s personal collection) figure 2 mri 3dt1 coronal section showing left trigeminal nerve, compressed by an aberrant loop of aica, with a reduced caliber in the contact site, compared with the normal caliber of the right trigeminal nerve (dr. b. dobrovat’s personal collection) correspondence bogdan dobrovat “grigore t. popa” university of medicine and pharmacy iași, romania e-mail: bogdandobrovat@yahoo.com references 1.adamczyk m, bulski t, sowińska j, furmanek a, bekiesińska-figatowska m. trigeminal nerve: artery contact in people without trigeminal neuralgia—mr study . med sci monit. 2007; 13:38 – 43. 2.amagasaki k, watanabe s, naemura k, shono n, nakaguchi h. safety of microvascular decompression for elderly patients with trigeminal neuralgia. clin neurol neurosurg. 2016; 141:77-81. 3.ashkan k, marsh h. microvascular decompression for trigeminal neuralgia in the elderly: a review of the safety and efficacy. neurosurgery. 2004; 55:840-848. 4.baechli h, gratzl o. microvascular decompression in trigeminal neuralgia with no vascular compression. eur surg res. 2007; 39:51-57. 5.barker fg 2nd.quality of life and individual treatment choice in trigeminal neuralgia. pain. 2007 131:234-236. romanian neurosurgery (2016) xxx 3: 334 341 | 339 6.barker fg 2nd, jannetta pj, bissonette dj, larkins mv, jho hd. the long-term outcome of microvascular decompression for trigeminal neuralgia. n engl j med. 1996; 334:1077-1083. 7.basser pj, pierpaoli c. microstructural and physiological features of tissues elucidated by quantitative-diffusion-tensor mri . j magn reson b. 1996; 111: 209 -219. 8.bathla g, hegde an. the trigeminal nerve: an illustrated review of its imaging anatomy and pathology. clin radiol. 2013; 68:203-213. 9.becker m, kohler r, vargas mi, viallon m, delavelle j. pathology of the trigeminal nerve. neuroimaging clin n am. 2008; 18:283–307. 10.bond ae, zada g, gonzalez aa, hansen c, giannotta sl.operative strategies for minimizing hearing loss and other major complications, associated with microvascular decompression for trigeminal neuralgia.world neurosurg. 2010; 74: 172-177. 11.broggi g, ferroli p, franzini a, servello d, dones i. microvascular decompression for trigeminal neuralgia: comments on a series of 250 cases, including 10 patients with multiple sclerosis. j neurol neurosurg psychiatry. 2000; 68:59-64. 12.chen jf, lee st, lui tn, yeh y, chen t, tzaan w. teflon granuloma after microvascular decompression for trigeminal neurologia. surg neurol. 2000; 53:281–287. 13.cheshire wp. trigeminal neuralgia: for one nerve a multitude of treatments. expert rev neurother. 2007; 7:1565-1579. 14.cheshire wp. can mri distinguish injurious from innocuous trigeminal neurovascular contact? j neurol neurosurg psychiatry. 2005; 76:1470-1471. 15.cohen-gadol aa. microvascular decompression surgery for trigeminal neuralgia and hemifacial spasm: naunces of the technique based on experiences with 100 patients and review of the literature. clin neurol neurosurg. 2011; 113:844-853. 16.dandy we. concerning the cause of trigeminal neuralgia. am j surg. 1934; 24:447-455. 17.docampo j, gonzalez n, muñoz a, bravo f, sarroca d, morales c. neurovascular study of the trigeminal nerve at 3 t mri. neuroradiol j. 2015; 28:28-35. 18.eller jl, raslan am, burchiel kj.trigeminal neuralgia: definition and classification. neurosurg focus. 2005; 18:e3. 19.elias wj, burchiel kj. microvascular decompression. clin j pain.2002; 18:35-41. 20.gardner wj. concerning the mechanism of trigeminal neuralgia and hemifacial spasm. j neurosurg. 1962; 19:947-958. 21.harsha kj, kesavadas c, chinchure s, thomas b, jagtap s. imaging of vascular causes of trigeminal neuralgia. j neuroradiol. 2012; 39: 281-289. 22.herweh c, kress b, rasche d, tronnier v, tröger j, sartor k, stippich c. loss of anisotropy in trigeminal neuralgia revealed by diffusion tensor imaging. neurology. 2007; 68: 776-778. 23.jannetta pj. arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia. j neurosurg. 1967; 26:159-162. 24.jannetta pj, mclaughlin mr, casey kf.technique of microvascular decompression. technical note. neurosurg focus. 2005; 18:e5. 25.kabatas s, albayrak sb, cansever t, hepgul kt. microvascular decompression as a surgical management for trigeminal neuralgia: a critical review of the literature. neurol india. 2009; 57:134-138. 26.kondo a. follow-up results of microvascular decompression in trigeminal neuralgia and hemifacial spasm. neurosurgery. 1997; 40:46-51. 27.kuncz a, vφrφs e, barzó p, tajti j, milassin p, mucsi z, elek p, benedek k, tarjányi j, bodosi m. comparison of clinical symptoms and magnetic resonance angiographic (mra) results in patients with trigeminal neuralgia and persistent idiopathic facial pain. mediumterm outcome after microvascular decompression of cases with positive mra findings. cephalalgia 2006; 26:266-276. 28.le bihan d. molecular diffusion, tissue microdynamics and microstructure. nmr biomed 1995; 8: 375-386. 29.leal pr, sindou m, hermier m, froment jc, souza ma, cristino-filho g. preoperative demonstration of the neurovascular compression characteristics with special emphasis on the degree of compression, using highresolution magnetic resonance imaging: a prospective study, with comparison to surgical findings, in 100 consecutive patients who underwent micro-vascular decompression for trigeminal neuralgia. acta neurochir. 2010; 152:817-825. 30.linn j, peters f, moriggl b, naidich tp, brückmann h, yousry i. the jugular foramen: imaging strategy and detailed anatomy at 3t. ajnr am j neuroradiol. 2009; 340 | turliuc et al neurovascular conflict in the trigeminal neuralgia 30: 34-41. 31.love s, coakham hb. trigeminal neuralgia: pathology and pathogenesis. brain. 2001; 124: 2347-2360. 32.love s, hilton da, coakham hb. central demyelination of the vth nerve root in trigeminal neuralgia associated with vascular compression. brain pathol. 1998; 8:1-11. 33.lutz j, linn j, mehrkens jh, thon n, stahl r, seelos k, brückmann h, holtmannspötter m. trigeminal neuralgia due to neurovascular compression: highspatial-resolution diffusion-tensor imaging reveals microstructural neural changes. radiology. 2011; 258: 524-530. 34.ma z. “nerve combing” for trigeminal neuralgia without vascular compression: report of 10 cases. clin j pain. 2009; 25:44-47. 35.mendoza n, illingworth rd. trigeminal neuralgia treated by microvascular decompression: a longterm follow-up study. br j neurosurg. 1995; 9:13-19. 36.merskey h, bogduk n. classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms. seattle: iasp press, 1994. 37.miller jp, acar f, burchiel kj. classification of trigeminal neuralgia: clinical, therapeutic, and prognostic implications in a series of 144 patients undergoing microvascular decompression. j neurosurg. 2009; 111:1231–1234. 38.moseley me, cohen y , kucharczyk j, mintorovitch j, asgari hs, wendland mf, tsuruda j, norman d. diffusion-weighted mr imaging of anisotropic water diffusion in cat central nervous system. radiology. 1990 ; 176: 439-445. 39.nurmikko tj, eldridge pr. trigeminal neuralgia: pathophysiology, diagnosis and current treatment . br j anaesth. 2001; 87:117 -132. 40.park js, kong ds, lee ja, park k. intraoperative management to prevent cerebrospinal fluid leakage after microvascular decompression: dural closure with a "plugging muscle" method. neurosurg rev. 2007; 30:139142. 41.peschillo s , delfini r. trigeminal neuralgia: a new neuroimaging perspective. world neurosurg. 2013; 80: 293-295. 42.premsagar ic, moss t, coakha hb. teflon-induced granuloma follow treatment of trigeminal neuralgia by microvascular decompression. report of two cases. j neurosurg. 1997; 87:454-457. 43.radoi m, stefanescu f, vakilnejad r, gheorghitescu l, rosu d. surgery of petroclival meningiomas. recent surgical results and outcomes. romanian neurosurgery. 2015; xxix (xxii) 1: 27-37. 44.rath sa, klein hj, richter hp. findings and longterm results of subsequent operations after failed microvascular decompression for trigeminal neuralgia. neurosurgery. 1996. 39: 933-938. 45.revuelta-gutierrez r, martinez-anda jj, coll jb, campos-romo a, perez-peña n. efficacy and safety of root compression of trigeminal nerve for trigeminal neuralgia without evidence of vascular compression. world neurosurg. 2013; 80: 385-389. 46.schaller b. trigemino-cardiac reflex during microvascular trigeminal decompression in cases of trigeminal neuralgia. j neurosurg anesthesiol. 2005; 17:45-48. 47.schaller b. trigeminocardiac reflex: a clinical phenomenon or a new physiological entity? j neurol. 2004; 251:658-665. 48.schaller b, probst r, strebel s, gratzl o. trigeminocardiac reflex during surgery in the cerebellopontine angle. j neurosurg. 1999; 90:215-220. 49.seoane er, rhoton jr al. suprameatal extension of the retrosigmoid approach: microsurgical anatomy. neurosurgery. 1999; 44:553-560. 50.sindou m. prediction of the vascular compression characteristics with magnetic resonance imaging for surgery of primary trigeminal neuralgias. world neurosurg. 2013; 80:298-299. 51.sindou m, leston j, howeidy t, decullier e, chapuis f. micro-vascular decompression for primary trigeminal neuralgia (typical or atypical). long-term effectiveness on pain; prospective study with survival analysis in a consecutive series of 362 patients. acta neurochir. 2006; 148: 1235-1245. 52.sindou m, howeidy t, acevedo g. anatomical observations during microvascular decompression for idiopathic trigeminal neuralgia (with correlations between topography of pain and site of the neurovascular conflict): prospective study in a series of 579 patients. acta neurochir. 2002; 144:1–12. 53.sindou m, leston j, decullier e, chapuis f. microvascular decompression for primary trigeminal neuralgia: long-term effectiveness and prognostic factors in a series of 362 consecutive patients with clear-cut neurovascular conflicts who underwent pure romanian neurosurgery (2016) xxx 3: 334 341 | 341 decompression. j neurosurg. 2002; 107:1144-1153. 54.singla v, modi m, singh p, khandelwal nk. dolichoectasia of vertebrobasilar system: a rare cause of tic douloureux. indian j med sci. 2007; 61:30-31. 55.theodosopoulos pv, marco e, applebury c, lamborn kr, wilson cb. predictive model for pain recurrence after posterior fossa surgery for trigeminal neuralgia. arch neurol. 2002. 59:1297-1302. 56.yousry i, camelio s , schmid ud, horsfield ma, wiesmann m, brückmann h, yousry ta. visualization of cranial nerves i-xii: value of 3d ciss and t2-weighted fse sequences. eur radiol. 2000; 10: 1061-1067. 57.zakrzewska jm, lopez bc, kim se, coakham hb. patients reports of satisfaction after microvascular decompression and partial sensory rhizotomy for trigeminal neuralgia. neurosurg. 2005; 56:1304-1312. 2adamd_incidentaldurotomy 20 adam et al incidental durotomy in lumbar spine surgery incidental durotomy in lumbar spine surgery incidence, risk factors and management d. adam1,3, t. papacocea2,3, r. iliescu3, i. hornea3, c. moisescu3 1associate professor, department of neurosurgery, “carol davila” university of medicine and pharmacy, bucharest, romania 2assistant professor, department of neurosurgery, “carol davila” university of medicine and pharmacy, bucharest, romania 3emergency clinical "st. pantelimon" hospital, bucharest, romania abstract: incidental durotomy is a common complication of lumbar spine operations for degenerative disorders. its incidence varies depending on several risk factors and regarding the intra and postoperative management, there is no consensus. our objective was to report our experience with incidental durotomy in patients who were operated on for lumbar disc herniation, lumbar spinal stenosis and revision surgeries. between 2009 and 2012, 1259 patients were operated on for degenerative lumbar disorders. for primary operations, the surgical approach was mino-open, interlamar, unior bilateral, as for recurrences, the removal of the compressive element was intended: the epidural scar and the disc fragment. 863 patients (67,7%) were operated on for lumbar disc herniation, 344 patients (27,3%) were operated on for lumbar spinal stenosis and 52 patients (5%) were operated for recurrences. the operations were performed by neurosurgeons with the same professional degree but with different operative volume. unintentional durotomy occurred in 20 (2,3%) of the patients with herniated disc, in 14 (4,07%) of the patients with lumbar spinal stenosis and in 12 (23%) of the patients who were operated on for recurrences. the most frequent risk factors were: obesity, revised surgery and the physician’s low operative volume. intraoperative dural fissures were repaired through suture (8 cases), by applying muscle, fat graft or by applying curaspon, tachosil. there existed 4 csf fistulas which were repaired at reoperation. incidental dural fissures during operations for degenerative lumbar disorders must be recognized and immediately repaired to prevent complications such as csf fistula, osteodiscitis and increased medical costs. preventing, identifying and treating unintentional durotomies can be best achieved by respecting a neat surgical technique and a standardized treatment protocol. key words: durotomy, dural tear, csf fistula; romanian neurosurgery (2015) xxix (xxii) 1: 20 26 21 introduction incidental injury of lumbar dura during surgery for lumbar herniated disc or lumbar spinal stenosis represents a serious problem which needs to be recognized and immediately repaired to prevent further complications, among which csf fistula is the most common. the occurrence of csf fistula increases the hospitalization period and also the costs of a new surgical intervention. the incidence of unintentional durotomy during spinal operations was estimated in different series between 1,6% 17,4%, depending on the complexity of the operation, the surgeon’s experience, the type of operation – primary or reoperation, patient’s age. (1,2,3,4,5). the purpose of this study is to evaluate the incidence of unintentional durotomy during operations for degenerative lumbar spinal disorders and also the intraoperative and postoperative management of this complication. material and method patient population medical records of 1259 patients who were operated during 2009-2012 in the department of neurosurgery by three senior neurosurgeons with a different surgical volume were retrospectively reviewed. every patient with lumbar disc herniation presented with radicular leg pain, paresthesia and the following neurological signs: straight leg raising pain under 45°, external or internal popliteal sciatic nerve paresis, depressed/ asymmetric reflexes. the lumbar disc herniations were visualized on mri imaging. in all cases the symptoms persisted for more than 6 weeks and did not respond to conservative therapy. patients with lumbar spinal stenosis presented with neurogenic claudication. some patients were operated on before in other institutions during the period in which the operation was performed by laminectomy. they were admitted for reoperation for they were diagnosed with lumbar disc herniaton or lumbar spinal stenosis at 2 or 3 levels. the operation primary surgery for lumbar disc herniation consisted of interlamar approach at the herniation site, followed by discectomy. for spinal stenosis we performed bilateral interlamar approach in case of foraminal stenosis and laminectomy in case of central spinal stenosis. there were cases with previous lumbar herniation operated by laminectomy, readmitted with recurrence of herniation associated with spinal stenosis. in these cases we tried to identify normal dura mater at the extremities of the laminectomy, in order to resect as much as possible from the fibrous scar and to remove the herniated disc. when incidental durotomy occurred, we tried to close the dural breach by primary suture if possible with 4-0 silk. the suture was covered with gel foam, fat graft, muscle graft or tachosil. in another cases the dural breach was small that the suture was unnecessary or impossible. in these cases we applied tachosil, tissucol or, in absence of these prefered materials, we applied muscle graft, fat graft, gel foam. 22 adam et al incidental durotomy in lumbar spine surgery subfascial drains were used according to the surgeon’s preference. in the past year, we used vancomycine which was placed in the epidural space at the end of the operation. postoperative management patients received antibiotics (cephazolyne) for three days. they remained at bed rest in prone position for 2 a 3 days, depending on the length of the durotomy and the quality of dural repair. results during the study period there were 1259 patients operated for lumbar degenerative diseases. incidental durotomy occurred in 46 cases, with an overall incidence of 3,6%. patients’ characteristics are presented in tabel i. table i patients’ characteristics characteristics number percentage age range 35-81 sex: • female; • male; 25 54,3% 21 46,7% comorbidities: • hypertension; • obesity; • chronic obstructive pulmonary disease (copd); 17 36,9% 12 26,08% 13 28,26% disease: • lumbar disc herniation; • spinal stenosis; • reoperation for reccurence; 863 67,7% 344 27,3% 52 5% level: • l3-l4; • l4-l5; • l5-s1; • 2 levels; • 3 levels; 3 6,52% 25 54,34% 14 30,43% 3 6,52% 1 2,17% type of operation: • unilateral interlamar; • bilateral interlamar; • hemilaminectomy; • laminectomy; 30 65,21% 6 13,04% 4 8,63% 6 13,04% durotomy: • disc herniation; • spinal stenosis; 20 2,3% 14 4,07% romanian neurosurgery (2015) xxix (xxii) 1: 20 26 23 • reoperation; 12 23% site of dural lesion: • lateral; • anterior; • root sheath; • root axilla; 39 84,78% 1 2,17% 3 6,52% 3 6,52% epidural drain: • with drain; • without drain; 12 26,08% 34 73,31% complications: • csf fistula; • osteodiscitis; • headache; • wound dehiscency; 4 8,69% 2 4,34% 3 6,52% 1 2,17% dural leak occurred in patients aged between 31 and 85 years, with a peak in the sixth decade. this peak corresponds to the decade of appearance and operation on patients with herniated disc, representing 67,7% of all cases. between the comorbidities, only obesity can be a risk factor because, regarding a “miniopen” approach like the interlamar approach, the depth of the lesion can create the condition of an unintentional dural rupture. all patients were operated under general anesthesia. when operations were occasionally performed under spinal anesthesia, we found that when the patient coughs during the operation there occurs a displacement and swelling of the dura due to increased intracanial pressure, which is why we are not partisans of spinal anesthesia because, during discectomy, sudden mobility may favor dural breaking. dural leak occurred more frequently during reinterventions (23%), compared with the primary approaches for herniated disc (2,3%) or spinal stenosis (4,07%). the extremely large number of dural leaks in cases of reinterventions is due to the fact that many of these patients were operated for herniated disc many years back through laminectomy performed at 1 or 2 levels. the postoperative scar was extensive and adherent. reintervention was performed for recurred hernia at the same level or adjacent levels, aiming to remove the fragment of the herniated disc and also the epidural scar. while studying the operation protocols, we observed that the dura mater was described as thin, translucent, even in cases without dural rupture. in such cases, if an adjustment of the superior articular facet after removing its internal third is not performed, puncture dural fissures may occur after closing the operative wound due to dural friction on the bone’s irregularities. the surgeon’s experience seems to influence the rate of unintended durotomies. we found that, although the surgeons have the same level of training, the operative volume is 24 adam et al incidental durotomy in lumbar spine surgery different and thus the frequency of dural rupture. the frequency has fluctuated between 2,8 and 8,1%, being higher in surgeons with a lower operative volume (5/61 cases) than those with a higher operative volume (20/738 cases). the most common locations of the dural injury were the lateral lesions (84,7%), followed by injuries of the root sheath and root axilla. a b postoperative mri, axial section demonstrates a csf fistula and site of dural tear: lateral (a) and anterior (b) in one case where the intervertebral disc was completely expelled into the spinal canal having 3,7 cm in cranio-caudal length, there occurred an anterior dural leak, unrecognized intraoperatively. after the appearance of csf fistula, mri showed the csf spill site in the tecal sack. primary dural repair was made by suturing the dura in 8 cases, supplemented by applying curaspon, fat, muscle or tachosil. in other cases (n=38, 82,6%), curaspon or autologous fat or muscle were used to cover the dural defect. a good sealant agent was tachosil. in these cases, the suture of the dura was not necessary because the breach was punctate. the epidural drain was used in 12 cases. in other cases it was considered that epidural bleeding promotes breach closure, but of course blood can also be a good medium culture and can lead to secondary infection. patients with intraoperative csf leak remained at bed rest in prone position for 3 days. during this period they received antibiotics to prevent infection. of the 4 csf fistulas, in 3 cases the dural leak was not recognized intraoperatively during the primary surgery. their repair was performed during reintervention by dural suture in 2 cases and by applying tachosil and tissucol in other 2 cases. another postoperative complication, osteodiscitis, occured in 2 patients with dural leak who had no epidural drainage after surgery. in the case of one patient who was operated on but had no fistula and no infection, a wound dehiscency appeared when the stitches have been removed. discussions incidental durotomy was reported in several series of patients operated for degenerative spinal injuries and it is a common complication of spinal surgery, even among surgeons with high professional romanian neurosurgery (2015) xxix (xxii) 1: 20 26 25 qualification. the current literature reports a wide incidence variation in rates of dural leaks in spine surgery. the reported incidence varies between 1,6% and 17,4%. our study reported an incidence of 3,6% which is located towards the lower limit of the incidence reported by current literature. dural leaks are more common in obese patients and among surgeons with lower operative volume. irregular bone surfaces in interlamar approach could explain the occurrence of csf fistula in cases when intraoperative there was not notified any dural break and the dura was thin, translucent. durotomies occurred more frequently within patients in the sixth decade of life, double the adjacent decades. unlike williams et. al, we cannot support an increased incidence in relation to age (1). the sixth decade of life is the period with the most frequently occurring herniated disc. we confirm that regarding operations for recurrent disc herniations there is a significantly higher incidence of unintetional durotomy, which has been reported previously (4, 5, 6, 7). in our series, the high incidence in revision operations can be explained through the fact that, in the past, the approach used for disc herniations was laminectomy, which left behind an extensive epidural scar at the level of the dura and the nerve roots. we aimed to remove the entire epidural scar and the disc herniation. if the dissection in the epidural space is lateral, at the level of the herniated disc, leaving scar on the posterior dural sac, the incidence rate of unintentinal durotomy decreases. in our series, durotomy did not associate with damage to the spinal nerves and has not created new neurological deficits postoperatively. wang et. al, jones et. al, cammisa et. al reached similar conclusions: dural tears do not have deleterious effects in outcomes, do not increase the risk of other perioperative morbidities or later outcome (4,5,7). saxler et. al had different results: in his group of 41 lumbar discectomy patients with intraoperative durotomies, they presented a poorer outcome after surgery (8). dural tear is detected intraoperative by the presence of csf in the epidural space. in punctiform dural tear, csf is in small quantity, mixed with blood, and dural fissure can remain unrecognised. anterior, small dural sac rupture is difficult to observe. in this case a postoperative mri can demonstrate the site of dural lesion. even after dural suture csf can be observed leaking in the epidural space through the repaired defect if valsalva maneuver is made. to decrease intradural pressure of csf when the dura mater is very thin or during the dural suture, we used the trendelenburg position and/or have blocked the csf circulation with a cotonoid placed at the superior pole of the interlamar approach. primary repair of durotomies, once recognised, should always be done to prevent the complications. in small punctiform durotomies, fat graft, muscle graft, tachocomb can be effective. larger durotomies have to be sutured. in all cases fibrin glue is recommended. to drain or not to drain? the use of drains is controversial. we used it in 26% of cases. wang et al placed a drain in all cases (5). eismont et al do not recommend subfascial drain because it could favor the 26 adam et al incidental durotomy in lumbar spine surgery formation of csf fistula (9). cammisa et al used a drain in case of adequate repair of the tear (4). a good repair of dural tear can be accompanied by postoperative bed rest. patients from our group remained in bed rest for 3 days, in prone position. in other series postoperative bed rest was used for a similar period of time but in supine position (4,5). hodges et al reported that 75% of the patients who had dural tears which were repaired during surgery did not need bed rest (10). in case of dural tear and intraoperative dural repair, postoperative bed rest and prolonged postoperative antibiotherapy were recommended to prevent complications. the rate of discitis in the present study was 0,65% (2 cases) and 1 case with dehiscent wound. weinstein et al reported an overall infection rate of 2,1% and 8,1% deep normal infection rate in durotomy cases (11). the presence of dural tears necessitates a prolonged hospital stay. the development of csf fistula or deep wound infection are serious dreaded complications of dural tear in lumbar surgery, which increase much more the period of hospitalization and medical costs. conclusions dural tear in lumbar surgery is not a benign event. in order to prevent or to minimize the incidental dural tear, spinal surgeries performed by experienced spine surgeons are advised. when is considered that a durotomy is possible to appear, a change in trendelenburg position of the patient is recommended. dural fissures have to be repaired intraoperatively to prevent complications. there is not a consensus regarding the protocol to follow. suture is the best way to treat dural tears. if this is not possible, there are various sealants to be used. tachosil and fibrin glue are the best. a non-aspirating drainage is proposed when dural tear is adequately repaired. to reduce the hidrostatic pressure of the csf, bed rest is recommended. antibiotic therapy with cefazoline or vancomycin for 72 hours is advised. references 1. williams bj, sansur ta, smith js, et al: incidence of unintended durotomy in spine surgery based on 108.478 cases. neurosurgery 68: 117 – 124, 2011 2. ruban d, o’toole ej: management of incidental durotomy in minimally invasive spine surgery. neurosurg focus 31 (4): e15, 2011 3. guerin p, el fegoun ab, obeid i, et al. incidental durotomy during spine surgery: incidence, management and complications. a retrospective review. injury 2011 4. cammisa jr fp, girardi fp, sangani pk, et al: incidental durotomy in spne surgery.spine 2000: 2663 – 2667 5. wang jk, bohlman hh, riew dk. dural tears secondary to operations on the lumbar spine: management and results after a two – year minimum follow-up of eighty – eight patients. j bone joint surg [am] 1998, 80: 1728 6. deyo ra, cherkin dc, loeser jd, et al: morbidity and mortality in association with operations on the lumbar spine. the influence of age, diagnosis and procedure. j bone joint surg [am] 74: 536 – 543, 1992 7. jones aa, stambough jl, balderstone ra, et al: longterm results of lumbar spine surgery complicated by unintended durotomy. spine (phila pa 1976) 14: 443 – 446, 1989 8. saxler g, kramer j, barden b, et al. the long term clinical sequelae of incidental durotomy in limbar disc surgery. spine 2005; 30: 2298 – 2302 9. eismont fj, wiesel sw, rothman rh. treatment of dural tears associated with spnal surgery. j bone joint surg [am] 1981; 63: 1132 – 1136 10.hodges sd, humphreys sc, eck jc, et al. management of incidental durotomy without manadatory bed rest: a retrospective review of 20 cases. spine 1999: 24: 2062 – 2064 11. weinstein ma, mc cabe jp, cammisa jr fp. postoperative spinal wound infection. proceedings of the 11th annual meeting of the north american spine society 1996, p. 254 13alvis-mirandahernando_thefalse romanian neurosurgery (2014) xxi 3: 329 333 329 the false falx and tentorium sign: case report of subdural haematoma and sickle cells disease hernando raphael alvis-miranda1, carlos fernando lozanotangua2, gabriel alcala-cerra2, andres m. rubiano3, luis rafael moscote-salazar2 1physician, universidad de cartagena 2neurosurgeon, universidad de cartagena 3neurosurgeon, hospital universitario de neiva abstract the increased density in the basal cisterns and the subarachnoid space on ct scans is a well-known characteristic of subarachnoid hemorrhage. have been described diverse conditions that can emulate subarachnoid hemorrhage, such as purulent leptomeningitis, intrathecal contrast material and leak of high doses of intravenous contrast material to the subarachnoid space. we present the case of a male patient who presented a subdural hematoma in the setting of non-diagnosed sickle cell disease. to this patient was performed a panangiography which discard any aneurismal hemorrhage origin key words: subarachnoid hemorrhage, sickle cell disease, subdural hematoma, false falx and tentorium sign. introduction subarachnoid hemorrhage (sah) appears characteristically in the ct scan as a hyperdensity in the basal cisterns and subarachnoid space (sas). diverse medical conditions can emulate sah appearance, such as hypoxic encephalopathy, hyperperfusion radical encephalopathy, extensive infarctions, viral meningoencephalitis, purulent meningitis, bilateral subdural haematoma and idiopathic intracranial hypertension (1–6), but without clinical or anatomopathological hemorrhage findings(7), this phenomena is called “pseudo-sah”. in 1980, osborn (8) described the “false falx and tentorium sign” as a finding of pseudo-sah. we present the clinical case of a patient with false falx and tentorium sign as a contribution to medical literature. case presentation male patient, 75 years old, who presents to the er of the hospital universitario del caribe with right hip pain that hinders the gait during the last week and a fast declining conscious level. he has not important antecedents, no smoke, and no alcohol habit. at physical examination is evidenced drowsiness, bradypsyquia, time and space disorientation, 330 alvis-miranda et al the false falx and tentorium sign glasgow coma scale (gcs) 13/15 (er: 3; vr: 4; mr: 6), obey orders, and has moderate neck stiffness. no motor or sensitive deficit at cranial nerves examination. ct scan is ordered, which evidences a left chronic laminar subdural hematoma without significant mass effect (figure 1, a and b). figures 1, a and b non-contrasted brain ct-scan showing a left hemispherical subdural collection with mass effect figure 2, a and b there is an interhemispherical fronto-parietal hemorrhagic collection, which extends toward the right side of the tentorium configuring sah probably from pericallus artery bleeding it is observed also a right frontoparietal interhemispheric hemorrhagic collection that extends to right tentorium cerebelli configuring a sah presumably from pericallosal artery (figure 2, a and b). the chronic subdural hematoma is considered an incidental finding. with a clinical impression of acute sah the patient is hospitalized in icu. the solicited laboratory test report: hemoglobin: 10g/dl, hematocrit: 34.1%, platelets: 104.000 mm3, wbc: 10.900 mm3, neutrophils: 8.900 mm3. cerebral aneurismal disease is suspected, and is considered perform a cerebral panangiography previous application of three platelets units, and sickle solubility test, wich result positive, then hemoglobin electrophoresis is performed confirming the sickle cell disease. the cerebral panangiography rule out any aneurismal alteration, and are evidenced secondary changes to the bilateral collection on right frontoparietal convexity. (figure 3, a and b). figure 3, a and b cerebral panangiography, discarding vascular pathology the patient has a temporal improvement of his neurological status. on the fourth day of admission appears diffuse abdominal pain, with prolonged control clotting times: ptt: 40 (control 28), mild conjunctival jaundice. are requested liver function tests: ast: 122 mg/dl (normal value 42), alt: 60mg/dl (normal value 40), ldh: 422.7 (normal value 180), romanian neurosurgery (2014) xxi 3: 329 333 331 hemoglobin 8.3 g/dl and hematocrit 25%. the internal medicine evaluation report an acute liver failure in a patient gcs 15/15 and no neurological focalization. fresh frozen plasma, compatible packed red blood cells and platelets are transfused. on the sixth day of admission, the patient develops right hemiparesis, dysphasia with motor predominance and deterioration of consciousness reaching coma. despite polytransfusion patient develops pancytopenia. bone marrow aspirate is performed on the left iliac crest showing no cellular infiltrate. there are no main changes on the simple ct scan respect the first. thus, it is considered that patient present sickle cell disease confirmed by hemoglobin electrophoresis, with transient ischemic brain events and infarctions that generate hip pain and acute progressive liver failure. patient died eight days after admission, the cause of death is considered fulminant hepatic encephalopathy as the brain scan shows no changes respect to the first, where the neurological status is normal. discusion sah is a serious entity that requires early and precise diagnosis and treatment. the wide availability of brain ct scans allow accelerate the diagnosis and the detection of early complications, due to its high sensibility and specificity in the first 24 hours of the event. however, occasionally in the simple ct scans can be appreciated images simulating bleeding in the sas, even without clinical or anatomopathological evidence of hemorrhage (9). this is a widely commented phenomenon in the medical literature, called "pseudo-sah" (10). the pseudo-sah hemorrhage in brain cisterns has received scarce attention in medical literature. however some authors had described weighted enhancement of falx cerebri and tentorium cerebelli in association with brain edema (11). this phenomenon has been described in cases of anoxic-ischemic encephalopathy with brain edema, bacterial meningitis, dural sinus thrombosis, brain metastasis, and as a complication of angiographic procedures, and even in healthy patients of all ages (11). causes are described in the box 1. spiegel et al (12) in 1989 were the first to note that in the brain edema secondary to encephalopathy, the ct scans images show a hyperdensity on basal cisterns and in the sas, similar to that observed during acute sah. they also reported that images of 10 patients with marked brain edema associated whether to tumor or to brain infarction, showed acute sah appearance, especially in the course of interhemispheric fissure and tentorium cerebelli, posteriorly in the autopsy findings sah was absent. in 1998, avrahmi et al (1), founded on the ct scans of 100 comatose patients with brain edema, similar findings of sah along cisterns and grooves, discarding in all of them this diagnosis. they also suggest the term “pseudo” for this phenomenon. list of common causes of pseudo-sah: cerebral gliomatosis bilateral subdural hematoma secondary polycythemia high doses of contrast material used in spinal angiographic procedures 332 alvis-miranda et al the false falx and tentorium sign intrathecally administered contrast material acute purulent leptomeningitis intracranial idiopathic hypertension or hypotension hipertensión o hipotensión intracraneal idiopática viral meningoencephalitis oters in a simple ct scan of a healthy individual, skull bones are immediately delineated by a thin layer of duramater, and this in turn by the sas, where is the cerebrospinal fluid (csf). there is wide variability of mean sas width, being greater in both life extremes. in the particular case of brain edema secondary to hypoxic encephalopathy, cerebral cortex begins to move into areas normally occupied by lcr, allowing neighbor vein congestion, and grooves convexity disappearance, being hyperdense on the simple ct scans, simulating sah (13). it is also envisaged that with severe brain ischemia the brain tissue density diminishes related to superficial cortex congestive veins, giving an impression of hyperdensity in the latter (14). contrasted ct scans can be useful to confirm the diagnosis of pseudo-sah, because of the basal cisterns abnormal enhancement (15). other useful tool for distinguish sah from pseudo-sah is the measurement of houndsfield (hu) units in the hyperdense region (16). in the al-yamani et al (17) study the mean value of accentuation quotients in the basal cisterns of patients with pseudo-sah and spontaneous intracerebral hemorrhage was 29-33hu, and in patients with aneurismal sah was of 60-70hu. conclusions the importance of this case is to consider in the cases of suspected subarachnoid bleeding and increased density of the sas, especially on the tentorium cerebelli and the falx cerebri, the presence of a false sah, corresponding to false falx and tentoium sign, which implies no aneurysmal rupture but forces us to discard with the complementary studies warranted in the vascular pathology evaluation. correspondence dr. luis rafael moscote. neurosurgeon. universidad de cartagena, cartagena de indias, colombia. e-mail: mineurocirujano@aol.com references 1. avrahami e, katz r, rabin a, friedman v. ct diagnosis of non-traumatic subarachnoid haemorrhage in patients with brain edema. eur j radiol 1998;28:222–5. 2. given ca, burdette jh, elster ad, williams dw. pseudo-subarachnoid hemorrhage: a potential imaging pitfall associated with diffuse cerebral edema. ajnr am j neuroradiol 2003;24:254–6. 3. cucchiara b, sinson g, kasner se, chalela ja. pseudosubarachnoid hemorrhage: report of three cases and review of the literature. neurocrit care 2004;1:371–4. 4. you js, park s, park ys, chung sp. pseudosubarachnoid hemorrhage. am j emerg med 2008;26:521.e1–2. 5. misra v, hoque r, gonzalez-toledo e, kelley re, minagar a. pseudo-subarachnoid hemorrhage in a patient with acute cerebellar infarction. neurol res 2008;30:813–5. 6. westwood aj, burns jd, green dm. teaching neuroimages: pseudo-subarachnoid hemorrhage. neurology 2012;78:e54. romanian neurosurgery (2014) xxi 3: 329 333 333 7. de la cruz-cosme c, barbieri g, vallejo-baez a. pseudo-subarachnoid haemorrhage. a need for clinicalradiological diagnostic criteria. neurología (english edition) 2010;25:463–5. 8. osborn ag, anderson re, wing sd. the false falx sign. radiology 1980;134:421–5. 9. agha a, al-hakami m. a case report of pseudosubarachnoid hemorrhage. maedica (buchar) 2011;6:210–2. 10. silberstein m. diagnosis of pseudosubarachnoid hemorrhage. ajnr am j neuroradiol 2003;24:1492; author reply 1492. 11. eckel ts, breiter sn, monsein lh. subarachnoid contrast enhancement after spinal angiography mimicking diffuse subarachnoid hemorrhage. ajr am j roentgenol 1998;170:503–5. 12. spiegel sm, fox aj, vinuela f, pelz dm. increased density of tentorium and falx: a false positive ct sign of subarachnoid hemorrhage. can assoc radiol j 1986;37:243–7. 13. thomas gl, stachowski er. pseudosubarachnoid haemorrhage on ct brain scan: an unusual presentation of diffuse hypoxic brain injury. intensive care med 2007;33:2038–40. 14. schievink wi, wijdicks ef, meyer fb, sonntag vk. spontaneous intracranial hypotension mimicking aneurysmal subarachnoid hemorrhage. neurosurgery 2001;48:513–6; discussion 516–7. 15. gutierrez lg, rovira a, portela lap, leite c da c, lucato lt. ct and mr in non-neonatal hypoxicischemic encephalopathy: radiological findings with pathophysiological correlations. neuroradiology 2010;52:949–76. 16. senthilkumaran s, balamurugan n, menezes rg, thirumalaikolundusubramanian p. role of hounsfield units to distinguish pseudo-subarachnoid hemorrhage. clin toxicol (phila) 2011;49:948. 17. al-yamany m, deck j, bernstein m. pseudosubarachnoid hemorrhage: a rare neuroimaging pitfall. the canadian journal of neurological sciences. le journal canadien des sciences neurologiques 1999;26:57–9. 03_paper romanian neurosurgery (2015) xxix 4: 397 409 397 doi: 10.1515/romneu-2015-0055 pseudotumour cerebri idiopathic intracranial hypertension and vascular intracranial hypertension st.m. iencean1, a.st. iencean2, a. tascu3 1“grigore t. popa” university of medicine and pharmacy, iasi, romania 2neurosurgery, “n. oblu” emergency hospital iasi, romania 3pediatric neurosurgical department, “bagdasar-arseni” clinical hospital, bucharest, romania abstract: from the first to use of “pseudotumor cerebri” by nonne in 1904, the historic evolution of the knowledge on pseudotumor cerebri has been marked by several periods (the otologic stage, the neurosurgical stage, the neuro-ophthalmologic stage); today there are clear diagnosis criteria for the idiopathic intracranial hypertension, there is a clear differentiation between idiopathic intracranial hypertension and vascular intracranial hypertension, also the comprehension of the illness pathogeny is based on the dynamics of the intracranial fluids, which allows the auto-regulation of the cerebral circulation within quasi-normal limits, despite the very high intracranial pressure. key words: idiopathic intracranial hypertension, pseudotumor cerebri, vascular intracranial hypertension vascular intracranial hypertension intracranial hypertension can occur in cerebral-vascular illnesses due to sanguine, cerebral or extra-cerebral, circulatory disorders, which modify the dynamics of the intracranial fluids and cause the intracranial pressure increase. there are disorders in the auto-regulation of the cerebral hemodynamics and the cerebral parenchyma volume continues to increase due to the brain edema or to the increase in the cerebral sanguine volume (brain swelling) with the secondary increase in the intracranial pressure. the volume of the cerebral parenchyma increases due to the modifications occurred at the level of the cerebral sanguine capillaries, which leads to: the occurrence of the extracellular brain edema due to the increased quantity of interstitial fluid: extracellular edema produced by a hydrostatic mechanism (ultra-filtration) in severe arterial hypertension, extracellular edema with oncotic induction (vasogenic edema) due to an increased permeability of the brain blood 398 iencean et al pseudotumour cerebri barrier (open brain-blood barrier) cerebral congestive edematization with an increase in the volume of the cerebral parenchyma by vascular dilatation. the vascular types of intracranial hypertension have characteristic etiologies and they occur by: slowing down or decreasing the intracranial venous flux in thrombophlebites and cerebral venous thrombosis, the decrease in the venous flux at the level of the superior longitudinal sinus (sls) directly in compressive lesions (hollowing fracture, etc.) or in sls shunting by an intracranial arterialvenous malformation, or the extra-cranial illnesses that block the returning venous circulation at the cervical level, reduce the cerebral venous drainage and cause the decrease in the absorption of the cranial-spinal fluid and then the occurrence of the brain edema. in hypertensive encephalopathy, when the hydrostatic brain edema occurs (by ultrafiltration), as well as a brain swelling (by vasodilatation). the cerebral ischemia or the ischemic stroke reduces the arterial sanguine contribution and causes an ischemic brain edema, which is a mixed brain edema, both a cellular edema (cytotoxic) and an extracellular brain edema with oncotic induction (vasogenic). cerebral venous thrombosis cerebral venous thrombosis reduce the returning venous circulation from the brain and the skull, a venous stasis is produced and the cerebral sanguine circulation is slowed down. there are areas of cerebral hypoanorexia concomitantly to areas of venous congestive edematization, and the cellular cerebral (cytotoxic) edema occurs, as well as the oncotic extracellular (vasogenic) edema, which evolves to a mixed brain edema. the venous sinuses also ensure the resorption of the cerebrospinal fluid, and the thrombosis of the venous sinuses leads to a diminished drainage of the cerebrospinal fluid. therefore, a progressive intra-ventricular accumulation of cerebrospinal fluid occurs, with a pressure increase in the ventricular system and the occurrence of the hydrocephalic brain edema. these phenomena happen slowly, in varied successions, but the evolution is progressive towards an intracranial pressure increase. the iatrogenic thrombosis of the internal jugular veins is quoted in cases of prolonged use of the jugular catheters for the intravenous administration of medication. in such cases, the same pathogenic processes occur, and the ich syndrome may appear. the symptomatology is caused by the initial causal lesion, after which neurological focal symptoms may occur related to the progression of the venous thrombosis, as well as symptoms caused by the intracranial pressure increase. a venous infarct often happens, which is associated to a cerebral hemorrhage, which also aggravates the neurological clinical presentation. usually, the clinic evolves to an incomplete or complete syndrome of intracranial hypertension. the main characteristics of the intracranial pressure increase in cerebral venous thrombosis are: a slow increase in the intracranial romanian neurosurgery (2015) xxix 4: 397 409 399 doi: 10.1515/romneu-2015-0055 pressure up to the normal limit value of 20 mm hg, usually during a period of a few days, over the value of 20 mm hg, the icp increase continues to be progressive, and it may reach maximum values of approximately 30 mm hg in a few hours or days. this gradual increase allows the compensating mechanisms to act more efficiently, and also for the applied therapy to encourage the intracranial pressure decrease and the improvement of the cerebral sanguine circulation. the maximum values that may be reached in cases of intracranial hypertension syndrome are of approximately 3035 mm hg (sometimes the maximum values may be of 40 mm hg) and the pathological pressure values may last for several weeks, with a slow return to normal pressure values and period of intermittent increases, usually, there is a recurrence to intracranial pressure values of about and above 20 mm hg, which causes the persistency of a prolonged attenuated symptomatology. the treatment of the venous thrombosis with an ich syndrome is: etiological and pathogenic for the vascular disorder, when possible, pathogenic for the intracranial hypertension syndrome. a particular pathogenic mechanism is the reduction of the venous flux at the level of the superior longitudinal sinus (sls) with an important blockage of the csf resorption: in the case of arterial-venous malformations of the galien vein (galien vein aneurisms), when there is a sls shunting by malformation and the cerebrospinal fluid resorption is diminished by the occurrence of the hydrocephalus. in infants and small children, the dominating symptomatology is the cardiac disorder due to the increased venous return, while the ich syndrome also occurs in older children. in the case of a median intrusive cranial fracture, which interests the third posterior part of the sls. in children with craniostenoses, there may be anomalies of the venous drainage, which interests the sigmoid sinus and the jugular vein, which may cause a venous hypertension, with a diminished drainage of the cerebrospinal fluid and the increase in the intracranial pressure. usually, the phenomenon occurs up to the age of 6 years old, after which a collateral venous drainage is developed by the stylomastoid plexus, leading to the normalization of the intracranial pressure. hypertensive encephalopathy high blood pressure is the most important predisposing factor for cerebral-vascular illnesses, and the most frequent complication is the cerebral hemorrhage. the exaggerated increase in the values of the systemic blood pressure also causes disorders of the cerebral circulation auto-regulation, with other secondary cerebral suffering. hypertensive encephalopathy is defined in the clinical presentation of induced intracranial hypertension by an acute episode of arterial hypertension. 1. the acute hypertensive encephalopathy is caused by the acute blood pressure increase in: 400 iencean et al pseudotumour cerebri severe high blood pressure, uncontrolled / untreated high blood pressurein pregnancy (eclampsia), high blood pressure in glomerulonephritis, pheochromocytoma, etc. the acute increase in the sanguine pressure values leads to the inefficiency of the cerebral vascular auto-regulation, a generalized cerebral vascular dilatation occurs and / or there is an increased permeability of the cerebral capillaries. the increased permeability in the brain blood barrier has been constant more frequently at the level of the gray matter. therefore, the increase in the volume of the cerebral parenchyma is caused by: brain swelling by vasodilatation, hydrostatic extracellular brain edema, by ultra-filtration when the brain blood barrier is intact (close brain-blood barrier) oncotic (vasogenic) extracellular brain edema by an injury of the brain blood barrier (open brain-blood barrier). the posterior reversible encephalopathy syndrome (pres) or the reversible posterior leuco-encephalopathy syndrome (rpls) with a hypertensive etiology is included in the acute form of vascular etiopathogeny ich. the clinical presentationis typical and the dwi exploration shows an extracellular brain edema by the increase in the water mobility with a posterior bilateral location, and a subcortical interest in the white matter too. the treatment consists of decreasing the systemic blood pressure. 2. the chronic hypertensive encephalopathy (binswanger encephalopathy) is a rare cerebral-vascular illness with a chronic extracellular brain edema: hydrostatic brain edema combined with the oncotic brain edema. the intracranial pressure increase in acute hypertensive encephalopathies are characterized by: the relatively high speed with which the intracranial pressure reaches the normal threshold value in approximately a few hours the icp continues to increase above the normal values for a period that is usually shorter than the previous interval, of few hours only the maximum values that the icp may reach are of 30 – 50 mm hg and the period with pathologic intracranial pressure values is usually of several hours, rarely of several days. the anti-hypertensive treatment improves the clinical condition. the unmonitored hypertensive patients, or those who are incompletely treated may present repeated episodes of hypertensive encephalopathy, or they may suffer from the most frequent complication, which is the cerebral hemorrhage. the clinical evolution of hypertensive encephalopathy is up to an incomplete syndrome of intracranial hypertension, and it has a regressive aspect. in the pathogeny of the syndrome, there is an auto-limiting mechanism: the intracranial pressure increase caused by the increase in the sanguine blood pressure and by occurrence of the cerebral vasodilatation generated the collapse of the walls of the intracranial sanguine vessels, and, to a certain extent, to a diminished cerebral sanguine volume. the mechanism consists of the direct action of the increased intracranial romanian neurosurgery (2015) xxix 4: 397 409 401 doi: 10.1515/romneu-2015-0055 pressure over a functional disorder that is secondary to the exceeded auto-regulation of the cerebral circulation, and it has a limited value. the treatment of the hypertensive encephalopathy is both etiologic and pathogenic: the treatment of the hypertensive episode, as an etiologic aspect, and the pathogenic treatment of the intracranial hypertension syndrome. ischaemic stroke the ischemic stroke represents 85 % of the cerebral-vascular illnesses. the large ischemic cerebral lesions are accompanied by the brain edema with cerebral herniation (subfalciform) and by the intracranial pressure increase. the extended cerebral ischemic infarct with phenomena of intracranial hypertension is caused by the occlusion or stenosis of a great cerebral artery: the internal carotid artery or a terminal branch that irrigates a vast territory, such as the middle cerebral artery. the extended ischemic infarct of the sylvian artery occurs in approximately 10 % of the patients with acute cerebral circulatory insufficiency, and it has been designated as the malign infarct of the sylvian artery due to the increased mortality, of up to 80 % of cases, despite the therapeutic means used. the massive cerebellum ischemic infarct can cause the collapse of the 4th ventricle with the occurrence of an acute obstructive hydrocephalus and an acute ich syndrome, and it has a direct compressive effect on the brainstem with the manifestation of vegetative disorders. in the case of the cerebral hemispheric ischemic stroke, the decreased sanguine flow in the territory of the middle cerebral artery leads to the occurrence of certain ischemic metabolic disorders at the level of the affected cerebral parenchyma. the permeability of the cerebral capillaries increases (open brainblood barrier) and the extracellular oncotic (vasogenic) edema occurs. the evolution is usually a rapid one, with the extension of the brain edema, the increase in the intracranial pressure and the occurrence of the subfalciform cerebral hernia (median line movement towards the unaffected cerebral hemisphere). although the intracranial pressure increasing mechanism is based on the cerebral ischemia with a hypoxic brain edema, which is characteristic for the parenchymatous lesions, while the etiology is represented by the impacts on a great cerebral artery, and it includes the ischemic stroke on vascular intracranial hypertension. since the moment of the arterial occlusion, the intracranial pressure increase is: rapid until it reaches the normal pressure limit of 20 mm hg, by the progression of the brain edema and the surpassing of the pressure compensating possibilities, with a duration of up to several hours above the normal pressure values, the icp increase is also a rapid one, and the maximum values are reached within a short interval of time: half an hour – several hours the maximum values of the intracranial pressure are of approximately 40 – 50 mm hg and the duration of these pathological values is of several days and it corresponds to the 402 iencean et al pseudotumour cerebri intensive care period. the evolution is rapid towards the decompensation of the intracranial hypertension with almost 80% unfavorable results despite the applied treatments. there is an attempt in using the etiological treatment of the arterial obstruction and the pathogenic treatment for the ich syndrome. during the first three hours from the beginning, there may be an intravenous administration of recombined tissue plasminogen activator (rtpa) in a dose of 0.9 mg/kg, maximum 90 mg; the administration of streptokinase or of other thrombolytic agents does not have the same efficiency as rtpa. the brain edema receives a pathogenic treatment with osmotic diuretics (mannitol), and hyperventilation if there is an imminent decompensation of intracranial hypertension and the production of a brain herniation etc. sometimes, there is an attempt of a surgical intervention: decompressive craniectomy of posterior cerebral fosse and of evacuation of a cerebellum infarct with a compressive effect on the brainstem, perhaps with a ventricular drainage, decompressive craniectomy and the evacuation of a cerebral hemispheric massive infarct, which may diminish the intracranial hypertension, but the surviving patients is left with major neurological deficits. a particular case of generalized cerebral ischemia is met in the post-resuscitation syndrome when the sanguine flux disorder includes the entire brain, with a complete ischemia throughout the stroke, followed by reperfusion disorders. the consequence of this cerebral circulatory failure, primary – before and during cardiopulmonary resuscitation, and secondary ischemic damage, during reperfusion is the development of the mixed brain edema: both cytotoxic and vasogenic, concomitantly to the production of the glialneuronal necrosis. the hyperemic reperfusion may exacerbate the brain edema. the mixed brain edema accentuates the elevated intracranial pressure and it exacerbates the brain injury. the treatment is complex and the results do not compensate the efforts. table i etio-pathogenic and evolutionary characteristics of the various forms of vascular ich cerebral venous thrombosis hypertensive encephalopathy ischemic stroke cerebral vascular pathology: thrombosis of dural sinuses thrombosis of cortical veins cerebral vascular pathology: dilatation of cerebral arteries cerebral vascular pathology: infarct of sylvian artery massive cerebellum infarct cerebral blood flow : reduced venous outflow cerebral blood flow : increase arterial inflow cerebral blood flow : reduced arterial inflow pathogenesis: venous dilatation; open bbb and vasogenic brain edema and pathogenesis: dilatation of cerebral vessels; closed bbb and hydrostatic brain edema, and pathogenesis: ischemic increased capillary permeability ; open bbb and vasogenic brain edema romanian neurosurgery (2015) xxix 4: 397 409 403 doi: 10.1515/romneu-2015-0055 diminished csf drainage with hydrocephalic brain edema -increased vascular permeability with open bbb and vasogenic brain edema icp increase: slow to the normal limit slow above the normal limit icp increase: rapid to the normal limit slow above the normal limit icp increase: rapid to the normal limit rapid above the normal limit sub-acute and chronic evolution possible decompensation acute and sub-acute evolution rarely decompensation acute evolution usually decompensation pathogenic treatment pathogenic and etiologic treatment etiologic and pathogenic treatment, decompressive craniectomy idiopathic intracranial hypertension idiopathic intracranial hypertension is a syndrome characterized by the intracranial pressure increase in the absence of an expansive intracranial process, of hydrocephalus, of an intracranial infection, of dural venous sinus thrombosis, of hypertensive encephalopathy and without a neurotoxic etiology. the idiopathic intracranial hypertension partially corresponds to the old designation of pseudotumor cerebri; the term of benign intracranial hypertension has also been used, but it was subsequently dropped as it was noticed that the evolution of this illness can be accompanied by complications that exclude the idea of benignity (visual acuity decrease to cecity in some cases). this medical condition is described as a specific entity in quincke’s papers from 1893 and 1897 and then by nonne in 1904, who is the first to use the term of pseudotumor cerebri. various hypotheses are delivered in order to explain the causes and the pathogenic mechanisms of the illness. in 1955, foley uses the term “benign intracranial hypertension”, which is to be used for several decades, and he defines this syndrome as follows: “prolonged intracranial hypertension without ventricular modifications, without focal neurological signs, without consciousness or intellectual disorders, the most important symptoms being a moderate cephalea, blurred sight, diplopia and sometimes tinnitus. the only signs are the papillary edema and the abducens paralysis. the cerebrospinal fluid has a normal composition. the prognosis is favorable, and the symptoms progressively diminish in several weeks or months.” according to foley’s classic definition, 1955, the idiopathic intracranial hypertension occurs as a diagnosis that may be established only by exclusion; moreover, even in dandy’s diagnosis criteria, modified by wall, one of the diagnosis elements is the non-identification of another cause for the intracranial pressure increase. the diagnosis of idiopathic intracranial hypertension can be given only after the intracranial pressure has been measured and after a complete neuroimagistic exploration. the diagnosis criteria of the idiopathic intracranial hypertension, which are standardized by friedman and jacobson, and which are currently accepted are: 404 iencean et al pseudotumour cerebri the pressure of the cerebrospinal fluid is higher than 25 cm h2o, that is higher than 18 20 mm hg (by lumbar manometry performed after the ct or mri exploration), the cerebrospinal fluid has a normal composition: normal or reduced cerebrospinal fluid proteins and normal cellularity, there are symptoms caused by the increased intracranial pressure: papillary edema, cephalea, with the absence of the neurological location signs (the abducens paresis is not a focal sign). the cerebral exploration using ct scan or mri reveals normal cranial-cerebral aspects, a ventricular system with reduced dimensions may also be revealed (with a collapsed aspect) – without significance, or an empty sella; moreover, there is no clinical or neuroimagistic suspicion of an intracranial venous sinus thrombosis. these criteria limit the diagnosis of idiopathic intracranial hypertension to patients who have an increased cerebrospinal fluid pressure without a noticeable etiology. although it is not a diagnosis criteria, a guiding element is the predominance of the feminine sex, with a women / men proportion of approximately 2-8 / 1, with an interest in the age groups 20 50 years old, and with the maximum incidence in the third decade of age. [10, 11, 12, 13] various pathologic conditions can also be taken into account, when the idiopathic intracranial hypertension occurs more frequently: thus the global incidence of the idiopathic ich is considered to be 1 2 cases / 100,000 but, in the case of young and obese women, it has been noticed that the incidence of idiopathic intracranial hypertension reaches 19-25 cases / 100,000. the idiopathic intracranial hypertension is defined by the clinical existence of the intracranial hypertension syndrome, with very high icp values and with a papillary edema in uncertain etiological conditions and due to pathogenic mechanisms that are difficult to establish. the term “associated factors” is used for the very diverse situations when the idiopathic intracranial hypertension occurs, without an etiopathogenic relationship. the pathological conditions where the idiopathic intracranial hypertension occurs are numerous: metabolic and endocrine disorders: if the global incidence of intracranial hypertension is estimated at 1 2/100,000, in young and obese women the incidence of idiopathic intracranial hypertension reaches 19 25/100,000. hypothyroidism, parathyroid anomalies, hypovitaminosis a; anemia due to fe deficiency; system illnesses – lupus eritematos; medicines: nalidixic acid, tetracycline, vitamin a, lithium carbonate, etc., in numerous cases, a possible association can be determined with various conditions that are pathogenically suggestive, with not etiological notification; but there are plenty of cases when no etio-pathogenic relation can be revealed. the pathogenic mechanisms are based on the dynamics of the intracranial fluids, and they correspond to the circuit of the fluids that justify the increased pressure of the cerebrospinal fluid and allow the maintenance romanian neurosurgery (2015) xxix 4: 397 409 405 doi: 10.1515/romneu-2015-0055 of the cerebral circulatory auto-regulation with a normal nervous functioning. the dynamics of the intracranial fluids in the case of the idiopathic intracranial hypertension can include several fluid circuits that concord to the brain edema and to the increased parenchymatous pressure, which is equal to the increased pressure of the cerebrospinal fluid, concomitantly to the maintenance of the cerebral sanguine circulation, which may explain the good clinical condition: hyper-production of interstitial fluid with increased resorption at the level of the brain blood barrier – which explains the increased parenchymatous pressure and the hyperproduction of cerebrospinal fluid, which may explain the increased pressure of the cerebrospinal fluid, with increased resorption at the level of the venous sinuses, as well as intense and rapid exchanges from the interstitial fluid towards the cerebrospinal fluid at the level of the ventricular wall, transependyma, and at the trans-cerebral pial level, which explains the pressure equilibrium between the cerebral parenchyma – ventricles, with a rapid venous drainage; hyper-production of cerebrospinal fluid, increased resorption at the level of venous sinuses with rapid venous drainage; hyper-production of interstitial fluid by modification of the brain-blood barrier, normal production of cerebrospinal fluid, but with increased exchanges from the interstitial fluid towards the trans-ependyma cerebrospinal fluid and at the trans-cerebral pial level, with a rapid venous drainage. the increased production of cerebrospinal fluid at the level of the choroid plexuses, and then with increased resorption, cannot explain the brain edema and the pressure equilibrium at the level of the nervous parenchyma – ventricular system. the brain edema occurs due to the impact on the brain-blood barrier, generating an increased flux of interstitial fluid, with an increase in the intra-parenchymatous pressure. the maintenance of the cerebral sanguine circulation within normal limits imposes the decrease in the parenchymatous pressure, which can be achieved through an increased resorption of the interstitial fluid and / or by the trans-ependyma passage in ventricles, and a trans-pial passage in the sub-arachnoid space. the resulting increased quantity of cerebrospinal fluid does not cause a ventricular dilatation because an increased resorption occurs; the ventricular system is usually reduced in volume, which suggests the fact that the trans-ependyma fluid circuit is predominant for the increase in the volume of cerebrospinal fluid, compared to the production at the level of the choroid plexuses. the increased resorption of the cerebrospinal fluid corresponds quantitatively to the transependyma exchange from the volume increased interstitial fluid, ensuring the intracranial circuit of fluids. the dynamics of the relations intracranial pressure – intracranial volume is expressed by the circulation of fluids, which allows the existence of an increased fluid pressure, although this pressure does not act significantly on the endocranial structures and 406 iencean et al pseudotumour cerebri on the cerebral circulation, which is maintained within normal limits. the most probable pathogenic mechanism is the impacts on the brain blood barrier of the hyper-production of interstitial fluid and an extracellular brain edema; the cerebrospinal fluid is produced normally; there are increased exchanges from the interstitial fluid towards the cerebrospinal fluid at the trans-ependyma level and at the trans-cerebral pial level; an increased resorption of the cerebrospinal fluid is produced, and there is a rapid venous efflux. the trans-ependyma exchange between the interstitial fluid of the edema from the cerebral parenchyma towards the cerebrospinal fluid, by means of which pressure is equalized, is followed by the increased resorption of the cerebrospinal fluid, maintaining the cerebral circulation, and representing a compensating mechanism. this mechanism is efficient and it allows the cerebral circulatory auto-regulation when there is a progressive injury of the brainblood barrier, the interstitial fluid volume increases slowly and the brain edema is also gradually installed. the trans-ependyma and trans-pial circuit of the interstitial fluid towards the cerebrospinal fluid is the fundamental element for this compensating mechanism of pressure increase. the increase in the intracranial pressure is extremely slow, with a chronic aspect. this very slow increase in the intracranial pressure allows good pressure compensation and an almost normal maintenance of the cerebral sanguine flux. the pathogenic icp values are very high, of up to 60 80 mm hg, values that may be maintained on a plateau for long periods. figure 1 hydrodynamic model of pathogeny in idiopathic intracranial hypertension romanian neurosurgery (2015) xxix 4: 397 409 407 doi: 10.1515/romneu-2015-0055 this pathogenic mechanism, which is based on the compensation of the fluid pressure increase by means of a gradual accentuation of the trans-ependyma circuit functioning and the trans-pial transfer of the interstitial fluid towards the cerebrospinal fluid, explains: the absence of hydrocephalus despite the increased pressure of the cerebrospinal fluid, through increased fluid resorption, the small dimensions of the ventricular system due to the initially increased pressure at the level of the nervous parenchyma, and subsequently balanced by the transfer of the interstitial fluid towards the cerebrospinal fluid, the good clinical condition due to the auto-regulation of the cerebral circulation, because the increased intracranial pressure has a reduced action on the endocranial structures in the dynamic conditions of the rapid fluid circuit; the brain edema frequently exists due to the dysfunction of the brain blood barrier and to the existence of an increased quantity of interstitial fluid; at the same time, in some cases, the brain edema may be reduced or even absent because the fluid transfer towards the cerebrospinal fluid is sufficiently rapid and intense for the brain edema not to be significant. treatment: the therapy is applied depending on the possible associated factors – metabolic and hormonal corrections, exclusion of certain medication, etc. a symptomatic treatment is applied for cephalea, and cerebral anti-edematous substances are administered, such as dexamethasone, or diuretics (acetazolamide, furosemide) in order to decrease the intracranial pressure. in some cases of obese patients, the weight loss is followed by an obvious clinical improvement, and by the progressive reduction of the papillary edema. moreover, repeated lumbar punctures and lumbar-peritoneal shunting have been used with good clinical results. an approximate quantity of 30 ml csf is evacuated by lumbar puncture or the cerebrospinal fluid is drained until the intracranial pressure, which is measured by the lumbar method, is seen to have decreased to approximately half of the initial value. the lumbar peritoneal shunting drains the excessive csf and the symptomatology disappears within less than a month; the shunting revising rate may reach to 50 %. in some cases of significant visual acuity decrease, there has been an attempt to decompress the optic nerve by performing fenestrations at the level of the optic nerve sheath in order to produce a decrease of the papillary edema, but the results are not always favorable. comparison between idiopathic ich and the vascular type of ich the recent literature data and the the above presentations allow the differentiation between the vascular type of ich and idiopathic ich. the name hyperemic ich has been suggested but the designation of vascular ich covers the etiology and pathogenesis better and more completely. although the symptoms may be similar in these two diseases, the imaging findings, therapy and evolution are different; therefore, 408 iencean et al pseudotumour cerebri the etiology and pathogenesis are different. vascular ich has a known etiology, such as cerebral vascular illness whereas idiopathic ich has no known etiology or has various nonspecific factors associated factors (e.g., metabolic and endocrine disorders, hypovitaminosis a, and medications). the imaging diagnosis for vascular ich showed a cerebral venous sinus thrombosis or stenosis or a cerebral venous thrombosis and either normal images or small ventricles in idiopathic ich. the imaging diagnosis of idiopathic ich excludes other diseases with similar symptoms. vascular ich involves vasogenic brain edema with papillary edema, whereas idiopathic ich commonly involves papillary edema and diminished visual acuity in some cases. there is also brain edema in idiopathic ich, but this appears to be balanced by the intraventricular pressure. the increase in icp is faster in vascular ich compared with the very slow icp increase in idiopathic ich, as demonstrated by the longer period until the complete clinical syndrome has developed. in addition, the icp values are higher in idiopathic ich. therefore, the critical icp values are lower in vascular ich until the decompensation of ich. the treatment is symptomatic, as well as etiologic and pathogenic in vascular ich but only symptomatic in idiopathic ich (including a lumboperitoneal shunt or decompression of the optic nerve). vascular ich may potentially include other syndromes, such as hypertensive encephalopathy, but this classification requires further study. in hypertensive encephalopathy, there is a dilatation of brain arteries with increased arterial inflow, increased vascular permeability, and disruption of the braineblood barrier; brain edema occurs as a result. in conclusion, ich caused by intracranial vascular damage is vascular ich and although it has clinical similarities to idiopathic ich, there are important differences: vascular ich has a known etiology, such as cerebral vascular illness, and the increase in icp is faster in vascular ich, but the critical icp values are lower compared with idiopathic ich. the therapy is etiologic, pathogenic and symptomatic in vascular ich, but is only symptomatic in idiopathic ich. correspondence a.st. iencean neurosurgery, “n. oblu” emergency hospital iasi, romania e-mail: andrei_steffan@yahoo.com references 1. pearce jm. from pseudotumour cerebri to idiopathic intracranial hypertension. pract neurol 2009;9:353e6. 2. johnston i. the historical development of the pseudotumor concept. neurosurg focus 2001;11:1e9. 3. degnan aj, levy lm. pseudotumor cerebri: brief review of clinical syndrome and imaging findings. ajnr am j neuroradiol 2011;32:1986e93. 4. brazis pw. pseudotumor cerebri. curr neurol neurosci rep 2004;4:111e6. 5. sylaja pn, ahsan moosa nv, radhakrishnan k, sankara sarma p, pradeep kumar s. differential diagnosis of patients with intracranial sinus venous thrombosis-related isolated intracranial hypertension from those with idiopathic intracranial hypertension. j neurol sci 2003;215:9e12. romanian neurosurgery (2015) xxix 4: 397 409 409 doi: 10.1515/romneu-2015-0055 6. friedman di, jacobson dm. diagnostic criteria for idiopathic intracranial hypertension. neurology 2002;59:1492e5. 7. wall m. idiopathic intracranial hypertension. neurol clin 2010; 28:593e617. 8. digre kb, nakamoto bk, warner je, langeberg wj, baggaley sk, katz bj. a comparison of idiopathic intracranial hypertension with and without papilledema. headache 2009;49:185e93. 9. biousse v, bruce bb, newman nj. update on the pathophysiology and management of idiopathic intracranial hypertension. j neurol neurosurg psychiatry 2012;83:488e94. 10. friedman di, liu gt, digre kb. revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. neurology 2013;81:1159e65. 11. leker rr, steiner i. features of dural sinus thrombosis simulating pseudotumor cerebri. eur j neurol 1999;6:601e4. 12. suzuki h, takanashi j, kobayashi k, nagasawa k, tashima k,kohno y. mr imaging of idiopathic intracranial hypertension. am j neuroradiol 2001;22:196e9. 13. hoffmann j, huppertz hj, schmidt c, kunte h, harms l, klingebiel r, et al. morphometric and volumetric mri changes in idiopathic intracranial hypertension. cephalalgia 2013;33: 1075e84. 14. iencean sm. simultaneous hypersecretion of csf and of brain interstitial fluid causes idiopathic intracranial hypertension.med hypotheses 2003;61:529e32. 15. iencean stm, av ciurea intracranial hypertension: classification and patterns of evolution j med life. 2008 apr 15; 1(2): 101–107. 16. iencean sm, poeata i, iencean as, tascu a cerebral venous etiology of intracranial hypertension and differentiation from idiopathic intracranial hypertension. kaohsiung j med sci. 2015 mar;31(3):156-62. doi: 10.1016/j.kjms.2014.12.007. 12_paper romanian neurosurgery (2015) xxix 4: 481 486 481 doi: 10.1515/romneu-2015-0064 cerebellar pilomyxoid astrocytoma somnath sharma1, bal krishan ojha2, anil chandra2, sunil kumar singh2, chhitij srivastava2, preeti agarwal3, kalpana sharma4 13rd year resident, department of neurosurgery, king george’s medical university chowk, lucknow, u.p., india 2department of neurosurgery, king george’s medical university chowk, lucknow, u.p., india 3department of pathology, king george’s medical university chowk, lucknow, u.p., india 4department of ent, sawai mansingh hospital, jaipur, rajasthan, india abstract: pilomyxoid astrocytomas (p.m.a) are new class of pilocytic astrocytoma (p.a.) which typically have their origin in hypothalamus and chiasmatic region. there are very few case reports of pmas arising from cerebellum. their imaging features are similar to pa but they behave more aggressively than pa. the authors report a case of 10 year old male child who presented with right cerebellar tumour diagnosed as pma on histopathology. introduction tihan et al, in year 1999, first reported pma as a new variant of pilocytic astrocytoma. (1) it has been recently defined as a distinct entity among brain tumours and is classified as a who grade ii glial tumour. (2, 3) pma may occur anywhere along the neuraxis but they are predominantly present in hypothalamic – chiasmatic region. (3-5) very few cases of cerebellar pma are mentioned in literature. (6-8) herein, we report a case of cerebellar pma in a 10 year old male child and discuss literature review. case report a 10 year old male child presented with history of unsteadiness of gait and frequent falls for last 3 months. also, he had developed severe headache and vomiting for last 20 days. physical examination revealed grade ii papilloedema in both eyes with right cerebellar signs. imaging: ncct head revealed a large solid-cystic mass in right cerebellum pushing the iv ventricle to the opposite side with hydrocephalus (figure 1). the tumour was heterogeneously iso to hypo intense on t1wi (figure 2a). dwi revealed anterior cystic and posterior solid tumor (figure 2b). solid portion was hyper intense on t2wi (figure 2c) and heterogeneous contrast enhancement was seen on gadolinium administration. the cyst wall was nonenhancing (figure 2d). 482 sharma et al cerebellar pilomyxoid astrocytoma figure 1 ct image shows solid cystic lesion in right cerebellum with hydrocephalus figure 2 a t1wi showing iso to hypointense lesion figure 2 b diffusion weighted image (dwi) revealing anterior cystic and posterior solid portion figure 2 c gadolinium enhancement present in solid portion romanian neurosurgery (2015) xxix 4: 481 486 483 doi: 10.1515/romneu-2015-0064 figure 2 d non-enhancing cystic portion on gadolinium administration figure 3 ct image showing gross total excision of tumour figure 4 section shows tumor cells displaying monomorphic nuclei with piloid morphology with perivascular arrangement of cells with myxiod areas. (h&e x200) figure 5 ihc gfap: tumor cells display diffuse cytoplasmic expression of gfap figure 6 ihc ki67: ki67 expression is low < 1% 484 sharma et al cerebellar pilomyxoid astrocytoma operation: patient underwent left sided ventriculo peritoneal shunt done to relieve raised intracranial pressure and further deterioration. after one week, right retromastoid suboccipital craniectomy was done with gross total excision of tumor (figure 3). tumour was greyish pink, moderately vascular, non suckable mass with clear cystic fluid. post operative: the post operative period was uneventful. headache and vomiting were relieved immediately after shunt surgery. child was discharged on 8th postoperative day. histopathological examination revealed it a case of pilomyxoid astrocytoma. in view of this report patient received 40 gray of radiation to whole brain with 14 gray boost to tumour bed. during follow up, his gait improved within 2 months. after one year of follow up, patient remained asymptomatic without any recurrence on contrast ct. histopathology: haematoxylin and eosin stained section displayed a tumor composed of piloid cells with monomorphic nuclei. cells were converged near blood vessels in myxoid background. rosenthal fibres and eosinophilic bodies were not observed (figure 4). these tumor cells displayed diffuse cytoplasmic immunoexpression for glial fibrillary acidic protein (gfap) (figure 5) with low ki-67 index; less than 1% (figure 6). neuronal markers like synaptophysin and neuron specific enolase were negative. discussion pma have been reported in the english literature and the overwhelming majority of the patients were children aged from 2 months to 4 years. (9) pmas were typically seen in the chiasmatic-hypothalamic region, but they were also found in other locations, including the spinal cord, the temporal lobe, occipital lobe and sellarsuprasellar region. (10-12, 19) recent reports have indicated that pmas can occur in adults; a tumor in the amygdala/uncus region has been reported in a 28-year-old man, (13) and a spinal cord pma has been reported in a 45-year-old woman. (14) the case of a 25-year-old man with a fourth ventricular pma has also been reported. (15) pma in cerebellum were reported from 2-12 years as in our case whose age was 10 years. pma has some specific features in histology, which include monomorphous growth of piloid cells with an angiocentric pattern, being rich in myxoid background, and lacking of rosenthal fibers or eosinophilic granular bodies. (16) similarly, pas also consist of piloid cells, but these cells grow in a biphasic pattern, mixed with rosenthal fibers and eosinophilic granular bodies. (16) occurrence of necrosis is more commonly associated with pma, while cyst formation, calcification and perilesional edema are more common in classic pa. (4) in immunohistochemical studies, pma stains strongly positive for glial fibrillary acidic protein and vimentin, and is negative for neuronal markers. (2) in our case tumor tissue was diffusely positive for gfap and negative for neuron-specific enolase. on mri, pmas also have similar signal patterns to pa, and they both show isointensity on t1w sequences, hyperintensity on t2w sequences and on flair images. however, some features could romanian neurosurgery (2015) xxix 4: 481 486 485 doi: 10.1515/romneu-2015-0064 be used to distinguish pma from pa on mri. pas are usually cystic with solid mural nodules and are surrounded by edema. when contrast medium was administered, pa often showed intense enhancement in the nodule or the cyst wall. on the contrary, pmas are often solid, rarely with peripheral edema. in pmas, 40% cases showed homogenous enhancement and 30%-60% cases displayed heterogeneous enhancement. (4, 17) in our case, the tumor showed cyst with a mural nodule. nodule displayed homogenous enhancement while cyst wall was non-enhancing. however, neuroimaging features cannot yet distinguish between pma and pa, (4) and the diagnosis of pma is made predominantly on the basis of distinctive histological features. (2, 4) for the patients with pma, regardless of total or partial resection, a majority of the postoperative recurrences took place within one year and the local recurrence rate was 76%. (18) the average survival time was 6 months when a recurred tumor was demonstrated by mri. (1, 12) our patient remained asymptomatic without any recurrence on contrast ct at one year of follow up. conclusion histopathologist should look for features of pmas whenever they consider the diagnosis of pas as this finding is important for patient and surgeon for prognostication and further treatment especially in cases of recurrence. disclosure the authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper. correspondence somnath sharma mbbs, ms soms.sms@gmail.com department of neurosurgery, king george’s medical university chowk, lucknow, u.p., india-226003 phone: 08799690407 fax: 0091-522-2257606 references 1.tihan t, fisher pg, kepner jl, et al. pediatric astrocytomas with monomorphous pilomyxoid features and a less favorable outcome. j neuropathol exp neurol 1999;58:1061–8. 2.brat dj, scheithauer bw, fuller gn, et al. newly codified glial neoplasms of the 2007 who classification of tumors of the central nervous system: angiocentric glioma, pilomyxoid astrocytoma and pituicytoma. brain pathol 2007;17:319–24. 3.komator rj, mocco j, carson bs, et al. pilomyxoid astrocytoma: a review. med gen med 2004;6:42. 4.komakula st, fenton lz, kleinschmidt-demasters bk, foreman nk: pilomyxoid astrocytoma: neuroimaging with clinicopathologic correlates in 4 cases followed over time. j pediatr hematol oncol 29:465–470, 2007 5.komotar rj, mocco j, jones je, zacharia be, tihan t, feldstein na, et al: pilomyxoid astrocytoma: diagnosis, prognosis, and management. neurosurg focus 18(6a):e7, 2005 6.ge pf, wang hf, qu lm, chen b, fu s, luo y. pilomyxoid astrocytoma in cerebellum .chin j cancer res. 2011 sep;23(3):242-4. 7.ajani oa, al sulaiti g, al bozom i. pilomyxoid astrocytoma of the cerebellum. j neurosurg pediatr. 2011 may;7(5):539-42. 8.forbes ja, mobley bc, o'lynnger tm, cooper cm, ghiassi m, hanif r, pearson mm. pediatric cerebellar pilomyxoid-spectrum astrocytomas. j neurosurg pediatr. 2011 jul;8(1):90-6. 9.morales h, kwock l, castillo m. magnetic resonance imaging and spectroscopy of pilomyxoid astrocytomas: 486 sharma et al cerebellar pilomyxoid astrocytoma case reports and comparison with pilocytic astrocytomas. j comput assist tomogr 2007; 31:682-7. 10.linscott ll, osborn ag, blaser s, et al. pilomyxoid astrocytoma: expanding the imaging spectrum. ajnr am j neuroradiol 2008; 29:1861-6. 11.omura t, nawashiro h, osada h, et al. pilomyxoid astrocytoma of the fourth ventricle in an adult. acta neurochir (wien) 2008; 150:1203-6. 12.buccoliero am, gheri cf, maio v, et al. occipital pilomyxoid astrocytoma in a 14-year-old girl--case report. clin neuropathol 2008; 27:373-7. 13.komotar rj, mocco j, zacharia be, wilson da, kim py, canoll pd, et al: astrocytoma with pilomyxoid features presenting in an adult. neuropathology 26:89– 93, 2006. 14.sajadi a, janzer rc, lu tl, duff jm: pilomyxoid astrocytoma of the spinal cord in an adult. acta neurochir (wien) 150:729–731, 2008 15.omura t, nawashiro h, osada h, shima k, tsuda h, shinsuke. a: pilomyxoid astrocytoma of the fourth ventricle in an adult. acta neurochir (wien) 150:1203– 1206, 2008 16.koeller kk, rushing ej. from the archives of the afip: pilocytic astrocytoma: radiologic-pathologic correlation. radiographics 2004; 24:1693-708 17.arslanoglu a, cirak b, horska a, et al. mr imaging characteristics of pilomyxoid astrocytomas. ajnr am j neuroradiol 2003; 24:1906-8. 18.tsugu h, oshiro s, yanai f, et al. management of pilomyxoid astrocytomas: our experience. anticancer res 2009; 29:919-26. 19.alimohamadi m, bidabadi ms, ayan z, ketabchi e, amirjamshidi a. pilomyxoid astrocytoma with involvement of the sella turcica in an adolescent. j clin neurosci. 2009 dec; 16 (12):1648-9. 19agrawal_letterextensive romanian neurosurgery (2014) xxi 4: 501 – 502 501 letter to the editor: extensive dilatation of third ventricle masking the diagnosis of aqueductal stenosis amit agrawal professor of neurosurgery, department of neurosurgery, mm institute of medical sciences & research, mullana (ambala), india dear sir, in 10% of adult patients with hydrocephalus, the cause is because of aqueductal stenosis (as), causing enlargement of the lateral and third ventricles. (1) 40 year gentleman presented with progressively increasing headache of three weeks duration with off and vomiting and mild relief in headache after vomiting. he had 3-4 episodes of loss of consciousness and it was associated with decerebrate posturing. there were no tonic clonic movements. at the time of presentation to emergency his general and systemic examination was normal. on examination, he was conscious and oriented. his higher mental functions were normal. fundus examination revealed bilateral papilloedema. there were no motor, sensory, or cerebellar signs, and no signs of meningitis. his plain ct scan showed dilated third and lateral ventricles and a hypodense lesion in the posterior third ventricular region (figure 1). a diagnosis of third ventricular tumor with obstructive hydrocephalus was suspected. in view of multiple hydrocephalic episodes he underwent right ventriculo-peritoneal shunt in emergency. he improved in his headache and doing well. he was planned for mri and it showed reduction in the size of the ventricles (figure 2 a-d). mass in the posterior third was disappeared and aqueductal stenosis was apparent. the fourth ventricle was disproportionately small. all these features were suggestive of adult onset aqueductal stenosis. figure 1: ct scan plain axial view showing extensive dilation of lateral and third ventricles and a lesion in the posterior part of third ventricle compressing the upper brain stem 502 agrawal letter to the editor figure 2 a-d post-operative mri of the same patient showing reduction in the size of the ventricles and aqueductal stenosis (a and d) aqueductal stenosis usually manifests in infancy or early adulthood with features suggestive of raised intracranial pressure syndrome. aqueductal stenosis in infancy usually manifests as failure to thrive and/or bulging fontanelle. (2) late onset idiopathic aqueductal stenosis (ias) may become manifest clinically either by headaches or by hydrocephalic symptoms such as gait disturbance, urinary urge, and cognitive impairment. (2) there are currently two alternate forms of surgical treatment for as; shunt surgery and ventriculostomy. shunt surgery is associated with high complication rates and many patients need revisions, but the effectiveness is high. (1, 3) endoscopic surgery is straightforward and effective in appropriately selected cases with obstructive hydrocephalus. (3) endoscopic third ventriculostomy (etv), re-establishing a physiological route of csf dynamics, has become the treatment of choice for as in most neurosurgical centers. etv has fewer complications and revisions are rare, but some patients need shunt surgery to improve despite a patent ventriculostomy. (1, 3) this case illustrates that if the facilities are available investigating these patients with mri would had helped in diagnosing aqueductal stenosis and etv is an effective option in these patients. references 1. tisell m. how should primary aqueductal stenosis in adults be treated? a review. acta neurol scand. 2005; 111(3):145-53. 2. fukuhara t, luciano mg. clinical features of lateonset idiopathic aqueductal stenosis. surg neurol 2001; 55:132-6. 3. choi ju, kim ds, kim sh. endoscopic surgery for obstructive hydrocephalus. yonsei med j. 1999; 40(6):600-7. doi: 10.33962/roneuro-2021-071 giant, primary, hydatid cyst of the gluteal region. case report g. iacob, r. rosiu, mihaela luchian, g. simion romanian neurosurgery (2021) xxxv (4): pp. 417-421 doi: 10.33962/roneuro-2021-071 www.journals.lapub.co.uk/index.php/roneurosurgery giant, primary, hydatid cyst of the gluteal region. case report g. iacob1, r. rosiu2, mihaela luchian2, g. simion3 1 professor of neurosurgery ‘‘carol davila’’ university of medicine and pharmacy, bucharest, romania 2 department of neurosurgery, emergency university hospital, bucharest, romania 3 department of histopathology, emergency university hospital, bucharest, romania abstract background: primary hydatid disease in the muscle is extremely rare, resulting in either the spread of cysts spontaneously or after operations for hydatidosis in distant regions. methods: report of an unusual case of primary hydatid cyst in the gluteus muscle, behaving as enlarging soft-tissue tumour, with a review of the literature. results: magnetic resonance imaging revealed an intramuscular cyst in the gluteus muscle; and no cyst existed in any other location. the cyst was excised totally, and the diagnosis of muscular cystic hydatidosis was confirmed by histopathologic examination. in follow-up of two years after the operation, there has been no recurrence in either patient. conclusion: the involvement of the gluteus maximus muscle without the evidence of hepatic or pulmonary disease is rare, characterized by slow development, but a major local extension must be considered in the differential diagnosis of a cystic mass with well-defined margins in the extremities of individuals from endemic regions. physical examination, serology results and radiological findings should be interpreted with care, especially in hydatid cyst endemic countries. surgery is still the treatment of choice, with total cyst excision. introduction human echinococcosis is a zoonotic disease, caused by ingestion of ova of the cestode echinococcus granulosus (eg) and formation of the larval stage in different organs and tissues. cystic echinococcosis (ce) has become an important burden on human population in endemic area and no endemic countries, by infected people migration and livestock exchange (1). ce is responsible for the loss of 1–3 million disability-adjusted life years per annum and severe economic losses to the livestock industry probably amounts to us$ 2 billion (2). romania was listed in 1995 among the countries with the highest prevalence of ce worldwide. nevertheless, latest study heracles fp7 eu project oct 2013 sept 2018 confirm that ce has a prevalence of 0.41%000 in keywords cystic echinococcosis, primary musculoskeletal location hydatid cyst, gluteal region hydatid cyst corresponding author: iacob gabriel “carol davila” university of medicine and pharmacy romania gbrl_cb@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 418 g. iacob, r. rosiu, mihaela luchian, g. simion romania (3). molecular characterization belonged to the g1-g3 complex (e. granulosus), which contains the most widespread and infective strains of the parasite, also a non-g1-g3 genotype of e. granulosus, likelihood, a g7 genotype, which is often found in pigs and dogs in most countries of eastern and south-eastern europe (4). primary musculoskeletal location hydatid cyst are rare: only 2 to 3%, possibly most affected sites are the neck, thigh and the paravertebral region, the psoas muscle, the thoracic wall muscles, sartorius, and quadriceps muscles. on the gluteal region hydatid cyst are very rare (5-19). clinical, diagnosis and therapeutic considerations are discussed. case presentation a 53 years old woman, seamstress in town, presents to his primary care provider with a 6 months history of lower back pain, stiffness. the pain was intermittent, improves after rest without medication, worse with activity and in the morning when changing the position of the body from supine position to orthostatism, at the effort of coughing, sneezing, defecation, sometimes with right irradiation on the back of the buttocks, thighs, left calves to the heels; but she was able to lean forward. also, the patient has been reporting for about 4 months a painful mass installed insidiously at the right gluteal region, firm consistency, normal skin, which has progressively increased in the last 2 weeks before admission. she does not have any known chronic medical conditions, also she has never smoked, but she does drink an occasional glass of wine with dinner. no significant family history of disease is reported. she has not noted any other masses on his body with self-examination, no history of rash, fever, malaise, anorexia, no weight loss, neither she nor other family members came in contact with pets. upon physical examination, this patient has a blood pressure of 131/75 mm hg and a heart rate of 65 beats/min. his respiratory rate is 7 breaths/min and his temperature is normal at 98°f (36.7°c). his cardiovascular and respiratory findings are normal; specifically, no murmurs or rubs are detected. the patient has no photophobia, eye redness, or decreased visual acuity. upon examination of the back, flexion of the lumbar spine is possible, without limited range of motion with rotation and lateral flexion at the lumbar spine. the right buttock is painful to the touch. on clinical examination we found a painful mass in the posterior lateral region of the upper third of the right thigh, with normal looking skin on top, of firm consistency, 30 cm long axis, 18 transversal axis, fixed to muscle with no evidence of local inflammation. no motor, sensitive deficit or abnormal hip mobility were encountered. the remainder of the physical examination is within normal limits. the biological assessment was unremarkable: it reveals a white blood cell count of 4.6 × 103 cells/μl (reference range, 4.5-11 × 103 cells/μl), a hemoglobin level of 13.7 g/dl (reference range, 13.517.5 g/dl), a hematocrit of 43% (reference range, 41% to 50%), eosinophilic count of 2.8 (reference range, 0.8-8.1 %), a platelet count of 120 × 103 cells/μl (reference range, 150-450 × 103 cells/μl); electrolyte values are within normal limits, only the erythrocyte sedimentation rate was 35 mm/hr (reference range, < 10 mm/h). the diagnosis was made by lumbar and pelvic magnetic resonance (mri) which brought into evidence of lumbar disc protrusions at l2-l5, without root conflict, lumbar vertebral marginal osteophytes; multiple cystic formations, single or partitioned cysts, on the posterior and lateral surfaces of the root of the right thigh and the gluteal region, mainly occupying the gluteus maximus and subaponeurotic fat. they had a thin wall in enhanced t2 hypo-intense after injection of gadolinium with variable signal fluid content, the largest measured 13 x 12 cm (fig.1). a. b. 419 giant, primary, hydatid cyst of the gluteal region c. figure 1. primary, multiple hydatid cysts of the right gluteal region mri, enhanced t2 hypo-intense after injection of gadolinium: a axial section, b & c coronal sections. a total resection under general anesthesia was performed by an extended posterior lateral approach of the thigh. intraoperative finding highlighted a very thick hydatid pericyst with tight adhesion to the gluteus maximus muscle bundles, composed of inflammatory tissue, the hydatid exocyst and the hydatid endocyst with irregularly shaped daughter cysts of different sizes and hydatid fluid. despite our anatomical exposure and delicate dissection of the cyst, a minimal breach with hydatid fluid exteriorization was found. the cyst content was appropriately evacuated and the surgical field was soaked with hypertonic saline (figure 2). a b c d e figure 2. intraoperative pictures: a. general aspect of the hydatid cyst during dissection, b&c several irregularly shaped daughter cysts of different sizes, d the hydatid exocyst, e thick hydatid pericyst with tight adhesion to the gluteus maximus muscle bundles completely dissected. a c a c b b a b a b a figure 3. the histopathologic examination in our case: a h.e col. obj. 20 x 10, a. the inner germinal layer, b. protoscolices, c. the middle-laminated membrane; 420 g. iacob, r. rosiu, mihaela luchian, g. simion b h.e col. obj. 20 x 20, a. protoscolices, b. the inner germinal layer, c. the middle-laminated membrane; c h.e col. obj. 20 x 20, a. the middle-laminated membrane, b. the inner germinal layer, c. daughter vesicle, attached by a pedicle to the germinal layer; d h.e col. obj. 20 x 10, a. the middle-laminated membrane, b. the inner germinal layer. the serology was positive for e.g., and the extension assessment: cerebral mri, pulmonary and abdominal ct were normal. the histopathologic examination (figure 3) confirmed the diagnosis of hydatid cyst. results the post-operative evolution was uneventful. the patient had completed a chemotherapy with an antihelminthic agent albendazole (zentel) 15 mg / kg /day, for the next 3 months postoperatively; 6 months after, there was no evidence of recurrence or complications. discussion hydatid cysts result from infection by the echinococcus tapeworm species and can result in cyst formation anywhere in the body. typically, the primary cyst locations hydatid are the liver and lungs. this can be explained by the significant vascularization of these structures that can be filters. rarely, the hydatid cyst occurs at the musculoskeletal tissues, with slow and relatively asymptomatic evolution, without hepatic involvement, as in our case. primary hydatid disease in the muscle is extremely rare, resulting either from the spread of cysts spontaneously or after operations for hydatidosis in distant regions.the most reported sites are the neck, thigh and the paravertebral region, very rare at the gluteal region (5-7)(10-20). in general recognition of hydatid disease is possible, sometimes even when serologic tests had been non-conclusive (9). in endemic areas the etiological diagnosis of the cyst can be difficult in some cases. accurate diagnosis could be made using pelvic radiograph, the usg exam, the first-line radiological examination in our case could have highlighted multiple hydatid cysts, within the stage 2 – septated cystic lesion and stage 3 cystic lesion with the daughter lesion, see the gharbi ultrasound classification (9). ct scan rarely shows typical characteristics of the hydatid cyst, possible wall calcifications, other hydatid cyst localizations and mri – the reference examination as in our case is useful, especially in the case of giant cysts, assessing the size of the mass, relationships with neighboring tissues and nervous and vascular structures (8), recognizing complications (e.g., rupture, infection of cysts)(6), correlated to macroscopic and microscopic pathology (20). also mri should be considered for differential diagnosis between slow-growing tumors, hematomas, myositis, and abscesses (19). total cyst excision is the primary treatment method, avoiding in suspected hydatid cysts biopsy and aspiration to prevent rupture and spread (8)(14)(20). in case of the hydatid cyst rupture hypertonic saline irrigation of the surgical field is the best method to prevent recurrences by antigens spreads to the muscles, inflammatory reaction complicated by a secondary bacterial infection (6)(20). as a particularity of the presented case there was a concomitant lesion generated by lumbar protrusions with right root irritation phenomena and buttock hydatid cyst. conclusions the involvement of the gluteus maximus muscle without the evidence of hepatic or pulmonary disease is quite rare, characterized by a slow development, but a major local extension must be considered in the differential diagnosis of a cystic mass with well-defined margins in the extremities of individuals from endemic regions. physical examination, serology results and radiological findings should be interpreted with care, especially in endemic areas. surgery is still the treatment of choice, with total cyst excision, followed by chemotherapy with an anti-helminthic agent. abbreviations echinococcus granulosus (eg) cystic echinococcosis (ce) ultrasonography (usg) tomograph computer (ct) magnetic nuclear resonance (mri) conflicts of interest there are no conflicts of interest. references 1. mamuti w., yamasaki h., et al. usefulness of hydatid cyst fluid of echinococcus granulosus developed in mice 421 giant, primary, hydatid cyst of the gluteal region with secondary infection for serodiagnosis of cystic echinococcosis in humans, clinical and diagnostic laboratory immunology 2002, 9, 3, 573–576. 2. torgerson p.r., craig p. “updated global burden of cystic and alveolar echinococcosis,” report of the who informal working group on cystic and alveolar echinococcosis surveillance, prevention and control, with the participation of the food and agriculture organization of the united nations and the world organisation for animal health, department of control of neglected tropical diseases who, geneva, switzerland, 2011. 3. cretu c.m., banu t. et al. – situation of cystic echinococcosis in humans and animals: a real alarming concern. heracles fp7 eu project oct 2013sept 2018. 4. piccoli l., bazzocchi c. et al. molecular characterization of echinococcus granulosus in southeastern romania: evidence of g1–g3 and g6–g10 complexes in humans, clinical microbiology and infection 2013, 19(6):578-582. 5. lamine a, fikry t, et al. primary hydatidosis of the peripheral muscles: 7 case reports. acta orthop belg. 1993;59(2):184-188. 6. aloui.y, saadana .j, et al.kyste hydatique géant de la région glutéale : a propos d’un cas, stpi & spilf congress 9-11.09.2021, www.infectiologie.org.tn. 7. jerbi o.s, abid f. et al. primary hydatid disease of the thigh: a rare location. orthop traumatol surg res. 2010;96(1):90-93. 8. von sinner wn. new diagnostic signs in hydatid disease; radiography, ultrasound, ct and mri correlated to pathology. eur j. radiol. 1991; 12 (2): 150-159. 9. stojkovic m, rosenberger k, et al. diagnosing and staging of cystic echinococcosis: how do ct and mri perform in comparison to ultrasound. plos negl too say, 2012; 6 (10): e1880. 10. haque f., harris s.h. et al. primary hydatidosis of gluteus maximus, j postgrad med 2006;52(4):300-301. 11. ates m., karakaplan m. hydatid cyst in the biceps and gluteus muscles: case report, surgical infections, 2007, 8.4.20. 12. kaplan m., aktoz t. et al. atypical renal and gluteal hydatid cysts: report of two cases, fırat tıp. dergisi 2009;14(4): 297-299. 13. eryilmaz ma, eroglu c, et al. gluteal hydatid cyst: case report. turkiye klinikleri j med sci. 2010;30:1380–1383. 14. mushtaque m., mohammad f. mir et al. solitary subcutaneous gluteal hydatid cyst: a case report, eastern journal of medicine 2010, 15, 2010, 76-79. 15. zeren s, kesici u, et al. gluteal hydatid cyst: report of a case. acta med iran, 2015;53(6):389–391. 16. aksakal n., kement m., et al unusually located primary hydatid cysts, ulus cerrahi derg. 2016; 32(2): 130–133. 17. hona bn, emami y.f. gluteal hydatid cyst: report of a case from iran, iran j parasitol 2017;12(2):305–308. 18. seyedsadeghi m. ghobadi j. t al. gluteal hydatid cyst: a case report, iran j parasitol 2019;14(3):487491. 19. şimşek s. hattapoğlu s. intramuscular hydatid cyst in the lower extremity: report of three cases, revista da sociedade brasileira de medicina tropical, 2021, 54 | (e0255-2021). 20. rabhi s., saadana j. et al. primary giant hydatid cysts of the thigh and the gluteal region: a case report. pan afr med j 2021, 5, 39:15, ecollection 2021. munteanuv_differential romanian neurosurgery (2016) xxx 2: 195-199 | 195 differential diagnostic problems in elderly chronic subdural hematoma patients valentin munteanu1, ionut luca-husti2, teodora camelia coman1, alexandru vlad ciurea2,3 1“bagdasar arseni” emergency hospital, bucharest 2sanador clinical hospital, bucharest 3“carol davila” university of medicine and pharmacy, bucharest abstract: chronic subdural hematomas (csdh) are recognized as common in older people (over 70 years). they are produced in minor injuries (falls on the same level). these csdh have minor symptoms (headache, memory disorders, balance disorders, cognitive disorders, etc. and are classified as signs for the onset of dementia, circulatory failure basilar vertebra, alzheimer, etc. a simple brain ct scan can highlight these hematomas and a neurosurgical intervention will achieve extremely favorable prognosis. there are many pitfalls in the differential diagnosis of csh especially with strokes being so common at this age. key words: chronic subdural hematoma, older patients, ct scan, gcs, gos, and neurosurgery introduction diseases with surgical recommendation in elderly patients, especially for those over 70 years old, involve significant risks both surgically and anesthetically, given the associated rich pathological context, as well as a very likely reduction in the body`s available capability to recover after as a resourceconsuming event, as surgery. the most common diseases of the elderly are obvious and indisputable, cardiovascular diseases accompanied by disorders of lipid metabolism with formation of atheroma plaques, leading most often to ictal neurological pathology like the hemorrhagic or ischemic strokes. in neurovascular pathology, the transitory ischemic stroke is an event that foresees severe lesions with permanent effects that can present itself later on. these considerations determine a more aggressive therapeutic approach from the neurological medical community in order to prevent events with significant consequences. in the case of neurosurgical pathology of these patients an important place is occupied by the chronic subdural hematoma. the main 196 | munteanu et al elderly chronic subdural hematoma etiological factor in the occurrence of subdural hematic collections is obviously the traumatic brain injury, but in the case of chronic subdural hematoma the traumatic factor is often unrecognized by patients or persons around them. the reason is that the traumatic event has taken place usually far away from the moment of the deceleration of the collection (usually at least 3 weeks) and the trauma is usually minor and overlooked immediately after production. the reasons favoring this particular type of intracranial fluid accumulation are related on one hand to the age-related involution of the brain parenchyma with subsequent atrophy and increased peri-cerebral spaces and on the other hand the long-term use of antithrombotic medication such as aspirin or other anticoagulants in the context of very likely associated cardiovascular diseases, which implies a more difficult hemostasis in case of any lesion in the “bridging” dural veins tensed the by reduction of the volume of the cerebral parenchyma. the most commonly used diagnostic method is computed tomography imaging which brings enough information to establish a diagnosis and a suitable treatment plan. chronic subdural hematomas occur classically under the form of a crescent hypo-dense collections located extra axially with mass effect on the adjacent brain parenchyma. depending on the time elapsed from the initial bleeding until the diagnosis the images can be different in relation to the adjacent parenchyma. this describes three phases of evolution: the first 7 days of collection has a hyper-dense appearance corresponding to the acute phase of bleeding, then for approx. 2 weeks iso-dense collection compared to the brain parenchyma, followed only after the third week of evolution to be described as having the classical hypo-dense fluid accumulation. thus between the first and third week of chronic subdural hematoma bilateral evolution can be very difficult to see on the native ct imaging, especially because the midline structures might not be deflected in this case. clinical symptoms that determines the patient to go to the doctor is nonspecific and often installs in an insidious way, some patients have minor symptoms. patients may complain of impaired consciousness with sleepiness, which is associated in varying proportions with headache, walk and balance disorders, cognitive disorders, personality changes or motor deficit or aphasia. often the onset symptoms are super-imposable on a clinical picture of transient ischemic stroke. the most common symptoms are headache, confusion syndrome and various degrees of neurological motor deficit. accordingly, when the ct imaging reveals iso-dense subdural collection hardly distinguishable from the brain parenchyma and it will not cause a significant mass effect, the differential diagnosis of minor neurological disorders and transient becomes difficult. within the neurological therapeutics the administration of anticoagulant and antiplatelet medication is very important in the prevention of acute ischemic events. a major disadvantage of taking this type of medication is that it predisposes to bleeding complications if the patients must undergo major surgery. romanian neurosurgery (2016) xxx 2: 195-199 | 197 the latter must be timed according to the medication administered, for varying time intervals that can reach up to several days. these delays in adopting surgical treatment solutions may have important consequences for the affected patients. on the other hand the administration of anticoagulant and antiplatelet therapy may increase the volume of intracranial hematic collections with the worsening of the accompanying neurological phenomena. material: case presentation in the following we want to present the case of a 72 years old patient with known hypertension in treatment, accusing short speech disorder episodes of “verbal barrage”, which were resolved at a minimum diuretic therapy, the allegations were recorded for approx. 2 weeks. the medical history revealed the existence of a head injury secondary to an accident, approx. 1.5 months prior to the installation of the symptoms. the injury was considered minor, followed by easy and fast reversible alteration of consciousness immediately posttraumatic with no obvious cranial trauma signs. the patient initially addressed the service of neurology, where the patient`s complaints were interpreted as the manifestation of transient ischemic strokes and was prescribed anti-platelet treatment with plavix. it is worth noting that the neurological consult ran a cerebral ct scan showing a subdural collection in the left cerebral hemisphere, without an obvious compressive character and was not considered to be an important factor of the symptom (figure 1). figure 1 – a.m. – ct aspect at admission given the absence of a favorable response to therapy by repeating the symptoms present at admission, the neurologist guided the patient to get a neurosurgical consult. after analyzing the ct imaging presented by the patient it is decided to adoption of a surgical therapeutic solution to evacuate the visualized collection. considering the introduction of treatment with plavix earlier, the surgical therapeutic solution, even if it involves a minimally invasive approach has high risks in terms of bleeding. for this reason it was decided to stop the plavix treatment for at least 7 days before surgery and replaced with low molecular weight heparin with clinical supervision to highlight any worsening of neurological status of the patient. surgery was performed safely, 7 days after discontinuation of anti-platelet medication, evacuating the collection through two drill holes and abundantly irrigating the subdural space (figure 2). 198 | munteanu et al elderly chronic subdural hematoma figure 2 – a.m. – ct native aspect 24 hours post operatory post operatory, given the associated pathology of the patient, she was monitored within the first 24 hours in the intensive care unit. the evolution was favorable with the relief of the neurological symptoms without repeating the episodes of verbal barrage. we can say that surgery was postponed with more than two weeks from the moment of the first consultation with the intention to minimize the potential irrigative effect of the ct visualizations – even though a little compressive corroborated with a possible „illusion” of the symptomatologycal interpretation seen through “the lens” of the known pathology treated as it currently is. this case had, fortunately, a very favorable evolution, with restoration of the optimal neurological functionality. however, by adopting – for a longer time period – of the wrong therapeutic attitude, it could have evolved towards severe neurological deficits. (figure 3). figure 3 – 3 days after surgery, patient discharged discussion chronic subdural hematoma (csdh) is one of the major co-morbidities in elderly resulting in disability and death. early recognition of csdh is important for early management. however, manifestations of csdh are nonspecific and subtle (8, 9). mixed density of csdh on radiological investigations results from multiple episodes of trauma, usually in the aged. although there were membranes within the mixed density hematomas, burr-holes were usually enough to drain the hematomas (6). surgical evacuation is the basis of management for symptomatic patients or hematomas exerting significant mass effect. although burr whole craniotomy is the most widely practiced technique worldwide, approximately 10-20% of surgically treated patients experience postoperative recurrence necessitating reoperation (2). recurrence rates romanian neurosurgery (2016) xxx 2: 195-199 | 199 in single and double-burr-hole groups were 6.15% and 4.83% respectively, which was not statistically significant. most of the subdural hematomas can be dealt by single burr-hole drainage (4). trepanation may be superior to craniotomy as primary surgery for sub-acute and chronic hematomas (1). a study on 45 patients 70 years of age or older relives that there was a significant improvement in the neurological status of patients from admission to follow up as assessed using the markwalder grading scale, yet no improvement in functional outcome was observed as assessed by glasgow outcome score (3). surgery for csdh is safe and positively recommended even in super-aged patients over 90 years old if the patient's physical status is fair. pre-illness status is the most important factor for considering operative indications and represents a limiting factor for postoperative outcomes in this age population (7). results of a new study on patients with anti-platelet therapy (recurrence occurred 8.9%, one of the lowest rates in the literature) relives the safety of early surgery for patients on the preoperative anti-platelet therapy without drug cessation or platelet infusion. patients with a previous history of infarction may need to be closely followed regardless of anti-platelet or anticoagulant therapy (5). conclusions we believe that the presence of pericerebral fluid collections which indicate the presence of a chronic subdural hematoma in the cranial-cerebral imaging investigations, should lead to the advice and guidance of the patients to a neurosurgical therapeutic attitude, prior to the initiation of therapy with anticoagulant or anti-platelet visa which may worsen the neurological status of the patients through the potential effect of augmentation of the collection by recurrent bleeding and difficult self-limiting of the bleeding. correspondence prof. dr. a.v. ciurea e-mail: prof.avciurea@gmail.com references 1. godlewski b, pawelczyk a, pawelczyk t, ceranowicz k, wojdyn m, radek m. retrospective analysis of operative treatment of a series of 100 patients with subdural hematoma. neurol med chir (tokyo). 2013;53(1):26-33. 2. kolias ag, chari a, santarius t, hutchinson pj. chronic subdural haematoma: modern management and emerging therapies. nat rev neurol. 2014 oct;10(10):570-8 3. mulligan p, raore b, liu s, olson jj. neurological and functional outcomes of subdural hematoma evacuation in patients over 70 years of age. j neurosci rural pract. 2013 jul;4(3):250-6 4. nayil k, altaf r, shoaib y, wani a, laharwal m, zahoor a. chronic subdural hematomas: single or double burr hole-results of a randomized study. turk neurosurg. 2014;24(2):246-8 5. okano a, oya s, fujisawa n, tsuchiya t, indo m, nakamura t, chang hs, matsui t. analysis of risk factors for chronic subdural haematoma recurrence after burr hole surgery: optimal management of patients on antiplatelet therapy. br j neurosurg. 2014 apr;28(2):204-8. 6. park hr, lee ks, shim jj, yoon sm, bae hg, doh jw. multiple densities of the chronic subdural hematoma in ct scans. j korean neurosurg soc. 2013 jul;54(1):38-41. 7. tabuchi s, kadowaki m. chronic subdural hematoma in patients over 90 years old in a super-aged society. j clin med res. 2014 oct;6(5):379-83. 8. teale ea, iliffe s, young jb. subdural haematoma in the elderly. bmj. 2014 mar 11;348:g1682 9. tseng jh, tseng my, liu aj, lin wh, hu hy, hsiao sh. risk factors for chronic subdural hematoma after a minor head injury in the elderly: a population-based study. biomed res int. 2014;2014:218646 sharmamukesh_intracranial 136 sharma et al intracranial arachnoid cyst intracranial arachnoid cyst: an institutional experience mukesh sharma, r.s. mittal, rajeev bansal, achal sharma department of neurosurgery,s.m.s. medical college and hospitals jaipur rajasthan (india) abstract: aim: in this study, symptoms at presentation, indication for surgery, surgical treatment modalities, postoperative results and complications were studied. material and methods: we retrospectively compiled the details of patients with iac from admission and operative records admitted through our opd during the period between january 1995 and january 2015. only those patients were admitted whose symptoms attributes to the cyst and asymptomatic patients were followed on opd basis. this is a single institutional study. results: this study includes 56 patients of iac who were operated. posterior fossa cysts (62.5%) were found more commonly symptomatic. headache (32%) was the most common symptom in a patient with iac. out of all, 24 patients presented with headache and underwent surgery subsequently; 20 showed satisfactory relief after surgery while four showed partial relief. size of cyst was significantly reduced after surgery in 52 patients after 12 weeks but four patients, who underwent cystoperitoneal shunt, required re-operation as patients showed no decrease in size of cyst due to shunt malfunction. head circumference was reduced following intervention in infant patients. three patients who presented with visual field defects with iac in sellar region showed improvement after endoscopic fenestration of cyst. one of the patient with cerebellopontine angle arachnoid was died immediately after marsupialization due to unexplained bleeding. conclusions: iac is not an uncommon finding on imaging but only few are symptomatic. patients with intracranial arachnoid cyst should be treated only if the patient’s symptoms are attributable to the cyst. key words: intracranial arachnoid cysts, cerebellopontine angle, neuroendoscopy, cystoperitoneal introduction intracranial arachnoid cysts (iac) are benign cystic lesions containing cerebrospinal fluid (csf) like material and are enclosed in arachnoid like membrane. the origin of arachnoid cyst is probably developmental in origin and these lesions become symptomatic either due to their progressive enlargement or due to haemorrhage into the cyst. with the increasing use of mri and ct, there has been a corresponding increase in the number of incidentally diagnosed arachnoid cysts. romanian neurosurgery (2016) xxx 1: 136 142 137 as per study done by wajd n. al-holou et al, the prevalence of arachnoid cyst in children was found to be 2.6 percent and in adults 1.4 percent. (1, 2) our study is a retrospective study and reports our experience with 56 patients of iac who underwent surgery. as patients of iac can be symptomatic or asymptomatic, asymptomatic patients are followed while symptomatic ones are evaluated so that it can be assured whether the symptoms are related with the cyst. as for instance delayed milestones, headache and hydrocephalus in children can be due to multiple others reasons also. so children were evaluated and investigated accordingly prior to surgery. for each patient we collected information regarding age, sex, symptoms at presentation, indication for imaging, location of intracranial arachnoid cyst and treatment modality used and outcome of patients. iac were considered symptomatic only if the patient’s symptoms are attributable to the cyst and only symptomatic patients were treated either by craniotomy, endoscopic or cystoperitoneal shunting. material and methods we retrospectively compiled the details of patients with iac from admission and operative records admitted through our opd during the period between january 1995 and january 2015. a detailed history of all patients of iac who attended opd whether newly registered or referred from other specialities taken. only those patients were admitted whose symptoms attributes to the cyst and asymptomatic patients were followed on opd basis. symptomatic cysts were operated. data was collected for age, sex, symptoms, location, and type of surgery. the follow-up period was 12 weeks. the aim of our study was to evaluate the symptoms at presentation, location of the iac, indications for surgery, surgical treatment modalities, postoperative results and postoperative complications. this is a single institutional study. results this study includes 56 patients of iac who were operated during the period between january 1995 and january 2015. out of 56, seventeen (30.36%) were adult males, 12(21.43%) adult females, 16(28.57%) males<18years of age and 11(19.64%) females<18 years of age. posterior fossa cysts (62.5%) were found more commonly symptomatic as shown in table 1. headache (32%) was the most common symptom in a patient with iac as shown in table 2. out of all, 24 patients presented with headache and underwent surgery; 20 showed satisfactory relief after surgery while four showed partial relief. size of cyst was significantly reduced after surgery in 52 patients after 12 weeks but four patients, who underwent cystoperitoneal shunt, required re-operation as patients showed no decrease in size of cyst due to shunt malfunction. seizure control was noted in all four patients who presented with seizures. however, it is unclear whether it is due to surgery or antiepileptic prescribed postoperatively. head circumference was reduced following intervention in infant patients. three patients who presented with visual field defects with iac in sellar region showed improvement after endoscopic fenestration of cyst. 138 sharma et al intracranial arachnoid cyst one patient having cyst in right cerebellopontine angle with acoustic neuroma presented with sensorineural hearing loss and facial palsy, in which facial palsy was improved after excision of cyst and acoustic neuroma. craniotomy for iac was done in 31 patients as shown in table 3. the surgery was fenestration, marsupialisation (figure 1), excision of cyst, cystoventriculostomy or cystocisternostomy. endoscopic procedure was done in 14 patients. four patients with sylvian fissure cyst, four patients with third ventricular region cyst (figure 2), three patients with suprasellar region cyst, and two cases of infratentorial cyst underwent it. endoscopic fenestration of iac in carotid-optico cistern and suprasellar cistern was done successfully for bilateral frontotemporal iac. cystoperitoneal shunting was done in 11 patients by using low pressure shunt (figure 3). six patient with supratentorial iac and five patients with infratentorial arachnoid cysts were shunted. table i distribution of cysts according to location table ii clinical features of different iacs table iii types of surgery figure 1a pre-operative ct brain of 60 year old female having left cerebellopontine angle arachnoid cyst presented with headache and gait disturbances. figure 1b ct brain of post-marsupialisation of arachnoid cyst showing reduction in size and craniectomy defect romanian neurosurgery (2016) xxx 1: 136 142 139 figure 2a pre-operative ct brain of 3 months male having third ventricle arachnoid cyst presented with vomiting and delayed milestones. figure 2b ct brain of post-endoscopic fenestration of third ventricle cyst with reduction in size seen after four weeks figure 3a pre-operative ct brain of 8 years female having suprasellar arachnoid cyst presented with vomiting, headache and diminution of vision. figure 3b ct brain of post-cystoperitoneal shunt showing reduction in size of suprasellar arachnoid cyst surgical treatment of arachnoid cysts results in complications in eight patients. one patient had csf leak which was controlled by conservative means. one patient developed wound infection which was treated with higher antibiotics. one patient developed subdural hygroma but fortunately it posed no problem in the patient. four patients developed shunt malfunction. in one patient shunt reposition was done in cyst and in another one ventriculoperitoneal shunt was done. in rest two patients marsupialisation of cyst was done successfully and shunt was removed. one of the patients with cerebellopontine angle arachnoid was died immediately after marsupialization due to unexplained bleeding. discussion arachnoid cysts are benign cystic lesions containing cerebrospinal fluid. the increasing use of intracranial imaging especially mri, has led to more frequent diagnosis of arachnoid cysts. (6, 13) as per study done by wajd n. alholou et al, the prevalence of arachnoid cyst in children was found to be 2.6% and in adults 1.4%. (1, 2) cysts in posterior fossa, quadrigeminal cistern and suprasellar cisterns were frequently symptomatic. majority of arachnoid cysts are asymptomatic and not all growing cysts may be symptomatic. (14) the intracranial arachnoid cyst can be asymptomatic or can present with symptoms depending on the location of cyst. however there are no guidelines regarding the operative indication or the best treatment modality or choice of surgery. patients can present with headache, seizures, gait disturbances, cognitive decline, focal neurologic deficits, cranial nerve palsy, visual disturbances, and increase in head circumference. the sign and symptoms depend on the location and size of cyst. iac can be supratentorial or infratentorial. in supratentorial region cyst can be in sylvian fissure, cerebral convexity, sellar or suprasellar, interhemispheric or quadrigeminal. in infratentorial region cyst can be in posterior midline, clival, 140 sharma et al intracranial arachnoid cyst cerebellopontine angle, vermis or in cistern magna. neurosurgeons agree that patients with iac with symptoms of intracranial hypertension, intractable seizures, and focal neurologic deficits warrant surgical management. (9) in patients with symptomatic arachnoid cysts, treatment may lead to lasting relief of focal neurological deficits. (4, 20) seizures and headaches, however, often persist despite adequate surgical treatment of the cyst, (15) as illustrated by the results of some studies but in our study seizures and headache were relieved following surgery. given the difficulty in properly identifying which cysts are symptomatic and the potential for surgical morbidity, further definition of treatment indications would be helpful. the operative indication for iac depends on signs and symptoms, site of cyst, size of cyst, features of raised intracranial pressure, and measurement of icp. the choice of surgery depends on the age of patient, the distance between the lesion and the neighbouring ventricle or cistern, presence of hydrocephalus, mass effect caused by cyst, relation with surrounding structures. surgical options available are open craniotomy for cyst removal or fenestration into adjacent arachnoid spaces, shunting or stenting of cyst contents into ventricle, endoscopic fenestration or cystoperitoneal shunt operation. (18) although any surgical technique to treat an arachnoid cyst may result in complication, the preference for any given surgical technique over another has been debated. (12, 15) among surgical options, primary endoscopic fenestration appears to be an ideal procedure. as the target membranes are avascular, csf provides optimal image transmission and the method of fenestration is familiar to those performing neuroendoscopy. (11) in our study, the principal of surgery was fenestration, marsupialisation, excision of cyst, cystoventriculostomy or cystocisternostomy, either by craniotomy or by endoscopy. cystoperitoneal shunting was also done in some cases. the results of our study of either endoscopy or craniotomy were similar but the endoscopic approach had advantage, as procedure was minimally invasive, associated with less bleeding and early recovery. cystoperitoneal shunting was effective for large cysts, particularly by using the low pressure shunt. however, recurrence of the cyst was noted and shunt related complications were also seen, thus cystoperitoneal shunting should not be the first choice as per our view. surgical treatment of arachnoid cysts may occasionally result in complications, including pseudomeningocele and csf leak, (15) wound related complications, (12, 15, 16) infection, (15) subdural hygroma, (15, 16) subdural hematoma (12, 16) seizure, (15) redo surgery (12, 15) and the risk of shunt dependency and its overdrainage. (17) johnson et al. (10) found that endoscopic treatment of middle cranial fossa arachnoid cysts resulted in subdural hygromas and subdural hematomas in 9% and 5% of cases, respectively. but only single patient in our study developed subdural hygroma during the romanian neurosurgery (2016) xxx 1: 136 142 141 follow-up. haemorrhage into the subdural space or into the arachnoid cyst has been reported in patients with arachnoid cysts. (3, 5, 19) the potential for haemorrhage has been used as a justification for prophylactic treatment of asymptomatic arachnoid cysts by some authors. (19) it is a rare event and not even a single patient in the natural history group experienced a haemorrhage, haemorrhages associated with arachnoid cysts have been reported in the literature are associated with generally good outcomes (19) and surgery may not eliminate the risk of future haemorrhage in these patients. (14, 21) we do not regard the potential for future haemorrhage as a justification for prophylactic surgical treatment. but if the patient presented with haemorrhage in cyst, surgical treatment was done. three patients (4%) presented with posttraumatic haemorrhage in cyst in our study. the cysts should be treated if they demonstrate evidence of local mass effect on imaging (7, 8) we do recommend surgery for cysts when there is an appearance of mass effect seen on imaging. conclusion arachnoid cysts are frequently discovered incidentally on intracranial imaging. most arachnoid cysts are asymptomatic. patients with intracranial arachnoid cyst should be treated only if the patient’s symptoms are attributable to the cyst. modality of surgery doesn’t create any difference in the outcome, though endoscopy has the advantage of minimal invasiveness. correspondence dr. mukesh sharma department of neurosurgery, s.m.s. medical college and hospitals jaipur rajasthan (india) 302004 telephone no. 91-9672209314 email: dr_mukki@yahoo.co.in references 1. al holou wn, yew ay, boomsaad ze, garton hj, muraszko km, maher co. prevalence and natural history of arachnoid cysts in children. j neurosurg pediatr 5 :578 85, 2010 2. al-holou wn, terman s, kilburg c, garton hj, muraszko km, maher co. prevalence and natural history of arachnoid cysts in adults. j neurosurg 118:22231, 2013 3. bilginer b, onal mb, oguz kk, akalan n: arachnoid cyst associated with subdural hematoma: report of three cases and review of the literature. childs nerv syst 25:119–124, 2009 4. boutarbouch m, el ouahabi a, rifi l, arkha y, derraz s, el khamlichi a: management of intracranial arachnoid cysts: institutional experience with initial 32 cases and review of the literature. clin neurol neurosurg 110:1–7, 2008 5. domenicucci m, russo n, giugni e, pierallini a: relationship between supratentorial arachnoid cyst and chronic subdural hematoma: neuroradiological evidence and surgical treatment. clinical article. j neurosurg 110:1250–1255, 2009 6. eskandary h, sabba m, khajehpour f, eskandari m: incidental findings in brain computed tomography scans of 3000 head trauma patients. surg neurol 63(6):550-3, 2005 7. go kg, houthoff hj, blaauw eh, havinga p, hartsuiker j: arachnoid cysts of the sylvian fissure. evidence of fluid secretion. j neurosurg 60:803–813, 1984 8. harsh gr iv, edwards ms, wilson cb: intracranial arachnoid cysts in children. j neurosurg 64:835–842, 1986 9. hellwig d, schulte m, tirakotai w. surgical management of arachnoid, suprasellar, and rathke’s cleft cysts. in: schmidek hh, roberts dw, editors. schmidek and sweet operative neurosurgical techniques. 5th ed., vol. 1. philadelphia: saunders elsevier; 2006. p. 455 76. 142 sharma et al intracranial arachnoid cyst 10. johnson rd, chapman s, bojanic s: endoscopic fenestration of middle cranial fossa arachnoid cysts: does size matter? j clin neurosci 18:607–612, 2011 11. kandasamy j, souweidane m. editorial: arachnoid cysts. j neurosurg pediatr 9:228‑30, 2012 12. kang jk, lee ks, lee iw, jeun ss, son bc, jung ck, et al: shunt-independent surgical treatment of middle cranial fossa arachnoid cysts in children. childs nerv syst 16:111–116, 2000 13. katzman gl, dagher ap, patronas nj: incidental findings on brain magnetic resonance imaging from 1000 asymptomatic volunteers. jama 282:36–39, 1999 14. lee jy, kim jw, phi jh, kim sk, cho bk, wang kc. enlarging arachnoid cyst: a false alarm in infants. childs nerv syst 28:1203 11, 2012 15. levy ml, wang m, aryan he, yoo k, meltzer h: microsurgical keyhole approach for middle fossa arachnoid cyst fenestration. neurosurgery 53:1138–1145, 2003 16. marin-sanabria ea, yamamoto h, nagashima t, kohmura e: evaluation of the management of arachnoid cyst of the posterior fossa in pediatric population: experience over 27 years. childs nerv syst 23(5):535-42, 2007 17. martínez-lage jf, ruíz-espejo am, almagro mj, alfaro r, felipe-murcia m, lópez-guerrero al: csf overdrainage in shunted intracranial arachnoid cysts: a series and review. childs nerv syst 25:1061–1069, 2009 18. oertel jm, wagner w, mondorf y, baldauf j, schroeder hw, gaab mr. endoscopic treatment of arachnoid cysts: a detailed account of surgical techniques and results. neurosurgery 67:824 36, 2010 19. parsch cs, krauss j, hofmann e, meixensberger j, roosen k: arachnoid cysts associated with subdural hematomas and hygromas: analysis of 16 cases, long-term follow-up, and review of the literature. neurosurgery 40:483–490, 1997 20. shim kw, lee yh, park ek, park ys, choi ju, kim ds: treatment option for arachnoid cysts. childs nerv syst 25 : 1459–1466, 2009 21. spacca b, kandasamy j, mallucci cl, genitori l: endoscopic treatment of middle fossa arachnoid cysts: a series of 40 patients treated endoscopically in two centres. childs nerv syst 26:163–172, 2010 chiriaca_ourexperience romanian neurosurgery (2016) xxx 1: 41 46 41 our first experience with cervical expandable cage for vertebral body reconstruction a. chiriac, z. faiyad1, c. popescu1, b. costachescu, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: vertebral body reconstruction after corpectomy using expandable cage has become a common surgical procedure especially at thoracic level. the recent published papers describe the successful use of expandable cages for cervical vertebral body reconstruction. in this paper we present our first experience with expandable cervical cage in the reconstruction of the cervical spine in a patient with cervical spondylotic myelopathy (csm) key words: corpectomy, expandable cage introduction cervical spine corpectomy is a frequent surgery in various pathological situations such as progressive degenerative process, spinal metastasis, infection, and trauma. the surgical procedure for anterior column reconstruction due to spinal instability, neurological deterioration, or failure of non-operative treatment was represented for a long period of time by using autogenous bone grafts such as iliac crest graft. also, pseudoarthrosis, donorsite morbidity, fatigue failure, graft subsidence and graft dislodgement are very well documented complications in the literature for the use of bone graft in spinal fusion. a solution for these issues was the developing of the first implant systems types for vertebral reconstruction to ensure goals of stability, axial load-bearing resistance, large interbodybone interface, sagittal alignment and height restore. although these titanium mesh cages have proved its usefulness some technical problems have been encountered in regards to optimal placement of a nonexpandable spacer. the exact matching of the implant into the corpectomy defect is often difficult because of predefined endplate angle and height of cage. if the need for a mechanical adjustment by cutting the cage is required correct rotation during placement must be ensured due to risks of implant tilting and finally of construct failure. in addition, the need of cage removal due to intraoperative displacement of the implant usually results in a severe deterioration of the vertebral end-plate integrity. in an attempt to overcome the 42 chiriac et al cervical expandable cage for vertebral body reconstruction technical problems of nonexpandable cages, various expandable cages have been developed. these devices offer the advantage of in situ height adjustment and opportunity for kyphosis correction. in the present study we report our first experience with a cervical expandable titanium cage for vertebral body reconstruction from ulrich medical, ulm, germany. implant characteristics the anterior distraction device (add) (ulrich medical, ulm, germany) is an implant made of titanium alloy (tial6v4). it is used for reconstructing the anterior column of the cervical and upper thoracic spine from c3 to t3 after complete or incomplete corpectomy. add is available in 3 outer diameters (12, 14, and 16 mm) with 0-degree (or 6-degree) fixed angulation of the cranial end piece and 0degree fixed angulation of the caudal end piece. the small central cavity can be filled with bone. an expansion instrument is inserted into a bore of the distraction ring, and the cage is distracted by counterclockwise rotation of the ring. the distraction ranges extend from 10 to 13 mm to 39 to 65 mm. a central screw is used to unlock the device to the desired size. additional anterior plating is necessary (figure 1) (5, 9). history and examination a 53-years-old male patient who suffered from five months by bilateral cervicobrachialgia had addressed to our emergency department for a progressive cervical myelopathy syndrome with numbness and weakness predominantly to left arm. he suffered from this progressive neurological deficit for four weeks and the modified joa score was 12 (moderate myelopathy) at admission (4). imaging plain radiographs and mri (figure 2) of the cervical spine revealed a c5c7 ossification of the posterior longitudinal ligament (opll), c5-c6 and c6-c7 median disc protrusion. the images revealed also a median subsidence of c6 vertebral with inflammatory reaction. figure 1 add anterior distraction device from ulrich medical, ulm, germany (9) romanian neurosurgery (2016) xxx 1: 41 46 43 figure 2 t2 irm images in axial and sagital projections showing c5-c6 and c6-c7 median disc protrusion and c5-c7 opll surgical technique – standard right anterior approach with corpectomy of c6 spinal cord decompression and opll resection at c5-c7 was performed. following the corpectomy procedure, the endplates are prepared and the measures of the defect size and endplate diameter are obtained. then, under fluoroscopic guidance the cage (filled with bone chips from corpectomy) is placed and expanded to a length close to that needed to be. before optimal cage placement into the defect, it is tightly packed with autogenous bone. when the ideal position is reached, the cage is carefully expanded to engage or fix into the endplates. for a correct lordosis or kyphosis the expandable cage can be supplementary adjusted. finally, anterior plating (unitas, ulrich medical, ulm, germany) is placed from c5 to c7. the xray confirms that the expandable cage is properly implanted and a good alignment of cervical spine is obtained by the anterior construction. postoperative course was uneventful. the patient was sent to a rehabilitation center 5 days after the surgery. at follow-up control, 2 months later the modified joa score was 15 (mild) (figure 3). 44 chiriac et al cervical expandable cage for vertebral body reconstruction figure 3 intraoperative images showing anterior distraction device kit from ulrich medical and different operative times romanian neurosurgery (2016) xxx 1: 41 46 45 figure 4 x-ray showing expandable cervical cage properly implanted and a good alignment of cervical spine by anterior cervical plate fixation discussions the uses of expandable cages were described in the literature within the past decade, but their use in the cervical spine has been limited. the most common reported indications of these implants are degenerative spondylosis, trauma, osteomyelitis, tumor, deformity, and ossification of the posterior longitudinal ligament. usually the cervical vertebral reconstruction technique with expandable cage involve additional placement of an anterior plate or posterior supplemental fixation. almost all manufacturing companies offer implant devices with modular construction and variable core diameters, heights, shape, size, angle and endcap footprint. this range on the characteristics of these implants offer to surgical team the possibility in creating an optimal sized and contoured construction for the corpectomy defect. most of the devices are made of titanium, but there are versions made of peek and some have an incorporated anterior fixation system. due to the complex biomechanical profile of cervical spine represented by marked flexion/extension, axial rotation, lateral bending and compression/ distraction, the major concern with the use of expandable cages is overdistraction of the cage, which could result in neurologic injury and/or structural damage (3, 5). the study published by yoganandan et al. (12) showed that excessive expansion of the cage with resulting injury is easier in the cervical spine, as a greater distraction is achieved at a significantly lower force. even so, the only complications mentioned by literature due to overdistraction were transient c5 palsy [arts and peul (1)] and a nerve root injury [shen et al. (8)] (5). the numerous previous studies have shown that supplementation of cervical vertebral reconstruction by expandable cage with anterior plating or posterior fixation system, or both, resulting in a decrease of range of motion in flexion-extension, lateral bending, and axial rotation compared with autograft alone. long studies also showed that supplemental fixation is necessary in two or three-level corpectomy and in most of the cases even for a one-level corpectomy. the majority of authors describe the use of only an anterior plate for a one-level corpectomy, while for a two-level corpectomy, additional posterior supplemental fixation is often required if there is poor bone quality (2, 5, 10). the lower fusion rate of expandable cages due to their limited surface area for fusion offered by a large footprint and less amount of bone graft that can be placed within the cage was another problem debated in the literature. 46 chiriac et al cervical expandable cage for vertebral body reconstruction the recent studies with longer periods of follow-up have shown that fusion rates for expandable cages are not significantly different than prior reported literature for structural bone grafts and fixed cages (4, 6, 7, 11). although, currently there are no large studies on the effect on lordosis and segmental height of expandable and fixed cages, most reported results showed that expandable cages generally allowed for a gain in cervical lordosis for both single and multilevel constructs (1, 2, 5). subsidence of the fixed cage is a widely recognized complication that has been observed at all levels of the spine. even if it is not always clinically significant this should be taken into attention. given these inconveniences, expandable cage may offer an advantage by their modular adjustable configuration making it easier to fit flush against the end plate, and the different end plate footprints may allow a more uniform distribution of stress over the end plate. conclusions the recent advances in spine surgery allow us a full mechanical reconstruction of the cervical spine. the cervical expandable cages offer to surgeon a viable solution for cervical vertebral body reconstruction. however, despite important progresses, cervical spinal interventions with restoration of lost functions still remain a challenge for most surgical teams. references 1. arts, m. p., & peul, w. c. (2008). vertebral body replacement systems with expandable cages in the treatment of various spinal pathologies: a prospectively followed case series of 60 patients. neurosurgery, 63(3), 537-545; 2. auguste ki, chin c, acosta fl, ames cp (2006) expandable cylindrical cages in the cervical spine: a review of 22 cases. j neurosurg spine., apr; 4(4):285-91; 3. awad, a. j., stidd, d. a., alkhalili, k., eli, i. m., & baaj, a. a. (2014). vertebral body reconstruction using expandable titanium cages after anterior decompression for cervical spondylotic myelopathy: a review. cureus, 6(3); 4. benzel ec, lancon j, kesterson l, hadden t. (1991) cervical laminectomy and dentate ligament section for cervical spondylotic myelopathy. j spinal disord.;4:286–95. 5. elder, b. d., lo, s. f., kosztowski, t. a., goodwin, c. r., lina, i. a., locke, j. e., & witham, t. f. (2016). a systematic review of the use of expandable cages in the cervical spine. neurosurgical review, 39(1), 1-11; 6. han yc, liu zq,wang sj, li lj, tan j (2014) is anterior cervical discectomy and fusion superior to corpectomy and fusion for treatment of multilevel cervical spondylotic myelopathy? a systemic review and metaanalysis. plos one 9(1):e87191. doi:10.1371/ journal.pone.0087191; 7. konig sa, spetzger u (2014) experience with a modular peek system for cervical vertebral body replacement. j spinal disord tech. doi:10.1097/bsd.0000000000000149; 8. shen fh,marks i, shaffrey c, ouellet j, arlet v (2008) the use of an expandable cage for corpectomy reconstruction of vertebral body tumors through a posterior extracavitary approach: a multicenter consecutive case series of prospectively followed patients. spine j off j n am spine so 8(2):329–339. doi:10.1016/j.spinee. 2007.05.002; 9.http://www.ulrichmedical.com/sites/default/files/down loads/add_f_dt_engl_r3_we b.pdf; 10. zhang ho yeol, thongtrangan issada, le hoang, park jon, kim h. daniel (2005) expandable cage for cervical spine reconstruction. j korean neurosurg soc 38 : 435-441; 11. zhang y, quan z, zhao z, luo x, tang k, li j, zhou x, jiang d (2014) evaluation of anterior cervical reconstruction with titanium mesh cages versus nanohydroxyapatite/polyamide66 cages after 1-or 2-level corpectomy for multilevel cervical spondylotic myelopathy: a retrospective study of 117 patients. plos one 9(5):e96265. doi:10.1371/journal.pone.0096265; 12. yoganandan n, pintar fa, maiman dj, cusick jf, sances a jr, walsh pr (1996) human head-neck biomechanics under axial tension. med eng phys 18(4):289–294. 10satyartheeguru_migration 192 satyarthee et al migration and coiling of shunt into subgaleal of scalp migration and sub-galeal coiling of distal components of v-p shunt in a 2-year-boy: does electrical stimulation as part of physiotherapy is cause or casual association? guru dutta satyarthee1, a.k. mahapatra2 department of neurosurgery 1neurosciences centre, aiims new delhi, 2aiims new delhi abstract: the ventriculo-peritoneal (vp) shunt surgery in resource constrained centre still remains, most common form of treatment for hydrocephalus. the v. p. shunt complications can occur along entire course of shunt, distal complications are obstruction of catheter, cerebrospinal fluid ascites, abscess and ulceration of skin. however, total cranial migration and getting coiled in subgaleal space, of peritoneal catheter end is very rare occurrence and is reported in only seven cases as isolated casereport in western literature, further more rare is associated extrusion of ventricular catheter and rarer is subgaleal coiling of both peritoneal and ventricular end. author reports a rare and unique case of complete migration of peritoneal catheter into subgaleal space in a 2-year old boy associated, with partial extrusion of ventricular end, the child was also given electric stimulation by untrained physiotherapist along the shunt tract, which might have facilitated cranial migration of distal catheter in our case. pertinent literature is briefly reviewed. key words: subgaleal coiling of shunt, shunt migration, hydrocephalus, extrusion introduction the ventriculo-peritoneal (vp) shunt surgery is the one of the most common form of treatment for hydrocephalus. the complications of ventriculo-peritoneal shunt may occur along cerebral ventricle to the peritoneal cavity. (1) distal shunt catheter related complications include cerebrospinal fluid ascites, catheter malfunction, intraperitoneal abscess and skin ulceration. (2) however, unusual complication of peritoneal catheter tip migration into stomach, urinary bladder, liver, colon, vagina, gall bladder and diaphragm are reported and may rarely migrate into heart chamber. (2, 3, 4) however, total cranial migration and getting coiled in subgaleal space, of peritoneal catheter end is very rare occurrence and is reported in few cases western literature. (3-7) romanian neurosurgery (2015) xxix 2: 192 195 193 case report a 2-year-old boy, presented with alteration in sensorium and vomiting of five days duration, who undergone low pressure ventriculo-peritoneal shunts surgery four months back for tuberculosis meningitis (tbm) with associated hydrocephalus. after the shunt surgery child had rapid recovery and was well in the follow-up period. one day prior to admission patient developed altered sensorium with progressive increasing swelling in the occipital region of seven days. child was given electrical stimulation by untrained physiotherapist in a remote village. examination at admission revealed a 5cm x 4cm size irregular swelling in the occipital region with overlying scalp without ulceration or discharge. the topogram revealed coiling of distal catheter in the subgaleal space causing soft tissue swelling. (figure 1) bone window of computerized tomography scan showed coiling of catheter in the scalp (figure 2). the ventricular end of ventriciloperitoneal shunt was in situ with enlarged size of lateral ventricles (figure 3) with marked periventricular lucency. the coiled catheter in the scalp was also caused artifact. figure 1 topogram showing coiling of distal catheter of ventriculo-peritoneal shunt in the scalp figure 2 – bone window c.t. scan showing coiling of catheter in the scalp figure 3 – computed tomography scan showing ventricular catheter almost extruded causing shunt malfunction leading to hydrocephalus. discussion shunt migration is rare but important cause of shunt malfunction. various types of migration is reported in literature. it may be partial, however, total migration of a ventriculo-peritoneal shunt into ventricles are also reported. (2, 4, 5) reduplication of ventriculo-peritoneal shunt catheter tip back through the shunt tract has been reported. (5) however, total migration of distal catheter of ventriculo-peritoneal shunt into subgaleal space in the scalp is an extremely rare complication, and only seven cases been 194 satyarthee et al migration and coiling of shunt into subgaleal of scalp reported in the literature reporting migration of the distal components of the vp shunt into a subgaleal pocket causing scalp swelling and associated shunt malfunction, further only three case report describes complete migration of proximal and distal components in subgaleal space. (3-7) current case is unique as having total migration of distal end and partial extrusion of ventricular catheter and getting coiled in subgaleal pocket. various hypotheses are proposed to explain the cranial migration of ventriciloperitoneal shunt. these include combination of mechanism formation of cyst at distal catheter, excessive head movement, low resistance, the shorter length of catheter between ventricular end and peritoneal ends specially in infant, inadequate fixation at cranial end and failure to properly put purse string suture at peritoneal end, relatively larger burr hole size and severe constipation causing upward displacement of peritoneal catheter due to raised intra-abdominal pressure. 8 the cranial migration of catheter can also be explained by gradient between intracranial and intra-abdominal pressure, and small peritoneal space in pediatric population. further postulates includes further explanation are windlass effect, inadequate shunt fixation, and increased intraabdominal pressures. dominguez et al. proposed migrated and coiled shunt in subgaleal pocket the occipital region in a tightly coiled manner mimicking as appearance to that of the pre-insertion shunt lying in the package as get supplied; and concluded that the migration was secondary to retained 'memory' of the shunt tubing. (3) the child was also given electric stimulation by untrained physiotherapist along the trunk which might have further facilitated other mechanism for cranial migration of distal catheter in our case, however large size reservoir might have prevented further cranial migration into the ventricle. placement of a purse string suture about the shunt catheter is common practice, which may reduce the chances of cranial migration of catheter. (2) correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: duttaguru2002@yahoo.com references 1. cheng jy, lo wc, liang hh, kun ih. migration of ventriculo peritoneal shunt into the stomach, presenting with gastric bleeding. acta neurochir (wien) 2007; 149(12):1269–70. 2. fewel me, garton hj. migration of distal ventriculoperitoneal shunt catheter into the heart. case report and review of the literature. j neurosurg. 2004; 100(2 suppl pediatrics): 206–11. 3. dominguez cj, tvagi a, hall g, timothy j, chumas pd. sub-galeal coiling of the proximal and distal components of a ventriculo-peritoneal shunt. an unusual complication and proposed mechanism. childs nerv syst. 2000; 16(8):493–5. 4. heim rc, kaufman ba, park ts. complete migration of peritoneal shunt tubing to scalp. childs nerv syst. 1994; 10(6):399–400. 5. kim kj, wang kc, cho bk. proximal migration and cutaneous coiling of a peritoneal catheter: report of two romanian neurosurgery (2015) xxix 2: 192 195 195 cases. childs nerv syst. 1995; 11(7):428–31. doi: 10.1007/bf00717412 6. pikis s, cohen je, shoshan y, benifla m ventriculoperitoneal shunt malfunction due to complete migration and subgaleal coiling of the proximal and distal catheters j clin neurosci. 2015 jan; 22(1):224-6. 7. brian t kloss, david m hart, lalainia secreti subgaleal coiling of the proximal and distal components of a ventriculoperitoneal shunt. int j emerg med. 2012; 5: 15. 8. taub e, lavyne mh: thoracic complications of ventriculo-peritoneal shunts: case report and review of the literature. neurosurgery 1994; 34:18 – 184. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-025 clinical spectrum of paediatric head injury. a prospective study from tribal region krishna govind lodha, tarun kumar gupta, gaurav jaiswal, yogendra singh romanian neurosurgery (2020) xxxiv (1): pp. 158-163 doi: 10.33962/roneuro-2020-025 www.journals.lapub.co.uk/index.php/roneurosurgery clinical spectrum of paediatric head injury. a prospective study from tribal region krishna govind lodha, tarun kumar gupta, gaurav jaiswal, yogendra singh rnt medical college udaipur, rajasthan, india abstract introduction: traumatic brain injury is considered as a major health problem which causes frequent deaths and disabilities in the paediatric population with special concern to tribal regions of developing countries like india where aetiology of traumatic brain injury in the paediatric population fall from height dominant over the road traffic accident as a major. aim & objective: the aim is to analyse the epidemiology, mechanism, clinical presentation, severity and outcome of paediatric head injury in the tribal region of northern india that could help to make preventive policies to improve their care. material methods: it is a prospective observational study of 345 children of up to 18 years of age admitted under department of neurosurgery from october 2017 to april 2019. results: the study population comprised of 345 paediatric patients. mean age was 9.25 years.36.81% patients were in 1-6-year age group and male to female ratio was 2.45. the most common cause for trauma was fall from height in 179(52%) cases followed by rta in 141(41%) cases. the most common radiological finding was depressed skull fractures in 97(50%) cases. there was 35% mortality in severe head injury patients. conclusion: this study through some light on the different scenario of head injury in tribal regions of developing country and will help to formulate effective strategies for prevention and better care of the patients. introduction traumatic brain injury (tbi) is a leading cause of death and disability in children worldwide. [1] young children are at relatively high risk of minimal and mild traumatic head injuries. an increase in the more severe and fatal traumatic brain injuries has been found in late adolescence. pediatric tbi has different pathophysiology due to higher vascularity, plasticity and less rigidity of scalp .pediatric brain has less degree of myelination which related to brain capacity to absorption of traumatic forces and increase the susceptibility to tbi.[2] tbi is classified as mild (glasgow coma scale [gcs] 13–15), moderate (gcs 9–12), or severe (gcs 3–8).[3] keywords tribal region, paediatric traumatic brain injury corresponding author: krishna govind lodha rnt medical college udaipur, rajasthan, india kg_ lodha@yahoo.co.in copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 159 clinical spectrum of paediatric head injury the study focuses on understanding the etiology, clinical presentation, treatment options, and outcome of these patients with special concern to tribal regions of developing countries like india where fall from height dominant over the road traffic accident as a major etiology of traumatic brain injury in paediatric population.[4] thus there is a critical need for effective fall and traffic accidents prevention strategies for children, and we should give attention to the predicting factors for more effective care of such patients material methods it is a prospective observational study of 345 children of upto 18 years of age admitted under department of neurosurgery from october 2017 to april 2019. study was started after obtaining the permission from ethical committee of the hospital. informed consent was obtained from the parent / guardian / relative of the patient. a detailed clinical history obtained from the parents/guardian/relative admitted in the hospital with head injury. analysis statistical analysis was performed using the collected data on incidence and clinical– radiologic correlation. analyses included the age and gender distribution of the children, the cause and location of the injury, medical status, and the part of the head injured and type of injury and the treatment provided. a comparison of types of head injuries sustained by gender, age, and cause was also carried out. results the study population comprised of 345 paediatric patients aged between 2 month to 18 years with a mean age of 9.25 years. there was 245 males (71.01%) and 100 females (28.98%) with male to female ratio of 2.45:1. table 1. outcome according to age age no % male female good outcome poor outcome <1yr 24 6.95 14 10 18(75%) 6(25%) 1-6yrs 127 36.81 95 32 108(85.03%) 19(14.07%) 7-12yrs 120 34.78 84 36 110 (91.7%) 10 (8.3%) 13-18yrs 74 21.44 52 22 62(83.8%) 12(16.2%) total 345 100% 245(71.1%) 100(28.9%) 298 47 the most common cause for trauma was fall from height in 179(52%) cases followed by rta in 141(41%) cases, bull horns in 11 (3%) cases; assault 7 (2%) cases. table 2. mode of injury mechanism no % mild moderate sever fall 179 52 93(52%) 73(41%) 13(7%) rta 141 41 38(27%) 72(51%) 31(22%) assault 7 2 5(72%) 1(14%) 1(14%) sport 7 2 7(100%) bull horn 11 3% 8(73%) 2(18%) 1(10%) rta: road traffic accident severity of injury was decided with gcs score at the time of admission and it was mild injury in 218 (63.19%), moderate in 92 (26.67%) and sever in 35 (10.14%) cases. outcome of injury was good in mild head injury group and poor outcome was associated with severe head injury group. table 3. severity and outcome gcs severity no good outcome poor outcome mortality 13-15 mild 218 210(96.33%) 8(3.67%) none 160 krishna govind lodha, tarun kumar gupta, gaurav jaiswal et al. 9-12 moderate 92 60(65.22%) 22(23.91%) 10(10.87%) 3-8 sever 35 9(25.71%) 15(42.86%) 11(31.43%) ct scan findings were positive in 195 cases and it was normal in 150 cases. most common radiological finding was depressed skull fractures in 97(50%) cases, extradural hematoma in 29 (15%), subdural hematoma in 20 (10%), contusion in 23 (12%), ich in 6 (3%), ivh in 2 (1%) cases. (figure-1 and 2) figure 1. ncct head of 8 yrs old child admitted with h/o of fall from roof with gcs e2v3m5 pupils b/l 3mm reacting to light. figure 2. ncct head of 6 yrs male child admitted with h/o fall from tree and gcs at admission e4v3m3, pupils b/l 3 mm reacting, after evacuation of edh child improved and at time of discharge gcs was e4v5m6. table 4. radiology positive in 195 cases and negative in 150 cases ct finding no % surgery conservative skull fractures 97 50% 40 57 edh 29 15% 10 19 sdh 20 10% 8 12 contusions 23 12% 11 12 ich 6 3% 2 4 ivh 2 1% 0 2 edema 18 9% 0 18 total 195 100% 71 124 edh: extradural hematoma, sdh: subdural hematoma, ich: intracerebral hematoma, ivh: intra ventricular hematoma out of 195 patients 71 patients’ required surgery and rest 124 patients were managed conservatively. fracture debridement or elevation done in 40 patients, hematoma (edh+ich) evacuation was done in 12 patients, contusectomy done in 11 patients and decompressive craniectomy done in 8 patients. (figure 3 and 4). 161 clinical spectrum of paediatric head injury figure 3 (a). ncct head of 15yrs male admitted with h/o rta with gcs e2v1m4 pupils b/l 3mm reacting to light undergone bifrontal craniectomy with evacuation of ehd. he discharged with gcs e4v5m6 and under gone 3d mold customized cranioplasty after 4 months. figure 3 (b). intraoperative photograph of 3d customised cranioplasty flap of above mentioned patient. table 5. intervention and outcome intervention total good outcome poor outcome hematoma evacuation 10(edh) +2(ich) 10(83.33%) 2(16.67%) contusectomy 11 5(45.4%) 6(54.5%) decompressive craniectomy 8 3(37.5%) 5(62.5%) fracture debridement or elevation 40 35(87.5%) 5(12.5%) total 71 53(74.65%) 18(25.35%) edh: extradural hematoma, ich: intracerebral hematoma 162 krishna govind lodha, tarun kumar gupta, gaurav jaiswal et al. while doing the survey for associated injuries, out of 345 patients 105 patients have associated injuries and most common associated injury was facial injury in 42 patients followed by long bone fracture in 24 patients, chest injury in 10 patients, multiple injury in 16 patients, spinal injury in 8 patients and abdominal injury in 5 patients. table 6. intervention and outcome associated injury good outcome poor outcome total nil 226(94.17%) 14(5.83%) 240 facial injury 38(90.48%) 4(9.52%) 42 limb fracture 22(91.67%) 2(8.33%) 24 spinal injury 5(62.5%) 3(37.5%) 8 chest injury 8(80%) 2(20%) 10 abdominal injury 4(80%) 1(20%) 5 multiple injuries 14(87.5%) 2(12.5%) 16 total 345 discussion in india children below 18 years of age constitute about 40% of the total population [5]. traumatic brain injury is listed as one of the most comman cause of death in pediatric population. our study on pediatric head injuries show male preponderance which also conformed in various studies [6]. in our study fall from height 179(52%) was the most comman cause of pediatric head injury [7]. this peculiarly occure due to fall from tree, unguarded rooftop while playing. this was followed by rta 141 (41%), bull horn 11(3%), assault 7(2%) and sport related injury 7 (2%) [8]. initial gcs score was the single most important factor affecting the out-come as described by beca et [9]. the patient who had a gcs of 13-15 (218) had a poor out come in 8 (3.67%), followed by gcs of 9-12 (92) who had a poor outcome in 22(23.91%) followed be gcs of 8 or less then 8 (35) who had poor outcome in 15(42.86%) which is similar as reported by astrand r et.al [10]. out of 345 patients in our study, ct scan findings were positive in 195 cases and it was normal study in 150 cases. we found isolated skull bone fracture as most comman ct findings in 97 (50%) cases, it was associated with good outcome (87.5%) similar results were described by suresh et al [11]. hematoma evacuation (edh, ich) was associated with good outcome in 83.3% and poor outcome in 16.67%, contusion was associated in good outcome in 45.4% and poor outcome in 54.6% cases and decompressive craniectomy was associated with poor outcome in 62.5% cases. tomberg et al also found the similar outcome in their study [12]. in our study, we found that 69.6% patient have isolated head injury with good outcome in 94.17% patient. facial injury was seen in 12.17%, limb fracture in 7%, spinal injury in 2.3%, chest injury in 3%, abdominal injury in 1.5% and multiple injuries seen in 4.6% patients. paret et al reported chest trauma in (62%), limb fracture in (32%), facial injury in (20%), and multiple injuries in (48%) cases. this difference is because we include all the childers in our study irrespective to severity of the injury while author include only sever cases of head injury in peadtric patient [13]. the overall outcome in our study was death in 21(6.09%), vegetative state in 10(2.90%), severe disability in 12(3.48%) and good outcome in 279(80.86%) of the cases which was similar to study conducted by abrar ahad wani et al [14]. table 7. glasgow outcome scale gos n (%) death (1) vegetative (2) sever disability (3) moderate disability (4) normal (5) 21 (6.09%) 10 (2.9%) 23 (6.67%) 12 (3.48%) 279 (80.86%) gos: glasgow outcome scale 163 clinical spectrum of paediatric head injury conclusion conclusion: our study highlights the different scenario of pediatric head injury in tribal regions of developing country, where even the minor head injuries are referred to tertiary care hospitals which can be easily managed by treating physicians. the findings of our study have implications for development of public health policy with especial reference to tribal regions of developing country. where more than half of pediatric head injury which are minor in nature can be prevented by just increasing public awareness. financial support and sponsorship: nil conflicts of interest: there are no conflicts of interest references 1. jagannathan j, okonkwo do, yeoh hk, dumont as, saulle d, haizlip j, et al.long term outcomes and prognostic factors in pediatric patients with severe traumatic brain injury and elevated intracranial pressure. j neurosurg paediatr. 2008; 2:237–9. [pub med: 18831656] 2. goldsmith w, plunkett j: a biomechanical analysis of the causes of traumatic brain injury in infants and children. am j forensic med pathol 25: 89–100, 2004 3. jennet b. epidemiology of head injury. arch dis child 1998; 78:403‑6 4. adirim ta, wright jl, lee e, lomax ta, chamberlain jm. injury surveillance in a pediatric emergency department. am j emerg med. 1999; 17:499–503. [pub med: 10530522] 5. international institute for population studies. mumbai, india: nf, india; 1998‑9. 6. mahapatra ak. head injury in children. in: mahapatra ak, kamal r, editors. a text book of head injury. delhi: modern publication; 2004.p. 156‑70. 7. sambasivan m. epidemeology‑pediatric head injuries. neurol india 1995; 43:57‑8. 8. osmond mh, brennan‑barnes m, shephard al. a 4‑year review of severe pediatric trauma in eastern ontario: a descriptive analysis.j trauma 2002; 52:8‑12.beca j, cox pn, taylor mj, bohn d, butt w, logan wj, et al. 9. somatosensory evoked potentials for prediction of outcome in acute severe brain injury. j pediatr. 1995; 126:44–9. [pub med: 7815222] 10. astrand r, undén j, hesselgard k, reinstrup p, and romner b. clinical factors associated with intracranial complications after pediatric traumatic head injury: an observational study of children submitted to a neurosurgical referral unit. pediatr neurosurg. 2010; 46:101–9. [pub med: 20664236] 11. suresh hs, praharaj ss, indira devi b, shukla d, sastry kolluri vr. prognosis in children with head injury: an analysis of 340 patients. neurol india. 2003; 51:16–8. [pub med: 12865508] 12. tomber g t, rink u, tikk a. computerized tomography and prognosis in pediatric head injury. acta neurochir (wien) 1996; 138:543-48. 13. paret g, ben abraham r, berman s, vardi a, harel r, manisterski y, et al. head injuries in children – clinical characteristics as prognostic factors. harefuah. 1999; 136:677–81. 755. [pubmed: 10955086] 14. abrar ahad wani, arif hussain sarmast, muzaffar ahangar pediatric head injury: a study of 403 cases in a tertiary care hospital in a developing country. j pediatr neurosci. 2017 oct-dec; 12(4): 332-337.doi: 10.4103/jpn_80_17. 6manishjaiswal_outcome romanian neurosurgery (2014) xxi 3: 283 291 283 outcome of operative intervention in intramedullary spinal cord tumours manish jaiswal, radhey shyam mittal department of neurosurgery, sms medical college and hospital, jln marg, jaipur (302004), rajasthan, india abstract objective: the authors analysed the outcome of intramedullary spinal cord tumour surgery, focusing on the preoperative & postoperative neurological status and influence of preoperative gait status on postoperative gait. methods: retrospective analysis of medical records of 53 intramedullary tumour patients, operated at our institute between jan 2006 and july 2012 was done. pre and postoperative neurological status was determined. preoperative mri was done. ambulatory status were evaluated using the modified mccormick scale. all the patients were operated using standard microsurgical techniques. extent of resection was quantified by direct visualization with microscope as: gross resection, subtotal resection, partial resection, and biopsy. results: 73.5% of the patients were in 40-60 years of age group (age range, 5-81 years; mean age 41 years). region most commonly affected was thoracic (40%). the preoperative mccormick grade was i in 20 (37.7%), ii in 16 (30.1%), iii in 7 (13.2%), iv in 9 (16.9%), and v in 1 (1.88%) patients. gross resection was possible in 54.7% of cases. gross resection rate was significantly higher in good preoperative gait (grade i). histologically 41.5% of the lesions were ependymomas. overall postoperative neurological status improved in 16 (30.3%) of the patients, remained unchanged in 27 (50.9%) of cases, and deteriorated in 10 (18.8%) patients. conclusions: better final outcome of walking ability correlated with good preoperative gait. higher gross resection rate was found in cases at an early stage. we favor early and optimal resection of tumour to give least morbidity and better quality of life. key words: intramedullary spinal cord tumour; intramedullary tumour outcome; spinal tumour introduction intramedullary spinal cord tumors (imsct) are relatively rare tumors, accounting for only 2% to 4% of central nervous system tumors. in adults imsct comprise 20% of all intraspinal spinal tumours while in children 35% of tumours are imsct [1]. the various cell types within the spinal cord are responsible for the similar variety of 284 jaiswal, mittal intramedullary spinal cord tumours histological subtypes of intramedullary tumors. astrocytes, oligodendrocytes, neurons, ependymal lining and blood vessels may all give rise to intramedullary tumors. the most frequent of these tumors are of glial origin, astrocytomas and ependymomas comprising the majority of them. unlike brain tumors, most cases, with a few exceptions, are pathologically benign. the clinical course of these tumors is most often an insidious process. by the time evident neurological signs are present, neurological compromise is irreversible and these tumors have often grown to an extent that makes surgical resection morbid or impossible [2]. the management of imsct remained controversial in the past, when these were often treated with biopsy or subtotal removal followed by radiotherapy but this therapy mode was usually associated with early tumour recurrence and progressive neurological deterioration [3]. with advent and later improvement of microsurgical procedures, complete or near total resection of imsct is possible with much better outcome and very less chances of recurrence and late neurological deterioration [4]. in this study, we analysed the outcomes of imsct surgery, focusing on the preoperative & postoperative neurological status in (imsct) and influence of preoperative gait status on postoperative gait. material and methods we retrospective analyzed medical records of 53 patients (30 males and 23 females) who were operated at our institute between jan 2006 and july 2012 and were histopathologically proven imsct. patients who lost follow-up before 6months and had not exact medical records or pathological reports were excluded from analysis. pathological reports were obtained from postoperative specimens for all patients. pre and postoperative neurological status was determined from their hospital records. preoperative diagnosis was made by gadolinium-enhanced mri. ambulatory status were evaluated using the modified mccormick scale, [grade i = normal gait, grade ii= mild gait disturbance not requiring support, grade iii= gait with support, grade iv= assistance required, grade v= wheel chair/ bed ridden]. all the patients were operated using standard microsurgical techniques. extent of resection was quantified by direct visualization with microscope by operating neurosurgeons as total resection: removal of 100% of the tumour as evidenced by a microscopically documented clean surgical field at the end of the procedure. when a small tumour fragment was deliberately left in place, the procedure was considered to be a subtotal resection (removal of 80–99% of tumour). in the same manner, we defined 50–80% resection as partial resection and < 50% resection was defined as a biopsy. confirmation of the extent of resection was done by gd-mri one month postoperatively. data was analyzed using spss-15. results in this study most of the patients (73.5%) were in 40-60 years of age group of life (age range, 5-81 years; mean age 41 years). romanian neurosurgery (2014) xxi 3: 283 291 285 distribution of tumour according to age is shown in (figure 1). most common preoperative symptoms or first clinical findings were: paraparesis in 31 (58.4%) cases, bladder bowel symptoms in 28 (52.%) cases, pain in 26 (49%) cases, numbness and quadriparesis each in 17 (32%) cases, brown sequard syndrome in 2 (3.7%) cases, and paraplegia in 1 (1.89%) case. our result demonstrates the most frequent tumour was ependymoma 22/53 (41.5%) and followed by astrocytoma 16/53 (30.1%) (table 1). figure 1 age group distribution of intramedullary spinal cord tumour table 1 histopathological subtypes of intramedullary spinal cord tumours histological subtypes number % of total ependymoma 22 41.5% astrocytoma 16 30.1% anaplastic astrocytoma 06 11.4% hemangioblastoma 04 7.5% ganglioglioma 02 3.8% teratoma 01 1.89% lipoma 01 1.89% epidermoid 01 1.89% 0 5 10 15 20 25 30 35 40 45 <20 20-40 41-60 61-80 n u m b e r o f p a ti e n ts age group in years no. of patients 286 jaiswal, mittal intramedullary spinal cord tumours region most commonly affected was thoracic (40%) followed by conus medullaris (30%), number and location of tumour showed in (table 2). the preoperative mccormick grade was i in 20 (37.7%), ii in 16 (30.1%), iii in 7 (13.2%), iv in 9 (16.9%), and v in 1 (1.88%) patients. neurological status was aggravated after surgery (assessed at the time of discharge) in 20 (37.7%) of the 53 patients. in patients who could not walk after surgery and whose mccormick scale grade was iv or v, the preoperative score was i in 2 patients (10%), ii in 4 (25%), iii in 1 (14.2%), and iv and v in 6 (60%). gait disturbance was almost absent after surgery-grade i or ii in 16 (80%) of the 20 cases with grade i status before surgery, 9 (56.2%) of the 16 with preoperative grade ii, 4 (57.1%) of the 7 with preoperative grade iii, 1 (11.1%) of the 9 with preoperative grade iv, and none of the 1 with preoperative grade v. on statistical analysis, postoperative gait was significantly better when the preoperative mccormick scale was i-iii (p< 0.001) (table 3). at 6 months after surgery, 19 (95%) of the 20 preoperative grade i cases, 12 (75%) of the 16 preoperative grade ii cases, 5 (71.4%) of the 7 preoperative grade iii cases, 2 (20%) of the 10 preoperative grade iv and v cases had almost no gait disturbance (grade i-iii), indicating that, when the preoperative grade was i-iii, the gait was favorable immediately to 6 months after surgery and the gait was improved at 6 months, compared with that at the time of discharge after surgery (table 4). regarding the relationship between the amount of tumour resection and preoperative neurological manifestation, gross resection was performed in 15 (75%) of the 20 patients with preoperative grade i status, 6 (37.5%) of the 16 with preoperative grade ii status, 3 (42.8%) of the 7 patients with preoperative grade iii status, 5 (50%) of the 10 patients with preoperative grade iv and v status, demonstrating that the total resection rate was significantly higher in patients with good preoperative gait (grade i) (p < 0.001) (table 5). table 2 intramedullary spinal cord tumour (imsct) location distribution location number percentage cervical 10 19% cervico-thoracic 06 11% thoracic 21 40% conus 16 30% romanian neurosurgery (2014) xxi 3: 283 291 287 table 3 summary of comparison between preoperative and postoperative mccormick grades at the time of discharge of patients pre-op grade postop. mccormick grade i postop. mccormick grade ii postop. mccormick grade iii postop. mccormick grade iv postop. mccormick grade v total i 11 05 02 01 01 20 ii 03 06 03 02 02 16 iii 01 03 02 00 01 07 iv 00 01 03 02 03 09 v 00 00 00 00 01 01 total 15 15 10 05 08 53 table 4 summary of comparison between preoperative and postoperative mccormick grades at 6 months follow-up of patients preop. grade postop. mccormick grade i postop. mccormick grade ii postop. mccormick grade iii postop. mccormick grade iv postop. mccormick grade v total i 15 04 01 00 00 20 ii 06 06 02 01 01 16 iii 02 03 02 00 00 07 iv 00 02 03 03 01 09 v 00 00 00 00 01 01 total 23 15 08 04 03 53 table 5 correlation of mccormick grade and extent of tumour resection in overall population of 53 patients with imscts preop mccormick grade gross resection (%) subtotal resection partial resection biopsy total no. of cases (%) i 15 (75%) 02 02 01 20 (37.7%) 288 jaiswal, mittal intramedullary spinal cord tumours ii 06 (37.5%) 03 05 02 16 (30.1%) iii 03 (42.8%) 01 02 01 07 (13.2%) iv 05 (55.5%) 00 02 02 09 (16.9%) v 00 (0%) 00 01 00 01 (1.88%) total 29 (54.7%) 06 (11.3%) 12 (22.6%) 06 (11.3%) 53 discussion first ever successful resection of an imsct was performed by anton von eiselsberg in 1907, but the first report about such resection appeared in 1911 by charles elsberg in new york who explained two-staged plan for surgery for the removal of these imscts [5]. only a few surgeons initially reported good outcomes [6]. several treatment protocols involving biopsies, decompressive laminectomies and adjuvant treatments such as radiation therapy became the norm up to as far as the 1960s [6] greenwood was one of these pioneering neurosurgeons and since his 1954 paper was an advocate of total resection of these tumors [7]. he was later joined by other accomplished surgeons such as yasargil, malis, stein and de sousa [8, 9, 10]. even though they had shown improved results with the help of the surgical microscope and bipolar coagulation, diagnosis was frequently established late in the clinical course of this condition, a situation that would only improve in the mid-1980s with the advent of magnetic resonance imaging (mri), improvement of microsurgical procedures. the widespread usage of cusa in intramedullary spinal cord tumour resection, and the usage of intraoperative neurophysiological monitoring have caused an increase in total resection rate to 90% and led to a significant change in the approach to imscts [11, 12, 13, 14, 15]. according to many authors, the aim of imscts surgery is optimal resection and protection of neurological function [11, 16, 17, 18, 19, 20, 21, 22]. we followed 53 surgically treated patients with imscts, investigated the outcomes, particularly the postoperative gait in relation to the various preoperative gait states, and identified the extent of tumor excision. in 1999 kane et al. [24] reported that the gait status was aggravated and unchanged in 6 (12%) and 45 (82%) of 54 patients with intramedullary tumors. in 1994 cristante and herrmann [25] reported that the outcome was aggravated, unchanged, and improved in 31, 55, and 17% of 69 intramedullary tumour cases, respectively. constantini et al.[1] reported the outcomes of aggravated, unchanged, and improved in 23.8, 60.4, and 15.8% of 164 cases of pediatric intramedullary tumor, respectively, and sandalcioglu et al.[14] reported that the outcome was aggravated in 27 (34.6%) and unchanged in 51 (65%) of 78 cases of intramedullary tumor. in our present series the outcome was aggravated, unchanged, and improved in 18.8, 50.9 and 30.3% of 53 intramedullary tumour cases respectively. despite advances in the surgical procedure, gait status became aggravated romanian neurosurgery (2014) xxi 3: 283 291 289 following surgery for intramedullary tumor in 20–30%. immediate postoperative neurological deterioration was observed in 20 (37.7%) cases, no change in 22 (41.5%) cases and improvement in11(20.7%) cases of our total 53 patients, but those patients who seek treatment early in their clinical course frequently reach their preoperative activity level or even improve beyond that (worsen patients number was reduced from 20 to 10, no change and improved status patients number increased from 22 to 27 and 11 to 16 respectively at 6 months follow-up), so in cases of imscts one should not wait for the onset of clinical deterioration but rather institute treatment as soon as possible. the earlier the diagnosis and the more radical the resection of an imsct, the greater the likelihood of preserving the patient’s neurological function [26]. it has been reported that gross total resection is usually sufficient to achieve recovery of the lesions or the long-term control of the tumour [2, 9, 12, 17]. as a result of a long-term followup study of 202 cases, raco et al.[22] reported that the surgical goal should be the removal of the entire spinal cord tumour. for malignant tumors, the primary objective was to achieve favorable postoperative gait as much as possible, not relying completely on total resection, but for benign tumors (ependymoma, hemangioma, and hemangioblastoma), total resection is desirable and should be attempted [1, 17, 27, 5, 26]. maintaining total resection may aggravate postoperative neurological manifestations, leading to poor gait (mccormick scale grades iii, iv, and v), which markedly affects the quality of life of the patient. no adjuvant treatments (including radiotherapy) were used in the postoperative period in our cases. the dominant opinion in the literature is that the standard treatment for is radical resection, and that radiation therapy after gross total resection is unnecessary [3, 17, 20]. however, when there is a possibility of residual tumours or a diagnosis of malignant pathology, postoperative radiotherapy is recommended [23]. in this series, no neurophysiological monitoring were available and we do not have any experience with intraoperative neurophysiological monitoring. some surgeons have shown these instruments to be helpful but not indispensable for a successful outcome. raco et al. [22] observed that intraoperative neurophysiological monitoring is not helpful for determining postoperative motor and sensory deficits. no doubt there are some limitations in our study. our study is retrospective, single institutional study and having large descriptive data. statistical analysis could not be performed between certain groups like tumour type and age group due to small number of patients. intra-operative usg and spinal cord monitoring facilities are not available at our institute, which limit extent of resection in our series and certainly there is room for improvement. conclusion better final outcome of walking ability correlated with good preoperative gait. higher gross resection rate was found in cases at an 290 jaiswal, mittal intramedullary spinal cord tumours early stage of preoperative mccormick grade. the postoperative gait was less aggravated in good preoperative mccormick grade cases. all of these inferences favour early and optimal resection to give least morbidity and better quality of life to imsct patients. correspondence dr. manish jaiswal a 33/48 a 2, omkareshwar varanasi, 221001, uttar pradesh, india phone – 091-9799980494 e-mail – manishmlnmc@gmail.com references 1.constantini s, miller dc, allen jc, rorke lb, freed d, epstein fj. radical excision of intramedullary spinal cord tumours: surgical morbidity and long-term follow-up evaluation in 164 children and young adults. j neurosurg 2000;93(2 suppl):183–93. 2.jellema k, overbeeke jj, teepen hljm. time to diagnosis of intraspinal tumors. eur j neurol 2005;12:621-624. 3.cooper pr, epstein f. radical resection of intramedullary spinal cord tumours in adults. recent experience in 29 patients. j neurosurg 1985;63:492–9. 4.ohata k, takami t, gotou t, el-bahy k, morino m, maeda m, et al. surgical outcome of intramedullary spinal cord ependymoma. acta neurochir (wien) 1999;141:341–6. 5.sala f, bricolo a, faccioli f, lanteri p, gerosa m. surgery for intramedullary spinal cord tumours: the role of intraoperative neurophysiological) monitoring. eur spine j 2007;16(suppl 2):s130–9. 6.poppen jl. an atlas of neurosurgical techniques. philadelphia & london: w.b. saunders & co 1960:424428. 7.greenwood jr j. total removal of intramedullary tumors. j neurosurg 1954;11:616-621. 8.chi jh, cachola k, parsa at. genetics and molecular biology of intra-medullary spinal cord tumors. neurosurg clin n am 2006;17:1-5. 9. malis li. intramedullary spinal cord tumors. clin neurosurg 1978;25: 512-539. 10.stein bm. surgery of intramedullary spinal cord tumors. clin neuro-surg 1979;26:529-542. 11.aghakhani n, david p, parker f, lacroix c, benoudiba f, tadie m: intramedullary spinal ependymomas: analysis of a consecutive series of 82 adult cases with particular attention to patients with no preoperative neurological deficit. neurosurgery 62: 1279-1285; discussion 1285-1286, 2008 12.hanbali f, fourney dr, marmor e, suki d, rhines ld, weinberg js, et al.: spinal cord ependymoma: radical surgical resection and outcome. neurosurgery 51: 11621172; discussion 1172-1174, 2002 13.nakamura m, ishii k, watanabe k, tsuji t, takaishi h, matsumoto m, et al.: surgical treatment of intramedullary spinal cord tumours: prognosis and complications. spinal cord 46: 282-286, 2008 14.sandalcioglu ie, gasser t, asgari s, lazorisak a, engelhorn t, egelhof t, et al.: functional outcome after surgical treatment of intramedullary spinal cord tumours: experience with 78 patients. spinal cord 43: 34-41, 2005 15.sun b, wang c, wang j, liu a: mri features of intramedullary spinal cord ependymomas. j neuroimaging 13: 346-351, 2003 16.chang uk, choe wj, chung sk, chung ck, kim hj: surgical outcome and prognostic factors of spinal intramedullary ependymomas in adults. j neurooncol 57: 133-139, 2002 17.epstain fj, farmer jp, freed d: adult intramedullary spinal cord ependymomas: the result of surgery in 38 patients. j neurosurg 79: 204-209, 1993 18.lin yh, huang ci, wong tt, chen mh, shiau cy, wang lw, et al.: treatment of spinal cord ependymomas by surgery with or without postoperative radiotherapy. j neurooncol 71: 205-210, 2005 19.mccormick pc, stein bm: intramedullary tumours in adults. neurosurg clin n am 1: 609-630, 1990 20. mccormick pc, torres r, post kd, stein bm: intramedullary ependymoma of the spinal cord. j neurosurg 72: 523-532, 1990 21.nakamura m, ishii k, watanabe k, tsuji t, takaishi h, matsumoto m, et al.: surgical treatment of intramedullary spinal cord tumours: prognosis and complications. spinal cord 46: 282-286, 2008 22. raco a, esposito v, lenzi j, piccirilli m, delfini r, cantore g: long-term follow-up of intramedullary spinal cord tumors: a series of 202 cases. neurosurgery 56: 972981; discussion 972-981, 2005 romanian neurosurgery (2014) xxi 3: 283 291 291 23. shaw eg, evans rg, scheithauer bw, ilstrup dm, earle jd: postoperative radiotherapy of intracranial ependymoma in pediatric and adult patients. int j radiat oncol biol phys 13: 1457-1462, 1987 24. kane pj, el-mahdy w, singh a, powell mp, crockard ha: spinal intradural tumors: part ii—intramedullary. br j neurosurg 13:558–563, 1999 25. cristante l, herrmann hd: surgical management of intramedullary spinal cord tumors: functional outcome and sources of morbidity. neurosurgery 35:69–76, 1994 26. shrivastava rk, epstein fj, perin ni, post kd, jallo gi: intramedullar spinal cord tumor in patients older than 50 years of age: management and outcome analysis. j neurosurg spine 2:249–255, 2005 27. kothbauer kf: intraoperative neurophysiological monitoring for intramedullary spinal cord tumor surgery. neurophysiol clin 37:407–414, 2007 doi: 10.33962/roneuro-2021-001 on thin ice. does season influence the ris k of haemorrhagic stroke from brain vascular malformations? ioan alexandru florian, teodora larisa timiș, lehel beni, larisa serban, ioan stefan florian, adrian bălașa, ioana berindan-neagoe romanian neurosurgery (2021) xxxv (1): pp. 7-13 doi: 10.33962/roneuro-2021-001 www.journals.lapub.co.uk/index.php/roneurosurgery on thin ice. does season influence the risk of haemorrhagic stroke from brain vascular malformations? ioan alexandru florian1,2, teodora larisa timiș3, lehel beni1, larisa serban1, ioan stefan florian1,2, adrian bălașa4, ioana berindan-neagoe5 1 clinic of neurosurgery, cluj county emergency clinical hospital, cluj-napoca, romania 2 department of neurosurgery, iuliu hatieganu university of medicine and pharmacy, cluj-napoca, romania 3 department of physiology, iuliu hatieganu university of medicine and pharmacy, cluj-napoca, romania 4 clinic of neurosurgery, tîrgu mureș county clinical emergency hospital and department of neurosurgery, tîrgu mureș university of medicine, pharmacy, science and technology, tîrgu mureș, romania 5 research center for functional genomics, biomedicine, and translational medicine, institute of doctoral studies, "iuliu hatieganu" university of medicine and pharmacy, cluj-napoca and department of experimental pathology "prof. ion chiricuta", the oncology institute, cluj-napoca, romania abstract introduction. brain vascular malformations (bvms) are congenital lesions with evolutive properties that possess a considerable chance of causing intracranial hemorrhage. the most common types are arteriovenous malformations (avms), aberrant entanglements of deformed vessels that shunt blood from the arteries directly into the veins, and cavernous malformations (cms), being mulberry-shaped sinusoid spaces filled with blood. the rate of hemorrhagic stroke varies between these two types of lesions, being the most common form of symptomatic presentation for avms, but a much rarer occurrence for cms. the purpose of our pilot study was to test whether the incidence of intracranial hemorrhage from bvms varies between seasons, as well as examining a possible causality for this event. material and methods. we performed a retrospective analysis on the cases of ruptured bvms of the brain operated by the senior surgeon in our department between january 2008 and december 2019. we then divided the patients according to type of lesion and gender, based on the month of the year when their pathologies caused hemorrhagic stroke. we performed pearson’s chi square test to verify the keywords arteriovenous malformation (avm), cavernous malformation (cm), rupture, haemorrhagic stroke, surgical removal, gender, season, meteorological conditions corresponding author: ioan alexandru florian department of neurosurgery, iuliu hatieganu university of medicine and pharmacy, cluj-napoca, romania florian.ioan.alexandru@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 8 ioan alexandru florian, teodora larisa timiș, lehel beni et al. relationship between season and rate of rupture of avms and cms, individual month and rate of rupture, season and gender, and individual month and gender. results. there were 87 ruptured vascular malformations, out of which 71 were avms and 16 were cms. there were 51 males (40 avms, 11 cms) and 36 females (31 avms, 5 cms). the majority of hemorrhagic strokes occurred in the months of july (10 avvms, 2 cms) and december (10 avms, 1 cm). we obtained a statistically significant correlation between the summer season and presentation with ruptured cavernous malformation, as well as the male sex and presentation with a ruptured avm in december, whereas the female sex presented a correlation with ruptured avms in the month of march. we also obtained a correlation between the male sex and presenting with a ruptured vascular malformation of any kind in december, as well as the female gender and hemorrhagic stroke from any vascular malformation in the months january and august. conclusion. despite promising statistical results, the relatively low number of cases may not be applicable to a larger patient population. it seems probable that meteorological conditions, especially extreme temperatures, might act as an additional risk factor for hemorrhagic stroke from vascular malformations, however these findings should be corroborated with supplementary case series from other centers, or a large prospective trial. introduction brain vascular malformations (bmvs) represent congenital aberrations of the cerebral blood vessels, having evolutive properties and a variable tendency to cause hemorrhagic stroke across its subtypes. the most common bmvs are arteriovenous malformations (avms), which consist of an entanglement of abnormal vessels that shunt blood from arterial feeders directly into one or more draining veins [4, 5, 10]. hemorrhagic stroke stands as their most common form of symptomatic presentation, avms being also the leading cause of spontaneous intracranial hemorrhage in the young population. cavernous malformations (cms), also referred to as cavernomas, have a lower prevalence than avms, are mulberry-shaped sinusoid caverns filled with blood in various stages of hemolysis and are generally asymptomatic upon discovery [1, 2, 9]. regarding symptoms, epilepsy is described as the most frequent for cms, hemorrhagic stroke being slightly less common. spontaneous intracranial hemorrhage (ich), or hemorrhagic stroke, is responsible for roughly 20% of all stroke types [15, 20]. despite medical and surgical advancements, it remains a mortifying pathology with a mortality as high as 30%, as well as a strikingly elevated morbidity among survivors. the influence of seasonal change on the propensity of hemorrhagic stroke has been widely investigated across several areas of the world, although the results are inconsistent and continuously debated. the majority of such studies described a rise in the incidence of stroke throughout the colder months of the year and a decline in the warmer months [3, 11, 12, 22]. since avm and cm rupture depends on both acquired and environmental factors, it is reasonable to assume that meteorological factors may indeed contribute to this event. nevertheless, our current comprehension of the individual environmental triggers is narrow at best. aside from risk factors such as smoking, alcohol and drug consumption, and various comorbidities like arterial hypertension and diabetes mellitus, we believe it important to also tackle the added influence of seasonal variation in hemorrhagic stroke from these lesions. in the present study, we examine the seasonal rates of rupture from bvms which were admitted in our hospital in a 12-year interval. materials and methods we conducted a retrospective analysis on the cases of ruptured bvms (avms and cms) operated by the senior surgeon in our department (the third author) between january 2008 and december 2019. patient data was gathered from the hospital internal electronic database (atlasmed), patient observation forms, surgery registry and the clinical imaging study database. we then divided the patients according to gender, age, and the histological type of lesion, based on the month of the year when their pathologies caused ich. inclusion criteria were the imaging and pathological confirmation of the vascular malformation, the presence of intracranial hemorrhage upon admission, as well as the surgical removal of the lesion. patients with bvms that did not present with rupture, were not confirmed as either avm or cm by the pathologist, did not have a visible bvm on imaging study, or that did not benefit from surgery in order to have a final diagnosis were excluded from the study. using microsoft® excel for mac, we made the appropriate value distribution graphs. we performed pearson’s chi square test to verify the relationship between season and rate of rupture of avms and cms, individual month and rate 9 does season influence the risk of haemorrhagic stroke from brain vascular malformations? of rupture, season and gender, and individual month and gender. results from the total of 202 bvms operated in the specified interval by our senior neurosurgeon, 87 had ruptured prior to admission, out of which 71 (81.61%) were avms and 16 (18.31%) were cms. there were 51 males (58.62%, with 40 avms and 11 cms, representing 45.98% and 12.64% respectively) and 36 females (41,38%, with 31 avms and 5 cms, accounting for 35.63% and 5.75% of cases respectively). the majority of ich occurred during the months of july – 12 bvms or 13.79% (10 avvms or 11.49%; 2 cms or 2.3%); followed by december – 11 bvms or 12.64% (10 avms or 11.49%; 1 cm or 1.15%). the months of march and november both accumulated 10 bvms each (11.49%), the former having a total of 9 avms (10.34%) and 1 cm (1.15%), whereas the latter amassed 7 avms (8.05%) and 3 cms (3.45%). figure 1 reveals the total number of cases presenting with ruptured avms and cms across each month. using pearson’s chi squared test, we first compared avms to cms in respects to the season they were most likely to rupture and obtained obtained a statistically significant correlation between the summer season and presentation with ruptured cm (chi2 value of 4.3291, p<.05). moreover, when taking each month individually, we found a statistically significant correlation between august and ruptured cms (chi2 value of 4.2902, p<.05) no other associations were statistically significant for this step. tables 1 and 2 show the all of the results emerging from this group of investigations. table 1. bvm risk of rupture according to histological type by season and period season/ period avms total/ month cms total/ month chi2 value p value interpre tation spring 19 1 1.905 8 1.9058 >.05 nonsignificant summer 17 8 4.329 1 .03746 7 <.05 significant autumn 18 5 0.233 6 .62890 3 >.05 nonsignificant winter 17 2 1.001 8 .31688 4 >.05 nonsignificant total 71 16 avms, arteriovenous malformations; cms, cavernous malformations table 2. bvm risk of rupture according to histological type by month month avms total /month cms total /month chi2 value p value interpre tation january 5 1 0.0128 .910048 >.05 nonsignificant february 2 0 could not be calculated march 9 1 0.53 .081428 >.05 nonsignificant april 6 0 could not be calculated may 4 0 could not be calculated june 4 3 3.0362 .096427 >.05 nonsignificant july 10 2 0.0276 .868123 >.05 nonsignificant august 3 3 4.2902 .038334 <.05 significant sept. 6 1 0.0855 .770012 >.05 nonsignificant october 5 1 0.0128 .910048 >.05 nonsignificant nov. 7 3 0.2564 .612595 >.05 nonsignificant dec. 10 1 0.7256 .394304 >.05 nonsignificant total 71 16 figure 1. diagram showing the cumulative incidence of ruptured brain vascular malformation based on type, according to calendar month. the ordinate shows the number of cases. avm – arteriovenous malformation; cm – cavernous malformation. next, we took into account only the patients with ruptured avms and compared the two genders in respects to rupture risks during all the same months combined. figure 2 shows the distribution of ruptured bvms for both sexes across each month. we found a statistically significant correlation between the male sex and presentation with a ruptured avm in the month of december (chi2 value 10 ioan alexandru florian, teodora larisa timiș, lehel beni et al. of 5.3617, p<.05), whereas the female sex was significantly correlated with ruptured avms in the month of march (chi2 value of 4.8766, p<.05). table 3 illustrates the complete results for this set of tests. figure 2. diagram showing the cumulative incidence of ruptured brain vascular malformation based on patient gender, according to calendar month. the ordinate shows the number of cases. vm – vascular malformation. table 3. avm risk of rupture according to gender by month month m. total /m. f. total /m. chi2 value p value interpretation january 1 4 2.8874 .089277 >.05 nonsignificant feb. 2 0 could not be calculated march 2 7 4.8766 .027223 <.05 significant april 4 2 0.2842 .593939 >.05 nonsignificant may 3 1 0.6001 .438524 >.05 nonsignificant june 1 3 1.6923 .193296 >.05 nonsignificant july 5 5 0.1901 .662852 >.05 nonsignificant august 1 2 0.6739 .411693 >.05 nonsignificant sept. 4 2 0.2842 .593939 >.05 nonsignificant oct. 4 1 1.2243 .268522 >.05 nonsignificant novem ber 4 3 0.002 963931 >.05 nonsignificant dec. 9 1 5.3617 .020584 <.05 significant total 40 31 avms, arteriovenous malformations; cms, cavernous malformations last, we considered all bvms, regardless of type, and again compared the hemorrhage risk for the two sexes along all of the same months. we discovered a statistically significant correlation between the male sex and a hemorrhage from a vascular malformation of any kind in december (chi2 value of 5.412, p<.05), as well as the female gender and hemorrhagic stroke from any vascular malformation in the months january and august (chi2 value of 4.6763 equally for each month, p<.05). no other significant associations could be established. the complete results of this step can be viewed in table 4. table 4. total bvm risk of rupture according to gender by month month m. total /m. f. total /m. chi2 value p value interpretation jan. 1 5 4.6763 .030582 <.05 significant feb. 2 0 could not be calculated march 3 7 3.8155 .05078 >.05 non-significant april 4 2 0.172 .678347 >.05 non-significant may 3 1 0.4637 .495889 >.05 non-significant june 4 3 0.0069 .934019 >.05 non-significant july 7 5 0.0005 .982633 >.05 non-significant aug. 1 5 4.6763 .030582 <.05 significant sept. 5 2 0.5148 .473064 >.05 non-significant oct. 5 1 1.6225 .202741 >.05 non-significant nov. 6 4 0.0089 .925001 >.05 non-significant dec. 10 1 5.412 .019999 <.05 significant total 51 36 discussions within seasons themselves, the differences regarding the total number of ruptured avms was minor, whereas cms tended to bleed more frequently during summer. the month of august showed a significantly higher relative frequency of ich from cms when compared to avms. males showed a clearer tendency of bvm rupture in the month of december, whereas female patients had a higher propensity for ich strictly from avms in march and from bvms in general in january and august. currently, there is a scarcity of studies dedicated to the effects of weather on the incidence of hemorrhagic stroke, especially those from preexisting vascular lesions such as aneurysms, avms or cms. to the extent of our knowledge, a single other article addresses the influence of seasons on the risk of spontaneous hemorrhage from avms [6]. hakan et al. discovered that the 11 does season influence the risk of haemorrhagic stroke from brain vascular malformations? highest incidence for avm rupture in istanbul ensued during winter, while its lowest occurred in summer, yet there were no proven statistical correlations to substantiate their results. with 78 ruptured malformations spread across 20 years, the difference between hemorrhagic stroke from avms was also higher for men during autumn and winter, although these were not as considerable the ones in our series. the authors concluded that aside from seasonal weather variations and individual risk factors such as alcohol consumption, the relative increase of the population during winter may also play a role in the upsurge of hemorrhagic stoke during winter. regarding cavernomas, our literature search did not yield any articles discussing the effect of meteorological conditions on their rupture patterns. stroke mortality was proven to rise in holiday seasons, at least in certain regions such as in the hiroshima prefecture of japan, or taiwan [8, 14]. yet the reason for this could not be accurately established due to a lack in more detailed clinical information like patient lifestyle, consumption of alcoholic beverages, smoking habits and so forth. in the heilongjiang province of china, the higher incidence of primary intracranial hemorrhage from hypertension within late spring and early autumn was attributed to the influence of daily mean ambient temperature, as well as its variation [22]. according to zheng et al, unexpected changes in temperature, such as sudden drops during the hot weather or climbs during the cold, were met with an increase in the incidence of primary intracranial hemorrhage. furthermore, in the same study, it was shown that the occurrence of sah escalated throughout days with lower ambient temperature. on the other hand, in the arab peninsula, ischemic stroke was correlated with the higher amount of solar radiations specific for the summer season which could not be elucidated by physiological events indicative of either dehydration or hemoconcentration [19]. therefore, the supposition that meteorological conditions influence the rates of stroke may not be far from true. the peaks occurring at the months of march, july and december might suggest a propensity for bvms to rupture whenever extreme temperatures are reached, or when there are large thermic variations. the more frequent hemorrhages could also be attributed to the stress related to the estival season or the festive holidays and their respective activities. the significant difference between genders within early winter remains intriguing and enigmatic, yet it cannot be entirely attributed to weather effects alone. one should also take into account the behavioral and socioeconomic aspects of the patients in the studied population. as such, there are clear trends of increasing alcohol consumption in the form of spirits and wine during late autumn and early winter in our country, possibly due to the lower temperatures occurring in this period, but also as a consequence of increased stress correlated with a progressively dynamic socioeconomic environment, as well as a widening poverty gap [16, 17]. although probable interference from other seasonal exposures such as dietary changes, hypovitaminosis or viral infections cannot be excluded. studies have also tried to pinpoint specific individual meteorological factors which may influence the occurrence of spontaneous ich. according to neidert et al., relative humidity presented a strong fluctuation in the 2 days prior to ich in patients with intracranial vascular lesions [15]. on the day of rupture relative humidity was significantly lower, suggesting that a low ambient humidity may promote hemodynamic and cardiocerebrovascular conditions associated with ich from these lesions. it has been shown that air humidity, along pollution and temperature, can influence the diameter of the brachial artery in patients with type 2 diabetes mellitus, with higher temperature and humidity acting as vasodilators [21]. conversely, it can be argued that a lower humidity may lead to vasoconstriction, although this might not suffice as a trigger for vascular malformation bleeds. low humidity and air pressure cause an increase of blood viscosity via insensible water loss [7]. this in turn can also alter the autoregulation properties of arterial feeders in avms, as well as promote shear stress [13, 18]. other reports revealed that low temperature is indeed a substantial risk factor for ich, significantly correlated with the higher incidence of these occurrences during winter and early spring [11, 12]. our findings are in line with these conjectures, showing that the increased incidence of ich from vascular malformations during the colder months may not be coincidental. nevertheless, it is as of yet unclear why so many our cases presented with rupture during summer and why the rate of rupture for cms remains higher during the warmer months. 12 ioan alexandru florian, teodora larisa timiș, lehel beni et al. nevertheless, these results should not be taken at face value. statistical bias can occur from the relatively small number of cases from each individual month. we can, however, speculate that there is indeed a higher tendency for bvms to rupture under certain environmental circumstances, such as high differences in temperature or atmospheric pressure. yet determining these parameters retrospectively within a large timeframe can be difficult and more inaccurate than acquiring the same data upon hospital admission. also, stress related to specific periods during the year may contribute to higher systemic blood pressure, ergo to an increase likelihood of these lesions to bleed. in order to resume and improve our research in the future, we intend to collect the meteorological data relevant to our patients on the same day in which they arrive. another problem in our approach is that the total number of lesions is spread too thin across the twelve months, thus even a seemingly impressive frequency peak may actually denote a negligible difference. a larger case series, or a collaboration with other neurosurgical centers in this field, may solve this predicament in the future. another limitation of this study is the lack of adequate meteorological data, particularly of the individual environmental factors such as temperature, relative humidity and air pressure in the days predating ich. in a future continuation of this study, we propose a collaboration with the national meteorological association in order to obtain such relevant data. despite this being a pilot study, we believe it could be further improved by enlarging the number of patients enrolled and by performing a multivariate analysis on the various individual meteorological, environmental, and geographical factors, as well as the individual characteristics of the patients and their bvms. conclusions according to our results, bvm rupture incidence is higher in the months of march, july and december. moreover, cms tend to rupture more frequently in the summer than avms. males tend to present with rupture from avms during early winter, whereas females had ruptures in early spring. despite the fact we achieved promising statistical results, due to the relatively low number of cases, our findings may not be applicable to a larger patient population. it may also be probable that our results are due to statistical bias, although we are optimistic regarding an actual relationship between meteorological conditions and an altered propensity of bvms to rupture. this may also depend on geographical variations in risk factors. it seems likely that seasonal changes in the environment, especially extreme temperatures, might act as an additional risk factor for hemorrhagic stroke from vascular malformations, however these findings should be corroborated with supplementary case series from other centers, or a large prospective trial. conflicts of interest the authors have no conflicts of interest to report. references 1. bertalanffy h, burkhardt jk, kockro ra, bozinov o, sarnthein j. resection of cavernous malformations of the brainstem. cavernous malformations nerv syst. 2011:143-160. doi:10.1017/cbo9781139003636.016. 2. choudhri o, chen rp, bulsara k. 21 cavernous malformations of the brain and spinal cord. fourth edition. elsevier inc. doi:10.1016/b978-0-323-431408.00021-4. 3. çevik y, doğan nö, daş m, ahmedali a, kul s, bayram h. the association between weather conditions and stroke admissions in turkey. int j biometeorol. 2015 jul;59(7):899-905. doi: 10.1007/s00484-014-0890-9. epub 2014 aug 22. pmid: 25145443. 4. florian is, barițchii a, trifoi sv. [arterio-venous mallformations]. in: popescu i, ciuce c, editors. tratat de chirurgie vol vi. 2nd edition. editura academiei române. 2014; 5: 402-410 [text in romanian]. 5. florian is, perju-dumbravă l. [therapeutic options in hemorrhagic strokes]. editura medicală universitară „iuliu hațieganu” cluj-napoca. 2007; 2.1: 331-346 [text in romanian]. 6. hakan t, kizilkilic o, adaletli i, karabagli h, kocer n, islak c. is there any seasonal influence in spontaneous bleeding of intracranial aneurysm and and/or avm in istanbul?. swiss med wkly. 2003;133(17-18):267-272. 7. hashiguchi n, takeda a, yasuyama y, chishaki a, tochihara y. effects of 6-h exposure to low relative humidity and low air pressure on body fluid loss and blood viscosity. indoor air. 2013 oct;23(5):430-6. doi: 10.1111/ina.12039. epub 2013 mar 28. pmid: 23464811. 8. huang hk, chang wc, hsu jy, et al. holiday season and weekend effects on stroke mortality: a nationwide cohort study controlling for stroke severity. j am heart assoc. 2019;8(8):e011888. 9. iliescu bf, poeata i. [cerebral cavernomas]. in: popescu i, ciuce c, editors. tratat de chirurgie vol vi. 2nd edition. 13 does season influence the risk of haemorrhagic stroke from brain vascular malformations? editura academiei române. 2014; 5: 402-410 [text in romanian]. 10. kalb s, gross ba, nakaji p. vascular malformations (arteriovenous malformations and dural arteriovenous fistulas). in: ellenbogen rg, sekhar ln, kitchen nd, editors. principles of neurological surgery. 4th edition. elsevier. 2018; 20: 313-324. 11. kim hj, kim jh, kim dr, kang hi, moon bg, kim js. age and meteorological factors in the occurrence of spontaneous intracerebral hemorrhage in a metropolitan city. j cerebrovasc endovasc neurosurg. 2014 sep;16(3):209-15. doi: 10.7461/jcen.2014.16.3.209. epub 2014 sep 30. pmid: 25340022; pmcid: pmc4205246. 12. magalhães r, silva m, c, correia m, bailey t. are stroke occurrence and outcome related to weather parameters? results from a population-based study in northern portugal. cerebrovasc dis 2011;32:542-551. doi: 10.1159/000331473. 13. morgan m, winder m. haemodynamics of arteriovenous malformations of the brain and consequences of resection: a review. j clin neurosci. 2001 may;8(3):216-24. doi: 10.1054/jocn.2000.0795. pmid: 11386794. 14. nakaguchi h, teraoka a. relationship between the occurrence of spontaneous intracerebral hemorrhage and holidays and traditionally unlucky days in fukuyama city, hiroshima prefecture, japan. j stroke cerebrovasc dis. 2007 sep-oct;16(5):194-8. doi: 10.1016/j.jstrokece rebrovasdis.2007.04.002. pmid: 17845915. 15. neidert mc, sprenger m, mader m, esposito g, hosp ja, bozinov o, regli l, burkhardt jk. a high-resolution analysis on the meteorological influences on spontaneous intracerebral hemorrhage incidence. world neurosurg. 2017 feb;98:695-703.e19. doi: 10.1016/j.wneu.2016.12.006. epub 2016 dec 10. pmid: 27965078. 16. petrovici da, ritson c. food consumption patterns in romania. british food journal. 2000; 102(4):290 – 308. 17. popescu a. changes and trends in wine production and consumption in the world and romania during the period 2007-2018. scientific papers series management, economic engineering in agriculture and rural development. 2019; 19(2): 345-362. 18. rossitti, s., svendsen, p. shear stress in cerebral arteries supplying arteriovenous malformations. acta neurochir. 1995; 137, 138–145. https://doi.org/10.1007/bf0218 7185. 19. salam a, kamran s, bibi r, et al. meteorological factors and seasonal stroke rates: a four-year comprehensive study. j stroke cerebrovasc dis. 2019;28(8):2324-2331. 20. wang k, li h, liu w, you c. seasonal variation in spontaneous intracerebral hemorrhage frequency in chengdu, china, is independent of conventional risk factors. j clin neurosci. 2013;20(4):565-569. doi:10.1016/j.jocn.2012.02.052. 21. zanobetti a, luttmann-gibson h, horton es, cohen a, coull ba, hoffmann b, schwartz jd, mittleman ma, li y, stone ph, de souza c, lamparello b, koutrakis p, gold dr. brachial artery responses to ambient pollution, temperature, and humidity in people with type 2 diabetes: a repeated-measures study. environ health perspect. 2014 mar;122(3):242-8. doi: 10.1289/ehp.1 206136. epub 2014 jan 7. pmid: 24398072; pmcid: pmc3948021. 22. [22] zheng y, wang x, liu j, zhao f, zhang j, feng h. a community-based study of the correlation of hemorrhagic stroke occurrence with meteorologic factors. j stroke cerebrovasc dis. 2016;25(10):2323-2330. microsoft word somilj_primary ewing_ romanian neurosurgery (2016) xxx 2             primary ewing sarcoma of squamous temporal bone with intracranial extension: a case report somil jaiswal1, pooja jaiswal2, bal krishna ojha1, anil chandra1 1department of neurosurgery king george’s medical university lucknow 2department of pathology, integral institute of medical sciences & research lucknow abstract: primary cranial ewing sarcoma (es) is rare and that of temporal bone is even rarer entity. only a few sporadic cases have been reported and no such case has been reported from eastern india in this report we describe a case of 18 yrs old male with primary cranial es of squamous temporal bone involving intracranial and extracranial compartment. the patient presented with swelling in zygomatic fossa and imaging studies showed a mass originating in the right temporal bone. gross total resection of the tumor was done and sent for histopathological study. the case was referred for radio-chemotherapy and had no recurrence up to eight months of follow up. key words: primary ewing sarcoma, squamous part of temporal bone, mri, histopathology introduction ewing sarcoma (es), also called peripheral primitive neuroectodermal tumor (pnet) commonly originates from bone and soft tissue of extremities and pelvis [1]. the skull is involved in less than two percent of cases [2,3]. till now only 14 such cases involving temporal bone have been reported in the literature .one such case is being reported. case history a 18 year old male child presented with history of swelling in his right temporal region since one year. the swelling was increasing in size and associated with pain since last one month. there was no preceding history of trauma and fever. physical examination suggested a palpable mass in right temporal region of 8 x 6 cm in size. the mass was firm and fixed to underlying bone. overlying skin was free and distended veins were seen over the swelling (figure 1). his general as well as systemic examination and neurological status was within normal limits. his routine haematological and biochemical investigations were normal. ultrasonographic evaluation of abdomen and thorax were normal. skeletal radiographs revealed no other extracranial lesion. ct scan of brain showed increased attenuating somil et al primary ewing sarcoma of squamous temporal bone with intracranial extension             enhancing lesion in right temporal area with involvement of inner and outer table of right squamous temporal bone with both intra and extracranial extension. mri study of brain revealed extra-axial mass in right temporal region with involvement of bone and extracalvarial soft tissue swelling showing marked enhancement on contrast study (figure 2). plan for excision of mass was decided. a right fronto-temporo-parietal craniotomy was performed. intraoperatively a firm tumor was noted which originated from the squamous part of temporal bone, extending extradurally under temporal lobe and involved dura. gross total excision of tumor and involved dura was done and sent for histopathological study. hematoxylin & eosin (h&e) stained sections revealed tumor mass composed of uniform small round cells with round nuclei containing fine chromatin, scanty cytoplasm and indistinct cytoplasmic membrane. immunohistochemistry for cd 99 was positive and negative for gfap and vimentin (figure 3). histopathological diagnosis was ewing sarcoma. the patient subsequently received induction chemotherapy with cyclophosphamide, vincristine and adriamycin alternating with ifophospamide and etoposide administered at 3 weeks. the local area was irradiated with 40–50 gy eight weeks later. this was followed by eight cycles of chemotherapy same as induction at 3-week intervals. patient was followed for eight months after radiochemotherapy where he developed no recurrence and later lost in follow up. figure 1 preoperative -right temporal palpable swelling extending to frontal and parietal region figure 2 axial contrast enhanced ct images show enhancing lesion in right temporal region with involvement of right squamous temporal bone and overlying scalp tissue romanian neurosurgery (2016) xxx 2             figure 3 t2w coronal and tiw axial contrast mri image reveals well defined extra-parenchymal and extra calvarial lesion maintaining distinct border with brain and shows marked contrast enhancement figure 4 a. tumor section showing small round cells (h&e, x400). b. tumor cells showing strong membranous staining for cd99 (immunoperoxidase, x400) discussion es is a highly malignant bone tumor arising from the pleuripotent cells in bone marrow or primordial bone marrow derived mesenchymal stem cells [4,5]. the tumor is now classified under ewing sarcoma family of tumor (esft) which includes classic ewing sarcoma, pnet, askin tumor and extra osseous ewing sarcoma [6]. median age of patient with esft is 15 years and more than 50% are adolescent. the tumor primarily involves lower extremity (41%), pelvis (26%), chest wall (16%) & upper extremity (9%) [7]. common presentations are localised bone pain and swelling, local tenderness, palpable mass. in the present case, the presenting symptom was a large swelling in the temporal region with no evidence of symptoms of elevated intracranial pressure suggesting extracranial extension was larger part of tumor. the predominant presenting feature in other such reported cases was scalp swelling, headache and findings of raised intracranial pressure. involvement of cranium by es is very rare. only 29 cases of primary es of cranium have been reported [8] and 14 cases pertaining to involvement of temporal bone. ct of ewing's sarcoma has often shown a diffusely enhancing hyperdense extra axial mass and extensive bone destruction involving both inner and outer table. the present case also had similar findings on the ct scan of brain [2,9,10,11]. differential diagnosis of such large and progressively increasing mass can be embryonal rhabdomyaosarcoma, lymphoma or metastatic neuroblastoma. es as diagnosis was confirmed by cd 99 positivity. management of such tumor is radical excision and radio-chemotherapy [12]. current standard chemotherapy includes vincristine, doxorubicin and cyclophosphamide alternating with ifosfamide and etoposide [13,14]. the prognosis for patient with es has improved considerably with current treatment protocol. however outcome for patient with metastasis or early relapse is poor. though primary cranial es of temporal bone is rare, it should be kept as differential diagnosis in cases of temporal scalp swelling. the present case is exceptional as it originates from the squamous part of temporal bone and no such tumor has been described from eastern india. somil et al primary ewing sarcoma of squamous temporal bone with intracranial extension             correspondence somil jaiswal address: 15/49 sector 15 indira nagar lucknow e-mail: dr.somil26@rediffmail.com phone: 7755075630 references 1.toskos m. peripheral primitive neuroectodermal tumor: diagnosis, classification and prognosis. perspect paediatric pathology. 1992; 16:27-98. 2.steinbok p, lodmark o f, norman mg, han kw c, fryer cj. primary ewing’s sarcoma of the base of skull. neurosurgery. 1986;19(1):104–107. 3.bhansali sk, desai pb. ewing sarcoma observation on 107 cases. j bone joint surg. 1963;45:541–553 4.suva ml, riggi n, stenle jc, et al. identification of cancer stem cells in ewing sarcoma. cancer res 69(5):1776-81,2009 5.tirode f, laudduval k, prieur a, et al. mesenchymal stem cells features of ewing sarcoma. cancer cell 11(5):421-9,2007 6.delattre o, zucmann j , melot t et al. the ewing family of tumorsa subgroup of small round cell tumors defined by specific chimeric transcripts n engl j. med 331(5): 294-9,1994 7.raney rb, asmer l, newton wa jr et al. ewing sarcoma of soft tissue in childhood: a report from intergroup rhabdomyosarcoma study1972 to 1991. j clin oncol 15(2):574-82;1997 8.primary intracranial ewing sarcoma with an unusually aggressive course: a case report. neuropathology 2012 jan, 32(3):293-300 9.davidson mjc, ewing's sarcoma of the temporal bone a case report oral surg oral med oral pathol 1991 nov; 72 (5): 534-6. 10.fitzer pm, steffy wr. brain and bone scans in primary ewing's sarcoma of the petrous bone. j neurosurgery may 1976; 44. 11.mansfield jb, primary ewing sarcoma of the skull. surg neurology 1982; 18: 286-8 12.primitive neuroectodermal tumor of head and neck : incidence, diagnosis and management. ann otol rhinol laryngol2004 jul; 113(7):533-43 13.cotterill s, malcolm a, et al. ifosfamide-containing chemotherapy in ewing's sarcoma: the second united kingdom children's cancer study group and the medical research council ewing's tumor study. j clin oncol. 1998;16:3628–3633. 14.grier he, krailo md, tarbell nj, et al: addition of ifosfamide and etoposide to standard chemotherapy for ewing sarcoma and primitive neuroctodermal tumor of bone. n engl j med 348(8):694-701,2003 2giovania_intraoperativeneuronavigation romanian neurosurgery (2015) xxix 2: 141 149 141 intraoperative neuronavigation integrated high resolution 3d ultrasound for brainshift and tumor resection control a. giovani1, f. brehar, narcisa bucur, d. martin1, r.m. gorgan 1phd student, “carol davila” university of medicine and pharmacy, bucharest “bagdasar-arseni” emergency clinical hospital, bucharest abstract: introduction: the link between the neurosurgeon’s knowledge and the scientific improvements made a dramatic change in the field expressed both in impressive drop in the mortality and morbidity rates that were operated in the beginning of the xxth century and in operating with high rates of success cases that were considered inoperable in the past. neuronavigation systems have been used for many years on surgical orientation purposes especially for small, deep seated lesions where the use of neuronavigation is correlated with smaller corticotomies and with the extended use of transulcal approaches. the major problem of neuronavigation, the brainshift once the dura is opened can be solved either by integrated ultrasound or intraoperative mri which is out of reach for many neurosurgical departments. method: the procedure of neuronavigation and ultrasonic localization of the tumor is described starting with positioning the patient in the visual field of the neuronavigation integrated 3d ultrasonography system to the control of tumor resection by repeating the ultrasonographic scan in the end of the procedure. discussion: as demonstrated by many clinical trials on gliomas, the more tumor removed, the better long term control of tumor regrowth and the longer survival with a good quality of life. of course, no matter how aggressive the surgery, no new deficits are acceptable in the modern era neurosurgery. there are many adjuvant methods for the neurosurgeon to achieve this maximal and safe tumor removal, including the 3t mri combined with tractography and functional mri, the intraoperative neuronavigation and neurophysiologic monitoring in both anesthetized and awake patients. the ultrasonography integrated in neuronavigaton comes as a welcomed addition to this adjuvants to help the surgeon achieve the set purpose. conclusion: with the use of this real time imaging device, the common problem of brainshift encountered with the neuronavigation systems is covered and any eventual tumor residue can be spotted by ultrasonography and resected. key words: high resolution 3d ultrasound, neuronavigation, glioma 142 giovani et al intraoperative neuronavigation introduction neurosurgery is a very fast changing field of medicine and keeping up to date with new technologies is a must. this link between the neurosurgeon’s knowledge and the scientific improvements made a dramatic change in the field expressed both in impressive drop in the mortality and morbidity rates that were operated in the beginning of the xxth century and in operating with high rates of success cases that were considered inoperable in the past. the neuronavigation systems are as useful for orienting in the operative field as is the operative microscope or endoscope for visualization and mri is for locating the lesion and designing an operative strategy. yet many of the experts rely on their orientation based on anatomical knowledge limiting the use of neuronavigation for small, deep seated lesions (less than 3 cm). in this cases it has been demonstrated that the use of neuronavigation is correlated with smaller corticotomies and with the extended use of transulcal approaches. a study in 2000 [1] presented for the first time the integration of neurosurgery into an ultrasound machine as a method to cope with normal anatomic changes during brain surgery , known as brainshift. compared to other methods against brainshift like intraoperative mri, interventional mri the ultrasound even in 2d or 3d offers real time images is much easier to use and needs less investment both of the time of the procedure and in the set up for the mri system and special operating rooms. [5, 6, 22] compared to the mri the ultrasound has a poor image quality and it is difficult to interpret, in part due to the fact that it is not regularly used in neurosurgery. the first neuronavigation integrated to a ultrasonography system was used since november 1997 at the university hospital in trondheim. [1] there are only a few studies to compare intraoperative mri with neuronavigation integrated ultrasonography and they conclude that imr is the most advanced and reliable intraoperative imaging modality but given to the limited applicability due to high costs and especially designed operating rooms intraoperative ultrasonography is an acceptable alternative. [8, 9, 17, 20] method in order to use this combined system a fine slice mri with fiducials applied on the scalp of the patient should be performed in the day before or the day of the surgery. we avoid performing this mri scan more than 1 day before surgery as the marks on the scalp may vanish giving an unacceptable error for navigation. we will chose for navigation from the acquired images the larger image series, either t1 or t2, or we can choose both and switch between them when needed. while loading the data into the sonowand system the patient’s head is fixed in a mayfield head holder. a mayfield frame with 4 reflecting spheres is fixed to the device and a nonsterile probe pointer with 4 reflecting spheres attached is used to register the points marked with fiducials on the scalp. usually romanian neurosurgery (2015) xxix 2: 141 149 143 after the first 3 or 4 points are registered in the frameless navigation system the pointer in the surgeon’s hand appears on the screen. during this procedure the three cameras of the video acquisition system should be pointed towards the surgeon’s hand as to include both the mayfield frame and the pointer device. an error less than 2 mm is acceptable. than the incision spot is drawn on the skin and the operative field is properly draped. before the craniectomy the sterile neuronavigation probe can be used again to avoid dural veins or dural lakes when performing the burr holes. before and after the dural incision both the neuronavigation pointer and the ultrasound probe can be used to identify the best spot for cortical incision. this should take into account the shorter path to the middle of the lesion and the avoidance of the eloquent cortex. the position of the ultrasound plane is shown on the monitor as the ultrasound probe has attached 4 reflecting spheres to integrate it into the neuronavigation system. the system can build 3d ultrasound images based on a slow freehand movement of the probe over the cortex for 15-30 seconds. the ultrasound image can be superimposed on the mri slices or can be seen in a separate screen. by rotating the neuronavigation or the ultrasound probe, different images are acquired the image shifts between the 3 planes (sagittal, coronal and horizontal). when the margin of the tumor facing the surgeon is reached the tip of the probe is used to mark it and after tumor removal the probe is inserted in the cavity to show the extent of removal. at this point when the resection is macroscopically total, the ultrasound is used again with continuous irrigation of the cavity to verify if there is any tumor remnant left. we have a limited experience with this device, only 7 patients, but it proved very useful in localizing and documenting the tumor resection. we used this device in cases of metastases, malignant or low grade gliomas or in cases of other intraparenchimal lesions like cavernomas especially when the lesion was located in or near the eloquent areas. depending on the mri sequence that is included in the study more information about the surroundings of the tissue can be gained. for some cases where we found important vessels in close contact with the tumor we used an angio mri sequence superimposed on the regular t1 image that we used for navigation. this proved very useful especially when performing the ultrasonography 3d acquisition. discussion since the first experiments with ultrasound on human brain in 1950, 20 years passed for the real time 2d imaging to be introduced into clinical trials and 10 more years till this technology became available on the market. nowadays most of the neurosurgical departments in high volume centers around the world have access to this technology. [11, 15, 20] its use is both in localizing the lesions, especially when these are small and located in eloquent cortex and in assessing the degree of tumor removal. in this era of evidence based medicine along with the microscope this device stands as a proof of the quality of surgery. [17, 21, 23] as demonstrated by many clinical trials on 144 giovani et al intraoperative neuronavigation gliomas, the more tumor removed, the better long term control of tumor regrowth and the longer survival with a good quality of life. of course, no matter how aggressive the surgery, no new deficits are acceptable in the modern era neurosurgery.[16,18,19] there are many adjuvant methods for the neurosurgeon to achieve this maximal and safe tumor removal, including the 3t mri combined with tractography and functional mri, the intraoperative neuronavigation and neurophysiologic monitoring in both anesthetized and awake patients. the ultrasonography integrated in neuronavigaton comes as a welcomed addition to this adjuvants to help the surgeon achieve the set purpose. [4, 7f] some authors used all these methods combined in a series of patients both with high grade and low grade gliomas reporting an increased rate of tumor resection compared to the cases without the use of this techniques, yet further long time studies on the recurrence of the tumors are needed to prove the benefit of using this advanced technologies for the life and the survival of the patients. [10, 12, 14] conclusion the ultrasound integrated neuronavigation system is an invaluable tool, cost benefit acceptable, compared to other methods, for the intraoperative detection and removal of tumor remnants, after achieving macroscopic gross total resection. with the use of this real time imaging device, the common problem of brainshift encountered with the neuronavigation systems is covered. figure 1 neuronavigation integrated ultrasonography system: the 3 video cameras are visible on an articulated arm above the touch screen monitor romanian neurosurgery (2015) xxix 2: 141 149 145 figure 2 in this case of parietal glioblatoma, the 52 yo woman presented for headache and left sided motor seizures; after performing the craniotomy the ultrasound probe scans the dura for the 3d image acquisition to be superimposed on the neuronavigation mri images. in this case we used both t1 and angio mri images and the relation of the tumor with the vessels om its surface is shown (orange) figure 3 the same case during tumor removal when macroscopic total resection was achieved. the green line is the neuronavigation probe touching the margins of the resection cavity. the tip of the instrument stops before reaching the deep margin of the tumor, indirect sign that there is some tumor residue 146 giovani et al intraoperative neuronavigation figure 4 the same case after tumor removal, on the central ultrasound image the resection cavity can be observed: under continuous irrigation with serum after h2o2 has been applied in the cavity to obtain hemostasis, oxygen bubbles can be seen inside the resection cavity. superimposing this set of images on the first set of images gives information about the degree of tumor resection figure 5 the same case in the end of the surgery when the rest of the tumor was removed and the tip of the probe is reaching the distal margin of the tumor. this check should be done for all the walls of the tumor romanian neurosurgery (2015) xxix 2: 141 149 147 figure 6 comparing the 3d acquisition data before (left) and after (right) the tumor resection showing a 4.8 mm brainshift. in order to limit the brain shift the head must be kept in a neutral position and the operating field should be continuously irrigated figure 7 navigating on a t2 mri sequence in this case of lung cancer metastasis in a 62 yo heavy smoker man. after the tumor removal the pointer touches the deep margin of the tumor 148 giovani et al intraoperative neuronavigation figure 8 oxygen bubbles on ultrasound filling the resection cavity of a pseudocystic hypocampal glioma in a 30 yo woman presenting with mesial temporal lobe epilepsy (mtle) for generalized seizures and temporal seizures with euphoric and aggressive behavior references 1.aage gronningsaeter, ph.d., atle kleven, m.s., steinar ommedal, b.s., tore erling aarseth, m.s., torgrim lie, m.s., frank lindseth, m.s., thomas langø, m.s., geirmund unsgård, m.d., sonowand, an ultrasoundbased neuronavigation system, neurosurgery 47:1373– 1380, 2000 2.claus eb, horlacher a, hsu l, schwartz rb, delloiacono d, talos f, et al: survival rates in patients with low-grade glioma after intraoperative magnetic resonance image guidance. cancer 103:1227–1233, 2005 3.smith js, chang ef, lamborn kr, chang sm, prados md, cha s, et al: role of extent of resection in the longterm outcome of low-grade hemispheric gliomas. j clin oncol 26: 1338–1345, 2008 4.holodny ai, schwartz th, ollenschleger m, liu wc, schulder m: tumor involvement of the corticospinal tract: diffusion magnetic resonance tractography with intraoperative correlation. j neurosurg 95:1082, 2001. 5. nimsky c, gansland o, cerny s, hastreiter p, greiner g, fahlbusch r: quantification of, visualization of, and compensation for brain shift using intraoperative magnetic resonance imaging. neurosurgery 47:1070– 1080, 2000. 6.nimsky c, gansland o, hastreiter p, fahlbusch r: intraoperative compensation for brain shift. surg neurol 56:357–365, 2001. 7.pierpaoli c, jezzard p, basser pj, barnett a, di chiro g: diffusion tensor mr imaging of the human brain. radiology 201:637–648, 1996. 8.unsgaard g, ommedal s, muller t, gronningsaeter a, nagelhus hernes ta: neuronavigation by intraoperative three-dimensional ultrasound: initial experience during brain tumor resection. neurosurgery 50:804–812, 2002. 9. auer lm, van velthoven v: intraoperative ultrasound (us) imaging: comparison of pathomorphological findings in us and ct. acta neurochir (wien) 104:84– 95, 1990 10.berger ms, deliganis av, dobbins j, keles ge: the effect of extent of resection on recurrence in patients with low grade cerebral hemisphere gliomas. cancer 74:1784– 1791, 1994 11.black pm, moriarty t, alexander e iii, stieg p, woodard ej, gleason pl, et al: development and implementation of intraoperative magnetic resonance romanian neurosurgery (2015) xxix 2: 141 149 149 imaging and its neurosurgical applications. neurosurgery 41:831–845, 1997 12. chacko ag, kumar nk, chacko g, athyal r, rajshekhar v: intraoperative ultrasound in determining the extent of resection of parenchymal brain tumours—a comparative study with computed tomography and histopathology. acta neurochir (wien) 145:743–748, 2003 13. chandler wf, knake je, mcgillicuddy je, lillehei ko, silver tm: intraoperative use of real-time ultrasonography in neurosurgery. j neurosurg 57:157– 163, 1982 14.fahlbusch r, samii a: a review of cranial imaging techniques lindner d, trantakis c, renner c, arnold s, schmitgen a, schneider j, et al: application of intraoperative 3d ultrasound during navigated tumor resection. minim invasive neurosurg 49:197–202, 2006 15. mäurer m, becker g, wagner r, woydt m, hofmann e, puls i, et al: early postoperative transcranial sonography (tcs), 16.nimsky c, ganslandt o, buchfelder m, fahlbusch r: intraoperative visualization for resection of gliomas: the role of functional neuronavigation and intraoperative 1.5 t mri. neurol res 28:482–487, 2006 17. nimsky c, ganslandt o, kober h, buchfelder m, fahlbusch r: intraoperative magnetic resonance imaging combined with neuronavigation: a new concept. neurosurgery 48:1082– 1091, 2001 18. regelsberger j, lohmann f, helmke k, westphal m: ultrasound guided surgery of deep seated brain lesions. eur j ultrasound 12:115–121, 2000 19. roth j, biyani n, beni-adani l, constantini s: realtime neuronavigation with high-quality 3d ultrasound sonowand in pediatric neurosurgery. pediatr neurosurg 43:185–191, 2007 20.rubin jm, quint dj: intraoperative us versus intraoperative mr imaging for guidance during intracranial neurosurgery. radiology 215:917–918, 2000 21. rygh om, nagelhus hernes ta, lindseth f, selbekk t, brostrup müller t, unsgaard g: intraoperative navigated 3-dimensional ultrasound angiography in tumor surgery. surg neurol 66:581–592, 2006 22.tronnier vm, bonsanto mm, staubert a, knauth m, kunze s, wirtz cr: comparison of intraoperative mr imaging and 3d-navigated ultrasonography in the detection and resection control of lesions. neurosurg focus 10(2):e3, 2001 23.unsgaard g, rygh om, selbekk t, selbekk t, brostrup müller t, unsgaard g: intra-operative 3d ultrasound in neurosurgery. acta neurochir (wien) 148:235–253, 2006 15moscotesalazar_an international 248 | moscote-salazar et al survey on perioperative use of tranexamic acid in neurotrauma an international based survey on perioperative use of tranexamic acid in neurotrauma luis rafael moscote-salazar1, amit agrawal2, andres m. rubiano3, mohammed al dhahir4, willem guillermo calderon-miranda5, nasly zabaleta-churio6, marco antonio blancas rivera7 1neurosurgeon-critical care, red latino latin american trauma & intensive neuro-care organization. bogota, colombia 2professor of neurosurgery, mm institute of medical sciences & research, maharishi markandeshwar university, mullana ambala, haryana, india 3neurosurgeon, professor of neuroscience and neurosurgery, universidad el bosque red latino latin american trauma & intensive neuro-care organization, bogota, colombia 4neurosurgeon, al-thawra modern general hospital, yemen 5national autonomous university of mexico. unam, mexico d.f, mexico 6nurse, universidd popular del cesar, colombia 7national autonomous university of mexico, unam, mexico d.f, mexico abstract: background: tranexamic acid is used to reduce bleeding, easy to use, affordable and relatively safe. there are few studies on the use of tranexamic acid in trauma and especially in neurosurgery. there is no published study on the trend the use of tranexamic acid in neurotrauma surgery among international doctors. the aim of this study was to evaluate the current practice for use of tranexamic acid during neurotrauma surgery. materials and methods: a 11-question electronic survey was sent to 25 practicing physicians worldwide. basic demographic information and estimated rates of use of tranexamic acid during neurotrauma surgery. results: twenty five physicians responded to our survey. very few trusts (12%) use tranexamic acid during neurotraumasurgery. conclusion: further studies are required to establish guidelines in neurosurgery and neurotrauma, especially. the use of this medicine potentially helps improve patient care with head injury and save lives. key words: neurotrauma surgery, survey, tranexamic acid, trauma romanian neurosurgery (2016) xxx 2: 248-251 | 249 introduction traumatic brain injury has been associated with significant mortality in the acute period. (1,2,3,4). there is great interest for the use of strategies that allow the decrease of bleeding within the surgical period. very few trends studies have evaluated the use of tranexamic acid in surgery. (5,6). until this date there is no study to assess the practical use of tranexamic acid in neuronal trauma surgery. the aim of this study was to record the use of tranexamic acid for neurotrauma surgery in physicians worldwide materials and methods to determine how physicians internationally use tranexamic acid in brain trauma surgeries; we developed a web-based structured survey with real time results through an online survey (http://www.neuropractice.com). survey invitations were sent by e-mail, and aimed physicians (neurosurgeons, intensivist, residents of neurosurgery/critical care, trauma surgeons and others) who manage patients with brain traumatic injury, during the month of august of 2015 to september of 2015. for ethical considerations was decided not to identify any of the physician surveyed. we used dichotomous choice questions, and multiple choice questions with single answers. the evaluated variables were: experience, occupation, place of training and use of ventriculostomy and placement of an intracranial pressure monitoring device. answers from the survey were compiled and entered into an excel database (microsoft, redmond, washington). each answer to a question was placed in a corresponding category and the frequencies of each category were computed. the data was analyzed by software 17.0 (spss. inc., chicago, il). the data obtained was analyzed statistically and was determined the frequency distribution of each of the variables. results twenty five international physician completed the survey, all physician practiced in many countries. the time, of experienced was analyzed: 0-5 years (16%; n= 4), 5-10 years (20%; n=5), 10-20 years (36%; n=9), 2130(28%; n=7) years. when asked about occupation the results were; neurosurgeon (32%; n=8), intensivist (36%; n=9), resident of neurosurgery/critical care (8%; n=2), trauma surgeon (8%; n=2), anesthesiologist (4%; n=1), rn critical care (4 %; n=1), others (8%; n=2). when asked about the use of tranexamic acid; yes (52%; n=13) and no (48%; n=12). when asked about the existence of an institutional policy for the use of tranexamic acid; yes (52%; n=13) and no (48%; n=12). when asked about the use tranexamic acid for all patients on neurotrauma surgery, (12%; n=3) and not (88%; n=22). when asked about the use of tranexamic acid in subdural chronic hematoma, yes (20%; n=5) and no (80%; n=20). when asked about the use tranexamic acid in recurrent subdural chronic hematoma; yes (12%; n=3) and no (88%; n=22). when asked about the use tranexamic acid in epidural hematoma; yes (36%; n=9) and no (64%; n=16). when asked about the use tranexamic acid in acute subdural 250 | moscote-salazar et al survey on perioperative use of tranexamic acid in neurotrauma hematoma; yes (44%; n=11) and no (56%; n=14). regarding the discontinuation of maintenance (tranexamic acid) at the time of skin closure was performed; yes (16%; n=4) and no (84%; n=21). other concern for the evaluation was the consideration of use with continuous infusion in the intensive care unit; yes (32%; n=8) and no (68%; n=17). discussion tranexamic acid is a synthetic derivative of the amino acid lysine that exerts its antifibrinolytic effect through the reversible blockade of lysine binding sites on plasminogen molecules. (6,7). the publication of the crash-2 trial opened a great interest in relation to the use of tranexamic acid and bleeding. (9). this has motivated the interest on the role of fibrinolysis in bleeding. it has been shown that the effect of tranexamic acid is greater the day of injury; it also reduces the risk of death from all causes by 20%. it has been established that survival is only evident in patients treated initially in the first 3 hours. until this day, no study has surveyed the use of tranexamic acid in patients with neuronal trauma. from this survey we can infer that 52% of respondents’ trusts routinely use tranexamic acid in neurosurgery. our results show an institutional policy for the use of tranexamic acid in 52%. there is disparity in the use of tranexamic acid; low use in neuronal trauma surgery in these cases may be beneficial. it is possible that some concerns about the possible complications derived from this drug are the reason of the low use of tranexamic acid. these complications have been estimated as too low. (10,11,12) despite evidence showing this drug is much useful and has low risk of side effects, it is clear that its use is not part of routine practice in many of the same neurosurgical centers. conclusion this survey shows on the current practice of physicians who specialize in neurotrauma surgery and tranexamic acid. as a relevant conclusion, further studies are required to achieve to provide a definitive dosing recommendations. also, to confirm the role of tranexamic acid in the management of neurotrauma surgery and so the improvement of patient care. references 1.baguley i. slewa-younan s. lazarus r. green a. longterm mortality trends in patients with traumatic brain injury. brain inj. 2000;14:505–512. 2.finkelstein e, corso p, miller t. the incidence and economic burden of injuries in the united states. new york: oxford university press; 2006. 3.mackenzie ej: epidemiology of injuries: current trends and future challenges. epidemiol rev 2000;22:112-119. 4.langlois ja, rutland-brown w, wald mm: the epidemiology and impact of traumatic brain injury: a brief overview. j head trauma rehabil 2006;21:375-378. 5.young b, moondi p. a questionnaire-based survey investigating the current use of tranexamic acid in traumatic haemorrhage and elective hip and knee arthroplasty. jrsm open. 2014;5(2):2042533313516949. doi:10.1177/2042533313516949. 6.bird s, mcgill n.blood conservation and pain control in scoliosis corrective surgery: an online survey of uk practice. paediatr anaesth. 2011 jan;21(1):50-3. 7.mccormack pl. tranexamic acid: a review of its use in the treatment of hyperfibrinolysis.drugs. 2012 mar 26;72(5):585-617. 8.dussel jn, zdankiewicz p.tranexamic acid: familiarity and use in the level ii trauma hospital.am surg. 2015 jan;81(1):e10-1 romanian neurosurgery (2016) xxx 2: 248-251 | 251 9.roberts i, shakur h, coats t, hunt b, balogun e, barnetson l, cook l, kawahara t, perel p, prieto-merino d, ramos m, cairns j, guerriero c.the crash-2 trial: a randomised controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and transfusion requirement in bleeding trauma patients. health technol assess. 2013 mar;17(10):1-79. 10. orpen nm, little c, walker g, crawfurd ej. tranexamic acid reduces early post-operative blood loss after total knee arthroplasty: a prospective randomised controlled trial of 29 patients. knee 2006; 13: 106–110 11.hynes m, calder p, scott g. the use of tranexamic acid to reduce blood loss during total knee arthroplasty. knee 2003; 10: 375–377 12.blake pg, lori jd, robert tt, mark wp, sierra rj. low risk of thromboembolic complications with tranexamic acid after primary total hip and knee arthroplasty. clin orthop relat res 2013; 471: 150–154 11satishkumar_appearance 100 satish kumar et al isolated thrombocytopenia in acute subdural hematoma appearance of isolated thrombocytopenia in a patient of acute subdural hematoma s. satish kumar1, m. srinivas1, k. raghu1, p. shashidhar1, amit agrawal2 1professor of emergency medicine, department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract: thrombocytopenia in critically ill patients probably reflects the severity of the underlying illness and these patients have a higher mortality due to the severity of overall clinical status. in present article we report a case of acute subdural hematoma who developed progressive thrombocytopenia resulting in fatal outcome. a 75 year gentleman presented with history of sudden onset headache and lapsed into altered sensorium. there was history of trivial fall before he developed headache. the patient was deeply comatose with pupils bilateral 2 mm and reacting to light. computerized tomography (ct) scan brain showed large right fronto-temporo-parietal acute subdural hematoma with mass effect and midline shift. post-operatively he was kept on elective ventilation. on following days the patient continues to develop thrombocytopenia (day3 platelet count 75,000, day-4 60,000, day-5 25,000). thrombocytopenia is a common but a potentially life-threatening condition problem and has been considered to play a role in worsening the prognosis of critically ill patients in intensive care unit. few studies statistically examine the strength of the association between risk factors and outcomes related to thrombocytopenia, additional research is recommended to identify putative molecular determinants. key words: thrombocytopenia, acute subdural hematoma, trivial, head injury introduction thrombocytopenia is a common but a potentially life-threatening condition problem and has been considered to play a role in worsening the prognosis of critically ill patients in intensive care unit. (1, 2) in present article we report a case of acute subdural hematoma who developed progressive thrombocytopenia resulting in fatal outcome. romanian neurosurgery (2015) xxix (xxii) 1: 100 102 101 case report a 75 year gentleman presented with history of sudden onset headache and lapsed into altered sensorium. he was in altered sensorium since then. he was a known hypertensive on regular medication. there was no history of diabetes. there was history of trivial fall before he developed headache. on examination in the emergency department pulse rate was 100/minute, blood pressure was 150/100 mmhg, saturation was 82% on room air, chest examination bilateral crepitations. the patient was deeply comatose with pupils bilateral 2 mm and reacting reacting to light. extraocular movements were full. blood investigations including coagulation profile and platelet count (1,65,000/mm3) were normal. computerized tomography (ct) scan brain showed large right fronto-temporoparietal acute subdural hematoma with mass effect and midline shift. post-operatively he was kept on elective ventilation. on following days the patient continues to develop thrombocytopenia (day-3 platelet count 75,000, day-4 60,000, day-5 25,000). the patient febrile (102of) but there was no clinical evidence of bleeding. coagulation profile was normal. then antibiotics were changed and platelet count was marginally improved (day6 60,000, day-7 1,00,000). however there was no improvement in general condition. peripheral smear was normal except mild thrombocytopenia. the patient did not improve and expired on 10th day post injury. discussion the mechanism of isolated thrombocytopenia in septicemia is largely unknown, (3) several mechanisms including compensated disseminated intravascular coagulation, (4) increased platelet destruction, (5) or some impairment of platelet production (6) have been proposed as the possible causes. septicemia, have been identified as the major independent risk factor for thrombocytopenia (2, 7-9) as thrombocytopenia can occur early in the course of septicemia even before the pathogen is cultured from the blood. 10 platelet counts are measured just as frequently as hemoglobin, in the critical care unit, still platelet counts have not been well studied among critically ill patients. (3) thrombocytopenia may occur in patients with septicemia without laboratory evidence of disturbed coagulation profile. (10-12) validity of platelet count as a predictor of bleeding and correction of thrombocytopenia with platelet transfusions, is uncertain, (3) as major bleeding has not been defined consistently across studies. (13, 14) just on the basis of laboratory findings alone, replacement therapy is not recommended and is required only in patients who are actively bleeding, who require an invasive procedure, or who are at risk for bleeding complications. (2, 15) conclusion thrombocytopenia in critically ill patients probably reflects the severity of the underlying illness and these patients have a higher mortality due to the severity of overall clinical status. (3, 1619) few studies statistically examine the strength of the association between risk factors and outcomes related to thrombocytopenia, (3) additional research is recommended to identify putative molecular determinants and pathogenetic mechanisms causing isolated thrombocytopenia in critically ill patients because of septicemia. (20) 102 satish kumar et al isolated thrombocytopenia in acute subdural hematoma correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1. shah ra, musthaq a, khardori n. vancomycininduced thrombocytopenia in a 60-year-old man: a case report. j med case reports 2009;3:7290. 2. stephan f, hollande j, richard o, cheffi a, maierredelsperger m, flahault a. thrombocytopenia in a surgical icu. chest 1999;115:1363-1370. 3. hui p, cook dj, lim w, fraser ga, arnold dm. the frequency and clinical significance of thrombocytopenia complicating critical illness: a systematic review. chest 2011;139:271-278. 4. neame pb, kelton jg, walker ir, stewart io, nossel hl, hirsh j. thrombocytopenia in septicemia: the role of disseminated intravascular coagulation. blood 1980;56:88-92. 5. harker la, slichter sj. platelet and fibrinogen consumption in man. n engl j med 1972;287:999-1005. 6. newsome tw, eurenius k. suppression of granulocyte and platelet production by pseudomonas burn wound infection. surg gynecol obstet 1973;136:375-379. 7. hanes sd, quarles da, boucher ba. incidence and risk factors of thrombocytopenia in critically ill trauma patients. ann pharmacother 1997;31:285-289. 8. yaguchi a, lobo fl, vincent jl, pradier o. platelet function in sepsis. j thromb haemost 2004;2:2096-2102. 9. baughman rp, lower ee, flessa hc, tollerud dj. thrombocytopenia in the intensive care unit. chest 1993;104:1243-1247. 10. corrigan jj, jr., ray wl, may n. changes in the blood coagulation system associated with septicemia. n engl j med 1968;279:851-856. 11. oppenheimer l, hryniuk wm, bishop aj. thrombocytopenia in severe bacterial infections. j surg res 1976;20:211-214. 12. riedler gf, straub pw, frick pg. thrombocytopenia in septicemia. a clinical study for the evaluation of its incidence and diagnostic value. helv med acta 1971;36:23-38. 13. arnold dm, donahoe l, clarke fj, et al. bleeding during critical illness: a prospective cohort study using a new measurement tool. clin invest med 2007;30:e93102. 14. kitchens cs. disseminated intravascular coagulation. curr opin hematol 1995;2:402-406. 15. baglin t. disseminated intravascular coagulation: diagnosis and treatment. bmj 1996;312:683-687. 16. brogly n, devos p, boussekey n, georges h, chiche a, leroy o. impact of thrombocytopenia on outcome of patients admitted to icu for severe community-acquired pneumonia. j infect 2007;55:136-140. 17. martin cm, priestap f, fisher h, et al. a prospective, observational registry of patients with severe sepsis: the canadian sepsis treatment and response registry. crit care med 2009;37:81-88. 18. vandijck dm, blot si, de waele jj, hoste ea, vandewoude kh, decruyenaere jm. thrombocytopenia and outcome in critically ill patients with bloodstream infection. heart lung 2010;39:21-26. 19. caruso p, ferreira ac, laurienzo ce, et al. shortand long-term survival of patients with metastatic solid cancer admitted to the intensive care unit: prognostic factors. eur j cancer care (engl) 2010;19:260-266. 20. khashu m, osiovich h, henry d, al khotani a, solimano a, speert dp. persistent bacteremia and severe thrombocytopenia caused by coagulase-negative staphylococcus in a neonatal intensive care unit. pediatrics 2006;117:340-348. 14bmoscotesalazar_spontaneous 230 moscote-salazar et al spontaneous chronic subdural hematoma spontaneous chronic subdural hematoma in a young male patient: case report luis rafael moscote-salazar1, hernando raphael alvis-miranda2, willen calderón-miranda3, gabriel alcala-cerra1, andres m. rubiano4 1neurosurgeon, universidad de cartagena, colombia 2physician, universidad de cartagena, colombia 3physician, universidad de magdalena, colombia 4neurosurgeon, hospital universitario de neiva, colombia abstract the chronic subdural hematoma is a common pathology in elderly patients. there is usually a history of head trauma. the diagnosis of chronic subdural hematomas in young patients is very rare and few cases have been reported in the literature. the authors present a case of a patient of 16 years old who presented headache of two months of evolution, which was conducted by tomography diagnosis of chronic subdural hematoma. the patient had no history of mild trauma. surgical management was performed, showing a satisfactory evolution. key words: chronic subdural hematoma, spontaneous, headache, young. introduction chronic subdural hematoma (csh) was described in 1857 by virchow, who was based in the hematic origin, and then named “internal hemorrhagic paquimeningitis.” csh is basically a blood collection located under the dural membrane and which is mainly characterized by the presence of capsule evolving the collection; generally occurring in elderly people, (1) currently is observed an increase in the frequency of occurrence of csh, probably due to increased life expectancy and the progress experienced in neuroimaging techniques that allow easy identification of lesions in the subdural space. (2) for the neurosurgeon, the csh is a condition of daily management, obtaining surgical resolution due to the relatively good performance in most cases. but beneath its apparent "goodness", mortality in patients with csh is usually between 0.5% and 8%, some reports reach a mortality of 20%. a better understanding of the pathophysiology of this entity, identifying risk factors, advances in diagnosis and advances in treatment options have significantly improved the prognosis.(3,4) however, this disease in young is unusual; we present a case of a young male patient with no trauma history who developed spontaneous csh. romanian neurosurgery (2014) xxi 2: 230 235 231 clinical case a 16-year-old male patient, without any relevant clinical record, presented holocraneal headache for 2 months, and was transferred from a local hospital that does not have access to neurosurgical care. the patient was admitted to our emergency department with a glasgow coma scale (gcs) score of 14 associated with right hemiparesis with motor strength grade 3. brain computed tomography (ct) and magnetic resonance imaging (mri) documented a large subdural collection in the left hemisphere. (figure 1). we decided to perform surgical evacuation of subdural hematoma with placement of a closed drainage system. the postoperative period was unremarkable at 2 months follow-up, the patient was in gcs 15. postoperative tc documented brain re-expansion and resolution of the subdural collection (figure 2). discusion physiopathology csh is a collection of encapsulated blood, situated below the dura, mainly characterized by the presence of a membrane composed of two layers, an outer and an inner layer. the outer layer undergoes a process which leads to a meningeal reaction due to hemorrhage, which involved blood vessels, smooth muscle cells, eosinophils, erythrocytes, and the collagen fibers subsequently it continuous with neovascularization in large sinusoids with fragile thin walls, with spaces between which passage of erythrocytes and blood plasma is allowed. so it behaves as a semipermeable structure that allows the entry of liquid, favoring the increase of the volume of hematoma. figure 1 brain mri; axial sections showing the presence of csh right frontoparietal convexity, determining a displacement of the middle line, without subfalcine hernia figure 2 postoperative tc at 60 days, showing brain re-expansion without any residual subdural collection 232 moscote-salazar et al spontaneous chronic subdural hematoma it has been determined that the two membranes surrounding the hematoma are originated between the first and the fourth week of the first collection of blood. this is followed by neocapilar growth and liquefaction of the hematoma associated with enzymatic fibrinolysis. furthermore it has been established that in the hematoma outer membrane occur local fibrinolysis, with low levels of fibrinogen and plasminogen. degradation products of fibrin which ultimately inhibit the hemostatic cascade are also increased. factors associated in most cases, sdh is a complication of traumatic brain injury, been rare the nontraumatic causes. at younger ages (child or adolescent), spontaneous chronic sdh is very unusual. the estimated incidence varies between 1.72 sdh, and 14.1 cases per 100,000 inhabitants / year, reaching 7.35 to 10.5 in the age group 70-79 years. (5–7) 83% occur in patients older than 40 years. several factors have been cited as causes, including head trauma, chronic alcoholism and anticoagulation. it has been suggested that a secondary alcohol leads to chronic liver damage coagulopathy and the probable risk of cranial trauma. in the literature it is present between 10 and 50% of cases. other described causes are primary tumors, metastases or vascular malformations, among others. reports spontaneous chronic sdh is a rare entity reported. carvalho et al.(4) in a review of the literature searching for spontaneous sdh, found the case of a 22-year-old patient who complained of persistent headaches and was neurologically intact on examination. cranial ct revealed the presence of a right-sided chronic subdural hematoma; the evaluation was followed by mri plus angiogram, aiming to rule out the presence of any vascular abnormality. as surgical treatment, a burrhole craniostomy procedure was used, resulting in resolution of symptoms. wang et al. (8) reported the case of sdh in a healthy 14-year-old girl who presented with severe headache following blurring of vision two weeks before the presentation without any history of head injury. ct and mri demonstrated a chronic sdh. the cause of the hematoma was not established. as in the case found by carvalho et al, after performing burr hole drainage of the hematoma, the patient made an uneventful recovery.(8) brennan et al. (9) present an unusual case of a 37-year-old healthy young male, who developed a spontaneous sdh. his clinical manifestations were headache was followed by blurring of vision and left upper limb symptoms. the diagnosis was made from a ct scan. symptoms resolved with surgical decompression.(9) this patient was a saxophonist, in who is believed as cause of the hematoma the increase in the venous pressure, as result of valsalva’s maneuver during music performance. clinical course chronic sdh typically occurs in individuals older than 60 years, men, alcoholics or with blood dyscrasias and romanian neurosurgery (2014) xxi 2: 230 235 233 frequent falls, complaining of a progressive clinical syndrome characterized by motor deficits, adding to signs and symptoms of intracranial hypertension. the course of chronic subdural hematoma is slowly progressive, allowing its accommodation around the brain and thereby prevents the sudden development of intracranial hypertension. it is recommended to start research through brain ct in all patients with brain qualitative disorder of consciousness, no matter if is an elderly patient. it can also present as a transient neurological deficit, headache, slurred speech, hemiparesis, seizures, etc. in the young patient the main symptoms are headache (59.5%) and seizures (21.4%), alterations in conscious level are marked in younger rather than elderly patients. (10) diagnosis and management it is extremely important to establish an accurate diagnosis, because it can be misinterpreted as ischemic event and be treated as such (oral anticoagulation or antiplatelet therapy) which is quite risky. simple brain tc is the current imagenology aid choice for the diagnosis of this entity. multiple treatments have been proposed, from mere observation, use of drugs (tranexamic acid, corticosteroids) and the different types of surgery. given the pathophysiology possibly the best option is the evacuation of the collection. conservative treatment is based on the osmotic theory of the formation and growth of chronic sdh by parenteral administration of hyperosmolar substances, which tend to reduce the absorption and volume of hematoma. what happen in young patients? there are very few publications about sdh in the younger population (10–12) because in this age group is not common to see 2 of the main predisposing factors for its development: brain atrophy and use of drugs that interfere with hemostasis. in young people there are a number of factors that we do not see in other age groups, among which: the coagulation disorders such as thrombocytopenic purpura (13) coagulation factors deficits (14) or hematological abnormalities from oncological nature. according to gelabert-gonzález et al. (15), in patients lesser than 40 years old, the mean age at diagnosis is 29.3±8.9 years (range: 4 to 39 years). some factors that facilitate the development of sch in young patients including arachnoid cysts, (17, 18) intracranial hypotension (e.g. ventriculoperitoneal shunt or traumatic/spontaneous spinal fistula) and the consumption of anabolic drugs (e.g. weightlifting). hesselbrock et al (16) review 21 patients with nontraumatic sdh, they found as risk factors: arterial hypertension, vascular malformations, neoplasia such as haematological malignancies causing thrombocytopaenia, solid tumour, dural metastases, infection, hypervitaminosis, coagulopathy and alcoholism. regarding our case, it is proposed that episodes of sudden increase in venous pressure can lead to subdural bleeding. this can happen during valsalva maneuvers as previously mentioned. in young patients taking anabolic drugs, it is believed that the subdural 234 moscote-salazar et al spontaneous chronic subdural hematoma hemorrhage is caused by vascular remodeling. our patient did not use steroids or recreational drugs, which also have been associated with subdural hematomas. (8,9) spontaneous chronic sdh is a rare entity, which treated by conventional neurosurgical management produces offers satisfactory results. correspondence: luis rafael moscote, md; e-mail: mineurocirujano@aol.com references 1. lo w-l, lee t-c, fang p-s, huang y-h. chronic subdural hematoma in patients under age 65 years: a comparative study of age cohort. formos j surg [internet]. 2013 feb [cited 2014 mar 21];46(1):10–4. available from: http://linkinghub.elsevier.com/retrieve/pii/s1682606x12 001193 2. arpino l, gravina m, basile d, franco a. spontaneous chronic subdural hematoma in a young adult. j neurosurg sci [internet]. 2009 jun [cited 2014 mar 21];53(2):55–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/19546844 3. lee k-s. natural history of chronic subdural haematoma. brain inj [internet]. 2004 apr [cited 2014 mar 21];18(4):351–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/14742149 4. de carvalho d, almenawer s, lozej m, noble h, murty nk. spontaneous chronic subdural hematoma in a 22-year-old healthy woman. world neurosurg [internet]. 2013 nov [cited 2014 mar 19];80(5):654.e9– 11. available from: http://www.ncbi.nlm.nih.gov/pubmed/23182734 5. foelholm r, waltimo o. epidemiology of chronic subdural haematoma. acta neurochir [internet]. 1975 jan [cited 2014 mar 19];32(3-4):247–50. available from: http://www.ncbi.nlm.nih.gov/pubmed/1225014 6. cousseau dh, echevarría martín g, gaspari m, gonorazky se. [chronic and subacute subdural haematoma. an epidemiological study in a captive population]. rev neurol [internet]. 2001 [cited 2014 mar 19];32(9):821–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/11424031 7. ducruet af, grobelny bt, zacharia be, hickman zl, derosa pl, anderson k, et al. the surgical management of chronic subdural hematoma. neurosurg rev [internet]. 2012 apr [cited 2014 mar 19];35(2):155–69; discussion 169. available from: http://www.ncbi.nlm.nih.gov/pubmed/21909694 8. wang hs, kim sw, kim sh. spontaneous chronic subdural hematoma in an adolescent girl. j korean neurosurg soc [internet]. 2013 mar [cited 2014 mar 21];53(3):201–3. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3638278&tool=pmcentrez&rendertype=abstract 9. brennan pm, fuller e, shanmuganathan m, keston p, fouyas i. spontaneous subdural haematoma in a healthy young male. bmj case rep [internet]. 2011 jan [cited 2014 mar 21];2011. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3149419&tool=pmcentrez&rendertype=abstract 10. liliang p-c, tsai y-d, liang c-l, lee t-c, chen h-j. chronic subdural haematoma in young and extremely aged adults: a comparative study of two age groups. injury [internet]. 2002 may [cited 2014 mar 19];33(4):345–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/12091031 11. aoki n. chronic subdural hematoma in infancy. clinical analysis of 30 cases in the ct era. j neurosurg [internet]. 1990 aug [cited 2014 mar 19];73(2):201–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/2366077 12. mauer um, kunz u. [chronic subdural hematoma in patients under 35 years of age]. nervenarzt [internet]. 2007 feb [cited 2014 mar 19];78(2):177–80. available from: http://www.ncbi.nlm.nih.gov/pubmed/17245586 13. seçkin h, kazanci a, yigitkanli k, simsek s, kars hz. chronic subdural hematoma in patients with idiopathic thrombocytopenic purpura: a case report and review of the literature. surg neurol [internet]. 2006 oct [cited 2014 mar 21];66(4):411–4; discussion 414. available from: http://www.ncbi.nlm.nih.gov/pubmed/17015125 14. albanese a, tuttolomondo a, anile c, sabatino g, pompucci a, pinto a, et al. spontaneous chronic subdural hematomas in young adults with a deficiency in coagulation factor xiii. report of three cases. j neurosurg [internet]. 2005 jun [cited 2014 mar 21];102(6):1130–2. available from: http://www.ncbi.nlm.nih.gov/pubmed/16028774 15. gelabert-gonzález m, frieiro-dantas c, serramitogarcía r, díaz-cabanas l, aran-echabe e, rico-cotelo romanian neurosurgery (2014) xxi 2: 230 235 235 m, et al. [chronic subdural hematoma in young patients]. neurocirugia [internet]. 2013 mar [cited 2014 mar 19];24(2):63–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/23158924 16. hesselbrock r, sawaya r, means ed. acute spontaneous subdural hematoma. surg neurol [internet]. 1984 apr [cited 2014 mar 22];21(4):363–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/6701770 17. chan j-y, huang c-t, liu y-k, lin c-p, huang j-s. chronic subdural hematoma associated with arachnoid cyst in young adults: a case report. kaohsiung j med sci [internet]. 2008 jan [cited 2014 mar 19];24(1):41–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/18218569 18. mori k, yamamoto t, horinaka n, maeda m. arachnoid cyst is a risk factor for chronic subdural hematoma in juveniles: twelve cases of chronic subdural hematoma associated with arachnoid cyst. j neurotrauma [internet]. 2002 sep [cited 2014 mar 21];19(9):1017–27. available from: http://www.ncbi.nlm.nih.gov/pubmed/12482115 doi: 10.33962/roneuro-2020-080 physiological alteration and anaesthetic drugs effects on intraoperative neurophysiological monitoring procedures mihaela coșman, andreea atomei, nina straticiuc, alexandru caragea, mihai soare, alina mihaela neacșu romanian neurosurgery (2020) xxxiv (4): pp. 475-481 doi: 10.33962/roneuro-2020-080 www.journals.lapub.co.uk/index.php/roneurosurgery physiological alteration and anaesthetic drugs effects on intraoperative neurophysiological monitoring procedures mihaela coșman1, andreea atomei2, nina straticiuc3, alexandru caragea1, mihai soare1, alina mihaela neacșu1,4 1 emergency county hospital, braila, romania 2 student. “grigore t. popa” university of medicine and pharmacy, iasi, romania 3 department of anaesthesia and intensive care. “n. oblu” emergency clinical hospital, iași, romania 4 “carol davila” university of medicine and pharmacy, bucharest, romania abstract intraoperative neurophysiological monitoring (iom) and especially motor evoked potentials represents an important tool in the evaluation of the nervous system integrity and particularly of the motor tracts. a real and correct registration of the potentials with a proper interpretation of the modification is mandatory for an optimal outcome in eloquent areas, tumours, brainstem and medullary lesions. for all this to happen a suitable anaesthetic protocol must be used. even though there is a large spectrum of anaesthetic agents at our disposal it is imperative to know their effect on the iom signals recordings and the fact that some of them are dosedependent. drugs effects and physiological changes produced intraoperatively must be corrected before a shift in the direction of the surgical lesion resection it is taken. we present an overview of the action of the anaesthetic agents, most used protocols and the physiological alteration encountered in the operative theatre. introduction nowadays tumors located in functional areas of the brain, brainstem and medullary lesions still represents a challenge for many neurosurgeons because of the high risk of postoperatively permanent neurological deficits, but the technological development comes in our aid and the golden standard of maximal resection with minimal neurological disfunction can be reached more often using functional technique perioperatively [12,34,35,41,46]. considering those date, intraoperative neurophysiological monitoring (iom) represents a suitable modality for the assessment of the integrity of the nervous system with a real time feedback [32,45,52]. keywords intraoperative neurophysiological monitoring, motor evoke potentials, eloquent areas, propofol, volatile agents, intravenous anaesthesia corresponding author: andreea atomei “grigore t. popa” university of medicine and pharmacy, iasi, romania atomei_andreea96@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 476 mihaela coșman, andreea atomei, nina straticiuc et al. this technique includes various evaluation possibilities e.g., direct cortical / subcortical stimulation and monitoring modalities like motor evoked potentials (meps), somatosensory evoked potentials (sseps), brainstem auditory evoked potentials (baeps), electromyography / free running emg. for proper recording of the motor /sensitive response special anesthetic drugs are used with differences between the induction step and the stage of maintaining of the sedation [4,9,24]. in order to record the motor response, the drugs used during surgery have a major role in data accuracy [11]. the vast majority of anesthetic drugs decrease the synaptic activity, this effect being dose dependent. they have a direct action on synaptic pathways or indirect effect by altering the influence of inhibitory or excitatory mediators: some anesthetic agents may bind to gamma-aminobutyric acid-a receptors, others may block the excitatory effect of glutamic acid and another group act at the neuromuscular junction level at the” n-type” acetylcholine receptors [43]. anesthetic agents’ effects on intraoperative evoked potentials. volatile anesthetics agents (sevoflurane, desflurane, halothane, nitrous oxide), dose dependently suppress the meps by inhibiting the pyramidal activation of spinal motor neurons, they increase the latency and decrease the amplitude (figure 1). meps are more sensitive to their action in comparison with seps [43]. some studies say that a concentration under 0,5-1 at the alveolar level (mac) it is safe for iom recording. nevertheless, for patients with preoperative neurologic disfunction, motor/sensitive alteration or neuropathy, lower doses may impede or even abolish the potentials [55]. a. b. figure i. a) cork-screw electrodes placement for transcranial meps recordings; b) morphology of meps from tibialis anterior muscle and abductor hallucis muscle: red star – time of the stimulus application, yellow arrow – latency (unit: seconds), red arrow – amplitude (unit: volts) (images form dr. coșman m. personal collection). between sevoflurane and desflurane the former has a bigger impact on decreasing the amplitude of meps. the recordings from the lower limbs seem to be more sensitive to anesthetics than the upper limbs [8]. the action mechanisms of desflurane are on different levels: on pre-postsynaptic receptors, on cellular ionic channels and on serotonin type 3 receptors [33,47] hence its capacity of maintaining proper anesthesia and amnesia at 0,5 mac [16]. sevoflurane, halothane, isoflurane are considerate “potent” agents and nitrous oxide is less “potent” being used at higher concentration. the latter is used for iom in combination with other drugs e.g. nitrous-narcotic technique and the effect depends on the agent already present [43]. his action determines a decrease in amplitude and no effect on cortical potentials latency, without changing the wave morphology [5,42]. intravenous agents such as propofol interact with seps and meps recordings, dose dependent, but in a smaller extent compared with volatile agents [44]. by comparison with the baseline the latency of the evoked potentials is prolonged and the amplitude is decreased after both isoflurane or propofol is administrated, but the former has a bigger inhibitory effect on iom than the latter [7]. propofol is been used commonly in tiva technique (calanci et al. 2001, deletis 2002, langeloo et al. 2003, chen et al. 2004, macdonald et al. 2006, sala et al. 2006, szeleny et al. 2007, lieberman et al 477 physiological alteration and anaesthetic drugs effects on intraoperative neurophysiological monitoring procedures 2017, marafona et al.2018, toossi et al. 2019) [6,7,10,18, 20,24,27,39,49,51] or with inhalant anesthetic agents to decrease their dosage [14,17,25,44]. although is the preferred drug in iom procedures, in a study from 2017 it was concluded that hemorrhage may alter the pharmacokinetic properties, the reduction of the cardiac output was associated with increase of the serum concentration which had the capacity to generate false positive results [20]. etomidate influence only the cortical seps (increases the amplitude) and ketamine enhance the response of both potentials, making those agents a good choice for patients with preoperatively functional deficit. nowadays the former is not used so frequently because of the risk of increasing the intracerebral pressure. etomidate produces the less depression over potentials amplitude but utilized in continuous infusion may induces adrenocortical suppression [30,42]. barbiturates (thiopental) influence significatively the meps, but they do not affect the seps registration so strongly. benzodiazepines – midazolam decreases the potential recordings, especially of meps but has an advantage by inducing amnesia [30]. dexmedetomidine ensure analgesia and sedation acting on α2 agonist receptors with minimal respiratory depression. in a study from 2015 published by rozet it is shown that this agent does not have a significant effect on the potential’s latency and amplitude [36]. as an adjuvant, when propofol is utilized for iom anesthesia, dexmedetomidine determine smaller changes on meps recordings in comparison with midazolam but alters in a bigger way the hemodynamical parameters [1]. also in a randomized double blinded study the use of dexmedetomidine before induction (1 µg/kg over 10 minutes) and at the maintenance stage (0,2µg/kg/hr) was associated with a need of lower doses of propofol and stable hemodynamical parameters [48]. from opioids, fentanyl may even improve the myogenic reaction when utilized for iom by reducing the spontaneous muscular contraction from the background [43]. another intravenous agent, remifentanil can be used in infusion, being an ultrashort action narcotic, but he has the disadvantage of opioid-induced hyperalgesia [14]. muscular relaxants have little effect on seps recordings but interact with meps registration. partial muscular blockade has the advantage of reducing the patient movements and facilitate the tissue retraction. to determine the degree of blockage we can use two methods: we measure the amplitude produced by supramaximal stimulation of the peripheral motor nerve – t1 (m wave) and compare with the baseline value obtained after the drugs where administrated. another technique requires to evaluate the motor response after 4 stimuli are delivered at 2 hz rate [43]. various anesthetic techniques were used and some combination have been tested with the aim of minimum effect on iom recordings. it was observed that at the same mac concentration volatile drugs have a greater suppression effect. however, the best protocol is still controversial [9,54]. however, it is important to know that: the most resistant type of potential at anesthetic drugs are baeps, visual evoked potentials are the most sensitive, meps can be totally blocked by skeletal muscle relaxants and the recordings of seps depends on type of the anesthetic drugs [15]. sometimes to assess the depth of the anesthesia can be a challenge for the anesthesiologist because the placement of the electrodes may coincide with the skin incision and so the type of the anesthesia must be chosen keeping in mind the site of the operation and the general status of the patient [17]. a summary of medications interactions with neurophysiological monitoring, especially with the meps recordings is presented in table 1. table 1. aesthetic drugs influence on motor evocated potentials [15,22,30]. anesthetic drug mep latency mepamplitude observation sevoflurane increase decrease use: mac – 0.5 nitrous oxide increase decrease strong effect, should be avoided fentanyl preserved slight depression dose dependent remifentanyl preserved decrease rapid metabolism – rapid titration propofol increase decrease dose dependent; 478 mihaela coșman, andreea atomei, nina straticiuc et al. rapid metabolism – rapid titration thiopentone high increase high decrease marked suppression etomidate decrease increase enhances the potentials ketamine increase increase enhances the potentials midazolam high increase high decrease marked suppression; indicated only in premedication administration dexmedeto midine increase decrease use to lower other tiva agents dose a combination of those drugs may be used as well with proper sedation and without impairing the iom measuring’s. gunter presented in 2016 a protocol which includes inhalant agent at a mac= 0,5 associated with remifentanil and dexmedetomidine. this technique has the advantage of a quick emergency from the general anesthesia due to the latter drug, which produces the sedation effect by acting in locus ceruleus [14]. another study presented by isik et al. in 2017, where optimal potentials recordings were obtained by using desflurane (0,5 mac) with remifentanil (0,05-0,3µg/kg/min at 50% o2) considers this association safe and an alternative for more used tiva technique [16]. in a randomized survey published by martin et al. in 2014 a comparison has been made between the two classes of drugs: the total intravenous technique (propofol – remifentanil) with volatile agents (desflurane – remifentanil). the results showed the necessity of a higher voltage to elicit response in volatile agent anesthesia [14,28]. similar results have been found by velayutham et al. in a study on spinal cord tumors from 2019 where the stimulation applied was 205 ± 55 volts for propofol anesthesia (6-8mg/kg/hr) and 274 ± 60 volts for isoflurane [53]. sloan et al. presents in 2015 a combination of inhalant and intravenous anesthesia (0,5 mac desflurane with propofol) with good results regarding electrophysiological monitoring and this technique may be an advantage for patients with opioid tolerance [3,44]. in a retrospective cohort study published in 2020 by oh et al. it was evaluated the postoperatively liver function in patients with preoperative transaminase alteration comparing the group cases operated using total intravenous anesthesia (propofol) with those operated using inhalator agents (sevoflurane). the halogenated inhalational drugs are frequently used but they are associated with hepatotoxicity which is less encountered in latest anesthetic agents like sevoflurane or desflurane. the study concluded that the changes in liver enzyme levels were obviously lower for patients from the tiva group and this type of anesthesia is indicated in neurosurgical intervention especially because of the longer time of the operation [2,31,37]. other study from 2020 presented by grau et al. discusses de impact of the anesthesia type on tumors recurrence and how the surgical stress can affect the mechanisms of the immune response inducing a vulnerable perioperative period. the idea started from the results obtain in vitro, where anesthetic drugs acted over tumor cells culture. propofol induced apoptosis in contrast with isoflurane which increased proliferation of glioblastoma stem cells, however the results have not been consistent because of the differences induced by the cell line [29,38]. the conclusion that grau et al. have reached shows no difference between volatile agents and tiva regarding glioblastoma recurrence (volatiles 8 vs. propofol 8,4 months) or overall survival (volatiles 16,9 vs. propofol 17,4 months) [13]. another thing to keep in mind when there is a oscillation between tiva and inhalational anesthesia is the fact that in a study from 2014 published by tamkus et al. volatile drugs were associated with obviously higher false positive responses (15% vs. 3,2%) compared with intravenous agents, when recording transcranial meps [50]. modification in potentials amplitude and the need of a higher voltage to elicit the same result was observed as independent of anesthetic drugs concentration during the intervention, phenomenon named “anesthetic fade”. this situation is produced by a long exposure of the nervous system to the drugs action [23]. in contrast with this decrease effect, it was observed and an increase impact called “anesthetic fade-in”. this may happen if the baseline measurements of the meps were recorded before the surgical procedure started and before the effect 479 physiological alteration and anaesthetic drugs effects on intraoperative neurophysiological monitoring procedures of the myorelaxants drugs used at induction disappeared [19]. therefore, the mainstay in anesthesia protocols are synthetic opioid (fentanyl, sufentanyl) and propofol which under continuous administration have the capacity to maintain a constant serum concentration. due to their pharmacokinetic properties the influence on amplitude, latency of meps and direct cortical stimulation is negligible [30]. this makes tiva (lo et al.2006, martin et al. 2014, tamkus et al. 2014, sloan et al.2015, malcharek et al. 2015, velayutham et al. 2019, oh et al.2020) more suitable for meps recording than inhalant anesthesia [ 21,26,28, 31,44,50,53]. physiological changes on intraoperative evoked potentials. temperature. cortical seps are the most vulnerable to temperature changes. brain irrigation with cold serum affects the potential recordings [15]. hyperthermia decrease the latency of meps where the hypothermia increases the latency. the effect of temperature on the conduction velocity of both meps and seps is raised in case of hyperthermy and reduced in case of hypothermia [27,40]. ventilation. on the one hand the most visible alteration induced by hypoxemia is on seps, on the other hand hypocapnia has a smaller effect on seps and meps [15]. hypercapnia has inhibitory effect on anterior horn cell and on cortical level, but the registration of the potential is altered only when extreme level of co2 is reached [22]. blood rheology. the blood viscosity and oxygenation depend on hematocrit values. studies have shown that mild anemia is associated with increase in seps amplitude, but no results are cited about meps [22,43]. intracranial pressure. intracranial hypertension decreases the amplitude of seps and prologs the latency. when the uncal herniation occurs the brainstem response is lost and mep signal can no longer be recorded [22,43]. blood pressure. of all the above, hypotension may induce severe potential alteration. at first when the perfusion pressure is raised again the changes restore to baseline. if the perfusion pressure is decreased under 15 ml/ min/100g tissue there are important changes, severe alteration and even the evoked potentials may be abolished [40]. usually mild to moderate changes do not affect meps values [22]. sometimes systemic blood pressure values may not predict regional ischemia induced by local factors like: prolong tissue retraction, vasospasm, positioning, head extension which can be discovered by potentials alterations [15,40,43]. conclusion a good neurological outcome for lesion located in eloquent area or for those with medullary development depends on the correct interpretation of the iom signals and surgical maneuvers. but all of those are interconnected with proper anesthesia management and a teamwork. so far, a standard anesthetic protocol is missing, but general recommendations have been made. even though the intravenous agents are more appropriate, the use of volatile anesthetic agents or a combination of them it is up to the anesthesiologist and the particularity of the case. references 1. aggarwal d, mahajan hk, chauhan pr. a comparative evaluation of dexmedetomidine with midazolam as an adjuvant to propofol anesthesia for spinal surgical procedures under motor evoked potential monitoring. anaesth pain & intensive care, 20(2):154-158, 2016. 2. ahmed z, ahmed u, walayat s, et al. liver function tests in identifying patients with liver disease. clin exp gastroenterol,11:301–307, 2018. 3. alkire mt, hudetz ag, tononi g. consciousness and anesthesia. science, 322(5903):876–80, 2008. 4. biscevic m, sehic a, krupic f. intraoperative neuromonitoring in spine deformity surgery: modalities, advantages, limitations, medicolegal issues – surgeons’ views. efort open rev, 5:9-16, 2020. 5. bithal pk. anaesthetic considerations for evoked potentials monitoring. j neuroanaesthesiol crit care, 1:2-12, 2014. 6. calancie b, harris w, brindle gf, green ba, landy hj. threshold-level repetitive transcranial electrical stimulation for intraoperative monitoring of central motor conduction. j neurosurg, 95(2 suppl.):161–8, 2001. 7. chen z. the effects of isoflurane and propofol on intraoperative neurophysiological monitoring during spinal surgery. j clin monit comput,18(4):303-8, 2004. 480 mihaela coșman, andreea atomei, nina straticiuc et al. 8. chong ct, manninen p, sivanaser v et a. direct comparison of the effect of desflurane and sevoflurane on intraoperative motor-evoked potentials monitoring. j neurosurg anesthesiol, 26(4):306-12, 2014. 9. deiner s. highlights of anesthetic considerations for intraoperative neuromonitoring. semin cardiothorac vasc anesth, 14(1):51-53, 2010. 10. deletis v. intraoperative neurophysiology and methodologies used to monitor the functional integrity of the motor system. in: deletis v, shils jl, editors. neurophysiology in neurosurgery. san diego: academic press; 2002. p. 25–51. 11. gheorghita e, ciurea j, balanescu e. considerations on anesthesia for posterior fossa-surgery. romanian neurosurg xix 3:183-192, 2012. 12. giamouriadis a, lavrador jp, bhangoo r et al. how many patients require brain mapping in an adult neurooncology service? neurosurg rev, 43(2):729-738, 2020. 13. grau sj, lohr m, taurisano v et al. the choice of anaesthesia for glioblastoma surgery does not impact the time to recurrence. sci rep 10: 5556, 2020. 14. gunter a, ruskin kj. intraoperative neurophysiologic monitoring: utility and anesthetic implications. curr opin anesthesiol, 29:539–543, 2016. 15. helal sa, abd elaziz aa, dawoud age. anesthetic considerations during intraoperative neurophysiological monitoring in spine surgery. menoufia med j. 31: 1187-92, 2018. 16. isik b, turan g, abitagaoglu s et al. a comparison of the effects of desflurane and total intravenous anaesthesia on the motor evoked responses in scoliosis surgery. int j res med sci,5(3):1015-1020, 2017. 17. kawaguchi m, iida h, tanaka s et al. a practical guide for anesthetic management during intraoperative motor evoked potential monitoring. j anesth, 34(1):5-28, 2020. 18. langeloo dd, lelivelt a, journée hl, slappendel r, de kleuver m. transcranial electrical motor-evoked potential monitoring during surgery for spinal deformity: a study of 145 patients. spine, 28:1043–50, 2003. 19. lee jy, lim bg, lee io. progressive enhancement of motor-evoked potentials during general anesthesia: the phenomenon of "anesthetic fade-in". j neurosurg anesthesiol, 25(1):87-9, 2013. 20. lieberman ja, feiner j, rollins m, lyon r. changes in transcranial motor evoked potentials during hemorrhage are associated with increased serum propofol concentrations. j clin monit comput, 32(3):541-548, 2018. 21. lo yl, dan yf, tan ye et al. intraoperative motor-evoked potential monitoring in scoliosis surgery: comparison of desflurane/nitrous oxide with propofol total intravenous anesthetic regimens. j neurosurg anesthesiol, 18:211–214, 2006. 22. lotto ml, banoub m, schubert a. effects of anesthetic agents and physiologic changes on intraoperative motor evoked potentials. j neurosurg anesthesiol, 16:32–42, 2004. 23. lyon r, feiner j, lieberman ja. progressive suppression of motor evoked potentials during general anesthesia: the phenomenon of "anesthetic fade”. j neurosurg anesthesiol ,17(1):13-9, 2005. 24. macdonald db. intraoperative motor evoked potential monitoring: overview and update. j clin monit comput, 20:347–77, 2006. 25. macdonald db, skinner s, shils j, yingling c. intraoperative motor evoked potential monitoring – a position statement by the american society of neurophysiological monitoring. clin neurophysiol ,124(12):2291-316, 2013. 26. malcharek mj, loeffler s, schiefer d et al. transcranial motor evoked potentials during anesthesia with desflurane versus propofol – a prospective randomized trial. clin neurophysiol, 126(9):1825-32, 2015. 27. marafona as, machado hs. intraoperative evoked potentials: a review of clinical impact and limitations. j anesth clin res, 9:2-11, 2018. 28. martin dp, bhalla t, thung a et al. a preliminary study of volatile agents or total intravenous anesthesia for neurophysiological monitoring during posterior spinal fusion in adolescents with idiopathic scoliosis. spine, 39(22):1318-1324, 2014. 29. meier, a. et al. isoflurane impacts murine melanoma growth in a sex-specific, immune-dependent manner. anesth analg. 126(6), 1910–1913, 2018. 30. nunes rr, bersot cda, garritano jg. intraoperative neurophysiological monitoring in neuroanesthesia. curr opin anesthesiol, 31:532–538, 2018. 31. oh sk, lim bg, kim ys, kim ss. comparison of the postoperative liver function between total intravenous anesthesia and inhalation anesthesia in patients with preoperatively elevated liver transaminase levels: a retrospective cohort study. ther clin risk manag, 16:223-232, 2020. 32. olesnicky bl, d’souza rj, jayram d et al. the establishment of an anaesthetist-managed intraoperative neurophysiological monitoring service and initial outcome data. anaesth intensive care, 46(1):74-78, 2018. 33. pavel ma, peterson en, wang h, lerner ra, hansen sb. studies on the mechanism of general anesthesia. pnas, 24: 13757-13766, 2020. 34. petrescu g, gorgan c, giovani a et al. preoperative mapping of the eloquent cortical areas using navigated transcranial magnetic stimulation combined with intraoperative neuronavigation for intracerebral lesions. romanian neurosurg xxxii 1: 16-14, 2018. 35. rossi m, nibali mc, vigano l et al. resection of tumors within the primary motor cortex using high-frequency stimulation: oncological and functional efficiency of this versatile approach based on clinical conditions. j neurosurg, 9;1-13, 2019. 36. rozet i, metzner j, brown m, et al. dexmedetomidine 481 physiological alteration and anaesthetic drugs effects on intraoperative neurophysiological monitoring procedures does not affect evoked potentials during spine surgery. anesth analg, 121:492–501, 2015. 37. safari s, motavaf m, seyed siamdoust sa, alavian sm. hepatotoxicity of halogenated inhalational anesthetics. iran red crescent med j,16(9):20153–20153, 2014. 38. saito j, masters j, hirota k, ma d. anesthesia and brain tumor surgery: technical considerations based on current research evidence. curr opin anaesthesiol, 32(5), 553–562, 2018. 39. sala f, palandri g, basso e et al. motor evoked potential monitoring improves outcome after surgery for intramedullary spinal cord tumors: a historical control study. neurosurgery, 58:1129–43, 2006. 40. sanders b, catania s, luoma am. principles of intraoperative neurophysiological monitoring and anaesthetic considerations. anesth & intensive care med, 21(1): 39-44, 2020. 41. sandu am, furtos ma, petrescu g et al. primary intramedullary spinal cord non-hodgkin lymphoma case report and review of the literature. romanian neurosurg xxxii 4: 538-546, 2018. 42. sloan tb. anesthesia management and intraoperative electrophysiological monitoring. in: kohta a, sloan tb, toleikis jr, editors. monitoring the nervous system for anesthesiologists and other healthcare professionals, 2nd ed. cham: springer; 2017. pp. 317–341. 43. sloan tb, heyer ej. anesthesia for intraoperative neurophysiologic monitoring of the spinal cord. j clin neurophysiol, 19(5):430-43, 2002. 44. sloan tb, toleikis jr, toleikis sc, koht a. intraoperative neurophysiological monitoring during spine surgery with total intravenous anesthesia or balanced anesthesia with 3 % desflurane. j clin monit comput, 29(1):77-85, 2015. 45. skinner s. the patient‑centered care model in ionm: a review and commentary. j clin neurophysiol, 30:204– 209, 2013. 46. so el, alwaki a. a guide for cortical electrical stimulation mapping. j clin neurophysiol, 35(2):98-105, 2018. 47. son y. molecular mechanisms of general anesthesia. korean j anesthesiol, 59(1): 3-8, 2010. 48. suvadeep s, chakraborty j, santra s, mukherjee p, das b. the effect of dexmedetomidine infusion on propofol requirement for maintenance of optimum depth of anaesthesia during elective spine surgery. indian j anaesth, 57:358-63, 2013. 49. szelényi a, kothbauer kf, deletis v. transcranial electric stimulation for intraoperative motor evoked potential monitoring: stimulation parameters and electrode montages. clin neurophysiol, 118:1586–95, 2007. 50. tamkus aa, rice ks, kim hl. differential rates of falsepositive findings in transcranial electric motor evoked potential monitoring when using inhalational anesthesia versus total intravenous anesthesia during spine surgeries. spine j, 14(8):1440-6, 2014. 51. toossi a, everaert dg, uwiera rre et al. effect of anesthesia on motor responses evoked by spinal neural prostheses during intraoperative procedures. j neural eng, 16(3):036003, 2009. 52. van der walt jjn, thomas jm, figaji aa. intraoperative neurophysiological monitoring for the anaesthetist. south afr j anaesth analg, 19(3):139-144, 2013. 53. velayutham p, cherian vt, rajshekhar v, babu ks. the effects of propofol and isoflurane on intraoperative motor evoked potentials during spinal cord tumour removal surgery a prospective randomised trial. indian j anaesth, 63(2): 92–99, 2019. 54. wang ac, than kd, etame ab, la marca f, park p. impact of anesthesia on transcranial electric motor evoked potential monitoring during spine surgery: a review of the literature. neurosurg focus, 27(4): e7, 2009. 55. wing-hay hy, chun-kwong ec. introduction to intraoperative neurophysiological monitoring for anaesthetists. atotw, 397, 2019. 6_oslobanua_anatomic romanian neurosurgery (2015) xxix 3: 269 275 269 anatomic locations in high grade glioma a. oslobanu1, st.i. florian2 university of medicine and pharmacy, “iuliu hatieganu” cluj-napoca 1assistant professor in neurosurgery, 2professor in neurosurgery abstract: the treatment options and prognosis in gliomas could be determined by anatomic topographic location, beside different subtypes of glioma. the aim of this study is to find if any correlation between anatomical location of a glioma and the different subtypes of high grade glioma exist, and if this differences exists, does this influence the treatment options in terms of surgery. to do this, a representative group of 318 adults with high grade glioma was used. the most frequent subtypes of high grade glioma were glioblastoma (76,1%) followed by anaplastic astrocytomas (19,1%), anaplastic oligodendrogliomas (2,2), anaplastic ependymomas (1,2%), anaplastic oligoastrocytomas (0,9%), and anaplastic oligoastrocyomas (0,3%). the most frequent locations of gliomas were in the right frontal lobe in 11,95% of the cases, followed by left frontal in 9,12%, left temporal in 9,12%, right parietal in 8,18%, left parietal in 6,60%, right temporal in 5,66% for one lobe location. for multiple lobe locations the left fronto-parietal and left temporo-parietal (5,03%) were the most frequent locations. deepseated locations were present in 1,56% of the cases, and brain stem location was in 3,46%. no significant difference was observed between left or right predominence. regarding the results among different subtypes of high grade glioma we noted that the anaplastic astrocytomas were more frequently located at the right frontal lobe in 18,03% compare to left frontal and left parietal lobe in 9,83%. in glioblastoma we found no significant differences in anatomical location as seen in anaplastic astrocytomas. these data results from our study could affect the therapeutic strategy regarding the extent of tumors resection. key words: brain tumors, location, high grade glioma, imaging. introduction incidence of glioma increased during the last 3-4 decades, and is around 5/100 000. they can develop at all ages, but the incidence is higher in the 5th and 6th decades of life. few several causes could explain this increase in incidence, the advance in neuroimaging possibilities being one of them along with a better access to neurosurgical services. [1] according to the who high grade glioma comprises glioblastoma – grade iv, anaplastic astrocytoma – grade iii, mixed anaplastic astrocytoma – grade iii, and anaplastic oligodendroglioma – grade iii. [2] the tumor grade is considered to be the most important prognostic factor, and glioblastomas carring the worst prognosis, oligodendroglioma tending to have the best outcome with higher response rates to chemotherapy and radiotherapy. anaplastic astrocytoma and mixed anaplastic oligoastrocytoma have an intermediate prognosis between glioblastoma and anaplastic oligodendroglioma. [1] locations of the gliomas have an impact to the treatment options and prognosis but even that, a few large-scale study have been 270 oslobanu, florian anatomic locations in high grade glioma published with detailed anatomic topographic locations of gliomas. [3] development of the gliomas in different lobes is believed to be relative to the volume of glial tissue, and revealing the diferencies in the anatomic location of gliomas could provide some details about gliomas etiology and pathogenesis. [4, 5, 6] for exemple, this can give clues in the role played by traumatic events or exposure to the electromagnetic radio-frequency fields form mobile phones to the development of gliomas. also, another possible situation is related to the functional differences among cells and tissues in different areas of the brain, or the possibilities of the existence of physiologic stimuli to the adjacent glial tissue by anatomic structures in developing high grade gliomas. some studies show the differences in the biologic characteristics in subsets of gliomas arising in different anatomic locations. [7, 8] using neuroradiological imaging we try to find some details about the posibilities of developing gliomas in specific anatomical locations. material and methods all cases included in the study were from the database of neurosurgical clinic in clujnapoca, and collecting the records of all patients diagnosed with high grade glioma during the period from january 2000 to december 2010. inclusion criteria in the study were based on the age of the patient and surgical treatment. those patients included in the study were required to be over 20 years, and all of them were treated by surgery. after surgical resection the department of pathology confirmed the diagnoses of high grade gliomafor patients included in the study. the diagnosis of high grade glioma was made using the pathological criteria offered by who, and they were classified into the following subgroups: glioblastomas, anaplastic astrocytomas, anaplastic ependymomas, anaplastic oligoastrocytomas, and anaplastic oligodendrogliomas. all patients or their family/relatives gave their consent to enter the study, and their identity was not revealed during or after the study. the topographic anatomic location of the glioma was specified using neuroradiologic imaging and the neuroradiologist indications. for the age standardization the world standard population was used. [9] the statistic analysis was done using the r project that provides a wide variety of statistical (linear and nonlinear modelling, classical statistical tests, tme-series analysis, classification, clustering) and graphical techniques. r is available as free software under the terms of the free software foundation’s gnu general public license in source code form. to compare distribution of different histological subtypes, high grade gliomas were grouped in different categories: anaplastic astrocytomas, glioblastomas, anaplastic oligodendrogliomas, and anaplastic oligoastrocytomas. results during the period of our study a number of 318 patients with high grade gliomas were diagnosed (table i). the vast majority were glioblastomas with 76,10% of the cases. at a distance, on the second place was anaplastic astrocytomas in 19,18% cases, followed by anaplastic oligodendrogliomas (2,2%), anaplastic ependymomas (1,26%), anaplastic oligoastrocytomas (0,94%), and finally anaplastic oligodendroastrocytomas with 0,31% of the cases. table 1 number and incidence of gliomas by histologic type pathology no. % gbm 242.00 76.10 aa 61.00 19.18 odga 7.00 2.2 ea 4.00 1.26 oaa 3.00 0.94 odaa 1.00 0.31 romanian neurosurgery (2015) xxix 3: 269 275 271 over all, the most frequent locations of the high grade gliomas were in the cerebral lobes (figure 1). gliomas of the right frontal lobe in 11,95% of the cases, followed by left frontal in 9,12%, left temporal in 9,12%, right parietal in 8,18%, left parietal in 6,60%, right temporal in 5,66% for single lobe location. for multiple lobe locations the left fronto-parietal and left temporo-parietal (5,03%) were the most frequent locations. deep-seated locations were present in 1,56% of the cases, and brain stem location was in 3,46%. lateralization of the gliomas showed a diference between right and left distribution with 47,16% of the case on the right, and 44,65% on the left. location in the center of the brain (considered for locations at the corpus callosum, thalamus and lateral ventricles) was in 7,54% cases, and only in 2 cases it was situated bilateral in the frontal lobes, both of them being glioblastoma (figure 2). between different lobes there were some differences in tumor frequencies. for glioblastomas, the most frequent single lobe location was at the right frontal lobe in 26 cases (10,33%), followed by right parietal and left frontal lobe in 23 cases (9,5%). for the multiple lobes location the most frequent location was at the left temporo-parietal lobes in 14 cases (5,78%), right fronto-parietal lobes in 13 cases (5,37%), and left fronto-temporal lobes in 12 cases (4,95%)(figure 3). anaplastic astrocytomas were most frequent located at the right frontal lobe in 11 cases (18,03%), followed by the left frontal, left parietal and left temporal lobes with 6 cases for each location (9,83%), and in multiple lobes location the left fronto-parietal lobes was the most frequent location with 6 cases (9,83%)(figure 4). involvement of the corpus callosum and bilateral frontal location was observed only in glioblastomas, but the location at the brain stem was more frequent for anaplastic astrocytomas then glioblastomas (5 vs. 3 cases). figure 1 incidence by tumors location for high grade gliomas 1 .5 7 0 .9 4 0 .6 3 1 1 .9 5 5 .0 3 4 .0 9 9 .1 2 3 .7 7 0 .3 1 3 .7 7 0 .6 3 0 .3 1 0 .6 3 0 .6 3 8 .1 8 0 .3 1 0 .3 1 3 .4 6 3 .1 4 6 .6 0 .6 3 0 .3 1 0 .3 1 1 .2 5 0 .3 1 3 .4 6 5 .6 6 1 .5 7 1 .2 6 3 .4 6 0 .6 3 0 .3 1 5 .0 3 9 .1 2 1 .2 6 0 2 4 6 8 10 12 14 c c c e re b e lu m f b il a te ra l f r ig h t f p r ig h t f p l e ft f l e ft f t r ig h t f t p l e ft f t l e ft n b r ig h t n b l e ft o r ig h t o l e ft p r ig h t p r ig h t + … p in e a l g l p o r ig h t p o l e ft p l e ft p t r ig h t p t o l e ft p t l e ft t h a la m u s r ig h t t h a la m u s le ft b ra in s te m t r ig h t t o r ig h t t o l e ft t p r ig h t t p o r ig h t t p o l e ft t p l e ft t l e ft l a te ra l… tumor location 272 oslobanu, florian anatomic locations in high grade glioma figure 2 left-right tumor location for high grade gliomas figure 3 incidence by location in glioblastomas 0.62 47.16 7.54 44.65 tumor location bilateral right central left romanian neurosurgery (2015) xxix 3: 269 275 273 figure 4 incidence by location in anaplastic astrocytomas for the rest of the high grade gliomas there were no significant differences between locations in the cerebral lobes. discussion according with the data presented in the central brain tumor registry of the united states, glioblastomas account for 51%, anaplastic astrocytomas for 8%, and oligodendrogliomas for 10% of all primary brain.[10] in our study, glioblastomas accounted for 76,10%, anaplastic astrocytomas for 19,18%, and oligodendrogliomas for 2,2% in high grade gliomas group. the number of high grade gliomas was substantially higher for the frontal lobe (21%), but the frequency are even distributed between parietal and temporal lobes (14,78%) with no regards to the right or left locations. at the frontal lobes the distributions of high grade gliomas shows a difference between right and left distribution with the predominence for the right location (11,95%) compare to the left (9,12%). at the other side, the occipital lobe was proved to be the location for high grade gliomas in only 0,63% of the cases. a study made by simpson et al. in 1993 found that 43% of glioblastomas were located in the frontal lobe, 28% in the temporal, 25% in the parietal, and 3% in the occipital lobe. [11] in our study, frontal location of glioblastomas was found in 20% of the cases, in the parietal and temporal lobes almost equally with 15%, and in the occipital lobe in 1% of the cases. bilateral occurrence of glioblastoma was found toward the frontal lobes, and the involvement more frequent on the right hemisphere as it has been reported in another study. [12, 13] anaplastic astrocytomas tend to have the same distribution in the cerebral lobes with the frontal lobe location in 28%, 14% in the temporal, 13% in the parietal lobe, and no pure 274 oslobanu, florian anatomic locations in high grade glioma occipital location only by extension from adjacent areas. the studies shows that tumors were distributed toward frontal subcortical areas. the subcortical areas contain the glial cells, whereas the cortical areas consist of gray material, and as gliomas develop from the glial cells, the difference between the cell types in separate areas partly could explain why tumors develop preferably from the subcortical sites. partly, involvement of developmental, neurochemical, or functional factors in the pathogenesis of gliomas could explaine this nonuniform anatomical distribution of gliomas. in another study, allelic loss was commonly found in oligodendroglioma located in the same areas were was found the highest tumor frequency.[14] it also has been suggested that tumors located in different parts of the brain may arise from different precursor cells or involvement of structural and functional differences between different brain regions, including energy metabolism, architectonic arrangements of the tissues, and interaction between neuronal and glial cells, has been postulated.[15] a slightly overestimated regarding the frequency of gliomas in some lobes is possible, because tumors in unspecific or deep brain location could be coded into the lobes. but all these issues could not explain the differences between gliomas distribution on cerebral lobes. the anatomical distribution of gliomas differs between adults and children. [16] in these regard findings of this study apply only for the gliomas in adults. conclusions the results of this study indicate that gliomas arise mainly from the anterior subcortical structures of the brain, with special regards for frontal lobes, followed by parietal and temporal lobes, and minor involvement of the occipital lobes. the predominance in the frontal lobes could not be explained only by tissue volume alone. a detailed analysis of a large case series will consolidate the knowledge about localization of gliomas, and will provide details about the development of gliomas. even more, details about development preferences of gliomas to different location of the brain will provide technical notes about surgical strategies in dealing with different types and/or subtypes of gliomas. correspondence dr. aurel oslobanu str. victor babes nr.43, cluj-napoca, romania tel-fax: 0040-264-450023 e-mail: oslobanu@yahoo.com references 1. r stupp, j-c tonn, m brada, g pentheroudakis and on behalf of the esmo guidelines working group. highgrade malignant glioma: esmo clinical practice guidelines for diagnosis, treatment and follow-up. ann oncol (2010) 21 (suppl 5): v190-v193.doi: 10.1093/annonc/mdq187 2. world health organization. international statistical classification of diseases and related health problems, icd-10. 2. geneva: world health organization; 2005 3. duffau h, capelle l. preferential brain locations of low-grade gliomas. cancer. 2004 jun 15; 100(12):26226. 4. larjavaara s, mäntylä r, salminen t, haapasal h raitanen, j jääskeläinen, j& auvinen a.(2007). incidence of gliomas by anatomic location. neurooncology, 9(3), 319–325. doi:10.1215/15228517-2007016 5. inskip p, linet ms, heineman ef. etiology of brain tumors in adults. epidemiol rev. 1995;17:382–414 6. ohgaki h, kleihues p (2005). epidemiology and etiology of gliomas. acta neuropathol (berl) 109: 93– 108 7. zlatescu mc, tehraniyazdi a, sasaki h, megyesi jf, betensky ra, louis dn, cairncross jg. tumor location and growth pattern correlate with genetic signature in oligodendroglial neoplasms. cancer res. 2001 sep 15; 61(18):6713-5. 8. mueller w, hartmann c, hoffmann a, et al. genetic signature of oligoastrocytomas correlates with tumor location and denotes distinct molecular subsets. am j pathol. 2002;161:313–319 9. bray f, guilloux a, sankila r, parkin dm. practical implications of imposing a new world standard population. cancer causes control. 2002 mar; 13(2):175-82. 10. cbtrus. statistical report: primary brain tumors in the united states, 1997–2001. central brain tumor registry of the united states. 2004. available at romanian neurosurgery (2015) xxix 3: 269 275 275 http://www.cbtrus.org/reports//20042005/2005report.pdf. 11. simpson jr, horton j, scott c, et al. influence of location and extent of surgical resection on survival of patients with glioblastoma multiforme: results of three consecutive radiation therapy oncology group (rtog) clinical trials. int j radiat oncol biol phys. 1993;26:239– 244 12. ali kahn a, o’brien df, kelly p, et al. the anatomical distribution of cerebral gliomas in mobile phone users. ir med j. 2003;96:240–242 13. inskip pd, tarone re, hatch ee, et al. laterality of brain tumors. neuroepidemiology. 2003;22:130–138. [pubmed] 14. laigle-donadey f, martin-duverneuil n, lejeune j, et al. correlations between molecular profile and radiologic pattern in oligodendroglial tumors. neurology. 2004;63:2360–2362 15. duffau h, capelle l. preferential brain locations of low-grade gliomas. cancer. 2004;100:2622–2626 16. legler j, gloecker ries la, smith ma, et al. brain and other central nervous system cancers: recent trends in incidence and mortality. j natl cancer inst. 1999;91:1382–1390 guzinozdemir_magnetic 98 ozdemir et al the changes of olfactory bulb volume in major depression magnetic resonance imaging study; does the olfactory bulb volume change in major depression? nuriye guzin ozdemir1, ibrahim burak atci1, sevda bag2, hakan yilmaz3, yesim karagoz4, adem yilmaz5 1istanbul education and research hospital, department of neurosugery, istanbul, turkey 2istanbul education and research hospital, department of phychiatry, istanbul, turkey 3duzce ataturk state hospital, department of neurosugery, duzce, turkey 4istanbul education and research hospital, department of radiology, istanbul, turkey 5sisli hamidiye etfal education and research hospital, department of neurosurgery, istanbul, turkey abstract: goal: the olfactory region function disorders and olfactory bulb volume changes in neurodegenerative and neuropsychiatric disorders are defined. in this study, the olfactory bulb values of patients diagnosed with major depression in accordance with dms-iv criteria, are measured with mri, and these values are compared with the values of healthy volunteers to see if there are any statistically significant changes. method: the study was carried out with 20 healthy volunteers and 20 patients who had been diagnosed with acute major depression in accordance with ‘diagnostic and statistical manual of mental disorders’ (dms) iv criteria and have been getting treatment for more than 2 years in istanbul education and research hospital. 1,5 tesla mri were used in 40 cases, and the olfactory bulb volume on two hemispheres were measured separately. results: contrary to the former studies, we found no statistically significant difference between the olfactory bulb volume measurements of the control group and the group diagnosed with major depression. key words: depression, magnetic resonance imaging, olfactory bulb introduction in the recent years, studies about olfactory bulb (ob) function and ob volume in neuropsychiatric disorders have become more and more frequent. it’s possible to examine the links between the limbic system, prefrontal cortex and olfactory region thanks to these studies (1, 6, 10). the most frequent type of neuropsychiatric disorder is major depression. its average incidence rate is 2.6%-6.2%. major depression is the most frequent disorder in psychiatry with its lifelong 15% of prevalence rate in the general society, and 25% of prevalence rate among women (4). major depression is seen romanian neurosurgery (2016) xxx 1: 98 103 99 twice as much among women, independent on culture or country of residence. the average age of onset for major depressive disorder is 40, and 50% of the patients first suffer from it between the ages of 20-50 (4). many reasons are defined for the development of major depressive disorder. the general opinion is that the cases with organic disorders are triggered by environmental causes. studies revealed that neurotransmitter changes in brain, and damage in especially affection functioned cortex regions are among the causes for the development of the disorder. in recent years, with the help of studies about ob volume and function, it’s thought that the ob volume of patients with depressive affect have differences from the ob volume of a healthy brain (1, 6, 8, 10). in this study, we examined 20 cases diagnosed with major depression and 20 healthy volunteers in terms of ob volumes using cranial magnetic resonance imaging, and we aimed to determine if there is a statistically significant difference between two groups. materials and method this study was carried out between 20132015 with the help of the psychiatry, radiology and neurosurgery clinics of istanbul education and research hospital. all patients took part in the study had given written consents and the ethics committee of the hospital had approved the study. 20 cases took part in the study; 14 males and 6 females, diagnosed with acute major depression in accordance with the ‘diagnostic and statistical manual of mental disorders’ (dms) iv criteria, and getting treatment for 3 months in average. the neurological examinations of the patients were carried out. then, with their eyes are closed, we used two pieces of scented cotton which does not damage the nasal mucosa to test their olfactory perceptions. this test was repeated with well-known (mintcoffee etc.) scents and the patients were asked to define what they had smelled. the cases with anosmia and olfactory disorders were left out of the study. before the neuroimaging stage, we had consulted the otorhinolaryngology clinic about the patients. the patients suffering from nasal problems such as septal deviation and sinusitis did not take part in the study. the control group consisting of 20 patients, 10 females and 10 males had been chosen amongst the patients applied to the hospital for various reasons. detailed neuropsychiatric examinations had been carried out before the study. patients with former psychiatric complaints, psychiatric disorder history in the family and head trauma history had been removed from the study. all mr imaging work were done using 8 channel head-coil with ge 1,5 tesla mr (ge, 2011, usa) device which belongs to istanbul education and research hospital. each participant was examined with cranial mri to exclude cranial organic disorders (5 mm thickstandard section 3 dimensional [3d] sequence). 2 mm thick and – t2 weighted fastspin-echo imaging was run to observe the anterior and central skull base for the ob measurements (figure 1). olfactory bulb (ob) volume measurements were calculated separately on lamina cribriform anterior on 100 ozdemir et al the changes of olfactory bulb volume in major depression each hemisphere. following the methods used in former studies; the ob’s longest part and the length that forms a right angle to that part were multiplied, and the result were multiplied with the number of sections ob’s observed on; thus the volume measurements were finalized (5, 6, 13). figure 1 ob measurements statistical analysis ncss (number cruncher statistical system) 2007&pass (power analysis and sample size) 2008 statistical software (utah, usa) program was used for statistical analysis. descriptive statistical methods (centering, standard deviation, median, frequency, ratio, minimum, maximum) were used when analyzing the study data. student’s t-test was used in order to analyze the relationship between variables. significance level was observed as p<0,05. results the study was carried out by measuring the ob volumes of 20 patients diagnosed with acute major depression; 14 being male (70%) and 6 being female (30%), and 20 volunteers; 10 being male (50%) and 10 being female (50%) using cranial magnetic resonance imaging (mri). the ages of the cases diagnosed with major depression varied between 17 to 65, with an average age of 38,1 years. the ages of cases in the control group varied between 20 to 60, with an average age of 34,5 years. the demographic attributes of the cases participated in the study is summarized (table 1). the patients with major depression had three months of past medical history in average. 14 patients had been using selective serotonin reuptake inhibitors (ssri: citalopram, escitalopram, paroxetine), 6 patients had been using tricyclic antidepressants (mirtazapine, doxepine, trimipramine). the right and left obs were measured separately for the patients in the depression group and the control group. patients with major depression had an ob volume of 39,15±12,82 mm3 in average for the right hemisphere, and 40,55±10,94 mm3 in average for the left hemisphere. volumes varied between 14 mm3and 66 mm3 for the right hemisphere, and between 23 mm3and 61 mm3 for the left hemisphere. patients of control group had an ob volume of 35,39±10,89 mm3 in average for the right hemisphere, and 36,55±12,8 mm3 in average for the left hemisphere. volumes varied between 22 mm3and 59 mm3 for the right hemisphere, and between 22 mm3and 65 mm3 for the left hemisphere (table 2). romanian neurosurgery (2016) xxx 1: 98 103 101 table 1 the demographic attributes of the cases participated in the study patients number female male age (average) major depression 20 (50%) 6 14 38,1 (17-65) control group 20 (50%) 10 10 34,5 (20-60) total 40 (100%) 16 (40%) 24 (60%) 36,3 (17-65) table 2 ob volume measurements of patients with major depression and control group patients ob volume (right) ob volume (left) range (right) range (left) major depression 39,15±12,82 mm3 40,55±10,94 mm3 14 mm3-66 mm3 23 mm3-61 mm3 control group 35,39±10,89 mm3 36,55±12,8 mm3 22 mm3-59 mm 3 22 mm3-65 mm3 total 37,27 mm3 (100%) 38,55 mm3 (100%) 14 mm3-66 mm3 22 mm3-65 mm3 there was no statistically significant difference found when the ob volume measurements were compared separately for the right and the left hemisphere of the major depression group and the control group p˃0,05. patients with major depression were split into two groups in terms of the type of medication they used. the two groups using medications with different active ingredients were first compared with each other statistically. there was no statistically significant difference found between patients using medications with different active ingredients. discussion depression is considered a frequent type of disorder and named as a public health problem in developed and developing communities. because it’s so frequent, most neuroscientists are interested in its causes. in the last two decades, it’s revealed that neurotransmitter pathways pave the way for and speed up the formation of many psychiatric disorders. having said that, some parts and regions of the brain have very important tasks regarding cognitive function and mood. prefrontal cortex and the limbic system form close relations with each other, thus, affect the clinical course and medication response (3, 6). with functional mri coming into the picture, in neuropsychiatric disorders, we can now examine and reveal the parts of the brain where there is a loss of function. brain imaging studies in major depression cases have been also carried out for years. we often see imaging studies mainly focusing on the frontal lobe which mostly deals with emotion regulation. personality changes often seen in cases dealing with frontal lobe trauma or frontal tumors prove the significance of the frontal lobe (2). studies in the recent years revealed that ob function losses cause a tendency to depression and may cause changes in medication 102 ozdemir et al the changes of olfactory bulb volume in major depression response. ob is an area that lies just below cribriform plate, in anterior cranial fossa with a 36,44±12,8 mm3average volume (7). it has fibers reaching out to thalamus. in 2001, the study by pause et al. detected reduced olfactory volume and reduced olfactory sensitivity. there are many theories aiming to explain olfactory deficit seen in major depression. pause et al. thought that the disinhibition in amygdala that affects emotional responses were in fact responsible for olfactory deficit. the abnormal functioning in the paralimbic cortex (especially amygdala and orbitofrontal cortex) were the main reasons for the concurrent early period olfactory area disinhibition in major depression cases (11). in 2010, with their studies, negoias et al. determined for the first time that depression score is correlated with olfactory function and volume (8). olfactory area volume and functions may also change due to psychiatric and neurodegenerative disorders. major depression and schizophrenia may be the cause of function or volume loss (7, 9, 11, 12, 14, 16). in addition to these, volume deficit and functional disorders may also be determined in multiple sclerosis and parkinson’s disease cases (15). not all cases of olfactory volume loss indicate a neuropsychiatric disorder. head trauma, sinonasal diseases, infections and upper respiratory pathologies may also cause changes in measurements. ob may function as a neurotransmitter. early period changes may also act as precursor symptom (7, 12). conclusion in our study, we measured the olfactory bulb volumes of major depression cases using neuroimaging, compared the findings with those of healthy volunteers and the results are examined to find out whether there is a statistically significant difference between them. contrary to the findings in former studies, we could not find any statistically significant difference. further studies with more patients are needed in order to come to a definite conclusion. correspondence op. dr. hakan yılmaz address: duzce ataturk state hospital, department of neurosugery, duzce, turkey tel: +90 506 621 18 29 e-mail: dr_hakanyilmaz@hotmail.com references 1.atanasova b, graux j, el hage w, hommet c, camus v, belzung c. olfaction: a potential cognitive marker of psychiatricdisorders. neurosci biobehav rev 2008;32(7):1315-25 2.cummings dm, knab br, brunjes pc. effects of unilateral olfactory deprivation in the developing opossum. j neurobiol 1997;33(4):429-38 3.curtis ma, kam m, nannmark u, anderson mf, axell mz, wikkelso c, et al. human neuroblasts migrate to theolfactory bulb via a lateral ventricular extension. science 2007;315(5816):1243-9 4.diagnostic and statistical manual of mental disorders 4th ed. washington dc, american psychiatric association 2000. 5.duprez tp, rombaux p. imaging the olfactory tract (cranialnerve 1). eur j radiol 2010;74(2):288-98 6.gul ai, sari k, ozkiris m, aydin r, simsek gg, serin hi, saydam l. correlation between olfactory bulb volume and chronic depression: a magnetic resonance imaging study. bulletin of clinical psychopharmacology 2015;25(3):280-6 romanian neurosurgery (2016) xxx 1: 98 103 103 7.mueller a, rodewald a, reden j, gerber j, von kummer r, hummel t. reduced olfactory bulb volume in post-traumatic and post-infectious olfactory dysfunction. neuroreport 2005;16(5):475-8 8.negoias s, croy i, gerber j, puschmann s, petrowski k, joraschky p, et al. reduced olfactory bulb volume and olfactory sensitivity in patients with acute major depression. neuroscience 2010;169(1):415-21 9.negoias s, hummel t, symmank a, schellong j, joraschky p, croy i. olfactory bulb volume predicts therapeutic outcome in major depression disorder. brain imaging behav 2015 may 15 [epub ahead of print] 10.oğuzhanoğlu nk, varma gs, karadağ f, tümakaya s, efe m, kıroğlu y. prefrontal cortex neurochemical metabolite levels in major depression and the effects of treatment: an 1 hmrs study. turkish journal of psychiatry 2014;25(2):75-83 11.pause bm, miranda a, goder r, aldenhoff jb, ferstl r. reduced olfactory performance in patients with major depression. j psychiatr res 2001;35:271–277 12.rombaux ph, mouraux a, bertrand b, nicolas g, duprez t, hummel t. olfactory function and olfactory bulb volumein patients with postinfectious olfactory loss. laryngoscope 2006;116(3):436-9 13.rombaux p, duprez t, hummel t. olfactory bulb volume inthe clinical assessment of olfactory dysfunction. rhinology 2009;47(1):3-9 14.schablitzky s, pause bm. sadness might isolate you in a non-smlelling world: olfactory perception and depression. front psychol 2014;7(5):45 15.tanik n, serin hi, celikbilek a, inan le, gundogdu f. olfactory bulb and olfactory sulcus depths are associated with disease duration and attack frequency in multiple sclerosis patients. j neurol sci 2015;15;358(12):304-7 16.youssem dm, geckle rj, doty rl, bilker wb. reproducibility and reliability of volumetric measurements of olfactory eloquent structures. acad radiol 1997;4(4):264-9 doi: 10.33962/roneuro-2022-013 anterior cervical discectomy and fusion in the era of motion preserving surgery. a retrospective study arun s., abhishek v., prakash goswami, sanu v., jyothish l.s., sunil kumar, suresh kumar, anil kumar, oommen p. mathew romanian neurosurgery (2022) xxxvi (1): pp. 73-83 doi: 10.33962/roneuro-2022-013 www.journals.lapub.co.uk/index.php/roneurosurgery anterior cervical discectomy and fusion in the era of motion preserving surgery. a retrospective study arun s., abhishek v., prakash goswami, sanu v., jyothish l.s., sunil kumar, suresh kumar, anil kumar, oommen p. mathew* department of neurosurgery, govt medical college, thiruvananthapuram, kerala, india * research investigator, population research centre, university of kerala, thiruvananthapuram, kerala, india abstract background. anterior cervical discectomy and fusion is accepted as the standard surgical treatment of cervical spondylotic myelopathy. cervical disc arthroplasty has gained widespread acceptance as an alternate choice for acdf. we intend to present the clinical and radiologic outcomes of patients who underwent acdf in our department. methods. designed as a retrospective study, the primary objective was to assess the nonunion in patients undergoing acdf and anterior cervical corpectomy and fusion. the article discusses the outcome for the discectomy group. all patients who underwent acdf for csm from january 2014 to december 2018 were included. patients who underwent posterior fusion in addition to anterior approach, revision surgery and congenital anomalies of the spine were excluded. of the 230 eligible patients,46 subjects were part of the study. they underwent neurologic and radiographic examination and their past records were examined. neurologic outcome was assessed using nurick grade and mjoa score. dysphagia was assessed using the bazaz score. neck radiographs were analyzed for fusion, adjacent segment disease, subsidence, cervical and segmental lordosis. results. the overall response rate was 25.65%. the mean follows up duration was 4 years. the mean age of the population was 47.1 years. the most common operating level was c5/6. the neurologic status of patients improved from the baseline. there was mild transient dysphagia in 5(10.9%) patients. the overall rate of fusion was 91.3%. subsidence was seen in 10.9%. degenerative changes were noted in postop x rays of 67.4% of patients. there was no mortality. conclusion. acdf achieves thorough decompression thereby resulting in neurologic improvement. it produces effective and sustained neurologic improvement. preoperative adjacent segment degenerative changes were significantly associated with the development of asd during follow up. this is can due to the progression of the disease. though the procedure improves the lordosis, it tends to decrease with follow up. keywords adjacent segment disease, anterior cervical discectomy and fusion, cervical spondylotic myelopathy, standalone cage corresponding author: abhishek v. govt medical college, thiruvananthapuram, kerala, india vijayan.abhishek@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 74 arun s., abhishek v., prakash goswami et al. introduction anterior cervical discectomy and fusion( acdf ) was pioneered by cloward and smith and robinson separately in 1950s for the surgical treatment for patients with cervical spondylotic myelopathy(1,2,3) .thorough and direct decompression of the pathology and subsequent bony fusion of the involved levels , as advocated by the cloward forms the fundamental principle of the surgery(2). anterior approach have became the standard treatment for cervical spondylotic myelopathy. anterior cervical corpectomy and fusion ( accf) was introduced by whitecloud and larocca to circumvent graft failure following discectomy following multilevel discectomy.( 4) though anterior cervical discectomy and corpectomy are excellent in achieving the decompression of the spinal cord and restoring the lordosis ; they are not without complications. variously reported complications include graft subsidence, graft migration , graft collapse , nonunion, loss of lordosis and adjacent segment disease (asd) (5,6,7,8 ). injury to neurovascular structures and oesophagus though rare have been reported (5,7) .the design of the anterior cervical plates introduced in 1980s to address the problem of graft migration and nonunion has evolved to the presently popular translational plates(9).the translational plates achieve graft loading by permitting controlled subsidence, a prerequisite for fusion (10). adjacent segment degeneration a described complication of fusion surgeries , was further elaborated by hilibrand et al as occurring at a rate of 2.5% per yr with cumulated rate of 25.9 % at 10 yrs (11) . the hypothesis that fusion increases the stress at the adjacent levels and subsequently accelerates degenerative changes at those levels ,brought back motion preserving surgery in to surgeon’s armamentorium. originally introduced by ulf fernstorm in 1966, artificial cervical disc was a stainless steel ball bearing device ,which was discontinued due to high failure rate (12,13) . the next era in motion preserving implants happened with introduction of frenchay ( prestige ) and bryan artificial disc .however both the devices were of different designs(14,15 ).first decade of 21 st century saw many arthroplasty devices completing trials and getting approval for use in cervical spondylotic myelopathy concurrent with expanding indications for their use(16). accruing evidence from long term results of rcts and multiple meta analyses suggested superiority of cda(cervical disc arthroplasty) over acdf in overall outcome , adjacent segment degeneration and secondary surgery at the index and adjacent levels(17,18) . dynamic cervical implant(dci), developed by dr g matge et al is a u shaped single piece implant with teeth for fixation into adjacent endplates, with u limb of the implant facilitating controlled flexion and extension, while preventing axial rotation and lateral bending ,thereby reducing the stress on facet joints. .matge et al reported excellent short term neurologic outcome and motion preservation in majority of the patients (19). though present day neurosurgical literature is replete with high quality evidence from many rcts which suggest better overall outcome of cdas over acdf all these trials however were nonblinded .recent analysis from a single blind trial for cda vs acdf found comparable results for prom( patient reported outcome measures ) as well as clinical adjacent segment disease(20).results of two double blinded trials comparing cda with acdf and acd, neck (netherlands cervical kinematics trial )and procon trial reported no advantage of cda over acdf in either patient outcome variables or in asd. data from the same trials show the incidence of heterotopic ossification( ho) in 68%-85% of patients ,with half of them being motion restricting severe ho ( 21). above all cda is the not the panacea for all patients needing anterior cervical fusion with only 47 % of all patients undergoing acdf for various indications being candidates for cda (22,24). regarding dci ,the outcomes reported by matge et al were not replicated in other series(23) . the present article discusses results of the subgroup analysis of the study conducted in the department to determine the rate of nonunion in patients undergoing anterior cervical fusion for spondylotic myelopathy including anterior cervical discectomy and corpectomy . the radiologic and clinical outcome of the discectomy and fusion subgroup is presented here. materials and methods patient population the study was designed as a retrospective design and was approved by institutional ethics committee. the primary objective was to determine the rate of 75 anterior cervical discectomy and fusion in the era of motion preserving surgery nonunion in patients undergoing anterior cervical fusion for cervical spondylotic myelopathy and included both discectomy and corpectomy subgroups. the patients operated between january 2014 to december 2018 in our department and willing to be part of study were included .those with history of previous cervical spine surgery , with congenital anomalies of spine and those who needed posterior approach in addition to anterior surgery were excluded. the patients underwent a detailed neurologic examination and radiographic examination with x rays of the cervical spine. their hospital records, previous images , and records of the follow up visit were examined. of the 256 eligible patients 59 patients who were willing to be part of the study and with complete data were included in the study. of these 46 patients had undergone discectomy while 13 had received corpectomy. the baseline data of the patients are summarised in table-1. surgical procedure the involved levels were approached using an oblique neck incision after identifying the level preoperatively with c arm. the caspar retractor system was used to retract the great vessals of the neck and the tracheoesophageal complex. the longus colli was detached from anterior vertebral surface. subsequent to reconfirming the level annulotomy and discectomy was done with microscopic assistance. the disc space spreader was used to widen the disc space during discectomy. after complete discectomy pll( posterior longitudinal ligament ) was inspected for any defect and disc fragments posterior to the pll was removed. the osteophytes were thinned using drill and removed using kerrison punches and was confirmed using c arm. after satisfactory decompression of the cord, the endplates were prepared and appropriately sized cages or standalone cages made of titanium filled with locally harvested bone pieces were impacted in to the disc space while avoiding overdistraction. the standalone cages have a side flange with a screw hole which allowed placement of a single screw in to the adjacent vertebral bodies. for those with conventional plates, a contoured plate of appropriate length was placed over the adjacent segment and fixed using 4 screws,2 each in to adjacent bodies. for patients undergoing corpectomy, the upper and lower discs were removed followed by median corpectomy. osteophytes were drilled thin and removed with punches .once decompression was confirmed, adequately sized titanium cages were impacted after filling them with bone harvested from the removed vertebra. patients were usually discharged on 5 th postoperative day. patients were given a cervical collar for 6 weeks. the follow ups were at 6 weeks,3 months,6 months and 1 year and annually thereafter .at 3 months,6 months and at 1 year f/u ,they undergo c spine x rays . clinical and radiologic outcome assessment nurick grade and mjoa (modified japanese orthopaedic association ) score were used to assess the neurologic outcome . radiologic assessment was done using plain and dynamic x rays . bazaz criteria was used for assessing dysphagia. the criteria used for fusion was absence of movement of >2 mm between spinous processes of the fused segment and absence of radiolucency between the implant and the bony surface and absence of bridging bone between the fused vetebrae. subsidence was interpreted as migration of the cage more than 2mm in to the adjacent bodies(25). the criteria proposed by chung et al was used to assess asd (26).the implant complications included screw pullout, screw breakage, plate loosening and plate breakage. global cervical lordosis was measured using cobb angle between inferior endplate of c2 and inferior endplate of c7(27).segmental angle was defined as the angle between the superior endplate of superior table 1 demographic details of patients age in years mean ± sd 47.1 ± 10.7 sex (m/f) 32/24 presence of other comorbidities( %) 16 (34.8) history of smoking( %) 14 (30.4 ) single level affected (%) 31 (67.4 ) presence of mri t2 hypertintensity (%) 19 (41.3 ) 76 arun s., abhishek v., prakash goswami et al. vertebra and inferior endplate of inferior vertebra (28) statistical methods categorical and quantitative variables were expressed as frequency (percentage) and mean ± sd respectively. chi-square test and fisher’s exact test were used to find association between categorical variables. mann-whitney u test was used to compare selected quantitative parameters between type of surgery. for all statistical interpretations, p&lt;0.05 was considered the threshold for statistical significance. statistical analyses was performed by using a statistical software package spss, version 20.0 results the discectomy subgroup included 46 patients.the demographic data of the patients is given in table 1. mean duration of follow up was 4 years. 31 (67.4%) % of patients had pathology affecting one level while 32.6% had pathologies at multiple levels. the details of the levels is given in table 2. cord signal changes ie, t2 hyperintensity were present in 41.3 %. plate extending in to adjacent disc space was present in 30.4 % patients in postop x ray . among patients with plate overlap majority of the overlap was at the cranial level (90.5%) and in 9.5% of subjects overlap was at the inferior level. degenerative changes at adjacent levels were present in preop x rays in 43.5 % of patients. regarding the height of cage most commonly used was 6 mm cages in 47.8% of patients, 7 mm in 34.8 %, 8 mm in 10.9% and 5 mm in 6.5% patients. table 2. level affected primary level count c3/4 8 (17.4)* c4/5 11 (23.9)* c5/6 19 (41.3)* c6/7 8 (17.4)* ( )* in percentages neurologic status of patients improved after surgery as reflected by the improvement in nurick grade and mjoa score ( table 2) and this improvement was sustained till final follow up. mild transient dysphagia occurred in 5 (10.9%) patients which improved in all during the postop period. regarding radiologic outcome ,the overall fusion rate was 91.3%( figure 1). degenerative changes were noted in postop x rays of 67.4% patients , 3 patients had implant related complications 2 had screw breakage and one suffered loosening of the screw.there was no mortality in the group.one patient had deteriorated neurologically in immediate postop period due to haematoma and required evacuation , following which patient improved gradually . 77 anterior cervical discectomy and fusion in the era of motion preserving surgery figure 1. a – sagital t2 image showing cord compression due to the disc. b -axial image .c ,d and e lateral radiographs preop ,postop and at 2 years f/u respectively . 2 yr radiograph shows solid fusion of the operated level. the lordosis both cervical and segmental angle improved after surgery , but there was partial loss of this improvement over the follow up period ( table 3 ). subsidence occurred in 5 patients .all of them had undergone fusion with standalone cage ( p = 0.026 ) the degenerative changes on x rays had increased from 43.5% in preop x rays to 67.4% in post op xrays. the affected level, no of operated levels, plate extending to the adjacent disc space , height of cage were not associated with postop degenerative changes .however preop degenerative changes had a significant association with postop x ray changes (p=0.025). table 3 cervical lordosis and segmental angle comparison mean ± sd median (iqr) pair p cervical lordosi pre op 18.2 ± 6.5 18 (15 23) post op 22.6 ± 7.5 23 (18 26) pre vs post p<0.01 follow up 19.8 ± 6.5 20 (15 23) pre vs follow up 0.007 segmental angle pre op 3.5 ± 2.3 3 (2 5) post op 4.7 ± 2.2 5 (3 6) pre vs post p<0.01 follow up 3.5 ± 2.2 3 (2 5) pre vs follow up 0.351 78 arun s., abhishek v., prakash goswami et al. table 4. mean ± sd media n (iqr) pair p nurick grade pre op 3.1 ± 1.1 3 (2 4) post op 2.4 ± 1.4 2 (1 4) pre vs post p<0.01 follow up 1.4 ± 0.9 1 (1 1) pre vs follow up p<0.01 m joa pre op 12.2 ± 3.2 13 (11 14) post op 12.8 ± 3.5 13 (11 15) pre vs post p<0.01 follow up 15.7 ± 3.1 17 (15 18) pre vs follow up p<0.01 discussion the participation rate in the study was (25.65%) .the travel restrictions imparted due to covid and the patient reluctance to attend the hospital opd which was a dedicated covid treatment centre might have contributed to low participation rate. anterior cervical discectomy and fusion remains as a standard surgical option for patients with spondylotic myelopathy despite the popularity of cervical disc arthroplasty . evidence from control arm of cda -ide( cervical disc arthroplasty – investigational drug exemption) trials provide high quality evidence about the outcome and complications of acdf (29).the fusion rate 97 % -98% along with excellent clinical outcome in 94% reported by cloward in his series of more than 2000 patients, operated for various pathologies underscores safety and efficacy of the procedure as well as the sound scientific basis of this procedure(3). the ability to achieve thorough decompression of the offending pathology and restoration of lordosis are the inherent advantages of the procedure .this is reflected in the neurologic outcome after fusion surgeries ,which shows a sustained improvement in neurologic function on long term follow up ( 30,31,32 ). a recent study by karim et al concluded that the neurologic improvement in all groups ie, mild ,moderate and severe myelopathy , though the improvement was more pronounced in severe group (33).in our study population the mean mjoa score improved from the 12.8 ( sd 2.5) to 16.5 (sd 1.9 ) at final follow up which is similar to the result from the past studies. all these results point to the efficacy of the procedure. postop dysphagia is a frequent complication reported after anterior cervical fusion with reported incidence ranging from 12% -35% (34).this subsides in majority of the patients though it can be troublesome for a minor group of patients various proposed etiological factors for dysphagia include design of the plate, female sex, number of levels operated and use of conventional plate (35,36,37).mild dysphagia for solid food present in 10.9% of our patients during immediate postop period resolved in follow up. cloward in his article stressed the role of fusion in acdf as equally important as decompression. he had used variously shaped allografts in his patients with an excellent fusion rates of up to 97% (3). though studies variously use absence of relative motion between the spinous processes of fused segments , the presence of bridging bone and absence of radiolucency between the endplate and implant as the criteria for fusion there is no uniformity in the definition for fusion. fraser et al in a metanalysis reported reported an overall fusion rate of 89.2% for anterior fusion surgeries which also included noninstrumented fusion and corpectomies(38). for instrumented acdf, the fusion rate varied from 82.5% for multilevel to 97.1% for single level(38). however information on fusion rates stratified according to the implant type was not availbale. noordhoek et al reported comparable fusion rates of >90 % for titanium and peek cages (38,39). our study population using titanium cages had a fusion rate of 91.3% . the cohort of patients who didn’t achieve radiologic fusion in our group were neurologically stable and were free of symptoms. (figure 2). 79 anterior cervical discectomy and fusion in the era of motion preserving surgery figure 2. a – nonunion after c5/6 fusionlateral radiographs (a ) preop, (b) postop,(c) at 2 yrs,(d) extension and (e) flexion images .flexion pronounces defect in the bridging bone and radiolucency around the implant. adjacent segment degeneration after anterior cervical fusion was noticed by several authors as the the procedure gained widespread popularity(40,41,42).hilibrand et al in a series of 409 patients followed up to 21 years reported the annual incidence of adjacent segment degeneration of 2.5% per year . using a survivorship analysis they estimated cumulative incidence of 25.9 % at 10 years. authors however had distinguished between adjacent segment disease and symptomatic adjacent segment disease which occured in 14.2 %.they recognized single operated level and c5/6 or c6/7 as risk factors for development of asd(11) .the etiology of the adjacent segment disease is the subject of a hitherto unsettled discussion. hilibrand et al after comparing the occurrence of asd in anterior and posterior surgery groups concluded asd as outcome of natural history of disease rather 80 arun s., abhishek v., prakash goswami et al. than an outcome precipitated by treatment(43). other risk factors emerged from further studies includes plate extending to the adjacent disc space plate to disc distance < 5 mm (44) , kyphotic postop sagittal alignment in patients with asd (45) ,preop needle localization at wrong level ( 46 ). 0.5 to 1 fold distraction on the other hand has been found to be protective against asd(47) .in our patient population the number of levels operated, plate overlap in to adjacent disc space and height of the cage were not associated with development of degenerative changes in postop x rays .however degenerative changes in pre op x rays( 43%) was significantly associated with development of further changes in post op x rays(67% )( p = .025).this finding supports the argument that the asd is an outcome of the natural history of the disease rather than a complication of the treatment. the height of the cage , an indirect marker of distraction had no association with the asd in our study . subsidence of the cage in to the adjacent vertebral body is not an infrequent phenomenan with the use of metal cages .there have been contrasting reports of subsidence unfavourably affecting clinical outcome(48,49) and having no impact on clinical outcome( 50,51). various authors have reported patient related, technique related a and implant related factors associated with subsidence.the risk factors include age, sex ,preop cervical alignment ,bone mineral density (52,53,54). truumees et al reported overdistraction and damage to endplates positively correlated with occurrence of subsidence(55).cage height and titanium cages , standalone cages were also reported to be significantly associated with subsidence (56).in our patients five developed subsidence ,all of them had undergone fusion with standalone cage compared to conventional cage and plate ,which was significant ( p=.026).however all the patients with subsided cages eventually attained fusion. both group had similar clinical outcome despite the subsidence. the finding in our patients possible might be due to 2 factors – titanium cages and greater graft loading with standalone cages compared to conventional cages. titanium cages have greater modulus of elasticity compared to peek and bone , with the resultant modulus mismatch playing a role in subsidence (57). restoration of lordosis is one of the advantages of the acdf over posterior procedures. the improvement in lordosis is reported to be associated with improvement ndi scores and joa recovery rate .the impact of the correction of lordosis on improvement of joa score is less clear as to whether this being a result of decompression or directly related to restoration of lordosis (58). katsuura et al reported the occurrence of local kyphosis in 43% of patients undergoing multilevel discectomy which was a predisposing factor for asd(59). reports differ on the long term maintenance of the postop lordosis (60,61).multilevel procedures tend to lose the lordosis compared to fewer operated segments. in our study the post op cervical lordosis(22.6 degrees ) and the segmental angle (4.7 degrees ) increased significantly compared to preop levels ( 18.2 and 3.5 ) .though the gain in the lordosis was partially lost over the follow up duration ,the final cervical lordosis( 19.8) was higher compared to preop levels and was significant for cervical lordosis ,though not segmental angle at final follow up. we attribute this to the progression of the degenerative disease which was present in 67% of our patients radiologically at final follow up. thus the occurrence of asd and loss of lordosis is closely related. however whether this loss of lordosis was due to the progression of the degenerative pathology couldn’t be conclusively verified from our study. conclusion anterior cervical discectomy and fusion is an effective option for the treatment for cervical spondylotic myelopathy . it produces a sustained neurologic improvement .preoperative adjacent segment degenerative changes was significantly associated with development of asd during follow up. this is can due to the progression of the disease rather being precipitated by the procedure. though the procedure improves the lordosis, it tends to decrease with follow up. references 1. smith gw, robinson ra. the treatment of certain cervical-spine disorders by anterior removal of the intervertebral disc and interbody fusion. j bone joint surg am. 1958 jun;40-a(3):607-24. 2. cloward rb. the anterior approach for removal of ruptured cervical disks. j neurosurg. 1958 nov;15(6):60217. 3. cloward rb. the anterior surgical approach to the cervical spine: the cloward procedure: past, present, and future. the presidential guest lecture, cervical spine 81 anterior cervical discectomy and fusion in the era of motion preserving surgery research society. spine (phila pa 1976). 1988 jul;13(7):823-7. 4. whitecloud ts, larocca h fibular strut graft in reconstructive surgery of the cervical spine. spine 1976;1: 33-43 5. sahjpaul rl. esophageal perforation from anterior cervical screw migration. surg neurol. 2007 aug;68(2):205-9; discussion 209-10. 6. jung a, schramm j, lehnerdt k et al. recurrent laryngeal nerve palsy during anterior cervical spine surgery: a prospective study. j neurosurg spine. 2005 feb;2(2):1237. 7. orlando er, caroli e, ferrante l. management of the cervical esophagus and hypofarinx perforations complicating anterior cervical spine surgery. spine (phila pa 1976). 2003 aug 1;28(15):e290-5. 8. fountas kn, kapsalaki ez, nikolakakos lg et al anterior cervical discectomy and fusion associated complications. spine (phila pa 1976). 2007 oct 1;32(21):2310-7. 9. böhler j, gaudernak t. anterior plate stabilization for fracture-dislocations of the lower cervical spine. j trauma. 1980 mar;20(3):203-5 10. steinmetz mp, benzel ec, apfelbaum ri. axially dynamic implants for stabilization of the cervical spine. neurosurgery. 2006 oct;59(4 suppl 2):ons378-88; discussion ons388-9. doi: 10.1227/01.neu.0000233901.53692.e1. 11. hilibrand as, carlson gd, palumbo ma, jones pk, bohlman hh. radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. j bone joint surg am. 1999 apr;81(4):519-28. 12. fernström u. arthroplasty with intercorporal endoprothesis in herniated disc and in painful disc. acta chir scand suppl. 1966;357:154-9. 13. fisahn c, burgess b, iwanaga j et al . ulf fernström (19151985) and his contributions to the development of artificial disc replacements. world neurosurg. 2017 feb;98:278-280. 14. cummins bh, robertson jt, gill ss. surgical experience with an implanted artificial cervical joint. j neurosurg. 1998 jun;88(6):943-8. 15. basho r, hood ka. cervical total disc arthroplasty. global spine j. 2012 jun;2(2):105-8. 16. turel mk, kerolus mg, adogwa o et al. cervical arthroplasty: what does the labeling say? neurosurg focus. 2017 feb;42(2):e2. 17. badhiwala jh, platt a, witiw cd et al. cervical disc arthroplasty versus anterior cervical discectomy and fusion: a meta-analysis of rates of adjacent-level surgery to 7-year follow-up. j spine surg. 2020 mar;6(1):217-232. 18. nunley pd, coric d, frank ka et al . cervical disc arthroplasty: current evidence and real-world application. neurosurgery. 2018 dec 1;83(6):1087-1106. 19. matgé g, berthold c, gunness vr et al . stabilization with the dynamic cervical implant: a novel treatment approach following cervical discectomy and decompression. j neurosurg spine. 2015 mar;22(3):23745. 20. johansen to, sundseth j, fredriksli oa et al .effect of arthroplasty vs fusion for patients with cervical radiculopathy: a randomized clinical trial. jama netw open. 2021 aug 2;4(8):e2119606.. 21. yang x, donk r, bartels rhma et al. comparing heterotopic ossification in two cervical disc prostheses. spine (phila pa 1976). 2020 oct 1;45(19):1329-1334. 22. leven d, meaike j, radcliff k et al . cervical disc replacement surgery: indications, technique, and technical pearls. curr rev musculoskelet med. 2017 jun;10(2):160-169. 23. li z, wu h, chu j et al . motion analysis of dynamic cervical implant stabilization versus anterior discectomy and fusion: a retrospective analysis of 70 cases. eur spine j. 2018 nov;27(11):2772-2780. 24. auerbach jd, jones kj, fras ci et al . the prevalence of indications and contraindications to cervical total disc replacement. spine j. 2008 sep-oct;8(5):711-6. 25. yang jj, yu ch, chang bs et al. subsidence and nonunion after anterior cervical interbody fusion using a standalone polyetheretherketone (peek) cage. clin orthop surg. 2011 mar;3(1):16-23. 26. chung jy, kim sk, jung st et al . clinical adjacent-segment pathology after anterior cervical discectomy and fusion: results after a minimum of 10-year follow-up. spine j. 2014 oct 1;14(10):2290-8. 27. chen y, liu y, chen h et al . comparison of curvature between the zero-p spacer and traditional cage and plate after 3-level anterior cervical discectomy and fusion: mid-term results. clin spine surg. 2017 oct;30(8):e1111-e1116. 28. chen y, lü g, wang b et al. a comparison of anterior cervical discectomy and fusion (acdf) using self-locking stand-alone polyetheretherketone (peek) cage with acdf using cage and plate in the treatment of three-level cervical degenerative spondylopathy: a retrospective study with 2-year follow-up. eur spine j. 2016 jul;25(7):2255-62. 29. zigler je, rogers rw, ohnmeiss dd. comparison of 1level versus 2-level anterior cervical discectomy and fusion: clinical and radiographic follow-up at 60 months. spine (phila pa 1976). 2016 mar;41(6):463-9 30. fehlings mg, wilson jr, kopjar b et al . efficacy and safety of surgical decompression in patients with cervical spondylotic myelopathy: results of the aospine north america prospective multi-center study. j bone joint surg am. 2013 sep 18;95(18):1651-8. d 31. badhiwala jh, witiw cd, nassiri fet al. efficacy and safety of surgery for mild degenerative cervical myelopathy: results of the aospine north america and international prospective multicenter studies. neurosurgery. 2019 apr 1;84(4):890-897. 32. fehlings mg, ibrahim a, tetreault l et al. a global perspective on the outcomes of surgical decompression in patients with cervical spondylotic myelopathy: results 82 arun s., abhishek v., prakash goswami et al. from the prospective multicenter aospine international study on 479 patients. spine (phila pa 1976). 2015 sep 1;40(17):1322-8. 33. karim sm, cadotte dw, wilson jr et al . effectiveness of surgical decompression in patients with degenerative cervical myelopathy: results of the canadian prospective multicenter study. neurosurgery. 2021 oct 13;89(5):844851. 34. rihn ja, kane j, albert tj et al. what is the incidence and severity of dysphagia after anterior cervical surgery? clin orthop relat res. 2011 mar;469(3):658-65 35. lee mj, bazaz r, furey cg et al. influence of anterior cervical plate design on dysphagia: a 2-year prospective longitudinal follow-up study. j spinal disord tech. 2005 oct;18(5):406-9. 36. riley lh 3rd, skolasky rl, albert tj et al. dysphagia after anterior cervical decompression and fusion: prevalence and risk factors from a longitudinal cohort study. spine (phila pa 1976). 2005 nov 15;30(22):2564-9. 37. zhou j, li j, lin h et al . a comparison of a self-locking stand-alone cage and anterior cervical plate for acdf: minimum 3-year assessment of radiographic and clinical outcomes. clin neurol neurosurg. 2018 jul;170:73-78. 38. fraser jf, härtl r. anterior approaches to fusion of the cervical spine: a metaanalysis of fusion rates. j neurosurg spine. 2007 apr;6(4):298-303. 39. noordhoek i, koning mt, vleggeert-lankamp cla. evaluation of bony fusion after anterior cervical discectomy: a systematic literature review. eur spine j. 2019 feb;28(2):386-399. 40. baba h, furusawa n, imura s et al. late radiographic findings after anterior cervical fusion for spondylotic myeloradiculopathy. spine 1993;18: 2167–73. 41. cherubino p, benazzo f, borromeo u et al. degenerative arthritis of the adjacent spinal joints following anterior cervical spinal fusion: clinicoradiologic and statistical correlations. ital j orthop traumatol 1990;16:533–43. 42. gore dr, sepic sb. anterior cervical fusion for degenerated or protruded discs. a review of onehundred forty-six patients. spine 1984;9:667–71. 43. hilibrand as, robbins m. adjacent segment degeneration and adjacent segment disease: the consequences of spinal fusion? spine j. 2004 nov-dec;4(6 suppl):190s194s. 44. park jb, cho ys, riew kd. development of adjacent-level ossification in patients with an anterior cervical plate. j bone joint surg am. 2005 mar;87(3):558-63. 45. park ms, kelly mp, lee dh et al. sagittal alignment as a predictor of clinical adjacent segment pathology requiring surgery after anterior cervical arthrodesis. spine j. 2014 jul 1;14(7):1228-34. 46. nassr a, lee jy, bashir rs et al . does incorrect level needle localization during anterior cervical discectomy and fusion lead to accelerated disc degeneration? spine (phila pa 1976). 2009 jan 15;34(2):189-92. 47. xiong w, zhou j, sun c et al. 0.5to 1-fold intervertebral distraction is a protective factor for adjacent segment degeneration in single-level anterior cervical discectomy and fusion. spine (phila pa 1976). 2020 jan 15;45(2):96102. 48. lee ys, kim yb, park sw. risk factors for postoperative subsidence of single-level anterior cervical discectomy and fusion: the significance of the preoperative cervical alignment. spine (phila pa 1976). 2014 jul 15;39(16):12807. 49. barsa p, suchomel p. factors affecting sagittal malalignment due to cage subsidence in standalone cage assisted anterior cervical fusion. eur spine j. 2007 sep;16(9):1395-400. 50. bartels rh, donk rd, feuth t. subsidence of stand-alone cervical carbon fiber cages. neurosurgery 2006;58:502–8 [discussion 502–8]. 51. wu wj, jiang ls, liang y, et al. cage subsidence does not, but cervical lordosis improvement does affect the longterm results of anterior cervical fusion with stand-alone cage for degenerative cervical disc disease: a retrospective study. eur spine j 2012;21:1374–82 52. lee ys, kim yb, park sw. risk factors for post-operative subsidence of single level anterior cervical discectomy and fusion: the significance of the preoperative cervical alignment. spine (phila pa 1976) 2014;39:1280–7 53. lim th, kwon h, jeon ch et al. effect of endplate conditions and bone mineral density on the compressive strength of the graft-endplate interface in anterior cervical spine fusion. spine (phila pa 1976) 2001;26:951– 6) 54. kao th, wu ch, chou yc, et al. risk factors for subsidence in anterior cervical fusion with stand-alone polyetheretherketone (peek) cages: a review of 82 cases and 182 levels. arch orthop trauma surg 2014;134:1343–51 55. truumees e, demetropoulos ck, yang kh et al . effects of disc height and distractive forces on graft compression in an anterior cervical discectomy model. spine (phila pa 1976). 2002 nov 15;27(22):2441-5. 56. igarashi h, hoshino m, omori k et al . factors influencing interbody cage subsidence following anterior cervical discectomy and fusion. clin spine surg 2019;32(7):297302. 57. heary rf, parvathreddy n, sampath s et al. elastic modulus in the selection of interbody implants. j spine surg. 2017 jun;3(2):163-167. 58. wu wj, jiang ls, liang y et al. cage subsidence does not, but cervical lordosis improvement does affect the longterm results of anterior cervical fusion with stand-alone cage for degenerative cervical disc disease: a retrospective study. eur spine j. 2012 jul;21(7):1374-82. 59. katsuura a, hukuda s, saruhashi y et al . kyphotic malalignment after anterior cervical fusion is one of the factors promoting the degenerative process in adjacent intervertebral levels. eur spine j. 2001 aug;10(4):320-4. 60. liang g, liang c, zheng x et al . sagittal alignment outcomes in lordotic cervical spine: does three-level anterior cervical discectomy and fusion outperform 83 anterior cervical discectomy and fusion in the era of motion preserving surgery laminoplasty? spine (phila pa 1976). 2019 aug 1;44(15):e882-e888. 61. park y, maeda t, cho w et al . comparison of anterior cervical fusion after two-level discectomy or single-level corpectomy: sagittal alignment, cervical lordosis, graft collapse, and adjacent-level ossification. spine j. 2010 mar;10(3):1. doi: 10.33962/roneuro-2020-063 ventriculoperitoneal shunt occlusion and cranioplasty. a case report lívio pereira de macêdo, arlindo ugulino netto, juan pablo borges r. maricevich, nivaldo s. almeida, hildo rocha cirne azevedo -filho romanian neurosurgery (2020) xxxiv (1): pp. 405-410 doi: 10.33962/roneuro-2020-063 www.journals.lapub.co.uk/index.php/roneurosurgery ventriculoperitoneal shunt occlusion and cranioplasty. a case report lívio pereira de macêdo1, arlindo ugulino netto1, juan pablo borges rodrigues maricevich2, nivaldo s. almeida1, hildo rocha cirne azevedo-filho1 1 department of neurosurgery, hospital da restauração, recife, pernambuco, brazil 2 department of plastic surgery, hospital da restauração, recife, pernambuco, brazil abstract decompressive craniectomy (dc) is an urgent neurosurgical procedure, effective in the reduction of intracranial pressure (icp) in patients with elevated icp and in complications of brain infarction that do not respond to clinical treatment; traumatic brain injury (tbi); intracerebral haemorrhage (ich) and aneurysmal intracerebral haemorrhage. symptomatic hydrocephalus is present in 2 to 29% of patients who undergo craniectomy. they may require a ventriculoperitoneal shunt (vps). the literature does not yet show standard management of cranioplasty in patients who have previously undergone a shunt, showing evidence of sinking skin flap syndrome. this case shows parenchymal expansion after vps occlusion and cranioplasty in the patient’s profile. the 23-year-old male patient, right-handed, went to the hospital in january 2017 due to severe traumatic brain injury following multiple traumas. the patient underwent urgent dc surgery for the management of elevated icp. the patient developed hydrocephalus. hydrocephalus. it was decided to perform the vps implant. after 2 years, and with quite a sunken flap, the patient was submitted to cranioplasty procedure after shunt occlusion was performed. the patient left the hospital receiving outpatient care with no more complaints. in spite of the favourable outcome, new studies are fundamental to decide upon the best approach. introduction decompressive craniectomy (dc) is efficient in reducing intracranial pressure (icp) in patients with intracranial hypertension in complications of brain infarction that do not respond to clinical treatment, traumatic brain injury (tbi), intracerebral hemorrhage and aneurysmal intracerebral hemorrhage.1,4 hydrocephalus is present in 2 to 29% of those who undergo craniectomy, possibly requiring ventriculoperitoneal shunt (vps) after the subacute stage. most of the patients needing craniectomy accompanied by vps develop sinking skin flap syndrome. this particular factor may be challenging during cranioplasty due to the difficulty in parenchymal expansion because of the shunt and the increased keywords cranioplasty, vps, vps occlusion corresponding author: lívio pereira de macêdo department of neurosurgery, hospital da restauração, recife, pernambuco, brazil livio21@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 406 lívio pereira de macêdo, arlindo ugulino netto, juan pablo borges r. maricevich et al. chances of material gathering in the vacant space created between the implant and brain parenchyma.12 the literature does not yet show a standard management of cranioplasty in patients who have previously undergone a shunt, showing evidence of sinking flap syndrome. the reported case demonstrates parenchymal expansion after vps occlusion and the cranioplasty that ensued for this patient. in spite of this favorable outcome, new studies are necessary for the best approaches to benefit these types of patients. case study a right-handed, 23-year-old male patient entered hospital in january 2017 due to a diagnosis of tbi accompanied by multiple traumas, which required decompressive craniectomy on the right side to control raised icp. hydrocephalus evolved in the patient and a ventriculoperitoneal shunt was performed. after a positive medical evaluation, he was able to leave the hospital for the cranioplasty to occur at a later stage. due to demanding workloads and loss of follow up procedures during 2018, the cranioplasty procedure was left until january, 2020. upon his second admission to hospital, the patient presented a quite sunken flap with a concave aspect (figure 1). in order to plan the surgery, a preoperative tomographic exam took place. the exam showed up parenchyma from the right side sheering off towards the side that had not been fractured, with structural deviances in the midline greater than 1 cm. the catheter of the vps was normally placed in the frontal position of the right lateral ventricle (figure 2). in the wake of parenchymal expansion after cranioplasty, caused by the existing vps, plans were made (after consulting the neurosurgery and plastic surgery departments) for shunt occlusion before performing cranioplasty during the same surgical period. electively, the patient was then submitted to occlusion of the distal end of the ventriculoperitoneal shunt catheter through clavicular incision. within the same surgical period, the cranioplasty proceeded with the customization of the polymethylmethacrylate (pmma) prosthesis created from a sterile mold based on the reconstruction of bones in the gaps with the help of a 3d printer (figures 3 and 4). no complications arose during the time of the procedure. immediately after the operation, the tomography of the cranium showed cerebral parenchyma that had not expanded and the presence of its gathering in the subdural area (figure 5). the patient was directed to the neurological intensive care unit (icu), with rigorous observations on level of consciousness and serial neurological exams. through the evolution of the patient’s recovery, the exams showed no alteration in level of consciousness, nor any physical changes. on the fourth and ninth days of the post-operative period, controlled observation by tomography showed gradual expansion of cerebral parenchemy until the point of total expansion in nine days (figure 5). the patient, in spite of ventricular ectasia, recovered with no additional complaints. after one-week of observation, he was released from hospital (figure 6). an outpatient follow-up was performed 3 times a week for 4 weeks. clinically, the patient remained stable. outpatient care has continued without any additional complaints. figure 1. figure 2. 407 ventriculoperitoneal shunt occlusion and cranioplasty figure 3. figure 4. figure 5. figure 6. discussion dc is indicated for the treatment of elevated intracranial pressure in grave situations of traumatic injury to the brain. this procedure consists of the removal of a significant part of the skullcap. the removal entails parts of the frontal, temporal, parietal, and part of the sphenoid from the affected side, permitting the free expansion of cerebral edema without exceeding limits inside the cranial vault. even though this procedure saves lives, in many cases it leaves behind grave aesthetic and functional disadvantages for the patient. even after the decrease in cerebral edema and when the 408 lívio pereira de macêdo, arlindo ugulino netto, juan pablo borges r. maricevich et al. patient has achieved a favorable clinical profile, cranial reconstruction is recommended. the surgery seeks to recover cerebral protection against traumas, recover the cranial contour and improve neurological symptoms by re-establishing physiological intracranial pressure. the restoration of the anatomic barrier between intracranial structures and the environment normalize the dynamics of csf and the blood flow inside the brain.1,4,5 even though the ideal moment for performing cranioplasty remains uncertain, recent studies show that it should be done between 3 to 6 months later, in order to allow for significant motor skill and cognitive recovery.4,12 cranioplasty after dc for management of elevated intracranial pressure is a neurosurgical procedure that seeks to restore stasis, improve the dynamic of csf and establish the conditions for protecting the brain. under these circumstances, the procedure can facilitate neurological rehabilitation and potentially improve neurological recovery.11,15 otherwise, cranioplasty can be associated with complications and even morbidity.2,13 a significant cranial defect after dc can alter the dynamics of the circulation of csf and turn itself into a risk factor in terms of hydrocephalus in relation to complications after dc in patients suffering tbi, hydrocephalus is present in between 2 to 29% of patients. in this context, patients submitted to dc may need cranioplasty and vps after the subacute stage.1,8,12 diagnostic of hydrocephalus in people who have had hemicraniectomy surgical procedures done is necessarily subjective, since criteria based on measuring intracranial pressure or details on ventricular structure are generally not reliable in the scenario of an open cranial vault. however, the almost universal disposition towards the progressive accumulation of csf in these individuals, frequently manifested as an increase in extra-axial gatherings over the hemispheric convexity, indicates an incapacity for adequately balancing the production of csf by draining the venous sinuses.3,14 the physiopathology of patients operated by craniectomy has still not been well established. however, it is believed that the absence of skull bone coverage near the arachnoid granulations modifies the hydrodynamics of fluid absorption. besides this, it is possible for other factors to contribute, besides alteration in the dynamics of intracranial pressure – for example, mechanical blockage or inflammation of arachnoid granulations because of post-surgical remains. furthermore, these patients could present other isolated risk factors for hydrocephalus – for example, subarachnoid hemorrhage.3,10 the management of the dynamic of fluids after hemicraniectomy can be quite a challenge as a result of problems in hemispheric change or compartmentalization, emphasizing that the definitive resolution for the accumulation of csf is a great priority. in patients with a bulging scalp flap and ventriculomegaly (vm), some authors indicate temporary management until cranioplasty by way of frequent lumbar puncture or the placement of a ventricular or external spinal tap. some studies demonstrate that cranioplasty, performed as early as possible, can promote an immediate solution for the problem of hydrocephalus. in spite of this, many patients possess a persistent hydrocephalus, especially when cranioplasty occurs at a late stage. this can make them predisposed for the necessity of a previous shunt, as described in this case study.8,10,12,14 in the patients who have gone through craniectomy and whose hydrocephalus is persistent, the literature’s point of view is still controversial as to the management of and the adequate time for applying shunt and cranioplasty. recent data suggest that patients submitted for cranioplasty procedures and vps by stages can benefit from less complicated results when compared to patients who go through the two procedures at the same time. some authors will defend the shunt for managing hydrocephalus and cranioplasty at a later stage.3,6,8,9 cranioplasty in patients with vps may be challenging, mainly in those patients presenting a sunken flap due to the shunt. in patients with the sunken flap, there is a technical difficulty at the time of operating during the separation of the cutaneous layer, dura mater and encephalic tissue. besides this, in these patients, due to the presence of the vps, a major difficulty can occur in the expansion of cerebral tissue, facilitating the gathering of material in the vacant space between prosthesis and encephalic tissue that has not expanded. until now, there are no randomized studies that can guide one through the knowledge in handling these situations. in the case described, what was chosen was the 409 ventriculoperitoneal shunt occlusion and cranioplasty closing of the vps in order to permit parenchymal expansion after the cranioplasty procedure.3,8,10,12,14 as in the majority of hydrocephalus cases, after decompressive craniectomy there is a spontaneous resolution with cranioplasty. vps occlusion was maintained after cranioplasty, and a rigorous postoperative observation was conducted with regard to expansion inside the brain and the necessity for a shunt. after one week of observation, involving more than one hospital, with good clinical improvement, a follow up was done on an outpatient basis, three times per week for 4 weeks. no worsening in the patient’s condition was observed.3,8,9 the literature is yet to offer a standard for managing cranioplasty in patients with previous shunt and sunken skin flap. in spite of the success in the case related, there is no relevant sample or previous works available to compare such a case. new studies are fundamental to pave the way for a better approach to these patients. conclusion therefore, the path chosen for cranioplasty procedure, associated with occlusion of the vps, is quite rare. we still do not know much about the best approach for cranioplasty in patients who have a previous shunt and sunken skin flap. in spite of the case’s favorable outcome, new studies are fundamental in order to discover the best way to approach the problem disclosure the authors report no conflicts of interest abbreviations and acronyms csf = cerebrospinal fluid; dc = decompressive craniectomy; ich = intracerebral hemorrhage; icp = intracranial pressure; pmma = polymethylmethacrylate; tbi = traumatic brain injury; icu = intensive care unit; vm = centriculomegaly; vps = ventriculoperitoneal shunt. references 1. campolina ac, orgill dp, logan mt, maricevich p. reconstruction of the skullcap with pmma prototyped implant after decompressive craniectomy. brazilian journal of implantology and health sciences, 2020;2(1):119.https://doi.org/10.36557/2674-8169.2020v2n1p1-19 2. carvi ynmn; hollerhage hg. combined cranioplasty and programmable shunt implantation. neurological research, 2006, volume 28, march. https://doi.org/10.1179/016164106x98008 3. chen s, luo j, reis c, manaenko a, zhang j. hydrocephalus after subarachnoid hemorrhage: pathophysiology, diagnosis, and treatment. biomed res int. 2017;2017:8584753. https://doi.org/10.1155/2017/8584753 4. de cola mc, corallo f, pria d, lo buono v, calabrò rs. timing for cranioplasty to improve neurological outcome: a systematic review. brain behav. 2018 nov;8(11):e01106. https://doi.org/10.1002/brb3.1106 5. foerch c, lang jm, krause j, raabe a, sitzer m, seifert v, steinmetz h, kessler kr: functional impairment, disability, and quality of life outcome after decompressive hemicraniectomy in malignant middle cerebral artery infarction. j neurosurg 101:248–254, 2004. https://doi.org/10.3171/jns.2004.101.2.0248 6. heo j, park sq, cho sj, chang jc, park hk: evaluation of simultaneous cranioplasty and ventriculoperitoneal shunt procedures. j neurosurg 121:313-318, 2014. https://doi.org/10.3171/2014.2.jns131480 7. kim sw, lee sm; shin ho. hydrocephalus developed after cranioplasty : influence of cranioplasty on the csf circulation. j korean neurosurg soc 40:193-195, 2006 https://www.jkns.or.kr/upload/pdf/0042006133.pdf 8. laccarino c,kolias ag, roumy lg, fountas k, adeleye ao. cranioplasty following decompressive craniectomy. front neurol. 2019; 10: 1357. https://doi.org/10.3389/fneur.2019.01357 9. meyer rm, morton rp, abecassis ij. risk of complications with simultaneous cranioplasty and placement of ventriculoperitoneal shunt. world neurosurg. 2017 nov;107:830-833. https://doi.org/10.1016/j.wneu.2017.08.034 10. pachatouridis d, alexiou ga, zigouris a. management of hydrocephalus after decompressive craniectomy.turk neurosurg. 2014;24(6):855-8. https://www.ncbi.nlm.nih.gov/pubmed/25448200 11. shahid, a. h., mohanty, m., singla, n., mittal, b. r., & gupta, s. k. (2018). the effect of cranioplasty following decompressive craniectomy on cerebral blood perfusion, neurological, and cognitive outcome. journal of neurosurgery, 128(1), 229–235. https://doi.org/10.3171/2016.10.jns16678 12. schuss p, borger v, güresir á, vatter h, güresir e. cranioplasty and ventriculoperitoneal shunt placement after decompressive craniectomy: staged surgery is associated with fewer postoperative complications. world neurosurg. 2015 oct;84(4):1051-4. https://doi.org/10.1016/j.wneu.2015.05.066 13. stiver si. complications of decompressive craniectomy for traumatic brain injury. neurosurg focus 26 (6):e7, 2009 https://doi.org/10.3171/2009.4.focus0965 14. waziri a, fusco d, mayer sa, mckhann gm 2nd, connolly es jr. postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. neurosurgery. 2007 sep;61(3):489-93; discussion 493-4. https://doi.org/10.1227/01.neu.0000290894.85072.37 410 lívio pereira de macêdo, arlindo ugulino netto, juan pablo borges r. maricevich et al. 15. winkler pa, stummer w, linke r, krishnan kg, tatsch k: the influence of cranioplasty on postural blood flow regulation, cerebrovascular reserve capacity, and cerebral glucose metabolism. neurosurgical focus 8:e9, 2000. https://doi.org/10.3171/jns.2000.93.1.0053. 20agrawal_lettercerebral romanian neurosurgery (2014) xxi 4 503 letter to the editor: cerebral salt wasting syndrome following neurosurgical intervention in tuberculous meningitis amit agrawal professor of neurosurgery, department of neurosurgery, mm institute of medical sciences & research, mullana (ambala), india dear sir, although rare but csws can develop in patients with hydrocephalus, cerebral infarction, tuberculous meningitis and can also complicate the postoperative course of surgery for brain tumors or for severe head injury. (1, 2, 3) the pathogenesis of csws is still not completely understood and it has been proposed that following acute insult sympathetic responses as well as some natriuretic factors play a role in the genesis of this syndrome. (4, 5) many time it is difficult to identify whether the csws occurred due to tuberculous meningitis per se or due to the neurosurgical intervention which was done on the day of admission. (1) we need to be aware of this potentially treatable complication, however the occurrence of the csws in the present cases probably can be the manifestation of complication of tubercular meningitis (basal arteritis leading to ischemic injury to the brain) rather than the complication of neurosurgical intervention. correspondence dr. amit agrawal professor of neurosurgery mm institute of medical sciences & research mullana (ambala) pin133203 haryana, india. phone: +9101731-274475 fax: +9101731-274375 email: dramitagrawal@gmail.com dramit_in@yahoo.com references 1. nagotkar l, shanbag p, dasarwar n. cerebral salt wasting syndrome following neurosurgical intervention in tuberculous meningitis. indian pediatrics 2008;45:598-601. 2. jiménez r, casado-flores j, nieto m, garcía-teresa ma. cerebral salt wasting syndrome in children with acute central nervous system injury. pediatr neurol. 2006;35(4):261-3. 3. ravishankar b, mangala , prakash gk, shetty kj, ballal hs. cerebral salt wasting syndrome in a patient with tuberculous meningitis. j assoc physicians india. 2006;54:403-4. 4. cerdà-esteve m, cuadrado-godia e, chillaron jj, pont-sunyer c, cucurella g, fernández m, goday a, cano-pérez jf, rodríguez-campello a, roquer j. cerebral salt wasting syndrome: review. eur j intern med. 2008 jun;19(4):249-54. 5. isotani e, suzuki r, tomita k, et al. alterations in plasma concentrations of natriuretic peptides and antidiuretic hormone after sub-arachnoid haemorrhage. stroke 1994;25:2198-203. 6. dass r, nagaraj r, murlidharan j, singhi s. hyponatraemia and hypovolemic shock with tuberculous meningitis. indian j pediatr. 2003;70(12):995-7. 14amitagrawal_falx 334 agrawal falx cerebelli meningioma falx cerebelli meningioma: technical note amit agrawal professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract the falx cerebelli is a small sickle-shaped fold of dura mater below the tentorium cerebelli, which projects forward into the posterior cerebellar notch. we report a rare case of 28 year female presented with the history of headache of six months duration off and it increased in severity and frequency over last 15 days. imaging findings were suggestive of meningiona arising from the falx cerebelli. the lesion could be excised totally and safely. key words: falx cerebelli, meningioma, posterior cranial fossa. introduction the falx cerebelli is a small sickle-shaped fold of dura mater below the tentorium cerebelli, which projects forward into the posterior cerebellar notch. normally, the falx cerebelli is between 2.8 and 4.5 cm in length and is approximately 1–2 mm thick and usually harbors a single occipital venous sinus at its posterior attachment. (4, 6) we report a rare case of meningiona arising from the falx cerebelli and review the relevant literature. case report a 28 year female presented with the history of headache of six months duration off and it increased in severity and frequency over last 15 days. she was also complaining of giddiness and swaying while walking. there was no history of blurring of vision, vomiting or loss of consciousness. neurological examination revealed no deficits or physical symptoms. computed tomography demonstrated a ill demarcated isodense mass, enhancing well after contrast administration with no calcification, in the cerebellar vallecula associated with obstructive hydrocephalus (figures 1 and 2). mr imaging showed that the lesion was an extra-axial mass, appearing homogeneously isointense on t1-weighted images, and hyperintense on t2-weighted images, compared to the adjacent cerebellum (figure 3). the preoperative diagnosis was posterior cranial fossa meningioma attached to the falx cerebelli. the lesion was exposed by median suboccipital craniectomy, the dura was opened in “y” shaped manner. occipital sinus was occluded by the tumor and there was no bleeding from the sinus. there was firm, grayish avascular mass attached to the falx cerebelli. the mass was initially completely detached from the falx. the arachnoid plane was well preserved. the dural attachment was also excised. total en bloc resection could be romanian neurosurgery (2014) xxi 3: 334 337 335 performed with minimal blood loss. the histological diagnosis was meningioma of the cerebellar falx. the patient's postoperative course was unremarkable, follow up ct scan showed complete excision of the lesion and reduction in the size of the ventricles (figures 4a and b). figure 1 ct scan brain plain study showing an isodense posterior fossa midline mass compressing the cerebellar vermis and fourth ventricle with obstructive hydrocephalus figure 2 the lesion was enhacing well after contrast administration figure 3 mri images sagittal t1-weighted image showing the homogeneously isointense lesion, the lesion was becoming hyperintense on t2-weighted images 336 agrawal falx cerebelli meningioma figures 4a and b ct brain plain and contrast showing complete excision discussion posterior cranial fossa meningiomas either involve cerebellar convexity or lateral tentorial meningiomas (8) and the incidences of tentorial and posterior fossa meningiomas have been described 5% and 10% of all intracranial meningiomas, respectively. (12) lesions arising from the falx cerebelli are rarely described in the engllish literature and include meningioma and cavernous hemangioma. (5) on mr imaging the appearance of posterior cranial fossa meningioma can mimic other tumors i.e. that of cavernous hemangioma and based only on radiological investigations one cannot distinguish dural cavernous hemangioma from meningioma. (3, 9) for the supratentorial falcine meningiomas it has been described that “falcine meningioma frequently have a dumbbell shape and invaginate into the medial aspects of both left and right hemispheres and in some patients the tumor grows into the inferior edge of the sagittal sinus and can completely be concealed by the overlying cortex and that typically these lesions do not involve the superior sagittal sinus”. (1, 2) the falx cerbelli lesion in present case had similar pattern of growth, however in contrary to the supratentorial parasagittal and falx meningiomas where these lesions are in the close vicinity of the venous vessels with crucial importance for the cerebral circulation that also make their surgical treatment is sometimes very challenging, (7) we found that it was easy to remove this tumor in present case. the tumor was excised based on the well know principles of meningioma surgery composed of four essential consecutive steps; devascularization, detachment, debulking, and dissection. (10) apart from this as has been described a large median suboccipital craniotomy exposes well the falx cerebellar and also there is well preserved arachnoid plane that makes the total en bloc resection possible with minimal blood loss. (5) the occipital sinus did not pose a problem as it was closed and as has been described probably there would had been development of enough romanian neurosurgery (2014) xxi 3: 334 337 337 venous drainage because of gradual but complete obstruction of the normal venous drainage due to invasion of meningioma. (11, 13) correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.chung sb, kim cy, park ck, kim dg, jung hw (2007) falx meningiomas: surgical results and lessons learned from 68 cases. j korean neurosurg soc 42:276-280 2.cushing h (1962) meningiomas: their classification, regional behaviour, life history, and surgical end results. hafner pub. co. new york, 3.goel a, achwal s, nagpal rd (1993) dural cavernous haemangioma of posterior cranial fossa. j postgrad med 39:222-223 4.gray h, standring s, ellis h, berkovitz bkb (2005) gray's anatomy : the anatomical basis of clinical practice. elsevier churchill livingstone edinburgh ; new york 5.ito m, kamiyama h, nakamura t, nakajima h, tokugawa j (2009) dural cavernous hemangioma of the cerebellar falx. neurol med chir (tokyo) 49:410-412 6.lang j (1991) clinical anatomy of the posterior cranial fossa and its foramina. g. thieme verlag ; thieme medical publishers stuttgart ; new york 7.nowak a, marchel a (2007) surgical treatment of parasagittal and falx meningiomas. neurol neurochir pol 41:306-314 8.roberti f, sekhar ln, kalavakonda c, wright dc (2001) posterior fossa meningiomas: surgical experience in 161 cases. surg neurol 56:8-20; discussion 20-21 9.sathi s, folkerth r, madsen jr (1992) cavernous angioma of the posterior fossa dura mimicking a meningioma: case report and review of literature. surg neurol 38:257-260 10.suga y, tsutsumi s, higo t, kondo a, abe y, yasumoto y, ito m (2008) [huge falx meningioma resected en bloc following acute brain swelling: a case report]. no shinkei geka 36:819-823 11.suzuki s, mizoi k, kato s, suzuki j (1988) [a successful removal of huge confluence meningioma]. no shinkei geka 16:289-294 12.tamaki m, tsuruoka s (1995) unusual recurrence pattern in peritorcular meningioma--case report. neurol med chir (tokyo) 35:92-95 13.tanaka y, sugita k, kobayashi s, hongo k (1985) straight sinus meningioma. surg neurol 24:550-554 15_satyartheeguru_surgical romanian neurosurgery (2015) xxix 3: 329 335 329 surgical management of combined fracture of atlas associated with fracture of axis vertebrae (caaf): case series guru dutta satyarthee, gaurang vaghani, a.k. mahapatra department of neurosurgery jpn apex trauma centre, aiims, new delhi, india abstract: combined fracture involving atlas together associated with axis (caaf) accounts for approximately 3 % of traumatic cervical spine injury, caaf are rarely reported, so modalities of management and outcome are not well understood, due to paucity of literature and only few reports reported in the form of isolated case report. caff management possess challenge as it is associated with high incidence non-union with previously conservative method. however, missed diagnosis and subsequent delay may be associated with catastrophic worsening in neurological deficit. so early diagnosis and management remains the key for successful neurological outcome. such fractures are rare. authors report five such cases of caff, all required surgical management with good outcome with no mortality. current study, all cases were males (n=5), commonest mode of injury was fall (n=3), time interval since injury was within 24 hours in (n=4), however rest one presented after a gap of eight months. commonest clinical feature was neck pain (n=3), neurological deficit (n=2), neck tenderness and swelling tenderness (n=3) neuroimaging including x-ray, ct scan and mri were carried out for all cases revealed fracture of arches of atlas (n=5), one case had multiple site fracture of both arches, odontoid fracture (n=2), lateral mass of atlas fracture in 1 cases. astonishingly two cases had disruption of transverse ligament. surgical procedures performed considering economic consideration included occipito-cervcial fusion (n=3), transarticular c1-c2 fusion and anterior odontoid screw fixation in one cases each. management options in caff and review of literature discussed in present study. key words: atlas fracture, axis fracture, atlantoaxial instability. introduction traumatic cervical spine injury is one of common injury accounting approximately 4.3 % of all patients with trauma. the incidence of combined fractures, as a subset of c-1 or c-2 fractures, is 43% and 16%, respectively (1, 2). atlantoaxial fractures are commoner in elderly but uncommon in young adults, however, most commonly caused by motor vehicle accidents (1). caff are often associated with higher incidence of neurological deficits or have higher chances of neurological deterioration when compared to isolated atlas or axis vertebra injuries. management is controversial. external immobilization or surgical intervention or initial trails of conservative therapy followed by delayed surgery have been advocated for management (1, 2, and 3). consensus regarding definitive management of caff is still lacking. in this view author retrospectively analyzed five 330 satyarthee et al combined atlas-axis fracture management cases of caff treated at level i trauma centre in india and literature reviewed. case illustration case 1: a 20-year old male presented with complaint of severe non-radiating pain and swelling in neck developed following a fall while doing exercise in the gym. detailed neurological evaluation on admission revealed swelling and tenderness in neck with restricted neck movements, however no associated neck deformity and rest of the neurological examination was unremarkable. xray and ct scan of craniovertebral junction revealed multiple fracture of atlas ring, being one over anterior arch and two fractures on posterior arch causing expansion of atlas ring with associate type ii odontoid process fracture causing reducible atlantoaxial dislocation (figures 1a, 1b). mri of craniovertebral junction revealed disruption of transverse ligaments with displaced fractured odontoid process causing thecal sac compression; however no associated cord contusions or edema was detected he was planned for surgical management and occipito-cervical fusion carried out with rod and polyaxial screws to occipital bones to c 3, c 4 lateral mass screws (figure 1 c). he was doing well at last follow-up 4 months following surgery. neck pain subsided completely. figure 1 ct scan imaging of craniovertebral junction, (a) axial section and (b) sagittal image showing multiple fractures of anterior and posterior arch of atlas vertebra associated with type ii odontoid fracture with displaced odontoid tip and (c) postoperative scan with in situ occipito-cervical fusion (co-c 4 ) case 2: a 50 –yearmale had history of fall ten feet height, presented with complaint of severe neck pain. neurological examination on admission revealed only restriction of neck movements and rest of examination were essentially within normal limits. ct scan of craniovertebral junction demonstrated type 2 odontoid fracture associate with right lateral mass of axis with anterior arch of atlas fracture (figure 2 a, b). mri revealed intact transverse ligament without cord signal alteration. he underwent anterior cervical odontoid screw placement (figure 2c). postoperative period was uneventful with complete relief at follow up of 3 months following surgery. figure 2 axial (a) and sagittal (b) section of ct scan of craniovertebral cv junction showing fracture of anterior arch c1 vertebra and associated type ii odontoid fracture (c) post -operative ct scan showing precisely placed odontoid screw through anterior approach. case 3a 30 –yearmale presented with history of progressive spastic quadriparesis and associated with respiratory distress following motor vehicle accident, he was incubated at peripheral hospital and after resuscitation, was referred to our institute for further management. examination on admission, he was quadriplegic with partial sensory impairment (asia grade b). x-ray and ct scan image revealed fracture of anterior arch on right side of c1 vertebra and fracture of vertebral body of c2, and c3; and associated fracture of lamina of c2, c3 and c4 causing significant cord compression (figure 3 a, b). patient undergone occipito-cervical rod and screw fusion, occiput-c3-4, on right side occipito-c2-3 fusion done on left romanian neurosurgery (2015) xxix 3: 329 335 331 side (figure 3 c). he needed tracheotomy in post-operative period for pulmonary toileting as he was on prolonged ventilator support. in postoperative period, he improved to asia grade c at the time of discharge at one month after definitive surgery. case 4: a 12year old boy after sustaining injury following fall from tree of 12 feet about eight months back, presented with progressive spastic quadriparesis in outpatient service department. examination on admission revealed neurological status was asia grade d, with hypertonia and exaggerated deep tendon reflexes and planter reflexes extensor bilaterally. on x-ray and ct scan evaluation of patient suggestive of right c1 posterior arch fracture with reducible atlanto-axial dislocation with transverse ligament injury (figure 4 a,b). patient underwent posterior c1-c2 trans-articular screw fixation (figure 4 c). post-operative period was uneventful and good fusion at follow up of 8 month following surgery. figure 3 axial section of ct scan of craniovertebral cv junction, (a), (b) depicting right side fracture of anterior c1 arch on and associated c2 body fracture with (c) post operative ct scan occipito-cervical fusion figure 4 axial (a) and sagittal (b) section of ct scan of cv junction shows posterior arch fracture c1 on right side with consequent atlanto-axial dislocation and (c) post operative x-ray showing c1c2 transarticular in position. case 5: a 19yearmale following motor vehicle accident and presented with pain ain in neck following trauma. detailed neurological examination revealed no deficits except tenderness in neck. ct scan of craniovertebral junction demonstrated fracture of posterior arch of atlas and body of c2 vertebrae with fracture of spinous process of c 7. mri examination revealed transverse ligaments injury. patient underwent occipitocervical rod and screw fusion (occipito – c34-5). post-operative period was uneventful and on follow up at 18 months, he had no deficits or pain. discussion sir geoffrey jefferson described burst fracture of atlas involving fracture of anterior and posterior arch on both sides in 1920 (1). he defined all types of c-1 fractures, and elaborated 19 cases of caff. its variants may include unilateral arch fractures, posterior ring fractures, and lateral mass fractures of atlas. it is most common type of atlas fracture; it is associated with high morbidity and mortality. atlas fracture accounts for about 25% of atlantoaxial and complex up to 10 % of upper cervical spine fracture. injuries involving the occipitocervical junction is often unstable and rapid diagnosis facilitates early stabilization reduce the risk of subsequent iatrogenic neurological deterioration (5). high-energy transmission during fall causes fractures of atlas, and commonly associated with contiguous cranio-cervical injuries in more than one third patients (6). it is commonly caused by road traffic accident or falling on to head especially in toddler. basic pathological mechanism is axial load producing the c-1 fracture is often coupled with a flexion force that leads fracture of axis, and odontoid process fracture constitutes one of the commonest association (1, 2, 3) the incidence is higher in the elderly due to brittleness of the bones caused by 332 satyarthee et al combined atlas-axis fracture management osteoporosis (7). in the current study majority were young and fall was commonest cause. caff is associated to higher incidence of neurological deficits in comparison to isolated atlas or axis fractures (1). treatment of caff is difficult, challenging and no definite guidelines provides difficulty in selection of ideal procedure, which led to multiple surgical approaches to treat caff and usually differs from isolated atlas or axis fractures. traditional conservative approaches which involved nonsurgical halo traction therapy (5). lipson (7) advocated initial immobilization of the cervical spine with a halo vest, which allow spontaneous healing of the c-1 fracture, could be followed by fusion of c1–2, if continued instability became evident. but dickman et al (1) advocated early surgery based on the type of type 2 odontoid fracture as there is high chances of non-union, especially in elderly and if displacement of fracture segment more than 6 mm, displaced, and early surgery is recommended for specially unstable fracture. guiot and fesseler (8) after analysis, observed about 50% of their case failed to show bony fusion, who were managed with halo immobilisation, so authors further noted nonsurgical management of caff would appear to have a high failure rate and so advocated “early” surgical intervention. age of patient, type of fracture of atlas ring, type of axis fracture and intactness of transverse ligament may help in selecting appropriate surgical approach and treatment for caff injuries; however treatment protocol should be individualised according type of injury, availability of intraoperative imaging facility, economic status of patients and associated comorbid illness, suitability for general anaesthesia. however major determinant is type of axis injury, rupture of transverse ligament of axis, associated atlanto-axial dislocation, reducibility. the selection of type of fusion depends on the basis of nature of c-2 fracture. treatment option further guided by degree of offset of c1 arch, injury to transverse ligament, associated fracture of c2 or odontoid fracture. caff injury may include hangman or type ii odontoid fracture. (8, 9, 10, 11) type ii odontoid fracture with greater than 6 mm displacement is itself a surgical indication. surgical option may include occipito-cervical fusion, c1 lateral mass and c2 pedicle screw, c1-c2 transarticular screws and anterior odontoid screw fixation anterior approach for odontoid screw fixation used with posterior sloping or horizontal fracture of odontoid. halo immobilisation following anterior odontoid screw fixation in complex c1–2 fractures involving a jefferson’s fracture with minimal displacement or bilateral anterior arch fracture and with intact the transverse ligament would be appropriate treatment, as in our case -2 limitation of anterior odontoid screw placement include forward sloping odontoid fracture making more suitable for posterior approach is preferred. posterior transarticular screw fixation as in our case – 4, although a posterior approach may be preferable because the difficulty of per forming fusion via an anterior approach, occipitocervical fusion has been advocated by several authors as rescue solution. the occipital bone is to be included in the fusion construct, if associated bilateral or multiple ring fractures of the atlas arches. if c1–2 transarticular screw fixation is not possible because of the position of the vertebral arteries, then occipitocervical fixation is the remaining surgical alternative. however, anterior subluxation of c1 on c 2 may indicate rupture of transverse ligament and again highlighting fact about transverse ligaments integrity is also important factor in selection of surgical approaches in management of caff groups of patients. an atlantoaxial dislocation or disruption of unstable c1-c2, with disrupted transverse ligament poses grave risk of injury to romanian neurosurgery (2015) xxix 3: 329 335 333 brainstem and upper cervical cord. if associated odontoid fracture, odontoid fragment may migrate up into foramen magnum. however, in case of disrupted transverse atlantal ligaments and in some cases of jefferson fracture of the atlas with widely splayed lateral masses, trans-articular screw fixation may be desirable. this procedure can be performed either via an anterior or posterior approach. these complex cases and our case no. 1, 4, 5, occipito cervical fusion extending to c2 or c3-4 may be necessary, as these construct stabilises ring. conclusion combined fracture of atlas associated with fracture of axis vertebrae (caaf) poses challenge for neurosurgeon. age of patient, type of fracture of c 1 arch, intactness of transverse ligament and type of c2 fracture may help in selecting appropriate surgical approach. early surgery is safe and effective especially, if transverse ligament is injured, displaced odontoid fracture, with unstable atalanto-axial dislocation carries high chances of non union. high index of suspicious, and prompt and emergent treatment can halt the development of catastrophic neurological deterioration. however ideal selection of fusion method demands detailed evaluation of x-ray, ct scan. mri imaging, age of patients, economic status of patient, expertise of surgical team and large number of surgical procedures in neurosurgical armamentarium further produces confusion as long term results are still awaited. however, in future study involving large number of cohorts will definitely provide eye opening solution. however, treatment for these injuries should be individualised according their type of injury. table 1 summary of our patients with combined fracture of atlas associated with fracture of axis vertebrae (caaf) sr no. age (years/ sex) mode of injury imaging of atlas vertebra with fracture of arch imaging of axis and transverse ligament associated other vertebral injury surgical approach remarks 1) 20 fall multiple site of anterior and posterior type ii odontoid fracture + transverse ligaments injury occipito-cervical fusion (o-c3-4) pain reduces completely 2) 50 fall from height arch of atlas fracture type ii odontoid fracture + lateral mass c2 odontoid screw. good fusion at 9 months 3) 30 motor vehicle accident anterior arch on right side c2 body fracture c3 body fracture lamina of c2,c3 and c4 fracture occipitocervical fixation (rtoc3-4, lt-o-c2-3) deficits improved post operatively. with good fusion at 20 months f/u 4) 12 fall from height right side posterior arch reducible atlantoaxial dislocation + transverse ligament injury posterior c1-c2 trans-articular screw fixation good bony fusion at 8 months. 5) 19 motor vehicle accident posterior arch fracture of c2 vertebrae body + transverse ligaments injury spinous process of c 7 fracture occipito-cervical rod and screw fusion (occiput – c3-4-5) no complaint at 18 month f/u. correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, #310, jai praksah apex trauam centre, and aiims, new delhi, india 334 satyarthee et al combined atlas-axis fracture management e-mail: duttaguru2002@yahoo.com references 1. jefferson g: fracture of the atlas vertebra. report of four cases, and a review of those previously recorded. br j surg 1920; 7:407-422. 2. gleizes v, jacquot f, signoret f, feron j m. combined injuries in the upper cervical spine: clinical and epidemiological data over a 14-year period. eur spine j.2000;9: 386–392 3. aïcha k. b, laporte c., akrout w.,. atallah a, kassab g, jégou d. surgical management of a combined fracture of the odontoid process with an atlas posterior arch disruption: a review of four cases. orthop traumatol surg res 2009; 95:3: 224–228. 4. dickman ca, hadley mn, browner c, et al. neurosurgical management of acute atlasaxis combination fractures. a review of 25 cases. j neurosurg 1989;70:45–49. 5. mccabe jp, waldron b, byrne j: occipitocervical fixation of a complex upper cervical 6. apostolides pj, theodore n, karahalios dg: triple anterior screw fixation of an acute combination atlas-axis fracture. case report. j neurosurg 1997; 87:96–99. 7. bellis y m, linnau k f, mann f a. a complex atlantoaxial fracture with craniocervical instability: a case with bilateral type 1 dens fractures. ajr 2001; 176:978. 8. lipson sj: fractures of the atlas associated with fractures of the odontoid process and transverse ligament ruptures. j bone joint surg (am) 1977; 59:940–943. 9. guiot b, fessler r g.complex atlantoaxial fractures j neurosurg (spine 2) 1999;91:139– 143. 10. liu c, kuang l, wang l, tian j management of combination fractures of the atlas and axis: a report of four cases and literature review. int j clin exp med. 2014 aug 15;7(8):2074-80. 11. wu am, wang xy, chi yl, xu hz, weng w, huang qs, ni wf. management of acute combination atlas-axis fractures with percutaneous triple anterior screw fixation in elderly patients. orthop traumatol surg res. 2012 dec; 98(8):894-9 10giovania_cerebral 454 giovani et al cerebral revascularization: direct versus indirect bypass cerebral revascularization: direct versus indirect bypass. case presentation and review a. giovani, f. brehar, r.m. gorgan “bagdasar arseni” university hospital, bucharest abstract: since 1985 when the ec-ic bypass study results were published and less procedures were performed for cerebral ischemia, the ec-ic bypass even high or low flow and the ic-ic bypass as flow replacement procedures gain acceptance for many neurosurgical pathologies, from extrinsic and intrinsic tumors requiring large vessels sacrifice to large giant and fusiform aneurysms. in recent years, after the results of carotid occlusion surgery study (coss) and the japanese ec-ic trial published their results the indications for extracranial-intracranial (ec-ic) by-pass expanded, including both extracranial carotid artery occlusive disease and intracranial atherosclerotic disease. the authors make a literature review of the indications for cerebral revascularization, with focus on the direct sta-mca and indirect (edams) revascularization techniques as a treatment for ischemic stroke. they present two cases of moyamoya disease one treated with combined approaches and one with indirect approach and discuss the technical skills the surgeon should acquire in order to perform an anastomosis, focusing on the details of sta-mca bypass, concluding that a combined approach gives better neurological results visible shortly after the surgery. key words: cerebral revascularization, extracranial-intracranial by-pass, stroke. introduction cerebral revascularization either surgical through very technical demanding bypasses or endovascular through pipeline embolisation devices, stenting or trombectomy devices refers to bringing cerebral perfusion in teritories where it is lacking due to vessel occlusion or where it will be lacking after the vessels involved in a large extra/intraaxial tumor or giant aneurysm will be sacrificed during the treatment of that specific condition (3, 7). in the first case we speak of a flow augmentation bypass while in the second it is a flow replacement bypass. for flow augmentation in the anterior circulation the most used bypass is a low-flow bypass, the superficial temporal artery (sta) to middle cerebral artery (mca), while for the posterior circulation occipital artery (oa) to posterior inferior cerebellar artery (pica) or sta to superior cerebellar artery (sta) are the romanian neurosurgery (2014) xxi 4: 454 – 464 455 alternatives. in cases of giant or complex aneurisms and skull base tumors where flow replacement is mandatory a high flow bypass is appropriate to replace the flow through the sacrificed vessel. even if the patient does not fail the balloon occlusion test there is a 30 % risk of subsequent ischemia and stroke. different types of bypasses have been described, from direct intra-intracranian (icic) like termino-terminal, reimplantation or laterolateral to ic-ic using short grafts like petrous carotid to mca or internal maxillary artery to mca, or ic-ec bypasses using long radial or safenous grafts to take blood from the common carotid artery to the middle or posterior cerebral artery (14). preoperative flow measurement is not readily available in many departments ours included which lack xenon ct, perfusion ct, perfusion mri, spect, transcrannial doppler or pet so in this centers the decision for the revascularization intervention is based only on the clinical and angiographic criteria. the normal cerebral blood flow (cbf) is 46 ml/100g/min and oxygen extraction fraction (oef) is 30/40% so the oxygen supply is two to three times greater than oxygen demand. the kyoto and st. louis trials based on hemodynamic criteria demonstrated that in stage ii hemodynamic failure defined as increased oef as measured by pet studies, the medical treatment results were poor and comparable to those reported for symptomatic severe carotid stenosis (12, 13). as the ec-ic bypass is known to normalize the oef in patients with increased oef distal to an occluded carotid artery it should be the treatment of choice for this subset of patients (2). the jet study measured the cbf and the reduced acetazolamide cerebrovascular reactivity with spect while the coss trial includes for eligibility clinical criteria, pet scan and arteriographic criteria, including angiography. after the patient has been included for the treatment a last line of physiological measurments must follow: the intraoperative flow measurement. this technique allows the surgeon to pick the appropriate sta branch for by pass and to check immediately the patency of the anastomosis. postoperative the state of the flow through the anastomosis should be checked by quantitative mr angiography. creating a bypass is very demanding technically and many days should be spent acquiring the required skill in the lab under the highest magnification of the microscope. lab training no in vivo anastomosis should be performed without previous intensive lab training. it is advised to use first swine heart coronary arteries than smaller chicken wing and only when comfortable with these the next step, anastomosis in anesthetized mice first on carotid than on inguinal arteries should be performed. all kinds of anastmosis, starting with termino-terminal (tt), than latero-lateral (l-l) termino-lateral (t-l) should be exercised. (figure 1 and figure 4) one must try to view any anastomosis as a l-l one as this concept allows the surgeon to perform tt and tl anastomosis in deep locations working in narrow corridors, without the need to rotate the anastomosis in order to make the second anastomotic line 456 giovani et al cerebral revascularization: direct versus indirect bypass visible. in the begging using separate 10-0 or 11-0 sutures is advised by most of the experts but one may find the continuous technique faster and easier. when the trainee feels he acquired enough experience he/she must use a continuous perfusion system and clips to make it as close as possible to in vivo conditions and only than anastomosis on anesthetized mice and then on humans can be performed. (figure 2 and figure 3). no high flow anastomosis should be tried unless dozens of low flow ones were previously done with success. a good exercise is to construct simulated aneurysms for clipping training as in video: https://www.youtube.com/watch?v=h6h4 nkbbhkk&index=5&list=uuac_q8qnpmd yqwbc6x_63wa https://www.youtube.com/watch?v=l4nb pcdg39c&list=uuac_q8qnpmdyqwbc6x_ 63wa&index=3 figure 1 latero-lateral anastomosis on chicken wing arteries – the back wall was sutured and the suture is continued on the front wall figure 2 a small aneurysm (black arrow) was reconstructed from a segment a vein. the aneurysm fills as the vessel is irrigated figure 3 a segment of an artery closed in one end is anastomosed at an artery bifurcation (black arrows) creating an aneurysm (white arrow) that is filled with water from the continuous infusion system and then clipped romanian neurosurgery (2014) xxi 4: 454 – 464 457 figure 4 two terminolateral anastomosis (black arrows); the two vessels are united by a laterolateral anastomose (white arrow) and the vessels are filled with water from the continuous infusion system showing no leakage sta-mca bypass one of the best indications for sta-mca bypass is moyamoya disease, yet the by-pass should be considered only in cases with lack of response to maximal medical treatment. the cerebral flow should be investigated preoperative using ct perfusion or xenon ct blood flow measurement or pet for oxygen extraction measurement. than the feasibility of the bypass should be evaluated measuring the caliber of the sta on a 6 vessels angiography. every step in performing an anastomosis is very important and any mistake can compromise the whole procedure. according to the team's preferences the head can be fixed in mayfield or left free on horseshoe with the head parallel to the floor. after identifying and mashin marking the sta and its branches by palpation or using a doppler probe a vertical linear incision in front of the ear is used with care not to injure the vessel. use of the operating microscope from the skin incision is advisable. during dissection small branches should be coagulated while lager ones should be ligated and cut. 458 giovani et al cerebral revascularization: direct versus indirect bypass figure 5 two ways of performing a termino-lateral anastomosis, using one thread that is sutured to its own tail in the end or two heel stiches that go continuously and are sutured to each other’s tail in the end the sta should not be completely denuded during dissection as this may cause injury. when this step is completed the artery is retracted and fixated posteriorly in a papaverine soaked cottonoid. then the temporal muscle is split with the cautery on the midline and desinserted from the bone. a 3/3 cm diameter craniectomy is performed and the dura is incised. after finding a proper caliber m3 or m4 vessel the sta is clipped proximally and cut as to assure a propper length for the anastomosis not to be in tension. at this step if a charbel doppler probe is available it should be used to measure the cut flow index. the distal end of the sta is fish mouthed to increase the diameter of the anastomosis. next a proximal 3mm clip should be placed on m3 or m4 followed by a distal clip. during this maneuver the blood pressure should be increased. the distance between the clips must be at least 1 cm to allow a good working space between the clips. then a linear incision is made along the axis of the m3/m4 vessel using a needle tip to make a puncture and a strait or angulated scissors to complete a 2,5 mm incusion (more than twice the diameter of the receiving vessel). the vessel must be irrigated with heparinised saline and some authors prefer a colored dye to see the margins. two sutures are placed at 0 and 180 degrees (heel and toe) and then the suture lines are runned continuously with 100, placing the stich as close to the edge as possible. the back wall is completed first and then the front, more proximal suture line. the anastomosis is continuously irrigated till the final closure. the distal clip is removed first than the proximal than the clip on sta. (fig 5) a little ooze from the anastomosis line is normal. if there is true bleeding the clips must be reapplied and another stich should close the opening. after the completion of the anastomosis the charbel doppler probe is used again to check the flow through the anastomosis. if the cut flow index is less than 0,5 it means there is a technical problem with the bypass and it may need revision. the next step of the surgery is applying the temporal muscle intimate on the pial surface with care not to occlude the sta coming between its two halves. the two layers are approximated to each other on the midline and to the suspended dura on the edges. case 1. combined direct/indirect approach a 32 yo male presented with left mild hemiparesis and dysarthria that worsened over the week prior to admission. a ct scan showed marked hypodensity areas in the right frontal and parietal lobes in the territory irrigated by right mca. (figure 6) the almost complete carotid occlusion was observed on the right internal carotid artery angiography romanian neurosurgery (2014) xxi 4: 454 – 464 459 and very few basal collaterals which corresponded to a grade vi moyamoya disease on suzuky classification. the patient opted for a combined direct-indirect approach. the surgical technique was described above. a video with the technique can be accessed here: https://www.youtube.com/watch?v=d_adljv o0-q&list=uuac_q8qnpmdyqwbc6x_ 63wa; https://www.youtube.com/watch?v=u60zurj -nfc&index=31&list=uuac_q8qnpmdyqw bc6x_63wa. the patient received heparine 1 day before and one day after the surgery and then was discharged on chronic aspirin treatment. given the small caliber of the anastomosed vessels hypotension should be avoided in the first postoperative days to maintain a good flow through the bypass. (figure 7) the outcome was favorable. dyasrthira and left hand deficit improved in the first postoperative week and the patient was able to ambulate without help at discharge after 1 week. at two months follow up the patient was able to hold his 4 yo daughter in his left hand, and he presented no speech impediment. (figure 8) figure 6 ct scan and angiography showing ischemia and complete intracranial ica occlusion corresponding to a grade vi moyamoya on suzuky classification 460 giovani et al cerebral revascularization: direct versus indirect bypass figure 7 intraoperative pictures with the technique (also see video) showing the linear cut in the recipient vessel, the first heel stich, and after the completion of the anastomosis the removal of the clips, in this case first the proximal one on the recipient vessel, note a little ooze from the anastomotic line and then note the increase in size of recipient vessel between the anastomosis place and the distal clip when the clip on the sta (black arrow) is removed, and the pulsating vessel with no leakage or stenosis after removal of the last clip 2 months ct scan 6 months angio ct figure 8 postop ct scan at two months shows no hypodensity in the territory of the right mca and the 6 months follow up angio ct shows many collaterals formed in the right fronto temporo parietal area romanian neurosurgery (2014) xxi 4: 454 – 464 461 case 2 encephaloarterioduromyosynagniosis (edams) a 36 years old woman presented with motor aphasia, left hemiparesis predominant in the arm, left central facial nerve paresis, facial paresthesia and visual deficit. the symptoms appeared and worsened over the last 2 weeks. the mri showed multiple ischemic frontal and parietal lesions, note ivi sign on the pial surface and the flow void signals given by the basal ganglia collaterals. angiography showed bilateral occlusion of the intracranial carotid artery with collaterals formation corresponding to a suzuky grade iv. (figure 9) the chosen treatment was bilateral encephaloarterioduromyosynagniosis (edams). using a linear temporal skin incision the sta was dissected from the surrounding tissue and preserved in continuity. a 3/3 temporal craniectomy was performed after the mobilization of the temporal muscle with care not to injure its vascular pedicle. the dura was opened and suspended circullary to the fascia. the arachnoid was opened over the cortical surface and the sta and then the temporalis muscle were applied on the pial surface. the muscle is then fixed in place with a few interrupted stiches to the reflected dura, and the skin was closed. (figure 10) at 6 months follow up the hemiparesis and aphasia recovered completely and the 7th nerve paresis recovered incompletely (figure 11). figure 9 preop ct and mri showing right frontal ischemia, and pial collaterals on t2 called ivi sign. the angiography shows an amputated flow in the mca and formation of basal collaterals, consistent with a suzuky 4 grade 462 giovani et al cerebral revascularization: direct versus indirect bypass figure 10 intraoperative images showing the technique figure 11 the postop ct shows the disappearance of frontal hypodensity at 6 months follow up discussion since 1985 when the ec-ic bypass study results were published and less procedures were performed for cerebral ischemia, the ecic bypass even high or low flow and the ic-ic bypass as flow replacement procedures gain acceptance for many neurosurgical pathologies, from extrinsic and intrinsic tumors requiring large vessels sacrifice to large giant and fussiform aneurysms (3). in recent years, after the results of carotid occlusion surgery study (coss) and the japanese ec-ic trial published their results the indications for extracranial-intracranial (ecic) by-pass expanded, including both extracranial carotid artery occlusive disease and intracranial atherosclerotic disease (7). as 10% of tia and 15-25% of ischemic strokes are caused by complete carotid artery occlusion and under the best medical treatment the two years risk of subsequent stroke is of 10%-15% surgical revascularization was reconsidered in diminishing this risk in many cerebrovascular centers. intracranial atherosclerotic disease accounts for 9% of all ischemic strokes and has a 2 years recurrence rates of 15%-20% (8, 9). even if coss trial didn't show clear evidence in favor to surgery the postoperative ischemic strokes (14/93) cannot be attributed to technical problems with the bypass, but to patient hemodynamic fragility due to age and inability of patients to tolerate surgery. thus decision making based on preoperative and intraoperative flow measurement is very important when selecting romanian neurosurgery (2014) xxi 4: 454 – 464 463 patients for by-pass, even direct indirect or combined. large metaanalysis showed that in one third of the cases the sta-mca anastomosis is combined with miosynangiosis with a growing tendency for this technique. when combined direct and indirect approach is used, it was shown that the bypass provides the patient with a immediate increase in blood flow and decrease of oef, translated in a recovery of the neurological symptoms, but in time , after the first 6 months postoperative the collaterals that form form the miosynangiosis take over the workload of the anastomosis and when this is checked with a qmri it will show a severe decreased flow through the anastomosis compared to the same measurement done in the first weeks after the surgery (1, 10). conflicting conclusions are found in different studies, some performed only on patients with indirect bypass criticize the stamca as prone to induce thrombosis at the place of stenosis and this thrombosis can occlude the lenticulostriate arteries giving rise to new neurologic deficit, and advocate the use of indirect bypass alone, either encephaloduroarteriosynangiosis (edas) or enecephaloduromioarteriosynangiosis (edams) (5). other studies performed on large numbers of patients who benefited from both direct and indirect approach show very good results in the rate of postoperative stroke (4.7%) combined to medical treatment or to indirect approach alone with even better results in pediatric compared to adult population (4, 6). in our poor experience with these techniques we noticed that the neurological recovery after the combined approach is better and comes more rapidly than with myosinangiosis alone. conclusions the refinement of anesthetic methods allows expert vascular neurosurgeons to operate with a high rate of success complex cases of giant aneurysms and tumors previously considered impossible, now even in awake setting. after a decline since 1985 revascularization procedures are reconsidered for cerebral ischemia. a combined direct – indirect approach is better than using each technique alone, for patients with simptomatic extracranial or intracranial carotid occlusion given the fact that sta-mca bypass provides early augmentation of flow and edams provides durable long term revascularization and one of the best indications for the technique is moyamoya disease. every high volume center should have a few vascular neurosurgeons very well trained in microanastomosis techniques. no bypass procedure should be performed without a good indication, yet moyamoya disease when symptomatic represents one of the best indications. correspondence andrei giovani giovani.andrei@gmail.com 464 giovani et al cerebral revascularization: direct versus indirect bypass references 1. amin-hanjani s, shin j, zhao m, et al : evaluation of extracranial-intracranial bypass using quantitative magnetic resonance angiography j neurosurg 106: 291298, 2007 2. amin hanjani s, charbel ft: is extracranialintracranial bypass surgery effective in certain patients? neurol clin 24: 729-743; 2006. 3. arthur l. day, m.d. ; indications for surgical intervention in middle cerebral artery obstruction ; neurosurg 60:296-304, 1984 4. james a. j. king, m.b., b.s., ph.d., f.r.a.c.s.,1 derek armstrong, m.b., b.s., f.r.c.p.,2 shobhan vachhrajani, m.d.,3 and peter b. dirk s, m.d., ph.d., f.r.c.s.c3 ; relative contributions of the middle meningeal artery and superficial temporal artery in revascularization surgery for moyamoya syndrome in children: the results of superselective angiography. ; j neurosurg pediatrics 5:000–000, 2010 5. joshua r. dusick, m.d.,1 david s. liebeskind, m.d.,2,4 jeffrey l. saver, m.d.,2,4 neil a. martin, m.d.,1 and nestor r. gonzalez, m.d.; indirect revascularization for nonmoyamoya intracranial arterial stenoses: clinical and angiographic outcomes; j neurosurg 117:94–102, 2012 6. ken kazumata, m.d.,1 masaki ito, m.d.,1 kikutaro tokairin, m.d.,1 yasuhiro ito, m.d.,1 kiyohiro houkin, m.d.,1 naoki nakayama, m.d.,1 satoshi kuroda, m.d.,2 tatsuya ishikawa, m.d.,3 and hiroyasu kamiyama, m.d.; the frequency of postoperative stroke in moyamoya disease following combined revascularization: a single-university series and systematic review; j neurosurg 121:432–440, 2014 7. maxim mokin, m.d., ph.d.,1,2 peter kan, m.d., m.p.h.,3,4 tareq kass-hout, m.d.,1,2 adib a. abla, m.d.,3,4 travis m. dumont, m.d.,3,4 kenneth v. snyder, m.d., ph.d.,3–6 l. nelson hopkins, m.d.,3–6 adnan h. sidd iqui, m.d., ph.d.,3–6 and elad i. levy, m.d.; intracerebral hemorrhage secondary to intravenous and endovascular intraarterial revascularization therapies in acute ischemic stroke: an update on risk factors, predictors, and management. neurosurg focus 32 (4):e2, 2012 8. maxim mokin, m.d., ph.d.,1 alexander a. khalessi, m.d., m.s.,3 j mocco, m.d., m.s.,4 giusepp e lanzino, m.d.,5 travis m. dumont, m.d.,1 ricardo a. hanel, m.d., ph.d.,6 demetrius k. lopes, m.d.,7 richard d. fessler ii , m.d.,8 andrew j. ringer, m.d.,9 bernard r. bendok, m.d.,10 erol veznedaroglu, m.d.,11 adnan h. sidd iqui, m.d., ph.d.,1,2 l. nelson hopkins, m.d.,1,2 and elad i. levy, m.d., m.b.a.1,2 ; endovascular treatment of acute ischemic stroke: the end or just the beginning? ; neurosurg focus 36 (1):e5, 2014 9. melanie g. hayden, m.d., m.a.s., marco lee, m.d., ph.d., f.r.c.s., raph ael guzman, m.d., and gary k. steinberg, m.d., ph.d.; the evolution of cerebral revascularization surgery, neurosurg focus 26 (5):e17, 2009. 10. raphael guzman, m.d.,1,3 marco lee, m.d., ph.d.,1,3 achal achrol, b.s.,1,3 teresa bell-stephens, r.n.,1,3 michael kelly, m.d.,1,3 huy m. do, m.d.,1–3 michael p. marks , m.d.,1–3 and gary k. steinberg , m.d., ph.d.1,3; clinical outcome after 450 revascularization procedures for moyamoya disease; j neurosurg 111:927–935, 2009 11. r. webster crowley m.d.,1 ricky medel, m.d.,1 and aaron s. dumont, m.d.1,2 evolution of cerebral revascularization techniques; neurosurg focus 24 (2):e3, 2008 12. richard leblanc, m.d., f.r.c.s.(c), jane l. tyler, m.d., g~rard mohr, m.d., f.r.c.s.(c), ernst meyer, ph.d., mirko diksic, ph.d., lucas yamamoto, m.d., ph.d., laughlin taylor, m.sc., serge gauthier, m.d., f.r.c.p.(c), and antoine hakim, m.d., ph.d., f.r.c.p.(c); hemodynamic and metabolic effects of cerebral revascularization; j neurosurg 66:529-535, 1987 13. sunil manjila, m.d.,1 tony masri, m.d.,2 tanzila shams , m.d.,2 shakeel a. chowdhry, m.d.,1 cathy sila, m.d.,2 and warren r. selman, m.d.1 ; evidence-based review of primary and secondary ischemic stroke prevention in adults: a neurosurgical perspective; neurosurg focus 30 (6):e1, 2011 14. sanai n, zador z, lawton mt: bypass surgery for complex brain aneurysms: an assessment of intracranial – intracranial bypass, neurosurgery 65: 670-683, 2009 doi: 10.33962/roneuro-2020-032 historical vignette: the first brain surgery performed by the first woman neurosurgeon in romania, dr. sofia ionescu-ogrezeanu andreea-anamaria idu, aurel-george mohan, mircea-vicentiu saceleanu, alexandru-vlad ciurea romanian neurosurgery (2020) xxxiv (1): pp. 209-212 doi: 10.33962/roneuro-2020-032 www.journals.lapub.co.uk/index.php/roneurosurgery historical vignette: the first brain surgery performed by the first woman neurosurgeon in romania, dr. sofia ionescu-ogrezeanu andreea-anamaria idu1,6, aurel-george mohan2,3, mircea-vicentiu saceleanu4,5, alexandru-vlad ciurea6,7 1 emergency university hospital of bucharest, bucharest, department of neurosurgery, romania 2 bihor county emergency hospital, department of neurosurgery, oradea, romania 3 oradea university – medical school, neurosurgical department, romania 4 emergency university hospital of sibiu, department of neurosurgery, sibiu, romania 5 “lucian blaga” university of medicine and pharmacy, sibiu, romania 6 sanador medical centre, department of neurosurgery, bucharest, romania 7 “carol davila” university of medicine and pharmacy, bucharest, romania abstract introduction. sofia ionescu-ogrezeanu (b. april 25, 1920, fălticeni d. march 21, 2008, bucharest), also known as the lady of romanian neurosurgery, became the first woman neurosurgeon in the world after performing a brain surgery during world war ii, a fact recognized as a world premiere during the 13th world congress of the world federation of neurosurgical societies (wfns) in morocco, in 2005. [1] materials and methods. sofia ionescu is the first woman neurosurgeon. she was born on the fields of bucovina, in fălticeni, and became part of the "golden team" of the romanian neurosurgery of the pioneering period. the decisive moment of her career took place in 1944, during the war when she was forced to perform an emergency operation on a child, a victim of the bombing. the article coagulates the reports regarding the description of the first brain surgery performed by the first woman neurosurgeon with the continuous activity integrated with the field of neurosurgery. both specialized articles, biographical books, and television interviews were used as references. results. the operation performed in the fifth year of faculty was the first step of a journey of 47 years of neurosurgical career, practised with high morality and devotion. the sacrifice of the pioneer of the first woman neurosurgeon was recognized in the press in the country and abroad, as well as by the recognition of different titles and distinctions. keywords neurosurgeon sofia ionescu (ogrezeanu), first brain surgery 1944, first woman neurosurgeon, neurosurgical history corresponding author: a.v. ciurea prof. md. phd. msc, dr.h.c. mult. “carol davila” university of medicine and pharmacy, bucharest, romania prof.avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 210 andreea-anamaria idu, aurel-george mohan, mircea-vicentiu saceleanu, alexandru-vlad ciurea introduction dr. sofia ionescu's professional career reveals the secret of the art of reversing the meaning of obstacles; according to the idea advocated by marcus aurelius, year 170: “the impediment to action advances action. what stands in the way becomes the way.” thus, she performed her integrated neurosurgical activity during 47 years, in the socio-political context of the second world war. she was part of the team that made the pioneering sacrifice in the romanian neurosurgery, also called the "gold team"; together with prof. dr. dimitrie bagdasar, the founder of the neurosurgical specialty in romania, formed by prof. dr. harvey williams cushing in boston, dr. constantin arseni and dr. ionel ionescu, who later became her husband and together they had two children [2],[3]. materials and methods in dr. sofia ionescu we discover a personality who practices great virtues, such as: courage to be the first woman neurosurgeon in romania and internationally renowned; reason to constantly perform the balance exercise in affective gymnastics and to practice for the first time in 1944, in the fifth year of study at the faculty of medicine, the drill procedure, in order to save the life of a boy in a coma, the victim of the bombings of world war ii; ingenuity and creativity to use in 1968 a sterile urinary well for external ventricular drainage, subsequently standardized procedure; compassion to the fellow patients, who she gave pieces of soul and days of their lives; humility to offer the sacrifice of her own existence in order to perpetuate neurosurgery as a specialty in romania, fulfilling the last wish of prof. dr. dumitru bagdasar. [4] about her first brain operation, which enrolled her in the history of world neurosurgery, she speaks in an interview with eugenia vodă, within the program "professionals" of the romanian television 1 (tvr1) in 2000, reporting: "this operation decided life for 47 years ahead, while i was in neurosurgery, and brought me to 180 degrees compared to what i had planned, a quiet life as an internist in my hometown, fălticeni. because at some point it was necessary to perform an emergency operation on a child after a bombing and he had no one to do it. dr. bagdasar had a suppuration in his hand, the other two secondary doctors, dr. arseni and dr. ionescu, each had a similar impediment to enter the operation, and the child was actually dying in front of us. and then bagdasar, who was very impressed, said. who can do this?ʺ he asked the intern who was a neurologist. and he said "no. no way." shaking his head. and then he asked me, too, and i agreed. although, in my mind, i thought ʺif he watches me operating, my hand will be shaking and he will look at me curiously”, as it was the first neurosurgery operation. dr. bagdasar, at the end of the operation, told me ʺmiss, you have the necessary skills. please stay with usʺ. figure 1. dr. sofia ionescu during surgery. also, in the biographical book "neodina binelui neurosurgeon sofia ionescu", written by rodica simionescu, published in 1998, at alas publishing house, călărași, there is a chapter that sets out the steps of initiating the operations in neurosurgery, fragments: "the year 1944. among the wounded emergency patients in the hospital at the neurosurgery department, a little boy is brought into a coma. dr. bagdasar consults him and decides that the child should be operated on immediately. the only valid persons were the intern sofia ogrezeanu and the intern constantin creţan. if they do not intervene urgently, the child dies in front of them. who can do a tripod? she defeats her chosen spirit, professional conscience and, of course, courage and states that she wants to operate. she operated safely and quickly as if she had been doing this for ever. she was operating on a child. she was 211 the first brain surgery performed by the first woman neurosurgeon in romania, dr. sofia ionescu-ogrezean performing brain surgery. no woman had done this before. she went into the operation with only one thought: to save the child. extraordinary peace, perfect peace and clarity have seized her soul. perfect concentration. her mind works without any emotion. everything is just calm and precision. that's how it was. that's how she always operated. professor bagdasar, dr. ionel ionescu, the staff of the operating room followed her breathlessly. she succeeded. dr. bagdasar immediately noticed that she had the skills and asks her to stay in neurosurgery. thus, prof. d. bagdasar baptized an exceptional physician, blessed a name that would remain in the history of romanian medicine in the honor gallery." [5] figure 2. “the golden team” during brain surgery. prof. dr. sebastian nicolau, head of the oncopediatrics section at fundeni hospital, referred to the worldwide validation of the operation performed by dr. sofia ionescu, in the article "dr. sofia ionescu primum inter pares the first woman neurosurgeon in romania", published in the repere iatro-istorice j.m.b magazine: "the undeniable truth has been brought to light after long iatrics-historical research of over 30 years, on september 17, 2005, at the world congress of neurosurgery in morocco (marrakesh), which confirmed that dr. sofia ionescu is the first woman neurosurgeon in the world. until then, it was believed that dr. eisenhardt from the u.s.a. holds this title of honor, but it has been proven that the one who practiced medicine in the first decades of the twentieth century was an anatomopathologist and not a neurosurgeon.”[6]. in the specialized literature, in the article entitled "sofia ionescu, the first woman neurosurgeon in the world", published in the journal "world neurosurgery" in march, 2013, it is also mentioned the place occupied by dr. sofia ionescu internationally: ”the nomination as first woman neurosurgeon took place in marrakech during the 2005 wfns congress. despite the fact that some claim mrs. diana beck to be the first woman neurosurgeon in the world, our theory suggests otherwise. while the first documented surgical intervention performed by mrs. diana beck dates since 1952, mrs sofia ionescu operated for the first time on a human brain as early as 1944. furthermore, mrs. diana beck's actions surfaced in the world in the year 1947, long after the war had ended and sofia ionescu became a neurosurgeon. last but not least, during the second world war mrs. diana beck had occupied the position of consultant for neurosurgery and not a fully entitled neurosurgeon.”[1] the years that followed the early initiation into the mysteries of neurosurgery were devoted entirely to the perpetuation of this specialty at the beginning, the work of dr. sofia ionescu being recognized in 1943 by the sign of distinction of the red cross. in 1972 she received the medal for the proclamation of the republic (25 years) decree no. 480, and in 1996 the diploma of honor a.n.f.d.u.r. for exceptional merits. in the general assembly of the academy of medical sciences she was elected honored member of the academy, the ing. elisa leonida zamfirescu award and the diploma of honor were offered by the national confederation of women in romania for outstanding merits in promoting romanian science and technology and everything else. in the same year, 1996, she became a member of the romanian society for the history of medicine. [7],[8]. the intraoperative effort has been doubled by the publication of scientific papers in journals in the country and abroad, such as acta chirurgica belgica 1958, journal de chirurgie 1958, psychiatry, neurology, neurosurgery 1960 amsterdam, wiener klinische wochenschr1ft 1962, journal of neurosurgery 1967, rev. roumaine de neurosurgery 1970, neurosurgery stuttgard 1970 and others, in a total of over 120 articles. also, dr. sofia ionescu is recognized in the national and foreign press as the first woman neurosurgeon.[9] 212 andreea-anamaria idu, aurel-george mohan, mircea-vicentiu saceleanu, alexandru-vlad ciurea figure 3. dr sofia ionescu, the lady of neurosurgery. conclusion at the world congress of neurosurgery in morocco, marrakech it was confirmed that dr. sofia ionescu is the first woman neurosurgeon in the world.[10] the life model of the lady of international neurosurgery, can be regarded as a true guide of life coaching through the objective judgment, the altruistic action and the power of acceptance that it manifests. the stories coagulated in the book illustrate the art of relentless zeal and ingenuity conflicts of interest the authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as potential conflict of interest. references 1. ciurea av. moisa h. mohan d. sofia ionescu. the first woman neurosurgeon in the world. world neurosurg. 80(5):650-3, 2013. 2. ciurea av. istoria neurochirurgiei române. editura viața medicală românească, bucurești, 1995. 3. aldea h: famous neurosurgeons [in romanian]. bucharest: glasul bucovinei publishing house; 1993. 4. dumitrescu c. lungul drum prin mii de nopti albe. flacăra, 1987. 5. simionescu rodica. neodihna binelui neurochirurg sofia ionescu. călărași: atlas publishing; 1998. 6. nicolau s. doctor sofia ionescu – primum inter pares – prima femeie neurochirurg din românia. repere iatroistorice, 84-6, bucurești, 1945. 7. arseni c, aldea h. milestones in the history of romanian neurosurgery [in romanian]. bucharest: romanian academy publishing house; 1988. 8. ogrezeanu irina, ciurea av. sofia ionescu – o biografie de excepție. textbook of neurosurgery, bucharest. romanian medical publishing house; vol.1:71-5, 2010. 9. glikesce. anaccount of the life and achievements of miss diana beck, neurosurgeon (1902 1956). neurosurgery 3:738-742, 2008. 10. ogrezeanu irina. women in neurosurgery. romania. the 13th wfns congress, marrakech, morocco, june 19 24, 2005. oral presentation mentioned in the abstract book of the congress. 04_paper romanian neurosurgery (2015) xxix 4: 411 416 411 doi: 10.1515/romneu-2015-0056 extensive spinal epidural abscess complicated with hydrocephalus corneliu balan, ovidiu carp, corina iordache department of neurosurgery, emergency clinical county hospital, constanta abstract: spinal epidural abscess is a rare but severe infection requiring prompt recognition in order to have a favorable outcome and appropriate treatment, mainly surgical. we present one of the largest extensions of such abscess in literature, involving the whole spine. no surgical treatment was tempted due to the involvement of 19 levels but antibiotics. the evolution of the lesion was complicated with hydrocephalus, by mechanism of cervical block of csf flow, and needed first external derivation and later ventriculo-peritoneal drainage. introduction spinal epidural abscess (sea) is a relatively rare pathology with an incidence of 1-2 cases per 10000 hospital admissions, however on the rise in the latest 10 years. classic teaching has generally maintained that sea represents a neurosurgical emergency, in which early diagnosis and urgent intervention are critical to prevent a neurologic catastrophe. however, over the past decade, there is a trend toward nonoperative management of sea in carefully selected patients with good outcomes. we present such a patient with an extensive sea involving the whole spine, treated with antibiotics due to poor general condition and extension of the lesion, complicated with hydrocephalus which required a ventriculoperitoneal drainage and good vital and functional results. case presentation mrs. g. sm, 61 years old, was admitted in the department of neurosurgery of the emergency clinical county hospital of constanta presenting pain irradiated to the whole spine, fever (38.2 c) lasting for two days and slight motor deficit of the lower limbs, mainly on the right side. non–insulin dependent diabetes mellitus was noticed as comorbid association, improper controlled, usually to 150-180mg/dl. however, on admittance, she presented 300 mg/dl glucose, with wbc = 20.3 k, anemia, esr = 99 mm/h suggesting an infectious process. later the same day, on thorough anamnesis from her family, we found that she had received an infiltration with corticoids for her chronic low back pain 10 days ago by a non neurosurgeon colleague. 412 balan et al extensive spinal epidural abscess complicated with hydrocephalus figure 1 figure 2 the mri performed initially for the lumbar segment then for the thoracic and cervical spine presented an epidural mass, located anterior from the dural sac, extending from l5 to c6 level (19 levels), hypo-intense on t1, high intensity in t2 and enhancing peripheral with gadolinium (figure 1, figure 2, figure 3). the same mri revealed an abscess situated deep in the lumbar muscles at l4 level, corresponding to the infiltration (figure 4). the germ was soon identified from blood cultures and direct puncture under ulstrasound control of the paravertebral abscess as a staphylococcus aureus multi sensible to antibiotics (non mrsa), which confirmed the hypothesis of an inoculation from the skin via the infiltration. figure 3 figure 4 romanian neurosurgery (2015) xxix 4: 411 416 413 doi: 10.1515/romneu-2015-0056 no surgical decision was taken in this case due to the extent of the sea and the patients’ general status, together with the absence of an important motor deficit. she received antibiotics, ceftriaxone + cyprofloxacine iv, according to antibiogram, with insulin to correct the hyperglycemia and she remained for the treatment in the neurosurgical department for better surveillance. the patient slowly improved clinical and biological for the first 3 weeks, followed later by a sudden alteration of conscience and confusion. we repeated her mri which surprised us by the augmentation of the volume of the collection in the cervical region (figure 5), despite proper antibiotics. however, the cerebral ct scan showed signs of active hydrocephalus by mechanisms of impaired flow of the csf and resorption by cervical block (figure 6). confronted with the clinical deterioration of the patient (gcs 12, wbc = 12k, esr = 86 mm/h), we tried to gain time with an external derivation of the csf, despite the high infectious risk. she first improved during the evd (csf clear, low opening pressure, 11 elem/mm3) but deteriorated again three days after the removal of the external derivation at 12 days since its introduction. figure 5 figure 6 at 6 weeks since the patients admission, after several debates with the neurosurgical /icu/ infectionists staff and after explaining the risk to the family we decided to perform a ventriculo-peritoneal drainage due to the fact 414 balan et al extensive spinal epidural abscess complicated with hydrocephalus that the csf was still sterile and to treat the patient like a potential shunt infection (meropenem 3 g/d as the patient had 52 kg). the surgical procedure went without complications as a unishunt with larger diameter tube than normally (1.2 mm) for the low pressure hydrocephalus. the patient improved slowly during the following month, both neurological, imagistic and biological, to gcs = 14, with no motor deficit excepting some bladder voiding difficulties which disappeared at the 6 months control). she was then discharged with biseptol for 3 weeks at home to a total of 13 weeks of antibiotherapy. control mri realized at 5 months from the onset revealed no collection in the cervical or dorsal region of the spine (figure 7) and little cicatriceal tissue in the lumbar region (figure 8). her cerebral ct scan reveals a functioning drain with no sign of hydrocephalus. figure 7 figure 8 discussion reports of sea, as a rare but severe infection, have two common threads poor outcome and appeals for earlier recognition and treatment to avoid this outcome. however, the diagnosis of spinal abscess can be tricky because of its rarity and the insidious presentation, time to a correct treatment being a key factor. the major prognostic factor for a favorable outcome is early diagnosis. [1, 2, 3, 4, 5, 6] the gold standard treatment, well supported by multiple published reports, consists of prompt surgical surgical debridement and drainage in combination with systemic antibiotic therapy [7, 8, 9]. final outcomes have been strongly and significantly correlated to both duration of the deficit and severity immediately prior to decompression, with morbidity of 33-46% and up to 22% definitive paralysis, even in 2013 papers [11]. romanian neurosurgery (2015) xxix 4: 411 416 415 doi: 10.1515/romneu-2015-0056 confronted with such statistics, there are few neurosurgeons who dare to try a conservative approach when surgery is possible and papers who present the results of non-surgical treatment are scarce or against such treatment. regarding the case presented, it has the particularities of the inoculation of the germ via infiltration with corticoids, seldom described in literature; even rare are the abscesses extended on such length (2 of 65 cases in the series presented by velissaris in 2009[12] and none in 77 cases reviewed by connor in 2013[11]). the onset of hydrocephalus as complication determined by such spinal epidural abscess was not found on pubmed. there were several key moments in the treatment of the patient when a risky decision had to be taken: after the first diagnosis of sea: most neurosurgical papers recommend surgical intervention with the evacuation of the purulent collection. we declined this option due to the extension of the sea which couldn’t allow multiple resections, the fact that staphylococcic pus is dense and not fluid to allow multiple level fenestrations for evacuation and the patient’s still good neurological status despite poor control of the diabetes. we preferred to keep the patient in a neurosurgical department (although with a long hospitalization) and not infectious diseases for better clinical surveillance in such patient. after the diagnosis of hydrocephalus – a trial with acetazolamide was initiated for a few days to lower the production of csf but the patient deteriorated and necessitated an evd. once again the infectious risk was high in a diabetic patient with a purulent collection and intraventricular implant. after removing the first evd – there was a choice between a second evd controlateral and a permanent vp drainage. our option was for the last, assuming it would better control the hydrocephalus and allow a quicker recovery than those of a patient connected to a temporary evd, immobilized in bed. conclusion spinal subdural abscess is a very rare but well described entity and associated with high morbidity and mortality. it is a neurosurgical emergency and as soon as diagnosis is established surgical treatment in collaboration to antibiotic therapy should be performed. the risks taken in our case proved worthy of the results, however, whenever an sea was admitted again in our neurosurgical department we would prefer the gold surgical standard than to wait and see for 3 months with medical treatment and all the complications which could happen. medical management of sea remains just for very selected cases, with no/slight neurological deficit, when anesthetical and surgical risks are too high to be assumed. references 1.darouiche ro : spinal epidural abscess. n engl j med 355: 2012–2020, 2006 2.pereira ce, lynch jc . spinal epidural abscess: an analysis of 24 cases. surg neurol 63 [suppl 1]: s26–s29, 2005 3.kumar k, hunter g : spinal epidural abscess. neurocrit care 2: 245–251, 2005 416 balan et al extensive spinal epidural abscess complicated with hydrocephalus 4.sendi p, bregenzer t, zimmerli w: spinal epidural abscess in clinical practice. qjm 101: 1–12, 2008 5.tunkel ar. subdural empyema, epidural abscess, and suppurative intracranial thrombophlebitis. in: mandell gl, bennett je, dolin r, eds. principles and practice of infectious diseases. 7th ed. philadelphia, pa: elsevier churchill livingstone; 2009:chap 89. 6.rigamonti d, liem l, sampath p, et al. spinal epidural abscess: contemporary trends in etiology, evaluation, and management. surg neurol. aug 1999;52(2):189-96 7.joshi sm, hatfield rh, martin j, taylor w. spinal epidural abscess: a diagnostic challenge. br j neurosurg. apr 2003;17(2):160-3 8.davis dp, salazar a, chan tc, vilke gm. prospective evaluation of a clinical decision guideline to diagnose spinal epidural abscess in patients who present to the emergency department with spine pain. j neurosurg spine. jun 2011;14(6):765-770 9.hooten wm, kinney mo, huntoon ma. epidural abscess and meningitis after epidural corticosteroid injection. mayo clin proc. may 2004;79(5):682-6 10.p harrington, p a millner, d veale inappropriate medical management of spinal epidural abscess, ann rheum dis 2001;60:218–222 11.david e. connor jr, prashant chittiboina, gloria caldito, anil nanda comparison of operative and nonoperative management of spinal epidural abscess: a retrospective review of clinical and laboratory predictors of neurological outcome:, j neurosurg spine 19:119–127, 2013 12.dimitris velissaris, diamanto aretha*, fotini fligou spinal subdural staphylococcus aureus abscess: case report and review of the literature, world journal of emergency surgery 2009, 4:31 doi: 10.33962/roneuro-2020-094 spontaneous spinal hematoma. experiences from a tertiary care centre in south india rajeev mandaka parambil, premkumar sasi, v.m. pavithran, v.j. byjo, akhil mohan romanian neurosurgery (2020) xxxiv (4): pp. 550-556 doi: 10.33962/roneuro-2020-094 www.journals.lapub.co.uk/index.php/roneurosurgery spontaneous spinal hematoma. experiences from a tertiary care centre in south india rajeev mandaka parambil, premkumar sasi, v.m. pavithran, v.j. byjo, akhil mohan department of neurosurgery, government medical college. kozhikode, kerala, india abstract background. spontaneous spinal hematoma (ssh) is a rare condition that can result in severe functional disability and even death. but early detection and prompt intervention can substantially reduce the morbidity. we present a series of seven operated cases of ssh. methods. all operated cases of ssh between 2017 and 2019 were studied. the demographic and clinical features, risk factors and imaging features were analyzed. the functional outcome at discharge and 6 months were assessed. results. seven operated cases of ssh with mean age 35(sd-20.9) were studied. six cases were spontaneous spinal extradural hematomas (ssedh) and one case was spontaneous spinal subdural hematoma (sssdh). the most common site was cervicothoracic. risk factors associated with ssh were thrombocytopenia, pregnancy, and necrotising pancreatitis. two patients had preoperative frankel’s grade a-b, three had grade c and two had d. the mean interval between the onset of symptoms and surgery was 4.7days. the functional outcome was dependent on the pre-operative functional status of the patient. patients with ssedh and thrombocytopenia had a poor outcome. conclusion. ssh even though spontaneous may be associated with risk factors. the presence of thrombocytopenia and preoperative functional status predicted outcome. this is the only single institution case series to report thrombocytopenia as a factor predicting poor outcome. introduction spontaneous spinal hematomas (ssh) are relatively rare and the majority of spinal hematomas are due to trauma. ssh includes both spinal extradural hematoma as well as subdural hematoma . the incidence of spontaneous spinal extradural hematoma (ssedh) is around 0.1/100000 and that of spontaneous spinal subdural hematoma (sssdh) is still rarer (1)(2). these conditions usually present as emergencies with rapidly progressive neurological deficits. prompt recognition and early intervention is very important for a better outcome. spinal hematoma was defined spontaneous when there was keywords spontaneous spinal hematoma, outcome, thrombocytopenia, pregnancy corresponding author: akhil mohan department of neurosurgery, government medical college. kozhikode, kerala, india akhilmohan84@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 551 spontaneous spinal hematoma. experiences from a tertiary care centre in south india no associated trauma, iatrogenic injury (secondary to procedures like lumbar puncture, epidural catheter insertion), or post-operative spinal hematoma. materials and methods setting: department of neurosurgery, government medical college, kozhikode, kerala which is a 3000 bedded teaching hospital in south india where around 2000 neurosurgical cases are operated annually. cases: all operated cases of spontaneous spinal hematomas during 2017-2019 all operated cases of ssh during the study period were studied. history was taken to assess any risk factors like hypertension, coagulopathies or bleeding diathesis. duration from the onset of symptoms to surgery was noted. a neurological examination was done and the preoperative functional status was assessed by frankel’s grade. all patients were evaluated with 1.5t mri with contrast and mr angiography. the site of the bleed was assessed from mri and the number of spinal segments involved was noted. all patients underwent standard decompressive laminectomy and evacuation of bleed. laminectomy was done at the level of maximal cord compression. a maximum of two-level decompressive laminectomy was done. after surgery, the functional status was reassessed at discharge and 6 months. all patients with improvement in frankel’s functional scores were taken as a good outcome. representative cases case 1 a 75-year-old male who was on treatment for necrotizing pancreatitis developed sudden onset of neck pain followed by weakness of bilateral upper limbs and lower limbs. the patient had numbness of the body up to the neck. there was also associated urinary retention. on examination, there was grade 3 power of upper limbs and grade 2 power of lower limbs and blunting of all sensations below the clavicles (frankels grade c). his routine blood workup showed elevated prothrombin time with an inr of 2.3, platelet count and activated partial thromboplastin time were normal. his s amylase was 4300. mri of the cervical spine showed t1 and t2 hyperintense signal from c2 to c6 with cord compression (figure 1) suggestive of sdh. after correcting the coagulopathy with fresh frozen plasma transfusions, we proceeded with c4c5 decompressive laminectomy. dura was bulging with underlying hematoma and was opened in the midline. thick sdh was evacuated. postoperatively the lower limb power improved to grade 3 (frankels grade c). at 6 months follow up both lower limbs and upper limbs had grade 4 power (frankels grade d). case 2 24-year-old 34 weeks pregnant lady presented with complaints of sudden onset neck pain and rapidly progressive weakness of both lower limbs. on examination, she had grade 2 power of both lower limbs and sensory loss below the nipple level (frankels grade c). her routine blood investigations were within normal limits. mr imaging of the spine showed t2 intermediate signal lesion noted involving left posterolateral epidural space at c7-t1 vertebral level suggestive of hematoma (figure 2). the management difficulty in view of 34 weeks completed pregnancy with regards to positioning as well as chances of intrauterine death were well explained. she was taken for ceaserian section and after the procedure, in the same sitting c7t1 laminectomy was done in the prone position and the hematoma was evacuated. postoperatively patient showed improvement in motor power. the baby was shifted to the neonatal icu for further care. at 6 months follow up the patient was able to walk with support and do her day-to-day activities (frankels grade d). case 3 a 25-year-old male patient presented with fever for 10 days and sudden onset of back pain for one day. he developed rapidly progressive weakness of lower limbs with urinary retention. on examination, he had grade 0 power of both lower limbs and there was sensory blunting below the nipple (frankels grade b). his lower limb reflexes were absent and plantar was mute bilaterally. on routine blood profile, his platelet count was 17000 but markers for dengue were negative. mr imaging of his spine showed cervicothoracic c5-t11 region spinal anterior extradural hematoma with spinal canal compromise and cord compression. after correcting the platelet count with platelet transfusion, we proceeded for surgery. t4 t5 two-level decompressive laminectomy was done (at the level of maximum cord compression). postoperatively patient remained 552 rajeev mandaka parambil, premkumar sasi, v.m. pavithran et al. with the same preoperative motor power. at six months follow up the lower limbs were spastic with flexor spasms and no spontaneous power (frankels grade b). he is still on a urinary catheter. figure 1. at1 t2 sagittal mr section of the cervical spine showing spinal sdh extending from c2-c6 bt1t2 axial mr sections c per operative image showing bluish bulging dura with underlying hematoma ddura is kept open with thick sdh. figure 2. a1, a2t1 and t2 sagittal mri of the cervical spine showing ssedh extending from c6-d2; baxial mr sections showing ssedh; c, d – per operative images of decompressive laminectomy and hematoma evacuation. 553 spontaneous spinal hematoma. experiences from a tertiary care centre in south india c a s e s age s e x risk factor platelet count/µl inr pre-op frankel’s grade type of ssh spinal level of ssh (segments) time from onset to maximal weakness (hours) duratio n till surgery (days) frankel’s grade at discharge frankel’s grade 6 months follow up 1 25 m thromboc ytopenia 17000 1.1 b edh c7-d11 (13) 6 1 b b 2 29 m nil 4.4 lakhs 1 d edh d1-d2 (2) 72 5 e e 3 24 f pregnanc y 4.2 lakhs 0.8 c edh c7-d1(3) 12 2 c d 4 75 m necrotisin g pancreatit is 3.3 lakhs 2.3 c sdh c2-c6 (5) 24 2 c d 5 30 m thromboc ytopenia 15000 1.2 a edh c7-d1(3) 8 2 a a 6 12 m thromboc ytopenia 10000 0.9 c edh c7-d3 (5) 10 2 c c 7 50 f nil 2 lakhs 1.1 d edh c5-d4 (8) 12 1 e e inrinternational normalized ratio table 1. demographic and clinical characteristics of the patients results of the 7 cases, the mean age was 35± 20.9 and 5 (71%) were males (table 1). thrombocytopenia was the most common risk factor and was present in three of our patients. one patient was 34 weeks pregnant and another had necrotising pancreatitis with coagulopathy. two of them had no known identifiable risk factor. one patient had sssdh while the rest had ssedh. the most common level affected for ssedh was cervicothoracic (n=5). the sssdh was purely cervical. the craniocaudal extension of the hematoma was variable with the longest involvement of 13 spinal segments and the shortest of two segments. of the ssedh one patient had anterior spinal edh and the rest had posterior spinal edh. all patients had local back pain as the first symptom which heralded the onset of neurological deficits. five of the patients with frankel’s grade less than ‘d’ had urinary retention. five patients had preoperative frankel’s grade a-c and two had ‘d’. all patients were operated at the earliest once the general conditions were favourable and the thrombocytopenia/ coagulopathy was corrected. the mean time between the onset of symptoms to maximal weakness was 20.5 hours. but in patients with thrombocytopenia, this was 8hours. the mean interval between the onset of significant symptoms and surgery in our series was 4.7days. of our seven cases, four had improvement in their frenkel score and were categorised as a good outcome. at 6 months, all the remaining patients remained in their same preoperative frenkel score. those who had thrombocytopenia as risk factor had a poor outcome. among the patients with thrombocytopenia two patients had fever with thrombocytopenia and for one patient thrombocytopenia was detected on the preoperative blood workup. also, when the pre-operative functional status was low (frenkel’s a, b, and c) the outcome was poor. the improvement of functional status was significantly dependent on the preoperative frenkel’s score. we couldn’t find any association between the number of segments involved or the time period between the onset of symptoms to surgery with postoperative outcome. discussion ssedh was first described by jackson and bain in the second half of the 19th century while sssdh was first reported by schiller (3)(4). ssh is a very rare clinical entity and its presentation can be variable from mild local pain to severe functional impairment in the form of weakness and bowel and bladder involvement. usually, spinal hematomas are associated with trauma, iatrogenic procedures or spinal surgeries but we studied the patients who had a spontaneous spinal hematoma. the risk factors for ssh include avms, coagulation abnormalities, 554 rajeev mandaka parambil, premkumar sasi, v.m. pavithran et al. anticoagulant use, vertebral haemangiomas, hypertension and pregnancy (5). however, in 40-60% of cases demonstrates no identifiable risk factor (6). in two of our patients, we could not identify any risk factors. thrombocytopenia was the most common risk factor for ssh in our study which was not reported before. thrombocytopenia may be associated with a febrile illness which is common in northern kerala where this study was conducted (7). in our series, two patients with thrombocytopenia had a preceding febrile illness, probably due to viral infection. the most common cause for viral infection with thrombocytopenia is dengue infection which was screened in all patients and was found negative. in a previous study from north kerala, 26% of cases of thrombocytopenia associated with febrile illness were due to viral infections other than dengue(7). viral infections causes thrombocytopenia both by decreased production of platelets from bonemarrow, as well as by the increased destruction by antibodies(8). ssedh is usually due to bleeding from posterior epidural venous plexus. but beatty and winson had postulated an arterial origin for ssedh particularly in the cervical region since the intrathecal pressure is higher than the venous pressure(9). in all of our cases, we did not find any evidence of vascular malformation with imaging (mr angiography) as well as perioperatively. bleeding from anterior epidural veins is rarer since they are smaller in caliber and are situated underneath the posterior longitudinal ligament. but anatomical variations are possible where the anterior epidural plexus can have a larger caliber. among our ssedhs one was located anterior to the thecal sac. the most common site of ssh in our series was cervicothoracic, probably due to mechanical factors as well as the prominence of epidural veins in the cervical and thoracic regions (6). the factors associated with poor outcomes were thrombocytopenia and pre-operative functional status. the post-operative recovery depends on the extend of ischemia to the cord which depends on various factors like rate, force, and duration of compression(10). we postulate that in patients with thrombocytopenia as the basic platelet plug formation is not happening to arrest the bleeding there will be a rapid accumulation of blood in the epidural space(11–13). also, the endothelial supporting function of the platelets is lost which heralds the bleeding in thrombocytopenia causing endothelial gaps for rbc extravasation(12). here the rate and force of compression may be very high on the cord and may result in neuronal death. all of our patients with thrombocytopenia had rapid deterioration of their motor power (mean-8hours). this shows the rate and force of compression of the spinal cord are high in these patients which resulted in poor postoperative outcomes. after a thorough literature search, this is the only single-institution case series to report thrombocytopenia as a factor predicting poor outcome. from the literature review, various studies have reported different values of platelet count below which there is a significant risk of major bleeding(14,15). we could not find any association between outcome and time took for surgical intervention from the onset of weakness. previous studies have shown that the most important factor determining the long-term outcome is the neurological status of the patient before surgical intervention. other bad prognostic factors are the onset of severe symptoms in a shorter time frame, the involvement of thoracic cord and lack of sensory sparing. the evacuation of the ssedh within 12 hours has been reported to predict the outcome(16). we found that the preoperative functional status predicted the outcome in our series. the presence of ssedh in pregnancy is even more rare and only 27 cases have been reported[16,17]. several theories are attributed to the occurrence of ssedh during pregnancy. usually, these hematomas tend to occur during the third trimester as the pressure in the vertebral venous plexus is normally elevated due to the compression by the gravid uterus(20). when there is a sudden change in pressure, as if when the patient sneezes, coughs, or during voiding there can be rupture of these veins resulting in ssedh. one of our cases was an sssdh, which was due to coagulopathy secondary to necrotising pancreatitis of unknown etiology. the pathophysiology of coagulopathy in severe pancreatitis is due to the activation of platelets and various inflammatory cytokines which will result in consumption coagulopathy(21,22). the sssdh is produced by the bleeding from subarachnoid vessels as the spinal subdural space is devoid of blood vessels unlike the cranial subdural space. the rupture of subarachnoid vessels may be due to trivial 555 spontaneous spinal hematoma. experiences from a tertiary care centre in south india trauma or sudden fluctuations in pressure due to coughing, sneezing, etc. recently radiculomedullary veins were also postulated to be involved in spinal subdural bleeds (23). conclusions the most important risk factor which caused ssh in our series was thrombocytopenia. the most common site was cervicothoracic. the outcome was dependent on preoperative functional status. thrombocytopenia was noted as a bad prognostic factor in our study. the outcome was not dependent on the extent of hematoma or time period between symptom onset and surgery. references 1. raasck k, habis aa, aoude a, simões l, barros f, reindl r, et al. spontaneous spinal epidural hematoma management: a case series and literature review. spinal cord ser cases. 2017;3(1):1–6. 2. joubert c, gazzola s, sellier a, dagain a. acute idiopathic spinal subdural hematoma: what to do in an emergency? neurochirurgie [internet]. 2019;65(2– 3):93–7. https://doi.org/10.1016/j.neuchi.2018.10.009. 3. schiller f, neligan g, budtz-olsen o. surgery in haemophilia; a case of spinal subdural haematoma producing paraplegia. lancet (london, england) [internet]. 2(6535):842–5. http://www.ncbi.nlm.nih.gov/ pubmed/18894192. 4. 4. jackson r. case of spinal apoplexy. lancet [internet]. 94(2392):5–6. https://linkinghub.elsevier .com/retrieve/pii/s014067360267624x. 5. groen rjm, ponssen h. the spontaneous spinal epidural hematoma. a study of the etiology. j neurol sci. 1990;98(2–3):121–38. 6. szkup p, stoneham g. spontaneous spinal epidural haematoma during pregnancy: case report and review of the literature. br j radiol. 2004 oct;77(922):881–4. 7. fawas n. m, beevi b. k, valliyot b, balakrishnan s. study of acute febrile illness with thrombocytopenia in a tertiary care centre. int j res med sci. 2018 jan 24;6(2):455. 8. kutty r, sreemathyamma s, sivanandapanicker j, mundhe v, chhabra k, peethambaran a. burden of dengue-related neurosurgical emergencies during an epidemic: a tertiary care experience. asian j neurosurg. 2019;14(1):211. 9. kim jk, kim th, park sk, hwang ys, shin hs, shin jj. acute spontaneous cervical epidural hematoma mimicking cerebral stroke: a case report and literature review. korean j spine. 2013;10(3):170. 10. raj r, seppälä m, siironen j. spontaneous spinal epidural hematoma: a surgical case series of ten patients. world neurosurg. 2016;93:55–9. 11. george jn. platelets [internet]. vol. 355, lancet. elsevier limited; p. 1531–9. https://linkinghub.elsevier.com /retrieve/pii/s0140673600021759. 12. ho-tin-noé b, jadoui s. spontaneous bleeding in thrombocytopenia: is it really spontaneous? [internet]. vol. 25, transfusion clinique et biologique. elsevier masson sas; p. 210–6. available from: https://linkinghub.elsevier.com/retrieve/pii/s12467820 18300624. 13. morowski m, vögtle t, kraft p, kleinschnitz c, stoll g, nieswandt b. only severe thrombocytopenia results in bleeding and defective thrombus formation in mice. blood. 2013 jun 13;121(24):4938–47. 14. neunert c, noroozi n, norman g, buchanan gr, goy j, nazi i, et al. severe bleeding events in adults and children with primary immune thrombocytopenia: a systematic review. j thromb haemost [internet]. 13(3):457–64. http://doi.wiley.com/10.1111/jth.12813 15. nagrebetsky a, al-samkari h, davis nm, kuter dj, wiener-kronish jp. perioperative thrombocytopenia: evidence, evaluation, and emerging therapies [internet]. vol. 122, british journal of anaesthesia. elsevier ltd; p. 19–31. http://bjanaesthesia.org/art icle/s0007091218307530/fulltext. 16. bakker na, veeger njgm, vergeer ra, groen rjm. prognosis after spinal cord and cauda compression in spontaneous spinal epidural hematomas. neurology. 2015;84(18):1894–903. 17. soltani s, nogaro mc, jacqueline kieser sc, wyatt mc, kieser dc. spontaneous spinal epidural hematomas in pregnancy: a systematic review. vol. 128, world neurosurgery. elsevier inc.; 2019. p. 254–8. 18. maurizio domenicucci, md, cristina mancarella, md, giorgio santoro, md, demo eugenio dugoni, md, alessandro ramieri, md, maria felice arezzo, ms a, paolo missori m. spinal epidural hematomas: personal experience and literature review of more than 1000 cases. j neurosurg spine [internet]. 27(2):198–208. https://thejns.org/spine/view/journals/j-neurosurgspine/27/2/article-p198.xml. 19. samali m, elkoundi a, tahri a, bensghir m, haimeur c. anesthetic management of spontaneous cervical epidural hematoma during pregnancy: a case report. j med case rep [internet]. 11(1):171. http://www.ncbi.nlm.nih.gov/pubmed/28648141. 20. kelly meb, beavis rc, hattingh s. spontaneous spinal epidural hematoma during pregnancy. can j neurol sci [internet]. 32(3):361–5. http://www.ncbi.nlm.nih.go v/pubmed/16225182. 21. kakafika a, papadopoulos v, mimidis k, mikhailidis dp. coagulation, platelets, and acute pancreatitis [internet]. vol. 34, pancreas. p. 15–20. http://journals.lww.co m/00006676-200701000-00002. 22. mimidis k, papadopoulos v, kotsianidis j, filippou d, spanoudakis e, bourikas g, et al. alterations of platelet function, number and indexes during acute pancreatitis. pancreatology [internet]. 4(1):22–7. 556 rajeev mandaka parambil, premkumar sasi, v.m. pavithran et al. https://linkinghub.elsevier.com/retrieve/pii/s14243903 04800048. 23. mattei ta, rehman aa, dinh dh. acute spinal subdural hematoma after vertebroplasty: a case report emphasizing the possible etiologic role of venous congestion. glob spine j [internet]. 5(5):e52-8. http://www.ncbi.nlm.nih.gov/pubmed/26430602. 13_paper romanian neurosurgery (2015) xxix 4: 487 491 487 doi: 10.1515/romneu-2015-0065 air in acute extradural hematoma: management and outcome analysis guru dutta satyarthee department of neurosurgery, neurosciences centre, aiims new delhi abstract: extradural hematoma with air bubbles has been described in literature. however the significance of it needs special attention with respect to prognosis. we report five case of extradural hematoma with air bubble and its management along with pertinent literature is reviewed briefly. key words: head injury, extradural hematoma, pneumocephalus, management introduction air in epidural hematoma is increasingly picked with the greater availability of newer generation computerized tomography for head injury patients. 1-5 however, its presence was previously evaluated by several authors, 4, 6-8 but the real significance of air inside the acute extradural hematoma was first clinically evaluated by aoki et al 1. however, there is paucity of literature in the western literature. 2, 3, 5 authors reviewed the computed tomography scan of 300 cases, who were operated at our institute, however, only five cases of extradural hematoma having air bubbles met the criteria. only those cases were selected, who sustained closed head injury but the overlying scalp adjacent to fracture and extradural hematoma did not have scalp laceration or open compound fracture. case illustration illustrated case 1 a-26-year-old male reported to our neurosurgical emergency after sustaining road traffic accident. he presented with headache with history of loss of consciousness. he had scalp contusion over parieto-occipital region on both side, more on right side. urgent computerized tomography revealed hematoma in the left temporo-occipital region having mixed attenuation density suggestive of actively forming extradural dermatome and containing gas bubbles. (figure 1), while left sided edh contained air bubble with underlying fracture of left temporo-occipital region bone extension into the posterior fossa. (figure 2), there was also fracture extending across the left mastoid bone. he underwent evacuation of extradural hematoma. he was doing well after twoyears following surgery at the last follow-up. 488 guru dutta satyarthee air in acute extradural hematoma figure 1 non-contrast computerized tomography scan head revealed bilateral temporooccipital extradural hematoma. extradural hematoma over the left temporo-occipital region having mixed attenuation density, suggestive of actively forming extradural dermatome and containing gas bubbles while left sided edh contained air bubble figure 2 the cranial computerized tomography scan, bone window view revealed bilateral temporooccipital extradural hematoma while left sided edh contained air bubble and underlying fracture involving left temporal – squamus with extension into left mastoid sinus figure 3 non-contrast computerized tomography scan head revealed bifrontal extradural hematoma with air aerocele over extradural hematoma spread over right basifrontal region figure 4 the cranial computerized tomography scan, bone window revealed fracture of orbital roof and ethmoid sinus with intracranial air pockets in cisterns illustrated case -2 a-16 year school going student had history of injury following assault by hit by colleagues in the playground. he had headache and romanian neurosurgery (2015) xxix 4: 487 491 489 doi: 10.1515/romneu-2015-0065 right ear otorrhoea. he was confused but rest of neurological examination was normal. the plain x-ray skull revealed linear fracture of right temporal bone. the cranial ct scan revealed acute extradural hematoma in the right temporal region with air bubbles. the bone window revealed linear skull fracture traversing the right mastoid bone. he underwent evacuation of extradural hematoma. the bleeding was through middle meningeal artery, which was coagulated during surgery. illustrated case 3 an 18 –year old boy with history of fall from height about seven hours ago reported tour hospital. he was comatose and decrebrating. both pupil were dilated and none reacting to light. the cranial ct scan revealed right frontal extradural hematoma with air pocket. (figure 3) the .right frontal skull fracture was extending to the ethmoid sinus. (figure 4) during surgery extradural hematoma was evacuated. he needed prolonged ventilatory support .later tracheostomy was required. he awes discharged 2 months later with tracheostomy tube and cerebrating motor response. illustrated case 4 a-10 year –old –boy was brought to our neurosurgical emergency after being run over by motor bike. he had headache and repeated episodes of vomiting with fracture of shaft of right femur. his neurological examination was normal. a thin extradural hematoma with air in extradural space was noted over right frontotemporal region, the fracture was involving right mastoid sinus. the source of bleeding middle meningeal artery, which was coagulated intraoperatively. he underwent intramedullary nailing for the fracture femur. he was doing well one year after surgery. illustrated case 5 a-30-old farmer presented to hospital 3 hours following hit by ox. on admission he was comatose with localizing to painful stimuli with history of aspiration of vomitus. he was immediately intubated in causality the right pupil was dilated with sluggish reaction to light. a cephalhematoma was present over right fronto parietal region. he was operated on after detection of right frontoparietal extradural hematoma. cranial ct scan displayed acuter extradural dermatome having mixed attenuation density suggestive of actively forming extradural dermatome with gas bubbles. the right basifronatal cortex showed contusion. the bone window ct scan revealed fracture of ethmoid sinus. he was neurologically normal without any csf rhinorrhoea. 490 guru dutta satyarthee air in acute extradural hematoma table 1 summary of five cases with extradural haematoma containing air bubbles case no. age(years) / sex mode of head injury origin of air infective /suppurative complications 1 26 m road traffic accident mastoid sinus none 2 16 m blow to head ethmoid sinus none 3 18 m fall mastoid sinus none 4 10 m road traffic accident mastoid sinus none 5 30 m blow to head ethmoid sinus none discussion extradural hematoma associated with gas bubbles is well known even prior to advent of ct scan. suwanwela et al (8) described extradural aerocele in 1962. even the 20 year long follow-up result of case, which was initially described by suwanwela et al (8) of extradural hematoma with pneumocephalus was reported by alexander et al (4) advocated the effectiveness of surgical closure of the fistula. nova et al in 1984 indicated that presence of black dot in hematoma indicated the role of localization of hematoma in the extradural space. air in acute extradural hematoma was increasingly picked with the advent of newer generation ct scan. the exact incidence is unknown, cossu et al. (5) retrospectively analyzed the actual incidence of gas bubble on ct scan was in 22.5 to 37 % cases, depending on older generation or current generation ct scanner were utilized, recent advanced generation scan being more sensitive in picking – up air pocket and minimizing beam hardening effect after analyzing 204 surgically verified extradural hematoma. shuto et al (2) reported incidence of air bubble in extradural hematoma up to 34.6 % in their study involving 78 cases, further also concluded that there was no statically difference in overall outcome or increase in the risk of enlargement of size of haematoma among the acute extradural haematoma with and a without air pocket as content. akoi was credited for first one, who stressed the significance air in the acute extradural hematoma and also pointed out the possibility of contamination of extradural hematoma leading to increased infection and also possible increase in mass effect subsequent to enlarging total volume of hematoma along with mixed air. however, aoki al observed an increase in volume of extradural hematoma in one of his case, which was diagnosed to have air pocket in the extradural hematoma, on repeat ct scan. regarding the possible contamination of extradural space and associated infection, there was no incidence of infective romanian neurosurgery (2015) xxix 4: 487 491 491 doi: 10.1515/romneu-2015-0065 complication in our series as well as those of reported cases in the literature. (2, 3, 5-7) however, one of the cases of suwanwela et al (8) having extradural aerocele with csf fistula developed meningitis. regarding the origin of gas trapped in the extradural hematoma may take entrance into hematoma either from the paranasal sinus, or mastoid sinus or direct overlying fracture of skull bone. nova et al (7) suggested that the gas trapped in an extradural hematoma is not related to the fracture of sinus, since air is collected in place which is away from the paranasal sinus or mastoid. but mastoid was implicated for the source of air from mastoid cell. (1, 9) shuto et al (2) observed in study of 27 cases the possible source of air was mastoid sinus (n=13), open compound fracture (n=5) and three cases each from following sources i.e. frontal sinus, sphenoid sinus, and unknown source. however, cossu et al (5) concluded that available data failed to clearly delineate the source of gas bubble. in present series, out of a total of 5 cases, three had fracture which was extending up to mastoid sinus while rest two had fracture involving ethmoid sinus. the presence of air in the epidural hematoma in case of closed head injury incites its probable location in the extradural space. however according to current literature, air in extradural hematoma is not associated with increased risk of infective complications, abscess formation or associated morbidity. further there is no possibility of increased incidence of raised mass effect caused by presence of air. however, relatively small sample of present study is limitation, however, a large study is needed to clearly establish or evaluate the exact role of air in the edh, in possibly increased risk of contamination, infection and contribution to the raised intracranial pressure or mass effect. correspondence dr. guru dutta satyarthee, mch associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: duttaguru2002@yahoo.com references 1.akoi n. air in acute extradural hematoma. report of two cases. j neurosurg 1986; 65: 555-556. 2.shuto t, kitsuto y, yoshida t, suzuki n, sugiyama m, yamamoto i. clinical study on air in epidural hematomas. no to shinkei 1997; 49; 977-981. 3.tewari mk, bhatoes hs, thakur rc, kak vk, khandelwal n. air in epidural hematoma. 1992; 36: 122128. 4. alexander e jr, davis ch jr, suwanwela c. extradural aerocele case report with 20year follow-up results. j neurosurg 1982; 56: 296-298. 5. cossu m, arcuri t, cagetti b, bas m, siccardi d, pau a. gas bubbles within acute intracranial epidural hamatomas. acta neurochir (wien) 1990; 102:22-24. 6. rahimiadeh a, hadadian k. acute extradural hematoma and pneumocephalus. neurosurg 1984; 15: 278-279. 7 nova hr. air in epidural hematoma. j neurosurg 1984, 60: 879 (letter) 8. suwanwela c, alexander e jr, davis ch jr. extradural aerocele. j neurosurg 1962; 19:401-404. 9. st john, french bn, traumatic hematomas of posterior fossa. a clinicopathological spectrum. surg neurol 1986; 25: 457466. 10. ersahin y, mutluer s air in acute extradural hematomas: report of six cases. surg neurol 1993; 40: 47 -50. doi: 10.33962/roneuro-2021-028 single versus double burr holes evacuation in the treatment of chronic subdural hematoma. a tertiary centre experience shrish nalin, anurag sahu, kanika gupta, kulwant singh romanian neurosurgery (2021) xxxv (2): pp. 180-188 doi: 10.33962/roneuro-2021-028 www.journals.lapub.co.uk/index.php/roneurosurgery single versus double burr holes evacuation in the treatment of chronic subdural hematoma. a tertiary centre experience shrish nalin1, anurag sahu2, kanika gupta3, kulwant singh2 1 department of neurosurgery, dr r.p.g.m.c. tanda, india 2 department of neurosurgery, ims, bhu, india 3 department of pain, palliative care and anaesthesia, ims, bhu, india abstract background: chronic subdural hematoma (csdh) is a well-known entity and common surgical disorder managed by the neurosurgeon and, if not recognized and treated timely, may prove fatal. it can be non-traumatic or post-traumatic and all of them need urgent attention irrespective of aetiology. it manifests with a progressive neurologic deficit that occurs ≥3 weeks following head injury. the principal techniques used in the treatment of csdhs presently are burr hole, twist drill craniostomy, craniectomy and craniotomy. objective: the aim of this study was to assess clinical outcome in unilateral chronic subdural hematoma patients treated by single or double burr-hole drainage. this prospective study was carried out at the department of neurosurgery, ims, bhu, varanasi from september 2016 to august 2018. a total of 60 patients with their age ranged from 22to 88 years with gcs 6 to 15 & hematoma thickness 10mmc were included in this study and randomly divided into two groups using random allocation software. in group a, patients with chronic subdural hematoma (csdh) were managed with single burr-hole drainage. in group b, patients were managed with double burr-hole drainage. clinical outcome was measured on the1st postoperative day, 3rd postoperative day and 7th postoperative day by gcs and at 1month followup by measuring the glasgow outcome scale (gos). result: in this study double burr-hole drainage and single burr-hole drainage surgery shows equal success in the management of csdhs with single burr hole taking less operative time. introduction chronic subdural hematoma (csdh) is a common neurosurgical disorder managed by neurosurgeons and if not recognized and treated timely, may prove fatal. it can be non-traumatic or post traumatic and all of them need urgent attention irrespective of etiology. 1it manifest with progressive neurologic deficit that occur ≥3 weeks following head keywords single burr hole craniostomy (sbhc), double burr hole craniostomy (dbhc), chronic sdh (csdh) corresponding author: shrish nalin department of neurosurgery, dr r.p.g.m.c. tanda, india nalinshrish@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 181 single versus double burr holes evacuation in the treatment of chronic subdural hematoma injury.2besides clinical suspicion various modalities has been used to diagnose csdh but ct scan of head is the investigation of choice. ct scan has revolutionized the ways in which patients with csdh may best be managed. 3some csdh known to resolve spontaneously as seen by the existence of calcified "hematomas". medical management has been advocated for old debilitating patient with csdh included bed rest, steroids and mannitol but it needs prolonged hospitalization for these patients. 4it is a common consensus that operative treatment would be more quickly, safely and effectively remove the mass. 5most of the neurosurgeons prefer to place two burr holes on the side of lesion and irrigate through small silicon catheters to wash out the subdural space with or without use of sterile closed drainage system.6few authors have suggested the use of a single burr hole and thorough irrigation for evacuation of csdh. instead of evacuation through a burr hole, evacuation through a twist drill hole in critically ill patients was found to be equally satisfactory by some surgeons.7evacuation of csdh by craniotomy is also indicated in certain situations and there are few surgeons who feel craniotomy has still a definite role in management of csdh. endoscopic evacuation of csdh can also be done.8in the light of current knowledge, there are various methods for surgical evacuation of csdh. described by different authors, all the methods have its merits and demerits. it is still debated that which is the best method for csdh. this study is planned to compare the intraoperative, postoperative complications and outcome of evacuation of csdh by two different techniques in the same set up ie single vs double burr hole evacuation of csdh. material and methods this prospective study was conducted on patients with csdh, admitted to trauma centre and ssh hospital(sir sundar lal hospital) department of neurosurgery ims, bhu varanasi, from september2016 to august2018. total 60 patients were enrolled in the study and divided in two groups .informed consent was taken from the patients or immediate relatives (first degree) .the patients who underwent single burr hole drainage were labeled as group a and those with a double burr holes were designated as group b. both groups included ‘thirty’ patients each who presented with diagnosis of csdh on monday, wednesday, saturday and on alternate sundays. all patients admitted in neurosurgery ward were evaluated by taking detailed history, clinical examination and investigations. diagnosis of csdh was confirmed by radiological (ct,mri) investigation. incidence of the csdh was recorded out of all admitted patients in a particular time period. after confirmation of csdh by ct/mri scan patients were operated alternatively by single and double burr holes respectively. inclusion criteria: • ct/mri proved symptomatic cases of csdh. • patients of both sexes and all age groups . • all the patients who were operated for the first time for the disease ( csdh). • all csdh patients with midline shift of 10 mm or more. • unilateral chronic sdh patients • hematoma thickness of 10 mm or more. exclusion criteria: • patients with recurrent disease after previous operation. • asymptomatic patients with very thin csdh (conservatively managed) • ventriculoperitoneal shunt in situ. • hematological disorder/anticoagulant drug use. • bilateral csdh. operations by “two burr holes technique” and “single burr hole were done under general anesthesia on emergency basis. procedure a written consent was taken from the patient or patient party after explaining the procedure. patients with csdh, treated at trauma centre & ssh, bhu varanasi in a neurosurgical unit during the years september 2016 to august 2018. on admission, in addition to the presenting history, details were obtained regarding previous head injury, alcohol abuse and medication. the patients underwent a neurological examination. routine laboratory tests, along with a complete coagulation profile and liver function tests, were done. radiological investigation of the brain ie ct and mri were the investigation to diagnose the csdh. the size, extentand density/intensity of the contents of the csdh were recorded.general anesthesia was given as the 182 shrish nalin, anurag sahu, kanika gupta et al. standard modality for anaesthesia. single and double burr hole procedure were performed randomly. the patients who underwent single burr hole drainage were labeled as group a and those with a double burr holes were designated as group b. the surgical procedure was as follows. double burr holes technique patient lied supine on operation table. head turned to side on which burr holes were made. parts cleaned and draped. two linear skin incision of two to three centimeters for burr holes were given on frontal and parietal region (precoronal and post coronal) along mid papillary line which correspond to maximum thickness of csdh ncct head. after the burr holes were made of dm 2.5 cm each , the dura was opened in a cruciate manner. the dural edges were coagulated completely. the subdural space was liberally irrigated with normal saline till the refluxing fluid started coming out clear. skin closure was done in two layers with vicryl 2-0 rb and nylon 2-0 cutting sutures respectively. no post-operative drains were used in our cases. single burr hole technique patient lied supine on operation table. head turned to side on which burr hole was made. parts cleaned and draped. single linear skin incision given after local infiltration along mid pupillary line over parietal bone correspond to maximum thickness of csdh over ncct head. after the burr hole was made of dm 2.5, the dura was opened in a cruciate manner. the dural edges were coagulated completely. the subdural space was liberally irrigated with normal saline till the refluxing fluid started coming out clear. skin closure was done in two layers with vicryl 2-0 rb and nylon 2-0 cutting sutures respectively no post-operative drains were used irrespective the fact weather brain expanded or not. post-operative course patients advised complete bed rest and were kept supine post-operatively for 3 days. the patients did not receive any specific medication, including steroids, anticonvulsants or excessive hydration. the operative procedure was standardized between the study groups. a repeat ct scan of the brain was performed in all patients on post-operative day 3 to confirm adequate drainage of the csdh.patients were discharged after first ct scan if no complication was found. in addition, a ct scan of the brain was performed at day 7 and 1-month after evacuation of the hematoma. all patients were followed-up for at least 1 month after surgery. both clinical and radiological criteria were used to evaluate the recurrence of csdh. the clinical criteria suggestive of a recurrence: • altered level of consciousness • persisting headache • appearance of new or worsening pre-existing neurological deficits. the radiological criteria of recurrence: • increased volume of subdural fluid • mass effect on the ipsilateral brain or ventricular system, • effacement of cerebral sulci to gross subfalcine herniation. reoperation in the form of rewashing ,craniectomy or additional burr hole was done in cases with recollection/recurrence on post operative ncct head. results the age ranges from 28 to 88 years in group a with mean of 58.77 ± 14.29 years while it is 30 to 88 years in group b with mean age 57.07 ± 15.02 years. out of total patients 44(73.3%) were males and 16 (26.7%)were females.in group a, 24(80%) were males and 6(20%)patients were females while in group b 20 (66.7%) were males and 10(33.3%) patient were females. headache was the most common presentation in both the groups with total 27 (45%) presented with it out of which 11(36.6%) were in group a and 16(53.3%) were in group b followed by altered sensorium which was presented by 5(16.7%) and 3(10%) patients in group a and b respectively. other presentations were hemiparesis presented in 4(13.3%) and 2(6.7%) ,aphasia (0%) and (3.3%), coma (10%) and (10%), gait disturbance (6.7%) and (3.3%), visual disturbance( 6.7 & 3.3%), incontinence (6.7% & 3.3%) and seizure (3.3 & 6.7%) patients of group a and b respectively (figure1). trauma was the most common etiology in both groups with total 48(80%) patients suffered with it.23(76.7%) in group a and 25 (80%) in group b patient gave history of trauma, while 6(20%) and 5 (18.3%) in group a and b respectively had history of 183 single versus double burr holes evacuation in the treatment of chronic subdural hematoma cva (cerebrovascular accident). history of avm (arteriovenous malformation) bleed was presented in one patient of group a. hypertension was the most common associated comorbidity found in 20% of total patients followed by dementia and diabetes mellitus (dm) which was found in 15% each in total patients. other comorbidities were copd, alcoholic, renal failure respectively. (figure2) figure 1. figure 2. the chronic sdh diagnosis was made on ct/mri brain. the thickness of chronic sdh in group a ranges from 10 to 18 mm with mean of 14.63± 2.46 mm while in group b the range was also from 1018mm with mean of 14.43t± 1. 18mm.the p value for thickness between two groups was 0.71 which was not significant. midline shift in group a ranges from 10-14 mm with mean of 10.80 ±1.03 mm while in group b the range was 10-14 mm with mean of 10.67±1.18 mm. the p value for midline shift on comparing two groups came out to be 0.64 which was not significant. on comparing the characteristics on hematoma membrane between two groups both groups had thin membrane in 26(86.67%) patients and thick membrane in 4(13.33%) patients the p value for membrane thickness was not significant. (table 1) hematoma characteristics gr. a mean gr. b mean p value (two tailed t test) midline shift (mm) 1014 10.80 ±1.03 1014 10.67± 1.18 .64 thickness(m m) 1018 14.63 ±2.46 1018 14.43± 1.59 .71 table 1. during intraoperative period bleeding from the fragile emissary veins occurred in 3(10%) patients of group a and 1(3.3%) patients of group b, while brain contusion during opening up of thick membrane occurred in 2(6.67%) patients’ of group a but none in group b. the brain after evacuation of hematoma not expanded in 4(13.33%) patients of group a and 3(10%) of group b while it expanded over time in 26(86.6%) of group a and 27(90%) of group b. the p value for intraoperative complications and non expansion of brain was >.05 which was not significant. the mean time for the duration of surgery was 31.13±5.01min in group a while in group b mean operating time was 47.07±4.75min,showing that the mean operating time in the groupa was significantly less as compare to the groupb.(p value=<.001). in group a (n=30), before surgery, mean glasgow coma scale (gcs) was 11.90 ± 2.76 (sd) where the range of the gcs was 6-15. in group b (n=30), mean glasgow coma scale (gcs) was 12.83 ± 2.23 (sd) where the range of the gcs was 8-15. so, the difference of mean pre-operative glasgow coma scale (gcs) between the two groups was not statistically significant (p-value >0.50). patients outcome on day one, three and seven was assessed with gcs. in group a (n=30), after surgery, mean glasgow coma scale (gcs) was 13.00 ± 2.01 (sd) ,13.93± 1.72 1nd 14.47±1.01 on day 1,3 and 7 respectively while it was 13.60±1.67.14.00±1.48 and14.30 ±1.29 respectively ingroup b (n=30). the range of the gcs was 10-15 in both the groups. so, in post-operative gcs level, there was no significant difference (p-value >0.05). (table2) gcs gr. a (mean ±sd) gr. b (mean ±sd) p value preop 11.90 ± 2.76 12.83 ± 2.23 0.15 day 1 13.00 ± 2.01 13.60 ± 1.67 0.21 0 5 10 15 20 n u m b e r o f p a t i e n t s presentations group a(n=30) group b(n=30) 0 2 4 6 8 10n u m b e r o f p a t i e n t s comorbidities group a group b 184 shrish nalin, anurag sahu, kanika gupta et al. day 3 13.93 ± 1.72 14.00 ± 1.48 0.87 day 7 14.47 ± 1.01 14.30 ± 1.29 0.58 table 2. clinical outcome of patients at one month on follow up was measured using glasgow outcome scale(gos) .in group a 17 (56.7%)&8(26.7%)had gos of 5 &4 respectively while in group b 15(50%)&8(26.7%) had gos of 5&4 respectively which is considered favorable gos score, while gos of 3 was present in 4(13.3%) patients in group a and 6 (20%) patients in group .one patient in group a died whose gos was one, while no mortality in group b.the p value of gos was s written in table below for various groups and is more than >.05 and statistically not significant (table 3). gos group a(n=30) percentage group b(n=30) percentage p value good outcome good recovery 5 17 56.7 15 50 .68 moderate disability 4 8 26.7 8 26.7 1 poor outcome severe disability 3 4 13.3 6 20 .68 persistent vegetative state 2 1 3.33 .92 death 1 1 3.33 .93 table 3. in both group a & b acute rebleed (from the dural stripping, subgaleal vessel) seen in one (3.3%) patient each. ,small brain haemorrhage seen in cva patients in 1(3.3%) patients of group a and 2(6.67%) patients of group b. pneumocephalus occurred in 3(10%) patients of group a and 4(13.33%) of group b. death(3.33%) occurred in one patient in group a while no death reported in group b. empeyma occurred in a 1(3.3%) patient of group b only .rest of complications like new onset seizure ,new focal neurological deficit, wound infection, meningitis also occurred in both groups as given in table below. on applying fisher exact test no post-operative complication was statistically significant p value >.05 on comparing both groups. (figure 3) figure 3. in group a 11(36.67%) patients were discharged on post operative day 4 & 5 while in group b 10(33.33%) were discharged. in 5 to 10 days interval 18(60%) patients were discharged in group a while in group b (16%) patients were discharged. after 10 days period only 1(3.33%) patients was discharged in group a ,while 4(13.33%) were discharged in group b .mean hospital stay was 5.67 ±2.15 in group a while it was 6.60 ±2.97 in group b.on comparing the hospital stay by t test 2 tailed ,p value was 0.17 which was not significant. ncct head was done on day 3 revealed recurrence in 3(10%) patients in group a while in group b 5(16.67%) patient had recollection/recurrence. on day 7 only 1(3.33%) patients had recollection in group a while in group b no patient had recollection. on follow up on 1 month 2(6.67) patients had recollection group a while in group b none had recollection. on comparing the recurrence on day 3,7 and 30 total recurrence was 20 %in group a and 16.67% in group band p value was .067 by pearson chi square test which was not significant. in group a, 4(13.33%) patients were reoperated during one month follow up for recurrence/recollection while in group b total 3(10%) patients were reoperated during the same period. in group a ,3(10%) patients were rewashed with the same craniostomy burr hole and improved and 1(3.3%) patients in which membrane was thick and brain not expanding had underwent craniectomy while in group b 2(6.67%) patients were rewashed for recollection and one (3.33%) patient sunderwent craniectomy for thick membrane and non-expanding brain due to which his gcs was not improving. no group needed extra burr hole for recollection. on comparing the both groups for 0 0.5 1 1.5 2 2.5 3 3.5 post-operative complications group a group b 185 single versus double burr holes evacuation in the treatment of chronic subdural hematoma reoperation the p value for wash group was .60 and for craniectomy was .37. both were more than .05 and not statistically significant. colour plate 1. ncct brain showing colour plate 1a: mri t1 image of brain. right sided chronic sdh showing right side chronic sdh. discussion the common occurrence of chronic subdural hematomas in older patient raises some diagnostic and therapeutic difficulties. despite general agreement about the indication of operation, the extent of surgery is still controversial. the treatment of chronic subdural hematomas has drastically evolved over time9,10,11,12,13,14. in the management of csdhs burr-hole craniostomy should be the method of choice for initial treatment. the treatment goal of csdh is complete drainage of the collection, using the least invasive technique without a high risk of recurrence. although burr hole drainage remains the commonest form of treatment of csdh,our literature search failed to yield an article that compared the results of single versus double burr hole drainage of csdh. however, double burr hole drainage was generally considered a better result, especially regarding recurrence of the subdural collection. the present study was performed to address this issue. colour plate 2. single burr hole incision marking. colour plate 3. single burr hole after dura opening. colour plate 4. single burr hole closure. 186 shrish nalin, anurag sahu, kanika gupta et al. colour plate 5. double burr holes after dura opening. the continuous search for the best method of surgery led us to carry out this study in the department of neurosurgery, ims, bhu, varanasi during the period of september 2016 to august 2018 in which we compared two groups of thirty patients each for intraoperative and postoperative complication, postoperative outcome with the help of gcs and gos. the mean age was 58.77±14.29 years in the group a and57.07 ± 15.02 years in group b respectively. these findings are consistent with the study of ernestus et al15 in which the mean age was 60 years, which correlates with this study. the higher incidence among the older age group is because of cerebral atrophy and slow accumulation of blood as well as increased incidences of falling down in elderly population. in the study out of 60 patients 16 (26.7%) were females and 44(73.3%) were males. in group a, 6(20%) patients were females and 24(80%) were males while in group b 10(33.3%) patient were females and 20 (66.7%) were males. on comparing. thus, male were mostly affected in both groups. the male-female ratio was 3:1: which correlates with the study of sanbasivan16where male–female ratio was 6:1 showing male preponderance in chronic sdh. cause of male preponderance could be because they are more prone to injuries because of more outing. the thickness of csdh in group a ranges from 10 to 18 mm with mean of 14.63± 2.46 while in group b the range was also from 10-18mm with mean of 14.43t± 1.18.. midline shift in group a ranges from 10-14 mm with mean of 10.80 ±1.03while in group b the range was 10-14 mm with mean of 10.67±1.18.the hematoma characteristics were similer to the p. taussky et al.17 whose study included cases with hematoma thickness of 1.8+0.7 cm and according to him hematoma thickness ,midline shift does not contributes to increased recurrence rate after surgery in both the groups. during intraoperative period bleeding from the fragile emissary veins occurred in 3(10%) pt. of group a and 1(3.3%) pt. of group b, while brain contusion during opening up of thick membrane occurred in 2(6.67%) pt.’s of group a but none in group b.the brain after evacuation of hematoma not expanded in 4(13.33%) pt. of group a and 3(10%) of group b while it expanded over time in 26(86.6%) of group a and 27(90%) of group b. thenon expansion of brain is due to long standing csdh and cerebral atrophy . the mean time for the duration of surgery was 31.13±5.01 min in group a while in group b mean operating time was 47.07±4.75 min, showing that the mean operating time in the group a was significantly less as compare to the group b. these findings were similer to findings of han et al18 whose study stated that one burr hole craniostomy takes shorter operation time and less invasive than that of two burr-hole craniostomy in group a (n=30), before surgery, mean glasgow coma scale (gcs) was 11.90 ± 2.76 (sd) where the range of the gcs was 6-15. in group b (n=30), mean glasgow coma scale (gcs) was 12.83 ± 2.23 (sd) where the range of the gcs was 8-15. so, the difference of mean pre-operative glasgow coma scale (gcs) between the two groups was not statistically significant (p-value >0.50). patients outcome on day one, three and seven was assessed with gcs. in group a (n=30), after surgery, mean glasgow coma scale (gcs) was 13.00 ± 2.01 (sd) ,13.93± 1.72 1nd 14.47±1.01 on day 1,3 and 7 respectively while it was 13.60±1.67.14.00±1.48 and14.30 ±1.29 respectively in group b (n=30). the range of the gcs was 10-15 in both the groups. so, in post-operative gcs level, there was no significant difference (p-value >0.05. the clinical assessment of patients through gcs findings were similer to findings of asaduzzamansm19et al who also studied patients preoperative and post operative gcs and find out that clinical outcome of csdh patients after sbh craniostomy was similer to dbh craniostomy. clinical outcome of patients at one month on follow up, measured using glasgow outcome scale(gos) at 1 month. .in group a 17 (56.7%)&8(26.7%)had gos of 5 &4 respectively while in group b 15(50%)&8(26.7%) had gos of 5&4 187 single versus double burr holes evacuation in the treatment of chronic subdural hematoma repectively which is considered favourable gos score.while unfavourable gos ie gos of 3 was present in 4(13.3%) patients in group a and 6 (20%) patients in group b .one patient in group a died whose cause of death was old age and poor gcs had gos 1,while no mortality in group b. the p value of gos was >0.05 and statistically not significant .the clinical outcome assessment with gos had proven the fact that single burr hole craniostomy is equally effective and less time consuming as compare to double burr hole craniostomy in selected group of patients as described by kansal et al20 in both group a & b rebleed (from the dural stripping, subgaleal vessel) seen in one (3.3%) pt. each, small brain haemorrhage seen in cva pt. in 1(3.3%) pt. of group a and 2(6.67%) pt. of group b which was due to uncontrolled hypertension. pneumocephalus occurred in 3(10%) pt. of group a and 4(13.33%) of group b. death (3.33%) occurred in one patient in group a, who had a preoperative gcs of 6 and after surgery he had rebleed for which washing done but patient dies due to multiorgan failure. empeyma occurred in a 1(3.3%) patient of group b only who was a known case of diabetes mellitus and prone to postsurgical infections. new onset seizure ,new focal neurological deficit were seen in one patient each(3.3%)of both groups while, wound nfection(3.3%&6.7%),meningitis(10%&6.67%) were also occurred in both groups. mean hospital stay was 5.67 ±2.15 in group a while it was 6.60 ±2.97 in group b. the hospital stay was shorter in the sbh group as compare to dbh group can be explained due to less operative time and early recovery of the patients. the study conducted by gupta sanja k.21had mean postoperative hospital stay was 5 days in single burr hole and 6.5 days in two burr hole technique. ncct head was done on day 3 revealed recurrence in 3(10%) patients in group a while in group b 5(16.67%) patient had recollection/recurrence. on day 7 only 1(3.33%) pt. had recollection in group a while in group b no patient had recollection. on follow up on 1 month 2(6.67) pt. had recollection group a while in group b none had recollection. on comparing the recurrence on day 3,7 and 30 p value was .067 by pearson chi square test which was not significant. the study by kansal et al 20in which they compare sbh with dbh recurrence rates had higher recurrence in sbh group but not statistically significant. in group a, 4(13.33%) patients were reoperated during one month follow up for recurrence/recollection while in group b total 3(10%) patients were reoperated during the same period. in group a ,3(10%) pts. were rewashed with the same craniostomy burr hole and improved and 1(3.3%) pt. in which membrane was thick and brain not expanding had underwent craniectomy while in group b 2(6.67%) pt. were rewashed for recollection and one (3.33%) .pt.underwent craniectomy for thick membrane and non expanding brain due to which his gcs was not improving. no group needed extra burr hole for recollection. on comparing the both groups for reoperation the p value for wash group was .60 and for craniectomy was .37. both were more than .05 and not statistically significant. a met analysis comparing single burr hole and double burr hole craniostomy for csdh was published by belkhair s22et al, whose conclusion was that suggest that sbhc is as good as dbhc in evacuating chronic subdural hematoma and is not associated with a higher revision rate compared to dbhc. no group needed second reoperation and recovered well. conclusion this study was undertaken with the aim to evaluate the results of treatment of csdh with single vs double burr hole craniostomy. with this study, we have found that single burr hole evacuation is similar to double burr hole evacuation of csdh in terms of intraoperative and postoperative complications in selected group of patients. the patients in both groups after intervention had almost similar outcomes and quality of life according to gcs and glasgow outcome scale also sbhc is a simple, less time consuming and less invasive treatment as it requires only one burr hole to be made. it was found that double burr-hole procedure is better than single burr-hole procedure in terms of recurrence; but the difference is not statistically significant. thus, our study recommends sbhc as equal and a good alternative to dbhc in the management of csdhs. limitations of the study. the sample size was small and patients with specific conditions were omitted, exampleuse of anticoagulants. investigations with larger sample size, inclusion of such patients are required to 188 shrish nalin, anurag sahu, kanika gupta et al. further assess the role of number of burr holes as an independent risk factor of csdh recurrence. references 1. weigel r, krauss jk, schmiedek p: concepts of neurosurgical management of chronic subdural haematoma: historical perspectives. br j neurosurg 18(1):8-18, 2004. 2. wilkins rh, rengachary ss: neurosurgery. 2nd ed. volume 3. new york: mcgraw-hill health professions division, 1996:2799-2801. 3. almenawer sa, farrokhyar f, hong c, alhazzani w, manoranjan b, yarascavitch b, et al. : chronic subdural hematoma management : a systematic review and metaanalysis of 34,829 patients. ann surg 259 : 449-457, 2014 4. suzuki j, takakua : nonsurgical treatment of chronic subdural hematoma. j neurosurg33 : 548-553, 1970. 5. berghauser pont lm, dippel dw, verweij bh, dirven cm, dammers r: ambivalence among neurologists and neurosurgeons on the treatment of chronic subdural hematoma: a national survey. acta neurologicabelgica 113: 55-59, 2013. 6. cenic a, bhandari m, reddy k: management of chronic subdural hematoma: a national survey and literature review.can j neurol sci 32(4): 501-506, 2005. 7. gazzeri r, galaraza m, neroni m, canova a, refice gm, esposito s: continuous subgaleal suction drainage for the treatment of chronic subdural haematoma. acta neurochir (wien) 149:487-493, 2007. 8. khursheed n, ramzan a, sajad a, zahoor s, wani a, nizami f, laharwal m, kirmani, bhat a: subdural hematomas: an analysis of 1181 kashmiri patients and review of literature. world neurosurg 77(1):103-110, 2012. 9. drapkin aj: endoscopy for chronic sdh. surg neurol48:427, 1997. 10. horn em, feiz-erfan, bristol re, spetzler rf, harringtontr: bedside twist drill craniostomy for chronic subdural hematoma: a comparative study. surg neurol 65:150-154, 2006. 11. lee jy, ebel h, ernestus ri, klug n: various surgical treatmentsof chronic subdural hematoma and outcome in 172 patients:ismembranectomy necessary? surg neurol 61:523-528, 2004. 12. mohamed ee: chronic subdural haematoma treated bycraniotomy durectomy outer membranectomy and subgalealsuction drainage. personal experience in 39 patients. br jneurosurg 17:244-247, 2003. 13. weisse a, berney j: chronic subdural haematomas: results ofa closed drainage method in adults. acta neurochir (wien)127:37-40, 1994. 14. zumofen d, regli l, levivier m, krayenbuhl n: chronicsubdural hematomas treated by burr hole trepanation and asubperiostal drainage system. neurosurgery 64: 1116-1122,2009. 15. ernestus ri, beldzinski p, lanfermann h, klug n. chronic subdural hematoma: surgical treatment and outcome in 104 patients. surg neurol. 1997; 48: 220-5. 16. sambasivan m. an overview of chronic subdural hematoma: experience with 2300 cases. surg neurol. 1997; 47: 418-22. 17. taussky p, fandino j, landolt h. number of burr holes as independent predictor of postoperative recurrence in chronic subdural haematoma. br j neurosurg. 2008 apr; 22(2):279-82 18. han hj, park cw, kim ey, yoo cj, kim yb, kim wk. one vs. two burr hole craniostomy in surgical treatment of chronic subdural hematoma. j korean neurosurg soc. 2009 aug;46(2):87-92. 19. asaduzzaman sm, islam kmt, hossain mn et al , comparative study between single versus double burrhole drainage of unilateral chronic subdural haematoma bangladesh med j. 2014 jan; 43. 20. kansal r, nadkarni t, goel a. single versus double burr hole drainage of chronic subdural hematomas. a study of 267 cases. j clin neurosci. 2010 apr;17(4):42. 21. sanjay, g., atul, j.k. . comparative study of evacuation of chronic subdural haematoma by two burr hole technique versus single burr hole with partial excision of membrane technique.international journal of medical science and education 2014;107. 22. 2belkhair s, pickett g. one versus double burr holes for treating chronic subdural hematoma meta-analysis. can j neurol sci. 2013 jan;40(1):56-60.1964 mar;21:172-7. calderon-miranda_traumatic 300 | calderon-miranda et al traumatic brain injury due to pressure cooker explosion in a child traumatic brain injury due to pressure cooker explosion in a child: case report willem guillermo calderon-miranda1, nidia escobar-hernandez2, luis rafael moscote-salazar3, andres m. rubiano4, marco antonio blancas-rivera5, amit agrawal6, zenem carmona-meza7, hernando raphael alvis-miranda8, gabriel alcala-cerra9 1resident of radiology, unam, school of medicine, mexico d.f, mexico 2chief of radiology, hospital general dr. manuel gea gonzalez, mexico d.f, mexico 3neurosurgeon-critical care, red latino. latin american trauma & intensive neuro-care organization 4neurosurgeon, universidad el bosque, colombia, red latino. latin american trauma & intensive neuro-care organization, colombia 5unam, school of medicine, mexico d.f, mexico 6professor of neurosurgery, mm institute of medical sciences & research, maharishi markandeshwar university, mullana ambala, 133-207, haryana, india 7chief of research, school of medicine, universidad de cartagen, cartagena de indias, colombia 8resident of neurosurgery, universidad de cartagena, cartagena de indias, colombia 9neurosurgeon, universidad de cartagena, cartagena de indias, colombia abstract: traumatic brain injury is a common condition in the emergency services, affecting the pediatric and adult population significantly. patterns of head injury as well as management principles in children are important differences compared to adults. traumatic brain injury by domestic pressure cooker is rare and has not been described in children, which to our knowledge is the first report in the literature of this nature. key words: cranio-cerebral injury, pressure cooker, blast injury, traumatic brain injury introduction pressure cookers consist of a pressurized vessel that is widely used to cook food faster. accidental malfunction of these vessels can be the cause of mild to severe injuries. domestic pressure related injuries are less commonly reported in literature with sporadic case reports. (1-8) we report a rare case of a one year old child who sustained traumatic brain injury due to pressure cooker explosion and mechanism, pathophysiology and management of such injuries. romanian neurosurgery (2016) xxx 2: 300-302 | 301 case report a 1 years old male child presented to the emergency room with the history of head trauma following an accidental blast of a pressure cooker. the child was unconscious since the time of injury and had multiple episodes of vomiting. the child was resuscitated in the emergency room and a neurosurgical consultation for head injury was asked. at the time of examination his glasgow coma scale (gcs) was 9/15 (eye opening nonee1, incomprehensible sounds-v3 and localizing to painful stimuli-m5). the child had paucity of movements of right side of grade 2/5. pupils were bilateral equal and reacting to light. the pulse rate was 140 beats/minute and blood pressure was 110/70 mmhg. in view of low gcs the child was intubated and kept on elective ventilation. local examination revealed an open wound over left parietal region without any underlying palpable fracture. computerized tomography (ct scan) of the brain with bone window showed diffuse cerebral edema, subarachnoid hemorrhage and multiple skull fractures (figure 1). his blood investigation including coagulation profile was normal. the child was managed conservatively in pediatric critical care unit. the child received tetanus prophylaxis, intravenous fluids, injectable antibiotics, antiepileptics, analgesics and sedations. the child made good recovery except right sided residual hemiparesis. discussion most of the accidental domestic pressure cooker related injuries related literature discuss ocular injuries (1, 4), burns (5, 7) or penetrating transorbital craniocerebral injuries (with mild traumatic brain injury). 6 accidental pressure cooker explosion can be compared to any other blast injury (9, 10, 11) i.e. release of gases (steam), release of metal fragments (lid or nozzle) and release of hot contents (food material and liquid). the metal fragments can act like bullet and can cause injuries at the site of impact (4, 6) there may be a blast wave and hot gases and contents can cause extensive burns. (5) management of a patient with pressure cooker related injuries follows the principal similar to a patient who had sustained injuries in blast and depends on the injuries sustained and is there any associated traumatic brain injury. the initial aim is to resuscitate the patient and maintain the airway and hemodynamic status. (6, 9) if there is an open wound with injuries to the underlying bony or neural structures the patient may need wound debridement and removal of devitalized brain tissue, removal of any foreign body, loose bone fragments followed by watertight closure of dura and closure of the wound. (9, 12) in present case the child did not require surgical and recovered well (except mild hemiparesis) with conservative management. conclusion in summary, accidental domestic pressure explosion can result in serious and potentially life threatening injuries. based on the available it is difficult to ascertain where there injuries are less common or have not been well addressed in literature. there is a need to recognize these injuries and promote safety measures to avoid such injuries. (1, 4, 5, 13) 302 | calderon-miranda et al traumatic brain injury due to pressure cooker explosion in a child figure 1 computerized tomography (ct scan) of the brain with bone window showed diffuse cerebral edema, subarachnoid hemorrhage and multiple skull fractures correspondence luis rafael moscote-salazar, colombia, red latino. latin american trauma & intensive neuro-care organization, bogota, colombia, southamerica e-mail: mineurocirujano@aol.com references 1.dobariya v, sheikh km, shastri m, desai s, savani m. an unusual case of penetrating ocular trauma with a pressure cooker whistle. delhi j ophthalmol 2014;24:207-208. 2.babar tf, khan mn, jan su, shah sa, zaman m, khan md. frequency and causes of bilateral occular trauma. j coll physicians surg pak 2007;17:679-682. 3.nwosu sn. domestic ocular and adnexal injuries in nigerians. west afr j med 1995;14:137-140. 4.chattopadhyay ss, mukhopadhyay u, saurabh k. an unusual case of penetrating ocular trauma with a pressure cooker. oman j ophthalmol 2010;3:89-90. 5.perera va, karunadasa k, perera c. a case series of domestic pressure cooker burns. ceylon med j 2012;57:49. 6.gupta op, roy k, ghosh s, tripathy p. an unusual penetrating transorbital craniocerebral injury. the indian journal of neurotrauma 2014;11:53-56. 7.gundeslioglu ao, yenidunya mo. burn and mandible fracture due to pressure cooker explosion. j craniofac surg 2010;21:1631-1633. 8.sandhir rk, sandhir m. accidental pressure cooker lid blow-out. burns 1992;18:438. 9.agrawal a, subrahmanyan bv, malleswara rao g. blast injury causing extensive brain injury and elevated skull fracture. the indian journal of neurotrauma 2014;11:64-67. 10.bhatoe hs. blast injury and the neurosurgeon. the indian journal of neurotrauma 2008;5:3-6. 11.wightman jm, gladish sl. explosions and blast injuries. ann emerg med 2001;37:664-678. 12.paiva ws, monaco b, prudente m, et al. surgical treatment of a transorbital penetrating brain injury. clin ophthalmol 2010;4:1103-1105. 13.mansouri mr, mirshahi a, hosseini m. domestic ocular injuries: a case series. eur j ophthalmol 2007;17:654-659. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-026 resection of giant invasive thoracic schwannoma. case report a. khelifa, f. aichaoui, i. assoumane, m. al-zekri, t. bennafaa, a. morsli romanian neurosurgery (2020) xxxiv (1): pp. 164-168 doi: 10.33962/roneuro-2020-026 www.journals.lapub.co.uk/index.php/roneurosurgery resection of giant invasive thoracic schwannoma. case report a. khelifa1, f. aichaoui1, i. assoumane2, m. al-zekri1, t. bennafaa1, a. morsli1 1 neurosurgical department of beo university hospital, algiers, algeria 2 department of surgery, national hospital of niamey, niger abstract even though spinal nerve sheath tumours, presented especially by schwannomas, are considered to be mostly benign; they can gain a huge size and have an invasive behaviour, causing spinal cord compression, bone destruction, and make the total removal of the tumour a real challenge for the surgeon. this type of tumours is recently described as giant invasive spinal schwannoma (giss), this type rarely reported in the thoracic region; deserve a special studying vis-a-vis the diagnosis and the management of both the tumour and the bone destruction. introduction even though spinal nerve sheath tumors, presented especially by schwannomas, are considered to be mostly benign; they can gain a huge size and have an invasive behavior, causing spinal cord compression, bone destruction, and make the total removal of the tumor a real challenge for the surgeon. this type of tumors is recently described as giant invasive spinal schwannoma (giss), this type rarely reported in the thoracic region (2); deserve a special studying vis-a-vis the diagnosis and the management of both the tumor, and the bone destruction. case presentation the patient is a girl of 30 years old without past medical history, who consulted for a weakness of the lower limbs appeared 5 months before she consults and with a recent worsening; the clinical exam at the admission found a patient who present paraplegia with urinary urgency. spinal ct then mri was performed, objectified a spinal cord keywords schwannoma, nerve sheath tumours, spinal cord compression corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 165 resection of giant invasive thoracic schwannoma compression by an intra and extra spinal giant dumped shape process extending to the left thoracic cavity at the level of th 8 and th 9, measuring: 73x47x45 mm; hypointense on t1 weighted images, with heterogeneous signal on t2 weighted images and intense enhancement after gadolinium injection; the process was responsible of a destructive scalloping on the left pedicle and partial destruction of the posterior wall of th 8, the tumor extends posteriorly to the left paraspinal muscles, and on the thoracic cavity in contact with the aorta (figures 1,2). there were no signs of neurofibromatosis. we operated the patient with the help of the thoracic surgery colleagues, under general anesthesia, and selective intubation of the right lung. together we performed a total removal of the tumor through a combined approach. first a posterior midline approach was performed through which a spinal cord decompression was obtained, and then through a left posterolateral thoracotomy passing through the sixth interrib space a total removal of the tumor was achieved (figure 3). the thoracic part of the tumor was well encapsulated and easily dissected, but the intra spinal part lacks a capsule and was totally excised with piecemeal removal. a thoracic drain was left. the histological exam found a who grade i schwannoma. on post operative the patient was diagnosed with an atelectasis of the left lung which was managed with fibroscopic aspiration and steroids. the patient was oriented to physical medicine where she progressively improved, gaining control on her urinary behavior, then 5 weeks later she was able to walk. post operative imaging performed 5 months later objectified a total removal of the tumor without residual or recurrence (figure 4). figure 1. preoperative thoracic ct; a: coronal reconstruction, b: sagittal reconstruction, c: axial slide; and d: 3d reconstruction. note the extension of the tumor (white arrow) and the amount of bone destruction on the axial and 3d views. 166 a. khelifa, f. aichaoui, i. assoumane et al. figure 2. preoperative t1 injected mri; a: coronal slide, b: axial slide. note the soft tissues infiltration (the arrow). figure 3. peroperative views, a: a view through the interrib approach after removing the tumor; b: the intrathoracic part of the tumor. note on the left image, the widened opening through which the tumor got through to invade the thoracic cavity; the black halo presents the parietal insert of the tumor. figure 4. post-operative images, a: axial slide of a thoracic ct, b: t2 wi mri coronal slide, c: t1 injected image axial slide, and d: t2 wi sagittal slide. note the total removal, no residual or recurrence tumor, and the spinal cord decompression (the star). 167 resection of giant invasive thoracic schwannoma discussion nerve sheath tumor could be either schwannoma or neurofibroma. neurofibromas produce a fusiform enlargement of the nerve where schwannomas are more smooth globoid tumors that develop eccentrically (1). histological exams of schwannomas find usually elongated bipolar cells with fusiform darkly staining nuclei arranged in compact interlacing fascicles that tend to palisade (1). nerve sheath tumors are mostly intradural but in 10% to 15% they are intra and extra dural in dumbbell shape (1). nerve sheath tumors are malignant in 2.5% of cases and half of these cases are neurofibromas (1). in 2001 sridhar et al proposed a classification for benign nerve sheath tumors with a precise definition of the giant and the invasive spinal schwannomas (table 1); in the same paper the authors reported for the first time, cases of giant thoracic invasive spinal schwannomas (2). giant invasive spinal schwannoma (giss) although a benign lesion put the surgeon face to many difficulties related to the size, the infiltration, and the invasive nature. big lesions need more exposure, though the selection of an adequate approach is mandatory. midline approach might be sufficient (2) but for more exposure a lateral extracavitary or extracavitary costotransversectomies approaches provide access to the extraforaminal extension of the tumor (3); for tumor extending beyond the vertebral body a combined approach is recommended (4). total removal is not possible in all cases (2,4), and that is mainly because the tumor might lack a capsule (2). the complications related to infiltration are represented especially by bone diffusion, in fact, some amount of bone destruction might jeopardize spinal stability and though the protection of neural structures, motion, and might cause some deformities. the evaluation of the consequences of bone infiltration classes these lesions into stable and unstable. classically spine surgeons use denis classification based on the three columns; kostuik divided those columns on tow, right and left zones and considered a destruction of three or more of these six zones as an unstable lesion (5). only instable lesions need spinal instrumentation. the lesion of our patient is considered stable, moreover some amount of infiltration is tolerable in the semi rigid spine (from th3 to th10) more than in the junctional or on the mobile spine, and that is the first criteria of stability evaluation in “the spinal instability neoplastic score (sins)” adopted by some spine surgeons (3,6). total removal of the tumor is the only factor related to long term outcome (2,4), in case where it is not possible, a decompression of neural structures is the priority, but a repeat surgery might be necessary (2). classification type i intraspinal tumor, < 2 vertebral segments in length; a: intradural; b: extradural. type ii intraspinal tumor > 2 vertebral segments in length (giant tumor) type iii intraspinal tumor with extension into nerve root foramen type iv intraspinal tumor with extraspinal extension (dumbbell tumors); a: extraspinal component < 2.5 cm; b: extraspinal component > 2.5 cm (giant tumor) type v tumor with erosion into the vertebral body (giant invasive tumor), lateral and posterior extensions into myofascial planes table 1. sridhar et al classification for benign nerve sheath tumors (2). conclusion giant invasive spinal schwannoma is a benign lesion with high bone destruction potential; its infiltration nature to the surrounding soft tissues could make the total resection a real challenge. knowing the real instable spinal lesions will orient the indication to spinal instrumentation. references 1. basheal m. agrawal, barry d. birch, paul c. mccormick, daniel k. resnick, e.c. benzel. intradural extramedullary spinal lesions. spine surgery. techniques, complication avoidance and management. 3d edition. chapter 102. p992. 2. sridhar k, ramamurthi r, vasudevan mc, ramamurthi b: giant invasive spinal schwannomas: definition and surgical management. j.neurosurg. 2001, 94:210–215. 3. edison p. valle-giler, juanita garces, roger d. smith, wale a. r. sulaiman. one-stage resection of giant invasive thoracic schwannoma: case report and review of literature. the ochsner journal 14:135–140, 2014. 4. nam hun yu, soo eon lee, tae-ahn jahng, chun kee chung. giant invasive spinal schwannoma: its clinical features and surgical management. neurosurgery, volume 71, issue 1, july 2012, pages 58–67, https://doi.org/10.1227/neu.0b013e31824f4f96. 5. william f. lavelle; e.c. benzel. thoracic and 168 a. khelifa, f. aichaoui, i. assoumane et al. thoracolumbar spinal tumors: regional challenges. spine surgery. techniques, complication avoidance and management. 3d edition. chapter 113. p1117. 6. shandy fox, michael spiess, luke hnenny, and daryl. r. fourney. spinal instability neoplastic score (sins): reliability among spine fellows and resident physicians in orthopedic surgery and neurosurgery. global spine journal. 2017, vol. 7(8) 744-748. doi: 10.1177/2192568217697691. 15amitagrawal_impropercoupling 236 agarwal improper coupling between inner nut and screw head improper coupling between inner nut and screw head leading to rod loosening and dislodgement amit agarwal professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) key words: lumbar spine, spinal fusion, instrumentation, fixation failure. although the true incidence is unknown, in a group of patients the construct failures may not actually be device failures but instead it can be a surgeonrelated error. (1, 2) a 45 year-old male patient was operated for l5-s1 fixation for grade ii lumbar spondylolisthesis one year back. he was apparently alright after surgery. for last three months he noticed recurrence of back pain. follow up x-ray showed rod loosening on right side (figure 1). figure 1 x-ray lumbo-sacral spine ap and lateral view showing dislodgement and migration of the right rod superiorly from screw head there were no focal neurological deficits. wound was healed well. the patient underwent re-exploration of the previous incision. screws and rod on right side were exposed. rod was slipped superiorly from both the screws heads. it was recognized that there was mismatch between inner nut and screw head as the nut was not tightened properly and it was oblique (figure 2). rod was located and removed. nuts were removed from both the screws. lower screw was loosened in the bone, was removed and replaced with a bigger size of screw. patient did well after surgery and doing well at follow up. figure 2 intra-operative images showing absence of rods between screw heads and (inset) improper coupling between inner nut and screw head romanian neurosurgery (2014) xxi 2: 236 237 237 pedicle screws are used achieve reduction and fixation of the spine which allows early mobilization of the patient without external support (3) in the treatment of fractures, degenerative disease, neoplasm, and congenital deformities. (4) in spite of the routine use of pedicle screws for spinal fixation, these devices can be associated with complications. (1, 5-7) the complications associated with pedicle screws include screw fracture, rod fracture, loose screw (8-11), screw loosening/pullout, rod breakage (with or without rod dislodgement. (3, 5, 8) the hardware failure at the junction of the hardware components (a rod sliding off a pedicle screw or fracture along the middle portion of a plate or rod (4) can be due to coupling failure (insufficient tightening of the blocking elements) resulting in loosening of the rod. (3, 12, 13) apart from insufficient tightening of the nut into the screw head, (as was seen in present case) the improper coupling between nut and screw head can also cause loosening and consequent dislodgment of the rod. (1) it has been suggested that, while tightening the nut, back off the adjusting nut and rotate counter-clockwise until it’s loose in the screw head and produces a tuck sound. following this the nut can be tighten to make sure that there is no mismatch in between the grooves in the screw head and the ridges of the nut. (1) correspondence: dr amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.agrawal a. pedicle screw nut loosening: potentially avoidable causes of spine instrumentation failure. asian spine j. 2014;8(2):224-226. 2.ahmed nms, ibrahim hb, farg a, sleem a. avoidable causes in pedicle instrumentation failure. pan arab journal of neurosurgery 2011;15:29-35. 3.pihlajamäki h, myllynen p, böstman o. complications of transpedicular lumbosacral fixation for non-traumatic disorders. journal of bone & joint surgery, british volume 1997;79:183-189. 4.slone rm, macmillan m, montgomery wj. spinal fixation. part 3. complications of spinal instrumentation. radiographics 1993;13:797-816. 5.harimaya k, mishiro t, lenke lg, bridwell kh, koester la, sides ba. etiology and revision surgical strategies in failed lumbosacral fixation of adult spinal deformity constructs. spine 2011;36:1701-1710. 6.aebi m, etter c, kehl t, thalgott j. the internal skeletal fixation system. a new treatment of thoracolumbar fractures and other spinal disorders. clinical orthopaedics and related research 1988;227:30-43. 7.olerud s, karlström g, sjöström l. transpedicular fixation of thoracolumbar vertebral fractures. clinical orthopaedics and related research 1988;227:44-51. 8.kim ht, hong sm, choi ih, jung jw. fixation failure of instrumentation for the spinal fusion in lumbar region. journal of korean society of spine surgery 1997;4:319-328. 9.davis h. increasing rates of cervical and lumbar spine surgery in the united states, 1979-1990. spine 1994;19:1117-1123; discussion 1123. 10.mulholland rc. pedicle screw fixation in the spine. the journal of bone and joint surgery british volume 1994;76:517-519. 11.west jl, ogilvie jw, bradford ds. complications of the variable screw plate pedicle screw fixation. spine 1991;16:576-579. 12.joseph v, al jahwari as, rampersaud yr. mediastinal migration of distal occipito-thoracic instrumentation. european spine journal 2008;17 suppl 2:s257-262. 13.faraj aa, webb jk. early complications of spinal pedicle screw. european spine journal 1997;6:324-326. 3giovania_surgicaltreatment 394 giovani et al surgical treatment and outcome of cerebral cavernomas surgical treatment and outcome of cerebral cavernomas – a 10 years’ experience a. giovani, aurelia sandu, angela neacsu, r.m. gorgan abstract: cavernous malformations (cavernomas) are congenital low flow angiographic occult vascular lesions with a high tencency to bleeding. the prevalence of cerebral cavernous vascular malformations is estimated to be 0.4% to 0.9%.2,7 cms in deep locations, including the brainstem, thalamus, and basal ganglia, account for 9% to 35% of all malformations in the brain. we performed a retrospective 10 years study on 130 operated cerebral cavernomas and discussed the clinical status at presentation, the choice and timing of the surgical approach and the short and longterm follow up. the 130 operated cases were divided into a supratentorial 102 (78.46%) group and an infratantorial group 28 (21.53%). the average age at presentation was 43,62 years old (17-76) and there was no sex predominance, male/female = 1,44 (77/53). only in 14 cases (10.76%) we could find multiple cavernomas which had relatives with multiple cavrnomas, but the familial inheritance was not studied, and only the symptomatic lesion was resected. we divided the outcome results reporting for agroup with superficial respectively profound lesions. the long term follow up for the patients in the profound lesions group showed that 31/37 (83,78%) of patients had a mrs between 0 and 2, and the rest had a poor long term outcome. after surgery there was no clinical deterioration in the superficial lesions group and 22 patients from those who presented in mrs 2 showed neurological improvement on long term follow up, meaning that 82,79% of patients had a 0 or 1 mrs. microsurgery is the treatment of choice in symptomatic brain cavernomas, total resection being the only curative treatment, capable to prevent further bleeding and to offer an efficient control of seizures. key words: cavernous malformation, microneurosurgery, seizures. introduction cavernous malformations (cavernomas) are congenital low flow vascular lesions, which can be associated with other lesions from the same spectrum like capillary telangiectasias and developmental venous anomalies, they account for 1% of intracranial vascular lesions an d 15% of vascular malformations. (1, 6) the prevalence of cerebral cavernous vascular malformations is estimated to be 0.4% to 0.9% (2, 7). malformations in deep locations romanian neurosurgery (2014) xxi 4: 394 – 404 395 including the brainstem, thalamus, and basal ganglia are of particular interest because their critical location renders them very challenging for surgical resection (3, 7, 10). cavernomas are well circumscribed, benign, low-flow vascular malformations, composed of irregular sinusoidal vascular channels, lacking smooth muscle and elastic fibers. they lack feeding arteries or draining veins and contain no neural tissue. by comparison to other vascular malformations included in mccormick classification (1966), angiography is not a good diagnostic tool as there is no blood flow inside these lesions, yet their characteristic mulberry shape on mri directs the diagnostic. (8, 9, 10) though the mechanism of growth of these lesions was not completely elucidated most studies sugest that repeated subclinical bleeding episodes inside the lesion and the subsequent thrombus formation and trombolisis create the “caverne” that give the name and the typical mulberry appearance on t2 mri. (5) after rigamonti’s first description of this aspect in 1986, zabramsky developed a 4 grade classification of cavernous malformations based on mri, in which grade 1are hyperintense grade ii are both hyper and hypointense, grade iii are hypointense and grade iv are small “black spot lesions” visible only on gradient echo these were considered capillary telangiectasies. (21, 25) cmin deep locations is not completely understood, but most reports suggest that they have a higher rate of hemorrhage than superficial cms as well as high rebleed rates. (2) treatment options include observation, and surgery, and a few authors in the past reported cases treated with radiosurgery but now it gained acceptance that radiosurgery has no positive long term impact in the treatment of cavernomas. especially superficial supratentorial lesions with a low risk of bleeding and producing neurologic deficit can be followed by observation alone but this approach is not safe for patients harboring deep seated lesions prone to produce new neurological deficits in case of rerupture. most of the studies report good outcomes with almost 100% complete removal, though this is not the case in the posterior fossa where the postoperative morbidity can be as high as 30%. (4) materials and methods the objectives of the study were to analyze the the factors that influence the short and long term outcome, to establish the best indications for surgery and to define the safe corridors to approach deep seated lesions. we retrospectively reviewed the clinical records the surgical details and the acute and delayed surgical complications for 130 consecutive patients operated between january 2000 and december 2009 in our department. the average follow up was around 5 years (between 6 months and 10 years). all the patients were investigated with ct scan and mri as the cavernomas are angiographically occult lesions. the outcome was evaluated comparing preoperative with postoperative modified rankin scale (mrs). the senior surgeon (r.m.g) did not feel the need to use neuronavigation or of stereotaxy for locating the lesions nor for those located immediately subcortical or for 396 giovani et al surgical treatment and outcome of cerebral cavernomas those in deep locations. we did not use motor, sensitive or cranial nerves evoked potentials. based on the information from the mri the surgical approach was directed on the shortest way to the lesion. the indication for surgery depends on the clinical state of the patient , for the supratentorial location either repeated seizures, motor or sensory deficit if the internal capsule or the thalamus are injured or visual disturbance if the optic radiations are injured. (20, 22) as the natural course of the brainstem cavernomas is more aggressive than of those located supratentorial and the risk of clinical significant hemorrhage is higher surgical resection is indicated in all symptomatic and accessible lesions. even if some studies report a 30% risk of new neurological deficit after surgery these make often a significant clinical recovery and there is no risk of rebleeding. (6, 8, 14) in almost all subcortical and deep seated supratentorial lesions the approach was transcortical with care not to injure eloquent areas or important veins, but respecting the rule of the shortest way to the lesion. the approaches used for the infratentorial lesions including those of the brainstem were retrosigmoid, supracerebelar infratentorial, suboccipital and suboccipital telovelar. all the lesions were approached from the point where they came closest to the surface (the 2 point method). (26, 27) the microsurgical technique included sharp dissection and piecemeal resection or one piece resection where possible in more superficial lesions. except for the deep seated lesions the surrounding hemosiderin rich gliotic ring was also removed, but the associated venous anomalies where it was the case were all left untouched. in cases with multiple cavernomas surgery is indicated for the lesions responsible for neurological deficit, the other lesions are just imagistically followed. (7) results between 2000 and 2009 130 consecutive patients with cavernomas were operated in our department. the mean age at presentation was 43,64 years range between 17 and 76. the 130 operated cases were divided into a supratentorial 102 (78.46%) group and an infratantorial group 28 (21.53%). the average age at presentation was 43,62 years old (17-76) and there was no sex predominance, male/female = 1,44 (77/53). only in 14 cases (10.76%) we could find multiple cavernomas which had relatives with multiple cavrnomas, but the familial inheritance was not studied, but only the symptomatic lesion was resected. the supratentorial cavernomas were located in frontal lobes in 52 patients (40%), in temporal lobes in 27 patients (20.76%) in parietal lobes in 25 patients (19,23%) in occipital lobes in 2 patients (1,53%) and deep in 24 (18,46%) the infratentorial cavernomas were distributed in cerebellum 15 patients (53.57%), and in brainstem and cerebellar peduncles in 13 patients (46,42%). out of these 13 patients, 3 were in medulla, 2 in the pontomedullary junction 4 in the pons and 4 in the mesencephalus. the clinical presentation was differentin the two groups: in the supratentorial one, seizures and headache while the dominant romanian neurosurgery (2014) xxi 4: 394 – 404 397 symptoms but in the infratentorial group where the cranial nerve deficits, hemiparesis, numbness and cerebellar syndrome were dominant (table 1). hemorrhage was present on mri in 40 patients (30.76%) in 38 (95%) as intraparenchymal hematoma, in 1 patient as intraventricular bleeding and in 1 as subarachnoid hemorrhage. 31 of these patients (77.5%) were in a poor preoperative mrs, having an altered mental state. the patients with seizures 66 p (50.76%) were stratified according to type and frequency (table 2). table i supratentorial cavernomas hemorrhage seizures headache hemiparesis numness aphasia visual deficits 29/102 (28,43%) 66/102 (64.70%) 58/102 (56,86%) 19/102 (18,62%) 19/102 (18,62%) 13/102 (12.74%) 3/102 (2.94%) infratentorial cavernomas hemorrhage cranial nerve deficits headache hemiparesis numbness cerebellar syndrome 14/28 (50%) 15/28 (53,57%) 13/28 (46,42%) 11/28 (39,28%) 11/28 (39,28%) 9/28 (32.14%) table ii type • generalized tonic-clonic seizures – 32 p (48.48%) • partial complexe seizures – 24 p (36,36% ) • partial simple seizures – 15 p (22.72%) • partial seizure, secondary generalized – 9 p (13.63%) • * some patients presented more than one type of seizures frequency • 1-2 seizures before surgery – 30 p (45,45%) • 1-2 seizures/year – 17 (25,75%) • 1 seizure/week – 9 (13.63%) • daily seizures – 11 (16.66%) 11 p (16.66%) presented refractory seizures mean time between seizure onset and surgery = 4 mo (0.4 → 40 mo) based on this data we identified a few risk factors for seizure reccurence. there were no seizures in deep locations. 398 giovani et al surgical treatment and outcome of cerebral cavernomas table iii risk factors for seizures occurrence: • cortical location • t location, especially temporomesial location • large lesions, including hemosiderinic ring • focal neurological deficits • left side cavernomas • acute hemorrhage • subacute hemorrhage • surrounding edema* were not confirmed as risk factors for seizures occurrence • sex, • age, • diameter of hemosiderinic ring, • diameter of surrounding edema, • multiple lesions outcome when we analyzed the outcome we studied the group of corticalised or superficial subcortical cavernomas and that of deep seated lesions, in brainstem, thalamus and basal ganglia. total resection was performed in all cases, but the surrounding hemosiderin ring was not removed in deep seated lesions where such a maneuver could harm grey matter nuclei and no mortality was registered on short or long term follow up in this series of 130 patients. both karnovsky and mrs improved after surgery. in patients with deep seated lesions (37 patients), 12 (32,43%) presented in a poor preoperative state mrs > 2. 10 patients from this group had worsened deficits immediately after surgery, 4 of these in brainstem cavernomas but all of them showed a good recovery with follow up 5 of them remained in mrs 2 and 3 with mrs>2. the complications included worsened hemiparesis, worsened ataxia, 7th nerve paresis and vi or iiird nerve paresis. the immediate postoperative status for this group was excellent in 10/37 (27,02%) of patients, good in 13/37 (35,13%) patients and poor in 14 (37,83%) patients. the long term follow up for these patients showed that 31/37 (83,78%) of patients had a mrs between 0 and 2, and the rest had a poor long term outcome. the situation was different in the group of superficial cavernomas where 55/93 (59.13%) of patients presented with a mrs of 0 or 1 and 36/93 (38,7%) presented with mrs of 2 and 2 patients with an mrs>2. after surgery there was no clinical deterioration in this group and 22 patients from those who presented in mrs 2 showed neurological improvement on long term follow up, meaning that 82,79% of patients had a 0 or 1 mrs. romanian neurosurgery (2014) xxi 4: 394 – 404 399 case presentations case 1: a 70 years old male was admitted for persistent headache and left homonymous hemianopsia that worsened in the week previous presentation. figure 1 mri – right occipital heterogenous lesion, with salt and pepper appearance suggestive for cavernoma the tumor was completely removed with the surrounding hemosiderin ring using a right suboccipital occipital-supratentorial approach. using the gravity with no need for mechanical retraction, the lesion was exposed corticalised on the tentorial surface of the right occipital lobe. the tumor was piecemeal removed and then the hemosiderin ring was resected. hemostasis was achieved with bipolar and intensive lavage with serum. after the dural closure the scalp is closed on epidural drain. the postoperative ct scan confirmed complete removal. figure 2 same patient with postop ct images of the occipital cavernoma – total removal 400 giovani et al surgical treatment and outcome of cerebral cavernomas case 2: a 45 years old female presented with altered mental state (14 p) and a history of headache, vomiting, swallowing disorders (liquid and solid food), gait disturbances (astasia-abasia), mild right faciobrachial paresis with onset 7 days before admission. the neurologic exam showed mild right faciobrachial paresis and ix, x, xi and xii cranial nerves paresis. figure 3 ct scan spontaneous hyperdense lesion within the right medulla, ø = 13 mm figure 4 mri: right medulla lesion, h-iso in t1 and h-ht2, ø = 13 mm, suggestive for cavernoma, with subacute bleeding romanian neurosurgery (2014) xxi 4: 394 – 404 401 the lesion was completely resected using a telovelar approach. a midline suboccipital craniectomy was performed, and after opening the cisterna magna a telovellar approach is used to access the medulla. as the lesion appeared subpial it was entered directly and then piecemeal resected completely. the surrounding yellow gliotic plane was left intact. dura mater was reconstructed with kolagen and then with the drain left in place the muscles plane and the skin were closed. the outcome was favorable with partial remission of the cranial nerves deficits and improvement of swallowing disorders at 2 months follow up. (figure 4) figure 5 postop. mri with complete resection of the cavernoma discussions the frequency of asymptomatic cavernomas can be as high as 40% (zabramsky), but the actual data is impossible to quantify. the most common presenting symptoms for the supratentorial group were seizures, headache, hemiparesis and numbnes. the most common infratentorial presentation were cranial nerve deficits followed by hemiparesis and numbness and cerebellar symptoms. compared to the infratentorial group where the hemorrhagic presentation was almost the rule (93%) only 39% of the supratentorial group patients had this presentation. the division into supratentorial and infratentorial groups is not enough and further studies should focus on the differences of the groups of patients with cortical or subcortical cavernomas compared to those 402 giovani et al surgical treatment and outcome of cerebral cavernomas with cavernomas seated in brainstem, thalamus or basal ganglia. (1, 3) the best method for preoperative and postoperative investigating the patient is the mri. it can show the borders of the lesion the intra or extralesional hemorrhage and the associated edema and also is invaluable in planning the aproach especially if neuronavigation or stereotaxy are not used for localization. angiography can be useful in defining associated lesions because cavernomas are not visible on it but we did not make a standard from using it and this may be a reason why venous associated anomalies escaped our view. as cavernomas in deep locations have an annual hemorrhage rate of 5,1% and a rebleed rate of 31,5% per patient per year, there was no time for wait and see in these cases. observation was reserved only to those cases we considered inoperable. complete removal was achieved in all cases but with the cost of new neurological deficits in 4 patients (3%), all of these presenting deep seated lesions. the postoperative mrs was good or excellent in 97% of patients compared to 64% preoperative and was even more evident in patients with deep seated lesions. the control of the seizures was achieved in all patients who presented with seizures, and almost 60% of them were free of medication after surgery. the dimensions of the lesions were not statistically different in the two groups but in the infratentorial group they correlated with the hemorrhage and neurologic deficit. some studies report larger sizes of cavernomas in children but our study included only adults. we could find an association with venous anomalies only in 3 patients which is in contrast to the reports of other studies. as prospective studies are lacking the hemorrhage rates which are the key to the surgical indication are calculated based on retrospective analysis considering cavernomas as congenital lesions, yet more and more studies document the appearance of de novo cavernomas in sporadic or familial cases. even the results of different studies differ it became clear that once symptomatic the cavernomas have a high rate of rebleeding causing new neurological deficits. (14, 18, 19) because of their tendency to bleed cavernomas are always in the surgical focus, yet surgery should not be proposed for all lesions, most of the supratentorial lesions can be treated conservatively if asymptomatic. most of the time the hemorrhage is inside the cavrnoma causing it’s enlargement in time, but when seated in deep nuclei even this enlargement can give neurological deficit, acting as a mass effect. when located in eloquent areas even small hemorrhage outside the lesion can be echoed in severe deficits. (11, 12) our study aimed at identifying those lesions with a higher tendency to produce deficits for which surgery is the best and the safest treatment but as is the case with many studies on cavernomas it is limited by its retrospective nature. as the most frequent manifestations of supratentorial lesions are repeated seizures, which disturb the patient’s life balance we identified a few risk factors for seizures like the cortical and more frequently the temporomesial location, the large cavernomas, romanian neurosurgery (2014) xxi 4: 394 – 404 403 the location in the left hemisphere, the acute or subacute hemorrhage and edema. in all supratentorial lesions we removed the hemosiderin ring as well and we believe this is one of the main reasons for the complete disappearance of seizures in most of the cases. (23, 24) we identified a few positive prognostic factors including a high preoperative karnofsky score coincident with a mrs of 0 or 1, the small size and the superficial location of the lesion. we did not consider radiosurgery an alternative to deep seated lesions because we considered the high rates of rebleeding after radiosurgery inacceptable and many studies showed that cavernomas can occur after radiation therapy. (12) conclusions symptomatic deep cavernous malformations in the brainstem, basal ganglia, and thalamus have a high bleed and rebleed rate and an aggressive natural history. early surgery provides excellent clinical results and protects against future hemorrhages. microsurgery is the treatment of choice in symptomatic brain cavernomas, total resection being the only curative treatment, capable to prevent further bleeding and to offer an efficient control of seizures. complete cavernoma resection and resection of surrounding hemosiderin is recommended except for cavernomas located in the brainstem or in eloquent areas acknowledgement: this paper was co-financed from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 "excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis", coordinator the bucharest university of economic studies. correspondence giovani andrei giovani.andrei@gmail.com references 1.abdulrauf si, kaynar my, awad ia. a comparison of the clinical profile of cavernous malformations with and without associated venous malformations. neurosurgery. 1999;44(1):41-46. 2.abla aa, lekovic gp, garrett m, et al. cavernous malformations of the brainstem presenting in childhood: surgical experience in 40 patients. neurosurgery. 2010;67 (6):1589-1598; discussion 1598-1599. 3.abla aa, lekovic gp, turner j, deoliveira jg, porter r, spetzler rf. advances in the treatment and outcome of brainstem cavernous malformation surgery: a singlecenter case series of 300 surgically treated patients. neurosurgery. 2011;68(2):403-414. 4.casazza m, broggi g, franzini a, avanzini g, spreafico r, bracchi m, valentini mc: supratentorial cavernous angiomas and epileptic seizures: preoperative course and postoperative outcome. neurosurgery 39:26–34, 1996. 5.clatterbuck re, elmaci i, rigamonti d: the nature and fate of punctate (type iv) cavernous malformations. neurosurgery 49:26–32, 2001. 6.cohen ds, zubay gp, goodman rr: seizure outcome after lesionectomy for cavernous malformations. j neurosurg 83:237–242, 1995. 7.dandy we. venous abnormalities and angiomas of the brain. arch surg. 1928;17 (5):715-793. 8.del curling o jr, kelly dl jr, elster ad, craven te: an analysis of the natural history of cavernous angiomas. j neurosurg 75:702–708, 1991. 9.engel jj: outcome with respect to epileptic seizures, in engel jj (ed): surgical treatment of the epilepsies. new 404 giovani et al surgical treatment and outcome of cerebral cavernomas york, raven press, 1987, pp 553–571. 10.ferroli p, casazza m, marras c, mendola c, franzini a, broggi g: cerebral cavernomas and seizures: a retrospective study on 163 patients who underwent pure lesionectomy. neurol sci 26:390–394, 2006. 11.ferroli p, sinisi m, franzini a, giombini s, solero cl, broggi g. brainstem cavernomas: long-term results of microsurgical resection in 52 patients. neurosurgery. 2005;56(6):1203-1212. 12.hasegawa t, mcinerney j, kondziolka d, lee jy, flickinger jc, lunsford ld. long-term results after stereotactic radiosurgery for patients with cavernous malformations. neurosurgery. 2002;50(6):1190-1197. 13.kondziolka d, lunsford ld, kestle jr. the natural history of cerebral cavernous malformations. j neurosurg. 1995;83(5):820-824. 14.kupersmith mj, kalish h, epstein f, et al. natural history of brainstem cavernous malformations. neurosurgery. 2001;48(1):47-53. 15.mathiesen t, edner g, kihlstrom l. deep and brainstem cavernomas: a consecutive 8-year series. j neurosurg. 2003;99(1):31-37. 16.mccormick wf: pathology of vascular malformations of the brain, in wilson cb, steihn bm (eds): intracranial arteriovenous malformations. baltimore,williams & wilkins, 1984, pp 44–63. 17.mizoi k, yoshimoto t, suzuki j. clinical analysis of ten cases with surgically treated brain stem cavernous angiomas. tohoku j exp med. 1992;166(2): 259-267. 18.nimjee sm, powers cj, bulsara kr: review of the literature on de novo formation of cavernous malformations of the central nervous system after radiation therapy. neurosurg focus 21:e4, 2006. 19.pozzati e, acciarri n, tognetti f, marliani f, giangaspero f: growth, subsequent bleeding, and de novo appearance of cerebral cavernous angiomas. neurosurgery 38:662–670, 1996. 20.quinones-hinojosa a, lyon r, du r, lawton mt. intraoperative motor mapping of the cerebral peduncle during resection of a midbrain cavernous malformation: technical case report. neurosurgery. 2005;56(2 suppl):e439. 21.rigamonti d, hadley mn, drayer bp, johnson pc, hoenig-rigamonti k, knight jt, spetzler rf: cerebral cavernous malformations. incidence and familial occurrence. n engl j med 319:343–347, 1988. 22.robinson jr, awad ia, little jr: natural history of the cavernous angioma. j neurosurg 75:709–714, 1991. 23.samii m, eghbal r, carvalho ga, matthies c. surgical management of brainstem cavernomas. j neurosurg. 2001;95(5):825-832. 24.vinas fc, gordon v, guthikonda m, diaz fg. surgical management of cavernous malformations of the brainstem. neurol res. 2002;24(1): 61-72. 25.zabramski jm, wascher tm, spetzler rf, et al. the natural history of familial cavernous malformations: results of an ongoing study. j neurosurg. 1994;80(3):422432. 26.wang cc, liu a, zhang jt, sun b, zhao yl. surgical management of brainstem cavernous malformations: report of 137 cases. surg neurol. 2003;59(6):444-454. 27.ziyal im, sekhar ln, salas e, sen c. surgical management of cavernous malformations of the brain stem. br j neurosurg. 1999;13(4):366-375. 11rahejaamol_chronicsubdural 196 raheja et al chronic subdural hematoma in accelerated phase of chronic myeloid leukaemia chronic subdural hematoma development in accelerated phase of chronic myeloid leukaemia presenting with seizure and rapid progression course with fatal outcome amol raheja1, guru dutta satyarthee1, ashok kumar mahapatra2 1department of neurosurgery, all india institute of medical sciences, new delhi, india 2all india institute of medical sciences, bhubaneswar, odisha, india abstract: occurrence of chronic subdural hematoma (csdh) in leukemia is rare, and most reported cases occurred in relation with acute myeloid leukaemia; however, occurrence is extremely rare in accelerated phase of chronic myelogenous leukaemia (cml). seizure as presentation of sdh development in cml cases is not reported in literature. authors report an elderly male, who was diagnosed as cml, accelerated phase of developing sdh. initially presented to local physician with seizure; urgent ct scan head was advised, but ignored and sensorium rapidly worsened over next day and reported to our emergency department in deeply comatose state, where imaging revealed chronic subdural hematoma with hypoxic brain injury with fatal outcome. seizure, progressive worsening of headache, vomiting and papilloedema are harbinger of intracranial space occupying lesion and requires ct head in emergency medical department for exclusion, who are receiving treatment of haematological malignancy. key words: chronic myeloid leukaemia, accelerated phase, chronic subdural hematoma, management, seizure introduction sdh is an important cause of morbidity and mortality and its common aetiology includes trauma, medications i.e. anticoagulants, antiplatelets, chemotherapy; arterio-venous malformation, aneurysms and post-craniotomy. it is very rarely associated with haematological malignancy, mostly known to occurring with acute myeloid leukaemia; however occurrence in chronic myelogenous leukaemia (cml) is unusual and about less than ten are reported to developing in accelerated phase. (1, 2, 3, 7, 10) management of sdh requires appropriate computed tomography (ct) scan of head to detect amount of hematoma, mass effect, and suitability of surgical intervention and presence of co-morbid illness. temporary measures may include administration of antiepileptic and cerebral decongestants. romanian neurosurgery (2015) xxix 2: 196 199 197 cornerstone of management is burr-hole drainage of sdh, rarely craniotomy is indicated if membranes are well organized and thick. case report 61 year old gentle man reported to emergency services in altered sensorium with history of respiratory distress for past two days. he had no previous history of trauma. although diagnosed as chronic remission phase of cml for eight years, unfortunately he developed accelerated phase since three months and kept on chemotherapy. comorbid illness included history of acute coronary ischemia two months back. he developed headache and one episode of generalised tonic-clonic seizure unassociated with aura or postictal weakness. evaluated by local physician at first encounter, ct scan head was advised but not done due to nonavailability of ct scan facility at native place. he notice progressive worsening of headache and lapsed into comma next day and he was brought to emergency services in altered sensorium and respiratory distress. examination in emergency department revealed pulse rate was 64 per minute and b.p. was 140/ 94 mm hg, with g.c.s. of 4, with dilated and non-reacting left pupil and sluggishly reacting right pupil, fundi showed with bilateral papilloedema. he was immediately intubated and kept on ventilator support. haematological evaluation showed anaemia with total leukocyte count (tlc) of 34100 and marked neutrophilia, peripheral blood smear showed anisocytosis with dimorphic r.b.c. bone marrow aspiration and biopsy findings were consistent with accelerated phase of cml. urgent ct scan head showed presence of large chronic subdural hematoma over left fronto-temporo-parietal region with significant compressed ipsilateral lateral ventricle, sub-falcine herniation, midline shift of about 9 mm towards right side, transtentorial herniation along with evolving ischemic-hypoxic injury of brain (figure 1). urgent left frontal and parietal burr hole and sdh evacuation and drain placement was carried out. post-operative ct head showed evidence of global ischemia (figure 2). he succumbed within 24 hours of admission despite optimal efforts. figure 1 ncct head showing large chronic subdural hematoma over left fronto-temporo-parietal region causing sub-falcine herniation and gross midline shift figure 2 post-operative ncct head scan showing diffuse hypoxic brain injury 198 raheja et al chronic subdural hematoma in accelerated phase of chronic myeloid leukaemia discussion cml is characterized by increased proliferation of the granulocytic cell line without loss of capacity to differentiate. its course is clinically sub-classified into three phases – chronic phase, accelerated and blast crisis. about 85 % cml patients remain in chronic phase, carrying favorable prognosis with maintenance chemotherapeutic agents, but can convert to other phases with unfavorable prognosis when untreated or chemotherapeutic resistant cases. predominant factor in differentiating between accelerated and blast crisis is percentage of myeloblasts present in blood or bone marrow study. (6, 14) although tyrosine kinase inhibitors have revolutionized cml therapy with 80-90 % longterm survival rates (8). few such cases on longterm chemotherapy can develop chronic sdh despite normal haematological parameters, and surgical treatment may be required if causing clinically symptomatic or producing mass effect. (7, 9) sdh is rarely reported in systemic haematological malignancies. (1, 2, 3, 7, 10, 11, 13) exact mechanisms of sdh development is not clear, however, possible mechanism include malignant cells deposition in duramater leading to dural blood vessels occlusion and causing rupture of occluded vessels into subdural space producing csdh. (11) other postulates are tumour necrosis in metastatic deposits, thrombocytopenia, development of disseminated intravascular coagulation, and secondary adverse effect of chemotherapy administration. (7, 9) druker et al, observed that incidence of intracranial haemorrhage in cml on medication is about 5 % in blast crisis, 1 % in accelerated phase and sharply falling to 0.6 % in chronic phase. (4) our case was in accelerated phase on chemotherapy. seizure may be presenting symptom of intrinsic brain pathology or extraaxial intracranial lesion. authors reported seizure can be the first presenting symptom in extra-axial lesions like pituitary adenoma. (12) hauser et al reported causes of first onset seizure in relation to age, idiopathic category accounted for more than 50 % of cases but, only 45 % of cases in the oldest age group. (5) amongst children, the greatest proportion were associated with neurological deficits, believed to be present since birth, among young age population (15-40 years) with an identified etiology included central nervous system (cns) infection, tumor, neurological deficit since birth and birth trauma were identified as a cause with equal frequency. in adult age (35-64 years) with presumed causes trauma and neoplasms were equally responsible, but less frequent with cerebrovascular disease. however in the elderly population, most common cause was cerebrovascular disease which account for 28 % of all new cases. so seizure is important warning signs of harbouring intracranial pathology especially in young or elderly age, which require full investigation and accordingly appropriate treatment, patient should be referred to neurologist or neurosurgeon. however in our case unfortunate delay in ct scan led to delay in detection of sdh, which was only picked up in the advanced stage and although urgent surgical intervention could not provide good outcome. hence authors recommend every case of seizure and associated symptoms of raised intracranial pressure need full clinical evaluation including appropriate neuro-imaging. romanian neurosurgery (2015) xxix 2: 196 199 199 conclusion this case report highlights the importance of urgent diagnosis and appropriate neurosurgical intervention in cases of underlying systemic haematological malignancies with high index of suspicion for raised icp owing to suspected intracranial bleed. seizure, progressive headache, vomiting and papilledema on fundus examination are warning signs of harbouring intracranial mass lesion, and every case should undergo at least ct head, which is economic, easily available and requires very short time to rule out life threatening intracranial pathology. proper awareness among physician in medical emergency department is of paramount importance to avoid such delay and providing lifesaving therapeutic intervention at the earliest opportunity. correspondence dr guru dutta satyarthee, associate professor, 714, department of neurosurgery and gamma knife, all india institute of medical sciences, new delhi, india 110029 telephone no. 9868398243 fax no. 91-11-26588663, 91-11-26588641 e-mail id duttaguru2002@yahoo.com references 1.abdulhamid mm, li ym, hall wa. spontaneous acute subdural hematoma as the initial manifestation of chronic myeloid leukemia. j neurooncol. 2011; 101(3): 513-516. 2.bromberg je, vandertop wp, jansen gh. recurrent subdural haematoma as the primary and sole manifestation of chronic lymphocytic leukaemia. br j neurosurg. 1998; 12(4): 373-376. 3. comănescu a, roşca e, bota m, ninulescu g chronic subdural hematoma in a patient with acute myeloid leukemia and dural metastatic infiltration. rom j morphol embryol. 2008; 49(2):259-262. 4. druker bj, sawyers cl, capdeville r, ford jm, baccarani m, goldman jm. chronic myelogenous leukemia. hematology am soc hematol educ program. 2001:87-112. 5. hauser wa, annegers jf, kurland lt. incidence of epilepsy and unprovoked seizures in rochester, minnesota: 1935-1984. epilepsia. 1993 may-jun; 34(3): 453-468. 6. karbasian em, morris el, dutcher jp, wiernik ph. "blastic phase of chronic myelogenous leukemia". current treatment options in oncology 2006; 7 (3): 189– 199. 7. kim ms, lee dh, lee yr, kim dk, bae sh, hwang jy et al. a case of subdural hematoma in patient with chronic myeloid leukemia treated with high-dose imatinib mesylate. korean j hematol. 2010; 45(1): 73-75. 8. mandal r, bolt dm, shah bk. disparities in chronic myeloid leukemia survival by age, gender, and ethnicity in preand post-imatinib eras in the us. acta oncol. epub 2012, nov 26. 9. matsue k, aoki t, odawara j, kimura s, yamakura m, takeuchi m. haemorrhagic complications associated with reduced alpha2-plasmin inhibitor during imatinib use in a patient with philadelphia chromosome-positive acute lymphoblastic leukaemia. leuk res. 2009; 33(6): 867-869. 10. minette se, kimmel dw. subdural hematoma in patients with systemic cancer. mayo clin proc. 1989; 64(6): 637-642. 11. prasad bc, chandra vv, varaprasad g. dural metastases in chronic myeloid leukaemia presenting as subdural hematoma. turk neurosurg. 2012; 22(6): 777778 12. satyarthee gd, mahapatra ak. seizure as presentation of pituitary adenoma: a series of four patients. neuroscience today 2002; 6: 167-169. 13. song kw, rifkind j, al-beirouti b, yee k, mccrae j, messner ha et al. subdural hematomas during cml therapy with imatinib mesylate. leuk lymphoma. 2004; 45(8): 1633-1636. 14. vardiman j, harris n, brunning r. "the world health organization (who) classification of the myeloid neoplasms". blood 2002; 100 (7): 2292–2302 munivenkatappa_doesindia 104 munivenkatappa, agrawal does india have national tbi data? does india have national tbi population based & economic burden data, is it essential? ashok munivenkatappa1, amit agrawal2 1scientist c, vrdl project, national institute of epidemiology (icmr), chennai – 77 2department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) india is world's fastest-growing major economy. the economic survey for 2014-15, reports that both central and state government combined spends 1.2% of gross domestic product (gdp) on healthcare (1). currently indians spend about 1,000 per capita on healthcare (2). traumatic brain injury (tbi) is a lead cause of neurological disability in our country, where neurological disability is expected to be third epidemic in india (3). our nation lacks population based tbi data. in 2002, it was estimated that nearly 1.5 to 2 million persons are injured and 1 million succumb to death every year in india (4). currently there are no available accurate data at national level on cost of tbi-related disability in india. the economic loss due to rta was estimated at nearly inr 550 billion every year (5). the tbi injuries and economic loss are only approximate values. rapid economic growth, better healthcare to public and more research activities will raise capital consumption, which is now highly expected. despite recent hikes in healthcare, data on tbi population survey and expenditure is relatively low or nil. developed countries have details of epidemiology, economic consequences and disease burden of tbi population. a study from netherlands has estimated tbi incidence of 213.6 per 100,000 person years. the total cost was €314.6 million per year and disease burden resulted in 171,200 disability-adjusted life years (on average 7.1 dalys per case) (6). a five year study from shahid rajaei trauma hospital, iran reported the economic burden of tbi; 6.2 billion rials of hospital costs, 6390 potential years of life lost, and 506 billion rials of productivity lost. the reports were very much helpful in optimizing healthcare policy and preventing tbi. india has around 362 medical colleges of them approximately 59 colleges have neurosurgical department (7). nearly 90 biological science research institutes focus mainly on basic research of them only few biological research institutes are involved in brain injury research. the burden of tbi is increasing every year due to rapid increase in motorization, industrialization and urbanization. with this enormous tbi resource and descent staff strength in our romanian neurosurgery (2016) xxx 1: 104 105 105 country the integrated insight on epidemiology, economic consequences and disease burden of tbi should be explored. multi institutional participation all over india is required to generate national level tbi population based data and economic burden. the data is very much crucial for developing country like india for better implementing health care guidelines and preventive strategies, as tbi is a major public health issue. correspondence dr. ashok munivenkatappa scientist c, vrdl project, national institute of epidemiology (icmr), chennai – 77 email id: ashokmphdns@gmail.com phone no. +91-9844250897 references 1. budget 2015: in search of an effective healthcare system. by neelam m kachhap on april 9, 2015. http://www.financialexpress.com/article/healthcare/cove r-story-healthcare/budget-2015-in-search-of-aneffective-healthcare-system/62145/b 2. government to hike health care investment to 2.5% of gdp by 2020. health cess recommended; public health care to be primary focus. nitin sethi, new delhi august 19, 2015. http://www.business-standard.com/article/economypolicy/government-to-hike-health-care-investment-to2-5-of-gdp-by-2020-115081900035_1.html 3. das a, botticello al, et al. neurologic disability: a hidden epidemic for india, neurology 2012, 79, 2146-7. 4. gururaj g. -epidemiology of traumatic brain injuries: indian scenario, neurological research 2002, 24, 24-8. 5. gururaj g. -road traffic deaths, injuries and disabilities in india: current scenario, natl med j india 2008, 21, 14– 20 6. scholten ac, haagsma ja, et al. traumatic brain injury in the netherlands: incidence, costs and disabilityadjusted life years. plos one 2014, 9, e110905. 7. ganapathy k. neurosurgery in india: an overview. world neurosurg 2013, 79, 621-8. 3radoimugurel_surgerypetroclival romanian neurosurgery (2015) xxix (xxii) 1: 27 37 27 surgery of petroclival meningiomas. recent surgical results and outcomes mugurel radoi1, florin stefanescu1, ram vakilnejad2, lidia gheorghitescu2, daniela rosu2 1umf “carol davila” bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases – bucharest 2neurosurgical department of the national institute of neurology and neurovascular diseases bucharest abstract: petroclival meningiomas represent only 10% of all meningiomas located in the posterior fossa, but are some of the most formidable challenges in skull base surgery. we described our recent experience (2005-september2014) regarding the surgery of these tumors. we retrospectively analyzed surgical results and outcome in 11 cases of petroclival meningiomas. most common symptoms in our series were headache and gait disturbance, while cranial nerves palsies represented the most common presenting signs. there were 8 females and 3 males, and the mean age was 52 years. surgical approaches chosen for petroclival meningiomas in our series were retrosigmoid (9 patients) and subtemporal transtentorial (2 patients). we achieved total tumor resection in 5 cases (45%) and subtotal resection in 6 cases (55%). overall outcome (total/subtotal resection) was good in 6 cases, fair in 3 cases and poor in one case. one postoperative death occurred due to hemorrhagic midbrain infarction (9%). complications were usually related to cranial nerve deficits: loss of hearing (2 patients), paresis of trochlear nerve (1 patient), trigeminal nerve (3 patients) and facial nerve (1 patient). in 4 patients these cranial nerves deficits were transient. in one case, a patient developed postoperative hydrocephalus and needed shunt placement. despite the fact that complications can be disastrous, we considered that an appropriate approach, combined with microsurgical techniques and a better understanding of the anatomy, greatly decrease the incidence and severity of complications and make feasible a total tumor resection. key words: petroclival meningiomas, surgery, retrosigmoid approach, subtemporal approach, outcome introduction of the meningioma of the basal posterior cranial fossa, petroclival meningiomas offer the greatest technical challenge to the neurosurgeon, because of their proximity to the brain stem, cranial nerves iii to xii, and 28 radoi et al surgery of petroclival meningiomas arteries of the posterior circulation. on autopsy, based on the site of their dural attachment, castellano and ruggiero classified meningiomas of the posterior fossa into five groups: cerebellar convexity, tentorium, posterior surface of the petrous bone, clivus and foramen magnum (4). based on intraoperative observations, yasargil et al. differentiated the posterior fossa meningiomas in clival (medial origin), petroclival (origin at the petrous tip, medial to the v nerve), sphenopetroclival (origin at meckel’s cave), foramen magnum and cerebellopontine angle (22). currently, the differentiation between clival, petroclival and sphenopetroclival meningiomas is based on natural history and surgical anatomy (1, 5, 6, 12). al-mefty and smith (2) emphasized that only those meningiomas arising medial to the trigeminal nerve should be included in the petroclival group to differentiate them from those arising more laterally; the latter may be included in the broad family of cerebellopontine angle meningiomas, which are easily removed. a more recent petroclival meningiomas classification was proposed by kawase in 1996 (10), according to the main attachment and trigeminal nerve deviation: upper clivus, cavernous sinus, tentorium and petrous apex meningiomas. in this study, we described our recent experience (2005-september2014) regarding the surgery of these tumors. material and methods we reported our experience referring on eleven consecutive cases of petroclival meningiomas operated in our department in the last ten years. we performed a retrospective review analyzing clinical and imaging data, surgical records, postoperative results and follow-up records. there were 8 females and 3 males in this series and the mean age was 52 years. preoperative clinical signs were as follows: headache (82%), cerebellar signs (63.6%), pyramidal signs (45.45%), facial pain (27.3%), facial numbness (45.45%), facial paresis (27.3%), hearing disturbances (54.54%), diplopia (27.3%) and lower cranial nerve dysfunction (18.2%). as preoperative evaluation, patients performed contrast cerebral tomography (ct), magnetic resonance imaging (mri) with or without gadolinium enhancement, and, in selected cases, cerebral angiography. imaging studies showed exact location and extent of the tumor, relationship to the surrounding neural structures (brain stem and cranial nerves) and possible encasement of cerebral vessels. there were 4 sphenopetroclival meningiomas and 7 petroclival meningiomas. all patients were treated surgically in one single operation. main aspects when choosing the surgical approach were goals of resection and extent of basal attachment (supra and/or infratentorial). in this series, most suitable and familiar approaches were chosen for surgical resection of meningiomas. a retrosigmoid approach was performed in 9 patients, while subtemporal transtentorial approach was suitable for 2 patients. degree of tumor extension was assessed by simpson grading scale for meningiomas. functional status was determined using karnofsky performance scale (kps). mean follow-up was 38 months (range 10 to 64 mo). romanian neurosurgery (2015) xxix (xxii) 1: 27 37 29 results there were 4 (36.37%) sphenopetroclival meningiomas and 7 (63.67%) petroclival meningiomas. we achieved total resection of the meningioma in 5 cases (45%) and subtotal resection in 6 cases (55%). macroscopically complete removal of the petroclival meningioma, simpson grade i to iii, was achieved in 5 out of 11 cases, as follows: grade i – 1 patient, grade ii – 3 patients and grade iii – 1 patient (table 1). in the rest of 6 patients, a partial removal of the meningioma was performed (simpson grade iv). most frequently encountered early surgical complication were related to cranial nerve paresis (ophthalmic paresis, facial paresis, hearing loss and ix, x cranial nerve deficits). most of them were transitory (table 2). table 1 grade of tumoral resection in our series meningioma extension surgical removal total total subtotal sphenopetroclival 2 (50%) 2 (50%) 4 (36.37%) petroclival 3 (43%) 4 (57%) 7 (63.67%) clival 0 0 0 total 5 (45%) 6 (55%) 11 (100%) table 2 surgical related complications in our series surgical related complication early late ophthalmic paresis 4 1 (n. iv) facial paresis 4 1 hearing loss 2 2 lower cranial nerve deficits 3 1 worsening of motor deficits 2 1 newly motor deficits 2 1 ataxia 1 0 hydrocephalus (vp shunt) 1 1 local csf leak 1 0 meningitis 0 0 total 21 9 postoperative hydrocephalus needing ventriculo-peritoneal shunt was encountered in one patient. there was one death recorded, in the 5th postoperative day, due to an important hemorrhagic midbrain infarction. according to karnofsky performance scale (kps), in our series, postoperative results were good in 7 (63.64%) patients (kps 80-100; patient is independent), poor in 2 (18.2%) patients (kps 50-70; patient requires assistance) and very poor in 1 (9%) patient (kps 30-40; patient severely disabled). 30 radoi et al surgery of petroclival meningiomas figure 1 (a, b, c, d, e, f) preoperative axial and coronal gadolinium enhanced mri images of a 52 years old female with a sphenopetroclival meningioma, admitted with 6th cranial nerve palsy and left trigeminal neuralgia; (g, h) postoperative axial and coronal gadolinium enhanced mri images after total resection of the meinigioma through a subtemporal approach with minimal incision of the tentorium romanian neurosurgery (2015) xxix (xxii) 1: 27 37 31 figure 2 (a) preoperative axial gadolinium enhanced mri images of a 43 years old female with petroclival meningioma, admitted with headache, facial numbness and hearing disturbances; (b) postoperative contrast cerebral ct scan showing complete microsurgical resection of the meningioma 32 radoi et al surgery of petroclival meningiomas figure 3 – (a) preoperative contrast cerebral ct scan showed a petroclival tumor, in a 60 years old female admitted with headache, ataxia, left facial numbness and hearing disturbances; (b) – postoperative contrast cerebral ct scan showed complete microsurgical resection of the tumor (histological result – trigeminal schwanoma) figure 4 – incomplete resection of a left petroclival meningioma in a 69 years old male. he was admitted with facial paresis, mild lower cranial nerves dysfunction, right hemiparesis and ataxia. we performed a subtotal resection through a left retrosigmoid approach; at 40 months follow-up control, he presented with hydrocephalus, but refused surgical treatment romanian neurosurgery (2015) xxix (xxii) 1: 27 37 33 discussion clival meningiomas arise from the superior two-thirds of the clivus and displaced the brainstem and basilar artery posteriorly. petroclival meningiomas are located along the superior two-thirds of the clivus and medial to the fifth cranial nerve; they displaced the brain stem and the basilar artery to the contralateral side (22). the sphenopetroclival meningiomas also arise along the spheno-occipital synchondrosis and displace the brain stem to the contralateral side; these tumors extend into the supratentorial compartment typically invading the lateral wall of the cavernous sinus (13). detailed preoperative radiologic work-up of a patient with petroclival meningioma is essential. magnetic resonance imaging (mri) with contrast enhancement provide information about exact location and extent of the meningioma, relationship to the surrounding neural structures (brain stem and cranial nerves), the possible encasement of cerebral vessels and any involvement of the cavernous sinus and temporal bone. cerebral angiography with visualization of the both carotid and vertebral circulation is a very important component of the preoperative plan. it demonstrates the blood supply of the meningioma and its angiographic relation with the basilar artery (frequently the basilar artery is pushed posteriorly and to one side), and the posterior cerebral and superior cerebellar arteries, which are usually elevated on the same side of the tumor (8). such tumors, often wedge in the brain stem, may encase cranial nerves and basilar and carotid arteries and their roots, perforate the dura, and invade the underlying bone (table 3 and table 4) (3). advances in microsurgery and approaches to the skull base have made their removal easier and less conducive to iatrogenic damage. surgical morbidity remains consistent in all contemporary published series (17, 21, 23), and in clinical reality there are still a number of patients, operated for this type of meningiomas, that are not satisfied with the “outcome and surgeon’s performance”. for the neurosurgeon there are two main aspects to consider: (a) – the tumor is benign and cause relative mild neurological symptoms with which the patient can learn to live and (b) – for their removal major surgery is required, with risk that the patient will be neurologically worse after surgery. (3). in surgery of petroclival meningiomas, bone removal may be necessary to facilitate medial exposure and minimize retraction of neural structures. more medial meningioma’s attachment, more lateral the bone removal is necessary for exposure. the best surgical approach is that which expose and enable immediate interruption of the tumor blood supply at the base of the skull (6). extension beyond the tentorial hiatus needs supratentorial exposure. we sustain that the best treatment for petroclival meningioma is trying to perform a radical surgical removal during the first operation. when subtotal removal of the meningioma must be accepted, a good outcome may still result, because these are slow-growing tumors, allowing the patient to have a functional survival. 34 radoi et al surgery of petroclival meningiomas table 3 position of the cranial nerves in posterior skull base meningiomas meningiomas cranial nerves iii iv v vi vii,viii ix,x,xi petroclival superior medial superior lateral posterior superior medial anterior posterior inferior posterior anterior petrous medial superior superior medial anterior medial medial anterior posterior inferior inferior posterior petrous anterior anterior anterior anterior inferior jugular foramen medial superior posterior lateral foramen magnum posterior superior posterior posterior superior (bricolo a, turazzi s. petroclival meningiomas. in schmidek and sweet (ed): operative neurosurgical techniques. new york: w.b. saunders company, 2000, pp. 932-955) (3) table 4 position of the arteries in posterior skull base meningiomas meningioma posterior cerebral artery superior cerebellar artery basilar artery aica pica vertebral artery petroclival superior medial superior medial posterior medial posterior medial posterior inferior posterior inferior anterior petrous superior medial medial medial anterior medial inferior medial medial posterior petrous anterior medial anterior anterior anterior medial jugular foramen medial superior inferior medial inferior foramen magnum superior posterior posterior lateral aica – anterior inferior cerebellar artery; pica – posterior inferior cerebellar artery (bricolo a, turazzi s. petroclival meningiomas. in schmidek and sweet (ed): operative neurosurgical techniques. new york: w.b. saunders company, 2000, pp. 932-955) (3) in elderly patients, small and asymptomatic meningiomas can be observed and followed with neurologic exams and mris. various approaches have been used to resect these meningiomas. most common of them are frontotemporal transsylvian (pterional) or subtemporal, posterior transcavernous (with removal of the petrous romanian neurosurgery (2015) xxix (xxii) 1: 27 37 35 apex), transtemporal approaches (presigmoid or transsigmoid retrolabyrinthine, translabyrinthine and transcochlear), retrosigmoid and petrosal approach (7, 14, 18). when choosing a surgical approach the following must be taken into consideration: (a) location of skull base attachment (upper/mid/lower clivus and medial/lateral), (b) extent of basal attachment (eg. supra/infratentorial), (c) preoperative cranial neuropathies (especially status of hearing) and (d) goals of resection. (6). for the most of our cases, we chose retrosigmoid craniotomy which is simple and rapid to perform offers access primarily to the midclival region and is well suited for tumors that are more laterally situated with a limited area of dural attachment. in two cases, with supratentorial extension of the tumor involving the internal carotid artery, we performed a frontotemporal craniotomy with wide splitting of the sylvian fissure, which offered access to the dorsum sellae and posterior clinoid region. in 1977, hakuba et al. (7), reviewing the neurosurgical literature found 44 cases of petroclival meningiomas, of which 31 had been treated surgically: total removal was achieved in only 3 patients, and 17 died within the first month of the postoperative period. in his personal series, hakuba had six cases of total removal and only one death. their results represented a turning-point in the use of surgery for these formidable lesions (7). in 1980, on a series of 20 cases of clival meningiomas, yasargil et al.(22) reported better results. there were 7 patients with total resection, and the outcome were good (selfsupporting and working) in five and fair in two. of the 13 subtotal resection, the outcome were good (fully employable) in six cases, fair in three cases, poor in two cases, with two mortalitie (22). in 1991, kawase et al. reported on a series of ten patients with sphenopetroclival meningiomas on whom they used the anterior transpetrosaltranstentorial approach; total resection was achieved in 7 patients with no postoperative mortality (11). based on a series of 52 patients with petroclival meningiomas, sekhar and javid (9) reported in 1991 their results using a variety of skull base approaches. they achieved total tumor resection in 38 cases (73%), subtotal resection in 11 (21%), and partial resection in 3 (6%) with 2 postoperative mortalities. in 1992, samii and tatagiba reported successful total removal in 27 (75%) of the 36 patients with petroclival meningiomas on whom they operated between 1978 and 1990; they had no postoperative death, and in 83%, no severe morbidity (16). more recent series have also reported zero mortality (1, 19, 20, 23). the reported rate of total tumor resection has increased from a low 25% up to 86% (1, 14, 20, 22). in our series, of 11 cases of petroclival meningioma, total resection was achieved in 5 patients (45%). good results were obtain in 7 (63.64%) patients (self-supporting), fair in 2 (18.2%) patients (require assistance), and very poor in 1 (9%) patient (severely disabled). complication related to surgical management of petroclival meningiomas remains as high as 50% and usually are related to cranial nerve deficits that are transient in the majority of cases (1, 15, 19, 20, 22). the most serious complications are related to brain 36 radoi et al surgery of petroclival meningiomas stem injury, which is very severe and is usually due to compromise of the blood supply to the brain stem (1, 15, 22). in the most recent series, these complications have decreased due to the use of microsurgical techniques and a better understanding of the anatomic behavior of these tumors (20). depending on the size of the petroclival meningioma, any of the cranial nerves can be injured during surgery in a retrosigmoid approach (17). the trochlear nerve can be injured because of its softness, especially in its subarachnoid course in the ambient cistern (18). complete injury to the trigeminal nerve is less frequent due to its large size, but a trigeminal nerve paresis is a frequent occurrence. because the facial nerve is usually displaced posteriorly by the tumor, it is injured especially in large size petroclival meningioma (17, 18, 20). loss of hearing is common with patients with petroclival meningiomas. if the hearing is normal, it is very important to use the appropriate approaches to preserve this function. injury to the vagus or glossopharyngeal nerves leads to significant compromise in the cough and gag reflex, and, as a result, serious pulmonary complications (13, 20). in our series, the mortality rate was 9% (1 patient) due to hemorrhagic midbrain infarction. paresis of the ophthalmic and facial nerve were the most frequent encountered (36,4%), but only 9% of patients presented permanent deficits. conclusions many surgical approaches have been advocated for complete resection of petroclival meningiomas. for each case, planning the safest approach should be sustained on: goals of resection, location and extent of basal attachment, preoperative cranial neuropathies. despite the fact that complications can be disastrous, we considered that an appropriate approach, combined with microsurgical techniques and a better understanding of the anatomy, greatly decrease the incidence and severity of complications and make feasible a total tumor resection. the conventional and easy suboccipital retrosigmoid approach is suitable for total removal of petroclival meningiomas, and, in selected cases, a combined, supra/infratentorial approach can be chose. correspondence mugurel radoi umf “carol davila” bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases bucharest email: muguradoi@yahoo.com references 1.al-mefty o, fox jl, smith rr. petrosal approach for petroclival meningiomas. neurosurgery 1988;22:510-517. 2.al-mefty o, smith rr. clival and petroclival meningiomas. in al-mefty o (ed): meningiomas. new york: raven press , 1991, pp 517-537. 3.bricolo a, turazzi s. petroclival meningiomas. in schmidek and sweet (ed): operative neurosurgical techniques. new york: w.b. saunders company, 2000, pp. 932-955. 4.castellano f, ruggiero g. meningiomas of the posterior fossa. acta radoil (suppl) 1953;104:1-157. 5.cherington m, schneck sa. clivus meningiomas. neurology 1966;16:86-92. 6.couldwell wt, weiss mh. surgical approaches to petroclival meningiomas. part i: upper and midclival approaches. contemp neurosurg 1994;16:1-6. 7.hakuba a, nishimura s, tanaka k, kishi h, nakamura t. clivus meningioma: six cases of total removal. neurol med chir (tokyo) 17:63, 1977 romanian neurosurgery (2015) xxix (xxii) 1: 27 37 37 8.iacob g, craciun m, tene s. microsurgical removal of posterior petrosal and petroclival meningiomas: a report of 8 cases. romanian neurosurgery 2011, vol. xviii,no.2 9.javid, t., sekhar, l. n. surgical management of clival meningiomas. acta neurochir. (wien.), 53: 171-182, 1991. 10.kawase t, shiobara r, ohira t, toya s. developmental patterns and characteristic symptoms of petroclival meningiomas. neurol med chir (tokyo) 1996 jan; 36(1):1-6. 11.kawase t, shiobara r, toya s. anterior transpetrosaltranstentorial approach for sphenopetroclival meningiomas: surgical method and results in 10 patients. neurosurgery 28:869, 1991. 12.mayberg mr, symon l. meningiomas of the clivus and apical petrous bone: report of 35 cases. j neurosurg 1986;65:160-167. 13.pieper dr, al-mefty o. the surgical management of petroclival meningiomas. in kaye ah and black pmcl (ed): operative neurosurgery. new york: churchill livingstone press, 2000, pp 559-574. 14.sakaki s, takeda s, fujita h, otha s. an extended middle fossa approach combined with a suboccipital craniectomy to the base of the skull in the posterior fossa. surg neurol 28:245, 1987. 15.samii m, ammirati m, mahran a, bini w, sephernia a. surgery of petroclival meningiomas:report of 24 cases. neurosurgery 24:12, 1989 16.samii m, tatagiba m. experience with 36 surgical cases of petroclival meningiomas. acta neurochir 118:27, 1992. 17.samii m, tatagiba m, carvalho ga. resection of large petroclival meningiomas by the simple retrosigmoid route. j clin neurosci 1999;6:27-30 18.sekhar ln, estonillo r. transtemporal approach to the skull base: an anatomical study. neurosurgery 19:799, 1986. 19.symon l. surgical approaches to the tentorial hiatus. in krayenbuhl h, ed. advances and technical standards in neurosurgery. vol 9. vienna: springer-verlag. 1982, pp. 69. 20.tahara a, de santana pa jr, calfat maldaun mv, panagopoulos at, da silva an, zicarelli ca, pires de aguiar ph. petroclival meningiomas: surgical management and common complications. j clin neurosci 2009, 16:655-65. 21.tatagiba m, acioly ma. retrosigmoid approach to the posterior and middle fossae. in ramina r, aguiar p, tatagiba m – samii’s essentials in neurosurgery, 2008;14, 146. 22.yasargil mg, mortara rw, curcic m. meningiomas of basal posterior fossa. in krayenbuhl h, ed. advances and technical standards in neurosurgery, vol. 7 vienna;springer-verlag, 1980;1-115. 23.wu zb, yu cj, guan ss. posterior petrous meningiomas: 82 cases. j neurosurg 2005;102: 284-9. doi: 10.33962/roneuro-2021-003 odontogen frontoparial epidural and subdural empyema complicated with frontal intracerebral abscess and covid. case report d. balasa, a. tunas, a.v. stan romanian neurosurgery (2021) xxxv (1): pp. 20-24 doi: 10.33962/roneuro-2021-003 www.journals.lapub.co.uk/index.php/roneurosurgery odontogen frontoparial epidural and subdural empyema complicated with frontal intracerebral abscess and covid. case report d. balasa, a. tunas, a.v. stan department of neurosurgery, clinical emergency hospital “sfantul andrei”, constanta, romania abstract introduction: cerebral infections (frontoparietal extradural and subdural empyema) following a dental abscess and multiple sinusitis is a rare and potentially devastating entity even in the era of modern diagnosis and treatment. case presentation: we present a patient with parietal epidural and subdural empyema and intracerebral frontal abscess, sinusitis and dental abscess, chronic consumer of alcohol and with neglected diabetes mellitus. he was initially diagnosed with encapsulated hematoma and sinusitis. the pus obtained at the intervention was certified by our laboratory as sterile with the consequent difficulty in antibiotic treatment and who induced a longer antibiotic treatment, a second surgical intervention for an encapsulated frontal abscess, a longer hospitalisation and favoured contamination with covid 19. despite these, the patient had a finally good evolution. conclusions: a frontoparietal extradural and subdural empyema and an intracerebral frontal abscess produced by a dental abscess and sinusitis is a rare and potentially lethal complication. the multidisciplinary approach between radiologist, neurosurgeon, otolaryngologist, dentist, microbiologists is mandatory for a proper diagnosis and treatment of these pathologies. introduction sinusitis is an important and underrated source of intracranial infection (41% to 67%) . even with modern improvements of diagnosys and treatment mortality from intracranial sinusitis-associated infection in the pre-ct era was 66%9but have decreased in the post-ct scan era to 5-40%. case report a 42 years old patient was admitted in our hospital for diffuse headache,vertigo, nausea, vomiting, ethanolic halene, amnesia. no signs of head trauma. anamnesis: chronic ethanolic consumer, glicemia 270 mg/dl in 2018 uncontrolled from diabetologist. emergent ct scan of the head revealed right parietal encapsulated subdural hematoma keywords subdural empyema, intracerebral abscess, sinusitis corresponding author: daniel balasa clinical emergency hospital “sfantul andrei”, constanta, romania balasadaniel100@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 21 odontogen frontoparial epidural and subdural empyema complicated with frontal intracerebral abscess and covid (7 mm initially), right frontal contusion, right maxilar, right frontal, sfenoidal sinusitis, superior right premolar abscess. the patient was initially treated conservative with analgetics, neurotrophics, b vitamines, antibiotics for sinusitis. the ent specialist and the dentist apreciated that they will treat the sinusitis and the dental abscess after the neurosurgical colection will be healed. despite the medical treatment the neurological status worsened within a few days with grand mal seizures, left hemiparesis, meningismus, photophobia . a new ct scan was performed and revealed the increasing of subdural colection with a maximum diameter of 14 mm in parietal area. figure 1. hypodense subdural right parietal collection (yellow arrow) he underwent evacuation of an epidural and subdural parietal empyema (mainly subdural) by right parietal craniectomy because of osteomielitis of cranial bone . frank pus (sterile-because of initial antibiotic treatment for acute sinusitis) was drained and cortical suface was proper washed with diluted betadine. post-operative, he was treated with intravenous antibiotics (meropenem, vancomycin and metronidazol.) despite of a favorable imediate postoperative evolution, the patient had multiple left motor jacksonian epilepsias. the ct scan with and without contrast revealed right dental abscess with lysis of right maxilar floor and medial maxilar wall, maxilar sinusitis, right frontal sinus and right frontal bone osteolysis, right frontal sinusitis, right frontal cerebral abscess. figure 2. axial ct scan. bone window. 1 5 right dental abscesses with lisis of the right maxilar floor and acute maxilar sinusitis (blue arrow). figure 3. axial ct scan. bone window. right frontal sinus and right frontal bone osteolysis (black arrow). figure 4. coronal ct scan. bone window ostyeolysis of the floor and medial wall of the right maxilar sinus, acute maxilar sinusitis (pink arrow). the mri scan of the head revealed encapsulated right cerebral frontal abscess compressive on the ventricular median structures. 22 d. balasa, a. tunas, a.v. stan figure 5. mri axial t2. encapsulated right frontal abscess (red arrow) compressive on the frontal ventricular horns. a new surgical intervention was performed with cerebral frontal abscess microsurgical exeresis and frontoparietal craniectomy. his neurological condition improved gradually and the follow up ct showed improvement of mass effect and cerebral edema. figure 6. postoperative axial ct scan -exeresis of empiema and frontal abscess. there is some residual edema. acute fronto-etmoidal sinusitis and dental abscess are not cured yet. after 8 weeks of treatment the patient developed cough, expectoration and hypoventilation (spo2 93%). ct scan of the chest revealed veiling areas “in matte glass” in the left upper lobe, subpleural with infectious substrate. the covid test was positive. the patient was transferred and treated 21 days in a covid hospital. the neurological status at the transfer moment was: residual left pyramidal syndrome, left brachial paresis (asia 4/5) in progressive recovery. after 21 days of treatment the patient was healed of covid and the brachial paresis disappeared. follow up: 3 months period we hope good result of ent and dental treatment to finally eradicate the infection and we scheduled a cranioplasty with titan mesh after one-year period. discussion ent brain abscess has a 3.2-to-i male predominance1. although there are many causes of infections of the head and neck, odontogenic are the most common type, with over 53% being found as the main source of deep neck infections2. sinusitis is an important and underrated source of intracranial infection (41% to 67%)3 . even with modern improvements of diagnosys and treatment mortality from intracranial sinusitis-associated infection in the pre-ct era was 66%4 but have decreased in the post-ct scan era to 5-40%5. in our case the patient has had amnesia, so we (neurosurgeons and radiologists) didn’t excluded a traumatic etiology, despite the absence of signs of cranial trauma and the presence of sinusitis. the rarely encountered complications of bacterial sinusitis are subdivided into local manifestations (like mucocele, pyocele and recurrence) and extension of sepsis to the adjacent orbital or intracranial structures. orbital complications include orbital cellulitis,subperiosteal abscess, intra-orbital abscess and osteomyelitis6,7. the intracranial complications comprise of meningitis, encephalitis,epidural or subdural empyema, cerebral abscess and cavernous or other dural venous sinuses thrombosis4. subdural empyema, however, is much strongly associated with underlying sinusitis and is also the most common sinusitis-associated intracranial infection6,7. from the sinonasal region the infection can spread through direct or indirect routes. the direct spread occurs following the erosion of sinus wall or through preformed pathways like congenital or acquired skull defects (as seen in ise associated with 23 odontogen frontoparial epidural and subdural empyema complicated with frontal intracerebral abscess and covid trauma and neurosurgical procedures8) and the natural skull foramina9. the more commonly implicated mechanism however is the indirect spread via retrograde septic thrombophlebitis of valveless emissary veins or endolymphatic channels10. compared with other causes of intracranial suppuration, a greater proportion of subdural empyemas (41% to 67%) result from sinusitis.3 brain abscesses and epidural abscesses typically have a more indolent presentation9. the anatomical considerations mentioned above are important determinants of the clinical course. for example, purulence in the epidural space is constrained by the dura, which is adherent to the calvarium. therefore, clinical presentation of epidural abscess is insidious with fever and headache evolving over weeks. by contrast, seeding of the subdural space leads to rapid spread of purulence because of lack of anatomical constraints4. the most common symptoms in patients presenting with intracranial complications are fever and headache4. altered mental status and focal neurological deficits are frequent. seizures occur in 8–20% of cases11. other symptoms include meningismus, decreased visual acuity or other ocular complaints including photophobia4. most intracranial complications result from frontal, ethmoid, or sphenoid3sinusitis; sinusitis is often bilateral11. long term sequelae of sde include hydrocephalus, residual hemiparesis and epilepsy. ct is the imaging modality of choice9. initial ct may be negative or nonspecific10. medical management of subdural empyema includes early initiation of antibiotic therapy, antioedema measures and treatment of associated seizures. in most cases the medical management alone is insufficient and associated with high mortality8,14. early surgical intervention by burr hole or craniotomy evacuation is the key to early recovery and salvage of maximal neurological function.4. in addition to drainage of intracranial purulence, definitive management of the infected sinuses should be done, preferably at the same time as empyema drainage4. odontogen abscess must be prevented by a rapid diagnosys and combined treatment surgical and medical of dental absess and sinusitis11 in our patient, the ent experts and dentists decided to treat (surgically) the sinusitis and dental infection after the healing of cerebral infection. the combination of improvement of investigations and management strategies have decreased mortality of intracranial infection to 49%12,13. the intracerebral frontal abscess formation was determined by the result of pus culture: sterile and in consequence the difficulty of finding an adequate antibiotic9,5 and the lack surgical treatment of synodental infections. prolonged spitalisation of this patient increased the risc of covid contamination. conclusions if the cranial ct scan reveals a sinusitis and a subdural/extradural hipodensity don’t forget the probability of empiema odontogen cerebral epidural and subdural empiema and cerebral abscess must be prevented by a rapid diagnosis and treated by combined concomitent treatment medical and surgical of empiema, dental absess and sinusitis as a gold standard. this should be realised by a mutidisciplinary approach between radiologist, neurosurgeon, otolaryngologist, dentist, microbiologist. consent written informed consent was obtained from the patient for publication of this case report and accompanying images. abbreviations ct scan computed tomography mri magnetic resonance imaging sde subdural empiema author’s contributions bd was the major contributor to writing the manuscript;tah: manuscript preparation, analysis, sav contributor of the manuscript preparation. all authors read and approved the final manuscript. acknowledgements this study received no funding conflicts of interest the authors declare no potential conflict of interest. references 1. pen-tung yen, shu-toa chan, tsun-sheng huang. brain abscess: with special reference to otolaringologic 24 d. balasa, a. tunas, a.v. stan sources of infection. otolaringology-head and neck surgery, july 1995,15. 2. martines et al. journal of medical case reports2014,8:2823.nathoo n, nadvi ss, van dellen jr, gouws e. intracranial subdural empyemas in the era of computed tomography: a review of 699 cases. neurosurgery 1999; 44: 529–35. 3. nathoo n, nadvi ss, van dellen jr, gouws e. intracranial subdural empyemas in the era of computed tomography: a review of 699 cases. neurosurgery 1999; 44: 529–35. 4. osborn mk, steinberg jp (2007) subdural empyema and other suppurative complications of paranasal sinusitis. lancet infect dis 7: 62-67. 5. moonis g, granados a, simon sl:epidural hematoma as a complication ofsphenoid 6.small m, dale ba. intracranial suppuration 1968–1982: a 15 year review. clin otolaryngol allied sci 1984; 9: 315–21. 6. small m, dale ba. intracranial suppuration 1968–1982: a 15 year review. clin otolaryngol allied sci 1984; 9: 315– 21. 7. younis rt, lazar rh, anand vk. intracranial complications of sinusitis: a 15-year review of 39 cases. ear nose throat j 2002; 81: 636–38. 8. yoon j, o’bryan cm, redmond m. intracranial subdural empyema – a mini review . j infectiology. 2020; 3(1): 1-5. 9. kombogiorgas d, seth r, athwal r, modha j, singh j (2007) suppurative intracranial complications of sinusitis in adolescence. single institute experience and review of literature. br j neurosurgery 21: 603-609. 10. kabilan chokkappan. rapidly developing subdural empyema in an adult with sinusitis-a neurosurgical threat alert!. emerg med (los angel) 2016, 6:2. 11. gallagher rm, gross cw, philips cd. suppurative intracranial complications of sinusitis. laryngoscope 1998; 108. 1635-42. 12. dill sr, cobbs cg, mcdonald ck. subdural empyema: analysis of 32 cases and review. clin infect dis. 1995; 20(2): 372-386. doi:10.1093/clinids/20.2.372. 13. widdrington jd, bond h, schwab u, et al. pyogenic brain abscess and subdural empyema: presentation, management, and factors predicting outcome. infection. 2018; 46(6): 785-792. doi:10.1007/s15010-018-1182. 14. bruner di, littlejohn l, pritchard a (2012) subdural empiema presenting with seizure, confusion, and focal weakness. west j emerg med 13: 509-511. gorganrm_raretype romanian neurosurgery (2016) xxx 1: 47 51 47 a rare type of tumor: orbital schwannoma. case report and literature review r.m. gorgan, angela neacsu, silvia mara baez rodriguez, g. popescu, catioara cristescu, a. giovani clinic of neurosurgery, “bagdasar – arseni” emergency clinical hospital, “carol davila” university of medicine and pharmacy, bucharest abstract: schwannomas arise in the cells responsible for the mielinating the neurons distal to the obersteiner-redlich zone. most of the intracranian schwannomas are in the posterior fossa, developed from the viiith or vth nerve stheath. the location on other cranian nerves is quite rare, only 6% of the orbital tumors being schwannomas. we review the case of a 52 years old male patient, presenting for right eye exophthalmia and visual field deficit, diplopia due to vith nerve paresis, and stubbing pain in the right eye, the mri showing a tumor, located in the orbital apex displaced the globe forward and superiorly, and the optic nerve medially and superiorly. a modified lateral orbital approach was preferred. the choice of the orbitotomy allowed us to maintain the integrity of the lateral rim of the orbit without the need of a bony reconstruction at the end of the intervention, as it faced the anterior margin of the temporal muscle, covering it and not the skin over the zigomatic bone. the technical approach for orbital schwanomas should be tailored to reach the lesion through an esthetic incision and orbitotomy, immediately under the resected bone, with no need retracting the ocular globe or the vasculonervous elements in the orbit. key words: schwannoma; lateral orbital approach introduction schwannomas arise in the cells responsible for the mielinating the neurons distal to the obersteiner-redlich zone. most of the intracranian schwannomas are in the posterior fossa, developed from the viiith or vth nerve stheath. the location on other cranian nerves is quite rare, only 6% of the orbital tumors being schwannomas. these tumors become symptomatic through the mass effect and usually the symptoms progress slowly over a few years mirroring the slow rate of growth. in a large series of 308 orbital tumors published in 1984 by j. maroon, the authors counted only 5 neurofibromas, the most often encountered orbital tumors being in order 48 gorgan et al orbital schwannoma metastasis, dermoid tumors, meningiomas and cavernomas. most patients with orbital tumors present with slowly progressive proptosis. a partial field cut, blurred vision and diplopia and papillary edema with or without optic atrophy can also be present though less frequent. differential diagnosis with other tumors or tumor like lesions should be obtained. the most common possible lessions resembling neurinomas are meningiomas, cavernomas and dermoid tumors, each presenting characteristic features on mri which should be sought with attention. the relation of the tumor with the optic nerve and the oculomotor muscles must be understood from the mri images before proceeding to resection. the tumor may be inside or outside the muscles cone, in the orbital apex or more excentrically situated. it may encircle the optic nerve or just displace it. the relation of the tumor with the orbit walls is very important in choosing the approach as the shortest way with the minimal risk of collateral damage should be chosen. in 1941 dandy introduced the subfrontal approach and nafzinger used the pterional transcranial approach for orbital tumors. over time with the tendency towards minimal invasiveness the extracranial approaches became more and more favored to transcranial approaches. these include lateral orbitotomy for tumors located lateral and basal to the optic nerve and in the orbital apex, transetmoidal for the extraconal tumors located medial to the, transmaxilary for basal lesions sitting on the maxillary sinus, or transconjunctival for basal intraconal tumors. the transcranial approaches remain in use nowadays for tumors developed both intracranian and intraorbitar or for tumors involving the optic canal. case report we review the case of a 52 years old male patient, presenting for right eye exophthalmia and visual field deficit, diplopia due to vith nerve paresis, and stubbing pain in the right eye. these symptoms evolved progressively during a few years. no signs and symptoms of recklinghausen disease were recognized. mri scan performed on admission showed a large inhomogeneous orbital tumor with central round areas of hypo intensity in both t1 and t2 and peripheral gadolinum enhancement. the tumor, located in the orbital apex displaced the globe forward and superiorly, and the optic nerve medially and superiorly. romanian neurosurgery (2016) xxx 1: 47 51 49 figure 1 preop mri showing a mix signal inferolateral orbital tumor that displaces superolaterally the optic nerve we preferred a modified lateral orbital approach. using an s shaped incision starting in the eyebrow and continued over the zigoma, we retracted the temporal muscle posteriorly and used a burr hole medial to the frontal process of the zigoma in the angle between the lateral and the inferior orbital walls. as this burr hole was performed over the tumor, only little enlargement of it with rongeurs was needed to mobilize the lesion circumferentially. using a small dissector, an extracapsular resection was performed detaching the tumor from the right lateral muscle displaced superiorly and from the optic nerve, displaced superomedially. the tumor was encapsulated, of a firm consistency and a pale white color. fortunately it was not attached to the surrounding structures and the capsule was easily dissected using a blunt instrument followed by a single piece excision of the lesion. the choice of the orbitotomy allowed us to maintain the integrity of the lateral rim of the orbit without the need of a bony reconstruction at the end of the intervention, as it faced the anterior margin of the temporal muscle, covering it and not the skin over the zigomatic bone. figure 2 enlarging the lateral orbital wall orbitotomy with a rongeur figure 3 extracapsular dissection of the tumor with a blunt instrument figure 4 total resection in a single piece 50 gorgan et al orbital schwannoma following an intradermal suture an ointment dressing was applied on the operated eye. the postoperative course was uneventful, the exophtalmy resolved almost completely as demonstrated on the postop. ct. and the visual field deficit improved. figure 5 postop ct showing complete tumor resection and lack of exoftalmus discussion the pathology diagnosis came much as a surprise as we expected a more frequent type of tumor like a metastasis, a meningioma or even a cavernoma yet the initial diagnosis was confirmed by the classic palisading pattern of tumor nuclei showed both on hematoxilineosine and s100 stain at the final exam. most of the orbital schwannomas develop from branches of the ophthalmic division of the trigeminal nerve thus being located superior and laterally or superior and medially to the optic nerve as described in an 18 years span study on 49 orbital schwannomas. the inferolateral location of the presented schwannoma indicates the abducens nerve as the site of origin. as the optic nerve is mielinated in a central like fashion from oligodendrocytes and not from schwan cells, it has been hypothesized that they arrise from the sympathetic plexus inervating the vessels feeding the optic nerve. (9, 10, 13) we described a modified krohnline approach with incomplete resection of the frontozigomatic arcade and an orbitotomy in the angle between the lateral and the inferior wall of the orbit after a good posterior retraction of the temporalis muscle. a classic lateral orbital approach would have been centered not on the tumor but on the superiorly displaced lateral rectus muscle. (2, 5, 6) most of the extracranian approaches to the orbit are based on the classical lateral orbitotomy described by kronlein in 1889. depending on the extension of the orbitotomy the lateral approach can open an extended though narrow surgical corridor from the lateral orbit to the superior orbital fissure, the optic canal and the cavernous sinus. (11, 12, 14) since the use of the ct scan and mri this tumors are diagnosed while they are confined to the orbit compared to the past when most of the orbital tumors presented an intracranian extension, henceforth the need for a transcranian approach either subfrontal preferred by dandy or pterional preferred by nafzinger. (3, 7, 8) the relation of the tumor with the optic nerve is the main thing to decide the approach romanian neurosurgery (2016) xxx 1: 47 51 51 as one should avoid an approach that crosses the on in its way to the tumor. in the presented case the tumor was behind the globe, under and lateral to the optic nerve. in 1993 a neurosurgical-ophtalmological team from duisburg described a transconjunctival approach for an intraconal orbitobasal large cavernoma. this technique allows tumor resection without bone or muscle resection. a transconjunctival approach could be taken into consideration in our case had the tumor been larger and bulging anteriorly from under the globe. the superior transcranian, transorbital roof approach and the endoscopic transetmoidal approach were not considered at all as the tumor was inferior and lateral to the optic nerve. as the tumor was intraconal with no intracranian or cavernous sinus extension there was no need for a transcranial approach. (1, 4) another combined approach with the help of an ent surgeon is the transmaxillary one, well suited for our case as the tumor was seated on the roof of the maxillary sinus. conclusion even if very rare, orbital schwannomas are well encapsulated tumors, which makes the resection simple and safe. the technical approach used should be tailored to reach the lesion through an esthetic incision and orbitotomy, immediately under the resected bone, with no need retracting the ocular globe or the vasculonervous elements in the orbit. references 1.abuzayed b, tanriover n, gazioglu n, eraslan bs, akar z: endoscopic endonasal approach to the orbital apex and medial orbital wall: anatomic study and clinical applications. j craniofac surg. 2009, 20:1594–1600. 2.al-mefty o, anand vk. zygomatic approach to skullbase lesion. j neurosurg. 1990;73(5):668-673. 3.arai h, sato k, katsuta t, rhoton al jr. lateral approach to intraorbital lesions:anatomic and surgical considerations. neurosurgery. 1996;39(6):1157-1162; discussion 1162-1163. 4.cappabianca p, cavallo lm, de divitiis e: endoscopic endonasaltranssphenoidal surgery. neurosurgery 55:933 941, 2004 5.ducic y: orbitozygomatic resection of meningiomas of theorbit. laryngoscope 114:164–170, 2004 6.fujitsu k, kuwabara t. zygomatic approach for lesions in the interpeduncular cistern. j neurosurg. 1985;62(3):340-343. 7.hakuba a, tanaka k, suzuki t, nishimura s. a combined orbitozygomatic infratemporal epidural and subdural approach for lesions involving the entire cavernous sinus. j neurosurg. 1989;71(5 pt 1):699-704. 8.maroon jc, kennerdell js. surgical approaches to the orbit. indications and techniques. j neurosurg. 1984;60(6):1226-1235. 9.nakayama k: studies on the myelination of the human optic nerve . jpn j ophthalmol. 1967, 11:18– 26. 10.natori y, rhoton al jr. microsurgical anatomy of the superior orbital fissure. neurosurgery. 1995;36(4):762775. 11.natori y, rhoton al jr. transcranial approach to the orbit: microsurgical anatomy. j neurosurg. 1994;81(1):78-86. 12.paluzzi a, gardner pa, fernandez-miranda jc, et al. “round-the-clock” surgical access to the orbit. j neurol surg b skull base. 2015;76(1):12-24. 13.pushker n, khurana s, kashyap s, sen s, shrey d, meel r, chawla b, bajaj ms: orbital schwannoma: a clinicopathologic study. int ophthalmol. 2014, 1-6. accessed: 4/10/2015: 14.sekhar ln, schramm vl jr, jones nf. subtemporalpreauricular infratemporal fossa approach to large lateral and posterior cranial base neoplasms. j neurosurg. 1987;67(4):488-499. tascual_newapproach romanian neurosurgery (2016) xxx 2: 147-153 | 147 new approach based on biomarkers in acute traumatic spinal cord injury al. tascu1, st.m. iencean2, a.st. iencean3 1“carol davila” university of medicine and pharmacy, bucharest, romania 2“grigore t. popa” university of medicine and pharmacy, iasi, romania 3neurosurgery, “prof n oblu” emergency hospital, iasi, romania abstract: spinal cord injury (sci) is one of the most devastating traumas for an individual because the complete traumatic spinal cord injury leads to paraplegia or tetraplegia. the mechanical injuries directly cause axonal destruction in fiber tracts, destruction of the neurons and of the glial cells, and their destruction releases substances whose presence, quantity and dynamics can be lesional biomarkers. the reactions of partially injured cells simultaneously start and the occurring substances and their quantity may be reaction biomarkers. the lesional biomarkers appear immediately postinjury and after several hours there are both lesional biomarkers and reaction biomarkers. the most important lesional biomarkers are the phosphorylated neurofilament subunits resulting from the axonal neurofilament destruction. the heavy phosphorylated neurofilament subunit (pnf-h) is a predictive lesional biomarker because its values pattern can show the reducing or stopping of the secondary lesions and the favorable outcome. the complete sci patients with a favorable development had a specific pattern of daily values of pnf-h: a sudden increase up to a maximum value then a progressive decrease to normal. the patients with unfavorable outcome or neurological stabilisation had two patterns: an increase to a plateau of pnf-h values or a progressive increase up to a peak followed by a progressive decrease to quasi-normal values. key words: lesional biomarker, phosphorylated neurofilament subunit, reactional biomarker, spinal cord injury introduction spinal cord injury (sci) is one of the most devastating traumas for an individual and their family because, depending on the level of injury, the complete traumatic spinal cord injury leads to paraplegia or tetraplegia. immediate traumatic spinal cord injury is the primary mechanical injury caused through the direct injury of the neurons, axons and blood vessels (compression, laceration, shearing and 148 | tascu et al biomarkers in acute traumatic spinal cord injury even transection of the spinal cord). after the injury event, the secondary injury mechanisms begin immediately and the secondary spinal cord lesions consist of hemorrhages, spinal cord edema, vasospasm and hypo-perfusion of the spinal cord and the damage of the spinal cord continues to progress for several days to weeks, and leads to the death of neurons and the interruption of the axonal tracts. many traumatic spinal cord injuries can be initially incomplete and the secondary damage completes the lesion of the spinal cord. spinal cord injuries are difficult to treat because of these secondary injuries. current therapy is unable to act on the primary mechanically lesion, but the secondary injury extension of the spinal cord could be stopped or reduced by an early efficient therapy. in sci the neurological examination brings the first very important information about the lesion and this directs imaging procedures to confirm the lesion. but because of the spinal shock, unstable condition of the patient, attendant injuries, alcohol or drugs etc., the clinical examination immediately following injury, even using the asia motor scores or other scales, cannot be considered reliable. these clinical examinations must be repeated, but they offer only static clinical states and no data about possible future development. biomarkers are measurable features that can be used to confirm the presence or to predict the severity of the disorders. biomarkers as biochemical indicators in sci can allow detection of the secondary lesion, can monitor its progress and predict the severity of sci and can also indicate the specific treatments required. in sci biomarkers detect the severity of injury within the first few hours and can direct the best patient care in a timely manner. in acute traumatic sci, the mechanical injuries directly cause axonal destruction in fiber tracts, destruction of the neurons in gray matter and of the glial cells. their destruction releases substances cellular constituents, whose presence, quantity and dynamics can be lesional biomarkers. detecting these protein changes, their quantity and dynamics may be biomarkers of response, or reaction biomarkers. correlating the lesional biomarkers and the reaction biomarkers with the clinical outcome and with the imaging techniques will enable understanding the complexity of the biological response to spinal cord injury and the establishment of appropriate therapies the lesional biomarkers appear immediately post-injury and their dynamics show the extension of the spinal cord injury and after several hours there are both lesional biomarkers and reaction biomarkers, involving the secondary cellular response to injury. biomarkers and the diagnostic value in sci in recent years a number of protein biomarkers have been evaluated to detect neuronal injury and recently there have been studies about their potential diagnostic and predictive value for spinal cord injuries. the concentration of specific proteins in blood or in the cerebrospinal fluid must be compared with the nervous tissue injury and these can be biomarkers for the pathologic processes in spinal cord injury. romanian neurosurgery (2016) xxx 2: 147-153 | 149 there are numerous experimental studies and a smaller number of clinical studies for determining and validating biomarkers in spinal cord injury: c-tau, myelin basic protein – mbp, neuron-specific enolase – nse, glial fibrillar acidic protein – gfap etc. new potential biomarkers were reported: the neurofilaments, the major cytoskeletal components in axon fibers. the most important are neurofilament subunit proteins (nf) that coassemble forming the cytoskeletal of axon fibers and they consist of five subunits of neurofilaments, named on the basis of molecular weight: heavy or highest (nfh, 200 – 220 kda), medium or middle (nf-m, 145-160 kda) and light or lowest (nf-l, 68-70 kda) subunits, also alpha-internexin subunit (nf66) discovered later than nf and the intermediate filament protein subunit peripherin. ueno et al. (2011) presented a rat model of acute spinal cord injury and they showed that the high-molecular-weight neurofilament subunit levels in plasma could be a biomarker for evaluating the efficacy of therapies for sci. hayakawa et al. (2012) studied the concentration of the phosphorylated neurofilament subunit nf-h (pnf-h) in plasma in patients with acute cervical sci and concluded pnf-h may be a prognostic biomarker for sci. the pnf-h concentration was measured by elisa test in csf in acute spinal cord injury patients and correlated the values of pnf-h with the clinical evolution. the phosphorylated form of the neurofilament subunit nf-h (pnf-h) is a biomarker in sci in humans and its increased values are consistent with an unfavorable outcome. the neurofilament subunit nf-h (pnf-h) is a lesional biomarker, it appears after the mechanical injury by axonal destruction in the fibers tracts. by now these studies have identified some potential biomarkers, but these biomarkers have not been validated and they still cannot be used in the clinical setting, for diagnosis, prognosis and evaluating therapeutic interventions. current status of biomarkers in traumatic spinal cord injury the research in traumatic spinal cord injury has been focused on the discovery of lesional biomarkers and lesser for reaction biomarkers. lesional biomarkers can be studied in patients with acute traumatic sci immediately after injury; reaction biomarkers occur after a short period post injury and after several hours post injury these two types of biomarkers coexist, and it is difficult to differentiate them. the study of reaction biomarkers involves cells around the lesion, which is not possible in patients with sci. therefore research is conducted on nerve cell cultures and there are experimental animal models, but the translation into human medicine is difficult because there are important differences. the most important studies on lesional biomarkers concerns the neurofilament subunit proteins (nf). the phosphorylated neurofilament subunit nf-h (pnf-h) was measured in the cerebro-spinal fluid of patients with spinal cord injury and it was demonstrated the correlation between the pnf-h levels and the severity of the injury. the study included subjects with acute traumatic spinal cord injury who underwent surgery during the first 150 | tascu et al biomarkers in acute traumatic spinal cord injury 24 hours post injury (decompression, stabilization): patients with complete spinal cord injury (sci) and patients with incomplete sci. the level of csf pnf-h was ten to a hundred times higher in complete sci than the level of csf pnf-h in cases with incomplete sci, where the level of this biomarker was close to normal. the patients with early surgery in complete spinal cord injury and with a favorable outcome had a specific pattern of daily values of pnf-h: a sudden increase up to a maximum value then a gradual decrease to normal; the peak was different in each case, from 10 times up to 170 times higher than normal. (figure 1) the same type of the pattern for the values of pnf-h appears in the incomplete spinal cord injury with favorable outcome, but with smaller values of pnf-h. there are two patterns in cases with unfavorable outcome or neurological stationary after the same early surgery and treatment: the second unfavorable pattern had a progressive increase up to a peak and then was followed by a progressive decrease to normal values, the peak was a hundred times higher than normal values (figure2), an increase to a plateau of pnf-h values, with increased values five or ten times higher than normal (figure 3). in patients with favorable development the progressive decrease of pnf-h values after the initial sudden increase, without extension of increased values in plateau or without a second peak, signifies a reduction or even a stop of the secondary lesion with evident effect on the favorable outcome in the spinal cord injury (figure 4). figure 1 pattern of daily value of pnf-h in patients with favorable outcome figure 2 pattern with progressive increase of pnf-h figure 3 pattern with increase up to a plateau of pnf-h romanian neurosurgery (2016) xxx 2: 147-153 | 151 figure 4 the three specific and predictive pattern of daily values of pnf-h in traumatic sci kato et al. (2015) investigated the phosphorylated form of the high molecular weight neurofilament subunit (pnf-h) levels in the serum in patients with cervical compressive myelopathy and they found an elevated serum level of pnf-h only in acute worsening of myelopathy and this study confirms that pnf-h is a lesional biomarker. kuhle et al. (2015) presented their results on a study of serum neurofilament light chain (pnf-l) in human spinal cord injury. they concluded that serum neurofilament light subunit (pnf-l) concentration in sci patients has a close correlation with acute severity and neurological outcome and it is of predictive value in sci patients. the presentation of these studies on biomarkers in sci highlights that the most important ones and those with significant results relate to lesional biomarkers, and first are the phosphorylated neurofilament subunits, light or heavy (pnf-l or pnf-h), resulting from the axonal neurofilament destruction. the research showed that the phosphorylated neurofilament subunit, light or heavy (pnf-l or pnf-h) in spinal cord injury is a specific lesional biomarker for spinal cord injury and it can distinguish the severity of sci. the heavy phosphorylated neurofilament subunit (pnf-h) is a predictive lesional biomarker because its values pattern can show the reducing or stopping of the secondary lesions and the favorable outcome. the complete sci patients with a favorable development had a specific pattern of daily values of pnf-h: a sudden increase up to a maximum value then a progressive decrease to normal. the patients with unfavorable outcome or neurological stabilization had two patterns: an increase to a plateau of pnf-h values or a progressive increase up to a peak 152 | tascu et al biomarkers in acute traumatic spinal cord injury followed by a progressive decrease to quasinormal values. conclusion these studies on biomarkers in spinal cord injuries highlights that the most important lesional biomarkers are the phosphorylated neurofilament subunits, light or heavy (pnf-l or pnf-h). the phosphorylated neurofilament subunits, (pnf-l or pnf-h) are specific lesional biomarkers for spinal cord injury and they can distinguish the severity of sci. the heavy phosphorylated neurofilament subunit (pnf-h) is a predictive lesional biomarker; its values pattern show the reducing or stopping of the secondary lesions and the favorable outcome. there is a specific pattern of daily values of pnf-h in complete sci patients with a favorable outcome: a sudden increase up to a maximum value then a progressive decrease to normal. also there are two patterns in the patients with unfavorable outcome: an increase to a plateau of pnf-h values or a progressive increase up to a peak followed by a progressive decrease to quasi-normal values. these specific patterns could be used to aid clinicians with making a diagnosis and establishing a prognosis, and evaluating therapeutic interventions. these studies should continue on larger groups of patients to prove the clinical usefulness. acknowledgements this work was funded by the cncs–uefiscdi romania, grant: “immediate neuroprotective therapy in acute traumatic spinal cord injury”, grant number: pn-ii-idpce-2011-3-0569. correspondence st.m. iencean “grigore t. popa” university of medicine and pharmacy, iasi, romania e-mail: mirceasteffan@yahoo.com references 1. burns as, marino rj, flanders ae, flett h. clinical diagnosis and prognosis following spinal cord injury. in: verhaagen j, mcdonald jw, editors. spinal cord injury. handbook of clinical neurology. volume 109, elsevier b.v; 2012. p. 47 – 62. isbn: 978-0-444-52137-8 2. tator ch, fehlings mg. review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. j of neurosurg. sp.suppl. 2010, vol. 112, no. 2 p15-26 3. liverman ct, altevogt bm, joy je, johnson rt, editors. spinal cord injury. progress, promise, and priorities. the national academic press, usa; 2005. 344p. isbn 0-309-09585-9 4. yokobori s, zhang z, moghieb a, mondello s, gajavelli s, dietrich wd, bramlett h, hayes rl, wang m, wang kk, bullock mr. acute diagnostic biomarkers for spinal cord injury: review of the literature and preliminary research report. world neurosurg. 2015; 83(5):867-78. 5. van dongen ep1, ter beek ht, boezeman eh, schepens ma, langemeijer hj, aarts lp. normal serum concentrations of s-100 protein and changes in cerebrospinal fluid concentrations of s-100 protein during and after thoracoabdominal aortic aneurysm surgery: is s-100 protein a biochemical marker of clinical value in detecting spinal cord ischemia? j vasc surg. 1998; 27(2):344-6. 6. van dongen ep, ter beek ht, schepens ma, morshuis wj, haas fj, de boer a, boezeman eh, aarts lp. the relationship between evoked potentials and measurements of s-100 protein in cerebrospinal fluid during and after thoracoabdominal aortic aneurysm surgery. j vasc surg. 1999;30(2):293-300. 7. kunihara t, shiiya n, yasuda k.changes in s100beta protein levels in cerebrospinal fluid after romanian neurosurgery (2016) xxx 2: 147-153 | 153 thoracoabdominal aortic operations.j thorac cardiovasc surg. 2001;122(5):1019-20. 8. basu s, hellberg a, ulus at, westman j, karacagil s. biomarkers of free radical injury during spinal cord ischemia. febs lett. 2001, 9; 508(1):36-8. 9. guéz m, hildingsson c, rosengren l, karlsson k, toolanen g. nervous tissue damage markers in cerebrospinal fluid after cervical spine injuries and whiplash trauma. j neurotrauma. 2003; 20(9): 853-8. 10. loy dn1, sroufe ae, pelt jl, burke da, cao ql, talbott jf, whittemore sr. serum biomarkers for experimental acute spinal cord injury: rapid elevation of neuron-specific enolase and s-100beta. neurosurgery. 2005; 56(2): 391-7. 11. kwon bk, casha s, hurlbert rj, yong vw. inflammatory and structural biomarkers in acute traumatic spinal cord injury. clin chem lab med. 2011;49(3):425-33. doi: 10.1515/cclm.2011.068. 12. kwon bk, stammers am, belanger lm, bernardo a, chan d, bishop cm, slobogean gp, zhang h, umedaly h, giffin m, street j, boyd mc, paquette sj, fisher cg, dvorak mf. cerebrospinal fluid inflammatory cytokines and biomarkers of injury severity in acute human spinal cord injury. j neurotrauma. 2010; 27(4): 669-82. doi: 10.1089/neu.2009.1080 13. pouw mh, hosman aj, van middendorp jj, verbeek mm, vos pe, van de meent h. biomarkers in spinal cord injury. spinal cord. 2009; 47(7): 519-25. doi: 10.1038/sc.2008.176. 14. ueno t, ohori y, ito j, hoshikawa s, yamamoto s, nakamura k, tanaka s, akai m, tobimatsu y, ogata t. hyperphosphorylated neurofilament nf-h as a biomarker of the efficacy of minocycline therapy for spinal cord injury. spinal cord. 2011; 49(3): 333-6. doi: 10.1038/sc.2010.116.. 15. hayakawa k, okazaki r, ishii k, ueno t, izawa n, tanaka y et al. phosphorylated neurofilament subunit nf-h as a biomarker for evaluating the severity of spinal cord injury patients, a pilot study. spinal cord 2012, 50, 493-496. doi:10.1038/sc.2011.184 16. iencean stm, adam d, ungureanu d, tascu al, cuciureanu d, costachescu b, iencean ast, poeata i. preliminary results of csf phosphorylated neurofilament subunit nf-h as biomarkers of acute spinal cord injury. romanian neurosurg.2013, xx; 4: 351 356 17. pouw mh, kwon bk, verbeek mm, vos pe, van kampen a, fisher cg, street j, paquette sj, dvorak mf, boyd mc, hosman aj, van de meent h. structural biomarkers in the cerebrospinal fluid within 24 h after a traumatic spinal cord injury: a descriptive analysis of 16 subjects. spinal cord. 2014; 52(6): 428-33. doi: 10.1038/sc.2014.26. 18. takahashi h, aoki y, nakajima a, sonobe m, terajima f, saito m, taniguchi s, yamada m, watanabe f, furuya t, koda m, yamazaki m, takahashi k, nakagawa k. phosphorylated neurofilament subunit nfh becomes elevated in the cerebrospinal fluid of patients with acutely worsening symptoms of compression myelopathy. j clin neurosci. 2014; 21(12): 2175-8. microsoft word 1florian_risk romanian neurosurgery (2013) xx 1: 5 21 5 risk factors for gliomas. an extensive review i.s. florian1,2, g. ungureanu1, c. berce2 1neurosurgery department,cluj county emergency hospital 2university of medicine and pharmacy cluj abstract primary brain tumors consist are a heterogenic group of malignancies. gliomas represent subtypes which include all tumors arising from glial cells. the risk factors for gliomas are until today unclear. the aim of this study was to summarize all possible connections between suspected risk factors and glial brain tumors. introduction primary brain tumors consist of a heterogenic group of malignancies. they have a relative small incidence when compared to other neoplasms. their incidence varies according to different classification techniques used. according to central brain tumor registry of the united states (cbtrus), in 2004-2008, their incidence in the us was 19.89 per 100,000 person-years (1). in the globocan 2008 series published by the international agency for research on cancer (iarc), brain tumors represented 1,9% of all cancers excluding nonmelanoma skin cancer (2)*. in the cbtrus statistics, gliomas represent 30% of all primary cns tumors and 80% of malignant ones (1). epidemiologic studies offer the possibility of understanding how a disease acts and who, when, where and why is exposed. they constitute the basis of understanding a disease and offer a chance on preventing and treating it. epidemiologic studies concerning risk factors for gliomas have studied a multitude of possible elements, but their results until now have been mostly inconclusive. this is due to the small number of cases, to the heterogeneity of study designs, inconsistent approach to suspected risk factors. the goal of this review is to provide up to date knowledge concerning risk factors for gliomas and offer an overview of epidemiologic literature data available for glial tumors. material and methods this article includes data from studies indexed by medline. we used the terms “brain tumors” or “gliomas” in combination with “epidemiology” or “risk factors”. all articles, including reviews were covered. articles published in the last five years were the first used when discussing a certain topic. when not available, older articles were included. all related abstracts to those initially used, were included. three large epidemiological reviews were extensively used in order to create specific categories of risk factors (3-5). we have to mention that our search did not exclude articles cited by these reviews. we also have to state that we used data from experimental research in order to highlight certain facts. for every category of risk factors the terms (e.g. ionizing radiation) combined with “brain 6 florian et al risk factors for gliomas. an extensive review tumors” and “gliomas” were again searched for on medline. age and race brain tumors affect more caucasians than african or asian descendants, this being true for all ages (4). the cbtrus report indicates that whites are affected twice more frequent than blacks. also, for all brain tumors, whites are affected more frequent than hispanics. the incidence in japan is half of that seen in northern europe (3). age-adjusted incidence tends to be higher in developed countries (4). for gliomas the peak incidence is situated in the 75-84 years interval (1). age-adjusted incidence rates follow an ascending route, except the decrease in incidence in the 85+ years (1). gender, hormonal status, exogenous hormones and risk for developing gliomas. the fact that glioma incidence varies according to gender is now admitted by most studies. given the fact that gliomas are less frequent in women, their age at diagnosis is higher, researchers have tried to study a possible link between female gender and gliomas (3). data available from the cbtrus shows a higher incidence in males than females (7.17/100 000 personyears vs. 5.07/100 000 person-years) (1). according to the same registry, gender is also important in survival, with females having longer survival rates for most types of tumors, except brain stem and pineal glands. while age alone should not disqualify patients from receiving complete treatment (6), a study found that women were older when diagnosed than men, and this was contraindication for treatment after surgery (7). data from globocan shows a higher incidence of new cases of brain tumors in men vs. women (127000 vs. 110000) (2). the number of deaths due to brain cancer is smaller in women vs. men (77000 vs. 97000) (2). experimental research, in which rats were transplanted with glial tumors, showed a slower rate growth in female rats, a longer survival for females and for the group estrogen treated group (both males and females) (8). a review of current knowledge between hormonal status and gliomas, published in 2010, included 15 articles concerning gliomas. the final conclusion of the study is that female sex hormones are protective against gliomas and constitute risk factors for meningiomas (9). in contradiction, in the epic study no connection between feminine hormones and gliomas was found (10). an older age at menarche was associated with a higher risk of gliomas in the nihaarp diet and health study (11). this conclusion was also drawn by researchers in other studies to (9). the nih-aarp diet and health study found no other link between female hormones and risk of gliomas (11). ever being pregnant had a protective effect in one study (12). some studies also found pregnancy to be a protective factor, while others found no relation between the two (9). research concerning the effect of exposure to exogenous hormones either by oral contraceptives or hormone replacement therapy and glioma risk had mixed results. studies found a slightly higher risk (13), no influence (10, 14) or a protective role of this therapy (9). the later study combines conclusions from 15 studies, and majority of these studies sustain a protective role of exogenous hormone therapy against gliomas (9). romanian neurosurgery (2013) xx 1: 5 21 7 genetic risk factors – family aggregation, genetic syndromes and gene polymorphism the existence of a family member with a glioma, could represent a risk factor for the other members. wrensch and all conducted a study were they showed that or of a primary brain tumor (pbt) in family members of patients with pbt was 2.3 (95% ci=1.0-5.8 (15).in a study of malmer, the authors obtained similar results (16). the same author investigated if genetic factors or genetic ones were the cause of a higher incidence of brain tumors in families having one member already affected by the disease (17). the study revealed that standardized incidence ratio (sir) among spouses of hgg patients was the same as in the general population, while sir was 2.30 (95% ci=1.66-3.11) for first degree relatives of patients diagnosed with hgg (17). segregation analysis showed that family aggregation could explain only 5% of glioma cases, and that a recessive gene model fits in about 2% of all cases (18, 19). on the other hand, family aggregation wasn’t confirmed by a study in iceland (20). there is strong evidence that some inherited genes influence the risk of developing a glioma. some familial cancer syndromes are associated with brain tumors (4). the most important of these syndromes and the associated genes are lifraumeni syndrome (tp53 mutations), type 1 and 2 neurofibromatosis (nf1 and nf2), tuberous sclerosis (tsc 1 and 2), retinoblastoma (rb1), and turcot syndrome (apc and hmlh1/hpsm2 mutations) (4, 5). li-fraumeni syndrome is characterized by a familial aggregation of tumors, with about 70% of cases carrying tp53 mutations (4). in the iarc database of lifraumeni syndromes, 14% of cases had a brain tumor, thus suggesting that familial gliomas could be related to p53 mutations (21). a study of 18 families with 2 or more cases of glioma, didn’t show any connection to p53 mutations, infirming this hypothesis (22). it must be said that these families did not meet classic li-fraumeni criteria. neurofibromatosis type 1 is an autosomal dominant disorder characterized by cafe-au-lait spots and multiple neurofibromas and an increased incidence of diffuse astrocitomas, gliomblastomas, optic nerve gliomas (4). neurofibromatosis type 2 is characterized by dysplastic and neoplastic lesions of the schwann cells, meningeal and glial ones (4). about 80% of gliomas that occur in nf2 patients are tumors of the spinal cord and cauda equine (4). turcot syndrome is also an autosomal dominant disease, characterized by colonic adenomatous polyps and nervous system tumors, usually meduloblastomas (23). gene polymorphism has been intensively studied by researchers. genes involved in dna repair are probably the most studied category, because their role in preventing carcinogenesis (5). the methylation status of mgmt is not only involved in gliomagenesis but also it can predict tumor response to temozolamide treatment (24, 25). mgmt methylation together with micrornas mir-21, mir181c, mir-195 are correlated to progression-free survival of gbm (26). mgmt f84l has been proven to be an important risk factor for gliomas (27). individuals carrying wild-type genotypes of mgmt f84l and parp1 a762va, exposed to ionizing radiation have a much higher risk (27).a genotype, rs1760944 gg of ape1/ref-1 promoter, involved both in dna repair and redox activity, has been 8 florian et al risk factors for gliomas. an extensive review show to exert protective roles in glioblastomas (28). a genetic variant of the chaf1a gene is linked to an increased risk of disease (29). an aa or ac variant of the 8092 nucleotide of errc1 was 4.6 times more frequent in individuals with oligoastrocytoma (30). another study showed that individuals homozygous for ercc1 c8092a and ercc2 k751q have an increasd risk for gliomas (31). other subtypes of errc2 were also incriminated (g3). chen identified that carriers of the two “cgt” haplotypes of vascular endothelial growth factor receptor 2 (vegfr 2) in a chinese population had a 42% reduced risk of developing gliomas compared to noncariers (32). other genetic variants of four genes rs4295627, a variant of ccdc26, rs4977756, a variant of cdkn2a and cdkn2b and rs6010620, a variant of rtel1were associated with glioma risk in a female population (33). tayrac and all identified a 4-gene signature (chaf1b, pdlim4, ednrb, and hjurp), that strongly correlated with survival of hgg patients (34). but this thesis needs to be verified, since it has been proven that susceptibility variants published in glioma genome-wide association studies (gwas) are different between gbm, low grade astrocitomas or oligodendrogliomas (35). exposure to ionizing radiation ionizing radiation is the only carcinogenic agent that has been classified by iarc as being a certain risk factor for brain tumors. studies have shown increased incidence of gliomas or pnets in children that received prophylactic cns irradiation for acute lymphoblastic leukemia (4). various studies conducted to observe the effects of ionizing radiation on children treated for tinea capitis found that risk for gliomas increased immediately postradiation, being higher even after ≥ 30 years, dose related, with no relation to gender or origin (4). different studies have analyzed effects of ionizing radiation after the exposure of the japanese population to atomic bomb irradiation in nagasaki and hiroshima (35). they all found an increased incidence of all brain tumor types, including gliomas. one study from hiroshima found a direct relation between risk and the distance from explosion epicenter (36). table i gene mutations, gene polymorphism, gene variants possibly implicated in glioma risk gene mutations/gene variants/genotypes relation to glioma risk no. of ref. tp53 increased or no connection 21,22mixed results mgmt methylation increased risk. predicts tumor response to temozolomide 24,25 parp1 a762va genotype increased risk 27 mgmt f84l increased risk 27 rs1760944 gg genotype of ape1/ref-1 decreased risk 28 chaf1a rs243356 increased risk 29 atr (mim 601215) rpa3 (mim 179837) could determine genetic glioma risk 29 ercc1c8092a and ercc2 k751q homozygous individual increased risk 31 cgt haplotypes of vegfr 2 increased risk 32 romanian neurosurgery (2013) xx 1: 5 21 9 the effect of medical exposure to ionizing radiation is yet to be clarified. various studies assessed effect of either occupational exposure to ionizing radiation by technicians, radiologists or low-dose irradiation for diagnostic proceduresdental x-rays, head and neck x-rays, or ct of those areas (37). an interphone study found an insignificant increased risk for meningiomas or acoustic neuromas, but an inexplicable statistically significant lower risk for gliomas after any kind of medical exposure (37). another study found an increased risk in a population that underwent ≥3 cts, but only in those with a family history of cancer (38). electromagnetic fields and use of mobile phones probably the most important debate our days, concerning risk factors for malignant brain tumors, lies in the use of mobile phones. several authors and institutions have conducted multiple studies that frequently show mixed results, and, moreover, results from one study are often contested by others conducting research in the same domain. one of the most active organizations that published studies regarding the use of mobile phones is the interphone group that functions under the auspices of iarc. their international study comprised 2708 glioma and 2409 meningioma cases, from 13 countries (39). the authors found no link between either glioma or meningioma risk and the use of mobile phones, even after 10 years of usage. the interphone study found only a higher risk for gliomas in the temporal lobe, and for those subjects that reported repeated use on the same side, but the ci varied in very large limits. the or was 0.81 (95% ci 0.70-0.94) in the regular mobile phone users group-defined by the authors as at least one call per week for more than six months. the or was 1.40 (95% ci 1.03-1.89) in the group that stated they used mobile phones more than 1640 h. but the authors of the study argued that values for mobile phone use in this group, was very unlikely. the results of the interphone study were extensively contradicted. in an article from 2008, by hardell and all (40) suggest that the results of the interphone study are largely affected by bias, so that results could not be considered valid. conclusions from the swedish team of the interphone group that concluded that no relation exists between mobile phone use and risk of developing gliomas (41) were challenged by several researchers (42-44). hardell conducted several studies were the researchers found a link between mobile phones and risk for developing severall types of tumors, including gliomas(45-48). in one study they found an increased risk for developing gliomas in people that used mobile phones for more than 10 years (or=2.7, 95% ci 1.9-3.7), this risk being even higher in those who started to use mobile phones before the age of 20 (or=4.9, ci = 2.2-11)(45). another study of the same author found a higher risk (or=3.4, 95% ci 1.6-7.1) for those who used mobile phones for more than 2000 hours (46). a latency period of more than 10 years was a risk factor for developing gliomas (or=2.0, 95% ci 1.2-3.4), even in a meta-analysis were results were compared with 16 other studies (49). results from five countries in the interphone group, showed a higher incidence of gliomas in people that had a higher exposure to radio frequency fields (rf) from mobile phones (or=1.91, 95% ci 1.05-3.47)(50). 10 florian et al risk factors for gliomas. an extensive review the conclusions of a long-term danish cohort study published in 2011, was that no link exists between mobile phones and malignant brain tumors (51). this research updates information from a 2006 study (52), which in turn is an update of a study started in 2001 (53). the results of these particular analysis were contested, partially for its design and extensive bias possibilities, and partially because the financing was done in part by companies that were involved in mobile telecommunications (54-56). in 2011, 30 scientists met at iarc, with the goal of establishing the impact that rf electromagnetic fields had on carcinogenesis. during that meeting, they established that rf magnetic fields are a potential risk factor for developing gliomas in humans (57). their conclusions were based mainly on two studies, cited in this paper, one being the interphone study and the other the study of hardell and all. the conclusions of the iarc group were compared by little and all with the effect of rf magnetic fields on glioma risk in the us population, based on 12 registries of the seer database (58). the conclusion was that the us data, could be compatible with the information obtained in the interphone study (moderate risk when mobile phones are excessively used) but in contradiction with the results of hardell’s study. finally we can say that the debate surrounding the influence of mobile phones on the risk of developing glial tumors is far from being over. in 2009, in a review of available data (59), kundi stated that four epidemiological aspects should be taken into account when analyzing this subject: temporal relation (the exact time when a brain tumor appeared), association (assessed as possible counterarguments for a possible relation), environmental factors (risk factors that could coexist with mobile phone usage) and finally population equivalence (both cases and controls should come from the same type of population). it is almost impossible for a case-control study, and most studies so far have been done using this approach, to follow these guidelines. a final conclusion on mobile phones-glioma risk relation will come probably, only when researchers will create a new model for a possible study. lifestyle factors there is still little evidence of an association between any lifestyle factors and an elevated risk for malignant gliomas. although certain factors like alcohol, diet, smoking have proven to be in relation to certain types of tumors (colonic, rectal, breast, lung) studies up to day were unable to identify any relevant link between a certain lifestyle and brain tumors. the main cause is the fact that gliomas are not a common disease in the general population. this means that cohort studies cannot gather sufficient information, which in turn determines that data can only be collected from case-control studies (60). diet and eating habits have not yet been proven to exert any certain influence on the development of gliomas. a study by hu and all, in a hospital based case-control showed a relation between certain foods and gliomas (61). consumption of fresh vegetables and fruits was inversely associated with gliomas (or=0.29). the same effect was found for fresh fish. the consumption of salted vegetables determines a high risk for brain tumors (or=2.54). this is explained by the high content of n-nitroso compounds (noc) and noc precursors. the study value is romanian neurosurgery (2013) xx 1: 5 21 11 limited, as it is a hospital-based case-control study of diet and by the low number of cases (73 glioma patients). a study conducted in california in 1997 among women with gliomas, also demonstrated a correlation between cured meat and an increased risk of gliomas, risk that was reduced by consumption of vegetables (62). vegetable intake also decreased risk in another large cohort study (63). two recent studies have shown that high coffee and tea intake are inversely correlated with glioma risk (64, 65). the first one reflects data from three independent cohort studies. tea (more than five cups a day) and coffee reduced the risk for glioma (rr=0.60, 95% ci 0.410.87). no association was found between decaffeinated coffee and risk of glioma, suggesting that caffeine has protective effects. in the second study, high coffee and tea intake (>100ml/day) were both associated with a significant lower risk for glial tumors. vitamin intake, especially vitamins a, d and e was correlated with a lower risk for gliomas, both in population and experimental studies. both food and supplement vitamins had this effect (61, 62, 66). retinoids, compounds related to vitamin a, have a significant anti oncogenic effect (66). alfacalcidol, a vitamin d analog also has anti proliferative effects on glioma cell cultures (67). tocopherols (vitamin e) also exert anti oncogenic effects on glioma cells (66). dietary minerals, especially calcium and zinc, have protective effects against tumors, including gliomas (68, 69). no correlation between acrylamide, present in several heat-prepared foods and glioma risk was found by a study (70). obesity and an increased body mass index (bmi) have been proven to be risk factors for gliomas in at least four studies (60). obesity and it’s direct consequences, hyperglycemia and type 2 diabetes mellitus, were also found to be independent risk factors for a poor outcome in patients with hgg (71,72) while an increased bmi didn’t influence survival in another study (73). caloric restriction may have an important role in improving outcome for gliomas (74). this is based on the fact that while normal glial cells can adapt their metabolism, tumor cells cannot do the same. dietary restriction reduced angiogenesis in a orthotopic mouse brain tumor model and also in human glioma cultures (75, 76). also normal nervous cells can use ketone bodies for energy, while tumor cells are highly dependent on glycolysis (77). this is the rationale for using a high-fat, low-carbohydrate diet (ketogenic diet) as adjuvant therapy for gliomas (77). the ketogenic diet also enhanced the anti-tumor effect of radiation in a study (78). caloric restriction with glucose withdrawal could cause phosphorylation of amp-activated protein kinase (ampk), and this may cause apoptosis in astrocytoma cells but not in normal cells under similar energy stress (79). there is no certain evidence linking alcohol or smoking to an increased risk for gliomas. this is due to the small number of cases in different studies, the incomplete research hypothesis and deficitary patient selection (80). in the melbourne collaborative cohort study, alcohol was associated with the risk for developing gliomas in a dose-response relation (81). but an older study from some of the members of the same team did not reveal any link between alcohol usage and gliomas 12 florian et al risk factors for gliomas. an extensive review (82). a study by devito and all, showed that ethanol inhibited the stimulation of icam-1 (an adhesion molecule) by tnf-α (83). icam-1 is an important molecule in the neuroimune response, and it’s inhibition by ethanol, could explain a lower response of the cns to injury, including gliomas (83). in a cohort study, efird and his team found an increased risk for gliomas in smokers, marijuana consumers, and coffee drinkers (>7 cups/day) (84). a study on a population of 22.946 icelanders, also found smoking as a risk factor of cancer for all sites, except endometrium (85). multiple studies did not find any relation between smoking and glioma risk (82, 86-88), while others have mixed conclusions (89). alcohol and cigarette smoking are not currently considered to be risk factors for malignant brain tumors (90). a review of studies concerning marijuana smoking and risk for cancer did not find any increase in the risk for gliomas (91), but some studies support the hypothesis of cannabinoids as an effective adjuvant therapy (92, 93). allergies, atopic conditions, infections, other disease, medication allergies have clearly been indicated by most studies regarding this subject, as protective conditions against gliomas (94101). in a meta-analysis published in 2011, by chen and coworkers, that included 12 studies, authors conclude that allergies could significantly decrease the risk of gliomas (102). moreover, some studies have shown that, the number of allergies for a patient is directly proportional with a smaller risk (98, 101). in a study risk decreased with 31-45% for every new atopic condition (98). antihistamine usage was not correlated with this risk (101). in most studies the levels of ige, an objective assessment tool for allergic conditions, correlated with the risk for glioma. the risk increased inversely with the levels of ige (100, 103-105). it seems that function of immune cells is altered in patients with gbm, in the sense that instead of preventing tumor appearance, immunity mechanisms support it (106). scd23, a soluble marker, part of the humoral immune system, that enhances inflammatory response, is lower in gbm patients than controls (107). sdc14 that inhibits inflammatory response, is higher in gbm group vs. controls (107). two subtypes of interleukin (il)-4 and il-3 were also associated with gbm, and or for gbm were opposite of the ones for asthma (108). in a study, gbm patients having high levels of ige survived 9 month longer, than those with normal levels (109). autoimmune disease were also inversely correlated with gbm, in one study (or=0.49, 95% ci= 0.35–0.69), the most significant being diabetes (96). another study showed that patients reporting a previous infectious disease had a rr of 0.72, 95% ci 0.61-0.85 of developing gbm (95). until now some viruses of the polyoma family, like bk virus, simian vacuolating virus 40 (sv40) and especially jc virus (jcv), have been proven to have oncogenic effect for gbm in experimental conditions (110). jcv proved oncogenic effect for malignant brain tumors in test animals. igg antibodies to the capsid of jcv, proved to increase or for developing gbm to 1.46, ci=0.61-3.5 in a group of patients (111). igg for varicella zoster was inversely correlated with glioma and some studies reported multiple hcmv gene products in glial tumors when compared to normal tissue (5). vzv igg levels were more romanian neurosurgery (2013) xx 1: 5 21 13 common in glioma cases vs. controls in another study (or=0.68, 95% ci= 0.411.13)(112). another condition investigated for a possible connection with hgg was epilepsy. a study found a 6-fold increase of risk for glioma in patients suffering from epilepsy in the last 2 years prior to diagnostic (95). the risk was highest for epilepsy for 20 years or less prior to diagnostic, although epilepsy > 20 years still had a higher risk. the interphone group also found a high risk of gliomas in patients with epileptic seizures (99). the authors conclude that seizures suggest a long preclinical evolution of gliomas, since they did not create two separate groups for low or high grade tumors. a family history of cancer could be a risk factor for developing brain tumors. a study found that risk of gliomas increases 1.4-3.4 fold familial history is positive for stomach, colon, prostate or hodgkin disease cancers (113). the authors found no connection between glioma risk and a family history of brain tumors. however a study from sweden found an increased risk for gliomas for people who had a parent suffering from this disease (114). a family history of brain tumors also increased risk for oligodendrogliomas in a mixt scandinavianus pooled analysis of 7 case-control studies (115). non-steroidal anti-inflammatory drugs (nsaid) were correlated with a lower risk for developing gbm. in a study by sivaksears and all, gbm cases reported a smaller use of nsaids than controls (116). the findings were strongest for aspirin and ibuprofen. another case-control study found a 33% lower risk for gbm in those reporting a regular use of nsaid (117). the authors failed in showing which nsaid had this effect. the influence of nsaid on gliomas, could be explained by the fact that they inhibit prostaglandins, inflammation mediators, that have a potential oncogenic effect (116). angiogenesis, a vital tumor growth process, is linked to cyclooxygenase-2 driven inflammation, and this enzyme is irreversibly blocked by aspirin for example (116). table ii medical conditions and relation to glioma risk condition relation to glioma risk no. of ref. allergies decreased risk 94-101 increased ige levels decreased risk 100,103-105 autoimmune disease decreased risk 96 polyoma virus infections increased risk (experimenal) 110 epilepsy increased risk 95,99 nsaid consumption decreased risk 116, 117 occupation and environment factors determining a relation between a certain occupation and the risk for brain tumors is difficult. in most professional areas, workers are exposed to more than one possible risk factor (3). it is hard to determine what is the total risk determined by all these factors together. for example, even if a certain chemical is proven to be an oncogenic agent, it’s interaction with other elements, could increase or decrease risk (3). moreover, chemicals that have been proven to favor tumor genesis, had that effect on lab animals, where they were directly implanted. their effect through another type of contact (touching, inhalation) could be different (3). all these things make it difficult to link certain professional factors with the risk of brain tumors. 14 florian et al risk factors for gliomas. an extensive review a case-control study from germany, did not find any association between a certain occupational field and the risk for developing gliomas. authors studied six occupational sectors -chemical, agricultural, transport, electric/electronic, construction, metalbut found no significant risk in any profession (118). in the san francisco bay area, physicians, surgeons, artists, foundry and smelter workers and petroleum and gas workers were at a higher risk for gliomas (119). a possible explanation is that health practitioners have raised access to diagnostic procedures that could explain some of the higher incidence (119). this is no longer a plausible factor because the access and quality of diagnostic procedures have increased dramatically. also, medical staff has contact with a large number of agents, i.e. disinfectants, biological agents, radiation, that could lead to an increased risk (119). parental work in agriculture, motor-vehicle related, electric domain determined an increased incidence in children in another study (120). this association was valid for both parents, while work in the textile industry was true only for mothers. a retrospective research found a positive association between children gliomas and father exposure to lead, cleaning solvents, pesticides from lawn care, during pregnancy period or immediately after birth (121). it must be noted that this study only took into consideration exposure resulting from hobbies, not occupational. exposure to pesticides was largely investigated as a risk factor for cancers. phenoxy herbicides were proven as a cause for malignant lymphoma and soft-tissue sarcoma (122). a hospital-based, casecontrol study did not prove any association between insecticides or herbicides and gliomas, although women exposed to herbicides were at a much larger risk of developing meningiomas than those that were not exposed to these substances (123). opposite results were obtained in a retrospective study from india, which showed that gliomas were much more frequent in orchard workers, residents or children playing in orchards that were exposed to numerous chemicals (chlorpyriphos, dimethoate, mancozeb and captan) for more than 10 years (124). a study of residents of rural zones from several us regions also proved that not washing or changing clothes immediately after applying pesticides constitutes a risk factor for developing gliomas (125). occupational exposure did not increase rsik of gliomas instead it determined a higher risk of meningiomas (126). a study noted a higher incidence of gliomas in professionals of the following domains: it, farm workers, financial, medicine, management, while it found a decreased incidence in childcare workers (127). a possible link between gliomas and physiological stress was also investigated, and found that major life events in a 5 years period prior to diagnostic, constituted a risk factor (128). studies trying to find a connection between sociodemographic variables and gliomas found mixed or inconclusive results (129). head trauma an association between trauma and brain tumors has not yet been clearly demonstrated. although that there are some reports of a positive association, the relation is either non-significant or inconsistent (4). associations have been made between perinatal or adult head trauma or combined perinatal and adult head trauma (4). in a study or for gliomas following any head injury was only 1.2 (95% ci 0.9-1.5) in men, and lower for females (130). in a romanian neurosurgery (2013) xx 1: 5 21 15 danish cohort study, that included patients hospitalized for concussion, fractured skull or any other head trauma, the incidence of gliomas was the same as for the general population (131). several authors reported cases that indicated head trauma as the cause of gliomas and its influence needs to be further investigated (132). other suspected risk factors there have been several sporadic studies investigating potential risk factors for gliomas. use of hair dye could increase the risk of bladder and hematopoietic cancers, but no association was found with glioma (133). high birth weight (>4000g) was associated with an increased risk for astrocytoma, and this risk was 19% higher for every 1000g (134). birth anomalies or season of birth were not associated with an increased risk for glial tumors (135). references 1.cbtrus (central brain tumor registry of the united states) (2012). statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2004-2008. central brain tumor registry of the united states. 2. ferlay j, shin hr, bray f, forman d, mathers c, parkin dm. estimates of worldwide burden of cancer in 2008: globocan 2008. int j cancer. 2010 dec 15;127(12):2893-917.doi:10.1002/ijc.25516. 3.wrensch m, minn y, chew t, bondy m, berger ms. epidemiology of primary brain tumors: current concepts and review of the literature. neuro oncol. 2002 oct;4(4):278-99. 4.ohgaki h, kleihues p. epidemiology and etiology of gliomas. acta neuropathol. 2005 jan;109(1):93-108. 5.bondy ml, scheurer me, malmer b, barnholtzsloan js, davis fg, il'yasova d, kruchko c, mccarthy bj, rajaraman p, schwartzbaum ja, sadetzki s, schlehofer b, tihan t, wiemels jl, wrensch m, buffler pa; brain tumor epidemiology consortium. brain tumor epidemiology: consensus from the brain tumor epidemiology consortium. cancer. 2008 oct 1;113(7 suppl):1953-68 6.iwamoto fm, cooper ar, reiner as, nayak l, abrey le. glioblastoma in the elderly: the memorial sloankettering cancer center experience (1997-2007). cancer. 2009 aug 15;115(16):3758-66. 7.verger e, valduvieco i, caral l, pujol t, ribalta t, viñolas n, boget t, oleaga l, blanco y, graus f. does gender matter in glioblastoma? clin transl oncol. 2011 oct;13(10):737-41. 8.kabat gc, etgen am, rohan te. do steroid hormones play a role in the etiology of glioma? cancer epidemiol biomarkers prev. 2010 oct;19(10):2421-7. 9.cowppli-bony a, bouvier g, rué m, loiseau h, vital a, lebailly p, fabbro-peray p, baldi i. brain tumors and hormonal factors: review of the epidemiological literature. cancer causes control. 2011 may;22(5):697-714. 10.michaud ds, gallo v, schlehofer b, tjønneland a, olsen a, overvad k, dahm cc, kaaks r, lukanova a, boeing h, schütze m, trichopoulou a, bamia c, kyrozis a, sacerdote c, agnoli c, palli d, tumino r, mattiello a, bueno-de-mesquita hb, ros mm, peeters ph, van gils ch, lund e, bakken k, gram it, barricarte a, navarro c, dorronsoro m, sánchez mj, rodríguez l, duell ej, hallmans g, melin bs, manjer j, borgquist s, khaw kt, wareham n, allen ne, tsilidis kk, romieu i, rinaldi s, vineis p, riboli e. reproductive factors and exogenous hormone use in relation to risk of glioma and meningioma in a large european cohort study. cancer epidemiol biomarkers prev. 2010 oct;19(10):2562-9. 11.kabat gc, park y, hollenbeck ar, schatzkin a, rohan te. reproductive factors and exogenous hormone use and risk of adult glioma in women in the nih-aarp diet and health study. int j cancer. 2011 feb 15;128(4):944-50. 12.wigertz a, lönn s, hall p, auvinen a, christensen hc, johansen c, klaeboe l, salminen t, schoemaker mj, swerdlow aj, tynes t, feychting m. reproductive factors and risk of meningioma and glioma. cancer epidemiol biomarkers prev. 2008 oct;17(10):2663-70. 13.benson vs, pirie k, green j, bull d, casabonne d, reeves gk, beral v; million women study collaborators. hormone replacement therapy and incidence of central nervous system tumours in the million women study. int j cancer. 2010 oct 1;127(7):1692-8. 14.wigertz a, lönn s, mathiesen t, ahlbom a, hall p, feychting m; swedish interphone study group. risk of brain tumors associated with exposure to exogenous female sex hormones. am j epidemiol. 2006 oct 1;164(7):629-36. 15.wrensch m, lee m, miike r, newman b, barger g, davis r, wiencke j, neuhaus j. familial and personal medical history of cancer and nervous system conditions among adults with glioma and controls. am j epidemiol. 1997 apr 1;145(7):581-93. 16.malmer b, grönberg h, bergenheim at, lenner p, henriksson r. familial aggregation of astrocytoma in 16 florian et al risk factors for gliomas. an extensive review northern sweden: an epidemiological cohort study. int j cancer. 1999 may 5;81(3):366-70. 17.malmer b, henriksson r, grönberg h. familial brain tumours-genetics or environment? a nationwide cohort study of cancer risk in spouses and first-degree relatives of brain tumour patients. int j cancer. 2003 aug 20;106(2):260-3. 18.malmer b, iselius l, holmberg e, collins a, henriksson r, grönberg h. genetic epidemiology of glioma. br j cancer. 2001 feb 2;84(3):429-34. 19.malmer b, haraldsson s, einarsdottir e, lindgren p, holmberg d. homozygosity mapping of familial glioma in northern sweden. acta oncol. 2005;44(2):114-9. 20.o'neill bp, blondal h, yang p, olafsdottir gh, sigvaldason h, jenkins rb, kimmel dw, scheithauer bw, rocca wa, bjornsson j, tulinius h. risk of cancer among relatives of patients with glioma. cancer epidemiol biomarkers prev. 2002 sep;11(9):921-4. 21.olivier m, goldgar de, sodha n, ohgaki h, kleihues p, hainaut p, eeles ra. li-fraumeni and related syndromes: correlation between tumor type, family structure, and tp53 genotype. cancer res. 2003 oct 15;63(20):6643-50. 22.paunu n, syrjäkoski k, sankila r, simola ko, helén p, niemelä m, matikainen m, isola j, haapasalo h. analysis of p53 tumor suppressor gene in families with multiple glioma patients. j neurooncol. 2001 dec;55(3):159-65. 23.jasperson kw, burt rw. apc-associated polyposis conditions. 1998 dec 18 (updated 2011 oct 27). in: pagon ra, bird td, dolan cr, stephens k, adam mp, editors. genereviews™ (internet). seattle (wa): university of washington, seattle; 1993-. available from http://www.ncbi.nlm.nih.gov/books/nbk1345/pubmed pmid: 20301519 24.hegi me, diserens ac, gorlia t, hamou mf, de tribolet n, weller m, kros jm, hainfellner ja, mason w, mariani l, bromberg je, hau p, mirimanoff ro, cairncross jg, janzer rc, stupp r. mgmt gene silencing and benefit from temozolomide in glioblastoma. n engl j med. 2005 mar 10;352(10):9971003. 25.hegi me, diserens ac, godard s, dietrich py, regli l, ostermann s, otten p, van melle g, de tribolet n, stupp r. clinical trial substantiates the predictive value of o-6-methylguanine-dna methyltransferase promoter methylation in glioblastoma patients treated with temozolomide. clin cancer res. 2004 mar 15;10(6):1871-4. 26.lakomy r, sana j, hankeova s, fadrus p, kren l, lzicarova e, svoboda m, dolezelova h, smrcka m, vyzula r, michalek j, hajduch m, slaby o. mir-195, mir-196b, mir-181c, mir-21 expression levels and o6-methylguanine-dna methyltransferase methylation status are associated with clinical outcome in glioblastoma patients. cancer sci. 2011 dec;102(12):2186-90. 27.liu y, scheurer me, el-zein r, cao y, do ka, gilbert m, aldape kd, wei q, etzel c, bondy ml. association and interactions between dna repair gene polymorphisms and adult glioma. cancer epidemiol biomarkers prev. 2009 jan;18(1):204-14. 28.zhou k, hu d, lu j, fan w, liu h, chen h, chen g, wei q, du g, mao y, lu d, zhou l. a genetic variant in the ape1/ref-1 gene promoter -141t/g may modulate risk of glioblastoma in a chinese han population. bmc cancer. 2011 mar 23;11:104. 29.bethke l, webb e, murray a, schoemaker m, johansen c, christensen hc, muir k, mckinney p, hepworth s, dimitropoulou p, lophatananon a, feychting m, lönn s, ahlbom a, malmer b, henriksson r, auvinen a, kiuru a, salminen t, swerdlow a, houlston r. comprehensive analysis of the role of dna repair gene polymorphisms on risk of glioma. hum mol genet. 2008 mar 15;17(6):800-5. 30.chen p, wiencke j, aldape k, kesler-diaz a, miike r, kelsey k, lee m, liu j, wrensch m. association of an ercc1 polymorphism with adult-onset glioma. cancer epidemiol biomarkers prev. 2000 aug;9(8):8437. 31.wrensch m, kelsey kt, liu m, miike r, moghadassi m, sison jd, aldape k, mcmillan a, wiemels j, wiencke jk. ercc1 and ercc2 polymorphisms and adult glioma. neuro oncol. 2005 oct;7(4):495-507. 32.chen h, wang w, xingjie z, song x, fan w, keke z, chen g, zhao y, mao y, lu d. association between genetic variations of vascular endothelial growth factor receptor 2 and glioma in the chinese han population. j mol neurosci. 2012 jul;47(3):448-57. epub 2012 jan 25. 33.wang ss, hartge p, yeager m, carreón t, ruder am, linet m, inskip pd, black a, hsing aw, alavanja m, beane-freeman l, safaiean m, chanock sj, rajaraman p. joint associations between genetic variants and reproductive factors in glioma risk among women. am j epidemiol. 2011 oct 15;174(8):901-8. 34.de tayrac m, aubry m, saïkali s, etcheverry a, surbled c, guénot f, galibert md, hamlat a, lesimple t, quillien v, menei p, mosser j. a 4-gene signature associated with clinical outcome in high-grade gliomas. clin cancer res. 2011 jan 15;17(2):317-27. 35.egan km, thompson rc, nabors lb, olson jj, brat dj, larocca rv, brem s, moots pl, madden mh, browning je, ann chen y. cancer susceptibility variants and the risk of adult glioma in a us casecontrol study. j neurooncol. 2011 sep;104(2):535-42. epub 2011 jan 4. erratum in: j neurooncol. 2011 romanian neurosurgery (2013) xx 1: 5 21 17 sep;104(2):543. 36.shintani t, hayakawa n, hoshi m, sumida m, kurisu k, oki s, kodama y, kajikawa h, inai k, kamada n. high incidence of meningioma among hiroshima atomic bomb survivors. j radiat res. 1999 mar;40(1):49-57. 37.blettner m, schlehofer b, samkange-zeeb f, berg g, schlaefer k, schüz j. medical exposure to ionising radiation and the risk of brain tumours: interphone study group, germany. eur j cancer. 2007 sep;43(13):1990-8. 38.davis f, il'yasova d, rankin k, mccarthy b, bigner dd. medical diagnostic radiation exposures and risk of gliomas. radiat res. 2011 jun;175(6):790-6. 39.interphone study group. brain tumour risk in relation to mobile telephone use: results of the interphone international case-control study. int j epidemiol. 2010 jun;39(3):675-94. epub 2010 may 17. erratum in: int j epidemiol. 2012 feb;41(1):328. 40.hardell l, carlberg m, hansson mild k. re-analysis of risk for glioma in relation to mobile telephone use: comparison with the results of the interphone international case-control study. int j epidemiol. 2011 aug;40(4):1126-8. 41.lönn s, ahlbom a, hall p, feychting m; swedish interphone study group. long-term mobile phone use and brain tumor risk. am j epidemiol. 2005 mar 15;161(6):526-35. 42.morgan l. re: "long-term mobile phone use and brain tumor risk". am j epidemiol. 2005 sep 15;162(6):599-600; author reply 601. 43.milham s. re: "long-term mobile phone use and brain tumor risk". am j epidemiol. 2005 sep 15;162(6):599; author reply 601. 44.hardell l, mild kh, kundi m. re: "long-term mobile phone use and brain tumor risk". am j epidemiol. 2005 sep 15;162(6):600-1; author reply 601. 45.hardell l, carlberg m, hansson mild k. pooled analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects. int j oncol. 2011 may;38(5):1465-74 46.hardell l, carlberg m, hansson mild k. mobile phone use and the risk for malignant brain tumors: a case-control study on deceased cases and controls. neuroepidemiology. 2010 aug;35(2):109-14 47.hardell l, carlberg m. mobile phones, cordless phones and the risk for brain tumours. int j oncol. 2009 jul;35(1):5-17. 48.hardell l, carlberg m, hansson mild k. epidemiological evidence for an association between use of wireless phones and tumor diseases. pathophysiology. 2009 aug;16(2-3):113-22. 49.hardell l, carlberg m, söderqvist f, mild kh, morgan ll. long-term use of cellular phones and brain tumours: increased risk associated with use for > or =10 years. occup environ med. 2007 sep;64(9):62632. 50.cardis e, armstrong bk, bowman jd, giles gg, hours m, krewski d, mcbride m, parent me, sadetzki s, woodward a, brown j, chetrit a, figuerola j, hoffmann c, jarus-hakak a, montestruq l, nadon l, richardson l, villegas r, vrijheid m. risk of brain tumours in relation to estimated rf dose from mobile phones: results from five interphone countries. occup environ med. 2011 sep;68(9):631-40 51.frei p, poulsen ah, johansen c, olsen jh, stedingjessen m, schüz j. use of mobile phones and risk of brain tumours: update of danish cohort study. bmj. 2011 oct 19;343:d6387 52.schüz j, jacobsen r, olsen jh, boice jd jr, mclaughlin jk, johansen c. cellular telephone use and cancer risk: update of a nationwide danish cohort. j natl cancer inst. 2006 dec 6;98(23):1707-13 53.johansen c, boice j jr, mclaughlin j, olsen j. cellular telephones and cancer--a nationwide cohort study in denmark. j natl cancer inst. 2001 feb 7;93(3):203-7. 54.hocking b. re: cellular telephones and cancer--a nationwide cohort study in denmark. j natl cancer inst. 2001 jun 6;93(11):877-8; author reply 878-9. 55.godward s, sandhu m, skinner j, mccann j. re: cellular telephones and cancer--a nationwide cohort study in denmark. j natl cancer inst. 2001 jun 6;93(11):878; author reply 878-9. 56.hardell l, mild kh. re: cellular telephones and cancer--a nationwide cohort study in denmark. j natl cancer inst. 2001 jun 20;93(12):952-3. 57.baan r, grosse y, lauby-secretan b, el ghissassi f, bouvard v, benbrahim-tallaa l, guha n, islami f, galichet l, straif k; who international agency for research on cancer monograph working group. carcinogenicity of radiofrequency electromagnetic fields. lancet oncol. 2011 jul;12(7):624-6. 58.little mp, rajaraman p, curtis re, devesa ss, inskip pd, check dp, linet ms. mobile phone use and glioma risk: comparison of epidemiological study results with incidence trends in the united states. bmj. 2012 mar 8;344:e1147. 59.kundi m. the controversy about a possible relationship between mobile phone use and cancer. environ health perspect. 2009 mar;117(3):316-24 60.benson vs, pirie k, green j, casabonne d, beral v; million women study collaborators. lifestyle factors and primary glioma and meningioma tumours in the million women study cohort. br j cancer. 2008 jul 8;99(1):185-90. 61.hu j, la vecchia c, negri e, chatenoud l, bosetti c, jia x, liu r, huang g, bi d, wang c. diet and brain cancer in adults: a case-control study in northeast 18 florian et al risk factors for gliomas. an extensive review china. int j cancer. 1999 mar 31;81(1):20-3. 62.blowers l, preston-martin s, mack wj. dietary and other lifestyle factors of women with brain gliomas in los angeles county (california, usa). cancer causes control. 1997 jan;8(1):5-12. 63.terry mb, howe g, pogoda jm, zhang ff, ahlbom a, choi w, giles gg, little j, lubin f, menegoz f, ryan p, schlehofer b, preston-martin s. an international case-control study of adult diet and brain tumor risk: a histology-specific analysis by food group. ann epidemiol. 2009 mar;19(3):161-71. 64.holick cn, smith sg, giovannucci e, michaud ds. coffee, tea, caffeine intake, and risk of adult glioma in three prospective cohort studies. cancer epidemiol biomarkers prev. 2010 jan;19(1):39-47. 65.michaud ds, gallo v, schlehofer b, tjønneland a, olsen a, overvad k, dahm cc, teucher b, lukanova a, boeing h, schütze m, trichopoulou a, lagiou p, kyrozis a, sacerdote c, krogh v, masala g, tumino r, mattiello a, bueno-de-mesquita hb, ros mm, peeters ph, van gils ch, skeie g, engeset d, parr cl, ardanaz e, chirlaque md, dorronsoro m, sánchez mj, argüelles m, jakszyn p, nilsson lm, melin bs, manjer j, wirfält e, khaw kt, wareham n, allen ne, key tj, romieu i, vineis p, riboli e. coffee and tea intake and risk of brain tumors in the european prospective investigation into cancer and nutrition (epic) cohort study. am j clin nutr. 2010 nov;92(5):1145-50. 66.kyritsis ap, bondy ml, levin va. modulation of glioma risk and progression by dietary nutrients and antiinflammatory agents. nutr cancer. 2011;63(2):17484. review. 67.trouillas p, honnorat j, bret p, jouvet a, gerard jp. redifferentiation therapy in brain tumors: long-lasting complete regression of glioblastomas and an anaplastic astrocytoma under long term 1-alphahydroxycholecalciferol. j neurooncol. 2001 jan;51(1):57-66. 68.tedeschi-blok n, schwartzbaum j, lee m, miike r, wrensch m; san francisco bay area adult glioma study. dietary calcium consumption and astrocytic glioma: the san francisco bay area adult glioma study, 1991-1995. nutr cancer. 2001;39(2):196-203 69.franklin rb, costello lc. the important role of the apoptotic effects of zinc in the development of cancers. j cell biochem. 2009 apr 1;106(5):750-7. review. 70.hogervorst jg, schouten lj, konings ej, goldbohm ra, van den brandt pa. dietary acrylamide intake and brain cancer risk. cancer epidemiol biomarkers prev. 2009 may;18(5):1663-6 71.chambless lb, parker sl, hassam-malani l, mcgirt mj, thompson rc. type 2 diabetes mellitus and obesity are independent risk factors for poor outcome in patients with high-grade glioma. j neurooncol. 2012 jan;106(2):383-9. 72.derr rl, ye x, islas mu, desideri s, saudek cd, grossman sa. association between hyperglycemia and survival in patients with newly diagnosed glioblastoma. j clin oncol. 2009 mar 1;27(7):1082-6. 73.jones lw, ali-osman f, lipp e, marcello je, mccarthy b, mccoy l, rice t, wrensch m, il'yasova d. association between body mass index and mortality in patients with glioblastoma mutliforme. cancer causes control. 2010 dec;21(12):2195-201. 74.seyfried bt, kiebish m, marsh j, mukherjee p. targeting energy metabolism in brain cancer through calorie restriction and the ketogenic diet. j cancer res ther. 2009 sep;5 suppl 1:s7-15. review 75.mukherjee p, el-abbadi mm, kasperzyk jl, ranes mk, seyfried tn. dietary restriction reduces angiogenesis and growth in an orthotopic mouse brain tumour model. br j cancer. 2002 may 20;86(10):161521. 76.mukherjee p, abate le, seyfried tn. antiangiogenic and proapoptotic effects of dietary restriction on experimental mouse and human brain tumors. clin cancer res. 2004 aug 15;10(16):5622-9. 77.maurer gd, brucker dp, bähr o, harter pn, hattingen e, walenta s, mueller-klieser w, steinbach jp, rieger j. differential utilization of ketone bodies by neurons and glioma cell lines: a rationale for ketogenic diet as experimental glioma therapy. bmc cancer. 2011 jul 26;11:315. 78.abdelwahab mg, fenton ke, preul mc, rho jm, lynch a, stafford p, scheck ac. the ketogenic diet is an effective adjuvant to radiation therapy for the treatment of malignant glioma. plos one. 2012;7(5):e36197 79.mukherjee p, mulrooney tj, marsh j, blair d, chiles tc, seyfried tn. differential effects of energy stress on ampk phosphorylation and apoptosis in experimental brain tumor and normal brain. mol cancer. 2008 may 12;7:37. 80.fisher jl, schwartzbaum ja, wrensch m, wiemels jl. epidemiology of brain tumors. neurol clin. 2007 nov;25(4):867-90, vii. review. pubmed pmid: 17964019. 81.baglietto l, giles gg, english dr, karahalios a, hopper jl, severi g. alcohol consumption and risk of glioblastoma; evidence from the melbourne collaborative cohort study. int j cancer. 2011 apr 15;128(8):1929-34. 82.hurley sf, mcneil jj, donnan ga, forbes a, salzberg m, giles gg. tobacco smoking and alcohol consumption as risk factors for glioma: a case-control study in melbourne, australia. j epidemiol community health. 1996 aug;50(4):442-6. 83.devito wj, stone s, mori k, shamgochian m. ethanol inhibits prolactinand tumor necrosis factor romanian neurosurgery (2013) xx 1: 5 21 19 alpha-, but not gamma interferon-induced expression of intercellular adhesion molecule-1 in human astrocytoma cells. j cell biochem. 2000 apr;77(3):45564. 84.efird jt, friedman gd, sidney s, klatsky a, habel la, udaltsova nv, van den eeden s, nelson lm. the risk for malignant primary adult-onset glioma in a large, multiethnic, managed-care cohort: cigarette smoking and other lifestyle behaviors. j neurooncol. 2004 may;68(1):57-69. 85.tulinius h, sigfússon n, sigvaldason h, bjarnadóttir k, tryggvadóttir l. risk factors for malignant diseases: a cohort study on a population of 22,946 icelanders. cancer epidemiol biomarkers prev. 1997 nov;6(11):863-73. 86.holick cn, giovannucci el, rosner b, stampfer mj, michaud ds. prospective study of cigarette smoking and adult glioma: dosage, duration, and latency. neuro oncol. 2007 jul;9(3):326-34. 87.lachance dh, yang p, johnson dr, decker pa, kollmeyer tm, mccoy ls, rice t, xiao y, ali-osman f, wang f, stoddard sm, sprau dj, kosel ml, wiencke jk, wiemels jl, patoka js, davis f, mccarthy b, rynearson al, worra jb, fridley bl, o'neill bp, buckner jc, il'yasova d, jenkins rb, wrensch mr. associations of high-grade glioma with glioma risk alleles and histories of allergy and smoking. am j epidemiol. 2011 sep 1;174(5):574-81. 88.mandelzweig l, novikov i, sadetzki s. smoking and risk of glioma: a meta-analysis. cancer causes control. 2009 dec;20(10):1927-38. 89.silvera sa, miller ab, rohan te. cigarette smoking and risk of glioma: a prospective cohort study. int j cancer. 2006 apr 1;118(7):1848-51 90.cogliano vj, baan r, straif k, grosse y, laubysecretan b, el ghissassi f, bouvard v, benbrahimtallaa l, guha n, freeman c, galichet l, wild cp. preventable exposures associated with human cancers. j natl cancer inst. 2011 dec 21;103(24):1827-39. epub 2011 dec 12. review 91.hashibe m, straif k, tashkin dp, morgenstern h, greenland s, zhang zf. epidemiologic review of marijuana use and cancer risk. alcohol. 2005 apr;35(3):265-75. review. 92.torres s, lorente m, rodríguez-fornés f, hernández-tiedra s, salazar m, garcía-taboada e, barcia j, guzmán m, velasco g. a combined preclinical therapy of cannabinoids and temozolomide against glioma. mol cancer ther. 2011 jan;10(1):90-103 93.foroughi m, hendson g, sargent ma, steinbok p. spontaneous regression of septum pellucidum/forniceal pilocytic astrocytomas--possible role of cannabis inhalation. childs nerv syst. 2011 apr;27(4):671-9. 94.wiemels jl, wiencke jk, sison jd, miike r, mcmillan a, wrensch m. history of allergies among adults with glioma and controls. int j cancer. 2002 apr 1;98(4):609-15. 95.schlehofer b, blettner m, preston-martin s, niehoff d, wahrendorf j, arslan a, ahlbom a, choi wn, giles gg, howe gr, little j, ménégoz f, ryan p. role of medical history in brain tumour development. results from the international adult brain tumour study. int j cancer. 1999 jul 19;82(2):155-60. 96.brenner av, linet ms, fine ha, shapiro wr, selker rg, black pm, inskip pd. history of allergies and autoimmune diseases and risk of brain tumors in adults. int j cancer. 2002 may 10;99(2):252-9. 97.schwartzbaum j, jonsson f, ahlbom a, prestonmartin s, lönn s, söderberg kc, feychting m. cohort studies of association between self-reported allergic conditions, immune-related diagnoses and glioma and meningioma risk. int j cancer. 2003 sep 1;106(3):4238. review. 98.il'yasova d, mccarthy b, marcello j, schildkraut jm, moorman pg, krishnamachari b, ali-osman f, bigner dd, davis f. association between glioma and history of allergies, asthma, and eczema: a case-control study with three groups of controls. cancer epidemiol biomarkers prev. 2009 apr;18(4):1232-8. 99.berg-beckhoff g, schüz j, blettner m, münster e, schlaefer k, wahrendorf j, schlehofer b. history of allergic disease and epilepsy and risk of glioma and meningioma (interphone study group, germany). eur j epidemiol. 2009;24(8):433-40. 100.wiemels jl, wilson d, patil c, patoka j, mccoy l, rice t, schwartzbaum j, heimberger a, sampson jh, chang s, prados m, wiencke jk, wrensch m. ige, allergy, and risk of glioma: update from the san francisco bay area adult glioma study in the temozolomide era. int j cancer. 2009 aug 1;125(3):680-7 101.mccarthy bj, rankin k, il'yasova d, erdal s, vick n, ali-osman f, bigner dd, davis f. assessment of type of allergy and antihistamine use in the development of glioma. cancer epidemiol biomarkers prev. 2011 feb;20(2):370-8. 102.chen c, xu t, chen j, zhou j, yan y, lu y, wu s. allergy and risk of glioma: a meta-analysis. eur j neurol. 2011 mar;18(3):387-95. doi: 10.1111/j.14681331.2010.03187.x. epub 2010 aug 16 103.wiemels jl, wiencke jk, patoka j, moghadassi m, chew t, mcmillan a, miike r, barger g, wrensch m. reduced immunoglobulin e and allergy among adults with glioma compared with controls. cancer res. 2004 nov 15;64(22):8468-73. 104.calboli fc, cox dg, buring je, gaziano jm, ma j, stampfer m, willett wc, tworoger ss, hunter dj, camargo ca jr, michaud ds. prediagnostic plasma ige levels and risk of adult glioma in four prospective cohort studies. j natl cancer inst. 2011 nov 20 florian et al risk factors for gliomas. an extensive review 2;103(21):1588-95. 105.schlehofer b, siegmund b, linseisen j, schüz j, rohrmann s, becker s, michaud d, melin b, bas bueno-de-mesquita h, peeters ph, vineis p, tjonneland a, olsen a, overvad k, romieu i, boeing h, aleksandrova k, trichopoulou a, bamia c, lagiou p, sacerdote c, palli d, panico s, sieri s, tumino r, sanchez mj, rodriguez l, dorronsoro m, duell ej, chirlaque md, barricarte a, borgquist s, manjer j, gallo v, allen ne, key tj, riboli e, kaaks r, wahrendorf j. primary brain tumours and specific serum immunoglobulin e: a case-control study nested in the european prospective investigation into cancer and nutrition cohort. allergy. 2011 nov;66(11):143441. 106.curran cs, bertics pj. eosinophils in glioblastoma biology. j neuroinflammation. 2012 jan 17;9:11. review. 107.zhou m, wiemels jl, bracci pm, wrensch mr, mccoy ls, rice t, sison jd, patoka js, wiencke jk. circulating levels of the innate and humoral immune regulators cd14 and cd23 are associated with adult glioma. cancer res. 2010 oct 1;70(19):7534-42. 108.schwartzbaum j, ahlbom a, malmer b, lönn s, brookes aj, doss h, debinski w, henriksson r, feychting m. polymorphisms associated with asthma are inversely related to glioblastoma multiforme. cancer res. 2005 jul 15;65(14):6459-65. 109.wrensch m, wiencke jk, wiemels j, miike r, patoka j, moghadassi m, mcmillan a, kelsey kt, aldape k, lamborn kr, parsa at, sison jd, prados md. serum ige, tumor epidermal growth factor receptor expression, and inherited polymorphisms associated with glioma survival. cancer res. 2006 apr 15;66(8):4531-41. 110.white mk, gordon j, reiss k, del valle l, croul s, giordano a, darbinyan a, khalili k. human polyomaviruses and brain tumors. brain res brain res rev. 2005 dec 1;50(1):69-85. epub 2005 jun 27. review. 111.rollison de, helzlsouer kj, alberg aj, hoffman s, hou j, daniel r, shah kv, major eo. serum antibodies to jc virus, bk virus, simian virus 40, and the risk of incident adult astrocytic brain tumors. cancer epidemiol biomarkers prev. 2003 may;12(5):460-3. 112.sjöström s, hjalmars u, juto p, wadell g, hallmans g, tjönneland a, halkjaer j, manjer j, almquist m, melin bs. human immunoglobulin g levels of viruses and associated glioma risk. cancer causes control. 2011 sep;22(9):1259-66. 113.hill da, inskip pd, shapiro wr, selker rg, fine ha, black pm, linet ms. cancer in first-degree relatives and risk of glioma in adults. cancer epidemiol biomarkers prev. 2003 dec;12(12):1443-8. 114.hemminki k, li x, collins vp. parental cancer as a risk factor for brain tumors (sweden). cancer causes control. 2001 apr;12(3):195-9. 115.mccarthy bj, rankin km, aldape k, bondy ml, brännström t, broholm h, feychting m, il'yasova d, inskip pd, johansen c, melin bs, ruder am, butler ma, scheurer me, schüz j, schwartzbaum ja, wrensch mr, davis fg. risk factors for oligodendroglial tumors: a pooled international study. neuro oncol. 2011 feb;13(2):242-50. 116.sivak-sears nr, schwartzbaum ja, miike r, moghadassi m, wrensch m. case-control study of use of nonsteroidal antiinflammatory drugs and glioblastoma multiforme. am j epidemiol. 2004 jun 15;159(12):1131-9. 117.scheurer me, el-zein r, thompson pa, aldape kd, levin va, gilbert mr, weinberg js, bondy ml. long-term anti-inflammatory and antihistamine medication use and adult glioma risk. cancer epidemiol biomarkers prev. 2008 may;17(5):1277-81. doi: 10.1158/1055-9965.epi-07-2621 118.samkange-zeeb f, schlehofer b, schüz j, schlaefer k, berg-beckhoff g, wahrendorf j, blettner m. occupation and risk of glioma, meningioma and acoustic neuroma: results from a german case-control study (interphone study group, germany). cancer epidemiol. 2010 feb;34(1):55-61. 119.carozza se, wrensch m, miike r, newman b, olshan af, savitz da, yost m, lee m. occupation and adult gliomas. am j epidemiol. 2000 nov 1;152(9):83846. 120.cordier s, mandereau l, preston-martin s, little j, lubin f, mueller b, holly e, filippini g, peris-bonet r, mccredie m, choi nw, arsla a. parental occupations and childhood brain tumors: results of an international case-control study. cancer causes control. 2001 nov;12(9):865-74. 121.rosso al, hovinga me, rorke-adams lb, spector lg, bunin gr; children's oncology group. a casecontrol study of childhood brain tumors and fathers' hobbies: a children's oncology group study. cancer causes control. 2008 dec;19(10):1201-7. 122.hardell l. pesticides, soft-tissue sarcoma and nonhodgkin lymphoma--historical aspects on the precautionary principle in cancer prevention. acta oncol. 2008;47(3):347-54. 123.samanic cm, de roos aj, stewart pa, rajaraman p, waters ma, inskip pd. occupational exposure to pesticides and risk of adult brain tumors. am j epidemiol. 2008 apr 15;167(8):976-85. 124.bhat ar, wani ma, kirmani ar. brain cancer and pesticide relationship in orchard farmers of kashmir. indian j occup environ med. 2010 sep;14(3):78-86. 125.ruder am, carreón t, butler ma, calvert gm, davis-king ke, waters ma, schulte pa, mandel js, romanian neurosurgery (2013) xx 1: 5 21 21 morton rf, reding dj, rosenman kd; brain cancer collaborative study group. exposure to farm crops, livestock, and farm tasks and risk of glioma: the upper midwest health study. am j epidemiol. 2009 jun 15;169(12):1479-91. 126.rajaraman p, stewart pa, samet jm, schwartz bs, linet ms, zahm sh, rothman n, yeager m, fine ha, black pm, loeffler j, shapiro wr, selker rg, inskip pd. lead, genetic susceptibility, and risk of adult brain tumors. cancer epidemiol biomarkers prev. 2006 dec;15(12):2514-20. 127.de roos aj, stewart pa, linet ms, heineman ef, dosemeci m, wilcosky t, shapiro wr, selker rg, fine ha, black pm, inskip pd. occupation and the risk of adult glioma in the united states. cancer causes control. 2003 mar;14(2):139-50. 128.cabaniols c, giorgi r, chinot o, ferahta n, spinelli v, alla p, barrie m, lehucher-michel mp. links between private habits, psychological stress and brain cancer: a case-control pilot study in france. j neurooncol. 2011 jun;103(2):307-16. 129.inskip pd, tarone re, hatch ee, wilcosky tc, fine ha, black pm, loeffler js, shapiro wr, selker rg, linet ms. sociodemographic indicators and risk of brain tumours. int j epidemiol. 2003 apr;32(2):225-33. 130.preston-martin s, pogoda jm, schlehofer b, blettner m, howe gr, ryan p, menegoz f, giles gg, rodvall y, choi nw, little j, arslan a. an international case-control study of adult glioma and meningioma: the role of head trauma. int j epidemiol. 1998 aug;27(4):579-86. 131.inskip pd, mellemkjaer l, gridley g, olsen jh. incidence of intracranial tumors following hospitalization for head injuries (denmark). cancer causes control. 1998 jan;9(1):109-16. 132.zhou b, liu w. post-traumatic glioma: report of one case and review of the literature. int j med sci. 2010 jul 29;7(5):248-50. review. 133.bluhm ec, zahm sh, fine ha, black pm, loeffler js, shapiro wr, selker rg, inskip pd. personal hair dye use and risks of glioma, meningioma, and acoustic neuroma among adults. am j epidemiol. 2007 jan 1;165(1):63-71. 134.harder t, plagemann a, harder a. birth weight and subsequent risk of childhood primary brain tumors: a meta-analysis. am j epidemiol. 2008 aug 15;168(4):366-73. 135.efird jt. season of birth and risk for adult onset glioma. int j environ res public health. 2010 may;7(5):1913-36. microsoft word 8.selectedabstracts_f_carpato.doc romanian neurosurgery (2012) xix 2: 145 – 167 145 the 2nd congress in the danube-carpathian region controversies in neurosurgery 29th may –1st of june, 2012, cluj-napoca, romania the second edition of the congress in the danube-carpathian region controversies in neurosurgery has been held between 29th of may and 1st of june, 2012 in clujnapoca, romania. the topics of the 2nd congress neurosurgical controversies in the danube-carpathian region were: • tumors around the sella: transcranial or transsphenoidal approach? • cranio-vertebral junction lesions: with or without fusion? • arterio-venous malformations: surgery, radiosurgery or embolization? • spontaneous intracerebral hemorrhage: conservative vs. surgery • what’s new in brain and spinal cord protection and recovery? • advances in electrophysiology prof. dr. ioan ştefan florian was the congress president and prof. dr. dafin fior muresanu was the co-president of the congress. the congress was proceeded by the german-romanian course. selected abstracts intracranial approach for sellar region tumors ștefan florian1,2, b.pintea1,2, z. andrasoni2 1university of medicine and pharmacy “iuliu hatieganu”, cluj-napoca, romania 2cluj county emergency hospital, department of neurosurgery, cluj-napoca, romania introduction: the principles in the surgical management of sellar and suprasellar tumors are to relieve mass effect, normalize pituitary hypersecretion, preserve or restore normal pituitary function, prevent tumor recurrence and to provide tissue for pathological and scientific study. selection of the approach is based on the size, configuration and location of the tumor. aim: this review consists in a case series of patients with suprasellar tumors operated by transcranial approach in 1st neurosurgical department of county emergency hospital cluj-napoca between 01.01.2000 31.12.2010. this study targets to add some arguments in favor of classical intracranial approach which could be the treatment of choice for many of these tumors. patients and methods: we present a retrospective study of a single centre single surgeon on 228 consecutive cases with large suprasellar tumors admitted and operated in our department between 01.01.2000 and 31.12.2010. 146 selected abstracts the 2nd congress in the danube-carpathian region results: all cases selected for this study had extrasellar extension, demonstrated on the preoperative neuroimagistic studies. like other reports on suprasellar tumors, the most common type of tumor in our study was pituitary adenoma, 118 of cases (52%), followed by tuberculum sellae and planum sphenoidale meningioma, 68 of cases (30%) and craniopharyngioma, 28 of cases (12%). other tumors encountered in this region was low grade glioma, 7 of cases, immature teratoma 2 cases, 3 cases of germ -cell tumor and 2 cases of metastasis. the peak incidence was in the 5th decade. sex ratio was 1, 28. the most common ophthalmic presentation was blurred vision, in 90% of cases. headache, the second most common presentation was presented in 68% of cases. the mean duration of symptoms was 12, 7 months. all our cases underwent surgery by transcranial approach, unilateral frontotemporal in 152 of cases (67%), unilateral subfrontal in 47 of cases (21%), bifrontopterional in 12 cases (5, 5%), and bifrontal in 9 cases (4%), interemispheric transcallosal in 5 cases (1,5%) and frontoorbitozigomatic in 3 cases (1%). surgical related complications were transient visual alteration in 3 cases, local infection in 4 cases, intracerebral hematoma in 3 cases, arterial vasospasm in 2 cases, transient diabetes insipidus in the large majority of pituitary adenomas and craniopharingiomas. only 4 cases of pituitary adenomas and 2 of craniopharingiomas recurred after subtotal resection, requiring re-intervention. gross total resection of the tumor was achieved in 83% of cases. mortality rate was 1,5%. concussions: the classical frontotemporal approach is enough for complete removal of large tumors in this region. there is no need for larger opening for multidirectional approach because that means multiple ways for brain injury. the key points are proper positioning, proper opening, brain relaxation and surgical experience. endoscopic approaches to the sellar region: endonasal, supraorbital or interhemispheric joachim oertel neurochirurgische klinik, universität des saarlandes, homburg / saar, germany the indication for endoscopic assisted surgery in skull base lesions is under controversial discussion. experienced skull base surgeons often consider the endoscope to be unnecessary while a younger generation of surgeons counts on the value of the endoscope. often it is forgotten that the endoscope is an instrument for visualization with distinct advantages and disadvantages. thus, the advantages of the endoscopic technique can only be appreciated in combination with an ideal approach and an adequate surgical technique. here, various approaches to the sellar regions such as endonasal transsphenoidal, supraorbital endoscopic, interhemipheric microsurgical with endoscopic assistance and pterional microsurgical with endoscopic assistance are presented. the distinct advantage with particular respect to application of the endoscopic of each approach is described. romanian neurosurgery (2012) xix 2: 145 – 167 147 after presentation of the various approaches, a detailed account on selected cases of each approach is given. exemplary lesion such as meningiomas, pituitary adenomas, rathke’s cleft cysts and craniopharyngiomas are presented. the peculiar advantages and disadvantages of the various approaches in each lesion are explained. in all, after careful selection of the approach, the endoscopic technique is a valuable tool in selected cases of skull base procedure within or next to the sellar region. in a small subgroup of these procedures, the endoscopic is indispensable. surgical management of sellar and parasellar menigiomas adrian balasa, rares chinezu, ors hajducsi neurosurgery department, targu mures clinical emergency hospital, targu mures, romania sellar and paraselarmeningiomas represent 4 – 10 % of all intracranial meningiomas. due to their close proximity to the arteries of the anterior circulation, anterior visual pathways, hypothalamus and pituitary stalk the have always been regarded as challenging cases. traditionally these cases have been operated via intracranial approaches (subfrontal, frontopterional, supraorbital) but advances hardware and technique have included this pathology in the indications of transsphenoidal endoscopic operations. material and method: patients operated in the past 5 years at the neurosurgery department of the targumures clinical emergency hospital. results: a number of 30 cases have been operated for sellar and parasellarmeningio mas: 13meningiomas of the 1/3 inner sphenoid wing and anterior clinoid, 12 tuberculumsellaemeningiomas, 5 planumsphenoidalemeningiomas. all cases have been operated by cranial approach (subfrontal, frontopterional) the mean age of the group is 51+/17 years, sex ratio f/m is 23/7. primary symptoms were visual disturbances (loss of sight or visual impairment, diplopia), followed by convulsive seizures and personality changes. 22 cases presented increase in visual acuity, in 5 cases preservation of sight has been achieved while in 3 casepatients postoperatively presented decreased visual acuity. we had 1 scalp infection that required surgical removal of the bone and later cranioplasty. in one case there was a severe thrombosis of the intracavernous carotid that resulted in the death of the patient. conclusion: microscopic intracranial approaches are a safe technique and widely used technique. endoscopic approaches have been proven to be effective in selected cases, but further studies are required. tumors around the sella easy and difficult microsurgical cases ion poeata1,2, b iliescu1, s. gaivas1, z. faiyad1, d. rotariu1 13rd department of neurosurgery “prof. dr.n.oblu” clinical emergency hospital, iasi, romania 2“gr.t. popa” university of medicine and pharmacy iasi, romania objectives: pituitary adenoma represents the most frequent tumour encountered in the sellar region. following our initial 148 selected abstracts the 2nd congress in the danube-carpathian region experience with endoscope assisted transphenoidal approach we compared the indications, technical aspects, and surgical results with the well-developed transcranial approach. material and method: we have analyzed retrospectively the cases of pituitary adenoma treated surgically between jan 2006 and dec 2010. we looked at the presenting symptoms, hormonal status, local extension, surgical approach, tumor histology, type of resection, tumor volume, cavernous sinus invasion, surgical corridors, recurrence rate, intraoperative and postoperative complications. results: 72 patients were included in the study, with an equal sex distribution. the pathology was dominated by pituitary macro adenomas in 47 cases. hormonal status evaluation showed 51.3% as being non-secreting pituitary adenomas. 65.2% of the cases underwent surgery. the surgical indication was based on the hormonal status and the involvement of the optic apparatus, which in our series was 51%. the invasion of the cavernous sinus has been classified according to the knosp criteria [7]. according to this grading system 44% of the cases were in grade 3 and 4. the most used surgical approach was the pterional approach in 83% and transsphenoidal approach in the remaining 17%. the most frequent postoperative complication encountered in our series was represented by meningitis, in 13% of the cases. the endocrine complications were represented by transitory diabetes insipidus in 23.4% and siadh in 4.2% (2 cases). the follow up at 3 months showed no cases of early recurrence, from the group of patient with str 6 were sent to radiotherapy. at the 1 year follow we documented 3 deaths, 3 cases of hydrocephalus (treated with ventriculoperitoneal shunt), 19 cases showed no imagistic or clinical signs of tumour reccurence, while 22 presented with imagistic evidence of stable residual tumour with no clinical symptoms. conclusions: the main surgical indication in pituitary adenomas is represented by the secreting hormonal status of the patient (excepting prolactin secreting tumours) and the impairment of the vision. the most frequent surgical approach was represented by the transcranial (pterional) approach due to the large dimensions and invasiveness of the tumours presented in our series but also the surgical team preference (in the absence of intracranial endoscopy at those times). keywords: pituitary adenoma, pituitary apoplexy, prolactinoma, sellar region controversies in adult brachial plexus surgery current concept in traction injuries lukas rasulic school of medicine, university of belgrade, serbia clinic of neurosurgery, clinical center, belgrade, serbia background: adult brachial plexus surgery still remains a long and hard task. traction injuries of the brachial plexus present a major problem in surgical management of peripheral nerve injuries. the reasons for this are difficult identification and differentiation of the level and extent of the injury, and a limited possibility for surgical reconstruction, especially in cases of avulsions of one or more spinal nerve roots. aim: this study analyzes the results of surgical treatment of traction injuries of the brachial plexus in 98 patients, 78 of whom were with avulsion of one or more spinal romanian neurosurgery (2012) xix 2: 145 – 167 149 roots, and the other 20 with peripheral traction injuries. methods: retrospective analysis. discussion: depending on the degree of nerve damage, the methods of surgical treatment are neurolysis, nerve grafting and nerve transfer. nerve transfer is also problematic because none of microsurgical techniques or methods regarding the choice of donor nerve have proven appropriate thus far. furthermore, there are several dilemmas that still remain in the field of the brachial plexus traction injures surgery which remains controversial up to date: 1. which is the best way to evaluate the viability of the proximal stump of the injured brachial plexus? physical examination, electrophysiology, image studies or histology? 2. grafts or distal transfers in the repair of postganglionic supraclavicular lesions? 3. flail arm: until when the surgical repair should be done? 4. treatment options in severe adult brachial plexus traction injuries: choice of nerve transfer. we have tried to resolve this dilemmas on the basis of our experience in 187 surgical procedures performed in accordance with functional priorities, including 146 nerve transfers. keywords: brachial plexus, nerve grafting, nerve transfer, neurolysis, traction injury. anterior dens and transarticular screws fusion for combined atlantoaxial fractures roxana matica neurochirurgie städtisches klinikum braunschweig brunswick, lower saxony, germany the treatment for combined dens fractures type anderson ii and jefferson fractures is controversial and there are no established guidelines. because reports of combination c1-c2 fractures are relatively infrequent until now sufficient studies to support treatment standards do not exist. a retrospective study of 3 cases with posttraumatic combined atlantoaxial factures stabilized with triple anterior screws was undertaken. all patients were over 70 years old. the accidents occurred by falling. the operations duration was between 1h30min and 2h50min. the ventral dens and transarticular fusion had good follow-up results in all 3 cases, none of the patients needed reoperation. the neurological outcome was favorable with no deficits. objectives: the treatment for combined dens fractures type anderson ii and jefferson fractures presents management challenges. because reports of combination c1-c2 fractures are relatively infrequent standards or guidelines haven’t been established. for relatively stable fractures immobilization is the first option. for instable c1 and c2 fractures with luxation fusion is recommended. cases of triple ventral fusion with dens and transarticular screws are uncommon. a retrospective study of 3 cases presenting these combined fractures stabilized in this manner in klinikum braunschweig was undertaken. aim: this study presents 3 cases of patients who were admitted with combined dens fractures type anderson ii and jefferson fractures. all patients were female, had no neurological deficit and were over 70 years old. anterior triple screw fusion was the chosen technique for stabilizing the fractures. these cases are proposed examples of the therapy option. the operations good results aim to point the 150 selected abstracts the 2nd congress in the danube-carpathian region need for a structured statistical study in order to obtain an indication consensus. report: a female patient 85 years old was admitted with anderson type ii odontoid fracture, jefferson fracture and additionally c4/5 pseudolisthesis and c5/6 subluxation. the patient had fallen at home and had no sensory or motoric deficits. the indication for ventral fusion given the multiple diagnoses was established. a triple anterior screw fusion was used for the upper cervical level: dens screw and 2 transarticular screws. the lower cervical level was fixed with two cages and titan plate. there was no significant blood loss. the operations duration was 2h50min. by the time of discharge no neurological deficit was noted. the patient wore for 6 weeks a miami-jcollar. the three months follow-up computer-tomography showed no implant dislocation or change, neurologically the patient showed no deficit. a female patient 83 years old was admitted with anderson type ii odontoid fracture, jefferson fracture after falling. the accident happened 2 weeks before and since then the patient complained about neck pain. the indication for ventral fusion was established. a triple anterior screw fusion was used: dens screw and 2 transarticular screws. the operations duration was 1h30min. by the time of discharge no sensory or motoric deficit was noted. the patient wore for 6 weeks a miami-j-collar. the three months follow-up computertomography showed no implant dislocation or change. a female patient 83 years old was admitted with anderson type ii odontoid fracture, jefferson fracture after falling. she had no neurological deficit but complained about acute neck pain. the indication for ventral fusion was established. a triple anterior screw fusion was used for the upper cervical level: dens screw and 2 transarticular screws. the operations duration was 2h10min. by the time of discharge no sensory or motoric deficit was noted. the patient wore for 6 weeks a miami-j-collar. the follow-up after one year computer-tomography showed no implant dislocation or instability, neurologically there were no deficits notable. method: the patients were all over 70 years old by the time of admission. all patients have fallen from a height lower than 2 meters. the primary diagnostic method was computer-tomography of the cervical spine. the first screw was in all operations was the stabilizing the dens fracture followed by the transarticular screws. the screws used were olerud 4x40mm for odontoid fixation and the transarticular screws varied between 4x17 and 4x20mm no significant blood loss was seen and no transfusion needed. in one case the head of the patient was fixed in mayfield-extension. result: all patients had no neurological deficit by then time of discharge and were stable over the follow up period. the follow up time was of 2 months, 4 months and 1 year respectively. the operations durations were 1h30min, 2h10min and 2h50min. one patient had additionally a c4/5 and c5/6 instability which was stabilized with plate and cages. there was minimal blood loss with no transfusion needed. all patients wore for one and a half months a miami-j-collar. no patient needed reoperation and no patient developed sensitive or motoric deficits. conclusion: the triple screw anterior fusion for combined anderson ii type odontoid fractures and jefferson fractures romanian neurosurgery (2012) xix 2: 145 – 167 151 had good postoperative outcome. the technique requires good operative skills. the outcome follow-up showed a good reposition with no notable implant loosening and no neurological deficit. a structured future study of this method in comparison with other therapeutic possibilities is needed in order to set standards. spinal epidural metastasis with unknown origin lászló fügedi, jános skapinyecz, csaba oláh, béla demeter department of neurosurgery borsod county university teaching hospital, miskolc, hungary introduction: spinal epidural metastases can be diagnosed in 1-5% of the systemic cancer patients. most of the cases come into recognition between the age of 40 and 65 years. these tumours can be found principally in the thoracic region. the origin of the spinal epidural metastasis is usually lung, breast, prostate cancer, nonhodgkin lymphoma or multiple myloma. it rarely occurs, that we can’t show any primary neoplasm. case report: we present a 54 years old male patient’s case who was admitted to our department with the clinical signs of severe paraparesis caused by a pure epidural spinal tumour at the level of th.iii.-v. vertebras. on mr imaging myelon compression was seen. histological exam verified solid anaplastic cancer. the patient underwent posoperative telecobalt irradiation and adjuvant medical treatment with bisphosphonate. results: in spite of the severe neurological deficit on admission the patient’s condition and his quality of life improved and he could reach a longer survival time than we expected. the circumstantial examination wasn’t suceed, we couldn’t find any origo of the spinal epidural metastasis. the histological revision supposed a large-cell neuroendocrin lung originated primary tumour but the selective evaluation couldn’t exhibit that. conclusions: considering the literature in such cases it is suggested to perform an urgent surgical decompression with radical tumour resection and postoperative irradiation and chemotherapy. it rarely occurs a favourable outcome with a better quality of life and longer survival time than expected. chiari malformations adrian bălașa, dorin nicolae gherasim neurosurgery departement, clinical emergency hospital, targu-mures, romania introduction: as described and classified over a century ago, herniation of the cerebellar tonsils more than 5 mm into the cervical spinal canal with obliteration of the cerebellomedullary cistern and obstruction of foramen magnum is the primary feature of chiari i malformation. pathophysiology: the chiari malformation constitutes an heterogeneous and multifactorial entity, in which congenital forms of isolated presentation or with a genetic background and forms of acquired etiology exist. no unitary clasification exists to this date. clinic and symptoms: one estimate based on extrapolations from a previous study suggested a prevalence of tonsillarectopiainthe general population of approximately 3.5%. the proportion of these individuals who go on to develop symptoms is unknown. nevertheless, the disorder can be associated with significant symptomatology, risk of secondary injury due to trauma and the risk of progression 152 selected abstracts the 2nd congress in the danube-carpathian region and damage of the spinal cord due to associated syringomyelia. clinical material and method: in the last 5 years we have treated 17 patients with chiari i malformation. 12 women, 5 men. the mean age was 43. (between 21 and 60 years). the symptoms were grouped in 6 syndroms: 1. brain stem and bulbar palsy syndrome, 2. cerebellar syndrome, 3. central cord syndrome, including pain (frequently “ burning”), 4. paroxysmal intracranial hypertension, 5. pyramidal syndrome, 6. scoliosis. surgical treatment: the goal of surgery is to relieve cord compression and to reestablish adequate csf flow. there have been no prospective studies in which one treatment form is directly compared with another. results: postoperative, the condition of the patient was reassessed at the last followup visit according to: symptom resolution; sign and symptom improvement; no change; sign and symptom worsening. conclusions: in light of the many theories of pathophysiology, broad clinical presentations, and multitude of surgical interventions with variable outcomes, it is no wonder that a single surgical approach does not exist. we recommend tailoring the surgical approach to treat the dominant clinical problem. early diagnosis and treatment is critical in obtaining the best outcome for the patient. the presence of syringomyelia is a sign of advanced structural abnormality, as it is associated with the presence of sensory and motor deficits, as well as with the presence of spinal deformity. the preoperative presence of deficit is a predictor of poorer neurological outcome, making a strong case for early surgical intervention. controversy of decompressive craniectomy (scandal in modern science) andrás csókay neurosurgery, baz county hosp. miskolc, hungary objectives: one of the weak points of the modern science may be the analysing of the efficacy of the medical treatment only by the rule of the evidence base medicine in the state around the death. it is an important topic as the scientific world often does not consider enough the rule of bioethics which says, “in life threatening illness the scientific rationale for the treatment must be sufficiently strong that a positive result would be widely accepted. “the history of dc is a very good example”. aim: to graduate up the dc from optional to recommendation cathegory in guidelines. report: we report additional consideration to improve the efficacy of dc. method: the status around the death is such a hundred or thousand? unknown equations that we must not fix only one or two constant in analysing the results as we probably make mistakes in our consequence. result: the evidence proved by decra (issued in 2011), which mixed the analysis of the status of far away from death and the status around the death in its conclusion. mixing the life threatening and curative characteristic it was obvious that the conclusion of the decra was questionable. the application of dc at the adults from icp 20 mmhg during 15-30 minutes is illogic because the surgical complication decreases the efficacy against the conservative therapy which is also effective in this icp status. conclusion: if we perform the dc routinely above 25 mmhg, probably we are going to operate many times in vain!!!, but romanian neurosurgery (2012) xix 2: 145 – 167 153 we can avoid the mindless death of the patients especially in child caused by a reversible curative pathological process called brain oedema. we have to know that in emergency care around the death we have to make efforts 10 times unnecessarily while it is worth doing the dc. the 10 dc causes less damage for the patients than the only one fatal death. the situation is quite similar to the situation of emergency conicotomy or reanimation. we should continue the debate not about the performance of dc, but how to increase the efficacy of the dc. spontaneous intracerebral hemorrhage – surgical or conservative treatment? ion poeata, cosmin apetrei, bogdan iliescu, bogdan chirita clinic of neurosurgery, “gr.t. popa” university of medicine and pharmacy iasi, romania according to current data spontaneous intracerebral hemorrhage is the cause of 1040% of stroke cases. surgical treatment of these hemorrhages is still a matter of debate despite the numerous randomized clinical trials looking at this problem. the first such study published in 1961 (mckissock w, richardson a, taylor j: primary intracerebral haematoma: a controlled trial of surgical and conservative treatment in 180 unselected cases) failed to show any advantage of surgery or conservative treatment. a metanalisys put together by prasad in 2000 looked at the 12 trials published to date and showed a slightly favorable outcome in the surgery group (0.85 odds ratio). we present the experience of our center retrospectively analyzing 42 cases treated during one year period (2011-2012). evaluated criteria was: location of the hematoma (lobar, cerebelar, putaminal, or deep), ethiopatogenesis (hbp, anticoagulant therapy, amyloidosis, age, cgs, neurological deficit, general status impairment, the intervals stroke presentation, presentation – surgery, outcome, complications. novoseven and thrombolysis were unavilable. we compare the results in two groups treated either surgically or conservatively according to current protocols. inclusion criteria in our study was same as stich i trial. endoscope-assisted haematoma evacuation in patients with spontaneous supraand infratentorial intra-parenchymal haemorrhages: initial results of a prospective monocentric trial yavor enchev1, tony avramov1, bogomil iliev1, tony kondev1, danail lichev2 1department of neurosurgery; 2department of anesthesiology and intensive care university hospital “sv. marina”, medical university varna, bulgaria objective: the endoscope-assisted haematoma evacuation in patients with spontaneous supraand infratentorial intraparenchymal hemorrhages, nowadays is considered investigational. aim: the purpose of the presented prospective trial is to determine the effectiveness of minimally invasive evacuation of intracerebral haemorrhage (ich) utilizing the endoscopic method. the authors analyzed the study design in terms of patient selection, surgical technique, clinical and radiological follow 154 selected abstracts the 2nd congress in the danube-carpathian region up, as well as their initial results. material and methods: the trial analyze prospectively the clinical and radiographic data obtained in patients treated with endoscope-assisted evacuation of spontaneous supraand infratentorial intraparenchymal haematomas. the study inclusion and exclusion criteria are defined and strictly implemented. the technical side of this report explains details of the procedure, the applied instruments and methods for hemostasis. hematoma evacuation degree is evaluated by comparing the preand postoperative ct scans. glasgow outcome scale scores is recorded at the 6-month postoperative follow-up. rebleeding, morbidity, and mortality are analyzed. the relevant literature is thoroughly reviewed and summarized. results: the trial start point is the 1st of april, 2012 as the fixed term of the study is 2 years with at least 100 patients. our primary results include 11 patients. all surgeries were performed within 36 hours of hemorrhage. the procedure related morbidity and mortality were 0%. conclusions: the authors acknowledge the limitations of these preliminary results in a insignificant small number of patients. however, the initially data suggest that early endoscope-assisted ich evacuation is safe and effective. spinal subdural empyema in childhood lászló fügedi, béla demeter department of neurosurgery borsod county university teaching hospital, miskolc, hungary introduction: among the spinal inflammatory diseases there are many types including spondylodiscitis, osteomyelitis, spinal epidural abscess, spinal subdural empyema and intramedullary abscess. it rarely occurs parasitic infections, otherwise nowadays we can see more and more cases with specific tuberculotic process (pott’s disease). in childhood first of all the haematogen spreading of bacterial meningitis or other inflammation can conduce to spinal epidural, subdural or intramedullary abscess. case report: we present a one year old girl, who was underwent surgery just after birth because of meningomyelocele and spina bifida aperta. she was often treated for urinary infections due to the renal disorder. in consequence of the haematogen spreading of the urocystitis an escherichia coli meningitis developed. in spite of the antibiotic treatment a very severe paraparesis occured in few days with other clinical signs of myelon compression. on mr imaging there was seen a spinal subdural empyema from the level of th.x. vertebra until the s.i. segment. we performed an urgent surgical decompression (right sided l.i.and l.iv. arcoflavotomy and radical evacuation of the abscess) and lumbal drainage for using intrathecal antibiotic treatment during 10 days. results: due to the immediate surgery, the intensive care and the expert rehabilitation therapy (massage, hydroand phisiotherapy) the paraplegic girl could be able to walk with orthesis. conclusions: the early diagnosis of spinal subdural empyema completed with a prompt surgical decompression, specified systemic and intrathecal antibiotic therapy, the adequate intensive care as well as the rehabilition treatment can lead better outcome and quality of life in spite of the bad prognosis. romanian neurosurgery (2012) xix 2: 145 – 167 155 the role of culture and spiritual life in neurosurgical innovations andrás csókay neurosurgery, baz county hosp. miskolc, hungary objectives: prayer, science, culture are three vastly different areas that in our personal experience complement one another. the quality of life of the patients and neurosurgeons is very tight junction aim: the presentation is intended as evidence thereof. method: more specifically over the course of the presentation we can learn how the spiritual life and culture aided neurosurgical work by discoveries operative innovations. result: direct examples show the reality of the above mentioned statements. conclusion: and where does faith come into the picture? religion and culture join forces in shaping a richly emotive inner life. it has been shown that such “internal wealth” is essential for remembering, and that it forms the basis of creativity. when solving a problem, the memories we recall most redly are those to which we can assign emotional import. to be able to do the latter, we need to have rich and emotive spiritual life. though important, learning itself is not enough to ensure creativity. we can freely choose to develop and improve our inner world. this is how we experienced culture and science united in the faith. neuromodulation v. masopust, k. saur department of neurosurgery military university hospital prague, czech republic introduction: neuromodulation is reversibile surgery process which blocks information of pain going to brain or blocks interneurons in brain cortex. there were realized 31 neuromodulation performances in our department in 2011. the most of these operations were perfomed for failed back surgery syndrom – 21. material and method: 31 patients were operated: 18 women a 13 men. methods of neuromodulation: dorsal colum stimulation (scs) peripheral nerve stimulation (pns) occipital nerve stimulation (ons) motor cortex stimulation (mcs) reason for implantation: 21 scs for failed back surgery syndrom 1 scs for post amputation pain 1 scs for periferal nerve denervation of lower leg 1 scs in cervical region for perifer nerve lesion 1 scs in cervical region for complex regional pain syndrom 1 pns for intercostal neuralgia 4 ons of headache 1 mcs for facial pain results: 1 stimulation was not efective. in 30 patients was effectivity of delta vas from 3 to 9. 1 neuromodulation system was removed for infection and returned after 2 months. in 2 cases was performed reinsertion of elektrod after electrod movement. conclusion: neuromodulation is very effective removable method for treatment of pain. only one problem exists and that is cost effectivity in our country. 156 selected abstracts the 2nd congress in the danube-carpathian region fbss in three perspectives saur karel, vanek petr department of neurosurgery military university hospital prague czech republic failed back surgery syndrome (fbss) is usuall mark for unsatisfactory result of any lumbar spine surgery in degenerative spine disease. management possibilities are as wide and numerous as possible etiologies of fbss and we can hardly proceed the patient according to any guideline or evidence based approach. from surgical perspective it is natural to search morphological basis of persistent pain and to suppose another surgery. in case of clearly proved morphological substrate is indication of another surgery obvious. but in case of lacking pain generator could be another surgery only next step to chronicity and one could consider another sort of intervention, or take a look of different perstective. from perspective of physiotherapist it is more about function than morphology, and numerous exercises could help to restore appropriate movement stereotype and function. the impact of malfunction is demonstrated on analysis of outcome of patient after lumbar spondylolistesis stabilization. from perspective of psychotherapy there is about 400 psychotherapeutic systems to approach the patient in different ways, in way of rationalism, or emotions and others. psychotherapy could be limited to relaxation and stress reduction or could address patient’s relationship to pain, or touch the deepest injuries. the main difference to surgery is the necessity of patient’s own activity and strong intention to change. in the case of patient’s passivity there is hardly any possibility to any change, or temper the pain. controversis in the therapeutical approach of pineal area lesions. an experience of 103 cases a.v. ciurea, a. tascu, m lisievici, f. brehar, h. moisa carol davila university school of medicine. the national center for excellency in neurosurgery; bagdasar-arseni teaching hospital, bucharest, romania. background: the pineal area (pa) is defined between the splenium of the corpus calosum and tella choroidea (dorsal), quadrigeminal plate and mesencephalum tectum (ventral), posterior part of the 3rd ventricule, (rostral) and cerebelar vermis (caudal). tumors of this region are more common in children (3-8% of primary brain tumours) than in adults (1%). germ cell tumors (gtc) are predominant in this area. materials & methods: the authors reviewed presentations, diagnostic problems, management and outcome in 103 cases of pineal area tumors admitted over a period of 17 years (1 jan. 1995 – 31 dec. 2011). the series comprises 59 male and 44 female patients, ranging in age from 0 to 59 years (media 26 y.o.). the clinical features were represented by intracranial hypertension (87 cases – 84.7 %), parinaud syndrome (72 cases – 70.2 %), convergence palsy (22 cases – 21.4 %), ataxia (35 cases – 34%), seizures (19 cases – 18,5 %), endocrine disturbances (16 cases – 15.4 %), consciousness disturbances (13 cases, 12,4%). diagnostic evaluation romanian neurosurgery (2012) xix 2: 145 – 167 157 consisted of a medical history, physical & detailed neurological examination, neurodiagnostic studies (ct and mri scan) and studies of serum and csf tumor markers. hydrocephalus was associated in 86 cases (83.5 %). generally, gct, ependymomas and pineal cell tumors metastasize easily through the csf (“drop metastases”). in that situation the all cns will be evaluated by mri scan preoperative and postoperative. there were 100 cases microsurgically approached, via the occipital transtentorial approach (85 cases (82.4 %)) or supracerebellar infratentorial approach (15 cases (14.4%)). three cases (3.4 %) in our data received only stereotactic procedures. histological diagnosis has revealed germ cell tumors in 48 cases (46,4%), pineal cell tumors in 19 cases (18,5 %), glial cell tumors in 33 cases (32 %) and miscellaneous tumors in 3 cases (3,1 %). total removal of the tumor was achieved in 30 cases (27.8 %), near total removal in 25 cases (24.7 %), partial removal in 37 cases (36.0 %); open biopsy was undertaken in 8 cases (8,2 %) and stereotactic biopsy in 3 cases (3,0%). there were four deaths in the first months (4.1 %). the postoperative complications included: ocular movement disorders (34 cases – 33 %), impaired consciousness (23 cases – 22.6 %), seizures (22 cases – 21.6 %), ataxia (18 cases – 17.5 %), pupillary abnormalities (18 cases – 17.8 %) and others. the majority of these complications were transient. forty-six patients (49 %) received craniospinal irradiation or focused radiotherapy (g.k.s.). radiation therapy was done always after the pathological diagnosis. craniospinal irradiation was administered only to those patients with the disease involving more than one intracranial site, demonstrated meningeal seeding or positive csf cytology. chemotherapy (cisplatin & bleomycin & actinomycin d) was received in 46 cases. the glasgow outcome scale (gos) at 6 months shows: good recovery 58 cases (56.7%), moderate disability 26 cases (24.7%), severe disability 13 cases (12,4%), persistent vegetative state 2 cases (2%), and death 4 cases (4.1%). conclusion: on the basis of this review, the authors consider that the outcome depends both by the histological type of tumor and the modality of treatment applied. there is no surgical approach superior to others, but the stereotactic approach is one of the good and minimal invasive option for obtain enough material for pathological diagnosis. the deep cerebral veins are not a major obstacle for operation (open or stereotactic) in these regions. keywords: pineal area tumors, mri, microsurgery, stereotactic biopsy, germ cell tumors and gamma knife surgery abreviation: pa = pineal area tumors pbt = pediatric brain tumors gct = germ cell tumors g.k.s. = gamma knife surgery g.o.s. = glasgow outcome scale csf = cerebral spinal fluid cns= central nervous system 158 selected abstracts the 2nd congress in the danube-carpathian region microsurgical approaches in cranio-vertebral junction area, a personal series of 29 cases andrei ștefan iencean, faiyad ziyad, marcel ivanovr, sergiu gaivas, alexandru chiriac, bogdan iliescu, ion poeata 3rd department of neurosurgery “prof. dr.n.oblu” clinical emergency hospital, iasi, romania objectives: the instability secondary to the cranio-vertebral junction lesions is important and states the question on the indication for stabilization. the question also arises about the incidence of postoperative instability and the need for treatment of this iatrogenic condition. we present our surgical experience in the treatment of 29 patients with nontraumatic lesions of the cranio-vertebral junction that were warded from 2007 to 2011 in our department. methods: in five years we treated twentynine patients with nontraumatic craniovertebral junction lesions: thirteen arnold– chiari malformations, five foramen magnum meningiomas, three vertebral tumors c1/c2 – posterior arch, two glomus jugulare tumors, two occipital condyle tumors, a c2 neurinoma, one case of odontoid panus, one case of cranio-cervical ependimoma and one cranio-spinal arteriovenous fistula. all patients were explored preoperatively by mri or ct exams and seldinger angiography was performed in two patients. results: the suboccipital (midline and paramedian) approach was performed in eighteen cases, sixteen of them required additional resection of the posterior arch of c1/ c2. in six patients the surgical approach implied only the resection of posterior arch of c1/c2; the far-lateral approach (accompanied with the resection of one third of the occipital condyle) was used in five patients. all patients benefited by a microsurgical approach; gross total removal was achieved in 9 out of 14 cases of tumors. there were no major clinical complications (except one case of hydrocephalus treated with ventriculoperitoneal shunting) and none of the patients developed instability of the region requiring stabilization. conclusions: the choosing of the surgical approach and the amount of bone resection must be customized to each patient, according to the size and localization of the lesion. the microsurgical approach allows the limitation of bone resection in case of cranio-vertebral junction lesions, thus avoiding the instability. apart from the cranio-vertebral junction lesions, potential unstable, the surgical approaches at this level may lead to the instability of the region. in our series none of the patients developed instability that should require consecutive stabilization. keywords: cranio-vertebral junction, instability, microsurgical approach. eosinophilic granuloma of the orbit: virtual endoscopy and 3d-ct scan of the bone distructions szabo ioan1, bianca szabo2, kakucs cristian1 1cluj county emergency hospital, neurosurgical department, cluj napoca, romania. 2“iuliu hatieganu” university, cluj county emergency hospital, ophthalmological clinic, cluj introduction: eosinophilic granuloma is a rare intraorbital tumor, we had only one case in our personal series of 825 orbital masses treated in the last 25 years. the advantages of modern neuroimagistical romanian neurosurgery (2012) xix 2: 145 – 167 159 techniques, such as 3d ct scan and virtual endoscopy are presented in this particular case. case report: the case of l.m., 26y old, male is presented. one month onset with right exophthalmos, superior palpebral swelling, orbital pain, diplopia. antibiotic and antiinflamatory treatment for a supposed orbital celullitis had no result. admitted in our departament, mri of the orbits revealed an intraorbital mass located in the superolateral part of the orbit, well delineated, nonincapsulated and distruction of the adjacent bony orbital wall. high definition ct scan of the skull was performed for better visualization of the bone deffect. 3d ct scan with osirix software revealed a cone-shape complete distruction in the greater wing of the sphenoid, from the periorbita to the dura mater in the right temporal pole. virtual endonavigation in the bone canal revealed 1,3 cm large deffect at the orbital and smaller, 0,9 cm deffect at the cranial end. the eroded walls of the bone were approximately smooth, with a sequestrum in the inferior part of the deffect. the tumor was completely removed, the walls of the bone communication drilled to healthy bone structure. pathologic finding eosinophilic granuloma, c 69.6 m 9752/1. postoperative total recovery. 3d ct scan of the orbit 30 days after surgery, smooth walls of the bone deffect. patient and method: we present the clinical case of a patient treated for right intraorbital eosinophilic granuloma. high definition ct scan with 3d secondary postprocessing of the images was made before and after operation. virtual endoscopy can clearly present the walls and margins of the bone defect. discussion: eosinophyilic granuloma is unusual in adult. our case presented a tunnel-shape bone distruction in the greater wing of the sphenoid, with direct communication between the orbit and temporal fossa. this bone lesion can be well localized with 3d ct. secondary postprocessing and 3d reconstruction of the images is recommended to be performed by every surgeon in certain cases. conclusions: eosinophilic granuloma of the orbit often produce adjacent bone erosions of the orbit. in our case, the erosion produced complete communication between the orbit and temporal fossa. 3d ct and virtual navigation permit a very good spatial localization and the inspection of the eroded bone, before and after surgery. keywords: eosinophilic granuloma, langerhans cell histiocytosis, orbital tumor, 3d ct scan, virtual endoscopy. a new approach for rational pharmacotherapy based on quantitative eeg source density mapping wilfried dimpfel justus-liebig university giessen, wetzlar, germany recording of voltage based electroencephalograms allows limited interpretation with respect to disease. it is strongly dependent on the experience of the physician. deviations from normality are difficult to recognize within the time dimension. mathematical quantitationof the signal using frequency analysis by fast fourier transformation (fft) provides the possibility to average data over time and to relate local frequency changesto 160 selected abstracts the 2nd congress in the danube-carpathian region neurotransmitter activity. for example, delta waves (up to 4.5 hz) are under the control of acetylcholine, alpha2 waves (9.75 to 12.5 hz) represent activity of the dopaminergic system. comparing data from an individual patient to a norm data base containing 250 files from healthy volunteers of different age allows discovering deviations from normality. recordings from 17 electrode positions and evaluation of 6 frequency ranges lead to 102 parameters. an aberration index is calculated which indicates the statistical probability with which the local frequency change deviates from normality. since many drugs have been characterized with respect to induction of frequency changes pre-clinically and clinically it is possible to find a drug which is able to modify the particular frequency recognized as deviated. this kind of matching provides a new approach in rational pharmacotherapy and allows control of therapeutic success. examples of patients suffering from epilepsy, migraine and parkinson’s disease will be given. quantitative eeg source density mapping should be of great help in practice. controversies in neurology: is the eeg burstsuppression pattern an epileptic behavior? florin amzica université de montreal, montreal, canada one of the typical electroencephalographic (eeg) patterns accompanying a comatose state is burstsuppression (bs). it was generally assumed that it would mark an almost complete deafferentation of the brain from its sensory inputs. recently it was shown that, at least in some iatrogenic comas, bs in fact results from a hyperexcitable state during which the bursting activity is triggered by low intensity stimuli that are unable to elicit overt responses under normal conditions (kroeger and amzica, 2007). on the other hand, the suppression episodes (isoelectric eeg) result from the exhaustion of cortical synaptic communication due to the transient depletion of extracellular calcium during the previous burst. it was further demonstrated that, contrary to the expected, bs is also associated with the suppression of cortical inhibition (ferron et al., 2009), thus promoting the idea that hyperexcitability is rather the result of abolished inhibition than increased excitation. an interesting issue concerns the similarity between symptoms associated either with bursts during bs or with spike– wave seizures. moreover, both conditions occur on a background of impaired inhibition. furthermore, in clinical practice there is often unclear delimitation between comatose bs behavior and epileptic manifestations (e.g., in hirsch et al., 2004). in addition, the antiepileptic medication obtains poor response (dan & boyd, 2006). this calls for one of the two possibilities: either bs is included in the already complex syndrome of epilepsies (with complicating issues regarding mechanisms and curative strategies) or it is regarded as distinct processes with distinct mechanisms. the latter alternative is supported by the fact that volatile anesthetics (isoflurane in particular) are used both to counteract status epilepticus and to induce bs, further suggesting that bursts of bs do not reflect an epileptic pathology. romanian neurosurgery (2012) xix 2: 145 – 167 161 transcranial magnetic stimulation an inside story on brain function tudor dimitrie lupescu transcranial magnetic stimulation is a useful neurophysiological technique that investigates the central nervous system, mainly the central motor pathways. it is used as a diagnostic tool, but also in research, therapeutics and neurorehabilitation. the method appeared 25 years ago, and has developed intensively throughout the world, so that nowadays a lot of scientific knowledge has been gathered. this presentation will try to describe the method, its physical and biological principles, and to show its major indications in clinical situations, as well as other more complex approaches regarding the central nervous system function in normal and pathological conditions. traumatic brain injury (tbi) – myths and facts christian matula neurosurgical department, medical university of vienna, austria the incidence and economic burden of traumatic brain injury (tbi) in all of its appearance is from undisputed high value all over the world. although a lot of work has been done in that field and still is ongoing, until nowadays a lot of “myths” are going around and most of the times (unfortunately) we’re still waiting for some “facts”. from a neurosurgeons perspective, it seems more than worthwhile to have an overview about the latest advances to offer more clearness respectively getting more facts into that jungle of recent perspectives and developments. one myth is that we can avoid trauma. fact is that there is no way to handle that. trauma is the leading cause of death ages 1-45, approximately 80,000 people per year are suffering on disability due to tbi and more that 3,100,000 are living with disabilities. precisely classify trauma is another myth. fact is, that time is ripe for a new, much more precise classification system based on the central questions: is “mild” really mild and differentiate “severe” due the possible outcome according to morphological findings in cct and mri. fact is that the admission gcs lost its predictive value for outcome so that nowadays there is a clear need for a new classification system. another myth is that the existing guidelines can solve the problems. fact is that the survey of compliance with the guidelines is rather bad. more than 65% shows no compliance, and although the relation gets better, it still remains rather low. a lot of myths are existing around decompressive craniotomy. fact is, that until now exept for problemtic studies in the 90’s there has never been a randomized trial studying decompressive craniotomy vs. other therapies. among others (e.g. cortison, prophilactic antiseizure therapy, etc.) the presentation will demonstrate that hard facts behind some other myths are missing. neurotrophicity, neuroprotection, neuroplasticity and neurogenesis are basic biological processes of paramount importance, overlapping and acting under genetic control to generate the endogenous defense activity (eda) which continually counteracts pathophysiological processes. illustrative clinical cases can prove a quiet remarkable outcome using cerebrolysin as a neuropretective drug and should 162 selected abstracts the 2nd congress in the danube-carpathian region probably motivate to novel our treatment concepts in case of tbi. moderate and severe traumatic brain injury (tbi) are characterize by a high rates of case fatality (15-20% in moderate tbi and 40% in severe tbi) and disability in survivors (3040% in moderate and 50-60% in severe tbi). biomarkers like gfap and s100b, but also others like erythropoetin, different statins or cyclosporin a could be proven as powerful adjuncts to the clinical assessment of brain damage and powerful predictors of outcome after tbi. there are a lot of myths on several topics in tbi (e.g. neuroprotection, biomarkers, stem cells, etc.) but not that many facts. what we need within the near future are reliable basic and clinical trials to get answers to questions mentioned above which probably will clear some of the above mentioned points. multimodal drugs and the new design for clinical trials in brain protection and recovery after tbi – captain trial dafin f. mureșanu chairman department of clinical neurosciences university of medicine and pharmacy “iuliu hatieganu” cluj -napoca, romania tbi is a field with many unmet needs in medicine and public health. it is a major cause of death and disability and also leads to huge direct and indirect costs to society. currently the incidence of tbi is increasing. tbi populations are heterogeneous in terms of mechanism of disease, baseline prognostic risk factors, clinical severity and evolution. this heterogeneity generates complex challenges. new pharmacological approach together with more basic and clinical research is needed for better targeting tbi therapy to the individuals. the frequent progression of contusive brain injury indicates that this may constitute a subpopulation of tbi more likely to benefit from acute neuroprotection (in the classic sense) by limiting processes involved in secondary brain damage. other mechanisms, and consequently different approaches may be more relevant in patients with diffuse axonal injury, and neuroprotection in a more broad sense also includes strategies and therapies aimed at promoting regeneration or replacement of lost neuronal and glial cells, neuronal circuits, and stimulation of neuroplasticity (neu-rorecovery). the primary goal of pharmacological support in tbi is to reduce secondary damage (neuroprotection) and to enhance repair (neurorecovery). the current presentation will highlight the limits of monomodal drugs, the advantages of multimodal drugs and the need for new designs for brain protection and recovery clinical trials in traumatic brain injury. as an example of new vision in the field of clinical research in brain protection and recovery after traumatic brain injury, the new design of related clinical trials will be presented – captain trail protocol: a large multicentric randomized controlled trial. romanian neurosurgery (2012) xix 2: 145 – 167 163 intracranial cavernous angiomas an experience on 109 cases a.v. ciurea1, a. tascu1, a. iliescu1, d. mohan2, f. stoica1, f. brehar1, r. rizea1, h. moisa1 1carol davila university school of medicine; the national center for excellency in neurosurgery; bagdasar-arseni teaching hospital, bucharest, romania 2oradea county emergency teaching hospital; university of oradea, faculty of medicine introduction: intracranial cavernomas (ic) count of 0.02 0.53% of all intracranial lesions and 8-15% of all avms. the association with avm is found in 10-30% cases. the lesions become symptomatic when the size of the lesion is bigger than 1 cm. these vascular malformations have started to be easily diagnosed with the introduction of routine mri scans. material and method: the cohort of 109 consecutive operated cases of intracranial cavernomas were admitted in the 1st department of neurosurgery of the bagdasar-arseni hospital & oradea county emergency hospital in the period of time between january 1998 january 2012 (14 years). all cases received a complex neuroimagistic diagnosis based on ct, mri & dsa angiography. the cases were operated and followed up in the bagdasararseni hospital in bucharest for a period ranging from 6 months to 9 years. the sex distribution was 55 males and 54 females aged between 11-56 years old with a peak of incidence in 31 year olds. the cavernomas localization was as follows: supratentorial in 75 cases (68,8%), infratentorial in 24 cases (22,0%), deep, basal ganglia & multiple 10 cases (9.1%). the lesions were located: frontal lobe 34 cases (31.2%), parietal lobe 15 cases (13.7%), temporal lobe 23 cases (21.1%), occipital lobe 3 cases (2.7%). multiple 3 cases (2.7%), deep and basal ganglia 7 cases (6.4%) brainstem 19 cases (17.4%), and cerebellum 5 cases (4.5%). in what concerns multiple cavernomas, we proceeded with surgery only for those either manifesting mass effect or presenting with hemorrhagic attack. the clinical symptoms were characterized by seizures 70 cases (64.2%), neurological deficits 16 cases (14.6%) hemorrhage 23 cases (21.1%). a special chapter of the study was dedicated to non-operated cases. they were: 7 cases multiple lesions, 9 asymptomatic and 5 lesions deep situated. in 2 cases of deep situated lesions, the therapy with gamma-knife surgery was applied. results: in this series of 109 operated patients, the global outcome scale (gos) at 6 months was: good recovery 82 cases (75.2%), moderate disability 18 cases (16.5%), severe disability 9 cases (8.2%), vegetative state 0 cases (0%) and death 0 cases (0%). the severe disability appears especially in brainstem cavernomas, but, in time, the cases improved exponentially. the follow-up period was between 6 months and 9 years, with a mean range of 7,6 years. out of the 70 cases exhibiting seizures, all cases were operated: in 52 cases (74,2%) we performed a lesionectomy with perifocal gliosis excision and in 18 cases (25,7%) only lesionectomy. conclusions: intracranial cavernous angiomas (cavernomas) are rare lesions 164 selected abstracts the 2nd congress in the danube-carpathian region characterized by epilepsy in the majority of cases or intracerebral hemorrhagic onset. when the main symptoms are seizures, the best prognosis results after the excision of the lesion and the perilesional gliosis. the neuronavigator-guided approach achieved in all cases the removal of the lesions with a good accuracy in the “target”, avoiding the post-operative deficits and improving the clinical outcome. furthermore, it avoids the discomfort of the stereotactic frame. in multiple lesions, the hemorrhagic or mass effect lesion must be managed. the option of gamma-knife surgery (gks) in cavernomas is disputed. in asymptomatic cavernomas, the best management is clinical follow-up and mri observation. keywords: intracranial cavernoma, epilepsy, mri, microsurgery, gos, neuronavigation, gamma knife surgery (gks). hemorrhagic complications after nonsurgical treatment of cerebral avm ion poeata1, a. chiriac1, n. dobrin2, z. faiyad2 1clinic of neurosurgery, “gr.t. popa” university of medicine and pharmacy iasi, romania 2clinic emergency hospital “prof. dr. n. oblu” iasi, romania non-surgical treatment of cerebral avms has been greatly enhanced. the three modalities of non-surgical treatment currently available include conservative management focused on imagistic and neurological monitoring, endovascular management by introduction of embolic agents for partially or totally avm occlusion and radiosurgery by stereotactic radiotherapy. the intracranial hemorrhage is known as the most important complication after non-surgical avm treatment. in this paper we review the result of non-surgical management of brain avms and present some representative cases treated at our institution. we retrospectively review 72 patients with cerebral avms admitted to clinc emergency hospital “prof. dr. n. oblu” iasi between january 2005 and april 2012 and who benefited of a single non-surgical treatment. the hemorrhagic complication correlated with treatment management, time interval, age, sex, presenting symptoms, and angiographic factors as avm size, deep venous drainage, and involvement of eloquent cortex were analyzed. according to results of the study the hemorrhagic complication of nonsurgically treated avms appears to be dependent of some predictor’s risk factors. difficulties and technical problems in endovascular treatment of cerebral vascular lesions, our experince in neuroendovascular surgery ion poeata1, patrick courtheoux2, nicolaie dobrin1, alexandru chiriac1, natalia ermalai1 13rd department of neurosurgery “prof. dr.n.oblu” clinical emergency hospital, iasi, romania 2chu-caen france first steps in endovascular neurosurgery in romania, iasi, were started in a mixed team formed by neurosurgeons and cardiologists under the coordination of professor patrick courtheoux, chu caen france, in the cardiology center from iasi where at that time were romanian neurosurgery (2012) xix 2: 145 – 167 165 two angiographical suites, after this in 2006 the endovascular cerebral pole was moved in the neurosurgical hospital with the inauguration of a modern angiographical interventional suite. introduction: the endovascular therapy of the craniocerebral and spinal diseases represents a very important aspect in solving efficiently a various type of pathology: cerebral aneurysm, arteriovenous malformations, arterial stenosis, tumoral etc. although this procedure requests an advanced infrastructure and many devices (as stents, coils, micro catheters, embolisation materials etc) it started to be used efficiently as well in romania. aim: our aim is to describe some interesting aspects and difficulties in treating patients with various vascular cerebral lesions. case report: aneurisms coiling, avm embolisations, dural fistulas, carotidcavernous fistulas are few type of lesions wich we want to show and some technical interventional difficulties were solved. material and methods: from 2006 to date in our clinics have been approached about 800 endovascular diagnostic and therapeutic procedures, were also organized annual courses with practical applications in collaboration with the medical center chu-caen france, on these occasions were different lesion types solved. results: endovascular neurosurgery in our country is only in the beginning however, we want to emphasize resolving outstanding bilateral bicavernos carotidocavrnous fistula, giant basilar artery aneurysms with emerging coletal branches, simptomatic internal carotid stenosis, intraarterial thromlolysis, also dural fistulas that were difficult to diagnose such clinical entities have become current, dynamic vascular studies have allowed to do a very correct surgical planning. conslusions: endovascular therapy is a full dynamic discipline, new devices try to solve problems of pathology that until now were unapproachable, the key is to heve a good team capable to treat both exo and endovascular strategies. cavernomas: our experience ioan ștefan florian, cristian pîrjol, horatiu ioani, petre kiss, sebastian-victor trifoi neurosurgical department, clujnapoca county hospital, clujnapoca, romania cavernomas are challenging lesions with a range of treatments that include combinations of microsurgery, radiosurgery, and endovascular approaches. in this paper we want to describe our surgical experience and strategy in this field and the current management of these lesions, which lead to successful surgical removal, in the absence of endovascular preoperative embolisation or neuronavigation facilities. the retrospective analysis of 60 cavernomas admitted and surgically treated in our department between june 1996 and december 2011. the diagnosis was established based on clinical findings, ct, mri and angiography and confirmed with pathological findings. the major clinical findings were as follows: hemorrhage, seizures, progressive neurological deficit, headache. we recorded a male preponderance of about 6:4 / male: female. the peak incidence has been found in the 5th decade. 16 cases were located in the brain stem and all were surgically approached with 166 selected abstracts the 2nd congress in the danube-carpathian region complete removal. postoperative complications were predominantly seizures (12%), and then hydrocephalus, and rebleeding. the outcome was good (gos 5 and 4) in 75% of the cases. the mortality rate for the entire series was 1.6% (meaning a case whit multiple cavernomas). objectives: for each patient the management resides in with moment we act conservative and when to operate. in surgery, cavernomas are more difficult to reach them than to resect. in the absence of endovascular embolisation or radiosurgery, surgery remains the single option to cure these lesions. most of these cases were admitted with a very severe neurological status, so the therapeutic decision was not how to operate but when to operate it. aims: cavernomas are challenging lesions with a range of treatments that include combinations of microsurgery, radiosurgery, and endovascular approaches. is to describe our surgical experience and strategy in this field and the current management of these lesions, which lead to successful surgical removal, in the absence of endovascular preoperative embolisation or neuronavigation facilities. material and methods: the retrospective analysis of 60 cavernomas admitted and surgically treated in our department between june 1996 and december 2011. the diagnosis was established based on clinical findings, ct, mri and angiography and confirmed with pathological findings. results: the major clinical findings were as follows: hemorrhage, seizures, progressive neurological deficit, headache. we recorded a male preponderance of about 6:4 / male: female. the peak incidence has been found in the 5th decade. 16 cases were located in the brain stem and all were surgically approached with complete removal. postoperative complications were predominantly seizures (12%), and then hydrocephalus, and rebleeding. the outcome was good (gos 5 and 4) in 75% of the cases. the mortality rate for the entire series was 1.6% (meaning a case whit multiple cavernomas). conslusions: for each patient the management resides in with moment we act conservative and when to operate. in surgery, cavernomas are more difficult to reach them than to resect. in the absence of endovascular embolisation or radiosurgery, surgery remains the single option to cure these lesions. most of these cases were admitted with a very severe neurological status, so the therapeutic decision was not how to operate but when to operate it. arteriovenous malformations: our experience ioan ștefan florian, cristian pîrjol, horatiu ioani, petre kiss, sebastian-victor trifoi neurosurgical department, clujnapoca county hospital, clujnapoca, romania intracranial arteriovenous malformations are challenging lesions with combined treatment: microsurgery, radiosurgery, and endovascular approaches. we want our surgical experience and strategy in this field and the current management of these lesions, which lead to successful surgical removal, in the absence of endovascular preoperative embolisation or neuronavigation facilities. the retrospective analysis of 184 intracranial arteriovenous malformations admitted and surgically treated in our department between june 1996 and romanian neurosurgery (2012) xix 2: 145 – 167 167 december 2010. from all intracranial vascular malformations this represents 67% (124) and cavernomas 33% (60 cases). the diagnosis was established based on clinical findings, ct, mri and angiography and confirmed with pathological findings. the major clinical findings were as follows: hemorrhage, seizures, progressive neurological deficit, and headache and according to spetzler-martin grading system most cases of avms were grade ii and iii (64%). we recorded a minor male preponderance for avms (55%). the peak incidence has been found in the 5th decade. postoperative complications were transient neurological deficits (10%), hydrocephalus (11%), and re-bleeding (10%). the outcome was gos 5 and 4 in 86% of the case. in 19% of the cases, the avms had associated aneurisms, treated in the same operatory session. most of these cases were admitted with a very severe neurological status, so the therapeutic decision was not how to operate but when to operate it. the best treatment of an intracranial vascular malformation is surgical resection and subtotal resection is not a good option in surgery. objectives: intracranial arteriovenous malformations are challenging lesions with combined treatment: microsurgery, radiosurgery, and endovascular approaches. aims: to describe our surgical experience and strategy in this field and the current management of these lesions, which lead to successful surgical removal, in the absence of endovascular preoperative embolisation or neuronavigation facilities. material and methods: the retrospective analysis of 184 intracranial arteriovenous malformations admitted and surgically treated in our department between june 1996 and december 2010. from all intracranial vascular malformations this represents 67% (124) and cavernomas 33% (60 cases). the diagnosis was established based on clinical findings, ct, mri and angiography and confirmed with pathological findings. results: the major clinical findings were as follows: hemorrhage, seizures, progressive neurological deficit, and headache and according to spetzler-martin grading system most cases of avms were grade ii and iii (64%). we recorded a minor male preponderance for avms (55%). the peak incidence has been found in the 5th decade. postoperative complications were transient neurological deficits (10%), hydrocephalus (11%), and re-bleeding (10%). the outcome was gos 5 and 4 in 86% of the case. in 19% of the cases, the avms had associated aneurisms, treated in the same operatory session. conslusions: most of these cases were admitted with a very severe neurological status, so the therapeutic decision was not how to operate but when to operate it. the best treatment of an intracranial vascular malformation is surgical resection and subtotal resection is not a good option in surgery. 7zuleicanavas-marrugo_estrogen 292 zuleica navas-marrugo et al estrogen, estrogen receptors and rupture of brain aneurysms estrogen, estrogen receptors and rupture of brain aneurysms: brief review of the literature sandy zuleica navas-marrugo, hernando raphael alvis-miranda, juan jose gutierrez-paternina, gabriel alcala-cerra, luis rafael moscote-salazar universidad de cartagena abstract estrogen, is involved in much of the life women lives, having great importance in many functions of the female body including the definition of secondary sexual characters, but also has been linked as protective factor regard to catastrophic events such as cerebral aneurysms, probably related to estrogen deficiency and described high incidence in menopausal women. it is known the effects of estrogen on vascular physiology and pathophysiologic mechanisms with potential therapeutic implications. we present a brief review focused in the role of estrogens and the rupture of cerebral aneurysms. key words: estrogen, cerebral aneurysms, deficiency, menopause. introduction about 20% of strokes are hemorrhagic events, from these subarachnoid hemorrhage (sah) accounts for 10% the remaining half corresponds tointracerebral hemorrhage. it is known that cerebral aneurysms are more common in women; numerous studies suggest the involvement of hormones in its pathogenesis. studies have shown that oral contraceptives and hormone replacement therapy may be protective against aneurysmal subarachnoid hemorrhage suggesting that cyclical hormonal fluctuations in the context of physiological menses are associated with cerebral vascular instability and then the formation of cerebral aneurysms. most causes sah are ruptured berry aneurysms. other causes include trauma, arteriovenous malformations, vasculitis, intracranial arterial dissections, amyloid angiopathy, bleeding diathesis, and illegal psychoactive substances such as cocaine and amphetamines. the aim of this work is to review the current kwnoledge regard aneurysms of the cerebral vasculature and their relationship with estrogen. subarachnoid hemorrhage sah is one of the most catastrophic intracranial events that may suffer an individual to whichneurosurgeons are routinely faced. it is defined as the occupation or invasion of blood in the subarachnoid space, where normally circulates the romanian neurosurgery (2014) xxi 3: 292 298 293 cerebrospinal fluid (csf). aneurysmal rupture leads the patient to a critical state, with high probability of mortality. the care and management of patients with subarachnoid haemorrhage is vital to the successful development, as well as a multidisciplinary approach where participating neurosurgeons and endovascular neurosurgeons should be experienced in the microsurgical management of cerebral aneurysms. epidemiology it is located within the pathologies that inevitably must handle any physician, affecting 6-10 people per 100,000 per year, although this range can varie (depending on the studies), in finland, there have been incidents that reach 20/100.000 patients/ year. (2) the most common age of onset is around 55 years, increasing incidence with increasing age. it is also more common in women. (2)according to retrospective studies, among all patients who attend the emergency department with headache, subarachnoid hemorrhage is the cause in 1% of cases. considering only patients with the worst headache of their lives and normal physical examination, this figure rises to 12%. this ratio increases again taking into account the patients with abnormal physical examination, reaching 25%. (3) it is a severe disease with a mortality rate of approximately 20 to 40% of inpatients plus 815% mortality in the first minutes or hours, in the prehospital phase. (3) etiology this process can be a pathological entity subsequent to trauma or occur spontaneously. being the main cause of the latter rupture of an aneurysm in the brain stem (85% of cases) (4). the causes of spontaneous sah are saccular aneurysm rupture (85%), ruptured arteriovenous malformation (8% -10%), unknown etiology (10%) and other rare (hypertension, arteritis, tumors, cardiac myxoma, and septic aneurysms). (4) cerebral aneurysms are saccular dilatations of the arterial wall that are located at the forks of the basal subarachnoid brain arteries or near the circle of willis. they originate from sites where there is a birth defect of the middle layer and the inner elastic membrane. several modifiable risk factors have been identified in relation to the hsa. clinical features the signs and symptoms of this disease are of sudden onset, in an individual who usually had no previous neurological disorders. the onset of symptoms is often preceded by intense physical activity or sexual activity, although it was noted that in a series of 500 patients with subarachnoid hemorrhage, in 34% of cases developed during stressful activities and 12% were produced during sleep. headache, which is the most common symptom, is presented as sudden onset and intense, usually referred as the worst. often is accompanied by nausea and vomiting. they can have any location, can be localized or generalized, may be mild and resolve spontaneously, may be relieved or nonrelieved by non-narcotic analgesics. facing the 294 zuleica navas-marrugo et al estrogen, estrogen receptors and rupture of brain aneurysms first or worst headache and an unusual headache in a patient with an established pattern of pain, sah should be suspected until proven otherwise. estrogen estrogens are female sex hormones that participate in a variety of actions on different tissues. among others, stimulate the development of female secondary sex characteristics, are involved in the characterization of the female physiognomy, adapting fatty deposits at the hips, thighs and development of internal and external genitalia. it acts on endometrial proliferation and growth of the uterus during the menstrual cycle in the cornification of the superficial cells of the vaginal mucosa, increases the secretion of cervical mucus to have the crossing of the sperm through the cervical mucus. estrogens alter serum lipid levels, the fibrinolytic system and coagulation, antioxidant systems, and the production of vasoactive molecules, influencing the development of vascular disease. (1). however, direct exert pleiotropic effects on endothelial cells, collagen vascular smooth muscle constituent, and a potent vasodilator called nitric oxide (no), thus contributing, together with other substances, the normal homeostatic process that allows endothelial remodeling arteries to maintain a constant diameter of the lumen, and therefore laminar blood flow strong enough for proper irrigation to distant structures. thanks to this, with any noxious event affecting the vasculature, endothelial cells have the ability to counteract all processes efficiently generated. atherosclerosis, which is a late consequence of all inflammatory and oxidative processes generated in endothelial cells has been associated with the formation, growth and ruptured aneurysms in any location. although not yet demonstrated a direct causal link between the two mechanisms, histopathological findings of the atheromatous plaque have been identified in some samples of intracranial aneurysm wall, a fact that has allowed these inflammatory phenomena gain importance, taking into account that could be a therapeutic target in the pathogenesis of aneurysmal cerebrovascular disease. the sequence of inflammatory phenomena at endothelial level can be described as follows: endothelial dysfunction, vasoconstriction, leukocyte and monocyte adhesion, increased vascular permeability, monocyte migration and leukocytes, programmed cell death, release of proteolytic enzymes. it is not known with certainty how the metabolic pathway of estrogen reduce vascular tone, by direct action of no and prostacyclin and inhibit monocyte adhesion to the endothelial wall by reducing plasma levels of the molecules vcam-1 and mcp -1. the latter is probably due to inhibition in the expression of genes that produce such molecules, after intercepting the nuclear transcription factor nf-κβ. furthermore, it is suspected that it is also responsible for the inhibition of mmp-2 and mmp-9, two major metalloproteinases that destroy the collagen and elastin of smooth muscle located in the arterial wall. all these actions are performed through the interaction of the hormone with its specific romanian neurosurgery (2014) xxi 3: 292 298 295 receptor. there are four different types: er-α, er-β (which are activated by ligands) ipg (also called gpr 30, which is coupled to protein g), and er-x , all available at level of the endothelial cells of the cerebral vasculature. estrogens are able to directly influence the fallopian tube, muscle, breast cancer, pituitary gland, bone, smooth muscle, ion transport mechanisms, among others. in the uterus, increases spontaneous contractions expanding the excitation of oxytocin in the tubes, increases in size, and breast in turn, lead to a proliferation of ducts. in the hypothalamus, are responsible for the secretion of lhrh and dopamine, through which reduced gonadotropin levels also stimulate the production of prolactin, however limit their actions on the breast, also favor the presence of receptors for fsh the hair and become more sensitive to their stimulating hormone pituitary hypothalamic lhrh. bones, provide mineralization, regularized long bone growth, cartilage conjunction closed and therefore cease growing. on the vascular system, estrogens may align or alter the ionic fluxes, receivers and reproduction property of vascular smooth muscle cells, and also regulate the release of endothelium-derived vasoactive factors. thus, estrogen increases competition gear dependent vasodilator no and prostacyclin, reduce the effectiveness of vasoconstrictors mechanisms, namely prostaglandins, raas (renin angiotensin aldosterone system), endothelin-1 (there is conflicting evidence on this ), involved in ion channel k + and ca2 + in the cells of the vascular smooth muscle (vsmc), prompting hyperpolarization and decreasing its contraction, worth noting the actions of estrogen on the lipid profile, they are able to reduce the plasma concentration of ldl and increase hdl. estrogens are hormones quintessential female puberty as they provide the characteristic distribution of body fat, which distinguish the female physiognomy predominantly around the hips and thighs of the male, which is mainly abdominal. it is seen that the activity of these hormones are present in most of women's lives, play an essential role in the biology of the vascular system and its mechanisms may represent beneficial results, however, is questioned their involvement in the pathophysiology of intracranial aneurysms (1). the fact that cerebral aneurysms are more common in women is not new. epidemiological data indicate a high incidence of cerebral aneurysms in postmenopausal women (2-3). numerous studies on the involvement of hormonal factors had treated the pathogenesis of aneurysms, is known the great participation of estrogen at different stages of the life of the woman, the great interaction between them and the vascular biology and although these interactions charities are largely still considers its involvement in the pathophysiology of cerebral aneurysms and catastrophic health of women. (4) (5) (1) endothelial and hormonal physiology the endothelium is a layer of tissue which covers all the vessels of the body. endothelial cells have a selective permeability, having non-thrombogenic properties, substantial 296 zuleica navas-marrugo et al estrogen, estrogen receptors and rupture of brain aneurysms metabolic activity and the ability to produce various vasoactive substances. in this way, the most important properties that can be identified on the endothelium are: • selective permeability: forms a highly selective permeability barrier, regulating the flow of nutrients, bioloigcamente active molecules and blood cells. (7). • maintenance balance between thrombosis and fibrinolysis. progression of the disease cerebrovascular disease is favored by oxidative stress, increases inflammation, and may trigger processes that contribute to the formation and subsequent rupture of an aneurysm, as direct endothelial injury, phenotypic change of smooth muscle cells to a phenotype of inflammatory and finally the radical apoptosis. free radicals are also able to activate the matrix metalloproteinases getting vessel remodeling and decomposition. these radicals in turn involved in all mechanisms responsible for cerebral aneurysm, such as atherosclerosis, hemodynamic stress and hypertensive pathology that makes it through the mechanism of peroxidation. thus, some preliminary studies involving targeted therapies to oxidative stress as a beneficial therapeutic option for treating cerebral aneurysms future, however, recent studies point to define the role of free radicals in the formation and rupture of a cerebral aneurysm. (6) estrogen and brain aneurysm formation the hypothesis regarding the alterations in hormone levels can influence the sah is gaining momentum rapidly. specifically, the concept that post-menopausal women are more susceptible to the condition has convinced many of the protective roles of estrogen and progesterone (7). the task of the estrogen is very important for vascular biology; its beneficial effects are well known but not participating in the pathogenesis of cerebral aneurysms (1). progression is associated with endothelial damage (2) to inflammation, impaired extracellular matrix and extracellular wall apoptosis, also in this process have been described as statins growth initiation mechanism and the aneurysm. (8) variations of estrogen level have been associated with the development and progression and rupture of cerebral aneurysms, which could explain the gender gap regarding the higher incidence found in women. in a case-control study which interviewed 4,682 women, mostly observed premature menopause (<40 years) associated with aneurysm formation, which suggests that reducing estrogen may be premature in training a cerebral aneurysm. this in turn may lead to a risk factor to explain the pathophysiology of cerebral aneurysms and for long term therapies. the growth in the incidence of cerebral aneurysms in postmenopausal women can relate diminished circulating estrogen levels. in a rat model, for example, which induced the formation of the aneurysm, the researchers found that in oophorectomized models increased incidence of cerebral aneurysms (9) involving the renin-angiotensin (ang)aldosterone in the pathology of vascular disease has also been described. however romanian neurosurgery (2014) xxi 3: 292 298 297 incommunicado mineralocorticoid receptor protects against vascular diseases, their influence on brain aneurysms is unclear. in a study used female rats which were induced by renal hypertension, increased hemodynamic stress, and they were subjected to insufficient estrogen for 3 months with the mineralocorticoid receptor blocker eplerenone (30 or 100 mg / kg per day) or vehicle (vehicle control) was observed as eplerenone reduced the incidence of cerebral aneurysms and saline intake without reducing blood pressure. on the wall of the aneurysm, increased production of ang ii and nitrotyrosine. mrna levels of ang-converting enzyme 1 and nadph (10) gender inequalities in the progression of aneurysmal subarachnoid hemorrhage (sah) are discussed, and the possible influence of estradiol on vasodilation is not well defined. (11) large number of studies suggests that hormones are important in the pathogenesis of an aneurysm. estrogen raises the normal physiological vascular endothelial employment, and waves during the menstrual cycle as well as drops significantly at menopause, which would explain such relationship (5). neuroprotective factors evidence for a protective role of estradiol in neurodegenerative diseases has increased steadily over the past decade, although the mechanisms of action and participation of estrogen receptors (er) showed a complex result. the protective effects of estrogens take place partly through pathways involving activation of canonical er, which is constitutively expressed in many brain regions and is capable of initiating transcription of genes after specifically bind estradiol. furthermore, non-genomic pathways (or alternative), involving extranuclear re respond to physiological concentration of estrogen to induce neuroprotection. often, rapid activation of intracellular signaling, such as mitogen activated protein kinase (mapk) and phosphatidylinositol 3-kinase (pi3k) underlying estrogen-induced neuroprotection alternative activation of specific binding sites in the plasma membrane. although the molecular characteristics of these unconventional ers are still largely unknown, the conventional wisdom holds that the plasma membrane er (mer) arises from or relates to, classical nuclear er. this article reviews some of the latest evidence that reveals the importance of alternative mechanisms for estrogen-dependent neuroprotection. special attention to models of cellular toxicity of betaamyloid in classical and alternative pathways activated by estrogens seem to exist to orchestrate neuroprotection. (12). conclusions knowledge of the cellular mechanisms involved in the possible involvement of estrogen and cerebral aneurysm formation will be an interesting line of research that may offer additional treatment alternatives for patients with incidental aneurysms or in patients at risk for brain aneurysms. correspondence dr. luis rafael moscote-salazar, university of cartagena, cartagena de indias, colombia, southamerica. e-mail: mineurocirujano@aol.com 298 zuleica navas-marrugo et al estrogen, estrogen receptors and rupture of brain aneurysms references 1. jamous ma, nagahiro s, kitazato kt, satomi j, satoh k. role of estrogen deficiency in the formation and progression of cerebral aneurysms. part i: experimental study of the effect of oophorectomy in rats. journal of neurosurgery [internet]. 2005 dec [cited 2013 may 26], 103 (6): 1046-51. available from: http://www.ncbi.nlm.nih.gov/pubmed/16381191 2. tamura t, jamous ma, kitazato kt, yagi k, tada y, uno m, et al. endothelial damage due to impaired nitric oxide bioavailability triggers cerebral aneurysm formation in female rats. journal of hypertension [internet]. 2009 jun [cited 2013 may 25], 27 (6) :1284-92. available from: http://www.ncbi.nlm.nih.gov/pubmed/19307983 3. ding c, toll v, ouyang b, chen m. younger age of menopause in women with cerebral aneurysms. neurointerv j surg [internet]. 2012 june 13 [cited 2013 may 15] available from: http://www.ncbi.nlm.nih.gov/pubmed/22700728 4. golledge j, biros e, warrington n, jones gt, cooper m, van rij am, et al. a population-based study of polymorphisms in genes related to sex hormones and abdominal aortic aneurysm. eur j hum genet [internet]. 2011 mar [cited 2013 april 11], 19 (3): 363-6. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3062004&tool=pmcentrez&rendertype=abstract 5. chen m, ouyang b, goldstein-smith l, feldman l. oral contraceptive and hormone replacement therapy in women with cerebral aneurysms. journal of neurointerventional surgery [internet]. 2011 jun [cited 2013 may 25], 3 (2): 163-6. available from: http://www.ncbi.nlm.nih.gov/pubmed/21990811 6. starke rm, chalouhi n, ali ms, jabbour pm, tjoumakaris si, gonzalez lf, et al. the role of oxidative stress in cerebral aneurysm formation and rupture. current neurovascular research [internet]. 2013 may 24 [cited 2013 jun 3] available from: http://www.ncbi.nlm.nih.gov/pubmed/23713738 7. young amh, karri sk, ogilvy cs. exploring the use of estrogen & progesterone replacement therapy in subarachnoid hemorrhage. current drug safety [internet]. 2012 jun [cited 2013 may 25], 7 (3) :202-6. available from: http://www.ncbi.nlm.nih.gov/pubmed/22950381 8. tada y, kitazato kt, yagi k, shimada k, matsushita n, kinouchi t, et al. statins promote the growth of experimentally induced cerebral aneurysms in estrogendeficient rats. stroke, a journal of cerebral circulation [internet]. 2011 jun [cited 2013 may 25], 42 (8) :2286-93. available from: http://www.ncbi.nlm.nih.gov/pubmed/21737796 9. jamous ma, nagahiro s, kitazato kt, tamura t, kuwayama k, satoh k. role of estrogen deficiency in the formation and progression of cerebral aneurysms. part ii: experimental study of the effects of hormone replacement therapy in rats. journal of neurosurgery [internet]. 2005 dec [cited 2013 may 26], 103 (6) :1052-7. available from: http://www.ncbi.nlm.nih.gov/pubmed/16381192 10. cl lin, shih hc, dumont as, kassell nf, lieu as, su yf, et al. the effect of 17beta-estradiol in attenuating experimental subarachnoid hemorrhage-induced cerebral vasospasm. journal of neurosurgery [internet]. 2006 feb [cited 2013 may 26], 104 (2) :298-304. available from: http://www.ncbi.nlm.nih.gov/pubmed/16509505 11. yang sh, he z, wu ss, he yj, cutright j, millard wj, et al. 17-beta estradiol can reduce secondary ischemic damage and mortality of subarachnoid hemorrhage. journal of cerebral blood flow and metabolism: official journal of the international society of cerebral blood flow and metabolism [internet]. 2001 feb [cited 2013 may 26], 21 (2): 174-81. available from: http://www.ncbi.nlm.nih.gov/pubmed/11176283 12. marin r, guerra b, alonso r, ramírez cm, diaz m. estrogen activates classical and alternative mechanisms flag to orchestrate neuroprotection. current neurovascular research [internet]. 2005 oct [cited 2013 may 26] 2 (4): 287-301. available from: http://www.ncbi.nlm.nih.gov/pubmed/16181121 agrawala_admission 252 | agrawal et al admission characteristics and outcome in traumatic brain injury patients admission characteristics and outcome in traumatic brain injury patients: a preliminary report from a tertiary care hospital amit agrawal1, ashok munivenkatappa2, b.v. subrahmanyam3, s. satish kumar4, p. ramamohan5 1department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2national institute of epidemiology (icmr), chennai 3department of forensic medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 4department of emergency medicine, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 5pharmacology, narayana medical college & hospitals, nellore; andhra pradesh, india abstract: introduction. traumatic brain injury (tbi) is affected by multiple factors. patient’s education, manifesting symptoms and surgical management play a significant role on discharge outcome. the literature of same from developing country is limited. the present pilot study aims to describe patient characteristics, presenting symptom and management aspects of tbi patients from a tertiary hospital. methods. the present study is a prospective study, where tbi patients were selected and data of injury was entered on standard proforma on electronic data base. the study was approved by institute ethical board. the data was analyzed using stats direct version 3.0.150 software. results. three hundred and thirty three patients were evaluated. eighty percent of patients were from rural areas. about 75% of patients were illiterates and married. patient employment was significant with discharge outcome. all the patients manifested with symptoms loss of consciousness (loc) was higher (73%) followed by vomiting (44%). loc and oral bleed was significant with outcome. associated injuries was higher in extremities (22.5%) followed by chest (4.4%). about 15% of patients require intracranial surgery that was significant with discharge outcome. conclusion. the present pilot study finding is similar to available literature data and adds knowledge to tbi data of a developing country like india. key words: illiterate, loss of consciousness, oral bleed, intracranial surgery, tbi, outcome romanian neurosurgery (2016) xxx 2: 252-257 | 253 introduction the injury characteristics for traumatic brain injuries (tbis) differ in important ways that has significant effect on outcome. (1, 2) the details of distribution of injured patient’s occupation and their marital status may be essential for outcome. (3, 4) outcome has significant association with manifesting symptoms like duration of loss of consciousness and oral bleed. (5) the management of tbi patient especially intra cranial surgery is very crucial for patient outcome. (6) the details of published data of above mentioned variables of tbi from our local environment are limited. the aim of the present pilot study is to describe the injured patients educational, presenting symptoms and treatment characteristics of traumatic brain injuries from our setting. methods the present study is a prospective study. the head injury patients attending emergency center of narayana medical college and hospital, nellore, andhra pradesh (india) was randomly selected. the study was approved by institute ethical committee and consent was taken by patient or by stander. the patient’s data was entered on standard head injury proforma which was comparable with computerized patient management system. patient’s data was mainly focused on education, employment, marital status, presenting symptoms and management aspects. the mentioned variable was checked for any significance with discharge outcome. the details of all variables was entered in simultaneous electronic data entry interface developed by filemaker pro advanced 13 (copyright © 1994-2015, filemaker, inc) and web data entry interface drupal cms. statistical analysis the study data was analyzed using statsdirect version 3.0.150 (statsdirect ltd. statsdirect statistical software. http://www.statsdirect.com. england: statsdirect ltd. 2015). frequencies and percentages were reported for categorical variables. mean and standard deviation was reported for continuous variables. the significance between discharge outcome (alive or dead) and mentioned variables was analyzed using chi square test. the significant level was <0.05. results totally 337 head injury patients were evaluated during the study period. twenty four (7.12%) patients expired during study period. the mean age was 36.26±15.86 years. males were four times more than females. fifty percent of patients had moderate to severe head injury. the details of patient’s education, employment and marital status with outcome are detailed in table 1. only employment status was significantly associated with patient outcome. table 2 highlights manifesting symptoms, other injuries, duration of loc, pulse rate and systolic blood pressure with outcome. the medical and surgical management of head injury patients and their discharge outcome is shown in table 3. 254 | agrawal et al admission characteristics and outcome in traumatic brain injury patients table 1 patients’ educational, occupational and marital status with outcome sl no. variables outcome p value alive dead 1 education 0.732 illiterate 225 19 primary 41 3 secondary 8 1 graduate 19 0 unknown 8 1 2 employment 0.007* farmer 132 9 student 19 1 laborer 16 0 employee in service 4 0 unemployed 2 2 housewife 10 3 unknown 5 0 3 marital status 0.867 married 262 21 unmarried 50 3 widow 1 0 *p value <0.05 table 2 symptoms and sigs presentation with outcome sl no. variables outcome p value alive dead 1 symptoms (present) loc 228 21 0.115 vomiting 138 11 0.868 ear bleed 125 13 0.172 nasal bleed 108 11 0.263 oral bleed 43 7 0.040* headache 52 2 0.287 seizures 22 3 0.324 post traumatic amnesia 14 2 0.391 2 duration of loc 1-29 minutes 176 4 30-59 minutes 60 11 0.021* 1-7 days 4 0 none 73 4 3 other injuries (present) neck 10 1 0.769 thorax 4 1 0.259 chest 13 2 0.339 abdomen 1 0 0.782 extremities 55 21 0.526 cervical spine 1 1 0.018* thorcaic spine 2 0 0.694 lumbar spine 1 0 0.782 4 pulse rate 0.016* <60 beats per minute 13 4 61-100 beats per minute 211 13 >100 beats per minute 43 6 5 systolic blood pressure 0.834 <90 14 1 >90 258 23 loc loss of consciousness; *p value <0.05 table 3 treatment with outcome sl no. variables outcome p value alive dead 1 medical treatment urinary catheter 180 22 0.001* nasogastric tube 58 12 0.001* tetanus toxoid 215 20 0.132 crystalloids 108 10 0.478 colloids 179 15 0.612 blood transfusion 1 0 0.782 cervical collar 12 3 0.047* cervical traction 1 0 0.782 bed rest 246 18 0.68 steroids 2 0 0.076 ventilation 39 7 0.022* 2 surgery intra cranial 40 9 0.003* extra cranial 17 2 0.576 *p value <0.05 romanian neurosurgery (2016) xxx 2: 252-257 | 255 discussion the study results report that majority of evaluated patients were illiterates (72.4%). farmers were about 37.4%. three fourth (75%) of patients were married. all the patients manifested with symptoms among them loss of consciousness (loc) was majorly reported (73.8%), followed by vomiting (44.2%), ear nose bleed (41%) and oral bleed (14.8%). post traumatic amnesia was reported in 4.7%. duration of loc and oral bleed was significant with discharge outcome (p<0.05). other than head extremities, chest and neck reported among 22.5%, 4.4% and 3.2% respectively. pulse rate was significant with discharge outcome. intracranial surgery was significant with discharge outcome. the study was conducted from a tertiary care hospital located in heart of the city. the hospital receives patients from local and surrounding areas. majority of patients were from rural areas (81%). our study reports that nearly three fourth of patients were not educated and there was no significance with outcome at discharge. a cross sectional study among moderate to severe tbi patients revel that higher education reduces the negative effect of tbi on cognitive outcome. patients with higher intellectual enrichment had positive on outcome. (7) about eighty five percent of patient’s age was above twenty years, so it’s obvious that 75% were married. tbi literature from both developed and developing countries reports that productive age group is commonly affected. the occupation of majority of patients were agriculture (37.4%) followed by 6% of students and 5% of labor class. as majority of patients are from rural set up where agriculture is main mode of occupation. a district level study of traumatic brain injury patients reported that students were higher (29%) followed by civil servants (16%) and casual labors (13%). (3) patients with tbi manifest with spectrum of symptoms. (8) tbi studies from india reports that brain injury patients manifest about 63% of loc, 48 to 40% of vomiting, 36% of ear, nose and throat bleed and 24% of traumatic amnesia. (8) the present study result reflects the literature results, but the post traumatic amnesia is less in our study as compared to above study. the post traumatic amnesia manifests for varying duration. (9) it may be due to the fact that the patients with low education might not have understood or have failed to understand. loc and its duration have significant association with outcome, longer the loc duration worse the outcome. (10) our study reports duration of loc has significance with outcome at discharge. the study reports that oral bleed has significance with discharge outcome. forty three percent of severe patients, 19% of moderate patients and 9% of mild group patients had oral group that was significant (p<0.001). a retrospective study from taiwan reports that severe the head injury patients with oronasal bleed had worse outcome. (11) associated injuries like involvement of neck, thoraco-abdominal, extremities and spine are common in tbi patients. our study reports associated injuries was higher in extremities (22.5%) followed by chest and neck. a tbi study from tertiary care center 256 | agrawal et al admission characteristics and outcome in traumatic brain injury patients reports higher neck injuries (95%), extremities on average of 32% and chest of 4.5%. (12) the management of patients with head injury is complex and requires a prompt, coordinated, comprehensive and multidisciplinary approach. early recognition and immediate treatment of surgically correctable intracranial lesion is essential for optimal patient outcome. (3, 14) the present study reports that intracranial surgical management of tbi patient was significant with discharge outcome. limitation the present study sample size is small with lack of data on long-term outcome. the statistics used are simple one, higher statistics like logistics to find detail association and risk factor that has significance with discharge outcome was note done. conclusion the pilot study reports that majority of patients were illiterates and married. loc was present among majority of patients and was significant with discharge outcome. associated injuries were present in majority of patients. intracranial surgery was significant with discharge outcome. studies with larger sample size and higher statistics should be considered to establish better prevention strategies and treatment protocols. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.nantulya vm, reich mr. the neglected epidemic: road traffic injuries in developing countries. bmj (clinical research ed) 2002;324:1139-1141. 2.masiira-mukasa n, ombito br. surgical admissions to the rift valley provincial general hospital, kenya. east african medical journal 2002;79:373-378. 3.kobusingye oc, guwatudde d, owor g, lett rr. citywide trauma experience in kampala, uganda: a call for intervention. inj prev 2002;8:133-136. 4.chalya pl, mabula jb, dass rm, et al. injury characteristics and outcome of road traffic crash victims at bugando medical centre in northwestern tanzania. journal of trauma management & outcomes 2012;6:1. 5.pruthi n, ashok m, kumar vs, jhavar k, sampath s, devi bi. magnitude of pedestrian head injuries & fatalities in bangalore, south india: a retrospective study from an apex neurotrauma center. indian j med res 2012;136:1039-1043. 6.horn sd, corrigan jd, beaulieu cl, et al. traumatic brain injury patient, injury, therapy, and ancillary treatments associated with outcomes at discharge and 9 months postdischarge. archives of physical medicine and rehabilitation 2015;96:s304-329. 7.sumowski jf, chiaravalloti n, krch d, paxton j, deluca j. education attenuates the negative impact of traumatic brain injury on cognitive status. archives of physical medicine and rehabilitation 2013;94:2562-2564. 8.munivenkatappa a, shukla dp, devi bi, kumarsamy ad, bhat di, somanna s. domestic animal-related neuro-trauma: an account, from a tertiary institute. journal of neurosciences in rural practice 2013;4:19. 9.ponsford jl, spitz g, mckenzie d. using posttraumatic amnesia to predict outcome after traumatic brain injury. journal of neurotrauma 2015. 10.shaklai s, peretz r, spasser r, simantov m, groswasser z. long-term functional outcome after romanian neurosurgery (2016) xxx 2: 252-257 | 257 moderate-to-severe paediatric traumatic brain injury. brain injury 2014;28:915-921. 11.liao c-c, tseng y-y, chen c-t. transarterial embolisation for intractable post-traumatic oronasal haemorrhage following traumatic brain injury: evaluation of prognostic factors. injury 2008;39:507-511. 12.munivenkatappa a, pruthi n, philip m, devi bi, somanna s. elderly pedestrian neurotrauma: a descriptive study from a premier neurotrauma center in india. journal of neurosciences in rural practice 2013;4:29. 13.marik pe, varon j, trask t. management of head trauma. chest journal 2002;122:699-711. 14.yattoo g, tabish s, rangrez r, afzal m, bukhari i, kirmani m. injuries profile of head trauma patients at a teaching hospital. jk-practitioner 2008;15:s31-s32. 3gorgan_vagusnerve 150 gorgan et al vagus nerve stimulation for the treatment of refractory epilepsy vagus nerve stimulation for the treatment of refractory epilepsy m.r. gorgan1,2, a. giovani1, f.m. brehar1,2 1“bagdasar-arseni” emergency clinical hospital, bucharest 2clinic of neurosurgery “carol davila” university of medicine and pharmacy, bucharest abstract: vagus nerve stimulation (vns) represents one of the main surgical options for the treatment of the refractory epilepsy in pediatric and adult patients. there are several mechanism involved in vagal nerve stimulation which could influence the pathophysiology of seizures like neuromodulation of the thalamic and subthalamic nuclei involved in seizure initiation and the modulation of the neurotransmitters pattern norepinefrin, gaba, and serotonin. the vns system is composed of the implanted components (the generator, the lead with the electrodes attached) and the programming system components (programming wand and handheld computer). the authors present their experience with 81 patients diagnosed with refractory epilepsy, investigated, selected and implanted with vagal neurostimulators between december 2012 and january 2015 in neurosurgery clinic, "bagdasar-arseni" emergency hospital. the surgical technique and the potential pitfalls are described in detail. there were 20 children (24,7%) and 61 (75,3%) adults in this series. there was no death in this series and no intraoperative incidence. one patient presented dysphagia postoperatively which completely remitted after two months of follow-up. the outcome in term of seizure frequency and severity was better for patients under 30 years compared with patients older than 30 years. vns represents now a safe, quick and efficient surgical procedure with a minimum period of hospitalization and a short recovery period. the good results on long term improve the quality of life of the patients and facilitate the social and professional reinsertion. key words: refractory epilepsy, vagus nerve stimulation introduction refractory epilepsy represents a severe clinic entity which involves a significant number of patients and has important economic and social implications. the consequences for the patients are numerous and severe and include: adverse effects with long-term aed use (1, 2-5), increased seizure severity (3), depression and anxiety (4), romanian neurosurgery (2015) xxix 2: 150 159 151 increased mortality and morbidity (6-8), seizure-related injuries, and increased healthcare utilization (eg, er visits, hospitalizations) (9-11). for all these patients the drug therapy fails and the epilepsy surgery remains the only option. one of the surgical techniques employed in the management of refractory epilepsy is vagus nerve stimulation. bremmer at al in 1938 were the first to investigate the use of vagus nerve stimulation and they recorded evoked response in thalamus after the nerve stimulation. the first effects of vagal nerve stimulation in animal models of chemical induced epilepsy were demonstrated in 1985 (12), this method relieving the subject from seizures by desynchronizing the cortical activity and decreasing the length and frequency of the seizures. there are several mechanism involved in vagal nerve stimulation which could influence the pathophysiology of seizures (13-23). first it should be underlined that vagus nerve contains an important contingent of afferent fibers to the dorsal nucleus of the vagus nerve located at the level of medulla oblongata. these inputs are directed to the locus coeruleus located in pons. this structure has multiple connections with several important cerebral structures. one important connection is with thalamic nuclei. another important connection is with amygdala and hippocampus. from the thalamus the nervous inputs are directed through the entire subcortical and cortical structures of the brain. therefore, in the end the vagus nervous stimuli are able to modulate the electric activity through the entire brain and to induce the desynchronization of the eeg rhythms (21, 22). also, it was demonstrated that vagus nerve stimulation works by neuromodulation of the thalamic and subthalamic nuclei involved in seizure initiation and by modifying the neurotransmitters pattern like norepinefrin (13,14, 19), gaba (15, 17, 18), serotonin and aspartate (16, 17). the neurotransmitters pattern is regulated in hippocampus through the over expression of brain derived neurotrophic factor and fibroblast growth factor (24). another important mechanism of action of vagus nerve stimulation is represented by the influence of the cerebral blood flow in thalamus and brain cortex, which indirectly may influence diffusely the electric activity of the entire brain cortex (20, 23). the vns system is composed of the implanted components (the generator, the lead with the electrodes attached (figure 1a)) and the programming system components (programming wand and handheld computer) (figure 1b). there are three electrodes which are attached to the vagus nerve: one positive, one negative and a neutral (tethered) electrode (fig. 1c). the electrodes are connected to the generator through a lead. the lead and the generator are placed subcutaneously. the generator can be interrogated wireless using a special emitter called wand. the wand is connected to a handheld computer. using these tools the doctor can turn on, turn off and more important can interrogate the generator to see the status of the battery and the impedance. this parameter is very useful to verify intraoperatively and postoperatively if 152 gorgan et al vagus nerve stimulation for the treatment of refractory epilepsy the electrodes are properly placed. postoperatively it can be checked if there is any discontinuity of the system. another important parameters which can be set up using the computer programmer and the wand are: intensity of the current, pulse width, the duty cycle (signal on/off time) and the frequency. tabel.1 shows the range of these parameters. figure 1a implanted components of the vns system. 1b. programming system components. 1c. the electrodes of the vns system tabel 1 the parameters of the vns stimulation romanian neurosurgery (2015) xxix 2: 150 159 153 intraoperatively the system is checked to see the proper function of it, and the impendence is measure to verify the correct placement of the electrodes around the vagus nerve, then the system is turned off. the system will be turned on at approximately two weeks after operation, in order to be sure that there is no risk of infections. then, the patients will be periodically called for follow-up (usually every two weeks) to progressively increase the parameters of stimulation until they reached the typical values showed in tabel 1. the authors present here the first series of patients with refractory epilepsy operated and implanted with vagal neurostimulators in romania, and describe the surgical technique and the preliminary results. patients and methods our study includes 81 patients diagnosed with refractory epilepsy, investigated, selected and implanted with vagal neurostimulators between december 2012 and january 2015 in neurosurgery clinic, "bagdasar-arseni" emergency hospital. we have implanted in all patients the latest model of vagal neurostimulator (model 103), excepting two patients operated in december 2012, for whom the previous model (model 102) was used. we perform in all cases a standard left latero-cervical surgical approach. we use an horizontal incision in the left latero-cervical region in one of the skin crest, located at approximately the midway between the sternum and mastoid tip (figure 2). after skin incision and platysma muscle division, we identify the anterior border of sternocleidomastoid muscle and the omohyoid muscle (figure 3) depending of the individual anatomy, we traction the omohyoid muscle out of the surgical corridor, or we divide it. the cervical left vasculo-nervous complex (common carotid artery and internal jugular vein) is identified and then we perform a microsurgical dissection of the left vagus nerv (figure 4). at that level, the vagus nerve is usually located between the common carotid artery (medially located) and the internal jugular vein (laterally located), but in deeper location. the surgical dissection is directed with great care to the connective tissue between the great vessels, using the microsurgical technique and optic magnification until the vagus nerve is identified. there are several principles which guide the vagus nerve dissection. first, we have to perform a minimum 3 cm long dissection of the nerve (ideally 5 cm). it is very useful to use two rubber pieces two anchor the nerve at the both ends of the portion of the nerve which is dissected (figure 5). figure 2 the position of the skin incisions 154 gorgan et al vagus nerve stimulation for the treatment of refractory epilepsy figure 3 intraoperative view of the platysma muscle dissection figure 4 the intraoperativ view of the common carotid artery and the internal jugular vein figure 5 the intraoperative view of the left vagus nerve applying gently a moderate tension on the nerve, we keep the portion of the nerve above the common carotid artery and internal jugular vein. second, in order to obtain a proper contact between electrodes and vagus nerve it is necessary to completely remove the connective tissue which surround the nerve. third, it is very important to not allow the nerve to dry out. therefore, the surgical field should be continuously irrigated with saline serum. after a minimum of 3 cm of the vagus nerve is dissected (ideally 5 cm), the electrodes can now be connected to the vagus nerve. a second incision is performed, usually located at the pre-pectoral area, then the leads is tunneled between this second incision and the latero-cervical incision in a way that the electrodes' end of the lead is placed at the level of the cervical incision . then, the electrodes are placed on the vagus nerve. there are, from proximal to distal, one anchor tether and two electrodes: one positive electrode and one negative electrode (figure 6). figure 6 intraoperative view of the electrodes placed on the left vagus nerve romanian neurosurgery (2015) xxix 2: 150 159 155 the order of electrodes placement depends on the surgeon's preference. the electrodes can be connected either from proximally to distally, or distally to proximally. after connecting the electrodes, a loop is made using the extra-length of the lead and the generator is inserted together with the extra-length of the lead in the subcutaneous pocket. at the end of the surgical procedure, before removing the sterile drapes, the system is checked to assure the proper function of it and also the correct positioning of the electrodes. results there were 20 children (24,7%) and 61 (75,3%) adults in this series (graphic 1). graphic 1: the percents of the children and the adults of the cohort 25% 75% children adults 156 gorgan et al vagus nerve stimulation for the treatment of refractory epilepsy the medium age was 25,2 years. the age distribution is represented in the graphic 2. graphic 2: age distribution of the patients in our series the gender distribution was: 39 females (48,1%) and 42 males (51,9%) (graphic 3). graphic 3: gender distribution of the patients in our series 46% 54% female male 1-10 y: 8 11-20 y: 16 21-30 y: 26 31-40 y: 21 41-50 y: 10 romanian neurosurgery (2015) xxix 2: 150 159 157 the average period of hospitalization was 3 days. the medium follow-up period was 11,5 months and the minimum follow-up period was 3 months postoperatively for all patients. there was no death in this series and no intraoperative incidence. one patient presented dysphagia postoperatively which completely remitted after two months of follow-up. eleven patients (13,5%) experienced for several days postoperatively hoarseness, which remitted completely within one week postoperatively. there were 50 patients under 30 years (61,7%) and 31 patients over 30 years (38,3%) in our series. we noticed that the percent of patients with 50% seizure frequency reduction was 58% (29 patients) at the end of the follow-up period in patients under 30 years compared with 48,4% (15 patients) in patients older than 30 years. seven patients (8,6%) were seizure free at 6 months postoperatively. discussions vns therapy was first approved for clinical use in 1994 in european union and canada, followed by the fda approval in 1997 for usa market. it should be noticed that this therapy is approved to be used for all kind of drug refractory epilepsy, both partial and generalized seizures (especially for partial seizures with secondary generalization). in order to be selected for this form of therapy the patients should fulfill two major requirements: 1. to be correctly diagnosed with drug refractory epilepsy (according with ilae consensus definition) and 2. do not have a surgically resectable epileptic focus/foci. according with ilae definition (published in 2010) the drug refractory epilepsy is "absence of complete seizures control of a properly diagnosed epilepsy syndrome, for a period of at least 12 months, following an adequate trial of two tolerated and appropriately chosen antiepileptic drugs" (25). the second condition is that patients, after a complete evaluation (including video eeg and cortical and deep electrodes monitoring) should not have a surgically resectable focus/foci. this means that it cannot be accurately identified the surgical focus/foci, or this/these are identified, but there are situated in eloquent areas of the brain. when the patients fulfills these criteria, they could be considered candidates for vagus nerve stimulation. because more than 80% of the parasimpatic fibers which innervate the cord are part of the right vagus nerve, the left nerve is targeted for vagus nerve stimulation, in order to reduce to the minimum the cardiac side effects. presently, the use of vns goes beyond intractable epilepsy, its use for depression being well spread in usa. since the fda approval of vagal nerve stimulation in 1997 the refractory epilepsy gained a valuable treatment tool. even if the cost is prohibitive for individuals, the efficacy of this treatment was proved in large scale trials. one of the largest meta-analysis in usa including 3321 patients from 74 clinical trials reported 50% reduction in seizures in half of the patients one year after the vns surgery (26). other series have communicated better results, with up to 10% becoming free of seizures at one year followup in pediatric population (27). these data underline the importance of a correct surgical pre-evaluation of the patients and a correct 158 gorgan et al vagus nerve stimulation for the treatment of refractory epilepsy selection in order to obtain a better outcome. we also find that children and young adults (under the age of 30 year-old) have a better response to vns therapy compared with older patients (over 30 year-old). a more recent meta-analysis included all the devices (51,882) implanted in usa from 1997 to 2012 and studied a rare complication, vocal cord paralysis, found in 193 cases (28). in our series we noticed only one case of temporary vocal cord paralysis, which remitted after two months of follow-up. there are several side effects related with vns therapy, and includes: dysphonia, dysphagia, hoarseness, cough and tingling sensation in the throat and all are related with stimulation. it is important to mention that the intensity of these side effects decrease in time and they are related with the parameters of the stimulation (29). conclusions vns represents now a safe, quick and efficient surgical procedure with a minimum period of hospitalization and a short recovery period. the outcome of the patients is better, in term of the frequency and severity of the seizures, for children and young adults (under the age of 30 year-old) compared with older patients. the good results on long term improve the quality of life of the patients and facilitate the social and professional reinsertion. references 1. schmidt d. the clinical impact of new antiepileptic drugs after a decade of use in epilepsy. epilepsy res. 2002;50:21–32 2. wheless jw. intractable epilepsy. a survey of patients and caregivers. epilepsy behav 2006; 8: 756-64 3. fisher rs, vickrey bg, gibson p, et al. the impact of epilepsy from the patient's perspective i. descriptions and subjective perceptions. epilepsy res 2000; 41:39 4. gilliam, f.. optimizing health outcomes in active epilepsy. neurology. 2002; 58, s9–s20 5. meador, k.j. cognitive outcomes and predictive factors in epilepsy. neurology.2002; 58(8 suppl.5), s21–s26 6. s d lhatoo, y langan, j w a s sander, sudden unexpected death in epileps, postgrad med j 1999;75:706709 7. annegers jf1, coan sp, hauser wa, leestma j, duffell w, tarver b., epilepsy, vagal nerve stimulation by the ncp system, mortality, and sudden, unexpected, unexplained death, epilepsia 1998;39:206-212 8. van ness pc., therapy for the epilepsies, arch neurol 2002;59:732-735 9. labiner, d.m., et al., generic antiepileptic drugs and associated medical resource utilization in the united states. neurology. 2010;74: 1566-1574 10. helmers sl, paradis pe, manjunath r, et al. economic burden associated with the use of generic antiepileptic drugs in the united states. epilepsy behav. 2010;18:43744 11. faught e, et al. impact of nonadherence to antiepileptic drugs on health care utilization and costs: findings from the ransom study, epilepsia 2009;50:501-509 12. zabara j: time course of seizure control to brief repetitive stimuli. epilepsia.1985; 26:518 13. roosevelt rw, smith dc, clough rw, jensen ra, browning ra. increased extracellular concentrations of norepinephrine in cortex and hippocampus following vagus nerve stimulation in the rat. brain res.2006; 1119(1):124 14. hassert dl, et al., the effects of peripheral vagal nerve stimulation at a memory-modulating intensity on norepinephrine output in the basolateral amygdala, behavioral neuroscience. 2004;118(1):79-88. 15. woodbury dm, woodbury jw. effects of vagal stimulation on experimentally induced seizures in rats. epilepsia. 1990;31(suppl 2): s7-s19 20 16. hammond bm, et al., neurochemical effects of vagus nerve stimulation in humans, brain research. 1992;583:300-3. romanian neurosurgery (2015) xxix 2: 150 159 159 17. ben-menachem e, manon-espaillat r, ristanovic r, et al, first international vagus nerve stimulation study group: vagus nerve stimulation for the treatment of partial seizures: 1-a controlled study of effect on seizures, epilepsy res .1995;20:221-7. 18. marrosu f, et al. increase in 20–50 hz (gamma frequencies) power spectrum and synchronization after chronic vagal nerve stimulation, epilepsy res. 2003;55:59-70. 19. krahl se, clark kb, smith dc, browning ra. locus coeruleus lesions suppress the seizure-attenuating effects of vagus nerve stimulation., epilepsia. 1998;39:709-714. 20. tr henry, rae bakay, pb pennell, cm epstein et al., brain blood‐flow alterations induced by therapeutic vagus nerve stimulation in partial epilepsy: ii. prolonged effects at high and low levels of stimulation, epilepsia. 2004;45(9):1064-1070. 21. de connor jr, m nixon, a nanda, b guthikonda, vagal nerve stimulation for the treatment of medically refractory epilepsy: a review of the current literature, neurosurgical focus, mar 2012 / vol. 32 / no. 3 / page e12 22. koo b: eeg changes with vagus nerve stimulation, j clin neurophysiol. 2001;18:434-441. 23. k vonck, v de herdt, t bosman, s dedeurwaerdere, thalamic and limbic involvement in the mechanism of action of vagus nerve stimulation, a spect study, seizure 2008; 17(8):699-706 24. follesa p, biggio f, gorini, caria s, talani g, dazzi l, et al: vagus nerve stimulation increases norepinephrine concentration and the gene expression of bdnf and bfgf in the rat brain. brain res.2007; 1179:28–34 25. kwan p, arzimanoglou a, berg at, brodie mj, allen hauser w, mathern g, moshé sl, perucca e, wiebe s, french j., definition of drug resistant epilepsy: consensus proposal by the ad hoc task force of the ilae commission on therapeutic strategy, epilepsia. 2010 jun;51(6):1069-77 26.dario j. englot, m.d., ph.d., edward f. chang, m.d., and kurtis i. auguste, m.d; vagus nerve stimulation for epilepsy: a meta-analysis of efficacy and predictors of response ; j neurosurg.2011; 115:1248–1255 27. re elliott, sd rodgers, l bassani, a morsi et al., vagus nerve stimulation for children with treatmentresistant epilepsy: a consecutive series of 141 cases, j neurosurg pediatrics.2011; 7: 491-500 28. leslie c. robinson, md, pharmd, mba, 1 and ken r. winston, md1–4, relationship of vocal cord paralysis to the coil diameter of vagus nerve stimulator leads ; j neurosurg. 2015 mar;122(3):532-5 29. morris gl, mueller wm, the vagus nerve stimulation study group eo1-eo5. long-term treatment with vagus nerve stimulation in patients with refractory epilepsy. neurology 1999;53:1731-5 16_patilrahul_pediclescrew 336 patil et al low lumbar burst fracture pedicle screw fixation for low lumbar burst fracture with grade 4 retrolisthesis without any neurological deficit rahul pramod patil1, gaurav jaiswal2, tarun kumar gupta3 department of neurosurgery, r.n.t. medical college, udaipur, rajasthan, india 1resident m.ch neurosurgery; 2neurosurgery, asst. prof. dept. of neurosurgery 3neurosurgery, prof. and head dept. of neurosurgery abstract: burst fractures of the spine account for 14% of all spinal injuries. lower lumbar burst fracture with retrolisthesis is a rare presentation of traumatic cause. management of this type of fracture are controversial and depends on plenty of factors like age of patient, type of injury, neurological deficit, associated comorbit injury. here we are discussing a rarest case of traumatic burst fracture of l4 vertebrae with grade 4 retrolysthesis of l4 on l5 vertebrae with severe secondary canal stenosis and neurologically intact, which was manage with pedicle screw fixation. key words: low lumbar burst fracture, pedicle screw fixation, retrolysthesis. introduction each year, there are approximately 5 million new vertebral fractures worldwide11.burst fractures of the spine account for 14% of all spinal injuries (11). most common site is thoraco-lumbar spine followed by cervical spine (11). burst fractures of the low lumbar (l4 and l5) spine represent a small percentage of all spine injuries. the ilio-lumbar ligaments, major muscle support and location in the pelvic brim and size of lumbar canal are main features unique to these fractures compared to those that occur at the thoraco-lumbar region (12). the rarity of these injuries is evident from their limited discussion in the literature. treatment must be individualised and the recommendations for thoraco-lumbar trauma management cannot necessarily been transferred to low lumbar fractures. management of this type of fracture are controversial and depends on plenty of factors like age of patient, type of injury, neurological deficit, associated comorbit injury. here we are discussing a rarest case of traumatic burst fracture of l4 vertebrae with grade 4 retrolysthesis of l4 on l5 vertebrae with severe secondary canal stenosis but neurologically intact, which was manage with pedicle screw fixation. case 35 year old male fell from tree and had severe back pain on admission to hospital. on examination power in both lower limbs was grade v, without sensory deficit, without bladder and bowel involvement and deep tendon reflexes were normal. local tenderness of lower lumbar spine was present. ct scan of lumbo-sacral spine showed burst fracture of l4 vertebra with retrolisthesis of l4 on l5 (figure 1). mri of lumbo-sacral spine showed burst fracture of l4 vertebra with retropulsion of fracture fragments into the bony spinal canal causing compression on ventral aspect of thecal sac and impingement on nerve root of filum terminale with obliteration of spinal canal with grade iv retrolisthesis of l4 over romanian neurosurgery (2015) xxix 3: 336 343 337 l5 vertebra with mild diffuse disc bulge at l34 and l5-s1 (figure 2). we had perform bilateral pedicle screw fixation at l3 and l5 with rod fixation with decompressive laminectomy via posterior approach (figure 3). to avoid canal compromise and development of iatrogenic cauda equina syndrome due to posterior migration of fracture fragments we had perform decompressive laminectomy. patient was mobilise with brace on postoperative day 3. post-operatively power in both lower limbs was 4+/5 and did not develop radiculopathy or cauda equina syndrome. discussion burst fracture of the lumbar spine is defined as a failure of at least the anterior and middle columns of a vertebral segment because of axial compression, usually associated with some flexion (2). burst fracture are offer associated with some degree of kyphotic deformity of lumbar spine with or without retrolisthesis. low lumbar burst fracture are rare spine injuries. they differ significantly from thoraco-lumbar fracture and their treatment must be individualised. the content and size of the neural canal distinguish the low lumbar area from other region of spine. the cauda equine, containing the nerve roots occupies the lumbar spinal canal below l2 vertebra. so any anatomical distortion due to injury at or below this level stimulates peripheral nerve injury with potential for spontaneous recovery unlike injury above this level which affects the conus medullaris or the spinal cord. additionally, the dimensions of the spinal canal are greater here than in any other region and, indeed, there have been several reports of decreases of as much as 90% in the cross-sectional area of the spinal canal without a neurological deficit especially at l4–l5. these features help to explain the infrequency of severe neurological deficits and the potential neurological recovery when such a fracture is present (8). treatments for low lumbar burst fractures are conservative or surgical, either posterior or by applying an anterior approach (1, 9). but, there is no strict guideline or consensus regarding the proper approach for such lesion. injury pattern, neurological status, age of patient, associated comorbid injury and anatomical approaches available should all be taken into consideration while deciding the line of management. in the neurologically intact patients, conservative care including initial bed rest with postural reduction, subsequent wearing of brace and ambulation has been an effective treatments for low lumbar burst fractures (3, 6). kostuik et al, suggested surgical stabilization is required in burst fracture of thoraco-lumbar and low lumbar region without neurological deficit, when there is canal compromise of more than 50% or there is local kyphosis (5). yazar et al, also share the same opinion, that anterior decompression and stabilization should be performed for low lumbar burst fractures in case of more than 70% of canal compromise due to risk of future displacement, even though there were no neurologic deficits (13). finn et al, reported no correlation of the degree of neurologic deficits with the amount of canal compromise at time of injury. he also said that there is no progression of posterior displacement of bone fragments in low lumbar burst fractures and no significant kyphosis with brace treatment (4). our patient had burst fracture of l4 vertebra with retrolysthesis of l4 over l5 causing more than 90% of canal compromises, but neurologically intact. we had performed pedicle screw fixation via a posterior approach as patient was neurologically intact. such surgery helps in immediate pain relief, elimination of donor site pain, reducing blood loss and short operative time, early mobilisation. there was no post-operative complication like displacement of bone 338 patil et al low lumbar burst fracture fragments causing neurological deterioration or cauda equina syndrome. kun soo jang et al, reported a similar case of l4 burst fracture with 85% of canal compromise and no neurological deficit, treated with short segment posterior fixation without bone fusion. he had convincing result in his patient (7). pelegri c et al, reported a retrospective study of 15 pt of thoraco-lumbar and lumbar burst fracture treated with percutaneous osteosynthesis via pedicle screw fixation without fusion with good results (10). romanian neurosurgery (2015) xxix 3: 336 343 339 340 patil et al low lumbar burst fracture romanian neurosurgery (2015) xxix 3: 336 343 341 342 patil et al low lumbar burst fracture conclusion there is no definitive correlation between the spinal canal compromise and neurological romanian neurosurgery (2015) xxix 3: 336 343 343 deficit in burst fracture of low lumbar vertebra fracture, unlike fracture at other vertebral levels. neurological deficit may not be present even if there is canal compromise of more than 90%. short segment posterior stabilization with pedicle screw is a simple and reliable method of treatment if patient is neurologically intact due to advantage of early pain relief and early mobilisation. correspondence rahul patil room no. 107-109, p.g. boys hostel, r.n.t.medical college, udaipur313001. rajasthan, india e-mail address: dr.rahulpatil@hotmail.com references 1. andreychik da, alander dh, senica km (1996) burst fractures of the second through fifth lumbar vertebrae. j bone joint surg am 78:1156–1166. 2.brant-zawadzki m, jeffrey rb, minagi h (1982) high resolution ct of thoracolumbar fractures. ajr am j roentgenol 138:699–704 3.chan dp, seng nk, kaan kt. nonoperative treatment in burst fractures of the lumbar spine (l2-l5) without neurologic deficits. spine. 1993;18:320–325 4.finn ca, stauffer es. burst fractures of the fifth vertebra. j bone joint surg am. 1992;74:398–403. 5.kostuik jp. anterior fixation for burst fractures of the thoracic and lumbar spine with or without neurological involvement. spine. 1988;13:286–293. 6.kraemer wj, schemitsch eh, lever j, mcbroom rj, mckee md, waddell jp. functional outcome of thoracolumbar burst fractures without neurological deficit. j orthop trauma. 1996;10:541–544. 7.kun soo jang, chang il ju, seok won kim, and sung myung lee; screw fixation without fusion for low lumbar burst fracture : a severe canal compromise but neurologically intact case; j korean neurosurg soc. 2011 feb; 49(2): 128–130. 8.mohanty sp, venkatram n. does neurological recovery in thoracolumbar and lumbar burst fractures depend on the extent of canal compromise? spinal cord. 2002;40:295–299. 9.okuyama k, abe e, chiba m, ishikawa n, sato k. outcome of anterior decompression and stabilization for thoracolumbar unstable burst fractures in the absence of neurologic deficits. spine. 1996;21:620–625. 10.pelegri c, benchikh el fegoun a, winter m, brassart n, bronsard n, hovorka i, de peretti f; percutaneous osteosynthesis of lumbar and thoracolumbar spine fractures without neurological deficit: surgical technique and preliminary results; rev chir orthop reparatrice appar mot. 2008 sep;94(5):456-63. 11.robert f heary and sanjeev kumar decision-making in burst fractures of the thoracolumbar and lumbar spine. indian j orthop. 2007 oct-dec; 41(4): 268–276. 12.seybold ea, sweeney ca, fredrickson be, warhold lg, bernini pm. functional outcome of low lumbar burst fractures. a multicenter review of operative and nonoperative treatment of l3-l5. spine.1999;24:2154– 2161. 13.yazar t, cebesoy o, soydan c, köse c. acute burst fracture of the low lumbar vertebra managed by anterior surgery. journal of ankara medical school. 2004;26:41– 45. radoimugurel_combined 200 | rădoi et al combined surgical and medical treatment of giant prolactinoma combined surgical and medical treatment of giant prolactinoma: case report mugurel rădoi1, florin stefanescu1, ram vakilnejad2, lidia gheorghitescu2 1umf “carol davila” bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases bucharest 2neurosurgical department of the national institute of neurology and neurovascular diseases bucharest abstract: the operative management of giant pituitary prolactinoma represents a significant challenge for neurosurgeons, due to the degree of local tumor infiltration into adjacent structures such as cavernous sinus. the degree of parasellar tumor extension can be classified according to the knosp grading system’ while suprasellar extension is qualified in accordance with the modified hardys classification system. this report describes the case of a male patient with a giant pituitary prolactinoma in which a partial tumor resection via a subfrontal approach was achieved. typically, resection rates of less than 50% have been reported following surgery on giant pituitary adenomas. prolactin levels were very high, consistent with invasive giant prolactinoma. our patient was treated with cabergoline which eventually normalized the prolactin level and significantly reduced the size of the residual tumor. this case serves to illustrate that in the presence of significant suprasellar and parasellar extension, multi-modal treatment strategies with surgery and dopamine agonist, is the gold standard in the management of locally aggressive pituitary prolactinomas. introduction pituitary adenomas are considered to be benign tumors and account for about 15% of primary intracranial tumors (14). tumors exceeding 10 mm are defined as macroadenomas, and those smaller than 10 mm are termed microadenomas (14). while microadenomas are located within the sella and do not cause visual loss, macroadenomas extend beyond the limits of the sella and may cause neuro-ophthalmologic manifestations by compression of adjoining structures (3). giant pituitary adenomas, defined as tumors 4 cm or greater in maximum diameter, account for 5%-14% of adenomas in surgical series (12, 18, 20). romanian neurosurgery (2016) xxx 2: 200-208 | 201 prolactinomas account for approximately 30% of pituitary adenomas and 50 to 60% of functional pituitary tumors (25). they are the most common type of functioning pituitary tumor and are second in frequency to nonfunctioning adenomas in overall incidence. men tend to present with a larger, more invasive and rapid growth prolactinomas than women, possibly because hypogonadism features are less evident (6). the degree of radical resection of giant adenomas is restricted to less than 50% in every published surgical study and is associated with a higher complication rate compared with non-giant pituitary adenomas (12, 18, 20). the most common surgical approaches used for the treatment of giant pituitary prolactinomas are the microscopic transsphenoidal or various frontal and frontotemporal transcranial routes (12, 17, 18, 20). additional therapies are usually necessary to obtain long-term control of tumor growth (18, 20). current recommendations suggest dopamine agonists as the treatment of choice for prolactinomas, including giant and invasive types as these drugs suppresses prolactin (prl) secretion and synthesis as well as lactotrope cell proliferation (24). we presented the case of a giant pituitary prolactinoma, which infiltrate the dura and cavernous sinus. we performed a subtotal resection through a subfrontal approach followed by dopamine agonist treatment. this combined treatment was very effective in normalizing serum prl levels and shrinking the tumor size. case presentation we presented the case of a 61 years old male patient, admitted in our clinic with a one year history of a reduction in his peripheral visual field. this was associated with a shorter history of gradual loss of movements and poor vision in the right eye, frontal headache and unsteady gait. prior to his admission he consulted an ophthalmologist with complaint of double vision. ophthalmological examination revealed important loss of visual acuity, especially in the right eye, a bilateral superior temporal quadrantanopsia and medial convergent squint due to the right sixth cranial nerve palsy. as his psychic was concerned, the patient was alert and oriented. a subsequent cerebral magnetic resonance imaging (mri) scan showed a giant (28/43mm.) enhancing tumor expanding in the pituitary fossa and extending into the suprasellar cistern (figure 1). the tumor, which demonstrated a relative homogenous enhancement, encased the right optic nerve and showed a lobular extension into the right sylvian fissure, invasion of the right cavernous sinus enclosing the cavernous carotid artery. the tumor elevated the floor of the third ventricle, extended to the perimesencephalic cisterns and contacted the right pons. the anterior vascular arcade (both a1 segments of the anterior cerebral arteries and anterior communicating artery) were displaced posteriorly. the degree of parasellar tumor extension was classified according to the knosp grading system (grade 4), while suprasellar extension 202 | rădoi et al combined surgical and medical treatment of giant prolactinoma was qualified in accordance to the hardys classification system (grade c). because of the irregular shape of the tumor and its extension into the subfrontal region, retrochiasmatic area and sylvian fissure we chose to perform a transcranial approach for this case. the patient underwent a subtotal tumor resection via a right subfrontal approach, achieving an approximately 30% reduction in tumor bulk, with focus on right optic nerve decompression. postoperatively, the patient’s bilateral superior quadrantanopsia improved and his headache resolved, but he developed diabetes insipidus. there were no other operative complications. the histopathological exam revealed a pituitary prolactinoma. preoperatively, laboratory studies revealed prolactin 4700 ng/ml (4.60-21.40), cortisol 1.64 μg/dl (6.2-19.4), testosterone 0.025 ng/ml (1.93-7.40), tsh 0.097uui/ml (0.27-4.20), low free thyroxine (ft4) 0.617 μg/dl (0.93-1.7). after surgery, beside the substitutional hormonal therapy, the patient started medical treatment with cabergoline (dostinex), a dopamine agonist, 0.25 mg twice per week, with gradual increase in the dose to 1 mg twice a week. after 3 weeks of endocrine treatment, laboratory studies revealed an important decrease in prolactin level to value of 343.50 ng/ml. after his discharge from hospital, the patient continued his treatment with cabergoline, which eventually normalized the prolactine level and significantly reduce the size of the tumor rest. mri images, obtained 5 months after surgery, showed important reduction of the tumor’s size. the right pons, the right temporal lobe and the floor of the third ventricle were completely decompressed (figure 2). there is still residual tumor in the right cavernous sinus. the visual symptoms were improved and the follow-up mri, 10 months after surgery, demonstrated that residual tumor has continued to collapse and minimize, under dopamine agonist therapy (figure 3). romanian neurosurgery (2016) xxx 2: 200-208 | 203 figure 1 preoperative axial (a1, a2, a3) and coronal (a4) mri images after contrast administration showed a giant (28/43 mm), homogenous tumor, which invaded the right cavernous sinus, extended over the upper clivus and in the temporal lobe, and elevated the floor of the third ventricle 204 | rădoi et al combined surgical and medical treatment of giant prolactinoma figure 2 images obtained 5 months after surgery and cabergoline treatment. axial (b1, b2, b3) and coronal (b4) mri images showed important reduction of the tumor’s size. the right pons, the right temporal lobe and the floor of the third ventricle were completely decompressed discussion giant macroadenomas are defined as lesions greater than 4cm in diameter and represent till 14-15% of all pituitary adenomas (20). since the original description of this pathological entity by jefferson in the 1940s, surgical treatment of giant pituitary adenomas has been extremely challenging (13). postoperative mortality rates as high as 35% has been reported (13, 19). giant pituitary adenomas can be extremely challenging to manage using surgery alone. in case of giant prolactinoma, the use of medical therapy and, possibly, radiation therapy, is crucial for achieving long-term tumor control. the main goals of surgery for giant pituitary adenomas are visual improvement, recovery from endocrinological and neurological symptoms, and maximal tumor resection (25). surgery, either transcranial or transsphenoidal approaches, is the first-line treatment in tumors with compression upon optic structures and visual impairment. the complexity of surgery for giant pituitary adenomas relate to the degree and direction of perisellar spread, because they tend to extend in either a suprasellar or parasellar trajectory (19). the degree of suprasellar tumor extension can be classified according to the modified hardys classification system, while parasellar extension is qualified in accordance with the knosp grading system (23). the completeness of microsurgical resection is inversely related to both the hardys and knosp grade of the tumor. in fact, true cavernous sinus invasion typically prohibits complete tumor resection (10, 18). it is generally accepted that the goal of surgical treatment for giant pituitary adenomas must be maximal tumor resection with minimal associated morbidity (9). total resection rate of giant pituitary adenoma vary between different series and the surgical approach used. on a large series, mortini et al (18) showed that total resection rate was 14.7%., while goel et al. (12) showed romanian neurosurgery (2016) xxx 2: 200-208 | 205 a total resection rate of 29.65%. koutourousiou (15) presented a near-total resection rate of 66.7%. the rate of gross and near-total tumor removal, in cases of giant pituitary adenomas, after transsphenoidal, transcranial or combined procedures range from 14.7% to 74% (12, 15, 18). with recent advances in the expended endoscopic endonasal approach and the associated benefits of improve panoramic visualization afforded, these resection rates will improve. the limitation of endoscopic endonasal approach is invasion of the lateral wall of the cavernous sinus and extension of the tumor to the temporal lobe. but, despite all this, as in our case, an open craniotomy may still be indicated in patients with dumbbell tumors extending far into the anterior cranial fossa, middle fossa or retro-chiasmatic space (13). safe complete resection of a giant pituitary adenoma lateral to the carotid artery remains nearly impossible with no regards to the surgical corridor used (8, 21). gross-total resection of giant pituitary adenomas was dependent on multiple factors, and the overall low resection rates confirm the difficulty in their management. in our opinion, even in case of giant pituitary prolactinoma, surgery could improve vision and its improvement is related with tumor resection rate. additionally, surgery could significantly improve the symptoms of headache and dizziness. however, surgery may not be effective for declined sexual function and amenorrhea (26). it is also believed that visual acuity improvement is significant during the first two postoperative weeks, with no further significant improvement after this period, while visual field defects significantly improve during the first two weeks postoperatively and continue to improve for the first three months but no later than that (21). maximum visual improvement after pituitary surgery is at three months postoperatively (4). although postoperative visual improvement varies among published series, it is more likely after transsphenoidal than transcranial surgery, with rates of approximately 80% (5, 15, 18). postoperative improvement of hypopituitarism after surgery for giant pituitary adenomas has not been studied in detail. the reported hormonal improvement rates of 35%-50% after transsphenoidal surgery are in reference to macroadenomas and cannot be applied to giant pituitary adenomas, in which hypopituitarism is usually long-standing and more difficult to be corrected after surgery (11). postoperative mri performed at different time points after surgery may affect the accuracy of tumor volume calculation. for example, mri performed within the first postoperative week may measure the volume of the hematoma while mri performed after 2 months or later may measure the adenoma recurrence. in general, giant pituitary adenomas have a higher surgical complication rate, highlighting the difficulty of their treatment. in cases of transsphenoidal or endoscopic endonasal approaches the most common complication was postoperative cerebrospinal fluid (csf) leak (16.7%), necessitating reoperation and/or lumbar drain placement (15). worsening of pituitary function occurred 206 | rădoi et al combined surgical and medical treatment of giant prolactinoma in 16.7% of patient after endoscopic endonasal surgery, which is comparable to new endocrinopathy after microscopic transsphenoidal surgery and lower than new pituitary dysfunction after transcranial surgery (5, 18, 20). diabetes insipidus is also another complication after surgery for giant adenomas. permanent postoperative diabetes insipidus vary between 8.2% and 10.4% (20). postoperative visual deterioration is also more common after transcranial than transsphenoidal surgery and can be as high as 22% (9, 18). postoperative cranial nerve dysfunction is a frequent complication after transcranial surgery for giant tumors involving the cavernous sinus, and it affects the oculomotor nerve most often (7). other complication such as syndrome of inappropriate antidiuretic hormone, hydrocephalus, pulmonary embolus, or cerebral ischemia may occur after transcranial or transsphenoidal surgery (microscopic or endoscopic) and are not correlated directly with the surgical approach. mortality rates after surgery are higher in giant pituitary adenomas compared with non-giant adenomas and range from 3.2% to 18.7% (16, 18). one of the leading causes of postoperative death is apoplexy of the residual adenoma. remarkable progress has been made with regards to the management of giant prolactionoma. sometimes, total resection can be achieved with a combined endonasal/transcranial approach or possibly with a staged endoscopic endonasal approach (2). the ultimate goal of a combined treatment (surgery, radiotherapy, endocrine medications) is to achieve eugonadism, euprolactinemia status, and reduction of tumor size (24). while radiotherapy is not the usual preferred treatment because of high complication rates, therapy with dopamine agonists (bromocriptine, cabergoline) are consistently promising in regression size of the pituitary prolactinoma, hypogonadal status reversal and prolactin level correction (6,27). once normalized, serum prl levels should be monitored annually (1). bromocriptine is started at 1.25 to 2.5 mg orally once a day and increased during 2 to 3 weeks to 5 to 10 mg daily in divided doses. cabergoline may be administered at doses ranging between 0.5 and 1.5 mg once or twice per week (1). after normalization of serum prl levels, bromocriptine can be reduced to the smallest effective dose. visual examination should be repeated approximately 1 month after initiation of therapy, and mri should be repeated at 6 weeks and again at 3 months after initiation of treatment (24, 27). some 10 to 25% of patients are partially or totally resistant to bromocriptine (22) and 5% to 10% of patients are intolerant to bromocriptine because of side effects (3, 22). in patients with giant or invasive prolactinomas, pretreatment with a dopamine agonist may improve the success of subsequent surgery. long-term treatment with dopamine agonists may alter the consistency of the tumor and make surgery more difficult (22). stereotactic radiosurgery is an option for patients with prolactinomas after failed transsphenoidal surgery or failed medical therapy and may be a primary treatment for prolactinomas in patients who are reluctant to undergo long-term medical therapy or surgery romanian neurosurgery (2016) xxx 2: 200-208 | 207 (22). this is not the case for a giant prolactinoma, in which stereotactic radiosurgery is only a postsurgical therapy. there is a risk of hypopituitarism, and there may be a radioprotective effect of dopamine agonist therapy; therefore, these medications should be stopped temporarily during radiosurgical treatment (12, 22, 24). conclusions prolactinoma is one of the pituitary tumors that significantly respond well to medical therapy. the main goal of surgical treatment of giant pituitary prolactinoma, through transsphenoidal or transcranial approach, is maximum possible tumor extirpation with minimal side effects. in our case, we used the transcranial approach, due to the dimension and extension of the tumor (temporal lobe and cavernous sinus) and the preference and experience of the operating team. our patient improved significantly after medical treatment, avoiding unnecessary reoperation, and preventing short and long term complications. multidisciplinary treatments should be applied during long-term follow-up periods for successful care and optimal outcomes. correspondence mugurel radoi umf “carol davila” bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases bucharest email: muguradoi@yahoo.com references 1.acharya sv, gopal ra, menon ps, bandgar tr, shah ns. giant prolactinoma: efficacy of medical management. endocr pract.24:1–14,2009. 2.alleyne ch jr, barrow dl, oyesiku nm: combined transsphenoidal and pterional craniotomy approach to giant pituitary tumors. surg neurol 57:380–390,2002 3.anderson d, faber p, marcovitz s, et al. pituitary tumors and the ophthalmologist. ophthalmology 90:1265-1270, 1983. 4.andreas k., kirchhofer d, handzel d, neuloh g, schramm j, mueller c-a, eter n: pre-existing chiasma syndromes do not entirely remit following transsphenoidal surgery for pituitary adenomas acta neurochir 153:26–32, 2011 5.buchfelder m, kreutzer j: transcranial surgery for pituitary adenomas. pituitary 11:375–384, 2008 6.delgrange e, trouillas j, maiter d, donckier j, tourniaire j. sex-related difference in the growth of prolactinomas: a clinical and proliferation marker study. j clin endocrinol metab. 82:2102–7, 1997. 7.dolenc vv: transcranial epidural approach to pituitary tumors extending beyond the sella. neurosurgery 41:542– 552, 1997 8.fahlbusch r, buchfelder m: present status of neurosurgery in the treatment of prolactinomas. neurosurg rev 8: 195-205, 1985 9.fahlbusch, r, buchfelder, m. transsphenoidal surgery of parasellar pituitary adenomas. acta neurochirurgica,92, 93-99, 1988 http://dx.doi.org/10.1007/bf01401978 10.fatemi, n., dusick, j.r., de paiva neto, m.a.,et al. the endonasal microscopic approach for pituitary adenomas and other parasellartumors: a 10-year experience. neurosurgery,63,244-56,2008. http://dx.doi.org/10.1227/01.neu.0000327025.03975.ba 11.fatemi n, dusick jr, mattozo c, mcarthur dl, cohan p, boscardin j, et al: pituitary hormonal loss and recovery after transsphenoidal adenoma removal. neurosurgery 63:709–719, 2008 12.goel a, nadkarni t, muzumdar d, desai k, phalke u, sharma p: giant pituitary tumors: a study based on surgical treatment of 118 cases. surg neurol 61:436–446, 2004 13.jefferson, a. chromophobe pituitary adenomata— the size of the suprasellar portion in relation to the safety of operation. journal of neurology, neurosurgery & psychiatry, 32, 633, 1969 14.jho hd, carrau rl, ko y, daly ma: endoscopic 208 | rădoi et al combined surgical and medical treatment of giant prolactinoma pituitary surgery: an early experience. surg neurol 1997, 47:213–222, 1997 15.koutourousiou m, gardner pa, fernandez-miranda jc, paluzzi a, wang ew, snyderman ch: endoscopic endonasal surgery for giant pituitary adenomas: advantages and limitations. j neurosurg 118:621–631, 2013 16.mohr g, hardy j, comtois r, beauregard h: surgical management of giant pituitary adenomas. can j neurol sci 17:62–66, 1990 17.mortini p, giovanelli m: transcranial approaches to pituitary tumors. op tech neurosurg 5:239–251, 2002 18.mortini p, barzaghi r, losa m, boari n, giovanelli m: surgical treatment of giant pituitary adenomas: strategies and results in a series of 95 consecutive patients. neurosurgery 60:993–1004, 2007 19.oluwafikayo f, shad a. a giant pituitary adenoma: surgical excision via a staged endoscopic an open approach. world journal of neuroscience 4:434-436, 2014 20.de paiva neto ma, vandergrift a, fatemi n, gorgulho aa, desalles aa, cohan p, et al: endonasal transsphenoidal surgery and multimodality treatment for giant pituitary adenomas. clin endocrinol (oxf) 72:512– 519, 2010 21.wang s, lin s, wei l, zhao l, huang y. analysis of operative efficacy for giant pituitary adenoma. bmc surgery 2014, 14:59. doi: 10.1186/1471-2482-14-59. 22.shimon i, benbassat c, hadani m. effectiveness of long-term cabergoline treatment for giant prolactinoma: study of 12 men. eur j endocrinol. 156:225–31, 2007. 23.shrestha, r., bao, g., wei, w. and wang, m. risk factor analysis on the predictors of the transsphenoidal pituitary surgery on marco-adenomas: a multivariate logistic regression analysis. nepal journal of neuroscience, 9, 10-16, 2012. 24.shrivastava rk, arginteanu ms, king wa, post kd. giant prolactinomas: clinical management and long-term follow up. j neurosurg. 97(2):299–306, 2002 25.vance mary lee, m.d. treatment of patients with pituitary adenoma: one clinican’s experience neurosurg focus 16 (4): article 1, 2004 26.wang s, lin s, wei l, zhao l, huang y. analysis of operative efficacy for giant pituitary adenoma. bmc surgery 2014, 14:59. doi: 10.1186/1471-2482-14-59. 27.wu zb, yu cj, su zp, zhuge qc, wu js, zheng wm. bromocriptine treatment of invasive giant prolactinomas involving the cavernous sinus: results of a long-term follow up. j neurosurg. 104(1):54–61, 2006. doi: 10.33962/roneuro-2020-081 complications after sciatic nerve defect repair in rats andrei marin, georgiana gabriela marin, carmen giuglea romanian neurosurgery (2020) xxxiv (4): pp. 482-487 doi: 10.33962/roneuro-2020-081 www.journals.lapub.co.uk/index.php/roneurosurgery complications after sciatic nerve defect repair in rats andrei marin1, georgiana gabriela marin2, carmen giuglea1,3 1 plastic surgery department, “st. john” emergency hospital, bucharest, romania 2 cardiology department, “c.c. iliescu” hospital, bucharest, romania 3 carol davila university of medicine and pharmacy, bucharest, romania abstract experimental microsurgery is a provocative field with great rewards. nerve microsurgery is particularly challenging because the results of the operation can only be tardily observed. during this time frame, multiple complications can appear to the laboratory rats, which can influence the final results. for this reason, when experimenting with wistar rats, one must be familiarized with the possible complications in order to know the suitable solutions for all the issues. lack of information and henceforth lack of action might result in compromising the final data. introduction on a simple internet search with the phrase “sciatic rat nerve”, there are a total of over 3,2 million results. [1] this goes to prove that there is a great interest in experimental surgery on the sciatic nerve conducted on laboratory rats. the rat, particularly the wistar rat, represents the most suitable candidate for experimental nerve surgery, as it is affordable, easy to manipulate and has a suitable anatomy for different types of experiments. furthermore, the faster nerve regeneration period (compared to that of humans) represents a major advantage in working with these laboratory animals. the anatomy of the sciatic nerve in rats is similar to that in humans: the main nerve divides into 3 branches common peroneal nerve, tibial nerve and sural nerve. [2] the anesthesia is another positive aspect for choosing wistar rats – it can be performed by the operator by direct intraperitoneal injection. there are more solutions which can be used, depending on the type and length of the operation. [3] in all experimental surgery performed on animals, a good collaboration with a veterinary is crucial, as he/she provides important expertise regarding anesthesia, post-operative evolution, solutions to problems; it is also stated in the law that in all animal projects, the keywords sciatic nerve, rats, microsurgery corresponding author: andrei marin plastic surgery department, “st. john” emergency hospital, bucharest, romania marin_dpt@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 483 complications after sciatic nerve defect repair in rats presence of a veterinary in the team is compulsory. furthermore, all types of animal experimentation require approvals from the ethics committee and the sanitary veterinary department. [4] material and method. the complications presented in the article were mostly observed and handled during an experimental project for a phd thesis, where 4 methods of defect nerve reconstruction were compared: • nerve graft, • nerve conduit made from a rat aorta (simple aortic conduit), • platelet-rich plasma (prp) inside an aortic conduit, • stem cells inside the aortic conduit. each batch consisted of 10 lab rats and 2 extra lab rats were sacrificed to obtain prp and aortic conduits. the anesthesia used was a mixture of xylazine 10mg/kg and ketamine 75mg/kg. after injecting the anesthesia and preparing the operation site (shaving the dorsal gluteal-thigh region), the wistar rat was placed in prone position and the incision was performed along the femur, 0,5cm inferior to it. a breach was created through the biceps femuri muscle and the sciatic nerve was exposed for a length of 4 cm to be able to observe the emerging branches. 2 separate incisions at a distance of 0,5cm were performed on the sciatic nerve, proximal to the emergence of its branches and the resulting defect was repaired using one of the above-mentioned methods. after nerve reconstruction, the muscle was close using absorbable suture and the skin was close using non-absorbable sutures. postoperatory, the rats were placed 2 in a cage, between the 2 existing a separating transparent plastic support. this was to prevent cannibalism between the rats. special designed plastic cages with a plastic support to create 2 separate compartments the post-operative treatment consisted of enroxil 0,003mg/kg and meloxicam 1mg/kg both injected subcutaneously for 3 days. the wounds were treated locally with betadine solution alternating with baneocin powder. the rats were monitored for 3 months and afterwards they were euthanized using an overdose of the anesthetic mixture and kcl injected intracardiac.[5] during this period, some rats experienced several complications which were treated accordingly. results out of the 40 rats included initially in the study, 2 rats were excluded due to major complications which could influence the final results – one due to postoperative death, the other one due to sciatic nerve rupture. the one death recorded was due to an anesthetic overdose – because the rat would not sleep under anesthesia, multiple doses were administered. this resulted in a profound anesthesia once the drugs took effect, and a prolonged anesthesia time (even after the surgery was over). the rat died the day after the operation. the first postoperative complication observed was wound dehiscence. this occurred in all batches 1-5 days after surgery due to chewing on the surgical knots. some dehiscence were partial, others were total. 2 different measures were taken, unfortunately without the desired effect. the first solution was to redo the suture under local anesthesia with the help of an assistant who would firmly restrain the rat not to bite during the procedure. this proved ineffective and dangerous as the rat would bite through the second knots as well. the second solution was to try to perform a dressing so that the operated rat could no longer reach the wound. this also proved ineffective, as the rat could easily slip out of the dressing and attempt to nibble on the knots. 484 andrei marin, georgiana gabriela marin, carmen giuglea sutured wound with different types of dressings the wounds were treated with different antiseptic solutions and they closed per secundam in maximum one week. a statistical analysis performed to see which batch presented more wound dehiscence revealed that there was a higher prevalence in the second batch (simple aortic conduit), followed by the stem cells batch. however, this analysis didn’t have statistical power (χ2 =1.479 (3); p=0.687). presence/absence of dehiscence wound in the 4 batches batch dehiscence total rats / batch no yes nerve graft no. 6 2 8 pct. 75% 25% 100% simple aortic conduit no. 5 5 10 pct 50% 50% 100% prp no. 7 3 10 pct 70% 30% 100% stem cells no. 6 4 10 pct 60% 40% 100% total per wound no. 24 14 38 pct 63.2% 36.8% 100% graphic of the wound dehiscence distribution in the 4 batches another complication encountered was that of selfmutilation of the affected limb. luckily, the mutilation was limited at the fingernails and like the wound dehiscence it was self-limiting. limb autophagy after sciatic nerve transection – erythema and swelling of the foot and mutilated fingernails (footprint covered with ink due to footprint test). presence/absence of self-mutilation in the 4 batches batch self-mutilation total rats/batch no yes nerve graft no. 7 1 8 pct. 87.5% 12.5% 100% simple aortic conduit no. 7 3 10 pct. 70% 30% 100% prp no. 8 2 10 pct. 80% 20% 100% stem cells no. 7 3 10 pct. 70% 30% 100% total selfmutilations no. 29 9 38 pct. 76.3% 23.7% 100% 485 complications after sciatic nerve defect repair in rats similar to the wound dehiscence percentage, the self-mutilation of the denervated limb was predominent in the prevalence in the second batch (simple aortic conduit) and the stem cells batch, without statistical difference. graphic of self-mutilation distribution in the 4 batches one month after the beginning of the project, all rats presented severe pruritus. as differential diagnoses, alergic dermititis and parasitologic contamination were taken into consideration. due to scratching, some rats presented crusts and erosions, especially around the neck and back. weight loss occured to all rats experiencing these symptoms. due to severe scratching, there was an important hair loss in the area with the pruritus. until the diagnosis was established, the wounds were treated locally with methylene blue, to prevent infection. scratching lesions with hair loss and methylene blue application. after a dermatologic consult, tape was applied on the skin and the sample was then examined under the microscope. the diagnosis of pediculosis with polyplax spp. was put and all rats underwent treatment with stronghold 15mg (selamectin). this treatment was repeated after 2 weeks. thorough mechanic sanitation of all cages was performed, as well as of the rooms where the cages laid. furthermore, the rooms were sterilized for 24 hours using a uv lamp. microscopic aspect of the parasite polyplax spp. after the first application of selamectin, there was a complete relief of the pruritus and a significant improvement of the scratching lesions. all rats recovered both locally (regaining the lost hair) as well as in terms of general state (in the following weeks there was a progressive weight gain). 3rd week after selamectin treatment 486 andrei marin, georgiana gabriela marin, carmen giuglea discussions proper anesthesia is the key to a successful surgery with optimal results. while it would help to sedate the animals using inhaling substances such as isoflurane before injecting them, direct intraperitoneal injection with ketamine, xylazine or acepromazine (or a mixture of these solutions) can be performed even without sedation but with proper contention. [6,7,8] correct calculation of the proper dose is crucial for the outcome. if a rat doesn’t fall asleep in 5 minutes after the normal dose is administrated, this doesn’t mean it has drug resistance, but rather that it takes the anesthetic a longer time to come into effect. therefore, if a rat doesn’t respond in the 5minute time frame, it should be left aside and another rat should be prepared for surgery. otherwise, administrating a new dose of anesthetic might result in a prolonged anesthesia or even death. after the rat is under anesthesia, another important aspect is the handling or moving of the rat. taking into consideration the muscle relation induced by the anesthesia, the rat is susceptible to aspiration if it is grabbed by the tail, with the head down. if this occurs, one should try freeing the airways using a small cannula attached to a vacuum. the typical symptoms a rat experiences in such cases are hiccup-like movement, with desaturation; if no prompt intervention is performed, this will also lead to its death. the best way to prevent this is to manipulate the rat by grabbing it by the back of its neck, heads up. although britto et all believe that total fasting or only-solids deprivation does not induce gastric emptying in mice, a preoperative total fasting for 6-8 hours could reduce this risk. [9] cannibalism immediately after surgery is another issue to be considered. the rats need to be separated a few days after the operation until the wound is closed. afterwards, they can be placed together and it would also be recommend not keeping them separated as they have a tendency to self-mutilate by chewing on the operated, senseless leg when left alone. one difficult complication to treat is selfmutilation – either limb mutilation (in case of peripheral nerve injuries) or wound dehiscence caused by biting the threads which hold the wound tight. hindlimb autotomy/autophagy represents the mutilation of the anesthetic foot by the animal which doesn’t feel the limb and therefore doesn’t recognize it as part of its body. wall et all described degrees of hindlimb autotomy differentiating on the type of nerve injury (cut nerve and encapsulated in polythene tube, sectioning with immediate repair, nerve ligation and nerve crush). [10] prevention of self-mutilation until nerve regeneration occurs is therefore a necessity. plastic head collars could be useful for dogs or other large animals but are not appropriate for the rat, as it can easily get out of this restraint due to its neck anatomy. repelling solutions (such as quinine) applied on the limb or on the wound could prove effective because of its bitter taste. al-adawi et all also proved the efficiency of 6-hydroxydopamine injected in the ascending noradrenergic bundle 1 week prior to transection or n-(2-) chloroethyl-nethyl-2-bromobenzylamine (dsp4) injection 24 h prior to transection. [11] picric acid is another solution that showed better results in reducing limb autophagy compared to the commercial bitedeterrent chemical (denatonium benzoate). [12] another possible complication which fortunately did not occur in this project is infection. although rodents are quite resistant to infection, it would be recommended that postoperative antibiotic be given and sterile conditions during the operation be used. graft versus host disease is another possible complication when using foreign allogen tissue. although no such reaction was noted during the project, even without the use of immunosuppressant medication, this could become a serious problem when transplanting tissues which determine a strong antigenic reaction. even though the project was conducted in a restricted environment in a building located in the veterinary university campus especially dedicated to this experiment, rat contamination occurred. there were 2 possible explanations. one would be the human factor – the people who come in contact with these animals to feed and clean after the rats. the second explanation, although unlikely, could be the 2 windows located at 2,5m altitude in the rooms where the experiments took place. a fast diagnosis and rapid intervention were the key in saving the animals and the project in this case. conclusions animal experimentation requires not only feeding and cleaning, but also attending to the possible 487 complications after sciatic nerve defect repair in rats complications generated by human intervention. when it comes to nerve surgery, the most frequent complications are self-mutilation (either wound dehiscence or autotomy of a limb that in no longer sensitive innervated). this study shows that the rats that presented wound dehiscence were predominantly in the simple aortic conduct batch; the same batch manifested self-mutilation of the denervated inferior limb. the laboratory animals present all possible complication of the surgical intervention, as well as health complications specific to the animals. however, some solutions which may apply to human patients may not be a proper solution for animals. references 1. https://www.google.com/search?q=sciatic+nerve+rat& rlz=1c1gcea_enro877ro877&oq=sciatic+nerve+&aqs =chrome.1.69i57j35i39j0l6.4694j0j7&sourceid=chrome &ie=utf-8. 2. marin andrei, mihai ruxandra ioana, marin georgiana gabriela. pitfalls and problems encountered in rat model sciatic nerve surgery. romanian neurosurgery (2019) xxxiii (4): pp. 396399doi: 10.33962/roneuro2019-064. 3. costea ruxandra, daniel lastofka, and mihai mehedinţu. “comparison of ketamine–medetomidinebutorphanol and ketamine – dexmedetomidine butorphanol anesthesia in rats.” agriculture and agricultural science procedia 6 (2015): 305-308. 4. marin a., marin g., patea a. and enescu d. (2019). timing, logistics and bureaucratic process in planning an experimental in vivo nerve project from a to z. modern medicine | 2019, vol. 26, no. 2. 5. montford jr, linas s. how dangerous is hyperkalemia?j am soc nephrol. 2017;28(11):3155–3165. doi:10.1681/asn.2016121344. 6. greenfield ea. administering anesthesia to mice, rats, and hamsters. cold spring harb protoc. 2019;2019(6):10.1101/pdb.prot100198. published 2019 jun 3. doi:10.1101/pdb.prot100198. 7. he s, atkinson c, qiao f, chen x, tomlinson s. ketamine-xylazine-acepromazine compared with isoflurane for anesthesia during liver transplantation in rodents. j am assoc lab anim sci. 2010;49(1):45-51. 8. lascar i., zamfirescu d. microchirurgie experimentala, 2000, 34-37. 9. brito mv, yasojima ey, teixeira rk, houat ade p, yamaki vn, costa fl. fasting does not induce gastric emptying in rats. acta cir bras. 2015;30(3):165-169. doi:10.1590/s0102-865020150030000001. 10. wall pd, devor m, inbal r, et al. autotomy following peripheral nerve lesions: experimental anaesthesia dolorosa. pain. 1979;7(2):103-111. doi:10.1016/03043959(79)90002-2. 11. al-adawi s, dawe gs, bonner a, stephenson jd, zarei m. central noradrenergic blockade prevents autotomy in rat: implication for pharmacological prevention of postdenervation pain syndrome. brain res bull. 2002; 57(5):581-586. doi:10.1016/s0361-9230(01)00747-x. 12. firouzi ms, firouzi m, nabian mh, et al. the effects of picric acid (2,4,6-trinitrophenol) and a bite-deterrent chemical (denatonium benzoate) on autotomy in rats after peripheral nerve lesion. lab anim (ny). 2015;44(4):141-145. doi:10.1038/laban.711. doi: 10.33962/roneuro-2021-072 important controversies in lumbar spine surgery: which patients benefit from lumbar spinal fusion and who should be fused? literature review f. urian, g. iacob, a.v. ciurea romanian neurosurgery (2021) xxxv (4): pp. 422-427 doi: 10.33962/roneuro-2021-072 www.journals.lapub.co.uk/index.php/roneurosurgery important controversies in lumbar spine surgery: which patients benefit from lumbar spinal fusion and who should be fused? literature review f. urian1, g. iacob1,3, a.v. ciurea2,3 1 university emergency hospital bucharest, neurosurgical department ii, romania 2 neurosurgical department, “sanador” clinical hospital, bucharest, romania 3 professor of neurosurgery, “carol davila” university school of medicine, bucharest, romania abstract considering the rising tendency in the application of lumbar spine devices, a rigorous selection of candidates for lumbar spinal fusion must follow the benefit of the patient in terms of a better outcome than classical techniques or conservatory treatment. we pulled essential information from scientific sources regarding the clinical results of patients who underwent fusion surgery to sift patients who do better from fusion. we found out that imagistic proof of instability such as spondylolisthesis associated with lumbar spinal stenosis and refractory pain takes the most from spinal fusion procedures. oswestry disability index improvement along with restoring the function and reduction of pain remained the postoperative desires of a successful fusion. clinical amelioration with bracing test prior to intervention was a predictor of better results after fusion. exclusion criteria like psychiatric disorders and prior lumbar spine surgery were highlighted since studies demonstrated that they are bad predictors of outcome in spinal fusion surgery. laminectomy was nowhere implemented in the literature as to be urgently fused since only about 20% of patients manifest instability after this classical procedure. iatrogenic segmental instability after laminectomy, radiologically proven should be a candidate for spinal fusion. these procedures have high costs and high rates of complications putting the patient’s functional status and quality of life at uncertainty since there is still a lot of debate in this area of spinal neurosurgery. motto: “outcome may be improved by more careful selection of patients and by performance of an adequate surgical decompression” (deen jr, 1995) introduction “which patients should be fused?” remains a big controversy. lumbar surgical interventions for disc herniation, lumbar stenosis, with or without scoliosis, spondylolisthesis are more frequent, especially for keywords lumbar spinal fusion, surgical outcomes, conservatory & surgical treatment, instability, spondylolisthesis, lumbar spinal stenosis, oswestry disability index corresponding author: iacob gabriel professor. university emergency hospital of bucharest. chief of neurosurgical department ii, bucharest, romania gbrl_cb@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 423 important controversies in lumbar spine surgery older patients, who request for a bigger autonomy (2-4). for several patients, on the medium and long term outcome, evolution may be complicated by postsurgical instability after extensive multilevel surgery, osteoporosis; the more rapid progression of degenerative changes, the suboptimal decompression of the contralateral side because of the impaired view of the target area and a slower postoperative rehabilitation may accentuate compression, especially to older patients, affecting their request autonomy (1)(5). figure 1. a case from our clinic (university hospital of bucharest). these are sagittal x-rays of a young 26 years old male who jumped off the 3rd floor in order to escape a domestic violence scenario. note the compression fracture at l4 in the pre-op image on the left and post-op aspects after lumbar fusion with rods and 4 screws at one level above and below the lesion (middle and right). material and methods radiological and clinical pictures of instability are key features in stratifying patients who gain the most from fusion procedures. spinal spondylodesis is suitable for deformities and instability but lacking proof of effectiveness in primary disc herniation and lumbar spinal stenosis without instability (3). spondylolisthesis represents the classical x-ray feature of spinal instability (6)(7). a meta-analysis made in 2017 on 302620 patients with lif demonstrated a major clinical improvement of individuals who were fused, while the complications and reintervention risk compared with simple decompression limited the benefits brought by spinal fusion in lumbar stenosis with rr of 1,17 for ci of 95% 1,06-1,28 compared with spondylolisthesis rr 0,75 for ci 95% 0,70-0,80 (8). authors and year class of evidence summary sport – 2007 2009 & 2018 ii randomized (n=304) and observational (n=303) spondilolysthesis surgical vs. conservatory. fusion offered a better outcome after 2, 4, and 8 years of follow-up. ghogawala et. al. – 2016 i 66 patients with spondylolisthesis grade i. simple decompression vs. decompression and lif. fusion improved the quality of life (4 years follow-up) chou et al. – 2009 ii a systematic review of 24 articles on fusion vs. conservatory for l lbp and spondilolysthesis surgery was equivalent to intense pm&r table 1. lumbar fusion in spinal canal stenosis with spondylolisthesis, modified after (9). lumbar back pain is common, unfortunately it’s a vague symptom and determining what patients benefit from fusion surgery can be delicate. about 20% of patients with lbp are unable to work (10). a detailed clinical exam and phi are essential in determining patients who have bigger chances of recovery after spinal fusion. multiple studies have demonstrated improvement after fusion in patients with lumbar stenosis and spondylolisthesis (tab.1). a multicentered randomized study with a 2 year follow-up on 294 subjects with chronic lbp and imagistic evidence of lumbo-sacral degeneration found that all surgical fusion procedures used reduced pain, oswestry score (tab.1) and improved function (10). exclusion criteria were: radiologically proven 424 f. urian, g. iacob, a.v. ciurea radicular compression, history of surgical intervention on lumbar spine and those with psychiatric disorders in treatment. all patients were refractory to conservatory treatment. another randomized study conducted in 2003 on 64 patients with ddd and lbp for more than 1 year demonstrated improvement of odi score similar to cognitive therapy and exercises (11). while patients with mild spondylolisthesis do well from postero-lateral fusion with no instrumentation, degenerative disc disease gains the most from postero-lateral fusion with instrumentation, therefore type of surgical treatment should be in relation with the diagnosis (12). a common outcome predictor of fusion in everyday practice is bracing test. important alleviation of pain after using a tlso indicates a good outcome for lumbar spinal fusion vs. conservatory treatment. this test has value only in patients with chronic low back pain with no prior spine surgery (5). 0%-20% minimum disability activities of daily living are performed normally. no special treatment is required 21%-40% moderate disability patient has pain when standing, sitting or lifting weights. normal activities are still performed well conservatory treatment is nedeed. 41%-60% severe disability daily activities are affected as pain is increasing and becoming constant 61%-80% infirmity daily activities are interrupted surgical intervention is mandatory 81%-100% “stuck in bed” patient lies in bed all day or dissimulates table 2. interpretation of oswestry disability index after filling a special questionnaire, modified after (4). discussions numerous descriptions regarding the stability of spinal column have been made still no defining consensus was reached. according to white-panjabi (13)(14): instability means a loss of spine’s ability to maintain under physiological conditions it’s normal anatomical relationships at risk causing signs of irritation spinal cord/nerve root, pain or crippling deformities and to louis (15) spinal stability is the cohesion of vertebral structures in all physiological positions. in contrast, spinal instability it’s an important cause of lumbar back pain and important disability. diagnosing spinal instability can be challenging. use of imaging like x-rays in flexion-extension and side-bending, standardised lumbo-sacral x-rays along with lateral flexion and extension radiographs – defining spinal instability as sagittal plane translation of 4 mm or more (13)(14), fluoroscopy, mri(standard and dynamic) and ct scans can provide useful information. dynamic x-rays in flexion and extension should not be replaced by mri and ct scans in the assessment of spinal instability (16). radiological documentation of instability should be performed preop, at 6 months and 3 years post op to demonstrate evidence of progressive segmental instability (2). instability could be responsible for stenosis; it could be associated with lss symptomatic with intermittent mechanical pain; iatrogenic with symptomatic instability or without clinical signs (17)(18). spondylolisthesis, lumbar scoliosis may generate instability (19-21), also after decompression, the possibility of segmental instability should always be considered. fusion procedures, especially those involving instrumentation are associated with increases in cost and complications, are used for preop, intraoperative instability or postop listhesis (2224). still there are several debatable aspects subject of controversy: the criteria of instability, the spondylolisthesis or scoliosis grade, what kind of stabilization should be used with or without motion preservation, minimally or invasive intervention, the approach used: posterior, anterior or “circumferential”, instrumentation increases the fusion rate?, implant failures and adjacent joints degeneration (25). spiking if stabilisation is needed, even if is better to stabilise without decompression, there are several aims to respect (2)(26): − treat a dynamic component patients with severe symptoms and radiographic evidence of excessive motion, greater than 4 mm translation or 10o of rotation, who fail to respond to a trial of nonsurgical treatment; − prevent postoperatory instability stabilization is needed for confirmed preoperatory instability, large resections and abnormal articular orientation; − fusion should be made to obtain a stabilization after arthrectomy, to correct a deformity, to avoid 425 important controversies in lumbar spine surgery a hypermobility, maintaining lordosis and foraminal size; − arthrodesis & instrumentation there are several options: open rigid stabilization systems with pedicle screw fixation, percutaneously, motion preservation: dynamic stabilization systems, facet arthroplasty tfas® total facet arthroplasty system; − lumbar interspinous implants: colfex, wallis, diam, x-stop, a.s.o. current guidelines reject stabilization by default on the basis of an extensive literature search (2)(23)(24). even after a laminectomy only 20% of cases need a fusion procedure (22). the reactive degenerative changes obviously prevent manifest segmental instability, even after decompression if more of 5066% of articular process or isthmus are conserved, without discal space violation (25). there are several surgical alternatives (27-32): − open: bone deposition, iliac bone graft, instrumentation rigid or dynamic with pedicular screws, inserted with the help of a spinal navigation system, interbody cages; − microscopic; − percutaneously; − facet arthroplasty; − interspinous spacers (x-stop, diam, coflex, helifix) with 45% improvements after two years, an intermediate option between conservative and surgical treatment “does not burn bridges”, for patients with mild symptoms, to those that can’t undergo or refuse more extensive surgery, as a temporary solution, “addressing the problem within the canal without entering the canal”. interspinous spacers advantages are: disc not removed, no pedicles used, opening of foramens, unloading of the posterior part of the disc, of the facets. there is also less risk of significant complications, no direct manipulation adjacent to the neural structures; the risk of neurological deficit (paralysis; dural tears; etc) decrease to a minimum. such interspinous spacers can’t be used in the following anatomic variants: markedly decreased interspinous distance (kissing spine– like), with concomitant facet joint hypertrophy, a posterior v-shaped interspinous area, limited accessibility of the space between the base and the tip of the spinous process because of facet joint hypertrophy and variations in the shape of the inferior surface of the spinous process. combined lss with degenerative spondylolisthesis and posterior arthrosis at one or several levels. in such cases it’s more frequent lateral lss associated with disc hernia. spondylolisthesis in itself is not an indication, except if there is > 4 mm translation in sagittal plane and 10° angulation flexion/extension. for such cases foraminal decompression, discectomy and fusion to all affected levels should be made (33). it is uncertain whether instrumentation: use of pedicle screws or metal cages help to fuse adjacent vertebrae or biologic agents bone morphogenetic protein should be used to enhance osseous fusion (2). combined lss with degenerative listhesis and posterior arthrosis at one or several levels. from the surgical point of view decompression in lss may affect isthmus and generate iatrogenic instability because of arthrectomy, especially in a lss with degenerative listhesis and posterior arthrosis. we should treat only the instable level (25). several complications could be seen: overlying stenosis (by recurrence of a degenerative spondylolisthesis, hypertrophic flavum ligaments), disassembly of osteosynthesis by fracture instrumentation on a short and medium term, as a sign of pseudarthrosis. conclusions interbody lumbar fusion indication should be established on imagistic proof of instability and substantiated by perpetual clinical suffering refractory to conservatory methods. it’s already demonstrated that large laminectomies should be avoided, lumbar decompression with fusion, at the symptomatic level should be made if medical treatment fails. there is still a lot of work to do in this field of research since there is a lack of randomized studies that compare surgical outcomes with natural history of lumbar pathologies, classical techniques and conservatory measures. on the other hand, there are some encouraging positive results of surgical fusion in patients with lumbar spine instability and associated degeneration, as a promising alternative detrimental to conservatory treatment, although psychiatric background and prior history of lumbar surgery should rise the alarm of surgeon, since the latter 426 f. urian, g. iacob, a.v. ciurea were proved to be negative predictors of outcome in spinal fusion. abbreviations ci confidence interval ct computed tomography ddd degenerative disk disease lbp low back pain lss lumbar spinal stenosis lif lumbar interbody fusion mri magnetic resonance imaging odi oswestry disability index phi personal history of illness pm&r physical medicine and rehabilitation rr relative risk tlso thoracic lumbar sacral orthosis acknowledgements this study received no funding. conflicts of interest the authors declare no conflict of interest. references 1. deen h. g. et al. analysis of early failures after lumbar decompressive laminectomy for spinal stenosis, mayo clin proc 1995, 70, 1, 33-36. 2. iacob g. craciun m personal experience in lumbar spinal stenosis (lss), romanian neurosurgery 2011, xviii, 4, 400-411. 3. omidi-kashani, farzad et al. “lumbar spinal stenosis: who should be fused? an updated review.” asian spine journal 2014, 8, 4, 521-530. 4. jalil n.a., sulaiman z, et al. retrospective review of outcomes of a multimodal chronic pain service in a major teaching hospital: a preliminary experience in universiti sains malaysia, malays j med sci 2009, 16(4), 55-65. 5. christensen fb. lumbar spinal fusion. outcome in relation to surgical methods, choice of implant and postoperative rehabilitation, acta orthop scand suppl. 2004, 75(313), 2-43. 6. beazell, james r et al. “lumbar instability: an evolving and challenging concept”, the journal of manual & manipulative therapy, 2010, 18, 1, 9-14. 7. roberto i, gianluigi g, et al. biomechanics of the spine. part i: spinal stability, european journal of radiology, 2013, 82, 118-126. 8. willems p. decision making in surgical treatment of chronic low back pain: the performance of prognostic tests to select patients for lumbar spinal fusion. acta orthop suppl. 2013, 84(349), 1-35. 9. reid. p.c. state of the union: a review of lumbar fusion indications and techniques for degenerative spine disease, j. neurosurg. spine 2019, 31:1-14. 10. fritzell p, hägg o, et al. swedish lumbar spine study group. chronic low back pain and fusion: a comparison of three surgical techniques: a prospective multicenter randomized study from the swedish lumbar spine study group, spine (phila pa 1976), 2002, 1, 27(11), 1131-1141. 11. brox ji, sørensen r, et al. randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. spine (phila pa 1976), 2003, 1, 28 (17), 1913-1921. 12. patrick c, simon m, et al. state of the union: a review of lumbar fusion indications and techniques for degenerative spine disease. jnspg 75th anniversary invited review article. j. neurosurg. spine 2019, 31, 1-14. 13. panjabi m. the stabilizing system of the spine. part ii. neutral zone and instability hypothesis, j spinal dis. 1992, 5, 390-397. 14. iqbal j. surgery for lumbar canal stenosis: micro or macro? dubai spinal course 2008. 15. louis r. – spinal stability and instability as defined by the louis three-column spine concept, spinal instability, springer verlag, 1993, 2, 21-22. 16. fernandes j., mauro a., et al. image correlation between facet facet effusion and lumbar instability. coluna/columna 2019, 18(3), 205-208, epub september 02, 2019. 17. paquisph. la scoliose dégénérative de l’adulte et canal lombaire étroit: comment décomprimer, course francophone bucarest 2014. 18. schramm j., kristof r., müller c.a. lumbar stenosis:operative techniques for simple stenoses and cases aggravated by other factors, spine congress dubai 2008. 19. yavin d, casha s, et al. lumbar fusion for degenerative disease: a systematic review and meta-analysis, neurosurgery, 2017, 1, 80(5), 701-715. 20. rezk, e.m.a., elkholy, a.r. & shamhoot, e.a. transforaminal lumbar interbody fusion (tlif) versus posterior lumbar interbody fusion (plif) in the treatment of single-level lumbar spondylolisthesis. egypt j neurosurg 2019, 34, 26. 21. robaina-padrón fj. controversias de la cirugía instrumentada y el tratamiento del dolor lumbar por enfermedad degenerativa. resultados de la evidencia científica [controversies about instrumented surgery and pain relief in degenerative lumbar spine pain. results of scientific evidence]. neurocirugia (astur). 2007, 18(5), 406-13. 22. sonntag vkh, marciano ff. is fusion indicated for lumbar spinal disorders ?, spine 1995, 20(suppl), 138s– 142s. 23. ian a, adrian t, et. al. lumbar spine fusion: what is the evidence? int. med. journal, 2018, 48, 12, 1421-1569. 24. martin, brook i. , mirza, sohail k.; et al. trends in lumbar fusion procedure rates and associated hospital costs for degenerative spinal diseases in the united states, 2004 to 2015, spine 2019, 44, 5, 369-376. 427 important controversies in lumbar spine surgery 25. duquesnoy b., mazel c. – le devenir du canal lombaire etroit (retrecit) opere, le 18-eme congres sfr. paris, 2005. 26. alan l, matthew f, et al. ct evaluation of lumbar interbody fusion: current concepts, american journal of neuroradiology 2005, 26, 8, 2057-2066. 27. caputy a et al. the role of spinal fusion in surgery for lumbar spinal stenosis: a review, neurosurg focus 1997, 3, 2. 28. burnett m.g. et al. cost-effectiveness of current treatment strategies for lumbar spinal stenosis: nonsurgical care, laminectomy and x-stop, j neurosurg spine 2010, 13 (1), 39–46. 29. barbagallo g,mv. et al. – analysis of complications in patients treated with the x-stop interspinous process decompression system: proposal for a novel anatomic scoring system for patient selection and review of the literature, neurosurgery 2009, 65, 111–120. 30. brussee p. et al. self-rated evaluation of outcome of the implantation of interspinous process distraction (x-stop) for neurogenic claudication, eur spine j 2008, 17, 200– 203. 31. kim ka, mcdonald m, et al. dynamic intraspinous spacer technology for posterior stabilization: case-control study on the safety, sagittal angulation and pain outcome at 1year follow-up evaluation, neurosurg focus 2007, 22, e7. 32. phillips f.m. effect of the total facet arthroplasty system after complete laminectomy-facetectomy on the biomechanics of implanted and adjacent segments, the spine journal, 2009, 9,1, 96-102. 33. grob d., et al.significance of simultaneous fusion and surgical decompression in lumbar spinal stenosis, orthopade 1993, 22, 243-249. doi: 10.33962/roneuro-2020-064 the idiopathic hypertrophic spinal pachymeningitis. a case report and review of literature surjeet singh, stuti kumari, abhijeet sachan, satish chandra verma romanian neurosurgery (2020) xxxiv (1): pp. 411-415 doi: 10.33962/roneuro-2020-064 www.journals.lapub.co.uk/index.php/roneurosurgery the idiopathic hypertrophic spinal pachymeningitis. a case report and review of literature surjeet singh1, stuti kumari2, abhijeet sachan3, satish chandra verma4 1 m.ch. neurosurgery, department of neurosurgery, sms medical college and hospital, jaipur, rajasthan, india 2 m.d. pathology, department of pathology, institute of medical sciences bhu varanasi, uttar pradesh, india 3 m.ch. neurosurgery department of neurosurgery, sms medical college and hospital, jaipur, rajasthan, india 4 m.ch. neurosurgery, department of neurosurgery, sms medical college and hospital, jaipur, rajasthan, india abstract idiopathic hypertrophic spinal pachymeningitis (ihsp) is a rare inflammatory condition characterized by chronic inflammatory hypertrophy of the dura mater. it can involve the entire spine. however, most cases are reported in the cervical and thoracic spine. it can progress from local pain to radiculopathy and eventually develop myelopathy. the aetiology of ihsp is not known. however, it has been suggested to be associated with many diseases. here we report a case of ihsp in 21year-old female who presented with paraplegia. the diagnosis was made on mri spine and histopathological examination. it was treated with surgical decompression, steroid therapy and patient improved gradually. introduction spinal ihp is a rare disease which causes chronic inflammatory hypertrophy of the duramater. its etiology is still unknown. it most commonly involves cervical and thoracic spine1,2,3. commonly presents in the age of 6th and 7th decade of life4. symptoms arises due to progressive compression of adjacent structures. we report a rare case of ihsp in a 21 year old women who presented with paraplegia. case report a 21 years old female presented with history of progressive weakness of bilateral lower limb since 2½ months, was admitted in department of neurosurgery, sms hospital jaipur. on examination, modified ashworth scale of spasticity was grade 2 in bilateral lower limb, medical research keywords chronic inflammatory spinal pachymeningitis, idiopathic, paraplegia, cord compression corresponding author: surjeet singh department of neurosurgery, sawai man singh medical college jaipur, rajashthan, india sujitgmc35@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 412 surjeet singh, stuti kumari, abhijeet sachan et al. council power grade was 0/5 in both lower limb, bilateral knee and ankle reflex was +3. bilateral babinski sign was positive and superficial abdominal reflex was absent. 70-80 % sensory loss of all modality below t2 dermatome level was present bilaterally. other systemic examinations were normal. mr imaging of the thoracic spine demonstrated an intradural extramedullary lesion extending from c7-d4 level that was hyperintense on t1 and hypointense on t2 and nonenhancing on contrast . the lesion was compressing the spinal cord with cord edema. all routine hematological investigations were within normal limit. all the relevant investigations related to the cause of spinal pachymeningitis were negative. after d1–d5 laminectomy, duramater was found to be thickened compressing spinal cord. posterior excision of duramater was done. a durafoam was placed posteriorly to expand the thecal sac and specimen was sent for histopathological examinations. chronic inflammation with lymphoplasmacytic infiltrate and fibrosis was found on histology. postoperative steroid therapy was given. patient was under follow up and after 8 months, patient developed some sensation in both lower limb and power of lower limb improved from 0/5 to 2/5. figure 1. mri cervico-dorsal spine sagittal preoperative (a) t1 imagea hyperintense intradural extramedullary lesion present at c7d4, compressing the spinal cord. (b) t2 imagea hypointense intradural extramedullary lesion present at c7d4, compressing the spinal cord. figure 2. mri cervicodorsal axial image post contrast: (a) minimal enhancing intradural extramedulla ry lesion present posterior to spinal cord (b) t2 weighted image hypointense lesion present posterior to spinal cord. figure 3. (a) intraoperativ e image showing a grossly thickened dura (b) histopatholo gical examination s showing fibrocollagen ous tissue with dense infiltrate of lymphocytes and plasma cells. 413 the idiopathic hypertrophic spinal pachymeningitis figure 4. postoperative mri of the cervico-dorsal spine, sagittal view: showing the expanded cord. discussion this disorder is rare and usually found intracranially and spinal form is extremely rare 5-8. friedman d et al found most cases of ihp intracranially2. it usually involves the cervical and thoracic dura or occurs as a craniospinal form (5,9,10). the first case of spinal ihsp was reported by charcot and joffroy named as "pachymeningitis hypertrophica cervicalis" in 1869(11,12). spinal ihsp is a rare cause of nerve root and spinal cord compression. it has been implicated in variety of inflammatory and infectious processes like tuberculosis, sarcoidosis, rheumatoid arthritis, wegener granulomatosis etc.(5-8) . so, other possibilities need to be ruled out as ihsp is a diagnosis of exclusion (5-7). in our case, we could not find any predisposing illnesses such as infectious diseases or autoimmune diseases in spite of thorough investigations. joffroy and rosenfeld et al, described three stages; local and radicular pain in first stage. signs of nerve root compression in second stage and spinal cord compression was described in third stage (12,13). haobin chen et al, reported age of the patients ranges from 28 years to 68 years (median age 56 years), and female being more commonly affected (male/female ratio: 6:9). thoracic spine being most commonly affected followed by cervical and lumbar spine14. friedman d and flanders described peripheral enhancement on mri which was present in all 3 patients as highly suggestive of hypertrophic pachymeningitis, which was also noted in another report2. dumont as and s.pai et al, proposed extramedullary mass extending over multiple vertebral levels, strongly hypointense signal on t2weighted images, and variable peripheral margin enhancement are suggestive of the ihsp15,16. in our case, extramedullary lesion was present in c7-d4 level which was hypointense on t2weighted image and hyperintense on t1 weighted image. spine. martin n et al reported good result of methotrexate treatment in cranial pachymeningitis7. treatment choices for ihsp include surgical decompression, administration of corticosteroids, radiation therapy, and immunosuppressive agents but relapses are common (5,17). surgical decompression provides some relief, and early surgical intervention can successfully alleviate neurologic sequelae1,9,10. naffziger and rosenfeld et al, recommended surgical decompression by laminectomy and excision of the involved dura for its management (13,15,18). dumont as and kitai ret al reported that biopsy with steroid therapy can reduce the thickness of the dura and can improve neurologic deficit(15,19).naffziger and dumont et al suggested laminoplasty instead of extensive laminectomy because it reduce back pain and increase spinal stability(15,18).in our case c7-d4 laminectomy with dural excision was done and post-operative steroid therapy was administered. after 8 months, power of lower limb improved from 0/5 to 2/5. conclusion we reported a rare case of cervico-dorsal compressive myelopathy caused by ihp. definite diagnosis needs thorough blood investigations, radiological and histopathological findings as ihsp is a diagnosis of exclusion. surgical decompression along with steroid therapy can be considered as an effective mode of treatment. early diagnosis and treatment can lead to better neurological outcomes. conflict of interests the authors declare no conflict of interests. abbreviations and acronyms ihsp: idiopathic hypertrophic spinal pachymeningitis; ihp: idiopathic hypertrophic pachymeningitis; mri: magnetic resonance imaging. 414 surjeet singh, stuti kumari, abhijeet sachan et al. table 1. idiopathic hypertrophic pachymeningitis – age, location, mode of treatment and its response. author ref no. age sex location treatment outcomes pai et al 16 68 f spinal: c6, c7 laminectomy, steroid spontaneous temporary resolution of symptoms, recurrence after surgery takahashi et al 20 67 m spinal c3, c7 corticosteroid at the 2-year follow-up, the patient could walk independently ranasinghe et al 21 65 m spinal t7, t8 laminectomy, corticosteroids mri improvement at 57 months yasuda et al22 28 m spinal: t1, t4, then l1, l3 laminectomy, corticosteroids recovered lai et al23 41 m spinal t2, t4 laminectomy, dura excision unavailable present study 21 f spinal c7-d4 laminectomy, dura excision partial recovery references 1. botella c, orozco m, navarro j, et al. idiopathic chronic hypertrophic craniocervical pachymeningitis: case report. neurosurgery 1994;35:1144 –49. 2. friedman d, flanders a, tartaglino l: contrast-enhanced mr imaging of idiopathic hypertrophic craniospinal pachymeningitis. ajr am j roentgenol 160:900–901, 1993. 3. hassin gb: histogenesis of cerebral hypertrophic pachymeningitis and its relation to syphilis. am j syphilis 2:715, 1918. 4. mikawa y, watanabe r, hino y, hirano k: hypertrophic spinal pachymeningitis. spine (phila pa 1976) 19:620– 625, 1994. 5. kupersmith mj, martin v, heller g, shah a, mitnick hj: idiopathic hypertrophic pachymeningitis. neurology 62:686– 694, 2004. 6. lee yc, chueng yc, hsu sw, lui cc: idiopathic hypertrophic cranial pachymeningitis: case report with 7 years of imaging follow-up. ajnr am j neuroradiol 24:119–123, 2003. 7. martin n, masson c, henin d, et al. hypertrophic cranial pachymeningitis: assessment with ct and mr imaging. ajnr am j neuroradiol 1989;10:477–84. 8. riku s, kato s. idiopathic hypertrophic pachymeningitis. neuropathology 2003;23:335–44. 9. ashkenazi e, constantini s, pappo o, et al. hypertrophic spinal pachymeningitis: report of two cases and review of the literature. neurosurgery 1991;28:730 –32. 10. mikawa y, watanabe r, hino w, et al. hypertrophic spinal pachymeningitis. spine 1994;19:620 –25. 11. charcot jm, joffroy a. deux cas d’atrophie musculaire progressive avec le´sions de la substance grise et des faisceaux ante´rolate´raux de la moelle e´pinie´re. arch physiol norm pathol 1869;2:354 –67, 629 –49, 744 –69. 12. joffroy a. deux cas d'atrophie musculaire progressive avec lesions de la substance grise et des faisceaux anterolateraux de la moelle epiniere. arch physiol norm path. 1869;2:354–367. 13. rosenfeld jv, kaye ah, davis s, gonzales m. pachymeningitis cervicalis hypertrophica. case report. j neurosurg. 1987;66:137–139. 14. haobin chena, yulong lib, nikita mehraa, sheela mehraa, david frescoc, joseph paula, chi p cheunga, d. idiopathic hypertrophic pachymeningitis as a rare cause of spinal cord compression.jornal of medical cases. volume 3, number 4, august 2012, pages 267-269. 15. dumont as, clark aw, sevick rj, myles st. idiopathic hypertrophic pachymeningitis : a report of two patients and review of the literature. can j neurol sci. 2000;27:333–340. 16. pai s, welsh ct, patel s, rumboldt z. idiopathic hypertrophic spinal pachymeningitis : report of two cases with typical mr imaging findings. ajnr am j neuroradiol. 2007;28:590–592. 17. smucker jd, ramme aj, leblond rf, bruch la, bakhshandehpour g. hypertrophic spinal pachymeningitis with thoracic myelopathy: the initial presentation of anca-related systemic vasculitis. j spinal disord tech 2011;24(8):525–532. 18. naffziger hc, stern we: chronic pachymeningitis; report of a case and review of the literature. arch neurol psychiatry 62:383–411, 1949. 19. kitai r, sato k, kubota t, kabuto m, uno h, kobayashi h. hypertrophic cranial pachymeningitis involving the pituitary gland : a case report. surg neurol. 1997;48:58– 62. discussion 62-63. 20. hiroshi takahashi, akihito wada, yuichiro yokoyama, maki ishii, kazutoshi shibuya, toru suguro. idiopathic hypertrophic spinal pachymeningitis: a case report. journal of orthopaedic surgery, 2010, 18(1), 113117. 21. moksha g. ranasinghe, omar zalatimo, elias rizk, charles s. specht, g. timothy reiter, robert e. harbaugh, and jonas sheehan. idiopathic hypertrophic spinal 415 the idiopathic hypertrophic spinal pachymeningitis pachymeningitis report of 3 cases. j neurosurg spine, 2011, 15, 195–201. 22. mio tsutsui. taketoshi yasuda. masahiko kanamori. takeshi hori.tomoatsu kimura. long-term outcome of idiopathic hypertrophic thoracic pachymeningitis. eur spine j, 2012, 21 (4), 404–407. 23. hui-ting hsu, shu-shong hsu, chu-chun chien, pinghong lai. teaching neuroimages: idiopathic hypertrophic spinal pachymeningitis mimicking epidural lymphoma. neurology, 2015, 84, 67-68. 7_adamd_microcystic 276 adam et al microcystic meningioma mimicking an arachnoid cyst microcystic meningioma mimicking an arachnoid cyst danil adam1*, ioana hornea1, cristiana moisescu1, dragos iftimie1, toma papacocea1* 1*”carol davila” university of medicine and pharmacy bucharest 1”saint pantelimon” emergency clinical hospital bucharest abstract: microcystic meningioma is a particular morphopathological form of benign meningiomas, with different imaging characteristics compared to other forms of meningiomas. it is presented the case of an 80 year old woman with repeated head injuries, initially operated for a right fronto-temporo-parietal pericerebral fluid collection. after four years, the patient returned with headache, confusional status, somnolence, symptoms wich appeared after a new head injury. cerebral ct scan revealed a hypodense lesion in the right sylvian fissure of 5.7/3.5 cm, without perilesional edema, which was interpreted as an arachnoid cyst. intraoperative, a soft, gelatin-fibrous tumor mass was identified, partially adherent to the dura mater and the underlying cortex, which was completely resected. the morphopathological diagnosis was microcystic meningioma. it is discussed the imaging aspect of the presented case compared to the literature data regarding the microcystic meningiomas and the relationship between head traumas and the occurrence of meningiomas. key words: microcystic meningioma, higroma, arachnoid cyst, computed tomography. introduction the meningioma represents 20-34% of the primary cerebral tumors (13, 16). the vast majority are solid benign tumors, more common among women, with classical typical imaging features: extraaxial well-defined mass, hyperdense on ct scan, sometimes with calcifications and adjacent bone hyperostosis, hypointense in t1-mri and hyperintense in t2-mri, with homogenous contrast enhancement. among the benign meningiomas there is a rare morphological type, with atypical imagistic features, with microcysts at the morphopathological examination, called microcystic meningioma. this constitutes a difficult preoperative diagnostic issue. we present the case of a patient who has had repeated head traumas and the diagnosis of this lesion was an intraoperative surprise. although miming a posttraumatic fluid collection on the preoperative investigation, in reality it was a tumor, a rare type of meningioma. we discuss the imaging aspects of the presented case in comparison with the literature data regarding the microcystic meningioma, mainly to eliminate the diagnosis confusion between the microcystic meningioma and the posttraumatic fluid collections frecquently encountered among the elderly patients. case presentation a 80 year old woman suffered in february 2011 a mild head injury by accidental fall on stairs. at admission she presented with headache and dizziness. the head ct scan did not reveal acute posttraumatic brain injuries, romanian neurosurgery (2015) xxix 3: 276 281 277 but a right temporo-parietal meningeal thickening was noted. after a month, the patient returned accusing headache and diplopia. the cerebral ct scan revealed a right fronto-temporoparietal hypodense extracerebral area with a maximum thikness of 12 mm at the level of the sylvian fissure, which determined a 5mm midline shift (figure 1). through a circular bone flap performed with a trephina, at the opening of the dura mater, a slightly xantocrom liquid was evacuated under pressure (figure 2). postoperative, the evolution was uneventful. after four years, the patient was readmitted after a mild head trauma, presenting headache, cognitive disorders exacerbated in recent months, somnolence. the cerebral ct scan revealed a right fronto-temporo-insular fluid collection of 5.7/ 3.5 cm with mass effect on the right ventricle which appeared almost completely collapsed, and which determined midline shift towards the left side. the density of the liquid from the fronto-temporo-insular collection was different (higher) than the liquid in the ventricular system, but there was no perilesional edema (figure 3). figure 1 axial head ct scan which reveals a right fronto-temporo-parietal hypodense extracerebral area with a maximum thikness of 12 mm at the level of the sylvian fissure, with a 5 mm midline shift figure 2 postoperative skull x-ray which reveals right parietal bone flap 278 adam et al microcystic meningioma mimicking an arachnoid cyst figure 3 head ct scan in axial (a), coronal (b) and sagittal (c) sections which reveals a right frontotemporo-insular fluid collection of 5.7/ 3.5 cm with mass effect on the right ventricle and midline shift towards the left side considering that it was a posttraumatic injury, a new fronto-temporal bone flap centered on the sylvian fissure was performed with the trephina (figure 4) and, intraoperative, an extraaxial, soft, gelatinous, grey violet, vascularized mass was identified, which was adherent to the dura mater, compressed the subjacent brain and in some places was adherent to the cortex and the sylvian fissure vessels. total tumor resection was performed with the coagulation of the adjacent dura mater (simpson ii resection). postoperative, the neurological evolution was influenced by the occurrence of lung infections and clostridium infections that have prolonged hospitalization. the patient was discharged in conscious state, without neurological deficits. the histopathological diagnosis was microcystic meningioma (figure 5). figure 4 postoperative cerebral ct scan which revelas the two bone flaps: right parietal and frontotemporal figure 5 h-e colored photomicrograph no.111090, original magnification 400x fragment of the surgically removed tissues showing numerous microcysts containing a pale eosinophilic fluid, surrounded by processes of neoplastic cells discussions although meningiomas have distinctive imagistic and morphological features, they are histologically heterogeneous. a unique morphopathological type is the microcystic meningioma. after the macroscopic appearance, masson named this type of meningioma using the term “humid meningioma”. the term “microcystic” was introduced by kleinmen and col. in 1980. although in the last century several classifications of meningiomas were made (2, romanian neurosurgery (2015) xxix 3: 276 281 279 4, 5, 20), this rare form of meningioma appears for the first time in the 1993 who classification (11). the microcystic meningiomas represent 1.6 % of the intracranian maningiomas (11). macroscopically, the tumor has a soft, gelatinous, spongy appearance, it is adherent to the dura mater and highly vascularized. microscopically, the tumor consists of polygonal eosinophilic cells with intracytoplasmic vacuoles and microcysts. in the tumor mass there can be identified extracellular microcystic spaces containing edematous fluid. even if the histological features of this tumor are well known to experts, the rarity of this type of meningioma generates diagnostic confusion regarding the radiological and imagistic data. based on the presented case and the literature data, we will discuss the characteristics of microcystic meningiomas in order to avoid incorrect preoperative diagnoses. the skull x-ray may reveal hyperostosis or osteolysis adjacent to the meningiomas, as well as calcifications. its role in guiding the diagnosis decreased once the ct scan has appeared. on ct scan images, the meningiomas appear as a hyperdense extracerebral mass with contrast enhancement. calcifications can be identified in over 20% of cases (19). hyperostosis is encountered more frequently in the skull base meningiomas, in up to 50% of the cases, and osteolysis in about 3% of cases (8). regarding the patients with symptoms appeared after head injuries who present at the emergency department, the routine investigation is the cerebral ct scan. in elderly patients with a history of mild head traumas, the cerebral ct scan may show a pericerebral fluid collection. at the first cerebral ct examination of the presented patient, two elements which need to be apprehended were described: the thickening of the dura mater in the fronto-temporal region and the highest thickness of the fluid collection at the level of this dural thickening. the evacuation of the fluid collection was followed by neurological improvement and a new cerebral ct scan was no longer necessary. at the last admission, the hypodense fluid collection was located at the level of the sylvian fissure. there were no elements to suggest a different diagnosis: perilesional edema, calcifications, requiring other imaging studies: contrast ct scan or brain mri. the clinical symptoms appeared after a new head trauma, which strengthened the diagnostic suspicion of fluid collection. peritumoral edema is the prerogative of malignant tumors, but it was observed in more than half of who grade i tumors. peritumoral edema was noted in 40 to 60% of all meningiomas (10). azizyan and col. found peritumoral edema in up to 66% of the 12 cases of pure micromeningiomas. the mechanism through which the peritumoral edema occurs is not completely understood. overexpression and secretion of vegf by the tumor is the most common theory on peritumoral edema production as vegf increases the permeability of capillaries and pial vascularization (6, 9, 18). yoshioka and col. believe that peritumoral edema only occurs when there is a brain-pial tumor vascularization, with vegf contribution. other theories relate to the production of fluid by the tumor through a tumor cell secreting activity, or mechanical or ischemic injury to the brain by the tumor (15). the trabecular tumor cells identified in microcystic meningiomas suggested to lantos and col. that the formation of microcysts was an attempt of tumor cells to restore the subarachnoid space. some authors have noted that in microcystic meningiomas there is a thickening of the dura mater adjacent to the tumor (3, 7, 12, 16). this aspect was also stated in our case, on the first cerebral ct scan. this suggests the fact that, at the first admission, the tumor was at the debut, small-sized, although the thickness of the hypodense pericerebral lesion was maximal at the level of the sylvian fissure, 280 adam et al microcystic meningioma mimicking an arachnoid cyst where subsequently the tumor resection was performed. if we do not admit the fact that the tumor pre-existed the first head trauma, we can assume that there is a relationship between head traumas and further development of meningioma, causal relationship commented even by cushing, afterwards admitted or denied by various authors. since a contrast ct scan or mri were not performed, otherwise unusual in a patient with head trauma, we cannot give a definite answer to the question whether there is a connection between head traumas and further development of meningiomas. conclusions in elderly patients with head traumas, the cerebral ct scan may reveal images suggestive for a pericerebral fluid collection. in very rare cases, this fluid collection may be associated with a rare type of meningioma, the microcystic one, some lesions appearing hypodense on these images. references 1. azizyan a, eboli p, drazin d, et al: differentiation of benign angiomatous and microcystic meningiomas with extensive peritumoral edema from high grade meningiomas with aid of diffusion weighted mri. biomed research international 2014, hindawi publishing corporation. http://dx.doi.org/10.1155/2014/650939. 2. bailey p, bucy pc: the origin and nature of meningeal tumors. am j cancer 1931, 15:15-54. 3. cho jh, yang kh, zhang hy: microcystic meningioma – unusual variant of meningiomas. j korean neurosurg soc, 2003, 34: 82-85. 4. cushing h: the meningiomas (dural endotheliomas): their source and favored seats of origin. brain 1992, 45:282-316. 5. cushing h, eisenhardt l: meningiomas: their classification, regional behaviour, life history and surgical end results. springfield, chargles c thomas, 1938. 6. ding y-s, wang h-d, tang k, et al: expression of vegf in human meningiomas and peritumoral brain areas. annals of clinical and laboratory science, 2008, 38: 344-351. 7. endert f: ueber geshwulste der dura mater. virchows arch 1900, 160:19-32. 8. gangadhar k, santrosh d, fatterpekar gh: imaging of intracranial meningiomas with histopathologial correlation: a relook into old disease. njr, 2013, 3(1): 14-32. 9. kalkanis sn, carroll rs, zhang j et al: correlation of vegf messenger rna expression with peritumoral vasogenic cerebral edema in meningiomas. j. neurosurg 1996; 85: 1095—1101. 10. kim ey, kim st, kim hj, jeon p, kim kh, byun hs: intraventricular meningiomas: radiological findings and clinical features in 12 patients. pubmed 2009 mayjune; 33(3):175-80. 11. kleihues p, burger pc, scheithauer bw: the new who classification of brain tumors. brain pathology 1993, 3:255-268. 12. kleinman gm, liszezak t, tarlov e, richardson ep jr. microcystic variant of meningioma: a lightmicroscopic and ultrastructural study. am j surg pathol. 1980; 4:383-389. 13. lantos pl, vandenberg sr, kleihues p. tumors of the nervous system. in: graham. lantos editors. greenfields, neuropathology. arnold: 1997, 732. 14. mahmood a, caccamo dv, tonrecekfj et al: atypical and malignant meningiomas: a clinicopathological review, neurosurgery, 1993, 33(6), 955-963. 15. michael pb, peter cb, james gs. typical, atypical and misleading features in meningioma. radiografics 1991; 11: 1087-1106. 16. michand j, gagne f: microcystic meningioma. clinicopathologic report of eight cases. arch pathol lob med 1983, 107:75-80. 17. perry a, louis d.n., scheithauer b.w. et al: worl health organization classification of tumours of the central nervous system. iarc, lyon, france, 4th edition, 2007. 18. provias j, claffey k, tang k, et al: meningiomas: role of vegf/vascular permeability factor in angiogenesis and peritumoral edema. neurosurgery 1997; 40: 1016-1026. 19. rohninger m, sutherland gr, louw df sima aaf. incidence and clinicopathological features of meningioma. jneurosurg 1989; 71:665-672. 20. russel ds, rubinstein lj: pathology of tumors of the nervous system. london, edward arnolo, 1971, 3rd edition. 21. yoshioka h, hama s, taniguchi s, et al: peritumoral brain edema associated with meningioma: influence of vascular boold supply. cancer 1999, 85(4): 936-994. 11adamd_gianthyperostosis romanian neurosurgery (2014) xxi 4: 465 – 470 465 giant hyperostosis after sphenoid ridge en plaque meningioma removal danil adam1, toma papacocea1, ioana hornea2, cristiana moisescu2 1university of medicine and pharmacy carol davila, bucharest 2“saint pantelimon” emergency hospital, bucharest abstract: meningioma is in most cases a benign tumor of the central nervous system with two growth patterns: en masse and en plaque. hyperostosis is associated in 13 – 49 % of the cases with en plaque meningioma. we describe the case of a 47 years old woman with meningotelial sphenoid ridge meningioma which was totally removed. at the first admission she presented with no neurological deficits, seizures and a mild right exophthalmos. this had an indolent growth. after 10 years, the patient was readmitted for headache, blurred vision and right exophthalmos. skull x-rays and brain mri revealed an important thickening of the right superior orbit wall and sphenoid ridge. she underwent a new surgery. there was no intradural tumor found. instead, bones of the superior and lateral right orbit walls were very hiperostotic. a hole of 3/2 cm in the right superior orbital wall was drilled and the orbital cavity was decompressed. in the postoperative period, the symptoms were remitted and the exophthalmos reduced. we discuss the causes and management of hyperostosis associated with meningiomas. key words: meningioma, hyperostosis, bone invasion. introduction meningioma is a primary tumor of the central nervous system which accounts for about 20 % of all intracranial tumors, more than 35 % of primary brain and central nervous system tumors and 53.8 % of nonmalignant brain and cns tumors (1). nomenclature of intracranial meningiomas refers to their location, pathological features and some growth characteristics. cushing and eisenhardt coined the terms meningioma en masse and en plaque (2). meningiomas en plaque represent 2 – 4 % of intracranial meningiomas. they are associated with hyperostosis in 13 – 49 % of the cases (3, 4). the association of meningiomas with adjacent bone hyperostosis was discussed for the first time in 1903 by brissaud and lererbaullet (5). we report the case of a patient with 466 adam et al giant hyperostosis after sphenoid ridge en plaque meningioma removal sphenoid ridge meningioma with massive hyperostosis extended to the orbit and floor of the middle cranial fossa. case report a 47 years old woman with right sphenoid ridge tumor was operated in 2003. tumor pathology was meningotelial meningioma. at that time, the patient presented a mild right exophthalmos. in the next 10 postoperative years she was under neurologist care for seizures and parkinson disease. right exophthalmos had an indolent growth. the patient was again admitted in our neurosurgical department in 2014 for headache, exophthalmos and blurred vision at the right eye. according to the ophthalmological examination, right exophthalmos had 29 mm in axial plane, was irreducible, extraocular eye movements were normal and visual acuity was 1/1. she had no neurological deficits. she presented a swelling of the zygomatic region. skull x-ray and axial t2-weighted and t1weighted mri images showed hyperostosis of the right sphenoid ridge and superior and lateral orbital bones extended to the middle cranial fossa (figures 1, 2, 3). the patient underwent a new surgery through the same pterional approach. an intradural tumor was not found but the orbital roof presented multiple osseous spiculi. with the aid of a drill, a hole was created in the superior orbital wall with the depth of 3 cm, which was enlarged until 3/2 cm, through which the periorbit herniated (figure 4). the optic canal was not uncovered. dura mater was closed with autologous fascia lata graft. the bone flap was replaced. figure 1 preoperative skull x-ray showing hyperostosis of the right sphenoid ridge and lateral orbital walls extended to the middle cranial fossa (highlighted by dotted circle) figure 2 romanian neurosurgery (2014) xxi 4: 465 – 470 467 figure 3 figures 1, 2 preoperative axial and sagittal cerebral mri showing important hyperostosis of the right sphenoid ridge and lateral orbital walls extended to the right anterior temporal lobe (highlighted by red arrows) figure 4 intraoperative image showing a hole created with the aid of a drill in the superior orbital wall 3 cm deep, enlarged until 3/2 cm through which the periorbit herniated (highlighted by dotted circle) figure 5 morpho-pathological aspects of tumor: monomorphic spindle cells with central round/ oval nuclei of meningothelial meningioma with bone infiltration (arrow) figure 6 postoperative skull x-ray showing radiolucency (highlighted by dotted circle) in the superior orbital wall instead of hyperostosis postoperative recovery was uneventful, with immediate 5 mm reduction of ptosis, disappearance of headache and of blurred vision. pathological examination revealed invasion of the bone with meningotelial cells (figure 5). skull x-ray showed radiolucency in the superior orbital wall instead of hyperostosis (figure 6). at the 6 months follow up the patient is without symptoms and exophthalmos remained stable. discussions intracranial meniongiomas develop from the arachnoid villi. in their development, they can form globular tumor masses or they can diffuse along the dura mater, creating what cushing and eisenhardt (2) have termed en plaque meningiomas. even though they do not exceed the leptomeninges, at the base of implantation the dura mater appears thickened and infiltrated with tumor cells. a sign associated to meningiomas is 468 adam et al giant hyperostosis after sphenoid ridge en plaque meningioma removal hyperostosis, which has a variable incidence and is more frequently observed in en plaque meningiomas. there were issued several hypothesis regarding the cause of hyperostosis. in 1934, echlin suggested that the bone adjacent to the tumor is infiltrated with tumor cells (6). in 1937, globus stated that neoplastic cells invade the bone through the haversian system (7). in order to avoid recurrence, other authors recommended excision of the tumor and of the hiperostotic bone (4, 8). simpson showed that in case of grade i resection (total removal of the tumor, of the dural attachment and of the invaded bone), the 10 years recurrence rate is 9 %, compared to 40 % in the case of subtotal tumor resection (8). recent histopathological studies demostrated bone infiltrated by tumor in the hiperostotic area (9, 10). kim and colab. described, according to the ct aspect, 4 different patterns of hyperostosis in en plaque meningiomas: homogeneous, periostal, diploic and threelayered. they consider that the tumor invasion of the periosteum stimulates the forming of the bone (11). others consider that the bone metabolism is hormonally and enzymatically controlled (12, 13). through recent immunohistochemical studies, matschke and colab. (13) demonstrated the presence of somatostatin 2a receptor in the meningiomas, which can have diagnostic implications. octreotide scintigraphy, a somatostatin analog, allows visualization of the meningioma and permits differentiating it from schwannoma or scar tissue. this method could be of great use in diagnosing patients with meningiomas without hyperostosis in which histopathological studies show bone invasion. timirgaz and colab. published the case of en plaque meningioma of the sphenoid ridge with easily resectable “soft” hyperostosis (15). the invasion of the sphenoid ridge and of the orbital walls by an en plaque meningioma may produce their osteolysis and easy decompression of the orbit (16). from the therapeutic point of view, the purpose of surgery is total removal of the tumor and aggressive resection of hiperostotic bone (17, 18). regarding en plaque meningioma developed at the cranial base, this objective is not possible. piepper and colab. reported a 69 % rate of tumor bone invasion in case of skull base meningiomas (19). extensive invasion of the orbital bone and middle fossa floor by an en plaque meningioma does not confer the character of histological malignancy. in the presented case, the hiperostotic superior orbital wall, with a thickness of 3 cm, had a very high density. even though there was no intradural tumor regrowth, histopathological studies showed that hiperostotic bone contained tumor cells, having the aspect of meningotelial meningioma. the total removal of the hiperostotic bone was not possible because of the extension of hyperostosis and infiltrated bone density: the superior and lateral orbit walls, anterior clinoida, medial wall of the sphenoid sinus, the floor of the middle cranial fossa as well as the zygomatic bone. the optic canal romanian neurosurgery (2014) xxi 4: 465 – 470 469 decompression was not performed because of fear of mechanical or thermal damage to the optic nerve. the preoperative visual acuity was 1/1 and postoperatively it maintained at the same value. the exophthalmos decreased. blurred vision disappeared. we consider that orbital decompression and intraorbital pressure reduction were sufficient measures to improve symptoms. a more aggressive resection may have produced optic nerve damage and enophthalmos. in the case of a less hiperostotic superior orbital wall, we believe that croping and milling it on both sides in order to reduce its thickness followed by restoring it into place, subdurally, without anchoring to adjacent bone structures, would be indicated. its final position will be influenced by intracranial and intraorbital pressure equalization. conclusions intracranial meningiomas are accompanied by ostosis, morphological changes of infiltrated bone, such as hyperostosis or osteomalacia. the case of an en plaque meningioma of sphenoid ridge accompanied by orbital walls and middle cranial fossa floor hyperostosis was presented. the surgical treatment of en plaque meningioma accompanied by hyperostosis should aim total removal of the tumor, of the infiltrated dura mater and, as far as possible, of the tumor infiltrated bone. total resection is unfeasible. references 1. quinn t. ostrom, haley gittleman, paul farah et al: cbtrus statistical report: primary brainand central nervous system tumors diagnosed in the united states in 2006-2010, neuro-oncology, 15 suppl 2: ii1-ii56, 2013. 2. cushing h, eisenhardt l: meningiomas. their cassification, regional behaviours, life history and surgical end results. charles c. thomas. springfield, il, 1938. 3. cushing h: the cranial hyperostosis produced by meningeal endotheliomas. arch.neurol.psychiatry 8: 139-154, 1922. 4. binnal j, thibault a, brotche j, born j: invading meningiomas of the sphenoid ridge. j neurosurg 53: 587599, 1980. 5. brissaud, lererbaullet p: deux cas d’hemicraniose rev neurol 11: 537-540, 1903. 6. echlin f: cranial osteomas and hyperostoses produced by meningeal fibroblastomas. arch surg 28: 357-405, 1934. 7. globus jh: the meningiomas. trans assoc res nerv ment dis 16: 210-265, 1937. 8. simpson d: the recurrence of intracranial meningiomas after surgical treatment. j neurol neurosurg psychiatry 20: 22-39, 1957. 9. akutsu h, sagita k, sonibe m, matsumura a: parasagital meningioma en plaque with extracranial extension presenting diffuse massive hyperostosis of the skull. surg neurol 61: 165-169, 2004. 10. gupta sk, mohindra s, radotra bd, klosla vk: giant calvarial hyperostosis with biparasagittal en plaque meningioma. neurol india 54: 210-211, 2006. 11. kim ks, rogers lf, goldblatt d: ct features of hiperostosing meningioma en plaque. ajr am j roentgenol 49: 1017-1023, 1987. 12. heick a, mosdal c, iorgensen k, klinken l: localized cranial hyperostosis of meningioma: a result of neoplastic enzymatic activity? acta neurol scand 87: 243-247, 1993. 13. oury f, yardav vk, wang y et al: creb mediates brain serotonin regulation of bone mass through its expression in ventromedial hypothalamic neurons. genes dev 24: 2330-2342, 2010. 14. matschke j, addo j, bernreuther c, zustin j: osseous chamges in meningioma en plaque. anticancer research 31: 591-596, 2011. 470 adam et al giant hyperostosis after sphenoid ridge en plaque meningioma removal 15. timirgaz v, crihan a: unele aspecte ale tratamentului chirurgical al meningiomului “en plaque” de aripa sfenoidala cu hiperostoza osoasa care a provocat exoftalmie. buletinul academiei de stiinte a moldovei. stiinte medicale. chisinau: 3/(22): 83-88, 2009. 16. jin-uk baek, young-dae cho, jae-chul yoo: an osteolitic meningioma en plaque of the sphenoid ridge. j korean neurosurg. soc. 43(1): 34-46, 2008. 17. maroon jc, kennerdell js, vidovich dv: sphenoorbital craniotomy for meningioma, in rengachary ss, wilkens rh (eds): neurosurgical operative atlas, park ridge, aans, 1993, vol 3, pp 249-257. 18. maroon jc, kennerdell js, vidovich dv et al: recurrent spheno-orbital meningioma. j neurosurg 80: 202-208, 1994. 19. pieper dr, al-mefty o, hanada y, buechner d: hyperostosis associated with meningioma of the cranial base: secondary changes of tumor invasion. neurosurgery 44: 742-747, 1999. doi: 10.33962/roneuro-2020-095 cervical extradural metastasis from follicular carcinoma thyroid after 14 years post-thyroidectomy with elsberg phenomenon vijayan peettakkandy, shanavas cholakkal, subrat kumar soren, harikrishnan s. romanian neurosurgery (2020) xxxiv (4): pp. 557-560 doi: 10.33962/roneuro-2020-095 www.journals.lapub.co.uk/index.php/roneurosurgery cervical extradural metastasis from follicular carcinoma thyroid after 14 years post-thyroidectomy with elsberg phenomenon vijayan peettakkandy, shanavas cholakkal, subrat kumar soren, harikrishnan s. department of neurosurgery, government medical college. kozhikode, kerala, india abstract background. follicular carcinoma thyroid usually metastasises to bone. common sites of bone metastasis include skull and spine. spinal metastasis are more common in the cervical region followed by dorsolumbar spine. cervical extradural lesions present with progressive quadriparesis, sensory loss, dysautonomia, and respiratory distress. typical elsberg phenomenon in a cervical extradural lesion is rare. elsberg phenomenon involves the involvement of ipsilateral upper limb, ipsilateral lower limb followed by contralateral lower limb and contralateral upper limb. case presentation. we are reporting a case of 47-year-old lady presented with progressive quadriparesis of 1-month duration. her weakness started in left upper limb followed by left lower limb, right lower limb and right upper limb weakness. she also had sensory loss below the level of c7. she had undergone near-total thyroidectomy for solitary thyroid nodule 14 years back and was on thyroid supplementation since then. histopathology at that time was reported as follicular adenoma with hashimoto thyroiditis. her right upper limb power was grade 4left upper limb grade 1 right lower limb grade 3, left lower limb grade 2 with hypertonia of both upper and lower limbs. she was evaluated with mri spine which showed a dumb bell-shaped extramedullary lesion involving the c5-c6 vertebra with significant cord compression and encasement of the left vertebral artery. usg neck showed left supraclavicular lymph node enlargement and small residual thyroid tissue in the left side of the thyroid. usg guided fnac from the thyroid tissue and neck nodes were inconclusive. the patient underwent c4 and c5 laminectomy and subtotal excision from the cervical lesion. histopathology was reported as metastasis from follicular carcinoma thyroid. postoperatively patient limb power improved to grade 3 left upper and lower limbs and was discharged and later referred for radioiodine ablation conclusion. cervical extradural metastasis from follicular carcinoma thyroid can present with elsberg syndrome even without any neck swelling even after decades of post thyroidectomy status for a benign aetiology. laminectomy and decompression may lead to clinical improvement. introduction carcinoma thyroid is the fifth common malignancy in women and can be broadly classified in to papillary, follicular, medullary and anaplastic. keywords thyroid, follicular carcinoma, cervical extradural, elsberg phenomenon corresponding author: shanavas cholakkal department of neurosurgery, government medical college. kozhikode, kerala, india shanavascholakkal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 558 vijayan peettakkandy, shanavas cholakkal, subrat kumar soren, harikrishnan s. (1) papillary carcinoma thyroid is the most common variety, which usually metastasise to neck nodes via lymphatic system. whereas the follicular carcinoma thyroid spreads hematogenously to lungs and bones.more than 80% of bone metastases from all tumors including dtc are located in the axial skeleton red marrow (vertebrae, ribs and hips) owing to high blood flow. (1)clinically, they present with bone pains, pathological fractures or signs of cord compression. progressive quadriparesis with typical elsberg phenomenon as the presenting manifestation of follicular carcinoma of thyroid in a post neartotal thyroidectomy for a benign etiology after several years of thyroidectomy is quite uncommon in medical literature related to this (2). case presentation a 47-year-old lady presented with complaints of neck pain of 4 months duration followed by progressive paraparesis of 1 month duration. weakness initially started as left upper limb weakness 1 month back followed by weakness of left lower limb, right lower limb and right upper limb. at the time of presentation, she was bed ridden. she also complained of numbness over all the four limbs and chest and abdomen and had urinary retention and constipation. she had underwent near total thyroidectomy for solitary thyroid nodule 14 years back and histopathology was reported as follicular adenoma with hashimoto thyroiditis. she was under follow up for next 2 years and was on thyroid hormone replacement. on examination, she was conscious, alert, hemodynamically stable. no signs of hyperthyroidism or hypothyroidism. she had a healed thyroidectomy scar in the neck with left supraclavicular lymphadenopathy and no other palpable swellings. her right upper limb power was grade 4 left upperlimb grade 1 right lower limb grade 3, left lower limb grade 2 with hypertonia of both upper and lower limbs. she had sensory loss below the c7 level. triceps jerk, knee jerk and ankle jerk were exaggerated bilaterally and plantar was extensor bilaterally. her routine blood investigations were normal. esr was slightly elevated (42 mm/hr). mantoux test was negative. she was evaluated with mri c-spine with screening of whole spine which showed an illdefined lobulated heterogenous enhancing dumbbell shaped probably extradural soft tissue lesion of size 3.5x3.3x3 cm (txapxcc) in the c5 and c6 vertebral level with infiltration in to the body of c6 vertebra. the lesion was extending intraspinally causing severe spinal canal compromise with compression over the spinal cord . the lesion was extending superiorly in to the posterior epidural space from c4 to c7 and was encasing the left vertebral artery at level of c5c6 vertebra. usg abdomen and chest x ray were normal. ultrasound neck showed thyroid tissue in the thyroid bed and left supraclavicular lymphadenopathy. fnac from the left supraclavicular lymphnode and recurrent thyroid were inconclusive. she underwent c5-c6 laminectomy and subtotal excision of the lesion. the intraoperative findings suggested an extradural lesion at c5-c6 level involving and destroying the c6 vertebra and compressing the spinal cord and encasing left vertebral artery. histopathology was reported as metastasis from the follicular carcinoma thyroid with ttf-1 positivity. patient improved clinically postoperatively. at the time of discharge, she had grade 3 power of left upper and lower limbs and grade 4 power of right upper and lower limbs. she underwent radio-iodine scanning followed by radioiodine ablation. she is presently on limb physiotherapy and rehabilitation. figure 1. mri c-spine showing an ill-defined lobulated heterogenous enhancing dumbbell shaped probably extradural soft tissue lesion 559 cervical extradural metastasis from follicular carcinoma thyroid figure 2a. intraoperative image showing extradural lesion with destruction of c5 and c6 vertebral body with encasement of left vertebral artery. figure 2b. histopathology was reported as metastasis from the follicular carcinoma thyroid with ttf-1 positivity. discussion follicular carcinoma usually forms osteolytic metastasis and are common in the skull and spine. usual site of spinal metastasis in follicular carcinoma is thoracic > lumbar> cervical. (1) presentation of follicular carcinoma thyroid spinal metastasis may vary. patient can present with destruction of the vertebral body, localised tenderness, radiculopathy and with features of myelopathy like quadriparesis or paraparesis, sensory deficits, sphincter disturbances, autonomic dysfunction and respiratory distress. in extradural lesions usually symptoms are progressive as the size of the lesion increases. (3,4) elsberg u phenomenon is the progressive quadriparesis with sequential involvement of ipsilateral upper limb, ipsilateral lower limb followed by contralateral lower limb and contralateral upper limb, often described as u-shaped or clockwise involvement of limbs. elseberg u phenomenon is commonly seen in cervical myelopathy due to cervical extradural lesions or in foramen magnum pathology and very rarely due to extradural metastasis from follicular carcinoma thyroid.(3,5,6,7) mri spine is the investigation of choice for spinal tumours. mri can help in differentiating the intramedullary tumours from extramedullary and extradural tumours. bony structure can be properly evaluated by ct spine. (8) contrast enhanced imaging helps in delineating the relationship of the cervical lesion with vertebral artery as well. if required vertebral artery reconstruction, along with bony reconstruction can help in perioperative planning. extradural lesions are most commonly tuberculous, myelomatous or metastatic. hence workup for primary is done routinely. surgical decompression and biopsy can help in confirmation of diagnosis and clinical improvement this case is reported in view of the rare clinical presentation of metastatic follicular carcinoma thyroid after 14 years post thyroidectomy without any neck swelling presenting with elsberg phenomenon. it also suggests the need for more regular followup in cases of follicular adenoma and hashimoto thyroiditis. conclusion cervical extradural metastasis from follicular carcinoma thyroid can present with elsberg syndrome even without any neck swelling even after decades of post thyroidectomy status for a benign etiology. laminectomy and decompression may lead to clinical improvement. postoperative radioablation may be required in case of incomplete excision. 560 vijayan peettakkandy, shanavas cholakkal, subrat kumar soren, harikrishnan s. abbreviations mri magnetic resonance imaging; ct computed tomography; dtc differentiated thyroid cancer; fnac fine needle aspiration cytology; esr erythrocyte sedimentation rate. declarations ethics approval and consent to participate. informed written consent for participation obtained from the patient and her caretakers. institutional ethics committee approval not obtained as the study did not involve any human trials. consent for publication informed written consent for publication obtained from the patient and her caretakers availability of data and material data and material available in the department of neurosurgery, govt medical college, kozhikode, kerala, india. competing interests authors declare that there is no competing interests funding nil authors' contributions all authors have contributed to the preparation of manuscript. all authors have read and approved the manuscript, and ensure that this is the case. acknowledgements nil references 1. parameswaran r, shulin hu j, min en n, tan wb, yuan nk. patterns of metastasis in follicular thyroid carcinoma and the difference between early and delayed presentation. ann r coll surg engl. 2017;99(2):151–4. 2. ríos a, manuel rodríguez j, balsalobre md, febrero b, tébar j, parrilla p. [distant metastases as the initial manifestation of follicular thyroid carcinoma]. endocrinol nutr. 2009 apr;56(4):213–4. 3. upreti v, sridhar m, dhull p, sen a. an unusual cause of progressive quadriparesis. indian j endocrinol metab. 2013 oct 1;17(7):155. 4. haghpanah v, abbas si, mahmoodzadeh h, shojaei a, soleimani a, larijani b, et al. paraplegia as initial presentation of follicular thyroid carcinoma. j coll physicians surg pak. 2006 mar;16(3):233–4. 5. dong p, chen n, li l, huang r. an upper cervical cord compression secondary to occult follicular thyroid carcinoma metastases successfully treated with multiple radioiodine therapies. med (united states). 2017 oct 1;96(41). 6. goldstein si, kaufman d, abati ad. metastatic thyroid carcinoma presenting as distal spinal cord compression. ann otol rhinol laryngol. 1988;97(4):393–6. 7. khan mn, sharfuzzaman a, mostafa mg. spinal cord compression as initial presentation of metastatic occult follicular thyroid carcinoma. j neurosci rural pract. 2014 apr;5(2):155–9. 8. çoban g, yildirim e, gemici k, erinanç h. mri findings of lumbosacral metastasis from occult follicular thyroid cancer: report of a case. surg today. 2014 mar;44(3):553–7. doi: 10.33962/roneuro-2021-040 letter to the editor. intracranial aneurysm: research in preclinical outcome models and human effectiveness of intraluminal devices tariq janjua, luis rafael moscote -salazar, amit agrawal romanian neurosurgery (2021) xxxv (2): pp. 239-240 doi: 10.33962/roneuro-2021-040 www.journals.lapub.co.uk/index.php/roneurosurgery letter to the editor. intracranial aneurysm: research in preclinical outcome models and human effectiveness of intraluminal devices tariq janjua1, luis rafael moscote-salazar2, amit agrawal3 1 medical director, aneuclose llc, mn, usa 2 neurosurgery department, cartagena, colombia 3 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india abstract endovascular treatment of intracranial aneurysms has become one of the most important preclinical research arenas. this influential progress is due to the incredible development of new devices and catheters technologies. one of the main outcomes for intraluminal devices used for treatment is the rate of occlusion of the aneurysm. dear editor, the endovascular treatment of intracranial aneurysms has become one of the most important preclinical research arenas. 1 this influential progress is due to incredible development of new devices and catheters technologies. one of main outcome for intraluminal devices used for treatment is the rate of occlusion of the aneurysm. coil embolization, stenting, flower diverter and intrasaccular disruptors cause progressive healing of the aneurysm.2 one of the most important challenges is recanalization resulting in retreatment in up to 20% of cases. 2 although the mechanisms of aneurysm healing are poorly understood, much of the information has been obtained from preclinical animal models. the latter do not emulate the conditions of the healing process that occurs in humans. 3 one recent biggest problem facing the world today is sars-cov-2 epidemic and the capability of sars virus to infect multiple cell types and thus several organs 4 varga et al, showed evidence of direct viral infection of the endothelial cell and diffuse endothelial inflammation. 5 although the 3 cases mentioned in the report did not include any cerebral vasculature histology though the same impact of keywords intracranial aneurysm, preclinical outcome models, intraluminal devices corresponding author: amit agrawal department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 240 tariq janjua, luis rafael moscote-salazar, amit agrawal virus can be there. this endotheliitis associated with covid-19 may have relevant implications for preclinical investigation, usually in animal models capable of being coronavirus-infected and in humans receiving treatment with devices such as stents, flow diverters, and intrasaccular disruptors. ravindran et al, published a systematic review where they evaluated the published literature regarding endothelialization after flow diverter deployment.6 for example, after pipeline embolization device (ped) deployment, progressive endothelialization occurs in two forms rapidly, at the parent artery and slowly at the aneurysmal neck. 7 at the histopathological level, the presence of inflammatory cells and thrombi have been determined, all of which contribute to the effectiveness of the devices. 8 the infection associated with sars-cov-2 leads to a hyperinflammatory response.9 the presence of a dysregulated macrophage response that injures the host. the role of this inflammatory response and its effect must be established on the endothelialization and healing process of intracranial aneurysms after treating with endovascular devices. 9 the clinical implication at this time is unknown with pandemic in full force. with time, patients who are getting devices placed for aneurysm treatment might not heal these aneurysms fully. more research is necessary to establish the effect of coronavirus on the healing and endothelialization of intracranial aneurysms. references 1. iosif c. neurovascular devices for the treatment of intracranial aneurysms: emerging and future technologies. expert review of medical devices. 2020;17(3): 173-188. https://doi.org/10.1080/17434440. 2020.1733409. 2. crobeddu e, lanzino g, kallmes df, cloft hj. review of 2 decades of aneurysm-recurrence literature, part 1: reducing recurrence after endovascular coiling. ajnr american journal of neuroradiology. 2013;34(2): 266-270. https://doi.org/10.3174/ajnr.a3032. 3. brinjikji w, kallmes df, kadirvel r. mechanisms of healing in coiled intracranial aneurysms: a review of the literature. ajnr american journal of neuroradiology. 2015;36(7): 1216-1222. https://doi.org/10.3174/ajnr.a 4175. 4. gu j, gong e, zhang b, et al. multiple organ infection and the pathogenesis of sars. j exp med. 2005;202(3): 415424. https://doi.org/10.1084/jem.20050828. 5. varga z, flammer aj, steiger p, et al. endothelial cell infection and endotheliitis in covid-19. lancet (london, england). 2020;395(10234): 1417-1418. https://doi.or g/10.1016/s0140-6736(20)30937-5. 6. ravindran k, salem mm, alturki ay, thomas aj, ogilvy cs, moore jm. endothelialization following flow diversion for intracranial aneurysms: a systematic review. ajnr american journal of neuroradiology. 2019;40(2): 295-301. https://doi.org/10.3174/ajnr.a5955. 7. ravindran k, distasio m, laham r, et al. histopathological demonstration of subacute endothelialization following aneurysm retreatment with the pipeline embolization device. world neurosurgery. 2018;118: 156-160. https://doi.org/10.1016/j.wneu.2018.07.090. 8. kallmes df, helm ga, hudson sb, et al. histologic evaluation of platinum coil embolization in an aneurysm model in rabbits. radiology. 1999;213(1): 217-222. https://doi.org/10.1148/radiology.213.1.r99oc16217. 9. merad m, martin jc. pathological inflammation in patients with covid-19: a key role for monocytes and macrophages. nature reviews immunology. 2020. https://doi.org/10.1038/s41577-020-0331-4. mandour_cystic trigeminal romanian neurosurgery (2016) xxx 2: 303-305 | 303 cystic trigeminal schwannoma. case presentation cherkaoui mandour, miloudi gazzaz, brahim el mostarchid department of neurosurgery – military hospital mohammed v – rabat – morocco abstract: trigeminal schwannoma is the second commonest intracranial schwannoma; they remain rare. a minority exhibit cystic changes, with even fewer an intracystic fluid level. we report a case of a 45-year-old man, presented with a progressive hearing loss, worsening right-sided facial spasms and facial numbness in the region of the right trigeminal nerve. neurological examination revealed hypoesthesia in the right facial region and intermittent rights sided hemi-facial spasms, without signs of raised intracranial pressure or achieve the mixed nerves or neurological deficit. a magnetic resonance imaging of the brain revealed a cystic mass in the right cerebello-pontine angle with extension forward towards the cavum meckel. the patient was operated by retro sigmoid approach, with a total resection of the tumor. intracranial cystic schwannomas constitute an uncommon subset of tumors with a distinct clinico-biological behavior. the presence of fluid–fluid levels within the tumors, although rare, confirms the cystic nature of the neoplasms. cystic areas are usually secondary to the coalescence of mucinous or microcystic regions in antoni b tissues. the treatment is surgical in the majority of cases and stereotactic radiosurgery has a clear role for adjuvant treatment of post-surgical recurrence of the tumor or residue. key words: cystic, trigeminal, schwannoma introduction schwannomas are uncommon nerve sheath tumors that may originate from any peripheral, cranial or autonomic nerve of the body with the exception of the olfactory and optic nerve. trigeminal schwannoma is the second commonest intracranial schwannoma; they remain rare. a minority exhibit cystic changes, with even fewer an intracystic fluid level (4). we report a case of this atypical histological presentation. case report a 45-year-old man, presented with a 2 year history of symptoms, of progressive hearing loss, worsening right-sided facial spasms and facial numbness in the region of the right trigeminal nerve. neurological examination revealed hypoesthesia in the right facial region 304 | mandour et al cystic trigeminal schwannoma and intermittent right sided hemi-facial spasms. there were no signs of raised intracranial pressure and it did not achieve the mixed nerves or neurological deficit. a magnetic resonance imaging of the brain revealed a cystic mass in the right cerebello-pontine angle with extension forward towards the cavum meckel (figure: panel a and b). the patient was operated on lateral position by retro sigmoid approach. the removal of the capsule was easy, after draining the cystic part. he was not of adhesions with vascular and nerve structures of the cerebello-pontine angle. seen extending into the middle cranial fossa, the exeresis was subtotal. post-operative course was favorable with no neurological sequelae and it was indicated radiosurgery for the remaining part. the final histopathology confirmed the diagnosis of a cystic schwannoma. figure: panel a: axial b: coronal: brain magnetic resonance imaging scan showing a cystic mass of the right cerebellar pontine angle discussion schwannomas usually arise from schwann cells and grow along cranial, peripheral, and autosomic nerves (9). they predominantly stem from sensory nerves rather than motor nerves (2). trigeminal schwannomas although rare, are the second commonest intracranial schwanomma (6), intracranial cystic schwannomas constitute an uncommon subset of tumors with a distinct clinico-biological behavior (4). the presence of fluid–fluid levels within the tumors, although rare, confirms the cystic nature of the neoplasms (5). cystic cranial nerve schwannomas are exceptionally uncommon (7). cystic areas are usually secondary to the coalescence of mucinous or microcystic regions in antoni b romanian neurosurgery (2016) xxx 2: 303-305 | 305 tissues of the schwannoma. speculative mechanisms include an insufficient vascular supply resulting in necrosis and cystic changes, hemorrhage into the tumor with blood resorption causing cyst formation, and hyaline degeneration leading to cyst formation (8, 10). the treatment is surgical to avoid progressive neurological deficits and the need to have a histological diagnosis.stereotactic radiosurgery (srs) has a clear role for adjuvant treatment of post-surgical recurrence of the tumor or residue (3). in addition, some advocate srs as a primary treatment modality for tumors less than 15 cm (1, 3). conclusion schwannoma of the trigeminal nerve is a benign tumor but dangerous by its topography and its relationship to vascular and nerve elements. we need to include cystic schwannoma in the list of differential diagnosis of cystic masses of the cerebellopontine angle. correspondence cherkaoui mandour e-mail: mandour1978@hotmail.com telephone: 212 06 45 76 34 23 miloudi gazzaz e-mail: gazzaznch@hotmail.com telephone: 212 06 40 46 34 20 brahim el mostarchid e-mail: elmostarchidnch@hotmail.com telephone: 212 06 48 34 89 45 references 1.vikas acharya, adam williams, william adams, david hilton, peter c whitfi eld. middle cranial fossa cystic schwannoma. bmj case reports 2012;10.1136. 2.g. s. carroll, b. g. haik, j. c. fleming, r. a. weiss, and m. f. mafee, “peripheral nerve tumors of the orbit. radiologic clinics of north america. 1999;37, 1,195– 202,. 3.yasuhiko hayashi, takuyawatanabe, daisuke kita, yutaka hayashi, masayuki takahira, and jun-ichiro hamada. orbital cystic schwannoma originating from the frontal nerve. case reports in ophthalmological medicine.2012, article id 604574, 4 pages. 4.colreavy mp, l acy pd, hughes j, e t al. head and neck schwannomas–a 10 year review. j laryngol otol. 2000; 114 : 119 – 24 . 5.h. kato, et al. fluid-fluid level formation: a rare finding of extracranial head and neck schwannomas. ajnr am j neuroradiol 2009 0: ajnr.a1511. 6.hasegawa t, k ida y, yoshimoto m, e t al. t rigeminal schwannomas: results of gamma knife surgery in 37 cases. j neurosurg 2007; 106 : 18 – 23 . 7.k. g¨und¨uz, r. a. kurt, and e. erden, “orbital schwannoma with fluid-fluid levels on mri, ophthalmic plastic & reconstructive surgery, 2011; 27, 3, pp. 51–54. 8.n. pushker, r. meel, s. sharma, m. s. bajaj, s. kashyap, and s. sen, “giant orbital schwannoma with fluid-fluid levels, british journal of ophthalmology, 2011; 95, 8, pp. 1180–1181. 9.fundová p, c harabi s, tos m, e t al. c ystic vestibular schwannoma: surgical outcome. j laryngol otol 2000 ; 114 : 935 – 9. 10.macnally sp, r utherford sa, ramsden rt, e t al. trigeminal schwannomas. br j neurosurg 2008 ; 22 : 729 – 38. 12gobrantaha_factors romanian neurosurgery (2015) xxix (xxii) 1: 103 110 103 factors associated with outcomes in ruptured aneurysmal patients: clinical study of 80 patients gobran taha ahmed alfotih, fang-cheng li, xin-ke xu, shang-yi zhang sun yat sen memorial hospital, neurosurgery department, sun yat sen medical university, guang zhou, guang dong province, people’s republic of china abstract: background: due to insufficient data in the literature, the optimal timing for surgical intervention for ruptured intracranial aneurysms is still controversial. some practitioners advocate early surgery, but others not. it is important to identify other factors that can be used to predict poor prognosis in ruptured intracranial aneurysm patients. objective: to determine the influence of timing of clipping surgery, and other factors on the outcomes of ruptured intracranial aneurysms in hunt & hess i~iii grade patients. method: we have performed a retrospective study involving 80 patients who were surgically treated for ruptured intracranial aneurysm between 2007 and 2012. the patient population consisted of 50(62.5%) females and 30(37.5%) males, with an age range of 12 to 75 years old, mean age 52.33 ± 10.63 years. we measured association between the glasgow outcome scores and sex, timing of clipping surgery, aneurysm location and pre-operative patient's neurological condition using famous hunt and hess grade system. results: we did not find any correlation between the outcomes of ruptured intracranial aneurysm patients and timing (early, intermediate, late stage) of clipping, sex, aneurysm location. whereas there is a significant correlation between patients outcomes and pre-operative patient neurological condition (hunt & hess grade). conclusion: timing of surgery (early, intermediate, late) does not affect outcomes in low hunt and hess grade patients i~iii. whereas neurological condition (hunt & hess) has strong impact on postoperative outcomes. others factors like sex, age, aneurysm location have no effect on outcomes in ruptured intracranial aneurysms. key words: subarachnoid hemorrhage, aneurysm, timing, hunt & hess, outcomes. introduction management of ruptured intracranial aneurysms is indispensable to prevent the risk of re-bleeding especially the first four weeks after the aneurysmal rupture, with a cumulative risk of 30% without intervention. 104 gobran taha et al factors associated with outcomes in ruptured aneurysmal patients the treatment options for securing the aneurysm is either to coil the aneurysm by packing it with platinum coils or by direct open surgery and application of a surgical clip. the optimal treatment for an aneurysm depends on the condition of the patient, the anatomy of the aneurysm, the ability of the surgeon, and must be weighed against the natural history of the condition. many factors had been studied to investigate the relation between the outcome in patients who performed clipping ruptured aneurysm with time of surgery, sex, hunt and hess grade and location of aneurysm. the timing of definitive management of acutely ruptured intracranial aneurysms (endovascular coiling or craniotomy and clipping) has been the subject of considerable debate[1][2].some authors advocated conservative treatment for all ruptured intracranial aneurysm patients till their condition is stable and perform late surgery, but some reports no significant different between early or late surgery in the outcomes[3]. in literature the concept of early stage surgery is defined between 1~3 days post subarachnoid hemorrhage (sah), late surgery, defined as ˃10 days post sah. some few studies raise what called “ultra-early” aneurysm treatment, within 24 hours of sah[4][5][6]. cerebral vasospasm, also known as delayed ischemic neurologic deficit (dind), a delayed ischemic neurologic deficit following sah. clinically characterized by confusion or decreased level of consciousness sometimes with focal neurologic deficit like speech or motor. typical at risk period is quoted as days 3-14 post-sah. always resolved by day 12 post-sah. because cerebral vasospasm never occur before day 3[7], many studies advocate early surgery treatment especially in good medical and neurological condition patients, hunt and hess ≤3. early surgery facilitates treatment of vasospasm which peaks in incidence between days 6-8 post sah by allowing induction of arterial hypertension and volume expansion without danger of aneurysmal rupture, and in the same time allows lavage to remove potentially vasospasmogenic agents from contact with vessels. to evaluate the most factors effecting the outcome of post-surgical clipping of intracranial aneurysm patients, we study some factors like: sex, hunt-hess grade, timing of surgery and location of aneurysm and their influence on glasgow outcome scores of hospitalization patients. it is important to identify factors that can be used to predict poor prognosis in ruptured intracranial aneurysm patients. method we have performed a retrospective study involving 80 patients who were surgically treated for ruptured intracranial aneurysm between 2007 and 2012. the patient population consisted of 50(62.5%) females and 30(37.5%) males, with an age range of 12 to 75 years old, mean age 52.33 ± 10.63 years. we measured associations between the glasgow outcome scores and sex, timing of clipping surgery, aneurysm location and pre-operative patient's neurological condition using famous hunt and hess grade system. for patients romanian neurosurgery (2015) xxix (xxii) 1: 103 110 105 selection, symptoms, aneurysm location, preoperative patient's neurological condition (hunt & hess) see table i. patients’ inclusion criteria: 1 patients with subarachnoid hemorrhage due to ruptured of intracranial aneurysm (ria), approved by computerized tomographic angiography (cta), magnetic resonance angiogram (mra) and digital subtraction angiography (dsa). 2 patients treated only by surgical clip placement. 3 the glasgow outcome scale is defined in our study as the outcome on the day of discharge from hospital [8]. 4 timing of surgery is defined in our study as: early stage surgery: 1~3 days, intermediate stage surgery: 4~10 days and late stage surgery: more than 11 days. 5 hunt and hess grade system is used to describe pre-operative neurological condition of ruptured aneurysm patients [9]. excluding criteria: 1 subarchnoid hemorrhage due to another cause like:trauma, arteriovenous malformation(avm), pretruncal nonaneurysmal sah and vasculitis or vasculopathy. 2 anuerysms combined with arteriovenous malformation (avm). 3 patients treated endovascularly. 4 incidentally discovered unruptured intracranial aneurysms. 5 patients with multiple systemic disease especially with coagulation disorders like: thrombocytopenia or liver dysfunction. 6 patients with uncompleted information. 7 rebleeding patients 7 hunt & hess iv and v except for large hematoma needs emergency evacuation. in this research to determine the relative risk affect the prognosis and outcome of postsurgical clip placement patients with four independent variables: sex, hunt & hess, aneurysm location and timing of surgery, spss 16.0: kruskal-wallis, chi-square tests were performed; significant difference when p＜0.05. table i sex cases (%) onset symptoms cases (%) hunt & hess cases (%) aneurysm location cases (%) female 50(62.5) male 30(37.5) headache 53(66.25) syncope 22(27.5) coma 2(2.5) seizure 1(1.25) aphasia & hemiparesis 2(2.5) i~iii 64(80) iv 11(13.75) v 5(6.25) lmca 20(25) rmca 11(13.8) lica 3(3.8) lpcoma 9(11.3) rpcoma 7(8.8) acoma 21(26.3) raca 2(2.5) lacha 2(2.5) racha 1(1.3) lopha 2(1.3) bta 2(2.5) raca+rica 1(1.3) 106 gobran taha et al factors associated with outcomes in ruptured aneurysmal patients abbreviation: acha: anterior choroid artery, aca: anterior cerebral artery, acoma: anterior communicating artery, bta: basilar tip artery, mca: middle cerebral artery, ica: intracranial carotid artery, opha: ophthalmic artery, pcoma: posterior communicating artery. results we did not find any correlation between the outcomes of ruptured intracranial aneurysm patients and timing (early, intermediate, late stage) of clipping, sex, aneurysm location. whereas there is a significant correlation between patients outcomes and pre-operative patient neurological condition (hunt & hess grade), table ii. outcomes in patients according to timing of surgery, table iii. table ii correlation between gos and sex, hunt & hess, aneurysm location and timing variable cases x2 p glasgow outcome scale (gos) sex: male female 30 50 2.37 0.122 hunt & hess: i~iii iv v 64 11 5 15.052 0.01 aneurysm location: lmca rmca lica lpcoma rpcoma acoma raca lacha racha lopha bta raca+rica 20 11 3 9 7 21 2 2 1 1 2 1 19.628 0.051 timing: 1~3d 4~10d ˃11d 54(67.5) 21(26.2) 5(6.2) 4.522 0.807 romanian neurosurgery (2015) xxix (xxii) 1: 103 110 107 table iii outcomes in patients according to timing of surgery outcomes timing total cases (%) 1~3d cases (%) 4~10d cases (%) ˃11d cases (%) death 3(60.0) 1(20.0) 1(20.0) 5(6.2) persistent vegetative state 3(100.0) 0(0.0) 0(0.0) 3(3.8) severe disability 7(58.3) 4(33.3) 1(8.3) 12(15.0) moderate disability 18(75.0) 5(20.8) 1(4.2) 24(30.0) good recovery 23(63.9) 11(30.6) 2(5.6) 36(45.0) total 54(67.5) 21(26.2) 5(6.2) 80(100.0) discussion many factors had been studied to investigate the relation between the outcome in patients who performed clipping ruptured aneurysm with time of surgery, sex, hunt and hess grade and location of aneurysm. the most controversial factor is timing of surgery. the timing of definitive management of acutely ruptured intracranial aneurysms (endovascular coiling or craniotomy and clipping) has been the subject of considerable debate [1][2]. in literature the concept of early stage surgery is defined between 1~3 days post subarachnoid hemorrhage (sah), late surgery, defined as ˃10 days postsah. some few studies raise what called “ultra-early” aneurysm treatment, within 24 hours of sah[2][3[10][11]. by the late 1980s, several reports suggested that early surgery was safe with good outcomes[12][13][14], especially in patients with good neurologic condition (hunt and hess (h&h) grade ≤3. early surgery eliminates the risk of re-bleeding which occurs most frequently in the period immediately following sah, and allows lavage to remove potentially vasospasmogenic agents from contact with vessels. however, early treatment (particularly of poor-grade patients) may increase the periprocedural complications beyond the rates reported in the international cooperative trial[3][15][16], and the acutely swollen, soft, hyperemic, poorly autoregulating brain was considered more prone to laceration, contusion, and infarction secondary to retraction [14][17]. the risk of intra-operative rupture is higher with early surgery, and possible increase incidence of vasospasm following early surgery from mechanotrauma to vessels, thus delayed ischemic neurological deficits can be started promptly[18][19][20]. period in 4 to 10 days after occurrence of sah also has been reported as a risky time for surgery[3].in one study by dorhout mees et al. they found clipped patients had no higher risk of delay cerebral ischemia when treated between 5 to 10 days if they compared to patients who treated with coils[21]. in one prospective study found the timing of surgery is no longer an important factor influencing surgical outcome in treating 108 gobran taha et al factors associated with outcomes in ruptured aneurysmal patients supratentorial circulation aneurysms[22]. cerebral ischaemia due to non-surgical causes (such as “vasospasm”) no longer seems to be the important issue governing the timing of surgery[23][24] some authors advocated conservative treatment for all ruptured intracranial aneurysm patients till their condition is stable and perform late surgery, but some reports no significant different between early or late surgery in the outcomes[3]. in our study we did not find any correlation between timing of surgery (early:1~3d,intermediate:4~10d, late:˃11d) and postoperative outcomes in the patients with good neurological conditions (hunt & hess ≤3) p˃0.05. in 2002, de gans et al. performed a systematic review, 1 randomized clinical trial and 10 observational studies, met the inclusion criteria. meta-analysis suggests that outcomes were better after early or intermediate surgery than after late surgery for patients in good clinical condition at admission[25] we think the hunt & hess grade on admission correlates with the risk of cvs. in our institute our strategy to eliminate the risk of peri/postoperative vasospasm and rebleeding of the aneurysm: pre/post-operative strategy :smooth muscle relaxants, calcium channel blockers(ccbs),which have neuroprotection more than preventing vasospasm, the most used agent is nimodipine (nimotop) 60 mg/iv/24h.the most seen side effect is systemic hypotension: which may be mitigated by iv volume expansion. triple-h therapy which includes: hypervolemia, hypertension and hemodilution[26]. for hypervolemia the target is euvolemia or very slight hypervolemia the most used agents: colloid: albumin, low molecular weight dextran, keep systolic blood pressure (sbp) between 160~180mmhg in all cases pre and postoperative. during operation, in case swelling of the brain, to avoid excessive brain retraction, surgical exposure requires sufficient bony removal, we use hyperventilation, csf drainage(ventriculostomy, lumbar spinal drainage and intra-operative drainage) and diuretics mannitol with decadron, furosemide and continuous irrigation of the operation field with normal saline (ns), nimotop can have some effect on vasospasmic vessels,we do not use papaverine because its side effects like hypotension ,bradycardia and even death[27][28]. the hunt and hess grade and world federation of neurological surgeons (wfns) scale are commonly used to predict mortality after aneurysmal subarachnoid hemorrhage, these scales are also used for prognostication purposes. hunt & hess in their experience the survival for patients admitted at grade 1, 2, or 3 was 70%, for grade 4 or 5 have historically fared poorly and many often were excluded from aggressive treatment. le roux et al demonstrated that 86% of patients with hunt and hess grades 1–3 return to independent function. this rate was 96% for the grade 1 patients[29].many studies indicates that very poor prognosis for high hunt & hess grade, in our study we find when patient with high hunt&hess grade the glasgow outcome scale (gos) will be low. no matter the timing of the clipping surgery, the most important factor is romanian neurosurgery (2015) xxix (xxii) 1: 103 110 109 the neurological condition of the patient. for i~iii grade the we advocate surgery no matter with time, but early surgery can eliminate the risk of re-bleeding, in a study of 33 patients who re-bled, the highest risk of re-bleeding occurred in the first 6 hours following sah[30]. for iv~v grade are excluded from our surgical clipping ,and are treated either conservatively or endovascular using guglielmi detachable coil (gdc) embolization .in the patients who are treated conservatively many techniques are use to improve outcome like: control elevated intracranial pressure (icp), prophylaxis of delay ischemic neurological deficit (dind), triple -h therapy. exceptions were made for patients with multiple, repeated bleeding episodes and those with significant mass effect from a hematoma. the gdc system was first made available for approved use in 1995. this device has since gained widespread acceptance as an alternative treatment technique for intracranial aneurysms. weir ru et al found[31]patients who are acutely ill with high hunt and hess grades after sah can undergo successful coil embolization despite their poor medical condition and a high frequency of vasospasm. many of these patients have a good clinical outcome. conclusion timing of surgery (early, intermediate, late) does not affect outcomes in low hunt and hess grade patients i~iii. the most advantage of early surgery is preventing re-bleeding, which is has high morbidity and mortality[32]. the most important factor that influencing on glasgow outcome scale is the neurological condition (hunt & hess) of ruptured intracranial aneurysms patients. urgent preoperative resuscitation, early surgery, and aggressive treatment of vasospasm to improved the outcome in patients with good grades[29]and conservative treatment or gdc system coiling for high grade hunt & hess grade iv~v[31]. correspondence gobran taha ahmed alfotih, sun yat sen memorial hospital, neurosurgery department, sun yat sen medical university, p.o. box 510120, guangzhou, guangdong province, people’s republic of china, tel: 008613066381670, email: gta_alfotih@yahoo.com references 1. adams hp, kassell nf, torner jc, et al. early management of aneurysmal subarachnoid haemorrhage. a report of the cooperative aneurysm study. j neurosurg 1981;54: 141–145. 2. chyatte d, fode nc, sundt tm jr .early versus late intracranial aneurysm surgery in subarachnoid haemorrhage. j neurosurg 1988; 69: 326–331. 3. kassell n, torner j, jane j, haley e, adams h. the international cooperative study on the timing of aneurysm surgery. ii, surgical results. j neurosurg. 1990;73:37–47. 4. stein s. brief history of surgical timing: surgery for ruptured intracranial aneurysms. neurosurg focus 2001;11:1–5. 5. laidlaw j, siu k.ultra-early surgery for aneurysmal subarachnoid hemorrhage: outcomes for a consecutive series of 391 patients not selected by grade or age.j neurosurg. 2002;97:250–258. 6. pan j, zhan r, wen l, tong y, wan s, zhou y. ultraearly surgery for poor-grade intracranial aneurysmal subarachnoid hemorrhage: a preliminary study. yonsei med j. 2009;50:521–524. 7. weir b, grace m,hansen j, et al. time course of vasospasm in man.j nenrosurg 1978; 48: 173-8. 110 gobran taha et al factors associated with outcomes in ruptured aneurysmal patients 8. jennett b, bond m. assessment of outcome after severe brain damage. lancet 1975;1(7905):480-4. 9. hunt we, hess rm. surgical risk as related to time of intervention in the repair of intracranial aneurysms. journal of neurosurgery 1968;28(1):14-20. 10. cha k, kim j, kang h,et al. aneurysmal rebleeding:factors associated with clinical outcome in the rebleeding patients.j korean neurosurg soc 2010;47:11923 11. hillman j, von essen c, leszniewski w,et al. significance of‘ultra-early’ rebleeding in subarachnoid hemorrhage. j neurosurg 1988;68:901–907. 12. suzuki j, onuma t, yoshimoto t. results of early operations on cerebral aneurysms. surg neurol 1979;11(6):407-412. 13. solomon ra, onesti st, klebanoff l. relationship between the timing of aneurysm surgery and the development of delayed cerebral ischemia. j neurosurg1991;75(1):56-61. 14. ohman j, heiskanen o. timing of operation for ruptured supratentorial aneurysms: a prospective randomized study. j neurosurg 1989;70(1):55-60. 15. haley ec jr, kassell nf, torner jc. the international cooperative study on the timing of aneurysm surgery. the north american experience. stroke 1992;23 (2):205214. 16. kassell nf, torner jc, haley ec jr, jane ja, adams hp, kongable gl. the international cooperative study on the timing of aneurysm surgery. part 1:overall management results. j neurosurg. 1990;73(1):18-36. 17. kassell n, torner j. the international cooperative study on timing of aneurysm surgery—an update. stroke 1984;15:566-70. 18. eddleman cs, hurley mc, naidech am, batjer hh, bendok br. endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm. neurosurg focus. 2009;26(3):e6. 19. bederson jb, connolly esjr, batjer hh, dacey rj,dion je,diringer mn,et al. guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the stroke council, american heart association. stroke 2009;40:994–1025. 20. weyer gw, nolan cp, macdonald rl. evidencebased cerebral vasospasm management. neurosurg focus 2006;21(3):e8. 21. dorhout mees sm, molyneux, aj, kerr rs, algera a, rinkel gj.timing of aneurysm treatment after subarachnoid hemorrhage: relationship with delayed cerebral ischemia and poor outcome. stroke 2012;43(8): 2126-2129. 22. ross n, hutchinson p, seeley h, kirkpatrick p. timing of surgery for supratentorial aneurysmal subarachnoid haemorrhage: report of a prospective study. j neurol neurosurg psychiatry 2002 ;72:480-484. 23. sano k, saito i. timing and indication of surgery for ruptured intracranial aneurysms with regard to cerebral vasospasm. acta neurochir (wien) 1978;41:49–60. 24. macdonald rl, wallace mc, coyne tj. the effect of surgery on the severity of vasospasm. j neurosurg 1994;80:433–9. 25. de gans k, nieuwkamp dj, rinkel gj, algra a.timing of aneurysm surgery in subarachnoid hemorrhage:a systematic review of the literature. neurosurgery 2002;5 :336-340. 26. origitano tc, wascher tm, reichman oh, anderson de.sustained increased cerebral blood flow with prophylactic hypertensive hypervolemic hemodilution ("triple-h" therapy) after subarachnoid hemorrhage. neursurgery 1990;27: 729-40. 27. conti a, angileri ff, longo m, pitrone a, granata f, la rosa ge. intra-arterial nimodipine to treat symptomatic cerebral vasospasm following traumatic subarachnoid haemorrhage. technical case report. acta neurochir ( wien ) 2008;150:1197 -1202. 28. baltaci b,basar h,ozcan a, gulhan y, aytunur cs. cardiac arrest after intracisternal papaverine instillation during intracranial aneurysm surgery. case report. j neurosurg 2 0 1 0;113:760-762. 29. le roux pd, elliott jp, downey l, newell dw, grady ms, mayberg mr. et al. improved outcome after rupture of anterior circulation aneurysms: a retrospective 10 year review of 224 good grade patients. j neurosurg 1995;83:394–402. 30. lnagawa t, kamiya k, ogasawara h. yano t. rebleeding of ruptured intracranial aneurysms in the actue stage. sarg neurol 1987;28: 93-9. 31. weir ru, marcellus ml, do hm, steinberg gk, marks mp. aneurysmal subarachnoid hemorrhage in patients with hunt and hess grade 4 or 5:treatment using the guglielmi detachable coil system. ajnr am j neuroradiol 2003;24:585-90. 32. hijdra a, vermeulen m, van gijn j, et al. rerupture of intracranial aneurysms: a clinicoanatomic study.j neurosurg.1987;67(1):29-33. doi: 10.33962/roneuro -2020-033 clinical spectrum of paediatric head injury. a prospective study from tribal region krishna govind lodha, tarun kumar gupta, gaurav jaiswal, yogendra singh romanian neurosurgery (2020) xxxiv (1): pp. 220-225 doi: 10.33962/roneuro-2020-033 www.journals.lapub.co.uk/index.php/roneurosurgery clinical spectrum of paediatric head injury. a prospective study from tribal region krishna govind lodha, tarun kumar gupta, gaurav jaiswal, yogendra singh rnt medical college udaipur, rajasthan, india abstract introduction: traumatic brain injury is considered as a major health problem which causes frequent deaths and disabilities in paediatric population with special concern to tribal regions of developing countries like india where etiology of traumatic brain injury in the paediatric population fall from height dominant over the road traffic accident as a major. aim and objective: the aim is to analyse the epidemiology, mechanism, clinical presentation, severity and outcome of paediatric head injury in the tribal region of northern india that could help to make preventive policies to improve their care. material methods: it is a prospective observational study of 345 children of up to 18 years of age admitted under department of neurosurgery from october 2017 to april 2019. results: the study population comprised of 345 paediatric patients. mean age was 9.25 years.36.81% patients were in 1-6-year age group and male to female ratio was 2.45. the most common cause for trauma was fall from height in 179(52%) cases followed by rta in 141(41%) cases. the most common radiological finding was depressed skull fractures in 97(50%) cases. there was 35% mortality in severe head injury patients. conclusion: this study through some light on the different scenario of head injury in tribal regions of developing country and will help to formulate effective strategies for prevention and better care of the patients. introduction traumatic brain injury (tbi) is a leading cause of death and disability in children worldwide. [1] young children are at relatively high risk of minimal and mild traumatic head injuries. an increase in the more severe and fatal traumatic brain injuries has been found in late adolescence. paediatric tbi has different pathophysiology due to higher vascularity, plasticity and less rigidity of scalp. paediatric brain has less degree of myelination which related to brain capacity to absorption of traumatic forces and increase the susceptibility to tbi.[2] tbi is classified as mild (glasgow coma scale [gcs] 13–15), moderate (gcs 9–12), or severe (gcs 3–8).[3] the study focuses on understanding the etiology, clinical presentation, treatment options, and outcome of these patients with special concern to tribal regions of developing countries like india keywords tribal region, paediatric traumatic brain injury corresponding author: krishna govind lodha rnt medical college udaipur, rajasthan, india kg_ lodha@yahoo.co.in copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 221 clinical spectrum of paediatric head injury. a prospective study from tribal region where fall from height dominant over the road traffic accident as a major etiology of traumatic brain injury in paediatric population.[4] thus there is a critical need for effective fall and traffic accidents prevention strategies for children, and we should give attention to the predicting factors for more effective care of such patients material methods it is a prospective observational study of 345 children of upto 18 years of age admitted under department of neurosurgery from october 2017 to april 2019. study was started after obtaining the permission from ethical committee of the hospital. informed consent was obtained from the parent/guardian/relative of the patient. a detailed clinical history obtained from the parents/guardian/relative admitted in the hospital with head injury. analysis statistical analysis was performed using the collected data on incidence and clinical– radiologic correlation. analyses included the age and gender distribution of the children, the cause and location of the injury, medical status, and the part of the head injured and type of injury and the treatment provided. a comparison of types of head injuries sustained by gender, age, and cause was also carried out. results the study population comprised of 345 paediatric patients aged between 2 months to 18 years with a mean age of 9.25 years. there were 245 males (71.01%) and 100 females (28.98%) with male to female ratio of 2.45:1. age no % male female good outcome poor outcome <1yr 24 6.95 14 10 18(75%) 6(25%) 1-6yrs 127 36.81 95 32 108(85.03%) 19(14.07%) 7-12yrs 120 34.78 84 36 110 (91.7%) 10 (8.3%) 13-18yrs 74 21.44 52 22 62(83.8%) 12(16.2%) total 345 100% 245(71.1%) 100(28.9%) 298 47 table 1. outcome according to age. the most common cause for trauma was fall from height in 179(52%) cases followed by rta in 141(41%) cases, bull horns in 11 (3%) cases; assault 7 (2%) cases. mechanism no % mild moderate sever fall 179 52 93(52%) 73(41%) 13(7%) rta 141 41 38(27%) 72(51%) 31(22%) assault 7 2 5(72%) 1(14%) 1(14%) sport 7 2 7(100%) bull horn 11 3% 8(73%) 2(18%) 1(10%) table 2. mode of injury. rta: road traffic accident severity of injury was decided with gcs score at the time of admission and it was mild injury in 218 (63.19%), moderate in 92 (26.67%) and sever in 35 (10.14%) cases. outcome of injury was good in mild head injury group and poor outcome was associated with severe head injury group. gcs severity no good outcome poor outcome mortality 13-15 mild 218 210(96.33%) 8(3.67%) none 9-12 moderate 92 60(65.22%) 22(23.91%) 10(10.87%) 3-8 sever 35 9(25.71%) 15(42.86%) 11(31.43%) table 3. severity and outcome. 222 krishna govind lodha, tarun kumar gupta, gaurav jaiswal, yogendra singh ct scan findings were positive in 195 cases and it was normal in 150 cases. most common radiological finding was depressed skull fractures in 97(50%) cases, extradural hematoma in 29 (15%), subdural hematoma in 20 (10%), contusion in 23 (12%), ich in 6 (3%), ivh in 2 (1%) cases. (figure 1 and 2) figure 1. ncct head of 8 yrs old child admitted with h/o of fall from roof with gcs e2v3m5 pupils b/l 3mm reacting to light. figure 2. ncct head of 6 yrs male child admitted with h/o fall from tree and gcs at admission e4v3m3, pupils b/l 3 mm reacting, after evacuation of edh child improved and at time of discharge gcs was e4v5m6. ct finding no % surgery conservative skull fractures 97 50% 40 57 edh 29 15% 10 19 sdh 20 10% 8 12 contusions 23 12% 11 12 ich 6 3% 2 4 ivh 2 1% 0 2 edema 18 9% 0 18 total 195 100% 71 124 table 4. radiology positive in 195 cases and negative in 150 cases. edh: extradural hematoma, sdh: subdural hematoma, ich: intracerebral hematoma, ivh: intra ventricular hematoma 223 clinical spectrum of paediatric head injury. a prospective study from tribal region out of 195 patients 71 patients’ required surgery and rest 124 patients were managed conservatively. fracture debridement or elevation done in 40 patients, hematoma (edh+ich) evacuation was done in 12 patients, contusectomy done in 11 patients and decompressive craniectomy done in 8 patients. (figure-3 and 4) figure 3a. ncct head of 15yrs male admitted with h/o rta with gcs e2v1m4 pupils b/l 3mm reacting to light undergone bifrontal craniectomy with evacuation of ehd. he discharged with gcs e4v5m6 and under gone 3d mold customized cranioplasty after 4 months. figure 3b. intraoperative photograph of 3d customised cranioplasty flap of above-mentioned patient. intervention total good outcome poor outcome hematoma evacuation 10(edh) +2(ich) 10(83.33%) 2(16.67%) contusectomy 11 5(45.4%) 6(54.5%) 224 krishna govind lodha, tarun kumar gupta, gaurav jaiswal, yogendra singh decompressive craniectomy 8 3(37.5%) 5(62.5%) fracture debridement or elevation 40 35(87.5%) 5(12.5%) total 71 53(74.65%) 18(25.35%) table 5. intervention and outcome. edh: extradural hematoma, ich: intracerebral hematoma while doing the survey for associated injuries, out of 345 patients 105 patients have associated injuries and most common associated injury was facial injury in 42 patients followed by long bone fracture in 24 patients, chest injury in 10 patients, multiple injury in 16 patients, spinal injury in 8 patients and abdominal injury in 5 patients. associated injury good outcome poor outcome total nil 226(94.17%) 14(5.83%) 240 facial injury 38(90.48%) 4(9.52%) 42 limb fracture 22(91.67%) 2(8.33%) 24 spinal injury 5(62.5%) 3(37.5%) 8 chest injury 8(80%) 2(20%) 10 abdominal injury 4(80%) 1(20%) 5 multiple injuries 14(87.5%) 2(12.5%) 16 total 345 table 6. associated injury and its outcome. discussion in india children below 18 years of age constitute about 40% of the total population [5]. traumatic brain injury is listed as one of the most comman cause of death in pediatric population. our study on pediatric head injuries show male preponderance which also conformed in various studies [6]. in our study fall from height 179(52%) was the most comman cause of pediatric head injury [7]. this peculiarly occure due to fall from tree, unguarded rooftop while playing. this was followed by rta 141 (41%), bull horn 11(3%), assault 7(2%) and sport related injury 7 (2%) [8]. initial gcs score was the single most important factor affecting the out-come as described by beca et [9]. the patient who had a gcs of 13-15 (218) had a poor out come in 8 (3.67%), followed by gcs of 9-12 (92) who had a poor outcome in 22(23.91%) followed be gcs of 8 or less then 8 (35) who had poor outcome in 15(42.86%) which is similar as reported by astrand r et.al [10]. out of 345 patients in our study, ct scan findings were positive in 195 cases and it was normal study in 150 cases. we found isolated skull bone fracture as most comman ct findings in 97 (50%) cases, it was associated with good outcome (87.5%) similar results were described by suresh et al [11]. hematoma evacuation (edh, ich) was associated with good outcome in 83.3% and poor outcome in 16.67%, contusion was associated in good outcome in 45.4% and poor outcome in 54.6% cases and decompressive craniectomy was associated with poor outcome in 62.5% cases. tomberg et al also found the similar outcome in their study [12]. in our study, we found that 69.6% patient have isolated head injury with good outcome in 94.17% patient. facial injury was seen in 12.17%, limb fracture in 7%, spinal injury in 2.3%, chest injury in 3%, abdominal injury in 1.5% and multiple injuries seen in 4.6% patients. paret et al reported chest trauma in (62%), limb fracture in (32%), facial injury in (20%), and multiple injuries in (48%) cases. this difference is because we include all the childers in our study irrespective to severity of the injury while author include only sever cases of head injury in peadtric patient [13]. the overall outcome in our study was death in 21(6.09%), vegetative state in 10(2.90%), severe disability in 12(3.48%) and good outcome in 279(80.86%) of the cases which was similar to study conducted by abrar ahad wani et al [14]. 225 clinical spectrum of paediatric head injury. a prospective study from tribal region gos n (%) death (1) 21(6.09%) vegetative (2) 10 (2.9%) sever disability (3) 23 (6.67%) moderate disability (4) 12 (3.48%) normal (5) 279 (80.86%) table 7. glasgow outcome scale. gos: glasgow outcome scale conclusion our study highlights the different scenario of pediatric head injury in tribal regions of developing country, where even the minor head injuries are referred to tertiary care hospitals which can be easily managed by treating physicians. the findings of our study have implications for development of public health policy with especial reference to tribal regions of developing country. where more than half of pediatric head injury which are minor in nature can be prevented by just increasing public awareness. conflicts of interest financial support and sponsorship: nil conflicts of interest: there are no conflicts of interest. references 1. jagannathan j, okonkwo do, yeoh hk, dumont as, saulle d, haizlip j, et al.long term outcomes and prognostic factors in pediatric patients with severe traumatic brain injury and elevated intracranial pressure. j neurosurg paediatr. 2008; 2:237–9. [pub med: 18831656]. 2. goldsmith w, plunkett j: a biomechanical analysis of the causes of traumatic brain injury in infants and children. am j forensic med pathol 25: 89–100, 2004. 3. jennet b. epidemiology of head injury. arch dis child 1998; 78:403‑6. 4. adirim ta, wright jl, lee e, lomax ta, chamberlain jm. injury surveillance in a pediatric emergency department. am j emerg med. 1999; 17:499–503. [pub med: 10530522]. 5. international institute for population studies. mumbai, india: nf, india; 1998‑9. 6. mahapatra ak. head injury in children. in: mahapatra ak, kamal r, editors. a text book of head injury. delhi: modern publication; 2004.p. 156‑70. 7. sambasivan m. epidemeology‑pediatric head injuries. neurol india 1995; 43:57‑8. 8. osmond mh, brennan‑barnes m, shephard al. a 4‑year review of severe pediatric trauma in eastern ontario: a descriptive analysis.j trauma 2002; 52:8‑12.beca j, cox pn, taylor mj, bohn d, butt w, logan wj, et al. 9. somatosensory evoked potentials for prediction of outcome in acute severe brain injury. j pediatr. 1995; 126:44–9. [pub med: 7815222]. 10. astrand r, undén j, hesselgard k, reinstrup p, and romner b. clinical factors associated with intracranial complications after pediatric traumatic head injury: an observational study of children submitted to a neurosurgical referral unit. pediatr neurosurg. 2010; 46:101–9. [pub med: 20664236]. 11. suresh hs, praharaj ss, indira devi b, shukla d, sastry kolluri vr. prognosis in children with head injury: an analysis of 340 patients. neurol india. 2003; 51:16–8. [pub med: 12865508]. 12. tomber g t, rink u, tikk a. computerized tomography and prognosis in pediatric head injury. acta neurochir (wien) 1996; 138:543-48. 13. paret g, ben abraham r, berman s, vardi a, harel r, manisterski y, et al. head injuries in children – clinical characteristics as prognostic factors. harefuah. 1999; 136:677–81. 755. [pubmed: 10955086]. 14. abrar ahad wani, arif hussain sarmast, muzaffar ahangar pediatric head injury: a study of 403 cases in a tertiary care hospital in a developing country. j pediatr neurosci. 2017 oct-dec; 12(4): 332-337.doi: 10.4103/jpn_80_17. 15amitagrawal_managementcraniofacial 338 agrawal et al management of craniofacial injuries management of craniofacial injuries: a primer for residents amit agrawal1, vijay mishra2, harsha jain3, umamaheshwar reddy v.4 1professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2senior lecturer, school of dental sciences, sharda university, greater noida (up) 3associate professor, school of dental sciences, sharda university, greater noida (up) 4assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract craniofacial injuries can occur in a significant proportion in traumatic brain injury patients and can be associated with many other concomitant life-threatening systemic injuries i.e. limbs fractures, chest injuries, spinal injuries and orbital injuries. an understanding of the presentations of craniofacial injuries, associated systemic injuries and patterns of traumatic brain injuries is crucial for improving care, survival and recovery of these patients. in present article we discuss the approach to craniofacial injuries which is based on time tested principles of surgery a good understanding of surgical anatomy, detailed history, accurate yet elaborative clinical evaluation, appropriate radiological investigations and decision to select management protocol for a given case. evaluation of these patients should include a coordinated and systematic examination to aim to evaluate of all areas and all the residents while examining these patients in emergency room should remember that facial swelling, altered sensorium, restless patient, presence of endotracheal and nasogastric tube can obscure the detail examination and distort the facial appearance. key words: craniofacial trauma, maxillofacial injuries, traumatic brain injury, head injuries. introduction craniofacial trauma is one of the most challenging injuries that are posed by prehospital care providers and personnel’s involved in emergency care. (1) these injuries can not only be life-threatening (as these can compromise airway or can cause significant hemorrhage) but also cause disfigurement. (2, 3) in present article we discuss the approach to craniofacial injuries which is based on time tested principles of surgery a good understanding of surgical anatomy, detailed romanian neurosurgery (2014) xxi 3: 338 344 339 history, accurate yet elaborative clinical evaluation, appropriate radiological investigations and decision to select management protocol for a given case. etiology craniofacial injuries can be life threatening (involvement of airway i.e. blood in oral cavity or in nose, injuries to neck vessels i.e. carotid and vertebral arteries or injuries to the brain and spine) requiring special attention or can be aesthetically significant. a number of etiologic factors (ranging from road traffic accidents to assaults), demographic properties and fracture patterns have been identified which varies widely (due to social, economic, cultural consequences) in different regions of the world. (4-8) leading cause of facial injuries include motor vehicle accidents, pedestrian collisions, stumbling, sports injuries, industrial accidents, assaults and warfare injuries. (9-13) however all the patients may not be attended by a singly facility i.e. may go to emergency room, may go to craniofacial faculties or may be seen by a neurosurgeon depending on the complexities of their injuries. (1, 14-16) clinical evaluation craniofacial skeleton can be divided into upper third (above superior orbital rim), middle third (midfacesuperior orbital rim down through maxillary teeth) and lower third – mandible. it is mainly composed of frontal bone, temporal bones, nasal bone, zygomas, maxilla and mandible. in addition ethmoid, lacrimal, sphenoid bones contribute to inner part of the orbits. (17) facial injuries can be categorized into soft tissue injuries, skeletal injuries and a combination of both. like any other discipline of medicine clinical evaluation start with details history taking. the details which need to be included are the mechanism of injury, any history of loss of consciousness, any history of previous medical or surgical disease. the detail history should include in what circumstances injury has occurred, ask details about the direction of the impact and speed of the vehicle. physical examination detail physical examination include careful but gentle palpation, assessment of mobility of bone fragments, and numbness or paresthesia, occlusal malfunction, assessment of integrity of the mandible, detail ocular examination including test for visual acuity (table 1). (1820) one need to remember that in juries to the facial skeleton are of special concern as these can be a marker for substantial transfer of energy to the intracranial contents. (21) associated injuries craniofacial injuries can be associated with many other concomitant life-threatening systemic injuries i.e. cranial trauma, limbs fractures, chest injuries, spinal injuries and orbital injuries. (22-30) evaluation of these patients should include a coordinated and systematic examination to aim to evaluate of all areas, local or general, in order not to miss any of the injuries. all the residents while examining these patients in emergency room should remember that facial swelling, altered sensorium, restless patient, presence of endotracheal and nasogastric tube can obscure the detail examination and distort the facial appearance. 340 agrawal et al management of craniofacial injuries table 1 key findings to suspect craniofacial injuries of physical examination type of injury examination findings general considerations • facial asymmetry or deformity • local tenderness • abnormal facial instability • step-offs • periorbital edema or crepitus • infraorbital numbness • epistaxis • csf rhinorrhea or otorrhoea • epiphora • exopthalmus or enopthalmus • nasal septum for position, integrity • any evidence of septal hematoma epistaxis mucosal disruption disruption of the membrane of maxillary sinus abnormal occlusion mandibular fracture preventing normal movements malar fracture infra orbital/upper lip numbness on the affected side the affected side of face may be flattened periorbital edema ecchymosis of the lower lid lateral sub-conjunctival hemorrhage zygomatic arch fractures a dimple palpable on the arch local tenderness restricted range of mouth opening ocular injuries suggest midface trauma check for ocular integrity telecanthus orbital muscle/nerve entrapment check extraoccular motility test visual acuity and visual fields check pupillary light reflex cranial nerves details neurological examination (including motor and sensory divisions) of all 12 cranial nerves traumatic brain injury (suspect intracranial hemorrhages, cerebral contusion or laceration, or skull fractures) history of vomiting loss of consciousness low glasgow coma scale investigations apart from the basic blood investigations (e.g. hb, pcv, esr, wbc estimations) the specific radiological investigations depend of the clinical indications and include plain radiographs, ct scan and on mri. romanian neurosurgery (2014) xxi 3: 338 344 341 plain radiographs plain radiographs have a limited role (less sensitivity to detect fractures of the skull base and facial skeleton) in the radiological evaluation of facial injuries and include skull radiographs (lateral as well as postanterior view), panorex radiographs (to evaluate the mandible), submentvertex view (to evaluate the zygomatic arch) cervical spine examination. while reading the radiographs a systematic approach (how the orbital outline, sinuses is are clear or is there any opacification or fluid levels suggestive of a fracture) will help to identify the facial fractures. computed tomography (ct scan) recently with the development of multislice ct and with significant technical advancement computed tomography (ct) has become the primary modality of imaging. ct scan detects craniofacial injuries in detail and can help to exclude intracranial hemorrhages and can assess, identify and classify associated bone injuries. (31, 32) ct scan can also help to differentiated fracture in anatomically difficult areas which cannot be seen on conventional radiographs (e.g., the orbits, the naso-orbitoethmoidal complex, the periand retroorbital skull base and the retromaxillary region). (24, 33) ct scan has the additional advantage that it can be extended to the cervical spine (if necessary whole spine, thorax and abdomen) in an unstable with polytrauma. ct scan also has the capacity to evaluate the facial skeleton in axial and coronal planes. (hassfeld et al. 1998; gellrich et al. 1999, 2003) computer assisted multiplanar reformatting allows to detect or exclude basal skull fractures, optic canal, orbital floor, maxilla, palate, and mandible fractures as well as the extent of different dislocations. (34, 35) magnetic resonance imaging (mri) mri may be used to investigate diffuse axonal injuries and in evaluating complications (i.e. csf rhinorrhea). (36) mri and mr angiography is helpful for the investigations of skull base trauma in cases of carotid-cavernous sinus fistula. mri has a limited role particularly in a polytrauma patient with traumatic brain injury as it is more time-consuming than ct and much less effective in detecting fractures than ct. presence of cardiac pacemakers and other implanted metals and electronic devices further limiting factors to perfume an mri. management initial management the initial management of any patient with the clinical suspicion of craniofacial who comes to the emergency room follows standard protocol i.e. airway management, breathing and circulation. once the general condition of the patient is stabilized further investigations and appropriate surgical intervention can be planned (table 2). maintenance of the airway in of primary importance (adequate suction, removal of nay foreign bodies or blood clot from the oral cavity), chin lift or jaw thrust to prevent tongue fall, pulling of the maxilla forward to disimpact the fracture, endotracheal intubation (or laryngeal mask airway) and if all these measures fail or not possible than an option to provide surgical airway needs to be considered (i.e. cricothyroidotomy or 342 agrawal et al management of craniofacial injuries tracheostomy). while securing the airway look for any active source of bleeding (injury to the major neck vessels, massive midface fractures, extensive scalp lacerations etc.) and take adequate measures to control the bleeding (i.e. local pressure application or suturing the scalp lacerations). table 2 summary of initial resuscitation approach and management primary survey • allows rapid assessment of vital functions (pulse, blood pressure and oxygen saturation) and help to identify lifethreatening conditions airway & breathing • assessment for airway patency • noisy breathing (gurgling or high-pitched noises) suggests partial airway obstruction • look for any broken or avulsed teeth • look for any fragments of loose bones • look for vomitus or blood in oral cavity • look for any tongue fall circulation • look for any source of massive bleeding scalp lacerations • severe midrace fractures may result massive blood loss • look for any associated injuries (hemothorax, hemoperitoneum, long bone fractures etc.) disability • assess of the patient's glasgow coma scale (gcs) score • any neurological deficits secondary survey (see table 1) • it should be performed once the primary survey is complete and life-threatening conditions have been ruled out or managed • a complete head-to-toe assessment so no injuries should be missed table 3 basic principal for the management of facial injuries • never shaved eyebrows • repair with precise attention to the normal shape and borders (lips, nose and eyebrows) • accurately restored the bony framework and soft tissue of the nose • nasal septum hematoma needs surgical draining as it can cause dissolution of the septal cartilage • epistaxsis can be controlled with head end elevation, cold compression and if necessary internal compression • while managing fractures either it should be done before a significant edema is develops or once the edema is resolved (5-7 days after the injury) romanian neurosurgery (2014) xxi 3: 338 344 343 surgical intervention once the patient general condition is stabilized, all the life threatening injuries are taken care off and a thorough clinical examination has been performed to rule out any intracranial injuries, surgery can be planned for facial injuries. before planning for surgery identifies the extent of injuries i.e. whether these are soft tissue injuries (contusions, abrasions, puncture wounds, lacerations or abrasions) or involve the facial skeleton (fractures of different bones) or it is a combination of both. the purpose of surgical intervention is to regain the function with good aesthetic outcome (table 3). open facial wounds need thorough cleaning, meticulous approximation, conservative debridement and if necessary graft to cover the raw surfaces. fractures will need rigid fixation of the fragments (by bone mini-plates and screws) to achieve perfect reduction, alignment and also needs good soft tissue cover and adequate time for bone healing to get completed. conclusion craniofacial injuries can occur in a significant proportion in traumatic brain injury patients and these will require prompt diagnosis and management. the management of these injuries is a challenge which is faced by residents in emergency room. an understanding of the presentations of craniofacial injuries, associated systemic injuries and patterns of traumatic brain injuries is crucial for improving care, survival and recovery of these patients. correspondence dr amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.malara p, malara b, drugacz j. characteristics of maxillofacial injuries resulting from road traffic accidents--a 5 year review of the case records from department of maxillofacial surgery in katowice, poland. head & face medicine 2006;2:27. 2.hull am, lowe t, finlay pm. the psychological impact of maxillofacial trauma: an overview of reactions to trauma. oral surgery, oral medicine, oral pathology, oral radiology, and endodontics 2003;95:515-520. 3.klotch dw. frontal sinus fractures: anterior skull base. facial plastic surgery 2000;16:127-134. 4.arslan ed, solakoglu ag, komut e, et al. assessment of maxillofacial trauma in emergency department. world journal of emergency surgery 2014;9:13. 5.aksoy e, unlü e, sensöz o. a retrospective study on epidemiology and treatment of maxillofacial fractures. the journal of craniofacial surgery 2002;13:772-775. 6.erol b, tanrikulu r, görgün b. maxillofacial fractures. analysis of demographic distribution and treatment in 2901 patients (25-year experience). journal of craniomaxillo-facial surgery 2004;32:308-313. 7.haug rh, foss j. maxillofacial injuries in the pediatric patient. oral surgery, oral medicine, oral pathology, oral radiology, and endodontics 2000;90:126-134. 8.wood eb, freer tj. incidence and aetiology of facial injuries resulting from motor vehicle accidents in queensland for a three-year period. australian dental journal 2001;46:284-288. 9.gassner r, tuli t, hächl o, rudisch a, ulmer h. cranio-maxillofacial trauma: a 10 year review of 9,543 cases with 21,067 injuries. journal of cranio-maxillofacial surgery 2003;31:51-61. 10.lee jh, cho bk, park wj. a 4-year retrospective study of facial fractures on jeju, korea. journal of craniomaxillo-facial surgery 2010;38:192-196. 344 agrawal et al management of craniofacial injuries 11.van den bergh b, karagozoglu kh, heymans mw, forouzanfar t. aetiology and incidence of maxillofacial trauma in amsterdam: a retrospective analysis of 579 patients. journal of cranio-maxillo-facial surgery 2012;40:e165-169. 12.gandhi s, ranganathan lk, solanki m, mathew gc, singh i, bither s. pattern of maxillofacial fractures at a tertiary hospital in northern india: a 4-year retrospective study of 718 patients. dental traumatology 2011;27:257262. 13.maliska mcds, lima júnior sm, gil jn. analysis of 185 maxillofacial fractures in the state of santa catarina, brazil. brazilian oral research 2009;23:268-274. 14.rosman dl, knuiman mw. a comparison of hospital and police road injury data. accident; analysis and prevention 1994;26:215-222. 15.rajendra pb, mathew tp, agrawal a, sabharawal g. characteristics of associated craniofacial trauma in patients with head injuries: an experience with 100 cases. journal of emergencies, trauma & shock 2009;2. 16.agrawal a, prasad r, shetty l, nachiappan s, manju m. characteristics of craniofacial trauma in a rural hospital in south india. annals of african medicine 2006;5:33-37. 17.gray j. gray's anatomy: random house llc, 2010. 18.eggensperger n, smolka k, scheidegger b, zimmermann h, iizuka t. a 3-year survey of assaultrelated maxillofacial fractures in central switzerland. journal of cranio-maxillo-facial surgery 2007;35:161-167. 19.lee kh, snape l, steenberg lj, worthington j. comparison between interpersonal violence and motor vehicle accidents in the aetiology of maxillofacial fractures. anz journal of surgery 2007;77:695-698. 20.kloss f, laimer k, hohlrieder m, et al. traumatic intracranial haemorrhage in conscious patients with facial fractures--a review of 1959 cases. journal of craniomaxillo-facial surgery 2008;36:372-377. 21.hohlrieder m, hinterhoelzl j, ulmer h, hackl w, schmutzhard e, gassner r. maxillofacial fractures masking traumatic intracranial hemorrhages. international journal of oral and maxillofacial surgery 2004;33:389-395. 22.béogo r, dakouré p, savadogo lb, coulibaly at, ouoba k. associated injuries in patients with facial fractures: a review of 604 patients. pan african medical journal 2013;16. 23.thorén h, snäll j, salo j, et al. occurrence and types of associated injuries in patients with fractures of the facial bones. journal of oral and maxillofacial surgery 2010;68:805-810. 24.scherbaum eidt jm, de conto f, de bortoli mm, engelmann jl, rocha fd. associated injuries in patients with maxillofacial trauma at the hospital são vicente de paulo, passo fundo, brazil. journal of oral & maxillofacial research 2013;4:e1. 25.udeabor s, akinmoladun vi, olusanya a, obiechina a. pattern of midface trauma with associated concomitant injuries in a nigerian referral centre. nigerian journal of surgery 2014;20:26-29. 26.alvi a, doherty t, lewen g. facial fractures and concomitant injuries in trauma patients. the laryngoscope 2003;113:102-106. 27.follmar ke, debruijn m, baccarani a, et al. concomitant injuries in patients with panfacial fractures. the journal of trauma 2007;63:831-835. 28.lim lh, lam lk, moore mh, trott ja, david dj. associated injuries in facial fractures: review of 839 patients. british journal of plastic surgery 1993;46:635638. 29.gwyn pp, carraway jh, horton ce, adamson je, mladick ra. facial fractures--associated injuries and complications. plastic and reconstructive surgery 1971;47:225-230. 30.tung tc, tseng ws, chen ct, lai jp, chen yr. acute life-threatening injuries in facial fracture patients: a review of 1,025 patients. the journal of trauma 2000;49:420-424. 31.bull h, choy m, manyonda i, et al. reactivity and assay restriction profiles of monoclonal and polyclonal antibodies to acid phosphatases: a preliminary study. immunology letters 1999;70:143-149. 32.lehmann ed. simulating glycosylated hemoglobin (hba1c) levels in diabetes using an interactive educational virtual diabetes patient simulator. diabetes technology & therapeutics 2001;3:517-524. 33.whitaker k, al k, abbasi k, dias p. compound anterior cranial base fractures classification using computerized to mograph scanning as a basis for selection of patients for dural repair. j neurosurg 1998;88:471-478. 34.joss u, piffko j, meyer u. behandlung von frontobasalen traumen und polytraumen. mund kiefer gesichtschir 2001;5:86-93. 35.probst w, fischer ja, binswanger u. intravenous 1,25(oh)2 vitamin d3 therapy in haemodialysis patients: evaluation of direct and calcium-mediated short-term effects on serum parathyroid hormone concentration. nephrology, dialysis, transplantation 1990;5:457-460. 36.yokota h, kurokawa a, otsuka t, kobayashi s, nakazawa s. significance of magnetic resonance imaging in acute head injury. the journal of trauma 1991;31:351357. doi: 10.33962/roneuro-2022-008 bilateral chronic subdural hematoma: clinical presentation, outcome and review literature. a single centre experience from india yadav kaushal, jaiswal gaurav, lodha krishna govind, gupta tarun kumar, patel pratik bipinbhai, kumawat suresh romanian neurosurgery (2022) xxxvi (1): pp. 43-48 doi: 10.33962/roneuro-2022-008 www.journals.lapub.co.uk/index.php/roneurosurgery bilateral chronic subdural hematoma: clinical presentation, outcome and review literature. a single centre experience from india yadav kaushal, jaiswal gaurav, lodha krishna govind, gupta tarun kumar, patel pratik bipinbhai, kumawat suresh department of neurosurgery, maharana bhupal government hospital & ravindra nath tagore (rnt) medical college, udaipur, rajasthan university of health sciences, jaipur (rajasthan), india abstract study design: prospective hospital-based study. background: annual incidence of bilateral chronic subdural hematoma (csdh) is increasing due to an increase in the ageing population, associated medical comorbidities such as haemodialysis, anticoagulant and/or antiplatelet therapy. objectives: 1. to determine the socio-demographic and clinical profile of bilateral csdh patients. 2. to determine treatment outcome and its association with the sociodemographic profile. method: a prospective hospital-based study was carried out on 100 confirmed patients of bilateral csdh. information of patients such as socio-demographic profile, clinical presentation and laboratory investigation, along with treatment and outcome were recorded and analysed. results: among 100 patients, male and female were 74% and 26%. the mean age of patients was 63.03±13.57 years. a history of head injury was reported by 49% of patients. the mean glasgow coma scale (gcs) was 12.14±2.38. common presenting symptoms were hemiparesis (69%), headache (58%), aphasia (18%) and complete loss of consciousness (16%). clinical improvement was observed in 81% while 09% had no change, 06% shows clinical deterioration and 04% of patients die during treatment. conclusion: bilateral csdh is common in the elderly and prognosis is poor with increasing age however gender has no association with poor outcomes. more than 80% of patients recover with timely interventions. key message: surgery leads to achieving good outcomes in cases of bilateral chronic sdh, but not all such patients will recover completely. similarly, good functional outcomes can also be achieved in those presented early after symptom onset when managed promptly. introduction a subdural hematoma (sdh) is collection of blood between the dura and the arachnoid membranes. sdh has been classified into three keywords bilateral csdh, glasgow coma scale, head injury, outcome corresponding author: gaurav jaiswal professor & head, department of neurosurgery, rnt medical college, udaipur, india drgauravjaiswal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 44 yadav kaushal, jaiswal gaurav, lodha krishna govind et al. verities i.e. acute, sub-acute and chronic types. acute sdh is usually caused by head injuries and is symptomatic within 24 hours of injury.13 the chronic subdural haematoma (csdh) are usually characterized by history of trivial head trauma.7 csdh is an encapsulated collection of old blood, which can be liquefied and located between the dura mater and arachnoid. csdh patient become symptomatic more than 2 weeks after the initial injury.14 it was first described by virchow in 1857 as “pachymeningitis haemorrhagica interna”. incidence of bilateral csdh is about 1-5.3 cases per one lac population. the incidence is increasing due to increase in aging population, associated medical comorbidities such as hemodialysis, anticoagulant and/or antiplatelet therapy.10,8 the presentation of csdh could vary from no symptoms to focal neurological signs such as hemiplegia, seizures, confusion, decreased memory, and signs of raised intracranial pressure such as headache, vomiting, and papilledema. patients may present with difficulty in speech, swallowing, and walking. there may be weakness or numbness of arms, legs, and face.16,19 csdh is usually diagnosed by ct scan. hematomas usually present as hypodense lesions, but sometimes isodense or mixed density lesions can also be observed. they are concavo-convex, but rarely may mimic acute epidural hematomas. csdh can be surgically treated, which has the potential for significant improvement or even resolution of symptoms postoperatively although multiple surgeries may required which leads to multiple hospitalization and deterioration of activities of daily living.6,18 there is lack of uniformity about the treatment strategies, such as the role of burr hole, twist drill, craniotomy, etc., in csdh amongst various surgeons. there is also disparity regarding use of drain, irrigation, and steroid. in addition, bilateral csdhs are operated unilaterally or bilaterally depending on symptoms or hematomavolume.17 bilateral sites of csdh are identified as a risk factor for recurrence by some researchers.11 materials and methods study design: a prospective hospital-based study. study setting: neurosurgery department of rnt medical college, udaipur, rajasthan, india study period: from july 2013 to june 2021. study population: all patients of bilateral csdh admitted at neurosurgery department during study period. inclusion criteria: patient of bilateral csdh showed isodense to hypodense hematomas with respect to the adjacent brain at computerized tomography (ct) scan. exclusion criteria: 1. patient had concomitant occurrences of other types of traumatic brain injury; 2) csdh had resulted from complications or history of prior neurosurgical procedures, such as craniotomy or cerebrospinal fluid shunting. sample size: 100 study tools: 1) individual case sheet. 2) ct scan report. method a prospective hospital-based study was conducted at neurosurgery department on patients of bilateral csdh admitted during july 2013 to june 2021. based on inclusion and exclusion criteria, records of 100 bilateral csdh patients were assessed and analysed. information of socio-demographic profile, clinical presentation at the time of admission, associated medical comorbidities, routine investigation along with neuro-image findings, treatment and outcome were assessed. all informations were entered in individual case sheet. ethical permission was taken from institutional ethic committee before starting of study. statistical analysis the collected data were compiled and tabulated using ms excel 2010 and analyzed using statistical software spss trial version 20. appropriated tables and figures were generated. the results were expressed in percentages. chi-square test was applied to determine association. p value of < 0.05 was considered statistically significant. results records of 100 patients with radiologically confirm cases of bilateral csdh were reviewed. among 100 patients, 74 (74%) were male and 26 (26%) were female. mean age of patient was 63.03±13.57 years. history of head injury was reported by 49% of patients. underlying medical condition such as hypertension, diabetes mellitus, stroke and end stage renal disease (esrd) with hemodialysis was found among 58%, 38%, 19% and 04% of patients 45 bilateral chronic subdural hematoma respectively. total 19% of patients were on antiplatelet therapy and 8% were on anticoagulant therapy at the time of admission. glasgow coma scale (gcs) was assessed for each patient at admission and mean gcs was 12.14±2.38. (table 1) table 1. socio-demographic and clinical characteristic of study participants variables male (n=74) female (n=26) total mean age 63.81±12.3 3 60.80±16.6 9 63.03±13.5 7 age (years) < 40 04 (5.4%) 02 (7.7%) 06 41 – 60 25 (33.8%) 10 (38.5%) 35 61 – 80 42 (56.8%) 10 (38.5%) 52 >80 03 (4.1%) 04 (15.4%) 07 history of head injury yes 37 (50%) 12 (46.15%) 49 no 37 (50%) 14 (53.85%) 51 underlying medical condition hypertension 35 (47.29%) 23 (88.46%) 58 diabetes mellitus 21 (28.38%) 17 (65.38%) 38 stroke 09 (12.16%) 10 (38.46%) 19 antiplatelet therapy 09 (12.16%) 10 (38.46%) 19 anticoagulan t therapy 05 (6.76%) 03 (11.53%) 08 esrd with hemodialysis 02 (2.70%) 02 (7.69%) 04 alcoholism 11 (14.86%) 02 (7.69%) 13 mean gcs at admission 11.72±2.44 12.82±2.32 12.14±2.38 table 2. neuro-image findings of study participants at admission neuro-image findings numbers (%) / mean±sd midline shift 12 (12%) mass effect 89 (89%) presence of layering 22 (22%) multiplicity of hematoma cavities 21 (21%) thickness of hematoma (mm) 32.09± 11.72 density of hematoma (hu) 34.82 ± 10.38 mean total hematoma volume in cm3 178.8 ± 71.4 neuro-image findings shows midline shift (12%), mass effect (89%), presence of layering (22%) and multiplicity of hematoma cavities (21%) among patients of bilateral csdh. mean thickness of hematoma was 32.09± 11.72 mm, mean density of hematoma was 34.82 ± 10.38 hu and mean total hematoma volume was 178.8 ± 71.4 cm3 among patients. (table 2). all patients of bilateral csdh were treated by biparietal burrhole with subgaleal drain placement. mean duration of hospital stay was 18.12±8.34 days. at the time of discharge, 81% patient shows clinical improvement, 09% had no change in condition while 06% shows clinical deterioration and 04% patients die during treatment. during follow up, 4% of patients shows recurrence of sdh. table 3. treatment and outcome of study participants variables numbers (%) treatment surgical 100 (100%) conservative 00 (0%) outcome (at discharge) improved 81 (81%) no change 09 (9%) worsened 06 (06%) death 04 (4%) mean hospital stay (day) 18.12±8.34 recurrence during follow up 04 (4%) table 4. association of treatment outcome with sociodemographic variables variables improved (n=81) others (no change, worsen and death) (n=19) total (n=10 0) p value * age (years) 0.013 < 40 06 (100%) 00 (0%) 06 41 – 60 31 (88.57%) 04 (11.43%) 35 61 – 80 42 (80.76%) 10 (19.24%) 52 46 yadav kaushal, jaiswal gaurav, lodha krishna govind et al. >80 02 (28.57%) 05 (71.42%) 07 gender 0.53 male 61 (82.43%) 13 (17.57%) 74 female 20 (76.92%) 06 (23.08%) 26 antiplatelet therapy yes 12 (63.16%) 07 (36.84%) 19 0.06 no 69 (85.18%) 12 (14.52%) 81 anticoagula nt therapy yes 05 (62.5%) 03 (37.5%) 08 0.35 no 76 (82.6%) 16 (17.4%) 92 presence of layering yes 16 (72.73%) 06 (27.27%) 22 0.26 no 65 (83.33%) 13 (16.67%) 78 multiplicity of hematoma cavities yes 14 (66.67%) 07 (33.33%) 21 0.059 no 67 (84.81%) 12 (15.19%) 79 thickness of hematoma (mm) 31.6±10.5 6 34.16±11. 88 32.09± 11.72 0.35 density of hematoma 34.61±10. 20 35.66±10. 76 34.82 ± 10.38 0.69 mean total hematoma volume in cm3 174.28±68 .2 196.6±72. 22 178.8 ± 71.4 0.20 *chi square and student t test were used as test of significance. for analysis purpose, outcome of patients was categorized into improved and others (no change, worsen and death). statistically significant (p=0.013) association was observed with age as outcome is favourable with younger age. no association was found between gender(p=0.53), antiplatelet therapy(p=0.06), anticoagulant therapy (p=0.35), presence of layering (p=0.26) and treatment outcome of bilateral csdh. association of multiplicity of hematoma cavities (p=0.059), thickness of hematoma (p=0.35), density of hematoma (p=0.69) and mean total hematoma volume (p=0.20) was insignificant with outcome of csdh. figure 1. symptoms of study participants at admission patients of bilateral csdh were present with multiple symptoms at admission. among them most common symptom was hemiparesis (69%) followed by headache (58%), aphasia (18%) and complete loss of consciousness (16%) excreta. (figure 1). discussion the increasing global incidence of bilateral csdh because of an aging population has a great disease burden.8,4 clinically, patients often present with a history of gradually increasing altered level of consciousness and/or focal signs. a relatively simple neurosurgical treatment can improve functional outcome; however, high mortality is still observed in patients.5 in present study, a prospective study was planned on 100 radiologically confirm cases of bilateral csdh. among 100 patients, 74% were male and 26% were female. age of patients varies from 35 years to 95 years with mean age of 63.03±13.57 years. head injury was precede csdh among 49% of patients. patients were present with multiple symptoms at admission such as hemiparesis (69%), headache (58%), aphasia (18%), complete loss of consciousness (16%) excreta. total 19% of patients were on antiplatelet therapy and 8% were on anticoagulant therapy at the time of admission. yuji 58 7 14 13 7 8 3 18 4 4 16 69 0 20 40 60 80 headache nausea or vomiting confusion convulsions focal seizures quadriplegia slurred speech aphasia unsteady gait (ataxia) dual incontinence complete loss of… hemiparesis symptoms 47 bilateral chronic subdural hematoma agawa et al2 study 368 cases of bilateral csdh. average age at onset of disease was 74.2±12.8 years and 246 (66.8%) patients were male and 122 (33.2%) were female. motor weakness (74.45%) was the most common clinical presentation followed by headache (19.56%). forty-one patients (11.1%) had warfarin use, 67 (18.2%) patients had a history of malignancy, 46 (12.5%) had dementia and 16 (4.3%) had history of depression. nina christine et al15 observed 291 patients of bilateral csdh and find that out of 291 patients, 71.1% were male and 28.9% were female. age is between 40 to 98 years, with a mean age of 73.0 years for males and 76.7 years for females. a history of head trauma was obtained in 53.3% patients. approximately half of the study population (47.8%) received anticoagulant or antiplatelet therapy upon admission. in this study, midline shift (12%), mass effect (89%), presence of layering (22%) and multiplicity of hematoma cavities (21%) was found in neuroimaging. mean thickness, density and mean total hematoma volume was 32.09± 11.72 mm, 34.82 ± 10.38 hu and 178.8 ± 71.4 cm3 among patients. in neuro imaging of 25 patients of bilateral csdh, yuhua huang et al20 found midline shift (12%), mass effect (96%), presence of layering (20%) and multiplicity of hematoma cavities (20%) among patients of bilateral csdh. mean thickness of hematoma was 32.16 ±10.81 mm, mean density of hematoma was 35.80±11.30 hu. in present study, management of all patients of bilateral csdh were remain surgical. mean duration of hospital stay was 18.12±8.34 days. at the time of discharge, clinical improvement was shown in 81% patient while 04% patients die during treatment. treatment outcome was significantly associated with age but not with gender of patient. nina christine treat 264 (90.7%) patients surgically while 27 (9.3%) patients conservatively. sakina mehboob rashid found improvement in 53.3%, worsening of condition among 6.6%, no change in 16.7% and deceased in 23.3% of patients. similar to our study, yuji agawa observed poor clinical outcome among 03 (5.7%) patients and yu-hua huang observed death among 01 (04%) of patients with bilateral csdh. olufemi babatola et al14 studied 73 patients with age range was 24 to 82 years. among 73 patients of bilateral csdh, in majority outcome was favourable (91.3%) in patients with a recurrence rate of 12.5% and mortality rate of around 6.3%. david kitya et al9 assess 205 patients of bilateral csdh and found that 202 patients underwent surgical intervention with burr holes and drainage and 22.8% (46) were admitted to the icu. two patients had a recurrence, 5 suffered postoperative wound infection, and 18 died. gcs score on admission was a significant predictor of the discharge gcs score (p = 0.004), icu admission (p < 0.001), and death (p < 0.001). presenting symptoms differed by age. hundred patients of bilateral csdh was managed by malaya patel et al,12 among them burr hole drainage was carried out in 94 patients (94%). primary craniotomy along with membrane excision was carried out in about 5 patients. secondary craniotomy was performed in 1 patient. with all efforts, total five deaths were reported. conclusion bilateral csdh are one of the most rewarding among neurosurgical procedures. bilateral csdh is common in elderly and prognosis is poor with increasing age however gender has no association with poor outcome. head injury was preceding in bilateral csdh among 49% of patients. patients were present with multiple symptoms at admission. with timely diagnosis and management, improvement was observed in more than 80% of patients. conflicts of interest the authors declare no conflict of interest. informed consent informed consent was obtained from all individual participants included in the study. references 1. adhiyaman v, asghar m et al. chronic subdural haematoma in the elderly. postgrad med j 2002;78:71– 75. 2. agawa y, mineharu y et al. bilateral chronic subdural hematoma is associated with rapid progression and poor clinical outcome. neurol med chir (tokyo) 56, 198– 203, 2016. 3. babatola o, salman a et al. chronic subdural haematoma: clinical presentation, surgical treatment and outcome at the lagos university teaching hospital. african journal of neurological sciences 2011 vol. 30, no 1. 4. balser d, farooq s, mehmood t, reyes m, samadani u. actual and projected incidence rates for chronic subdural hematomas in united states veterans administration and civilian populations. j neurosurg 2015;123:1209–15. 48 yadav kaushal, jaiswal gaurav, lodha krishna govind et al. 5. bankole ob, yusuf as, kanu oo, ukponwan e, nnnadi mn, arigbabu so. chronic subdural haematoma: clinical presentation, surgical treatment and outcome at the lagos university teaching hospital. afr j neurol sci 2011;30:10–7. 6. dekker mcj, urasa sj, howlett wp. neurological letter from kilimanjaro. practneurrol. 2017;5:412–6. 7. jobse ic, feitsma mt. presentation of chronic subdural hematoma in the elderly. tijdschrgerontolgeriatr. 2011;42:139–43. 8. karibe h, kameyama m, kawase m, hirano t, kawaguchi t, tominaga t. epidemiology of chronic subdural hematoma. no shinkeigeka. 2011;39:1149–53. 9. kitya d, med m et al. causes, clinical presentation, management, and outcomes of chronic subdural hematoma at mbarara regional referral hospital. neurosurg focus volume 45:october 2018. 10. krupa m. chronic subdural hematoma: a review of the literature. part 1. ann acad med stetin. 2009;55:47–52. 11. kurokawa y, ishizaki e, inaba k. bilateral chronic subdural hematoma cases showing rapid and progressive aggravation. surgneurol 2005;64(5):444e9. 12. malaya patel et al., clinical presentation and surgical outcome in chronic subdural haemorrhage patients. journal of clinical and diagnostic research, 2021 mar, vol-15(3): pc08-pc12. 13. mayer s, rowland l. head injury. in: rowland l, editor. merritt’s neurology. philadelphia: lippincott williams & wilkins; 2000. p. 401. 14. miller jd, nader r. acute subdural hematoma from bridging vein rupture: a potential mechanism for growth. j neurosurg. 2014;120(6):1378–84. 15. nina christine andersen-ranberg et al. bilateral chronic subdural hematoma: unilateral or bilateral drainage. j neurosurg 126:1905–1911, 2017. 16. rashid s m , deliran s s et al. chronic subdural hematomas: a case series from the medical ward of a north tanzanian referral hospital egyptian journal of neurosurgery (2019) 34:29. 17. santarius t, lawton r, kirkpatrick pj, hutchinson pj. the management of primary chronic subdural haematoma: a questionnaire survey of practice in the united kingdom and the republic of ireland. br j neurosurg. 2008;22:529– 34. 18. takahashi s, yamauchi t et al. proposal of treatment strategies for bilateral chronic subdural hematoma based on laterality of treated hematoma. asian journal of neurosurgery | volume 13 | issue 4 | octoberdecember 2018. 19. yadav y r, parihar v et al. chronic subdural hematoma. asian j neurosurg. 2016 oct-dec; 11(4): 330–342. 20. y.-h. huang et al. bilateral chronic subdural hematoma: what is the clinical significance? international journal of surgery 11 (2013) 544e548. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 342 | moldovan et al diagnostic criteria in invasive pituitary adenomas diagnostic criteria in invasive pituitary adenomas ioana-maria moldovan1,2, carmen melincovici1, carmen mihaela mihu1, sergiu susman1, anne-marie constantin1, stefan ioan florian2 1histology discipline, morphological sciences department, “iuliu hațieganu” university of medicine and pharmacy, cluj-napoca, romania 2neurosurgery clinic, cluj-napoca, romania abstract: pituitary adenomas are benign pituitary primary tumors, the most frequent type of tumor in the pituitary fossa. an important part, around 1/3 of the pituitary adenomas manifests an aggressive behavior, growing faster and invading into parasellar areas (cavernous sinus, neural tissues and bones). objectives: the first aim of this paper is to review the last findings about invasiveness diagnostic criteria, imagistic and biomarkers, which can be used in the classification of pituitary tumors and also to predict the probability of invasiveness, tumor recurrence and suspicion of malignancy. the second aim is to highlight the morphological and clinic types of invasive pituitary adenomas. materials and methods: we performed a systematic review and analysis of the published articles, searching pubmed between january 1985 and december 2015. there were selected articles published in english, reviews and abstracts. during the advanced search type in pubmed, combinations of the following keywords were used: “pituitary adenoma”, “invasive”, “aggressive”, “biomarkers”, “classification”, “histological subtypes”, ‘”immunohistochemical markers”. results: 215 articles were selected, regarding diagnostic, prognostic and therapeutic aspects. there were some histological subtypes of pituitary adenomas known as having an aggressive clinical behavior. several biomarkers were identified as being associated with the invasive feature: proliferation markers (ki-67 index, number of mitoses, p53 & p27 expression, microvascularization density, telomerase, topoisomerase 2 alpha), matrix metalloproteinases, protein kinase c, cyclooxygenase-2, e-cadherin, transcription factors, genetic alterations (pttg gene, galectin-3 protein/ lgals3 gene), apoptosis markers. based on their invasion and proliferation characteristics, pituitary tumors are proposed to be classified into five grades (1a, 1b, 2a, 2b, 3), the grade 2b tumor with high risk of recurrence being considered as tumor suspected of malignancy. conclusions: using a set of specific biological markers for invasive process, there is hope to establish an early diagnosis and prevention of invasive pituitary adenomas. due to the fact that aggressive pituitary romanian neurosurgery (2016) xxx 3: 342 355 | 343 tumors are generally difficult to manage, unresponsive to therapy, quickly recurrent and associated with poor prognosis, the early diagnosis and the search for new therapeutic approaches is becoming mandatory. instead of using “invasive” or “aggressive” adenoma, the term “tumor suspected of malignancy” would be used for more accuracy. key words: pituitary adenoma, invasive, aggressive, biomarkers, classification, histological subtypes, immunohistochemical markers introduction the pituitary primary tumors, originating from adenohypophyseal cells, can be benign (adenomas) and malignant (carcinomas). the pituitary adenomas’ incidence is about 10–15% of all brain tumors, being on the third place, after gliomas and meningiomas. the pituitary carcinomas represent only 0.1% of all pituitary tumors (1). invasion represents the phenomenon in which the cells from a malignant neoplasm extend to the adjacent healthy tissues, infiltrating and destructing them. for epithelial neoplasms, invasion signifies infiltration beneath the epithelial basement membrane. although pituitary adenomas are non-metastasizing tumors, invasive local growth occurs in 35% of cases (2). atypical adenomas are small subset of pituitary adenomas, tumors with a more aggressive behavior, which have potential to grow faster than typical adenoma and have also potential of invasion into vascular (cavernous sinus), neural tissues and bones (1). most of the neurosurgeons agree that a key feature in defining an ‘‘aggressive’’ pituitary tumor is the rapidity of growth, which often may cause an early recurrence. a tumor that re-grow in 6 months is considered ‘‘aggressive’’, compared with a recurrence in 10 years after a complete resection, which might be considered as a benign behavior (2). materials and methods an extensive medical literature research was performed in pubmed, years of publication from january 1985 – december 2015. the analyzed articles were published in english language, in abstract or in extenso and 20 articles were excluded. there were selected articles focusing on classification of pituitary tumors, biomarkers of invasiveness, diagnostic criteria, morphologic types of invasive pituitary tumors, imagistic criteria, on tumor recurrence and suspicion of malignancy. for the research, there were used combinations of 2 or 3 of the biomarkers identified as being associated with the invasive feature: proliferation markers (ki-67 index, number of mitoses, p53 & p27 expression, microvascularization density, telomerase, topoisomerase 2 alpha), matrix metalloproteinases, protein kinase c, cyclooxygenase-2, e-cadherin, transcription factors, genetic alterations (pttg gene, galectin-3 protein/ lgals3 gene), apoptosis markers. results from clinical point of view, in the studied articles was found that the pituitary tumors are 344 | moldovan et al diagnostic criteria in invasive pituitary adenomas classified into functioning – acromegaly syndrome with growth hormone (gh) secretion, or amenorrhea-galactorrhea with prolactin (prl) secretion, or cushing’s disease with adrenocorticotropic hormone (acth) secretion) and nonfunctioning tumors – secreting mainly follicle-stimulating hormone (fsh) and luteinizing hormone (lh). the functional tumors represent 75% of pituitary adenomas, but the non‑secreting tumors are usually larger (3). beside the increased secretion of some hormones, the pituitary tumors are usually causing a subsequent “mass effect” on surrounding structures (optic chiasm and/or the cavernous or sphenoid sinuses), with symptoms and signs such as: headaches; epistaxis (due to downward extension through the floor of sella) (4); visual field impairment (typically bi‑temporal field loss or diplopia) or even proptosis (due to a mass extended to orbit) or other neurological deficits (cranial nerve palsies, due to invasion into cavernous sinus) (4). headaches or vision loss with sudden onset can be due to hemorrhage or necrosis of tumor (5). in the studied articles we identified several hormone-secreting and morphological subtypes of pituitary adenomas, which tend to have a more aggressive clinical behavior. these include: 1) aggressive prolactinsecreting pituitary tumors (sparsely granulated somatotroph and acidophil stem cell adenomas); 2) aggressive corticotroph pituitary tumors (silent corticotroph adenomas, thyrotroph adenomas, crooke’s cell adenomas); 3) aggressive growthhormone secreting pituitary tumors(more common are densely and sparsely granulated somatotroph adenomas); 4) aggressive gonadotroph and thyrotroph pituitary tumors (tumors immunohistochemical positives for the fsh and/or lh gonadotrophins or the oncocytomas); and 5) aggressive plurihormonal tumors (silent subtype 3 adenomas). tumor invasion was defined based on one or more of the following parameters: preoperative imaging (mri or ct), intraoperative findings, and histology (6). by size, pituitary adenomas are classified by size into microadenoma (b<10 mm) and macroadenomas (≥10 mm). it was shown that the invasion of the cavernous sinus space occurs in 6 to 10% of all pituitary adenomas. it is only considered an unequivocal invasion of the cavernous sinus, when the percentage of encasement of the internal carotid artery by the tumor is 67% or greater, or for grades 3 or 4 of knosp’s classification (7). in case of such large invasive macroadenoma, the total surgical resection is unobtainable. the proliferation markers for aggressive pituitary tumorsidentified were: ki-67 index, number of mitoses, p53 & p27 expression, microvascularization density, telomerase, topoisomerase 2 alpha. the main diagnostic criteria for atypical pituitary adenoma, included in all the studied articles, included: pleomorphism, elevated mitotic index, increased nuclear reaction for the p53 protein, and a ki-67 proliferative index >3% (8). increasing levels of ki-67 correlate with rate of tumor growth, invasion, responsiveness to pharmacological treatment, tumoral romanian neurosurgery (2016) xxx 3: 342 355 | 345 remission and recurrence (8). a threshold of 3% ki-67 index can distinguish between invasive and noninvasive adenomas, with 97% specificity and 73% sensitivity and has indeed a prognostic value (9). the mean values of ki67, reported by thapar et al. (1996) were 1.37% in noninvasive pituitary adenomas, 4.66% in invasive adenomas and 11.91% in carcinomas (9). a number of mitoses higher than 2/10 hpfs (10 hpf: high power field=2 mm2, at least 40 fields, at 40× magnification, evaluated in areas of highest mitotic density) indicate the proliferative characteristic of a tumor (10). several studies showed an increased p53 expression in ‘aggressive-invasive’ pituitary tumors: significantly higher (p=0.0001) or of 15% in invasive pituitary adenomas and of 100% in pituitary carcinoma metastases (11, 12). p27 kip1 expression was found lower in recurrent adenomas compared with nonrecurrent ones, especially in corticotroph adenomas, and in carcinomas compared with invasive adenomas (13). in invasive pituitary tumors vidal et al. described a higher microvascular density, but without statistical significance (14). also, salehi et al. obtained inconsistent association between the expression of vascular endothelial growth factor (vegf) and the tumor invasiveness and proliferation (15). harada et al. (16) and yoshino et al. (17) detected a telomerase expression in 13% of large, invasive adenomas, therefore telomerase detection may be also useful for identifying aggressive adenomas. also, in pituitary adenomas, there were reported low values of topoisomerase ii alpha, results similar to those of ki-67, however further studies are requested to establish if this enzyme is a valid marker of tumor aggressiveness (18). other characteristics modifications in aggressive pituitary tumors identified in the studied articles were: matrix metalloproteinases, protein kinase c (pkc), cyclooxygenase-2, e-cadherin, genetic alterations (pttg gene, galectin-3 protein/ lgals3 gene), apoptosis markers. in aggressive/invasive pituitary tumors, it was demonstrated that mmp9 expression level and activity is higher than in noninvasive pituitary tumors (19). in invasive pituitary adenomas was shown by a point mutation of pkc-α and a higher total pkc activity and expression (20) and in some cases of prolactinomas that responded favorably to dopamine agonists therapy was observed a reduced pkc activity. cyclooxygenase-2 (cox-2) presents an increased expression evident particularly in pituitary carcinomas, compared with adenomas and normal pituitary (21), in a study of van roy and berx it was observed that in pituitary aggressive/invasive adenoma, cells e-cadherin and β-catenin expression was downregulated and a decreased e-cadherin expression can lead to development of metastases (22). also, they were demonstrated accumulations of new chromosomal alterations which may transform an “aggressive” pituitary tumor into a pituitary carcinoma, as in the case of prl aggressive tumors (grade 2b), that became malignant and 346 | moldovan et al diagnostic criteria in invasive pituitary adenomas developed metastasis during follow-up (the 11p region was usually deleted, the 11q arm was loss and in the 1q arm was a gain) (23). zhang et al. noted significantly higher levels of pituitary tumor transforming gene (pttg) expression in hormone-secreting invasive tumors compared with non-invasive ones (24). in both prl and acth functioning pituitary tumors (adenomas and carcinomas) was shown that lgals3 has a higher expression, with the highest level in acth carcinomas (25). higher apoptotic activity was reported in aggressive, drug-resistant adenomas by kontogeorgos et al. (26) and in pituitary carcinomas compared with adenomas, kulig et al. (27) reported a four-fold increase in apoptotic activity. discussions imagistic diagnostic criteria for aggressive pituitary tumors recent anatomical and ultrastructural studies have shown that the medial wall of the cavernous sinus is composed of dura. dural invasion is not considered a feature of invasion because previous studies demonstrated that it is not related to the recurrence rate. suprasellar growth is considered an extension, rather than an invasion. according to hardy’s neuroradiological classification, tumors with a suprasellar expansion that were frequently lined by non-tumoral pituitary, are not considered as invasive. any tumor growth into the cavernous sinus would therefore represent a sign of invasiveness without histological proof, such as the invasion into the sphenoid sinus confirmed by the infiltrated respiratory mucosae on histology. new methods of immunohistochemistry, by staining with ki-67, a significantly higher proliferation rate were demonstrated in invasive adenomas; this was not only true in pituitary adenomas with histologically proven invasion of the dura, but also in pituitary adenomas macroscopically invading the cavernous sinus space (28). mri importance mri offers detailed information on the anatomical relationship of the tumor with the surrounding structures; therefore, it is considered as the method of choice in the diagnosis of pituitary adenomas and it also become the gold standard for diagnosis and follow-up of pituitary adenomas. the application of gadoliniumdiethylenetriaminepentaacetic acid (gddtpa) enhances precisely the cavernous venous plexus, which allow the precise distinction between the medial, superior, inferior, and lateral compartments (29). although it is common to wait 3–4 months after surgery to obtain the first mri, even immediate postoperative imaging is useful to provide information regarding the presence of residual tumor, in order to start early specific therapeutic strategies. but despite the mri improvements, there are authors who consider that the invasion into the cavernous sinus space cannot be proved only by mri and that the invasion of the cavernous sinus space remains a surgical diagnosis, because only the surgeon can distinguish between compression of the romanian neurosurgery (2016) xxx 3: 342 355 | 347 venous spaces and real infiltration of the medial wall of the cavernous sinus space (30). proliferation markers for aggressive pituitary tumors there are evidences at the molecular level which indicate that pituitary tumors accumulate abnormalities over time, fact that contribute to their progression from ‘‘benign’’ adenoma to aggressive recurrent pituitary tumors and even to a pituitary carcinoma (15). proliferation is defined as the presence of at least two of the three markers: mitoses or ki67 index which exceeded the defined thresholds, or positive p53 detection. ki-67 index the protein ki-67 is a marker of cell proliferation present in the nuclei of cells in g1, s, and g2 cell division cycle phases and in mitosis. the ki-67 expression is detected by the monoclonal antibody mib-1 and is quantified as ki-67 proliferation index being a percentage of immunopositive nuclei (31). the ki-67 index >1 or c3% according to the bouin-hollande or formalin fixative and the number of mitoses n>2/10 hpfs had been defined previously in pituitary and/or endocrine tumors (10). for pituitary adenoma, ki-67 is a routinely examined marker of cell proliferation. in clinical practice, ki-67 index is daily used to select the patients who need a strict follow-up, because a very high proliferation index suggests the presence of a carcinoma in situ or premetastatic carcinoma, with potential for a rapidly progressive and fatal course. the above mentioned data have led to a proposal that pituitary tumors exhibiting ki-67 index greater than 10% should routinely be classified as atypical independent of other criteria (21). even if ki-67 index >3% is considered a good proliferation marker, its values exhibit a certain variability. they vary depending of immunohistochemical (ihc) type and in functional pituitary tumors are higher than in nonfunctioning ones. also, there are authors who found no correlation between ki-67 index and pituitary tumor invasiveness (21). therefore, it is recommended the use of other makers for more accurate prediction of the tumor behavior. number of mitoses beside ki-67 index, also the presence and the number of mitoses can represent important predictive factors of proliferation and rapid growth in endocrine tumors. p53 expression p53 is a tumor suppressor gene that plays an important role in cell proliferation, apoptosis and genomic stability. there are also reports about a non-conclusive correlation between p53 increased expression and aggressive adenoma behavior (31), but it is possible to exist differences in p53 evaluation between laboratories and pathologists. therefore, only the p53 positivity or negativity is considered, because, actually, there is no validated prognostic cut-off for it (11), but a p53 positive immune reaction has been found in all pituitary carcinomas (9,11) and, also, p53 is one of the criteria to classify ‘‘atypical adenomas’’ (6). p27 expression p27 kip1 is a cyclin-dependent kinase inhibitor, involved in regulation of cell-cycle 348 | moldovan et al diagnostic criteria in invasive pituitary adenomas progression.because p27 kip1 expression was inversely correlated with the ki-67’s one, it was suggesting that p27 kip1 is an additional predictive marker of pituitary tumor behavior (32). telomerase telomerase is a reverse transcriptase enzyme carrying its own rna molecule, which elongates telomeres and contributes to the preservation of the senescence-crisisapoptosis cycle. because this represent one of the fundamental defense mechanisms against cancer development, this can be a valuable exploration in aggressive pituitary tumors. topoisomerase 2 alpha topoisomerase ii alpha is a key enzyme involved in dna replication and cell-cycle progression, not found in resting cells; its expression correlates with cell proliferation (18), fact which can also be valuable in exploring aggressive tumor comportment. other characteristics modifications in aggressive pituitary tumors angiogenesis the “angiogenic switch”, the imbalance between stimulating and inhibiting angiogenetic factors, becoming predominant promoting factors, represents an important phenomenon in tumorigenesis: the formation of new blood vessels sustains the tumor growth. it was observed that in pituitary adenomas, they are less vascularized than the normal pituitary tissue; this can explain the slow growth and lack of metastasis, and lead to the development of the hypothesis that pituitary adenoma evolve through a non-angiogenic pathway. in carcinomas it was observed a higher vascularization than in the adenomas, finding which supports the idea that the development of metastasis is correlated with the neo-angiogenesis (33). but nevertheless, vegf is an important angiogenic factor up-regulated by pttg and future studies could confirm its link with invasive pituitary adenomas (15). other enzymes matrix metalloproteinases the matrix metalloproteinases (mmp) are a family of proteolytic enzymes cleaving the extracellular matrix molecules. mmps play a role in invasiveness of many neoplasms and the mmp study underlines the importance of the pituitary tumor environment. the expression of mmp9 may be correlated with the activation of protein kinase c (pkc), which is also known to indicate invasion and aggressive behavior of pituitary tumors (34). protein kinase c pkc is a ubiquitous family ofisoform enzymes, playing important roles in controlling the function of other proteins and in signal transduction cascades. therefore, pkc are associated with a variety of cellular responses, including cell growth and invasion (19). pkc activation has been shown to increase mmp-9 expression in some tumor cells. because pkc activates mmp-9 in a highly celltype-specific manner, the differential expression of pkc isozymes may involve various signal transduction pathways; therefore, it is important to identify which romanian neurosurgery (2016) xxx 3: 342 355 | 349 pkc isozyme is regulating the mmp-9 expression of in pituitary adenomas (19). cyclooxygenase-2 cox-2 is a key enzyme of prostaglandin synthesis, involved in inflammatory responses. there were studies who reported that cox-2 presents an increased expression also in the gonadotrophic tumors, compared with other pituitary neoplasms (35). the observations sustain the cox-2 implication in tumor invasiveness, angiogenesis and progression; indeed, it was observed that cox-2 expression shows a strong correlation with microvessel density (21). e-cadherin e-cadherin is a calcium-dependent cell adhesion protein, playing an important role in epithelial cell behavior and tissue development and having a strong anti-invasive and antimetastatic role. in normal pituitary cells ecadherin is strongly expressed (22). transcription factors/regulators for immunonegative or silent tumors, the transcription factors involved in pituitary cell differentiation may be used to confirm the diagnosis. pit-1 is expressed in gh, prl, and thyroid stimulating hormone (tsh) tumors; t-pit in acth tumors with and without cushing’s disease and sf-1 in fsh and lh tumors (36). rarely, some pituitary tumors differentiate functionally and produce hormones belonging to different cell lineages (acth-omas with gh production, or gh-omas with acth production); this abnormal differentiation could be caused by an aberrant expression of transcription factors (37). ikaros is a transcriptional regulator and an important factor implicated in chromatin remodeling that can influence hypothalamicpituitary cell development, differentiation and proliferation (38). genetic alterations despite the pituitary tumors are in majority sporadic, they characterized some genetic forms of pituitary adenoma in familial cases. pttg gene the pituitary tumor transforming gene (pttg) is another less well studied marker, found in 90% of pituitary tumors. 2.9% or more of pttg expression can be also considered an indication of a more aggressive behavior of pituitary adenomas. comparing pttg expression in 54 pituitary tumors, zhang et al. found no correlation with radiological tumor stage in clinically non-functioning adenomas, even they founded significantly higher levels in invasive tumors (24). h-ras gene mutation several proto-oncogenic events, as the p53 and p27kipl expression, the function of telomerase, and the role of h-ras gene mutation, can represent central events in the pathogenesis and spread of pituitary carcinomas (15, 16, 17). galectin-3/ lgals3 gene galectin-3 is a protein encoded by the lgals3 gene, expressed in pituitary gland by both folliculostellate cells and normal prolactin (prl) and adrenocorticotropin (acth)-producing cells, but not by most other cell types. lgals3 is a useful 350 | moldovan et al diagnostic criteria in invasive pituitary adenomas immunohistochemical marker for differentiating silent from functioning acthsubtype adenomas. lgals3 represents a reliable marker for predicting the aggressive tumor behavior (assessing a high risk of progression or recurrence) (12). prl and acth functioning pituitary tumors (adenomas and carcinomas) are aggressive subtypes of tumors, in which the invasive growth with suprasellar extension, a high ki-67 index, and lgals3 expression levels are the most important pathologic features, therefore a target therapy against galectin-3 protein may be useful. apoptosis apoptosis, the programmed cell death, is a sequence of events characterized by cellular shrinkage and nuclear demarcation, which ends with the elimination of damaged cells. in neoplasms, there is a misbalance between mitotic and apoptotic activity, apoptosis is generally suppressed and there is an increased tumor growth (15). apoptosis may be a useful prognostic marker; the expression of anti-apoptotic factor bcl2 and proapoptotic factor bax also correlates with apoptotic indices. a lower expression of bcl2 was also reported in pituitary carcinomas compared with adenomas and the non-tumoral pituitary gland (27). the new classification criteria for atypical adenomas until the 1980’s, the classification of pituitary tumors included three types, based on tinctoriality correlated with the clinical disease: acidophilic with acromegaly, basophilic with cushing’s disease, and chromophobic adenomas. the advancements in electron microscopy (em) and immunohistochemistry (ihc) changed the classification of pituitary tumors into five immunocytochemical types and a dozen ultrastructural subtypes, based on their organelles appearance (granulations and mitochondria) and their hormonal secretion (39). the new 2004 who classification for endocrine tumors define 3 types of pituitary tumors: benign adenoma, atypical adenoma, and carcinoma (1,8). wolfsberger and knosp criticized the who 2004 classification; they stated that ‘‘the definition of invasiveness is needed and should be included in this classification’’ and underline the need to also include proliferation, evaluated by markers of the cell cycle with well-defined thresholds (40). considering invasion potential for atypical adenomas at a threshold of ki-67 index >3% and p53 >5%, saeger et al. found only 2.7% of among 241 tumors from the german registry (1). actually, it is recognized that there is no reliable distinction between carcinoma and adenoma based on distinct standard histological criteria or electron microscopic features, distinct that would permit a reliable early prediction of future aggressive behavior of a pituitary adenoma, even if invasive. based on above mentioned characteristics of atypical adenomas, recently, a new clinicopathological classification has been proposed, which takes into account tumor size, immunocytochemical type (hormonal immunoexpression profile), tumoral invasion romanian neurosurgery (2016) xxx 3: 342 355 | 351 (invasion to the cavernous and sphenoid sinuses, evaluated by magnetic resonance imaging (mri) or histology), and tumor cell proliferation markers (ki-67 and p53) (41). therefore, based on their invasion and proliferation characteristics, the tumors were classified into five grades: grade 1a: noninvasive tumor, grade 1b: non-invasive and proliferative tumor, grade 2a: invasive tumor, grade 2b: invasive and proliferative tumor, grade 3: metastatic tumor). trouillas proposed to consider the grade 2b tumors with high risk of recurrence as tumors suspected of malignancy (41). the aggressive subtypes of pituitary adenomas aggressive prolactin-secreting pituitary tumors prolactinomas represent about 40% of all pituitary adenomas. two histological subtypes are clinically relevant (42): 1 – the sparsely granulated lactotroph adenoma is the most common form, more aggressive in men than in women, which can reach considerable size, high prl serum levels and invasive features at mri. in many cases, this type responds dramatically to dopamine agonist therapy; 2 – the densely granulated lactotroph adenoma, with diffuse cytoplasmic positivity to prl it is very rare; 3 – the acidophil stem cell adenomas presents weakly acidophilic cells producing prl and gh, oncocytic changes, and giant mitochondria. it often has an aggressive clinical behavior, with hyperprolactinemia and/or acromegaly (1). clinically, some mass effect features are observed, such as visual field restriction or dull headache at presentation and symptoms of amennorrhea and galactorrhea in females and erectile dysfunction in males. the aggressive prolactinomas present serum prl levels which can vary widely (6– 21,560 ng/ml in one series). imagistic studies often put into evidence a pituitary macroadenoma with invasion of one/both cavernous sinuses, which extent and often encase the internal carotid arteries (43,44). aggressive corticotroph pituitary tumors 10–15% of all pituitary adenomas are acth-secreting adenomas. two morphologic variants have been identified at electron microscopy level: subtype 1 densely granulated basophilic tumors, similar to functional acth secretory tumors and subtype 2 different by electron microscopy, chromophobic, sparsely granulated and their secretory granules are smaller and irregular in shape and lack cytoplasmic intermediate filaments (45).the densely granulated corticotroph subtype is the most common (42,45), usually present in patients with cushing’s disease and nelson’s syndrome. crooke cell tumors is a rare form of acth producing adenoma, tumor cells presenting a variable but often characteristic crooke's intracytoplasmic accumulation of cytokeratin. clinicopathologically, these tumors represent a distinct entity from typical endocrinologically active corticotroph adenomas; they may produce acth-causing cushing’s disease or may be endocrinologically silent. pituitary tumors composed of crooke cells exhibit aggressive clinical behavior, with high recurrence rate, 352 | moldovan et al diagnostic criteria in invasive pituitary adenomas and invasiveness (46), and nearly always these recurrent invasive macroadenomas may progress to corticotroph carcinomas (46). the crooke’s cell adenoma must not be confused with keratin deposition in the normal corticotrophs (crookes hyaline change), first described in 1935 by endocrinologist ac crooke. clinically, patients with aggressive pituitary corticotroph tumors present cushing’s disease, with acth dependent hypercortisolism, including central obesity, rounded facies, abdominal and proximal limb striae, hypertension, altered menses, osteoporosis and delayed wound healing (40). a second clinical onset is observed in nelson’s syndrome, the rapid enlargement (likely to occur within the first 3 years) of a pre-existing acth-secreting pituitary adenoma that occurs after bilateral adrenalectomy to control hypercortisolismin patients with cushing’s disease (47). thirdly, they are recurrent but ’’silent’’ corticotroph tumors, which present variable immunopositivity for acth. clinically, are nonfunctional adenomas, which do not secrete excess acth, but have a more aggressive course than most functional acth-secreting tumors (48) and recur more frequently than tumors with hypercortisolism (48). aggressive growth-hormone secreting pituitary tumors gh-secreting adenomas represent 10–15% of all pituitary adenomas and are classified into five histological subtypes; the more common are densely and sparsely granulated somatotroph adenomas (42). usually, these adenomas are small or medium in size, and gh serum levels are moderate increased; they respond to treatment with long-acting somatostatin analogs. quantification of somatostatin receptors 2 and 5 (sstr2, sstr5) can be useful to predict the response to medical treatment (49): all tumors (gh, tsh, acth, and fsh-lh secreting) with a low sstr2 expression are at a higher risk of resistance to octreotide / lanreotide and those with high sstr5r expression are more likely to respond to pasireotide treatment. this detection is always negative in prl tumors (49). the sparsely granulated somatotroph adenomas are larger and more invasive (proved by mri); this lead to an incomplete resection and in some cases, they are resistant to long-acting somatostatin analog therapy (50). aggressive gonadotroph and thyrotroph pituitary tumors almost all pituitary tumors (up to 97 % in some studies) are immunohistochemical positive for the fsh and/or lh gonadotrophins, even 30–35 % of them are clinically nonfunctioning (do not cause a clinical endocrine syndrome). often those tumors are large invasive macroadenomas, with pressure on the optic chiasm, varying degrees of hypopituitarism; and fsh and lh serum levels which may be elevated or not (51). the clinically nonfunctioning tumors are rarely encountered as aggressive tumors, but can behave aggressively and they were reported cases of clinically nonfunctioning pituitary carcinoma. romanian neurosurgery (2016) xxx 3: 342 355 | 353 the oncocytomas are fsh-lh adenomas with high concentration of mitochondria. the null cell adenomas are tumors immunonegatives for adenohypohysialhormones, they represent only 1% from all pituitary tumors. tsh-producing adenomas are less than 2% of all pituitary adenomas (1, 42, 45). aggressive plurihormonal tumors the silent subtype 3 adenomas are plurihormonal tumors, usually immunohistochemical positive for gh, prl and tsh, with nuclear inclusions called spheridia (electron microscopy revealed). clinically, they are usually silent, but may be associated with hyperprolactinemia, acromegaly or hyperthyroidism. these tumors can also have an aggressive behavior (52). conclusions for pituitary gland, it would be more correctly from oncological point of view (adenoma means benign) to use instead of “atypical” or ”aggressive” adenoma, the term “tumor suspected of malignancy” (tumor grade 2b). there is not a single specific biomarker able to confidently predict the aggressive/invasive behavior for pituitary tumors. the correct histological diagnosis of pituitary adenomas may identify adenomas’ subtypes known as having an aggressive clinical behavior: sparsely granulated somatotroph, acidophil stem cell, silentcorticotroph, with crooke’s cell, thyrotroph or silent subtype 3. there is hope that establishing specific biological markers for invasive process, would became possible an early diagnosis and prevention of invasive pituitary adenomas. because aggressive pituitary tumors are difficult to manage, generally unresponsive to therapy, tend to recur quickly and are associated with poor prognosis, the early diagnosis and the search of new therapeutic approaches is becoming mandatory. references 1.saeger w, lüdecke dk, buchfelder m, fahlbusch r, quabbe hj, petersenn s. pathohistological classification of pituitary tumors: 10 years of experience with the german pituitary tumor registry. eur j endocrinol 2007; 156: 203-216. 2.scheithauer bw, kovacs kt, laws er jr, randall rv. pathology of invasive pituitary tumors with special reference to functional classification. j neurosurg 1986;65:733–744. 3.raju kv, ruby mv. pituitary macroadenoma: a case presentation. kerala j ophthalmol, 2006; 18:58‑60. 4.kovacs k, horvath e. pathology of pituitary tumors. endocrinol metab clin north am 1987; 16:529‑551. 5.riskind pn, richardson ep. clinicopathologic conference‑sn. n engl j med 1986; 314:229. 6.lloyd rv, kovacs k, young jr wf, et al. pituitary tumours : introduction. in: delellis ra, lloyd rv, heitz pu, eng c (eds) tumours of the pituitary, chapter 1. pathology and genetics of tumours of endocrine organs. world hearth organization classification of tumours. iarc press, lyon, 2004; 10–13. 7.knosp e, steiner e, kitz k, matula c. pituitary adenomas with invasion of the cavernous sinus space: a magnetic resonance imaging classification compared with surgical findings. neurosurgery 1993; 33(4):610–617 (discussion 617–618). 8.zada g, woodmansee ww, ramkissoon s, amadio j, nose v, laws re. atypical pituitary adenomas: incidence, clinical characteristics, and implications. j neurosurg 2011; 114: 336-344. 9.thapar k, kovacs k, scheithauer bw, et al. proliferative activity and invasiveness among pituitary adenomas and 354 | moldovan et al diagnostic criteria in invasive pituitary adenomas carcinomas: an analysis using the mib-1 antibody. neurosurgery 1996; 185(38):99-107. 10.rindi g, kloppel g, alhman h, et al. tnm staging of foregut (neuro)endocrine tumors: a consensus proposal including a grading system. virchows arch 2006; 449(4):395–401. 11.thapar k, scheithauer bw, kovacs k, pernicone pj, laws er jr. p53 expression in pituitary adenomas and carcinomas: correlation with invasiveness and tumor growth fractions. neurosurgery, 1996; 38(4):765–770. 12.pernicone pj, scheithauer bw, sebo tj, et al. pituitary carcinoma: a clinicopathologic study of 15 cases. cancer,1997; 79:804-812. 13.scheithauer bw, gaffey ta, lloyd rv, et al. pathobiology of pituitary adenomas and carcinomas. neurosurgery 2006; 59: 341-353. 14.vidal s, kovacs k, horvath e, scheithauer b, kuroki t, lloyd r. microvessel density in pituitary adenomas and carcinomas. virchows arch. 2001; 438:595–602. 15.salehi f, augur a, scheithauer bw, kovacs k, lloyd rv, cusimano m. biomarkers of pituitary neoplasms: a review—part ii. neurosurgery, 2010; 67:1790-1798. 16.harada k, arita k, kurisu k, tahara h. telomerase activity and the expression of telomerase components in pituitary adenoma with malignant degeneration. surg neurol, 2000; 53:267-274. 17.yoshino a, katayama y, fukushima t, et al. telomerase in pituitary adenomas: significance in predicting pituitary adenoma recurrence. j neurooncol 2003; 63: 155-162. 18.vidal s, kovacs k, horvath e, et al. topoisomerase ii alpha expression in pituitary adenomas and carcinomas in relation to tumor behavior. mod pathol, 2002; 15:12051212. 19.hussaini im, trotter c, zhao y, et al. matrix metalloproteinase-9 is differentially expressed in nonfunctioning invasive and noninvasivepituitary adenomas and increases invasion in human pituitary adenoma cell line. am j pathol. 2007;170(1):356-365. 20.alvaro v, levy l, dubray c, et al. invasive human pituitary tumors express a point-mutated alpha-protein kinase-c. j clin endocrinol metab. 1993; 77:1125–1129. 21.sav a, rotondo f, syro lv, et al. biomarkers of pituitary neoplasms. anticancer res 2012;32(11):46394654. 22.van roy f, berx g. the cell-cell adhesion molecule ecadherin. cell mol life sci. 2008; 65:3756-3788. 23.wierinckx a, roche m, raverot g, et al. integrated genomic profiling identifies loss of chromosome 11p impacting transcriptomic activity in aggressive pituitary prl tumors. brain pathol 2011; 21: 533-543. 24.zhang x, horwitz ga, heaney ap, et al. pituitary tumor transforming gene (pttg) expression in pituitary adenomas. j clin endocrinol metab, 1999; 84: 761-767. 25.ruebel kh, leontovich aa, jin l, et al. patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative pcr, and protein expression. endocrine 2006; 29:435-444. 26.kontogeorgos g, sambaziotis d, piaditis g, karameris a. apoptosis in human pituitary adenomas: a morphologic and in situ end-labeling study. mod pathol, 1997; 10(9): 921-926. 27.kulig e, jin l, qian x, et al. apoptosis in nontumorous and neoplastic human pituitaries: expression of the bcl2 family of proteins. am j pathol, 1999; 54(3): 767-774. 28.knosp e, kitz k, perneczky a. proliferation activity in pituitary adenomas: measurement by monoclonal antibody ki-67. neurosurgery, 1989; 25:927-930. 29.yilmaz m, vural e, koc k, ceylan s. cavernous sinus invasion and effect of immunohistochemical features on remission in growth hormone secreting pituitary adenomas.turk neurosurg. 2015;25(3):380-388. 30.knosp e, kitz k, steiner e, matula ch. pituitary adenomas with parasellar invasion. acta neurochir (wien) [suppl], 1991; 53:65-71. 31.salehi f, augur a, scheithauer bw, kovacs k, lloyd rv, cusimano m. ki-67 in pituitary neoplasms: a review—part i. neurosurgery, 2009; 65:429-437. 32.lloyd rv, erickson la, jin l, et al. p27kip1: a multifunctional cyclindependent kinase inhibitor with prognostic significance in human cancers. am j pathol, 1999; 154(2): 313-323. 33.ragel bt, couldwell wt. pituitary carcinoma: a review of the literature. neurosurg. focus. 2004; 16:e7. 34.blevins ls jr, verity dk, allen g. aggressive pituitary tumors. oncology (williston park),1998; 12(9):13071312, discussion 1315-1318. 35.vidal s, kovacs k, bell d, horvath e, scheithauer bw, lloyd rv. cyclooxygenase-2 expression in human pituitary tumors. cancer, 2003; 97(11): 2814-2821. 36.asa sl, bamberger am, cao b, wong m, parker kl, ezzat s. the transcription activator steroidogenic factor1 is preferentially expressed in the human pituitary romanian neurosurgery (2016) xxx 3: 342 355 | 355 gonadotroph. j clin endocrinol metab, 1996; 81: 21652170. 37.tahara s, kurotani r, ishii y, sanno n, teramoto a, osamura ry. a case of cushing’s disease caused by pituitary adenoma producing adrenocorticotropic hormone and growth hormone concomitantly: aberrant expression of transcription factors neurod1 and pit‑1 as a proposed mechanism. mod pathol 2002; 15:1102‑1105. 38.ezzat s, asa sl. the emerging role of the ikaros stem cell factor in the neuroendocrine system. j mol endocrinol 2008; 41(2):45-51 39.trouillas j, girod c. pathology of pituitary adenomas. in: landolt am, vance ml, reilly pl (eds) pituitary adenomas. churchill livingstone, new york, 1996; 27– 46. 40.wolfsberger s, knosp e. comments on the who 2004 classification of pituitary tumors. acta neuropathol, 2006; 111(1):66–67; 10-47. 41.trouillas j. in search of a prognostic classification of endocrine pituitary tumors. endocr pathol 2014; 25:124–132. 42.asa sl. tumors of the pituitary gland. afip fascicle 15/4. 1st ed, washington, dc, usa, 2011; 275. 43.zemoura i, wierinckx vasiljevic a, jan m, trouillas j, francois p. aggressive and malignant prolactin pituitary tumors: pathological diagnosis and patient management. pituitary, 2013; 16:515–522. 44.florian is, ghervan c. opțiuni terapeutice în adenoamele hipofizare. ed. medicală universitară “iuliu hațieganu”, cluj-napoca, 2009. 45.asa sl, ezzat s. the pathogenesis of pituitary tumors. annu rev pathol 2009;4:97-126 46.rotondo f, cusimano m, scheithauer bw, coire c, horvath e, kovacs k. atypical, invasive, recurring crooke cell adenoma of the pituitary. hormones (athens) 2012; 11(1):94-100. 47.assie g, bahurel h, coste j, et al. corticotroph tumor progression after adrenalectomy in cushings disease: a reappraisal of nelson’s syndrome. j clin endocrinol metab, 2007; 92:172–179. 48.cooper o, melmed s. subclinical hyperfunctioning pituitary adenomas: the silent tumors. best pract res clin endocrinol metab, 2012; 26:447–460. 49.chinezu l, vasiljevic a, jouanneau e, et al. expression of somatostatin receptors, sstr2a and sstr5, in 108 endocrine pituitary tumors using immunohistochemical detection with new specific monoclonal antibodies. hum pathol 2014; 45(1):71-77. 50.fougner sl, casar-borota o, heck a, et al. adenoma granulation pattern correlates with clinical variables and effect of somatostatin analogue treatment in a large series of patients with acromegaly. clin endocrinol (oxf) 2012;76(1):96-102. 51.mccutcheon ie, piper dr, fuller gn, benjamin rs, friend ke, gagel rf. pituitary carcinoma containing gonadotrophins: treatment by radical excision and cytotoxic chemotherapy: case report. neurosurgery, 2000; 46:1233–1239. 52.mete o, asa sl. clinicopathological correlations in pituitary adenomas. brain pathol 2012;22(4):443-453 16saurabhjain_traumatic 238 saurabh jain et al traumatic pseudoaneurysm of superficial temporal artery traumatic pseudoaneurysm of superficial temporal artery a case report with review of literature saurabh jain1, vinod sharma2, r.s. mittal3 1resident, department of neurosurgery, sms hospital, jaipur, rajasthan, india 2assistant professor, department of neurosurgery, sms hospital, jaipur, rajasthan, india 3professor and head, department of neurosurgery, sms hospital, jaipur, rajasthan, india abstract superficial temporal artery (sta) pseudoaneurysm is uncommon and usually is the result of trauma to the front temporal region. the appearance of a pulsatile preauricular mass chronologically related to trauma is highly suggestive of the diagnosis. here we discuss a case of trauma to head presented with pseudoaneurysm of frontal branch of temporal artery and its management. key words: trauma, pseudoaneurysm, cerebral angiography, superficial temporal artery. introduction superficial temporal artery is one of the two terminal branches of external carotid artery. it supplies scalp of frontal and parietal region. this artery is one of the most common arteries vulnerable for trauma in scalp injuries due to relatively exposed course over the temporal bone2. few reports are available for development of aneurysm in this artery after trauma. superficial temporal artery (sta) pseudoaneurysm is uncommon and usually is the result of trauma to the front temporal region. the appearance of a pulsatile preauricular mass chronologically related to trauma is highly suggestive of the diagnosis. here we discuss a case of trauma to head presented with pseudoaneurysm of frontal branch of temporal artery and its management. case a 20 year old male with history of trauma to the head causing laceration in frontal region two month back came to our out patient facility with history of pulsatile swelling in left frontal region. on detailed questioning patient revealed that two month back he met an accident while riding a motorbike. he got a lacerated wound over the scalp frontal region. this wound was repaired in emergency department. for about one and a half month patient was doing well when he noticed a pulsatile swelling in his frontal region away from the wound scar. the swelling was progressively increasing in size and pulsatile. on examination there was a healed scar at left frontal region of about 2 cm oriented vertically (figure 1). romanian neurosurgery (2014) xxi 2: 238 240 239 figure 1 figure 2 figure 3 figure 4 there was a swelling in left frontal region about six cm away from the upper margin of scar. the swelling was single, situated in left frontal region of about 1.5 cm length and one cm breadth, pulsatile, warm to touch and compressible. a formal diagnosis of superficial temporal artery aneurysm of frontal branch was made. patient was subjected for ct angiography head with three dimensional reconstructions (figures 2, 3 and 4). ct angiography confirmed the diagnosis. surgical excision of aneurysm with ligation of both ends was done under local anesthesia. discussion superficial temporal artery is a terminal branch of external carotid artery. it is of the most important artery of the scalp. most of the scalp flaps raised for various craniotomies are based on it. it is the sole artery for st-mc bypass procedure. pseudoaneurysm of sta is uncommon with approximately 200 cases reported in the literature (1, 3). 240 saurabh jain et al traumatic pseudoaneurysm of superficial temporal artery bartholin was the first one to report such an aneurysm in 1740 secondary to trauma. the most important cause of this pathology remains to be trauma whether it is war related, contact sports, road accident or iatrogenic1. sta aneurysms are usually solitary though multiple aneurysms following a craniotomy in hemophiliac have been reported. the sta, after originating from the external carotid artery at the base of the parotid gland runs through a relatively exposed course over the temporal bone2. the diagnosis of sta aneurysms can usually be made by history and physical examination. the usual presenting symptom is a pulsating swelling in the temporal region or a throbbing headache. the treatment of sta aneurysms varies from a conservative method such as repeated compression of the lesion to surgical excision of the lesion (2). correspondence: dr. saurabh jain 33, uniara gardens, near trimurti circle, jaipur, rajasthan, india emaildrsaurabh_jain@rediffmail.com mobile+91 9828954850 references 1. cheng ca, southwick eg, lewis ec ii. aneurysms of the superficial temporal artery: literature review and case reports. ann plast surg 1998;40:668-671 2. fox jt, cordts pr, gwinn bc. traumatic aneurysms of the superficial temporal artery: case report. j trauma 1994;36:562-4. 3. porcellini m, bernardo b, spinetti f, carbone f. outpatient management of superficial temporal artery aneurysms. j cardiovasc surg 2001;42:233-236 05_paper romanian neurosurgery (2015) xxix 4: 417 426 417 doi: 10.1515/romneu-2015-0057 small and medium size intracranial aneurysms a 5 years retrospective analysis trial and multimodal treatment valentin munteanu1, mircea radu gorgan2 1ph.d. student in neurosurgery, university of medicine and pharmacy “carol davila” bucharest, faculty of medicine, department of neurosurgery, clinic of neurosurgery, m.d. emergency clinical hospital “bagdasar – arseni” 2professor in neurosurgery md, phd, university of medicine and pharmacy “carol davila” bucharest, faculty of medicine, department of neurosurgery, clinic of neurosurgery; head of department clinic of neurosurgery ,emergency clinical hospital, “bagdasar – arseni”, bucharest abstract: clinical context. subarachnoid hemorrhage (sah) due to rupture of an aneurysm is one of the most common neurosurgical emergencies who account for onethird of stroke .in the sah cases , aneurysms accounted for 70%. aneurysms had a bleeding rate of 12 per 100,000 population per year, and in particular between 50 to 60 years of age with a high morbidity and mortality, especially in the first episode of bleeding at about 43% of cases (1, 4, 14). surgery is indicated to prevent rebleeding. 2.5% of patients in the general population may have unbroken aneurysms with a prevalence of 0.65%, with a preponderance of aneurysms in a 2: 1 in women. aci aneurysms are more common in women and acom aneurysms are more common in men and in 15-30% of patients with presence of multiple aneurysms. surgical timing, the assessment in each individual case for rebleeding usage of endovascular techniques (3, 12), neurological status, the presence or absence of intraparenchymal hematoma or intraventricular hemorrhage with or without vasospasm, have an influence on the result. over a period of 5 years from january 2010 to november 2014, 317 cases of patients with intracranial aneurysms in four clinics of neurosurgery in bagdasar -arseni hospital have been studied. the follow up period range between 6 month and 4 years and 3 month. key words: aneurysm size, sah, timing, microneurosurgery. introduction the authors of this work are concerned with the correlations between small and medium size aneurysms, shape and location and their real risk of bleeding and rebleeding. the data obtained are safe choices for both patient and surgeon in choosing the right surgical technique or for abstention from surgery. nothing replaces clinical judgment (6, 11, 12). 418 munteanu, gorgan small and medium size intracranial aneurysms it is therefore necessary to advice each patient individually. it is necessary to consider and take into account all the variables of the patient life and clinical aspects of current aneurysmal lesions. (size, location, hta, patient age, alcohol, smoking, a history of bleeding drugs, hereditary history, fungal and bacterial infections, comorbidity, cystic kidneys, sex). based on all this information, the individuality of the patient can be appreciate (7, 8). intracranial sacular type aneurysms occur in about 1-2% of the population. intracranial aneurysms are found more and more often with non-invasive imaging acquisition techniques in clinical practice. once an aneurysm is detected unruptered, decisions on the optimal management will be based on careful comparison of shortand long-term risk of rupture of the aneurysm through natural history with risks associated with the intervention itself, whether is open surgery or endovascular technique. several factors should be carefully considered, including the size and location of the aneurysm, family history of the patient and medical history, and the availability of interventional possibilities that has an acceptable risk (9, 13). patient information about having an unruptered intracranial aneurysm can led to stress and cause significant anxiety. is it of utmost importance choosing right treatment type? controversy remains regarding the optimal management and detailed assessment of the risks and benefits for the patient. benchmarking with other similar studies will enable us to ensure correct positioning among other neurosurgical departments. for example: description of 128 patients with subarachnoid hemorrhage parameter n = 128 age (mean years ± sd) 53.1 ± 12.1 hunt and hess grades grade 1 47.3% grade 2 20.5% grade 3 18.1% grade 4 14.2% aneurysms identified 74.2% acoma 30.5%, mca 22.7%, aca 13.3%, ophthalmic artery 4,7% ba 4.7% pica 1.6% sca 0,8% va 2,3% multiple aneurysms 6,2% fisher grades (n = 125) grade 1 10% grade 2 46% grade 3 17% grade 4 27% hydrocephalus on admission 35.9% recurrent hemorrhage 7.8% surgery 64.1% coil embolization 9.4% temporary clipping during surgery 28% aca = anterior cerebral artery, acoma = anterior communicating artery, ba = basilar artery, mca = middle cerebral artery, pica = posterior inferior cerebellar artery, sca = superior cerebellar artery, sd = standard deviation, va = vertebral artery. data from three patients are missing. journal of clinical neuroscience 16 (2009) 1409–1413 clinical study the prediction of long-term outcome after subarachnoid hemorrhage as measured by the short form-36 health survey wolfram scharbrodt, matthias f. oertel* department of neurosurgery, university hospital giessen, klinikstrasse 29, giessen 35385, germany clinical material and method this study is dedicated to small and medium intracranial aneurysms. the study covers a period of 5 years between january 2010 and november 2014, using the neurosurgery clinics of the bagdasararseni hospital experience data. is a retrospective study including 317 patients romanian neurosurgery (2015) xxix 4: 417 426 419 doi: 10.1515/romneu-2015-0057 admitted into the hospital. our intention is both to establish the variability of cases in our clinic departments, and effectiveness of used therapeutic methods, with real benefit for the patient an attempt to establish an effective therapeutic algorithm. the observation period varies between 24 hours and 4 years and 3 month. between studied patients, because some of them overturned surgery, others were transferred to other hospitals or just could not follow any data, had been excluded 27 patients. the study comprises 317 patients from whom correct data have been achieved. in this group are 185 women account for 58.3%, 132 men -41.7% with ages between 29 and 82 years old. the symptoms for this patients at presentation are extremely variable, from almost asymptomatic patients, mild transient headaches, cranial nerve and motor deficits up to coma gcs = 3p. scaling system and evaluating patients are according with international systems: glasgow coma scale, scale wfns, hunt & hess scale, glasgow outcome scale, motor deficits asia fisher scale. classification of vascular lesions is of international usage: size: microaneurysms <2 mm, small ø = 2-7mm, medium ø =712mm, large ø = 13-24mm, huge ø> 25mm aneurysms by form: saccular (berry), fusiform, dissecting (pseudo-aneurysms). 240 of the cases studied, presents on admission with bleeding phenomena such as subarachnoid hemorrhage accounting for 75.70%. depending on the severity were assessed by glasgow coma scale (figure 1). figure 1 neurological status assessed by gcs scale figure 2 sah cases assessed by hunt & hess scale table 1 neurological status at admission in sah patients nr pacienti 109 149 13 32 14 h&h 1 2 3 4 5 the 317 patients have been studied by imaging technique at their admission in the hospital. the main investigation was cerebral angiography (figure3, 4), generaly achieved after 24 hours but in some cases angio ct with or without 3d reconstruction (figure 5, 6) – cases were the catheter could not be inserted into the internal carotid artery, mri with angio mri in unruptured aneurysms (figure 7, 8). 420 munteanu, gorgan small and medium size intracranial aneurysms figure 3 ant. comm. artery aneurysm figure 4 anterior communicating artery aneurysm with daughter sac figure 5 ct angiographyshowing right posterior communicating artery aneurysm figure 6 ct angiogram 3d left sylvian aneurysm romanian neurosurgery (2015) xxix 4: 417 426 421 doi: 10.1515/romneu-2015-0057 figure 7 mriinternal carotid artery aneurysm figure 8 mr angiography-multiple aneurysms results a series of 237 aneurysms with various locations have been described. from all, 27 cases were multiple intracranial aneurysms. among multiples diagnosed, 21 aneurysms were with 2 aneurisms, and 6 cases with more than two -with a maximum of 8 aneurysms (rm, female 39 years old, addressed in 2013 sah, h & h = 1, gcs = 15, fisher ct = 1, cerebral angiography 4 vessels: 1) saccular mca right aneurysm ø max = 4, 95 mm and neck = 6,94 mm 2) ophthalmic right artery microaneurysm, 3) internal carotid aneurysm left sausage-like section c7)4)5) two aneurysms segment c6 left, 6) posterior communicating artery microaneurysm left 7) basilar bifurcation aneurysm size ø = 1, 78 mm neck = 1.37 mm 8) anterior communicating artery aneurysm size neck = 2,7 mm ø = 2,13 mm – mca aneurysm wrapping technique used). depending on the type of lesion discovered after investigations, especially after the angiography, management has been adapted as follow (table 2). table 2 various procedure for treatment treatment type surgery clipping wrapping endovascular evd no cases 79 7 63 16 surgical procedure in 86 selected patients. for each patient the operation was adjusted depending on the aneurysm location. most frequently used approaches were pterional, frontopterional, suboccipital for posterior fossa lesions. 422 munteanu, gorgan small and medium size intracranial aneurysms site and size of the aneurysm, but also the neck direction contribute for the procedure used. intraparenchymal hematoma, accompanying lesions, multiple aneurysms led to the modification of approaches. in all cases, we have used optical magnification systemssurgical microscope. unruptured aneurysms are more easily to dissect (figure 9). figure 9 intraoperative image-unruptured aneurysm intraoperative capture using leyca microscope: figure 10 intraoperative image – aneurysm after clipping the clips are very effective in taking out an aneurysm (figure 10). regrowth of an aneurysm after an adequate clipping is as small as 1%. this is one of the biggest advantages over endovascular coiling. in addition, after clipping only one angiographic follow-up is required. the main disadvantage of the clipping is of course the brain operation itself (including scarring, infection, bleeding) and the risk of brain damage. once the clip in place and the aneurysm secured, the patient is considered cured (figure 11). if the treatment of an aneurysm by means of an endovascular approach (coiling) is not possible the aneurysm should be clipped (figure 12). figure 11 small 3,5 mm aneurysm clipped figure 12 tools for aneurysms treatment romanian neurosurgery (2015) xxix 4: 417 426 423 doi: 10.1515/romneu-2015-0057 surgery is a more traditional treatment of cerebral aneurysms which, has proven its effectiveness and safety. the aneurysm is dissected and the neck closed with a titanium clip (figure 13). surgery is safe and has a low risk in small aneurysm -5% complication rate. figure 13 postoperative result for a larger aneurysm or an aneurysm located in an eloquent area or brain stem the risk of the operation is much higher (20 to 30% complication). a number of 38 cases of total has died. 16 of cases studied, refused treatment.19 of cases are worsening during admittance and have been discharged following families request. between latest, 3 cases after endovascular treatment and 5 cases after surgery and two cases in which dve has been installed. in 9 cases any kind of intervention has been applied. description of selected 116 cases for the comparative study with subarachnoid hemorrhage (figure 14). figure 14 brain ct showing subarachnoid hemorrhage from a ruptured posterior cerebral artery aneurysm 424 munteanu, gorgan small and medium size intracranial aneurysms table 3 a number of 116 cases selected in our study with complete clinical data parameter n=116 age (mean years ± sd) 53.1 ± 12.1 age 56,5 sex 68 pac 48 pac female 58,3 % male 41,7 % hunt and hess grades grade 1 79 cases 68,1 % grade 2 15 cases 13 % grade 3 5 cases 4,3 % grade 4 17 cases 14,65 % aneurysms identified 87 cases with aneurvsm 75% from total. acoma 20 cases 23% mca 21 cases 24,1% ophthalmic artery 4 cases 4,5 % ba 4cases 4,5 % pica 8 cases 9,1 % ica 23 cases 26,43% post. com . 3 cases 3,44% post. 6 cases 6,89% multiple aneurysms 10 cases 3 cases 8,6 % 2,5 % more than 2 fisher grades grade 1 12 cases 13,79 % grade 2 8 cases 9,19% grade 3 15 cases 17,24% grade 4 26 cases 29,88 % hydrocephalus on admission 28 cases 32,18 % recurrent hemorrhage 4cases 4,59 % surgery 29 cases 33,33% coil embolization 23 cases 26,43% temporary clipping during surgery 15 cases 17,24 % aca = anterior cerebral artery, acoma = anterior communicating artery, ba = basilar artery, mca = middle cerebral artery, pica = posterior inferior cerebellar artery, sca = superior cerebellar artery, sd = standard deviation, va = vertebral artery. aci internal carotid, a com post-post. comm, a cerebrala post posterior cerebral discussions aneurysms must be occluded fast in order to make an immediate and aggressive treatment of symptomatic vasospasm to have a proper neurological recovery and prevent infarction. intraoperative aneurysm rupture, feeding artery occlusion, cerebral contusion due to brain retraction, intracerebral hematoma evacuation, necessary decompression lobectomy, inexperienced surgeon, are factors for inadequate technical surgery and bad outcome (2, 5, 12). aneurysm size, location, morphology, calcified necks associate a poor prognosis and postoperative complications, even for patients with a favorable prognosis class. they can also have neuropsychological deficits, cognitive inpairement, after surgery (12, 13). special circumstances like patients with advanced age, very young age, posttraumatic or mycotic aneurysms, pregnant women, the romanian neurosurgery (2015) xxix 4: 417 426 425 doi: 10.1515/romneu-2015-0057 association of aneurysms with arteriovenous malformation, fusiform aneurysms or micro aneurysms must be treated with caution. surgical concept and decision making: interventional endovascular department development, has changed the management of the emergencies with subarachnoid hemorrhage (10, 11). unruptered intracranial aneurysm cases diagnosed outside the hospital after preliminary noninvasive investigations change the natural history of aneurysms and course of treatment (8, 9). in the study carried out (table 3), 81% rate of all patients underwent cerebral angiography within 24 hours of admission and 30% of patients undergoing endovascular intervention within 48 h of admission. for the decision on microsurgery in the first 48 hours of hospitalization for subarachnoid hemorrhage cases operability percent rising from 2% with an increase between the 5th and the 14th day to 91% of cases. in the remaining 7% of patients, surgery was performed over 14 days. the serious condition of the patient with subarachnoid hemorrhage requires rapid hospitalization, pace of investigation and decision making timing (14). aneurysms type and location, angiographicaly confirmed vasospasm with clinical expression, neurological status prior consultation between the surgeon and interventional radiologists will make the decision for individually kind of treatment. it has been estimated that nearly 3% of the population may develop an aneurysm. at the moment the angio-mri can set non-invasive diagnosis of brain aneurysm by population screening (4, 5). as a result one could expect in the coming years, a large number of patients with intracranial aneurysms diagnosed and for that, a decision on the treatment must be taken. to this end, a reliable estimate risk of intracranial aneurysm natural history and treatment risk should be available. intracranial aneurysms unruptured international studies (isuia) published in 2003 attempted to get light in this field and shows that the cumulative risk over a period of 5 years from a previous ruptured aneurysm ø <7 mm is 0%.is this the right conclusion or is it wrong? patients with subarachnoid hemorrhage are usually in a very serious clinical condition and associate other factors, such as hypertension, diabetes, vascular degenerative diseases, vasospasm and other medical complications (9). this co-morbid changes lead to surgery complications and postoperative sequelae and so, prolonging time for returning to family life and intellectual abilities previously had. international studies (isat), a randomized trial comparing results of surgery with endovascular interventions in the treatment of aneurysms had been published in the lancet in 2002. the results showed that the endovascular treatment is less risky (6.9 percent) than open surgery. these results are informative, but they must be interpreted with caution, since the study was the first of its kind and patient follow-up was short, for only one year. long-term results of endovascular treatment was not yet been established. in terms of open intervention study showed no difference in mortality rate between microneurosurgery and embolization. therefore, the superiority of one treatment over the other, had no definitive conclusion at that time (10). a recent study largest, showed that for ruptured aneurysms who have indication for 426 munteanu, gorgan small and medium size intracranial aneurysms both, microsurgery and endovascular treatment, patients who underwent endovascular treatment had better results, at least in the short term. (rate of death or disability at one year is 23.5 percent, compared with 30.9). how can you decide which procedure is best for a brain aneurysm? the treatment of choice for aneurysms, like all medical decisions should be agreed between doctor and patient. if it is unruptured or ruptured aneurysms, the doctor should discuss the risks and benefits of each treatment option (13). the doctor will usually recommend one treatment or another, depending on the individual case .since here we are speaking about small and medium size aneurysms , and all data in this study show that good results can be obtained after accurate surgery we advise this kind of treatment over endovascular procedures especially for emergency cases and a very good selection of cases for unruptered aneurysms. conclusions although controversy over the best treatment option for some patients remain unresolved both surgical and endovascular treatment options as viable treatment options in the management of cerebral aneurysms today. outcome of patients depend largely from team experience. if both departments are available, surgical and endovascular, the patient can benefit from individualized treatment and real chances to be healed. references 1. connolly es jr, et al. guidelines for the management of aneurysmal subarachnoid bleeding: a guide for health professionals from the american heart association / american stroke association. stroke. published online 3 may 2012. 2. morgenstern lb et al. guidelines for the management of spontaneous intracerebral hemorrhagic. stroke, 41 (9): 2108 2129,2013. 3. weir b. unruptured intracranial aneurysms: a review. j neurosurg.;96:3-42, 2002. 4. wiebers do, whisnant jp, huston j iii, et al, international study of unruptured intracranial aneurysms investigators. unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. lancet; 362: 103110, 2003 5. wardlaw jm, white clock. the management of unruptured intracranial aneurysms and recognition. brain.; 123 (pt 2): 205-218,2000. 6. s. takahashi neurovascular imaging, mri & microangiography. springer verlag. isbn: 1848821336th,2010. 7. wiebers do, whisnant jp, huston et al j. ruptured intracranial aneurysms: natural history, clinical findings and surgical and endovascular treatment of risks.; 362 (9378): 103-10. lancet. 2003 8. makio kaminogo, masahiro yonekura, shobu shibata. incidence and outcome of multiple intracranial aneurysms in a defined population. stroke;34;1621,2003 9. ropper ah, samuels ma. cerebrovascular diseases. in adams and victor's principles of neurology, 9th ed., pp. 746-845. new york: mcgraw-hill. 2009 10. winn hr, mk rosner, campbell va. youmans neurological surgery. 6th edition. saunders 2011 11. raaymakers tw, rinkel gj, limburg m, algra a. mortality and morbidity of unruptured intracranial aneurysms for surgery: a meta-analysis. stroke.; 29 (8): 1531-8, august1998. 12. quinones-hinojosa 12 a. schmidek and sweet: operational neurosurgical techniques: notes 6th edition. saunders, 2012 13. choi ds, mc kim, lee sk, willinsky ra, terbrugge kg.clinical and angiographic long-term follow-up of completelycoiled using intracranial aneurysms endovascular technique. j neurosurg.112 (3): 575-581, march 2010 ellamushi he, grieve jp, jager hr, kitchen nd.risk factors for the formation of multiple intracranial aneurysms. j neurosurg; 94: 728 –732, 2001 doi: 10.33962/roneuro-2021-004 management of a double basilar tip aneurysm a. chiriac, n. dobrin, georgiana ion, i. poeata romanian neurosurgery (2021) xxxv (1): pp. 25-28 doi: 10.33962/roneuro-2021-004 www.journals.lapub.co.uk/index.php/roneurosurgery management of a double basilar tip aneurysm a. chiriac1, n. dobrin2, georgiana ion2, i. poeata1 1 “gr. t. popa” university of medicine and pharmacy, iasi, romania 2 “n. oblu” emergency clinical hospital, iasi, romania abstract complex basilar tip aneurysms are still challenging to secure with coils or stentassisted coiling. double aneurysms at the basilar bifurcation and the basilar arterysuperior cerebellar artery are a rare particular situation that usually requires more appropriate treatment. this case reports details of our experience with a double basilar tip aneurysm treated in two steps by coiling repair and stent-assisted coiling. introduction the basilar tip aneurysm (bta) is still represents a real challenge for a microsurgical approach due to the deep location and proximity to delicate neuro-vascular anatomical structures. thus, endovascular techniques remain the most commonly used option for the treatment of these lesions. a double basilar tip aneurysm is a very complex lesion usually characterized by a wide neck that often involves the origins of more vascular branches. this special vascular pathological condition makes even endovascular treatment a major challenge for most interventionists. in such cases, usually preservation techniques using a stent(s) or balloon can be attempted for a one or two steps intervention. therefore, a proper diagnosis of these double aneurysms and an optimal technique selection are the most important facts in achieving complete obliteration of these lesions. in this paper we intended to report our experience with such rare case of double basilar tip aneurysm successfully treated while reviewing the literature to improve the understanding of this particular clinical situation. case presentation a 38-year-old man was addressed to our emergency room from a service in another hospital on 31 december 2020. a head ct exam in ation at th e lo cal h o s pi tal s u gg es ted fis h er grade 3 subarachnoid haemorrhages and the contrast administration revealed a complex basilar artery aneurysm. the patient was transferred to our hospital for further diagnosis and treatment. at admission patient presented severe headache accompanied by episodes of nausea and keywords double basilar tip aneurysm, stent-assisted coiling corresponding author: a. chiriac “n. oblu” emergency clinical hospital, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 26 a. chiriac, n. dobrin, georgiana ion, i. poeata vomiting. the patient had a ten-year history of multiple sclerosis and hypertension with regular treatment. a ruptured large basilar tip aneurysm was confirmed on brain ct angiography, and subsequent subtraction catheter cerebral angiography confirmed a double basilar tip aneurysm at the basilar bifurcation and the basilar artery-superior cerebellar artery junction. a two steps aneurysms embolization treatment was decided. based on predominant haemorrhage location and aneurysms characteristics the basilar artery-superior cerebellar artery junction aneurysm was considered the ruptured one. under general anaesthesia, 6f merit medical introducer sheath was placed into the right femoral artery. using biplane roadmap fluoroscopy a 6f chaperon guiding catheters (microvention) were advanced over 0.035 glidewire up to the mid-v2 portion of the left vertebral artery. based on 3d ct images analysis a working angle roadmap for the target aneurysm was obtained. a prowler 10 microcatheter was then advanced over a 0.014 transed microwire (boston scientific) into the basilar artery-superior cerebellar artery junction aneurysm to allow placement of coils inside the aneurysm dome. five galaxy g3 xsft microcoils (cerenovus johnson&johnson) were then sequentially inserted and detached into aneurysm. on final angiography, both pcas were fully saved and the aneurysm was completely packed. the patient was placed into intensive care and received 75mg clopidogrel and 100mg aspirin daily. figure 1. a first head ct examination at the local hospital showing a sah; b brain ct angiography revealing a double basilar tip aneurysm; c – cta 3d reconstruction; d – dsa in working projection; e – dsa control after basilar artery-superior cerebellar artery junction aneurysm coil occlusion. after 7 days a second endovascular intervention was decided for associated unrupted basilar bifurcation aneurysm occlusion. a chaperon guiding catheters (microvention) was passed to the right femoral artery and securely advanced up to the half-v2 segment of the left vertebral artery. to pass an enterprise 2 stent a b c d e 27 management of a double basilar tip aneurysm (4/23mm), a prowler select plus microcatheter (codman &shurtlett, inc.) was carefully inserted into the right pca under the guidance of a 0.014 transed microwire. the stent was deployed over the pcom/pca junction point and both aneurysms necks. the prowler select plus microcatheter is than retracted and a prowler 10 microcatheter is advanced into the basilar tip aneurysm through the stent using a 0.014 transed microwire. three galaxy g3 xsft microcoils were used for complete angiographic occlusion of the aneurysm. the patient was safely returned to intensive care and antihypertensive therapy, antiplatelet therapy, volume expansion therapy, and medication for the prevention of vasospasm were continued. the patient recovered without any complications, and was discarded home 10 days later. he is currently under follow-up as an outpatient. figure 2. a – microcatheterization of right pca for stent placement; b,c – dsa control after stent detachment and trans-stent coil embolization of basilar bifurcation aneurysm. discussion the basilar tip aneurysm is most commonly associated with a complex anatomical configuration. the main pitfall in the treatment of a basilar tip aneurysm consists in the presence of thalamoperforating arteries and numerous vascular branches in relation with a wide-neck or polylobated aneurysmal dome. presence of a double basilar tip aneurysm at the basilar bifurcation and the basilar artery-superior cerebellar artery junction is a more complex treatment condition. tanaka et al reported in 2001 the incidence of double basilar tip aneurysm as 5.3% and concluded that they were not extremely rare if accurately diagnosed by the use of modern techniques[4]. at the same time, hernisniemi in an analysis of the article on double basilar aneurysms reported a much lower incidence of them (3 cases of double basilar aneurysms from a total of 112 patients)[2,3,4]. due to a high reported morbidity of surgical clipping for basilar tip aneurysm, endovascular interventional therapy became commonly used for majority of these clinical situations. for complex basilar tip aneurysm several endovascular techniques such as stent assisted coiling, waffle cone technique and balloon remodelling can be used to increase aneurysm packing during aneurysm coiling [1]. the technique of balloon-assisted coil embolization, firstly introduced by moret et al., even if it initially showed a high rate of aneurysmal occlusion, many delayed coil compaction and aneurysm recurrence were reported in time.[4,5] the emergence of various stent assisted coiling has offered a safe and effective clinical solution for this type of complex wide-necked bifurcation aneurysm[1,2,3]. these techniques provide scaffolding for stable and dense coil embolization and blood flow diversion effect away from aneurysm. the most representative stent remodelling techniques in coil embolization of basilar apex aneurysms include classical curvilinear stenting technique, double y-stenting technique, and waffle cone technique. the waffle-cone technique first reported by horowitz et al has proved in time a satisfactory protection of the parent arteries origins but not an optimal blockage of the aneurysmal neck. y-stent assisted coiling technique firstly proposed by chow et al. in 2004, showed a good clinical prognosis for the treatment of basilar tip aneurysm by 28 a. chiriac, n. dobrin, georgiana ion, i. poeata effectively reduction of the aneurysmal neck, protection of the parent arteries and by changing the angle of the blood vessels at the bifurcation. even if the y stent configuration has many advantages, it also has several important disadvantages represented by potential thrombus formation and the need for long-term application of double antiplatelet agents. the thrombotic complications associated with this procedure were reported in literature to be approximately 2-21.4%[4,6]. given the above, there is clear evidence that the single stenting technique associated to basilar tip aneurysms coil occlusion is much easier and with much lower morbidity rates than the double stenting technique. representative unique stent remodelling techniques of the basilar apex include a curvilinear or horizontal implant positioning. treatment of basilar tip aneurysms by horizontally stenting was firstly described by cross and colab. they used a unique retrograde approach with horizontally stent deployment to both p1 segments perpendicular to the aneurysm, using the ica-pcom route[2,3,4]. this approach is completely dependent on the tortuosity and size of the posterior communicating artery. in case of the double basilar apex aneurysms that implicate also the basilar artery-superior cerebellar artery junction, the horizontal stent deployment must start from arterysuperior cerebellar artery to cover the both aneurysms neck. our experience as well as the few data reported in the literature has shown that single curvilinear stenting is the most optimal technique in the treatment of double basilar apex aneurysms. this consists of positioning a stent from the p1 segment opposite the junction aneurysm (ba-pca) over the necks of both aneurysms to the distal segment of the basilar trunk. however, the stent placement strategy is also determined by a precisely differentiation of a double basilar aneurysm from a bilocular aneurysm at the basilar apex pre-intervenionally. conclusion double wide-neck basilar tip aneurysms are a challenge to repair, but the unique stent assisted coiling technique is proved to be quite effective whether performed in one or two separate sessions. references 1. ahmad s. basilar tip aneurysm in takayasu arteritis. bjr case rep. 2019 nov 15;5(4):20180114. doi: 10.1259/bjrcr.20180114. pmid: 31938555; pmcid: pmc6945252. 2. drake cg, peerless sj, hernesniemi ja: surgery of vertebrobasilar aneurysms: london, ontario, experience on 1,767 patients. vienna, springer-verlag, 1995, p 251. 3. hernesniemi j. double aneurysms at distal basilar artery: report of nine cases. neurosurgery. 2001 jul;49(1):229231. doi: 10.1097/00006123-200107000-00048. 4. hongo, k., tanaka, y., & kobayashi, s. (2001). double aneurysms at distal basilar artery: report of nine cases: in reply. neurosurgery, 49(1), 230-231. 5. tanaka, y., hongo, k., nagashima, h., tada, t., & kobayashi, s. (2000). double aneurysms at distal basilar artery: report of nine cases. neurosurgery, 47(3), 587593. 6. sekhar ln, tariq f, morton rp, ghodke b, hallam dk, barber j, kim lj. basilar tip aneurysms: a microsurgical and endovascular contemporary series of 100 patients. neurosurgery. 2013 feb;72(2):284-98; discussion 298-9. doi: 10.1227/neu.0b013e3182797952. pmid: 23147787. 4gorganrm_unilateralextended 38 gorgan et al unilateral extended suboccipital approach for a c1 dumbbell schwanoma unilateral extended suboccipital approach for a c1 dumbbell schwanoma r.m. gorgan, angela neacşu, a. giovani clinical emergency hospital “bagdasar arseni”, bucharest abstract: craniovertebral junction tumors represent a complex pathology carrying a high risk of injuring the vertebral artery and the lower cranial nerves. dumbbell c1c2 schannomas are very rare tumors in this location. we present a case of a 66 years old male accepted for left laterocervical localized pain, headache and vertigo, with a large c1 dumbbell schwannoma extending in lateral over the c1 arch and displacing the c3 segment of the vertebral artery superiorly and anteriorly. complete removal of the tumor was achieved using a far lateral approach. the approach is discussed with focus on the vertebral artery anatomy as the approach should give enough space to gain control of the artery without creating instability. safe removal of c1 nerve root schwanomas can be achieved even if they compress and displace the vertebral artery by entering a fibrous tissue plane between the tumor and the vertebral artery. key words: dumbell schwanoma, craniocervical junction, far lateral. introduction meningiomas and chordomas are the most frequent pathology at the level of the craniocervical junction. even if scwanomas represent 5-10 % of all intracranial tumors most of them being located on the vestibular nerve, their location at the craniospinal junction is quite rare. [1] with the rapid advancing of neurosurgical technology the goal of resecting these tumors shifted from lowering mortality to lowering morbidity and preservation of the vascular and nervous elements involved by the tumor [2, 3]. most sudies report using some variant of far lateral approach for removal of these tumors as it gains access to the posterior, lateral and anterolateral aspect of the foramen magnum, the upper cervical spinal canal and even the clivus where the lesion has an important anterior extension. [4, 5] case presentation a 66 years old male presented for left laterocervical localised pain, headache and vertigo. he showed no motor or sensitive impairment on neurological exam. a contrast mri showed a dumbell gadolinophil tumor with a 3,3 cm largest diameter located extradurally inside the spinal canal with romanian neurosurgery (2015) xxix (xxii) 1: 38 42 39 extension outside the canal above the c1 arch. the tumor displaced superiorly the vertebral artery. (figure 1) figure 1 t1 mri with contrast showing a large filling tumor extending laterally from the spinal canal, displacing anteriorly and superiorly the vertebral artery which feeds the tumor through a few small branches an angiography showed that the tumor was highly vascularized, injected from the vertebral artery and the displacement and narrowing of the v3 portion of the vertebral artery. as no other comorbidities were encountered the patient was accepted for surgery. surgical technique the patient was positioned prone with the head slightly rotated to bring the lesion closer to the surgeon, flexed and fixed with tape to the horseshoe headrest. the table is than flexed to place the lesion higher in the operating field. a hockey stick incision centered on the lesion was used to access the craniospinal junction starting from the c4 over the midline, curved over the superior nuchal line and ended over the mastoid. 40 gorgan et al unilateral extended suboccipital approach for a c1 dumbbell schwanoma the posterior neck muscles are detached from the occipital bone leaving a muscle cuff on the superior nuchal line and the paravertebral muscles are skeletonized bilateral from c1 to c3. a suboccipital craniectomy extended to the left occipital condile and a posterior c1 arch resection were performed in order to gain access and control to the vertebral artery before it pierces the dura. the operative microscope was introduced at this step of the surgery. a well encapsulated 2/3 dumbell shaped, redisch tumor is seen over the c2 vertebral arch and pushing on the vertebral artery. the tumor was firm and elastic and appeared to have developed from the c1 nerve steath. the tumor was covered by fibrous attachments and dissecting it from these created a superior clavage plane. a cottonoid introduced in these plane protected the vertebral artery over the rest of the surgery. after the internal debulking the tumor is than circumferentially dissected to see the c1 nerve entering and exiting the tumor .the tumor was completely resected using a distal and a proximal cut in the nerve. in order to avoid a csf fistula, the nerve was ligated before the proximal cut. (see figure 2) as the tumor was extradural there was no need to open the suboccipital dura. no fixation was needed as the bone resection did not include the occipital condile. hemostasis from muscles was achieved with the bipolar and saline solution and tight muscles and fascia suture was performed. the postoperative course was uneventful and the patient did not complain of the headache and cervical pain. a the ferm tumor was detached from the surrounding fibrous adherences and internally debulked b a branch from the vertebral artery irigating the tumor was coagulated and disected and a cottonoid was inserted over the superior aspect of the tumor to separate it from the vertebral artery romanian neurosurgery (2015) xxix (xxii) 1: 38 42 41 c the c1 nerve root was sectioned imediatelly lateral to the tumor. and then the proximal c1 nerve root was ligated and cut d total tumor removal figure 2 intraoperative images – total tumor resection discussions in order to access the lesions coming in relation to the v3 segment of the vertebral artery different teams reported a few positions, including the park bench position, the lateral decubitus position (half and half), three qarter prone and supine position with the head turned towards the lesion. in our department we use the supine position with a roll under the shoulder and the head slightly flexed and turned to the side of the lesion and fixed with tape in a horseshoe. [8, 11] the head rotation is not always adviced as it may change the relation of the vertebral body to the tumor by stretching it, and enough space can be gained in a neureal position with enough bone removal and turning the table opposite to the surgeon. some authors prefer an s shape incision but we like using the hockey stick incision as we can better identify the bony landmarks which are very useful in identifying the vertebral artery. the disadvantage of this approach is that the view can be obstructed by the bulk of muscles especially when a more lateral trajectory is chosen. [6, 10] the classic far lateral approach is a suboccipital craniectomy including the margin of the foramen magnum which extends lateral and anteriorly to the occipital condile. the bone resection includes the site where the vertebral artery enters the dura, so removing the bone in the area of the foramen magnum is the essential part of the craniectomy. the last part of the craniectomy near the occipital condile should be drilled as it becomes vertical and can’t be removed with the cloward. care should be taken not to injure the posterior emissary condilar vein in the condilar fossa. bleeding from this vein can 42 gorgan et al unilateral extended suboccipital approach for a c1 dumbbell schwanoma be important in tumors of the craniovertebral junction as was the case here, because it is the communication between the sigmoid sinus and the perivertebral venous plexus. in our approach we identified than coagulated, ligated and dissected this vein. we hold the opinion of other authors that opening the mastoid air cells should be avoided as this increases the risk of postoperative csf fistula. as the schwanoma in this case was attached to the vertebral artery and by the suboccipital craniectomy and by removing the arch of the c1 there was no need for condyle resection. in order to avoid injuring the vertebral artery over the atlantal arch we palpated the posterior margin of the arch becoming thin and sharp under the vertebral artery. [9] the main complications that could be encountered using this approach were injuring the vertebral artery which was intimately attached to the superior part of the tumor and having a csf fistula. both of them were prevented, the second by ligating the c1 nerve and sectioning it between the ligature and the tumor, and the first was prevented by early identifying the vertebral artery and dissecting it up to the point where it pierced the dura and by creating a dissection plane in the fibrous plane between the vertebral artery and the dura and protecting the artery with a cottonoid during the tumor resection. as craniovertebral junction instability can appear with extended resections, we avoided removing the occipital condyle and the resection of the posterior arch was stopped at the medial margin of the vertebral artery. performing a careful multilayer closure of the muscles of fascia is important to avoid having postoperative csf leaks. conclusions this case report shows that c1 nerve root schwanomas even if they compress and displace the vertebral artery can be safely removed by entering a fibrous tissue plane between the tumor and the vertebral artery. references 1. arnautovic ki, al-mefty o, husain m: ventral foramen magnum meningiomas. j neurosurg 92:71-80, 2000 2. banerji d, behari s, jain vk, pandey t, chhabra dk: extreme lateral transcondylar approach to the skull base. neurol india 47:22–30, 1999 3. bertalanffy h, gilsbach jm, mayfrank l, klein hm, kawase t, seeger w: microsurgical management of ventral and ventrolateral foramen magnum meningiomas. acta neurochir suppl (wien) 65:82–85, 1996. 4. goel a, desai k, muzumdar d: surgery on anterior foramen magnum meningiomas using a conventional posterior suboccipital approach: a report on an experience with 17 cases. neurosurgery 49:102–107, 2001. 5. hakuba a, komiyama m, tsujimoto t, ahn ms, nishimura s, ohta t, kitano h: transuncodiscal approach to dumbbell tumors of the cervical spinal canal. j neurosurg 61:1100–1106, 1984. 6. hida k, iwasaki y, seki t, yano s: two-stage operation for resection of spinal cord astrocytomas: technical case report of three cases. neurosurgery 58:ons-e373, 2006. 7. hori t, takakura k, sano k: spinal neurinomas: clinical analysis of 45 surgical cases. neurol med chir (tokyo) 24:471–477, 1984 8. mccormick pc: surgical management of dumbbell tumors of the cervical spine. neurosurgery 38:294–300, 1996. 9. rhoton al jr: the far-lateral approach and its transcondylar, supracondylar, and paracondylar extensions. neurosurgery 47[suppl 3]:s195–s209, 2000. 10. samii m, klekamp j, carvalho g: surgical results for meningiomas of the craniocervical junction. neurosurgery 39:1086–1095, 1996. 11. sen cn, sekhar ln: an extreme lateral approach to intradural lesions of the cervical spine and foramen magnum. neurosurgery 27:197–204, 1990. turliucdana_ararecase 52 turliuc et al suprasellar arachnoid cyst with giant perimesencephalic extension a rare case of suprasellar arachnoid cyst with giant perimesencephalic and mesial temporal extension physiopathological mechanisms dana mihaela turliuc1,2, a.i. cucu2, b. dobrovăț1,2, daniela trandafir1,3, ş. turliuc1, gabriela florența dumitrescu2, claudia florida costea1,2 1“grigore t. popa” university of medicine and pharmacy iasi, romania 2“prof. dr. n. oblu” emergency clinical hospital iasi, romania 3“sf. spiridon” emergency clinical hospital iasi, romania abstract: the arachnoid cyst is a lesion commonly encountered in neurosurgery, especially in pediatric pathology. we are presenting the case of an adult patient with a suprasellar arachnoid cyst with giant perimesencephalic and mesial temporal extension discovered incidentally, where there is a discrepancy between the spectacular neuroimaging and the non-specific symptomatology. some of the physiopathological mechanisms which led to the evolution of the cyst will also be presented. key words: giant arachnoid cyst, sellar cyst, enlargement basal cisterns background the arachnoid cyst (ac) is a congenital collection of cerebrospinal fluid (csf) contained within the arachnoidal membrane and the subarachnoid space (21, 27, 28). the first case of ac to be described was located in the middle cranial fossa and was published for the first time in 1831 by the english physician richard bright (1789-1858) (24), best known for his studies on kidney diseases (bright’s albuminuric nephritis). bright defined ac as “serous cysts forming in connection with the arachnoid and apparently lying between its layers” (7). the incidence of ac ranges between 0.2 and 1.7% (11, 20, 22, 38, 37), but is continuously growing due to the increasing use of magnetic resonance imaging (mri) and computed tomography (ct) (2, 37, 38). moreover, some studies report an incidence of 2.6% (3). most arachnoid cysts (acs) are diagnosed incidentally after imaging explorations such as ct or mri after a mild head injury (26). the predominance is greater in males, with a male female ratio of 2:1. the multiple or bilateral forms of ac are unusual, and some studies even report a familial occurrence (15, 19, 24, 39). romanian neurosurgery (2016) xxx 1: 52 56 53 case presentation we are presenting the case of a male patient, aged 34 years old, who sought medical attention for a right hemicrania-like migraine, anxiety and neurotic syndrome, as well as subjective neurovegetative symptoms. further to a head ct scan, a sharply demarcated, nonenhancing, extra-axial cyst, with csf density, located at the level of the basal cisterns and the medial temporal lobe was observed. the exploration was completed by a mri scan, which highlighted large and relatively symmetrical cystic lesions in the middle cranial fossa, on the medial aspect of temporal lobes which follow csf signal on all sequences (figure 1). given the fact that the symptoms were non-specific and very few compared with the neuroimaging, a conservative treatment was chosen, consisting in clinical and imaging follow-up of the patient. discussions as mentioned, most acs, regardless of their location, are an incidental finding, usually after a brain imaging performed for non-specific symptoms, as in our case. other non-specific symptoms encountered in patients with ac are mild headache, dizziness or balance impairment (14, 34). if the acs become symptomatic, the symptoms occur especially in early childhood, as 60-90% of patients with acs being children (9, 24). several ac occurrence mechanisms were proposed, among which head injury in childhood (8, 10), the splitting or duplication of the arachnoid membrane (25, 27-29, 33), as well as some genetic factors (1, 4, 6, 16-18, 23). in our patient’s case, neuroimaging did not highlight any signs of intracranial hypertension with cerebral compression, and the absence of abnormal brain development made us consider the existence of cystic lesions with progressive development. moreover, in mri imaging, even though a slight volume reduction of both hippocampal areas (figure 2) was observed, the patient had no cognitive deficits. in terms of the physiopathological mechanisms of ac, some studies (12, 31) suggest that the membrane of liliequist plays an important role in the development of the suprasellar arachnoid cyst. normally, it is perforated and separates the incomplete interpeduncular and chiasmatic parts of the suprasellar cistern, stretching between its attachments points at the dorsum sellae, hypothalamus, ventral midbrain and oculomotor nerves (13). if this membrane is imperforated, either as a result of congenital neurodevelopment or of an acquired adhesive arachnoiditis, the csf obstruction from infratentorial to supratentorial subarachnoid spaces (12) occurs. the continuous flow of csf from the fourth ventricle through the subarachnoid space in the posterior side of the spinal cord and then in the anterior side will produce upward expansion of the membrane in the suprasellar cistern with the appearance of a diverticulum. the progressive dilatation of the suprasellar cyst will lead to a widening of the suprasellar cistern extending towards the basal cisterns (figure 3) and further into the crural and carotidian cisterns, widening the subarachnoid spaces on the inferior and medial region of the temporal lobe (13). (figure 1). the occurrence of clinical symptoms is closely related to the intracytic pressure (17, 18). for this reason, in case of increased intra 54 turliuc et al suprasellar arachnoid cyst with giant perimesencephalic extension cystic pressure (e.g. hemorrhage, cyst expansion), the most common clinical symptoms are headache, seizures and dizziness (5). moreover, perfusion studies showed that increased intra-cystic pressure will eventually compromise the function of the adjacent cortex by reducing blood perfusion and neuronal metabolism (5, 32, 35, 36). the therapeutic options consist of monitoring the patient or surgical treatment: cyst excision, fenestration, endoscopic fenestration or stereotactic suction (9, 30). many authors recommend ac follow-up in case there are no symptoms or imaging signs of intracranial hypertension, regardless of the size or location of the cyst (9, 30). figure 1 the middle cranial fossa contains large an relatively symmetrical cystic lesions, on the medial aspect of temporal lobes; the lesions follow csf signal on all sequences figure 2 there is a slightly volume reduction of both hippocampal areas due to the mass effect of the cystic lesions (blue arrows) figure 3 simetrical enlargement of ambiens and quadrigeminal cisterns (blue arrows) romanian neurosurgery (2016) xxx 1: 52 56 55 conclusions to the best of our knowledge, this case of ac with giant perimesencephalic and mesial temporal extension is the first of its kind to be reported in the literature, given its discrepancy between the spectacular neuroimaging and the nonspecific clinical image. in the absence of neurological symptoms, the clinical and imaging follow-up is recommended, due to the fact that an ill-timed surgery could produce an imbalance between the multiloculated spaces of ac maintaining an intracranial hypertension syndrome. correspondence a.i. cucu “prof. dr. n. oblu” emergency clinical hospital iasi, romania e-mail: andreiucucu@yahoo.com references 1.aarhus m, helland ca, lund-johansen m, wester k, knappskog pm. microarraybased gene expression profiling and dna copy number variation analysis of temporal fossa arachnoid cysts. cerebrospinal fluid res. 2010; 7:6. 2.al-holou wn, terman s, kilburg c, garton hj, muraszko km, maher co. prevalence and natural history of arachnoid cysts in adults. j neurosurg. 2013; 118:222–231. 3.al-holou wn, yew ay, boomsaad ze, garton hj, muraszko km, maher co. prevalence and natural history of arachnoid cysts in children. clinical article. j neurosurg pediatr. 2010; 5:578–585. 4.arriola g, de castro p, verdu a. familial arachnoid cysts. pediatr neurol. 2005; 33:146–148. 5.b gjerde p, schmid m, hammar a,wester k. intracranial arachnoid cysts: impairment of higher cognitive functions and postoperative improvement. j neurodev disord. 2013; 5 (1): 21. 6.bayrakli f, okten ai, kartal u, menekse g, guzel a, oztoprak i, pinarbasi e, kars hz. intracranial arachnoid cyst family with autosomal recessive trait mapped to chromosome 6q22.31-23.2. acta neurochir. 2012; 154:1287–1292. 7.bright r. serous cysts in the arachnoid, in rees, orme, brown, green (eds): diseases of the brain and nervous system. part i. london: longman group ltd, 1831. 8.choi ju, kim ds. pathogenesis of arachnoid cyst: congenital or traumatic? pediatr neurosurg. 1998; 29:260–266. 9.ciurea av, tascu a, iliescu a, mihalache c, brehar f, palade c, spatariu a, intracranian arahnoid cysts in children. romanian neurosurgery. 2011; xviii 1: 68-76. 10.contreras c, copty m, langelier r, gagne f. traumatic suprasellar arachnoid cyst. surg neurol. 1977; 8:196–198. 11.eskandary h, sabba m, khajehpour f, eskandari m. incidental findings in brain computed tomography scans of 3000 head trauma patients. surg neurol. 2005; 63:550– 553. 12.fox jl, ai-mefty o. suprasellar arachnoid cysts: an extension of the membrane of liliequist. neurosurgery.1980; 7:615-618. 13.gentry lr, smoker wr, turski pa, menezes ah, ramirez l, cornell sh. suprasellar arachnoid cysts: 1. ct recognition. am j neuroradiol. 1986; 7(1):79-86. 14.greenberg ms. handbook of neurosurgery, 6th edition. new york: thime, 2006. 15.handa j, okamoto k, sato m. arachnoid cyst of the middle cranial fossa: report of bilateral cysts in siblings. surg neurol. 1981; 16:127–130. 16.helland ca, lund-johansen m, wester k. location, sidedness, and gender distribution of intracranial arachnoid cysts in a population-based material. j neurosurg. 2010; 113:934–939. 17.helland ca, wester k. intracystic pressure in patients with temporal arachnoid cysts: a prospective study of preoperative complaints and postoperative outcome. j neurol neurosurg psychiatry. 2007; 78:620–623. 18.helland ca, wester k. monozygotic twins with mirror image cysts: indication of a genetic mechanism in arachnoid cysts? neurology. 2007; 69:110–111. 19.jamjoom za, okamoto e, jamjoom ah, al-hajery o, abu-melha a. bilateral arachnoid cysts of the sylvian region in female siblings with glutaric aciduria type i. report of two cases. j neurosurg. 1995; 82(6):1078-81. 56 turliuc et al suprasellar arachnoid cyst with giant perimesencephalic extension 20.katzman gl, dagher ap, patronas nj. incidental findings on brain magnetic resonance imaging from 1000 asymptomatic volunteers. jama. 1999; 282:36–39. 21.lemire r, loeser j, leech r, alvord ej. normal and abnormal development of the human nervous system. new york: harper & row, 1975. 22.morris z, whiteley wn, longstreth wt jr, weber f, lee yc, tsushima y, alphs h, ladd sc, warlow c, wardlaw jm, al-shahi sr. incidental findings on brain magnetic resonance imaging: systematic review and metaanalysis. bmj. 2009; 339:b3016. 23.pomeranz s, constantini s, lubetzki-korn i, amir n. familial intracranial arachnoid cysts. childs nerv syst. 1991; 7:100–102. 24.pradilla g, jallo g. arachnoid cysts: case series and review of the literature. neurosurg focus. 2007; 22(2):e7. 25.rabiei k, tisell m, wikkelsø c, johansson br. diverse arachnoid cyst morphology indicates different pathophysiological origins. fluids barriers cns. 2014; 11:5. 26.rajendra s, reeka p, xu j, you c. arachnoid cyst complicated by spontaneous chronic subdural hematoma in the infant. romanian neurosurgery. 2012; xix 1. 27.rengachary ss. parasagittal arachnoid cyst: a case report. neurosurgery. 1981; 9:70-75. 28.rengachary ss, watanabe i. ultrastructure and pathogenesis of intracranial arachnoid cysts. j neuropathol exp neurol. 1981; 40:61–83. 29.rengachary ss, watanabe i, brackett ce. pathogenesis of intracranial arachnoid cysts. surg neurol. 1978; 9:139– 144. 30.di rocco c. sylvian fissure arachnoid cysts: we do operate on them but should it be done? childs nerv syst. 2010; 26:163-172. 31.sansregret a, ledoux r, duplantis f, lamoureux c, chapdelaine a, leblanc p. suprasellar subarachnoid cysts: radioclinical features. am j roentgenol radium ther nucl med. 1969; 105:291-297. 32.sgouros s, chapman s. congenital middle fossa arachnoid cysts may cause global brain ischaemia: a study with 99tchexamethylpropyleneamineoxime single photon emission computerised tomography scans. pediatr neurosurg. 2001; 35:188–194. 33.starkman sp, brown tc, linell ea. cerebral arachnoid cysts. j neuropathol exp neurol. 1958; 17:484– 500. 34.tascu a, florea sm. surgical decompression of arachnoid cysts: a study on 44 pediatric patients. romanian neurosurgery. 2013; xx 3: 264-270. 35.tsurushima h, harakuni t, saito a, tominaga d, hyodo a, yoshii y. symptomatic arachnoid cyst of the left frontal convexity presenting with memory disturbance – case report. neurol med chir (tokyo). 2000; 40:339–341. 36.de volder ag, michel c, thauvoy c, willems g, ferriere g. brain glucose utilisation in acquired childhood aphasia associated with a sylvian arachnoid cyst: recovery after shunting as demonstrated by pet. j neurol neurosurg psychiatry. 1994; 57:296–300. 37.vernooij mw, ikram ma, tanghe hl, vincent aj, hofman a, krestin gp, niessen wj, breteler mm, van der lugt a. incidental findings on brain mri in the general population. n engl j med. 2007; 357:1821–1828. 38.weber f, knopf h. incidental findings in magnetic resonance imaging of the brains of healthy young men. j neurol sci. 2006; 240:81–84. 39.wester k. gender distribution and sidedness of middle fossa arachnoid cysts: a review of cases diagnosed with computed imaging. neurosurgery. 1992; 31:940– 944. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-027 the tumour volume influence on tumour recurrence and progression-free survival in the case of atypical meningiomas. our experience on a series of 81 cases a.i. cucu, claudia florida costea, mihaela dana turliuc, cristina gena dascalu, ioana jitaru, r. dinu, gabriela dumitrescu, anca sava, b. dobrovat, camelia bogdanici, t. andrei, i. stirban, i. poeata romanian neurosurgery (2020) xxxiv (1): pp. 52-57 doi: 10.33962/roneuro-2020-027 www.journals.lapub.co.uk/index.php/roneurosurgery the tumour volume influence on tumour recurrence and progression-free survival in the case of atypical meningiomas. our experience on a series of 81 cases a.i. cucu1, claudia florida costea1,2, mihaela dana turliuc1,2, cristina gena dascalu2, ioana jitaru1, r. dinu1, gabriela dumitrescu1, anca sava1,2, b. dobrovat1,2, camelia bogdanici2, t. andrei1, i. stirban1, i. poeata1,2 1 "prof. dr. n. oblu" emergency clinical hospital iasi, romania 2 "grigore t. popa" university of medicine and pharmacy, iasi, romania abstract objective: the objective of our study was to evaluate a possible relation between the volume of atypical meningiomas (ams) and the risk of tumour recurrence, as well as progression-free survival (pfs). material and methods: we evaluated 81 patients diagnosed with ams (who grade ii meningioma) who have undergone surgery at the "prof. dr. n. oblu" emergency clinical hospital iasi between january 1, 2010, and december 31, 2019. the recorded data were demographic and imagistic (mri, contrast-enhanced t1wi). we calculated the tumour volume prior to the surgery and evaluated the tumour recurrence using mri at 12, 24, 36, 48 and 60 months after the surgery. results: 50.6% of patients had meningioma volume < 26.4 cm3. women had larger tumour volumes than men (52.6%). patients of age ≤ 60 years old, had tumour volumes ˃ 26.4 cm3 in 58.5% of cases and meningiomas with volumes ˃ 26.4 cm3 recurred earlier (p=0.010). also, patients who had tumour volumes ˃ 26.4 cm3, had a shorter pfs (40.976 months), compared to patients with tumour volumes < 26.4 cm3, who had better pfs (53.4 months). conclusions: the tumour volume of ams ˃ 26.4 cm3 represents a negative prognostic factor for both early tumour recurrence and reduced pfs. introduction meningiomas are the most common primary intracranial tumors in adults and represent about one third of them (26). out of the histopathological grades of meningiomas, ams (who grade ii meningiomas) represent approximately 20-30% of them (27, 28, 33), and their incidence has increased in the last years (10, 33). keywords atypical meningiomas, tumour volume, progression-free survival corresponding author: claudia florida costea "grigore t. popa" university of medicine and pharmacy, iasi, romania costea10@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 53 the tumour volume influence on tumour recurrence regarding the multiple prognostic factors of tumor recurrence in case of ams (8, 12, 13, 27, 30, 31), some studies have reported that the size and volume of the tumor would also represent a prognostic factor (16, 17, 22). thus, some authors have proved that larger size of ams (for example, over 4.5 cm) are associated with early tumor recurrence (16). other authors have reached the conclusion that the size of the meningioma is not only a prognostic factor of tumor recurrence, but also of the survival of patients, both in the case of ams, as well as in the case of anaplastic meningiomas (17). this study is aimed to evaluate the influence of the tumor volume on early tumor recurrence, as well as on the survival period up to the tumor recurrence. material and methods we evaluated the tumor volume of 81 patients diagnosed with atypical meningioma (am), who had undergone surgery at the neurosurgery department, "prof. dr. n. oblu" emergency clinical hospital iasi, followed between january 1, 2010 and december 31, 2019. each patient had the following recorded: demographic data regarding age and sex, and imaging studies (mri). the tumor volume was calculated using the formula: volume = π /6 x legnth x wirdth x height (5, 18, 21, 29), and was analysed on magnetic resonance images prior to the surgery (contrast-enhanced t1wi). the mean tumor volume calculated was of 26.4 cm3, and depending on it, patients were grouped into two samples: (1) patients whose volume was < 24 cm3 and (2) patients whose volume was ˃ 26.4 cm3. we also performed a qualitative evaluation of the ams volume and evaluated the relation between the tumor volume, the rate of recurrence and pfs. the patients had an annual imaging examination (mri), for a period of 5 years, and the tumor reccurence/tumor progression was defined as any contrast-enhancement at the level of the remaining tumor bed, or the increase in size of the the remnant tumor. in the cases of subtotal tumor resections, we named and classified the tumor progression as a tumor recurrence. depending on its location in the intracranian space, the meningiomas were classified as: (1) skull base meningiomas, (2), convexity meningiomas, (3) parasagittal/falcine meningiomas, (4) posterior fossa meningiomas, and (5) intraventricular meningiomas. in the group of skull base meningiomas were included only those located at the level of the anterior and middle fossa. posterior fossa meningiomas included all infratentorial meningiomas, including tentorium meningiomas or those located on the cerebellopontine angle or the petroclival junction. the statistical data processing was made in spss 24.0 (spss inc., chicago, il). the data were characterized through descriptive statistics and frequency distributions. the data normality was checked using the kolmogorovsmironov fitting test; after this, we used t-student and anova tests to compare the samples of normally distributed data and mann-whitney and kruskal-wallis tests to compare the other samples. the qualitative data were characterized through frequency distributions and contingency tables, and the comparisons were made using the chi-squared test. all p values were 2-tailed; a p value of 0.05 was considered significant. the actuarial data were represented with kaplan-meier plots, and the cumulative incidence curves were compared using the log-rank test. the study was approved by the reasearch ethics committee of the "grigore t. popa" university of medicine and pharmacy of and by the ethical committee of the "prof. dr. n. oblu" emergency clinical hospital of iași. results demography (age, sex) the study group included 81 patients, of which most cases of ams were in men, in a percentage of 53.1% (n = 43). the age of the patients in the total group ranged from 37 to 87 years, with a mean age of 61 years. when we evaluated the age of patients by sex, we noticed that women have a mean age of onset younger than men (58.42 years), compared to those who have a mean age of disease onset of 63.47 years (p=0.0052). 50.6% of patients had ages ≤ 60 years old (figure 1). there were no statistically significant differences between the sexes in terms of age distribution. all patient characteristics can be seen in table i. characteristics n (%) gender male female 43 (53.1%) 38 (46.9%) age ≤ 60 years ˃ 60 years 41 (50.6%) 40 (49.4%) tumor localization convexity parasagittal/falcine skull base posterior fossa 34 (42%) 21 (25.9%) 17 (21%) 6 (7.4%) 54 a.i. cucu, claudia florida costea, mihaela dana turliuc et al. intraventricular 3 (3.7%) tumor volume < 26.4 cm3 ≥ 26.4 cm3 41 (50.6%) 40 (49.4%) table i. characteristics of 81 patients with atypical meningiomas. figure 1. female, 60 years-old with atypical meningioma. a. well-cellularized tumor, infiltrative into adjacent dura mater, consisting of meningothelial cells arranged in syncytial pattern, with oval nuclei and fine granular chromatin (3 mitoses/10 high-power fields) (he, x 400). b and c. two different fields of the same tumor showing high expression of ki-67 li (mean 12%) (immunohistochemical staining, x400). tumor localization regarding the localization of meningiomas at the skull level, most were located on the convexity level (42%, n=34), followed by parasagittal/falcine localization (25.9%) and at the level of the skull base (21%). smaller percentages were located at the level of the posterior fossa (7.4%) or at the intraventricular level (3.7%) (table i). following the qualitative analysis of the tumor volume, although there was no statistically significant difference between the tumor volume and the location of the meningioma at the level of the intracranial space, we found, however, that the largest tumors were located at the base of the skull, with a mean of 53.724 cm3 (ranging between 3.444149.094 cm3). these were followed by intraventricular meningiomas (mean of 47.927 cm3), convexity meningiomas, (mean of 41.396 cm3), posterior fossa meningiomas (mean of 39.172 cm3) and those with parasagittal/falcine localization (mean of 36.596 cm3) (figure 2). figure 2. the mean tumor volume depending on location (personal collection of authors, public domain). tumor volume the mean tumor volume was 26.4 cm3 and 50.6% of patients had meningioma volumes of < 26.4 cm3. analyzing the differences between genres, although we did not identify any statistically significant values, we found that women had larger meningioma volumes than men (52.6%). also, patients with ages ≤ 60 years old, had tumor volumes ˃ 26.4 cm3 in 58.5% of cases. we identified a statistically significant relation between the meningioma volume and the tumor recurrence (p=0.010). tumors with volumes ˃ 26.4 cm3 recurred earlier, and within this group the tumor recurrence rate was 17.1% at 12 months, 19.5% at 24 months and 41.5% at 60 months. on the other hand, tumors with volumes < 26.4 cm3 had no recurrence in the first 12 months, and the recurrence rate at 24 months was 5%. moreover, 65% (n=26) of meningiomas with volumes < 26.4 cm3 had a slow recurrence, at 60 months. also, recurrent meningiomas had a larger mean volume (49.438 ± 41.771) compared to meningiomas that did not recur (35.323 ± 35.524). in regards to pfs, we identified a statistically significant relation between it and the tumor volume (p=0.030). patients who had tumor volumes ˃ 26.4 cm3 had shorter pfs (40.976 months). patients who had tumor volumes < 26.4 cm3, had better pfs (53.4 months) (figure 3). 55 the tumour volume influence on tumour recurrence figure 3. pfs depending on the tumor volume. it is notable that patients with tumor volume < 26.4 cm3 had better pfs. discussions the influence of tumor volume on the tumor recurrence risk in our study we observed a predominance of convexity meningiomas, in agreement with our previous studies (9, 11). we also noticed that a higher tumor volume has a negative influence on the rate of recurrence. thus, in cases of meningiomas with tumor volumes ˃ 26.4 cm3, the recurrence rate was higher than in the case of tumors with volumes below this value. this correlation between a larger size of the meningioma and the existence of the risk of tumor recurrence has also been observed by other authors in previous studies (16, 17, 19). fernandez et al. reported that the size of over 4.5 cm of am is associated with a risk of early recurrence (16). moreover, garzon-muvdi et al. also observed in his study that the size of the tumor can be considered an important factor not only for pfs, but also for overall survival. nakasu et al. also reported the mean size of 4.4 ± 1.4 cm to influence tumor recurrence compared to non recurrent tumors which had a diameter of 3.5 ± 1.5 cm (25). moreover, various authors reported that smaller sized ams can represent a protective factor against tumor recurrence (4, 14, 16). this relation between the larger tumor volume and the risk of tumor recurrence may be explained by the fact that a larger size meningioma makes a complete tumor resection more difficult due to the potential invasion of adjacent structures (3, 15, 20, 23). another interesting aspect was observed by magill et al., who proved in a study conducted on 1113 meningiomas (905 grade i meningiomas and 208 grade ii meningiomas) that the larger the size of the tumor, the higher the risks that it would be a grade ii meningioma (24). in order to explain this, magill et al. considered that there would be two possibilities: one would be that the grade ii meningiomas grow faster than grade i meningiomas, and a second that once the slow growth tumor reaches a larger size, it develops a microenvironment due to hypoxia, which leads to the phenotype of this tumor becoming more aggressive (24). in recent years, progress has been made in establishing the genetic factors that govern the growth of meningiomas or leading to their transformation into a more malignant histological grade, and in this sense, in addition to nf2, mutations in smo, pi3k, traf7, klf4 and akti have been identified (1, 6, 7). in the case of recurrent meningiomas, mutations in polr2a have also been identified (7). the influence of tumor volume on pfs we found that the tumor volume of the meningioma influences the survival period until the tumor recurrence (p=0.030). thus, tumor volumes ˃ 26.4 cm3 had a shorter pfs. this can be explained by the fact that larger sized tumors invade more neurovascular structures, which make complete tumor resection more difficult, leaving a remnant tumor sometimes. in this sense, wang et al. also found that tumors with dimensions ˃ 41.5 mm are associated with a higher risk of tumor recurrence (32). similarly, nakasu et al. 1999 also reported that meningiomas with a mean diameter ˃ 44 ± 14 mm have a significantly shorter pfs, consistent with other authors who consider that the tumor size is significantly associated with tumor recurrence in the case of patients diagnosed with ams (2, 14, 17). conclusions our patients’ series demonstrated that the tumor volume of ams ˃ 26.4 cm3 increases the tumor recurrence rate and decreases pfs. moreover, mean tumor volumes had bigger values in case of recurrent ams. we consider the tumor volume 56 a.i. cucu, claudia florida costea, mihaela dana turliuc et al. represents a prognostic factor not only for tumor volume, but also for pfs. references 1. abedalthagafi m, bi wl, aizer aa, et al. oncogenic pi3k mutations are as common as akt1 and smo mutations in meningioma. neuro oncol 2016; 18:649-55. 2. aizer aa, arvold nd, catalano p, et al. adjuvant radiation therapy, local recurrence, and the need for salvage therapy in atypical meningioma. neuro oncol 2014; 16(11):1547-53. 3. buttrick s, shah ah, komotar rj, ivan me. management of atypical and anaplastic meningiomas. neurosurg clin n am 2016; 27(2):239-47. 4. champeaux c, houston d, dunn l. atypical meningioma. a study on recurrence and disease-specific survival. neurochirurgie 2017; 63(4):273-81. 5. char dh, kroll s, phillips tl. uveal melanoma. growth rate and prognosis. arch ophthalmol 1997; 115:1014-18 6. clark ve, erson-omay ez, serin a, et al. genomic analysis of non-nf2 meningiomas reveals mutations in traf7, klf4, akt1, and smo. science 2016; 339:1077-80. 7. clark ve, harmancı as, bai h, et al. recurrent somatic mutations in polr2a define a distinct subset of meningiomas. nat genet 2016; 48:1253-59. 8. cucu ai, costea cf, turliuc md, et al. are there any correlations between demographic characteristics, tumor location, and ki-67 labeling index in intracranial atypical meningiomas (who grade ii)? rom j morphol embryol 2019; 60(2):567-72. 9. cucu ai, costea cf, turliuc md, et al. anatomical localization of intracranial grade ii meningiomas in north-eastern romania. our 25-years experience. rom neurosurg 2019; 33(3):232-38. 10. cucu ai, costea cf, carauleanu a, et al. meningiomas related to the chernobyl irradiation disaster in northeastern romania between 1990 and 2015. rev chim (bucharest). 2018; 69:1562-65. 11. cucu ai, costea cf, poeată i, et al. anatomical localization of atypical meningiomas: our experience on 81 patients. med surg j rev med chir soc med nat iaşi 2018; 122(4):744-52. 12. cucu ai, turliuc md, carauleanu a, et al. chemical aspects of peritumoral cerebral edema in atypical meningiomas. rev chim (bucharest), 2018; 69(10):280407. 13. cucu ai, costea cf, poeata i, et al. prognostic factors in atypical meningioma. rom neurosurg. 2017; 31(2):16571. 14. detti b, scoccianti s, di cataldo v, et al. atypical and malignant meningioma: outcome and prognostic factors in 68 irradiated patients. j neurooncol. 2013; 115(3):42127. 15. durand a, labrousse f, jouvet a, et al. who grade ii and iii meningiomas: a study of prognostic factors. j neurooncol 2009; 95(3):367-75. 16. fernandez c, nicholas mk, engelhard hh, slavin kv, koshy m. an analysis of prognostic factors associated with recurrence in the treatment of atypical meningiomas adv radiat oncol 2016; 1(2):89-93. 17. garzon-muvdi t, yang w, lim m, brem h, huang j. atypical and anaplastic meningioma: outcomes in a population based study. j neurooncol 2017; 133(2):32130. 18. gass jd. comparison of uveal melanoma growth rates with mitotic index and mortality. arch ophthalmol 1985; 103:924-31. 19. go kg, kamman rl, wilmink jt, mooyaart el. a study on peritumoural brain oedema around meningiomas by ct and mri scanning. acta neurochir (wien) 1993; 125:4146. 20. goyal lk, suh jh, mohan ds, et al. local control and overall survival in atypical meningioma: a retrospective study. int j radiat oncol biol phys 2000; 46(1):57-61. 21. guthoff r. modellmessungen zur volumenbestimmung des malignen aderhautmelanoms. graefe arch klin ophthalmol 1980; 214:139-46. 22. hale at, wang l, strother mk, chambless lb. differentiating meningioma grade by imaging features on magnetic resonance imaging. j clin neurosci 2018; 8:71-75. 23. hanft s, canoll p, bruce jn. a review of malignant meningiomas: diagnosis, characteristics, and treatment. j neurooncol 2010; 99(3):433-43. 24. magill st, young js, chae r, et al. relationship between tumor location, size, and who grade in meningioma. neurosurg focus 2018; 44(4):e4. 25. nakasu s, nakasu y, nakajima m, matsuda m, handa j. preoperative identification of meningiomas that are highly likely to recur. j neurosurg 1999; 90(3):455-62. 26. ostrom qt, gittleman h, liao p, et al. cbtrus statistical report: primary brain and other central nervous system tumors diagnosed in the united states in 2010-2014. neuro oncol 2017; 19(suppl 5):v1-v88. 27. pasquier d, bijmolt s, veninga t, rezvoy n, villa s et al. atypical and malignant meningioma: outcome and prognostic factors in 119 irradiated patients. a multicenter, retrospective study of the rare cancer network. int j radiat oncol biol phys 2008; 71(5):1388-93. 28. pearson be, markert jm, fisher ws, et al. hitting a moving target: evolution of a treatment paradigm for atypical meningiomas amid changing diagnostic criteria. neurosurg focus 2008; 24(5):e3. 29. richtig e, langmann g, müllner k, richtig g, smolle j. calculated tumour volume as a prognostic parameter for survival in choroidal melanomas. eye (lond) 2004; 18(6):619-23. 30. ros-sanjuan a, iglesias-moroño s, carrasco-brenes a, bautista-ojeda d, arraez-sanchez ma. atypical meningiomas: histologic and clinical factors associated with recurrence. world neurosurg 2019; 125:e248-e256. 57 the tumour volume influence on tumour recurrence 31. roser f, nakamura m, bellinzona m, et al. the prognostic value of progesterone receptor status in meningiomas. j clin pathol 2004; 57(10):1033-37. 32. wang yc, chuang cc, wei kc, hsu yh, hsu pw et al. skull base atypical meningioma: long term surgical outcome and prognostic factors. clin neurol neurosurg 2015; 128:112-26. 33. willis j, smith c, ironside jw, erridge s, whittle ir et al. the accuracy of meningioma grading: a 10-year retrospective audit. neuropathol appl neurobiol 2005; 31(2):141-49. 4iacobg_spinalintramedullary romanian neurosurgery (2014) xxi 4: 405 – 413 405 spinal intramedullary cavernomas. personal experience reffering to six cases g. iacob, angela olarescu neurosurgery clinic, university emmergency hospital, bucharest despite cavernous malformations of the cns are pathologically similar, intramedullary cavernous malformations are very rare lesions, increasingly recognized after introduction of magnetic resonance image, generating gradual neurological decline, with severe deficits or acute loss of spinal function. we report our experience on six patients with intramedullary cavernomas defining the spectrum of presenting symptoms and signs analyzing the role of surgery as a treatment for these lesions. we present our experience with 2 cervical and 4 thoracal spinal intramedullary cavernoma from 2010 to 2014 searching history, onset of clinical manifestation, neurological status, radiological findings, operation, and clinical outcome. among 6 patients male were 2 cases; female 4 cases; mean age was 42 years (range 25-72 years); mean duration of symptoms were 1,5 years (range 5 days and 2 years) with slowly progressive neurological decline. in two cases there was acute onset of neurological compromise. in all cases diagnosis was made on mri and lesions were possible to be radically excised and gently extracted from the hemosiderin-stained bed inside of the spinal cord via a laminectomy and midline myelotomy with microsurgical techniques. the surgical outcome on a mean duration of follow up of 12 months were: for 4 cases the patients neurological conditions remarkably improved 1 month later, for 2 cases no improvement were remarked. no recurrent hemorrhages were recorded. a follow-up mri examination was made in all cases to confirm complete removal of the cavernous angioma. spinal intramedullary cavernoma should be early recognized by mri, can be positioned in a precarious position and generate significant neurologic deficits than cranial cavernomas. for symptomatic intramedullary cavernous malformations extended to the dorsal surface of the spinal cord, total resection with microsurgical techniques can offer good or excellent outcome, restoring neurological status and to stop chronic deterioration and acute rebleeding. to asymptomatic patients with deeper lesions which entail a higher operative risk, but also a surgically manageable cause of myelopathy a closed observation is mandatory. key words: intramedullary cavernous malformation, spinal mri magnetic susceptibility sequences, microsurgical resection. 406 iacob, olarescu spinal intramedullary cavernomas introduction cavernous malformations are well-defined lesions composed of abnormally dilated blood vessels, vascular channels with structurally incomplete vessel walls, lined by a thin endothelium without intervening normal nervous tissue, surrounded by gliotic medullar tissue, often stained with hemosiderin, expresion of previous hemorrhage. intramedullary spinal cord cavernous malformations are unusual: solitary or multiple lesions discovered in both the brain and spinal cord using mri and justified by genetic basis (1, 2), causes neurological symptoms due to the higher density of eloquent structures in the spinal cord and have an unknown natural course (3-7). methods and results we present our personal experience concerning 2 cervical (c3 and c5) and 4 thoracal (t2-t3, t6, t7 and t9) spinal intramedullary cavernoma from 2000 to 2014. among 6 patients male were 2 cases; female 4 cases; mean age was 42 years (range 25-72 years) at presentation; mean duration of symptoms were 1,5 years (range 5 days and 2 years) with slowly progressive neurological decline (stade 2 according to ogilvy classification) (8) and symptoms (mild paraparesis, hypoesthesia, gait, trophic and sphincterian disturbances) evaluated on the frankel scale. in two cases the onset of neurological compromise was acute: 3 hours respective 18 hours (stade 3 according to ogilvy classification). in all cases diagnosis was made on mri and lesions were possible to be radically excised and gently extracted from the hemosiderin-stained bed inside of the spinal cord via a laminectomy and midline myelotomy with microsurgical techniques. the surgical outcome on a mean duration of follow up of 12 months were: for 4 cases the patients neurological conditions remarkably improved 1 month later, for 2 cases (c3 and t2t3) no improvement were remarked. no recurrent hemorrhages were recorded. a follow-up mri examination was made in all cases to confirm complete removal of the cavernous angioma. illustrative case: a 48-years-old, complained of thoracolumbar pains, bilateral leg weakness, especially on the left leg, legs numbness 1 year before admission, with sudden deteriorating legs weakness and urinary retention 2 weeks before admission. he presented with a brownsequard syndrom: spastic paraparesis especially on left side, left babinski and foot clonus signs, with impaired right thermo-algic sensation below the t8 dermatome. the patient underwent cranial and spinal mr examinations and postoperative mr imaging in a 1,5-tesla mr imager. sagittal t1 and t2 weighted images and axial t2 – weighted mr images of the thoraco-lumbar spine reveal an intramedullary t6, 11/9 mm, well-marginated lesion, with heterogenous signal abnormality in both t1 and t2 – weighted images, representing blood products romanian neurosurgery (2014) xxi 4: 405 – 413 407 of various ages. the lesion was surrounded by low signal intensity, representing iron storage products and medullary perilesional oedema, occupying most of the thoracic spinal cord, suggesting the diagnosis of an intramedullary thoracal cavernoma. figure 1, figure 2 after induction of general anesthesia, the patient was positioned prone. the patient underwent a t6-t7 laminectomy. the dura was sharply incised on the midline, reflected to expose the lesion and retained laterally using no 4-0 silk sutures between its edges and the paraspinous muscles. using the operating microscope, the arachnoid was opened; the widened, brown colored spinal cord becomes apparent at the lesion level. a midline mielotomy to preserve the fine vascular network is performed, lacate blood was aspirated and an entirely intramedullary yellowdark red mass, clearly demarcated from the adjacent spinal cord tissue, was excised and gently extracted from the the hemosiderin-stained bed inside of the spinal cord. after the lesion has been completely resected, the walls of the cavity remaining in the spinal cord collapse. the dura was closed in a watertight manner. the muscular, fascial, subcutaneous and cutaneous layers were closed in the standard fashion. the resected material showed thin-walled vascular spaces, variable in caliber and fibrous tissue content, occlusive thrombus attached to the vascular wall, revealing a cavernoma. (figures 3-6.) the clinical course was uneventful: the patient was encouraged to begin ambulation the following morning and his neurological condition remarkably improved: 1 week later he recovered motor strength and sensation in his left foot and was able to walk without cane and climb stairs. a 3 day postoperative mri showed a postoperative status, a little intramedullary zone with magnetic susceptibility effect, suggesting post operatory intramedullary hemorrhagic remnants at t6 level, surrounded by a minimal intramedullary oedema. at 1 month follow up, the patient's spasticity has diminished and he was able to walk without difficulty. a a b figure 1 a axial t2w images show low signal intensity on the lesion susceptibility effect and hiperintense signal intensity in the perilesional edema; b axial t1w images reveal mixt hiperintense and hipointense t1w signal, representing an intramedular lesion with methemoglobin contain, c t6 spinal intramedular mixt signal lesion and perilesional edema of the spinal cord 408 iacob, olarescu spinal intramedullary cavernomas figure 2 a axial t2w images show low signal intensity on the lesion susceptibility effect and hiperintense signal intensity in the perilesional edema b axial t1w images reveal mixt hiperintense and hipointense t1w signal, representing an intramedular lesion with methemoglobin contain a b c d figure 3 a the surface of the left medulla, at t6-t7 , is widened, brown colored, from previous hemorrhages, making intramedullary cavernoma apparent, b after a median myelotomy, lacate blood was aspirated and the cavernous malformation is sharply dissected from its surrounding bed, mobilized and removed, c the pathologic specimen is shown, d after the lesion has been removed completely, the walls of the cavity remaining in the spinal cord collapse a b fiure 4 h&e staining a vascular spaces variable in caliber and fibrous tissue content; the extraluminal interstices are chinked with fibrous connective tissue, note no intermingled nervous tissue. original magnification ×100b detail of an occlusive thrombus attached to the vascular wall. original magnification ×100 figure 5 van gieson staining.fibrosclerotic perivascular tissue, marked fibrosis in vascular wall, original magnification x100 romanian neurosurgery (2014) xxi 4: 405 – 413 409 a b figure 6 gomori staining: a fibrotic vascular wall; occlusive thrombus, original magnification x100, b detail of fibrotic wall, original magnification x200 discussion cavernous angiomas also known as cavernous malformations, cavernous hemangiomas (9) or cavernomas occur throughout the central nervous system, representing 10% of all snc vascular abnormalities are considered to be congenital hamartromas in contrast to true vascular neoplasms (3)(10). although they are most commonly found in the brain, the intramedullar cavernoma accounts for approximately 5 to 12% of all adult intramedullary lesions in adults (11) and 1% of intramedullary lesions in children (12)(13). usually solitary they may be associated with cavernous angiomas in other organs or in the central nervous system where they frequently originate in the vertebrae with occasional extension into the extradural space (14) (15). the first spinal cavernoma was reported in a 27-year-old girl who died 212 days after an acute occurrence at 1901; schultze reported the first total resection in 1912 and mccormick was first advocated with complete microscopic resection in 1988 (16) intramedullary cavernoma tend to become clinically symptomatic during the third and the fourth decade of life, like cerebral cavernous malformations (4), but they are more aggressive than cranial cavernomas, probably because the spinal cord is less tolerant of mass lesions. reports of familial incidence and multiple localizations, involving both brain, spinal cord and other organs (skin, retina), suggest the possibility of genetic mechanisms in the development of such lesions (1) (2). they are more common in women in two thirds of cases, in the cervical and thoracic regions of the spinal cord, as in our series (17). there is a male preponderance in pediatric patients (12) intramedullary cavernomas are slow-growing lesions, the risk for hemorrhage range was estimated from 1.7 to 4.5 %, per year (3) (11) and may enlarge in three different ways which may coexist: small bleedings, (chronic hemorrhages) often clinically silent, which create a small cavity around the blood vessels, causing hemosiderin deposition in the surrounding neural tissue with reactive gliosis budding of new capillaries as reactive angiogenesis with new vessel formation, the nidus may grow over time, increasing the mass 410 iacob, olarescu spinal intramedullary cavernomas of the malformation, the so-called hemorrhagic angiogenic proliferation acute massive hemorrhage with rapid expansion and acute mass effect or repeated intralesional hemorrhage and thrombosis, with expansion of a hemorrhagic cyst cavity. sometimes cavernomas are associated with cryptic venous malformations (18). histopathological features of intramedullary cavernomas are similar to those of cranial lesions (19) (20): -macroscopy: a dark red or purple spongy mass composed of vessels and blood on gross examination, surrounded by discolored glial tissue. the size is reported to vary between less than 1 mm up to more than 10 mm in diameter; -microscopy: vascular channels, blood-filled, with hyalinized thin walls, without elastica interna, closely apposed, abnormal venous channels, without intervening medullar tissue. those cavernous malformations that lack calcification has a greather tendency to bleed. intramedullary cavernomas simptomatology (pain, weakness, paraesthesias, slowly progressive myelopathy, subarachnoid hemorrhage) (11) (21-23) are related on: tumor location with respect to the spinal topography, but also to the spinal cord; abnormal vessels which may lead to spinal cord compression; cord expansion or oedema, ischemia generated by arterial steal, repeated hemorrhage and venous hypertension. our findings are similar to those of others (24) (25); several patterns of intramedullary cavernomas clinical presentation are known: asymptomatic, accidentally found at autopsy in patients with multiple cavernous angiomas; gradual slow neurological deterioration over months to years (8), with acute episodes lasting for hours to days, with possible neurological recovery between episodes generated by small hemorrhages or acute thrombosis with organization and recanalization mild neurological symptoms, with progressive myelopathy, the most frequent mode of presentation, of gradual decline during weeks to months or even acute onset, events related to changes in the microcirculation surrounding the lesions and to the neurotoxic effect of hemosiderin; acute complete paralysis, fortunately not common but seen in pediatric population (13), due to hemorrhage extension into the spinal parenchyma, similar to cauda equine cavernoma (26) where intratumoral microbleeding may generate acute onset. intramedullary cavernomas are occult angiographcally and often ct, but mri is the current study of choice both for the diagnosis and for surgical planning, with particularly high sensitivity blood oxygenation level (27). typical manifestation: “popcorn appearance” a webbed core, composed of blood and blood products in various states of evolution of mixed spinal intensity on both t1 and t2 weighted images, with moderate, occasionally strong absorption of contrast medium after an infusion of gadolinium. as a sign of previous hemorrhage in the t1-weighted image, as well as in the t2-weighted image, a black ring of low signal intensity around the cavernoma, consistent with hemosiderin deposits from old hemorrhages indicates disturbances of susceptibility caused by the iron in romanian neurosurgery (2014) xxi 4: 405 – 413 411 hemosiderin. blood products are identified depending the age of a hemorrhage: isointense to slightly hypointense on t1 weighted images and hypointense on t2 weighted images susceptibility effect. if edema is present, the signal outside the hemosiderin rim is increased on the t2-weighted images. small cavernous malformations may appear only as petechial areas of decreased signal density, “black dots”. although large vessels are uncharacteristic of cavernous malformations, a coexistent large draining vein is occasionally identified (16). in the subacute hemorrhage stade, few days later, the lesion that contains methemoglobine are hyperintense on t1 weighted images and hypointense on t2 weighted images (susceptibility effect). several weeks later, in the hemosiderin chronic stade, old blood products are hypointense “blooming” on both t1 and t2 weighted images. changes in volume and gradient echo (ge) mri characteristics are frequent seen, that is the result of hemorrhage evolution. small intramedullary cavernomas have usually no edema; differential diagnosis should rule out cryptic avms and hemorrhagic neoplasms. even when small, with characteristic surrounding edema. the natural history of untreated cavernomas (6) (28-30) is still unclear: after (23) intramedullary cavernomas tend to be clinically progressive, neither the indication for the optimal timing for surgery are known: it’s preferable to operate intramedullary cavernoma in the subacute stage before rapide decline of symptoms and when gliosis surrounding lesion protects the normal spinal cord facilitating removal (5) (14). early microsurgical en bloc resection should be considered for: asymptomatic intramedullary cavernous angiomas in children, for the potential devastating hemorrhage particularly significant (12) for all symptomatic patients, especially to those lesions that extend to the dorsal surface of the spinal cord, before enlargement or rebleeding; generating gradual clinical improvement or to halt the progressive neurological decline; prognosis are depending on the severity and duration of the preoperative status (31)(32). a subtotal resection should be considered for deeper lesions (despite possible future hemorrhages with adverse consequences); when neurological function is at risk, since rebleeding of the residual lesion can occur. to limit surgical trauma intraoperative ultrasonography is able to localize the hyperechogenic malformation, guiding the extent of myelotomy, also intraoperative somatosensory and motorevoked potential monitoring must be used (11) (33). after dura opening, the presence of anomalous vascular reticule or swelling on pia mater could suggest an underlying hemorrhagic lesion. using the shortest path approach midline cordotomy or a postero-lateral approach the wellcircumscribed dark-bluish lesion as the small low-flow feeding vessels should be identified and coagulated and lesion should be carefully dissected and removed in one piece. the outcomes of surgery for cavernous malformations are related to the preoperative neurological status and total removal of the lesion. although patients could transiently 412 iacob, olarescu spinal intramedullary cavernomas experience neurological worsening after surgery, complete removal is generally possible with minimal morbidity. also surgery cannot cure the chronic myelopathy from cavernoma, but can halt its progression. these facts emphasize the need for early diagnosis. delayed complications were the result of incomplete resection (5) (18) (34) (35). the resultant hemorrhage: the reported risk is 9% (15) or 17,6% (18) required reexploration, which led to tethering of the spinal cord. most patients who underwent resection, however, had improved neurologically at long-term follow-up. conclusions spinal intramedullary cavernoma can be positioned in a precarious position, may generate significant neurologic deficits than cranial cavernomas and should be early recognized by mri for symptomatic intramedullary cavernous malformations extended to the dorsal surface of the spinal cord, total resection with microsurgical techniques can offer good or excellent outcome, restoring neurological status and stop chronic deterioration and acute rebleedng. for asymptomatic patients with deeper lesions entail a higher operative risk, also a surgically manageable cause of myelopathy a closed observation is mandatory. similar residual lesion possible masked by surrounding gliosis impose a careful follow up. references 1.cohen-gadol aa, et al. coexistence of intracranial and spinal cavernous malformations: a study of prevalence and natural history, j neurosurg 2006, 104:376-381 2.lee s.t. et al. identification of an arg35x mutation in the pdcd10 gene in a patient with cerebral and multiple spinal cavernous malformations, j neurol sci 2008, 267:177-181 3.kondziella d. et al. – cavernous hemangioma od the spinal cord – conservative or operative management? acta neurol scand 206, 114: 287-290. 4.santoro a. et al. intramedullary spinal cord cavernous malformations: report of ten new cases, neurol rev. 2004, 27: 93-98 5.aoyama t. et al. – intramedullary cavernous angiomas of the spinal cord: clinical characteristics of 13 lesions, neurol. med. chir. (tokyo) 2011, 51, 561-566 6.kharkar s. et al. –the natural history of conservatively managed symptomatic intramedullary spinal cord cavernomas, neurosurgery 2007, 60: 865-872. 7.knipe h., wein s. spinal cavernous malformation, neurosurg focus. 2010 sep;29(3):e12 8.ogilvy c.s. et al. – intramedullary cavernous angiomas of the spinal cord: clinical presentation, pathological features and surgical management, neurosurgery 1992, 31: 219-230 9.park g.y., seo h.j. et al. intramedullary cavernous hemangioma as a cause of paraplegia: two cases report, abstract, journal of the korean academy of rehabilitation medicine 2002; 26(6): 815-818 10.robinson j.r.et al. – natural history of cavernous angioma, j. neurosurg. 1991, 75, 709-714. 11.grasso g. et al. thoracic spinal cord cavernous angioma: a case report and review of the literature, journal of medical case reports 2014, 8:271 doi:10.1186/1752-1947-8-271 12.nagib m.g. et al. – intramedullary cavernous angiomas of the spinal cord in the pediatric age group: a pediatric series. pediatr. neurosurg 2002, 36; 57-63; 13.noudel r. et al. – intramedullary spinal cord cavernous angioma in children: case report and literature review.childs nerv. syst 2008, 24, 259-263. 14.hatiboglu m.a. et al. – epidural spinal cavernous hemangioma case report, neurol med chir (tokyo) 2006, 46, 455-458. 15.zevgaridis d. et al. cavernous hemangiomas of the spinal cord. a review of 117 cases, acta neurochir. (wien), 1999, 141: 237-245 romanian neurosurgery (2014) xxi 4: 405 – 413 413 16.iacob g. olarescu a spinal intramedullary cavernomas.personal experience reffering to six cases, romanian neurosurgical congress bucharest 2014 17.harrison m.j. et al. – symptomatic cavernous malformations affecting the spine and spinal cord neurosurgery 1995, 37: 195-205. 18.vishteh ag, et al. surgical resection of intramedullary spinal cord cavernous malformations: delayedcomplications, long-term outcomes and association with cryptic venous malformations. neurosurgery 1997, 41:1094-1100 19.jellinger k: vascular malformations of the central nervous system: a morphological overview, neurosurg rev 1986, 9:177-216. 20.rigamonti d, et al. cerebral venous malformations, j neurosurg 1990, 73:560-564 21.young k.a, min jeong m.h et al. a case of spinal cord cavernoma mimicking transverse myelitis, case – report, abstract, journal of the korean child neurology society 2010; 18(1) : 153-157 22.miyoshi y, et al. infantile cervical intramedullary cavernous angioma manifesting as hematomyelia. case report, neurol med chir (tokyo) 2010, 50:677-682 23.bian lg, et al. intramedullary cavernous malformations: clinical features and surgical technique via hemilaminectomy, clin neurol neurosurg 2009, 111:511-517 24.deutsch h. et al. – spinal intramedullary cavernoma: clinical presentation ans surgical outcome, j. neurosurg. 2000, 93, 65-70 25.sandalcioglu i.e. et al. intramedullary spinal cord cavernous malformations; clinical features and risk of hemorrhage neurosurg. rev. 2003, 26: 253-256 26.popescu m. et al. – cauda equina intradural extramedullary cavernous haemangioma: case report and review of the literature, neurol medchir (tokyo) 2013, 53, 890-895 27.weinzierl mr, et al. mri and intraoperative findings in cavernous haemangiomas of the spinal cord, neuroradiology 2004, 46:65-71 28.huffmann b.c. et al. – treatment strategies and results in spinal vascular malformations, neurol med chir suppl (tokyo) 1998, 38, 231-237 29.badhiwala j.h. et al. surgical outcomes and natural history of intramedullary spinal cord cavernous malformations: a single-center series and meta-analysis of individual patient data, journal of neurosurgery: spine, july 25, 2014; doi: 10.3171/2014.6.spine13949. 30.gross b.a., et al. intramedullary spinal cord cavernous malformations, .neurosurg focus 2010, 29:e14. 31.jallo g.i – clinical presentation and optimal management for intrameullary cavernous malformations neurosurg. focus 2006, 21(1): e10 32.cho y.j. et al. surgical treatment of intramedullary spinal cord cavernous malformation, abstract, journal of korean neurosurgical society 2003; 33(5): 466-471 33.matsuyama y. et al. surgical results of intramedullary spinal cord tumor with spinal cord monitoring to guide extent of resection.j neurosurg spine 2009, 10:404-413 34.labauge p. et al. outcome in 53 patients with spinal cord cavernomas, surg neurol 2008, 70:176-181 35.knipe h., wein s. spinal cavernous malformation, neurosurg focus. 2010 sep;29(3):e12. 14_paper romanian neurosurgery (2015) xxix 4: 493 502 493 doi: 10.1515/romneu-2015-0066 step training in a rat model for complex aneurysmal vascular microsurgery dan martin1, mircea radu gorgan2 1phd student, university of medicine and pharmacy “carol davila”, emergency clinical hospital “bagdasar arseni”, bucharest 2professor of neurosurgery, clinic of neurosurgery, emergency clinical hospital “bagdasar arseni”, university of medicine and pharmacy “carol davila”, bucharest this paper was co-financed from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/187/1.5/s/155605 abstract: introduction: microsurgery training is a key step for the young neurosurgeons. both in vascular and peripheral nerve pathology, microsurgical techniques are useful tools for the proper treatment. many training models have been described, including ex vivo (chicken wings) and in vivo (rat, rabbit) ones. complex microsurgery training include termino-terminal vessel anastomosis and nerve repair. the aim of this study was to describe a reproducible complex microsurgery training model in rats. materials and methods: the experimental animals were brown norway male rats between 10-16 weeks (average 13) and weighing between 250-400g (average 320g). we performed n=10 rat hind limb replantations. the surgical steps and preoperative management are carefully described. we evaluated the vascular patency by clinical assessment-color, temperature, capillary refill. the rats were daily inspected for any signs of infections. the nerve regeneration was assessed by foot print method. results: there were no case of vascular compromise or autophagia. all rats had long term survival (>90 days). the nerve regeneration was clinically completed at 6 months postoperative. the mean operative time was 183 minutes, and ischemia time was 25 minutes. key words: microsurgery, training, replantation introduction with the increasing use of microsurgical techniques in neurosurgery, regular laboratory training has become essential. microneurosurgical operations differ from other surgery. longer operative time, narrow 494 martin, gorgan step training in a rat model for complex aneurysmal vascular microsurgery and deep-seated operative corridors, hand-eye coordination, fine manipulation, and physiologic tremor present special problems. proper understanding of visual feedback, control of physiologic tremor, better instrument design, and development of surgical skills with better precision is important for optimal surgical results. sufficient clinical case volume or opportunity during routine operative hours may not be available in the beginning for young neurosurgeons and microsurgical training using various models can enable them to gain experience. training models using deep-seated and narrow operative corridors, drilling, knottying technique, and anastomosis using fine sutures under high magnification can be practiced for skill improvement. training laboratory and simulation modules can be useful for resident training and skill acquisition. the knowledge of ergonomics, proper training, observing hand movements of skillful surgeons, and the use of operative videos can improve skill (1). the aim of this article is to describe the surgical steps in limb replantation in a rat model as complex microsurgical training. material and methods the study was done in the microsurgery laboratory in the emergency clinical hospital in bucharest. the experimental animals were brown norway male rats between 10-16 weeks (average 13) and weighing between 250-400g (average 320g). we performed n=10 rat hind limb replantations. the surgical steps and preoperative management are carefully described. we evaluated the vascular patency by clinical assessment-color, temperature, capillary refill. the rats were daily inspected for any signs of infections. the nerve regeneration was assessed by foot print method. for anesthesia the animals were placed into the induction chamber with anesthetic gas inflow. the rats were anesthetised with xylazine (0,02 ml ) and ketamine (0,01ml). monitoring throughout anesthesia was done using the tail pinch reflex, respiratory rate, heart/pulse rate and tissue color. the whole operation is performed under aseptic conditions and antibiotic prophylaxis was administered using clavulox 0.1 ml/100 g. s.c. at the commencement of the operation. fluid loss during the operation was compensated with 6-7 ml 0.9% sodium chloride solution given by intraperitoneal injection. no vasodilatant or anticoagulation drugs were used except for the limb perfusion. surgical procedure a circumferential skin incision of the hind limb was made at the mid-thigh level (figure 1). the inguinal fat flap with pedicle a. and v. epigastrica superficialis and sensory nerve branch from n. saphenus was sharply dissected and after isolation of the pedicle flap was reflected distally. the saphenus nerve was prepared and transected proximally at the level of its branching from n. femoralis. the femoral artery and vein were then identified and skeletonized (figure 2). the femoral artery was clamped with a double microvascular clamps and transected. the femoral vein was clamped and transected. perfusion washout was performed with 4oc cold heparinized romanian neurosurgery (2015) xxix 4: 493 502 495 doi: 10.1515/romneu-2015-0066 solution (1500 ui of heparin in 500 ml of 10% dextran 40 intravenous infusion bp in 0.9% sodium chloride intravenous infusion). the thigh muscles were sharply cut approximately 1 cm distally from the level of the femoral nerve branching into the muscular branches and n. saphenus. this muscle dissection must be performed very carefully as it is close to the branching of the femoral artery and vein into the saphenous and popliteal vessels. during muscle dissection the sciatic nerve was solicitously protected when it emerged between thigh adductors and m. quadratus femoris on the one side and m. biceps femoris on the opposite side (figure 3). this nerve was isolated and cut proximally. skeletonisation of the middle third of the femoral bone was done. the femur was then divided in the middle using a bone saw. after amputation, muscles, bone, vessels and nerves of the limb were meticulously washed down with 0.9% sodium chloride solution (figure 4). for the replantation, first, femoral bone fixation was achieved by a combined technique using intramedullary rod made from a 19-gauge stainless steel needle and osteosuture using 28 swg monofilament stainless steel suture wire. muscles were then sutured with 4/0 nylon interrupted stitches with emphasis on precise adaptation of functional muscle groups. an epiperineural suture of the sciatic nerve was performed an-block either from the anterior or posterior access under the operating microscope using 10/0 nylon before muscle suture completion (figure 5). femoral vessels were washout with 0.9% sodium chloride solution and the ends were precisely trimmed before anastomosis. revascularisation started with vein suturing. both vessels were sutured under the microscope using 10/0 nylon single stitches (figure 6). clamps were removed first from the artery and after a few seconds, when femoral vein began to expand with blood, the clamps were removed from the vein. firstly the distal vein clamp was taken away to allow dilatation of the vein anastomosis and then the proximal clamp was removed. the initial bleeding from both anastomoses stopped after a few seconds of gentle compression with a wet gauze swab. after restoration of the blood flow in the reconnected vessels the suturing of n. saphenus was done under the microscope using the same technique as for the sciatic nerve. an ample washout of the wound with 0.9% sodium chloride solution was performed and the replantation was completed by skin closure with running 4/0 nylon sutures. note it is important to include subcutaneous fat into this suturing to prevent bleeding from large vessels in the subcutaneous fat mainly in the hypogastric and inguinal area. after completion of the surgery, the skin suture was wiped down with povidone-iodine 10% solution and no wound covering or limb splint was used. the animals after awakening from anesthesia were put in a clean, dry, warmed box on a folded towel in a quiet post-operative room (30-32oc) away from strong light. immediately post recovery the animals were housed with a companion and allowed free access to food and water. no collar or other special device was used to prevent selfmutilation. 496 martin, gorgan step training in a rat model for complex aneurysmal vascular microsurgery figure 1 skin incision figure 2 femoral vessel dissection figure 3 sciatic nerve identification figure 4 limb ready for replantation figure 5 epineural sciatic nerve repair figure 6 arterial anastomosis romanian neurosurgery (2015) xxix 4: 493 502 497 doi: 10.1515/romneu-2015-0066 results there were no case of vascular compromise or autophagia. all rats had long term survival (>90 days). the nerve regeneration was clinically completed at 6 months postoperative. the mean operative time was 183 minutes, and ischemia time was 25 minutes. discussions while microvascular suturing technique was the province of neurosurgeons a couple of decades ago, nowadays almost every surgical specialty uses this technique for its one pathology. many programs have integrated training in microvascular anastomosis techniques in their curricula. the surgeons are either trained at their own institution, if this happens to have a microvascular animal laboratory, or they are sent to centers that conduct microsuturing courses. materials that are initially used for learning microsurgical suturing and knot techniques are latex (2) and silicon tubules (2), (3), (4). however, the ‘‘feel’’ of manipulating viable biological tissue is achieved only in small animal laboratories (4) (5). the available models for training microvascular anastomosis techniques may be classified into three categories: (1) the nonbiological and nonfunctional, (2) the biological and nonfunctional, and (3) the vital small animal model, which demands investment and maintenance (6). each of these models has its advantages and disadvantages, which are very well-known. recently abouod et al. proposed a model of a perfused human cadaver head for training neurosurgical procedures (7). the success of a microvascular suture, irrespective of the technique, can only be proved through surviving replanted parts in chronic experiments, e.g., tail and limb replantation or organ transplantation in rats (5), (8), (9) (10), (11), (12), (13). since 1968s when komatsu and tamai reported first successful digit replantation with repair of micro blood vessels, the laboratory microsurgical training on rats become popular model in microvascular surgery. having in mind that microsurgery is a precise surgical skill that requires an extensive training period of time and creates a simulated surgical environment that allows gifted surgeon to make and recognize mistakes in microsurgery techniques and thus shifts any related risks of the early training period from the real case on the operating room to the lab allowing in this way achieving a high level of skill acquisition. the classical training schemes in microsurgery lab experimental on the rat model was to take surgeon through a series of microsurgical maneuvers that would develop his skills utilized the femoral artery and vein, the epigastric artery and vein, and the sciatic nerve working at mid –to high-range magnification. sun lee's manual fifty years ago describing microsurgery techniques in the rat to respond the aspirations of the surgeons of that time, the surgical field is again in need of further microsurgical training interventions with the advent of new horizons in microsurgery that will and be applied in vascular microvascular surgery (14). 498 martin, gorgan step training in a rat model for complex aneurysmal vascular microsurgery they are many papers and studies that presents the utility and beneficiates of the classical rat model of microsurgery training centres and the new prospects that this versatile and not suchexpansive training model offers. it is motivated and supported the idea that practice is key to microsurgery skill maintenance and improvement, at least at a trainee level where a laboratory based surgical skills can significantly improve skill. the widespread use of microsurgery in numerous surgical fields has increased the need for basic microsurgical training outside of the operating room. this stage is basic and the most important; the aim is to develop the fundamental skills of using microsurgical instruments under a magnified field. the minimum requirements would be an operating microscope, microsurgical instruments, suture materials and non-living models. advances in microsurgery continue to be based on the experimental animal models. ilie et al. organized microsurgical models into five main groups: 1) basic manipulation, movement, and orientation in the microscopic field. 2) knot placement/tying principles, apposition of edges, non-dominant hand usage, and deformable volumes. 3) threedimensional models/completing the anastomosis. 4) the real tissue experience (15). the distinctive emphasis that microsurgery places on advanced technical skills gives it particular challenges for training. currently, there is no universal system by which surgical skills are assessed, but generally there are considered to be three broad categories: cognitive/clinical skills, technical skills, and social/interactive skills (16). the distribution of these skills is debated and depends upon the specialty and the particular operation being undertaken (17). as in any other domain more so in microsurgery the past and everything go well in this field must be remembered, updated and taken as a landmark. the limited time, resources and opportunities to practice microsurgical technique in clinical settings, along with the serious consequences of failure, have led to the establishment of microsurgical training courses. reviews of microsurgical training centers worldwide shows that basic microsurgery courses range in duration and intensity from 20 to 1,950 hours. on average (18), a basic microsurgical training course lasts 40 hours (5 days) costing $1,500 (usd). so it is worth remembering the rat model in microsurgery education and development of this practice along other training courses: paris school of surgery (paris, france), northwick park workshops (london, uk), and columbia university (new york, usa). the paris school of surgery is the longest serving out of eighteen training courses on the record to date in france, all of which are either basic 'certificate' courses or advanced university 'diploma' courses. the training lab was established in 1976 by dr. alain gilbert, gisèle amichot, and josette legagneux as instructors. currently, the course is directed by professor alain masquelet, the course with two parts: basic and advanced teaches about 60-70 surgeons per year (19). romanian neurosurgery (2015) xxix 4: 493 502 499 doi: 10.1515/romneu-2015-0066 in the united kingdom (working within home office guidelines for the use of animals), basic microsurgery workshops were established at northwick park institute of biomedical research in 1979 by professor colin green and sandra shurey (20). at columbia university (cu), the microsurgery research and training lab was established in the early 1980s by dr. harold m dick in the department of orthopedic surgery, and now it is under the leadership of dr. melvin p. rosenwasser and dr. yelena akelina, training over 150 surgeons every year, from 12 specialties and more than 45 countries. all of the courses emphasise the importance of the right attitude and psychology set in achieving a successful outcome in microsurgery. classical exercises were developed to take surgeons through a series of microsurgical maneuvers that would develop their skill (21). vascular microsurgery training, maybe more than others surgical fields, across the world is very heterogeneous. ex-vivo prosthetic models such as the latex glove, silicone sheets and tubing can be for some level a common starting point in microsurgical training, followed by a variety of non-living animal models, such as the turkey coronary artery, and chicken wing artery, the advantages of non-living and prosthetic models are: portability, minimal maintenance over a favorable shelf life, and with no biological hazards or regulations for their usebut they may not be as realistic as living models. recently the most commonly used animal model in microsurgical courses is the rat. microvascular end-to-end and end-to-side anastomoses are common to most basic models, with half the practice on larger arteries (>1 mm diameter) prior to practice on smaller arteries (≤1 mm diameter). in vivo vascular microsurgery models offers an opportunity for reviewing the functional results of anastomoses while taking account that nerve models demand a different dissection and tissue handling. amputated rat limbs storage by wet and cold (4°c) showed no macroscopic changes or weight increase rate. limbs preserved by wet and cold appeared to have insufficient blood circulation, causing limb necrosis within 3 days of surgery. the current method of preserving amputated limbs involves simply wrapping them with saline-moistened gauze and then cooling them on ice (22). this method is basically similar to allen’s, which was reported more than 70 years ago (23).new methods modified of preserving muscle tissues have not been developed for a long time. at this moment replantation it is considered to be successful not only when there is vascular circulation to the amputated limb but also when limb function is restored. some animal experiments have evaluated functional recovery of ischemia–reperfusion limbs. song et al. (24) reported good functional recovery of rat limb allografts after the immediate limb transplantation by using a cutaneous reaction test, walking track analysis, and electrophysiological evaluation. 500 martin, gorgan step training in a rat model for complex aneurysmal vascular microsurgery tsuji et al (25) performed an electrophysiological study after rat limb transplantation in several ischemia periods and found that the distal motor latencies of the sciatic nerve at 3 weeks increased with increasing limb ischemia time. the results may depend on not only muscle function recovery but also sciatic nerve regeneration. preservation solutions can protect muscle function and morphology in ischemiareperfusion limbs and improve recipient survival rates after transplantation of longterm-preserved limbs (26). replantation of major extremities after long periods of ischemia can lead to viable replants in many cases, but functional restoration is often poor owing to fibrosis of the muscle (27). intermittent blood flow provided a much better outcome than continuous ischemia for rat limb preservation at room temperature. only a short period of time (on average 10min) perfusion every 4 hour appeared to result in insufficient blood supply, but was nonetheless effective in preserving the limb (28). it is postulate that as in health under normal physiologic conditions, there is a safety margin of oxygen delivered to the tissues (29). having this as information, we revised a series of limb preservation studies with oxygen carriers. autologous blood is often used in such experiments but the clinical utility of this approach is limited (30). in systematic review done by ghanem et al to identify randomized control trials looking for educational and training interventions that objectively improved microsurgical skill acquisition, although there is significant paucity in the literature reviewed to support microsurgical course and training practices, simulated training on fidelity models in microsurgery is an effective intervention that leads to acquisition and refining of transferable skills and improved technical performance (31). sutherland et al, looked at 30 randomized control trials, all of methods of delivering surgical education, such as computer simulation, video simulation, and physical models against classic predominant current teaching summarizing that computer and video simulation did not significantly enhance training but that model and cadaveric training showed promise expectation (32). sturm et al. carried a systematic review comparing whether skills acquired in simulation training were transferable to the operating room in the surgical field, they concluded that on the whole simulation training does transfer to the operative setting and is a safe and effective means for adjunct surgical education particularly in novice trainees, as it helps eliminate part of the steep learning curve, and improve visuo-spatial awareness (33). szalay et al. showed that novice surgeons had to perform between 40 and 48 vessel anastomoses to achieve 100% patency on live rats two weeks after the procedure (34). zhaowei zhu et al used showed that limbs rats with a minimal amount of muscle tissue can be successfully replanted. because of its complexity, cryopreservation of muscle tissue is challenging and injury during the cryopreservation process and from reperfusion results in swelling and elimination of blood flow (35). in our study, the mean romanian neurosurgery (2015) xxix 4: 493 502 501 doi: 10.1515/romneu-2015-0066 ischemia time was acceptable and no cryopreservation was done, only a moist gauze was applied over the limb to avoid tissue desiccation. hin-lun liu reveled that consistent size and anatomy of the femoral vessels in a rat model allow very easy and quick dissection of vessels, which is particularly useful for surgeons who want intensive training of submillimeter vessels anastomosis (36). in our study we performed the microvascular arterial anastomosis in a classical method on femoral artery with a mean diameter of 0.5 mm. conclusions we successfully descried step by step the surgical procedure of a limb replantation in a rat model. several options of training and assessing microanastomosis have been described previously. methods of assessment included long-term evaluation of patency of the micro-anastomosis performed in animals models (37), as well as structured video assessment by expert microsurgeons (38) (39). the use of these training models and assessment modalities validated improvement while training (40). performing a complex operation such as a limb replantation is a highly demanding procedure for the young neurosurgeon. important operative skills as microvascular arterial and venous anastomosis are trained, useful tools in daily clinical work. correspondence dan martin emergency hospital “bagdasar arseni” bucharest berceni street 10-12, bucharest, romania e-mail: danmartinmd@yahoo.com references 1. microneurosurgical skills training.yadav yr, parihar v, ratre s, kher y, iqbal m. j neurol surg a cent eur neurosurg. 2015 apr 27. 2. lee s, coppersmith wj. a microvascular surgical practice disc for beginners. microsurgery 1983 and 4:67-69. 3. senior ma, southern sj, majumder s. microvascular simulator— a device for micro-anastomosis training. ann r coll surg engl 2001 and 83:358_360. 4. habal sm, fitzpatrick hf, green ge. training in microvascular surgery. surgery 1977 and 81:596_598. 5. 1995, bao jy. rat tail: a useful model for microvascular training. microsurgery and 16:122_125. 6. lannon da, atkins ja, butler pe. non-vital, prosthetic, and virtual reality models of microsurgical training. microsurgery 2001 and 21:389_393. 7. aboud e, al mefty o, yasargil mg. new laboratory model for neurosurgical training that simulates live surgery. journal of neurosurgery 2002 and 97:1367_1372. 8. araico-laguillo j, andrade-gomez f, arambulaalvarez ih, ochoa-diaz le. training program for free transfer of skin grafts by microvascular anastomosis. archives of invested medicine (mex) 1981 and 12:323_339. 9. zhang f, chin bt, ho pr, costa ma, lineaweaver wc, buncke hj. rat tail replantation as a training model for microvascular procedures of digit replantation. microsurgery 1998 and 18:364_367. 10. amara b, fernandez jj, newlin l, buncke hj. transfer of the rat tail: an experimental model for free osteocutaneous transfer. j reconstr microsurg 1998 and 14:359_362. 11. 1993, rosslein r. experimental approaches towards testicular autotransplantation. european journal of pediatriacs and 152:47_49. 12. schonauer f, la ri, gonzales yr, romagnuolo m, molea g. laboratory model of a microvascular free flap in rat: the epigastric flap. minerva chirurgia 2002 and italian]., 57:537_541 [in. 13. matsumura n, hamada h, yamatani k, hayashi n, hirashima y, endo s. side-to-side arterial anastomosis model in the rat internal and external carotid arteries. journal of reconstructive microsurgery 2001 and 17:263_266. 14. koshima i, inagawa k, urushibara k, et al. supermicrosurgical lymphaticovenular anastomosis for the treatment of lymphedema in the upper extremities. j reconstr microsurg. 2000 and 16:437–442. 15. ilie vg, ilie vi, dobreanu c, et al. training of microsurgical skills on nonliving models. 502 martin, gorgan step training in a rat model for complex aneurysmal vascular microsurgery microsurgery.2008;28:571–577. 16. aucar ja, groch nr, troxel sa, et al. a review of surgical simulation with attention to validation methodology. surg laparosc endosc percutan tech. 2005;15:82–89. 17. spencer f. teaching and measuring surgical techniques: the technical evaluation of competence. bull am coll surg. 1978;64:9–12. 18. wokes j. microsurgery training courses: a review. face mouth jaw surg. 2012;2:12–15. 19. cabrol c, gilbert a. training of microsurgery in the laboratory of the hopitaux de paris. chirurgie.1991;117:145–148. 20. green c, simpkin s. clinical research centre (harrow, london, england) basic microsurgical techniques: a laboratory manual. harrow, middlesex, uk: surgical research group, mrc clinical research centre; 1986. 21. the rat model in microsurgery education: classical exercises and new horizons, sandra shurey,1 yelena akelina,2 josette legagneux,3 gerardo malzone,4 lucian jiga,5 and ali mahmoud ghanem; arch plast surg. 2014 may; 41(3): 201–208). 22. lloyd ms, teo tc, pickford ma, et al. preoperative management of the amputated limb. emerg med j. 2005;22:478–480 . 23. allen fm. surgical considerations of temperature in ligated limbs. am j surg. 1939;45:459–464. 24. song yx, muramatsu k, kurokawa y, et al. functional recovery of rat hind-limb allografts. j reconstr microsurg. 2005;21:471–476 . 25. ( tsuji n, yamashita s, sugawara y, et al. effect of prolonged ischaemic time on muscular atrophy and regenerating nerve fibres in transplantation of the rat hind limb. j plast surg hand surg. 2012;46:217–221. 26. muscle is a target for preservation in a rat limb replantation model, iijima y1, ajiki t1, teratani t1, hoshino y1, kobayashi e1; plast reconstr surg glob open. 2013 dec 6;1(8):e70. 27. preservation of skeletal muscle in tissue transfers using rat hindlimbs, kihira, masayasu m.d.; miura, takayuki m.d.; ishiguro, naoki m.d, plastic & reconstructive surgery. 88(2):275-284, august 1991. 28. normothermic preservation of the rat hind limb with artificial oxygen-carrying hemoglobin vesicles ; jun araki,1 hiromi sakai,2,3 dai takeuchi,1,4 yu kagaya,1,5 kensuke tashiro,1 munekazu naito,6 makoto mihara,1 mitsunaga narushima,1 takuya iida,1 and is. 29. thomas d. the physiology of oxygen delivery. vox sang. 2004; 87(suppl 1):70. 30. müller s, constantinescu ma, kiermeir dm, et al. ischemia/reperfusion injury of porcine limbs after extracorporeal perfusion. j surg res 2013; 181:170. 31. ghanem am1, hachach-haram n, leung cc, myers sr.a systematic review of evidence for education and training interventions in microsurgery. archives of plastic surgery. 2013 jul and 40(4):312-9. 32. sutherland lm, middleton pf, anthony a, et al. surgical simulation: a systematic review. annals of surgery 2006 and 243:291–300. 33. sturm lp, windsor ja, cosman ph, et al. a systematic review of skills transfer after surgical simulation training. ann surg. 2008 aug and 248(2):16679. 34. szalay d, macrae h, regehr g, et al. using operative outcome to assess technical skill. american journal of surgery 2000 and 180:234–237. 35. zengtao wang bo he, yongzhuang duan,yun shen, lei zhu, xiaolei zhu,zhaowei zhu. cryopreservation and replantation of amputated rat hind limbs. european journal of medical research. 2014 and 28., 19(1):. 36. hin-lun liu. microvascular anastomosis of submillimeter vessels—a training model in rats. journal of hand and microsurgery. june 2013, volume 5, issue 1, pp 14-17. 37. s. komatsu, k. yamada, s. yamashita, n. sugiyama, e. tokuyama, k. matsumoto, a. takara, y. kimata. evaluation of the microvascular research center training program for assessing microsurgical skills in trainee surgeons. arch plastic surg, 40 (2013), pp. 2. 38. j.c. selber, e.i. chang, j. liu, h. suami, d.m. adelman, p. garvey, m.m. hanasono, c.e. butler. tracking the learning curve in microsurgical skill acquisition. plastic reconstr surg, 130 (2012), pp. 550e– 557e. 39. e. nugent, c. joyce, g. perez-abadia, j. frank, m. sauerbier, p. neary, a.g. gallagher, o. traynor, s. carroll. factors influencing microsurgical skill acquisition during a dedicated training course. microsurgery, 32 (2012), pp. 649–656. 40. w.y. chan, a. figus, c. ekwobi, j.r. srinivasan, v.v. ramakrishnan. the 'round-the-clock' training model for assessment and warm up of microsurgical skills: a validation study.j plastic reconstr aesthet surg, 63 (2010), pp. 1323–1328. 41. nov, doi k. homotransplantation of limbs in rats. a preliminary report on an experimental study with nonspecific immunosuppressive drugs.plast reconstr surg. 1979 and 64(5):613-21. cucua_falx romanian neurosurgery (2016) xxx 2: 209-213 | 209 falx cerebri tuberculoma mimicking en plaque meningioma – case report a.i. cucu1, dana mihaela turliuc1,2, anca sava1,2, gabriela florența dumitrescu1, ș. turliuc2, claudia florida costea1,2 1“prof. dr. n. oblu” emergency clinical hospital iasi, romania 2“grigore t. popa” university of medicine and pharmacy iasi, romania abstract: background: the involvement of falx cerebri in tuberculosis is extremely rare, with only three cases reported so far in the literature. the diagnosis is most often difficult to establish, given the location of the lesion, making surgical intervention necessary for a definite histopathologic diagnosis. methods: we present the case of a 49-year old female patient who was admitted for a right jacksonian seizure, followed by a right crural monoparesis, without a history of tuberculosis. the lesion mimicked a falx cerebri en plaque meningioma in the imaging tests. results: a complete surgical excision was performed through a left fronto-parietal parasagittal approach. the histopathological examination revealed a case of cerebral tuberculosis. the surgical treatment was complemented postoperatively with antituberculous therapy. conclusion: in this article, we emphasize the rarity of the lesion at this level and also presenting similar cases from the literature. moreover, we also discuss epidemiological, clinical, imaging, therapeutic as well as pathological aspects of en-plaque dural tuberculoma. key words: falx cerebri tuberculoma, en plaque tuberculoma, neurotuberculosis introduction the prevalence of central nervous system tuberculosis (tb) is constantly increasing worldwide (4). the incidence of intracranial tuberculomas varies between 0.15-0.18% in developing countries and represents between 5% and 30.5% of all intracranial space occupying lesions (6, 12). in this paper, we present the case of a falx cerebri tuberculoma mimicking en plaque meningioma extremely well, in 49-year-old women, discussing epidemiological, pathological, clinical and radiological findings and treatment according to this exceptional localization. short case report a 49-year-old women with no medical past history, was admitted for a right crural monoparesis, which occurred further to a right jacksonian seizure, in apparent health status. 210 | cucu et al falx cerebri tuberculoma mimicking en plaque meningioma results the clinical examination and the chest xray revealed normal findings. the cranial computed-tomography (ct) scan performed on admission revealed a falx cerebri tumor with a perilesional edema. magnetic resonance imaging (mri) aspect showing the presumptive diagnosis of falx cerebri en plaque meningioma (figure 1, figure 2). the surgical procedure consisted of a left frontoparietal parasagittal craniotomy with complete resection (figure 3). the histopathological examination objectified the diagnosis of leptomeningeal tuberculosis (figure 4). although mycobacterium tuberculosis was not revealed in the cerebrospinal fluid (csf) cultures and in the excised tissue, due to the histopathological exam which disclosed the tuberculoma, the antituberculosis therapy (att) was continued with a combination of four drugs (isoniazid, rifampicin, pyrazinamide and ethambutol) following conventionally recommended treatment regimens. the neurological evolution was favorable with the remission of the motor deficit. romanian neurosurgery (2016) xxx 2: 209-213 | 211 figure 1 a, b preoperative magnetic resonance imaging; c, d postoperative imaging aspect after 4 months figure 2 leptomeninges thickened by the presence of numerous granulomas of tuberculosis with the tendency to confluence, with central caseous necrosis surrounded by multinucleated giant cells and epithelioid cells, as well as numerous peripheral lymphocytes. the lesion infiltrates the adjacent nerve tissue (bottom-left) (col.h-e, x100) figure 3 langerhans multinucleated giant cell alongside numerous lymphocytes (col.h-e, x 400) discussion despite the fact that there have been reports of intracranial en plaque tuberculoma located at the cerebral convexity (9, 10), tentorium cerebelli (1) or cavernous sinus (6), the falx cerebri en plaque tuberculoma remains an extremely rare condition in literature. en plaque tuberculoma was described for the first time in 1927 by pardee and knox as a lesion similar to en plaque meningioma, located in the frontoparietal region (10). only three cases of falx cerebri en plaque meningioma have been published so far in the literature, located in the frontoparietal (5), frontal, towards the top of the falx cerebri (3) and interhemispheric, in the pericallosal cistern (1), but none located in the high frontoparietal region, as in the case of our patient. the intracranial location at this level is the result of a hematogenous spread from a primary dormant locus at the level of the lungs, which becomes active in the brain through a rich focus (13). several hypotheses 212 | cucu et al falx cerebri tuberculoma mimicking en plaque meningioma according to which the the mycobacterium tuberculosis bacillus reaches the brain have been considered: by narrowing of the arterioles supplying the cortex as they enter the white matter or by the spreading of the infection from the level of the csf in the adjacent parenchyma, via the cortical veins or the virchow–robin perivascular spaces at the level of the small penetrating arteries (7). in the case in which the tuberculoma develops en plaque, it remains, for the most part, attached to the dura mater; it does not produce a central cavity of caseation and does not calcify (8), a behavior also adopted by the dural-based en plaque tuberculoma which we presented. of all patients with pulmonary tuberculosis, only 1% develops an intracranial tuberculoma which occurs in most cases within miliary tuberculosis. the map of intracranial tuberculomas locations shows that they can develop anywhere in the brain, but they occur most often the cerebrum and cerebellum lobes. the rare locations include the brainstem, the sellar region, the cerebellopontine angle, the basal ganglia, the thalamus, the pineal region and the cavernous sinus. the most common locations for en plaque tuberculoma are the frontal and parietal convexity, the tentorium cerebelli and the posterior fossa (3, 9, 14). en plaque tuberculoma can be described as a solid and well-defined lesion that is able to compress the adjacent structures, with a creamy-white macroscopic aspect, without areas of caseation or calcification (3, 9, 14). the clinical symptomatology depends on the location of the tuberculoma. the most common symptoms are: cephalalgia, vomiting, blurred vision, seizures or motor neurological deficits. in 50% of the patients, the symptoms persist less than 6 months until onset. in 33% of the patients with cerebral tuberculomas, the lung radiography is normal, as in the case of our patient. moreover, the esr is also a questionable paraclinical test, due to the fact that it reveals a high value only in 15% of the patients and it shows a high value in the case of gliomas as well (3). furthermore, the laboratory analysis of saliva, urine, gastric juice and csf rarely isolate the tubercle bacilli (2). in mri imaging, in the case of cerebral tuberculomas, a thickening of the dura mater with the characteristic appearance of the dural tail found in meningiomas can be observed (2), thus creating a common confusion between an en plaque tuberculoma and a meningioma, especially if it is located in the frontoparietal (5), pericallosal (1), pontine and suprasellar regions. calcification is not an indicator of the inactivity of the lesion and the contrast enhancement can be absent in patients with aids due to the absence of immune response. this was not an issue in our case, as the patient was hiv negative. the imagining of the dural en plaque tuberculoma is not characteristic and differential diagnosis, which is often impossible, is made with lesions such as: meningioma, cerebral metastases, astrocytoma, lymphoma, sarcoidosis, neurosyphilis, empyema, intracranial fibromatosis, leptomeningeal carcinomatosis, arteriovenous malformation, etc. the att is the main form of treatment. poonnoose et al. concluded in their studies romanian neurosurgery (2016) xxx 2: 209-213 | 213 that in over 2/3 of patients placed under att and with a partial resection or biopsy, the ct revealed persistent lesions, even after 18 months of drug therapy (11). surgical treatment is recommended in atypical cases (when histopathologic diagnosis is required) and in symptomatic cases, as in the case we presented (the patient had right crural monoparesis). conclusion intracranial tuberculomas, although rare in developed countries, should be taken into consideration in the differential diagnosis of the intracranial space-occupying process, especially in the geographical regions in which tuberculosis is endemic. correspondence dana mihaela turliuc “prof. dr. n. oblu” emergency clinical hospital iasi, romania e-mail: turliuc_dana@yahoo.com references 1.adachi k, yoshida k, tomita h, niimi m, kawase t. tuberculoma mimicking falx meningioma-case report. neurol med chir 2004; 44: 489-492. 2.castro cc, barros ng, campos zm, cerri gg. ct scans of cranial tuberculosis. radiol clin north am 1999; 33: 753–769. 3.elisevich k, arpin ej. tuberculoma masquerading as a meningioma. case report. j neurosurg 1982; 56(3): 435438. 4.gropper mr, schulder m, duran hl, wolansky l. cerebral tuberculosis with expansion into brainstem tuberculoma. report of two cases. j neurosurg 1994; 81: 927–931. 5.isenmann s, zimmermann dr, wichmann w, moll c. tuberculoma mimicking meningioma of the falx cerebri. pcr diagnosis of mycobacterial dna from formalinfixed tissue. clin neuropathol 1996; 15: 155–158. 6.jaimovich sg, thea vc, guevara m, gardella jl. cavernous sinus tuberculoma mimicking a neoplasm: case report, literature review, and diagnostic and treatment suggestions for tuberculomas in rare locations. surg neurol int 2013; 4:158 7.mcguinness fe: intracranial tuberculosis. in: clinical imaging in non-pulmonary tuberculosis. mcguinness fe. springer, berlin heidelberg new york 2000: 5–25 8.mullener er. six geneva physicians on meningitis. j hist med allied sci 1965; 20 (1): 1-26. 9.ng sh, tang lm, lui tn, ko sf, wong hf, wai yy, wan yl. tuberculoma en plaque: ct. neuroradiology 1996; 38(5):453-455. 10.pardee i, charlton l. tuberculoma en plaque. arch neur psych 1927. 17(2): 231-238. 11.poonnoose si, rajshekhar v. rate of resolution of histologically verified intracranial tuberculomas. neurosurg 2006; 53(4): 873-879 12.ramamurthi b, varadarajan mg. diagnosis of tuberculomas of the brain: clinical and radiological correlation. j neurosurg 1961; 18: 1-7. 13.rich a. the basis of symptoms in tuberculous meningitis. in: the pathogenesis of tuberculosis. oxford: blackwell scientific publications 1951: 893–894. 14.vengsarkar us, pisipaty rp, parekh b, panchal vg, shetty mn. intracranial tuberculoma and the ct scan. j neurosurg 1986; 64: 568-574. 8_tascua_growing skull 282 tascu et al growing skull fracture in a 2 months old child growing skull fracture in a 2 months old child a. tascu1, iulia e.b. vapor1, a. iliescu1, irina tudose1, st.m. iencean2 1pediatric neurosurgical department, “bagdasar-arseni” clinical hospital, bucharest, romania 2“gr. t. popa” university of medicine and pharmacy, iassy, romania abstract: a growing skull fracture, also called posttraumatic leptomeningeal cyst, is a rare complication of skull fractures less than 1%, usually encountered in children younger than 3 years old. although rare, this complication must be recognized early and treated to prevent permanent neurologic deficits. we present the case of a 2 months old child who had suffered a closed head trauma in a car accident 2 weeks before he was admitted in our clinic with a left parietal growing skull fracture. he was submitted to surgery and leptomeningeal cyst was evacuated, dural defect repaired and bone fragments fixed. child was discharged 6 days postoperative without neurologic deficits. growing skull fractures represent a rare complication of head trauma in small children. it is imperious to be recognized and treated in early phases to prevent debilitating permanent neurologic deficits in that category of population. key words: growing skull fracture, leptomeningeal cyst. introduction growing skull fracture is a rare complication of paediatric skull fracture. it is a poorly understood complication of head trauma and it results in dural tear and brain lesion that can enlarge the initial linear fracture. it is also called posttraumatic leptomeningeal cyst and the usual site is parietal bone, with a palpable bony defect. we present the case of a 2 months old child with a closed head trauma in a car accident 2 weeks before the admission in our clinic. case presentation in this paper we present the case of a child who was admitted in our clinic at the age of 11 weeks with a big subgaleal fluid collection in the left parietal region. two weeks before admission in our clinic the child suffered a head trauma in a car accident. ct-scan performed at that time revealed a left parietal hemorrhagic contusion and left parietal fracture. the child was discharged one week after trauma with good neurologic condition. at admission in our clinic the child was alert, had no neurologic deficits and at the local exam of the scalp was noticed a tumefaction approximately 5/6 cm, with fluid consistency. ct-scan performed revealed a diastatic left parieto-occipital skull fracture with an underlying porencephalic cyst and subgaleal fluid collection (figures 1, 2). the child underwent surgery. after incision of the scalp approx 50 ml clear liquid were evacuated. we noticed a diastatic parietal skull fracture from coronal suture to lambdoid suture and part of occipital bone. through fracture edges herniated cerebral tissue (figure 3). the craniotomy was made considering the fact that ruptured dura mater usually is retracted under the edges of the fracture. after removing the bone flap, margins of dura were adjusted, romanian neurosurgery (2015) xxix 3: 282 285 283 leptomeningeal cyst evacuated and scarred brain tissue removed (figure 4). after that we made duraplasty using pericranium. the two bone fragments were rigidly fixed (figure 5). ct-scan performed 24 hours postoperatively revealed total evacuation of leptomeningeal cyst without subgaleal fluid collection and fixation of bone flap. child was discharged 6 days postoperative alert, without neurologic deficits and normal healing of wound. figure 1 preoperative ct scan showing a distatic left parietal fracture figure 2 preoperative ct scan showing diastatic fracture with an underlying porencephalic cyst and subgaleal fluid collection figure 3 through fracture edges can be noticed cerebral tissue figure 4 intraoperative aspect before the duraplasty was made figure 5 intraoperative aspect after fixation of bone flaps 284 tascu et al growing skull fracture in a 2 months old child figure 6 postoperative 3d reconstruction ct-scan figure 7 postoperative 3d reconstruction ct-scan figure 8 postoperative ct-scan discussions a growing skull fracture is a rare but significant complication of pediatric head trauma, occurring almost exclusively in children who are younger than 3 years of age. it usually develops from a linear skull fracture, as sometimes occurs in a closed-head injury. therefore, it is often misdiagnosed or the treatment is either wrong or delayed. first condition in recognizing and proper treating a gsf is understanding of pathogenesis of this condition. it is unanimously accepted that a skull fracture, with underlying dural tearing and entrapment of the arachnoid membrane or brain tissue within the fracture margins, is the most important factor for gsf pathogenesis. in small children brain growing leads to increasing bone defect and herniation of cerebral tissue through the bone defect. in the early stage of gsf, the main damages to the brain and bone are caused by the injury itself. however, the damages as well as the neurological deficits will increase during the progression of gsf, especially in the late stage. the neurological deficits cause the main disruption in the quality of life for most patients with gsf. against this background, reasonable classification of the progression of gsf as well as early diagnosis and rational surgical treatment for gsf will lead to improvement in prognosis. xue-song liu classified gsf in 3 stages: prephase of gsf from the time of injury until the beginning of enlargement of fracture; early phase of gsf 2 months from beginning of enlargement of fracture and late phase of gsf that begins at 2 months after initial enlargement. best surgical results are obtained in the first two stages. stanford proposes a strategy he used for 35 years to prevent development of gsf. he explores surgically all linear fractures wider than 5 mm, in which brain irm reveals herniated brain tissue through fracture margins. regarding surgery, there are certain aspects you must take into consideration. romanian neurosurgery (2015) xxix 3: 282 285 285 scalp incision must be made so that whole fracture must be visualized and included in bone flap. after inspection of fracture, bone flap is made considering that dural margins are retracted 1-2 cm under fracture margins. after removing bone flaps intact dura is identified and carefully freed from herniated brain tissue. the most important step of surgery is watertight closure of the dural defect. pericranium, fascia lata, cadaveric dural grafts, and artificial dura have been used in this step. in our opinion, the autologous material is the best choice because of its tissue compatibility, convenience, inexpensiveness, and low rate of infection. rigid bone fixation is also important or else pulsating brain will lead to bone resorbtion. in small children new lateral bone growth will leave no defect over time. in case of persistent bone defect cranioplasty will be made. conclusion follow-up after head injury is very important to avoid misdiagnosis in gsf. most delays in diagnosis and treatment of gsf’s are related to the lack of knowledge and awareness of the condition among doctors, parents and caregivers. the parents should be informed about the possibility of gsf and be instructed to watch for any persistent or progressive scalp swelling and onset of any neurological signs and symptoms. references 1. howship j: practical observations in surgery, and morbid anatomy. london: a. strahan, 1816 2. khandelwal s, sharma g l, gopal s, sakhi p. growing skull fractures/leptomeningeal cyst. indian j radiol imaging 2002;12:485-6 3. naim-u-rahman, jamjoom z, jamjoom a, murshid wr. growing skull fractures: classification and management. br j neurosurg;8: 667-79. 1994 4. robert a. sanford: prevention of growing skull fractures. j neurosurg pediatrics 5:000–000, 2010 5. xue-song liu, m.d., chao you, m.d., ph.d., ma lu, m.d., ph.d., and jia-gang liu, m.d. growing skull fracture stages and treatment strategy j neurosurg pediatrics 9:670–675, 2012] 6. ziyal im, aydin y, türkmen cs, salas e, kaya ar, ozveren f: the natural history of late diagnosed or untreated growing skull fractures: report on two cases. acta neurochir (wien) 140:651–654, 1998 romanian neurosurgery (2019) xxxiii (3): pp. 329-331 doi: 10.33962/roneuro-2019-056 www.journals.lapub.co.uk/index.php/roneurosurgery overview of neurosurgical capacity in st. lucia emil zhalmukhamedov1, christopher magloire2, e. maidyrov3, aleric soans4, latisha elijio5, nikita nossov6, shameea mahbub7 1 scientissimum medical group (richmond hill, ny, usa.), new york chiropractic college (seneca falls, ny, usa) 2 scientissimum medical group (richmond hill, ny, usa.), suny downstate (brooklyn, ny, usa) 3 scientissimum medical group (richmond hill, ny, usa.), central almaty clinic department of interventional cardiology (almaty, kazakhstan) 4 international american university college of medicine (st. lucia, west indies) 5 cuny city college (brooklyn, ny, usa) 6 kent state university (kent, oh, usa) 7 cuny baruch college (new york, ny, usa) abstract when we talk about the most scenic caribbean islands, st. lucia is one of those islands that certainly come into our mind. it is a beautiful tourist destination and the place of post-volcanic paradise on earth. however, just like many remote caribbean islands, st. lucians (name for local population) used to have its own difficulties of obtaining on demand basic neurosurgical services in their homeland. this beautiful caribbean island, socioeconomically falls in the same category as most low-and middle-income countries (lmics) and unfortunately echoes the same unmet surgical and anaesthesia needs as the rest of them. introduction out of any specialized medical professions, neurosurgery requires diversely prepared physicians and specialized operating rooms and experienced staff, who can handle variety of cranial and spinal cases on demand. in this paper we provided an overview of current neurosurgical capacity in st. lucia, a caribbean island that recently defined its neurosurgical scope of work. our research included a systematic survey, in-person data mining and observation of neurosurgical capacity on the island from 2018 to 2019. the state of neurosurgery services on the island as of 2019 population census reported a count of 180,287 st. lucians living on the island [1]. it’s very hard to imagine that population which is getting closer to 200,000 people didn’t have an adequate access to keywords caribbean neurosurgery, neurosurgery capacity in lmics corresponding author: emil zhalmukhamedov scientissimum medical group (richmond hill, ny, usa.), new york chiropractic college (seneca falls, ny, usa) scientissimum@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 330 emil zhalmukhamedov, christopher magloire, e. maidyrov et al. the lifesaving specialized surgical procedures. up until august 2016 st. lucian’s population who suffered from complex neurosurgical diseases or traumas, had to be evacuated by air to the nearest and more medically developed island such as barbados, in order to receive a competent neurosurgical care. with this model in mind, it’s not hard to figure out that majority of critical patients who needed an immediate intervention, simply didn’t make pass the receiving hospital’s doors. presently, st. lucia has 2 fully functioning board certified neurosurgeons, namely dr. curby dwaine sydney who is native st. lucian and dr. esteban roig fabré – a distinguished professor from cuba. both neurosurgeons provide a broad (general) spectrum of adult and paediatric neurosurgical services on the island (figure 1), which are not limited to [2]: 1. brain and spine microsurgical procedures 2. craniotomy and cranioplasty for traumatic brain injuries 3. cerebrovascular accident treatments. 4. ventriculostomy and ventriculoperitoneal shunt placements. 5. spinal procedures include: discectomy, microdiscectomy and laminectomy. on the diagnostic/imaging side, the following equipment is utilized: • computed tomography (ct). • magnetic resonance imaging (mri). • electroencephalogram (eeg). • intracranial pressure (icp) monitoring. • 3d volume rendering and multi-planar reconstruction software. figure 1. proportion of available neurosurgeons to population of st. lucia due to a scarce nature of neurosurgeons on the island, both neurosurgeons also cover neuro-consult services in public victoria and private tapion hospitals for referred emergency patients. both hospitals function as level 1 trauma centres and are equipped with generalist physicians in the emergency room. additionally the ministry of health of st. lucia is working with u.s non-profit organization “wpp” which stands for world paediatric project. the wpp organization provides volunteer specialized paediatric surgeons from u.s to address the need of surgically sick children in the caribbean islands. the majority of ongoing wpp surgeries in st. lucia were addressing congenital scoliosis. those children with more complex spinal deformities have an opportunity to be flown to u.s for ongoing treatment and monitoring. prevalence of neurosurgical disease upon our discovery, st. lucia along with other lmics such as haiti has the same prevalence of neurosurgical disorders [3]. the number one spot takes traumatic brain injury (tbi) followed by cerebrovascular accidents (cva) [4][5], spinal deformities and congenital pediatric cases (figure 2). during our research findings it was interesting to note that st. lucia has low percentage of tumour prevalence in both adult and paediatric patients. figure 2. graphical representation of neurosurgical cases in st. lucia the most obvious reason for high incidence of traumatic brain injury prevalence is uncoordinated 331 overview of neurosurgical capacity in st. lucia and unstructured road infrastructure. there is no evidence of dedicated traffic police or clear markings on the pavement for traffic to flow on some major highways (figure 3). therefore every driver and pedestrian is guided according to his/her own intuition. the second largest prevalence of neurosurgical disease is cerebrovascular accidents. the cerebrovascular accidents in st. lucia directly correlate to lack of primary care screening. even though shortage of primary care doctors is not evident, citizens are not exposed to ongoing physical check-up or simply neglect doctor’s visits. our findings showcased that majority of st. lucian population older than 50 years old are found to have diabetes mellitus or uncontrolled hypertension; which can explain why it contributes to cva and makes up to 28.6% of all neurosurgery related diseases. figure 3. st. jude highway in vieux fort conclusion this paper showcased an overview of current state of neurological surgery that could be used as a guidance to further neurosurgical development in st. lucia. as st. lucian government in collaboration with world bank continues to invest capital in public healthcare [6], further studies are suggested to assess advancement of neurosurgical care from this point on. declarations consent for publication the consent for publication is not applicable for this review article. competing interests authors declared no competing interests to declare. availability of data and material data sharing is not applicable for this review article. funding funding is not applicable to this study. acknowledgements author would like to acknowledge the contributing neurosurgeons who are actively involved in improving neurosurgical care worldwide. ethics approval and consent to participate the approval and consent is not applicable to this study. references 1. saint lucia population (live). worldometers. http://www.worldometers.info/world-population/saintlucia-population/. accessed april 17, 2019. 2. sydney cd. business focus. business focus the magazine for decision makers. http://businessfocusstlucia.com/ neurosurgery-going-farther-dont/. published june 6, 2018. accessed april 17, 2019. 3. barthélemy ej, gabriel pj, lafortune y, clervius h, pyda j, park kb. the current state of neurosurgery in haiti. world neurosurgery. 2019;124:208-213. doi:10.1016/j.wneu. 2018.12.205. 4. lavados pm, hennis aj, fernandes jg, et al. stroke epidemiology, prevention, and management strategies at a regional level: latin america and the caribbean. the lancet neurology. 2007;6(4):362-372. doi:10.1016/s14744422(07)70003-0. 5. smeeton nc, heuschmann pu, rudd ag, et al. incidence of hemorrhagic stroke in black caribbean, black african, and white populations. stroke. 2007;38(12):3133-3138. doi:10.1161/strokeaha.107.487082. 6. saint lucia to improve its health coverage. world bank. https://www.worldbank.org/en/news/pressrelease/2018/09/28/saint-lucia-to-improve-its-healthcoverage. published september 28, 2018. accessed april 17, 2019. 17_sharmaanand_longsegment 344 sharma et al long segment composite split cord malformation long segment composite split cord malformation with double bony spur anand sharma, achal sharma, r.s. mittal sms medical college, jaipur, india abstract: a composite type of scm is very rare and only a few cases have been reported until today. the frequency of compositetype scm is lower than 1% in the literature. in this report, we presented an unusual case of long segment composite type split cord malformation with double level bony spur with multiple associated bony anomalies. key words: composite split cord malformation, double bony spur introduction split cord malformations (scm) are rare, congenital spinal anomalies involving splitting of the cord. here, a segment or whole of the spinal cord is divided into two parts by a rigid or a fibrous septum. these are usually diagnosed in children, up to 20% may be present in adulthood (6). scoliosis and skin lesions are the main physical findings in patients with scms. composite type scm is very rare and results from two separate foci of ectoendodermal adhesions and endomesenchymal tracts (7) leading to development of different scm types with intervening normal cord in the same patient (4). only a few cases of composite type scm have been reported in literature. in this report, we presented an unusual case of long segment composite type split cord malformation with double level bony spur and multiple associated bony anomalies. case report a 4-year girl with hypertricosis over lower back since birth came to our institute. there is no history of delayed milestone, fever and bladder and bowel involvement. on physical examination, excessive hairs were present at lower lumber region without other cutaneous stigmata. muscle tone and power was normal bilaterally in the lower limbs. deep tendon reflexes and uroflometry were also normal. ncct scan shows evidence of two large bony spurs located at d6 and l2 vertebral levels with multiple fused vertebrae at d7, d8, and d9 with spina bifida at l1. (figures 1, 3a, 3b, and 3c). mr imaging revealed two bony septum at d6 and l2 with fibrous band at d7 with long segment of split cord without intervening normal single cord extending from d5 vertebral body level to l3 and the conus medullaris at l4. (figures 2, 3d, 3e) romanian neurosurgery (2015) xxix 3: 344 348 345 figure 1 – coronal and sagittal ct whole spine figure 2 – mri spine coronal sections showing long segment splitting of cord extending from d5 vertebral level to l4 vertebral level with double bony spurs 346 sharma et al long segment composite split cord malformation figure 3 – ct scan a, b – axial images at d6 level showing bony spur. c – axial images showing another located bony spur at l2 level. d, e – mri t2 axial images at d6 (a) and l2 (e) level management surgery was performed to prevent the progress of the neurologic damage resulting from tethering of the conus. the patient underwent laminectomies at d5–7, and l2, l3, l4 to remove the splitting lesions. specifically, two spinal cords with their own dural sheaths were noted at d-5 and l2 and two hemicords in single dural sac were observed at d7. we resected bony spurs and fibrous band, reconstruction of dural sac done with the released of conusmedullaris by cutting the terminal filum via a l-4 laminectomy. postoperatively patient develop csf leak from operative site, which were managed by reexploration and repair of dural defect with fibrin glue. discussion scms are rare congenital malformations of the spinal cord and it’s covering that were first described by ollivier (5) in 1837 and which he termed diastematomyelia. he used this term to describe an abnormality of the spinal cord in which the dura is separated by a bone spur or rigid fibrous bands to create 2 sleeves, each containing a portion of spinal cord divided sagittally into 2 parts. bruce et al (1) used the term “diastematomyelia” to describe a spinal cord split by a midline bony spur, and reserved the term “diplomyelia” for a true doubling of the spinal cord without a spur. pang (8) in 1992 gave a new classification recommending the term “scm” for all double spinal cord malformations. in type i the hemi cords are always invested with individual dural sacs and the medial walls of the sacs always ensheath a rigid (bony or cartilaginous) midline spur, whereas in type ii the hemicords are always within a single dural sac and the midline septum is always composed of nonrigid fibrous or fibro-vascular tissues. a composite type of scm is very rare and only a few cases have been reported. the frequency of compositetype scm is lower than 1% in the literature (3). the most constituents of composite scm are a type 1-type 2-type 1 combination (9). pang et al (6, 7) proposed a unified theory to explain the embryogenetic mechanisms of all variants of scms. according to the theory, the formation of an “accessory neurenteric canal” between the yolk sac and amnion through the midline embryonic disc was the main cause of the defects. this canal gets subsequently invested with the mesenchyme to form an endomesenchymal tract, which causes the splitting between the notochord and neural romanian neurosurgery (2015) xxix 3: 344 348 347 plate. the accessory neurenteric canal is the key point of this malformation. this canal may be alone, or multiple canals may occur. the presence of multiple accessory neurenteric canals results in two or more septa that divide the spinal cord into two hemi-cords. according to this theory, one or more types of scm may develop in patients at many different levels. pang (6) reported on 2 cases of composite-type scm among 39, and erşahin et al. (2) reported on 4 cases of this type among 74 patients. our case represent unusual variant of scm comprising of composite split cord malformation with two level bony spur. another important finding were long segment of split cord (d5 to l4), usually the two hemi cords reunite caudally to the split, but in our case the split did not reunite and represents the true duplication of the spinal cord, so it has three elements two bony spur at ends and one fibrous band with long segment of split cord malformation. these three elements are continuous, suggesting that entire lesion results from a single (but very large) endomesenchymal tract in which meninx primitive precursor cells have been included at both ends to cause type 1 lesion, but not in midline where medial septa remain fibrous (9). mr imaging is the diagnostic modality of choice for such lesions and imaging of the whole spine is essential to rule out other associated anomalies. ct scan is complimentary to mri and is helpful in evaluating the nature of the spur and associated vertebral body anomalies. the location of the bony spur was thoracic and lumbar in our case. surgery is the treatment of choice wherein the bony spur should be excised microsurgically. low‐lying conus should also be addressed along with the excision of bony spur and dural sac reconstruction. exploration and excision of the bony spur was followed by filum detethering in the same stage using standard microneurosurgical principles. conclusion composite scms are uncommon, complex conditions of spinal dysraphism. etiology and pathogenesis is not clearly defined. the clinical radiological findings in our patient could not be explained by multiple accessory neurenteric canal theory. physical and neurological signs of scm in a patient should prompt the neurosurgeon to consider performing the screening mri of whole spine with brain to rule out other composite type scm and associated anomaly. correspondence dr. anand sharma mch neurosurgery associate consultant, neurosurgery artemis health sciences, gurgaon, 122003(india), ph: +91-9873190047 email: dranandsharma100123@gmail.com references 1.bruce a, m’donald s, pirie jh. a second case of partial doubling of the spinal cord. rev neurol psychiatry. 1906;4:6–19. 2.erşahin y, mutluer s, kocaman s, demirtas e: split spinal cord malformations in children. j neurosurg 1998; 88: 57–65. 3.harwwod-nash dc, mchugh k: diastematomyelia in 172 children: the impact of modern neuroradiology. pediatr neurosurg 1990; 16: 247–251. 4.khandelwal a, tandon v, mahapatra ak:an unusual case of 4 level spinal dysraphism: multiple composite type 1 and type 2 split cord malformation, dorsalmyelocystocele and hydrocephalous.j pediatr neurosci. 2011;6:58-61. 5.ollivier c: traité des maladies de la moelle épinière. paris, mequignon-marvis, 1837. 6.pang d, dias ms, ahab-barmada m: split cord malformation. i. a unified theory of embryogenesis for double spinal cord malformations. neurosurgery 1992; 31:451–80. 7.pang d: split cord malformation: part ii: clinicalsyndrome. neurosurgery.1992;31:481–500. 8.pang d. split cord malformation, proposal for a new clinicoradiological.neurosurg clin n am. 1995;3:339– 52. 348 sharma et al long segment composite split cord malformation 9.schmidek & sweet operative neurosurgical techniques. elsevier saunders 2012,727-728. govindmangal_intradural 106 govind et al intradural extramedullary spinal cord tumors intradural extramedullary spinal cord tumors: a retrospective study at tertiary referral hospital mangal govind, mittal radheyshyam, sharma achal, gandhi ashok department of neurosurgery, sms medical college and hospitals jaipur, india abstract: introduction: intradural extramedullary (idem) spinal cord tumours account two thirds of all intraspinal tumours. the objective of this study was to determine shortand long-term outcomes of surgical patients with idem spinal cord tumours, and to see clinical features that could be helpful in management of patients with these lesions (operated by single senior surgeononly). methods: a retrospective review of 201 operative idem spinal cord tumours cases between 1993 and 2014 was performed. outcomes were scored at one month and at mean follow-up of 8.5 months postoperatively. in addition, patient demographics, tumour types and locations were also collected. statistical analysis was conducted utilizing chi-square and student's t-tests. results: there were 93 men and 108 women (mean age 48 yrs, range 5 -87 yrs). men presented at a younger age than women (42 vs 51 yrs, p<0.02). 165 (82.08 %) patients presented with severe radiculopathy and myelopathy. the 36 (17.91 %) had symptoms of radiculo -pathy. mean duration of symptoms prior to diagnosis was 11 months. schwannomas (113 patients) had the longest mean duration of symptoms (14.9 months), followed by meningiomas (68 patients, 8.4 months), and ependymomas (20 patients, 2 months). hundred and eighty nine (94%) of patients demonstrated significant improvement at one-month and 186 (92%) at 6-month mean follow-up. only 39/201 (19.4%) patients had residual focal deficits on long term follow-up. conclusions: surgery for idem should be expected to produce significant and dramatic improvement in most of patients. demographic, tumor-specific and anatomic considerations will be clinically useful while managing idem. key words: intradural extramedullary tumors (idem), spinal cord, surgical outcomes introduction spinal tumors account for only approximately 5-15% of the nervous system neoplasms (13, 18). intradural extramedullary (idem) spinal cord tumours account for about 60% of the intraspinal tumors, (17) and include schwannomas (1, 6) (30%; incidence rate, 0.3-0.4 cases annually per 100,000 people), meningiomas (6, 22) (25%; incidence romanian neurosurgery (2016) xxx 1: 106 112 107 rate, 0.32 cases annually per 100,000 people), neurofibromas, teratomas, lipomas, and metastatic tumors. the primary aim of this study was to examine surgical outcomes of idem spinal cord tumours in a large retrospective cohort of patients operated by single surgeon. secondary objectives includes examination of clinical data related to demographics, symptoms, tumor location and type that could be helpful in clinical decision making while managing these tumours. materials and methods in this retrospective study of 201 surgical patients who underwent surgery for idem spinal cord tumours between january 1993 and november 2014 were included. parameters recorded include patients demographics, symptoms (severity and duration), tumor characteristics (anatomic and pathologic), postoperative follow-up and surgical outcomes. surgical intervention was indicated by a combination of presenting symptoms (radiculopathy and/or myelopathy) and radiographic findings of mri. the neuroimaging procedure of choice was contrast-enhanced mri. surgical outcomes were scored at 1 month and then at the mean follow-up period. the mean follow-up was calculated from the interval between surgery and the last complete clinical examination in the patient chart (in this study, 8.5 months). patient records were carefully reviewed and surgical outcomes were scored strictly according to the modified criteria of odom, et al (table 1) (16). table i excellent complete relief of pain and other symptoms, return to full activity. good partial relief of pain and other symptoms, return to full activity. fair improvement with persistent limitation of activities. poor no improvement or further deterioration. descriptive statistics, chi-square test and student's ttest were utilized for data analysis. statistical significance was set at alpha = 0.05. note: other symptoms paresthesias, paresis, sensory loss results in this study there were 93 men and 108 women (mean age 48 yrs, range 5 -87 yrs). overall men presented at a younger age than women (42 vs 51 yrs, p<0.02). the age distribution was bimodal with a major peak around 41 yrs and a minor peak around 70 yrs. the second peak around age 70 represents predominantly because of older meningioma patients, whereas the peak around age 41 due to schwannoma and ependymoma patients. there were three primary tumor types: schwannomas (113/201), meningiomas (68/201), and myxopapillary ependymomas (20/201) (table 2a). schwannomas were noted to be more common in men, meningiomas more common in women, and ependymomas distributed equally among men and women (table 2a). patients with meningiomas tends to be older (57 yrs) than those patients with schwannomas (44 yrs) and ependymomas (40yrs, p<0.01) (table 2b). tumor locations varied between the three tumour subtypes in a predictable fashion (table 2c) schwannomas were distributed 108 govind et al intradural extramedullary spinal cord tumors fairly evenly among the three anatomic regions (cervical, thoracic, and lumbosacral), meningiomas common in cervical and thoracic regions and ependymomas were commonly localized to the lumbar region. the ratio of schwannomas to meningiomas to ependymomas was approximately 4:2:1 in this study (actual ratio 113:68:20). the mean duration of symptoms before diagnosis was 11 months. schwannomas had a statistically longer duration of symptoms (14.9 months) than meningiomas (8.4 months, p<0.05) for cervical and thoracic tumors. ependymomas had shorter duration of symptoms (2.0 months) than schwannomas (10.8 months, p<0.05) for lumbosacral tumors. results of one month follow up excellent good fair poor 75 (37.3%) 114 (56.7%) 9 (4.5%) 3 (1.5%) results of six months follow up excellent good fair poor 123 (61.2%) 66 (32.8%) 12 (6%) three patients had multiple idem, all of which were schwannomas. two of these patients were nf-ii positive. four patients had recurrence of their idem spinal cord tumours. three of these were schwannomas and one was an ependymoma. two patients with recurrent dumbbell-shaped schwannomas within the soft tissues of the neck underwent surgical treatment with acceptable results (one patient returned with new symptoms 5 years after initial tumor excision while another patient presented 15 years after the initial surgery). one patient with recurrent ependymoma at 4 years following initial surgery underwent a successful course of radiotherapy, and one patient with schwannoma underwent non-operative semiannual observation for a localized radiographic recurrence. while no metastases were noted during the 8.5 month mean follow-up period (range 1.5 to 30 months), this study did not specifically examine whether metastatic disease did appear at a later time. one mortality was noted in this series, in case of large cervical c1-c2 schwannoma due to respiratory complications, and the only complications included a superficial wound infection. table 2 histologic, demographic, and anatomic considerations for idem spinal cord tumours a. distribution of tumours by histologic type and patient gender in this series patient gender total men women schwannoma 113 (56.21%) 69 44 meningeoma 68 (33.83%) 14 54 ependymoma 20 (9.9%) 10 10 total 201 93 108 b. tumour incidence by age group age <40 40-60 >60 schwannoma 47 47 19 meningeoma 4 39 25 ependymoma 10 4 6 total 61 90 50 c. tumour incidence by anatomic location location cervical thoracic lumbar schwannoma 31 38 44 meningeoma 19 49 0 ependymoma 0 0 20 total 50 87 64 romanian neurosurgery (2016) xxx 1: 106 112 109 figure 1 t1w mri sagittal view showing l1-2 neurofibroma figure 2 t2w mri sagittal view showing l1-2 neurofibroma figure 3 ct abdomen showing left l1-2 neurofibroma 110 govind et al intradural extramedullary spinal cord tumors discussion intradural extramedullary tumors account for two-thirds of primary spinal tumors (12). most intradural extramedullary tumors are benign, and they exhibit no specific symptoms. radicular pain and worsening sensory and motor loss are common manifestations. therefore, most of the patients are wrongly diagnosed with cervical spondylopathy or intervertebral disk herniation. mri is very crucial to confirm the diagnosis of intradural extramedullary tumors. once the diagnosis is confirmed, the best treatment for nonmalignant intradural extramedullary tumor is surgery. the goal of surgery is complete surgical resection while preserving spinal stability, without worsening the preoperative neurological status. all the processes of conventional surgical tumor resection are carried out without using microscope, which may lead to a greater likelihood of incomplete tumor resection, as well as more damage to the spinal cord and vessels surrounding the spinal canal. with the improve ement of medical devices, surgeons are increasingly using microscopy to perform surgical tumor resection. mis can provide a clearer visual operative field and more delicate operative maneuvers, which can avoid the damage to the spinal cord and peripheral nerves as far as possible, reduce intraoperative blood loss and postoperative complications, and increase the rate of complete removal of tumors. it was reported that mis allowed removal of the tumor with minimal impairment from cutting of nerve fibers at the nerve root (14). no poor results were noted in this study at the mean 8.5 month follow-up. our findings are similar with those of other authors, with majority of clinical improvement noted either immediately or within 6 months of the operative intervention, with less notable clinical change after this initial period (13, 19). other studies reported that duration of preoperative symptoms appears to correlate with postoperative improvement, and that successful complete microsurgical tumor excision is of utmost importance (11, 13, 21). in terms of mortality, our result correlate well with other authors, with a reported range between 04.4% (2, 4, 13). approximately 20% of patients in our study had residual focal deficits, none of which were disabling. other authors report similar outcome among patients with similarities to our patient sample, with significant improvement in 62-88% of cases and clinical worsening in only a minority of patients (15%) (13). the demographics in our study are similar to those in previous studies (13, 19). we found that schwannomas affected younger male patients, meningiomas tended to occur in women and older patients. patients with myxopapillary ependymomas were younger than patients with schwannomas. the reported frequencies of schwannomas among idem spinal cord tumours vary from 43% to 67% in other studies as copared to 56.21% in our series (7, 10, 13, 19). schwannomas tend to produce localized pain, radiculopathy, and cauda equina syndrome. most report schwannomas to be solitary, with a 2.5% malignancy rate, which carries a poor prognosis (8). in our study, schwannomas romanian neurosurgery (2016) xxx 1: 106 112 111 were the only group of tumors without a predominant location of occurrence, and constituted 75% of recurrent tumors. in this study, patients with meningiomas were older than those with other tumor types. findings in this series agree with the literature in that meningiomas are the second most common idem, with approximately 80% localized to the thoracic region (72.05% in this study) (8, 9, 11). between 75% and 85% of patients with meningiomas are women (79.41% in this study), who tend to be older than patients with schwannomas or ependymomas (8, 11, 19). consistent with previous reports, we found meningiomas to be more aggressive in younger patients, with the higher incidence of myelopathy likely due to predilection of meningiomas for the thoracic region (5). others describe higher operative morbidity associated with idem spinal cord tumours located in the thoracic region 19. meningiomas tend to produce the “dural tail” sign on mri scans in sagittal, axial, and coronal planes, and it is recommended that all three planes of visualization be used 20. we follow this recommendation because as many as 10% of meningiomas can be both intradural and extradural (12). myxopapillary ependymomas constitute 9.9 % of idem spinal cord tumours in this study, and although in this study ependymomas had equal distribution among men and women, another series reported twice as many men as women (24). in this study, the mean age of the ependymoma group was lower than the mean age of patients with meningioma or schwannoma. symptomatically, ependymomas tended to produce cauda equina syndrome, localized pain, and radiculopathy. a 4:2:1 ratio of schwannomas to meningiomas to ependymomas was observed in this series. although not specifically described by others, similar ratio of tumor types can be noted in previous reports (10, 13, 19). limitations of this study include its retrospective nature, lack of patient follow up data beyond the 8.5-month mean follow up period, lack of complete data on recurrences or metastases beyond the end of the study period, and the drawbacks of the odom's modified criteria as a measurement tool for morbidity. the odom's modified scale is a very ‘rough' instrument of outcome assessment and does not have the capacity to truly delineate actual morbidity. the odom's scale was chosen for this study because of standard and uniform reporting of this scale on our patient charts. although the use of scales such as sf-36 or nurick grading would greatly enhance this study, the long period of this study as well as the difficulty of assigning these scales in a retrospective fashion to every patient in this study, make their applicability impractical (3, 15). conclusions surgery for idem spinal cord tumours, with goal of complete tumor removal, is a safe and effective option. at the 8.5 month mean followup, majority of patients had complete or near complete relief of symptoms and return to full activity schwannomas and ependymomas were the only histologic types to recur. demographic, tumor-specific and anatomic considerations may be clinically useful when approaching idem spinal cord tumours. 112 govind et al intradural extramedullary spinal cord tumors references 1.abul‑kasim k, thurnher mm, mckeever p, sundgren pc. intradural spinal tumours: current classification and mri features. neuroradiology 2008;50:301‑14. 2.allen jc, aviner s, yates aj, boyett jm, cherlow jm, turski pa, et al. treatment of high-grade spinal cord astrocytoma of children with "8 in 1" chemotherapy and radiotherapy: a pilot study of ccg-945. children's cancer group. j neurosurg. 1998;88:215-220. 3.brazier je, harper r, jones nm, o'cathain a, thomas kj, usherwood t, westlake l. validating the sf-36 health survey questionnaire: new outcome measure for primary care. bmj 1992;305:160-4. 4.cohen ar, wisoff jh, allen jc, epstein f. malignant astrocytomas of the spinal cord. j neurosurg. 1989;70:5054. 5.cohen-gadol aa, zikel om, koch ca, scheithauer bw, krauss we. spinal menin giomas in patients younger than 50 years of age: a 21-year experience. j neurosurg. 2003;98:258-63. 6.duong lm, mccarthy bj, mclendon re, dolecek ta, kruchko c, douglas ll, et al. desc riptive epidemiology of malignant and nonmalignant primary spinal cord, spinal meninges, and cauda equina tumors, united states, 2004–2007. cancer 2012;118:4220‑7. 7.el-mahdy w, kane pj, powell mp, crockard ha: spinal intradural tumors: part i extramedullary. br j neurosurg. 1999;13:550-557. 8.fromme k, miltner fo, klawki p, friedrich m. spinal cord monitoring during intraspinal extramedullary tumor operations (peroneal nerve evoked responses). neurosurg rev. 1990;13:195-9. 9.gelabert-gonzalez m, garcia-allut a, martinezrumbo r. spinal meningiomas. neurocirurgia (astur). 2006;17:125-131. 10.garrido p, laher-mooncey s, murphree nl, jonker n, levy lf, and makarawo s. neoplasms involving the spinal cord in zimbabweans: an analysis of 262 cases. cent afr j med. 1994;40:201-204. 11.gelabert-gonzalez m. primary spinal cord tumors. an analysis of a series of 168 patients. rev neurol. 2007;44:269-274. 12.helseth a, mørk sj (1989) primary intraspinal neoplasms in norway, 1955 to 1986: a population-based survey of 467 patients. journal of neurosurgery. 71(6): 842–845. 13.hufana v, tan jsh, tan kk. microsurgical treatment for spinal tumors. singapore med j. 2005;46:74-77. 14.kobayashi s, uchida k, kokubo y, yayama t, nakajima h, et al. (2007) a schwannoma of the s1 dural sleeve was resected while the intact nerve fibers were preserved using a microscope. report of a case with early mri findings. minimal invasive neurosurgery. 50(2): 120–123. 15.nurick s. the pathogenesis of the spinal cord disorder associated with cervical spondylosis. brain 1972; 95:87100. 16.odom gl, finney w, woodhall b. cervical disk lesions. jama. 1958;166:23-28. 17.osbom ag. handbook of neuroradiology. st louis: mosby; 1991. p. 380‑2. 18.porchet f, sajadi a, villemure jg. spinal tumors: clinical aspects, classification and surgical treatment. schweiz rundsch med prax. 2003;92:1897-1905. 19.prevedello dm, koerbel a, tatsui ce, truite l, grande cv, ditzel lf, araujo jc. prognostic factors in the treatment of the intradural extramedullary tumors: a study of 44 cases. arq neuropsiquiatr. 2003;61:241-247. 20.queckel lg, versteege cw. the "dural tail sign" in mri of spinal meningiomas. j comput assist tomogr. 1995;19:890-2. 21.sandalcioglu ie, gasser t, asgari s, lazorisak a, engelhorn t, egelhof t, stolke d, wiedemayer h. functional outcome after surgical treatment of intramedullary spinal cord tumors: experience with 78 patients. spinal cord. 2005;43:34-41. 22.seppälä mt, haltia mj, sankila rj, jääskeläinen je, heiskanen o. long‑term outcome after removal of spinal schwannoma: a clinicopathological study of 187 cases. j neurosurg 1995;83:621‑6. 23.souweidane mm, benjamin v. spinal cord meningiomas. neurosurg clin north am. 1994;5:283291. 24.wippold fj 2nd, smirniotopoulos jg, moran cj, suojanen jn, vollmer dg. mr ima-ging of myxopapillary ependymoma: findings and value to determine extent of tumor and its relation to intraspinal structures. ajr am j roentgenol. 1995;165:1263-7. microsoft word 2ienceanstm_rational_ 22 iencean et al rational management of intracranial hypertension rational management of intracranial hypertension st.m. iencean1, a.st. iencean2, m.r. gorgan3 1“grigore t. popa” university of medicine and pharmacy iasi 2emergency hospital “n. oblu” iasi 3“carol davila” university of medicine and pharmacy bucharest the treatment of intracranial hypertension depends on the type of intracranial hypertension and on the developmental stage of the illness. the treatment is first of all an etiologic one in order to remove the cause that has caused the intracranial pressure increase; simultaneously, there is an attempt to stop the pathogenic mechanisms that impact on the nervous structures, and a symptomatic treatment is applied in order to reduce the intensity of the clinical syndrome. the term of etiologic treatment refers to the etiology of the intracranial hypertension, that is to the immediate cause that generates the intracranial pressure increase: for instance, in the case of a cerebral metastasis leading to ich, the name of etiologic treatment is given to the action of metastasis extirpation, and it has no connection to the etiology and the therapy of the original neoplasia (1, 2, 3, 4, 15). the intracranial hypertension treatment can be complex by combining three therapeutic methods used concomitantly or successively, or only the pathogenic therapy and the symptomatic one are used, depending on the clinical stage and the paraclinical explorations. the type of intracranial hypertension establishes the treatment that must be applied: 1. the treatment is etiologic in: expansive intracranial processes: cerebral tumors, intracranial hematomas, cerebral abscesses, hydatid cyst, etc., in the case of parenchymatous intracranial hypertension, hypertensive encephalopathy in the case of vascular intracranial hypertension, thrombosis of intracranial vessels, venous or arterial, in the case of vascular intracranial hypertension, csf circulation disorders due to the existence of a ventricular or paraventricular tumor with the occurrence of an obstructive hydrocephalus, csf resorption disorders in acute meningitis. 2. the pathogenic treatment is applied in: the ich cases with known etiology, which are mentioned above, in order to stop the development of the pathogenic mechanisms that have already started, the parenchymatous intracranial hypertension due to posttraumatic brain edema, hypoxic brain edema caused by secondary posttraumatic cerebral ischemia or in the case of sub-arachnoid hemorrhage, general intoxications with neurotoxins (endogenous or exogenous), etc. the vascular intracranial hypertension due to cerebral venous thrombosis, thrombosis of superior sagittal sinus with a decrease in the venous drainage and the blockage of the csf absorption, or in the case of the secondary ischemic brain edema romanian neurosurgery (2013) xx 1: 22 28 23 in the ischemic stroke caused by the occlusion or the stenosis of the great cerebral vessels, intracranial hypertension due to csf dynamic disorder idiopathic intracranial hypertension especially in order to block the development of certain complications depending on possible pathogenic mechanisms. 3. symptomatic treatment: all the cases of intracranial hypertension, when the etiologic and/or pathogenic therapy is applied, benefit from the symptomatic treatment, depending on the presented symptomatology, in idiopathic intracranial hypertension. (1, 2, 15, 27, 28) based on the manifested clinical syndrome, there may be several situations that correspond to the evolutionary stages of intracranial hypertension: the patient is conscious and the cerebral exploration reveals a lesion that may cause the development of an intracranial hypertension syndrome – the treatment is etiologic and it addresses the lesion that may cause ich, the patient is conscious with incipient ich signs, therefore with a compensated ich syndrome, with or without focal neurological signs – the treatment is etiologic, pathogenic and symptomatic, the patient is in a critical condition, with consciousness disorders, with a decompensating ich syndrome or in a coma due to the decompensation of the intracranial hypertension – the treatment is etiologic, pathogenic and symptomatic, and it is applied immediately. therapeutic recommendations etiologic treatment i. if there is an expansive intracranial process that caused the intracranial hypertension syndrome, the etiologic treatment consists in the surgical intervention for the lesion removal. in numerous situations, the neurosurgical techniques allow the ablation of that particular expansive intracranial process: the extirpation of the cerebral tumors is complete or partial, depending on the tumor location relative to the eloquent nervous structures, and depending on the benign or malign character of the neoformation. the removal of the neoformation makes the supplementary endocranial volume disappears as a first moment in the development of the intracranial hypertension, as well as removing the compressive effect on the csf circulation paths and the edematous effect on the adjacent nervous parenchyma. (figure 1) the expansive traumatic lesions, with or without a traumatic brain edema, are surgically solved by the evacuation of the traumatic hematomas, the removal of the edematous cerebral dilaceration, etc., (figure 2) other expansive intracranial lesions, non-tumor or non-traumatic lesions, such as the cerebral abscess, the dural empyema, the hydatid cyst, etc., are surgically solved, usually by a complete evacuation. (4, 6, 8) ii. in the case of hypertensive encephalopathy, the etiologic treatment is the treatment of the hypertensive crises with a gradual, but fast enough, return, to normal values of the blood pressure, concomitantly to the brain edema decrease and the clinical improvement of the ich syndrome. iii. in the case of the vascular intracranial hypertension, due to cerebral 24 iencean et al rational management of intracranial hypertension venous thrombosis, thrombosis of superior sagittal sinus, etc., anti-thrombotic and anticoagulant substances may be used. iv. in the ischemic stroke caused by the occlusion or stenosis of the great vessels, substances with fibrinolytic action may be used: intravenous thrombolysis, fibrinogen degrading enzymes, etc. the thrombotic occlusion of the sylvian artery can benefit from an extra-intracranial anastomosis with the superficial temporal artery. the carotid endarteroctomy and the angioplasty, with the mechanic removal of the sanguine coagulum or with the installation of an arterial stent, have been used in emergency cases, but certain procedures are presented especially as prophylactic surgical treatments for the cerebral stroke in patients with repeated transitory ischemic cerebral vascular accidents. v. the intracranial hypertension, due to csf resorption disorders, secondary to an acute meningitis benefits from the etiologic treatment of the bacterial meningitis, which decreases the meningeal inflammation and reduces the changes in csf resorption. vi. in intracranial hypertension of acute liver failure with endotoxic etiology, the etiologic treatment consists of performing a hepatic transplant. the decision on the performance of the hepatic transplant is made based on the neurological prognosis monitoring the intracranial pressure in the fulminating case of a hepatic failure of a degree ≥ 3, (west haven criteria of altered mental status in hepatic encephalopathy). vii. in the intracranial hypertension of the posterior reversible encephalopathy syndrome (pres) with a non-hypertensive etiology, due to the neurotoxic action of certain immuno-suppressors or cytostatics, the treatment is etiologic, and it consists of interrupting the causing medication, with the progressive improvement within a few days. a b figure 1. olfactory groove meningioma: mri preoperative (a) with secondary intracranial hypertension and postoperative (b) image with normal cerebral ventricles romanian neurosurgery (2013) xx 1: 22 28 25 figure 2. ct image of right subdural hematoma and secondary intracranial hypertension pathogenic treatment the pathogenic treatment is used in all types of intracranial hypertension in order to stop the pathogenic mechanisms by means of which various causes bring about the intracranial pressure increase, and which cause the compensating capacities of the endocranial pressure increases to be exceeded. (3, 4, 9, 19, 20, 22) the purpose of the pathogenic treatment is: to act on the development of the brain edema, and once this has occurred, it must be reduced by medication therapies or there must be an attempt to decrease the effect of the neoformation or of the perilesional brain edema on the rest of the nervous parenchyma by surgical decompression, to prevent the occurrence of internal hydrocephalus and, in the case of an already existing obstructive hydrocephalus, to decrease the volume of the ventricular csf, to prevent endocranial circulatory disorders or to bring back to normal values the already affected cerebral sanguine circulation, in order to stop the development of the cerebral ischemia, in the case of certain signs that announce a complication, to stop the development of that particular process (decompression of the optic nerve in idiopathic ich in order to stop the evolution of cecity, etc.), before the occurrence, or at the first signs of intracranial hypertension decompensation through the appearance of a cerebral hernia, to try various maneuvers for the protection of the nervous parenchyma by using methods such as ventricular drainage, sub-temporal decompressive craniectomy, craniectomy of posterior cerebral fosse with the excision of the posterior arch of the atlas, etc. ( 9, 23, 26, 30, 31) symptomatic treatment the symptomatic treatment is necessary in most cases of intracranial hypertension in order to decrease the intensity of the symptoms until the etiopathogenic therapy comes into effect, and then concomitantly with it. antalgics, antiemetics, antivertigos, anticonvulsants, antithermics, sedatives, etc., are used, depending on the existing symptomatology. (1, 2, 21) therapeutic schemes in intracranial hypertension treatment of the brain edema the pathogenic treatment of the brain edema depends on the type of edema: the cellular cerebral (cytotoxic) edema occurs due to the intra/extracellular osmotic pressure disequilibrium, with an intact brain-blood barrier, and it is reduced by 26 iencean et al rational management of intracranial hypertension diuretics; the hydrostatic extracellular brain edema in hypertensive encephalopathy is caused by the increase in the hydrostatic pressure from the cerebral capillaries secondary to a severe aht, and it is produced by an ultra-filtration mechanism with an intact brain-blood barrier; the oncotic (vasogenic) extracellular brain edema represents a severe alteration of the brain blood barrier (open brainblood barrier), it has a peri-tumor development or in other lesions by through a vasogenic mechanism, and it responds favourably to corticosteroids; the mixed brain edema, cellular and extracellular, is the most frequent type of brain edema; the typical features occur from the start in the case of the traumatic brain edema. diuretics and corticosteroids are used in order to decrease the brain edema.(2, 5, 7, 8, 10) the mannitol is an osmotic diuretic, and it is used in a dose of 0.25 – 1 g / kgc intravenously; the effect occurs after 10 – 15 minutes, it lasts for approximately two hours and it may be repeated after 6 hours. it is efficient in the case of the brain edema with intact brain-blood barrier. the administration of larger doses does not reduce the intracranial pressure further, but there is a longer period of action. the mannitol must be carefully administered in order not to increase a hematoma by decreasing the volume of the parenchyma with an edema around. during the mannitol therapy, one must verify the serous osmolarity, which must be maintained between 300 – 315 mosm / l.the osmolarity can be calculated, and must be maintained below 320 mosm/ l. the classical belief is that mannitol can be administered in sufficiently large doses, taking into account the serous osmolarity, in order to prevent a possible secondary renal insufficiency. recent studies have specified the fact that the renal insufficiency, which can occur after the mannitol administration, is related more to the preexisting high blood pressureor to the existence of a diabetes mellitus, than to osmolarity or to the mannitol doses. (2, 12, 20, 25, 29) furosemide is an ansa diuretic, it is used in a dose of 10 – 40 mg, which is administered intravenously or as an initial dose of 0.5 – 1 mg / kgc; it also decreases the csf production. the combination of these two diuretics is more efficient and it requires the monitoring of the sanguine electrolytes (potassium). corticosteroids (dexamethasone) are efficient in the vasogenic brain edema as they repair the brain-blood barrier. a quantity of 4 – 20 mg of dexamethasone is administered intravenously, and the effects are felt in a few hours. (12, 16, 18, 29) decrease in csf secretion and excess the acetazolamide and corticosteroids reduce the production of cerebrospinal fluid, and they are used in order to reduce the csf volume. acetazolamide is a sulfonamide that specifically inhibits the carbonic anhydrase at the level of the renal tube, ciliary body, choroid plexus, and in the digestive mucous membrane. the acetazolamide administration in doses of 250 – 1000 mg / day gradually reduces the csf production; it is necessary to monitor the electrolytes and the sanguine ph. (3, 5, 7, 11, 28, 31) a reduced csf secretion also happens after the administration of mannitol and furosemide. romanian neurosurgery (2013) xx 1: 22 28 27 the rapid removal of the csf excess can be performed by means of a ventricular drainage during the intracranial pressure monitoring, which ensures the intracranial pressure control, or by means of an external ventricular drainage in emergency cases. the csf drainage by lumbar puncture or by lumbar catheter is not used due to the risk of cerebral herniation. in the case of an idiopathic intracranial hypertension syndrome, the lumbar-peritoneal shunt is sometimes used, while, in the case of an obstructive hydrocephalus, ventricularperitoneal shunting systems may be used. (3, 6) maintaining a normal cerebral sanguine perfusion the sanguine arterial pressure increase is recommended in order to maintain an appropriate cerebral perfusion pressure when the monitoring reveals a significant increase in the intracranial pressure. the hypertensive therapy for the systemic blood pressure increase includes the administration of colloidal solutions, intravenous vasopressors, such as dopamine or phenylephrine. (1, 8, 10, 15, 26) in the case of the intracranial hypertension syndrome in traumatic brain injury, the systemic arterial pressure may usually increase up to 150 – 170 mm hg. in the case of decreased values of the cerebral perfusion pressure, sanguine pressure increasing measures can be applied even with the risk of an icp increase as the purpose is to maintain the normal values of the cerebral perfusion pressure. (3, 5, 6, 9, 10) in the case of non-traumatic intracranial hypertension syndrome and in the absence of the cerebral hemorrhage, the blood pressure can increase up to 180 mm hg. corresponding author: a.st. iencean emergency hospital “n. oblu” iasi andrei_steffan@yahoo.com references 1. adelson pd, bratton sl, carney na, chesnut rm, du coudray he, et al the use of barbiturates in the control of intracranial hypertension in severe pediatric traumatic brain injury. pediatr crit care med. 2003; 4: s49-52. 2. adelson pd, bratton sl, carney na, chesnut rm, et al the role of cerebrospinal fluid drainage in the treatment of severe pediatric traumatic brain injury. pediatr crit care med. 2003, 4(3 suppl): s38-9. 3. adelson pd, bratton sl, carney na, chesnut rm, et al use of hyperosmolar therapy in the management of severe pediatric traumatic brain injury. pediatr crit care med. 2003; 4(3 suppl): s40-4. 4. adelson pd, bratton sl, carney na, chesnut rm, et al surgical treatment of pediatric intracranial hypertension. pediatr crit care med. 2003; 4(3 suppl): s56-9. 5. adelson pd, bratton sl, carney na, chesnut rm, et al the use of corticosteroids in the treatment of severe pediatric traumatic brain injury. pediatr crit care med. 2003; 4(3 suppl): s60-4. 6. adelson pd, bratton sl, carney na, et al critical pathway for the treatment of established intracranial hypertension in pediatric traumatic brain injury. pediatr crit care med. 2003; 4(3 suppl): s65-7. 7. allan r, chaseling r. subtemporal decompression for slit-ventricle syndrome: successful outcome after dramatic change in intracranial pressure wave morphology. report of two cases. j neurosurg. 2004; 101( suppl): 214-7. 8. battison c, andrews pj, graham c, et al randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. crit care med. 2005; 33(1): 196-202. 9. berger s, schwarz m, huth r. hypertonic saline solution and decompressive craniectomy for treatment of intracranial hypertension in pediatric severe traumatic brain injury. j trauma. 2002 53(3): 558-63. 10. coppage kh, sibai bm. treatment of hypertensive complications in pregnancy. curr pharm des. 2005; 11(6): 749-57. 11. cruz j, minoja g, okuchi k. major clinical and physiological benefits of early high doses of mannitol for intraparenchymal temporal lobe hemorrhages with abnormal pupillary widening: a randomized trial. neurosurgery. 2002, ; 51(3): 628-37. 28 iencean et al rational management of intracranial hypertension 12. demchuk am, burgin ws, christou i, et al. thrombolysis in brain ischemia (tibi) transcranial doppler flow grades predict clinical severity, early recovery, and mortality in patients treated with intravenous tissue plasminogen activator. stroke. 2001; 32: 89–93. 13. diener hc, ringelstein eb, von kummer r, et al. treatment of acute ischemic stroke with the lowmolecular-weight heparin certoparin: results of the topas trial: therapy of patients with acute stroke (topas) investigators. stroke. 2001; 32: 22–29. 14. donnan ga, davis sm. surgical decompression for malignant middle cerebral artery infarction: a challenge to conventional thinking. stroke. 2003; 34(9): 2307. 15. el-watidy s. bifrontal decompressive craniotomy in a 6-month-old infant with posttraumatic refractory intracranial hypertension. pediatr neurosurg. 2005; 41(3): 151-4. 16. figaji aa, fieggen ag, peter jc. early decompressive craniotomy in children with severe traumatic brain injury.childs nerv syst. 2003; 19(9): 666-73. 17. fraser jf, hartl r. decompressive craniectomy as a therapeutic option in the treatment of hemispheric stroke. curr atheroscler rep. 2005; 7(4): 296-304. 18. georgiadis al, suarez ji. hypertonic saline for cerebral edema. curr neurol neurosci rep. 2003; 3(6): 524-30 19. gupta r, connolly es, mayer s, elkind ms. hemicraniectomy for massive middle cerebral artery territory infarction: a systematic review. stroke. 2004; 35(2): 539-43 20. iencean st m a new classification and a synergetical pattern in intracranial hypertension. medical hypotheses, 2002; 58(2): 159-63. 21. iencean st m brain edema a new classification. med hypotheses. 2003; 61(1): 106-9. 22. iencean st m ciurea av intractranial hypertension, nova science publishers, new york, 2009. 23. kontopoulos v, foroglou n, patsalas j, et al decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered? acta neurochir (wien).2002; 144(8): 791-6. 24. lee ag, pless m, falardeau j, et al the use of acetazolamide in idiopathic intracranial hypertension during pregnancy. am j ophthalmol. 2005; 139(5): 855-9. 25. owler bk, parker g, halmagyi gm, pseudotumor cerebri syndrome: venous sinus obstruction and its treatment with stent placement. j neurosurg. 2003; 98(5): 1045-55. 26. schneider gh, bardt t, lanksch wr, unterberg a. decompressive craniectomy following traumatic brain injury: icp, cpp and neurological outcome. acta neurochir suppl. 2002; 81: 77. 27. shiozaki t, nakajima y, taneda m, etc all. efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia. j neurosurg. 2003; 99(1): 47-51. 28. togay-isikay c, kim jy, meads d, tegeler c. lumbar drainage affects transcranial doppler pulsatility and waveforms in the presence of elevated intracranial pressure.eur j neurol. 2005; 12(5): 407-9. 29. videtta w, villarejo f, cohen m, et al effects of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure. acta neurochir suppl. 2002; 81: 93-7. 30. watling cj, cairncross jg. acetazolamide therapy for symptomatic plateau waves in patients with brain tumors. report of three cases. j neurosurg. 2002; 97(1): 224-6. 31.woodworth gf, mcgirt mj, williams ma, rigamonti d. the use of ventriculoperitoneal shunts for uncontrollable intracranial hypertension without ventriculomegally secondary to hiv-associated cryptococcal meningitis. surg neurol. 2005; 63(6): 529531. doi: 10.33962/roneuro-2020-075 cerebrospinal fluid dynamics with its surgical implications harold e. vasquez, yeider a. durango-espinosa, ezequiel garcia-ballestas, b.v. murlimanju, andrei fernandes joaquim, luis rafael moscote-salazar, amit agrawal romanian neurosurgery (2020) xxxiv (1): pp. 459-462 doi: 10.33962/roneuro-2020-075 www.journals.lapub.co.uk/index.php/roneurosurgery cerebrospinal fluid dynamics with its surgical implications harold e. vasquez1, yeider a. durango-espinosa2, ezequiel garcia-ballestas2, b.v. murlimanju2, andrei fernandes joaquim4, luis rafael moscote-salazar2, amit agrawal5 1 faculty of medicine, university of sinu, cartagena, colombia 2 center for biomedical research (cib). faculty of medicine university of cartagena, cartagena, colombia 3 department of anatomy, kasturba medical college, manipal academy of higher education, manipal, karnataka, india 4 prof. of neurosurgery. university of campinas (unicamp), campinas-sp, brazil 5 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india abstract cerebrospinal fluid (csf) is largely (70-80%) produced by the choroids plexus of the ventricles and is considered as the plasma ultrafiltrate. while csf formation, circulation, and composition appear to be physiological and physical, its absorption appears to be mainly physical. the formation, composition, circulation, absorption, and changes in pathological conditions of csf are discussed briefly in this review article. the csf pressure dynamics studies provide information about the tightness, elastance, or outflow resistance of the csf in the cns. we believe that the present study shall help to provide essential details of csf physiology which are important to many disciplines including radiology, neurology, and neurosurgery. introduction thorough knowledge of csf dynamics is essential for understanding the intracranial -intraspinal changes due to pathologic conditions. perhaps, the first time described was by dandy in 1919 (1). however, years later three components of csf dynamics was stablished by czosnyka et al, wich are csf formation, circulation, and composition. this, appears to be physiological and physical, and its absorption may be mainly physical. since most of the surgical treatments involve manipulating the physical principles, it is important to understand the studies, which are emerged on the dynamics of csf (2). studies in patients with hydrocephalus and traumatic brain injury has contributed to understand the strong association between csf dynamics, physical keywords cerebrospinal fluid, hydrocephalus, ventricles corresponding author: luis rafael moscote-salazar center for biomedical research (cib). faculty of medicine university of cartagena, cartagena, colombia rafaelmoscote21@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 460 harold e. vasquez, yeider a. durango-espinosa, ezequiel garcia-ballestas et al. and surgical components (3). the main objective of this review is to review csf dynamics and the association with surgical components. physiology of csf dynamics physiological principles include vascular, neurohumoral, and sub-cellular regulation, while physical principles include all the fluid dynamics. some of the well-known physiological principles include cushing’s reflex, which affects the cerebrovascular system. pressure on ventricular walls affects the secretion of csf at the aquaporin level of the choroid plexus. sco-spondin, the peptide secreted by the sco (subcommissural organ) will regulate the flow of csf across the aqueduct of sylvius. however, scospondin is rudimentary in humans. there are approximately 150 ml of csf, with a rate of 0.3-0.6 ml/min of production in an adult, distributed between 120 and 30 ml in cranial and spinal subarachnoid spaces, with daily volume produced between 500-600 ml (4). the extracellular space is about 15% of the brain volume and about 1500 ml of adult intracranial space consists of 1100 ml of intracellular space, 200 ml extracellular space, 140 ml of cerebrospinal fluid, and about 60 ml of blood at a given time (5). the choroid plexus in the ventricles is the main production site of csf formation. however, there is a strong association between resistance of csf and formation, which in many studies has shown to be the first parameter to consider in patients with intracranial hypertension (6–8). perhaps, large amounts of csf are drained primarily into the blood through the arachnoid villi by penetrating the sinus, mainly into the superior sagittal sinus. understanding this process, may contribute to be the key to comprehend surgical components. as surgery component, according to monro-kellie theory; a disbalance between csf reabsorption and resistance may be the key to develop every illness related to csf dynamics (9,10). physiological responses hypothermia decreases the csf volume by 11%, with each one-degree reduction in the temperature and hyperthermia increases the csf volume. in general, the drugs that increase the cerebral blood flow consequently increase the csf production; on the other hand, the aging process and some infections cause reduce in the csf formation (11–14). however, the total csf volume increases with age in both sexes, mainly due to the contribution by the cortical sulcal volume. these pressure gradients which are being created by continuous csf secretion and facilitated by the arterial pressure pulsations have an important role for csf circulation and absorption through the venous system (15). the respiratory variations and vascular pulsations emanating from the choroid plexus and cerebral arteries cause the ventricles to pulsate providing the additional movement to csf. although trans-mural migration of csf across the pial arteries has been demonstrated in the animals, these do not contribute to the bulk of csf absorption (16). functions of csf this bloodcsf barrier maintains a chemically precise environment, which is necessary for the neurotransmitter and removes the metabolic products, unwanted drugs and pathological substance that may result in cns injury (17,18). changes in csf ca, mg, k produce changes in the sympathetic and autonomic response, ventilation, muscle tone, and emotional state. in continuity with the brain interstitial fluid, csf provides a stable supply of substrates, primarily glucose, even though the plasma concentration of the substrate is continuously changing. transport of endorphins, hormones of the hypothalamus and pineal gland is facilitated by the csf. specialized ventricular cells and brain parenchymal neurons secrete neuroendocrine factors (19,20). laboratory investigation of csf important information on csf can be derived from the following parameters, opening pressure, gross appearance, total and differential cell count, bacterial culture and sensitivity, protein and glucose, analysis of immunoglobulins (to detect chronic cns inflammatory conditions) and cytology (to detect malignant cells). increased neutrophils in the csf indicate bacterial meningitis (21). other causes of increased neutrophil count include a cerebral abscess, seizures, and cns hemorrhage. increased lymphocytes in the csf indicate viral meningitis. lymphocyte counts are also elevated in meningitis, tuberculosis, syphilis, fungal and parasitic infections. increased plasma cells is a feature of tb meningitis and chronic inflammatory disorders like multiple sclerosis. the presence of leukemic cells in the csf indicates meningeal infiltration by leukemic cells (22). 461 cerebrospinal fluid dynamics with its surgical implications leukemic cells typically appear in the csf after several remissions have been achieved by chemotherapy. tumor cells can be detected by cytological studies and the sources of tumor cells can be from primary cns tumors like medulloblastoma, or metastatic cns tumors from lung, breast, gi tract, and melanoma. it may be necessary to determine if a nasal or ear fluid is found as a content in the csf. csf fluid contains a modified transferrin protein called β2-transferrin (tau protein), which is not present in plasma or other fluids. the presence of β2-transferrin in a fluid strongly suggests that the fluid is csf, which may be used, by instance, to identify csf leak after sinus surgery (22,23). studies of csf dynamics in clinical practice, external lumbar drainage (taptest) is widely used to evaluate normal pressure hydrocephalus (nph). infusion tests, bolus injections, and isotope dilution methods are employed most often in experimental studies. icp monitoring in acute conditions such as head injury and chronic conditions such as nph is widely used. in the study on csf dynamics by ramesh et al. a simple, safe, and cost-effective method of infusion method to predict the vps effectiveness was devised (24). not only in nph and pth but also postmeningitic hydrocephalic patients seems to correlate and benefit from the preoperative saline infusion studies. ct cisternography consists of the injection of radioactive agents into the subarachnoid space and serial ct scans are taken at different times depending on the clinical problem, such as csf fistulae, nph, etc. it is also used to evaluate the shunt function. it can also help in the evaluation of patients receiving intrathecal chemotherapy, evaluation of brain fluid-filled structures (arachnoid cysts, etc.), evaluation of csf pumps for continuous delivery of medication. ct and mri are useful to estimate intracranial compliance (25). conclusion this review briefs about the formation, composition, circulation and absorption of the csf. the changes in csf due to pathological conditions are highlighted. it is believed that the present study will offer the details about the physiology and dynamics of csf, which is essential to the broad specialties including radiology, neurology, and neurosurgery. references 1. dandy we. internal hydrocephalus. an experimental, clinical and pathological study. ann surg [internet]. 1919;70(2):129–42. available from: https://www-ncbinlm-nih-gov.ep.fjernadgang.kb.dk/pmc/articles/pmc14 10318/pdf/annsurg00745-0001b.pdf 2. czosnyka m, czosnyka z, momjian s, pickard jd. cerebrospinal fluid dynamics. physiol meas. 2004;25(5). 3. johanson ce, duncan ja, klinge pm, brinker t, stopa eg, silverberg gd. multiplicity of cerebrospinal fluid functions: new challenges in health and disease. cerebrospinal fluid res. 2008;5:1–32. 4. sakka l, coll g cj. anatomy and physiology of cerebrospinal fluid. eur ann otorhinolaryngol head neck dis. 2011;128:309–16. 5. orešković d, radoš m, klarica m. role of choroid plexus in cerebrospinal fluid hydrodynamics. neuroscience. 2017;354:69–87. 6. bradbury mw, cserr hf wr. drainage of cerebral interstitial fluid into deep cervical lymph of the rabbit. am j physiol. 1981;240:329–36. 7. pollay m. the pathophysiology of the cerebrospinal fluid circulation. neurosurgery, sci basis clin pract (eds crockard a, hayward r, hoff jt) blackwells sci publ oxford. 1985;279–96. 8. linninger aa, tsakiris c, zhu dc, xenos m, roycewicz p, danziger z, et al. pulsatile cerebrospinal fluid dynamics in the human brain. ieee trans biomed eng. 2005;52(4):557–65. 9. segal mb pm. the secretion of cerebrospinal fluid. exp eye res. 1977;127–48. 10. klarica m, orešković d. enigma of cerebrospinal fluid dynamics. croat med j. 2014;55(4):287–90. 11. brierley jb; field ej. the connexions of the spinal subarachnoid space with the lymphatic system. j anat. 1948;82:153–66. 12. welch k; pollay m. the spinal arachnoid villi of the monkeys cercopithecus aethiops sabaeus and macaca irus. anat rec. 1963;145:43–8. 13. cutler rw; page l; galicich j; watters gv. formation and absorption of cerebrospinal fluid in man. brain. a j neurol. 1968;91:707–20. 14. ahmed a; hickey sm; ehrett s. et al. cerebrospinal fluid values in the term neonate. pediatr infect dis j. 1996;15:298–303. 15. kc b. cerebrospinal fluid pressure. j neurol neurosurg psychiatry. 1970;33:387–97. 16. milhorat th; hydrocephalus and the cerebrospinal fluid. williams & wilkins. 1972; 17. milhorat th. the third circulation revisited. j neurosurg. 1975;42:628–45. 18. sahar a; hockwald gm; ransohoff j. cerebrospinal fluid and cranial sinus pressures. relationship in normal and hydrocephalic cats. arch neurol. 1975;23:413–8. 19. leusen i. regulation of cerebrospinal fluid composition with reference to breathing. physiol rev. 1972;52:1–52. 20. nakada t, kwee il. fluid dynamics inside the brain 462 harold e. vasquez, yeider a. durango-espinosa, ezequiel garcia-ballestas et al. barrier: current concept of interstitial flow, glymphatic flow, and cerebrospinal fluid circulation in the brain. neuroscientist. 2019;25(2):155–66. 21. shapey j, toma a, saeed sr. physiology of cerebrospinal fluid circulation. curr opin otolaryngol head neck surg. 2019;27(5):326–33. 22. j. skypr. ural sinus pressure. in normal and hydrocephalic dogs. arch neurol. 1964;10:575.580. 23. greitz d; hannerz j; rahn t; bolander h; ericsson a. mr imaging of cerebrospinal fluid dynamics in health and disease. on the vascular pathogenesis of communicating hydrocephalus and benign intracranial hypertension. acta radiol. 1994;35:204–11. 24. wasserstrom wr; glass jp; posner jb. diagnosis and treatment of leptomeningeal metastases from solid tumors: experience with 90 patients. cancer. 1982;42:759–72. 25. ramesh vg; narasimhan v; balasubramanian c. cerebrospinal fluid dynamics study in communicating hydrocephalus. asian j neurosurg. 2017;12:153–8. martind_vivo 154 | martin et al ex vivo aneurysm models ex vivo aneurysm models mimicking real cases for the preoperative training of the clipping technique d. martin*, a. giovani, narcisa bucur, r.m. gorgan *phd student abstract: training in a specialty like cerebrovascular neurosurgery becomes more and more difficult as the access to training is limited by the increasing number of neurosurgical departments and the lack of expert centers for specific pathology. this is why an increased investment in experimental training is encountered in many centers worldwide. the best models for training the clipping technique are ex vivo on cadaveric heads aneurysm models, animal models or augmented reality models. we present a few ex vivo models of aneurysms mimicking acoa, acm bifurcation and basil are tip aneurysms using a pulsed continuous perfusion system. clipping training on aneurysm models is an invaluable tool both for the residents and for the specialists with a special interest in cerebrovascular surgery. key words: aneurysm model, clipping, microanastomosis introduction cerebrovascular surgery, as a very challenging subspecialty of neurosurgery requires both a thorough knowledge of anatomy and skull base approaches, and refined technical skills. if the anatomy and the usual neurosurgical approaches can be learned from books and online video materials, and the skull base approaches can be learned by assisting in the surgery or hands on courses, there is no way of acquiring the required technical skill needed in complex vascular cases through learning on human patients at least, without having a long list of failure. in order to address this training issue, the resident with a special interest in cerebrovascular surgery should attend many hands on courses of skull base surgery and microneurosurgery, but more importantly should have access to training in a neurosurgical laboratory with ex vivo and in vivo animal models, cadaveric heads and if available virtual reality and 3d printed models on a weekly basis. a good model is one that comes closer to the real operative experience, and this is only possible in cadaveric surgical simulation where real vessels are used to build the models and a pulsed flow system is used after the vascular malformation model has been implanted in a cadaveric head, or in romanian neurosurgery (2016) xxx 2: 154-161 | 155 augmented reality computer models. although the haptic performances of the virtual reality and the 3d reconstruction of the cerebral arteries, veins and malformation models bring this closer to the real experience it is nonetheless lacking brain manipulation and the realistic surgical feedback. [1,5] method we used chicken wings to create different aneurysm models. in all cases we dissected both the main artery and the main vein past the bifurcation. than we implanted a vein or an artery segment at different sites, either at the main artery bifurcation or past this spot. because we used an ex vivo model there was no need for ethical approval. all the aneurism models were checked by inserting first water and then air to identify the eventual leaking points. in some cases we used a colored dye to perfuse the vessels to make sure. in some of the cases we connected the main arterial branch to a pulsed continuous infusion system using a processor to open and close a valve interposed in the tubing system coming from a pressured perfusion sac with variable pressure, between 80 mmhg and 180 mmhg. building the aneurysm we used the microsurgical technique of vessel dissection and we first exposed the artery which lies deep in the bone, past it's bifurcation and the superficial lying vein and it's quadrifurcation in every case. we performed different types of aneurysm models, starting with a fusiform one which is made by interposing a vein segment in an artery using two termino-terminal anastomosis. the simplest type of sacular aneurysm is made with only a terminolateral anastomosis using a fishmouthed vein segment, but this does not meet the criteria of resembling the real cases where the aneurism forms at a bifurcation. as the main artery bifurcation is in sharp angle, this allowed us to implant an aneurysm in this bifurcation. for this a linear incision was made from one branch to the other on the internal edge, than a vein segment with one end ligated was anastomosed in a continuous fashion starting with the back wall. the vein segment has to be prepared either by one incision or by two 180° incisions so that the cut edge perimeter equals that of the incision in the artery. in order to make this anastomosis easier, the two branches can be split apart using two adventiceal stitches so that it is reduced to a simple yet longer terminoterminal anastomosis. in order to create a basilar bifurcation aneurysm model we terminolaterally implanted two ends of the same long arterial segment at 0° and 180° immediately proximal to the main artery bifurcation and then we performed a 5 branched incision in all 5 vessels. we then performed a running suture to anastomose the free end of an augmented edge vein to this branched incision. this anastomosis is technically quite difficult and it cannot be performed using only one continuous suture. using a terminolaterally anastomosis a long arterial branch is implanted in the bifurcation of the main branch to resemble a 156 | martin et al ex vivo aneurysm models mca trifurcation. than we performed a y incision in all three branches. a “v” incision in the cut edge of the vein segment approximates its shape. than a continuous or interrupted sutures were performed. in all of these cases the aneurysm can be fixed to the arterial branches using many adventiceal stitches in order to give it the required shape and orientation. an mca quadrifurcation aneurysm can be built making an incision in both walls of the main artery starting from the bifurcation than extending this incisions on the internal margin of both branches. following, a vein segment is split open on its longitudinal axis and an anastomosis is started on the back wall of the cut artery, than the vein is reflected onto itself and the front wall of the aneurysm is anastomosed to the anterior cut edge of the artery. before completing the anastomosis both free edges of a long arterial segment are tl anastomosed between the artery and the vein at 180 degrees. this construct can be used as both a mca quadrifurcation or as a basilar bifurcation giant aneurysm with the neck implanted on both pca’s and both sca’s. one of the most technically difficult model is a giant acom aneurysm, irrespective of the dome orientation when the neck comprises both a2 segments and the acom on the entire length. in order to build this kind of model a short arterial segment is recolted and cut open on its length. two liniar mirroring incisions are cut in the branches at a distance of half a centimeter distal from the bifurcation. the "acom" segment is sutured continuously to the inferior edge of the branches' incisions. this h shaped anastomosis is impossible to perform with continuous sutures on all walls so we continued ligating the back wall of the aneurysm to the back wall of the "acom". then, the lateral side of the aneurysm is anastomosed to the both a2' s starting with the back wall. once constructing the aneurysm was finished, the flow through it was verified with serum and to check for eventual leaks. at this step we usually encounter some leaks from small branches that were missed during vessel harvest or vessel skeletonising. figure 1 a model of blister aneurysm implanted at an artificially created bifurcation. a straight clip parallel to parent vessel was applied romanian neurosurgery (2016) xxx 2: 154-161 | 157 another cause for leakage is either the distance between stitches is different between the vessels, especially when an artery to vein anastomosis is executed, or if continuous suture was used it was not properly tightened. the problem when using continuous suture is that it can narrow the lumen but this problem can be easily prevented by fishmouthing the donor vessel depending on how large we want the aneurysm neck. figure 2 a bilobed aneurysm was implanted in a natural bifurcation of the arteries. the clip is closed on the neck of the aneurysm with the blades inserted between the two arterial branches figure 3 model of basilar tip bifurcation aneurysm performed by anastomosing the vein segment on a 5 branched incison in the reconstructed pca’s-sca’s compelx. this is difficult to occlude with a single clip 158 | martin et al ex vivo aneurysm models figure 4 a mca quadrifurcation/ basilar tip bifurcation giant aneurysm. incompletely occlusion with one clip. a rupture in the aneurysm dome is simulated and a stacked clip technique is used, inserting multiple clips between the 4 branches, such as the flow is patent in all of them figure 5 the flow through a acoa aneurysm model at 80mmhg and 140mm hg using a continous pulsed flow system figure 6 clipping an acoa aneurysm using either two clips which occlude the acoa and using a single curved clip between the “a2” branches to completely occlude the neck romanian neurosurgery (2016) xxx 2: 154-161 | 159 figure 7 building an mca quadrifurcation aneurysm model inserted on all 4 branches: we used a two bifurcated arteries, both cut in a y shape. than we kept them open using by fixating in the muscle walls with two stiches and after anastomosing these two vessels we implanted the aneurism between them. the aneurism was checked with a colored solution and clipped using a between branches technique discussion based on the thorough full study of the angiography and angioct studies the surgeon should make an image of the steps implied in successful clipping of an aneurysm. the surgical approach should be chosen as to allow a good visibility to the vessels proximal and distal to the aneurysm and a good access to the aneurysm neck. also the approach should take into consideration the orientation of the aneurysm and the relation of the dome with the surrounding vessels, and with parenchima, cranial nerves and tentorium. once the operative corridor has been established the surgeon should correlate all the information given by the angio, mri and angioct images and during the arachnoid dissection around the aneurysm he should compare the setting in his mind with the real setting. the more experienced the surgeon, the less the difference between the real and the imagined. yet there are a few methods to surpass this difference which is to have a perfect operative understanding of the aneurysm, including training on a virtual reality model or training in an animal model or training of a sintetic 3d printed model. [9,10] the best aneurysm models reported so far in the literature are those testing both the 160 | martin et al ex vivo aneurysm models anatomical knowledge and the technical skills. lawton et all used a model of 3d printed aneurysm implanted into cadaver and prepared for surgical simulation, while a group from little rock designed a “live cadaver” model using a pulse generator, and vein segments to create aneurisms in cadaver heads connected to a closed flow system. [1,4,8] the accuracy of reproducing the real aneurysm surgery in an experimental setting should be balanced with the cost , thus training on chicken wing on rat , bigger animals like rabbit or swine or human placenta models is the cheapest , while training on cadaveric heads with vein models, 3dprinted models can increase the cost to more than 2000 $ per model . the virtual reality model for training, even if the most expensive, around 300000$ for a surgery rehearsal platform is the farthest away from the real surgery. [2,7,12,13] all of these experimental methods of training have their shortcomings. the synthetic and the virtual models are far from reaching the real feel sense one can develop only training with real vessels and also one cannot train dissecting around the aneurysm using these models. the in vivo animal model can approximate relatively simple aneurysm conformations and in larger vessels than we usually encounter in brain as it is difficult to build an aneurysm model in a living animal and it takes too much time to reperfusion to be feasible in smaller animals like rats where the vessels resemble those in the brain. the ex vivo model lacks the flow and the real vessels reactivity to manipulation but this shortcoming can be exceeded by connecting the vessels to a pulsating flow system. also it allows building of complex giant aneurysms to resemble giant acom, ica, mca trifurcation or quadrifurcation aneurysms. there is no aneurism model so far to take into consideration the perforating vessels we routinely use chicken wings for aneurysm and avm models as their vessels have a similar calibre with the a1 and a2 segments. the wall of the chicken wing arteries have a slightly better developed muscular tunica than those in the brain. [2] excepting the fact that aneurism models are a useful tool to practice clipping the aneurysm implantation technique is a good practice for vessel dissection and practicing microanastomosis. this study has an important limitation in that it does not take into account the skull base and the cisternal anatomy. the 3d printers are limited by the impossibility to reproduce aneurism models smaller than 1mm and given the fact that it is based on information from the angio mri, the printed model cannot include the perforators, which should be the main concern for a successful surgery. as more performant mri machines will be available for clinical use the perforators may become visible in the 3d reconstruction and can be used for the printed models. using cadaveric models is the most appropriate experimental model as it tests the anatomical knowledge and the arachnoid dissection technique, but it cannot mimic an in vivo environment, even if the arteries are connected to a continuous perfusion system. [3,8] the virtual reality aneurysm clipping simulation provides a realistic haptic virtual romanian neurosurgery (2016) xxx 2: 154-161 | 161 reality clipping of patient based cerebral aneurysm. the system is designed to give the user the sense of the force of the clip and the tissue deformation as the clip is positioned on the aneurysm neck. conclusion clipping training on aneurysm models is an invaluable tool both for the residents and for the specialists with a special interest in cerebrovascular surgery. using ex vivo models allows constructing a complex shape aneurysms to resemble real cases, which are time consuming, and thus difficult to build in in vivo models and also is the less resource consuming method with advantages comparable to the other experimental models described in literature. references 1. "live cadavers" for training in the management of intraoperative aneurysmal rupture emad aboud, md1, ghaith aboud2, ossama al-mefty, md3, talal aboud2, stylianos rammos, md1, mohammad abolfotoh, md, phd3,4, sanford p. c. hsu, md5, sebastian koga, md6, adam arthur, md, mph7, and ali krisht, md1 , journal of neurosurgery nov 2015 / vol. 123 / no. 5 / pages 1339-1346 2. abla aa, uschold t, preul mc, zabramski jm. comparative use of turkey and chicken wing brachial artery models for microvascular anastomosis training. j neurosurg. 2011;115(6):1231-1235. 3. anatomical reproducibility of a head model molded by a three-dimensional printer. kondo k, nemoto m, masuda h, okonogi s, nomoto j, harada n, sugo n, miyazaki c.neurol med chir (tokyo). 2015;55(7):592-8 4. e. aboud, o. al-mefty, and m. g. ya?argil, "new laboratory model for neurosurgical training that simulates live surgery," journal of neurosurgery, vol. 97, no. 6, pp. 1367-1372, 2002. 5. güvençer m, sayhan s, ay dereli n, tetik s, yücesoy k, arda mn: simulation of cerebrovascular circulation in the human cadaver for surgical neuroanatomy training. turk neurosurg 17:243-246, 2007 6. hino a. training in microvascular surgery using a chicken wing artery. neurosurgery. 2003;52(6):14951497; discussion 1497-1498. 7. human placenta aneurysm model for training neurosurgeons in vascular microsurgery. oliveira magaldi m, nicolato a, godinho jv, santos m, prosdocimi a, malheiros ja, lei t, belykh e, almefty ro, almefty kk, preul mc, spetzler rf, nakaji p.neurosurgery. 2014 dec;10 suppl 4:592-600 8. implantation of 3d-printed patient-specific aneurysm models into cadaveric specimens: a new training paradigm to allow for improvements in cerebrovascular surgery and research.; benet a, platabello j, abla aa, acevedo-bolton g, saloner d, lawton mt.; biomed res int. 2015;2015:939387. doi: 10.1155/2015/939387. epub 2015 oct 11. 9. j. olabe, j. olabe, and v. sancho, "human cadaver brain infusion model for neurosurgical training,"surgical neurology, vol. 72, no. 6, pp. 700-702, 2009. 10.m. t. lawton and r. du, "effect of the neurosurgeon's surgical experience on outcomes from intraoperative aneurysmal rupture," neurosurgery, vol. 57, no. 1, pp. 915, 2005. 11.mucke t, holzle f, wolff kd, harders a, scholz m. microsurgically induced pure arterial aneurysmmodel in rats. cent eur neurosurg. 2011;72(1):38-41. 12.olabe j, roda j. microsurgical cerebral aneurysm training porcine model. neurol india. 2011;59(1):78-81. 13.yatomi k, yamamoto m, mitome-mishima y, et al.. new experimental model of terminal aneurysms in swine: technical note. j neurol surg a cent eur neurosurg. 2012;73(6):397-400. 12alatasi_threelevel romanian neurosurgery (2014) xxi 4: 471 – 473 471 three level spinal dysraphism: multiple composite type 1 and type 2 split cord malformatıon i. alatas1, m. gundag2, h. canaz1*, e. emel3 1spina bifida center, florence nightingale bilim university, istanbul, turkey 2department of neurosurgery, bezmi alem vakif gureba school of medicine, istanbul, turkey 3department of neurosurgery, bakirkoy psychiatry and neurology research and training hospital, istanbul, turkey abstract: it has reported an uncommon case a 3 year-old girl a composite split cord malformation (scm) with two different levels of scm type1 and one level scm type2, tight filum and sacral dermal sinus. the patient was admitted with a hypertrichosis and hyperpigmented patch. mri of whole spine and brain was done. scm type1 at t 7 and l2 levels and scm typ2 at t11 level were removed then tight filum was cut and dermal sinus was excised at different sites during the same surgery. key words: split cord malformation, 3 levels spinal dysraphism. introduction diastematomyelia literally means spinal cord splitting, while diplomyelia represents cord duplication. in 1992, pang at all suggested that terms such as diastematomyelia and diplomyelia be abandoned, to make way for a new classification of scm into two types, based on the state of the dural tube and the nature of the median septum. type 1 has an osseous or osteocartilagineous midline septum splits the spinal cord into two tubes each containing a hemicord. type 2 has no osteocartilagineous spur, consist of two hemicords, but they are contained in a single dural sheath, rarely, thin fibrous septa may form. (5) composite type is very rare and result from two seperate foci of ectoendodermal adhesions and endomesenchymal tracts leading to development of different scm types with intervening normal cord in the same patient. only very few cases of composite scm have been reported in literature. (6, 8) we present a case of composite type of scm with two levels scm type 1 and single level scm type 2, tight filum and sacral dermal sinus. case: a 3 year-old girl was admitted hyperpigmented patch and hypertrichosis. there was no history of bladder, bowel and limbs disturbances. neurological examination was normal. the urodynamic test showed overactive detrusor and increased bladder capacity. mri revealed the scm type 1 at level 472 alatas et al three level spinal dysraphism t7 and l2, scm type2 at t11 level and lowlying conus (figure 1, 2). a skin incision was made from t5 to l5. then t7 laminoplasty was done and the dural sheath was incised and the bony spur was removed and dura was unified. afterthat t11 laminoplasty was performed and the thin fibrous septum was excised. then l2 laminoplasty was done, the dural sheath was incised and the bony spur was removed and dura was unified. then l5 laminoplasty was done and dural sheath was incised and the filum terminale was cut and the unification of the dura was done (figure 3). the control urodinamic test was normal after six month’ surgery. figure 1 mri sagittal t2 weighted image showing scm type 1 at level t7 and l2, scm type 2 at t11 level figure 2 mri axial t2 weighted image shows scm type 1 at t7 , scm type 2 at t11 and type 1 at l2 figure 3 at the operation photograph showing three level scm discussion diastematomyelia was introduced by olliver the disease of the spinal cord and its covering published in 1837. later cohen and sledge emphasised that this term only defines the cleft in the spinl cord or not, as often written, the osseous spur or fibrocartilaginous tract that separates both hemicords. (1) diplomyelia was invented by von recklinghausen, applies to a completely different malformation where one finds a totally formed spinal cord, situated dorsally or ventrally to the original spinal cord, mostly at the lumbo-sacral level. (9) pang gave a new classification recommending the term scm for all double spinal cord malformations. he also described the unified theory, explains the embryologic mechanism of development of all variants of scm. according to the theory, the formation of an “accessory neuroenteric canal" between the yolk sac and amnion through the midline embryonic disc, which is subsequently invested with mesenchyme to form an endomesenchymal tract that splits the notochord and neural plate. the location of romanian neurosurgery (2014) xxi 4: 471 – 473 473 this abnormal fistula is variable, but it must be rostral to the primitive neuroenteric canal, because the primitive pit into which the latter normally opens, ultimately comes to lie opposite the coccyx. in type 1 scm, the precursor cells within endomesenchymal tract may form a bony spur in the midline, attached to the bone of developing vertebral column, while in type 2 scm the mesenchymal tract forms a thin fibrous septum in the space between the hemicords. (7) accessory neuroenteric canal maybe single or multiple, and the presence of multiple accessory neuroenteric canals results in two or more septa that divide the spinal cord into hemicords. one or both types of scm at different levels have been reported in the same patients as we have seen in our case. pang reported about two such cases of composite type of scm, out of total 39 case studies. (7) ersahin et al. reported on 4 such cases out of 74 cases of scm in their study. (2) kumar et al labeled the complex spina bifida and feel it is necessary to make minor modification to pang’s classification to accommodate the pure/combined anomalies together. (3) kumar and singh were put forward that meningomyelocele and scm are seen together 40.8 %. thus, they emphasized spinal dysrafism together with occult and also open types. (4) our patient has a composite split cord malformation (scm) with two different levels of scm type1 and one level scm type 2, tight filum and sacral dermal sinus. our surgery was performed well in a one-stage operation. we did not have any complication during surgery. conclusion composite type scm is seen rare. not only neurological deficits, but also neuro-urological findings should be noted. our case’s neurological examination was normal, however, the urodynamic test showed overactive detrusor and increased bladder capacity. control urodinamic test was done after six month surgery and test result was normal. it should be remembered if presence of tethered cord syndrome other congenital spinal malformation can be exist. correspondence huseyin canaz spina bifida center, florence nightingale bilim university, sisli, istanbul, turkey +905065307853, drcanaz@gmail.com references 1. cohen j, sledge cb diastematomyelia. an embryological interpretation and report of a case. am j dis child 1960;100: 257-263 2. ersahin y, demirtas e, mutluer s, tosun ar, saydam s. split cord malformations: report of three unusual cases. pediatr neurosurg. 1996;24:155-9. 3. kumar r, bansal kk, chhabra dk. occurrence of split cord malformation in meningomyelocele: complex spina bifida. pediatr neurosurg. 2002;36:119-27. 4. kumar r, singh v, singh sn. split cord malformation in children undergoing neurological intervention in india: a descriptive study. j pediatr neurol. 2004;2:21-7. 5. pang d, dias ms, ahab-barmada m. split cord malformation: part i: a unified theory of embryogenesis for double spinal cord malformations. neurosurgery 1992; 31:451-480. 6. pang d split cord malformation. ii. clinical syndrome. neurosurgery 1992; 31:481-500. 7. pang d. split cord malformation, proposal for a new clinicoradiological. neurosurg clin n am. 1995;3:339-52. 8. vaishya s, kumarjain p. split cord malformation: three unusual cases of composite split cord malformation. childs nerv syst. 2001;17:528-30 9. von recklinghausen f untersuchungen über die spina bifida. virchows arch path anat 1885;105:243-330 4iongeorgiana_temporo 160 ion et al temporo-sylvian anastomosis and aneurysm clipping temporo-sylvian anastomosis and aneurysm clipping in a case of left m1 aneurysm with progressive evolution after initial embolization; case report georgiana ion1, a. chiriac, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: a giant unrupted middle cerebral artery aneurysm partially thrombosed, previously endovascularly treated after a mild right hemiparesis remitted. after 12 months, in routine check we discovered a reperfusion of the aneurysm and decide ecic bypass and clipping, with a good outcome. introduction complex intracranial aneurysms are among the most challenging lesions faced by neurosurgeons. among them are mentioned giant aneurysms and those with an intraluminal thrombus that can dislodge emboli into the vascular territory. partially thrombosed aneurysms, is defined to be those aneurysms in which the diameter of the aneurysm as detected by cross-sectional studies is larger than the diameter of the perfused aneurysm detected by digital subtraction angiography. it is suggested that the giant intracranial aneurysm grows by recurrent hemorrhage into its wall and behaves like growing encapsulated hematomas. the neurosurgical approach often requires techniques other than conventional clipping, such as bypass and clip reconstruction. disadvantage of coiling is the migration of coils into the thrombus during follow-up. case report a 53-years-old female first presented 1 year ago with headache, right hemiparesis and aphasia, remitted in a few days. brain computer tomography imaging raised suspicion of a mca aneurysm. the diagnosis was confirmed by the angio-ct and by the digital subtraction angiography. it was observed a 12x18mm left m1 segment, saccular aneurysm with broad-based neck. the aneurysm was treated by coil embolization. under local lidocaine anesthesia, a 6.0 fr guiding catheter was introduced into the left carotid artery via the transfemoral approach. then a coaxial microcatheter under fluoroscopic guidance romanian neurosurgery (2015) xxix 2: 160 165 161 was introduced through the left carotid artery, into the mca and finally into the aneurysm. figure 1 initial ct scanhyperdense area on the topography of the left sylvian fissure figure 2 angio-ct reconstruction after the first coil placement 5000 u of intravenously heparin were used for systemic anticoagulation and another 5000 u at the end of the procedure. to achieve occlusion were placed five coils. post embolization angiography showed a approximately 90% occlusion, with a a portion of the neck of the aneurysm not closed. further packing of the aneurysm would have carried a high risk of parent artery compromise because of the large aneurysm neck that appeared to be incorporated into the parent artery. ct scan follow-up 4 month later showed nothing abnormal, but after 12 month ct scan, angioct and cerebral mri point-out a giant mca aneurysm, partially thrombosed. the next step was to perform an angiography, were is observed an m1 segment giant aneurysm near the one previous occluded. figure 3 angio-ct reconstruction after 12 months follow-up figure 4 t2 and tof weighted sequences 12 months after embolization it can be seen that the coils are scattered and have a different conformation, showing a regrowth and recanalization of the aneurysm. figure 5 top images-control angiography after embolization; bottom image-control angiography after 12 month 162 ion et al temporo-sylvian anastomosis and aneurysm clipping it was decided that the best method of treatment in this case would be the surgical one, clip reconstruction and obliteration of the aneurysm and a by-pass between superficial temporal artery and sylvian atery. first we studied angiographically sta and then we have identified it with doppler ultrasound. a left pterional approach was performed, the afferent (ica and mca), and efferent vessels were then dissected and the aneurysmal neck was exposed. a temporary clip was placed on the m1 segment for less than 2 minutes,and the aneurysm was closed with multiple fenestrated clips. after securing the aneurysm, the sac was opened for endarterectomy and reconstruction of the arterial wall with suture. sta-mca bypass is a technique that allows the blood supply from the extracranial carotid circulation to be routed to the distal middle cerebral artery branches, to increase flow to the distal mca territory. first stamca anastomoses were made by yasargil for the treatment of complex intracranial aneurysms or for cerebrovascular occlusive disease. procedure preoperative preparation consists of computed tomography scan and digital subtraction angiography the sta, in the most cases bifurcates in the preauricular region into a frontal and parietal branch, with some anatomic variations: one branch dominant, both branches of the same caliber, or atresia of the parietal branch. the donor artery branch of the sta must to be more than 1mm in diameter and is identified by doppler ultrasound. to expose and isolate the sta branch, after the skin incision and dissection of an acceptable length of the artery then is irrigated with heparinized saline, temporary clipped at the distal extremity and stored in a wet gauze. a suitable m4 branch of the mca is dissected, mobilized for 2 cm and isolated in a rubber barrier. the blood pressure is elevated and the cerebral metabolic activity is reduced with barbiturates or propofol. after the small temporary clip is placed on the m4 branch, the vessels are irrigate with papaverine solution. an end to end anastomosis, a running suture with an 90/10-0 nylon microsuture with noncutting needle.after the suture is ready the temporary clamps are removed from the recipient and donor vessels, and flow is established. a small amount of leakage of blood at the suture site is acceptable and can be diminish with an application of a small amount of surgicel. when closing, have to rongeur an adequate portion of the craniotomy flap and to suture the temporalis muscle loosely to prevent compression of the graft. the patient’s blood pressure is kept above 110 systolic to prevent graft occlusion. postoperatively, in the first 24h, pacient was with a right central facial paresis and right sided hemiparesis (4/5 mrc), that resolved in a few days. at the control ct scan was observed a hypodense area in the left caudate nucleus. for a better view of the permeability of the anastomosis was performed an angio-ct scan. romanian neurosurgery (2015) xxix 2: 160 165 163 figure 7 before and after surgical treatment angiography figure 6 top images-angioct images with stamca by-pass (arrow); bottom images-native ct scan no complication was observed during or after surgery. clinically, the patient was discharged only with a right facial paresis. after 2 months, for a better analysis of the anastomosis and the circulation and cerebral perfusion we thought that the angiography is more conclusive. it highlights the complete closure of the aneurysm and left two-thirds of the m1 segment, and repermeabilisation of the left mca territory at an sca-mca anastomosis and by collateral circulation from the left anterior cerebral artery and posterior circulation (pca). the occlusion of the parent vessel (m1) can be caused by a thrombus or the atherosclerotic plaque. figure 8 control angiography 2 months after surgery figure 9 clinical outcome 2 months after surgical treatment; right facial paresis discussion the first question we must ask is whether there it originally was a giant aneurysm or if it developed further. initial catheter angiography and angio-ct scans failed to disclose a giant aneurysm partially thrombosed or a blister aneurysm that may progress to a giant aneurysm to time. the residual neck observed on the angiographic control may be associated with aneurysm 164 ion et al temporo-sylvian anastomosis and aneurysm clipping regrowth. although statistical data are not sufficient, there are studies that support this theory. in a study of murayama, et al.it was reported that aneurysms with a neck remnant after embolization 30% remained unchanged, 30% thrombosed and 30% showed recanalization. interlocking detachable coils were deposited into the patent portion of the aneurysm, resulting in 95% obliteration of the aneurysm and preservation of the parent artery. reperfusion is not a rare complication following coiling. some studies regarding endovascular treatment of the partially thrombosed intracranial aneurysms showed that this is not the first or the best treatment option. reopening after coiling is frequent 21% in the literature and retreatment was often needed (10%) and this is due to the migration of the coil mass into the thrombus. in cases in where chrurgical treatment or parent vessel occlusion is not possible, placement of a flow diverter is an option. 86% of aneurysms treated by carotid artery ligation were not visualized postoperatively or reduced in dimensions, after a study of roski and spetzler. partially thrombosed aneurysm pathophysiology is controversial. some suggest that in the development of this aneurysms by proliferation,inflammation and and rupture is involved vasa vasorum of the wall, but most of the theories concludes that the growth of these aneurysms is determined by the dissection of the aneurysm wall. so, this explains why in case of endovascular treated partially thrombosed aneurysms, dissection may continue at the level of the remaining neck. review of the patient previous images we realize that probably would have been required an mri exploration at the first presentation in the hospital. regarding the initial symptomatology, given that the right hemiparesis and aphasia were transient, probably were caused by small thrombus that had migrated into the distal circulation and less likely determined by the mass effect of the aneurysm. on the initial ct scan there were no signs of sah. follow-up angiography (2 months later) revealed obliteration of the aneurysm and the parent vessel, but with a good compensation through the collateral circulation and from the external carotid artery via the anastomosis, all these evidenced by the absence of symptomatology. conclusion in the future, angiographic and long-term clinical follow-up is needed, not for a routine but in case of expansive aneurysms, with known residual necks or broad-based ones. vascular by-pass of aneurysm with subsequent clipping was the best option in this case. in selected cases of partially thrombosed aneurysms the best treatment option may be the use of flow-diverting stents. if on follow-up imaging growth of the aneurysm is detected, surgical or endovascular procedures should be considered because the prognosis of this patients is poor. references 1.david w. newell, m.d, superficial temporal artery to middle cerebral artery bypass. 1 skull base. 2005 may; 15(2): 133–141. romanian neurosurgery (2015) xxix 2: 160 165 165 2.h. hunt batjer, m.d., alan i. frankfurt, m.d., phillip d. purdy, m.d., shirley s. smith, m.d., and duke s.samson, m.d., .use of etomidate, temporary arterial occlusion, and intraoperative angiography in surgical treatment of large and giant cerebral aneurysms, university of texas health science center 3.carlos a. david, m.d., a. giancarlo vishteh, m.d., robert f. spetzler, m.d., michael lemole, m.d., michael t.lawton, m.d., and shahram partovi, m.d., late angiographic follow-up review of surgically treated aneurysms, . journal of neurosurgery,september 1999 / vol. 91 / no. 3 / pages 396-401 4.robert a. mericle, m.d., ajay k. wakhloo, m.d., ph.d., demetrius k. lopes, m.d., giuseppe lanzino, m.d., lee r. guterman, ph.d., m.d., and l. nelson hopkins, m.d, delayed aneurysm regrowth and recanalization after guglielmi detachable coil treatment, journal of neurosurgery,july 1998 / vol. 89 / no. 1 / pages 142-145 5.motoharu hayakawa, m.d., yuichi murayama, m.d., gary r. duckwiler, m.d., y. pierre gobin, m.d., guidoguglielmi, m.d., and fernando viñuela, m.d., natural history of the neck remnant of a cerebral aneurysm treated with the guglielmi detachable coil system, journal of neurosurgery,october 2000 / vol. 93 / no. 4 / pages 561-568 6.. murayama y, viñuela f, duckwiler gr, et al: embolization of incidental cerebral aneurysms by using the guglielmi detachable coil system. j neurosurg 90:207–214, 1999 7.kakarla uk,maughanph, deshmukh vr, spetzler rf., giant,partially thrombosed aneurysm develops after remote angographically negative subarachnoid hemorrhage: case report ,neurosurgey 2007mar60(3):e572 8.s. kobayashi, neurosurgery of complex vascular lesions and tumors 9.t. krings, h. alvarez, p. reinacher,a. ozanne, c.e. baccin, c. gandolfo,w.-y. zhao, m.h.t. reinges,and p. lasjaunias, . growth and rupture mechanism of partially thrombosed aneurysms, interv neuroradiol. 2007 jun; 13(2): 117–126. 10. h. richard winn, md and h. richard winn, md, youmans neurological surgery, 6th edition 13agrawalamit_gliosarcoma romanian neurosurgery (2015) xxix (xxii) 1: 111 115 111 temporal gliosarcoma: case report and review of literature amit agrawal1, vissa shanthi2, baddukonda appala ramakrishna3, kuppili venkata murali mohan3 1professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2associate professor of pathology, department of pathology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 3professor of pathology, department of pathology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract: first characterized by stroebe, the gliosarcomas are highly malignant and rare primary tumor of the brain composed of neoplastic glial cells in association with spindle cell sarcomatous elements (biphasic tissue patterns). in spite of being recognized as two different pathologies studies have not shown any significant differences between gliosarcoma and glioblastoma with regard to age, sex, size, clinical presentation, and median survival. in summary, gliosarcoma is an aggressive tumor with a propensity to recur and re-grow with poor outcome. future studies are needed to understand the true pathology of these biphasic tumors. key words: gliosarcoma, radiotherapy, survival, temporal gliosarcoma introduction first characterized by stroebe, (1) the gliosarcomas are highly malignant and rare primary tumor of the brain composed of neoplastic glial cells in association with spindle cell sarcomatous elements (biphasic tissue patterns). (1-9) world health organization characterizes primary gliosarcoma as a grade 4 neoplasm and a variant of glioblastoma multiform (10, 11) and gliosarcomashave an incidence of 1.8%-2.8% of that of glioblastomas. (5, 12, 13) case report a 50-year female presented with fever of 20 days duration, right sided headache and right hypochondrial pain of similar duration. she lapsed into altered sensorium three hours before presenting to emergency room and had two episodes of vomiting. she lapsed into altered sensorium after vomiting. her general and systemic examination was unremarkable. neurologically glasgow coma scale (gcs) was e1v1m4, pupils were bilateral equal and reacting. she was moving all four limbs equally to deep painful stimuli. pulse rate was 112 agrawal et al temporal gliosarcoma 56 per minute regular. the patient was intubated in emergency and ventilated. computerized scan (ct) of brain revealed a well-circumscribed heterogeneous isoto hyperdense lesion in the right temporal lobe with significant peri-lesional edema, mass effect and midline shift (figure 1). total leucocytes count was 26,500 per mm3 (n-86, l-09, e-01, 04. esr was 36 mm in 1st hour. she was started on anti-edema measures. she underwent emergency right temporal craniotomy and total excision of the lass. the mass was avascular and firm to hard in consistency (figure 2). based on clinical features and intra-operative findings a diagnosis of tuberculoma was suspected. figure 1 ct scan brain plain showing a heterogeneously lesion in the right temporal lobe with significant peri-lesional edema, mass effect and midline shift figure 2 intra-operative image showing (a) well defined mass lesion in right temporal lobe, (b) total excision of the mass (see inset) figure 3 following up ct showing complete removal of the mass lesion figure 4 (a) spindle shaped tumor cells with one foci showing necrosis and pseudopalisading pattern (h&e,x100), (b) tumor with spindle shaped tumor cells, multinucleated tumor giant cells and congested blood vessels (h&e, x100), (c) tumor with spindle shaped tumor cells and multinucleated tumor giant cells (h&e, x100), (d) spindle shaped tumor cells (h&e,x100), (e) tumor cells with vacuolated cytoplasm (h&e, x100) and (f) spindle shaped tumor cells with vesicular nuclei, prominent nucleoli and an atypical mitotic figure (h&e, x400) romanian neurosurgery (2015) xxix (xxii) 1: 111 115 113 figure 5 (a) spindle shaped tumor cells positive for gfap (gfap, x100) and (b) spindle shaped tumor cells positive for gfap (gfap, x400) in addition to broad spectrum antibiotics she was stated on att. postoperative ct showed total excision of the tumor and reduction in cerebral edema, mass effect and midline shift (figure 3). multiple section studies showed lesion composed of spindle shaped cells arranged in fascicles. in some foci they are arranged irregularly. the tumor cells are having oval elongated vesicular nuclei with prominent nucleoli and eosinophilic cytoplasm. in some foci tumor cells show vacuolated cytoplasm. few foci show tumor cells having eccentrically placed nuclei with abundant eosinophillic cytoplasm. mononucleated and multinucleated tumor giant cells are seen. numerous atypical mitotic figures are noted. occasional foci show necrosis and pseudo-pallisading pattern of arrangement of tumor cells. glial component was seen in some foci (figures 4 and 5). the patient received radiotherapy and chemotherapy. she is doing well at follow up. discussion gliosarcomas are usually located in the cerebral cortex (the temporal, frontal, parietal, and occipital lobes in decreasing frequency), most common in adults males in the fourth to sixth decades of life. (3, 5, 8, 12-16) clinically these patients present with features of raised intracranial pressure due to an expanding space occupying lesion (i.e. headache, hemiparesis, seizures, and cognitive decline). (15, 17) the pathogenesis of gliosarcoma has been a topic of controversy and various theories have been proposed (1) the sarcomatous component originates from neoplastic transformation of hyperplastic blood vessels found in high-grade glioma, and (2) the recent theory suggests monoclonal origin of sarcomatous component originating via aberrant mesenchymal differentiation of the malignant glioma. (15, 18-20) histologically, the gliosarcoma is composed of 2 distinct malignant cell populations (biphasic tissue pattern), one component being gliomatous (heterogeneous infiltrative areas with hemorrhage and necrosis and stains for gfap compatible with glioblastoma) and the other with malignant mesenchymal differentiation (a firm discrete mass compatible with sarcoma). wrinkler, 2000 #179} (3, 19-23) the presence of identical genetic alterations in both gliomatous and sarcomatous components strongly supports monoclonal origin of gliosarcomas, however the absence of amplification/over expression of the egfr gene, a genetic hallmark of primary glioblastomas. 24 appearance of gliosarcoma on ct is extremely variable and these lesions generally appear as a well-defined hyperdense mass with heterogeneous or ring enhancement due to a fibrous component with intense peritumoral edema and necrotic areas. (13, 15, 25-28) on magnetic resonance imaging (mri) gliosarcoma appear as a heterogeneous mass both in t1and t2 114 agrawal et al temporal gliosarcoma weighted images with irregular contrast enhancement with marked peritumoral edema (15, 25, 26) management of gliosarcoma includes maximum surgical decompression with post-operative radiotherapy. (7, 9, 15, 29) the possible role of chemotherapy in gs is still undefined and could be explored in future studies. (7, 8, 13, 15, 20, 30) metastases has been reported in up to one third of cases, mainly to the lungs, pleura, lymph nodes, bone marrow, liver, spinal cord, kidney and peripancreatic areas. (15, 17, 25) in spite of being recognized as two different pathologies studies have not shown any significant differences between gliosarcoma and glioblastoma with regard to age, sex, size, clinical presentation, and median survival. (3, 7, 8, 14-16, 19, 20, 31) the predominance of the sarcomatous component has been shown to be associated with a better prognosis and a greater recurrence-free interval. (19) in summary, gliosarcoma is an aggressive tumor with a propensity to recur and re-grow with poor outcome. future studies are needed to understand the true pathology of these biphasic tumors. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.stroebe h, stupp r, mason wp, bent mj. uber entstehung und bau der gehirngliome. beitr pathol anat allg pathol van den radioth 1895;18 src googlescholar:405-485. 2.feigin i, gross sw, j., fischer s, lee w, aulisi e. sarcoma arising in glioblastoma of the brain. am pmcid pmc557 pubmed 14388124 1942;31 src googlescholar:633-653. 3.morantz ra, feigin i, ransohoff j. clinical and pathological study of 24 cases of gliosarcoma. journal of neurosurgery 1976;45:398-408. 4.goldstein sj, young b, markesberry wr. congenital malignant gliosarcoma. ajnr american journal of neuroradiology 1981;2:475-476. 5.parekh hc, o'donovan dg, sharma rr, keogh aj. primary cerebral gliosarcoma: report of 17 cases. british journal of neurosurgery 1995;9:171-178. 6.güney y, hiçsönmez a, yilmaz s, adas yg, andrieu mn. gliosarcoma: a study of four cases. rare tumors 2010;2. 7.kumar p, singh s, kumar p, krishnani n, datta nr. gliosarcoma: an audit from a single institution in india of 24 post-irradiated cases over 15 years. journal of cancer research and therapeutics 2008;4:164-168. 8.meis jm, martz kl, nelson js. mixed glioblastoma multiforme and sarcoma. a clinicopathologic study of 26 radiation therapy oncology group cases. cancer 1991;67:2342-2349. 9.basmaci m, hasturk ae, ayata t, canbay s, cobanoglu m. primary gliosarcoma: clinical and pathological evaluation of four cases. journal of neurological sciences (turkish) 2011;28:402-409. 10.louis dn, ohgaki h, wiestler od, et al. the 2007 who classification of tumours of the central nervous system. acta neuropathologica 2007;114:97-109. 11.kleihues p, cavenee wk. pathology and genetics of tumours of the nervous system: international agency for research on cancer, 2000. 12.lutterbach j, guttenberger r, pagenstecher a. gliosarcoma: a clinical study. radiotherapy and oncology : journal of the european society for therapeutic radiology and oncology 2001;61:57-64. 13.okami n, kawamata t, kubo o, yamane f, kawamura h, hori t. infantile gliosarcoma: a case and a review of the literature. child's nervous system : chns : romanian neurosurgery (2015) xxix (xxii) 1: 111 115 115 official journal of the international society for pediatric neurosurgery 2002;18:351-355. 14.galanis e, buckner jc, dinapoli rp, et al. clinical outcome of gliosarcoma compared with glioblastoma multiforme: north central cancer treatment group results. journal of neurosurgery 1998;89:425-430. 15.han sj, yang i, tihan t, prados md, parsa at. primary gliosarcoma: key clinical and pathologic distinctions from glioblastoma with implications as a unique oncologic entity. journal of neuro-oncology 2010;96:313-320. 16.kozak kr, mahadevan a, moody js. adult gliosarcoma: epidemiology, natural history, and factors associated with outcome. neuro-oncology 2009;11:183191. 17.witwer bp, salamat ms, resnick dk. gliosarcoma metastatic to the cervical spinal cord: case report and review of the literature. surgical neurology 2000;54:373378; discusiion 378. 18.boerman rh, anderl k, herath j, et al. the glial and mesenchymal elements of gliosarcomas share similar genetic alterations. journal of neuropathology and experimental neurology 1996;55:973-981. 19.salvati m, caroli e, raco a, giangaspero f, delfini r, ferrante l. gliosarcomas: analysis of 11 cases do two subtypes exist? journal of neuro-oncology 2005;74:59-63. 20.winkler pa, büttner a, tomezzoli a, weis s. histologically repeatedly confirmed gliosarcoma with long survival: review of the literature and report of a case. acta neurochirurgica 2000;142:91-95. 21.koul r, tai p, dubey a. five patients with gliosarcoma. j hk coll radiol 2008;11:116-121. 22.borota oc, scheie d, bjerkhagen b, jacobsen ea, skullerud k. gliosarcoma with liposarcomatous component, bone infiltration and extracranial growth. clinical neuropathology 2006;25:200-203. 23.sarkar c, sharma mc, sudha k, gaikwad s, varma a. a clinico-pathological study of 29 cases of gliosarcoma with special reference to two unique variants. the indian journal of medical research 1997;106:229-235. 24.reis rm, könü-lebleblicioglu d, lopes jm, kleihues p, ohgaki h. genetic profile of gliosarcomas. the american journal of pathology 2000;156:425-432. 25.moreira jn, gaspar r. antagonist g-mediated targeting and cytotoxicity of liposomal doxorubicin in nci-h82 variant small cell lung cancer. brazilian journal of medical and biological research = revista brasileira de pesquisas medicas e biologicas / sociedade brasileira de biofisica [et al] 2004;37:1185-1192. 26.alatakis s, stuckey s, siu k, mclean c. gliosarcoma with osteosarcomatous differentiation: review of radiological and pathological features. journal of clinical neuroscience : official journal of the neurosurgical society of australasia 2004;11:650-656. 27.nitta h, hayase h, moriyama y, yamashima t, yamashita j. gliosarcoma of the posterior cranial fossa: mri findings. neuroradiology 1993;35:279-280. 28.rees jh, smirniotopoulos jg, jones rv, wong k. glioblastoma multiforme: radiologic-pathologic correlation. radiographics : a review publication of the radiological society of north america, inc 1996;16:14131438; quiz 1462. 29.maeda d, miyazawa t, toyooka t, shima k. temporal gliosarcoma with extraneural metastasis: case report. neurologia medico-chirurgica 2010;50:343-345. 30.balasubramaniam s, tyagi dk, sawant hv, epari s. posterior fossa involvement in a recurrent gliosarcoma. journal of neurosciences in rural practice 2012;3:60-64. 31.hasegawa t, yamamoto s, yokoyama r, umeda t, matsuno y, hirohashi s. prognostic significance of grading and staging systems using mib-1 score in adult patients with soft tissue sarcoma of the extremities and trunk. cancer 2002;95:843-851. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 356 | chiriac et al associated intracranial meningioma and aneurysm associated intracranial lesions: meningioma and anterior communicating aneurysm a. chiriac, georgiana ion1, z. faiyad1, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi, romania 1“prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract: asymptomatic associated intracranial lesions are more frequently diagnosed with the utilization of high-resolution imaging. the occurrence of brain tumors together with intracranial aneurysms are a very rare situation. this coexistence is still a diagnostic and therapeutic challenge as no consensus concerning imaging that may cover both type of intracranial lesion was established. we report a case of a 62 years old patient with a meningioma and aneurysm treated in one session with good outcome. key words: associated intracranial lesions, aneurysm, meningioma introduction the coexistence of brain tumors together with intracranial aneurysms is a relatively rarely condition but not considered as a new phenomenon. there are few case reports published in the literature documenting the association between brain tumors and aneurysms. different types of brain tumors as pituitary adenoma, glioma, meningioma, lipoma or metastatic tumor were identified in association with intracranial aneurysm. the estimated incidence was reported between 0.30.7%. however, intracranial meningioma was found to be the most common tumor entity associated with intracranial aneurysm. the aim of this article is to present our treatment strategies in these particular cases and to identify possible explanations of this coexistence (1, 3, 5, 7). case report a 62-year-old female patient, with a history hypertension and noninsulin-dependent diabetes, was suffering from episodes of loss of consciousness and headache for several months. she was admitted to another hospital and a magnetic resonance (mr) revealed an extra-axial mass in left frontal lobe with planum sphenoidale implantation. because the most likely imaging diagnosis was meningioma, she was admitted to our department of neurosurgery. a preoperative cerebral ct-angiography was performed for the purpose of analysis of the relationship with large vessels in the region and neoplastic vessels. following this investigation an anterior communicating artery aneurysm was revealed. there were no significant tumor vessels and any involvement of large vessels in relation to tumor mass. (figure 1a, b). on the next days, with the patient´s consent, a left fronto-pterional approach was performed with total tumor resection and aneurysm clipping. the ct scan control performed the next day after surgery shows complete tumor romanian neurosurgery (2016) xxx 3: 356 359 | 357 resection and the clip artifacts. the outcome of the patient was well and she was discharged home after seven days. discussions association of meningioma and intracranial aneurysm is the most common situation that was first reported by arieti and all in 1944. the reported incidence of meningioma and intracranial aneurysm varied from 0.3% to 0.7% (1, 3, 4, 9). 358 | chiriac et al associated intracranial meningioma and aneurysm figure 1: a, b – mri images on sagital and coronal view showing a planum sphenoidale menigioma; c, d – ct – angiography showing an acoa associated aneurysm; e, f – ct control showing complete resection of meningioma and aneurysm clip artifact however, the real incidence is probably higher because an angiography investigation is not usually performed in patients with brain meningioma. now, advanced imaging techniques like the noninvasive mra method become increasingly available and applied for brain tumors investigation. consequently, the reported prevalence of intracranial aneurysms has also increased to approximately 2%–5% in patients with brain tumors. (7, 8) there have been several proposed possible mechanisms that have been published trying to explain the relationship between tumors and aneurysms. thus, local hemodynamic factors, hormonal influence, genetic factors and direct invasion of tumor cells to the vessel wall were considered responsible for this clinical coexistence. the first mechanism is due to the phenomenon of maintaining a constant cerebral perfusion pressure by an increased arterial blood pressure to equal the increased intracranial pressure caused by the tumor volume expansion. this chronic increase in arterial blood pressure could cause an increase in hemodynamic stress on cerebral arteries around slowly growing meningiomas or even in the entire brain. that may explain the degenerative changes to arterial walls leading to intracranial aneurysm formation. some scientific researches have reports a hormonal influence in association of brain tumors and intracranial aneurysm. growth factors like estrogen have been suggested in association with both meningioma and aneurysms. pia et al. (3) had reported in the literature an association between a dysgenetic factor and the coexistence of brain tumors together with intracranial aneurysm. the klippeltrenaunay syndrome might explain a high incidence of meningiomas associated with aneurysms. klippel-trenaunay syndrome is a rare neurocutaneous disorder in which skeletal hypertrophy, vascular nevi and vessel anomalies coexist. the conclusion of pia analysis showed an insufficient evidence of dysgenetic factor hypothesis. kandel et al. (5) had published a case of a typical mca aneurysm associated with a fronto temporal meningioma. the authors explain the formation of the aneurysm by the damage that the meningioma caused to the wall of the artery based on tumor adhesion to the arterial adventitia. the treatment options of this particular situation vary from conservative management to treating both pathologies simultaneously or sequentially. if the aneurysm is in close romanian neurosurgery (2016) xxx 3: 356 359 | 359 proximity to the tumor both can be accessed simultaneously in the same sitting. if the aneurysm occurs in the other hemisphere, most of the specialists recommend treating first the pathology that causes the symptoms (1, 2, 3, 4, 5, 7). conclusions the coexistence of intracranial aneurysms and menigiomas is not a new phenomenon and the association between the two lesions is still under debate. even some of the assumptions underlying mechanisms of such an association were stated, their low incidence suggests a rather due to chance. regarding the treatment, if both lesions are in a close proximity they can be managed simultaneously and if they are located contra lateral usually it will be approached in two steps starting with the symptomatic one. references 1. de eulate-beramendi, s. a., alvarez-vega, m. a., gutierrez-morales, j. c., & lópez-garcía, a. (2016). meningioma associated with brain aneurysm: report of two cases. turk neurosurg. 2. fischer, b. r., palkovic, s., holling, m., niederstadt, t., jeibmann, a., & wassmann, h. (2009). coexistence of cerebral aneurysm and meningioma—pure accident?. clinical neurology and neurosurgery, 111(8), 647-654. 3. javadpour, m., khan, a. d., jenkinson, m. d., foy, p. m., & nahser, h. c. (2004). cerebral aneurysm associated with an intracranial tumour: staged endovascular and surgical treatment in two cases. british journal of neurosurgery, 18(3), 280-284. 4. .javalkar, v., guthikonda, b., vannemreddy, p., & nanda, a. (2009). association of meningioma and intracranial aneurysm: report of five cases and review of literature. neurology india, 57(6), 772. 5. kim, y. h., lee, y. j., han, j. h., ahn, s., lee, j., kim, j. h., ... & kwon, o. k. (2015). association of intracranial aneurysms and meningiomas: a case-control study. journal of neurosurgery, 123(2), 357-361. 6. paraskevopoulos, d., magras, i., balogiannis, i., & polyzoidis, k. (2011). anterior clinoidal meningioma coincidental with bilateral intracranial aneurysms.hippokratia, 15(4), 353. 7. spitler, k., drazin, d., hanna, g., patel, a., & chu, r. (2013). association of intracranial aneurysms with meningiomas, pituitary adenomas, and gliomas: review of possible interrelationships. isrn neurology, 2013. 8. suslu, h. t., & bozbuga, m. (2010). primary brain tumors associated with cerebral aneurysm: report of three cases. turkish neurosurgery, 21(2), 216-221. 9. tancioni, f., egitto, m. g., & tartara, f. (1998). aneurysm occurring within a meningioma: case report. british journal of neurosurgery, 12(6), 588-591. 10. zhong, z., sun, y., lin, d., sun, q., & bian, l. (2013). surgical treatment of brain tumor coexisted with intracranial aneurysm—case series and review of the literature. neurosurgical review, 36(4), 645-656. doi: 10.33962/roneuro-2021-035 c7 contribution to the ulnar nerve. literature review l.p. de macêdo, a.u. netto, k. franke, p.v. oliveira eugenio, l.r. de moraes freitas, f.a.s. de lima júnior j.v.r. de paula, s.n. bernardino, f.h.m. de souza, n.s. almeida, h.r.c. azevedo-filho romanian neurosurgery (2021) xxxv (2): pp. 215-218 doi: 10.33962/roneuro-2021-035 www.journals.lapub.co.uk/index.php/roneurosurgery c7 contribution to the ulnar nerve. literature review l.p. de macêdo1, a.u. netto1, k. franke1, p.v. oliveira eugenio2, l.r. de moraes freitas2, f.a.s. de lima júnior2, j.v.r. de paula3, s.n. bernardino4, f.h.m. de souza5, n.s. almeida1, h.r.c. azevedo-filho6 1 department of neurosurgery, hospital da restauração, recife, pernambuco, brazil 2 centro de ciências médicas, universidade federal da paraíba, joão pessoa, paraíba, brazil 3 faculdade pernambucana de saúde, recife, pernambuco, brazil 4 neurophysiologist, department of neurology, hospital getúlio vargas, recife, pernambuco, brazil 5 chief of peripheral nerves section, department of neurosurgery, hospital da restauração, recife, pernambuco, brazil 6 chairman of department of neurosurgery, hospital da restauração, recife, pernambuco, brazil abstract introduction. classic anatomical literature frequently describes c7 contribution to ulnar nerve (un) formation as a casual event. however, surgical practice and dissections frequently reveal a recurrent presence of a lateral cord component of the un. this study aimed to seek through literature to establish the frequency and degree of this contribution. methodology. we ran a literature review searching on pubmed, medline, embase and web of science databases for ulnar nerve anatomy and described discursively the results. results and discussion. we found 9 articles that described quantitatively and qualitatively the contribution of c7 on the formation of the un. the prevalence described ranged from 2 to 100%, depending on the methodology used and population characteristics. when present, studies described a contribution from 9,9% to 30,4%, sending even more fibres than t1 root on average. conclusion. the c7 root can be considered a frequent and important component of the ulnar nerve, explaining un territory repercussions on c7 radiculopathies. this knowledge is important on surgical approaches, maybe avoiding iatrogenic lesions and negative outcomes. introduction the anatomical literature reports the origin of the ulnar nerve (un) as the medial fascicle (c8-t1), but often receiving fibers from the ventral branch of c7. it is also mentioned its path through the axilla, initially keywords ulnar nerve, brachial plexus, neuroanatomy corresponding author: lívio pereira de macêdo hospital da restauração, recife, pernambuco, brazil livio21@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 216 l.p. de macêdo, a.u. netto, k. franke et al. medial to the axillary artery and between this and the vein, continuing distally medial to the brachial artery up to the middle third of the arm, where the un punctures the medial intermuscular septum and leans medially as it descends anteriorly to the medial head of the triceps muscle towards the interval between the medial epicondyle and the olecranon, with the superior ulnar collateral artery. its relationship with the brachial artery and medial epicondyle makes it easy to map in its proximal path; a line from the medial epicondyle to the lateral margin of the pisiform bone represents its distal path1,2,3,4,5. although its path and function are known, there are few records in the literature about the frequency and the way c7 contributes to the formation of the un. it should also be noted that there are differences between the anatomical study and the electromyographic diagnosis of the nerve. the objective of this study was to seek, through a literature review, to clarify the frequency and the degree of c7's contribution to the formation of the un. methods an integrative review of the literature was carried out, seeking articles that described qualitatively and/or quantitatively the formation of the un from the brachial plexus. for this, we searched at medline, embase and web of science, using the descriptors "ulnar nerve" and "anatomy", with no language or publication date restrictions. the results of the search were discursively described. results and discussion hur et al. (2013) analyzed 100 brachial plexus (bp) from korean adult cadavers. the extracted samples were immersed in guanidine-hcl for 2 weeks. after the contribution of c7 was proven, 20 samples were processed with a routine histological staining (h&e) procedure to count the number of myelinized axons using imbroglio modometer software. in all 100 bps, there was a contribution of c7 to the formation of the ulnar nerve. moreover, it was unanimous the ramification of the c7 fascicles in the distal portion of the fascicles that compose the lateral root of the median nerve, decussing with the medial root of the median nerve. the contribution of c7 to the ulnar nerve was 1.452 ± 429 (9.9%) myelinized axons, c8 was 11.448 ± 1.473 (78.3%) and t1 was 1.720 ± 382 (11.8%) in the 20 samples processed in h&e6. in contrast, fuss (1989) investigated 158 bps and reported in his study a 56% contribution of c7 to the formation of the ulnar nerve, highlighting that this collaboration may be accompanied by fibers of the median nerve (type 1) or may occur separately (type 2). considering the 56:44% relationship between ulnar nerves with and without lateral root, the author highlights that both possibilities should be considered as normal variations7. pyun, kang and kwon (2010), after dissection of 38 bps, reported 13.1% contribution of c7. it is worth mentioning that, for having performed an associated electrophysiological study, this study showed a high prevalence of alterations in the electromyography of m. flexor ulnar carpi in patients with c7 radiculopathy (13/17 = 76.5%)8. kumar and ranganath (2014) also described only 1 (2%) out of 100 bps with the contribution of the lateral cord of c7 to the formation of the un; more precisely, the branches for the un came from the union of the medial and lateral roots of the median nerve9. guru et al. (2015) dissected 50 upper limbs to observe un variations. in all, 4 variations were observed, all on the right side. the notable contribution of the bp side cord to the formation of the un was observed unilaterally in 2 (4%) members. the contributing branch passed from the lateral side to the medial side deeply to the formation of the median nerve and joined the ulnar nerve at its lateral aspect. in the two remaining cases, the ulnar nerve had abnormal communications with the neighboring nerves, radial nerve, and medial cutaneous nerve of the forearm nerve10. emamhadi et al. (2016) dissected 64 fresh bps in order to evaluate possible anatomical variations, excluding damaged specimens or ante mortem surgical interventions. during the investigations, it was found collaboration of the lateral cord of bp for the formation of the un in 3 (9.38%) of the 32 cadavers11. koo and lee (2007) analyzed the composition of the terminal branches of bp, dissecting 32 upper limbs. regarding the un, four different patterns were observed. the most frequent type was c7, c8 and t1 (75% of cases). in the average diameter, c8 was the thickest, measuring 2.64 ± 0.57 mm, and t1 was the thinnest with 0.06 ± 0.56 mm12. 217 c7 contribution to the ulnar nerve the oldest studies found, performed with even more rudimentary cadaveric dissection techniques, were those of harris (1904)13 and linell (1921)14, which showed the presence in, respectively, 86% and 57% of the brachial plexus of an exchange of fibers between the medial and lateral plexus strands, specifically the c7 fibers contributing to the formation of the ulnar nerve. author, date sample (n) methodol ogy qualitative analysis quantitative analysis hur et al., 2013 100 bps h&e + imbroglio modomet er 100 (100%, c7) 1,452 ± 429 (9,9%) axônios koo, lee, 2007 32 bps cadaveric dissection 24 (75%, c7) 1,18 ±0.59 mm fuss, 1989 158 bps cadaveric dissection 56% (lateral cord) n/a pyun et al., 2010 38 bps cadaveric dissection 13,1% (lateral cord) n/a kumar, ranganat h, 2014 50 bps cadaveric dissection 1 (2%,lateral cord) n/a guru et al., 2015 50 bps cadaveric dissection 2 (4%, lateral cord) n/a emamhad i et al., 2016 64 bps cadaveric dissection 3 (9,38%,latera l cord) n/a ramchan dran et al., 2006 1 bp case report 1 (lateral root of the median) n/a linnel, 1921 42 bps cadaveric dissection 57%, c7 n/a harris, 1904 60 bps cadaveric dissection 86%, c7 n/a figure 1. summary of the findings of the review on c7 contribution it is noticeable that the studies that performed quantitative analysis, especially hur et al. (2013) and koo and lee (2007), showed a higher prevalence of c7 contribution than the studies with cadaveric dissection, except for those of harris (1904) and linnel (1921) 6,12,13,14. this can be justified by an eventual iatrogenic loss of the lateral contribution during dissection or by the sophistication of quantitative methods. in this context, it is frequent a sub-quantification of the contribution of c7 to the nerve during dissection, justifying the absence of root representation in most of the classic anatomic literature 1,2,3,4,5. in practice, however, the repercussions of c7 radiculopathies on electromyographic variables in part of the un territory can be seen, as pyun et al. (2010) have shown8. this knowledge becomes essential in neurosurgical practice, since unadvised dissection can cause iatrogenicity. the authors themselves came across the contribution of the lateral cord to the formation of the un during surgical dissection in the treatment of a brachial plexopathy (figure 2), which motivated this review. figure 2. conclusion the c7 root can be considered a frequent component of the ulnar nerve, although its contribution may be underestimated in less sophisticated dissection studies. there is even a high incidence of c7 radiculopathy causing repercussions in the nerve territory. knowledge of this participation is indispensable for peripheral nerve surgery, avoiding iatrogenic lesions and possible negative outcomes for the patient. references 1. baehr m, frotscher m. duus topical diagnosis in 218 l.p. de macêdo, a.u. netto, k. franke et al. neurology. 5th ed. rio de janeiro, rj: guanabara koogan; 2014. 2. ellis h. clinical anatomy: a revision and applied anatomy for clinical students. 8th ed. london: blackwell scientific publications; 1992: 209. 3. moore kl, dalley af. clinically oriented anatomy. 5th ed. baltimore: lippincott williams & wilkins; 2006: 777. 4. romanes gj. cunningham’s textbook of anatomy. 12th ed. new york, ny: oxford university press; 1981: 328329. 5. standring s. gray’s anatomy. 39th ed. edinburgh: elsevier churchill livingston; 2005: 847-877. 6. hur ms, woo js, kim hj, lee ks. frequency and quantity of the c7 contribution to the ulnar nerve. korean j phys anthropol. 2013;26(3):101-104. 7. fuss fk. die radix lateralis des nervus ulnaris [the lateral root of the ulnar nerve]. acta anat (basel). 1989;134(3):199-205. 8. pyun sb, kang s, kwon hk. anatomical and electrophysiological myotome corresponding to the flexor carpi ulnar is muscle. j korean med sci. 2010; 25:454-57. 9. kumar sv, ranganath p. morphology of the ulnar nerve in axilla and arm and its variations. int j anat res. 2014;2(4):677-680. 10. guru a, kumar n, ravindra shanthakumar s, et al. anatomical study of the ulnar nerve variations at high humeral level and their possible clinical and diagnostic implications [published online july 12, 2015]. anat res int. doi:10.1155/2015/378063 11. emamhadi m, chabok sy, samini f, et al. anatomical variations of brachial plexus in adult cadavers; a descriptive study. arch bone jt surg. 2016;4(3):253-258. 12. koo jh, lee ks. anatomic variations of the spinal origins of the main terminal branches of the brachial plexus. korean j phys anthropol. 2007;20(1):11-19. 13. harris w. the true form of the brachial plexus, and its motor distribution. j anat physiol. 1904;38(pt 4):399-422. 14. linell ea. the distribution of nerves in the upper limb, with reference to variabilities and their clinical significance. j anat. 1921;55(pt 2-3):79-112. 15. ramachandran k, kanakasabapathy i, holla sj. multiple variations involving all the terminal branches of the brachial plexus and the axillary artery – a case report. eur j anat. 2006;10(3):61-66. alatasi_statisticalanalysis 258 | alatas et al associated vertebra and costal anomalies in spina bifida patients statistical analysis of associated vertebra and costal anomalies in spina bifida patients ibrahim alatas1, huseyin canaz1, ayten saracoglu2, haluk kafali2, gokhan canaz3, mehmet tokmak4 1spina bifida research center, sisli florence nightingale hospital, istanbul bilim university, istanbul 2department of anesthesiology, sisli florence nightingale hospital, istanbul bilim university, istanbul 3department of neurosurgery, haseki training and research hospital, istanbul 4department of neurosurgery medipol university, istanbul abstract: objective: spina bifida is one of the most severe birth defects and can happen as a result of disrupted primary neurulation. congenital vertebra and costa anomalies are more frequently seen with spina bifida, and associated anomalies significantly affect the prognosis of affected children. in this study, we aimed to determine the incidence of scoliosis, costal anomalies, and vertebral deformations seen at the time of diagnosis and to statistically evaluate their concomitancies. methods: gender and mean ages of the patients were determined. the spina bifida patients were examined for deformation anomalies, butterfly vertebra, hemivertebra, wedge vertebra, costal anomalies and scoliosis. the relationships between these anomalies were evaluated. results: 94 patients with a mean age of 11,5 months examined. the incidence of scoliosis was 21.8% among female infants and 17.9% among males. rates of scoliosis with vertebra anomalies (hemivertebra, wedge vertebra) and costal anomalies did not differ significantly (p > 0.05). wedge vertebra were the most frequent vertebra anomaly type with 38.2% ratio. costal anomalies were detected in 25.5% of females and 20.5% of male infants. hemivertebra and wedge vertebra were seen significantly more frequently in this group. gender distribution did not differ between with and without any vertebra types. conclusion: congenital vertebra and costa anomalies are more frequently seen with spina bifida. we believe that these anomalies and relationship with spina bifida may demonstrate differences among different ethnic groups or locations. more detailed multi-centered studies performed on this issue will aid in the determination of etiologies, genetics, and treatment principles of these congenital anomalies. key words: costal anomalies, scoliosis, spina bifida, hemivertebrae, wedge vertebrae romanian neurosurgery (2016) xxx 2: 258-266 | 259 introduction spina bifida can happen as a result of the disruption of any stage of primary neurulation, which terminates at the 4th week of intrauterine life, or secondary neurulation, which terminates at the 11th week. in patients with spina bifida, higher incidence of vertebral formation, segmentation anomalies, scoliosis, kyphosis, and costal anomalies have been detected. associated anomalies significantly affect the prognosis of children with myelomeningocele. congenital vertebral anomalies can affect any vertebral segment or involve one or more than one segment (31). vertebral anomalies lead to skeletal deformities and consequently complicate the clinical picture (19). vertebral anomalies complicate primary surgery and affect pathogenesis and monitorization of tethered spinal cord syndrome during long-term follow-up. costal anomalies are usually associated with vertebral anomalies in patients with spina bifida. congenital costal anomalies complicate vertebral surgery, lead to pulmonary problems at an early stage, and increase mortality rates. in patients with spina bifida, scoliosis can be congenital or develop secondary to paresthesis. in this patient group, scoliosis has a progressive course and induces severe restriction of the range of motion. in this case, re-planning of rehabilitation and treatment processes can be necessary. in this study, we aimed to determine the incidence of scoliosis, costal anomalies, and vertebral deformations seen at the time of diagnosis in children with open or closed spinal dysraphism, independently of the type of spinal dysraphism. the concomitancies were statistically evaluated. material and method the spina bifida patients included in the study were delivered in bakırkoy, yenimahalle, women’s & children’s hospital and kanuni sultan suleyman training and research hospital and diagnosed firstly on an ambulatory basis. gender and mean ages of the patients were determined. the patients were examined for spinal deformations, scoliosis, and costal anomalies associated with spina bifida. the relationships between associated anomalies were evaluated. the mean, standard deviation, rate, and frequencies were used as descriptive statistics of the data. distribution of variables was controlled with the kolmogorov-smirnov test. the mann-whitney u test was used in the quantitative analysis of data. qualitative analysis of data was performed using a chisquare test. when the criteria for this test were not met, fisher’s exact test was used. statistical analysis was performed using spss 21.0. results a total of 94 patients with a mean age of 11.5 months (55 female and 39 male) were included in the study. vertebra were examined for deformation anomalies, which revealed butterfly vertebra (n=8; 8.6%), hemivertebra (n = 13; 13.8%), and wedge vertebra (n = 31; 33%) (table 1). costal anomalies (n = 22; 23.4%) and scoliosis (n = 19; 20.2%) were also found. 260 | alatas et al associated vertebra and costal anomalies in spina bifida patients the incidence of scoliosis was 21.8% among female infants and 17.9% among males. the mean ages of those with and without scoliosis were 9.7 and 11.9 months, respectively. the distributions of age and gender of those with and without scoliosis were not significant (p ˃ 0.05). rates of scoliosis in patients with and without butterfly vertebra, hemivertebra, wedge vertebra, and costal anomalies did not differ significantly (p ˃ 0.05) (table 2). costal anomalies (rib anomalies) were detected in 25.5% of females and 20.5% of male infants. the mean ages of the patients with and without costal anomalies were 7.68 and 12.64 months, respectively, without any significant difference between the two groups (p ˃ 0.05). the rate of butterfly vertebra was significantly higher in patients with costal anomalies when compared to those without (p < 0.05). hemivertebra were seen significantly more frequently in infants with costal anomalies relative to those without (p < 0.05). wedge vertebra were significantly more frequently observed in the group with costal anomalies when compared to those without (p < 0.05) (table 3). hemivertebra were detected in 14.5% of females and 12.8% of male infants. the mean ages of the patients with and without hemivertebra were 7.85 and 12.06 months, respectively. gender distribution in patients with and without hemivertebra did not demonstrate significant differences (p ˃ 0.05). butterfly vertebra were detected in 7.3% of females and 10.3% of male infants. mean ages of the patients with and without butterfly vertebra were 5.88 and 12.00 months, respectively. gender distribution among patients with and without butterfly vertebra did not demonstrate significant differences (p ˃ 0.05). wedge vertebra were detected in 38.2% of females and 38.2% of male infants. mean ages of the patients with and without wedge vertebra were 11.13 and 11.65 months, respectively. gender distribution among patients with and without wedge vertebra did not demonstrate significant differences (p ˃ 0.05) (table 4). table i numbers of patients according to diagnosis table ii analysis of scoliosis scoliosis (-) scoliosis (+) p med. ± sd./n-% med.± sd./n-% age 11,9 ± 17,2 9,7 ± 16,4 0,371 butterfly vertebrae 6 %75 2 %25 0,661 n % butterfly vertebrae 8 %8,6 hemivertebrae 13 %13,8 wedge vertebrae 31 %33 rib anomalies 22 %23,4 scoliosis 19 %20,2 romanian neurosurgery (2016) xxx 2: 258-266 | 261 hemivertebrae 9 %69,24 4 %30,76 0,307 wedge vertebrae 22 %73,3 8 %27,7 0,135 rib anomalies 15 %68,2 7 %31,8 0,121 table iii analysis of rib anomalies (costal anomalies) r.a.(-) r.a. (+) p med. ± sd med. ± sd age 12,64 ± 18,17 7,68 ± 11,86 0,591 butterfly vertebrae 2 %2,8 6 %27,3 0,002 hemivertebrae 6 %8,3 7 %31,8 0,005 wedge vertebrae 18 %25,0 13 %59,1 0,003 table iv distribution of scoliosis, rib anomalies and vertebrae formation anomalies according to gender female (n=55) male (n=39) n % n % p butterfly vertebrae 4 %7,3 4 %10,3 0,61 hemivertebrae 8 %14,5 5 %12,8 0,811 wedge vertebrae 21 %38,2 10 %25,6 0,203 rib anomalies 14 %25,5 8 %20,5 0,577 scoliosis 12 %21,8 7 %17,9 0,645 discussion for comprehension of the congenital anomalies of vertebra and their associated anomalies, normal embryological development of the vertebral axis should be known. a complex association exists between neural elements of the spinal cord and its supportive mesenchymal elements (19). development of vertebra and the spinal cord begins from the third week of embryonic life and is completed at 20 years of age (24). problematic development for any reason causes incomplete closure of any region of the neural tube, which generally takes place within critically important days after fertilization (i.e., the 23rd. and 28th days) and leads to the formation of neural tube defects. neural tube defects are heterogeneous and complex congenital anomalies of the central nervous system. neural tube defects constitute a group of cerebral and spinal cord anomalies caused by incomplete closure of cerebral and spinal cord structures within the first weeks of 262 | alatas et al associated vertebra and costal anomalies in spina bifida patients embryonic life. normally, closure of the neural tube is simultaneously realized irregularly in five different regions of the spinal cord, both towards the cephalad and in the caudal direction. the cephalad and caudal openings of the neural tube are closed at 25 and 27 days after fertilization, respectively. dysfunctional primary neurulation causes formation of open neural tube defects (spina bifida aperta), while disruption of the secondary neurulation leads to the development of closed neural tube defects (spina bifida occulta). exposure to teratogenic agents can lead to specific anomalies during certain phases of embryonic life. these include impairments in the development of notochords, unsegmented mesoderm, and differentiation of sclerotomes (24). during progression of the neurulation process, the notochord aids in the formation of mesenchymal elements of the spinal cord (5). mesodermal layers on both sides of the notochord mainly differentiate into paraxial, middle, and lateral regions (10, 20). the notochord also induces differentiation of the mesoderm into somites through a longitudinal segmentation process (22, 23, 26). somites are paired structures localized on both sides of the embryonic midline that are constructed from mesoderm-derived epithelial blocks. they take their final shape following segmentation of the presomitic mesoderm (2, 4, 9, 25, 27). vertebrae, ribs, intervertebral discs, related skeletal muscles, and connective tissue originate from these somites. segmental alignment of the vertebrae stems directly from the segmental structure of the somites (15). deformations develop as a result of a deficiency of structural elements of the vertebrae. anterior, anterolateral, posterior, posterolateral, or lateral parts of the vertebral ring can be affected. malformations can be partial or complete. partial malformation manifests as wedge-shaped vertebrae, while its complete forms can appear as hemivertebra, butterfly vertebrae, or vertebral aplasia (19). hemivertebra are one of the most frequently seen vertebral anomalies. since one side of the vertebra is not formed, it is characterized by an incomplete vertebral body, a single pedicle, and hemilamina. a hemivertebra is not an extra vertebra but a partially developed vertebral remnant (figure 1a, 1b) (17). butterfly vertebra result from an inability of bilateral ossification foci. with a central cleft, they resemble a cleaved bilateral hemivertebra. normally, the notochord is localized in the central part of a disc, and persistence of the notochord during the formation of vertebrae leads to the development of butterfly vertebra (figure 1c) (19). wedge vertebra form as a result of dysplasic development of the vertebral body. however, on the affected side, the presence of the pedicle is maintained. it stems from onesided partial developmental impairment of one of the chondrification foci (figure 1d) (19). total aplasia of the vertebral body can rarely be seen and leads to the development of kyphosis. the embriological pathology leading to this anomaly is not yet clearly defined. however, in this condition, late or early ossification phases of the central part of the vertebral body could conceivably be romanian neurosurgery (2016) xxx 2: 258-266 | 263 dysfunctional. clear-cut data are not available about the incidence of concomitancy between congenital vertebral anomalies and myelomeningocele. however, there is a correlation between multifocal complex anomalies and the risk of neural tube defect formation (13). figure 1 illustrating defects of formation. a. lateral hemivertebrae. b. dorsal hemivertebrae. c. butterfly vertebrae. d. wedge vertebrae in the literature, vertabral malformations have been more frequently reported in patients with myelomeningocele, but there is no literature data concerning the incidence in all patients with spina bifida. in our study, all study populations with the diagnosis of open (spina bifida aperta) or closed (spina bifida occulta) neural tube defects were reviewed. the most frequently encountered vertebral malformation was wedge vertebra (33%), followed by hemivertebra (13.8%) and butterfly vertebra (8.5%). gender distribution among patients with vertebral malformation did not demonstrate any statistically significant difference. non-coincidental correlations between costovertebral malformations and neural tube defects have been reported (6, 7). costal anomalies associated with myelomeningocele have been described as costal deficiency, costal fusion, and irregular or bicephalic ribs (3, 30). in our series, costal anomalies were detected in 22 patients (23.4%). gender distribution did not demonstrate a statistically significant difference among patients with costal anomalies, but the rates of hemivertebra, butterfly vertebra, and wedge vertebra were significantly higher. as discussed, embriological development of the ribs and vertebra stems from the same origin, and an interaction persists between the two structures. as a result of this phenomenon, the incidence of costal anomalies increases in conditions that affect embriological development and lead to the formation of vertebral anomalies. vertebral anomalies progress to scoliosis, kyphosis, lordosis, and mixed skeletal anomalies and lead to clinical symptoms and signs (19). scoliosis is a three-dimensional deviation of the spine on a frontal plane of more than 10 degrees (cobb angle > 10o). this deformity can develop secondary to idiopathic factors, congenital vertebral malformations, tumors, or neuromuscular diseases. adolescent idiopathic scoliosis is the most frequently seen form. however, neuromuscular scoliosis 264 | alatas et al associated vertebra and costal anomalies in spina bifida patients causes more severe spinal deformities and demonstrates a progressive course. in combination with the effects of the underlying disease, it leads to more severe restriction of mobility (1). the incidence of scoliosis, kyphosis, and lordosis is higher in children with myelomeningocele (8). among these, the most frequently seen is scoliosis, while kyphosis is the rarest (11). most of these deformities occur during pediatric ages and secondary to paralysis, and nearly 15% of them are congenital (28). spinal curvature in myelomeningocele emerges at an earlier age relative to many developmental anomalies. it is seen at 2 and 3 years of age and can worsen at 7 years of age (8, 12, 28). helpful definitions for the incidence and prevalence of scoliosis in children with myelomeningocele have been developed by trivedi et al. (29)(28). in their survey, a patient population with a cobb angle of more than 20 degrees was determined as cases with scoliosis. most of the spinal curvatures develop during early stages of life, while nearly 40% of them occur after age 9. a small proportion is seen after age 15 (29). scoliosis in patients with myelomeningocele can develop secondary to congenital, idiopathic, or spinal dysraphism. it can also be directly or indirectly related to subsequent paralysis. in patients with spinal dysraphism involving thoracic vertebrae, the incidence of scoliosis rises to 90% (12, 28, 29). 85% of these curvatures are greater than 45 degrees. the incidence of scoliosis in patients decreases with paralysis involving lower vertebral levels. the incidence of scoliosis stemming from l4 level drops down to 60%, and only 40% require surgical intervention. when the level of deficit involves levels below l4, the incidence of scoliosis regresses to 10% (14, 29). acquired scoliosis in patients with myelomeningocele has a greater tendency to regress. muller et al. reported that acquired scoliosis in these patients worsens at a mean annual rate of 5 degrees (21). the angle of curvature and the patient’s age are risk factors for disease progression. various etiological factors for scoliosis have been described in patients with myelomeningocele. c-shaped scoliosis can generally stem from muscle weakness due to high-level paraplegia. paralysis affecting asymmetrical levels or spastic hemiplegia due to hydrocephalus can cause this type of scoliosis. these types of scoliosis accompany kyphosis rather than lordosis. these curvature patterns typically first appear at a younger age and frequently during infancy and lead a progressive course. if present in these cases with scoliosis a surgical procedure aiming at severe spasticity can be required (16). another reason for scoliosis in this population is uncompensated hydrocephalus secondary to hydromyelia or hydrosyringomyelia. in these patients, sshaped scoliosis is typically observed at the thoracic and thoracolumbar levels. shunt dysfunction or hydomyelia can present with scoliosis at any age even during early childhood. typical symptoms of hydromyelia may not be detected in the affected patient. in patients with scoliosis with a cobb angle of less than 50 degrees, shunt replacement has been romanian neurosurgery (2016) xxx 2: 258-266 | 265 demonstrated to have a regressive effect on congenital deformations from scoliosis. segmentation defects of vertebrae are also among the etiological factors in children with scoliosis. these malformations can accompany hydromyelia, tethered cord, or muscle paralysis. therefore, the attending physician should consider each one of the components of scoliosis when arranging a treatment program (18). we detected scoliosis in 19 (20.2%) out of 75 patients. a statistically significant difference was not seen in the age and gender distribution of patients with and without scoliosis. the rates of scoliosis did not demonstrate differences among patients with and without costal anomaly, butterfly vertebrae, hemivertebrae, or wedge vertebra. the lower incidence of scoliosis in our study compared with the literature findings was evaluated, which revealed to be related to the inclusion of both patients with myelomeningocele and those with closed spinal dysraphism. our patient population was also younger than 12 years of age. when the progressive pattern of neuromuscular scoliosis in patients with spina bifida is considered, we can admit that assessments in future years might detect increased incidence of scoliosis in this patient group. since our study had a retrospective design, and some of the patients did not attend the follow-up visits after a while, we could not include follow-up results of all patients in this study. our study did not aim to determine the incidence of overall rates of scoliosis in patients with open and closed neural tube defects. on the contrary, we statistically evaluated patients for the presence of scoliosis at the time of diagnosis of neural tube defects. because of a lack of demographic and followup data of some patients, we could not differentiate between congenital and neuromuscular scoliosis in all patients, and our data relevant to these issues were not included in this study. conclusion vertebral deformities associated with or developed secondary to spinal dysraphism make the clinical picture of this disease more challenging or even complicate treatment and follow-up planning. the incidence of neural tube defects with their partially elucidated embriological and genetic mechanism demonstrate regional differences. we think that neural tube defects and associated anomalies of the vertebrae and other organ can demonstrate differences with respect to their locations and ethnic groups. more detailed multi-centered studies performed on this issue will aid in the determination of etiologies, genetics, and treatment principles of these congenital anomalies. correspondence dr. gokhan canaz haseki reseach and training hospital department of neurosurgery 34087 fatih/i̇stanbul türkiye +90 212 529 44 00 e-mail: gokhancanaz@mail.com references 1.allam am, schwabe al. neuromuscular scoliosis. pm & r: the journal of injury, function, and rehabilitation 2013; 5: 957-963. 266 | alatas et al associated vertebra and costal anomalies in spina bifida patients 2.aulehla a, pourquie o. oscillating signaling pathways during embryonic development. current opinion in cell biology 2008; 20: 632-637. 3.cetinkaya m, ozkan h, koksal n, et al. spondylocostal dysostosis associated with diaphragmatic hernia and neural tube defects. clinical dysmorphology 2008; 17: 151-154. 4.dequeant ml, pourquie o. segmental patterning of the vertebrate embryonic axis. nature reviews genetics 2008; 9: 370-382. 5.egelhoff j, prenger ec. the spine, in ball ws (ed), pediatric neuroradiology, philadelphia, lippincottraven, 1997. 6.etus v, ceylan s, ceylan s. association of spondylocostal dysostosis and type i split cord malformation. neurological sciences: official journal of the italian neurological society and of the italian society of clinical neurophysiology 2003; 24: 134-137. 7.giacoia gp, say b. spondylocostal dysplasia and neural tube defects. journal of medical genetics 1991; 28: 51-53. 8.herring ja, tachdjian mo. tachdjian's pediatric orthopaedics, philadelphia, saunders, 2002. 9.iimura t, denans n, pourquie o. establishment of hox vertebral identities in the embryonic spine precursors. current topics in developmental biology 2009; 88: 201234. 10.jinkins jr. atlas of neuroradiologic embryology, anatomy, and variants, philadelphia, lippincott williams & wilkins, 2000. 11.karol la. orthopedic management in myelomeningocele. neurosurgery clinics of north america 1995; 6: 259-268. 12.lindseth re. myelomeningocele, in lovell ww, winter rb, morrissy rt, weinstein sl (eds), lovell and winter's pediatric orthopaedics, philadelphia, lippincott williams & wilkins, 2001, pp601-632. 13.loder rt. congenital scoliosis and kyphosis, in dewald rl (ed), spinal deformities: the comprehensive text, new york, thieme, 2003, pp684-693. 14.mackel jl, lindseth re. scoliosis in myelodysplasia. the journal of bone & joint surgery 1975; 57: 1031. 15.makino y, kaneko k, yamaguchi a, et al. developmental biology and etiology of axial skeleton: lessons from a mouse model of spondylocostal dysostosis and spondylothoracic dysostosis. journal of oral biosciences 2013; 55: 175-179. 16.mclaughlin tp, banta jv, gahm nh, et al. intraspinal rhizotomy and distal cordectomy in patients with myelomeningocele. the journal of bone and joint surgery american volume 1986; 68: 88-94. 17.mcmaster mj, david cv. hemivertebra as a cause of scoliosis. a study of 104 patients. the journal of bone and joint surgery british volume 1986; 68: 588-595. 18.autho: management of vertebral problems and deformities, in memet özek m, cinalli g, maixner wj (eds): the spina bifida management and outcome. milano: springer-verlag italia, 2008, pp305-318. 19.memetözek m, belirgen m. vertebral anomalies and spinal malformations in myelomeningocele, the spina bifida, springer milan, 2008, pp185-196. 20.moore kl, persaud tvn. formation of germ layers and early tissue and organ differantiation, philadelphia, wb saunders, 1998. 21.muller eb, nordwall a, oden a. progression of scoliosis in children with myelomeningocele. spine 1994; 19: 147-150. 22.muller f, o'rahilly r. the development of the human brain, the closure of the caudal neuropore, and the beginning of secondary neurulation at stage 12. anatomy and embryology 1987; 176: 413-430. 23.o’rahilly r, benson dr. the development of vertebral column, in bradford ds, hensinger rn (eds), the pediatric spine, new york, thieme, 1985, pp3-17. 24.oi s. malformations of the vertebrae, in rocco cd, raimondin aj (eds), principles of pediatric neurosurgery, new york, springer-verlag, 1989, pp1-18. 25.ozbudak em, pourquie o. the vertebrate segmentation clock: the tip of the iceberg. current opinion in genetics & development 2008; 18: 317-323. 26.phillips wa. sacral agenesis, in weinstein sl (ed), pediatric spine: principles and practice, new york, raven press, 1994, pp259-273. 27.pourquie o. vertebrate segmentation: from cyclic gene networks to scoliosis. cell 2011; 145: 650-663. 28.samuelsson l, eklof o. scoliosis in myelomeningocele. acta orthopaedica scandinavica 1988; 59: 122-127. 29.trivedi j, thomson jd, slakey jb, et al. clinical and radiographic predictors of scoliosis in patients with myelomeningocele. the journal of bone & joint surgery 2002; 84: 1389-1394. 30.vazquez-lopez me, lopez-conde mi, somoza-rubio c, et al. anomalies of vertebrae and ribs: jarcho levin syndrome. description of a case and literature review. joint, bone, spine: revue du rhumatisme 2005; 72: 275277. 31.wynne-davies r. congenital vertebral anomalies: aetiology and relationship to spina bifida cystica. journal of medical genetics 1975; 12: 280-288. doi: 10.33962/roneuro-2022-015 a clinico-radiological study of diagnostic accuracy of special clinical tests in diagnosing compressive myelopathy in patients of early cervical spondylitis symptoms along with its radiological correlation anshul galav romanian neurosurgery (2022) xxxvi (1): pp. 88-91 doi: 10.33962/roneuro-2022-015 www.journals.lapub.co.uk/index.php/roneurosurgery a clinico-radiological study of diagnostic accuracy of special clinical tests in diagnosing compressive myelopathy in patients of early cervical spondylitis symptoms along with its radiological correlation anshul galav department of neurosurgery. st. john's medical college hospital, bengaluru. kota medical college, kota, india abstract background. cervical spine myelopathy occur due to compression of the spinal cord is present is quite common with a prevalence of around 90. diagnosis of in the early stages of the condition, the patient may be symptomatic as neck pain, myelopathy or radiculopathy signs clinical examination findings, correlated by mri findings. aims and objectives. to study the clinic-radiological correlation between these clinical signs and radiological imaging in patients with early cervical spondylotic symptoms. methods and measures. a minimum of 100 cases shall be considered in this study. all the patients of either sex above the age of 12 years with early cervical spondylotic symptoms of sjmch during the study period will be considered in this study thorough clinical history including past medical, treatment and personal history is taken. the following clinical signs are assessed in them: clonus, hoffman’s, trömner, wartenberg's sign, deep tendon reflexes, plantar reflexes the results of these tests are tabulated. mri cervical spine is performed and cervical myelopathy is graded. mri findings are correlated with the clinical signs and thus sensitivity, specificity and accuracy of each of these tests is calculated. results. four clinical diagnostic tests were found to have been quite reliable. none of the tests was self-diagnostic. among various diagnostic tests babinski, clonus sign has the highest specificity but low sensitivity. conclusion. this study denotes those 6 tests used to diagnose myelopathy are interdependent, none is fully diagnostic. introduction degenerative cervical spondolytic myelopathy (csm) is a progressive disease of the spinal cord. the clinical signs, symptoms and radiology play a key role in diagnosis.1 in the early stages diagnosis is difficult due to subtle signs . various clinical test considered for diagnostic purpose.mri cervical spine is considered the best method for diagnosis keywords myelopathy, wartenbergs, spondylitis, hoffmann, tromner. radiculopathy, interforaminal corresponding author: anshul galav st. john's medical college hospital, bengaluru, india dranshul33@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 89 accuracy of special clinical tests in diagnosing compressive myelopathy of cervical stenosis, cord compression, or myelomalacia elements .spondylosis is common ageing process seen between age of 25 to old age . most patients are asymptomatic most common symtoms are : neck pain ,cervical radiculopathy, and cervical myelopathy. neck pain may be due to degenerative disc or facet changes. cervical radiculopathy can be acute, subacute, or chronic. radiculopathy may be due to disc or osteophyte which causes motor or sensory deficits2 cervical myelopathy due to long tracts involvement due to various static, dynamic factors and ischemic changes. early subtle signs like hyperreflexia, babinski’s sign, hoffman’s reflex,tromner’s sign and/or clonus . other characteristic signs and symptoms include weakness of the hands, hand parathesia,gait disturbances ,bowel and bladder involvement. signs of lmn at site of lesion and umn at below level. clinical tests various clinical tests have been used to diagnose cervical myelopathy – hyperreflexia, hoffman’s, tromners, the babinski sign, wartenbergs sign, clonus.3 controversy is there regarding reliability of these tests. sensitivity and specificity of these tests depends on various factors like inter observer variation ,stage of disease,age of patient,associated comorbidities .positivity of these tests in normal people not known.combination of these tests are more reliable then single test. hoffmann's sign 4 stabilise proximal ip joint followed by flicking nail with thumb positive response is flexion of fingers and thumb. deep tendon reflex tests in biceps tendon testing, the patient is in sitting position ,examiner strikes bicep tendon on his thumb normal response is flexion of elbow. babinski sign 5 -patient in sitting position ,strike foot from lateral to medial ,positive response is fanning of fingers and dorsiflexion of thumb. tromner sign – on flicking volar apect of middle finger flexion of thumb and index finger. wartenberg sign 6–involuntary abduction of little finger when hands r outstretched due to unopposed action of extensor muscles digiti minimi,digitorum communis. clonus7 –on rapid passive dorsiflexion of foot, repititive foot movement due to stretch on achilles tendon. radiological studies the radiological diagnostic workup often includes static or dynamic plain cervical x-rays, magnetic resonance imaging (mri) [8]. magnetic resonance imaging (mri) mr is useful for evaluating the spinal canal diameter, spinal cord, intervertebral discs,and vertebral ligaments signal changes on t2-weighted mri scans at the level of spinal compression are often increased in patients with cervical spondylotic myelopathy. this represents edema, inflammation, ischemia, myelomalacia, or gliosis .9 in dcm, the following are 3 key characteristics that indicate the severity of disc degeneration: loss of t2wi hyperintensity of the nucleus pulposus and resulting loss of delineation between the nucleus pulposus and annulus fibrosus on t2wi, narrowing of the ivd space, and migration of disc material into the spinal canal10. methods this is a descriptive prospective study conducted department of neurosurgery at sjmch bengaluru and kmc, kota study period: 2018 to 2020 study population/sample size/ inclusion/exclusion criteria minimum of 100 cases shall be considered in this study.all the patients of either sex above the age of 12 years with early cervical spondolytic symptoms of during the study period will be considered in this study. children less than 12 yrs and other non spondylotic cause of myelopathy. procedure patients presenting with symptoms of neck pain, radiating pain to upper limbs, paraesthesia, weakness & stiffness in the limbs and fulfilling the inclusion criteria are included in this study.thorough clinical history including past medical, treatment and personal history is taken.the following clinical signs are assessed in them : clonus ,hoffman’s, trömner ,wartenberg's sign, deep tendon reflexes, plantar reflexes. the results of these tests are tabulated.mri cervical spine is performed and extent of cervical myelopathy changes are graded.mri findings are 90 anshul galav correlated with the clinical signs and thus sensitivity, specificity, accuracy of each of these tests is calculated .the following parameters will be assessed -patients age and sex, occupation, complete symptomatology ,co morbidities like htn,dm, thyroid disorder, ra, as etc mri cervical spine and assessing for degree of cord compression correlating mri findings with the clinical signs. statical evaluation as this is a descriptive study, all the mentioned data will be collected and analysed using the parameters described above. specificity and sensitivity of the clinical tests analysed through the collected data. results 100 patient studied from 2018 to2020, who satisfied inclusion criteria conformed by mri. mri taken on basis of presence of clinical signs. among total patients majority 55 females and 45males,with 35 patients associated with various comorbidities . patient included having symptoms of radiculopathy, myelopathy, and cervical strains. 73%admitted with complains of neck pain ,64%admitted with diagnosis hand numbness and gripping weakness and 45 %admitted with gait disturbances. four tests are highly diagnostic : hoffmann’s sign , deep tendon reflexes ,tromner and clonus sign. other 2 wartenbergs and babinski sign have moderate diagnostic capacity. most frequent level affected in mri are c5-c6 and c6-c7 levels. combining clinical examination tests provided significant improvements in the diagnostic accuracy of the clinical tests. patient associated with various comorbidities has higher positive value of sensitivity and specificity of clinical tests. age gender presence of comorbidities {35 patients} 30 to 80 yrs male =46 male =15 mean age 50 female =54 female=20 neck pain 73 loss of hand dexterity and medial numbness 64 clumsiness while walking and gait disturbances 45 clinical test sensitivity specificity hoffmann test 43 76 tromners sign 45 77 deep tendon reflex 43 70 babinski reflex 32 93 clonus 15 96 wartenberg sign 18 78 discussion there is high level of agreement for these clinical tests in two examiners .among these 4 tests highly substantiates diagnosis and other 2 with moderate efficacy. mri is used to confirm diagnosis,presence of myelomalcia,cord signal changes are highly diagnostic. tromner sign more sensitive to hoffman as hoffman elicited by nipping of nail having no nerve endings while tromner elicited by tapping volar aspect of skin at terminal phalynx of middle finger.11 as more nerve endings present at volar aspect .most widely accepted explanation for clonus is that it is hyperactive tendon reflexes caused by self excitation. it is caused by interruption of umn fibres, having low sensitivity but high specificity. babinski sign having low sensitivity but high specificity indicates high chances of correctly diagnose cervical myelopathy.wartenberg sign also have low sensitivity value but good specificity.12 conclusion our various clinical test shows moderate reliability to diagnose cervical myelopathy. this means these tests may be false negative in presence of myelopathy.there accuracy may be increased by using multiple tests for diagnosis. limitations there are chances of interobserver variability of diagnosing clinical sign ,some interpretations may be wrong .there are chances of variability of signs according to age ,some signs may be more ominous with old age. there is variability in timing of mri in different patients with different symptom profile. 91 accuracy of special clinical tests in diagnosing compressive myelopathy references 1. batzdorf u, flannigan bd. surgical decompressive procedures for cervical spondylotic myelopathy. a study using magnetic resonance imaging. spine. 1991;16:123127. 2. bednarik j, kadanka z, dusek l, et al. presymptomatic spondylotic cervical cord compression. spine. 2004;29:2260-2269. 3. berger jr, fannin m. the "bedsheet" babinski. south med j. 2002;95:1178-1179. 4. bossuyt pm, reitsma jb, bruns de, et al. towards complete and accurate reporting of studies of diagnostic accuracy: the stard initiative. ann intern med. 2003;138:40-44. 5. braga-baiak a, shah a, pietrobon r, braga l, neto ac, cook c. intraand inter-observer reliability of mri examination of intervertebral disc abnormalities in patients with cervical myelopathy. eur j radiol. 2008;65:91-98. http://dx.doi. org/10.1016/j.ejrad.2007. 04.014. 6. brennan pf, hays bj. the kappa statistic for establishing interrater reliability in the secondary analysis of qualitative clinical data. res nurs health. 1992;15:153158. 7. browder da, erhard re, piva sr. intermittent cervical traction and thoracic manipulation for management of mild cervical compressive myelopathy attributed to cervical herniated disc: a case series. j orthop sports phys ther. 2004;34:701-712. 8. estanol bv, marin os. mechanism of the inverted supinator reflex. a clinical and neurophysiological study. j neurol neurosurg psychiatry. 1976;39:905-908. 9. fujiwara k, yonenobu k, ebara s, yamashita k, ono k. the prognosis of surgery for cervical compression myelopathy. an analysis of the factors involved. j bone joint surg br. 1989;71:393-398. 10. fukushima t, ikata t, taoka y, takata s. magnetic resonance imaging study on spinal cord plasticity in patients with cervical compression myelopathy. spine. 1991;16:s534-538. 11. ghosh d, pradhan s. "extensor toe sign" by various methods in spastic children with cerebral palsy. j child neurol. 1998;13:216-220. 12. glaser ja, cure jk, bailey kl, morrow dl. cervical spinal cord compression and the hoffmann sign. iowa orthop j. 2001;21:49-52. kankanekumar_applyofwhats 306 | kankane et al apply of whatsapp in neurosurgery apply of whatsapp: a quick, simple, smarty and cost competent method of communication in neurosurgery vivek kumar kankane, gaurav jaiswal, tarun kumar gupta department of neurosurgery, r.n.t. medical college & m.b. hospital, udaipur, rajasthan, india abstract: objective: neurosurgeons habitually have to hinge on judgments of subordinate staffs to build an assessment on patients whom they cannot be present at immediately. whatsapp is a no charge to use application for image transfer on internet. we evaluated the use of whatsapp in neurosurgical milieu, to show it is economical, quick, available, reliable and practicable. materials and methods: we coordinate a prospective observational study from december 2014 to june 2015. residents were skilled to take sharp pictures and upload them immediately using whatsapp on internet. primary conclusion was difference between opinion of residents and consultants on whatsapp images and time delay in decision-making. conflict was evaluated significant if it changed management decision. results: in the study period, 1356 (mean age: 35.53 years, 71.28% males) patients were included in study those admitted in after hospital hours. internet packs of smart phone available in market in very economical cost. judgment could be made on images received on whatsapp at an average of 4.06 min. there was conflict in 7.22% cases between residents’ reports and images on whatsapp. all radiological imaging modalities, were associated with statistically insignificant difference (p >0.05). conclusion: this study suggests that apply of whatsapp in neurosurgery can be a simple quick reliable and almost free mode of communicating images enabling a quick decision. though this cost-effective method should be used with concern particularly with radiological imaging modalities, which require dispensation and appraisal on console. key words: multimedia messaging service, communication, neurosurgery, whatsapp, smart phone introduction radiological imaging (ri) conflict has been often reported when junior doctors or residents report on imaging done during off hours. [1‑5] this ri conflict has been found to have significant clinical impact. [1‑5] to be capable to make an assessment on a neurosurgical patient as soon as his primary management is complete, will not only accelerate the definitive care but also improve romanian neurosurgery (2016) xxx 2: 306-312 | 307 the final outcome. such an approach will have an impact on the residency training program. smart phones are broadly available. whatsapp is a free of charge to use application, which can be used over an extensive number of mobile and enable one to talk as well as send pictures over wi-fi or 3g or 2g network. 3g or 2g internet packs available in market in very economical rate. this study was coordinate to look at the option of using this free app in communicating information related to neurosurgical emergencies. the objective of this study was to observe if use of whatsapp is economical, quick, easy to get to, reliable and realistic in neurosurgery mainly in reporting emergency cases in off hours of hospital. materials and methods a prospective observational study was coordinate in the department of neurosurgery, r.n.t. medical college & m.b. hospital, udaipur, and rajasthan, india from december 2014 to june 2015. all patients observing emergency department in off hours of hospital and assessment by neurosurgical residents were included in the study. personal smart phones with facility of camera (resolution at least 5 megapixel) and whatsapp installed were used in the study. residents were trained to take clear pictures and upload them immediately using whatsapp over internet [figure 1]. images were taken in close and distant mode. there was no restriction on number of images however uploading big number of images took more time. radiological images transferred include those of x-rays, computed tomography (ct) scans, magnetic resonance imaging (mri) scans; ct angiography scans [figure 2]. these images were studied by consultant neurosurgeon and afterward compared with the reporting done by resident. ri reported by residents was considered as group 1, by the consultant neurosurgeon on whatsapp as group 2, by residents’ radiologist as group 3, by the consultant neurosurgeon on actual images as group 4 and by consultant radiologist as group 5. outcome variables primary endpoints were conflict of opinion between group 1 and 2, and compared to group 2& 4 and group 3 & 5 and time delay in decision-making on whatsapp. conflict was considered significant if it changed management decision. afterward analysis involved which ri modality was difficult to study on whatsapp using chisquare test. statistical software for social sciences (spss) version 17 was used for analysis of data. figure 1 resident captivating snapshot on smart headset 308 | kankane et al apply of whatsapp in neurosurgery figure 2 dissimilar category of smart phones used in the study with whatsapp on display ethical issues as this study instructed collecting data and did not entail direct intervention on patients, there were no ethical issues involved. patients enrolled were not provided with economic incentives, as this study did not require any extra investigation. results a total of 1356 (mean age: 35.53 years, range 3 month days to 91 years, 71.28% males) patients were included in the study. all patients with accidents, 997 (73.52%) patients had road traffic accidents, 171 (12.61%) had fall and 188 (13.86%) had physical assault. 610 (44.98%) patients presented with headache, 132 (9.73%) with weakness, 680 (50.14%) with altered sensorium and 162 (11.94%) with seizure. of the 1356 different types of ri transferred on whatsapp included: 828 (61.06%) cranial ct scans, 155 (11.43%) xrays, 13 (0.95%) ct angiography images, 360 (26.54%) mri images and respectively. decision could be made on images sent on whatsapp after a mean delay of 4.06 ± 1.482 min (range 3‑12 min) from availability of images for upload. this delay involved taking pictures, uploading and communicating to consultant. using whatsapp, conflict between ri reporting by residents (group 1) and consultant neurosurgeon (group 2) was 7.22% (98 cases). in 58 cases (4.27%), residents could not comment due to confusion in diagnosis, in 14 cases (1.03%) they could not identify surgical indications, in 17 cases (1.25%) they missed critical findings and in the last 9 cases (0.66%) they missed surgical requirement as well as critical findings. resident usually missed location as well as differentials in romanian neurosurgery (2016) xxx 2: 306-312 | 309 hypodense lesions on ct scans. they frequently missed critical findings that had bearing on deciding time of surgery as well as approach. this conflict was clinically significant in 80 cases out of 98 cases (81.63%) where management of patients changed. this change in management plan from medical to surgical intervention or adding osmotic diuretics of all imaging modalities, conflict between group 1 and group 2 was highest for ct angiography head (30.76%) followed by xray of cervical spine (21.93%) followed by mri (8.33%) and ct head (3.623%). there was 100% accord between group 3 and 4 however there was 5.16% conflict between images seen on whatsapp (group 2) and actual image interpretation (group 4) and there was 7.81% conflict between image seen on consultant radiologist (group 3) and image seen by resident radiologist (group 5). it was found that of all the ri modalities, had statistically insignificant difference between group 1 and group 2 compare to group 2 and group 4 (p value > 0.05) and also all ri modalities, had statistically insignificant difference between group 1 and group 2 compare to group 3 and group 5 (p value > 0.05) [table -1]. of 1356 patients, 351 patients (25.88%) underwent surgery and rest 74.12% were managed conservatively. as this app is freely available on internet and can be used on any mobile or pc platform, using this app and service was free of cost. moreover due to very cost effective 3g or 2g internet packs available in market. effect of time of day when images were sent for consultation was studied to know whether exhaustion induced during duty hours and consequent slowness during off hours has effect on delay in reporting or increase in difference between ri reporting. table i comparison of conflict between group 1, 2 and group 2 & 4 and comparison of conflict between group 1 & 2 and group 2 & 4 according to different images sent on whatsapp comparison of groups x ray ( skull &cervical spine) ncct head ct angiogram mri (brain & spine) yes no yes no yes no yes no conflict between group 1 & 2 34 121 30 798 4 9 30 330 conflict between group 2 & 4 25 130 20 808 3 10 22 338 p value 0.193 0.07 0.658 0.249 conflict between group 1 & 2 34 121 30 798 4 9 30 330 conflict between group 3 & 5 25 132 40 788 2 11 39 321 p value 0.107 0.222 0.352 0.225 310 | kankane et al apply of whatsapp in neurosurgery table ii drawback and dealings to settle drawback dealings to settle deprived resolution when taking images with a smart phone camera, try to go as close as possible to the subject rather than zooming in when you take a shot. you will get better-resolution photos cropped, than zoomed in. images of flash/ neighboring luminosity camera flash you have on your phone is almost always too harsh and rarely helpful. instead try increasing your camera’s exposure and iso levels. alternatively you could use an external flash like iblazer or light strap so close flash light keep away from any direct luminosity over image while taking snap missing fractures learn on bone windows of real images under reporting angiography learn on console/3d difficulty in beginners to taking snaps residents were skilled to take clear pictures & gave basic knowledge about focus, exposure, white balance and iso. discussion neurosurgical care is limited in many parts of the world to one or two hospitals serving a large geographic area. the quality of neurosurgical response to emergencies depends on the reliability and completeness of the information received from referral hospitals. first time servadei f et.al conducted a study from january 1998 to december 2000, the aim of this study is to show how application of guidelines for head injury management in an entire area can be usefully combined with transmission of images from the peripheral to the central hospital. in conclusion of this study is unnecessary transfers can be avoided and the neurosurgeons can evaluate the images of a number of patients who have always been treated outside our units. this results in more work for the neurosurgeons on duty, but also in a better quality service for the whole area [9]. during the last decade, there is an increasing demand to discuss diagnostic images and reports of difficult cases with experienced staff. a possible solution besides physically transporting patients and material is to use high-speed communication networks to transfer images and reports electronically. with the web application pacs flow we have developed a solution to transfer images, reports, and messages as a single package in a one-step procedure. the pacs flow is an interoperable and standard compliant webbased application, which gives clinicians a user-friendly interface for their work on a daily basis, so clinicians have tried sending images using kis, ris and pacs after office hours in specialties such as radiology [6, 3], medicine and cardiology[2,11,12,]. patients archiving and communication system (pacs) which is time consuming and requires expensive hardware’s or definite system. the advance of communicating images using whatsapp only requires taking appropriate pictures and romanian neurosurgery (2016) xxx 2: 306-312 | 311 uploading on internet. this process is speedy as it takes only fractions of minutes to upload as well download on the recipient workstations. in this study it took a mean of 4.06 min. to decide on images. this was much faster than reported delay in actual image interpretation by radiologist in literature (8.6 h). [5]. using other modes of communications like sending images by using multimedia messaging service (mms) is used by neurosurgical residents to transmit scan images to the attending neurosurgeon in conjunction with telephone consultation. this service has been well received by the attending neurosurgeons, who felt that after viewing scan images on their phones, they felt increased confidence in clinical decision making and that it reduced the need for recall to the hospital. bullard tb et al. investigated whether head ct images captured using a mobile phone would be of sufficient quality for neurosurgeons at a level 1 trauma center to make decisions about whether to transfer patients from referring hospitals. mobilephone images of ct scans appear to provide adequate images for triaging patients and helping with transfer decisions of neurosurgical cases [4]. pick j.et al introduce image transfer by mobile phones into clinical practice to improve communication between neurosurgeons. most images were transferred from the resident on call to the senior neurosurgeon backing him up. overall, the system was extremely reliable, quick, and enabled immediate decisions in all emergency situations [8]. thapa a et al [10] used viber in neurosurgical scenario, to show it is cheap, fast, accessible, reliable and feasible. this study suggests that the use of viber app in neurosurgery can be an easy fast reliable and almost free mode of communicating images enabling a quick decision. our study is similar to this study, except number of patient and number of groups is more in our study and we used different apps of smart phone. conflict between resident and consultant (consultant neurosurgeon) was comparable to other studies, published particularly by emergency physicians [5, 1] and radiologist.[7,13] in our study, we found that in 81.63% cases where there was between resident report and image interpretation on whatsapp, treatment was significantly altered. medical imaging sent over mobile phones has been found to be constantly interpretable as in our study. in only 4.08% cases images reported on whatsapp required further modification on actual image interpretation, which was found to be in cases of ct angiography and mri spine. our study shows that whatsapp not only helped in early and proper decision making but also take required interventions. it was found that those medical imaging modalities, which required maneuvering on console especially ct angiography head, required careful analysis on whatsapp and we recommend that it should not exclusively be reported on whatsapp. hence this study shows that use of whatsapp in communicating neurosurgical emergencies is economical, speedy, handy, reliable and realistic; however there is drawback as noted in table 2. 312 | kankane et al apply of whatsapp in neurosurgery conclusion this study, a first of its way recommends use of whatsapp in neurosurgery; an easy fast reliable and almost free mode of communicating radiological images enabling a quick decision. however this cost effective method should be used with concern particularly with radiological imaging modalities, which necessitate dealing out, and evaluation on console. the mobile phone system is adequately useful for early diagnosis and start of treatment in emergent cases. this is attributable to its low cost and eases of handling for sending images to remote areas and between hospitals, despite the small dimensions of the monitor. correspondence vivek kumar kankane m.ch.neurosurgery resident, r.n.t. medical college & m.b. hospital, udaipur, rajasthan, india. email address: vivekkankane9@gmail.com address: c/o dr. khamesara 59 sardarpura, udaipur, rajasthan, india, pincode 313001 mobile no. 8955337812 references 1. alfaro d, levitt ma, english dk, williams v, eisenberg r. accuracy of interpretation of cranial computed tomography scans in an emergency medicine residency program. ann emerg med 1995; 25:169‑174 2. balasingham i, ihlen h, leister w, røe p, samset e. communication of medical images, text, and messages in inter-enterprise systems: a case study in norway ieee trans inf technol biomed. 2007 jan; 11(1):7-13 3. boochever ss. his/ris/pacs integration: getting to the gold standard. radiol manage. 2004 may-jun; 26(3):16-24 4. bullard tb, rosenberg ms, ladde j, razack n, villalobos hj, papa l. digital images taken with a mobile phone can assist in the triage of neurosurgical patients to a level 1 trauma centre. j telemed telecare. 2013 feb; 19(2):80-83 5. friedman sm, merman e, chopra a. clinical impact of diagnostic imaging discrepancy by radiology trainees in an urban teaching hospital emergency department. int j emerg med 2013; 6:24-28 6. klose kj, schäfer c, kail s, röthke m, zhang l. [kisris-pacs integration: the marburg approach]. radiologe. 2005 aug; 45(8):671-681 7. le ah, licurse a, catanzano tm. interpretation of head ct scans in the emergency department by fellows versus general staff non‑neuroradiologists: a closer look at the effectiveness of a quality control program. emerg radiol 2007; 14:311‑316 8. piek j, hebecker r, schütze m, sola s, mann s, buchholz k. image transfer by mobile phones in neurosurgery. zentralbl neurochir. 2006 nov;67(4):193196 9. servadei f, antonelli v, mastrilli a, cultrera f, giuffrida m, staffa g. integration of image transmission into a protocol for head injury management: a preliminary report. br j neurosurg. 2002 feb; 16(1):36-42 10.thapa a, shrestha d, shrestha d, giri s. use of viber app: a fast, easy and cost effective method of communication in neurosurgery. neurol india. 2013 nov-dec; 61(6):610-613 11. vogl r. [teleradiology and pacs--strategy of the innsbruck university hospital]. radiologe. 2005 aug; 45(8):704-711 12. 6. wirth s, treitl m, villain s, lucke a, nissen-meyer s, mittermaier i, pfeifer kj, reiser m. [pacs: storage and retrieval of digital radiological image data].radiologe. 2005 aug; 45(8):690-697 13. wysoki mg, nassar cj, koenigsberg ra, novelline ra, faro sh, faerber en. head trauma: ct scan interpretation by radiology residents versus staff radiologists. radiology 1998; 208:125‑8. doi: 10.33962/roneuro-2020-082 surgical management of rolandic area meningioma in the era of intraoperative neurophysiological monitoring mihaela coșman, ionuț mihail panțiru, andrei ionuț cucu, andreea lenuța atomei, gabriela florența dumitrecu, ion poeată romanian neurosurgery (2020) xxxiv (4): pp. 488-494 doi: 10.33962/roneuro-2020-082 www.journals.lapub.co.uk/index.php/roneurosurgery surgical management of rolandic area meningioma in the era of intraoperative neurophysiological monitoring mihaela coșman1, ionuț mihail panțiru2, andrei ionuț cucu2, andreea lenuța atomei3, gabriela florența dumitrecu4, ion poeată5 1 department of neurosurgery. emergency county hospital, braila, romania 2 department of neurosurgery. "n. oblu" emergency clinical hospital, iași, romania 3 6th-year student. gr. t. popa university of medicine and pharmacy, iași, romania 4 department of anatomopathology. "n. oblu" emergency clinical hospital, iași, romania 5 department of neurosurgery. gr. t. popa university of medicine and pharmacy, iași, romania abstract introduction. the advantages and the necessity of intraoperative neurophysiological monitoring (iom) in the surgery of motor area infiltrative tumours is well known. the use of this technique for rolandic meningioma is still debatable. the absence or the loss of the cleavage plan and an infiltrative border make the dissection exceedingly difficult and increase the risk of new postoperative motor disfunction. materials and methods. we evaluated the impact of iom, especially direct cortical stimulation on the degree of resection, new postoperative deficits, symptom remission and clinical-imagistic aspects at one-year follow up of 19 cases of rolandic meningioma admitted in third department of neurosurgery,” prof. dr n. oblu” emergency clinical hospital, yassi, romania, between january 2014 and july 2018. results. more than half of the cases (57,88%) had epileptic manifestations as the main clinical symptom with the jacksonian seizures being on the first place (31,57%), followed by progressive paresis (26,31%) and other nonspecific symptoms. intraparenchymal preoperative oedema was observed in 36,84% of patients. the intensity of direct cortical stimulation was between 6-13 ma (median = 9ma; mode = 12ma). simpson degree of resection was dominated by s3– 47,36% and s4 was obtained in 15,78% of cases. postoperative the outcome was favourable for 73,68% patients with 5,26% motor aggravation and 10,52% new deficits. at one-year follow up no imagistic recurrence was observed and the permanent motor deficit was maintained in one of the three cases (5,26%). conclusion. even though meningiomas are extranevraxial lesions and those located on the convexity have a low risk of complication, the absence of a clear dissection plan between the tumour and the adjacent motor cortex is associated with a high risk for new postoperative neurological deficits. therefore, it is important to perform keywords rolandic area, intraoperative neurophysiological monitoring, meningioma, tumour resection, motor cortex, cortical mapping corresponding author: ionuț mihail panțiru "n. oblu" emergency clinical hospital, iași, romania ionut.mihail26@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 489 surgical management of rolandic area meningioma in the era of intraoperative neurophysiological monitoring cortical mapping for rolandic meningioma, to determine the location of the primary motor area and to protect it from mechanical and vascular trauma, during tumour resection. introduction resection of lesion located in eloquent areas e.g., primary motor area is associated with an increased risk of postoperatively neurologic deficits. for a good outcome it is mandatory, for us, to know the location of this area and to protect it from mechanical and vascular intraoperative injures. the landmarks offered by the preoperative radiological images are of great help, but not sufficient [10,35]. the continuous development of medical technology comes in our aid to perform maximal resection with minimal motor dysfunction, knowing the impact on overall survival and on the progression free survival [8,29,32]. on this line, intraoperative neurophysiological monitoring (iom) which includes mapping procedures (direct / subcortical stimulation) and monitoring technique (evoked potentials) offers a real time feedback and helps to establish the location of the functional area from the operative field. if the use of iom is clear for infiltrative lesions like gliomas, the necessity of it in cases of meningiomas remains questionable [2,21,31]. one functional area in which this lesion may appear is the central gyrus region. the definition of rolandic meningioma is represented by the direct anatomical contact, observed on t2 weighted magnetic resonance imaging (t2w-mri) of the tumour with the precentral and postcentral gyrus [25]. the presence of the cleavage plan around the eloquent brain help protect it during resection. when this landmark is lost or its not present mechanical trauma and vascular alterations over the cortex may generate new motor deficits. an intraoperative evaluation of the surrounding brain with the enhancement of the primary motor area is important, with the purpose of maximal resection with minimal neurological dysfunction. this goal is desirable especially when the most common symptoms of presentation are the epileptic seizures and the nature of the lesion is with good prognosis [6,21,31]. we proposed in this article to present the impact of using iom in meningioma surgery located in central gyrus region regarding the clinical and radiological postoperative evolution first day after surgery and at one year follow up period along with a review of the literature. materials and methods the study group included patients with meningioma located in central region, diagnosed using contrast enhancement head mri imaging, admitted in the 3rd neurosurgery department of ‘prof. dr n. oblu’ clinical emergency hospital iasi, between 1 january 2015 and 1 july 2018, who underwent surgical resection. inclusion criteria in the study group: meningioma located in central gyrus region, imagistic diagnosed and histologically confirmed; age over 18 years; intraoperative use of iom; consent to be included in the study. exclusion criteria from the study group: other histological tumour subtypes localized in central region; cases to which conservative management was performed; patients with pacemaker; patients who failed to come for their one-year follow-up examination and incomplete cases data. this technique was performed using the nim eclipse device from medtronic. direct cortical / subcortical stimulation was achieved by means of the short-train technique or train of five. the parameters used were: 3hz, interstimulus interval = 4mseconds, length = 500µseconds. the intensity was included in the interval 6 – 13ma. the recording electrodes were placed in abductor pollicis brevis muscle (m.), biceps brachii m., orbicularis orris and oculi m., tibialis anterior m. and abductor hallucis m, depending on tumour precise location. results 76 patients with various histological tumour types were initially enrolled in the study group, but 6 of them were excluded because they did not come to the one-year follow-up examination after surgery and 4 were excluded because they had a pacemaker and we could not perform iom. in the end, the group included 19 cases of meningioma with rolandic location. the age distribution interval was between 25 – 73 years with a female dominance – 52,63% of all the cases. most frequent symptom was jacksonian seizure (31,57%), followed by motor deficit – progressive brachial/ crural paresis (26,31%), partial seizures (15,73%) and nonspecific manifestation like headache, intracranial hypertension and grand mall seizure (each 10,52%). 490 mihaela coșman, ionuț mihail panțiru, andrei ionuț cucu et al. from the anatomical point of view 47,36% (9 cases) were located on the convexity, 47,36% were parasagittal and 5,26% (one case) had the insertion of the falx cerebri. 5,26% of the patients underwent preoperative embolization. intraparenchymal oedema was observed in t2 / flair mri sequences in a proportion of 36,84% (7 cases). an illustrative is presented in figure 1. figure 1. clinical case: female, 48 years, jacksonian seizures, no motor deficit, rolandic lesion. (a) preoperative mri (t1wi with enhancement and t2wi), yellow star = contralateral primary motor area (omega sign), no clear demarcation of the ipsilateral motor area, no perilesional oedema. (b) one-year postoperative follow-up mri (t2 dark-fluid), pink star=reshaping of the motor area with normal morphology. (c) meningioma grade ii (who classification): densely cellularized lesion with meningothelial cells arranged in wide cords. (hemalaun-eozina staining, x20). according to world health organisation (who) the histological result was classified as who grad i: 84,21% and who grade ii: 15,78%. simpson degree of resection was: s1 – 2 patients (10,52%), s2 – 5 patients (26,31%), s3– 9 cases (47,36%) and s4 – 3 cases (15,78%). the intensity of direct cortical stimulation was between 6-13 ma, with the following statistical parameters: median = 9ma and the mode = 12ma. postoperative the outcome was favourable with symptoms resolution for 73,68% cases, stationary for 10,52% cases and with functional alteration for 15,78% cases (2 patients presented new neurologic deficit and one aggravated the initial motor disfunction). one-year evaluation reveal favourable outcome in 89,47% and stationary in 10,52%. from the three cases with postoperative motor disfunction, in 5,26% of them persisted the deficit. no recurrence was observed on the control mri and no tumour growth on the 15,78% of simpson iv cases. discussions meningioma represent the most common benign primary brain tumour with an increasing incidence, being more frequent in elderly and in women [1,11,16]. usually between the brain and the lesion there is a cleavage plan which allows a safe resection. when this plan is lost or it does not exist, vascular impairment and mechanical trauma of the brain tissue may be a consequence of tumour ablation. this is very important when the perilesional tissue is represented by functional areas, e.g., central gyrus region, hence the higher postoperatively motor deficit and an increased rate of complication for rolandic meningioma compared with other convexity meningioma [3,9,18,23]. perioperatively imaging techniques characterizes the relationship between the tumour and the eloquent cortex. standard mri, functional mri, 3d tractography and neuronavigation system are important tools regarding the resection of lesions located in eloquent cortex, planning the approach and guiding further tumour ablation [20,22,27,30]. in some meningioma cases, the landmarks may not correspond intraoperatively because of the displacement of the normal anatomy induced by the tumour growth. in others the cleavage plan may be lost near the central gyrus region and the arachnoid may be invaded [5]. to avoid such situation where the dissection is difficult to realise without harming the surrounding cortex intraoperative neurophysiological monitoring is being used for a real time functional feedback. in a study from 2019 published by raffa et al., it is evaluated even the advantage of combining the navigated transcranial magnetic stimulation with iom for detection of the presence or the absence of the arachnoid cleavage plan and the functional tissue. the correspondence with the iom results was in a percentage of 94,2% [28]. with all those tools available, in the literature there is still a controversy about the techniques association and intraoperative necessity of neurophysiological monitoring for all meningioma [25,26,31]. 491 surgical management of rolandic area meningioma in the era of intraoperative neurophysiological monitoring from the anatomical point of view rolandic meningioma compresses convexity meningioma, falx, falx-sinus lesions of middle one third of the sagittal sinus in contact with precentral and postcentral gyrus and sinus. beside the surrounding functional areas, the vascular representation is of the same importance e.g., rolandic draining vein [6]. because these lesions have a tendency of being smaller, the difficulty of the intervention can be underestimated and so may be associated with higher complication [25]. motor area meningioma need special anaesthesia protocols when iom is used, the aim being to avoid the medication that interacts with muscle relaxation. synthetic opioids such as fentanyl and sedative-hypnotic agents (propofol) are preferred when cortical stimulation or evoked potentials are recorded, since those drugs can maintain a constant serum concentration with insignificant effect over motor response registration [14,15,24]. usually, one of the most common presentation symptoms is represented by epileptic seizure (47,6% ostry et al.,2012; 38,46% bi et al., 2013; 42% deng et al.,2014) [4,6,25]. in our study this manifestation occurred in 57,88% of patients, with a dominance of jacksonian seizures (31,57%). especially for these patients with no motor deficit preoperatively it is important to determine the relation between the meningioma and the surrounding brain tissue. the dominance of this clinical presentation is explained by the tumour mechanism of action. being an extranevraxial lesion, it compresses the brain tissue inducing hemodynamical changes at the level of myelin, oxygenation and intracellular water. this is important because there is not a real loss of neurons and explains the remission of the symptoms after resection. even the patients with preoperative motor deficits may improve the muscle strength postoperatively [17]. though the meningioma is completely resected in some patients the outcome after the operation is stationary. the persistence of the seizures after the surgery is explained, in some cases by the cerebral changes induced by a slow-growing tumour with the appearance of epileptogenic foci e.g., hippocampal scleroses and cortical dysgenesis, beside local microenvironment abnormal discharges. in these cases, it seems that only the removal of the central gyrus region tumour is not enough [7,33]. in a study published by deng et al., in 2014 from all 26 patients presented with epilepsy, after tumour resection 88, 46% were seizures free at mean follow up of 16 months under antiepileptic drug medication and one patient had seizures recurrence in less than 6 months postoperatively [6]. in our study, after symptoms remission the patient did not report any new seizure at the one-year follow up or recurrence. when there is pial adhesions, brain invasion or irregular borders intracapsular resection is recommended to preserve the functional cortex which is usually identified by direct cortical stimulation (e.g., monopolar anodic stimulation – ostry et al.,2012) [25]. in our study we performed brain mapping before starting to remove the meningioma to identify the primary motor area. usually, this aria was modified being push by the tumour growth and surrounded the lesion. the intensity interval was between 6 – 13 ma, the most frequent threshold value which generated motor response was 13 ma. the cortical stimulation was repeated every time when the junction brain-tumour was reached, to ashore that further dissection does not affect the eloquent cortex. intermittent minimal traction was applied. the surgical aim is symptom remission and if it is the case to leave the smallest cortical layer of tumour to prevent neurological alteration, even though this means subtotal resection – simpson iv [12,19]. on the one hand this approach is preferable because of the slow growth pattern of the lesion and because gross resection is associated with increased morbidity for the infiltrative borders type, on the other hand some studies found that simpson resection grade is a predictor factor for recurrence. in this condition the intraoperative decision is tailored depending on the particularities of the case [13,36]. in our study simpson iv was obtained at 15,74% of patients, all of them were located parasagittal with no cleavage plan and with positive stimulation response surrounding the tumour. other characteristic of those three cases was the fact that it was observed an important venous component involvement, with the rolandic vein being encased in tumour capsule and the superior sagittal sinus being partially obstructed. in other publication various result of subtotal resection were presented from 26,2% (ostry et al., 2012) to 1,1% (ottenhause et a., 2018) [25,26]. ostry et al., mentioned that in some 492 mihaela coșman, ionuț mihail panțiru, andrei ionuț cucu et al. patients the remanent tumour was not even detected on the postoperative mri, the estimated volume being of 0,1cm³ and the simpson iv grade of the case was based on surgeons’ report. usually, the residual layer was less than 0,5cm³ [25]. even though simpson grad iv was present in our result one the first place from the point of view of resection was simpson grade ii (47,36%) matching with the literature results. it is important to keep in mind that clinical presentation with preoperative muscular strength dysfunction may alter the stimulation response, decreasing the technique accuracy. from our patients 26,31% presented progressive paresis and the intensity used to generate motor response was the highest from the study group. an aggressive traction and dissection, when the cleavage plan is lost, is associated postoperatively with a higher risk for motor deficit [17,34]. ostry et al., in a study from 2012 observed that the difference of the threshold value between the direct cortical stimulation and the value obtained after stimulating through the mass lesion was ≤ 2 ma has an impact over outcome. in this situation he stopped the resection even though it was intracapsular, to prevent new motor deficits. when the motor evoked potentials are used, the need for an increased threshold to generate response is a warning signal [25]. how is to be expected, the motor preservation is the main goal in surgical resection of rolandic meningioma. starting from this idea some authors studied the prognostic factors for the risk of motor impairment (aggravation of the symptoms or new ones). ottenhausen et al., found that a high rate of neurological deficit was associated with parafalcine insertion, large tumoral mass and perilesional oedema. another negative prognostic factor was found to be the necessity for preoperative embolization and the involvement of the rolandic drainage vein [26]. from our group of patients in one case it was necessary to perform an endovascular procedure, tumour’s location being on the falx cerebri to facilitate the resection. progressive paresis as an admitting symptom beside disturbing the iom is considered to be a negative prognostic factor for the motor outcome (47,2 % vs 22,2%, p = 0,017, ottenhausen et al., 2018) [26]. in our group of patients in one case we had aggravation of the pre-existent deficit and new deficit was observed in 10,52% of the cases. the image control showed central gyrus region oedema and no haemorrhage. other values from the literature regarding the new motor deficit range from 7,69% (lee et al., 2016) to 34,61% (bi et al., 2013) [4,17]. the latter reference presents the results from 26 parasagittal central region meningioma microsurgical resected. no simpson grade iv was found, only grade i (30,8%), grade ii (46,2%) and grade iii (23,1%) but as mentioned the aggravation was observed in one third of the cases. therefor complete tumor removal was associate with a higher negative outcome. another important fact is that the authors do not report the use of cortical stimulation or evoked potential generation [4]. the main postoperative outcome of our patients was favourable with symptom remission in 73,68%. almost the same percentage was obtained and by lee at al., in 2016 – 76,92%. the first place for clinical evolution is maintained and with 60,3% (ottenhausen et al., 2018), 65,39% (bi et al., 2013) and the high clinical amelioration was 81% (ostry et al., 2012) [4,17,25,26]. an important remark it that at one year follow up period just one patient of the three with postoperatively aggravated or new deficit maintained the motor disfunction. practically the permanent neurologic deficit for our group was 5,26%. overall, the neurological outcome was favourable in 89,47% of the cases, no imagistic recurrence was observed on the control mri but further follow up must be done. conclusions rolandic meningiomas, even though are extranevraxial lesions represents a challenge from the surgical point of view. a careful dissection is mandatory, the venous drainage must be preserved and the surrounding functional tissue must be protected from mechanical trauma. when the cleavage plan is lost precentral and postcentral cortex may be affected and secondary after the resection new motor deficits may appear. to prevent unwanted cortical damage intraoperative neurophysiological monitoring is used and if necessary, a thin layer of meningioma is left over the cortex. 493 surgical management of rolandic area meningioma in the era of intraoperative neurophysiological monitoring disclosures the authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper. references 1. achey rl, gittleman h, schroer j et al. non-malignant and malignant meningioma incidence and survival in the elderly from 2005-2015 using the central brain tumor registry of the united states. neuro oncol, 21(3):380-391, 2019. 2. bander de, shelkov e, modik o et al. use of the train-offive bipolar technique to provide reliable, spatially accurate motor cortex identification in asleep patients. neurosurg focus, 48: 1-6, 2020. 3. berg-johnes j, hogestol ea. supplementary motor area syndrome after surgery for parasagittal meningiomas. acta neurochir (wien), 160(3):583-587, 2018. 4. bi n, xu rx, liu ry et al. microsurgical treatment for parasagittal meningioma in the central gyrus region. oncol lett 6: 781-784, 2013. 5. cimino pj. malignant progression to anaplastic meningioma: neuropathology, molecular pathology, and experimental models. exp mol pathol, 99(2):354-9, 2015. 6. deng ws, zhou xy, li zj et al. microsurgical treatment for central gyrus region meningioma with epilepsy as primary symptom. j craniofac surg, 25: 1773-1775, 2014. 7. dhiman v, rao s, sinha s et al. outcome of lesionectomy in medically refractory epilepsy due tonon-mesial temporal sclerosis (non-mts) lesions. clin neurol neurosurg, 115(12):2445-53, 2013. 8. duffau h. diffuse low-grade glioma, oncological outcome and quality of life: a surgical perspective. curr opin oncol, 30:383-389, 2018. 9. elzarief aa, ibrahim mf. long-term follow-up of motor function deterioration following microsurgical resection of middle third parasagittal and falx meningioma. egypt j neurol psychiatr neurosurg, 54(1):9, 2018. 10. giamouriadis a, lavrador jp, bhangoo r et al. how many patients require brain mapping in an adult neurooncology service? neurosurg rev, 43:729-738, 2020. 11. holleczek b, zampella d, urschart s et al. incidence, mortality and outcome of meningiomas: a populationbased study from germany. cancer epidemiol, 62:101562, 2019. 12. hou w, ma y, xing h, yin y. imaging characteristics and surgical treatment of invasive meningioma. oncol letters, 13: 2965-2970, 2017. 13. hwang wl, marciscano ae, niemierko a et al. imaging and extent of surgical resection predict risk of meningioma recurrence better than who histopathological grade. neuro oncol, 0:1-10, 2015. 14. isik b, turan g, abitagaoglu s et al. a comparison of the effects of desflurane and total intravenous anaesthesia on the motor evoked responses in scoliosis surgery. int j res med sci,5(3):1015-1020, 2017. 15. kawaguchi m, iida h, tanaka s et al. a practical guide for anesthetic management during intraoperative motor evoked potential monitoring. j anesth, 34(1):5-28, 2020. 16. ko cc, chen ty, lim sw et al. prediction of recurrence in parasagittal and parafalcine meningiomas: added value of diffusion-weighted magnetic resonance imaging. world neurosurg, worl neurosurg, 124: e470e479, 2019. 17. lee sj, hwang sc, im sb, kim bt. surgical resection of non-glial tumors in the motor cortex. brain tumor res treat, 4 (2):70-76, 2016. 18. lemee jm, corniola mv, broi md et al. early postoperative complications in meningioma: predictive factors and impact on outcome. world neurosurg, 128: e851-e858, 2019. 19. lin q, ling f, xu g. invasive benign meningioma: clinical characteristics, surgical strategies and outcomes from a single neurosurgical institute. exp ther med, 11(6):2537-2540, 2016. 20. low d, lee ck, dip llt et al. augmented reality neurosurgical planning and navigation for surgical excision of parasagittal, falcine and convexity meningiomas. br j neurosurg, 24(1):69-74, 2010. 21. magill st, han sj, li j et al. resection of primary motor cortex tumors: feasibility and surgical outcomes. j neurosurg, 129:961-972, 2018. 22. morin o, chen wc, nassiri f et al. integrated models incorporating radiologic and radiomic features predict meningioma grade, local failure, and overall survival. neurooncol adv, 1(1):011, 2019. 23. nanda a, bir sc, konar s, maiti tk, bollam p, world health organization grade i convexity meningiomas: study on outcomes, complications and recurrence rates, world neurosurg, 89:620-627.e2, 2016. 24. nunes rr, bersot cda, garritano jg. intraoperative neurophysiological monitoring in neuroanesthesia. curr opin anesthesiol, 31:532–538, 2018. 25. ostry s, netuka d, beneš v. rolandic area meningioma resection controlled and guided by intraoperative cortical mapping. acta neurochir (wien), 154:843-53, 2013. 26. ottenhausen m, rumalla k, younus i et al. predictors of postoperative motor function in rolandic meningiomas. j neurosurg, 1:1-6, 2018. 27. panesar ss, abhinav k, yeh fc et al. tractography for surgical neuro-oncology planning: towards a gold standard. neurotherapeutics, 16: 36–51, 2019. 28. raffa g, picht t, scibilia a et al. surgical treatment of meningiomas located in the rolandic area: the role of navigated transcranial magnetic stimulation for preoperative planning, surgical strategy, and prediction of arachnoidal cleavage and motor outcome. j neurosurg, 14;1-12, 2019. 29. ritaccio al, brunner p, schalk g. electrical stimulation 494 mihaela coșman, ionuț mihail panțiru, andrei ionuț cucu et al. mapping of the brain: basic principles and emerging alternatives. j clin neurophysiol, 35: 86–97, 2018. 30. romero-garcia r, erez y, oliver g et al. practical application of networks in neurosurgery: combined 3d printing, neuronavigation, and pre-operative surgical planning. world neurosurg, 137:1-22, 2020. 31. rossi m, nibali mc, vigano l et al. resection of tumors within the primary motor cortex using high-frequency stimulation: oncological and functional efficiency of this versatile approach based on clinical conditions. j neurosurg, 9:1-13, 2019. 32. sala f. penfield’s stimulation for direct cortical motor mapping: an outdated technique? clin neurophysiol, 129:2635-2637, 2018. 33. spencer s, huh l. outcome of epilepsy surgery in adults and children. lancet neurol 7: 525-37, 2008. 34. tang h, xu f, lin l et al. intra-operative motor function preservation for resection of primary motor cortex meningioma. transl cancer res, 7(6):1666-1674, 2018. 35. thon n, tonn jc, kreth fw. the surgical perspective in precision treatment of diffuse gliomas. onco targets ther,12: 1497–1508, 2019. 36. winther wl, torp sh. the significance of the extent of resection in modern neurosurgical practice of who grade i meningiomas. world neurosurg, 99:104-110, 2017. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-035 coccydynia a medical condition with multiple causes and different management strategies. a local experience amin sabry, ashraf s. zidan, mohemed abdel bari, hesham el sobky romanian neurosurgery (2020) xxxiv (1): pp. 232-237 doi: 10.33962/roneuro-2020-035 www.journals.lapub.co.uk/index.php/roneurosurgery coccydynia a medical condition with multiple causes and different management strategies. a local experience amin sabry, ashraf s. zidan, mohemed abdel bari, hesham el sobky department of neurosurgery, faculty of medicine, mansoura university, egypt abstract background: coccydynia is a common complaint which is usually self-limited and tolerable. although most of these patients respond dramatically to conservative measures, some patients need more complex plane of treatment. in these conditions, the cause of coccydynia can be complex and multifactorial. patients and methods: a total of 8 cases were included in the study. all cases received medical treatment for 9 months before surgery. complete coccygectomy was performed for all cases. post-operative outcomes were measured according to the degree of pain relief. results: the mean age of the included cases was 43.87 years (range, 39 – 52). a total of 5 females (62.5%) and 3 males (37.5%) were included. the mean preoperative vas score was 9 (range, 8 – 10), while post-operatively, it decreased significantly down to 2 (range, 1 – 3). excellent postoperative outcomes were achieved in 6 cases (75%) whereas good outcomes were obtained in the remaining 2 cases (25%). conclusion: although conservative medical measures are effective for treating coccydynia, but surgical excision is still a valid treatment option in resistant cases. introduction although being a small bone the coccyx has many important functions. as we all know it gives insertion for many muscles, ligaments, and tendons which play a main role in the pelvic floor support and actively share in voluntary bowel control. it is also considered one limb of the tripod—in addition to the two ischial tuberosities—that represents weight-bearing support to a person while setting [14]. coccydynia is pain in the region of the coccyx. simpson first announced the definition in 1859, but reports about this pain dated back to the 16th century. although this condition is well known since a long time, its management may be a dilemma and a real controversial issue in resistant cases as it is multifactorial in nature. several organic and psychological causes contribute to its occurrence. most of these keywords coccydynia, coccygectomy, surgical excision corresponding author: amin sabry department of neurosurgery, faculty of medicine, mansoura university, egypt amin_ sabryneuro@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 233 coccydynia a medical condition with multiple causes and different management strategies cases resolve within a short time with or without conservative measures, but for a small percent of these patients, the condition may become chronic and debilitating [19]. the accurate incidence of this condition has not been known exactly; however, high risk factors for coccydynia include obesity and female sex. female to male ratio is about five times. children are less likely to develop this condition than adolescents and adults. marked rapid loss of weight as in bariatric surgery may increase the risk of this condition due to loss of subcutaneous fat and mechanical cushioning [12]. coccydynia is commonly caused by external or internal trauma. the external trauma is usually caused by a backwards fall, childbirth, especially associated with obstructed or instrumented labor, sitting for long time on hard, or uncomfortable seats. nontraumatic coccydynia may be caused by degenerative affection of joint or disc disease, infection and variants of coccygeal morphology. coccydynia may be caused by nonorganic etiologies, such as somatization and other psychological disorders [13]. although most cases respond to conservative treatment, few patients fail to show a good response and hence, surgery may be an option [17]. historically, the surgical management of such condition has been discussed with caution as it was associated with poor results and high complication rates. nevertheless, better outcomes have been reported recently [18]. this study was conducted at mansoura university hospitals aiming to evaluate the surgical outcomes of coccygectomy for coccydynea refractory to conservative treatment. patient and methods study design this is a prospective study that was conducted at mansoura university hospitals during the period between december 2016 and december 2018. study cases a total of 8 cases (n = 8) with coccydynia who showed no response to 9-month duration of failed all conservative measures including physical therapy, coccydynia exercise, medications, injections, and even psychotherapy were included in our study. all of our cases had a history of trauma to the coccyx. inclusion criteria patients older than 18 years, no contraindication for anaesthesia or surgery, having pain at the region of coccyx, tenderness over the same area, or the presence of coccygeal abnormalities. exclusion criteria patients younger than 18 years, and patients who are not candidates for anaesthesia or operation were excluded from our study. patient consent a pre-operative written informed consent was obtained from all cases after the explanation of advantages and drawbacks of the surgical approach. moreover, the study was approved by the local ethical committee. patient preparation all cases were subjected to complete history taking, thorough physical examination, and routine laboratory investigations. digital rectal examination was also performed to exclude the presence of rectal pathology. during rectal examination the coccyx was grasped between the forefinger and thumb then we started to manipulate the coccyx to detect pain, hypermobility or hypomobility of the sacrococcygeal joint. the reported normal range of movement is about 13 degrees [10]. besides, an x-ray was ordered for all cases to assess the lumbar and sacrococcygeal regions. ct sacrum and coccyx with 3d reconstruction or mri were done in some cases to exclude inflammatory or infiltrative lesions. operative procedure patients were instructed to take a low residue diet for four days prior to surgery and an enema was done the night before surgery. unsayn 1.5 gm i.v. was administered on call for surgery and repeated every 8 hours for 48 hours after surgery. all surgeries were done in prone position. the surgical strategy was similar to that technique described by key [9]. the buttocks were separated and strapped laterally with adhesive plaster to open the cheeks of the buttocks for wide exposure. about 1 cm superior to the gluteal cleft, a 5cm skin incision was created at the midline. after skin incision we dissected through the layers down to the posterior surface of the coccyx. then we bluntly dissected to expose the coccygeal tip. then 234 amin sabry, ashraf s. zidan, mohemed abdel bari, hesham el sobky we exposed and cut the anococcygeal ligament and then we elevated the coccygeal tip. then we dissected and cut the attachment of the coccygeus and iliococcygeus muscle from the coccyx while taking great care not to injure the rectum. then the coccyx was totally removed. after meticulous hemostasis, we removed the straps retracting the buttock cheeks. the wound was closed in layers taking care to minimize the dead space as much as possible. suction drains were left for at least forty-eight hours postoperatively. post-operative care early ambulation was encouraged, and postoperative pain was managed by paracetamol or nsaids. all cases were discharged on the 1st or 2nd post-operative day. ct and x rays were done postoperatively to ensure total excision of the coccyx. follow up regular follow up visits were arranged for our cases for one year after surgery (1 week after surgery, then after 1 month, 3 months, 6 months, and finally 12 months). their current level of pain was assessed via vas score. moreover, cases were asked to evaluate their general pan symptoms as; complete relief, significant improvement, moderate relief, unchanged, or worsened. surgical outcome was also measured according to table (1). outcome criteria excellent complete absence or significant pain improvement and vas ≤ 2/10. good significant pain improvement and vas ≤ 3 /10. satisfactory moderate pain improvement with vas ≤ 6/10. poor unchanged symptoms or vas > 6/10. table 1. outcome categories [1]. statistical analysis the collected data were coded, processed and analysed using the spss (statistical package for social sciences) version 22 for windows® (ibm, spss inc, chicago, il, usa). normally distributed quantitative data (vas score) were expressed as mean (range) and comparison between preoperative and postoperative values was compared using paired samples t-test. p value (< 0.05) was considered significant. results the mean age of the included cases was 43.87 years (range, 39 – 52). we included 5 females (62.5%) and 3 males (37.5%). the mean pre-operative vas score was 9 (range, 8 – 10), while post-operatively, it decreased significantly down to 2 (range, 1 – 3) (p < 0.001). excellent post-operative outcomes were achieved in 6 cases (75%) whereas good outcomes were obtained in the remaining 2 cases (25%). in this study, there were two cases of wound infection. one of them had superficial infection which improved on antibiotics and frequent dressing. the other case had deep wound infection and sinus discharging pus and she underwent surgical debridement and repair by plastic surgeon. these data are illustrated at table (2). case no. ag e gender preoper ative vas postoperativ e vas outcome 1 43 female 8 2 excellent 2 48 female 9 1 excellent 3 52 female 9 2 excellent 4 40 female 10 3 good 5 44 female 8 2 excellent 6 39 male 10 2 excellent 7 42 male 9 3 good 8 43 male 9 1 excellent table 2. overview of the included cases. figure 1. sagittal ct sacrum and coccyx in patient with post traumatic anterior angulation of the coccyx and coccydynia. 235 coccydynia a medical condition with multiple causes and different management strategies figure 2. intraoperatove exposure of the coccyx during coccygectomy. figure 3. sagittal ct sacrum and coccyx after coccygectomy. figure 4. preoperative sagittal ct sacrum and coccyx in patient with showing anterior angulation of the coccyx. discussion coccydynia seems to be emerging as a major medical condition in the current millennium due to the increasing number of populations that spend a long time setting in front of computers. many patients complain of severe pain during sexual intercourse or defecation. pain and tenderness over the coccyx is usually diagnostic for this condition [7]. figure 5. the excised coccyx. first line of conservative measures includes nsaids, sitting aids, hot fomentations, and physiotherapy. these conservative measures are effective in about 60% to 66% of patients. when these measures fail, fluoroscopic or us guided local steroid administration and coccygeal manipulation showed success rates ranging between 75% and 85%. so surgical excision of the coccyx is still needed to treat the resistant cases not responding to previous measures [16]. this study was conducted at mansoura university hospitals aiming to evaluate the role of coccygectomy in the management of coccydynia. we included a total of 8 cases with a mean age of 43.87 years (range, 39 – 52). another study handling the same perspective included 31 cases with coccydynia with a mean age of 41.5 years (range, 20 – 65) [4]. in the current study, we included 5 females (62.5%) and 3 males (37.5%). other studies reported that this disease has a higher prevalence in women [6]. on the other hand, another study conducted by antoniadis and his colleagues included 6 males (60%) and 4 females (40%) [1]. this contradicts with our study results. regarding outcomes in the current study, the mean pre-operative vas score was 9 (range, 8 – 10), 236 amin sabry, ashraf s. zidan, mohemed abdel bari, hesham el sobky while post-operatively, it decreased significantly down to 2 (range, 1 – 3). excellent post-operative outcomes were achieved in 6 cases (75%) whereas good outcomes were obtained in the remaining 2 cases (25%). another study also confirmed our findings as it reported a marked decrease in vas score, and all cases included have achieved good or excellent outcomes (100%) [1]. this correlates with also with other studies that stated that more than 90% of cases were having a good or very good surgical outcomes after coccygectomy [11, 21, 22]. cheng and his associates reported that excellent outcomes were achieved in 20 cases (64.5%) while good outcomes were present in 7 cases (22.6%). additionally, 3 cases had moderate outcome (9.7%) whereas only one case reported poor outcome (3.2%) [4]. another recent study reported that there was a significant decrease in vas score following operation (2.25 vs. 9.62 preoperatively – p < 0.001). moreover, excellent or good outcomes were achieved in 87.5% of the included cases [18]. of note, some authors have reported that better surgical outcomes could be achieved in patients with traumatic coccydynia compared with idiopathic cases [2, 14]. however, others have found no difference between the surgical outcomes of the two types [15]. another larger study also reported that the short form 36 (sf-36), the oswestry disability index (odi) and the visual analogue scale (vas) showed a significant improvement after surgery (p < 0.0001). successful outcome was obtained in 70.4% of cases while failure occurred in 25.5% of cases. the rest of cases were lost during follow up [7]. cebesoy et al. reported no infection in 21 patients all of whom received prophylactic antibiotics for 5 days [3]. doursounian et al. had no infection in his series of 80 patients all of whom received two prophylactic antibiotics over 48 hours and preoperative rectal enema [5]. although coccygectomy appears to be a technically easy procedure, multiple complications have been documented in the literature. its rate ranges between 0 and 50% [3, 20]. the most common encountered complication is wound infection, followed by healing problems (dehiscence) [1]. other rare complications may include rectal injury [8]. in the study conducted by cheng and his colleagues, post-operative wound infection was encountered in 2 cases (6.45%) [4]. other reports assume that the infection rates associated with coccygectomy have ranged from 14% to 30%, including superficial and deep wound infections and dehiscence [21]. this is comparable to our results as we had two cases of wound infection 25%. the main drawback of this study is the small number of cases and short duration of follow up. therefore, additional studies including more cases with longer follow up periods should be conducted. conclusion although conservative medical measures are effective for treating coccydynia but surgical excision is still a valid treatment option in resistant cases. authors contributions this work was carried out in collaboration between all authors. they designed the study and researched literature. they approved the protocol. all the surgeries were done by the same surgical team. they all shared in data collection and manuscript finalization. all authors read and approved the final manuscript. references 1. antoniadis a, ulrich n h-b, and senyurt h: coccygectomy as a surgical option in the treatment of chronic traumatic coccygodynia: a single-center experience and literature review. asian spine journal 2014, 8(6),705. 2. bayne o, bateman j e, and cameron h u: the influence of etiology on the results of coccygectomy. clinical orthopaedics and related research 1984, (190),266-72. 3. cebesoy o, guclu b, kose k, basarir k, guner d, and us a: coccygectomy for coccygodynia: do we really have to wait? injury 2007, 38(10),1183-8. 4. cheng s-w, chen q-y, lin z-q, wei w, zhang w, kou d-q, yue s, ying x-z, cheng x-j, and lü c-z: coccygectomy for stubborn coccydynia. chinese journal of traumatology (english edition) 2011, 14(1),25-8. 5. doursounian l, maigne j-y, cherrier b, and pacanowski j: prevention of post-coccygectomy infection in a series of 136 coccygectomies. international orthopaedics 2011, 35(6),877-81. 6. fogel g r, cunningham iii p y, and esses s i: coccygodynia: evaluation and management. jaaosjournal of the american academy of orthopaedic surgeons 2004, 12(1),49-54. 7. hanley e, ode g, jackson iii j, and seymour r: 237 coccydynia a medical condition with multiple causes and different management strategies coccygectomy for patients with chronic coccydynia: a prospective, observational study of 98 patients. the bone & joint journal 2016, 98(4),526-33. 8. karadimas e j, trypsiannis g, and giannoudis p v: surgical treatment of coccygodynia: an analytic review of the literature. european spine journal 2011, 20(5),698705. 9. key j a: operative treatment of coccygodynia. jbjs 1937, 19(3),759-64. 10. maigne j-y, doursounian l, and chatellier g: causes and mechanisms of common coccydynia: role of body mass index and coccygeal trauma. spine 2000, 25(23),3072-9. 11. maigne j-y, lagauche d, and doursounian l: instability of the coccyx in coccydynia. the journal of bone and joint surgery british volume 2000, 82(7),1038-41. 12. maigne j, pigeau i, aguer n, doursounian l, and chatellier g: chronic coccydynia in adolescents. a series of 53 patients. european journal of physical and rehabilitation medicine 2011. 13. nathan s, fisher b, and roberts c: coccydynia: a review of pathoanatomy, aetiology, treatment and outcome. the journal of bone and joint surgery british volume 2010, 92(12),1622-7. 14. pennekamp p h, kraft c n, stütz a, wallny t, schmitt o, and diedrich o: coccygectomy for coccygodynia: does pathogenesis matter? journal of trauma and acute care surgery 2005, 59(6),1414-9. 15. postacchini f, and massobrio m: idiopathic coccygodynia. analysis of fifty-one operative cases and a radiographic study of the normal coccyx. the journal of bone and joint surgery american volume 1983, 65(8),1116-24. 16. ramsey m l, toohey j s, neidre a, stromberg l j, and roberts d a: coccygodynia: treatment. orthopedics 2003, 26(4),403-5. 17. saleh i, and reksoprodjo a y: coccygeal excision for treatment of coccyx instability. jurnal orthopaedi dan traumatologi indonesia-the journal of indonesian orthopaedic & traumatology 2018, 1(3). 18. sarmast a h, kirmani a r, and bhat a r: coccygectomy for coccygodynia: a single center experience over 5 years. asian journal of neurosurgery 2018, 13(2),277. 19. simpson j: coccygodynia and diseases and deformities of the coccyx. med times gaz 1859, 40,1-7. 20. traub s, glaser j, and manino b: coccygectomy for the treatment of therapy-resistant coccygodynia. journal of surgical orthopaedic advances 2009, 18(3),147-9. 21. wood k b, and mehbod a a: operative treatment for coccygodynia. clinical spine surgery 2004, 17(6),511-5. 22. zayer m: coccygodynia. the ulster medical journal 1996, 65(1),58. 16dhavalshukla_decompressive romanian neurosurgery (2014) xxi 3: 345 348 345 decompressive craniectomy for acute stroke: the good, the bad, and the ugly of it dhaval shukla1, amit agrawal2 1additional professor of neurosurgery, department of neurosurgery, national institute of mental health and neurosciences, bangalore, karnataka (india) 2professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract large hemispheric infarctions have malignant course and constitute a major cause of severe morbidity and mortality after stroke. the medical management is usually not effective in these cases. decompressive craniectomy is a salvage therapy for medically refractory icp. this paper discusses the merits and demerits of decompressive craniectomy for large hemispheric infarctions. hemicraniectomy is a life-saving but nonrestorative surgery. surgery should be done before clinical signs of brain herniation to obtain maximum benefit. the relatives of the patient should be explained clearly about possibility of survival with disability before offering the surgery. key words: hemispheric infarctions, decompressive craniectomy, hemicraniectomy, brain herniation, stroke. introduction large hemispheric infarctions have malignant course and constitute a major cause of severe morbidity and mortality after stroke. it is usually due to occlusion of distal internal carotid artery (ica) or proximal middle cerebral artery (mca) trunk without sufficient collateral flow. atrial fibrillation and ica dissection are major causes of these occlusions. [6] the incidence of malignant cerebral infarction is 10 to 20 per 100 000 per year. [2] neurological deterioration due to edema occurs in 10% of all strokes. neurological decline occurs in 36% patients within 24 hrs and in 68% within 48 hrs. [2] the first sign of neurological decline is nausea and vomiting followed by drowsiness, and pupillary asymmetry. if not aggressively treated death occurs within 5 days in 41 to79% patients.[8] the clinical predictors of malignant infarction are: younger age, female gender, absence of history of previous stroke, systolic bp >180mmhg during first 12 hours, and national institutes of health stroke scale (nihss) score >20. the radiological predictors are: hypodensity in mca territory ct >50%, ica bifurcation occlusion, involvement of additional vascular territories, hyperdense mca sign, perfusion deficit of 346 shukla, agrawal decompressive craniectomy for acute stroke more than 66% of mca territory on ct scan performed within 6 hours of stroke, and diffusion weighted imaging (dwi) volume on mri more than 145 ml within 14 h of stroke onset. [2] the medical management is usually not effective in these cases. intravenous thrombolysis is less likely to reperfuse large cerebral artery occlusions. the patients require management of raised intracranial pressure (icp), which include: endotracheal intubation, mechanical ventilation, sedation,and medical management of cerebral edema. the addition of hypothermia is also not much beneficial, and mortality is still high at 43 – 47%. [8] decompressive craniectomy decompressive craniectomy (dc) is a salvage therapy for medically refractory icp. it consists of removal of large bone flap over frontal, temporal, and parietal lobe at infarct site. as dc for infarct is usually unilateral i.e. on the side of infarct, it is called as hemicraniectomy. the basic steps of hemicraniectomy are following: [7] skin incision: a large reverse question mark skin incision is made. the incision begins 2 to 3 cm lateral to midline behind the hairline, extends at least 15 cm posteriorly, and then curves around and down to the posterior root of zygoma. the skin and temporalis muscle are reflected anteriorly as a myocutaneous flap. bone removal: the limits of bone removal are 2-3 cm from midline, avoiding frontal sinus and superior sagittal sinus, till middle cranial fossa base. the anteroposterior extent is atleast 12 cms. dural opening:the dura is opened in a stellate fashion to maximize cerebral decompression. the bulging brain can be covered with pericranium or dural substitute for augmented duraplasty. dc helps by reversing brain shifts, and relieving ventricular and vascular compression. this allows edematous brain to expand extracranially instead of compressing the normal opposite cerebral hemisphere and brain stem. hemicraniectomy is also believed to improve cerebral perfusion pressure (cpp), increase retrograde flow in mca, preserve cerebral blood flow (cbf), andprevent further ongoing ischemia. good about dc the outcome of dc is quoted from french decimal (decompressivecraniectomy in malignant middle cerebral-artery infarcts), german destiny (decompressive surgery for the treatment of malignant infarction of the middle cerebral artery), and dutch hamlet (hemicraniectomy after middle cerebral artery infarction with lifethreatening edema trial) trials. [4] the survival is improved from29% with medical treatment to 78% resulting in absolute risk reduction arr of 50%. among survivors the good functional outcome (modified rankin scale (mrs) score ≤4) is increased from 24% to 75% with arr of 51%. the number needed to treat (nnt) is 2 for survival. [4] hemicraniectomy is lifesaving surgery in patients with malignant hemispheric infarction. bad about dc the outcome discussions are often dichotomized into simply survival or death. the above mentioned trial included a mrs romanian neurosurgery (2014) xxi 3: 345 348 347 score of 4 (moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance) as a favourable outcome, hence apparent result of these trials showed good number of patients with favorable outcome. such a class of mrs should not be clubbed with patients with good outcome. the nnt for survival with better function defined as mrs≤3 (moderate disability; requiring some help, but able to walk without assistance) is 4, i.e. out of 4 patients who survive after surgery only 1 will have good functional outcome. [5] including mrs 4 about 40%of survivors have severe disability. very little attention is paid about disability after surgery. there is very limited time prior to surgery for patients to understand the benefits and outcome of dc. the decision to operate is not always made in the light of the real probabilities of surviving with severe disability. [5] the patients are not prepared to accept the risk of unacceptable badness after surgery. the operating neurosurgeon and referring neurologist, before hey consign a patient to survival with a severe disability, have an obligation to establish that this would have been acceptable to them. [5] the american headdfirst study (hemicraniectomy and durotomy upon deterioration from infarction related swelling trial) and philippine hemmi trial (hemicraniectomy for malignant middle cerebral artery infarcts) have included quality of life as a outcome measure and will give more answers to this problem of disabled survivors. [8] another problem with dc is delayed mortality. most of the patients who are manged medically die during initial few days. the preliminary results of headdfirst study showed that mortality after dc approximated to that of medical treatment after 6 months. this delayed mortality may be due to complications associated with dc. [8] the timing of surgery has mixed results, with some studies showing that early surgery decreases mortality, others reporting no difference or worse outcomes. the functional outcome is uncertain in the studies dealing with timing of surgery. the results of hamlet show that surgical decompression within 4 days of symptom onset does not reduce poor outcome in patients. as many of our patients are referred late after neurological deterioration and development of clinical signs of brain herniation, we can offer a little by operating upon these patients. [4] the benefit of surgery in older individuals is also not clear. in an earlier study, though the mortality was reduced, none of survivors have a barthel index (bi) score >60 or a mrs score< 4. a recent study showed no significant difference between mortality. the nihss score before surgery contributed to the sixmonth mortality. hence when surgery is offered to elderly patients factors other than age should be considered and the treatment should be individualized in elderly patients. an upcoming destiny-ii trial will study patients older than 60 years and will clarify the issues of surgery for elderly population. [8] ugly about dc hemicraniectomy sounds a very simple surgical procedure, but is not without complications. none of the above mentioned studies discussed about complications of dc in detail. the incidence of any complication after dc is 50% to 55%. [3] the complications include hemorrhagic infarction, necrosis, 348 shukla, agrawal decompressive craniectomy for acute stroke hematomas and edema at the site of the craniectomy in about 25% cases. [3] paradoxical cerebral oedema after dc is attributed to possible reduction in the interstitial pressure within the brain after decompression, resulting in a greater hydrostatic pressure gradient between the intravascular and interstitial spaces. other complications are infection and seizures in 7– 20% cases. [3] the delayed complications are cerebrospinal fluid absorption disorders including subdural hygroma in 6–21% and hydrocephalus in 10–40% cases. [3] a complciation specific to dc is syndrome of the trephined (also called as sunken flap syndrome) which is due to subatmospheric pressure, irritation of neural parenchyma at bone edges, and adhesion of brain to subcutaneous tissue. the clinical manifestation of this syndrome is headache, seizures, mood swings, and behavioral disturbances. this syndrome can be prevented by early bone flap replacement (cranioplasty). [3] cranioplasty is filling of skull defect. this is usually performed after 6 weeks to 6 months of surgery. this procedure is also not without complications, which are reported in about 34% cases. [1] the common complications after cranioplasty are infection, wound breakdown, intracranial hemorrhage, bone resorption, and sunken cranioplasty. there is no difference in infection rate irrespective of autologous/ allogenic (bone substitutes, titanium) material used, method of bone flap preservation, and timing of replacement of bone flap. [1] conclusion hemicraniectomy is a life-saving but nonrestorative surgery. surgery should be done before clinical signs of brain herniation to obtain maximum benefit. the relatives of the patient should be explained clearly about possibility of survival with disability before offering the surgery. correspondence dr. dhaval shukla (mch) additional professor of neurosurgery department of neurosurgery national institute of mental health and neurosciences bangalore karnataka (india) emailneurodhaval@rediffmail.com phone+91-8026995411 references 1.gooch mr, gin ge, kenning tj, german jw. complications of cranioplasty following decompressivecraniectomy: analysis of 62 cases. neurosurg focus. 2009;26:e9. 2.hofmeijer j, algra a, kappelle lj, van der worp hb. predictors of life-threatening brain edema in middle cerebral artery infarction. cerebrovasc dis. 2008;25:176184. 3.honeybul s, ho km. long-term complications of decompressive craniectomy for head injury. j neurotrauma. 2011;28:929-935. 4.huttner hb, schwab s. malignant middle cerebral artery infarction: clinical characteristics, treatment strategies, and future perspectives. lancet neurol. 2009;8:949-958. 5.kelly ag, holloway rg. health state preferences and decision-making after malignant middle cerebral artery infarctions. neurology. 2010;75:682-7. 6.kimberly wt, sheth kn. approach to severe hemispheric stroke. neurology. 2011;76(suppl 2):s50-6. 7.staykov d, gupta r. hemicraniectomy in malignant middle cerebral artery infarction. stroke. 2011;42:513-6. 8.wartenberg ke. malignant middle cerebral artery infarction. curr opin crit care. 2012;18:152-63. doi: 10.33962/roneuro-2020-096 surgical options for traumatic fractures of the thoracic and lumbar spine. a series of 20 patients elhawary e. mohamed, aljboor ghaith s., buzantian p. armand romanian neurosurgery (2020) xxxiv (4): pp. 561-569 doi: 10.33962/roneuro-2020-096 www.journals.lapub.co.uk/index.php/roneurosurgery surgical options for traumatic fractures of the thoracic and lumbar spine. a series of 20 patients elhawary e. mohamed1, aljboor ghaith s.2, buzantian p. armand2 1 benha university hospital, neurosurgery department, benha, egypt 2 emergency hospital of saint pantelimon, neurosurgery department, bucharest, romania abstract background context. thoracolumbar fractures represent a large number of spine injuries in adults. such fractures are a result of traumatic accidents with high-energy impacts, such as falls from height or following motor vehicle accidents, often resulting in some degree of neurological deficit. purpose. to report a total of 20 cases of thoracolumbar fractures in young adults with various neurological manifestations. the majority had indications for transpedicular fixation. study design. series of 20 cases and review of the literature. patient sample. a series of 20 patients with a history of falling from a height or after motor vehicle accidents (rta) with complicated fractures at the level of the thoracolumbar vertebrae which present with neurological deficits. methods. we report here on a total of 20 patients with a history of falls from height or following rta. patients presented to the hospital complaining of back and abdominal pain. fractures at the thoracolumbar vertebral level were confirmed with imaging studies revealing post-traumatic spinal deformities. all cases were initially considered for conservative medical treatment. however, unstable complicated cases with bone fragment migration as well as spinal canal compression were deemed candidates for surgical intervention via posterior spinal fusion with transpedicular screw fixation. written informed consent was gathered from all patients. detailed history, clinical examination, as well as x-ray, computed tomography and magnetic resonance imaging of the dorsolumbar spine were obtained in all cases. neurological status was assessed using the frankel grading for spinal cord injury. results. the patients tolerated the operations without complications and remained in stable postoperative condition. conclusion. surgical treatments via transpedicular fixation are extremely efficient for treating unstable and complicated thoracolumbar spinal fractures. nevertheless, conservative medical treatment is still of high value and should be considered as the first treatment option, especially in stable cases. the patients who underwent surgery showed excellent outcomes and improvement of neurological deficits. the surgical procedure preferred in the present study was the posterior spinal fusion with pedicle screw fixation. keywords spine, fractures, surgery, fixation, thoracic and lumbar, screw, tarnspedicular, treatment corresponding author: aljboor ghaith s. emergency hospital of saint pantelimon, neurosurgery department, bucharest, romania ghaith_gtr@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 562 elhawary e. mohamed, aljboor ghaith s., buzantian p. armand introduction the biomechanical properties of the thoracic spine and thoracolumbar junction directly predispose this anatomically unique region to various types of traumatic injuries. high-energy trauma produced by road traffic accidents (rta) is the primary cause of injury, followed by falls from a height and sportsrelated injuries (1). the thoracolumbar vertebrae are associated with a high risk of post-traumatic compression fractures due to the effects of axial loading, which under normal conditions contribute to the natural kyphotic curvature of the thoracic spine (2) (3). the management of traumatic fractures of the thoracolumbar (t1-l5) spinal column remains controversial. there are a number of publications outlining various treatment strategies aimed at obtaining normal mobilization and stability of spinal fractures. despite the variety of treatment options presented in medical literature, there has as yet been no definitive consensus with regards to a goldstandard management protocol (4)(5). nor have there been any reported advantages with respect to patient outcome, despite several operative strategies being currently employed to achieve fracture reduction and fixation. furthermore, there is a scarcity of supporting evidence in the available literature for choosing conservative versus surgical management or vice versa (6) (7). while patients with limited vertebral body compression, for example, can benefit from nonoperative treatment such as thoracolumbar orthosis, restriction of activities and administration of analgesics (8), surgical management is generally considered of utmost necessity in patients presenting with severe biomechanical spinal instability or acute or chronic neurologic deficit (9). indications for surgical treatment include unstable injuries associated with neurological deficits, complicated fractures with dislocation or progressive deformations associated with compression of neural structures (10) (11) (12) (13). the primary objectives of surgical treatment of unstable thoracolumbar fractures are optimizing neural decompression, early stabilization, pain relief and adequate nursing care (6) (14). a number of classification systems have been devised to categorize thoracolumbar fractures. one of the most commonly used classification systems in clinical practice today is the scheme proposed by francis denis in 1983, which has aided in the communication and description of thoracolumbar fractures and their respective treatment strategies among medical practitioners [figure 1] (15). denis maintained that complete rupture of the posterior ligamentous complex alone would be insufficient to create spinal instability in flexion, extension, rotation and shear, and that spinal instability at least in flexion would develop only in the presence of additional disruption of the posterior longitudinal ligament and posterior annulus fibrosis (15) (16). in the denis classification system, the spine is subdivided into three columns as follows: anterior column (anterior longitudinal ligament [all] and anterior two-thirds of the vertebral body and annulus), middle column (posterior one-third of the vertebral body and annulus, posterior vertebral wall and posterior longitudinal ligament [pll]), and posterior column (all posterior structures of the pll which include: posterior bony arch and posterior ligamentous complex (supraspinous and interspinous ligaments, capsule, and ligamentum flavum). figure 1. two-column model compared with three-column model (denis). in addition to the positions of ssl, pll and all. the denis "3-column model" relied on anatomic divisions to guide surgical planning, whereas more modern classification systems such as the thoracolumbar injury classification system (tlics) emphasize the initial neurologic status and structural integrity of the posterior ligamentous complex as a 563 surgical options for traumatic fractures of the thoracic and lumbar spine guide for surgical decision-making and have demonstrated a high intraand inter-observer reliability. other systems, such as the load-sharing classification, also aid as useful tools in planning the extent of instrumentation and fusion (15) (17) (18) (12) (19). this case study is aimed at presenting our experiences in adult traumatic spinal injury. radiological findings, treatment strategies, and clinical outcomes were evaluated retrospectively and compared with the available literature. cases and methods study design this is a retrospective study conducted at benha university hospital, benha, egypt, between 2016 and 2020. we report here a total of 20 patients with thoracolumbar injuries sustained by falling from a height or following rta, of which 16 had presented with indications for surgical management via transpedicular fixation, i.e., with unstable and complicated fractures associated with neurological deficits. four cases had no indication for surgical treatment and were treated conservatively. as per standard procedure for all patients admitted to our clinic, detailed patient histories were gathered, comprehensive physical examinations were performed, and all relevant laboratory investigations were completed for each case. pre and postoperative neurological status was assessed using the frankel grade classification for spinal cord injury, a functional grading of impairment in activities of daily living, and analysis of gait disturbances (20) (21). after performing an initial clinical and neurological examination, the diagnosis was confirmed radiologically, i.e., bony structure injury of the thoracolumbar spine was confirmed with computerized tomography (ct), while neural and ligamentous involvement was confirmed with additional magnetic resonance imaging (mri). the length of time, from the day of patient admission to the operation, ranged from 3-7 days, depending on the clinical and neurological status of the patient, as well as on trauma severity. all patients were fully informed with regard to treatment options to manage their injuries, including the aim and scope of the treatment, possible operative and perioperative risks, as well as potential shortand long-term complications. informed written consent forms were signed and submitted by all patients upon hospital admission. case reports surgical procedures all patients in the present study with surgical indications were treated with pedicle screw fixation, which is generally considered a safe procedure through which adequate reduction and stability can be achieved, and provides patients with early pain relief and mobility (22). although either anterior or posterior approaches can be used in spinal fusion surgery, posterior approaches are associated with lower postoperative morbidity rates. less aggressive than the anterior approach, posterior fixation is associated with several advantages, including less intraoperative bleeding and fewer postoperative complications, while still achieving excellent spinal stabilization (23) (24). preoperative intravenous antibiotic prophylaxis was administered to each patient. the posterior approach was utilized for each case in the present study. each patient was placed in a prone position. a midline posterior incision centered over the affected area was performed with the aid of preoperative x-ray imaging planning. an initial laminotomy was performed on each patient. using anatomical landmarks such as the facet joints and transverse processes, it was possible to establish insertion points on the pedicles [figure 2]. for example, an entry point can be identified by drawing a horizontal line through the middle of the transverse processes, or from the intersection of the upper one-third of the transverse process and a vertical line drawn through the prominent ridge on the superior articular facet. figure 2. the transpedicular insertion; insertion point of the screw. 564 elhawary e. mohamed, aljboor ghaith s., buzantian p. armand cortical bone was nibbled off at the point of the intersection of these two lines, pilot holes were created using a burr, and a ball handle probe was passed through the cancellous channel in the pedicle and into the vertebral body. screw angulation and placement were performed using c-arm-guided fluoroscopy. a transpedicular screw fixation and fusion approach was then employed, with bilateral, twolevel pedicle screw placement, followed by bilateral rod placement situated on the fracture level and on at least one adjacent level superiorly or inferiorly, based on the location of the intact endplate. for example, in cases where the inferior endplate was intact and the superior endplate was fractured, screws were inserted caudally to the inferior endplate at an angle of approximately 5°. transpedicular screw fixation was complemented by placement of adjoining rods with cross-connecting rod reinforcement. distraction was performed and locking nuts were tightened. the surgical wound was thoroughly irrigated and closed over a suction drain. postoperative monitoring and follow-up postoperative imaging studies were performed in order to ensure the efficacy of the surgical procedure. following surgery, patients were transferred to the post-anesthesia care unit for 24 hours. postoperative patient mobilization was initiated on the first day. the average time for suture removal was approximately 12 days. patients wore a taylor brace until the 10th–12th postoperative day, or longer in cases with injuries involving all three columns. regular physiotherapy and assisted mobilization were continued until the patient was discharged from the hospital. a detailed neurological examination was repeated on the day of patient discharge. all patients with unstable injuries were monitored with regular follow-up visits: at 4–6 weeks postoperation, and bi-monthly afterwards, for an average total period of 24-36 months. follow-up visits included clinical, neurological and radiological examinations, as well as documentation of any postoperative complications. results the posterior spinal fixation approach was used in the surgical treatment of 16 cases with unstable thoracolumbar burst fractures. of the patients treated surgically, 12 had no neurological deficits at the time of hospital presentation. transient leg numbness, tingling sensation and pain, immediately after the traumatic event, were reported by eight of these 12 patients, with symptoms subsiding by the time of admission into the emergency department. persistent neurological deficit was reported by four cases in the study. six cases presented with a t12-level fracture, three cases with a t10-level fracture, one case with t9-level fracture and one case of t11-level fracture. three cases presented with a fracture at the l3-level, and two cases presented with a fracture at the l2 level. there were no cases of dural tears in the present study. of the four patients with stable injuries who were managed conservatively, two cases presented with t10-level fractures, one case with a t11-level fracture and one case with a fracture at the l2-level. the mean duration of hospitalization was approximately four weeks. preoperatively, eight of the patients presented with normal motor function (frankel grade e). six patients presented with preserved, functionally useful voluntary motor function (frankel grade d). two cases presented with preserved, nonfunctional voluntary motor function (frankel grade c). in follow-up visits at 24-36 months postoperatively, the majority of patients had neurological recovery with either frankel grade of e or d scores, while one patient had a persistent motor deficit, with a frankel grade of c score. 565 surgical options for traumatic fractures of the thoracic and lumbar spine figure 3. case 1: a, preoperative sagittal ct of a 26-year-old male patient who sustained a t10 burst fracture without neurological deficit at time of admission (frankel grade e). b, preoperative axial ct scan image confirming the presence of a fracture at the t10 vertebral level. c, preoperative mri demonstrating t10-level fracture. d, postoperative sagittal ct imaging taken 24h after the patient underwent a transpedicular fixation procedure. the ct scan demonstrated correct screw placement at two levels (t9 and t11). 566 elhawary e. mohamed, aljboor ghaith s., buzantian p. armand figure 4. case 2: a1, preoperative sagittal ct of a 20-year-old male patient who sustained an l2 burst fracture without neurological deficit at time of admission (frankel grade e). a2, preoperative axial ct image confirming the presence of a fracture at the l2 vertebral level. b1, preoperative sagittal t1weighted mri revealing l2 fracture. b2, preoperative axial mri showing the aspect of the fracture at l2. c1, postoperative sagittal ct scan obtained 24h after the patient underwent a transpedicular fixation procedure. the ct scan demonstrated correct screw placement at two levels superiorly (t12, l1) and two levels inferiorly (l3, l4). there is no significant correction of local post-traumatic kyphosis c2, postoperative axial t1weighted mri, 12 months after surgery, at which point the patient had a frankel grade of e. 567 surgical options for traumatic fractures of the thoracic and lumbar spine figure 5. case 3: a, preoperative sagittal ct of a 29-year-old female patient who suffered a t12 burst fracture without neurological deficit at time of admission (frankel grade d). b, preoperative axial mri confirming the presence of a fracture at the t12 vertebra level. c, preoperative coronal ct scan confirming the t12-level fracture. d, preoperative sagittal mri demonstrating the fracture at t12. e1, postoperative sagittal ct scan acquired 24h after the patient underwent a transpedicular fixation procedure. the ct scan demonstrated correct screw placement at two levels superiorly (t10, t11) and one level inferiorly (l1). e1 and e2, postoperative sagittal and axial t1weighted mri revealing correct screw insertion. serial followup ct scans were performed after surgery, with the patient having a frankel grade of d. 568 elhawary e. mohamed, aljboor ghaith s., buzantian p. armand figure 6. case 4: a, preoperative sagittal ct of a 17-year-old female patient who was admitted with a burst fracture at the level of l3, with bilateral motor deficit (frankel grade a). b, preoperative axial mri confirming spinal cord compression at the l3-level due to the fracture. c, preoperative sagittal mri demonstrating the presence of the fracture with evidence of spinal cord injury at the l3-level. d, postoperative sagittal ct scan revealing screw insertion at one level superiorly (l2) and at one level inferiorly (l4) relative to lesion. e, postoperative axial t1-weighted mri revealing correct screw insertion (l2). serial follow-up ct scans were performed after surgery, with the patient having a frankel grade of c. discussion the mechanism of injury in the present case series was via fall from a height or road traffic accidents (rta) (20 cases), resulting in thoracolumbar fractures. four patients presented with uncomplicated stable fractures, in which conservative management was indicated. the majority of the patients in the study (16 cases) had complicated unstable fractures. the patients were operated using the posterior approach with transpedicular screw fixation within 3-7 days from hospital admission. in our study, the most common site of fracture was located at the t12 vertebral level (6 cases). the surgical interventions proceeded uneventfully with no major intraor postoperative complications. all patients who underwent surgery were assessed neurologically preand post-operatively at regular intervals. the frankel grade classification was used to evaluate neurological function of the patients. preoperatively, eight cases had frankel grades of e, six cases had frankel grades of d and two cases had frankel grades of c. following surgical intervention, only one patient had a persistent frankel grade of c, while the majority of our cases had frankel grades of d or e, which indicate acceptable results with posterior fixation for unstable thoracolumbar fractures. conclusion the main objectives of surgical treatment of thoracolumbar fractures are to improve neurological deficits as classified by the frankel scale, to prevent spinal cord injuries, and to achieve stability by screw fixation. our case study demonstrates that posterior transpedicular screw fixation is an effective and safe surgical method to obtain stabilization of the spine. the approach is associated with good surgical outcomes and minimal complications. references 1. epidemiology of incident spinal fracture in a complete population. c. burns, r. hu, c.a. mustard,. 15;21, feb 1996, spine, vol. 4, pp. 492-9. 2. the contribution of the three columns of the spine to spinal stability. m.f. lospinuso, et al., t.r. haher, j.m. tozzi,. 27, 1989, a biomechanical model., vol. paraplegia, pp. 432-439. 10.1038/sc.1989.69. 3. surgical treatment of traumatic fractures of the thoracic and lumbar spine: a systematic review of the literature on techniques, complications, and outcome. e. buskens, et al, j.j. verlaan, c.h,\. diekerhof,. 7, 1 april 2004, wolters kluwer health, inc., vol. spine, pp. 803-814. 10.1097/01.brs.0000116990.31984.a9. 4. surgical vs. conservative treatment of fractures of the thoracolumbar transition. klampfer h, et al., resch h, rabl m,. 103, 2000, vol. unfallchirurg, pp. 281-288. 5. thoracolumbar burst fracture. a biomechanical investigation of its multidirectional flexibility. t w mcgowen, m m panjabi t r oxland,. 19, 1994, vol. spine, pp. 578 –585. 8184353. 6. the three column spine and its significance in the classification of acute thoracolumbar spinal injuries. denis f. 8, nov-dec 1983, vol. spine (phila pa 1976)., pp. 817-31. 7. spinal instability as defined by the three-column spine concept in acute spinal trauma. f. denis. 189, oct 1984, clinic ortho related research, vol. spine, pp. 65-76. pmid: 6478705. 8. stability of spinal fractures and fracture dislocations. g. m. bedbrook. 1, 9 may 1971, vol. paraplegia, pp. 23-32. doi: 10.1038/sc.1971.3.. 9. pathophysiology and management of traumatic spinal injuries. andy shores, dvm, ms, phd. 195, 4 july 1992, diseases of the spine, vol. spinal trauma, pp. 859-890. 10. pediatric spinal injury review of 174 hospital admissions. hamilton mg myles st. 5, 1992, j. neurosurg, vol. 77, pp. 700–704. 11. spinal fractures and dislocations in children and adolescents. mcphee ib. 6, 1981, vol. spine, pp. 533537. 10.1097/00007632-198111000-00001. 12. a prospective multicenter study of cervical spine injury in children. pressman bd, shah mn, p viccellio simon h,. 2, 2001, vol. pediatrics 108, p. e20. 13. treatment of unstable thoracolumbar junction burst fractures with shortor long-segment posterior fixation in magerl type fractures. dogan o, tabak ay, altay m, ozkurt b, aktekin cn, ozturk am,. 8, 2007, eur spine j off publ, vol. 16, pp. 1145-1155. 14. cortical bone trajectory for lumbosacral fixation: penetrating s-1 endplate screw technique: technical note. takashi kato, keitaro matsukawa keitaro matsukawa 1 , yoshiyuki yato,. 2, 2014, j neurosurg spine, vol. 2014 aug;21, pp. 203-9. 10.3171/2014.3.spine13665. 569 surgical options for traumatic fractures of the thoracic and lumbar spine 15. thoracolumbar spine trauma: review of the evidence. j jallo, . 2, jun 2013, j. neurosurgery sci, vol. 57, pp. 11522. 16. brad j. chauvin, . denis classification. s.l. : statpearls publishing, 2020. nbk544310. 17. incomplete burst fractures of the thoracolumbar spine: a review of literature. c josten, . 12, 25 may 2017, eur spine j ., vol. 26, pp. 3187-319. 10.1007/s00586-0175126-3. 18. management of thoracolumbar spine fractures. weishi li, . 1, jan 2014, spine j., vol. 14, pp. 145-64. 10.1016/j.spinee.2012.10.041. 19. does surgical intervention or timing of surgery have an effect on neurological recovery in the setting of a thoracolumbar burst fracture? so kato. 4, sep 2017, j orthop trauma, vol. suppl, pp. s38-s43. doi: 10.1097/bot.0000000000000946.. 20. a comparison of diagnostic stability of the asia impairment scale versus frankel classification systems for traumatic spinal cord injury. amanda botticello, . 9, sep 2020, multicenter study, vol. arch phys med rehabilitation, pp. 1556-1562. 10.1016/j.apmr. 2020.05.016. 21. posterior short-segment fixation including the fractured vertebra for severe unstable thoracolumbar fractures. jin wu, zhida chen, bin lin. 1, 15 jan 2018, zhongguo xiu fu chong jian wai ke za zhi, vol. 32, pp. 59-63. 10.7507/1002-1892.201708082.. 22. surgical outcome of posterior short segment transpedicle screw fixation for thoracolumbar fractures. vijay sharma,. 4, dec 2013, j orthop, vol. 10, pp. 162– 167. 10.1016/j.jor.2013.09.010. 23. steffee variable screw placement system in the management of unstable thoracolumbar fractures: a third world experience. r bahadur,. 10, dec 1998, vol. injury 29, pp. 737-42. 10.1016/s0020-1383(98)00173-9. 24. prognostic factors and optimal management for patients with cervical spinal cord injury without major bone injury. ippei kitade, hideaki nakajima, ai takahashi,. 2, may 2019, j orthop sci, vol. 24, pp. 230236. 10.1016/j.jos.2018.10.001. romanian neurosurgery (2019) xxxiii (3): pp. 287-294 doi: 10.33962/roneuro-2019-048 www.journals.lapub.co.uk/index.php/roneurosurgery primary central nervous system sarcomas. clinical, radiological and pathological features in our institution wael k. zakaria, ahmed n. taha, mohamed state neurosurgery department; mansoura university, egypt abstract objective: primary cns sarcomas are very rare tumours with no defined standard of care. patients and methods: this study was a retrospective review of seven patients diagnosed with a primary cns sarcoma at neurosurgery department, mansoura university hospital between 2006 and 2018. we reviewed the clinical, radiological, and pathological data of these patients. there were 2 female (28.6%) and 5 male (71.4%) with age ranged from 8 years to 73 years (mean age 25.4 years). three patients (42.9%) had an intracranial sarcoma, and four (57.1%) had intraspinal tumours. all intracranial tumours located in supratentorial region. results: we have characteristic imaging findings inform of osteolytic bony erosion in 3 patients and marked enhancement of the tumour in 5 (71.4%) patients. we operated upon all patients to remove the tumour surgically with our aim is gross tumour resection. tumour was totally resected in 5 patients (71.4%) and subtotal in another 2 patients (28.6%). tumour has dural attachment in 5 cases (71.4%) and brain invasion was present in all intracranial 3 patients (42.9%). postoperative radiotherapy was used in 5 patients and postoperative chemotherapy was used in all patients. we used immunohistochemical studies for all patients with the most consistent finding being strong desmin positivity. the mean length of patients survival was 4.6 years (range from 3 month to 8 years). conclusions: primary cns sarcomas are very rare cns tumours, total surgical resection and post-operative radio and chemotherapy provided encouraging outcomes. introduction primary cns sarcomas are rare tumours. there are many theories of the cell of origin of these tumour. tumour may arise from pluripotential primitive mesenchymal cells which located in the dura, or originated from the leptomeningial cells or their extensions via the pia into the brain and the spinal cord along the stroma of the choroid plexus, the tela choroidea, or the periadventitial spaces and these considered as widely accepted theory. we can defined sarcomas that have originated from metastases of soft tissue or bone sarcomas to the cns as secondary cns sarcomas. these tumours result from direct extension of sarcoma located at places neighbouring the cns. keywords primary cns, sarcoma corresponding author: wael k. zakaria neurosurgery department; mansoura university, egypt drwaelmusa@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 288 wael k. zakaria, ahmed n. taha, mohamed state patients and methods we looking for all types of primary cns sarcomas between 2006-2018 at mansoura university hospital through retrospective analysis of our cns tumor database which archived in our neurosurgery department in these period. the research ethical committee at mansoura medical school give us permission to use these patients’ data. in this study, we defined primary cns sarcomas as tumours that originated primary in the cns from non-neuronal, non-glial, and non-reticular elements, and we not include any previously diagnosed benign tumour with sarcomatous transformation. the medical data of these patients included in our definition of a primary cns sarcoma were then analysed for clinical, radiological and pathological features. all primary cns sarcoma were investigated for any possibility of the presence of extra cns sarcomas at the time of study. the work-up study were chest x-ray, chest ct, abdominal and pelvic ct, and abdominal ultrasound. all cases surgical specimens were examined in pathology department by light microscopy using eosin and hematoxylin stain, periodic acid-schiff, and reticulin. we used immune histochemical studies in all cases. the range of follow up varied from 3 month to 8 years (mean 2.9 years). we calculated the length of survival from the date of diagnosis of the disease and the end points were the patient death day or the last follow-up visit. 289 primary central nervous system sarcomas 290 wael k. zakaria, ahmed n. taha, mohamed state patient age/ sex location ct m r i extent of resection radiotherapy chemotherapy dural attachment brain invasion survival 1 73/f d10 enhanceme nt ++, bone destruction total yes yes no no alive 1 years then absent 2 8/f d11-12 enhanceme nt +++, cystic near total no yes yes no alive 1years 6 months 3 8/m frontal lobe enhanceme nt +++, bone destruction total yes yes yes no alive 8years 4 47/ m occipital lobe cystic, enhanceme nt++,bone destruction total yes yes yes yes alive 3month s 5 8/m l2-5 enhanceme nt +++, bone destruction ,cystic total no yes no no alive 7years 6 18/ m bifrontal lobe cystic, enhanceme nt++, near total yes yes yes yes alive 7month s 7 16/ m d4-6 enhanceme nt +++, bone destruction total yes yes yes no alive 2years results clinical pictures we summarized the clinical pictures in this study in table 1. there were 2 female (28.6%) and 5 male (71.4%) ranged in age from 8 years to 47 years (mean age 19.4 years). three patients in this study (42.9%) were in the first decade of life. three sarcoma patients (42,9%) were intracranial and 4 patients (57.1%) were intraspinal. all intracranial sarcomas in this series were supratentorial in location, two of them presented bilaterally either in frontal or occipital lobes. three of intraspinal tumours (75%) were located in the dorsal area and the remaining presented in the lumbar region. the clinical presentation of these patients varied from symptoms and signs of icp as vomiting, headache and papillodema and other presentation as focal neurological deficit such as dysphasia, fits, hemiparesis for intra cranial tumours and paraparesis for the intra spinal tumours. radiological features we summarized the radiological data in table 1. ct and mri used for investigation (fig. 1). ct was performed in all patients, tumour enhancement with contrast had been obtained. all intracranial tumours patients in this study showing osteolytic bony destruction. 5 patients (71.4%) showed marked humoral enhancement. magnetic resonance imaging in selected cases revealed increased signal on t2 images on these lesions, and irregularly enhancement after contrast study (fig. 2). surgery all patients in these series underwent at least one surgical procedure with the aim of surgery is gross tumoural resection; only 2 cases underwent another surgical operation due to recurrence of the tumour. surgical tumoural resection was total in 5 cases (71.4%) and subtotal in the remaining 2 patients (28.6%). we performed true cut needle biopsy in just a patient of intracranial tumour with extra cranial extension prior to surgical excision. postoperative radiotherapy was used in 5 patients (71.4%) and postoperative chemotherapeutic agents were used in all patients (100%). 291 primary central nervous system sarcomas table 1 showed the operative details of the patients included in this series. at surgery, we found dural attachment of the tumour in 5 patients (71.4%) and parenchymal invasion of the tumour in 2 patients (28.6%). we found a well-defined demarcation plane of dissection around the lesion in four patients, two of them were intracranial sarcoma and the other were intra spinal. pathological features in this series, we found similar histological characters of the different intracranial and extra cranial sarcomas. we did immunohistochemical studies for all cases (table 2). the most consistent data in immunohistochemical studies were strong positive results of vimentin and general negative results for both neuronal and glial markers. all patients showed positive desmin with more rhabdomyoblastic differentiation. all patients tumour examined by electron microscopic studies. there are many feature as the spindle shape of the cells, lack of well-developed junctions, dilated rough endoplasmic reticulum, and absence of microvilli and neurosecretory granules. the final pathological diagnosis in these series was a ewing's sarcoma in 2 (28.6%) patients, a embryonal rhabdomyosarcoma in 2 (28.6%), an otherwise low grade chodrosarcoma (14.3%), synovial sarcoma and an undifferinated sarcoma in the remaining three patients alternatively. patient no desmi n neurone specific enolase bdl-2 lca,cd3,cd9 9 1 negativ e positive negativ e na 2 negativ e negative positive na 3 positiv e negative na na 4 negativ e negative na negative 5 negativ e positive na na 6 na na na na 7 positiv e na na negative survival we calculate the length of survival from the day of the diagnosis of the disease (table 1). we have data on survival for 6 patients and lack information in just one patient. the longest survival time in these study was eight years and the shortest survival time was three month (mean 3.2 years). the durations of patient survival in intracranial tumours ranged from three months to eight years (mean 2.9 years), while the intraspinal tumours ranged from 18 months to 7 years (mean 3.5 years). three months to 8 years (mean 4 years) was the length of survival in the cases with gross surgical resection of the lesion; and the range of length of survival in cases with subtotal tumour resection was 18 months to 2 years (mean 1, 8 years). adjuvant therapy we used postoperative radiation in 5 patients; with a radiation dose ranged from 4,500–5,900 gy. on the other hand we used postoperative chemotherapy in all patients. the most used chemotherapeutic agents were ifosfamide, carboplatin, vincristine and cyclophosphamide. discussion the occurrence of a primary cns sarcoma described firstly by bailey in 1929.2 cns sarcoma with all forms considered as rare tumours.⁶⁻¹⁴⁻³ºthe survival in sarcoma patients increased than in the past due to advances technique in chemotherapy. ⁶⁻²⁶⁻⁴⁵in different studies, we found variation in the incidence of primary cns sarcomas which ranged from 0.1% to 4.3%.³⁻¹⁹⁻²⁷⁻³¹⁻³³⁻³⁶ this variation happened due to the term of a primary cns sarcoma were inconsistent in different series. previous reported studies included different forms such as giant cell sarcoma, circumscribed sarcoma of the posterior fossa, reticulum cell sarcoma, and hemangiopericytoma, and this gave a false result in high incidence of these tumour type.⁷⁻²º⁻²¹⁻²⁵⁻³⁵ in other series, they considered cases of primary glial, neuronal, neuroectodermal, and/or previously diagnoesd benign meningeal tumours with. sarcomatous features as sarcomas and this lead to falsely high incidence of these tumour type .²³⁻³¹finally, many studies not used immunohistochemistry that could be helpful to resolve diagnostic issues for many examined sarcomatous tumors.²³⁻³³⁻³⁶⁻⁴³ the origin of sarcoma have many theories, the most accepted theory assumed the origin of these 292 wael k. zakaria, ahmed n. taha, mohamed state tumour to pluripotential primitive mesenchymal cells, the leptomeninges or their extension into the brain and the spinal cord via the pia along the. periadventitial spaces, the stroma of the choroid plexus and the tela choroidea.²⁻⁴⁻¹⁻²⁴⁻²⁵⁻³¹⁻³⁻³⁵⁻⁴⁵ the causes for occurrence of the primary cns sarcoma is not known yet well accepted inciting agent of sarcoma in the literature is radiation therapy¹⁹⁻²³⁻²⁷⁻³⁴⁻⁵⁻³⁸⁻⁴⁴. there are another predisposing factor as trauma¹⁷⁻¹⁹⁻²⁷⁻²⁸⁻²⁹⁻³¹, genetic and familial factors¹⁹⁻³¹ and viruses such as rsv.⁸⁻²¹⁻²⁷⁻³¹ primary cns sarcomas may happen at any life decade, with high incidence in children ²³⁻³¹⁻⁴⁴. in these series sarcomas were exist in the age range 8– 73 years, with the youngest case was 8 years old. primary intracranial sarcoma clinically presented as other intracranial tumours. however, it can present with intracranial hemorrhage due to their extreme vascularity¹⁻¹⁵⁻²⁷⁻³º. the clinical presentation of primary intraspinal sarcoma had the same clinical presentation of other intraspinal tumours. there are nonspecific image of primary cns sarcomas on radiology as ct or mri. in our series, tumour was large and with different heterogeneous density, cystic (hypodense), or solid and in one patient presented bilaterally in intracranial. two of the 7 tumours had both solid and cystic components. mri of sarcoma was available with an inhomogeneous signal. solid parts of the tumour usually enhanced after administration of intravenous contrast. enhancement of the tumour after contrast in the mri has been a feature of sarcomas in the many series in literature ³⁴⁻³⁵. an important characteristic feature of sarcoma is the location near to the surface of the brain or the meninges, and it existed in four patients in our studies `. cns sarcoma have high incidence of leptomeningeal spread ¹¹⁻¹³⁻⁴⁵. there are many differential diagnosis of primary cns sarcoma on radiology as ct and mri includes glioma, medulloblastoma in posterior fossa, cranial and spinal meningioma, and ependymoma ¹⁹⁻²⁷⁻³²⁻³⁶. in current study, our paients tumor are located in supratentorial region with the most common sites of origin is the frontal lobes which is not match with other studies in literature ¹³⁻²²⁻²³⁻³²⁻³⁶⁻⁴⁵. none of our patients presented with their tumour in intraventricular region, although in many series reported intraventricular sarcomas which originated from the choroid plexus²³⁻²⁶⁻²⁸⁻⁴º⁻⁴¹⁴⁵. a common feature of primary cns sarcoma is dural involvement⁵⁻¹⁷⁻³⁶⁻⁴⁴⁻⁴⁵⁻⁴⁷. we have dural involvement of the tumour in 3 patients which considered as a half of the cases in our study. we did not report any malignant glial tumour within or adjacent to the primary sarcoma on our series. although some series document that reactive glioma can be happened in a primary cns sarcoma ¹⁶⁻²³⁻²⁹⁻⁴⁶. primary sarcomas of cns has the ability to send metastasis outside the central nervous system, as the liver, bone, and lung with a poor prognosis³⁻¹²⁻¹³⁻². it is difficult to determine the incidence of the different histological subtypes of these tumour. this is due rare incidence of the lesion, and the deficient criteria for including specific subtypes in the patients who documented in study ³⁻⁴º. we have frequent changes happened in the classification system for primary cns sarcomas due to appearance of new histological subtypes such as malignant fibrous histiocytoma, and in the literature its considered as most common soft tissue sarcoma⁴⁻⁵⁻¹⁶⁻²⁷⁻³⁸ . undifferentiated sarcoma considered as the most common pathological type in our study, and this not matched with others series ⁷⁻⁴⁵. other series reported fibrosarcomas and mfh as the most pathological tumoural subtype ¹⁻²⁻⁹⁻³⁶. primary cns sarcomas characteristic with a bad prognosis, although the long duration of postoperative survival is well reported in many series in literature¹³⁻³¹⁻³²⁻³⁴⁻⁴º⁻⁴⁵. many studies in the literature reported that gross surgical resection is considered as the best treatment of choice. we can use postoperative radiation or chemotherapy for prolonged the patient survival ¹⁻³⁻¹¹⁻¹³⁻¹⁷⁻¹⁶⁻³⁶⁻⁴º⁻⁴⁵⁻⁴⁶. in our study, we found that maximal surgical resection of the tumour followed by post-operative radiotherapy help the patient to receive his best choice of management. although, there are many side effects of radiation on young patient category. the aim of postoperative chemotherapy could not be exactly reported in our study. conclusion the primary central nervous system sarcoma is a rare tumour that mainly originated in the 293 primary central nervous system sarcomas supratentorial region with ability to be exist in the intraspinal region. csf dissemination and dural attachment of the tumour are frequently exist. metastases outside the cns associated with bad prognosis. for long term survival we advised gross surgical resection followed by postoperative radiotherapy. chemotherapy regimens may be considered as one of the factor that prolong the survival if they are tolerated by the patient. future studies should be focused to understand the histopathological subtypes of primary cns sarcoma to use different chemotherapeutic agents which be helpful to give patients long survival and best choice of treatment. references 1. anderson wr, cameron jd, tsai sh (1980) primary intracranial leiomyosarcoma. case report with ultrastructural study. j neurosurg 53:401– 405pubmedgoogle scholar 2. arumugasamy n (1969) some neuropathological aspects of intracranial sarcomas. med j malaya 23:169– 173pubmedgoogle scholar 3. asai a, yamada h, murata s, matsuno a, tsutsumi k, takemura t, matsutani m, takakura k (1988) primary leiomyosarcoma of the dura mater. case report. j neurosurg 68:308–311pubmedgoogle scholar 4. bahr al, gayler bw (1977) cranial chondrosarcomas. report of four cases and review of the literature. radiology 124:151–156pubmedgoogle scholar 5. berry add, reintjes sl, kepes jj (1988) intracranial malignant fibrous histiocytoma with abscess-like tumor necrosis. case report. j neurosurg 69:780– 784pubmedgoogle scholar 6. bryant bm, wiltshaw e (1980) central nervous system involvement in sarcoma: a presentation of 12 cases, a review of the literature, and a discussion of possible changing patterns with the use of chemotherapy, placing special emphasis on embryonal tumours. eur j cancer 16:1503–1507pubmedgoogle scholar 7. cassady jr, wilner hl (1967) the angiographic appearance of intracranial sarcomas. radiology 88:258– 263pubmedgoogle scholar 8. charman hp, lowenstein dh, cho kg, dearmond sj, wilson cb (1988) primary cerebral angiosarcoma. case report. j neurosurg 68:806–810pubmedgoogle scholar 9. christensen e, lara d (1953) intracranial sarcomas. j neuropathol exp neurol 12:41–56pubmedgoogle scholar 10. cybulski gr, russell ej, d’angelo cm, bailey ot (1985) falcine chondrosarcoma: case report and literature review. neurosurgery 16:412–415pubmedgoogle scholar 11. dropcho ej, allen jc (1987) primary intracranial rhabdomyosarcoma: case report and review of the literature. j neurooncol 5:139–150pubmedgoogle scholar 12. el-gindi s, abd-el-hafeez m, salama m (1974) extracranial skeletal metastases from an intracranial meningeal chondrosarcoma. case report. j neurosurg 40:651–653pubmedgoogle scholar 13. gaspar le, mackenzie ir, gilbert jj, kaufmann jc, fisher bf, macdonald dr, cairncross jg (1993) primary cerebral fibrosarcomas. clinicopathologic study and review of the literature. cancer 72:3277–3281pubmedgoogle scholar 14. gercovich fg, luna ma, gottlieb ja (1975) increased incidence of cerebral metastases in sarcoma patients with prolonged survival from chemotherapy. report of cases of leiomyosarcoma and chondrosarcoma. cancer 36:1843–1851pubmedgoogle scholar 15. heros rc, martinez aj, ahn hs (1980) intracranial mesenchymal chondrosarcoma. surg neurol 14:311– 317pubmedgoogle scholar 16. hirato j, nakazato y, sasaki a, yokota m, nojiri k, toyoda o, nakajima h (1994) intracranial malignant fibrous histiocytoma: characterization of gfap-positive cells in the tumor. clin neuropathol 13:315–322pubmedgoogle scholar 17. ho ys, wei ch, tsai md, wai yy (1992) intracerebral malignant fibrous histiocytoma: case report and review of the literature. neurosurgery 31:567– 571pubmedgoogle scholar 18. hockley ad, joffman hj, hendrick eb (1977) occipital mesenchymal tumors of infancy. report of three cases. j neurosurg 46:239–244pubmedgoogle scholar 19. ironside jw (1991) classification of primary intracranial sarcoma and other central nervous system neoplasms. histopathology 18:483–486pubmedgoogle scholar 20. kernohan jw, uihlein a (1962) sarcomas of the brain. thomas, springfieldgoogle scholar 21. kishikawa t, numaguchi y, fukui m, komaki s, ikeda j, kitamura k, matsuura k (1981) primary intracranial sarcomas: radiological diagnosis with emphasis on arteriography. neuroradiology 21:25–31pubmedgoogle scholar 22. kubota t, hayashi m, yamamoto s (1982) primary intracranial mesenchymal chondrosarcoma: case report with review of the literature. neurosurgery 10:105– 110pubmedgoogle scholar 23. lalitha vs, rubinstein lj (1979) reactive glioma in intracranial sarcoma: a form of mixed sarcoma and glioma (“sarcoglioma”): report of eight cases. cancer 43:246–257pubmedgoogle scholar 24. lam rmy, malik gm, chason jl (1981) osteosarcoma of meninges: clinical, light, and ultrastructural observations of a case. am j surg pathol 5:203–208pubmedgoogle scholar 25. legier jf, wells jr ha (1967) primary cerebellar rhabdomyosarcoma. case report. j neurosurg 26:436– 438pubmedgoogle scholar 26. louis dn, richardson jr ep, dickersin gr, petrucci da, rosenberg ae, ojemann rg (1989) primary intracranial leiomyosarcoma. case report. j neurosurg 71:279– 282pubmedgoogle scholar 27. martinez-salazar a, supler m, rojiani am (1997) primary intracerebral malignant fibrous histiocytoma: 294 wael k. zakaria, ahmed n. taha, mohamed state immunohistochemical findings and etiopathogenetic considerations. mod pathol 10:149–154pubmedgoogle scholar 28. matsukado y, yokota a, marubayashi t (1975) rhabdomyosarcoma of the brain. j neurosurg 43:215– 221pubmedgoogle scholar 29. mayo cm, barron kd (1966) concurrent glioma and primary intracranial sarcoma. a report of two cases and a review of the literature. neurology 16:662– 672pubmedgoogle scholar 30. mcdonald p, guha a, provias j (1997) primary intracranial fibrosarcoma with intratumoral hemorrhage: neuropathological diagnosis with review of the literature. j neurooncol 35:133–139pubmedgoogle scholar 31. mena h, garcia jh (1978) primary brain sarcomas: light and electron microscopic features. cancer 42:1289– 1307google scholar 32. mena h, ribas j, enzinger fm, parisi je (1991) primary angiosarcoma of the central nervous system: study of eight cases and review of the literature. j neurosurg 75:73–76pubmedgoogle scholar 33. min kw, gyorkey f, halpert b (1975) primary rhabdomyosarcoma of the cerebrum. cancer 35:1405– 1411pubmedgoogle scholar 34. niwa j, hashi k, minase t (1996) radiation induced intracranial leiomyosarcoma: its histopathological features. acta neurochir 138:1470–1471google scholar 35. onofrio bm, kernohan jw, uihhelein a (1962) primary meningeal sarcomatosis: a review of the literature and report of 12 cases. cancer 15:1197–1208pubmedgoogle scholar 36. paulus w, slowik f, jellinger k (1991) primary intracranial sarcomas: histopathological features of 19 cases. histopathology 18:395–402pubmedgoogle scholar 37. raskind r, grant s (1966) primary mesenchymal chondrosarcoma of the cerebrum. report of a case. j neurosurg 24:676–678pubmedgoogle scholar 38. roosen n, cras p, paquier p, martin jj (1989) primary thalamic malignant fibrous histiocytoma of the dominant hemisphere causing severe neuropsychological symptoms. clin neuropathol 8:16– 21pubmedgoogle scholar 39. roy s, bhatia r, nanda nr (1980) primary rhabdomyosarcoma of the cerebellum. j pathol 132:235–241pubmedgoogle scholar 40. rueda-franco f, lopez-corella e (1995) sarcomas in the central nervous system of children. 1982 [classical article]. pediatr neurosurg 22:49–55pubmedgoogle scholar 41. scott rm, dickersin r, wolpert sm, twitchell t (1976) myxochondrosarcoma of the fourth ventricle. case report. j neurosurg 44:386–389pubmedgoogle scholar 42. shuangshoti s, piyaratn p, viriyapanich pl (1968) primary rhabdomyosarcoma of cerebellum—necropsy report. cancer 22:367–371pubmedgoogle scholar 43. smith mt, armbrustmacher vw, violett tw (1981) diffuse meningeal rhabdomyosarcoma. cancer 47:2081–2086pubmedgoogle scholar 44. stone jl, zavala g, bailey ot (1979) mixed malignant mesenchymal tumor of the cerebellar vermis. cancer 44:2165–2172pubmedgoogle scholar 45. tomita t, gonzalez-crussi f (1984) intracranial primary nonlymphomatous sarcoma in children: experience with eight cases and review of the literature. neurosurgery 14:529–540pubmedgoogle scholar 46. vecchio f, giordano r, zanche ld, caro rd, maggioni f, zanchin g (1988) intracranial sarcoma with reactive glioma: a clinicopathological case report. eur neurol 28:301–305pubmedgoogle scholar 47. waga s, matsushima m, ando k, morii s (1972) intracranial chondrosarcoma with extracranial metastases. case report. j neurosurg 36:790– 794pubmedgoogle scholar 48. younis ga, sawaya r, demonte f, hess kr, albrecht s, bruner jm (1995) aggressive meningeal tumours: review of a series. j neurosurg 82:17–27pubmedgoogle scholar 49. zwartverwer fl, kaplan am, hart mc, hertel ga, spataro j (1978) meningeal sarcoma of the spinal cord in a newborn. arch neurol 35:844–846pubmedgoogle scholar. 06_paper romanian neurosurgery (2015) xxix 4: 427 434 427 doi: 10.1515/romneu-2015-0058 spontaneous cervical epidural hematoma with incomplete brown-sequard syndrome mugurel radoi1, florin stefanescu1, ram vakilnejad2, lidia gheorghitescu2 1“carol davila” umph, bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases, bucharest 2neurosurgical department of the national institute of neurology and neurovascular diseases, bucharest introduction cervical epidural hematoma, without a traumatic etiology, is a rare clinical entity. in the neurosurgical literature it is called spontaneous cervical epidural hematoma (sceh) and, both the venous and arterial theories provide plausible explanations for its occurrence. the potential causes include coagulopathies, hypertension, vascular malformations and conditions that increase venous pressure such as sneezing, coughing or vomiting (25). the clinical presentation is usually characterized by acute radicular pain followed by progressive paralysis and sensory loss of symmetric nature. the brown-sequard syndrome is an exceptional result of sceh (7, 16, 28). surgical evacuation of the hematoma is the standard therapy, although conservatively treated sceh cases have been reported (9). we presented a case of a cervical spontaneous epidural hematoma presenting with an incomplete brown-sequard syndrome and treated by surgical evacuation. case report the patient, a 68-year old female, presented to our hospital with a history of acute neck pain and left side weakness, symptoms that started 3 weeks earlier, after she did a mild physical effort. she complained pain on her posterior neck and left shoulder while neck rotation. her past medical history was significant for hypertension, she had taken aspirin due to chronic cardiac ischemia. on neurologic examination, she had 3/5 motor strength in muscle groups of the left upper and lower limbs and reduced sensation of pain contralaterally below the c5 level (incomplete brown-sequard syndrome). sensation of light touch was present. deep tendon reflexes were brisk and plantar response was extensor on the left side. she had normal coagulation values. at her first admission, in another hospital, the patient, known with a prolonged history of hypertension, was misdiagnosed as infarction on right hemisphere and was delayed in diagnosis. 428 radoi et al spontaneous cervical epidural hematoma with incomplete brown-sequard syndrome a computed tomography (ct) scan of the brain was normal. cervical magnetic resonance imaging (mri) showed a large left posterolateral extradural mass extending from c2 to c6 with spinal cord compression and rightward displacement. the mass demonstrated low signal intensities on t1weighted images and intermediate to high signal intensities on t2-weighted images (figures 1a, 2a and 3a). no contrast enhancement or signs or signs of vascular malformation were found. a cervical spinal angiography was performed in order to diagnose an underlying pathology but it was normal (figure) the patient underwent a c3-c5 hemilaminectomy of left side. a dark blood clot was noted in the epidural space and was evacuated under microscope. no evidence of vascular malformation was found. figure 1 (a) preoperative t1 weighted saggital images (black arrows) show intermediate signal left extradural mass extending from c2-c6 (higher intensity that the signal of the spinal cord) (b) postoperative t1 weighted saggital images after evacuation of hematoma (white arrows) romanian neurosurgery (2015) xxix 4: 427 434 429 doi: 10.1515/romneu-2015-0058 figure 2 (a) preoperative t2 weighted saggital image show intermediate signal of an extradural mass extending from c2-c6 (black arrows); posterior compression of the spinal cord with interruption of the intense signal of the csf at this level. (b) postoperative t2 weighted saggital images after evacuation of hematoma and decompression of cervical spinal cord; presence of the intense signal of csf in the posterior aspects of the c2-c6 vertebrae (white arrows) 430 radoi et al spontaneous cervical epidural hematoma with incomplete brown-sequard syndrome figure 3 (a) preoperative t2 weighted axial images show intermediate signal of an left posterolateral extradural mass with spinal cord compression (black arrow), (b) postoperative t2 weighted axial images showing no compression on cervical spinal cord and resumption of csf flow after evacuation of the hematoma (white arrow) postoperatively, the patient recovered well until prompt return of her sensory symptoms. her motor function gradually improved within the next 48 hours. postoperative mri showed complete evacuation of the hematoma (figures 1b, 2b and 3b). on her six months follow-up, she was doing well, with no residual neurological deficits. discussion spontaneous cervical epidural hematomas (scef) are well recognized but rare surgical conditions (28). it was first described in 1869 by jackson (19) and the first surgical approach was performed in 1946 by ver brugghen (31). one of the first extensive reviews on spontaneous spinal epidural hematoma was reported by groen in 1996 (15). a more recent one, by kim et al in 2011 (9), identified a total of 107 cases of spontaneous spinal epidural hematoma published in neurosurgical series between 1996 and 2011. in the majority of reports, the hematoma is considered to be “spontaneous” if it develops without known case (i.e. trauma, fractures, spinal lesion or medical procedure). usually, sceh develops because of a predisposing condition, including anticoagulant therapy (11, 24), vascular malformations (5,30), neoplasm (17), immunovasculitis (10,20), hypertension (11),or bleeding tendencies of all kinds (12,26). however, the cause of bleeding remains unknown in 40% of the cases and are called idiopathic spontaneous cervical epidural hematoma (11). in our case, the patent had a medical history for hypertension.. it is still debated if the bleeding that lead to the occurrence of spontaneous epidural hematoma is arterial or venous. both the venous and arterial theories provide plausible explanations, but, most likely, the sceh results from a venous bleeding, because the epidural veins have thin walls and no valves (32). the posterior epidural venous plexus (22) lies directly between the dura and the ligamentum flavum making rupture more likely than in the anterior venous plexus which is covered by the posterior longitudinal ligament. given that the epidural venous plexus is devoid of valves, sudden changes of romanian neurosurgery (2015) xxix 4: 427 434 431 doi: 10.1515/romneu-2015-0058 intra-thoracic and intra-abdominal pressure, after valsalva maneuvers can determine lacerations in the venous plexus, causing epidural hemorrhage. in contrast, beatty suggested that bleeding occurs from epidural arteries (6). he argued that hemorrhage from an epidural vein would not create enough pressure to compress the dural sac, observing that the normally expanded epidural sac may tamponade epidural bleeding, encountered during surgical procedures (6). beatty and winston sustained that is more logical that epidural arteries are likely causative, especially in the light of the compression of the cord that can occur and the posterolateral location of most cervical epidural hematomas (2). they have explained that the c6 and c7 segments are the most common region of cervical epidural hematomas and extreme compelling movements could therefore cause tearing of these arteries (2). lowery has defined an active bleeding arterial structure under the hematoma in one of the operated cases (21). the clinical picture of sceh is characterized by sudden onset of neck pain, with or without radicular radiation, followed by rapidly progressive symptoms and signs of cord compression. rarely, however, patients may present with slowly progressive symptoms which can lead to difficulties in diagnostic (3). pain radiation varies according to the localization of the hematoma on the spinal cord and nerve roots. the second most common symptom is weakness of the limbs, seen below the compressed spinal cord. the neurologic deficits may be mild or complete (11,24) and, based on the location of the hematoma, they can be bilateral, show features of a brown-sequard syndrome (7,30), or, rarely, anterior cord syndrome (11). paresis increase within minutes or days, or, rarely, recover spontaneously (2). we presented the case of a female patient, with the neurological signs of an incomplete brown-sequard syndrome. cervical epidural hematoma presenting with brown-sequard syndrome is a rare condition (8), but has been reported in the literature (16, 27, 28, 32). this unusual presentation can be confused with a cerebrovascular accident, as in our case, when the patient, known with a prolonged history of hypertension, was misdiagnosed as infarction on right hemisphere and was delayed in diagnosis. acute cervical disc herniation, transverse myelitis, spondylitis, epidural neoplasia, dissection of aortic aneurysm should be considered in the differential diagnosis (1, 28). magnetic resonance imaging (mri) is considered the first choice of diagnostic method for sceh. it gives accurate information not only concerning the location and extension of the hematoma, but also the degree of the cord compression, as well as any preexisting lesion that might have been the source of the bleeding, such as arteriovenous malformations (18, 28). before 48 hours, the signal intensity of the acute cervical epidural hematoma on t1-weighted images is varying from hyper-intense to iso-intense. on t2weighted images, acute cervical epidural hematoma demonstrates focal hypo-intensity, in contrast with the heterogenous hyperintensity of the cord. old hematoma (more than 21 days) shows, in contrast, high signal 432 radoi et al spontaneous cervical epidural hematoma with incomplete brown-sequard syndrome intensity on the t2w1 and mixed (low and iso-) signal intensity on t1w1 (18). on t1weighted post-contrast images, peripheral contrast enhancement due to adjacent dural hyperemia may be seen (4, 28). the t1 and t2 signals of sceh vary based on the clot, age, size and oxygenation (14). mri has greatly facilitated the diagnostic of sceh allowing for more cases, with a benign natural course to be diagnosed (20). surgery is the treatment of choice in sceh. emergent surgical decompression and evacuation of the hematoma is needed, especially in cases with neurological deterioration. some authors consider that total laminectomy is the best choice as a surgical approach but hemilaminectomy on two or third cervical levels, can be preferred according to the localization of the hematoma (1, 28, 32). in our case, we performed a c3-c5 left hemilaminectomy, and under microscope magnification we completely evacuate the left posterolateral epidural hematoma. in recent years, there have been increased reports of spontaneously resolving spinal epidural hematomas, due to quick diagnosis by higher resolution mri (9). a conservative treatment under close neurologic observation is recommended for patients with no, or mild neurologic deficits and for patients who show definite progressive improvement prior to the mri diagnosis of sceh (9, 13, 27). the major factors determining neurological recovery after spontaneous cervical epidural hematoma are the localization of the hematoma (cervical segments involved), the preoperative neurological condition and the operative interval (9, 15). initial neurological dysfunction was the strongest predictor for a patient’s outcome. patients presenting with severe or worsening conditions usually did not recover as wells as those presenting with minor symptoms (9). furthermore, the timing of decompressive laminectomy and evacuation of the hematoma was more significant factor in patients initially presenting with frankel grades a or b. patients with a better neurological function (scores of d or e) frequently showed substantial improvement regardless of time of operation (9, 28, 32). in complete preoperative sensori-motor loss, surgery within 36 hours correlated with favorable outcome; in incomplete preoperative sensori-motor deficit, favorable outcome correlated with surgery within 48 hours (15). also, those patients with a shorter interval to operation had a better prognostic than those with longer intervals. cho y.e et al (29) and kim dk et al (9), on a large reviews of cases with spontaneous spinal epidural hematomas, showed that neurological outcome was good in those patients that had their hematoma evacuated within 24 hours, and the patients with a preoperative incomplete neurological deficits, who had a surgical operation performed within 12 hours, had an excellent surgical outcome. in our case, surgery was performed within 36 hours after admission, but eight days after the development of hemiparesis. postoperative, a gradual recovery in neurological status and improvement of sensation and motricity was observed within the next 48 hours. even patients with significant comorbidities did achieve functional recovery, romanian neurosurgery (2015) xxix 4: 427 434 433 doi: 10.1515/romneu-2015-0058 comparable with patients without comorbidities. a relevant past medical history does not predict poor outcome, but may be associated with worse initial neurological dysfunction than others (9, 20). conclusions spontaneous cervical epidural hematoma is a rare neurosurgical emergency and prompt diagnosis using cervical mri is very important. both the venous and arterial theories provide plausible explanation for the occurrence of sceh. the development of a brown-sequard syndrome due to a sceh is very are, and is usually incomplete. the clinical presentation of the cervical epidural hematomas with hemiparesis can be misdiagnosed as a cerebrovascular accident. surgical decompression must be preferred in patients presenting with neurological deterioration. patients with less initial neurological deficits and those with shorter time to operation show better neurological prognostic. in our opinion, a prompt diagnostic and an appropriate surgical treatment is essential for a favorable functional neurological recovery. correspondence mugurel radoi “carol davila” umph, bucharest; neurosurgical department of the national institute of neurology and neurovascular diseases bucharest e-mail: muguradoi@yahoo.com references 1.adamson dc, bulsara k, bronec pr. spontaneous cervical epidural hematoma: case report and literature review. surg neurol 62(2):156-160, 2004. 2.beatty rm, winston kr. spontaneous cervical epidural hematoma. a consideration of etiology. j neurosurg 61:143-148, 1984. 3.boyd hr, pear bl. chronic spontaneous spinal epidural hematoma. j neurosurg 36:239-242, 1972. 4.crisi g, sorgato p, scarpa f, falasca a, angiari p. gadolinium-dtpa-enhanced mri imaging in the diagnosis of spinal epidural hematoma. neuroradiology 32:64-6, 1990. 5.d’angelo v, bizzozero l, talamonti g, ferrara m, colombo n. value of magnetic resonance imaging in spontaneous extradural hematoma due to vascular malformation: case report. surg neurol 34:343-4, 1990. 6.di lorenzo n, rizzo a, fortuna a. spontaneous spinal epidural hematoma: preoperative diagnosis by mri. clin neurol neurosurg 92:357-9, 1990. 7.egido herrero ja, saldana c, jimenez a, vazquez a, varela de seijas e, mata p. spontaneous spinal epidural hematoma with brown-sequard syndrome and spontaneous resolution. case report. j neurosurg sci 36:117-179, 1992. 8.emery dj, cochrane dd. spontaneous remission of paralysis due to spinal extradural hematoma: case report. neurosurgery 23:762-4, 1988. 9.feodor m, kim es, ding k, muizelaar jp, kim kd. spontaneous spinal epidural hematoma: a retrospective study on prognostic factors and review of the literature. korean j spine 8(4):272-282, 2011. 10.flaschka g. akutes spinales epiduralhamatom bei imunvaskulitis. neurochirurgia (stuttg) 25:174-6, 1982. 11.foo d, rossier ab. preoperative neurologic al status in predicting surgical outcome of spinal epidural hematomas. surg neurol 15:389—401, 1981. 12.futawatari k, katsouka s, kowada m. a case of spinal epidural hematoma associated with idiopathic thrombocytopenic purpura. no shinkei geka 19:1187-90, 1991 13.galzio rj, zenobii m, d’ecclesia g. spontaneous spinal epidural hematoma: report of a case with complete recovery. surg neurol 14:263-265, 1980. 14.gomori jm, grossman ri, yu-ip c, asakura t. nmr relaxation times of blood: dependence on field strength, oxidation state, and cell integrity. j comput assist tomogr 11:684-90, 1987. 15.groen rj, van alphen ha. operative treatment of spontaneous epidural hematomas: a study of the factors 434 radoi et al spontaneous cervical epidural hematoma with incomplete brown-sequard syndrome predicting postoperative outcome. neurosurgery 39(3):494-509, 1996. 16.hancock jb, field em, gadam r. spinal epidural hematoma progressing to brown-sequard syndrome: report of a case. j emerg med 15:309-312, 1997. 17.harris d, fornasier v, livingstone k. hemangiopericytoma of the spinal canal: report of three cases. j neurosurg 49:914-920, 1978. 18.imamura t, tsuburaya k. chronic cervical epidural hematoma diagnosed by magnetic resonance imaging. no to shinkei 42:857-61, 1990. 19.jackson r. case of spinal apoplexy. lancet 2:538-539, 1869. 20.jamjoom zab. acute spontaneous spinal epidural hematoma: the influence of magnetic resonance imaging on diagnosis and treatment. surg neurol 46:345-9, 1996. 21.lowrey jj. spinal epidural hematomas: experiences with three patients. j neurosurg 16:508-513, 1959. 22.marmey g, doyon d, david p. diagnostic irm d’un hematome epidural cervical: apropos d’une observation. j radiol 71:549-553, 1990. 23.matsumura a, namikawa t, hashimoto r, okamoto t, yanagida i, hoshi m, et al. clinical management for spontaneous spinal epidural hematoma: diagnosis and treatment. spine j 8:534-537, 2008. 24.mattle h, sieb jp, rohner m, mumenthaler m. nontraumatic spinal epidural and subdural hematomas. neurology 37:1351-6, 1987. 25.miyagi y, miyazono m, kamikaseda k. spinal epidural vascular malformation presenting in association with spontaneously resolved acute epidural hematoma. j neurosurg 88:909-911, 1998. 26.muller h, schramm j, roggendorf w, brock m. vascular malformations as a cause of spontaneous spinal epidural hematoma. acta neurochir (wien) 62:297-305, 1982. 27.neetu r, chandra ms, rashmi m. cervical spinal epidural hematoma with acute brown-sequard presentation. neurol india 54:107-108, 2006. 28.ofluoglu e, ozdemir a, toplamaoglu h, sofuoglu e. spontaneous cervical epidural hematoma causing brownsequard syndrome: case report. turkish neurosurgery vol. 19 (1):99-102, 2009. 29.shin jj, kuh su, cho ye. surgical management of spontaneous spinal epidural hematoma. eur spine j 15(6):998-1004,2006. 30.takano s, saitoh m, motoori t, miyasaka y, yoda k, takagi h. a case of acute cervical spinal epidural hematoma caused by extradural arteriovenous malformation. no shinkei geka 21:1119-23, 1993. 31.ver brugghen a. extradural spinal hemorrhage. ann surg 123:154-159, 1946. 32.yoon bh, park sk, jung ss, park ms, kim s-m, chung s-y, chung j-c, kim hk. spontaneous cervical epidural hematoma causing brown-sequard syndrome. korean j spine 9(3):297-299, 2012. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 473-477 doi: 10.33962/roneuro-2019-075 www.journals.lapub.co.uk/index.php/roneurosurgery quality and reliability of the information on youtube videos about botox injection on spasticity aysel gürcan atci i̇stanbul baltalimanı bone and joint research and education hospital, physical medicine and rehabilitation department, turkey abstract background: this study analyzes the botox injection on spastisite videos that have the highest views and likes on youtube, and attempts to reveal the video qualities in order to contribute to the literature. methods: for review, “botox injection on spastisite” was written to the standard youtube search bar, and the videos with the highest views were ranked using advanced search preferences. the 69 most widely viewed videos were watched and scored by one physician. results: the mean modified discern score of the videos was 2,66+/-1,032 (the lowest: 1; the highest: 4) while the mean gqs score was 2,876+/-1,06 (the lowest: 1; the highest:4). in addition, the mean discern score and the mean gqs value were 3,51 and 3,82, respectively, for the informational videos that were uploaded by health professionals but did not contain actual surgery. conclusion: we think that medical associations and state authorities in medicine should check the validity and accuracy of the information on the internet and should support the society in access to the most correct information. introduction in recent years, the rate of receiving information from the internet has increased in almost every subject in daily practice due to the developing and increasing frequency of internet usage. patients and health professionals apply to the internet for information on many healthrelated issues. among these sources of application, youtube is the biggest video archive website in the world and attracts 95% of internet users with 30 million active users every day(1). there are also many health-related videos in the archive. generally, patients apply to a physician and get detailed information about recommended treatments but they are also inclined to watch on youtube the operation to be carried out. therefore; the quality of a video, the persons who shot it and whether such video contains correct information are matters of great importance. spasticity is characterized by an increase in muscletone resulting from upper motor neuron lesions. it is a common condition in the upper keywords spasticity, botox, youtube corresponding author: aysel gürcan atci i̇stanbul baltalimanı bone and joint research and education hospital, physical medicine and rehabilitation department, turkey lesyag2002@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 474 aysel gürcan atci and lower extremity muscles after stroke in general cerebrovascular events (2). it is observed in 16% of patients after stroke (3). the increase in muscletone is a condition that makes mobilization and positioning difficult, delaying recovery to function that makes patients' daily life difficult. spasticity is tried to be treated by various methods. botulinium toxin is the most common invasive treatment method. this study analyzes the botox injection on spastisite videos that have the highest views and likes on youtube, and attempts to reveal the video qualities in order to contribute to the literature. material and method search strategy and data collection for review, “botox injection spastisite ” was written to the standard youtube search bar, and the videos with the highest views were ranked using advanced search preferences. the 69 most widely viewed videos were watched and scored by 1 physician. inclusion and exclusion criteria the videos that were not in english language or did not have subtitles or speech or that did not explain the operation were eliminated. variables extracted views, upload dates, like rates, uploaders, video lengths, comment numbers, like numbers and dislike numbers were identified as well as whether they were actual or animated videos. inaddition, video powerindex (vpi) values [(number of likes/number of likes þ number of dislikes) 100] were calculated to evaluate thepopularity of the videos. assessment of usefulness all videos were independentlye valuated by one physician for usefulness and categorized into the following mutuall exclusive categories. 1. useful information : videos designated as useful information were mainly focused on information delivery. they contained accurate information and were useful for learning how to do botox. 2. misleading information :the videos contained incorrect information or did not contain usefull information. 3. useful patient opinion: the videos in this group have the discern and gqs scores as 3 or above and clearly explain the patient experiences, the performance of operations, and preoperational and postoperational pain scores. 4. misleading patient opinion: the videos in this group have the discern and gqs scores as 2 or lower and do not clearly explain patient experiences (table 1). scoring system video reliability was scored using a modified fivepoint discern tool (4), which was adapted from the original discern toolforthe assessment of written healthin formation by charnock et al(5). the overall quality of each video was rate dusing the five-point global qualityscale (gqs). the gqs was developed as an evaluation tool for websiteresourcesand it assesses the flowandease of use of the information presented online, and the quality of video (table 2) [4]. table 1: analyses of video characteristics by usefulness category usefulli̇nformation (gr1) misleadingi̇nformation (gr2) usefullpatientopinion(g r3) misleadingpatientopinio n(gr4) video number n:11(15,9%) n:33(47,8%) n:1(2%) n:24(34,7%) viewspeerday 2,21 +/-0,31 1,257+/-0,12 4,32 +/-1,55 3,4+/-1,3 video lenght 24,562min(2,0432,01 min) 6,50 min(0,20-7,17 min) 12,31 min 7,25 min(4,01-12,08 min) like 22+/-14 18,14+/-12,1 29,08+/-2,01 33,4+/-3,33 dislike 1,32+/-0,45 2,74+/-1,1 1,02+/-0,32 1,47+/-1,21 comments 26,8+/-2,33 27,2+/-1,33 92,1+/-7,41 113,4+/-11,2 discernscore 3,4 2,2 3,3 0,5 gqs score 3,9 2,3 3,8 1,6 475 quality and reliability of the information on youtube videos about botox injection on spasticity statistical analysis the results were statistically analysed using a nonparametric kruskal–wallis test. a p value of 0.05 or less was considered significant. the statistical package for thesocial sciences version 23 software (spss, chicago, il, usa) was used for all statistical analyses (table 2). gr1-gr2 gr1-3 gr1-4 gr2-3 gr2-4 gr3-4 discernscore p value 0,518 0,708 0,001 0,652 0,332 0,0018 gqs score p value 0,125 1,00 0,001 0,069 0,852 0,001 * values of p 0,05 was accepted table 2: pairwise comparisons of video groups according to usefulness results 69 videos with the highest views were analyzed while 31 videos were later excluded from the analysis for they were neither in english language nor contained subtitles. there were 36 technically-narrated and actual videos by professionals, 25 patient view and 8 videos were botox processing. the oldest video was uploaded in 2010 while the newest one was added to the system in 2019. the videos were uploaded by hospitals (25 videos), health professionals and physicians (20 videos), and personal accounts (21 videos) (figure 1). figure 1: uploaded videos by youtube the mean time of the video lengths was 41,623 sec (the shortest: 19 sec; the longest: 54.16 sec) , and the mean view was 88,293+/-9,75 (the least viewed: 4075; the most viewed: 825.731). the daily mean view of the videos was 42.444+/-72,77 (the least viewed: 5; the most viewed: 37405). the mean like rate was 23.27+/-,52 (the most liked:360 the least liked: 0), and the mean dislike rate was 1,34+/-0,21 (the most disliked: 15; the least disliked: 0).as for the comments, the mean number was 4,54+/-1,23 (the least commented: 0; the most commented: 65).similarly, video power index (vpi) analyses showed that the mean vpi value of the 69 videos was 0,71+/-0,14 . the mean modified discern score of the videos was 2,88+/-0,318 (the lowest: 1; the highest: 4) while the mean gqs score was 3,56+/-1,206 (the lowest: 1; the highest:4) . in addition, the mean discern score and the mean gqs value were 2,13 and 3,25, respectively, for the informational videos that were uploaded by health professionals. similarly, the mean discern score and the mean gqs value were 1,33 and 1,71, respectively, for the patient videos in which personal experiences were shared. no statistically significant correlation was found between the gqs and discern scores according to both researchers and vpi values (p > 0.05). discussion youtube is a video hosting site headquartered in san bruno / california, usa. the site was founded in 2005 and started to be operated by google in 2006. the primary purpose of the site is to download and share videos on any subject. many health professionals, hospitals and patients share more intensive videos on medical issues. while using these videos to make inferences from the experience of the patients, the method and possible risks of the treatment to be performed by patients and their relatives; health professionals try to learn the interventional procedure live. however, there may also be incorrect, low-quality and prejudiced videos on this platform where everyone can upload videos free-ofcharge without being subject to any inspection. pubmed reviews reveal 1089 studies that measure the quality of youtube videos on health issues(8,9). physician %23 health channe 56% patient 21% physician health channe patient 476 aysel gürcan atci the first of these is a study from 2007 that evaluate the training of health professionals (7). botulinium toxin-related treatment applications started in 1980. it has been used in the treatment of spasticity for the last 15 years. botulinum a is a successful method used to increase theeffectiveness of pain, restlessness and physical therapy in spasticity(10,11). botulinium a toxin is the most common market name in the world as botox © and dysport ©. botox application is performed in spasticity in our country. when theliterature is screened, there are 3 controlled randomized studies on botox(12,13,14). in our study, it was to question whether a patient with spasticity who is planned to use botox is able to get reliable information when watching the youtube video in order to obtain information and ideas before the procedure. apart from this, it is aimed to evaluate the quality of the information that the health professionals who want to make the initiative can learn theoretically and visually from the videos. the literature review we made did not produce any study concerning the subject in question. there are various scales and measures to evaluate the quality of the information in videos and on the internet. in this study, one researcher assesses the videos using modified discern scoring system, global quality index and video power index (vpi). according to the analysis of the 69 videos with the highest views and vpis, it was found out that the videos presented weak and poor-quality information to patients, patient relatives and professionals who desire to learn the narrated operation. however, it was also observed that 60.9% of the videos were uploaded by health professionals and institutions. in 8 (11.5%) videos with actual surgeries, it was seen that the average time was 15,24 seconds, the operators did not satisfactorily explain the methods before and after the operations, they did not clearly specify alternative treatments and effects and possible complications, and the videos were not supported with subtitles. it was observed that the videos did not explain the operations in simple language to convey the processes to patients and patient relatives but only the course was expressed, and that there were dialogs with patients during operations. furthermore, it was revealed that 11 (15.9%) videos with the highest results of evaluation were animated or notional surgery videos, made theoretical powerpoint presentations and were supported with anatomic cross-sections. when the 5 most watched videos were examined, it was seen that there were 3.73 impressions per day on average and these videos belonged to hospitals installing botox application. the videos with the highest vpi values but had 2 or below in discern and gqs scoring were found to convey inadequate information. in contrast with the foregoing, the videos with the highest scores had 2,21 views every day, on average, and did not appear on the first page when searched on youtube. however, the videos that had the highest views but contained insufficient information appeared on top in youtube searches. apart from these, the video comment analyses demonstrated that the highest number of comments were entered to the uploads with patient experiences. in the content of the comments, it was seen that the regression rate of complaints and the duration of the complaint-free period were examined. accordingly, the videos with the highest like numbers were those that contained patient remarks. the videos were divided into 4 groups in terms of usefulness, and only 11 videos were found to contain useful and valid information. all these were uploaded by health professionals and were generally about physician remarks. the mean time of these videos was 24,562 seconds. useful patient remarks were identified only in 1 videos, and their mean view time was 12,31 seconds. the limitations of this study include the crosssectional design (popularity based on number of views changes constantly), and the inclusion of only the 69 most widely viewed videos (an arbitrary cut point). conclusion as a result, it may not always be accurate to believe that the medical videos with high view, comment and like numbers on youtube contain reliable, comprehensible and correct information. although the access to information and videos on medical subjects is very easy in today’s world, it is more appropriate to apply to experienced health professionals in order to get information. we think that medical associations and state authorities in medicine should check the validity and accuracy of the information on the internet and should support the society in access to the most correct information. 477 quality and reliability of the information on youtube videos about botox injection on spasticity compliance with ethical standards this study does not include any human participants or animals. videos that were available to every one were evaluated for this study. therefore, ethics committee approval was not required. table 3: discern and gqs modifiy discern (1 point per question answered yes) 1. is the video clear, concise, and understandable? 2. are valid sources cited? (from valid studies, physiatrists or rheumatologists) 3. is the information provided balanced and unbiased? 4. are additional sources of information listed for patient reference? 5. does the video address areas of controversy /uncertainty? global quality scale 1. poor quality, poor flow, most information missing, not helpful for patients; 2. generally poor, some information given but of limited use to patients; 3. moderate quality, some important information is adequately discussed; 4. good quality good flow, most relevant information is covered, useful for patients; 5. excellent quality and excellent flow, very useful for patients; references 1. youtube. youtubestatisticpage. https://www. omnicore agency.com/youtube-statistics/. accessed october 25, 2018. 2. lance jw. symposium synopsis. in: feldman rg, young rr koella wp, editors. spasticity: disordered motor control. chicago: year book medical publishers. 1980. p. 485-94. 3. turkel c, sissins p. functional activities affected by poststroke spactisity (abstract). arch phys med rehabil 2004;85:e52. 4. singh ag, singh s, singh pp (2012) youtubeforinformation on rheumatoidarthritis—a wakeupcall? j rheumatol 39(5):899–903. https://doi.org/10.3899/jrheum.111114 (epub 2012 apr 1) 5. charnock d, shepperd s, needham g, gann r (1999) discern: an instrumentforjudgingthequality of writtenconsumerhealthinformation on treatmentchoices. j epidemiolcommunityhealth 53(2):105–111 6. bernard a, langille m, hughes s, rose c, leddin d, veldhuyzenvanzanten s (2007) a systematicreview of patientinflammatoryboweldiseaseinformationresources on the world wide web. am j gastroenterol 102(9):2070– 2077 7. skiba dj (2007) nurseducperspect. nursingeducation 2.0: youtube 2007 mar-apr;28(2):100-2. 8. ovenden cd, brooks fm. anterior cervical discectomy and fusionyoutubevideos as a source of patient education. asianspine j. 2018;12:987-991. 9. drozd b, couvillon e, suarez a. medical youtube videos and methods of evaluation: literature review. jmir mededuc. 2018;4:e3. 10. sheean g. botulinum toxin treatment of adult spasticity. a benefitrisk assessment. drug safety 2006;29:31-48. 11. naumann m, toyka kv, moore p. history and current applications of botulinum toxin: from poison to remedy. in: naumann p, moore p, editors. handbook of botulinum toxin treatment. 2nd ed. cambridge (ma). blackwell science, 2003. p. 3-8. 12. richardson d, sheean g, werring d, desai m, edwards s, greenwood r, et al. evaluating the role of botulinum toxin in adults. j neurol neurosurg psychiatry 2000;69:499-506. 13. simpson dm, alexander dn, o’brien cf, tagliati m, aswad as, leon jm. botulinum toxin type a in the treatment of upper extremity spasticity: a randomized, double-blind, placebo-controlled trial. neurology 1996;46:1306-10. 14. brashear a, gordon mf, elovic e, kassicieh vd, marciniak c, do m, et al. intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke. n engl j med 2002;347:395-400 balasad_acute 214 | balasa et al acute cerebral mca ischemia acute cerebral mca ischemia with secondary severe head injury and acute intracerebral and subdural haematoma. case report d. balasa1, a. tunas1, i. rusu1, a. hancu2, g. butoi3, v. gramanschi4 1neurosurgery, “sfantul andrei” hospital, constanta, romania 2neurology, “sfantul andrei” hospital, constanta, romania 3medimar clinic, constanta, romania 4resuscitation department, “sfantul andrei” hospital, constanta, romania abstract: generally, according to international literature, cerebral ischemia is a secondary posttraumatic lesion produced by direct compression in the context of a cerebral herniation syndrome or indirect by vasospasm produced by posttraumatic subarachnoid, subdural or intraventricular hemorrhages. we present the case of a patient with an acute mca ischemia with severe head injury due to a fall with subsequent intracranial acute intracerebral and subdural hematoma which evolved with acute left uncal, parahipocampal and subfalcinecerebral herniation (coma, gcs 6, left mydriasis, right severe hemiparesis). surgical emergency aspiration of the hematomas was performed. postoperative treatment of cerebral ischemia and residual hematomas was properly done. we consider important and underdiagnosed the association of cerebral ischemia and secondary posttraumatic brain injuries. abbreviations: mca-middle cerebral artery, gcsglasgow coma scale, ica-internal carotid artery, pca-posterior cerebral artery, aca-anterior cerebral artery. conclusion: we present a case of a patient with an acute mca ischemia with secondary head injury due to a fall with subsequent intracranial acute intracerebral and subdural hematomas. surgical emergency aspiration of the hematomas was performed. the treatment was performed for both lesions (cerebral ischemia and posttraumatic hematomas) with vitamins b, neurotrophycs, pain killers, antibiotics. unfortunately, due to aggravation of the mendelson syndrome, the patient died 7 days later. key words: cerebral ischemia, secondary head injury, acute intracerebralsubdural hematoma. romanian neurosurgery (2016) xxx 2: 214-218 | 215 introduction generally, according to the international literature, cerebral ischemia is a secondary posttraumatic lesion produced by direct compression in a cerebral herniation syndrome, by perfusion failure in cerebral micro or macro circulation, by increased icp due to swelling or expanding hemorrhagic mass (2), and or indirect by vasospasm produced by posttraumatic subarachnoid, subdural and intraventricular hemorrhages. we present the case of a patient with an acute mca ischemia with cranial trauma due to a fall with subsequent intracranial acute intracerebral and subdural hematomas who evolved with acute left uncal, parahipocampal and subfalcine herniation. case report a 66 year old female was admitted as an emergency after a fall with secondary head injury, followed by rapid deterioration of neurologic status (drowsiness-stupor-coma), vomiting, right severe hemiparesis. within a few hours, gcs reached 6 points, with left eye mydriasis. the patient has 3 vomiting episodes which lead to suspicion of incidental aspiration of vomitus. emergency ct scan revealed an acute intracerebralfrontotemporo-parietal hyperdense hemorrhagic lesion (1) and acute fronto-parietal subdural haematoma on a large perilesional hypodense lesion with aspect of an acute ischemia in left mca territory, left uncal, parahipocampal and subfalcine herniation (1) emergency surgery was performed (fronto-parietal craniectomy, aspiration of intracerebral and subdural hematomas). after a 36 hours of neurological improvement (the patient recovered from superficial coma and became obnubilated gcs11, recovery of the motor function on the right side, moderate hemiparesis), the patient deteriorated (gcs 9, became hypertensive, with right hemiplegia). new emergency ct scan revealed acute partial ischemia on mca left territory and a small amount of intracerebral hematoma, significantly smaller than the preoperative scan, and a small acute subdural residual hematoma. figure 1 | figure 2 preoperative ct scan: acute left fronto-temporoparietal intracerebral haematoma and left acute subdural frontal hematomas (black double peak arrows). left uncal and parahipocampal herniation (black arrow).large hypodense lesion with aspect of stroke within the left mca territory around intracerebral hematoma (white arrow) 216 | balasa et al acute cerebral mca ischemia figure 3 | figure 4 preoperative ct scan: acute left fronto-temporoparietal intracerebral hematoma and acute left subdural frontal haematomas (black double peak arrows).large hypodense lesion with aspect of a stroke in the left mca territory (white arrow).left subfalcine herniation (black arrow) figure 5 | figure 6 postoperative ct scan: large hypodense lesion with aspect of stroke in left mca area (white arrow). small amount of intracerebral hematoma (black double peak arrow) the patient was treated simultaneously for both lesions (mca ischemia and residual posttraumatic intracranial hematomas) with neurotrophic, aspirin, vitamin b, antibiotics. despite the correct treatment the patient dies 3 days later due to aggravation of mendelson syndrome. discussion generally, according to international literature, cerebral ischemia is a secondary posttraumatic lesion produced by direct compression in a cerebral herniation syndrome, by perfusion failure in cerebral micro or macro circulation, by increased icp due to swelling or expanding hemorrhagic mass(2) and or indirect by vasospasm produced by posttraumatic subarachnoid, subdural and intraventricular hemorrhages. we have not found a similar case in medical literature. the patients with stroke has romanian neurosurgery (2016) xxx 2: 214-218 | 217 a relative high risk of falling (6). after ugur et all (6) the patients between 55-69 years have the highest risk of falling. we believe that the association between cerebral ischemia and severe troubles of equilibrium with a secondary cerebral trauma, intracranial hematomas is underdiagnosed. but, for clinical and radiological reasons this coexistence can be proved with great difficulty: •clinical reasons: the patients are admitted in the hospital with deterioration of consciousness, hic syndrome, cerebral herniation syndromes produced by the coexistence of intracranial posttraumatic lesions and cerebral ischemia. for these reasons anamnesis is not always clear to argue the 2 cerebral entities (cerebral ischemias and intracranial hematomas) and precise succession. •radiological reasons: is well known that ct is the golden standard for head injuries (1, 4). but the images of cerebral ischemia may by invisible or indirect in the first 24 hours on ct, or may be masked by the presence of the traumatic intracranial lesions: intracerebral hematoma, subdural, extradural hematoma. head trauma after stroke generally have small consequences, skin abrasions, ecchymosis(6).we present the case of a 66 year old lady which was admitted as an emergency, after a fall, with secondary cranial impact. the patient described hic syndrome (frequently vomiting), signs of left uncal, parahipocampal and subfalcine herniation syndromes (severe hemiparesis, left eye mydriasis, coma gcs 6 points). emergency head ct scan revealed an acute intracerebralfronto-parietal lesion and acute fronto-parietal subdural hematoma surrounded by a large perilesional hypodense lesion with the aspect of an acute stroke within the left mca territory, left uncal, parahipocampal and subfalcine herniation(1,5). based on anamnesis and preoperative ct scan we performed emergency surgery of the hematomas and had the presumption of coexistent mca ischemia as a first cerebral lesion. * we made the differential diagnosis with a cerebral ischemia with hemorrhagic modification based on the anamnesis (fall and secondary head injury) and the presence on cranial ct of the acute subdural hematoma. it was not possible for us to obtain a preoperative emergency mri because of the neurological status of the patient (coma gcs 6, acute lateral supratentorial herniation syndromes left mydriasis, right hemiparesis). the second postoperative ct scan, performed 3 days later, revealed the left mca ischemia, in a very clear manner, with a small amount of residual intracerebral and subdural hematoma. despite of the intensive treatment patient died 3 days later due to aggravation of mendelson syndrome. we advise as a routine an emergency mri investigation in all patients which: •have a cranial trauma due to severe troubles of equilibrium followed by secondary fall, if anamnesis is clear; •have a cranial ct scan that shows posttraumatic cerebral lesions (intracerebral hematomas, contusion, subdural or extradural hematoma, associated with a significant perilesional hypo density), if the neurological status of the patient allows. 218 | balasa et al acute cerebral mca ischemia the importance of a correct and early radiological diagnosis has a clear impact on the treatment and following investigations: •we may add aspirin within the classic treatment of the operated hematomas (neurotrophic, b vitamins, ocasionally antiepiepileptic medication, pain killers, antibiotics) •we will investigate the etiology of cerebral ischemia and treat it accordingly. correspondence daniel balasa bulevardul 1 mai, 50 bis, bloc i2, apartament 19, constanta phone: 004 0744682613 e-mail: daniel_balasa@hotmail.com references 1. albanèse j, portier f, léone m. tomodensitométrie du traumatismecrânien. in: sfar, eds: conférencesd’actualisation, paris, elsevier, 2000, 367 – 387 2. blumbergs p. c. neuropathology of traumatic brain injury in neurosurgical neurosurgery youmans, sixth edition, 3288-3300 3. chesnut rm, marshall lf, klauber mr. the role of secondary brain injury in determining outcome from severe head injury. j trauma 1993; 34: 216-222. 4.jacobs b, beems t, van der vliet tm, diaz-arrastia r, borm gf, vos pe. computed tomography and outcome in moderate and severe traumatic brain injury: hematoma volume and midline shift revisited. journal of neurotrauma 2011; 28: 203 – 215. 5.narayan rk, mass ir, servadei f, skolnick be, tillinger mn, marshall lf et al. progression of traumatic intracerebral hemorrhage: a prospective observational study. journal of neurotrauma2008; 25: 629-639 6.ugur c., gücüyener d., uzuner n., özkan s., özdemir g., characteristics of falling in patients with stroke, j neurolneurosurg psychiatry 2000;69:649–651 adamd_odontoid romanian neurosurgery (2016) xxx 1: 57 64 57 odontoid fracture that is not listed in the existing classifications a new subtype of odontoid fracture: case report d. adam1,2, r. cergan1,2, d. iftimie2, cristiana moisescu2 1“carol davila” university of medicine and pharmacy, bucharest 2“saint pantelimon” clinical emergency hospital, bucharest abstract: background: there is a significant variety of odontoid fracture classifications along with corresponding treatment strategies. there are though cases which cannot be framed within the existing classifications. clinical presentation: we report the case of a 91 years old female patient who suffered a cervical trauma secondary to a ground level fall. the cervical ct scan revealed a particular type of odontoid fracture, unframeable within existing classifications. the fracture line was at the base of the odontoid process and continued in an oblique trajectory through the right pedicle of the axis. as treatment strategy, we opted for external immobilization in a minerva jacket and, after 3 months, the patient is symptom free, with partial bone fusion. conclusion: we named this rare case of odontoid fracture type ii b for which external immobilization seems sufficient. key words: odontoid fracture, classification types, external immobilization. introduction odontoid fractures have always aroused the interest of many researchers, given their high incidence, multiple classifications and treatment modalities. (1-9) odontoid fractures represent 10 – 15% of cervical fractures. among people over 65 years old, they are the most common type of fracture, their incidence increasing with age (9). the first classification of these types of fractures was proposed by anderson and d’alonzo in 1974. according to these authors, there are three types of odontoid fractures: type i, an oblique fracture through the upper part of the odontoid process itself, type ii, a fracture at the junction of the odontoid process with the vertebral body of the second cervical vertebra, type iii, a fracture through the body of the atlas (1). in 1988, hadley describes a new subtype of odontoid fracture characterized by comminution at the base of the odontoid process, which he names type ii a. it 58 adam et al a new subtype of odontoid fracture represents 5 % of type ii odontoid fractures, is highly unstable and usually associated with ligamental injuries (4). in 2005, grauer & col. propose a new classification of odontoid fractures, bringing modifications to ii and iii fracture types proposed by anderson and d’alonzo. in type ii fractures, with three subtypes, the trajectory of the fracture, although including the vertebral body of c2, it does not extend to the superior articular facets. in type iii fractures, the trajectory includes the superior articular facets of c2 (2). in 2006, jea & col. describe type iii a odontoid fractures characterized by a horizontal fracture line through the body of c2 extended through c1-c2 facet joints (6). the treatment of patients with odontoid fractures is controversial. the multiple therapeutic strategies, conservatory versus surgical by anterior or posterior approach, must be adapted to the type of fracture. we present the case of a patient with odontoid fracture that cannot be framed using the aforementioned classifications. case report a 91 years old female patient suffered a cervical trauma secondary to a ground level fall. at admission, the patient presented with intense upper cervical pain and restriction of neck movements. the cervical radiograph was negative for cervical fractures. the cervical ct scan showed a fracture at the level of c2, which includes the body/ dens junction as well as the right side of the vertebral body of the axis, at the level of the right lateral pedicle. there is also a 4 mm anterior and caudal displacement of the cranial bone fragment (figure 1, figure 2). a b figure 1 cervical ct scan at admission in (a) coronal and (b) sagittal plane showing fracture at the level of c2, which includes the body/ dens junction as well as the right side of the vertebral body of the axis, at the level of the right lateral mass figure 2 schematic representation in coronal and sagittal plane highlighting the fracture trajectory considering the age and the associated comorbidities (osteoporosis, high blood romanian neurosurgery (2016) xxx 1: 57 64 59 pressure) as well as the patient and family members’ preference, external immobilization of the fracture in a minerva jacket was decided. after 3 months of immobilization, a control ct scan showed minimal bone union, reason for which maintaining the external immobilization was decided (figure 3). a b c figure 3 comparative coronal cervical ct scans at admission (a), after 2 (b) and 3 months of external immobilization (c) respectively showing an initially minimal, but progressive bone fusion the patient continued to be without neurological deficits. discussion there are different lines of fracture through the odontoid process which, in the last decades, many researchers tried to classify in order to recommend the optimal treatment in each case (table i). the fractures near the tip of the odontoid process, above the transverse ligament, are type i fractures (figure 4) in all classifications and the recommended treatment is external immobilization using a hard cervical collar, as they are generally stable. there is a very low incidence of non-union and surgery is seldom indicated in these cases, mainly if the displacement is greater than 6 mm and the patient is over 60 years of age (1). the fracture lines at the base of the odontoid process, between the level of the transverse ligament and the body of the axis, are known as type ii fractures (figure 5) in anderson and d’alonzo classification. they are highly unstable and, regarding their management, longenduring controversies exist (1). figure 4 type i odontoid fractures figure 5 type ii odontoid fractures 60 adam et al a new subtype of odontoid fracture table i classifications of odontoid fractures author year type of fracture treatment anderson – d’alonzo (1) 1974 i: the tip of the dens; ii: fracture of the odontoid base; iii: broad-base fracture involving the c2 body; cervical collar; halo immobilization/ odontoid screw fixation/ atlanto-axial arthrodesis if displacement > 6 mm or patient > 60 years old external immobilization; roy – camille (8) 1981 i: oblique fracture with anterior displacement; ii: oblique fracture with posterior displacement; iii: horizontal fracture with anterior or posterior displacement; wiring and polyethylene spacer anterior screw fixation posterior fusion and c2-c1 screw fixation levine – edwards (7) 1985 i: fracture with less than 3.0 mm anteroposterior displacement, without angular deviation; ii: fracture with more than 3.0 mm antero-posterior displacement, with significant angular deviation; transverse ligament dislocation; iia: oblique or horizontal fracture with significant angular deviation, without anterior or posterior displacement; iii: a variety of type i fracture with bilateral dislocation; external immobilization anterior screw fixation romanian neurosurgery (2016) xxx 1: 57 64 61 author year type of fracture treatment hadley (3,4) 1988 i: through tip, above the transverse ligament – rare; ii: through base of neck the most common dens fracture; iia: similar to type ii but with large bone chips at fracture site – represents ~ 5% of type ii fractures; iii: through body of c2 (usually involves narrow space); cervical collar, halo-vest; anterior or posterior fixation/ halo-vest for 12 weeks; early posterior fixation and c1c2 fusion; cervical collar, halo-vest; grauer (2) 2005 -he redefined types ii and iii of anderson – d’alonzo classification: ii: the fracture line involves the body of c2 but it does not affect de superior articular facets: iia: transverse fracture without comminution and less than 1.0 mm displacement; iib: fracture that passes from anterosuperior to postero-inferior or a transverse fracture with displacement greater than 1.0 mm; iic: fracture that passes from anteroinferior to postero-superior or a fracture with significant comminution of the dens iii: the line of fracture involves the superior c2 articular facets; external immobilization anterior screw fixation posterior atlantoaxial fixation jea (6) 2006 iiia: horizontal fracture through the body of c2 extending into the c1–c2 facet joints; adam cergan 2016 fracture at the base of the odontoid process, with oblique inferior right trajectory, passing through the c2 pedicle extending to the right transverse process, determining in coronal plane a 10º angulation and ventral displacement of the bone fragment to the odontoid of ~ 5 mm in sagittal plane; external immobilization (???) 62 adam et al a new subtype of odontoid fracture the fractures at the base of the odontoid process which extend into the vertebral body are known as type iii fractures (figure 6). they are relatively stable unless significantly displaced and usually external immobilization is a successful treatment option (1). figure 6 type iii odontoid although this is the most widely accepted classification, two limitations of this classification have been highlighted. first is the difficulty in precise differentiation between a low type ii and a high type iii fractures; the second is the lack of distinction between fractures in terms of fracture line obliquity, displacement and comminution which has an impact on subsequent management (5). to address the first limitation, in 1988, hadley introduced a type iia fracture subclass to the classification, defined as a type ii fracture complicated by an additional chipfracture fragment at the anterior or posterior aspect of the base of the odontoid (figure 7). it is highly unstable and represents 5% of type ii odontoid fractures (3). figure 7 type iia odontoid in order to address the second limitation of the anderson and d’alonzo classification, in 2005 grauer further classified types ii and iii, highlighting the fact that in type ii fractures the superior facet joints of the axis are not interested, while in type iii fractures they are affected. he also classified type ii fractures into three subtypes: type iia was defined as a transversal line of fracture, with no comminution and a displacement of the dens < 1mm; type iib was a displaced fracture extending from anterior–superior to posterior-inferior, or a transverse fracture with a displacement > 1mm; type iic was a fracture extending from anterior–inferior to posterior superior or a fracture with significant comminution (figure 8) (2,5). no comminution and displacement of dens < 1mm transverse fracture with displacement of dens > 1 mm or displaced fracture extending from antero-superior to postero-inferior romanian neurosurgery (2016) xxx 1: 57 64 63 displaced fracture extending from antero-inferior to postero-superior or fracture with significant comminution figure 8 the grauer modifications of type ii fractures in 2006, jea described type iii a as a horizontal fracture through the body of c2 extending into the c1–c2 facet joints (6). in the presented case, the fracture line passes at the base of the odontoid process and it descends on one side only, separating the body of the axis of the lateral mass. this fracture cannot be framed in the aforementioned classifications because: • it is not a simple transverse fracture at the base of the odontoid process to be considered type ii fracture (anderson and d’alonzo); • it is not accompanied by comminution to be considered type ii a fracture (hadley); • it does not pass through both superior articular facets (in fact, none of the facets are interested) to be classified as type iii fracture (grauer); • on the coronal section, in does not affect de body of the axis on both sides for it to be classified as type iii fracture (anderson and d’alonzo); • the transversal fracture continues on only one side, separating the body of the axis and the lateral mass, so it cannot be considered type ii a fracture (grauer); • it does not have an oblique trajectory through the dens to be considered type ii b or c (grauer); in roy – camille classification, the level of the odontoid fracture trajectory is not specified (8). none of the described fracture types include the body of c2, pedicle (as in the presented case) or lateral mass. also, we can affirm that the presented fracture trajectory cannot be framed in any of the fracture types proposed by levine– edwards classification (7). we can conclude that the described fracture is rarely seen, not found in cases that we treated and also not described in the literature. conclusions the presented case shows a new subtype of odontoid fracture, undefined using the aforementioned classifications. we name this type ii b odontoid fracture, for which an external immobilization was the treatment of choice. references 1.anderson ld, d’alonzo rt: fractures of the odontoid process of the axis. the journal of bone and joint surgery 1974; 56(8): 1663 – 1674. 2.grauer jn., shafi b., hilibrand as., et al.: proposal of a modified, treatment-oriented classification of odontoid fractures. spine journal 2005; 5(2): 123 – 129. 3.hadley mn, browner c, sonntag vkh: axis fractures: 64 adam et al a new subtype of odontoid fracture a comprehensive review of management and treatment in 107 cases. neurosurgery 1985; 17: 281 – 290. 4.hadley mn, browner c, liu ss, sonntag vkh: new subtype of acute odontoid fractures (type iia). neurosurgery 1988; 22: 67 – 71. 5.jaiswal ak., sharma ms., behari s., et al.: current management of odontoid fractures. indian journal of neurotrauma 2005; 2(1): 3 – 6. 6.jea a., levi ad.: vertically unstable type iii odontoid fractures: case report. neurosurgery 2006; 59 (5): e1152. 7.levine am, edwards cc: the management of traumatic spondylolisthesis of the axis. j bone joint surg am. 1985; 67(2): 217 – 226. 8.roy-camille r, saillant g, judet t et-al. factors of severity in the fractures of the odontoid process (author's transl). rev chir orthop reparatrice appar mot. 1981;66 (3): 183-6. pubmed citation. 9.pal d., sell p., grevitt m.: type ii odontoid fractures in the elderly: an evidence-based narrative review of management. european spine journal 2011; 20(2): 195– 204. 9_iong_ruptured fusiform 286 ion et al ruptured fusiform aneurysm of the proximal anterior cerebral artery ruptured fusiform aneurysm of the proximal anterior cerebral artery in young patient case report georgiana ion*, a. chiriac, n. dobrin*, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi *“prof. dr. n. oblu” clinic emergency hospital, iasi abstract: a 16-year old male presented with a ruptured aneurysm of the proximal segment of the anterior cerebral artery, with symptoms like sudden headache. paraclinical explorations revealed a fusiform aneurysm of the right a1 segment. the optimal treatment used was the microsurgical one via right pterional approach. the aneurysm was associated with a saccular pseudoneurysm at the proximal part. the saccular portion was clipped and the fusiform one was wrapped with muscle. the postoperative evolution was favorable, without neurological deficits. key words: fusiform aneurysm, wrapping, dissecting aneurysm, child. introduction in children, fusiform aneurysms typically affect a major intracranial artery and involve a segment several centimeters long. regarding the treatment, these aneurysms are difficult to manage both endovascular and microsurgical. sometimes a combination of these methods may be needed. trapping by ligation proximal and distal to the aneurysm may be an option if the perfusion is maintained by a collateral blood flow. this technique should lower the risk of rebleeding. fusiform aneurysms represents 1% of all intracranial aneurysms, the incidence in a1 segment is about 0,76-3,4%,often associated with vascular anomalies. in children are four times more common. the most frequent location is vetebrobasilar system, then internal carotid artery, middle cerebral artery and in more rare casesanterior cerebral artery. these aneurysms are characterized by the spindle shape dilatation sometimes associated with a saccular expansion-beer belly. our case is a saccular aneurysm developed on the proximal a1 fusiform aneurysm. case report history and presentation a 16 year old boy suddenly complained of severe headache and vomiting followed by loss of consciousness. he was brought to our hospital with hunt&hess score of 2, fisher 2. the neurological and general examinations were unaltered. personal history with no other conditions associated or alcohol and cigarettes consuming. is important to note the family history of subarachnoid hemorrhage in a parental uncle. brain computer tomography revealed subarachnoid hemorrhage in bilateral sylvian fissure and carotid cistern. romanian neurosurgery (2015) xxix 3: 286 290 287 native ct scan at admission ct angio reconstructions ct angio exploration and 3d reconstructions demonstrated a fusiform aneurysm in the proximal part of the a1 segment. for a better visualization of the configuration of the aneurysm and relationship with adjacent vessels, seldinger angiography was necessary. a bilateral internal carotid artery catheterization was performed, demonstrating the right aca aneurysm and the right a1 dominant. right carotid artery angiography after review by the multidisciplinary neurovascular team, was decided that the best treatment option is the microsurgical one. surgery was performed in day 1 after the rupture and was used a right pterional transsylvian approach. during the sylvian fissure proximal dissection is distinguished some arachnoiditis changes fronto-basal, around optic nerves and right internal carotid. then is identified the bifurcation, a1 segment up to anterior communicating complex. the right a1 segment included a saccular aneurysm developed on a fusiform dilatation that extends approximately 10mm. the saccular dilatation was surrounded by a fresh clot. one perforator was identified branching proximal from the aneurysm. at first the saccular aneurysm is closed with a yasargil straight phynox clip, then the fusiform dilatation was wrapped with muscle and aponeurosis going between the aneurysm and supraoptic recess and fixed on the anterior part 288 ion et al ruptured fusiform aneurysm of the proximal anterior cerebral artery with an oblique phynox clip. the rupture point was identified on the anterior surface of the saccular aneurysm. after wrapping the blod flow through the distal aca was maintained. aneurysmal wall was not so thin, there were no perforators branching from the dilatation, therefore wrapping was considered the best option to achieve adequate hemostasis. intraoperative view –arachnoiditis a. intraoperative aspect of the aneurysm b. saccular dilatation clipped c. fusiform dilatation is wrapped with muscle the postoperative evolution was favorable, without vasospasm during the 3 weeks of hospitalization. the ct scan 24 hours after surgical treatment demonstrated a hypodense area located at the level of basal ganglia. pacient was discharged without neurological deficits or psychiatric symptoms. postoperative 48 h ct scan discussion natural history of unrupted fusiform aneurysms is not very well studied, but in case of rupture the rebleeding rate is about 10% per year. first it has to be discussed the term of fusiform aneurysm and the clear differentiation from the dissecting ones, due to the difference regarding the natural history and optimal therapy. some consider that fusiform aneurysms may be predisposant for a dissecting aneurysm. angiographic characteristics of dissecting lesions are represented by the double lumen sign, the pearl and string sign, retention of contrast media in false lumen, intimal flap or vascular occlusion. in the case presented was found none of these criteria. based on angiographic images and the intraoperative ones the morphological diagnosis was fusiform aneurysm. they may be caused by collagen and elastin affections, infections or neoplastic invasion of the arterial wall. in younger population, according to a recent study comorbid conditions found in the goup weretrauma, immune dysfunction, cardiovascular malformation, dermatologic disorder, hormonal abnormality and genetic syndromes romanian neurosurgery (2015) xxix 3: 286 290 289 like polycystic kidney disease, tuberous sclerosis, osler-weber–rendu disease, klippel-trenaunay-weber syndrome, alpha 1antitrypsin deficiency. aterosclerotic origin in the development of these lesions is well known but not mandatory. histopathological studies revealed a thinning of the media, atrophy of the muscle fibers, hyalinization of the connective tissue or deficiency of reticular fiber. these aneurysms located on a1 segment, usually are symptomatic by neural compression, ischemia and rarely due to bleeding. these aneurysms may expand gradually transforming into saccular or spherical shape. if the aneurysm is rupted, then treatment is required. clipping only the neck of the saccular dilatation is not sufficient. regarding the circumferential fusiform dilatation, clipping is not an option, but trapping or wrapping are. trapping is recommended if there is a confirmation of a good collateral blood flow and if the preservation of the perforating artery is possible. therefore if these criteria are not fulfilled, wrapping may be the next treatment option. the ideal procedure in the case presented was to clip the saccular dilatation and wrapping (reinforcement) of the fusiform segment especially that intraoperative, the aneurysmal wall was not so thin. incomplete wrapping can be the cause of re-rupture and regrowth. some studies (vivek rd, udaya kk, joseph robert 2006) shown that half of the patients treated by wrapping, the follow-up angiography showed no changes regarding the configuration and the size of the aneurysm. is safe to mention that, in pediatric population development of new and enlarging aneurysms (many within 3 years) is hard to quantify, but is more common in patients with fusiform aneurysms. should be considered and the risk of rebleeding which is between 12-18 %, according to many studies. other complications may be obstruction of one of the branches that emerge from a1 segment-medial lenticulostriate arteries or occurrence of a new aneurysm adjacent to the previously treated one. these perforantes supply the globus pallidus and medial portion of putamen. intraoperative could observe the recurrent artery of heubner and a small branch running proximal to the aneurysm. however, 48 hour postoperative ct scan revealed an ischemic area at the level of basal ganglia, probably because of affecting a small medial lenticulostriate branch, without clinical manifestation. conclusion brain aneurysms in pediatric population may be considered as a potentially aggressive chronic progressive condition. this impose a rigorously follow-up with mri or ct angiography at three year interval, for a long period of time considering the long life expectancy. however, more data should be gathered to reach a consensus about the nature of this pathology. references 1. de steven e. roach, warren d. lo,geoffrey heyer (2012), pediatric stroke and cerebrovascular disorders, third edition, demosmedical; 2. aoki y, nemoto m, yokota k, kano t, goto s, sugo n. (2007) ruptured fusiform aneurysm of the proximal anterior cerebral artery (a1 segment), neurol med chir (tokyo). aug;47(8):351-5. 3. hetts sw, narvid j, sanai n, lawton mt, gupta n, fullerton hj, dowd cf, higashida rt, halbach vv. (2009) intracranial aneurysms in childhood: 27-year single-institution experience, ajnr am j neuroradiol. 2009 aug;30(7):1315-24. 4. hetts, s. w., english, j. d., dowd, c. f., higashida, r. t., scanlon, j. t., & halbach, v. v. (2011). pediatric intracranial aneurysms: new and enlarging aneurysms after index aneurysm treatment or observation. american journal of neuroradiology, 32(11), 2017-2022. 5. sorteberg, a., & dahlberg, d. (2013). intracranial nontraumatic aneurysms in children and adolescents. current pediatric reviews, 9(4):343–352. 6. shigemori, m., kawaba, t., yoshitake, y., miyagi, j., & kuramoto, s. (1988). fusiform aneurysm of the proximal anterior cerebral artery. journal of neurology, neurosurgery, and psychiatry, 51(3), 451. 290 ion et al ruptured fusiform aneurysm of the proximal anterior cerebral artery 7. anson, j. a., lawton, m. t., & spetzler, r. f. (1996). characteristics and surgical treatment of dolichoectatic and fusiform aneurysms. journal of neurosurgery, 84(2), 185-193. 8. drake, c. g., & peerless, s. j. (1997). giant fusiform intracranial aneurysms: review of 120 patients treated surgically from 1965 to 1992. journal of neurosurgery, 87(2), 141-162. 9. fuentes, s., levrier, o., metellus, p., dufour, h., fuentes, j. m., & grisoli, f. (2004). giant fusiform intracranial a2 aneurysm: endovascular and surgical treatment. case illustration. journal of neurosurgery, 101(4), 704. 10. kan, p., liu, j. k., & couldwell, w. t. (2007). giant fusiform aneurysm in an adolescent with phaces syndrome treated with a high-flow external carotid arterym3 bypass: case report and review of the literature. journal of neurosurgery: pediatrics, 106(6), 495-500. 18_agrawalamit_intraventricular romanian neurosurgery (2015) xxix 3: 349 352 349 intraventricular entrapment of shunt catheter causing shunt malfunction amit agrawal1, umamaheswara reddy v.2, yashwant sandeep3 1professor of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 2assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) 3resident of neurosurgery, department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract: intraventricular septations can lead to compartmentalization of the ventricles that can result in “complex or loculated hydrocephalus”. we report a case of 7 year old female child who underwent multiple shunt revisions where there was intraventricular entrapment of shunt catheter leading to obstruction of the shunt and malfunction. in present case we placed the ventricular catheter in contra-lateral ventricle with good clinical outcome. with the recent advancements endoscopic guided removal of the old malfunctioning ventricular catheters is considered the safest option. key words: shunt malfunction, mechanical failure, loculation, entrappement introduction many complications can be associated with vp shunt procedures requiring multiple shunt revisions during lifetime. (1-3) out of many, mechanical failure (obstruction either proximal or distal and displacement) and shunt infection are most commonly encountered problems. (3-6) we report a case of female child where intraventricular entrapment and subsequent obstruction lead to the malfunctioning of the shunt and worsening in contra lateral hydrocephalus. case report a 7 year old female child underwent right ventriculo-peritoneal shunt for congenital hydrocephalus (presented with increase in head size at that time) at the age six months. she presented with headache associated with vomiting and medial deviation of eye balls. there was no history of fever, seizures or abnormal posturing. on examination the child was dull and apathetic. she was opening eyes to call, obeying command and moving all four limbs. she had bilateral rectus palsy with medial deviation of both eyes. motor and sensory examination was normal. on pressing the shunt chamber it was not filling well. she had similar episode one month back and a shunt revision was performed (figure 1, a-f). during surgery lower end of the catheter was retrieved from the peritoneal cavity and there was a good flow of csf. it was suspected that the obstruction was distal and the abdominal end of the catheter was placed in fresh position. a repeat ct scan was performed and it showed asymmetrical dilation of the ventricles (left more than right) and shunt tube was trapped in the right lateral ventricle probably causing functional ventricular shunt catheter obstruction responsible for features of shunt malfunction. her blood investigations 350 agrawal et al intraventricular entrapment of shunt catheter causing shunt malfunction and csf analysis were normal. following the fresh revision the child is doing well at follow up. figure 1 plain axial ct images of brain (a-f) showing ventriculoperitoneal shunt inserted through parietal burr hole and inserted into the frontal horn. there is peristence of hydrocephalus, close observation revealed adhesions in the midportion of right ventricle causing entrapment of shunt resulting in improper drianage romanian neurosurgery (2015) xxix 3: 349 352 351 figure2 repeat plain ct of the brain (a-d) showing no significant reduction in the hydrocephalus, however notice the asymmetry or upper portion the right lateral ventricle due to preferential drainage discussion intraventricular septations can lead to compartmentalization of the ventricles leading to a challenging neurosurgical problem called “complex or loculated hydrocephalus”. (7, 8) although silicone catheter is supposed to be chemically inert and should not provoke inflammatory reactions. however, these silicone made catheters may contain many impurities and when it comes in contact with csf (which can also contain cells or blood) or tissue (choriods plexus, ventricular ependyma or debris) there may be an inflammatory response leading to gliosis and blockage of shunt catheter. (9-11) apart from that the intraventricular inflammatory response may lead to septations, these can alter the ventricular anatomy and normal csf flow leading to loculated accumulation of csf with progressive and asymmetric dilatation of the ventricles and mass effect. (12) patients with shunt malfunction present with features of raised intracranial pressure (headache, vomiting, deviations of the eye balls suggestive of sixth nerve paresis). on local examination where shunt malfunctions is suspected due to the blockage of the ventricular catheter, on pumping of the shunt chamber it is slow to refill, or may not refill at all. plain ct scan of the brain is the initial investigation of choice in suspected cases of shunt malfunction. (12) it will show the disproportionately dilated ventricular system and position of the ventricular catheter. (12) however for the delineation of the intraventricular septations mri (with gadolinium) of the brain is a superior modality of imaging. (12) neurosurgical intervention is aimed to convert multiple compartments into a single communicating cavity and neuroendoscopic procedures can best achieve this goal. (7, 8, 13, 14) with the recent advancements endoscopic guided removal of the old malfunctioning ventricular catheters is considered the safest option as the scarred or adherent tissue can be easily separated and the catheter can be withdrawn safely without risk of intraventricular hemorrhage. (15) correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramit_in@yahoo.com mobile+91-8096410032 references 1.chiriac a, poeata i, iliescu b. mechanical failures of ventriculo-peritoneal shunts. romanian neurosurgery 2012; xix:226 229. 2.agrawal a, rao gm. subcutaneous shunt catheter calcification: an uncommon cause of shunt failure. saudi journal of medicine and medical sciences 2014;2. 3.dickerman rd, mcconathy wj, morgan j, et al. failure rate of frontal versus parietal approaches for proximal catheter placement in ventriculoperitoneal 352 agrawal et al intraventricular entrapment of shunt catheter causing shunt malfunction shunts: revisited. journal of clinical neuroscience 2005;12:781-783. 4.di rocco c, marchese e, velardi f. a survey of the first complication of newly implanted csf shunt devices for the treatment of nontumoral hydrocephalus. child's nervous system 1994;10:321-327. 5.ventureyra ec, higgins mj. a new ventricular catheter for the prevention and treatment of proximal obstruction in cerebrospinal fluid shunts. neurosurgery 1994;34:924926. 6.satow t, saiki m, kikuchi t. complications associated with surgical treatment of hydrocephalus: intech open access publisher, 2012. 7.ross da, muraszko k, dauser r. a special cyst puncture catheter for use in thick-walled or mobile intracranial cysts. neurosurgery 1994;34:191-192. 8.schultz p, leeds ne. intraventricular septations complicating neonatal meningitis. journal of neurosurgery 1973;38:620-626. 9.ivan lp, choo sh, ventureyra ec. complications of ventriculoatrial and ventriculoperitoneal shunts in a new children's hospital. canadian journal of surgery 1980;23:566-568. 10.mclaurin rl. ventricular shunts: complications and results. pediatric neurosurgery saunders, philadelphia 1989;219. 11.kalsbeck je, desousa al, kleiman mb, goodman jm, franken ea. compartmentalization of the cerebral ventricles as a sequela of neonatal meningitis. journal of neurosurgery 1980;52:547-552. 12.nida ty, haines sj. multiloculated hydrocephalus: craniotomy and fenestration of intraventricular septations. journal of neurosurgery 1993;78:70-76. 13.oi s, abbott r. loculated ventricles and isolated compartments in hydrocephalus: their pathophysiology and the efficacy of neuroendoscopic surgery. neurosurgery clinics of north america 2004;15:77-87. 14.browd sr, gottfried on, ragel bt, kestle jrw. failure of cerebrospinal fluid shunts: part ii: overdrainage, loculation, and abdominal complications. pediatric neurology 2006;34:171-176. 15.leszek h, regina s, józef r, aleksandra h, leszek s. fluoroscopy neuro-guided endoscopic removal of a lost ventricular catheter in hydrocephalic girl with staphylococcal shunt infection. open journal of modern neurosurgery 2012;2012. iacobg_writing romanian neurosurgery (2016) xxx 1: 3 5 3 writing in neurosurgery g. iacob bucharest, romania motto: "god doesn’t require us to succeed; he only requires us to try." mother teresa 1910-1997 "there are many paths to the top of the mountain, but the view is always the same." chinese proverb neurosurgery today is an open discipline based on technological innovations referring on information processing, imaging, nanotechnology with molecular engineering, neural prosthetics, proliferation of capabilities with regard to minimally invasive surgical techniques, endovascular surgical procedure, radio-surgical methods. the actual neurosurgeon should become a conductor of professionals oriented for a successful intervention to restore function by modulation, rather by injury a structure; assuming primary the utility for information management, future emerging technologies, but also for the practicing neurosurgeon for daily procedures (1). in such a spirit, writing in neurosurgical papers is important for several reasons (2-4): support the education of future neurosurgery investigators, fix the research opinion on certain point, establish new ideas cancelling a previously established fact, share experience, anticipate readers’ needs, establish strong links between neurosurgeons, even some sort of friendship is an essential job skill, permit improving quality of life by incorporating an evidencebased view of neurosurgery practice, transfer experience, solve local problems organize the knowledge into clinically useful forms, via the publication of metaanalyses and dissemination of clinical practice guidelines in electronic formats, offer ethical and procedural safeguards for a young neurosurgeon, write afford to be appreciated for intellectual activity and personality making clear, visible personal ideas, opinions; giving others the possibility for feedback or even for the author to reflect upon them later writing is an art, good writings are usually an expression of maturity, intellectual flexibility, the ability to pose worthwhile questions. for medical community, articles should pin point work, hitting one target at a time; without changing for the sake of change. such articles should be original, reflecting personal experience, establishing an easy 4 iacob writing in neurosurgery solution for a difficult situation: randomized trials, cooperative studies, observational cohort study a case report, a controversial point, an analytic study, a descriptive or review article, experimental or animal studies, a technical note, even a letter to the editor. most cited works in neurosurgery cover cerebrovascular diseases followed by trauma, stereotactic and functional neurosurgery and neuro-oncology (5). to stimulate readers’ interest, making a neurosurgical article, several keys are mandatory to respect (2-4): the title should be directly related to the content, attracting attention, be concise, impressive, mentioning the real authors names who did the article and order depending on their contribution the abstract must be synthetic (not exceed 250 words), written in the past tense, containing comprehensive information, pointing the originality of the paper, providing a brief summary of the main section of the paper without abbreviation and anything that is not in the paper introduction data must explain the objective of a specific subject, related to literature review, with the aim to enable the reader why and how to appreciate the significance of author findings, an historical review is necessary to point evolution in knowledge of the paper subject material and methods should describe the details needed to clarify the used idea, presenting only facts, avoiding exaggeration; especially animal experiment, enabling other researcher to reproduce the same experience, performing statistical analysis, disseminate information and convince readers using tables (generally one table for every thousands words), illustrations with explicit text content, remember the ethical aspect results should reflect with accuracy and precision statements, with statistical significance; even negative results if significant. discussions should assess the validity and significance of the results obtained, comments, comparing results; establishing conclusions as clearly as possible, summarize the evidence, pointing out any results that suggest new lines of study. references must consider vancouver guidelines, without including unpublished data: author, name of the article, name of the journal, year of publication, volume, no., page; for book: title of the book, place of publication, publisher, year of publication chap, page no. argues for accepted papers: real original work, concise, precise, reflecting controlled clinical trials, double blind study, experimental work. argues for rejected papers: the article is difficult to read, validity of results is doubtful, nothing original, too long despite available information it contains. in conclusion my plea for writing neurosurgical articles are addressed to young neurosurgeons: don’t hesitate to write read in full reputable papers on the subject you are interested get reports on ethical issues of research presenting honestly results compared with similar work romanian neurosurgery (2016) xxx 1: 3 5 5 ask a senior writer assistance, presenting topic clearly and simply as possible, giving confidence and understanding how truth is established in neurosurgery; even today failures doing an neurosurgical article are tomorrow pillars of success avoid spelling and grammar mistakes, confusions, difference between tables, illustrations and the text, no abbreviations dissipate fear to be accepted sending your article to a well-known journal and read their remarks carefully offering visibility of achievements and a future plan. references 1. apuzzo m.l.j., liu c.y. 2001: things to come, neurosurgery 2001, 49: 765–778 2. amadio j.p., oyesiku n.m. the role of neurosurgery journals in evidence-based neurosurgical care, neurosurgery clinics of north america 11/2014; 26(2). doi: 10.1016/j.nec.2014.11.001 3. why is writing important brown university and the university of missouri brochures 4. hamdan a.t. why arab spine journal? 16th dubai spine conference 2015 5. ponce f.a., lozano a.m. highly cited works in neurosurgery. part i: the 100 top-cited papers in neurosurgical journals, j neurosurg. 2010 feb;112(2): 223-232 gangeshgunjan_asymptomatic romanian neurosurgery (2016) xxx 1: 113 117 113 asymptomatic posterior cervical myelomeningocele with tethered cord in an adolescent: a rare form of spinal dysraphism with rare presentation gangesh gunjan, sumit sharma, s.k. jain, s. chopra department of neurosurgery, sms medical college & hospital, jaipur, rajasthan, india abstract: unlike lumbar spinal dysraphism, cervical spinal dysraphism with or without tethered cord are rare lesions. these lesions are generally asymptomatic at birth, but with progression of time symptoms develop. these may be associated with various other anomalies. not much have been reported in literature about cervical myelomeningocele (mmc) in adults or adolescents. we report a case of a 17 years old adolescent boy with cervical myelomeningocele with tethered cervical cord, who was completely intact neurologically even at this age and was without any associated anomaly. he came to us only for cosmetic reasons. the tethering band, which was evident on imaging was confirmed intra-operatively. key words: cervical myelomeningocele, spinal dysraphism, tethered cord. introduction cervical meningocele and myelomeningocele are rare lesions accounting for 1-8% of all neural tube defects. diagnosis of these lesions are obvious at birth: a mass protrudes from the posterior midline of the neck. children with cervical mmc with tethered cord can be asymptomatic and thus the subtle features of cervical cord tethering or any other associated anomaly may be overlooked on imaging. if left untreated, the tethered cervical cord may cause gradual neurological deterioration with progression of time, with motor function in the upper extremities being primarily affected. in our case the patient an adolescent, came only for cosmetic reasons and was neurologically intact; had we not done thorough pre-op evaluation and tried to remove the protruding posterior cervical midline mass, we would have landed the patient in trouble. in order to avoid any future neurological deficit, any cervical region mass mandates a thorough clinical and radiographic pre-op evaluation regardless of patient’s age. case report a 17 years old adolescent boy with rural background was admitted to our department with a mass lesion in the posterior cervical 114 gunjan et al asymptomatic posterior cervical myelomeningocele region. it has been present there since his birth. he was asymptomatic and got admitted only for cosmetic reasons. physical examination revealed normal findings except a partially spherical swelling over the nape of his neck in mid cervical region, 2.5 x 3.5cm x 2 cm in dimensions with an elevated nodule of 1x0.5cm. it was covered with full thickness skin and was compressible, non fluctuant, non tender and without any csf leak. neurological, orthopedic and urological evaluations were normal. mr imaging (figure 1 & figure 2) of the cervical spine was performed and high resolution t1, t2w serial sections obtained in the sagittal and axial planes. it showed spina bifida at c4 vertebral level and a heterogenous lesion in subcutaneous tissue at this level communicating with the spinal canal with evidence of focal bulge in posterior surface of cord at this level. a low-signal connection between the posterior bulge of the cord and the dorsal dural sac, which could represent the tethering stalk, was identified. ct scan of brain (figure 3) was within normal limits. excision of sac and c3 & c4 laminectomy with intradural exploration and detethering of cord was performed under general anesthesia. whitish, fibrous tissues connecting the dorsal cervical cord to the sac of the myelomeningocele were present. these fibrous tissues were taut, further confirming the suspicion of tethered cord. the fibrous tissues on the dorsal cord were attached at the rostral end of the sac. all were subsequently excised and the spinal cord detethered. histopathological examination revealed epidermis on the external aspect, which in most part was thin and attenuated. the underlying tissue comprised of fibrocollagenous tissue with focal collection of meningothelial cells present irregularly in nest and cords with foci of psammomatous calcification. there were areas of glial tissue, small nerve twigs and blood vessels. overall morphology suggestive of meningomyelocele. figure 1 t1w sagittal section of cervical spine romanian neurosurgery (2016) xxx 1: 113 117 115 figure 2 t2w sagittal section of cervical spine showing the posterior cervical mass lesion with elevated dorsal cord surface and the connecting band discussion cervical meningocele and myelomeningocele are rare lesions that comprise only a small proportion of neural tube anomalies. previous studies have reported that these rare entities account for approximately 1-8% of all neural tube defects [3, 4, 6, 7, 9, 10, 11, 12, 13].cervical dysraphism lesions are structurally distinct lesions than myelomeningoceles of the thoracic and lumbar regions [2, 5, 8]. the neural placode is absent in cervical mmc. they are more limited and more protuberant and are usually covered by normal skin tissue to a certain extent of the defect excluding the dome of the cervical mmc, which is lined by squamous epithelium or with scar tissue [10]. neural structures are not exposed through the defect and csf leak is not usual [9]. however, tethering of the neural structures to nearby dural or intrasaccular structures may be present [7]. neurological examinations in patients with cervical mmc are usually normal in newborns [2, 6, 8, 10, 12]. although cervical mmc causes tethering of the spinal cord, neurological functions of the patients are generally preserved below the level of lesions [9].if left untreated, the tethered cervical cord is likely to cause gradual neurological deterioration over the years, with motor function in the upper extremities being primarily affected. posterior fossa distortions and hindbrain herniations if associated, may lead to intellectual dysfunctions [7]. in case of cervical mmc, the neurulation process is uneventful except for fusion of the two sides of the neural fold [3]. imperfect closure of the neural tube and deficient separation of the cutaneous ectoderm from neural ectoderm results in dorsal myeloschisis [9]. another theory regarding failure of closure is fusion of the cutaneous ectoderm properly while attachment of neural ectoderm to cutaneous ectoderm incurs maldevelopment of the skin [12]. other anomalies associated with cervical mmc include hydromyelia, hydrocephalus, chiari malformations, diastematomyelia, lipomyelomeningoceles, thickened filum terminale, klippel-feil syndrome and thoracic hemivertebra etc [1, 2, 4, 7, 8, 12]. 116 gunjan et al asymptomatic posterior cervical myelomeningocele figure 3 ct scan of brain of the same patient romanian neurosurgery (2016) xxx 1: 113 117 117 conclusion even adult patients with cervical mmc with a cervical tethered cord can be fully intact neurologically. a thorough preoperative evaluation clinically and radiologically is required. mri is recommended for patients with cervical mmc to depict the morphological properties of the lesions and to detect any other associated cranial or spinal anomaly. future neurological deterioration can be prevented if extensive surgical treatment with untethering of neural structures in and around the defect together with management of the associated anomaly is provided. we acknowledge that further longterm follow-up is needed to assess the natural history of the posterior cervical mmc with tethered cord more accurately. correspondence dr. gangesh gunjan department of neurosurgery sms medical college & hospital jaipur, rajasthan, india pin 302004 e mail: dr_gunjangangesh@yahoo.com phone no. +91 7727834367 references 1.delashaw jb, park ts, cail wm, vollmer dg: cervical meningocele and associated spinal anomalies.childs nerv syst.3(3):165-169, 1987 2.etus v, sarisoy ht, ceylan s: surgical technique and outcome in cervical and thoracic myelomeningocoele surgery clinical study. journal of clinical neuroscience 13: 643–647, 2006 3.habibi z, nejat f, tajik p, kazmi ss, kajbafzadeh a-m: cervical myelomeningocele. neurosurgery 58: 11681175,2006 4.konya d, dagcinar a, akakin a, gercek a, ozgen s, pamir mn: cervical meningocele causing symptoms in adulthood. case report and review of the literature. j spinal disord tech 19: 531-533, 2006 5. kasliwal mk, dwarakanath s, mahapatra ak: cervical meningomyelocele-an institutional experience. childs nerv syst 23(11): 1291-1293, 2007 6.may d, rilliet b, berney j: cervical meningocele and meningomyelocystocele. apropos of 4 cases. neurochirurgie 38(6):347-352, 1992 7.meyer-heim ad, klein a, boltshauser e: cervical myelomeningocele follow-up of five patients. european journal of paediatric neurology 7: 407-412, 2003 8.nishio s, morioka t, hikino s, fukui m: cervical (myelo)meningocoele: report of 2 cases. j clin neurosci. 8(6):586-7, 2001 9.pang d, dias ms: cervical myelomeningoceles. neurosurgery 33: 363-373, 1993 10.salomao jf, cavalheiro s, matushita h, leibinger rd, bellas ar, vanazzi e, souza lam, nardi ag: cystic spinal dysraphism of the cervical and upper thoracic lesion. childs nerv syst 22: 234-242, 2006 11.steinbok p, cochrane d: the nature of congenital posterior cervical or cervicothoracic midline cutaneous mass lesions. j neurosurg 75: 206-212,1991 12.steinbok p: dysraphic lesions of the cervical spinal cord. neurosurgery clinics of north america 6(2): 367376, 1995 13.vogter dm, culberson jl, schochet ss, gabriele of, kaufman hh: “high spinal dysraphism” case report of a complex cervical meningocele. acta neurochir (wien) 84: 136-139, 1987 5mittler-maticaroxana_ontraumatic romanian neurosurgery (2015) xxix (xxii) 1: 43 50 43 on traumatic brain injury epidemiological data collected from a county hospital in romania and an estimation of psychiatric consequences thereof roxana mittler-matica phd student in medicine, university of oradea, romania neurosurgery resident, neurochirurgische klinik, städtisches klinikum braunschweig, germany abstract: introduction: many aspects justify the increasing attention upon tbi and post tbi sequels. material and methods: the paper resumes statistics on traumatic brain injury (tbi) from a romanian country district, collected throughout five years. statistics in the literature that demonstrated the link between tbi and psychiatric disorders are extrapolated. results: tbi is considered to be a risk factor for psychiatric disorders. as consequence, estimation of some post tbi psychiatric sequels is computed aiming to emphasize the need for psychiatric support and treatment in more organized multidisciplinary neuro-trauma management teams. conclusions: tbi is considered to be a risk factor for psychiatric disorders which are a major cause of post tbi disability. the size of these psychiatric sequels in accordance with the existing literature can be approximated in a given population. tbi epidemiology analysis reveals hazardous impact on the overall health condition of patients. key words: psychiatric sequels, aetiology. introduction traumatic brain injury (tbi) has been identified and established as a real public health problem. it is shown that approximately 6.6% results in death in the case of tbi patients, of which 91.4% less than 7 days after tbi. [1] a percentage of 3.5% to 4% of tbi cases of all patients who have survived a tbi, are followed by permanent disability with socio-economic impact, most of these cases involving psychiatric disabilities. [2] corroborating recent data, it is found that every two minutes one eu citizen dies of an injury and annually approximately one million eu people remain permanently disabled due to an injury, [3] most of which are tbi. in the geographical area targeted by our paper (i.e. bihor county, romania), it was determined a ratio of 1/5 of the incidence of severe tbi versus moderate tbi, for 44 mittler-matica tbi epidemiological data collected from a county hospital in romania hospitalized patients, and 1/22 of the moderate tbi versus uncomplicated tbi. [6] it is known that a psychiatric sequel post tbi can occur even after a longer period of time. [4] establishing a causal relationship between psychiatric disorders and tbi is especially important for understanding the pathophysiology of such possible sequels, in order to treat these diseases. also, it contributes to understand the pathogenesis and define the causality of mental suffering in general. if the psychiatric disorders highlight the causes of psychiatric morbidity, this should alert physicians to consider the tbipsychiatric sequel causality and to try to prevent such consequences. such a finding regarding causality would be more important in the case of legal disputes concerning the consequences of tbi compared to simple situations when an individual presents only post tbi motor difficulties. frequently reported, psychiatric disorders after tbi are greater than on general population and prospective follow-up studies have found that the most common post tbi psychiatric disorders are depression and anxiety, although the causality association remains unclear. [5] the occurrence of generalized anxiety disorder was associated with post tbi greater physical and emotional problems, with negative impact on the active role in social life and general health. numerous definitions and measures were used to assess "successful outcome" of tbi treatment, including return to work or social functional recovery.[4; 5] the result of the treatment is multi-dimensional and complex and cannot be comprehensively understood by a single score achieved on certain scales (such as the glasgow outcome scale). causality of psychiatric sequel after tbi is not fully elucidated. approaches to explaining the causality could account on the high incidence of somatic sequels after tbi. in order to improve the outcome after tbi, it is important to have an overview of epidemiological data on tbi and their psychiatric impact. the analysis of locally adapted epidemiological data provides the opportunity to form a more realistic idea of the size of the studied pathology and guides the clinician in the decision making for treatments. therefore an epidemiological analysis of tbi, in a given district and correlation with data from the literature on the psychiatric consequences of post tbi, both provide an overview of the pathological phenomenon in question. material and methods this paper presents the analyze of tbi cases in the bihor county, romania, reported in the city of oradea, at emergency regional hospital, for 5 years along. it consists of a retrospective study on demographic and clinical data. it was followed parameters like tbi etiology, patient age, health status at discharge... all patients treated in the neurosurgery department of this county hospital, on which a chart of the patient was drawn, were included in statistics. data processing method involved coding information in a database and then processed in excel management database (for each year a file was filled in, and the years submitted for analysis are 2005, 2006, 2007, 2008 and 2009). romanian neurosurgery (2015) xxix (xxii) 1: 43 50 45 results various diagrams are presented below by means of which we intend to highlight the evolution of tbi casuistry, reported at emergency regional hospital, bihor county, and various characteristics of their prevalence and incidence. the total number of tbi cases varied over the five years, [6] see table 1. the number of patients, diagnosed with tbi, reported in rural versus urban area is balanced, table 1. analysis by gender, shown in table 2, highlights the following observation: women represent a smaller percentage of cases, compared with men. table 1 patients diagnosed with tbi, reported in rural versus urban residential area year 2005 2006 2007 2008 2009 all patients 608 603 628 640 597 rural 261 250 269 322 306 urban 347 353 359 318 291 table 2 number of patients by gender, admitted to the neurosurgery department of the county hospital, diagnosed with tbi year 2005 2006 2007 2008 2009 all patients 608 603 628 640 597 men 405 397 432 456 412 women 203 206 196 184 185 computing the association of tbi with multiple trauma (since it complicate the treatment and may be marks of more important lesions), for 2005, the percentage is 4.23% from tbi total cases, for 2006 the percentage is 3.98%, for 2007 the percentage is 15.29%, for 2008 the percentage is 5.78% and for 2009 it is 1.84%. the number of post tbi deaths is relatively small, so per each year the percentages of tbi fatal cases were as follows: 2.96%; 2.82%; 3.98%; 4.36%; 4.52%. the distribution of cases by the tbi in relation with age was determined for the age groups, according to the following data, as shown in table 3. the etiology of tbi has a diversified distribution, as shown in table 4. the association with alcoholism is of interest because of the increased susceptibility regarding those patients to be victims of accidents and incidents with cerebral adverse consequences. the percentage of those patients with alcoholism is about 7%, for the five years studied. the alcoholism is a risk factor for tbi (p=0.1) and the evolution of patient after tbi treatment is not favorable (p=0.05). analyzing the patients’ post tbi health condition at discharge from hospital, we find several patients with post traumatic deficits, especially neuro-motor deficit, see table 5 below. the favorable development is conventionally defined as an intact neurological status. 46 mittler-matica tbi epidemiological data collected from a county hospital in romania table 3 distribution of tbi cases by age groups year: 2005 2006 2007 2008 2009 aged < 1 year 0 1 0 4 3 aged 1 to 4 3 5 10 14 18 aged 5 to 14 old 36 39 27 32 30 aged15 to 18 62 63 48 54 38 aged 18 to 24 59 54 45 45 31 aged 25 to 34 83 76 92 73 76 aged 35 to 54 81 69 94 82 66 aged 45 to 54 86 87 94 105 92 aged 55 to 64 82 80 99 79 87 aged 65 to 74 55 62 67 84 83 aged 75 to 84 52 59 41 54 61 aged > 85 9 8 11 14 12 all patients 608 603 628 640 597 table 4 etiology of tbi, for whole time analyzed (%) aetiology 2005 2006 2007 2008 2009 accidentally hitting with a blunt object 7.50% 7.30% 11.20% 8.80% 7.03% traffic accidents 9.10% 8.60% 12.60% 6.70% 16.42% fall from same level 53% 60% 43.60% 61.60% 39.87% fall from height 12.40% 8.50% 5.40% 4.10% 0.84% aggression 11.60% 9.30% 12.90% 9.20% 10.55% unspecified 5.40% 5.30% 8.30% 5.90% 20.26% fall from bike 0.50% 0.70% 3% 2.80% 2.68% horse kick 0.50% 0.30% 0.30% 0.20% 0.00% fall from tram 0.00% 0.00% 0.50% 0.00% 0.00% fall from motorcycle 0.00% 0.00% 1.40% 0.00% 0.00% sports accident 0.00% 0.00% 0.00% 0.20% 1.51% accident at work 0.00% 0.00% 0.00% 0.50% 0.84% romanian neurosurgery (2015) xxix (xxii) 1: 43 50 47 table 5 patients post tbi health status at discharge from hospital, concerning patients with tbi (%) patients health status 2005 2006 2007 2008 2009 improved 2.06% 1.91% 1.84% 6.41% 87.60% slow progressive 84.39% 85.03% 82.03% 84.84% 4.36% favorable development 7.63% 7.48% 7.22% 4.06% 1.84% surgical intervention healed 0.93% 0.32% 3.84% 1.09% 1.51% transferred to another hospital 0.52% 0.64% 0.61% 0.47% 0.50% discharged on request 3.92% 3.98% 3.84% 2.81% 3.85% deficit neuro-motor 0.55% 0.64% 0.61% 0.31% 0.34% table 6 number of deaths per year (during 2005-2009) year number of severe tbi number of deaths deaths in total patients with severe tbi (%) total number patients with tbi deaths in total patients with tbi (%) 2005 98 18 18.37% 608 2.96% 2006 95 17 17.89% 603 2.82% 2007 83 25 30.12% 628 3.98% 2008 74 26 35.14% 640 4.36% 2009 63 27 42.86% 597 4.52% discussions traumatic brain tbi is a significant cause of hospitalizations and remains a major cause of death, especially in the case of young people. the highest number of patients with tbi is included in this age group, i.e. aged 15 to 24 years old, see fig.1, (per each year of the five years study time span, i.e. 2005-2009). the number of deaths in patients who have had tbi is shown in table 6. the probability of survival after severe tbi, considering the first 7 days (the majority of deaths occurred in this period) is represented in the figure 2 below, considering kaplanmeier method, (after one day 94.18% of patients survive having severe tbi, 89.35% after two days, after three days the rate of survival was 84.99%, and 81.84% after another day). the mortality graph, after severe tbi, is represented in figure 3 below (after the first day 5.82% of the patients with severe tbi deceased, 10.65% deceased after two days, with a daily death rate increase as follows: 15.01%; 18.16%; 20.82%; 23.24%; 25.42%; 27.36%). the percentage of total number of deaths, recorded after the first seven days from a severe tbi, was 7.08%. a tbi case may have devastating consequences. [710] 48 mittler-matica tbi epidemiological data collected from a county hospital in romania figure 1 tbi cases number of patients aged 15 to 24 years old (days) figure 2 graph of survival after severe tbi (kaplan-meier curve) (days) figure 3 graph on mortality after severe tbi (kaplan-meier curve) most post tbi disability involves psychiatric disorders. for example about 70% of cases were followed by a post tbi depression. among post tbi psychiatric disorders, one could list the following ones (see table 7 below): major depression in more than 14% of tbi cases; bipolar disorder in more than 2% (and up to 17%) of the tbi cases; generalized anxiety disorder in more than 3% (and up to 28%) of the tbi cases; panic disorder in more than 4% of the tbi cases; phobic disorders in more than 1% tbi cases; obsessive-compulsive disorder in more than 2% tbi cases; post-traumatic stress disorder (ptsd) in more than 3% tbi cases; substance abuse or dependency in more than 5% of patients who have suffered a tbi, and schizophrenia in about 1% of tbi cases. [4, 10] it is shown [10] that the headaches occur in more than 25% (up to 90%) of tbi cases; dizziness or vertigo, as the second incidence of sequel after tbi, has been reported to occur in more than 24% (up to 78%) of tbi cases; sleep disorders or drowsiness in up to 73% of tbi cases, compared with 32% in the general population. tiredness was reported in up to 73% of patients who have suffered a tbi, [10] with negative implications for social integration, activities, productivity and quality of life. considering the number of patients with post tbi psychiatric sequels or other post tbi health problems, and based on this epidemiological data of the patients from bihor county treated in the emergency regional hospital, the expected number of patients presenting post tbi psychiatric sequels was estimated, see table 7 below. 113 107 93 97 69 608 603 628 640 597 0 100 200 300 400 500 600 700 1 2 3 4 5 romanian neurosurgery (2015) xxix (xxii) 1: 43 50 49 table 7 estimates on the number of patients with possible post tbi psychiatric sequels or other post tbi health problems, based on the literature name of post tbi disorder specified percentage value estimated number of possible patients post tbi sleep disorders and sleepiness 41% 1011 post tbi tiredness 73% 1,801 post tbi migraine (headaches) 25% 617 post tb vertigo i 24% 592 post tbi depression 70% 1,827 post tbi major depression 14% 345 post tbi bipolar disorder 2% 49 post tbi generalized anxiety disorder 3% 74 post tbi panic disorder 4% 98 post tbi phobic disorders 1% 24 post tbi obsessive-compulsive 2% 49 post tbi ptsd (post traumatic stress disorder) 3% 74 post tbi substance dependence 5% 123 post tbi schizophrenia 1% 24 the estimated total number of tbi psychiatric sequel or other post tbi health problems is more than 6700 new cases. in various studies, [3; 7] the causality (though less explicit in pathophysiological mechanisms) between tbi and some psychiatric disorders was proved. the neuro psychiatric consequences of tbi are numerous in terms of life quality impact or results at workplace e.g. return to job when compared to others disorders; therefore the prevention, rapid detection and effective treatment are highly recommended. [7; 8] at the moment, there is no standard psychiatric management algorithm for acute and sub-acute tbi. so far, this study aimed to emphasize the importance of psychiatric component in the treatment of traumatic brain injury (tbi). correspondence roxana mittler-matica e-mail: roxana.mittler-matica@live.de references 1. bhr pharma, traumatic brain injury fact sheet. bhr pharma, a besisa healtcare company, may, 2012. 2. bryant r, et all, the psychiatric sequelae of traumatic injury. am. journal psychiatry, 2010 , 167:312-3. 3. eurosafe, summary of injury statistics for the year 2008-2010. european association for injury prevention and safety promotion (eurosafe), injuri in the eu. 2012, rijswijkstraat 2, 1059 gk amsterdam, the netherlands, isbn: 978-90-6788-464-8. 50 mittler-matica tbi epidemiological data collected from a county hospital in romania 4. hall ec, lund e, brown d, murdock kr, gettings l, scalea tm, stein dm, how are you really feeling? a prospective evaluation of cognitive function following trauma. j. trauma acute care surg., 2014, mar; 76(3):859-64; discussion 864-5. doi: 10.1097/ta.0000000000000148. 5. http://www.cdc.gov/ncipc/pubres/tbi_congress/01_executive_summary.htm 6. matica roxana, actualităţi ȋn traumatismele cranio cerebrale. lucrare de licenţă, universitatea din oradea, 2010, romania. 7. sansonetti d, hoffmann t, cognitive assessment across the continuum of care: the importance of occupational performance-based assessment for individuals post-stroke and traumatic brain injury. aust. occup. ther. j., oct; 60(5):334-42. doi: 10.1111/14401630.12069. epub. 2013, sep. 1. 8. schwarzbold m, 2008, psychiatric disorders and traumatic brain injury. neuropsychiatric disease and treatment, 4 (4) 797-816. 9. sommer jb, norup a, poulsen i, mogensen j, cognitive activity limitations one year post-trauma in patients admited to sub-acute rehabilitation after severe traumatic brain injury. rehabil. med., 2013, 45: 778–784. 10. whelan-goodison r, ponsford j, schonberger m, association between psychiatric states following traumatic brain injury and outcome. journal rehabil. med., 2008, 40:850-85. 13sumeetsingh_bilateral 474 singh et al bilateral post traumatic thalamic infarct bilateral post traumatic thalamic infarct: rare case report sumeet singh, r.s. mittal, achal sharma sms medical college, jaipur, india dept. of neurosurgery abstract: bilateral thalamic infarction is rarely seen in cases with artery of percheron embolization. artery of percheron is a rare variant of arterial supply to both thalamus and midbrain. occlusion of this artery following trauma and causing bilateral thalamic infarction is rare and very few cases are reported in world literature. key words: bilateral thalamic infarct, artery of percheron, mri. introduction occlusion of artery of percheron is a rare phenomenon and causes bilateral thalamic infarction. it can occur due to embolism to this artery following crush injury of the lower limbs. occlusion of this artery can be the cause of patient loss of consciousness and must be known to attending neurosurgeon to think of this phenomenon other than infectious, inflammatory or malignant cause. case report a 28-year-old man was admitted to accidental emergency with history of road side accident. the patient was conscious oriented with gcs 15. ct brain was normal (figure 1). the initial respiratory and hemodynamic parameters were normal. he had crush injury of right leg which was highly contaminated. his peripheral pulses of right lower limb were not palpable. color doppler shows no flow distal to injured segment. othopedician performed amputation. after 6hours of the surgery patient becomes unconscious. within few hours his glasgow coma score (gcs) decreased to 7 (e2 m4 v1) patient was shifted to icu and was ventilated. medical causes ruled out to know cause of unconsciousness. mri with dwi done reveals abnormal signal intensity in the paramedian thalami as shown in figures 2, 3, 4. dwi confirmed infarction in bilateral thalamic region shown in figure 5. patient was seen by neurologist who was of the same opinion. after neurology consultation patient was started on intravenous methyl prednisolone 1 gm/day administered for five days. ventilation and other supportive treatment were continued. neurologist advised for thrombolytic agents but could not be started because of amputation done. after clinical correlation and radiology of the patient a diagnosis of bilateral paramedian thalamic and midbrain infarction due to occlusion of the artery of percheron by the embolism probably from crushed limb was made. patient died due to septicemia because of infection of amputated wound. romanian neurosurgery (2014) xxi 4: 474 – 477 475 figure 1 ct brain axial image non contrast figure 2 t2 mri image showing hyperintensity in bilateral thalamic region figure 3 t2 mri flair image showing hyperintensity in bilateral thalamic region figure 4 t1 mri image showing mixed hypo and hyperintensity in bilateral thalamic region 476 singh et al bilateral post traumatic thalamic infarct figure 5 dwi mri image showing hyperintensity in bilateral thalamic region discussion during the 70s of the past century, g percheron, the french neurologist (5-7) published three papers describing the vascular anatomy of the posterior circulation, which supplies the human thalamus. according to percheron, there are four variants of paramedian perforating arteries to the thalami. in most people, these arteries arise from the proximal segments of both posterior cerebral arteries, on each side; this is type i variant. when paramedian penetrating arteries arise directly from the proximal segment of one of the posterior cerebral arteries, type iia is found. however, in some people, a single arterial trunk stems off the p1 segment of one of the posterior cerebral arteries and this trunk then divides to supply both thalami and the upper midbrain (type iib); this is the artery of percheron. type iii is defined by the presence of a single arterial arc that links the proximal segments of both posterior cerebral arteries, and from this arc, the paramedian thalamic perforating arteries arise. therefore, percheron artery exemplifies the presence of a small single artery that supplies bilateral vital structures. bilateral paramedian thalamic infarction with/without midbrain infarction due to involvement of the aop supplying thalamus is uncommon. with respect to the prevalence of percheron artery in the general population, the pertinent literature provides scarce information. bogousslavsky and co-workers (2) analysed 1000 consecutive patients with first stroke and found that isolated thalamic infarcts as a presenting feature comprised 11% of all strokes in the posterior circulation while midbrain ischemic infarctions constituted 7% only. uz (8) examined the brains of 15 cadavers; percheron artery was found in one specimen only. to assess the incidence of bilateral thalamic strokes, kumral and colleagues (3) studied the registry of 2750 stroke patients; bithalamic infarctions occurred in 0.6% of their patients only. lazzaro et al (4) identified four patterns of ischemic infarctions when percheron artery is occluded. they retrospectively reviewed the clinical presentation and imaging findings of 37 patients with arterial occlusion. approximately, 43% of their patients demonstrated damage to both paramedian thalami and midbrain (this was the most common pattern), while 38% had ischemic damage to paramedian thalami only, without midbrain involvement. around 14% of patients, the damage involved the anterior thalamic nuclei in addition to paramedian thalami and upper midbrain. the least common pattern (5%) was ischemic damage of bilateral paramedian and anterior thalami; the midbrain was spared here. the sudden loss of consciousness, romanian neurosurgery (2014) xxi 4: 474 – 477 477 respiratory distress in our patient suggested brainstem stroke. however, the initial brain ct scan of the patient showed normal study. the subsequently done mri revealed infarction in both paramedian thalami and the left half of the midbrain. the latter observation explains the involvement of artery of percheron. prior to his presentation, the patient was conscious; there was no explanation for this young patient's ischemic stroke. to date, through conventional angiography, only four authors were able to visualise this artery (1). conclusion artery of percheron occlusion remains an uncommon event and can be the cause of brain stem stroke and thalamic infarction in patient with crush injury. the initial brain ct scan may be normal and brain mri imaging shows abnormal signal intensities in the paramedian thalami with/without anterior thalamic or midbrain extension. the treating neurosurgeon should be aware of this condition. references 1. a, wright b, castillo m, et al. artery of percheron infarction: imaging patterns and clinical spectrum. ajnr am j neuroradiol 2010; 31:1283–9. 2. bogousslavsky j, van melle g, regli f. the lausanne stroke registry: analysis of 1,000 consecutive patients with first stroke. stroke 1988; 19:1083–92. 3. kumral e, evyapan d, balkir k, et al. bilateral thalamic infarction. clinical, etiological and mri correlates. acta neurol scand 2001; 103:35–42. 4. lazzaro na, wright b, castillo m, et al. artery of percheron infarction: imaging patterns and clinical spectrum. ajnr am j neuroradiol 2010; 31:1283–9. 5. percheron g. the anatomy of the arterial supply of the human thalamus and its use for the interpretation of the thalamic vascular pathology. z neurol 1973;205:1–13. 6. percheron g. arteries of the human thalamus. i. artery and polar thalamic territory of the posterior communicating artery. rev neurol (paris) 1976;132:297– 307. 7. percheron g. arteries of the human thalamus. ii. arteries and paramedian thalamic territory of the communicating basilar artery. rev neurol (paris) 1976;132:309–24. 8. uz a. variations in the origin of the thalamoperforating arteries. j clin neurosci 2007; 14:134–7. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 513-516 doi: 10.33962/roneuro-2019-083 www.journals.lapub.co.uk/index.php/roneurosurgery microscopic trans-cerebellar approach for infratentorial cavernous malformation near the lateral recess associated with developmental venous anomaly. case report samer s. hoz1, awfa a. aktham2, hassan m. bdaiwi3, alyaa a. khadim2, zainab a. jihan2, mohammed maan abdulazeez4 1 neurosurgeon, frcs neurosurgery glasgow, department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 neurosurgery resident, department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 3 neurosurgeon, department of meurosurgery, alramadi teaching hospital, anbar, iraq 4 medical student, university of baghdad, college of medicine, baghdad, iraq abstract background: reports showed the intimate association of the developmental venous anomaly with infra-tentorial cavernous malformation. this association has several clinical and surgical implications, sometimes this association will be a surgical challenge and affect the selection of the safest approach to the lesion. surgery for infratentorial cavernoma is indicated for accessible symptomatic lesion only. case scenario: we present a case of deep cerebello-pontine cm adjacent to the lateral recess, presented with acute clinical deterioration to the emergency department of the neurosurgery teaching hospital in baghdad, iraq, with the only possible approach was trans-cerebellar approach because of the medial location of the associated dva. conclusion: the association of developmental venous anomaly with infratentorial cavernous malformation has a pivotal role in selection the most appropriate and safe surgical approach which should be based upon the individualized patient anatomy and the location of the target lesion. introduction developmental venous anomaly is also called venous angiomas, although the latter is abandoned at time being (1). dva drains normal brain tissue, and its formation is still controversial, with most studies suggest that dva represent an arrested development of primitive keywords cavernous malformation, developmental venous anomaly, trans-cerebellar approach corresponding author: mohammed maan abdulazeez university of baghdad, college of medicine, baghdad, iraq mohammed.wwt@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 526 samer s. hoz, awfa a. aktham, hassan m. bdaiwi et al. medullary venous system (1). other emerging studies suggesting the acquired nature of this vascular lesion with possible causation of the associated cm by alteration of the local hemodynamics (2,3). before the introduction of brain ct scan and brain mri, the association between developmental venous anomaly (dva) and cavernous malformation (cm) was not well established. the initial report was at 1984 after introduction of ct scan then followed by frequent reports supporting and confirm this association especially when the brain mri included as a common investigating tool for intracranial vascular lesions (4-6). recent reports showed that up to 30% of dva are associated with cm, and up to 100% of cm are intimately associated with dva (710). the mri features of the cm include the classic “popcorn appearance” due to the presence of hemorrhages at different ages. the dva are usually angiographically evident in the form of the classic caput medusa and may be very clear on mri also especially when being large in size. developmental venous anomalies may be visible only after excision of the associated cm (10). surgery for infratentorial cavernoma is indicated for accessible symptomatic lesion only. we present a case of deep cerebello-pontine cm adjacent to the lateral recess with the only possible approach was trans-cerebellar approach because of the medial location of the associated dva. case scenario a twenty-nine years old male, a known case of cm, presented to the emergency department of the neurosurgery teaching hospital, baghdad, iraq, with acute onset of drowsiness, left side ataxia and cerebellar signs, nystagmus with previous two mild attacks. imaging revealed a new and larger deep cerebello-pontine hemorrhage as compared with previous imaging, the mri suggest confirmation of the previous diagnosis as hemorrhagic cavernoma, associated with very large dva that runs medial then superior to the cm to be drained into the galenic venous system, with no hydrocephalus (figure 1a,1b). based on the acute presentation, the location and size of the hematoma, the history of recurrent hemorrhages, we decide to evacuate the hematoma urgently. with the patient in prone position, left trans-cerebellar approach was done through left suboccipital craniectomy, the hematoma and the cm are totally removed using microsurgical technique. the associated dva is preserved to avoid any unwanted events. the patient improved gradually over the first 5 days’ post operatively and discharged home 10 days after the admission with significant improvement. three months follow up mri show the complete evacuation of the cm with preservation of the adjacent dva. the patient was conscious, neurologically intact apart from very mild ataxia of the left side on follow up visits (figure 1c). a b 527 microscopic trans-cerebellar approach for infratentorial cavernous malformation c figure 1: deep cerebello-pontine hemorrhagic cm associated with very large dva that runs medial then superior to the cm to be drained into the galenic venous system, with no hydrocephalus. pre-operative sagittal (a) and axial (b) mri with contrast, showed both the cm and the large dva. (c): postoperative axial t1 mri, showed the resection cavity. discussion the usual surgical approaches for infratentorial cm near the lateral recess include trans-lateral recess telovellar approach, transcerebellomedullary fissure approach, presigmoid approach, or rarely the anterior endoscopic approach (11,12). the presence of a dva associated with the cm may render the common approaches not feasible. our case of cerebello-medullary cm adjacent to the lateral recess with the only possible approach was trans-cerebellar approach because of the medial location of the associated dva. the surgical strategy for infratentorial cm involves two critical goals: 1. cm should be totally excised to prevent the risk of recurrent hemorrhages without affecting the surrounding normal parenchyma. 2. extreme care should be taken to preserve the associated dva to prevent venous disasters to the normal brain tissue. thus, the usual approach that should be preferred according the accessibility of the cm, will be greatly affected by the location of the associated dva. the usual entry zones may be disturbed by the overlying vascular tissue. although there are frequent reports showed that coagulating some parts of the dva when mandatory during surgery of cm, may pass peacefully especially if the dva is already detected in the preoperative imaging and considered during presurgical planning (10,13). to note that till now there is no approved research comparing dva resection against dva preservation during cm resection surgery (10,14,15). although the trans-cerebellar approach is not always a preferable approach as it involves transgression of important anatomical structure especially deep cerebellar nuclei, but in this case, the advantage of hematoma evacuation outweighs other disadvantages. also, the use of meticulous microsurgical technique with good planning that take in consideration the anatomical landmarks and the possible obstacles, this approach remain a viable option particularly when other approaches are not possible or not safe. conclusion the association of developmental venous anomaly with infratentorial cavernous malformation has a pivotal role in selection the most appropriate and safe surgical approach which should be based upon the individualized patient anatomy and the location of the target lesion. abbreviations list: cm: cavernous malformation dva: developmental venous anomaly ct: computerized tomography mri: magnetic resonance imaging funding information: nothing to declare. conflict of interest declaration: nothing to declare. references 1. lasjaunias p, burrows p, planet c. developmental venous anomalies (dva): the so-called venous angioma. neurosurgical review. 1986 sep 1;9(3):233-42. 2. comey ch, kondziolka d, yonas h. regional parenchymal enhancement with mixed cavernous/venous malformations of the brain: case report. journal of neurosurgery. 1997 jan 1;86(1):154-8. 528 samer s. hoz, awfa a. aktham, hassan m. bdaiwi et al. 3. rothbart d, awad ia, lee j, kim j, harbaugh r, criscuolo gr. expression of angiogenic factors and structural proteins in central nervous system vascular malformations. neurosurgery. 1996 may 1;38(5):915-25. 4. takamiya y, takayama h, kobayashi k, mine t, suzuki k. familial occurrence of multiple vascular malformations of the brain. neurologia medico-chirurgica. 1984;24(4):2717. 5. rigamonti d, spetzler rf. the association of venous and cavernous malformations. acta neurochirurgica. 1988 mar 1;92(1-4):100-5. 6. wilms g, bleus e, demaerel p, marchal g, plets c, goffin j, baert al. simultaneous occurrence of developmental venous anomalies and cavernous angiomas. american journal of neuroradiology. 1994 aug 1;15(7):1247-54. 7. abdulrauf si, kaynar my, awad ia. a comparison of the clinical profile of cavernous malformations with and without associated venous malformations. neurosurgery. 1999 jan 1;44(1):41-6. 8. marasco r, spagnoli m, leonardi m. association between developmental venous anomalies and cavernous angiomas: a retrospective mr study. the neuroradiology journal. 2009 apr;22(2):179-85. 9. perrini p, lanzino g. the association of venous developmental anomalies and cavernous malformations: pathophysiological, diagnostic, and surgical considerations. neurosurgical focus. 2006 jul 1;21(1):1-4. 10. porter rw, detwiler pw, spetzler rf, lawton mt, baskin jj, derksen pt, zabramski jm. cavernous malformations of the brainstem: experience with 100 patients. journal of neurosurgery. 1999 jan 1;90(1):50-8. 11. akiyama, o., matsushima, k., nunez, m., matsuo, s., kondo, a., arai, h., rhoton, a.l. and matsushima, t., 2018. microsurgical anatomy and approaches around the lateral recess with special reference to entry into the pons. journal of neurosurgery, 129(3), pp.740-751. 12. deshmukh vr, rangel-castilla l, spetzler rf. lateral inferior cerebellar peduncle approach to dorsolateral medullary cavernous malformation. journal of neurosurgery. 2014 sep 1;121(3):723-9. 13. wurm g, schnizer m, fellner fa. cerebral cavernous malformations associated with venous anomalies: surgical considerations. operative neurosurgery. 2005 jul 1;57(suppl_1):42-58. 14. pozzati e, marliani af, zucchelli m, foschini mp, dall'olio m, lanzino g. the neurovascular triad: mixed cavernous, capillary, and venous malformations of the brainstem. journal of neurosurgery. 2007 dec 1;107(6):1113-9. 15. pereira vm, geibprasert s, krings t, aurboonyawat t, ozanne a, toulgoat f, pongpech s, lasjaunias pl. pathomechanisms of symptomatic developmental venous anomalies. stroke. 2008 dec 1;39(12):3201-15. doi: 10.33962/roneuro-2020-061 can routine biochemical tests be a short-term prognostic biomarker in patients operated for chronic subdural hematoma? ulaş yüksel, mustafa öğden, i̇brahim umud bulut, bülent bakar, ucler kisa romanian neurosurgery (2020) xxxiv (1): pp. 391-399 doi: 10.33962/roneuro-2020-061 www.journals.lapub.co.uk/index.php/roneurosurgery can routine biochemical tests be a shortterm prognostic biomarker in patients operated for chronic subdural hematoma? ulaş yüksel1, mustafa öğden1, i̇brahim umud bulut1, bülent bakar1, ucler kisa2 1 kırıkkale university, faculty of medicine, department of neurosurgery, kırıkkale, turkey 2 kırıkkale university, faculty of medicine, department of biochemistry, kırıkkale, turkey abstract objectives: the effect of routine blood biochemistry parameters on the short-term prognosis of patients with chronic subdural hematoma (csdh) has not been evaluated in literature before. in this study, it was aimed to establish markers for determination of short-term prognosis using data of patients who were operated for csdh. methods: during admission to hospital, data of patients including age, sex, antiaggregan and/or anticoagulant drugs usage, comorbidity, glasgow coma scale (gcs) and glasgow outcome scale scores were evaluated. location and thickness of csdh were recorded using brain ct or mr images. blood leukocyte, neutrophil, lymphocyte, eosinophil, basophil, platelet count results, neutrophil-lymphocyte ratio and platelet-lymphocyte ratio results, activated prothrombin time and inr values, serum glucose, aspartate aminotransferase, alanine aminotransferase, c-reactive protein, sodium, potassium, blood urea nitrogen and creatinine level values were also recorded. patients were divided into two groups according to csdh located “unilaterally (n=19)” and “bilaterally (n=12)”. in addition, patients with unilateral csdh were divided into two groups as csdh located at the "right hemisphere (n=6)” and "left hemisphere (n=13)". results: it was concluded that short-term prognosis of patients with unilateral or bilateral csdh was similar. correlation analysis showed no correlation between short-term prognosis and demographic, clinical and laboratory findings. however, likelihood ratio test revealed that gcs score could be a biomarker in order to predict short-term prognosis of these patients, albeit weak (x2=6.138, p=0.046). conclusion: it was thought that gcs scores could be effective in predicting shortterm prognosis in patients with csdh but routine biochemistry laboratory parameters could not predict short-term prognosis of these patients. introduction chronic subdural hematoma (csdh) is characterized by the presence of fluid trapped in the capsule or membrane in the subdural space its annual incidence is 5-8.2 / 100000 and generally seen in patients older than 65 years. [1,2] keywords biochemistry, chronic subdural hematoma, prognosis corresponding author: ulaş yüksel kırıkkale university, faculty of medicine, department of neurosurgery, kırıkkale, turkey ulasyksl@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 392 ulaş yüksel, mustafa öğden, i̇brahim umud bulut et al. several studies have reported that the cause of bleeding is often previous head trauma, brain atrophy, advanced age, alcohol abuse and anticoagulant use.[2,3] the rate of surgical treatment in csdh patients is 2.7-33% and burr-hole drainage is the most commonly used surgical technique.[4] however, there is still some controversial in literature in deciding the short-term prognosis in csdh patients. it has been suggested in some studies that midline shift thickness and volume of fluid accumulated in the subdural space may be prognostic markers.[5] in addition, it has been emphasized that the lower the modified rankin scale scores may make the prognosis worse.[6,7] it has been also demonstrated in studies in which csdh cases were evaluated immunologically that interleukin-6 and "vascular endothelial growth factor (vegf)" values measured in hematoma fluid were found to be higher than serum values.[8-10] however, to the best of our knowledge, there is no study in literature to demonstrate the effect of routine blood biochemical parameters on short-term prognosis of patients with csdh. therefore, in this study, demographic, clinical and routine laboratory biochemistry results of patients operated for csdh were investigated and markers were established to determine short-term prognosis. materials and methods materials this retrospective study was conducted after the approval of the “local ethics committee for clinical trials”. the hospital records were scanned using “the international statistical classification of diseases and related health problems (icd-10)” coding (i62: intracerebral hemorrhage (non-traumatic), other hemorrhage) i62.1: extradural hemorrhage (nontraumatic); i62.9: intracranial hemorrhage (nontraumatic), undefined; s06.5: traumatic subdural bleeding). patients who were treated surgically (i.e. burr-hole evacuation) between january 2017 and june 2019 after the determination of the chronic subdural hematoma on brain computed tomography (ct) and / or magnetic resonance imaging (mri) were included in this study. patients with intracranial mass, patients with acute and / or subacute subdural hematoma, patients whose csdh was evacuated by craniectomy or patients whose csdh was not treated surgically but followed-up were excluded from the study. the patients were also excluded from this study if data were incomplete, if they had another intracranial bleed secondary to the trauma (e.g., epidural hematoma, subarachnoid hemorrhage etc), if they had been incorrectly coded with icd-10, did not have subdural hematoma, or were in the pediatric age group (<16 years) patients were divided into two groups according to the subdural hematoma located “unilaterally (n = 19)” or “bilaterally (n = 12)”. in addition, patients with unilateral subdural hematoma were divided into two groups as subdural hematoma located at the "right hemisphere (n = 6)” and "left hemisphere (n = 13)". patients were also divided into two groups according to age (<70 years and <70 years) or gender (female = 6, male = 25). methods during admission to hospital, age, sex, antiaggregan and anticoagulant drugs use, history of comorbidity, glasgow coma scale (gcs) scores and glasgow outcome scale (gos) scores of the patients were recorded. the location and thickness of the chronic subdural hematoma were evaluated using by brain ct or mr images. blood leukocyte, neutrophil, lymphocyte, platelet, eosinophil, basophil count results, neutrophil-lymphocyte ratio (nlr) and platelet-lymphocyte ratio (plr) results, activated prothrombin time and “international normalized ratio” (inr) values, serum glucose, aspartate aminotransferase (ast), alanine aminotransferase (alt), c-reactive protein (crp), sodium (na), potassium (k), blood urea nitrogen (bun) and creatinine level values were recorded. the scales used in this study are listed below: glasgow coma scale (gcs): this scale is used to determine and simply define the consciousness level and neurological status of patients.[11] the scale consists of three subscales (eye findings, speech content, motor response) and is evaluated over 15 points. the higher the patient's score, the better the state of well-being. glasgow outcome scale (gos): it is evaluated over 5 points and is used to identify patients' current neurological levels, levels of help / care, and awareness at the time of discharge from hospital.[12] as the 393 can routine biochemical tests be a short-term prognostic biomarker for chronic subdural hematoma? scale score increases, the patient's level of well-being increases. surgical procedure after sedation anesthesia, frontal and parietal skin incisions of approximately 3 cm were performed in the supine position. subsequently, burr-holes were opened to the cranium using a drill (midas rex®, usa). first, the cross-shaped incision was made to the dura mater in the frontal localized burr-hole and after the chronic hematoma content started to discharge, then cross-shaped incision was made to the dura mater in the parietal localized burr-hole and the hematoma content was completely removed. subdural space was then irrigated with saline solution using foley catheter and then suction drain was left to the frontal region from the parietal burrhole and the galea and skin were sutured anatomically before the operation was terminated (figure 1). in patients with bilateral csdh, a similar procedure was performed on the other side (figure 2). biochemical analysis biochemical data of the study were obtained from the analysis of patients' venous blood samples which were taken during their admission to the hospital. serum glucose (reference range 74-109 mg / dl), crp (reference range 0.15-5 mg / dl), alt (reference range 5-41 u / l), ast (reference range 5-40 u / l), creatinine (reference range 0.84-1.24 mg / dl) and bun (reference range 17-43 mg / dl) level values were measured of the "immunoturbidimetric method" and levels of serum sodium (reference range 136-146 mmol / l) and potassium (reference range 3.5-5.1 mmol / l) were determined by ion selective electrode (ise) method using commercial kits (roche) and an analyzer device (roche diagnostic cobas c501). blood leukocyte (reference range 4400-11300 ul), neutrophil (reference range 1,1009600 ul), lymphocyte (reference range 500-6000 ul), eosinophil (reference range 0-1000 ul), basophil (reference range: 0-300 ul) and platelets (reference range 150000-500000 ul) count values were determined using an analyzer (mindray bc-6800, shenzen, china). activated prothrombin time (reference range 24.0-39.2 minutes) and inr (0.8-1.2) values were measured using an analyzer (acltop700, usa). statistical analysis mann-whitney u test was used to compare the nonparametric data between the groups. independent samples t test was used to compare the parametric data between the groups (p <0.05). spearman's rho correlation test was used to determine the relationship between the parameters (p <0.05). likelihood ratio test was used to find the best parameter to predict the short-term prognosis of the patients (p <0.05). results a total of 31 patients (female = 6, male = 25) were included in this study. demographic, clinical and laboratory findings of all patients are summarized in table 1 and figure 3. at the end of the medical past history, it was found that 3 patients had coronary artery disease, 5 had essential hypertension, 4 had diabetes mellitus, 4 had chronic obstructive pulmonary disease, 3 had a history of cerebral stroke, and 1 had atrial fibrillation. six of the patients were using antiaggregant and two of the patients were taking anticoagulant drugs, but activated prothrombin time and inr values were within normal limits. it was observed that new onset left hemiparesis was detected in 5 patients, new onset right hemiparesis in 5 patients, new onset dysphasia in 3 patients, and new onset stupor in 4 patients at their admission to the hospital. at the end of the correlation analysis of all parameters of all patients, there was found no correlation between short-term prognosis and demographic, clinical and laboratory findings. however, at the end of likelihood ratio test, it was seen that gcs scores could be a good parameter in predicting the short-term prognosis of patients with csdh (x2 = 6.138, p = 0.046). when patients were divided into two groups according to unilateral or bilateral localization of chronic subdural hematoma, comorbidity was found to be higher in patients with unilateral csdh (x2 = 4.288, p = 0.038). in addition, the thickness of rightsided hematoma was higher in patients with bilateral csdh (z = -4.169, p <0.001). other demographic, clinical and laboratory data was not different between the groups (table 2). at the end of the correlation analysis applied to the parameters of each group, no study parameter was found to be correlated with the patient's neurological status and post-treatment short-term prognosis. 394 ulaş yüksel, mustafa öğden, i̇brahim umud bulut et al. in addition, when the patients with unilateral csdh were divided into two groups according to the hematoma located on the right side hemisphere or the left side hemisphere, the gos scores of the patients with right side hemisphere hematoma were found to be lower (z = 2.156, p = 0.031), while platelet count values were higher (t = 2.243, p = 0.040). however, there was no statistical difference between the groups in terms of other demographic findings and laboratory values (table 3, figure 2). at the end of the correlation analysis of the parameters belonging to each group, no study parameter was found to be correlated with the patient's neurological status or postoperative short-term prognosis. however, at the end of the likelihood ratio test, it was concluded that gcs score (x2 = 12.079, p = 0.002) and plr values (x2 = 8.578, p = 0.014) could be a biomarker for predicting the short term prognosis of the patients with unilateral csdh. when the patients were divided into two groups according to age distribution and gender, the demographic, clinical and laboratory findings of the patients was not statistically different between the groups and it was observed at the end of the correlation test and likelihood ratio test that these parameters could not be a predictive biomarker in determining the short-term prognosis of these patients. table 1. it shows the demographic data and blood biochemistry findings of the patients (sd: standard deviation, min: minimum, max: maximum). variable mean±sd/ number (%)/ median (min-max) age (year) 72.19±14.62 gender female 6 (19.4) male 25 (80.6) comorbidity no 16 (51.6) yes 15 (48.4) drug usage no 23 (74.2) yes 8 (25.8) convulsion no 29 (93.5) yes 2 (6.5) glasgow coma scale score 15 (8-15) glasgow outcome scale score 5 (1-5) right sided hematoma thickness (mm) 15.61±11.21 left sided hematoma thickness (mm) 12.39±11.59 leukocyte (ul) 8726.79±3517.66 neutrophil (ul) 6686±3199.51 lymphocyte (ul) 1460±739.55 monocyte (ul) 495±257.46 eosinophil (ul) 121±121.42 basophil (ul) 57±86.75 platelet (ul) 244035±88146.97 neutrophil-lymhocyte ratio 5.79±4.04 platelet-lymphocyte ratio 195.75±91.86 c-reactive protein (mg/dl) glucose (mg/dl) 130.04±44.14 blood urine nitrogen (mg/dl) 52.80±29.53 creatinine (mg/dl) 1.13±0.89 sodium (mmol/l) 134.93±17.25 potassium (mmol/l) 4.36±0.86 alanine aminotransferase (u/l) 12.28±3.80 aspartate aminotransferase (u/l) 23.93±13.73 international normalized ratio (inr) 1.15±0.23 activated protrombine time 28.29±11.91 395 can routine biochemical tests be a short-term prognostic biomarker for chronic subdural hematoma? table 2. this table shows the results of the demographic, radiographic and biochemical analyses of the patients according to the subdural hematoma located “unilaterally” or “bilaterally” (t: t score, x2: chi-square, z: z score, sd: standard deviation, min: minimum, max: maximum). unilateral hematoma bilateral hematoma variable mean±sd/ number (%)/ median (min-max) mean±sd/ number (%)/ median (min-max) t/x2/z p age (year) 74.32±15.12 68.83±13.75 1.017* 0.317 gender female 4 (12.9%) 2 (6.5%) 0.091† 0.763 male 15 (48.4%) 10 (32.3%) comorbidity no 7 (22.6%) 9 (29.0%) 4.288† 0.038 yes 12 (38.7%) 3 (9.7%) drug usage no 14 (45. 2%) 9 (29.0%) 0.007† 0.935 yes 5 (16.1%) 3 (9.7%) convulsion no 18 (58.1%) 11 (35.5%) 0.115† 0.735 yes 1 (3.2%) 1 (3.2%) glasgow coma scale score 15 (8-15) 15 (8-15) -0.709‡ 0.478 glasgow outcome scale score 5 (1-5) 5 (4-5) -0.983‡ 0.326 right sided hematoma thickness 6.84±10.77 21.17±6.25 -4.169* <0.001 left sided hematoma thickness 16.42±13.09 14.33±7.71 0.499* 0.622 leukocyte (ul) 8532±3892.01 9027±3001.62 -0.358* 0.723 neutrophil (ul) 6535±3302.91 6918±3176.02 -0.304* 0.764 lymphocyte (ul) 1415±872.74 1530±499.34 -0.392* 0.698 monocyte (ul) 469±296.07 534±189.44 -0.647* 0.523 eosinophil (ul) 140±126.54 91±112.14 1.047* 0.305 basophil (ul) 53±69.02 62±112.43 -0.266* 0.792 platelet (ul) 240823±110146.06 249000±39020.51 -0.235* 0.816 neutrophil-lymhocyte ratio 5.99±3.64 5.49±4.76 0.312* 0.758 platelet-lymphocyte ratio 203.06±100.54 184.45±79.89 0.516* 0.610 c-reactive protein (mg/dl) 14.50 (2.00-65.00) 2.58 (1.14-71.00) -1.791‡ 0.073 glucose (mg/dl) 138.75±50.03 116.50±30.84 1.191* 0.247 blood urine nitrogen (mg/dl) 57.85±32.12 44.21±23.56 1.167* 0.254 creatinine (mg/dl) 1.20±1.03 1.02±0.61 0.497* 0.623 sodium (mmol/l) 133.09±21.38 138.06±5.47 -0.716* 0.481 potassium (mmol/l) 4.34±1.01 4.39±0.57 -0.145* 0.886 alanine aminotransferase (u/l) 12.46±4.29 12.03±3.18 0.269* 0.790 aspartate aminotransferase (u/l) 26.90±16.25 19.47±7.44 1.347* 0.191 international normalized ratio 1.18±0.18 1.12±0.29 0.666* 0.512 activated protrombine time 30.39±16.48 25.98±1.49 0.841* 0.397 right sided hematoma left sided hematoma variable mean±sd/ number (%)/ median (min-max) mean±sd/ number (%)/ median (min-max) t/x2/z p age (year) 81.17±9.60 71.15±16.44 1.374* 0.187 gender female 0.0% 4 (21.1%) 2.338† 0.126 male 6 (31.6%) 9 (47.4%) comorbidity no 3 (15.8%) 4 (21.1%) 0.652† 0.419 yes 3 (15.8%) 9 (47.4%) drug usage no 4 (21.1%) 10 (52.6%) 0.223† 0.637 yes 2 (10.5%) 3 (15.8%) convulsion no 6 (31.6%) 12 (63.2%) 0.487† 0.485 yes 0 (0.0%) 1 (5.3%) glasgow coma scale score 15 (8-15) 15 (9-15) -0.203‡ 0.839 glasgow outcome scale score 4.50 (1-5) 5 (4-5) -2.156‡ 0.031 hematoma thickness (mm) 21.67±5.68 24.00±7.75 -0.657* 0.520 396 ulaş yüksel, mustafa öğden, i̇brahim umud bulut et al. table 3. this table shows the results of demographic, radiographic and biochemical analyses of the patients according to the subdural hematoma located “right hemisphere” or “left hemisphere” (t: t score, x2: chi-square, z: z score, sd: standard deviation, min: minimum, max: maximum). figure 1. ct images of a patient with chronic subdural hematoma unilaterally; (1a) on admission to hospital; (1b) early postoperative image. figure 2. ct images of a patient with chronic subdural hematoma bilaterally; (2a) on admission to hospital, and (2b) early postoperative image and (2c) at discharge from the hospital. leukocyte (ul) 9916±4933.55 7955±3456.79 0.943* 0.361 neutrophil (ul) 7372±4350.28 6187±2921.63 0.662* 0.518 lymphocyte (ul) 1640±754.62 1322±931.92 0.672* 0.512 monocyte (ul) 628±280.93 403±287.41 1.477* 0.160 eosinophil (ul) 198±146.70 116±115.43 1.232* 0.237 basophil (ul) 52±45.50 54±78.58 -0.062* 0.952 platelet (ul) 323800±127609.56 206250±85391.21 2.243* 0.040 neutrophil-lymhocyte ratio 5.27±2.37 6.29±4.12 -0.514* 0.615 platelet-lymphocyte ratio 225.66±130.63 193.6±590.38 0.586* 0.567 c-reactive protein (mg/dl) 16.00 (5-65) 13.00 (2-53.14) -0.570‡ 0.569 glucose (mg/dl) 154.31±77.67 132.52±38.13 0.723* 0.484 blood urine nitrogen (mg/dl) 67.47±34.68 53.85±31.69 0.787* 0.444 creatinine (mg/dl) 1.01±0.17 1.28±1.23 -0.486* 0.634 sodium (mmol/l) 140.04±3.54 130.19±25.09 0.858* 0.404 potassium (mmol/l) 4.77±0.48 4.16±1.13 1.155* 0.266 alanine aminotransferase (u/l) 14.42±5.54 11.68±3.74 1.087* 0.299 aspartate aminotransferase (u/l) 21.28±8.03 28.95±18.25 -0.798* 0.439 international normalized ratio 1.24±0.26 1.16±0.14 0.772* 0.455 activated protrombine time 29.27±5.74 30.81±19.44 -0.132* 0.898 397 can routine biochemical tests be a short-term prognostic biomarker for chronic subdural hematoma? figure 3. graphics show the “glasgow coma scale” and “glasgow outcome scale” scores, chronic subdural hematoma thickness located at the left and right-side hemisphere of all patients. discussion the aim of this study was to determine how its surgical treatment affected the short-term prognosis of the patient using their demographic, clinical and laboratory findings. for this purpose, gos scores of patients included in the study were used to establish the short-term prognosis of these patients. furthermore, in this study, it was aimed to determine short-term prognostic indicators in the patients with csdh using simple, inexpensive and easily applicable blood biochemistry tests in almost every health institution. it has been reported in the literature that the prognosis of the patient with intracranial hemorrhage who has a gcs score of 7 or less is worse.[13-15] in the studies conducted on this subject, the mean gos score was found to be 1 point in cases with gcs score of 7 and below, while the gos score was found in the range of 4-5 points in cases with gcs score above 7.[16-19] in addition, it has been shown that the advanced patient age and comorbidity such as vascular pathology, coagulation disorder and diabetes mellitus adversely affects the prognosis in patients with chronic subdural hematoma.[20] the most commonly preferred surgical treatment method in patients with chronic subdural hematoma is the burr-hole evacuation technique.[21-23] it has been reported that the mortality rate after surgical treatment is 10% in patients with csdh, but in some studies, this rate can reach up to 32% and morbidity may occur in up to 20% of these patients.[23] in our study, it was found that the additional diseases detected in the study patients had no effect on the short-term prognosis but bilateral subdural hematoma was more common in patients with additional disease. in addition, it was found that anticoagulan and / or antiaggregant drug use did not affect short-term prognosis in these patients. with these findings it could be said that comorbidity and / or anticoagulan and / or antiaggregant drug use may not affect on the short term prognosis in surgically treated patients with csdh. on the other hand, short-term prognosis was similar in patients with unilateral or bilateral csdh. therefore, the presence of unilateral or bilateral csdh had no effect on the short-term prognosis of these patients. however, in patients with unilateral csdh, right-sided subdural hematoma was thought to adversely affect to the short-term prognosis. on the other hand, in our study, no significant correlation was found between the gcs scores of the patients at the time of hospital admission and gos scores at the end of the treatment. in addition, no direct or indirect relationship was found between these gos scores and other parameters including demographic or laboratory parameters. however, likelihood ratio test applied to the data of all patients revealed that the gcs scores of patients could be a parameter in predicting prognosis of these patients in the short-term period, albeit in a weak character. as a matter of fact, 2 operated patients died in the hospital (mortality rate of 6.4%) despite the gcs score of 15/15 while 3 operated patients whose gcs scores were 8, 13, 14 were discharged from the hospital with the help of daily life (gos score was 4, morbidity of 10.34%). furthermore, all of the 398 ulaş yüksel, mustafa öğden, i̇brahim umud bulut et al. remaining patients left the hospital with a gos score of 5 regardless of gcs scores. on the other hand, routine blood biochemistry results have been examined in studies conducted to determine the prognosis in patients with csdh and it has been argued that hscrp, albumin, prealbumin, inr elevations may be associated with poor prognosis but other routine blood biochemistry values have no effect on prognosis.[24] in our study, unfortunately, none of the simple routine blood biochemistry value had any effect on the short-term prognosis of the patients, postoperatively. however, it was concluded at the end of the likelihood ratio test that gcs scores and plr values may be a biomarker in predicting the prognosis of these patients in the early postoperative period. as a matter of fact, two of the patients with unilateral subdural hematoma died postoperatively. one of these 2 patients had no additional disease and laboratory values were within normal limits. the other patient had chronic obstructive pulmonary disease and high leukocyte and lymphocyte count values. both patients had no history of anticoagulant and / or antiaggregant drug use. therefore, no parameter could be found to correlate the existing mortality with csdh. in addition, gcs values were found to be similar in patients with csdh which located on the right or left hemisphere and it did not show any statistical relationship with any study parameter. however, unilateral csdh was thought to cause a relative increase in platelet count in patients and this could lead to an increase in plr values. however, this increase in platelet count remained within the normal range of laboratory values. furthermore, gos scores, platelet and lymphocyte count and plr values were not different between groups and there was no direct or indirect relationship with the gos scores and platelet and lymphocyte count and plr values. therefore these parameters could not be a biomarker in predicting the short-term prognosis of patients with csdh. limitations this study had some limitations. firstly, the study was of a retrospective character and the number of patients included in the study was not sufficient because the patients' data was obtained from single health center. secondly, patients with chronic subdural hematoma followed without performing surgery was not included in this study. therefore, in this study, it could not be determined how chronic subdural hematoma itself affected the short-term prognosis of these patients. thirdly, because ultrastructural methods such as histopathological and biochemical investigation of the hematoma and / or cerebrospinal fluid could not be included in this study, the effects of these investigation findings on short term prognosis could not be evaluated in this study. finally, patients with chronic subdural hematoma evacuated by craniotomy were not included in the study. therefore, the differentiation of the short term prognosis between the patients performed burr-hole evacuation and patients treated using craniotomy could not be discussed. conclusion in conclusion, gcs values of patients with chronic subdural hematoma which were measured during the admission to the hospital could be weakly effective in predicting the short-term prognosis after surgical treatment of these patients. however, it was found that routine biochemical laboratory parameters were not successful in determining the short-term prognosis of these patients. conflict of interest and financial disclosure statements the authors declare that they have no conflict of interest. there no any funding. they also declare that they have not engaged in any financial relationship with any company whose product might be affected by the research described or with any company that makes or markets a competing product. references 1. adhiyaman v, asghar m, ganeshram kn, et al. chronic subdural haematoma in the elderly. postgrad med j. 2002;78:71-5. 2. markwalder tm. chronic subdural hematomas: a review. j neurosurg. 1981;54:637-45. 3. christopher e, poon mtc, glancz lj, et al. outcomes following surgery in subgroups of comatose and very elderly patients with chronic subdural hematoma. neurosurg rev. 2019;42:427-31. 4. baechli h, nordmann a, bucher hc, et al. demographics and prevalent risk factors of chronic subdural haematoma: results of a large single-center cohort study. neurosurg rev. 2004;27:263-6. 5. santos rgd, xander paw, rodrigues lhds, et al. analysis of predisposing factors for chronic subdural hematoma recurrence. rev assoc med bras. 2019;65:834-8. 6. agawa y, mineharu y, tani s, et al. bilateral chronic subdural hematoma is associated with rapid 399 can routine biochemical tests be a short-term prognostic biomarker for chronic subdural hematoma? progression and poor clinical outcome. neurol med chir (tokyo). 2016;56:198-203. 7. shen j, shao x, wang q, et al. comparison of clinical and radiologic characteristics and prognosis of patients with chronic subdural hematoma with and without a history of head trauma. world neurosurg. 2019;132:391-8. 8. frati a, salvati m, mainiero f, et al. inflammation markers and risk factors for recurrence in 35 patients with a posttraumatic chronic subdural hematoma: a prospective study. j neurosurg. 2004;100:24-32. 9. hohenstein a, erber r, schilling l, et al. increased mrna expression of vegf within the hematoma and imbalance of angiopoietin-1 and -2 mrna within the neomembranes of chronic subdural hematoma. j neurotrauma. 2005;22:518-28. 10. suzuki m, endo s, inada k, et al. inflammatory cytokines locally elevated in chronic subdural haematoma. acta neurochir (wien). 1998;140:51-5. 11. teasdale g, jennett b. assessment of coma and impaired consciousness. a practical scale. lancet. 1974;2(7872): 81-4. 12. mcmillan t, wilson l, ponsford j, et al. the glasgow outcome scale 40 years of application and refinement. nat rev neurol. 2016;12:477-85. 13. auer lm, deinsberger w, niederkorn k, et al. endoscopic surgery versus medical treatment for spontaneous intracerebral hematoma: a randomized study. j neurosurg. 1989;70:530-5. 14. juvela s, heiskanen o, poranen a, et al. the treatment of spontaneous intracerebral hemorrhage. a prospective randomized trial of surgical and conservative treatment. j neurosurg. 1989;70:755-8. 15. waga s, yamamoto y. hypertensive putaminal hemorrhage: treatment and results. is surgical treatment superior to conservative one? stroke. 1983;14:480-5. 16. elhechmi yz, hassouna m, chérif ma, et al. prognostic value of serum c-reactive protein in spontaneous intracerebral hemorrhage: when should we take the sample? j stroke cerebrovasc dis. 2017;26:1007-12. 17. garton ala, gupta vp, christophe br, et al. biomarkers of functional outcome in intracerebral hemorrhage: interplay between clinical metrics, cd163, and ferritin. j stroke cerebrovasc dis. 2017;26:1712-20. 18. shimizu k, sadatomo t, hara t, et al. importance of frailty evaluation in the prediction of patients with chronic subdural hematoma. geriatr gerontol int. 2018;18:11736. 19. nouvenne a, ticinesi a, lauretani f, et al. the prognostic value of high-sensitivity c-reactive protein and prealbumin for short-term mortality in acutely hospitalized multimorbid elderly patients: a prospective cohort study. j nutr health aging. 2016;20:462-8. 20. yasuda cl, morita me, nishimori fy, et al. chronic subdural hematoma: study of 161 patients and the relationship with coagulation abnormalities. arq neuropsiquiatr. 2003;61:1011-4. 21. lind cr, lind cj, mee ew. reduction in the number of repeated operations for the treatment of subacute and chronic subdural hematomas by placement of subdural drains. j neurosurg. 2003;99:44-6. 22. motiei-langroudi r, stippler m, shi s, et al. factors predicting reoperation of chronic subdural hematoma following primary surgical evacuation. j neurosurg. 2018;129:1143-50. 23. ramachandran r, hegde t. chronic subdural hematomas--causes of morbidity and mortality. surg neurol. 2007;67:367-73. 24. wang s, ma y, zhao x, et al. risk factors of hospital mortality in chronic subdural hematoma: a retrospective analysis of 1117 patients, a single institute experience. j clin neurosci. 2019;67:46-51. romanian neurosurgery (2019) xxxiii (3): pp. 332-336 doi: 10.33962/roneuro-2019-057 www.journals.lapub.co.uk/index.php/roneurosurgery ewing’s sarcoma of the mobile spine. three unusual observations a. khelifa1, i. assoumane2, s. bachir3, l. berchiche1, n. benmedakhene1, t. bennafaa1, a. morsli1 1 neurosurgical department of beo university hospital, algiers, algeria 2 neurosurgical department of niamey, niger 3 neurosurgical department of laghouat hospital, laghouat, algeria abstract background. ewing’s sarcoma is a bony highly malignant tumour, it occurs most frequently in the second decade of life. ewing’s sarcoma is a rare affection, located usually in the pelvis, the femur, the humerus, the ribs, the mandible and clavicle, other location are rare especially in the spine. we report three cases of spinal ewing’s sarcoma, two primary spine locations and one on young adult with unusual clinical presentation. cases presentation case 1. the first patient is a girl of 14 years old without past medical history. she presented initially two months before consultation a neck pain followed days after by a weakness of the left upper limb; the spine imaging performed objectified a destructive process of c2 with a spinal cord compression. the patient was operated beneficiating of a spinal cord decompression and a subtotal removal of the tumour. the pathologist’s results were in favour of ewing’s sarcoma and the patient was oriented to oncology. case 2. the second patient is a man of 31 years old operated five years before he consulted for shoulder ewing’s sarcoma followed by chemotherapy and radiotherapy, he presented two months before consultation a cauda equina syndrome. spine mri objectified a double location of an epidural tumour at t3-t4 and s1-s2 levels. the patient was operated beneficiating of subtotal removal of the tumour. the laboratory exam results were in favour of ewing’s sarcoma and the patient was oriented to oncology. case 3. the third patient is a 6 years old boy who presented a 1 month history of low back pain followed by a rapidly deteriorating weakness of both lower limbs over a weak. on examination there was bilateral spastic paraplegia, hypoesthesia below the level of th10 and a urinary retention. the mri imaging revealed a lesion on the levels th8, th9 and th10 vertebras involving the body, pedicle, lamina, and the transverse process on the left side with an epidural invasion compressing the spinal cord. the tumour was radically removed. pathology report was in favour of ewing’s sarcoma. two weeks after surgery the patient was able to walk. he was referred for adjuvant systemic chemotherapy. conclusion. ewing’s sarcoma is rare malignant tumour. the location in the spine exposes the patient to more complications because of the neurostructures compression. the surgical total removal followed by radio and chemotherapy is the only option with the best prognostic and guaranties an acceptable life quality. keywords ewing’s sarcoma, spinal cord compression, child malignancy corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 333 ewing’s sarcoma of the mobile spine introduction ewing’s sarcoma is a bony highly malignant tumour, it occurs most frequently in the second decade of life (1,3,4,5,7,8,10). ewing’s sarcoma is a rare affection (4), located usually in the pelvis, the femur, the humerus, the ribs, the mandible and clavicle (7), other location are rare especially in the spine(4,8). we report three cases of spinal ewing’s sarcoma two primary spine locations and one on young adult with unusual clinical presentation. figure 1 patient 1 imaging. a: sagittal t1 wi sequence cervical mri; b: sagittal t2 wi sequence; c: axial t2 wi sequence; d: sagittal bone window ct; e: axial bone window ct; f: postoperative x rays. case presentation case 1 the first patient is a girl of 14 years old without past medical history. she presented initially two months before she consults a neck pain followed days after by a weakness of the left upper limb; the spine ct and mri performed objectified a destructive process of c2 with a spinal cord compression (figure 1). the patient was operated beneficiating of a spinal cord decompression and a subtotal removal of the tumour, the lesion is considered to cause a spinal instability so an occiptocevical fixation was put. the pathologist’s results were in favour of ewing’s sarcoma and the patient was oriented to oncology for adjuvant treatment. case 2 the second patient is a man of 31 years old operated five years before for shoulder ewing’s sarcoma followed by chemotherapy and radiotherapy, he presented two months before consultation a cauda equina syndrome. spine ct and mri objectified a double location of an epidural tumour at t3-t4 and s1-s2 levels (figure 2). the patient was operated beneficiating of subtotal removal of the both lesions through th3 and th4 then s1 and s2 lamenectomy. the laboratory exam results were in favor of ewing’s sarcoma and the patient was oriented to oncology. 334 a. khelifa, i. assoumane, s. bachir et al. figure 2. patient 2 imaging. a: sagittal cervical t1 wi mri; b: sagittal cervical t2 wi mri; c: axial cervical t2 wi mri; d: sagittal lumbosacral t2 wi mri; e: sagittal lumbosacral bone window ct. case 3 the third patient is a 6 years old boy who presented a 1 month history of low back pain followed by a rapidly deteriorating weakness of both lower limbs over a weak. on examination there was bilateral spastic paraplegia, hypoesthesia below the level of th10 and a urinary retention. the mri imaging revealed a lesion on the levels th8, th9 and th10 vertebras involving the body, pedicle, lamina, and the transverse process on the left side with an epidural invasion compressing the spinal cord (figure 3). the tumour was radically removed. pathology report was in favour of ewing’s sarcoma. two weeks after surgery the patient was able to walk. he was referred for adjuvant systemic chemotherapy. figure 3. patient 3 spine mri. a: preoperative t1 injected sequence; b: postoperative t2 wi. discussion ewing sarcoma (es) was first described by james ewing in 1921(2,6). it is a small round blue neoplastic cells (1,2,3,4,5,6,7,8,9) with clear to lightly eosinophilic cytoplasm, evenly dispersed chromatin, and indistinct nucleoli (3,7). es is found in bones or in the surrounding soft tissues (1,3,4,5,6,7,8). es is usually diagnosed in the second decade of life (1,3,4,5,7,8,10), the occurrence in adulthood is sporadic (1,6,3,8). ewing’s sarcoma present 4% of paediatric malignant tumours (4), it arises mostly in the long bones in 47% of cases, pelvis in 19%, and on ribs in 12% of cases (7), vertebral location is seen in less than 6% of cases (4,8), and mostly located in sacrococcygeal region (5,6,7), its presence on nonsacral spine is found in only 0.9% of all cases (7) with extremely rare involvement of the cervical spine (5,7). the primary location on the spine is unusual (4,6,7). being a primary bone tumour, extra osseous locations are rare in a review between 1969 and 2015 only 119 cases of extra osseous es was reported among them 76 cases of epidural es (3). the clinic is summarized in the triad of local pain, palpable mass and neurologic deficit depending on the site of compression (1,7). radiographic exams in spinal es are not specific (3,6,8). mostly it is a lytic lesion, sclerotic changes are rarely seen (7,8,9) especially in primary lesions(8). spinal es is located on posterior elements in 70% of cases and on the body in 30% of cases which could lead to vertebral collapse (8), extraossous location is limited to some reported cases (3,8). plain radiography shows the lytic lesions tardively (7,9) usually after the neurological signs became obvious (9). ct is very helpful to assess the amount of destruction of the vertebral body and posterior element (7,9). soft tissue lesions are better 335 ewing’s sarcoma of the mobile spine outlined by mri, es have hypo or isointense signal on t1 weighted imaging and a hyperintense signal on t2 weighted imaging with heterogeneous enhancement after gadolinium injection (3,8). there is no standard management described for the spinal es and no difference between child and adult treatment strategy (1,6). usually it associates surgery chemotherapy and radiotherapy. the surgery assures biopsy, the local control of the tumour, spinal cord decompression and spinal stabilization. because of the intimate relationship with neurological structures some surgeons prefer intralesional excision or debulking of the tumour in order to prevent long term morbidity (4) but many studies suggest that gross total resection is associated with better outcome (1,2,3,4,6,9). tumours excised with 2 cm of normal tissue are considered to have safe surgical margins (2) otherwise radiotherapy is highly indicated (1,2,3,4,5,6,7,9). radiation doses could not exceed 45 gy (3,4,9). radiotherapy could be used alone to assure the local control of the tumour (2,3,4,6), but with high risk of deterioration and less overall survival (2,3,4). when surgery and radiotherapy assure the local control of the tumour, chemotherapy is indicated to eradicate systemic micro metastasis (1,2,3,4,5,9). with patients who have no neurological deterioration and if the diagnosis is made before by needle biopsy a neoadjuvant chemotherapy could be proposed in order to shrink the tumour which could facilitate its removal (1,2,6,7,9). the classical chemotherapy protocol of es is vaca (vincristine, actinomycin, cyclophosphamide and doxorubicin) (3,9) many other drugs have been added like ifosfamide and or etoposide (vac/ie) which improved the outcome (1,2,3). prognosis is poor in the spinal es compared to other locations (1,4), other factors are related to a bad prognosis like the presence of metastasis (1,5,7) the adult age (3,7) and extra osseous location (3). in the other hand tumours located in the sacrum are associated with a poor prognosis due to the late stage diagnosis (4) and those located in cervical spine due to the difficulties of the total resection (7). the local control of the tumour with en bloc resection is associated with the best survival outcome (1,3,4,6,9). overall median survival in spinal es is 26 months, the survival rates for 5-year is at 41% and for 10-year 34% (4,10). conclusion ewing’s sarcoma is rare malignant tumor. the location in the spine exposes the patient to more complications because of the neurostructures compression. the surgical total removal followed by radio and chemotherapy is the only option with the best prognostic and guaranties an acceptable life quality. references 1. shoubash l, nowak s, vogelgesang s, schroeder hw, müller ju. surgical management of an adult manifestation of ewing sarcoma of the spine—a case report. ame case rep 2018;2:34. doi: 10.21037/acr.2018.06.07. 2. toshifumi ozaki. diagnosis and treatment of ewing sarcoma of the bone: a review article. j orthop sci (2015) 20:250–263. doi 10.1007/s00776-014-0687-z. 3. mark bustoros, cheddhi thomas, joshua frenster, aram s. modrek, n. sumru bayin, matija snuderl, gerald rosen, peter b. schiff, and dimitris g. placantonakis. adult primary spinal epidural extraosseous ewing’s sarcoma:a case report and review of the literature. hindawi publishing corporation case reports in neurological medicine volume 2016, article id 1217428, 8 pages. http://dx.doi .org/10.1155/2016/1217428. 4. manjusha nair, reghu kesavapillai sukumaran nair, rajeev kavalakararaghavan, kusumakumary parukkutty, renu sukumaran. primary ewing’s sarcoma of the spine in pediatric patients: a case series analysis and literature review. middle east journal of cancer; april 2015; 6(2): 115120. 5. kyriakos paraskeva, dimitrios giakoumettis, ioannis nikas, george georgoulis, george sfakianos, marios s. themistocleous. primary ewing sarcoma of the axis-c2: a case report and the review of the literature. neurologia i neuroc h irurgia polska 52 (2018) 534 – 542. https://doi.org/10.1016/j.pjnns.2018.02.005. 6. maurizio iacoangeli,mauro dobran, alessandro di rienzo, lucia giovannamaria di somma, lorenzo alvaro, elisamoriconi, niccol `onocchi, maurizio gladi, andmassimo scerrati. non metastatic ewing’s sarcoma of the lumbar spine in an adult patient. hindawi publishing corporation case reports in oncological medicine volume 2012, article id 165289, 5 pages. doi:10.1155/2012/165289. 7. adil aziz khan, sehrish nadeem, iqra kanwal, sameer raja. an unusual case of ewing’s sarcoma of cervical spine. journal of rawalpindi medical college; 2019;23(s-1):56-58. 8. patnaik s, yarlagadda j, susarla r. imaging features of ewing’s sarcoma: special reference to uncommon features and rare sites of presentation. j can res ther 2018;14:1014-22. doi: 10.4103/jcrt.jcrt_1350_16. 336 a. khelifa, i. assoumane, s. bachir et al. 9. leandro i. dini, rodrigo mendonça, pasquale gallo. primary ewing’s sarcoma of the spine. arq neuropsiquiatr 2006;64(3-a):654-659. 10. mukherjee d, chaichana kl, gokaslan zl, aaronson o, cheng js, mcgirt mj. survival of patients with malignant primary osseous spinal neoplasms: results from the surveillance, epidemiology, and end results (seer) database from 1973 to 2003. j neurosurg spine. 2011 feb;14(2):143-50. doi: 10.3171/2010.10.spine10189. epub 2010 dec 24. doi: 10.3171/2010.10.spine10189. 14aakumar 116 kumar et al post-traumatic acute bilateral facial nerve palsy post-traumatic acute bilateral facial nerve palsy a management dilemma rakesh kumar1, jitin bajaj1,2, devendra purohit1,3, radheshyam mittal1,4 1department of neurosurgery, sawai man singh medical college, jaipur, rajasthan, india 2resident; 3professor; 4professor & head abstract: acute bilateral facial nerve paralysis is a rare clinical entity, and its management remains very controversial (operative or conservative). here we are presenting a case of acute onset bilateral facial nerve palsy following head injury with bilateral temporal bone fracture with clinico-radiographic contrary. patient was managed conservatively with complete recovery. by this article, authors want to stress on combining clinical examination and radiological findings for decision making of this rare entity and tried to evaluate the management. key words: acute, post-traumatic, bilateral, facial nerve palsy. introduction acute bilateral facial nerve paralysis is a rare clinical entity. nearly 5% of all facial palsy is due to trauma [1]. in all the patients of bilateral facial nerve palsy only three per cent of cases are due to temporal bone fractures and rest all have medical disease, infections or tumours [2]. out of all post traumatic temporal bone fractures, which occur in 14 to 22% of all skull injuries, only 9% of patients will have bilateral temporal bone fractures [3].on reviewing the english literature posttraumatic acute bilateral facial nerve palsy is rare after closed head injury, and its management remains very controversial (operative or conservative). here we are reporting a case of acute onset post traumatic bilateral facial nerve palsy, which recovered completely following conservative treatment. case report a twenty seven year old male presented three hours after road traffic accident with a history of transient loss of consciousness and left ear bleed. on examination his gcs was 15/15 and there was bleeding from left ear. no csf leak was seen. the patient had bilateral lmn type facial nerve palsy (house brackmann grade iv) (figure 1). his lacrimal and taste sensations were found to be intact indicating the lesion of the facial nerve distal to origin of chorda tympani nerve in petrous romanian neurosurgery (2015) xxix (xxii) 1: 116 119 117 bone. all other cranial nerves were normal. audiometric examination, showed no conductive/ sensorineural hearing loss. his ct scan of head (figure 2) revealed right temporal contusion without any mass effect. ct right temporal bone (figure3b) was suggestive of longitudinal fracture of squamous & petrous part involving anterior margin of middle ear cavity reaching up to lateral margin of meatal segment of facial nerve canal, and longitudinal fracture of squamous & petrous part of left temporal bone with fracture line extending in anterior part of middle ear cavity and involving meatal segment of facial nerve canal (figure 3a). electro diagnostic study of facial nerve was found to be normal with no distal axonal degeneration. patient was managed conservatively with oral steroids and on followup. he gradually improved to complete facial nerve functions within 8 weeks (figure 4). figure 1 photograph of patient showing bilateral lmn type facial nerve palsy figure 2 ncct head showing right temporal contusion a b figure 3 ct left temporal bone showing longitudinal fracture (3a) and ct right temporal bone (3b) was suggestive of longitudinal fracture of squamous & petrous part of temporal bone fracture line 118 kumar et al post-traumatic acute bilateral facial nerve palsy figure 4 photograph of patient showing recovery figure 5 linear line diagram showing clinico radiographic contrary discussion the facial nerve is the second most common cranial nerve, after olfactory nerve, involved in head injuries [4], while some authors report it to be the most common [5,6]. unilateral facial nerve palsy is more common with transverse fractures (40-50%), and less with longitudinal fractures (20%). in cases of facial nerve palsy with longitudinal fractures intraneural hematoma or contusion is found in 43%, bony impingement in 33%, transection in 15%, and as idiopathic in 12%. in contrast, facial nerve palsy due to transverse fractures, transection is found in 92% and bony impingement in 8% [7]. de villers et al [8] proposed that the longitudinal fracture of petrous part of temporal bone can lead to backward displacement of the petrous apex and coronal splitting of the body of sphenoid leading to mirror image fracture in the opposite temporal bone producing bilateral facial nerve palsy, while a transverse fracture of the petrous bone will not involve bilateral facial nerves [8]. in our case we could not found backward displacement of sphenoid bone. for better correlation with hearing impairment temporal bone fracture is categorized in the otic capsule sparing (ocs) versus otic capsule disrupting (ocd) fractures [3].in our case the fracture was otic capsule sparing type hence patient has no hearing impairment. high resolution computed tomography (hrct) 1mm thin cuts of temporal bone is a useful diagnostic tool for traumatic facial nerve palsy, as it can visualize the fracture line and its relationship to the fallopian canal. as advised by darrouzet et al, immediate onset facial nerve palsy with a fracture line running through the fallopian canal is considered a definite indication for early surgical intervention [9]. many researchers advocate no exploration for non-penetrating trauma for intra-temporal facial nerve palsy [9]. patients with delayed onset facial romanian neurosurgery (2015) xxix (xxii) 1: 116 119 119 weakness or incomplete facial weakness should be managed conservatively with steroids and vasodilators [9]. late surgery may be recommended in cases of non-recovery within 6 months after trauma. hence the management of these patient is still controversial. the preservation of lacrimal and taste sensations indicate the injury of facial nerve distal to origin of chorda tympani nerve, while on ct scan the fracture line can be seen running over the roof of middle ear bilaterally (figure 6). hence it appears that it may be the contusion injury to bilateral facial nerve leading to acute bilateral facial nerve palsy. decision of conservative management of the patient was consider due to this clinico radiographic contrary. on the conservative management patient recovered completely. we advocate that all the patient of facial nerve palsy(acute/delayed) should be given conservative management first with steroid and physiotherapy and if there is no recovery at the end of three months then surgery (nerve anastmosis) may be consider. electroneurography doesn’t provide any information about the level of injury in acute injury, but in long term follow up it is valuable for prognosis of recovery [10]. conclusion traumatic acute bilateral facial nerve palsy is a rare clinical entity. in patients with immediate palsy, possibility of transection should be considered, which can be ruled out with hrct 1 mm thin cuts of temporal bones. it can be combined with clinical examination and findings of electrical testing to help characterize the site, degree and prognosis of nerve injury. in patients with acute facial nerve palsy with anatomic continuity of the nerve, outcome ought to be excellent in most patients, and should be initially managed conservatively. acknowledgement we acknowledge our patient for giving his consent to publish this matter. correspondence dr. rakesh kumar 4kh2, shastrinagar, jaipur, rajasthan, india, 302004. e-mail: rksingh2226@gmail.com references 1. steenerson l. bilateral facial paralysis. the american journal of otolarytigology, 7: 99-103, 1986. 2. glasscock e, wiet j, jackson g, dickins jr. rehabilitation of the face following traumatic injury to the facial nerve. the laryngoscope, 89: 1389-1404,1979. 3. ki-hong kevin ho, tomoko makishima. temporal bone fracture source: grand rounds presentation, utmb, dept. of otolaryngology. march 31, 2010. 4. coello af, canals ag, gonzalez jm, martín jj. cranial nerve injury after minor head trauma. j neurosurg. 2010 sep;113(3):547-55. doi: 10.3171/2010.6.jns091620. 5. dolan kd: temporal bone fractures. semin us ct mr 10:262-279,1989 6. haberkamp tj, harvey sa, daniels dl: the use of gadolinium-enhanced magnetic resonance imaging to determine lesion site in traumatic facial paralysis. laryngoscope 100:1294-1300, 1990. 7. chang cy, cass sp. management of facial nerve injury due to temporal bone trauma. the american journal of otology; 20: 96-114, 1999. 8. de villiers jc. fracture-dislocation of the petrous temporal bone. j neurol neurosurg psychiatr. 1971;34:104–109. 9. darrouzet v, duclos jy, liguoro d, truilhe y, de bonfils c, bebear jp. management of facial paralysis resulting from temporal bone fractures: our experience in 115 cases. otolaryngol head neck surg. 2001;125:77–84. 10. sertac y. total facial nerve decompression for severe traumatic facial nerve paralysis: a review of 10 cases. int j otolaryngol. 2012:5. papacoceatoma_factors 162 | papacocea et al factors influencing the recurrence rate of operated chronic subdural hematomas factors influencing the recurrence rate of operated chronic subdural hematomas toma papacocea1,2, danil adam1,2, raisa croitoru2, ionut rusu2, alexandru papacocea3 1“carol davila” university of medicine and pharmacy, bucharest, romania; 2neurosurgical department, emergency “saint pantelimon” hospital, bucharest, romania 3neurosurgical department, county general hospital, ploiesti, romania abstract: in this study we are trying to establish a correlation between the surgical technique used for the treatment of chronic subdural hematomas and the risk of recurrence. between 01.06.2008 and 31.05.2014, 123 patients with 138 chronic subdural hematomas (csdh) were operated on and followed-up in our department. among them, 16 hematomas (11,6%) recurred. factors related to the patients (gender, age, location of the hematoma) are analyzed as possible predictors of recurrence. several surgical techniques were used in the treatment of chronic subdural hematomas. each of them is analyzed to find possibly connections with the recurrence risk of the size of the approach, the reposition of the bone flap, the suture of the dura and other aspects. there are obvious, statistically significant correlations between the risk of recurrence and some elements of the surgical technique employed. key words: chronic subdural hematoma, recurrence, surgical technique introduction chronic subdural hematomas (csdh) represent a frequent encountered pathological condition in neurosurgery. despite this fact, there still are, nowadays, controversies and unclear aspects concerning the best management of this particular type of intracranial hemorrhage (4,8). technically, a csdh is located in the otherwise potential intradural space as a consequence of the disruption of the dural border cell layer from the deep pachymeninges (11). blood in this space provokes an inflammatory reaction, which results in an enveloping surrounding membrane (14) although some csdhs evolve from acute subdural hematomas, most experimental models have failed to produce an enlarging csdh from a solid clot. (13,18). most of the time, there is no clear traumatic history that precedes the discovery of a csdh. in the cases in which there is no trauma involved, other etiologies, such as coagulopathy, vascular romanian neurosurgery (2016) xxx 2: 162-167 | 163 malformations, metastasis, meningiomas or inflammatory lesions must be considered (20). although spontaneous resolution of csdh can occur, patients with a neurologic deficit should undergo surgical evacuation. the patients complaining of headache, but otherwise neurologically intact should be referred to a neurosurgical service, where they can be monitored with serial ct scans (15). the collection will often become smaller and disappear. should there be an increase in the size of the csdh and/or of the symptomatology, the patient should undergo surgical intervention (17). the efficacy of the standard procedures for evacuation of a csdh (twist drill, burr hole, craniotomy with or without irrigation and drainage of the subdural space) can be reflected by the recurrence rate of the csdh after these procedures postoperative recurrence of csdh still represents an important issue. among published series, the recurrence rates usually vary between 3,7% and 21,5% (19). there are some factors that clearly influence recurrence, such as coagulopathy, brain atrophy, alcoholism, intracranial hypotension, bilateral surgery (5). the involvement of other factors is still debatable. the aim of this study was to identify risk factors correlated with the recurrence of csdh. we analyzed 2 categories of such presumptive risk factors: related to individual features of the patients (age, gender, bilaterality of lesions) and related to the operative technique. material and methods this is a retrospective study conducted in the neurosurgical department of “saint pantelimon” emergency hospital from bucharest, romania encompassing patients operated on for csdh between 01.06.2008 and 31.05.2014. the inclusion criteria were: patients with unior bilateral csdh with: at least 3 weeks of free interval after an identifiable trauma, if any ctscan showing homogenous iso/hypodensity without signs of rebleeding or important layering by arachnoid septae intraoperative aspect of dark “motor oil” fluid cases with subacute sdh, or with fresh bleeding on the ct images, or csdh complicated with thick septal or calcified membranes were excluded from this study, in an attempt to clear out recurrence risk factors related to the hematoma density and architecture. according to the inclusion criteria listed above, there were 123 consecutive patients recruited in the study. among them, 15 patients were operated on bilateral, so there were an overall of 138 csdh operated on. there were 16 csdh that recurred, giving an 11,6 % overall recurrence rate. the gender distribution was 83 males versus 40 females, meaning a sex ratio of 2.1/ 1 m/w. most of the patients (48) were more than 70 years old, 38 were between 60 and 69 years old and 37 were younger than 60. several surgical techniques were used for the operative treatment of the csdh in our 164 | papacocea et al factors influencing the recurrence rate of operated chronic subdural hematomas department. we employed 4 main approaches with different technical variants of dural closure summarized below: a. burr-hole b. 2.5 cm large craniectomy cross-shaped incision of the dura bipolar coagulation used to shrink the dura to the full width of the bony opening c.2.5 cm large craniotomy with trephine and re-emplacement of the bone flap c1. without dural suture c2. with partial dural suture c3. with complete dural suture d. 4cm large craniotomy d1. with partial dural suture d2. with complete dural suture beside this technical differences between the variants exposed above, there were also some common steps always employed in the surgical treatment of csdh in our department: the complete evacuation of the hematoma with abundant irrigation and aspiration coagulation of the outer membrane of the hematoma at the bony opening margins epidural non-aspirating drain for 36-72 hours postoperatively the attitude concerning the inner membrane was not unitary: in 58 cases it was resected or coagulated and in 80 cases it was not touched. postoperatively, all patients were kept in bed-rest restriction with the head of the bed flat and mild overhydration until 24-48 hours after the drain was removed. results we compared the recurrence rate between different categories of patients. firstly, we analyzed the individual features of the patients in an attempt to observe any predisposition to recurrence related to gender or age. we found no significant differences, as one can see in figures 1 and 2, respectively. figure 1 – gender distribution romanian neurosurgery (2016) xxx 2: 162-167 | 165 figure 2 – age distribution “st. pantelimon” emergency hospital, bucharest (neurosurgical department) figure 3 – results “st. pantelimon” emergency hospital, bucharest (neurosurgical department) we also analyzed bilaterality of csdh as a possible risk factor for recurrence and we found that, among the 15 cases of bilateral hematomas operated, 3 patients needed reoperation on both sides, giving a 20% recurrence rate, significant more than the average recurrence of the whole group (11,6%) afterwards, we compared the recurrence rates of each surgical variant presented above in the text. the results are exposed in figure 3. it is obvious that there is a very high recurrence rate for variants a and c3, and also a high recurrence rate (rr) for variant d2. we can also observe that there is a low, under average recurrence rate for variants b and d1, 166 | papacocea et al factors influencing the recurrence rate of operated chronic subdural hematomas and an outstanding 0% rr for variants c1 and c2. the controversial topic of touching or avoiding the inner membrane is illustrated in the table in figure 4 which shows that rr in cases when the inner membrane is resected or coagulated is much higher (17,2%) than in cases where this membrane is left alone (7,5%). figure 4 – inner membrane “st. pantelimon” emergency hospital, bucharest (neurosurgical department) discussions a symptomatic recurrence means the reappearance of neurologic signs and symptoms together with a volume increase of the csdh with mass effect on ct-scan within weeks to months after surgery (2). this situation must be distinguished from residual collections that are asymptomatic, do not demonstrate pressure effects on ct and can be followed with serial studies until their complete or nearly complete resolution without surgical intervention (3). a clinical improvement in the status of the operated patients can be obtained when the subdural pressure is reduced to close to zero, which usually occurs after 20% of the collection is removed (7). ct scans can show persistent fluid collection in 78% of cases on post-op day 10 and in 15% after 40 days (1), and it may take up to 6 months for complete resolution (5). it is, therefore, recommended not to treat a persistent fluid collection unless it increases in size on ct or if the patient shows no recovery or deteriorates (6). an ongoing debate concerns optimal surgical management of a csdh. in this topic the meta-analysis by weigel and colleagues is of great interest. this study is based on a review of 48 publications and covers a period of time between 1981 and 2001. the authors of this meta-analysis conclude that craniotomy is associated with the lowest recurrence rate but a higher morbidity rate compared to more limited approaches (twist drill and burr hole) (12,19). in the patients included in this study we didn’t use subdural drainage; data in the literature suggests that this maneuver can decrease the rr from 19% to 10% (9). conclusions 1. individual factors like gender and age don’t influence the rr. 2. bilateral csdh are more prone to recur than unilateral ones. 3. the single burr-hole technique without subdural aspirating drainage is associated with a high recurrence rate and should be avoided 4. the best technique for decreasing the risk of recurrence seems to be the 2.5 cm. craniotomy without any or only with partial suture of the dura. 5. the complete suture of the dura increases the risk of recurrence especially in smaller approaches and should be avoided. 6. a larger than 2.5 cm approach for uncomplicated csdh brings no improvement of the rr. romanian neurosurgery (2016) xxx 2: 162-167 | 167 7. there are no significant differences related to the rr between 2.5 cm craniectomy and craniotomy, but the cosmethic aspect should be taken into account. 8. the inner membrane of the csdh shouldn’t be touched during the operation in order to avoid a higher rr. correspondence toma papacocea “carol davila” university of medicine and pharmacy, bucharest, romania e-mail: tpapacocea@hotmail.com references 1. adeolu aa, rabiu tb, adeleye ao: post-operative day two versus day seven mobilization after burr-hole drainage of subacute and chronic subdural haematoma in nigerians. br j neurosurg 26:743-746, 2012. 2. berghauser pont lm, dippel dw, verweij bh, dirven cm, dammers r: ambivalence among neurologists and neurosurgeons on the treatment of chronic subdural hematoma: a national survey. acta neurol belg 113:5559, 2013. 3. berghauser pont lm, dirven cm, dippel dw, verweij bh, dammers r: the role of corticosteroids in the management of chronic subdural hematoma: a systematic review. eur j neurol 19:1397-1403, 2012. 4. bozkurt g, ahyan s, akbay a, palaoglu s. treatment of chronic subdural hematoma by twist drill craniostomy with irrigation. turkish neurosurgery 2006; 16:19-24. 5. cenic a, bhandari m, reddy k: management of chronic subdural hematoma: a national survey and literature review. can j neurol sci 32:501-506, 2005. 6. chari a, clemente morgado t, rigamonti d: recommencement of anticoagulation in chronic subdural haematoma: a systematic review and metaanalysis. br j neurosurg 28:2-7, 2014. 7. delgado pd, cogolludo fj, mateo o, cancela p, garcia r, carrillo r: early prognosis in chronic subdural hematomas. multivariate analysis of 137 cases rev neurol 30:811-817, 2000. 8. ducruet af, grobelny bt, zacharia be, hickman zl, derosa pl, anderson k, sussman e, carpenter a, connolly es, jr.: the surgical management of chronic subdural hematoma. neurosurg rev 35:155-169, 2012. 9. erol fs, topsakal c, faik ozveren m, kaplan m, tiftikci mt: irrigation vs. closed drainage in the treatment of chronic subdural hematoma. j clin neurosci 12:261-263, 2005. 10. etminan n, vergouwen md, ilodigwe d, macdonald rl: effect of pharmaceutical treatment on vasospasm, delayed cerebral ischemia, and clinical outcome in patients 11. haines d,harkey h,al-mefty o: the subdural space: a new look at an outdated concept. neurosurgery 32: 1120, 1993 12. ibrahim i, maarrawi j, jouanneau e, guenot m, mertens p,sindou m. evacuation of chronic subdural hematomas with the twist-drill technique: results of a randomized prospective study comparing 48-h and 96-h drainage duration. neurochirurgie 2010; 56:23-7. 13. ito h, yamamoto s, komai t, mizukoshi h. role of local hyperfibrinolysis in the etiology of chronic subdural hematoma. j neurosurg 1976; 45:26-31. 14. jones s, kafetz k. a prospective study of chronic subdural haematomas in elderly patients.age and ageing 1999; 28:519-21. 15. lin x. comparing twist-drill drainage with burr hole drainage for chronic subdural hematomachin j traumatol 2011; 14(3):170-173 16. nakajima h, yasul t, nishikawa m, kishi h, kan m. the role of postoperative patient posture in the recurrence of chronic subdural hematoma: a prospective randomized trial. surg neurol 2002; 58:385-7. 17. pruna v, bucur n, neacsu a, andrei g, sandu a, gorgan m calcified chronic subdural hematona – case report romanian neurosurgery vol xv nr 2 pag 22-25 18.watanabe s, shimada h, ishii s : production of clinical form of chronic subdural hematoma in experimental animals. j neurosurg 37: 552-561, 1972 19. weigel r, schmiedek p, krauss j : outcome of contemporary surgery for chronic subdural hematoma : evidence based review. j neurol neurosurg psychiatry 74:937943, 2003 20. wilberger j. pathophysiology of evolution and recurrence of chronic subdural hematoma.neurosurg clin n am 2000; 11:435438. doi: 10.33962/roneuro-2021-005 the impact and causes of negative cortical mapping in primary motor area tumours mihaela coșman, bogdan florin iliescu, anca sava, gabriela florența dumitrecu, ion poeată romanian neurosurgery (2021) xxxv (1): pp. 29-35 doi: 10.33962/roneuro-2021-005 www.journals.lapub.co.uk/index.php/roneurosurgery the impact and causes of negative cortical mapping in primary motor area tumours mihaela coșman1, bogdan florin iliescu2,3, anca sava4, gabriela florența dumitrecu4, ion poeata3 1 emergency county hospital, department of neurosurgery, braila, romania 2 department of neurosurgery, “n. oblu” emergency clinical hospital, iași, romania 3 “gr. t. popa” university of medicine and pharmacy, department of neurosurgery, iași, romania 4 department of anatomopathology, “n. oblu” emergency clinical hospital, iaşi, romania abstract introduction: intraoperative neurophysiological monitoring is the golden standard for lesions located in eloquent areas of the brain. on the one hand, positive mapping offers a view of the relationship between the anatomo-functional cortical organisation of the patient and the lesion, facilitating the choice of the cerebrotomy entry point and the resection until the functional borders are found. on the other hand, negative mapping does not offer certainty that the absence of the motor response, from the operative field, is the real feedback or is the result of the falsenegative response. in such a situation, a differentiation between those two must be done. materials and methods: we evaluated the results of direct cortical stimulation of lesion located in or near the primary motor area, which were diagnosticated with contrast-enhancement head mri and admitted to the third department of neurosurgery, "prof. dr n. oblu” emergency clinical hospital, iasi, romania, between january 2014 and july 2018. special attention was given especially to the negative mapping cases, regarding the histological type, imagistic localisation, symptoms and neurological outcome immediate postoperative, at 6 months and one-year follow-up. results: from all 66 patients meeting the inclusion and exclusion criteria in 9,09% (6 cases) we did not obtain any motor response after direct cortical stimulation. the imagistic localisations of those cases were: 3 – rolandic, 2 – pre-rolandic and one retro-rolandic. tumors histological types were: glioblastoma, anaplastic astrocytoma, oligoastrocytoma and oligodendroglioma each one case and two cases of fibrillary astrocytoma. the intensity range was between 6 – 18ma, the mode – 12ma and the median – 10ma. postoperatively the neurological condition of 3 patients worsened (4,54% from all the cases), while 3 had a favourable evolution with symptom remission. at 6monts and one-year follow-up in one case (1,51%), we observed no improvement in contrast with the other two, where dysfunction remission was highlighted. conclusion: the possible technical, surgical and anesthesiologic causes of falsenegative motor response must be eliminated to be able to differentiate from the real keywords negative mapping, positive mapping, direct cortical stimulation, primary motor area, brain tumour corresponding author: mihaela coșman emergency county hospital, department of neurosurgery, braila, romania mihaelacosman@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 30 mihaela coșman, bogdan florin iliescu, anca sava et al. absence of the functional area from the operative field. in the first scenario, the resection may be associated with permanent postoperative neurologic deficit and major life quality alteration while in the second one the patient presents no motor dysfunction after surgery and the resection may be extensive with multiple oncological benefits. introduction intraoperative neurophysiological monitoring (iom) remains across time in the first line and have gotten the title of the golden standard procedure for lesion located in functional areas, even though we are witnessing a high development of functional imaging techniques especially 3d diffusion tractography and functional magnetic resonance imaging [1,9, 11]. a young age of presentation, paucisymptomatic cases, lesions with good survival rate make the life quality of the patients one of the main medical priorities and so an intraoperative real time feedback it is mandatory for a maximal surgical resection with a minimal neurological dysfunction. the presence of the tumour with its perilesional oedema modifies the normal functional cortical organisation and the topography of the eloquent areas is distorted. brain mapping with direct cortical stimulation helps identify the functional tissue and differentiate the false-eloquent lesion from the real-eloquent ones, with a considerable impact over the degree of resection [4,5]. positive mapping is recommended because reveals the anatomical-functional patients brain organisation, which has an interindividual degree of variability helping in choosing the best approach for the tumour resection considering the functional borders [31]. a negative mapping which means the absence of identification of the functional sites in the operative fields has the advantages of o smaller craniotomy, less time in performing the cortical stimulation and decrease the intervention time. a disadvantage of this technique is represented by the fact that negative is not equal with a shore absence of the functional tissue because of the possibility of occurrence of false negative response. the latter is associated with new, eventually permanent motor deficit. hence the importance of clearing the false negative recordings and the real absence of functional cortex from the operative filed [27,33]. in the following article we present and discuss the poststimulation response after direct cortical stimulation performed on patients with tumors located in central area. the cases in which we did not obtain any response, even though radiologically the primary motor area was located in the operating field were study from clinical, histological and imagistic point of view. materials and methods we present a study group which included patients with surgical lesions in primary motor area or in its vicinity, diagnosed using contrast-enhancement magnetic resonance imaging (mri), who underwent surgery in the 3rd neurosurgery department of prof. dr. n. oblu clinical emergency hospital of iasi, between 1 january 2015 and 1 july 2018. 76 patients were initially enrolled in the group, but 6 of them were excluded because they did not come to the 6month and one-year follow-up examination after surgery, and 4 were excluded because they had a pacemaker. in the end, the group included 66 patients. inclusion criteria in the study group: tumor located in the primary motor area radiological diagnosed; age over 18 years; intraoperative use of iom; presentation at the 6 months and one-year followup; consent to be included in the study. exclusion criteria in the study group: tumor located in the motor area, but inoperable; cases in which only stereotactic biopsy was performed; patients with pacemaker; incomplete patient data. intraoperative neurophysiological monitoring was performed using the nim eclipse device from medtronic. direct cortical stimulation was achieved by means of the short-train technique or train of five. the values of the parameters used in all patients were the following: frequency = 3 hz, number of pulses = 5, duration = 500μsec, inter-stimuli interval = 4 msec, intensity interval: 6-18ma.the recording muscles were: abductor pollicis brevis, biceps brachii, deltoid, abductor hallucis and tibialis anterior muscle. results 76 patients were initially diagnosticated with a lesion in primary motor area, but after applying the inclusion and the exclusion criteria the study group included 66 patients. the age group distribution was 18 – 79 years and the male/female ratio: 32 (48.48%) / 34 (51.51%). as far as the clinical manifestation is concerned, jacksonian seizures ranked first. the anatomopathological findings revealed a 31 the impact and causes of negative cortical mapping in primary motor area tumours glioblastoma (gb) predominance – 21 cases (31.81%), followed by meningioma (mg) – 19 patients (28.78%), metastases (mts) – 12 patients (18.18%), anaplastic astrocytoma (aa) – 4 cases (6.06%), fibrillary astrocytoma (af) – 4 cases, oligoastrocytoma (oa) – 4 cases and oligodendroglioma (odg) – 2 cases (3.03%). the most frequent stimulation value that generated motor response was 12ma, then 8ma, followed by 10 ma and 9 ma; 13ma, 14ma, 15ma and 16ma, respectively, were necessary in a smaller number of cases. the peak value 18ma was used only when the stimulation produced no motor response at inferior values. the intensity range was between 6 – 18ma, the mode – 12ma and the median – 10ma. no direct cortical stimulation response was received in 6 of all patients (9.09%). preoperative lesions localization revealed by head mri were: 3 – rolandic, 2 – pre-rolandic and one retro-rolandic. from the anatomopathological point of view, there were 2 patients with af and one case each following histological type: glioblastoma, anaplastic astrocytoma, oligoastrocytoma and oligodendroglioma. after surgery, the neurological condition of 3 patients worsened (4,54% from all the cases), while 3 had a favourable evolution with symptom remission. the functional status and extent of resection overlapped. thus, 3 cases who underwent gtr showed motor deficit, while in the other 3 cases, where the resection was subtotal, the clinical manifestation improved. overall, favourable outcome was achieved in 65,15% of the patients from the study group and new deficits or worsening of the pre-existent one was observed in 15,15% cases. at 6-months and one-year follow up, one case (1,51%) from those with no intraoperative motor response was stationary from the neurological point of view and the other two shown some functional improvement. an illustrative case is presented in figure 1. figure 1. 28 years old female with right prerolandic oligodendroglioma (a-c) has presented with jacksonian seizures which became drug resistant 2 years after the onset. she was operated using and iom. postoperatively she installed left brachial paresis even though intraoperative no cortical motor response was found at direct cortical stimulation (d). she slightly recovered the motor deficit at one year follow up. (a) preoperative head mri: t2 and flair weighted-images, the star – rolandic area. (b) postoperative mri hypersignal in hand area. (c) one year follow up images, oedema remission. (d) no motor response (intensity-18ma), standard baseline muscular recordings (biceps brachii, abductor hallucis, tibialis anterior muscle). 32 mihaela coșman, bogdan florin iliescu, anca sava et al. discussion for lesion with imagistic location in or near eloquent areas of the brain is extremely important to determine the precise relationship between the tumour and the functional cortex. in comparison with negative, positive cortical sites bring a higher confidence in choosing the cortectomy entry zone and in performing the maximal degree of resection with the aim of minimal postoperative neurological deficits. when in the operative field we do not have the presumed eloquent area is sometimes more stressful because we do not know its location and we are not sure of the postoperative neurologic status for cases with extensive resection [6, 36]. in our study group we had 6 cases in which we did not obtain the motor response. the percentage of 9,09% overlaps over the literature findings (magill et al., reported 91% of positive mapping) [24]. the absence of the expected motor response or negative mapping creates uncertainty because we must differentiate form the false negative response over real absences of the functional cortex. the former is associated with new postoperative motor dysfunction and has technical, anaesthesiologic and surgical causes. the latter is often the result of neuroplasticity process and the patient remains neurological intact after tumour resection. chang et al., revealed that 36% of his presumed eloquent cases, based on the radiological images, where in fact false-eloquent. this characterisation is associated with good outcome, because allows to perform an extended degree of resection. the impact of lesion location is considered especially in low grade glioma patients regarding the tumour ablation and progression free survival [5,8]. so et al., published an article in 2018 in which he showed that the motor response is not restricted only to the primary motor area, in 7% of the patient’s motor response was observed and posterior to the central sulcus. in one-fourth of them positive sites were discovered anterior to the central sulcus. tumours growth may be associated with displacement of the normal anatomy and of course of the functional areas, like in two-third of the tested patients [36]. our results shown that only 3 lesions from those with negative mapping were situated strictly rolandic and the other three were preand retro-rolandic. regarding technical causes, those can be prevented by preoperative evaluation of the equipment quality, necessary for the procedure, e.g., the electrodes, the stimulation probe. verification of the precise placement of the electrodes is particularly important for a correct recording with real assessment of the eloquent area, especially after the patient was positioned, looking for detachments. another significative step is represented by performing the technique correctly intraoperatively, direct stimulating the cortex, avoiding other structures like blood vessels or through a high amount of cerebrospinal fluid [20, 21,25]. other causes of negative mapping may be: stimulation with an intensity below the threshold value, shorter pulse duration, electric current transmission through the cerebrospinal fluid and stimulation during the refractory period (pallud et al., 2017, eseonu et al., 2018) [10, 27]. therefor the parameters settings of the stimulation current are important and it’s good to know de differences form the two methods of motor network assessment. the traditional technique – penfield method uses a low frequency (lf) 50 – 60 hz, a stimulus train of 1 – 4s of biphasic pulse, while short train technique or train of five (tof, hf) uses a high frequency 250 – 500hz, a stimulus train of 10 – 18milliseconds of monophasic pulse [3, 30, 32]. those parameters are usually selected before the surgery and remain the same, the only variable being the value of the stimulus intensity. for our cases we chose the train of five technique and the intensity range was between 6 – 18ma, the mode – 12ma and the median – 10ma, for direct cortical stimulation. in the speciality literature we usually find papers regarding one technique, but a comparison was made between the lf and hf used on the same patients, in an article from 2020 presented by bander et al., and the results showed that bipolar hf technique allowed to identify the primary motor cortex in a proportion of 100% (13 cases) vs. 31% obtained using the bipolar lf stimulation [2]. beside choosing from the two methods of performing iom, we used, for brain mapping, the technique of stimulating the entire exposed cortex with a constant current value starting from an intensity of 6 ma, which was subsequently progressively increased with 1 ma until the motor response was generated or at a peak value of 18 ma. another brain mapping technique consist in stimulating every single site with progressive higher current until the response is generated. this is based 33 the impact and causes of negative cortical mapping in primary motor area tumours on the interindividual and intraindividual threshold variability [6, 22, 29]. pourtain et all, in 2004 observed significative differences between frontal motor response, parietal/temporal language response and frontal language mapping, the mean stimulation threshold was: 8,4± 2,8ma, 12,3 ±2,9 ma, 9,3 ±3,6ma. this type of mapping has the disadvantage of an increased risk of producing the afterdischarge potentials which may induce intraoperative seizures. maximizing the current intensity may be associated with less specific cortical eloquent sites identification due to adjacent and subcortical functional stimulation. another drawback may be represented by the fact that is not time efficient. both approaches are able to determine the functional sites and the absence of the response is not dependent of which method we use but on knowing the advantages and disadvantages of both of them. in general, if the current intensity is used in order to prevent the appearance of afterdischarge potentials and the threshold is less than the minimum necessary to identify the functional sites, then false negative response will be generated [12, 14]. the bias generated by false negative response may be due to the learning curve of the team including the surgeon, the anesthesiologist and the neurophysiologist. the knowledge and the ability of response interpretation has a great impact on the postoperative neurological status and on the degree of tumor resection. in a paper from 2020 pan et al., reveal that the run-in period for his team was around two years and the unexpected postoperative new motor deficit happened in the first three year from the technique application [28]. in our study all the patients had been operated by the same members of the team and the technical aspects were under the responsibility of the same person. discussing the surgical aspects one cause for the absence of a response after stimulation may also be due to a smaller craniotomy with more limited cortex exposure. the literature study showed that intraoperative eloquent sites were identified in a proportion of 30% to 100% of the cases: e.g., positive mapping (pm) 58% (eseonu et al., 2018), 65% (kim et al., 2009), 91% (magil et al., 2018) the new postoperative deficit was 51,5% in pm patients vs. 12,5% negative mapping (nm) patients (eseonu et al., 2018), 12% pm vs. 9% nm (kim et al., 2009), 60% new / worsen deficit, not specified regarding the pm nor nm (magil et al.,2018) [10, 19, 24]. in our study group positive mapping was achieved in 90,91% of the patients. the postoperative outcome was represented by new dysfunction in 15,15% of the cases, 4,54% being from those how did not respond after stimulation. at one-year follow-up in just one case, from the study group, the motor deficit persisted. it is clear that small craniotomy may limit the identification of the eloquent sites but as showed before the new postoperative motor deficit was higher in positive mapping patients, this suggesting that is not mandatory to perform a large bone flap just for cortical stimulation. tailored craniotomy which includes the tumor and the adjacent cortex may be enough [24, 33]. in literature it is mentioned that in some limited number of cases, not the dimension of the bone flap is the cause of the negative mapping or of the new installed motor deficit but rather omission or not including a group of muscle from recording setup. most often it is citated transient orofacial paresis [25]. other surgical manoeuvres like dissection in the proximity of the corticospinal tract, vascular occlusion of the rolandic artery or vein may create inadvertence in recording motor evocated potentials. for centres where the subdural grid /stipe electrode is used more attention must be offered to the possible device displacement [37]. the third possible reason for negative mapping is represented by anaesthesia, which has an important role in obtaining the proper result after stimulation. special protocols have been used in order to avoid the medication that causes muscle relaxation which is associated with false negative recordings [16, 18, 26]. those agents (lystenon®) were used by our anaesthesia team, in general, at the induction step of the orotracheal intubation, just to facilitate the procedure. the drug’s effects are over until the beginning of the operation. because a large spectrum of drugs decreases the synaptic activity, the effect being dose dependent, other criteria for the anaesthetic agents to be included in the protocol are represented by the impact on the latency and the response amplitude. currently there are two directions represented by total intravenous anaesthesia (tiva) and the use of volatile agents [23, 38]. the latter determines an increase of response latency and a decrease of amplitude, inducing pyramidal inhibition, dose 34 mihaela coșman, bogdan florin iliescu, anca sava et al. dependent. a concentration at the alveolar level of 0,5-1 have been found to be safe. the impact of tiva is also dose dependent but in a smaller extent. hence, due to their pharmacokinetic properties influence on motor response recordings, synthetic opioids such as fentanyl and sedative-hypnotic agents represented by propofol are preferred when iom is used [13, 17]. these were included in the protocol used on the patients from our study. from a histological point of view, even though our cases have a large category of tumor type, they have a common feature, namely slow development. this tumor characteristic allows for the neuroplasticity process to start. a consequence of this is function preservation, the main symptom of presentation of our patients being the jacksonian seizures and not motor deficit. studying the neuroplasticity and searching for the reasons of paucisymptomatic cases it is important to understand the functional organisation of the primary motor area which depends on the strict equilibrium from inhibitory and excitatory intrinsic local mechanism. the main system involved in reorganization is represented by the horizontal connections. the redundant motor sites within this map may be reviled using gabaergic inhibition [34, 35]. usually just this type of reshaping is not sufficient to maintain the function intact so other regions are recruited. first ipsilateral areas are involved e.g., premotor area, supplementary motor area and posterior parietal cortex. as a last resort contralateral “mirror” area participate to this process. in those situations, negative mapping may be found and the tumour resection is not associated with motor deficits [7, 15]. conclusion in cases where we do not have a motor response after direct cortical stimulation is applied, for lesion located in or near primary motor area is necessary to consider the step of the intervention to delineate the false negative recordings from real absence of the feedback. the three categories of causes must be eliminated starting with technical problems, anaesthesia and surgical issues. the differentiation from real absence of the motor response has an impact over the degree of resection and this in turn affects the survival rate and the progression free survival. references 1. azad td, duffau h. limitations of functional neuroimaging for patient selection and surgical planning in glioma surgery. neurosurg focus 2020; 42: 1-5. 2. bander de, shelkov e, modik o et al. use of the train-offive bipolar technique to provide reliable, spatially accurate motor cortex identification in asleep patients. neurosurg focus 2020; 48: 1-6. 3. bello l, riva m, fava e et al. tailoring neurophysiological strategies with clinical context enhances resection and safety and expands indications in gliomas involving motor pathways. neurooncol 2014; 16: 1110–1128. 4. brennan np, peck kk, holodny a. language mapping using fmri and direct cortical stimulation for brain tumor surgery. top magn reson imaging 2016; 25:1–9. 5. chang ef, clark a, smith js et al. functional mapping– guided resection of low-grade gliomas in eloquent areas of the brain: improvement of long-term survival. j neurosurg 2011; 114: 1-17. 6. corley ja, nazari p, rossi vj et al. cortical stimulation parameters for functional mapping. seizure 2017; 45: 3641. 7. duffau h. brain plasticity: from pathophysiological mechanisms to therapeutic application. j clin neurosci. 13 (9): 885-897, 2006. 8. duffau h. surgery of low-grade gliomas: towards a ‘functional neurooncology’. curr opin oncol 2009; 21:543–549. 9. ellis dg, white ml, hayasaka s et al. accuracy analysis of fmri and meg activations determined by intraoperative mapping. neurosurg focus 2020; 48:1-9. 10. eseonu ci, rincon-torroella j, lee ym et al. intraoperative seizures in awake craniotomy for perirolandic glioma resections that undergo cortical mapping. j neurol surg a 2018; 79:239–246. 11. giamouriadis a, lavrador jp, bhangoo r et al. how many patients require brain mapping in an adult neurooncology service? neurosurg rev, 43:729-738, 2020. 12. gollwitzer s, hopfengärtner r, rössler k et al. afterdischarges elicited by cortical electric stimulation in humans: when do they occur and what do they mean? epilepsy behav 2018; 87:173-179. 13. gunter a, ruskin kj. intraoperative neurophysiologic monitoring: utility and anesthetic implications. curr opin anesthesiol, 29:539–543, 2016. 14. hamberger mj, williams ac, schevon ca. extraoperative neurostimulation mapping: results from an international survey of epilepsy surgery programs. epilepsia 2014; 55: 933–939. 15. hayashi y, nakada m, kinoshita m. functional reorganization in the patient with progressing glioma of the pure primary motor cortex: a case report with special reference to the topographic central sulcus defined by somatosensory-evoked potential. world neurosurg 2014; 83:1-4. 16. helal sa, abd elaziz aa, dawoud age. anesthetic considerations during intraoperative neurophysiological 35 the impact and causes of negative cortical mapping in primary motor area tumours monitoring in spine surgery. menoufia med j. 31: 118792, 2018. 17. isik b, turan g, abitagaoglu s et al. a comparison of the effects of desflurane and total intravenous anaesthesia on the motor evoked responses in scoliosis surgery. int j res med sci,5(3):1015-1020, 2017. 18. kawaguchi m, iida h, tanaka s et al. a practical guide for anesthetic management during intraoperative motor evoked potential monitoring. j anesth, 34(1):5-28, 2020. 19. kim ss, mccutcheon ie, suki d et al. awake craniotomy for brain tumor near eloquent cortex: corelations of intraoperative cortical mapping with neurological outcomes in 309 consecutive patients. neurosurg 64: 836-846, 2009. 20. kombos t, suss o, kern bc et al. comparison between monopolar and bipolar electrical stimulation of the motor cortex. acta neurochir (wirn) 1999; 141: 12951301. 21. kombos t, suss o. neurophysiological basis of direct cortical stimulation and applied neuroanatomy of the motor cortex: a review. neurosurg focus 2009; 27:1-7. 22. kovac s, kahane p, diehl b. seizures induced by direct electrical cortical stimulation – mechanisms and clinical considerations. clin neurophysiol 2016; 127:31-39. 23. lotto ml, banoub m, schubert a. effects of anesthetic agents and physiologic changes on intraoperative motor evoked potentials. j neurosurg anesthesiol, 16:32–42, 2004. 24. magill st, han sj, li j et al. resection of primary motor cortex tumors: feasibility and surgical outcomes. j neurosurg, 129:961-972, 2018. 25. neuloh g, schramm j. are there false-negative results of motor evoked potentials monitoring in bran surgery? cent eur neurosurg, 70:171-175, 2009. 26. nunes rr, bersot cda, garritano jg. intraoperative neurophysiological monitoring in neuroanesthesia. curr opin anesthesiol, 31:532–538, 2018. 27. pallud j, rigaux-viode o, corns r et al. direct electrical bipolar electrostimulation for functional cortical andsubcortical cerebral mapping in awake craniotomy. practical considerations. neurochirurgie 2017; 63:164174. 28. pan sy, chen jp, cheng wy et al. the role of tailored intraoperative neurophysiological monitoring in glioma surgery: a single institute experience. j neurooncol 2020; 146:459-467. 29. pourtain n, cannestra af, bookheimer sy et al. variability of intraoperative electrocortical stimulation mapping parameters across and within individuals. j neurosurg 2004; 101:458–466. 30. ritaccio al, brunner p, schalk g. electrical stimulation mapping of the brain: basic principles and emerging alternatives. j clin neurophysiol 2018; 35: 86–97. 31. rossi m, nibali mc, vigano l et al. resection of tumors within the primary motor cortex using high-frequency stimulation: oncological and functional efficiency of this versatile approach based on clinical conditions. j neurosurg 2019; 9:1-13. 32. sala f. penfield’s stimulation for direct cortical motor mapping: an outdated technique? clin neurophysiol 2018; 129:2635-2637. 33. sanai n, mirzadeh z, berger ms. functional outcome after language mapping for glioma resection. n engl j med 2008; 358:18-27. 34. sanes jn, donoghue jp. plasticity and primary motor cortex. annu rev neurosci 2000; 23:393–415. 35. schellekens w, petridou n, ramsey nf. detailed somatotopy in primary motor and somatosensory cortex revealed by gaussian population receptive fields. neuroimage 2018; 179:337-347. 36. so le, alwaki a. a guide for cortical electrical stimulation mapping. j clin neurophysiol 2018; 35: 98–105. 37. szelenyi a, hattingen e, weidauer s et al. intraoperative motor evoked potential alteration in intracranial tumor surgery and its relation to signal alteration in postoperative magnetic resonance imaging. neurosurgery 2010; 67: 302-313. 38. tamkus aa, rice ks, kim hl. differential rates of falsepositive findings in transcranial electric motor evoked potential monitoring when using inhalational anesthesia versus total intravenous anesthesia during spine surgeries. spine j, 14(8):1440-6, 2014. 5adamd_topicalvancomycine 414 adam et al topical vancomycine prevents postoperative osteodiscitis topical vancomycine and bacterial culture from intervertebral herniated disc prevent postoperative osteodiscitis danil adam1, toma papacocea1, ioana hornea2, cristiana moisescu2 1carol davila university of medicine and pharmacy, bucharest 2“saint pantelimon” emergency hospital, bucharest abstract: osteodiscitis represents a serious complication of lumbar disc herniation operations. the treatment of osteodiscitis is controversial and expensive to society. it extends over a period of several months from diagnosis.reducing postoperative osteodiscitis by using simple measures may limit patient's suffering and reduce costs. the purpose of this study is to evaluate the early diagnosis of bacterial infections of the intervertebral disc by isolating germs located in the herniated disc fragment and topical vancomycine powder application, along with the conventional anti-infective therapy. medical files of patients who were operated on for lumbar disc herniations during 01.01.2013 30.06.2014 were reviewed. the diagnosis of lumbar disc herniation was established based on the clinical evaluation, confirmed by mri results. the surgical intervention was performed by mini-open approach: fenestration and foraminotomy completed with removal of the herniated disc fragment and disc remnants from the intervertebral space. a group of 162 patients (group a) received conventional therapy for prevention of post-operative infections with 2 doses of cephalosporin. in the second group of 137 patients (group b), after the removal of the herniated disc fragments, 1g of vancomycine powder was topically applied and the disc fragments were bacteriologically analyzed. they received the conventional treatment of preventing post-operative infections with cephalosprin 2 doses. the two groups of patients were similar in terms of demographic characteristics: age, sex, operative level. out of the 162 patients of group a, one patient developed postoperative osteodiscitis and was treated for 3 months with antibiotics. regarding patients in group b, in four cases staphylococcus was isolated from the disc fragments. postoperative treatment for these patients with prolonged antibiotic therapy over the standard period avoided the developement of the clinical picture of osteodiscitis. postoperative osteodiscitis requires prolonged antibiotherapy. by using simple measures, like topical vancomycine powder application and early isolation of germs from the herniated intervertebral disc, followed by the immediate establishment of appropriate antibiotic treatment, this serious complication is avoided. key words: herniated disc, osteodiscitis, vancomycine, microbiological examination. romanian neurosurgery (2014) xxi 4: 414 – 419 415 introduction among nosocomial infections, those that occur at the place of the surgical intervention are the most common. they have not only a socio-economic impact but affect both the patient whose quality of life is reduced, and the treating surgeon whose professional prestige suffers. postoperative osteodiscitis has an incidence of 0.2 to 3.0% (1, 2) among interventions for lumbar disc herniations, and 0.2-0.4% in recent series. (3, 4) the treatment for osteodiscitis, conservative or surgical debridement, is in both cases long-termed and expensive. prevention of postoperative infections is accomplished by using simple aseptic measures and short-term prophylactic antibiotics. topical application of vancomycine powder proved to be effective in reducing post-operative infection rate. (5) microbiological disc examination and culture and sensitivity together with lab tests (count of white blood cells, erythrocyte sedimentation rate and c-reactive protein) help in early diagnosis and treatment of infection especially regarding patients with risk factors. the aim of the study is to evaluate the role of topical vancomycine powder application and microbiological examination of the disc fragments comparing a group of patients operated on for lumbar disc herniations where these measures were applied, with another group of patients operated on for lumbar disc herniations where the conventional prophylactic antibiotherapy was applied. material and methods a series of 299 patients were operated on for lumbar disc herniations during a period of 18 months (january 2013 june 2014), through a mini-open approach previously described. (6) briefly, we performed a unilateral interlamar approach with fenestration and foraminotomy followed by removal of the herniated fragment and curettage of the disc space. regarding group a consisting of 162 patients, prevention of postoperative infection was made using the conventional classical methods: intra and postoperative strict asepsis associated with prophylactic antibiotherapy (two doses of cephalosporin). regarding group b consisting of 137 patients, in addition to the means of prevention postoperative infection applied to group a, at the surgical site it was applied 1 g of vancomycine powder before wound closure. in this group of patients, a microbiological examination of the resected disc fragments was made. for patients with positive microbiological results, specific antibiotherapy was continued, based on the sensitivity of isolated pathogens. several risk factors have been identified by several studies in the literature related to postoperative infections. (7) among them, the most common risk factors are obesity, diabetes, smoking, existence of previous infection before surgery on the skin or urinary infections. 416 adam et al topical vancomycine prevents postoperative osteodiscitis results the two groups of patients were similar in terms of demographic characteristics. (table i) lumbar disc herniation was more common among men. the median age was 53.3 years in group a and 45.8 years in group b. patients at the peak of their professional activity represented 71% in group a and 74.4% in group b. the most common sites of lumbar disc herniations have been at l4-l5 and l5-s1 in both groups. one patient from group a developed postoperative osteodiscitis. symptoms appeared 18 days after surgery with local pain, low grade fever, elevated esr and crp. mri examination showed a hyperintense image in the l4-l5 disc space. the patient required surgical debridement, staphylococcus aureus was isolated and antibiotic treatment with cefazoline followed for 3 months. during this period of time the patient wore a boston brace. in 4 patients from group b, staphylococcus was isolated from the intervertebral disc fragments (table ii). out of these, 1 patient presented staphylococcal skin infection, another one type ii diabetes and the third one obesity, as risk factors. patient 2 had underwent surgery for lumbar disc herniation at the same level 3 months earlier. table i patients’ characteristics characteristics group a no., % group b no., % number of cases 162 (54.1%) 137 (45.8%) gender male 93 (57,4%) 86 (62,7%) risk factors obesity diabetes smoking 17 (5.6%) 26 (8.6%) 20 (6.6%) 13 (4.3%) 17 (5.6%) 29 (9.6%) age (years) mean age 20-29 30-39 40-49 50-59 60-69 70-79 53,3 7 (2.3%) 36 (12.04%) 27 (9.03%) 44 (14.7%) 24 (8.02%) 23 (7.6%) 45,8 5 (1.6%) 27 (9.03%) 41 (13.7%) 29 (9.6%) 26 (8.6%) 9 (3.01%) level l2-l3 l3-l4 l4-l5 l5-s1 5 (1.6%) 10 (3.3%) 70 (23.4%) 77 (25.7%) 3 (1.003%) 71 (23.7%) 63 (21.07%) osteodiscitis 1 (0.61%) positive disc cultures 4 (1.33%) romanian neurosurgery (2014) xxi 4: 414 – 419 417 table ii characteristics of patients with pathogens isolated from the intervertebral disc no. gender age level risk factors pathogen treatment 1. m 58 l4-l5 staphylococcal skin coagulase positive staphylococci cefort + ciprofloxacin 1 week ciprofloxacin + biseptol 2 weeks 2. m 61 l3-l4 recent surgery at the same level coagulase positive staphylococci ciprofloxacin 10 days 3. f 42 l4-l5 grade iii obesity smoker staphylococcu s aureus ciprofloxacin+ biseptol one month 4. m 52 l5-s1 type ii diabetes staphylococcu s aureus tavanic 3 weeks immediately after the pathogens were isolated and their sensitivity to antibiotics was tested, appropriate antibiotherapy for a period of 10 to 30 days was initiated. no patient had clinical symptoms specific to osteodiscitis. one patient presented changes in the erythrocyte sedimentation rate (37mm/h) and c-reactive protein (10.6 ng/ml) which normalized after a month of treatment. patient no. 3, who presented with varicose veins in the legs, developed after surgery a superficial thrombophlebitis in the left leg. in this patient with grade iii obesity, partial wound dehiscence occurred which required resuture at the inferior pole. all patients were discharged after 7 days. postoperative course was uneventful after discharge. at the 1 month postoperative follow-up, no patient showed any specific symptoms of osteodiscitis, laboratory tests were normal and the symptoms of a herniated disc had an improvement between 80% and 100% after patients’ evaluation. discussion infection of intervertebral disc creates a serious suffering for patients operated for lumbar disc herniations, prolonging antibiotic treatment for several months, whether it is treated conservativly or surgically. pathogen inoculation can be done directly during surgery from an infection of the skin, or hematogenously from an infectious outbreak in the body, most often from a neglected genitourinary infection or an infection of the intestinal tract. in over half of the cases, the source of infection remains unidentified. (8) the most common pathogen isolated in cases of osteodiscitis is staphylococcus. (9) the clinical picture of osteodiscitis appears 418 adam et al topical vancomycine prevents postoperative osteodiscitis on average after 2-3 weeks with back pain and spinal stiffness accompanied by low-grade fever or fever and sweating. the biological markers of osteodiscitis, erythrocyte sedimentation rate and c-reactive protein values are above normal and can serve both as tests to monitor disease progression and treatment effectiveness. leukocytosis is inconsistent. (8) early detection of changes that occur at the disc space and adjacent end-plates is done by modern imaging means, mri. isolation of the pathogens is done by puncture biopsy or open biopsy, in which case inflamed tissue debridement is also performed. antibacterial treatment consists of antibiotics intravenously administrated for 23 weeks and, after the improvement of the erythrocyte sedimentation rate and c-reactive protein, orally administrated for 6 weeks to 3 months. in the prevention of postoperative osteodiscitis strict aseptic measures have an important role. as for surgery for lumbar disc herniation is rarely an emergency, preoperative diagnosis and appropriate treatment of possible genitourinary infections or infections in other sites is important for reducing the incidence of osteodiscitis. the first step in this regard is a proper history and general and local clinical examination. in recent years, it was shown that topical vancomycine powder application before suturing the lumbar aponeurosis is effective in reducing postoperative infections (5). since 2012 we have applied this policy to reduce postoperative infections in spine interventions. since 2013, regarding surgical interventions for lumbar disc herniations, we studied the presence of microbial pathogens in the herniated intervertebral disc. in the present study we analyzed the outcome of patients who underwent surgery for lumbar disc herniations and the incidence of postoperative osteodiscitis comparing two groups of patients. one group received 2 doses of cephalosporins to prevent postoperative infection. in the second group, we microbiologically analyzed the presence of bacteria in the herniated disc fragments. in the cases where the microbiological examination confirmed the presence of microbial pathogens, germ sensitivity appropriate antibiotherapy was continued from 10 to 30 days. from the first group of patients, one patient developed osteodiscitis. from the second group, in 4 cases there was revealed the presence of staphylococcus in the disc fragments. antibiotherapy immediately instituted prevented the development of postoperative osteodiscitis and the modification of the biological markers of inflammation in all cases but one. regarding this patient, erythrocyte sedimentation rate and c-reactive protein normalized after one month. comparing patients from the two groups regarding the developement of postoperative osteodiscitis, it seems that patients from group b were more likely to develop osteodiscitis than patients from group a, despite the topical romanian neurosurgery (2014) xxi 4: 414 – 419 419 vancomycine powder application in addition to the conventional antibiotic treatment and early detection of germs in disc fragments, followed by adequate antibiotic administration. we do not know if, had these patients not have been treated with antibiotics, clinical and biological changes of discitis would have developed. in reality, only one patient presented changes of the biological inflammatory tests. further studies focused on the evolution of patients with positive microbiological tests using a comparison between the treated and the non-treated ones, which seems highly unethical. there are several limitations regarding our study. firstly, this is a retrospective study which implies the fact that a full characterization of isolated germs is missing. secondly, we suspect that the microbiological tests were not immediately worked which possibly permitted bacterial contamination of the sample. our initial results have yet to be confirmed by further prospective studies. conclusions postoperative osteodiscitis is a rare but serious complication of lumbar disc herniation surgery. its treatment, conservative or surgical, is both resource and time consuming. for the prevention of postoperative osteodiscitis, in addition to the conventional measures, topical vancomycine powder application, in the wound, and the search for the presence of microbial pathogens in the disc fragments followed by appropriate antibiotherapy, are proving effective. references 1. brussatis f: osteomyelitis nach operation lumbaler disckuchernien. acta neurochir (wien) 2: 209-230, 1953. 2. pilgaard s: discitis following removal of lumbar intervertebral disc. jbonejoinsurg (am) 511: 713-716, 1969. 3. boden sd, davis do, dina ta, et al: postoperative diskitis: distinguishing early mrimaging findings from normal postoperative disk space changes. radiology 184: 765-771, 1992. 4. roth sa, neff u, schneider o, richter hp: neurosurgical management of thoracic and lumbar vertebral osteomyelitis and discitis in adults. neurosurgery 1996: 38: 926-933. 5. rw molinari, oa khera, wj molinari iii: prophylactic intraoperative powdered vancomycin and postoperative deep spinal wound infection: 1,512 consecutive surgical cases over a 6-year period. european spine journal, 2012 springer 6. adam d, nica d: hernia de disc lombară. neurologia medico-chirurgicală 2000, 1: 8-13. 7. albert f. pull ter gunne, david b. cohen.: incidence, prevalence, and analysis of risk factors for surgical site infection following adult spinal surgery. spine 34:13, 1422-1428. 8. jensen ag, espersen f; skinhj p, et al: bacteremic staphylococcus aureus spondylitis. arch intern med, 158: 509-517, 1998. 9. dufour v, feydy a, rillardon l, et a: comparative study of postoperative andspontaneous pyogenic spondylodiscitis. lemin arthritis rheum, 34: 766-771, 2005. anuragp_factors affecting romanian neurosurgery (2016) xxx 2: 267-271 | 267 factors affecting outcome in posterior fossa edh: an analytical study at tertiary referral hospital pateriya anurag1, bansal rajeev1, mittal radheyshyam2 1mch resident in neurosurgery, sms medical college and hospitals jaipur. india 2professor and head of department, department of neurosurgery; sms medical college and hospitals, jaipur, india abstract: introduction. posterior fossa extradural hematomas (pfedhs) are uncommon as compared to supratentorial edh and these patients can deteriorate very rapidly due to compression over brainstem. thus early identification and intervention can save the lives of these patients. methods. we prospectively studied 114 patients of posterior fossa injury for mode of injury, neurological status during admission, radiological findings, management, and outcomes of patients suffered posterior fossa extradural hematoma. all statistical analyses were determined using the spss 22.0.0.0 version. statistical analysis was conducted utilizing chi-square test. results. out of 114 posterior fossa trauma patients 28 patients (24.56%) having posterior fossa edh. gcs on admission (p value=0.002), volume of posterior fossa edh (p value= 0.000) were significant factors for the outcome of posterior fossa edhs. on comparing the data patients who survived and those who did not survive, the gcs on admission (p value=0.004) and brain stem compression (p value=0.000) were two factors found to affect the mortality significantly. conclusion. early detection with high degree of suspicion and immediate evacuation of pfedhs should be done if causing fourth ventricle, basal cistern or brain stem compression. key words: posterior fossa extradural hematomas (pfedhs), glasgow coma scale (gcs), brainstem compression introduction posterior fossa injury is rare, it accounts for less than 0.3 % of all head injuries. in comparison to supratentorial epidural hematomas are much less common and constitutes nearly 1.2 -15 % of all intra cranial epidural hematomas. (1, 3) the stable looking patient deteriorates very rapidly due to compression over the brainstem usually without any prior warning sign. thus early intervention before progression to herniation is lifesaving. we prospectively studied mode of injury, neurological status during admission, radiological findings, 268 | anurag et al factors affecting outcome in posterior fossa edh management, and outcomes of patients suffered posterior fossa extradural hematoma. material and methods study design from august 2013 to july 2014, total one hundred fourteen posterior fossa injury patients admitted in department of neurosurgery at our institution. out of them 28 (25%) patients were suffered by posterior fossa edh. all patients were divided in two groups. group a were those who had mass effect on fourth ventricle (n=14) and decompression surgery was performed as an emergency procedure. in group b were those patients without fourth ventricle shift and hence treated conservatively by continuous watching of patients neurological status, there vital parameters and serial ct scans as and when indicated. patients were evaluated age, gender, mode of injury neurological status cranial ct findings were noted at the time of admission and follow up to find outcome. we assessed the prognosis of posterior fossa edh depending on the compression over the fourth ventricle, basal cistern and brain stem. clinical data for each patient, the clinical data, mechanism of head injury, neurological findings, treatment, and outcome were noted carefully. radiological data radiological data including volume of hematoma, its mass effect, associated skull fractures and other intracranial lesions were noted. volume was measured by empirical formula of volume = (0.5×lenght× depth× height) and the mass effect over fourth ventricle, basal cisterns were noted carefully. statistical analysis all statistical analyses were determined using the spss 22.0.0.0 version. factors like gcs on admission , volume of posterior fossa edh , mortality and time of hospital stay were compared between group with mass effect over fourth ventricle and group without mass effect and there statistical significance was evaluated and analyzed by chi square test. results patient characteristics out of total posterior fossa trauma patients 28 patients (24.56%) having posterior fossa edh. age of the patients ranged from 4yrs to 80 yrs with average age of 25yrs. there were eighteen males (64.29%) with ten female (35.71%) (figure 1). the cause of injury were vehicular accidents in 24 patients and fall from height in four patients. figure 1 bar diagram showing age and sex wise distribution of patient population romanian neurosurgery (2016) xxx 2: 267-271 | 269 radiographic findings among all the total number of post traumatic posterior fossa edhs, skull fractures was seen in 71% cases, supratentorial contusions in 43%, associated supratentorial edhs in 21.45% cases, and cerebellar ich found in 14.28 % patients (figure 2) and fifty percent patients were in group a (mass effect over fourth ventricle and basal cisterns). figure 2 bar diagram showing intracranial injuries associated with posterior fossa edhs statistical analysis comparisons of clinical features, neurological findings and neuroimaging findings between patients with mass effect over fourth ventricle and without mass effect during hospitalization are listed in table i. statistical analysis of gcs at admission, average time of stay at hospital, mortality and neuroimaging findings between two groups revealed that gcs on admission (p value=0.002), volume of posterior fossa edh (p value= 0.000) were significant factors for the outcome of posterior fossa edhs. on comparing the data patients who survived and those who did not survive, the gcs on admission (p value=0.004) and brain stem compression (p value=0.000) were two factors found to affect the mortality significantly. table i comparison of variables in patients with mass effect and without mass effect group and their significance patient with mass effect (mean) patient without mass effect (mean) p value correlation gcs on admission 7.89±3.48 14.2±1.09 0.002 -0.747 volume of pfedh in cubic cms 17.22±5.54 5.2±2.1 0.000 0.798 average time of hospital stay 7.57±0.787 4.4±0.548 0.000 0.925 mortality 28.57% none 0.29 0.304 table ii statistical analysis of various variables and their significance survivors non survivors p value correlation age 24.83±13.05 46.5±15.46 0.152 0.404 gcs 11.33±3.17 3 0.004 0.72 volume of pfedh 11.92±7.63 19±1.41 0.229 4th ventricle compression 14 4 0.290 0.304 basal cistern effacement 10 4 0.147 0.408 brain stem compression none 4 0.000 1 270 | anurag et al factors affecting outcome in posterior fossa edh discussion post traumatic posterior fossa hematoma is the most commonly encountered after posterior fossa injury. in this study posterior fossa edhs accounted for 25% of total cases of posterior fossa injuries. overall mortality of posterior fossa edhs was 14.28%. the outcome of pfedhs was mainly influenced by gcs on admission and the mass effect over brain stem. bor seng shu et al reported that radiologic findings precedes clinical findings so patients suspected of having posterior fossa edh should be monitored thoroughly and patients with external injuries in occipital region should be followed with regular ct scans (4, 5). we advocate early surgical intervention as the size of edh increases rapidly and thus patients deteriorates quickly and may not be able to decompress by surgical intervention during such a short time. the outcome of posterior fossa edh depends on the volume of hematoma, or the mass effect over 4th ventricle, but van den brink et al postulated that hematoma volume is not the sole criteria for surgical intervention. (7) we suggest that the decision for surgery should be based on the gcs of the patient on admission, any further deterioration in neurological status, mass effect on 4th ventricle, effacement of basal cisterns and the compression over brain stem. in the literature the mortality in posterior fossa edh ranges from 4% to 26.5% (5, 6, 7) and lesser the gcs more is the mortality, in our study we found mortality rate of 14.28%. along with the gcs, age of the patient, duration from injury to operation also affects mortality. we found that the mortality along with the gcs on admission, the mass effect over 4th ventricle, effacement of basal cisterns and the compression over brain stem should also be considered as the potential factors suggesting poor prognosis, the later was associated with the poorest outcome (p value=0.000). therefore we recommend early detection with high degree of suspicion and immediate evacuation of pfedhs if causing fourth ventricle, basal cistern or brain stem compression. bozbuga (3) and colleagues also postulated that the obliteration of perimesencephalic cisterns and compression of fourth ventricle were evidences of brain stem compression in cases of pfedhs. in cases of posterior fossa edhs there are associated supratentorial injuries in greater than 55 % of cases. in one study by zucarello et al, he reported 87.5% of these associated intra cranial post traumatic lesions (8). we documented 78.57% of other intracranial lesions like contusions in frontal and temporal region, supra tentorial edhs. conclusion this study concludes that the patients with mass effect over fourth ventricle, perimesencephalic cistern and brain stem should undergo evacuation of hematoma as early as possible. gcs on admission and mass effect over above mentioned structures are the factors of statistical significance for the outcome. romanian neurosurgery (2016) xxx 2: 267-271 | 271 correspondence dr. anurag pateriya mch neurosurgery resident sms medical college and hospitals jaipur, india +91-9828019723 dr.anurag1984@gmail.com references 1.ammirati m, tomita t: posterior fossa epidural hematoma during childhood. neurosurgery 1984; 14: 541–44. 2.ateş ö, koçak a, önal ç, tarım ö, çaylı s, tektaş ş: travmatik posterior fossa hematomları. i̇nönü üniversitesi tıp fakültesi dergisi 2002; 9: 205 –9. 3.bozbuga m, izgi n, polat g, gürel i: posterior fossa epidural hematomas: observations on a series of 73 cases. neurosurg rev 1999; 22: 34–40. 4.bor-seng-shu e, aguıar ph, leme rjda, mandel m, andrade afd, marın rjr: epidural hematomas of the posterior cranial fossa. neurosurg focus 2004; 16: 1 – 4. 5.bor-seng-shu e, aguiar ph, matushita h, manreza la, ferreira aa: actual asymptomatic epidural hematomas in childhood. report of three cases. childs nerv syst 1997;13: 605–7. 6.ersahin y, mutluer s. posterior fossa extradural hematomas in children. pediatr neurosurg 1993; 19: 31– 33 7.van den brink w a, zwienenberg m, zandee s m, van der meer l, maas a i r, avezaat c j j: the prognostic importance of the volume of traumatic epidural and subdural haematomas revisited. acta neurochir (wien) (1999) 141: 509-514 8.zuccarello m, pardatscher k, andrioli gc, fiore dl, iavicoli r, cervellini p: epidural hematomas of posterior cranial fossa. neurosurgery 1981; 8: 434–7. doi: 10.33962/roneuro-2020-065 a thoracic intradural intramedullary epidermoid in a 12-years old female without any evidence of spinal dysraphism. a rare case report and review of literature abhijeet singh sachan, prakrati sachan, sateesh chandra verma, surjeet singh romanian neurosurgery (2020) xxxiv (1): pp. 416-420 doi: 10.33962/roneuro-2020-065 www.journals.lapub.co.uk/index.php/roneurosurgery a thoracic intradural intramedullary epidermoid in a 12-years old female without any evidence of spinal dysraphism. a rare case report and review of literature abhijeet singh sachan, prakrati sachan, sateesh chandra verma, surjeet singh sms medical college and hospital, jaipur, rajasthan, india abstract the spinal epidermoid lesion is an extremely rare benign condition, seen in < 1% of all spinal tumours and are most commonly associated with spinal dysraphism. they are more common in young children and have female preponderance. they can be either congenital or acquired with congenital being more common. they are most commonly located in the thoracic region. they grow slowly and present with back pain and progressive neurological deficit with or without bladder bowel involvement. we present a case of a 12-year-old female child with gradually progressive neurological deficit in the form of spastic paraparesis and decreased sensation with early bladder involvement. her contrast mri dorsolumbar spine showed a welldefined intradural intramedullary lesion hypointense on t1 image, hyperintense on t2 image with no contrast enhancement at d10-d11 level. the patient was managed by surgical intervention with d9-d10-d11 laminectomy with total excision of the mass. postoperatively on follow up patient had gradually improved motor and sensory symptoms with no improvement in bladder symptoms. her histopathological study was confirmative of an epidermoid cyst. introduction spinal epidermoid tumors are rare occurrence found in < 1% of all spinal tumors in adults and 3% in childrens .1-3 they are benign lesion with slow and indolent growth. they are derived from epidermal elements and can be congenital with entrapment of ectodermal cells during development and acquired by iatrogenic injury after surgery, trauma (penetrating injuries), lumbar puncture, myelography .4-5 they are most commonly associated with spinal dysraphism. it was first reported by chiari in 1833. 6-7 there most common location is thoracic followed by lumbosacral region. most of these lesions are found extramedullary and intramedullary location is a rarity .8-9 keywords ectodermal cells, spinal epidermoid, spinal dysraphism, intramedullary, intradural corresponding author: abhijeet singh sachan sawai man singh medical college and hospital, jaipur, rajashthan, india abhijeet1711@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 417 a thoracic intradural intramedullary epidermoid in a 12-years old female without any evidence of spinal dysraphism case report a 12 year old female child presented with complaints of gradual progressive ascending weakness and numbness of both lower limbs for 6 months with difficulty in walking and bladder involvement in the form of intermittent retention of urine for last 3 months .there was no history of back pain ,fever, trauma , any previous spinal procedure , cutaneous manifestation of spinal dysraphism .her neurological examination revealed spastic paraparesis with increased tone ( grade 3 modified ashworth scale )in both lower limbs , power 3/5 in both lower limbs . reflexes were +3 in both knee, ankle. dtr were brisk and planter was bilateral extensor. sensory examination showed decreased pain, touch and temperature sensation of around 60% below l2 spinal segments with decreased perianal sensation. her systemic, general, local, spine and upper limbs were normal in examination. mri dorsolumbar spine revealed a well-defined, homogenous, oval, cystic intramedullary lesion seen at d10-d11 level. it was hypointense on t1 image (figure 1a), hyperintense on t2 image (figure 1b,1c,) with no contrast enhancement (figure 2a,2b). d9d10-d11 laminectomy was performed with bulging dura seen. after opening of dura, a 1.5 x .8 x .5 cm intramedullary lesion, bulging out from the cord, and attached to cord on right lateral aspect was seen, it was well encapsulated, pearly white in color, smooth, soft to firm, avascular in nature. the cord was thinned out and shifted to left side. total excision of mass was done with watertight closure of dura was performed. figure 1a. t1 weighted mri axial view showing hypointense lesion. figure 1. t2 weighted mri b) sagittal view c) axial view showing single, cystic, hyperintense intradural lesion at d10 –d11 level, with cord shifted anteriorly and towards left side. figure 2. post gadolinium contrast image a) sagittal, b) axial view with no contrast enhancement. image 1. intraoperative image with dural bulge (arrow head). post-operative period was uneventful with mild improvement in power and tone. post op mri was done and revealed complete excision of mass (figure 3a, 3b, 3c). pt was discharged and followed up at 3 and 6 months. her power improved gradually to 4+/5 in both lower limbs and tone was decreased, sensory symptoms also improved but there was no 418 abhijeet singh sachan, prakrati sachan, sateesh chandra verma et al. improvement in bladder symptom. her histopathological study showed a fibrous capsule with stratified squamous epithelium with degenerated epithelial tissue (figure 4) confirming it to be epidermoid cyst. figure 3. post-operative mri image 3a) t2 weighted showing complete excision of mass, post gadolinium contrast 3b) axial image, 3c) sagittal view. figure 4. histopathological image with (h & e x 100) stained section shows the classical features of epidermoid cyst lined with keratinizing stratified squamous epithelium with anucleate squamous debris. discussion spinal epidermoids are uncommon lesions and very rare without any evidence of spinal dysraphism. its first description was given by cruveilhier in 1835 , who described them as tumors perlees (pearly tumors) .10 its first surgical removal was done by gross in 1934 .11 an incidence of .7% was reported by guidetti and gagliardi .12 in 1956 choremis et al described 6 case in childrens receiving subarachnoid injections of streptomycin for treatment of tbm . roux et al in 1992 presented 47 cases of intramedullary epidermoid .13 manno et al reported a total of 90 cases, of which 39 were acquired and 51 congenital .14 these are most commonly seen in thoracic spine in d4-d6 and d11-d12 region followed by lumbosacral region. they are benign lesion which arise when epidermal cells are trapped into the thecal sac. this can occur congenitally or acquired. congenital causes are spectrum of spinal dysraphism including spina bifida , myelomeningocele , split cord malformationdiastematomyelia ,dermal sinus ,syringomyelia , hemivertebrae .15 -17-18 love and kernohan in 1936 described them as congenital epithelial tumors .16 they are believed to arise from displaced ectodermal inclusions in early development resulting from defective closure of neural tube between 3rd to 5th week of fetal life .17 dias and walker corroborated a defect at the gastrulation stage .18 on the other hand acquired lesions develop after iatrogenic displacement of epithelial cells after trauma , lumbar puncture ,previous surgery .14,19 gibson and norris found epidermal tissue in needle bevels after skin puncture and needles with well fitted stylet did not carry any fragments with production of intramuscular dermoid in rats after injection of these skin fragments .20 oblu experimented development of intraspinal epidermoid cyst by introduction of dermoepidermal fragment into subrachnoid space of dogs by lumbar puncture .21 a study by van gilder and schwartz in rats showed , 89% of young rats develop intraspinal epidermoid and they failed to develop in adult rats .22 repeated punctures are thought to increase the risk of developing intraspinal epidermoid cyst . since 1970 incidence has decreased because of use of styletted needles lumbar puncture. the signs and symptoms are dependent on location of tumor and size of lesion. slow and indolent growth causes the usual delay in diagnosis. they can range from back pain, painful radiculopathy to umn signs below the level of lesion including weakness, spasticity, increased tone from involvement of corticospinal tract to sensory deficit, numbness and bladder -bowel dysfunction. rarely they can also present with chemical meningitis .23 malignant transformation has not been documented so far in intraspinal epidermoid. radiologically, the x-ray of these patients are usually normal but may show the evidence of spinal 419 a thoracic intradural intramedullary epidermoid in a 12-years old female without any evidence of spinal dysraphism dysraphism, and scalloping of the vertebral bodies, and scoliosis. on ct spine they show widening of spinal canal, scalloping of the vertebral bodies, thinning of lamina. mri of spine usually shows a welldefined homogenous lesion that is hypointense on t1 image , hyperintense on t2 image , shows intense diffusion restriction on dwi image and no significant enhancement on t1 gadolinium image 6,24,25,26,27,28,29. occasionally their margin may look “shaggy” due to leak of content causing chronic inflammatory response and gliosis along the margin . diagnosis is primarily done by proper history and clinical examination and established with preoperative radiological investigation and confirmed by postoperative histopathological findings. the differential diagnosis of these tumors includes dermoid, neurofibroma, meningioma, lipoma. on hpe examination stratified squamous epithelium and an outer layer of collagenous tissue. with progressive desquamation, keratin breakage the inner part of tumor is filled with soft white material, rich in cholesterol .13,28,30 treatment: in symptomatic patients. total excision of mass without any neural damage is the primary goal. in asymptomatic cases found incidentally, it can be managed conservatively. mostly their capsule is attached to the cord element, so some authors (including rand and rand 31) believe in subtotal resection of tumor with preservation of neural structures. subtotal resection frequently results in early relapse of symptoms and leak of contents causing more distressing meningitis. total microsurgical excision with intact capsule is the best possible treatment option available 13,32,33, but may lead to some neurological injury. this can be prevented by using intraoperatively neurophysiological monitoring guided by emg and somatosensory evoked potential .34 these lesions have high recurrence rate because of its dense adherence to neural tissue and the risk of recurrence is approximately equal to patients age plus 9 months .35,36 surgery remains the treatment of choice for recurrent lesions also. radiotherapy was given to 1 patient with repeated relapses with good result .37 radiotherapy can be offered to multiple recurrence .37 so, it can be considered an option for pts not fit to undergo surgery. despite all this most pt treated surgically enjoy a normal life with good neurological function. conclusion spinal epidermoid tumors are extremely rare slow growing lesions with non-specific presentation. most commonly these are congenital lesions seen in children. mostly they present with gradually progressive neurological deficit. diagnosis is predicted mri with dwi features and are confirmed by histopathological evidences. early diagnosis and prompt treatment limit the neurological deterioration. surgical excision is the treatment of choice. the preoperative neurological status is the prime determinant of functional outcome. maximal safe resection results in cessation of clinical progression and remission of symptoms. subtotal resection results in tumor recurrence and surgery is the treatment option. radiotherapy can be offered to multiple recurrence. references 1. baba h, wada m, tanaka y, imura s, tomita k. intraspinal epidermoid after lumbar puncture. int orthop 1994;18:116-8. 2. chandra ps, manjari t, devi bi, chandramouli ba, srikanth sg,shankar sk. intramedullary spinal \epidermoid cyst. neurol india2000;48:75-7. 3. guidetti b, gagliardi fm. epidermoid and dermoid cyst:clinical evaluation and surgical results. j neurosurg 1977;47:12-8. 4. gonzalvo a, hall n, mcmahon jh, fabinyi gc. intramedullary spinal epidermoid cyst of the upper thoracic region. j clin neurosci 2009;16:142-4. 5. boyd hr : iatrogenic intraspinal epidermoid. report of a case. j neurosurg24 : 105-107, 1966. 6. penisson-besnier i, guy g, gandon y. intramedullary epidermoid cyst evaluated by computed tomographic scan and magnetic resonanceimaging: case report. neurosurgery 1989;25:955-9. 7. mishra ss, satapathy mc, deo rc, tripathy sr,senapati sb. isolated thoracic (d5) intramedullary epidermoid cyst without spinal dysraphism: a rare case report. j pediatr neurosci 2015;10:133-6. 8. cincu r, lázaro jf, liesa jl, callizo jr. dorsal intramedullary spinal epidermoid cysts: report of two cases and review of literature. indian j orthop 2007;41:395-7. 9. bloomer cw, ackerman a, bhatia rg. imaging for spine tumors and new applications. top magn reson imaging 2006;17:69‑87. 10. cruveilhier j. anatomie pathologique. vol. 2. paris: bailliere jb; 1835. 11. gross sw :concerning intraspinal dermoids and epidermoids with report of a case . j nerv ment dis 80:274-284, 1934 420 abhijeet singh sachan, prakrati sachan, sateesh chandra verma et al. 12. guidetti b, gagliardi fm. epidermoid and dermoid cyst:clinical evaluation and surgical results. j neurosurg 1977;47:12-8. 13. roux a, mercier c, larbrisseau a, dube l-j, dupuis c, carpio rd :intramedullary epidermoid cysts of the spinal cord : case report. j neurosurg 76 : 528-533, 1992. 14. manno nj, uihlein a, kernohan jw. intraspinal epidermoids. j neurosurg 1962;19:754–65. 15. gormley wb, tomecek fj, qureshi n, malik jm: craniocerebral epidermoid and dermoid tumors: a review of 32 cases. acta neurochir 128:115121, 1994. 16. love j, kernohan j: dermoid and epidermoid tumors (cholesteatomas) of central nervous system. jama 107:18761883, 1936. 17. pang d, ahab-barmada m: split cord malformations. parts 1 and 2. a unified theory of embryogenesis for double spinal cord malformations. neurosurgery 31:451 500, 1992. 18. dias m, walker m: the embryogenesis of complex dysraphic malformations: a disorder of gastrulation? pediatr neurosurg 18:229-253, 1992. 19. halcrow sj, crawford pj, craft aw: epidermoid spinal cord tumour after lumbar puncture. arch dis child 60:978979, 1985. 20. gibson t, norris s : skin fragments removed by injection needles.lancet 2 : 983-985, 1958. 21. oblu n, wasserman l, sandulescu g, onofrei t : experimental investigation of the origin of intraspinal epidermoid cysts. acta neurol scand 43 : 79-86, 1967. 22. van gilder jc, schwartz hg : growth of dermoids from skin implants to the nervous system and surrounding spaces of the newborn rat. j neurosurg 26 : 14-20, 1967. 23. dobre mc ,smoker wr ,moritani t ,et al. spontaneously ruptured intraspinal epidermoid cyst causing chemical meningitis .j clin neurosci 2012;19:587-9. 24. cornu p, manai r, foncin jf, philippon j, boukobza m, metzger j: intramedullary epidermoid cyst diagnosed by magnetic resonance imaging] rev neurol (paris) 145:248250, 1989. 25. elazhari a, sami a, naja a, ouboukhlik a, el kamar a, boucetta m: [thoracic medullary epidermoid cyst. apropos of a case with mri and review of the literature] neurochirurgie 42(6):309-311, 1996 . 26. wang mt, wu tc, chen jc, tsai tc, chen ty, zeng w, et al: magnetic resonance imaging of intramedullary epidermoid cyst of low thoracic spinal cord: a case report. chin j radiol 30:109-113, 2005. 27. kallmes df, provenzale jm, cloft hj, mcclendon re: typical and atypical mr imaging features of intracranial epidermoid tumors. am j roentgenol 169:883887,1997. 28. gonzalvo a, hall n, mcmahon jh, fabinyi gc. intramedullary spinal epidermoid cyst of the upper thoracic region. j clin neurosci 2009;16:142‑4. 29. phillips j, chiu l: magnetic resonance imaging of intraspinal epidermoid cyst: a case report. j comput assist tomogr 11:181-183, 1987 30. kumar a, singh p, jain p, badole cm. intramedullary spinal epidermoid cyst of the cervicodorsal region: a rare entity. j pediatr neurosci 2010;5:49‑51. 31. rand rw ,rand cw : intraspinal tumors of childhood . springfield,iii:charles c thomas ,1960,pp 349-381. 32. ogden at, khandji ag, mccormick pc, kaiser mg. intramedullary inclusion cysts of the cervicothoracic junction. j neurosurg spine 2007;7:236-42. 33. lunardi p, missori p, gagliardi fm, fortuna a. long-term results of the surgical treatment of spinal dermoid and epidermoid tumors. neurosurgery 1989;25:860-4. 34. liu h , zhang jn , zhu t .microsurgical treatment of spinal epidermoid and dermoid cysts in the lumbosacral region . j clin neurosci 2012 ;19:712-17. 35. stevens ww, schlesinger eb: intramedullary epidermoid tumors of the thoracic spinal cord. report of two cases. j neurosurg 29:296-299, 1968. 36. alvord ec: growth rates of epidermoid tumors. ann neurol 2:367-370, 1977. 37. bretz a, van den berge d, storme g. intraspinal epidermoid cyst successfully treated with radiotherapy case report. neurosurgery 2003;53:1429-31. 5sanduaurelia_experimental 166 sandu et al experimental model of arteriovenous malformation experimental model of arteriovenous malformation in vitro using biological grafts aurelia mihaela sandu1,2, a. giovani1,2, m.r. gorgan2,3 1phd student, university of medicine and pharmacy “carol davila”, bucharest 2fourth department of neurosurgery, emergency clinical hospital bagdasar arseni, bucharest 3university of medicine and pharmacy “carol davila”, bucharest abstract: introduction: brain arteriovenous malformations (avms) represent a serious health problem all around the world. experimental models help to better understand the pathophysiology of these lesions. experiment: we performed an experimental model of avm using biological grafts, arteries and veins harvested from chicken wings at the elbow joint. we used 14 vessels and we performed 20 end-to-end anastomoses to create a nidus with a single feeding artery and a single draining vein. the system was irrigated with colored solution. the experiment was done according with law in force regarding experimental research activity. conclusions: experimental models allow us to understand the hemodynamics and predict the outcome of brain avms in humans. this experimental model is a useful tool in understanding the hemodynamic properties of brain avms. it is very useful in vascular anastomosis training. key words: arteriovenous malformations, biologic grafts, chicken wings, experimental model introduction vascular malformations of the brain represent a serious health problem.(8;29) brain arteriovenous malformations (avms) are not very frequently encountered, having an incidence of 0.89-1.34 cases/100.000 inhabitants/year (3;4;20) and a prevalence of 0.02-0.2% (1;2;20;31;34). although they are no common pathology, brain avms represent a continuous and prolific field of research (810;27-29), because social impact of this disease is high. they become clinically manifest in young and active people, mean age at diagnosis varying from 29 to 33 years.(25;29) brain avms carry high morbidity and mortality. they are the most common cause of spontaneous hemorrhagic stroke in young people.(7;11) hemorrhagic stroke has devastating consequences, being a major cause of mortality, morbidity and long-term neurological deficits. thus, after avms rupture with intraparenchymatal hemorrhage, mortality reaches 10% and morbidity accounts for 30-50%.(11;14;16) other clinic forms romanian neurosurgery (2015) xxix 2: 166 171 167 specific to brain avms are with seizures and neurological deficits. brain avms are composed by a network of dysplastic vessels (dilated arteries, arterialized veins, interconnected through shunts), from which arterial blood flows from arteries directly into draining veins, without any capillary bed.(11;21;32;35) avms have complex hemodynamic effects, impairing normal brain blood flow. the aim of this article is to make an experimental in vitro model of brain avm, using biological grafts. experiment we used vessels (arteries and veins) harvested from chicken wings, at the elbow joint. short chicken wing anatomy is summarized below. surprisingly, chicken wing anatomy resembles human upper limb anatomy. bones are represented by humerus, radius, ulna, carpal bones, metacarpals, alula and phalanges. muscles of the arm are biceps and triceps and of the forearm are radialis longus and ulnaris muscles. at the elbow joint humeral artery bifurcates into radial and ulnar arteries. radial and ulnar veins join into brachial vein. we harvested 14 vessels (arteries and veins) from the elbow joint, at the point where they bifurcate. so all vessels were “y” shaped. after harvesting, vessels were kept in a normal saline solution. we performed 20 end-to-end anastomoses, under operating microscope, using microsurgical instruments, according to the scheme shown in figure 1. anastomoses were done according to the classical principals of vascular surgery. two sutures were placed on the lateral sides, joining the two vascular ends together. the posterior wall of the anastomosis was sewed first, using a prolene 11-0 continuous suture, followed by suturing of the anterior wall in the same fashion. this model mimics an avm nidus with a single feeding artery and single draining vein. the afferent artery was catheterized using an intravenous cannula and the system was irrigated with colored solution (normal saline and blue ink) in a pulsatile fashion. the experiment was done according with law in force regarding experimental research activity. figure 1 schematic view of the experimental model of avm figure 2 part of experimental model of avm 168 sandu et al experimental model of arteriovenous malformation figure 3 final view of the experimental model of avm figure 3 experimental model of avm irrigated with colored solution, by catheterizing the afferent vessel with an intravenous cannule disscusions over the time, researchers from the field of medicine, tried to build experimental models of brain avms.(5;6) experimental models can be true or virtual. true experimental models can be built in vitro or in vivo. grafts used to recreate the network of a brain avm can be synthetic (dacron or goretex) or biological. true in vivo models were done in experimental animals. massoud et al performed an experimental avm in swine, using a side-to-side carotid-jugular anastomosis and ipsilateral endovascular occlusion of occipital artery, external carotid artery and muscular branch of the ascending pharyngeal in the pig’s neck, with subsequent forming of a rete mirabilis, mimicking a nidus, with feeding artery and draining veins.(22-24) qian et al. performed an in vivo experimental avm model in sheep, making a side-to-side carotid-jugular anastomosis, jugular vein ligation above the arteriovenous fistula and ligation of common carotid artery proximal to the anastomosis.(26) schumacher et al. designed an experimental model in dogs, performing a bilateral high-flow carotid to external jugular vein fistula, which was later occluded with a coated stent on one side, whereas the contralateral side remained patent.(30) other experimental models in animals were performed in rats. herman et al. performed an anastomosis between common carotid artery and external jugular vein, accompanied by occlusion of the sagittal sinus and of the vein draining the transverse sinus.(15) romanian neurosurgery (2015) xxix 2: 166 171 169 experimental models were used not only to design an anatomical network of vessels with specific hemodynamic properties, but also to explain consequences secondary to associated avms, such as normal perfusion pressure breakthrough.(12) animals models proved to be faithful copy of brain avms.(33) animal models of avms can be used to apply several therapies, such as radiosurgery ot endovascular embolization.(6) also virtual models of brain avms were designed for research purposes. computer and biomathematical models were used to imitate a brain avm and its consequences.(13;36) computer and biomathematical experimental models are a theoretical method of investigating avm. hademenos et al. constructed an electrical networks based on the biomathematical avm model, in order to provide an accurate rendering of transnidal and intranidal hemodynamics.(13) computer models are useful for pathophysiological studies. the advantage of these models is the flexibility, which cannot be found in an intact system.(36) the disadvantage is that they are dependent on the assumptions made by their constructors.(36) kerber et al. performed an experimental model of brain avm using an open pore cellulose sponge and a wax wire, 4.5-6.5 in diameter, simulating single draining vein and one to three wax wires, 2.6 mm in diameter, simulating feeding arteries, attached to the sponge with adhesive elastomer.(18) inagawa et al. created an artificial nidus model, using one milliliter syringe, in which they put small beads, 2.5x4.5 mm in size, which was connected through tubes to a active, pulsatile flow circuit.(17) human placenta was used as an ex vivo vascular model in research because its vessels resemble brain avm.(19) conclusions experimental models allow us to understand the hemodynamics and predict the outcome of brain avms in humans. this experimental model is a useful tool in understanding the hemodynamic properties of brain avms. it is very useful in vascular anastomosis training. acknowledgement this paper was co-financed from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 “excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis”, coordinator the bucharest university of economic studies. correspondence aurelia mihaela sandu, address: emergency clinical hospital bagdasar-arseni, no. 10-12, berceni street, sector 4, bucharest; e-mail: aurasandu@gmail.com; tel. 0724.263.023 references 1. al-shahi r, bhattacharya jj, currie dg, papanastassiou v, ritchie v, roberts rc, sellar rj & warlow cp. (2003). prospective, population-based detection of intracranial vascular malformations in adults: the scottish intracranial vascular malformation study (sivms). stroke 34, 1163-1169. 170 sandu et al experimental model of arteriovenous malformation 2. al-shahi r & warlow c. (2001). a systematic review of the frequency and prognosis of arteriovenous malformations of the brain in adults. brain 124, 19001926. 3. apsimon ht, reef h, phadke rv & popovic ea. (2002). a population-based study of brain arteriovenous malformation: long-term treatment outcomes. stroke 33, 2794-2800. 4. berman mf, sciacca rr, pile-spellman j, stapf c, connolly es jr, mohr jp & young wl. (2000). the epidemiology of brain arteriovenous malformations. neurosurgery 47, 389-396. 5. carvi y & nievas mn. (2005). experimental cerebral arteriovenous fistulas. neurol res 27, 857-863. 6. chen w, choi ej, mcdougall cm & su h. (2014). brain arteriovenous malformation modeling, pathogenesis, and novel therapeutic targets. transl stroke res 5, 316-329. 7. choi jh & mohr jp. (2005). brain arteriovenous malformations in adults. lancet neurol 2005, 299-308. 8. giovani a, sandu a, neacșu a & gorgan rm (2014). surgical treatment and outcome of cerebral cavernomas – a 10 years’ experience. rom neurosurg 21, 394-404. 9. gorgan mr, bucur n, neacșu a, sandu am, brehar fm, prună vm & giovani a. (2014). aspecte clinice și microchirurgicale în cavernoamele cerebrale (clinical aspects and microsurgery in brain cavernomas. the xvii-th national conference of stroke (avc) with international participation, 15-17 october 2014, brașov, romania. abstract was published in rev rom stroke (avc) 17, 62-64. 10. gorgan mr, ciubotaru vg, tătăranu lg, tașcu a, iliescu a, bucur n, neacșu a, brehar fm & sandu am. (2014). our experience in a series of 277 brain avms, microsurgical treatment and outcome. the 40th congress of the romanian society of neurosurgery with international participation, 25-27 september 2014, bucharest, romania. abstract was published in rom neurosurgery 21, 525-526. 11. greenberg ms. (2010). vascular malformations. in greenberg ms (ed), handbook of neurosurgery (10981142). new york: thieme medical publisher. 12. gutierrez-gonzalez r, perez-zamarron a & rodriguez-boto g. (2014). normal perfusion pressure breakthrough phenomenon: experimental models. neurosurg rev 37, 559-568. 13. hademenos gj, massoud tf & vinuela f. (1996). a biomathematical model of intracranial arteriovenous malformations based on electrical network analysis: theory and hemodynamics. neurosurgery 38, 1005-1014. 14. hartmann a, mast h, mohr jp, koennecke hc, osipov a, pile-spellman j, duong dh & young wl. (1998). morbidity of intracranial hemorrhage in patients with cerebral arteriovenous malformation. stroke 29, 931-934. 1998. 15. herman jm, spetzler rf, bederson jb, kurbat jm & zabramaki jm. (1995). genesis of a dural arteriovenous malformation in a rat model. j neurosurg 83, 539-545. 16. hillman j. (2001). population-based analysis of arteriovenous malformation treatment. j neurosurg 95, 633-637. 17. inagawa s, isoda h, kougo h, isogais s & sakahara h. (2003). in-vitro simulation of nbca embolization for arteriovenous malformation. interv neuroradiol 9, 351358. 18. kerber cw, hecht st & knox k. (1997). arteriovenous malformation model for training and research. ajnr am j neuroradiol 18, 1229-1232. 19. kwok jc, hunag w, leung wc, chan sk, chan ky, leung km, chu ac & lam ak. (2014). human placenta as an ex vivo vascular model for neurointerventional research. j neurointerv surg 6, 394-399. 20. laakso a & hernesniemi j. (2012). arteriovenous malformations: epidemiology and clinical presentation. neurosurg clin n am 23, 1-6. 21. marciano ff, vishteh ag, apostolides pj & spetzler rf. (2000). arteriovenous malformations – supratentorial. in kaye ah, black p (eds), operative neurosurgery (1079-1091). london: harcourt publishers limited. 22. massoud tf, ji c, guglielmi g & vinuela f. (1996). endovascular treatment of arteriovenous malformations with selective intranidal occlusion by detachable platinum electrodes: technical feasibility in a swine model. ajnr am j neuroradiol 17, 1459-1466. 23. massoud tf, ji c, vinuela f, guglielmi g, robert j, duckwiler gr & gobin yp. (1994). an experimental arteriovenous malformation model in swine: anatomic basis and construction technique. ajnr am j neuroradiol 15, 1537-1545. 24. massoud tf, vinters hv, chao kh, vinuela f & jahan r. (2000). histopathologic characteristics of a chronic arteriovenous malformation in a swine model: romanian neurosurgery (2015) xxix 2: 166 171 171 preliminary study. ajnr am j neuroradiol 21, 12681276. 25. ondra sl, troupp h, george ed & scawab k. (1990). the natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. j neurosurg 73, 387-391. 26. qian z, climent s, maynar m, uson-garallo j, limarodriguez mav, calles c, robertson h & castanedazuniga wr. (1999). a simplified arteriovenous malformation model in sheep: feasibility study. ajnr am j neuroradiol 20, 765-770. 27. sandu a & gorgan m. (2015). microsurgery and outcome in 277 brain avms, a common cause of hemorrhagic stroke in young people. the 9th world congress on controversies in neurology (cony), 26-28 march 2015, budapest, hungary. 28. sandu am. (2015). electronic national registry of brain arteriovenous malformations a useful tool in monitoring patients with cerebral vascular pathology. congress of university of medicine and pharmacy carol davila, 28-30 may 2015, bucharest, romania. 29. sandu am, ciubotaru vg, tătăranu lg, tașcu a, bucur n, neacșu a & gorgan mr. (2014). clinical aspects, management and oucome of brain arteriovenous malformations result with microsurgery first policy. rom neurosurg 21, 369-383. 30. schumacher m & schellhammer f. (1999). experimental pseudo arteriovenous malformation. a model for training and research. interv neuroradiol 5, 213-217. 31. soderman m, andersson t, karlsson b, wallace mc & edner g. (2003). management of patients with brain arteriovenous malformations. eur j radiol 46, 195-205. 32. spagmolo e. (2012). surgical management of cerebral arteriovenous malformations. in quinones-hinojosa a (ed), schmidek & sweet operative neurosurgical techniques: indications, methods, and results (10031018). philadelphia: elsevier-saunders. 33. tu j, karunanayaka a, windsor a & stoodley ma. (2010). comparison of an animal model of arteriovenous malformation with human arteriovenous malformation. j clin neurosci 17, 96-102. 34. weber f & knopf h. (2006). incidental findings in magnetic resonance imaging of the brains of healthy young men. j neurol sci 240, 81-84. 35. yasargil mg. (1987). microneurosurgery. iiia. avm of the brain, history, embryology, pathological considerations, hemodynamics, diagnostic studies, microsurgical anatomy. stuttgart: georg thieme verlag; new york: thieme medical publishers, inc. 36. young wl, gao e, hedemenos gj & massoud tf. (2007). use of modeling for the study of cerebral arteriovenous malformations. in stieg pe, batjer hh, samson d (eds): intracranial arteriovenous malformations (49-71). new york: informa health care. doi: 10.33962/roneuro -2020-042 long term study on the effects of microsurgical drezotomy for chronic pain control f. aichaoui, a. khelifa, m. al-zekri, w. bennabi, s. meyara, a. morsli romanian neurosurgery (2020) xxxiv (1): pp. 288-293 doi: 10.33962/roneuro-2020-042 www.journals.lapub.co.uk/index.php/roneurosurgery long term study on the effects of microsurgical drezotomy for chronic pain control f. aichaoui, a. khelifa, m. al-zekri, w. bennabi, s. meyara, a. morsli neurosurgical department of beo university hospital, algiers, algeria abstract the drezotomy (dorsal root entry zone tomy) is an analgesic procedure. the analgesic effect is evaluated on 30 patients with chronic pain resulting from respectively: brachial plexus avulsion (66.6%), postherpetic pain (10%), hyperspastic states (6.6%), phantom pain (6.6%), the pain in the stump (6.6%), and spinal cord injuries (3.3%). pain intensity was evaluated using a visual analogue scale (vas). at last evaluation, between 12 and 60 months, after drezotomy, 93% had a good or excellent global pain relief after surgery. according to the component types of pain, 9.6% of patients had good or excellent control of the paroxysmal pain, and 84% of the continuous pain. kaplan–meier prediction of lasting global pain control at 60 months of follow-up was calculated at 75.5%. comparison of the 2 corresponding kaplan–meier curves at long term, namely, pain control in 82.8% for the paroxysmal component and in 51.7% for the continuous component, showed a statistically significant difference (p < 0.0001). functional effects are improved by more than 70% according to patients. introduction chronic pain is a major public health problem, causing disability and of considerable human suffering. depressive states are frequently associated with it; without counting the health costs it generates. there are, however, situations where conservative methods such as conventional drugs and psychotherapies are not effective and where the use of "lesional" neurosurgical management can provide an effective solution. this is the case for certain microsurgical techniques including drezotomy (drez: dorsal root entry zone). this technique consists in interrupting the so-called nociceptive fibers and destroying by coagulation the hyperactive neurons located in the dorsal horn, corresponding to the area of pain, respecting the other fibers. it has been shown to be effective in some cases of chronic pain [2-5, 8, 9]. keywords neuropathic pain, chronic pain, brachial plexus avulsion, neurosurgery of pain, microsurgical drezotomy corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 289 long term study on the effects of microsurgical drezotomy for chronic pain control methods we conducted a prospective study of 30 patients who underwent microsurgical drezotomy for chronic pain resistant to medical treatment. this work was carried out between july 2007 and january 2015. our series included 2 women and 28 men, who had an average age of 46 years with extreme ages of 25 and 79 years. all patients had a detailed clinical assessment including the characteristics of their pain, its intensity using the visual analog scale (vas), as well as an assessment of the psychological impact of the pain. imaging, represented by ct scan and / or spinal mri, was performed before the surgery to assess the extent of the lesions. etiologies the chronic pain that affected our patients was caused by sequelae of brachial plexus avulsion (bpa) in 20 cases (66.6%) (figure 1), postherpetic neuralgia in 3 cases (10%), stump pain in 2 cases ( 6.6%), the phantom limb in 2 cases (6.6%), spasticity in 2 cases (6.6%) and one case (3.3%) of spinal cord injury. pain description in our study, more than half of the patients (56.7%) experienced pain initially, and 33.3% two months after the onset of the lesions. the time between onset of pain and surgery is on average 5 ± 1 year. three patients had a dn4 (douleur neuropathique en 4 questions, french for neuropathic pain in 4 questions), lower than 3, including 2 with stump pain and one patient with phantom limb pain. in fact, during the interrogation, we noted in 25 patients (83.3%) the presence of tingling. these latter involved 18 patients with bpa (90%), all patients with postherpetic neuralgia, spinal cord injury and a patient with phantom limb pain (50%). numbness was reported in 3 patients (10%) including two patients with bpa (10%) and a patient with spasticity (50%). dysesthesia was present in one patient who has bpa. analogous visual scale (vas) of our patients was initially on average 9.20 ± 1.06 with extreme values of 7 and 10. two categories of pain were noted, in particular electrical shooting-like paroxysmal pain, and the continuous pain realizing a painful background most often a burning type. the two components combined were present in 83% of patients. the paroxysmal and background components alone interested 6.7% and 10% of the patients, respectively. in the bpa, the pain concerned c6 and c7 dermatomes in all cases, and c8 and t1 dermatomes, in 95% and 90% of cases, respectively. for stump pain, the dermatomes affected by the pain range from c6 to t1. for the phantom limb, the pain areas extend from c5 to t1. in the three patients with postherpetic neuralgia, the dermatomes concerned range from c7 to t1 and from t3 to t8 at a frequency of 33.33% of cases for each one, associated in cases with allodynia. in the patient who suffered from chronic pain due to spinal cord injury, the dermatomes involved range from l2 to s2. as for patients suffering from spastic pain, the dermatomes concerned are l1 and l2 but also l4, l5 and s1. whatever the causal etiology of chronic pain, there is a noticeable impact on several aspects of life, whether individual, social or professional. medical treatment all of our patients received simultaneous treatment with who class i and ii anticonvulsants, tricyclics and analgesics. however, we note that 5 (16.6%) of our patients took at least occasional who class iii analgesics during their previous management. two of our three patients with postherpetic neuralgia used topical lidocaine as a patch in the allodynic areas. although the duration of treatment was 5 years ± 1 year, there was no reported improvement. surgical management microsurgical drezotomy was performed under general anesthesia. the patients were placed in the prone position. the laminectomy was homolateral to the corresponding painful dermatomes and bilateral when the symptomatology concerned both sides. after opening the dura mater, micro-incisions under an operating microscope were performed at the spinal cord dorsolateral sulcus at the entrance of the posterior roots. the incision was of 2 mm deep at an angle of 35 ° anteriorly and medially when it was the cervical and thoracic levels and 45 ° when it was the lumbar region. these incisions were followed by lowintensity micro-coagulations (figures 2 and 3). results the effects of drezotomy on pain are evaluated when the patient is discharged from the hospital, in average, 15 days after surgery, but also evaluated at 3 months and at long term (beyond 6 months). whatever the etiology, the results of drezotomy are mainly excellent for 26 patients (86.6%) at discharge, 290 f. aichaoui, a. khelifa, m. al-zekri et al. for 25 patients (86.2%) at 3 months, and for 20 patients (68.9%) in the long term; the good results interested 4 patients (13.3%) at discharge, 4 patients (13.7%) at 3 months and 7 patients (24.1%) in the long term; poor results are rare and concerned only 2 patients (6.8%) in the long term (figure 4). the longterm overall pain control defined by excellent to good results is studied by the kaplan-meier curve; this one shows 75.7% pain control over a 60 month follow-up period (figure 5). in our study, the results are excellent on allodynia, especially in patients with postherpetic neuralgia. the correlation between the number of painful dermatomes and the results of microsurgical drezotomy is statistically significant; the fewer the number of dermatomes, the more excellent the results of the drezotomy (p = 0.0093). the control of the pain components defined by excellent and good results is analyzed using the kaplan-meier curve; this one shows that the control of the paroxysmal and continuous components is estimated respectively at 82.8% and 51.7% over a period of 60 months (figures 6 and 7). this analysis demonstrates the effectiveness of the technique on the various components of pain with a predilection on the paroxysmal component compared to the continuous component (p <0.0001). surgical drezotomy improves the quality of life in all its aspects and whatever the etiology. this improvement is statistically significant in all cases (p = 0.00000). there is an average improvement of 83 ± 15% in daily activity, 79 ± 14% in walking, 85 ± 14% in the mood, 77 ± 15% in social relationships, and 85 ± 14% in sleep quality. the reduction in the doses of the drugs was performed gradually until stopping, in 3-4 weeks. analgesic treatment at low doses was continued in 6 patients. complications are generally few and quickly resolve; limited essentially to neck pain in 15.4% of cases, and in much rarer cases there was: csf fistula in 3.3% of cases, ataxia, tactile hypoesthesia, transient or permanent arthrokinesthesia, transient dysthesia, and mild motor disorder in 3.7% of cases for each of these complications. we regret a death of one patient which occurred during hospitalization caused by a pulmonary embolism. figure 1. preoperative cervical spine mri in t2 weighted images, in patient suffering from brachial plexus avulsion pain; a: axial slide, b: coronal slide, c: sagittal slide; the arrow shows a pseudoméningocèle characteristic lesion of brachial plexus avulsion. figure 2. per operative pictures in patient suffering from brachial plexus avulsion; a: before drezotomy, b: after drezotomy. the 291 long term study on the effects of microsurgical drezotomy for chronic pain control black arrows show the drezotomy zone for an avulsed c6 root, the white arrows show micro blood vessels entering the drez zone, the full star shows the c5 root, the empty star shows the spinal cord, and the ring the denticulate ligaments. figure 3. per operative pictures in a patient suffering from postherpetic neuralgia; a: before drezotomy, b: after drezotomy. the black arrows show the drezotomy zone, the white arrows show atrophied c7 root. figure 4. good to excellent results of drezotomy on overall pain at discharge, at 3 months and in the long term, all etiologies taken together (excellent: improvement greater than 75%; good: improvement between 75% and 50%, and poor improvement less than 50%). figure 5. kaplan meier curve describing in percentage the longterm overall pain control (excellent to good). pain control is estimated at 75.7% over a 60-month follow-up period. excellent: improvement greater than 75%; good: improvement between 75% and 50%. figure 6. the kaplan meier curve describing in percentage the control of the paroxysmal component of pain (excellent to good) in the long term. pain control is estimated at 82.8% over a period of 60 months. excellent: improvement greater than 75%; good: improvement between 75% and 50%. figure 7. the kaplan meier curve describing in percentage the control of the continuous component of pain (excellent to good) in the long term. pain control is estimated at 51.7% over 0 20 40 60 0 0.2 0.4 0.6 0.8 1 douleur globale 0 20 40 60 0 0.2 0.4 0.6 0.8 1 0 20 40 60 0 0.5 1 0 50 100 86.6 86.2 68.9 13.3 13.7 24.1 6.8 excellent good poor 292 f. aichaoui, a. khelifa, m. al-zekri et al. a period of 60 months. excellent: improvement greater than 75%; good: improvement between 75% and 50%. discussion we believe that the effectiveness of drezotomy on pain reinforces the hypothesis that the dorsal horn plays a main role in the genesis of pain [4]. guenot et al report the appearance of hyperactive neurons after the experimental rhizotomy performed in animals [13]. drezotomy significantly suppresses autotomy behavior in animals that have undergone rhizotomy. neuron hyperactivity has also been recorded using microelectrodes implanted in the dorsal horn during the drezotomy procedure for bpa pain [12, 14, 16]. the fact that the paroxysmal component is often reduced by drezotomy, suggests that its origin predominates in the dorsal horn. central sensibilisation by the phenomenon of denervation cannot in itself explain the mechanism generating pain within the dorsal horn. like other authors, we have frequently observed intraoperatively, the presence of hemosiderin deposits, microcavitations and gliotic tissue within the gray matter of the dorsal horn in the cases of bpa and spinal cord injury [4,10,17]. these lesions can cause a change in normal activity within this region and consequently cause dysfunction of the pain pathways at the spinal or cerebral level [16]. however, it is quite clear that not all pain-generating centers are located at the dorsal horn. as for the mechanism of the continuous component, dominated by the burning sensation which is less influenced by drezotomy than the paroxysmal component, it remains less clear; however, several hypotheses can be put forward. bpa causes more or less extensive necrosis of cells belonging to the dorsal horn that participate in the spinothalamic tract ascending pathway, as well as in the case of spinal cord trauma. this results in some degree of spino-reticulo-thalamic pain responsible of the continuous component [4]. the mechanisms of postherpetic neuralgia are similar to the abovementioned mechanisms; the presence of the varicella zoster virus in the sensory neurons of the dorsal ganglion [1] causes inflammation and cell destruction within it [7,15, 23]. the inflammatory process extends along the sensitive fibers to the dorsal horn, causing lesions similar to those observed in the bpa [3], which explains the beneficial effect of drezotomy on the two components, in particular the component paroxysmal as well as allodynia. drezotomy acts by suppressing the collaterals of the aβ fibers which are oriented towards the nociceptive layers of the dorsal horn. several hypotheses are suggested in the stump pain and the phantom limb pain. in fact, the loss of the afferent influx from the periphery leads to irritation of the neurons of the dorsal horn and their hyperexcitability and reduction of inhibitory processes [11,18, 25]. this gives the drez area a therapeutic interest. according to the series, paraplegic pain is mostly secondary to the conus medullaris lesion which often accompanies spinal trauma [21], probably in relation with the site corresponding to the thoraco-lumbar junction which is exposed to frequently to fractures. the thoracolumbar junction corresponds to numerous spinal segments condensed on a small poorly vascularized (adamkiewicz artery) explaining their concomitant involvement during the trauma. the mechanism of spastic pain may be linked to painful spasms, painful contracture and neuropathic pain [21]; which occurs in multiple sclerosis [8,9], and spinal cord injury [10]. this neuropathic disorder is secondary to a demyelization of the spino-thalamic tract [6,24] and the posterior horn where the paroxysmal and continuous components are usually present. the beneficial effect of drezotomy, on the various components of pain in particular the paroxysmal component was obtained by interrupting the myotatic fibers (monosynaptics), and the nociceptive fibers (polysynaptics), thus depriving the somatosensitive relays of the dorsal horn of all excitatory afferents [22]. conclusions drezotomy has a satisfactory operating risk / benefit ratio with few side effects. it is suitable for chronic refractory pain especially bpa and spinal cord injury. it significantly attenuates chronic pain in its paroxysmal but also continuous components with supremacy for paroxysmal pain, including in allodynic phenomena. conflict of interest none references 1. ada delaney, lesley a. colvin, marie t. fallon, robert g. dalziel, rory mitchell, and susan m. fleetwood-walker. postherpetic neuralgia: from preclinical models to the 293 long term study on the effects of microsurgical drezotomy for chronic pain control clinic. neurotherapeutics: the journal of the american society for experimental neurotherapeutics. october 2009. vol. 6, 630–637. 2. adam f. et le bars d. voies de la douleur. in: martin c., riou b. et vallet b. (2006). physiologie humaine appliquée. arnette, rueil-malmaison, 845-857. 3. allan h. friedman, blaine s. nashold, and janice ovelmen-levitt. dorsal root entry zone lesions for the treatment of post-herpetic neuralgia. j neurosurg 60:1258-1262, 1984. 4. aichaoui f, mertens p, sindou m. dorsal root entry zone lesioning for pain after brachial plexus avulsion: results with special emphasis on differential effects on the paroxysmal versus the continuous components. a prospective study in a 29-patient consecutive series. pain_ 152 (2011) 1923–1930 5. han zs, zhang et, craig ad. nociceptive and thermoreceptive lamina i neurons are anatomically distinct. nat neurosci 1998 ;1 :218-25.). 6. dahm.p.o, nitescu.p.v, appelgren.l.k and curelaru.l. long-term intrathecal (i.t.) infusion of bupivacaine relieved intractable pain and spasticity in a patient with multiple sclerosis. european journal of pain (1998) 2: 8185. 7. d’hardemare vincent, margot-dclot anne, bruxelle jean, bachelart maximillien, thiébaut jean-baptiste.chirurgie de la douleur de la lésion à la neuromodulation. springer 2014; 33 :374-387. 8. devor m. sodium channels and mechanisms of neuropathic pain. j pain 2006;7(suppl. 1): 3-12. 9. dickenson a. the inhibitory effects of thalamic stimulation of the spinal transmission of nociceptive information on the rat) (gerhart kd, yezierski rp, fang zr, willis wd. inhibition of primate spinothalamic tract neurons by stimulation in ventral posterior lateral (vplc) thalamic nucleus: possible mechanisms. j neurophysiol 1983; 49 :406-23. 10. dreval on. ultrasonic drez-operations for treatment of pain due to brachial plexus avulsion. acta neurochir 1993;122:76–81. 11. flor h. phantom-limb pain: characteristics, causes, and treatment. lancet neurol 2002;1:182 9. 12. guenot m, bullier j, rospars jp, lansky p, mertens p, sindou m. single-unit analysis of the spinal dorsal horn in patients with neuropathic pain. j clin neurophysiol 2003;20:143–50. 13. guenot m, bullier j, sindou m. clinical and electrophysiological expression of deafferentation pain alleviated by dorsal root entry zone lesions in rats. j neurosurg 2002;97:1402–9. 14. guenot m, hupe jm, mertens p, ainsworth a, bullier j, sindou m. a new type of microelectrode for obtaining unitary recordings in the human spinal cord. j neurosurg spine 1999;91:25–32. 15. hökfelt t, zhang x, wiesenfeld-hallin z. messenger plasticity in primary sensory neurons following axotomy and its functional implications. trends neurosci 1994;17:22–30. 16. jeanmonod d, sindou m, magnin m, boudet m. intraoperative unit recordings in the human dorsal horn with a simplified floating microelectrode. electroencephalogr clin neurophysiol 1989;72:450–4. 17. kandel ei, ogleznev kia, dreval on. destruktsiia vkhodnoi zony zadnykh koreshkov kak metod lecheniia khronicheskoi boli pri traumaticheskikh povrezhdeniiakh plechevnogo spleteniia. zh vopr neirokhir im n n burdenko 1987;6:20–7. 18. kerr, 1975a. snyder, 1977 ; livre ablative. 19. lazorthes y, sallerin-caute b, verdie jc, et al. chronic intrathecal baclofen administration for control of severe spasticity. j neurosurg. 1990; 72:393-402. 20. penn rd, kroin js. continuous intrathecal baclofen for severe spasticity. lancet 2:125-127, 1985) (lazorthes y, sallerin-caute b, verdie jc, et al: chronic intrathecal baclofen administration for control of severe spasticity. j neurosurg 72:393-402, 1990. 21. sindou marc p., and mertens patrick. surgery in the dorsal root entry zone for spasticity in adults. operative technique in neurosurgery.2005. elsevier. inc. 22. sindou.m, e blondet, e emery, and p mertens. microsurgical lesioning in the dorsal root entry zone for pain due to brachial plexus avulsion : a prospective series of 55 patients. j neurosurg 102 : 1018-1028. 2005. 23. smith mt, edwards rr, mccann ud, haythornthwaite ja. the effects of sleep deprivation on pain inhibition and spontaneous pain in women. sleep 2007;30:494–505. 24. thomas rj. excitatory amino acids in health and disease. j am geriatr soc 1995; 43:1279-89. 25. woolf cj, ma q. nociceptorsnoxious stimulus detectors. neuron 200 ; 55 : 353-64. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-001 management of a patient with acute internal hydrocephalus, ventriculitis and bronchopneumonia. case report balasa daniel, tunas alexandru romanian neurosurgery (2020) xxxiv (1): pp. 17-19 doi: 10.33962/roneuro-2020-002 www.journals.lapub.co.uk/index.php/roneurosurgery management of a patient with acute internal hydrocephalus, ventriculitis and bronchopneumonia. case report balasa daniel, md, phd; tunas alexandru, md department of neurosurgery, clinical county hospital, constanta, romania abstract a 69-year-old patient, with a long history of lung tuberculosis, with lymphopenia was emergently admitted in our hospital for bronchopneumonia, ventriculitis, acute internal hydrocephalic. he was aggressively treated with iv meropenem and vancomycin, intraventricular high doses of vancomycin, aerosols, dexametazone with healing of internal hydrocephalus, ventriculitis and improvement of bronchopneumonia. object the international data in the literature regarding the treatment of ventriculitis is limited. the authors aimed to share their experience in the treatment of ventriculitis and using intraventricular (ivt) and intravenous antibiotherapy. case report the patient was a 69 year-old man, with a previous history of lung tuberculosis. he was adressed to the emergency department for 2 days of fever (39 degrees c), 4 days of productive cough with purulent expectoration, dyspnea with tachypnea, respiratory failure (spo2 87%), altered mental status (stupor, gcs 10 ), neck stifness. the patient was treated by his family doctor with oral cefuroxyme , 4 grams daily . the patient was imunodepressed (lymphocytes 470/microliter) chest x-rays and ct scan revealed bronchopneumonia (fig. 1) head ct scann: acute hidrocephalus, ventriculitis, parafluid purulent deposits in occipital horns, bilateral. (fig 2 blue arrows) the lumbar puncture revealed a purulent csf with 4690 white cells/mm3, 92% of neutrophils. the patient underwent emergency surgery, extraventricular drainage (evd) with double purpose: treatment of acute hydrocephalus and treatment of ventriculitis. the ventricular csf samples were purulent. for this reason we considered unnecesarry a keywords bronchopneumonia, intraventricular vancomycin, limphopenia, ventriculitis corresponding author: balasa daniel university of medicine and pharmacy “carol davila”, bucharest, romania balasadaniel100@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 18 aurelia mihaela sandu, adrian mircea fürtös, radu mircea gorgan complementary head mri scan. bacteriologic examination of the csf revealed: streptococcus pneumoniae. intravenous antibiotherapy with meropenem 6 grams/day and vancomycin 2 grams /day, intraventricular antibiotics (vancomycin 50 mg/day in the first postoperative day and 100 mg/day in the following days), iv dexametasone (6 mg q 6 hours), aerosols with salbutamol 5mg/ml, 1 ml. after 22 days of treatment, control ct scann revealed disappearance of the acute hydrocephalus and the occipital purulent debris (fig 3). figure 1. bronchopneumonia. multiple perihilar opacities, bilateral. figure 2. figure 3. postoperative contrast ct scann. no internal hidrocephalus, no ventriculitis. moderate ventriculomegaly. the neurological status of the patient progressively improved and the neck stiffness dissapeared, also the respiratory status improved. follow time period: 5 months discussion ventriculitis is defined by high fever, clinical signs of meningitis (nuchal rigidity, photophobia, decreased mental status, seizures), a positive csf culture, positive gram stain, decreased csf glucose, increased csf proteins, csf pleocytosis (at least 11 leukocytisis/ml with 50% or more polymorphonuclear neutrophils) 1,2 in the preantibiotic era, the great majority of patients died from bacterial meningitis/ventriculitis at the end of the first week of ventriculitis3. nowadays, the incidence of this complication lowered. central nervous system infections requiring treatment with intraventricular (ivt) vancomycin are becoming increasingly common with advent of intracranial devices and increasing prevalence of multi-drug resistant and nosocomial organisms4. administering vancomycin via ivt route bypasses the blood-brain barrier and allows controlled delivery directly to the desired site of action, achieving higher concentrations for a more reliable bactericidal action4. indications for ivt vancomycin include meningitis unresponsive to intravenous antibiotics, ventriculitis, and intracranial device infections4. recommended dosages of antimicrobial agents 19 overview of patients with vascular pathology and cost analysis administered by the intraventricular route are vancomycin (5–20 mg/d). dosages reported in literature ranged from 0.075-50 mg/day, with the most evidence for dosages of 5 to 20 mg/day. duration of therapy most commonly ranged from 7 to 21 days4. for this patient, considering the imunodepression, bronchopneumonia, ventriculitis our option was to administer a higher dose of ivt vancomycine.the patient received aditional dexamethasone according to current guidelines, as soon as possible when the lumbar puncture reveals a purulent csf 6. such a treatment has been proven to be beneficial in preventing hearing loss and neurological sequelae in adult purulent bacterial meningitis, particularly those due to streptococcus pneumoniae6,7 the mean time to obtain csf sterilisation in medical literature was 24hours. this time was achieved in this case too. the fever disapeared in the first postoperative day. there were no adverse effect of antibiotics administered ivt. conclusion intraventricular and intravenous antibiotics lead very quickly to csf sterilisation in this critical ill patient. the ivt vancomicyne administration appears to be safe and have high efficacy together with iv administration of vancomicyn and meropenem. the ivt vancomycin dose , higher than the literature data, dramaticaly hastened the healing of ventriculitis and shortened the hospitalisation period of the patient. financial support and sponsorship nil. conflicts of interest there are no conflicts of interest references 1. sundbarg g, kjallquest a, lundberg n, et al. complications due to prolonged ventricular fluid pressure recording in clinical practice. in: brock m, dietz h, eds. intracranial pressure i: experimental and clinical aspects—international symposium on intracranial pressure, hannover, 1972. berlin: springer-verlag:348– 35, 1972. 2. sundbarg g, nordstrom ch, soderstrom s. complications due to prolonged ventricular fluid pressure recording.br j neurosurg;2:485–495, 1988. 3. adams rd, kubik cs, bonner fj. the clinical and pathological aspects ofinfluenzal meningitis. arch pediatr;65:354–76, 1948. 4. ng k, mabasa vh, chow i, ensom mh. systematic review of efficacy, pharmacokinetics, and administration of intraventricular vancomycin in adults. neurocrit care. feb;20(1):158-71, 2014. 5. bijlsma mw, brouwer mc, kasanmoentalib es, kloek at, lucas mj, tanckmw, et al. community-acquired bacterial meningitis in adults in thenetherlands, 2006-14: a prospective cohort study. lancet infect dis.2016;16:339– 447. 6. brouwer mc, mcintyre p, prasad k, van de beek d. in: van de beek d, editor.corticosteroids for acute bacterial meningitis: cochrane database syst. rev;2015.https://doi.org/10.1002/14651858.cd004405.p ub5. 7. tunkel ar, hartman bj, kaplan sl, kaufman ba, roos kl, scheld wm, et al.practice guidelines for the management of bacterial meningitis. clin infectdis.;39(9):1267–84, 2004. 8. w pfisterer, m mühlbauer, t czech, a reinprecht early diagnosis of external ventricular drainage infection:results of a prospective study . j neurol neurosurg psychiatry;74:929–932, 2003. 9. ricard jd, wolff m, lacherade jc, mourvillier b, hidri n, barnaud g, et al. levels of vancomycin in cerebrospinal fluid of adult patients receiving adjunctive corticosteroids to treat pneumococcal meningitis: a prospective multicenter observational study. clin infect dis;44:250-5, 2007. 10. nagl m, neher c, hager j, pfausler b, schmutzhard e, allerberger f. bactericidal activity of vancomycin in cerebrospinal fluid. antimicrob agents chemother;43:1932-4, 1999. 11. rybak mj, lomaestro bm, rotschafer jc, moellering rc, craig wa, billeter m, et al. vancomycin therapeutic guidelines: a summary of consensus recommendations from the infectious diseases society of america, the american society of health-system pharmacists, and the society of infectious diseases pharmacists. clin infect dis;49:325-7, 2009. 12. wen dy, bottini ag, hall wa, haines sj. infections in neurologic surgery. the intraventricular use of antibiotics. neurosurg clin n am;3:343-54, 1992. 13. fukui mb, williams rl, mudigonda s. ct and mr imaging features ofpyogenic ventriculitis. ajnr am j neuroradiol.22(8):1510–6, 2001. doi: 10.33962/roneuro-2020-083 endodermal cyst of the cranio-cervical junction. a case report bogdanović ivan, ilić rosanda, milićević mihajlo, aleksić vuk, milosavljević filip,miljković aleksandar, šćepanović vuk, stanimirović aleksandar, nedeljković žarko, todorović marko, joković miloš, grujičić danica romanian neurosurgery (2020) xxxiv (4): pp. 495-497 doi: 10.33962/roneuro-2020-083 www.journals.lapub.co.uk/index.php/roneurosurgery endodermal cyst of the cranio-cervical junction. a case report bogdanović ivan1, ilić rosanda1, milićević mihajlo1, aleksić vuk1,2, milosavljević filip1, miljković aleksandar1, šćepanović vuk1, stanimirović aleksandar1, nedeljković žarko1, todorović marko1, joković miloš1, grujičić danica1 1 neurosurgery clinic, clinical centre of serbia, medical school, university of belgrade, serbia 2 department of neurosurgery, clinical hospital centre zemun, belgrade, serbia abstract we report an extremely rare case of an endodermal cyst of the cranio-cervical junction located dorsally to the brainstem and upper cervical spine in a 27-year-old female presented with occipital headache, vertigo and pain in both shoulders. neurological examination showed neck stiffness with bilateral xith nerve palsy. magnetic resonance imaging revealed a cystic lesion at the cranio-cervical junction and slight compression of the brain stem. the lesion was totally removed through the posterior approach. the histological diagnosis was endodermal cyst. to our knowledge, the only one such case has been reported in the literature. introduction endodermal cysts can be found in literature by a variety of different names including neurenteric, epithelial, bronchogenic, enterogenous, respiratory and foregut cysts. these cysts are a benign congenital condition resulting from the persistence of an abnormal communication between endoderm and neuroectoderm at 3 weeks life of the embryo. this malformation is encircled by a mucosal secreting epithelioma mimicking the normal gastrointestinal epithelioma tractus (1). exact histopathological diagnosis may be hard to establish, since there are many similarities with other cystic lesions such as rathke cysts, colloidal cysts, and/or cystic teratomas (9). intracranial locations are rare, and location of such cysts in the cranio-cervical junction is exceptional. they are located in the midline, in ventral or ventrolateral locations. endodermal cysts may occur at any age, but there is a slight predominance of male patients in their forties. since they are slow growing tumours, many patients have only mild symptoms relative to the tumour size. the main symptoms are due to compression and mass keywords endodermal cyst, cranio-cervical junction corresponding author: vuk aleksić department of neurosurgery, clinical hospital centre zemun, belgrade, serbia aleksicvuk@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 496 bogdanović ivan, ilić rosanda, milićević mihajlo et al. effect. however, cases of recurrent aseptic meningitis can be found in literature (2). neurenteric cysts are treated surgically. with only partial resection, endodermal cysts may recur at the original site on long-term follow-up (3-6). the incomplete resection may be associated with postoperative malignant transformation or widespread cranial-spinal dissemination. almost all authors advocate the aggressive resection to reduce the possibility of endodermal cyst recurrence (7, 8). case report we present a case of a 27-year-old woman admitted with a history of recurrent episodes of occipital headache, vertigo and pain in region of both shoulders of six months duration prior to admission. she had no difficulty with swallowing or speech, and the strength of all extremities, gait, and coordination were normal. the neurological examination presented only moderate neck stiffness with bilateral xith nerve palsy. there was neither sensibility deficit nor extra neurologic signs. magnetic resonance imaging (mri) of the craniocervical junction revealed a well-defined, round, intradural cystic lesion located dorsally to the spinal cord and the medulla, extending from the foramen magnum to the upper level of c1 lamina, with neither bony nor soft tissue associated abnormalities. t2weighted images displayed a hypointense signal, and t1-weighted mri demonstrated a hyperintense mass without enhancement. the lower medulla and c1 spinal cord were found to be slightly compressed in the posterior aspect in the sagittal image. this intradural extraaxial process was measuring 20,7 x 12,7 x 8,3 mm (figure 1). preoperative ct scan showed a high density area at the cranio-vertebral junction, well delimited, dorsal to the medulla and upper cervical spine. in our case the cyst appeared spontaneously hyperdense. figure 1. cranio-cervical junction mri showing intradural cystic lesion located dorsally to the spinal cord and the medulla. the patient was operated in a prone position through a posterior approach and midline incision. surgery consisted in a reduced suboccipital craniotomy associated to partial c1 laminectomy. after opening of the dura a thin-walled yellowish cyst was noted below atlanto-occipital membrane, in the region of cerebellomedullaris cistern. it was floating in liquor, attached with bulbo-medulary junction only with thin aracnoidal connection. the lesion had not adhered to any other surrounding structures. surgical excision was complete in one piece. on pathohistological examination, the cyst membrane was underlined by unistratified cylindrical enteroid cells with basal nucleus and apical muco-secreting pole, with supra-nuclear acumulation of alcain-blue positive mucine. the diagnosis was endodermal cyst. postoperatively, the patient showed no neurological deficits. in the next few months’ clinical signs resolved completely. postoperative ct (figure 2) and mri revealed no evidence of a residual cyst. figure 2. postoperative ct scan showing complete resection of cyst. discussion endodermal cysts are congenital abnormalities belonging to notochordodysraphies which are result of an abnormal adherence between ectoderm and 497 endodermal cyst of the cranio-cervical junction endoderm. a failure during embryogenic development is probably responsible for cyst formation (1,9,10,11). the pathogenesis of this lesion is not clarified. however, the most convincing hypothesis is a dysgenesis of the endoderm from the neuroectoderm in the 3rd week of foetal development (12). usually, these lesions occur at the lower cervical and upper thoracic region, and their ventral origin is suggested by defects in the vertebral bodies. the lesions may be either intradural or extradural (13). the present case is unusual because cyst is found in the cranio-cervical junction and exceptionally unusual because of dorsal location, representing the only one such case reported in the literature (14, 15, 16). they show slow growing rate, remaining asymptomatic for a long time, but without surgical removal they can produce a brain stem and spinal cord compression syndrome followed-up by a neurological impairment. in this case, according to our opinion, surgery was justified in order to achieve total removal of the cyst and to prevent recurrence, malignant transformation or subarachnoid dissemination. references 1. harris cp, dias ms, brockmeyer dl, et al: neurenteric cysts of the posterior fossa: recognition, management, and embryogenesis. neurosurg 1991, 29(6): 893-897; 2. goel a, muzumdar d, chagla a. endodermal cyst anterior and anterolateral to the brainstem: a report of an experience with seven cases. br j neurosurg 2005;19(2):163–6. 3. chavda sv, davies am, cassar-pullicino vn enterogenous cysts of the central nervous system: a report of eight cases. clin radiol. 1985; 36(3):245-51. 4. fuse t, yamada k, kamiya k, inagaki h (1998) neurenteric cyst at the craniovertebral junction: report of two cases. surg neurol. 1988; 50: 431–436. 5. de oliveira rs, cinalli g, roujeau t, sainte-rose c, pierre-kahn a, zerah m j review neurenteric cysts in children: 16 consecutive cases and review of the literature. neurosurg. 2005;103(6 suppl):512-23. 6. abe k, oyama k, mori k, ishimaru s, eguchi m, maeda m neurol med chir (tokyo). review neurenteric cyst of the craniocervical junction--case report. 1999; 39(12):875-80. 7. gessi m, legnani fg, maderna e, casali c, solero cl, pollo b, dimeco mucinous low-grade adenocarcinoma arising in an intracranial enterogenous cyst: case report. f neurosurgery. 2008; 62(4):e972-3; 8. perry a, scheithauer bw, zaias bw; aggressive enterogenous cyst with extensive craniospinal spread: case report. minassian hv neurosurgery. 1999; 44(2):401-4; discussion 404-5. 9. filho fl, tatagiba m, carvalho ga, weichhold w, klekamp j, samii m. neurenteric cyst of the craniocervical junction. report of three cases. j neurosurg. 2001 jan;94(1 suppl):129-32. 10. houssine ghannane, m laghmari, k aniba, m lmejjati, s ait benali . craniocervical intradural neurenteric cyst: case report. pan arab journal of neurosurgery. 2011; 15(1)(p64-67) 11. yunoki m, hirashita k, gohda y, et al: true intraspinal neurentric cyst in the lumbosacral region case report. neurol med chir (tokyo) 2007, 47(5): 237-239. 12. malcolm g, symon l, kendall b, pires m: intracranial neurenteric cysts. report of two cases. j neurosurg 1991;75(1): 115-120. 13. pierot l, dormont d, oueslati s, et al: gadolinium-dtpa enhanced mr imaging of intradural neurenteric cyst. j comput assist tomgr 1998;12(5):762-764. 14. s. ohba, t. akiyama, r. kanai, s. onozuka, t. kawase. endodermal cyst of the cranio-cervical junction. acta neurochirurgica. 2008;150:257-263 15. zahos pa, goodman la, onesti st, michelsen wj. dorsal endodermal cyst of the upper cervical spine. j spinal disord. 1996;9(6):536-9. 16. king nk, joshi sm, marino s, yeh js, ellamushi h. dorsally located endodermal cyst: case report and review. br j neurosurg. 2009;23(3):318-20. doi: 10.33962/roneuro-2020-097 intradural migration of bullet in vertebra corpus after meningitis halil i̇brahim gündüz, turan kandemir romanian neurosurgery (2020) xxxiv (4): pp. 570-573 doi: 10.33962/roneuro-2020-097 www.journals.lapub.co.uk/index.php/roneurosurgery intradural migration of bullet in vertebra corpus after meningitis halil i̇brahim gündüz1, turan kandemir2 1 eskişehir city hospital, department of neurosurgery, eskisehir, turkey 2 yunus emre state hospital, department of neurosurgery, eskisehir, turkey abstract in a gunshot injury, the spinal cord of the thoracic region is usually the most affected and damaged part of the body. in most cases, the bullet cannot be removed without causing more damage to the injury. over time, the bullet tends to travel in different areas of the body. moreover, cases on bullet movements in the spinal canal were reported in the literature. in this study, we reviewed the diagnosis and treatment of a 27-year-old male patient with a bullet detected in his vertebra corpus, which is caused by a gunshot injury. during the follow-up period, an intradural migration of the bullet from the vertebra corpus was observed. furthermore, we performed surgery to prevent any future neural damage. in this study, we focused on a case with a gunshot injury, presenting an intradural migration of a bullet from the vertebra corpus after meningitis. introduction gunshot injuries (gsi) are the third most common cause of spinal cord injuries after traffic accidents and falls from height. although the incidence of spinal cord injuries caused by gsi changes according to the countries’ level of development, the most common causes of it are suicides, accidents and attacks. moreover, in developed countries, the approximate percentage of spinal cord injuries caused by gsi among all kinds of spinal cord injuries was reported to be 15% [1,2]. aside from the aforementioned damages on the spinal cord, secondary injuries, such as the degradation of the spinal cord vascularisation, autoregulation deficiency and hypotension, also worsen the neurological presentation due to systemic effects [3]. in the literature, cases of bullets travelling through the intraspinal canal were reported. in our case, the bullet was first stuck in the vertebra corpus, and removing it through manipulation was not feasible during the surgical operation. but in the follow-up period, it was observed that the bullet had left the corpus and travelled through the spinal canal after meningitis. keywords gunshot injury, intradural migration, spinal cord corresponding author: turan kandemir yunus emre state hospital, department of neurosurgery, eskisehir, turkey turankandemir26@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 571 intradural migration of bullet in vertebra corpus after meningitis case presentation a 27-year-old male patient was admitted to the emergency service following the gunshot injury in the chest area. a chest tube was then inserted as the patient had hemopneumothorax. a hole in the patient’s body due to the bullet which entered his thorax from right axillary lower region was observed. based on the neurological examination, the patient had paraplegia in the lower extremity, and anaesthesia was administered below t10; moreover, an anal sphincter reflex was not observed. the steroid protocol treatment from the nascis protocol was performed. a bullet was stuck in the t10 corpus was observed using the spinal tomography (figure 1). therefore, an urgent surgery was performed. during the surgery, it was observed that the dura and medulla were partially disintegrated. two-third of the bullet was in the t10 corpus. however, the bullet could not be removed despite further manipulation. the operation was then ended following duraplasty. as no change in the postoperative neurological examination was observed, the patient was required to undergo physical therapy and rehabilitation and was discharged afterwards. figure 1. image of the bullet in the t10 corpus following the gunshot injury. due to wound drainage and high fever, the patient was re-admitted a month after the discharge. a meningeal irritation was observed, and the white blood count and c-reactive protein were high. due to the presence of meningitis, antibiotherapy was started. moreover, the patient was reoperated since serous wound discharge continued to persist. during the surgery, it was observed that the discharge was coming from an intradural distance. the bullet was stuck in the corpus could not be removed through manipulation. duraplasty was then performed again, and the wound discharge ended postoperatively. after the antibiotherapy was completed and the wound recovered completely, the patient was discharged and was required to undergo physical therapy and rehabilitation. based on the medical imaging performed nearly a year later, it was observed that the bullet in the t10 corpus was dislocated and moved in an intradural distance; it reached the s1 level (figure 2). moreover, the neurological deficit of the patient regressed, and the muscle strength of the lower right extremity was evaluated as 4/5 and the lower left extremity 2/5. the patient underwent surgery in order to remove the bullet. during the operation, it was observed that the bullet had reached the l4 level when checked based on the results of the fluoroscopy (figure 3). l4 total laminectomy was performed after opening the l4 level. when the dura was opened, it was observed that the bullet was in the l3 level. when the patient was in a reverse trendelenburg position, the bullet moved towards the dural opening and was removed. the dura was closed via primary suturing. furthermore, no additional deficit was observed in the postoperative neurological examination. figure 2. ct image showing the bullet at the s1 level. figure 3. fluoroscopy image before intraoperative laminectomy 572 halil i̇brahim gündüz, turan kandemir discussion spinal gunshot injuries occur mostly in the thoracic region. another common place for it to occur is the lumbar region, with the cervical region being the less common [4]. injuries in the cervical region have a more mortal course. in the thoracic region, the spinal canal/cord ratio is lower and the neural damage is higher compared with that in other levels. in the literature, studies showing a bullet migration in the intervertebral disc level and in the paraspinal mass tissue into the spinal canal were included. kuijlen et al. presented a case of bullet migration from the paraspinal muscles to the spinal canal at the l3 level [5]. conway et al. presented a case showing a cauda equina development after a bullet migration from the l4 to l5 intervertebral disc level [6] . ceylan et al. presented a case who had back pain caused by a bullet migration anteriorly between the l2 and l3 intervertebral disc levels [7]. in our case, the bullet was stuck in the t10 corpus and migrated through the spinal canal in a span of nearly 1 year since the injury. in our case, in contrast to the other cases, two-third of the bullet was stuck in the vertebra corpus which could not be removed by manipulation during the two surgical operations performed, and the bullet spontaneously migrated to the canal following the patient’s meningitis treatment. in a gunshot injury, leaving the bullet inside the body rarely causes infection, neurological deficit and lead poisoning [8]. in the case of our patient, the infection occurred followed by a to cerebrospinal fluid (csf) leakage after the first operation. moreover, gunshot injury treatment is still a disputed and complex subject. surgery is necessary if csf leakage, progressive neurological deficit and infection formation co-occur with the infection. aside from gravity, respiratory movements and csf fluidity are also factors that affect the bullet movement inside the spinal canal. a neurological deficit may also occur if the bullets move in the spinal canal; in our case, no signs of newly developed neurological deficits were observed. however, a neurological deficit may develop later due to the fibrotic reactions forming in the pia and arachnoid. it was also shown that axon and myelin damage and lead and copper implantation causes induces gliosis in the spinal cord [9,10]. therefore, we decided to remove the bullet piece although our patient lacked any symptom or additional neurological finding. computed and direct tomography are usually the first diagnostic options for gunshot injuries. kafadar et al. reported that a magnetic resonance imaging (mri) can be performed since the bullet is covered with non-ferromagnetic metals just like copper in low-speed gunshot injuries [11]. although mri is the appropriate option for the evaluation of neurological tissue damage and causes less artefact compared to computed tomography (ct), its use is limited depending on the patient. since such cases are required to undergo an urgent operation, a ballistic examination cannot be performed for the bullet as mri is more commonly used. moreover, the patient did not have an mri scan since we did not have the sufficient information about the bullet structure. when our patient was positioned on the operation table, the results of the endoscopy showed that the bullet was moving. the bullet which was at the s1 level based on the preoperative ct scan had reached the l4 level, and we determined our incision accordingly. in the case presented by genç et al., the bullet moved intraoperatively, and its location was determined via ultrasonography [12]. we then performed laminectomy after determining the location of the bullet via endoscopy. however, we did not have to perform a long-level laminectomy and refrained from stabilisation. based on the findings of this study, it should be noted that despite being stuck in the bone, most foreign objects can move in later stages. overall, no neurological deficit following the bullet migration was observed in our patient and necessary measures were taken to prevent any possible neurological deficit. in addition, the individual who caused the injury was also identified by the researchers. references 1. aarabi b, alibaii e, taghipur m, kamgarpur a. comparative study of functional recovery for surgically explored and conservatively managed spinal cord missile injuries. neurosurgery 1996;39(6):1133-40. 2. young j. spinal cord injury statistics: experience of the regional spinal cord injury systems. 1982. 3. bono cm, heary rf. gunshot wounds to the spine. the spine journal 2004;4(2):230-40. 4. calik s, calik m, esme h. intraspinal bullet migration: a rare case report. chest 2017;152(4):a44. 5. kuijlen jm, herpers mj, beuls ea. neurogenic claudication, a delayed complication of a retained bullet. spine 1997;22(8):910–914. 573 intradural migration of bullet in vertebra corpus after meningitis 6. conway je, crofford tw, terry af, protzman rr. cauda equina syndrome occurring nine years after a gunshot injury to the spine. a case report. jbjs 1993;75(5):760– 763. 7. ceylan d, cosar m. migration of a bullet in the lumbar intervertebral disc space causing back pain. neurologia medico-chirurgica 2008;48(4):188-90. 8. yoshida gm, garland d, waters rl. gunshot wounds to the spine. orthop clin north am 1995;26(1):109-16. 9. bordon g, burguet girona s. gunshot wound in lumbar spine with intradural location of a bullet. case rep orthop 2014;2014:698585. 10. esnal-baza e, zaldua-unanue m, etxebarria-foronda i. neurological symptoms secondary to the intraspinal migration of a bullet. revista española de cirugía ortopédica y traumatología (english edition) 2007;51(6):351-3. 11. kafadar am, kemerdere r, isler c, hanci m. intradural migration of a bullet following spinal gunshot injury. spinal cord 2006;44(5):326-9. 12. genç a, usseli mi, pamir mn. when the bullet moves! surgical caveats from a migrant intraspinal bullet. neurologia i neurochirurgia polska 2016;50(5):387-91. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 360 | turliuc et al biblical descriptions of spinal neurological and neurosurgical pathology biblical descriptions of spinal neurological and neurosurgical pathology s. turliuc1, claudia florida costea1,2, a.i. cucu2, ana-maria dumitrescu1, gabriela florenta dumitrescu2, dana mihaela turliuc1,2 1“grigore t. popa” university of medicine and pharmacy iași, romania 2“prof. dr. n. oblu” emergency clinical hospital iași, romania abstract: the holy bible includes descriptions of the spine with both neurosurgical and neurological implications and most spinal disorders presented have been briefly described and display a mystical nature. the holy bible is a book full of sacred precepts and not a medical encyclopedia as it was written in the context of that age, and in a language that had to be understood by people of that era. this paper aims to give a short presentation of several diseases of the spine mentioned in the holy scripture in order to identify the most common disease among the jews during biblical times and attempts to provide their diagnosis. key words: spine diseases, religion, history of medicine, neuroscience introduction the holy bible or the holy scripture contains only short descriptions of spinal disorders as medical knowledge was scarce and limited at the time when sacred books were written. even though there have been existed medical schools since the 15th century bc, israelites ancestors did not have a proper medical education during biblical times (11), the priest playing also the role of the physician. the priests practiced medicine by applying the percepts of leviticus which was not only a true moral code, but also a preventive medicine and public health treaty. they had knowledge about the contagiousness of most diseases (especially leprosy), knowing how to recognize and isolate them. due to this “health legislation”, israel was a fairly healthy land compared to neighboring countries (11). this paper aims to identify the spinals disorders described briefly in the holy scripture in order to identify the most common diseases among the israelites during biblical times. spine trauma the first book of the kings in the old testament presents a spine injury that caused immediate death: “when he mentioned the ark of god, eli fell backward from his chair beside the gate, and his neck was broken and he died, for the man was old and heavy.” (first book of kings, 4, 17) (22). since death occurred instantly after cervical spine trauma, we can suspect an odontoid fracture caused by hyperreflexia in the elderly as eli was 98 years romanian neurosurgery (2016) xxx 3: 360 365 | 361 old. in the elderly, even a minor trauma of the cervical spine (including a fall from the same level) can produce a fatal odontoid fracture at the moment of impact (1, 17). eli had been a judge of israel for 40 years and high priest in shiloh, one of the largest religious centers of hebrew antiquity (10)and died when philistines had stolen the holy ark and had killed hundreds of israelites among which were his two brothers, hophni and phinehas (15). another episode about a spinal cord injury could be identified in the new testament. without providing details, the evangelists matthew, mark and luke described a full cross section of cervical spinal cord, namely the beheading of st. john the baptist (figure 1) ordered by king herod: „and immediately the king sent an executioner, and commanded his head to be brought: and he went and beheaded him in the prison, and brought his head in a charger, and gave it to the young lady: and the young lady gave it to her mother.” (mark, 6, 27-28) (22, 23). figure 1 salome with the head of saint john the baptist (c.1507-09), andrea solario metropolitan museum of art, new york, usa), public domain degenerative spine pathology the third books of kings tells about king asa, the third king of the kingdom of judah, about which we are told that at the end of life he had a disease of the lower limbs, perhaps due to a spinal cord injury: “all other acts of asa, and all his might, and all that he did and the cities which he built, are written in the chronicles of the kings of judah, except that in his old age he was diseased in his feet. then he slept with his fathers and was buried together with his fathers in the city of david, his ancestor.” (third book of kings, 15, 23-24) (22). the second book of paralipomena mentions again „in the thirty-ninth year of his reign asa became diseased in his feet. his disease was severe, yet even in his disease he did not seek the lord, but the physicians” (the second book of paralipomena, 16, 12-13) (22). in both sources, king asa's disease is just mentioned without any details, but based on the claim that it broke at „old age”, „in the thirty-ninth year of his reign”, when the patient could have been aged 60, we cannot exclude a degenerative spinal pathology (for example, a lumbar stenosis), that could have caused walking disorders or a neoplastic spinal pathology with a progressive setting of an incomplete motor deficit (18). falk (1996) believes that it is a paralysis of the lower limbs (9), but we may take into consideration the existence of a polyradiculoneuritis. it is interesting, however, that king asa was the first patient who saw a physician and was not a supporter of the idea that a disease is just a sin for which you have to suffer. 362 | turliuc et al biblical descriptions of spinal neurological and neurosurgical pathology infectious pathology of the spine distress related to spinal kyphosis (“the hunchback”) refers mainly to pott's disease, which is the spinal location of tuberculosis, about which hebrew priests had knowledge that it was contagious (3).thus, among the main diseases that did not allow a person to become a priest, which are listed in the third book of moose of the leviticus in the old testament, included “the hunchback”: “none of your descendants who has a defect may approach to offer gifts to god. for no one who has a blemish shall draw near, a man blind or lame, or one who has a mutilated face or a limb too long, or a man who has a broken foot or broken hand, or a hunchback or a dwarf, or one who has a defect in his eye or eczema or scabs or crushed testicles (leviticus, 21, 17-20) (22). the gospels of matthew, mark and luke mentioned another condition of the spinal cord: ”many gathered together so that there was no longer room for them(…), and they came, bringing to him a paralytic carried by four men. they lowered the stretcher on which the paralytic was lying. and jesus seeing their faith said to the paralytic, „son, your sins are forgiven!”(mark, 2, 2-5) (22) and this, „taking his bed, and went forth before all, that they were all pleased and glorified god, saying, these things i have ever seen.”(mark, 2, 12) (22). we have few information about his disease: it could have been a tumor or fracture of the spine with paraplegia. jesus christ addressed to the sufferer with the appellation of „son” to refer to someone who was probably of a young age. this makes us to believe that the disease was a pathology specific to young people, maybe a birth trauma (3), or a myelitis lesion type (11). spinal disease and its consequent paraplegia were considered a consequence of certain facts far from moral code of the time as savior first tells him: “your sins are forgiven!” and he healed him and the former paralytic man began to walk. as it was a disease of the spine believed to be the consequence of a „sin”, we could suspect a lesion of neurosyphilis: syphilitic myelitis (6), erb paraplegia (21) or tabes dorsalis. we meet in the gospel of luke another case of spine pathology that is much discussed in the literature. luke, being a physician, provides the best medical descriptions in this holy book: „and behold, a woman who had a spirit of infirmity for eighteen years, and which was bowed together, for she could not stand up at all. when jesus saw her, he called her and said to her, woman, thou art loosed from thine infirmity. and he laid his hands on her, and she immediately went and glorified god.”(luke, 13, 11-13) (22) (figure 2). figure 2 the woman who had an infirmity (c.1886-1896) james tissot (brooklyn museum, new york, usa), public domain romanian neurosurgery (2016) xxx 3: 360 365 | 363 as the gospel says that she had a long-term suffering (18 years), we deduce that this spinal disorder was a chronic one. the main diseases causing spinal kyphosis are chronic infectious diseases (tuberculosis of the spine, or ankylosing spondylitis), and degenerative (spondylosis, spine fractures, or osteoporosis of the spine). in this case, the main differential diagnoses can be made with: multiple osteoporotic spine fractures, spinal tuberculosis and ankylosing spondylitis. in general, infectious pathology of the spine affects young people and the degenerative one the elderly. in the case of „bent woman”, considering that her kyphotic condition had a history of over 18 years, we may suspect that the disease may have occurred as a result of spine fractures, possibly because of osteoporosis, especially that even today, in israel, the incidence of osteoporosis is over of 7% in men and 25% in women, being a public health problem (24). although the prevalence of osteoporosis in jewish women during biblical times is not known, ethnic considerations, genetic determinants and external factors make us believe that in ancient palestine, the incidence of osteoporosis in palestinian women was much higher. however, in ancient times, the jews, like all other peoples, lacked vitamins and minerals in their diet so they were vulnerable both to epidemic infectious diseases, as well as to endemic parasitic diseases as there are many biblical references to this pathology (14).moreover, the present rate of osteoporosis is almost two times higher in women in asian countries, than in the european countries or united states of america (13). on the other hand, considering that in ancient israel life expectancy of men was of about 40 years(12), and of women in poor rural areas of 30-40 years (7, 8),we could suspect that woman’s kyphosis was rather caused by ankylosing spondylitis or spinal tuberculosis, because the disease began when she was in her youth. spine tuberculosis existed in ancient near east as the most evidence has come from egyptian mummies (5), but it is however unlikely that the bent women could have spinal tuberculosis as she had a long-termkyphosis of the spine (for 18 years). if she have had spinal tuberculosis, the woman would have died soon and could not have lived for so many years. we consider that it is most likely that the woman's disease was an ankylosing spondylitis kyphosis as the patients develop a progressive kyphotic severe deformity of the spine and have a life expectancy similar to that of the general population, except severe cases (2, 19). paraparesis gospel of john talks about a paraplegic man who was healed by jesus (figure 3), “now there is in jerusalem, at the sheep market, a pool, which is called in the hebrew language bethesda, having five porches. in these place, a great number of invalid people, blind, halt, or withered, waited for the moving of the water. for an angel of the lord went down at appointed seasons into the pool and moved and stirred up the water; after the stirring up of the water, who then first stepped in the water was cured of whatever disease he was afflicted. there had been an invalid for thirty 364 | turliuc et al biblical descriptions of spinal neurological and neurosurgical pathology eight years. when jesus saw him lying there and founding out that he had been in this condition for a long time, he asked him: do you want to get well? the invalid replied: i have no one to help me to get into the pool when the water is stirred. while i am trying to get in, someone else goes down ahead of me. jesus said unto him: rise, take up thy bed, and walk.” (john, 5, 2-9) (20, 22).having only this scarce description, we conclude that the patient from bethesda could suffer from progressive muscular atrophy, most likely an amyotrophic lateral sclerosis (3)and not from a complete neurological deficit as the man could move on crutches. brachial monoplegia neuromuscular pathology of upper limb is another pathology found in the bible: “on another sabbath, he entered the synagogue and was teaching, and a man was there whose right hand was withered. and the scribes and the pharisees watched him, to see whether he would heal the man in the sabbath, so that they might find a reason to accuse him. but he knew their thoughts, and he said to the man with the withered hand: come and stand here. and he rose and stood there (….).and after looking around at them all he said to him: stretch out your hand. and he did so, and his hand was restored” (luke, 6, 6-11) (22). we cannot say exactly what kind of disease have this man, but can surmise a paralytic form of polio (anterior poliomyelitis), an atrophic paralysis caused by a shoulder plexopathy (4) or even a cervical spine pathology. figure 3 christ healing the paralytic at the pool of bethesda (c.1667), bartolome esteban murillo (the national gallery, london, uk), public domain conclusions most spinal conditions presented in the bible have been briefly described and display a mystical nature. so, an exact diagnosis could be made with difficulty. the bible is a book full of sacred precepts and not a medical encyclopedia as it was written in the context of that age, and in a language that had to be understood by people of that era. spinal diseases are rarely mentioned because two thousand years ago the rate of survival of patients with spine injuries or other spine conditions was very low. only those with incomplete lesions caused by syphilis, spina bifida, leprosy, spinal tuberculosis or other spinal infectious diseases survived (16).but, a careful reading of the brief details may suggest the spinal disorders that affected the israelites in biblical times, such as trauma, degenerative diseases, bone infections, spinal neuromuscular diseases and even tumors. romanian neurosurgery (2016) xxx 3: 360 365 | 365 correspondence claudia florida costea “grigore t. popa” university of medicine and pharmacy, iași, romania e-mail: costea10@yahoo.com references 1.adam d, cergan r, iftimie d, moisescu c. odontoid fracture that is not listed in the existing classifications. a new subtype of odontoid fracture: case report romanian neurosurgery. 2016; xxx (1): 57-64. 2.bot sdm, caspers m, vn royen bj, toussaint hm, kingma i. biomechanical analysis of posture in patients with spinal kyphosis due to ankylosing spondylitis: a pilot study. rheumatology. 1999; 38: 441443. 3.bromiley gw. international standard bible encyclopedia. wm. b. eerdmans publishing, 1995, p. 646. 4.budrys v. neurology in holy scripture. european journal of neurology. 2007; 14: 1-6. 5.cave aje. demonstrator a. the evidence for the incidence of tuberculosis in ancient egypt. british journal of tuberculosis. 1939; 33: 142. 6.cintron r, pachner ar. spirochetal diseases of the nervous system. curr opin neurol. 1994; 7(3): 217-222. 7.corrine l, carvalho cl. encountering ancient voices. saint mary's press, 2006, p. 345. 8.day l, pressler c. engaging the bible in a gendered world. presbyterian publishing corp, 2006, p. 207. 9.falk a. a psychoanalytic history of the jews. fairleigh dickinson univ press, 1996. p. 151. 10.finkelstein i, bunimovitz s, lederman z. shiloh: the archaeology of a biblical city.tel aviv, 1993. 11.hastings j . a dictionary of the bible. honoloulu: the minerva group, 2004, pp.321-326. 12.king p j, stager le. life in biblical israel. westminster john knox press, 2001, pp.37. 13.menczel j, makin m, robin g, steinberg r, lender m. interrelationship between osteoporosis and fractures of neck of femur. calcif tissue res. 1976; 21: 462-466. 14.meyers c. rediscovering eve: ancient israelite women in context. oxford university press, 2013, pp. 53-55. 15.moskopp d. neurosurgery and the holy bible. neurosurg rev. 1996; 19: 97-104. 16.ohry-kossoy k, ohry a. the portrayal of paralysis in some masterpieces by european painters. paraplegia. 1990; 28: 489-495. 17.pal d, sell p, grevitt m. type ii odontoid fractures in the elderly: an evidence-based narrative review of management. european spine journal. 2011; 20 (2): 195 204. 18.rahman hasa, iacob g. general considerations in lumbar spinal stenosis. romanian neurosurgery. 2015; xxix (xxii) (1): 77-84. 19.ramiro s, stolwijk c, van tubergen a, van der heijde d, dougados m et. al. evolution of radiographic damage in ankylosing spondylitis: a 12 year prospective follow-up of the oasis study. ann rheum dis. 2015; 74(1): 52-59. 20.rosner f . neurology in the bible and talmud. isr j med sci. 1975; 11(4): 385-397. 21.sharma c, nath k, kumawat bl, khandelwal d, jain d. erb's paraplegia with primary optic atrophy: unusual presentation of neurosyphilis: case report and review of literature. ann indian acad neurol. 2014; 17(2): 231233. 22.the holy bible or the holy scripture. bucharest: the biblical and missionary institute of the romanian orthodox church, 2008. 23.tubbs rs, loukas m, shoja mm, cohen-galdol aa, wllons iii jc et. al. roots of neuroanatomy, neurology, and neurosurgery as found in the bible and talmud. neurosurgery. 2008; 63: 156–163. 24.werner p. self-reported prevalence and correlates of osteoporosis: results from a representative study in israel. arch gerontol geriatr. 2003; 37(3): 277-292. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 317 320 | 317 biomarkers in spinal cord compression ethics and perspectives a.st. iencean1, a. tascu2, st.m. iencean3 1neurosurgery, “prof. n. oblu” emergency hospital, iasi, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania 3“grigore t. popa” university of medicine and pharmacy, iasi, romania abstract: the phosphorylated form of the high-molecular-weight neurofilament subunit nf-h (pnf-h) in serum or in cerebro-spinal fluid (csf) is a specific lesional biomarker for spinal cord injury. the lesional biomarkers and the reaction biomarkers are both presented after several hours post-injury. the specific predictive patterns of lesional biomarkers could be used to aid clinicians with making a diagnosis and establishing a prognosis, and evaluating therapeutic interventions. diagnosis, prognosis, and treatment guidance based on biomarker used as a predictive indicator can determine ethical difficulties by differentiated therapies in patients with spinal cord compression. at this point based on studies until today we cannot take a decision based on biomarker limiting the treatment of neurological recovery in patients with complete spinal cord injury because we do not know the complexity of the biological response to spinal cord compression. key words: ethics, lesional biomarkers, reaction biomarkers, spinal cord compression introduction spinal compression with radicular or spinal cord injury is caused by inflammatory diseases, disk degeneration, spinal injuries or other causes as tumors, infections etc. the phosphorylated form of the high-molecularweight neurofilament subunit nf-h (pnf-h) in serum or in cerebro-spinal fluid (csf) is a specific biomarker for spinal cord lesion. in spinal cord injury the direct mechanical injuries cause axonal destruction and destruction of the neurons and their destruction releases the lesional biomarkers. the reactions of other injured cells start simultaneously and the produced substances are the reaction biomarkers. the lesional biomarkers and the reaction biomarkers are both presented after several hours post-injury. a comparison between degenerative diseases of the nervous system (amyotrophic lateral sclerosis or multiple sclerosis) and traumatic spinal cord injuries shows that the same biomarker: pnf-h can be a lesional biomarker in traumatic injuries and is a reaction biomarker in degenerative diseases, because of the different pathophysiological mechanisms: direct injury or secondary response caused by other factors. 318 | iencean et al biomarkers in spinal cord compression. ethics a new proposed approach in spinal compression is based on the biomarkers as pnf-h; the heavy phosphorylated neurofilament subunit concentration can be a predictive lesional biomarker because the pattern in its values can show the reduction or stoppage of the secondary lesion in spinal cord injury with a favorable result. a b c figure 1 mri of three-level disc herniation with cervical myelopathy: a. sagital image; b. normal transversal image of cervical spinal cord; c. transversal image of compression of cervical spinal cord the studies on biomarkers in spinal cord injuries highlight that the most important lesional biomarkers are the phosphorylated neurofilament subunits, light or heavy (pnf-l or pnf-h). the phosphorylated neurofilament subunits (pnf-l or pnf-h) are specific lesional biomarkers for spinal cord compression and they can distinguish the severity of sci. the heavy phosphorylated neurofilament subunit (pnf-h) is a predictive lesional biomarker; its values pattern shows the reducing or stopping of the secondary lesions and the favorable outcome. there is a specific pattern of daily values of pnfh in complete spinal cord compression patients with a favorable outcome: a sudden increase up to a maximum value then a progressive decrease to normal. also there are two patterns in the patients with unfavorable outcome: an increase to a plateau of pnf-h values or a progressive increase up to a peak followed by a progressive decrease to quasi-normal values. these specific patterns could be used to aid clinicians with making a diagnosis and establishing a prognosis, and evaluating therapeutic interventions. romanian neurosurgery (2016) xxx 3: 317 320 | 319 figure 2 the three specific and predictive pattern of daily values of pnf-h in traumatic sci (from ref. 12) the studies on lesional biomarkers in spinal cord compression should continue on larger groups of patients to prove the clinical usefulness. also the studies on reaction biomarkers are very important, but obtaining cells from the site of spinal cord compression is problematic in humans. a new approach in the management of acute traumatic spinal cord injury has been proposed that could enable obtaining cells from the site of spinal cord injury without adverse consequences for the patient. in the cases with a predictive pattern of unfavorable outcome or neurological stationary after decompression and stabilization during the first 24 hours, a new approach was proposed based on the predictive pattern of daily values of pnf-h. if the clinical neurologic evolution is unfavorable and imaging techniques (mri) show a complete sci and the daily values of pnf-h as lesional biomarker form predictive unfavorable pattern, a second microneurosurgery in the spinal cord injury site can create favorable conditions for functional recovery of the remaining spinal cord: opening the spinal cord in the midline and microsurgical debridement of the necrotic tissue. at the same time this second microneurosurgical approach in the spinal cord injury site could enable obtaining cells from this site without adverse consequences for the patient. the use of these cells (neurons and glial cells around the lesion) for cell culture techniques will allow the study of the changes in the spinal cord compression at the molecular and structural levels in humans. diagnosis, prognosis, and treatment guidance based on biomarker used as a predictive indicator can determine ethical difficulties by differentiated therapies in patients with spinal cord compression. it is difficult to stop or to limit the treatment of neurological recovery in patients with complete spinal cord injury, with paraplegia or tetraplegia, with complete spinal cord lesions on imaging techniques and unfavorable 320 | iencean et al biomarkers in spinal cord compression. ethics patterns of predictive lesional biomarkers. we do not currently know the value of the lesional predictive biomarkers, and also the reaction biomarkers, for the neurological outcome several years after the injury. at the moment, we cannot take a decision limiting the treatment of neurological recovery in patients with complete spinal cord injury because we do not know the complexity of the biological response to spinal cord injury. this requires extensive and profound research both on lesional biomarkers and on reaction biomarkers correlated with genetic and molecular response in spinal cord compression and we hope further research will deliver effective treatments. acknowledgments this work is within the grant: “immediate neuroprotective therapy in acute traumatic spinal cord injury”, grant number: pn-iiidpce-2011-3-0569, funded by the cncs– uefiscdi romania. correspondence a. tascu “carol davila” university of medicine and pharmacy, bucharest, romania e-mail: tascu_alexandru@yahoo.com references 1. burns as, marino rj, flanders ae, flett h. clinical diagnosis and prognosis following spinal cord injury. in: verhaagen j, mcdonald jw, editors. spinal cord injury. handbook of clinical neurology. volume 109, elsevier b.v; 2012. p. 47 – 62. isbn: 978-0-444-52137-8 2. liverman ct, altevogt bm, joy je, johnson rt, editors. spinal cord injury. progress, promise, and priorities. the national academic press, usa; 2005. 344p. isbn 0-309-09585-9 3. yokobori s, zhang z, moghieb a, mondello s, gajavelli s, dietrich wd, bramlett h, hayes rl, wang m, wang kk, bullock mr. acute diagnostic biomarkers for spinal cord injury: review of the literature and preliminary research report. world neurosurg. 2015; 83(5):867-78. 4. basu s, hellberg a, ulus at, westman j, karacagil s. biomarkers of free radical injury during spinal cord ischemia. febs lett. 2001, 9; 508(1):36-8. 5. guéz m, hildingsson c, rosengren l, karlsson k, toolanen g. nervous tissue damage markers in cerebrospinal fluid after cervical spine injuries and whiplash trauma. j neurotrauma. 2003; 20(9): 853-8. 6. kwon bk, casha s, hurlbert rj, yong vw. inflammatory and structural biomarkers in acute traumatic spinal cord injury. clin chem lab med. 2011;49(3):425-33. 7. kwon bk, stammers am, belanger lm, bernardo a, chan d, bishop cm, slobogean gp, zhang h, umedaly h, giffin m, street j, boyd mc, paquette sj, fisher cg, dvorak mf. cerebrospinal fluid inflammatory cytokines and biomarkers of injury severity in acute human spinal cord injury. j neurotrauma. 2010; 27(4): 669-82. doi: 10.1089/neu.2009.1080 8. hayakawa k, okazaki r, ishii k, ueno t, izawa n, tanaka y et al. phosphorylated neurofilament subunit nf-h as a biomarker for evaluating the severity of spinal cord injury patients, a pilot study. spinal cord 2012, 50, 493-496. doi:10.1038/sc.2011.184 9. iencean stm, adam d, ungureanu d, tascu al, cuciureanu d, costachescu b, iencean ast, poeata i. preliminary results of csf phosphorylated neurofilament subunit nf-h as biomarkers of acute spinal cord injury. romanian neurosurg.2013, xx; 4: 351 356 10. pouw mh, kwon bk, verbeek mm, vos pe, van kampen a, fisher cg, street j, paquette sj, dvorak mf, boyd mc, hosman aj, van de meent h. structural biomarkers in the cerebrospinal fluid within 24 h after a traumatic spinal cord injury: a descriptive analysis of 16 subjects. spinal cord. 2014; 52(6): 428-33. doi: 10.1038/sc.2014.26. 11. takahashi h, aoki y, nakajima a, sonobe m, terajima f, saito m, taniguchi s, yamada m, watanabe f, furuya t, koda m, yamazaki m, takahashi k, nakagawa k. phosphorylated neurofilament subunit nfh becomes elevated in the cerebrospinal fluid of patients with acutely worsening symptoms of compression myelopathy. j clin neurosci. 2014; 21(12): 2175-8. 12. tascu al, iencean st m, iencean ast. new approach based on biomarkers in acute traumatic spinal cord injury. romanian neurosurgery (2016) xxx 2: 147-153 romanian neurosurgery (2019) xxxiii (3): pp. 295-298 doi: 10.33962/roneuro-2019-049 www.journals.lapub.co.uk/index.php/roneurosurgery tentorial dural arteriovenous fistulae presenting as transient ischemic attack. case illustration marco zenteno1, mohamed m. arnaout2, angel lee3, amit agrawal4, mohammed maan abdulazeez5, hayder ali al-saadi6, osama m. al-awadi6, samer s. hoz6, luis rafael moscote-salazar7 1 departamento de terapia endovascular neurológica, instituto nacional de neurología y neurocirugía, universidad nacional autónoma de mexioco 2 neurosurgeon, department of neurosurgery, zagazig university, zagazig, egypt 3 departamento de terapia endovascular neurológica, instituto nacional de neurología y neurocirugía, universidad nacional autónoma de mexico 4 professor of neurosurgery, mm institute of medical sciences & research, maharishi markandeshwar university, haryana, india 5 medical student, college of medicine, baghdad university, baghdad, iraq 6 neurosurgeon, department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 7 neurosurgeon, university of cartagena, cartagena de indias, columbia abstract dural arteriovenous fistulae are vascular lesions of the dura mater, usually acquired, consisting of abnormal connections between the dural arteries with the venous sinuses or the cortical veins. a case report presents a case with an unusual form of presentation of the dural (tentorial) arterio-venous fistula simulating a transient ischemic attack in a 60-year-old male patient. abbreviations davfs: dural arteriovenous fistulas, tdavfs: tentorial dural arteriovenous fistulas mri: magnetic resonance imaging, mra: magnetic resonance arteriography ct: computerized tomography. introduction as described and characterized angiographically, dural arteriovenous fistulas (davfs) are lesions generally acquired and progressive with an keywords dural arteriovenous fistulae, transient ischemic attack; endovascular treatment corresponding author: mohammed maan abdulazeez college of medicine, baghdad university, baghdad, iraq mohammed.wwt@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 296 marco zenteno, mohamed m. arnaout, angel lee et al. incidence of 10 to 15% of all cerebral vascular lesions (1-3). they are divided into two main types: davfs that drain into a venous sinus with direct reflux to a cortical vein, or not of the venous sinus type (3). the first type includes those that drain into the cavernous sinus, the sigmoid-transverse sinus, the sinuses confluence, superior sagittal sinus, and petrous sinuses. the second type, include tentorial, ethmoidal, cranio-cervical davfs (4-9). the most frequent davfs is at the transversesigmoid junction (38%), and the cavernous sinus, followed by deep veins, the superior sagittal sinus, superior petrous sinus, ethmoidal sinus, inferior petrous sinus and ethmoidal davfs (2,10). the etiology is controversial and the location of the davfs in very specific sites, and not throughout the dura mater. case report a 60-year-old male patient came to the emergency department with the complaint of acute onset of slurred speech that started 15 minutes prior to his arrival. he denied any associated headache or visual, motor, balance, sensory symptoms, or any previous similar episode, and his family denied witnessing any loss of consciousness, abnormal body movement or odd behavior when inquired. relevant history included hypertension for 10 years for which the patient was prescribed a lisinopril 10 mg once daily taken regularly as the patient emphasized. the initial evaluation demonstrated a conscious, oriented patient with a blood pressure of 130/85, afebrile, with dysarthria. other aspects of the neurologic examination were normal. the routine investigation showed normal blood sugar, electrocardiography showed sinus rhythm and native brain ct-scan. meanwhile, the patient reported complete resolution of his speech difficulty and requested if he can go home. his initial abcd2 score was 3 (1 for age, 1 for his dysarthria & 1 for less than 60 minutes duration of symptoms), and was deemed low risk for recurrent tia (transient ischemic attack) or stroke within the next 48 hrs., kept on antiplatelet and statin tablets, sent for full stroke workup including cardiac telemetry, given mri/mra appointment and was discharged home. 36 hours later, he presented again with disorientation that soon evolved into a stupor with a blood pressure of 200/110 mm hg, and was suspected to have suffered from a hemorrhagic stroke. aspirin was stopped and urgent ct scan was done, it showed left tempo-occipital hematoma. evaluated by neurosurgeon and neuro-endovascular specialist. mri/mra and ctangiography were performed (figure. 1 and 2), suggested the presence of tentorial vascular malformation. the next day, cerebral digital subtraction angiography was performed, showed the dural arteriovenous fistula of the tentorium. during the procedure, histoacryl embolization was performed without any complications (figure. 3). the patient was transferred to an intensive care unit. he was discharged after 15 days without neurological deficit. figure 1. ct angiography 3d reconstruction study showed tentorial davf, the fistulous connection was between the middle meningeal artery, tentorial branches of the meningohypophysial trunk of the internal carotid artery with the transvers-sigmoid sinuses junction and the straight sinus, with venous varices that render the lesion as a high risk for haemorrhage davfs. figure 2. cerebral mri showing posterior left temporal intraparenchymal hematoma. 297 tentorial dural arteriovenous fistulae presenting as transient ischemic attack figure 3. (a, b) cerebral digital subtraction angiography (dsa) of the left external carotid artery showing the medial tentorial davf supplied by the middle meningeal artery and drained into the transverse-sigmoid junction and the the straight sinus, with the venous varices. (c) post embolization image showing the histoacryl used in relatively large amount due to multiple fistulous connections. discussion dural arteriovenous fistulas (davfs) are relatively rare, representing 10% to 15% of intracranial vascular malformations. their usual locations are tentorium (26%), cavernous sinus (26%), transverse/sigmoid sinus (25%), convexity and superior sagittal sinus (11%), and frontal cranial vault (9%). the tentorial dural arteriovenous fistulas (tdavf) clinically present with hemorrhage, with reported rates from 58% to 92%, and neurological deficits in 79% to 92% of patients. the pathophysiology is retrograde leptomeningeal venous drainage with ensuing venous congestion (1, 2, 11-13). common presentations include intracranial hemorrhage, urinary incontinence, paresis, and sensory loss affecting the extremities (14,15). transarterial endovascular treatment of davfs showed symptomatic improvement in about 78% of the cases, with a complication rate of 5% (16). in our patient, digital subtraction angiography revealed a fistulous connection located at the medial tentorium draining directly into cerebellar veins and finally into the straight sinus. davfs clinical presentation includes specific and nonspecific neurological symptoms. non-specific manifestations such as headache are usually attributed to cerebrospinal fluid malabsorption due to increased pressure in the superior sagittal sinus, venous sinus thrombosis or meningeal scarring due to repeated small subarachnoid hemorrhages. cranial nerve deficits are probably related to arterial steal phenomena. specific neurological manifestations may be the result of venous ischemia, venous mass effect, venous rupture or venous thrombosis due to passive venous hypertension, congestion or both (17-20). many non-hemorrhagic neurological deficits due to tdavfs have been reported, including gait instability, bruit, personality changes, depression, trigeminal neuralgia, syncopal events, slurred speech, cranial nerve vii weakness (3), visual symptoms. (including bilateral proptosis, bilateral episcleral and retinal venous congestion, optic disc pallor, quadrantanopia and concentric narrowing of the visual field) (10), hemifacial spasm (3), progressive myelopathy, hemisensory disturbance, brainstem dysfunction and obstructive hydrocephalus (4). the mechanism of brainstem dysfunction may be related to arterial steal phenomena, brainstem venous congestion or compression due to dilated veins or cerebellar edema (15). the vast majority of these lesions can be successfully treated with selective endovascular embolization (3,17,21). conclusion the clinical symptoms of davfs depend on the location and pattern of the venous drainage. the transient ischemic attack should be kept in mind as an uncommon presentation of tentorial davfs. endovascular, surgical, radiosurgery, and even observation in certain cases are valid options in the treatment of different grades davfs. references 1. gupta ak, periakaruppan al. intracranial dural arteriovenous fistulas: a review. indian j radiol imaging. 2009; 19:43-8. 2. panagiotopoulos v, kastrup o, wanke i. endovascular 298 marco zenteno, mohamed m. arnaout, angel lee et al. treatment resolves non-hemorrhagic brainstem dysfunction due to tentorial dural av fistula. journal of clinical neuroscience. 2009 feb 1;16(2):317-20. 3. forsting m, wanke i. sinovenous thrombosis and dural av fistulas: related diseases from a neuroradiological point of view. aktuelle neurologie. 2004 jan 1;1(6):342-8. 4. pannu y, shownkeen h, nockels rp, origitano tc. obliteration of a tentorial dural arteriovenous fistula causing spinal cord myelopathy using the cranio-orbito zygomatic approach. surgical neurology. 2004 nov 1;62(5):463-7. 5. valderrama j, garcia r, satyarthee g, calderon w, hoz s, narvaez-rojas a, moscote l. intracranial pial arteriovenous fistula mimicking a vein of galen aneurysm with hydrocephalus managed with endovascular method: case report. iranian journal of neurosurgery. 2017 sep 15;3(2):67-3. 6. gobin yp, rogopoulos a, aymard a, khayata m, reizine d, chiras j, merland jj. endovascular treatment of intracranial dural arteriovenous fistulas with spinal perimedullary venous drainage. journal of neurosurgery. 1992 nov;77(5):718-23. 7. herman jm, spetzler rf, bederson jb, kurbat jm, zabramski jm. genesis of a dural arteriovenous malformation in a rat model. journal of neurosurgery. 1995 sep;83(3):539-45. 8. picard l, bracard s, islak c, roy d, moreno a, marchal jc, roland j. dural fistulae of the tentorium cerebelli. radioanatomical, clinical and therapeutic considerations. journal of neuroradiology. journal de neuroradiologie. 1990;17(3):161-81. 9. kajita y, miyachi s, wakabayashi t, inao s, yoshida j. a dural arteriovenous fistula of the tentorium successfully treated by intravascular embolization. surgical neurology. 1999 sep 1;52(3):294-8. 10. wajnberg e, spilberg g, rezende mt, abud dg, kessler i, mounayer c. endovascular treatment of tentorial dural arteriovenous fistulae. interventional neuroradiology. 2012 mar;18(1):60-8. 11. tomak pr, cloft hj, kaga a, cawley cm, dion j, barrow dl. evolution of the management of tentorial dural arteriovenous malformations. neurosurgery. 2003 apr 1;52(4):750-62. 12. byrne jv, garcia m. tentorial dural fistulas: endovascular management and description of the medial dural-tentorial branch of the superior cerebellar artery. american journal of neuroradiology. 2013 may 9. 13. van lindert e, hassler w, kühne d, henkes h. combined endovascular-microsurgical treatment of tentorialincisural dural arteriovenous malformations. report of five cases. min-minimally invasive neurosurgery. 2000 sep;43(03):138-43. 14. lawton mt, sanchez-mejia ro, pham d, tan j, halbach vv. tentorial dural arteriovenous fistulae: operative strategies and microsurgical results for six types. operative neurosurgery. 2008 mar 1;62(suppl_1):ons110-25. 15. van rooij wj, sluzewski m, beute gn. tentorial artery embolization in tentorial dural arteriovenous fistulas. neuroradiology. 2006 oct 1;48(10):737-43. 16. paredes i, martinez-perez r, munarriz pm, castaño-leon am, campollo j, alén jf, lobato rd, lagares a. fístulas durales arteriovenosas intracraneales. experiencia con 81 casos y revisión de la literatura. neurocirugia. 2013 jul 1;24(4):141-51. 17. khan s, polston dw, shields jr rw, rasmussen p, gupta r. tentorial dural arteriovenous fistula presenting with quadriparesis: case report and review of the literature. journal of stroke and cerebrovascular diseases. 2009 nov 1;18(6):428-34. 18. davies ma, ter brugge k, willinsky r, wallace mc. the natural history and management of intracranial dural arteriovenous fistulae: part 2: aggressive lesions. interventional neuroradiology. 1997 dec;3(4):303-11. 19. tubbs rs, nguyen hs, shoja mm, benninger b, loukas m, cohen-gadol aa. the medial tentorial artery of bernasconi–cassinari: a comprehensive review of its anatomy and neurosurgical importance. acta neurochirurgica. 2011 dec 1;153(12):2485-90. 20. shin m, kurita h, tago m, kirino t. stereotactic radiosurgery for tentorial dural arteriovenous fistulae draining into the vein of galen: report of two cases. neurosurgery. 2000 mar 1;46(3):730-. 21. lewis ai, tomsick ta, tew jm. management of tentorial dural arteriovenous malformations: transarterial embolization combined with stereotactic radiation or surgery. journal of neurosurgery. 1994 dec 1;81(6):851-9. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 478-481 doi: 10.33962/roneuro-2019-076 www.journals.lapub.co.uk/index.php/roneurosurgery skull metastasis of hepatocellular carcinoma in normal liver. case report a. khelifa1, i. assoumane2, bachir s.3, l. berchiche1, t. bennafaa1, a. morsli1 1 neurosurgical department of beo university hospital, algiers, algeria 2 national hospital of niamey, niger 3 neurosurgical department of laghouat hospital, laghouat, algeria abstract background: so far hepatocellular carcinoma (hcc) is the most common liver malignant tumour; it is rarely encountered on a healthy liver (9). the metastasis from hcc cancer are seen in lymph nodes (16%–40%) and lungs (34%–70%), (1,3,4,5,7,8), bone metastasis is unusual and some locations stay rare among them the skull (2,4,5). we report here a case of a patient operated in our department for skull metastasis. that patient was followed for hepatocellular carcinoma in digestive surgery department. case presentation: the patient is a 57 years old male presenting hcc on healthy liver, the patient was referred to our department by digestive surgery colleagues to manage a parietal subcutaneous mass; brain ct scans were performed objectified a calvarial osteolytic process. we remove the tumour and we put a cranioplasty using surgical cement, later the histological studies were in favour of secondary location of hepatocellular carcinoma. conclusion: skull metastasis from hepatocellular carcinoma is rare, reporting such cases strengthen the idea of evoking hcc metastasis in the differential diagnosis of cranial subcutaneous mass. introduction the development of hepatocellular carcinoma on a healthy liver is unusual and skull metastasis from this type of cancer is rare; this make evoking the diagnostic of a metastatic hepatocellular carcinoma for a skull lesion difficult, we report a case of skull metastatic lesion from a hepatocellular carcinoma on patient with a healthy liver. case presentation the patient is a male of 57 years old who presented weeks before he consulted an epigastric pain, then one month later a cranial left parietal subcutaneous mass. first an abdominal ct was performed objectified a tissue mass of 57 mm on the segment ii of the liver extended to the gastro-hepatic omentum reaching the lesser curvature of the stomach, keywords hepatocellular carcinoma, metastasis, skull tumour corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 479 skull metastasis of hepatocellular carcinoma in normal liver the surrounding hepatic tissue appeared to be normal; and all laboratory tests was initially normal. the patient was scheduled to a surgical resection meanwhile he was referred to our department to manage the cranial mass. the clinical exam at the admission found a conscious patient without neurological deficit presenting a left parietal mass with a diameter of 5 cm, soft, painless, fixed, pulsing, and without cutaneous defect. the brain ct objectified a tumor interesting the left parietal bone without cerebral invasion intensely enhanced after injection of the contrast product, on bony window the lesion is an irregular erosion measuring 48 x 53 mm, (figure 1). on the brain mri the tumor was hypointense on t1 weighted images intensely enhanced by gadolinium, the t2 weighted images have a heterogeneous signal, the angio-mri images objectify a multiple thin vessels inside the tumor, there was a shift effect on the dura but there was no invasion to either dura or cutaneous tissues (figure 2). bone scan with tc99m objectified a calvarial left parietal lake of fixation without any other skeleton locations. we operated the patient and we remove the lesion with the surrounding normal bone, it was a soft brown cauliflower-like mass highly vascularized, easily dissected from the cutaneous tissue pushing the dura witch was eroded at some spots, so we performed a dura plasty using a galea and a bone plasty using surgical cement to repair the bone defect. the histological study of the specimen found a predominance of pseudo glandular trabecular tissue and in the immunohistochemical examination there was a high expression of the hepatocyte antigen, so the diagnosis was in fact a secondary location of a fibro lamellar hcc. there was a full postoperative recovery. the patient was discharged from our department 7 days after the operation without any neurological deficits. we referred him back to general surgery where the liver tumor was resected with 2 cm of security marge and a portion of the stomach lesser curvature; the postoperative recovery was optimal. the patient is still followed in our external consultation since 24 months and there is no tumor recurrence on brain ct scans. figure 1: preoperative brain ct scan. a: injected axial slide; b: bony window axial slide; c: sagittal bony window, showing an osteolytic left parietal lesion intensely enhanced after injection of the contrast product (red arrow). figure 2: preoperative brain mri. a: t1 weighted imaging sagittal; b: t2 weighted imaging coronal; c: t1 enhanced; d: angio mr, showing that the tumor is limited at skull plan without brain invasion and its hyper vasculazation nature 480 a. khelifa, i. assoumane, bachir s. et al. figure 3: preoperative brain ct. bone plasty (red arrow), there is no tumor recurrence discussion so far hepatocellular carcinoma is the most frequent malignant liver tumor; the incidence in a healthy non cirrhotic liver is rare, according to different series it is between 1.7% and 14% (9). skull metastasis are most commonly seen from breast, lung, prostate, and thyroid cancers (2, 4), metastasis from hepatic cancer is rare (5,2,4) it was reported in 0.5 to 1.6% of patients with hcc in most studies (3,4,1), in a review performed in 2014, a total of 59 patients with solitary skull metastasis from hcc were published (1).males are largely more exposed to this affection than females (1,4).metastases occurring in the calvarial site were more frequent than those occurring in the skull base and facial skeleton (1).the most common clinical presentation is a subcutaneous mass with occasional painful sensation (57%), followed by neurological deficits(51%), headache (15%) and seizure (3%) (1). the subcutaneous mass is usually firm solitary painless or occasionally painful rapidly evolving neglected by the patient (1,6,4,3). the tumor size and location are related to the neurologic deficit which is rather present in the skull base tumors (visual disturbance, dysphagia, deafness and facial numbness), than in the volt tumors where the weakness of the limbs is more frequent (4,5,7). although rare cases of tumor bleeding were reported, the per operative hemorrhage risk should be kept in mind and preventive measures should not be neglect (2,3,4,6). in plane x rays the lesion appears to be osteolytic in all reported patients (1,2,3,4,5,6,7,8). the brain ct shows the bone defect, and a significant homogenous enhancement in all cases (1,4,5). in mri the lesion appears as iso or hypo intense in t1 and t2 weighted images. the treatment for skull metastasis, includes radiotherapy, chemotherapy, surgery and palliative care. a single calvarial metastasis can be treated surgically (4). although many reports suggest that the life expectancy is related to the liver failure and the presence of hcc skull metastasis don’t change it significantly (7); all studies suggest that the surgical treatment for hcc metastasis may relief the patient, esthetic, reduce the risks of neurological sequelae, and thus improve the quality of life (1,2,3,4,5). preoperative embolisation is preferred (4). conclusion hepatocellular carcinoma (hcc) is responsible in rare reported cases of cranial metastasis, which clinical presentation is a subcutaneous mass and appears as an osteolytic lesion on radiological investigations. although the vital prognostic is depending on the initial lesion, early diagnostic and surgical removal of the metastasis may improve the life quality. declarations of interest none. funding this research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. references 1. xieliguo.jiangliuyin,yugang jiang. solitary skull metastasis as the first symptom of hepatocellular carcinoma: case report and literature review. neuropsychiatric disease and treatment 2014:10. http://dx.doi.org/10.2147/ndt.s58059 2. jun-ichi kuratsu, masaji murakami, shozaburo uemura and yukitaka ushio. brain and skull metastases of hepatic or pancreatic cancer; report of six cases. neuro med chir (tokyo) 30, july, 1990. 3. dumindasubasinghe, chathurangatisarakeppetiyagama, hemanthasudasinghe, samanwadanamby,niranthiperera and sivasuriyasivaganesh. solitary scalp metastasis – a rare presentation of hepatocellular carcinoma. annals of surgical innovation and research (2015) 9:4. doi 10.1186/s13022-015-0013-2. 4. c.-t. hsieh, j.-m. sun1, w.-c. tsai, t.-h. tsai, y.-h. 481 skull metastasis of hepatocellular carcinoma in normal liver chiang,and m.-y. liu. skull metastasis fromhepatocellular carcinoma. actaneurochir (wien) (2007) 149: 185–190. doi 10.1007/s00701-006-1071-3. 5. takashi goto, takahiro dohmen, kouichi miura, shigetoshi ohshima, kazuo yoneyama, tomomi shibuya, eikataoka, daisuke segawa, wataru sato, yumiko anezaki, hajime ishii, daigokon, ikuhiroyamada, kentarokamada, hirohide ohnishi. skull metastasis from hepatocellular carcinoma with chronic hepatitis b. world j gastrointestoncol2010 march 15; 2(3): 165-168. doi:10.4251/wjgo.v2.i3.165. 6. v. r. ferraz, j. l. vitorino-araújo, l. sementilli, j. f. neto, and j. c. e. veiga. lesion in scalp and skull as the first manifestation of hepatocellular carcinoma. hindawi publishing corporation case reports in neurological medicine volume 2016, article id 2897048, 4 pages. http://dx.doi.org/10.1155/2016/2897048. 7. yu shik shim, jung yong ahn, jun hyung cho and kyu sung lee. solitary skull metastasis as initial manifestation of hepatocellular carcinoma.world journal of surgical oncology 2008, 6:66. doi:10.1186/1477-7819-6-66. 8. vc shakya, cs agrawal, sr pandey, rk rauniyar, k dhungel and s adhikary. multiple skeletal metastases as unusual manifestations of hepatocellular carcinoma in a noncirrhoticliver. nepal med coll j 2010; 12(3): 198-200. 9. lamia kabbage, meryem el kouhen, ahmed taghy, kaoutarznati, nawalkabba. a rare presentation of hepatocellular carcinoma in non-cirrhotic liver pan african medical journal – issn: 19378688. doi:10.11604/pamj. 2017.28.69.13512. ungureanuraluca_subarachnoid romanian neurosurgery (2016) xxx 1: 65 69 65 subarachnoid hemorrhage mimicking acute myocardial infarction: case presentation raluca ungureanu1, gabriel iacob2 1department of anesthesiology and intensive care, emergency university hospital, bucharest 2department of neurosurgery, emergency university hospital, bucharest abstract: we present a patient with a subarachnoid hemorrhage (sah) on the computed tomography and electrocardiogram changes compatible with myocardial infarction. sah is a medical emergency, but it can be initially misdiagnosed. diagnosis may be delayed due to atypical presentations of sah and this may endanger the life of the patient. electrocardiogram abnormalities have been described previously in sah and may obscure the correct diagnosis. key words: subarachnoid hemorrhage sah, acute myocardial infarction introduction subarachnoid hemorrhage (sah) represents a life-threatening medical emergency; therefore patients suffering from it are generally admitted to an intensive care unit (1, 4, 7). with a worldwide incidence of 9 per 100.000 persons per year, this condition has an average mortality of 51%, with one third of survivors needing lifelong care (1, 4). although approximately 70% of deaths are due to direct complications of sah, such as primary bleeding (about 15% die at the time of the ictus), rebleeding and vasospasm; up to 23% of deaths are mainly caused by cardiopulmonary complications (1, 4, 7, 16). cardiac dysfunction has been frequently described in conjunction with intracranial pathologies, such as ischemic stroke, meningitis and epilepsy. yet, sah is the most common intracranial condition associated with cardiac abnormalities (1, 2, 5, 6, 10-12, 16, 18). the mechanisms of these abnormalities are not yet completely understood, but they are thought to be related to the autonomic imbalance, in particular to direct autonomic discharge to the heart or to increased levels of circulating catecholamines induced by the intracranial hemorrhage (1, 2, 4-9, 12). injury in the insular area has particularly been noted to be associated with ecg abnormalities (2, 5, 6, 8, 10). the absence of significant coronary lesions in such patients has been demonstrated by coronary angiography (1, 4, 17). byer cited by (1, 3) is the first to describe ecg abnormalities associated with cerebrovascular diseases, since 1947. it has been estimated that around 50% to 100% of patients suffering from 66 ungureanu, iacob subarachnoid hemorrhage mimicking acute myocardial infarction sah present ecg abnormalities, including t wave abnormalities, peaked p waves, prolonged qtc (greater than 440 ms), stsegment elevations/depressions and in some cases, even q waves (1, 3, 4, 6, 8, 10, 12). prolongation of qt interval is one of the most common changes during sah (1, 2). these changes are often observed in patients without a known preexisting heart disease, therefore they represent a real challenge to cardiologists, anesthetists and intensivists, since the variety of these st/t changes during sah are indistinguishable from those identified during acute myocardial ischemia or injury (1, 2-4, 10, 16). a misdiagnosis may lead to unfortunate consequences, since treatment of myocardial ischemia is aimed at reperfusion of the myocardium with double antiplatelet therapy, anticoagulants, with or without acute coronary angioplasty or fibrinolytic drugs (2, 10, 16). case presentation a 80-year-old-man, with a medical history of hypertension, type 2 diabetes mellitus and dementia, was found drowsy by his family. at the emergency department of the first hospital he was brought to, neurological examination showed a glasgow coma scale of 8 points (e2m5v1), with normal isochoric pupils and bilateral reactive light reflexes. he had spontaneous breathing with no need of intubation or ventilatory support. his physical examination revealed a heart rate of 70 beats per minute and a blood pressure of 110/65 mmhg. his first ecg (figure 1) showed atrial fibrillation and st elevation in lateral leads d i, avl, v 4-v 6, with st depression in leads d ii, d iii, avf, which indicated an acute anterolateral myocardial infarction. next, an echocardiography was performed, showing diffuse hypokinesis of the left ventricle, with an ejection fraction of 40%. his ctni value was 1.9 ng/ml (normal value < 0.4 ng/ml). creatinine and serum potassium were within normal range (1,1 mg/dl and 4,2 mmol/l respectively. based on the abnormalities seen on the patient’s ecg, the result of the echocardiography and his ctni value, he was diagnosed with acute antero-lateral myocardial infarction. an emergency coronary angiography was performed but there was no significant stenosis. next, an emergency cerebral ct scan was done. it revealed the presence of sah and a 5 mm subdural hematoma, without the need of an urgent neurosurgical intervention. a few hours later, the patient’s family decided to transfer him at the emergency university hospital in bucharest. here a cerebral angiography could not be performed. during the patient's follow-up his left ventricle ejection fraction improved (45-50%) and his ctni value decreased (0,9 ng/ml on day 4). moreover his ecg traces improved (fig. 2) and negative/biphasic t waves appeared (day 4). a control cerebral ct scan showed some resorption of the intracranial blood. unfortunately, the patient died the fifth day following a respiratory arrest which could not be resuscitated. the family refused the necropsy. romanian neurosurgery (2016) xxx 1: 65 69 67 figure 1 atrial fibrillation: d i, avl, v4-v6 st elevation; d ii, d iii, avf st depression figure 2 st elevations in ecg traces improved and negative/biphasic t waves appeared (after 4 days) discussion although electrocardiographic abnormalities are not uncommon in patients with cerebrovascular disease including subarahnoid hemorrhage, subdural hematoma and ischemic stroke, typical st segment elevation is rare. up to date, there are only a few cases of intracranial pathologies mimicking acute myocardial infarction described in the literature (13-17). as described earlier, the physiopathology is still not known. there are two mechanisms thought to produce such ecg changes in patients with cerebral lesions: autonomic neural stimulation from the hypothalamus/insula and/or elevated circulating catecholamines. hypothalamic 68 ungureanu, iacob subarachnoid hemorrhage mimicking acute myocardial infarction stimulation might cause ecg changes without associated myocardial damage, whereas elevated circulating catecholamines might induce tachycardia, coronary vasospasm and direct myocardial toxicity due to increased intracellular calcium (1-5)(8)(9). in the present case, the coronary angiography excluded an acute myocardial infarction. thus the left ventricular dysfunction seen on echocardiography may have a toxic effect upon the myocardium leading to contractile dysfunction, necrosis and apoptosis. during a follow-up period, the cardiovascular status of the patient showed almost complete recovery. serial ecg revealed resolution of the st elevations, repeated echocardiography demonstrated cvasi-normal left ventricular function. reversible left ventricular systolic dysfunction associated with intracranial hemorrhage may be due the neurogenic stunned myocardium. the present case tries to emphasize the fact that there may be diagnostic problems in differentiating between intracranial hemorrhage and acute myocardial infarction among unconscious patients. differentiating myocardial infarction from neurogenic left ventricular dysfunction associated with intracranial hemorrhage is very important for initiating appropriate therapy for the relevant condition. antiplatelet, anticoagulant and fibrinolytic drugs are essential in stemi treatment, while they are contraindicated in intracerebral hemorrhages. in conclusion, doctors should always be aware of the cardiac manifestations of acute cerebrovascular events such as sah, especially in unconscious patients, where coronary angiography might prove extremely important in the differential diagnosis. references 1.okabe t., kanzaria m., et al. cardiovascular protection to improve clinical outcomes after subarachnoid hemorrhage: is there a proven role?, neurocrit care 2013, 18, 271-284 2.takeuci s., nagatani k. et al. electrocardiograph abnormalities in intracerebral hemorrhage, journal of clinical neuroscience 2015, 22, 1959-1962 3.sakr y.l., lim n. et al. relation of ecg changes to neurological outcome in patients with aneurysmal subarachnoid hemorrhage, international journal of cardiology 2004, 96, 369-373 4.urbaniak k., merchant a.i. et al. cardiac complications after aneurysmal subarachnoid hemorrhage. surgical neurology 2007, 67, 21-29 5.juntilla e., vaara m. et al. repolarization abnormalities in patients with subarachnoid and intracerebral hemorrhage: predisposing factors and association with outcome. neuroscience in anesthesiology and perioperative medicine 2012, 116 (1), 190-197 6.huang c.c., huang c.h. et al. the 12-lead electrocardiogram in patients with subarachnoid hemorrhage: early risk prognostication. the american journal of emergency medicine 2012, 30, 732-736 7.diringer m.n., citerio g. understanding the disease: aneurysmal subarachnoid hemorrhage. intensive care med 2014, 40, 1940-1943 8.chen w-l., huang c-h. et al. ecg abnormalities predict neurogenic pulmonary edema in patients with subarachnoid hemorrhage, american journal of emergency medicine 2016, 34, 79-82 9.schuiling w.j., algra a. et al. ecg abnormalities in predicting secondary cerebral ischemia after subarachnoid haemorrhage, acta neurochirurgica 2006, 148, 853-858 10.van bree m.d.r., roos y.b.w.e.m. et al. prevalence and characterization of ecg abnormalities after intracerebral hemorrhage, neurocrit care 2010, 12, 5055 romanian neurosurgery (2016) xxx 1: 65 69 69 11.crago e., kerris k. et al. cardiac abnormalities after aneurysmal subarachnoid hemorrhage: effects of βblockers and angiotensin-converting enzyme inhibitors, am j crit care 2014, 23(1), 30-39 12.brouwers p.j.a.m., wijdicks e.f.m. et al. serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage, stroke 1989, 20, 1162-1167 13.van der bilt i. a. c., raaphorst j. et al. ischemic stroke mimicking acute myocardial infarction, a diagnostic dilemma, international journal of cardiology 2006, 109, 127-128 14.hamilton j.c., korn-naveh l., crago e.a. case studies in cardiac dysfunction after acute aneurysmal subarachnoid hemorrhage, journal of neuroscience nursing 2008, 5 (40), 269-274 15.heo w.j., kang j.h. et al. subarachnoid hemorrhage misdiagnosed as an acute st elevation myocardial infarction, korean circ j 2012, 42, 216-219 16.benninger f., raphaeli g., steine i. subarachnoid hemorrhage mimicking myocardial infarction, journal of clinical neuroscience 2015, 22, 1981–1982 17. köklü e., yüksel i. ö. et al. subarachnoid hemorrhage that electrocardiographically mimics acute coronary syndrome: a case report, turk kardiyol dern ars 2015, 43(8), 730-733 a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-036 outcome analysis of upper and lower limb motor functions after anterior cervical discectomy and fusion for degenerative cervical disc disease ninad n. srikhande, v.a. kiran kumar, n.a. sai kiran, amrita ghosh, ranabir pal, luis rafael moscote-salazar, v. anil kumar, vishnu vardhan reddy, amit agrawal romanian neurosurgery (2020) xxxiv (1): pp. 238-244 doi: 10.33962/roneuro-2020-036 www.journals.lapub.co.uk/index.php/roneurosurgery outcome analysis of upper and lower limb motor functions after anterior cervical discectomy and fusion for degenerative cervical disc disease ninad n. srikhande1, v.a. kiran kumar1, n.a. sai kiran1, amrita ghosh2, ranabir pal3, luis rafael moscote-salazar4, v. anil kumar5, vishnu vardhan reddy1, amit agrawal1 1 department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 2 department of biochemistry, calcutta medical college, 88, college street, kolkata-700073, india 3 department of community medicine, mgm medical college and lsk hospital, kishanganj -855107, bihar, india 4 neurosurgery-critical care, red latino, organización latinoamericana de trauma y cuidado, neurointensivo, bogota, colombia 5 department of anaesthesia, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract background: anterior cervical discectomy and fusion (acdf) is the most commonly performed surgical procedure for symptomatic cervical disc disease. in this study, we analysed the upper and lower limb motor functions after acdf for disc prolapse in patients with degenerative cervical disc disease. methods: one hundred consecutive adult patients who underwent acdf for single or two-level cervical disc prolapse during the study period (october 2015 to october 2017) were included in the study. results: preoperative motor deficits in limbs were noted in 73% (73/100) of the patients. enhance recovery of motor deficits was noted in 72.6% (53/73) of these patients and persisting motor deficits in the remaining patients (20/7327.4%). five patients (5/2718.5%) without any preoperative motor deficits developed motor deficits after acdf. detailed pre and postoperative (at the time of discharge) motor power (graded by mrc grade) in all 4 limbs (shoulder abduction / adduction / flexion / extension, elbow flexion / extension, wrist flexion / extension, hip abduction / adduction / flexion / extension, knee flexion/extension, ankle flexion/extension) was recorded. statistically significant improvement in motor power (as recorded at the time of discharge) was noted in all the tested muscle groups after acdf. conclusion: early improvement in preoperative motor deficits can be expected in the majority of the patients with cervical pivd following acdf. keywords anterior cervical discectomy and fusion, outcome, cervical disc degeneration corresponding author: v. a. kiran kumar assistant professor of neurosurgery, narayana medical collegehospital chinthareddypalem, nellore, andhra pradesh, india drananth21@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 239 outcome analysis of upper and lower limb motor functions after anterior cervical discectomy and fusion introduction acdf is most commonly done to treat a symptomatic cervical pivd. (1, 16, 20, 22, 23, 25) acdf is a safe procedure and is rarely associated with postoperative complications. (2, 7, 9, 12, 17) significant proportion of patients shows remarkable recovery in motor deficits following acdf. (11, 16) authors in this publication analysed in detail the early recovery of motor deficits following acdf for single or two level degenerative cervical pivd. material and methods one hundred consecutive adult patients who underwent acdf for degenerative cervical pivd during the study period (october 2015 to october 2017) were included in the study. patients with traumatic pivd were excluded. approval from the institutional ethical committee was taken for this study. detailed pre and postoperative (at the time of discharge) motor power (graded by mrc grade except hand grip which was subjectively graded from 0-100%) in all 4 limbs (shoulder abduction / adduction / flexion / extension, elbow flexion / extension, wrist flexion / extension, hip abduction / adduction / flexion / extension, knee flexion / extension, ankle flexion / extension) were analysed. statistical analysis data analysis was done by using statistical software spss statistics version 24.0. descriptive statistics including mean and standard deviation for continuous variables, and frequency and percentage for categorical variables were used for data expression. appropriate tests like chi-square test, wilcoxon signed rank test etc. were used for checking statistically significant correlation. a probability (p) value of <0.05 was considered significant. results preoperative motor deficits in limbs were noted in 73% (73/100) of the patients. at the time of discharge, enhance recovery of motor deficits was noted in 72.6% (53/73) of these patients and persisting motor deficits in the remaining patients (20/7327.4%). five patients (5/2718.5%) without any preoperative motor deficits developed motor deficits after acdf. pre and postoperative (at the time of discharge) motor power in all 4 limbs is compared in tables 1-4. statistically significant improvement in motor power at the time of discharge was recorded in all the tested muscle groups after acdf. right upper limb preoperative (n=100) postoperative (n=100) p-value mean# median# range# iqr mean# median# range# iqr shoulder should er abducti on 3.80±1.4 4 0-5 2 4.15±1.29 5 0-5 1 0.001 (s)* should er adducti on 3.80±1.4 4 0-5 2 4.16±1.29 5 0-5 1 0.001 (s)* should er flexion 3.81±1.4 4 0-5 2 4.18±1.29 5 0-5 1 0.001 (s)* should er extensi on 3.80±1.4 4 0-5 2 4.17±1.32 5 0-5 1 0.001 (s)* 240 ninad n. srikhande, v.a. kiran kumar, n.a. sai kiran et al. table 1. comparison of preoperative and postoperative motor power in right upper limb. #power graded according to mrc grade. *obtained using wilcoxon signed rank test; † obtained using chi square test; s: significant. left upper limb preoperative (n=100) postoperative (n=100) pvalue* mean# median# range# iqr mean# median# range # iqr shoulder shoulder abduction 3.75±1.4 1 4 0-5 2 4.12±1.36 5 0-5 1 0.001 (s)* shoulder adduction 3.74±1.4 1 4 0-5 2 4.14±1.34 5 0-5 1 0.001 (s)* shoulder flexion 3.72±1.4 2 4 0-5 2 4.13±1.34 5 0-5 1 0.001 (s)* shoulder extension 3.72±1.4 5 4 0-5 2 4.13±1.32 5 0-5 1 0.001 (s)* elbow elbow elbow flexion 3.73±1.5 4 0-5 1 4.17±1.32 5 0-5 1 0.001 (s)* elbow extensi on 3.71±1.5 4 0-5 2 4.16±1.33 5 0-5 1 0.001 (s)* wrist wrist flexion 3.71±1.6 4 0-5 1 4.14±1.27 5 0-5 1 0.001 (s)* wrist extensi on 3.72±1.6 4 0-5 2 4.14±1.29 5 0-5 1 0.001 (s)* right hand grip preoperative (number of patients) postoperative (number of patients) p-value 0-25% 11 4 0.001 (s)† 25-50 % 11 13 50-75 % 29 22 75100% 49 61 241 outcome analysis of upper and lower limb motor functions after anterior cervical discectomy and fusion elbow flexion 3.70±1.4 8 4 0-5 2 4.13±1.30 5 0-5 1 0.001 (s)* elbow extension 3.70±1.4 8 4 0-5 2 4.13±1.29 5 0-5 1 0.001 (s)* wrist wrist flexion 3.64±1.5 1 4 0-5 1 4.2±1.26 5 0-5 1 0.001 (s)* wrist extension 3.64±1.5 3 4 0-5 2 4.14±1.3 5 0-5 1 0.001 (s)* left hand grip preoperative (number of patients) postoperative (number of patients) p-value 0-25% 12 3 0.001 (s)† 25-50 % 11 13 50-75 % 34 16 75-100% 43 68 table 2. comparison of preoperative and postoperative motor power in left upper limb. #power graded according to mrc grade *obtained using wilcoxon signed rank test; † obtained using chi square test; s: significant right lower limb preoperative (n=100) postoperative (n=100) p-value* mean# median# range# iqr mean# median# range# iqr hip hip abduction 3.42±1.85 4 0-5 2 3.90±1.59 5 0-5 2 0.001(s) hip adduction 3.43±1.88 4 0-5 2 3.91±1.59 5 0-5 1 0.001(s) hip flexion 3.43±1.88 4 0-5 2 3.91±1.59 5 0-5 1 0.001(s) hip extension 3.42±1.88 4 0-5 2 3.88±1.59 5 0-5 2 0.001(s) knee 242 ninad n. srikhande, v.a. kiran kumar, n.a. sai kiran et al. knee flexion 3.40±1.86 4 0-5 2 3.90±1.60 5 0-5 2 0.001(s) knee extension 3.38±1.86 4 0-5 2 3.90±1.59 5 0-5 2 0.001(s) ankle ankle flexion 3.33±1.85 4 0-5 2 3.84±1.58 4.5 0-5 2 0.001(s) ankle extension 3.35±1.86 4 0-5 2 3.85±1.58 5 0-5 2 0.001(s) table 3. comparison of preoperative and postoperative motor power in right lower limb. #power graded according to mrc grade *obtained using wilcoxon signed rank test; s: significant left lower limb preoperative (n=100) postoperative (n=100) p-value* mean median range iqr mean median range iqr hip hip abduction 3.32±1.86 4 0-5 2 3.98±1.53 5 0-5 1 0.001 (s) hip adduction 3.33±1.87 4 0-5 2 3.99±1.52 5 0-5 1 0.001 (s) hip flexion 3.32±1.86 4 0-5 2 4.00±1.49 5 0-5 1 0.001 (s) hip extension 3.29±1.84 4 0-5 2 3.98±1.49 5 0-5 1 0.001 (s) knee knee flexion 3.27±1.83 4 0-5 2 3.95±1.52 5 0-5 1 0.001 (s) knee extension 3.27±1.84 4 0-5 2 3.94±1.51 5 0-5 1 0.001 (s) ankle ankle flexion 3.22±1.89 4 0-5 3 3.88±1.55 5 0-5 2 0.001 (s) ankle extension 3.20±1.89 4 0-5 3 3.89±1.56 5 0-5 2 0.001 (s) table 4. comparison of preoperative and postoperative motor power in right lower limb. #power graded according to mrc grade *obtained using wilcoxon signed rank test; s: significant discussion cervical pivd is a common degenerative disc disease affecting millions of people. (24) cervical disc herniation can occur as a result of ageing, wear and tear, or sudden stress from an accident.(5) majority of these patients present with neck pain radiating to upper limbs. (24) other presenting symptoms include motor deficits, stiffness in limbs, sensory deficits, paresthesias in limbs etc. (16, 24) majority of the patients presenting with only neck pain or radicular pain can be managed with medicationas and conservative measures like physiotherapy, cervical collar etc. patients with significant pain not responding to conservative measures and patients with neurological deficits like sensory/motor deficits and bladder symptoms respond well to surgery. (10, 16, 21) acdf is a common surgical procedure performed for symptomatic degenerative cervical disc disease. (6, 16) it helps to relieve the pressure on nerve roots and/or on the spinal cord, (14) thus resulting in improvement in various clinical symptoms including 243 outcome analysis of upper and lower limb motor functions after anterior cervical discectomy and fusion neck pain, radicular pain, motor weakness, sensory symptoms, tightness in limbs and bladder disturbances. (10, 13, 16) various complications reported with acdf include dysphagia, hoarseness of voice, wound hematoma, graft migration, pseudoarthrosis, wound infection etc. (13) patients can rarely have sensory or motor deficits after acdf due to small risk of damage to the spinal cord, nerve roots or both. (10, 13, 16) improvement in neurological deficits ranging from 36-93% has been reported in various series after acdf.(3, 13, 15, 16, 18) lehman et al (16) reported preoperative motor deficits in 55% of the patients and reported recovery of these deficits in 95% of them at 1 year. chiles et al(4) reported strength improvement rates ranging form 79.1% to 90.9% in various individual muscle groups of upper and lower limbs following acdf. in the present study very high proportion of patients (73%) presented with motor deficits and early complete recovery of these deficits were noted in 72.6% (53/73) of these patients. majority of the studies on acdf have graded neurological deficits using various scores like nurick’s grade, joa, modified joa scores etc. which combine both sensory and motor deficits. (4, 8, 16, 19) detailed assessment of motor deficits with grading of motor power for various muscle groups has not been done in most of the studies on acdf. (8, 16) in the present study we compared the preoperative motor power and early postoperative (at the time of discharge) motor power following acdf in all major groups of muscles of lower and upper extremity and found that significant improvement in motor power in early postoperative period. long term follow-up studies in patients following acdf is required as they can develop new deficits secondary to adjacent segment disease. (16) conclusion early improvement in preoperative motor deficits can be expected in majority of the patients with degenerative cervical pivd following acdf. references 1. bhaganagare as, nagesh sa, shrihari bg, naik v, nagarjun mn, pai bs: management of cervical monoradiculopathy due to prolapsed intervertebral disc, an institutional experience. journal of craniovertebral junction & spine 8:132, 2017. 2. boakye m, mummaneni pv, garrett m, rodts g, haid r: anterior cervical discectomy and fusion involving a polyetheretherketone spacer and bone morphogenetic protein. journal of neurosurgery: spine 2:521-525, 2005. 3. bohlman hh, emery se, goodfellow db, jones pk: robinson anterior cervical discectomy and arthrodesis for cervical radiculopathy. long-term follow-up of one hundred and twenty-two patients. jbjs 75:1298-1307, 1993. 4. chiles iii bw, leonard ma, choudhri hf, cooper pr: cervical spondylotic myelopathy: patterns of neurological deficit and recovery after anterior cervical decompression. neurosurgery 44:762-769, 1999. 5. chung jy, park j-b, seo h-y, kim sk: adjacent segment pathology after anterior cervical fusion. asian spine j 10:582-592, 2016. 6. dardis rm, saxena a, shad a, chitnavis b, gullan r (2012) disc replacement technologies in the cervical and lumbar spine. elsevier, pp 1777-1788. 7. davis ra: a long-term outcome study of 170 surgically treated patients with compressive cervical radiculopathy. surgical neurology 46:523-533, 1996. 8. emery se, bohlman hh, bolesta mj, jones pk: anterior cervical decompression and arthrodesis for the treatment of cervical spondylotic myelopathy. two to seventeen-year follow-up. jbjs 80:941-951, 1998. 9. fountas kn, kapsalaki ez, nikolakakos lg, smisson hf, johnston kw, grigorian aa, lee gp, robinson jr js: anterior cervical discectomy and fusion associated complications. spine 32:2310-2317, 2007. 10. gore dr, sepic sb: anterior discectomy and fusion for painful cervical disc disease: a report of 50 patients with an average follow-up of 21 years. spine 23:2047-2051, 1998. 11. hessler c, boysen k, westphal m, regelsberger j: functional and radiological outcome after acdf in 67 cases. zeitschrift fur orthopadie und unfallchirurgie 149:683-687, 2011. 12. jacobs wc, anderson pg, limbeek j, willems pc, pavlov p: single or double-level anterior interbody fusion techniques for cervical degenerative disc disease. cochrane database syst rev 4:cd, 2004. 13. jagannathan j, shaffrey ci, oskouian rj, dumont as, herrold c, sansur ca, jane sr ja: radiographic and clinical outcomes following single-level anterior cervical discectomy and allograft fusion without plate placement or cervical collar. 2008. 14. kim w-k (2011) role of minimally invasive cervical spine surgery in the aging spine. elsevier, pp 198-203. 15. lebl dr, hughes a, cammisa fp, o’leary pf: cervical spondylotic myelopathy: pathophysiology, clinical presentation, and treatment. hss journal 7:170-178, 2011. 16. lehmann cl, buchowski jm, stoker ge, riew kd: neurologic recovery after anterior cervical discectomy and fusion. global spine j 4:41-46, 2014. 17. levinthal r: anterior cervical discectomy with and 244 ninad n. srikhande, v.a. kiran kumar, n.a. sai kiran et al. without fusion. results, complications, and long-term follow-up. spine 19:2343-2347, 1994. 18. murrey d, janssen m, delamarter r, goldstein j, zigler j, tay b, darden b: results of the prospective, randomized, controlled multicenter food and drug administration investigational device exemption study of the prodisc-c total disc replacement versus anterior discectomy and fusion for the treatment of 1-level symptomatic cervical disc disease. the spine journal 9:275-286, 2009. 19. nurjck s: the pathogenesis of the spinal cord disorder associated with cervical spondylosis. brain 95:87-100, 1972. 20. orr rd, zdeblick ta: cervical spondylotic myelopathy: approaches to surgical treatment. clinical orthopaedics and related research 359:58-66, 1999. 21. saldua ns, okafor c, harris eb, vaccaro ar (2011) the role of spinal fusion and the aging spine: stenosis without deformity. elsevier, pp 329-335. 22. truumees e, herkowitz hn: cervical spondylotic myelopathy and radiculopathy. instr course lect 49:339360, 2000. 23. wu t-k, wang b-y, deng m-d, hong y, rong x, chen h, meng y, liu h: a comparison of anterior cervical discectomy and fusion combined with cervical disc arthroplasty and cervical disc arthroplasty for the treatment of skip-level cervical degenerative disc disease: a retrospective study. medicine 962017. 24. yolas c, ozdemir ng, okay ho, kanat a, senol m, atci ib, yilmaz h, coban mk, yuksel mo, kahraman u: cervical disc hernia operations through posterior laminoforaminotomy. journal of craniovertebral junction and spine 7:91, 2016. 25. yu j, ha y, shin jj, oh jk, lee ck, kim kn, yoon dh: influence of plate fixation on cervical height and alignment after one-or two-level anterior cervical discectomy and fusion. british journal of neurosurgery:18, 2017. 22_grandhibhavana_follicular romanian neurosurgery (2015) xxix 3: 373 375 373 follicular carcinoma of thyroid presenting as brain metastasis bhavana grandhi1, byna syamasundara2, amit agarwal3, p. umamaheshwara reddy4 narayana medical college and hospital, nellore, andhra pradesh 1assistant professor, department of pathology; 2associate professor, department of pathology; 3professor, department of neurosurgery; 4assistant professor, department of radiology abstract: metastatic brain tumors are a major cause of mortality in cancer patients. the primary tumor is most commonly seen in the lung, breast, colon and kidney and very rarely in the thyroid. we discuss a case of a 55year old lady with presenting complaints of seizures. there is a past history of carcinoma thyroid for which she had underwent total thyroidectomy. craniotomy was done and histopathological examination revealed metastatic deposits from follicular carcinoma thyroid. key words: brain tumors, follicular carcinoma, metastasis, thyroid. introduction brain masses are mostly metastatic in origin, accounting for more than 50% of hospital admissions for brain tumors. the most common primary sites are tumors from the lung, breast, colon, kidney (2). follicular carcinoma of thyroid is the second most common thyroid malignancy with distant metastasis to bone, lungs, and rarely to the brain, skin and adrenals. (1) most of the cns tumors are symptomatic at the time of diagnosis with most common being seizures and localized motor deficits. (3, 4) we report a case of a 55yr old female who presented to the neurosurgery opd with seizures and was diagnosed, metastasis from follicular carcinoma thyroid. case history a 55 year old female came to the emergency with history of seizures. mri brain was done showing parasagittal hypodense lesion and was admitted under neurosurgery with a provisional diagnosis of meningioma or secondary deposits. previous history of carcinoma thyroid for which total thyroidectomy was done twenty years back. left parasagittal craniotomy was done with tumour excision and the specimen was sent for histopathological examination. microscopic examination revealed glial tissue with adjacent tumor tissue showing well-formed follicles lined by epithelium showing nuclear atypia. vascular invasion also seen and the diagnosis of metastatic deposits, probably of follicular carcinoma thyroid was given. discussion brain metastasis is seen in 16-18% of cancer patients and in about 9% cases, it represents the only site of cancer. the intracranial compartment is of particular interest as most of the foci are symptomatic with highly lethal manifestations if left untreated. (8) hematogenous spread is commonest route spread. the acute angle of the branching of pulmonary vessels makes the corticomedullary gray white junction, the commonest site of metastasis within the brain parenchyma. (5) metastasis from thyroid carcinoma is rare and accounts for 0.1-5% of 374 grandhi et al follicular carcinoma of thyroid presenting as brain metastasis cases in the reported series. thyroid carcinoma is divided into 3 types, follicular, papillary and anaplastic carcinoma. the metastatic potential is a function of the tumour size, capsular and vascular invasion. (8) disseminated metastasis as an initial presentation is very rare in follicular thyroid carcinoma. (2) brain metastasis has been reported from thyroid adenomatous nodules. (7) distant metastasis from follicular thyroid carcinoma to the lumbar vertebrae, skull bone and meninges have been documented. (6) mc. william et al published the largest series of metastatic thyroid carcinoma to brain with 16 patients, out of which only two of them were diagnosed as follicular thyroid cancer which speaks about its rarity. (8) thus, we report this case because of its rare occurrence. figure 1 axial t2w images (a, b, c) showing well defined iso-hypointense extra-axial lesion in left parafalcine location with extensive vasogenic edema. on susceptibility weighted images (d) there was no blooming, diffusion weighted images and corresponding adc map (e, f) show no restriction within the lesion figure 2 a normal glial tissue with adjacent tumor tissue (hematoxylin and eosin, scanner view) figure 2 b tumor tissue composed of thyroid follicles filled with colloid (hematoxylin and eosin, 10x) figure 2 c tumor cells with hyperchromatic nuclei and moderate amount of cytoplasm. (hematoxylin and eosin, 40x) romanian neurosurgery (2015) xxix 3: 373 375 375 conclusion follicular carcinoma of thyroid is a rare tumour that presents with cerebral metastasis and thyroid carcinoma should be considered in the differential diagnosis of contrast enhancing mass lesions in the cns. correspondence dr. bhavana grandhi 1/1278, nawabpeta, bunglathota nellore andhra pradesh, india mobile: 9642111209 e-mail: drbhavana.grandhi@gmail.com references 1. alper sevinc, follicular thyroid cancer presenting initially with soft tissue metastasis. jpn j.clin.oncol 2003;30(1)27-29. 2. douglas c miller. metastatic neoplasms in brain parenchyma in. modern surgical pathology. new york: cambridge university press, 2009;206-207. 3. kamar fg, posner jb. brain metastases. semin neurol 2010;30:217-35. 4. lagerwaard fj, levendag pc, nowak pj, eijkenboom wm, hanssens pe, schmitz pi. identification of prognostic factors in patients with brain metastases: a review of 1292 patients. int j radiat oncol biol phys1999;43:795-803. 5. melike pekmezci, arie perry neuropathology of brain metastases sni: neuro-oncology 2013, vol 4, suppl 4 a supplement to surgical neurology international. 6. p. krishnappa, s. ramakrishnappa, m. kulkarni, s. giriyan. follicular carcinoma of the thyroid presenting as distant metastasis: a case report and review of literature. the internet journal of laboratory medicine. 2012;5(1). 7. tadashi terada: brain metastasis from thyroid adenomatous nodules or an encapsulated thyroid follicular tumor without capsular and vascular invasion: a case report. cases journal 2009, 2:7180. 8. yusuf, engin, doga, erol, turkish neurosurgery 2005, vol: 15, no: 3, 132-135brain metastasis from follicular thyroid carcinoma: case report and literature review. sharmaarvind_teacup 118 sharma et al tea cup in the brain tea cup in the brain, a rare case of penetrating brain injury in pediatric patient arvind sharma, s.k. jain, sanjeev chopra department of neurosurgery, s.m.s medical college, jaipur, rajasthan, india abstract: head injuries are very common in children. all over the world, the most common mechanism is fall. these injuries are more prevalent in developing countries due to lack of education, poverty, lack of standard and scientific ways to child upbringing. penetrating injuries in pediatric patients is extremely uncommon and usually occur due to sharp objects like knife, screw driver, drills, nails. we are reporting a rare case of a child with penetrating head injury due to tea cup, very commonly used crockery in every house hold. to the best of our knowledge, no similar case has ever been reported in world literature. our case also emphasized the need for educating people about child care. key words: penetrating, crockery, tea-cup introduction head injuries due to fall from height are not uncommon in pediatric patients in developing countries. a variety of foreign bodies penetrating the cranium has described in literature like wooden stick, drill bits, electric socket, low and high velocity pallets, stone. but we are describing a very rare case of penetrating injury to cranium due to a tea-cup, a very common crockery item used in day today life. case report a four year old female child presented to us with history of fall from 10 feet of height in his house while playing. there was no history of loss of consciousness, vomiting and seizures. his vitals was within normal range with pulse was 90 per minute and blood pressure was 100/70 millimeter of mercury. he was maintaining oxygen saturation at room air. his pupil was bilateral equal, round and regular and reacting to light. child was conscious, actively playing and having left side hemiparesis with motor power 4/5. child was able to identify his mother. on examination of scalp there was multiple lacerated wound over right parietal region with visible depressed bone fragment and penetrating foreign body. non-contrast enhanced ct scan of brain (figure 1)done and showed right parietal depressed fracture with penetrating foreign body with under laying contusion of brain. romanian neurosurgery (2016) xxx 1: 118 121 119 figure 1 ncct brain showing penetrating foreign body with under-laying contusion no systemic injuries were noted. patient was investigated and blood samples were drawn. surgery was performed promptly with craniectomy done all around the penetrating object followed by removal of foreign body (figure 2) without any side to side movement. figure 2 showing penetrated piece of tea-cup in brain 120 sharma et al tea cup in the brain all devitalized tissue and depressed bone segment taken out. there was a piece of teacup (a type of crockery used in kitchen to serve tea) that was taken out. there was a dural tear with underlying brain contusion, but no active bleeding from brain parenchyma. wound toileting done and dural tear repaired using pericranial patch. postoperatively patient did well with no neurologic deficit. postoperative non contrast enhanced ct scan of brain showed no residual foreign body or bone fragment. there was no hematoma but only residual contusion. post operatively patient’s left side weakness improved. discussion head trauma is exceedingly common in children and the most common mode of injury is fall from height results in coup and countercoup injuries but penetrating injuries in pediatric patients are rare(2). most of penetrating injuries caused by sharpnels and bullets. the most common is due to knife injury, although several cranio-cerebral perforating injuries have been reported, like those caused by nails, keys, pencils, pen metal poles, ice picks, chopsticks, and power drills(3,4,5,7,8,9). these penetrating foreign bodies may breach the dura and can cause damage to brain parenchyma and major vessels within hence these injuries may be fatal. local bone thickness and angle of impact of penetrating object determines the severity of injury (1). neurologic deficit might occurred if eloquent areas of brain are involved. in cases of non-eloquent part of brain involved without any major vascular injury, prognosis is relatively good. these patients should be evaluated with x ray skull that can showed penetrating foreign body with bone defect in cranium. non-contrast enhanced ct scan of brain is investigation of choice and that may showed depressed bone fragment with underlying brain injury. ct angiography of brain should be performed whenever there is high suspicion of any major vascular injury. mri of brain may be hazardous as penetrating object may be ferromagnetic and can cause additional damage to brain. preoperative assessment should be done and any other systemic injuries should be rule out. there is high risk of infection and seizures hence surgical intervention should be done as early as possible. the aim of surgical management is prompt action with removal of any extradural or subdural hematoma, removal of foreign body and involved bone, evacuation of brain contusion or any devitalized tissue and proper dural closure to prevent brain fungus and csf leak (6, 10). postoperatively these patients should be treated with intravenous antibiotics and short course of antiepileptics & closely watch for sign and symptoms of intracranial infection. contrast enhanced ct scan should be performed to rule out brain abscess whenever there is suspicion. conclusion pediatric head injuries are very common in developing countries and most common mode of injury is fall. penetrating head injury in children is very uncommon and mostly occurs due to shrapnel. these patients should be promptly evaluated and treatment should be given as early as possible. our case is very romanian neurosurgery (2016) xxx 1: 118 121 121 special as no case has been reported in world literature in which cause of injury was due to a tea-cup. our case also emphasize the need to educate people in developing world about child care so that these type of injuries can be prevent. references 1. aarabi b. history of the management of craniocerebral wounds. in: aarabi b, kaufman hh, dagi tf, george ed, levy ml, editors. missile wounds of the head and neck. vol. 1. park ridge, ill: american association of neurological surgeons; 1999. pp. 281–92. 2. atabaki sm. pediatric head injury. pediatr rev. 2007;28:215–24. 3. bakay l, glausuer fe, grand w. unusual intracranial foreign bodies: report of five cases. acta neurochir (wien) 1977;39:219–31. 4. herring cj, lumsden ab, tindall c. transcranial stab wounds: a report of three cases and suggestions for management. neurosurgery. 1988;23:658–62. 5. jennifer k, reza k. penetrating head injury in children: a case report and review of the literature. j emerg med. 2001;21:145–50. 6. kaufman hh, schwab k, salazar am. a national survey of neurosurgical care for penetrating head injury. surg neurol. 1991;36:370–7. 7. nakayama y, tanaka a, arita t, kumate s, yoshinga s. penetrating head injury caused by weed: case report. brain and nerve. 1995;47:1192–94. 8. pascual jm, navas m, carrasco r. penetrating ballistic like frontal brain injury caused by a metallic rod. acta nurochirurgica. 2009;151:689–91. 9. salar g, costella gb, mottaran r, mattana m, gazzola l, munari m. multiple craniocerebral injuries from penetrating nails. j neurosurg. 2004;100:963. 10. trask tw, narayan rk. civilian penetrating head injury. in: narayan r, wilberger j, povlishock j 2nd, editors. neurotrauma. new york, ny: mcgraw hill; 1996. pp. 868–89. doi: 10.33962/roneuro-2022-016 osmotherapy in patients with severe brain trauma: which agents should we take into account? randy reina-rivero, gustavo gaitán-herrera, aixa eliana garcía-garcía, amalia molina-trujillo, manuel a. jaramillo-acosta, juliana paniagua-aguirre, alfonso barón-sánchez, antonio luis castro-castro, mohamed argüello-manrique, michael gregorio ortega-sierra romanian neurosurgery (2022) xxxvi (1): pp. 92-97 doi: 10.33962/roneuro-2022-016 www.journals.lapub.co.uk/index.php/roneurosurgery osmotherapy in patients with severe brain trauma: which agents should we take into account? randy reina-rivero1, gustavo gaitán-herrera1, aixa eliana garcía-garcía2, amalia molina-trujillo3, manuel alejandro jaramillo-acosta4, juliana paniagua-aguirre5, alfonso barón-sánchez6, antonio luis castrocastro7, mohamed argüello-manrique8, michael gregorio ortega-sierra9 1 school of medicine, universidad de cartagena, cartagena, colombia 2 school of medicine, universidad de santander, bucaramanga, colombia 3 school of medicine, universidad de ciencias aplicadas y ambientales, bogotá, colombia 4 school of medicine, universidad del quindío, armenia, colombia 5 school of medicine, universidad de caldas, manizales, colombia 6 school of medicine, universidad de boyacá, tunja, colombia 7 centro médico especializado cemes, saravena, colombia 8 school of medicine, universidad juan n corpas, bogotá, colombia 9 medical and surgical research centre, future surgeons chapter, bogotá, colombia abstract traumatic brain injury is still a major cause of mortality and morbidity in the world and is considered a public health problem that needs to be well attended to. cerebral oedema due to brain injury compromises the delivery of essential nutrients and alters normal intracranial pressure, whose increase has been shown to be strongly associated with poor neurological outcomes and mortality for patients with head trauma. intravenous fluids are a fundamental component of trauma care and fluid management influences patient outcomes. thanks to advances in the research of osmotic agents, mortality has been reduced and there has been greater control in intracranial pressure. the osmotic agents most used for the control of intracranial pressure in patients who have suffered severe brain trauma are mannitol and hypertonic saline. however, in recent years have been studying the benefits that sodium lactate can generate in these cases. it has been found that sodium lactate has generated a greater decrease in intracranial pressure values and lower mortality rates with respect to mannitol and hypertonic saline. this still has been disputed as an application of mannitol, hypertonic saline or sodium lactate for treating patients who have suffered some head trauma. this review aims to show the advantages, disadvantages and recommendations of the different hyperosmolar solutions mentioned previously based on current evidence. keywords osmotherapy, traumatic brain injury, intracranial pressure, mannitol, sodium lactate, hypertonic saline solution corresponding author: michael gregorio ortega-sierra medical and surgical research centre, future surgeons chapter, bogotá, colombia mortegas2021@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 93 osmotherapy in patients with severe brain trauma introduction severe traumatic brain injury (tbi) initially causes an injury to the brain by an impact as force propagates towards the cranial cavity, resulting in a stretching and loosening of neural and vascular structures. these direct injuries into the brain parenchyma or blood vessel, prompt inflammation or edema which can be accompanied by bleeding; all these factors ultimately result in an increase in intracranial pressure (icp) (1,2). fluid resuscitation in patients with severe head trauma is vital because of the need to avoid hypotension and secondary neurological injury (3). the increased icp can generate several consequences. on one hand, as the icp increases, the cerebral perfusion pressure (cpp) (initially conserved by regulatory mechanisms) when stopping the self-regulating capacity, the cpp will decrease, which implies a risk of secondary hypoxic brain injury. moreover, the brain can herniate between intracranial compartments and can also lead to secondary brain injury compression and territorial arterial ischemia or by direct compression of the brainstem, becoming in a very mortal issue (1). the main objective of osmotherapy is to preserve or restore the physiology and minimize secondary brain damage, through conservation of cpp and decreased icp. moreover, the brain tissue tension of oxygen (pbto2) has emerged adds as an additional therapeutic goal in the treatment of these patients (3-5). osmotherapy has limited efficacy, so prophylactic use should be avoided and must be carefully removed after the maximum period of edema (6). in addition, it is important to pay attention to signs of rebound edema (7). the major hyperosmolar solutions used in patients with traumatic brain injury include hypertonic saline, mannitol and sodium lactate (2). in view of the above, the objective of this review is to synthesize evidence on the use of osmotherapy in the management of patients with traumatic brain injury and related aspects. methods a bibliographic search was carried out in the pubmed and science direct databases and in the google scholar search engine using the following terms: “osmotherapy”; “traumatic brain injury”; “intracranial pressure”; “mannitol”; “sodium lactate”; “hypertonic saline solution”. articles in spanish and english were included, emphasizing in the benefits of different osmotic agents in the treatment of severe brain trauma, regardless of the publication date. a total of 325 articles were identified from original articles, topic reviews, systematic reviews, letters to the editor, case reports, and case series. 41 articles were selected (3 in spanish and 38 in english) that were adjusted to the objective of the article. results mannitol mannitol is an osmotic agent associated with the treatment of intracranial hypertension (ih), used for clinical purposes in 1962 (3). currently it is highlighted among its indications decreasing refractory icp, elevated icp, oliguria and in some cases of acute renal failure. concentrations ranging from 5% g/100 ml at 25% g/100 ml at an osmolality between 274 and 1372 mosm/l. as for the dose, it was observed a significant reduction in icp and more durable responses to treatment when doses are administered between 0.5 and 1.4 g/kg (8,9). the objective is to maintain osmotherapy normal volemia or mild hypervolemia, and maintain serum osmolality between 300 and 320 mosm/l, so particular vigilance is required to treatment (3,10,11). mannitol acts on ih after about 20 minutes to be administered and reaches its maximum effect in the brain 30 minutes after; effect duration ranging from 90 minutes to 6 hours depending on the etiology. by decreasing the blood viscosity and the hematocrit and increase the flow of oxygenated blood brain leads to vasoconstriction of cerebral arterioles, and this in turn leads to a reduction in icp and increasing the cpp. broadly speaking, also generates a reduction in systemic vascular resistance (and afterload) combined with a transient increased preload and a slight positive inotropic effect, therefore, it improves cardiac output and ventilation (3,12). however, osmotic diuresis with mannitol can cause intravascular dehydration and hypotension (7). in the brain, the mannitol remains in the vascular fluid compartment (13); after prolonged use, it may cross the blood brain barrier and accumulate in the brain tissue, causing an inverse osmotic change, which increases icp (rebound phenomenon) (7). mannitol is filtered at the glomerulus and reabsorbed in the nephron as an osmotic diuretic, it 94 randy reina-rivero, gustavo gaitán-herrera, aixa eliana garcía-garcía et al. is excreted unchanged (3). it can induce acute renal failure (arf) due to renal vasoconstriction, decreased intravascular volume and hyperosmolarity (4). usually it produces no permanent injury; then removing the drug this is reversed. several studies report the lowest total dose of mannitol that can cause arf is 200 g/day (3). other side effects include electrolyte disorders (hyponatremia, hypochloremia, hyperkalemia), acidosis, heart failure and pulmonary edema (3,7). restrict the use of mannitol in patients with signs of trans-tentorial hernia or progressive neurological deterioration causes not attributable to extracranial (14). hypertonic saline hypertonic saline (hs) was used in clinical practice for the first time in 1926 by silver, who used a 5% hs to treat burger's disease. currently, it is positioned as the most popular osmo-agent for hyperosmolar therapy, this due to the multiple complications associated with the use of mannitol (3,15). continuous hs can be early to reduce brain swelling and ih (16). it is also used in cases of subarachnoid hemorrhage, stroke and liver failure. it is used as adjunctive therapy with mannitol or as an alternative treatment in those patients who failed prior therapy with mannitol (3,7,17). it is offered in different concentrations (2%, 3%, 7.5% and 23.4%) and is recommended to administer via a central line and should be used at a concentration > 2%, avoiding the risk of thrombophlebitis and peripheral venous thrombosis (3). it is commonly administered as a bolus of 30 ml saline 23.4% (7) or in addition to continuous infusion therapy, decreasing the icp over a period <72 hours, but this effect extended not maintained for a while (3). similar to the action of mannitol, hs causes the liquid passage from the parenchyma into the intravascular space, reduces the rate of cerebrospinal fluid (csf) production and having a lower diuretic effect causes expansion of the intravascular volume, increasing cerebral blood flow and reducing the icp at the same time. also it has an anti-inflammatory effect reducing leukocyte adhesion (3,18,19). continuous and frequent use of hypertonic saline lead to the development of hyperchloremic metabolic acidosis, which can be prevented by using hypertonic sodium/acetate (7,20). other problems include arf, arrhythmias, hemolysis and acute pulmonary edema (3). mannitol vs. hypertonic saline mannitol and hs are the two most commonly used hyperosmolar solutions (7). no class i evidence showing the superiority of one over another in the treatment of cerebral edema and intracranial hypertension of different etiologies in critically ill patients (3,21). in 2012, mortazavi et al. (22) performed a meta-analysis studying the results of hs for the management and control of ih. this review included 36 articles; of these, 9 showed that hs controlled ih better, compared to mannitol. in 6 articles, a reduction in icp values was present when hs was administered after the use of mannitol. the potential advantages of hypertonic saline include intravascular volume expansion, to produce less osmotic diuresis, maintains a more stable patients with brain injury systemic and cerebral hemodynamics, and not only decreases the icp and maintains the cpp, but also increases pbto2 (7,23,24). as for intracranial hemorrhage have in the acute phase there is an elevated icp, suggesting a poor prognosis in these patients. currently it is not known which of these two agents has better performance in this condition (3,25). there are no strong recommendations on which of the two hyperosmolar agents should be used. mannitol is most often used as first line therapy for ih caused by cerebral trauma, as second line therapy the hs is used when no response to the first. several authors report that both agents have a similar effect in equimolar dose, and others affirm that the hs is more efficient and safer than mannitol to decrease icp in severe traumatic brain injury (3,26). although the evidence regarding these solutions and their impact on patients is low, there have been studies that have examined various aspects of these fluids with significant results. pelletier et al. performed a meta-analysis which determined that when comparing the use of hs with other solutions such as mannitol, ringer's lactate, hypertonic sodium and 0.9% saline, it was found that there is no difference in mortality and maintenance of the icp (27). sodium lactate to control the elevated icp as a result of severe brain trauma, it is necessary to use safe and effective osmotic agents. one of these has been mannitol, which has been for many years, solving lesson (27); however, there have been various adverse effects 95 osmotherapy in patients with severe brain trauma attributable to this solution. within these adverse effects are: hypovolemia, hypotension, renal failure, a transient effect, among others (28). meanwhile, hypertonic saline emerged showing high efficacy in the management of patients neurocritical ill; some of the benefits that this solution is the easy monitoring of its infusion, its high potency and longer duration of effects, his great role as a stabilizer and systemic hemodynamics intracranial, among others. however, hs can cause negative effects that could limit their use; within these it has generated hypernatremia (independent marker of mortality in critically ill patients), osmotic nephropathy, phlebitis, hypokalemia, rhabdomyolysis, and many more (28,29). therefore, in recent years it has been emerging hypertonic fluid promising for the treatment of severe ih associated with cerebral trauma, sodium lactate. to understand the mechanism of action sodium lactate, it is important to analyze the pathophysiological mechanism by which brain damage occurs in severe brain trauma. this causes trauma injuries dividing two phases: primary and secondary; said phases depend on the time elapsed since the trauma occurred (29,30). the primary stage is given the exact time when the brain injury is generated, and will be characterized by presenting vascular damage, followed by a bleeding in the brain tissue, generating a mass effect in the brain and subsequent ih. as late consequences, at this stage an imbalance of the neurotransmitter regulation, axonal damage and cell death occurs (30). in the secondary phase will be altered cerebral autoregulation mechanisms; generating power failures, which are to be supplied momentarily by increased glycolysis and oxidative phosphorylation; out of atp stores, anaerobic metabolism begins until this process is unsatisfactory (30,31). there is a theory that suggests that astrocytes use the process of glycolysis to lactate production; once said lactate enters neuronal cells, this is transformed into pyruvate by the action of lactate dehydrogenase, and thus involved in oxidative metabolism and energy generating (27,32). under physiological conditions, lactate contributes 8% of the energy required by the brain; however, in cases where there is brain damage, and decreased levels of glucose, lactate can contribute over 60% (31). for this reason, sodium lactate has been a very promising method in controlling the ih in cases of severe brain trauma, requiring more research that yield firm conclusions about the use of this solution with respect to the other, analyzing their effects beneficial and adverse effects. sodium lactate acts primarily by decreasing the blood viscosity by increasing plasma volume, resulting in an increased blood flow and brain tissue oxygenation (31). once increased perfusion of the brain tissue, vasoconstriction occurs reflects which contributes to decrease icp by limiting blood supply to the brain. due to its hypertonic properties, sodium lactate causes an increase in the osmotic pressure within the blood vessels and a great extent of osmotic gradient between the intraand extravascular spaces. as a result, decrease the edema fluid introduced in the intravascular space, helping equally to decrease icp (32,33). sodium lactate vs. mannitol in 2009, ichai et al. (34) compared the mannitol and sodium lactate in 34 patients who had suffered traumatic brain injury and had ih; in this study it was determined that sodium lactate compared to mannitol, icp decreased more (p = 0.016), longer (p = 0.009) and performed with greater success patients (p = 0.053). in 2013, ichai et al. (35) conducted a double-blind, randomized and controlled 60 patients who received a continuous infusion of 0.5 ml/kg/h for 48 hours sodium lactate or normal saline (control group). the results obtained showed that the sodium lactate reduced ih episodes compared to control group (p <0.05); this suggests that sodium lactate can be used as an alternative treatment for preventing post ih traumatic brain injury. moreover, in patients receiving sodium lactate, better urine output and an optimal fluid balance she was found (4,31). within the future perspectives on osmotherapy in patients with tbi, it is necessary to mention that the use of one agent or another will vary according to the availability and level of complexity of the hospital where the patient is located (35-38). therefore, many more studies are needed to evaluate the outcomes of the use of osmotic agents for the management of ih, according to the context of each country, team of professionals and hospital institutions (39,40). this research should be promoted more strongly in low and middle-income countries, where there is a high incidence of neurotrauma cases, and where hightech tools that have been shown to further improve neurosurgical outcomes of neurotrauma are not available (35,41). 96 randy reina-rivero, gustavo gaitán-herrera, aixa eliana garcía-garcía et al. conclusions traumatic brain injury is a public health problem worldwide. management and control of intracranial hypertension back to this type of trauma has been being an aspect in which health professionals need to improve as the years pass. osmotherapy has been a very important mechanism for achieving this objective using fluids such as mannitol and hypertonic saline, which have had great results for patients; however, there have been multiple adverse effects that affect their health. in search of better methods to treat this condition has been introduced as sodium lactate osmotherapy, which has proved very effective in counteracting the secondary damage generated by the traumatic brain injury. similarly, it has shown better results regarding the cognitive effects after injury. however, conducting research on which these solutions are compared with respect to the benefits and disadvantages that can generate in patients is necessary. references 1. wells aj, hutchinson pja. the management of traumatic brain injury. surgery. 2018; 1–8. 2. ramos vy, bedoya oh, gómez rmc, corrales sh, moscote slr. osmotherapy in patients with severe brain trauma. rev cuba med intensiva y emergencias. 2018; 17:53–6. 3. llorente g, claudia m. mannitol versus hypertonic saline solution in neuroanaesthesia. rev colomb anestesiolgía. 2015; 43(s-1):29–39. 4. rossi s, picetti e, zoerle t, carbonara m, zanier er, stocchetti n. fluid management in acute brain injury. curr neurol neurosci rep. 2018; 1–9. 5. jagt m van der. fluid management of the neurological patient: a concise review. crit care. 2016; 20(126):1–11. 6. diringer m. treatment of fever in the neurologic intensive care unit with a catheter-based heat exchange system. neurol crit care. 2004; 32(2):559–64. 7. shah s, kimberly wt. today's approach to treating brain swelling in the neuro intensive care unit. semin neurol. 2016; 36(6):502-507. 8. sorani md, manley gt. dose-response relationship of mannitol and intracranial pressure: a metaanalysis. j neurosurg. 2008; 108:80–7. 9. sorani md, morabito d, rosenthal guy, giacomini km, manley gt. characterizing the dose-response relationship between mannitol and intracranial pressure in traumatic brain injury patients using a highfrequency physiological data collection system. j neurotrauma. 2008; 298:291–8. 10. gondim f de a, aiyagari v, shackleford a, diringer m. osmolality not predictive of mannitol-induced acute renal insufficiency. j neurosurg. 2005; 103:444–7. 11. garcía-morales ej, cariappa r, parvin ca, scott mg, diringer mn. osmole gap in neurologic-neurosurgical intensive care unit: its normal value, calculation, and relationship with mannitol serum concentrations. crit care med. 2004; 32(4):986–91. 12. rickard ac, smith je, newell p, bailey a, kehoe a, mann c. salt or sugar for your injured brain? a meta-analysis of randomised controlled trials of mannitol versus hypertonic sodium solutions to manage raised intracranial pressure in traumatic brain injury. emerg med j. 2014; 31(8):679-83. 13. hong y, yingying s. hemodynamic effects of mannitol infusion in patients with acute intracerebral hemorrhage. acta cirúrgica bras. 2013; 28(2):106–11. 14. carney n, totten am, reilly co, ullman js, bell mj, bratton sl, et al. guidelines for the management of severe traumatic brain injury 4th edition. brain trauma found. 2016. 15. mangat hs, chiu yl, gerber lm, alimi m, ghajar j, härtl r. hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury. j neurosurg. 2015; 122(1):202-10. 16. lazaridis c, neyens r, bodle j, desantis sm. highosmolarity saline in neurocritical care: systematic review and meta-analysis. crit care med. 2013; 41(8):1353–61. 17. kerwin aj, schinco ma, tepas jj 3rd, renfro wh, vitarbo ea, muehlberger m. the use of 23.4% hypertonic saline for the management of elevated intracranial pressure in patients with severe traumatic brain injury: a pilot study. j trauma. 2009; 67(2):277-82. 18. chen h, song z, dennis ja. hypertonic saline versus other intracranial pressure-lowering agents for people with acute traumatic brain injury. cochrane database syst rev. 2020; 1(1):cd010904. 19. rizoli sb, rhind sg, shek pn, inaba k, filips d, tien h, et al. the immunomodulatory effects of hypertonic saline resuscitation in patients sustaining traumatic hemorrhagic shock: a randomized, controlled, doubleblinded trial. ann surg. 2006; 243(1):47-57. 20. fatima n, ayyad a, shuaib a, saqqur m. hypertonic solutions in traumatic brain injury: a systematic review and meta-analysis. asian j neurosurg. 2019; 14(2):382391. 21. hooman k, navi b, nakagawa ka, hemphill c. hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. crit care med. 2011; 39(3):554–9. 22. mortazavi m, romeo a, deep a, griessenauer c. hypertonic saline for treating raised intracranial pressure: literature review with meta-analysis. j neurosurg. 2012; 116:210–21. 23. anstey jr, taccone fs, udy aa, citerio g, duranteau j, ichai c, et al. early osmotherapy in severe traumatic brain 97 osmotherapy in patients with severe brain trauma injury: an international multicenter study. j neurotrauma. 2020; 37(1):178–84. 24. jagannatha at, sriganesh k, devi bi, rao gsu. an equiosmolar study on early intracranial physiology and long term outcome in severe traumatic brain injury comparing mannitol and hypertonic saline. j clin neurosci. 2016; 27:68–73. 25. huang x, yang l, ye j, he s, wang b. equimolar doses of hypertonic agents (saline or mannitol) in the treatment of intracranial hypertension after severe traumatic brain injury. medicine (baltimore). 2020; 99(38):e22004. 26. gu j, huang h, huang y, sun h, xu h. hypertonic saline or mannitol for treating elevated intracranial pressure in traumatic brain injury: a meta-analysis of randomized controlled trials. neurosurg rev. 2019; 42(2):499-509. 27. gantner d, moore em, cooper dj. intravenous fluids in traumatic brain injury: what’s the solution? curr opin crit care. 2014; 20:385–9. 28. aramendi i, biestro wma. lactato de sodio 0,5 molar: ¿el agente osmótico que buscamos? med intensiva. 2015; 40(2):113-117. 29. alnemari am, krafcik bm, mansour tr, gaudin d. a comparison of pharmacologic therapeutic agents used for the reduction of intracranial pressure after traumatic brain injury. world neurosurg. 2017; 106:509–28. 30. reza m, zuhro a, ibrahim a, hafid a. role of hypertonic sodium lactate in traumatic brain injury management. asian j neurosurg. 2018; 13:971–5. 31. betancur-calderón jm, veronesi-zuluaga la, casta f. terapia con lactato sódico hipertónico en trauma cráneoencefálico: ¿se convertirá en la mejor alternativa de manejo? rev colomb anestesiol. 2017; 5(s-2):51–57. 32. millet a, cuisinier a, bouzat p, batandier c, lemasson b, stupar v, et al. hypertonic sodium lactate reverses brain oxygenation and metabolism dysfunction after traumatic brain injury. br j anaesth. 2018; 9:1–9. 33. berger-pelleiter e, émond m, lauzier f. hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials. can j emerg med care. 2016; 18(2):112–20. 34. ichai c, berthier f, samat-long c. sodium lactate versus mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients. intensive care med. 2009; 35:471–9. 35. ichai c, leverve xm. half-molar sodium lactate infusion to prevent intracranial hypertensive episodes in severe traumatic brain injured patients: a randomized controlled trial. intensive care med. 2013; 39:1413–22. 36. pérez-fontalvo nm, de arco-aragón ma, jimenez-garcía jdc, lozada-martinez id. molecular and computational research in lowand middle-income countries: development is close at hand. j taibah univ med sci. 2021; 16(6):948-949. 37. ortega-sierra mg, prado-grajales v, martinez-imbett r, unás-perea k, lozada martinez id. research career in neurosurgery: a challenge for future neurosurgeons. j neurosurg sci. 2021. aug 3. 38. blanco-teherán c, quintana-pájaro l, narvaez-rojas a, martínez-pérez r, garcía-ballestas e, moscote salazar l, et al. evidence-based medicine in neurosurgery: why and how? j neurosurg sci. 2021 aug 3. 39. silva-rued ml, ramírez-romero a, guerra-maestre lr, forero-hollmann ám, lozada-martínez id. the need to develop specialized surgical centers: the evidence that surgical diseases cannot wait. int j surg. 2021; 92:106036. 40. ortega-sierra mg, durán-daza rm, carrera-patiño sa, rojas-nuñez ax, charry-caicedo ji, lozada-martínez id. neuroeducation and neurorehabilitation in the neurosurgical patient: programs to be developed in latin america and the caribbean. j neurosurg sci. 2021 jun 10. 41. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0062 article tinnitus after traumatic brain injury: an overview b. ushasree reddy, ranabir pal, amrita ghosh, luis rafael moscote-salazar, vishnu vardhan reddy, amit agrawal india, colombia      romanian neurosurgery (2018) xxxii 3: 487 490 | 487             doi: 10.2478/romneu-2018-0062 tinnitus after traumatic brain injury: an overview b. ushasree reddy1, ranabir pal2, amrita ghosh3, luis rafael moscote-salazar4, vishnu vardhan reddy1, amit agrawal1 1department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 2department of community medicine, mgm medical college and lsk hospital, kishanganj, bihar, india 3department of biochemistry, calcutta medical college, india 4neurosurgery-critical care, red latino, organización latinoamericana de trauma y cuidado neurointensivo, bogota, colombia abstract: tinnitus is a frequent clinical feature encountered during follow up of traumatic brain injury (tbi) that can be incapacitating in the long run. literature suggests that post-tbi carries a higher psychological burden than tinnitus patients presenting with other non-traumatic or unknown etiologic. posttraumatic tinnitus is of longer duration, frequently associated with hyperacousis and occurs in younger age group. if the symptoms are severe post-traumatic tinnitus can affect quality of life of the patients. the management of these patients needs detail evaluation and comprehensive rehabilitation plan. key words: tinnitus, traumatic brain injury, auditory dysfunction introduction traumatic brain injury can lead to the damage to auditory nerve and cochlear structures resulting in hearing loss and labyrinthine dysfunction.1,2 injury to cochlear hair cells can result in tinnitus which can persist a long time after tbi as a part of postconcussive symptoms.3,4 many advancements have been made in the management of tbi, however little has been understood regarding the pathophysiology of post-traumatic tinnitus. traumatic brain injury (tbi) has been reported to be associated with a spectrum of sequel and the post-tbi tinnitus has been reported as a frequent yet difficult to treat symptom.5,6 it has been suggested that forces generated during trauma leads to neuronal dysfunction7 including injury to the otic capsule.8,9 or damage to the medullary somatosensory nuclei can cause tinnitus.10 clinical spectrum tinnitus is a subjective feel and there is no specific test to confirm, all the details e.g. location, character, presence of hyperacusis, any rhythmicity or pulsatile component needs 488 | reddy et al tinnitus after traumatic brain injury             to be obtained from the patient.11,12 obviously these patients have history suggestive of traumatic brain injury and shall need standardized assessment to rule out other nontraumatic causes of tinnitus.13 details needs to obtained include is the tinnitus affecting quality of life, whether it is disturbing sleep or concentration and increasing the psychological stress.14-16 post-traumatic tinnitus needs to be differentiated from other non-traumatic causes of tinnitus. usually post-traumatic tinnitus occur in younger patients, more severe in nature and accompanied by many other co-symptoms including frequent headache, impaired memory and concentration and transient episodes of depression. 4,17 diagnosis selected audiological investigations will help to rule out treatable pathologies i.e. disruption of the ossicular chain disruption or any perilymphatic fistulas.18 pure-tone audiometry shall help to assess any hearing impairment.19 in a patient who present with pulsatile tinnitus, we need to rule out trauma induced carotid-cavernous fistulas, arteriovenous malformations, and carotid artery dissections where the treatment approach will be entirely different. 18 appropriate imaging will help to rule out cervical spine injuries and any intracranial lesions as an underlying cause of tinnitus.11,18 management the management of post-traumatic tinnitus is to control underlying pathology, management of any treatable cause and to suppress the tinnitus perception and thus to improve the quality of life of the patient.20,21 several categories of drugs have been used to manage post-traumatic tinnitus including drugs acting on vestibular system as well drugs to help to reduce concomitant psychological stress.22-24 drugs which improve microcirculation in auditory systems have also not shown to be much effective.25-27 betahistine, has been used to increase cochlear blood flow with variable success.28 the management of post-traumatic tinnitus is largely conservative and surgery is reserved for the cases where there are underlying structural lesions as the cause of tinnitus (i.e. carotidcavernous fistulas, arteriovenous malformations, and carotid artery dissections etc.)18 or there are any other underlying pathologies (i.e. otosclerosis or meniere’s disease etc.).29-34 brain stimulation techniques including repetitive transcranial magnetic stimulation are under investigation as noninvasive tool to manage tinnitus.34-39 role of laser therapy has been explored in the management of tinnitus however how it works and much it is effective both are controversial.40 conclusion findings from this review hopefully going to help the health care providers and stakeholders working in this area of rehabilitation of tbi cases. patients with tinnitus need extensive investigations regarding etiology and functional assessments to devise tailor-made plan of interventions to treat not only the auditory problems but also to address the associated deficits in patients recovering from tbi. presently the treatment of post-traumatic tinnitus is directed towards romanian neurosurgery (2018) xxxii 3: 487 490 | 489             improving the quality of life as still there is not advancements to achieve definitive cure. in the clinical practice guidelines of the office practice of clinicians we need standard operative procedures (sop) to help patients with tinnitus in an empathetic manner. correspondence dr. amit agrawal professor of neurosurgery department of neurosurgery narayana medical college hospital chinthareddypalem nellore-524003 andhra pradesh (india) emaildramitagrawal@gmail.com dramitagrawal@hotmail.com mobile+91-8096410032 references 1.henry ja, dennis kc, schechter ma. general review of tinnitus: prevalence, mechanisms, effects, and management. journal of speech, language, and hearing research 2005;48:1204-1235. 2.schuknecht hf. mechanism of inner ear injury from blows to the head. annals of otology, rhinology & laryngology 1969;78:253-262. 3.fitzgerald dc. persistent dizziness following head trauma and perilymphatic fistula. archives of physical medicine and rehabilitation 1995;76:1017-1020. 4.ferber‐viart c, postec f, duclaux r, dubreuil c. perilymphatic fistula following airbag trauma. the laryngoscope 1998;108:1255-1257. 5.kreuzer pm, landgrebe m, frank e, langguth b. repetitive transcranial magnetic stimulation for the treatment of chronic tinnitus after traumatic brain injury: a case study. the journal of head trauma rehabilitation 2013;28:386-389. 6.jury ma, flynn mc. auditory and vestibular sequelae to traumatic brain injury: a pilot study. n z med j 2001;114:286-288. 7.ommaya ak, hirsch ae. tolerances for cerebral concussion from head impact and whiplash in primates. journal of biomechanics 1971;4:13-21. 8.grimm rj, hemenway wg, lebray pr, black fo. the perilymph fistula syndrome defined in mild head trauma. acta oto-laryngologica 1989;108:1-40. 9.claussen c, constantinescu l. tinnitus in whiplash injury. the international tinnitus journal 1995;1:105. 10.levine ra. somatic (craniocervical) tinnitus and the dorsal cochlear nucleus hypothesis. american journal of otolaryngology 1999;20:351-362. 11.baguley d, mcferran d, hall d. tinnitus. the lancet 2013;382:1600-1607. 12.khalfa s, dubal s, veuillet e, perez-diaz f, jouvent r, collet l. psychometric normalization of a hyperacusis questionnaire. orl 2002;64:436-442. 13.kreuzer pm, landgrebe m, schecklmann m, staudinger s, langguth b. trauma-associated tinnitus: audiological, demographic and clinical characteristics. plos one 2012;7:e45599. 14.newman cw, jacobson gp, spitzer jb. development of the tinnitus handicap inventory. archives of otolaryngology–head & neck surgery 1996;122:143-148. 15.hoare dj, gander pe, collins l, smith s, hall da. management of tinnitus in english nhs audiology departments: an evaluation of current practice. journal of evaluation in clinical practice 2012;18:326-334. 16.meikle mb, henry ja, griest se, et al. the tinnitus functional index: development of a new clinical measure for chronic, intrusive tinnitus. ear and hearing 2012;33:153-176. 17.folmer rl, griest se. chronic tinnitus resulting from head or neck injuries. the laryngoscope 2003;113:821827. 18.møller ar, langguth b, deridder d, kleinjung t. textbook of tinnitus: springer science & business media, 2010. 19.fowler ep. the “illusion of loudness” of tinnitus—its etiology and treatment. the laryngoscope 1942;52:275285. 20.dobie ra. a review of randomized clinical trials in tinnitus. the laryngoscope 1999;109:1202-1211. 21.jastreboff pj, gray wc, gold sl. neurophysiological approach to tinnitus patients. otology & neurotology 1996;17:236-240. 490 | reddy et al tinnitus after traumatic brain injury             22.baldo p, doree c, lazzarini r, molin p, mcferran dj. antidepressants for patients with tinnitus. cochrane database syst rev 2006;4. 23.johnson rm, brummett r, schleuning a. use of alprazolam for relief of tinnitus: a double-blind study. archives of otolaryngology–head & neck surgery 1993;119:842-845. 24.jalali mm, kousha a, naghavi se, soleimani r, banan r. the effects of alprazolam on tinnitus: a cross-over randomized clinical trial. medical science monitor 2009;15:pi55-pi60. 25.jayarajan v, coles r. treatment of tinnitus with frusemide. j audiol med 1993;2:114-119. 26.mora r, salami a, barbieri m, et al. the use of sodium enoxaparin in the treatment of tinnitus. international tinnitus journal 2003;9:109-111. 27.davies e, knox e, donaldson i. the usefulness of nimodipine, an l-calcium channel antagonist, in the treatment of tinnitus. british journal of audiology 1994;28:125-129. 28.james a, burton mj. betahistine for meniere's disease or syndrome. the cochrane library 2001. 29.de ridder d, elgoyhen ab, romo r, langguth b. phantom percepts: tinnitus and pain as persisting aversive memory networks. proceedings of the national academy of sciences 2011;108:8075-8080. 30.atik a. pathophysiology and treatment of tinnitus: an elusive disease. indian journal of otolaryngology and head & neck surgery 2014;66:1-5. 31.foyt d, wazen jj, sisti m. selective cochlear neurectomy for debilitating tinnitus. annals of otology, rhinology & laryngology 1997;106:568-570. 32.pulec jl. cochlear nerve section for intractable tinnitus. ear, nose, & throat journal 1995;74:468,-470466. 33.baguley dm, atlas md. cochlear implants and tinnitus. progress in brain research 2007;166:347-355. 34.shi y, burchiel kj, anderson vc, martin wh. deep brain stimulation effects in patients with tinnitus. otolaryngology—head and neck surgery 2009;141:285287. 35.eggermont jj, roberts le. the neuroscience of tinnitus. trends in neurosciences 2004;27:676-682. 36.noreña aj. an integrative model of tinnitus based on a central gain controlling neural sensitivity. neuroscience & biobehavioral reviews 2011;35:1089-1109. 37.norena aj, eggermont jj. changes in spontaneous neural activity immediately after an acoustic trauma: implications for neural correlates of tinnitus. hear res 2003;183:137-153. 38.meng z, liu s, zheng y, phillips js. repetitive transcranial magnetic stimulation for tinnitus. the cochrane library 2011. 39.cheung sw, larson ps. tinnitus modulation by deep brain stimulation in locus of caudate neurons (area lc). neuroscience 2010;169:1768-1778. 40.kleinjung t. low-level laser therapy. textbook of tinnitus: springer, 2011: 749-752. faheem_isolated 272 | faheem et al isolated thoracic intramedullary epidermoid cyst isolated thoracic intramedullary epidermoid cyst a rare entity mohd faheem1, qazi zeeshan1, bal krishna ojha1, anil chandra1, sunil kumar singh1, chhitij srivastava1, mala sagar2, noor us saba3 1department of neurosurgery, king george’s medical university, chowk, lucknow, u.p., india 2department of pathology, king george’s medical university, chowk, lucknow, u.p., india 3department of anatomy, king george’s medical university, chowk, lucknow, u.p., india abstract: intramedullary epidermoid cysts of the spinal cord are rare tumours, especially those not associated with spinal dysraphism. around 60 cases have been reported in the literature. of these, only 10 cases have had magnetic resonance imaging (mri) studies. here, we report a case of isolated intramedullary epidermoid tumour at d2-d3 level. the etiology, pathology, clinical features, mri characteristics and surgical treatment of such rare intramedullary tumours are discussed. key words: intramedullary, epidermoid cyst, thoracic introduction spinal epidermoid tumours are rare and comprises < 1% of all spinal tumours. these are mostly located in intradural and extramedullary position and commonly associated with congenital malformations like syringomyelia, dermal sinus, spina bifida or may be iatrogenic following procedures such as surgery for bullet wounds, myelography or lumbar puncture. (1) isolated intramedullary epidermoid tumours without any congenital malformations are even rarer. thoracic region is the commonest site of intramedullary cysts followed by lumbar and rarely cervical region. we encountered a patient, where epidermoid was not only intramedullary, it was not associated with any congenital stigmata or malformation. only 60 cases of intramedullary epidermoid have been reported till now. (2) rarity of such lesion prompted us to report this case. case report a 27 year old man presented with gradually progressive and descending weakness of bilateral lower limbs for the past one year. it was associated with spasticity and paraesthesia in both lower limbs. there was no history of fever, back pain, bowel/bladder involvement, trauma, any surgical procedure involving spine or any congenital malformation of spine. romanian neurosurgery (2016) xxx 2: 272-276 | 273 clinical examination revealed spastic paraparesis with power of grade 4/5 mrc in both lower limbs, with maximum weakness at right ankle joint (2/5). reflexes were 3+ bilaterally at knee and ankle and plantars were bilateral extensors. sensory examination revealed decrease in pain and touch sensation of up to 20-30% from d4 to d9 spinal segments along with decreased proprioception below d4 with intact perianal sensations. examination of upper limbs revealed no abnormality. magnetic resonance imaging (mri) dorsal spine revealed a well-defined intramedullary cystic lesion at d2-d3 level. the lesion was hypointense on t1 and hyperintense on t2 weighted image with no enhancement of lesion after administration of gadolinium (figure 1, figure 2). patient underwent d2-d3 laminectomy and cord was found to be widened at the level of lesion. a midline dorsal myelotomy was performed. a 2cmx1.5cm sized intramedullary pearly white lesion was found. lesion was encapsulated, soft, nonvascular and gross total excision was performed using microsurgical technique and electrophysiological monitoring. the part of capsule which was attached densely to the cord was left behind. immediate post-operative period was uneventful without any deterioration of neurological symptoms. at 6 months of follow up, spasticity reduced in both lower limbs and power too improved to 3/5 mrc at right ankle joint. there was no improvement in sensory loss. on histopathological examination, the lesion had a thin fibrous capsule encircled by gliotic tissue. cyst was lined by compressed stratified squamous epithelium and contained degenerated squamous tissue, thereby confirming the diagnosis of epidermoid cyst (figure 3). figure 1 saggital ti and t2 weighted image showing lesion at d2-d3 level 274 | faheem et al isolated thoracic intramedullary epidermoid cyst figure 3 axial t1 and t2 mri showing intramedullary lesion figure 3 microphotograph showing epidermoid cyst filled with lamellated keratin. h&e 40x discussion epidermoid tumour was first described by cruveilhier in 1835, who called them ‘’tumors perlees’’ (pearly) tumour. (3) the first description of an intramedullary epidermoid cyst belongs to hans chiari in 1883. incidence of epidermoid cysts among intracranial tumours in most large series is estimated to be 0.2%-1%. it is approximately 0.7% of all spinal epidermoid cysts. (4) symptoms of epidermoid cyst vary with the level of involvement but same as other compressive lesions in spinal column. presentation is usually in the form of progressive neurological deterioration like paraparesis sensory loss urological manifestation and back pain. epidermoids grow very slowly in path of the least resistance and may lead to delay in diagnosis. duration of symptoms before diagnosis may extend for years. it is generally believed that congenital epidermoid cysts originate from displaced ectodermal inclusion arising in early fetal life and possibly may be associated with defective closure of the dural tube. (5) acquired epidermoid cysts are thought to result from iatrogenic proliferation of skin fragments especially after lumbar puncture or menigomyelocele repair. (6, 7) epidermoid cysts are generally characterized on mri by variable signal intensity, they are usually slightly hyperintense as opposed to cerebrospinal fluid, and their lobulated aspect helps differentiating these lesions from other cysts. this disparity in signal intensity most likely reflects variable lipid and protein composition in these lesions. other features romanian neurosurgery (2016) xxx 2: 272-276 | 275 include well defined palne of cleavage, calcification and absence of surrounding edema. additionally, it has been noticed that the margins of these lesions are shaggy, possibly because of chronic inflammatory response to squamous tissue leak through the capsule and variable gliosis along the margin, extending into the cord. diagnosis of epidermoid cyst is usually based on inspection due to typical aspect of their content. histologically, epidermoid cyst is lined by stratified squamous epithelium supported by another layer of collagenous tissue, and progressive desquamation of keratin from epithelial lining toward the interior of the cyst produces a soft whitish material. to the best of our knowledge, there have been only seven cases of intramedullary epidermoid with mri features reported till date in the literature. (8, 9, 10, 11, 12, 13, 14). management of intramedullary epidermoid cyst is surgical. decompression of the cyst material is easily performed, but tumour capsule is usually adherent to the cord and complete removal may cause permanent neurological deficit, so it should be left behind. the risk of recurrence exists, however, in most cases even partial removal of the intramedullary epidermoid resulted in total remission of symptoms. if recurrence occurs again, surgery is the treatment of choice. prognosis of these tumours is good because of their histologically benign nature and surgical intervention should be done as soon they are diagnosed. conclusion epidermoid tumours are infrequent, without any specific clinical features. due to atypical features and delay in the onset of symptoms, high index of suspicion should be kept in mind and detailed neurological examination along with mri of the spinal cord is warranted to diagnose these cases at the earliest. generous reporting of such cases is to be done to better understand this rare entity. correspondence mohd faheem mbbs, ms faheemjnmc@gmail.com resident, department of neurosurgery, king george’s medical university chowk, lucknow, u.p., india-226003 phone no: +919368480100 fax: 0091-522-2257606 references 1.gonzalvo a, hall n, mcmahon jh, fabinyi gc. intramedullary spinal epidermoid cyst of the upper thoracic region.j clin neurosci 2009;16:142-4. 2.gardner dj, o'gorman am, blundell je. intraspinal epidermoid tumour: late complication of lumbar puncture. cmaj 1989;141:223-5 3.chandra ps, manjari t, devi bi, chandramouli ba, srikanth sg, shankar sk. intramedullary spinal epidermiod cyst. neurol india 2000;48:75-7. 4. guidetti b, gagliardi fm: epidermoid and dermoid cysts. clinical evaluation and late surgical results. j neurosurg 1977; 47: 12-18. 5. roux a, claude m, larbrisseau a et al: intramedullary epidermoid cysts of the spinal cord: a case report. j neurosurg 1992; 76: 528-533. 6.manno nj, uihlein a, kernohan jw: intraspinal epidermoids. j neurosurg 1962; 19: 754-765. 7.halcrow sj, crawford pj, craft aw: epidermoid spinal cord tumour after lumbar puncture. arch dis child 1985; 60: 978-979. 276 | faheem et al isolated thoracic intramedullary epidermoid cyst 8.penisson ib, gilles g, gandon y: intramedullary epidermoid cyst evaluated by computed tomographic scan and magnetic resonance imaging: case report. neurosurgery 1989; 25: 955-959. 9.cornu p, manai r, foncin jf et al: kyste epidermoide intra medullaire. apport de 1' imagerie par resonance magnetique. rev neurol 1989; 145: 248-250. 10.gallina p, roux fx, lo re f et al: a rare case of intramedullary epidermoid cyst diagnosed by mri. neurochirurgie 1992; 38(6): 372-375. 11.phillips j, chiu l: magnetic resonance imaging of intraspinal epidermoid cyst: a case report. j comput assist tomogr 1987; 11: 181-183. 12.roux a, claude m, larbrisseau a et al: intramedullary epidermoid cysts of the spinal cord: a case report. j neurosurg 1992; 76: 528-533. 13.scholz m, marzheuser bs, gottschalk j et al: intramedullary epidermoid cyst: a case report. neurosurg rev 1994; 17(1): 89-93. 14.zavanone m, guerra p, rampini pm et al: a cervicodorsal intramedullary epidermoid cyst. case report and review of the literature. j neurosurg sci 1991; 35: 11-15. doi: 10.33962/roneuro-2021-048 analysis of functional outcome of single and double level lumbar discectomy surendra k. gupta, deepak k. singh, anuj chhabra, mohd kaif, kuldeep yadav, rakesh k. singh romanian neurosurgery (2021) xxxv (3): pp. 285-293 doi: 10.33962/roneuro-2021-048 www.journals.lapub.co.uk/index.php/roneurosurgery analysis of functional outcome of single and double level lumbar discectomy surendra k. gupta1, deepak k. singh2, anuj chhabra3, mohd kaif2, kuldeep yadav2, rakesh k. singh2 1 department of neurosurgery. all india institute of medial sciences, raipur, india 2 department of neurosurgery. dr. ram manohar lohia institute of medical sciences, lucknow, india 3 department of neurosurgery. kalpana chawla government medical college, karnal, haryana, india abstract introduction: functional improvement in lumbar pivd patients can be assessed either objectively like improvement in slrt, relief in pain, etc or subjectively using different types of scales. in our study, we have used revised oswestry disability index (rodi) score, ronald–morris disability questionnaire (rdq), the back bournemouth questionnaire (bq) to analyse functional outcome in single and double level lumbar pivd patients pre-operatively and post-operatively. method: it is a prospective study including 80 patients of lumbar pivd who failed to respond to conservative treatment. patients were clinically evaluated and disability scales vizrodi, rdq & bq were recorded. after lumber discectomy, patients were again assessed and scored as per disability scales at 1 month, 6 months and 1 year postoperatively. result: rodi, rdq and bq scores were calculated at pre-operatively and postoperatively 1, 6 and 12 months and statistically analysed. the mean rodi scores at pre-operative and postoperative 1, 6, and 12 months were 72, 18, 10, and 6 respectively. the mean rdq scores at pre-operative and postoperative 1, 6, and 12 months were 15, 5, 3, and 2 respectively. similarly, the mean bq scores at preoperative and postoperative 1, 6, and 12 months were 51, 12, 8, and 4 respectively. statistically, significant improvement was seen in mean scores of all 3 functional scales and maximum changes were observed after 1 month. statistically, significant improvements were observed in 54 out of 62 patients (87%). three questions of bq related to the patient social and family activities, anxiety and depression were separately compared pre and post-operatively and they showed a statistically significant improvement. conclusion: overall 87% of patients had a significant improvement in functional assessment using rodi, rdq and bq scales. on comparing single and double level discectomy patients, the functional improvement was similar in follow up of one year. social and family activities (sfa), depression and anxiety of the patients improved significantly over 1 year. keywords lumbar pivd, functional outcome, rodi, rdq, bq corresponding author: anuj chhabra department of neurosurgery. kalpana chawla government medical college, karnal, haryana, india dranujchhabra123@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 286 surendra k. gupta, deepak k. singh, anuj chhabra et al. introduction lumbar disc prolapse has been thoroughly evaluated in terms of its epidemiology [14], physiology [33] and outcome after discectomy [22, 26, 34]. proper patient selection and surgical technique can provide an excellent outcome. different discectomy procedures are carried out for the treatment of lumbar disc prolapse. postoperatively 75-90% of patients get relief from radicular pain [4,5,9,17,20,21]. according to asch et al, in a prospective study of 200 patients, the outcome was significant, which was determined by six parameters including preoperative odi (oswestry disability index) and the odi at 1 and 10 days, 6 weeks, and 6 months and 12 months postoperatively. one of the most common causes of the poor outcome is the poor definition of selection criteria for surgery, which varies fourfold to fivefold between different communities and countries [3]. risk factors associated with poor outcome include work off over 3 months, psychosocial problems including poor educational level, smoking, and obesity (30). according to weber’s study, the first symptom to improve following successful surgery is the radicular pain, typically followed by improvement in motor function, and finally the resolution of sensory loss. sensory loss may be permanent persisting at 10-years follow-up in 35% of patients [31, 32]. the restoration of normal function after discectomy in lumbar pivd patients is considered a key outcome. assessment of functional improvement can be done either objectively, like improvement in slrt, relief in pain, improvement in movement, or subjectively with the help of different types of scales. functional assessment scales are comprised of a self-reported questionnaire and having a standardised format that yields a measure with known reliability and validity. thus, we performed our study to analyse the functional outcome after lumbar discectomy using the revised oswestry disability index (rodi) score, ronald–morris disability questionnaire (rdq) and the back bournemouth questionnaire (bq). we are also comparing the degree of improvement after single and double level lumbar discectomy along with the effect of surgery on sfa, depression and anxiety. methodology this prospective study was conducted in the department of neurosurgery at our institute between february 2017 to september 2018. eighty patients with symptoms and signs of lumber pivd, diagnosed as a case of single and double level lumbar pivd by magnetic resonance imaging (mri) were enrolled in the study after informed consent. the study was approved by the institutional ethical committee. inclusion criteria: • signs and symptoms of lumbar pivd correlating with mri findings. • not responding to conservative management of 6 weeks or more. • needs primary lumbar discectomy without fusion. exclusion criteria: • previous spinal surgery. • more than 2 level discs prolapsed. • lumbar disc prolapsed associated with spondylolisthesis or severe degenerative disease. • the patient having red flag signs. spinal fractures primary malignancy, metastasis or infection cauda equine syndrome or severe neurological compromise • intra-op complications – dural tear, root injury. patients were clinically evaluated and disability scales vizrodi, rdq & bq were recorded. after lumber discectomy, patients were again assessed and scored as per disability scales at 1 month, 6 month and 1 year postoperatively. data were summarised as mean ± se (standard error of means). groups were compared by repeated measures one-way analysis of variants (anova) and the significance of the mean difference between the groups were compared by tuckey’s hsd (honestly significant difference) post hoc test. a two-tailed pvalue < 0.05 was considered as statistically significant. the analysis was performed on stata software. functional status questionnaires: the following functional status questionnaires, completed by the patients, were taken into account for this study. the 287 functional outcome analysis in lumbar pivd patients after discectomy researcher was present during the measurements (at pre-op, post-op 1 month, 6 months, and 1 year) to help patients complete the questionnaires. functional status questionnaires: 1. revised oswestry disability index (rodi): the oswestry disability index is an index derived from the oswestry low back pain questionnaire used by clinicians and researchers to quantify disability for low back pain. this validated questionnaire was first published by jeremy fairbank et al. in physiotherapy in 1980. the self-completed questionnaire contains ten topics. each topic category is followed by 6 statements describing different potential scenarios in the patient's life relating to the topic. the patient then checks the statement which most closely resembles their situation. each question is scored on a scale of 0–5 with the first statement being zero and indicating the least amount of disability and the last statement is scored 5 indicating the most severe disability. the scores for all questions answered are summed and then multiplied by two to obtain the index (range 0 to 100). zero is equated with no disability and 100 is the maximum disability possible. scoring: • 0% –20%: minimal disability • 21%–40%: moderate disability • 41%–60%: severe disability • 61%–80%: crippling back pain • 81%–100%: these patients are either bed-bound or have an exaggeration of their symptoms 2. the roland-morris disability questionnaire (rdq) contains 24 yes/no items. patients are asked whether the statements apply to them that day (the last 24 hours). the rdq-24 score is calculated by adding up the number of “yes” items, ranging from 0 (no disability) to 24 (maximum disability). the clinical improvement over time can be graded based on the analysis of serial questionnaire scores. total improvement can be reflected as a percentage of initial score. 3. the back bournemouth questionnaire (bq) is a comprehensive multi-dimensional core outcome tool assessing patients’ outcomes of care in a routine clinical setting. it is a short, self-report questionnaire, developed by j. bolton. the questionnaire consists of seven core items, which are: pain intensity, function in activities of daily living, function in social activities, anxiety, depression levels, fear-avoidance behaviour and locus of control behaviour. each item is rated on a numeric rating scale (nrs) from 0 to 10: 0= much better 5= no change 10= much worse. the score for each measure is added. this can produce a value between a minimum score of 0, and a maximum score of 70. a higher score reflects a higher degree of impact on a patient’s life. results out of 80 patients, 10 patients were lost in the followup, 5 patients showed intra-operative mobility which needed stabilization, two patients had post-op foot drop and one patient had intra-operatively csf leakage due to dural tear. after exclusion of these patients, 62 patients were studied. post-operative ct scan, 6 out of 62 patients, 47 (76%) patients were male and 15 (24%) were female. age ranged between 22 years to 63 years. the mean age was 38.8± 9.88 years (mean±sd). thirty-four (55%) patients had history of insidious onset of pain and twenty-eight (45%) patients had history of sudden onset pain. patients were categorised into 4 categories based on the duration of pain i.e. <3 months, 3 months – 1 year, 1year3 years and > 3 years. twenty (32%) patients had complaints of radicular pain for less than 3 months, fourteen (26%) had pain since one year, thirteen (21%) patients had history of pain since 3 years and fifteen (21%) patients had pain for more than 3 years. knee reflex was decreased in 4 (6%) and normal in 58 (96%) patients but ankle reflex was total no. of patients enrolled in study = 80 total no. of patients followed after surgery = 72 excluded from study because of intr-op complication and findings = 8 total no. of patients studied = 62 total no. of patients lost in follow up = 10 288 surendra k. gupta, deepak k. singh, anuj chhabra et al. decreased in 59 (95%) and normal in 3 (5%) patients. plantar reflex was absent in 45 (73%), equivocal in 13 (21%), absent in 2 (3%) and normal in 2 (3%) patients. 31 (50%) patients had paraspinal muscle spasm on examination. 7 (11%) had lumbosacral scoliosis because of unilateral pain and muscular spasm. out of 80 patients, 60 (97%) had positive straight leg raising test (slrt) while 2 (3%) had negative slrt. 25(40%) patients had bilateral positive slrt whereas 17 (27%) patients had left-sided positive slrt and 18 (29%) patients had right-sided positive slrt (table 1). table 1. clinical parameters of patients parameter no. of patients age profile of the study population number of cases 62 sex male 47 female 15 minimum age (years) 22 maximum age (year) 63 mean age ± sd 38.80 ± 9.88 clinical parameters occupation light work 20 moderate work 19 heavy work 23 pain onset insidious 34 sudden 28 duration < 3 month 20 3month1year 14 1year 3 year 13 >3 year 15 knee reflex normal 58 decrease 4 ankle reflex normal 3 decrease 59 planter reflex normal 2 decrease 2 equivocal 13 absent 45 paraspinal muscle spasm present 31 absent 31 spinal deformity (scoliosis) present 7 absent 55 slrt positive 25+17+18 (b/l+lt+r t) negative 2 out of 62 patients, 27 (44%) patients were diagnosed as a case of l4-l5 pivd, 27 (44%) patients had l5-s1 pivd and 8 (12%) patients had both l4-l5, l5-s1 pivd. at l4-l5 disease level, 15 patients had central disc herniation, 5 had right paracentral and 7 had left paracentral disc herniation on mri lumbosacral spine. out of 27 l5-s1 pivd patients, 19 had central disc herniation, 10 had right paracentral disc herniation and 8 had left paracentral disc herniation (table 2). table 2. level of disease and methods of surgery parameter no. of patients l4—l5 pivd central 15 rt paracentral 5 lt paracentral 7 total 27 l5-s1 pivd central 19 rt paracentral 10 lt paracentral 8 total 27 l4-l5, l5-s1 8 method of discectomy open 41 microscopic 18 endoscopic 2 percutaneous 1 patients underwent different types of discectomies that are by open method, microscopic endoscopic, and percutaneous. open laminectomy and discectomy were performed in 41 (66%) patients. microscopic, endoscopic and percutaneous discectomies were performed in 18 (29%), 2 (3%) and one (2%) patient respectively (table 2). the mean rodi scores at pre-operative and postoperative 1, 6, and 12 months were 72, 18, 10, and 6 respectively. the mean rdq scores at preoperative and postoperative 1, 6, and 12 months were 15, 5, 3, and 2 respectively. similarly, the mean bq scores at pre-operative and postoperative 1, 6, and 12 months were 51, 12, 8, and 4 respectively. a one way repeated measures anova was run on the 62 patients to determine, if there were any changes in the mean rodi, rdq, bq scores over time (pre-op; post-op at 1 month, 6 month, and 1 year) (figure 1 and 2). results showed that there was a statistically significant difference in the mean rodi, rdq, bq scores over time that is pre-op vs post-op 1 month, 6 month, and 1 year period (p=0.000). tukey’s post-hoc test revealed no statistically significant differences between the rodi, rdq, bi scores observed 1-month post-op vs 6-month post-op, and 6-month post-op vs 1-year post-op (p>0.05). however, a statistically 289 functional outcome analysis in lumbar pivd patients after discectomy significant difference was observed between mean rdq scores 1-month post-op vs 1-year post-op (p=0.013), whereas, mean rodi and bq scores 1month post-op vs 1-year post-op were statistically non-significant (table 3). figure 1. changes in rodi, rdq, bq scores and their mean table 3. pre-op versus post-op changes in different functional score system changes in mean rodi scores in single/ double level discectomy patients time contrast s.d tukey pvalue 1 month post-op vs pre-op -54.516 2.73 0.000 6 month post –op vs pre-op -54.064 2.73 0.000 1 year post-op vs pre-op -55.000 2.73 0.000 changes in mean rdq scores in single/ double level discectomy patients 1 month post -op vs pre-op -9.032 0.654 0.000 6 month post –op vs pre-op -10.322 0.654 0.000 1 year post-op vs pre-op -11.032 0.654 0.000 changes in mean bq scores in single/ double level discectomy patients 1 month post-opvs pre-op -34.516 2.142 0.000 6 month post –op vs pre-op -37.484 2.142 0.000 1 year post-op vs pre-op -38.612 2.142 0.000 figure 2. mean of odi, rdq and bq figure 3. changes in mean of rodi scores in single level vs double level discectomy patients patients were categorised in 2 categories based on the level of discectomy performed, i.e single level discectomy (sldg) and double level discectomy (dldg). in sldg patients (n=54), the mean rodi scores were 65.67±2.76, 16.18±1.06, 11.92±1.58, and 10.95±2.05, at pre-operative, and postoperative 1month, 6 month, 1 year respectively. similarly, the mean rdq scores were 14.42±4.79, 5.38±2.38, 4.11±3.16, 3.44±3.64, and mean bq score 46±18.10, 12.35±6.11, 9.16±8.01, 7.85±10.63 at pre-operative and respective post-operative follow up. in dldg patients (n=8), the mean rodi scores were 75.75±5.57, 18.75±3.42, 19.50±7.87, and 18.87±9.10, at pre-operative, and postoperative 1month, 6 month, 1 year respectively. similarly, the mean rdq scores were 15.63±4.0, 6.62±3.11, 5.20±3.73, 4.25±5.03 and mean bq score 50.38±16.12, 14.63±8.19, 13.12±12.73, 13.25±17.99 at pre 290 surendra k. gupta, deepak k. singh, anuj chhabra et al. operative and respective post-operative follow up (figure 3, 4 and 5). changes in rodi, rdq, and bq scores at the respective intervals were compared between these two groups using a mixed anova test. the difference of change in rodi, rdq, and bq scores over time in both groups was found to be statistically non-significant (p=0. 701, p=0.992, p=0.962 respectively). this finding showed that a similar degree of improvement occurred in both sldg and dldg. sub questions of bq related to patient’s anxiety, depression, social, and family activities (sfa) were compared pre-operatively and post-operatively. the mean ± s.d sfa scores at pre-operative and postoperative at 1 year were 7.65 ± 2.26 and 3.32±1.40 and this difference was statistically significant (p=0.000) (table 4 and figure 6). figure 4. changes in mean of rdq scores in single level vs double level discectomy patients figure 5. changes in mean of bq scores in single level vs double level discectomy patients table 4. changes in psychosocial status (sub-questions of bq) subquestion of bq pre-op post-op pvalue mean of diff. s.d mean of diff. s.d social and family activities 7.650 2.26 3.32 1.40 0.000 anxiety 5.50 2.53 1.42 1.37 0.000 depression 5.50 2.53 0.71 1.08 0.000 similarly, the pre and 1 year post-op anxiety scores were 5.73 ± 2.53 and 1.42± 1.37 respectively and the difference was statistically significant (p=0.000). the pre-op and 1 year post-op depression scores were 5.50 ± 2.53 and 0.71± 1.08 respectively and the difference was statistically significant (p=0.000) (table 4 and figure 6). figure 6. changes in psychosocial status (sub question of bq) figure 7. functional assessment of not significantly improved patients discussion patients were assessed functionally with rodi, rdq, and bq at admission and after surgery at 1 month, 6 months, and 12 months. the rodi scores at preoperative, post-operative 1, 6, and 12 months were 72, 18, 10, and 6 respectively. the rdq scores at preoperative, post-operative 1, 6, and 12 months were 15, 5, 3, and 2 respectively. similarly, the bq scores at pre-operative, post-operative 1, 6, and 12 months were 51, 12, 8, and 4 respectively. a gradual statistically significant improvement was seen in mean scores of all 3 functional scores. maximum changes were observed after 1 month follow up in most of the patients as mentioned in the statistical table and diagram (table 2 and figure 1). pre 291 functional outcome analysis in lumbar pivd patients after discectomy operative functional scores of each patient were compared with post-operative scores separately and the result showed that gradual, statistically significant improvement seen in 54 (87%) patients and 8 (13%) patients did not show statistically significant improvement, after the initial decrease in scores (figure 7). among the patients who did not show improvement, four patients were in the rodi category 5 and 4 patients were in rodi category 3 pre-operatively. these patients were evaluated with mri lumbosacral spine and among these two patients had developed spondylolisthesis at operated level, four patients had foraminal stenosis due to facet joint hypertrophy and two patient’s mri showed increase degenerative changes at the operated level. among two patients those who had developed post-op listhesis, one patient had undergone l4-l5 discectomy through open method and another patient had undergone l4-l5, l5-s1 double level discectomy (table 5). table 5. mri findings in patients not showing significant improvement spondylolisthesis 2 foraminal stenosis 4 canal stenosis 2 many previous studies measured functional assessment with the help of different tools like sf-36, sf-24, prolo scores, odi scores or self-made objective criterias of improvement and many other [1,2,8,10,11,12,15,18,23,25,27,28,29]. joel n abramowitz categorized patient's outcome into 3 groups good, fair & poor. a good outcome was defined as a situation where the patient had returned to the premorbid level of activity and was not limited by residual symptoms and was not taking narcotic medications. a fair outcome was defined as a situation where the patient did not return to work or was taking narcotic medications but improved after surgery. a poor outcome was defined as a situation where the patient had no improvement. in his study of 108 patients, 72 patients showed good outcome, whereas 34 patients showed fair and 2 showed poor outcome [19]. lewis et al (1987) divided the outcome as completely relieved, same or worse. 100 patients were followed for 5 10 years [16]. the results of lumbosacral discectomy appeared favourable as compared to weber’s study [31, 32]. in the study of junge et al out of 381 patients 89% and 86% were followed up for 6 months and 12 months respectively. low back pain of 6 or more on visual analog scale, reduced working ability of more than half a year, no return to the previous job, regular visits to treating physicians, or hospital stay have been chosen as a criteria for the bad outcome. the outcome was categorized into good, moderate, and bad. goodnone of the above-mentioned criteria, moderate -one or two of the criteria if back pain is between 0 and 3. bad two criteria and back pain more than 3 or all of these criteria. 51.5% had a good outcome, 28.4% moderate, and 20.11 % bad outcome at 12 months follow up. there was no difference in 6 months outcome and 12 months outcome [13]. it is evident from above that for analyzing the outcome of lumbar disc disease various authors have chosen criteria that differ from study to study and the duration of follow up also differs significantly. these assessments were done by clinicians, so functional assessment of patients can be overestimated. that’s why in our study, the functional assessments of the patients were done with the help of rodi, rdq, and bq scores. these questionnaires were filled by patients themselves; hence there were chances to plot their functional assessment in a better way. our results were comparable to other studies. most of the long term studies with follow up of more than 5 years are retrospective and most of the short term studies with short follow up of 2 years and less are prospective. studies with short term follow up showed better outcomes than long term results. further studies that included patients with severe degenerative spine or with neurological deficit showed unsatisfactory results. salenius and laurent reported satisfactory early results in 70% of patients that was decreased to 56% after 6 to 11 years of observation[24]. frymoyer et al, in a retrospective study with a minimum 10-year follow-up, reported a 38% failure rate because of persistent symptoms or the need for reoperation [7]. dvorak et al found that 23% of patients still complained of severe low-back pain and 45% had residual sciatica after 4 to 17 years follow-up [34]. in spangfort’s analysis of 2504 patients, more than 30% of patients complained of persistent low back pain, while sciatic pain was found in 23% of the patients [26]. 292 surendra k. gupta, deepak k. singh, anuj chhabra et al. single and double level discectomy patients were compared along with changes in the mean of rodi, rdq, and bq scores over the defined follow-up time. both groups of patients showed significant improvement over time. further, both these groups were compared to see the degree of improvement over 1 year with the help of difference in the mean rodi, rdq, and bq scores measured at preoperatively and one-year postoperatively and both these groups showed a similar degree of improvement (figure 3, 4, and 5). some patients of lumbar disc disease had anxiety and depression and some patients had affected their social and family activities. hence 3 questions of bq related to the patient social and family activities, anxiety and depression were separately compared pre and post-operatively. mean of differences of means at pre-op and post-op 1 year of these subquestions showed the statistically significant improvement over time. (table 4 and figure 6) complication: four patients experienced complications in our study. the intra-operative cerebrospinal fluid leak was present in one patient due to a dural tear, two patients had unilateral post-operative foot drop, and 1 patient developed postoperative superficial wound infection (table 6). table 6. complications complication no of patients csf leak due to dural tear 1 post-op foot drop 2 superficial wound infection 1 limitations: this is a single centred study so the study population is less. follow up period is one year as this is a prospective study and having time limitation. further, prospective study is needed, which include large sample size and long follow up period so the results can be better plotted on population. conclusion 87% (n= 54) of patients had statistically significant improvement on functional assessment scales i.e rodi, rdq, and bq. most of the patients who did not show statistically significant improvement were in odi category 4 or 5. no statistically significant differences were seen on comparing single and double level discectomy on follow up of one year i.e similar trends of improvement were seen in single level versus double level discectomy patients. sfa, depression, and anxiety of the patients improved significantly over 1 year. acknowledgements i am thanking dr arvind kumar singh, associate professor, deptt. of community medicine, dr rmlims, lucknow for statistics and valuable advice during my study. abbreviations odi: disability index pivd: prolapsed intervertebral disc rodi: revised oswestry disability index score, rdq: ronald–morris disability questionnaire bq: the back bournemouth questionnaire mri: magnetic resonance imaging anova: one-way analysis of variants. hsd: honestly significant difference se: standard error of means. slrt: straight leg raising test sldg: single level discectomy dldg: double level discectomy sfa: social and family activities references 1. ankur mittal, a. chandrasekhar, ram mohan, ramprasad rallapalli, siva prasad y: analysis of the functional outcome of discectomy in lumbar disc prolapse. iosr journal of dental and medical sciences (iosr-jdms) 14: 5, 73-80. 2015. 2. ansari ishtyaque abdul aziz, ansari muqtadeer abdul aziz: functional outcome of microscopic lumbar discectomy for the treatment of lumbar disc prolapse; int j res orthop. 4(3): 389-394. 2018. 3. asch hl, lewis pj, moreland db, egnatchikjg, yu yj, clabeaux de, hyland ahj: prospective multiple outcomes study of outpatient lumbar microdiscectomy: should 75 to 80% success rates be the norm? j neurosurg. 96(1 suppl): 34-44. 2002. 4. aslam m, khan fr, huda n, pant a, julfiqar m, goel a: outcome of discectomy by fenestration technique in prolapsed lumbar intervertebral disc. ann int med den res 1: 286–90. 2015. 5. chakrabarty ps. excision of lumber disc through fenestration : a prospective study to analyse functional results. ind j med res pha sci. 2(1): 10–13. 2015. 6. dvorak j, gauchat mh, valach l: the outcome of surgery for lumbar disc herniation: a 4 to 17-year follow-up with emphasis on somatic aspects. spine 13:1418–22. 1988. 7. frymoyer jw, hanley en, howe j, kuhlmann d, matteri re: 293 functional outcome analysis in lumbar pivd patients after discectomy disc excisionand spine fusion in the management of lumbar disc disease. a minimum ten-year follow-up. spine 3: 1–6. 1978. 8. gaetani paolo, aimar enrico , panella lorenzo, debe rnardi alberto , tancioni flavio , rodriguez y baena riccardo : surgery for herniated lumbar disc disease; factors influencing outcome measures: an analysis of 403 cases. functional neurology 19: 43-49. 2004. 9. garg m, kumar s: interlaminar discectomy and selective foraminotomy in lumbar disc herniation. j orth surg. 9: 15–18. 2001. 10. george a. loupasis, konstadinos stamos, paul g. katonis, george sapkas, dimitrios s. korres, and george hartofilakidis: sevento 20-year outcome of lumbar discectomy; spine 24: 22, 2313–2317. 1999. 11. hurme m and alaranta h: factors predicting the result of surgery for lumbar intervertebral disc herniation. spine 12: 933-938. 1987. 12. imran b.m, pisudde p.m, aravind kumar: study on analysis of functional outcome of fenestration technique; int j cur res rev 7: 22 , 2015. 13. junge a ,dvork j. ahren: predictors of bad and good outcomes of lumbar disc surgery. spine 20, 4: 460 68, 1995. 14. kelsey jl: an epidemiological study of acute herniated lumber disc. rheumatol rehabil 14:144-159, 28a. 1975. 15. kotryna veresciagina, bronius spakauskas, kazys vytautas ambrozaitis: clinical outcomes of patients with lumbar disc herniation, selected for one-level opendiscectomy and microdiscectomy. eur spine j. 19(9): 1450–1458. 2010. 16. lewis, p., weir, b. a., broad, r. w., & grace, m. g. (1987). long-term prospective study of lumbosacral discectomy, journal of neurosurgery, 67(1), 49-53. retrieved mar 9, 2019. 17. manoharababu kv: surgical management of lumbar disc prolapse by fenestration technique. j.orthopaedics. 3(4): e6. 2006. 18. mariconda m, galasso o, secondulfo v, rotonda gd, milano c: minimum 25-year outcome and functional assessment of lumbar discectomy. spine (phila pa 1976). 31(22): 2593-9; discussion 2600-1. 2006. 19. n. abramovitz, joel & r. neff, samuel: lumbar disc surgery: results of the prospective lumbar discectomy. neurosurgery. 29: 301-7, 1991. 20. nahar k, srivastavark: prospective study of prolapsed lumbar intervertebral disc treatment by fenestration. int j res med. 2(2): 170–73. 2013. 21. nygaard op, kloster r, solberg t:duration of leg pain as a predictor of outcome after surgery for lumbar disc herniation: a prospective cohort study with 1-year follow up. j neurosurg. 92(2 suppl): 131-4. 2000. 22. peul wc : surgery versus prolonged conservative treatment for sciatica. n engl j med 356: 2245-2256, 2007. 23. rothoerl rd: when should conservative treatment for lumbar disc herniation be ceased and surgery considered. neurosurg rev 25: 162-165. 2002. 24. salenius p, laurent le: results of operative treatment of lumbar disc herniation. a survey of 886 patients. acta orthop scand 48: 630–4. 1977. 25. sanath kumar shetty , arjun ballal , lawrence john mathias & h. ravindranath rai: a study of functional outcome of laminectomy and discectomy in lumbar intervertebral disc prolapse (a comparison of retrospective and prospective analysis); nujhs 5: 4, 2015. 26. spangfort ev: the lumbar disc herniation: a computer aided analysis of 2,504 operations. acta orthop scand 142(suppl): 1–95. 1972. 27. sun ec, wang jc, endow k, delamarter rb: adjacent twolevel lumbar discectomy: outcome and sf-36 functional assessment. spine (phila pa 1976) 29(2): e22-7. 2004. 28. toms jacob, u sudheer, c jayaprakash: functional outcome of patients underwent lumbar microdiscetomy: international journal of scientific study 4: 4, 2016. 29. ujjwal gowardhan wankhade, mahesh kotehal umashankar, b.s. jayakrishna reddy: functional outcome of lumbar discectomy by fenestration technique in lumbar disc prolapse – return to work and relief of pain. journal of clinical and diagnostic research. 10(3): rc09-rc13. 2016. 30. volker schade, norbert semmer, chris j main, josef hora, norbert boos: the impact of clinical, morphological, psychosocial and work-related factors on the outcome of lumbar discectomy. pain 80: 1–2, 239–249.1999. 31. weber h. lumbar disc herniation: a controlled, prospective study with ten years of observation. spine. 8: 131–140. 1983. 32. weber h. spine update: the natural history of disc herniation and the influence of intervention. spine 19: 2234-8. 1994. 33. weber h: the natural course of disc herniation. acta orthop scand suppl, 251: 19-20, 1993. 34. weinstein jn, tosteson td, lurie jd, toteston ana, hanscom b: surgical vs. non-operative treatment for lumbar disc herniation – the spine patient outcome research trial (sport): a randomized trial. jama. 296(20): 22–29. 2006. microsoft word 3ienceanst_mid-term romanian neurosurgery (2018) xxxii 4: 547 551 | 547             doi: 10.2478/romneu-2018-0070 mid-term results in continuous intracranial pressure monitoring in severe traumatic brain injury in children era-net neuron grant st.m. iencean1,2, a. tascu3,4, c.a. apetrei2, c. gheorghita5, tsz-yan milly lo6, ian piper7, a.st. iencean2 1neurosurgery, “grigore t. popa” university of medicine and pharmacy iasi, romania 2neurosurgery, “prof. dr. n. oblu” clinical emergency hospital iasi, romania 3neurosurgery, “bagdasar-arseni” clinical emergency hospital bucharest, romania 4neurosurgery, “carol davila” university of medicine and pharmacy bucharest, romania 5neurosurgery, “sf. maria” children clinical emergency hospital iasi, romania 6university of edinburgh (child life & health) / royal hospital for sick children (paediatric critical care medicine), uk 7brainit group coordinator, principal health care scientist, neuro-intensive care monitoring research, uk abstract: this article presents the mid-term results of the multi-center grant “paediatric brain monitoring with information technology (kidsbrainit). using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety”, acronym kidsbrainit, of the romanian team. continuous real-time intracranial pressure monitoring is a standard in tbi intensive-care management and icp-lowering therapy is recommended when icp is elevated above 20 mmhg or more. paediatric tbi patients requiring intensive care are recruited from more contributing centres in 4 different countries and the romanian team includes doctors ca apetrei, c gheorghita and a tascu as principal investigators. children aged 2 to 16 years who require intensive care management after sustaining traumatic severe brain injury are included in this study in three neurosurgical hospital: "prof. dr. n. oblu" clinical emergency hospital iasi, "sf. maria" children clinical emergency hospital iasi and "bagdasar-arseni" clinical emergency hospital bucharest. continuous icp and mean arterial blood pressure (map) monitoring allow calculation of cerebral perfusion pressure (cpp) and establish of an optimal cpp. the aim of this study is to improve the treatments in severe traumatic brain injury in children. key words: cerebral perfusion pressure, children brain injury, intracranial pressure, paediatric brain monitoring 548 | iencean et al mid-term results in continuous intracranial pressure monitoring             introduction traumatic brain injuries in children represent an important cause of morbidity and the main cause of death in children older than one years of age. as it is presented in the scientific project proposal the “majority of children who survives a life threatening brain trauma have new disabilities that affect how they function throughout the rest of their lives. currently the best option to improve survival and recovery of children with life threatening brain trauma is to improve their early hospital treatments including intensive care”. also “the current best therapeutic option to improve severe traumatic brain injury in children outcome is to optimise physiological support in the intensive-care to minimise secondary physiological insults which are proven to negatively affect outcome. we urgently need clinically relevant and readily translatable research that optimises paediatric brain trauma treatment”. material and methods children aged 2 to 16 years who require intensive care management after sustaining accidental tbi are included in this study in three neurosurgical hospital: "prof. dr. n. oblu" clinical emergency hospital iasi, "sf. maria" children clinical emergency hospital iasi and "bagdasararseni" clinical emergency hospital bucharest. this neurosurgical units have same treatment protocols, which include: defined raised icp treatment guidelines using osmodiuretics as a first line medical treatment; sedation and muscle relaxant protocol; mechanical ventilation to control paco2 to low normal values; using intravenous infusions of vasopressive drugs to drive mean arterial blood pressure to achieve a target cpp; actively controlling core body temperature to normothermia. patients’ anonymised clinical data are collected with the cause and nature of injury, age, glasgow coma score (gcs) on admission and after acute non-surgical resuscitation, pupillary responses, initial radiological and computerized tomography (ct), operative and other treatment details. as planned in the scientific project cppopt calculation and icp dose-response visualisation analyses are performed and determine if tbi patients with favourable outcome have longer periods of measured cpp within the calculated cppopt ranges and an enhanced tolerance of raised icp. figures 1, 2 and 3 show a case of a 2 years old children with severe tbi and contiuous intracranial pressure monitoring intensive care unit. figure 1 case of 2 years old children with severe tbi and contiuous intracranial pressure monitoring romanian neurosurgery (2018) xxxii 4: 547 551 | 549             figure 2 the same case of a children with severe tbi and contiuous intracranial pressure monitoring figure 3 medical devices used for contiuous intracranial pressure monitoring results there were a total of 624 children with traumatic brain injury during 8 months in these three neurosurgical departments and 20 patients needed intensive care and 6 children have been icp and blood pressure monitored, but onky three patients were included in this scientific project. in two cases the values of icp were high and very high and cerebral decompression was performed; unfortunately, the initial clinical condition was extremely severe and evolution was not favorable in these two cases. the third patient monitored showed elevated icp values up to 28-30 mm hg, which were medically treated and had a favorable evolution. figure 4 a. child with with severe tbi and contiuous intracranial pressure monitoring with intraventricular catheter and cerebral decompression; b. ct of the same case with efficient decompressive craniectomy 550 | iencean et al mid-term results in continuous intracranial pressure monitoring             discussion the number of cases of pediatric tbi vary across clinical and epidemiological studies and our number of over 600 cases in 8 months should be interpreted by reference to only two neurosurgical centers : two hospitals in iasi and one in bucharest, so only for two areas from the country. the cases with icp and cpp monitoring are few and a statistical analysis is not yet conclusive. with regard to cases that needed icp monitoring, the gender distribution is predominantly male, and the most common cause was the road traffic accident. intracranial pressure monitoring is an invasive method but it assured an early detection of increased icp in children with severe tbi. in our cases of monitored traumatic intracranial hypertension the performed maneuvers were decompressive craniectomy, drug therapy and csf drainage in accordance with modern therapeutic guidelines. the relationship between icp elevation and cpp values is known in the adult, but in the pediatric tbi the studies are not conclusive; so “chambers et al. proposed agestratified critical levels of cpp: in the age groups 2–6, 7–10, and 11–16 years, cpp values of 43 mmhg, 54 mmhg and 58 mmhg, respectively, were associated with normal values of icp and good outcomes”. treatment used sedatives, analgesics; hyperosmolar therapy as intravenous mannitol and hypertonic saline to control intracranial hypertension; mild hyperventilation; barbiturates, temperature control and prophylactic anticonvulsants. the routine steroid treatment in children with severe tbi is not conclusive; it has to be individualized and rather it is not indicated because the potential harm from infectious complications. decompressive craniectomy was performed for controlling intracranial hypertension and it was effective at icp reduction. our study will continue with the inclusion of patients and icp and cpp monitoring with the hope of obtaining conclusive and beneficial results for setting standards in care of severe traumatic brain injury in children. conclusion the best care of severe traumatic brain injury in children requires a multidisciplinary approach in each phase of management. the initial evaluation with prompt diagnosis and multimodal monitoring must be followed by the management of intracranial hypertension (icp and cpp) to minimize the pathophysiological damage to the brain. intracranial pressure monitoring assured an early detection of increased icp in children with severe tbi. the findings from our study are directly transferable to a wider clinical audience because no special equipment is required, beyond that is currently used for the routine minute-by-minute physiological bedside monitoring. this study is within the grant: “paediatric brain monitoring with information technology (kidsbrainit): using it innovations to improve childhood traumatic brain injury intensive care romanian neurosurgery (2018) xxxii 4: 547 551 | 551             management, outcome, and patient safety”, grant: cofund-neuron iii eranet kidbrainit, funding no.2 / 01/06/2017. correspondence a tascu, "carol davila" university of medicine and pharmacy bucharest, romania e-mail: tascu_alexandru@yahoo.com references 1. tsz-yan milly lo. paediatric brain monitoring with information technology (kidsbrainit): using it innovations to improve childhood traumatic brain injury intensive care management, outcome, and patient safety. proposal application form era-net neuron, 2016 2. iencean st m, tascu a, apetrei ca, gheorghita c, iencean a st. continuous intracranial pressure monitoring in severe traumatic brain injury in children. romanian neurosurgery, vol xxxii, sept 2018, supplement pp.73 3. chambers ir, jones pa, lo tym et al. critical thresholds of intracranial pressure and cerebral perfusion pressure related to age in paediatric head injury. j neurol neurosurg psychiatry 2006. 77(2): 234-240. 4. depreitere b, güiza f, van den berghe g, schuhmann m, maier g, piper i, meyfroidt g. pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in severe traumatic brain injury patients based on minute-by-minute monitoring data. j. neurosurgery 2014 jun; 120(6): 14511457. 5. güiza f, meyfroidt g, lo tym, jones pa, greet van den b, depreitere b. continuous optimal cpp based on minute-by-minute monitoring data: a study on a pediatric population. acta neurochir 2015. 6. guiza f, depreitere b, piper i et al. visualizing the pressure and time burden of intracranial hypertension in adult and paediatric traumatic brain injury. intensive care medicine 2015. 41(6): 1067-1076. 7. hutchison js, frndova h, lo tym et al. impact of hypotension and low cerebral perfusion pressure on outcomes in children treated with hypothermia therapy following severe traumatic brain injury: a post hoc analysis of the hypothermia pediatric head injury trial. dev neurosci. 2010; 32(5-6): 406-12. 8. araki t, yokota h, morita a pediatric traumatic brain injury: characteristic features, diagnosis, and management. neurol med chir. 2017; 57(2): 82–93. 9. ommaya ak, goldsmith w, thibault l: biomechanics and neuropathology of adult and paediatric head injury. br j neurosurg 16: 220– 242, 2002 10. suttipongkaset p, chaikittisilpa n, vavilala ms et al. blood pressure thresholds and mortality in pediatric traumatic brain injury, pediatrics, 2018; 142(2). pii: e20180594. doi: 10.1542/peds.2018-0594. adamd_aretrospective 6 adam et al comparison of laminectomy and fenestration in lumbar spinal stenosis a retrospective comparison of laminectomy and unilateral fenestration with foraminotomy on outcome of patients with lumbar spinal stenosis d. adam1,2, ioana hornea1, gina burduşa1, d. iftimie1, cristiana moisescu1 1“saint pantelimon” emergency clinical hospital, bucharest 2“carol davila" university of medicine and pharmacy, bucharest abstract: background: neural decompression for lumbar spinal stenosis (lss) can be performed, besides conventional lumbar laminectomy, by many other surgical techniques. objective: the goal of this study is to analyze the results of laminectomy versus unilateral fenestration and foraminotomy with bilateral neural decompression in lss patients. methods: a number of 58 patients with lumbar spinal stenosis were divided into two groups: group a (no.=22) consists of patients that underwent a laminectomy procedure and group b (no.=36) of cases where unilateral fenestration with foraminotomy was used. outcome was assessed at 1, 6 and 12 months postoperatively. two parameters were evaluated: level of pain with the vas (visual analogue scale) score and the odi (oswestry disability index) scale for functional improvement. results: the level of pain was reduced in both patient groups. cases in group a maintained higher levels of back pain in the first postoperative month versus group b. improvement was faster for those operated by unilateral approach. at 6 months and 1 year follow-ups, vas values were very similar. all patients presented functional recovery evaluated with the odi scale, that showed continuous improvement at 6 months and 1 year. conclusions: bilateral decompression by unilateral approach is an efficient method that represents the first option of treatment for patients with lateral lumbar spinal stenosis with unilateral or predominantly unilateral symptoms. for patients with severe central stenosis, classic laminectomy remains the first surgical choice. key words: lumbar spinal stenosis, laminectomy, unilateral approach with improvement in overall life expectancy and widespread use of mri, an increasing number of patients are diagnosed with lumbar spinal stenosis (lss), a frequent condition among the elderly population. prior to the emergence of modern imagistic techniques, in the de sèze classification based on clinical presentation, it corresponded to romanian neurosurgery (2016) xxx 1: 6 14 7 stage iv and had conservative treatment as the sole therapeutic method. ct-scan and mr images have brought on clearer information regarding the morphology of the spinal canal and revealed its stenosis, which can be central or lateral (of the lateral recess or foraminal). the failure of conventional therapy has fostered the discovery of different surgical techniques for decompression of the affected nervous elements, which have proven superior to conservative treatment options. (1, 2, 3) laminectomy has been the gold standard of surgical treatment for central lumbar spinal stenosis. subsequently, less invasive techniques have been conceived: unilateral laminectomy, bilateral fenestration and foraminotomy, unilateral fenestration and foraminotomy with ipsilateral and contralateral nerve root decompression. the goal of the study is to investigate if by using bilateral decompression performed with unilateral foraminotomy, the same or even better results can be obtained compared to the classical technique of laminectomy. material and methods the study was conducted on 58 consecutive patients with lumbar spinal stenosis operated in the year 2013 by the senior neurosurgeon (d.a.). diagnosis was based on clinical symptoms (e.g.: neurogenic claudication, leg pain) and signs, correlated with mr images. preoperatively, conservative therapy for 3 to 6 months failed to improve symptoms for all cases included. patients were investigated using lumbar mri that confirmed lumbar spinal stenosis. cases with a clinical diagnosis of polyradiculopathy with a variable clinical presentation at different preoperative examinations and clinical-imagistic discrepancy, were further investigated with emg (electromyography) in order to objectively establish the most affected level. in cases with neurogenic claudication and a central lss on mr scan, a standard lumbar laminectomy was performed. for patients that presented unilateral or predominantly unilateral radicular pain and lumbar mri showed lateral recess and/or foraminal stenosis, a unilateral fenestration at the most affected side and bilateral decompression of nerve roots at the level of interest was performed. on the ipsilateral side, the ligamentum flavum and the internal third of the superior facet were resected. contralaterally, the ligamentum flavum was resected after the ablation of a portion of the spinous process, tilting of the operating table and protection of the dural sac with a spatula. all surgical interventions were performed under general anesthesia. for both groups of patients, a retrospective analysis was carried out on operative time, postoperative hospital length of stay and complications that occurred (e.g.: incidental durotomy, wound infection). neurological examinations performed preoperatively and during follow-up assessed vas (visual analogue scale) score and odi (oswestry disability index) scale at 1, 6 and 12 months. spinal instability signs were sought for with the use of conventional x-rays in neutral (anteroposterior and profile) and dynamic positions. the characteristics of the two treatment groups were compared at the time of admission and during follow-up (table i). 8 adam et al comparison of laminectomy and fenestration in lumbar spinal stenosis table i patient characteristics number of cases: 58 group a (no.=22) laminectomy no. (%) group b (no.=36) unilateral approach no. (%) mean age male no. comorbidities • hypertension • diabetes • osteoporosis • depression symptoms • leg pain • back pain • neurogenic claudication stenosis type • central • lateral level of stenosis • l2 l3 • l3 l4 • l4 l5 • l5 s1 no. of operated levels • 1 • 2 • 3 68 12 (54%) 12 (54%) 3 (13%) 4 (18%) 2 (9%) 15 (68%) 20 (90%) 19 (86%) 22 (100%) 0 1 (4%) 3 (13%) 11 (50%) 7 (31%) 7 (31%) 10 (45%) 5 (22%) 69 22 (55%) 16 (44%) 6 (16%) 5 (13%) 3 (8%) 29 (80%) 36 (100%) 7 (19%) 0 36 (100%) 3 (8%) 7 (19%) 16 (44%) 10 (27%) 18 (50%) 12 (33%) 6 (16%) incidental durotomy infections operative time (min.) • mean • range 1 (4,55%) 0 105 70 135 0 0 70 45 95 romanian neurosurgery (2016) xxx 1: 6 14 9 figure 1 vas back pain score (patients with unilateral approach benefited more in terms of back pain relief at 1 month postoperative) figure 2 vas leg pain score (postoperative leg pain reduction was important in both groups, with a nonsignificant difference between them) 10 adam et al comparison of laminectomy and fenestration in lumbar spinal stenosis figure 3 odi scale during follow-up table ii postoperative results group a group b hospitalization days 7 3 vas back pain preoperative 1 month 6 months 1 year 7,1 6,1 2,6 2,2 6,9 3,2 2,3 2 vas leg pain preoperative 1 month 6 months 1 year 7,9 4,2 3,2 2,5 8,1 3,0 2,2 1,6 odi score preoperative 1 month 6 months 1 year 69 37 26 20 65 31 23 19 romanian neurosurgery (2016) xxx 1: 6 14 11 results sex distribution for the two groups of patients was similar, in both cases the male gender being more frequently affected (54% and 55%, respectively). the average age and number of comorbidities that constitute preoperative risk factors were evaluated using the asa (american society of anesthesiologists) classification and proved to be similar in both groups. neurogenic claudication was predominant in group a (19 versus 7), while radiculopathy was more common in group b (29 versus 15). the lumbar level most frequently affected by spinal stenosis was l4-l5, followed by l5s1. there were 22 cases of central stenosis and 36 cases of lateral stenosis. the lateral recess and foraminal stenosis were grouped together under the name of lateral stenosis. the two types of surgery were performed: at 1 level in group a for 7 cases versus 18 patients in group b, at 2 levels in 10 and 12 cases respectively, and at 3 levels in 5 and 6 cases respectively. there have been cases in which patients presented with a history of bilateral alternating radiculopathy or bilateral radiculopathy, but prevalent on one side at the time of presentation. one patient for whom decompression was performed with the laminectomy technique, with a severe central stenosis, suffered an incidental durotomy that was repaired by dural suturing. the average duration of surgery was higher in the case of laminectomy (a mean duration of 105 versus 70 minutes), but also varied with the number of levels operated on (70 – 135 minutes versus 45 – 95 minutes, respectively). the duration of postoperative hospital stay was higher in the laminectomy group (a mean of 7 versus 4 days). patients presented alleviation of pain levels during the postoperative period, regardless of the method used for nervous decompression. (table ii) for patients in group a, a lesser degree of back pain reduction was achieved 1 month after surgery compared to group b patients. (figure 1) the decrease of vas score for leg pain had close values in both patient groups. (figure 2) functional recovery assessed using the odi scale appears almost superimposable, which demonstrates that both methods are efficient and equally beneficial for patients with lss. during the one-year follow-up period, only two patients from group b required a supplementation of the decompression by unilateral approach, contralateral to the first intervention. discussion lumbar spinal stenosis, a pathological entity whose prevalence has risen in the last decades, is now more frequently diagnosed and treated surgically. in the category of degenerative diseases of the spinal column, the preeminence of spinal stenosis is disputed with that of spinal disc herniation. 12 adam et al comparison of laminectomy and fenestration in lumbar spinal stenosis in a german study, surgical interventions for lumbar spinal stenosis at the present time are three times more frequent that those for disk herniations when compared to 1999. (4) in the us, the incidence of surgeries for this condition has risen 8 times in the period between 1972 and 1992. (2) recent studies have demonstrated that lumbar spinal stenosis is better treated surgically than by nonsurgical means. (1, 5, 6, 7) laminectomy is the classical technique in the surgical treatment of lumbar spinal stenosis. this approach allows for decompression of nervous elements at 1 or more levels. the disadvantages of this method consist of: prolonged postoperative pain, atrophy of the paravertebral muscles, a greater risk of incidental durotomy and spinal destabilization when discectomy or fecetectomy are associated. different surgical techniques for decompression have been implemented, among them being bilateral or unilateral fenestration at the stenosed level. the unilateral approach was initially described in 1988 by young et al. (8). we are now applying the two techniques (laminectomy or unilateral fenestration) depending on the type of lss. in the case of a severe central lumbar spinal stenosis, the decompression is achieved with the use of bilateral laminectomy, with ablation of the ligamentum flavum and the internal third of the facet (facetectomy). by using this method, decompression of the dural sac and nerve root for approximately 15 mm is obtained. a discectomy is associated only if a disc protrusion of appropriate size is present. in the case of lateral recess or foraminal stenosis, decompression is performed with the use of fenestration and fecetectomy at the respective level. these patient have either an alternating radiculopathy, or a bilateral radiculopathy predominant on one side. all patients were operated on by unilateral fenestration with foraminotomy, undercutting of the base of the spinous process and resection of the contralateral ligamentum flavum. the same type of approach is used for patients with strictly unilateral radiculopathy, for which mri scan shows a bilateral stenosis to prevent an ulterior new contralateral surgical intervention. this type of approach is mini-open, with a skin incision of 3-4 cm depending on the patient’s bmi (body mass index). bilateral decompression by unilateral approach is also performed in other neurosurgical centers. (4, 9, 10) the average operative duration was significantly higher in the laminectomy group (105 versus 70 minutes). in recent years, several studies on minimally invasive interventions for lss have been published, with results comparable to those of “open” interventions. (3, 10, 11, 12) in our opinion, by unilateral approach, results as good as in the case of laminectomy can be obtained, in regard to medium and long term outcomes. by using this approach, lumbar pain levels are reduced faster and operative time and post-operative hospital length of stay are shortened. however, each technique targets a different category of patients: laminectomy for central romanian neurosurgery (2016) xxx 1: 6 14 13 lss and unilateral approach for lateral lss. regarding the latter, especially when the symptoms are unilateral, an “open”, wide approach may be waived. patients with bilateral laminectomy continue to experience higher levels of pain for the first postoperative month when compared to cases with a unilateral approach. for the former, pain may be caused by ischemia of the paravertebral muscle, an opinion shared by datta et al (13). in cases with a fenestration and foraminotomy approach, the paravertebral muscles are retracted unilaterally and the operative time is shorter. they present reduced postoperative hospitalization and begin recovery earlier. evaluation of vas and odi scores during follow-up has shown continuous improvement, so that at 1 year postoperative, vas leg pain score was 2,5 in group a versus 1,6 in group b. similar results have been reported by other studies1 (4, 15), improvement obtained with fenestration and foraminotomy, a less invasive method, being grater when compared to bilateral laminectomy, although the difference in results at 6 months and 1 year is not statistically significant. niggermeyer et al (16) have shown that better results were obtained by using less invasive surgical techniques to decompress lss. incidental durotomy occurred in only one patient with severe lumbar spinal stenosis. the immediate dural suture avoided the development of a cerebrospinal fluid fistula and the patient did not present any other neurological complication. desai et al. (17) have found that incidental durotomy in the sport study did not have any long term effects on affected patients. this is a retrospective study with its inherent limitations. a larger number of patients is necessary to perform a statistical analysis representative for the general population. longer follow-up would be helpful in evaluating if additional surgery becomes necessary for both groups, because lss is a progressive condition. conclusions neurogenic claudication, back and leg pain of patients with lss are alleviated by surgical treatment. laminectomy is indicated for patients with severe lumbar spinal stenosis. in the case of foraminal stenosis, by using a unilateral approach with ipsilateral and contralateral decompression, similar results can be obtained. both techniques led to significant improvement in clinical outcome. the unilateral approach is faster, safer and not inferior regarding neural decompression and overall pain relief. references 1.athiviraham a, yen d: is spinal stenosis treated better surgically or nonsurgically? clin orthop relat res. 458: 490-493, 2007. 2.ciol ma, deyo ra, howell e, kreif s: an assessment of surgery for spinal stenosis: time trends, geographic variations, complications and reoperations, j am geriatr soc. 44: 285-290,1996. 3.khoo lt, fessler rg: microendoscopic decompressive laminotomy for the treatment of lumbar stenosis. neurosurg 51 (suppl 5): 146-154, 2002. 14 adam et al comparison of laminectomy and fenestration in lumbar spinal stenosis 4.papavero l, thiel m, frityche e, et al.: lumbar spinal stenosis: prognostic factors for bilateral microsurgical decompression using unilateral approach. neurosurgery 65 (ons suppl 1): ons 182-ons 187, 2009. 5.chang y, singer de, wu ya, et al.: the effect of surgical and nonsurgical treatment on longitudinal outcomes of lumbar stenosis over 10 years. j am geriatr soc. 53: 785792, 2005. 6.malmivaara a, slätis p, heliövaara m et al.: finnish lumbar spinal research group: surgical or nonoperative treatment for lumbar spinal stenosis? a randomized controlled trial. spine 32: 1-8, 2007. 7.weinstein jn, tosteson td, lurie jd, et al.: surgical versus nonsurgical therapy for lumbar spinal stenosis. n engl j med. 358: 794-810, 2008. 8.young s, veerapen r, o’laoire sa: relief of lumbar canal stenosis using multilevel subarticular fenestration as an alternative to wide laminectomy: preliminary report. neurosurgery 23: 628-633,1988. 9.oertel mf, ryang ym, korinth mc, et al.: long-term results of microsurgical treatment of lumbar spinal stenosis by unilateral laminotomy for bilateral decompression. neurosurgery 59:1264-1270, 2006. 10.alimi m, njoku i jr, cong gt, et al.: minimally invasive foraminotomy through tubular retractors via a contralateral approach in patients with unilateral radiculopathy. operative neurosurgery 10: 436-4477, 2014. 11.yano s, hida k, seki t, et al.: a new ceramic interspinous process spacer for lumbar spinal canal stenosis. neurosurg. 63 (suppl 1) ons108–ons113, 2008. 12.ahn y, oh hk, kim h, lee sh, lee hn: percutaneous endoscopic lumbar foraminotomy: an advanced surgical technique and clinical outcomes. neurosurgery 75: 124133, 2014. 13.datta g, gnanalingham kk, peterson d: back pain and disability after lumbar laminectomy: is there a relationship to muscle retraction? neurosurgery 54(6):1413-1420. 2004. 14.palmer s, turner r, palmer r: bilateral decompression of lumbar spinal stenosis involving a unilateral approach with microscope and tubular retractor system. neurosurg. 97 (suppl 2): 213-217, 2002. 15.mayer hm, list j, korge a, wiechert k: microsurgery of acquired degenerative lumbar spinal stenosis. bilateral over-the-top decompression through unilateral approach. orthopade. 32: 889-895, 2003. 16.niggemeyer o, strauss jm, schulitz kp: comparison of surgical procedures for degenerative lumbar spinal stenosis: a meta-analysis of the literature from 1975 to 1995. eur spine j.: 423-429, 1997. 17.desai a, ball pa, lurie j, et al.: sport: does incidental durotomy affect long-term outcomes in cases of spinal stenosis? neurosurgery 69: 38-44, 2011. prunaviorel_particular aspects romanian neurosurgery (2015) xxix 4 particular aspects of cerebral metastases secondary to malignant melanoma in comparison with other brain metastases viorel mihai pruna1,2, m.r. gorgan2,3 1phd student, university of medicine and pharmacy “carol davila”, bucharest 2clinic of neurosurgery, emergency clinical hospital “bagdasar-arseni”, bucharest 3university of medicine and pharmacy “carol davila”, bucharest abstract: authors present a retrospective study of 427 patients with brain metastases admitted and treated in third and fourth neurosurgical departments of emergency clinical hospital “bagdasar-arseni” bucharest, from january, 2005 until december, 2014. 62.1% of all patients were men and 37.9% were women, with a medium age of 56.8 years, ranging between 17 and 85 years. 311 patients (72.8%) had a single metastasis, 79 patients (18.5%) developed 2 or 3 metastases and 37 patients (8.7%) had more than 3 metastases. the biggest four metastases in multiple cases were noted in database regarding location, either reported to left / right hemisphere, either related to site (frontal parietal etc.), and dimensions. in the case of malignant melanoma (22 men and 24 women) the status of the primary tumor was noted: the malignant melanoma was operated in 32 cases (69.6%) and in 7 patients (15.2%) the primary tumor was not operated. in another 7 cases the status of the primary tumor was not noted. the most frequent location for malignant melanoma was the legs in women and anterior thorax in men. in conclusion, cerebral metastases from malignant melanoma have most frequent intratumoral hemorrhages, comparative with other primary sources. common primary sites founded in this study is legs in women and anterior thorax in men. treatment of cerebral metastases is complex, multimodal, implying neurosurgeons, oncologists and radiotherapists. key words: brain metastases, malign melanoma, intratumoral hemorrhages. introduction brain metastases are the most frequent cerebral tumors and represent the main cause for morbidity and mortality among patients with systemic cancer. between 20 – 40% of patients develop one or more brain metastases during neoplastic disease. the most of the brain metastases arise from lung cancer, breast cancer, malign melanoma and kidney cancer. pruna, gorgan particular aspects of cerebral metastases secondary to malignant melanoma all studies report a maximum incidence in sixth and seventh decades of life. among all systemic cancer, malign melanoma has the greatest propensity for brain metastases. modern treatment for brain metastases includes currently not only whole brain radiotherapy, but more complex approach, consisting in classic surgery, stereotactic radiosurgery and chemotherapy. surgical resection represents the gold standard for brain metastases therapy, because it provides local control of diseases, releases the symptoms and accurate establish histopathological diagnosis. unfortunately, not all patients with brain metastases are good candidates for surgical treatment. material and methods authors present a retrospective study of 427 patients with brain metastases admitted and treated in third and fourth neurosurgical departments of emergency clinical hospital “bagdasar-arseni” bucharest, from january, 2005 until december, 2014. clinical data were collected from clinical observation sheets and surgical protocols recorded for each patient, including demographic data (age, sex), symptoms, karnofsky performance scale, number and location of tumors, systemic disease, imaging, surgical treatment and outcome. furthermore, location of primary cancer was noted for malign melanoma, as well as the presence of intratumoral hemorrhage visible on ct or mri scan. results 62.1% of all patients were men and 37.9% were women, with a medium age of 56.8 years, ranging between 17 and 85 years. demographic data are shown in table 1, figure 1. the maximum incidence of brain metastases was observed in sixth and seventh decades of life, 35.4% and 30.7% respectively, as it is shown in table 1, figure 2. figure 1 sex distribution figure 2 histogram from age distribution m, 265 f, 162 0 50 100 150 200 250 300 romanian neurosurgery (2015) xxix 4 311 patients (72.8%) had a single metastasis, 79 patients (18.5%) developed 2 or 3 metastases and 37 patients (8.7%) had more than 3 metastases. the biggest four metastases in multiple cases were noted in database regarding location, either reported to left / right hemisphere, either related to site (frontal parietal etc.), and dimensions. in 70.3% of cases (300 patients) tumors were located supratentorial, and in 18.5% (79 patients) brain metastases were located infratentorial. both supraand infratentorial location was seen in 11.2% of cases (48 patients) (figure 3). the medium size of the largest metastasis was 31.6 mm (varying from 4 to 80 mm). the medium size for the second metastasis was 10.6 mm, 9 mm for third tumor and 8.9 mm for fourth tumor. lung cancer was the starting point for brain metastases in almost half of the cases (196 patients, 45.9%), and most of them were men (84.7%). next source for brain metastases was breast cancer (68 patients, 15.9%) 95.6% of the patients with breast cancer were women and 4.4% were men (3 patients). the third starting point for cerebral metastases was malignant melanoma (46 patients, 10.8%). other primary sites were noted: colon cancer (24 patients), kidney cancer (19 patients), ovarian cancer (8 patients), cervix cancer (7 cases), and prostate cancer (4 cases). in 40 patients (9.4%) the investigations failed to reveal the source for brain metastases (table 2, figure 4). figure 3 location of cerebral metastasis pruna, gorgan particular aspects of cerebral metastases secondary to malignant melanoma table 1 characteristics of patients with cerebral metastasis characteristic of patients with brain metastasis count sex m 265 (62.1%) f 162 (37.9%) age <20 years 3 (0.7%) 21-30 years 6 (1.4%) 31-40 years 27 (6.3%) 41-50 years 72 (16.9%) 51-60 years 151(35.4%) 61-70 years 131(30.7%) 71-80 years 33 (7.7%) >81 years 4 (0.9%) number of brain metastases 1 311 (72.8%) 2 50 (11.7%) 3 29 (6.8%) >3 37 (8.7%) location supratentorial 300 (70.3%) infratentorial 79 (18.5%) supra/infratentorial 48 (11.2%) intracranial hypertension 402 (94.6%) neurological deficits hemiparesis 130 (30.7%) hemiplegia 28 (6.6%) seizures generalized seizures 51 (12.0%) focal seizures 45 (10.6%) facial nerve palsy 24 (5.6%) cranial nerve palsies 36 (8.5%) aphasia broca’s aphasia 46 (10.8%) werniche’s aphasia 16 (3.8%) dyshartria 14 (3.3%) memory disorders 41(9.6%) visual problem 49 (11.5%) personality disorders 36 (8.5%) confusion 34 (8.0%) bone metastasis 17 (4.0%) lung metastasis 38 (8.9%) liver metastasis 18 (4.2%) kidney metastasis 5 (1.2%) genital metastasis 10 (2.3%) adrenal metastasis 9 (2.1%) other organs 11 (2.6%) romanian neurosurgery (2015) xxix 4 table 2 primary site of cancer total pacients masculin feminin lung cancer 196 (45.9%) 166 (84.70%) 30 (15.30%) breast cancer 68 (15.9%) 3 (4.4%) 65 (95.6%) melanoma malign 46 (10.8%) 22 (47.8%) 24 (52.2%) kidney cancer 19 (4.4%) 15 (78.9%) 4 (21.1%) colon cancer 24 (5.6%) 15 (62.5%) 9 (37.5%) unspecified cancer 1 (0.2%) 1 (100%) 0 (0%) prostate cancer 4 (0.9%) 4 (100%) 0 (0%) ovary cancer 8 (1.9%) 0 (0%) 8 (100%) unknown cancer 40 (9.4%) 30 (75%) 10 (25%) sarcoma 2 (0.5%) 1 (50%) 1 (50%) laryngeal cancer 2 (0.5%) 2 (100%) 0 (0%) uterine cancer 7 (1.6%) 0 (0%) 7 (100%) bladder cancer 2 (0.5%) 2 (100%) 0 (0%) mediastinal cancer 2 (0.5%) 2 (100%) 0 (0%) malignant timoma 1 (0.2%) 0 (0%) 1 (100%) testicular cancer 1 (0.2%) 1 (100%) 0 (0%) gastric cancer 3 (0.7%) 1 (33.3%) 2 (66.7%) thyroid cancer 1 (0.2%) 0 (0%) 1 (100%) total 427 (100.0%) 265 (62.1%) 162 (37.9%) pruna, gorgan particular aspects of cerebral metastases secondary to malignant melanoma figure 4 primary site figure 5 differences in symptomatology between patients with single metastasis and patients with multiple metastases the most frequent symptoms were related to raise of intracranian pressure, founded in 94.6% of the patients. motor deficits (paresis or palsy) were noted in 37.3% of cases (158 166 3 22 15 15 1 4 0 30 1 2 0 2 2 0 1 1 0 30 65 24 4 9 0 0 8 10 1 0 7 0 0 1 0 2 1 200 150 100 50 0 50 100 lung cancer breast cancer malign melanoma kidney cancer colon cancer unspecified cancer prostate cancer ovary cancer unknown cancer sarcoma laryngeal cancer uterine cancer bladder cancer mediastinal cancer malignant timoma testicular cancer gastric cancer tyroid cancer masculin feminin 9 4 .5 0 % 9 5 .7 0 % 3 0 .9 0 % 3 0 .2 0 % 8 .4 0 % 2 .6 0 % 1 1 .0 0 % 1 4 .7 0 % 8 .7 0 % 1 5 .5 0 % 6 .8 0 % 2 .6 0 % 8 .4 0 % 8 .6 0 % 1 1 .6 0 % 8 .6 0 % 4 .2 0 % 3 .4 0 % 2 .9 0 % 4 .3 0 % 9 .6 0 % 1 0 .3 0 % 1 1 .6 0 % 1 1 .2 0 % 8 .7 0 % 8 .6 0 % 7 .7 0 % 8 .6 0 % 0.00% 20.00% 40.00% 60.00% 80.00% 100.00% 120.00% 1 metastasis >2 metastases ihc syndrome hemiparesis hemiplegia generalized seizures partial seizures facial nerve palsy other nerve palsy broca's aphasia werniche aphasia dysarthria memory disorders abnormal vision p=0.9 romanian neurosurgery (2015) xxix 4 patients) and 22.6% of patients presented with seizures. altered consciousness was encountered in 34 cases (8%), with giant metastases or posterior cranial fossa locations (figure 5). differentiated analysis of patients with one vs multiple metastases failed to reveal any statistical significant difference regarded to symptomatology (p=0.99), as shown in figure 5. in the case of malignant melanoma (22 men and 24 women) the status of the primary tumor was noted: the malignant melanoma was operated in 32 cases (69.6%) and in 7 patients (15.2%) the primary tumor was not operated. in another 7 cases the status of the primary tumor was not noted. the most frequent location for malignant melanoma was the legs in women and anterior thorax in men, as shown in figure 6. cerebral imaging (ct or mri scan with and without contrast enhancement) revealed intratumoral hemorrhage in 13 cases of brain metastases secondary to malignant melanoma, which meant the highest incidence, followed by cerebral metastases from lung cancer, with 3 cases of intratumoral hemorrhage (figure 7). figure 6 location of malign melanoma figure 7 mri aspect of intratumoral hemorrhage (brain metastases from malignant melanoma) all patients received steroids, while anticonvulsants were administrated in patients with supratentorial metastases. 335 of all patients (79.2%) underwent surgery for brain metastases. surgical resection was performed in 34 of all patients diagnosed with malignant melanoma (73.9%), while surgery was not considered an option in 4 patients with multiple brain metastases, who had a poor biologic status. 1 patient refused surgery and was referred to oncologist. 8 patients underwent stereotactic gamma-knife radiosurgery. most patients had a good postoperative outcome. only in 6.8% of cases the neurologic status worsened. the most common postoperative complication was cerebral hematoma, encountered in 17 patients (4.7%). worsening of motor and sensitive deficits was noted in 8 cases (2.2%). 7 patients were complicated with pneumonia and 1 patient developed pulmonary embolism. pruna, gorgan particular aspects of cerebral metastases secondary to malignant melanoma discussions cerebral metastases are the most frequent tumors of the brain. they arise mainly from lung cancer (50%), breast cancer (15-20%), malignant melanoma (5-20%), and colon and kidney cancer (1, 2). common clinical manifestations derive from raising of the intracranian pressure, focal neurologic deficits, seizures and altered consciousness. occurrence of brain metastases dramatically lowers the survival rate. if untreated, medium survival is approximately one month. corticotherapy increase survival at 2 months (3). association of corticotherapy with whole brain radiotherapy increase survival at 3 to 6 months (4-7). surgical resection of the tumors raise life expectancy at 9 – 14 months, depending of primary cancer, karnofsky performance scale, presence or absence of other systemic metastases (6-10). major changes in the treatment for brain metastases had seen over time. the main goals of the treatment are lowering morbidity and mortality, with improvement of quality of life. corticotherapy relief symptomatology by reducing peritumoral edema (11, 12). all patients in this study received steroids (dexamethasone sodium phosphate 8 mg daily). surgical treatment is usually indicated in patients with karnofsky performance scale > 70, with a single brain metastasis, which can be approached such that no additional motor or sensitive deficit be caused postoperative. cerebral metastases are usually well demarcated form surrounding cerebral tissue. the 3 main goals of the surgical treatment are establishing of accurate histologic diagnosis, quick relief of symptoms and local cure of disease. modern surgery, using of microsurgical techniques, neuronavigation and intraoperative monitoring had lead today to drops of intraand postoperative complications (13, 14) and dramatically decreased immediate postoperative mortality under 1% (15). patchell, tibbs, 1990 (7) showed that surgical resection of brain metastases increases survival in comparison with whole brain radiotherapy alone (7). furthermore, whole brain radiotherapy after surgical removal reduces the risk of recurrence compared with surgery alone (16). stereotactic radiosurgery (srs), used since 1980 in north america (17) revolutionized treatment for cerebral metastases and not only. in the present, prospective randomized studies shows that, for selected cases, with 3 or 4 brain metastases, smaller than 2 cm, stereotactic radiosurgery combined with whole brain radiotherapy increase survival in comparison with wbrt alone (18, 19). stereotactic radiosurgery has several advantages, such as: it is easily tolerated by patients, can treat deep sites or tumors located in eloquent areas, that cannot be approached surgical, and may be tried in treatment of some cerebral metastases considered radioresistant, such as those derived from malignant melanoma and kidney cancer (20). postoperative radiation has the main goal to destroy residual tumoral cells from tumor bed or other occult locations. patchell et all showed that when surgical treatment were applied alone, without wbrt, tumor recurred in medium in 27 weeks after surgery in 46% of patients, in whom complete surgical resection was confirmed on mri. romanian neurosurgery (2015) xxix 4 postoperative wbrt decreased recurrence at 10% and prolonged time of recurrence over 52 weeks (16). conclusions cerebral metastases from malignant melanoma have most frequent intratumoral hemorrhages, comparative with other primary sources. common primary sites founded in this study is legs in women and anterior thorax in men. treatment of cerebral metastases is complex, multimodal, implying neurosurgeons, oncologists and radiotherapists. surgical resection combined with postoperative radiotherapy (wbrt or srs) represent the gold standard of treatment for brain metastases. in cases of multiple brain metastases, the particular metastasis which is responsible of main symptomatology has surgical priority and should be resect first. references 1.barnholtz-sloan js, sloan ae, davis fg, vigneau fd, lai p, sawaya re. incidence proportions of brain metastases in patients diagnosed (1973 to 2001) in the metropolitan detroit cancer surveillance system. journal of clinical oncology: official journal of the american society of clinical oncology. 2004;22(14):2865-72. 2.schouten lj, rutten j, huveneers ha, twijnstra a. incidence of brain metastases in a cohort of patients with carcinoma of the breast, colon, kidney, and lung and melanoma. cancer. 2002;94(10):2698-705. 3.ruderman nb, hall tc. use of glucocorticoids in the palliative treatment of metastatic brain tumors. cancer. 1965;18:298-306. 4.cairncross jg, kim jh, posner jb. radiation therapy for brain metastases. annals of neurology. 1980;7(6):529-41. 5.kurtz jm, gelber r, brady lw, carella rj, cooper js. the palliation of brain metastases in a favorable patient population: a randomized clinical trial by the radiation therapy oncology group. international journal of radiation oncology, biology, physics. 1981;7(7):891-5. 6.sause wt, crowley jj, morantz r, rotman m, mowry pa, bouzaglou a, et al. solitary brain metastasis: results of an rtog/swog protocol evaluation surgery + rt versus rt alone. american journal of clinical oncology. 1990;13(5):427-32. 7.patchell ra, tibbs pa, walsh jw, dempsey rj, maruyama y, kryscio rj, et al. a randomized trial of surgery in the treatment of single metastases to the brain. the new england journal of medicine. 1990;322(8):494500. 8.sundaresan n, galicich jh. surgical treatment of brain metastases. clinical and computerized tomography evaluation of the results of treatment. cancer. 1985;55(6):1382-8. 9.galicich jh, sundaresan n, arbit e, passe s. surgical treatment of single brain metastasis: factors associated with survival. cancer. 1980;45(2):381-6. 10.burt m, wronski m, arbit e, galicich jh. resection of brain metastases from non-small-cell lung carcinoma. results of therapy. memorial sloan-kettering cancer center thoracic surgical staff. the journal of thoracic and cardiovascular surgery. 1992;103(3):399-410; discussion -1. 11.vecht cj, hovestadt a, verbiest hb, van vliet jj, van putten wl. dose-effect relationship of dexamethasone on karnofsky performance in metastatic brain tumors: a randomized study of doses of 4, 8, and 16 mg per day. neurology. 1994;44(4):675-80. 12.wolfson ah, snodgrass sm, schwade jg, markoe am, landy h, feun lg, et al. the role of steroids in the management of metastatic carcinoma to the brain. a pilot prospective trial. american journal of clinical oncology. 1994;17(3):234-8. 13.black pm, johnson md. surgical resection for patients with solid brain metastases: current status. journal of neuro-oncology. 2004;69(1-3):119-24. 14.paek sh, audu pb, sperling mr, cho j, andrews dw. reevaluation of surgery for the treatment of brain metastases: review of 208 patients with single or multiple brain metastases treated at one institution with modern neurosurgical techniques. neurosurgery. 2005;56(5):1021-34; discussion -34. 15.sawaya r, hammoud m, schoppa d, hess kr, wu sz, shi wm, et al. neurosurgical outcomes in a modern series of 400 craniotomies for treatment of parenchymal pruna, gorgan particular aspects of cerebral metastases secondary to malignant melanoma tumors. neurosurgery. 1998;42(5):1044-55; discussion 55-6. 16.patchell ra, tibbs pa, regine wf, dempsey rj, mohiuddin m, kryscio rj, et al. postoperative radiotherapy in the treatment of single metastases to the brain: a randomized trial. jama. 1998;280(17):1485-9. 17.pike b, peters tm, podgorsak e, pla c, olivier a, de lotbiniere a. stereotactic external beam calculations for radiosurgical treatment of brain lesions. applied neurophysiology. 1987;50(1-6):269-73. 18.andrews dw, scott cb, sperduto pw, flanders ae, gaspar le, schell mc, et al. whole brain radiation therapy with or without stereotactic radiosurgery boost for patients with one to three brain metastases: phase iii results of the rtog 9508 randomised trial. lancet. 2004;363(9422):1665-72. 19.kondziolka d, patel a, lunsford ld, kassam a, flickinger jc. stereotactic radiosurgery plus whole brain radiotherapy versus radiotherapy alone for patients with multiple brain metastases. international journal of radiation oncology, biology, physics. 1999;45(2):427-34. 20.muacevic a, kreth fw, mack a, tonn jc, wowra b. stereotactic radiosurgery without radiation therapy providing high local tumor control of multiple brain metastases from renal cell carcinoma. minimally invasive neurosurgery : min. 2004;47(4):203-8. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 521-528 doi: 10.33962/roneuro-2019-084 www.journals.lapub.co.uk/index.php/roneurosurgery romanian neurosurgery at european standards. the 45th congress of the “romanian society of neurosurgery” dr. andreea gavrilei2, stud. stefan gradinaru2, stud. mihai-stelian moreanu1, prof. dr. msc. alexandru vlad ciurea3,4 1 “carol davila” university of medicine and pharmacy, bucharest, romania 2 “lucian blaga” university, faculty of medicine and pharmacy, sibiu, romania 3 sanador clinical hospital, department of neurosurgery, bucharest, romania 4 “carol davila” university of medicine and pharmacy, department of neurosurgery, bucharest, romania in romania, neurosurgery has started to develop as a separate speciality since 1935, when prof. al. moruzi set up the first neurosurgery service, at the ”socola” hospital in iassy. then prof. d. bagdasar set up the neurosurgery service at the central hospital in bucharest in 1936. the years have passed and the bucharest clinic of neurosurgery in „gh.marinescu” hospital was developing under the leadership of acad. prof. constantin arseni, and later under the leadership of prof. alexandru constantinovici. contemporary romanian neurosurgery benefiting from the technological explosion and the openness to european neurosurgery , has evolved toward performance. the romanian society of neurosurgery was founded in 1982, the first president being acad. prof. constantin arseni until 1991. the first congress of rsn was held in the same year, and after that the rsn activity raised year by year. today (2019), the committee of romanian society of neurosurgery is formed by: president (assoc. prof. horia ples,md, phd) , honorary president (prof. a.v. ciurea, md,phd, msc, dr.h.c.mult.) three vicepresidents (prof.r.m. gorgan,md,phd ; prof.i. poeata ,md,phd ; lecturer v. saceleanu, md, phd), ex-president (prof. dr. i.s. florian) ,secretary , treasurer,residents representative and three other members. the comitee of rsn is chosen at a period of 2 years (20182020). keywords romanian neurosurgery, the 45th congress of the “romanian society of neurosurgery” corresponding author: alexandru vlad ciurea sanador clinical hospital, department of neurosurgery, bucharest, romania prof.avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 534 andreea gavrilei, stefan gradinaru, mihai-stelian moreanu, alexandru vlad ciurea the rsn congress is held anually, in the autumn season, in the city chosen by vote at the last congress in 2018, the 44th congress of r.s.n. was organized in timisoara between 5 and 8 of september, and was chaired by asocc. assoc. prof. horia ples, md, phd; there, was took the decision that the next annual congress will take place in sibiu. the 45th congress of the romanian society of neurosurgery ((rsn) was held in sibiu, (a historical framework recognized as german burg – hermannstadt founded in 1191), at ramada hotel between 16 and 19 of october, including the 4th francophone medical course and the 3rd symposion of nurses. the 45th congress of the rsn had the full support of ’’lucian blaga’’ university of sibiu and the sibiu city hall. the congress works were opened on the 17th of october, at 9.00, by the congress president, lecturer vicentiu mircea saceleanu, who addressed a welcome word to all participants and stressed the importance of this event to the sibiu neurosurgery center and to romania. (picture 1). picture 1. the welcome words at the 45th congress of romanian society of neurosurgery the whole participation at the rsn congress was impressive 420 participants starting from students in medicine (21%), young residents (18%) to university professors (49%) from both the country and abroad. (picture 2). the entire pathology of tumor neurosurgery, vascular, pediatric, spinal pathology, etc. were addressed. during the scientific event, the whole neurosurgical pathology was adressed: tumoral, vascular,pediatric, spinal, etcthrough 18 scientific sessions, 112 oral presentations (aprox. 20 minute each) and 30 e-posters. among the presentations that have recorded an increased interest there are: abdessamad el ouahabi (maroc)– multimodal treatment of pituitary adenomas, alexandru vlad ciurea (romania) – craniopharingyomas in children / overview of pediatric intracranial arachnoid cysts , stefano ferraresi (italia) – accessory nerve injuries/ lumbosacral plexus injuries, ioan-stefan florian (romania) – posterior fossa tumors at the pediatric age/ neurovascular malformation at the pediatric age, radu mircea gorgan (romania) – prognostic factors associated with survival for brain metastases, 535 romanian neurosurgery at european standards lukas rasulic (serbia) – new horizons in brachial plexus surgery , keki turel (india) complications in skull base surgery, victor volovici (olanda) microvascular education from the lab to the or, from basics to bypass, peter a. winkler (austria) – epilepsy surgery seven steps to improve the results ,grigore zapuhlih (moldova) – hunterian proximal arterial occlusion for giant unclippable intracranial aneurysms, etc. picture 2. an impressive number of participants at the congress of “romanian society of neurosurgery”, 45th edition, sibiu picture 3. special speech transmitted from the president of romania, klaus werner iohannis in the evening, after the first day of congress, the participants were invited to a cocktail reception at the sibiu city hall. lecturer vicentiu saceleanu, as the host of the event, has held a welcome speech. the mayor of sibiu, madame astrid fodor, invited as a 536 andreea gavrilei, stefan gradinaru, mihai-stelian moreanu, alexandru vlad ciurea special guest, has pointed out the importance of the 45th rsn congress for romania and especially for sibiu. to the astonishment of everyone, counselor prof.dr.diana paun came with an encouraging message for the congress events, message especially sent from the president of romania klaus werner iohannis. the organizers were honoured to recieve such a praise. (picture 3). the congress events took place in three halls simultaneously , diverse papers being presented at a time. besides the classical neurosurgical elements that took place during the three days of congress, there were also a young neurosurgeons corner (picture 4) and sessions of the medical assistants (12 % of the congress participants were nurses). picture 4. young neurosurgeons corner – session i in the period of preparations of the congress prof. dr. ioan-stefan florian (picture 5) and prof. dr. alexandru vlad ciurea (picture 6) continuously collaborated to coagulate all the factors that followed the good scientific and organizational development of this event. picure 5. ex-president of rsn prof. ioan ștefan florian, md, phd, head of neurosurgery clinic cluj-napoca 537 romanian neurosurgery at european standards picure 6. honorary president of rsn prof. alexandru vlad ciurea, md, phd, head of neurosurgery department at clinical hospital sanador, bucharest. the congress president, lecturer vicentiu saceleanu, md, phd (picture 7), the president of romanian neurosurgery society – assoc. prof. horia ples, md, phd (picture 8) and the organizing firm medevents have created an appropriate scientific and social framework for such a valuable event. furthermore, a truly remarkable organizational involvement had the sibiu students circle of neurosurgery coordinated by dr. vicentiu saceleanu. such congress should be an example of scientific elevation, organization and social-touristic presentation for the next scientific neurosurgical manifestations. picure 7. vice-president of rsn s.l. dr. vicențiu săceleanu, lecturer at ulb sibiu, head of the neurosurgery department at sibiu county hospital. 538 andreea gavrilei, stefan gradinaru, mihai-stelian moreanu, alexandru vlad ciurea picure 8. president of rsn conf. dr. horia pleș. in the last day of the congress, a session with two special presentations was held : prof. amir samii, md,phd (picture 9) (germania) – “current concepts in the treatment of vestibular schwannomas /auditory midbrain implant: a new approach for hearing restoration in neural deafness”; and prof. saleem abdulrauf, md, phd (picture 10) (sua) – „future directions in microneurosurgery” prof. abdulrauf, using his speaker talent, has fascinated the audience with interactive case presentations, and also created a special and strong bond between him and the young students who attended his lecture. a special praise for akio morita (picture 11) (japan) who presented the top neurosurgical equipment and new elements of science fiction robotics in japanese neuroscience, a dream difficult to accomplish, but not impossible. picture 9. prof. amir samii, md,phd, vice-president of the neuroscience institute hanovra, germany ‘head of the program’ intraoperative mapping and visualization of the human brain” , professor of neurosurgery in hanover; next to lecturer vicențiu săceleanu, md,phd, the rsn congress president 2019. 539 romanian neurosurgery at european standards picture 10. prof. saleem abdulrauf, md,phd , chairman of the department of neurological surgery at saint louis university school of medicine. picture 11. prof. akio morita, md,phd , nippon medical school · department of neurosurgery japan · tokyo 540 andreea gavrilei, stefan gradinaru, mihai-stelian moreanu, alexandru vlad ciurea all of these astonishing presentations were carefully assembled in a very useful book of abstracts that was included in the october edition of the official journal of ’’romanian society of neurosurgery’’. the congress works ended on the 19th of october, where, at the closing ceremony,a surprisingly large number of participants took part, and where the closing remarks offered by prof. al. vlad ciurea ,prof. horia ples and by the congress president, lecturer vicentiu saceleanu underlined once more the high quality of all scientific and social manifestations and the excellent organization, thus making the 45th congress of rsn one of the most successful scientific events organized by far. next year , in the autumn of 2020 we invite you in bucharest, the capital city of romania, to participate at the works of the 46th congress of romanian society of neurosurgery – in memoriam of the founder prof.dr.constantin arseni, organised by prof.dr.r.m.gorgan – the head of the ’’bagdasararseni’’ neurosurgical clinic. ultimately , we go back to the first statements and we consider the remark of dr. madjid samii (ini center, hanovra) presented at 43rd congress of romanian society of neurosurgery held in clujnapoca (2017): ”romanian neurosurgery is situated at european level”. 6prunavioleta_therapeutic romanian neurosurgery (2015) xxix (xxii) 1: 51 58 51 therapeutic results in sixth nerve palsy violeta ioana pruna1, daniela cioplean2, liliana mary voinea3 1ph.d student in ophthalmology “carol davila” university of medicine and pharmacy bucharest, faculty of medicine, department of ophthalmology 2oftapro clinic, bucharest 3universitary emergency hospital, bucharest abstract: authors aim to assess through a retrospective study the efficiency of different therapeutic methods used in vith nerve palsy. 60 patients with vith nerve palsy, admitted and treated in oftapro clinic, were divided into two groups: a group with partial dysfunction (paresis) of sixth nerve and a group with the complete abolition of neuromuscular function (vith nerve palsy). initial examination included assessment of neuromuscular function, binocular vision and existence of medial rectus muscle contracture (ipsiand contralateral) and contralateral lateral rectus inhibitory palsy. neuromuscular dysfunction was graded from 8 (paralysis) to 0 (normal abduction). therapeutic modalities ranged from conservative treatment (occlusion, prism correction), botulinum toxin chemodenervation and surgical treatment: medial rectus recession + lateral rectus resection, in cases of paresis, and transposition procedures (hummelscheim and full tendon transfer) in cases of sixth nerve palsy. functional therapeutic success was defined as absence of diplopia in primary position, with or without prism correction, and surgical success was considered obtaining orthoptic alignment in primary position or a small residual deviation (under 10 pd). 51 patients had unilateral dysfunction, and 9 patients had bilateral vi-th nerve dysfunction. 8 patients had associated fourth or seventh cranial nerves palsy. the most common etiology was traumatic, followed by tumor and vascular causes. there were 18 cases of spontaneous remission, partial or complete (4-8 months after the onset), and 6 cases enhanced by botulinum toxin chemodenervation. 17 paretic eyes underwent surgery, showing a very good outcome, with restoration of binocular single vision. the procedure of choice was recession of medial rectus muscle, combined with resection of lateral rectus muscle. all patients with sixth nerve palsy underwent surgery, except one old female patient, who refused surgery. hummelscheim procedure was applied in 19 cases, and full tendon transfer in 6 cases. in 13 cases partial results were obtained, who needed further prismatic correction or reintervention. in 12 cases the outcome was very good, with restoration of binocular single vision, without prismatic correction. therapeutic success in sixth nerve palsy depends on accurate assessment of neuromuscular dysfunction and appropriate choice of therapeutic modality for each case. interdisciplinary collaboration is mandatory for correct etiologic diagnosis of sixth nerve palsy. key words: paresis, paralysis, nerve vi, recession, resection, botulinum toxin. 52 pruna et al therapeutic results in sixth nerve palsy introduction sixth nerve palsy is one of the most common cranial nerves palsies, because of the long intracranial route of this nerve. patel, mutyala, leske, hodge, and holmes found an incidence of 11,3/100000 in a population – based study (1). the most frequent causes they described are: undetermined (26%), hypertension alone (19%), coexistent hypertension and diabetes (12%), trauma (12%), multiple sclerosis (7%), neoplasm (5%), diabetes alone (4%), cerebrovascular accident (4%), post neurosurgery (3%), aneurysm (2%), and other (8%). peters et all. founded in their work central nervous system mass lesions and multiple sclerosis as the most common causes for a sixth nerve palsy in a 20 – 50 years age group (traumatic cases were excluded) (2). they reported that patients with tumoral etiology had the lowest rate of spontaneous recovery (3). in other publication trauma was the most common etiology, followed by viral infections, tumors and cerebral ischemia. although positive diagnosis is obvious in almost all cases, sometimes differential diagnosis may raise difficulties. thyroid eye diseases, myasthenia gravis, duane’s syndrome, spasm of the near reflex, and medial orbital wall fracture may mimic an isolated sixth nerve palsy (4). treatment may be conservative and/or surgical, but a waiting period of at least 6 months to 1 year should be consider prior to any surgery, for the eventuality of spontaneous recovery (5). objective the authors aim to assess trough this retrospective study the efficiency of different therapeutic methods used in sixth nerve palsy. material and methods the records of 60 patients with sixth nerve palsy, admitted and treated in oftapro clinic between january 2009 and december 2013, were reviewed, in order to assess the efficiency of different therapeutic methods used in sixth nerve palsy. the etiology was correlated with age and the degree of neuro-muscular dysfunction. in the evaluation criteria of sixth nerve palsy were included: measuring of primary and secondary deviation (in prism diopters), evaluating the degree of abduction (from 0 = full abduction, to – 8 = complete abolition of abduction, with the eye immobilized in extreme adduction), finding of ipsilateral and contralateral medial rectus contracture and contralateral lateral rectus inhibitory paresis (active and passive duction tests). the associated neuro-muscular dysfunctions were, also, noted (other cranial nerves paresis or palsies), as association of optic nerve atrophy (partial or total). the treatment was differentiated according to degree of neuro-muscular dysfunction, to the purpose and the intended result, and according to patient’s expectations and options. conservative treatment consisted of alternating occlusion, follow up and/or prismatic correction. minimally invasive treatment meant botulinum toxin chemodenervation. surgical treatment were applied as follows: ipsilateral medial rectus recession, combined with ipsilateral lateral rectus resection in cases with partial neuromuscular dysfunction and transfer procedures (hummelscheim, combined or not with contralateral medial rectus recession, full tendon transfer simple or augmented, or combinations of these). surgical success was romanian neurosurgery (2015) xxix (xxii) 1: 51 58 53 defined as orthoptic alignment in primary position or a residual esotropia, less than 12 pd, and surgical failure was considered when postoperative deviation was greater than 12 pd. functional therapeutic success was defined as absence of diplopia in primary position, either partial, in which cases binocular single vision was achieved by prismatic correction for distance or for both, distance and near, or complete, with no need for prismatic correction. results 31 men and 29 women, aged between 4 months and 81 years, had sixth nerve palsy, unilateral in 59 cases and bilateral in 9 patients (59 eyes). in 43 eyes the deficit was partial (paresis) and 26 eyes manifested complete abolishment of neuro-muscular function (sixth nerve palsy). most cases had traumatic etiology (32 patients), especially by car crashes (24 cases), followed by fall from height (7 cases) and one perinatal craniocerebral trauma. next frequent etiology was vascular (12 cases), hta being most commonly incriminated, either alone (6 eyes), or in association with diabetes mellitus, dyslipidemia and/or cardiac insufficiency (6 cases). tumoral etiology had almost equal frequency, involving 11 eyes. multiple sclerosis was not insignificant, being responsible of 5 cases of sixth nerve palsy. in 2 cases, sphenoidal sinusitis was incriminated as etiology, one case after empyema and klebsiella meningitis, one case after repeated febrile relapses with seizures, and one case post immunization. the etiology were unable to be determined in 3 cases (to note that among these, one female patient gave birth to 10 times). table i etiology (age related) etiology age <10 years 11-20 years 21-30 years 31-40 years 41-50 years 51-60 years 61-70 years >71 years car crashes 0 1 5 7 2 2 2 0 fall from height 0 1 1 2 0 1 0 0 perinatal trauma 1 0 0 0 0 0 0 0 cns tumors 2 1 2 1 2 1 1 0 hta 0 0 0 0 0 0 3 3 hta in association 0 0 0 0 0 1 2 3 multiple sclerosis 0 0 1 1 2 1 0 0 sphenoidal sinusitis 0 1 1 0 0 0 0 0 empyema 1 0 0 0 0 0 0 0 febrile seizures 1 0 0 0 0 0 0 0 postvaccinal 0 1 0 0 0 0 0 0 multiparity 0 0 0 1 0 0 0 0 unknown 0 0 1 1 0 0 0 0 54 pruna et al therapeutic results in sixth nerve palsy graph 1 neuromuscular deficit on each eye both tumors and trauma had predilection for younger ages (third and fourth decades), while vascular etiology was most frequent among the elders. traumatic etiology interested a little more male than female patients (14 of 25), and was responsible for all bilateral cases and for most cases with complete abolition of abduction (17 of 32 eyes). tumoral and vascular causes produced more paresis. 8 patients had associated neuromuscular dysfunctions: 4 of them had a fourth nerve palsy, and the other 4 had an associated seventh nerve palsy. 5 patients had optic atrophy in the affected eye (4 partial and one total optic nerve atrophy). the primary deviation in paresis cases varied from 12 to 55 pd (prism diopters) esotropia (average 29,30 pd) for distance and from 8 to 50 pd (average 23,67) for near, while secondary deviation was about 30 pd for distance and 27,68 pd for near. in cases of sixth nerve palsy, deviations was greater than in paresis cases, varying from 35 to 80 pd esotropia (average 56,20 pd) at distance and from 30 to 70 pd at near (average 49,20 pd). secondary deviation was just slightly larger than primary deviation (57,20 pd at distance and 50,2 pd at near) which is explained by the fact that waiting period before surgery was greater, thereby medial rectus contracture and, in some cases, contralateral lateral rectus inhibitory paresis had time to install, reducing thus incomitance. ipsilateral medial rectus contracture was present in 19 cases and contralateral medial rectus contracture was shown in 13 cases. contralateral lateral rectus inhibitory paresis developed in 7 cases. limitation of abduction in paresis ranged from – 1 to – 6 (average – 3,13) and was quasicomplete in palsies – 8 (2 cases with – 7), average – 7,92. 0 5 10 15 20 25 paresis palsies 22 11 21 15 neuromuscular deficit od os romanian neurosurgery (2015) xxix (xxii) 1: 51 58 55 table ii means of measurements of deviations (in prism diopters) paresis palsies initial primary et at distance 29,30 56,2 initial primary et at near 23.67 49,29 initial secondary et at distance 33 57,20 initial secondary et at near 27,68 50,2 final primary et at distance 3,34 9,32 final primary et at near 1,55 5,4 final secondary et at distance 3,82 9,24 final secondary et at near 1,97 5,16 conservative treatment was applied in 18 cases of sixth nerve paresis, consisting in alternating occlusion (10 cases) with follow up and prismatic correction 8 cases). 7 of these patients showed partial recovery at 5 to 6 months from beginning and needed permanent prismatic correction, for distance (5 patients) or both, for distance and near (2 patients). 11 patients demonstrated complete recovery, without need for prismatic correction, at 3 to 11 months from onset. spontaneous recovery rate without any treatment but alternating occlusion or prismatic correction was 30%. when botulinum toxin was used to enhance the recovery of neuro-muscular deficit, the rate of remission was raised up to 40%. vascular and mild traumatic etiology, as well as young patients showed highest recovery rate. botulinum toxin chemodenervation was used in 6 paretic and 1 paralitic eyes (one bilateral case paresis – palsy). in all cases, btxa potentiated partial (one case) or complete recovery (5 cases), except the last one, who needed further surgery. the waiting period was at least 8 months before surgery, to permit the chance of eventual spontaneous recovery of deficit. in one case with bilateral sixth nerve paresis after empyema and klebsiella meningitis, bilateral medial rectus recession was performed, with excellent outcome. in the rest of paretic eyes, medial rectus recession combined with lateral rectus resection was the procedure of choice. in one of these eyes, the surgery was performed after botulinum toxin chemodenervation (at 8 months). an inferior oblique muscle surgery (one inferior oblique recession and one miectomy) was associated in 2 cases. surgical results were good, except one case who needed further reintervention (lateral rectus re-resection). functional outcome showed partial recovery in 5 eyes and complete remission in 13 eyes. postoperative deviations were significantly reduced to an average of 3,34 pd at distance and 1,55 pd at near, thus resulting a correction of approximately 25,96 pd for distance and 22,12 pd for near. abduction was enhanced from an average of – 3,13 to – 0,53, showing an improvement about 83,06%. in paralytic group, a 78 years old patient refused surgery, because poor perception of diplopia, due to a very large deviation, and because she was not concerned with aesthetics. hummelsheim procedure alone was performed in 7 eyes, and in other 7, who developed contralateral medial rectus contracture, it was combined with contralateral medial rectus recession. in another case, hummelscheim technique was 56 pruna et al therapeutic results in sixth nerve palsy performed after botulinum toxin chemodenervation (the bilateral case paresis – palsy). 2 patients underwent associated surgery on the inferior oblique muscle, for fourth nerve palsy. one case had a reintervention after failed recession – resection procedure. full tendon transfer was done in 6 cases one simple, one augmented (foster technique), 3 combined with ipsilateral medial rectus recession and 1 combined with bilateral medial rectus recession. reoperation was necessary in one case (with full tendon transfer alone), and bilateral medial rectus recession was done. surgical failure appeared in 2 cases one above mentioned, and one who refused further surgery. partial correction was the outcome in 9 cases, 6 of them needed prisms for distance, and 3 patients needed prisms for both distance and near, in order to achieve binocular vision. in 10 cases, a good postoperative result was achieved, with restoration of binocular vision, both for distance and near. postoperative esodeviation measured an average of 9,23 pd for distance and 5,4 pd at near that means a reduction of 46,88 respective 43,8 pd of esotropia. the degree of abduction was improved from – 7,92 preoperative to – 3,4 postoperative. graph 2 overall functional results no operative or postoperative complications were noted. discussions in contrast to literature data, showing the main etiology as vascular or unidentified, we found a higher proportion of traumatic etiology, and, also, a significant number of tumoral causes in our patients (6). this may be due to the fact that many vascular patients arrived first in neurological services, and vascular etiology cases having a higher rate of spontaneous recovery, these patients do not get the ophthalmologist, since they see their condition improves in time. most of the functional recovery, 36 prisms for distance, 14 prisms for distance and near, 8 functional failure, 2 0 5 10 15 20 25 30 35 40 romanian neurosurgery (2015) xxix (xxii) 1: 51 58 57 patients with sixth nerve paresis have indication for botulinum toxin chemodenervation (7, 8), but many of them refuse this option, because of fear of muscle damage, or because this is a temporary solution and last but not least for financial reasons. nevertheless, our findings that coincide with literature data, shows that botulinum toxin chemodenervation promotes an accelerated recovery of the deficit, inhibit the development of medial rectus contracture, and relieves symptoms of diplopia (8). the waiting period recommended in specialized books should be respected, as we found many patients (30%) who have recovered their lost function even after 11 months of disease onset. when surgery is recommended, it should be done, as postoperative results are very good, with restoration of binocular vision in most of the cases. our postoperative results show a very good outcome in 60,60% of cases, 18,18% of patients needed prismatic correction just for distance, and same percent needed prisms for both distance and near. only 3,03% were considered functional failure. this outcome is in agreement with published results of holmes et all (5), in which shows an overall surgical success rate of 75%. when cases are carefully selected and surgical indication is well chosen, the results are excellent and reintervention rate is greatly diminished. holmes in his studies found some predictive factors for spontaneous recovery and stated that “in acute traumatic sixth nerve palsy or paresis, failure to recover by 6 months after onset was associated independently with inability to abduct past midline at presentation and bilaterality. although the overall recovery rate is high in acute traumatic sixth nerve palsy or paresis, a complete or bilateral case has a poor prognosis and is more likely to need strabismus surgery.” (9) king et all found a spontaneous recovery rate in their series of 78.4%, but traumatic etiology was excluded (10). on the other hand, mutyala and holmes stated that “spontaneous recovery from isolated traumatic sixth-nerve palsy may be lower than previously reported. a prospective study is needed to provide a more accurate estimate of recovery rate” (11). volpe searched the mechanism of spontaneous recovery in tumoral sixth nerve palsies and found that “possible mechanisms for recovery include remyelination, axonal regeneration, relief of transient compression (eg, resorption of hemorrhage), restoration of impaired blood flow, slippage of a nerve previously stretched over the tumor, or immune responses to the tumor” (12). conclusions the functional and surgical success in sixth nerve palsy depends on accurate assessment of degree of neuromuscular dysfunction and appropriate choice of therapeutic modality for each case. a waiting period of at least 6 months to 1 year should be consider prior to any surgery, to track the event of spontaneous recovery of neuro-muscular function. interdisciplinary collaboration is mandatory for correct etiologic diagnosis of sixth nerve palsy. vascular etiology should be remain an exclusion diagnosis, after more serious and life-threatening conditions have been ruled-out. botulinum toxin chemodenervation for paretic cases should be 58 pruna et al therapeutic results in sixth nerve palsy encouraged, both by ophthalmologist and neurologist, as it provide the chance for earlier recovery and is a minim invasive and reversible procedure. references 1. patel sv, mutyala s, leske da, hodge do, holmes jm. incidence, associations, and evaluation of sixth nerve palsy using a population-based method. ophthalmology. feb 2004;111(2):369-375. 2. peters gb, 3rd, bakri sj, krohel gb. cause and prognosis of nontraumatic sixth nerve palsies in young adults. ophthalmology. oct 2002;109(10):1925-1928. 3. bagheri a, babsharif b, abrishami m, salour h, aletaha m. outcomes of surgical and non-surgical treatment for sixth nerve palsy. journal of ophthalmic & vision research. jan 2010;5(1):32-37. 4. gunter k. von noorden ecc. binocular vision and ocular motility: theory and management of strabismus. 6th edition ed. 5. holmes jm, leske da. long-term outcomes after surgical management of chronic sixth nerve palsy. journal of aapos : the official publication of the american association for pediatric ophthalmology and strabismus / american association for pediatric ophthalmology and strabismus. oct 2002;6(5):283-288. 6. moster ml, savino pj, sergott rc, bosley tm, schatz nj. isolated sixth-nerve palsies in younger adults. archives of ophthalmology. sep 1984;102(9):1328-1330. 7. dutton jj, fowler am. botulinum toxin in ophthalmology. survey of ophthalmology. jan-feb 2007;52(1):13-31. 8. holmes jm, beck rw, kip ke, droste pj, leske da. botulinum toxin treatment versus conservative management in acute traumatic sixth nerve palsy or paresis. journal of aapos : the official publication of the american association for pediatric ophthalmology and strabismus / american association for pediatric ophthalmology and strabismus. jun 2000;4(3):145-149. 9. holmes jm, beck rw, kip ke, droste pj, leske da, pediatric eye disease investigator g. predictors of nonrecovery in acute traumatic sixth nerve palsy and paresis. ophthalmology. aug 2001;108(8):1457-1460. 10. king aj, stacey e, stephenson g, trimble rb. spontaneous recovery rates for unilateral sixth nerve palsies. eye. 1995;9 ( pt 4):476-478. 11. mutyala s, holmes jm, hodge do, younge br. spontaneous recovery rate in traumatic sixth-nerve palsy. american journal of ophthalmology. dec 1996;122(6):898-899. 12.volpe nj, lessell s. remitting sixth nerve palsy in skull base tumors. archives of ophthalmology. oct 1993;111(10):1391-1395. doi: 10.33962/roneuro-2020-062 chondrosarcoma in petroclival synchondrosis without visual change. a case report messias villa mendonça, joão italo fortaleza de melo, raphael oliveira r. f. netto, victor augusto r. fernandes, luiz dias dutra, marina de farias g. mendonça, micaias conde simões romanian neurosurgery (2020) xxxiv (1): pp. 400-404 doi: 10.33962/roneuro-2020-062 www.journals.lapub.co.uk/index.php/roneurosurgery chondrosarcoma in petroclival synchondrosis without visual change. a case report mesías villa mendonça1, joão italo fortaleza de melo1, raphael oliveira ramos franco netto1, victor augusto ramos fernandes², luiz dias dutra1, marina de farias guelfi mendonça1, micaias conde simões1 1 radiology and diagnostic imaging center, cerdil, dourados-ms, brazil 2 laboratory of tissue morphology, faculty of medicine of jundiaífmj, jundiaí-sp, brazil abstract chondrosarcomas are a heterogeneous group of malignant bone tumours that share the production of the chondroid matrix in common. at the base of the skull, they are most commonly found in the region of the various synchondroses with an affinity for the petroclival fissure, they are locally invasive tumours, with little capacity to perform metastasis. the age group affected is variable, however, they frequently occur in middle-aged adults. its clinical manifestation depends on the location and local extent; headache or paralysis of cranial nerves, particularly of the vi nerve is a frequent sign. as the petrous apex cannot be viewed directly, imaging studies such as computed tomography and magnetic resonance imaging play an important role in the evaluation of injuries. we present a case of a 36-year-old patient with chondrosarcoma of petroclival syndromes without visual changes. for the identification of this pathology, a battery of imaging tests was used and the diagnosis was made assertively, preserving the best choices for the treatment of the patient. introduction chondrosarcomas (cs) is a heterogeneous group of malignant bone tumors that share in common the production of the chondroid (cartilaginous) matrix. cartilaginous tumors are almost always found in bones that arise from endochondral ossification, noting in the growth plate, the proliferation and hypertrophic cell differentiation of chondrocytes, which undergo apoptosis, followed by subsequent local invasions by vessels and osteoblasts, thus initiating the matrix formation, which consequently leads to longitudinal bone growth. chondrosarcomas of the skull are rare and have a higher incidence in keywords tomography, x-ray computed, diagnostic imaging, chondrosarcoma corresponding author: raphael oliveira ramos franco netto radiology and diagnostic imaging center, cerdil, dourados-ms, brazil raphael_ fn@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 401 chondrosarcoma in petroclival synchondrosis without visual change male patients in a 2:1 ratio. they are usually diagnosed around the third and fourth decades of life(1,2). at the base of the skull, they are most commonly found in the region of the various synchondroses that remain after ossification of the embryonic chondroid matrix, with an affinity for the petrooccipital (petroclival) fissure. therefore, they present as para-sagittal tumors. these tumors are locally invasive, with little capacity to metastasize. they spread through the petroclival fissure, involve the clivus, the petrous portion of the temporal bone, and are more prominent in cisterns or soft tissues at the base of the skull (5,6). case report a 36-year-old female patient enters a private clinic in the city of dourados-ms-brazil with headache, otalgia, runny nose, dysphonia, hyposmia, postural vertigo, weight loss of 5 kg and without visual changes. rhinoscopy procedure was performed after clinical examination, which detected a “vegetating” lesion in the nasopharynx. a biopsy of the rhino pharynx tumor was then requested, with the removal of numerous irregular fragments of tissues with a light-brown surface, finely granular and fibroelastic, sent for anatomopathological analysis and initial imaging investigation with multislice computed tomography of the skull and magnetic resonance (mr) of the brain. the anatomopathological result suggested cartilaginous neoplasia with hypercellularity and nuclear hyperchromasia, concluding a histological aspect that could correspond to grade 1-2 chondrosarcoma depending on the correlation with clinical and radiological data. the multislice computed tomography of the skull (figures 1 and 2) showed an expansive, heterogeneous and predominantly hypodense lytic lesion, with foci of calcification in the aspect of “popcorn” in-between, with irregular contours and defined limits, which presents a slight enhancement and predominantly peripheral after the infusion of the contrast medium, with an epicenter in the right petroclival synchondrosis. this formation invades the petrous region of the temporal bone and part of the sphenoid wing anterolaterally, without invading the orbital accumulation; extends medially and inferiorly through the jugular foramen, widening it, to the cerebellar point angle, right lateral wall of the cavum, part of the clivus and without cleavage planes with the internal carotid artery, sphenoid sinus, and lateral retropharyngeal space, with consequent obliteration of the corresponding parapharyngeal space; it later compromises part of the cerebellum and the occipital condyle; finally, it affects the locoregional temporal lobe superiorly. the result of brain nuclear magnetic resonance figure (3 and 4) suggested an expansive lesion whose epicenter is in the right petroclival synchondrosis, with erosion and bone destruction, characterized by an intermediate signal in t1, marked hypersignal in t2-weighted sequences, with some foci hypointense inside (calcification) and intense impregnation utilizing paramagnetic contrast. this lesion exhibits a component extending anteriorly and inferiorly to the retropharyngeal region and carotid space, maintaining close contact with the internal carotid artery and with the internal jugular vein, displacing the posterior wall of the rhino pharynx. subsequently, the lesion occupies the cistern of the cerebellar-cerebellar and cerebellar-bulbar angles, causing an impression on the right anterolateral face of the bridge and bulb and the anterior face of the cerebellar hemisphere, extending further to the jugular foramen, petrous apex and part of the condyle occipital rights. superiorly it extends to the parasellar region where it probably involves the cavernous sinus and circumferentially the internal carotid artery, also determining the impression on the medial aspect of the corresponding temporal lobe. figure 1. a. axial ct scan using computed tomography, showing an expansive lytic lesion predominantly hypodense, with an epicenter in the right petroclival synchondrosis. b. post-contrast axial and coronal section ct, showing slight and heterogeneous contrast to the contrast medium. 402 messias villa mendonça, joão italo fortaleza de melo, raphael oliveira ramos franco netto et al. figure 2. a, bct axial axial section in bone window, showing the lytic aspect of the lesion, and calcifications in “popcorn”. figure 3. a-axial t1-weighted mri showing an intermediate sign of the expansive lesion in petroclival synodrosis. baxial and coronal mri, weighted in t1 after contrast, showing enhancement by gadolinium. 403 chondrosarcoma in petroclival synchondrosis without visual change figure 4. a-axial t2-weighted mri, showing a high sign of the referred lesion. bdiffusion-weighted axial mri showing a high signal in the adc values. discussion chondrosarcoma is a cancer of chondral origin, rare, slow-growing, locally advanced and with aggressive behavior, constituting 0.15% of all intracranial neoplasms, making up the third most common cause of primary bone malignancy, after multiple myeloma and the osteosarcoma. approximately 25% of all cranial chondrosarcomas occur at the base, representing 6% of all neoplasms at this site (1). this type of tumor has a slow growth, constituting locally 404 messias villa mendonça, joão italo fortaleza de melo, raphael oliveira ramos franco netto et al. aggressive neoplasms that makeup 0.15% of all intracranial tumors, being capable of generating bone, cartilage or even tissues without cartilage constituents (1,2). embryology findings suggest the hypothesis that cranial-based chondrosarcomas may originate from multipotential mesenchymal cells or remnants of embryonic cartilage from cranial synchondrosis. the various plaques that remain after ossification of the chondroid fissures remain as growth sites for these tumors, and the most common tumor origin sites described were petroclival, petro-occipital, sphenocecipital, and spheno-petrous synchon-droses, with a propensity for the first, that is, constituting parasagittal tumors in the majority. other locations of expected impairment are the midline, more specifically in the basisphenoid/basioccipital, which are structures related to sphenoccipital cleft, and less commonly the junction between the nasal septum and the sphenoid face (1,3). histologically, chondrosarcomas are divided into conventional subtypes (myxoid and hyaline type), differentiated, clear cells and mesenchymal (1). the conventional form is the most common type at the base of the skull, being further subdivided into three classes: well-differentiated (grade i), moderately differentiated (grade ii) and poorly differentiated (grade iii) (1). the age range affected is variable; however, they often occur in middle-aged adults. the presentation depends on the location and the local extension; headache or paralysis of cranial nerves, particularly of the vi (abducent) nerve is a frequent sign. however, the patient, in this case, showed no signs and symptoms of visual impairment despite being diagnosed with petroclival chondrosarcoma (5). as the petrous apex cannot be viewed directly, the radiological image plays a crucial role in the evaluation of injuries (4). computed tomography (ct) presents a varied pattern, depending on the amount of the chondroid matrix. generally, there are components of soft parts with a dense appearance in the non-contrast phase and enhanced by the iodinated agent. calcifications are characteristic, but not always present. a magnetic resonance imaging (mri), these tumors usually present an intermediate signal at t1, a high signal at t2, with heterogeneous impregnation after the gadolinium injection (5,6). the main differential diagnoses include cholesteatoma of the petrous apex, calcified meningioma, chondromyxoid fibroma, chordoma, plasmacytoma, nasopharynx carcinoma, and metastases. conclusion imaging examinations such as computed tomography and magnetic resonance become an important means of evaluation in this type of injury due to its difficult anatomical presentation. the indicated treatment combines surgery with several types of radiation; eventually, it consists exclusively of radiotherapy. complete surgical excision is usually not feasible due to its location and proximity to neurovascular structures. however, as the growth pattern is slow, the prognosis is good (99% in 10 years). although the vi cranial pair is affected in this type of injury, no characteristic visual symptoms were observed in the studied patient, highlighting the importance of the case report presented. references 1. sbaihat a, bacciu a, pasanisi e, sanna m. skull base chondrosarcomas: surgical treatment and results. ann otol rhinol laryngol 2013; 122: 763–70. 2. pinna f de r, wiikmann c, chung d, lessa mm, voegels rl, botugan o. condrossarcoma nasal: relato de caso. rev bras otorrinolaringol 2003; 273–6. 3. hu j, van valckenborgh e, menu e, de bruyne e, vanderkerken k. understanding the hypoxic niche of multiple myeloma: therapeutic implications and contributions of mouse models. dis model mech 2012; 5: 763–71. 4. razek aa, huang by. lesions of the petrous apex: classification and findings at ct and mr imaging. radiographics 2012; 32: 151–73. 5. harnsberger ric h. diagnostic ima-ging: head and neck. elsevier saunders 2005; 1st edition; i-3: 58-61. doi: 10.33962/roneuro-2021-006 single-session treatment of bilateral, tandem, internal carotid artery aneurysms with pipeline flex with shield technology rares cristian filep, lucian marginean, andrei florin bloj, istvan szikora romanian neurosurgery (2021) xxxv (1): pp. 36-39 doi: 10.33962/roneuro-2021-006 www.journals.lapub.co.uk/index.php/roneurosurgery single-session treatment of bilateral, tandem, internal carotid artery aneurysms with pipeline flex with shield technology rares cristian filep1, lucian marginean1, andrei florin bloj1, istvan szikora2 1 university of medicine, pharmacy, sciences and technology “george emil palade”, phd school of medicine, targu mures, romania 2 national institute of clinical neurosciences, department of neurointerventions, budapest, hungary abstract the treatment of intracranial aneurysms (ia) has been transformed by the development of flow-diversion (fd) devices. initially, these revolutionary devices were conceived for giant and fusiform aneurysms located on the internal carotid artery (ica). technological improvements have expanded their indications. distal middle cerebral, anterior cerebral artery aneurysms, or even posterior fossa aneurysms can now benefit from this technology. one other category of aneurysms that can be treated is multiple ia’s. multiple ia’s are encountered in approximately one-quarter of patients presenting with subarachnoid haemorrhage. endovascular management of such cases is complex, requiring different devices and treatment strategies to secure all lesions. fd’s can be successfully employed to reconstruct vessels, which harbour more than one aneurysm, especially multiple ica lesions. multiple aneurysms located on both ica’s are generically known as tandem aneurysms. we present the case of a patient with tandem aneurysms located on both intracranial internal carotid arteries that we treated simultaneously with the pipeline flex with shield technology in one single session. to the best of our knowledge, this is the first case reported in the literature so far. introduction multiple intracranial aneurysms (ia) are found in up to 30% of patients with subarachnoid haemorrhage.1 endovascular cure of multiple ia’s by simple coiling with or without balloon or stent assistance, performed in one single session, has been assessed in previous studies, as having high procedural success rates and a low number of complications. 2,3 alternatively, only small patient series have explored the safety and efficacy of flow-diverters for multiple ia, especially as a one-stage treatment.4 keywords multiple intracranial aneurysms, flow-diversion, surface modification corresponding author: lucian marginean university of medicine, pharmacy, sciences and technology “george emil palade”, phd school of medicine, targu mures, romania go2lucian@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 37 single-session treatment of bilateral, tandem, internal carotid artery aneurysms our case highlights the treatment of three intracranial aneurysms located on both internal carotid arteries (ica), with two pipeline flex with shield technology devices implanted bilaterally in one single session. this is, to the best of our knowledge, the first case reported in the literature pertaining to the use of this device in bilateral, tandem intracranial aneurysms. case report a 53-year-old female was brought in the emergency department with acute onset headache, dizziness, and nausea. neurological examination revealed a conscious patient, gcs 15, with 1 point on the hunt&hess scale. ct showed mfisher 2 subarachnoid hemorrhage and multiple intracranial aneurysms (not shown). catheter angiography was performed the next day demonstrating 5 aneurysms, one on the anterior communicating artery (aca), one on the basilar tip, and 3 on both ica’s, in the ophthalmic segments. based on the morphologic characteristics and the distribution of the blood on ct, a decision was made to coil the basilar tip and the aca aneurysms, while the ica lesions remained to be treated with flow-diversion in a further session. simple coiling was performed under general anaesthesia for the two aneurysms mentioned above, without clinical complications and a good neurological outcome (fig. 1 b, c). due to the lack of flow-diverter devices in our department at that time, the patient was scheduled nine months later for endovascular treatment of the remaining 3 ica aneurysms in one single session. the patient received 75mg aspirin, and 75mg clopidogrel for 2 weeks before the intervention. no platelet function test was used before the intervention. under general anaesthesia, a 7f destination long sheath (terumo, tokyo, japan) was placed consecutively in the left and right common carotid arteries, and a 6f navien intracranial support catheter (medtronic, california, usa) was navigated in the intracranial ica. phenom 27 microcatheters with 0,014” avigo guidewires (medtronic, california, usa) were used for distal navigation and flowdiverter implantation. based on the vessel measurements, two pipeline flex with shield technology devices (medtronic, california, usa), 4x20mm on the left and 4x25 mm on the right, were successfully deployed in both ica’s without periprocedural complications (fig. 1, 2 b, c). the patient was discharged two days later without neurological deficits, mrs 0. dual antiplatelet therapy was continued for 6 months, and a control angiogram was performed. it showed complete obliteration of all aneurysms. (figures 1, 2 d). afterwards, clopidogrel was discontinued, while aspirin remained as a life-long treatment. figure 1. a. volume rendered depiction of the right ica shows the broad-neck aneurysm located in the ophthalmic segment. b, c. dsa and unsubtracted image in the “working” projection. note the two coil masses at the top of the images, representing the previously coiled anterior communicating and basilar tip aneurysms. d. at 6-months the aneurysm is completely occluded. ica=internal carotid artery; dsa=digital subtraction angiogram. 38 rares cristian filep, lucian marginean, andrei florin bloj et al. figure 2. a. virtual rendered angiogram of the left ica denoting the two elongated aneurysms located in the ophthalmic segment. b, c. dsa and unsubtracted view in the “working” projection showing the position of the device. d. 6-months control angiogram highlighting the complete obliteration of the two aneurysms. ica=internal carotid artery; dsa=digital subtraction angiogram discussions flow-diverter devices have revolutionised the treatment of intracranial aneurysms. large, widenecked, even fusiform, or dissecting, can benefit from the concept of flow-diversion, progressive intra-aneurysmal thrombosis, endothelialisation of the aneurysm neck and subsequent vessel reconstruction5,6. one of the first devices to implement these notions was the pipeline embolization device (ped) (medtronic, california, usa). currently at its third generation, the pipeline flex with shield technology, incorporates a phosphorylcholine surface modification, that acts to reduce the risk of platelet aggregation and thrombosis7. the use of this device for the cure of ica aneurysms is safe and efficacious, with low complication rates, as reported in a recent study8. however, its employment, as a solution for multiple ia, especially in both ica’s, in one single treatment session, has not been reported before. we based our decision to implant two devices for all five aneurysms as a one-shot therapy, based on a number of arguments: one single procedure implies the use of general anaesthesia and femoral artery puncture once, consequently avoiding their inherent risks; furthermore, only one set of devices for access and flow-diverter deployment during the same hospital admission would be more cost-effective. on the other hand, bilateral flow-diverter implantation can expose the patient to a higher risk of specific complications. in-stent thrombosis and distal thromboembolic events were encountered in 4.7% of cases in the intreped study,9 although older generation ped’s, without surface modification, were used. the phosphorylcholine surface theoretically ensures a smaller rate of thromboembolic complications, confirmed in a more recent prospective trial.8 the more dreaded haemorrhagic complications of flow-diverter treatment, delayed aneurysm rupture and delayed intraparenchymal bleeding, can be a reason for concern if a singlesession, bilateral implantation is contemplated. spontaneous aneurysm rupture can occur in up to 1% of cases,9 especially if large or giant aneurysms are treated, which was not the case in our patient, the largest aneurysm having a maximal diameter less than 10 mm. intraparenchymal haemorrhage and its pathophysiological mechanisms are still a matter of debate. if haemorrhagic transformation of small infarcts generated by microemboli are the main cause, the surface modification of the device, can potentially, reduce the likelyhood of such events. otherwise, the “windkessel” effect is another mechanism incriminated. it relates mainly to the aneurysm size and its capacitance role, which in our case would not be a matter of concern due to their small to medium size.10 conclusion flow-diversion can be a safe and effective therapeutic alternative for multiple intracranial aneurysms, with low periprocedural complication rates. bilateral, multiple internal carotid artery aneurysms can benefit from this technique, even in one single treatment session. in this regard, the pipeline flex with shield technology offers a potential advantage due to its phosphorylcholine surface modification. nonetheless, further studies are mandatory to confirm the safety and efficacy of bilateral, singlesession internal carotid artery flow-diverter vessel reconstruction. ethical requirements no personal data of the patient is available for identification. conflicts of interest szikora i. offered professional guidance on behalf of medtronic for this case. acknowledgements “renasterea” foundation has generously donated both flowdiverter devices. references 1. mcdowell mm, zhao y, kellner cp, et al. demographic and clinical predictors of multiple intracranial aneurysms in patients with subarachnoid hemorrhage. j neurosurg; 128: 961–968. 2. shen x, xu t, ding x, et al. multiple intracranial aneurysms: endovascular treatment and complications. interv neuroradiol; 20: 442–447. 39 single-session treatment of bilateral, tandem, internal carotid artery aneurysms 3. xavier ar, rayes m, pandey p, et al. the safety and efficacy of coiling multiple aneurysms in the same session. j neurointervent surg; 4: 27–30. 4. awad a-w, moon k, yoon n, et al. flow diversion of tandem cerebral aneurysms: a multi-institutional retrospective study. neurosurgical focus; 42: e10–5. 5. nelson pk, lylyk p, szikora i, et al. the pipeline embolization device for the intracranial treatment of aneurysms trial. ajnr am j neuroradiol; 32: 34–40. 6. rajah g, narayanan s, rangel-castilla l. update on flow diverters for the endovascular management of cerebral aneurysms. neurosurgical focus; 42: e2–11. 7. girdhar g, ubl s, jahanbekam r, et al. thrombogenicity assessment of pipeline, pipeline shield, derivo and p64 flow diverters in an in vitro pulsatile flow human blood loop model. eneurologicalsci; 14: 77–84. 8. martínez-galdámez m, lamin sm, lagios kg, et al. treatment of intracranial aneurysms using the pipeline flex embolization device with shield technology: angiographic and safety outcomes at 1-year follow-up. j neurointervent surg; 11: 396–399. 9. kallmes df, hanel r, lopes d, et al. international retrospective study of the pipeline embolization device: a multicenter aneurysm treatment study. ajnr am j neuroradiol; 36: 108–115. 10. rouchaud a, brinjikji w, lanzino g, et al. delayed hemorrhagic complications after flow diversion for intracranial aneurysms: a literature overview. neuroradiology; 58: 171–177. doi: 10.33962/roneuro-2023-021 an insight into artificial intelligence and its role in neurosurgery ahtesham khizar romanian neurosurgery (2023) xxxvii (1): pp. 124-127 doi: 10.33962/roneuro-2023-021 www.journals.lapub.co.uk/index.php/roneurosurgery an insight into artificial intelligence and its role in neurosurgery ahtesham khizar punjab institute of neurosciences, lahore, pakistan abstract to acquire a wide range of technical skills, neurosurgeons undergo extensive and drawn-out training. additionally, neurosurgery necessitates a significant amount of preoperative, intraoperative, and postoperative clinical data collection, decisionmaking, care, and recovery. the significance of artificial intelligence in neurosurgery has significantly increased during the past ten years. the potential of artificial intelligence to improve diagnostic and prognostic outcomes in neurosurgery is quite promising. it is important to clinical therapy because it helps neurosurgeons make crucial decisions during surgical interventions to improve patient outcomes and it enhances their abilities to give patients the finest interventional and noninterventional care possible. furthermore, the acquisition, processing, and storage of clinical and experimental data are all greatly influenced by artificial intelligence. its application in neurosurgery can lower surgical care expenses and offer top-notch medical treatment to a larger population. this article examines the use of artificial intelligence in preoperative, intraoperative, and postoperative care for both interventional and non-interventional aspects of neurosurgery, including diagnosis, clinical decision-making, surgical operation, prognosis, data collection, and research in the field. introduction in the context of medicine, "artificial intelligence" (ai) literally refers to "a robotic doctor" and can be understood as "a machine capable of thinking." neuroscience is still far from comprehending human intelligence, and ai technology is still far from constructing an "artificial brain." currently, "artificial intelligence" methods use wholly new technologies to solve very conventional and logistical problems.1 the field of neurosurgery is grueling work. neurosurgeons must have significant training, endurance, physical dexterity, outstanding hand-eye coordination, the ability to make wise decisions, leadership and organisational abilities, compassion, communication skills, and the ability to operate in a team.2 in 1988, kwoh and colleagues performed the first robotic brain surgery that was guided by computerised tomography.3 the gap between people and machines has been closed by recent technological advancements, allowing computers to replicate and even surpass natural human ability to produce so-called "artificial intelligence."4 keywords artificial intelligence, machine learning, deep learning, neurosurgery corresponding author: ahtesham khizar punjab institute of neurosciences, lahore, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 125 an insight into artificial intelligence and its role in neurosurgery ai technologies may make it possible to quickly and thoroughly analyse the vast amounts of clinical data produced in contemporary healthcare settings at a level that is otherwise not attainable for humans. by pushing the boundaries of clinical diagnosis, clinical decision-making, and prognostication, ai may subsequently improve clinical practice. moreover, ai may enter the operating theatre and provide more accurate procedures with fewer errors if integrated with surgical robotics and other surgical adjuncts like image guidance. there has been little published about potential drawbacks to increased clinical automation, despite the great hoopla surrounding the imminent medical ai revolution. both direct and indirect effects could be among them. directly, flawed, insufficiently taught, or poorly comprehended algorithms may yield false results, which may have a significant effect. a clinical workflow that is increasingly automated may unintentionally worsen the deskilling of human doctors due to over-reliance, inadequate understanding, overconfidence, and a lack of necessary monitoring.5 in comparison to people, machines, algorithms, and ai have a higher level of safety since they can work continuously without experiencing physical or mental exhaustion. additionally, machines are better able to learn and recognise patterns that are not immediately apparent to humans6, revealing difficult-to-discern linkages7. ai can help neurosurgeons by decreasing surgical mistake rates, cutting expenses for prognosis, diagnosis, and treatment, increasing access to high-quality healthcare, and giving patients more control over their own decision-making processes. discussion artificial intelligence and neurosurgery the clinical speciality of neurosurgery generates a lot of data due to the routine usage of cutting-edge medical technologies and medical information systems. these elements make the application of ai technology in the field of neurosurgery more likely to succeed. to design an ai-based project in neurosurgery, it is necessary to first analyse the present demand for and implementation of these technologies, as well as to identify research areas that have the potential to benefit from ai.8 neurosurgery could be transformed by ai, machine learning (ml), and deep learning (dl). while ml, a subfield of ai, integrates computer science and statistics to enable computers to discover patterns through direct studying of data via experience, independent of external programming, ai tries to imitate the behaviour of intelligent individuals in computers.9,10 ai has the potential to increase the precision of neurosurgery diagnosis and treatment, as well as give neurosurgeons fast access to useful and efficient tools for preoperative, intraoperative, and postoperative care. ai is able to identify tiny abnormalities and deformities in clinical data and neuroradiological images that are invisible to human sight. a subtype of machine learning called dl is built on neural networks, which has numerous layers of learning algorithms.11 by giving recommendations to foster consensus among neurosurgeons on surgical approaches, ai can lower variances in patient outcomes while also improving prognosis and cutting expenses. role of ai in preoperative, intraoperative and postoperative phases of neurosurgery ai can support surgeons in the preoperative stage of neurosurgery by helping to diagnose the condition, choosing patients for the best course of treatment, and guiding patients in making the best choices.10 ai can improve surgeon performance and lower neurosurgery-related errors during the intraoperative stage of the procedure. ai in postoperative care can forecast outcomes, spot potential issues after surgery, and monitor data for better recovery and aftercare. role of ai to push the boundaries of neurosurgical research ai and artificial neural networks can be helpful tools for understanding how intricate the nervous system is. over the past ten years, increased data processing capacity and data accumulation have improved ai's performance in surgical research. combining braincomputer interface (bci) and ai can enable the creation of future robots and help paralysed individuals regain some of their sensory and movement abilities.12 a major drawback of ai-assisted research in neurosurgery is a small sample size when compared to the huge data that machine learning has processed in other fields of science and industry. it is 126 ahtesham khizar crucial to follow the guidelines of evidence-based medicine when organising research that makes use of ai technology, since these guidelines ensure the accuracy of the results and, as a result, boost their value for patients. challenges associated with use of ai in neurosurgery neurosurgical use of ai is not entirely risk-free. when ai is used too heavily in neurosurgery, there may be both direct and indirect harmful effects. at the most basic level, hardware and software issues can result in blunders during surgical procedures as well as incorrect interpretations of clinical data, lab results, and image scans that result in incorrect diagnoses.5 at the secondary level, a surgeon may become discouraged from gaining the skills necessary to master surgical techniques if they rely too heavily on ai for surgical interventions. it can be dangerous to rely too much on algorithms to diagnose and treat disorders of the neurological system.4 the idea that ai will replace professionals in the medical field has been one of the concerns surrounding its adoption. it is crucial to keep in mind that the patient is at the centre of medicine, and the benefit to the patient should be the main factor in determining whether ai can benefit medicine or not. ai shouldn't replace humans, but rather should collaborate with them to complement their abilities and enhance their performance in order to deliver the best care possible.4 the cost of using ai in neurosurgery is another issue. the long-term advantages of lessening surgeons' effort, enhancing data management, and decreasing mistake, however, can offset the initial expense of ai training and operation.4 in order to uphold ethical standards, the introduction of ai in neurosurgery needs to be carefully regulated and monitored.13 to prepare the next generation of surgeons with cutting-edge technology, ai should be used in medical and surgical training as early as possible even at undergraduate level.4 conclusions to provide patients with the best results possible, neurosurgery can use ai to its advantage. ai has the potential to improve surgeons' preoperative, intraoperative, and postoperative skill sets in neurosurgery. humans and machines can collaborate to improve healthcare delivery quality by acquiring, processing, and interpreting images, selecting patients for the most appropriate surgeries, improving intraoperative work, postoperative follow-up, and facilitating access to high-quality healthcare. future widespread adoption of ai in neurosurgery will necessitate further study, funding, and multidisciplinary cooperation. list of abbreviations ai: artificial intelligence ml: machine learning dl: deep learning bci: brain-computer interface references 1. danilov gv, shifrin ma, kotik kv, et al. artificial intelligence technologies in neurosurgery: a systematic literature review using topic modeling. part ii: research objectives and perspectives. sovrem tekhnologii med. 2021;12(6):111-118. 2. wise j. life as a neurosurgeon. bmj. 2020 feb 28;368. 3. kwoh ys, hou j, jonckheere ea, hayati s. a robot with improved absolute positioning accuracy for ct guided stereotactic brain surgery. ieee transactions on biomedical engineering. 1988 feb;35(2):153-60. 4. mofatteh m. neurosurgery and artificial intelligence. aims neuroscience. 2021;8(4):477. 5. panesar ss, kliot m, parrish r, fernandez-miranda j, cagle y, britz gw. promises and perils of artificial intelligence in neurosurgery. neurosurgery. 2020 jul 1;87(1):33-44. 6. obermeyer z, emanuel ej. predicting the future—big data, machine learning, and clinical medicine. the new england journal of medicine. 2016 sep 9;375(13):1216. 7. cruz ja, wishart ds. applications of machine learning in cancer prediction and prognosis. cancer inform. 2007;2:59–77. 8. danilov gv, shifrin ma, kotik kv, et al. artificial intelligence in neurosurgery: a systematic review using topic modeling. part i: major research areas. sovrem tekhnologii med. 2021;12(5):106-112. 9. jordan mi, mitchell tm. machine learning: trends, perspectives, and prospects. science. 2015 jul 17;349(6245):255-60. 10. senders jt, staples pc, karhade av, zaki mm, gormley wb, broekman ml, smith tr, arnaout o. machine learning and neurosurgical outcome prediction: a systematic review. world neurosurgery. 2018 jan 1;109:476-86. 11. lecun y, bengio y, hinton g. deep learning. nature. 2015 may;521(7553):436-44. 12. zhang x, ma z, zheng h, li t, chen k, wang x, liu c, xu l, 127 an insight into artificial intelligence and its role in neurosurgery wu x, lin d, lin h. the combination of brain-computer interfaces and artificial intelligence: applications and challenges. annals of translational medicine. 2020 jun;8(11). 13. collins jw, marcus hj, ghazi a, sridhar a, hashimoto d, hager g, arezzo a, jannin p, maier-hein l, marz k, valdastri p. ethical implications of ai in robotic surgical training: a delphi consensus statement. european urology focus. 2021 apr 30. martinandra_nervesheath romanian neurosurgery (2016) xxx 2: 219-229 | 219 nerve sheath tumor, benign neurogenic slow-growing solitary neurilemmoma of the left ulnar nerve: a case and review of literature andra elena martin1,2, d. martin1,2, aurelia mihaela sandu3, angela neacsu3, oana rata3, cristina gorgan3, m.r. gorgan3,4 1phd student, university of medicine and pharmacy “carol davila”, emergency clinical hospital “bagdasar arseni”, bucharest 2phd student, university of medicine and pharmacy “carol davila”, emergency clinical hospital “bagdasar arseni”, bucharest 3clinic of neurosurgery, emergency clinical hospital “bagdasar arseni”, bucharest 4professor of neurosurgery, clinic of neurosurgery, emergency clinical hospital “bagdasar arseni”, university of medicine and pharmacy “carol davila”, bucharest abstract: this paper represent a report of a case with ulnar nerve schwannoma(neurilemmoma), benign neurogenic slow-growing, tumors originating from schwann cells along the course of a nerve (1) (2) (3). schwannomas are the most common tumors of the peripheral nerves which occur in the adults (0.8–2%) (5). usually they progress slowly and so they can remain painless swellings for a few years before other symptoms appear. most of these lesions could be diagnosed clinically, are mobile in the longitudinal plane along the course of the involved nerve but not in the transverse plane (7). emg, mri, and ultrasonography are useful tools in the diagnosis. the definitive treatment of benign peripheral nerve schwannomatosis is complete enucleation of the tumor mass without damaging the intact nerve fascicles followed by confirmatory hystopathological examination (12). we present the case of a 62 years old right hand-dominant female who notice a slow increasing bulge over the inner aspect of her distal volar left forearm superior to the wrist, for a longer period of time not exactly specified; this was tracked and associated by pain, tingling and numbness over inner one and half fingers of her left hand in progress until the presentations. a diagnosis of softtissue tumor was presumed clinically. the other investigations were ultrasonography (us), nerve conduction studies (ncss) such as sensory nerve action potential (snap) and compound muscle action potential (cmap). in this case irm was suggestive of a benign growth in her left ulnar nerve in the forearm region. microsurgical techniques were used for ample enucleation of the tumor the distal volar left forearm. subsequent histopathological examination confirmed the presumed diagnosis of a benign cellular 220 | martin et al benign neurogenic slow-growing solitary neurilemmoma schwannoma. at her last follow-up one month after surgery, the patient was neurological gradually improving sensory and motor function and she is highly satisfied with the results of surgery. key words: nerve tumor, schwannoma, ulnar nerve, enucleation introduction ulnar nerve is a division of medial cord of brachial plexus with a root value of c8-t1.this nerve passes superficially to the flexor retinaculum and go into the palm of the hand through the guyon's canal. in the hand, it provides motor (hypothenar, 3rd/4th lumbricals, palmar/dorsal interossei muscles) and sensory (fifth digit and the medial half of the fourth digit) innervations (17). nerve sheath tumor originate from the cells of the schwann sheath and, thus, are also called schwannomas (neurilemoma), is the most common benign neoplasm of peripheral nerve sheaths, are tumors that can affect any nerve in the body. microscopically they are composed of two cell patterns antoni type a and antoni type b. they usually arise from a single fascicle within the nerve sheath and grow circumferentially displacing the intact nerve fascicles, are located eccentrically on the nerve root and surrounded by a true capsule consisting the epineurium. neurofibromas and schwannomas are two benign nerve sheath tumors that commonly occur in adults. neurofibromas are more common than schwannomas. schwannomas affect all the age groups and grow very slowly most often, they are solitary tumors ranging from 1.5 to 3 cm in diameter and are frequently located in the extremities, with upper extremity account for 12 to 19% and in the lower extremity for 13.5 to 17.5% of all cases (18) (19) (20) (11) (21) (22). these tumors account for 5% of all soft tissue tumors (23) (24) the typical clinical presentation triad (mass, positive tinels sign and differential motility) is infrequently encountered in daily practice. in most patients the lesion is detected as a painless bulk. clinically it is extremely difficult to differentiate schwannoma from a neurofibroma, still intraoperative form of the tumor mass, its gross morphological appearances and the subsequent histopathological and immunohistochemical examination can set the diagnosis in almost all the cases. preoperative conclusion is sometimes difficult and the tumor may resemble a ganglion when it presents on the volar side near the wrist joint. the important clinical differentials that are often confused with a benign solitary schwannoma of an extremity include traumatic neuroma, neurofibroma,lipoma, cold abscess muscle hernia, haemangioma and synovial cyst (25) (26) (27) magnetic resonance imaging (mri) is a wanted imaging technique in the diagnosis of tumors of peripheral nervous system. on romanian neurosurgery (2016) xxx 2: 219-229 | 221 imaging scans, benign tumor of peripheral nerve presents as well-defined mass, usually fusiform in shape located within a nerve, isointense to surrounding muscles on t1weighted images, and hyperintense on t2weighted images .neurogenic tumors usually show signal enhancement after intravenous administration of contrast medium (28) (29). they are typically located on the flexor surfaces of the extremities, and the upper extremities are twice as likely to be involved as the lower limbs. neurilemmomas are mobile in a plane transverse to the course to the nerve but the show to be immobile in the longitudinal plane. there is a higher incidence in the flexor surface of the upper extremity, since the concentration of nerve fibres is higher over that region (11). the treatment of choice is extracapsular or intracapsular removal under magnification or under operating microscop (6) (30) (31) (32) (31) (21) .satisfactory surgical outcomes can be achieved without the risk of recurrence. (27) (33) case report we present the case of a 62 years old right hand-dominant female who notice a slow increasing bulge over the inner aspect of her distal volar left forearm superior to the wrist level for a longer period of time not exactly specified. she also presents paresthesia in the form of tingling and numbness in the distribution of left ulnar nerve. there was no history of fever, weight loss or any preceding trauma. he had pain over the left forearm which radiated to the fingers. on local examination, there was a swelling over the medial aspect of the forearm measuring 2 cm × 2 cm with ill-defined borders. the swelling was firm and tender on deep palpation with free mobility horizontally and restricted mobility vertically. the skin over the swelling was free of signs of inflamation. there was no axillary lymphadenopathy.a positive tinel sign at the wrist and palm and a phalen sign were noted. superficial sensory function impairment (s3/s3+) and motor deficit bmrc (m2+/m3) preoperative were detected. clinical examination not revealed café-aulait spots, axillary and inguinal freckling, multiple cutaneous neurofibromas, learning disabilities, scoliosis, tibial dysplasia and vasculopathy (34). a diagnosis of soft-tissue tumor was presumed clinically. ultrasonography (us) was made and it revealed an oval lesion, hyperperfused, hypoechoic, with dimensions of 14/10/18 mm, net contoured, along ulnar nerve, with peripheral vascular septa and with mass effect on the ulnar artery. nerve conduction studies (ncss) were performed: sensory nerve action potential (snap): conduction slowing with low amplitude on median nerve and absent on ulnar nerve. compound muscle action potential (cmap): amplitude and distal motor latency is normal in median and ulnar nerve bilateral. a contrast magnetic resonance imaging (mri) showed distal volar left forearm, 2.4 cm superior to the wrist, enhancing lesion measuring 1.2/1.9 cm, along ulnar nerve, 222 | martin et al benign neurogenic slow-growing solitary neurilemmoma between flexor carpi ulnaris muscle and flexor digitorum profundus with intermediate signal on t1-weighted images and hyperintense signal on t2-fat weighted images with the central portion of the lesion hyperintense t2 and hypointense t1.characteristic “target sign” was also present on mri. there was no infiltration into surrounding tissues, and there was no perilesional edema on mri (figure 1, 2, 3). figure 1 mr imaging of the nerve sheath tumor t1 weighted image coronal section: isointense mass along median nerve figure 2 mri imaging of the tumor (axial sections) t2 weighted axial section: hyperintense mass ulnar nerve figure 3 mri imaging of the tumor (axial sections) t1 weighted axial section: hyperintense mass ulnar nerve figure 4 intraoperative view of the ulnar nerve tumor romanian neurosurgery (2016) xxx 2: 219-229 | 223 figure 5 tumor aspect after enucleation figure 6 pathology slide peripheral nerve schwannoma with antony a cells (the compact array with spindle cells) and palisading cells of verocay body figure 7 pathology image with antony b cells (less compact array) a complete surgical enucleation of the tumor mass followed by histopathological analysis was intended. after general anesthesia being induced and the patient intubated and remain in supine position, he is given intravenous ceftriaxone sodium after being tested in advance. the entire left upper extremity is prepped with betadine all the way to the axilla and draped in a sterile fashion. a sterile tourniquet was placed higher on the arm. the arm is then exsanguinated with ace bandage and tourniquet inflated to 250 mmhg. under the operating microscope with microsurgical techniques the tumor mass was exposed through skin incision centered on the long axis of lesion at the level of the distal volar left forearm. adequate exposure of the nerve both proximal and distal to the tumor was made. the nerve fascicles stretched over the tumor mass. a surgical plane was developed between the intact nerve fascicles and tumor mass, to expose the actual tumor mass. the complete enucleation of the tumor mass was possible without any obvious structural damage to the intact nerve fascicles. was conducted primary repair of the ulnar nerve segment involved after resection of tumor mass with perineural neurorrhaphy establishing the continuity of the schwann sheath with a minimal number of monofilament 10-0 nylon sutures under the operating microscope. the wound was then irrigated with normal saline and wound edges were reapproximated with interrupted with interrupted vicryl subcutaneously and monocryl to the skin. meanwhile the patient is awakened and extubated in the operating room and returned to the recovery room in good condition. histopathological examination of the masses revealed typical features of benign schwannoma, that showed an encapsulated 224 | martin et al benign neurogenic slow-growing solitary neurilemmoma hypercellular tumor of pleomorphic spindle cells with tapering nuclear ends, growing in the uniform fascicular pattern with prominent palisading at most places antoni a pattern and areas antony b pattern. at the last follow-up one month after surgery the patient was neurological gradually improving sensory and motor function and she highly satisfied with the results of surgery. discussion schwannomas (neurilemmoma) are neurogenic slow-growing tumors, wellencapsulated witch mostly develop as solitary tumors (35) (11) (36) (21). microscopically, two kinds of cells have been described namely antoni a and antoni b, which are found in archetypal schwannomas (24) (6). the tumor cells are considered to be strongly immunopositive for the s-100 protein (37). the pathological variants of schwannomas include the most common conventional variety followed by, cellular, plexiform and the melanotic schwannoma. histological conditions that must differentiation from schwannomas include palisaded leiyomyoma, palisaded myofibroblastoma of inguinal lymph nodes, gastro-intestinal stromal tumors, plexiform neurofibroma, palisaded encapsulated neuroma, neurotropic melanoma, clear cell sarcoma ofs oft parts etc. excluding the conventional variant there is no risk of malignant transformation of schwannomas (25). lee sh et al. described that the (31) most frequently affected peripheral nerve in schwannoma is the median nerve (2). the upper and lower extremity ratio of schwannoma is 2:1 as seen in major series (38) (33). commonly schwannomas present as sporadic solitary peripheral nerve mass and, when multiple are usually seen in association with nf2 or schwannomatosis (39). typical neurological symptoms of schwannomas are mentioned tinel sign, numbness, and pain (4). considered to be uncommon tumors, however they are still the most common primary nerve sheath tumors of the hand and wrist they account for about 5% of all the benign soft-tissue neoplasms because of this rarity they usually carriage a challenge to have correct preoperative diagnosis (40). siqueira et al. mentioned in the upper extremity 12 cases of tumor place in ulnar nerve, 12 cases of tumor location in median nerve, and 3 cases of tumor site in radial nerve (41). date et al. observed tumors of the upper extremity in descending order of frequency in ulnar, median and radial nerves (31). in the opinion of adani et al. the most common sites of tumor origin, in descending order of frequency are: ulnar nerve (14 tumors), median nerve (4 tumors), musculocutaneous nerve (3 tumors), and digital nerves (3 tumors) (11). correct clinical history and examination tracked by investigations like ultrasonography, mri and electromyographic studies may sometimes help in a correct preoperative diagnosis, but this is not the truth in a substantial proportion of cases (42) (43). the main reason why solitary benign peripheral nerve schwannoma can be romanian neurosurgery (2016) xxx 2: 219-229 | 225 enucleated securely without any structural damage to the nerve trunk is that tumor mass is less intermingled with the normal tissue. benign solitary schwannomas have first-rate prognosis and unless incompletely excised, there is no risk of recurrence (11). mri is considered to be the most important radiological imaging technique for diagnosing the nerve, that can detect the nerve of origin, dimensions, encapsulation, place of the nerve trunk in the tumor mass, perilesional edema, and the distinguishing target sign (28) (44). preoperatively the possibility of iatrogenic nerve injury with neurological deficits subsequent must be taken into account and discussed with the patient. neurological deficits occurred postoperative urging to a careful clinical and imaging examinations are essential (45). an accurate surgical plane is essential to prevent any unwanted injury to the intact nerve fascicles with postoperative neurological deficit (11) (27) (26) (46) since schwannomas have an eccentric location, non-infiltrating growth it can often be excised without or with only slight damage to nerve structure (11) (47) (48) (49) surgical complication might be the result of a difficult enucleation, the correlation of operative findings with neurological symptoms and surgical complications were not fully discussed. moreover, numbness goes on with small tumor had the strong impact on and the postoperative neurological deficit. tumors arising in the extremities or those with a small volume (<4 cm3) are correlated with spontaneous pain and tinel sign and the location of tumor also might influence the symptomatology (50). postoperative neurological problems such as numbness, palsy, and sensory disturbances are severe problems, with a range of 0.05–76.7 % (51) (2) (52). regarding early postoperative period, adani et al. mentions worsening of paresthesias in 23 out of 24 patients with schwannomas enrolled in the study (11). it has been established by numerous studies that schwannomas can hardly induce damaged motor function and yet if this happens should always raise a high suspicion of malignancy of that neural tumors (21) (53). kang et al. described permanent sensory impairment present in 1 out of 20 patients (54). knight et al. reports serious postoperative complications in 5 out of 198 treated patients (55). outlook of atraumatic tumor enucleation does not eliminate the risk of developing new postoperative neurological deficits, their contributing causes can be varied (56).]. donner et al support a different opinion, claiming as argument intraoperative stimulation, that fascicles entering the tumor are ordinarily nonfunctional and their transection does not cause additional neurological deficits (57). park et al. advocate that 73.2 % of all tumors induce postoperative neurological symptoms and that the symptoms persist in 30 % cases (58). whitaker and drouli as argue that temporary muscle weakness or diminished sensory perception occurs at the time when performing dissecting nerve fibers (59). 226 | martin et al benign neurogenic slow-growing solitary neurilemmoma kim et al. reported that extensive tumor growth is a predisposition in determining a higher percentage of postoperative neurological deficits, this being due to the fact that these lesions look to have a higher frequency of fascicular injury during dissection (51). it is assumed on the basis of the results that schwannoma accompanying numbness correlated with the effort of the enucleation (50).the use of microscope and microsurgical techniques might contribute to facilitate the normal nerve and to avoid the postoperative neurological deficit (60). adani et al. in 2008, publish a study that included 24 schwannomas situated in the upper extremity, in 20 cases the authors were able to remove tumors without damage of the fascicular structure (11). the surgical techniques described in the literature are also controversial. extracapsular tumor removal is an operative technique commonly used for removal of neurilemmoma (6) (30) (31) (32). however, date et al. pick out the intracapsular technique (31) (21) hussain et al. underline “tumor release by incising the capsule far lateral to the path of the nerve and dissecting the tumor circumferentially from its capsule. the epineural capsule is then left behind and acts as a protective covering of the nerve” (32). regardless the reports of h.j. kang (54) according to which the majority of schwannomas can be completely enucleated harmless the nerve because the nerve fibers are relocated and do not penetrate the tumor, chris yuk kwan tang et al. state that a large amount of the fibers had fascicular involvement. more exactly, 75% of the involved nerve fascicles while 25% schwannoma could be completely enucleated without nerve fascicles involvement (61). the actual data shows contradictory outcomes regarding the function of nerve fascicles running through the tumor. the study done by donner et al. (57) indicate that there was no nerve action potential transmission through the tumor nerve fascicles, proposing that division of the affected ones will not induce neurological deficit. however, m. j. park et al. (56) disclosed that 75% of patients had immediate neurological deficit once the tumor it has been removed. conclusion schwannoma (neurilemmoma) located in extremities, a benign neurogenic slowgrowing lesions is a rare nerve sheath tumor commonly diagnosed after a histopathological examination of a soft-tissue neoplasm most commonly of the ulnar and median nerves. tumor enlargement causes amplification of compression on adjacent to nerve structure. magnetic resonance imaging (mri) is a wanted imaging technique in the diagnosis of tumors of peripheral nervous system and nerve conduction studies (ncss): sensory nerve action potential (snap), compound muscle action potential (cmap) can be helpful. microsurgical techniques for tumor resection with nerve preservation is the treatment of choice as chance of recurrences is very low, frequently progress in peripheral romanian neurosurgery (2016) xxx 2: 219-229 | 227 nerve function after excision of schwannoma is reached. the possibility of new permanent or transitional postoperative neurological deficits is low (16). references 1. gosk j, zimmer k, rutowski r (2004) peripheral nerve tumors-diagnostic and therapeutical basics. folia neuropathol 42:31–35. 2. lee sh, hg jung, park yc, kim hs (2001) results of neurilemoma treatment: a review of 78 cases. orthopaedics 24:977–980. 3. (rosenberg ae, dick hm, botte mj (1991) benign and malignant tumors ofperipheral nerve. in: richard h, gelberman (eds) operative nerve repair and reconstruction, vol 2. jb lipponcot company 2, philadelphia). 4. (zhou j, man xy, zheng m, cai sq (2012) multiple plexiform schwannoma of a finger. eur j dermatol 22:149–150. . 5. (j. c. harkin and r. s. reed :, tumors of the peripheral nervous system, armed forces institute of pathology, washington, dc, usa, 1968). 6. (ozdemir o, ozsoy mh, kurt c, coskunol e, calli i. schwannomas of the hand and wrist: long term results and review of the literature. j ortho surg (hong kong). 2005 dec;13(3):267–72. 7. (n. b.white, “neurilemomas of the extremities,” journal of boneand joint surgery a, vol. 49, no. 8, pp. 1605–1610, 1967. 8. rosenberg et al. 1991 ,oberle et al. 1997; pivlavaki et al. 2004. 9. c. l. forthman and p. e. blazar, “nerve tumors of the hand and upper extremity,” hand clinics, vol. 20,no. 3, pp. 233–242, 2004. 10. (d. s. louis and f. m.hankin, “benign nerve tumors of the upper extremity,” bulletin of thenewyorkacademy ofmedicine, vol. 61,no. 7, pp. 611–620, 1985). 11. adani, a. baccarani, e. guidi, and l. tarallo, “schwannomas of the upper extremity: diagnosis and treatment,” la chirurgia degli organi di movimento, vol. 92, no. 2, pp. 85–88, 2008. 12. ajay pant, julfiqar, najmul huda, m. aslam benign solitary schwannoma of right ulnar nerve – a case report , acta medica international, jan jun 2015, vol 2 | issue 1. 13. a. l. dellon, “the moving two-point discrimination test: clinical evaluation of the quickly adapting fiber/receptor system,” journal of hand surgery, vol. 3, no. 5, pp. 474–481, 1978. 14. g. e. omer jr., “report of the committee for evaluation of the clinical results in peripheral nerve injury,” journal of hand surgery, vol. 8, no. 5, pp. 754– 758, 1983. 15. h. j. p¨azold and k. henkert, “operative behandlung von verletzungen peripherer nerven,” zentralblatt f¨ur chirurgie, vol. 115, pp. 677–684, 1990. 16. jerzy gosk,olga gutkowska,maciej urban, witold wnukiewicz,paweb reichert, and piotr zióbkowski results of surgical treatment of schwannomas arising from extremities , , biomed research international volume 2015, article id 547926). 17. bekler h, wolfe vm, rosenwasser mp. a cadaveric study of ulnar nerve innervation of the medial head of triceps brachii. clin orthop relat res. 2009;467:235–8, polatsch db, melone cp, jr, beldner s, incorvaia a. ulnar nerve anatomy. hand clin. 2007;23:283–. 18. kang hj, shin sj, kang es. schwannomas of the upper extremity. j hand surg br 2000;25:604–7. 19. white nb. neurilemomas of the extremities. j bone joint surg am 1967;49:1605–10. 20. tang jb, ishii s, usui m, naito t. multifocal neurilemomas in different nerves of the same upper extremity. j hand surg am 1990;15:788–92. 21. k. malizos, m. ioannou, and v. kontogeorgakos, “ancient schwannoma involving the median nerve: a case report and review of the literature,” strategies in trauma and limb reconstruction, vol. 8, no. 1, pp. 63–66, 2013. 22. m. j. kransdorf, “benign soft-tissue tumors in a large referral population: distribution of specific diagnoses by age, sex, and location,” american journal of roentgenology, vol. 164, no. 2, pp.395–402, 1995. 23. mackinnon se, dellon al. surgery of peripheral nerve. new york: thieme medical publishers; 1988: 53540.); their incidence in the upper extremity varies as does their clinicalpresentation, knight dm, birch r, pringle j. benign solitary schwannomas: a revi. 24. trãistaru r, enãchescu v, manu cd, gruia c, ghiluşi m. multiple right schwannoma. rom j morphol embryol. 2008;49(2):235–9. 228 | martin et al benign neurogenic slow-growing solitary neurilemmoma 25. o. kurtkaya-yacipier, bschithauer, j.m. woodruff . the pathological spectrum of schwannomas. histol histopathol 2003;18:925-934. 26. ekkernfkamp a, wol jd, muller km, wiebe v. myxoid schwannoma of the forearm-a case report. handchir mikrochir plast chir 1990 nov; 22(6):316-20. 27. di lorenzo s, corradino b, cordova a, moschella f. unexpected ulnar nerve schwannoma. the reasonable risk of misdiagnosis. acta chir plast 2007;49(3):77-9. 28. t. ergun, h. lakadamyali, a. derincek, n. c. tarhan, and a.ozturk, “magnetic resonance imaging in the visualization of the benign tumors and tumor-like lesions of hand and wrist,”current problems in diagnostic radiology, vol. 39, no. 1, pp. 1–16, 2010. 29. s. k. thawait, v. chaudhry, g. k. thawait et al., “high resolution mr neurography of diffuse peripheral nerve lesions,” the american journal of neuroradiology, vol. 32,no. 8, pp. 1365– 1372, 2011. 30. s. m. kim, s.w. seo, j. y. lee, and k. s. sung, “surgical outcome of schwannomas arising from major peripheral nerves in the lower limb,” international orthopaedics, vol. 36, no. 8, pp. 1721– 1725, 2012. 31. r.date, k.muramatsu, k. ihara, andt.taguchi, “advantages of intra-capsular micro-enucleation of schwannoma arising from extremities,” acta neurochirurgica, vol. 154, no. 1, pp. 173–178, 2012. 32. m. a. hussain, h. jhattu, a. pandya, q. chan, and w. c. a. pandya, “a precise excision technique for schwannomas,” european journal of plastic surgery, vol. 36, no. 2, pp. 111–114, 2013. 33. tapas k das gupta, richard d brasfi eld. tumours of peripheral nerve origin-benign and malignant solitary schwannomas. ca-a cancer journal for clinicians. 1970 20; 4:228-233. 34. jm friedman, md, phd (2014). neurofibromatosis 1. genereviews® . pagon ra, adam mp, ardinger hh, et al., editors.seattle (wa): university of washington, seattle; 1993-2016. 35. beaman fd, kransdorf mj ,menke dm. schwannoma: radiologic–pathologic cor¬relation. radiographics. 2004 sep–oct; 24(5):1477–81. 36. n. j. s. kehoe, r. p. reid, and j. c. semple, “solitary benign peripheral nerve tumors,” the journal of bone & joint surgery b, vol. 77, no. 3, pp. 497–500, 1995. 37. karamchandani, jason r. md *; nielsen, torsten o. md, phd +; van de rijn, matt md, phd *; west, robert b. md, phd *.sox10 and s100 in the diagnosis of softtissue neoplasms .applied immunohistochemistry & molecular morphology.20(5):445-450, october 2012. 38. nicholas jh kehoe, robin p reid, j campbell semple. solitary benign peripheral nerve tumours-review of 32 years experience. j bone joint surg [br]. 1995:77-b; 3:497500. 39. harun kütahya, 1 ,* ali güleç, 2 yunus güzel, 3 burkay kacira, 4 and serdar toker 5 .schwannoma of the median nerve at the wrist and palmar regions of the hand: a rare case report. case rep orthop. 2013; 2013: 950106. 40. vanherendael b, heyman s, schepper am, gielen j, parizel pm. schwannoma of left ulnar nerve. jbr-btr. 2006 may–jun; 89(3):156–7. 41. m. g. siqueira, m. socolovsky, r. s. martins et al., “surgical treatment of typical peripheral schwannomas: the risk of new postoperative deficits,” acta neurochirurgica, vol. 155, no. 9, pp. 1745–1749, 2013. 42. j. gosk, k. zimmer, and r. rutowski, “peripheral nerve tumours—diagnostic and therapeutical basics,” folia neuropathologica, vol. 42, no. 1, pp. 31–35, 2004. 43. m. pilavaki, d. chourmouzi, a. kiziridou, a. skordalaki, t. zarampoukas, and a. drevelengas, “imaging of peripheral nerve sheath tumors with pathologic correlation: pictorial review,” european journal of radiology, vol. 52, no. 3, pp. 229–239, 2004. 44. koga h, matsumoto s, defi nition of target sign and its use for diagnisis of schwannomas. clin orthop relat res 2007aug;464:224229. 45. kehoe njs, reid rp, semple jc (1995) solitary benign peripheral-nerve tumours. review of 32 years’ experience. j bone joint surg br 77:497–500 kim sm, sei sw, lee jy, sung ks (2012) surgical outcome of schwannomas arising from major peripheral nerves in t. 46. boustany ashley,mcclellan, w. thomas. schwannoma of the ulnar nerve: a case report and review of the literature. west virginia medical journal. march/april 2012 vol 108, issue 2; p36. 47. g. m. rockwell, a.thoma, and s. salama, “schwannoma of the hand and wrist,” plastic and reconstructive surgery, vol. 111, no. 3, pp. 1227–1232, 2003. 48. g. jerzy, r. roman, and r. jerzy, “peripheral nerve tumours in own material,” folia neuropathologica, vol. 42, no. 4, pp. 203– 207, 2004. romanian neurosurgery (2016) xxx 2: 219-229 | 229 49. c. y. k. tang, b. fung, m. fok, and j. zhu, “schwannoma in the upper limbs,” biomed research international, vol. 2013, article id 167196, 4 pages, 2013. 50. kensaku abe,hiroyuki tsuchiya (2015) symptomatic small schwannoma is a risk factor for surgical complications and correlates with difficulty of enucleation. springerplus (2015) 4:751 doi 10.1186/s40064-015-1547-9. 51. kim sm, sei sw, lee jy, sung ks (2012) surgical outcome of schwannomas. 52. sawada t, sano m, ogihara h, omura t, miura k, nagano a (2006) the relationship between preoperative symptoms, operative findings and postoperative complications in schwannomas. j hand surg br 31:629– 634. 53. a. ogose, t. hotta, t. morita et al., “tumors of peripheral nerves: correlation of symptoms, clinical signs, imaging features, and histologic diagnosis,” skeletal radiology, vol. 28, no. 4, pp. 183–188, 1999. 54. h. j.kang, s. j. shin, and e. s.kang, “schwannomas of the upper extremity,” journal of hand surgery, vol. 25, no. 6, pp. 604–607,2000. 55. d. m. knight, r. birch, and j. pringle, “benign solitary schwannomas: a review of 234 cases,” the journal of bone & joint surgery b, vol. 89, no. 3, pp. 382–387, 2007. 56. m. j. park, k. n. seo, and h. j. kang, “neurological deficit after surgical enucleation of schwannomas of the upper limb,” journal of bone and joint surgery—series b, vol. 91,no. 11,pp. 1482–1486, 2009. 57. t. r. donner, r. m. voorhies, and d. g. kline, “neural sheath tumors of major nerves,” journal of neurosurgery, vol. 81, no. 3, pp. 362–373, 1994. 58. park mj, seo kn, kang hj (2009) neurological deficit after surgical enucleation of schwannomas of the upper limb. j bone joint surg br 91:1482–1486. doi:10.1302/0301-620x.91b11.22519. 59. whitaker wg, droulias c (1976) benign encapsulated neurilemoma: a report of 76 cases. am j surg 42:675–678. 60. omezzine sj, zaara b, ben ali m, abid f, sassi n, hamza ha (2009) a rare cause of non discal sciatica: schwannoma of the sciatic nerve. orthop traumatol surg res 95:543–546. doi:10.1016/j.otsr.2009.05.007. 61. chris yuk kwan tang, boris fung,margaret fok, and janet zhu. schwannoma in the upper limbs. biomed research international,volume 2013, article id 167196. adamd_diagnosticchallenge 168 | adam et al dumbbell-shaped lumbar non-hodgkin’s lymphoma diagnostic challenge in a patient with primary bilateral dumbbell-shaped lumbar non-hodgkin’s lymphoma d. adam1,2, gina burduşa2, d. iftimie2, ioana hornea2, camelia dobrea1,3, sorina nicoleta badelita4 1„carol davila” university of medicine and pharmacy, bucharest 2department of neurosurgery, „saint pantelimon” clinical emergency hospital, bucharest 3department of pathology, monza hospital, bucharest 4department of hematology, „fundeni” clinical institute, bucharest abstract: objective: primary bilateral dumbbell-shaped lumbar non-hodgkin lymphomas with epidural and extraspinal involvement, are rare occurrences. patients presenting at advanced stages and rapid evolution towards neurological impairment lead to diagnostic dilemmas for which only immunohistochemistry can provide a correct, although delayed solution. case report: we report the first case of a bilateral, dumbbellshaped, lumbar lymphoma in a 65-year-old man with a medical history of chronic viral hepatitis type b and d under interferon treatment. the patient presented with back pain radiating down the right leg, with rapid progression to paraplegia and sphincter dysfunction. ct and mri revealed a large dumbbell mass (approx. 5/5/10 cm) in the right paraspinal musculature, at the l4-l5 level, with intraspinal epidural extension. a similar mass of smaller size was described on the left side, almost mirroring the first lesion, the imagistic aspect suggesting a neural sheath tumor. intraoperatively, in the right lumbar paraspinal musculature, a soft, yellowish region was discovered, the macroscopic appearance being rather suggestive for a diffuse infection. clinical, imagistic and surgical findings were not conclusive, nor was the histological examination in light microscopy of the surgical specimen or of the bone marrow biopsy. immunohistochemistry identified the presence of large b cells, leading to the diagnosis of b cell lymphoma. although the patient was treated with systemic chemotherapy, his condition rapidly deteriorated and he died within 3 months. conclusions: in the case of a lumbosacral, dumbbell shaped mass, developed both epidural and extraspinal, the differential diagnosis must include lymphoma. the histological examination, especially immunohistochemistry provided the final diagnosis. delays in establishing a diagnosis, associated with a malignant evolution of lymphoma, diminish the chances of determining and applying a treatment strategy that could prolong survival. key words: dumbbell shaped tumor, non-hodgkin lymphoma, lumbar spine, sciatica, paraspinal musculature romanian neurosurgery (2016) xxx 2: 168-176 | 169 case report a 65-year-old patient was referred to our department for low back pain radiating to the posterior aspect of right thigh down to the heel associated with numbness and tingling on the plantar aspect of the right foot. symptoms were resistant to nsaid treatment and were more pronounced during the night. his gait was difficult due to pain. significant medical history included chronic viral hepatitis type b and d treated with interferon up until 3 months prior to admission and diabetes mellitus type ii. physical examination was normal, except for a firm region located superficially on the right paravertebral lumbar spine. he presented no fever, nor lymphadenopathy or weight loss. neurologic examination was normal at presentation with negative sciatic nerve stretch test. notable laboratory results included an esr of 42 mm/h, total white cell count of 8720/µl, neutrophils 5940/µl (68.20%), lymphocytes 2030/µl (23.30%), eosinophils 100/µl (1.12%), basophils 20/µl (0.20%). no atypical lymphocytes were encountered. lumbar computer tomography revealed swelling of the iliopsoas muscle and the right paraspinal muscles adjacent to l4 and l5 vertebras, with post-contrast enhancement and enlargement of the corresponding neural foramina (figure 1). figure 1 axial ct image at the level of the l4 vertebra that shows swelling of the iliopsoas muscle and the right paraspinal muscles with post-contrast enhancement mri showed a polylobed dumbbell-shaped mass, posterior to the insertion of the right psoas, extended in the right paraspinal muscles in close contact with the l4 and l5 posterior arches, entering the spinal canal through the l4-l5 and l5-s1 foramina, compressing and left-displacing the dural sack. within the spinal canal, the tumor presented epidural extension over the entire length of the sacral canal. the mass, measuring 5/5/10 cm, appeared homogenous, with t1, t2 and stir hyperintensity and homogenous enhancement. on the left side, an identical mass of smaller size was identified, located lateral to the l4-l5 intervertebral foramen, extending in the paraspinal musculature (figure 2). 170 | adam et al dumbbell-shaped lumbar non-hodgkin’s lymphoma figure 2 lumbar spine mri, t1 weighted images after contrast administration in coronal plane that show a bilateral dumbbell shaped hyper intense mass that extends in the paravertebral muscles (a); the tumor enters the spinal canal at the l4-l5 level, with left displacement of the dural sack (b); axial image at s1 level reveals the epidural extension in the sacral canal (c) chest, abdomen and pelvic contrast ct scans as well as abdominal ultrasound were negative for enlarged lymph nodes or additional masses. the patient underwent decompression of the l5 and s1 right spinal roots performed via l4 and l5 right hemilaminectomy. at this level the epidural tissue mass was debrided and its extension in the paraspinal musculature was partially resected. intraoperatively, in the central area of the paraspinal tumor, a mass of yellowish color and soft consistency was found, the macroscopic aspect being rather that of a diffuse infection in a very infiltrative mass. immediately following the surgical decompression, the patient’s pain was alleviated. he was able to walk with the aid of a cane. bacteriological examination of the debrided muscular tissue isolated staphylococcus aureus, sensitive to gentamicin, linezolid and trimethoprim/sulfamethoxazole. two weeks later the patient presented a difficult gait due to foot drop on the right side. he also showed sensory impairment of the l5 and s1 radicular territories. no sphincter disturbances were encountered. the general physical examination revealed a painless, 1 cm diameter inguinal adenopathy of firm consistency, adherent to the adjacent planes. organomegaly was absent. romanian neurosurgery (2016) xxx 2: 168-176 | 171 histological examination of the specimen with light microscopy was inconclusive, indicating an undifferentiated tumor, with medium/large cells, proliferating in a discohesive manner (figure 3). bone marrow obtained through biopsy showed at histopathological examination hematogenous marrow with age appropriate cellularity with the presence of all cellular series, light megakaryocytic reactive hyperplasia and extremely rare, small cell, mature lymphoid interstitial infiltrate (reactive aspect). immunostaining was used in order to establish the diagnosis. the microscopic characteristics made necessary an investigation of cell type as vimentin and cytokeratin mnf116 were the first applied markers. the cytokeratin mnf116 was negativ and vimentin was positive in a fashion suggesting a lymphoid proliferation. the common leukocyte antigen cla (cd45) and cd20 were diffusely positive while cd3 showed only rare positive cells. for typing the lymphoid b cell proliferation cd10 (for germinal center subtype) and mum1 (for activated b cell type) were applied. mum1 was diffusely positive, indicating the activated b cell and that the final diagnosis was diffuse large b cell non-hodgkin’s lymphoma activated subtype, infiltrating skeletal muscle. a high proliferative cell index reveals the aggresive nature of the tumor. (figure 4). the origin of the lymphoid proliferation is more difficult to establish; it may be in a lymph node near the muscle, near the bone or even in the bone marrow of the vertebra. figure 3 light microscopy examination of the tumor specimen revealing skeletal muscle with diffuse tumor invasion. tumor cells are large, with scant cytoplasm and rounded nuclei with dispersed chromatin and with a discohesive feature (he staining, 20x magnification) 172 | adam et al dumbbell-shaped lumbar non-hodgkin’s lymphoma figure 4 immunostaining of the tumor tissue. a: cd20 appears diffusely positive, revealing the lymphoid nature of the tumor proliferation. (cd20 staining, 20x magnification); b: mum1 staining is positive for activated b cells (mum1 staining, 20x magnification); c: the proliferative cell index is very high (~90%), illustrating the aggressive character of the tumor (ki67 staining, 20x magnification) figure 5 postoperative (1 month) contrast lumbar ct at the level of the l5 vertebra showing the increase in size of both paravertebral masses neurological deficits rapidly progressed to paraparesis and urinary retention. a lumbar ct was repeated at 1 month after surgery that showed the increase in size of both paravertebral masses with central necrosis and also bony erosion of the right iliac bone and sacrum (figure 5). repeated laboratory tests revealed an increased crp of 47,2 mg/dl and ldh of 719 mmol/l. the patients’ postoperative course included pain relief medication, antibiotherapy, dexamethasone, zoledronic acid, filgrastim and 3 cycles of chemotherapy with cyclophosphamide and doxorubicin. the patient’s general condition progressively worsened, in parallel with gradual neurological impairment, followed by death at 3 months postoperatively. discussion basic notions regarding the immune system and non-hodgkin lymphomas the human body has defensive immune mechanisms through which it triggers immune responses: •the innate immune response consists of macrophages, monocytes, granulocytes and natural killer cells that detect pathogens and rapidly respond to the nonspecific signals that appear in case of infection and tissue damage •the adaptive immune response is provided by lymphocytes. they are immunocompetent cells that present specificity and memory for foreign agents. lymphocytes present specific receptors: b cell receptor or t cell receptor. the adaptive immunity can be humoral or cellular, depending on the receptor type expressed by lymphocytes. (1) the humoral immune system consists primarily of b cells and plasma cells that romanian neurosurgery (2016) xxx 2: 168-176 | 173 secrete antibodies. the b cell receptor is located at the surface of the cell and has specificity for antigens. antibodies represent the weapons of the humoral immune system, secreted by b cells. the cellular immune system is provided by t cells that can express cd4 or cd8 coreceptors. cd8+ t-cells are also called cytotoxic lymphocytes. cd4+ t-cells are known as t-helper cells that regulate the function of other immune cells via the cytokines that they secrete. non-hodgkin lymphomas (nhls) are caused by lymphocytic proliferation in the lymph nodes, spleen or bone marrow. nhls can develop in any site of the body where lymphatic tissue is present. (2, 3) the non-hodgkin lymphoma is a systemic condition that has the tendency to disseminate even at the level of the central nervous system, both intra and extracranial, spine (4), spinal epidural space, at the level of the nerve roots, nerve plexuses, even cranial or peripheral nerves (5–9) and can be primary or secondary lesions of the nervous system. because it is capable of mimicking any other condition at affected sites, the diagnosis is sometimes delayed, and the outcome is grim, despite therapeutic advances in recent years. nhls are heterogeneous, blood cell tumors composed of b and t cells. there are several types of lymphoma that are classified by the who in: • large, diffuse b-cell lymphomas • t-cell lymphomas • plasmablastic lymphomas • natural killer t-cell lymphomas (nk/t-cell) there are approximatively 30 subtypes of non-hodgkin lymphomas, with variable severity, from mild to aggressive. non-hodgkin lymphomas with spinal cord compression are often aggressive (10– 13). nhl is the seventh most common cancer in the united states (14). monnard et al (15) have reported that 4% of spinal epidural lymphomas were developed at the lumbosacral level and 27% in the lumbar area. spinal cord compression occurred in 0,1% to 3,3% of patients with non-hodgkin lymphomas (15, 16) and up to 10,2% in aggressive forms (11, 12). while their cause is unknown, several risk factors have been identified. although nhls can develop at any age, they most frequently occur in the seventh and eight decades. men are more frequently affected than women. various risk factors are mentioned in the literature: viral or baterial infections (epsteinbarr virus, hiv), immune system defficiencies in immunosupressed patients, under immunosupresive theraphy, after organ transplant, autoimmune diseases and radiation exposure (8, 17, 18). immune system compromise in the presence of a risk factor predisposes patients to develop lymphomas. surgical intervention followed by chemotherapy and radioterapy, can improve neurological function and can prolong the patient’s lifespan (19). differential diagnosis in the presented case, the patient was under interferon treatment for chronic viral hepatitis type b and d. the presence of this element in recent case history was not a sufficiently powerful aspect to guide towards the diagnosis 174 | adam et al dumbbell-shaped lumbar non-hodgkin’s lymphoma of lymphoma at the time of admission. ct and mri revealed a bilateral, dumbbellshaped mass, at the level of the lumbar spine, extending in the paraspinal muscles and intrapinally that raised the suspicion of malignant nerve sheath tumor at the l4 and l5 level. according to tsai (5), lymphomas can grow in patterns that are indistiguishable from nerve sheath tumors. the radiological characteristics of the lession are not fully consistent with the diagnosis of malignant nerve sheath tumor because it is highly unlikely for this tumor type to develop bilaterally, at two levels simultaneously and also extend epidurally along the entire length of the sacral canal, while also presenting an extraspinal globular shape and not stretched along the length of the sciatic nerve roots. also, nerve sheath tumors appear iso or hypointense in t1 weighted images and hyperintense in t2 with heterogenous enhancement. in the presented case, the tumor showed hyperintensity in t1 and t2 sequences and homogenous enhancement. increased lab test values corellated with the inflamatory aspect of the central area of the lesions developed in the paraspinal muscles along with the bacteriological examination positive for stafilococcus aureus suggest a defficiency of the patient’s immune system. all these elements sustained the diagnosis of an infectious process and to begin treatment according to the germ’s sensitivity, but at the same time further strengthened the diagnostic dilemma. bobba et al (20) reported a hodgkin lymphoma with a bilateral fluid collection in the epidural space and paraspinal region at the l4-l5 level which was initially treated with vancomycin. the diagnosis of nhl was not solved with the help of histopathological examination in light microscopy. we include in the differential diagnosis soft tissue tumors like rhabdomyosarcoma or metastases but these were ruled out by histopathological examination in light microscopy. the diagnosis of lymphoma could only be made with the help of immunohistochemistry. the tumor cells were positive for vimentin that suggested a lymphoid proliferation, also diffusely positive for cla and cd 20, while only rare cd3 positive cells were encountered. mum1 was diffusely positive, establishing the final diagnosis of diffuse large b cell nonhodgkin lymphoma, activating subtype, infiltrating skeletal muscle. not even immunostaining could pinpoint the origin of the lymphoid proliferation. the fact that at the time of admission no adenopathies were found at general physical examination, nor organomegaly and the thoracic, abdominal and pelvic ct scan did not reveal enlarged lymph nodes, demonstrates that this particular tumor is a primary lymphoma with an uncommon radiological appearance, presenting a lumbar, bilateral, dumbbell-shaped development. swelling of the inguinal lymph node appeared as the condition progressed and so was not the origin of the lymphoma. the purpose of the surgical procedure was to obtain a tissue sample for histopathologic examination ant to decompress the neural roots in accordance with recommendations of hong et al (21). romanian neurosurgery (2016) xxx 2: 168-176 | 175 postoperative survival was short because, although primary lymphomas are sensitive to chemotherapy, only 3 cycles could be administered, without iradiation. radiotherapy, some authors claim, is no longer justified (22, 23). conclusions primary non-hodgkin lymphomas have to be taken into consideration in the differential diagnosis of patients presenting with low back pain and radiculopathy. we report a very rare case of primary lumbosacral and paraspinal lymphoma with late discovery which was correctly diagnosed only after immunhistochemical examination. late presentation associated with an aggressive form of disease prevent an optimal and complete treatment protocol with a chance to prolong survival. in the diagnosis and treatment of patients with primary non-hodgkin lymphoma, a multidisciplinary team is necessary. references 1. prins rm, liau lm. immunology and immunotherapy in neurosurgical disease. neurosurgery. 2003;53(1):144152; discussion 152-153. http://www.ncbi.nlm.nih.gov/pubmed/12823883. accessed may 4, 2016. 2. eeles ra, o’brien p, horwich a, brada m. nonhodgkin’s lymphoma presenting with extradural spinal cord compression: functional outcome and survival. br j cancer. 1991;63(1):126-129. http://www.ncbi.nlm.nih.gov/pubmed/1989650. accessed may 16, 2016. 3. mora j, wollner n. primary epidural non-hodgkin lymphoma: spinal cord compression syndrome as the initial form of presentation in childhood non-hodgkin lymphoma. med pediatr oncol. 1999;32(2):102-105. http://www.ncbi.nlm.nih.gov/pubmed/9950197. accessed may 16, 2016. 4. tahiri l, benbouazza k, amine b, allali f, el mesbahi o, hajjaj-hassouni n. primary non-hodgkin’s lymphoma presenting as radicular syndrome: report of two cases. rheumatol int. 2009;30(1):113-117. doi:10.1007/s00296-009-0898-3. 5. tsai m-c. non-hodgkin’s b-cell lymphoma of a lumbar nerve root: a rare cause of lumbar radiculopathy. j clin neurosci. 2013;20(7):1029-1031. doi:10.1016/j.jocn.2012.06.017. 6. cappellari m, benedetti f, fiaschi a, benedetti md. multiple radiculopathy as the presenting manifestation of primary spinal leptomeningeal b cell lymphoma detected by flow cytometry of cerebrospinal fluid. neurol sci. 2011;32(6):1171-1174. doi:10.1007/s10072-011-0613-5. 7. gonzalvo a, mckenzie c, harris m, biggs m. primary non-hodgkin’s lymphoma of the radial nerve: case report. neurosurgery. 2010;67(3):e872-e873; discussion e873. doi:10.1227/01.neu.0000374852.65670.7d. 8. abdel aziz km, van loveren hr. primary lymphoma of meckel’s cave mimicking trigeminal schwannoma: case report. neurosurgery. 1999;44(4):859-862; discussion 862-863. http://www.ncbi.nlm.nih.gov/pubmed/10201312. accessed may 16, 2016. 9. da cunha-bang sa, crone c, christensen t. nonhodgkin lymphoma presenting with foot drop. clin neurol neurosurg. 2012;114(8):1201-1203. doi:10.1016/j.clineuro.2012.02.051. 10. barnard m, perez-ordoñez b, rowed dw, ang lc. primary spinal epidural mantle cell lymphoma: case report. neurosurgery. 2000;47(5):1239-1241; discussion 1242. http://www.ncbi.nlm.nih.gov/pubmed/11063119. accessed may 16, 2016. 11. epelbaum r, haim n, ben-shahar m, ben-arie y, feinsod m, cohen y. non-hodgkin’s lymphoma presenting with spinal epidural involvement. cancer. 1986;58(9):2120-2124. http://www.ncbi.nlm.nih.gov/pubmed/3756827. accessed may 16, 2016. 12. perry jr, deodhare ss, bilbao jm, murray d, muller p. the significance of spinal cord compression as the initial manifestation of lymphoma. neurosurgery. 1993;32(2):157-162. http://www.ncbi.nlm.nih.gov/pubmed/8437651. accessed may 16, 2016. 176 | adam et al dumbbell-shaped lumbar non-hodgkin’s lymphoma 13. cho h-j, lee j-b, hur jw, jin s-w, cho t-h, park jy. a rare case of malignant lymphoma occurred at spinal epidural space: a case report. korean j spine. 2015;12(3):177-180. doi:10.14245/kjs.2015.12.3.177. 14. alterkruse sf, kasary c, kraycho m, et al. seer cancer statistics review, 1975-2007.; 2010. http://seer.cancer.gov/csr/1975-2007/. 15. monnard v, sun a, epelbaum r, et al. primary spinal epidural lymphoma: patients’ profile, outcome, and prognostic factors: a multicenter rare cancer network study. int j radiat oncol biol phys. 2006;65(3):817-823. doi:10.1016/j.ijrobp.2006.01.002. 16. vanneuville b, janssens a, lemmerling m, de vlam k, mielants h, veys em. non-hodgkin’s lymphoma presenting with spinal involvement. ann rheum dis. 2000;59(1):12-14. http://www.ncbi.nlm.nih.gov/pubmed/10627420. accessed may 16, 2016. 17. boffetta p, de vocht f. occupation and the risk of non-hodgkin lymphoma. cancer epidemiol biomarkers prev. 2007;16(3):369-372. doi:10.1158/1055-9965.epi06-1055. 18. roug ik, mccartney lb. metastatic non-hodgkin lymphoma presenting as low back pain and radiculopathy: a case report. j chiropr med. 2012;11(3):202-206. doi:10.1016/j.jcm.2012.05.008. 19. tang y, yang x, xiao j, et al. clinical outcomes of treatment for spinal cord compression due to primary non-hodgkin lymphoma. spine j. 2013;13(6):641-650. doi:10.1016/j.spinee.2012.11.054. 20. bobba rk, arsura el, sawh ak, naseem m. diagnostic challenge posed by the clinical presentation of foot drop in a patient with hodgkin’s lymphoma. eur j intern med. 2006;17(8):572-574. doi:10.1016/j.ejim.2006.07.010. 21. hong b, hermann ej, reuter c, brandis a, krauss jk. outcome of surgical decompression of spinal mass lesions in non-hodgkin’s lymphoma and plasmacytoma. clin neurol neurosurg. 2013;115(12):2476-2481. doi:10.1016/j.clineuro.2013.09.037. 22. mcallister ld, doolittle nd, guastadisegni pe, et al. cognitive outcomes and long-term follow-up results after enhanced chemotherapy delivery for primary central nervous system lymphoma. neurosurgery. 2000;46(1):51-60; discussion 60-61. http://www.ncbi.nlm.nih.gov/pubmed/10626935. accessed may 16, 2016. 23. davis ta, horning sj. advances in the management of hodgkin’s and non-hodgkin's lymphoma. curr opin hematol. 1998;5(4):259-263. http://www.ncbi.nlm.nih.gov/pubmed/9747632. accessed may 16, 2016. romanian neurosurgery (2019) xxxiii (3): pp. 337-344 doi: 10.33962/roneuro-2019-058 www.journals.lapub.co.uk/index.php/roneurosurgery supratentorial hemangioblastoma without von hippel-lindau syndrome in an adult. a rare case report oguz baran1, omur kasimcan2, aydin sav3, hakan oruckaptan4 * 1 haseki research and training hospital, neurosurgery clinic, istanbul, turkey 2 istinye university, neurosurgery clinic, istanbul, turkey 3 department of pathology, school of medicine, yeditepe university, istanbul, turkey 4 memorial hospital, neurosurgery clinic, ankara, turkey * our senior author was deceased in the writing process of the article abstract hemangioblastomas (hbls) are highly vascular and cystic benign neoplasms. they form very small part of intracranial tumours and are often localized in the posterior fossa. although most of them are sporadic, a significant group is accompanied with von hippel-lindau (vhl) syndrome. this case report presents a 57-year-old woman treated with total resection using micro-surgical technique and was diagnosed as hbl based on histopathologic findings. contrast-enhanced cranial mri of the patient with the complaints of spasms in the right side of body showed a right paracentral mass that caused midline shift. in literature, the previously reported cases of supratentorial hbl unaccompanied with vhl syndrome were searched in pubmed, compiled and presented. it should be borne in mind that rare hbls manifesting with various neurological symptoms may occur in the supratentorial region, and may not accompany with vhl syndrome. introduction hemangioblastoma (hbl) is a benign vascular tumour of the central nervous system consisting of veins and neoplastic stromal cells (1). it usually occurs after the third decade (2). it may arise sporadically (6680%) or along with von hippel-lindau (vhl) syndrome (20-33%), a familial neoplasia syndrome. although hbls are located in infratentorial site, rare supratentorial cases are present. (3). the most common infratentorial localizations in order of decreasing frequency are cerebellum, brain stem, and spinal cord, and less frequently in the cerebral hemispheres along the optical pathways in supratentorial region (4). although they have benign histology, hbls can cause symptoms such as peritumoral edema, cyst formation, and as a result of the mass effect occurring in adjacent structures due to tumour growth (5). keywords supratentorial, hemangioblastoma, von hippel-lindau syndrome corresponding author: oguz baran haseki research and training hospital, neurosurgery clinic, istanbul, turkey oguzbaran@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 338 oguz baran, omur kasimcan, aydin sav, hakan oruckaptan our case was a 57-year-old female patient and was worth of reporting due to the presence of hbl manifesting supratentorial localization without an accompanying vhl syndrome. the current literature mostly consists of case reports and series of hbl associated with vhl disease. due to its rarity, detailed information on the clinical features, treatment, and prognosis of supratentorial hbl is limited. case report a 57-year-old female patient was admitted to our clinic with complaints of spasms in the left side of her body that began about a month ago, frequent awakenings that lasted for about ten minutes. neurological examination revealed left 3/5 hemiparesis. her medical history revealed no known comorbidities and medication use, but a previous surgery for varicose veins. upon conducting contrast-enhanced cranial mri, a mass lesion in the right paracentral region with dense contrast enhancement of 6x5.5x5.5cm causing a midline shift (figures 1 and 2). patient was operated upon a provisional diagnosis of meningioma, and lesion was observed to be hypervascularized. the lesion was totally resected without any complication utilizing microsurgical technique. histopathologic examination showed a tumour rich in vascular framework harbouring granular cells in where some nuclei revealing “degenerative atypia. immunohistochemical examination, showed certain pathognomonic findings with specific antibodies verifying hbl. the reactivities for egfr and inhibin were significant, while the gfap reactivity was dubious. although it is not a general rule, mast cell tryptase activity used to reveal the presence of mast cells embedded in tumour tissue for supporting the diagnosis. furthermore, rare nuclear progesterone reactivity is a finding that helps with the diagnosis of hbl (figure 3). in the post-operative examination of the patient, neurological deficit diminished. in the early post-operative period, contrast-enhanced cranial mri revealed total removal of the lesion. additional tests showed no stigmata consistent with vhl syndrome after the discharge of the patient. figure 1. in preoperative axial contrast enhanced cranial mri sections, a mass lesion with dense contrast enhancement that caused edema in the periphery of paracentral region and a shift in midline is observed. 339 supratentorial hemangioblastoma without von hippel-lindau syndrome in an adult figure 2. in cranial mri sections with postoperative contrast, the lesion is observed to have been totally resected. 340 oguz baran, omur kasimcan, aydin sav, hakan oruckaptan figure 2. (a) tumour consisting of capillaries surrounded by atypical cells bearing nuclei with rough chromatin pattern and granular cytoplasm typical for hemangioblastoma. (hematoxylin-eosin, x200). (b) higher magnification reveals cells with “atypical nuclei” consistent with “degenerative atypia” with no effect on prognosis. (hematoxylin-eosin, x400). (c) a dense reticulin framework surrounding tumour cells as clusters typical for hemangioblastoma, reticular variant. (x100, reticulin stain). (d) an intense cytoplasmic egfr reactivity. (egfr, streptavidin biotinylated complement, x100). (e). eye-catching mast cells randomly distributed in tumour tissue (mast cell tryptase [mtc], streptavidin biotinylated complement, x100). (f). ki-67/mib-1 labeling index is low (4%). (ki-67/mib-1, streptavidin biotinylated complement, x200). discussion hbls of the central nervous system are rare, benign and vascularized neoplasms of unknown origin (6). most of the hbls that are generally macroscopically well limited, are cystic in nature, however, can be 20% solid. for this reason, they mostly show cystic mural nodule adjacent to tumour tissue (7). hbl is generally considered as a non-metastatic tumour, and in many cases, diagnosis is delayed due to the absence of clinical findings (8). they account for approximately 1.5-2.5% of all primary intracranial tumours and 7-10% of primary posterior fossa tumours (9). this is observed in both sexes at approximately equal ratios and most often at the age 341 supratentorial hemangioblastoma without von hippel-lindau syndrome in an adult of 35-45 years. they are most commonly observed in the cerebellum, less frequently in the brain stem and in the spinal cord, and rarely in the supratentorial region (2,4 ). the uncommon supratentorial hbl was first defined by bielschowsky in 1902 (10). the frontal lobe of the cerebrum is followed by the parietal and temporal lobes according to the incidence (8). the clinical presentation of supratentorial hbls is anatomically dependent on the site and growth pattern. in some cases, the endothelia of the vascular component of the tumour secrete erythropoietin-like substance, and correspondingly, such paraneoplastic syndromes as polycythemia may be observed (11). in general, supratentorial hbls have long-term minor symptoms or symptoms may not appear at all. in most cases, sudden exacerbations requiring urgent surgical intervention may occur (12). it is reported that 5-31% of cerebellar hbl cases, 11% of supratentorial cases, and 80% of spinal cord cases are associated with vhl disease. rare supratentorial hbls account for 1-6% of hbls that accompany vhl disease (6). hbls are macroscopically well-circumscribed neoplasms with solid and varying sizes containing cystic components. due to its ability to manifest cystic mural nodules, a differential diagnosis specifically from pilocytic astrocytomas is mandatory (13). hbl is usually observed frequently in the form of enhancing mural nodule accompanied by cystic component in computed tomography. mri is the gold standard imaging method in the differential diagnosis. in contrast-enhanced t1-weighted sections, the tumour nodule is prominent and hyperintense in homogeneous form however, in t2weighted images, the cystic area is displayed as hyperintense. hbl is characteristically of a highly vascular tumour and is located in the avascular cyst, and is directly fed from the vessels originating from dural arteries (14). histological features of hbl are distinctive. vessels of various sizes are important components of tumour tissue and are furnished with a single row of endothelial cells. stromal cells in the interstitial area contain lipid droplets and glycogen in varying proportions (6). stromal cells constituting the main component of the tumour show pleomorphism and diverse levels of nuclear hyperchromasia. mastocytes may be found and mitosis is very rare. in “reticular” variant the stromal cells are dominantly located around the veins whereas wider groups are formed in “cellular” variant (15). if there is evidence of the progression of the lesion, due to bleeding or mass effect, then surgery is primary choice of treatment. removal of nodules in cystic lesions during surgical resection is vital (9). for solid lesions, procedures similar to the management of arteriovenous malformation should be performed. surgical treatment is considered certainly curative (16). in the relevant literature, there are infrequent supratentorial hbl cases those of which are unaccompanied vhl. concisely, table 1 shows a compilation of hbl cases reported in the medical literature. author (year) age sex supratentorial location gross bielschowsky (1902) (10) 24 y f frontal solid berger and guleke (1927) (17) 24 y m parietal cystic schley (1927) (18) 48 y f occipital cystic marrioti (1936) (19) n/a n/a posterior part of the corpus callosum solid zeitlin (1942) (20) 54 y m meningeal parasaggital solid kautzky and vierdt (1953) (21) 55 y m right cerebrum‑occupied thalamus, globus pallidus, basal surface of brain solid floris et al. (1954) (22) 32 y m frontal solid grattarola (1955) (23) 18 y m temporal cystic morello and bianchi (1958) (24) 10 y m temporal solid stein et al. (1960) (25) 49 y m temporal solid stein et al. (1960) (25) 12 y f frontal cystic morello and bianchi (1960) (24) 27 y m parieto‑occipital solid papo et al. (1961) (26) n/a n/a frontal n/a 342 oguz baran, omur kasimcan, aydin sav, hakan oruckaptan morello and bianchi (1960) (24) 27 y m parieto‑occipital solid rivera and chason (1966) (27) 16 y m meningeal parietal solid ishwar et al. (1971) (28) 62 y f meningeal falx, occipital solid perks et al. (1976) (29) 21 y f frontal highly vascular grisoli et al. (1984) (30) 28 y f pituitary stalk n/a katayama et al. (1987) (31) n/a n/a third ventricle n/a neuman et al. (1989) (32) 35 y f pituitary stalk n/a black et al. (1991) (33) 15 y m third ventricle solid sharma et al. (1995) (34) 72 y m meningeal parietal solid kachhara et al. (1998) (35) 57 y f sella sphenoid sinus n/a choi et al. (1998) (36) 26 y f meningeal parietal solid isaka et al. (1999) (5) 47 y f third ventricle solid tarantino et al. (2000) (37) n/a f cerebral n/a yamakawa et al. (2000) (38) 17 y m parietal cystic kim et al. (2001) (39) 45 y m meningeal convexity, frontal solid ikeda et al. (2001) (16) 62 y m suprasellar n/a ozveren et al. (2001) (40) 40 y f right supratentorial lesion near the splenium solid‑cystic acikalin et al. (2003) (4) 43 y m frontal cystic rumboldt et al. (2003) (14) 60 y m sellar suprasellar n/a agostinelli et al. (2004) (41) 10 y f meningeal convexity, frontal solid iyigun et al. (2004) (13) 61 y m meningeal convexity, frontal solid peker et al. (2005) (42) 54 y m suprasellar n/a tekkök and sav (2006) (43) 18 m f lateral ventricle cystic cosar et al. (2006) (44) 50 y m meningeal parasaggital, parietal solid ohata et al. (2006) (11) 27 y f hippocampus solid murali et al. (2007) (12) 57 y m meningeal parasaggital solid sherman et al. (2007) (3) 52 y f meningeal convexity, frontal solid jang (2007) (45) 68 y f meningeal convexity, frontal solid takeuchi et al. (2008) (8) 58 y m meningeal parasaggital, frontal solid jaggi et al. (2009) (46) 30 y m third ventricle solid peyre et al. (2009) (47) 3 m m lateral ventricle cystic elguezabal et al. (2010) (48) 67 y f meningeal falx frontal solid‑cystic crisi et al. (2010) (49) n/a n/a hippocampus n/a schär et al. (2011) (50) 80 y f pituitary n/a yang et al. (2011) (2) 19 y f temporal‑occipital lobe solid‑cystic kaloostian and taylor (2012) (7) 49 y f meningeal falx frontal solid sarkari and agrawal (2012) (51) 45 y f midline basifrontal solid she et al. (2013) (9) 60 y f cerebral falx solid‑cystic she et al. (2013) (9) 24 y m temporal, choroidal fissure solid she et al. (2013) (9) 21 y m frontal cystic kishore et al. (2013) (15) 50 y m parietal solid‑cystic al‑najar et al. (2013) (52) n/a n/a lateral ventricle n/a xie et al. (2013) (53) 64 y f suprasellar solid 343 supratentorial hemangioblastoma without von hippel-lindau syndrome in an adult raghava et al. (2014) (1) 50 y m frontal solid pandey et al. (2016) (6) 39 y m parietal cystic baran et al. (2019) 57 y f right paracentral region solid table 1. reported cases of supratentorial hemangioblastoma without vhl. conclusions infratentorial hemangioblastoma cases are inherently observed at high rates along with von hippel-lindau disease. however, it should be borne in mind that a small percentage of supratentorial hemangioblastoma cases may be presented with various neurological symptoms due to mass in imaging studies. hemangioblastoma should be considered as an entity among other possible tumorous masses occupying supratentorial area. references 1. raghava m, joshi u, mathur a. hemangioblastoma of cerebral cortex unusual presentation and review of literature. int j basic appl med sci. 2014;4:165 7. 2. yang b, luan s, cao x, bao w. supratentorial hemangioblastoma. neurosciences (riyadh). 2011;16:150 2. 3. sherman jh, le bh, okonkwo do, jane ja. supratentorial dural based hemangioblastoma not associated with von hippel lindau complex. acta neurochir (wien). 2007;149:969 72. 4. acikalin mf, oner u, tel n, pasaoglu o, altinel f. supratentorial hemangioblastoma: a case report. arch pathol lab med. 2003;127:e382 4. 5. isaka t, horibe k, nakatani s, maruno m, yoshimine t. hemangioblastoma of the third ventricle. neurosurg rev. 1999;22:140 4. 6. pandey s, sharma v, pandey d, kumar v, kumar m. supratentorial haemangioblastoma without von hippel– lindau syndrome in an adult: a rare tumor with review of literature. asian j neurosurg. 2016;11:8-14. 7. kaloostian p, taylor c. supratentorial dural based haemangioblastoma in a native american patient without von hippel lindau syndrome. j surg case rep. 2012;2012(6):11. 8. takeuchi h, hashimoto n, kitai r, kubota t. a report of supratentorial leptomeningeal hemangioblastoma and a literature review. neuropathology. 2008;28:98 102. 9. she dj, xing z, liu y, cao dr. supratentorial hemangioblastomas: three case reports and review of the literature. clin neuroradiol. 2013;23:243 7. 10. bielschowsky m. for histology and pathologic the gehirngeschwiilste. dtsch z nervenheilkd. 1902;22:54 99. 11. ohata k, takami t, tsuyuguchi n, hara m, haque m. hemangioblastoma of hippocampus without von hippel lindau disease: case report and review of literature. neurol india. 2006;54:89 90. 12. murali r, jones wi, ma wyatt j. a 57 year old man with a dural based parietal lobe tumor. brain pathol. 2007;17:460 463, 474. 13. iyigun ol, cogluk c, aydin k, yildiz l, rakunt c, celik f. supratentorial leptomeningeal hemangioblastoma mimicking a meningioma without von hippel lindau complex. turk neurosurg. 2004;14:25 7. 14. rumboldt z, gnjidic z, talan hranilovic j, vrkljan m. intrasellar hemangioblastoma: characteristic prominent vessels on mr imaging. ajr am j roentgenol. 2003;180:1480 1. 15. kishore pv, ratnan h, dharmapuri a, ravinder t, srinivas v. supratentorial hemangioblastoma: a case report and review of literature. j chalmeda anand rao inst med sci. 2013;6:67 9. 16. ikeda m, asada m, yamashita h, ishikawa a, tamaki n. a case of suprasellar hemangioblastoma with thoracic meningioma. no shinkei geka. 2001;29:679 83. 17. berger, guleke. about brain tumors and their surgical treatment. dtsch z chir. 1927;203-204:104-167. 18. schley w. about the occurence a gehirncysten with simultaneous formation of tumors. virchows arch. 1927;265:665 82. 19. marrioti d. angioreticuloma of corpus callosum. pathologica. 1936;28:1 8. 20. zeitlin h. hemangioblastomas of meninges and their relation to lindau’s disease. j neuropathol exp neurol. 1942;1:14 23. 21. kautzky r, vierdt n. an angioblastoma of the cerebrum. zbl neurochir. 1953;13:158 63. 22. floris v, severini p, castorina g. angioreticuloma of brain. contribution clinical and angiographic. riv neurol. 1954;24:642 58. 23. grattarola fr. hemangioblastoma of the brain. clinical and anatomical pathology. cancer. 1955;8:3-28. 24. morello g, bianchi m. cerebral hemangioblastomas: review of literature and report of two personal cases. j neurosurg. 1963;20:254 64. 25. stein aa, schilp ao, whitfield rd. the histogenesis of hemangioblastoma of the brain. a review of twenty one cases. j neurosurg. 1960;17:751 61. 26. papo i, colombo f, dorizzi a. considerations about 45 344 oguz baran, omur kasimcan, aydin sav, hakan oruckaptan cases of angioreticuloma brain. historical introduction. minerva neurochir. 1961;5:90 100. 27. rivera e, chason jl. cerebral hemangioblastoma. case report. j neurosurg. 1966;25:452 4. 28. ishwar s, taniguchi rm, vogel fs. multiple supratentorial hemangioblastomas. case study and ultrastructural characteristics. j neurosurg. 1971;35:396 405. 29. perks wh, cross jn, sivapragasam s, johnson p. supratentorial haemangioblastoma with polycythaemia. j neurol neurosurg psychiatry. 1976;39:218 20. 30. grisoli f, gambarelli d, raybaud c, guibout m, leclercq t. suprasellar hemangioblastoma. surg neurol. 1984;22:257 62. 31. katayama y, tsubokawa t, miyagi a, goto t, miyagami m, suzuki k. solitary hemangioblastoma within the third ventricle. surg neurol. 1987;27:157 62. 32. neumann hp, eggert hr, weigel k, friedburg h, wiestler od, schollmeyer p. hemangioblastomas of the central nervous system. a 10 year study with special reference to von hippel lindau syndrome. j neurosurg. 1989;70:24 30. 33. black ml, tien rd, hesselink jr. third ventricular hemangioblastoma: mr appearance. ajnr am j neuroradiol. 1991;12:553. 34. sharma rr, cast ip, o’brien c. supratentorial haemangioblastoma not associated with von hippel lindau complex or polycythaemia: case report and literature review. br j neurosurg. 1995;9:81 4. 35. kachhara r, nair s, radhakrishnan vv. sellar sphenoid sinus hemangioblastoma: case report. surg neurol. 1998;50:461 3. 36. choi dh, kim hs, mok jh, kim dh, lee kc, lee yb. supratentorial meningeal hemangioblastoma: case report. j korean neurosurg soc. 1998;27:1299 303. 37. tarantino r, isidori a, raco a, missori p. supratentorial hemangioblastoma in a patient with breast cancer. a case report. j neurosurg sci. 2000;44:137 9. 38. yamakawa n, noda m, ohyama t, furuno m, tsutsumi a, taki w. a cellular variant of supratentorial hemangioblastoma. brain tumor pathol. 2000;17:15 9. 39. kim hs, park sh, cho bm, kim dh, oh sm. supratentorial hemangioblastma, occurred after total removal of recurrent cerebellar hemangioblastoma – case report. j korean neurosurg soc. 2001;30:348 51. 40. ozveren mf, topsakal c, erol fs, kaplan m, uchida k, tanik c. tentorial vascularization in solid hemangioblastoma – case report. neurol med chir (tokyo). 2001;41:201 5. 41. agostinelli c, roncaroli f, galassi e, bernardi b, acciarri n, tani g. leptomeningeal hemangioblastoma. case illustration. j neurosurg. 2004;101 1 suppl:122. 42. peker s, kurtkaya yapicier o, sun i, sav a, pamir mn. suprasellar haemangioblastoma. report of two cases and review of the literature. j clin neurosci. 2005;12:85 9. 43. tekkök ih, sav a. supratentorial cystic hemangioblastoma with infratentorial extension – a unique location and a rare infant case. childs nerv syst. 2006;22:1177 81. 44. cosar m, hatiboglu ma, iplikcioglu ac, ozcan d. parasagittal leptomeningeal hemangioblastoma – case report. neurol med chir (tokyo). 2006;46:294 7. 45. jang h. supratentorial leptomeningeal hemangioblastoma: case report. yeungnam univ j med. 2007;24:770 4. 46. jaggi rs, premsagar ic; abhishek. hemangioblastoma of the lateral ventricle. neurol india. 2009;57:677 9. 47. peyre m, di rocco f, varlet p, giraud s, richard s, sainte rose c, et al. supratentorial hemangioblastoma in the neonatal period. pediatr neurosurg. 2009;45:155 6. 48. elguezabal a, díaz ml, landeyro j, gené m, boutayeb l, escosa m, et al. solid cystic supratentorial hemangioblastoma affecting the falx cerebri. report of a case. neurocirugia (astur). 2010;21:401 4. 49. crisi g, giombelli e, ventura e. non von hippel lindau hemangioblastoma in the hippocampus: characterization with time resolved mra using tricks sequence at 3t. a case report. neuroradiol j. 2010;23:416 9. 50. schär rt, vajtai i, sahli r, seiler rw. manifestation of a sellar hemangioblastoma due to pituitary apoplexy: a case report. j med case rep. 2011;5:496. 51. sarkari a, agrawal d. midline basifrontal solid hemangioblastoma in non von hippel lindau syndrome patient. j neurosci rural pract. 2012;3:399 401. 52. al najar m, al hadidy a, saleh a, al tamimi a, al darawish a, obeidat f. sporadic lateral ventricular hemangioblastoma presenting with intraventricular and subarachnoid haemorrhage. sultan qaboos univ med j. 2013;13:597 600. 53. xie t, zhang x, hu f, wang x, wang j, yu y, et al. suprasellar hemangioblastoma mimicking a craniopharyngioma: result of extended endoscopic transsphenoidal approachcase report. neurol med chir (tokyo). 2013;53:735 9. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-010 surgical challenges and outcome of endoscopic endonasal approaches in the management of recurrent pituitary adenomas ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed romanian neurosurgery (2020) xxxiv (1): pp. 77-84 doi: 10.33962/roneuro-2020-010 www.journals.lapub.co.uk/index.php/roneurosurgery surgical challenges and outcome of endoscopic endonasal approaches in the management of recurrent pituitary adenomas ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed neurosurgery department, mansoura college of medicine, mansoura university, egypt abstract background: various surgical approaches for the management of midline anterior skull base meningiomas exist in the literature. the main surgeon target is proper selection the appropriate approach that achieves total removal of the lesion without causing morbidity or mortality and facilitates safe effective removal of the tumor. objectives: to evaluate the role of the extended pterional approach for excision of midline anterior skull base meningiomas as regard the effectiveness, extent of resection and surgical outcome. patients and methods: this retrospective study involved 23 cases with midline anterior skull base meningiomas resected through the extended pterional approach. patients' clinical data, operative notes, imaging studies and clinical follow-up data were analyzed and evaluated. results: tumors studied were 9 olfactory groove meningiomas, 8 tuberculum sellae meningiomas, 4 planum sphenoidale meningiomas and 2 diaphragma sellae meningiomas. gross total resection tumor excision in 15 cases (64.5%), subtotal excision in 5 cases (21.5%) and partial excision in 3 cases (14%). complications were diabetes insipidus (2 cases 8.6%), csf rhinorrhea (3 cases 12.9%) and visual deterioration (3 cases 12.9%). we had two cases of mortality. conclusion: the extended pterional approach allows safe and effective removal of midline anterior skull base meningiomas. it expands the exposure offered by the classic pterional approach and minimizing the necessity for applying fixed brain retraction with good cosmetic outcome and less approach related morbidities in comparison with the extensive skull base approaches. introduction pituitary adenomas are relatively common brain tumor with benign features, and, in fact, they are found in 10%-17% of the general population. surgical resection continues to be the preferred treatment except for prolactin-secreting tumors. the nature of the pituitary adenoma itself suggests the possibility of tumor recurrence, regardless of its endocrinological characteristics. recurrence rate keywords extended pterional, meningioma, skull base, extent of resection corresponding author: mahmoud saad mohamed neurosurgery department, mansoura collage of medicine, mansoura university, egypt dr_ mhmodsaad@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 78 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed of pituitary adenoma after surgical resection has been reported up to 30%, and regrowth after incomplete tumor removal was reported in up to 75% of cases (2,5,10,12,16). recurrent tumors can be managed with observation, medical therapy, radiotherapy, radiosurgery, or revision surgery. additionally, the combined treatment paradigm is essential in some cases because all treatment modalities have advantages and disadvantages. surgery for a recurrent lesion is burdened by increased risk of mortality and morbidity, and it often results in incomplete resection compared with initial surgery. radiosurgery and stereotactic radiotherapy can be recommended as adjuvant treatments to obtain long-term control with low procedure-related morbidity in selective cases. however, the repeated surgical resection is crucial in cases of sizable adenomas compressing the optic apparatus, or hormone-secreting adenomas (1,2,3,4,7,9,14). nearly a century ago, harvey cushing realized the limitations of microsurgical approaches for treating pituitary adenomas. cushing and his colleagues used a radium bomb to deliver a single-session, focused radiation to treat pituitary adenomas. henceforth, neurosurgeons and radiation oncologists have employed repeat resection or ionizing radiation to treat selected patients with recurrent or residual pituitary adenomas(1,6,22,24). during the last century, pituitary surgery has been developed with various technical modifications and instrumental advances, and the outcome has been generally excellent, with high rates of clinical improvement and endocrinological remission and minimal rates of morbidity and mortality. the introduction of endoscopy in the transsphenoidal approach (tsa) has tremendously advanced the midline skull base surgery. in the literatures, the efficacy and safety of endoscopic tsa in the management of pituitary adenomas have been proven and the complication rates of endoscopic tsa are at least comparable with those of microscopic series. however, the reports on endoscopic tsa as a revision surgery have been less commonly published (6,8,11,13,15,19,26,28). we retrospectively evaluated the efficacy and safety of the endoscopic tsa for recurrent pituitary adenomas as regard extent of resection, ica injury and csf leakage and related reconstruction obstacles. material and methods a retrospective study is conducted on 30 patients with recurrent pituitary adenomas that were reoperated up on via endoscopic endonasal transsphenoidal approach at the neurosurgery department, mansoura university over the period from 2013 to 2019. patients who did a previous transsphenoid either via microscopic or endoscopic technique are included in the study. the indications to do another endoscopic endonasal transsphenoidal approach were big residual or recurrent tumor compressing the chiasm, persistent endocrinological problem due to residual adenoma. patient demographic and previous surgery data were collected and analyzed including any previous medical treatment, radiation treatment and any previous surgery related morbidities. routine preoperative complete ophthalmological assessment was done for all cases and was repeated after surgery to assess the outcome. preand postoperative endocrinological assessment were done for all cases including serum prolactin, free cortisol, acth, free thyroxine, tsh, gh and insulinlike growth factor 1 (igf-1). serum electrolytes and fluid chart were done for all cases with diabetes insipidus that present either prior or after the surgery. pre-operative contrast-enhanced mri were done for all the patients and then 3 months after surgery and then yearly for follow up. the tumors were assessed regarding its size and extension. tumor volumes were assessed by the ellipsoid model “(abc)/2” equation. the degree of cavernous sinus invasion was evaluated based on knosp criteria. the extent of tumor resection (eor) was assessed based on a post-contrast mri study done 3 months after surgery. surgical technique we utilize the standard endoscopic approach for pituitary adenoma surgery which is widely described in the literature, and we will stress on our steps in relation to surgery for recurrent cases. lumbar drain was utilized for cases with history of previous csf rhinorrhea with the initial surgery and for cases we have encountered intra-operative csf leakage and was left for 1 to 3 postoperative days for postoperative drainage. the important steps to ensure efficient safe surgery for recurrent cases were binostril four handed endoscopic technique with wide sphenoidotomy and obtaining adequate 79 surgical challenges of endoscopic endonasal approaches in the management of recurrent pituitary adenomas sellar exposure to have the full panoramic view ofthe carotid prominences, medial and lateral opticocarotid recesses, planum and clivus. our biggest challenge was the way to achieve adequate reconstruction after tumor resection. options were reusing prior flap from the previous surgery, obtaining a contralateral nasoseptal flap but in many cases with extensive adhesions and disturbed normal anatomyespecially those previously irradiated;abdominal fat graft or fascia lata graft was utilized to achieve sellar reconstruction. results thirty patients involved in this study were operated up on via endoscopic endonasal transsphenoidal surgery for recurrent or residual pituitary adenomas. 18 were females and 12 were males. age ranged from 29 to 61 years (mean 50 years). twenty-four patients (80%) had single prior endoscopic endonasal transsphenoidal surgery. the remaining 6 patients (20%) had 2 previous transsphenoidal surgeries. in 23 patients; the initial surgery was done at neurosurgery department, mansoura university hospitals while the remaining seven cases were previously operated up on in other hospitals. the initial surgery was done microscopically in 13 cases while the other 17 cases were operated up on via the endoscopic approach (table 1). the mean interval between the previous surgery and the redo endoscopic endonasal surgery was 30 months (ranged from 19 months to 42 months). 19 patients (63.3%) presented with tumor growth on follow up mri brain before the onset of clinical symptoms andwere re-operated uponbecause of growth of the residual tumor or persistent symptoms related to a persistent hormone hypersecretion. in 11 patients (36.6%); the tumor recurred after previous total resection documented on postoperativemri brain. 21 patients (70%) had macro-adenomasat recurrence while the remaining nine patients (30%) had giant adenomas. the clinical presentation was visual affection in 9 patients (30%), headache in 3 patients (10%), amenorrhea galactorrhea in 5 patients(16.6%)and persistent acromegalic features in 8 patients (26.6%).only 4 patients received adjuvant radiotherapy following first surgery (table 1).17 patients (56.6%) had nonfunctional pituitary adenomas. 8 patients (26.6%) had gh adenomas and 5 patients (16.6%) had a prolactinoma. tumor locations varies at time of presentation and determined radiologically with contrast enhanced mri brain and distributed into: confined to sella in 7 cases (23.3%), sellarwithsuprasellar extension in 12 cases (40%), sellar with parasellarextension in 6cases (20%) and sellar, suprasellar and parasellar extension in 5 cases (16.6%) (table 2). overall gross total resection was achieved in 17 patients (56.6%) while subtotal and partial resection in 13 patients (43.4%) confirmed by gadolinium enhanced magnetic resonance imaging of the brain done 3 months after surgery (table 3). total resection was achieved in 11 cases of non-functioning adenoma, 3 cases of growth hormone secreting adenomas and 3 cases of prolactinomas. total resection was achieved in 9 (47.3%) residual adenomas and in 8 (72.7%) recurrent adenomas.according to the tumor extension; total resection was feasible in 5 out of 6(83.3%) cases where the tumor is confined to sellae, in 10 out of 12 (83.3%) cases where is tumor is sellar and suprasellar extension and in 1 out of 11 (9.09%) of cases that had parasellar extension into the cavernous sinus. subtotal resection was done in 6 cases of nonfunctioning adenoma, 5 cases of growth hormone secreting adenomas and 2 cases of prolactinomas. subtotal resection was achieved in 10 (52.6%) residual adenomas and in 3 (27.2%) recurrent adenomas. according to the tumor extension; subtotal resection was done in 1 out of 6 (16.6%) cases where the tumor is confined to sellae, in 2 out of 12 (16.6%) cases where is tumor is sellar and suprasellar extension and in 10 out of 11 (90.9%) of cases that had parasellar extension into the cavernous sinus (table 3). no further treatment was required for the 17 cases with total tumor resection. among 6 cases of non-functioning adenoma with incomplete resection; 4 cases were done via microscopic transcranial approach and 2 of them offered 3dimensional radiotherapy after the transcranial surgery while the other 2 cases were treated with gamma knife radiosurgery. we have 5 cases of acromegaly with incomplete resection; one was offered additional microscopic transcranial approach followed by conformal radiotherapy, 3 offered gamma knife radiosurgery and one died from ruptured carotid pseudoaneurysm from intraoperative vascular injury. 2 cases of residual prolactin secreting adenomas were treated 80 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed medically with dopamine agonists and one of them received conformal radiotherapy after failed trail of medical treatment. we have a case of mortality from carotid injury in a case of recurrent growth hormone secreting adenoma. 3 cases had post-operative csf rhinorrhea; 2 passed conservatively and one required another endoscopic repair. 4 cases developed post-operative diabetes insipidus (2 required permanent treatments). 3 cases developed post-operative hypopituitarism requiring long term hormonal replacement therapy. improvement of the visual manifestations occurred in 5 (55.5%) out of the 9 cases presented with visual affection regarding visual acuity and visual field disturbances (table 4). regression of acromegalic features and normalization of growth hormone and insulin-like growth factor occurred in 3 (37.5%) out of 8 acromegalic cases while the other 5 (62.5%) cases failed to improve necessitating further treatment to control endocrinological problem. restoration of normal menstrual cycle and cessation of galactorrhea occurred in 3 cases after total tumor removal while the other 2 cases with residual tumor were kept on medical treatment and one case received radiotherapy. table 1. clinical and demographic distribution of recurrent adenoma patients illustrated cases case 1: forty-two years old male patient with recurrent non-functioning pituitary adenoma (fig. 1 a & b) with visual compression totally resected (fig. 1 c & d) with marvelous visual improvement. case 2: fifty-four years old female patient with recurrent growth hormone secreting adenoma with visual compression (fig. 2 a & b); subtotal resection due to cavernous sinus invasion with good optic apparatus decompression (fig. 2 c & d) and followed by gamma knife radiosurgery. discussion recurrent or residual pituitary adenomas after transsphenoid approach whether done microscopically or endoscopically represent a potential challenge in deciding the best appropriate treatment. many options of treatment are available including just follow up, medical treatment for some functioning adenoma, radiotherapy including gamma knife, microscopic transcranial resection and repeat the transsphenoid approach. the decision is based up many factors including size of the residual or recurrent adenomas, pattern of the tumor extension, nature and function of the adenoma, clinical presentation and data regarding previous operation, surgery related morbidities and if any adjuvant treatment was given after the initial surgery (1,3,8,21,23,25,29). feature number (%) gender: male 12 (40%) female 18 (60%) pathology: nonfunctioning 17 (56.6%) gh producing 8(26.6%) prolactinoma 5 (16.6%) number of previous surgeries: 1 24 (80%) 2 6 (20%) previous resection: recurrent tumor 11 (36.6%) residual tumor 19 (63.3%) clinical presentation: tumor regrowth (mri) 14 (46.6%) visual 9(30%) acromegaly 8 (26.6%) headache 3 (10%) amenorrhea galactorhea 5 (16.6%) 81 surgical challenges of endoscopic endonasal approaches in the management of recurrent pituitary adenomas tumor extension total residual adenoma recurrent adenoma sellar 7 2 5 sellar& suprasellar 12 6 6 sellar&parasellar 6 6 0 sellar&suprasellar& parasellar 5 5 0 table 2. pattern of tumor extension extent of previous resection number of cases gross total resetion tumor extension residual tumor 19 9 (30%) 2 sellar, 6 sellar & supra sellar, 1 sellar &p arasellar recurrent tumor 11 8 (26.6%) 4 sellar, 4 sellar & suprasellar table 3. pattern of tumor extension extent of tumor resection correlated to pattern of tumor extension table 4. outcome of surgery of recurrent pituitary adenomas correlated to literature reports in this study we evaluated our results of endoscopic transsphenoid approach for recurrent and residual pituitary adenomas. among the 30 cases involved in this study; 19 cases were residual tumors and 11 cases were recurrent after initial total resection. among the 19 cases with residual tumors; 11 (57.9%) cases had tumor extension to the cavernous sinus and this reflects that the extent of tumor resection was more related to the pattern of tumor extension rather than the nature of the adenoma or the technique of surgery whether microscopic or endoscopic. in 8 patients with residual adenomas; the tumor was confined to sella in 2 cases and sellar with suprasellar extension in 6 cases and the reason for incomplete tumor removal was inadequate opening all the sphenoid septationswith limited delineation of the sellar floor with less room for manipulating the endoscope and the instrument. series no. of cases eor (no. of cases, %) no. of cases, % of cases other complications gtr str complications hypopit. di csf leak curent study 30 17, 56.6% 13, 43.4% 8, 26.6% 0 4, 13.3% 3, 10% mortality: 1 (carotid injury) negm et al. 2017 41 24, 55.5% 2, 4.9% 8, 19.5% 4, 9.7% 2, 4.9% 1, 2.4% hematoma: 1 (2.4%) wang et al. 2015 29 16, 55% 11, 38% 5, 17% 0 1, 3.4% 1, 3.4% 2 (6.9%) cases of deerioration of vision due to hemorrhage in tumor bed & intracranially; 6th nerve palsy: 1 (3.4%) tajudeen et al. 2015 27 17, 63% 7, 26% 6, 22% 1, 3.7% 2, 7.4% 0 abducent palsy: 1 (3.7%) cavallo et al. 2012 59 37, 63% 9, 15% 8, 13.5% 4, 6.7% 3 (5%) 1 (1.7%)† hematoma: 1 (1.7%) rudnik et al. 2006 20 8, 40% 0 4, 20% 3, 15% 0 1, 5% hwang et al. 2013 30 15, 50% 7, 23% 5, 16% 1, 3.3% 4 (13.3%) 0 mengitis: 2 (6.7%) yamada et al. 2010 53 31, 58.5% 0 5, 9% 1, 2% 1, 2% 1, 2% epistaxis: 1 (2%), pituitary abscess: 1 (2%) alahmadi et al. 2011 39 18, 46% 21, 54% 6, 13% 0 0 1 (2.6%)† 1 mi, 1 hcp, 1 sinusitis, 1 crushing 82 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed mattozo et al. 2006 30 17, 57% 0 5, 17% hypoth: 1, 3.3% 1, 3.3% 1, 3.3% sinusitis: 1 (3.3%), hyponatremia: 1 (3.3%) benveniste et al. 2005 96 0 0 29, 30% 15, 15.6% 5, 5.2% 1, 1% cn palsy: 1, graft site infection: 1, sinusitis: 5, epistaxis: 1 cn = cranial nerve; hcp = hydrocephalus; hypopit = hypopituitarism; hypoth = hypothyroidism; mi = myocardial infarction; pe = pulmonaryembolism. * represents a case of hypocortisolemia. † patient also had meningitis. the importantsurgical step to facilitate efficient tumor resection was the use of binostril four handed endoscopic technique with wide sphenoidotomy and obtaining adequate sellar exposure to have the full panoramic view ofthe carotid prominences, medial and lateral optico-carotid recesses, planum and clivus. with this technique we achieved total resection of the all 8 cases with residual adenomas and 8 out of 11 recurrent cases involving the sellar and suprasellar area (2, 4, 9,18,20,24,27,29). extensive tumor extension into the cavernous sinus is a barrier against total resection of pituitary adenoma disregarding the nature of the adenoma and whether it is de novo or recurrent. some pituitary adenomas like growth hormone secreting adenomas had aggressive inherent biology enabling them to more easily invade surrounding dural and/or bony structures with early parasellar extension into cavernous sinus. the challenge of surgery inside the cavernous sinus increase markedly in recurrent cases particularly if the tumor is fibrous or if the patient was given radiation after the initial surgery. aggressive attempts of tumor resection inside the cavernous sinus is hazardous and increase the potential surgical risks of vascular injuries and ocular cranial nerves palsy. among the 19 cases with residual tumors; 11 (57.9%) cases had tumor extension to the cavernous sinus and from the 11 cases with residual tumor in the cavernous sinus; we were able to achieve total tumor resection in one case at the 2nd surgery and in 10 cases; a residual tumor was left in the cavernous sinus for further adjuvant treatment and the reason for doing the redo surgery was that the tumor growth after the initial surgery and reduction of the tumor size has the advantage of reducing the mass effect to improve the visual manifestation, better achieving hormonal control in functioning adenomas and would improve the response and reduce the associated morbidities of subsequent adjuvant treatment(1,2,4,5,7,8,17,21,28). the extent of tumor resection for recurrent adenomas is addressed in many studies in the literature and the growth total resection could be achieved endoscopically in 40% to 63%. the studies of microscopic resection of recurrent pituitary adenomas had similar results with chance of total adenoma resection up to 60%. although the similarity of the results in the literature; we did all the recurrent cases endoscopically as the we had 19 cases (63.3%) of residual tumor that kept growing after the initial surgery and in 11 of them (57.9%); the residual tumor was in the parasellar region which is a hidden location for the microscopic view. moreover, the extended endoscopic transsphenoidal approach allowed better visualization and hence removal of the sellar and suprasellar component of the tumor than what could be done microscopically. regardless of the better visualization and tumor manipulation, cavernous sinus invasion remained our greatest limiting factor. the overall gross total resection in our study was achieved in 17 patients (56.6%) while subtotal and partial resection in 13 patients (43.4%) which is similar to what achieved in other reports in the literature (3,4,6,11,13,14,15,18,20,22,26,27). reoperations on any recurrent tumor had a higher incidence of complication in comparison for operating a newly developed tumor. rates of complications for recurrent pituitary tumors in many studies the literature ranged from 9.4% to 31.3%. presence of scars and adhesions interfere with natural dissection plans adding difficulties for surgery. the challenge is valid for reoperation on recurrent adenomas with higher incidence of morbidities. one critical complication is the occurrence of csf rhinorrhea after surgery. intraoperative csf leakage could be encountered easily because of scaring of the initial surgery and easily injuring the arachnoid during tumor 83 surgical challenges of endoscopic endonasal approaches in the management of recurrent pituitary adenomas dissection. multilayer reconstruction is crucial and if vascularized flaps could be obtained during the redo surgery; it was the best to prevent post-operative csf leakage. in cases we were not able to harvest vascularized flap; we obtained fascialata and fat graft with fibrin glue to do solid reconstruction when we faced intra-operative csf leakage. then lumbar drain was left up to 3 days after surgery. despite our aggressive reconstruction plan; 3 cases had postoperative csf rhinorrhea; 2 passed conservatively and one required another endoscopic repair. the incidence of post-operative pituitary hormonal insufficiency was slightly higher with surgery for recurrent adenomas. a meta-analysis of the result endoscopic surgery for recurrent adenomas reported transient di in 7%, permanent di in 2.5%, and anterior pituitary hormonal insufficiency in 1.5%. we had 2 cases (6.6%) of transient di, 2 cases (6.6%) of permanent di, 3 cases (10%) developed postoperative hypopituitarism requiring long term hormonal replacement therapy. we had a case of mortality from vascular injury during doing a case of recurrent growth hormone secreting adenomas (1,7,8,10,16,17,19,22,23,29). conclusions endoscopic endonasal approach for recurrent or residual pituitary adenomas allows optimum visualization and better delineation of all hidden corridors to achieve the safest maximum resection. although cavernous sinus involvement still prevents total resection but aggressive safe tumor debulking is essential to reduce the compression manifestation, improve hormonal control and optimize the result of any further adjuvant treatment including radiotherapy or radiosurgery. adequate endoscopic exposure is crucial to improve the extent of resection and minimize the potential morbidities. solid reconstruction plan is very important to minimize post-operative csf leakage. (a) (b) (c) (d) figure 1. preoperative mri image of recurrent nonfunctioning pituitary adenoma sagittal view (a), axial view (b), postoperative follow-up mri images sagittal view (c), axial view (d). (a) (b) (c) (d) figure 2. preoperative mri image of recurrent growth hormone secreating adenoma sagittal view (a), axial view (b), postoperative follow-up mri images sagittal view (c), axial view (d). abbreviations eor=extent of resection, coz= cranio-orbito-zygomatic, ict= intracranial tension, csf= cerebrospinal fluid, ogm= olfactory groove meningioma, gtr= gross total resection, str= subtotal resection, tsm= tuberculum sellae meningioma, psm= planum sphenoidale meningioma. references 1. yamada s, fukuhara n, oyama k et al. repeat transsphenoidal surgery for the treatment of remaining 84 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed or recurring pituitary tumors in acromegaly. neurosurgery 67:949–956, 2010 2. tajudeen ba, mundi j, suh jd, bergsneider m et al. endoscopic endonasal surgery for recurrent pituitary tumors: technical challenges to the surgical approach. j neurolsurg b skull base 76:50–56, 2015 3. wang s, xiao d, wang r et al. repeated transsphenoidal surgery for resection of pituitary adenoma. j craniofacsurg 26:452–455, 2015 4. mclaughlin n, eisenberg aa, cohan p et al. value of endoscopy for maximizing tumor removal in endonasaltranssphenoidal pituitary adenoma surgery. j neurosurg 118:613–620, 2013 5. krings jg, kallogjeri d, wineland a et al. complications following primary and revision transsphenoidal surgeries for pituitary tumors. laryngoscope 125:311–317, 2015 6. hwang jm, kim yh, kim jw et al. feasibility of endoscopic endonasal approach for recurrent pituitary adenomas after microscopic transsphenoidal approach. j korean neurosurgsoc 54:317–322, 2013 7. jahangiri a, wagner j, han sw et al. morbidity of repeat transsphenoidal surgery assessed in more than 1000 operations. j neurosurg 121:67– 74, 2014 8. dhandapanis, singh h, negm hmet al. endonasal endoscopic reoperation for residual or recurrent craniopharyngiomas. j neurosurg2016. 9. ferrelif, turri-zanoni m, canevarifret al. endoscopic endonasal management of non-functioning pituitary adenomas with cavernous sinus invasion: a 10year experience. rhinology 53:308–316,2015 10. hofstettercp, nanaszko mj, mubita llet al.volumetric classification of pituitary macroadenomas predicts outcome and morbidity following endoscopic endonasaltranssphenoidal surgery. pituitary 15:450–463, 2012 11. cavallo lm, solarid, tasiouaet al. endoscopic endonasaltranssphenoidal removal of recurrent and regrowing pituitary adenomas: experience on a 59patient series. world neurosurg 80:342–350, 2013 12. dehdashti ar, ganna a, karabatsou k et al.pureendoscopic endonasal approach for pituitary adenomas: early surgical results in 200 patients and comparison with previous microsurgical series. neurosurgery 62:1006–1017,2008 13. alahmadi h, dehdashti ar, gentilif: endoscopic endonasal surgery in recurrent and residual pituitary adenomas after microscopic resection. world neurosurg 77:540–547,2012 14. cappabiancapandsolari d: the endoscopic endonasal approach for the treatment of recurrent or residual pituitary adenomas: widening what to see expands what to do? world neurosurg 77:455–456,2012 15. rudnik a, zawadzki t, galuszka-ignasiak b et al. endoscopic transsphenoidal treatment in recurrent and residual pituitary adenomas-first experience. minim invasneurosurg 49:10-14, 2006 16. santoro a, minniti g, ruggeri a et al. biochemical remission and recurrence rate of secreting pituitary adenomas after transsphenoidaladenomectomy: longterm endocrinologic follow-up results. surgneurol 68:513518, 2007 17. karabatsou k, o’kelly c, ganna a et al. outcomes and quality of life assessment in patients undergoing endoscopic surgery for pituitary adenomas. br j neurosurg 22:630-635, 2008. 18. kelley rt, smith jl, rodzewicz gm.transnasal endoscopic surgery of the pituitary: modifications and results over 10 years. laryngoscope 16:1573-1576, 2006. 19. kitano m, taneda m, shimono t et al. extended transsphenoidal approach for surgical management of pituitary adenomas invading the cavernous sinus. j neurosurg 108:26-36, 2008. 20. knosp e, steiner e, kitz k et al. pituitary adenomas with invasion of the cavernous sinus space: a magnetic resonance imaging classification compared with surgical findings. neurosurgery 33:610617, 1993. 21. kurosaki m, luedecke dk, abe t: effectiveness of secondary transnasal surgery in gh-secreting pituitary adenomas. nedcor j 50:635-642, 2003. 22. laws erjr, foda nc, redmond mj: transsphenoidal surgery following unsuccessful prior therapy. an assessment of benefits and risks in 158 patients. j neurosurg 63:823-829, 1985. 23. losa m, mortini p, barzaghi r et al. early results of surgery in patients with nonfunctioning pituitary adenoma and analysis of the risk of tumor recurrence. j neurosurg 108:525-532, 2008. 24. mattozo ca, dusick jr, esposito f et al. suboptimal sphenoid and sellar exposure: a consistent finding in patients treated with repeat transsphenoidal surgery for residual endocrine-inactive macroadenomas. neurosurgery 58:857-865, 2006. 25. benveniste rj, king wa, walsh j et al. repeated transsphenoidal surgery to treat recurrent or residual pituitary adenoma. j neurosurg 102:1004-1012, 2005. 26. negm hm, al-mahfoudh r, pai m et al. reoperative endoscopic endonasal surgery for residual or recurrent pituitary adenomas. j neurosurg 127:397–408, 2017 27. cappabianca p, alfieri a, colao a et al. endoscopic endonasal transsphenoidal surgery in recurrent and residual pituitary adenomas: technical note. minim invasneurosurg 43:38-43, 2000. 28. cappabianca p, cavallo lm, colao am et al. surgical complications associated with endoscopic endonasaltranssphenoidal approach for pituitary adenomas. j neurosurg 97:293-298, 2002. 29. chang ef, zada g, kim s et al. long-term recurrence and mortality after surgery and adjuvant radiotherapy for nonfunctional pituitary adenomas. j neurosurg 108:736745, 2008. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 482-485 doi: 10.33962/roneuro-2019-077 www.journals.lapub.co.uk/index.php/roneurosurgery surgical consideration in posterior c1-2 instrumentation in case of vertebral artery anomaly harshad patil1, nitin garg2 1 consultant, department of neurosurgery, bansal hospital, bhopal madhya pradesh, india 2 senior consultant, department of neurosurgery, bansal hospital, bhopal madhya pradesh, india abstract anatomical variations in the course of the vertebral artery have been previously described in the literature. generally, these predictable patterns of variations commonly observed in lower cervical vertebral artery anatomy and less commonly described for upper cervical vertebral artery anatomy. due to presence of these variations, treatment options for upper cervical spine pathology may be influenced and sometimes prevent commonly performed stabilization procedures. herein author presented a case of vertebral artery anatomic variation at the craniovertebral junction and management option for such variations. introduction steady advances have been made in fixation of an unstable atlantoaxial complex over the last century. there are many options for fixation of the atlantoaxial complex like posterior clamps or wiring techniques, c1c2 transarticular screw fixation, posterior c1 lateral mass screw with c2 pars or pedicle screw fixation, and anterior transoral c1 lateral mass to c2 vertebral body fixation1. advantage of the c1-2 screw technique is that it can completely obliterate rotational, flexion or extension motion of the atlantoaxial joint. however, the disadvantages of this technique are the steep learning curve and risk of serious complications like injury to spinal cord, hypoglossal nerve or vertebral artery laceration. to avoid these complications, pre-operative computerized tomography (ct) scanning of the cervical spine is necessary. this is mainly to identify an anomalous vertebral artery course, bony status of the intended site of screw fixation, or unacceptably small c2 pars1. to minimize the risk of vertebral artery injury, screw placement should be done only if the preoperative ct scan confirms the normal anatomic position of the vessel. if aberrant vessel present on unilateral side then screw placement should be done on normal side. if vertebral artery injury occurred during screw placement, then screw placement keywords vertebral artery anomaly, cervico-vertebral junction, cervical stabilization corresponding author: harshad patil department of neurosurgery, bansal hospital, bhopal madhya pradesh, india dr.harshadpatil@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 483 surgical consideration in posterior c1-2 instrumentation in case of vertebral artery anomaly should be done to tamponade the bleeding and contralateral screw placement should be avoided in order to prevent the risk of bilateral vertebral artery injury1,2. herein we presented a case of type 2 vertebral artery anomaly which was managed by placing c1 lateral mass and c2 translaminar screw on normal side and sublaminar wiring on abnormal side. case report 16 years old male admitted in neurosurgery department with chief complaints of heaviness in neck and weakness in all four limbs for 4 months. on examination, his power was 4/5 in all four limbs as per mrc (medical research council) grading. tone was increased in all four limbs and hyperreflexia was present. bladderbowel was normal. magnetic resonance imaging (mri) cervical spine showed compression over cervicomedullary junction with hyperintense signals in cord (image 1). dynamic ct of craniovertebral (cv) junction showed reducible atlantoaxial dislocation (aad) with os odontoidum (image 2). mri angiogram neck showed anomalous origin of left posterior inferior cerebellar artery (pica) at c1-c2 level and intradural entry from left side at c1-2 interlaminal space (image 3). thus preventing safe placement of c1 and c2 screw from left side. to minimize the risk of vertebral artery injury, we placed c1 lateral mass screw (40x34mm) and c2 translaminar screw (35x28 mm) (c2c system) on right side and sublaminar wiring with iliac crest graft on left side (image 4). patient tolerated the procedure well and showed improvement. image 1: preoperative mri cervical spine showed compression over cervicomedullary junction with hyperintense signals in cord. image 2: dynamic ct of craniovertebral junction showed reducible atlantoaxial dislocation (aad) with os odontoidum. 484 harshad patil, nitin garg image 3: mri angiogram neck showed anomalous origin of left posterior inferior cerebellar artery (pica) at c1-c2 level and intradural entry from left side at c1-2 interlaminal space. image 4: c1 lateral mass & c2 translaminar screw on right side and sublaminar wiring with iliac crest graft on left side. discussion the presence of vertebral artery variation at the craniovertebral junction may influence treatment options so it should be identified preoperatively. this helps the surgeons for planning of surgery and minimizes the risk to the vertebral artery injury3. three types of vertebral artery variation at the craniovertebral junction have been described in the literature. the most common variant is a persistent first intersegmental artery (fia), in this the aberrant vertebral artery have taken an anomalous course and enter the spinal canal between c1 and c2 and the normal vertebral artery branch is absent. it found in 3.2% of patients. the second most common variation is an extracranial c1/2 origin of the posterior inferior cerebellar artery (pica). it present in 1.1% of patients. in this variant, the fia continues to the pica without reuniting with the vertebral artery. the third variant is fenestration of the vertebral artery and it is also the least common variant. it presents in 0.9% of patients. all 3 of those variants could have an effect on screw placement because the abnormal vertebral artery passes directly dorsal to the c1 lateral mass. other less common variants have been described but are beyond the scope of this article 3,4,5. there is no algorithm for surgical consideration in posterior c1-2 instrumentation in case of vertebral artery anomaly. only few case reports are available in the literature. hong jt et al used as c1 superior lateral mass as an entry point in case of type 1 vertebral artery anomaly [5]. abtahi am et al performed occiput-c3 fusion in case of type 1 vertebral artery anomaly [6]. yamazaki m performed 485 surgical consideration in posterior c1-2 instrumentation in case of vertebral artery anomaly occiput c2 fusion in case of type 3 (fenestration of vertebra artery) vertebral artery anomaly [7]. song et al in his case series conclude that unilateral c1-2 facet screw fixation with interspinous bone graft wiring is an excellent alternative in the treatment of atlantoaxial instability when bilateral screw fixation is contraindicated. but in his case series there was no vertebral artery anomaly presents [8]. in our case there was type 2 vertebral artery anomaly on left side so c1 lateral mass and c2 translaminar screw insertion was done from right side and sublaminar wiring with iliac crest graft from left side. there are multiple reports of injury to the vertebral artery during anterior cervical decompression surgery exist in the literature. five studies reported rates of 0.10 to 1.96%, depending on the type of anterior cervical spine procedure. there is paucity of literature with respect to vertebral artery injury associated with a posterior cervical surgical exposure. molinari et al recently reported vertebral artery injury in two cases involving a persistent first intersegmental artery in the region of c1–c2. both injuries were occurred with routine posterior exposure of the c1–c2 anatomy 8,9,10. conclusion this particular vertebral artery anomaly produces great risk to the conventional placement of c1 lateral mass screws through previously described techniques. these anomalies can be identified preoperatively by computed tomography angiography. to minimize the risk of complications, thorough assessment of the vascular anatomy is recommended before operative intervention in the upper cervical spine pathology. acknowledgements: none footnotes: no conflict of interest references 1. mummaneni pv, haid rw. atlantoaxial fixation: overview of all techniques. neurol india 2005;53:408-15. 2. huang dg, hao dj, he br, wu qn, liu tj, wang xd, guo h, fang xy. posterior atlantoaxial fixation: a review of all techniques. spine j. 2015 oct 1;15(10):2271-81. doi: 10.1016/j.spinee.2015.07.008. epub 2015 jul 10. review. 3. padget d h. the development of cranial arteries in the human embryo. contrib embryol. 1948;32:207–261. 4. tokuda k, miyasaka k, abe h. et al. anomalous atlantoaxial portions of vertebral and posterior inferior cerebellar arteries. neuroradiology. 1985;27(5):410–413. 5. hong jt, jang wy, kim is, yang sh, sung jh, son bc, lee sw. posterior c1 stabilization using superior lateral mass as an entry point in a case with vertebral artery anomaly: technical case report. neurosurgery. 2011 mar;68(1suppl operative):246-9; discussion 249. doi: 10.1227/neu.0b013 e318207b6e6. 6. abtahi am, brodke ds, lawrence bd. vertebral artery anomalies at the craniovertebral junction: a case report and review of the literature. evid based spine care j. 2014 oct;5(2):121-5. doi: 10.1055/s-0034-1386751. 7. yamazaki m, okawa a, aramomi ma, hashimoto m, masaki y, koda m. fenestration of vertebral artery at the craniovertebral junction in down syndrome: a case report. spine (phila pa 1976). 2004 dec 1;29(23):e551-4. 8. song gs, theodore n, dickman ca, sonntag vk. unilateral posterior atlantoaxial transarticular screw fixation. j neurosurg. 1997 dec;87(6):851-5. 9. curylo l j, mason h c, bohlman h h, yoo j u. tortuous course of the vertebral artery and anterior cervical decompression: a cadaveric and clinical case study. spine (phila pa 1976) 2000;25(22):2860–2864. 10. molinari r, bessette m, raich a l, dettori j r, molinari c. vertebral artery anomaly and injury in spinal surgery. evid based spine care j. 2014;5(1):16–27. 12rahmanabdul_treatment 200 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome treatment of lumbar spinal stenosis (lss) and outcome hawis abdul salam abdul rahman1, gabriel iacob2 1siria, 2neurosurgery clinic bucharest romania “outcome may be improved by more careful selection of patients and by performance of an adequate surgical decompression” deen g. et al. mayo clin proc 1995, 70, 33-36 the natural history of lumbar spinal stenosis is critical to treatment decisions, since it is unlikely that symptoms will worsen or that neurologic function will deteriorate rapidly, prophylactic treatment is not warranted; also there are no specific recommandations: see randomized prospective controlled trials of surgical vs nonsurgical treatment (1-18). because spontaneous improvement is uncommon, watchful waiting is an unsatisfactory strategy for patients with intolerable symptoms, surgical attitude lukes like natural to alleviate pains, to improve fonctional capacity, to obtain symptoms resolution (1)(2)(4)(7)(8)(11-13)(17)(18). the clinical coursevaries considerably: in most patients, is chronic, benign, stagnating – see also emg changes (16), partially controllable by conservative treatment or is expected to progress slowly, with neurogenic claudication or although rare, with a cauda equine syndrome – with sensory and motor deficit, saddle anesthesia, bowel and bladder dysfunction, imposing a causal treatment of spinal canal stenosis (10)(14-16)(20). if disk prolapse tends to regress spontaneously, the causative degenerative changes associated with spinal stenosis will progress slowly (15)(21-23). in most patients (60% to 70%), the pain seems to stagnate in the medium term (5)(6); of the natural course of 31 patients with lss over 49 months reports: unchanged symptoms in 70%, improvement, even walking capacity in 15%, worsening in 15%(5). in patients with pronounced symptoms, a high degree of stenosis and spondylolisthesis, a progressive disease course may be assumed and surgery is consistent with clinical experience, showing several advantages in terms of disability, leg pain, backache, for symptoms recurrencies at least in the short term, most surgically treated patients would again choose surgery and quality of life at 3-6 months, remained for up to 2-4 years (13)(6)(7)(11-13)(17-23). there are also unclear aspects too: why there is no no difference in the outcomes of patients who underwent surgery earlier vs later in the disease; several outcome parameters are unknown: the duration of follow-up, the outcome measures, level of pain, use of analgesics, walking capacity, fluctuating evolution, medical and surgical treatments frequently interference, time for surgery (2-8)(10-14) (16-23). also nonsurgical management is effective: up to one third of patients treated surgically romanian neurosurgery (2015) xxix 2: 200 229 201 for residents responded to non-surgical treatment: 70% satisfactory at 6 months, 57% satisfactory at 4 yrs; it’s generating a slight to moderate improvement for a time, it is advisable initial for most patients (1)(7)(8)(10). a recent publication in the new england journal of medicine (2), the spine patient outcomes research, 13h trial (sport) from the us, supported these results in a larger group of 289 patients, in a randomized cohort and 365 patients in an observational cohort. surgery resulted in faster and significantly better alleviation of complaints than conservative treatment. interestingly, patients who did not have surgery also experienced a reduction in symptoms, albeit at a slower rate. however, this study showed that surgery is superior to conservative treatment in the longer term, decompression should be advocated whenever history, symptoms, findings and imaging clearly indicate its use in patients with lss refractory to conservative treatment for at least 3 months, the patient should be informed about results. similar results has also malmivaara (1), but no current recommendations. the conservative treatment are based on observations, clinical judgments; should be applied in a stepwise pathway that progresses from least invasive treatments: activity restrictions, physical therapy, analgesics, antiinflammatory medications, lumbo-sacral orthoses, to most invasive epidural or intratecal injection with corticoid products, calcitonin, peripheral vasodilators medication with a success rate of 50-65% of cases, prostaglandin e (3)(6)(7)(10-12)(17)(2330)(32). there are also reports, but not highquality trials, reporting no substantial change over the course of 1 year to majority of symptomatic patients with lumbar spinal stenosis whose are managed non operatively (5)(7)(13)(19)(22)(23). decompression is more effective than other alternative ? (8)(21) the conservative treatment indications are (16): as initial treatment for radiculopathies cases, without significant deficits, reducing pain, augmenting walking distance; a therapeutic option to those patients who cannot be operated. several alternatives are deployed as a multimodal therapeutic concept: physical therapy(16)(19)(20)(23)(27) gives symptomatic relief of root or low back pain with the goals of improving strength, endurance and flexibility, significant benefit concerning: standing time, pain score, roland disability score, walking distance; maintaining a better posterior pelvic tilt. using a customized program several therapeutic alternatives could be used: � active exercises in the form of stretching to increase lumbo-pelvic muscular stabilization, distraction, manipulation and neural mobilization, encouraging lumbar flexion and flattening of the lumbar lordotic curve; also exercises performed during lumbar flexion, such as bicycling are better tolerated than walking, avoid hyperextension and side bending � massage, ultrasound, tens, braces, supports, lumbar corsets for a limited number of hours per day, to avoid atrophy of paraspinal muscles, 202 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome in patients with symptomatic spinal stenosis with pain, maintaining a posture of slight lumbar flexion; although there are no trial data to guide this decision; treadmill and ergometer training acupuncture; biofeedback; hot or cold packs; traction or chiropractic manipulation. these therapies (14) have not been compared in any randomized controlled trial and there is considerable variability among practitioners in their use. for pain: medication such as acetaminophen, non-steroidal anti-inflammatory drugs (nsaids), anti-cox 2–debatable efficacy, used for short time (2)(4)(13)(23)(27-30), tolerance mediocre, although there is no clear rationale, but are strongly contraindicated in patients with a history of congestive heart failure, peptic ulcer or kidney disease; muscle relaxants – used when pain is not controlled by antalgic drugs, nsaids, but no proofs; also mild narcotic analgesics. lumbar epidural corticosteroid injections (24)(25-28) are justified to control severe roots symptoms on the assumption that symptoms may result from inflammation at the interface between the nerve root and the compressing tissues. data on the efficacy of epidural injections are sparse and mixed; on low time, especially in older patients is a lack of consistent evidence of efficacy (24). in patients with predisposing conditions, such as diabetic patients and in repeated infiltrations, infections are possible, which may have severe consequences (31). no efficacy or even negative results with foraminal or even intrathecal, made blind or under fluoroscopic control (28) -relational causes treatement: anxiolytic, antidepressive, relaxation, education (reassure the patient, explain) long-term opioid therapy (28) should be considered for older patients with unsatisfactory response to other medical therapies and who are not surgical candidates with the following caveats: assess for pain control and functional improvement in walking, standing, self-care activities, may generate complications: constipation and in the older patient may adversely affect cognition. -calcitonin could be tried in patients with lumbar spinal stenosis administered by nasal spray to improve pain and walking tolerance, usually apparent within 4 to 6 weeks, despite double blind, randomized, placebo-controlled trial (29)(30). the calcitonin’s mechanism of action is unknown: nonspecifically by raising the level of endogenous opioids beta endorphins or by enhancing circulation to an ischemic cauda equine (22). prostaglandin e was credited by yoshihara (32) useful in lss treatment, based on same raising the endogenous opioids level. the conservative treatment conclusions: conservative treatment is a therapeutic option for lss without major risks see nsaids complications it’s acceptable for the patient several options could be used to those patients who cannot be operated it must be applied as the first treatment the surgical treatment is not only a solution for resistant symptoms in patients romanian neurosurgery (2015) xxix 2: 200 229 203 for residents with lss, but even useful: in cases of consistent clinical and radiological findings after adequate conservative therapeutic measures have failed for a time at least three months, to patients with realistic expectations; certified although by few evidence-based insights into the treatment options (1)(2)(4)(68)(12)(17)(19)(23)(33-41). surgical treatment in lss means (33)(34)(38)(40-55): -a functional surgery – never operate pictures with the aim to alleviate symptoms, to normalize daily life activities, improving functional capacity, achieving a good quality of life -difficult surgery – most aged patients, with chronic illness; there are still 20% unsatisfactory results -experience surgical treatment should be applied to each patient, with a perfect correspondence between neuro-radiological and clinical findings there are several points to consider into the preoperative planning (33)(50)(51)(56): � medical status & physiologic age of the patient � clinical and morphologic aspects, associated pathology – it’s rational to consider a disturbed balance between the capacity of the spinal canal and its contents at the time of presentation must be responsible for the insidious onset of neurogenic claudication; also is usually symptomatic at a particular side & motion segment/s rather than affecting bilateral multiple radiological involved levels; careful evaluation of all available data proved that the number of nerve roots requiring decompression is often less than what appears in radiological studies alone � the timing for surgery has not been clearly decided. data comparing the outcomes of patients who underwent surgery earlier vs later in the disease suggest no difference in outcome � is there deformity/instability too ?, the suggested decompression technique alone may lead to segmental instability ? � a fusion technique should be performed to all cases ? – see loss of mobility of the operated segment, possible adjacent segment decompensation or unless instability is present pre-op; for older patients ability to fuse may be compromised, also fixation may not be adequate � the proposed surgical procedure should be correlated with long-term results relating especially to modern techniques, which are still often lacking � should this operation to be the “last surgery”? � it’s also art of surgery– adequacy for enlarged lumbar spinal canal it’s a balance between doing too much and not doing enough: suppressing the conflict between the lumbar spinal canal with disco-ligamentous structures and the content represented by the dural sac and radicular nerves, decompressing the neural foramina, eliminating pressure 204 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome on the spinal nerve roots, without generating spinal instability, never prophylactic in the absence of randomized prospective controlled trials of surgical vs nonsurgical treatment several ideas should be underlined (1)(2)(4)(11)(12)(16)(19)(20)(23)(33)(34)(39) (41) (50)(54)(56): -stenotic symptoms improved significantly more often in surgically treated patients; there is an advantage at least in the short term than in conservatively treated patients -most surgically treated patients would again choose surgery; no difference in outcomes of patients who underwent surgery earlier vs later in the disease; but over 10 years outcome was most favorable with surgery -however, up to one third of patients treated non surgically also do well and an initial nonsurgical approach was advisable for most patients the aims of surgical techniques (50)(51)(53)(54) in degenerative lumbar spinal stenosis should be critical evaluated since the aims of the procedure are clearly explained in the written consent, especially to old-aged patients: � to restore functional capacity acting on neuro-vascular compression, with no or limiting complaints: neurogenic claudication + mono or multi roots resting or in efforts pain; subjective neurologic signs + neurologic deficit during walking, to improve leg and low back symptoms, to increase the pain free walking distance � to achieve a good quality of life using a technique for “maximum effect with minimum trauma”: minimize tissue disruption, decompress the lumbar channel and the roots, avoid to destabilize, no stabilization, no instrumentation, minimize time of surgery and length of hospital stay, minimize post operative morbidity, avoiding complications, to permit a rapid patient mobilization, almost addressability is for old, fragile patients think to an unique surgical procedure it’s better to inform the patient, that surgical treatment has no action on (33)(51)(54): focal or diffuse low back pain and/or stiffness “degenerative” illness no patient will be completely free of complaints no patient will have a new lumbar spine after the operation surgical indications are depending on case to case evaluation (37)(38-41)(50): -general indications related to age without a priori contraindications, comorbidities, surgeon experience which predicts failure of conservative therapy or patients intolerant to conservative therapy, younger age and somatic co-morbidity were independently associated with life dissatisfaction -specific indications related to: degree of stenosis, mri findings, with evidence of good correlation between severity of symptoms, radiological concordance and surgical outcome and poor correlation between degree of stenosis with degree of symptoms; degree of romanian neurosurgery (2015) xxix 2: 200 229 205 for residents disability (odi, pain analog scales, walking distance, daily life activities), degree of instability and associated neurological deficit, surgical option and the timing for surgery individualized on patient request. establishing indications, there are several situations (50)(54): � incidental finding of lss and those with no limitation of life style; not bothered by symptoms (mild): explanation of findings, reassurance and “watchful waiting” treat any co-morbidities or other conditions contributing to symptoms of stenosis treat low back pain with nsaid’s (selective cox2 inhibitors) � symptomatic lss: patients with cauda equine syndrome (52) should be operated on emergency – rare cases � symptomatic lss with persistent or worsening symptoms of neurogenic claudication and/or radiculopathy (reduced walking distance but can manage daily activities with medication) despite conservative therapy for at least 3 months, with minimal co-morbidities, radiologically demonstrated severe stenosis the best patients to benefit from surgery. also in cases with recurrent symptoms (56) proofed clinically and radiologically of: residual stenosis at operative site due to inadequate first surgery, stenosis at adjacent levels to surgical site, new herniated disc, epidural and arachnoidal adhesions, instability and/or spondylolisthesis following first surgery, in the absence of demonstrated stenosis, further investigations are warranted: contrast studies, emg and ncs. for symptomatic lss evidence in the literature is poor for correlating degree of stenosis with degree of symptoms, but there is a good correlation between severity of symptoms and surgical outcome (34). because the timing for surgery has not been clearly decided (50), option for early surgical management is based, in selected patients, on surgeon experience who predicts failure of conservative therapy, to those patients failing or intolerant to conservative therapy or patients with associated instability and neurological deficit. � symptomatic lss in patients with comorbidities that increase surgical risk (46) severe medical conditions (severe pulmonary disease or unstable cardiac status) morbid obesity, diabetic severe osteoporosis extremely advanced age: treat with conservative measures, use adaptive techniques for restoring mobility, utilize rehabilitation services such patients should be treated with conservative measures, adaptive techniques for restoring mobility, utilize rehabilitation services 206 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome � patients with lss candidates for instrumentation and fusion (35)(36)(48): pre-existing spondylolisthesis, instability; if proposed operation may compromise spinal integrity (about 5% laminectomies in most series ended up requiring stabilization) a consent should be obtained. lss surgical tactic strategy should respond to 5 problems (33)(43)(45)(48-51): 1. should we decompress ? yes, in a majority of cases no in cases with instability; hypermobility may accentuate compression – it’s better to stabilise without decompression 2. what kind of surgery should be done ? micro or macro ? it’s better to choose the best operative technique, avoid reintervention, never preventive. the operative technique should minimize tissue disruption (smaller incisions, less tissue trauma), minimal blood loss, minimize time of surgery, length of hospital stay, post operative morbidity, with earlier return to activities and work; easier operative approach in obese patients. it should be used local or regional anesthesia combined with conscious sedation, less postoperative pain medication is required. what to do in the meantime requirements: continue with current best practice surgical expertise and experience for patient selection & for surgical skills, inform patients of surgical choices and availability of resources and facilities in institution informed consent 3. which roots should be decompressed ? electrophysiological testing correlated to through neurological examination is more accurate than radiological evaluation alone in choosing the roots to be decompressed. in practice we deal with several situations: -central lumbar canal stenosis even with unilateral radiculopathy, during walking or effort – decompress all roots -lateral recess stenosis bilateral with unilateral radiculopathy, at one level decompress both roots -lateral recess stenosis multilevel, with unilateral radiculopathy – radical fenestration and foraminotomy technique, decompressing only the symptomatic side & level -foraminal stenosis decompress affected root 4. stabilisation is needed ? there are several aims to respect: -treat a dynamic componentpatients with severe symptoms and radiographic evidence of excessive motion, greater than 4 mm translation or 10o of rotation, who fail to respond to a trial of nonsurgical treatment prevent a postoperatory instability stabilization is needed for: confirmed preoperative instability, extent of bone resection, articular processes orientation, spinal static condition 5. what type of stabilisation should be used? preoperatory instability, see also articular processes orientation spinal static the extent of bone resection caveats: no systematic stabilization ! stabilization should be limited ! no stabilization for lumbar associated pains ! romanian neurosurgery (2015) xxix 2: 200 229 207 for residents -fusion should be made to obtain a stabilization after arthrectomy, to correct a deformity, to avoid a hyper-mobility, maintaining lordosis and foraminal size -arthrodesis &instrumentation open rigid stabilization systems with pedicle screw fixation percutaneous motion preservation: dynamic stabilization systems facet arthroplasty tfas® total facet arthroplasty system lumbar interspinous implants: colfex, wallis, diam, x-stop surgical interventions for lss a variety of surgical techniques can be used depending on patient selection (informed written choice and consent) surgical skills, surgeon expertise and experience, but also availability of resources and facilities in each institution (50)( 54)(55)( 57)(58)(60-133) a. for lumbar spinal stenosis 1. “the gold standard technique” – microsurgery using microscope and micro instruments to realize microsurgical decompression without instrumented fusion and with segmental stabilization. microsurgical decompression of the spinal canal or “internal laminoplasty” (50)(51)(60)(61)(66)(71)(72)(75)(76)(78)(79) (82)(129)(133) is defined as a mono or multi segmental, unilateral or bilateral internal enlargement of the central and/or lateral volume of the spinal canal, without performing a laminectomy. surgical principle the spinal canal is approached through a modified microsurgical inter-laminar route usually from the (most) symptomatic side. in cases with associated degenerative lumbar scoliosis, the approach from the convex side is preferred. the inter-laminar window is opened ipsilateral by resection of the hypertrophied yellow ligament. the insertions of the yellow ligament are resected by osteoclastic undercutting of the cranial and caudal lamina. subarticular ipsilateral decompression is achieved by undercutting or partial resection of the medial parts of the superior facet of the infradiacent vertebra. enlargement of the central parts of the spinal canal, controlateral decompression of the lateral recess is performed without the risk of destabilization of the motion segment by a limited and modified approach bringing in the working instruments through an “over-the top” approach which means undercutting of the laminae and resection of the ventral parts of the interspinous ligament. this approach was proposed by poletti (73) and refined by mcculloch (75) for the treatment of lumbar disc herniations. micro surgery for lss has both technical as well as clinical advantages, but also limitations; using para-spinal approach introduced by wiltse in 1973 (63) are many advantages: technical advantages: permit bilateral decompression of the spinal canal through a unilateral approach, also the spinal nerves on both sides; from their dural sleeve exits to their entrance into the foramen decreased trauma to paravertebral muscles on the ipsilateral side, preserving skin vascularisation which is dependent on two networks joigned at 30 mm from midline, no 208 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome trauma to paravertebral muscles on controlateral side, preserve the posterior spinal elements: limiting the iatrogenic disruption of ligaments (supraspinous, interspinous), spinous processes, paraspinal muscles on the contro-lateral side as well as complete preservation of the laminae, the two thirds of the facet joint on the ipsilateral side and more than 75% of the facet joint of the contro-lateral side -avoids iatrogenic multifidus denervation, devascularization, atrophy if approach are median, diminishing low back pain about to this muscle which is a key position -allows decompression, pedicle fixation under visual control (no need fluoro), tlif, elif, plf -offer direct access to articular process, entry point of pedicle fixation, transverse process and sacral alar decreased operative blood loss even in multi segmental approaches clinical advantages result from the technical advantages: -decrease postoperative pain & infection rate, minimize rates of developing de novo postoperative changes in spinal alignment segmental motion is similar to the intact spine, avoiding iatrogenic « instability » -decrease hospital stay & duration for rehabilitation, increase patient satisfaction and confort, quicker return to normal activities -early mobilization by decreased trauma to paravertebral muscles; important argue to decrease postoperative complications: such as deep venous thrombosis, urinary tract infection or pneumonia due to prolonged immobilization; especially in aged patients >70 years, without stability operation indication reduce surgical morbidity in a frequently high-risk patient group. reported success rates of surgery vary considerably in uncontrolled trials (50), but data from long-term studies are lacking. over the past several years, minimally invasive surgical techniques have been introduced that use smaller incisions and more limited removal of the laminae and facet joints to achieve decompression. early results from small observational studies are promising (51) limitations: longer surgery: 45 to 60 min per level -an insufficient exposure lead to intempestive manipulation of the thecal sac and cauda equina, generating temporary and/or permanent neurological deficits unfavorable clinical outcomes by inadequate decompression, especially of the controlateral side -radiation exposure -dural tear -learning curve before micro surgery for lss, the patient must sign the informed consent on the risks of microsurgical mono or multilevel approaches to the lumbar spinal canal: nerve root, cauda equina and/or conus medullaris lesions with postoperative neurological deficits, inclusive bladder and bowel dysfunction; dural tears with menigocele and/or csf fistulas, postoperative epidural hematoma, meningitis, spondylodiscitis with epidural abscess, compressive epidural scarring with permanent sciatica or even neurological deficits, segmental instability, chronic low back pain romanian neurosurgery (2015) xxix 2: 200 229 209 for residents and radicular symptoms (“failed back surgery syndrome”) requiring stabilizing surgical procedures. micro surgery for lss indications: -symptomatic lss patients, congenital or acquired, with spinal claudication, stiffness of low back pain, loss of lumbar lordosis, uni or bilateral crural symptoms, with or without vertebral body translations -proof of neuroradiology of a narrowing of the central and/or lateral spinal canal, in relation to the topography of the affected lumbar nerve roots: dynamic mri, myelo-ct, saccoradiculography (measurement of the sagittal and/or transverse diameter of the spinal canal are not helpful for the indication for surgery, since it is not the absolute width of the spinal canal). for a differential diagnosis, see peripheral radiculopathy: electromyograms – emg (80), nerve conduction studies or somato-sensory-evoked potentials (sse) are useful to rule out other diagnosis. -decompression without stabilization is performed in all patients without radiological signs of vertebral body translation, in patients without low back pain despite vertebral body translation or degenerative scoliosis, in patients older than 75 years, with severe osteoporosis and multi segmental pathology -decompression with segmental stabilization (usually posterior–anterior 270° fusion or tlif) is performed in patients exhibiting grade i or higher type spondylolisthesis on rest or functional x-rays with significant low back pain, as well as in patients with unstable lumbar degenerative scoliosis. micro surgery for lss contraindications: unstable angina pectoris, severe arterial hypertension, severe respiratory insufficiency micro surgery for lss surgical technique (60) preoperative planning is based on: -clinical -neuroradiologic studies: -x-rays of the lumbar spine using ap and lateral views -for instability functional x-rays in flexion and extension to reveal a degenerative scoliosis, segmental rotational or translational instability -mri the imaging technique of choice, using standard facilities: the thickness of the yellow ligament, its extension underneath the adjacent laminae as well as the thickness of the lamina itself; the size and topography of the neural structures at the level of compression as well as above and below to avoid damage during decompression; the epidural fat distribution which may lead to enter the spinal canal through a more medial posterior route where more epidural fat protecting the thecal sac especially in a extremely narrow lumbar canal; the shape of the spinal canal (round, oval, trefoil) and estimate whether it is mainly soft tissue (yellow ligament, joint capsule, intervertebral disc) or bone (superior facet, lamina, osteophytes) which leads to a compression of neural structures, preserving the bony structures as much as possible or dynamic facilities to discover instability -ct scan/post-myelographic ct-scan -electrophysiologic studies especially in a multilevel stenosis: emg, ncv, somatosensory-evoked potentials (sse) 210 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome the operation is performed under general anesthesia, requiring arterial blood pressure monitoring, central venous line, the introduction of a urinary catheter. if a multilevel decompressions is intended, blood collection for retransfusion or blood transfusions are nedded. the patient should be positioned as similar for lumbar micro discectomy in a prone “mecca” position, restricting head rotation, padding the eyes, forehead and nose; also protecting shoulders, brachial plexus, ulnar nerve, the knees with as many gel cushions or pads as are needed. the level(s) which have to be approached for microsurgical decompression are localized. the skin incision is centered exactly over the lumbar segment of interest. for two or more adjacent levels the skin incision is enlarged; for nonadjacent levels two separate skin incisions are recommended. after the interlaminar space is approached a new intraoperative reperage is performed and under microscope, fascia is opened in a semicircular manner, leaving the medial parts attached to the supraspinous ligament and the lamina. the paravertebral muscles are retracted after subperiosteal elevation. retraction does not extend beyond the lateral border of the facet joint in order to avoid disruption of segmental innervation. the laminae of the adjacent vertebrae are exposed, the interlaminar window is cleaned of soft tissue, the speculumretractor is inserted, the interspinous ligament is exposed, verifying that the visual axis toward the midline is not obstructed by a hypertrophied or dysplastic spinous process. microsurgical ipsilateral decompression is started with the removal of the inferior parts of the cephalic lamina, using a high-speed burr. laminotomy is extended laterally and caudally. depending on the size ofthe inferior facet, its medial aspect is removed until the medial parts of the superior facet can be identified. the yellow ligament is removed with rongeurs including the ventral parts of the interspinous ligament. adhesions of the dura to the yellow ligament are gently dissected from medial to lateral. after removal of the yellow ligament and its insertion underneath the lamina in most of the cases the central portion of the spinal canal is already decompressed. however, if there is still narrowing by a hypertrophied lamina, undercutting has to be continued in cranial and caudal directions. “subarticular” decompression can be the most difficult part of the operation. usually there is no space between the lateral parts of the thecal sac, the nerve root and the superior facet. with a blunt micro dissector, the neural structures are gently mobilized from the yellow ligament, the lateral recess is opened with a 1.5 or 2 mm kerrison rongeur, proceed first in a caudal direction, minimizing the risk of dural laceration or nerve injury. decompression continue along the nerve until the medial border of the pedicle can be visualized and completed until the inferior border of the exiting nerve root can be identified or palpated with the blunt nerve hook. in cases with pronounced narrowing of the intervertebral space there is often impingement of the exiting nerve root by the tip of the superior facet. this tip can now be removed with a rongeur thus achieving a complete decompression of the exiting nerve root in the foramen. romanian neurosurgery (2015) xxix 2: 200 229 211 for residents microsurgical controlateral decompression is realized tilting the table and adjusting the microscope to give an oblique view into the spinal canal. the ventral parts of the interspinous ligament, sometimes even ventral parts of the base of the spinous process should be resected, also the transition zone into the fibers of the contralateral yellow ligament are resected; the yellow ligament of the contralateral side are resected. it is necessary to continue undercutting of the supra and infradjacent lamina to increase the spinal canal volume as well as to have a free visual axis toward the controlateral recess and foramen entrance. decompression is facilitated if the medial border of the controlateral inferior pedicle is identified by minimum retraction of the thecal sac. then decompression by subarticular undercutting as well as by undercutting of the supradjacent lamina can be accomplished using a blunt dissector, a nerve hook or a metal sucker probe to temporarily retract the dura. at the end of the procedure the surgical field is irrigated with saline solution, hemostasis is achieved with small amounts of bone wax for the bone surface, avoiding to place into the spinal canal gelfoam, surgicel; fascia and the skin are closed with absorbable sutures. for the lumbar lateral recess stenosis a bilateral lateral recess decompression via subarticular fenestrations (57) is a less invasive technique, which enables to decompress the neural structures while preserving as much of the bony structures and ligamentum flavum as preferred. these technique will lead to early mobilization of patients without impending instability, less postoperative pain and immobility, minimal epidural fibrosis, providing an easier reoperation of the same area if required. 2. endoscopic: not superior to “gold standard”(51)(54)(61)(62)(65-70).the micro endoscopic decompression technique used in spinal lumbar stenosis is a less invasive form of surgery, based on the micro endoscopic discectomy as developed by foley and smith in 1996 (70). using this method, it is possible to address problems on the controlateral side in addition to those on the ipsilateral side. therefore there is no valid evidence from randomized controlled trials on the effectiveness of transforaminal endoscopic surgery for lumbar stenosis (67): • comprehensive systematic literature review • no randomized controlled trials, seven observational studies. • studies were of poor methodological quality • heterogeneous regarding patient selection, indications, operation techniques, follow-up period and outcome measures. • re-operation rate varied from 0 to 20%. the micro endoscopic decompression technique is characterized by several advantages: -require local or regional anesthesia combined with conscious sedation -a small skin incision, useful even for two neighboring segments approach -less invasion of paraspinal muscle because the paraspinal muscle is not detached from the lamina, less tissue trauma, a small dead space -affords a safe procedure, minimizes resection 212 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome of the pathologic compression tissues -the ipsilateral approach and controlateral endoscopic decompression can be performed under the midline posterior structures the same as microsurgical decompression or even more easier tilting the tubular retractor about 20° to 30° medially -damaged areas inaccessible by direct vision can be reach by an endoscope angled at 25°; it’s possible to see the compressed nerve root directly under the hypertrophied superior facet -minimal blood loss -less postoperative pain medication -earlier return to activities and work -easier operative approach in obese patients -excellent clinical outcome and patient satisfaction in most cases the micro endoscopic decompression technique disadvantages: -demanding technique, a steep learning curve; for lss should be applied only after mastering the endoscopic procedure for lumbar disc herniation -the field of view through the endoscope is limited, which makes it difficult to appreciate the amount of bony resection that has been performed indications: -initially for lateral recess stenosis, because the inter laminar space is relatively wide -for moderate central canal stenosis the micro endoscopic decompression technique in lss: -after radiologic control, tubular retractor is inserted and a minimal skin incision is performed -different types of endoscopes angulations are used -using a curved chisel, the inferior part of the ipsilateral lamina and the medial side of the inferior facet is cut, the remnants of lamina are removed with kerrison rongeurs -the ligamentum flavum is cut transversely, with a sheathed knife blade and removed piece by piece with the kerrison rongeur the tubular retractor is moved to the medial side through and beneath the interspinous ligament controlateral; the ligamentum flavum and medial facet are removed by using the kerrison rongeur always oriented away from the nerve root during the decompression procedure, exposing the dural tube, ipsi and controlateral nerve roots, which could be retracted, using the penfield retractor using a curved chisel the additional medial facet are removed -also a small chip of shaved lamina could be removed by the use of a pituitary rongeur -hemostasis is realized using a bipolar coagulator, bone wax. 3. conventional several techniques have been used, depending the lss topography: central stenosis, lateral stenosis and mixed stenosis. for central stenosis there are (33)(39)(43)(4951)(55)(56)(83)(87)(9597)(98)(99)(105) (108)(109)(111): -laminectomy with bilateral foraminotomy (yellow ligament removal, inferior facetectomy, respecting isthm, discectomy if needed, it could be made in block or by fragmentation = “the recalibration” – “the windows technique” romanian neurosurgery (2015) xxix 2: 200 229 213 for residents laminectomy is still considered to be the treatment of choice in degenerative spinal stenosis without instability, used for adequate and safe decompression of lumbar stenosis, with highly significant reduction of symptoms and disability and improved health-related quality of life. laminectomy is the traditional standard operation in lumbar spinal stenosis decompression, to remove the roof of the spinal canal. if no preoperative instability, laminectomy does not require fusion or fixation; only about 5% laminectomies (in most series) ended up requiring stabilization, if facet and discal anatomy is compromised. for congenital central spinal stenosis wide laminectomies are indicated because that narrowing of the spinal canal not only affects the interlaminar interval but also the sublaminar space in multiple segments. in a meta analysis, the success rate of this procedure has been shown to be 92.2% fair to excellent result (finneson + cooper criteria), 9.8% complications, including 6.8% durotomies, 11.2% re-operation rate (restenosis, instability, complications)(76) nerve compression is usually limited to the height of the intervertebral space in the area of the hypertrophied joint facets and the ligamentum flavum. removing long sections is therefore not necessary, which has – aided by enormously increasing numbers of surgical procedures – resulted in the development of newer, less invasive techniques. -unilateral and bilateral laminotomy „recalibrage“ means lumbar decompression by partial removal of laminae. there are several techniques variants: unilateral hemilaminotomy (66) (one or several levels), partial decompressive lamino-arthrectomy uni/bilateral, hemilaminotomy + arthrectomy with ligamentectomy & recess decompression (87-90). there are several alternatives to laminectomies: the “port-hole”technique is a surgical procedure for spinal stenosis developed by dr. kleeman in 1992 (88); instead of performing a laminectomy and removing the spinous processes, the spinal canal was decompressed through openings or “port holes” that left the spinal structures intact. weiner et al. (100) used a procedure for lumbar decompression, with unilateral periosteal dissection of multifidus, to minimise denervation and subsequent atrophy. a modified weiner technique is ”the hinge osteotomy technique” applied by elabed k. et al. (101)(107); a safe unilateral approach for multi-level lumbar stenosis, allowing wide decompression of lumbar spine with significant symptom and functional improvement and no iatrogenic spinal instability ”the hinge osteotomy technique” incorporate: unilateral subperiostal muscle dissection with osteotomy of the of the base of the spinous processes of the involved segments, just superficial to their junction with the lamina, bilateral complete laminectomies avoiding over-resection of the facet joints (less than 30%) and complete resection of the ligamentum flavum thereby providing excellent exposure, preserving the integrity of the posterior elements, while maintaining posterior column stability 214 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome a variant of bilateral laminotomies are “the transspinous median sublaminar decompression” which means bilateral laminotomies, with unilateral periosteal dissection of multifidus, to minimise denervation and subsequent atrophy, osteotomy of the spinous processes of the involved segments, just superficial to their junction with the lamina weiner procedure, (111) in most outcome parameters, bilateral laminotomies was associated with a significant benefit and thus constitutes a promising treatment alternative. -radical fenestration (93) as an alternative to laminectomy, interlaminar fenestration techniques have become established that spare the midline structures and thus the dorsal tension band, decompressing the nerve roots, by resecting the ligamentum flavum and parts of the medial facet joint; exceptionally disc removal. encouraging results have been shown for bilateral fenestration and unilateral fenestration with undercutting controlateral decompression. -foraminotomy (50)(51)(133) means radicular nerve decompression by classic or minimal invasive decompression technique removing ligamentum flavum, partial inferior arthrectomy. it can be associated with discectomy -open door expansive lumbar laminoplasty is another decompressive lumbar spinal canal technique without impairement of instability (50)(51) today's conventional technique should provides excellent exposure, a safe approach even for multiple level stenosis, maintaining posterior column stability. this techniques are generally based on: -clinical evaluation, inclusive: -leg pain validation vas (0-10), -self-reported functional status based on likert scale (srfs: pain interference with normal work:1 not at all 5 extremely) -likert symptom-specific well-being score (sswbs: 1 very dissatisfied 5 very satisfied) -likert general well-being score (gwbs how would you rate your quality of life? 1 very bad 5 very good) -oswestry disability index for leg pain (odi) -radiologic evaluation, lumbar spine ct and rm, standardised lumbo-sacral x-rays along with lateral flexion and extension radiographs – defining spinal instability as sagittal plane translation of 3 mm or more white and panjabi (1990) clinical bio-mechnics of spine (cited by 54); performed preop, at 6 months and 3 years post op to demonstrate evidence of progressive segmental instability. -operation is made under general anesthesia, using magnifying loops -the patient is placed in prone position, midline incision is made, after radiological level confirmation. -periosteal multifidus muscle dissection is carried out unilaterally -the electric pen burr is used to delineate the base of spinous process -the integrity of the posterior elements: the spinous process, interspinous/supraspinous romanian neurosurgery (2015) xxix 2: 200 229 215 for residents ligaments, and facet capsules are preserved -surgical retractors are spread to hinge the spinous process(es) off the midline -the spinal canal, the foraminal zones and nerve root canals are decompressed after bilateral laminectomies and complete excision of ligamentum flavum, as completely as possible, avoiding over-resection of the facet joints less than 30% -fat pad is laid on the dura to avoid subsequent fibrosis -supraspinous ligament is sutured to dorsolumbar fascia -drain is used in general conventional open posterior lumbar approach and laminectomy generate tendon disruption, muscle devascularisation, atrophy, denervation, dysfunction, dysconfort, crusch injury; also produces the greatest changes in segmental motion during flexion, extension, left and right axial rotation. (85)(86)(92)(9599)(102)(105)(106) for lateral stenosis: (81) in lateral lumbar spinal canal stenosis, radiculopathy is well recognized as expression a spinal nerve entrapment in the three zones: entrance zone, mid zone and exit zone. for entrance zone stenosis the most common causeis hypertrophic osteoarthritis of the facet joint, particularly involving the superior articular process. the appropriate surgical decompression technique are medial fatectomy, ranging from one-third to one-half. for mid zone stenosis localized facet degeneration under the pars interarticularis where the ligamentum flavum is attached are due by osteophyte formation, periarticular calcification, articular narrowing of the joint space, subchondral erosion and fibrocartilaginous hypertrophy at a spondylolytic defect. the surgical techniques focused on the symptomatic stenotic side have common hallmark of medial fatectomy, careful excision and curettage under the pars interarticularis; osteophytes trimming along the superior margins of the superior articular process and along the lateral margins of the corresponding inferior articular process or even laminectomy with total fatectomy. for exit zone stenosis the main causes are: hypertrophic osteoarthritis changes of the facet joints with subluxation and osteophytic ridge formation along the superior margin of the disc. the suggested technique are foramen approach from the interlaminar space below the level of the root. it’s to be remarked in congenital lateral recess stenosis a trefoil-shaped, the nerve root is entrapped under the superior articular facet by facet hypertrophies or by disk bulging, disk margin enlarges because of endplate spur. surgical management consists of decompressing the nerve root emerging from the thecal sac along its entire course in the radicular canal with laminotomy and medial facetectomy. if lumbar disc herniation accompanies the pathology, removal of disc material is needed additionally. there is also a second form with an angled shape of the recess by progressive facet, endplate and disk margin changes with subsequent pinch of the nerve root. if early facet hypertrophy occurs, an acquired trefoilshaped canal ensues. -for mixed stenosis: laminectomy + partial artrectomy; the wiltse 216 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome approach (63) with foraminotomy for isolated foraminal stenosis 4. fusion: current guidelines reject stabilization by default on the basis of an extensive literature search (33)(34)(48)(51)(54-56)(58)(113-127). even after a laminectomy only 20% of cases need a fusion procedure (58). the reactive degenerative changes obviously prevent manifest segmental instability, even after decompression if more of 50-66% of articulary or isthme are conserved, without discal space violation (56) after white-panjabi (cited by 54): instability means a loss of spine 's ability to maintain under physiological conditions its normal anatomical relationships at risk causing signs of irritation spinal cord/nerve root, pain or crippling deformities ". instability could be responsible of stenosis; it could be associated with lss symptomatic – with intermittent mechanical pains; iatrogene with symptomatic instability or without clinical signs (50)(51)(54)(55)(133). spondylolisthesis, scoliosis may generate instability; also after decompression, the possibility of segmental instability should always be considered. fusion procedures, especially those involving instrumentation, are associated with increases in cost and complications, are used for pre-op, intraoperative instability or postoperatory listhesis (58). still there are several debatable aspects subject of controversy: the criteria of instability, the spondylolisthesis or scoliosis grade, what kind of stabilization should be used with or without motion preservation, minimally or invasive intervention, the approach used: posterior, anterior or “circumferential”, instrumentation increases the fusion rate ?, implant failures and adjacent joints degeneration (56). there are several surgical alternatives (50)(51)(113-128)(131)(133)(135): -open: bone deposition, iliac bone graft, instrumentation rigid or dynamic with pedicular screws, inserted with the help of a spinal navigation system, inter body cages -microscopy -percutaneous -facet arthroplasty -interspinous spacers (x-stop, diam, coflex, helifix) with 45% improvements after two years, an intermediate option between conservative and surgical treatment “does not burn bridges”, for patients with mild symptoms, to those that cannot undergo or refuse more extensive surgery, as a temporary solution, “addressing the problem within the canal without entering the canal”. interspinous spacers advantages are: disc not removed, no pedicles used, opening of foramens, unloading of the posterior part of the disc, of the facets. there are also less risk of significant complications, no direct manipulation adjacent to the neural structures; the risk of neurological deficit (paralysis; dural tears; etc) decrease to a minimum. such interspinous spacers can’t be used in the following anatomic variants: markedly decreased interspinous distance (kissing spine–like), with concomitant facet joint hypertrophy, a posterior v-shaped interspinous area, limited accessibility of the space between the base and the tip of the spinous process because of facet joint romanian neurosurgery (2015) xxix 2: 200 229 217 for residents hypertrophy and variations in the shape of the inferior surface of the spinous process. the technique used for microsurgical decompression with instrumented fusion are based on the same principles (113)(114): -preoperative planning includes the acquisition of ct-scan, mri data for intra operative navigation general anesthesia: with the introduction of a central venous line, to perform arterial blood pressure monitoring, as well as the introduction of a urinary catheter, blood transfusion are not usually necessary. patient positioning: in a prone, comfortable position, on a soft foam frame, on a radiolucent table; respecting the protection of neural structures and the skin. the hips and knees are slightly flexed (20–30°) and the anterior iliac crest is padded in order to avoid pressure on the lateral femoral cutaneous nerve. screw insertion with the help of an intra operative navigation system or under fluoroscopic control -insertion of mono or multi segmental internal fixation system -reduction and reconstruction of normal curvature -microsurgical decompression (see above) -drain insertion and wound closure. -wound drains are inserted underneath the fascia without applying suction. wound closure. several complications could appear (38)(54)(56)(59)(60)(61)(95)(137): dural tears leading to a pseudomeningocele or even csf fistulas are the most common complications nerve roots lacerations (the nerve roots could be vulnerable by chronic compression for years in lss; by temporary direct compression of the cauda equina roots during decompression of the controlateral side; also the arterial supply may be diminished by other concomitant diseases: diabetic microangiopathy, microangiopathy due to arterial hypertension, etc.) segmental instability destabilization of the adjacent segment arachnoiditis epidural scar formation epidural hematoma complications secondary to positioning, especially postoperative blindness or corneal lesions after pressure on the eyes higher as compared to microsurgical discectomy, since microsurgical decompression requires longer operating times deep venous thrombosis upper respiratory tract infection urinary tract infection superficial wound infection b. lumbar stenosis + aggravating factors (55)(56)(133) there are several situations which should be discussed: 1.co-existing multiple disk prolapses or single level disk prolapsed with a multistage lumbar 218 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome spinal stenosis, without scoliosis: more common there is a single or two level prolapsed discs with lss; the patient may present lombalgia, intermittent radicular claudication (walking perimeter, the caddie sign), isolated radicular pain, sciatic pain or cural nevralgia: for such cases medical treatment should be tried, in case of failure surgical attitude with lss decompression plus disk surgery 2.combined lss with degenerative listhesis and posterior arthrosis at one or several levels. in such cases it’s more frequent lateral lss associated with disc hernia. spondylolisthesis in itself is not an indication, except if there is > 4 mm translation in sagittal plane and 10° angulation flexion/extension for such cases foraminal decompression, discectomy and fusion to all affected levels should be made (50)(132). it is uncertain whether instrumentation: use of pedicle screws or metal cages help to fuse adjacent vertebrae or biologic agents bone morphogenetic protein should be used to enhance osseous fusion (50). 3.combined lss with scoliosis scoliosis and lss can be explained in two ways: spinal deformation induce lss or by arthrosis, massive joint hypertrophy may generate lss and degradation of scoliosis. saccoradiculography, dynamic mri, eos system osteodensitometry, electromyogramme are particularly useful examinations of reference for assessing instability and to measure the extent of curvature (54). lss with scoliosis with a small radius of curvature: decompression should not be associated with fusion. lss with scoliosis and a big radius of curvature installed in adolescence, it’s stable and has similar therapeutic strategy lss with scoliosis and a big radius of curvature, with rapid evolution 5-100 in one year generating both radiculalgia and instability can not be neglected; also in scoliosis with rotation and rapid evolution to 30-500, with arthrosis in concavity which should be decompressed and fused (55). if scoliosis affect several levels a multilevel fusion should be tried (133). 4.combined stenosis and facet joint cyst should be decompressed as usual, but the major risk is a dural tear which should be avoided 5. lss with severe polineuropaty with or without uni/bilateral paresis should be decompressed and fused as well, but prognosis is different and should be explained to the patient (133) the outcome in operated lumbar spinal stenosis despite several published studies, a lot of aspects should be clarified: -functional outcome valuation should be made using (107)(135): self-reported leg pain on vas (0-10), self-reported functional status based on likert scale (srfs)(pain interference with normal work:1 not at all 5 extremely), likert symptom-specific well-being score(sswbs) if you had to spend the rest of your life with the symptoms you have right now (1 very dissatisfied 5 very satisfied), likert general well-being score (gwbs) how would you rate your quality of life? (1 very bad 5 very good), oswestry disability index (odi) for leg pain, dallas pain romanian neurosurgery (2015) xxix 2: 200 229 219 for residents questionnaire (dpq) lawlis et al. spine, 1989, low back pain rating scale (lbpr) manniche et al. pain, 1994, sf-36 ware, spine 2000, eq5d, swiss spinal stenosis stucki et al, spine 1996, oxford claudication score makan et al, jbjs, 1998. -time – mean follow up 24 months or more: advantage of surgery was noticeable at 3-6 months, remained for up to 2-4 years (4)(44)(128-130). cohort studies indicate that although more than 80% of patients have some degree of symptomatic relief after surgery for spinal stenosis, 7 to 10 years later, at least one third of patients report back pain (33)(56). patients with the most severe nerve-root compression preoperatively are the most likely to have symptomatic relief. reoperation rates are on the order of 10 to 23% over a period of 7 to 10 years of follow-up. systematic review are necessary to compare the effectiveness of surgery vs. conservative treatment on pain, disability, loss of quality of life (19)(38)(50)(51)(136). 739 citations reviewed, several publications studies, showed surgery better results for pain, disability and quality of life, although not for walking ability. results were similar among patients with and without spondylolisthesis. advantage of surgery was noticeable at 3-6 months, remained for up to 2-4 years (1-17). 32,152 operations for lumbar stenosis in the first 11 months of 2007 (137): surgical rates declined slightly from 2002-2007, rate of complex fusion procedures increased 15-fold, life-threatening complications increased 2.3% to 5.6%, rehospitalization within 30 days, 7.8% decompression and 13.0% complex fusion, medical expenses were $23,724 compared with $80,888, preoperatory predictors for post operative outcome in lumbar spinal stenosis based on 21 prospective studies (4)(38)(4345)(52)(56)(133), despite reported success rates of surgery vary considerably in trials: � good preoperatory walking predict a better walking capabilities two years later � less co-morbidities: patients with cardio-vascular co-morbidities, severe scoliosis, lumbar spine surgery history had bad prognosis; also preop. depression predict: pain, less good satisfaction, less walking capabilities � surgery appears to lead to better outcomes if there are ongoing symptoms after three to six months of conservative treatment, in those who worsen despite conservative treatments, surgery leads to improvement in 60–70% of cases (3)(50)(51)(76)(138)(139) � poor pre operatory indications for surgery are bad predictors for outcome � age < 65 years good post operative outcome � back pain predominance compared with radicular pain has bad prognosis � pre operatory motor deficit monoradicular and unilateral, installed less than 6 weeks has complete recovery 40%, no recovery 20% � stenosis to one level with real compressive disc herniation, predict a better function especially on walking and pain 220 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome � insufficient decompression are a bad predictor � an important stenosis: a-p diameter < 6 mm predict less pain to 5 years � therefore the timing for surgery has not been clearly decided. data comparing the outcomes of patients who underwent surgery earlier vs later in the disease suggest no difference in outcome -overall rating of post-operatory results of operated lss: improved – 85% better quality of life-walking distance improvement 95%, pain improvement (vas) 85%, low improvement – 5%, no improvement – disability 5%, worse – very rare, mortality 0 3% (12)(33)(38)(56). daily life activities are post-operatory: normal 82%, modification of life/work style 13%, stopped working 5% (17)(133)(140). in general surgery affords earlier and greater pain relief and improvement in functional status and that these gains begin to narrow over the course of follow-up. -although technical errors during time were noted, they seemed to have less influence on the outcome than did appropriate selection of patients; also complication rates did not differ based on patient age or fusion. the most common complications (up to 3%) (50)(133)(136)(137) are: epidural haematoma, csf fistula +/ pseudomeningocele, inadequate insufficient decompression, decompression at wrong level, root trauma or avulsion, infection up to 4%, arachnoiditis, epidural fibrosis, recurrence of stenosis with reoperation rates as high as 21%, instability, pseudarthrosis, flat back syndrome, general complications such as deep venous thrombosis, pulmonary embolism, urinary infection, wound healing disturbances; also by the co-morbidity of the patients. -if operated patients present recurrent symptoms it’s mandatory to resume lumbar mri and ct, contrast studies, emg and ncs to demonstrate (50)(51)(133): residual stenosis at operative site due to inadequate first surgery, stenosis at adjacent levels to surgical site, new disc herniations, epidural and arachnoidal adhesions, instability and/or spondylolisthesis following first surgery -outcome depends on surgical type of operation used; also the pathological situation (56)(133): � one level lumbar stenosis or a multistage lumbar spinal stenosis, without scoliosis there are several meta analyseses : turner (38) on retrospective studies reffering to surgery for lumbar spine stenosis between 1970-1993 revealed 64% satisfied people by surgery marjerko (cited by 56) on degenerative lumbar spondylosis between 1970-1993 find 69% satisfaction by decompression without fusion and more than 80% satisfaction if decompression was made with fusion. updated cochrane review 2005 (34) several studies, for a short time, are reffering to different techniques applied, to pain symptomatology, but few informations about functional results, with limited conclusions. amundsen (7) on 19 patients operated of 50 patients, assert that conservatory treatment is compared with immediately post op on 4/5 romanian neurosurgery (2015) xxix 2: 200 229 221 for residents patients without a significative diffference; after 10 years good surgical results in 5/11 patients, compared to 4/14 treated conservatory. postacchini 1993 (87) laminectomy versus staged laminotomies no difference ; herkowitz 1991 (94), grob 1995 (131) laminectomy with or without fusion no difference on 139 patients during 3 years. fritzell spine 2001 (cited by 56) fusion versus physiotherapy 294 patients of which 98% were reevaluated at two years; in 46% of cases surgery has good or very good results, compared with 18% good results by physiotherapy, p<0,0001. brox spine 2003, keller spine 2004 (cited by 56) postero-lateral fusion with transpedicular screws compared with physiotherapy alone demonstrate the value of physiotherapy on avoidance beliefs, flexion, force and muscular endurrancy. another 3 studies with idet without encouraging results ; also studies mcafee spine 2003, zigler j.spin disord 2003, geisler j neurosurg 2004 (cited by 56) reffering to disc prothesis no superiority versus simple fusion cochrane updated review 2005 (34) surgery for degenerative lumbar spondylosis conclusion: few controlled trials, most retrospective, few are interested about symptoms. zucherman (120) made a prospective multicentric randomised study on 191 patients during 15 months; patients were >50 years with sciatalgic predominance, with or without lombalgia, intermitent claudication, surgical treatment consist in laminectomy with spacer versus medical traitement – at least one epidural infiltration before the study and 1-4 infiltration during study. at 2 years for operated patients 45% amelioration on severity score versus 7% in control groupe p<0,001); 56 of 93 operated patients has significant amelioration compared with 15 of 81 medically treated patients with a satisfaction index of 73% versus 36%. he foud that predictive factors were influenced by comorbidities. conclusion: the first precise study on methodological aspects is a plea to proof surgical treatment superiority versus conservatory in intermitent radicular claudication. atlas (4) published in spine 2005 a prospective study on 10 years on 105/148 patients of which 97 are survivors; inclusion criteria: lss on clinical argues, half of the patients with a radiculalgia monitorised at 3, 6, 12 months, after that annually. he found surgery superiority for radiculalgia 67% versus 41% p=0,04; satsfaction 42% versus 28% p=0,24; 23% of patients have a second spinal operation and 39% of medically treated patients were operated too. duquesnoy & assaker (56)(62) on 168 operated cases: excellents results : retourn to anteriorly life condition, good results: good waking, retourn to professional activities, medium results: persistent invalidity, bad results: no amelioration. 124 patients at 2 months at 2 years excellent results 68% 21% good results 33% 41% medium results 17% 19,5% bad results 12% 18,5% 222 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome on intermittent claudication: excellents results in 47% of cases and good results in only 28% of cases; reffering on radiculalgia: excellents results in only 26% of cases; good results in 44% of cases. for an operated multistage lumbar spinal stenosis, without scoliosis, without arthrodesis, walking troubles may be generated by (56): iterative stenosis (rare, by osseous aposition, forestier illness) insufficient decompression to only symptomatic level, lateral partial decompression especially by incomplete lateral flavum ligament resection iatrogene instability (articulary resection, even isthm rupture may generate radiculalgia) concomitant cervical canal stenosis (if walking troubles are persistent, correlated with profound sensibility troubles) coxartrosis could be concomitant with lss. surgical indication for spinal decompression should be made on clinics and dynamic mri or saculography. in conclusion: for a multistage lumbar spinal stenosis, without scoliosis, surgery even to oldest patients has proved his efficacy in intermittent medullar claudication and radiculalgia on one or several levels, decompressing lss, also performing discectomies, fusions techniques; the patients should be inform that lombalgia is not treated. � combined lss with degenerative listhesis and posterior arthrosis at one or several levels for surgical point of vue decompressing roots in a lss may affect isthm, may generate iatrogene instability because of arthrectomy, especially in a lss with degenerative listhesis and posterior arthrosis. we should treat only the instable level (56). several complication could be seen : overlying stenosis (by recurrence of a degenerative spondylolisthesis, hypertrophic flavum ligaments), disassembly of osteosynthesis by fracture instrumentation short and medium term as a sign of pseudarthrosis. in conclusion: large laminectomies should be avoided, lumbar decompression with fusion, at the symptomatic level should be made if medical traitement fails. � combined lss with scoliosis may be generated by two mechanisms: -deformation generate stenosis – see stable scoliosis since adolescence -degeneration induce a hypertrophic articular process with lss evolutive scoliosis with severe torsion always deformation should be evaluated, severe scoliosis should be operated (55)(133) if deformation is responsible for lss the reduction arthrodesis treats claudication if the deformation is not the cause of lss rahisynthesis is imperative to avoid iatrogenic instability after decompression laminectomy for old patients with severe ostheoporosis, lss with scoliosis may generate complications: romanian neurosurgery (2015) xxix 2: 200 229 223 for residents -fails of rahisynthesis 15-20% especially in the lumbo-sacral area -overlying osteoporothic fracture or settlement may be seen in 10-15% of cases, imposing : arthrodesis extension, vertebroplasty disorder sagittal echilibre should be corrected by subtraction osteotomy a scoliosis research society (srs) database: 10.329 patients with lss, treated with either decompression alone (64%) or decompression with concomitant fusion (36%) between 2004 – 2007 (140): complications (7.0%), including 13 deaths (0.1%); complication rates did not differ based on patient age or fusion. in conclusion in lss with scoliosis: limited surgical indication; indisputably effective surgery in intermittent claudication root and radicular pain, but surgical indications are on demand; surgery measuring if the predominant low back pain or joint pain; preeminence of the clinic on neuro-radiologic data; no proved superiority of multistage laminectomy compared to one level laminectomy, adjusted to the demand, with rahisynthesis final conclusions � initial management in lss should be non-surgical unless very severe; also conservative treatment is able to give satisfactory results even for 10 years. it’s important to survey scoliosis after climax, to use a lombostat. � clinical argues for surgical traitement: severe lumbar stenosis with waking perimeter limited, radicular pain and claudication, to a patient in good health condition, without comorbidities clinical findings are prevalent compared with neuro radiological data. � surgical interventions are more frequent corresponding to increasing number of older patients and to their request for a bigger autonomy � lss surgery is a functional one, balance bony and soft tissue decompression while maintaining spinal stability, surgical interventions have to be tailored and rigourous applied to the unique pathological situation in the persistently symptomatic patient; explored by mri, dynamic flexion and extension x-rays, emg (electrophysiological testing correlated to thorough neurological examination is more accurate than radiological evaluation alone in choosing the roots to be decompressed) � adaptation of the surgical strategy according to the therapeutic objectives, constraints and physiological analysis of imbalances: never preventive, minimize tissue damage minimally invasive decompressive technique and/or fusion technique, clearly precised in the informed consent who correspond with patients expectations. � selective decompression only at the neurological responsible level improved neurogenic intermittent claudication in the majority of patients, un operated radiological 224 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome stenotic levels or previously borderline stenotic level rarely became symptomatic in later follow up � there is still a lack of evidence based data regarding the different surgical techniques for lumbar spinal decompression, this explains why the success rate of decompression for lss ranges from 57% to 95%; microsurgical decompression is useful in pain decrease and analgesic consumption, but also in functional improvement � surgery for lss is efficacy for short and medium term; compared with medical treatment; for short time, surgery is better, nearly 80% of patients enjoyed excellent results: less pain and better functional status than those who had non operative treatment. � randomized trials are required to produce better guidelines for minimally invasive procedures, avoiding more extensive surgery � the outcome after surgical decompression of lss could be influenced by general complications such as deep venous thrombosis, pulmonary embolism, urinary infection, wound healing disturbances; also by the comorbidity of the patients. each additional decade could increase the asa score and could worsen the postoperative result of the patients in their 60s to 90s. most aggravating factors do not really make outcome worse; in particular degenerative spondylolisthesis and disk prolapses do not affect outcome. the medium and long term outcome may be complicated by postsurgical instability after extensive multilevel surgery, osteoporosis; the more rapid progression of degenerative changes, the suboptimal decompression of the contro-lateral side because of the impaired view of the target area and a slower postoperative rehabilitation. references 1.malmivaara a, slätis p, heliövaara m,et al. surgical or nonoperative treatment for lumbar spinal stenosis? a randomizedcontrolled trial, spine 2007, 32, 1-8 2.weinstein j.n. et al. surgical vs nonsurgical therapy for lumbar spinal stenosis, n engl jmed 2008, 358, 794810 3.djurasovic m, et al. contemporary management of symptomatic lumbar spinal stenosis, orthop. clin. north am. 2010, 41 (2), 183–191 4.atlas s.j. et al. long-term outcomes of surgical and non surgical management of lumbar spinal stenosis : 8 to 10 year results form maine lumbar spine study, spine 2005, 30, 936-943 5.johnsson ke, et al. -the natural course of lumbar spinal stenosis, clin orthop 1992, 279, 82–86 6.johnsson k.e. lumbar spinal stenosis, a retrospective study of 163 cases in southern sweden, acta orthop scand 1995, 66, 403–405 7.amundsen t, et al. lumbar spinal stenosis: conservative or surgical management? a prospective 10year study, spine 2000, 25, 1424–1436 8.athiviraham a, yen d is spinal stenosis better treated surgically or nonsurgically?, clin orthop relat res 2007, 458, 90–93 9.schulte tl, bullmann v, lerner t et al. lumbal spinal kana lstenose, orthopäde 2006, 35, 675–694 10.mazanek d.j. et al. lumbar canal stenosis: start with nonsurgical therapy,cleveland clinic journal of medecine, 2002, 69, 11, 909-917 romanian neurosurgery (2015) xxix 2: 200 229 225 for residents 11.atlas sj, et al. the maine lumbar spine study, part iii. 1-year outcomes of surgical and nonsurgical management of lumbar spinal stenosis, spine 1996, 21, 1787-1794 12.atlas sj, keller rb, robson d, et al.surgical and nonsurgical management of lumbar spinal stenosis: fouryear outcomes from the maine lumbar spine study, spine 2000, 25, 556–562\ 13.atlas sj, delitto a. spinal stenosis versus non surgical treatment, clin orthop relat res 2006; 443: 198-207 14.fritz jm, et al. lumbar spinal stenosis: a review of current concepts in evaluation, management and outcome measurements, arch phys med rehabil 1998, 79(6), 700-708 15.thomé c. et al. degenerative lumbar spinal stenosis, dtsch arztebl int 2008, 105(20), 373–379 16.haig a.j. et al. a prospective, masked 18 month minimum follow-up on neurophysiologic changes in persons with spinal stenosis, low back pain and no symptoms, pm r. 2009, 1(2), 127–136 17.kovacs f.m., et al. – surgery versus conservative treatment for symptomatic lumbar spinal stenosis, spine 2011, 9 18.johnsson k.e., et al. the effect of decompression on the natural course of spinal stenosis. a comparison of surgically treated and untreated patients spine 1991, 16, 615–619 19.herno a et al. lumbar spinal stenosis: a matchedpair study of operated and nonoperated patients, br j neurosurg 1996, 10, 461–465 20.katz j, et al. seven to 10 year outcome of decompressive surgery fordegenerative lumbar spinal stenosis, spine 1996, 21:92–98 21.katz j, et al.-the outcome of decompressive laminectomy for lumbar stenosis, j bone joint surg 1996, 73, 809–816 22.katz j.n., harris m.b. lumbar spinal stenosis, www.nejm.org 2008, 21, 818-825 23.verbeek j. et al. patient expectation of treatment for back pain. a systmatic review of qualitative and quantitative studies, spine 2004, 29, 2309-2318 24.cooper g, lutz ge, et al. effectiveness of transforaminal epidural steroid injections in patients with degenerative lumbar scoliotic stenosis and radiculopathy, pain physician 2004, 7, 311-317 25.fukusaki m, kobayashi i, et al. – symptoms of spinal stenosis do not improve after epidural steroid injection, clin j pain 1998, 14, 148-151 26.armon c, argoff ce, et al. assessment: use of epidural steroid injections to treat radicular lumbo-sacral pain: report of the therapeutics and technology assessment subcommitteeof the american academy of neurology, neurology 2007, 68, 723-729 27.simotas c.a. et al.-nonoperative treatment for lumbar spinal stenosis. clinical and outcome results and a 3-year survivorship analysis, spine 2000, 25, 197–203 28.costandi s., chopko b. et al. – lumbar spinal stenosis: therapeutic options review, pain practice 2015, 15, 1, 68-81 29.porter rw, miller cg neurogenic claudication and root claudication treated with calcitonin. a double-blind trial spine 1998, 13, 1061–1064 30.podichetty vk, et al. effectiveness of salmon calcitonin nasal spray in the treatment of lumbar canal stenosis: a double-blind, randomized, placebo-controlled, parallel grouptrial, spine 2004; 29, 2343–2349 31.hooten wm, mizerak a, et al. discitis after lumbar epidural corticosteroid injection: a case report and analysis of the case report literature, pain med 2006, 7, 46–51 32.yoshihara h. – prostaglandin e, treatment for lumbar spinal canal stenosis, review of the literature, pain practice 2015 33.marty m., guigui p – controverse: canal lombaire etroit, retrecit ou mixte. traitement conservateur ou chirurgical ? 19-eme congres francais de rhumatologie, dec. 2006 34.gibson j.n. – cochrane database syst rev 2005, cd 001352 35.friedly j, chan l, deyo r. increases in lumbo-sacral injections in the medicare population: 1994 to 2001, spine 2007, 32, 1754-1760 36.murphy d.r. et al. a non-surgical approach to the management of lumbar spinal stenosis: a prospective observational cohort study, bmc musculoskeletal disorders 2006, 7, 16 37.athiviraham a., yen d. is spinal stenosis treated better surgically or nonsurgically?, clin orthop relat res 2007, 458, 490–493 38.turner ja, ersek m, et al. surgery for lumbar spinal stenosis. attempted meta-analysis of the literature, spine 1992, 17, 1–8 226 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome 39.chang y, singer de, the effect of surgical and nonsurgical treatment on longitudinal outcomes of lumbar spinal stenosis over 10 years, j am geriatr soc 2005, 53, 785–792 40.malmivaara a, et al. finnish lumbar spinal research group: surgical or nonoperative treatment for lumbar spinal stenosis? a randomized controlled trial, spine 2007, 32, 1–8 41.atlas sj, keller rb, et al. surgical and nonsurgical management of lumbar spinal stenosis:four-year outcomes from the maine lumbar spine study, spine 2000, 25, 556-562 42.benoist m. the natural history oflumbar degenerative spinal stenosis, jointbone spine 2002, 69, 450-457 43.treatment of degenerative lumbarspinal stenosis summary. evidence report/technology assessment number 32.rockville, md: agency for healthcare research and quality, 2001, ahrqpublication no.01e047,accessed january28, 2008 athttp: /www.ahrq.gov/ clinic/epcsums/stenosum.htm 44.katz j.n, et al. predictors of surgical outcome in degenerative lumbar spinal stenosis, spine 1999, 24, 2229–2233 45.aalto tj et al. preoperative predictors for postoperative clinical outcome in lumbar spinal stenosis: systematic review spine 2006, 31, e648–e663 46.sinikallio s. et al. somatic comorbidity and younger ageare associated with life dissatisfactionamong patients with lumbar spinalstenosis before surgical treatment, eur spine j 2007, 16, 857–864 47.irwin zn, hilibrand a, gustavel m et al. variation in surgical decision making for spinal disorders. part i: lumbar spine, spine 2005, 30, 2208–2213 48.caputy a et al. the role of spinal fusion in surgery for lumbar spinal stenosis: a review, neurosurg focus 1997, 3, 2 49.benz rj et al. current techniques of decompression of the lumbar spine, clin orthop relat res 2001, 384, 75– 81 50.iacob g. craciun m personal experience in lumbar spinal stenosis (lss), romanian neurosurgery 2011, xviii, 4, 400-411 51.iacob g. neurochirurgia in managementul coloanei dureroase, congresul asociatiei romane pentru studiul durerii, “managementul durerii acute pentru medicii din ambulator” howard-johnson grand plaza, bucuresti, 1415. 10. 2011 52.schatzker j, pennal gef. spinal stenosis, a cause of cauda equina compression, j bone joint surg br 1968, 50, 606–618 53.toyonne et al. – patients expectations in lumbar spine surgery, spine 2005 54.iqbal j. surgery for lumbar canal stenosis: micro or macro?, dubai spinal course 2008 55.paquisph. la scoliose dégénérative de l’adulte et canal lombaire étroit: comment décomprimer, course francophone bucarest 2014 56.duquesnoy b., mazel c. – le devenir du canal lombaire etroit (retrecit) opere, le 18-eme congres sfr. paris 2005 57.k. iwatsuki et al. bilateral interlaminar fenestration and unroofing for the decompression of nerve roots by using a unilateral approach in lumbar canal stenosis, surgical neurology 2007, 68, 487–492 58.sonntag vkh, marciano ff. is fusion indicated for lumbar spinal disorders ?, spine 1995, 20(suppl), 138s– 142s 59.jakola et al. clinical outcomes and safety assessment in elderly patients undergoing decompressive laminectomy for lumbar spinal stenosis: a prospective study, bmc surgery 2010, 10:34 60.mayer h.m. microsurgical decompression of acquired (degenerative) central and lateral spinal canal stenosis, in mayer h.m. minimally invasive spine surgery, a surgical manual, second edition springerverlag berlin heidelberg 2006, 397408 61.rosen d.s. et al. – minimally invasive lumbar spinal decompression in the elderly: outcomes of 50 patients aged75 years and older, neurosurgery 2007, 60, 3, 503 62.assaker r. lumbar stenosis, minimal invasive decompression, spinal congress dubai 2012 63.wiltse l.l., kirkaldy-willis wh, mcivor gw. the treatment of spinal stenosis, clin orthop relat res 1976, 83–91 64.vialle r. et al. the wiltse paraspinal approach to the lumbar spine revisited, clin orthop and related research, 2006: 445, 175-80 65.court c. rationale for wiltse approach for l5-s1 mini-invasive arthrodesis, dubai spinal congress 2008 66.khoo lt, fessler rg. microendoscopic decompressive laminotomy for the treatment of lumbar stenosis neurosurgery 2002, 51, s146–154 romanian neurosurgery (2015) xxix 2: 200 229 227 for residents 67.nellensteijn j. et al. – transforaminal endoscopic surgery for lumbar stenosis: a systematic review, eur. spine j. 2010, 19(6), 879-886 68.endoscopy guidelines from ismiss, feb. 2008 69.yoshida m. et al.surgical procedures and clinical results of endoscopic decompression for lumbar canal stenosis, in dezawa a., chen p.q., chung j.y. state of the art for minimally invasive spine surgery, springerverlag tokyo 2005, 18-25 70.foley kt, smith mm microendoscopic discectomy, techniques neurosurg 1997, 3, 301–307 71.guiot bh, khoo lt, fessler rg. a minimally invasive technique for decompression of the lumbar spine. spine 2002, 27, 432–438 72.papavero l et al. – lumbar spinal stenosis: prognostic factors for bilateral microsurgical decompression using a unilateral approach, neurosurgery 2009, 65[ons suppl 1], ons182–ons187 73.poletti ce central lumbar stenosis caused by ligamentum flavum: unilateral laminotomy for bilateral ligamentectomy.preliminary report of two cases, neurosurgery, 1995, 37, 343–347 74.yoshida m, shima k, taniguchi y, et al hypertrophied ligamentum flavum in lumbar spinal canal stenosis. pathogenesis, morphologic and immunohistochemical observation, spine 1992, 17:1353– 1360 75.mcculloch ja – microsurgery for lumbar spinal canal stenosis,in: mcculloch ja, young ph (eds) essentials ofspinal microsurgery, lippincott-raven, philadelphia, 1998, 453–486 76.oertel m.f., ryang y.m., et al. long-term results of microsurgical treatment of lumbar spinal stenosis by unilateral laminotomy for bilateral decompression, neurosurgery 2006, 59, 1264–1269 77.bresnahan l., ogden a.t. et al. – a biomechanical evaluation of graded posterior element removal for treatment of lumbar stenosis, comparison of a minimally invasive approach with two standard laminectomy techniques, spine 2008, 34, 1, 17-23 78.rosen d.s., o’toole j.e., eichholz k.m.,et al. minimally invasive lumbar spinal decompression in the elderly: outcomes of 50 patients aged 75 years and older, neurosurgery2007, 60, 503-510 79.weiner bk, walker m, brower r, et al microsurgery for lumbar spinal canal stenosis, spine 1999, 24, 2268– 2272 80.see d.h., kraft g.h. electromyography in paraspinal muscles following surgery for root compression, arch phys med rehabil 1975, 56, 80–83 81.colak a. et al. a less invasive surgical approach in the lumbar lateral recess stenosis: direct approach to the medial wall of the pedicle, eur spine j 2008, 17, 1745– 1751 82.mayer h.m. microsurgical anterior approaches for anterior interbody fusion of the lumbar spine, in: mccullochja, young p.h. (eds) essentials of spinal microsurgery. lippincott-raven, philadelphia, 1998, 633–649 83.silvers h.r, lewis p.j, asch h.l. decompressive lumbar laminectomy for spinal stenosis, j neurosurg 1993, 78, 695–701 84.yoshida m, sumiya h, iwasaki k, et al initial clinical outcomes of microendoscopic discectomy for lumbar disc herniation, spine spinal cord 2001, 14:381–388 85.podichetty v.k., spears j., et al.complications associated with minimally invasive decompression for lumbar spinal stenosis, j spinal disord tech 2006, 19, 161-166 86.wang j.c., bohlman h.h., riew k.d. dural tears secondary to operations on the lumbar spine, j bone joint surg am 1998, 80, 1728–1732 87.postacchini f. surgical management of lumbar spinal stenosis, spine 1999, 24, 1043–1047 88.kleeman t.j., hiscoe a.c., berg e.e.. patient outcomes after minimally destabilizing lumbar stenosis decompression: the “port hole” technique, spine 2000, 25, 865–870 89.aryanpur j., ducker t. multilevel lumbar laminotomies: an alternative to laminectomy in the treatment of lumbar stenosis, neurosurgery 1990, 26, 429–432 90.lin p.m. internal decompression for multiple levels of lumbar spinal stenosis: a technical note,neurosurgery 1982, 11, 546–549 91.aryanpur j., ducker t. multilevel lumbar laminotomies: an alternative to laminectomy in the treatment of lumbar stenosis, neurosurgery 1990, 26, 429–433 92.sihvonen t., herno a., paljarva l., et al local denervation atrophy of paraspinal muscles in postoperative failed back syndrome, spine 1993, 18, 575– 581 228 rahman, iacob treatment of lumbar spinal stenosis (lss) and outcome 93.young s, veerapen r, o’laoire sa. relief of lumbar canal stenosis using multilevel subarticular fenestrations as an alternative to wide laminectomy: preliminary report,neurosurgery 1988, 23, 628–633 94.herkowitz h.n., kurz l.t.degenerative lumbar spondylolisthesiswith spinal stenosis. a prospective study comparing decompression and intertransverse process arthrodesis, j bone joint surg am 1991, 73, 802–808 95.herno a., airaksinen o., saari t. long-term results of surgical treatment of lumbar spinal stenosis, spine 1993, 18:1471–1474 96.silvers h.r., lewis p.j., asch h.l. decompressive lumbar laminectomy for spinal stenosis. j. neurosurg 1993, 78, 695–701 97.tuite g.f., et al outcome after laminectomy for lumbar spinal stenosis. part i. clinical correlations, j. neurosurg 1994, 81, 699–706 98.tuite g.f., et al. outcome after laminectomy for lumbar spinal stenosis. part ii: radiographicchanges and clinical correlations, j. neurosurg. 1994; 81, 707–715 99.tuite g.f., et al. diagnosis and treatment of surgery for lumbar spinal stenosis, burr ridge (il): north american spine society (nass), 2007, 262, 394 references 100.weiner b.k., fraser r.d., peterson m. spinous process osteotomies to facilitate lumbar decompressive surgery,spine 1999, 24, 62-66 101.el-abed k. et al. – multilevel lumbar spinal stenosis decompression: midterm outcome using a modified hinge osteotomy technique, j.spinal disord. tech 2010, 8 102.ciol m.a., deyo r.a., howell e., kreif s. an assessment of surgery for spinal stenosis: time trends, geographic variations, complications, and reoperations, j am geriatr soc 1996; 44:285–290 103.lee c.k. lumbar spinal instability (olisthesis) after extensive posterior spinal decompression, spine 1983, 8, 429–33 104.johnsson k.e., redlund-johnell i., uden a. preoperative and postoperative instability in lumbar spinal stenosis. spine 1989, 14, 591–593 105.iguchi t., kurihara a., nakayama j., et al minimum 10-year outcome of decompressive laminectomy for degenerative lumbar spinal stenosis, spine 2000, 25, 1754–1759 106.nakai o, ookawa a, yamamura if long-term roentgenographic and functional changes in patients who were treated with wide fenestration for central lumbar stenosis, j bone joint surg 1991, 73a, 1184–1191 107.khaldoun el abed hinge osteotomy for decompression lumbar spinal stenosis: mid-term outcome using a modified surgical technique, dubai spinal cngress 2008 108.iwatsuki k., yoshimine t., aoki m. bilateral interlaminar fenestration and unroofing for the decompression of nerve roots by using a unilateral approach in lumbar canal stenosis, surg neurol 2007, 68, 487-92 109.mariconda m., et al. unilateral laminectomy forbilateral decompression of lumbar spinal stenosis: a prospective comparativestudy with conservatively treated patients, j spinal disord tech 2002,15:39–46 110.cavusoglu h, et al. midterm outcome after unilateral approach for bilateral decompression of lumbar spinal stenosis: 5-year prospective study, eur spine j 2007, 16:2133–2142 111.jayarao et al, transspinous median sublaminar decompression, spine 2010 112.katz j.n., lipson s.j., lew r.a., et al. lumbar laminectomy alone or with instrumented or noninstrumented arthrodesis in degenerative lumbar spinal stenosis: patient selection, costs and surgical outcomes, spine 1997, 22, 1123-1131 113.wimmer c percutaneous lumbar spine fusion. a comparison study, dubai spinal congress 2008 114.alves oscar l. role of percutaneous interspinous process dynamic stabilization in the treatment of lumbar spine stenosis, dubai spinal congress 2008 115.resnick d.k., choudhri t.f., dailey a.t. et al. guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine, part 9: fusion in patients with stenosis and spondylolisthesis, j neurosurg spine 2005, 2, 679–685 116.resnick dk, choudhri tf, dailey at et al. guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. part 10: fusion following decompression in patients with stenosis without spondylolisthesis, j neurosurg spine 2005, 2, 686–691 117.laine t., schlenzka d., et al. improved accuracy of pedicle screw insertionwith computer-assisted surgery, spine 1997, 22, 1254–1258 romanian neurosurgery (2015) xxix 2: 200 229 229 for residents 118.berlemann u, monin d, et al. planning and insertion of pedicle screws with computer assistance, j spinal disord 1997, 10, 117–124 119.schnake kj, schaeren s, jeanneret b dynamic stabilization in addition to decompression for lumbar spinal stenosis with degenerative spondylolisthesis, spine 2006, 31, 442–449 120.zucherman jf, hsu ky, hartjen ca, et al. a prospective randomized multi-center study for the treatment of lumbar spinal stenosis with the x stop interspinous implant: 1-year results. eur spine j 2004, 13, 22-31 121.zucherman j.f., hsu k.y., hartjen c.a. et al.: a multicenter, prospective, randomized trial evaluating the x stop interspinous process decompression system for the treatment of neurogenic intermittent claudication: two-year follow-up results, spine 2005, 30, 1351–1358 122.siddiqui m., smith f.w., wardlaw d. one-year results of x stop interspinous implant for the treatment of lumbar spinal stenosis, spine 2007, 32, 1345–1348 123.burnett m.g. et al. cost-effectiveness of current treatment strategies for lumbar spinal stenosis: nonsurgical care, laminectomy and x-stop, j neurosurg spine 2010, 13 (1), 39–46 124.barbagallo g,mv. et al. – analysis of complications in patients treated with the x-stop interspinous process decompression system: proposal for a novel anatomic scoring system for patient selection and review of the literature, neurosurgery 2009, 65, 111–120 125.brussee p. et al. self-rated evaluation of outcome of the implantation of interspinous process distraction (xstop) for neurogenic claudication, eur spine j 2008, 17, 200–203 126.kim ka, mcdonald m, et al. dynamic intraspinous spacer technology for posterior stabilization: case-control study on the safety, sagittal angulation and pain outcome at 1-year follow-up evaluation, neurosurg focus 2007, 22, e7 127.phillips f.m. effect of the total facet arthroplasty system after complete laminectomy-facetectomy on the biomechanics of implanted and adjacent segments, the spine journal, 2009, 9,1, 96-102 128.herron i.d., mangelsdorf c.-lumbar spinal stenosis:results of surgical treatment, j spinal disord. 1991, 4, 26–33 129.kovacs f.m. et al. – surgery versus conservative treatment for symptomatic lumbar spinal stenosis, spine 2011, 9 130.thome c., zevgaridis d., et al. outcome after lessinvasivedecompression of lumbar spinal stenosis: a randomized comparisonof unilateral laminotomy, bilateral laminotomy and laminectomy, j neurosurg spine 2005, 3, 129–141 131.grob d., et al.significance of simultaneous fusion and surgical decompression in lumbar spinal stenosis, orthopade 1993, 22, 243-249 132.fischgrund j.s., et al. degenerative lumbar spondylolisthesis with spinal stenosis: a prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation, spine 1997, 22, 2807-2812 133.schramm j., kristof r., müller c.a. lumbar stenosis:operative techniques for simple stenoses and cases aggravated by other factors, spine congress dubai 2008 134.bolger c. ‘day case’ decompressive surgery for spinal stenosis, technique, results verses laminectomy, spine congress dubai 2012 135.christensen f.b. the importance of assessment and outcome measures in spine surgery, spine congress dubai 2008 136.deyo r.a., et al morbidity and mortality in association with operations on the lumbar spine: the influence of age, diagnosis,and procedure, j bone joint surg am 1992;74:536-43 137.deyo r.a. et al. – trends, major medical complications and charges associated with surgery for lumbar spinal stenosis in older adults, jama 2010, 7, 303(13): 1259-1265 138.martin b.i.et al. reoperation rates following lumbar spine surgery and the influence of spinal fusion procedures, spine 2007, 32, 382–387 139.aslto t.j. et al. – preoperative predictors for postoperative clinical outcome in lumbar spinal stenosis.systematic review. spine 2006; 31: e648-e663 140.fu k.m. et al. – morbidity and mortality in the surgical treatment of 10329 adults with degenerative lumbar stenosis, spine 2010, 12(5): 443-446 romanian neurosurgery (2019) xxxiii (3): pp. 260-267 doi: 10.33962/roneuro-2019-043 www.journals.lapub.co.uk/index.php/roneurosurgery “the silk road” via subarachnoid cisterns. cerebrospinal fluid dissemination of meningiomas a.i. cucu1, mihaela dana turliuc1,2, claudia florida costea1,2, b. costăchescu1,2, cristina mihaela ghiciuc2, b. dobrovăț1,2, camelia margareta bogdănici2, daniela maria tănase2, gabriela florența dumitrescu1, anca sava1,2, i. poeată1,2 1 “prof. dr. nicolae oblu” emergency clinical hospital iași, romania 2 “grigore t. popa” university of medicine and pharmacy iași, romania abstract meningiomas are generally slow-growing extra-axial benign tumours and in rare cases they can metastasize both neural and extra-neural. intracranial meningiomas with leptomeningeal dissemination are extremely rare and the exact pathogenesis still remains unknown. the aim of this review is to analyse the pathways of intracranial and spinal metastatic spread of intracranial meningiomas and to discuss their particular clinical and pathological features. we highlight the fact that there is a possibility of leptomeningeal dissemination, even if cerebrospinal fluid cytology is negative, in patients with a medical history of a resected meningioma. we identified three possible ways of dissemination: haematogenous, through the csf, or during surgery. from a histopathological point of view, the more malignant the meningioma, the more likely its leptomeningeal dissemination. introduction meningiomas are generally benign intracranial tumours and represent approximately 30% of all primary central nervous system tumours, with an incidence that has increased in recent years (1, 2, 3, 4, 5). usually occurring on the surface of the brain as they originate in the arachnoid cells, meningiomas are generally slow-growing extra-axial benign tumours. in very rare cases, especially when the tumours become malignant, meningiomas can metastasize both in neural and extraneural sites (6). only 0.1% of meningiomas are thought to metastasize (7), and usually these cases were atypical and anaplastic meningiomas (8, 9, 10), also known for their tendency to relapse after surgery (2, 11, 12, 13). ather enam et al. report an overall metastatic risk of 5% for atypical meningiomas and of 30% for anaplastic meningiomas (8), although keywords meningioma, metastatic spread, csf disseminated meningioma corresponding author: mihaela dana turliuc “grigore t. popa” university of medicine and pharmacy iași, romania turliuc_dana@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 261 “the silk road” via subarachnoid cisterns other authors consider these percentages to be overestimated (11, 14, 15). meningiomas can metastasize in various organs (lung, liver, spleen, adrenal gland, thyroid, parotid gland) or bones, skin and deep soft tissue (16), but also in the intracranial or spinal space through cerebrospinal fluid (csf) pathways. according to the existing literature, metastatic dissemination of meningiomas through csf is a rare presentation (17, 18, 19, 20, 21) and, since 1950, only 45 cases have been reported (22). nevertheless, different other authors consider that the csf dissemination risk of meningiomas is an uncommon event, as it may occur in 4% of metastasizing meningiomas (17, 23). however, the first historical description of leptomeningeal metastasis was made by oliver in 1837, followed by eberth in 1870 (24, 25) also, the first description of carcinoma cells in the csf was realized by dufour (26) and, in 1912, berman was the first who used the term "meningeal carcinomatosis" (27). however, kalm, in 1950, was the first who published a case of a malignant tentorium tumour, i.e. an anaplastic meningioma that metastasized in the medulla oblongata and in the leptomeningeal space (28). pathways of metastatic spread in meningiomas meningioma cells gain access to the subarachnoid space in several ways: haematogenous pathway, through the csf, or during surgery. more frequently, the spread is haematogenous via the venous system and tumour cells gain access to the csf through the dural sinuses or epidural plexus, especially in meningiomas that invade dural sinuses (29, 30). a figure 1. cerebrospinal fluid circulation: (1) superior sagittal sinus, (2) arachnoid granulation, (3) convexity subarachnoid space, (4) choroid plexus (site of csf production), (5) lateral ventricle, (6) interventricular foramen (monro), (7) third ventricle, (8) cerebral aqueduct (sylvius), (9) fourth ventricle, (10) lateral aperture (foramen of luschka), (11) median aperture (foramen of magendie), (12) ventral subarachnoid space, (13) dorsal subarachnoid space. (adapted after ropper ah et al., adams and victor’s principles of neurology, 11th edition) 262 a.i. cucu, mihaela dana turliuc, claudia florida costea et al. second route of dissemination is by csf with the tumour spreading throughout the neuroaxis (figure 1). in a review, rawat et al. highlighted the fact that approximately 75% of patients with meningiomatous metastasis regardless of the route they followed have had previous operation for the primary tumour (31). also, it was hypothesized that tumour cells gain access to the vascular channels and meningeal surface by seeding during surgery (32). although this theory has earlier been rejected (33, 34), now it is accepted that surgical manipulation may release tumour cells into the csf (30, 31). metastatic spread during or after surgery exists theoretically, even though this theory is unlikely. but the incidence of leptomeningeal dissemination after meningiomas surgery is low and there are also cases with leptomeningeal dissemination through csf without surgical intervention (35). regarding malignant transformation of meningiomas after surgical resection, there is also the theoretical one (22). koenig et al. reported that at the site of surgical injury, the growth factors can promote malignant changes inside the meningeal tumour (36) and this event was observed by morantz and shain in an experimental rat model (37). intracranial and spinal cord dissemination through csf pathways there are variable sites of meningioma metastasis through csf pathways. the metastasis occurred due to leptomeningeal seeding from the neighboring meningioma, and the spinal canal is the second most common site (17) (table 1). in literature, spinal metastasizing meningiomas are rarely reported (17, 38, 39, 40, 41). in spinal intradural dissemination, the tumour cells have a tendency to accumulate more frequently at dorsal nerve root level, especially in the medullary cone and cauda equine, probably due to directional active flowing of the csf throughout the neuroaxis, and also to the effect of gravity (42, 43). in a large study on 200 consecutive meningiomas, of who grade i, which were followed prospectively during a median time of 8.5 years, chamberlain and glantz reported that 4 patients (2%) were diagnosed with spinal metastasis (21). vries et al. also reported csf or drop metastasis in 5% of non-benign meningiomas (44). meningioma metastasis may be simultaneous, both in the intracranial space and in the spinal cord (17, 45). in 1992, akimura et al. reported a malignant meningioma metastasizing through the csf pathways, both in the cerebellopontine angle cistern and in the thoracic spinal cord. the primary tumour was a parasagittal malignant meningioma two-times operated, the second time for recurrence. at the first surgery, the frontal horn of the lateral ventricle was opened because the meningioma infiltrated into the deep frontal brain. the authors concluded that this artificial communication between the meningioma cavity and the csf pathways enhanced the probability for tumour metastasis into cerebellopontine angle cistern and thoracic spinal cord (17). neoplastic meningitis it is well known that neoplastic meningitis is more common with solid carcinoma such as lung, breast and gastrointestinal cancer (46), but literature also reported few malignant meningioma cases with csf dissemination into the brain ventricles (47). there were only eight cases (47, 48) with intracranial or intraspinal malignant meningioma arising from lowgrade meningiomas, which disseminated throughout the csf (47). in neoplastic meningitis, csf dissemination of malignant meningioma cells may cause a variety of neurological symptoms such as disturbances of multiple cranial nerves, hydrocephalus, cerebellar dysfunction and multiple spinal nerve roots or cauda equine symptoms (49). brainstem damage by csf dissemination of malignant cell is rare, literature reporting a few cases with central hyperventilation, wallenberg syndrome and diplopia, facial nerve palsy and unsteadiness of gait secondary of csf dissemination of malignant tumour cells (20, 47, 50). it is important to mention, in terms of diagnosis, that only 54% of all cases with leptomeningeal meningiomatous dissemination revealed malignant cells in the csf on initial lumbar puncture, and only 8% of these cases remained negative, even after repeated examinations (51). the reason for this low specificity of the lumbar puncture remains unclear, although fujimaki et al. speculate the fact that malignant cells adhere rather than float freely in the csf (47). although identification of malignant cells by csf cytology has been considered the diagnostic gold standard, these paradigms have changed nowadays due to limited sensitivity of cytology. 263 “the silk road” via subarachnoid cisterns histopathology of csf-disseminated meningiomas even though the pathogenesis of csf disseminated meningiomas is not completely understood, over time researchers have issued various theories. in this regard, engelhard proposed three different pathways of dissemination: (1) tumour cells could be "shed" away directly into the csf due to direct contact between an anaplastic meningioma and csf pathways; (2) tumour cells might invade the leptomeningeal space during its progression; 3) the tumour cells might be inoculated within the csf at the time of the surgery (52). other authors, such as russel and rubinstein, considered that tumour friability may play an important role in meningioma dissemination within csf (42). however, considering that meningiomas arise from arachnoid cells and are naturally exposed to csf during their growth, it is difficult to explain the scarcity of meningioma dissemination through csf (22) as chamberlain and glantz reported that only 4% of the meningiomas could present leptomeningeal dissemination and positive csf cytology at the time of the diagnosis (21). more theoretically, the risk of intraventricular meningiomas to metastasize through csf pathways should be high, but literature reports only nine cases of intraventricular meningiomas (22). as an explanation, miller and ramsden considered that the dynamics of the csf pathways might prevent fragment formation and deposition of tumour cells (22, 53). however, in a review of 45 cases of meningioma with leptomeningeal dissemination through csf, park et al. noticed that the period of time needed for leptomeningeal dissemination in cases with intraventricular meningiomas is the shortest when compared to other intracranial and spinal meningiomas (22). all histological subtypes of meningiomas can metastasize (table 1), even benign meningiomas (45, 54, 55, 56, 57, 58), but meningeal tumours with clearly malignant features have a higher metastatic rate (59). metastatic meningiomas are associated more frequently with aggressive meningiomas (who grade 2, and who grade 3), with a range of occurrence of 10-25% (21), i.e. the more malignant the meningioma, the more likely its leptomeningeal dissemination (9, 17, 41, 60). according to literature, from a histological point of view, several factors are predictive of meningioma metastasis, including high cellularity, nuclear pleomorphism (figure 2), high mitosis rate, tumour necrosis, and invasion of blood vessels (7, 8). on the other hand, other authors consider that the metastasizing behaviour of these tumours is not correlated with their histological features (30, 31). figure 2. microphotographs of atypical meningioma, who grade ii. a. a tumour made up of meningothelial cells arranged in a sheet-like pattern, with increased cellularity, pleomorphism, and areas with small cells having high nucleus/cytoplasm ratio (he staining, x20); b. ki67 labelling index has high values and indicates a malignant neoplasia (anti-ki67 antibody immunohistochemical staining, x40). conclusion intracranial meningiomas with csf dissemination are extremely rare and, despite reports from literature, their pathogenesis remains unknown. in the case of a patient with a resected meningioma, the possibility of csf dissemination of tumour cells should be borne in mind, even if csf cytology is negative. also, a spinal mri should be performed, especially when spinal signs and symptoms are present. 264 a.i. cucu, mihaela dana turliuc, claudia florida costea et al. table 1. literature review of meningioma cases with csfdissemination year of publication, author primary site of meningioma who grade intracranial metastasis spinal metastasis time to csf disseminated disease 2013, tsuda et al. (43) t10-11 intradural i →ii + 12 years 2011, wu et al. (61) convexity iii + 1.7 years 2011, kim et al. (62) posterior fossa iii + 0 2011, peng et al. (63) medial temporal iii + 2 years 2009, kuroda et al. (64) skull base i→ii→ii i + + 6.3 years 2009, eom et al. (6) lateral ventricle ii→iii + 1.3 years 2008, erkutlu et al. (65) posterior fossa iii + 2.7 years 2008, santhosh et al. (65) convexity iii + + 9 months 2007, shintaku et al. (67) lateral ventricle i→iii + 4.3 years 2006, chuang et al. (68) convexity iii + 3 months 2005, cramer et al. (60) c1-c3 intradural ii + 1.4 years 2005, al-habib et al. (69) not mentioned iii + + 2 months 2005, chamberlain and glantz (21) not mentioned, 8 cases i + (8 cases) + (6 cases) 2005, wakabayashi et al. (70) frontal convexity iii + 13 years 2005, koenig et al. (36) temporal lobe iii + 1 month 2005, darwish et al. (71) lateral ventricle ii→iii + + 7 months 2002, ramakrishnamurthy et al. (35) lateral ventricle i + 4 years 2001, conrad et al. (72) convexity i→ii→ii i + + 6.4 years 2000, meinsma-vdtuin et al. (73) c2-c4 intradural iii + + 6 months 2000, lee et al. (74) convexity iii + + 9 years 1998, lee and landy (41) convexity skull base convexity iii i iii + + + + + 1.5 years 3.8 years 8.5 years 265 “the silk road” via subarachnoid cisterns 1995, peh and fan (39) lateral ventricle iii + + 5 years 1993, greenberg et al. (75) lateral ventricle iii + + 2 months 1992, satoh et al. (18) skull base i + + 0 1992, akimura et al. (17) convexity iii + + 1.8 years 1989, kamiya et al. (76) lateral ventricle iii + 6 months 1987, strenger et al. (77) third ventricle iii + 1.5 months 1985, kleinschmidtdemasters and avakian (20) lateral ventricle iii + + 1.7 years 1975, ludwin and conley (78) convexity iii + + 10 months 1972, miller and ramsden (53) convexity iii + 1971, riley et al. (22, 78) convexity i→iii + 1970, shuanghoti et al. (22, 78) convexity iii + 1963, russell et al. (22, 78) skull base i + 1960, hoffman et al. (22, 78) convexity i→iii + + 1954, winkelman (22, 78) skull base i + 1950, kalm (22, 78) posterior fossa iii + references 1. louis dn, scheitauer bw, budka h, von deimling a, kepes jj. meningiomas. in: kleihues p, cavenee wk (eds). pathology and genetics of tumors of the nervous system. lyon: iarc press, 2000. 2. cucu ai, costea cf, poeata i, et al. prognostic factors in atypical meningioma. rom neurosurg. 2017; 31(2):165171. 3. cucu ai, costea cf, poeata i, et al. anatomical localization of atypical meningiomas: our experience on 81 patients. rev med chir soc med nat iasi. 2018; 122:744-752 4. cucu ai, costea cf, carauleanu a, et al. meningiomas related to the chernobyl irradiation disaster in northeastern romania between 1990 and 2015. revista de chimie bucharest. 2018; 69:1562-1565. 5. cucu ai, turliuc md, carauleanu a, et al. chemical aspects of peritumoral cerebral edema in atypical meningiomas. rev chim (bucharest). 2018; 69:2804-2807. 6. eom ks, kim dw, kim ty. diffuse craniospinal metastases of intraventricular rhabdoid papillary meningioma with glial fibrillary acidic protein expression: a case report. clin neurol neurosurg. 2009; 111(7):619-623. 7. figueroa be, quint dj, mckeever pe, chandler wf. extracranial met¬astatic meningioma. br j radiol. 1999; 72:513-516. 8. ather enam s, abdulrauf s, mehta b, et al. metastasis in meningioma. acta neurochir. 1996; 138: 1172-1178, discussion 1177-1178. 9. gezen f, kahraman s, canakci z, bedük a. review of 36 cases of spinal cord meningioma. spine (phila pa 1976). 2000; 25: 727-731. 10. scognamiglio g, d’antonio a, rossi g, et al. cd90 expression in atypical meningiomas and meningioma metastasis. am j clin pathol. 2014; 141:841-849. 11. forest f, berremila sa, gyenes c, et al. metastatic meningiomas: an unusual clinical and pathological diagnosis with highly variable outcome. j neurooncol. 2014; 120(2): 411-421. 12. cucu ai, costea cf, turliuc md, et al. mirror, mirror on the wall, who’s the fairest of them all? atypical meningioma associated with multiple meningiomas. romanian neurosurgery. 2018; 32:563-572. 13. cucu ai, turliuc md, costea cf, et al. atypical meningiomas of cerebellopontine angle. a five case series. rev med chir soc med nat iasi. 2018; 122: 533-545. 266 a.i. cucu, mihaela dana turliuc, claudia florida costea et al. 14. gordon a, maloney a. a case of metastasizing meningioma. j neurol neurosurg psychiatry. 1965; 28:159-162. 15. kabus d, sidhu gs, wieczorek rl, choi hs. metastatic meningioma. hemangiopericytoma or angioblastic meningioma? am j surg pathol. 1993; 17:1144-1150. 16. cucu ai, turliuc dm, costea cf, et al. pathways of metastatic spread in meningiomas. romanian neurosurgery. 2019; 33(1):12-16. 17. akimura t, orita t, hayashida o, et al. malignant meningioma metastasizing through the cerebrospinal pathway. acta neurol scand. 1992; 85(5):368-371. 18. satoh t, kageyama t, yoshimoto y, et al. intra¬thecal dissemination of meningiomas; a case report. no shinkei geka. 1992; 20:805-808. 19. noterman j, depierreux m, raftopoulos c, brotchi j. metastases of meningioma. apropos of 2 cases. neurochirurgie. 1987; 33:184-189. 20. kleinschmidt-demasters bk, avakian jj. wallenberg syndrome caused by csf metastasis from malignant intraventricular meningioma. clin neuropathol. 1985; 4:214-219. 21. chamberlain mc, glantz mj. cerebrospinal fluiddisseminated meningioma. cancer. 2005; 103(7):14271430. 22. park ks, kim kh, park sh, et al. intracranial meningioma with leptomeningeal dissemination: retrospective study with review of the literature. j korean neurosurg soc. 2015; 57(4):258-265. 23. ludwin sk, rubinstein lj, russell ds. papillary meningioma: a malignant variant of meningioma. cancer. 1975; 36(4):1363-1373. 24. cantillo r, jain j, singhakowinta a, vaitkevicius v. blindness as initial manifestation of meningeal carcinomatosis in breast cancer. cancer.1979; 44:755-757. 25. eberth c. zur entwick pung des ephlheliomas (cholesteatomas) der pia and der lung. virchow s arch. 1870; 49:51-63. 26. dufour h. meningite sarcomateuse diffuse avec envahissement de las melle et das racines: cytologie positive et speciale du liquide cephalorachidien. rev. neurol. 1904; 12:104-106. 27. berman wf. meningeal carcinomatosis. jama. 1912; 58:1437-1439. 28. kalm h. ein malignes tentoriummeningeom mit metastasierung in die medulla oblongata und in die subarachnoidalen liquorräume. deutsche zeitschrift für nervenheilkunde. 1950, 163:131-140. 29. deangelis lm. current diagnosis and treatment of leptomeningeal metastasis. j neurooncol. 1998; 38(23):245-252. 30. fulkerson dh, horner tg, hattab em. histologically benign intraventricular meningioma with concurrent pulmonary metastasis: case report and review of the literature. clin neurol neurosurg. 2008; 110(4):416-419. 31. rawat b, franchetto aa, elavathil j. extracranial metastases of meningioma. neuroradiology. 1995; 37:38-41. 32. gyepes mt, dangio gj. extracranial metastases from central nervous system tumors in children and adolescents. radiology. 1966; 87:55-63. 33. christensen e, kiaer w, winblad s. meningeal turnouts with extracerebral metastases. br j cancer. 1949; 3:485-493. 34. wilkenman nw jr., cassell c, schlesinger b. intracranial tumors with extracranial metastases. j neuropathol exp neurol. 1952; 11:149-168. 35. ramakrishnamurthy tv, murty av, purohit ak, sundaram c. benign meningioma metastasizing through csf pathways: a case report and review of literature. neurol india. 2002; 50:326-329. 36. koenig ma, geocadin rg, kulesza p, et al. rhabdoid meningioma occurring in an unrelated resection cavity with leptomeningeal carcinomatosis. case report. j neurosurg. 2005; 102(2):371-375. 37. morantz ra, shain w. trauma and brain tumors: an experimental study. neurosurgery. 1978; 3(2):181-186. 38. wippold ii fj, smirnoitopoulus jg, pilgram tk. lesions of the cauda equina: a clinical pathology review from the armed forces institute of pathology. clin neurol neurosurg. 1997; 9:229-234. 39. peh wc, fan yw. case report: intraventricular meningioma with cerebellopontine angle and drop metastases. br j radiol. 1995; 68(808): 428-430. 40. solero cl, fornari m, giombini s, et al. spinal meningiomas: review of 174 operated cases. neurosurgery. 1989; 125:153-160. 41. lee tt, landy hj. spinal metastases of malignant intracranial meningioma. surg neurol. 1998; 50(5): 437441. 42. russel ds, rubinstein lj. pathology of tumors of the nervous system, 3rd. london: edward arnold, 1971. 43. tsuda k, akutsu h, yamamoto t, et al. benign spinal meningioma without dural attachment presenting delayed csf dissemination and malignant transformation. brain tumor pathol. 2013; 30(3):185-191. 44. de vries j, wakhloo ak. repeated multifocal recurrence of grade i, grade ii, and grade iii meningiomas: regional multicentricity (primary new growth) or metastases? surg neurol. 1994; 41(4):299-305. 45. miller dc, ojemann rg, proppe kh, et al. benign metastasizing meningioma. j neurosurg. 1985; 62:763-766. 46. clarke jl, perez hr, jacks lm, et al. leptomeningeal metastases in the mri era. neurology. 2010; 74:1449-1454. 47. fujimaki m, takanashi m, kobayashi m, et al. cerebrospinal fluid dissemination of anaplastic intraventricular meningioma: report of a case presenting with progressive 267 “the silk road” via subarachnoid cisterns brainstem dysfunction and multiple cranial nerve palsies. bmc neurol. 2016; 16:82. 48. tao cy, wang jj, li h, you c. malignant intraventricular meningioma with craniospinal dissemination and concurrent pulmonary metastasis. world j surg oncol. 2014; 12:238. 49. maria gp, teodoro s, jenny f, et al. leptomeningeal metastasis from solid tumors: a diagnostic and therapeutic challenge. neurol sci. 2015; 36:117-123. 50. toyooka t, miyazawa t, fukui s, et al. central neurogenic hyperventilation in a conscious man with csf dissemination from a pineal glioblastoma. j clin neurosci. 2005; 12:834-837. 51. william rw, j peter g, jerome bp. diagnosis and treatment of leptomeningeal metastases from solid tumors: experience with 90 patients. cancer. 1982; 49:759-772. 52. engelhard hh, corsten la. leptomeningeal metastasis of primary central nervous system (cns) neoplasm. in: abrey le, chamberlain mc, engelhard hh (eds.). leptomeningeal metastases. cancer treatment and research. vol 125. boston: springer, 2005. 53. miller aa, ramsden f. malignant meningioma with extracranial me¬tastases and seeding of the subarachnoid space and the ventricles. pathol eur. 1972; 7:167-175. 54. erman t, hanta i, haciyakupolu s, et al. huge bilateral pulmonary and pleural metastasis from intracranial meningioma: a case report and review of the literature. j neurooncol. 2005; 74:179-181. 55. aumann j, vandenbosch j, elbers j, wagenaar j. metastatic meningioma of the lung. thorax. 1986; 41:487-488. 56. kovoor j, jayakumar pn, srikanth sg, et al. solitary pulmonary metastasis from intracranial meningiothelial meningioma. australas radiol. 2002; 46:65-68. 57. som pm, sacher m, strenger sw, et al. "benign" metastasizing meningiomas. ajnr. 1987; 8:127-130. 58. cerda-nicolas m, lopez-givens c, perez-bacete m, et al. histologically benign metastatic meningioma: morphological and cytogenetic study. j neurosurg. 2003; 98:194-198. 59. kaminski j, movsas b, king e, et al. metastatic meningioma to the lung with multiple pleural metastases. am j clin oncol. 2001; 24:579-582. 60. cramer p, thomale uw, okuducu af, et al. an atypical spinal meningioma with csf metastasis: fatal progression despite aggressive treatment. case report. j neurosurg spine. 2005; 3:153-158. 61. wu yt, ho jt, lin yj, lin jw. rhabdoid papillary meningioma: a clinicopathologic case series study. neuropathology. 2011; 31:599-605. 62. kim jp, park bj, lim yj. papillary meningioma with leptomeningeal seeding. j korean neurosurg soc. 2011; 49:124-127. 63. peng j, liang zg, li kc. intracranial malignant meningioma with ce¬rebrospinal fluid dissemination: a case report. chin med j (engl). 2011; 124:1597-1599. 64. kuroda h, kashimura h, ogasawara k, et al. malignant intracranial meningioma with spinal metastasis--case report. neurol med chir (tokyo). 2009; 49:258-261. 65. erkutlu i, buyukhatipoglu h, alptekin m, et al. spinal drop metastases from a papillary meningioma : a case report and review of the literature : utility of csf sampling. med oncol. 2009: 26:242-246. 66. santhosh k, kesavadas c, radhakrishnan vv, et al. rhabdoid and papillary meningioma with lepto¬meningeal dissemination. j neuroradiol. 2008; 35:236-239. 67. shintaku m, hashimoto k, okamoto s. intraventricular meningioma with anaplastic transformation and metastasis via the cerebrospinal flu¬id. neuropathology. 2007; 27:448-452. 68. chuang hc, lee hc, cho dy. intracranial malignant meningioma with multiple spinal metastases--a case report and literature review: case report. spine (phila pa 1976). 2006; 31:e1006-e1010. 69. al-habib a, lach b, al khani a. intracerebral rhabdoid and papillary meningioma with leptomeningeal spread and rapid clinical progression. clin neuropathol. 2005; 24:1-7. 70. wakabayashi k, suzuki n, mori f, et al. rhabdoid cystic papillary meningioma with diffuse subarachnoid dissemination. acta neuropathol. 2005: 110:196-198. 71. darwish b, munro i, boet r, et al. intraventricular meningioma with drop metastases and subgaleal meta¬static nodule. j clin neurosci. 2004: 11:787-791. 72. conrad md, schonauer c, pelissou-guyotat i, et al. recurrent lumbosacral metastases from intracranial menin¬gioma. report of a case and review of the literature. acta neurochir (wien). 2001: 143: 935-937. 73. meinsma-vdtuin m, molenaar wm, mooij jj. spinal papillary menin¬gioma: a case report and review of the literature. acta neurochir (wien). 2000; 142:703-708. 74. lee wh, chen a, chao dg, et al. malignant meningioma with rhabdoid transformation. zhonghua yi xue za zhi (taipei). 2000; 63:492-497. 75. greenberg sb, schneck mj, faerber en, kanev pm. malignant menin¬gioma in a child: ct and mr findings. ajr am j roentgenol. 1993; 160:1111-1112. 76. kamiya k, inagawa t, nagasako r. malignant intraventricular menin¬gioma with spinal metastasis through the cerebrospinal fluid. surg neurol. 1989; 32:213218. 77. strenger sw, huang yp, sachdev vp. malignant meningioma within the third ventricle: a case report. neurosurgery. 1987; 20:465-468. 78. ludwin sk, conley fk. malignant meningioma metastasizing through the cerebrospinal pathways. j neurol neurosurg psychiatry. 1975; 38:136-142. doi: 10.33962/roneuro-2021-015 retrospective study on early outcomes of carotid stenting. institutional experience saurabh sharma, prashant raj singh, ram kumar goyal, raghavendra kumar sharma, yashuhiro yamada, yoko kato romanian neurosurgery (2021) xxxv (1): pp. 94-97 doi: 10.33962/roneuro-2021-015 www.journals.lapub.co.uk/index.php/roneurosurgery retrospective study on early outcomes of carotid stenting. institutional experience saurabh sharma1, prashant raj singh2, ram kumar goyal3, raghavendra kumar sharma4, yashuhiro yamada5, yoko kato6 1 m.ch. neurosurgery. associate consultant, max hospital, delhi, india 2 d.n.b. neurosurgery. assistant professor, a.i.i.m.s. raipur, c.g. india 3 m.ch. neurosurgery. consultant, gnrc hospital, guwahati, assam, india 4 m.ch. neurosurgery. assistant professor, a.i.i.m.s. raipur, c.g. india 5 md. phd. consultant neurosurgeon, department of neurosurgery, bantane hospital, fujita health university, nagoya, japan 6 prof. dr md. phd. consultant neurosurgeon, department of neurosurgery, bantane hospital, fujita health university, nagoya, japan abstract objective: this study is conducted to evaluate the early events after carotid artery stenting (cas) among our patients in a single institute. methods: this study was conducted on 40 patients. these patients underwent stenting of extracranial carotid arteries. stenting was performed on symptomatic patients with carotid artery stenosis of more than 50 per cent of asymptomatic patients with more than 70 per cent carotid artery stenosis on doppler ultrasonography. follow up period for this study was of one month. results: 40 patients who underwent cas between august 2018 and june 2019 were included in the study. self-expandable hybrid stents were implanted in all patients and pre or poststent-dilatation was performed if required after implantation. none of the patients suffered from a stroke, myocardial infarction or death due to cas during their hospital stay. only one patient had a minor stroke during follow up, which was managed conservatively. no transient ischemic attack (tia), myocardial infarction or death during the follow-up period. re-stenosis was not observed in the follow-up carotid doppler ultrasonography; flow rates were within normal limits. conclusions: carotid stenting is a safe alternative to cea (carotid endarterectomy) in the treatment of carotid stenosis regardless of age. cas with cerebral protection can be performed safely in patients who are at high surgical risk, with low perioperative morbidity and mortality. the durability of the procedure must be determined with a longer follow-up. further high-quality rcts are required to address other shortcomings and controversies. introduction in the industrialized world, the leading cause of death is stroke. [1] keywords carotid stenosis, stents, stroke corresponding author: raghavendra kumar sharma a.i.i.m.s. raipur, c.g., india sdr.raghavendra@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 95 retrospective study on early outcomes of carotid stenting stroke is also the major culprit of disability in the affected individuals. about 6.5 million strokes occur per year. atherosclerosis and embolization from stenosed carotid arteries are one of the most common causes of vascular stroke. bifurcation of the common carotid artery is the common site of stenosis and the atherosclerotic plaques found in this stenosed area. it accounts for nearly 20 % of strokes. this embolization can lead to tia, brain ischemia, and other neurological manifestations. [2,3] carotid atherosclerosis is often asymptomatic until a disabling or fatal stroke occurs. predisposing factors for carotid atherosclerosis are diabetes mellitus, hypertension, hyperlipidemia, and smoking. there is a strong association between the severity of stenosis and stroke risk exists. medical treatment, interventional angioplasty, and carotid endarterectomy (cea) are some treatment options for symptomatic carotid artery stenosis.[4] as compared to cea, carotid artery stenting (cas) is a minimally invasive alternative for the treatment of carotid artery stenosis. however, the safety and efficacy of cas have been approved by various randomized trials (rcts). the incidence of restenosis after cas is comparatively low but periprocedural stroke after cas is a little concern.[4] in this article, we are sharing our institutional experience with cas, its complication, and early outcome. material and methods we conducted a retrospective study on patients who underwent carotid artery stenting from august 2017 to june 2019 to determine the various outcomes of the procedure and to find out the different outcomes in asymptomatic and symptomatic patients. the total number of patients undergone carotid stenting in our study was 40. as per our departmental protocol the patients who underwent cas, required to have symptoms with more than 50% of carotid artery stenosis. asymptomatic patients who had more than 70% carotid artery stenosis on doppler ultrasonography were also selected for cas. patients who suffered transient ischemic attacks (defined as focal neurological dysfunction due to focal brain ischemia without cerebral infarct), minor nondisabling stroke, or amaurosis fugax, considered as symptomatic. those patients, who have a history of severe stroke, were excluded from the study. before the procedure, detailed history and clinical and laboratory examinations were performed. routinely electrocardiography (ecg) was done in all patients and detailed interpretation performed by the cardiology team. all patients underwent carotid doppler ultrasound, magnetic resonance angiography (mra) of the carotid arteries, or computed tomography angiography (cta) of the carotid arteries. data were collected for both rights and left carotid arteries, regardless of which carotid artery was stented. the degree of stenosis was grouped into ranges using velocity criteria in doppler ultrasound. the categories were: < 70% stenosis and >70% stenosis or occluded. in this procedure, we used self-expandable stents and both proximal and distal embolic protection devices (figure 1). in all patients, a stent with a distal or proximal protection device was placed after accessing a femoral artery. predilatation before stent placement and post dilatation after stenting was performed depending upon the surgeon's choice and requirement. every patient received standard medical care post-procedural, including the treatment of hypertension, hyperlipidemia, and diabetes. in our study, a detailed neurologic evaluation was performed at baseline, during the hospital stay. any complications such as transient ischemic stroke, myocardial infarction, visual deterioration, and death were reported. follow up period of our study was 30 days. figure 1. showing self-expandable stent with diastal embolic protection device. 96 saurabh sharma, prashant raj singh, ram kumar goyal et al. results forty patients who underwent cas between the study periods were included in the study conducted at bantane hospital, fujita health university, nagoya, japan. the mean age was 71.61 years (range: 48-89 years old) and the percentage of male participants was 90%. 40% of our patients were less than 70 years of age. 72.5% of patients were having a history of hypertension which was considered as the most common cardiac risk factor. 60 % of our patients had stenosis > 70 percent and among them 41.66 % were symptomatic. the most common neurologic sign was hemiparesis (stroke8 patients) followed by transient ischemic attack (tia-5 patients) and amaurosis fugax (2 patients). the ratio of males and females in our study was 9:1. 38% patients were symptomatic and the rest was asymptomatic. embolic protection devices (epds), as well as selfexpandable hybrid stents, were used in all cases. distal epds were used in 25% cases whereas, proximal epds in 75% cases. there was no stroke, mi, or death in our study population during the period of hospital stay. patients were followed up and the mean follow-up period was 30 days after discharge. only one patient had a minor stroke in the follow-up period, which was managed conservatively. no tia, myocardial infarction, or death during the follow-up period. doppler ultrasonography was used to look for re-stenosis (observed by flow rate) of carotid vessels during the follow-up periods. no evidence of restenosis was noticed during this period. discussion before the introduction of embolic protection devices and hybrid selfexpandable stents, the postprocedural complications used to be high but with the uses of these devices, morbidity and mortality were remarkably reduced. setacci et al. observed in his prospective study that the combined stroke and death rate at 30 days for symptomatic patients who underwent cas was about 10 percent.[5] gray et al. analyze the data from 2 prospective multicentric studies. analysis from these 2 post-market surveillance studies (exact, capture-2) on 6,320 high-risk patients, showed a 3.6 percent death and stroke rate over a period of 30 posts procedural days.[6] the mean age of patients in our study was 71.61 years. one patient in our study developed a minor no disabling stroke which was managed conservatively and successfully. no associated mortality in our cases as compared to other studies. 30 days stroke rate is also comparable to other studies on exclusive carotid stenting.[5] the absolute perioperative risks we observed when considering cas is that there is a lower absolute risk of stroke in asymptomatic patients than for symptomatic carotid stenosis. previous studies have suggested that prophylactic revascularization for asymptomatic carotid stenosis may not have clear advantages over medical management when the procedural risk exceeds 3%.[7] in our center procedural risk is less than 3%. according to a study, the 30-day stroke of 16% for symptomatic primary-cas patients but no stroke in the asymptomatic group.[8] their 16% stroke rate significantly exceeds the 2.5% rate reported in the current study. in a study by hobson et al, cas was successful in all 17 cases and produced no periprocedural neurologic deficits or deaths.[9] similar favorable results were reported by yadav et al, with only one minor stroke in 25 cas procedures in 22 symptomatic patients.[10] naggara et al showed that the use of an embolic protection device (epd) lowers the risk of stroke at the time of cas. in our study, we used distal or proximal embolic protection devices and selfexpandable stents.[11] according to some studies, the use of closed-cell stent design decreases the operative and postoperative stroke rates.[12] calvin et al stated that high volume operators had the lowest operative stroke and death rates.[13] in sapphire and crest studies post-cas myocardial infarction (mi) was associated with 2.4 and 1.1 % cases respectively.[14,15] antiplatelet therapy when initiated early can reduce the recurrence of neurological events after non-cardioembolic tia/stroke.[16] in our study, one patient developed minor strokes which was not disabling and there was no effect on hospital stay and all patients were discharged in stable conditions. as compared to other studies, there was no mortality or myocardial infarction in our groups. a 2012 cochrane review of 7572 patients from 16 trials reported that endovascular treatment was associated with significantly lower risks of mi, cranial nerve palsy, and haematomas.[17] conclusion stroke is a major contributor to the global health 97 retrospective study on early outcomes of carotid stenting burden. cas is a good alternative treatment for carotid artery stenosis. according to many studies, periprocedural stroke is more commonly associated with cas but mi and other complications are far less in post-cas patients. the present analysis emphasizes that cas can be performed with high procedural success and reasonable procedural safety in a high-volume center with experienced interventionists, utilization of appropriate devices, and under embolic protection devices. however, an expert operator is needed to avoid cardiovascular complications in high-risk patients. guidelines for performing cas, use of instruments, embolic devices, dual or single antiplatelet therapy pre and post-procedure, and use of closed or open cell stents are variable and need to be defined. high-quality rct is required so that cas can be performed for specific reasons and with specific instruments. this procedure is less invasive and better tolerated, and is a better future treatment option for carotid stenosis. moreover, in comparison with cea, cas is an effective as well as a safe treatment option for the high-risk patients with carotid artery stenosis, and hence it is expected that more institutes will opt for this intervention in upcoming years. acknowledgements authors thank all staffs of bantane hospital, fujita health university, nagoya, japan for supporting us. declarations financial support and sponsorship: nil conflict of interest: there are no conflicts of interest references 1. merchán-baeza ja, gonzalez-sanchez m, cuesta-vargas a. clinical effect size of an educational intervention in the home and compliance with mobile phone-based reminders for people who suffer from stroke: protocol of a randomized controlled trial. jmir research protocols. 2015;4(1):e33. 2. benjamin ej, blaha mj, chiuve se, et al. heart disease and stroke statistics-2017 update: a report from the american heart association. circulation. 2017;135(10):e146–e603. 3. diao z, jia g, wu w, wang c. carotid endarterectomy versus carotid angioplasty for stroke prevention: a systematic review and meta-analysis. journal of cardiothoracic surgery. 2016;11(1):142. 4. jonas de, feltner c, amick hr, et al. screening for asymptomatic carotid artery stenosis: a systematic review and meta-analysis for the us preventive services task force. annals of internal medicine. 2014;161(5):336– 346. 5. setacci c, chisci e, setacci f, iacoponi f, de donato g, rossi a. siena carotid artery stenting score: a risk modelling study for individual patients. stroke. 2010;41(6):1259–1265. 6. gray wa, chaturvedi s, verta p. thirty-day outcomes for carotid artery stenting in 6320 patients from 2 prospective, multicenter, high-surgical-risk registries. circulation: cardiovascular interventions. 2009;2(3):159– 166. 7. goldstein l, bushnell c, adams r, et al. american heart association stroke council; council on cardiovascular nursing; council on epidemiology and prevention; council for high blood pressure research; council on peripheral vascular disease, and interdisciplinary council on quality of care and outcomes research. guidelines for the primary prevention of stroke. headache. 2011;51(6):1011–1021. 8. aburahma af, abu-halimah s, bensenhaver j, et al. primary carotid artery stenting versus carotid artery stenting for postcarotid endarterectomy stenosis. journal of vascular surgery. 2009;50(5):1031–1039. 9. hobson ii rw, goldstein je, jamil z, et al. carotid restenosis: operative and endovascular management. journal of vascular surgery. 1999;29(2):228–238. 10. yadav js, roubin gs, king p, iyer s, vitek j. angioplasty and stenting for restenosis after carotid endarterectomy: initial experience. stroke. 1996;27(11):2075–2079. 11. naggara o, touzé e, beyssen b, et al. anatomical and technical factors associated with stroke or death during carotid angioplasty and stenting: results from the endarterectomy versus angioplasty in patients with symptomatic severe carotid stenosis (eva-3s) trial and systematic review. stroke. 2011;42(2):380–388. 12. bosiers m, de donato g, deloose k, et al. does free cell area influence the outcome in carotid artery stenting? european journal of vascular and endovascular surgery. 2007;33(2):135–141. 13. calvet d, mas j-l, algra a, et al. carotid stenting: is there an operator effect? a pooled analysis from the carotid stenting trialists’ collaboration. stroke. 2014;45(2):527– 532. 14. bonati lh, ederle j, mccabe dj, et al. long-term risk of carotid restenosis in patients randomly assigned to endovascular treatment or endarterectomy in the carotid and vertebral artery transluminal angioplasty study (cavatas): long-term follow-up of a randomised trial. the lancet neurology. 2009;8(10):908–917. 15. brott tg, hobson rw, howard g, et al. stenting versus endarterectomy for treatment of carotid-artery stenosis. new england journal of medicine. 2010;363(1):11–23. 16. brott tg, howard g, roubin gs, et al. long-term results of stenting versus endarterectomy for carotid-artery stenosis. new england journal of medicine. 2016;374(11):1021–1031. 17. bonati lh, lyrer p, ederle j, featherstone r, brown mm. percutaneous transluminal balloon angioplasty and stenting for carotid artery stenosis. cochrane database of systematic reviews. 2012;(9). a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-003 accuracy of 2d fluoroscopy with preoperative ct fused neuronavigation in thoracic and lumbar pedicle screw insertion adrian bălașa, corina-ionela hurghiș, flaviu tămaș, ioanalexandru florian, levente peter, rareș chinezu romanian neurosurgery (2020) xxxiv (1): pp. 20-25 doi: 10.33962/roneuro-2020-003 www.journals.lapub.co.uk/index.php/roneurosurgery accuracy of 2d fluoroscopy with preoperative ct fused neuronavigation in thoracic and lumbar pedicle screw insertion adrian bălașa1,2, corina-ionela hurghiș2, flaviu tămaș2, ioan-alexandru florian3,4, levente peter2, rareș chinezu1,2 1 university of medicine, pharmacy, science and technology “george emil palade”, tirgu mures, romania 2 neurosurgery clinic, clinical emergency hospital, tirgu mures, romania 3 university of medicine and pharmacy “iuliu hatieganu”, cluj napoca, romania 4 neurosurgery clinic, clinical emergency hospital, cluj napoca, romania abstract aim: pedicle screw fixation is an established technique in the lumbar and thoracic area. fluoroscopy-guided screw placement and subsequently navigation have decreased the rate of misplaced screws, but no technique has wholly eliminated this risk. this paper aims to study the difference between the accuracy of the fluoroscopic guided screw placement to that of the 2d fluoroscopypreop ct fused neuronavigation guided technique, a lesser-used navigation technique. material and methods: this retrospective study reflects our results using both techniques between march 2018 and march 2019 in both degenerative or traumatic spinal pathology for thoracic and lumbar regions. the accuracy of the screw placement was measured using mirza grading system on postoperative ct images. results: a total number of 56 patients underwent spinal instrumentation surgery. a total of 274 screws were placed with a mean number of 4.89 screws per patient; 199 screws were implanted using neuronavigation and 75 using the freehand-2d fluoroscopy-guided technique. the accuracy rate of pedicle screw placement in the freehand technique guided by 2d fluoroscopy was 88,00%. with the use of neuronavigation, the accuracy increased to 89,96%. conclusion: pedicle screw placement accuracy is higher when guided by ct-fluoro matching neuronavigation compared to freehand fluoroscopy-guided technique and can be used in departments where there is no intraoperative o-arm or 3d fluoroscopy available. introduction in the past 30 years, spinal surgery has seen a significant increase in the keywords 2d fluoroscopy, ct-fluoro matching, image guided surgery, screw accuracy, transpedicular screw fixation corresponding author: adrian bălașa university of medicine, pharmacy, science and technology “george emil palade”, tirgu mures, romania adrian.balasa@umfst.ro copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 21 ct fluoro matching neuronavigation technique development of surgical techniques and instrumentation. pedicle screw fixation is an established technique in the lumbar and thoracic area (3). there are many techniques of pedicle screw placement starting from the "free hand technique" described by kim and lenke (5,17) to modern techniques that use intraoperative image guidance: 2d fluoroscopy, 2d/3d fluoroscopy navigation, cone beam intraoperative ct navigation or intraoperative mri navigation (11). fluoroscopy-guided screw placement has decreased the rate of misplaced screws from 55% to 21% in the thoracic region and from 40% to 12% in the lumbar region (14). neuronavigation in spinal surgery further decreased the rate of misplaced screws, but no intraoperative navigation technique has wholly eliminated this risk (4,7,13). neuronavigation using 2d fluoroscopyct fusion is a technique used for pedicle screw placement that was described by sakai (12). this technique uses a preoperative ct thin cut slice scan that is linked via neuronavigation to a set of intraoperative fluoroscopic images and allows for navigation even in the absence of 3d fluoroscopic c-arms or intraoperative ct machines (12). despite being introduced more than ten years ago, this technique has not seen wide adoption, and no relevant studies are available to assess its efficacy. this paper aims to study the difference between the accuracy of the fluoroscopic guided screw placement to that of the 2d fluoroscopy-ct fused neuronavigation guided technique. figure 1: fusion between the intraoperative fluoroscopy and a 3d model of a vertebra (based on the ct scan) and subsequently registration of the defined vertebra. materials and methods this retrospective study was performed between march 2018 and march 2019 at the department of neurosurgery of the tîrgu mureș clinical emergency 22 adrian bălașa, corina-ionela hurghiș, flaviu tămaș et al. hospital, romania. patients were operated by a team of multiple neurosurgeons, all with proper levels of spinal instrumentation expertise. the study has included traumatic and degenerative cases in the thoracic and lumbar spine; redo surgeries or repositioning of misplaced screws were not included. all patients were operated in a prone position using a bertchtold translucent table (stryker, michigan, usa). intraoperative fluoroscopy was performed in all cases with a siemens siremobil compact l 200 machine (siemens, munich, germany). for cases in which the neuronavigation guided technique was used, a preoperative ct thin cut slice (under 3 mm slices) scan of the operated area was obtained before surgery. a curve brainlab (brainlab, munich, germany) neuronavigation system was used in conjunction with a spine and trauma software (brainlab, munich, germany) (figure 1). a fusion between the intraoperative fluoroscopy and a 3d model of a vertebra (based on the ct scan) and subsequently registration of the defined vertebra was performed using sakai’s (12) previously described technique (figure 1). medtronic polyaxially titanium screws (medtronic, minnesota, usa) or stryker (stryker, michigan, usa) monoaxial and polyaxially titanium screws with diameters ranging from 4 to 6 mm, and lengths between 40 and 60 mm were used, depending on the spinal level and pedicle width. there are two commonly used grading systems used for measuring screw placement accuracy: zdichavsky (18), (9) and mirza (10) which use postoperative ct images to analyze the pedicle screw placement accuracy. we have chosen to use in our study the mirza scoring system (table 2). table 1. demographic distribution. no. patients 56 sex male 36 (64, 28%) female 20 (35, 72%) age (years) mean 52,76 range 20-75 years pathology/level traumatic degenerative conditions thoracic 15 patients (26,78%) 0 patients (0%) thoraco-lumbar 1 patients (1,78%) 0 patients (0%) lumbar 18 patients (32,14%) 17 patients (30,35%) lumbo-sacral 0 patients (0%) 5 patients (8,92%) number of screws implanted ct-fluoro matching neuronavigatio n 2d fluoroscopy freehand thoracal 46 (23.11%) 32 (42.66%) lumbar 153 (76.88%) 43 (57.33%) table 2. mirza et al. 2 mm increment grading system. classification borders grade 0 (optimal) the screw correctly fits the pedicle grade 1 (minor) under 2 mm of displacement grade 2 (moderate) between 2 to 4 mm of displacement grade 3 ( severe) over 4 mm of displacement postoperative imaging was analyzed by the senior author (ab) and an independent radiologist. statistical analyses included descriptive (frequency, mean, standard deviation) and inferential statistics. the shapiro-wilk test was applied to determine the distribution of the analyzed data series. for analyzing the quantitative variables the t-student test was applied for unpaired data and for analyzing the qualitative variables the fisher test was applied. the significance threshold chosen for the p value was 0.05. statistical analysis was performed using the graphpad prism trial variant. results between march 2018 and march 2019, a total number of 69 patients underwent spinal instrumentation surgery in the thoracolumbar regions for degenerative or traumatic pathology. out of these, 56 patients (81.16%) had complete documentation and were included in our study. second surgery for repositioning of screws was necessary in 2 screws (2 cases). a total of 274 screws were placed with a mean number of 4.89 screws per patient, ranging from 4 screws to a maximum of 10 screws. in our study, traumatic pathology was represented by 60.71% (n=34 ) of cases, and the lumbar spine was the most frequent region involved with 39.29% of cases (n=35). table 1 summarizes the clinical data and demographic distribution of the patients. the ct fluoro matching neuronavigation method was used in 72.63% of cases, which resulted in a total 23 ct fluoro matching neuronavigation technique of 199 screws implanted; the rest of 75 (27.37%) screws were implanted using the” freehand” technique under fluoroscopy guidance. the distribution of screws by region and the type of technique used is seen in table 1. the results of the mirza 2 mm increment staging system are presented in table 3 for medial and lateral displacement and table 4 for the correlation between the severity of displacement and anatomic region. from 20 mispositioned screws implanted under neuronavigation guidance, 11 screws were in the lumbar area and 9 screws in the thoracic area. the misplaced screws in the thoracic area represented 19.57% of the total number of 46 screws implanted, whilst in the lumbar area, the misplaced screws represented 7.19% of the total of 153 screws implanted. all severly placed screws were in the thoracic area (table 4). there is a statistically significant association between the region of screw implantation and the malposition rate (p = 0.023, fischer’s test). table 3. grade of screw misplacement using the 2 mm increment (mirza score) classification and screws direction tendency of cortex perforation. severity minor (%) moderate (%) severe (%) total (%) p lateral misplacement with neuronavigation 6 (3.01%) 4 (2,01%) 1 (0,50%) 11(5,52%) 0.55 lateral misplacement with fluoroscopy 1 (1,33%) 1 (1,33%) 1 (1,33%) 3 (4%) medial misplacement with neuronavigation 8 (4.02%) 1 (0,50%) 0 (0%) 9 (4,52%) 0.99 medial misplacement with fluoroscopy 5 (6,66%) 1 (1,33%) 0 (0%) 6 (8%) table 4. grade of screw misplacement using the 2mm increment (mirza score) classification relative to the vertebral region. 2d fluoroscopy freehand number of screws (%) misplacement rate (%) p value minor moderate severe thoracal 32 (42.66) 4 (8.69%) 4 (8.69%) 1 (2.17%) 0.1585 lumbar 43 (57.33) 10 (6.53%) 1 (0.65%) 0 (0.00%) total 75 20 ctfluoromatching neurnavigation thoracal 46 (23.11%) 4 (12.50%) 1 (3.12%) 1 (3.12%) 0.0231 lumbar 153 (76.88%) 2 (4.65%) 1 (2.32%) 0 (0.00%) total 199 9 discussions this study tries to reflect our experience in transpedicular screw implantation. we focused on the accuracy of transpedicular screw implantation using the two implantation procedures that are used at our institution: freehand technique under fluoroscopy guidance and neuronavigation with ct 2d fluoro-matching. there are few articles in the literature about pedicle screw implantation that include ct-fluoromatching neuronavigation or compare this technique with the freehand technique under fluoroscopic guidance (15), and to our knowledge this is the first series presented. this might be because intraoperative 3d fluoroscopy or intraoperative ct has become widely available. scoring the screw misplacement is still a difficult task as there are reported more than 35 classifications that analyze pedicle screw misplacement and, in most of them, there is no clear description of the assessment methods used to determine the accuracy of the pedicle screw positioning (2,6). evermore there are publications showing that moderate lateral or medial displacement of the screws with violation of the pedicle cortex does not commonly relate with neurologic, vascular, and/or visceral complications (8). 24 adrian bălașa, corina-ionela hurghiș, flaviu tămaș et al. we have chosen mirza scoring system(10) because this seems to be the most widely accepted and one of the most precise scale for scoring pedicle screw placement. (1) our overall accuracy rate of pedicle screw placement using the freehand technique guided by 2d fluoroscopy was 88.00%. with the use of the neuronavigation, the accuracy increased to 89.96%. nevertheless, our results are comparable to different other papers: the screw misplacement rate in our study was of about 12% in the fluoroscopy technique group, and pedicle cortex perforation over 4 mm (severely misplaced screw) was seen in 1.33%, comparable to the results previously published by guedes and verma (2),(16). in our ct-fluoro navigation group, a slight increase in the overall accuracy was noted. even if this increase in accuracy is not statistically significant, these results are similar to the ones of kosmopoulous (6), showing over 90% accuracy rate for both techniques, and might be partially explained by good fluoro screw positioning technique. gelalis (3) concluded that neuronavigation increases the accuracy of pedicle screw placement and when using freehand technique there is an increased tendency of medial perforation of pedicle cortex as opposed to neuronavigation where the tendency is to perforate the cortex laterally which decreases the risk of neurological complication even in case of inaccuracy. our results seem to reconfirm this as in the ct-fluoro group we noted a slight increase in the lateral displacement (5,52% vs. 4%) but also a 50% reduction of medial misplacement (4.52% vs. 8%) (table 3.) there are also inherent limitations to ct-fluoro matching neuronavigation technique: due to the acquisition of the preoperative spine ct in the supine position and the prone position in the operating room, a spine displacement most likely occurs and interferes with the accuracy(8). scanning patients in prone position or spine curvature detection algorithms might further improve this technique. inaccuracies are also given by the need to fuse a 3d vertebral body model to a 2d intraoperative fluoroscopy, and a less than perfect thoracic imaging allows for navigation errors and screw misplacement that is higher than the rate we obtained in lumbar spine, but still lower than freehand fluoroscopy technique. conclusion despite its shortcomings, the ct-fluoro matching technique has similar or slightly better results than freehand fluoroscopy and can be used in departments where there is no intraoperative o-arm or 3d fluoroscopy available and a more affordable neuronavigation solution is required. conflicts of interest the authors of this paper state that they have no conflict of interests to disclosure. abbreviations mri: magnetic resonance imaging ct: computer tomography 2d: two-dimensional 3d: three-dimensional references 1. aoude aa, fortin m, figueiredo r, jarzem p, ouellet j, weber mh: methods to determine pedicle screw placement accuracy in spine surgery: a systematic review. eur. spine j. 24: 990–1004, 2015. 2. de paula guedes v, manffra ef, aguiar lr: image-guided surgery in the spine: neuronavigation vs. fluoroscopy. coluna/ columna 14: 181–185, 2015. 3. gelalis id, paschos nk, pakos ee, politis an, arnaoutoglou cm, karageorgos ac, ploumis a, xenakis ta: accuracy of pedicle screw placement: a systematic review of prospective in vivo studies comparing free hand,fluoroscopy guidance and navigation techniques. eur. spine j. 21: 247–255, 2012. 4. karhade a, vasudeva, pompeu, lu: image guided spine surgery: available technology and future potential. austin neurosurg open access 3: 1043–1, 2016. 5. kim yj, lenke lg, bridwell kh, cho ys, riew kd: free hand pedicle screw placement in the thoracic spine: is it safe. spine (phila. pa. 1976). 29: 333–342, 2004. 6. kosmopoulos v, schizas c: pedicle screw placement accuracy. spine (phila. pa. 1976). 32: e111–e120, 2007. 7. laine t, mäkitalo k, schlenzka d, tallroth k, poussa m, alho a: accuracy of pedicle screw insertion: a prospective ct study in 30 low back patients. eur. spine j. 6: 402–405, 1997. 8. liu h, chen w, liu t, meng b, yang h: accuracy of pedicle screw placement based on preoperative computed tomography versus intraoperative data set acquisition for spinal navigation system. j. orthop. surg. 25: 1–8, 2017. 9. marios theologou1 2, , theologos theologou1 , dimitrios 25 ct fluoro matching neuronavigation technique zevgaridis1 , nikolaos skoulios2 , slavisa matejic3 ct: pedicle screw placement accuracy impact and comparison between grading systems marios. surg. neurol. int. 8: 1–7, 2017. 10. mirza sk, wiggins gc, kuntz iv c, york je, bellabarba c, knonodi ma, chapman jr, shaffrey ci: accuracy of thoracic vertebral body screw placement using standard fluoroscopy, fluoroscopic image guidance, and computed tomographic image guidance: a cadaver study. spine (phila. pa. 1976). 28: 402–413, 2003. 11. moses zb, mayer rr, strickland ba, kretzer rm, wolinsky j-p, gokaslan zl, baaj aa: neuronavigation in minimally invasive spine surgery. neurosurg. focus 35: e12, 2013. 12. sakai y, matsuyama y, yoshihara h, nakamura h, nakashima s, ishiguro n: simultaneous registration with ct-fluoro matching for spinal navigation surgery. a case report. nagoya j med sci 68: 45–52, 2006. 13. shin mh, hur jw, ryu ks, park ck: prospective comparison study between the fluoroscopy-guided and navigation coupled with o-arm guided pedicle screw placement in the thoracic and lumbosacral spines. j. spinal disord. tech. 28: e347–e351, 2015. 14. tehli o, harman f, temiz c, kacar y, kazanci b, daneyemez m, solmaz i, kural c: the use of neuronavigation and intraoperative imaging in spinal stabilization surgery. turk. neurosurg. 26: 771–776, 2016. 15. tjardes t, shafizadeh s, rixen d, paffrath t, bouillon b, steinhausen es, baethis h: image-guided spine surgery: state of the art and future directions. eur. spine j. 19: 25, 2010. 16. verma sk, singh pk, agrawal d, sinha s, gupta d, satyarthee gd, sharma bs: o-arm with navigation versus c-arm: a review of screw placement over 3 years at a major trauma center. br. j. neurosurg. 30: 658–661, 2016. 17. wagner sc, morrissey pb, kaye id, sebastian a, butler js, kepler ck: intraoperative pedicle screw navigation does not significantly affect complication rates after spine surgery. j. clin. neurosci. 47: 198–201, 2018. 18. zdichavsky m, blauth m, knop c, graessner m, herrmann h, krettek c, bastian l: accuracy of pedicle screw placement in thoracic spine fractures part i: interand intraobserver reliability of the scoring system. eur. j. trauma 30: 234–240, 2004. doi: 10.33962/roneuro-2020-088 pre-hospital care: demography, current profile and future trends. improving the health of traumatic brain injury patients sateesh chandra verma, abhijeet singh sachan, surjeet singh, prakrati sachan romanian neurosurgery (2020) xxxiv (4): pp. 518-523 doi: 10.33962/roneuro-2020-088 www.journals.lapub.co.uk/index.php/roneurosurgery pre-hospital care: demography, current profile and future trends. improving the health of traumatic brain injury patients sateesh chandra verma, abhijeet singh sachan, surjeet singh, prakrati sachan department of neurosurgery, sawai man singh medical college, jaipur, india abstract introduction. traumatic brain injury (tbi) is a major public health problem throughout the world. it is one of the leading causes of mortality and disability as a consequence results in a great financial burden on societies. damage to the brain following trauma does not occur only at the moment of injury but also develops over a period of hours to days with the further secondary insult of the brain. methods. this was a prospective study done between april 2017 to march 2019. a total of 2134 patients were enrolled for this study with a collection of data in a formatted proforma. all the patients of trauma with clinical or radiological evidence of head injury coming to the trauma centre were included. results. in our study patient, mortality was 6.79% in patients receiving pre-hospital care compared to 12.03% in patients not receiving adequate pre-hospital care. 29.42% were in the age group of 21–30 years. rta (overall 64.45%) was the most common mode of injury in the age group 21–30 years with 81.36% cases. mortality in first emergency care provider by ambulance paramedics was 5.69% and member of the public was 10.10%. conclusion. it was observed that mortality was higher in patients not receiving adequate pre-hospital care. early resuscitation facilities at the site of the accident have to be introduced and improved with the execution of rapid transportation to trauma care centres. . introduction traumatic brain injury (tbi) is a major burden on the health care system in developing countries like india. it is one of the leading causes of mortality and disability worldwide as a consequence results in a great financial burden on societies. research in the area of neurological trauma has shown that the totality of damage to the brain following trauma does not occur at the moment of injury but develops over a period ranging from hours to days. brain injury occurs with further insult from secondary causes like hypotension, hypoxia, cerebral keywords pre-hospital care, hypoxia, hypotension, ambulance, intubation, traumatic brain injury corresponding author: surjeet singh department of neurosurgery, sawai man singh medical college, jaipur, india sujitgmc35@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 519 pre-hospital care: demography, current profile and future trends edema, raised intracranial pressure, and expansion of the mass lesion. the incidence of tbi has increased significantly in the last 30 years but the mortality has decreased as a result of better management and availability of health care services.1,2 in developing countries there is a large number of lives lost due to lack of pre-hospital care whereas in developed countries life expectancy has increased 3 due to advancements in pre-hospital and better understanding of pathophysiological processes in tbi. to achieve better outcomes an early critical intervention in delaying or preventing secondary brain insults and maintaining cerebral perfusion is of paramount importance. this can be done with simple measures done just after trauma following atls guidelines with the prevention of hypotension and hypoxia. evidence-based guidelines have been developed for the management of traumatic brain injury and implemented over the past decade, particularly within the intensive care unit (icu) environment. however, the uncertainty of the efficacy of pre-hospital advanced life support interventions remains as such. in pre-hospital care, the standard management procedure for severe traumatic brain injury varies from case to case due to divergent scene conditions and characteristics. multiple factors such as mechanism of injury, severity, and pattern, location of the accident, mode of transport, the time interval between trauma and first care and experience and skill level of paramedic contribute to this varied response.4 as a consequence of this uncertainty in the efficacy, further investigations and researches are the need of the hour. while pre-hospital management of severe tbi has become progressively more advanced, many challenges are remaining especially in the early recognition and treatment of severe brain trauma by ambulance paramedics. the expeditious transport of patients with brain injuries to an appropriate facility and the prevention of secondary insult is of increasing importance in the reduction of mortality and morbidity in brain trauma patients.5 it is crucial that the first health care provider must be familiar with the complex presentation of severe traumatic brain injury patients in the initial stages of injury. early recognition and response to traumatic brain injury can significantly impact on neurological outcome. paramedics must have a sound knowledge of the interventions which may minimize secondary insult with the pre-hospital treatment of hypoxemia and hypotension being crucial components of traumatic brain injury management. this study can be used to formulate new guidelines and plans to tackle the delay in first care to patients with tbi. methodology the study was conducted at a level 1 trauma center of sms medical college, jaipur, india between april 2017 to march 2019. overall, 2134 patients were enrolled for this study with a collection of data in a formatted proforma from admission to discharge. the data was collected from patients and their relatives. the ethical committee clearance was obtained prior to the commencement of the study. all the patients of trauma with clinical or radiological evidence of head injury or associated other injury coming to the trauma center were included. it was a prospective observational study. data of individual patients were collected in the form of age, sex, mode of injury, mode of transportation, distance from the hospital, care providers, safety equipment used by the vehicle, duration in reaching the hospital, pre-hospital care, glasgow coma scale (gcs), saturation of peripheral oxygen (spo2), systolic blood pressure (sbp) at admission and glasgow outcome score (gos) at time of discharge. based on gcs, tbi cases were graded as mild (13-15), moderate (9-12), and severe (<8). this neurosurgical center is one of the leading institutes of india and asia catering to both urban and rural populations. after researching various literature published, we could conclude that this study is one of the largest in the world and is unique with maximum variations in population. results during the period from april 2017 to march 2019 data from 2134 tbi patients was collected. the mean age was 31.65+ 15.1 years. in our study 69.89% were males and 31.11% were females (table 1). males were 2.21 times more common than females. most patients affected were in the age group of 21–30 years (29.42%) followed by 31–40 years (22.68%). road traffic injury (64.45%) was seen as the most common mode of injury in the age group 21–30 years (81.36%) followed by injury due to fall (21.41%) which mostly affected the age group of 0–10 years 520 sateesh chandra verma, abhijeet singh sachan, surjeet singh, prakrati sachan (71.44%) and above 60 years (33.80.%) (table 2). most of the patients were attended by the members of public as a first responder (77.41%) (table 3) and transported to definitive treatment centers in ambulances (66.82%) (table 4) but most of them not received care in the form of vitals monitoring, intravenous (iv) fluid administration and airway protection at the site of trauma and during transportation. safety devices such as helmets, seat belts, and child restraint were used in 27.03% patients only (table 5). alcohol consumption while driving is 14.53% (table 6). time duration to reach definitive treatment centers was <1 hour in 3.13% of patients, between 1 and 4 hours in 16.16% of patients, between 4 and 12 hours in 56.04% and >12 h in 24.65% of patients (table 7). 32.29%, patients were primary referrals, and 67.71%, patients were secondarily referred to our study center (table 8). the overall mild injury was seen in 49.11% cases, moderate in 31.02%, and severe in 19.87% (table 9). table 1. different age groups and outcome age in years the total no. of cases n (%) out come alive death n=1901(%) n=233 (%) age yrs.(mean) 31.65+ 15.1 33.24 + 14.5 41.36 + 17.8 0-10 191(8.95) 183 (8.58) 8(4.18) 11-20 233(10.91) 221 (10.36) 12(5.15) 21-30 628(29.42) 554 (25.96) 74(11.78) 31-40 484(22.68) 428 (20.06) 56(11.57) 41-50 232(10.87) 192 (8.99) 40(17.24) 51-60 153(7.17) 139 (6.51) 14(9.15) >60 213(9.98) 184 (8.62) 29(13.61) total male female 1470(68.89) 664(31.11) 1311(89.19) 590(88.85) 159(10.81) 74(11.14) table 2. incidence of mode of injury in different age groups age (years) total cases n(%) n=2134 mode of injury rta fall assault sports others n(%) n(%) n(%) n(%) n(%) 0-10 191 (8.95) 41 (21.47) 130 (68.06) nil 12 (6.28) 8 (4.19) 11-20 233 (10.92) 128 (54.93) 54 (23.17) 15 (6.43) 24 (10.3) 12 (5.15) 21-30 628 (29.43) 511 (81.36) 43 (6.85) 29 (4.61) 5 (0.79) 40 (6.36) 31-40 484 (22.68) 357 (73.76) 69 (14.26) 34 (7.02) nil 24 (4.96) 41-50 232 (10.87) 144 (62.06) 54 (23.27) 26 (11.20) nil 8(3.44) 51-60 153 71 35 45 nil 2(1.31) (7.17) (46.41) (22.87) (29.41) >60 213 (9.98) 124 (58.21) 72 (33.80) 13 (6.10) nil 4 (1.88) total 2134 (100) 1376 (64.48) 457 (21.41) 162 (7.59) 41 (1.92 98 (4.60) table 3. first emergency care provider care providers no of patient n ( %) outcome alive death n (%) n (%) member of public 1652 (77.41) 1485 (89.89) 90 (80.35) ambulance officer or paramedic 123 (5.76) 116 (94.30) 7(5.69) relatives 247 (11.57) 210 (85.02) 37 (14.98) medical retrieval team nil nil nil unknown 112 (5.24) 90 (80.35) 22 (19.64) table 4. mode of transportation mode first hospital total no of cases n=1445(%) study center total no of cases n(%) outcome alive death n(%) n(%) ambulance 432 (29.90) 1426 (66.82) 398 (92.13) 34 (7.8) private vehicle 1013 (70.10) 708 (33.18) 1503 (88.30) 199 (11.69) table 5. safety equipment used equipment no of patient n(%) outcome alive death n(%) n(%) helmet urban rural 204(20.90) 139(68.13) 65(31.87) 189(92.64) 131(94.24%) 58(89.23%) 15(7.35) 8(5.76%) 7(10.77%) seatbelt 168(78.50) 157(93.45) 11(6.54) child restraint nil nil nil unknown 495(23.20) 447(9.03) 48(96.97) table 6. substance abuse no of patient n(%) outcome alive death n(%) n(%) alcohol involvement 310(14.53) 243(78.39) 67(21.61) alcohol breath on admission 213(10.00) 184(86.38) 29(13.62) 521 pre-hospital care: demography, current profile and future trends drug involvement 10(0.47) 8(80.00) 2(20.00) using mobile phone at time of accident 43(2.00) 35(81.40) 8(18.60) prior head injury 43(2.00) 33 (76.74) 10(23.25) multiple addiction 46(2.16) 33(71.74) 13(28.26) none 1469(68.84)) 1365(92.92) 104(7.08) table 7. time to arrival at hospital time to arrival at hospital – first hospital n (%) study center n (%) outcome alive, n(%) death, n(%) <1 hrs 1364(63.92) 67 (3.13) 59 (88.05) 8 (11.94) 1-4 hrs 585 (27.41) 345 (16.16) 328 (95.07) 17 (4.92) 4-12 hrs 123 (5.76) 1196(56.04) 1040 (86.96) 156 (15.00) >12 hrs 62 (2.91) 526 (24.65) 474 (90.11) 52 (09.89) table 8. correlation of sbp and spo2 and outcome systolic blood pressure no of patient (%) outcome alive, n(%) death, n(%) >90 mmhg 1885(88.33)) 1745(92.57) 140(7.43) <90 mmhg 249(11.69) 156(8.20) 93(37.35) spo2 <90% 339(15.89) 216(63.72) 123(36.28) >90% 1785(84.11) 1675(93.84) 110(6.16) first ct primary hospital 456(21.36) 425(93.20) 31(6.79) study center 1678(78.63) 1476(87.96) 202(12.03) referral primary 689(32.29) 632(91.73) 57(8.27) secondary 1445(67.71) 1269(87.82) 76(12.18) table 9. severity of injury gcs on admission total no of cases, n (%) outcome alive, n (%) deaths, n (%) mild (13-15) 1048 (49.11) 1036(98.85) 12 (1.1) moderate (912) 662(31.02) 608(91.84) 54 (8.15) severe (<8) 424 (19.87) 257(60.61) 167(39.38) discussion with rapid industrialization, the cases of tbi are rising, and so does its severity. but the advancement in pre-hospital care is lacking in developing countries. different studies have shown that early resuscitation and pre-hospital care are cardinal to better outcomes in tbi. mortality and morbidity of the severely injured patient can be reduced significantly by directly transporting them from the scene to level i trauma centers. early identification and prompt management lead to a better survival rate in cases of tbi. this can be achieved through pre-hospital care which was non-existent in india.6-8 in our study, the incidence of head injury was highest in the age group 21-30 years i.e. 29.42% and commonest mode of injury were as rta in 64.45% cases followed by fall from height in 21.41%. similar studies conducted by meena et al.9 and phonprasert et al.10 showed 69.52% and 58% of cases were due to rta respectively. gururaj et al.11 in his study claimed 60% of cases were due to rta and 20-25% cases were of falls. thus, rta was found to be the most common mode in almost all studies. 9-11 it was most probably due to excessive congestion of traffic on roads, less traffic sense, poor conditions of the road, not using helmet by bike riders, and not following the road traffic rules. alcohol consumption while driving is also a contributing factor for increasing rtas in young adults. in studies by esser et al.12 and gururaj13 the percentage of alcohol consumption was 17.9% and 14.50% respectively which is comparable to our study which is 14.53%. the patient using a helmet more often sustain milder head injuries, whereas, a patient without a helmet was having more severe injuries. alcohol consumption was associated with more severe head injuries and high mortality of 21.61% compared to 7.08% in patients not using any drug and alcohol. in our study private vehicle was the most common mode of transport at the first hospital while the ambulance was the most common mode at the study center. there was clearly a decrease in mortality of patients transported by ambulance (7.80%) than by private vehicle (11.69%), the difference was due to early identification and less time taken to reach the hospital and early treatment resulting in decreased secondary insults. prevention of hypoxia and hypotension is of utmost importance with the maintenance of cerebral perfusion. the presence of leads to multiple cascades of events leading to increased cerebral edema decreased cerebral perfusion, decreased 522 sateesh chandra verma, abhijeet singh sachan, surjeet singh, prakrati sachan tissue, and vital organ perfusion. these all contribute to poor outcomes. in our study patients with sbp, less than 90 mmhg on admission had a mortality of 37.35% than patients with sbp, more than 90 mmhg 7.43 % mortality. the mortality in patients with spo2 less than 90% was 36.28% compared to 6.16% in patients with spo2 above 90%. our study suggested that most of the primary or first hospitals overlooked the importance of monitoring oxygen saturation and blood pressure with increased chances of missing hypoxia, hypotension, thereby undervaluation of important secondary changes in the brain ultimately increasing the risk of worse outcomes. in the primary hospital ct scan had done in 21.36% and mortality 6.79% and study center 78.63% and mortality 12.03 %. patients with their ct brain done at the first hospital within 4 hours after injury performed better. early ct brain is a critical step in managing tbi cases with early information about operative intervention required, thus preventing further insult to the brain. thus it is very critical for the emergency staff to be well versed with an indication of ct brain in trauma patients. for providing good pre-hospital care there are needs for intensive training of medical personnel and adequate resources at primary and secondary level health care facilities. time lapsed in reaching the hospital is also a significant factor determining the outcome. there is a major part of critical time lost in transportation. the prognosis of tbi is excellent if the patients get appropriate treatment in the golden hour. our study noted that around 3.13%, 16.16%, 56.04%, and 24.65% of patients reached the hospital in less than 1 hour, 1-4 hour, 4-12 hour, and more than 12 hours respectively. in a comparative study by gururaj,13 only 25% reached hospital within 3 hours and 20% reached after 24 hours. the time interval between the time to arrive at the injury site and the hospital is one of the deciding factors between life and death. the overall mortality was found to be 10.92% as compared to 16% by both phonprasert et al.10 and narwade et al.14 the maximum severity of the injury was shifted to the hospital by private vehicle, without any vital monitoring. it was observed that mild, moderate, and severe tbi cases were 49.11%, 31.02%, and 19.87% respectively. a study by natarajan et al.15 showed the total number of mild, moderate, and severe injuries were 42%, 30%, and 28%, respectively. in our study, it was observed that mortality was highest in severe tbi (39.38%) and 1.1% in mild tbi. in our study patient, mortality was 6.79% in patients receiving pre-hospital care compared to patients 12.03% in patients not receiving adequate pre-hospital care. this clearly signifies that prehospital care is a crucial step in managing tbi patients. chennai had 8.16% mortality, bangalore had 8.6% and 5.5% mortality rate in 2002 and 2005 respectively whereas the mortality rate in delhi was 10.49%. in recent years the mortality has decreased due to the availability of better health care facilities. with intensive studies and data registry in the usa and other western countries, they have formed better pre-hospital guidelines for trauma patients thus are able to avoid preventable deaths and disability. our study showed that patient with tbi need aggressive management in the form of, victims reaching the hospital in the shortest possible time, taking care of airway by use of laryngeal mask/endotracheal tube intubation, oxygenation and iv infusion for maintaining perfusion pressure for prevention of secondary brain injuries like hypoxia, hypotension, and cerebral edema. we can apply this data to develop new action plans and public awareness programs and developing adequate neurotrauma care protocols for aggressive management of patients with poor admission gcs score. conclusion it is recommended that essentially, the outcome in tbis can be improved by attending to priorities of reaching the victims in the shortest possible time, and evacuating them to hospital, taking care of airway, oxygenation and maintaining total perfusion pressure through judicious iv infusions. depending upon the skills of emergency medical technician / paramedic, the use of laryngeal mask airway / endotracheal tube can be considered. infrastructure in the form of dedicated trauma centers, wellequipped ambulances with trained trauma staff, should be developed. abbreviation tbitraumatic brain injury, icuintensive care unit, gos glasgow outcome score, gcsglasgow coma scale, sbpsystolic blood pressure, spo2 saturation of peripheral oxygen. 523 pre-hospital care: demography, current profile and future trends financial support and sponsorship nil conflicts of interest there are no conflicts of interest. references 1. who. world report on the road traffic injury prevention. geneva: world health organization; 2004. 2. maas ai, stocchetti n, bullock r. moderate and severe traumatic brain injury in adults. lancet neurol. 2008;7:728–41. 3. stocchetti n, paternt r, citerio g, beretta l, colombo a. traumatic brain injury in an aging population. j neurotrauma. 2012;29:1119–25. 4. boulger, c. t., & werman, h. a. (2010). controversies in emergency medical services. emergency medicine reports, 31(7), 77-87. 5. badjatia, n., carney, n., crocco, t. j., fallat, m. e., hennes, h. m. a., jagoda, a. s., wright, d. w. (2007). guidelines for the prehospital management of traumatic brain injury. prehospital emergency care, 12(1), s1-s52. 6. sampalis js, denis r, fré chette p, brown r, fleiszer d, mulder d. direct transport to tertiary trauma centers versus transfer from lower level facilities: impact on mortality and morbidity among patients with major trauma j trauma 1997; 43:288-95. 7. dash hh. pre-hospital care of head injured patients. neurol india 2008; 56:415-9. 8. saxena mk, sahoo s, vibha p, rahman a. pre-hospital determinants of outcome in traumatic brain injury: experiences from first comprehensive integrated prehospital care providers in india: gvk – emri experience.indian j neurotrauma. 2010;7:129–34. 9. meena us, gupta a, sinha vd. prehospital care in traumatic brain injury: factors affecting patient's outcome. asian j neurosurg. 2018;13(3):636–639. 10. phonprasert c, suwanwela c, hongsaprabhas c, prichayudh p, o’charoen s. extradural haematoma: analysis of 138 cases. j trauma. 1980;2:679-83. 11. gururaj g. road traffic deaths, injuries and disabilities in india: current scenario. natl med j india. 2008;21:14– 20. 12. esser mb, et al. characteristics associated with alcohol consumption among emergency department patients presenting with road traffic injuries in hyderabad, india. injury (2015). 13. gururaj g. epidemiology of traumatic brain injuries: indian scenario. neurol res. 2002;24:24-8. 14. narwade n, narwade p, ghosalkar m, shaikh tp, sharma y, khan n, ansari s. clinical profile and management of head injury at tertiary health care center in rural area, india. int j res med sci 2015;3:313740. 15. natarajan m. adjustmental problems of head injured patients, indian council of medical research, 1987. doi: 10.33962/roneuro-2020-084 dolichoectatic middle cerebral artery masquerading as cerebral cavernous malformation. a case report and review of literature zahraa f. al-sharshahi, saja a. albanaa, ahmed m. jawad, noor k. al-waely, noor a. hummadi, samer s. hoz romanian neurosurgery (2020) xxxiv (4): pp. 498-503 doi: 10.33962/roneuro-2020-084 www.journals.lapub.co.uk/index.php/roneurosurgery dolichoectatic middle cerebral artery masquerading as cerebral cavernous malformation. a case report and review of literature zahraa f. al-sharshahi1, saja a. albanaa2, ahmed m. jawad3, noor k. al-waely4, noor a. hummadi5, samer s. hoz1 1 department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 medical student, college of medicine, baghdad university, baghdad, iraq 3 medical student, royal college of surgeons in ireland, dublin, ireland 4 fibms-diagnostic radiology. al-nahrain university. college of medicine, department of surgery, iraq 5 c.a.b.h.s-diagnostic radiology. al-imamain al-kadhmain medical city, iraq abstract background. intracranial dolichoectasia (iade) is a rare vascular disease characterized by distension, elongation and tortuosity of an artery. iade rarely involves paediatric aged groups. it is either asymptomatic or manifests as ischemic or haemorrhagic attacks. case description. a healthy, 30-year-old, female teacher presented with recurrent attacks of bi-frontal headaches associated with dizziness and dropping attacks of twoweek duration. she was referred by her general physician to our institution of neurosurgery teaching hospital in baghdad, iraq with a suspicion of medial temporal lesion on a cranial computed tomography (ct) scan. magnetic resonance imaging study excluded the diagnosis suggesting a dolichoectatic middle cerebral artery that was confirmed by ct-angiography. conclusion. dolichoectasia of the middle cerebral artery is a rare and benign lesion. however, it can masquerade as cerebral cavernous malformation or intracranial arterial aneurysm. thus, careful radiological evaluation with the suggested diagnostic criteria are of paramount importance to prevent its misdiagnosis. background intracranial arterial dolichoectasia (iade) is sporadic angiopathy characterized by dilatation, elongation and tortuosity of an intracranial artery. iade is approximately 0.1-6.5% prevalent in the general populakeywords dolichoectasia, middle cerebral artery, anterior circulation, arteriopathy, tortuous artery corresponding author: saja a. albanaa college of medicine, baghdad university, baghdad, iraq sajaalbanaa@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 499 dolichoectatic middle cerebral artery masquerading as cerebral cavernous malformation tion and 12 % in stroke patients [1]. iade preferentially involves the basilar artery and posterior circulation; anterior circulation iade constitutes only one third of all cases [2]. iade is usually an incidental finding but symptoms may arise due to ischemia, hemorrhage or cranial nerve compression [3]. although uncommon, hydrocephalus was also reported as a manifestation of iade due to the obstruction of cerebrospinal fluid flow through the foramen of monro or the cerebral aqueduct [4]. iade may co-exist with several vascular pathologies such as abdominal aortic aneurysms, intracranial aneurysms and coronary artery disease [5]. a diagnostic criterion for dolichoectatic basilar artery was suggested by smoker et al, but no criteria for dolichoectasia in other intracranial arteries have been validated thus far [6]. herein, we present a case of middle cerebral artery dolichoectasia, initially diagnosed as cerebral cavernous malformation along with proposed diagnostic criteria based on reviewing the available literature. case scenario a healthy, 30-year-old, female teacher presented with recurrent attacks of pulsatile bifrontal headache of two-week duration. each attack lasts for more than one-hour and significantly impacted her daily activities. the headache is associated with profound dizziness and “dropping attacks”; assumed to be seizures by her general physician. the patient’s eeg and video eeg were both normal. she was referred to the neurosurgery outpatient clinic at our institution with a suspicious medial temporal lesion on a cranial ct scan. on examination, the patient was pale but fully oriented with no remarkable neurologic deficits. her brain ct scan showed a small rounded heterogeneous lesion with calcification at the medial temporal area; there was no evidence of peri-lesional edema. initially, the diagnosis of uncal cavernous malformation was pondered. (fig.1). in order to confirm this diagnosis, brain mri with t2gradient echo and mra studies were ordered. the t2-weighted mri study revealed lesional flow-void, the t2-gradient echo was negative and the mra showed an abnormal vascular loop of the mca within the lesion. these findings excluded the diagnosis of cavernous malformation and strongly suggested mca aneurysm or dolichoectasia (fig.2). next, a computed tomography angiography (cta) of the brain was obtained. the cta revealed that the proximal part of the mca was dilated, elongated, tortuous and formed a superior blind loop; findings that were consistent with the diagnosis of mca dolichoectasia (fig.3). moreover, catheter cerebral angiography can be used to confirm the diagnosis in such situation but it is not feasible in our facility nor in many neurosurgical institutions around the world. thereafter, patient was reassured that she had a “benign variation in the brain circulation rather than a critical pathology and that no intervention was indicated at the time”. laboratory investigations normal except for iron deficiency anemia. the patient was discharged and a follow-up was scheduled with her physician. at 6-month follow-up, patient was generally well, had already resumed her normal daily activities and received treatment for anemia. the headache was both minimal and occasional at this stage. both cta and mri revealed no new significant findings. figure 1. cranial ct scan showing a heterogeneous, deep left-sided, temporal lesion of mixed density with no perilesional edema. here, the initial diagnosis was cerebral cavernous malformation. 500 zahraa f. al-sharshahi, saja a. albanaa, ahmed m. jawad et al. a. b. c. d. figure 2. brain mri showed deep left temporal lesion. a: flair axial section: the lesion is hypointense with no perilesional edema. b: t2 axial section: the lesion contains signal voids that denoted the presence of vessels within the lesion. c: t2gradiant echo axial view showing the absence of blood clots. d: mra showing an enlarged and tortuous left mca (sphenoidal segment) as compared with the right mca with a superiorly projecting loop or a possible aneurysm. figure 3. brain ct angiography 3d reconstructed image showing an enlarged and tortuous left mca (sphenoidal segment) as compared with the right mca with a superiorly projecting loop, confirming the diagnosis of left mca dolichoectasia and excluding the presence of an aneurysm. discussion the vertebrobasilar system is the most common site of iade followed by internal carotid artery. iade is a disease of all ages although its presentation in the pediatric age group is rare. it affects females more than males [2]. iaed may be asymptomatic or masked by an array of inconclusive manifestations such as headaches, strokes, seizures and focal deficits [4]. in this report, a 30-year-old female presented with recurrent bouts of headache and dizziness. a brain ct-scan revealed a calcified lesion, leading to a provisional diagnosis of an uncal cavernous malformation. further imaging studies including mra and t2-gradient echoprovided a better visualization of the vasculature and the brain parenchyma narrowing the differential diagnosis to an aneurysm or a dolichoectasia. finally, cta images showed dilated, distended and tortuous vessels and excluded the differential of an aneurysm. iade is commonly mistaken with other vascular pathologies, such as dural fistulas or arteriovenous malformations [7]. therefore, multiple imaging modalities are often required to reach the definitive diagnosis of dolichoectasia especially if it is located distally in the anterior circulation. nakahara et al 501 dolichoectatic middle cerebral artery masquerading as cerebral cavernous malformation reported a case of mca dolichoectasia, initially diagnosed as a terminal-ica, saccular aneurysm using antero-posterior and lateral cta views. however, the reverse waters view suggested the correct diagnosis of a dolichoectatic mca rather than an ica aneurysm; this study highlights the importance of multiple cta views in the diagnosis of iade [8]. several efforts attempted to establish a solid platform for diagnosing anterior circulation dolichoectasia depending on a multi-modal diagnostic approach. some authors have recommended the co-utilization of additional radiological techniques such as digital subtraction angiography to capture the real-time flow properties of the aberrant vessel [9,10]. dolichoectatic mca is a benign lesion in general. however, treatment is usually indicated when there is a co-existing pathology. surgical manipulation of the enlarged vessel may lead to complications such as hemorrhage or ischemia [10]. in this study, we treated the patient conservatively using simple analgesics which enabled her to resume her normal activities. our approach is comparable to the one described in the literature of mca dolichoectasia (table 1). however, the initial false interpretation of medial temporal cavernous malformation, then mca aneurysm rendered this case report to be of a critical value regarding differential diagnosis of mca dolichoectasia [8,10]. based on the aforementioned literature analysis, we suggest 3 features that can be considered as alarming criteria for the diagnosis of mca dolichoectasia, these include: atypical clinical presentation, enlarged parent vessel and unusual location of the lesion. we recommend a multi-modal diagnostic approach to determine the most appropriate management along with long-term clinical and radiological follow-up for monitoring of a less likely but possible lesion enlargement. table1: literature review of dolichoectatic middle cerebral artery author sex age, year presentation radiologic findings treatments brinjikji et al [11] f 19 asymptomatic, found incidentally mca dolichoectasia with superimposed multilobulated aneurysm, mild preceding stenosis conservative feliciano et al [12] m 42 headache associated with left-sided weakness and intermittent nausea and vomiting mca dolichoectasia and a cluster of aneurysms with right basal ganglia hemorrhage conservative abe et al [13] m 32 asymptomatic, found incidentally after a motor-vehicle accident mca dolichoectasia — nakahara et al [8] f 59 left hyposmia and mild intermittent occipitalgia mca dolichoectasia no surgery, no medication kanemoto et al [14] f 41 seizures and anxiety mca dolichoectasia with cavernous hemangioma cavernous hemangioma resection 502 zahraa f. al-sharshahi, saja a. albanaa, ahmed m. jawad et al. tokunaga et al [15] f 58 right hemiplegia, homonymous hemianopia, hypertension left putamen hematoma and bilateral mca dolichoectasia — puca et al [16] f 32 ischemic stroke at the age of 7 y old ischemic lesion and mca dolichoectasia no surgery, no medication maruya et al [17] f 40 subarachnoid hemorrhage a saccular aneurysm on a dolichoectatic mca surgical clipping of the aneurysm guo et al [10] m 43 ischemic stroke 3 y ago mca dolichoectasia no surgery, antiaggregating therapy current study f 30 headache and dizziness mca dolichoectasia conservative m = male; f = female; mca = middle cerebral artery conclusion mca dolichoectasia is a rare and benign lesion. however, it can masquerade as cerebral cavernous malformation or intracranial aneurysm. thus, careful radiological evaluation along with the suggested diagnostic criteria are of a paramount importance to prevent its misdiagnosis. abbreviations iade; intracranial arterial dolichoectasia, eeg; electroencephalogram, ct; computed tomography, mri; magnetic resonance imaging, cta; computed tomography angiography, mca; middle cerebral artery. declarations acknowledgements: none. authors’ contributions: sa wrote the primary manuscript. za, sh participated in its coordination, supervision, and revision of the manuscript. sh conceived of the study and collected the data. za, aj helped to draft the manuscript. sh, na, nh diagnosed the case. all authors read and approved the final manuscript. funding: none. availability of data and materials: not applicable. ethics approval and consent to participate: not applicable. consent for publication: not applicable. competing interests: the authors declare that they have no competing interests. references 1. jia zy, zhao lb, lee dh. localized marked elongation of the distal internal carotid artery with or without phace syndrome: segmental dolichoectasia of the distal internal carotid artery. american journal of neuroradiology. 2018 may 1;39(5):817-23. 2. baran, b., kornafel, o., guziński, m., & sąsiadek, m. dolichoectasia of the circle of willis arteries and fusiform aneurysm of basilar artery–case report and review of the literature. polish journal of radiology. 2012;77(2):54-59. 3. yuan y, xu k, luo q, yu j. research progress on vertebrobasilar dolichoectasia. international journal of medical sciences. 2014;11(10):1039-1048. 4. kansal r, mahore a, dange n, kukreja s. dolichoectasia of vertebrobasilar arteries as a cause of hydrocephalus. journal of neurosciences in rural practice. 2011 jan;2(01):062-4. 5. del brutto vj, ortiz jg, biller j. intracranial arterial dolichoectasia. frontiers in neurology. 2017 jul 17; 8:344. 6. smoker wr, corbett jj, gentry lr, keyes wd, price mj, mckusker s. high-resolution computed tomography of the basilar artery: 2. vertebrobasilar dolichoectasia: clinical-pathologic correlation and review. american journal of neuroradiology. 1986 jan 1;7(1):61-72. 503 dolichoectatic middle cerebral artery masquerading as cerebral cavernous malformation 7. smith k, bardenheier j. aneurysm of the pericallosal artery caused by closed cranial trauma. journal of neurosurgery. 1968;29(5):551-554. 8. nakahara i, taki w, tanaka m, matsumoto k, kikuchi h. dolichoectasia of the middle cerebral artery. neurologia medico-chirurgica. 1995;35(11):822-824. 9. sharawat ik, kumar a, goswami jn, sankhyan n. dolichoectasia of the anterior cerebral arteries: a rare cause of headache in a young child. child's nervous system. 2018 mar 1;34(3):389-91. 10. guo l, zhang x, ge j, qiu y. middle cerebral artery dolichoectasia with radiologic follow-up. journal of craniofacial surgery. 2014 may 1;25(3): e269-71. 11. brinjikji w, nasr dm, flemming kd, rouchaud a, cloft hj, lanzino g, kallmes df. clinical and imaging characteristics of diffuse intracranial dolichoectasia. american journal of neuroradiology. 2017 may 1;38(5):915-22. 12. feliciano ce, pamias-portalatin e, mendoza-torres j, effio e, moran y, rodriguez-mercado r. color-coded digital subtraction angiography in the management of a rare case of middle cerebral artery pure arterial malformation: a technical and case report. interventional neuroradiology. 2014 nov;20(6):715-21. 13. abe t, singer rj, marks mp, kojima k, watanabe m, uchida m, hayabuchi n. arterial vascular abnormality accompanying cerebral cortical dysplasia. american journal of neuroradiology. 1997 jan 1;18(1):144-6. 14. kanemoto y, hisanaga m, bessho h. association of a dolichoectatic middle cerebral artery and an intracranial cavernous hemangioma—case report—. neurologia medico-chirurgica. 1998;38(1):40-2. 15. tokunaga t, yamamoto t. hemorrhage with dolichoectatic middle cerebral arteries. neurology. 2003 jul 22;61(2):e4. 16. puca a, marchese e, esposito g, calcagni ml, di lazzaro v. middle cerebral artery dolichoectasia in a young woman with a previous stroke. european journal of neurology. 2007 jan;14(1):109-11. 17. maruya j, nishimaki k, minakawa t. hyperperfusion syndrome after neck clipping of a ruptured aneurysm on a dolichoectatic middle cerebral artery. journal of stroke and cerebrovascular diseases. 2011 may 1;20(3):260-3. doi: 10.33962/roneuro-2022-076 pica ischemic stroke. the importance of urgent neurosurgical treatment razvan adrian covache-busuioc, horia petre costin, vicentiu mircea saceleanu romanian neurosurgery (2022) xxxvi (4): pp. 418-422 doi: 10.33962/roneuro-2022-076 www.journals.lapub.co.uk/index.php/roneurosurgery pica ischemic stroke. the importance of urgent neurosurgical treatment razvan adrian covache-busuioc3, horia petre costin3, vicentiu mircea saceleanu1,2 1 neurosurgery department, sibiu county emergency hospital, sibiu, romania 2 neurosurgery. “lucian blaga” university of medicine, sibiu, romania 3 general medicine, “carol davila” university of medicine and pharmacy, bucharest, romania abstract the posterior inferior cerebellar artery (pica) has a unique anatomical complexity, which is of great clinical importance and is involved in many pathologies, such as aneurysm, ischemic stroke, neurovascular compression syndrome (nvcs), arteriovenous malformation (avm) and brain tumour (1). pica has a sinuous and variable trajectory, divided into 5 segments. pica infarction usually manifests lateral bulbar syndrome and is more likely to cause mass effects. pica frequently compresses the bulb and cranial nerves, resulting in various neurovascular compression syndromes (nvcs) (2). the ischemic stroke caused by thromboembolism in the pica segment is accounted for more than 2% of all cases of ischemic stroke (3). moreover, it tends to be underdiagnosed due to the symptomatology, represented usually by vertigo which mimics a possible peripheral vestibulopathy (4). . case report the patient aged 50 years old, known with venous thrombosis of the transverse and sigmoid sinuses, proximal internal jugular vein on the right, hta, thrombophilia, mild mitral insufficiency, without chronic treatment at home, presents herself in upu sibiu for balance disorder and postural instability with a sudden on-set, on 01.11.2022, around 22:00. the symptomatology debuted due to the sudden voluntary stop of the anticoagulation medication by the patient, against the recommendation of the attending physician. the patient had another 2 similar episodes 2 days ago and 7 days ago, respectively, spontaneously remitted. it was decided to hospitalize the patient in the neurology department for further investigations and specialized treatment. keywords pica, urgent neurosurgical treatment, ischemic stroke corresponding author: vicentiu mircea saceleanu assoc. prof. m.d, phd. "lucian blaga" university of sibiu, faculty of medicine, romania vicentiu.saceleanu@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 419 pica ischemic stroke the patient presents altered general condition, norm ponderal, conscious, uncharacteristic facies, warm skin and mucous membranes, normally coloured and hydrated, normally represented adipose connective tissue, normal superficial ganglion system, osto-articular system mobile integrity; normal conformed thorax, vesicular murmur present bilaterally, spo2 = 98% spontaneous; heart noise rate, arterial pressure = 150/90mmhg, cardiac frequency = 73bpm; spontaneous and on palpation painless abdomen; liver and spleen nonpalpable; egfr= 88,66 ml/min/1,73 m2, giordano sign negative bilateral, cooperative, temporo-spatial oriented. neurological examination at admission upon admission, the neurological examination reveals the following: • no signs of meningeal irritation, no involuntary movements • orthostatism and difficulty walking • cranial nerves: preserved ocular motricity, without nystagmus, without amputations of visual field • negative paresis samples • no coordination disorder in bilateral i-n and c-g tests • osteotendinous reflexes symmetrical triggered • negative babinski sign • no sensibility disorder • normal control of sphincters • fluent language • conscious, cooperative, temporo-spatial oriented • guss scale = 5/5 points • rankin score before = 0 points • rankin score after = 1 point • nihss score = 0 points pre-operative status on 01.11.2022, a native emergency head ct scan was performed. hypodense areas with the appearance of patchy ischemic strokes can be detected at the left cerebellar and right parasagittal cerebellar level. on 02.11.2022, a head mri is performed, which reveals an acute ischemic vascular lesion located in the inferior cerebellar (vermian and bihemispherical predominantly on the left side) in the left pica vascularization territory, established in flair. left retrobulbar swan hyposignal image, along the path of the left pica artery, is suggestive for the presence of thrombus at this level. figure 1. native ct head performed on 01.11.2022. figure 2. mri head performed on 02.11.2022. on 03.11.2022, the second native head ct is performed, which shows a hypodense area in the right paramedian, vermian cerebellum and at the level of the lower left cerebellar hemisphere, with the deletion of the differentiation between white and gray matter and the cortical grooves, with mass effect on the brain stem and the iv ventricle. 420 razvan adrian covache-busuioc, horia petre costin, vicentiu mircea saceleanu the patient has an episode of worsening of the symptoms, after which she complains of intense frontal headache and nausea. figure 3. native ct head performed on 03.11.2022. on 04.11.2022, a native head ct scan is performed, in which an extensive cerebellar ischemic stroke can be observed, with infratentorial mass effect, with supratentorial hydrocephalus; the ventricular system is on the median line, asymmetric, enlarged supratentorial. also, during the neurological examination, the patient is conscious, drowsy, answers questions with difficulty, opens her eyes spontaneously and on command with difficulty, spontaneously mobilizes bilateral inferior member, presents divergent strabismus of the right eye, squeezes the examiner's fingers with bilateral superior member on command; urgent neurosurgical consultation is requested. figure 4. native ct head performed on 04.11.2022. the 50-year-old patient is transferred from the neurology ward, in critical condition, comatose, gcs score 4 points and equal pupils and admitted to the neurosurgery department for investigations and specialized treatment. operation stage on 04.11.2022 at 07:25 a.m., neurosurgical intervention takes place under general anaesthesia by performing an occipital craniectomy, to reduce the infratentorial and supratentorial mass effect, caused by the massive cerebral edema due to bilateral ischemic pica stroke, having a history of previous thrombosis of transverse and sigmoid venous sinus and right internal jugular vein. post-operative evolution the evolution on the icu and neurosurgery ward is favourable under painkillers, anti-inflammatory, antibiotic and hemostatic treatment with a clean, exposed surgical wound, without celsian signs, the wound being closed with sutures suture to the skin. the native head ct is re-performed on 05.11.2022 post-operatively, in which an extended infratentorial hypodense area and patchy occipital craniectomy area are observed, with a reduction of the infra and supratentorial compressive effect. figure 5. native ct head performed on 05.11.2022. post-intervention haematological status for massive cerebral edema, due to ischemic stroke. patient had a history of thrombosis of transverse and sigmoid venous sinus and internal jugular vein, hyperhomocysteinemia and lupus anticoagulant for which she took warfarin and later aspenter and plavix, later discontinued. due to the increased risk score for thrombosis, required anticoagulation with clexane 0.6 x230 days + therapy of the neurological and neurosurgical department. after in 30 days, it will be decided whether to switch to sintrom or another anticoagulant. 421 pica ischemic stroke on 11.11.2022, the transfer to the neurology ward was decided, the patient being conscious, cooperative, temporo-spatial oriented, in good general condition, afebrile with neurological symptoms in remission. discussions the conservative medical approach is a factor that leads to an increase in the mortality rate among patients with extensive bilateral ischemic strokes, because these patients have a very high risk of developing massive cerebral edema with mass effect if the neurosurgical treatment is delayed (5). these aspects are important to be taken into consideration since the therapeutic benefit requires early intervention, before the adjacent brain structures are affected by the mass effect (6). the thromboembolism represents a key point when speaking about an ischemic stroke. it is usually seen in atrial cardiopathy, such as atrial fibrillation, which cause is determined by a systemic vascular disease that affects the tissue of the atria (7). the atrial fibrillation represents one of the main factors that can determine an ischemic stroke due to the formation of the thrombus inside the left atrium. due to this situation, it is shown the importance of following the treatment with anticoagulant, without a voluntary sudden stop by the patient (8). the recent studies show that the decompressive craniectomy approach represents that golden standard for space occupying infarctions, but it must be performed up to 48 hours since the first sign of ischemic stroke for the best results (9). moreover, the goal of a very quick, "ultra-early" surgical intervention is to reduce the mortality rate, not the disabilities that are permanent consequences of the strokes (10). conclusions the goal of a very quick, "ultra-early" surgical intervention is to reduce the mortality rate, not the disabilities that are permanent consequences of strokes. decompressive craniectomy remains the only chance of survival for patients who develop malignant edema after an episode of stroke. decompressive craniectomy is not a therapeutic method but a life-saving one when other methods have failed. decompressive surgical treatment reduces mortality, but the family must know that this intervention does not guarantee a quick and spectacular recovery and that the patient will present a certain degree of disability. the procedure should be performed within the first 48 h from the onset of the heart attack or as soon as possible. in patients with suspected tia or stroke, general and neurological examination, followed by diagnostic brain imaging should be performed immediately upon arrival at the hospital so that treatment can be initiated promptly. post-operative recovery also depends on the comorbidities that the patient has before the onset of the stroke references 1. uchino a, saito n, ishihara s. double origin of the posterior inferior cerebellar artery diagnosed by mr angiography: a report of two cases. neuroradiol j. 2015 apr;28(2):187–9. 2. miao h-l, zhang d-y, wang t, jiao x-t, jiao l-q. clinical importance of the posterior inferior cerebellar artery: a review of the literature. int j med sci. 2020;17(18):3005– 19. 3. won d, lee jm, park is, lee ch, lee k, kim j-y, et al. posterior inferior cerebellar artery infarction originating at c1-2 after c1-2 fusion. vol. 15, korean journal of neurotrauma. korea (south); 2019. p. 192–8. 4. kim js, caplan lr. 26 vertebrobasilar disease. in: grotta jc, albers gw, broderick jp, day al, kasner se, lo eh, et al., editors. stroke (seventh edition) [internet]. seventh edition. philadelphia: elsevier; 2022. p. 368-403.e7. available from: https://www.sciencedirect.com/science/article/pii/b9780 323694247000260 5. reinink h, jüttler e, hacke w, hofmeijer j, vicaut e, vahedi k, et al. surgical decompression for space-occupying hemispheric infarction: a systematic review and individual patient meta-analysis of randomized clinical trials. jama neurol. 2021 feb;78(2):208–16. 6. demchuk am, krieger dw. mass effect with cerebral infarction. curr treat options neurol. 1999 jul;1(3):189– 99. 7. schmidt h, heinemann t, elster j, djukic m, harscher s, neubieser k, et al. cognition after malignant media infarction and decompressive hemicraniectomy a retrospective observational study. bmc neurol [internet]. 2011;11(1):77. available from: https://doi.org/10.1186/1471-2377-11-77 8. boehme ak, esenwa c, elkind ms v. stroke risk factors, genetics, and prevention. circ res. 2017 feb;120(3):472– 95. 422 razvan adrian covache-busuioc, horia petre costin, vicentiu mircea saceleanu 9. hossain-ibrahim mk, tarnaris a, wasserberg j. decompressive craniectomy – friend or foe? trauma [internet]. 2012;14(1):16–38. available from: https://doi.org/10.1177/1460408611412685 10. shah db, paudel p, joshi s, karki p, sharma gr. outcome of decompressive craniectomy for traumatic brain injury: an institutional-based analysis from nepal. asian j neurosurg. 2021;16(2):288–93. romanian neurosurgery (2019) xxxiii (3): pp. 299-304 doi: 10.33962/roneuro-2019-050 www.journals.lapub.co.uk/index.php/roneurosurgery quality and reliability of information available on youtube videos pertaining to transforaminal lumbar epidural steroid injections aysel gürcan atci1, ibrahim burak atci2 1 md. specialist. baltalimanı bone and joint research and education hospital, department of physical therapy rehabilitation, turkey 2 md. assoc. prof. istanbul training and research hospital, department of neurosurgery, turkey abstract background. this study analyses the transforaminal lumbar steroid injection videos that have the highest views and likes on youtube, and attempts to reveal the video qualities in order to contribute to the literature. methods. for review, “transforaminal lumbar steroid injection” was written to the standard youtube search bar, and the videos with the highest views were ranked using advanced search preferences. the 50 most widely viewed videos were watched and scored by 2 physicians. results. the mean modified discern score of the videos was 2,66+/-1,032 (the lowest: 1; the highest: 4) while the mean gqs score was 2,876+/-1,06 (the lowest: 1; the highest:4). in addition, the mean discern score and the mean gqs value were 3,51 and 3,82, respectively, for the informational videos that were uploaded by health professionals but did not contain actual surgery. conclusion. we think that medical associations and state authorities in medicine should check the validity and accuracy of the information on the internet and should support the society in access to the most correct information. introduction in daily practice, internet search rates have increased in almost every subject due to developing information technologies that are used more and more every day. in health practices, professionals and patients make internet researches in order to get information and gain experience. among these sources of application, youtube is the biggest video archive website in the world and attracts 95% of internet users with 30 million active users every day (1). there are also many healthrelated videos in the archive. generally, patients apply to a physician and get detailed information about recommended treatments but they are also inclined to watch on youtube the operation to be carried out. keywords youtube, videos, transforaminal lumbar epidural steroid injections, discern, global quality index corresponding author: ibrahim burak atci istanbul training and research hospital, turkey drburakatci@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 300 aysel gürcan atci, ibrahim burak atci therefore; the quality of a video, the persons who shot it and whether such video contains correct information are matters of great importance. lumbar disc herniation is frequently observed among people. recently, fluoroscopy injections have been increasingly applied with success for nerve roots that cause pressure on patients whose pains do not regress with medical treatment and rehabilitation programs and who are not appropriate for operation (11). this study analyses the transforaminal lumbar steroid injection videos that have the highest views and likes on youtube, and attempts to reveal the video qualities in order to contribute to the literature. material and methods search strategy and data collection for review, “transforaminal lumbar steroid injection” was written to the standard youtube search bar, and the videos with the highest views were ranked using advanced search preferences. the 50 most widely viewed videos were watched and scored by 2 physicians. inclusion and exclusion criteria the videos that were not in english language or did not have subtitles or speech or that did not explain the operation were eliminated. variables extracted views, upload dates, like rates, uploaders, video lengths, comment numbers, like numbers and dislike numbers were identified as well as whether they were actual or animated videos. in addition, video power index (vpi) values [(number of likes / number of likes þ number of dislikes) 100] were calculated to evaluate the popularity of the videos. assessment of usefulness all videos were independently evaluated by two physicians for usefulness and categorized into the following mutual exclusive categories. 1. useful information: videos designated as useful information were mainly focused on information delivery. they contained accurate information and were useful for learning how to do transforaminal lumbar steroid injection. 2. misleading information: the videos contained in correctin formation or did not contain useful information about transforaminal lumbar steroid injection. 3. useful patient opinion: the videos in this group have the discern and gqs scores as 3 or above and clearly explain the patient experiences, the performance of operations, and preoperational and post operational pain scores. 4. misleading patient opinion: the videos in this group have the discern and gqs scores as 2 or lower and do not clearly explain patient experiences. scoring system video reliability was scored using a modified fivepoint discern tool (2), which was adapted from the original discern tool for the assessment of written health information by charnock et al. (3). the overall quality of each video was rate during the five-point global qualityscale (gqs). the gqs was developed as an evaluation tool for website resources and it assesses the flow and ease of use of the information presented online, and the quality of video (table 1) [4]. statistical analysis the results were statistically analysed during a nonparametric kruskal–wallis test. a p value of 0.05 or less was considered significant. the statistical package forth esocial. sciencesversion 23 software (spss, chicago, il, usa) was used for all statistical analyses. results 60 videos with the highest views were analyzed while 10 videos were later excluded from the analysis for they were neither in english language nor contained subtitles. among these, 10 videos were animations while 32 consisted of actual images. there were 22 surgery, 10 patient view and 13 technically-narrated animated and actual videos. on the other hand, 6 videos were uploaded by physicians and gave theoretical information about the processes they applied (figure 2). the oldest video was uploaded in 2007 while the newest one was added to the system in 2017. the videos were uploaded by hospitals (27 videos), health professionals and physicians (13 videos), and personal accounts (10 videos) (figure 1). the mean time of the video lengths was 4.22 sec (the shortest: 0,20 sec; the longest: 12,08 sec), and the mean view was 88,293+/-9,75 (the least viewed: 4075; the most viewed: 825.731). the daily mean 301 quality of youtube videos to transforaminal lumbar epidural steroid injections view of the videos was 42,975+/-4,442 (the least viewed: 4,45; the most viewed: 323,8). the mean like rate was 53,6+/-3,52 (the most liked:3000; the least liked: 0), and the mean dislike rate was 28+/-2,21 (the most disliked: 758; the least disliked: 0).as for the comments, the mean number was 42,8 (the least commented: 0; the most commented: 423).similarly, video power index (vpi) analyses showed that the mean vpi value of the 50 videos was 82,557+/-9,766 (the lowest vpi: 60,1; the highest vpi: 95,8). the mean modified discern score of the videos was 2,66+/-1,032 (the lowest: 1; the highest: 4) while the mean gqs score was 2,876+/-1,06 (the lowest: 1; the highest:4). in addition, the mean discern score and the mean gqs value were 3,51 and 3,82, respectively, for the informational videos that were uploaded by health professionals but did not contain actual surgery. similarly, the mean discern score and the mean gqs value were 1,08 and 1,29, respectively, for the patient videos in which personal experiences were shared. no statistically significant correlation was found between the gqs and discern scores according to both researchers and vpi values (p > 0.05). table 1. analyses of video characteristics by usefulness category useful i̇nformation (gr1) misleading i̇nformation (gr2) useful patient opinion (gr3) misleading patient opinion (gr4) video number n:16(32%) n:24(48%) n:4(8%) n:6(12%) views peer day 35,2+/-7,31 53,7+/-8,1 40,3+/-4,55 42,7+/-8,3 video lenght 4,01 min (2,04-5,91 min) 3,50 min (0,20-8,17 min) 6,03 min (5,02-8,54 min) 7,25 min (4,01-12,08 min) like 216+/-24 27,14+/-2,1 43,08+/-2,01 33,4+/-3,33 dislike 189,5+/-24,5 46,3+/-4,44 20,2+/-1,35 15,2+/-1,56 comments 26,8+/-2,33 27,2+/-1,33 92,1+/-7,41 113,4+/-11,2 discern score 3,4 2,2 3,2 0,5 gqs score 4,1 2,3 4,2 1,6 table 2. pairwise comparisons of video groups according to usefulness gr1-gr2 gr1-3 gr1-4 gr2-3 gr2-4 gr3-4 discern score p value 0,518 0,708 0,001 0,652 0,332 0,0018 gqs score p value 0,125 1,00 0,001 0,069 0,852 0,001 values of p 0,05 was accepted figure 1. video disseminator physician 26% health channe 54% patient 20% physician health channe patient 302 aysel gürcan atci, ibrahim burak atci modify discern (1 point per question answered yes) 1. is the video clear, concise, and understandable? 2. 2. are valid sources cited? (from valid studies, physiatrists or rheumatologists) 3. 3. is the information provided balanced and unbiased? 4. 4. are additional sources of information listed for patient reference? 5. 5. does the video address areas of controversy/uncertainty? global quality scale 1. poor quality, poor flow, most information missing, not helpful for patients 2. generally poor, some information given but of limited use to patients 3. moderate quality, some important information is adequately discussed 4. good quality good flow, most relevant information is covered, useful for patients 5. excellent quality and excellent flow, very useful for patients figure 2. video contents discussion youtube is a video sharing website based in san bruno, california, the usa. the website was founded in 2005 and was later acquired by google in 2006. the primary purpose of the website is that the users can upload and share any video in any subject freeof-charge (5). the first video uploaded to the website was the video showing jawed karim, one of the founders of the website, in which he appears in a zoo (5). concerning medical subjects; health professionals, hospitals and patients have a heavier traffic of video uploading activity. patients and patient relatives refer to these videos in order to see treatment methods and possible risks and to make inferences from the experiences of cases. on the other hand, health professionals use operation videos to learn by watching (10). however, there may also be incorrect, low-quality and prejudiced videos on this platform where everyone can upload videos free-of-charge without being subject to any inspection. pubmed reviews reveal 1089 studies that measure the quality of youtube videos on health issues (8,9). the first of these is a study from 2007 that evaluate the training of health professionals (6). the first publication concerning transforaminal steroid application with fluoroscopy was made by lutz ge in 1998. the study follows up 69 cases for about 80 weeks and describes the results thereto. the study was described as an effective attempt on cases with radiculopathy due to non-surgical disc herniation (7). after the article, pubmed also 0 5 10 15 20 25 general introduction injection technique animation patient experience 303 quality of youtube videos to transforaminal lumbar epidural steroid injections published a paper indicating that the attempt was a positive one. many physicians who deal with pain studied this attempt and applied the same to their patients. in this sense, the purpose of the present study is to find out whether patients can get reliable information from youtube channels prior to their transforaminal operations applied to lumbar disc herniation cases that do not require or are not recommended surgery. the second purpose is to evaluate the quality of the theoretical and visual information health professionals can get from such videos. the literature review we made did not produce any study concerning the subject in question. there are various scales and measures to evaluate the quality of the information in videos and on the internet. in this study, 2 researchers assess the videos using modified discern scoring system, global quality index and video power index (vpi). according to the analysis of the 50 videos with the highest views and vpis, it was found out that the videos presented weak and poor-quality information to patients, patient relatives and professionals who desire to learn the narrated operation. however, it was also observed that 80% of the videos were uploaded by health professionals and institutions. in 16 (32%) videos with actual surgeries, it was seen that the average time was 3,44 seconds, the operators did not satisfactorily explain the methods before and after the operations, they did not clearly specify alternative treatments and effects and possible complications, and the videos were not supported with subtitles. it was observed that the videos did not explain the operations in simple language to convey the processes to patients and patient relatives but only the course was expressed, and that there were dialogs with patients during operations. furthermore, it was revealed that 6 (12%) videos with the highest results of evaluation were animated or notional surgery videos, made theoretical powerpoint presentations and were supported with anatomic cross-sections. although 6 of 10 videos with patient experiences contained information about pain statuses in postop early stage and the post-op 2nd day, these were not found sufficient in terms of quality. the mostviewed 5 videos had approximately 300 views every day, on average, and 3 of these were actual surgeries while the other 2 were about patient experiences. the videos with the highest vpi values but had 2 or below in discern and gqs scoring were found to convey inadequate information. in contrast with the foregoing, the videos with the highest scores had 60 views every day, on average, and did not appear on the first page when searched on youtube. however, the videos that had the highest views but contained insufficient information appeared on top in youtube searches. apart from these, the video comment analyses demonstrated thatthe highest number of comments were entered to the uploads with patient experiences. the comments notably asked the regression rate of complaints, the length of the period without complaints and whether the operations were painful. accordingly, the videos with the highest like numbers were those that contained patient remarks. the videos were divided into 4 groups in terms of usefulness, and only 16 videos were found to contain useful and valid information. all these were uploaded by health professionals and were generally about physician remarks. the mean time of these videos was 2,44 seconds. useful patient remarks were identified only in 4 videos, and their mean view time was 2,31 seconds. the limitations of this study include the crosssectional design (popularity based on number of views changes constantly), and the inclusion of only the 50 most widely viewed videos (an arbitrary cut point). conclusion as a result, it may not always be accurate to believe that the medical videos with high view, comment and like numbers on youtube contain reliable, comprehensible and correct information. although the access to information and videos on medical subjects is very easy in today’s world, it is more appropriate to apply to experienced health professionals in order to get information. we think that medical associations and state authorities in medicine should check the validity and accuracy of the information on the internet and should support the society in access to the most correct information. compliance with ethical standards this study does not include any human participants or animals. videos that were available to everyone were evaluated for this study. therefore, ethics committee approval was not required. 304 aysel gürcan atci, ibrahim burak atci references 1. youtube. youtube statistic page. https://www. omnicoreagency.com/youtube-statistics/. accessed october 25, 2018. 2. singh ag, singh s, singh pp (2012) youtube for information on rheumatoid arthritis—a wakeup call? j rheumatol 39(5):899–903. https://doi.org/10.3899/jrheu m.111114 (epub 2012 apr 1). 3. charnock d, shepperd s, needham g, gann r (1999) discern: an instrument for judging the quality of written consumer health information on treatment choices. j epidemiol community health 53(2):105–111. 4. bernard a, langille m, hughes s, rose c, leddin d, veldhuyzen van zanten s (2007) a systematic review of patient inflammatory bowel disease information resources on the world wide web. am j gastroenterol 102(9):2070–2077. 5. https:// tr . wikipedia.org/wiki/youtube history. 6. skiba dj (2007) nurs educ perspect. nursing education 2.0: youtube 2007 mar-apr;28(2):100-2. 7. lutz ge, vad vb, wisneski rj .(1998) arch phys med rehabil. fluoroscopic transforaminal lumbar epidural steroids: an outcome study. nov;79(11):1362-6. 8. ovenden cd, brooks fm. anterior cervical discectomy and fusion youtube videos as a source of patient education. asian spine j. 2018;12:987-991. 9. drozd b, couvillon e, suarez a. medical youtube videos and methods of evaluation: literature review. jmir med educ. 2018;4:e3. 10. tackett s, slinn k, marshall t, gaglani s, waldman v, desai r. medical education videos for the world: an analysis of viewing patterns for a youtube channel. acad med. 2018;93:1150-1156. 11. hassan kz, sherman al.(2018)epidural steroids. statpearls [internet]. treasure island (fl): statpearls publishing; 2019 jan-. 2018 dec 19. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 321 328 | 321 the role of the basal cisterns in the development of posterior fossa skull base meningiomas ioan stefan florian1,2, gheorghe ungureanu1, alexandru florian2 1neurosurgery department, cluj county emergency hospital, cluj-napoca, romania 2university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, romania abstract: meningiomas account for more than 30% of all intracranial brain tumors, with 25% of them originating somewhere along the skull base and about 20% of these located in the posterior fossa. the intimate relation of these tumors with neural and vascular structures make them difficult to treat, both surgically and nonsurgically. their treatment is further hampered by the lack of definitive recommendations, which is partially due to the fact that there is no general accepted model of classification. the present report proposes a new concept of classification of posterior fossa skull base meningiomas, one that takes into account the intimate relation of these tumors with arachnoid structures, simplifies the overcrowded landscape of their systematization and can be extended to oher skull base locations. introduction meningiomas are the most frequent type of primary brain tumors, accounting for more than 30%, with an estimated prevalence of 6.0 in 100000 in the us (1). these tumors can originate in any cranial and spinal region where there are arachnoid cells, with about 25% of them originating somewhere along the skull base (2). the treatment philosophy changed significantly during the last two decades (3). because of their intimate relation with neural and vascular structures, their treatment is challenging and gross total removal is not feasible in some cases, so a combination of surgery, endoscopy and srs is employed to achieve a good outcome (4). the terms used in the various classifications of skull base meningiomas are a subject of debate, as diverse locations are subjected to various terminologies with no accepted classification (5). from anterior to posterior these tumors are classified according to bony landmarks and include olfactory groove, planum sphenoidale, tuberculum sellae, optic nerve sheath, sphenocavernous, sphenoorbital, cavernous sinus, tentorial, clival and petroclival, cerebellopontine angle, jugular foramen, lower clivus and foramen magnum tumors (2). this classification is often confusing and doesn’t provide a clear grouping of skull base meningiomas, although various studies have tried to offer different sorting systems (5, 6, 7, 8). because of the complexity of the categories of these classifications, it is difficult to assign tumors to a certain group. for example, cerebello 322 | florian et al classification of posterior fossa skull base meningiomas pontine angle tumors are included in the larger group of petroclival meningiomas in some studies, and this is debated by other authors (6). simmilarly, meningiomas originating in the lower clivus are not distinguishable from foramen magnum ones, because of the anatomical continuity of these areas (9). the present report focuses on proposing a novel model for the classification of posterior skull base meningiomas, one in which tumors are grouped according to the perilesional subarachnoid cysterns. concept 1. rationale of the classification a) origins of meningiomas meningiomas originate in the progenitor cells of the arachnoid cap cells, which are positioned ouside the arachnoid membrane (10). the main function of these cells is the reabsorbtion of csf, and in order to carry out this task, they exibit numerous forms of cellular junctions (11, 12). the reason that meningiomas are thought to originate from these cells is the fact that they both express similarities in function and ultrastructure (10). tight junctions, desmosomes, pynocitic vesicles, extracellular spaces resembling cisterns, are for example, some of the features found in both cells (13, 11). current knowledge regarding adhesion, cell-to-cell communication, cell survival, homeostasis in meningiomas is still lacking, although new research gives hope in understanding the multiple singnaling pathways and mechanisms implicated in the development of these tumors and their similarities with arachnoid cap cells (13). b) subarachnoid cysterns under the brain, around the brainstem and in the tentorial incisura, the subarachnoid space expands, forming cavities filled with csf, which are separated through a large number of septae, trabeculaes and membranes into cisterns (14). these cisterns offer the pathway through which all the major vessels and cranial nerves pass and are also corridors for the neurosurgeon as most procedures can be performed noninvasevely by using these natural access routes (15). the cisterns of the posterior fossa, the vessels and nerves that pass through them are detailed in figure 1. the arachnoid membranes provide landmarks for dissection and provide the “need-to-know” limits for neurosurgeons, both in transcaranial and, more importantly, endoscopic procedures (16). the membranes of the posterior fossa are (14): liliequist’s membrane, separating the chiasmatic and interpeduncular cisterns; anterior pontine membrane, between the prepontine and cerebellopontine cisterns; lateral pontomesencephalic membrane, between the ambient and cerebellopontine cisterns; medial pontomedullary membrane, between the premedullary and prepontine cisterns; lateral pontomedullary membrane, between the cerebellopontine and cerebellomedullary cisterns. romanian neurosurgery (2016) xxx 3: 321 328 | 323 figure 1 posterior fossa cysterns and their neurovascular content 2. the concept of the classification our concept of classification proposes to classify skull base meningiomas according to the subarachnoid cisterns proximal to the tumors. it is based both on our clinical experience and a wide study of literature. in a retrospective study conducted over a period of 15 years, including 934 new cases of meningioma, with 985 locations (some cases with multiple meningiomas), 51 tumors were located in the petro-clival region and 11 cases in the anterolateral portion of the foramen magnum. posterior fossa meningiomas accounted for 144 cases, 15.4% of all new cases. petro-clival meningiomas represent 34.5% of the posterior fossa meningiomas, while those located in the foramen magnum around 10%. as it has been shown previously, meningiomas originate from the arachnoid capp cells. as yasargil stated more than twenty years ago “meningiomas and schwannomas originate in the subdural space and extend subdurally, but epiarachnoidally. they are covered by two or more cisternal layers depending on the number of cisterns traversed” (17). the cisterns of interest for the development of meningiomas of the posterior fossa skull base are the interpeducular cistern, prepontine cistern, cerebellopontine cisterns, cerebellomedullary cisterns and the premedullary cistern. the limitations of meningiomas into a specific cistern are demonstrated by the similar aspects of the tumors, for a period of time, regardless of factors like age, gender, histology. in time, maligancny influences the growth pattern, but the membranes and other arachnoidal structures, along with the neurovascular structures, will conduct the further expansion of the tumors. below are some examples of how tumors follow growth patterns with a relative respect to the arachnoid and neurovascular surrounding structures: tumors originating at the level of the prepontine cistern will grow predominantly on the median line, with a lateral extension depending on the location of the basilar artery, their upward expansion being limited by liliequist’s membrane; meningiomas originating at the level of the superior cerebellopontine cistern, predominantly grow laterally and superiorly 324 | florian et al classification of posterior fossa skull base meningiomas along the oculomotor nerve, into meckel’s cave, displacing laterally the acusticovestibular and facial bundle; meningiomas originating outside the cerebellopontine cistern, on the petrous bone, will displace medially the facial and acusticovestibular cranial nerves, and in larger tumors also the glosopharingeal and vagus nerve and can be included in the category of posterior petrous meningiomas, in order to be distinguished by those located in the middle fossa; meningiomas originating at the level of the premedullary cistern will further develop anteromedially, in an ascending and descending direction, their growth being limited posteriorly by the dentate ligament. as they grow, they will displace laterally the glosopharingeal, vagus and accessory nerves; those tumors mostly located in the cavernous sinus, with a secondary involvement of the posterior fossa cisterns are those included in the current sphenopetroclival category; 3. importance for neurosurgeons the surgical implication of this classification relies in the fact that it offers a justification and reasoning for the idea that, with the exception of sphenopetroclival meningiomas, all other meningiomas in this location, could be resected trough a “classic” lateral posterior fossa approach, namely the retrosigmoidian approach, for those located superiorly, and a lateral approach, for those located inferiorly. taking advantage of the surgical corridor created by the tumor growth, using progressive internal debulking, basal devascularization, mobilization of the nerves and arteries in their arachnoid layer, the surgeons can usually obtain a complete removal of the tumor. in some instances, in which the tumor invades the brainstem piamater, the concept of leaving in place some of the tumor, in order to preserve quality of life applies. a classification according to the basal cisterns allows, on one hand an easier anatomical framework and also offers an anticipation of tumor relations with neurovascular elements contained in a specific cistern, relations valid at least for medium size tumors. at the same time it allows an explanation of the pattern of tumor development. as the tumor grows, it will gradually exceed the natural barriers posed by arachnoidal membranes, invading the adjacent cisterns and consequently, the adjacent neurovascular structures. romanian neurosurgery (2016) xxx 3: 321 328 | 325 figure 2 schematic representation of posterior fossa cisterns and case examples discussion our study offers a novel approach in classifying meningiomas of the posterior fossa skull base. considering the origin of meningioma cells, the anatomic locations of these tumors, and the “simplicity” of relating these tumors to the subarachnoid cysterns, we see this as a viable classification system. the importance of the arachnoid membrane in the growth pattern and expansion of meningiomas is probably most visible in the case of clinoidal tumors. when meningiomas occur proximal to the carotid cistern, where the carotid lacks an arachnoid wraping, the meningioma will adhere directly to the vessel adventia (18). this is just an instance that proves that meningiomas cannot be viewed outside their relation with the arachnoid membrane that is both the origin of the tumors and also a very important surgical limit. skull base meningiomas probably represent one of the most formidable challenges to a neurosurgeon. with the development of microsurgery, came an initial enthusiasm, in which performing radical surgery for lesions previously seen as inoperable was viewed as a major advancement, even if this lead to major postoperative morbidity (19). in various series, surgery resulted in permanent cranial nerve deficits ranging from 20.3% to 86% (20). in time, as patients and physicians began asking for preservation of quality of life and deficit free survival, the treatment paradigm 326 | florian et al classification of posterior fossa skull base meningiomas shifted towards subtotal removal combined with some kind of radiotherapy (21). slowly, with the advent of endoscopic neurosurgery and radiosurgery, this evolved into a concept of “minimally invasive neurosurgery” (19, 21). this view was challenged, as an innapropriate treatment through a minimally invasive surgery can become maximally invasive for the patient, and so the concept of treatment slowly settled in applying a combination of skull base surgery, endoscopy and radiosurgery (19, 22, 23, 24). usually, surgery can achieve gtr, but this should be a secondary goal of surgery, the first being the improvement or at least preservation of life quality. comparing results of various treatments coming from different groups, is complicated by the lack of a simple, straight forward classification system. it is impossible to compare outcomes of a certain medical procedure, as long as the understanding of the disease is different between those who compare the procedures. this is especially true in the case of skull base lesions. in an area of just a few centimeters, a variety of tumors can be encountered. just in the clival region, some studies define tumors with distinct anatomical differences as “true” petroclival, sphenopetroclival, midclival, and posterior petrosal tumors (7). other grading and classification systems that were proposed for tumors in this location have a different view and offer another perspective, providing other classifications and recommended approaches, frequently with conflicting opinions regarding similar tumors (25, 26, 27). the same difference in views is also encountered in foramen magnum lesions (28, 29, 30, 31, 32). as one would expect, differentiating between tumors originating in an area of a couple of cm is not easy, as the anatomical “landmarks” are not clearly defined, and furthermore it’s easy to mistake one category for another. if treatment prognosis is different between these tumors, it’s obvious to see why different groups will obtain different results even when comparing the same technique. in the era of evidence based medicine, the treatment of skull base tumors, has still not been the subject of prospective, randomized trials, applying similar therapies to similar lesions. a review found that their rarity, the variety of the reported data and treatment diversity of these tumors, only lead to a very complicated picture (24). the majority of recommendations come from “master surgeon” series, which do not reflect the overall quality of surgeons, and thereby may provide divergent results when applied to the entire community (33). furthermore, these studies reach results by analyzing patients operated using various, preferred approaches by the surgeons (6) (34, 25, 35, 27, 26). this, combined with the various classification systems, make the decision process towards a certain therapy or approach even more difficult. using a “simple” sorting mechanism like ours, would prove beneficial in this regard. the majority of posterior fossa meningiomas can be managed through “classic” approaches, with minimal traction of the neural and vascular elements, if one considers this cisternal classification. our classification concept offers the advantage of being a true “anatomical” and simple classification. it divides tumors using a romanian neurosurgery (2016) xxx 3: 321 328 | 327 constant peritumoral trait, the subarachnoid cisterns. because the neurovascular elements are found in these cisterns, it’s easy to look for the clinical deficits that the tumors will cause as they grow and compress them. the pericisternal location also anticipates the elements that will be encountered during surgery. the growth pattern of benign tumors could also be investigated using this system, as it’s possible that they expand by these natural pathways. last, but not least, this classification pattern can be applied to other skull base tumors, eg. sellar region tumors. conclusion our report proposes a new classification system of posterior fossa meningiomas. it’s, for the best of our knowledge, the first system of classification that divides this tumors using the subarachnoid cisterns and the various membranes as anatomical and clinical landmarks. its simplicity and clarity make it easy to use and also applicable to other skull base lesions. correspondence gheorghe ungureanu victor babes, no. 43/7, cluj-napoca, cluj county, romania e-mail: ungureanugeorge@gmail.com references 1. porter kr, mccarthy bj, freels s, kim y, davis fg. prevalence estimates for primary brain tumors in the united states by age, gender, behavior, and histology. neuro oncol 2010; 12:520–7. doi: 10.1093/neuonc/ nop066. 2. di maio s, ramanathan d, garcia-lopez r, rocha mh, guerrero fp, ferreira m, et al. evolution and future of skull base surgery: the paradigm of skull base meningiomas. world neurosurg 2012;78:260–75. doi:10.1016/j.wneu.2011.09.004. 3. seifert v. clinical management of petroclival meningiomas and the eternal quest for preservation of quality of life: personal experiences over a period of 20 years. acta neurochir (wien) 2010;152:1099–116. doi:10.1007/s00701-010-0633-6. 4. nanda a, javalkar v, banerjee ad. petroclival meningiomas: study on outcomes, complications and recurrence rates. j neurosurg 2011;114:1268–77. doi:10.3171/2010.11.jns10326. 5. kawase t, toya s. developmental patterns and characteristic symptoms of petrolival meningiomas. neurol med chir (tokyo) 1996;36:1–6. doi:10.1016/j.wneu.2010.12.035. 6. ichimura s, kawase t, onozuka s, yoshida k, ohira t. four subtypes of petroclival meningiomas: differences in symptoms and operative findings using the anterior transpetrosal approach. acta neurochir (wien) 2008;150:637–45. doi:10.1007/s00701-008-1586-x. 7. almefty r, dunn if, pravdenkova s, abolfotoh m, almefty o. true petroclival meningiomas: results of surgical management. j neurosurg 2014;120:40–51. doi:10.3171/2013.8.jns13535. 8. boulton mr, cusimano md. foramen magnum meningiomas: concepts, classifications, and nuances. neurosurg focus 2003;14:e10. doi:10.3171/ foc.2003.14.6.10. 9. kano t, kawase t, horiguchi t, yoshida k. meningiomas of the ventral foramen magnum and lower clivus: factors influencing surgical morbidity, the extent of tumour resection, and tumour recurrence. acta neurochir (wien) 2010;152:79–86. doi:10.1007/s00701009-0511-2. 10.yamashima t. on arachnoid villi and meningiomas: functional implication of ultrastructure, cell adhesion mechanisms, and extracellular matrix composition. pathol oncol res 1996;2:144–9. 11.arishima h, sato k, kubota t. immunohistochemical and ultrastructural study of gap junction proteins connexin26 and 43 in human arachnoid villi and meningeal tumors. j neuropathol exp neurol 2002;61:1048–55. 12.mehta bc, holman dw, grzybowski dm, chalmers jj. characterization of arachnoidal cells cultured on three-dimensional nonwoven pet matrix. tissue eng 2007;13:1269–79. doi:10.1089/ten.2006.0233. 328 | florian et al classification of posterior fossa skull base meningiomas 13.pećina-šlaus n, kafka a, lechpammer m. molecular genetics of intracranial meningiomas with emphasis on canonical wnt signalling. cancers (basel) 2016;8:67. doi:10.3390/cancers8070067. 14.rhoton al. chapter10 the posterior fossa cisterns. neurosurgery 2000;47:s287–97. doi:10.1097/00006123200009001-00029. 15.lü j. arachnoid membrane: the first and probably the last piece of the roadmap. surg radiol anat 2015;37:127– 38. doi:10.1007/s00276-014-1361-z. 16.anik i, ceylan s, koc k, tugasaygi m, sirin g, gazioglu n, et al. microsurgical and endoscopic anatomy of liliequist’s membrane and the prepontine membranes: cadaveric study and clinical implications. acta neurochir (wien) 2011;153:1701–11. doi:10.1007/s00701-011-0978-5. 17.yasargil mg. microneurosurgery. 1st ed. new york: georg thieme verlag; 1984. 18.al-mefty o, abdulrauf si, haddad gf. meningiomas. in: winn rh, editor. youmans neurol. surg. sixth edit, philadelphia: elsevier b.v.; 2011, p. 1426–50. 19.misra bk. the paradigm of skull base meningiomas: what is optimal? world neurosurg 2012;78:220–1. doi:10.1016/j.wneu.2011.11.018. 20.xu f, karampelas i, megerian c a, selman wr, bambakidis nc. petroclival meningiomas: an update on surgical approaches, decision making, and treatment results. neurosurg focus 2013;35:1–10. doi:10.3171/2013.9.focus13319. 21.stippler m, kondziolka d. skull base meningiomas: is there a place for microsurgery? acta neurochir (wien) 2006;148:1–3. doi:10.1007/s00701-005-0667-3. 22.brito h, pridgeon js. skull base meningiomas: aggressive resection 2015;62:30–49. doi:10.1227/neu.0000000000000803. 23.li d, hao sy, wang l, tang j, xiao xr, jia gj, et al. recurrent petroclival meningiomas: clinical characteristics, management, and outcomes. neurosurg rev 2015;38:71–87. doi:10.1007/s10143-014-0575-1. 24.maurer aj, safavi-abbasi s, cheema aa, glenn ca, sughrue me. management of petroclival meningiomas: a review of the development of current therapy. j neurol surgery, part b skull base 2014;75:358–67. doi:10.1055/s-0034-1373657. 25.m. p, s. v, m.r. p, d. k. novel classification for surgical approach of petroclival meningiomas: a singlesurgeon experience. neurol india 2015;63:718–22. doi:10.4103/0028-3886.166551. 26.tao j, wang y, qiu b, ou s, wang y, wu p. selection of surgical approaches based on semi-quantifying the skull-base invasion by petroclival meningiomas: a review of 66 cases. acta neurochir (wien) 2014;156:1085–97. doi:10.1007/s00701-014-2084-y. 27.steiger hj. surgical management of medium and large petroclival meningiomas: benchmark and limits. acta neurochir (wien) 2016;158:407–8. doi:10.1007/s00701015-2686-z. 28.mostofi k. foramen magnum meningioma: some anatomical and surgical remarks through five cases. asian spine j 2015;9:54–8. doi:10.4184/asj.2015.9.1.54. 29.dobrowolski s, ebner f, lepski g, tatagiba m. foramen magnum meningioma: the midline suboccipital subtonsillar approach. clin neurol neurosurg 2016;145:28–34. doi:10.1016/j.clineuro.2016.02.027. 30.bruneau m, george b. classification system of foramen magnum meningiomas. j craniovertebral junction spine 2010;1:10–7. doi:10.4103/09748237.65476. 31.bruneau m, george b. classification system of foramen magnum meningiomas. j craniovertebral junction spine 2010;1:10–7. doi:10.4103/09748237.65476. 32.wu z, ren c, hao s, wang l, xiao x, tang j, et al. foramen magnum meningiomas: surgical results and risks predicting poor outcomes based on a modified classification 2016:1–4. doi:10.3171/2016.2.jns152873. 33.sughrue me, sayegh et, parsa at. towards a hypermodern theory of meningioma surgery. clin neurol neurosurg 2014;126:69–75. doi:10.1016/j.clineuro.2014.06.002. 34.yamahata h, tokimura h, hirahara k, ishii t, mori m, hanaya r, et al. lateral suboccipital retrosigmoid approach with tentorial incision for petroclival meningiomas: technical note. j neurol surgery, part b skull base 2014;75:221–4. doi:10.1055/s-0034-1373656. 35. ambekar s, amene c, sonig a, guthikonda b, nanda a. quantitative comparison of retrosigmoid intradural suprameatal approach and retrosigmoid transtentorial approach: implications for tumors in the petroclival region. j neurol surgery, part b skull base 2013;74:300– 4.doi:10.1055/s-0033-1348025. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note 366 | atanasov, popov predictors for outcome in traumatic acute subdural hematoma predictors for outcome after surgery for traumatic acute subdural hematoma vladimir a. atanasov, rumen v. popov department of neurosurgery, university hospital “tsaritsa yoanna” sofia, bulgaria abstract: introduction: acute traumatic subdural hematoma (asdh) is one of the most frequent conditions in neurosurgery demanding emergency surgery. the aim of the study was to identify factors influencing outcome in patients who had surgery for evacuation of asdh. methods: from 2005 to 2012 eighty-five patients at age above 18 years had surgery for evacuation of asdh. outcome was measured according gos at discharge and was dichotomized as “favorable outcome” (gos 4 to 5) and “unfavorable outcome” (gos 1 to 3). these factors were evaluated with univariate and logistic regression analysis for significance with outcome. results: the mean age of the 85 patients was 62.7 years (sd±18.5). 45.9% patients were with favorable outcome and 54.1% had unfavorable outcome. patients with gcs score 3-8 (54.1%) had 80.4% unfavorable outcome whereas 78.6% of patients with gcs score 13-15 (32.9%) had favorable outcome. all patients with nonreactive pupils (bilaterally or unilaterally 31.8%) had unfavorable outcome whereas patients (36.5%) with both reactive pupils (36.5%) had in 80.6% favorable outcome. all patients (40%) with rotterdam ct scores 5 and 6 had unfavorable outcome. the factors determining outcome were admission gsc score, rotterdam ct scores, and prothrombin time. conclusion: patients who have gsc score of 3, unresponsive pupil(s) or have rotterdam ct scores 5 and 6 have little chance of survival. patients with coagulopathy have two times more unfavorable outcome. the patients with asdh should have surgery as soon as possible after correction of vital parameters in order to avoid deterioration which can be very rapid and irreversible. key words: acute traumatic subdural hematoma, factors, outcome, surgery introduction traumatic subdural hematoma is one of the most frequent neurosurgical condition, demanding emergency surgery (figure 1 and figure 2). the mortality is still high – between 40 and 90% (4, 10, 11, 15, 23, 29, 33) despite the progress in the care of the patients – early in-field resuscitation and rapid transfer to the hospital, staffed with experienced trauma surgeons and neurosurgeons. a numerous factors has been reported to have influence on the outcome after surgery in these patients and include age (4, 10, 12, 15, 22, 28), comorbidities (7, 16), injuries in other body romanian neurosurgery (2016) xxx 3: 366 374 | 367 areas (17), gcs score (1, 4, 8 12, 15,19, 23, 28, 31, 33), pupils reactivity (4, 8, 10, 11, 15, 33, 34), different ct characteristics of the asdh (1, 19, 25, 33), time of surgery (1, 4, 8 10, 12, 24, 26, 28, 31, 34). the goal of the study was to evaluate factors that had influence on the outcome after surgical management of asdh and to allow prediction for functional outcome in such patients. figure 1 acute subdural hematoma figure 2 acute subdural hematoma with traumatic subarachnoid hemorrhage materials and methods this is a retrospective study on 85 patients who had surgery between 2005 and 2012 at the department of neurosurgery in queen joanna hospital isul – sofia. criteria for inclusion were age over 18 years and patients subjected to surgery for asdh where informed consent was given by the patient or patients’ relatives or caregivers. criteria for exclusion were patients with penetrating injury, asdh due to aneurismal rupture, asdh in posterior fossa, secondary bleeding in chronic subdural hematoma, and refusal of surgery by the patient or by his/her relatives. surgery was performed in a standardized manner using a trauma flap. patients were further managed in the intensive care unit using a standard protocol. data for age, gender, and mechanism of trauma were collected from emergency medical service records, patients, accompanied persons, and from referral hospital documentation. all patients underwent evaluation of the vital signs (pulse oximetry, blood pressure, heart rate, gcs score, pupils reactivity) and neurological examination at admission. comorbidities were evaluated according charlson comorbidity index (3). consultations were made with other specialists (general surgeons, trauma surgeons, cardiologists, ear, nose and throat surgeons) in cases with concomitant injuries (evaluated with injury severity score, iss) or health problems. standard computerized tomography (ct) protocol was used. for classification of the ct 6-point rotterdam ct score (16) was used. routine 368 | atanasov, popov predictors for outcome in traumatic acute subdural hematoma laboratory tests were done. patients with traumatic shock or with impaired consciousness were stabilized in the resuscitation room at the emergency department and intubated and ventilated prior to transfer to ct suite. outcome was measured according gos (5) and was dichotomized in “favorable” (gos 4 and 5) and “unfavorable” (gos 1-3). statistical analysis was performed using ibm spss software ver. 20.0 (spss inc. chicago, il, usa) for windows. significance was defined at p < 0.05. results full data sets were available for 85 patients. these data are presented in table 1. the mean age of the patients was 62.7 years (standard deviation, sd±18.5), the patients over the 65 years were 50.6% and they had more frequently unfavorable outcome (62.8%) than patients in younger group (45.2%) but this was not of significance.significant effect (p=0.519). table i demographic data, mechanism of injury, and comorbidities in 85 patients parameter no of patients % favorable outcome % unfavorable outcome % p sig age ≤64 ≥65 42 43 49.4 50.6 23 16 54.8 37.2 19 27 45.2 62.8 0.519 no sex males females 61 24 71.8 28.2 31 8 50.8 33.3 30 16 49.2 66.7 0.149 no mech.of injury fall mva 72 13 84.7 15.3 36 3 50 23.1 36 10 50 76.9 0.128 no charlson comorbidity index 0 2 ≥3 30 55 35.3 64.7 16 23 53.3 41.8 14 32 46.7 58.2 0.059 no outcome favorable unfavorable 39 46 45.9 54.1 romanian neurosurgery (2016) xxx 3: 366 374 | 369 table ii characteristics of overall severity of injury and severity of brain injury, ct characteristics and time from injury to admission and to surgery + no of patients % favorable outcome % unfavorable outcome % p sig iss ≤25 ≥26 ≤33 ≥34 70 15 73 12 85.9 14.1 36 3 37 2 51.4 20 50.7 16.7 34 12 36 10 48.6 80 49.3 83.3 0.013 yes gcs 3-8 9-12 13-15 46 11 28 54.1 12.9 32.9 9 8 22 19.6 72.7 78.6 37 3 6 80.4 27.3 21.4 <0.0005 yes pupillary abnormalities nonreactive unilat. reactive sluggish both reactive 14 13 27 31 16.5 15.3 31.8 36.5 14 25 51.9 80.6 14 13 13 6 100 100 48.1 19.4 <0.0005 yes map1 ≤70 mmhg ≥70 mmhg 1 84 1.2 98.8 39 46.4 1 45 100 53.6 0.891 no rotterdam ct score 2 3 4 5 6 19 14 18 14 20 22.4 16.5 21.2 16.5 23.5 17 11 11 89.5 78.6 61.1 2 3 7 14 20 10.5 21.4 38.9 100 100 <0.0005 yes time injury to surgery ≤ 240 min ≥ 240 min 17 68 20 80 4 35 23.5 51.5 13 33 76.5 48.5 0.002 yes time admission to injury ≤60 min ≥61 min 22 63 25.9 74.1 7 32 31.8 50.8 15 31 68.2 49.2 0.028 yes outcome favorable unfavorable 39 46 45.9 54.1 1map mean arterial pressure 370 | atanasov, popov predictors for outcome in traumatic acute subdural hematoma table iii laboratory parameters in 85 patients parameter no of patients favorable outcome % unfavorable outcome % p sig hb1 males < 130 females < 115 both 21 9 55 8 2 29 38.1 22.2 52.7 13 7 26 61.9 77.8 47.3 0.519 no wbc2 <3.5 3.5-10.5 >10.5 1 38 46 21 18 55.3 39.1 1 17 28 100 44.7 60.9 0.231 no plt3 <130 130-440 >440 14 70 1 3 36 21.4 51.4 11 34 1 78.6 48.6 100 0.097 no glucose 3.3-6.0 >6.0 12 73 10 29 83.3 39.7 2 44 16.7 60.3 <0.0005 yes sodium <135 135-145 >145 14 65 6 8 30 1 57.1 46.2 16.7 6 35 5 42.9 53.8 83.3 0.232 no pt4 <70 70-120 >120 45 37 3 12 24 3 26.7 64.9 100 33 13 73.3 35.1 <0.0005 yes 1hemoglobine; 2white blood cells; 3platelets; 4prothrombine time predominant gender was male (71.8%) but this had no effect on outcome. predominant mechanism of trauma was fall (84.7%) and motor vehicle accident (mva) carried more unfavorable outcome (76.9%) but mechanism had no effect on outcome. fifty-five patients had charlson comorbidity index more than 2 but this was not of significance. more than half of the patients were with gcs score group 3 to 8 and they had unfavorable outcome in 80.4% contrary to the group with highest scores (gcs 13-15), where 21.4% of patients were with unfavorable outcome (table 2). 63.6% of patients had abnormalities in pupillary reaction, 16.5% with bilaterally unresponsive and 15.3% with unilaterally responsive pupils and all patients in these two groups were with unfavorable outcome. about half of the patients in the group with sluggish reaction had unfavorable outcome and pupillary reaction was a significant factor in univariate analysis. romanian neurosurgery (2016) xxx 3: 366 374 | 371 there was only one patient with hypotension on admission so mean arterial pressure (map) had no significant effect on outcome. in the only patient hypotension was lethal, possibly due to irreversible brain damage. the patient was with bilaterally nonresponsive pupils and gcs score 3. ct abnormalities were of significance for outcome and there were no patients with favorable outcome among patients (40%) with highest score of 5 and 6 whereas 89.5% of patients with rotterdam ct scores 2 had favorable outcome. time injury to surgery up to 240 min had 20% of patients and 23.5% of them had favorable outcome. time admission to injury up to 60 min had 25.9% of patients and 31.8% of them had favorable outcome. results for laboratory data analysis are shown in table 3. there was no effect on outcome except for blood glucose (p<0.0005) and prothrombin time (p<0.0005). amongst all patients 8 were with diabetes and 2 were with use of acenocumarol (both with unfavorable outcome). discussion our results show a favorable outcome in 45,9% and unfavorable one in 54,1%. the main factors, influencing outcome in this study were gcs score on admission, rotterdam ct score and pt. patients with lowest scores had the worst outcome and in (4) all patients with gcs score of 3 had unfavorable outcome whereas all patients with gcs 7 to 14 made functional recovery. in (10) patients with gcs scores less than 8 had 55.4% mortality and with scores 9 to 15 had 11.1%. in our study all but one patients with gcs 3 had unfavorable outcome and in the group with gcs scores 3 to 8 (54.1% of all patients) only 19.6% had favorable outcome. in the group with gcs scores 9-12, favorable outcome was achieved in 72.7% and in the group with gcs 13 to 15 in 78.6% of cases. the main question raised is whether patients with gcs scores 13 to 15 are candidates for surgery. the ct characteristics (rotterdam ct score takes into consideration midline shift, width of the basal cisterns, other intracranial traumatic lesions) along with the gcs scores play significant role in decision making for conservative management. some authors (20) proposed criteria for conservative management of such patients but only 3% of the population they had studied were candidates for conservative management and later 6 of 23 patients required surgery. the main indication for conservative management was the thickness of the asdh. when (32) treated conservatively 31 patients with midline shift less than 10 mm and gcs 15, six of them required urgent surgery after short period of observation. they came to conclusion that a midline shift more than 5 mm heralds failure of the intracranial compensatory mechanisms. not only a patient with certain ct parameters but with gcs scores (greater than 8) might have good outcomes in carefully selected patients younger than 65 years (2). we did not manage any patient with thickness of the asdh more than 10 mm conservatively and cannot advise conservative management because such patients deteriorated quickly and all had unfavorable outcome. 372 | atanasov, popov predictors for outcome in traumatic acute subdural hematoma the group with most lethal combination of factors was the group of patients with bilaterally unresponsive pupils and gsc scores of 3 and this group comprised 28.2% of all patients. in (21) only 8 out of 92 patients with gcs scores 3 and bilaterally unresponsive pupils had favorable outcome and they found that in this group the only factor having significance was ct characteristics. in most of the studies age is the factor in the outcome with significantly higher mortality in older patients but in ours it was not. this may be due to the fact that the age of our population was higher than in many others studies because in some studies (4, 7, 8, 23) younger patients were included. (17) did not find statistically significant correlation also. in a carefully selected aged population (27) demonstrated promising results. older patients had more comorbidities and (7) found that this affected mortality when more than 2 comorbidities were encountered. since (24) many studies evaluated the time elapsed from injury and favorable outcome with earlier surgery (up to 240 min after injury). this was supported by (5, 6) but (4, 11, 12, 26, 31) did not. (28) and (34) found a tendency toward lesser mortality and they had more patients with favorable outcome with earlier surgeries but without significance. in our study 25.9% of patients were admitted up to 60 min after injury but only 20% had surgery up to 240 min after injury and time of surgery was of significance in univariate analysis bur not in logistic regression analysis. some authors (1, 10) suggested that patients with most severe brain injuries were sent to a neurosurgical unit more rapidly. (12) found that patients operated later than 12 hours had the lowest mortality rate due to lesser severity and thought that patients who might have benefit from earlier surgery died in a hospital at remote distance from a hospital capable of dealing trauma patients. our policy is to operate as early as possible after resuscitation and full evaluation of a trauma patient and we do not suggest any time delay in managing patients with asdh. in the laboratory parameters routinely determined on admission we found significance in univariate analysis only in blood sugar (p<0.0005), and protrombin time (p<0.0005) but in logistic regression analysis the only laboratory parameter of significance was protrombin time (p=0.013). a significantly worse outcome was found by (16) in patients with coagulopathy defined as inr more than 1.2 or partial thromboplastin time more than 37 sec. in their group of patients 54.1% were had coagulopathy but only 9.7% were on oral anticoagulation therapy and there were no significant difference in gcs scores between coagulopathic and noncoagulopathic patients. in our group 2 patients were on acenocumarol and both were with unfavorable outcome. in the group with elevated levels of blood sugar 8 were with diabetes with only one with favorable outcome. we did not find any data regarding the influence of laboratory parameters on outcome in patients with asdh. limitations the major limitation of the study is that it is a retrospective one. this study represents a single institution experience and was done in a romanian neurosurgery (2016) xxx 3: 366 374 | 373 university hospital so the results obtained may differ in other type of institution. conclusion in this study 45.9% of patients had favorable outcome and 54.1% were with unfavorable one. the main factors of significance in determining outcome in patients with ash who had surgery were gcs score on admission, rotterdam ct score and pt. patients with gsc score of 3 had little chance of survival, especially if they had unresponsive pupil. all patients with rotterdam ct scores 5 and 6 had unfavorable outcome. patients with pt less than 70 had two times more unfavorable outcome than patients with pt within normal range. the patients with asdh should have surgery as soon as possible after correction of vital parameters in order to avoid deterioration which can be very rapid and irreversible. correspondence vladimir a. atanasov university hospital “tsaritsa yoanna” 8 bjalo more st 1527 sofia, bulgaria phone: +359 2 9432 605 e-mail: vovaatanasov@yahoo.com references 1.dent d, croce m, menke p, young b, hinson m, kudsk k, et al. prognostic factors after acute subdural hematoma. j trauma. 1995;39:36–42. discussion 42-43. 2.feliciano c, de jesús o. conservative management outcomes of traumatic acute subdural hematomas. p r health sci j. 2008 sep;27(3):220-3. 3.charlson m, pompei p, ales k, mackenzie c. a new method of classifying prognostic comorbidity in longitudinal studies: development and validation. journal of chronic diseases 1987; 40:373-383. 4.hatashita s, koga n, hosaka y, takagi s. acute subdural hematoma : severity of injury, surgical intervention, and mortality. neurol med chir (tokyo) 1993;33:13–18. 5.howard m, gross a, dacey r, jr, winn h. acute subdural hematomas: an age-dependant clinical entity. j neurosurg. 1989;71:858–863. 6.jennett b, bond m. assessment of outcome after severe brain damage. lancet 1975 mar 1;1(7905):480-4. 7.kalanithi p, schubert r, lad s, harris o, boakye m. hospital costs, incidence, and inhospital mortality rates of traumatic subdural hematoma in the united states. j neurosurg. 2011 nov;115(5):1013-8. 8.karasu a, civelek e, aras y, sabanci pa, cansever t, yanar h, sağlam g, imer m, hepgül kt, taviloğlu k, canbolat a. analyses of clinical prognostic factors in operated traumatic acute subdural hematomas. ulus travma acil cerrahi derg. 2010 may;16(3):233-6. 9.kiboi j, kitunguu p, angwenyi p, mbuthia f, sagina l. predictors of functional recovery in african patients with traumatic intracranial hematomas.world neurosurg. 2011 may-jun;75(5-6):586-91. 10.kim k. predictors for functional recovery and mortality of surgically treated traumatic acute subdural hematomas in 256 patients. j korean neurosurg soc. 2009 march; 45(3): 143–150. 11.koç r, akdemir h, oktem i, meral m, menkü a. acute subdural hematoma : outcome and outcome prediction. neurosurg rev 20 : 239-244, 1997. 12.kotwica z, brzezinski j. acute subdural hematoma in adults: an analysis of outcome in comatose patients. acta neurochir (wien) 1993;121:95–99. 13.kotwica z, jakubowski jk: head-injured adult patients with gcs of 3 on admission -who have a chance to survive? acta neurochir (wien) 133:56–59, 1995. 14.lefering r, paffrath t, linker r, bouillon b, neugebauer ea; deutsche gesellschaft für unfallchirurgie/german society for trauma surgery. head injury and outcome--what influence do concomitant injuries have? j trauma. 2008 nov;65(5):1036-43; discussion 1043-4. 15.leitgeb j, mauritz w, brazinova a, janciak i, majdan m, wilbacher i, rusnak m. outcome after severe acute subdural hematoma. j neurosurg 2012 117:324–333. 16.lemcke j, al-zain f, von der brelie c, ebenau m, meier u. the influence of coagulopathy on outcome after traumatic subdural hematoma: a retrospective single 374 | atanasov, popov predictors for outcome in traumatic acute subdural hematoma center analysis of 319 patients. blood coagul fibrinolysis. 2014 jun;25(4):353-9. 17.lingsma h, andriessen t, haitsema i, horn j, van der naalt j, franschman g, maas a, vos p, steyerberg e. prognosis in moderate and severe traumatic brain injury: external validation of the impact models and the role of extracranial injuries. j trauma acute care surg. 2013 feb;74(2):639-46. 18.maas a, hukkelhoven c, marshall l, steyerberg e. prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. neurosurgery. 2005 dec;57(6):1173-82; discussion 117382. 19.massaro f, lanotte m, faccani g, triolo c. one hundred and twenty-seven cases of acute subdural haematoma operated on. correlation between ct scan findings and outcome. acta neurochir (wien). 1996;138(2):185-91 20.mathew p, oluoch-olunya d, condon b, bullock r. acute subdural haematoma in the conscious patient: outcome with initial non-operative management. acta neurochir (wien). 1993;121(3-4):100-8 21.mauritz w, leitgeb j, wilbacher i, majdan m, janciak i, brazinova a, rusnak m. outcome of brain trauma patients who have a glasgow coma scale score of 3 and bilateral fixed and dilated pupils in the field. eur j emerg med. 2009 jun;16(3):153-8. 22.munro p, smith r, parke t. effect of patients’ age on management of acute intracranial haematoma: prospective national study. bmj. 2002;325:1001-1006. 23.phuenpathom n, choomuang m, ratanalert s. outcome and outcome prediction in acute subdural hematoma. surg neurol. 1993; 40:2225 24.seelig j, becker d, miller j, greenberg r, ward j, choi s. traumatic acute subdural hematoma: major mortality reduction in comatose patients treated within four hours. new engl j med. 1981;304:1511-1518. 25.servadei f, nasi m, giuliani g, cremonini a, cenni p, zappi d, taylor g. ct prognostic factors in acute subdural haematomas: the value of the 'worst' ct scan. br j neurosurg. 2000 apr;14(2):110-6. 26.stone j, rifai m, sugar o, lang r, oldershaw j, moody r. subdural hematomas. i. acute subdural hematoma: progress in definition, clinical pathology, and therapy. surg neurol. 1983 mar;19(3):216-31. 27.taussky p, hidalgo e, landolt h, fandino j. age and salvageability: analysis of outcome of patients older than 65 years undergoing craniotomy for acute traumatic subdural hematoma. world neurosurg. 2012 sep-oct;78(3-4):306-11 28.tian h, chen s, xu t, hu j, rong b, wang g, et al. risk factors related to hospital mortality in patients with isolated traumatic acute subdural hematoma: analysis of 308 patients undergone surgery. chin med j 2008;121:1080–1084. 29.tien h, jung v, pinto r, mainprize t, scales d, rizoli s. reducing time-to-treatment decreases mortality of trauma patients with acute subdural hematoma. ann surg. 2011 jun;253(6):1178-83. 30.van beek j, mushkudiani n, steyerberg e, butcher i, mchugh g, lu j, marmarou a, murray g, maas a. prognostic value of admission laboratory parameters in traumatic brain injury: results from the impact study. j neurotrauma. 2007 feb;24(2):315-28. 31.wilberger j, harris m, diamond d. acute subdural hematoma: morbidity and mortality related to timing of operative intervention. j trauma. 1990 jun;30(6):733-6. 32.wong c. criteria for conservative treatment of supratentorial acute subdural haematomas. acta neurochir 1995;135:38-43. 33.yanaka k, kamezaki t, yamada t, takano s, meguro k, nose t. acute subdural hematoma : prediction of outcome with a linear discriminant function. neurol med chir (tokyo) 1993;33:552–558. 34.zhao h, bai x. influence of operative timing on prognosis of patients with acute subdural hematoma. chin j traumatol. 2009 oct;12(5):296-8. doi: 10.33962/roneuro-2023-026 endoscopic endonasal transsphenoidal surgery for pituitary adenomas. a single centre initial experience mahmut sertdemir, fatih erdi romanian neurosurgery (2023) xxxvii (2): pp. 150-154 doi: 10.33962/roneuro-2023-026 www.journals.lapub.co.uk/index.php/roneurosurgery endoscopic endonasal transsphenoidal surgery for pituitary adenomas. a singlecentre initial experience mahmut sertdemir, fatih erdi necmettin erbakan university, meram faculty of medicine, department of neurosurgery, konya, turkey abstract endoscopic endonasal transsphenoidal surgery (eets) is a widely accepted technique for the surgical resection of pituitary tumours. in this report, we present our singlecentre experience with eets for pituitary adenomas, mainly focusing on its efficacy and postoperative complications. among 100 patients who underwent eets, 57 (57%) were female and 43 were (43%) male. the mean age of the patients was 51.55 ± 13.51 years. nonfunctional adenoma was found in 61 (61%) patients, acromegaly was found in 29 (29%) patients, cushing’s disease in six (6%), and prolactinoma was found in four (4%) patients. on average, a 75.8% decrease in the postoperative tumour volume was observed in nonfunctional adenomas. surgical cure was achieved in 51.7% of patients with acromegaly, 50% of those with cushing’s disease, and 25% of those with prolactinoma. the most common postoperative complication was found to be cerebrospinal fluid fistula. introduction pituitary adenomas, accounting for 10%–15% of all primary intracranial tumors, develop from the adenohypophysis and are considered benign neoplasms.1 the prevalence of pituitary adenoma was reported to be between 1/865 and 1/2688 persons in different clinical studies.2-4 despite their benign nature, pituitary adenomas may cause significant morbidity and mortality because of their endocrine activity and mass effect.5 the diagnosis, treatment, and follow-up of pituitary adenomas require a multidisciplinary approach, including neurosurgery, endocrinology, and radiosurgery. the primary aim in the surgical treatment of pituitary adenomas is to excise the tumor without damaging the surrounding anatomical structures. initially, the transcranial surgical approach was adopted in treating pituitary adenomas. however, less invasive methods have been developed later on because of the high morbidity and mortality rates associated with this method.6 recently, the endonasal approach for the surgical excision of pituitary adenomas has gained great popularity and has been considered the “gold standard.”7 currently, the endoscopic endonasal transsphenoidal surgery (eets) technique, keywords adenoma, endoscopy, pituitary, transsphenoidal corresponding author: fatih erdi necmettin erbakan university, meram faculty of medicine, department of neurosurgery, konya, turkey mferdinrs@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 151 endoscopic endonasal transsphenoidal surgery for pituitary adenomas which provides a wide panoramic view of the surgical field and anatomical structures, has become a preferred surgical method.8,9 in this study, we report our initial experience with eets in patients with pituitary adenoma, mainly focusing on its efficacy and postoperative complications. materials and methods study population in this study, 100 patients diagnosed with pituitary adenoma who underwent eets at our clinic between february 2014 and december 2020 were included. patients with missing data, pediatric cases, and those operated with the transcranial route were excluded from the study. the records of the patients included in this study were retrospectively reviewed, and their clinical, radiological, and biochemical findings were recorded. microadenomas were defined as adenomas that have a maximum diameter of 10 mm, and macroadenomas were defined as those with a diameter of at least 10 mm. tumor volumes were calculated by measuring the largest tumor diameters in the axial, sagittal, and coronal axes in the cranial magnetic resonance imaging (mri), as described previously in macroadenomas.10 all patients with nonfunctional adenoma underwent cranial mri within the first 3 months after surgery, and the postoperative volumetric decrease was calculated. the knosp grade of the tumor was determined using preoperative mri.11 the efficacy of surgical treatment in functional adenomas was evaluated according to the pituitary diseases diagnosis, treatment and follow-up guideline published by the society of endocrinology and metabolism of turkey.12 accordingly, in patients with acromegaly, a serum growth hormone level of <0.4 µg/l at the third month after surgery was accepted as a marker of surgical remission and a value of <1 µg/l was accepted as a marker of surgical control of the disease. in patients with cushing’s disease, a morning serum cortisol level of <2 µg/dl within the first week after the operation was accepted as surgical remission. initial remission was defined as a measured prolactin level that had returned to normal.13 the study protocol was approved by the local ethics committee (2021/3019), and written informed consent was obtained from all participants or their legal successors. surgical procedure all patients underwent eets under general anesthesia by the same surgical team. neuroradiological images of the patients were analyzed before the procedure. computed tomography of the paranasal sinuses was examined to evaluate the sellar access route and to detect pathologies related to this pathway. anatomical relationships between the internal carotid arteries (icas) and pituitary adenomas were evaluated. any suprasellar and intrasellar vascular pathologies were excluded. in the operating room, the patients were placed in the supine position, and their head was fixed using a skull clamp. image guidance was used in all patients using the medtronic ®stealthstation (medtronic, mn, usa) surgical navigation system. subsequently, the patient’s face, both nasal cavities, and abdominal region were cleaned with povidoneiodine solution. the vasoconstrictor agent, adrenaline, was applied to the nasal mucosa. the surgical procedures were performed through the binostril approach with a diameter of 4 mm, length of 18 cm, and rigid scopes of 0° and 30° (karl storz gmbh & co. kg, tuttlingen, germany), and related endoscopic skull base instruments were used. initially, the middle nasal turbinate was accessed by passing the lower turbinate and choanae. the middle nasal turbinate was dissected laterally using a dissector, and the surgical corridor was established. then, the superior turbinate was accessed by moving posteriorly between the middle turbinate and the septum. the natural ostium of the sphenoid sinus was identified between the superior turbinate and the septum. then, the vomer was opened, and a binostril corridor was achieved. the anterior wall of the sphenoid sinus was opened following clear identification of the sphenoid ostium. using a kerrison rongeur or micro-drill, the anterior wall of the sphenoid sinus was opened laterally. the mucosa covering the sellar floor was excised. then, the base of the sella and neighboring structures were revealed. then, the base of the sella was opened and widened using a micro-drill and kerrison rongeur, and the dura mater was exposed. to not damage the icas, intraoperative doppler ultrasonography was performed, as necessary. after 152 mahmut sertdemir, fatih erdi that, the dura mater was incised and opened using scalpel blades and micro-scissors. the tumor was identified and evacuated using an aspirator, ring curettes, and micro-forceps (fig. 1). if cerebrospinal fluid (csf) leakage was observed during the procedure, fat and fascia grafts taken from the abdomen were placed on the field. additional nasoseptal flaps, which were prepared in early stages of the operation, were engrafted in some cases (particularly those with large macroadenomas). multilayer closure was achieved, and the operation was terminated. figure 3 different stages of the endoscopic endonasal approach in a case of macroadenoma. a: revealing the osseous structures belonging to the base of the sella. b: opening of the dura and excision of the tumor. c: control of the residual tumor. d: sagging of the diaphragm sella toward the surgical field after radical resection. statistical analysis statistical package for the social sciences, version 22.0, was used for data analysis. categorical data are expressed as numbers and percentages, while continuous data are presented as means ± standard deviations. results among the 100 patients who underwent eets, 57 (57%) were female, and 43 (43%) were male, and the mean age of the patients was 51.55 ± 13.51 years. macroadenoma was detected in 84 (84%) patients, and microadenoma was found in 16 (16%) patients. nonfunctional adenoma was found in 61 (61%) of the operated patients, acromegaly in 29 (29%), cushing’s disease in six (6%), and prolactinoma in four (4%). when the patients were classified according to their sex, among female patients, 34 (59.6%) had nonfunctional adenoma, 16 (28.1%) had acromegaly, five (8.8%) had cushing’s disease, and two (3.5%) had prolactinoma. meanwhile, among male patients, nonfunctional adenoma was found in 27 (62.8%), acromegaly in 13 (30.2%), cushing’s disease in one (2.3%), and prolactinoma in two (4.7%). of all patients, 25 (25%) had knosp stage 0 lesions, 23 (23%) had knosp stage 1 lesions, 16 (16%) had knosp stage 2 lesions, seven (7%) had knosp stage 3a lesions, nine (% 9) had knosp stage 3b lesions, and 20 (20%) had knosp stage 4 lesions. patients with nonfunctional adenomas the mean preoperative volume of nonfunctional adenomas was 9.84 ± 9.79 cm³, which decreased to 2.35 ± 3.79 cm³ within the first 3 postoperative months. when the preoperative and postoperative volumes were compared, on average, there was a 75.8% decrease in the tumor volume postoperatively. patients with acromegaly surgical remission was achieved in six (20.7%) of the 29 patients with acromegaly, and surgical control was achieved in 15 (51.7%) patients. of the patients with surgical remission, four had microadenomas and two had macroadenomas. again, of the 15 patients with surgical control, eight had microadenomas and seven had macroadenomas. patients with cushing’s disease and prolactinoma according to the criteria stated in the methods section, remission was achieved in three (50%) of the six patients with cushing’s disease, and all cured patients had microadenomas. surgical remission was achieved in only one (25%) of the four patients with prolactinoma who underwent surgery. all patients with prolactinoma were found to have macroadenomas, which were resistant to medical therapy. postoperative complications permanent di occurred in one patient with acromegaly and one patient with cushing’s disease, who all had microadenomas. these patients received desmopressin treatment, which was adjusted after endocrinology consultation. 153 endoscopic endonasal transsphenoidal surgery for pituitary adenomas postoperative rhinorrhea was observed in eight (8%) patients within the first month after surgery. csf leakage was ceased with external lumbar drainage in three patients. two patients underwent reoperation, and the remaining three patients underwent both external lumbar drainage and endoscopic reoperation. all csf leaks were treated successfully using these methods. meningitis occurred in two patients and was treated with appropriate antibiotics. discussion in this study, we presented our single-center experience with eest, a widely used technique for the surgical resection of pituitary adenomas. in our series of 100 patients with pituitary adenomas, we observed a reasonable remission rate, low incidence of postoperative complications, and no mortality. this study contributes to the current literature regarding the safety and efficacy of eets. the demographic characteristics of our study population revealed a mean patient age of 51.55±13.51 years and female preponderance. these findings were comparable with the data reported in previous surgical series for pituitary adenomas.9,14,15 furthermore, our findings demonstrated that 84% of the study group had macroadenomas and 61% had nonfunctional adenomas. in a previous surgical series, eseonu et al. have reported that 71.6% of their patients had macroadenomas and 63.6% had nonfunctional adenomas.14 in another series, singh et al. have reported that 86% of their patients had macroadenomas and 79% had nonfunctional adenomas.9 all these data show that our patient group had similar demographic and clinicopathological features with those in previous surgical series in the literature. transsphenoidal surgery is the primary therapeutic option for pituitary adenomas, except for prolactinomas, and is associated with high remission rates, particularly in patients with microadenomas (80%–90%).5,16 we evaluated the preoperative and postoperative tumor volumes in patients with nonfunctional adenomas and found a 75.8% decrease in tumor volume postoperatively. similarly, eseonu et al. have reported a 85.1% decrease in tumor volume postoperatively using the eets technique in a previous study.14 in our patient group, surgical control was achieved in 51.7% of patients with acromegaly. in a similar series, including patients with acromegaly, yildirim et al. have reported that biochemical remission was achieved in 80.0% of patients with microadenomas and 64.7% of patients with macroadenomas. the total remission rate was found to be 66.1%.17 in another series, hazer et al. have revealed that biochemical cure was achieved in 62.6% of patients with acromegaly following eets.18 all these data suggest that eets is associated with a reasonable remission rate in patients with acromegaly and that there are minor differences between different series regarding its efficacy. in addition to its efficacy, eets has also shown to be associated with low complication rates following the surgical removal of pituitary tumors.19,20,21 csf leakage, di, vascular complications, hypopituitarism, meningitis, and visual complications were most commonly reported complications in other series.5,19 in our patient group, we detected rhinorrhea because of csf leakage in 8% of the patients. all these patients were successfully managed with endoscopic repair and/or external lumbar drainage. in previous reports, csf leakage following eets was reported in 2.4%–24% of patients.20,22 death is a rare complication of eets and usually occurs because of carotid artery injury and meningitis.5,19 no carotid injury was observed in our series. this report has some limitations. first, this was a single-center study and has a retrospective nature, lacking prospective follow-up data. this situation restricts the generalization of the results of this study. second, there was no control group of patients operated with another surgical technique, such as microscopic endonasal transsphenoidal surgery, to compare perioperative outcomes of eets. however, we suggested that eets is a safe and efficient method for treating pituitary adenomas. although learning is relatively steep, augmented experience and throughout knowledge of the neurosurgical anatomy make significant differences. conclusions eets is an effective technique frequently used for resecting pituitary tumors. this report revealed that eets is associated with a good remission rate, low incidence of postoperative complications, and low mortality rates. these findings support the previous 154 mahmut sertdemir, fatih erdi data regarding the safety and efficacy of eets for the surgical treatment of pituitary adenomas. references 1. terada t, kovacs k, stefaneanu l, et al. incidence, pathology, and recurrence of pituitary adenomas: study of 647 unselected surgical cases. endocr pathol. 1995 winter;6(4):301-10. pubmed pmid: 12114812. epub 1995/01/01. 2. tjornstrand a, gunnarsson k, evert m, et al. the incidence rate of pituitary adenomas in western sweden for the period 2001-2011. eur j endocrinol. 2014 oct;171(4):519-26. pubmed pmid: 25084775. epub 2014/08/03. 3. agustsson tt, baldvinsdottir t, jonasson jg, et al. the epidemiology of pituitary adenomas in iceland, 19552012: a nationwide population-based study. eur j endocrinol. 2015 nov;173(5):655-64. pubmed pmid: 26423473. epub 2015/10/02. 4. daly af, rixhon m, adam c, et al. high prevalence of pituitary adenomas: a cross-sectional study in the province of liege, belgium. j clin endocrinol metab. 2006 dec;91(12):4769-75. pubmed pmid: 16968795. epub 2006/09/14. 5. molitch me. diagnosis and treatment of pituitary adenomas: a review. jama. 2017 feb 7;317(5):516-24. pubmed pmid: 28170483. epub 2017/02/09. 6. collins wf. hypophysectomy: historical and personal perspective. clin neurosurg. 1974;21:68-78. pubmed pmid: 4608911. epub 1974/01/01. 7. nishioka h. recent evolution of endoscopic endonasal surgery for treatment of pituitary adenomas. neurol med chir (tokyo). 2017 apr 15;57(4):151-8. pubmed pmid: 28239067. pubmed central pmcid: pmc5409268. epub 2017/02/28. 8. swearingen b. update on pituitary surgery. j clin endocrinol metab. 2012 apr;97(4):1073-81. pubmed pmid: 22337908. epub 2012/02/18. 9. singh a, grewal ss, kumar n. endoscopic endo-nasal trans-sphenoidal excision of pituitary tumors: an institutional experience. indian j otolaryngol head neck surg. 2018 mar;70(1):98-101. pubmed pmid: 29456951. pubmed central pmcid: pmc5807291. epub 2018/02/20. 10. chuang cc, lin sy, pai pc, et al. different volumetric measurement methods for pituitary adenomas and their crucial clinical significance. sci rep. 2017 jan 18;7:40792. pubmed pmid: 28098212. pubmed central pmcid: pmc5241871. epub 2017/01/18. 11. knosp e, steiner e, kitz k, et al. pituitary adenomas with invasion of the cavernous sinus space: a magnetic resonance imaging classification compared with surgical findings. neurosurgery. 1993 oct;33(4):610-7; discussion 7-8. pubmed pmid: 8232800. epub 1993/10/01. 12. pituitary study group. pituitary diseases diagnosis, treatment and follow-up guideline. in karaca z editor. the society of endocrinology and metabolism of turkey, 2022, ankara, turkey 13. wilson cb. surgical management of pituitary tumors. j clin endocrinol metab. 1997 aug;82(8):2381-5. pubmed pmid: 9253304. epub 1997/08/01. 14. eseonu ci, refaey k, rincon-torroella j, et al. endoscopic versus microscopic transsphenoidal approach for pituitary adenomas: comparison of outcomes during the transition of methods of a single surgeon. world neurosurg. 2017 jan;97:317-25. pubmed pmid: 27742515. epub 2016/10/16. 15. hsu c-p, chang c-k, chiang m-f, et al. endoscopic endonasal trans-sphenoidal approach for pituitary fossa tumor: outcome analysis of 39 consecutive procedures. journal of cancer research and practice. 2016;3(2):39-44. 16. ammirati m, wei l, ciric i. short-term outcome of endoscopic versus microscopic pituitary adenoma surgery: a systematic review and meta-analysis. j neurol neurosurg psychiatry. 2013 aug;84(8):843-9. pubmed pmid: 23243265. pubmed central pmcid: pmc3717601. epub 2012/12/18. 17. yildirim ae, sahinoglu m, divanlioglu d, et al. endoscopic endonasal transsphenoidal treatment for acromegaly: 2010 consensus criteria for remission and predictors of outcomes. turk neurosurg. 2014;24(6):906-12. pubmed pmid: 25448208. epub 2014/12/03. 18. hazer db, isik s, berker d, et al. treatment of acromegaly by endoscopic transsphenoidal surgery: surgical experience in 214 cases and cure rates according to current consensus criteria. j neurosurg. 2013 dec;119(6):1467-77. pubmed pmid: 24074496. epub 2013/10/01. 19. singh h, essayed wi, cohen-gadol a, et al. resection of pituitary tumors: endoscopic versus microscopic. j neurooncol. 2016 nov;130(2):309-17. pubmed pmid: 27161249. epub 2016/11/03. 20. o'malley bw, jr., grady ms, gabel bc, et al. comparison of endoscopic and microscopic removal of pituitary adenomas: single-surgeon experience and the learning curve. neurosurg focus. 2008;25(6):e10. pubmed pmid: 19035697. epub 2008/11/28. 21. goudakos jk, markou kd, georgalas c. endoscopic versus microscopic trans-sphenoidal pituitary surgery: a systematic review and meta-analysis. clin otolaryngol. 2011 jun;36(3):212-20. pubmed pmid: 21752205. epub 2011/07/15. 22. karppinen a, kivipelto l, vehkavaara s, et al. transition from microscopic to endoscopic transsphenoidal surgery for nonfunctional pituitary adenomas. world neurosurg. 2015 jul;84(1):48-57. pubmed pmid: 25731792. epub 2015/03/04. 10_baritchii_impactofsurgery romanian neurosurgery (2015) xxix 3: 291 304 291 the impact of surgery in high grade gliomas a literature review adriana baritchii1, a. gubian1,*, st.i. florian1,2 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery 2cluj county emergency hospital, department of neurosurgery *student abstract: malignant gliomas are aggressive brain cancers. after many decades of intensive research they represent a major cause of cancer related mortality and morbidity. management of malignant gliomas is very difficult. none of the current treatments are curative. high grade gliomas are optimally treated with surgery followed by radiotherapy and chemotherapy. the impact of surgery on progression free survival and overall survival was a constant preoccupation and debate for decades among neurosurgeons. different studies published in the last 25 years have provided evidence that the extent of resection of high grade gliomas can influence time to progression and median survival, although so far there is no class i prospective randomized trial to fully answer this question. some of the most important studies are reviewed here. the modern neurosurgery relay on some tools that proved to be very helpful in guiding the surgeon to achieve the maximal tumoral cytoreduction with minimum impact on the brain’s eloquent areas. imri has been proved to be safe and became an important tool during tumor surgery, used alone or in conjuction with other important techniques: intraoperative neurophysiology, awake cortical mapping, 5-ala fluorescence etc. although so far the prognostic of high grade gliomas is still disappointing, further understanding of the biology of these tumors and a patient-tailored treatment could be the keys of finding a cure in the future. introduction malignant gliomas are aggressive brain cancers. after many decades of intensive research high grade gliomas represent a major cause of cancer related mortality and morbidity. they are the most common primary brain tumors and account for about of 2% of all cancers. [36, 23]. due to the fact that glial cells undergo mitosis, they can present with abnormal proliferation, which may result in glial tumors. the origin of the tumor is thought to be a common pluripotent neuro-ectodermal precursor. this cell has the ability to differentiate along the astrocytic lineage, up to a grade iv. primary glioblasomas are tumors that appear de novo [10]. the world health organization classifies the glial tumors into four grades. grade i is reserved for special types of astrocytomas that are better delineated. the more typical astrocytic neoplasm is graded ii through iv. there are some histological criteria that affect the prognosis like: cellularity, presence of giant cells, anaplasia, mitosis, vascular proliferation with or without endothelial proliferation, necrosis and pseudopalisading [42]. grades iii and iv are the malignant ones. 292 baritchii et al the impact of surgery in high grade gliomas they represent approximately 70% of all gliomas and affect predominantly patients between 40 and 70 years [33]. glioblasoma multiforme (grade iv) is the most aggressive primary brain tumor. despite all the effort of trying to improve the treatment, the median survival is 12-15 months, with a 2 year survival rate of 15% up to 26% [49]. currently there are no prevention strategies for malignant gliomas, except reducing the exposure of the head to high doses ionizing radiation. among other studied risk factors supposed to be involved in the development of this type of brain tumors (radiation, chemical carcinogens, infection/ viruses) only radiation exposure has been established to be causal [35, 58]. some genetic syndromes, for exemple lifraumeni, are also more frequent associated with the development of malignant gliomas [35]. management of malignant gliomas is very difficult. none of the current treatments are curative [40]. recent studies concentrate on understanding the molecular mechanism and gene mutation. combined with clinical trials this work will be able to provide us a new promising and individual approach. standard treatment consist of maximal surgical resection, radiotherapy and concomitant and adjuvant chemotherapy with temozolomide [43,15]. among all the treatment option available for malignant gliomas the surgery is the first step and maybe the most important one. beside the fact that it provides tumoral tissue for pathological examination and reduces the tumor volume and edema, surgery also serve the purpose of treating the patient with bcnu implantable wafers and also developing in vitro drug sensitivity assay with the goal of predicting the clinical response to chemotherapy. surgery how much the first step in the treatment of malignant gliomas is the surgery. the mechanical cytoreduction of the tumor mass can help the patient to gain some time for other therapeutic intervention (radiotherapy, chemotherapy). the beneficial effect of tumor resection was observed both on cerebral blood flow and metabolism even at distant sites of the tumor. 30 to 60 g of tumor mass will create a neurologic symptom while 100 g of tumor is lethal. a 90% resection of a 50 g (5x 1010 cells) tumor theoretically reduces the tumor burden to 5 g (5 x 109 cells). after the total resection of the gadolinium enhancing regions on mri 1 g of tumor (or 1x 109 cells) may be left in place. the other therapies are also involved in the tumor destruction: radiotherapy can kill two logs of cells while chemotherapy is believed to destroy one to two logs of cells. the body immune system will reduce the tumor burden to less than 1x105 cells [32]. although tumor cytoreduction appears to be vital, the presence of the viable tumor cells beyond the enhancing margins of the tumora cause for future recurrences explain why surgery is more effective as part of multimodality treatment strategy [27,14] the impact of surgery of high grade gliomas on progression free survival and overall survival was a constant preoccupation and debate for decades among neurosurgeons. the infiltrative nature of these tumors makes impossible the curative resection. a wider margin resection coupled with adjuvant therapy creates the condition of delaying the recurrence and prolonging the survival [4]. an early retrospective study by simpson et al [47] included 645 patients with glioblastoma from the radiations therapy oncology group database. the authors analyzed the survival with respect to known prognostic factors, such as age and karnofsky performance status, as well as extent of surgery, site, and size. the median survival was 11.3 months in patients with complete resection, 10.4 months for partial resection and 6.6 months for biopsy only. some factors that offered survival benefit were identified: age romanian neurosurgery (2015) xxix 3: 291 304 293 <40, karnofsky performance score (kps)>70, frontal lobe location and total resection. the conclusion of the study was that biopsy only yields inferior survival to more extensive surgery for patients with glioblastoma multiforme treated with surgery and radiation therapy. in 2003 metcalfe and grant, after the research of 2100 documents, were unable to draw a conclusion, due to the fact that they didn’t found enough randomized data for analysis. the authors underlined the idea that treatment must be considered on an individual basis. although there was no good evidence that resection offers any clear advantage over biopsy, the indication of using biopsy for certain deep seated lesions is still standing, while small superficial placed frontal tumors can be resected completely with little difficulty [34]. evaluation of the extent of resection and its influence on the survival using a 5 aminolevulinic acida non-fluorescent prodrugwas described by stummer and al [50]. ala is a precursor of haemoglobin that leads to the synthesis of porphyrins in malignant gliomas. the intracellular accumulation of fluorescent porphyrins which appear in red fluorescence under blue lightenable more complete resection of contrastenhancing tumour.. 322 adult patients with radiographically suspected malignant gliomas were randomized, comparing cytoreductive surgery using ala (n=161) versus conventional white light (n=161). the authors concluded that surgery using 5-aminolevulinic acid enabled more complete resections of contrast-enhancing tumor. this was associated with a significant improvement in progression-free survival in patients with newly diagnosed malignant glioma undergoing cytoreductive surgery. one of the most comprehensive studies that attempt to find a correlation between the extent of the resection and survival comes from lacroix et al [26]. 416 patients who underwent resection for glioblastoma over a period of 6 years were included. the tumoral volume pre and postoperative was assessed using computer assisted image analyses. five independent predictors of survival were identified by the authors following multivariate statistical analyses: age, karnofsky performance scale (kps) score, extent of resection, and the degree of necrosis and enhancement on preoperative mr imaging studies. when a resection of 98% or greater of the tumor was achieved a significant survival advantage was associated. the median survival was 13 months in patients with gross or near gross total resection (98% or greater) compared with 8.8 months for patients with less than 98% resection (p=0.02). a clinical outcome scale ranging from 0 to 5 was proposed based on age, kps and radiographic evidence of necrosis. a significantly improved survival was observed in patients with lower scores (1-3) who underwent aggressive resections and a trend toward slightly longer survival was found in patients with higher scores (4-5). this study supports the concept of aggressive cytoreductive surgery as part of the management of high grade gliomas, yet not at the expense of neurologic function or surgical complications. starting from almost 3 decades ago some authors suggested that partial tumor resection could be associated with a greater risk in terms of postoperative neurological worsening compared with radical resection or stereotactic biopsy. today is very well known that partial resection of glioblastoma carries significant risk of postoperative haemorrhage and edema so called wounded glioma syndrome. in the series of ciric et al [8] 42 patients with supratentorial gliomas were studied pre and postoperatively with ct scan. a gross total or nearly gross total resection was performed in the majority of patients (86%). the postoperative neurological status was stabile or improved in 97% of these patients. 40% of patients with partial resection presented a 294 baritchii et al the impact of surgery in high grade gliomas neurological worsening after the operation. fadul et al [13] examinated prospectively morbidity and mortality in 104 patients who underwent surgery for supratentorial gliomas. the authors reported that patients with complete resection had fewer acute neurologic complications and no greater risk of being neurologically impaired at 1 week compared with patients that were treated with biopsy or less extensive procedures. another retrospective analysis performed on 66 patientsvecht et al [55]found that extensive surgery was correlated with a better immediate postoperative performance, a lower onemonth mortality rate and a longer survival in high grade gliomas. because of the retrospective nature of the study the authors concluded that a more extensive surgery does not lead to more postoperative neurological deterioration. abrudan et al [1] published a study on 266 patients showing that age and type of surgery were prognostic factors that significantly influenced the survival at 12, 18 and 24 months. the authors found that the global survival rate was 47 % at 12 months, 26,3% at 18 months and 16,7% at 24 months and the difference of mean survival at 12, 18 and 24 months monitoring was 2,8 months, 4,4 months and 5,1 months respectively for the patients that underwent gross total resection of the tumor. this study adds a new argument in favor of maximal cytoreductive surgery whenever possible. although the management of elderly patients with high grade gliomas is mainly focused on the optimal use of radiotherapy and chemotherapy, it is important first to address the patient to neurosurgical resection. age and number and severity of additional illness are vital when considering the extent of resection in older patients, due to surgical risks and potential postoperative complication. there are some useful data regarding management of high grade gliomas in elderly patients, namely those over 65 years. in the study of vuorinen et al [56] 30 patients older than 65 years were randomized into two groups: stereotactic biopsy and open craniotomy and resection of the tumor. ultimately only 23 tumors proved to be a malignant glioma (19 glioblasoma and 4 anaplastic astrocytoma). 13 patients had a stereotactic biopsy and in 10 cases a resection was performed. all the patients were referred to radiotherapy. the estimated median survival time was 85 days in the first group compared with 171 days in the second one. the estimated survival time was 2.757 longer after tumor resection. radiotherapy had a significant effect on survival (p= 0.001). the authors didn’t find a significant difference in the time of deterioration between these two treatment (p=0.057) and concluded that in this population the survival was improved by the resection of the tumor although the overall benefit is modest [56]. in 2010 chaichana et al [7] reported a retrospective study were they found that patients who underwent surgical resection had median survival of 5.7 months, while patients who underwent needle biopsy without resection had median survival of 4.0 months. for patients aged 70 years and older median survival was 4.5 months for 26 patients with surgical resection as compared with 3.0 months for 26 patients who underwent needle biopsy (p = 0.03). the authors found no significant differences in postoperative outcomes among the two groups. as a conclusion this study demonstrates that older patients tolerate aggressive surgery without increased surgery-related morbidity and have prolonged survival as compared with similar patients undergoing needle biopsy. a study of zouaoui et al [59] in 2014 describes oncological patterns of care, prognostic factors, and survival for patients with glioblastoma multiforme older than 70 years in france. 265 patients were included. 95 of them underwent surgical resection and 107 biopsy. adjuvant therapy was also performed chemotherapy alone (ct), radiotherapy alone romanian neurosurgery (2015) xxix 3: 291 304 295 (rt) or concomitant radiochemotherapy (crc). in the group of patients with biopsy median survival was 199 days in those who received only ct, 318 days in those who received crc and 149 days in patients who received rt. in the group of patients that underwent surgical resection the median survival (in days) was as following: 245 with ct, 372 with crc and 26 with rt. a hypothesis of the authors was that elderly patients are undertreated. the authors concluded that karnofsky performance status seems to be the most relevant clinical predictive factor and rs and crc have a positive impact on survival for elderly gbm patients in the general population, at least when feasible. mariniello et al [31] compared the effects of combined treatments (surgery and radiochemotherapy) on the outcome and survival between elderly (≥ 65 years) patients with glioblastoma and younger ones (<65 years). the median survival of older patients was 14.5 months, significantly lower than patients < 65 years (17 months) (p = 0.02). the conclusion of the study was that when several criteria of selection to surgery are respected (good karnofsky performance status (kps), largely resecable tumor, and no significant co morbidity) the difference of survival is less significant. age is one of the most important prognostic factor in patients diagnosed with malignant gliomas. a study of uzuka et al [54] suggested that postoperative kps score is an important prognostic factor for glioblastoma patients aged ≥ 76 years. based on statistical analyses of 79 glioblastoma patients aged ≥ 76 years (median age 78.0 years; 34 men and 45 women) that were treated with tumor resection or biopsy followed by chemotherapy or radiotherapy, the authors reported a median overall progression free survival of 6.8 months and a median overall survival of 9.8 months. patients aged ≥ 78 years were significantly less likely to receive radiotherapy (p = 0.004) and patients with a postoperative kps score of ≥ 60 were significantly more likely to receive maintenance chemotherapy (p = 0.008). two independent prognostic factors were identified: postoperative kps score ≥ 60 ( p = 0.017) and temozolomide therapy (p < 0.001) konqlund et al [24] included in their study 80 patients over 60 years old diagnosed with high grade gliomas and operated at oslo and haukeland university hospitals between 2008-2009. clinical outcome was assessed at six months and overall mortality at 2 years. surgical morbidity included neurological sequels (10%), postoperative hematomas (3.8%), hydrocephalus (1.3%) while the surgical mortality reported was 1.3%. median overall survival was 8.4 months. adjuvant radiochemotherapy increased significantly the survival. in univariate analyses couple of factors were identified to reduce survival: age ≥ 80 years, subtotal resection, american society of anesthesiology (asa) scores 3-4, karnofsky performance scale (kps) < 70, and mini-mental state examination (mmse) score < 25. authors conclusions were that surgical treatment of high grade gliomas carries low mortality and acceptable morbidity in patients aged ≥ 60 years and maximum tumor resection should be attempted. the benefit of total tumor resection in elderly patients is supported by others studies in the literature. after analyzing 437 patients ≥70 years scott et all [45] identified 4 prognostic subgroups with markedly different median survivals: subgroup i =patients <75.5 years of age who underwent surgical resection (9.3 months); subgroup ii = patients ≥75.5 years of age who underwent surgical resection (6.4 months); subgroup iii = patients with karnofsky performance status of 70 to 100 who underwent biopsy only (4.6 months); and subgroup iv = patients with karnofsky performance status <70 who underwent biopsy only (2.3 months). grossman et al [17] published a study aiming to compare surgical outcome of elderly patients undergoing 296 baritchii et al the impact of surgery in high grade gliomas awake-craniotomy to that of younger patients. a total of 334 young (45.4 ± 13.2 years, mean ± sd) and 90 elderly (71.7 ± 5.1 years) patients were studied. the authors found no significantly higher rate of mortality, or complications in the elderly group and concluded that gross total tumor resection in elderly patients with high grade was associated with prolonged survival. gulti et al [18] explored the survival and treatment provided to elderly patients diagnosed with glioblastoma in a population-based setting, from the norwegian cancer registry. 2882 patients who were diagnosed with glioblastoma between 1988 and 2008 were included. the following factors were identified as independent predictors of reduced survival: increasing age, no tumor resection, no radiotherapy, and no chemotherapy. in the authors opinion despite multimodal treatment the gain for the oldest seems at best very modest and the prognosis remains very poor. another study published in 2012 underlines the importance of total resection regardless of age. oszvalt et al [37] collected data from 361 patients with newly diagnosed cerebral glioblastoma. depending on tumor size, location and karnofski performance scale score the patients underwent resection (complete, subtotal and partial) or biopsy. after the surgery all the patients received adjuvant treatment. the overall survival of elderly patients (>65 years) (9.1 ± 11.6 months) was significantly lower than that of younger patients (<65 years) (14.9 ± 16.7 months; p = 0.0001). age was a negative prognostic factor in patients undergoing biopsy (4.0 ± 7.1 vs 7.9 ± 8.7 months; p = 0.007), but not in patients undergoing tumor resection (13.0 ± 8.5 vs 13.3 ± 14.5 months; p = 0.86), which lead the authors to conclude that resection should not be withheld from patients only on the basis of age. one of the most extensive study comparing biopsy, partial resection and gross total resection in older patients was published by almenawer et al at the beginning of this year [2]. the authors undertook a meta-analysis of the outcome, overall survival (os), postoperative karnofsky performance status (kps), progression-free survival (pfs), mortality, and morbidity in patients over 60 years old after the surgical procedure. 12607 participants from 34 studies were included. when comparing the tumor resection (of any extent) with biopsy overall survival (md 3.88 mo, p < .001), postoperative kps (md 10.4, p < .001), progression free survival (md 2.44 mo, p < .001), mortality (rr = 0.27, p = .002), and morbidity (rr = 0.82, p = .514) were in favor of the resection group. gross total resection was found to be superior to subtotal resection in terms of overall survival (md 3.77 mo, p < .001), postoperative kps (md 4.91 mo, p = .016), and progression free survival (md 2.21 mo, p < .001) with no difference in mortality (rr = 0.53, 95% ci: 0.05-5.71, p = .600) or morbidity (rr = 0.52, 95% ci: 0.181.49, p = .223). these findings support the idea of increasing extent of safe resection in elderly patients, which can lead to an upward improvement in survival time, functional recovery, and tumor recurrence rate at this group of age (>60 years). recurrent glioma resection has also been debated in the literature and there are many class iii studies that show the improvement of survival with re-resection. a study of rostomily et al [41] was focused on 51 adult patients with recurrent malignant gliomas that were treated in a phase ii trial of multidrug chemotherapy. 31 patients underwent radical tumor resection before chemotherapy. higher karnofsky scores, lower grade initial histology, lack of prior chemotherapy, greater degree of myelotoxicity, smaller postoperative tumor volumes, greater extent of surgical resection, and a local versus diffuse recurrence pattern were associated with a longer overall median time to tumor progression. the overall median survival time was increased in patients with higher karnofsky scores, lower grade romanian neurosurgery (2015) xxix 3: 291 304 297 histology at the time of recurrence, greater degree of myelotoxicity and lobar versus deep tumor location. helseth et al [19], after studying 516 patients with glioblastoma who underwent primary surgery in 2003-2008 found an overall survival (os) of 9.9 months and negative prognostic factors like increasing age, poor neurological function, bilateral tumor involvement, biopsy instead of resection, and radiotherapy alone compared to temozolomide chemoradiotherapy. the authors concluded that in a carefully selected group of patients, repeat surgery significantly prolongs os. park et al [38] based on clinical and radiographic data of 34 patients who underwent re-operation of recurrent gbm tumors validated a preoperative scale that identifies patients likely to have poor, intermediate, and good relative outcomes after surgical resection. the authors found that the factors associated with poor postoperative survival were: tumor involvement of prespecified eloquent/critical brain regions (p = .021), karnofsky performance status (kps) < or = 80 (p = .030), and tumor volume > or = 50 cm (3) (p = .048). sughrue et al [53] published a paper where they showed that repeat surgery for glioblastoma is beneficial in many cases providing the patient with a satisfying disease free period but is difficult to reliably predict who these patients are. useful tools in the surgical treatment of high grade gliomas the use of intra operative fluorescence in gliomas surgery is a recent innovation. in living mammalian cells 5-ala is a natural biochemical precursor for heme synthesis [12]. each cell metabolizes 5-ala along a set pathway toward heme production. the synthesis of the endogenous fluorescent molecule, protoporphyrin ix (ppix), is induced through metabolic conversion in the mitochondria [5]. given via oral route 5 ala does not usually cross the intact blood-brain barrier but it can easily pass through the disrupted bbb found in gliomas [51]. the principle is simple: 5-ala acts as a diagnostic fluorescent marker; given orally it assists the surgeons to visualize directly the extent of tumor resection when lighting up the operative field with a specific wavelength light source. the tumor cells that accumulates ppix can be easily discerned from the surrounding normal cell. the fluorescent dye peak is 2-6 hours after oral administration and disappears from the tumor tissue after 12 hours [28]. 5-ala mediated-photodynamic therapy (5 ala mediated pdt) has revealed a promising adjuvant tool in the treatment of malignant gliomas [43]. the rapid pdt response in vivo is due to three types of mechanisms: 1. pdt can directly damage and kill the cancer cells; 2. alteration of the tumoral blood flow: stasis, vascullar collapse/ leakage; 3. the induction of an inflammatory response due to the release of cytokines and other inflammatory mediators from target cells [30]. other studies have shown that 5–ala pdt causes mitochondrial and nuclear dna damage with cytochrome c release and activation of caspase-3 and caspase-9 in glioma cells [22]. the lack of randomized controlled trials and an optimal 5-ala-pdt regimen may be the reason why 5-ala-pdt is not a standard treatment for malignant gliomas. some challenging side effects that neurosurgeons have to deal with are cerebral edema and long-lasting skin photosensitivity. 5-alapdt could be regarded as a promising alternative in glioma treatment if the specificity and selectivity of 5-ala-pdt in glioma tissue would be improved [28]. hirschberg et al [21] evaluated the effects of 5-aminolevulinic acid (ala)-mediated photodynamic therapy (pdt) on the invasiveness of human glioma cells migrating from implanted multicell human tumor spheroids. the authors found that 5-ala mediated pdt inhibited the invasiveness of 298 baritchii et al the impact of surgery in high grade gliomas the gliomal cells by a migratory inhibition effect rather than by a cytotoxic one a study of puppa et al [9] showed that 5ala guided resection of high grade gliomas permits an overall gross total resection of 90% in 100% of patients, and 98% in 93% of patients. in the same study the authors found that in 43% of patients the boundaries of fluorescent tissue exceeded those of tumoral tissue detected by neuronavigation and concluded that 5-ala fluorescence in the surgery of high grade gliomas enables a gross total resection in 100% of cases even if selection of patients remains a main bias. stummer et al [52] published a study where they showed that fluorescence appears superior to contrast enhancement on mri for indicating residual tumor. a systemic review and meta-analysis of 10 studies from the literature made by zhao et al [58] showed a level 2 evidence of superior efficiency of fluorescence guided resection to neuronavigation guided surgery with respect to diagnostic accuracy, extent of tumor resection, safety and survival. finally, a study of slof et al [48] showed that 5-ala guided resection is a cost effective option for the treatment of high grade gliomas. intra operative mri (imri) is an imaging tool used primarily to increase the extent of tumour resection (eotr) while minimizing the impact of the surgery on the brain’s eloquent areas. with stereotactic frameless neuro-navigation, imri shows changes occuring in the brain as the resection goes on. this is very important as changes occur during the resection: brain shift diminishes, the effect of gravity may be different than on the pre-op scans, etc. those factors render the “conventional” navigation inaccurate and the extent of resection may suffer from it. a review by liang and schulder [29] showed that imri enabled a significant increase of eotr, and was a safe tool used in combination with other techniques such as intra-operative neurophysiology, awake cortical mapping, 5-ala fluorescence, etc. for the treatment of high grade gliomas. the same ideea is supporterd by schatlo et al [44] in a recent article focusing on the impact of gross total resection on progression and survival in patients with high-grade glioma and how this can be achieved using imri in combination with 5-ala. although some studies like the one published by senft et al [46] showed evidence supporting the use of the technology in gliomas, other studies seem to disapprove this use or at least to show its limits. it is the case of kubben et al [25] which states that there is, at best, a level 2 evidence to support the use of this technology compared with conventional neuronavigation-guided surgery in increasing eotr, enhancing quality of life, or prolonging survival after resection of glioblastoma multiforme. on the other side imri is an extremely expensive technology and require the upgrading of the operating room, thus inducing a huge cost to the health system. intra operative mapping is a technique which aims to delimitate the tumoral margins and thus to limitate the resection to non eloquent tissues. it is of great importance because of the infiltrative nature of gliomas, where these lesions not only grow but also migrate along white matter tracts. this technique helps maximize the extent of tumor resection while minimizing postsurgical morbidity, in order to increase the median survival as well as to preserve quality of life [11]. a review from garrett et al [16] shows the utility of this technique in the resection of gliomas in eloquent brain regions. another study of hervey-jumper sl et al [20] analyzed retrospectively a single surgeon experience on 859 patients undergoing awake brain tumor surgery between 1986 and 2014. perioperative risk factors like asa classification, body mass index, smoking status, psychiatric or emotional history, seizure frequency and duration and tumor site, size, and pathology were assessed. the overall perioperative romanian neurosurgery (2015) xxix 3: 291 304 299 complication rate was 10% and the authors concluded that awake brain tumor surgery can be safely performed with extremely low complication and failure rates. brown et al [6] found that awake craniotomy results in a shorter hospital stay and less frequent postoperative deficits compared with general anesthesia. the data collected retrospectively from 1970 until 2012 suggests an expanded role for awake craniotomy in brain tumor surgery regardless of tumor location. different techniques used for functional mapping of the brain have largely replaced invasive techniques such as awake craniotomy [39]. non invasive evaluation of the brain include bold-functional mri (fmri) magnetoencephalography (meg), and transcranial magnetic stimulation (tms). a case study by asim f. choudri et al [3] showed that tri-modality functional brain mapping allows non-invasive localization of motor, sensory, and language centers as well as white matter pathways helping the surgical planning. conclusions after three decades of intensive research the prognosis for patients with hggs is still disappointing. the infiltrative nature of these cancers precludes a surgical cure but nevertheless surgery remains the first and more important step for achieving a good quality of life. different studies published in the last 25 years have provided evidence that the extent of resection of high grade gliomas can influence time to progression and median survival, although so far there is no class i prospective randomized trial to fully answer this question. a maximal resection is preferred but not with any cost. the standard of care for elderly patients with high grade gliomas remains controversial and undefined. although high grade gliomas can develop at any age, elderly population represents half of the glioblastoma population. the increasing age remains the most powerful negative prognostic factor in high grade gliomas, being related with less favorable tumor biology, less aggressive care and co morbid disease in order to achieve a maximum resection current concept of surgical decision-making takes in consideration multimodal pre and intraoperative information. imri has been proved to be safe and became an important tool during tumor surgery. used in conjuction with other important techniques, such as intraoperative neurophysiology, awake cortical mapping, 5-ala fluorescence etc., imri can help the surgeon to obtain the highest levels of tumor resection while minimizing neurologic injury. references 1. abrudan c, cocis adriana , cernea dana, suciu b , cheptea marinela , florian i. st.. surgery of high grade gliomas pros in favor of maximal cytoreductive surgery. romanian neurosurgery (2011) xviii 1: 38 – 53 2.almenawer sa, badhiwala jh, alhazzani w, greenspoon j, farrokhyar f, yarascavitch b, algird a, kachur e, cenic a, sharieff w, klurfan p,gunnarsson t, ajani o, reddy k, singh sk, murty nk. biopsy versus partial versus gross total resection in older patients with high grade glioma: a systematic review and metaanalyses. neuro oncol. 2015 jan 3. pii: nou349. [epub ahead of print]. 3. asim f. choudhri, shalini narayana,roozbeh rezaie,matthew t. whitehead, samuel s. mcafee, samuel s. wheless, frederick a. boop, andrew c. papanicolaou . same day tri-modality functional brain mapping prior to resection of a lesion involving eloquent cortex: technical feasibility. neuroradiol j. 2013 nov; 26(5): 548–554 4.boon-chuan pang, wei-hwang wan, cheng-kiang lee, kathleen joy khu,wai-hoe ng. the role of surgery in high-grade glioma – is surgical resection justified?a review of the current knowledge:ann acad med singapore 2007;36:358-63. 5. bottomley, s. s, & muller-eberhard, u. (1988). pathophysiology of heme synthesis. seminars in hematology. 0037-1963, 25(4), 282-302. 6. brown t, shah ah, bregy a, shah nh, thambuswamy m, barbarite e, fuhrman t, komotar rj. awake craniotomy for brain tumor resection: the rule rather than the exception? j neurosurg anesthesiol. 2013 jul;25(3):240-7. 7.chaichana k l, garzon-muvdi t, parker s, weingart jd, olivi a, bennett r, brem h, a quinones-hinojosa 300 baritchii et al the impact of surgery in high grade gliomas a. supratentorial glioblastoma multiforme: the role of surgical resection versus biopsy among older patients, ann surg oncol (2010) published on-line in 10 august 2010 8.ciric i, ammirati m, vick n, mikhael m (1987). supratentorial gliomas: surgical considerations and immediate postoperative results. gross total resection versus partial resection. neurosurgery 21: 21 ± 26. 9. della puppa, a., ciccarino, p., lombardi, g., rolma, g., cecchin, d., & rossetto, m. (2014, january 24). 5aminolevulinic acid fluorescence in high grade glioma surgery: surgical outcome, intraoperative findings, and fluorescence patterns. biomed res int. 2014; 2014: 232561. 10.diamandis p., sacher a.g., tyers m., dirks p.b. new drugs for brain tumors? insights from chemical probing of neural stem cells. med hypotheses. 2009 jun;72(6):683–687. 11. duffau h . brain mapping in tumors: intraoperative or extraoperative? epilepsia. 2013 dec;54 suppl 9:79-83. 12. eljamel, m. s, goodman, c, & moseley, h. (2008). ala and photofrin fluorescenceguided resection and repetitive pdt in glioblastoma multiforme: a single centre phase iii randomised controlled trial. lasers in medical science. 0268-8921, 23(4), 361-367. 13.fadul c, wood j, thaler h, galicich j, patternson rh, jr, posner jb. morbidity and mortality of craniotomy for the excision of supratentorial gliomas. neurology 1988;38:1374–9. 14.fransen p., tribolet n. surgery of supratentorial tumors. current opinion in oncology. 1993;5: 450 ± 457 15.furnari fb, fenton t, bachoo rm, mukasa a, stommel jm, stegh a, et al. malignant astrocytic glioma: genetics, biology, and paths to treatment. genes dev. nov 1 2007;21(21):2683-710. 16. garrett, m., pouratian, n., & liau, l. (2012, july 1). use of language mapping to aid in resection of gliomas in eloquent brain regions. neurosurg clin n am. 2012 jul; 23(3): 497–506. 17.grossman r, nossek e, sitt r, hayat d, shahar t, barzilai o, gonen t, korn a, sela g, ram z. outcome of elderly patients undergoing awake-craniotomy for tumor resection. ann surg oncol. 2013 may;20(5):17228. 18.gulati s1, jakola as, johannesen tb, solheim o. survival and treatment patterns of glioblastoma in the elderly : a population based study. world neurosurg. 2012 nov;78(5):518-26 19.helseth r, helseth e, johannesen tb, langberg cw, lote k, ronning p, et al. overall survival, prognostic factors, and repeated surgery in a consecutive series of 516 patients with glioblastoma multiforme. acta neurol scand 2010;122:159-67. 20. hervey-jumper sl1, li j, lau d, molinaro am, perry dw, meng l, berger ms. awake craniotomy to maximize glioma resection: methods and technical nuances over a 27-year period. j neurosurg. 2015 apr 24:1-15 21. hirschberg, h. (2006, december). effects of alamediated photodynamic therapy on the invasiveness of human glioma cells. lasers surg med. 2006 dec;38(10):939-45. http://www.statistics.gov.uk/statbase/product.asp?vlnk= 8843 22. inoue, h, kajimoto, y, shibata, m. a, miyoshi, n, ogawa, n, miyatake, s, otsuki, y, & kuroiwa, t. (2007). massive apoptotic cell death of human glioma cells via a mito‐ current applications of 5–ala in glioma diagnostics and therapy http://dx.doi.org/10.5772/52428 257 chondrial pathway following 5-aminolevulinic acid-mediated photodynamic thera‐ py. j neurooncol. 0016-7594x, 83(3), 223-231 23. kohler, b. a. et al. annual report to the nation on the status of cancer, 1975–2007, featuring tumors of the brain and other nervous system. j. natl cancer inst.2011;103, 714–736. 24.konglund a1, helseth r, lund-johansen m, helseth e, meling tr. surgery of high grade gliomas in the aging. acta neurol scand. 2013 sep;128(3):185-93. 25. kubben, p., & al, e. (2011, october 12). intraoperative mri-guided resection of glioblastoma multiforme: a systematic review. lancet oncol. 2011 oct;12(11):1062-70 26.lacroix m, abi-said d, fourney dr et al (2001) a multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. j neurosurg 95(2):190–198 3. 27.laws jr er. radical resection for the treatment of glioma. clin neurosurg 1995;42: 480-487. 28. lei teng, mitsutoshi nakada, yutaka hayashi, takeshi yoneyama, shi-guang zhao and jun-ichiro hamada (2013). current applications of 5-ala in glioma diagnostics and therapy, clinical management and evolving novel therapeutic strategies for patients with brain tumors, dr. terry lichtor (ed.), isbn: 978953-51-1058-3, intech, doi: 10.5772/52428. available from: http://www.intechopen.com/books/clinicalmanagement-and-evolving-novel-therapeutic-strategiesfor-patients-with-brain-tumors/current-applications-of-5ala-in-glioma-diagnostics-and-therapy 29. liang d, schulder m. the role of intraoperative magnetic resonance imaging in glioma surgery. surg neurol int.2012;3:320–7. [pubmed] 30. macdonaldi.j. & dougherty, t.j. ((2001). basic principles of photodynamic therapy. j porphyr phthalocya. 1088-4246, 5(2), 105-129. 31.mariniello g, peca c, de caro mdel b, giamundo a, donzelli r, maiuri f. glioblastoma in the elderly: the impact of advanced age on treatment and survival. j neurol surg a cent eur neurosurg. 2014 jul;75(4):27681. romanian neurosurgery (2015) xxix 3: 291 304 301 32.max kole and jack rock malignant glioma surgery: complication avoidance neurosurgery quarterly. 2002 ;12(3):251–258. 33.mb1 no 37–cancer registration statistics. 2006. 34.metcalfe se, grant r (2003) biopsy versus resection for malignant glioma (cochrane review). the cochrane library 35.ohgaki h., kleihues p. epidemiology and etiology of gliomas. acta neuropathol. 2005 jan;109(1):93–108 36. ohgaki, h. & kleihues, p. population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas. j. neuropathol. exp. neurol.2005; 64,479–489. 37.oszvald a, güresir e, setzer m, vatter h, senft c, seifert v, franz k. glioblastoma therapy in the elderly and the importance of the extent of resection regardless of age. j neurosurg. 2012 feb;116(2):357-64. 38.park jk, hodges t, arko l, shen m, dello iacono d, mcnabb a, olsen bailey n, kreisl tn, iwamoto fm, sul j, auh s, park ge, fine ha, black pm. scale to predict survival after surgery for recurrent glioblastoma multiforme. j clin oncol. 2010 aug 20;28(24):3838-43. 39. pillai jj, zaca d, choudhri a. clinical impact of integrated physiologic brain tumor imaging. technol cancer res treat. 2010;9(4):359–380. [pubmed] 40.preusser m, de ribaupierre s, wohrer a, et al. current concepts and management of glioblastoma. ann neurol. jul 2011;70(1):9-21. 41.rostomily rc, spence am, duong d, mccormick k, bland m, berger ms. multimodality management of recurrent adult malignant gliomas: results of a phase ii multiagent chemotherapy study and analysis of cytoreductive surgery. neurosurgery 1994;35:378-88. 42.russell d. s., rubenstein l. j. pathology of tumors of the nervous system. william and wilkins, baltimore, 5th ed., 1989: pp 83-161. 43.sathornsumetee s, reardon da, desjardins a, quinn ja, vredenburgh jj, rich jn. molecularly targeted therapy for malignant glioma. cancer. jul 1 2007;110(1):13-24. 44. schatlo b, fandino j, smoll nr, wetzel o, remonda l, marbacher s, perrig w, landolt h, fathi ar . outcomes after combined use of intraoperative mri and 5-aminolevulinic acid in high-grade glioma surgery. neuro oncol. 2015 apr 8. 45.scott jg, bauchet l, fraum tj, nayak l, cooper ar, chao st, suh jh, vogelbaum ma, peereboom dm, zouaoui s, mathieu-daudé h, fabbro-peray p,rigau v, taillandier l, abrey le, deangelis lm, shih jh, iwamoto fm. recursive partitioning analysis of prognostic factors for glioblastoma patients aged 70 years or older. cancer. 2012 nov 15;118(22):5595-600 46. senft c, bink a, franz k, vatter h, gasser t, seifert v. intraoperative mri guidance and extent of resection in glioma surgery: a randomised, controlled trial. lancet oncol.2011;12:997–1003. [pubmed] 47.simpson jr, horton j, scott c, curran wj, rubin p, fischbach j, et al. influence of location and extent of surgical resection on survival of patients with glioblastoma multiforme: results of three consecutive radiation therapy oncology group (rtog) clinical trials. int j radiat oncol biol phys 1993;26:239-44 48. slof, j., & al, e. (2014, january 24). costeffectiveness of 5-aminolevulinic acid-induced fluorescence in malignant glioma surgery. neurologia. 2015 apr;30(3):163-8 49. soderberg-naucler c, rahbar a, stragliotto g. survival in patients with glioblastoma receiving valganciclovir. nejm. sep 5 2013;369(10):985-6. 50.stummer w, pichlmeier u, meinel t, wiestler od, zanella f, reulen hj (2006) fluorescence-guided surgery with 5-aminolevulinic acid for resection of malignant glioma: a randomised controlled multicentre phase iii trial. lancet oncol 7(5):392–401 51. stummer, w, reulen, h. j, novotny, a, stepp, h, & tonn, j. c. (2003). fluorescenceguided resections of malignant gliomas--an overview. acta neurochir suppl. no. 0065-1419, 88, 9-12. 52.stummer, w., & al, e. (2014, march 1). 5aminolevulinic acid-derived tumor fluorescence: the diagnostic accuracy of visible fluorescence qualities as corroborated by spectrometry and histology and postoperative imaging. neurosurgery. 2014 mar; 74(3): 310–320. 53.sughrue me1, sheean t, bonney pa, maurer aj, teo c.aggressive repeat surgery for focally recurrent primary glioblastoma: outcomes and theoretical framework. neurosurg focus. 2015 mar;38(3):e11. 54.uzuka t, asano k, sasajima t, sakurada k, kumabe t, beppu t, ichikawa m, kitanaka c, aoki h, saito k, ogasawara k, tominaga t, mizoi k, ohkuma h,fujii y, kayama t; tohoku brain tumor study group. treatment outcomes in glioblastoma patients aged 76 years or older: a multicenter retrospective cohort study. j neurooncol. 2014 jan;116(2):299-306. 55.vecht cj, avezaat cj, van putten wl, eijkenboom wm, stefanko sz the influence of the extent of surgery on the neurological function and survival in malignant glioma. a retrospective analysis in 243 patients. j neurol neurosurg psychiatry (1990)53(6):466–471. 56.vuorinen v, hinkka s, farkkila m, jaaskelainen j (2003) debulking or biopsy of malignant glioma in elderly people—a randomised study. acta neurochir (wien) 145(1):5–10 11. 57.wrensch m., bondy m. l., wiencke j. et al. environmental risk factors for primary malignant brain tumor: a review. j. neurooncol 1993;17:47-64. 58. zhao, s., & al, e. (2013, may 28). intraoperative fluorescence-guided resection of high-grade malignant gliomas using 5-aminolevulinic acid-induced porphyrins: a systematic review and meta-analysis of prospective studies. plos one. 2013; 8(5): e63682. 302 baritchii et al the impact of surgery in high grade gliomas 59.zouaoui s1, darlix a, fabbro-peray p, mathieudaudé h, rigau v, fabbro m, bessaoud f, taillandier l, ducray f, bauchet f, wager m, faillot t, capelle l,loiseau h, kerr c, menei p, duffau h, figarellabranger d, chinot o, trétarre b, bauchet l. oncological patterns of care and outcomes for 265 elderly patients with newly diagnosed glioblastoma in france. neurosurg rev. 2014 jul;37(3):415-23. moscotesalazar_traumaticsubarachnoid romanian neurosurgery (2016) xxx 2: 277-283 | 277 traumatic subarachnoid pleural fistula in children: case report, algorithm and classification proposal luis rafael moscote-salazar, osvaldo koller, sergio valenzuela, claudia cataldo, juan jose marengo, gabriel campos, jose joaquin muller, cristobal vergara department of pediatric neurosurgery, “asenjo” institute of neurosurgery, santiago, chile abstract: subarachnoid pleural fistulas are rare. they have been described as complications of thoracic surgery, penetrating injuries and spinal surgery, among others. we present the case of a 3-year-old female child, who suffer spinal cord trauma secondary to a car accident, developing a posterior subarachnoid pleural fistula. to our knowledge this is the first reported case of a pediatric patient with subarachnoid pleural fistula resulting from closed trauma, requiring intensive multimodal management. we also present a management algorithm and a proposed classification. the diagnosis of this pathology is difficult when not associated with neurological deficit. a high degree of suspicion, multidisciplinary management and timely surgical intervention allow optimal management. key words: subarachnoid pleural fistula, spinal cord trauma, dura mater, polytrauma introduction traumatic subarachnoid pleural fistulas are an infrequent connection between the pleura and subarachnoid space. the diagnosis is difficult when not associated with neurologic deterioration. there are few cases reported in the literature and their current management is controversial (1, 2, 3) we present the case of a female child who was surgically managed in our service for a subarachnoid pleural fistula secondary to a dorsal column fracture. upon review of the clinical and fundamental neuroradiologic characteristics, we propose a classification strategy and present a management algorithm, as well as the therapeutic options for this kind of injury. clinical case a 3-year-old patient was admitted in the asenjo neurosurgery institute (chile), for assessment and management, after being diagnosed with a politraumatism. no medical or surgical history was relevant, not pharmacological history. on the physical examination paraplegia was found. there were 278 | moscote-salazar et al traumatic subarachnoid pleural fistula in children no alterations on the cranial nerves. spine ct showed a fracture on d2-d3 (figures 1a and 1b). magnetic resonance imaging confirmed the injuries that were seen in the ct (figures 2a and 2b). the injury produced compression of the dural sac, which was treated with arthrodesis and placement of transpedicular fixation. subsequently, transparent fluid drainage through the pleurostomy was present, therefore the presence of cerebrospinal fluid was suspected. a myelography was performed and the diagnosis of subarachnoid pleural fistula was confirmed (3). a new neurosurgical intervention was performed by posterior approach at dural level and a 360-degree injury was identified. it was corrected with an adipose tissue graft, dura mater patch and fibrin seal. during the intervention, significant bleeding occurred and transfusion of two globular packages were required. at the same time a lumbar drainage was placed that stayed there for a week. after the surgery, progressive decrease of cerebrospinal fluid through the pleurostomy was seen, this was retired on the 7th day. the patient showed satisfactory progress, and a dorsal lumbar orthosis was placed. the patient was discharged with an intensive rehabilitation scheme. on the posterior controls the patient has presented satisfactory evolution with motor deficit reduction. figure 1a dorsal spine ct, coronal cuts, showing fracture in the body of vertebrae t2 romanian neurosurgery (2016) xxx 2: 277-283 | 279 figure 1b dorsal spine ct, axial cuts, showing fracture in the body of vertebrae t2 figure 2a dorsal spine mri, sagittal cuts with vertebral involvement figure 2b dorsal spine mri, coronal cuts, showing fracture in the body of vertebrae t2 figure 3 myelography showing subarachnoid pleural fistula. the white arrow points the contrast material leak from subarachnoid space into pleural space 280 | moscote-salazar et al traumatic subarachnoid pleural fistula in children figure 4 dorsal spine mri, sagittal cuts, posterior to surgery, decompression of dural sac is seen discussion the first case of subarachnoid pleural fistula was reported on 1959 by milloy and cols (4). subarachnoid pleural fistulas are pathologic continuities between the spinal canal and pleural cavity, and require the production of a sprain in the region adjacent to the dura mater and pleura. the primary causes of such fistulae are; post-surgical, iatrogenic or traumatic. these injuries are rare, with few reported cases in the english literature. (5, 6, 7, 8, 9, 10). in this case, as reported by other authors, the release of vertebral fragments may be the cause of dural injury. in the literature, most of them have been cause by traumatic events and by surgical complications. election of the treatment strategy is the hardest challenge in these cases. some authors have mentioned that surgical repair is essential in these injuries. in our case, surgical resolution was definitive. (11, 12, 13, 14, 15, 16, 17, 18). this case illustrates a unique multidisciplinary treatment strategy applied to a subarachnoid pleural fistula secondary to pediatric trauma. among the complementary tests to confirm the existence of a fistula is pleural fluid analysis, evaluating the characteristics of a serous clear with few cells, normal glucose and low protein content. the measure of ferritin in cerebrospinal fluid may be useful, although false negative results may be present. the mechanism of persistence of a subarachnoid pleural fistula is linked to respiration, as intrapleural negative pressure during respiration pulls cerebrospinal fluid into the pleural space. beta-2-transferrin is a protein that is produced by the activity of neuraminidase in the brain and it’s found in cerebrospinal fluid and perilymph of internal ear, becoming an important marker for cerebrospinal fluid fistulas. sensitivity of beta2-transferrin ranges from 94%-100% and specificity ranges from 98%-100%. although infrequently reported in the literature, it can be utilized as a non-invasive strategy in the romanian neurosurgery (2016) xxx 2: 277-283 | 281 pediatric patient. (19) among the surgical techniques to be used, the election depends on the size and extension of the dural injury. in those cases, where there are few available autologous tissues, fibrin and methyl methacrylate seals may be used. in those cases, where extensive injury is present with complete sac translocation, the injury may be repaired by bonding the proximal part of the sac to the medullar spine. it’s interesting that all the surgical techniques reported have been effective to repair the injury without recurrences, the injury in this case was repaired with a graft of lipid tissue and fibrin seals, obtaining similar results. (20, 21, 22, 23, 24, 25) traditional post-surgery management based on bed rest and seriated lumbar punctures are also usual in these injuries. in this case, we used as a complementary measure, a continuous lumbar drainage. (26, 27, 28, 29). as described, lumbar drainage offers advantages such as: decreased repeated invasive procedures and continuous decompression of subarachnoid space. we propose a management algorithm as outlined in diagram 1. a classification of these injuries was published by liang and coworkers; they define type i fistulas as being the most frequent, associated with cerebrospinal fluid and pleural effusion; and type ii fistulas as less frequent, associated with tension pneumothorax and subarachnoid outpouring. we consider this classification to be impractical as it doesn’t allow to plan the therapeutic approach. (14) we propose a classification for subarachnoid pleural fistulas, based in the literature; we consider type a fistulas those that are only evidenced by imaging methods; type b, low output that will resolve spontaneously, and depending on the etiology type b fistulas may be divided into b1, b2 and b3; type c are those with high output and may be classified in c1, c2 and c3. this is a practical classification that will help the neurosurgeon, thoracic surgeon and spine surgeon to define these injuries facilitating better management. table i subarachnoid pleural fistulas classification • type a fistulas evidenced by image studies. mri. • type b fistulas active fistula. low output. resolve spontaneously. o b1 – related to closed thoracic trauma. o b2 – related to open thoracic trauma. o b3 – non-associated to high-energy trauma. • type c fistulas – active fistula. high output. higher degree of severity. o c1 – related to closed thoracic trauma. o c2 – related to open thoracic trauma. o c3 – non-associated to high-energy trauma. 282 | moscote-salazar et al traumatic subarachnoid pleural fistula in children diagram 1 management algorithm suspected subarachnoid pleural fistula ct mielography and/or ct cisternographyfistula? β2-transferrin lumbar drainage for 5 to 7 days lumbar peritoneal shunt open surgery/direct approach discard pleural effusion or hemothorax yesno no yes active fistula? active fistula? conclusions subarachnoid pleural fistulas are a rare complication of diverse traumatic, tumor or iatrogenic injuries. this classification and management algorithm offers a simple management approach for these unusual injuries and the classification proposal allows describing each injury. correspondence dr. luis rafael moscote e-mail: mineurocirujano@aol.com references 1.labadie el, hamilton rh, lundell dc, bjelland jc. hypoliquorreic headache and pneumocephalus caused by thoraco-subarachnoid fistula. neurology 1977;27:9935. 2.assietti r, kibble mb, bakay rae. iatrogenic cerebrospinal fluid fistula to the pleural cavity: case report and literature review. neurosurgery 1993;33:1104-8. 3.quereshi nm, roble dc, gindin ra, et al. subarachnoid-pleural fistula. case report and review of the literature. j thorac cardiovasc surg 1986;91:238-41 4. milloy fj, correll no, langston ht. persistent subarachnoid-pleural space fistula; report of a case. j am med assoc 1959; 169:1467. 5. campos ba, silva lb, ballalai n, negrão mm. traumatic subarachnoid-pleural fistula. j neurol neurosurg psychiatry. 1974 mar;37(3):269–270. 6. beutel ew, roberts jd, langston ht, barker wl. subarachnoid-pleural fistula. j thorac cardiovasc surg. 1980 jul;80(1):21–24. 7.overton mc, 3rd, hood rm, farris rg. traumatic subarachnoid-pleural fistula. case report. j thorac cardiovasc surg. 1966 may; 51(5):729–731. romanian neurosurgery (2016) xxx 2: 277-283 | 283 8. bramwit dn, schmelka dd. traumatic subarachnoidpleural fistula. radiology. 1967, oct;89(4):737–738. 9.zilkha a, reiss j, shulman k, schechter mm. traumatic subarachnoid-mediastinal fistula; case report. j neurosurg. 1970 apr;32(4):473–475. 10. cantu rc. value of myelography in thoracic spinal cord injuries. int surg. 1971 jul; 56(1):23–26. 11. higgins cb, mulder dg. traumatic subarachnoidpleural fistula. chest. 1972 feb;61(2): 189–190. 12. hofstetter kr, bjelland jc, patton dd, woolfenden jm, henry re. detection of bronchopleuralsubarachnoid fistula by radionuclide myelography: case report. j nucl med. 1977 oct;18(10):981–983. 13. depinto d, payne t, kittle ce. traumatic subarachnoid-pleural fistula. ann thorac surg. 1978 may;25(5):477–478. 14. liang mk, moore ee, williams am, marks jl. traumatic subarachnoid pleural fistula. j trauma 2008;65:1155-61. 15. lloyd c, sah sa. subarachnoid pleural fistula due to penetrating trauma. case report and review of literature. chest 2002; 122: 2252–56. 16. joanes v. iatrogenic cerebrospinal fluid fistula to the pleural cavity: case report and review of literature. neurosurgery 1994; july (35)(1): 171–72. 17. güllüpınar b , topaçoğlu h, subarachnoid pleural fistula due to gunshot wound turk j emerg med. 2014; 14(2): 87-89. 18. peter jc, rode h. traumatic subarachnoid pleural fistula. j trauma. 1993;34:303–304. 19.moorehead rj, spence raj, gibbons jrp, stevenson hm. traumatic subarachnoidpleural fistula. injury. 1985;16:482. 20. huggins jt, sahn sa. duro-pleural fistula diagnosed by beta2-transferrin. respiration 2003;70:423-5. 21.godley cd, mccabe cj, warren rl, rosenher ws. traumatic subaracnoid-pleural fistula: case report. j trauma 1995:38;808. 22.epstein bs, epstein ja. extra pleural intrathoracic apical traumatic pseudomennnningocele. ajr 1974:120;887. 23.osaka k, hanada h, watanabe h. traumatic intrathoracic meningocele (traumatic subarachnoidpleural fistula). surg neurol 1981:15;137. 24.zilkha a, reiss j, schulman k, et al. traumatic subarachnoid-mediastinal fistula: case report, j neurosurg 1970:32;473. 25.beutel ew, roberts jd, langston ht, barker wl. subarachnoid-pleural fístula. j thorac cardiovasc surg 1980:80;21. 26. higgins cb, mulder dg. traumatic subarachnoidpleural fístula. chest 1972:61;18. 27. lesoin f, delandsher e, thomas iii ce, viaud c, jomin m. persistent pleural effusion and traumatic subarachnoid-pleural fistula, lancet 1982:2;772. 28. wilson c, jumer m. traumatic spinal-pleural fistula. jama 1962:179;168. 29. lovaas me, castillo ro, deutschman cs. traumatic subarachnoid-pleural fistula. neurosurgery 1985:17;650. doi: 10.33962/roneuro-2023-007 black cumin 0.3 gram and 0.4 gram on apoptotic levels in cerebral contusions rattus norvegicus wistar tommy alfandy nazwar, farhad balafif, donny wisnu wardhana, muhammad annas, agus chairul anab, m. istiadjid e.s. romanian neurosurgery (2023) xxxvii (1): pp. 54-58 doi: 10.33962/roneuro-2023-007 www.journals.lapub.co.uk/index.php/roneurosurgery black cumin 0.3 gram and 0.4 gram on apoptotic levels in cerebral contusions rattus norvegicus wistar tommy alfandy nazwar1,2, farhad balafif1,2, donny wisnu wardhana1,2, muhammad annas2, agus chairul anab3, m. istiadjid e.s.4 1 division of neurosurgery. department of surgery. brawijaya university/saiful anwar hospital malang east java, indonesia 2 department of surgery. brawijaya university/saiful anwar hospital malang east java, indonesia 3 national hospital surabaya, indonesia 4 department of neurosurgery and plastic surgery. faculty of medicine, brawijaya university, malang, indonesia abstract background. apoptosis is one of the indicators to check for following brain damage. along with this trend, treatment in the form of herbal and phytopharmaca therapy is required more frequently to treat brain injury complications. black cumin possesses a function that opposes the apoptotic mechanism. objectives. this study sought to determine the effect of black seed on an animal model of brain damage using apoptotic measures. methods. four treatment groups were created from the experimental animals as follows: group bc1: for 7 days following the brain contusion, they were given [0.3 gram] g/kg bw of black cumin extract daily. group bc2: for 7 days following the brain contusion, they were given [0.4 gram] g/kg bw of black cumin extract daily. following the brain contusion, group k received 3 ml of nacl 0.9% daily for 7 days. the tunel dna fragmentation method was used to count the amount of apoptotic cells and analysis was conducted using anova with f-test and tukey hsd. results. the control group had the greatest amount of apoptosis at 30.4. apoptosis averages for bc1 (0.3 g), and bc2 (0.4 g) groups of rats were 25.0, and 18.8, respectively. black cumin anova test with apoptosis was present while a higher dose of black cumin will minimize the amount of apoptosis. conclusions. injecting black cumin extracts into rats with head injuries reduced apoptosis, albeit not significantly. in rats with experimental head injuries, black cumin extract induces a connection through the apoptosis mechanism. introduction the progression of a brain injury is not random, but rather a continuous process between primary and secondary brain injuries1. consequently, the initial diagnosis, treatment, and prognosis of brain injury are not keywords black cumin, cerebral contusion, apoptosis, neuronal injury corresponding author: tommy alfandy nazwar brawijaya university/saiful anwar hospital malang east java, indonesia nsubtommy@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 55 black cumin 0.3 and 0.4 grams on apoptotic levels in cerebral contusions simple, despite the fact that methods of diagnosis and management of brain injury are constantly evolving2. numerous research have demonstrated the advantages of black cumin seeds, which include analgesic, antibacterial, anti-inflammatory, antimicrobial, antioxidant, anti-pyretic, anti-tumor, immunomodulatory, and neuroprotective activities 3–5. experimental animals receiving black cumin seed extract for cerebral ischemia have lower levels of mda (malondialdehyde)6. black cumin prevents formaldehyde from causing neuronal apoptosis when administered to animals7. it is believed that black cumin inhibits calcium channel blockers, hence decreasing calcium flow8. black cumin research as a neuroprotectant in nontraumatic settings has been validated. black cumin has not yet been investigated as a neuroprotectant in models of head injury (cerebral contusion) or trauma. this study aimed to examine the effect of black cumin on apoptotic neuron cells following head damage in rattus norvegicus wistar rats. methods in this laboratory investigation, mice were utilized as the experimental animals, and the experiment was designed to be entirely randomized. the ethical clearance no. 351/kepkvii/2012 commission for health research ethics granted permission for this line of investigation. dr saiful anwar general hospital malang indonesia. four treatment groups were created from the experimental animals as follows: group bc1: for 7 days following the brain contusion, they were given [0.3 gram] g/kg bw of black cumin extract daily. group bc2: for 7 days following the brain contusion, they were given [0.4 gram] g/kg bw of black cumin extract daily. following the brain contusion, group k received 3 ml of nacl 0.9% daily for 7 days. the rattus norvegicus wistar strain was used in this experiment, and the average age and weight of the animals used were 12-14 weeks and 200-250 grams, respectively. the male experimental animal was in good health and was freely moving around. supplies needed to sustain experimental animals for 10 days. black cumin extract is manufactured by. salinity of seawater, typical of normal (0.9% saline) (otsuka). apoptosis examination material: mouse brain tissue, apoptec (proteinase-k enzyme, apoptag, dab liqud), assay diluent a, assay diluents b, tetramethyl benzidine (tmb) one step substrate reagent, stop solution. cerebral contusion model: cerebral contusion was done on experimental animals 9, which has been modified. a load of 0.2 kg was dropped through a cylindrical tube from a height of 0.8 m (impact energy of 1.6 joules) over the head of a stereotactic framemounted experimental animal. previously, 1 mg/kg of body weight (i.m.) of ketamine was administered intramuscularly to sedate the test animals 10. the tunel dna fragmentation method was used to count the amount of apoptotic cells and the results are as follows: slides were cleaned in pbs ph 7.4 and then treated with proteinase k (20 ug/ml) for 15 minutes at 37 °c. three times, each for five minutes, wash with pbs ph 7.4. 15 minutes of 3% h2o2 incubation. three times, each for five minutes, wash with pbs ph 7.4. typical commercially available black cumin extract formulations contain 100 mg/cc of a suspension prepared by dissolving 600 mg of black cumin extract from capsules in 6 cc of 0.9% nacl. group bc1 0.3 grams (g), and group bc2 0.4 grams (g) via nasogastric tube. following the administration of black cumin extract, specimen collection (harvesting) was performed on the seventh day for each group (n=5) in the study. infusions of ketamine at a dose of 1 mg/kg body weight were used to induce anesthesia. after performing a decapitation on the animal model, a ventriculostomy procedure with a spinal needle placed 27.3 mm in front of the central sulcus and 3 mm lateral to the fissure was used to withdraw cerebrospinal fluid from the animal model. half of the right and left brains were removed sterilely and placed in a petri dish with 10% formalin. the computation method utilizes spsstm software tools. a statistical analysis was conducted: examine the difference between black cumin extract treatments. in each group, analysis was conducted using anova with f-test and tukey hsd for multiple comparisons. results four treatment groups present data. the bc1 group fed black cumin at 0.3 g/kgbw, the bc2 group fed 0.4 g/kgbw, and the control group fed 0.9% 3cc ns. brain tissue on a macroscopic level from rats who had head trauma a head injury model was used for the experimental 56 tommy alfandy nazwar, farhad balafif, donny wisnu wardhana et al. group bc1, bc2, as well as the control, and it had an energy of 1.6 joules. a macroscopic examination of the animal model's brain tissue did not reveal any signs of cranial fracture, subdural hemorrhage, subarachnoid or intracerebral bleeding. on a macroscopic scale, there was no discernible difference between the treatments; more specifically, the structural characteristics of the brain parenchyma were identical across all treatment groups (figure 1). figure 1. shows a macro view of the parenchyma of rat brain tissue. after seven days of treatment with either black cumin (bc), the macroscopic picture of the rat brain parenchyma did not reveal any differences between the two groups. table 1. average and one way anova test for apoptosis treatment average standart deviation f value p 2,761 0,076 bc1 (0.3 g) 25,00 7,91 bc2 (0.4 g) 18,80 5,67 control 30,40 7,77 total 25,35 6,42 table description; from the table above, it was found that the control group had the highest degree of apoptosis (mean 30.40) bc1 (mean 25.00) and bc2 (mean 18.80). the results of the anova test with p=0.076 are not significant. the correlation between black cumin and the death of neurons (apoptosis) the analysis of tunnel apoptosis revealed that there were differences between the treatment groups, with the amount of apoptosis decreasing with increasing the dose of black cumin. the table shows that the quantity of apoptosis decreases with increasing doses of black cumin. comparing all of the groups of rats administered black cumin, the control group had the greatest amount of apoptosis at 30.4. apoptosis averages for bc1 (0.3 g), and bc2 (0.4 g) groups of rats were 25.0, and 18.8, respectively. the table below displays the outcomes of the black cumin anova test with apoptosis, even though descriptively it was discovered that the higher the dose of black cumin will minimize the amount of apoptosis. table 2 shows that no significant differences between treatments were found at the 0.05 level or lower, although descriptively, the control group and feeding normal saline caused the most apoptosis (average 30.4), the group bc1 with black cumin feeding 0.3 g/kg body weight per day for 7 days (average 25), and the group bc2 with (average 18.8). the difference between the means of apoptosis in each treatment group was not statistically significant, but p = 0.076 indicates that the risk of failure of 7 treatments in 100 clinical trials is extremely high. table 2. tukey hsd apoptosis test results treatment n subset alpha=0.05 1 bc1 5 18,8000 bc2 5 25,0000 control 5 30,4000 sig ,058 note: from the tukey hsd test, it appears that the three treatments have no significant difference even though they have different mean values. discussion in this experiment, a male rat rattus norvegicus weighing between 250 and 300 grams was employed. the choice of these experimental animals was made in accordance with kanter7 research. the low mortality rate of rats, cost-effectiveness, and simplicity of the brain contusion model all contribute to the usage of this experimental rodent11. in this particular experiment, only male experimental animals were utilized. when there is a difference between the sexes, the results will be different. xiap production was more in female rats than in male rats, resulting in reduced apoptosis in female rats compared to male rats. it is believed that increased estrogen levels in female rats contribute to higher xiap levels protein12 the head injury model was executed by impacting the head of the experimental animal with an energy of 1.6 joules, specifically by lowering a 200gram weight through a 0.80-meter-tall cylindrical pipe. this agrees with model of brain contusion of previous study10, which assumes an impact of 1.62– 1.89 joules. there is bleeding inside the skull (either subdural, subarachnoid, or intracerebral) but no visible fractures of the skull. increased permeability of the cerebral vasculature, decreased cerebral blood flow, and raised intracranial pressure are all 57 black cumin 0.3 and 0.4 grams on apoptotic levels in cerebral contusions possible outcomes of the contusion model. mild bleeding will start after 48 hours of impact. these animal models are reproducible and can be used to simulate mild or moderate head trauma in humans, depending on the weight of the load, the height of the fall, and the weight of the experimental animal. this study employs 1.6 joules of energy, hence the brain contusion model in this study is consistent with the usual cerebral contusion model10. using a probe, black cumin (bc) was administered orally using the following dosages: bc1 0.3 g/kgbw, bc2 0.4 g/kgbw, and a control with 3 cc normal saline. the 0.4 g/kg bw dosage is based on research conducted by kanter7. however, a dose of 0.3 grams per kilogram of body weight is a dose that falls between a low dose and a high dose7. since black cumin's use is predicated on the idea that scavengers need to be present before free radicals appear or are generated, it is administered as soon as possible after injury. after 4 hours post-traumatically, cerebrovascular leakage and inos/no expression both began to rise 11,13. when a person suffers a head injury, the intracranial pressure rises, which can alter the physiology of the brain. blood flow in the brain is interrupted, which can lead to ischemic processes and brain metabolic diseases. brain edema will result from secondary brain injury caused by this mechanism up to 48–72 hours after the incident. the load inside the skull will rise as a result. the process through which black cumin extract increases the quantities of endogenous proteins that has been researched focuses on its anti-oxidant properties. black cumin, which acts as a chelating agent against free radicals, boosts the activity of the acetylcholinesterase enzyme in the central nervous system14. in experimental chicken erythrocytes, black cumin administration dramatically decreased mda levels (p0.002) and increased gsh levels (p0.005)15. additionally, black cumin suppresses inflammation by inhibiting the 5-lipoxygenase enzyme, hence inhibiting different inflammatory leukotrienes. lps-induced inos (inducible nitric oxide synthase) expression is suppressed, resulting in decreased no generation by macrophages, which improves the inflammatory response and reduces cell damage due to fewer free radicals16. black cumin's anti-apoptotic effects were observed in this investigation; however, they were not statistically significant (p 0.076). the mechanism through which black cumin extract reduces neuronal cell death is currently unknown. the treatment of black cumin extract to rats with brain injuries was observed to reduce the levels of mda (malondialdehyde) p0.001, an end product of lipid membrane peroxidation, possibly through its anti-oxidant activity7. a dose of 0.4 g/kgbb black cumin extract was proven to dramatically reduce apoptosis (p0.0001) in a nontrauma model (formaldehyde induced neuronal damage). the tunel technique revealed brown apoptotic entities, which included condensed cytoplasm, degeneration of cell nuclei, and dark, picnotic nuclei. the mechanism of prevention of neuronal cell apoptosis inhibitory pathways has not been thoroughly disclosed in a study on the effect of black cumin extract as an anti-apoptotic neuron cell model of non-trauma. degenerative changes in neurons are typically accompanied by elevated oxidative stress. high oxidative metabolic ability, a high concentration of polyunsaturated fatty acids, and a low antioxidant capacity make the brain, and particularly the cortex and hippocampus, particularly vulnerable to oxidative stress13. thymoquinone (2-isopropyl-5methylbenzo-1,4-quinone), which makes about 30% of black cumin's composition, has been shown to promote apoptosis in colon carcinoma cells by upregulating the activation of the mapk pathway and erk and jnk signaling (mitogen). active protein kinases)17. thymoquinone can also initiate apoptosis by p53-dependent and p53-independent pathways in addition to these methods. thymoquinone is a double-edged blade that acts as both a proand an anti-oxidant due to its two potentials. thymoquinone may be reduced to semiquinone (1 electron) or thymohydroquinone, depending on the structure of the thymoquinone molecule (2 electrons). thymohydroquinone has anti-oxidant properties, whereas semiquinone has pro-oxidant properties17. this study found that giving black cumin extract to experimental rats with head traumas raised neuronal apoptotic levels. in experimental rats with head injuries, injection of black cumin extracts reduced apoptosis, albeit not significantly. in experimental rats with head injuries, treatment of black cumin extract causes a connection through apoptosis mechanism. it is necessary to do pharmacological study on the various methods of extracting black cumin in order to increase levels of 58 tommy alfandy nazwar, farhad balafif, donny wisnu wardhana et al. understanding regarding thymohydroquinone. to learn more about thymohydroquinone, pharmacological research on black cumin extraction methods is needed. acknowledgment the authors would like to thank of the contribution of all the members of the neurosurgery team in saiful anwar hospital rssa, malang, east java, indonesia. references 1. dash, h. h. & chavali, s. management of traumatic brain injury patients. korean j. anesthesiol. 71, 12–21 (2018). 2. graham, d., cooper p, & golfinos g ed. pathology of brain damage after head injury. (mcgraw-hill professional, 2000). 3. ismail, m. therapeutic role of prophetic medicine habbat el baraka (nigella sativa l.) a review. (2009). 4. roshan, abdullah khan, tazneem, & sadath ali. to study the effect of nigella sativa on various biochemical parameters on stress induced in albino rats. int. j. pharm. pharm. sci. 2, (2010). 5. padhye, s., banerjee, s., ahmad, a., mohammad, r. & sarkar, f. h. from here to eternity the secret of pharaohs: therapeutic potential of black cumin seeds and beyond. cancer ther. 6, 495–510 (2008). 6. hosseinzadeh, r., shokrieh, m. m. & lessard, l. damage behavior of fiber reinforced composite plates subjected to drop weight impacts. compos. sci. technol. 66, 61–68 (2006). 7. kanter, m. protective effects of nigella sativa on the neuronal injury in frontal cortex and brain stem after chronic toluene exposure. neurochem. res. 33, 2241– 2249 (2008). 8. najaran, z. t.-, hamid reza sadeghnia 1,2, , mozhgan asghari 3, & seyed hadi mousavi. neuroprotective effect of nigella sativa hydro alcoholic extract on serum/glucose deprivation induced pc12 cells death. physiol. pharmacol. 13, 263–270 (2009). 9. bates, j. f. & goldman-rakic, p. s. prefrontal connections of medial motor areas in the rhesus monkey. j. comp. neurol. 336, 211–228 (1993). 10. cernak, i. animal models of head trauma. neurorx j. am. soc. exp. neurother. 2, 410–422 (2005). 11. dohare, p., garg, p., sharma, u., jagannathan, n. r. & ray, m. neuroprotective efficacy and therapeutic window of curcuma oil: in rat embolic stroke model. bmc complement. altern. med. 8, 55 (2008). 12. bramlett, h. m. et al. sex differences in xiap cleavage after traumatic brain injury in the rat. neurosci. lett. 461, 49–53 (2009). 13. noor neveen, a. & iman, m. mourad. evaluation of antioxidant effect of nigella sativa oil on monosodium glutamate-induced oxidative stress in rat brain. j. am. sci. 6, (2010). 14. yassin, m. m. prophylactic efficacy of crushed garlic lobes, black seed or olive oils on cholinesterase activity in central nervous system parts and serum of lead intoxicated rabbits. turk. j. biol. (2005). 15. tuluce, y., halil özkol, & bünyamin söğüt. effects of nigella sativa l. on lipid peroxidation and reduced glutathione levels in erythrocytes of broiler chickens. cell membr. free radic. res. 1, (2009). 16. ilaiyaraja, n & khanum, f. nigella sativa l: a review of therapeutic applications. j. herb. med. toxicol. (2010). 17. el-najjar, n. et al. reactive oxygen species mediate thymoquinone-induced apoptosis and activate erk and jnk signaling. apoptosis int. j. program. cell death 15, 183–195 (2010). romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0063 article bone flap preservation in abdominal wall after decompressive craniectomy in head injury: a single institute experience pavan kumar, ashok kumar, gaurav jaiswal, tarun kumar gupta india      romanian neurosurgery (2018) xxxii 3: 491 495 | 491             doi: 10.2478/romneu-2018-0063 bone flap preservation in abdominal wall after decompressive craniectomy in head injury: a single institute experience pavan kumar, ashok kumar, gaurav jaiswal, tarun kumar gupta department of neurosurgery, r.n.t. medical college, udaipur, raj, india abstract: objective: the objective of this study is to study factors associated with infection of calvarial bone flap preserved in subcutaneous tissue of abdominal wall after decompressive craniectomy (dc) in head injury. associated factors include age, sex, nutrition of patient, gcs of patient at time of surgery, vacuum drain placement, type of paramedian abdominal incision, site of decompressive craniectomy and associated comorbid conditions. method: this is a prospective study carried out in department of neurosurgery, tertiary care centre of southern rajasthan (india) from july 2016 to december 2018. total of 66 patient with head injury were enrolled, who underwent dc and bone flap preservation in abdominal wall. result: out of 112 patients who underwent dc in this study period 66 were included in this study. out of 66 patient 7(10.6%) patient develop bone flap infection. bone flap infection was more in poor nutrition patient, poor gcs (5-8), patient in which vacuum drain was not placed, patient with bifrontal decompressive craniectomy and associated comorbid condition. conclusion: bone flap preservation in subcutaneous abdominal wall after dc is safe and efficient. cranioplasty with autologous bone graft has lower cost, good cosmetic results and is well accepted by patient. key words: bone flap, decompressive craniectomy, infection introduction decompressive craniectomy (dc) defined as the removal of a large area of skull with opening of dura to increase the volume of cranial cavity, facilitating a reduction in icp. dc is surgical option in the management of refractory intracranial hypertension when maximal medical treatment has failed to control it, especially in head injury, stroke, and post-operative edema after brain surgery. the technique of storing calvarial bone flap in subcutaneous abdominal wall offer a theoretical advantage in that patient’s own body provide a storage environment, thereby reducing graft devitalization. 492 | kumar et al bone flap preservation after decompressive craniectomy in head injury             other preservation techniques include deep freezing, preservation in bactericidal solution and preservation in a subgaleal pouch. aim and objective the objective of this study is to study factors associated with infection of calvarial bone flap preserved in subcutaneous tissue of abdominal wall in head injury patient. associated factors include age, sex, nutrition of patient, gcs of patient at time of surgery, vacuum drain placement, type of paramedian abdominal incision (transverse/ longitudinal), site of dc (ftp or bifrontal) and associated comorbid conditions (obesity and diabetes). material and method this is a prospective study carried out in department of neurosurgery, tertiary care centre of southern rajasthan (india) from july 2016 to december 2017. out of 112 patients who underwent decompressive craniectomy in this study period 66 patient with head injury were enrolled, who underwent decompressive craniectomy with bone flap preservation in abdominal wall. inclusion criteria include-(1) dc in patient of head injury, (2) age between 10 and 70 year. exclusion criteria include (1) comminuted fracture of skull, (2) patient expired early (within 5 days) after dc, (3) dc in patient of stroke or post-operative edema after brain surgery, and (4) gcs ≤4. the abdomen must be prepared before the craniectomy was performed to avoid flap contamination. a paramedian abdominal incision, with dissection of a space under the subcutaneous tissue and placing of the bone flap was made. bone flap placement in parietal wall was same side of dc (e.g right side dc bone flap was placed in right side of abdominal wall) because if post traumatic hydrocephalous develop then it became easy to do vp shunt in opposite side. results a total of 112 decompressive craniectomy done in study period of 18 months. out of 112 patient with dc 66 enrolled in study and other are excluded. out of 66 patient enrolled in study 7(10.6%) patient develop bone flap infection preserved in abdominal wall. bone flap infection was more in poor nutrition patient(21.42%) vs good nutrition patient(7.69%), gcs 5-8 (13.88%) vs gcs >8(6.66%), patient in which vacuum drain was not placed(21.05%) vs vacuum drain placed(6.38%), bifrontal dc(20%) vs frontoparietotemporal dc(9.83%) and associated comorbid condition as obesity(16.67%) and diabetes(25%) shown in table 1. age, sex and type of paramedian abdominal incision (transverse or longitudinal) was not significantly associated with infection rate (table 2). most of bone flap infection develop between 8-15 days after surgery. in most of cases autologous bone cranioplasty done between 3-6 month with good result. incision and infected bone flap shown in figure 1-5. decompressive craniectomy done for acute subdural haematoma and contusion of brain. romanian neurosurgery (2018) xxxii 3: 491 495 | 493             table 1 associated factor no. of patient (total no. of pt.-66) no. of pt. with bone flap infection (%) nutrition status good poor 52 14 4 (7.69) 3 (21.43) gcs 5-8 >8 36 30 5 (13.88) 2 (6.66) vacuum drain placed not placed 47 19 3 (6.38) 4 (21.05) site of dc fpt bifrontal 61 5 6 (9.83) 1 (20.00) comorbid condition obesity diabetes 6 4 1 (16.67) 1 (25.00) table 2 associated factor no. of patient (total no. of pt.-66) no. of pt. with bone flap infection (%) age(year) 10-20 21-40 41-60 61-70 11 36 16 3 1 (9.09) 4 (11.11) 2 (12.5) 0 sex male female 46 20 5 (10.86) 2 (10.00) paramedian abdominal incision transverse longitudinal 55 11 6 (10.90) 1 (9.09) figure 1 transverse paraabdominal incision figure 2 ftp decompressive craniectomy incision figure 3 infected paraabdominal wound 494 | kumar et al bone flap preservation after decompressive craniectomy in head injury             figure 4 infected abdominal wound with exposed bone flap figure 5 infected abdominal wound with bone flap discussion decompressive craniectomy (dc) is performed in medically refractory situations involving elevated intracranial pressure (icp), such as intracerebral bleeding, traumatic brain injury (tbi), and ischemic brain lesion leading to severe brain swelling (1,2). given the ultimate goal of cranioplasty to reproduce the structure and function of absent calvaria to the greatest degree possible, the merits of autologous bone are obvious, including marked strength and elasticity, biocompatibility, general availability, and resistance to infection. given the low cost of conservation, lower rates of infection compared with many other types of prostheses, and assured biocompatibility, the autologous cranial flap remains the gold standard in calvarial repair (3). in the literature, four possible fates are possible for the bone flap after craniotomy: 1) placing of the bone under the subcutaneous abdominal tissue, 2) preservation of the bone in the subgaleal space on the edges of the craniotomy, 3) freezing of the bone flap and 4) dumping the flap for delayed cranioplasty with synthetic material or bone graft resulting from cranial vault split. movassaghi et al. (4) evaluated the efficacy of bone flap placement in the abdomen of 53 patients, being successful in 49 with one time reconstruct. one patient needed a surgical revision for cosmetic purposes and three had flap infection, one of them with the flap still in the abdomen. they concluded that the abdominal bone flap preservation is effective and has a low complication rate. hauptli et al. (5) related 43 cases of bone flap placement in the subcutaneous abdominal tissue, obtaining only three unfavorable outcomes: one patient presented bone infection and two had local absorption. they emphasized that this technique was better then the freezing with less bone loss by absorption. tybor et al. (6) after studying 36 cases of flap implants preserved in the abdominal wall (median 14 days between the surgeries), had one case of flap infection in 28 implants. two patients had the flap removed out of the romanian neurosurgery (2018) xxxii 3: 491 495 | 495             abdomen for subcutaneous hematoma other by abdominal wall inflammation. they considered that bone flap preservation in the abdomen has cosmetic, financial, and technical advantages when compared to the use of synthetic prosthesis and has low inflammatory complication events. in our study bone flap infection seen in 10.6% of cases. higher bone flap infection was associated with poor nutritional status of patient, low gcs (5-8) at time of surgery, vacuum drain not placed in abdominal wall, bifrontal decompressive craniectomy and associated comorbid condition as obesity and diabeties. patient with gcs >8 recover early. in patient with poor gcs (5-8) bone lap infection was 13.88% compare to good gcs (>8) patient (6.66%). vacuum drain placement in abdominal wall prevent haematoma formation under bone flap so it prevent infection as seen in which vacuum drain placed infection rate was 6.38% as compare to patient in which vacuum drain not placed (21.05%). shape of bifrontal craniectomy bone flap is more convex compare to ftp craniectomy bone flap so more dead space available under bifrontal bone flap for haematoma formation leading to infection. infection rate in bifrontal bone flap was 20% compare to 9.83% in ftp craniectomy bone flap. in our study bone flap infection was not significantly associated with age and sex of patient. conclusion bone flap infection is more common in poor nutrition patient, poor gcs (5-8), patient in which vacuum drain not placed, site of dc (ftp or bifrontal) and patient with associated comorbid condition. bone flap preservation in subcutaneous abdominal wall after decompressive craniectomy is safe and efficient. cranioplasty with autologous bone graft has lower cost, good cosmetic results and is well accepted by patient. correspondence dr. pavan kumar 323 p g boy’s hostel, r n t medical college, udaipur, rajasthan, india emai: pavanbarh@rediffmail.com phone: +919588229198 references 1. diedler j, sykora m, blatow m, jüttler e, unterberg a, hacke w. decompressive surgery for severe brain edema. j intensive care med 24:168-178, 2009 2. meyer mj, megyesi j, meythaler j, murie-fernandez m, aubut ja, foley n, et al. acute management of acquired brain injury part ii: an evidence-based review of pharmacological interventions. brain inj 24:706-721, 2010 3. artico m, ferrante l, pastore fs, ramundo eo, cantarelli d, scopelliti d, et al: bone autografting of the calvaria andcraniofacial skeleton: historical background, surgical results in a series of 15 patients, and review of the literature. surg neurol 60:71–79, 2003. 4. movassaghi k, ver halen j, ganchi p, amin-hanjani s, mesa j, yaremchuk mj. cranioplasty with subcutaneously preserved autologous bone grafts. plast reconstr surg 2006;117(1):202-6. 5. hauptli j, segantini p. new tissue preservation method for bone flaps following decompressive craniotomy. helv chir acta 1980;47(1-2):121-4. 6. tybor k, fortuniak j, komunski p, papiez t, andrzejak s, jaskólski d, et al. supplementation of cranial defects by an autologous bone flap stored in the abdominal wall. neurol neurochir pol 2005;39(3):220-4. 21selectedabstracts 504 selected abstracts of the 40th congress of the rsn selected abstracts of the 40th congress of the romanian society of neurosurgery with international participation, september 18th 21th 2013 microsurgery of ventricular lesions: an experience with 309 patients prof. basant kumar misra, chairman, department of neurosurgery and gamma knife radiosurgery, p. d. hinduja national hospital & medical research centre, mumbai, india president elect, world federation of skull base societies secretary, wfns chairman, education committee, asian australian society of neurological surgeons past president, skull base surgery society of india introduction: microsurgical experience with the management of lateral and anterior third ventricular tumors is presented. the surgical approach to the lesions at posterior third ventricle and suprasellar tumors like craniopharyngioma is not included here. material and method: three hundred nine ventricular lesions, 214 anterior third ventricular and 95 lateral ventricular, were operated by the first author from 1987 till 2014 june. these were mostly primary intraventricular lesions. 90% of the third ventricle lesions were benign as was most of the lateral ventricular lesions. colloid cyst (153 cases) was the commonest 3rd ventricular lesion and neurocytoma (25 cases) the commonest lateral ventricular tumor. results: while the majority of the third ventricular tumors were operated by the transcallosal route, the transcortical was the preferred route for the lateral ventricular tumor. following transcallosal transventricular entry there were four options of entering the third ventricle, the transforaminal, interforniceal, subchoroidal and subforniceal suprachoroidal. our preferred route is the transforaminal followed by subforniceal suprachoroidal; the later was first time developed and reported in the literature by the author in 1994. the approaches to the lateral ventricle are more varied and was dependent on the location of the lesion in the ventricle: lateral temporo parietal, middle temporal gyrus, anterior temporal lobectomy, occipital incision, superior parietal, middle frontal gyrus, and transcallosal. changing trends in the management of petroclival meningioma prof. basant kumar misra, chairman, department of neurosurgery and gamma knife radiosurgery, p. d. hinduja national hospital & medical research centre, mumbai, india president elect, world federation of skull base societies secretary, wfns romanian neurosurgery (2014) xxi 4: 504 – 546 505 chairman, education committee, asian australian society of neurological surgeons past president, skull base surgery society of india the initial enthusiasm of achieving eradication of a seemingly ‘inoperable’ meningioma by novel skull base approaches led many neurosurgeons to employ radical surgery. the accompanying high morbidity was accepted as inevitable. over the years, however, many started questioning this philosophy and the last decade saw the pendulum swing to the other extreme with the popularity of endoscopic surgery and radiosurgery. thus, minimally invasive neurosurgery became the fashion. however, it is important to remember “the pearl” that inadequate treatment through a less invasive approach is maximally invasive. realization has now dawned that endoscopic surgery and radiosurgery cannot replace microsurgery for meningioma. a judicious use of various microsurgical techniques, including skull base approaches, with appropriate adjuncts like neuroendoscope and image guidance is the best way forward in dealing various meningioma. measures preventing neurovascular damage during surgery, adequate closure to prevent csf leaks, the bugbear of skull base surgery, and quick remedial measures to treat csf leaks will go a long way to achieve acceptable results. radical but safe excision in skull base tumors followed by adjunct radiosurgery, if necessary, will result in long-term control. examples of meningioma at various sites managed will be demonstrated on video. our philosophy is that of optimally invasive neurosurgery, individualizing the approach to suit the given patient with a goal to achieve maximal result with minimal damage to the patient. neuroendoscope, image guidance and radiosurgery are all utilized as pillars on the foundation of microsurgery! we will try to answer some of the following decision dilemmas in this lecture: (1) to treat or not, (2) microsurgery or radiosurgery, (3) which surgical approach and (4) total or subtotal excision “radiating” multiple subpial transection for refractory epilepsy reduces rate of complications christian raftopoulos background: multiple subpial transection (mst) is a potential surgical treatment for patients with epileptogenic foci located in cortical areas with higher functions. as neurosurgical teams have become more experienced with mst, the original technique has adapted. objective: to report our 6-year experience with a modified mst technique. methods: the population included 62 consecutive patients with medically refractory epilepsy treated by mst, with a follow-up period ranging from 2 to 9 years. mst was performed on gyri under neuronavigation and guided by intraoperative electrocorticography. we performed radiating mst from a single cortical entry point. the mst technique was 506 selected abstracts of the 40th congress of the rsn described according to the number of transections performed and the brodmann areas (bas) involved. any mst-related complications were registered and followed up. clinical outcome was described in terms of seizure suppression or reduction according to the engel modified classification. results: twelve patients underwent mst alone (msta), and 50 had mst with another procedure. the main mst sites were ba 4 (61%) and 3, 1, 2 (58%); in 22% of cases, mst was performed in ba 44, 22, 39, and 40. permanent neurological deficits were observed in 4 (6.4%) patients; 2 minor deficits were mst related (3.2%). a reduction in the seizure rate of at least 50% was seen in 79% of patients (msta group, 75%), and 42% became seizure free (msta group, 33%). conclusion: this study demonstrates the efficacy and low morbidity of radiating mst performed under neuronavigation and intraoperative electrocorticography. preservation of function in acoustic neuroma surgery prof. basant kumar misra, chairman, department of neurosurgery and gamma knife radiosurgery, p. d. hinduja national hospital & medical research centre, mumbai, india president elect, world federation of skull base societies secretary, wfns chairman, education committee, asian australian society of neurological surgeons past president, skull base surgery society of india introduction: an attempt is made to present the management protocol in acoustic neuroma (an) patients and outline the steps for preservation of cranial nerve function during acoustic neuroma surgery. material & method: a detailed analysis of 1454 cases of cerebellopontine angle lesions operated by the first author between 1987 and 2014 june yielded 913 cases of an. microsurgery was the primary option in 634 and gammaknife radiosurgery was done in 296, of which 66 were previously operated by the author. a detailed analysis of microsurgically managed patients in two different periods (100 consecutive patients each before 1993 and 2008) were compared to see the changing trend and document current results. in the initial experience (1990s), the emphasis in microsurgery was preserving life, total excision of tumor and preservation of function in that order. in the 21st century, the emphasis in microsurgery has been all about functional preservation. in 100 consecutive cases of vs (excluding neurofibromatosis-2) that were treated microsurgically between 2005-08, there were four small tumors (<2 cm), 14 medium – sized tumors (2-3 cm) and 82 large tumors (≥ 3 cm). the total excision rates was 83%. the facial nerve anatomical preservation rate was 96% and function was grade iii house-brackmann (hb) or better in 87%. both the total excision rate and facial function of grade ii hb or better were 100% in cases with tumor size less than three cm. functional hearing preservation was achieved in ten cases. there was no operative mortality. the risk of injury to cranial nerves 7th and 8th can be: (i) just medial to iam, (ii) at the brain stem and (iii) inside iam. the causes of injury just medial to iam is because of mechanical injury while romanian neurosurgery (2014) xxi 4: 504 – 546 507 dissecting because of well-known maximal adherence between tumor and the nerve and the sharp angle the nerves make between the iam and cisternal component. at the brainstem, the risk of injury is because of venous injury and subsequent loss of anatomical definition. inside the iam, the main causes of injury to vii and viii are vascular jeopardy, thermal injury by drilling or coagulation and injury to labyrynth causing deafness. recognizing the risk factors is the first step towards prevention of injury to 7th and 8th cranial nerves. microsurgery of giant intracranial aneurysms prof. basant kumar misra, chairman, department of neurosurgery and gamma knife radiosurgery, p. d. hinduja national hospital & medical research centre, mumbai, india president elect, world federation of skull base societies secretary, wfns chairman, education committee, asian australian society of neurological surgeons past president, skull base surgery society of india introduction: giant intracranial aneurysms (gia) are treacherous lesions with significant risks in management. in spite of the great advances in endovascular therapy the results of evt in giant aneurysms has been suboptimal. a retrospective analysis of our strategy and results with microsurgery of gia in the 21st century is presented. material and method: the author has operated on 123 gia microsurgically till june 2013, 99 since 2000 and the material of this presentation. age ranged from 2 to 73 years and the female to male ratio was 2:1. 80% were in the anterior circulation and 20% in the posterior circulation. intra operative neuroprotection measures included mild hypothermia, propofol induced burst suppression and hypertensive anesthesia during temporary arterial occlusion. peroperative parent artery/bypass patency was checked by microvascular doppler, catheter angiography / icg dye angiography. postoperative check angiogram was routinely performed. results: exclusion of the aneurysm from the circulation by direct repair (clipping, aneurysmorrhaphy, excision & suture) was done in 60. flow diversion and ecic bypass was done in 29, high flow bypass in 27 and stmc in 2. trapping was done in 10. temporary ecic protective bypass was done in 3. hypothermic cardiac arrest was used in 3 cases of giant basilar artery aneurysm with femoro-femoral bypass for direct repair. dedicated skull base approach and lumbar drainage helped in avoiding brain retraction. postoperative outcome was good in 79%, poor in 16% and 5 patients died. conclusions: judicious surgical strategy and appropriate technology can result in good outcome in more than 80% of cases of gia. majority of the gia can be treated microsurgically, the preferred modality today. 508 selected abstracts of the 40th congress of the rsn fourth ventricle tumors i.s. florian1,2, m. balaci2, s.i. fofana2, c. kakucs1,2 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, department of neurosurgery 2cluj county emergency hospital, department of neurosurgery introduction: fourth ventricle tumors are rare and challenging lesions with nonspecific clinical manifestations, with a native ct scan usually irrelevant in the early stages and with common rapid neurological deterioration due to brainstem compression or hydrocephalus. the purpose of this study is to present our surgical experience in the management of fourth ventricle lesions. material methods: we retrospectively evaluated the epidemiological aspects, indications, approaches, the histopathological findings, clinical outcomes and other specific characteristics of 102 patients diagnosed with fourth ventricle tumor that were operated in our service in a 15 year period between january 1999 and december 2013, representing 51% of all intraventricular operated tumors and 2,8% of 3609 operated intracranial tumors by the main author in this period. results: the gender distribution in this study was 45% females and 55% males. over 50% of the tumors were found in the 4-18 years aged group population. regarding the pathological findings there was a high variety with the predominance of medulloblastomas (35%), followed by ependymomas (28%), pilocytic astrocytomas (17%), other tumors being more rare. while medulloblastomas represented 50% of fourth ventricle tumors in pediatric patients, for the adult population in our experience ependymomas represent 41%, astrocytoma 18% and medulloblastomas 7%. all the cases were operated in the sitting position with no significant air-embolism complications related to the position. there was a slight predominance in favor of transvermian approach, compared with telovellar approach. complete removal was achieved in large majority of the cases, except the exophytic from the brain stem. the main complication was pneumocephalus, but only in 3% of cases was noted a tension pneumocephalus. another complications were persistent hydrocephalus (requiring definitive vps) and csf leakage, but only 1% developed meningitis. cerebellar mutism, pres were uncommon in our experience, and the mortality was 2% in our experience, higher than in supratentorial procedures. conclusions: the surgical results are directly correlated with the surgical expertise, the proper selection of the cases and of the approach. sitting position is, in our opinion, the proper position for posterior fossa surgery. cerebellar mutism is more related to retraction forces that can be encountered in both of the main approaches for fourth ventricle tumors: transvermian or telovellar approach. despite of their frightening aura, majority of fourth ventricle tumors can be totally removed, offering the cure in benign lesions. the amount of tumor removal is directly correlated with survival in malignant tumors. romanian neurosurgery (2014) xxi 4: 504 – 546 509 key words: intraventricular tumors, telovelar approach, transvermian approach, hydrocephalus, sitting position. surgical management and outcome of mca bifurcation aneurysms r.m. gorgan2, narcisa bucur1, angela neacsu1, aurelia mihaela sandu1, v.m. pruna1, f. m. brehar2, a. giovani1 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: a shift in paradigm in the treatment of mca bifurcation aneurysms was encountered in recent years since the pipeline embolisation device became available. the objective is to evaluate the role of surgical clipping for the mca bifurcation aneurysms in this changing era. patient and methods: this study analyzes the 5 years results on mca bifurcation aneurysms in 4th neurosurgical department with a mean follow up of 28 months, dedicated especially to surgical treatment results/result: between january 2009 and december 2013, 59 mca bifurcation artery aneurysms were treated by surgical clipping and 2 by endovascular embolisation in our department. the incidence was twice in women than in men, 35% of the aneurysms were ruptured; the postoperative mortality was 10%: 1 death out of 39 in the sah group and 7 out of 20 in the hematoma group, 4 patients died before surgery. 63,7% of the aneurysms were located on the right side. the average dimensions were 3,99 neck and 7.68 for dome with increased dimensions in the hematoma group. in the sah group 4 patients developed new neurological deficits postoperative. most of the patients who died presented in wfns 5. most of the patients in the sah group presenting in wfns 3 grade recovered the neurological deficit postoperative. the postop rankin scale averaged to 1 in the sah group. conclusions: surgical clipping remains the only curative treatment especially in acute cases of ruptured aneurysms or in cases where the broad neck prevents embolisation or where the aneurysm is thrombosed and acts by mass effect. key words: mca bifurcation; clipping; hematoma posterior fossa meningiomas – an overview st. florian1,2, b. pintea1,2, a. kiss1, i. irimescu2, andrasoni zorinela2 1university of medicine and pharmacy “iuliu hatieganu” cluj-napoca, discipline of neurosurgery 2cluj county emergency hospital, department of neurosurgery introduction: posterior fossa meningiomas have a frightening aura mostly because of the high vascularizationand intimate relation with numerous neurovascular structures in a quite small space. from a surgical point of view the most difficult locations are clival meningiomas, those 510 selected abstracts of the 40th congress of the rsn situated medial to the acoustic meatusand the tentorial notch. aim: the purpose of this retrospective study is to present our strategies in the management of these difficult tumors and to deliniatethe technique’s advantages and ait in achieving an improved extent of tumor resectionand enhancing the patient’s outcome. materials and methods: from a total of 765 locations of intracranial meningiomas operated by the main author between 2001 – june 2014, 118 were located in the posterior fossa. all patients were evaluated by mri and ct scans before surgery, and tumor location, size and relation to neighbouring anatomical structures were determined. we discussed the tumor’s characteristics that could influence treatment decisionand the choice of the most reliable approach. results: 118 posterior fossa meningiomas represent 15% of all new cases of intracranial meningiomas operated by the main author. the specific locations were: cerebello pontine angle: 40 cases; tentorial 23 cases; tentorial notch: 3 cases; petro-clival: 20 cases; foramen magnum: 13 cases; convexity: 19 cases. all cases were operated in semi-sitting position. simpson’s grade i resection was not a goal, but grade ii was achieved in most of the cases. the most frequent complication related to semi-sitting position was pneumocephalus. local postoperative complications were pseudomeningocelle, hematomas (5%) and csf fistulas (4%). postoperative mortality was 2%. conclusions: despite their scary appearance, most of the posterior fossa meningiomas can be safely resected without major complications. avoiding is a matter of adherence to the general principles of meningioma surgery: early devascularization, preservation of arachnoidal layer, internal debulking, circumferential dissection and preservation of all normal vasculature and nervous structures. all these objectives could be achieved with microsurgical techniques in semi-sitting position. key words: posterior fossa, meningiomas, semi-sitting, tentorial notch, retrosigmoid approach, gross total removal. posterior fossa cavernous malformations – clinical characteristics, management and prognostic factors ligia tataranu¹˒², v. ciubotaru¹, m. chelsoi¹, adriana solomon¹˒², d. paunescu¹˒² ¹neurosurgical clinic, “bagdasar – arseni” emergency clinical hospital, bucharest, romania ²“carol davila” university of medicine and pharmacy, bucharest, romania introduction: cavernous malformations represent clusters of abnormal, dilated sinusoidal channels with a single layer of endothelium. material and methods: between july 2004 and july 2014, 38 patients were diagnosed with posterior fossa cavernous malformations and treated in our neurosurgical department from “bagdasar – arseni” emergency clinical hospital, bucharest, romania. there were 25 women (65.8%) and 13 men (34.2%) with age between romanian neurosurgery (2014) xxi 4: 504 – 546 511 28 and 69 years old. the mean age at admission was 49.8 years. results: there were 38 patients with 48 posterior fossa cavernous malformations (cm), 7 patients had multiple cavernous malformations (18.4%), 3 patients with both supra and infratentorial lesions and 4 with cavernous malformations located exclusively in the posterior fossa. 3 patients (7.9%) had associated developmental venous anomalies. from 48 posterior fossa cavernous malformations, 22 were located in the cerebellar hemispheres, 3 in vermis, 10 in pons, 6 in midbrain, 1 in medulla and 6 in cerebellar peduncles. the most common signs and symptoms at presentation were headache 35 patients (92.1%), cerebellar symptoms (ataxia, dysarthria, vertigo) 25 patients (65.7%), motor weakness 10 patients (26.3%), paresthesia 8 patients (21%), and cranial nerve dysfunction 15 patients (39.5%). 37 cavernomas were approached microsurgically. removal of the lesion was attempted in all patients. some degree of transient neurological deterioration was detected in 10 patients (27%). a significant permanent neurological deterioration from surgery was detected in 6 patients (16,2%): two patients had third nerve palsy following resection of a midbrain cavernoma, one experienced unilateral hearing loss after surgical resection of a pontine cavernoma, two patients retained minor sensitive symptoms, and one patients had postoperative pulmonary thromboembolism and died. overall, preoperative symptoms improved in a large number of patients: cerebellar symptoms improved in 20 patients (52,6%), motor weakness in 5 patients (13.2%), paresthesia in 1 patient (2,6%), cranial nerve palsy in 3 patients (7.9%), and headache in 33 patients (86.8%). the histopathological examination confirmed the diagnosis of cavernous malformations in all 37 operated patients, one patients refused the surgical treatment. from 48 posterior fossa cavernous malformations, 36 had at least one hemorrhagic episode prior to hospital admission. conclusions: cavernous malformations are more frequent present in the younger population. individualized surgical strategies ensure decreased postoperative hemorrhage rates and favorable long-term outcomes. key words: cavernous malformations, posterior fossa the preference for transcallosal or transcortical approach in surgery of lateral ventricle tumors m. radoi2, ram vakilnejad1, lidia gheorghitescu1, f. stefanescu1, c. popescu1, l. danaila2 1national institute of neurology and neurovascular diseases bucharest, neurosurgery, romania 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: tumors of the lateral ventricle are rare and could originate in the ventricular wall or arising and expanding within the lateral ventricle from the surrounding neural structures. based on a 10 years retrospective study, we analyze postoperative results and factors that 512 selected abstracts of the 40th congress of the rsn affected the preference for transcallosal or transcortical approach. patient and methods: we performed a retrospective study, lasted between january 2004 june 2014, that comprised 29 consecutive patients who underwent operation for lateral ventricle tumors. the main clinical symptoms and signs were associated with the localization and size of the tumors. the transcortical approach was used in 18 patients and the transcallosal approach was used in 11 patients. results/result: total tumor resection was achieved in 21 patients (72.5%). in cases with subtotal resection, transcortical approach was used in 6 cases (20.5%) and transcallosal approach in 2 cases (7.5%). most frequent histological tumor’s type was glioblastoma, choroid plexus papilloma, ependymoma and meningioma. one patient died because of postoperative intraventricular hemorrhage. additional neurological deficits were seen in 4 patients and postoperative seizure occurred in five patients. two patients with preoperative hydrocephalus required ventriculo-peritoneal shunting after tumor’s resection. two patients developed postoperative epidural hematoma and one required reoperation. the mean duration of postoperative evaluation was 26,45 months (range 4-96). conclusions: the nature, size, location and vascularization of intraventricular tumors are the most important elements influencing the choice of surgical approach. surgeons must evaluate all these factors and prefer the short and safe way to remove the tumor. key words: lateral ventricle tumors, transcallosal approach, transcortical approach. discussing post-op complications: cerebellar mutism and postoperative visual loss after posterior fossa surgery, a case report a. budu1, b. iliescu1, d. rotariu2, b. chirita2, c. apetrei2, i. poeata1 1“gr. t. popa” university of medicine and pharmacy, iasi, romania 2“prof. dr. n. oblu” clinical emergency hospital, iasi, romania cerebellar mutism has been associated with injury to midline cerebellar structures secondary to degenerative disease, tumors, hemorrhage, or surgery. this syndrome typically arises 48 hours after the initiating event and resolves approximately 7 to 8 weeks later. another rare post-op complication that can appear after posterior fossa surgery is the postoperative visual loss syndrome which has a very low incidence (∼1/60 000–1/125 000 cases) and usually occurs after long prone patient positioned surgery. we present the case of a 10 year old child that presented to our hospital with signs of icp due to a large 4th ventricle ependymoma. after endoscopic third ventriculostomy and surgery he developed cerebellar mutism and post-op visual loss syndrome. the possible etiology of this complications along with an in depth look romanian neurosurgery (2014) xxi 4: 504 – 546 513 about the pathophysiology of such post-op complications is discussed. surgery of petroclival meningiomas. recent surgical results and outcomes m. radoi2, ram vakilnejad1, lidia gheorghitescu1, f. stefanescu1 1national institute of neurology and neurovascular diseases bucharest, neurosurgery, romania 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: petroclival meningiomas represent only 10% of all meningiomas located in the posterior fossa, but are some of the most formidable challenges in skull base surgery. we described our recent experience (2000-2014) regarding the surgery of these tumors. patient and methods: we retrospectively analyzed surgical results and outcome in 11 cases of petroclival meningiomas. most common symptoms in our series were headache and gait disturbance, while cranial nerves palsies represented the most common presenting signs. there were 8 females and 3 males, and the mean age was 52 years. surgical approaches chosen for petroclival meningiomas in our series were retrosigmoid (9 patients) and subtemporal transtentorial (2 patients). results/result: we achieved total tumor resection in 5 cases (45%) and subtotal resection in 6 cases (55%). overall outcome (total/subtotal resection) was good in 6 cases, fair in 3 cases and poor in one case. one postoperative death occurred due to hemorrhagic midbrain infarction (9%). complications were usually related to cranial nerve deficits: loss of hearing (2 patients), paresis of trochlear nerve (1 patient), trigeminal nerve (3 patients) and facial nerve (1 patient). in 4 patients these cranial nerves deficits were transient. in one case, a patient developed postoperative hydrocephalus and needed shunt placement. conclusions: despite the fact that complications can be disastrous, we considered that an appropriate approach, combined with microsurgical techniques and a better understanding of the anatomy, greatly decrease the incidence and severity of complications and make feasible a total tumor resection. key words: petroclival meningiomas, surgery, retrosigmoid approach, subtemporal transtentorial approach. decompressive craniectomy in severe brain injury guided by intracranial pressure monitoring. n. oblu emergency hospital experience c. apetrei1, a. iordache1, b. chirita2, a. budu2, m. cosman2, i. poeata1 1“gr. t. popa” university of medicine and pharmacy, iasi, romania 2“prof. dr. n. oblu” clinical emergency hospital, iasi, romania severe brain injury is a devastating entity for the patient. it often leads to neurological and anatomical troubles with severe and permanent deficiency that affects the patient’s quality of life on long term or can even cause 514 selected abstracts of the 40th congress of the rsn death. intracranial pressure monitoring seems to be an indispensable stage in management of severe traumatic brain injured patients. our days this technique completes trauma protocol in our center. we compared two groups of patients with severe traumatic brain injury who received a decompressive craniectomy: in the first group the surgical decision was made on clinical signs and imaging, in the second group of patients decompressive craniectomy was performed after invasive monitoring of intracranial pressure. the first group studied includes a total of 77 patients. in this group, mortality was very high, namely 75%. in the last two years in 20 patients with severe brain injury we monitored intracranial pressure with camino systems. in this group the overall mortality was 45%. among the 20 patients monitorred in 8 patients we had performed a decompressive craniectomy. in this second group of 8 patients we found a mortality of 62%. (lower then those in the first group). the main complication was bronchopneumonia occurred in both groups studied. in conclusion, monitoring of intracranial pressure seems to be indispensable in the management of severe brain injuries as guides for an aggressive treatment including the decompressive craniectomy. mild head injury: epidemiology, management, outcome, costs d. adam “carol davila” university of medicine and pharmacy neurosurgery, bucharest, romania introduction: mild traumatic brain injuries represent 80% of the total traumatic brain injuries. their management is conducted as recommended by ebic (european brain injury consortium) or wfns (world federation of neurosurgical societies). the aim of the study is to analyze the management of patients with mild traumatic brain injuries who present at the emergency department (ed), of the admitted ones, the paraclinical investigations used and the cerebral lesions which these identify. patient and methods: during a 3 months period, 533 patients with mild traumatic brain injuries presented at the ed. we have followed these patients regarding the demographic data, the causes that led to the mild traumatc brain injuries and the paraclinical investigations used. regarding the admitted patients, we have taken into consideration risk factors, neurological symptoms, the need to repeat a paraclinical investigation, their management and outcome. results/result: out of the 533 patients who presented at the ed, 248 (65%) were adults and 158 (29.64%) were third age patients. the remaining 27 (5%) were aged between 0-18 years old. male patients (359; 67%) were more frequently affected than female patients (174; 32.6%). the top three causes were aggressions (57%), car accidents (27%) and same level falls (6.3%). the patients were investgated by skull x-rays (47.8%) and head computed tomography (ct) scans (52.35%). out of the total number of patients, 198 were admitted; these had the following risk factors: age > 65 years old (31%), alcohol use (18.6%), seizures (7.57%) and the romanian neurosurgery (2014) xxi 4: 504 – 546 515 following clinical symptoms: headaches (71%), vomiting (9.6%), dizziness (36.8%), loss of consciousness (31.8%). out of the admitted patients, only 12 presented cerebral lesions: hemorrhagic brain contusions (n=5), small subdural blood collections (n=3), traumatic subarachnoid hemorrhages (n=2), acute subdural hematoma (n=1) and intraventricular hemorrhage (n=1). the patient with acute subdural hematoma was operated on and had a favorable outcome. the patient with intraventricular hemorrhage, who was 90 years old and presented with coagulopathy, has deceased. all the other patients were discharged after a mean hospitalization period of 3 days. conclusions: out of the patients with mild traumatic brain injuries, only a small number present cerebral lesions. for their diagnosis, expensive paraclinical investigations are used in both the ed and the neurosurgical department. careful monitoring of the evolution of the neurological status and performing a head ct scan only in case of neurological deterioration would save resources that could be targeted for the therapeutic stage. key words: mild head injury, head ct scan. reccurence of chronic subdural hematomas: the importance of the surgical technique t. papacocea emergency clinical “st. pantelimon” hospital, neurosurgery, bucharest, romania introduction: in this study we are trying to establish a correlation between the surgical technique used for the treatment of chronic subdural hematomas and the risk of reccurence. patient and methods: between 01.04.2008 and 30.06.2014, 138 patients were operated on and followed-up for chronic subdural hematomas. among them, 18 patients (13%) had one or several reccurencies. factors related to the patients (gendre, age,location of the hematoma) are analysed as possible predictors of reccurence. results/result: several surgical techniques were used in the treatment of chronic subdural hematomas. each of them is analysed to find possibly connections with the reccurence risk of the size of the approach, the reposition of the bone flap, the suture of the dura and other aspects conclusions: there are obvious, statistically significant, correlations between the risk of reccurence and some elements of the used surgical technique. key words: chronic subdural hematomas, reccurence, surgery. traumatic injuries of the spine in paedriatic population a. tascu2, f. exergian1, d. serban1, a. iliescu1, c. pascal1, g popescu1 11-st neurosurgery clinicpediatric department, emergency hospital “bagdasar-arseni”, bucharest, romania, av berceni 10-12, sector 4, cod 041915 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: traumatic pediatric spine injuries represents a subject poorly debated in the literature. 516 selected abstracts of the 40th congress of the rsn the authors aim is to realize an extended study addressing this theme. patient and methods: authors present a retrospective study including 434 pediatric patients admitted with traumatic spine injuries in the first and second neurosurgical clinics in "bagdasar-arseni" clinical hospital, from 2003 to 2013 (11 years). the diagnosis was established throughout clinical examination and radioimagistic investigations. the study group was divided in 4 age-related categories (0-3y, 47y,8-14y and 15-18y) taking into consideration specific age related risk factors. out of the 434 admitted patients, 172 had no proven osseous or disc lesions, 149 had spinal fractures with or without spinal cord involvement, 51 had spinal luxations and 24 had other spinal pathologies. neurological diagnosis was establish using frankel classification grading system. also the etiology and the localization of the spinal level where included in the study. 68,5% of the patients were treated conservative, while 31,5% needed surgery. results/result: based on the information noted in the medical records, a distinct injury profile, explained by anatomical and biomechanical features, differentiates the young patient with an immature spine from the older adolescent with a more mature, adult like spine. conclusions: traumatic spine injuries in pediatric patients have a low incidence, mainly due to a more flexible spine. anatomical particularities in children spine allows a better applicability of conservative treatment. the prognosis depends on the severity of spinal cord injuries, with neurofunctional recovery noticeably increased in pediatric population compared to adult population. key words: spine trauma, children, outcome. brachial plexus surgery long and a hard task rasulic lukas, samardzic miroslav, bascarevic vladimir, micovic mirko, cvrkota irena, savic andrija, zivkovic bojana corresponding author: associated professor lukas rasulic clinic of neurosurgery, clinical centre of serbia, koste todorovica 4, 11000 belgrade, serbia e-mail: lukas.rasulic@kcs.ac.rs surgery of the brachial plexus is demanding field of surgery. in recent years, development of microsurgery improvements in optics, electrodiagnostic, equipment, magnetic resonance imaging, surgical instruments, and new suture material evolved surgery of brachial plexus. the most common condition in this section of neurosurgical expertise that requires surgical treatment is brachial plexus injury. in 90% of cases cause of brachial plexus injury is vehicular accident. this said, it is obvious that this type of injury usually occurs in previously healthy and relatively young population. the fact that untreated brachial plexus injury may cause permanent disability of these previously healthy young people, demands development of even better treatment plans and new surgical techniques. timing of the surgical treatment is of the romanian neurosurgery (2014) xxi 4: 504 – 546 517 outmost importance. most experts in this field of surgery recommend conservative treatment for patients who have showed spontaneous recovery within the first few week after the trauma. surgical treatment is indicated for patients who have an associated vascular lesion and for sharp wounds, in which a nerve lesion can be expected, exploration and repair of the divided neural elements should be undertaken as soon as the patient’s condition permits. the patient with a root avulsion injury should undergo surgery within the first few months after the injury. a closed injury without evidence of root avulsion should be treated by surgery, if there is no sign of recovery within 6 months. in cases of brachial plexus traction injuries only possibility is neurotization (nerve transfer). if indicated, surgical treatment consists of neurolysis, nerve grafting, nerve transfer and combination of these procedures. goal of the treatment is achieving good shoulder and elbow control, than elbow, wrist and finger extension, and finally sensibility of the hand and the forearm. combined use of donor nerves in reinnevation of the musculocutaneus or axillary nerves results with high rate and better quality of recovery when compared to the other modalities of nerve transfer. the use of intraplexal and contralateral plexal neurotization along with a better understanding of central-peripheral function integration may provide improved results and purposeful hand function for our patients in the future. the other, much rarer pathology are tumors of brachial plexus. they pose a great challenge to the neurosurgeon. radical to complete excision of the tumor with preservation of neurological function of the involved nerve is an ideal surgical treatment option with brachial plexus tumor surgery. key words: nerve transfer, nerve transplantation, peripheral nerve surgery, brachial plexus tumors. surgery of the peripheral nerves in children rasulic lukas, samardzic miroslav, bascarevic vladimir, micovic mirko, cvrkota irena, savic andrija, zivkovic bojana corresponding author: associated professor lukas rasulic clinic of neurosurgery, clinical centre of serbia, koste todorovica 4, 11000 belgrade, serbia e-mail: lukas.rasulic@kcs.ac.rs modern surgical treatment of peripheral nerves begins with introduction of operative microscope in 1964 (curtze). pathology of peripheral nerves is a complex field of neurosurgery, and includes injuries, tumors and compressive neuropathies. nerve injuries: in neonatal period the most frequent type of injury is obstetric brachial plexus injury. after this period and until 3rd year of age child is prone to falls and cuts, while still insecure on his feet. from age 3 to 8, frequent type of injury are secondary peripheral nerve injuries after fracture (compression of radial nerve after humerus fracture, ulnar and median nerve after supracondylar fracture, and injuries of the knee that affect peroneal nerve). from age 9 to 15 the most frequent 518 selected abstracts of the 40th congress of the rsn mechanisms are motorcycle accidents, cuts, missile injuries and stab wounds. indications for operative treatment are open injuries with undoubtable nerve injury and neurological deficit, closed injuries that show no sign of recovery even three months after injury, and pain that is resistant to therapy. good preoperative evaluation and multidisciplinary approach is an imperative. in our clinic, many different procedures are done: neurolysis, direct suture, nerve transplantation, nerve transfer. treatment of choice is different for every patient and it is individually selected. after surgery, of outmost importance for neurological recovery is physical rehabilitation. in children, greater regeneration ability contributes to better treatment results (especially in children less than 10 years old). poorer results are when mixed nerves are involved, traction injuries and higher lesions. best results are accomplished when defect is less than 5cm. also, better recovery is noticed in early surgical treatment, however delay no longer than 6 months doesn’t affect outcome significantly. obstetric brachial plexus injury: specific type of peripheral nerve injury in children is obstetric brachial plexus injury. risk factors are: shoulder dystocia, macrosomia (over 4kg), small stature/cephalopelvic disproportion, breech presentation). the generally accepted mechanism of this injury is traction to the neck during delivery, where the neck on the side of the anterior shoulder is stretched and this stretch causes a “strain” on the brachial plexus on that side, causing a varying degree of injury. initial treatment consists of detailed clinical examination, including a check for associated injuries. electrophysiological diagnostic is recommended at 4 weeks initially to confirm the diagnosis and get a baseline reading. repeat examinations are carried out every 4–6 weeks until 3 months. surgery should be performed when there are no clinical signs of recovery three months after surgery; partial lesions of brachial plexus are usually treated conservatively. in majority of cases, 70-80% of children spontaneous recovery is expected. early recovery, during first two weeks is good prognostic sign. if treated surgically after 9 months of injury outcome is significantly poorer. after surgery, physical rehabilitation is conducted. functional usage of injured arm and child feeding itself are the most important recovery criteria. peripheral nerve tumors in children: tumors of peripheral nerves are rare lesions, and even rarer in children. however, around 14% of all soft-tissue tumors in children arise from peripheral nerve system. they are even more frequent in phakomatoses. symptoms and signs of peripheral nerve tumors are caused by direct nerve invasion, involvement of surrounding tissues, or mass effect. the duration and progression of symptoms or signs is important as most benign tumors have a longer duration and a slow rate of progression, while malignant tumors tend to progress rapidly in size, romanian neurosurgery (2014) xxi 4: 504 – 546 519 amount of pain, and neurologic deficit. a careful family history is important in the assessment of an underlying neurogenetic disorder, such as neurofibromatosis. peripheral primitive neuroectodermal tumors (ppnets) account for 4-17% of all pediatric soft tissue tumors and often exhibit aggressive clinical behavior. in several large series, the rates of metastases range from 2031%, with long-term survival rates (< 25%). obtaining a complete resection of tumor with negative margins is paramount in surgically treating primitive neuroectodermal tumors. key words: pediatric peripheral nerve surgery, peripheral nerves, pediatric peripheral nerve tumors. minimal invasive spine surgery with robotic intraoperative 2/3d fluoroscopy and computer assisted navigation christian raftopoulos (belgium) many surgical treatments for chronic low back pain that is refractory to medical treatments focus on spine stabilization. one of the main surgical procedures consists of placing an interbody cage with bone grafts associated with pedicle screws. this technique can be performed using different approaches: a large open posterior approach, tubular approaches (minimal open) or percutaneously (minimally invasive percutaneous or mip). one of the main difficulties is to precisely locate the screws into the pedicle avoiding especially infero-medial pedicle breaches. this difficulty is even greater when working percutaneously. this lecture focuses on percutaneously placed pedicle screws (pps), reports the use of a robotic multi-axis 2d/3d fluoroscopy and neuronavigation to enhance the accuracy of pedicle screw placement and reviews other strategies and results reported in the literature. wrong site surgery in the realm of neurosurgery y. enchev, t. kondev, b. iliev, d. handjiev, t. avramov, p. trendafilov department of neurosurgery, medical university of varna, university hospital “st. marina, varna, bulgaria recently there is a surge in patient safety awareness, nevertheless preventable harm to neurosurgical patients remains problematic. wrong site surgery with its subtypes permanently exists in the realm of neurosurgery, however it is often underreported or underestimated due to the associated legal claims. wrong-patient, wrong-side, wrong-level and wrongprocedure surgeries could be catastrophic to patients, healthcare professionals and institutions. these sentinel events are generally preventable according to the literature. different approaches are developed in an attempt to solve this problem. one of the most promising tool is the neurosurgical safety checklist. it represents low-cost, time-saving, cost-effective and easy to apply and to modify solution. 520 selected abstracts of the 40th congress of the rsn the multicentric critical analysis of the long-term experience with such checklists will be fateful for their future. microsurgery of posterior cranial fossa meningiomas m.r. gorgan1,2, narcisa bucur1, angela neacsu1, f.m. brehar1,2, v.m. pruna1, aura sandu1, catioara cristescu1 1“bagdasar-arseni” emergency clinical hospital, bucharest 2clinic of neurosurgery “carol davila” university of medicine and pharmacy, bucharest introduction: the authors of this study presents a retrospective study based on 48 case series of posterior fossa meningiomas operated in the fourth department of neurosurgery of “bagdasar-arseni” clinic emergency hospital between june 2009 and june 2014. material and methods: data was collected and analyzed from electronic data base and hospital registry. there were 17 man and 31 women with a median age of 54.8 years old. all patients underwent open tumor resection. 12 patients benefited from a ventriculoperitoneal shunt, 4 in an acute phase. results: tumor size was between 3-5 cm in 29 cases, and over 5 cm in 19 cases. 2 of this category of patients supported 2 and respectively 3 stages of resection. according to simpson scale, grade i resection was achieved in 20,8%, grade ii in 34.6 %, grade iii in 35.4 %, and grade iv in 9.2%. the most frequent location was cerebellar convexity (37.5%) followed by pontocerebellar angle (27.1%) and petroclival area (24.1%). most frequent pathological samples showed transitional meningioma (33.9%) followed by meningothelial (25.2%) and fibrous type (22.5%). they were 6 cases with atypical and anaplastic meningiomas (12,5%). in 94.6 % of cased the postoperative neurological status remained the same or improved. 3 cases (5.6%) presented neurological deterioration, 2 reversed on the follow-up period, and 1 remained permanent. one case with a giant hemifossa tumor deceased by complications related to brain stem decompression. they were 2 csf postoperative fistulas, one postoperative wound infection, one postoperative cerebellar hematomas, and 3 patients presented decompensations of previous illnesses (heart and lung). they were recorded 4 tumor re-growth in malignant meningiomas, and 2 in the non-malignant group. all cases benefited of treatment: 4 casesgamma-knife and 2 cases-open surgery. mean general follow up period was 34 months. conclusion: general results of the treatment of posterior fossa meningioma are very good in our clinic, due to homogenous neurosurgical attitude, experienced teams and adequate perioperative treatment. the rate of total resection is significant decreased by lesions over 5 cm diameter and lesions located in petroclival area. romanian neurosurgery (2014) xxi 4: 504 – 546 521 the interhemispheric transcallosal approach for ventricular tumors. personal considerations i. poeata1,2, z. faiyad2, a. chiriac1, b. iliescu1, d. rotariui2, a. budu2 1“gr. t. popa” university of medicine and pharmacy, iasi, romania 2“prof. dr. n. oblu” clinical emergency hospital, iasi, romania the optimal approach for lateral and third ventricular mass lesions depends on many considerations, among which: location, size, aim of surgery, neurosurgeon’s experience and preferences. maximal safe resection is generally the goal together with a minimally invasive surgical corridor. in this presentation we review our last series of 34 supratentorial ventricular tumors operated on during a 5 years period (9 glioblastomas, 8 low grade gliomas, 6 coloid cysts, 3 metastasis, 2 meningiomas, 2 neurocytomas,1 cavernoma, 1 subependimoma, 1 choroid plexus tumor, 1 pineocytoma). 21 of these were approached through an interhemispheric transcalosal route. we present videos with our techniques for nervous tissue (i.e. fornicis) and vessel preservation (collateral of the sagittal sinus, pericallosal and calosomarginal arteries, thalamostriate veins, posterior choroidal arteries) tumor dissection, intra and extracapsular debulking, and removal together with pre/post op imaging. diffusion tensor imaging: implications for target volume delineation in high grade glioma radiotherapy and follow up i.c. chiricuta1, m. medrea2, c. popa3 1amethyst radiotherapy center, otopeni 2centrul de diagnostic romano-german medinst, bucuresti 3innbn, clinica de neurologie, bucuresti aims: radiotherapy treatment planning for high-grade gliomas (hgg) is hampered by the inability to visualize peritumoral white matter infiltration and to individualize radiotherapy target volumes. diffusion tensor imaging (dti) is able to show white-matter abnormalities resulting from tumor infiltration not visualized by conventional imaging methods as ct and mri. the gross tumor volume (gtv) and the subclinical disease volume considered as the clinical target volume (ctv) should include the macroscopic and the peritumoral whitematter infiltration. methods: in ten patients with biopsyproven hgg who were refered and treated by high dose radiotherapy at our center were retrospectively analysed regarding the information obtained by dti tractography. using a siemens mr facility a dti tractography was obtained before and after high dose radiotherapy. the follow up dti were performed in 4 patients. results: a comparison of the gtv and ctv delineation based only on the conventional methods used for imaging of high grade gliomas for external beam radiotherapy and the additional information 522 selected abstracts of the 40th congress of the rsn obtained on white matter peritumoral infiltration provided by the dti tractography was performed. postradiotherapy changes in tract configuration were analysed. conclusion: dti tractography can be used to individualise radiotherapy target volumes. changes in the shape of the radiotherapy used target volumes make the individualization of treatment possible. agressive or conservative management in extradural hematomas in children 0-3 yo – a challenging neurosurgical choice a. tascu2, r.e. rizea2, a. iliescu1, c. pascal1, iulia vapor1, p. petrescu1, catalina lipan1, simona mihaela florea1 11-st neurosurgery clinic-pediatric department, emergency hospital „bagdasar-arseni”, bucharest, romania, av berceni 10-12, sector 4, cod 041915 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: epidural hematomas (edh) in children appear as a consequence of head trauma. although emergency surgical intervention was the classical neurosurgical treatment for edh, lately there has been observed a tendency to replace operation by conservative management, whenever the neurological status and imaging appearance allows it. the aim of this article is to present our experience in treating edh in children 03 years old and to establish a management protocol for edh in infants, by evaluating the clinical and neuroimaging status, of both surgically and conservatively treated patients, from hospital admission to discharge. patient and methods: retrospective study that includes 52 patients diagnosed with an extradural hematoma, admitted in the first neurosurgical clinic, clinical hospital ‘bagdasar-arseni’ in bucharest, from january 2004 to december 2013. the patients were identified by diagnosis from the clinic’s database; clinical and imaging data was extracted from the patient’s individual records and crosschecked with the operating protocols. cerebral ct scan was the preferred imaging investigation for diagnosis. results/result: our study includes 52 patients (26 boys and 26 girls), with a mean age of 14.5 months (range 6 weeks – 3 years old). 25 patients were surgically treated, while the other 27 received symptomatic medication and were monitored clinically and by imaging exams. the most frequent clinical manifestations were intracranial hypertension (21 patients) and psychomotor agitation (19 patients). the traumatic mechanisms were: accidental falling (38 patients), blunt head trauma (3 patients), road accident (2 patients), unspecified (8 patients) other causes (1 patient). based on the glasgow coma scale classification of tbi, 39 patients suffered a mild tbi, 7 a moderate tbi and 6 patients suffered a severe tbi. most of the patients had a good recovery; there was a total of two deaths. the most common location for the edhs was parietal (20 pa tients) and temporalparietal (11 patients). conclusions: both surgical treatment and conservative management of edh have a good clinical outcome. clinical and neuroimaging evaluation at admission and romanian neurosurgery (2014) xxi 4: 504 – 546 523 dynamic imaging surveillence plays an imperative role in deciding the appropriate therapeutic attitude for each patient. key words: extradural hematoma, children, head trauma. complex surgery in cervical spine trauma t. maior department of neurosurgery, cluj county emergency hospital this paper aims to present the surgical protocol of the traumatic spine injuries, of the injuries belonging to the occipital cervical junction area as well of those in subaxial and transition cervical dorsal area. the advantages and disadvantaged, indications and contraindications, tips and tricks of the different types of approach are comparatively presented, by showing several cases from the personal database of the author. key words: odontoid surgery, anterior fusion, posterior – transarticular fusion, combined approaches. thoracic spine type c injuries according to ao classification: injury profile, management and outcome c. filip, d. serban, n. calina, g. checiu, m. podea, c. zamfir, f. exergian emergency hospital “bagdasar–arseni”, department of neurosurgery, bucharest, romania introduction: in the last years we observed an increased number of patient with multiple lesions after high energy accidents. type c injuries of the thoracic spine are the most severe lesions, with the worse prognosis. patient and methods: this study analises the injury profile, management and outcome of all pacients with thoracic spine, from t1 to t10, type c injuries treated in the spinal surgery department of "bagdasararseni" emergency hospital, in the last 5 years. results/result: there were 26 patiens admitted, mostly male = 77%, mean age 33.8 years. all of them were victims of high energy accidents. all the 26 patients presented had spine injury associated with multiple lesions (head, thoracic, abdominal and limbs). we have chosen a posterior approach in all cases, with laminectomy or hemilamnectomy, permitting us to resolve all the major objectives of the surgery with the advantage of lower blood loss and a smaller operating time. the purpose of surgery was to achieve decompression of the spinal cord and the stability of the thoracic spine. we treated surgically 19 patients and conservative 4 patients. conclusions: thoracic spine type c fractures remain a challenge for the spinal surgeon. these lesions require a multidisciplinary team approach for the treatment of the associated lesions. the main goal of the surgery is to achieve stability of the fractured segments. the timming for surgery is indicated mainly by the associated respiratory problems. key words: thoracic spine, type c injuries. 524 selected abstracts of the 40th congress of the rsn percutaneous transpedicular stabilization in thoraco-lumbar fractures patients g. zapuhlih institute of neurology&neurosurgery department of neurosurgery, chisinau, moldova introduction: we present our preliminary results of using percutaneous transpedicular stabilization in thoraco-lumbar fractures patients. patient and methods: four patients with spinal fractures in thoraco-lombar region, were operated on using stabilizing procedures in our institution during the period of time since february 2013 till august 2014. results/result: in all 4 cases we obtained good stabilization using monoaxial screws , and no mobility limitations conclusions: percutaneous 4 screws fixation time in thoraco-lumbar region is faster and the intraoperative bleeding is less in comparison with open surgery , with average operative time of 45-60 minutes, and bloodshed of about 200 ml, instead 135 minutes and 1 liter. key words: percutaneous, transpedicular, thoraco-lumbar fractures immunohistochemical expression of gfap-δ and nestin in cerebral astrocytomas correlates with tumor invasiveness felix brehar1, mircea gorgan1, dorel arsene2, lacramioara brinduse3 1clinic of neurosurgery “carol davila” university of medicine and pharmacy, bucharest 2victor babes” national institute of pathology, splaiul independenţei 99 – 101, bucharest 3public health and management, “carol davila” university of medicine and pharmacy, bucharest introduction: gfap-δ, the delta isoform of glial fibrilary acid protein (gfap), is particularly expressed in the subventricular zone (svz) of the brain. gfap-δ positive cells in the svz co-express the neural stem cells (nscs) marker nestin. according to the theory of glioma oncogenesis transformation of a cell population with stem features which resides in the svz could be the origin of astrocytomas. the working hypothesis of this paper is that cerebral astrocytomas retain the molecular signature of precursor cells and express the gfap-δ and nestin. material and methods: we investigated the immunostaining of gfap-δ and nestin in cerebral astrocytomas and evaluated the correlation between the positive cell ratio of these markers and the neuroimaging features associated with tumor invasion in forty-four cases of grade ii, iii and iv cerebral astrocytomas (world health organization's classification). tissue samples were obtained by stereotactic biopsies in all cases. gfap-δ and nestin immunostaining were graded in a semi-quantitative manner taking into account the ratio of positive cells. according to the neuroimaging criteria, tumors were categorized in highly-invasive and low-invasive. results: there were thirty-seven highgrade astrocytomas (thirty-five glioblastomas and two anaplastic astrocytomas) and seven low-grade (diffuse) astrocytomas included in romanian neurosurgery (2014) xxi 4: 504 – 546 525 this study. most of the low-grade and highgrade astrocytomas express gfap-δ and nestin. there is a statistically significant correlation between the neuroimaging invasiveness of cerebral astrocytomas and gfap-δ immunostaining grade (rho=0,484, n=44, p=0,001) and nestin immunostaining grade (rho=0,362, n=44, p=0,012). conclusions: our results show that gfap-δ and nestin positive cell ratio in biopsy samples of cerebral astrocytomas correlates with tumour invasiveness assessed by preoperative neuroimaging investigations. therefore, we suggest that gfap-δ and nestin could have potential clinical implications as markers associated with tumor invasiveness in cerebral astrocytomas. key words: cerebral astrocytomas, gfap-δ, nestin, immunostaining. acknowledgments: this work was supported by grant no.28487/30.10.2012 of university of medicine and pharmacy “carol davila”, bucharest, romania. preservation of passing-through vessels during brain tumor resemoval i. poeata1,2, z. faiyad2, a. chiriac1, b. iliescu1, c. apetrei2, a. iencean2 1“gr. t. popa” university of medicine and pharmacy, iasi, romania 2“prof. dr. n. oblu” clinical emergency hospital, iasi, romania cranial base meningiomas and high grade gliomas are the most frequent tumors that can incorporate brain vessels into the tumor mass. sometimes tumors lobs just cover the vessels with or without vessel wall infiltration, other times the vessel trunk (i.e. carotid artery, pericallosal artery, sylvian artery, rolandic artery or important venous trunks) cross the tumor mass giving vascular supply for the tumor or collaterals traversing the tumor with brain destination to more or less important areas. for the big trunks preop images, neuronavigation and intraop echodopler can give indications about the position but not about the cleavage plane between the vessel wall and the tumor tissue. for perforators and other small branches careful dissection can provide identification and preservation. for big vessels reconstruction is sometimes possible with suture or tangential clips. at the end the balance between the decision to maximize the tumor resection continuing dissection or to live bigger or smaller part of the tumor for avoiding vessels potential damage remains a challenge in all this cases. we present videos from our surgeries to document our attitude concerning this topic. our experience in a series of 277 brain avms, microsurgical treatment and outcome m.r. gorgan2, v.gh. ciubotaru1, ligia gabriela tataranu2, al. tascu2, a. iliescu1, narcisa bucur1, angela neacsu1, f.m. brehar2, aurelia mihaela sandu1 1clinic of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest, romania 2university of medicine and pharmacy “carol davila” bucharest, romania introduction: brain arteriovenous malformations (avms) are congenital tangle 526 selected abstracts of the 40th congress of the rsn of dysplastic vessels. method: we reviewed medical records of patients with brain avms operated from 1999 to june 2014, in clinic of neurosurgery, emergency clinical hospital bagdasar-arseni. results: 277 patients with brain avms underwent surgery. mean age was 29.82 years. fourty five patients (16.25%) had grade i spetzler-martin avms, 100 patients (36.10%) grade ii, 81 patients (29.24) grade iii, 39 patients (14.08%) grade iv and 12 patients (4.33%) grade v. in 250 patients (90.25%) avms were supratentorial and in 27 cases (9.75%) were infratentorial. 195 patients had ruptured avms, 86 presented seizures and 111 cases had motor deficits. we performed total resection of avms in 228 cases (82.31%). following surgery modified rankin score improved in 202 patients (73%), remained unchanged in 41 (15%) and deteriorated in 34 patients (12%) (wilcoxon test p=0.000, z=9.248). short term morbidity rate was 37%. long term follow-up revealed favorable outcome in 241 patients (86.7%). mortality was 6.1%. conclusions: microsurgery is the treatment of choice in avms. in the majority of cases the outcome was favorable. surgical results were good, with low morbidity and mortality. patients with poor results belonged to the group admitted with severe altered state of consciousness, massive hematomas and acute brainstem dysfunction. acknowledgement: this paper was cofinanced from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 “excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis”, coordinator the bucharest university of economic studies. phosphorylated neurofilament subunit nf-h in csf is biomarker in acute traumatic spinal cord injuries st.m. iencean1, a. tascu2, a.st. iencean3, i. poeata1, r.m. gorgan2 1gr.t. popa university of medicine and pharmacy, iasi, neurosurgery, iasi, romania 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania introduction: the objective of this study was to measure the phosphorylated neurofilament subunit nf-h (pnf-h) in cerebro-spinal fluid of patients with spinal cord injury and to determine the correlation between the pnf-h levels and the severity of the injury. patient and methods: the study included 15 subjects with acute traumatic spinal cord injury: eight patients with complete spinal cord injury (sci) and seven patients with incomplete sci. all patients were classified according to the american spinal injury association impairment scale (asia) and all patients underwent surgery during the first 24 hours (decompression, stabilization). we measured daily the heavy phosphorylated neurofilament subunit (pnf-h) concentration by sandwich elisa test in csf romanian neurosurgery (2014) xxi 4: 504 – 546 527 in all patients and and we correlated the values of pnf-h with the clinical evolution. results/result: for all patients with sci pnf-h was detectable in csf samples and the values were different in the cases of complete sci toward the cases of incomplete sci and the cerebro-spinal pnf-h level was more elevated in cases of complete sci. the level of csf pnf-h was of ten till hundred times higher in complete sci than the level of csf pnf-h in cases with incomplete sci, where the level of this biomarker was close to normal. the patients with a favorable neurological evolution after treatment had a specific pattern of daily values of nfp-h: a sudden increase up to a maximum value then a progressive decrease until normal. the maximum values were different in each case, from 10 times up to 170 times higher than the normal. conclusions: the phosphorylated form of the high-molecular-weight neurofilament subunit nf-h (pnf-h) in cerebro-spinal fluid can be a specific biomarker for spinal cord injury and it can distinguish the severity of sci. pnf-h is a predictive biomarker because of its values pattern can show the reducing or stopping of the secondary lesion and the favorable result. key words: biomarker, cerebro-spinal fluid, phosphorylated neurofilament subunit nf-h, spinal cord injury spinal intramedullary cavernomas. personal experience reffering to six cases g. iacob university emergency hospital, department of neurosurgery – suub, bucharest, romania introduction: despite cavernous malformations of the cns are pathologically similar, intramedullary cavernous malformations are very rare lesions, increasingly recognized after introduction of magnetic resonance image, generating gradual neurological decline, with severe deficits or acute loss of spinal function. patient and methods: we present our experience with 2 cervical and 4 thoracal spinal intramedullary cavernoma from 2010 to 2014 searching history, onset of clinical manifestation, neurological status, radiological findings, operation, and clinical outcome. results/result: among 6 patients male were 2 cases; female 4 cases; mean age was 42 years (range 25-72 years); mean duration of symptoms were 1,5 years (range 5 days and 2 years) with slowly progressive neurological decline. in two cases there was acute onset of neurological compromise. in all cases diagnosis was made on mri and lesions were possible to be radically excised and gently extracted from the hemosiderin-stained bed inside of the spinal cord via a laminectomy and midline myelotomy with microsurgical techniques. the surgical outcome on a mean duration of follow up of 12 months were: for 5 cases the patients neurological conditions 528 selected abstracts of the 40th congress of the rsn remarkably improved 1 month later, for 1 case no improvement were remarked. conclusions: spinal intramedullary cavernoma should be early recognized by mri, can be positioned in a precarious position and generate significant neurologic deficits than cranial cavernomas. for symptomatic intramedullary cavernous malformations extended to the dorsal surface of the spinal cord, total resection with microsurgical techniques can offer good or excellent outcome, restoring neurological status and to stop chronic deterioration and acute rebleedng. to asymptomatic patients with deeper lesions which entail a higher operative risk, but also a surgically manageable cause of myelopathy a closed observation is mandatory. key words: intramedullary cavernous malformation, microsurgical resection. first results of cyberknife radiosurgery of meningiomas compared to international workgroups fabian fehlauer, thomas schneider, karen piefel, simone glessmer-junike, torsten maass, oliver bislich, nelem lange, michael heinrich seegenschmiedt the radiation oncology clinic hamburg, hamburg, germany introduction: outcome-report about cyberknife-radiosurgery experience of intracranial meningeomas (im) from hamburg, germany in comparison to published datas. patient and methods: 28 patients (2011–2014) with im were treated with robotic cyberknife radiosurgery (ck-srs) in our centre. resection before srs was performed in 5/28 (21%) cases. ck-srs as primary option in 22/28 (78%), recurrent disease in 5/28 (22%). one patient was treated after incomplete resection. target volumes varied from 20–130ccm. patients were treated in 1-5 fractions, depending on size and location. 30% of lesions were meningiomas at high risk (hrm) areas closed to optical nerves, pathways or brainstem were treated in five fractions. mri follow-up was at 3/ 6/ 12/ 18 and 24 month after treatment. results/result: follow-up extended from 6 to 40 months (median 24 months). only minor srs–toxicities was observed: mortality: 0%, morbidity: 3% (grade 1: headache 3%, no grade 2 ≥ side effects). no patients underwent salvage resection after cksrs. no recurrence until today. no side effect on hrm. results will be comparable to literature. non-robotic systems have equal local control but significant higher morbidity (2– 9% vs. 0.5–1% ck). conclusions: high precision, high tumor coverage and the steep dose gradients make ck-srs efficient and safe. even for larger and more complex volumes near organs at risk cyberknife offers a noninvasive srstreatment option. all patients showed excellent clinical outcome in terms of high local control, minor side effects and good quality of life. romanian neurosurgery (2014) xxi 4: 504 – 546 529 key words: radiosurgery, meningiomas, cyberknife intramedullary tumors: clinical features and outcomes 5 years experience m. catana1, v.m. prună1,2, a. giovani1, oana rata1, mariana cochior1, m.r. gorgan3 1clinical hospital “bagdasar-arseni”, bucharest, romania 2ph.d. student in neurosurgery university of medicine and pharmacy “carol davila”, bucharest 3clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: intramedullary tumors rare lesions. this study discusses the clinical features at presentation, the outcomes, giving a few hints on tehnical nuances and complications. patient and methods: this is a retrospective review of the data of 41 patients with intramedullary tumors admitted for treatment in the ivth neurosurgical department of bagdasar arseni university hospital between january 2009 and december 2013. only 36 patients were evaluated with preoperative and postoperative magnetic resonance imaging (mri) and underwent microsurgery. the diagnosis of certainty was made on pathological criteria. asia score and modified mccormick classification was applied to assess neurological function before and after surgery. results/result: there were 17 males and 19 females with a mean age of 46.8 years. twelve tumors were located in the cervical cord, 19 in the thoracic cord, and 5 in the conus medullaris. gross total resection (gtr) of the tumor was achieved in 29 cases, and subtotal resection (str) was achieved in 7 cases. the histopathology proved 25 tumors to be ependimomas,6 hemangioblastomas, 5 astrocitomas. patients presented with nonspecific symptoms and the mean duration of symptoms was 37.4 months.. during a mean follow-up period of 62.4 months, no recurrence or regrowth of the residual tumors was observed in the 7 cases of subtotal resection on mri. 92% of patients experienced an improvement in the mccormick grade and asia score and 8 % of patients maintained their preoperative status. conclusions: excepting high grade astrocitomas, intramedullary tumors are benign lesions with a tendency to grow and to develop neurological deficit. . the accurate diagnosis depends on pathology. for symptomatic patients, early surgery should be performed before neurological deficits deteriorate. when gtr cannot be achieved, str of the tumor for decompression is advised as in the current series no regrowth or reccurence was observed after str. postoperative radiotherapy is not recommended for these benign tumors. with few exceptions tumor resection is associated with a good outcome. key words: intramedullary tumors, ependimoma, astrocytoma. 530 selected abstracts of the 40th congress of the rsn frontotemporal versus bifrontal approach for anterior cranial fossa meningiomas m.r. gorgan2, narcisa bucur1, angela neacsu1, aurelia mihaela sandu1, f.m. brehar2, v.m. pruna1, catioara fanica cristescu1, a. giovani1, silvia mara1, anamaria gheorghiu1, adrian barari1 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: meningiomas of anterior cranial fossa are represented by olfactory groove, tuberculum selae, planum sphenoidale, anterior clinoid process and orbital roof meningiomas. patient and methods: we reviewed medical records of patients that underwent surgery for anterior fossa meningiomas from 2009 to 2014, in the fourth department of neurosurgery, emergency clinical hospital bagdasar-arseni. results/result: there were 59 patients operated in our department. mean age was 55.58 years, sex ratio m/f was 27/32. according to grade of resection 46 patients (77.97%) had simpson grade ii, 6 patients (10.17%) simpson grade ii, 6 patients (10.17%) simpson grade iv and 1 patient (1.69%) simpson grade v. we performed frontotemporal approach in 41 cases (69.49%), bifrontal approach in 13 patients (22.03%) and frontal unilateral approach in 5 cases (8.47%). we compared mrs (modified rankin score) before and following surgery, using wilcoxon test, and we found that 46 patients improved, 10 patients remained with the same score and only 3 patients got worse (z=-5.352, p=.000). we found no difference between frontotemporal and bifrontal approaches regarding degree of tumor resection, using mann-whitney test (u=235, p=.394), but frontotemporal approach had fewer complications. morbidity was 13.55% and mortality 1.69%. tumor rest/recurrence was found in 11 patients (18.64%), and 5 underwent second surgery and 6 stereotactic radiosurgery. conclusions: anterior fossa meningioma can be operated with favorable outcome. frontotemporal approach offers the same chance of complete tumor resection as bifrontal approach, but with lower surgical risks. choosing the appropriate approach must be individualized. preserving optic nerves, optic chiasm, oculomotor nerves and, if possible, olfactory nerves is mandatory. key words frontotemporal approach, bifrontal approach, anterior cranial fossa. gelastic seizures in a patient with right paracentral tumour g. iacob university emergency hospital, department of neurosurgery – suub, bucharest, romania introduction: gelastic seizure (gs) also known as “gelastic epilepsy” is a rare type of seizure associated with several different conditions such as tumors hypothalamic hamartromas, tuberous sclerosis, hemangiomas, post infectious foci, cortical temporal dysplasia we report one case of this rare condition generated by a right gyrus cinguli gr.ii astrocytoma. romanian neurosurgery (2014) xxi 4: 504 – 546 531 patient and methods: clinical presentation: a 27 years, old male, right handed, was admitted for a 2 years history of very frequent gelastic seizures accompanied sometimes by simple motor partial seizures in both arms, more often being involved his left arm, without impairment of his consciousness state. his neurological examination was normal. diagnosis was made on native ct scan: minimal hypodense frontal right paramedian lesion, cerebral mri showed a small right, parenchymal, homogeneous lesion (16/22/15mm), well delimited, involving gyrus cinguli, without perilesional edema and mass effect, hyperintense both on t1 and t2 mr sequences, non-enhancing after gadolinium. the cerebral lesion was also documented on eeg and video-eeg recordings. results/result: using an interhemispheric microsurgical approach, above the corpus callosum and the right pericallosal artery, at the level of gyrus cinguli, a yellow-gray, infiltrative tumour, having a moderate vascularisation had been identified and totally removed. the anatomo-pathological analysis revealed a grade ii astrocytoma. the patient recovered very well, without deficits, no gelastic seizures or epileptic manifestations; three months after operation he is still free of seizures. conclusions: a case of gelastic seizures accompanied by simple motor partial seizures in both arms, without impairment of his consciousness state induced by a grade ii right gyrus cinguli astrocytoma is described and documented by radiological and electrophysiological studies. using microsurgical resection, the tumor was totally removed, the patient clinical condition improved. without an affective connotation as in temporal or hypothalamus topography, gelastic seizures are not patognomonic for hypothalamic hamartomas and in the case of frontal localization of the lesion they can be associated with motor involvement of the limbs as in our case. key words: gelastic seizures (gs), cerebral astrocytoma. choline in spinal cord predicts functional outcome in cervical spondylotic myelopathy s.c. craciunas1, m.r. gorgan2, c.m. cirstea3 1neurosurgery department, bagdasar-arseni hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy neurosurgery, bucharest, romania 3psychological sci. and physical med. & rehabil, univ. of missouri, columbia, mo, usa introduction: csm is the most common spinal cord dysfunction in patients over the age of 50. although neuroimaging has undergone spectacular development in recent years, no group of predictors has proven reliable enough for an accurate prediction of long-term functional outcome and/or individual gain following surgery in these patients. magnetic resonance spectroscopy (1h-mrs) assesses metabolites associated with various neural events involved in spinal cord pathology (e.g., n-acetylaspartate naa, reflective of neuronal integrity; choline cho – marker of inflammation; lactate lac, a marker of anaerobic metabolism). since neurological 532 selected abstracts of the 40th congress of the rsn recovery appears to be influenced by residual spared function, we proposed that the 1hmrs measurements of radiologically normalappearing (or spared) spinal cord (c2 level) can provide valuable prognostic information of recovery after decompressive surgery. methods: patients underwent clinical (functional) evaluations modified japanese orthopedic association scale (mjoa), 9-hole peg test (9-htp) and walking test (wt) / time and # steps one day prior to surgery (time1) and 6 months (time2) postsurgery. also, at time 1 all patients underwent mri and mrs. high resolution thin-sliced sagittal t2-image (tr=1500ms, te=125ms, fov=200mm, voxel size=0.6 x 0.6 x 0.6) has been acquired to reconstruct the spinal anatomy. a volume of interest (voi) with dimension of about 10 x 10 x 30 mm3 has been placed along the main axis of the cord at c2 level. for mrs acquisition we used a pointresolved spectroscopy sequence (press, te=30ms, tr=1500ms, averages=200, flip angle 90, spectral width=1000 hz) with chemical shift selective water suppression. three metabolites were quantified: naa functional recovery has been defined as the change (δ) between sessions ii and i for 9htp and wt scores (i.e., δ9-hpt = 9hptsesionii – 9-hptsessioni) and the recovery rate [rr=(mjoa sessionii mjoa sessioni)x100/(18 mjoa sessioni)] for mjoa. spearman correlation coefficient was used to determine the correlations between metabolites and functional recovery. at the moment, 10 patients have been enrolled in the study and four already accomplished the full (6 months) time course of study. results: our preliminary results suggest that high cho correlates negatively with rr and positively with δ9-hpt. a similar trend has been found between naa and functional tests, but without statistical significance. walking test did not correlate in any way with metabolical alterations. also, the lac peaks were difficult to be detected and poorly correlated with functional recovery. however, the whole group of patients needs to finalize the study in order to draw statistical conclusions. conclusions: high cho suggests remote increased membrane turnover due to inflammation/gliosis. inflammatory response in normally appearing cervical spinal cord was related to functional recovery. thus, 1h-mrs might be a sensitive method to quantify relevant metabolite changes in csm, and consequently increase our knowledge of the factors leading from these changes to neurological deficits. such objective data would help clinicians to set realistic therapeutic goals, by selection of individualized rehabilitation strategies based on the prediction of functional potential. in addition, they can also be helpful as an individual prognostic indication to relatives and patients. aknowledgments: this study was supported by eurospine – the spine society of europe. neuroendocrine carcinoma of the bran invading the frontal sinus. a microsurgical resection. romanian neurosurgery (2014) xxi 4: 504 – 546 533 the role of diffusion tensor imaging in the evaluation of the cervical spinal cord trauma b.f. iliescu1, m. dabija1, d. andronic2, p. gutu1, i. poeata1 1“gr. t. popa” university of medicine and pharmacy, iasi, romania 2“prof. dr. n. oblu” clinical emergency hospital, iasi, romania these authors contributed equally to this work cervical spine trauma with the involvement of spinal cord represents a major cause of devastating neurologic morbidity amongst the young population. the management of this condition is undermined by a poor level of evidence regarding the possible evolution and long-term outcome. numerous efforts have been made in the last decades to find the clinical and imaging indicators for the neurological and overall prognostic of these complex patients. however, little can be predicted today and the information that reaches the patient and his family rely mostly on experience and clinical flair. we wanted to analyze the quantifiable measures comprised within the diffusion tensor mri images and to see how well they correlate with the clinical status. we looked at the data from 15 patients with cervical spinal cord trauma, subaxial, and measured diffusion anisotropy, anisotropy diffusion coefficient, and fiber length and studied their grade of correlation with the neurological performance (measured on slic scale). the results showed a strong correlation between clinical and imaging data, suggesting that measures of the diffusion tensor imaging are a good indicator of the level of neurological damage. we present the results and discuss the biological and clinical implications. topical vancomycine and bacterial culture from intervertebral herniated disc prevent postoperative osteodiscitis d. adam “carol davila” university of medicine and pharmacy neurosurgery, bucharest, romania introduction: osteodiscitis represents a serious complication of lumbar disc herniation operations. the treatment of osteodiscitis is controversial and expensive to society. it extends over a period of several months from diagnosis. reducing postoperative osteodiscitis by using simple measures may limit patient's suffering and reduce costs. the purpose of this study is to evaluate the early diagnosis of bacterial infections of the intervertebral disc by isolating germs located in the herniated disc fragment and topical vancomycine powder application, along with the conventional antiinfective therapy. the purpose of this study is to evaluate the early diagnosis of bacterial infections of the intervertebral disc by isolating germs located in the herniated disc fragment and topical vancomycine powder application, along with the conventional antiinfective therapy. patient and methods: medical files of patients who were operated on for lumbar disc herniations during 01.01.2013 534 selected abstracts of the 40th congress of the rsn 30.06.2014 were reviewed. the diagnosis of lumbar disc herniation was established based on the clinical evaluation, confirmed by mri results. the surgical intervention was performed by mini-open approach: fenestration and foraminotomy completed with removal of the herniated disc fragment and disc remnants from the intervertebral space. a group of 162 patients (group a) received conventional therapy for prevention of post-operative infections with 2 doses of cephalosporin. in the second group of 137 patients (group b), after the removal of the herniated disc fragments, 1g of vancomycine powder was topically applied and the disc fragments were bacteriologically analyzed. they received the conventional treatment of preventing post-operative infections with cephalosprin 2 doses. results/result: the two groups of patients were similar in terms of demographic characteristics: age, sex, operative level. out of the 162 patients of group a, one patient developed postoperative osteodiscitis and was treated for 3 months with antibiotics. regarding patients in group b, in four cases staphylococcus was isolated from the disc fragments. postoperative treatment for these patients with prolonged antibiotic therapy over the standard period avoided the developement of the clinical picture of osteodiscitis. conclusions: postoperative osteodiscitis requires prolonged antibiotherapy. by using simple measures, like topical vancomycine powder application and early isolation of germs from the herniated intervertebral disc, followed by the immediate establishment of appropriate antibiotic treatment, this serious complication is avoided. key words: herniated disc, osteodiscitis, vancomycine, microbiological examination. vagus nerve stimulation (what is it, how does it work, how to implant, results) m.r. gorgan1,2, f.m. brehar1,2 1“bagdasar-arseni” emergency clinical hospital, bucharest 2clinic of neurosurgery “carol davila” university of medicine and pharmacy, bucharest introduction: refractory epilepsy represents a severe clinic entity which affects an important number of patients. one of the surgical techniques employed in the management of refractory epilepsy is vagal neurostimulation (vns). the authors present here the first series of patients with refractory epilepsy operated and implanted with vagal neurostimulators in romania, and described in detail the surgical technique and the preliminary results. material and methods: our study included 50 patients diagnosed with refractory epilepsy, investigated, selected and implanted with vagal neurostimulators between october 2012 and august 2014 in neurosurgery clinic, "bagdasar-arseni" emergency hospital. we have implanted in all patients the latest model of vagal neurostimulator (model 103) using a left latero-cervical surgical approach. results: there were 13 children and 37 adults in this series. the gender distribution was: 23 females and 27 males. the medium age romanian neurosurgery (2014) xxi 4: 504 – 546 535 was 24,8 years. the average period of hospitalization was 3,5 days. the medium follow-up period was 14 months. there was no death in this series and no intraoperative incidence. one patient presented dysphagia postoperatively which completely remitted after two months. conclusions: vns represents now a safe, quick and efficient surgical procedure with a minimum period of hospitalization and a short recovery period. key words: refractory epilepsy, vagal neurostimulation. cerebral venous etiology of intracranial hypertension st.m. iencean1, a.st. iencean2 1gr.t. popa university of medicine and pharmacy, iasi, neurosurgery, iasi, romania 2emergency prof. dr. n. oblu hospital, neurosurgery iii, iasi, romania introduction: the aim of this study was to present the characteristics that differentiate between idiopathic intracranial hypertension and intracranial hypertension caused by intracranial vascular damage. patient and methods: this study included twenty-one patients, 14 women and 7 men of 18 – 61 years old. the main symptoms and the imaging findings diagnosed intracranial hypertension in the absence of an expansive intracranial process, hydrocephalus and intracranial infection. results/result: cerebral angiography with venous phases showed whether there was cerebral vascular disease (cerebral venous thrombosis, venous sinus thrombosis or stenosis). the pressure of the cerebro-spinal fluid was determined by repeated lumbar puncture with manometry after the exclusion of endocranial lesions by cerebral explorations. the analysis of the symptomatology correlated with the values of intracranial pressure, and the imaging findings revealed significant differences between these two types of intracranial hypertension. conclusions: vascular intracranial hypertension has a known etiology, such as cerebral vascular illness, and a relatively rapid increase in intracranial pressure of approximately 21 cm h2o. intracranial hypertension caused by intracranial vascular damage is named vascular intracranial hypertension. the treatment of vascular intracranial hypertension is etiologic, pathogenic and symptomatic, but that of idiopathic intracranial hypertension is only symptomatic. key words: intracranial pressure, vascular intracranial hypertension, venous sinus stenosis, venous sinus thrombosis the endovascular, minimal invasive, cerebral aneurysms treatment with vascular remodeling techniques with stents and balloons st. dima1, m. lucian2 1interventional neuroradiology, department of angiography, national institute of neurology and cerebrovascular diseases bucharest 2clinic of neurosurgery university of medicine and pharmacy tg. mures 536 selected abstracts of the 40th congress of the rsn introduction: the large neck cerebral aneurysms can be treated endovascular way, helped by the remodeling techniques with balloons and stents. patient and methods: 89 cerebral aneurysms at 83 patients treated endovascular, minimal invasive, with coils and remodeling techniques with 64 balloons and 36 stents. we used the balloons and stents to keep the coils inside the aneurysm sac. results/result: all the 89 aneurysm were coiled and the parent vessels remained patent. the recanalization rate of the aneurysm at 6 and 12 months follow up was 6%. 2 cases of stent occlusion because the patients did not take the double antiplatlet inhibition (with plavix and aspirin) after stent implantation. conclusions: most of the cerebral aneurysm can be treated safe in this moment, minimal invasive, endovascular way, helped by remodeling techniques with stents and balloons. key words: cerebral, aneurysm, endovascular, stent, balloons. second neurosurgical masterclass clujnapocaintroduction to vascular neurosurgery cristina caterina aldea1, v. volovici2, i. caravan1, i.s. florian1 1“iuliu hatieganu” university of medicine and pharmacy, cluj-napoca, romania 2erasmus university medical center, rotterdam, netherlands introduction: the second neurosurgical masterclass, “introduction to vascular neurosurgery” was held between 28th february and 1st march 2014 in clujnapoca. it was organized by the students’ scientific circle of neurology and neurosurgery under the auspices of the neurosurgical department of cluj-napoca. it was addressed to students and residents. the previous edition of this event was the first known neurosurgical course dedicated to medical students, held in july 2013. patient and methods: our course was designed to offer first-hand guidance from experienced speakers. before the course, participants received a textbook specially written for this occasion by students and residents under the guidance of the main author. the lectures were divided into three days. results/result: 281 medical students from 8 university centers from romania and abroad participatedin this course. our speakers comprised of a professor of neurosurgery, an endovascular specialist, residents and students. the lecturers encompassing three generations meant that the auditorium could witness different stages of neurosurgical evolution, the importance of experience and mentorship. the first day was dedicated to the history of vascular neurosurgery. on the second, a review of relevant anatomy and neuroimaging were provided. on the last day we discussed intracranial vascular lesions and case presentations. conclusions: the goal of the course, to give participants a guide to the field of vascular neurosurgery, was accomplished. we managed to create a bridge not only between romanian neurosurgery (2014) xxi 4: 504 – 546 537 the present and the future generation of neurosurgeons, but also between university centers. considering the positive feedback provided by the participants these courses will continue. key words: vascular neurosurgery, course, students. multiple cranial tumors in a 26year-old male with neurofibromatosis type 2 francesca gabriela ochea2, dana pisica2, adriana solomon1, v. ciubotaru1, ligia – gabriela tataranu2 1clinical hospital “bagdasar-arseni”, bucharest 2clinic of neurosurgery university of medicine and pharmacy “carol davila”, bucharest introduction: neurofibromatosis type 2 is an autosomal dominant inherited disorder predisposing to multiple benign tumors of the nervous system, such as meningiomas, ependymomas, vestibular shwannomas and other cranial nerve and peripheral schwannomas. bilateral vestibular schwannomas are found in 90–95% of the cases and it is reported that 99% of them are benign. however, they remain an important cause of mortality due to their location. patient and methods: in this paper we present a case report of a 26-year-old male admitted with ataxia, headache, nausea, emesis and bilateral sensorineural hypoacusis, intracranial hypertension syndrome and cerebellar syndrome. the patient also presented with significant congenital hypotrophy of the lower and upper limbs. the cerebral mri scan revealed multiple cranial tumors, schwannomas and meningiomas, located in both cerebellopontine angles, right lateral ventricle (temporal horn), right frontal lobe (paramedial), left frontal lobe (parasagittal). the overall aspect suggested the diagnosis of neurofibromatosis type 2. over the course of one year, the patient underwent 3 different neurosurgical interventions, in order to improve the neurological symptomatology. results/result: the postoperative clinical evolution was favorable, without subsequent motor deficits. the ct scan performed 6 months after the last neurosurgical intervention showed no tumoral recidivation and no changes in tumor size. conclusions: due to the benign nature of the tumors associated with neurofibromatosis type 2, neurosurgical resection was used only as a cure for complications caused by tumor growth. the typical treatment strategy is „watch and wait then rescan”, meaning that close monitoring of the patient’s neurological status and periodic scanning are recommended. key words: meningioma, schwanomma, neurofibromatosis. prognosis value of computer tomography for patients with cerebellar hemorrhage in good neurological status gcs = 13-15 al.v. papacocea1, t. papacocea3, l. danalia2 1emergency clinical hospital, neurosurgery, ploiesti, romania 2“carol davila” university of medicine and pharmacy neurosurgery, bucharest, romania 538 selected abstracts of the 40th congress of the rsn 3emergency clinical “st. pantelimon” hospital, neurosurgery, bucharest, romania introduction: for patients with cerebellar hemorrrhage in good neurological status (gcs=13-15) sometimes terapeutical management may be difficult. in many studies, different authors tried to find predictors for outcome and determine what the best choice is for these patients: surgery or medical treatment only. patient and methods: we made a retrospectiv study of 66 patients with primary cerebellar hemorrrhage, admitted in hospital in good neurological status (gcs=13-15). we have considered three ct factors suitable for predicting patient outcome: largest diameter of hemorrhage (measured on axial ct), shape of the fourth ventricle and aspect of the cvadrigeminal cistern. results/result: all patients with cerebellar hemorrhage with maximum diameter less than 3cm and only 79% of those with diameter higher than 3cm had a good prognosis. good prognosis has been related in all cases with normal shape of the fourth ventricle, in 88% of patients with partial compression of v4 and only in 56% of patients with complete obliteration. good prognosis has been related in in all cases with normal cvadrigeminal cistern, in 84% of patients with partial obliteration and only in 63% of patients with complete obliteration. conclusions: 1. patients in gcs=1315 with cerebellar hemorrhage having maximum diameter less than 3 cm, normal shape of the fourth ventricle and cvadrigeminal cistern can receive only medical treatment 2. patients with complete obliteration of the fourth ventricle or cvadrigeminal cistern have better prognosis with early surgery key words: cerebellar hemorrhage ct prognosis. neuroendocrine carcinoma of the bran invading the frontal sinus. a microsurgical resection v. munteanu, r. stanescu neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania neuroendocrine tumors are rare, accounting for less than one percent of all malignant disorders. these tumors can only be accurately diagnosed when a pathologist examines a tissue sample using specialized stains that help clarify the cells’ subtype. urine also may be tested for elevated levels of specific products that are related to this type of cancer. neuroendocrine carcinomas can originate in different locations including the gastrointestinal tract, lung, and brain. some tumor cells produce hormones, while other cells cause no symptoms. case report: a 60 years old male presented in our hospital for loss of smell, headache and for the appearance of an epicranial tumor in the frontal region. the ent doctor discovered a tumor inside his nose. irm study discovered a tumor with ethmoidal origins that invaded the ethmoidal cells, the left frontal sinus, the duramater and with mass effect upon the cerebral parenchyma. romanian neurosurgery (2014) xxi 4: 504 – 546 539 results: the tumor was resected via a frontal approach. it had infiltrated the ethmoidal cells, the frontal sinus and the duramater. we evacuated pus from the frontal sinus. histophatological exam showed a neuroendocrine carcinoma. post-op evolution was uneventfull, the pacient being kept for 10 days under. key words: neuroendocrine carcinoma, microsurgical resection, pus in the frontal sinus. multiple brain cavernomas: microsurgical resection of two lesions v. munteanu, r. stanescu neurosurgical clinic, “bagdasar – arseni” clinical hospital, bucharest, romania background: cavernomas of the brain are congenital lesions clinically divided into hereditary and sporadic forms. multiple lesions are usually observed in the familial form, whereas the sporadic variant generally shows a single cavernoma. in this case we describe the case of a patient with two left side cavernomas, one pontomezencephalic and the other temporoinsular that were treated surgically. case description: a 43 years old male was admitted in our hospital for right hemiparesis, right cranial nerve iv paresis, headache and vomiting. the irm study identified two lesions that were treated surgically. the pontomezencephalic lesion showed signs of bleeding. results: both lesions were treated surgically, the temporoinsular one by opening the sylvian valley and the brain stem one by a subtemporal approach. post-op evolution was uneventfull.the patient had no additional neurological deficits. key words: hemangioma, cavernous, central nervous system, hemmmorage, familial cerebral cavernous malformation. posterior fossa cavernous malformations: treatment and surgical outcome – a 5 years experience a. giovani clinical hospital “bagdasar-arseni”, bucharest introduction: only 15% of cavernous malformations are located in the posterior fossa, yet this location is associated with important neurological deficits and even death if left untreated. we review here the experience of our department with a series of 15 consecutive cases. patient and methods: we reviewed the case files of 15 consecutive cases of brainstem and cerebellar cavernous malformations operated between january 2009 and december 2013. special attention was paid to the accuracy of diagnosis as predicted by the mri, to the operative protocol and to the follow up. the patients were followed on average for 26 months using karnovsky performance score. results/result: we reviewed the case files of 15 consecutive cases of brainstem and cerebellar cavernous malformations operated between january 2009 and december 2013. special attention was paid to the accuracy of 540 selected abstracts of the 40th congress of the rsn diagnosis as predicted by the mri, to the operative protocol and to the follow up. the patients were followed on average for 26 months using karnovsky performance score. conclusions: total removal should be the standard treatment of posterior fossa cavernomas and where there is no danger of injuring the brainstem, the surrounding hemosiderin ring should be removed as well. “this paper was co-financed from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 "excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis", coordinator the bucharest university of economic studies” key words: brainstem; cavernous malformation; surgery. analysis of 98 patients with apoplexy in a pituitary adenoma: clinical characteristics, management and prognostic factors adriana solomon¹˒², ligia tataranu¹˒², vasile ciubotaru¹ ¹neurosurgical clinic, “bagdasar – arseni” emergency clinical hospital, bucharest, romania ²“carol davila”university of medicine and pharmacy, bucharest, romania introduction: pituitary apoplexy is a clinical syndrome characterized by abrupt and occasionally catastrophic occurrence of hemorrhagic or ischemic infarction of a pituitary adenoma. material and methods: between january 2009 and december 2013, 98 patients were diagnosed with pituitary apoplexy and treated in our neurosurgical department from “bagdasar – arseni” emergency clinical hospital, bucharest, romania. adequate follow-up was obtained for all patients of the study. there were 62 women (63.3%) and 36 men (36.7%) with age between 17 and 75 years old. the mean age at admission was 49.9 years. results: there were 98 tumors with pituitary apoplexy, 14 tumors were microadenomas (14.3%) and 84 were macroadenomas (85.7%). in our study there were 64 non-functional adenoma (65.3%), 24 prolactinomas (24.5%), 7 somatotroph adenoma (7.1%) and 3 corticotroph adenomas (3.1%). in all cases urgent transnasal transsphenoidal approach was made and hormonal replacement when needed. the histopathological examination confirmed the diagnosis of pituitary apoplexy. in all cases ocular motility improved after surgical decompression, deficits in visual acuity and visual field deficits were partially resolved after surgery, with better results when surgery was done in the first week after diagnosis. conclusions: pituitary apoplexy represents a true neurosurgical emergency for which rapid diagnosis and glucocorticoid replacement are the first important steps. urgent transsphenoidal decompression is recommended to save life, visual function and to have the chance to regain pituitary function. romanian neurosurgery (2014) xxi 4: 504 – 546 541 acknowledgement: this paper was co-financed from the european social fund, through the sectorial operational program human resources development 2007-2013, project number posdru/159/1.5/s/138907 "excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis", coordinator the bucharest university of economic studies. key words: apoplexy, pituitary adenoma. planum sphenoidale meningioma – case report and review of the literature b.c. dumitrescu1,2, tabita larisa cazac2, v. ciubotaru¹, ligia tataranu1,2 ¹department of neurosurgery, emergency clinical hospital “bagdasar-arseni”, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania background: meningiomas of the central subfrontal region originate either from the olfactory groove, planum or jugum sphenoidale or suprasellar area, accounting for about 5% to 10% of all intracranial meningiomas in a review of the world literature. they represent a subgroup of anterior skull base meningiomas, planum sphenoidale meningiomas being located more anterior and in proximity of the olfactory groove location. objective: we are reporting a case of a planum sphenoidale meningioma successfully resected using a classical left pterional approach. methods: a 64-year-old woman presented with symptoms of opto-chiasmatic syndrome, with progressive visual disturbance, headache and nerve compression from a planum sphenoidale meningioma. preoperative magnetic resonance imaging showed a well-defined suprasellar solid mass with homogenous enhacement and a broad dural attachement to the planum sphenoidale. surgical resection was performed using a left pterional approach. the intraand postoperative courses were uneventful with a partial recovery. the opto-chiasmatic syndrome persisted but the postoperative computer tomography investigation showed total surgical removal with no residual tumor. conclusion: in order to obtain a better postoperative outcome, the planum sphenoidale meningiomas must be diagnosed early and the operative procedures are to be performed with utmost care and in time. egfr inactivation in combination with temozolamide induced synergistic cytotoxicity in low passage glioblastoma cell line: in vitro study ada maria georgescu1, ligia gabriela tataranu2,3, florentina serban1, oana alexandru1, vrajitoru alisa1, roxana folcuti1, v. ciubotaru2, anica dricu1 1university of medicine and pharmacy of craiova, biochemistry unit 2”bagdasar-arseni” emergency clinical hospital, bucharest, neurosurgery department 3“carol davila” university of medicine and pharmacy, bucharest, romania 542 selected abstracts of the 40th congress of the rsn the central nervous system (cns) tumours are the most common solid tumours. despite the successful introduction of multimodal therapy approaches (modern surgery, etc) and new cytostatics, the prognosis of many brain tumous, especially high-grade brain tumours remains grim. drug failures in the clinic may be due to the fact that preclinical models do not represent the heterogeneity that is observed in human tumours. compared to established cell lines, low passage cell lines were reported to better preserve features of cancer. at low passage, cancer cell lines are a mixture of several cell populations and should better mimic the tumour heterogeneity in vivo. for this reason, they are supposed to have better value as tumor models. in this study, we used a low passage primary brain tumour cell line derived from glioblastoma tumours, to analyze the effect of ag556 (a egfr inhibitor) alone or in combination with temozolmide (tmz) (a common drug for brain cancer). both ag556 (1, 5 and 10μm) and tmz (1 and 5μm) treatment, induced significant cytotoxic effect on glioblastoma cells in a doseand timedependent manner. dual treatment with ag556 and tmz resulted in synergistic cytotoxicity at a frequency of 93%, when compared to single treatment. the emerging role of alternative therapy in targeting brain tumours ligia tătăranu2,3, ştefana oana purcaru1, g. d. mogoşanu1, sandra alice buteică1, ada maria georgescu1, anica dricu1* 1university of medicine and pharmacy of craiova, romania 2emergency hospital “bagdasar–arseni”, department of neurosurgery, bucharest, romania 3“carol davila” university of medicine and pharmacy, bucharest, romania *corresponding author e-mail: anica.dricu@live.co.uk, anica.dricu@webmail.umfcv.ro recent studies have shown that more than 50% of cancer patients use plant compounds for alternative and complementary therapies. ligustrum vulgare hydroalcoholic extract (lhae) is used for prevention or treatment of several diseases including cancer. the aim of this study was to investigate the effect of lhae on the brain tumor cell viability. in the present study, we have analyzed the effect of lhae alone and in combination with temozolomide (tmz) or doxorubicin (doxo) on four primary brain tumor cell lines in vitro. we found that lhae displayed inhibition property against brain tumor cell lines including: glioblastoma (gb1b, gb2b, gb8b) and astrocytoma (ac1b). depending on drug concentration, period of treatment, lhae induced 40–60% cytotoxicity in glioblastoma cells and 60–80% cytotoxicity in low-grade astrocytoma cells. at the higher concentration used in this study (100 μl/ml), lhae induced more pronounced cytotoxic effects than both doxo and tmz in all brain tumor cell lines analyzed. in general, cytotoxic drugs are proposed to act selectivity by targeting cells that proliferate rapidly. in our study, we found that low proliferative astrocytoma cells were romanian neurosurgery (2014) xxi 4: 504 – 546 543 more sensitive to single treatment compared to rapid proliferative glioblastoma cells. the treatment with lhae failed to exhibit a real benefit when combining with a second agent tmz or doxo, except in the case of gb1b cell line where combinatorial treatment, resulted in synergistic response in 44% and additive response in 22% of the combinations. this study underlines the need for identification of new molecules able to kill brain tumor cells that would facilitate the development of better therapeutic approaches. indoor environmental quality study in an emergency hospital from bucharest ilinca nastase1, cristiana croitoru1, andreea vartires1, ligia tătăranu2,3 1technical university of civil engineering bucharest, cambi research centre 2emergency hospital “bagdasar–arseni”, department of neurosurgery, bucharest, romania 3“carol davila” university of medicine and pharmacy, bucharest, romania email: ilinca.nastase@gmail.com introduction: for the medical staff, the hospital is an ongoing environmental work space, while for the patients the hospital means a temporary space to be healed, before returning home. in this context, indoor microclimate conditions are perceived differently by the patients and the medical staff. methods: two types of questionnaires were used: for operating rooms and other areas, like wards and medical and non-medical offices. in parallel, measurements of ieq most important parameters were performed in the analyzed building. results: the questions in this survey are mostly addressed to evaluate the indoor environmental quality and the implications on the medical activity. regarding the air quality, it is perceived as low in some medical wards and relatively high in the operating zone. measurements of air quality confirmed the results of the enquiry. thermal comfort was found to be variable in function of the occupants’ activity level. measured values of the predicted mean vote and of the draft risk were confronted with data collected from questionnaires. conclusions: as it can be observed, the survey results are partially in agreement with measurements of comfort. in both cases, we recorded disagreement between the various categories and the experienced comfort sensation. it follows the importance of finding new strategies for air distribution and ventilation in operating rooms: zonal ventilation and changing the conception of the perforated panels used laminar flow ceilings for instance. acknowledgments: this work was supported by the grants of the romanian national authority for scientific research, cncs – uefiscdi, project number: pniipt-pcca-2011-3.2-1212. key words: field survey, healthcare, indoor comfort. our experience in a series of 57 patients with colloid cysts of the third ventricle d. paunescu1,2, m.r. gorgan1,2, v. ciubotaru1, 544 selected abstracts of the 40th congress of the rsn ligia gabriela tataranu1,2 1clinic of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest, romania 2university of medicine and pharmacy “carol davila” bucharest, romania objective: a variety of surgical approaches have been described to access and remove colloid cysts. endoscopic approaches are least invasive but are used especially in cases with ventriculomegaly. transcallosal interhemispheric and transcortical approaches are typically reserved for patients with symptomatic or large asymptomatic cysts without any significant hydrocephalus. for selected cases ventriculoperitoneal shunt is an option. materials and methods: we retrospectively analyzed the surgical outcome and complications of 57 patients with colloid cysts of the third ventricle operated at bagdasar arseni emergency hospital, bucharest, between 2000 and 2014. a detailed preand post-operative neurological assessment was done in all patients. ct or irm scan of the brain was done before and after surgery. results: an analysis was performed for resection rates, morbidity and mortality based on treatment strategy. a total of 32 patients were included in the microsurgical group and 25 patients in the endoscopic group. the median maximal cyst diameter was 11.3 mm (range 5-37 mm) with no significant differences between the two groups. total resection was achieved in 93.75% of the microsurgical group compared to 64% of endoscopic group (p < 0.001), but with higher morbidity in the first group (18.75% compared to 12%). the median hospital stay was 5 days for endoscopic group and 8 days for microsurgical one. there were no deaths related to the surgery. conclusion: microsurgical resection of colloid cysts is associated with a higher rate of complete resection but a higher morbidity rate than with endoscopic removal. with increasing experience, most of the complications are avoidable. key words: colloid cyst; third ventricle; complications; microsurgery; endoscopy. acknowledgement: this paper was cofinanced from the european social fund, through the sectorial operational programme human resources development 2007-2013, project number posdru/159/1.5/s/138907 “excellence in scientific interdisciplinary research, doctoral and postdoctoral, in the economic, social and medical fields excelis”, coordinator the bucharest university of economic studies. reperfusion syndrome in early childhood – case report a. iordache2, mihaela cosman*, alexandra mihaila2 1emergency hospital "n.oblu" iasi 2university of medicine and pharmacy "gr.t.popa" iasi reperfusion syndrome in children is a rare situation. we present the case of 6 month old child who had fallen from his mother arms. he presented for complete motor deficit 72 hours after the traumatic event. we have operated him and immediately he improved his motor romanian neurosurgery (2014) xxi 4: 504 – 546 545 deficit and afterwards 6 12 hours postop he became again hemiplegic. we have performed angio ct scan which shows signs of reperfusion. we follow up the infant and he had a good clinical outcome although he maintained sequels on the ct scan. the role of virtual endoscopy in planning endoscopic transsphenoidal surgery for pituitary adenomas d. rotariu1, z. faiyad1, b. iliescu1,2, a. budu1, i. poeata1,2 1“prof. dr. n. oblu” clinical emergency hospital, iasi, romania 2“gr. t. popa” university of medicine and pharmacy, iasi, romania objectives: to realize and navigate the 3d model from cts of patients and compare them to the intraoperative endoscopic images. design: prospective observational study methods: the cts of 15 patients proposed for endoscopic approach for pituitary adenoma werereconstructed using osirix (pixmeo sarl). virtual endoscopy (ve) was performed prior surgery to assess the surgical corridor and particularanatomy. we evaluated the inferior and middle turbinate, sphenoid ostia (so), choanal arch, sphenoethmoidal recess, sphenoid septa, sellarfossa, paraclival carotid prominences. the intraoperative endoscopic images were compared to the virtual images. results: the virtualimages had a good resemblance with the actual surgical images, all the structures from the nasal cavity were identified and had a perfectmatching except the so which was identified in 8 cases in ve vs. 12 intraoperative. all the structures from the sphenoid sinus were identifiedwith perfect matching except the ipsilateral parcalival carotid (10 cases in ve vs. 5 intraoperative) the ve could not appreciate the state of thesellar floor in none of the cases. conclusions: the preoperative knowledge of the nasal and sphenoid anatomy may generate benefits duringthe performance of surgeries, anyhow detailed information concerning the integrity of structures could not be offered by this technique and it offers no additional information in cases where the sphenoid sinus is fully occupied by tumor or not aerated. awake craniotomy for eloquent areas tumors – case report m. cosman1, a. iordache1,2, g. ion1, c. apetrei1, a. cucu1, a. rotaru3, i. poeata1,2 1“prof. dr. n. oblu” clinical emergency hospital, iasi, romania 2“gr. t. popa” university of medicine and pharmacy, iasi, romania nowadays the role of brain tumors surgery is to maximize the tissue resection and to minimize the postoperative morbidity. lesions located in eloquent area have a high risk for a neurological impairment. we present the case of a 31yearsold male admitted in our department with right-sided body hypoesthesia since one month associated with general seizures. mri showed an infiltrative lesion located on the left temporoparietal region. because the language area was 546 selected abstracts of the 40th congress of the rsn trapped in the tumor and due to imagistic difficulty in specifying the involvement of the motor area we managed surgically this patient using the technique of awake craniotomy. the outcome was favorable with no neurological deficit. the histology was low grade glioma. because remnant infiltrative part of the tumor exists on postop images, chemo and radiotherapy was applied. the patient has a 2 years neurological free outcome until now and not imagistic modifications. we present this case together with pre/postop images; follow up images, histology, anesthesia for awake craniotomy protocol and treatment protocol. this method allows intraoperative brain mapping with identification and protection of functional cortex and it provides a good alternative for intraoperative functional monitoring in lesion located in eloquent areas. doi: 10.33962/roneuro-2020-092 dorsolumbar angiolipoma. a rare case report and review of literature surendra kumar gupta, anuj chhabra, hanuman kumar prajapati, faran ahmad romanian neurosurgery (2020) xxxiv (4): pp. 540-543 doi: 10.33962/roneuro-2020-092 www.journals.lapub.co.uk/index.php/roneurosurgery dorsolumbar angiolipoma. a rare case report and review of literature surendra kumar gupta1, anuj chhabra2, hanuman kumar prajapati3, faran ahmad4 1 mch neurosurgery. assistant professor. department of neurosurgery, aiims raipur, india 2 assistant professor. department of neurosurgery. kalpana chawla government medical college, karnal, haryana, india 3 mch neurosurgery. assistant professor. department of neurosurgery, uttar pradesh university of medical sciences, saifai, etawah, india 4 dnb neurosurgery. senior resident. department of neurosurgery, dr ram manohar lohia institute of medical sciences, lucknow, india abstract a 55-year-old female was presented with complaints of tingling sensations of the bilateral lower limb with spastic paraplegia for last one year. her pre-operative contrast mri study of dorsolumbar spine was suggestive of extradural angiolipoma. she underwent d11, d12 and l1 laminectomy and a mildly vascular yellowish globular extradural mass was found which was excised completely and dural decompression was achieved. post-operatively, the patient’s neurologic symptoms improved. conclusion: spinal angiolipoma is considered a rare benign entity which emulates malignancy. it should be included as a differential diagnosis of the spinal epidural tumour with fat component and a high degree of vascularisation. surgical removal of this epidural tumour through a proper and comprehensive approach provides complete and permanent recovery. introduction spinal angiolipoma and angiomyolipoma are rare tumors, there incidence was noted only 0.14% of all tumors of the spinal axis. it is difficult to distinguish them from spinal lipoma, as they are found mainly in adults. they are localised almost exclusively in the dorsal epidural space of the thoracic spine [4]. they are not associated with any malformation. these lesions usually show no tendency to involve the surrounding tissue although some may show infiltrative process into the bony compartment of the vertebral column [5, 14]. we are reporting a rare case of angiolipoma of the dorsolumbar spine in a 55-year-old female patient that was diagnosed by pathological examination following surgical resection, and discuss the imaging findings of angiolipoma published in literature. keywords spinal extradural tumour, spinal angiolipoma, angiomyolipoma corresponding author: anuj chhabra assistant professor. department of neurosurgery. kalpana chawla government medical college, karnal, haryana, india dranujchhabra123@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 541 a rare case of dorsolumbar angiolipoma case report a 55-year-old female were admitted in our hospital with complaints of tingling sensation of bilateral lower limb with spastic paraplegia for last one year. her neurological examination was showing paraplegia with diminished sensations over b/l lower limbs. knee and ankle jerks were exaggerated with significant increase in tone. her mri (magnetic resonance imaging) dorsolumbar spine was showing signal of the fat and blood vessels. the fatty content was hyperintense on both t1and t2-weighted images (similar to the signal of subcutaneous adipose tissue) and hypointense on fat-suppressed images. the vascular component was hypointense on t1-weighted and hyperintense on t2-weighted, and showed intense enhancement with gd-dtpa infusion (figure 1). figure 1. spindle shaped extradural contrast enhancing on t1w contrast (1a, d) and hyperintense on t2w (1b,c,e). she was planned for laminectomy with decompression of cord under general anaesthesia. she underwent d11, d12 and l1 laminectomy and a mildly vascular yellowish globular extradural mass was found which was excised completely and dural decompression was achieved on histopathological examination. microscopic examination revealed sheets of mature adipocytes arranged in lobules divided by delicate intervening fibrous septae showing numerous thick-walled blood vessels without elastic lamina. no evidence of malignancy was noted, so histopathology diagnosis of angiolipoma was given (figure 2). figure 2. photomicrographs show mature adipose tissue and proliferated vascular tissue with thin septation and foci of fibrosis (a; h&e, 100x, b; h&e, 400x). post-operative course. the patient’s neurologic symptoms improved immediately. on second postoperative day, her power in bilateral lower limb improved to 4/5. she was discharged on fifth postoperative day. on two months follow up, no signs of recurrence and neurological deficits were noted. discussion howard and helwig described angiolipoma as one entity in 1960 [7]. they said that the majority of these a b c d e a b 542 surendra kumar gupta, anuj chhabra, hanuman kumar prajapati, faran ahmad tumors are found in subcutaneous vessel, muscle, bone and kidney and it was noted that they have no tendency to recur after excision. more than 50 cases of spinal angiolipoma and angiomyolipoma have been reported [1-3, 6, 8-11]. after reviewing following clinical and radiologic characteristics were noted: 1) these tumors are occurs in middle aged patients usually; 2) these are mostly located in the dorsal epidural space; 3) they grow in a spindle shape along the spinal canal; 4) they lack the associated malformations; and 5) they are mostly benign and result in a good postoperative outcome. most of spinal angiolipomas are found to be nonfiltrating hence complete excision is the rule. in a few reported cases the tumor merges to the extradural fat so that it is difficult to differentiate tumor from the fat [12]. the pathogenesis of angiomyolipoma (aml) and angiolipoma is not clear. two major theories have been given previously regarding the pathogenesis. one is that primitive pluripotent mesenchyme cells (which provides a common origin to adipose, smooth muscle, and vascular endothelial elements) are developed into tumor by ill-defined stimuli (trauma or other causes). another theory is that the tumor is a congenital malformation or true hamartoma [7]. it was noted in most patients with spinal aml and angiolipoma that they have complaints of neurological symptoms related to spinal cord compression, such as weakness of the extremities and abnormal sensation below the level of lesion [3]. it was observed that there exists a relationship between pregnancy and accelerated onset of neurologic symptoms in several cases of epidural spinal angiolipoma [13]. for radiological assessment of spinal aml and angiolipoma, previously conventional radiograph, myelography, or ct were used for the purpose of preoperative diagnosis. recently in such cases mri were employed. both spinal aml and angiolipoma appear as elliptical shaped soft tissue mass with heterogeneous marked enhancement at epidural space of thoracic spine. fat component with high signal intensity on t1-weighted image is often visualized in cases of spinal angiolipoma [8]. however, infiltrative properties such as invasion to adjacent bone or extension to perilesional space and ventral location have been mentioned as distinctive features of aml compared to major patterns of angiolipoma according to sakaida et al [14]. such kind of lesions includes differential diagnosis of fat-containing tumor (such as lipoma, lipomatosis, and liposarcoma), prominently vascular tumor (such as spinal epidural hemangioma), and other t1-high signal intensity lesion (such as epidural hematoma). epidural lipoma or lipomatosis is an abnormal accumulation of unencapsulated adipose tissue in the extradural space. because of their fat components, they also display hyper intensity on t1weighted images and intermediate intensity on t2weighted images [12]. however, they present with typical y configuration (with circumferentially compressed dural sac) and show no definite contrast enhancement pattern. well-differentiated liposarcoma is a rare fat-containing tumor of the spinal canal. it frequently has irregular thick-ended septa. it contains regions of hyperintense signal (compared to fat) on t2-weighted images which are rare in spinal aml [8, 12, 14]. conclusion spinal angiolipoma is considered as rare benign entity which emulates malignancy. a sufficient attempt must be made to reach a correct preoperative diagnosis by using reliable imaging techniques such as mri. it should be included as a differential diagnosis of spinal epidural tumor with fat component and high degree of vascularisation. it can be believed that surgical removal of this epidural tumor through proper and comprehensive approach provides complete and permanent recovery. references 1. anson ja, cybulski gr, reyes m. spinal extradural angiolipoma, a report of two cases and review of the literature.surg neurol 1990;34: 173-8. 2. bender jl,van ladinghum jh,manno nj.epidural lipoma producing spinal cord compression:report of two cases.j neurosurg 1974;41:100-3. 3. geers c, lecouvet fe, behets c, malghem j, cosnard g, lengelé bg. polygonal deformation of the dural sac in lumbar epidural lipomatosis: anatomic explanation by the presence of meningovertebral ligaments. ajnr am j neu¬roradiol 2003;24:1276-1282. 4. goldblum jr, weiss sw, folpe al. enzinger and weiss’s soft tissue tumors. 6th ed. philadelphia: elsevier saunders, 2013:897-899. 543 a rare case of dorsolumbar angiolipoma 5. gonzalezz-crussi f, enneking wf,arean vm; infiltrating angiolipoma.j bone joint surg[am] 1966;48:1111-23. 6. griebel rw, khan m,rozdilski b. spinal extradural angiolipoma: a case report and literature review.spine 1986;11: 47-8. 7. howard wr,helwig eb. angiolipoma.arch derm(chicago)1960; 82:924-33. 8. hu s, hu ch, hu xy, wang xm, dai h, fang xm, et al. mri features of spinal epidural angiolipomas. korean j radiol 2013;14:810-817. 9. kuroda s,abe h, akino m, et al. infiltrating spinal angiolipoma causing myelopathy: case report. neurosurgery 1990;27:315-8. 10. padovani r, tongnetti f, speranza s,et al.spinal extrathecal hemangiolipomas: report of two cases and review of the literature.neurosurgery 1982;11:674-7. 11. pearson j, stellar s, feigin i. angiomyolipoma: long term cure following a radical approach to malignant appearing benign intraspinal tumor:report of three cases.j neurosurg 1970;33: 466-70. 12. provenzale jm, mclendon re. spinal angiolipomas: mr features. ajnr am j neuroradiol 1996;17:713-719 13. rubin g, gornish m, sandbank j, et al. spinal extradural angiolipoma:case report and review of the literature.spine 1992;17:719-24. 14. sakaida h, waga s, kojima t, kubo y, matsubara t, yama¬moto j. thoracic spinal angiomyolipoma with extracanal extension to the thoracic cavity. a case report. spine (phila pa 1976) 1998;23:391-39. doi: 10.33962/roneuro-2022-083 ventriculoperitoneal shunt surgery in a nigerian city. a single institutional experience ukpong secundus udoffa, stephen agbomhekhe oga, folafoluwa ayokunle aduloju, okezie obasi kanu romanian neurosurgery (2022) xxxvi (4): pp. 460-464 doi: 10.33962/roneuro-2022-083 www.journals.lapub.co.uk/index.php/roneurosurgery ventriculoperitoneal shunt surgery in a nigerian city. a single institutional experience ukpong secundus udoffa1, stephen agbomhekhe oga2, folafoluwa ayokunle aduloju1, okezie obasi kanu3 1 department of surgery federal medical centre lokoja, niger state, nigeria 2 mount gerizim medical centre, lokoja nigeria 3 neurosurgery division, department of surgery, college of medicine, university of lagos, idi-araba, lagos state, nigeria abstract introduction. improvements in surgical techniques and advancements in antibiotic management have significantly reduced the complications associated with ventriculoperitoneal shunting which is still the most common procedure for the treatment of hydrocephalus. these complications are believed to be highest in low and middle-income countries due to delayed presentation to care facilities. the authors report our experience of managing paediatric hydrocephalus in an institution with evolving neurosurgical practice in north central nigeria. material and methods. we retrospectively reviewed all cases of vp shunting from 2011 to 2018 taking into consideration the demographics, aetiologies of hydrocephalus, length of hospital stay, postoperative morbidity and mortality, and overall outcome. complications sought included, surgical site infections, shunt exposure, obstruction or any other cause of shunt malfunction. the minimum followup period was 24 months results. there were 27 vps procedures done in 25 patients of whom 15 were males and 10 females (m:f ratio of 1.5:1). the age range was 8 days to 9 years with a median age of 5 months. of the 25 cases, 24 (96%) were non-tumoral in origin comprising 17 congenital and 7 acquired hydrocephalus. at 2 years post shunt insertion, 21 (84%) of the 25 initial cases were still functional. the total complication rate was 28%, comprising surgical site infection, shunt exposure, shunt obstruction, seizure, and one death, there were 3 (12%) shunt failures from shunt obstruction (2) and shunt exposure (1). conclusion with meticulous control of the surgical environment and improved experience in ventriculoperitoneal shunting, the complication rate can be significantly reduced. there is a need to increase the awareness of the population to the availability of care for seemingly hopeless conditions. the burden of the cost of care on individuals should be lightened through better health insurance coverage. keywords ventriculoperitoneal shunt, hydrocephalus, paediatric hydrocephalus corresponding author: ukpong udoffa department of surgery, federal medical centre, lokoja kogi, state, nigeria ukpongudoffa1811@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 461 ventriculoperitoneal shunting introduction hydrocephalus is one of the most common clinical conditions affecting children in neurological surgery. ventriculoperitoneal (vp) shunt placement is the mainstay of treatment for hydrocephalus in both adult and paediatric patients.(1, 2) hydrocephalus accounts for over 69,000 hospital admissions and over 30,000 procedures performed every year in the united states.(3-7) with failure rates of 30–40% at 1 year and approximately 50% at 2 years in pediatric patients.(8) some recent studies report a relatively lower rate of shunt failure.(1, 9, 10) it is believed that vp shunting complications are highest in africa and other developing countries.(11) this is not unconnected with delayed presentation to care facilities as a result of poverty, ignorance and other socio-cultural factors. hereby, we report our experience of managing pediatric hydrocephalus in an institution with evolving neurosurgical practice in north central nigeria. materials and method the authors present a three-year-old female patient who accidentally sustained a phi with a screwdriver through the right orbit (figure 1). the patient did not lose consciousness or vomit after the injury. she was previously examined by an ophthalmologist and a pediatric surgeon at the local hospital. during the neurosurgical examination, on admission, the patient was conscious, oriented to time, space and person (glasgow coma scale score of 15), cardiopulmonary stable, without any recorded gross neurological deficits. results demographics there were 27 vps procedures done in 25 patients of whom 15 were males and 10 females with a malefemale ratio of 1.5:1. the age range was 8 days to 9 years with a mean age of 1.2 years and a median of 5 months. all patients had clinical features of hydrocephalus and confirmation was made with diagnostic scan. the occipito-frontal circumference ranged betwwn 39cm to 65cm. all patients were treated with cchabra slit and spring shunt. length of post-operative hospital stay was 3 days to 16 days with a mean duration of 9.2 days. aetiology of hydrocephalus of the 25 cases of hydrocephalus, 24 (96%) were non-tumoral in origin with only one case (4%) caused by posterior fossa tumour in a 9 year-old child, who coincidentally is the oldest patient in this series. seventeen (68%) of the 25 cases were congenital in origin, comprising of aqueductal stenosis (11), arnold-chiari malformation (4) and dandy-walker malformation (2). the major cause of acquired hydrocephalus was post-meningitic (5 of 8). there were 2 cases of aqueductal stenosis with no history of infection. (table 1b) table 1. demographic profile of hydrocephalus variables (total number n=25) frequency (%) a) males females 15 (60) 10 (40) b) congenital a) acqueductal stenosis b) arnorld-chiari malformation c) dandy-walker malformation acquired a) post-infective b) acqueductal stenosis c) post fossa tumor 17 (68) 11 (44) 4 (16) 2 (8) 8 (32) 5 (20) 2 (8) 1 (4) c) diagnostic imaging mri ct scan tfus 6 (24) 17 (68) 2 (8) diagnostic imaging diagnosis was made in 17 cases (68%) with computerized tomographic (ct) scan. magnetic resonance imaging (mri) was deployed in 6 (24%) while trans-fontanel ultrasonographic scan (tfuss) was used in 2 (8%) patients (table 1c) outcome at 2-year post shunt insertion, 21 (84%) of the 25 initial cases were still functional. there were 3 (12%) shunt failures from shunt obstruction (2) and shunt exposure (1). two of the shunt failures were revised. there was one post-operative death (4%). there were 3 (12%) cases of surgical site infection (ssi) at the scalp region noted in the first week postoperative period, all of which grew staphylococcus 462 ukpong secundus udoffa, stephen agbomhekhe oga, folafoluwa ayokunle aduloju et al. aureus that was treated with amikacin and rifampicin. one of the cases of ssi led to shunt exposure which was promptly removed but the parents declined revision surgery and requested discharge from the facility. the child was lost to follow-up. one patient (4%) died on the third postoperative day accounting for the shortest period of hospital stay. permission for autopsy was not granted by the parents. one patient developed seizure disorder post op. whereas shunt complication was seen in 28% of all patients, only 12% required shunt revision (table 2). the other 2 cases of shunt failure were marked by increasing head circumference and reduced activities. these occurred within 6 months of the surgery. shunt was promptly revised and the cause of failure was determined in both cases to be obstruction of the ventricular catheter by debris. these two patients have remained clinically stable. table 2. outcome and complications of ventriculoperitoneal shunting (*one case of ssi led to shunt exposure) a) summary of outcome (n=25) frequency (%) comments favourable outcome poor outcome 21 (84) 4 (16) satisfactory 3 failed, 1 died a. complications (7 of 25) frequency (%) comments surgical site infection (ssi)* shunt exposure* shunt obstruction seizure death 3 (12) 1 (4) 2 (8) 1 (4) 1 (4) antibiotics declined treatment revised anticonvulsant post-op day 3 discussion ventriculoperitoneal shunting remains the mainstay for treatment of hydrocephalus despite recent advances in neurological surgery practice. (1-3) in this study the age range was between 8 days to 9years with a median of 5 months. ninety two percent of the patients were below the age of 1 year and it is mainly caused by congenital anomalies. hydrocephalus is predominantly a disease of infants and this is a common finding in sub-saharan africa. (6, 11-15) the male to female ratio of 1.5:1 is in keeping with the male preponderance noted in many studies. (6, 12-14, 16) the occiptofrontal circumference (ofc) ranged from 39cm to 65cm. increase in the ofc is the commonest sign of hydrocephalus seen in infants.(17) grotesque head enlargement is common in underdeveloped countries due to late presentation and head circumference greater than 60cm is associated with higher rates of shunt failure.(11) about 70% of the cases of hydrocephalus were congenital with acqueductal stenosis being the commonest cause. (table 1b) this is at variance with some of the studies cited (11, 12, 14-16, 18) and the reason may be partly related to volume of the study population. the other reasons may be geographical in nature. many mothers who had infection during pregnancy in rural areas may not have been adequately looked after, thereby increasing the risk of maternal-to-fetal transmission. neural tube defects (arnold-chiari malformations with spina bifida, and congenital posterior fossa anomalies) are still a challenge in low-income communities where adherence to folic acid supplementation is suboptimal.(15, 19) the preferred imaging modality is mri but this was used in only 24% of patients (table 1c). ct scan was the most commonly used imaging modality in this study because of affordability. transfontanel ultrasonography has been used very frequently is our region for the similar reasons.(20, 21) the overall complication rate in this series was 28%. (table 2) the commonly reported incidence of complication is between 20 to 40%(10) though there are reported failures as high as 85%.(6) the incidence has reduced in more recent publications. the infection rate was 12% in this study. this is similar to the rate recorded by yusuf et al(13) in an earlier study though they had a relatively higher volume in their series. the weighted average shunt infection rate across multiple studies is about 5.1% but could be as high as 39% in some studies.(18, 22-28) staphylococcus aureus is one of the most implicated bacterial organisms in shunt infections.(29) shunt infection has been reduced with advent of newer techniques including double gloving, prophylactic antibiotics and antibiotic-impregnated shunts (commonly with rifampicin and clindamycin)(30) most of the shunts used in developing countries are fixed-pressure types of shunt; antibioticimpregnated shunts are not affordable to most patients in underdeveloped countries where the 463 ventriculoperitoneal shunting citizens are not adequately covered by health insurance and health care is paid on out-of-pocket basis.(20, 21) other established factors that influence the shunt infection rate are the age of the patients, aetiology of the hydrocephalus, operating room settings to prevent infection, total operating time and experience of the surgeon.(26) sharing the experience of the senior author in center with large volume has helped to cut down shunt failure rates in the country. there were 3 (12%) failed shunts though 2 (8%) shunt revision surgeries were done in this study. one was caused by infection, while the other two were caused by shunt obstruction. the incidence of shunt failure is commonly seen in children younger than 6 months and often noticed within the first month of shunt placement.(18, 31) seizure was seen in one patient in our series, accounting for 4% and this was controlled with anticonvulsant. seizure is a known complication of vp shunting accounting for 48%. it is believed that seizure is not due to direct placement of the vp shunt but to the underlying neurologic disorder.(32) one patient (4%) died in the first week following vp shunt placement. the cause of death could not be determined because the parents declined postmortem. the shunt-related mortality has been reported to be 3.4% to 13.7%.(13, 33). though endoscopic third ventriculostomy is available in the country as shown in many studies, (13, 14, 16) this facility is not available in our center at the time of this study. it is expected that the face of hydrocephalus treatment will improve as soon as this is done. conclusion with meticulous control of the surgical environment and improved experience in ventriculoperitoneal shunting, the complication rate can be significantly reduced. there is need to increase the awareness of the population to the availability of care for seeming hopeless conditions. the burden of the cost of care on individuals should be lightened through better health insurance coverage. references 1. khan f, shamim ms, rehman a, bari me. analysis of factors affecting ventriculoperitoneal shunt survival in pediatric patients. childs nerv syst. 29(5):791-802,2013. 2. khan f, rehman a, shamim ms, bari me. factors affecting ventriculoperitoneal shunt survival in adult patients. surg neurol int. 6:25,2015. 3. bondurant cp, jimenez df. epidemiology of cerebrospinal fluid shunting. pediatr neurosurg. 23(5):254-8; discussion 9,1995. 4. merkler ae, ch'ang j, parker we, murthy sb, kamel h. the rate of complications after ventriculoperitoneal shunt surgery. world neurosurg. 98:654-8,2017. 5. borgbjerg bm, gjerris f, albeck mj, borgesen se. risk of infection after cerebrospinal fluid shunt: an analysis of 884 first-time shunts. acta neurochir (wien). 136(1-2):17,1995. 6. stone jj, walker ct, jacobson m, phillips v, silberstein hj. revision rate of pediatric ventriculoperitoneal shunts after 15 years. j neurosurg pediatr. 11(1):15-9,2013. 7. simon td, riva-cambrin j, srivastava r, bratton sl, dean jm, kestle jr, et al. hospital care for children with hydrocephalus in the united states: utilization, charges, comorbidities, and deaths. j neurosurg pediatr. 1(2):1317,2008. 8. hanak bw, bonow rh, harris ca, browd sr. cerebrospinal fluid shunting complications in children. pediatr neurosurg. 52(6):381-400,2017. 9. khan f, rehman a, shamim ms, bari me. ventriculoperitoneal (vp) shunt survival in patients developing hydrocephalus after cranial surgery. turk neurosurg. 26(3):369-77,2016. 10. reddy gk, bollam p, caldito g. long-term outcomes of ventriculoperitoneal shunt surgery in patients with hydrocephalus. world neurosurg. 81(2):404-10,2014. 11. gathura e, poenaru d, bransford r, albright al. outcomes of ventriculoperitoneal shunt insertion in subsaharan africa. j neurosurg pediatr. 6(4):329-35,2010. 12. komolafe eo, adeolu aa, komolafe ma. treatment of cerebrospinal fluid shunting complications in a nigerian neurosurgery programme. case illustrations and review. pediatr neurosurg. 44(1):36-42,2008. 13. yusuf as, omokanye hk, adeleke na, akanbi ro, ajiboye so, ibrahim hg. management and outcome of infantile hydrocephalus in a tertiary health institution in nigeria. j neurosci rural pract. 8(2):249-53,2017. 14. bankole ob, ojo oa, nnadi mn, kanu oo, olatosi jo. early outcome of combined endoscopic third ventriculostomy and choroid plexus cauterization in childhood hydrocephalus. j neurosurg pediatr. 15(5):5248,2015. 15. adebayo bo, kanu oo, bankole ob, ojo oa, adetunmbi b, morgan e. early outcome of endoscopic third ventriculostomy with choroid plexus cauterization versus ventriculoperitoneal shunt as primary treatment of hydrocephalus in children with myelomeningocele: a prospective cohort study. oper neurosurg (hagerstown). 21(6):461-6,2021. 16. ojo oa, bankole ob, kanu oo, okubadejo nu. efficacy of endoscopic third ventriculostomy in the management of hydrocephalus in children under 2 years of age: 464 ukpong secundus udoffa, stephen agbomhekhe oga, folafoluwa ayokunle aduloju et al. experience from a tertiary institution in nigeria. niger j clin pract. 18(3):318-22,2015. 17. pan p. outcome analysis of ventriculoperitoneal shunt surgery in pediatric hydrocephalus. j pediatr neurosci. 13(2):176-81,2018. 18. kulkarni a, drake j, lamberti-pasculli m. cerebrospinal fluid shunt infection: a prospective study of risk factors. j neurosurg. 94(2):195-201,2001. 19. bankole ob, arigbabu so, kanu oo. spinal neural tube defects in lagos university teaching hospital, nigeria. nig q j hosp med. 22(1):22-4,2012. 20. kanu oo, nnoli c, olowoyeye o, ojo o, esezobor c, adeyomoye a, et al. infantile subdural empyema: the role of brain sonography and percutaneous subdural tapping in a resource-challenged region. j neurosci rural pract. 5(4):355-9,2014. 21. kanu oo, esezobor ci, ojo oa, asoegwu cn, nnoli c, dawang y, et al. infantile supratentorial subdural empyema managed by percutaneous aspiration: an outcome study in a nigerian city. sudan j paediatr. 19(1):37-43,2019. 22. raygor kp, oh t, hwang jy, phelps rrl, ghoussaini k, wong p, et al. ventriculoperitoneal shunt infection rates using a standard surgical technique, including topical and intraventricular vancomycin: the children's hospital oakland experience. j neurosurg pediatr.1-9,2020. 23. choux m, genitori l, lang d, lena g. shunt implantation: reducing the incidence of shunt infection. j neurosurg. 77(6):875-80,1992. 24. drake j, kestle j, milner r. randomized trial of cerebrospinal fluid shunt valve design in pediatric hydrocephalus. neurosurgery. 43(2):294-305,1998. 25. enger p, svendsen f, wester k. csf shunt infections in children: experiences from a population-based study. acta neurochir (wien). 145(4):243-8,2003. 26. reddy g, bollam p, caldito g. ventriculoperitoneal shunt surgery and the risk of shunt infection in patients with hydrocephalus: long-term single institution experience. world neurosurg. 78(1-2):155-63,2012. 27. rehman a-u, rehman t-u, bashir h, gupta v. a simple method to reduce infection of ventriculoperitoneal shunts. j neurosurg pediatr. 5(6):569-72,2010. 28. edwards n, engelhart l, casamento e, mcgirt m. costconsequence analysis of antibiotic-impregnated shunts and external ventricular drains in hydrocephalus. j neurosurg. 122(1):139-47,2015. 29. wu x, liu q, jiang x, zhang t. prevention options for ventriculoperitoneal shunt infections: a retrospective analysis during a five-year period. int j clin exp med. 8(10):19775-80,2015. 30. brown em, edwards rj, pople ik. conservative management of patients with cerebrospinal fluid shunt infections. neurosurgery. 58(4):657-65; discussion 65,2006. 31. faillace wj. shunt infection. j neurosurg. 94(6):101920,2001. 32. klepper j, busse m, strassburg hm, sorensen n. epilepsy in shunt-treated hydrocephalus. dev med child neurol. 40(11):731-6,1998. 33. tuli s, tuli j, drake j, spears j. predictors of death in pediatric patients requiring cerebrospinal fluid shunts. j neurosurg. 100(5 suppl pediatrics):442-6,2004. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-011 spinal intramedullary cysticercosis mimicking spinal tumour ahmed ansari, sheshank agrawal, sadaf riyaz romanian neurosurgery (2020) xxxiv (1): pp. 89-91 doi: 10.33962/roneuro-2020-011 www.journals.lapub.co.uk/index.php/roneurosurgery spinal intramedullary cysticercosis mimicking spinal tumour ahmed ansari1, sheshank agrawal2, sadaf riyaz3 1 assistant professor, department of neurosurgery, upums, saifai, up, india 2 resident neurosurgery, upums, saifai, up, india 3 department of microbiology, upums, saifai, up, etawah, up, india abstract neurocysticercosis is a relatively uncommon entity with even more rare spinal intramedullary variety. we present a case of cervicodorsal intramedullary ncc mimicking spinal tumour with per operative finding mimicking abscess. introduction cysticercosis is caused by larval stage of tape worm taenia solium and is the single most common parasitic cause of epilepsy in resourse-poor endemic region. prevalence of ncc may reach up to 4% in endemic population with about 1.5-3% prevalence of all ncc as spinal cysticercosis. most common site for ncc as described is subarachnoidal space with intramedullary involment, and extremely rare in spinal ncc scenario. case report a 17years old female presented with lower back ache for last 8 months with bilateral lower limb weakness for last 1 months which was gradual in onset and progressive with bowel disturbance and urinary complaints. on neurological examination, there was motor weakness with 0/5 power in bilateral lower limb with exaggerated deep tendon reflexes in lower limbs. the mri reveled a solitory focal well defined rounded intramedullary mass lesion at c7-d1 level. the lesion showed t2 hyperintens rim with central t2 hyperintesity and was isointense on t1 images (figure 1). mild perifocal hyperintensity suggestive of edema but no other focal lesion observed. she underwent c7 to d1 laminectomy with mid-line myelotomy with drainage of yellow coloured pus material with biopsy of contained margins (figure 2). afterwards irrigation was done and dura was repaired. keywords neurocysticercosis, intramedullary, spinal tumour corresponding author: ahmed ansari department of neurosurgery, upums, saifai, up, india ahmed.ansari2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 90 ahmed ansari, sheshank agrawal, sadaf riyaz neuropathological examination revealed examined biopsy specimen with invaginated scolex of cysticercosis with hooklets and surrounding tissue with fibrocollagenous wall with an area of inflammatory reactions comprising of modified histiocytes, few plasma cells and neutrophils. in early post-operative analysis, no foci of other sources of cysticercosis were found. her neurological status remained stable and no additional deficits occurred. patient was discharged with relief in pain symptoms with bilateral lower limb power improvement to 1/5 with elevation of bladder and bowel symptoms. at two months follow up, the patient developed power of 4/5 in bilateral lower limbs. figure 1. mri t1 wi showing hyperintense lesion at c7-d1 level. figure 2. yellowish coloured fluid draining out of the intramedullary component of the lesion. discussion worldwide, cysticercosis is the most common parasitic infection affecting the cns. ncc typically involves the brain parenchyma, intracranial subarachnoid space, or ventricular system and is often self-limited unless hydrocephalus requires surgical intervention. spinal ncc is rare even in endemic regions, and may require more aggressive management because of the natural confines of the spinal canal. the location and the size of the lesion, and the inflammatory response generated by cyst breakdown are the important factors in the management of spinal ncc. spinal cysticercosis can be leptomeningeal, intramedullary or epidural. leptomeningeal is the most frequent, intramedullary is quite rare and epidural is an extremely rare form. spinal involvement is quite rare and the migration of the cysticercus through the ventriculo-ependymal pathway and hematogenous dissemination has been hypothesized to be the possible mechanism. however, queiroz et al. did not find any evidence for ependymal route of spread of intramedullary cysticercosis. rokitansky, in 1856, firstly described intramedullary cysticercosis. because of limited space in the spinal canal, mass effect of these lesions is poorly tolerated necessitating for aggressive management. blood flow to the brain is approximately 100-fold greater than that of the spine explaining the lower incidence of spinal cysticercosis. in the spine, thoracic cord has higher incidence due to high blood flow in this segment. queiroz et al. estimated the location of cysticerci in spine as: cervical-34%, thoracic44.5%, lumbar-15.5% and sacral-6% . mri is the investigation of choice. mathuriya et al. described mri findings for various stages of intramedullary cysticercosis. usually, mri is described as hypointense rim with hyperintense core on t2wi and hypointense or isointense lesion on t1wi as is our case. however, these are not specific and the same changes can also be present in neoplastic, inflammatory, demyelinating, vascular, and granulomatous diseases. the entire neuraxis should be evaluated to find additional lesions. in the present case, an isolated intramedullary cystic lesion was demonstrated at c7-d1 with absence of cranial cysticercosis.this is in contrast with the previous hypothesis that concomitant intracranial lesions are present in all patients with 91 spinal intramedullary cysticercosis mimicking spinal tumour spinal cysticercosis. our finding is supported by parmar et al. who found only 2 patients with brain neurocysticercosis among 6 patients with intramedullary cysticercosis. perifocal edema was present in all of their 6 patients as in ours. surgical treatment is indicated in spinal ncc in which patients had severe and progressive neurological dysfunction regardless of whether medical therapy has been attempted. the inflammatory process may be so severe that some cysts cannot be readily or completely resected. excision of intramedullary ncc lesions has been described as being possible after myelotomy or requiring microsurgical dissection from the parenchyma prior to removal. we performed a 3level laminectomy plus midline myelotomy to reach the lesion and removed it subtotally in order to preserve the neural tissue. albendazole or praziquantel, with or without steroids are used. albendazole is preferred because its blood levels are improved by corticosteroids, whereas those of praziquantel are diminished. finally, we conclude that spinal intramedullary cysticercosis represents a diagnostic challenge and surgery is required to decompress the cord, confirm the diagnosis and provide a route for definitive therapy. patient recovery may be variable. despite promising reports, the safety and efficacy of medical treatment remains unproved. references 1. alsina ga, johnson jp, mcbride dq, et al. spinal neurocysticercosis. neurosurg focus 2002; 12: e8. 2. sheehan jp, sheehan j, lopes mb, et al. intramedullary spinal cysticercosis. case report and review of the literature. neurosurg focus 2002; 12: e10. 3. singh p, sahai k. intramedullary cysticercosis. neurol india 2004; 52: 264-5. 4. mathuriya sn, khosla vk, vasishta rk et al. intramedullary cysticercosis: mri diagnosis. neurol india 2001; 49: 71-4. 5. homans j, khoo l, chen t, et al. spinal intramedullary cysticercosis in a five-year-old child: case report and review of literature. pediatr infect dis j 2001; 20: 904-8. 6. de souza queiroz l, filho ap, callegaro d, et al. intramedullary cysticercosis. case report, literature review and comments on pathogenesis. j neurol sci 1975; 26: 6170. 7. torabi am,quiceno m, mendelsohn db, et al. multilevel intramedullary neurocysticercosis with eosinophilic meningitis. arch neurol 2004; 61: 770-2. 8. parmar h, shah j, patwardhan v, et al. mr imaging in intramedullary cysticercosis. neuroradiology 2001; 43: 961-7. 9. mohanty a,venkatrama sk, das s. spinal intramedullary cysticercosis. neurosurgery 1997; 40: 82-7. 10. sharma bs, banerjee ak, kak vk. intramedullary spinal cysticercosis. case report and review of literature. clin neurol neurosurg 1987; 89: 111-6. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 404-410 doi: 10.33962/roneuro-2019-085 www.journals.lapub.co.uk/index.php/roneurosurgery preliminary study of thrombogenicity induced by the nanoparticle surface coating of intracranial stents a. chiriac1, georgiana ion1, g. stan2, t. popescu2, mihaela sofronie2, i. poeata1 1 “gr. t. popa” university of medicine and pharmacy, iasi, romania 2 national institute of materials physics, bucharest-magurele, romania abstract endovascular treatment of intracranial aneurysms with intracranial stents was proven to be clinically safe and effective, but is still associated with a risk of thromboembolic complications. stent thrombosis could be a sever complication associated with specific stent surface coatings and designs. standardized in vitro tests for investigation of thrombogenicity induced by different nanomaterials were used as the basic method in carrying out the present study. therefore, the aim of this study was to evaluate the thrombogenicity of three different nanomaterials (zno, tio2 si fe3o4) possible used as surface coating for intracranial stents. this study is based on a procedure for in vitro analyses of plasma coagulation time. to measure the plasma coagulation time, platelet-poor plasma from human whole blood was in vitro exposed to nanoparticles and analysed in prothrombin (pt) and activated partial thromboplastin (aptt). introduction a variety of intracranial stents are used in permanent blood contact. thrombogenicity is the property of a material to induce a thrombus formation, which may result in partial or complete blood vessel occlusion. thus, thrombogenicity of intracranial stent may have important implication in the long-term outcome of neurosurgical patients that may lead to a life-threatening condition such as stroke. stent / blood contact surface activity has been a widely subject discussed and reported and, notwithstanding the clinical significance of this phenomenon is still controversial. moreover, the surface coatings of these implants that are in permanent contact with blood are often subjected to tests on coagulation in order to use the least thrombogenic materials. activated partial thromboplastin time (aptt), prothrombin time (pt) and the international normalized ratio (inr) are indicated as the techniques of choice used to help detect and diagnose a bleeding disorder or excessive clotting disorder. in ou r study, an in vitro model was established, which allows investigation of neurovascular stents with keywords intracranial stents, thrombogenicity, nanomaterials, surface coating corresponding author: a. chiriac “gr. t. popa” university of medicine and pharmacy, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 405 preliminary study of thrombogenicity induced by the nanoparticle surface coating of intracranial stents regard to thrombogenicity and coagulation activation. the preliminary study was designed to compare these 3 methods to address the coagulation property of three biomaterials (zno, tio2 si fe3o4) with emphasis on the sensitivity and reproducibility of the test. these three biomaterials prepared in the form of nanoparticles were evaluated for their coagulation profile during incubation in human plasma. the study presents a revised version of these methods to include updated details on sample preparation of nanoparticles, selection of nanoparticle concentration for in vitro study, and updated details on test controls [4,5,6]. materials and methods platelet rich plasma (prp) is obtained from fresh human blood derivative incubated with nanoparticles for 15 minutes at 37 ° c. this probe is subsequently analysed by evaluating the plasma coagulation time and how the nanoparticles affect this part of the haemostasis control system. the materials listed below are required for coagulation tests for the study of nanoparticles (fig. 1): 1. vacuum test tubes for coagulation testing; 2. 12% sodium citrate. 3. thermostat bath; 4. special centrifuge with tubes test stand; 5. fresh human blood completely anti-coagulated with sodium citrate and obtained from at least three healthy donors known to be out of any antiinflammatory and antihistamine drug, blood thinning agents and birth control pills; 6. aptt and pt / inr test cards for abrazo cascade equipment; 7. coagulation tester analyzer abrazo cascade system from helena laboratories; 8. nanoparticle sample for analysis. a b c d e 406 a. chiriac, georgiana ion, g. stan et al. figure 1: aaptt tester card; bpt / inr tester card; cabrazo cascade coagulation test equipment; dcentrifuge; e vacuum test tubes with citrate; fthermostatic bath. preparation of the study samples the concentrations used in these assays are based on an estimated plasma concentration in a mediumsized human patient at the desired therapeutic dose. in our study, we refer to this concentration as the theoretical concentration of plasma. the hypotheses and considerations for estimating theoretical plasma concentration have been reviewed in the literature [4] and are summarized below. for the calculation of nanoparticle concentration, we used in vitro test reports in mice. if the mouse dose used is approximately 123 mg / kg in this example the human dose can be calculated as follows: it is known that blood volume accounts for about 8% of body weight (for example, an adult of 70 kg has about 5.6 l (8% of 70) blood. this allows an extremely crude estimate of maximum blood concentration. each test evaluates a nanoparticle formulation of three different materials at preset concentrations. when the predicted therapeutic concentration is not known, the highest final concentration is 1 mg per ml. figure 2: ablood collection; bcentrifuge with multiple cartridges; cvacutainer tubes with centrifuged plasma. plasma preparation when the blood collection procedure is started the first 10 ml of blood must be discarded [fig.2] due to necessity to prevent the activation of cells and plas ma bioch em ic al c as cades by th e v eno us puncture procedure. exposure and storage of blood or plasma at extreme temperatures (<20 c or> 37 c) can affect the quality of test results and should be avoided. two types of plasma can be obtained to perform this experiment: platelet rich plasma (prp), platelet poor plasma (ppp). plasma from individual donors can be analyzed separately or collected together. the combined plasma is prepared by mixing plasma from at least two individual donors. f 407 preliminary study of thrombogenicity induced by the nanoparticle surface coating of intracranial stents normal test plasma preparation fresh whole blood must be used within 1 hour after collection. the blood is then centrifuged for 10 min at 3000 g at 20–22 c and plasma is collected from at least two donors. the combined plasma is stable for 8 hours at room temperature. the assay can also be performed in plasma from individual donors, when needed for mechanical tracking experiments. two duplicates (four total samples) of plasma test are analyzed in each of the coagulation tests. a duplicate is performed prior to analyzing the nanoparticle samples and the second duplicate at the end of each run to verify that plasma functionality is not affected throughout the experiment. nanoparticle-treated test plasma preparation in a micro-tube, 0.125 mg of nanoparticles and 1 ml of plasma are combined. mix well on a shaker and incubate for 30 min at 37 ° c. three test tubes are prepared for each test sample (ie, when each nanoparticle is tested at four concentrations, one needs three test tubes for each concentration for a total of 12 test tubes per nanoparticle test). plasma coagulation tests (fig. 3) 1. prepare the cascade abrazo equipment as described in the manufacturer's manual. 2. preheat all tubes to 37 c. 3. configure the instrument test parameters for each of the two tests (aptt and pt / inr). 4. add to the micro-tubes with pre-loaded nanoparticles 1 ml of plasma. 5. stir micro-tubes for 5 minutes. 6. scan each specific tester card (aptt and inr / pt) before testing; 7. insert the test card into the cascade abrazo device; 8. allow the instrument to warm up before use. 9. extract the test solution with the micropipette. 10. when the test timer starts, transfer the solution to the test card's geode by pressing the pip button to activate the pipette. 11. when the time is up, the device will beep and the recording of coagulation time will remain displayed on the screen until further testing begins. 12. the average of the three values must be calculated for each control or test. 13. the average for each control and test sample should be between 25%. 14. if two duplicates of the same study sample showed different results more than 5%, this sample was reanalysed. figure 3: schematic diagram of coagulation time measurement. donors fresh blood plas ma control samples with nanoparticles test settings data recording and analysis card scan card insertion add test solution 408 a. chiriac, georgiana ion, g. stan et al. results the results shown in this study indicate that zno nanoparticles administered in the blood vessels can adsorb the coagulation factors in a specific form to the surface functional group, without activating these factors and that the adsorbed coagulation factors are not functional. also, zno nanoparticles delayed the coagulation time with the size or surface functional group specificity, because all types of zno nanoparticles adsorbed the coagulation factors of the common pathway, some types of nanoparticles adsorbing more factors than others. the thrombogenicity study of tio2 and fe3o4 nanoparticles suggests that nanoparticles should be an effective agent in prolonging the blood clotting time, thus exerting an anti-coagulant effect, thus improving the hemocompatibility of the coating. the ability of tio2 and fe3o4 nanoparticles to regulate platelet adhesion and plasma coagulation was thus demonstrated in vitro. discussions treatment of neurosurgical patients with functionalized coating surfaces stents continues to evolve with the current emergence of nanoparticle functionalization technology that offers a combination of pharmacological and mechanical approaches to prevent thrombosis and arterial restenosis. despite the promising short term and mid-term outcomes of surface coated stents, there are serious concerns about adverse clinical effects of late stent thrombosis. certain nanoparticles intended for drug delivery application are designed pt coagulation test for nanoparticles 0 2 4 6 8 10 12 14 16 n o rm a l p o s it iv e c o n tr o l z n o : m n 5 0 p p m z n o : m n 5 0 p p m z n o : m n 5 0 0 p p m z n o : m n 2 0 0 0 z n o : m n 5 0 0 p p m z n o : m n 2 0 0 0 id v (f e 3 o 4 ) d b / h 2 4 (t io 2 ) d b 1 / 4 5 0 c b 1 4 5 0 (t io 2 ) appt coagulation test for nanoparticles 0 20 40 60 80 100 120 n o rm a l p o s it iv e c o n tr o l z n o : m n 5 0 p p m z n o : m n 5 0 p p m z n o : m n 5 0 0 p p m z n o : m n 2 0 0 0 z n o : m n 5 0 0 p p m z n o : m n 2 0 0 0 id v (f e 3 o 4 ) d b / h 2 4 (t io 2 ) d b 1 / 4 5 0 c b 1 4 5 0 (t io 2 ) 409 preliminary study of thrombogenicity induced by the nanoparticle surface coating of intracranial stents to reduce the effect of thrombogenicity of an intracranial stent in the bloodstream for a prolonged coagulation time in the circulatory system. thus, a larger therapeutic window is offered until systemic anti-aggregation is administered. studies evaluating nanoparticles effects on plasma coagulation time and their tendency to initiate vascular thrombosis are useful to assess nanoparticle thrombogenicity [1,2,3]. a number of nanotechnology approaches have been borrowed and applied in stent technology. stents with biofunctionalized surfaces with nanoparticles with high stability and carrier capacity, able to reduce the interaction with blood components and to incorporate substances as carriers for bioactive factors and drugs have been manufactured. there are already implants in the form of drug-eluting or biodegradable stents that induce healing reactions by triggering the body's natural processes [2,3]. at present, there is not much data on the thrombogenicity of stent materials dictated by nanoscale observations. because thrombogenicity is a multiparametric process, our study tests the hypothesis of the influence of surface nanotopography on platelet activation, in order to produce nano-coatings with less thrombogenic stent by adapting their surface properties. it is in fact intended to implement a real-time study of platelet response to biomaterials to improve hemocompatibility. the primary phenomenon of blood-material interaction was the rapid and selective adsorption of proteins through a three-step process represented by the transport to the interface, the adsorption reaction and the conformational rearrangement. thus, the engineering of the surface properties (physical and chemical characteristics) of the implants aims to reduce the adsorption of proteins and cellular interactions resulting in the improvement of implant biocompatibility. platelets are the main cells present in the blood that play the most important role in blood-material interactions. the adhesion of platelets to a surface is conditioned by two independent mechanisms. these are the transport of platelets to the surface, which depends on the flow conditions and the reaction of platelets with the surface, which depends on the nature of the surface and the adsorbed proteins. in this paper, we want to verify the influence of nanotopography and surface characteristics on the thrombogenicity of different possible types of nanocoatings (zno, tio2 and fe3o4). thus, the results obtained by us are in line with previous hemocompatibility studies in the literature regarding the influence of these nanoparticles on coagulation. these lead us to the conclusion that nanotopography and surface roughness of biomaterials influence their biological behaviour. the studies within our project will be continued by thrombogenicity analyses on nanoparticle-coated metal bands. this study about thrombogenicity induced by the nanoparticle is the subject of the grant: "new diagnostic and treatment methodologies: current challenges and technological solutions based on nanoparticles and biomaterials", that won the 2017 complex projects completed in consortia cdi, grant number: pn-iii-p1-1.2-pccdi-2017-0062, funded by cncs – uefiscdi romania. references 1. hansi, c., arab, a., rzany, a., ahrens, i., bode, c., & hehrlein, c. (2009). differences of platelet adhesion and thrombus activation on amorphous silicon carbide, magnesium alloy, stainless steel, and cobalt chromium stent surfaces. catheterization and cardiovascular interventions, 73(4), 488-496. 2. karagkiozaki, v. c., logothetidis, s. d., kassavetis, s. n., & giannoglou, g. d. (2010). nanomedicine for the reduction of the thrombogenicity of stent coatings. international journal of nanomedicine, 5, 239. 3. krajewski, s., neumann, b., kurz, j., perle, n., avci-adali, m., cattaneo, g., & wendel, h. p. (2015). preclinical evaluation of the thrombogenicity and endothelialization of bare metal and surface-coated neurovascular stents. american journal of neuroradiology, 36(1), 133-139. 4. neun, b. w., & dobrovolskaia, m. a. (2011). method for in vitro analysis of nanoparticle thrombogenic properties. in characterization of nanoparticles intended for drug delivery (pp. 225-235). humana press. 5. scott e. mcneil (ed.), characterization of nanoparticles intended for drug delivery, methods in molecular biology,cvol. 1682, doi 10.1007/978-1-4939-7352-1_10, © springer science+business media llc 2018; 6. weber, m., steinle, h., golombek, s., hann, l., schlensak, c., wendel, h. p., & avci-adali, m. (2018). blood-contacting biomaterials: in vitro evaluation of the hemocompatibility. frontiers in bioengineering and biotechnology, 6. 7. yang, j. y., bae, j., jung, a., park, s., chung, s., seok, j., ... & jeong, j. (2017). surface functionalization-specific binding of coagulation factors by zinc oxide nanoparticles delays 410 a. chiriac, georgiana ion, g. stan et al. coagulation time and reduces thrombin generation potential in vitro. plos one, 12(7), e0181634. 8. xue, l. l., long, p., wei, h., & liang, y. (2011). hemocompatibility of tio2 nanoparticles composite ptfe coating for medical devices. in advanced materials research (vol. 299, pp. 600-603). trans tech publications. chiriaca_superiorophthalmic 230 | chiriac et al superior ophthalmic vein approach the superior ophthalmic vein approach for the treatment of carotid-cavernous fistulas: our first experience a. chiriac, n. dobrin1, georgiana ion1, v. costan2, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi 1“prof. dr. n. oblu” clinic emergency hospital, iasi 2“sf. spiridon” clinic emergency hospital, iasi abstract: complex cavernous sinus fistulae (ccf) are still a technical challenge to neurovascular team. the most commonly performed treatment consists in endovascular embolization of the lesion through an arterial or venous approach. not always these conventional routes are feasible, requiring alternative routes. we report a case of a 44year-old woman with a complex indirect (barrow d) carotid cavernous sinus fistula treated by two interventional sessions that imposing a retrograde direct transvenous approach via the superior ophthalmic vein. key words: cavernous sinus fistulae, superior ophthalmic vein introduction intracranial dural arteriovenous fistulae are predominantly idiopathic arteriovenous shunts located inside the dura-mater. they account for 10–15% of all intracranial arteriovenous malformations. carotidcavernous fistulas (ccf) are abnormal vascular communications between the cavernous sinus and the carotid artery and/or its branches. these vascular lesions are broadly grouped into two: direct and indirect types [1, 3, 8]. the direct ccf are direct shunt between the cavernous sinus and the internal carotid artery whereas the indirect ccf are dural fistulas between the cavernous sinus and extradural branches of the internal carotid artery, the external carotid artery, or both. over time and development of new embolization materials, the endovascular therapy has become the treatment of choice for ccfs. the most commonly performed endovascular treatment consists in transarterial or transvenous embolization of cavernous sinus. in special cases with complex ccf a combined microsurgical and endovascular treatment via a superior ophthalmic vein approach can be necessary. a direct operative cannulation of the superior ophthalmic vein ensures a direct, fast and reasonable route to the cavernous sinus. in this article, we describe the treatment of a type d ccf, using a combined microsurgical and endovascular treatment via a superior ophthalmic vein approach performed in two session [1, 3]. romanian neurosurgery (2016) xxx 2: 230-236 | 231 case presentation a female patient of 44 years old was admitted in our clinic in august 2015. the clinical presentation of our patients was left periocular pain, episodes of diplopia, ocular injection, proptosis, periocular swelling, low visual acuity and a pulsatile mass. these symptoms occurred evolving a month. the tof mri of the head demonstrated enlargement of the left sov posterior to the eye globe and vascularization around left cavernous sinus (figure 1). figure 1 tof mri showing an enlarged left sov and vascularization around left cavernous sinus figure 2 dsa angiography showing a left carotid cavernous fistula with fed braches from bilateral eca and left ica a cerebral angiography showed a complex barrow type d dural carotid cavernous sinus fistula. the fistula is fed by multiple meningeal branches of the external carotid artery on both sides and by the internal carotid artery on the left side (figure 2). the ccf drained from the cavernous sinus into the right sov. the left inferior petrosal sinus could not be angiographically detected. the treatment required two sessions. 232 | chiriac et al superior ophthalmic vein approach operative technique the first session consisted in bilateral menigeal branches of the external carotid artery occlusion with glue injection. the patient was with local anesthesia. both eca were cauterized turn with a 6f launcher guiding catheter (medtronic, usa) supported by 0.035 poseidon hydrophilic guidewire (sp medical, denmark). 6 meningeal branches were approached and occluded by glubran 2 injection via 6 marathon™ flow directed microcatheter (ev3 neurovascular, usa). almost complete occlusion of the supply from eca was obtained (figure 3). external manual carotid compression was performed for a period of 3 weeks. figure 3 dsa angiography showing different time of first embolization session of branches from bilateral eca because the neurologic deficits of the patient did not completely improve, the patient was treated 3 weeks later in a second session while under general anesthesia. thus, a microsurgical approach in the catheter laboratory, with exposure of the sov on the left side, was chosen. we performed a 2-cm skin incision in the upper eyelid and the orbital septum was opened by the craniofacial surgeon. microsurgical preparation of the orbital fat and exposure of the dilated sov were done. romanian neurosurgery (2016) xxx 2: 230-236 | 233 the sov was punctured with a 0.018gauge cannula (braun, melsungen, germany) and temporarily fixed with a 4.0 suture. this was used as a sheath for introducing a excelsior sl-10 (stryker neurovascular) with a 0.014-in transendex microguidewire (boston scientific, fremont, ca). 14 gdcs were introduced and detached into the left cavernous sinus with completely angiographic occlusion. after the embolization, the cannula was removed and the opening in the sov was closed by using a 7.0 suture. in the end, the skin was closed with interrupted 5.0 nylon sutures (figure 4). figure 4 intra-operative aspects of left sov microsurgical exposure and canulation; coil occlusion of left cavernous sinus via sov 234 | chiriac et al superior ophthalmic vein approach figure 5 photo and fluoroscopic aspects of ccf evolution at admission, after treatment and at one month control discussion complex cavernous sinus fistulae are complex vascular lesions still considered a technical challenge to most neuro-vascular teams. according to barrow et al [1], carotid cavernous fistulae are divided into 4 categories: type a ccf are high flow direct shunts between the cavernous sinus and the internal carotid artery usually caused by traumatic laceration of the internal carotid artery; type b ccf are fistulae between meningeal branches of the internal carotid artery and the cavernous sinus; type c are dural abnormal communications between meningeal branches of the external carotid artery and the cavernous sinus; type d are fistulae between meningeal branches of both the internal carotid artery and external carotid artery and the cavernous sinus. etiology ccfs can be classified based on etiology (traumatic or spontaneous), rate of flow (high versus low flow), or the angiographic architecture (direct or indirect). clinical symptoms the clinical presentations of carotid cavernous fistulae are usually represented by neuro-ophtalmologic symptoms due to indirect arterialization of the ophthalmic veins. thus, the most common symptoms encountered are the chemosis (88%), exoftalmos (70%), iii cranial nerve palsy (35%), vi nerve palsy (64%) and bruit (47%) as the klisch et al reported in their series [1,3]. acute-onset fistulae, high flow fistulae or those with fulminant evolution may be associated with periocular swelling and sever visual deterioration witch require emergency intervention to preserve their visual function. once the loss of vision is complete, even with treatment, optic nerve function is difficult to recover. in case of cortical vein drainage implication the risk of intra-parenchymal hemorrhage must be taken in to consideration [3, 8]. diagnosis first steps for diagnostic imaging requires an initial evaluation by cranio-cerebral ct scan and/or mri. the noncontrasts ct scan in patient with carotid cavernous fistulae are usually normal, in rare cases can highlight a dilated superior ophthalmic vein or edema due to venous congestion. on contrast-enhanced ct scan is more likely to identify a dilated superior ophthalmic vein or an enlarged cavernous sinus. routine t1 and t2, spin echo romanian neurosurgery (2016) xxx 2: 230-236 | 235 weighted mr images can show dilated vessels or vascular enhancement without an identifiable parenchymal nidus, venous pouches and signs of venous hypertension in high-grade lesions (as white matter hyperintensity, venous infarction or intracranial hemorrhage). conventional ct and mri are less successful for arterial pedicle identification and direct visualization of the exact fistula site. for any suspicions mentioned above supplementary evaluation by dynamic cta, mra, or dsa are indicated. even if cta is specifically useful for a clear diagnostic of carotid cavernous fistulae presence it is characterized by a low sensitivity for endovascular interventional planning. mra is a reliable imaging technique for carotid cavernous fistulae detection and screening but it is limited by low resolution, restricted fov and saturation artifacts. conventional angiography remains the most accurate method for detection and classification of carotid cavernous fistulae by precise location and delimitation of fistula site and superior visualization of arterial feeders and venous outflow [1, 3, 4, 8]. treatment over time it has been reported different types of approaches for the management of carotid cavernous fistulae such as conservative treatment, surgery, endovascular intervention, radiosurgery or combination of them. external manual carotid compression is a classically non-invasive method for carotid cavernous fistulae treatment. its questionable efficiency and potential complications represented by vaso-vagal attack or even isquemic stroke made this technique not frequently used today. surgical ligation of the internal carotid artery or packing of the cavernous sinus was the successful surgical techniques described for the treatment of carotid cavernous fistulae [hamby and gardner in 1933]. however sacrifice of the ica is performed carefully due to significant risk of cerebral infarction even after successful balloon test occlusion studies [2, 3, 5]. with the advent and development of embolization techniques and materials, endovascular treatment has become the treatment of choice in case of ccfs. currently endovascular treatment in ccfs can be done about both arterial and venous route. the first and simple arterial endovascular approach were performed since the introduction of detachable balloons and demonstrate its efficiency for a long period of time especially in type a fistulae. since the introduction of gdcs embolization, transarterial occlusion of the cavernous sinus through the fistulous site became the recommended treatment. however, indirect ccfs are more complex vascular lesions requiring more advanced techniques. trans-arterial particulate embolization of indirect ccfs may be performed with a success rate of up to 50% of cases. in these cases delayed recanalization or change in drainage pattern were reported. this technique is specially indicated in ccfs fed by only few meningeal branches of the external carotid artery. also, arterial embolization by glue injection can be performed especially in simple fistulae with clear arterial fed pedicles. a distal catheterization with good flow control especially at the venous side allows a complete 236 | chiriac et al superior ophthalmic vein approach treatment. with the introduction of transvenous embolization trough the femoral vein and inferior petrosal sinus by uflacker et al. in 1986 these technique become the treatment of choice for such lesions [1, 3, 6, 8]. so, transvenous embolizations by occlusion of the cavernous sinus with coils become treatment of choice for barrow type b–d indirect ccfs. in highly complex fistulas combinations of endovascular treatment by transarterial and transvenous approach and/or additional stereotactic radiosurgery were reported. in case of thrombosis or anatomic particularities, such as tortuosity, plexiform inferior petrosal sinus or absence of connection with the jugular vein, the transfemural venouse approach is compromised. an alternative technique in such cases was represented by direct superior ophthalmic vein catheterization after its surgical exposure. this approach offers a reasonable and safe route to cavernous sinus occlusion with coils or onyx. complication the most known potential surgical complications of the sov approach are hemorrhage, damage to the trochlea or other orbital structures, and infections. the technical complication of this approach is the over-packing of the cavernous sinus resulting in nerve palsies, dural dissections, or penetrations. retrograde sov thrombosis was also reported. conclusions our case shows that a complex ccf requires interdisciplinary treatment. when the classical routes are not available, the direct surgical superior ophtalmic vein catheterization is a feasible approach and carries a low risk of complications. references 1. berlis, a., klisch, j., spetzger, u., faist, m., & schumacher, m. (2002). carotid cavernous fistula: embolization via a bilateral superior ophthalmic vein approach. american journal of neuroradiology, 23(10), 1736-1738.1. 2. ellis, j. a., goldstein, h., connolly jr, e. s., & meyers, p. m. (2012). carotid-cavernous fistulas. neurosurgical focus, 32(5), e9. 3. gandhi, d., chen, j., pearl, m., huang, j., gemmete, j. j., & kathuria, s. (2012). intracranial dural arteriovenous fistulas: classification, imaging findings, and treatment. american journal of neuroradiology, 33(6), 1007-1013. 4. gemmete, j. j., ansari, s. a., & gandhi, d. m. (2009). endovascular techniques for treatment of carotidcavernous fistula. journal of neuro-ophthalmology, 29(1), 62-71. 5. korkmazer, b., kocak, b., tureci, e., islak, c., kocer, n., & kizilkilic, o. (2013). endovascular treatment of carotid cavernous sinus fistula: a systematic review. world j radiol, 5(4), 143-155. 6. nadarajah, m., power, m., barry, b., & wenderoth, j. (2011). treatment of a traumatic carotid–cavernous fistula by the sole use of a flow diverting stent.journal of neurointerventional surgery, neurintsurg-2011. 7. tjoumakaris, s. i., jabbour, p. m., & rosenwasser, r. h. (2009). neuroendovascular management of carotid cavernous fistulae. neurosurgery clinics of north america, 20(4), 447-452. 8. wajnberg, e., spilberg, g. z., & gasparetto, e. l. (2009). superior ophthalmic vein puncture: an alternative approach to treat complex cavernous sinus fistulae. arquivos de neuro-psiquiatria, 67(2b), 523-526. doi: 10.33962/roneuro-2023-020 global neurosurgery: the need of the hour for developing countries ahtesham khizar, soha zahid romanian neurosurgery (2023) xxxvii (1): pp. 120-123 doi: 10.33962/roneuro-2023-020 www.journals.lapub.co.uk/index.php/roneurosurgery global neurosurgery: the need of the hour for developing countries ahtesham khizar1, soha zahid2 1 punjab institute of neurosciences, lahore, pakistan 2 the aga khan university hospital, karachi, pakistan abstract global neurosurgery is relatively a new sub-discipline of global surgery. it is an area of study, research, practice, and advocacy that focuses on enhancing health outcomes and promoting health equity for all individuals around the world who are afflicted by neurosurgical disorders or require neurosurgical care. lowand middleincome countries (lmics) around the world have not benefited from advances in neurosurgery; most have little or no neurosurgical capacity in their entire country. the need of the hour is that a global problem necessitates a global response with a common vision and objectives. introduction global neurosurgery is relatively a new sub-discipline of global surgery.1 "global neurosurgery" can be defined as an area of study, research, practice, and advocacy that focuses on enhancing health outcomes and promoting health equity for all individuals around the world who are afflicted by neurosurgical disorders or require neurosurgical care.2 it should be made sure that neurosurgery is completely integrated into the growth of the global surgery movement. every year, 5 million crucial neurosurgical cases go untreated, all of which are in lowand middle-income countries.3 a sufficient number of medical professionals, facilities, and training programs for neurosurgery are still lacking in the majority of underdeveloped countries. the world health organization (who) and world federation of neurosurgical societies (wfns) have had a very positive role in global neurosurgery. research is an integral part of global neurosurgery and according to studies, despite having a high disease burden, lowand middle-income countries have a poor representation in research publications.2 the need of the hour is that a global problem necessitates a global response with a common vision and objectives. discussion global neurosurgery is a subset of global surgery that lives in relative obscurity in the context of global health. despite its recent popularity, global neurosurgery has been around for decades, with amazing work keywords global neurosurgery, developing countries, lowand middle-income countries corresponding author: ahtesham khizar punjab institute of neurosciences, lahore, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 121 global neurosurgery: the need of the hour for developing countries being done all over the world. because of the individual and collective efforts of neurosurgeons around the world, modern neurosurgery has become one of the most complex specialties in healthcare. massive advances in patient care have transformed the field, transforming previously inoperable cases into standard practice. this progress has affected countless lives, but its impact has been disproportionate. lowand middle-income countries (lmics) around the world have not benefited from advances in neurosurgery; most have little or no neurosurgical capacity in their entire country.4 when it comes to surgical subspecialties such as neurological surgery, access to care ranges from uneven to non-existent in some cases. many parts of the world, particularly in lmics, have one neurosurgeon for every 10 million people, making access to neurosurgical care a luxury rather than a right.2 research is an essential component of global neurosurgery. it can help to shape policy, support training, and spread new ideas. furthermore, and particularly in the developing world, research educates the public about disease trends, interventions, outcomes, and potential barriers to quality, safe, accessible, and affordable care. but according to studies, despite having a high disease burden, lowand middle-income countries have a poor representation in research publications.2 the global neurosurgery committee (gnc) action plan aims to advance relevant research, particularly in developing countries.5,6 the lancet commission on global surgery was formed in 2013 with the mission of "developing and assembling the best evidence on the state of surgery worldwide". the following is a summary of their report's findings: ● 5 billion people worldwide do not have access to “safe, affordable surgical, and anesthesia services when needed”. ● 9 out of 10 people in lmics lack access to basic surgical treatment. ● 18.6 million people die each year due to lack of essential surgical care, more than 3 times the number of deaths due to hiv/aids, tuberculosis, and malaria. ● 143 million additional surgical procedures are needed in lmics each year. ● 2.2 million more surgeons, anesthetists, and obstetricians are needed. ● the cost of addressing this need is estimated at us $350 billion by 2030. ● the cost of not responding to this need will result in losses estimated at us $12.3 trillion over next 15 years.6 the first step in addressing the global demand for safe, affordable, and equitable neurosurgical care is to identify current resources and needs. to provide the necessary data, research efforts at both the global and local levels are required. the wfns gnc is actively involved in studies to determine the global neurosurgical workforce, broken down by countryspecific numbers and markers, in order to determine where the greatest need exists and where additional efforts should be directed to address those needs. knowing the density of neurosurgeons in a country, however, is only the first step; educational programmes are required to train more neurosurgeons. the distribution of training centres around the world is being studied, but the barriers to training access are still being investigated. once a sufficient number of neurosurgeons have been trained, the issue of limited resources and the need for appropriate neurosurgical equipment that is both suitable and sustainable in various lmics remains. programs such as the wfns foundation neurosurgical equipment support aim to provide donated equipment to lmic neurosurgeons who would not otherwise be able to afford it. the gnc is currently analysing the wfns programme to determine the suitability and sustainability of such equipment in lmic settings, as well as the effectiveness of such equipment donation programmes.5 role of who in global neurosurgery who is the united nations (un) health technical branch, and its primary functions include: 1. provide leadership and engaging partnerships 2. shape the research agenda 3. develop norms and standards 4. articulate ethical, evidence-based policy options 5. provide technical support 6. monitor and assess health situations and trends.7 most of the world's populations face ongoing challenges in gaining access to safe, timely, and affordable surgical care, as well as financial risk protection. global neurosurgery, in particular, has a 122 ahtesham khizar, soha zahid significant need to increase the neurosurgical workforce, which includes all sub-specialty fields, particularly paediatric neurosurgery. furthermore, good imaging and other equipment are required to provide an optimal means of providing comprehensive neurosurgical service delivery. despite ongoing challenges at who, persistent underfunding, political wrangling, bureaucracy, and significant criticism, there have been significant successes and positive ongoing efforts to make the world a healthier, better place. there is no other international body or member state capable of providing coordinated global leadership or commanding such global respect; no other body can bring all 194 ministers of health together in an international forum to set global health priorities. most lmics rely on who at all levels, particularly the country office, which is viewed as an essential ally of the local health ministry; who remains a vital asset to achieving a healthier world. by working directly with who at all levels and optimising wfns interactions, including the who liaison committee, global neurosurgery would do well to consider who as an advantageous, strong, and willing partner.7 role of wfns in global neurosurgery wfns is the largest neurosurgical organisation, with over 49,000 neurosurgeons from almost every existing neurosurgical society worldwide. it was founded in 1955 to promote neurosurgery camaraderie among neurosurgeons. several committees play critical roles under the auspices of the wfns. the foundation's activities are organised around three pillars: 1. education 2. development of network of training centers 3. provision of neurological equipment to developing countries.8 recommendations and future directions in global neurosurgery ● expand the accumulation of human resources. ● by increasing capacity at existing training facilities and launching new programmes, more neurosurgeons, nurses, operating room staff, and anaesthetists need to be taught. ● to address the current deficit as soon as feasible, the idea of task-sharing training for nonneurosurgeons in basic and emergency neurosurgery should be investigated. ● encourage lmics to conduct research in neurosurgery. for contributions coming from lmics, removing the financial obstacles to publication should be taken into consideration. ● encourage innovative ideas that are useful and economical. ● by cultivating personal connections with significant organisations, neurosurgery can become a prominent player in the global surgery community.2 more articles on the outcomes of global neurosurgery measures implemented in lowresource countries will aid in the formulation of future strategies. it is a source of pride that neurosurgeons from developed regions have banded together to spread the benefits, love, and joy of neurosurgery to their underserved brothers and sisters. the collaboration and coordination of various societies such as the world federation of neurological surgeons (wfns), the asian congress of neurological surgeons (acns), the neurosurgery outreach foundation (nof), and the foundation for international education in neurological surgery (fiens) would be a watershed moment in making neurosurgery truly global.9 a sufficient number of medical professionals, facilities, and training programmes for neurosurgery are still lacking in the majority of underdeveloped nations. dedicated neurosurgical beds, beds in intensive care units, and hospitals with the capacity for neurosurgery are all in short supply. computed tomography, magnetic resonance imaging, and specialist neurosurgery tools are further amenities. additionally, there are the same issues with neurosurgeons being overrepresented in metropolitan areas as opposed to suburban ones. the main causes of the delayed progress in neurosurgery services in underdeveloped nations have been recognised as poor coordination amongst neurosurgical societies, limited funding, and poor development in neurosurgery education programmes by the governing bodies in those countries. the current measures taken by numerous institutions, organisations, societies, and people, particularly those from high income nations, have led to an increase in the number of qualified neurosurgeons in lmics. to assure the sustainability of neurosurgery services, self-reliance with 123 global neurosurgery: the need of the hour for developing countries committed education and training should be built in every nation. the ultimate goal of structuring neurosurgery education, human resources, and facilities in all nations around the world should be the equality of access to neurosurgical treatments by all people.10 a worldwide solution with a common vision and objectives is necessary for a global problem. the authors call on like-minded neurosurgeons to get together, begin the process of developing consensus within the international neurosurgery community, and work with other stakeholders in the provision of global surgical care. conclusion the world's lowand middle-income countries have not profited from advancements in neurosurgery. the majority of developing countries still struggle with a lack of medical professionals. however, in recent years, the sector has started to coalesce and important initiatives have been taken to create a cohesive voice. large-scale collaboration through multilateral, multinational participation is the only real answer to the problems we face in global neurosurgery. the future of global neurosurgery looks promising as the key actors have started working together toward this final resolution. list of abbreviations lmic: lowand middle-income country lmics: lowand middle-income countries gnc: global neurosurgery committee un: united nations wfns: world federation of neurosurgical societies who: world health organization acns: asian congress of neurological surgeons nof: neurosurgery outreach foundation fiens: foundation for international education in neurological surgery references 1. lartigue jw, dada oe, haq m, rapaport s, sebopelo la, ooi sz, senyuy wp, sarpong k, vital a, khan t, karekezi c. emphasizing the role of neurosurgery within global health and national health systems: a call to action. frontiers in surgery. 2021;8. 2. park kb, johnson wd, dempsey rj. global neurosurgery: the unmet need. world neurosurgery. 2016 apr 1;88:325. 3. dewan mc, rattani a, fieggen g, arraez ma, servadei f, boop fa, johnson wd, warf bc, park kb. global neurosurgery: the current capacity and deficit in the provision of essential neurosurgical care. executive summary of the global neurosurgery initiative at the program in global surgery and social change. journal of neurosurgery. 2018 apr 27;130(4):1055-64. 4. haglund mm, fuller at. global neurosurgery: innovators, strategies, and the way forward: jnspg 75th anniversary invited review article. journal of neurosurgery. 2019 oct 1;131(4):993-9. 5. rolle m, ammar a, park kb. global neurosurgery: a call to action. journal of global neurosurgery. 2021 apr 23;1(1):86-8. 6. meara jg, leather aj, hagander l, alkire bc, alonso n, ameh ea, bickler sw, conteh l, dare aj, davies j, mérisier ed. global surgery 2030: evidence and solutions for achieving health, welfare, and economic development. the lancet. 2015 aug 8;386(9993):569-624. 7. johnson wd. the role of who in global neurosurgery. journal of global neurosurgery. 2021 apr 23;1(1):80-2. 8. arraez ma. global neurosurgery: the role of wfns foundation. journal of global neurosurgery. 2021 apr 23;1(1):62-3. 9. agrawal a, mishra r. current status of global neurosurgery in south-east asia. journal of global neurosurgery. 2021 apr 24;1(1):43-6. 10. kato y, liew bs, sufianov aa, rasulic l, arnautovic ki, dong vh, florian is, olldashi f, makhambetov y, isam b, thu m. review of global neurosurgery education: horizon of neurosurgery in the developing countries. chinese neurosurgical journal. 2020 sep 10;6(03):178-90. 7mittler-maticaroxana_about romanian neurosurgery (2015) xxix (xxii) 1: 59 67 59 about symptoms of patients with post traumatic brain injury psychiatric sequels roxana mittler-matica phd student in medicine, university of oradea, romania neurosurgery resident, neurochirurgische klinik, städtisches klinikum braunschweig, germany abstract: introduction: because of high incidence, even if not permanently, some post traumatic brain injury (tbi) psychiatric sequels, are analysed. material and methods: the paper refers to 1185 patients who were admitted to section i psychiatry, neurology and psychiatry hospital, oradea, during 2013 year. it was analysed the symptoms of those who suffered a tbi in the past; patients called: patients in the analysis group. the linear correlation coefficient was computed, in purpose to determine the relationship between duration relapses and number of symptoms. results: it is observed a strong correlation between the years number of relapse (of post-tbi psychiatric disease) and the number of psychiatric symptoms associated. for 80% of psychiatric relapses after a tbi with loss of conscious (about patients in the analysis group), the tbi were suffered in infancy; such an incident in infancy may have severe influence on mental health. the psychiatric disease (for which they were admitted in hospital) worsened general health status at a percentage of 83.58% patients in the analysis group. the average by hospitalization days was 11.58; with approximation it was 12 days. discussion: the most common symptoms of post-tbi psychiatric disease, which affects physical functionalities of patients in the analysis group, were: insomnia, fatigue, headache (64.66% have accused insomnia; 41.18% have accused weakness and / or fatigue; 33.34% have accused headache). average by age of the patients in the analysis group with reduced instincts was 45.08 years. women patients preserve better the instincts excepting defense instinct which diminishes more often compared to men patients in the analysis group. key words: linear correlation coefficient, years number of relapse, loss of conscious. introduction establishing causality between tbi and psychiatric disorders, it is important in terms both clinically and scientifically, [5] especially in purpose to treat them effectively. [2] for some patients, [1] the consequences of tbi are particularly serious. many cases of tbi are followed [4] by 60 mittler-matica symptoms of patients with post tbi psychiatric sequels permanent disabilities with socio-economic impact, ones of these involve psychiatric disorders. for example, reported incidence rate of 15.3 to 33% were followed by a post-tbi major depression or other psychiatric disease such as: [7] posttraumatic stress disorder, personality change, aggression, inconsequent or immature behavioural, hyperactivity, mania, psychosis. the spectrum of neuro-psychiatric sequels includes various manifestations, both somatic and psychiatric manifestations. these psychiatric symptoms may be divided into two categories: [6] cognitive and behavioral presentations. materials and methods the paper refers on the 1185 patients who were hospitalized in section i psychiatry, neurology and psychiatry hospital, oradea, during 2013. a number of 67 patients have declared an antecedent tbi, so they are suspected to suffer of post-tbi psychiatric sequels. these 67 patients are named: patients in the analysis group. linear correlation coefficient (bravaispearson) [3] was calculated in purpose to identify interdependence of two phenomena, as well as intensity of the connections, according with next formula: � = ± ∑���∙ � �∑��� �∙�∑� � � (1) the notations are: r is correlation coefficient, with x' deviations from the arithmetic average of x phenomenon values; with y' deviations from the arithmetic average of the y phenomenon values. about correlation coefficient value, it is advisable to interpret (according to the theory guilford) as follows: [3] an absolute value between 1 and 0.9 denotes a very strong correlation; between 0.9 and 0.7 denotes a strong correlation; between 0.7 and 0.4 denotes a correlation of medium intensity; between 0.4 and 0.2 denotes a low intensity correlation; between 0.2 and 0 denotes a very weak intensity correlation that it can be considered as non-existent. results general health status of patients in the analysis group, were damaged by the psychiatric disorders for 46 of them, so at a percentage of 83.58%. for other 21 patients (16.42%) in the analysis group, the state of general health was evaluated to be reliably. on admission to hospital, besides psychiatric disorder, a number of 38 patients in the analysis group were suffering by other chronic diseases. of them, 31 patients had more than another chronic condition, figure 1. as well as psychiatric disorder, a percentage of 46.26% of patients in the analysis group were suffering of two or more chronic disease. romanian neurosurgery (2015) xxix (xxii) 1: 59 67 61 figure1 chronic diseases (others than psychiatric) for patients in the analysis group the symptoms described by patients in the analysis group are diverse. on the symptoms of patients in the analysis group were defined those vectors, comprising following: a) physical functionalities vector of symptoms which includes the following symptoms: vertigo, dizziness or balance disorders, tremors, tingles, retardation in movement, neck pain, back pain, limb pain or physical pain in general, chest pain, palpitations, sweating, lack of appetite, asthenia, fatigue, insomnia, etc.; b) cognitive functionalities vector of symptoms which determines the capability to work and to have a job and includes the following symptoms: low capability to memorize, aboulia (decrease of the will), voluntary activity reduction, spatial or/and temporal disorientation, etc.; c) emotional vector of symptoms which includes the following symptoms: fear, worries over everyday existence, psychomotor inhibition, psychomotor restlessness, psychomotor agitation, etc.; d) social vector of symptoms which determines the socio-affective functionalities and which includes the following symptoms: verbose, depressed mood, sad mood, aggressiveness, verbal aggression, mental degradation, etc. for a percentage of 5.97% patients in the analysis group, some motor skills, corresponding physical functionalities vector, were affected by tremor of the extremities, sudden involuntary limb movements or false sensation of tingling, numbness, etc. (that occurs in some neurological disorders). headache was accused by a percentage of 33.34% patients in the analysis group. vertigo was accused by a percentage of 10.45% the patients in the analysis group; dizziness was accused by a percentage of 16.41%; vertigo and dizziness was accused by a percentage of 26.86% patients in the analysis group, figure 2. neck pains and / or lumbar pains were accused by a percentage of 7.46%; limb pains a percentage of 1.49%; generally physical pains 10.45% 46.26% 43.29% psychiatric disease without other cronic disease psychiatric disease and two or more cronic diseases psychiatric disease and one cronic disease 62 mittler-matica symptoms of patients with post tbi psychiatric sequels were accused a percentage of 2.98% patients in the analysis group. chest pains (in the thoracic region that is above the heart) were accused by a percentage of 4.47% patients in the analysis group (at one of these patients was reported duodenal ulcer, the other chest pains are not correlated with any other diseases than the psychiatric disease). palpitations were accused by a patient of 61 years old, which among other diseases found (cervical spondylosis, thyroid dysfunction) was essv arrhythmia (over ventricular extra systole arrhythmia). fatigue was blamed by a percentage of 14.93%; fatigue and asthenia were blamed by a percentage of 23.88% of patients in the analysis group, figure 3. sweating was accused by a percentage of 2.98% of patients in the analysis group. lack of appetite was accused by a percentage of 8.96%; lack of appetite and weight loss were accused a percentage of 4.47%. so, a percentage of 13.45% patients in the analysis group have accused lack of appetite (followed or not by weight loss). feeling lump in the throat was accused by one female patient of 48 years old, who suffered a tbi two year ago, with the diagnosis recurrent depressive disorder (rdd), severe depressive episode. sound phobia was accused by a male patient of 48 years old, who suffered a tbi one year ago, diagnosed with rdd, severe depressive episode. frequently, insomnia was accused by patients in the analysis group; mixed insomnia accused a number of 31 patients (a percentage of 42.27%); wake insomnia was accused by a percentage of 14.93%; insomnia about the sleep start (dyssomnia) was accused by a percentage of 7.46%; figure 4. about the instincts analysis, it was observed diminished instincts at a percentage of 17.91% patients in the analysis group. for year 2013, hospitalization days of patients in the analysis group were 776. a percentage of 22.39% patients in the analysis group have declared a tcc with loss of conscious; a percentage of 33.33% those cases of tcc with loss of conscious represents psychiatric relapses; for example: a male patient of 49 years old, with diagnostic: recurrent depressive disorder, moderate depressive episode and psychiatric relapses along last 24 years. romanian neurosurgery (2015) xxix (xxii) 1: 59 67 63 figure 2 symptoms of vertigo and dizziness figure 3 symptoms of fatigue and asthenia figure 4 on complaints of insomnia vertigo and dizziness 26.86% vertigo 2.99% dizziness 7.46% others symptoms that vertido and dizziness 62.69% fatigue 14.96% fatigue and astenia 23.88% other symptoms then fatigue and astenia 61.16% mixed insomnia 42.27% dyssomnia 7.46% wake insomnia 14.93% other symptoms than insomnia 35.34% 64 mittler-matica symptoms of patients with post tbi psychiatric sequels discussions for a small percentage, 16.42% patients in the analysis group, the general health status was evaluated as good. a percentage of 56.72% patients in the analysis group, besides psychiatric disease, they suffer from other chronic diseases, which complicate their treatment, sometimes. those diseases were: • hypertensive cardiomyopathy (4 patients), ischemic cardiomyopathy (2 patients), metabolic cardiomyopathy (2 patients), arrhythmia essv (1 patient), mitral (heart) in-sufficient (2 patients), arterial hyper pressure (10 patients); • cervical spondylosis (6 patients), herniated disc (3 patients); • chronic gastritis (2 patients), duodenal ulcer (2 patients), state postoperative colon cancer (1 patient); • biliary dyskinesia (2 patients), gallstones (1 patient); • liver disease (3 patients), toxic liver disease (2 patients), hepatic stenosis (2 patients); • renal impairment (2 patients); • alcohol abuse syndrome (2 patients), alcohol withdrawal syndrome (2 patients); • anemia (1 patient), obesity (1 patient), diabetes (3 patients); • sinusitis (3 patients), bronchitis chronic asthmatic (1 patient), chronic obstructive broncho pneumonia (1 patient); • thyroid dysfunction (2 patients). a percent of 20,89% patients in the analysis group have a diagnostic that involve a damaged functioning of the brain; those diagnostics were: organic disorder of personality and post-tcc behavior, cod f079, at a percentage of 2.98% patients in the analysis group (for example, a male patient of 51 year old, who suffered a severe tbi and brain contusion, 20 year ago), personality disorder of organic type, at 4.47%, (male patient of 42 years old, who suffered a severe tbi, one month ago), personality disorder of mixt type, at 2.98%, organic delusional disorder, cod f062 (at male patient of 55 years old, who suffered a severe tbi and cerebral hematoma, 11 month ago), cognitive disorder and brain atrophy (at a female patient of 69 year old, who suffered a tbi a week ago), organic mental disorder, cod f069, at 2.98% (for example, a male patient of 48 years old who suffered a tbi 3 year ago, with symptoms: psychomotor restlessness, low capability to memorize, low capability to process the information, mmse test: 27 points, anxiety, low tolerance on frustration, social withdrawal tendencies). the symptoms described by patients in the analysis group are different. it was analyzed the correlation between years number of psychiatric relapses were noticed and number of symptoms (about hospitalization in 2013). average by years, for which patients in the analysis group have registered psychiatric relapses, was 11 years (more accurate 10.82353). average by number of symptoms was 6 (more accurate 6.05882). the computation of linear correlation coefficient includes the determination of romanian neurosurgery (2015) xxix (xxii) 1: 59 67 65 deviation from the arithmetic average of two phenomena. it was performed according to table 1, (where it is written only values different from zero of achievement number, so it was detected at least one case). the result of correlation coefficient value is: r=-29/(10,95445*34,32200)=-0,07713; consequently, a strong correlation between those (but not a very strong correlation). table 1 correlation between number of symptoms and time period (years) of psychiatric relapses years 1 2 6 8 9 13 14 19 23 24 deviation (average=11) 10 9 5 3 2 -2 -3 -6 -12 -13 the two events pairs values multiplied of achievements number symptoms/ deviation 3 / 3 (average=6) 3x10 x1 =30 3x -3 x1 3x -6 x1 3x -13 x1 4 / 2 2x9 x1=18 2x2 x1=4 5 / 1 1 x 3 x1=3 1 x(-2) x1=-2 6 / 0 0 x 5 x2=0 0 x -2 x1=0 0x -12x1 9 / -3 -3 x10 x2 10 / -4 -4x10 x1 =-40 -4 x -6 x1 11 / -5 -5 x -12x1 total 30 60 40 18 0 3 4 -2 +0 -9 -18 +24 60 -39 + 0 total general -29 it is noticed that a percentage of 88.24% patients (in the analysis group) with psychiatric relapse (who suffered a tbi before psychiatric disease) has accused insomnia as symptom and a percentage of 41.18% has accused weakness and / or fatigue (for other 5.97% the psychiatric relapses was before the tbi). about those who have not accused weakness and / or fatigue, a percentage of 40% have accused lack of appetite or lack of 66 mittler-matica symptoms of patients with post tbi psychiatric sequels appetite with weight loss. it is noticed that a percentage of 52.94% of patients (in the analysis group) with psychiatric relapses (who suffered a tbi before psychiatric disease) suffers from other chronic disease; among those diseases were: cervical spondylosis, arterial hypertension, arthrosis, chronic gastritis, diabetes, hepatic stenosis, renal impairment. regarding physical functionalities vector of symptoms, headache was accused, frequently. a percentage of 65.22% patients in the analysis group specified a constant location of pain. it was complaints about a frontal headache (sometimes with left frontal headache specification) or occipital headache, for most of them. uncommon, it was accused left parietal headaches. further descriptions of these pains were earpiece, mixed, persistent or diffuse. of the patients who experienced headache, only one suffered from cervical spondylosis, his diagnosis was: cognitive disorder in observation, (mmse: 17 points). headache and vertigo were accused by a percentage of 71.43% of patients with vertigo. headache and dizziness and were accused by a percentage of 45.45% patients with dizziness. for example, a patient of 66 years old, with diagnostic: organic mental disorder, who underwent a tbi with 8 months before hospitalization in section i psychiatry; other symptoms were psychomotor restlessness, limitation of movements by involuntary contraction, fixing and evoking amnesia, ideas of guilt. fatigue and weakness represent symptoms that have been reported frequently, more accurate by a percentage of 38.81% patients in the analysis group. it can be observed that insomnia is the most common symptom; a percentage of 64.66% patients in the analysis group accused insomnia, that it means a rate of two out of three patients, fig.4. arithmetic average by age of the patients with reduced instincts was 45 years (45.08). of these patients, 33.33% were women and 66.66% were men; it is noticed that the proportion of women / men is not the same as the patients in the analysis group, (a percentage of 41.79% were women and 58.21% were men); women preserved better all instincts (the difference is 8.46%). instinct of defense was found to be decreased to 8.95% of patients in the analysis group. average by age of patients with diminished instinct of defense was 58.5 years, while women represent a percentage of 83.33%, the difference is 41.54%; much more than the percentage of female patients in the analysis group. it is observed that women lose much easier the defense instinct than men. exacerbated defense instinct was observed at a 68 year old male patient, with diagnostic: personality disorder mixed type; which suffered a tbi, 21 years ago. food instinct was observed to be exacerbated at a female patient of 49 years suffering a severe tbi in childhood, or it was observed to be diminished at two male patients of 48 and 62 years old. food instinct was observed to be abolished at a female patient of 61 years old, whose psychiatric disease started immediately after a tbi, 13 years ago. instinct for alcohol romanian neurosurgery (2015) xxix (xxii) 1: 59 67 67 consumption it is noticed at a percentage of 4.47% patients in the analysis group, for example at a patient of 51 year old, his psychiatric disease started immediately after a severe tbi, due to a traffic accident (cerebral hematoma), 24 years ago, with psychiatric diagnostic: organic mental disorder. in conclusion, women preserve better the instincts, excepting defense instinct which diminishes more often comparing to men. a percent of 20.89% patients in the analysis group have a psychiatric diagnostic that involve an anatomically damaged functioning of the brain; correlation between tbi and psychiatric disease was considered evident; for example: organic disorder of personality and post-tbi behavior, cod f079; organic delusional disorder, cod f062; organic mental disorder, cod f069. it is recommended an increasing attention on risk of post-tbi psychiatric disorder, especially during convalescence after a tbi. a good response to treatment with good result of each patient social integration, depend of each patient motivation; it is noticed the case of a 60 years old male patient with diagnostic: organic disorder of personality and post-tcc behavior, which suffered a severe tbi due an traffic accident, 14 years ago (the expert consult revealed: fluctuation of concentration and mobilization of attention, mental fatigue… and ct image reveals posttbi brain sequels), but has a job. correspondence roxana mittler-matica e-mail: roxana.mittler-matica@live.de references 1. anderson, v., & spencer-smith, m & coleman, l., & anderson, j. & greenham, m. & jacobs, r. & lee, k. & leventer, r., (2014), predicting neurocognitive and behavioural outcome after early brain insult. dev. med. child. neurol., apr., 56(4):32936;doi:10.1111/dmcn.12387 2. bhalerao, s.u. & geurtjens, c & thomas g.r. & kitamura, c.r. & zhou, c. & marlborough, m., (2013), understanding the neuropsychiatric consequences associated with significant traumatic brain injury. brain. inj., 27(7-8):767-74, doi: 10.3109/02699052.2013.793396 3. dugaciu, n. & moise, gh. & doroftei, s., (1997), elemente de biostatisticǎ. arad, editura vasile goldis, isbn 973-98196-1-3 4. greenberg, m.s., (2010), handbook of neurosurgery. new-york, thieme medical publishers, isbn 978-160406-326-4 5. kinnungen, k.m. & greenwood, r. & powell, j.h. & leech, r. & hawkins, p.c. & bonnelle, v. & patel, m.c. & counsell, s.j. & sharp, d.l., (2011), white matter damage and cognitive impairment after traumatic brain injury. brain, (a journal of neurology), vol.134, issue 2, doi: http://dx.doi.org/10.1093/brain/awq347 6. riggio, s., & wong, m., (2009), neurobehavioral sequelae of traumatic brain injury. mt sinai j of med, apr; 76(2):163–172, doi:10.1002/msj.20097 7. schwarzbold, m. & diaz, al. & martins, e.t. & rufina, a. & amante, l.n. & thais, m.e. & quevedo, j. & hohl, al. & linhares, m.n. & wals, r., (2008), psychiatric disorders and traumatic brain injury. neuropsychiatric disease and treatment, aug, v.4(4): 797-816 8. whelan-goodison, r. & ponsford, j. & schonberger, m., (2008), association between psychiatric states following traumatic brain injury and outcome. journal rehabil. med., 40:850-85, doi:10.2340/16501977-0271 doi: 10.33962/roneuro-2022-041 study of association of serum vitamin d and serum calcium with spontaneous aneurysmal subarachnoid haemorrhage in a tertiary care centre kuldeep singh, sharad pandey, pankaj kumar, l.n. gupta, amit mehto, ravi prakesh romanian neurosurgery (2022) xxxvi (2): pp. 230-236 doi: 10.33962/roneuro-2022-041 www.journals.lapub.co.uk/index.php/roneurosurgery study of association of serum vitamin d and serum calcium with spontaneous aneurysmal subarachnoid haemorrhage in a tertiary care centre kuldeep singh1, sharad pandey1, pankaj kumar1, l.n. gupta1, amit mehto2, ravi prakesh3 1 department of neurosurgery, a.b.v.i.m.s. and dr ram manohar lohia hospital, new delhi, india 2 department of community medicine vcsg government institute of medical science and research, srinagar, uttrakhand, india 3 department of community medicine, dr baba saheb ambedker medical college & hospital, delhi, india abstract background: aneurysmal subarachnoid haemorrhage (asah) is a disease associated with high mortality and morbidity. recent studies have postulated a correlation between vitamin d deficiency and asah, however, the mechanism of which remains obscure. vitamin d and calcium in patients withasah has not been formally investigated. therefore, the aim of this study was to evaluate the incidence of hypovitaminosis d and hypocalcemia in patients with asah. methods: an observational study was conducted at the department of neurosurgery at tertiary care centre, new delhi, india. 40 patients with spontaneous aneurysmal sah were enrolled during the period january 2019 to 15th april 2020. the standard protocol of care was given to all patients included in the study. laboratory investigations including vitamin d and calcium levels; clinical examination and grading were done for each patient. the data thus collected was used to see the clinicdemographic profile of patients of asah with an emphasis on vitamin d and calcium levels. results: the study reported mean vitamin d level of 17.4 ± 7 ng/ml; mean calcium level of 8.3 ± 0.9 mg/dl amongst the study participants. out of 40 patients, 8 patients (20%) were severely deficient, 24 patients (60%) were mild to moderate deficient and 8 patients (20%) were having normal vitamin d levels. 50% of the patients (n=20) were hypocalcaemic and 50% were normocalcaemic. conclusion: a higher incidence of vitamin d deficiency was observed in our study along with an equal incidence of hypocalcemia vs normocalcemia. further studies with a comparison group and a bigger sample size are needed to validate this evidence. introduction subarachnoid haemorrhage (sah) is the extravasation of blood into subarachnoid space of the cns, which i s normally filled with keywords hypocalcaemia, hypovitaminosis, asah (aneurysmal subarachnoid haemorrhage), bleeding corresponding author: sharad pandey department of neurosurgery, a.b.v.i.m.s. and dr ram manohar lohia hospital, new delhi, india drsharad23@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 231 serum vitamin d and serum calcium with spontaneous aneurysmal subarachnoid haemorrhage cerebrospinal fluid (csf). the prevalence of subarachnoid haemorrhage (sah) is approximately 9 per 100,000 person per year1. there is a slight preponderance in women as compared to men, and this increases with age. peak incidence has been observed in 5th and 6th decade of life2. the commonest cause of sah overall is trauma, whereas commonest cause of spontaneous sah is rupture of intracranial aneurysms3. about 80% of nontraumatic sah happens due to aneurysms4. most common symptom of sah is headache, which is referred to by the patient as the worst headache he/she has ever experienced in his/her life. it can also be accompanied by nausea, vomiting, loss of consciousness. aneurysmal subarachnoid haemorrhage (asah) is a disease associated with a high mortality and morbidity. a study from netherlands reported that the overall mortality rate of non-traumatic sah has been found out to be 30%5. sah because of the rupture of an intracranial aneurysm is a potentially fatal event .altough it accounts for 5% of all strokes but its burden is relevant due to high mortality ,high disability and higher incidence in the young6. even after good outcome of sah, long term cognitive deficits (commonly in memory, language and executive functions) may happen to patients. further, a study reported that approximately 40% of sah survivors may not be able to return back to their previous jobs7.even after successful aneurysmal clipping in patients with asah, overall quality of life was found to be decreased as compared to controls in a study8. recent studies have postulated a correlation between vitamin d deficiency and asah, however the mechanism of which remains obscure9,10,11. probable mechanisms that have been postulated are indirect variations in blood pressure9, antiproliferative and anti-inflammatory action of vitamin d on smooth muscle of blood vessels10. these effects of vitamin d becomes more important as cerebral vasospasm has been implicated as a major causative factor for long term neurological deficits present in patients with sah. in the past decade, there has been a surge of interest in the impact of vitamin d levels on various conditions ranging from bony fractures to malignancy. a growing body of evidence also implicates hypovitaminosis d in cerebral smallvessel disease and stroke12,13.recent investigations, primarily in the cardiothoracic14,15and vascular surgeryliterature, have suggested a concordance of hypovitaminosis d and arterial disease, including aneurysmal dilation of the aorta16.this relationship is believed to be mediated by a variety of mechanisms, including modulation of vessel wall inflammation, changes in vascular smooth muscle cell development, and numerous systemic effects such as changes in insulin resistance and lipid processing17. hypocalcaemia has been significantly associated with extent of bleeding in patients with intracerebral haemorrhage because magnesium and calcium have roles in platelet function and coagulation cascade18. however, research regarding the association of intracranial aneurysm rupture risk in hypocalcaemia and hypomagnesemia are lacking. vitamin d and calcium in patients with cerebral aneurysms and aneurysmal sah has not been formally investigated. therefore, the aim of this study was to evaluate the incidence of hypovitaminosis d and hypocalcemia in patients with asah. methods this was an observational study conducted at the department of neurosurgery at tertiary care centre new delhi, india. 40 patients with spontaneous aneurysmal sah were enrolled during the period january 2019 to 15th april 2020. all cases of spontaneous aneurysmal sah admitted in the institute during the study period were included and patients who had a previous history of renal disease; history of liver dysfunction; history of chronic intestinal malabsorption; and those taking vitamin d and calcium supplementation for any reason were excluded from the study. informed written consent was taken from each eligible patient before his/her enrolment. the baseline evaluation included personal and family history including any comorbidities or prior surgical intervention; general physical examination and thorough neurological evaluation; laboratory tests including complete blood count (cbc), liver function tests (lfts), renal function tests (rfts); non-contrast enhanced ct (ncct) head; ct angiography/ mr angiography/dsa; serum calcium levels; and vitamin d (25-hydroxyvitamin d) levels using radioimmunoassay method. standard protocol of care was given across to all patients included in the study. grading was done by 232 kuldeep singh, sharad pandey, pankaj kumar et al. the world federation of neurological societies (wfns) grading of sah, modified fisher grade, hunt and hess grade and glasgow coma scale (gcs). mayo medical laboratories reference ranges for total serum 25-hydroxyvitamin d were adhered to for classifying the patients in terms of vitamin d levels which are severe deficiency <10ng/ml; mild to moderate deficiency – 10-24.9 ng/ml; optimal – 25-80 ng/ml; possible toxicity >80 ng/ml; calcium reference levels used at our institute arenormal total calcium level 8.5 mg/dl – 10.5 mg/dl; normal ionized calcium level 4.5-5.6 mg/dl. data collection all enrolled patients of spontaneous aneurysmal sah had these tests as part of their routine investigations during their treatment (conservative management or operative management). statistical analysis all statistical calculations were conducted with standard statistical programs (ibm spss version 26) . shapiro wilk test was applied to check the normality of variables that were included in the study. parametric data was assessed with help of student’s t-test, one way anova test. nonparametric data was analyzed with help of chi square, mann whitney u test, kruskalwallistest. p-value of <0.05 was considered to be of statistical significance in the study. results out of 40 patients with asah, 18 were males (45%). 15 patients (37.5%) were in age group of 25-45 years, 16 (40%) were in age group of 46-60 years, 9 (22.5%) were in the age group of 61 -75 years. the mean age of patients was 51 years. in our study 10 patients were current smokers (25%); 22 patients (55%) were hypertensive;and 14 patients (35%) were diabetic. the most common site of aneurysm was found to be anterior communicating artery (47.5%) and the least common was cerebellar artery (2.5%). the study reported mean vitamin d level of 17.4 ± 7 ng/ml; mean calcium level 8.3 ± 0.9 mg/dl. the study reported that out of 40 patients, 8 patients (20%) were severely deficient, 24 patients (60%) were mild to moderate deficient and 8 patients (20%) were having normal vitamin d levels. amongst males, 61.1% were vitamin d deficient whereas amongst females, 77.3% were deficient and this difference was found to be statistically insignificant (p-value=0.2). mean vitamin d levels in males and females were 19.4 ± 6.7 ng/ml and 15.7 ± 7.0 ng/ml respectively. as vitamin d levels in the study participants were found to be not normally distributed, therefore independent sample mann-whitney-u test was applied to check the mean difference of vitamin d among gender and it was found to have no significant difference in the two groups (p-value = 0.106) (figure 1). figure 1. independent sample mann whitney u test showing the mean difference of vitamin d among gender. figure 2. kruskal wallis test showing the mean difference of vitamin d among wfns grade. 233 serum vitamin d and serum calcium with spontaneous aneurysmal subarachnoid haemorrhage mean vitamin d level in smokers and non-smokers were 18.9 ± 7.1 ng/ml and 16.9 ± 7.0 ng/ml respectively and this difference was found to be nonsignificant, (p value 0.45). similarly, mean vitamin d levels in diabetics and non-diabetics; and hypertensives and non-hypertensives patient were 17.2 ± 6.6 ng/ml and 17.4 ± 7.4 ng/ml; and 17.3 ± 6.6 ng/ml and 17.4 ± 7.7 ng/ml respectively and these differences were found to be statisticallynonsignificant (p value – 1 and 0.757 respectively) (table 1). table 1. mean vitamin d levels in smokers non-smokers, diabetics –non diabetics and hypertensive and normotensive patients. gender no of patients mean (vitamin d) sd p value female 22 15.7 7.0 0.106 male 18 19.4 6.7 smoking no of patients mean (vitamin d) sd p value no 30 16.9 7.0 0.45 yes 10 18.9 7.1 diabetes mellitus no of patients mean (vitamin d) sd p value no 26 17.4 7.4 1.00 yes 14 17.2 6.6 hypertens ion no of patients mean (vitamin d) sd p value no 18 17.4 7.7 0.757 yes 22 17.3 6.6 the mean vitamin d levels in the various wfns grades (figure 2), modified fischer grades and hunt and hess gradesof patients were found to be statistically non-significant using the kruskal-wallis test (p value =0.412, 0.568, 0.529 respectively) (table 2). table 2. vitamin d levels across wfns grades, modified fischer grades and hunt & hess grades. wfns grades mean (vitamin d) sd p value i 18.9 7.4 0.412 ii 20.4 7.0 iii 16.9 8.6 iv 17.3 6.7 v 10.7 2.8 modified fischer grades mean (vitamin d) sd p value i 19.2 6.9 0.568 ii 16.8 9.7 iii 15.7 6.0 iv 17.7 7.1 hunt & hess grades mean (vitamin d) sd p value i 13.7 0 0.529 ii 20.6 7.0 iii 19.7 8.0 iv 15.5 8.0 v 16.6 5.8 the present study reported that half of the patients (n=20) were hypocalcaemic and the other half were normocalcaemic. mean calcium levels in males and females were 8.5 ± 1.0 mg/dl and 8.2± 1.0 mg/dl respectively and this difference was not statistically significant (p value=0.3) similarly, the mean calcium levels in smokers and non-smokers; diabetics and non-diabetics; hypertensives and non-hypertensives were 8.4 ± 0.9 mg/dl and 8.3 ± 1.0 mg/dl;8.0 ± 0.9 mg/dl and 8.5 ± 1.0 mg/dl; 8.3 ± 0.9 mg/dl and 8.4 ± 1.0 mg/dl respectively and these differences were not statistically significant (p value=0.8, 0.07, 0.65) (table 3). table 3. mean serum calcium levels across gender, smokers non-smokers, diabetics –non diabetics and hypertensive and normotensive patients. gender no of patients mean(calcium) sd p value female 22 8.2 1.0 0.3 male 18 8.5 1.0 smoking no of patients mean(calcium) sd p value no 30 8.3 1.0 0.8 yes 10 8.4 0.9 234 kuldeep singh, sharad pandey, pankaj kumar et al. diabetes mellitus no of patients mean(calcium) sd p value no 26 8.5 1.0 0.07 yes 14 8.0 0.9 hypertension no of patients mean(calcium) sd p value no 18 8.4 1.0 0.65 yes 22 8.3 0.9 the mean serum calcium amongst the different wfns grades did not differ statistically significantly (p value = 0.07) whereas the mean serum calcium levels were found to differ statistically significantly amongst the various modified fischer grades hunt & hess grades with p values 0.002 and 0.04 respectively (table 4). table 4. serum calcium levels across wfns grades, modified fischer grades and hunt & hess grades. wfns grades mean(calcium) sd p value i 8.6 0.14 0.07 ii 9.0 0.87 iii 8.3 1.3 iv 8.2 0.83 v 7.3 0.4 modified fischer grades mean(calcium) sd p value i 9.0 0.8 0.002 ii 8.9 0.4 iii 7.8 0.9 iv 7.9 0. 9 hunt & hess grading mean (calcium) sd p value i 8.7 0 0.04 ii 8.4 0.3 iii 8.8 1.4 iv 8.6 0.7 v 7.7 0.8 discussion despite recent advances in thediagnostic modalities, management and availability of plenty of literature, a substantial mortality as well as morbidity rate is attributable to unfavourable overall outcomes in patients following asah. various factors have been implicated in occurrence and poor outcome in asah patients. however only handful of those have been found to reliably predict the incidence of asah . this study was designed to identify the mean serum vitamin d and serum calcium levels and its any association in asah patients. the mean age of patients was 51 years. weir et al19studied 945 patients of cerebral aneurysm and they found mean age of patients was 46 years. aarhus et al20studied 444 patients of cerebral aneurysm and the median age of patients was 56 years . in our study out of 40 patients, 18 were males (45%) and 22 patients were females (55%) , which is comparable to the available literature suggesting that cerebral aneurysm is more common in females. in our study 10 patients were chronic smoker (25%) and 30 patients (75%) were non smoker. 22 patients (55%) were hypertensive and 18 patients (45%) were non hypertensive. 14 patients (35%) were diabetic and 26 patients (65%) were non diabetic. tuenissen et al21reviewed 9 longitudinal and 11 case control studies to identify the risk factors for asah and they found smoking ,hypertension and alcohol consumption were significantly related to the risk of spontaneous sah . we observed that the mean vitamin d levels in males and females were 19.4±6.7 ng/ml and 15.7±7.0 ng/ml respectively and this difference was not statistically significant (p value=0.106). in our study in males, 61.1% were vitamin d deficient whereas in females, 77.3% were deficient and however this difference was not statistically significant (p value=0.2). guan j et al10in a retrospective study found the mean serum vitamin d level in patients with aneurysm was 23.3± 12.3 ng/ml whereas control group had mean level of 28.7± 14.1 ng/ml which was statistically significant .they used multivariable poisson regression and backward elimination to identify the risk factors .they found patients in the aneurysm group were older ,mostly females ,tobacco users ,hypertensive and had hypovitaminosis d but race ,body mass index and diabetes were not significantly different. there was no statistically significant difference in mean vitamin d levels across wfns grading (p value = 0.412) , modified fischer grading (p value = 0.568) and hunt & hess grading (pvalue-0.529). we noted that the mean serum calcium level in males and females was 8.5 ± 1.0 mg/dl and 8.2 ± 1.0 235 serum vitamin d and serum calcium with spontaneous aneurysmal subarachnoid haemorrhage mg/dl respectively and this difference was not statistically significant (p value=0.3).in our study 9 male patients and 11 female patients had calcium deficiency and it was not statistically significant (p value =1.0). anil can et al22did a multivariate analysis of serum calcium and magnesium levels to see the association with the ruptured aneurysm and they found hypomagnesemia and hypocalcemia were significantly associated with ruptured aneurysms. in our study there was no significant difference in mean calcium levels across wfns grades (p value = 0.07) (figure 3). however, we found significant difference in mean calcium levels across modified fischer grades (p value = 0.002) and hunt & hess grades (p value=0.04) (figure 4) which means low serum calcium level was associated with the higher grades. figure 3. one-way anova test showing the mean difference of calcium among wfns grade. figure 4. one-way anova test showing the mean difference of calcium among hunt & hess grading. van heuven et al23in a retrospective study validated the prognostic value of wfns grading on admission in determination of the outcome . lindvall et al24found a significant correlation of fischer scale and hunt & hess scale with the outcome of patient although the predictive value of limited due to low sensitivity and specificity of these scales . we observed that the serum calcium has moderate positive correlation with vitamin d and gcs . this correlation was statistically significant with a p value of 0.006 which explains the direct effect of serum vitamin d level in calcium absorption and its metabolism. conclusion aneurysmal subarachnoid hemorrhage is associated with high mortality and morbidity. we observed higher incidence of serum vitamin d and serum calciumdeficiencyin asahpatients .we found statistically significant difference in mean calcium levels across modified fischer grades (p value = 0.002) and hunt & hess grades (p value=0.04) .however further studies need to be undertaken to evaluate the role of vitamin d and serum calcium in asah. also studies with a control group could help further validate this data. conflict of interest the authors have no conflict of interest to declare. acknowledgement the authors acknowledge the support of department of biochemistry. references 1 de rooij, n.k., linn, f.h.h., van der plas, j.a., algra, a., rinkel, g.j.e. incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends. j neurolneurosurg psychiatry. 2007;78:1365–1372. 2 ingall t, asplund k, mahonen m, bonita r. a multinational comparison of subarachnoid hemorrhage epidemiology in the who monica stroke study. stroke. 2000;31:10541061. 3 van gijn j. subarachnoid haemorrhage: diagnosis, causes and management. brain. 2001;124:249-278. 4 suarez j, tarr r, selman w. aneurysmal subarachnoid hemorrhage. new england journal of medicine. 2006;354:387-396. 5 risselada r, de vries l, dippel d, van kooten f, van der lugt a, niessen w et al. incidence, treatment, and case 236 kuldeep singh, sharad pandey, pankaj kumar et al. fatality of non-traumatic subarachnoid haemorrhage in the netherlands. clinical neurology and neurosurgery. 2011;113:483-487. 6 bansal m , mittal r s .clinical demographic association and outcome in patients with aneurysmal subarachnoid hemorrhage.indian j neurosurg2015;4:63–68. 7 timour al-khindi, r loch macdonald, tom a. schweizer. cognitive and functional outcome after aneurysmal subarachnoid hemorrhage. stroke. 2010;41:519-536. 8 preiss m, netuka d, koblihova j, bernadova l. quality of life 1 year after aneurysmal subarachnoid hemorrhage in good outcome patients treated by clipping or coiling. journal of neurological surgery, central european neurosurgery. 2012;73:217-23. 9 lai pm, dasenbrock h, du r. the association between meteorological parameters and aneurysmal subarachnoid hemorrhage: a nationwide analysis. plos one. 2014;9:112961. 10 guan j, karsy m, eli i, bisson ef, mcnally s, taussky p, park ms. increased incidence of hypovitaminosis d among patients requiring treatment for cerebral aneurysms. world neurosurgery. 2016;88:15-20. 11 alvarado y, perez a. effects of vitamin d deficiency in aneurysmal subarachnoid hemorrhage. critical care medicine. 2015;43:138 . 12 chung pw, park ky, kim jm, shin dw, park ms, chung yj, et al. 25hydroxyvitamin d status is associated with chronic cerebral small vessel disease. stroke. 2015;46:248-251. 13 poole ke, loveridge n, barker pj, halsall dj, rose c, reeve j, et al. reduced vitamin d in acute stroke. stroke. 2006;37:243-245. 14 giovannucci e, liu y, hollis bw, rimm eb. 25 hydroxyvitamin d and risk of myocardial infarction in men: a prospective study. arch intern med. 2008;168:11741180. 15 wang tj, pencina mj, booth sl, jacques pf, ingelsson e, lanier k, et al. vitamin d deficiency and risk of cardiovascular disease. circulation. 2008;117:503-511. 16 wong yy, flicker l, yeap bb, mccaul ka, hankey gj, norman pe. is hypovitaminosis d associated with abdominal aortic aneurysm, and is there a dose response relationship? eur j vascendovasc surg. 2013;45:657-664. 17 kassi e, adamopoulos c, basdra ek, papavassiliou ag. role of vitamin d in atherosclerosis. circulation. 2013;128:2517-2531. 18 inoue y, miyashita f, toyoda k, minematsu k. low serum calcium levels contribute to larger hematoma volume in acute intracerebral hemorrhage. stroke. 2013;44:2004– 2006. doi: 10.1161/strokeaha.113.001187. 19 weir b. unruptured intracranial aneurysms: a review. j neurosurg. 2002;96:3–42. 20 aarhus, m., helland, c.a. & wester, k. differences in anatomical distribution, gender, and sidedness between ruptured and unruptured intracranial aneurysms in a defined patient population. actaneurochir 151, 1569 (2009). 21 teunissen ll, rinkel gj, algra a, van gijn j. risk factors for subarachnoid hemorrhage: a systematic review. stroke1996; 27: 544–9. 22 can a, rudy rf, castro vm, dligach d, finan s, yu s, gainer v, shadick na, savova g, murphy s, cai t, weiss st, du r. low serum calcium and magnesium levels and rupture of intracranial aneurysms. stroke. 2018 jul;49(7):1747-1750. doi: 10.1161/strokeaha.118.020963. 23 van heuven a, dorhoutmees s, algra a, rinkel g. validation of a prognostic subarachnoid hemorrhage grading scale derived directly from the glasgow coma scale. stroke. 2008;39(4):1347-13. 24 lindvall p, runnerstam m, birgander r, koskinen l. the fisher grading correlated to outcome in patients with subarachnoid haemorrhage. british journal of neurosurgery. 2009;23(2):188-192. doi: 10.33962/roneuro-2022-062 coexistence of ipsilateral ulnar and median nerve entrapment turan kandemir, serdar ercan, zeki serdar ataizi romanian neurosurgery (2022) xxxvi (3): pp. 365-369 doi: 10.33962/roneuro-2022-062 www.journals.lapub.co.uk/index.php/roneurosurgery coexistence of ipsilateral ulnar and median nerve entrapment turan kandemir1, serdar ercan2, zeki serdar ataizi1 1 eskişehir yunus emre state hospital, department of neurosurgery, eskisehir, turkey 2 eskişehir city hospital, department of neurosurgery, eskisehir, turkey abstract objective: carpal tunnel syndrome (cts) and cubital tunnel syndrome (cuts) are the median nerve compressions under the carpal ligament and ulnar nerve at the wrist, the most common peripheral nerve entrapment of the upper extremity. the fatty tissue due to the high body mass index (bmi) differs the severity of the entrapment symptoms. the study aims to evaluate the association between bmi and symptoms of cts and cuts by analyzing the patients whose entrapments are at the same extremity and onset at the same time. method: the patients were divided into two groups according to the neuropathy sit (cts and cuts) and four subgroups according to the bmi (overweight, grade 1 obese, grade 2 obese, and morbidly obese). all patients were followed up with emg and performance scale before and after surgical treatment. results: a total of 31 patients were included in the study. the mean bmi of the patients was 29.63 kg/m2. the average bmi of male patients was 29.02 kg/m2, while the average bmi of female patients was 30.3 kg/m2. conclusion: in contrast to the previous hypotheses that claim the high body mass index increases the severity of cts but reduces the formation of cuts, our study revealed that body mass index was not related to the severity of symptoms. introduction entrapment neuropathies occur when nerves are exposed to pressure during their course in rigid anatomical structures. carpal tunnel syndrome (cts) occurs due to compression of the medial nerve under the flexor retinaculum ligament in the wrist, while compression of the ulnar nerve at the elbow level causes cubital tunnel syndrome (cuts). while cts is the most common neuropathy among entrapment neuropathies (annual incidence 424/1000000), cuts is observed in the 2nd frequency (annual incidence 20.9 / 100000) [1,2]. in the initial phase of peripheral entrapment neuropathies, epineural blood flow is reduced due to ischemic block. as a result, the nerve slowed down the conduction velocity, and a conduction block may develop. at this stage, wallerian degeneration has not yet begun, and the patient benefits from conservative treatment. in the late stage, keywords peripheral nerve, carpal tunnel, cubital tunnel, entrapment, body mass index corresponding author: turan kandemir eskisehir yunus emre state hospital, department of neurosurgery, tepebası, 26200 eskisehir, turkey turankandemir26@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 366 turan kandemir, serdar ercan, zeki serdar ataizi epineural edema, endoneurial edema, and segmental demyelination begin to develop. as this situation becomes chronic, wallerian degeneration now occurs, and clinical findings such as sensory defects and muscle atrophy can be seen [3]. patients with cts complain of pain, numbness, and tingling in the first three fingers of the hand, while patients with cuts have pain in the medial of the elbow and arm, numbness in the 4th and 5th fingers, and loss of strength in the intrinsic muscles of the hand. the definitive diagnosis of both syndromes is made by electromyography (emg) and neurological examination. conservative treatment is given primarily to patients with mild and moderate nerve compression. in addition to anti-inflammatory drugs, splits restricting wrist movements for cts and elbow movements are used for cuts. surgical intervention is required for cases resistant to conservative treatment, severe hypoesthesia, atrophy, and loss of strength. the trap channel is surgically opened, and nerve compression is decompressed. in individuals with a high body mass index, the amount of adipose tissue around the median nerve increases, which increases the risk of entrapment neuropathy [4]. studies have shown the coexistence of cts and cuts, but the frequency of median and ulnar nerve entrapment neuropathy in the same extremity and at the same time has not been reported [5,6]. in this study, it was aimed to compare the severity of entrapment neuropathies and to evaluate their demographic structure according to the body mass index of patients who were admitted to our clinic with ipsilateral cts and cuts complaints at the same time and who were treated with surgical intervention in the same session. material and methods cts and cuts patients who were treated with ipsilateral surgical intervention between january 2015 and december 2019 in the neurosurgery department of our hospital were retrospectively analyzed. the local ethics committee approved each stage of the study, and consent was obtained from all patients. patients with numbness, weakness, and thenar muscle atrophy in the 1st, 2nd, and 3rd fingers due to median nerve entrapment, and patients with the same symptoms in the 4th and 5th fingers and hypothenar muscle atrophy due to ulnar nerve entrapment, and whose symptoms started on the same side and at the same time were included in the study. cubital tunnel and carpal tunnel syndromes were diagnosed according to the patients' neurological examination and emg results. numbness, tingling, and pain sensation in the palmar face of all the fingers were questioned. tinel test was performed on the median nerve at the wrist and the ulnar nerve at the elbow, and the phalen test was also performed on patients with suspected carpal tunnel syndrome. patients with carpal and cubital tunnel syndrome at the same time were determined by evaluating physical examination findings and emg results together. cervical pathologies were excluded by performing a cervical magnetic resonance imaging. among these patients, patients whose complaints did not recover despite using medical treatment and splint and who underwent ulnar nerve and median nerve decompression surgery under local anesthesia in the same session were evaluated. patients with symptoms of the cts and cuts occur at different times, in different extremities, patients with cervical vertebral root lesions and/or discopathy findings in cervical magnetic resonance imaging, patients with thoracic outlet syndrome and polyneuropathy, cases secondary to trauma such as fractures, nerve injury and tumor and cases with cts and cuts secondary to pregnancy were excluded from the study. parameters evaluated data of the patients were collected to evaluate the age, gender, which side of the surgery, presence of atrophy, smoking, diabetes, presence of thyroid disease, hypertension, educational status, occupation, and dominant hand. preoperative emg results of the patients were collected. body mass index (bmi) was calculated in kg / m2 by measuring the patients' height and weight. calculated bmis were grouped using the world health organization (who) classification. statistical analysis spearman test was used to evaluate the correlation between bmi and severity of cts and cuts in statistical analysis. p <0.05 was considered statistically significant. 367 coexistence of ipsilateral ulnar and median nerve entrapment results a total of 31 patients were included in the study (17 men (55%), 14 women (45%)). the average age of all patients was 51.29 ± 13.2 (male 51.65 (min: 23-max: 70), female 50.86 (min: 14max: 72). nine patients were operated on from the left side, 22 from the right side, and the right/left ratio was 2.44. there was only one male patient with the left dominant hand, and the pathology of this patient was on the right side. ipsilateral involvement of 30 right dominant patients was 22 (73.3%). smoking was present in 17 (55%) of the patients. the number of patients with diabetes was 10 (32%). the number of patients with thyroid dysfunction was 6 (19%). the number of patients with hypertension was also 6. the mean bmi of the patients was 29.63 kg/m2. the average bmi of male patients was 29.02 kg/m2, while the average bmi of female patients was 30.3 kg/m2. while 3 of the patients were morbidly obese, one was 2nd degree obese, and ten were first-degree obese. as a result, 45% of the patients were obese (table 1). table 1. the distribution of patients according to the body mass index and gender body mass index total normal overwei ght grade 1 obese grade 2 obese morbi d obese gender male 2 10 3 0 2 17 female 3 2 7 1 1 14 total 5 12 10 1 3 31 the education level of the patients is that 3 of them did not go to school, 24 of them were primary school graduates, and 4 of them were secondary education graduates. 13 of the patients were housewives, 8 of them were workers, 5 of them were farmers, and the rest were in the other occupational groups (office worker, trader, students). physical examination of the patients revealed 17 thenar atrophy. in the emg evaluation, 9 of the patients had mild, 14 had moderate, 8 had severe carpal tunnel syndrome, eight had mild, 15 had moderate, and 8 had severe cubital tunnel syndrome. in carpal tunnel syndrome, the average bmi was found to be 29.86 kg/m2 in patients with mild emg findings, 28.94 kg/m2 in moderate, and 30.59 kg/m2 in severe ones. while the mean bmi in mild cubital tunnel syndrome was 31.15 kg/m2, it was found to be 28.08 kg/m2 in moderate patients and 31.03 kg/m2 in severe ones (table 2). according to body mass indexes and emg findings, there was no significant correlation between carpal tunnel syndrome and cubital tunnel syndrome severity (p> 0.05). table 2. the severity of entrapment neuropathies in different body mass index groups body mass index mean cubital tunnel syndrome minor 31,15 moderate 28,08 severe 31,03 carpal tunnel syndrome minor 29,86 moderate 28,94 severe 30,59 discussion carpal tunnel syndrome and cubital tunnel syndrome are the most common entrapment neuropathies of the upper extremity. it has been reported that 93% of patients benefit from decompression surgery [7]. there are epidemiological studies in the literature separately for these two syndromes, but there are few publications regarding the operation of these two syndromes in the same session. the most known risk factors for carpal tunnel syndrome are female gender, obesity, advanced age, and repetitive hand movements [8]. risk factors for cubital tunnel syndrome have been reported as advanced age and high bmi for men, while low bmi for women [9]. it is known that diabetes mellitus is a risk factor for both carpal tunnel syndrome and cubital tunnel syndrome. diabetes increases the severity of entrapment neuropathy after collagen solidifying after neural ischemia due to diabetic microangiopathy and non-enzymatic collagen glycolysis [10]. naran et al. found dm in 23% of patients with cubital tunnel syndrome [11]. it was present in 32% of our patients. in our study, the average age of all patients was 51.2, and the number of male patients was higher than female patients, similar to the literature. carpal tunnel syndrome is more common in females than cubital tunnel syndrome [12,13]. 13 (41.9%) of our patients were housewives, 8 (25.8%) were workers, and 5 (16.1%) were farmers. 79% of female patients with carpal tunnel syndrome were determined to be 368 turan kandemir, serdar ercan, zeki serdar ataizi housewives in a study [14]. consistent with our study, it has been shown that homemakers performing activities such as cleaning and handicraft intensively and male patients work in professions with intense, repetitive hand movements increase the risk of entrapment neuropathies [13,14]. the literature has reported that entrapment neuropathies are more common in the dominant hand and arm. wilson et al. claim that while ulnar entrapment was determined in the left side with a rate of 51.8%, entrapment was observed in 53% of the dominant arm [15]. in our study, the right side/left side ratio was found to be 2.44, and the entrapment rate on the dominant side was 73.3%. in the literature, it has been suggested that a high body mass index increases the severity of cts. it has been thought that supportive fat tissue around the nerve may cause stenosis in the carpal canal in people with high bmi [4,10]. also, they showed that the fatty tissue in the carpal canal increased hydrostatic pressure [16]. the situation is the opposite in cubital tunnel syndrome. it has been thought that the increased fatty tissue at the height of the bmi creates a protective filling around the nerve against external effects [9]. in our study, no significant correlation was found between body mass index and the severity of entrapment neuropathy. while only 5 of our patients had average body weight, other patients were overweight and obese. contrary to expectations, mild entrapment neuropathy in emg results is observed in patients with high bmi (29.86), severe entrapment neuropathy was observed as a result of emg in patients with cuts with high bmi (31.03), and it is not compatible with the hypotheses in the literature. the study results of sahin et al. were consistent with ours, and no significant difference was found between increased bmi and the severity of carpal tunnel syndrome [17]. there are not many publications examining the association of carpal and cubital tunnel syndrome in the literature. similar to our study, cross et al. applied decompression procedures to patients with cubital and carpal tunnel syndrome in both pathologies in the same session [18]. surgical intervention in two entrapment neuropathies in the same session prevents the patient from receiving anesthesia twice, decreases the duration of hospital stay, and decreases workforce loss. conclusions when cts and cuts patients are evaluated separately in the literature, although it is hypothesized that high body mass index and thick adipose tissue increase the severity of cts by increasing the median nerve compression, but the same adipose tissue reduces the formation of cuts, in our study when patients with the same extremity and simultaneous onset of symptoms were evaluated, it was revealed that body mass index was not related to the severity of symptoms. although bmi does not change the severity of neuropathy, it is an important etiological factor in entrapment formation. references 1. gelfman r, melton lr, yawn b, wollan p, amadio pc, stevens j. long-term trends in carpal tunnel syndrome. neurology. 2009;72(1):33-41. 2. bartels r, verbeek a. risk factors for ulnar nerve compression at the elbow: a case control study. acta neurochirurgica. 2007;149(7):669. 3. lundborg g, dahlin lb. the pathophysiology of nerve compression. hand clinics. 1992;8(2):215-227. 4. kouyoumdjian ja, zanetta dm, morita mp. evaluation of age, body mass index, and wrist index as risk factors for carpal tunnel syndrome severity. muscle & nerve: official journal of the american association of electrodiagnostic medicine. 2002;25(1):93-97. 5. chimenti pc, mcintyre aw, childs sm, hammert wc, elfar jc. combined cubital and carpal tunnel release results in symptom resolution outside of the median or ulnar nerve distributions. the open orthopaedics journal. 2016;10:111. 6. day cs, makhni ec, mejia e, lage de, rozental td. carpal and cubital tunnel syndrome: who gets surgery? clinical orthopaedics and related research®. 2010;468(7):17961803. 7. ettema am, amadio pc, cha ss, harrington jr, harris am, offord kp. surgery versus conservative therapy in carpal tunnel syndrome in people aged 70 years and older. plastic and reconstructive surgery. 2006;118(4):947-958. 8. geoghegan j, clark d, bainbridge l, smith c, hubbard r. risk factors in carpal tunnel syndrome. journal of hand surgery. 2004;29(4):315-320. 9. richardson jk, green df, jamieson sc, valentin fc. gender, body mass and age as risk factors for ulnar mononeuropathy at the elbow. muscle & nerve: official journal of the american association of electrodiagnostic medicine. 2001;24(4):551-554. 10. moghtaderi a, izadi s, sharafadinzadeh n. an evaluation of gender, body mass index, wrist circumference and wrist ratio as independent risk factors for carpal tunnel 369 coexistence of ipsilateral ulnar and median nerve entrapment syndrome. acta neurologica scandinavica. 2005;112(6):375-379. 11. naran s, imbriglia je, bilonick ra, taieb a, wollstein r. a demographic analysis of cubital tunnel syndrome. annals of plastic surgery. 2010;64(2):177-179. 12. altun g, kurtulmuş t, oltulu i̇, sağlam n. kübital tünel sendromu tedavisinde in situ dekompresyon. medical journal of suleyman demirel university. 2018;25(2). 13. mondelli m, giannini f, giacchi m. carpal tunnel syndrome incidence in a general population. neurology. 2002;58(2):289-294. 14. tanik n, ümit s, çelikbilek a, et al. karpal tünel sendromu: 350 hastanın klinik ve sosyodemografik özelliklerinin değerlendirilmesi. dicle tıp dergisi. 2014;41(3). 15. wilson tj, tubbs rs, yang lj. the anconeus epitrochlearis muscle may protect against the development of cubital tunnel syndrome: a preliminary study. journal of neurosurgery. 2016;125(6):1533-1538. 16. werner ra, albers jw, franzblau a, armstrong tj. the relationship between body mass index and the diagnosis of carpal tunnel syndrome. muscle & nerve. 1994;17(6):632-636. 17. sahin n, albayrak i, ugurlu h. association between intensity of carpal tunnel syndrome and body mass index values in obese patients. tubav bilim. 2009;2(4):484-488. 18. cross d, matullo ks. concomitant endoscopic carpal and cubital tunnel release: safety and efficacy. hand. 2014;9(1):43-47. romanian neurosurgery (2019) xxxiii (3): pp. 268-271 doi: 10.33962/roneuro-2019-044 www.journals.lapub.co.uk/index.php/roneurosurgery a rare case of metastatic esthesioneuroblastoma emilia marciuc1,2, m. barcan1, s. popa1, b.i. dobrovăț1,2, r.m. popescu1,2, r. buga1,2, d. haba1,2 1 department of radiology and medical imaging of emergency hospital “prof. dr. n. oblu”, iasi, romania 2 “grigore t. popa” university of medicine and pharmacy, iasi, romania abstract olfactory neuroblastoma, also known as esthesioneuroblastoma (enb), is a rare malignant tumour of the basal layer of the olfactory epithelium, which originally develops unilaterally, accounting for 3-6% of all intranasal tumours. we present the case of a patient with a voluminous ethmoidal lesion that invaded the left basal frontal lobe and left orbit. the biopsy revealed a stage c kadish, grade iii neuroblastoma. the patient followed a multimodal treatment with chemotherapy and radiation therapy to which he responded partially, then returned after 11 months for sphincter disorder and bilateral sciatic type pain. an mri showed metastasis of the filum terminale, the anatomopathological exam identifying also neuroblastoma. ct and mri imaging are required for a correct assessment of the regional extension of olfactory neuroblastoma, response to oncological treatment but also for the detection of secondary lesions found in a small number of cases. introduction enb is a rare malignancy, includes 3% of all intranasal tumours (1), was first described in 1924 (2), and it develops from the olfactory epithelium of the cribriform plate. these tumours are initially located unilaterally, and then invades orbit, nasal fossa, skull base, and intracranial space. the risk factors are unknown and there is a bimodal incidence at 10-15 years and 40-50 years. the most common symptoms are nasal congestion, anosmia, epistaxis, headache, and diplopia. these tumours have a high potential for regional and distance extension and multimodal treatment may help patients and increase their survival rate (3). case presentation a 33-year-old patient presented to the emergency room with headache and vomiting. ct exploration was recommended which showed hydrocephalus and a lesion that occupied the ethmoidal air cells, an extension in the nasal fossa, the anterior cranial fossa with bone lysis. a gadolinium enhanced mri was performed that showed a 33/34/23 keywords neuroblastoma, olfactory, spinal metastasis corresponding author: bogdan ionuț dobrovăț university of medicine and pharmacy "gr.t.popa" iasi, romania bogdan.dobrovat@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 269 a rare case of metastatic esthesioneuroblastoma mm (ap/cc/t) lesion, with a heterogeneous enhancement, with calcified areas, occupying mostly of the nasal fossa and all ethmoid cells, most likely developing from the cribriform plate, invading the orbit (with mass effect on the internal muscles) and frontal lobes, more evident in the left side (fig. 1, fig. 2, fig. 3, fig. 4). figure 1. sag t2wi. the tumour occupying the nasal fosa, originating from cribriform blade with superior extension. figure 2. mri cor gd-t1wi. figure 3. sag ct (bone window): bone lysis. figure 4. (a) axial t2wi-extension of the frontal lobe; (b) axial t2wi mass effect on the internal muscles in the left orbit. after the biopsy, the anatomopathological exam concluded stage iii kadish group c neuroblastoma. in this case the patient followed two chemotherapy cycles but abandoned it later because he was known to have hepatitis b and the viremia level was increasing. therefore, he continued only with radiotherapy. the patient returned to control after six months when the mri scan showed a decrease in tumour size, with the same characteristics as before, and was kept under control for one year. after one year the patient came back with bilateral sciatica and major sphincter dysfunctions. the mri exam of lumbar region highlighted a hyperintense t1 and t2, hypointense stir lesion in the s1 vertebral body and a nodular vivid enhancing lesions of cauda equina in s1 and s2 region, suggestive of secondary lesion (fig. 5, fig. 6); the anatomopathological examination confirmed the diagnosis of metastasis from neuroblastoma. 270 emilia marciuc, m. barcan, s. popa, b.i. dobrovăț et al. figure 5. mri axial stir s1 vertebral body level. figure 6. s1 secondary lesion (a – t1wi; b – gd enhanced-t1wi)) after 10 episodes of lumbar radiotherapy, the patient returned accusing headache, diplopia and diffuse cervico-lumbar pain. mri exploration revealed a stationary aspect of the tumor compared to the previous exam. the patient wanted to be discharged and unfortunately, he died shortly afterwards. discussions olfactory neuroblastoma is a tumour which originates from the olfactory cells of the cribriform blade and, although it develops initially in an unilateral manner, it invades afterwards the bilateral intracranial spaces. kadish classifies these tumours in three classes (4): a limited to the nasal cavity, b infiltrated into the nasal cavity and paranasal and c extended beyond the nasal and paranasal cavity. our case was classified in stage c and histologically in class iii. there are four histological classes that divide this type of tumour by histological cellularity and histochemical analysis. according to some authors, enb it is most likely congenital, and it develops even in intrauterine life (5). the role of imaging in the staging of enb is very important. in 40% of cases, it extends in the paranasal sinuses, in 30% extension is intracranial, and in 30% extension is orbital (6). mri is the most used technique in staging because the report on the extension of the tumour in the adjacent tissues can be very thorough. very important are the cect and pet-ct exams of lymph nodes because esthesioneuroblastoma disseminates in cervical and laterocervical lymph nodes which are asymptomatic and undetectable on physical exam. cect and pet-ct can highlight these lymph nodes by marked contrast enhancement on cect and moderate to highly avid of fdg on pet/ct. some studies highlight a cervical dissemination in the lymph nodes in 30% of cases and the presence of secondary lesions are rare and very rare for spine (7). in our case there was secondary involvement of vertebral body of s1 and also a metastasis of cauda equina in s1 and s2 region. many studies show that patients treated with surgery have a 5-year survival rate of about 50%, while surgery combined with chemotherapy prolong survival to 65% at 5 years in the case of local esthesioneuroblastoma (8,9). in local advanced enb, resection of the cervical lymph nodes is performed to reduce the risk of recurrences. postoperative chemotherapy and radiotherapy in patient with lymph nodes metastasis have decreased recurrences and the survival rate at 10 years was 80%. chemotherapy combined with radiotherapy is widely accepted recently, with a survival rate of 35%. despite lymph node resection, radiotherapy and chemotherapy, in most cases of advanced enb lymph node recurrence is detected 12 months after completion of treatment. currently, radiotherapy in enb is used in combination with surgery and chemotherapy because there are no randomized trials to guide radiotherapy treatment, but radiotherapy plays an important role in the treatment plan in early stages with definitive cure and good tumour control. the 271 a rare case of metastatic esthesioneuroblastoma doses used are 50-60 gy with intensity‐modulated radiation therapy to minimize doses to the optic structures, pituitary gland and brain (10). conclusions olfactory neuroblastoma is a rare tumour that originates from olfactory epithelium and extends into the orbit, nasal fossa, skull base and intracranial space. the combined use of ct and mri techniques is excellent in providing necessary information for treatment planning. recognizing the limitation of current data, surgical resection and postoperative radiation therapy for resectable lesions is the most commonly used management approach. for unresectable tumours, radiation alone or chemoradiation therapy are also viable treatment options. palliative chemotherapy has not shown a clear survival benefit in patients with recurrent and/or metastatic disease. considering the metastatic potential of this type of tumour, a rigorous imaging examination is required for an early diagnosis and a more effective treatment. references 1. berger l, luc r, richard d. l’esthesioneuroepitheliome olfactif. bull assoc fr etude cancer 1924; 13: 410-421. 2. kumar m, fallon rj, hill js, davis mm. esthesioneuroblastoma in children. j pediatr hematol oncol 2002; 24: 482-487. 3. chao ks, kaplan c, simpson jr, et al. esthesioneuroblastoma: the impact of treatment modality. head neck 2001. 4. kadish s, goodman m, wang cc. olfactory neuroblastoma: a clinical analysis of 17 cases. cancer.1976;37(3):1571-6. 5. thompson ld. olfactory neuroblastoma. head neck pathol. 2009;3(3):252–259. doi:10.1007/s12105-009-01252. 6. morita a, ebersold mj, olsen kd, foote rl, lewis je, quast lm. esthesioneuroblastoma: prognosis and management. neurosurgery 1993; 32: 706-714; discussion 714-715. 7. shirzadi as, drazin dg, strickland as, bannykh si, johnson jp. vertebral column metastases from an esthesioneuroblastoma: chemotherapy, radiation, and resection for recurrence with 15-year followup. case rep surg 2013; 2013: 107315. 8. yan-feng chen, an-kui yang, quan zhang, dian ouyang, wen-kuan chen and fu-jin chen. clinical analysis of 53 cases of esthesioneuroblastoma; chinese journal of cancer 2009; 28:3, 259-262. 9. gupta s, husain n, sundar s. esthesioneuroblastoma chemotherapy and radiotherapy for extensive disease: a case report. world j surg oncol. 2011;9:118. published 2011 oct 5. doi:10.1186/1477-7819-9-118. 10. patel sg, singh b, stambuk he, et al. craniofacial surgery for esthesioneuroblastoma: report of an international collaborative study. j neurol surg b skull base. 2012;73(3):208–220. doi:10.1055/s-0032-1311754. doi: 10.33962/roneuro -2020-037 prognostic factors of ruptured middle cerebral artery aneurysms treated with surgical clipping samer s. hoz, saja a. albanaa, ali m. neamah, farah w. abdulmohsin, zahraa al-sharshahi romanian neurosurgery (2020) xxxiv (1): pp. 245-253 doi: 10.33962/roneuro-2020-037 www.journals.lapub.co.uk/index.php/roneurosurgery prognostic factors of ruptured middle cerebral artery aneurysms treated with surgical clipping samer s. hoz1, saja a. albanaa2, ali m. neamah2, farah w. abdulmohsin2, zahraa al-sharshahi3 1 neurosurgeon, department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 medical student, college of medicine, baghdad university, baghdad, iraq 3 mb, bch bao (nui, rcsi), lrcp & si, royal college of surgeons in ireland (alumnus), dublin, ireland abstract background: spontaneous subarachnoid haemorrhage is an emergent condition that leads to profound morbidity and mortality. it is mainly caused by a ruptured intracranial aneurysm. herein we described the relationship of different factors and their impact on the outcome of patients who underwent a surgical clipping exclusively to the ruptured middle cerebral artery aneurysm. methods: we retrospectively analyzed the medical records of patients admitted to the neurosurgery teaching hospital (nth) in baghdad for the period between january 2017-april 2019 of patients who underwent microsurgical clipping for ruptured middle cerebral artery aneurysm. demographic, clinical, radiological and surgical data were extracted. a univariate analysis was used to illustrate the relationship between the variables and outcome which was assessed using the five scores of the glasgow outcome scale where patients were dichotomized into two groups; favourable (iv + v) and unfavourable (i, ii, iii). results: within this cohort, a total of 50 patients were studied and the analysis revealed that 92% (n=46) had a favourable outcome and 8% (n=4) had an unfavourable outcome at discharge. the in-hospital mortality was 6%(n=3). factors that were significantly associated with poor outcome were giant aneurysms, the presence of other unruptured aneurysms, post-operative clinical vasospasm, presence of contralateral weakness, lower pre/post-operative glasgow coma scores, higher hunt and hess, world federation of neurosurgical societies (wfns) and modified-wfns grades. conclusion: the factors with a significant impact on the outcome of patients with surgically clipped ruptured middle cerebral artery aneurysms were gcs, wfns, mwfns, h&h, contralateral muscle weakness, size of the aneurysm, presence of other unruptured aneurysms and clinical vasospasm. introduction subarachnoid hemorrhage (sah) constitutes about 5% of all strokes. more than 80% of all spontaneous sah is due to ruptured intracranial aneurysms (7,13). ct scan is the best initial test for detecting sah, ct keywords intracranial aneurysm, subarachnoid haemorrhage, surgical clipping, middle cerebral artery aneurysm corresponding author: zahraa al-sharshahi royal college of surgeons in ireland (alumnus), dublin, ireland zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 246 samer s. hoz, saja a. albanaa, ali m. neamah et al. angiography (cta) is often used to characterize the aneurysm. however, the catheter angiography is the best diagnostic modality to define the aneurysm characteristics preoperatively whenever possible (10,16). middle cerebral artery (mca) aneurysms account for 20% of all intracranial aneurysms (26). up to 81% of mca aneurysms are located at the bifurcation. in addition, 30% present with symptoms related to mass effect (14). the mca aneurysm is the most common aneurysm that co-present with intracerebral hematoma (ich) (30-50%) due to its anatomic and hemodynamic features (21). several grading scales have been used for ruptured sah including hunt and hess (h&h), world federation of neurosurgical societies (wfns) grading and modified wfns which were reported to be valuable outcome prediction tools (1,2). complications of ruptured aneurysms can be categorized as early or late. such complications include rebleeding, symptomatic vasospasm and hydrocephalus at the rates of 30%, 30% and 20%, respectively (4). rebleeding is the most serious acute complication and is, at the same time, the most preventable (8). the rate of rebleeding has been declining significantly in association with the establishment of prompt management of sah by early surgical clipping or endovascular coiling (16). mca aneurysm is the most feasible aneurysm for surgical clipping, owing to its accessible location as well as its morphology with a wide neck. additionally, the mca aneurysm is unfavorable to be treated with endovascular coiling due to its distal location that renders the difficult (3,9,15,23). in this study, we present a case series which is the first to be reported from iraq regarding the surgical clipping of ruptured mca aneurysms. patients and methods in this retrospective cohort study, data were recruited from 50 patients with sah attributed to a ruptured mca aneurysm. all cases were treated with surgical clipping within 72 hours of aneurysm rupture at neurosurgery teaching hospital in baghdad/iraq between january 2017 and april 2019. the inclusion criteria were as follows: age >18 years, confirmed diagnosis of aneurysmal sah by ct-scan and cta, ruptured mca aneurysms and surgically treated groups. cases of traumatic, idiopathic sahs, unruptured aneurysms and non-mca aneurysms were excluded from this series. the analyzed parameters included: age, sex, co-morbidities, reported sudden severe headache as part of the index presentation, pre or post-operative contralateral weakness (mrc grade), seizure, vomiting, neck stiffness, similar previous attacks, clinical vasospasm, pre or post-operative gcs (gcs categorized into; mild ≥13, moderate 12-9 and severe≤8), location and size of the mca aneurysms, the presence of other unruptured aneurysms, ich, aneurysmal remnant of post-operative cta, size of the aneurysm (giant >25mm, large 11-25mm, medium 5-10mm and small <5mm), the need for temporary clipping, intraoperative rupture, m-wfns scale, wfns scale, h&h scale, glasgow outcome scale at the time of discharge and at six-month follow-up period. at six months follow-up; two cases were lost to follow up in which they were excluded from the analysis. fisher exact test was used to evaluate the relationship between the aforementioned factors and gos at both discharge and six-month intervals. patients were divided into 2 categorical groups based on the 5 scores of the gos into favorable (good recovery v+ moderate disability iv) and unfavorable (severe disability iii + vegetative state ii+ dead i) prognostic groups. the paired data of gos at discharge and follow-up were also tested for any statistical difference using a wilcoxon signed-rank test. the correlation between sah grading scales and gos was assessed using kendall's tau correlation coefficient. the level of significance decided on pvalue. all statistical analysis was done using commercially available software (spss, version 23.0). results the study sample included 50 patients, 68% (n=34) of whom were females with a female: male ratio of 2:1. the mean age was 40.32 ± sd, with 80% (n= 30) of the females being over 40 years of age and 93.8% (n=15) of the males being younger than 40 years of age. results for patients parameters corresponding to the outcome are shown in tables 1,2 and 3. overall, 92% (n=46) of the patients had favorable outcome at discharge (good recovery in 82% (n=41) and moderate disability in 10% (n=5)) while 8% (n=4) had unfavorable outcome including 2% (n=1) discharged with severe disability and 6% (n=3) pronounced dead. the mortality was attributed to 247 prognostic factors of ruptured middle cerebral artery aneurysms treated with surgical clipping ischemic stroke in two patients and pulmonary embolism in one patient. the factors that were associated with unfavorable outcome (gos scores of i to iii) included giant aneurysms, the presence of other unruptured aneurysms, the need for temporary clipping during surgery, the presence of postoperative clinical vasospasm, the presence of pre/post-operative contralateral muscle weakness (decreased mrc grading), lower gcs scores and higher h&h, wfns and m-wfns scores. in analyzing the correlation between these scales and gos, m-wfns had the best negative rank-order correlation coefficient with respect to higher gos and the overall order was as: m-wfns then wfns then h&h. h&h showed the least negative correlation with respect to higher gos (table 4). the remaining parameters were not considered as independent risk factors that influence the outcome because they showed no statistical significance. higher pre-operative mrc scores were significantly associated with the absence of hematoma (p = 0.035). a higher post-operative mrc grade was notably associated with the absence of post-operative clinical vasospasm (p <0.001). 64% (n=32) of patients presented with an ich, 12.5% (n=4) of whom had unfavorable outcomes, compared to the patients without ich where none of them had a poor outcome. the factors that showed statistical significance at discharge have also proven significant at six-month follow-up with the exception of temporary clipping which was not significant at the 6-month follow-up. temporary clipping which was an infrequent adjunct applied only in 22% (n= 11) of all cases for a period of fewer than 10 minutes. 45.5% of patients in our study with temporary clipping developed vasospasm (p = 0.017). a wilcoxon signed-rank test showed that the gos at discharge differed significantly from the gos at 6 months follow-up (z = -2.33, p = .031). table 1 patient’s charecteristics favorable outcome (%) unfavorable outcome (%) total no. of cases p value at discharge p value at follow-up age ≤40 18 (36%) 1 (2%) 19 (38%) 1.000 1.000 >40 28 (56%) 3 (6%) 31 (62%) sex male 14 (28%) 2 (4%) 16 (32%) 0.584 0.254 female 32 (64%) (4%)2 34 (86%) hypertension yes 15 (30%) 3 (6%) 16 (32%) 0.127 0.547 no 31 (62%) 1 (2%) 32 (64%) diabetes mellitus yes 10 (20%) 2 (4%) 14 (24%) 0.240 0.150 no 36 (72%) 2 (4%) 38 (76%) sudden severe headache yes 44 (88%) 3 (6%) 47 (94%) 0.226 0.180 no 2 (4%) 1 (2%) 3 (6%) vomiting yes 43 (86%) 3 (6%) 46 (92%) 0.291 1.000 no 3 (6%) 1 (2%) 4 (8%) 248 samer s. hoz, saja a. albanaa, ali m. neamah et al. table 1 patient’s charecteristics neck stiffness yes 44 (88%) 3 (6%) 47 (94%) 0.226 0.180 no 2 (4%) 1 (2%) 3 (6%) history of previous attack yes 2 (4%) 1 (2%) 3 (6%) 0.226 0.180 no 44 (88%) 3 (6%) 47 (94%) pre-op seizure yes 8 (16%) 1 (2%) 9 (18%) 0.560 0.472 no 38 (76%) 3 (6%) 41 (82%) post-op seizure yes 4 (8%) 1 (2%) 5 (10%) 0.353 0.286 no 42 (84%) 3 (6%) 45 (90%) post-op clinical vasospasm yes 5 (10%) 4 (8%) 9 (18%) 0.001* 0.005* no 41 (82%) 41 (82%) pre-op mrc grading 0 1 (2%) 1 (2%) 0.002* 0.004* 1 3 (6%) 2 (4%) 5 (10%) 2 4 (8%) 1 (2%) 5 (10%) 3 1 (2%) 1 (2%) normal 38 (76%) 38 (76%) post-op mrc grading 0 2 (4%) 2 (4%) < 0.001* < 0.001* 1 1 (2%) 1 (2%) 3 2 (4%) 2 (4%) normal 44 (88%) 1 (2%) 45 (90%) initial gcs mild 42 (84%) 1 (2%) 43 (86%) < 0.001* < 0.001* moderate 4 (8%) 4 (8%) severe 3 (6%) 3 (6%) post-op gcs mild 46 (92%) 1 (2%) 47 (94%) < 0.001* < 0.001* severe 3 (6%) 3 (6%) mrc,medical research council ; gcs,glasgow coma scale ; pre-/post-op, pre-/post-operative significance was determined according to chi-square test. * statstically significant 249 prognostic factors of ruptured middle cerebral artery aneurysms treated with surgical clipping table 2 radiological & surgical data favorable outcome (%) unfavorable outcome (%) total no. of cases p value at discharge p value at follow-up aneurysm location right mca bifurcation 27 (54%) 4 (8%) 31 (62%) 0.445 0.624 left mca bifurcation 16 (32%) 16 (32%) right m2 1 (2%) 1 (2%) right m2 bifurcation 1 (2%) 1 (2%) left m2 1 (2%) 1(2%) aneurysm size small 8 (16%) 1 (2%) 9 (18%) 0.004* 0.003* medium 30 (60%) 30 (60%) large 7 (14%) 1 (2%) 8 (16%) giant 1 (2%) 2 (4%) 3 (6%) other unruptured aneurysm yes 2 (4%) 2 (4%) 0.005* 0.003* no 46 (92%) 2 (4%) 48 (96%) ct-ich yes 28 (56%) 4 (8%) 32 (64%) 0.283 0.543 no 18 (36%) 18 (36%) ich in dominant hemisphere yes 12 (37.5%) 2 (6.3%) 14 (43.8%) 1000 576 no 16 (50%) 2 (6.3%) 18 (56.3%) temporary clipping yes 8 (16%) 3 (6%) 11 (22%) 0.029* 0.127 no 38 (76%) 1 (2%) 39 (78%) intra-op rupture yes 24 (48%) 3 (6%) 27 (54%) 0.614 1.000 no 22 (44%) 1 (2%) 23 (46%) remnant of post-op cta yes 1 (2%) 1 (2%) 2 (4%) 0.155 1.000 no 45 (90%) 3 (6%) 48 (96%) 250 samer s. hoz, saja a. albanaa, ali m. neamah et al. table 2 radiological & surgical data favorable outcome (%) unfavorable outcome (%) total no. of cases p value at discharge p value at follow-up ct, computed tomography; ich, intracerebral hematoma; cta; computed tomography angiography significance was determined according to chi-square test. statistically significant table 3 neurological grading scales favorable outcome (%) unfavorable outcome (%) total no. of cases p value at discharge p value at followup hunt&hess level ii 38 (76%) 38 (76%) 0.002** 0.013* level iv 8 (16%) 4 (8%) 12 (24%) wfns i 37 (74%) 37 (74%) 0.002* 0.006* ii 1 (2%) 1 (2%) iii 4 (8%) 1 (2%) 5 (10%) iv 4 (8%) 3 (6%) 7 (14%) modified -wfns i 37 (74%) 37 (74%) 0.002* 0.003* ii 5 (10%) 1 (2%) 6 ( 12%) iv 4 (8%) 3 (6%) 7 (14%) wfns; world federation of neurosurgical societies significance was determined according to chi-square test. * statistically significant 251 prognostic factors of ruptured middle cerebral artery aneurysms treated with surgical clipping table 4 rank-order correlation coefficients of different grading systems on higher gos rank order correlation coefficient p value modified-wfns 0.56 < 0.001 wfns 0.55 < 0.001 hunt&hess 0.54 < 0.001 wfns; world federation of neurosurgical societies, discussion aneurysmal sah is one of the most serious and often deadly phenomena (12). mca aneurysm is one of the commonest causes of aneurysmal sah (6). it is commonly located at the bifurcation and constitutes 81% of all unruptured mca aneurysm and 87% of the ruptured ones (24). patient's characteristics: our data showed a female predominance with a female: male ratio of 2:1. although there appears to be a tendency towards a more favorable outcome in both females and younger patients, this failed to achieve statistical significance in our study; a finding that was also reported by similar studies (11,17,24). the presence of co-morbidities is often cited as a significant risk factor for aneurysm rupture, but their prognostic significance is still uncertain (14,25). in our data, concomitant diseases, history of previous attacks and seizures were not found to be significantly associated with an unfavorable outcome. vasospasm is classified as one of the major complications associated with mca aneurysm clipping (26). in this study, we exclusively evaluated post-operative clinical vasospasm which was defined as a deterioration in the neurologic status (speech or motor) along with the presence of new ischemic ct changes or ct-angiography-defined vessels spasm. vasospasm was only evident in 18%(n= 9) of patients and was noted to be associated with worse outcomes. motor weakness is also a known neurological complication that follows aneurysmal sah with an incidence of 14-29% (12). hereby, we evaluated the presence of contralateral limb weakness both pre and post-operatively, using the mrc grading score. all patients showed a more marked weakness in the upper limbs compared to the lower limbs which reflects the anatomical territory supplied by the mca. patients with pre or post-operative mrc grading scores for muscle power of (0,1) showed a significant tendency toward a poorer outcome and those with no weakness showed a significant tendency toward a better prognosis. additionally, higher pre-operative mrc scores were associated with the absence of hematoma whereas post-operative mrc was associated with postoperative clinical vasospasm. these findings were consistent with other studies reporting vasospasm and cerebral ischemia as the most common mechanisms that may lead to motor weakness in aneurysmal sah (12). cerebral vasospasm is directly linked to cerebral ischemia and patients may present with stroke-like symptoms including motor weakness, hence low mrc scores are not uncommon in patients with cerebral vasospasm. the presence of lower (severe) pre or post-operative gcs scores was found to be significantly associated with a lower gos in contrast to the higher (mild) gcs scores which were significantly associated with higher gos. radiological and aneurysmal characteristics: aneurysm characteristics such as aneurysm location, size and the presence of other unruptured aneurysms are important factors that impact the prognosis of ruptured cranial aneurysms (14,25). most reports inversely correlate aneurysmal size with the outcome (11). our data showed that giant aneurysms were associated with unfavorable outcome whereas medium-sized aneurysms were associated with a more favorable outcome. notably, ruggeri et al reported that the diameter of the 252 samer s. hoz, saja a. albanaa, ali m. neamah et al. aneurysm didn't significantly affect the outcome which is in contrast to what most reports (19). our study took the side of the aneurysm (right vs left) into account. 62% of the aneurysms were located on the right mca bifurcation and were noted to be associated with unfavorable outcomes; this observation did not, however, achieve statistical significance. this can be attributed to the fact that most of the cases in our sample are right-handed, with a left dominant hemisphere. however, brawanski et al reported that the side of the aneurysm did not affect the outcome directly, but rather determined the side of infarction (5). in addition to the aneurysm size and location, the presence of other unruptured aneurysms was found to significantly associated with an unfavorable outcome (p = 0.005). this finding is in contrast to the study performed by rodrıguez-hernandez et al who stated that the number of aneurysms did not impact the outcome; although this series did not take into account the status of the aneurysm whether it was ruptured or not (25). mca aneurysm is known to be the most common intracranial aneurysm that is associated with an ich (24).in a paper by shimoda et al which studied 47 patients presented with ruptured mca aneurysm associated with a hematoma, it was found that 42% (n=20) had an ich in the dominant hemisphere that led to a poor outcome but was reported to be non-significant similarly to the findings of this cohort (22). surgical parameters: intra-operative rupture was reported as a factor that doesn't impact the surgical outcome (20). this finding is consistent with our results where intra-operative rupture showed a nonsignificant trend toward a poorer outcome. the application of temporary clipping was significantly associated with lower gos at discharge but not at follow-up. this can be attributed to the fact that temporary clipping was noted to increase the risk of postoperative clinical vasospasm significantly where 45.5% of patients in our study with temporary clipping developed vasospasm (p = 0.017). therefore, temporary clipping was found to be a dependent factor regarding follow-up. we observed that the absence of post-operative cta remnants led to a favorable outcome but this was not statistically significant. grading scales: wfns, mwfns, and h&h are commonly used neurological scales that aid in surgical decision and predict the outcome of patients with aneurysmal sah (1).h&h scale showed the least negative correlation in respect to higher gos since it relies only on general subjective terms that depend on the judgment and interpretation, leading to a blurring of the lines between grades which in return would increase the inter-rater reliability (2,18). therefore, this scale is more useful in the selection of surgical candidates than outcome prediction. wfns scale is superior to h&h as it depends on both gcs and the absence/presence of neurologic deficits. when both wfns and m-wfns were compared in terms of correlation with gos, m-wfns correlated slightly stronger. regarding m-wfns, none of the cases in our study scored grade iii, 12% (n= 6) scored grade ii and the rest scored grade i and iv. hence grades ii and iii are the only different grades between the 2 scales, explaining the slight preference of m-wfns over wfns (table 4). limitations: first, this is a retrospective cohort from a single neurosurgical center with a small sample size that only included univariate analysis, making the conclusions non-generalizable. second, the absence of intravascular coiling facilities made surgical clipping the only available treatment option in iraq, limiting our ability in comparing the results to those of intravascular coiling. conclusion factors that may predict poorer outcomes in ruptured mca aneurysm clippinginclude: higher mwfns, wfns, and h&h scores, lower gcs scores, the presence of clinical vasospasm, the presence of hemiparesis, the presence of other unruptured aneurysms and aneurysm size (giant aneurysms). mwfns was found to be slightly superior to the other neurologic scales in predicting the outcome. conflicts of interest the authors declare no conflict of interests abbreviations ct: computerized tomography mca: middle cerebral artery sah: subarachnoid haemorrhage h and h: hunt and hess scale wfns: world federation of neurosurgical societies scale references 1. adams jr hp. clinical scales to assess patients with stroke. instroke 2011 jan 1 (pp. 307-333). wb saunders. 253 prognostic factors of ruptured middle cerebral artery aneurysms treated with surgical clipping 2. aggarwal a, dhandapani s, praneeth k, sodhi hb, pal ss, gaudihalli s, khandelwal n, mukherjee kk, tewari mk, gupta sk, mathuriya sn. comparative evaluation of h&h and wfns grading scales with modified h&h (sans systemic disease): a study on 1000 patients with subarachnoid hemorrhage. neurosurgical review. 2018 jan 1;41(1):241-7. 3. alreshidi m, cote dj, dasenbrock hh, acosta m, can a, doucette j, simjian t, hulou mm, wheeler la, huang k, zaidi ha. coiling versus microsurgical clipping in the treatment of unruptured middle cerebral artery aneurysms: a meta-analysis. neurosurgery. 2018 feb 9;83(5):879-89. 4. bakker na, metzemaekers jd, groen rj, mooij jj, van dijk jm. international subarachnoid aneurysm trial 2009: endovascular coiling of ruptured intracranial aneurysms has no significant advantage over neurosurgical clipping. neurosurgery. 2010 may 1;66(5):961-2. 5. brawanski n, kashefiolasl s, won sy, tritt s, berkefeld j, senft c, seifert v, konczalla j. does aneurysm side influence the infarction side and patients´ outcome after subarachnoid hemorrhage?. plos one. 2019;14(11). 6. chyatte d, porterfield r. nuances of middle cerebral artery aneurysm microsurgery. neurosurgery. 2001 feb 1;48(2):339-46. 7. dabilgou aa, drave a, kyelem jm, naon l, napon c, kabore j. spontaneous subarachnoid haemorrhage in neurological setting in burkina faso: clinical profile, causes, and mortality risk factors. neurology research international. 2019;2019. 8. danière f, gascou g, de champfleur nm, machi p, leboucq n, riquelme c, ruiz c, bonafé a, costalat v. complications and follow up of subarachnoid hemorrhages. diagnostic and interventional imaging. 2015 jul 1;96(7-8):677-86. 9. de gans k, nieuwkamp dj, rinkel gj, algra a. timing of aneurysm surgery in subarachnoid hemorrhage: a systemic review of the literature. neurosurgery. 2002;50:336-40. 10. đilvesi đ, cigić t, papić v, horvat i, karan m, vuleković p. the fisher grade in predicting a degree of cerebral vasospasm in patients after intracranial aneurysm rupture. vojnosanitetski pregled. 2016;73(4):349-52. 11. hamdan a, barnes j, mitchell p. subarachnoid hemorrhage and the female sex: analysis of risk factors, aneurysm characteristics, and outcomes. journal of neurosurgery. 2014 dec 1;121(6):1367-73. 12. jang sh, do lee h. the pathogenic mechanisms of motor weakness following aneurysmal subarachnoid hemorrhage: a review. neurology asia. 2017 sep 1;22(3). 13. javadpour m, silver n. subarachnoid haemorrhage (spontaneous aneurysmal). bmj clinical evidence. 2009;2009. 14. oh jw, lee jy, lee ms, jung hh, whang k, brain research group. the meaning of the prognostic factors in ruptured middle cerebral artery aneurysm with intracerebral hemorrhage. journal of korean neurosurgical society. 2012 aug;52(2):80. 15. qin s, sun x, hui p, li j, wang z. analysis on prognostic factors of patients with ruptured intracranial aneurysms. int j clin exp med. 2017 jan 1;10(1):1303-8. 16. rahmanian a, derakhshan n, alibai ea. outcome of inhospital rebleeding and early aneurysm rupture at the referral center. iranian journal of neurosurgery. 2018 jul 15;4(2):93-100. 17. rodríguez-hernández a, sughrue me, akhavan s, habdank-kolaczkowski j, lawton mt. current management of middle cerebral artery aneurysms: surgical results with a "clip first" policy. neurosurgery. 2012 nov 30;72(3):415-27. 18. rosen ds, macdonald rl. subarachnoid hemorrhage grading scales. neurocritical care. 2005 apr 1;2(2):110-8. 19. ruggeri ag. ruptured middle cerebral artery aneurysms: retrospective study and multivariate analysis of 105 patients treated by surgical clipping. journal of neurosurgery research and reviews. 2017 nov 25;1(1). 20. sandalcioglu ie, schoch b, regel jp, wanke i, gasser t, forsting m, stolke d, wiedemayer h. does intraoperative aneurysm rupture influence outcome? analysis of 169 patients. clinical neurology and neurosurgery. 2004 mar 1;106(2):88-92. 21. santiago-dieppa dr, pannell js, khalessi aa. endovascular and surgical options for ruptured middle cerebral artery aneurysms: review of the literature. stroke research and treatment. 2014;2014. 22. shimoda m, oda s, mamata y, tsugane r, sato o. surgical indications in patients with an intracerebral hemorrhage due to ruptured middle cerebral artery aneurysm. journal of neurosurgery. 1997 aug 1;87(2):170-5. 23. taha mm, alawamry a, abdelbary th. outcome of microsurgical clipping of anterior circulation aneurysms during the period of vasospasm: single center experience in egypt. egyptian journal of neurosurgery. 2019 dec 1;34(1):5. 24. ulm aj, fautheree gl, tanriover n, russo a, albanese e, rhoton jr al, mericle ra, lewis sb. microsurgical and angiographic anatomy of middle cerebral artery aneurysms: prevalence and significance of early branch aneurysms. operative neurosurgery. 2008 may 1;62(suppl_5):ons344-53. 25. wang gx, yu jy, wen l, zhang l, mou kj, zhang d. risk factors for the rupture of middle cerebral artery bifurcation aneurysms using ct angiography. plos one. 2016 dec 15;11(12):e0166654. 26. yang w, huang j. treatment of middle cerebral artery (mca) aneurysms: a review of the literature. chinese neurosurgical journal. 2015 dec;1(1):1. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-004 a rare case of pituitary macroadenoma with synchronous suprasellar meningioma. case report, surgical strategy and review of literature bogdan ionut david, ligia gabriela tataranu, vasile gheorghe ciubotaru, aurelia mihaela sandu, radu mircea gorgan romanian neurosurgery (2020) xxxiv (1): pp. 26-30 doi: 10.33962/roneuro-2020-004 www.journals.lapub.co.uk/index.php/roneurosurgery a rare case of pituitary macroadenoma with synchronous suprasellar meningioma. case report, surgical strategy and review of literature bogdan ionut david1,3, ligia gabriela tataranu2,3, vasile gheorghe ciubotaru3, aurelia mihaela sandu3, radu mircea gorgan2,3 1 phd student, university of medicine and pharmacy “carol davilaˮ, bucharest, romania 2 university of medicine and pharmacy “carol davilaˮ, bucharest, romania 3 department of neurusurgery, emergency clinical hospital bagdasar-arseni, bucharest, romania abstract synchronous tumours can be found all along the entire neuraxis, however, some lesions are far less likely to coexist. one of these extremely rare associations is between gh-pituitary adenomas and suprasellar meningiomas. a wide spectrum of transcranial and transsphenoidal approaches were described in the literature for either sellar, suprasellar and parasellar lesions, but no agreement has been reached for the cases of simultaneous occurring lesions. we present a rare case of a woman with gh-secreting pituitary adenoma and concomitant suprasellar meningioma. the strategy chosen was sequential transsphenoidal surgeries. however, after the first surgery, the remaining tumour mass did not mobilize as expected due to gravity, hence we decided to perform a transcranial subfrontal unilateral approach. surprisingly, the second surgery revealed a different histopathological result. association of a gh-pituitary adenoma and suprasellar meningioma is very rare, only 17 cases being reported in the relevant literature so far. different authors prefer different strategies, ranging from only transsphenoidal to simultaneous transsphenoidal and transcranial approaches, but no general consensus was established. in conclusion, the existence of synchronous tumours of the sellar region should be taken into account when imaging studies reveal an intracranial mass developing both sellar and suprasellar. the surgical strategy should be tailored to every specific patient and experience of the neurosurgeon. introduction synchronous tumors are found along the entire neuraxis, however some lesions are far less likely to coexist (1). one of these unlikely associations is between pituitary adenomas and suprasellar menin keywords pituitary macroadenoma, synchronous, staged surgery, suprasellar meningioma corresponding author: bogdan ionut david university of medicine and pharmacy “carol davilaˮ, bucharest, romania david.bogdan.med@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 27 a rare case of pituitary macroadenoma giomas. few cases have been reported in literature, most of the pituitary tumors being gh secreting adenomas. (1) however, a syndrome has yet to be defined consisting of this association, and, with the exception of the previously radio-treated pituitary adenomas that develop subsequent meningiomas, no pathophysiological connection exists. even though each type of tumor has distinct radiological findings, there are cases in which they can easily be misdiagnosed or even confused for one single lesion. this rare occurrence must be taken into account by neurosurgeons planning tumor resection in such cases. a wide spectrum of transcranial and transsphenoidal approaches have been described in literature for either sellar, suprasellar and parasellar lesions, but no agreement has been reached for the cases of simultaneous occurring lesions. (2) the purpose of this article is to present a rare case of a simultaneous gh secreting pituitary adenoma and a supradiafragmatic meningioma, the strategy behind the surgical approach and review of literature. case presentation a 57 years old woman, with history of stage ii hypertension, type ii diabetes mellitus, nyha ii heart failure was admitted with intense headache, visual field disturbances and hormonal disturbances (elevated gh levels: igf-1 = 98 ng/ml, n = 10 ng/ml). the cerebral ct scan showed a contrast enhancing sellar mass which extended suprasellar, slightly eccentric to the left. (figure 1) the presumed diagnosis was gh-secreting pituitary macroadenomma with suprasellar extension. we decided to perform surgery via transsfenoidal approach. due to large size of the tumor and high risk of rupturing the sellar diaphragm, only partial resection was performed and a second transsfenoidal surgery was scheduled for the upcoming three months. the rationale was that the suprasellar part of a tumor originating in the sellar region will gravitationally fall in the sella over the next three months, thus enabling a second minimally invasive surgery. the first histopathological exam was acidophilic pituitary adenoma with capsular invasion. (figure 2) initial postoperative outcome was uneventful, without any additional neurological deficits. after three months, the cerebral ct scan showed a surprising stationary suprasellar tumor. (figure 3) we changed our initial strategy, and we decided to operate the tumor via the subfrontal approach on the nondominant side (right). intraoperative we found a suprasellar meningioma. we achieved tumor complete resection, with no intraoperative incidents. the second histopathological exam revealed meningothelial meningioma with transitional components. (figure 4) after removal of the suprasellar tumor, visual field impairment improved. the patient required substitute hormonal therapy for transient diabetes insipidus for the first three months, which was gradually lowered in dosage. at three months postop, ct showed complete tumor removal and the patient was hormonally stable. even if standard post-surgical strategy is to administer oral corticoids, these were interrupted after only one month, and no further hormonal therapy was required. the particularity of the case was simultaneous development of a gh-secreting pituitary macroadenoma and suprasellar meningioma, a rare association of two types of histological tumors, with no apparent link between them. figure 1. cerebral ct scan showing a sellar and suprasellar contrast enhanced tumor. 28 bogdan ionut david, ligia gabriela tataranu, vasile gheorghe ciubotaru et al. figure 2. acidophilic pituitary adenoma; he; 40x. figure 3. cerebral ct scan, performed 3 months after the first surgery, showing suprasellar contrast enhanced tumor with no sellar tumor. figure 4. meningothelial meningioma with transitional components; he; a. 20x; b. 40x. review of literature mesh terminology consists of two different situations which describe simultaneous development of brain tumors. thus, one can encounter either collision tumors, in which case one tumor infiltrates the other one, or coincidental tumors, tumors being synchronous, but with different histogenesis, being situated one next to the other or at a distance. (3) we performed a search in pubmed and google scholar for simultaneous occurring brain tumors out of which one would be a pituitary adenoma and we found 43 publications and a total of 63 patients. (1) furthermore, a search of similar cases to ours found that the rare situation of simultaneous development of a pituitary adenoma and suprasellar or sphenoid wing meningioma has been reported in 32 cases. (4) moreover, only 17 cases of strictly suprasellar meningiomas were described in the literature, our case being the 18th. (1) discussions tumors of the sellar region have mesenchymal, neural or epithelial origin, along with cystic and inflammatory processes. out of all these tumors, pituitary adenomas are the most common, accounting for about 10-15% of all intracranial tumors. (5) most of the patients treated in our clinic present with both endocrine symptoms, but also intracranial hypertension and optic chiasm symptoms due to large size of the tumor. thus, most of the patients suffer from macroadenomas (> 10 mm) at the time of diagnosis, and most of the tumors extending beyond the sella turcica, either parasellar or suprasellar. the existence of simultaneous pituitary adenoma and supradiafragmatic meningioma is a very rare situation. search of relevant literature performed in pubmed and google scholar revealed only 17 other cases, ours being the 18th. (1) even though a plethora of possible mechanisms have been forwarded in relation to multiple brain tumors occurring simultaneously and having different histology origins, none have been widely recognized by the neurosurgery community. while some authors suggest a common receptor activator that triggers both lesions, others believe that one of the tumors might secrete a growth factor responsible for the initiation of aberrant cell growth in the second tumor. although growth hormone 29 a rare case of pituitary macroadenoma secreting adenomas have been suggested to induce arachnoid cell transformation, this hypothesis has yet to be confirmed. (6) other authors consider favorable factors for synchronously developing adenoma and meningioma variables such as genetic factors, prior trauma or surgery and even exposure to offending biochemical substances. (7) it is essential to distinguish between cases of pituitary adenoma with a suprasellar component, and cases of a co-existing sellar adenoma and suprasellar meningioma, because different surgical strategies might be adequate for these two different situations. (2) this is particularly difficult, because in most of the times the two lesions are indistinguishable from a radio-imaging point of view, our case did not show any pathognomonic imaging characteristic. most authors prefer to perform both tumor resections in either one surgical procedure, or combined transsphenoidal and transcranial approach under the same single general anesthesia. however, sometimes this might not be possible, and a decision must be made on which lesion to perform resection on first. surgical strategy is tailored according to the symptomatic lesion. so, in such cases it must be seen to whom the symptoms are due. both tumors were located in the same area, sellar and suprasellar region and both can cause slightly similar neurological complains. headache is a nonspecific symptom, visual fields deficits are common findings in both pituitary macroadenomas and suprasellar meningiomas, but hormonal imbalances are specific for a pituitary adenoma. so, in cases when lesions cannot be resected using the same approach, the surgeon must first operate the symptomatic tumor. regarding the existence of an agreement as to the best surgical approach to be used, we could only find one: use the best approach tailored to the specific case of the patient. therefore, some authors prefer to perform a transsphenoidal approach for both the lesions (3), others use a combined approach under the same anesthesia, others prefer a two timed transsphenoidal (4), transcranial, and so on. two-stage surgery is not an uncommon practice for large pituitary adenomas. in our case, both sellar and suprasellar components were considered to be part of the same pituitary macroadenoma. the treatment of choice for pituitary adenomas is tumor resection via transphenoidal route. during transsphenoidal surgery the sellar part of the tumor is resected, and the soft suprasellar component descends, with the aid of gravity and csf pulsation and develop itself to the surgeon. when the tumor is more firm this cannot happen during surgery. vigorous attempts to pull the suprasellar tumor into the sella can be dangerous, due to possibility of adherence to neurovascular structures. more sellar diaphragm can be teared, leading to postoperative csf fistula. in such cases a two-stage transsphenoidal surgery can be performed, because after a period of time of a few months the suprasellar will descend and through planned elective surgery the tumor can be complety resected via same surgical approach with minimal risks. even more, first histopathological examination confirmed the nature of the tumor as being gh-secreting pituitary adenoma. that was the rationale for our decision not to extend the resection to the suprasellar component, but rather consider a second transsphenoidal approach 3 months later, in order to allow the rest of the tumor to gravitationally descend in the sella. however, the ct scan at 3 months showed a stationary suprasellar component. the decision was made to perform subfrontal approach in order remove this component. this second lesion turned out to be a meningioma. this case perfectly illustrates the need for approaching every sellar tumor through the path that offers the most advantages. thus, a transsfenoidal approach would not have allowed the surgeon to resect the suprasellar component without major risks, whilst a subfrontal approach would not have been possible to resect the entire sellar component. overall, the patient had favorable outcome, because he harbored two benign, slow-growing tumors. conclusions synchronous gh-secreting macroadenoma and suprasellar meningioma developing simultaneously in the sellar and suprasellar region are very rare findings. in selected cases, both minimally invasive transsfenoidal approach and transcranial microsurgical approach must be considered simultaneously in order to achieve complete resection. moreover, the existence of two different lesions developing in the same region should be 30 bogdan ionut david, ligia gabriela tataranu, vasile gheorghe ciubotaru et al. considered in all the cases of pituitary adenomas with a suprasellar component. further research is needed with genetic profile of patients with synchronous tumors. conflicts of interest the authors declare no conflict of interests. founding none references 1. amirjamshidi a, mortazavi sa, shirani m, saeedinia s, hanif h. coexisting pituitary adenoma and suprasellar meningioma a coincidence or causation effect report of two cases and review of the literature. j surg case rep, 2017 (5):rjx039. doi: 10.1093/jscr/rjx039. 2. lim kz, goldschlager t, chandra rv, hall j, uren b, pullar m. co-occurrence of pituitary adenoma with suprasellar and olfactory groove meningiomas . basic clin neurosci, 2016. 7:361-365. 3. prevedello dm, thomas a, gardner p, snyderman ch, carrau rl, kassam ab. endoscopic endonasal resection of a synchronous pituitary adenoma and a tuberculum sellae meningioma: technical case report. neurosurgery, 2007. 60(4 suppl 2):e401. 4. guaraldi f, prencipe n, di giacomo v, scanarini m, gasco v. association of craniopharyngioma and pituitary adenoma. endocrine, 2013. 44:59-65. 5. cannav s, curt l, fazio r, paterniti s, blandino a, marafioti t, trimarchi f. coexistence of growth hormone-secreting pituitary adenoma and intracranial meningioma: a case report and review of the literature. j endocrinol, 1993. 16:703-8. 6. mathuriya sn, vasishta rk, dash rj, kak vk. pituitary adenoma and parasagittal meningioma: an unusual association. neurol india, 2000. 48:72-4. 7. goldberg mb, sheline ge, malamud n. malignant intracranial neoplasms, following radiation therapy for acromegaly. radiology, 1963. 80:465-470. flat panel detector-ct with endovenous injection. description of a novel technique for obtaining cerebral arteries imaging: technical note romanian neurosurgery (2016) xxx 3: 375 378 | 375 complete 3rd cranial nerve dysfunction postdeflation/excision of an encasing pituitary macroadenoma intrasellular cyst: a case report c.s. ng1, s. norlela2, k. nor azmi2 1registrar of internal medicine 2endocrinology, university kebangsaan malaysia medical centre, kuala lumpur, malaysia abstract: central nervous system injury in particular cranial nerve palsy has been reported to be as high as 2%. such prevalence of palsy generally attributed to surgical manipulation at the cavernous sinus, especially incurring the abducens nerve. we report the first case of acute oculomotor nerve sequel to the release of cystic fluid wrapping the nerve following a transsphenoidal excision of pituitary macroadenoma in a 57-year-old woman. she attended with the presentation of acute excruciating headache associated with partial drooping of right eye. the computed tomography and magnetic resonance imaging (mri) were consistent with pituitary apoplexy of an underlying pituitary macroadenoma. urgent transsphenoidal hypophysectomy was done. intra-operatively, cystic fluid was aspirated during pituitary tumour dissection. at the same time, curettage was employed to removal residual tumour after the tumour biopsy. immediate post-operative assessment noted complete right eye ptosis, with clinical evidence of complete right third and fourth nerve palsies. mri was repeated a week later in view of such palsy non-resolution. however, no local compression or edema noted. observation and monitoring were opted versus surgical revision. propitiously the aforementioned cranial nerve palsies persist for a month and subsequently subsided. in this case, we highlight the potential deleterious impact of aspirating cystic component and curettaging during pituitary surgery. likely postulated accounts for such occurrence include sudden release of fluid pressure with resultant cystic traction on its enfolding cranial nerves and subsequent neuropraxia. we aim to invite comments that could enlighten us on this gray area. key words: pituitary tumour, cranial nerve palsy, intraoperative cyst aspiration introduction pituitary macroadenoma could often lead to apoplexy requiring emergency operative intervention, i.e. transsphenoidal. transsphenoidal hypophysectomy has attained wide popularity ensuing 1962, with the debut of operative microscope (1). reported sequelae from such approach include carotid artery injury, meningitis, haemorrhage, cns injury, csf leak, nasal septal perforation, endocrine complications of diabetes insipidus and anterior pituitary 376 | ng et al third cranial nerve dysfunction post macroadenoma surgery insufficiency, and even death. the risks, however, depend on surgeon’s experience, ranging from 0.4 % to 20 %. of these, vision loss and ophthalmoplegia are common cranial nerve dysfunction, with the peril of 0.4 to 2.4 % (2). these have been directly related to inevitable intrasellar attempt to reach the pituitary tumour from medial cavernous sinus (2). nonetheless, cyst breakdown with consequent third nerve palsy has yet to be reported. case illustration a 57 years old woman with underlying dyslipidemia, came as outpatient with affliction of intermittent episodic headache of 2-year duration. nevertheless, the headache became worse and generalized over the past five months, with associated left upper eye visual disturbance. few ct brain imaging examinations in several private centers during this period of time were told to be unremarkable. she was then seen by an ophthalmologist who arranged for an mri brain, which showed pituitary macroadenoma, and referred her to our center: figure 1. elective admission for transsphenoidal hypophysectomy was ordered by neurosurgeon. however, 10 days prior to admission, she developed severe right sided headache but no evidence of apoplexy based on ct brain ordered via neurosurgeon. following that, a day prior to admission she complained of partial drooping of right eye. clinical examination revealed a right partial ptosis with the rest of cranial nerves remained intact. repeat ct brain confirmed clinical diagnosis of pituitary apoplexy and she was rushed by neurosurgeon for an urgent transsphenoidal hypophysectomy. pituitary mass was noted to be identified with brain lab igs system. sphenoid was noted to be seen and excised. bilateral optic and carotid indentation as well as sella were found to be recognized. cystic component of soft gelatinous tumour was aspirated during tumour dissection. the remaining pituitary tumour was curettaged out. the tumour was removed from posterior, lateral and anterior, without involving medial aspect. the operation lasted 3 hours without intra-operative sequelae. histopathological examination of brain tissue (excluding cystic component) showed pituitary adenoma. notwithstanding, immediately after the surgery, she complained of complete right eye ptosis, with clinical evidence of complete right third and fourth nerve palsies. mri brain was repeated a week later in view of such palsy non-resolution. however, no local compression or edema noted. observation and monitoring were opted versus surgical revision/decompression. the cranial nerve palsy resolved completely after one month during follow-up. romanian neurosurgery (2016) xxx 3: 375 378 | 377 figure 1 mri brain cystic component of the pituitary tumour wrapping the cranial nerves/cavernous sinus ct brain pre-op (pituitary apoplexy) mri brain one week post-op (residual pituitary lesion at right cavernous sinus, no massive local compression or edema noted) figure 2 preand post-op complete right eye ptosis post-op: lack of right eye’s medial gaze, with right eye in “up and out” position, indicating both oculomotor and trochlear nerves palsy figure 3 discussion visual dysfunction and cns impairment have been recognized as part of complications from pituitary surgery (2). usually it is related to tracing the pituitary tumour that is located medial to the cavernous sinus (2) whereby all the vital structures of cranial nerves situated. however, cases of cranial dysfunction related to intraoperative cyst aspiration have not been reported. in contrary, it has been advocated back in 1987, that transspenoidal cyst puncture was a routine therapeutic measure for symptomatic expanding cyst (3). in this patient, the excision did not involve the medial aspect. cyst enclosing the oculomotor nerve’s area was indeed aspirated. 378 | ng et al third cranial nerve dysfunction post macroadenoma surgery adapted from netter’s atlas of human anatomy figure 4 diagramatic and imaging representations of pituitary cyst in proximity to cranial nerves iii and iv the removal of the cystic fluid could have resulted in traction along with the cyst the underlying vital cranial nerves that it has wrapped upon. this has led to the clinical apparent third and fourth cranial nerve palsy immediately post-op. furthermore, concurrent curettage of the tumour could have compounded the nerve dysfunction by creating transient local tissue edema and pressure. mutually, perhaps this case did not involve scar tissue with resultant axonal compromise, in which case the symptoms will begin rather later (3-4 days from onset). the resulting neuropraxia could have explained the speedy recovery of this case. thus, observation will be sufficient in this case. otherwise, if axonotmesis or even neurotmesis is to happen, the potential outcome will be dismal. this case illustrated perhaps practice of cystic aspiration should be revised. or at least, to formulate an effective preventive and immediate surgical approach should severe cranial nerve dysfunction arise from such puncture. conclusion again this case underscores the importance of understanding the clinical neuro-anatomy and the potential harm of aspirating cyst intraoperatively. such outcome needs to be foreseen and addressed ahead prior and during the operative intervention. correspondence dr. ng choon seong department of internal medicine, hospital canselor tuanku muhriz, university kebangsaan malaysia medical centre, jalan yaacob latif, bandar tun razak, 56000, cheras, kuala lumpur, malaysia telephone: 6013-6981188 e-mail: csng2009@gmail.com references 1. hardy j: transsphenoidal removal of pituitary adenomas. union med can 91:933-945, 1962 2. ciric i, ragin a, baumgartner c, pierce d. complications of transsphenoidal surgery: results of a national survey, review of the literature, and personal experience. neurosurgery 40(2):225, 1997. 3. lundberg po, muhr c, bergström k, bergström m, deuschl h, enoksson p, hagelquist e, thuomas ka & wide l. transsphenoidal therapeutic puncture of a cystic pituitary adenoma. upsala journal of medical sciences 92(1):59-64, 1987. 1tascua_adult quality romanian neurosurgery (2015) xxix 3: 235 238 235 adult quality of life in congenital hydrocephalus operated cases. a twenty years retrospective study a. tascu1, a. iliescu1, r.e. rizea1, irina tudose1, st.m. iencean2 1pediatric neurosurgical department, “bagdasar-arseni”clinical hospital, bucharest, romania 2“gr. t. popa” university of medicine and pharmacy, iassy, romania abstract: congenital hydrocephalus is a health problem in many countries and in romania the pediatric neurosurgical department of the emergency hospital “bagdasararseni” has a large number of such patients. this is a retrospective study and it includes the patients with congenital hydrocephalus operated between 1992 and 2012 in the pediatric neurosurgical department of the emergency hospital “bagdasar-arseni”. the functional outcome was assessed using karnofsky performance scale, hydrocephalus outcome questionnaire and glasgow outcome scale. the total number of the patients was 372, with a predominance of boys (212 boys versus 160 girls) and at the time of our study 168 patients were over 16 years old. functional outcome of the children over 16 years old assessed using karnofsky performance scale, showed that 73 patients were above 80 and leading independent lives, and 95 were less than 80 points. the results would be better if all these patients would benefit from schooling for children with special needs. key words: congenital hydrocephalus, quality of life, retrospective study. introduction congenital hydrocephalus is a health problem in many countries, with an incidence of 0,2 to 0,8/1000 live births in usa. the techniques of shunting have permanently evolved since the early days of holter. they became routine in many pediatric neurosurgical departments but the data that describe mortality and morbidity and that certify the improvement in the quality of life of these patients are a few. the old saying: “once a shunt, always a shunt” hasn’t, till now, been completely contradicted. even further, data regarding the remote prognosis of these children that reach adulthood are even less. accordingly, clinical scores have been designed to assess the functional and vital outcome of the children and adults that have been operated in childhood for congenital hydrocephalus. there is no definite consensus over the best scale to use, making comparison between different series difficult. material and methods for many years the pediatric neurosurgical department of the emergency hospital “bagdasar-arseni” was the only unit in romania that could take in charge children with congenital hydrocephalus. also, the children who were fortunate to become adults were treated in the same hospital. the study that we have designed is a retrospective one. there were selected the patients with congenital hydrocephalus without any other pathology, operated between 1992 and 2012 in the pediatric neurosurgical department of the emergency hospital “bagdasararseni”. the 236 tascu et al adult quality of life in congenital hydrocephalus operated cases follow-up of the patients is a life-long one and patients were invited to check-up once a year. the hospital protocol is to revise any shunt that has been ruptured, has become short, or otherwise nonfunctional, provided that the patient is dependent on the shunt. the functional outcome was assessed using karnofsky performance scale, hydrocephalus outcome questionnaire and glasgow outcome scale. on the karnofsky scale, 100 is asymptomatic, 80 able to assume normal life, 0= dead. with glasgow coma scale, according to the wfns, 1 is normal life and 5 is dead. schooling was appreciated as normal, school with special help or none at all. social status depended on the employment or nonemployment of the patients. results the total number of the patients was 372, with a predominance of boys (212 boys versus 160 girls). the reoperation was due to shunt obstruction and infection. there were 1190 reoperations with an average of 3,19 reoperations for a patient. in 68 patients, reoperation was made for shunt infection with an average of 3 reoperations for a patient. a minimum of 2 operations and a maximum of 23 operations for a patient were performed. only 10 patients were without sequelae. a large number, 131 patients had motor deficits and even more, 245, had cognitive deficits. unfortunately, 31 patients died. at the time of our study, 168 patients were over 16 years old. no one of our patients gained independency from their shunts. as we can see from the graphic, for the children operated when they were under 1 year of age, first reoperation was mainly between 4 and 7 years of age (162 cases). functional outcome of the children over 16 years old assessed using karnofsky performance scale, showed that 73 patients were above 80 and leading independent lives, and 95 were less than 80 points. concerning schooling, there was a disappointing 27,1% (101) of the children that followed normal school, with 12,9% (48) of the children who could not attend any school. as for the rest, 223 children (59,9%) needed special schooling. unemployment in the group of 168 patients that were over 16 years old, was pretty high, of over 50%, with patients that over the years had a job and had lost it, and patients that have never worked. discussion it is well known that shunt malfunction is a permanent risk for the hydrocephalic patients that were treated with shunts. earlier the shunt, worse the prognosis. as we have seen, the reoperation for different reasons for shunt malfunction, is greater between 4 and 7 years old and then, between 8 and 11 years old, if the children were shunted before age of 1 year old. as for the children who were treated with etv (5 cases), the number is to small to draw a conclusion, but it seems that an obstruction of the stomy is more dangerous than a merely shun obstruction, as acute hydrocephalus leads to coma and impending death. concerning the shunt infection, the most frequent germ was staphyloccocus epidermidis, which means that proper care is mandatory for these patients. infection of the shunt is usually heralded by the appearance on the abdominal ultrasound of a peritoneal cyst which precludes the normal absorption of the csf. a special problem is that of an asymptomatic patient that has been shunted for years and presents with a ruptured shunt. there are 2 ways to deal with. the first is to revise the shunt, and even there is a large gap between the stumps of the shunt, and the surgeon sees only one csf drop drooling from the proximal stump, than the shunt is to be considered needed and the gap should be repaired. the second is to ligate the shunt at the neck of the patient and see if he would be romanian neurosurgery (2015) xxix 3: 235 238 237 asymptomatic. that is a dangerous maneuver, because the shunt might be in fact functional and the patient would be in deep coma in short time. we should stress, as we have already said, that shunt independence is rather exceptional. mortality is a fact that cannot be overlooked. 31 of our patients died of shunt malfunction, mostly because of obstruction of the shunt. this is why the close follow-up of the shunts is the only way to prevent such an occurrence. speaking about sequelae, the cause of hydrocephalus and frequent shunt malfunctions are the main causes of neurological sequelae and psychological disturbances. conclusions prolongation of life span, with or without sequelae, depending on a shunt, is usually all that we could do for these patients. life-long follow-up is the only way to prevent shunt malfunction and sudden death and this is the work of a dedicated. the education system should provide a repeated psychological evaluation and a system schooling for children with special needs. references 1. matthieu vinchon, marc baroncini, isabelle delestret. adult outcome of pediatric hydrocephalus childs nerv syst. 2012 june; 28(6): 847–854 2. matthieu vinchon, harold rekate, abhaya v kulkarni. pediatric hydrocephalus outcomes: a review. fluids barriers cns. 2012; 9: 18. 3. n. k. venkataramana hydrocephalus indian scenario – a review j pediatr neurosci. 2011 october; 6(suppl1) 4. arvind sinha, anuj sharma, charitesh gupta pediatric hydrocephalus: does the shunt device pressure selection affect the outcome? j indian assoc pediatr surg. 2012 apr-jun; 17(2): 54–57. 5. tadanori tomita pediatric neurosurgery—science, art, and humility: reflection of personal experience childs nerv syst. 2013; 29(9): 1403–1414. 6. m. mataro, m. a. poca, j. sahuquillo, a. cuxart, j. iborra, m. d. de la calzada, c. junque, cognitive changes after cerebrospinal fluid shunting in young adults with spina bifida and assumed arrested hydrocephalus j neurol neurosurg psychiatry. 2000 may; 68(5): 615– 621. 7. matheus fernandes de oliveira, fernando campos gomes pinto, koshiro nishikuni, ricardo vieira botelho, alessandra moura lima, josé marcus rotta revisiting hydrocephalus as a model to study brain resilience front hum neurosci. 2011; 5: 181. 8. ricardo m fernandes, johanna h van der lee, martin offringa a systematic review of the reporting of data monitoring committees' roles, interim analysis and early termination in pediatric clinical trials bmc pediatr. 2009; 9: 77 9. hannah m tully, william b dobyns infantile hydrocephalus: a review of epidemiology, classification and causes eur j med genet. 2014 august; 57(8): 359– 368. 10. mcallister jp 2nd, williams ma, walker ml, kestle jr, relkin nr, anderson am, gross ph, browd sr; hydrocephalus symposium expert panel. an update on research priorities in hydrocephalus: overview of the third national institutes of health-sponsored symposium "opportunities for hydrocephalus research: pathways to better outcomes". j neurosurg. 2015 jun 19:1-12 238 tascu et al adult quality of life in congenital hydrocephalus operated cases 11. shannon cn, carr kr, tomycz l, wellons jc, tulipan n. time to first shunt failure in pediatric patients over 1 year old: a 10-year retrospective study. pediatr neurosurg. 2013;49(6):353-9. 12. kulkarni av, riva-cambrin j, butler j, browd sr, drake jm, holubkov r, kestle jr, limbrick dd, simon td, tamber ms, wellons jc 3rd, whitehead we; hydrocephalus clinical research network. outcomes of csf shunting in children: comparison of hydrocephalus clinical research network cohort with historical controls: clinical article. j neurosurg pediatr. 2013 oct;12(4):334-8. romanian neurosurgery (2019) xxxiii (3): pp. 305-309 doi: 10.33962/roneuro-2019-051 www.journals.lapub.co.uk/index.php/roneurosurgery spontaneous cerebrospinal fluid rhinorrhea in patient with pallister–hall syndrome milicevic mihajlo1,2, aleksic vuk1, ilic rosanda1,2, scepanovic vuk1, stanimirovic aleksandar1, paunovic aleksandra1, milic marina, nedeljkovic zarko, matteo sacco1, grujicic danica1,2 1 neurosurgery clinic, clinical center of serbia, belgrade, serbia, serbia 2 faculty of medicine, university of belgrade, belgrade, serbia abstract pallister-hall syndrome (phs) is extremely rare autosomal dominant disorder with typical clinical features such as presence of polydactyly, hypothalamic hamartoma, bifid epiglottis, anal, renal, genitourinary and pulmonary abnormalities, mainly located in the midline of the body. spontaneous cerebrospinal fluid (csf) rhinorrhea is also a rare condition, and it is used to describe nasal discharge of csf unrelated to previous trauma, localized tumour, surgery, or previous radiation therapy. the exact cause is not yet fully understood. we report a case of adult female patient previously diagnosed with phs and late onset of spontaneous nasal liquorrhea, due to defect in the anterior skull base. although it can be incidental finding, we believe that described defect in the body midline can be another presentation of congenital craniofacial abnormality which are common in phs. introduction pallister hall syndrome (phs) is extremely rare autosomal dominant disorder usually diagnosed in infants and children, but it can be seldomly seen in adulthood (1). in 1980, judith hall and philip pallister described 6 cases of infants with a neonatally lethal malformation syndrome of hypothalamic hamartoblastoma, postaxial polydactyly, and imperforate anus, and after several simmilar cases were described by other authors, this syndrome was named after pallister and hall (2, 3). typical clinical features of phs are presence of polydactyly and hypothalamic hamartoma, however, in recent years, many patients were reported expanding the phenotype, and more rare features may also be seen, such as bifid epiglottis, anal, renal, genitourinary, and pulmonary abnormalities, nonpolydactyly skeletal anomalies, and dev elo pmental delay. even rearly epilepsy, hypo pituitaris m, aganglonosis of colon, congenital cardiac defect, and adrenal abnormalities can also be found (4). clinical suspicion of phs is confirmed by genetic testing of the gli3 zinc finger transcription factor keywords pallister-hall syndrome, spontaneous csf rhinorrhea, nasal liquorrhea corresponding author: aleksic vuk neurosurgery clinic, clinical center of serbia, belgrade, serbia aleksicvuk@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 306 milicevic mihajlo, aleksic vuk, ilic rosanda et al. gene on 7p14 (2). the importance of this gene located on chromosome 7 is that it regulates downstream genes of the hedgehog pathway important to the formation of the neural tube, otic vesicles, craniofacial structures, and distal limb buds (4). we report a case of adult female patient previously diagnosed with phs and late onset of spontaneous nasal liquorrhea. case report we present a case of a 56-year-old woman admitted to the neurosurgery clinic of the clinical center of serbia, with signs of spontaneous nasal liquorrhea. she was born from healthy and non-consanguineous parents after normal pregnancy and delivery. on birth examination, she was found to have polysyndactyly on both hands. at the age of 2, she was operated, and ablation of redundant fingers and soft tissue was performed with surgical reconstruction and good appearance in size and shape of both hands was achieved (picture 1). after few years, in early childhood, patient developed epilepsy with laughing, gelastic seizures, and she was placed on two antiepileptic drugs after which seizures resolved. later on, during fertility testing she was found to have bilateral renal hypoplasia, as well as uterine hypoplasia. in the late 40’s, during the clinical testing due to signs of polyneuropathy, suspicion of phs was made by attending neurologist, and brain magnetic resonance imaging (mri) showed typical hypothalamic hamartoma (picture 2). patient underwent genetic testing, and mutation of gli3 gene in the short arm of chromosome 7 was found. at the age of 50, the patient noticed spontaneous watery discharge from left nostril, and occasional sweet taste in her mouth, usually in the morning or after a long bed rest. there was no history of head trauma. after 4 years of neglecting this symptom patient was referred to our hospital. at admission her neurologic exam was indicative of distal polineuropathy without signs of motor weakness. high glucose concentration, and detection of β-2transferrin in clear fluid collected from left nostril confirmed the diagnosis of cerebrospinal fluid rhinorrhea. head mri was performed and communication of the frontobasal liquor space with the upper nasal corridor at the level of the left olfactory nerve was found. also, presence of hypothalamic hamartoma in the projection of tuber cinereum, 19 x 13 mm in diameter was confirmed. a non-contrast ct scan with bone window revealed mucosal thickening in the left cribriform plate in conjunction with the olfactory fila presenting possible defect in the adjacent skull base (picture 3). we performed endonasal endoscopic repair of csf rhinorrhoea under general anaesthesia. operatively identified bone defect in the left cribriform plate with signs of csf leak was closed by dura matter, fascia lata, and tissue glue. the mucosa of middle turbinate and adjacent septum was made raw and bolgerisation was performed. valsalva manoeuvre did not show signs of csf leakage. after haemostasis was achieved nose was bagged for five days. avoidance of coughing or sneezing, the use of stool softeners, elevation of the head, and bed-rest were given in the post-operative period. patient was on prophylactic antibiotics for one week. on the 5th post-operative day patient was discharged from the hospital. at 2 year follow-up patient is asymptomatic, without signs of nasal liquorrhea. also, nasal cavities healed well, with no breathing difficulties. picture 1. present look of patient’s hands, 54 years, after ablation of redundant fingers and soft tissue due to polysyndactyly. 307 spontaneous cerebrospinal fluid rhinorrhea in patient with pallister–hall syndrome picture 2. brain mri showing hypothalamic hamartoma in our patient picture 3. ct scan (bone window) showing mucosal thickening in the left cribriform plate in conjunction with the olfactory fila presenting defect in the adjacent skull base discussion phs is extremely rare autosomal dominant disorder usually diagnosed in infants and children, but it can be seldomly seen in adulthood (1). dramatic beginning of phs started in 1980, when judith hall and philip pallister described 6 lethal cases of infants with typical combination of hypothalamic hamartoblastoma, postaxial polydactyly, and imperforate anus (2, 3). today, this clinical features of phs in the terms of the clinical findings are considered to be just a tip of the iceberg, since many others rare features may also be seen, such as bifid epiglotis, polydactyly, dysmorphic face in the form of small ears pointing backwards, small retroverted nose, flat nasal bridge, and small tongue. also, different cardiac, anal, renal, adrenal, genitourinary, and pulmonary abnormalities can be found. hypothalamic hamartomas are typically found, and can be asymptomatic or in the origin of epilepsy, hypopituitarism, lethargy, hypoglycaemia, electrolyte dysfunction, and metabolic acidosis. so far, about 100 cases of phs with variable manifestations are reported in literature (4-6). we reported a case of adult female patient previously diagnosed with phs and late onset of spontaneous nasal csf rhinorrhoea. to our knowledge this is a 308 milicevic mihajlo, aleksic vuk, ilic rosanda et al. first case of phs patient with skull base bone defect, presented with spontaneous cerebrospinal fluid rhinorrhoea. also, this is the first described case of phs in serbian population according to our knowledge. our patient is a 56-year-old woman with previously operated polysyndactyly on both hands, well controlled epilepsy with typical gelastic seizures, bilateral renal and uterine hypoplasia, and hypothalamic hamartoma. these are usual signs and symptoms found in phs. about ninety-five percent of phs patients have gli3 gene mutation in the short arm of chromosome 7 (6). this was also case in our patient, since definite diagnosis was confirmed after molecular testing showing mutation of gli3 gene. hypothalamic hamartoma represents a benign tumour of the hypothalamus and does not need treatment from a tumour biological perspective. however, other problems can be associated with hypothalamic hamartoma such as pharmacoresistant epilepsy, behavioural problems, and endocrine disturbances (7). an mri of the brain in our patient revealed presence of hypothalamic hamartoma in the projection of tuber cinereum, 19 x 13 mm in diameter. in presented case patient developed epilepsy with laughing, gelastic seizures. after introduction of two different antiepileptic drugs, our patient was in total remission. the term spontaneous csf rhinorrhoea has been used to describe nasal discharge of csf unrelated to previous trauma, localized tumour, surgery, or previous radiation therapy, and it represents a rare medical condition (8). our patient had first onset of watery discharge from left nostril at the age of 50, without history of previous trauma, and after neglecting symptoms for about 4 years, patients was referred to our hospital. also, other possible causes of spontaneous csf rhinorrhoea were excluded in our patient. in the study of schuknecht et al, more than 70% of patients with spontaneous csf leak had osteodural interruption at the site of cribriform plate leading into the olfactory cleft (8). this was also a case in our patient. in the case of osteodural interruption surgical repair is recommended to prevent complications such as meningitis. endonasal endoscopy is the preferred and minimally invasive approach and it has been accepted worldwide as the method of choice. the advantages of this approach are: excellent visualization, precise placement of graft, minimal surrounding tissue damage, preservation of olfactory nerves and their function, shortened operating time, and faster recovery. this approach has a high success rate up to 97% (9, 10). we performed surgical endonasal endoscopic repair of previously found osteodural deffect along the cribriform plate leading into the left olfactory cleft. on two years fallow-up, patient is without signs of cfs rhinorrhoea recurrence. phs is a rare, autosomal dominant, genetic disorder with a mutation in the gli3 gene on the short arm of chromosome 7. this gene regulates pathways important for the formation of the neural tube, craniofacial structures, otic vesicles, and limbs (11). many different congenital abnormalities are found in patients with phs, and hypothalamic hamartoblastoma, bifid epiglottis, polydactyly, epilepsy, imperforate anus and other genital anomalies being most common, with predominance of anomalies in the midline of the body (4, 12). about 100 case reports of phs are found in the literature, but to our knowledge this is the first case of phs with spontaneous csf rhinorrhoea, due to defect in the anterior skull base. although it can be incidental finding, we believe that described defect in the body midline can be another presentation of congenital craniofacial abnormality which are common in phs. endoscopic endonasal approach is minimally invasive and successful treatment approach for described congenital osteodural defect. references 1. talsania m, sharma r, sughrue me, scofield rh, lim j. familial pallister-hall in adulthood. neuro endocrinol lett. 2017;38(5):329-331. 2. courtney e, swee ds, ishak d, ngeow j. a delayed diagnosis of pallister-hall syndrome in an adult male following the incidental detection of a hypothalamic hamartoma. hum genome var. 2018;5:31. 3. hall jg, pallister pd, clarren sk, beckwith jb, wiglesworth fw, fraser fc, cho s, benke pj, reed sd. congenital hypothalamic hamartoblastoma, hypopituitarism, imperforate anus and postaxial polydactyly--a new syndrome? part i: clinical, causal, and pathogenetic considerations. am j med genet. 1980;7(1):47-74. 4. hayek f. pallister-hall syndrome with orofacial narrowing and tethered cord: a case report. j med case rep. 2018;12(1):354. 5. biesecker lg, graham jm jr. pallister-hall syndrome. j med genet. 1996;33(7):585-9. 309 spontaneous cerebrospinal fluid rhinorrhea in patient with pallister–hall syndrome 6. chandra sr, daryappa mm, mukheem mudabbir ma, pooja m, arivazhagan a. pallister-hall syndrome. j pediatr neurosci. 2017;12(3):276-279. 7. mundlos s, horn d, mundlos s, horn d. limb malformations. berlin: springer; 2014. pallister–hall syndrome; pp. 61–62. 8. schuknecht b, simmen d, briner hr, holzmann d. nontraumatic skull base defects with spontaneous csf rhinorrhea and arachnoid herniation: imaging findings and correlation with endoscopic sinus surgery in 27 patients. ajnr am j neuroradiol. 2008;29(3):542-9. 9. kljajić v, vuleković p, vlaški l, savović s, dragičević d, papić v. endoscopic repair of cerebrospinal fluid rhinorrhea. braz j otorhinolaryngol. 2017;83(4):388-393. 10. gonen l, monteiro e, klironomos g, alghonaim y, vescan a, zadeh g, gentili f. endoscopic endonasal repair of spontaneous and traumatic cerebrospinal fluid rhinorrhea: a review and local experience. neurosurg clin n am. 2015;26(3):333-48. 11. hall jg. the early history of pallister–hall syndrome— buried treasure of a sort. gene. 2016;589(2):100–103. 12. biesecker lg, graham jm, jr. pallister-hall syndrome. j med genet. 1996;33(7):585. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 486-491 doi: 10.33962/roneuro-2019-078 www.journals.lapub.co.uk/index.php/roneurosurgery management of spinal dural arterio venous fistula with peri-medullar drainage. experience of a north-african centre assoumane ibrahim1,2, loucif houari1, sanoussi samuila3, sidi said abderahmane1, abdelhalim morsli1 1 department of neurosurgery, chu bab el oued, algiers, algeria 2 department of neurosurgery, maradi reference hospital, niger republic 3 department of neurosurgery, niamey national hospital, niger republic abstract introduction: spinal dural arterio venous fistula (sdavf) is an arteriovenous communication on the spinal dura with peri-medullar venous drainage. it is a curable cause of myelopathy and the most common form of spinal arterio venous malformation (avm). the average age of revelation is the fifth decade; it is a diagnostic and therapeutic emergency. materials and methods: this is a retrospective study conducted in the neuro surgical department of chu bab el oued in algiers during a five years time from november 2013 to september 2018. we assessed the clinical status of patients according to the aminoff-logue disability score before and after surgery. all patients did a total spine mri followed by a medullar angiography which facilitated the pinpointing of the exact location of the dural fistula. the mean follow-up is 30 months. results: there were five males and two females, all of them older than 45 years of age. at the admission, patients presented with signs of neurological deficits. after the diagnosis of sdavf the surgical intervention consisted of a disconnection of the arteriovenous communication by coagulation and section of the fistula at the foot of the vein after a laminectomy. functional rehabilitation was prescribed for all patients and they were regularly followed-up. conclusion: treatment of avf is surgical or endovascular. results depend largely on preoperative neurological status. introduction the spinal dural arterio venous fistula (sdavf) with peri-medullar venous drainage is an abnormal communication within an afferent artery and an adjacent vein without interposition of capillary bed. this communication occurs at the spinal dura and is followed by a peri medullar venous drainage. individualize by kendall and merland in the 1980 th , it is a rare pathology even if it represente the most frequent spinal arteriovenous malformation accounting about 60–80% of all spinal vascular malformations [1,2,3,4]. keywords arteriovenous fistula, arteriovenous malformation, myelopathy corresponding author: assoumane ibrahim department of neurosurgery, chu bab el oued, algiers, algeria as_ibrah2006@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 487 management of spinal dural arterio-venous fistula with peri-medullar drainage arterial blood flow is shunted directly into the venous plexus, under arterial pressure. the venous plexus subsequently becomes “arterialized,” and obstruction of venous outflow leads to venous congestion, venous hypertension, and progressive ascending myelopathy [5] the average age of revelation is the fifth decade. clinical signs are not specific, that is the reason of the diagnosis delay causing sometimes severe disability; for that reason, sdavf constitute a diagnostic and therapeutique emergency. treatment of avf is usually surgical or endovascular. the objective of our study is to assesses the surgical treatment of sdavf and the clinical outcome of patients operated for sdavf in the neurosurgical department in chu beo algiers. materials and methods this is a retrospective study conducted in the neuro surgical department of chu bab el oued in algiers during a five years time from november 2013 to september 2018. we analyze clinical data of patients operated for sdavf. we assessed the clinical status of patients according to the aminoff-logue disability score before and after surgery (table 1). table 1: aminoff-logue disability score this score has 4 grades: grade 1: 0-2; grade 2: 3-5; grade 3: 6-8; grade 4: 9-11 we performed a total spinal mri which suspect the sdavf and spinal digital subtraction angiography (dsa) that facilitated the pin-pointing of the exact location of the dural fistula. all patients underwent microsurgical approach; the day before surgery we perform a plan x ray on a metallic landmark to guide the skin incision. the microsurgical approach consisted of a disconnection of the arteriovenous communication by coagulation and section of the fistula at the foot of the vein after a laminectomy. patients presenting disabilities were send for functional rehabilitation. results during the time of our study we registered 7 patients suffering of sdavf, there is predominance of male with a sex ratio of 5/2; the mean age of our patients is 56 years with extreme from 49 to 68 years. the time before consultation is fifty one month’s with extreme from 6 to 60 months. all patients suffered for motor disturbance (100%), a leg weakness is found in 5 patients representing 71, 42%, one patient require a stick for walking and another one require walker to move. urination disturbance is present in all patients (100%) as occasional incontinence is found in 3patients (42, 85%), frequency urination is found in 2 patients (28, 57%) and occasional retention in 2 patients (28, 57%). six patients presented defecation disorders representing 85, 75 % of patients, like moderate constipation for 4 patients (57, 14%), severe constipation for one patient, another one presented occasional incontinence. three (3) patients present sensibility disorder which represent 42, 85% of patients. the pre-operative disability scale of aminoff-logue is iii for 2 patients (28, 57%) and ii for 4 patients (57, 14%), and i for one patient. all patients did a total spine mri, this investigation objectified serpiginous images and flow void sign of peri medullar vessels dilation; also, an intra medullar hyper intensity (figure 1). figure 1: a: mri sagittale t2 weithed showing flow void sign (yellow arrow) and intramedullar hyper intensity (red arrow). 488 assoumane ibrahim, loucif houari, sanoussi samuila et al. to locate the communication, we performed medullar angiography for all patients; angiography has facilitated the pin-pointing of the exact location of the dural fistula. the investigation permits us to see the afferent pedicles, the peri medullar drainage vein which is dilated and serpiginous, also the dural fistula (figure 2). all our patients presented thoracic single fistula. figure 2: dsa: after catheterisation of left t6 showing a fistula (red arrow) and an arterialized vein (yellow arrow). figure 3: per operative image, after durotomy showing the fistula (yellow arrow) and the tortuous varterialized veins (red arrow). for all our patients we performed microsurgical approach; under general anesthesia, on prone position, a median skin incision is made at the level of the fistula; we perform a laminectomy one level above and one below the fistula to expose the work field before a median durotomy and suspension of the dural edges. under microscope the arterialized veins are found tortuous and colored in red and the fistula is found communicating aradicular artery (figure 3). we performed the coagulation of the fistula and section of it at the foot of the vein. at the end of the procedure we spent about 30 minutes after the section of the fistula to make sure that the arterialized vein become progressively blue, which is the vein normal color. the dural closure is assured with continuous running suture. patients presenting disabilities were send for functional rehabilitation. the post-operative outcome 7 days and 6 months after surgery is summarized in the following table. initial aminofflogue grade day 7 after surgery 6 months later patient 1 iii iv iii patient 2 iii iv ii patient 3 ii iii i patient 4 ii ii ii patient 5 ii ii i patient 6 i i i patient 7 ii ii i table 2: post-operative outcome of patients at day 7 and 6 months later. the mean follow-up is 30 months; patients are seen in the clinic weekly for the first month and every month for three months and every trimester until one year. discussion in our study there is predominance of male with the average age of revelation the fifth decade as reported by many authors [6, 7]. the time before consultation is long about 51 months in our series; it is comparable to the time reported in the literature [8, 9,]. this is due to the difficulty to diagnose the sdavf because of lack specific signs. the diagnosis delay reduces the chance of recuperation even after the treatment. the most frequent signs in our series is motor and sphincter disturbance representing 100% of patients followed by sensibility disturbance which represent 42, 85% of patients. many authors 489 management of spinal dural arterio-venous fistula with peri-medullar drainage reported the predominance of motor disturbance follow by sensory disturbance and sphincter disturbance [2, 10, 26]. we performed mri for all our patients, in case of sdavf suspicion a dsa is performed to confirm and locate the level and number of fistula, the feeders as well. yamaguchi [11] reported that spinal ct angiography could be used to demonstrate the fistula localization. in practice it is not safe because of the radiation quantity, before getting the exact location of the fistula. mri images signs on t1weighted scans, the swollen cord is slightly hypointense and enlarged. following contrast administration, diffuse enhancement may be seen within the cord as a sign of chronic venous congestion with a breakdown of the blood spinal cord barrier [13, 14]. on t2-weighted sequences, the cord edema is depicted as a centromedullary not well-delineated hyperintensity over multiple segments that is often accompanied by a hypointense rim, most likely representing deoxygenated blood within the dilated capillary vessels surrounding the congestive edema spin echo [3d-tse]) compared with standard t2 tse sequences [12]. the help of mr angiography in the positive diagnostic was emphasized by some authors. for efrat saraf-lavi [15] the principal advantage of mr angiography is the improved detection of the fistula level, with the correct level ± one level identified in 73% of true positive cases. they supported that overall, the combination of mr imaging and mr angiography provides improved screening for dural avf and benefits the subsequent radiographic dsa study by helping target the level of the fistula. we performed for all our patients a total spine mri, this investigation objectified suspicion signs of sdavf but to confirm the diagnostic the dsa was used , this investigation allow us to locate the fistula , the number of afferent arteries. many authors recognize the digital angiography as a helpful tool that can give a map of the vascularisation and help to plan the endovascular treatment. it is the gold standard for the diagnostic of sdavf [16, 17, 18, 19]. all our patients presented thoracic single fistula, many authors reported that the thoracic level is the most frequently affected [2,26,34] and most of patients present a single fistula, the multiple are rarely reported[2,9]. all patients underwent microsurgical approach; the surgical technique consisted of a disconnection of the arteriovenous communication by coagulation and section of the fistula at the foot of the vein after a laminectomy. permanent vascular clips could be used [22].authors reported the use of microsurgery or endovascular to be effective [7, 20, 21].many authors reported a rate of recanalization after embolization with polyvinyl alcohol, in up to 83% of cases [27,28].but with the evolution of material use endovascular embolization with liquid adhesive material is reported to have a very low rate of recanalization [29,30]. the success rates of endovascular therapy have been reported to vary between 25% and 75% [31, 32] but for j. marc et al the advantages of the endovascular technique are its noninvasiveness and the possibility of an immediate angiographic control of the treatment [10]. steinmetz mp et al in a recent meta-analysis suggested complete occlusion of the fistula following surgery in 98% [33]. the outcome was marqued by a worsening of the aminoff–logue disability scale in three patients in the first week after the surgery. but after six months of occupational therapy five patients (71.42%) improved their aminoff–logue disability scale while two patients remain stable. they did not improve their disability after two years. approximately 75% of patients get a degree of satisfaction as report in the literature [22]. in their series of 17 patients treated by microsurgery jakub w et al reported that functional improvement or good stable condition was achieved in 65% of the patients at discharge and in 76% in long-term follow-up [34]. chibbaro s et al advocated multidisciplinary approach based on direct cooperation between endovascular specialists and neurosurgeons before the choice of the treatment option. they obtained the excellent result of 100% cure rate with no procedural complications after patient’s selection for microsurgical treatment [21] the most complications of the microsurgical treatment are csf leak, infection, haematoma, and neurological sequelae [23, 24, 25]. in our study we did not experiment such complications. conclusion sdavf is a rare pathology, with unspecific clinical signs leading to diagnostic difficulties. to avoid misdiagnosis a multidisciplinary collaboration is required. the neuroradiologist help is very 490 assoumane ibrahim, loucif houari, sanoussi samuila et al. important using mri and dsa to get the exact location of the fistula and guide the treatment, either surgical or endovascular. after our series we conclude that microsurgery is a good option for the treatment but the post-operative outcomes depend largely on preoperative neurological status. conflict of interest: none references 1. houdart e, chapot r, boissonnet h et merland jj. fistules artérioveineuses durales rachidiennes.encycl méd chir (editions scientifiques et médicales elsevier sas,paris, tous droits réservés), neurologie,17-490-b-20, 2000, p. 4. 2. lee j et al. clinical presentation, imaging findings, and prognosis of spinal dural arteriovenous fistula. j clin neurosci 2015 elsevier. 3. robert f. spetzler, m. yashar s. kalani, peter nakaji, neurovascular surgery. thieme publishers new york 2015 4. nozar aghakhani; fabrice parker; philippe david; pierre lasjaunias; marc tadie, curable cause of paraplegia spinal dural arteriovenous fistulae. american heart association, inc. 2008. 5. jennifer e. fugate, d.o. giuseppe lanzino and alejandro a. rabinstein. clinical presentation and prognostic factors of spinal dural arteriovenous fistulas: an overview. neurosurg focus 32 (5):e17, 2012. 6. muralidharan r, saladino a, lanzino g, et al. the clinical and radiological presentation of spinal dural arteriovenous fistula. spine (phila pa 1976) 2011;36:e1641–7. 7. saladino a, atkinson jl, rabinstein aa. surgical treatment of spinal dural arteriovenous fistulae: a consecutive series of 154 patients. neurosurgery 2010;67:1350–7 [discussion 1357–8]. 8. narvid j, hetts sw, larsen d, neuhaus j, singh tp, mcswain h,et al. spinal dural arteriovenous fistulae: clinical features andlong-term results. neurosurgery. 2008;62:159—67. 9. donghai w, ning y, peng z, shuo x, xueen l, peng z, et al. the diagnosis of spinal dural arteriovenous fistulas. spine.2013;38: e546—53. 10. j. marc c. van dijk; karel g. terbrugge; robert a. willinsky; richard i. farb; m. christopher wallace. multidisciplinary management of spinal dural arteriovenous fistulas clinical presentation and long-term follow-up in 49 patients. 2002 american heart association, inc. 11. yamaguchi s, eguchi k, kiura y, et al. multi-detector-row ct angiography as a preoperative evaluation for spinal arteriovenous fistulae. neurosurg rev 2007;30:321–26, discussion 327. 12. krings t, lasjaunias pl, hans fj, et al. imaging in spinal vascular disease. neuroimaging clin n am 2007;17:57–72. 13. chen cj, chen cm, lin tk. enhanced cervical mri in identifying intracranial dural arteriovenous fistulae with spinal perimedullary venous drainage. neuroradiology 1998;40:393–97. 14. terwey b, becker h, thron ak, et al. gadolinium-dtpa enhanced mr imaging of spinal dural arteriovenous fistulas. j comput assist tomogr 1989;13:30–37. 15. efrat saraf-lavi, brian c. bowen, robert m. quencer, evelyn m.l. sklar, alan holz, steve falcone, richard e. latchaw, robert duncan, and ajay wakhloo. detection of spinal dural arteriovenous fistulae with mr imaging and contrast-enhanced mr angiography: sensitivity, specificity, and prediction of vertebral level. ajnr am j neuroradiol 23:858–867, may 2002. 16. morris jm. imaging of dural arteriovenous fistula. radiol clin north am 2012;50:823–39. 17. muralidharan r, saladino a, lanzino g, et al. the clinical and radiological presentation of spinal dural arteriovenous fistula. spine (phila pa 1976) 2011;36:e1641–7. 18. marcus j, schwarz j, singh ip, et al. spinal dural arteriovenous fistulas: a review. curr atheroscler rep 2013;15:335. 19. hacein-bey l, konstas aa, pile-spellman j. natural history, current concepts, classification, factors impacting endovascular therapy, and pathophysiology of cerebral and spinal dural arteriovenous fistulas. clin neurol neurosurg 2014;121:64–75. 20. patsalides a, santillan a, knopman j, et al. endovascular management of spinal dural arteriovenous fistulas. j neurointerv surg 2011;3:80–4. 21. chibbaro s, gory b, marsella m, et al. surgical management of spinal dural arteriovenous fistulas. j clin neurosci 2015;22:180–3. 22. antoine nachanakian, antonios el helou, ghassan abou chedid and moussa alaywan. spinal dural arteriovenous fistulas — treatable cause of myelopathy. 2013, http://dx.doi.org/10.5772/56725. 23. schick u and hassler w. treatment and outcome of spinal dural arteriovenous fistulas. eur spine j. 2003; 12(4): 350– 355. 24. song jk, vinuela f, gobin yp, duckwiler gr, murayama y, kureshi i, frazee jg, martin na. surgical and endovascular treatment of spinal dural arteriovenous fistulas: long-term disability assessment and prognostic factors. j neurosurg. 2001; 94(2 suppl): 199–204. 25. ropper ae, gross ba, du r. surgical treatment of type i spinal dural arteriovenous fistulas. neurosurg focus 2012; 32(5): e3 26. ortega-suero g, etessam jp, gamazo mm, rodríguez-boto g. fístulas arteriovenosas espinales del adulto.manejo de una serie de casos desde una planta de neurología. neurología. 2018. https://doi.org/10.1016/j.nrl.2016.12. 001 27. hall wa, oldfield eh, doppman jl. recanalization of spinal arteriovenous malformations following embolization. j neurosurg. 1989;70: 714–720. 28. morgan mk, marsh wr. management of spinal dural arteriovenous malformations. j neurosurg. 1989;70:832– 836. 491 management of spinal dural arterio-venous fistula with peri-medullar drainage 29. song jk, gobin yp, duckwiler gr, murayama y, frazee jg, martin na, vinuela f. n-butyl 2-cyanoacrylate embolization of spinal dural arteriovenous fistulae. ajnr am j neuroradiol. 2001;22:40–47. 30. anson ja, spetzler rf. spinal dural arteriovenous malformations. in: awad ia, barrow dl, eds. dural arteriovenous malformations. parkridge, ill: american association of neurological surgeons; 1993:175–191. 31. van dijk jm, terbrugge kg, willinsky ra, et al. multidisciplinary management of spinal dural arteriovenous fistulas: clinical presentation and longterm follow-up in 49 patients. stroke 2002;33:1578–83 32. niimi y, berenstein a, setton a, et al. embolization of spinal dural arteriovenous fistulae: results and follow-up. neurosurgery 1997;40:675– 82, discussion 682–83 33. steinmetz mp, chow mm, krishnaney aa, et al. outcome after the treatment of spinal dural arteriovenous fistulae: a contemporary single-institution series and meta-analysis. neurosurgery 2004;55:77– 87, discussion 87–88 34. jakub wojciechowski, przemysław kunert *, arkadiusz nowak, tomasz dziedzic, tomasz czernicki, katarzyna wójtowicz, kamil leśniewski, andrzej marchel. surgical treatment for spinal dural arteriovenous fistulas: outcome, complications and prognostic factors. neurologia neurochirurgia polska (2017) 446-453. http://dx.doi.org/10.1016/j.pjnns.2017.07.001 0028-3843/. doi: 10.33962/roneuro-2020-085 the two stages surgery in the management of central neurocytoma. case series of 10 patients w. bennabi, a. khelifa, y. felissi, l. houari, a. morsli romanian neurosurgery (2020) xxxiv (4): pp. 504-508 doi: 10.33962/roneuro-2020-085 www.journals.lapub.co.uk/index.php/roneurosurgery the two stages surgery in the management of central neurocytoma. case series of 10 patients w. bennabi, a. khelifa, y. felissi, l. houari, a. morsli department of neurosurgery. el oued university hospital, algiers, algeria abstract central neurocytoma is an uncommon benign tumour of the central nervous system. the intraventricular location close to the monro foramina and the attachment to septum pellucidum are characteristics for diagnosis. the encasement of vascular structures represents a surgical challenge. we report a series of 10 cases of central neurocytoma operated at our department 06 of those was operated in two stages intentionally in order to avoid post-operative complications and to obtain complete removal. introduction central neurocytoma (cn) is an extremely rare benign tumour of central nervous system accounting for only 0.1 to 0.5% of brain tumours [1]; although described for the first time by hassoun et al in 1982 [2]; since then, we dispose poor data about theses tumours in the literature [1]. the intraventricular location is the main site of development of these lesions [1, 3]. the brain mri is an important tool for diagnosis; however, the certainty is obtained by histological examination; in which the differential diagnosis is made with oligodendroglioma and ependymoma. surgery represents the only effective option to deal with this kind of lesions, with usually good results, associated with conventional radiation or radiosurgery in case of atypical finding. materials and methods we report a retrospective study of 10 cases of central neurocytoma treated in our department over a period extending from 2003 to 2019. all patients underwent computerized tomography (ct) scans and magnetic resonance imaging (mri) on t1, t2, flair, and t1 injected sequences. results the study includes 10 patients aged between 22-60 years old, with average age of 30.5 years. the sex ratio was 3f/2m. keywords central neurocytoma, ventricular tumour, immunohistochemical markers corresponding author: walid bennabi department of neurosurgery. el oued university hospital, algiers, algeria walidneurosurgeon@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 505 the two stages surgery in the management of central neurocytoma clinical presentation increasing intracranial pressure (icp) symptoms were the main clinical presentation observed in six patients, associated to visual disorder in seven patients; other symptoms were less frequent: seizures were found in two patients, cognitive disturbance in sthree patients, and decreased consciousness in one patient. imaging the computerized tomography (ct scan) showed in the majority of cases heterogeneous lobulated lesion, located frequently in the frontal horn of the lateral ventricle adherent to the septum pellucidum and frequently invading this one, the lesion was associated in most cases with biventricular dilation. the magnetic resonance imaging (mri) showed the characteristic aspect of this lesion: isointense on t1 weighted imaging, iso or hyperintense on t2 weighted imaging with heterogeneous enhancement due to the cystic and calcic components after gadolinium injection; showing a “soap bubble” characteristic aspect. treatment hydrocephalus management six patients consulted with hydrocephalus treated with different modalities: ventriculo-peritonealshunt (vp-shunt) was used in two patients; endoscopic third ventriculostomy (etv) was performed in one patient; rickham reservoir was placed in one patient (table 1). table 1: hydrocephalus managements method number of patients vp-shunt 2 etv 1 rickham reservoir 2 direct approach 1 vp-shunt: ventriculo-peritoneal shunt, etv: endoscopic third ventriculostomy management of the lesion all patients were operated with open approaches, the trans-frontal trans-ventricular approach was used in all patients combined to the trans-callosal approach in three patients. six patients were operated intentionally in two stages. a complete resection was obtained in six (06) patients and subtotal resection in four (04) patients. the resection was limited in the remaining four (04) cases because of the infiltration of the trigone and encasement of the major venous vessels. table 2: surgical approaches patients approach outcome and complications 1st stage 2nd stage patient 1 tftv tftv recidivism patient 2 tftv tftv worsening of the cognitive disturbance patient 3 tftv none none patient 4 tftv transcallosal none patient 5 tftv tftv none patient 6 tftv none none patient 7 tftv transcallosal none patient 8 tftv transcallosal none patient 9 tftv none none patient 10 tftv none none tftv: trans-frontal trans-ventricular pathological findings the diagnosis of cn was based on microscopic examination and several immunohistochemistry markers such as synaptophysin, gfap, olig2, nse, chromatogramine, ps100. patients with ki-67 antigen (mib1) ≥8% was considered as atypical cn. this finding was observed in three patients. adjuvant therapy conventional radiotherapy was used for the three patients with atypical cn whereas surgery was preferred in recurrence with low grade lesion. we didn’t experience stereotactic radiosurgery in our series as well as chemotherapy. mortality and morbidity we noted that one patient presented a worsening of his cognitive disturbance (memory loss) while we didn’t observe any death in our series. although we reoperated one patient for recidivism three years later. (table2) 506 w. bennabi, a. khelifa, y. felissi et al. figure 1. 30 years old female, with six months history of headache vertigo and visual disturbance with progressive worsening, at the admission the patient was conscious presenting visual acuity at 1/10 and 5/10, there was also a stage iii papilledema in both eyes. brain mri objectified a 55 mm intraventricular process located on the left lateral horn, isointense on t1 wi, hyperintense on t2 and flair sequences, with heterogeneous enhancement due to those images were defined a “soap bubble” aspect characteristic for neurocytoma (a, b, c, and d). the patient was operated and the lesion was totally removed through a left trans-frontal transventricular approach. pathological study confirmed the diagnosis of benign neurocytoma in post-operative there was a disappearance of headache and vertigo; the control imaging performed four years later showed no recidivism (e, f, g, and h). (a and e: t1 wi; b and f: t2 wi; c and g: flair sequences; d and h: t1 injected images). 507 the two stages surgery in the management of central neurocytoma figure 2. 22 years old male with one-month history of severe headache clinical exam at the admission found conscious patient without neurologic deficit there was no papilledema. brain mri objectified a process in the left ventricular frontal lateral horn measuring 33 x 45 mm with heterogeneous isosignal in t1wi, t2 wi, and flair sequences with heterogeneous enhancement after gadolinium injection (a, b). the patient was operated and the lesion was subtotaly removed through a left trans frontal trans ventricular approach. one year later a control brain mri objectified a re-expansion of the lesion it measured 50 x 50 x 42 mm (c, d), this time a total removal of the tumour was planned to be performed in two stages first a subtotal removed was performed through the same approach. three years later the brain mri objectified the persistence of the residual amount of the tumour measuring 23 x 34 mm (e, f) so the second stage of the removal was lunched and as planed the total removal obtained through the same approach. the brain mri control images performed four later objectified no evidence of recurrence (g, h). a, c, e, and g axial t2 wi b; b, f, and h injected sequences; and c: flair sequence). discussion the central neurocytoma represents a very small proportion of brain tumours (0.1-0.5%), mostly in the lateral ventricle (77%),[2] with sometimes extension to the third ventricle (26%) [6] and rarely an exclusive localization in the third ventricle. as in our series it occurs frequently at the third decade with extremities ranging from (8 to 67) years old [7,8]. most studies attest that there is no correlation between gender and incidence of central neurocytoma [5,9,10,11]; a slight female predominance was noted in our study, also higher incidences of this lesion was mentioned in some studies in japan, korea and india [8,12,13]. the clinical presentation is dominated by increasing intracranial pressure signs due to obstructive hydrocephalus by obliteration of the foramen of monro associated to cognitive disturbance. seizures, decreased consciousness and vision problems are less frequent. we consider that the cognitive disturbance is due to the close relation of the tumour to the trigone which is frequently infiltrated by the lesion (..).in radiological findings this lesion is mostly located in the anterior half of lateral ventricle appears to be isodense in computerized tomography (ct) scans associated to hyperdensities indicating calcifications which occur in up to 50% of all cases[5, 14].in magnetic resonance imaging (mri) the central neurocytoma appears isointense on t1 weighted imaging, iso-hyperintense on t2 weighted imaging; and with heterogeneous moderate enhancements after contrast agent injection which is the classic “soap bubble” aspect [15]. surgery is the only effective treatment for this kind of lesions and complete resection is associated with better rates of survival and local control, with five-year survival rate of 99% for gross total resection (gtr) and 86% for subtotal resection (str) [19]. the trans-frontal transventricular approach as well as the anterior trans-callosal approach offers the best surgical corridor to all lesions located in the frontal horn of the lateral ventricle [20]. we noted in patients operated in two stages that the resection was safer and easier comparing with those operated in single stage, this can be explained by the devascularization of the lesion in the first stage. due to its histological similarities with other ventricular tumors such as ependymoma oroligodendroglioma the cn is frequently not easy to diagnose, the immunohistological markers are very useful in the diagnosis of this lesion and synaptophysin is the most specific one [13]. adjuvant therapies are indicated in case of atypical, incomplete resection or inoperable recurrence neuocytoma; tow modalities are used conventional radiotherapy and stereotactic radiosurgery; with no statistically difference between both therapies. [16, 18] conclusion the cn is usually a benign tumour of the central nervous system in which the surgical treatment is the only efficient option with very good results in term of survival rates and local control. conventional radiotherapy or stereotactic radiosurgery can be considered in cases of atypical neurocytoma. the two stages surgery adopted in our department can be a good and safe strategy to deal with this kind of haemorrhagic tumours. references 1. waters jd, gonda d, chen cc, carter bs. evidencebased management of central neurocytoma (gross total resection versus subtotal resection and the role of adjunctive therapies). in: alfredo quinoneshinojosa, shaan m.raza, editors. best evidence medicine for brain tumor surgery, 1st edition. new york, stuttgart: thieme medical publishers; 2014. p. 155-61. 2. hassoun, j., gambarelli, d., grisoli, f., et al. central neurocytoma. an electronmicroscopic study of two cases. acta neuropathol 1982; 56, 151–156. 3. peltier j, baroncini m, le gras d, lejeune jp. central 508 w. bennabi, a. khelifa, y. felissi et al. neurocytoma of the lateral ventricule. a series of 35 cases with review of the literature. neurochirurgie 2011; 57: 215-9. 4. kerkeni a, benlakhdher z, rkhami m, sebai r, belguith l, khaldi m, et al. central neurocytoma: study of 32 cases and review of the literature. neurochirurgie 2010; 56: 408-14. 5. hassoun, j., söylemezoglu, f., gambarelli, d., et al. central neurocytoma: a synopsis of clinical and histological features. brain pathol 1993; 3, 297–306. 6. moussa r, abadjian g, nader m, rizk t, samaha e, nohra g, et al. central neurocytoma. four patients. neurochirurgie 2004 ; 50 n6: 639-46. 7. figarella-branger d, soylemezoglu f, kleihues p, hassoun j. central neurocytoma. in: kleihues p, cavenee wk. pathology and genetics of tumors of the nervous system. lyon: iarc press; 2000.p.107-9. 8. sharma mc, deb p, sharma s, sarkar c. neurocytoma: a compre¬hensive review. neurosurg rev 2006;29:27085; discussion 285. 9. maiuri f, spaziante r, de caro ml, cappabianca p, giamundo a, ia¬conetta g. central neurocytoma: clinico-pathological study of 5 cases and review of the literature. clin neurol neurosurg 1995; 97:219-28. 10. patel dm, schmidt rf, liu jk. update on the diagnosis, pathogene¬sis, and treatment strategies for central neurocytoma. j clin neurosci 2013; 20: 1193-9. 11. vasiljevic a, françois p, loundou a, et al. prognostic factors in cen¬tral neurocytomas: a multicenter study of 71 cases. am j surg pathol 2012; 36:220-7. 12. kim dg, chi jg, park sh, et al. intraventricular neurocytoma: clini-copathological analysis of seven cases. j neurosurg 1992; 76:759-65. 13. lee sj, bui tt, chen jhc, lagman c, chung lk, sidhu s et al. central neurocytoma: a review of clinical management and histopathological features. brain tumor res treat 2016; 4(2):49-57. 14. goergen sk, gonzales mf, mclean ca. interventricular neurocyto¬ma: radiologic features and review of the literature. radiology 1992 ; 182:787-92. 15. chen, c.l., shen, c.c., wang, j., et al., 2008. central neurocytoma: a clinical, radiological and pathological study of nine cases. clin neurol neurosurg 110, 129– 136. 16. barani, igor j., raleigh, david r., et larson, david. the management of central neurocytoma: radiotherapy. neurosurgery clinics, 2015, vol. 26, no 1, p. 45-56. 17. garcia rm, evan mi, oh t, barani i, parsa at. intraventricular neurocytoma: a systematic review of stereotactic radiosurgery and fractionated conventional radiotherapy for residual or recurrent tumors. clinical neurology and neurosurgery 2014; 117: 55-64 18. rades, d., & schild, s. e. (2006). value of postoperative stereotactic radiosurgery and conventional radiotherapy for incompletely resected typical neurocytomas. cancer: interdisciplinary international journal of the american cancer society, 106(5), 11401143. 19. rades d, fehlauer f. treatment options for central neurocytoma. neurology 2002; 59:1268-70. 20. mortazavi mm, adeeb n, ellenbogen rg. microsugical removal of intraventricular tumors. in: sekhar ln, fessler rg, editors. atlas of neurosurgical techniques, 2nd edition. new york, stuttgart, delhi, rio de janeiro: thieme medical publishers; 2016.p.154-71. doi: 10.33962/roneuro-2022-070 steps towards neuro-excellence alexandru vlad ciurea, andrei adrian popa romanian neurosurgery (2022) xxxvi (4): pp. 387-388 doi: 10.33962/roneuro-2022-070 www.journals.lapub.co.uk/index.php/roneurosurgery steps towards neuro-excellence alexandru vlad ciurea1,2,3, andrei adrian popa4 1 chief of the neurosurgical department and scientific director of sanador clinical hospital, bucharest, romania 2 professor of neurosurgery. “carol davila” university of medicine and pharmacy, bucharest, romania 3 honorary member of the romanian academy, medical science section 4 student of general medicine. “carol davila’’ university of pharmacy and medicine bucharest, romania abstract between september 28 and october 1, 2022, took place the 47th national congress of the romanian society of neurosurgery. it was organized in iasi, at the palace of culture. on this occasion, the 26th francophone course and the 4th national congress of modern neuroscience were held. these three events represent the quintessence of all current modern neurosurgical problems. extremely important topics were disputed which helped to grow the passion in the hearts of young enthusiasts and their mentors. the entire organization of this very special event was realized with the help of dimas events represented by mr. sebastian draghici together with the management of the romanian society of neurosurgery (president assoc. prof. dr. hab. horia ples). a major role had the current management of the emergency clinical hospital "prof. dr. nicolae oblu" iasi – manager – conf. univ. dr. lucian eva. the event was fully supported by the mayor of iasi – mihai chirica and by the management of the county council – president: costel alexe, vice-president marius sorin danga, sorin alexandru afloarei, but also by the prefect of iasi – petru bogdan cojocaru. this year, the national congress of the romanian society of neurosurgery managed to gather an important number of 47 guest speakers from the country and abroad, 110 primary physicians and specialists in the field of neurosurgery, including also an important number of resident physicians and students from various years of general medicine. keywords 47th national congress of the romanian society of neurosurgery, 26th francophone course, 4th national congress of modern neuroscience corresponding author: alexandru vlad ciurea professor. “carol davila” university of medicine and pharmacy, bucharest, romania prof.avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 388 alexandru vlad ciurea, andrei adrian popa figure 1. the structure of participants the entire congress was organized and held in english, and the presentations were held in the famous halls of the palace of culture (unesco monument), henri coanda hall and the voivodes' hall. the halls presented exceptional architectural aspects, with historical significance such as "bois cement", a material imitating wood, invented by henri coanda, but also modern aspects, which made the audience feel in a world of science and discoveries. a very relevant element was the 26th french course of neurosurgery, quite exceptional, in which prof. carmine mottolese and prof. olivier klein from france, revealed modern and current aspects of pediatric neurosurgical pathology. for the 47th congress of the romanian society of neurosurgery, we note that an important number of personalities of the world participated directly or online. among the international personalities we mention prof. amir samii – germany, prof. samy youssef – usa of america, prof. michael buchfelder – germany, prof. marcos tatagiba – germany, prof. ihsan solaroglu – turkey, prof. franco servadei – italy, prof. virendra deo sinha – india, prof. grigore zapuhlic – moldova, prof. sorin aldea – france, prof. marcel ivanov – england etc. the foreign guests through the special works and the interventions constituted an element of major lifting of the neurosurgical quality of the congress. among the works and university centers in romania we notice the presence of prof. horia ples – timisoara, prof. stefan florian – cluj, prof. mircea gorgan – bucharest, conf. corneliu toader – bucharest, conf. balasa adrian – tg. mures, prof. aurel mohan – oradea etc. we also consider the major progress in intracerebral vascular pathology through the multiple works allocated to endovascular treatment, works presented in a totally fantastic and didactic manner by dr. cristian mihalea (paris) and dr. nicolae dobrin (iasi). one of the works that impressed was that of prof. marcos tatagiba, who presented “surgical treatment of vestibular schwannomas in the era of radiosurgery” bringing a new vision about evolution of pathology and treatment in neurosurgical field. cristian mihalea, an expert in radiological field, kept the audience focused when started to present the neuro-vascular pathologies from his point of view. his works and those of nicolaie dobrin gave to this congress a special value due to their endovascular method used in neuro-vascular pathologies. figure 2. prof. marcos tatagiba presenting his works at the 47th national congress of the romanian society of neurosurgery the young neurosurgeons had a number of sections of development (young neurosurgeon corner) where they had the opportunity to present their surgical and scientific work, carried out with so much devotion and enthusiasm. in these sessions, some of the bravest students presented papers through which they brought to the attention of the entire audience about the dreams and young hopes in the neurosurgical field. an important section was dedicated to the 4th congress of neuroscience in which a whole series of topical elements in neuroscience were reviewed: the accumbens nucleus, the evolution of neural theory, the management of the covid-19 pandemic and many other very impressive papers. at the end of the congress, it was possible to outline as an idea that the entire romanian neurosurgery has made important steps for the european integration, and the future of a center of excellence in neuroscience belongs entirely to the emergency hospital "prof. dr. nicolae oblu" which in these moments possesses elements of robotic neurosurgery, gamma knife surgery and department of neuroscience. doi: 10.33962/roneuro-2022-078 cerebrospinal fluid leak after combat penetrating gunshot wound to the head yurii perekopaiko romanian neurosurgery (2022) xxxvi (4): pp. 430-434 doi: 10.33962/roneuro-2022-078 www.journals.lapub.co.uk/index.php/roneurosurgery cerebrospinal fluid leak after combat penetrating gunshot wound to the head yurii perekopaiko shupyk national healthcare university of ukraine, neurosurgery department, kyiv, ukraine abstract introduction: cerebrospinal fluid leak is a common complication after head gunshot wounds, which commonly leads to infectious complications. this complication may prolong hospital staying and prevents soldiers from return to operation theatre as soon as possible. the purpose of this article is to determine the impact of the quality of primary surgical debridement and other factors that influenced the presence of cerebrospinal fluid leak in the military stuff with gunshot wounds to the head. materials and methods: this is a retrospective study of 20 military cases with cerebrospinal fluid leak, which were admitted during the combat actions in eastern ukraine in the period from march 2014 to the end of december 2017. information was collected on demographics, evacuation assistance, type of injury and infectious complications. r commander version 4.2.0 (http://www.r-project.org) was used for statistical analysis. statistical significance was defined as p<0.05. results: cerebrospinal fluid fistulas were detected in 20 cases (25,31%). factors affecting the rate of leaks are number of re-operations (p<0.001), multiple sites of injury (p=0.002), ventricular injury (p<0.005). csf leakage significantly lengthens hospitalization time. conclusions: csf fistula influenced significantly rate of infection complication. reoperation should follow initial surgery in cases of csf leak development. to avoid development of cerebrospinal fluid fistulas, the operation should be performed by neurosurgeons in specialized department. introduction cerebrospinal fluid leak (csfl) is a common complication of gunshot wounds to the head, which in many cases lead to infectious complications [3, 8]. such patients should receive high-quality and comprehensive medical care, but not all front-line hospitals have neurosurgeons and trained personnel capable of correctly diagnosing and determining tactics. in the conditions of war presence of csfl is often ignored, which can have even fatal consequences [19]. the effectiveness of medical care that will be provided in the next stages, and how quickly the injured personnel will return to combat missions, d e p e n d s o n t h e c o r r e c t d i a g n o s i s a n d t h e c h o s e n t a c t i c s . the purpose of this article is to determine the impact of the quality of primary surgical debridement and other factors that influenced the keywords csf fistula, infection complication, gunshot wound, surgical debridement corresponding author: yurii perekopaiko shupyk national healthcare university of ukraine, neurosurgery department, kyiv, ukraine yuraperekopayko@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 431 cerebrospinal fluid leak after combat penetrating gunshot wound to the head presence of cerebrospinal fluid leak in the military personnel with gunshot wounds to the head. materials and methods the study is based on medical records of patients that were treated at national military medical clinical centre “main military clinical hospital” (nato role iv) from 1st of may 2014 until 31st of december 2017. all patients were servicemen who were injured during military action in the eastern ukraine. medical information was collected from patient records and include demographics, clinical examination findings during evacuation and at the treating hospitals, laboratory results, computed tomography scans. surgical and medical interventions after injury also were collected. statistical analysis was performed using r version 4.1.2 (http://www.r-project.org). in univariable analysis, variables were compared between groups by fisher’s exact test for categorical variables and the wilcoxon signed-rank test for numerical variables. statistical significance was defined as p<0.05. local ethics committee approval was obtained before the study. results among 79 patients with penetrating head injury, we found 20 cases (25,31%) with csfl who were treated in our department and participated in military conflict in eastern ukraine. the average age of the wounded was 28.5±8,69 years (min 19.9, max 54.5), all injured were males. the average number of days in the hospital was 68.4 ±40,89 (min 6, max 157). the average number of days in intensive care unit is 15.2 ±24,87 (min. 2, max. 88). the type of csf leak was defined as one nasal, one orbital, two cases of otorrhea and 16 wound leaks. the most of wounded on battlefield received assistance in the form of self-help or mutual aid, a sterile bandage was applied to stop the bleeding, painkillers were administered. antibiotics were not administered in all cases, but no exact details could be extracted from medical records. consciousness upon admission to the hospital was assessed using the glasgow coma scale (gcs) and presented in table 1. the neurological status was evaluated in all patients, pyramidal signs were detected in 14 wounded which correlated with traumatic origin of the injury. table 1. gcs score on admission to main hospital gcs number 15 14 11 13-12 4 10 1 6 2 4 1 not evaluated 1 the vast majority, 13 observations, were injured with missile fragments, five observations injured with bullets and two patients were injured due to the blast wave. type of injury included: penetrating (11), perforating (4), ricochet (2), tangential (1), and blast wave related injuries (2). injuries reached or passed through the ventricular system were found in nine cases. isolated craniocerebral trauma was diagnosed in 10 cases, in five cases injuries of more than two anatomical areas were found, average injury severity score (iss) was 28.8 ±7,42 (min 18, max 49). all patients underwent head computed tomography (ct) on admission. epidural hematomas were visualized in two cases, subdural hematomas in seven, intracerebral hemorrhage in eight, depressed fractures in three, and intraventricular hemorrhages were found in five cases. according to ct, bone fragments were detected in 16 cases, in 10 cases, bone fragments remained unremoved after the first surgery during previous stage. metal fragments were revealed in 14 patients, and in 6 patients these fragments were removed at the previous stage. all victims underwent surgery. reoperation was performed in 16 cases. the terms of reoperation were different (table 2). table 2. patients which were reoperated because of different causes and types of infection complications id. number ais type of complication type of csfl number of reoperati ons 12383 25 meningitis wound 2 12691 33 wound 2 12823 25 meningoencep halitis wound 1 15287 29 rhinorrh ea 2 20064 35 wound 1 432 yurii perekopaiko 9126 26 abscess, ventriculitis wound 2 21745 25 encephalitis wound 1 24244 25 abscess, ventriculitis wound 2 14020 34 rhinorrh ea 1 28726 26 meningoencep halitis wound 2 32057 25 meningitis wound, otorrhe a 1 13255 25 meningitis wound 1 21464 26 abscess, ventriculitis, empyema wound 1 20429 26 meningitis wound 2 161 26 meningoencef alytis wound 3 24493 45 meningitis rhinorrh ea 2 fourteen patients (70%) developed infectious complications (table 2). diagnosis of infectious complications was based on the following data: clinical symptoms, hyperthermia, redness around the wound, leukocytosis, neutrophilic pleocytosis in the csf, positive meningeal signs, and ct data. in 9 cases the culture was sent from the wound, and in 3 of them pseudomonas aeruginosa was detected. two patients with otorrhea were managed conservatively with dehydration and antibiotic therapy. one of them was also diagnosed with purulent otitis. the otorrhea spontaneously disappeared in these two patients on the 5th and 7th posttraumatic day respectively. one patient with nasal csf leak was also treated conservatively. a patient with transorbital csf leak underwent reoperation by multidisciplinary team with the reconstruction of the anterior cranial fossa. treatment outcomes were assessed using glasgow outcome score (gos) and are shown in table 3. table 3. outcomes in patients with csf fistula gos1 1 gos2 1 gos3 11 gos4 6 gos5 1 table 4. analysis of factors that influence rate of infection csf fistulas yes csf fistula n=20 no csf fistula n=59 p value year of admission 2014 2015 2016 2017 9 (45%) 7 (35%) 3 (15%) 1 (5%) 19 (32.2%) 18 (30.5%) 12 (20.3%) 10 (16.9%) 0.502 gcs on admission to main hospital1 gcs 3-5 gcs 6-12 gcs 13-15 1 (5.3%) 5 (26.3%) 13 (68.4%) 3 (5.2%) 7 (12.1%) 48 (82.8%) 0.294 type of penetrating agent bullet missile blast wave 5 (25%) 13 (65%) 2 (10%) 11 (18.6%) 45 (76.3%) 3 (5.8%) 0.542 multiple site of injury 9 (45%) 7 (11.9%) 0.003 iss on admission 26 (25-30) 25(25-31) 0.357 ventricular injury 9 (45%) 9 (15.3%) 0.011 repeated surgeries 16 (80%) 14 (23.7%) <0.001 discussion based on the literature data, csfl varies from 4.75% to 25.6% [6; 7]. the frequency of csfl in our study was 25.31%. this is most likely due to the fact that the evacuation and medical care system was not well established in the early stages of the war. wound csf leak, otorrhea and rhinorrhea negatively affect treatment outcomes [2; 3; 8; 11; 15]. in our study it was not a significant factor (p=0.196) but we found significant correlation between presents of csf leak and the number of hospitalization days (p=0.007). the most common type of csf leak was csf leak from the wound, less commonly diagnosed were csf otorrhea and rhinorrhea. some authors also distinguish transorbital csf leak [2; 8]. in our series we also had one case. some authors reckon that there is a direct relationship between the patient's condition on admission and the development of csf leak [18]. they state that a lower gcs score has an influence on the rate of csf fistulas. we could not find such a relationship, likely due to lack of information about gcs score on admission at the third and second 433 cerebrospinal fluid leak after combat penetrating gunshot wound to the head echelon, where they mainly hospitalized from combat theatre. in nine patients canal passed through or reached the ventricular system, and the postoperative clinical course after the first surgery was accompanied by wound csfl. our and literature data [2; 3] show that injury to the ventricular system contributes significantly to the risks of csf leak (p = 0.01). early detection of csfl is crucial to prevent the possible development of meningitis or abscess [16]. in 20 wounded with csfl, the number of infection complications reached 70% (14 patients), its twice as many as in the group without csf leak, and this is definitely influence rate of infection complications (ic) in wounded cohort (p = 0.002). the most common cause of wound csf leak is misinterpretation during primary surgical examination (pse) of the wound and the impossibility of transferring an open penetrating wound into a closed one. if, after pse, there is csf leak from the wound, then preference is given to early reoperations before the development of infectious complications. same was also recommended by some authors [11]. neurosurgical treatment should be performed in specialized neurosurgical departments, after a precise examination of the patient, assessment of the general and neurological conditions and nature of the wound. these measures work as a prevention of csf leak and ic, with chances to reduce mortality [3; 10; 11; 17]. high level of wound csf leak in our study in the early period of hostilities may be due to the fact that interventions were mainly carried out in frontline hospitals, where working conditions are quite tense, complicated by massive admissions, which usually affects the quality of care [9]. evidence of this is the large number of repeated surgeries (p<0.001) associated with the presence of wound csf leak, which is comparable to other reports [2; 13]. watertight closure and dural reconstruction is mandatory during surgery [8, 19]. in all our surgeries, we performed reconstruction with the fascia lata. though we agree that other options like using the pericranium and temporal fascia [2 4; 14] or an allograft [7; 8], and artificial dura [20] are also valuable. in addition, plastic of meningea prevents the risk of epilepsy and facilitate cranioplasty in the future, prevents brain prolapse in the wound [4]. all reoperations were performed using magnifying techniques, which in our opinion improves the results and allows to better sewing the defects [12]. in the presence of csf leak our strategy includes multiple lumbar punctures and insertion of continuous lumbar drain. thirty-degree head elevation, antibiotic prophylaxis, control of hydration, electrolytes are important. similar approach was reported by other authors [2; 6-9; 13]. one case of otorrhea was diagnosed on the first day after injury and closed spontaneously within 72 hours after injury. two wounded, who were diagnosed with otorrhea, received medical treatment (moderate dehydration therapy). in other series where the conservative approach and continuous lumbar drain were ineffective, patients underwent surgery [14]. described cases with manifestation of otorrhea within 48 hours of injury [11], also described cases with later manifestations of otorrhea after craniofacial injury [21]. conclusion csf leaks are the risk factor of infectious complications after head gunshot wounds. the presence of csf leaks prolongs hospitalization time. primary surgical treatment of penetrating gunshot wounds to the head is the main element in the prevention of csf leak and infectious complications. it is important to transfer a gunshot wound from a penetrating to a closed nonpenetrating; it is the first step to avoid csfl. primary surgical wound exploration better to perform in specialized neurosurgery departments, after a precise examination of patients using not only x-ray, but also ct. limitations this study has several limitations. firstly, some of the data were missing due to its retrospective design. in addition, the relatively small sample size did not allow us to analyze the contribution to csf leak of other important factors. references 1. aarabi, b. (1987). comparative study of bacteriological contamination between primary and secondary exploration of missile head wounds. neurosurgery, 20(4), 610–616. 2. aarabi, b. (1989). causes of infections in penetrating head wounds in the iran-iraq war. neurosurgery, 25(6), 923–926. 3. aarabi, b., taghipour, m., alibaii, e., & kamgarpour, a. 434 yurii perekopaiko (1998). central nervous system infections after military missile head wounds. neurosurgery, 42(3), 500–509. 4. ameen, a. a. (1984). the management of acute craniocerebral injuries caused by missiles: analysis of 110 consecutive penetrating wounds of the brain from basrah. injury, 16(2), 88–90. 5. bhatoe, h. s. (2001). retained intracranial splinters: a follow up study in survivors of low intensity military conflicts. neurology india, 49(1), 29–32. 6. brandvold, b., levi, l., feinsod, m., & george, e. d. (1990). penetrating craniocerebral injuries in the israeli involvement in the lebanese conflict, 1982-1985. analysis of a less aggressive surgical approach. journal of neurosurgery, 72(1), 15–21. 7. coşar, a., gönül, e., kurt, e., gönül, m., taşar, m., & yetişer, s. (2005). craniocerebral gunshot wounds: results of less aggressive surgery and complications. minimally invasive neurosurgery, 48(2), 113–118. 8. gönül, e., baysefer, a., kahraman, s., çiklatekerlioǧlu, ö., gezen, f., yayla, o., & seber, n. (1997). causes of infections and management results in penetrating craniocerebral injuries. neurosurgical review, 20(3), 177– 181. 9. hagan, r. e. (1971). early complications following penetrating wounds of the brain. journal of neurosurgery, 34(2 pt 1), 132–141. 10. hammon, w. m. (1971). retained intracranial bone fragments: analysis of 42 patients. journal of neurosurgery, 34(2 pt 1), 142–144. 11. hecimovic, i., dmitrovic, b., kurbel, s., blagus, g., vrane, j., & rukovanjski, m. (2000). intracranial infection after missile brain wound: 15 war cases. zentralblatt fur neurochirurgie, 61(2), 95–102. 12. kivelev, j., & hernesniemi, j. (2013). four-fold benefit of wound closure under high magnification. surgical neurology international, 4, 115. 13. meirowsky, a. m., caveness, w. f., dillon, j. d., rish, b. l., mohr, j. p., kistler, j. p., & weiss, g. h. (1981). cerebrospinal fluid fistulas complicating missile wounds of the brain. journal of neurosurgery, 54(1), 44–48. 14. melada, a., marcikić, m., mrak, g., štimac, d., & šćap, m. (2002). cerebrospinal fluid fistula as a consequence of war head injury. military medicine, 167(8), 666–670. 15. nguyen, t. l., & bui, n. t. (1994). prevention of infective complications of craniocerebral war wounds in vietnam (1978-79). journal of clinical neuroscience, 1(2), 118–120. 16. oh, j.-w., kim, s.-h., & whang, k. (2017). traumatic cerebrospinal fluid leak: diagnosis and management. korean journal of neurotrauma, 13(2), 63. 17. rahimi-movaghar, v., jazayeri, s. b., alimi, m., abbassioun, k., & amirjamshidi, a. (2013). lessons learned from war: a comprehensive review of the published experiences of the iranian neurosurgeons during the iraq-iran conflict and review of the related literature. world neurosurgery, 79(2), 346–358. 18. rish, b. l., caveness, w. f., dillon, j. d., kistler, j. p., mohr, j. p., & weiss, g. h. (1981). analysis of brain abscess after penetrating craniocerebral injuries in vietnam. neurosurgery, 9(5), 535–541. 19. starcha v., polishchuk m. (2006) gunshot wounds to the head, kyiv 1996, 117p. 20. white-dzuro, g., entezami, p., wanna, g., russell, p., & chambless, l. (2016). single operation to repair multifocal cerebrospinal fluid fistulae following gunshot wound: a case report. journal of neurological surgery reports, 77(02), e89–e93. 21. yildirim, a. e., dursun, e., divanlioglu, d., ozdol, c., nacar, o. a., corapci, o. e., & belen, a. d. (2014). unusual posttraumatic delayed cerebrospinal fluid rhinorrhea due to gunshot wound. turkish neurosurgery, 24(2), 276–280. 08_paper romanian neurosurgery (2015) xxix 4: 445 457 445 doi: 10.1515/romneu-2015-0060 massive cerebellar infarction: a neurosurgical approach luis rafael moscote salazar1, hernando raphael alvis-miranda2, amit agrawal3, gabriel alcala-cerra1, williem calderon-miranda4, umamaheswara reddy v.5 1neurosurgeon, university of cartagena, colombia 2resident of neurosurgery, university of cartagena, colombia 3professor of neurosurgery, department of neurosurgery, narayna medical college hospital, chinthareddypalem, andhra pradesh (india) 4resident of radiology, unam, mexico df, mexico 5assistant professor of radiology, department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh (india) abstract: cerebellar infarction is a challenge for the neurosurgeon. the rapid recognition will crucial to avoid devastating consequences. the massive cerebellar infarction has pseudotumoral behavior, should affect at least one third of the volume of the cerebellum. the irrigation of the cerebellum presents anatomical diversity, favoring the appearance of atypical infarcts. the neurosurgical management is critical for massive cerebellar infarction. we present a review of the literature. key words: cerebellar infarction, stroke, infratentorial infarction introduction massive cerebellar infarction is less frequent than ischemic strokes in anterior circulation; there is a huge variability on the definition. it is more frequent in younger individuals and those with less comorbidities than those that occur in the anterior circulation, generally having an embolic origin, although principal arteries occlusion of posterior circulation are distinguished. clinically it will depend on the extension of the cerebellar compromise and the simultaneous injury to the encephalic trunk, although the clinical manifestation is non-specific. the ct and mri are still the initial imaging studies. the most useful mode to identify the ischemic area are the diffusion sequences (dwi-adc), given the great sensitivity. the management always emphasizes the patient stabilization, airway protection, appropriate oxygenation, arterial pressure management, glycemic control, euthermia and prevention of deep venous thrombosis and pulmonary thromboembolism. despite all the diagnostic and therapeutic tools, described in this review, the mortality due to ischemic events in the 446 moscote salazar et al massive cerebellar infarction posterior fossa is still high, around 43%, this make us follow up to define the etiology, diagnostic and therapeutic processes, specially in the critical stage. ischemic strokes injuring cerebellum are less frequent that those involving anterior cerebral circulation. according to the findings from different observational studies, it is estimated that infratentorial strokes correspond approximately to 3% of all ischemic events (from 1,9% to 27,2%); (1-7) however, the consequences can be devastating, in many cases, fatal. nowadays, the exact proportion of patients with cerebellar strokes that will develop massive edema is unknown, however, it is estimated that from 17% to 54% of cases can develop edema and threat life. (8) massive cerebellar or space-occupying infarction: in search of a definition in the actuality there is no concrete definition that includes objective criteria to consider a cerebellar infarction as massive or space-occupying. these criteria are variable among specialized centers, which constitute one of the principal limitations for the design, handling, and generalization of investigation works. generally, the presence of cerebellar edema, associated to obstructive hydrocephalus, posterior fossa cistern artery or cerebral trunk compression, is a condition infallible to most definitions, which generally, do not consider the clinical state of the patient, leaving the definition to be linked only to the imaging findings. however, not all the patients with these findings will develop clinical deterioration. in a follow up by koh and coworkers to 35 patients that developed caudal displacement of cerebellar amygdala or rostral displacement of the aqueduct of sylvius or pontocerebellar junction on medium sagittal mri, only 50% developed consciousness deterioration, defined by the study as decrease of 2 points in ecg from the initial assessment. (9) this is why a definition that includes only radiologic findings is imprecise and insufficient to determine the therapeutic conducts. etiology the clinical and etiologic characteristics of patients with infratentorial infarction are different from those with injury to anterior circulation. the national acute stroke israeli survey (nasis) study showed that these patients are generally younger and have less comorbidities, specially heart failure and atrial fibrillation that predispose to cardioembolic events. (10) also it has been found that arterial dissections are less frequent. (11,12) in a follow up of 293 patients by tohgi and coworkers, demonstrated that approximately 24% of cerebellar infarctions are from embolic origin. additionally, they found that most of the cerebellar infarctions were caused by obstruction of superior cerebellar artery (sca) and posterior inferior cerebellar artery (pica), 52% and 49% respectively; while anterior inferior cerebellar artery is only responsible in 20% of the cases. (7) physiopathology after blood flow decrease to the brainstem and cerebellum, a diminution of neural parenchyma and glia capacity to carry on aerobic metabolism occurs, this causes a reduction of atp molecules available for the na/k pump to maintain homeostasis of these romanian neurosurgery (2015) xxix 4: 445 457 447 doi: 10.1515/romneu-2015-0060 electrolytes. at the same time, the osmotic pressure imbalance favors the increase on cellular content of water molecules, generating cytotoxic edema; while hematoencephalic barrier disruption develops vasogenic edema. (13) posterior fossa is a non-distensible space, whose approximate volume is between 165cm3 and 196cm3 and therefore, the tolerance limit is reduced by any expansive process, this may lead to accelerated increase in infrantentorial pressure. (14) because of this, around 81% of cerebellar infarctions may develop radiologic signs of mass effect. (15) increase of edematous cerebellar tissue volume causes compression of adjacent structures, especially of fourth ventricle and brainstem; this can lead to acute obstructive hydrocephalus and major compromise to arterial flow. as the clinical picture get worse and the infratentorial pressure increases, cerebellar amygdala herniation through the foramen magnum may be present, which present clinically with deep coma, ataxic breathing, irregular shape of pupils in medial position, loss of motor response to pain stimuli and absence of ocular cephalic and ocular vestibular reflexes. the other type of cerebellar herniation is the displacement of superior vermis to supratentorial space through the tentorial foramen, also known as ascending or transtentorial herniation. this phenomenon is causes by increase of pressure gradient between anterior fossa and supratentorial space, presenting clinically as consciousness quantitative compromise, ocular motor compromise, ascending conjugated eye movement paresis is frequent, or more characteristic, paresis of conjugated descending eye movements (looking upwards spontaneously). decerebrate and decorticate rigidity are also seen. it may lead to infarction of posterior cerebral artery. (16-18) this event may present as a complication related to the performance of procedures that decrease supratentorial pressure, such as ventricular punctures, ventriculostomies or ventriculoperitoneal shunt, however, the complication of any of these procedures is in low. both types of cerebellar herniation conctitutes terminal stages of the onfratentorial hypertension process, and its prognosis is generally fatal. it is the most frequent cause of dead in the acute state. (8, 19-21) clinical presentation the clinical manifestations will depend on the extension of the cerebellar compromise and especially of the simultaneous injury to the brainstem. the majority of distal arterial infarctions that compromise the cerebellar parenchyma cause few specific symptoms, such as vomit, walking abnormalities, cephalea and vertigo. furthermore, the clinical signs such as dysarthria, ataxia and nystagmus are often hard to detect or may be confused with other benign disorders of peripheral vestibular system. (3) thus, it is not surprising that about 30% of patients receive a wrong diagnosis at the moment the symptoms begin, especially when the patients are younger than 60 years old or have vertebral artery dissections or medial branch obstruction of the posterior inferior cerebellar artery, whose neurologic symptoms and signs may be subtle. (22-24) among the clinical variables that must 448 moscote salazar et al massive cerebellar infarction increase the suspicion of a cerebellar infarction there is the presence of moderate to severe unbalance, the presence of vertigo for more that 72 hours since the beginning of the symptoms and abnormalities in the neurologic examination. (25) nevertheless, up to 10% of cases may present vertigo as the only symptom and in these cases, more than 90% are secondary to infarction in the medial branch of the posterior inferior cerebellar artery. (26) for proper identification of these cases, one of the most useful maneuvers is cephalic impulse test, in which, the absence of a corrective shake highly decreases the probability that symptoms are caused by peripheral injuries of the vestibular system (vestibular neuritis, ménière’s disease, etc). (23, 27) another sign with highly diagnostic value is spontaneous nistagmus, especially if it has a vertical or rotational component, or variable direction. (25) these signs have to be systematically examined in all patients with acute vertigo in order to rule out cerebellar infarctions, because when overlooked, there is a high risk of complications related to poor clinical examination, with a mortality that can go as high as 40%. (24) table 1 syptom sca aica pica deafness absent frequent absent dizziness frequent absent frequent abnormalitis of consciousness frequent frequent rarely tinnitus rarely frequent absent vertigo frequent frequent very common nausea/vomiting frequent very common very common hallucinations rarely rarely absent cephalea/facial pain rarely absent rarely pain in extremities and trunk absent frequent absent aica: anterior inferior cerebellar artery; sca: superior cerebellar artery; pica: posterior inferior cerebellar artery modified from manto, et al. (28) radiologic assessment when a cerebellar infarction is suspected, a computed tomography scan without contrast material is still the first election imaging study; it allows differentiation of ischemic events from hemorrhagic events. (image 1) nevertheless, it must be considered that bone structures that form the base of skull highly decrease the sensibility to assess the posterior fossa. (3, 29) this explains why in a significant group of patients with ischemic events no abnormality is detected in the initial evaluation, therefore when a cerebellar ischemic event is suspected a magnetic resonance imaging (mri) scan without contrast material should be performed to complete the diagnostic approach. (9, 29) however, the sensibility of standard sequences (t1, t2 and flair) to detect early ischemic romanian neurosurgery (2015) xxix 4: 445 457 449 doi: 10.1515/romneu-2015-0060 changes is also low. (30) (image 2) at the present time the most useful modality to identity the ischemic area is the diffusion sequences (dwi-adc) which have a sensibility around 88% and 100%, even when performed during the first 24 hours after the symptoms have started. its sensibility is also high, between 95%-100%, because of this it must be performed specifically when a cerebellar infarction is suspected. (3, 13, 30, 31) the total extension to the cerebellar tissue with diffusion restriction correlates to the final infarction territory, allowing the distinction of vascular territory that is compromised; it also allows estimating the risk of deterioration, related to the addition of hydrocephalus and/or conversion to hemorrhagic event, in the early stages. (31) additionally, these sequences help to identify small cortical and subcortical injuries that make us suspect a cardioembolic etiology. (30) besides the diagnostic significance, some findings in neurologic imaging allow to estimate the risk of neurological deterioration in the acute phase. koh and coworkers identified several factors related to adverse clinical outcomes, with their respective odds ratio (or), among these there is brainstem deformities, (or=15,1) and the presence of obstructive hydrocephalus (or=26). also, a displacement greater that 5 mm of the fourth ventricle from the middle-clival line may be helpful to estimate the clinical evolution, however, the impact seems to be lower that the one of those previously mentioned signs. (9) the assessment of the cisterns in the posterior fossa is also a strong factor to predict deterioration. it has been demonstrated that those patients in whom they are compressed, the probability of presenting consciousness deterioration is 20 times higher. (9) taneda and coworkers developed a scanning scale to classify the severity of compression based on the appearance of the quadrigeminal cistern in the patients with cerebellar hemorrhage, this scale has also been used for ischemic injury, including: grade i (normal), grade ii (compresses) or grade iii (absent). this scale correlates to the prognosis and not necessarily to the volume of affected tissue or hematoma; for this it is an indicator of infratentorial hypertension, useful in the selection of therapeutic conducts. (32) other imaging characteristics that predict adverse outcome are the compromise of more than two thirds of a cerebellar hemisphere and the conversion to a hemorrhagic event. (9, 33, 34) the risk of conversion to a hemorrhagic event is closely related to the diameter and total cerebellar tissue with infarction. sakamoto and coworkers showed that infarctions with a diameter bigger than 2,7 cm or a volume greater that 4,5 cm3 have a probability of hemorrhagic conversion of 7-11 times superior to those whose extension is smaller. (31) therefore, a strict follow-up by imaging is advisable during hospitalization, since up to 55% of them will develop a hemorrhagic conversion that is clinically significant. (3, 31) because of the different etiologies associated with cerebellar infarctions, different authors have recommended an imaging evaluation of the arterial system in search of underlying injuries when identification of a cardioembolic etiology is not possible in the 450 moscote salazar et al massive cerebellar infarction initial evaluation. (3) however, other study groups recommend performing them systematically, knowing that alone or coexisting alterations may be found along with other potential etiologies in up to 20% of the cases. (12,35) the most recent guidelines from the american stroke society suggest the anatomic vascular assessment as integral component of the initial evaluation of patients with neurologic symptoms that may be attributed to the posterior circulation or those with subclavial steal syndrome (class i recommendation). (35) in the actuality, there are many diagnostic modalities available to identify arterial injuries; among these the digital subtraction angiography stands out; as well as other noninvasive methods such as ultrasonography and ct or mri guided angiography. (36-38) the usefulness of doppler ultrasonography is very limited, specially to assess the ostium and v1 segment of vertebral arteries, where the atherosclerotic injuries are more frequent, thus, it is not recommended for the assessment of posterior circulation. (12, 35) digital subtraction angiography is still the gold standard to assess the intraand extra cranial arterial system; however, it has several deficiencies such as availability, opportunity, requirement of contrast material, ionizing radiation exposure, costs and the risks related to the procedure itself. (39,40) therefore, there have been several advances in non-invasive techniques with ct and mri, which have shown that the specificity and sensibility of imaging obtained by ct are good enough to be recommended as first election method in the assessment of patients with cerebellar infarction. (35-38, 41) although ct angiography is widely available and it is performed rapidly, the patient is exposed to high doses of ionizing radiation and contrast material and may be potentially toxic; this may be a very important limitation, specially for patients in risk of developing contrast material induced nephropathy. despite these limitations, the spatial resolution of ct angiography is way superior to that of mri, especially in the assessment of infratentorial arteries. (42) in the other hand, acquisition of imaging through mri does not require exposure to contrast material and ionizing radiation, making it an alternative choice when other modalities represent an unacceptable risk. however, it must be considered that most of the studies have demonstrated their sensibility is not higher than 70%. (35-38) therapeutic approach the medical treatment of patients with cerebellar infarction is very similar to that recommended for supratentorial infarction, it includes airway protection, proper oxygenation, arterial pressure management, glycemic control, euthermia, prevention of deep venous thrombosis and pulmonary thromboembolism. also, the conventional treatment with antiaggregant and statints, is also recommended in these patients. (30, 35) the intensive control of patients with massive cerebellar infarction is similar to the one of patients with infarct in the middle cerebral artery, which has been deeply reviewed previously. (13) despite the start of an appropriate complementary medical treatment, the romanian neurosurgery (2015) xxix 4: 445 457 451 doi: 10.1515/romneu-2015-0060 available observational studies have demonstrated that the conservative treatment as the only measure is associated with a high mortality rate, close to 43% and can go as high as 85% in those patients that reach deep coma. (8) in the other hand, the result of a complementary treatment that includes appropriate required surgical procedures tends to have favorable results. the surgical treatment is the cornerstone of massive cerebellar infarction management. according to a review by neugebauer et al. the survival rate of patients treated surgically was superior that 75%. the subgroup analysis found that for those who were treated only with ventriculostomy the survival rate was 81,6%, for those who underwent decompression of the posterior fossa, 76,8%, an 77,5% for those who underwent both procedures simultaneously. (8) because of the mentioned previously, multidisciplinary assessment and management is recommended, ideally in a unit that specializes in the management of patients with infarction whose characteristics allow early surgical intervention if needed. when there is no infarction specialized unit available, an alternative choice is intensive care unit. the rigorous monitoring is essential, especially during the acute stage of the event, because about 50% of patients will deteriorate during the infarction, especially in the first five to seven days after the beginning of symptoms. (2, 6, 8, 43, 44) the neurological complications that may present during this stage are: recurrent ischemic events, large brainstem infarction, brainstem-encephalon compression by the infarcted hemisphere, obstructive hydrocephalus, and descending or ascending cerebellar herniation. the surgical treatment of patients with cerebellar infarction has as main goal to control supratentorial obstructive hydrocephalus and infratentorial intracranial pressure. although there are several therapeutic approaches, the superiority of each of them is not know for sure, because there are no clinical trials that allow to clear the uncertainty. thanks to this, there is a remarkable variability between the therapeutic approaches used in each medical center. (45) we propose an algorithm for the clinical management of massive posterior infarct that can be used by the treating medical team. (see algorithm below). in the actuality, there are no comparative studies that evaluate the effectiveness of surgical decompression and cerebrospinal fluid diversification procedures, alone or in combination, and the conservative treatment in each particular circumstance. therefore, only through a detailed analysis, the information obtained from the clinical examination and the findings from neurologic imaging may determine the best therapeutic option for each patient. in the neurologic images it must be evaluated carefully the aspect of peritruncal cisterns, the appearance of fourth ventricle, the size and morphology of supratentorial ventricular system. acute obstructive hydrocephalus is one of most frequent complications of cerebellar infarctions, presenting in 10,9 to 27,2% of cases. (2, 44) its evolution is generally progressive; reaching abrupt changes in the state of consciousness whose consequences may even be lethal if treatment is not started 452 moscote salazar et al massive cerebellar infarction promptly. the management of hydrocephalus must be aggressive; as soon as dilation of temporal horns of lateral ventricles becomes evident. in the actuality, control of hydrocephalus may be accomplished through several techniques; among these techniques there is ventriculoperitoneal shunting, external ventricular shunting, ventriculostomy, endoscopic ventriculocisternostomy of third ventricle. however, some authors have recommended surgical decompression of posterior fossa as treatment, based on the concept that the cause of hydrocephalus is the asymmetrical deformation of the fourth ventricle. (30, 34, 36) in the absence of comparative studies, the most accepted conduct in the majority of centers is to perform a cerebrospinal fluid shunt. also, the latest guidelines from the american stroke association recommend the implantation of catheters for ventricular draining of patients with acute hydrocephalus secondary to ischemic infarction (class i recommendation). (30) nevertheless, the clinical status posterior to the control of hydrocephalus must be monitored strictly, specially during the first hours after surgery, because in case that there is no clinical improvement additional exams should be performed in order to determine whether there is compression of infratentorial structures and the functional status. (8, 30, 47) in the absence of hydrocephalus, the neurologic causes of persistent deterioration in the state of consciousness are: 1. brainstem compression by the infarcted hemisphere. 2. repetitive ischemic events, supraor infratentorial. 3. extensive infarctions of brainstem. 4. descending (transforaminal) or ascending (transtentorial) herniation. the importance of performing an accurate differential diagnosis is preponderant for subsequent decision making in the therapy. for this, there are basically 2 approaches: 1) decompressive craniectomy of posterior fossa. the american stroke society recommends this procedure in combination with aggressive medical treatment to relieve brainstem compression and as therapeutic strategy in those cases that show clinical or imaging signs of cerebral herniation (class i recommendation; evidence level b). (30) the ideal indication for the procedure is those cases that represent deterioration in the state of consciousness, associated with radiological signs of hypertension within the posterior fossa, such as compression of basal cisterns or displacement from the middle-clival midline, in those who do not have active hydrocephalus and no irreversible injury to the brainstem is present. (6, 8) identification of brainstem reflexes in the clinical examination. 2) perform control mri, which is very useful to identify if whether there are changes in the intensity in the brainstem that confirm the presence of ischemic injury in the anatomical region that contains the reticular activating substance. also, it allows identification of new ischemic events, which are specially frequent in those patients whose embolism has a cardiogenic origin. it has been shown that in the cases that mri confirms an extended infarction in the brainstem, the romanian neurosurgery (2015) xxix 4: 445 457 453 doi: 10.1515/romneu-2015-0060 survival and functionality prognosis is adverse, therefore, the literature recommends limiting therapeutic effort. (6, 8) however, performing a mri in the critical patient may be unpractical because it requires great acquisition time and wide electromagnetic field, which is incompatible with several life support and monitoring elements. to avoid this, an alternative that is becoming highly acceptable is the functional evaluation of brainstem through neurophysiologic exams, which can be performed even bedside in the intensive care unit. (48, 50) in patients with cerebellar and brainstem infarction, the brainstem auditory evoked response and somatosensory evoked response generally give accurate estimations about survival and functional prognosis. brainstem auditory evoked response measure transmission through the cochlear nerve, superior olive, lateral lemniscus and inferior colliculus; these allow extension of ischemic compromise in the auditory pathways that are found in the pons. (51) the somatosensory evoked response is more reliable than brainstem auditory evoked response. figure 1 brain ct scan showing infarction in the posterior fossa figure 2 mri showing cerebellar infarction 454 moscote salazar et al massive cerebellar infarction cephalic impulse test. a) normal response. when rapid cephalic rotation is performed, conjugated look remains focused on the look’s target. b) abnormal response or “positive test”. license creative commons non-commercial attribution. (26) http://creativecommons.org/licenses/by-nc/3.0/ conclusions despite the large variability of massive cerebellar infarction definitions, this is characterized by cerebellar edema associated with obstructive hydrocephalus, compression of cisterns in the posterior fossa or brainstem; however, it does not consider the patient’s clinical status. massive cerebellar infarction is more frequent in younger individuals than those infarctions involving anterior circulation, in patients with less comorbidity, and generally they have an embolism as etiology, although obstructions in the principal arteries of posterior circulation are distinguished. the clinical presentation will depend on the extension of cerebellar injury and specially, the simultaneous injury to the brainstem, although the clinical picture is nonspecific. ct and mri are still the first choice imaging studies, considering bone findings in the posterior fossa when assessed by ct scan. the most useful mode to identify the ischemic territory is the diffusion sequence (dwiadc), due to the high sensibility even when performed during the first 24 hours after the symptoms have started. the management is similar to that in supratentorial ischemic events, emphasizing at all time patient stabilization, airway protection, proper oxygenation, arterial pressure control, glycemic control, euthermia, prevention of deep venous thrombosis and pulmonary thromboembolism. despite the knowledge of all these diagnostic and therapeutic tools, previously discussed in the review, the mortality caused by ischemic events in the posterior fossa is still high, around 43%, this force us to follow up to establish an etiology, diagnostic and therapeutic processes, specially in the critical patient. correspondence dr. luis rafael moscote university of cartagema colombia e-mail: mineurocirujano@aol.com references 1. shenkin ha, zavala m. cerebellar strokes: mortality, surgical indications, and results of ventricular drainage. lancet [internet]. 1982 aug 21 [cited 2014 jul 10];2(8295):429–32. available from: http://www.ncbi.nlm.nih.gov/pubmed/6124817 2. baldauf j, oertel j, gaab mr, schroeder hws. endoscopic third ventriculostomy for occlusive hydrocephalus caused by cerebellar infarction. neurosurgery [internet]. 2006 sep [cited 2014 jul 10];59(3):539–44; discussion 539–44. available from: http://www.ncbi.nlm.nih.gov/pubmed/16955035 3. edlow ja, newman-toker de, savitz si. diagnosis and initial management of cerebellar infarction. lancet neurol [internet]. 2008 oct [cited 2014 jul 10];7(10):951– romanian neurosurgery (2015) xxix 4: 445 457 455 doi: 10.1515/romneu-2015-0060 64. available from: http://www.ncbi.nlm.nih.gov/pubmed/18848314 4. jauss m, krieger d, hornig c, schramm j, busse o. surgical and medical management of patients with massive cerebellar infarctions: results of the germanaustrian cerebellar infarction study. j neurol [internet]. 1999 apr [cited 2014 jul 10];246(4):257–64. available from: http://www.ncbi.nlm.nih.gov/pubmed/10367693 5. andoh t, sakai n, yamada h, hattori t, miwa y, hirata t, et al. [cerebellar infarction: analysis of 33 cases]. no shinkei geka [internet]. 1990 sep [cited 2014 jul 10];18(9):821–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/2234303 6. raco a, caroli e, isidori a, salvati m. management of acute cerebellar infarction: one institution’s experience. neurosurgery [internet]. 2003 nov [cited 2014 jul 10];53(5):1061–5; discussion 1065–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/14580272 7. tohgi h, takahashi s, chiba k, hirata y. cerebellar infarction. clinical and neuroimaging analysis in 293 patients. the tohoku cerebellar infarction study group. stroke [internet]. 1993 nov [cited 2014 jul 10];24(11):1697–701. available from: http://www.ncbi.nlm.nih.gov/pubmed/8236346 8. neugebauer h, witsch j, zweckberger k, jüttler e. space-occupying cerebellar infarction: complications, treatment, and outcome. neurosurg focus [internet]. 2013 may [cited 2014 jul 10];34(5):e8. available from: http://www.ncbi.nlm.nih.gov/pubmed/23634927 9. koh mg, phan tg, atkinson jl, wijdicks ef. neuroimaging in deteriorating patients with cerebellar infarcts and mass effect. stroke [internet]. 2000 sep [cited 2014 jul 10];31(9):2062–7. available from: http://www.ncbi.nlm.nih.gov/pubmed/10978030 10. korn-lubetzki i, molshatzki n, benderly m, steiner i. the relatively good outcome of cerebellum-brainstem ischemic strokes. eur neurol [internet]. 2013 jan [cited 2014 jul 10];69(1):8–13. available from: http://www.ncbi.nlm.nih.gov/pubmed/23146821 11. putaala j, haapaniemi e, kaste m, tatlisumak t. how does number of risk factors affect prognosis in young patients with ischemic stroke? stroke [internet]. 2012 feb [cited 2014 jul 10];43(2):356–61. available from: http://www.ncbi.nlm.nih.gov/pubmed/22052508 12. glass ta, hennessey pm, pazdera l, chang h-m, wityk rj, dewitt ld, et al. outcome at 30 days in the new england medical center posterior circulation registry. arch neurol [internet]. 2002 mar [cited 2014 jul 10];59(3):369–76. available from: http://www.ncbi.nlm.nih.gov/pubmed/11890839 13. godoy d, piñero g, cruz-flores s, alcalá cerra g, rabinstein a. malignant hemispheric infarction of the middle cerebral artery. diagnostic considerations and treatment options. neurologia [internet]. 2013 apr 16 [cited 2014 jul 10]; available from: http://www.ncbi.nlm.nih.gov/pubmed/23601756 14. bagci am, lee sh, nagornaya n, green ba, alperin n. automated posterior cranial fossa volumetry by mri: applications to chiari malformation type i. ajnr am j neuroradiol [internet]. 2013 sep [cited 2014 jul 10];34(9):1758–63. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3773013&tool=pmcentrez&rendertype=abstract 15. amarenco p. the spectrum of cerebellar infarctions. neurology [internet]. 1991 jul [cited 2014 jul 10];41(7):973–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/2067660 16. adamson dc, dimitrov df, bronec pr. upward transtentorial herniation, hydrocephalus, and cerebellar edema in hypertensive encephalopathy. neurologist [internet]. 2005 may [cited 2014 jul 10];11(3):171–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/15860139 17. lankford j, butler ij. transient tonic upgaze deviation: a neuro-ophthalmological complication of acute cerebellitis. j child neurol [internet]. 2013 jul [cited 2014 jul 10];28(7):942–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/22914381 18. gurol me, st louis ek. treatment of cerebellar masses. curr treat options neurol [internet]. 2008 mar [cited 2014 jul 10];10(2):138–50. available from: http://www.ncbi.nlm.nih.gov/pubmed/18334136 19. amarenco p, hauw jj. cerebellar infarction in the territory of the superior cerebellar artery: a clinicopathologic study of 33 cases. neurology [internet]. 1990 sep [cited 2014 jul 10];40(9):1383–90. available from: http://www.ncbi.nlm.nih.gov/pubmed/2392223 20. amarenco p, hauw jj. [edematous cerebellar infarction. a clinico-pathological study of 16 cases]. neurochirurgie [internet]. 1990 jan [cited 2014 jul 10];36(4):234–41. available from: http://www.ncbi.nlm.nih.gov/pubmed/2277660 21. keidel m, galle g, wiedmayer j, taghavy a. [malignant cerebellar infarct]. fortschr neurol psychiatr 456 moscote salazar et al massive cerebellar infarction [internet]. 1984 aug [cited 2014 jul 10];52(8):277–83. available from: http://www.ncbi.nlm.nih.gov/pubmed/6479828 22. masuda y, tei h, shimizu s, uchiyama s. factors associated with the misdiagnosis of cerebellar infarction. j stroke cerebrovasc dis [internet]. 2013 oct [cited 2014 jul 10];22(7):1125–30. available from: http://www.ncbi.nlm.nih.gov/pubmed/23186911 23. lee h. neuro-otological aspects of cerebellar stroke syndrome. j clin neurol [internet]. 2009 jun [cited 2014 jul 10];5(2):65–73. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=2706413&tool=pmcentrez&rendertype=abstract 24. savitz si, caplan lr, edlow ja. pitfalls in the diagnosis of cerebellar infarction. acad emerg med [internet]. 2007 jan [cited 2014 jul 10];14(1):63–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/17200515 25. casani ap, dallan i, cerchiai n, lenzi r, cosottini m, sellari-franceschini s. cerebellar infarctions mimicking acute peripheral vertigo: how to avoid misdiagnosis? otolaryngol head neck surg [internet]. 2013 mar [cited 2014 jul 10];148(3):475–81. available from: http://www.ncbi.nlm.nih.gov/pubmed/23307911 26. nelson ja, viirre e. the clinical differentiation of cerebellar infarction from common vertigo syndromes. west j emerg med [internet]. 2009 nov [cited 2014 jul 10];10(4):273–7. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=2791733&tool=pmcentrez&rendertype=abstract 27. maranhão et, maranhão-filho p. vestibulo-ocular reflex and the head impulse test. arq neuropsiquiatr [internet]. 2012 dec [cited 2014 jul 10];70(12):942–4. available from: http://www.ncbi.nlm.nih.gov/pubmed/23295423 28. manto m. cerebellar stroke. cerebellar disorders a practical approach to diagnosis and management. cambridge: cambridge university press; 2010. p. 88–101. 29. simmons z, biller j, adams hp, dunn v, jacoby cg. cerebellar infarction: comparison of computed tomography and magnetic resonance imaging. ann neurol [internet]. 1986 mar [cited 2014 jul 10];19(3):291–3. available from: http://www.ncbi.nlm.nih.gov/pubmed/3963774 30. jauch ec, saver jl, adams hp, bruno a, connors jjb, demaerschalk bm, et al. guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the american heart association/american stroke association. stroke [internet]. 2013 mar [cited 2014 jul 10];44(3):870–947. available from: http://www.ncbi.nlm.nih.gov/pubmed/23370205 31. sakamoto y, kimura k, iguchi y, shibazaki k, aoki j. hemorrhagic transformation in acute cerebellar infarction. cerebrovasc dis [internet]. 2011 jan [cited 2014 jul 10];32(4):327–33. available from: http://www.ncbi.nlm.nih.gov/pubmed/21921595 32. taneda m, hayakawa t, mogami h. primary cerebellar hemorrhage. quadrigeminal cistern obliteration on ct scans as a predictor of outcome. j neurosurg [internet]. 1987 oct [cited 2014 jul 10];67(4):545–52. available from: http://www.ncbi.nlm.nih.gov/pubmed/3655893 33. reddy ak, saradhi v, panigrahi m, rao tn, tripathi p, meena ak. decompressive craniectomy for stroke : indications and results. neurol india [internet]. 2002 dec [cited 2014 jul 10];50 suppl:s66–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/12665881 34. michel p, arnold m, hungerbühler h-j, müller f, staedler c, baumgartner rw, et al. decompressive craniectomy for space occupying hemispheric and cerebellar ischemic strokes: swiss recommendations. int j stroke [internet]. 2009 jun [cited 2014 jul 10];4(3):218– 23. available from: http://www.ncbi.nlm.nih.gov/pubmed/19659825 35. brott tg, halperin jl, abbara s, bacharach jm, barr jd, bush rl, et al. 2011 asa/accf/aha/aann/aans/acr/asnr/cns/sai p/scai/sir/snis/svm/svs guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary. stroke [internet]. 2011 aug [cited 2014 jul 10];42(8):e420–63. available from: http://www.ncbi.nlm.nih.gov/pubmed/21282494 36. nguyen-huynh mn, wintermark m, english j, lam j, vittinghoff e, smith ws, et al. how accurate is ct angiography in evaluating intracranial atherosclerotic disease? stroke [internet]. 2008 apr [cited 2014 jul 10];39(4):1184–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/18292376 37. bash s, villablanca jp, jahan r, duckwiler g, tillis m, kidwell c, et al. intracranial vascular stenosis and occlusive disease: evaluation with ct angiography, mr angiography, and digital subtraction angiography. ajnr romanian neurosurgery (2015) xxix 4: 445 457 457 doi: 10.1515/romneu-2015-0060 am j neuroradiol [internet]. 2005 may [cited 2014 jul 10];26(5):1012–21. available from: http://www.ncbi.nlm.nih.gov/pubmed/15891154 38. skutta b, fürst g, eilers j, ferbert a, kuhn fp. intracranial stenoocclusive disease: double-detector helical ct angiography versus digital subtraction angiography. ajnr am j neuroradiol [internet]. 1999 may [cited 2014 jul 10];20(5):791–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/10369348 39. leffers am, wagner a. neurologic complications of cerebral angiography. a retrospective study of complication rate and patient risk factors. acta radiol [internet]. 2000 may [cited 2014 jul 10];41(3):204–10. available from: http://www.ncbi.nlm.nih.gov/pubmed/10866072 40. willinsky ra, taylor sm, terbrugge k, farb ri, tomlinson g, montanera w. neurologic complications of cerebral angiography: prospective analysis of 2,899 procedures and review of the literature. radiology [internet]. 2003 may [cited 2014 jul 10];227(2):522–8. available from: http://www.ncbi.nlm.nih.gov/pubmed/12637677 41. hirai t, korogi y, ono k, nagano m, maruoka k, uemura s, et al. prospective evaluation of suspected stenoocclusive disease of the intracranial artery: combined mr angiography and ct angiography compared with digital subtraction angiography. ajnr am j neuroradiol [internet]. 2002 jan [cited 2014 jul 10];23(1):93–101. available from: http://www.ncbi.nlm.nih.gov/pubmed/11827880 42. graf j, skutta b, kuhn fp, ferbert a. computed tomographic angiography findings in 103 patients following vascular events in the posterior circulation: potential and clinical relevance. j neurol [internet]. 2000 oct [cited 2014 jul 10];247(10):760–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/11127530 43. cano lm, cardona p, quesada h, mora p, rubio f. [cerebellar infarction: prognosis and complications of vascular territories]. neurologia [internet]. [cited 2014 jul 10];27(6):330–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/22341984 44. khan m, polyzoidis ks, adegbite ab, mcqueen jd. massive cerebellar infarction: “conservative” management. stroke [internet]. [cited 2014 jul 10];14(5):745–51. available from: http://www.ncbi.nlm.nih.gov/pubmed/6658959 45. mostofi k. neurosurgical management of massive cerebellar infarct outcome in 53 patients. surg neurol int [internet]. 2013 jan [cited 2014 jul 10];4:28. available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?ar tid=3604818&tool=pmcentrez&rendertype=abstract 46. adams hp, adams rj, brott t, del zoppo gj, furlan a, goldstein lb, et al. guidelines for the early management of patients with ischemic stroke: a scientific statement from the stroke council of the american stroke association. stroke [internet]. 2003 apr [cited 2014 jul 10];34(4):1056–83. available from: http://www.ncbi.nlm.nih.gov/pubmed/12677087 47. kudo h, kawaguchi t, minami h, kuwamura k, miyata m, kohmura e. controversy of surgical treatment for severe cerebellar infarction. j stroke cerebrovasc dis [internet]. 2007 [cited 2014 jul 10];16(6):259–62. available from: http://www.ncbi.nlm.nih.gov/pubmed/18035243 48. itoh a, kim ys, yoshioka k, kanaya m, enomoto h, hiraiwa f, et al. clinical study of vestibular-evoked myogenic potentials and auditory brainstem responses in patients with brainstem lesions. acta otolaryngol suppl [internet]. 2001 jan [cited 2014 jul 10];545:116–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/11677723 49. deftereos sn, panagopoulos g, eleftheriadou a, korres s, georgonikou d, kandiloros d, et al. using vestibular evoked myogenic potentials to localise brainstem lesions. a preliminary report. b-ent [internet]. 2008 jan [cited 2014 jul 10];4(4):215–9. available from: http://www.ncbi.nlm.nih.gov/pubmed/19227026 50. burghaus l, liu w-c, dohmen c, bosche b, haupt wf. evoked potentials in acute ischemic stroke within the first 24 h: possible predictor of a malignant course. neurocrit care [internet]. 2008 jan [cited 2014 jul 10];9(1):13–6. available from: http://www.ncbi.nlm.nih.gov/pubmed/17982737 51. sand t, kvaløy mb, wader t, hovdal h. evoked potential tests in clinical diagnosis. tidsskr nor laegeforen [internet]. 2013 may 7 [cited 2014 jul 10];133(9):960–5. available from: http://www.ncbi.nlm.nih.gov/pubmed/23652144 romanian neurosurgery (2019) xxxiii (3): pp. 272-276 doi: 10.33962/roneuro-2019-045 www.journals.lapub.co.uk/index.php/roneurosurgery idiopathic normal pressure hydrocephalus. a brief review d. adam1,2, d. iftimie1, cristiana moisescu1 1 department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania abstract idiopathic normal pressure hydrocephalus (inph) is a neurodegenerative disease which affects the elderly, with a significant prevalence in the general population (0,2% 5,9%), thus a common pathology encountered by neurologists and neurosurgeons, alike. although the widespread availability of modern imaging techniques has facilitated the diagnosis of this disorder, the clinical manifestations can often be misleading. also, an overlap with other degenerative or psychiatric diseases can make the differential diagnosis even more challenging. cerebrospinal fluid (csf) diversion procedures are the first line of treatment for inph. nowadays, there are several shunting options available, including: ventriculoperitoneal (the most commonly used), ventriculoatrial, ventriculopleural, ventriculosternal, lumboperitoneal, endoscopic third ventriculostomy. choosing a procedure tailored to the individual patient is essential for therapeutic success. although they are generally straightforward surgical interventions, they associate a high rate of failure, regardless of procedure used, which emphasizes the need for regular clinical and imagistic follow-up. thus, inph remains a disease where there is significant room for improvement, both in diagnosis and treatment. definitions hydrocephalus is produced by an excessive accumulation of cerebrospinal fluid (csf) at the level of the ventricular system that determines a specific clinical picture (depending on the patient’s age) and enlargement of ventricles on imaging studies. normal pressure hydrocephalus, also known as chronic adult hydrocephalus, is clinically characterized by the classic triad: gait, urinary and cognitive dysfunction, associated with ventriculomegaly. normal pressure hydrocephalus can be idiopathic or secondary. idiopathic normal pressure hydrocephalus (inph) is a neurodegenerative disease which affects the elderly, representing a treatable cause of dementia with a prevalence of 0,2% up to 5,9%1,2. clinical picture in 1965, hakim and adams described the clinical picture of this disease, characterized by walking, urinary and cognitive dysfunction (3). keywords idiopathic normal pressure, hydrocephalus, csf shunting corresponding author: dragos iftimie department of neurosurgery, “saint pantelimon” clinical emergency hospital, bucharest, romania iftimie.dragos@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 273 idiopathic normal pressure hydrocephalus: a brief review the patients present an ataxic gait, bradykinetic, with small steps and low cadence, as well as balance disorders. they have difficulty in ascending or descending stairs, in getting up from a sitting position or turning around. in advanced stages, patients become hypertonic, bradykinetic. urinary disfunctions generally manifest as incontinence. in the early stages of the disease, the urinary symptoms consist of urgency in emptying the bladder, but subsequently it is replaced by urinary incontinence, more frequently than fecal incontinence. in advanced stages, patients become indifferent to their urinary disorders. cognitive disorders consist of memory impairment, slow ideation, attention deficits, apathy, depression and aggressiveness. it is important to obtain a correct diagnosis because other diseases present a similar clinical picture. inph symptoms are also encountered in other disorders that must be included in the differential diagnosis, such as: parkinson’s disease, alzheimer’s disease and vascular dementia. similar cognitive impairment can be encountered in schizophrenic patients and the two conditions can also coexist. in vanhala’s opinion, inph is three times more frequent in this category of patients4.a list of other disorders that must be differentiated from inph is presented by bechazeddine5. according to israelsson et al, the prevalence of depression is four times higher in patients with inph compared to the elder population without inph2. imagistic diagnosis modern imagistic methods reveal ventriculomegaly. the size and span of ventricles can be appreciated by calculating certain indices: • evans index (bifrontal index) is the distance between the lateral walls of the frontal horns of the ventricle divided by the internal diameter of the skull at the same level. in inph, the value of this index is ≥ 3 • bicaudate index is equal to the ratio between a line drawn between the two ends of the caudate nuclei and the internal diameter of the skull at the same level • fronto-occipital horn index represents the ratio between the sum of the distances between the lateral walls of the frontal horns and occipital horns of the ventricles respectively and twice the largest internal diameter of the calvaria in the horizontal plane csf physiology and inph physiopathology briefly, it is known that csf is produced at the level of the choroid plexus located in the ventricular system with a rate of 0,3 0,5 ml/min, representing approximately 500 ml every 24 hours. csf travels from the lateral ventricles to the fourth ventricle through the aqueduct of sylvius and subsequently, through the magendie foramen reaches the subarachnoid spinal space and cerebral convexities. csf is reabsorbed at the level of pacchioni’s granulations located parasagitally on the cerebral convexities and afterwards reaches the superior sagittal sinus, entering the blood stream. in the case of inph, one hypothesis suggests that enlargement of ventricles compresses or deforms the axons of the central motor neurons that pass through the medial portion of the corona radiata. parkinson’s disease type symptoms of inph patients are caused by the dysfunction of the nigrostriatal dopaminergic pathways caused by abnormal csf pulsations which affect the substantia nigra and determine the disorder of motor planning.6 the cognitive disorders are produced by involvement of the frontostriatal system, of the projection fibers which pass in the proximity of the lateral ventricles. treatment the majority of inph patients benefit from surgical treatment of csf diversion. preoperatively, there must be a careful selection of patients that respond to this treatment. in order to do so, there are multiple methods to evaluate potential responsiveness and tests which evaluate the degree of clinical improvement: 1) csf pressure: is measured during a lumbar puncture, with the patient positioned in left lateral decubitus, with the help of a manometer. in healthy individuals, the opening pressure is 122 mmh2o, while in inph patients, the pressure varies between 60 – 240 mmh2o, with a mean of 150 mmh2o. this pressure is not constant, a value higher than 245 mm mmh2o indicating secondary noncommunication hydrocephalus, not inph1,7. 2) alleviation of symptoms after repeated 274 d. adam, d. iftimie, cristiana moisescu lumbar punctures with removal of 40 ml csf is a common method for estimating responsiveness, but nonetheless a subjective one. 3) external csf drainage for 72 hours, which determines clinical improvement. it is carried out by inserting an intrathecal catheter in the lumbar area and drainage of 10 ml csf every hour for 72 hours8. 4) postoperative clinical improvement can be evaluated by comparing results of several tests: • timed up and go (tug) • timed up and go cognition (tug-c) • berg balance scale (bbs) • performance oriented mobility assessment (tinetti) • mini mental status examination (mmse) • nph japanese scale • minimal clinically important difference (mcid) • geriatric depression scale 15 surgical treatment is not risk free. therefore, a riskbenefit evaluation must be carried out for each patient. patients under anticoagulant treatment associate a high risk for intracranial haemorrhage. those with cerebrovascular disease have a low rate of response to csf drainage. types of csf drainage • ventriculoperitoneal (vp) shunt is the most frequently used. there are however other shunt options, each with its advantages and disadvantages: • ventriculoatrial (va) • ventriculopleural • ventriculosternal • lumboperitoneal (lp) • endoscopic third ventriculostomy (etv) ventriculoperitoneal shunting is not recommended for patients with a history of multiple abdominal surgery or peritonitis, due to the presence of adhesions and low csf absorption. also, vp shunting is difficult to perform in obese patients. ventriculoatrial shunting can be associated with chronic infections, which if undiagnosed, can lead to shunt nephritis. lumboperitoneal shunt has a similar efficiency compared to ventriculoperitoneal shunt in inph treatment. it is indicated for inph patients who are not ideal candidates for intracranial procedures. lp shunts are technically more difficult to perform in obese patients, in ones with spinal deformity (kyphosis, scoliosis), degenerative lumbar stenosis. in these patients, repeated lumbar dural sac punctures may be necessary, which can lead to venous plexus lesions with blood-stained csf and also radicular lesions.9 endoscopic third ventriculostomy can be performed “d’emblée” or in the case of vp shunt malfunction. a rigid neuroendoscope is introduced through a burr hole placed in the right kocher point (10-13 cm posterior from the nasion and 2-3 cm lateral from the median line) up to the third ventricle, through monro’s foramen. the floor of the third ventricle is entered between the mammillary bodies and the infundibular recess and the fenestration is enlarged by inflating a fogarty catheter’s balloon, thus creating a communication between the third ventricle and the prepontine cistern, representing a 4-6 mm diameter ventriculostomy. the patients who, intraoperatively, immediately after etv present no pulsations on the floor of the third ventricle (“flag signal”), will not improve after etv and need immediate vp shunting10. ventriculosternal shunting in critical situations, when vascular access cannot be performed, intraosseous fluid infusion is a procedure that has been performed for many years11. from this technique, tubbs conceived ventriculosternal shunting. the distal catheter is implanted in the sternal manubrium, after a 4 cm tunnelization. from this point, csf is drained through the internal mammary veins and the azygos vein12. the ventriculosternal shunt represents an alternative to other types of shunting, when they are contraindicated. risks of fat embolism, sternal iatrogenic fracture, brachiocephalic vein injury or vagus nerve injury are disadvantages of this method13. types of valves csf pressure must be measured intraoperatively and a valve corresponding to that pressure must be chosen or in the case of a programmable valve, the opening pressure will be adjusted to the measured pressure. there are low, median and high pressure valves with a range of opening pressure of 20 40 mmh2o, 50 90 mmh2o and 100 – 140 mmh2o, respectively. 275 idiopathic normal pressure hydrocephalus: a brief review csf overdrainage can occur in the case of vp shunts because of the hydrostatic pressure of the liquid column, when the patient is standing. antisiphon systems, placed distally from the valve, prevent overdrainage and intracranial pressure decrease. in the case of programmable valves, pressure values can be adjusted noninvasively, thus avoiding revision surgery to replace the existing valve with a different pressure one. postoperative course preoperatively, patients that will benefit from the shunting procedure must be selected and the surgery must be tailored to the patient’s particularities (type of shunting/valve). in the postoperative period, all patients need clinical and imagistic follow-up in order to evaluate their response to surgical treatment and to obtain an early diagnosis of shunt system malfunction or possible complications. out of the cardinal symptoms of inph, gait disturbances are the first to improve. evaluation of the cognitive component requires psychometric testing. stein and laughfitt scale, black scale or rankin scale can be used14,15. approximatively ¼ of operated patients experience shunt malfunction in the first year after surgery and up to 60% require shunt revision during the next years. the rate of shunt failure in the first year is 20 50%, with a mean of 40%16. two causes contribute to shunt malfunction: inadequate catheter placement and infection. in order to prevent proximal catheter malposition, when the catheter is located paraventricularly or partially intraventricular, adequate placement of ventricular catheter can be achieved with the help of image guidance, stereotaxis, neuronavigation or endoscopy. a correctly placed catheter must float at equal distance from the ventricular walls, far from the choroid plexus and must have a straight trajectory from the burr hole. all catheter perforations must be located intraventricularly in order to prevent its obstruction with paraventricular tissue16. recently, the concept of prevention of readmission and reoperation has been introduced in neurosurgery, from which preventable shunt revision rate was derived and introduced in the us in 2016. the fact that a part of shunt failures are caused by intraventricular catheter malposition was noted. therefore, at the end of each operation a control of catheter position with imagistic guidance is recommended. the rate of shunt infection reported in the literature varies between 1% and 15%. this rate is lower when: antibiotic impregnated catheters are used, 2 layers of gloves are worn by the operators, the number of medical personnel in the operating room is limited, prophylactic antibiotherapy is administered, antibiotics are applied in the surgical wound (bacitracine) etc. all these aforementioned measures can prevent bacterial inoculation during surgery. in the case of febrile patients (temperature > 38oc) with meningeal irritation signs, csf must be obtained through lumbar puncture in order to obtain cultures and determine the microorganisms that are present as well as their antibiotic sensitivity. overdrainage, which occurs more frequently in standing position, in the case of an inadequate valve can determine the formation of a subdural fluid collection, followed by the development of subdural hematoma. in other patients, the drainage is insufficient and the valve must be replaced with a low pressure one. conclusions inph is a frequently encountered condition that is still challenging to diagnose and treat despite significant progress in imaging diagnosis and development of different surgical techniques. although surgical treatment consists of generally straightforward procedures, it associates a high rate of failure, regardless of technique used, which emphasizes the need for regular clinical and imagistic follow-up. thus, inph remains a disease where there is significant room for improvement, both in diagnosis and treatment. references 1. relkin n, marmarou a, klinge p, bergsneider m, black pm. diagnosing idiopathic normal-pressure hydrocephalus. neurosurgery. 2005;57(suppl_3):s2-4-s2-16. doi:10.1227/ 01.neu.0000168185.29659.c5 2. israelsson h, allard p, eklund a, malm j. symptoms of depression are common in patients with idiopathic normal pressure hydrocephalus. neurosurgery. 2016;78(2):161-168. doi:10.1227/neu.0000000000001093. 276 d. adam, d. iftimie, cristiana moisescu 3. hakim s, adams rd. the special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure. observations on cerebrospinal fluid hydrodynamics. j neurol sci. 1965;2(4):307-327. doi:10.1016/0022-510x(65)90016-x. 4. vanhala v, junkkari a, korhonen ve, et al. prevalence of schizophrenia in idiopathic normal pressure hydrocephalus. neurosurgery. 2019;84(4):883-889. doi:10.1093/neuros/nyy147. 5. bech-azeddine r, waldemar g, knudsen gm, et al. idiopathic normal-pressure hydrocephalus: evaluation and findings in a multidisciplinary memory clinic. eur j neurol. 2001;8(6):601-611. http://www.ncbi.nlm.nih.gov/pubmed/11784345. 6. stolze h, kuhtz-buschbeck jp, drücke h, jöhnk k, illert m, deuschl g. comparative analysis of the gait disorder of normal pressure hydrocephalus and parkinson’s disease. j neurol neurosurg psychiatry. 2001;70(3):289-297. doi:10.1136/jnnp.70.3.289. 7. marmarou a, bergsneider m, klinge p, relkin n, black pm. the value of supplemental prognostic tests for the preoperative assessment of idiopathic normal-pressure hydrocephalus. neurosurgery. 2005;57(3 suppl):s17-28; discussion ii-v. doi:10.1227/01.neu.0000168184.01002.60. 8. haan j, thomeer rtwm. predictive value of temporary external lumbar drainage in normal pressure hydrocephalus. neurosurgery. 1988;22(2):388-391. doi:10.1227/00006123-198802000-00020. 9. tucker a, kajimoto y, ohmura t, et al. fluoroscopic-guided paramedian approach for lumbar catheter placement in cerebrospinal fluid shunting: assessment of safety and accuracy. oper neurosurg (hagerstown, md). 2019;16(4):471-477. doi:10.1093/ons/opy176. 10. gangemi m, maiuri f, buonamassa s, colella g, de divitiis e. endoscopic third ventriculostomy in idiopathic normal pressure hydrocephalus. neurosurgery. 2004;55(1):129134; discussion 134. doi:10.1227/01.neu.0000126938.128 17.dc. 11. koschel mj. sternal intraosseous infusions: emergency vascular access in adults. am j nurs. 2005;105(1):66-68. http://www.ncbi.nlm.nih.gov/pubmed/15660000. accessed august 4, 2019. 12. tubbs rs, bauer d, chambers mr, loukas m, shoja mm, cohen-gadol aa. a novel method for cerebrospinal fluid diversion. neurosurgery. 2011;68(2):491-495. doi:10.1227/neu.0b013e3181ffa21c. 13. ming woo py, hung pang pk, chan ky, ching kwok jk. ventriculosternal shunting for the management of hydrocephalus: case report of a novel technique. neurosurgery. 2015;11 suppl 3(supplement3):371-375; discussion 375. doi:10.1227/neu.0000000000000861. 14. stein sc, langfitt tw. normal-pressure hydrocephalus. j neurosurg. 1974;41(4):463-470. doi:10.3171/jns.1974.41.4 .0463. 15. black pm. idiopathic normal-pressure hydrocephalus. j neurosurg. 1980;52(3):371-377. doi:10.3171/jns.1980.52.3. 0371. 16. hayhurst c, beems t, jenkinson md, et al. effect of electromagnetic-navigated shunt placement on failure rates: a prospective multicenter study. j neurosurg. 2010;113(6):1273-1278. doi:10.3171/2010.3.jns091237. doi: 10.33962/roneuro-2022-085 tangential gunshot wound to the head. a case report with review of literature ruqayah a. al-baidar, mustafa ismail, osman elamin, mustafa k. ahmed, alkawthar m. abdulsada, ali m. neamah, aktham o. alkhafaji, samer s. hoz romanian neurosurgery (2022) xxxvi (4): pp. 470-475 doi: 10.33962/roneuro-2022-085 www.journals.lapub.co.uk/index.php/roneurosurgery tangential gunshot wound to the head. a case report with review of literature ruqayah a. al-baidar1, mustafa ismail1, osman elamin2, mustafa k. ahmed3, alkawthar m. abdulsada4, ali m. neamah1, aktham o. alkhafaji1, samer s. hoz5 1 college of medicine, university of baghdad, baghdad, iraq 2 department of neurosurgery, jordan hospital, amman, jordan 3 department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 4 azerbaijan medical university. baku, azerbaijan 5 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract introduction. tangential gunshot wounds (tgsw) to the head is the high-velocity bullet that does not penetrate the cranium but passes through the tissue adjoining the cranial cavity, creating a “gutter” wound and indirectly causing cerebral injury. this article presents a reporting case of tgsw to the head, discusses the mechanism underlying this traumatic injury and the possible complications resulting from it, and reviews of literature. case description. a thirteen-year-old schoolboy was admitted to the emergency department (er) of the neurosurgery teaching hospital in baghdad, iraq, with a tangential gunshot to the head of an unknown source during civilian protests in baghdad. in addition to a seizure attack in the er, his glasgow coma (gcs) scale was 13 initially. the computed tomography showed multiple bilateral brain contusions, interhemispheric haemorrhage, partially depressed fracture of the frontal bone midline, and a paramedian to the left with a significantly depressed skull fracture. then, an urgent decompressive craniectomy was performed. the postoperative course was uneventful, with rapid improvement in gcs of 15 one hour after surgery. on the six-month follow-up, the patient reported no further attacks of seizure. conclusion. tgsws are associated with good gcs and favourable prognosis in most cases unless the patient has been deteriorating or has an associated ich. moreover, in our case, the history taking, mechanism of the injury, rapid evolution, and radiological imaging have an essential effect on the outcome. introduction gunshot injuries to the head represent a driving cause of 6,000 deaths in the united states annually [17]. the majority of all these injuries are deadly, as two-thirds of them die immediately [10]. tangential gunshot wounds (tgsw) to the head were first described by sir geo h. makins, a british surgeon involved in the army from 1899-1902 [5,9]. moreover, keywords tangential gunshot wound, head, skull, ich corresponding author: samer s. hoz department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 471 tangential gunshot wound to the head in tgsw to the head, the high-velocity bullet does not penetrate the cranium. however, it passes through the tissue adjoining the cranial cavity, creating a "gutter" wound and indirectly causing cerebral injury [5]. the absence of intracranial metallic parts of the bullet gives the possibility of a single entry-exit wound in the form of a continuous abrasion, and the presence of underlying intracranial damage on radiological evaluation without direct penetration by the missile is the most characteristics of tgsws. furthermore, tgsws usually present with multiple degrees of brain contusion with or without skull fractures, which, if present, can sometimes contain in-driven bone parts, with or without evidence of skull fracture in imaging studies [5]. this article presents an illustrative case of tgsw to the head, discusses the mechanism underlying this traumatic injury and its possible complications, and reviews the literature. case scenario a thirteen-year-old schoolboy was admitted to the emergency department of the neurosurgery teaching hospital in baghdad, iraq, with a tangential gunshot to the head of an unknown source during civilian protests in baghdad. the patient underwent a primary survey and was immediately sent to take a computed tomography (ct) scan. however, he was aware of the time, place, and date, but he and his escort could not remember the way of the injury. on examination, a grazing head wound was recognized alongside a depressed fracture of the right frontal part of the head with no csf leak. in addition, the patient was fully conscious and aware, obeying commands with a glasgow coma score (gcs) of 15, and no further findings were noticed on neurological examination. along with wound cleaning, the bone fragments were removed, and the patient was kept under observation. after one hour, his condition began to deteriorate, becoming drowsy with a gcs of 13 (eyeopening 4, verbal response 3, and motor response 6). the patient developed multiple attacks of tonicclonic seizures. besides, an urgent non-contrast ct scan of the brain revealed multiple bilateral brain contusions and interhemispheric hemorrhage (figure 1. a) and partial depressed fracture of the frontal bone midline, and a paramedian to the left with a significant depressed skull fracture (figure 1. b). he received prophylactic antiepileptic drugs to control the attacks of seizures and prepare for urgent decompressive craniectomy to restrain rising intracranial pressure and relieve brain swelling. the underlying dura was intact, and no intraoperative complications were encountered. postoperatively the patient rapidly improved with a gcs of 15 one hour after surgery. the patient was discharged one week later with no seizures reported during hospitalization. the patient reported no further seizure attacks during the six-month follow-up appointment, and the radiological evaluation did not show any new abnormalities. figure 1. a: non-contrast ct scan shows an axial section of the brain and bone window showing depressed left frontal skull fracture with underlying multiple bilateral brain contusion and interhemispheric hemorrhage, b: 3d reconstruction brain ct scan showing partial depressed fracture of the frontal bone midline and paramedian to the left with multiple comminution reveals the presence of significant depressed skull fracture. discussion gunshot head injuries are the second leading cause of post-traumatic mortality in the united states [12]. they are categorized into perforating, penetrating, and tangential injuries with different mechanisms and prognoses [5]. however, the tgsw of the head represents a moderate-severe blunt injury with a high-velocity missile that does not penetrate the cranial cavity with/without intracranial damages [1,10,17]. the penetrating gunshot wound (pgsw) has no meaningful differences according to age and education from the tgsws to make them demographically comparable [15]. however, there is little difference between these two groups. pgsw holds high severity compared with tgsw as the pgsw mortality rate is equal to 78% compared with tgsws, which are approximately 18% [6,12]. although hotz ga et al. found in their study that the duration of hospitalization was longer in pgsw than in tgsw, they both have a significant neurological deficit. furthermore, it is necessary to mention that 472 ruqayah a. al-baidar, mustafa ismail, osman elamin et al. if the patient survives the severe stage, which has a higher incidence in the pgsw, they will have the same prognosis [12,14]. patients with tgsws commonly present with a good gcs ranged from13 to 15 in most cases with loss of consciousness which is relatively uncommon [1,6,7,14]. moreover, in typical cases, the bullet does not breach the skull, and no significant fracture is present. furthermore, there is a considerable force directed into the brain that has the potential of causing brain pathologies such as intracranial hematoma (ich) and cerebral contusions which result from disrupted vessels that following the primary damage, site of hematoma related to site tgsws can be temporal, parietal or posterior fossa [1,4,8,16]. on the other hand, some cases may present with forced depressed fracture and tissue loss according to the distance and the missile velocity. in both of the previous presenting categories, many cases are associated with a neurological deficit that requires rehabilitation facilities [7,8].in contrast, the presentation can be only a foot drop as atac et al. [3]. it should be noted that the severity and the prognosis of each patient depend on several factors; the type of the used gun, the velocity of the bullet, and the distance from the target, which is demonstrated clearly in i. b. copley et al. report. accordingly, a very high-velocity missile passes through the adjacent tissue and produces brain damage without penetrating it, while low velocity is associated with tissue loss [1,4]. also, the injured area has a special role anatomically, as adeloy et al. demonstrate the association between the tgsws in the frontoparietal areas of the brain and the features of "longitudinal sinus syndrome" which is a misnomer since the main underlying cause is a cortical injury in which patients presented with limbs paresis and also a cortical form of sensory impairment was noted without venous any occlusion or thrombosis (8, 14). consequently, in the emergency department, the initial management goes with immediate resuscitation and urgent brain ct scan. prophylactic antibiotics and antiepileptic drugs have a unique role in the management. besides that, repeated neurological assessment and radiological imaging are very important [4,14]. it is essential to mention that history taking in such injuries is the mechanism; the rapid evolution and management play a crucial role in the outcome and prognosis of such patients. moreover, the prognosis is also affected by the presence or absence of depressed fracture and intracranial hemorrhages such as subdural (sdh), epidural hematoma (edh), traumatic sah, and ich [13]. however, anglin d et al. found that approximately 25% of patients with tgsw have ich. that means there is a case of ich in every four cases of tgsw. many authors try to generate criteria to predict the presence of ich along with tgsw, but obviously, no clear association is stated. however, if the patient present with one or more of the following conditions along with tgsw, he will have an increased risk of developing ich. the condition is; gcs less than 15 on a presentation or/and if he has a history of a loss of consciousness [4,7,13,14]. according to the mentioned findings, if there is no intracranial pathology, a 12-24h repeated ct scan is a must; as stone et al. demonstrate in their study, a late ich in some cases could be present [1,3,4]. while if there is any acute brain pathology, the time should be less, and the repeated scan should be done in 6h or less if there is any change during the neurological assessment [4]. the line of management and treatment depends on patient status and associated risk. to a much lesser extent, if the patient is alert and oriented about the time and the place, nonoperative management with prophylactic antibiotics and antiepileptic are preferable besides wound cleaning and debridement [1,14]. while in more severe cases with a significant hemorrhage that needs an urgent decompression, surgery will be an option [4,16]. accordingly, in our case, the patient was fully conscious with 15 gcs, then deteriorated to 13 with multiple seizure attacks. the urgent scan show findings necessitate operative management. a craniectomy managed the patient with an elevation of depressed fracture; the superior sagittal sinus (sss) was intact intraoperatively. in addition, the operation went well without complications, and no neurological deficits were documented in the followup period. in general, the overall prognosis in the tgsws is good; özkan ü et al. found in their study that's nearly 60% of patients achieve a good prognosis while the mortality rate less than 19% in other studies, according to the previously mentioned factors and the severity of such cases [1]. 473 tangential gunshot wound to the head without a doubt, we highlight the importance of the history taking in such injures, the mechanism of the injury, the immediate evolution and management and its effect on the outcome. conclusion tgsws are associated with good gcs and favorable prognosis in 60% of cases unless the patient has been deteriorating or has an associated ich. moreover, in our report, the history taking, mechanism of the injury, the immediate evolution, and radiological imaging have an important effect on the outcome. furthermore, the management line and treatment are individualized and dependable on the patient's status and the associated risk factors. all patients of tgsws need close observation in a medical facility for at least the first 24 hours post-trauma. table 1 literature review for tangential gunshot wound to the head (case series) no authors year of publication number of cases insinuation major finding 1 adeloye a [8] 1971 6 nigeria fronto-praitial region of the brain is most likely associated with superior sagittal sinus syndrome 2 copley, i. b. [1] 1991 27 southern africa 1mortality =18.5% 2tangential bullets (especially high velocity) are associated with considerable brain damage, and their effect may delay from a few hours to days 3brain damage can occur in the absence of a skull fracture 4fracture of the inner table may go unnoticed. 3 anglin d [13] 1998 240 los angeles county + university of southern california medical center 125% of all patients with tgsws to the head had ichs. 2there is a higher risk of having ich if the patient has gcs < 15 on presentation or/and a history of a loss of consciousness. 4 hotz ga [12] 2000 11 usa 1penetrating gunshot wound is a more severe and costly injury than a t-gsw to the head 2tgsw possesses significant deficits, and, if the patient survives past the acute phase of recovery 3tgsw has less length of stay compared with penetrating gunshot wounds. 5 özkan ü [15] 2002 39 turkey 159% of them have a good prognosis 2importance of periodical followed up with ct scans. 3in icu, patients’ vital functions should be closely monitored. 4immediate follow-up if an infection is suspected tgsw; tangential gunshot wound to the head, ich; intracerebral hemorrhage, gcs; glasgow coma scale, ct; computed tomography, icu; intensive care unit. table 2 literature review for tangential gunshot wound to the head (case reports) case type /age/sex presentation gcs* imaging management outcome hadas et al. 1990 [7] civilian 27 y male wound in lt temprozygmatic region (lt temporal); 15 minutes later, 15/15 15 minutes later, 8/15 ct scan / lt temporal subdural hematoma craniotomy with hematoma evacuation gos =5 474 ruqayah a. al-baidar, mustafa ismail, osman elamin et al. several vomiting spells stone et al., 1991 [16] civilian 16 y male wound over rt occipital 10/15 one hour later became less than 8/15 ct scan/subdural hematoma in the posterior fossa with rt cerebellar hematoma suboccipital craniectomy with hematoma evacuation gos =5 atac k et al. 2004 [3] civilian 21 y male wound over the scalp with only weakness of left dorsiflexion 15/15 mri/ hyperintense contusion of the rt sfg with mild subdural hematoma conservative management gos =5 robles 2012 [14] military 22 y male rt parietal, posterior linear wound about 12 cm; fracture was observed in the same area 15/15 after 1.5 hours 11/15 ct scan/intracranial occipital hematoma bone fragment, hematoma causing mass effect evacuation of hematoma gos =5 farhat 2012 [14] 19 y male left temple & near small midline wounds 15/15 small left sdh with traumatic sah (small) minor temporal contusion, 8 hours later brain edema conservative management gos =5 the present case 2022 civilian 13 y male right frontal area with a depressed fracture 15/15, one hour later 13/15 with tonic-clonic seizure multiple bilateral brain contusion and interhemispheric urgent decompressive craniectomy gos =5 glasgow outcome score (gos) 1. death, 2. persistent vegetative state, 3. severe disability, 4. moderate disability, 5. low disability glasgow coma scale (gcs) on initial presentation abbreviations tgsw; tangential gunshot wound to the head, pgsw; penetration gunshot wound, ich; intracerebral hemorrhage, gcs; glasgow coma scale, ct; computed tomography. references 1. adeloye a, odeku el. a syndrome characteristic of tangential bullet wounds of the vertex of the skull. journal of neurosurgery. 1971 feb 1;34(2):155-8. 2. anglin d, hutson hr, luftman j, qualls s, moradzadeh d. intracranial hemorrhage associated with tangential gunshot wounds to the head. academic emergency medicine. 1998 jul;5(7):672-8. 3. atac, kaan, et al. foot drop due to cranial gunshot wound. military medicine, 2004, 169.7: 568-569. 4. bratton sl, chestnut rm, ghajar j, et al. guidelines for themanagement of severe traumatic brain injury. vi. indications for intracranial pressure monitoring. j neurotrauma 2007;24(suppl1):s37– 44. 5. copley ib. cranial tangential gunshot wounds. british journal of neurosurgery. 1991 jan 1;5(1):43-53. 6. farhat hi, hood b, bullock mr. a tangential gunshot wound to the head: case report and review of the literature. the journal of emergency medicine. 2012 aug 1;43(2):e111-4. 7. hadas na, schiffer ju, rogev ma, shperber ye. tangential low-velocity missile wound of the head with acute subdural hematoma: case report. the journal of trauma. 1990 mar 1;30(3):358-9. 8. hotz ga, stewart kj, petrin d, villanueva pa, cohn sm, nedd kj, puentes g, duncan r. neurobehavioural outcomes of penetrating and tangential gunshot wounds to the head. brain injury. 2000 jan 1;14(7):649-57. 9. izci y, kayali h, daneyemez m, koksel t. comparison of clinical outcomes between anteroposterior and lateral penetrating craniocerebral gunshot wounds. emergency medicine journal. 2005 jun 1;22(6):409-10. 10. kaufman hh. gunshot wounds to the head. in: ivatury rr, cayten cg. the textbook of penetrating trauma. baltimore: williams & wilkins, 1996, pp 431-3. 11. makins gh. surgical experiences in south africa18991900. smith, elder, london 1901:241 12. martins rs, siqueira mg, santos mt, zanon-collange n, 475 tangential gunshot wound to the head moraes oj. prognostic factors and treatment of penetrating gunshot wounds to the head. 13. özkan ü, kemaloğlu m, özateş m, aydin m. analysis of 107 civilian craniocerebral gunshot wounds. neurosurgical review. 2002 aug 1;25(4):231-6. 14. robles la. high-velocity gunshot to the head presenting as initial minor head injury: things are not what they seem. the american journal of emergency medicine. 2012 nov 1;30(9):2089-e5. 15. stone jl, lichtor t, fitzgerald lf, gandhi yn. civilian cases of tangential gunshot wounds to the head. journal of trauma and acute care surgery. 1996 jan 1;40(1):57-60. 16. stone, james l., et al. hematoma in the posterior fossa secondary to a tangential gunshot wound of the occiput: case report and discussion. neurosurgery, 1991, 28.4: 603-606. 17. trask tw. civilian penetrating head injury. neurotrauma.. 1996:869-89. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0064 article sporadic hemangioblastoma of the filum terminale: case report and review of literature prashant s. gade, vernon velho, harish naik, laxmikant bhople india      496 | gade et al sporadic hemangioblastoma of the filum terminale             doi: 10.2478/romneu-2018-0064 sporadic hemangioblastoma of the filum terminale: case report and review of literature prashant s. gade, vernon velho, harish naik, laxmikant bhople department of neurosurgery, grant government medical college, mumbai, india abstract: hemangioblatomas are low grade, highly vascular tumors usually associated with vhl syndrome and most commonly occurs in the cerebellum. they very rarely occur in the spinal nerve roots and an origin in the filum terminale is exceptionl. a 47 year old man presented with low back pain, paresthesias and stiffness of the both lower limbs. he also had urinary retention and constipation. mri showed an enhancing mass at the l5 vertebral level with multiple dilated and tortuous vessels at both poles of the tumor. digital subtraction angiogram showed the tumor to be supplied by the anterior spinal artery and dural branches of lumbar arteries. at surgery, a well-defined tumor with orange red hue was found to be arising from the filum terminale. the tumor was excised en bloc. histopathological examination showed hemangioblastoma which was confirmed with immunohistochemistry. clinical symptoms improved significantly after surgery. a sporadic hemangioblastoma arising from the filum terminale should be considered as a rare cause of back pain and sciatica. total excision of the tumor usually cures the patient. key words: cauda equina, extramedullary, filum terminale hemangioblastoma sporadic, von hippel-lindau syndrome abbreviations: vhl von hippel-lindau; ct computed tomography; mri magnetic resonance imaging; who world health organization introduction tumors of the cauda equina are uncommon and those arising from the filum terminale are even rarer. most common tumors affecting this region include ependymoma, schwannoma, neurofibroma and meningioma. hemangioblastoma is a rare occurrence at this site, most of them affecting the cervical or thoracic spine. hemangioblastoma of the filum terminale is extremely rare and only a few cases are reported in the literature. here we describe a rare case of hemangioblastoma arising from filum terminale, diagnosed in a patient without clinical criteria of von hippel-lindau (vhl) romanian neurosurgery (2018) xxxii 3: 496 501 | 497             syndrome and briefly review the relevant literature. case report a 47 year old male presented with low back pain radiating to both lower limbs since 5 years. pain was insidious in onset, gradually progressive, ill defined, moderate in intensity and increased in recumbent position. since last 2 years pain increased in intensity especially at night times and became more continuous. he also developed stiffness and paresthesias in both lower limbs. he had to strain to pass urine and also had constipation. family history was unremarkable. on examination, lower limbs were spastic. there was no motor weakness or sensory deficit. screening for vhl syndrome was negative. magnetic resonance imaging (mri) of the lumbosacral region revealed a well-defined intradural lesion at the level of sacralised l5 vertebra. tumor was isointense on t1weighted and hyperintense on t2-weighted images with intense contrast enhancement and numerous flow voids within. multiple dilated, tortuous vessels are seen in the intradural extramedullary compartment extending from d8 to l5 level (figure 1). spinal angiogram showed highly vascular tumor at l5 pedicular level supplied predominantly by anterior spinal artery. other feeders to the tumor were the dural branches from bilateral lumbar arteries. patient underwent l4 to s1 laminectomy through midline incision. thecal sac was found to be expanded and thinned out. durotomy revealed well defined, firm, lobulated mass with orange-red hue. there were dilated venous channels at both poles of the tumor. tumor was arising from the filum terminale and displacing the nerve roots of the cauda equina laterally. tumor was dissected circumferentially, preserving all nerve roots of the cauda equina and removed in an en bloc manner. the dilated venous channels which were entering and leaving the tumor capsule were coagulated and sharply divided (figure 2). histopathology showed a highly vascular tumor composed of vascular channels of various sizes with intervening stromal cells. there were foci of hemorrhage and some vessels were thrombosed. no atypias or mitotic figures were found (figure 3). histopathological diagnosis of hemangioblastoma (reticular variant) was made and confirmed with immunohistochemistry. immunohistochemical stains showed positivity for cd31, cd34 in endothelial cells while stromal cells were neagative for cd34. stromal cells were positive for neuron specific enolase but negative for glial fibrillary acidic protein. s-100, epithelial membrane antigen and cytokeratin stains were negative. postoperatively, he had no new neurological deficit. at 1 month follow-up, he reported significant pain relief with no need for further analgesic. postoperative mri confirmed the complete excision of the tumor. discussion hemangioblastomas are benign, slow growing, highly vascular tumors and considered as grade i in the who classification of cns tumors. 498 | gade et al sporadic hemangioblastoma of the filum terminale             hemangioblastomas account for 1.6 to 2.1 % of all spinal cord tumors. (3) these tumors may occur sporadically (67-75%) or as a part of multisystem involvement in vhl syndrome (25-33%). (3) majority of these lesions are intramedullary, affecting all spinal levels and all compartments. extramedullary disease is relatively uncommon and represents approximately one fifth of all spinal cord hemangioblastomas. (2) the incidence of isolated hemangioblastomas of the cauda equina is unclear. our literature review revealed 26 previously reported cases of sporadic hemangioblastoma occurring in the cauda equina, out of which 15 are described to be arising from the filum terminale. (table 1) table 1 reported cases of sporadic filum terminale hemangioblastomas* authors & year age (yrs) sex spinal level symptoms mr imaging angiogra phy treatment & outcome 1. wyburnmason, 1943 25 f l2-s2 radicular pain na na surgery, improved 2. norstrom et al., 1961 nr nr nr na na nr 3. sloof et al., 1964 51 m l4-s1 nr na na surgery, outcome nr 4. wolbers et al., 1985 36 m l1 radicular & lumbar pain, cauda equina syndrome na, diagnosis by ct na surgery, improved 5. silverman et al., 1986 66 m l2 back & leg pain, partial cauda equina syndrome na, diagnosis based on myelogram na surgery, improved 6. tibbs et al., 1999 35 m l2-l3 lumbar pain, worse on sitting enhancing mass with serpentine flow voids na surgery, improved 7. arbelaez et al, 1999 73 m l1-l2 lumbar & radicular pain enhancing mass with serpentine flow voids na surgery, improved 8. farnetti et al., 2001 57 m l4 lumbar & radicular pain, worse while recumbent enhancing mass with serpentine flow voids na surgery, improved 9. biondi et al., 2005 61 m l3 motor & sensory disturbances enhancing mass with serpentine flow voids yes surgery, unknown 10. nr m nr only sensory disturbances enhancing mass with serpentine flow voids yes surgery, unknown 11. nadkarni et al., 2006 52 m l2-l3 lumbar pain, paresthesias, sphincter disturbances enhancing mass with serpentine flow voids yes surgery, improved 12. ortegamartinez et al., 2007 41 f l3 & s1 lumbar pain, worse in recumbent,better after abortion iso& hyperintense masses with flow voids, no contrast yes surgery, minimal hypesthesia 13. ciapetta et al., 2007 62 f l2-l3 lumbar pain, paresthesias enhancing mass, no flow voids no surgery, improved 14. wong et al., 2007 64 m l4 lumbar pain enhancing mass with serpentine flow voids yes surgery, transient urinary incontinence 15. sergides et al., 2009 75 m l3 asymptomatic, incidental enhancing mass, no flow voids no surgery, no complication 16. present case m l5 lumbar pain, paresthesias, sphincter disturbances enhancing mass with serpentine flow voids yes surgery, improved romanian neurosurgery (2018) xxxii 3: 496 501 | 499             figure 1 magnetic resonance imaging shows intradural extramedullary mass at the level of sacralised l5 vertebra. mass appears isointense on t1 weighted images (a) and hyperintense with flow voids on t2 weighted images (b). t1 weighted contrast images shows enhancing mass with tortuous feeding vessels (c) figure 2 intraoperative photographs showing the surgical steps.(a) duratomy exposed a firm, lobulated, reddish tumor (*)with dilated and tortuous vessels on the surface.(b) tumor was originating from the filum terminale(**).(c)final step showing en bloc resection of the tumor.(d)surgically excised specimen of hemangioblastoma (d) 500 | gade et al sporadic hemangioblastoma of the filum terminale             figure 3 histological section shows a highly vascular tumor composed of vascular channels of varying sizes with intervening vacuolated stromal cell (haematoxylin and eosin, original magnification x 300) filum terminale hemangioblastomas can remain asymptomatic for several years. however as they grow in size, they may cause compression of the surrounding neural structures and cause symptoms. most common symptoms are progressive low back pain, radiating to lower limbs and weakness of the lower limbs. most of the previously reported patients have radicular symptoms except the patient reported by tibbs et al. (7) with further increase in size it may also cause cauda equina syndrome. on mri of the lumbosacral region, hemangioblastoma appears isointense on t1w and hyperintense on t2w. the hyperintensity is characteristically heterogenous due to the flow voids resulting from high vascularity. schwannoma, on the other hand, shows a uniform homogenous hyperintesity on t2w, thus differentiating it from hemangioblastoma. on contrast study, there is marked tumoral enhancement; however, the patterns do not help in differentiating it from other neurogenic tumors. the most characteristic finding on mri is serpentine flow voids of tortuous and convulated vessels (4) which was seen in our case and was also reported by most other authors. spinal angiography is the gold standard in the diagnosis of spinal vascular malformations. it is more sensitive and specific in differentiating solid tumor from vascular malformations. angiography can better define the lesion, provides information about feeding arteries/venous drainage and help in the preoperative embolization. however preoperative embolization was not considered in our case. total surgical resection is the treatment of choice. (5) these tumors should be dissected circumferentially and removed en bloc; intralesional debulking should not be done as it may lead to profuse bleeding. incomplete resection has been associated with a high rate of recurrence. radiosurgery has been used in cases of residual tumor after subtotal tumor excision. (1) histopathologically, hemangioblastomas are benign lesions, partly cystic, consisting of stromal cells and endothelium-lined vascular channels. two histological variants are described; reticular and cellular. in reticular type, stromal cells are evenly distributed around the vascular network while in cellular variant, they are arranged in larger sheets or clusters. on immunohistochemistry, the endothelial cells stain positive for cd34 whereas stromal cells stain negative for the same. (6) immunohistochemistry is also helpful in differentiating it from other tumors. absence of s-1oo, epithelial membrane antigen and cytokeratin rules out the romanian neurosurgery (2018) xxxii 3: 496 501 | 501             schwannoma and meningioma. stromal cell positivity for neuron specific enolase along with absent glial fibrillary acidic protein rules out hemangiopericytoma. inhibin alpha is useful for differentiating hemangioblastoma from other vascular tumors such as capillary hemangioma. conclusion the present case report shows the rare occurrence of intradural extramedullary spinal hemangioblastoma originating from the filum terminale, not associated with vhl syndrome. spinal angiography remains the gold standard for the diagnosis. based on neuroimaging, tumor associated with serpentine flow voids of tortuous and convulated vessels appeared to be the best diagnostic indicator. in addition to the histopathological examination, immunohistochemical stains are needed to make the diagnosis. complete resection of the tumor is considered as the treatment of choice, as recurrence is common with incomplete excision. filum terminale hemangioblastoma even though rare should be included in the differential diagnoses of the tumors of the cauda equina. correspondence dr. prashant s. gade mbbs, dnb (gen surg), mch, dnb (neurosurg) senior resident, department of neurosurgery, grant government medical college, mumbai dr.prashantgade@gmail.com mob. no. 9890129901 references 1. blaty d, malos m, palmrose t, mcgirr s: sporadic intradural extramedullary hemangioblastoma of the cauda equina: case report and literature review. world neurosurg 109: 436-441, 2018 2. brisman jl, borges lf, olgilvy cs: extramedullary hemangioblastoma of the conus medullaris. acta neurochir (wien) 142(9): 1059-1062, 2000 3. browne tr, adams rd, roberson gh: hemangioblastoma of the spinal cord. review and report of five cases. arch neurol 33: 435-441, 1976 4. kunihiro n, takami t, yamagata t, tsuyuguchi n, ohata k: spinal hemangioblastoma of the cauda equina origin not associated with von hippel-lindau syndromecase report. neurol med chir (tokyo) 51(10): 732-735, 2011 5. nadkarni td, menon rk, desai ki, goel a: hemangioblastoma of the filum terminale. j clin neurosci 13: 285-288, 2006 6. taniguchi s, ogikubo o, nakamura t, yamagishi i, hayakawa k, otsuka t, katoh t: a rare case of extramedullary-intradural hemangioblastoma in the thoracic spine. spine 34(26): e969-e972, 2009 7. tibbs re jr, harkey hl, raila fa: hemangioblastoma of the filum terminale: case report. neurosurgery 44(1): 221-223, 1999 doi: 10.33962/roneuro-2021-007 the evolution of eloquent located low grade gliomas surgical approaches, their natural history and molecular classification mihaela coșman, andrei ionuț cucu, alin constantin iordache, bogdan florin iliescu, gabriela florența dumitrecu, dana mihaela turliuc romanian neurosurgery (2021) xxxv (1): pp. 40-47 doi: 10.33962/roneuro-2021-007 www.journals.lapub.co.uk/index.php/roneurosurgery the evolution of eloquent located lowgrade gliomas surgical approaches, their natural history and molecular classification mihaela coșman1, andrei ionuț cucu2, alin constantin iordache2,3, bogdan florin iliescu2,3, gabriela florența dumitrecu4, dana mihaela turliuc2,3 1 department of neurosurgery, emergency county hospital, braila, romania ² department of neurosurgery, “n. oblu” emergency clinical hospital, iași, romania ³ “gr. t. popa university of medicine and pharmacy”, department of neurosurgery, iași, romania 4 department of anatomopathology. “n. oblu” emergency clinical hospital, iaşi, romania abstract low-grade glioma is characterized by slow growth, infiltrative pattern through white matter tracts and progression to a malignant tumour type. the traditional classification is newly replaced by molecular stratification. this reorganisation gathers glioma with similar prognosis and treatment protocols. the preferential location of that tumour in eloquent areas constituted, over time, a real challenge regarding the best surgical approach. because of the high risk of postoperative neurological deficits initially a more conservative management was adopted. once with the development of preoperative and intraoperative functional assessment techniques, a higher degree of resection was possible in the limits of corticosubcortical eloquence, being well known that this is a statistically significant factor for survival. we present in this paper the natural evolution of low-grade glioma, their new molecular classification, prognostic factors and the various approach proposed for eloquent ones. natural history and the new molecular classification diffuse low-grade gliomas or world health organisation grade ii gliomas (lgg) represents a group of tumours developed from oligodendrocyte and astrocytic precursors, with a slow and continuously growth pattern, infiltrative character, usually along white matter tracts and progression towards a malignant histological type. traditionally this includes diffuse astrocytoma, oligodendroglioma and oligoastrocytoma [35,66]. keywords low-grade glioma, lgg, molecular markers, functional area tumour, intraoperative neuropsychological monitoring corresponding author: andrei ionuț cucu department of neurosurgery, “n. oblu” emergency clinical hospital, iași, romania andreiucucu@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 41 the evolution of eloquent located low-grade gliomas surgical approaches in the new classification of central nervous system tumours from 2016, the phenotypical and genotypical manifestation are in the foreground. the molecular markers like isocitrate dehydrogenase (idh) mutant / wild type, codeletion of chromosome 1p and 19q, α thalassemia mental retardation xlinked (atrx) and tumour protein p53 (tp53) genes stratify patients in groups with the same prognostic and guides the cases to a specific therapeutic protocol [36,43]. according to those markers, nowadays, lgg grade ii includes: oligodendroglioma ihd mutant and 1p / 19q codeleted, diffuse astrocytoma idh mutant and diffuse astrocytoma idh wild type. in patients to which these molecular markers cannot be evaluated the histological diagnosis will be oligodendroglioma not otherwise specified (nos) or diffuse astrocytoma, nos [16,35]. lgg occurs usually in young adult, 30-35 years old being the incidence peak [61]. regarding the natural history of these lesions, it may be summarized in four steps. the first one consists in biological glioma tumoral cells transformation with no clinical manifestation and no routine head mri detection [34]. the chronological order, from a molecular point of view is represented by idh mutation, which is thought to be the first, next codeletion of chromosome 1 and 19 (1p/19q) occur and after telomerase reverse transcriptase (tert) promotor mutation is produced. some germ lines are associated with tumour grade, the former being found in low-grade glioma and the latter in highgrade glioma [3]. in the second step, the silent stage, the patient is asymptomatic but with imagistic alterations. in this period glioma may be incidentally diagnosed. in the literature, the percentage of incidental lgg (ilgg), from all lggs, is approximatively similar between studies: 3-10% (smits et al.,2019) – 3,8%-9,6% (ius et al., 2020) [27,62]. they have a smaller volume and usually are within non-eloquent brain areas. even though the diagnostic is obtained after imagistic head investigation for other reasons than a tumour, 36% of all the patient with lgg had the workload decreased for at list one year before lesion discovery [62]. in a study from 2013, pallud et al., evaluated 148 ilgg cases and observed that the mean time duration until the next phase was 14 ± 7,8 years [46]. concerning the growth rate of ilgg which was obtained after at list two mri investigation evaluation at 3 months interval was found to be ranging from 2,93 mm/year (opoku – darko et al., 2019) to approximately 4mm/year (pallud et al., 2013) [43,46]. in the third step, the symptomatic stage, the lesion generates clinical manifestation, most frequently epileptic seizures, which are a proof of somatotopic organization of the cortex where the tumor locates. for example, pericentral region induce jacksonian motor or somatosensory seizures; temporal lobe – déjà vu phenomena, memory dysfunctions, auditory hallucinations; wernicke area – sensitive aphasia; broca area – speech arrest, mutism; insula – paraesthesia, dysarthria, abdominal and thoracic discomfort [47,62]. the average period of this stage is about 7 years and sometimes subtle cognitive impairment may be associated. in general, the cognitive performance is similar to that of healthy population, but specific neurophysiological assessment protocols may highlight memory, attention and executive function disturbance [14,15,49]. the fourth step, the malignant stage consists in tumor malignant progression to a higher histological grade. this happens over a period of 2-3 years and the clinical manifestations are more complex, with neurological degradation and in the final stage death occurs [16,19,34]. survival and prognostic factors the survival rate of lgg grade ii it is variable, ranging from a few months to over 15 years. the possible factors which may influence the overall survival (os) are represented by the neurosurgical and oncological management, the histological type or more precise by molecular markers and by clinical parameters [2,22]. some of them are independent and cannot be changed, but on others we may act. taking this into account, zhao et al., proposed in 2019 a nomogram to predict individual 5and 9years os, using 7 clinical and paraclinical parameters [67]. a meta-analysis published in 2019 by brown et al., confirms that extent of resection has a statistically significant impact over survival rate and progression free survival at 2, 5, 10 years. this parameter constitutes an independent predictor, not being influenced by age or preoperative tumor volume [8,16]. the same results are confirmed and by choi et al., in a paper from 2020 where he showed that for patients in whom gross total resection (gtr) could not be performed presented recurrence more 42 mihaela coșman, andrei ionuț cucu, alin constantin iordache et al. frequently after radiotherapy (idh wild type: 57,9% and idh mutant: 47,6%) [12]. regarding the precise value of the extent of resection, there are no exact values, positive effects were observed even from a debulking of 40 % of the tumor and a residual volume <15cm³ (roelz et al., 2016), but is well known the statistical significance of a higher resection [2,52]. this is confirmed in a paper of ius et al., in which 190 cases of lgg located in functional areas were included. a resection less than 70% compared with one of more than 90% had a risk of death 19,7 times higher, tumour progression was found to be 13,6 times higher and malignant transformation 9,7 times higher [28]. the best prognostic is carried by oligodendroglioma idh mutant and 1p/19q codeleted and the worse by astrocytoma idh wild type [8,35]. the negative prognostic was associated with a tumor volume > 5 cm (nitta et al., 2015), functional area location (gousias et al., 2014), karnofsky performance scale ≤ 80% (gousias et al., 2014), age ≥ 40 years (franceschi et al., 2018) and idh wild-type genetics (lombardi et al., 2020) [22,25,35,42]. clinical manifestation with neurological deficits, the absence of seizures, tumour crossing the midline, short time of symptoms before diagnosis, rapid growth rate and the astrocytic type carry an unfavourable impact [16,19,24,30,44]. in table i we have a schematic representation of the new classification of lgg grade ii with their specific molecular markers, the impact over survival rate and some specific characteristics. table 1. low grade glioma, the molecular diagnosis markers, and survival impact [1, 16,19, 32,36, 38, 40]. tumor nomenclature molecular markers and prognosis notes oligodendroglioma, idh mutant and 1p/19q codeleted idh mutant (70-80% of the tumors) – longer os 1p/19q codeleted tp53 (5% of the tumors) -the best prognosis. -more sensitive to chemotherapy. oligodendroglioma, nos no molecular marker evaluated diffuse astrocytoma, idh mutant idh mutant – mandatory. tp53 mutation –may be found, shorter os. atrx loss – may be found. -the classical variants protoplasmic and fibrillary astrocytoma were deleted. small difference in os compared to anaplastic astrocytoma idh mutant*. gemistocytic astrocytoma, idh mutant tp53 mutation in >80% of cases -the only type of astrocytoma recognized diffuse astrocytoma, idh wild type no mutation present of idh1 codon 123 and or idh2 codon 172 usually, uncommon. not all have poor prognosis. some have similar manifestation as glioblastoma. diffuse astrocytoma, nos no molecular marker evaluated oligoastrocytoma, nos oligodendroglioma and astrocytic elements only in the absence of molecular assessment under previous entities “true” lesion with spatial distinct of both elements in the same tumor are reported. * os for diffuse astrocytoma idh mutant was 10,9 years and for anaplastic astrocytoma idh mutant 9,3 years in a large series similar regarding the age distribution (reuss et al., 2015) [51]. surgical approach the infiltrative feature of these lesions determined duffau to describe them as” an infiltrating chronic disease that progressively invades the central nervous system”, usually the subcortical pathways are affected, and so different neurological functions may be altered [19]. regarding their location, usually are found in eloquent areas, especially in supplementary motor area and insula, followed by language centres. the preferential development may be explained by cytoarchitectonic (agranular – dysgranular – granular cortex) and functional 43 the evolution of eloquent located low-grade gliomas surgical approaches similarities between these brain regions [17]. as far their position, the surgical management remain a challenge for every neurosurgeon. over time, the strategies changed aiming a higher degree of resection with minimal neurologic postsurgical deficits [6]. because of the increased risk of postoperative neurologic dysfunction for gliomas located in eloquent areas, functional preoperative and intraoperative techniques use is mandatory. the evolution of surgical strategies for these lesions was corelated with the rapid and continuous development of imagistic diagnosis modalities and intraoperative functional assessment techniques. even though the extent of resection is corelated with survival, nowadays the quality of patient’s life is one of the main goals [21, 50, 53]. the surgical management of eloquent lgg suffered many changes over the time. initially, the approach “wait and see” was applied, but nowadays we can talk even about supratotal resection. the conservative treatment was indicated for incidental glioma and for young patients with minor symptoms [9,21,54]. after a period, when “wait and see” policy was the only measure taken, biopsy become a part of the surgical management, especially for young patients with no neurological deficits, no mass effect and with minor symptoms. this type of treatment has one drawback: because of the tumors heterogeneity, even image-guided stereotactic samples may impair the histological diagnoses, undergrading the lesion. muragaki et al., highlighted in an article from 2008 that tumors with low proliferative activity, mib-1 less than 3% and mixt gliomas are more susceptible to this error. this situation may induce a wrong inclusion of the case in a protocol treatment and a misinterpretation of the prognosis. on the one hand, a way to lower this possibility is to perform multiple sampling from various parts of the tumor. on the other hand, for neoplasms located in functional areas this action may be associated with postoperative neurological dysfunctions [41]. nowadays the bias, in histological interpretation induced by stereotactic biopsy sampling compared with the specimens obtained from a classical intervention is reduced because of molecular analysis and new classification of the gliomas [29]. clinical studies concluded that early surgery may delay malignant transformation and increases overall survival in low grade glioma patients. maximal resection in functional limits is indicated and for tumours located in functional areas of the brain. the development of intraoperative neurological functions assessment technologies e.g., neurophysiological monitoring (magil et al., 2018; bander et al., 2020), 3d tractography integrated in neuro-navigation system (romero-garcia et al., 2020), awake craniotomy (saito et al., 2018; wang et al., 2019), fluorescein-based surgery (coburger et al., 2019), intraoperative mri (caras et al., 2020; scherer et al., 2020) help in obtaining a maximal resection with minimal postoperative dysfunction [ 6, 10, 13, 31, 37, 53, 56, 59, 63]. jackola et al., highlighted the important survival advantage when comparing wait and see approach with early tumor resection. for the first group the median of os was 5,8 years and 14,4 years for the second group [29]. in a metanalysis performed by yang et al., in 2018 a comparison was made between biopsy and surgical resection (gtr and subtotal resection – str). os was found to be 3,7 years in biopsy patients’ group, 6,6 years for str cases and 10,6 years for gtr cases. statistical significance was obtained comparing biopsy with any degree of resection, in favour of surgical debulking [65]. considering the ones above, only biopsy is performed in patients who have contraindication for an open surgery because of severe medical pathologies or when even subtotal resection is not feasible [19]. as mentioned before, the study of lgg literature considers eloquence as a negative prognostic factor. chang et al., showed that this parameter induced over the 281 functional located diffuse glioma cases an increased hazard ratio with shorter os and pff [11]. a shift from image – guided surgery to functional – guided resection made possible to perform a higher degree of resection by delineating the preoperative presumed eloquent situated lesion form the ones truly eloquent. when cortical mapping was negative and the functional area was actually relocated and not in contact with the tumour, the survival of those cases was longer and similar to those in non-eloquent areas [4,11]. even if the glioma is developing in eloquent area, the slow growth pattern, is considered as an advantage which allows the neuroplasticity process to act. this concept was at the base of the proposal of individualized multistage surgery. a better 44 mihaela coșman, andrei ionuț cucu, alin constantin iordache et al. understanding of brain plasticity, development of neurocognitive protocol assessment for cerebral tumours and personalized postsurgical cognitive and functional rehabilitation increased the chance for a better outcome. duffau presented the steps of this approach. after the first operation, where a subtotal resection was performed, limited by the functional borders, the patient was evaluated periodically clinically and radiologically and a second surgery was scheduled, if needed, considering the tumor regrowth and cortical remapping. this allows to increase the extent of resection and to maintain the neurological integrity [18,19,21]. one of the first presentation of this technique performed over 19 cases of eloquent lgg was from 2009. the results of martino et al. showed the safety of this strategy. the patients were operated two times with a median time of 4,1 years between intervention and intraoperative neurophysiological monitoring was used. the functional guided surgery resulted in allowing 94,7% of the cases to have a normal socio-professional life [39]. another strategy proposed for eloquent lggs was the safe margin technique resection. this policy was based on the development of perioperative assessment methods, especially functional magnetic resonance imaging (fmri) and brain mapping. in the early 90s, using intraoperative neurophysiological monitoring, ojemann recommended a 7-10 mm secure margin preservation around positive sites, after observing that this is associated with fewer postoperative neurological deficits. the results were based on the fact that for cortical mapping the electrodes from the subdural grid were placed at one-centimetre distance from each other [26, 57]. in the same surgical direction are presented the results of 54 motor area tumour resection using the fusion of preoperative f mri with neuro-navigation, in an article of krishnan et al. published in 2004. in 83,33% of the cases gross total resection was achieved and subtotal (80-95% of the tumour volume) was performed to the rest of the patients, the postoperative new deficits were recorded in 16,7% of the cases. the author observed and concluded that a distance less than 5 mm from the tumour to the active functional site is associated with high risk of motor dysfunction and a greater distance than 10 mm is safe for gross total resection [33]. new fmri studies confirmed the relationship between the tumour borders and the location of the eloquent sites, regarding the postoperative new neurologic deficits. in 2011 wood et al. observed some difference between the behaviour of the motor and primary language areas regarding the distance to the lesion. for motor strip when the distance was 1 2 cm compared to greater than 2 cm, the incidence of neurological dysfunction was 39%, a 34% increase was observed when less than 1cm was meet. as for language area a nonlinear manifestation was found. the prevalence of aphasia increased significatively when the distance was less than 1 cm. the difference of the functional and structural organization of the motor area and language areas may explain these results, beside the high grade of individual variability of the latter [64]. it is well known that not only the cortical functional sites are important and need to be preserved but also the subcortical motor and language pathways. in 2015 bailey et al. evaluated if the lesion to distance activation (lad) is a predictor factor for the perioperative language and motor deficits. he used fmri and assessed the superior longitudinal fasciculus (slf) and corticospinal tract (cst) with diffusion tensor imaging (dti) on 76 cases of functional located tumours. postoperative, the only significative difference was noted for motor lad with a trend level effect. the involvement of cst was significantly statistically for pre and postoperative motor deficit, in comparation slf involvement had a significance only between asymptomatic and symptomatic preoperative cases [5]. sollman et al. presented in 2020 the results of evaluating the impact of the distance from the lesion to cst or arcuate fascicle (af) of 250 functional located tumours which were assessed using navigated transcranial magnetic stimulation and dti fibre tracking. the most statistically significative postoperative neurological impact observed for cst was for a distance less than 12mm, for af less than 16mm and the value of 25 mm for any other language tract [61]. in an previews study from 2019, sollman et al. found that a distance greater than 8 mm from the tumour to the af and one greater than 11mm for the other fascicle involved in the language pathways were associated with permanent aphasia. these differences may be explained by the difference between the two studies regarding the cases numbers and the fact that the permanent deficit was not so high, hindering the statistical evaluation [60]. 45 the evolution of eloquent located low-grade gliomas surgical approaches white matter dissection, development of 3d tractography helped in discovering and understanding the subcortical pathways anatomy. a functional atlas of white matter fibres was proposed after evaluating 130 eloquent tumours operated awake and with intraoperative neurophysiological monitoring [58]. the anatomo-functional structure of the brain is the bases of the next type of approach used for functional located gliomas: cortical subpial dissection. duffau and gil-robles compared the results regarding the postoperative deficits of the patient with eloquent glioma operated with and no safe margins around the functional area. they did not find a significative difference between the two techniques when the permanent deficit was evaluated (1-2,5% vs. 1,7%), even though the transient deficit was higher for the latter technique, this suggesting that subpial dissection and intraoperative mapping is a safe strategy for eloquent lgg. the assessment of cortical areas along with the projection tracts, long distance association fibres and short association fibres (ufibre) increase the degree of resection while preserving and minimizing the postoperative deficits [23]. a tailored intraoperative monitoring may improve the neurological outcome, but the survival rate was found to be the same (pan et al., 2020) [48]. even though it seems utopian, the question about the feasibility of supramarginal resection for presumed eloquent glioma was asked. this concept has at the basis the observation made after biopsy tissue, from beyond the abnormal flair-mri signal, was evaluated and tumor cells were found, even at a distance of 20 mm from the preoperative images lesion demarcation. the first study with a long followup period (132 months) showed no case of malignant transformation and no relapse at half of patients, highlighting the impact of supramarginal resection over tumor progression [ 7, 20, 45]. an extensive analyse was performed by rossi et al., in an article from 2020 regarding this supposition. the study group included 449 glioma cases, 413 of them imagistic located in functional areas. the results showed that the most important and statistically significant factor associated with achieving this degree of resection was the duration of the symptoms longer than 6 months and was independent of age, sex and tumor volume. the safety of this procedure for lesion preoperatively presumed to be in eloquent area and a good neurological outcome is explained by the activation of neuroplasticity processes with a high reorganisation of the cortico-subcortical pathways and intraoperative identification of the functional sites outside the tumors margins. smaller odd of obtaining this result was for parietal lesions compared with temporal and frontal location. from all four hundred forty-nine patient supratotal resection was obtained in 32,2% and total resection in 40,8% of the cases. regarding the postoperative new deficits, the transient type remitted in 1-2 week and the permanent one was lower in comparison with those from the patient’s group where subtotal or partial removal was performed (6,6% vs 0,55%; 6,6% vs 0.68%, p<.001) [55]. conclusion considering the natural history, the continuous, slow growth and histological progression make the surgical treatment of low-grade gliomas to be the first choice in their management. the development of preoperative radiologic evaluation and intraoperative function assessment techniques, especially cortical and subcortical mapping helps in performing a higher degree of resection with minimal neurological dysfunction and for eloquent located lgg. we witness the evolution and the advance made regarding the surgical approach of these tumours from wait and see policy to even evaluation the feasibility of supramarginal resection. references 1. aibaidula a, chan aky, shi z et al. adult idh wild type lower-grade glioma should be further stratified. neuro oncol, 19(10): 1327-1337, 2017. 2. albuquerque laf, almeida jp, filho ljm et al. extent of resection in diffuse low-grade gliomas and the role of tumor molecular signature-a systematic review of the literature. neurosurg rev, 8:1-19, 2020. 3. arcela a, limanaqi f, ferese r et al. dissecting molecular features of glioma: genetic loci and validated biomarkers. int j mol sci, 21:685-702, 2020. 4. azad td, duffau h. limitations of functional neuroimaging for patient selection and surgical planning in glioma surgery. neurosurg focus, 42: 1-5, 2020. 5. bailey pd, zaca d, basha mm et al. presurgical fmri and dti for the prediction of perioperative motor and language deficits in primary or metastatic brain lesions. j neuroimag, 25:776-784, 2015. 6. bander de, shelkov e, modik o et al. use of the train-offive bipolar technique to provide reliable, spatially accurate motor cortex identification in asleep patients. 46 mihaela coșman, andrei ionuț cucu, alin constantin iordache et al. neurosurg focus, 48: 1-6, 2020. 7. boissonneau s, duffau h. identifying clinical risk in lowgrade gliomas and appropriate treatment strategies, with special emphasis on the role of surgery. expert rev anticancer ther, 17 (8): 703-716, 2017. 8. brown tj, bota da, van den bent mj et al. management of low-grade glioma: a systematic review and metaanalysis. neurooncol pract, 6(4): 249-258, 2019. 9. carabenciov id, buckner jc. controversies in the therapy of low-grade glioma. curr treat options in oncol, 20:2537, 2019. 10. caras a, mugge l, miller wk et al. utility and impact of intra-operative imaging for glioma resection on patient outcome and extent of resection: a systematic review and meta-analysis. world neurosurg, 134: 98-110, 2020. 11. chang ef, clark a, smith js et al. functional mapping– guided resection of low-grade gliomas in eloquent areas of the brain: improvement of long-term survival. j neurosurg, 114: 1-17, 2011. 12. choi j, kim sh, ahn ss et al. extent of resection and molecular pathologic subtype are potent prognostic factors of adult who grade ii glioma. sci rep, 10:2086-94, 2020. 13. coburger j, witz cr. fluorescence guided surgery by 5ala and intraoperative mri in high grade glioma: a systematic review. j neurooncol, 141:533-546, 2019. 14. cosman m, pantiru im, serban r et al. correlation between histological subtypes and neurocognitive assessment of language tumors. our 43 cases series and review of the literature. rom j morphol embryol, 60(4): 1143-1151, 2019. 15. de witte e, satoer d, robert e et al. the dutch linguistic intraoperative protocol: a valid linguistic approach to awake brain surgery. brain lang,140:35-48, 2015. 16. delgado-lopez pd, corrales-garcia em, martino j et al. diffuse low-grade glioma: a review on the molecular classification, natural history, and current management strategy. clin transl oncol, 19(8): 931-944, 2017. 17. duffau h, capelle l. preferential brain locations of lowgrade glioma. cancer, 100(12):2622-2626, 2004. 18. duffau h. awake surgery for incidental who grade ii gliomas involving eloquent areas. acta neurochir (wien), 154:575–584, 2012. 19. duffau h, taillandier l. new concepts in the management of diffuse low-grade glioma: proposal of a multistage and individualized therapeutic approach. neuro oncol, 17(3): 332-342, 2015. 20. duffau h. long-term outcomes after supratotal resection of diffuse low-grade gliomas: a consecutive series with 11-year follow-up. acta neurochir (wien), 158:51–58, 2016. 21. duffau h. functional mapping before and after low-grade glioma surgery: a new way to decipher various spatiotemporal patterns of individual neuroplastic potential in brain tumor patients. cancer, 12:2611-2632, 2020. 22. franceschi ef, mura a, de biase d et al. the role of clinical and molecular factors in low-grade gliomas: what is their impact on survival? future oncol, 14(16):1559-1567, 2018. 23. gil-robles s, duffau h. surgical management of world health organization grade ii gliomas in eloquent areas: the necessity of preserving a margin around functional structures. neurosurg focus, 28:1-9, 2010. 24. gorlia t, wu w, wang m et al. new validated prognostic models and prognostic calculators in patients with lowgrade glioma diagnosed by central pathology review: a pooled analysis of eortc/rtog/ncctg phase iii clinical trials. neuro oncol, 15(11): 1568-1579, 2013. 25. gousias k, schramm j, simon m. extent of resection and survival in supratentorial infiltrative low-grade gliomas: analysis of and adjustment of treatment bias. arta neurochir, 156: 327337, 2014. 26. haglund mm, berger ms, shamseldin m, lettich e, ojemann ga. cortical localisation of temporal lobe language sites in patients with glioma. neurosurg, 34(4):567-76, 1994. 27. ius t, cesselli d, isola m et al. incidental low-grade gliomas: single institution management based on clinical, surgical, molecular data. neurosurg 0: 1-9, 2020. 28. ius t, isola m, budai r et al. low-grade glioma surgery in eloquent areas: volumetric analysis of extent of resection and its impact on overall survival. a single institute experience in 190 patients. j neurosurg, 117: 1039-1052, 2012. 29. jakola as, skjulsvik aj, myrmel ks et al. surgical resection versus watchful waiting in low-grade gliomas. ann oncol, 28:1942-1948, 2017. 30. jakola as, sagberg lm, gulati s, solheim o. advancements in predicting outcomes in patients with glioma: a surgical perspective. expert rev anticancer ther, 20(3): 167-177, 2020. 31. jooma r, waqas m, khan i. diffuse low-grade glioma – changing concepts in diagnosis and management: a review. asian j neurosurg, 14(2):356-363, 2019. 32. kalidindi n, or r, babak s, mason w. molecular classification of diffuse glioma. can j neurol sci, 47(4): 463-473, 2020. 33. krishnan r, raabe a, hattingen e et al. functional magnetic resonance imaging integrated neuronavigation: correlation between lesion-to-motor cortex distance and outcome. neurosurgery, 55:904-914, 2004. 34. lima gl, zanello m, mandonnet e et al. incidental diffuse low-grade gliomas: from early detection to preventive neuro-oncological surgery. neurosurg rev, 39(3): 377-84, 2016. 35. lombardi g, barresi v, castellano a et al. clinical management of diffuse low-grade glioma. cancer, 12:308, 2020. 36. louis dn, perry a, reifenberger g et al. the 2016 world health organization classification of tumors of the central nervous system: a summary. acta neuropathol,131:803-820, 2016. 47 the evolution of eloquent located low-grade gliomas surgical approaches 37. magill st, han sj, li j et al. resection of primary motor cortex tumors: feasibility and surgical outcomes. j neurosurg, 129:961-972, 2018. 38. malzkorn b, reifenberger g. integrated diagnostics of diffuse astrocytic and oligodendroglial tumors. pathologe, 40: 9-17, 2019. 39. martino j, taillandier l, moritz-gasser s et al. reoperation is a safe and effective therapeutic strategy in recurrent who grade ii gliomas within eloquent areas. acta neurochir (wien), 151: 427-436, 2009. 40. mirchia k, richardson te. beyond idh mutation: emerging molecular diagnostic and prognostic features in adult diffuse gliomas. cancer 12: 1817-1839,2020 41. muragaki y, chernov m, maruyama t et al. low-grade glioma on stereotactic biopsy: how often is the diagnosis accurate. minim invas neurosurg, 51: 275-279, 2008. 42. nitta m, muragaki y, muruyama t et al. proposed therapeutic strategy for adult low-grade glioma based on aggressive tumor resection. neurosurg focus, 38(1): e7, 2015. 43. opoku-darko m, eagles me, cadieux m et al. natural history and growth patterns and incidentally discovered diffusely infiltrating low-grade gliomas: a volumetric study. world neurosurg, 132: 133-139, 2019. 44. paiva ws, fonoff et, beer-furlan a et al. evaluation of postoperative deficits following motor cortex tumor resection using small craniotomy. surg j, 5: e8-e13, 2019. 45. pallud j, varlet p, devaux b et al. diffuse low-grade oligodendrogliomas extent beyond mridefined abnormalities. neurol, 74:1724-7431, 2010. 46. pallud j, capelle l, taillandier l et al. the silent phase of diffuse low-grade gliomas. it is when we missed the action? acta neurochir, 155: 2237-2242, 2013. 47. pallud j, mckhann gm. diffuse low-grade glioma related epilepsy. neurosurg clin n am, 30(1): 43-54, 2019. 48. pan sy, chen jp, cheng wy et al. the role of tailored intraoperative neurophysiological monitoring in glioma surgery: a single institute experience. j neurooncol, 146:459-467, 2020. 49. papagno c, casarotti a, comi a et al. measuring clinical outcomes in neuro-oncology. a battery to evaluate lowgrade gliomas (lgg). j neurooncol,108:269–275, 2012. 50. patel sh, bansal ag, young eb et al. extent of surgical resection in low-grade gliomas: differential impact based on molecular subtype. am j neuroradiol, 40:1149-1155, 2019. 51. reuss de, mamatjan y, schrimpf d et al. idh mutant diffuse and astroplastic astrocytoma have similar age at presentation and little difference in survival: a grading problem for who. 129: 867-873, 2015. 52. roelez r, strohmaier d, jabbarli r et al. residual tumor volume as best outcome predictor in low grade glioma – a nine-years near-randomized survey of surgery vs. biopsy. sci rep, 6:32286-95, 2016. 53. romero-garcia r, erez y, oliver g et al. practical application of networks in neurosurgery: combined 3d printing, neuronavigation, and pre-operative surgical planning. world neurosurg, 137:1-22, 2020. 54. rossi m, nibali mc, vigano l et al. resection of tumors within the primary motor cortex using high-frequency stimulation: oncological and functional efficiency of this versatile approach based on clinical conditions. j neurosurg, 9:1-13, 2019. 55. rossi m, ambrogi f, gay l et al. is supratotal resection achievable in low-grade glioma? feasibility, putative factors, safety, and functional outcome. j neurosurg, 132:1692-1705, 2020. 56. saito t, tamura m, chernov mf et al. neurophysiological monitoring and awake craniotomy for resection of intracranial gliomas. chernov mf, muragaki y, kesari s, mccutcheon ie (eds): intracranial gliomas. part i – surgery. prog neurol surg. basel, karger, 2018, vol 30, pp 117–158. 57. sanai n, mirzadeh z, berger ms. functional outcome after language mapping for glioma resection. n engl j med, 358:18-27, 2008. 58. sarubbo s, de benedictis a, merler s et al. towards a functional atlas of human white matter. hum brain mapp, 36: 3117-3136, 2015. 59. scherer m, ahmet h, roder c et al. surgery for diffuse who grade ii gliomas: volumetric analysis of a multicenter retrospective cohort from the german study group for intraoperative magnetic resonance imaging. neurosurgery, 86:64-74, 2020. 60. sollmann n, fratini a, zhang h et al. association between clinical outcome and tractography based on navigated transcranial magnetic stimulation in patients with languageeloquent brain lesions. j neurosurg, 15: 1-10, 2019. 61. sollmann n, zhang h, fratini a et al. risk assessment by presurgical tractography using navigated tms maps in patients with highly motoror languageeloquent brain tumors. cancer, 12:1264-1283, 2020. 62. smits a, jackola as. clinical presentation, natural history, and prognosis of diffuse low-grade gliomas. neurosurg clin n am, 30(1):35-42, 2019. 63. wang yc, lee cc, takami h et al. awake craniotomies for epileptic gliomas: intraoperative and postoperative seizure control and prognostic factors. j neurooncol, 142:577-586, 2019. 64. wood jm, kundu m, utter a et al. impact of barin tumor location on morbidity and mortality: a retrospective functional mr imaging study. am j neuroradiol, 32 (8): 1420-1425, 2011. 65. yang k, nath s, koziarz a et al. biopsy versus subtotal versus gross total resection in patients with low-grade glioma: a systematic review and meta-analysis. world neurosurg, e1-e14, 2018. 66. youseef g, miller jj. low-grade glioma. curr neurol neurosci rep, 20:21-30, 2020. 67. zhao yy, chen sh, hao z et al. a nomogram for predicting individual prognosis of patients with low-grade glioma. world neurosurg, 130: e605-e612, 2019. doi: 10.33962/roneuro-2022-063 commentary: controlling high blood pressure with intravenous sedation in mechanically ventilated neurosurgical patients in the intensive care unit. is it a correct practice? ebtesam abdulla, bassam al-aradi, sabrina rahman, md moshiur romanian neurosurgery (2022) xxxvi (3): pp. 370-371 doi: 10.33962/roneuro-2022-063 www.journals.lapub.co.uk/index.php/roneurosurgery commentary: controlling high blood pressure with intravenous sedation in mechanically ventilated neurosurgical patients in the intensive care unit. is it a correct practice? ebtesam abdulla1, bassam al-aradi1, sabrina rahman2, md moshiur3 1 department of neurosurgery, salmaniya medical complex, manama, bahrain 2 department of public health, independent university bangladesh, dhaka, bangladesh 3 department of neurosurgery, holy family red crescent medical college, dhaka, bangladesh abstract this commentary discusses the effect of misuse of intravenous sedation regimens in lowering the systemic blood pressure in mechanically ventilated neurosurgical patients in the intensive care unit. intravenous sedation regimens are widely used in a neuro-intensive care unit (neuro-icu) for specific neurologic purposes.1-4 among these purposes are intracranial pressure control, seizures management, targeted temperature management, reduction of pain, agitation control, and patient-ventilatory asynchrony.1-4 the effect of sedatives on blood pressure is that they lower systemic blood pressure.5 thus, some would intensify sedation intending for systemic blood pressure control.5 the problem is, when the sedatives are stopped, the risk of systemic rebound hypertension will exacerbate intracranial pressure in patients with low brain compliance.6 improper management of systemic blood pressure (bp) can ultimately lead to encephalopathy, cardiac and renal complications.7,8 moreover, the misuse of sedatives in neurocritical patients has deleterious effects in terms of eliminating neuro-assessment and potential cardiovascular depression; thus, it increases hospital stay, morbidity, mortality and delays the clinical decision process.1-4 keywords hypertension, neuroicu, sedation corresponding author: ebtesam abdulla department of neurosurgery, salmaniya medical complex, manama, bahrain dr.ebtesam@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 371 controlling high blood pressure with intravenous sedation prompt bp control in mechanically ventilated patients with neurological emergencies in neuro-icu is necessary.7-10 nicardipine, labetalol, clevidipine, and urapidil are examples of fast-acting, soluble intravenous medicines that are feasible and recommended as first-line antihypertensive medications.8 invasive bp monitoring is required, especially in the setting of intracranial hypertension.8,9 the 2013 american stroke association (asa) guidelines state no exact bp target for which intravenous antihypertensive agents should be started.10 when the systolic bp surpasses 220 or the diastolic bp surpasses 120 during the first 24 hours after an acute ischemic stroke, the asa recommends reducing the blood pressure.10 when fibrinolytic therapy is attempted, the recommended bp target is a systolic bp less than 180 or diastolic bp less than 110.10 references 1. watts, charles r. md, phd; kelley, parker pa-c sedation and analgesia in neurosurgery/neurocritical care, contemporary neurosurgery: september 15, 2016 volume 38 issue 13 p 1-6 doi: 10.1097/01.cne.0000502657.11174.29 2. paul bs, paul g. sedation in neurological intensive care unit. ann indian acad neurol. 2013 apr;16(2):194-202. doi: 10.4103/0972-2327.112465. pmid: 23956563; pmcid: pmc3724073. 3. roberts dj, hall ri, kramer ah, robertson hl, gallagher cn, zygun da. sedation for critically ill adults with severe traumatic brain injury: a systematic review of randomized controlled trials. crit care med. 2011;39(12):2743-2751. doi:10.1097/ccm.0b013e318228236f 4. oddo, m., crippa, i. a., mehta, s., menon, d., payen, j.-f., taccone, f. s., & citerio, g. (2016). optimizing sedation in patients with acute brain injury. critical care, 20(1). doi:10.1186/s13054-016-1294-5 5. woolcombe, s., koshal, s., bryant, c. and rood, p. (2009), use of intravenous sedation in the management of patients with high blood pressure. oral surgery, 2: 116125. https://doi.org/10.1111/j.1752-248x.2010.01069.x 6. salah, j., grgurich, p., nault, k., & lei, y. (2020). identification of risk factors for hypertension and tachycardia upon dexmedetomidine discontinuation. journal of critical care. doi:10.1016/j.jcrc.2020.06.006 7. anderson cs, heeley e, huang y, et al. rapid bloodpressure lowering in patients with acute intracerebral hemorrhage. n engl j med 2013;368:2355-65. 10.1056/nejmoa1214609 8. aronow ws. treatment of hypertensive emergencies. ann transl med. 2017;5(suppl 1):s5. doi:10.21037/atm.2017.03.34 9. manning l, robinson tg, anderson cs. control of blood pressure in hypertensive neurological emergencies. curr hypertens rep 2014;16:436. 10.1007/s11906-014-0436-x 10. jauch ec, saver jl, adams hp, jr, et al. guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the american heart association/american stroke association. stroke 2013;44:870-947. 10.1161/str.0b01 3e318284056a doi: 10.33962/roneuro-2020-060 intracisternal papaverine toxicity in anterior circulation aneurysm clipping surgery. a literature review zahraa f. al-sharshahi, samer s. hoz, mustafa e. almurayati, zahraa m. kareem, zahraa ameen romanian neurosurgery (2020) xxxiv (1): pp. 386-390 doi: 10.33962/roneuro-2020-060 www.journals.lapub.co.uk/index.php/roneurosurgery intracisternal papaverine toxicity in anterior circulation aneurysm clipping surgery. a literature review zahraa f. al-sharshahi1, samer s. hoz2, mustafa e. almurayati3, zahraa m. kareem3, zahraa ameen3 1 mb, bch bao (nui, rcsi), lrcp & si, royal college of surgeons in ireland (alumnus), dublin, ireland 2 neurosurgeon, frcs (neurosurgery) glasgow, department of neurosurgery, neurosurgery teaching hospital, baghdad. iraq 3 medical student, college of medicine, university of baghdad, baghdad. iraq abstract introduction. cerebral vasospasm is a major cause of mortality in patients with subarachnoid haemorrhage. irrigation of intracisternal papaverine has been adopted as a strategy to reduce the incidence of aneurysm-surgery-associated vasospasm. aim. the aim of this literature review is to summarize the reported complications associated with intracisternal papaverine administration. patients and methods. we searched the following databases: pubmed, google scholar, cochrane library, clinical key, embase, emerald, health business elite, medline at ovid, ebm reviews and research gate. the following keywords were used: intracisternal papaverine, topical papaverine, direct papaverine, a vasodilator for aneurysm surgery, papaverine in aneurysm clipping, papaverine complications and papaverine side effects. the search criteria included all articles published between 1980-2019, in the english language. results. our search yielded a total of 19 articles describing 43 cases. the most common reported complication was ipsilateral oculomotor nerve palsy. other local complications included: bilateral oculomotor nerve palsy, ipsilateral facial nerve palsy, and monocular blindness. although less common, reports pointing to papaverine systemic toxicity did exist. examples of such complications included: profound hypotension, bradycardia, hypertension and tachycardia, hyperthermia and metabolic acidosis, cardiac arrest and even death. conclusion. intracisternal papaverine irrigation is an effective strategy in reducing peri-operative vasospasm associated with aneurysm surgery. although uncommon, both local and systemic side effects have been linked to papaverine use, calling for careful dosing and close monitoring to enhance its safety profile. introduction the use of intracisternal papaverine to prevent vasospasm during aneurysm surgery was first described in the fifties of the 19th century (1). papaverine is a vasodilator that can be installed directly onto the keywords intracisternal papaverine toxicity, anterior circulation aneurysm, clipping surgery corresponding author: zahraa f. al-sharshahi royal college of surgeons in ireland (alumnus), dublin, ireland zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 387 intracisternal papaverine toxicity in anterior circulation aneurysm clipping surgery the vessels in the exposed cisterns during aneurysm clipping. papaverine's main role is to prevent intraoperative and postoperative vasospasm and to alleviate its deleterious consequences (1). the application of intracisternal papaverine is considered to be a safe procedure as compared to other routes of administration such as the intra-arterial, and intravenous routes along with the slow release pellets as these routes often entail several serious direct side effects (2-4). to date, there are few reports that describe the complications associated with the installation of intracisternal papaverine. in this article, we reviewed the available literature regarding the adverse effects related to the intracisternal papaverine use during aneurysm surgery. patients and methods we conducted a literature review of all articles published on pubmed, google scholar, cochrane library, clinical key, embase, emerald, health business elite, medline at ovid, ebm reviews and research gate from 1980-2019. the following keywords were used: intracisternal papaverine, topical papaverine, direct papaverine, vasodilator for aneurysm surgery, papaverine in aneurysm clipping, papaverine complications and papaverine side effects. the reported cases were analyzed in relation to the location of the aneurysm, the association with subarachnoid hemorrhage (ruptured or unruptured aneurysm), the dose of papaverine used, the reported side effects, the resolution time of these effects and the fenestration status of the lamina terminals. the demographic data and the surgical approaches were excluded from the results as these parameters were not mentioned in the majority of the reported cases. results our search yielded 19 articles, with a total of 43 aneurysms. as for the types of articles; there were two original articles (5,6), two case reports and reviews (7, 8), one case series (9), nine case reports (10-18), and five letters to the editor (19-23). the two most common aneurysm locations that were associated with topical papaverine complications were the middle cerebral artery (mca) and the anterior communicating artery (acoma) with 18 and 17 cases, respectively. other reported locations included posterior communicating artery aneurysm (6 cases), internal carotid artery bifurcation aneurysm (one case), and ophthalmic artery aneurysm (one case). there was one report where the location of the aneurysm was not specified. notably, amongst the 43 reported papaverine toxicity cases, 42 cases were associated with ruptured aneurysms while only one case was associated with an un-ruptured aneurysm (13) while the remaining cases did not specify the status of aneurysm rupture. this literature review showed that intracisternal papaverine can cause ipsilateral (6, 9, 11-13, 18), contralateral (6, 7, 21), and even bilateral oculomotor nerve palsy (7-10, 19). the ipsilateral oculomotor palsy in the form of mydriasis with a non-reacting pupil was the most common reported complication of intracisternal papaverine installation (18 out of 43 patients). temporary facial nerve palsy was the only other reported cranial nerve paresis after the oculomotor nerve (13). hemodynamic and metabolic adverse effects were reported in a total of 15 cases. these effects included profound hypotension (5, 20, 22), bradycardia (5), both hypotension and bradycardia (14, 16, 23), and hypertension and tachycardia (17). two of the three reported cases of intracisternal papaverine complications in the form of both hypotension and bradycardia progressed to cardiac arrest and death (16, 23); these were the only reported deaths related to cisternal papaverine. mcloughlin et. al described the unique toxicity of papaverine as hyperthermia and metabolic acidosis (12). one other rare complication was permanent monocular blindness resulting from choroidal infarction with an unknown mechanism of causation (15). (table 1) out of all the reviewed reports on the complications of the intracisternal papaverine, only three reports by rath et al. 2006 (14), singla et al. 2009 (22), and baltaci et al. 2010 (16) included the fenestration of the lamina terminalis within the parameters under study; the authors described serious complications related to intracisternal papaverine installation after the fenestration of the lamina terminalis; namely, profound hemodynamic changes, severe hypotension, and cardiac arrest respectively. the resolution time of the adverse effects of papaverine was variable. the oculomotor-related complications usually resolved within the first day 388 zahraa f. al-sharshahi, samer s. hoz, mustafa e. almurayati et al. with the majority of patients recovering within the first 5 hours. however, in three cases the resolution extended beyond 4-7 days and even up to 23 days in one report (8, 10, 12). as compared to cranial nerve paresis, the hemodynamic complications of intracisternal papaverine were more abrupt with the majority of reports charting a resolution time of few minutes; only two cases, that reported hypotension, recorded a resolution time of more than one hour (20, 22). our review revealed that papaverine hydrochloride ampule was used in all cases. the concentration used ranged between 30 and 300 mg of 3% papaverine, diluted in 10 up to 100 ml of warm 0.9% normal saline or ringer lactate with only a few cases reporting the use of undiluted (60 mg)of papaverine. the recommended papaverine regimen, based on our review, was 2 cc of 3% papaverine (60 mg) diluted in 10-20 ml of warm 0.9% normal saline or ringer lactate at room temperature (35-37 °c). table 1: review of the reported complications of intracisternal papaverine adverse effects number of reported cases percent of the total reported cases with toxicity ipsilateral oculomotor nerve palsy 18 42% bilateral oculomotor nerve palsy 7 16% contralateral oculomotor nerve palsy 3 7% ipsilateral facial nerve palsy 1 2% monocular blindness 1 2% profound hypotension 7 16% bradycardia 3 7% severe hypotension and bradycardia* 3 7% hypertension and tachycardia 1 2% hyperthermia and metabolic acidosis 1 2% *two of the cases end with cardiac arrest and death. discussion the topical papaverine installation on the dissected cisterns after aneurysm clipping and just prior to dural closure can cause rare but diverse adverse effects ranging from temporary cranial nerve paresis to cardiac arrest and even death. the association of these complications with papaverine use was confirmed in all reports after the exclusion of all possible anesthetic and surgical causes. furthermore, the temporal association between the application of papaverine and the development of side effects confirmed that the primary cause was the drug itself rather than other factors. also, the type of papaverine formula used had no neurotoxic solvent in its composition (14). it is worth noting that although the distribution of the reported aneurysm locations was found to follow the classic pattern of incidence of the surgically managed intracranial aneurysms, one cannot deny the possibility of papaverine related complications may increase with both acoma and mca aneurysms as the surgery for such locations entails more arachnoid dissection and involve the opening of more subarachnoid cisterns than surgeries in other proximal locations. additionally, we suggest that aneurysm rupture may be one of the factors that contribute to papaverine toxicity as subarachnoid hemorrhage may render the brain and the cranial nerves more sensitive for the direct effect of papaverine, increasing the rate of complications. the most commonly cited theory for the reason behind papaverine-associated cranial nerve paresis is that papaverine likely exerts direct chemical toxicity, working in synchrony with the subarachnoid blood to irritate the already-sensitized cranial nerves. the hemodynamic and metabolic changes were explained in the literature by the possible effect of papaverine while in contact with vital centers in the hypothalamus and brainstem. as for the three reports that linked papaverine toxicity to the anterior thi rd ventriculostomy (opening of lamina terminalis), the authors of these reports hypothesized that the introduction of papaverine into the ventricular cavity through the 389 intracisternal papaverine toxicity in anterior circulation aneurysm clipping surgery fenestrated lamina terminalis may have resulted in direct chemical irritation to the hypothalamus and midbrain in the walls of the third ventricle and the vagal nucleus in the walls of the fourth ventricle (14, 16, 22). these complications can occur when papaverine is installed in the cistern after the fenestration of lamina terminalis (anterior third ventriculostomy or anterior ventriculocisternostomy). thus, papaverine can easily enter the third ventricle and become in direct contact with the hypothalamic nuclei in the ventricular wall. papaverine can also reach the fourth ventricle through the aqueduct of sylvius and exert its effect on the brainstem nuclei in the floor of the fourth ventricle. these complications would, inevitably, be more evident when papaverine is used in a nondiluted form or in a relatively high dose. considerable variability was found in the description of the used doses (concentration and amount) of papaverine to be installed into the cisterns during aneurysm clipping surgery. whether to dilute the papaverine or not and what is the best diluting fluid are still debatable issues and the decisions currently based on the surgeon's personal experience. conclusion intracisternal papaverine use is an effective method for the prevention of perioperative vasospasm during intracranial aneurysm clipping surgery. however, this is not a completely safe intervention and may be associated with toxicity, mainly in the form of temporary paresis to the adjacent cranial nerves or variable hemodynamic consequences. thus, precautions regarding dosing and monitoring must be contemplated when introducing topical papaverine into the surgical field. references 1. pool jl, jacobson s, fletcher ta. cerebral vasospasmclinical and experimental evidence. journal of the american medical association. 1958 jul 26;167(13):1599601. 2. dalbasti t, karabiyikoglu m, ozdamar n, et al. efficacy of controlled-release papaverine pellets in preventing symptomatic cerebral vasospasm. j neurosurg 2001; 95 (1): 44–50 3. majoie cb, van boven lj, van de beek d, et al. perfusion ct to evaluate the effect of transluminal angioplasty on cerebral perfusion in the treatment of vasospasm after subarachnoid hemorrhage. neurocrit care 2007; 6 (1): 40–44 4. vajkoczy p, horn p, bauhuf c, et al. effect of intra-arterial papaverine on regional cerebral blood flow in hemodynamically relevant cerebral vasospasm. stroke 2001; 32 (2): 498–505 5. sabouri m, rahmani p, rezvani m, nikbakht h, rafiee a, torkashvand m, eshraghi n, nourian n, moradi m. the effect of irrigation of intracisternal papaverine on cerebral blood flow in subarachnoid hemorrhage. advanced biomedical research. 2013;2. 6. zhou w. intraand post-operational changes in pupils induced by local application of cisternal papaverine during cerebral aneurysm operations 7. sheshadri v, surve r, chandramouli ba. papaverine is a confounding factor in neurological assessment after cerebral aneurysm clipping: report of three cases and review of the literature. journal of neuroanaesthesiology and critical care. 2016 jan;3(01):040-2. 8. zhou x, alambyan v, ostergard t, pace j, kohen m, manjila s, ramos-estebanez c. prolonged intracisternal papaverine toxicity: index case description and proposed mechanism of action. world neurosurgery. 2018 jan 1; 109:251-7. 9. zygourakis cc, vasudeva v, lai pm, kim ah, wang h, du r. transient pupillary dilation following local papaverine application in intracranial aneurysm surgery. journal of clinical neuroscience. 2015 apr 1;22(4):676-9. 10. ausman ji, slavin kv, charbel ft. pupillary changes after intracisternal injection of papaverine. surg neurol. 1994; 41:283. 11. pritz mb. pupillary changes after intracisternal injection of papaverine. surgical neurology. 1994 apr 1;41(4):2812. 12. mcloughlin al. intracisternal papaverine administration associated with acute onset of hyperthermia and metabolic acidosis in a craniotomy. journal of neurosurgical anesthesiology. 1997 jan;9(1):21-4. 13. lang ew, neugebauer m, ng k, fung v, clouston p, dorsch nw. facial nerve palsy after intracisternal papaverine application during aneurysm surgery. neurologia medico-chirurgica. 2002;42(12):565-7. 14. rath gp, prabhakar h, dash hh, suri a. hemodynamic changes after intracisternal papaverine instillation during intracranial aneurysmal surgery. bja: british journal of anesthesia. 2006 sep 19;97(6):848-50. 15. reddy s, goldman dr, kaines a, hubschman jp, sarraf d. intracisternal irrigation of papaverine leading to choroidal infarction. archives of ophthalmology. 2009 nov 9;127(11):1547-53. 16. baltaci b, basar h, ozcan a, gulhan y, aytunur cs. cardiac arrest after intracisternal papaverine instillation during intracranial aneurysm surgery: case report. journal of neurosurgery. 2010 oct 1;113(4):760-2. 17. srivastava vk, agrawal s, sahu s. association of acute onset hypertension and tachycardia following intracisternal papaverine administration during intracranial aneurysm surgery: a case report and review of the literature. journal of clinical anesthesia. 2011 may 390 zahraa f. al-sharshahi, samer s. hoz, mustafa e. almurayati et al. 1;23(3):224-6. 18. chittiboina p, willet o, nanda a, guthikonda b. transient oculomotor nerve palsy after topical administration of intracisternal papaverine. acta neurochirurgica. 2011 feb 1;153(2):431-3. 19. bala i, ghai b, kumar a, pratap m. bilateral pupillary dilatation after intracisternal papaverine application. anesthesia & analgesia. 2006 mar 1;102(3):965. 20. reddy km, rao gu, kolluri vs. profound hypotension after intracisternal papaverine. journal of neurosurgical anesthesiology. 2006 jul 1;18(3):221. 21. pritz mb. contralateral pupillary dilatation after intracisternal papaverine instillation. surgical neurology. 2007 may;67(5):546. 22. singla n, mathuriya sn, mohindra s, umredkar aa, adhikari s, gupta sk, gupta v. severe hypotension with intracisternal application of papaverine after clipping of an intracranial aneurysm. surgical neurology. 2009 dec;72(6):770-1. 23. chowdhury fh, haque mr. severe hypotension, cardiac arrest, and death after intracisternal instillation of papaverine during anterior communicating artery aneurysm clipping. a case report. acta neurochirurgica. 2013 feb 1:1-2. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-020 early diagnosis and management of traumatic dura tear with brachial plexus injury without spinal lesions in childhood a. khelifa, l. berchiche, i. assoumane, m. al-zekri, b. yakoubi, a. morsli romanian neurosurgery (2020) xxxiv (1): pp. 137-140 doi: 10.33962/roneuro-2020-020 www.journals.lapub.co.uk/index.php/roneurosurgery early diagnosis and management of traumatic dura tear with brachial plexus injury without spinal lesions in childhood a. khelifa1, l. berchiche1, i. assoumane2, m. al-zekri1, b. yakoubi1, a. morsli1 1 neurosurgical department of beo university hospital, algiers, algeria 2 national hospital of niamey, niger abstract although the dura is a thick membrane, it could be severed in spine surgery and less frequently by a traumatism (7,8,10); in this case, it is usually accompanied with bone or ligamentous injury (2). rare cases are reported of a traumatic dura tear without spinal lesion and would suspect in the first place a brachial plexus injury (2,8). dura tears are rarely seen in childhood (3). we report a case of early diagnosis of dura tear in brachial plexus injury without bone or ligamentous lesions on a child of 4 years old and we discuss the diagnostic and treatment modalities. introduction although the dura is thick membrane it could be severed in spine surgery and less frequently by a traumatism (7,8,10), in this case it is usually accompanied with bone or ligamentous injury (2). rare cases are reported of a traumatic dura tear without spinal lesion and would suspect in the first place a brachial plexus injury (2,8). dura tears are rarely seen in childhood (3). case presentation the patient is a 04 years old girl without past medical history; victim of traffic collision accident; clinically the patient was conscious presenting a left upper limb monoparesis. simple x-ray, ct, and then dynamic xrays found no more than a simple straightening of the cervical spine (figure 1). we complete by a cervical mri witch objectified a left epidural collection expanding from c2 to c5, hypointense on t1 weighted images hyperintense t2 weighted images causing spinal cord and roots compression (figure 2). we operate the patient approaching the collection through a laminoplasty from c3 to c7. the collection appeared to be a csf leak through a dura tear which was repaired with a watertight closure. in post-operative the patient was oriented to physical medicine where she recovered totally from her motor deficit in two months. keywords dura tear, paediatric spinal trauma, brachial plexus injury corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 138 a. khelifa, l. berchiche, i. assoumane et al. figure 1. a: simple spine x-ray. b: cervical spine ct (bone window). c: dynamic x-ray on flexion. d: dynamic x-ray on extension; those images showed a straightening of the cervical spine without bone lesions or instabilities. figure 2. preoperative mri showing an epidural collection (the arrow). a: sagittal t2 weighted image, b: axial t1 weighted image, c: axial t2 weighted image. discussion the dura mater is a thick membrane of connective tissue that covers the brain and the spinal cord composed of collagen and elastin fibers, it’s biomechanical proprieties was frequently studied especially in the lumbar region, but there is no available study of the difference in those proprieties between adults and children (1).the dura tear (dt) can be in the first place iatrogenic and less frequently traumatic or congenital. in fact dts have an incidence that could reach 17% of all spine surgeries according to some series (2,4). a large study held by hiroyuki yoshihara and daisuke yoneoka in 2009 included 190,021 patients who underwent a cervical spine surgery a dt was found during surgery in 855 patients (0.45% of all patients), this sample include 880 patients under 17 years old and no one was diagnosed with dt (3). traumatic dts are rarer than iatrogenic (7,8,10), even though they still complicate 18% to 36% of all spine injuries (2). traumatic dt can be divided into penetrating and blunt traumas. burst fractures associated with laminar fracture are predictive 100% of sensitivity and 74% of specificity to a dt (6). luszczyk et al published a study including 1615 spinal traumas, 187 patients of theme was diagnosed with traumatic dt; 36% (67 patients) of these dts were in the cervical spine; 26.2% are burst fractures (ao type a3), 16% flexion distraction lesions (ao type b), and 36.4% are fracture dislocations (ao type c); other lesions included atlanto axial dislocations, flexion compressions lesions, extension lesions, and sacral fractures; the study did not report dts without spinal lesion (2). in absence of spine lesion traumatic dt can complicates brachial plexus injuries, in fact dt can be the result of the stretching of spinal roots between two mobile parts (8,10). dt resulting of brachial plexus injuries are rarely reported (8). in those cases the dt is located in the transition zone (11). according to bonney’s classification of the pregonglionar injuries of the brachial plexus, roots lesions distal to the transition zone (type b) could be complicated by an intra or extra spinal dt (13). the dt will allow under hemodynamic pressure the csf leakage along the nerve course and in the epidural space (11). the dt by itself doesn’t present a clinical problem (6) and it could heal spontaneously (11). but in some cases this collections will spread and gain an arachnoid covering forming what most authors call pseudomeningocele (2,3,5,7,8,10,11) causing compression of nerve structures and responsible of neurologic deficit appearing months or years after the traumatism (8,10). other complications are seen: spinocutaneous fistula (2,3,4 ,6,7,8), meningitis (2,3,4,8), arachnoiditis (2,7,8), epidural abscess (2,7), and intracranial hypotension (2,7,8,9,10). large part 139 early diagnosis and management of traumatic dura tear of dts could pass asymptomatic (8,10). neurologic deficit could happen due to the compression or even the entrapment of the roots or nerves by a pseudomeningocele, appearing months or years after the traumatism (6,7,8,10,11); other clinical presentations could include: subcutaneous palpable masse that might be painful, collection or fistula (7,8,10), cervical pain, headache, or sciatalgia (7,8). as in our case, conventional ct is unhelpful to the diagnosis and mri should be performed in presence of neurologic deficit non explained by the ct. mri sensitivity could reach 97% and 100% in some studies (7,9), it shows an epidural collection hypointense in t1 weighted images and hyperintense in t2 weighted images. that collection is considered a diminution of dura sac volume rather than an epidural fluid, t.hosoya et al proposed to call it “the floating dura sign” (9,12). t. yagi et al classified epidural fluid collections in three types according to their relation with the dural sac: type v, for ventral location; type c, for circularly; and type d for dorsally (9). fat suppression sequences are very helpful to differentiate the collection from the epidural fat (9,12). when a dt is highly suspected invasive imaging modalities might be performed like ct myelography or retrograde radionuclide myelography (7,8,10,11,12). the management of patients with dura tears differs whether the dura tear was diagnosed in pre, per, or in post-operative. away from the operating room, in preor postoperative; if a csf leak was found, the bed rest in the trendelenburg position could be effective; the body is laid supine, or flat on the back with a 15 to 30-degree inclination and the feet elevated (3,8,9,10). another option that showed to be effective is to put a subarachnoide lumbar drain for 4 days collecting from 200 to 300 ml per 24 hours (2,3,4,7,8). recently blood patch has been reported as very effective technique, by injecting 20 ml of precubital venous blood in the epidural space and in contact with the csf it will form a clot that obstructs the dt (7,8,9,10). with an intraoperative dt and in any case a watertight closure should be tented as long as possible and a in addition gelfoam and surgicel are recommended (2,3,4,7,8,10). hermetic fascia closure is mandatory (7).in case of brachial plexus injury the dura tear could be far lateral and thus a direct closure is difficult, in such cases mayfield and kurokawa proposed to open the dura medially and plunge a piece of fat or muscle with witch the lateral tear is obstructed from the intradural space (7). the fibrine glue is an easy effective complement or alternative if the suture is not possible (2,4,5,7,8). a subfascial drain is preferred (7). conclusion dura tear is an unfortunate accident that could happen in several conditions including spinal traumatism. although it’s not a problem by itself and could heal spontaneously or stay asymptomatic, some complications could appear later, though spinal mri with adequate sequences should be a part of the diagnosis protocol even if the lesion is well defined by the spinal ct. declarations of interest none. funding this research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. references 1. chauvet d, carpentier a, allain jm, polivka m, crépin j, george b. histological and biomechanical study of dura mater applied to the technique of dura splitting decompression in chiari type i malformation. neurosurg rev. 2010 jul;33(3):287-94; discussion 295. doi: 10.1007/s10143-010-0261-x. epub 2010 may 4. 2. myles j. luszczyk et al. traumatic dural tears: what do we know and are they a problem? the spine journal 14 (2014) 49–56. http://dx.doi.org/10.1016/j.spinee. 2013.03.049 3. hiroyuki yoshihara, and daisuke yoneoka. incidental dural tear in cervical spine surgery analysis of a nationwide database. j spinal disord tech _ volume 28, number 1, february 2015. 4. m. lopesa, t. faillot b. dural tears: regarding a series of 100 cases. neurochirurgie 61 (2015) 329–332. http://dx.doi.org/10.1016/j.neuchi.2015.06.005 5. soo eon lee, chun kee chung, tae-ahn jahng, chi heon kim. dural tear and resultant cerebrospinal fluid leaks after cervical spinal trauma. eur spine j. doi 10.1007/s00586-014-3332-9. 6. by frank p. cammisa, jr, frank j. eismoni, and barth a. green. dural laceration occurring with burst fractures, and associated laminar fractures. the journal of bone and joint surgery.1989. 7. stephen j. bosacco, michael j. gardner, and james t. guille. evaluation and treatment of dural tears in lumbar spine surgery a review. clinical orthopaedics and related research. number 389, pp. 238–247.2001. 8. mark w. hawk, and kee d. kim. review of spinal 140 a. khelifa, l. berchiche, i. assoumane et al. pseudomeningoceles and cerebrospinal fluid fistulas. neurosurg. focus / volume 9 / july, 2000. 9. takashi yagi, toru horikoshi, nobuo senbokuya, hiroaki murayama, and hiroyuki kinouchi. distribution patterns of spinal epidural fluid in patients with spontaneous intracranial hypotension syndrome. neurol med chir (tokyo) 58, 212–218, 2018. doi: 10.2176/nmc.oa.2017-0227. 10. samantha knight. pseudomeningocele. encyclopedia of clinical neuropsychology. 25 march 2017. doi: https://doi.org/10.1007/978-3-319-56782-2_9036-2. 11. lt col hariqbal singh, maj vljai chandran, col sk khanna, lt col l satija. post traumatic pseudomeningocele. mjafi 1999; 55 : 151-152. 12. hosoya t, hatazawa j, sato s, kanoto m, fukao a, kayama t. floating dural sac sign is a sensitive magnetic resonance imaging finding of spinal cerebrospinal fluid leakage. neurol med chir (tokyo). 2013;53(4):207-12. 13. sophie.j. camp. peripheral nerve injury. neurosurgery: cases with expert commentary. page 179. e.book: books.google. doi: 10.33962/roneuro-2022-082 penetrating head injury caused by a screwdriver. a case report jovan ilić, vesna nikolov, marija djordjević, aleksandar kostić, miloš stojanović romanian neurosurgery (2022) xxxvi (4): pp. 456-459 doi: 10.33962/roneuro-2022-082 www.journals.lapub.co.uk/index.php/roneurosurgery penetrating head injury caused by a screwdriver. a case report jovan ilić1, vesna nikolov1,2, marija djordjević2, aleksandar kostić1,2, miloš stojanović2 1 department of neurosurgery, university clinical centre of niš, niš, serbia 2 faculty of medicine, university of niš, niš, serbia abstract background: penetrating head injuries (phi) caused by sharp objects are associated with a high risk of potentially life-threatening complications and are estimated to account for approximately 0.4% of all head injuries. since not many cases of phi with a screwdriver have been described in the literature, the treatment of these patients is quite controversial and non-standardized. therefore, the aim of this paper was to present our experience with treating a patient with a phi caused by a screwdriver. case description: the authors present a three-year-old female patient who accidentally sustained a phi with a screwdriver through the right orbit. a computed tomography scan of the head was performed, which demonstrated the presence of the metal end of a screwdriver in the anterior cranial fossa. the patient underwent emergency surgery and the foreign body was evacuated with the repair of dura and brain injury. the intervention was followed by a complete postoperative recovery without any gross neurological deficits. follow-up examinations were performed up to three years after the injury, while the patient's condition remained unchanged. our patient's case supports immediate neurosurgical intervention and removal of a foreign object from the endocranium. introduction penetrating head injuries (phi) of non-missile origin caused by sharp objects are associated with a high risk of potentially life-threatening complications and are estimated to account for 0.4% of all head injuries (3). areas with cranial openings and with a thinner bone, such as the orbit and the squamous portion of the temporal bone, are more susceptible to penetrating injuries caused by sharp objects (2). however, these injuries constitute only a small number in the pediatric population and the transorbital localization of phi has been reported in about 45% of pediatric cases, while it occurs in 25% of adult phi cases (1,6). although penetrating head injuries caused by a screwdriver are rare, these injuries should not be neglected due to the length of the screwdriver and the spiral force, as well as the fact that the metal end of the tool can rotate in the skull and cause serious trauma. moreover, keywords craniocerebral trauma, craniotomy, paediatric brain injury, penetrating head injury corresponding author: jovan ilić department of neurosurgery, university clinical centre of niš, serbia jovanilicneuro@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 457 penetrating head injury caused by a screwdriver the superficial skin wound does not correspond to the severity of intracranial trauma, so the extent of trauma can be easily overlooked (10). these injuries may be accompanied by rare contrecoup lesions and radiating skull fractures, depending on the dimensions of the screwdriver (8). since not many cases of phi with a screwdriver have been described in the literature, the treatment of these patients is quite controversial and nonstandardized. case report the authors present a three-year-old female patient who accidentally sustained a phi with a screwdriver through the right orbit (figure 1). the patient did not lose consciousness or vomit after the injury. she was previously examined by an ophthalmologist and a pediatric surgeon at the local hospital. during the neurosurgical examination, on admission, the patient was conscious, oriented to time, space and person (glasgow coma scale score of 15), cardiopulmonary stable, without any recorded gross neurological deficits. figure 1. the metal part of the screwdriver passes through the medial part of the orbit. a computed tomography (ct) scan of the head was performed, which demonstrated the presence of a metal end of a screwdriver in the anterior cranial fossa (figure 2, figure 3). the ct scan did not detect any vascular or brain parenchyma injuries. figure 2. the axial (a), sagittal (b) and coronal (c) ct tomograms demonstrate a metallic foreign body, penetrating the medial wall of the right orbit and partially through the roof of the ipsilateral orbit, with the metal tip extending along the cerebral falx. the brain parenchyma was without evident and detectable injury. figure 3. a 3-d ct scan revealed the penetrating injury in the anterior cranial fossa. after an adequate preoperative examination, the patient underwent an emergency surgery. during the operation, the head was positioned for a pterional craniotomy with little deflection and greater rotation of the head by using the skull fixation device and an arcuate incision was made starting from the projection of the zygomatic arch anterior to the tragus in the length of about 15 cm and behind the hairline area. the dissection of the temporal muscle was done in the interfacial fashion. afterwards, the fronto-temporo-sphenoidal craniotomy was performed with the three points of trepanation. 458 jovan ilić, vesna nikolov, marija djordjević et al. following an adequate hemostasis and the incision of the dura mater, the prophylactic dural tenting sutures (dts) were placed through the perforations made along the edges of the pterional craniotomy. upon accessing the anterior cranial fossa and the olfactory cistern, a metal end of the screwdriver was encountered, which superficially injured the right olfactory bulb and right gyrus rectus, as well as the right medial frontobasal artery, while the metal tip was extending along the cerebral falx. moreover, the screwdriver was then removed by pulling the handle outwards, with taking special consideration about the potential twisting of the screwdriver, which must not occur. furthermore, the authors managed the superficial injuries of the previously mentioned areas of the brain tissue and blood vessels with the use of regenerated oxidised cellulose (surgicel®). a penetrating bone defect was irrigated with hydrogen peroxide and normal saline profusely. the dura mater was repaired with simple interrupted absorbable vicryl sutures and collagen-based dural graft (duragen®), an epidural drain was placed, while the bony lid was returned with titanium plates. the patient was treated with dual antibiotic therapy (ceftriaxone in the dose of 750 mg once a day and metronidazole in the dose of 100mg three times a day) as well as with prophylactic anticonvulsant therapy (levetiracetam-oral solution in the dose of 150mg twice a day). both tetanus toxoid and tetanus immunoglobulin were administered due to the unknown immunization status of the patient. the intervention was followed by a complete postoperative recovery without any gross neurological deficits. follow-up examinations were performed up to three years after the injury, while the patient's condition remained unchanged. discussion due to the lack of adequate recommendations in the scientific literature, insufficient retrospective data collection, as well as described complications arising from such a rare mechanism of injury, there is no consensus on the adequate treatment of patients with phi with a screwdriver. although head ct indicated that there was no injury to brain and vascular structures, non-operative screwdriver extraction was initially rejected due to the possibility of injuring numerous structures of the brain base as well as the formation of a cerebrospinal fluid fistula. depending on the characteristics and dimensions of the screwdriver, whether the screwdriver has a larger or smaller cross-sectional area of the tip, taking into account the sharpness of the tip and the applied stabbing force, these objects make a disproportionately small skin stab wound in comparison to the injuries of the intracranial structures they cause (8). our patient reportedly tripped and fell head first on the tip of a screwdriver, sustaining a penetrating injury through the right orbit. although the gold standard in the diagnostic assessment of these patients is brain ct with ct angiography if blood vessels injury is suspected (7), no brain injuries were reported on the brain ct, while superficial brain lesions were determined during the operation. the most common complications of these injuries are vascular injuries, which occur in 19% of patients, and often in the form of pseudoaneurysms (46%) and cutting of blood vessels (32%), and therefore require treatment (5). after a penetrating brain injury occurs, thromboplastin is released, which promotes blood coagulation, while on the other hand, intracerebral bleeding can occur as well. disseminated intravascular coagulation, acute respiratory distress syndrome and neurogenic pulmonary edema may develop. if the screwdriver is not surgically removed 48 hours after injury, the chance of acquiring meningitis and brain abscess increases from 4.6% to 36.5% (8,9). for those reasons, the authors decided on an urgent operation and removal of the screwdriver from the anterior cranial fossa with preventive irrigation of the operative field and administration of dual antibiotic therapy. moreover, about 50% of these patients develop a late post-traumatic epilepsy (8,9). consequently, we decided on convulsion prophylaxis for a year, and the patient has not experienced any form of convulsions to this day. although when deciding on a surgical approach, one could opt for the right frontal approach, the right subfrontal approach and other approaches (3), we decided on the pterional approach because it allowed us to see all the structures affected by the injury and enabled the repair of the dura mater lesion. aesthetic reasons also played a role as most 459 penetrating head injury caused by a screwdriver of the scar would be covered by hair after the wound had healed. the use of dts in hemostasis is an important technique, which can lead to unnecessary complications if they are placed before opening of the dura. in elderly patients, subdural hygromas may occur after placement of dts (4). we decided therefore to place dts after opening the dura and visualizing the brain tissue through a microscope. conclusion in conclusion, this is a very peculiar case of a phi with a screwdriver, while the authors of this paper have not found a similar case described in the literature. it is necessary to make an adequate diagnosis as soon as possible and urgently surgically evacuate the screwdriver from the endocranium with adequate medical therapy in order to prevent possible complications. references 1. awori j, wilkinson da, gemmete jj, thompson bg, chaudhary n, pandey as. penetrating head injury by a nail gun: case report, review of the literature, and management considerations. j stroke cerebrovasc dis 2017;26(8):e143-149. https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.04.0 04 2. bodwal j, sreenivas m, aggrawal a. intracranial penetrating injury by screw driver: a case report and review of literature. j forensic leg med 2003;20(8):972975. https://doi.org/10.1016/j.jflm.2013.09.010 3. de tommasi a, cascardi p, de tommasi c, luzzi s, ciappetta p. emergency surgery in a severe penetrating skull base injury by a screwdriver: case report and literature review. world j emerg surg 2006;1(1):1-4. https://doi.org/10.1186/1749-7922-1-36 4. eroglu u, zaimoğlu m, sayacı ey, ugur hc, attar a, kahilogullari g, bozkurt m, ünlü ma, özgüral o, doğan i̇, seçinti kd. is placing prophylactic dural tenting sutures a dogma? world neurosurg 2021;153:e403-407. https://doi.org/10.1016/j.wneu.2021.06.131 5. harrington bm, gretschel a, lombard c, lonser rr, vlok aj. complications, outcomes, and management strategies of non-missile penetrating head injuries. j neurosurg 2020;134(5):1658-1666. https://doi.org/1 0.3171/2020.4.jns20122 6. karim t, topno m. an unusual case of penetrating head injury in a child. j emerg trauma shock 2010;3(2):197. https://doi.org/10.4103/0974-2700.62113 7. moussa wm, abbas m. management and outcome of low velocity penetrating head injury caused by impacted foreign bodies. acta neurochir 2016;158(5):895–904. https://doi.org/10.1007/s00701-016-2764-x 8. pavlidis p, karakasi mv, birbilis ta. traumatic brain injury due to screwdriver assaults: literature review and case report. am j forensic med pathol 2016;37(4):291-298. https://doi.org/10.1097/paf.0000000000000267 9. rutherford gw, corrigan jd. long-term consequences of traumatic brain injury. j head trauma rehabil 2009;24(6):421–423. https://doi.org/10.1097/ htr.0b 013e3181c13439 10. shi j, mao y, cao j, dong b. management of screwdriverinduced penetrating brain injury: a case report. bmc surg 2017;17(1):1-4. https://doi.org/10.1186/s12893-0160195-5 https://doi.org/1 doi: 10.33962/roneuro-2023-017 mature cystic teratoma of spinal cord in an adult. a rare tumour rajneesh misra, sushil kumar, sandeep sharma romanian neurosurgery (2023) xxxvii (1): pp. 107-110 doi: 10.33962/roneuro-2023-017 www.journals.lapub.co.uk/index.php/roneurosurgery mature cystic teratoma of spinal cord in an adult. a rare tumour rajneesh misra1, sushil kumar2, sandeep sharma3 1 robert jones and agnes hunt royal orthopaedic hospital, oswestry, uk 2 st. stephens hospital, tis hazari, delhi, india 3 safdarjung hospital, ansari nagar east, new delhi, india abstract aim: reporting a rare case of mature cystic teratoma of spinal cord in an adult background: teratomas of the central nervous system are rare lesions accounting for less than 0.5-2% of all cns tumors. most of these are found in pediatric age group and favor sellar suprasellar, pineal and sacro-coccygeal regions. their occurrence in spinal cord in an adult is incredibly rare. case presentation: a 22-year-old male presented with low back ache and weakness of both lower limbs. clinical examination and radiological workup revealed presence of a cystic lesion causing diffuse enlargement of the cord from l1 to l5-s1. histopathological examination of the excised lesion revealed it to be teratoma. conclusion and clinical significance: mature teratoma of the spinal cord in adults is extremely rare occurrence. however, this diagnosis should be kept in mind when evaluating a cystic lesion of cord even in adults. maximal safe resection of the lesion results in prolonged deficit free survival. background teratomas of the central nervous system are rare lesions. barring the sacro-coccygeal region, their occurrence in spinal cord is a rarity. they constitute only 0.5% of intraspinal tumors. case presentation: a 22-year-old male had presented with complaints of weakness of both lower limb in the last three months. he had difficulty in clearing the feet off the ground. this was associated with altered sensation in the left leg in a below knee distribution where he was not able to feel the temperature of water properly when bathing. he had a history of low back ache on and off for 4 years which was relieved by rest and analgesics. there were no ‘red flags’ till his presentation with weakness. he denied any history of trauma, lumbar puncture, bowel or bladder incontinence or fever. he was not forthcoming about his sexual history probably due to cultural reasons. on examination, his vitals were normal, and the local examination of spine did not reveal any stigmata of spinal dysraphism. there was no keywords spinal teratoma. adult teratoma, cauda equina, conus medullaris corresponding author: rajneesh misra st. stephens hospital, tis hazari, delhi, india misra_rajneesh@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 108 rajneesh misra, sushil kumar, sandeep sharma deformity. the power in both ankle dorsiflexors and great toe extensors was 3/5. it was largely unaffected in all other muscle groups. sensory examination revealed almost complete loss to touch, pain, and temperature in left l4 to s1 distribution and by about 25-30% in s2 to s4 distribution. bilateral knee and ankle jerks were absent, and planters were mute. mri imaging revealed a large irregular intradural lesion of spine extending from l2 to l5-s1 junction which was hypointense on t1 and hyper intense on t2 with irregular enhancement on contrast (fig. 1) figure 1. preoperative mri shows the lesion extending from upper border of l2 vertebra to lower border of l5.it has typical cystic appearance , hypo intense on t1 (a & d) with enhancement of walls on contrast (b & e). the contents are hyperintense on t2 (c & f) along with a syrinx in the cord. the lesion itself is pointed with hollow arrows. the patient underwent l1-l5 laminectomy. on dural opening, a thick-walled lesion was found adherent to the conus and cauda roots. on opening the cavity, greenish pus-like fluid was drained. the wall was dissected piecemeal, and a small residual was left over one of the roots. the intraoperative picture was indicative of an epidermoid cyst. histopathogical picture showed presence of all three germ cell layer derivatives indicative of a mature teratoma. post operative period was complicated by presence of csf leak which abated after removal of drain , pressure dressing and keeping the patient in prone position for 3 days. before discharge on 10th day, the patient’s motor status had improved to 4/5 in both ankle dorsiflexors and great toe extensors. he had a residual sensory loss of about 50% in left l5 and s1 distribution. he has been followed up for last seven years and he has recovered a power of 5/5 in all muscle groups with minimal sensory loss in left s1 distribution. follow up mri showed presence of a residual lesion at the tip of conus which was mildly hyperintense on t1 with no contrast enhancement and hypointense on stir (fig2). this is consistent with fatty tissue which may have been the small fragment that was left attached to one of the roots intraoperatively. figure 2. mri image at eight years follow up shows residual lesion (marked with hollow arrows) opposite the lower half of l3 vertebra which is hyperintense on t1(a&d) and hypointense on stir (b & e) indicating fatty tissue. there is no evidence of syrinx. discussion the spinal tumors are classified according to their location. the idem lesions constitute about 55% of all spinal tumors. the most common idem tumors in 109 mature cystic teratoma of spinal cord in an adult adults are nerve sheath tumors and meningioma [1]. virchow reported the first spinal teratoma. this occurs more frequently in children with spinal dysraphism and is associated with various malformations like spina bifida, tethered cord, and split cord malformations of various types [2-7]. sloof et al in their series of 1322 patients of spinal cord tumors, identified only 2 patients with teratoma [8]. al-sarraj et al had seven cases with a histological diagnosis of teratoma in a series of 25,000 cases over a period of 15 years [9]. thus, spinal cord teratomas are in general very rare. moreover, they occur far less frequently in adults. spinal teratoma in adults can have variable presentation and in general have a set of presenting symptoms like other idem lesions. however, there is a significant alteration in frequency of these symptoms compared to idems in general. usually, there is nothing in presentation that points specifically to the diagnosis. in our case, the patient presented with syndrome suggestive of a conuscauda lesion. poeze et reviewed 31 cases of intramedullary teratomas and found motor dysfunction to be the most common presentation (71%), followed by changes in reflexes, sensory changes, urinary changes, and pain [6]. far less common were sexual disturbances and anal sphincter disturbances. on the other hand, a prospective study in 107 patients of idem tumors by tarantino et al found pain to be the most common presentation followed by sensory deficits. the motor deficits at presentation were distant third (12%) [10]. specific diagnosis of teratomas on imaging is difficult. they, in general have a picture like other idem tumors. on mri, they appear lobulated or cystic, with variable signal intensity and enhancement consistent with the different solid and cystic components of the tumor [11, 12]. ct imaging is nonspecific and reveals differences in densities within the tumor consistent with different tissue types [13]. the role of imaging is more for preoperative planning and the decision regarding location of the tumor in relation to the cord rather than a definitive diagnosis. ultimately, the diagnosis of teratoma rests on histopathological demonstration of all the three germ layers in the specimen. currently there are two proposed theories for the origin of spinal teratoma, the misplaced germ cell theory and the dysembryogenic theory [14, 15]. regardless of the origin, the prognosis of teratoma is dictated by the classification into mature, immature, and malignant. the mature ones have an overall benign course once resected. however, the malignant teratoma as the name suggests, have an aggressive and stormy course with poor prognosis. the primary mode of treatment is surgical resection, and the goal is decompression of the neural tissue without causing further deficits. however, complete resection is a realizable goal in about 50% of cases and should always be attempted with patient safety in mind [16]. however, many authors suggest not attempting a complete resection citing the logic that these are slow growing tumors affording a large window period for picking up a recurrence and that the rate of recurrence with partial and complete resection is very similar (11% vs 9%) [17,18]. the overall prognosis for mature teratoma of spine is good following surgical resection with most patients reporting either improvement or stabilization of symptoms. however, most case reports [3, 6] have a short follow up. the patient in our case was followed up for approximately 8 years and showed improvement of all symptoms except mild sensory abnormality in left s1 dermatome. the rarity of these lesions in adults makes it difficult to design a long-term study of disease progression. currently, there is no evidence supporting any role for chemotherapy or radiotherapy for mature teratoma following resection [19]. conclusion and clinical significance spinal mature teratomas in adults are very rare. the clinical presentation is like any other idem tumor or conus-cauda lesion. imaging modalities also do not offer any specific distinguishing features from other similar lesions in the region. however, this differential diagnosis must always be considered when evaluating a radiological picture of cystic lesion of the spinal cord. the treatment rests on maximal safe surgical resection with an attempt for complete resection. these patients are likely to have a prolonged near deficit free course even in the long term. list of abbreviations mri: magnetic resonance imaging t1wi: t2 weighted image t2wi:t1 weighted image idem: intradural extramedullary 110 rajneesh misra, sushil kumar, sandeep sharma ct: computer tomography csf: cerebrospinal fluid stir: short tau inversion recovery references 1. gebauer gp, farjoodi p, sciubba dm, gokalsan zl, riley lh 3rd, wasserman ba, et al.(2008) magnetic resonance imaging of spine tumors: classification, differential diagnosis, and spectrum of disease. j bone joint surg am;90 suppl 4:146-62. 2. ak h, ulu mo, sar m, albayram s, aydin s, uzan m.(2006) adult intramedullary mature teratoma of the spinal cord: review of the literature illustrated with an unusual example. acta neurochir (wien);148:663-9. 3. guvenc bh, etus v, muezzinoglu b.(2006) lumbar teratoma presenting intradural and extramedullary extension in a neonate. spine j;6:90-3. 4. makary r, wolfson d, dasilva v, mohammadai a, shuja s.(2007) intramedullary mature teratoma of the cervical spinal cord at c1-c2 associated with occult spinal dysraphism in and adult. case report and review of literature. j neurosurg spine; 6:579-84. 5. nonomura y, miyamoto k, wada e, hosoe h, nishimoto h, ogura h, et al. (2002) intramedullary teratoma of the spine: report of two adult cases. spinal cord; 40:40-3. 6. poeze m, herpes mj, tjandra b, freling g, beuls ea.(1999) intramedullary spinal teratoma presenting with urinary retention: case report and review of literature. neurosurgery; 45:379-85. 7. sung ks, sung sk, choi hj, song yj.(2008) spinal intradural extramedullary mature cystic teratoma in an adult. j korean neurosurg soc; 44:334-7. 8. koen jl, mclendon re, george tm.(1998) intradural spinal teratoma: evidence for dysembryogenic origin. report of four cases. j neurosurg; 89(5):844-51. 9. al-sarraj st, parmar d, dean af, phookun g, bridges lr.(1998) clinicopathological study of seven cases of spinal cord teratoma: a possible germ cell origin. hispathology; 32:51-6 10. tarantino r, donnarumma p, nigro l, rullo m, santoro a, delfini r. (2014) surgery of intradural extramedullary tumors: retrospective analysis of 107 cases. neurosurgery; 75(5):509-14. 11. li y, yang b, song l, yan d.(2013) mature teratoma of spinal cord in adults: an unusual case. onco let;6(4):9426. 12. monajati a, spitzer rm, wiley jl, heggeness l.(1986) mr imaging of spinal teratoma. j comput assist tomogr;10(2);307-10 13. hamabuchi m, hasegawa r, murase t.(1989) teratoma of the spinal cord. a case report with ct scans. j bone joint surg br;71(3):390-2. 14. kalani my, iyer s, coons sw, smith ka.(2012) spinal intradural teratomas: developmental programs gone awry? neurosurg focus;33(4):e1. 15. koen jl, mclendon re, george tm.(1998) intradural spinal teratoma: evidence for dysembryogenic origin. report of four cases. j neurosurg; 89(5):844-51. 16. rosenbaum tj, soule eh, onofrio bm.(1978) teratomatous cyst of the spinal canal. case report. j neurosurg;49(2):292-7. 17. nonomura y, miyamoto k, wada e, hosoe h, nishimoto h, ogura h, et al.(2002) intramedullary teratoma of the spine: report of two adult cases. spinal cord; 40:40-3. 18. hejazi n, witzmann a.(2003) spinal intramedullary teratoma with exophytic components: reports of two cases with review of literature. neurosurg rev:26(2):1136. 19. allsopp g, sgouros s, barber p, walsh ar.(2000) spinal teratoma: is there a place for adjuvant treatment? two cases and review of literature. br j neurosurg;14(5):4828. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0056 article post traumatic biparietal mirror extradural haematoma – a case report and review of literature g. venkateswara prasanna, sathish kumar vandanapu, hima bindu india      458 | prasanna et al post traumatic biparietal mirror extradural haematoma             doi: 10.2478/romneu-2018-0056 post traumatic biparietal mirror extradural haematoma – a case report and review of literature g. venkateswara prasanna1, sathish kumar vandanapu2, hima bindu3 1,2consultant neurosurgeon, 3consultant radiologist simhapuri institute of neurological sciences, simhapuri hospital, nellore, andhra pradesh, india abstract: bilateral extradural haematomas [edh] are rare and it is an uncommon consequense of cranio cerebral trauma. the mortality is higher than unilateral extradural haematoma and management of extradural haematomas requires careful planning, judicial surgical exposure and most important is timing of evacuation of extradural haematomas. emergency evacuation of bilateral extradural haematomas were performed in this case with uneventful postoperative period. the pathophysiology and surgical nuances of this rare entity been discussed. key words: extradural haematoma, biparietal, symmetric introduction biparietal mirror extradural haematoma is extremely rare with only a handful of cases reported in literature.1,2,8,9,12 incidence of bilateral edh ranges from 2 to 25%.3 bifrontal edh is most common among bilateral edh. biparietal mirror extradural haematoma is a rare entity. emergency evacuation of bilateral extradural haematomas with bilateral craniotomies is the treatment of choice. biparietal extradural haematoma is associated with low gcs and associated with higher mortality than solitary edh if not timely interfered. authors report a case, who had low gcs on admission, been subjected to emergency bilateral craniotomies with uneventful postoperative period, with good outcome. case report a 25year-old male was brought to our emergency department, 24 hours following a motor vehicle accident. initially treated in a local hospital, been referred following neurological deterioration. history of loss of consciousness is present. history of multiple episodes of vomiting is present. on assessment, he had a gcs of 5/15 for which he was intubated. pupils were asymmetric with sluggish reaction to light. examination of scalp suggestive of diffuse subgaleal hamaetoma. his computed tomography (ct) scan brain showed a symmetrical biparietal edh with bilateral parietal linear fractures. emergency evacuation of bilateral extradural haematoma was done. with the patient in prone bilateral romanian neurosurgery (2018) xxxii 3: 458 461 | 459             horse shoe scalp flaps over the parietal eminences were raised. bilateral parietal craniotomies were done and haematoma evacuation was done. arterial bleeders were identified and coagulated. dural hitches were taken. complete haemostasis been achieved. bilateral parietal bone flaps were replaced. post-operative scan showed no residual haematoma. post-operative period was uneventful. he made a gradual recovery and was discharged on 10th postoperative period in good condition, with gcs of 15/15. discussion contact injuries resulting from blunt trauma cranium results in edh. extradural haematoma is the most common manifestation of traumatic brain injury. roy in 1884 reported the first case of bilateral edh. the incidence of bilateral edh ranges from 2 25%.3,7 of these bilateral edhs bilateral frontal edh is the most common.7 male to female ratio is 5:1.12 very few cases of symmetric bilateral edh were reported in literature.1,8,9,12 various theories were postulated for bilateral injuries, the impact tend to be on anteroposterior direction rather than lateral direction.4 dura is detached from two sites by a unidirectional force. stripping of dura can ocuur at the site of impact by inbending or outbending of skull or due to motion of skull. it can be due to extension of fracture line across midline, which is most commonly seen in bifrontal and bilateral posterior fossa edh.9 coup and countra coup injuries to the skull can also cause bilateral edh.11 bilateral edhs are different from solitary edh. they are associated with significant trauma, evolve rapidly, and are associated with high mortality.6,7 patients with bilateral edhs less frequently have a lucid interval, have a lower gcs, lateralization is frequently absent, and deteriorate more frequently than individuals with unilateral edh.4,7,8,10 one entity similar to bilateral edh is the double edh. in double edh, edh is found in two locations irrespective of laterality and symmtricity.7 in this case we report bilateral symmetric biparietal edh, were only few cases have been reported. table 1 summarizes the reported cases. table 1 literature review on traumatic symmetric biparietal extradural hematomas author no of cases age/sex mode of injury gcs treatment final outcome (gcs) idei et al1 1 72/m fall na surgery b/l good (15) ramzan et al2 2 na na na na 14 8 surgery b/l surgery b/l good(15) fair(12) udoh et al3 2 64/m rta 11 left-surgery; right-resolved good(15) 460 | prasanna et al post traumatic biparietal mirror extradural haematoma             60/m rta 7 surgery b/l died agrawal et al4 1 55/f fall of object 9 surgery b/l good(15) prasad et al13 2 60/m 30/m rta rta 4 7 surgery b/l surgeryb/l good(15) good(15) prasanna et al (present) 1 25/m rta 5 surgery b/l good(15) abbreviationsgcs -glasgow coma scale; b/l-bilateral; na-not available; rtaroad traffic accident figure 1 plain ct brain showing bi parietal edh edhs secondary to blunt trauma with skull bone fractures, the fracture detaches the dura and injures blood vessels, once bleeding begins the extradural space is filled with blood. arterial bleeding produces hydrostatic water pressure, leading to stripping away of dura from the skull and widening the perimeter of the haematoma. venous bleeding is slower, tends to be smaller in size and less severe due to ease of spontaneous arrest.12 in this case cause of biparietal edhs is linear skull fractures injuring the arterial vessels which were coagulated during haematoma evacuation. figure 2 – post-operative image showing bi parietal craniotomies with complete evacuation of haematomas surgical evacuation of haematoma should be done on emergency basis. side of surgery depends on volume of hematoma. it has been suggested that with similar volumes bilaterally, craniotomy and evacuation need to be performed on both sides, initially on dominant side or simultaneously by two groups of neurosurgeons.1,3,8 agrawal suggested use of bicoronal skin flap, performing of craniotomies on both sides and then evacuation of hematoma sequenitially.1 in our case, patient is placed in prone position bilateral horse shoe scalp incisions centered on romanian neurosurgery (2018) xxxii 3: 458 461 | 461             the parietal eminences were taken. scalp flaps been elevated. craniotomy done initially on dominant side followed by non-dominant side. haematoma evacuation was done. arterial bleeders were coagulated, dural hitches taken. complete haemostasis been achieved. bone flaps were replaced. drains were put on both sides before closing of the scalp flaps. on first post-operative period drains were removed. post-operative ct brain showed complete evacuation of haematoma. conclusion symmetric biparietal edhs are rare and carry high mortality when compared with solitary edh. emergency evacuation of haematomas should be done. good intensive care is needed post operatively, as these are severe traumatic head injuries. timing of haematoma evacuation is important for good outcome. correspondence dr. sathish kumar vandanapu simhapuri institute of neurological sciences simhapuri hospital, chinthareddypalem nellore524003 andhra pradesh (india) emailsathishvandanapu@gmail.com mobile+91-8008222342 references 1. agrawal a.bilateral symmetrical parietal extradural hematoma.j surg tech case rep2011;3:34-36. 2. cirak b, mut m, akalan n. bilateral epidural hematoma in a pyknodysostotic child. pediatric neurosurg 1999; 30: 33-34 3. dharker sr, bhargava n. bilateral epidural haematoma. acta neurochir (wien) 1991; 110: 29–32 4. frank e, berger ts, jew jm. bilateral epidural hematoma. surg neurol 1982;17:218-22 5. g.lakshmi prasad, sumit sinha et al.traumatic symmetric biparietal extradural haematoma: report of two cases.neurological surgeon’s society of india 2016 6. gorgulu a, cobanoglu s, armagan s, karabagli h, tevruz m. bilateral epidural hematoma. neurosurg rev 2000;23:30-3 7. huda mf, mohanty s, sharma v, tiwari y, choudhary a, singh vp. double extradural hematoma: an analysis of 46 cases. neurol india 2004; 52: 450–452 8. idei m, shima t, nishida m, yamanae k, mihara c, hatayama t, onda h, et al. symmetrical bilateral epidural hematoma after head injury in the mid parietooccipital region: case report. no shinkei geka 2004; 32: 379–382 9. ramzan a, wani a, malik ah, kirmani a, wani ma. acute bilateral extradural hematomas. neurol india 2002; 5: 217–218 10. rasmussen gl, holme s. bilateral epidural hematomas. ugeskr laeger 1991;154:20 11. subrahmanian mv, rajendraprasad gb, dibbala br. bilateral extradural hematomas. br j surg 1975; 62: 397400 12. udoh do. bilateral post-traumatic acute extradural hematomas: a report of four cases and review of literature. niger j clin pract 2012; 15: 104-107 doi: 10.33962/roneuro-2023-015 combined endoscopic-microscopic trans-nasal trans-sphenoidal approach for pituitary adenomas. an institutional experience mohammad kaif, kuldeep yadav, amit upadhyay, deepak kumar singh, rakesh kumar singh, ashish chandra agarwal, kshitij sinha romanian neurosurgery (2023) xxxvii (1): pp. 95-100 doi: 10.33962/roneuro-2023-015 www.journals.lapub.co.uk/index.php/roneurosurgery combined endoscopic-microscopic transnasal trans-sphenoidal approach for pituitary adenomas. an institutional experience mohammad kaif, kuldeep yadav, amit upadhyay, deepak kumar singh, rakesh kumar singh, ashish chandra agarwal, kshitij sinha dr ram manohar lohia institute of medical sciences, lucknow, uttar pradesh, india abstract objective. to obtain evidence that the use of endoscopy along with a microscope in the surgical management of pituitary tumours improves intraoperative visualization and significantly impacts operative outcomes in the trans-nasal approach. material and methods. each patient underwent endonasal transsphenoidal microscopic tumour resection. the procedure was modified by the use of intrasellar endoscopy as an adjunctive imaging modality. following complete microscopic resection of tumour, rigid 0° and 30° 4.0-mm endoscopes were used to conduct a final survey of the sellar and parasellar spaces. residual tumour fragments identified during this endoscopic examination were removed. results. in 50 patients with pituitary macroadenomas, the rigid 30 ° angled rigid endoscope was found to be highly beneficial. hidden areas could be visualized and tumour residues were detected. in the majority of the patients with detected tumour residues, adenomatous remnants were safely removed by meticulous endoscopic dissection under optimum visual control after the main part of the tumour had been removed with the operating microscope. conclusions. endoscopy provides distinct advantages over microscopy in imaging intrasellar and parasellar structures during pituitary tumour resection which are often missed by microscopy alone. introduction since sir victor horsley1 performed the first surgery for pituitary tumor, different approaches have been described for it. the transnasal-transsphenoidal route by schloffer 2 and cushing3 sublabial trans-septal route had been widely used. this surgery was further improved with the introduction of the microscope by hardy4 and the use of endoscope in management the first time for such lesions, by jankowski5. with the evolution in the technology of endoscope, it’s use has become much more frequent6. keywords pituitary macroadenomas, micro-endoscopy, trans-nasal surgery, endoscopy corresponding author: kshitij sinha dr ram manohar lohia institute of medical sciences, lucknow, uttar pradesh, india kshitij.sinha0023@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 96 mohammad kaif, kuldeep yadav, amit upadhyay et al. the endoscopic transsphenoidal approach requires different surgical skills from those needed for microsurgery. surgeons need to handle surgical instruments in a relatively narrow working space with a two−dimensional view. added to this, an unfamiliarity of neurosurgeons with sino-nasal surgery is also an obstacle to widespread use of the endoscopic transsphenoidal approach for pituitary lesions. in this study we have applied microscopic endonasal septal pushover technique described by griffith and veerapen7. since this approach consists of relatively simple surgical procedures, access to the sphenoid sinus is quick and causes minimum disruption of normal tissue in the nasal cavity. we, later convert this microsurgical technique into endoscopic method by using a rigid endoscope after reaching the sellar floor. in this study, we describe our experience using this technique in 50 patients. patients and methods this is a retrospective review of case records of patients who had undergone endonasal transsphenoidal surgery for pituitary tumors from january 2018 to december 2021. a total of 50 patients with pituitary tumors underwent endoscope-assisted endonasal trans-sphenoidal microsurgery in our institute. all patients underwent a complete endocrinological, neurological, neuroophthalmological and neuro-radiological work-up prior to surgery. figure 1. (a & b) show intra-op use of microscope and endoscope during resection of pituitary adenoma. operative technique our endonasal trans-sphenoidal surgery for pituitary tumors is performed using combined microscope and endoscope in order to exploit the advantages of each modality. primarily, we perform the surgeries with an operating microscope. the endoscope is used in later stage to inspect and excise the residual tumor. the surgical procedure is performed under general endotracheal anesthesia with the patient supine. the oropharyngeal cavity is packed with 3-in moist gauze. the head is cradled in a horseshoe head-holder and tilted toward the surgeon. a navigation system is used for providing intraoperative guidance in the sphenoid sinus and the sella turcica. the lateral side of the thigh is prepared to harvest fat and fascia graft. the procedure in the nasal cavity is primarily performed with a microscope, and later assisted by an endoscope to observe lateral anatomy including carotid prominences, especially in the sphenoid sinus with complicated structure. a nasal speculum is used to inspect the nasal cavity and identify the middle turbinate. an incision 97 combined endoscopic-microscopic trans-nasal trans-sphenoidal approach for pituitary adenomas is made in the nasal septum just opposite to the middle turbinate at the junction of the bony and cartilaginous nasal septum. the mucosa of the intact contralateral nasal cavity is also elevated off the septum laterally. the nasal mucosa is elevated to expose the sphenoid sinus ostia bilaterally, in order to achieve the classical an “owl’s eye” view. a hardy nasal speculum is placed to achieve a wider surgical field. the perpendicular plate of the vomer is fractured with the blade of the hardy speculum and dislocated toward the contralateral side. then, the keel bone of the vomer and the sphenoid rostrum are exposed, which are the distinct landmarks of the midline. it is essential to have the midline orientated to the sella at this point of the surgery. neuronavigation is used as for assessing the real time location of the surgical exposure. the anterior wall of the sphenoid sinus is removed with alligator forceps and kerrison rongeurs. the intra-sinus septa are also removed and the floor of the sella turcica is exposed and removed subsequently. the dura is coagulated and incised in a cruciate manner. a highspeed drill is sometimes used on the thick bone or incomplete pneumatization of the sphenoid sinus and the sellar floor to achieve adequate exposure. the sella is entered and the tumor is debulked using curettes, forceps, and suction. during or after removal of the tumor, an endoscope is used to inspect the tumor cavity, especially in the blind spot of the microscope. the residual tumor is often extirpated under an endoscope (2.7 mm and 4 mm in diameter with viewing angles of 0 and 30 degrees, olympus, tokyo, japan). at the end of surgery, the tumor bed is packed with surgicel (ethicon, somerville, nj, usa) and fibrin glue. in case of relatively significant cerebrospinal fluid (csf) leakage, a fascia lata and fat graft harvested from the patient’s thigh is also packed with fibrin glue. the speculum is withdrawn and the residual nasal septum and nasal mucosa is returned to the midline. nasal packing done to prevent formation of the posterior synechiae. table 1. summary of pituitary adenoma tumor characteristics no. of patients sellar only 20 microadenoma 10 suprasellar extension 30 parasellar extension 12 non-secretory tumor 30 secretory tumor 11 table 2. post-complications of procedure complications no. of patients treatment csf leak 4 thigh fat graft placement diabetes insipidus temporary permanent 8 2 temporary use of desmopressin desmopressin worsening of anterior pituitary function 6 hormone replacement asymptomatic synechia of nasal mucosa 2 none chronic sphenoidal sinusitis 3 5day oral antibiotic course meningitis 2 injectable antibiotic observations from a total of 50 pituitary adenomas, 11 (22%) were hormonally active, while 39(78%) were nonfunctioning. mean follow-up period was 9 months. the average length of hospital stay was 4 days. the most common indications for longer hospitalization included temporary diabetes insipidus and prior comorbid conditions which required extended monitoring or rehabilitation. all patients had postoperative mri/ct studies to assess residual or recurrent disease; all patients with hormonally active tumors had additional postoperative hormonal studies. remission, being defined as no hormonal or radiological evidence of recurrence within the timeframe of the follow-up. remission was demonstrated in 45/50 (90%) of adenomas. there were 26 males (52%) and 24 females (48%). the age ranged from 18 years to 56 years, with a mean of 26.4 years. other than hormonal symptoms, the most common presenting complaints includes visual symptoms, changes in visual acuity or visual field deficits (44) (88%) headache (38) (76%) menstrual cycle disturbance or impotence (18) (36%), and acromegalic features (6) (12%). forty patients had 98 mohammad kaif, kuldeep yadav, amit upadhyay et al. macroadenoma (80%) and 10 had microadenomas (20%). thirty patients out of 40 macroadenoma had suprasellar extensions (60%). only 10 patients (20%) had lumbar drain inserted prior to commencement of the surgery and the majority of these were macroadenomas. all cases were performed under general anesthesia. postoperatively all of our patients who underwent this procedure, recovered well with normal and unobstructed nasal airways. postoperative pain was reported to be minimal and the patients often did not require analgesic medication beyond second day post-operatively. because of the potential occurrence of diabetes insipidus, every patient was kept in the hospital at least 3 days. among the 50 endonasal procedures performed, 37 operations were completed with the patients needing to stay 4 days in the hospital. thirteen procedures were accomplished with the patients requiring a 7 days hospitalization. the mean follow-up duration for these patients was 9 months. the common complications encountered were diabetes insipidus (8) (16%), cerebrospinal fluid leak (4) (8%), meningitis (2) (4%), epistaxis (2), septal perforation or synechia (2) (4%), and anterior pituitary insufficiency (6) (12%). mean operative time was 90 min. our study reveals that hybrid transsphenoidal approach is a safe and effective method of management of pituitary adenomas. patient outcomes were determined from post-operative assessment of tumor resection, postoperative hormonal levels. mr imaging studies were performed for all patients during the early postoperative period, to be repeated after 6–12 months and then annually for the rest of their followup period. this combined microscopic and endoscopic transnasal technique demonstrated remission (being defined as no hormonal or radiological evidence of recurrence within the timeframe of follow-up) in 40/50 (80%) patients. five of the patients demonstrating recurrent tumor had a mass ranging from 5 to 8 mm on an mri scan performed postoperatively, 6 of them underwent revision surgery and 3 of them having recurrence located in the cavernous sinus were referred for radiosurgery. there was no mortality in our series. discussion the surgery for pituitary tumors has evolved significantly in the past few decades from transcranial approach to microscopic trans-nasal approach and then to endoscopic trans-nasal approach. gerard guiot8 popularized the use of endoscope in the trans-sphenoidal approach. apuzzo et al.9 used an endoscope as an adjunct in the microscopic resection of pituitary lesions with extrasellar extension. axel perneczky10 has been credited to describe the micro-anatomy not apparent with the microscope, by endoscope, and introduced the concept of minimally-invasive neurosurgery. both, microscope and endoscope have some advantages and disadvantages. the microscope offers a single, unobstructed and continuous threedimensional field of vision where depth perception is more accurate. however, field of view is relatively narrow as compared to that of endoscope. most of the neurosurgeons are familiar and more comfortable with microscope. on the other hand, endoscope provides panoramic view with better illumination. angled scope can enhance vision and provide better view at lateral part of tumors and cavernous sinus which helps surgeons to work more efficiently. however, field of view in endoscope is two dimensional and often obstructed by surgical debris and since nasal speculum is not used, maneuvering in nasal cavity is difficult. in this study we have expressed our experience of combined use of microscope and endoscope where surgery is started with microscope and endoscope is used to excise the residual tumor which is not accessible with microscope. in present study, we found that residual tumor after microscopic excision could be easily identified with endoscope. similar findings have also been reported in separate studies of endoscope assisted microscopic surgery, in which after microscopic tumor resection endoscope was introduced into the sella to look for the residual tumour.11 in this series, an average of 40% of patients were found to have after microscopic resection and were discovered and resected during the endoscopic surveys. thus, microscope alone was successful only in 60% of cases for complete tumor removal12. in our hybrid technique the surgical procedure is started with microscope. here, an incision is made at nasal septum mucosa at the junction of bony and cartilaginous part, opposite to middle turbinate and 99 combined endoscopic-microscopic trans-nasal trans-sphenoidal approach for pituitary adenomas this junction is fractured. the septal mucosa on opposite side is dissected off the bony septum to expose the keel of vomer. a hardy nasal speculum is then inserted for adequate retraction and proper visualization of both sphenoid ostia as classical owl’s eye appearance. it also provides an appropriate surgical corridor through which surgical instruments can be taken in and out without hindrance. our experience with 50 patients, operated through hybrid technique, shows that it is accurate, convenient and time efficient approach for complete resection of sellar tumours. in majority of the cases, sellar floor was reached within 10-15 minutes of starting the procedure. the most crucial step is to reach sphenoid ostium for which most of the neurosurgeons are unaccustomed, especially during early stage of their practice. in purely endoscopic technique, nasal speculum is not used to achieve sphenoidotomy and thus it needs several other surgical steps to achieve adequate corridor to reach sphenoid ostia. maneuvering endoscope in nasal cavity is often cumbersome due to limited space, especially for those who are naïve in endoscopic surgery. in microscopy the approach to sphenoid ostia is direct and most of the sino nasal procedures performed in endoscopy are omitted. a potential advantage of the purely endoscopic approach over the microscopic direct endonasal approach remains to be discussed since these two techniques adopt the same surgical route to the sella. it is accepted that the microscopic direct endonasal approach has the advantage of a simpler and less time consuming sphenoidotomy with fewer postoperative rhinological complications13. the microscopic approach also has the drawback in that it does not provides access to the lateral margins of the sellar cavity and the surgical trajectory is deviated from the midline14. surgical microscopes also need the retraction of superficial structures (i.e., the nostrils), which otherwise hinder the entry of the light beam. the nasal speculum used in the microscopic approach has a wider opening of its blade which can cause excessive stretch force on the nostril, and at time needs a relaxing alar incision. this incision was reported in a 20% of the patients by was zada et al.15 in his study of 100 patients. in contrast, endoscopes can provide a more panoramic view without any need of such incision. in our series of 50 patients, we needed alar release incision in only 5 cases that is less than 10% of patients. our technique exploits a more simplistic and familiar approach to pituitary tumors with added advantage of endoscopic visualization of the residual tumor in the lateral part of the sella as well as those trapped in the arachnoid folds. despite a limited number of cases, the present study also suggests that this simplified hybrid technique is a safe and time efficient technique where judicious use of microscope and endoscope can reduce the operative time and post-op rhinological complication with comparable surgical outcome. conclusions we consider that the endoscope, which allows visualization of areas not seen with the operating microscope, should be used actively in conjunction with the operating microscope that provides threedimensional visualization and is timesaving. our surgical method for pituitary tumors provides good results with minimal invasion, by exploiting the advantages of a microscope and an endoscope at the same time. references 1. sachs e. sir victor horsley. br med j 1957;1:916 – 1917. 2. schloffer h. zur frage der operationen an der hypophyse. beitr klin chir 1906;50:767 – 817. 3. cushing h. partial hypophysectomy for acromegaly: with remarks on the function of the hypophysis. ann surg 1909;50: 1002 – 17. 4. hirsch o. symptoms and treatment of pituitary tumors. arch otolaryngol 1952;55:268 – 306. 5. jankowski r, auque j, simon c, et al. endoscopic pituitary tumour surgery. laryngoscope 1992;102:198 – 202. 6. kennedy dw, zinreich sj, rosenbaum ae, johns me. functional endoscopic sinus surgery. theory and diagnostic evaluation. arch otolaryngol 1985;111:576 – 82. 7. griffith hb, veerapen r. a direct transnasal approach to the sphenoid sinus. technical note. j neurosurg 1987; 66: 140-2 8. guiot g. trans-sphenoidal approach in surgical treatment of pituitary adenomas: general principles and indications in non-functioning adenomas. excerpta med int congr series 1973;303: 159 – 78. 9. apuzzo mlj, heifetz m, weiss mh, kurze t. neurosurgical endoscopy using the side-viewing telescope. technical note. j neurosurg 1977;16:398 – 400. 10. fries g, perneczky a. endoscope-assisted brain surgery: part 2 analysis of 380 procedures. neurosurgery 1998;42:226 – 32. 11. helal mz. combined micro-endoscopic trans-sphenoid 100 mohammad kaif, kuldeep yadav, amit upadhyay et al. excisions of pituitary macroadenomas. eur arch otorhinolaryngol 1995;252:186 – 9. 12. jarrahy r, berci g, shahinian hk. assessment of the efficacy of endoscopy in pituitary adenoma resection. arch otolaryngol head neck surg 2000;126:1487 – 90. 13. cooke rs, jones rac. experience with the direct transnasal transsphenoidal approach to the pituitary fossa. br j neurosurg 1994; 8: 193–196. 14. kawamata t, iseki h, ishizaki r, hori t. minimally invasive endoscopic-assisted endonasal trans-sphenoidal microsurgery for pituitary tumors: experience with 215 cases comparing with sublabial trans-sphenoid approach. neurol res 2002;4: 259 – 65. 15. jho h-d, carrau rl. endoscopic endonasal transsphenoidal surgery: experience with 50 patients. j neurosurg 1997; 87: 44–51. doi: 10.33962/roneuro-2023-010 intramedullary cavernoma. a case report mamadou bata dianka, farida abdoulkader geudi, djama houssein omar, goumaneh omar housein, filsan omar ali romanian neurosurgery (2023) xxxvii (1): pp. 67-70 doi: 10.33962/roneuro-2023-010 www.journals.lapub.co.uk/index.php/roneurosurgery intramedullary cavernoma. a case report mamadou bata dianka1, farida abdoulkader geudi1, djama houssein omar1, goumaneh omar housein2, filsan omar ali2 1 hôpital général peltier, djibouti 2 hôpital cheiko, djibouti abstract the cavernoma is a vascular malformation made of well-circumscribed agglomeration of pseudo-capillaries. bone marrow localization is rare and accounts for about 5% of spinal cord vascular lesions. clinical symptomatology is marked by progressive bone marrow compression syndrome. the diagnosis is strongly evoked in magnetic resonance imaging and confirmed by histology. the management is essentially surgical. we report a case of bone marrow cavernoma in a 38-year-old man seen in consultation, paraplegic for 2 weeks. the spinal cord mri revealed a lesion opposite d11, evoking a cavernoma. the patient was operated on with total removal of the lesion; histology confirmed the diagnosis of cavernoma. the immediate postoperative follow-up was marked by the partial recovery of the deficit. we discuss, through this clinical case, the clinical, radiological and especially therapeutic aspects of the medullary cavernoma. introduction cavernomas are benign vascular abnormalities consisting of cavities into which blood circulates at low flow and low pressure. intramedullary localization is unusual, represents about 5 to 12% of spinal vascular malformations and 3% of intramural vascular malformations (5% of spinal vascular malformations) (1). unlike cerebral cavernomas, intramedullary cavernomas often have a more aggressive clinical course due to acute or rapidly progressive alteration of spinal cord functions. asymptomatic forms are common. the diagnosis is strongly evoked by imaging, in particular by magnetic resonance, and confirmed by the anatomo-pathological study. surgery is essential especially in symptomatic forms. we report a case of dorsal intramedullary cavernoma and analyses in the light of literature, the clinical, radiological and surgical aspects of the spinal cavernoma. case report this is a 38-year-old man patient with no significant medical history and who had a low back pain for 1 year. one year after back pain, it showed keywords cavernoma, microsurgery, spinal cord corresponding author: mamadou bata dianka hôpital général peltier, djibouti mb1dianka@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 68 mamadou bata dianka, farida abdoulkader geudi, djama houssein omar et al. a b c d a total functional impotence of the lower limbs of rapidly progressive installation. we received him in consultation, coming from a neighbouring country, two weeks after the establishment of the deficit. the clinical examination found a conscious patient, a urinary tube in place (because of urine retention), paraplegic at 0/5, hypoaesthesia under umbilical region, a positive babinski sign, sharp osteotendinous reflexes. magnetic resonance imaging showed an irregular intramedullary lesion (previous reverse) opposite d11, in hyper signal in both t2 and t1 and surrounded by a hypo signal halo and myelopathy extended up to l1. the set evoked recent bleeding and the diagnosis of cavernoma was mentioned. the patient was operated on, a laminectomy d11 and d12 was performed. after opening the hard mother, we discovered intramedullary in depth a globular, reddish and little hemorrhagic lesion. we realized a complete single-block removal. the immediate postoperative follow-up at 24 hours were simple and marked by a clear improvement in neurological deficit, in particular, the removal of the urinary catheter and correct urination without retention, the improvement in the motor deficit whose rating increased to 1/5 in proximal (quadriceps) and 3/5 in distal (toes). three months after the surgery, the patient presents an improvement, 4/5 in extension and 3/5 in flexion of the lower limbs. the anatomopathological study confirmed the diagnosis of cavernoma discussion the definition of cavernoma is histological, it is a vascular malformation made of dystrophic and ectasic blood vessels without interposition of tissue between the vessels (2). it is an unusual vascular malformation of the central nervous system. it occurs sporadically or hereditaryly. cavernomas are generally not associated with other pathological entities. however, one case of cavernoma associated with oligodendroglioma, two cases associated with an nf1 and one case, with klippel-trenaumay syndrome, have been reported (3, 4). medullary cavernomas are considered rare (5) and thoracic localisation is the most common (2, 6). the origin of these malformations is poorly known, they are said to be more common in women with a peak frequency between 30 and 60 years (6). the risk of bleeding is on average 2 to 3% each year (7). the rate of re-bleeding increases to 9 to 10% each year in case of cavernoma larger than 1cm, symptomatic patients and those with a history of haemorrhage (8). picture a: t1 sequence in the sagittal plane: intradural intramedullary lesion, in projection of d11-d12, in spontaneous t1 hypersignal associated with intramedullary haemorrhagic changes. picture b: t1 fs sequence after injection of gadolinium in the sagittal plane: absence of notable enhancement of the intramedullary intradural lesion. picture c: t2 sequence in the sagittal plane: the intradural intramedullary lesion 2cm in height is of heterogeneous signal with alternating zones in hypo and hypersignal t2 realizing the appearance of salt and pepper; it is associated with a range of edema in t2 hypersignal. picture d: se t2 sequence in the axial plane: the intradural intramedullary lesion is lateralized to the left, pushing the marrow to the right, of heterogeneous signal with zones in hypo/hypersignal t2 in pepper and salt. the clinic for intramedullary cavernomas is not pathognomonic. they can remain asymptomatic for a very long time or be responsible for a slowly progressing alteration of neurological functions or reveal themselves abruptly (9). acute forms occur in 69 intramedullary cavernoma order of a hemorrhagic context while progressive forms (60%), can be reversible during the first month or be accompanied by a progressive pseudotumour worsening (10). classical symptomatology is made of moderate spinal pain followed by muscle weakness in the lower limbs of progressive worsening, responsible for walking disorders (1, 3). in children, the clinical picture is most often acute in the form of a very rapid neurological deficit (3). radiological diagnosis is essentially based on magnetic resonance imaging (11). mri currently represents the most efficient imagery for both dignostic and evolutionary monitoring (12, 13, 11). technically, we must emphasize the interest of t2 in gradient echo (t2*). the typical aspect is that of a heterogeneous hyper signal lesion on the t1 and t2 sequences, surrounded by a hypointense peripheral area in t1 and t2 (12). bone angiography is most often normal but retains its place in differential diagnosis especially with arteriovenous malformations (13, 14) or haemorrhagic spinal cord tumors (15). computed tomography is less in demand and rarely poses diagnostic (13, 16). the treatment of medullary cavernoma is neurosurgical with complete microsurgical resection of the malformation. surgery improves the functional prognosis and very often allows a permanent cure without major sequelae (14, 5). the removal of the lesion must be done in operational theatre by bipolar coagulation of the surface, which decreases its volume and makes removal easier (17). our case consisted of block removal without much coagulation. the basic principle is to avoid bleeding of the lesion during its removal to operate in a clean field so as not to lose sight of the border with the marrow (9). in the absence of surgical treatment, the evolution can be chronic myelopathy (14, 11). it is indeed essential in case of surgical indication to know the exact situation of the cavernoma, schematically near or in contact with the ventral surface, the lateral surface, or the dorsal surface of the marrow (18). topography is therefore one of the determining criteria for the surgical indication and the expected clinical results (19). the superficial posterior forms make it possible to consider complete removal, most often without long-term neurological worsening. centromedullary localisations are accessible through a classic median commissural myeloma with a transient probability of posterior cord damage. an anterior or anterolateral distribution is often respected in paucisymptomatic forms, in the case of a surgical approach (severe or recurrent deficit), a previous approach may be considered (10). this last localisation corresponds to that of our case but a later approach was enough for a complete excision. unanimity seems to be around abstention in asymptomatic forms while symptomatic forms hardly lend for discussion (18). however, a distinction must be made between haemorrhagic, deficit forms and only painful forms. the disappointing post-surgical results observed in painful forms make surgical indications cautious in this context (20). post-operative results are variable. a multicentre series (10) of 19 operated patients obtained 47% improvement, 42% aggravated and 5% unchanged. another series (9) of 24 operated patients, did not get any improvement, however, notes 2 patients aggravated while 22 patients kept a condition similar to that observed before surgery. she recommends rapid surgery for any cavernoma associated with neurological disorders consistent with the localisation of the lesion. picture e: histological appearance of a cavernous hemangioma. hematoxylin and eosin coloring. low magnification (x20). conclusion the bone marrow localization of the cavernoma is unusual. the thoracic site is the most common. the origin of these vascular malformations is poorly known. the clinic is not pathognomonic, it is that of a rapidly progressive installation medullary compression. mri is the most efficient examination for the diagnosis, topographical assessment and monitoring of cavernoma. the diagnosis of certainty 70 mamadou bata dianka, farida abdoulkader geudi, djama houssein omar et al. is histological. the management of symptomatic spinal cavernomas is surgical with complete resection of malformation followed by quality physiotherapy. references 1. n.d.a bankole, h. selhi, y. oudrihiri, a. melhaoui, m. boutarbouch, a. el ouahabi. cavernome intramédullaire: à propos d’un cas et revue de la littérature. neurochirurgie 65 (2019) 106-144. 2. j.-f. mosnier, j. brunon, c. nuti. anatomie pathologique des cavernomes du système nerveux central. neurochirurgie 53 (2007) 131-135. 3. g. lena, j. ternier, a. paz-paredes, d. scavarda. cavernomes du système nerveux central chez l’enfant. neurochirurgie 53 (2007) 223-237. 4. m. boutarbouch, l. gire, n. vigon, d. ben salem, b. cote, n. baudouin, f. ricolfi. syndrome de klippel-trenaunayweber et cavernomes intramédullaires dorsaux : une association très rare. journal of neuroradiology, volume 34, issue 1, march 2007, page 26-27. 5. khalil ayadi, fatma kolsi, najar haitham, anis hachicha, kammoum brahim, mohamed zaher boudawa. les cavernomes intramédullaires: etude de sept cas. revue neurologique, volume 177, supplement, april 2021, page s95. 6. jetan h. badhiwala, b.h.s.c., forough farrokhyar, waleed alhazzani, blake yarascavitch et al. surgical outcom and natural history of intramedullary spinal cord cavernous malformations : a single-center series and meta-analysis of individual patient data. j neurosurg spine 2014, 21:662-676. 7. gross ba, du r, popp aj, day al. intramedullary spinal cord cavernous malformations. neurosurg focus. 2010; 29 (3): e14. 8. matha ap, turner jd, spetzler rf. surgical approche to intramedullary cavernous malformations of the spinal cord. oper neurosurg. 2011; 68 (suppl_2): ons 317 – ons 324. 9. f. lefranc, d. balériaux, j. brotchi. les cavernomes intramédullaires: série personnelle de 24 cas. neurochirurgie 53 (2007) 203-207. 10. f. parker, j-p. lejeune, s. bouly, m. lonjon, e. emery, f. proust, j. auque, h. loiseau, s. gallas, s. boetto, p. labauge. neurochirurgie 53 (2007) 208-216 11. i. ben hamouda, s. masmoudi, n. ben ali, a. mrabet. cavernome médullaire : à propos d’une observation. revue neurologique, volume 163, issue 4, supplement 1, april 2007, page 18. 12. h. ghannane, t. khalil, l. sakka, j. chazal. analyse d’une série de cavernomes du système nerveux central: 39 cas non opérés, 39 cas opérés et un cas décédé. neurochirurgie 53 (2007) 217-222. 13. j. gabrillangues, f.-g barral, b. claise, l. manaira, e. chabert. imagerie des cavernomes du système nerveux central. neurochirurgie 53 (2007) 141-151. 14. marie giroud, guillaume fargeix, pauline vallet, hassan katrandji, thierry moulin, elisabeth medeiros de bustos. cavernome médullaire : une cause rare de myélopathie. revue neurologique, volume 168, suplement 2, april 2012, page a87. 15. stuart lee, spetzler r. spinal cord cavernous malformation in a patient with familial intracranial cavernous malformations. neurosurgery 1990, 26: 877880. 16. turjman f., joly d. mri of intramedullary cavernous haemangiomas. neuroradiology 1995, 37: 297-302. 17. brotchi, jacques m.d., ph. d.; lefranc, florence m.d. current management of spinal cord tumors. contemporary neurosurg 21, 26. 18. j. chazal, t. khalil, l. sakka. indications thérapeutiques des cavernomes du système nerveux central. neurochirurgie 53 (2007) 251-255. 19. cristante l., hermann h.-d. surgical management of intramedullary spinal cord tumors : functional outcome and sources of morbidity. neurosurgery 35, 69-76. 20. kim j.n., klopfenstein j.d., zabramski j.m., sonntag v.k., spetzler r.f. analysis of pain resolution after surgical resection of intramedullary spinal cord cavernous malformations. neurosurgery 58, 106-111. doi: 10.33962/roneuro-2020-071 very late recovery of vision after removal of giant pituitary tumour forhad h. chowdhury, mohammod raziul haque romanian neurosurgery (2020) xxxiv (1): pp. 441-443 doi: 10.33962/roneuro-2020-071 www.journals.lapub.co.uk/index.php/roneurosurgery very late recovery of vision after removal of giant pituitary tumour forhad h. chowdhury, mohammod raziul haque 1 neurosurgery, national institute of neurosciences and hospital, shere-e-bangla nagar, dhaka, bangladesh 2 neurosurgery, dhaka medical college and hospital, dhaka, bangladesh abstract visual impairment is the most common clinical presentation of the pituitary tumour. visual recovery usually occurs within days to months after surgical removal of the tumor. we report a case of a giant pituitary tumour where preoperatively there was severe visual impairment. postoperatively he recovered vision in one eye within three months and the other eye remained completely blind for 5 years, then it began to recover very slowly to a serviceable vision in the next six years. a 22 years old young man presented with progressive loss of vision in both eye for last 2 years. he was near totally blind on right side and could see with to some extent by the left eye. clinical examination showed, there were only pl and pr on right side where as visual acuity was 6/36 on left side. confrontation test revealed blind right eye with temporal hemi field cut on left side, which was confirmed by perimetry. fundoscopy revealed early atrophic changes in left eye and atrophic changes in right eye. contrast mri showed giant pituitary adenoma extending into suprasellar and subfrontal region. his hormonal study was normal. he under-went transnasal transspenoidal removal of tumor first but it failed to remove the tumor satisfactorily. so second surgery was done within few days to remove the tumor through right lateral supraorbital frontal craniotomy. postoperatively his vision on left side began to recover quickly. by the end of three month after operation, visual acuity and visual field on left side recovered completely whereas on the right side it remained as preoperative without any improvement. he was on regular follow up. five year after operation his vision on right eye began to recover very slowly. it continued to recover for next four years and perimetry showed central and nasal field recovery on the left side [figure1]. by the end of 09 years after operation, his visual acuity was 6/6 on left side where as on the right side it was 6/20. mri showed small residual tumor without further growing for last 09 years [figure2]. keywords very late recovery of vision, giant pituitary tumour corresponding author: forhad hossain chowdhury assistant professor, neurosurgery, national institute of neurosciences and hospital, shere-e-bangla nagar, dhaka-1207, bangladesh forhadchowdhury74@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 442 forhad h. chowdhury, mohammod raziul haque many factors influences in visual recovery after pituitary surgery such as types of tumor, size of tumor, consistency of tumor, extension and location of tumor, preoperative duration and severity of symptoms, preoperative state of fundus, type and approach of surgery, type of resection, optic canal and optic apparatus decompression etc. 1 most of the visual recovery occurs with 3-6 month but it may continue several years.2 although a previous study has reported that the recovery of visual field progresses over several years and that most of the recovery (>50%) occurs in the first 3 to 6 months after surgery, the time course of visual function recovery after transsphenoidal surgery for pituitary adenomas is unclear.3,4 but after scleral buckling procedure of rhegmatogenous retinal detachment involving the macula the vision may continue to recover up to 10 years.5 to best of our knowledge there is no report (of post pituitary surgery) where visual recovery started 5 years after surgery and that continued for another four years. in our case in early postoperative period less severely affected eye recovered with in three month but blind eye remained blind for five years after operation and there after it went for slow recovery. how and why such thing happened, it’s a big question. figure 1. visual fields analysis (vfa). abefore pituitary surgery, left nasal field was the only remaining field of vision. b04 years after operation, vfa showing left eye fields recovered whereas right eye was totally blind. c07 years operation, vfa showing recovery of left sided central and nasal field of vision. d-9 years after operation vfa showing recovery of left sided central and nasal field of vision. figure 2. contrast mri of brain. a&b –preoperative mri; sagittal and coronal view showing giant pituitary tumor. c&dpost operative mri 09 years after operation; sagittal and coronal view showing small residual tumor. 443 very late recovery of vision after removal of giant pituitary tumour references 1. carlson ap, stippler m, and myers o. predictive factors for vision recovery after optic nerve decompression for chronic compressive neuropathy: systematic review and meta-analysis. j neurol surg b skull base. 2013 feb; 74(1): 20–38. doi: 10.1055/s-0032-1329624. 2. cohen ar, cooper pr, kupersmith mj, flamm es, ransohoff j.visual recovery after transsphenoidal removal of pituitary adenomas. neurosurgery. 1985 sep;17(3):446-452. 3. okamoto y, okamoto f, yamada s, honda m, hiraoka t, oshika t. vision-related quality of life after transsphenoidal surgery for pituitary adenoma. investigative ophthalmology & visual science july 2010, vol.51, 3405-3410. doi:10.1167/iovs.09-3763. 4. johnson md woodburn cj vance ml . quality of life in patients with a pituitary adenoma. pituitary. 2003;6:81– 87. 5. chang sd, kim it. long-term visual recovery after scleral buckling procedure of rhegmatogenous retinal detachment involving the macula. korean j ophthalmol. 2000 jun;14(1):20-6. romanian neurosurgery (2019) xxxiii (4): pp. 355-362 doi: 10.33962/roneuro-2019-059 www.journals.lapub.co.uk/index.php/roneurosurgery a neurosurgical challenge: awake mapping in „critical” language area tumours mihaela cosman1, ionut mihail pantiru2, bogdan florin iliescu1,2, nina straticiuc3, iulia aldea4, vlad buraga4, gabriela florenta dumitrecu5, ion poeata1,2 1 “gr. t. popa” university of medicine and pharmacy of iași, department of neurosurgery, romania 2 “n. oblu” emergency clinical hospital, iași, department of neurosurgery, romania 3 “n. oblu” emergency clinical hospital, iași, department of anaesthesia and intensive care, romania 4 “n. oblu” emergency clinical hospital, iași, department of neurosurgery, psychologist, romania 5 “n. oblu” emergency clinical hospital, iași, department of anatomopathology, romania abstract introduction. despite the technological development lesion located in or near language area still represent a challenge for every neurosurgeon. awake craniotomy and intraoperative neurophysiological monitoring come to our help. different techniques variation exists among specialized centres. we present our experience and the set up for this procedure. materials and methods. we conducted a retrospective analysis of collected data from 10 patients with brain tumours located in or near language area to which we performed awake craniotomy and intraoperative neurophysiological monitoring. they were admitted in third department of neurosurgery,” prof. dr. n. oblu” emergency clinical hospital, yassi, romania, between january 2014 and july 2018. results. presenting symptoms had a duration more than a month in 60 % of patients. in 80% of them were represented by epileptic seizures and the rest of 20 % had transient aphasia elements. the median age of presentation was 28 years old with a male dominance. the histological reports indicated: fibrillary astrocytoma – 40%, anaplastic astrocytoma – 30%, oligodendroglioma – 20% and metastases – 10%. gross total resection was performed in half of the cases and subtotal in just one case, in which the spontaneous speech and object naming showed repeated impairment in time of tumour debulking. the surgical intervention was well tolerated by all the patients. the intensity of cortical stimulation used was between 4 – 10 ma. postoperatively two patients had neurological aggravation, with full recovery at 3 months follow up period, two were stationary and six had symptoms remission. conclusion. a young age of presentation, a paucity of symptoms, the chance for an increase in overall survival and progression free survival impose the need for direct keywords awake craniotomy, language area tumours, intraoperative neurophysiological monitoring, glioma, neurocognitive evaluation corresponding author: mihaela coșman gr. t. popa” university of medicine and pharmacy of iași, department of neurosurgery, romania mihaelacosman@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 356 mihaela cosman, ionut mihail pantiru, bogdan florin iliescu et al. communication and feedback with the patient in time of tumour resection. thus, awake craniotomy and intraoperative neurophysiological monitoring is the golden standard for selected cases of language area tumours. introduction the role of surgery in the management of brain tumors is nowadays more and more prominent. this results from the fact that the extent of resection, e.g. in glioma cases is linked to increased survival rate and progression free survival [30]. the most challenging cases of them all are those located in and near eloquent areas, because of the high risk of producing new neurological deficit or worsen the previous ones, after surgery. for this reason, traditionally, the approach of those lesion was less invasive and with great caution [2, 11, 25]. to obtain the goal of a higher degree of resection with minimal neurological impairment, in language area surgery it is used the technique of awake craniotomy (ac) and intraoperative neurophysiological monitoring (iom) [7, 17]. this is helpful especially for those with preserved speech function like for example those manifested through epileptic seizures. for a proper selection of the cases, suitable for this technique, preoperative neurocognitive assessment is crucial and special battery of tests must be applied. [5, 15]. despite the fact that the principals of those intraoperative techniques are the same worldwide there are some difference in implementing them. in this study we present our experience and method from surgical, anesthetic, neurocognitive and intraoperative brain mapping point of view. materials and methods we conducted a retrospective analysis of collected data from 10 patients with brain tumors who underwent awake craniotomy and were admitted in the third department of neurosurgery,” prof. dr. n. oblu” emergency clinical hospital, yassi, romania, between january 2014 and july 2018. inclusion criteria were: (1) patients diagnosed by contrast enhancement mri with tumors located in or near language areas, (2) age > 18 years old, (3) preserved preoperative language function or slightly affected, (4) presented at 1 and respectively 6 months postoperative evaluation. every patient proposed for this surgical technique, from the neurosurgical point of view was evaluated by the psychologist and the anesthesiologist to confirm that it’s completely eligible. before the intervention they were prepared for 3 days, repeating and working with the psychologist on the items used intraoperatively. the initial assessment consisted in a battery of tests with an accent on reviling even the slit language dysfunction (spontaneous and automatic speech, word repetition, objects/images/forms naming and reading special texts from speech exercises). other function tested include: executive function, praxis, memory, calculus and the writing. the neuroanesthesia consisted in asleep-awakeasleep variant. after the induction step, the patient was positioned in a manner that allowed an easy access to the airway, comfortable for him and for the surgeon and also permitted communication with the psychologist. after the patient’s head fixation, the skin incision was infiltrate with a mixt of lindocaine and epinephrine. when the craniotomy was finished and we started to open the dura mater the procedure of awakening the patient begun and throughout the tumor resection it was used total intravenous anesthesia (tiva, propofol -50 – 150 µg /kgc/min, the opioid used was fentanyl 0, 5 1µg/kgc/h). the neurocognitive intraoperative assessment was made by the same psychologist who evaluated the language function, testing patient’s spontaneous speech, counting, object / images naming and depending on the case, limb muscle strength. in all cases we performed direct cortical and subcortical brain stimulation with a bipolar probe (ball tips ends 5 mm apart, nimeclipse system, medtronic) and we chose the high frequency technique. the start stimulation intensity was increased gradually with 0,5ma. we preferred to stimulate all the expose brain with the same intensity and after that to rise it. a site was considered positive if 2 of 3 stimulation lead to language tests dysfunction. the stimulation was repeated in time of resection, the subcortical pathways were tested more often at the end of debulking. the quantification of resection was made using intraoperative echography (esaote system). results at the beginning of our study we identified a total of 58 cases of tumors located in or near language area, 357 awake mapping in „critical” language area tumours but only 10 of them have met all the criteria, the vast majority had important speech dysfunction (45 cases with motor or sensitive aphasia, in 2 cases we performed only biopsy and one patient was under 18 years old). the gander ratio showed male dominance; the median age distribution of the group was 28 years old. the clinical manifestation was represented by transient language disturbance with aphasia elements (2 patients) and epileptic seizures (8 patients). the symptoms duration was more than a month in 60% of cases. other patient’s characteristic are presented in table 1. no. age gender location histology degree of resection postop evolution 6mo postop mri + c rctx 1. 66 f left t mts total fav no c.e. + 2. 46 m left t odg iii ntr fav no c.e. + 3. 37 f left t fa str stat stat 4. 27 m left t aa gtr stat no c.e. + 5. 37 m left f fa ntr fav stat,no rec 6. 38 m left t odg iii ntr fav p.c.e. + 7. 20 m left f aa gtr agg p.c.e. + 8. 22 f left t aa ntr fav p.c.e. + 9. 28 m right t fa gtr agg no rec. 10. 28 m left f fa gtr fav no rec table 1. some characteristic of patients from the study: ffemale, m-male, t-temporal lobe near/in wernicke area, f-frontal lobe near/in broca area, mtsmetastasis, odg-oligodendroglioma, fafibrillary astrocytoma, aaanaplastic astrocytoma, favfavorable, statstationary, aggaggravation , no c.e. – no contrast enhancement, p.c.eperipheral contrast enhancement, no recno recurrence. rctxradio-chemotherapy. a. b. 358 mihaela cosman, ionut mihail pantiru, bogdan florin iliescu et al. c. d. figure 1. a. anesthesia and patient’s positioning; b. awake stage, psychologist showing images/cards for naming test; c. brain mapping direct cortical stimulation with bipolar probe, choosing the site for cerebrotomy; d. deep tumor resection and subcortical stimulation of white matter tracts, no motor respons (upper left) on electomyographic registration of abductor policis and tibialis anterior muscle (nimeclipse, medtronic). all patient tolerated well the surgery. the stimulation intensity used was between 4-10ma. in one case, in time of tumor resection we registered language dysfunction with tests performance decreasing. no intraoperative seizures were found. the interval from starting the process of awakening and proper communication was between 20 and 40 minutes. in figure 1 are presented the intraoperative steps of the intervention, from anesthesia to cortical mapping and tumor debulking. in two cases we registered postoperative neurologic aggravation as follow: one patient had transient sensitive aphasia elements which remitted completely until discharge, under anti-edematous drugs administration and another case manifested with motor aphasia which needed logopedic therapy. at 6 moths’ evaluation the resolution of symptoms was completed. all patients were monitored al list one year postoperatively (clinical and imagistic). two of our cases first enrolled in the study presented neurologic deterioration associated with imagistic sign of recurrence and needed reoperation, at 4 and respectively 5 years after the first intervention. the histological reports reveal tumor progression from anaplastic astrocytoma to glioblastoma. recurrence with no surgical solution was found in one case of grade iii odg, at three and a half years evaluation. discussion maximizing the extent of resection and minimizing the postoperative neurological and neurocognitive disturbance becomes nowadays mandatory in the surgical treatment of brain tumors [6, 27]. due to oncological impact on overall survival and progression free survival in low-grade glioma (lgg) cases some suggested an early surgical approach or resection when those lesions are discovered incidentally [21]. to support this statement duffau presented the idea of supratotal cytoreduction in diffuse gliomas. even though the study included only 15 patient and the follow up period was short it was registered a reduction in the malignant transformation rate compared with the group of only complete resection [40]. another proposal from kamp et al. consisted in the supramarginal resection of metastases. the cases in which it was practiced this technique had a one-year local recurrence rate of 29,1% compared with 58,6% for those with only gross total resection [22]. although there are some controversies about the modern treatment of high-grade-glioma (hgg) cytoreductive surgery still represents a key element in their management [1, 3, 16]. this is shown by lacroix et al. how observed on a study of 416 glioblastoma (gb) that the reduction of tumor volume more than 98% is associated with a significant survival advantage [24]. other study on 500 glioblastomas from 2011 published sanai et al. noticed a significant increase in survival rate (p<0, 0001) even when the degree of resection was 78% [32]. it’s well known that oligodendroglial tumors have an increase sensitivity to chemotherapy and there is 359 awake mapping in „critical” language area tumours a development of the oncological treatment with introduction of radiotherapy and immunotherapy in their protocols, however the first step in the management of those lesion is still represented by surgical resection. studies shows that more than 90% of tumor volume reduction is associated with increase in the overall survival and progression free survival. having a relatively good prognostic, the quality of life and the neurological status must be one of the neurosurgeon priorities [35, 38, 39]. to achieve such a goal, we need improvement and development of techniques designed to help use us in evaluating and detecting in real time the functional brain tissue and to set the relationship with the lesion. another reason to implement those methods lays in the fact that brain tumors with a high incidence are usually located in or near eloquent areas. one example is represented by lggs which are usually found in those locations, because of chemoarchitectonic and cytoarchitectonic similarities [13, 28]. the third most common gliomas – oligodendroglioma are located with predilection in those regions as well (frontal lobe 50-65%, temporal lobe 45%, parietal lobe 7-20%) [35]. although our number of patients is small, there is a dominance from the histological point of view of lggs (i.e., fibrillary astrocytoma, 40%) followed by high-gradeglioma (hgg i.e. anaplastic astrocytoma, 30%) and oligodendroglioma (20%), matching the literature data. there is a shift from imagine guided surgery (intraoperative functional mri and neuronavigation) towards functional guided interventions (awake craniotomy and intraoperative neuropsychological monitoring). this is because neuroimaging concept is based on reduction only not taking into account the functional feedback. preserving the classical anatomical landmarks for eloquent cortex, which have a wide variability interindividual is not enough. also, it is hard to differentiate primary critical region from secondary or compensatory ones whose resection wont produces permanent neurological or neurocognitive deficits, thus reducing the degree of resection and the chance of prolonged free survival [12]. hence the utility of combining the neurocognitive assessment during awake craniotomy and the result form direct cortical/subcortical mapping (dcm). the history and the development of awake craniotomy starts in 1886 and was done by victor horsley, first being used in epileptic surgery. special anesthetic protocol are needed for this type of surgery and different variants are available by now. the improvement and introduction to asleep-awakeasleep (aaa) method was performed by penfield, ingvar and hall in 1950, later hansen described and used the awake-awake-awake anesthesia. the third option is represented by asleep-awake variant [36, 41]. our anesthetic team chose and utilized the aaa variant. even though the number of patient with lesion located near/in language area was initially 58 only 10 meet all the inclusion criteria. because of the complexity and potential risks of this procedure the contraindication must be evaluate wisely. of the relative ones we enumerate: neurological causes: aphasia, confusion, agitation and cognitive disorders; psychiatric diseases; highly vascular tumors; airway problems; history of difficult intubation, obstructive sleep apnea; morbid obesity [23, 41]. for these reasons in our practice, before deciding to perform this procedure, the psychologist and the anesthetist evaluate the case too and together discuss the eligibility for this type of intervention. while awake craniotomy provides a close communication and an accurate evaluation, there is still room for other functional intraoperative tools. in a study published in 2010 de benedictis et al. it is shown that the association between awake craniotomy and dcm increases the extent of resection and secondary the overall survival in patients with lggs. this is achieved by resecting all the affected tissue up to critical individual limits with no need for safety margin around the eloquent area [10, 11]. kelm et al. evaluated 61 gliomas located in language area in which it was performed awake craniotomy and observed that gtr was higher in the patient operated and with iom (61, 7% vs. 28, 6%). beside the maintaining the integrity of the eloquent cortex, conservation of the subcortical pathways and tracts it’s even more important because in this part of the brain the potential for neuroplasticity and reshaping is much smaller comparing to the cortical surface. damaging the white matter tracts increases the risk for permanent neurological deficits. although the preoperative imaging modalities have developed and we have many information about de language function localization and about the cortical and subcortical network involvement in this process, 360 mihaela cosman, ionut mihail pantiru, bogdan florin iliescu et al. mapping remains an essential step along with awake craniotomy in the surgical management of language area tumors [7, 18, 20, 23]. the advantage of using both methods was reflected in the degree of resection of our cases too. so, because we had a real time assessment of neurologic and neurocognitive performances, we could achieve gross total resection in half of the patients, with more confidence in the postoperative functional and imagistic status. this had a favorable impact especially for fibrillary astrocytoma cases because: first of all the patients were young (28 yo) whose quality of life was an extremely important outcome factor and secondly the risk of malignant transformation was reduced. those cases were followed up 2 years with no signs of recurrence. still in the light of quality of life preservation and because the admission symptoms were epileptic seizure in 90% of cases, the maintenance of language integrity was essential. therefore, in one case were decided to perform only subtotal resection. it’s about a 37 years old female, with the histological report of fibrillary astrocytoma, in which we had intraoperative language disturbance manifested by speech blockage and even sensitive aphasia when the tumor margins were stimulated and further resect was attempted. until now we talked about the role and advantages of an extensive resection, but this dogma should not be obtained by sacrificing the functional status. in 2015 duffau published an article where is presented the multistage surgical resection. the idea is based on the action of neuroplasticity process. a functional reorganization and the chance for a new intervention without postoperative permanent deficits, in individual cases may be obtain. the reshaping may be induced by the surgery itself and other contributing factor may be represented by the rehabilitation therapy and tumor growth [8, 14]. it’s important to know when is the proper time for the patient to stat the testing. meskelevicius et al. published in 2019 a study in which it’s shown the strong correlation between the speed of reaction and the patient’s age and the fact that the speed of reaction it’s at list two times slower than in the preoperative period, being the slowest in the first 1020 minute after the awaking. although we had a small number of cases none of them failed and we could perform the awake surgery in all. our patients started to react better after minimum of 20 minutes after awakening. during resection the psychologist communicated and evaluated continuously the language and motor function. we didn’t find the positive cortical sites for language in all the cases. one possible reason must be the fact that the size of the craniotomy wasn’t very big and so the exposed surface of the brain was limited. another plausible reason is represented by the neural reshaping induced by the neuroplasticity process and so the imagistic landmarks for the eloquent area didn’t match with the cortical ones. some surgeon prefers a larger exposer to find the eloquent cortical sites not basing on these negative language sites [26, 29]. the stimulation technique and the value of stimulus parameters varies between different studies. the discrepancy comes from the fact that there are an interand intra-individual factor which determine this, for instance: tumor histological type and symptoms duration [9]. usually a biphasic current it is used, the intensity it’s raised gradually with 0,5 or 1 ma at a maximum of 10 ma. to find the threshold which generates the response and not to generate the after-discharge byproducts it’s a matter of perseverance, skill and a challenge [19, 31, 37]. we used the same parameters and in situation were no response was found we didn’t raise the intensity higher than 10 ma, because of the increased risk for seizure induction, especially in the patients with these symptoms in meta-analysis published by satoer et al in which he evaluated the studies about the possibility of cognitive preservation in eloquent area glioma surgery, in the postoperative period, language function was found altered in seven out of nine studies. at 3 months follow up period five out of six studies have revealed improvement in language deficit to a preoperative level [4, 34]. the percentage of postoperative deficit reposts varies: sanai found a rate of 14% new speech deficit, and 8, 4% aggravation; duffau noticed a high degree of impairment 33%-100%, but with no severe permanent disability [11, 33]. in our cases postoperative speech deterioration were observed in two patients but full recovery was obtained after logopedic therapy. one of them remitted the symptoms even before discharge and the other one at 6 months evaluation returned to the initial stat. 361 awake mapping in „critical” language area tumours conclusions there is a diversity of histological types of tumors located in eloquent areas of the brain, some of them have a relatively slow growth pattern allowing the neuroplasticity process to act. for this reason, the patients presenting symptoms are just mild dysfunction instead of severe problems as in the cases of rapid growth rate tumors. with this in mind and with the chance for a prolonged overall survival, the importance of quality of life impose the necessity for a balanced decision between the degree of resection and the possibility of new postoperative neurologic deficits. despite the obvious development of preoperative functional evaluation only a direct approach and communication with the patient through tumor removal may increase the chances for a good postoperative functional status outcome and a higher degree of resection. awake craniotomy and intraoperative neurophysiological monitoring meet those criteria and are the golden standard for selected cases of ‘critical’ language area tumors. disclosures the authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper. references 1. abrudan c, cocis a, cernea d, suciu b, cheptea m, florian si. surgery of high-grade gliomas pros in favor of maximal cytoreductive surgery. romanian neurosurgery, 18(1): 38 – 53, 2011. 2. antonsson m, longoni f, jakola a, tisell m, thordstein m, hartelius l. pre-operative language ability in patients with presumed low-grade glioma. j neurooncol, 137(1):93-102, 2018. 3. baritachii a, gubian a, florian si. the impact of surgery in high grade gliomas a literature review. romanian neurosurgery, xxix 3: 291 – 304, 2015. 4. barzilai o, moshe bs, sitt r, sela g, shofty b, ram z. improvement in cognitive function after surgery for lowgrade glioma. j neurosurg, 1:1-9, 2018. 5. bondari s, bondari d, pîrşcoveanu m, moroşanu dv, muşetescu ae, tudorică v, pîrşcoveanu dfv. study on cognitive decline in patients diagnosed with brain tumors. rom j morphol embryol, 58(4):1185–1192, 2017. 6. bogaciu ns, teleanu d, ciurea av. new technologies for low-grade glioma surgery. romanian neurosurgery, 33(2), 122-126, 2019. 7. chang wh, pei yc, wei kc, chao yp, chen mh, yeh ha, jaw fs, chen py: intraoperative linguistic performance during awake brain surgery predicts postoperative linguistic deficits. journal of neuro-oncology, 139:215–223, 2018. 8. charras p, herbet g, deverdun j, de champfleur nm, duffau h, bartolomeo p, bonnetblanc f. functional reorganization of the attentional networks in low-grade glioma patients: a longitudinal study. cortex, 63: 27 – 41, 2015. 9. corley ja, nazari p, rossi vj, kim nc, fogg lf, hoeppner tj, stoub tr, byrne rw. cortical stimulation parameters for functional mapping. seizure. , 45:36-41, 2017. 10. de benedictis a, moritz-gasser s, duffau h. awake mapping optimizes the extent of resection for low-grade gliomas in eloquent areas. neurosurgery. 66(6):1074-84, 2010. 11. duffau h. is non-awake surgery for supratentorial adult low-grade glioma treatment still feasible? neurosurg rev, 41(1):133-139, 2018. 12. duffau h. a new philosophy in surgery for diffuse lowgrade glioma (dlgg): oncological and functional outcomes. neurochirurgie, 59: 2–8, 2013. 13. duffau h, capelle l. preferential brain location of low-grade glioma comparison with glioblastomas and review of hypothesis. cancer, 100(12):2622-6, 2004. 14. duffau h, taillandier l. new concepts in the management of diffuse low-grade glioma: proposal of a multistage and individualized therapeutic approach. neuro-oncol 17(3), 332–342, 2015. 15. dwan tm, ownsworth t, chambers s, walker dg, shum dhk. neuropsychological assessment of individuals with brain tumor: comparison of approaches used in the classification of impairment. front.oncol, 5:56, 2015. 16. flechl b, sax c, ackerl m, crevenna r, woehrer a, hainfellner j, preusser m, widhalm g, kiesel b, lütgendorfcaucig c, dieckmann k, steffal c, marosi c, hassler mr. the course of quality of life and neurocognition in newly diagnosed patients with glioblastoma. radiother oncol, 125(2):228-233, 2017. 17. gerritsen jkw, lidia arends l, klimek m, dirven cmf,vincent ajpe. impact of intraoperative stimulation mapping on high-grade glioma surgery outcome: a metaanalysis. acta neurochir, 161(1): 99–107, 2019. 18. ghinda cd, duffau h. network plasticity and intraoperative mapping for personalized multimodal management of diffuse low-grade gliomas. front surg, 4:1-8, 2017. 19. gollwitzer s, hopfengärtner r, rössler k, müller t, olmes dg, lang j, köhn j, onugoren md, heyne j, schwab s, hamer hm. afterdischarges elicited by cortical electric stimulation in humans: when do they occur and what do they mean? epilepsy behav., 87:173-179, 2018. 20. ille s, engel l, kelm a, meyer b, krieg sm. languageeloquent white matter pathway tractography and the course of language function in glioma patients. front oncol., 8:572, 2018. 21. jakola as, skjulsvik aj, myrmel ks, sja˚vik k, unsga˚rd g, torp sh, aaberg k, berg t,dai hy, johnsen k, kloster r, solheim o. surgical resection versus watchful waiting in low-grade gliomas. annals of oncology, 28: 1942–1948, 2017. 362 mihaela cosman, ionut mihail pantiru, bogdan florin iliescu et al. 22. kamp ma, dibué m, niemann l, reichelt dc, felsberg j, steiger hj, szelényi a, rapp m, sabel m. proof of principle: supramarginal resection of cerebral metastases in eloquent brain areas. acta neurochir (wien). , 154(11):1981-6, 2012. 23. kelm a, sollmann n, ille s, meyer b, ringel f, krieg sm. resection of gliomas with and without neuropsychological support during awake craniotomy-effects on surgery and clinical outcome. front oncol. , 7:176, 2017. 24. lacroix m, abi-said d, fourney dr, gokaslan zl, shi w, demonte f, lang ff, mccutcheon ie, hassenbusch sj, holland e, hess k, michael c, miller d, sawaya r. a multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. j neurosurg., 95(2):190-8, 2001. 25. leal rtm, barcellos bm, landeiro ja.technical aspects of awake craniotomy with mapping for brain tumors in a limited resource setting. world neurosurg, 113:67-72, 2018. 26. meskelevicius d, schäfer a, weber jk, hegmann l, haddad l, kamp ma, mainzer b, rapp m, steiger hj, sabel m. determination of optimal time window for cortical mapping in awake craniotomy: assessment of intraoperative reaction speed. neurosurg rev. 15, 2019 27. monticelli m, zeppa p, zenga f, altieri r, mammi m, bertero l, castellano i, cassoni p, melcarne a, la rocca g, sabatino g, ducati a, garbossa dthe post-surgical era of gbm: how molecular biology has impacted on our clinical management. a review. clin neurol neurosurg., 170:120126, 2018. 28. oslobanu a, florian si. anatomic location in high grade gliomas. romanian neurosurgery, xxix 3: 269 – 275, 2015 29. pallud j, rigaux-viode o, corns r, muto j, lopez lopez c, mellerio c, sauvageon x, dezamis e. direct electrical bipolar electrostimulation for functional cortical and subcortical cerebral mapping in awake craniotomy. practical considerations. neurochirurgie. 63(3):164-174, 2017. 30. roelz r, strohmaier d, jabbarli r, kraeutle r, egger k, coenen av, weyerbrock a, reinacher pc. residual tumor volume as best outcome predictor in low grade glioma – a nine-year near-randomized survey of surgery vs. biopsy. scientific reports, 6:32286, 2016. 31. saito t, muragaki y, maruyama t, tamura m, nitta m, okada y. intraoperative functional mapping and monitoring during glioma surgery. neurol med chir (tokyo)., 55 suppl 1:1-13, 2015. 32. sanai n, berger ms. extent of resection influences outcomes for patients with gliomas. rev neurol (paris). 167(10):648-54, 2011. 33. sanai n, mirzadeh z, berger ms. functional outcome after language mapping for glioma resection. n engl j med, 358:18-27, 2008. 34. satoer d, visch-brink e, dirven c, vincent a. glioma surgery in eloquent areas: can we preserve cognition? acta neurochir (wien). 158(1):35-50, 2016. 35. simonetti g, gaviani p, botturi a, innocenti a, lamperti e, silvani a. clinical management of grade iii oligodendroglioma. cancer manag res., 27(7):213-23, 2015. 36. sitnikov ar, grigoryan ya, mishnyakova lp. awake craniotomy without sedation in treatment of patients with lesional epilepsy. surg neurol int., 9:177, 2018. 37. so el, alwaki a. a guid for cortical electrical stimulation mapping. j clin neurophysiol, 35: 98–105, 2018. 38. thon n, kreth fw, tonn jc. the role of surgery in grade ii/iii oligodendroglial tumors. cns oncol, 4(5), 317–323, 2015. 39. torensma r. the dilemma of cure and damage in oligodendroglioma: ways to tip the balance away from the damage. cancers (basel), 10(11): 431, 2018. 40. yordanova yn, duffau h. supratotal resection of diffuse gliomas – an overview of itsmultifaceted implications. neurochirurgie, 63(3):243-249, 2017. 41. zhang k, gelb aw. awake craniotomy: indications, benefits, and techniques. rev colomb anestesiol., 46(supp):46-51, 2018. https://www.ncbi.nlm.nih.gov/pubmed/?term=niemann%20l%5bauthor%5d&cauthor=true&cauthor_uid=22875595 https://www.ncbi.nlm.nih.gov/pubmed/?term=reichelt%20dc%5bauthor%5d&cauthor=true&cauthor_uid=22875595 https://www.ncbi.nlm.nih.gov/pubmed/?term=felsberg%20j%5bauthor%5d&cauthor=true&cauthor_uid=22875595 https://www.ncbi.nlm.nih.gov/pubmed/?term=steiger%20hj%5bauthor%5d&cauthor=true&cauthor_uid=22875595 https://www.ncbi.nlm.nih.gov/pubmed/?term=szel%c3%a9nyi%20a%5bauthor%5d&cauthor=true&cauthor_uid=22875595 https://www.ncbi.nlm.nih.gov/pubmed/?term=rapp%20m%5bauthor%5d&cauthor=true&cauthor_uid=22875595 https://www.ncbi.nlm.nih.gov/pubmed/?term=sabel%20m%5bauthor%5d&cauthor=true&cauthor_uid=22875595 https://www.ncbi.nlm.nih.gov/pubmed/22875595 https://www.ncbi.nlm.nih.gov/pubmed/?term=kelm%20a%5bauthor%5d&cauthor=true&cauthor_uid=28868255 https://www.ncbi.nlm.nih.gov/pubmed/?term=sollmann%20n%5bauthor%5d&cauthor=true&cauthor_uid=28868255 https://www.ncbi.nlm.nih.gov/pubmed/?term=ille%20s%5bauthor%5d&cauthor=true&cauthor_uid=28868255 https://www.ncbi.nlm.nih.gov/pubmed/?term=meyer%20b%5bauthor%5d&cauthor=true&cauthor_uid=28868255 https://www.ncbi.nlm.nih.gov/pubmed/?term=ringel%20f%5bauthor%5d&cauthor=true&cauthor_uid=28868255 https://www.ncbi.nlm.nih.gov/pubmed/?term=krieg%20sm%5bauthor%5d&cauthor=true&cauthor_uid=28868255 https://www.ncbi.nlm.nih.gov/pubmed/28868255 https://www.ncbi.nlm.nih.gov/pubmed/?term=lacroix%20m%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=abi-said%20d%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=fourney%20dr%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=gokaslan%20zl%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=shi%20w%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=demonte%20f%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=lang%20ff%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=mccutcheon%20ie%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=hassenbusch%20sj%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=holland%20e%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=hess%20k%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=michael%20c%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=miller%20d%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=sawaya%20r%5bauthor%5d&cauthor=true&cauthor_uid=11780887 https://www.ncbi.nlm.nih.gov/pubmed/11780887 https://www.ncbi.nlm.nih.gov/pubmed/11780887 https://www.ncbi.nlm.nih.gov/pubmed/?term=leal%20rtm%5bauthor%5d&cauthor=true&cauthor_uid=29452315 https://www.ncbi.nlm.nih.gov/pubmed/?term=barcellos%20bm%5bauthor%5d&cauthor=true&cauthor_uid=29452315 https://www.ncbi.nlm.nih.gov/pubmed/?term=landeiro%20ja%5bauthor%5d&cauthor=true&cauthor_uid=29452315 https://www.ncbi.nlm.nih.gov/pubmed/?term=meskelevicius%20d%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=sch%c3%a4fer%20a%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=weber%20jk%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=hegmann%20l%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=haddad%20l%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=haddad%20l%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=kamp%20ma%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=mainzer%20b%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=rapp%20m%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=steiger%20hj%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=sabel%20m%5bauthor%5d&cauthor=true&cauthor_uid=30877481 https://www.ncbi.nlm.nih.gov/pubmed/?term=determination+of+optimal+time+window+for+cortical+mapping+in+awake+craniotomy%3a+assessment+of+intraoperative+reaction+speed https://www.ncbi.nlm.nih.gov/pubmed/?term=monticelli%20m%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=zeppa%20p%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=zenga%20f%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=altieri%20r%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=mammi%20m%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=bertero%20l%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=bertero%20l%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=castellano%20i%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=cassoni%20p%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=melcarne%20a%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=la%20rocca%20g%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=sabatino%20g%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=sabatino%20g%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=ducati%20a%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=garbossa%20d%5bauthor%5d&cauthor=true&cauthor_uid=29777944 https://www.ncbi.nlm.nih.gov/pubmed/29777944 https://www.ncbi.nlm.nih.gov/pubmed/?term=pallud%20j%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=rigaux-viode%20o%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=corns%20r%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=muto%20j%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=lopez%20lopez%20c%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=mellerio%20c%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=sauvageon%20x%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=dezamis%20e%5bauthor%5d&cauthor=true&cauthor_uid=28162255 https://www.ncbi.nlm.nih.gov/pubmed/28162255 https://www.ncbi.nlm.nih.gov/pubmed/?term=saito%20t%5bauthor%5d&cauthor=true&cauthor_uid=26236798 https://www.ncbi.nlm.nih.gov/pubmed/?term=muragaki%20y%5bauthor%5d&cauthor=true&cauthor_uid=26236798 https://www.ncbi.nlm.nih.gov/pubmed/?term=maruyama%20t%5bauthor%5d&cauthor=true&cauthor_uid=26236798 https://www.ncbi.nlm.nih.gov/pubmed/?term=tamura%20m%5bauthor%5d&cauthor=true&cauthor_uid=26236798 https://www.ncbi.nlm.nih.gov/pubmed/?term=nitta%20m%5bauthor%5d&cauthor=true&cauthor_uid=26236798 https://www.ncbi.nlm.nih.gov/pubmed/?term=okada%20y%5bauthor%5d&cauthor=true&cauthor_uid=26236798 https://www.ncbi.nlm.nih.gov/pubmed/26236798 https://www.ncbi.nlm.nih.gov/pubmed/26236798 https://www.ncbi.nlm.nih.gov/pubmed/21903234 https://www.ncbi.nlm.nih.gov/pubmed/?term=satoer%20d%5bauthor%5d&cauthor=true&cauthor_uid=26566782 https://www.ncbi.nlm.nih.gov/pubmed/?term=visch-brink%20e%5bauthor%5d&cauthor=true&cauthor_uid=26566782 https://www.ncbi.nlm.nih.gov/pubmed/?term=dirven%20c%5bauthor%5d&cauthor=true&cauthor_uid=26566782 https://www.ncbi.nlm.nih.gov/pubmed/?term=vincent%20a%5bauthor%5d&cauthor=true&cauthor_uid=26566782 https://www.ncbi.nlm.nih.gov/pubmed/26566782 https://www.ncbi.nlm.nih.gov/pubmed/26566782 https://www.ncbi.nlm.nih.gov/pubmed/?term=simonetti%20g%5bauthor%5d&cauthor=true&cauthor_uid=26251628 https://www.ncbi.nlm.nih.gov/pubmed/?term=gaviani%20p%5bauthor%5d&cauthor=true&cauthor_uid=26251628 https://www.ncbi.nlm.nih.gov/pubmed/?term=botturi%20a%5bauthor%5d&cauthor=true&cauthor_uid=26251628 https://www.ncbi.nlm.nih.gov/pubmed/?term=innocenti%20a%5bauthor%5d&cauthor=true&cauthor_uid=26251628 https://www.ncbi.nlm.nih.gov/pubmed/?term=lamperti%20e%5bauthor%5d&cauthor=true&cauthor_uid=26251628 https://www.ncbi.nlm.nih.gov/pubmed/?term=silvani%20a%5bauthor%5d&cauthor=true&cauthor_uid=26251628 https://www.ncbi.nlm.nih.gov/pubmed/26251628 https://www.ncbi.nlm.nih.gov/pubmed/?term=sitnikov%20ar%5bauthor%5d&cauthor=true&cauthor_uid=30221022 https://www.ncbi.nlm.nih.gov/pubmed/?term=grigoryan%20ya%5bauthor%5d&cauthor=true&cauthor_uid=30221022 https://www.ncbi.nlm.nih.gov/pubmed/?term=mishnyakova%20lp%5bauthor%5d&cauthor=true&cauthor_uid=30221022 https://www.ncbi.nlm.nih.gov/pubmed/?term=awake+craniotomy+without+sedation+in+treatment+of+patients+with+lesional+epilepsy https://www.ncbi.nlm.nih.gov/pmc/articles/pmc6265865/ doi: 10.33962/roneuro-2020-093 comparative analysis of anterior third ventricle approaches deepak kumar singh, kuldeep yadav, rakesh kumar, arun kumar singh, vipin kumar chand romanian neurosurgery (2020) xxxiv (4): pp. 544-549 doi: 10.33962/roneuro-2020-093 www.journals.lapub.co.uk/index.php/roneurosurgery comparative analysis of anterior third ventricle approaches deepak kumar singh, kuldeep yadav, rakesh kumar, arun kumar singh, vipin kumar chand department of neurosurgery. dr ram manohar lohia institute of medical sciences, lucknow, india abstract background. third ventricle tumors are uncommon and account for only 0.6 0.9% of all the brain tumors7. in 1921, dandy was the first neurosurgeon who successfully removed a colloid cyst from the third ventricle through a posterior transcallosal approach. despite their unfavourable locations, these tumours can be removed successfully by proper knowledge of anatomical landmarks and by choosing the appropriate approach. methods. we performed a retrospective analysis of all patients (17 patients) who underwent surgery for anterior third ventricular masses between march 2018 to march 2020 in the dr ram manohar lohia institute of medical science lucknow, uttar pradesh. results: the most common symptom in our cases was headache, which was present in all (100%) patients, nausea/vomiting in 7 (41%), history of recurrent episodes of drop attacks in 4 (23%), h/o seizure in 2 (11.7%), visual disturbance in 1 (5.4%), memory disturbance in 1 (5.4%) and urinary incontinence in 1 (5.4%) patient. 6 patients were operated with transcallosal-transforaminal approach, 1 patient was operated with transcallosal interforniceal approach, 3 patients were operated with transcortical-transforaminal approach, 1 patient was operated with subfrontal translamina terminalis approach, 1 patient was operated with transcallosaltranschoroidal approach, 5 patients were operated with endoscopically. gross total excision was achieved in 15 (88%) patients while in 2 (11.7%) patients subtotal resection was done due to their adherence to choroid plexus and optic chiasm. the most common post-operative complication was endocrine dysfunction in the form of diabetes insipidus. conclusions. anterior third ventricular tumours are mostly benign and best treatment modality is surgical resection. when we analyzed the results of various approaches, we found that despite their unfavourable location, the results were satisfactory for different tumours of different location in the anterior third ventricle, when treated with the carefully planned microsurgical or endoscopic approach with proper knowledge of anatomical landmarks. introduction third ventricle tumors are uncommon and account for only 0.6 0.9% of all the brain tumors7. third ventricle includes wide variety of lesions ranging from benign to malignant. majority of intra-ventricular tumors keywords third ventricle, transcallosal corresponding author: arun kumar singh department of neurosurgery. dr ram manohar lohia institute of medical sciences, lucknow, india aks30041990@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 545 comparative analysis of anterior third ventricle approaches are benign, surgery is therefore preferred and is curative. most common entities for this location are colloid cysts, astrocytomas and craniopharyngiomas. others lesions for this location are arachnoid cysts, pituitary adenomas, subependymomas, germinomas, central neurocytoma, teratomas, dermoids, meningiomas and choroid plexus papillomas12,18. third ventricle can be divided into anterior and posterior third ventricle on the basis of an imaginary line connecting foramen monro to aqueduct sylvius. common tumors originating from anterior third ventricle are astrocytomas and craniopharyngiomas; from the posterior third ventricle are meningiomas, choroid plexus papillomas and colloid cysts at the level of foramen monro8. anterior third ventricular tumors can be classified as primary and secondary tumors. primary tumors: originating purely intraventricular ependymoma, choroid plexus papilloma, colloid cysts. secondary tumors: originating adjacent to third ventricle and secondarily expand within the ventricular cavity – pituitary adenoma, craniopharyngioma, meningioma. patients of anterior third ventricular mass usually presents with symptoms secondary to hydrocephalus such as headache, vomiting, blurring or diminution of vision. in 1921, dandy was the first neurosurgeon who successfully removed a colloid cyst from the third ventricle through a posterior transcallosal approach, and stated that no treatment short of total removal could have any possible value in the treatment of tumors in this region10. the anterior transcallosal approach was suggested by ehni who used this approach for different pathological entities11. third ventricular tumors are difficult to treat due to their deep location and proximity to vital neural structures such as thalamus, hypothalamus and vascular structure such as internal cerebral vein and medial posterior choroidal artery. despite their unfavorable locations, these tumors can be removed successfully by proper knowledge of anatomical landmarks, pre-operative planning and by choosing appropriate approach. there are various approaches to anterior third ventricle including transcortical-transventricular approach through foramen of monro22, interhemispheric – transcallosal interforniceal approach2,5, interhemispheric transcallosaltranschoroidal trans-velum interpositum approach9,14, subfrontal trans laminaterminalis approach21and endoscopic approach. common surgical complications are seizure following transcortical approach, memory deficit and venous cortical infarct following transcallosal approach. other postoperative complications are mutism, hematoma, and hemiparesis. some study suggests that unilateral damage to fornix produces no deficit. the inter-forniceal approach to a lesion of third ventricle carries the potential risk for bilateral damage o fornix, but memory deficit is usually transient by this approach4,3. method we performed a retrospective analysis of all patients who underwent surgery for anterior third ventricle mass between march 2018 to march 2020 in the dr ram manohar lohia institute of medical science lucknow uttar pradesh. 17 patients underwent for surgery of anterior third ventricular mass. we reviewed case sheets, radiological images, pathological reports, surgical reports of all the patients. we also collected data regarding their demographic data, preoperative symptoms and signs, surgical approaches, histopathological reports and postoperative complications. results in our study we reviewed case sheets of 17 patients, who were operated for anterior third ventricle approaches in dr ram manohar lohia institute of medical sciences lucknow during a time period from march 2018 to march 2020. in our study there were 12 males and 5 females, age ranged from 9 years to 54 years with mean age of 27 years. maximum patients (9) were in the age group of 20-30 years. the most common symptom in our cases was headache, which was present in all (100%) cases, nausea/vomiting in 7(41%), history of recurrent episodes of drop attacks in 4(23%), h/o seizure in 2(11.7%), visual disturbance in 1(5.4%), memory disturbance in 1(5.4%), urinary incontinence in 1(5.4%). one patient presented with altered mental status [table-1]. symptoms no of patients headache 17(100%) nausea/vomiting 7(41%) h/o drop attacks 4(23%) 546 deepak kumar singh, kuldeep yadav, rakesh kumar et al. h/o seizure episode 2(11.7%) visual disturbance 1(5.4%) memory disturbance 1(5.4%) urinary incontinence 1(5.4%) table 1. clinical presentation of patients of anterior third ventricle mass. surgical approaches no of patients transcortical transforaminal 3 transcallosal transforaminal 6 transcallosal interforniceal 1 transcallosal subchoroidal 1 subfrontal translaminar 1 endoscopic excision 5 table 2. surgical approaches in patients with anterior third ventricle mass. histopathological report no of patients colloid cyst 11 craniopharyngioma 4 central neurocytoma 2 table 3. histopathological report. 6 patients were operated with transcallosaltransforaminal approach, 1 patient was operated with transcallosal interforniceal approach, 3 patients were operated with transcortical-transforaminal approach, 1 patient was operated with subfrontal translamina terminalis approach, 1 patient was operated with transcallosal-transchoroidal approach, 5 patients were operated endoscopically [table 2]. gross total excision was achieved in 15(88%) patients while in 2(11.7%) patients one of craniopharyngioma and one of colloid cyst subtotal resection was done due to their adherence to choroid plexus and optic chiasm. the most common post-operative complication was endocrine dysfunction in the form of diabetes insipidus in 4 patients and cortisol insufficiency and hypothyroidism in 1 patient due to hypothalamic injury. all four patients of post op endocrine dysfunction were of craniopharyngioma. 3 patients develop post-op seizure in the evening of day of surgery, 2 patients in which post-operative seizure developed were operated by transcortical approach and 1 patient was operated with transcallosal approach. histopathological reports of 11 patients were colloid cyst, craniopharyngioma was found in 4 patients and central neurocytoma was seen in 2 patients [table 3]. discussion in current study of anterior third ventricular mass, in maximum patients 11(64%) the diagnosis was colloid cyst and most common symptom was headache seen in 100 % patients, vomiting in 41% patients and history of recurrent drop attacks in 23 % of patients. similar results were reported by many authors13,20. the choice of the third ventricular tumors approach basically depends on the location of tumor, differential diagnosis, size, patient’s clinical status and anatomical knowledge. it should be underlined that, although several corridors to the third ventricle exist, they all demand the incision of the neural tissue which may be relatively free from the underlying disease. endoscopic approach remains the commonly used approach for the treatment of colloid cyst with chances of reoperation for residual cyst, but more cost effective and safer than open craniotomy for the resection of colloid cyst. surgical approaches transcallosal approach transcallosal approach allow removal of tumor from anterior third ventricle by incising the corpus callosum longitudinally in the direction of corpus callosum less than 2.5 cm (to avoid disconnection syndrome) between the two pericallosal artery at the level of foramen of monro. genu of internal capsule touches the wall of ventricle in the area lateral to foramen of monro near the anterior pole of thalamus. retraction should be done at this level minimally to avoid hemiplegia. after incising the corpus callosum we have multiple options to reach the third ventricle. we use trans-foraminal approach in 6 patients, in which 4 patients were of colloid cyst, 1 was of craniopharyngioma and 1 was of central neurocytoma, in all the cases foramen monro was already dilated, there was no need of enlarging the foramen of monro. gross total excision was achieved in 5 cases; in one patient of craniopharyngioma gross total resection was not achieved due to adherence to choroid plexus and chiasma. radiotherapy was given later to this patient. we used inter-forniceal approach in 1 patient of craniopharyngioma, located just behind the foramen of monro in midline. the point of entry was approximately 2 cm posterior to 547 comparative analysis of anterior third ventricle approaches foramen of monro to preserve the hippocampal commissure to avoid temporary or permanent problems with memory function. in this approach the body of the fornix is split in the midline, in the direction of its fibers, to expose the velum interpositum3,15,27. we used transchoroidal approach in 1 patient of craniopharyngioma, the entry was through the tenia fornicis as it has advantage that large veins like a thalamostriate vein which drains the internal capsule and central part of hemisphere and choroidal arteries can be dissected laterally, avoiding injury to these vessels. the transchoroidal and interforniceal approaches have the advantage of giving access to the central portion of the third ventricle behind the foramen of monro by displacing it, rather than transecting the fibers in the fornix19,29. transcallosal approach is superior to transcortical approach as it is not dependent on ventricle size, more direct and avoid incision over cortex. (figure 1) figure 1. (a) pre-operative contrast mri axial scan showing contrast enhancing third ventricular mass (b) anterior callosotomy between two pericallosal artery (c) opening the right lateral ventricle(d) lateral ventricle entered and tumor( )identified (e) post-operative ct scan showing complete tumor removal. transcortical approach we used transcortical-transforaminal approach in 3 patients. out of 3, the diagnosis in 2 patients was colloid cyst and in one patient it was central neurocytoma. we entered through right middle frontal gyrus, after reaching lateral ventricle we used transforaminal corridor to remove the tumor as it is a natural orifice to enter third ventricle. enlargement of foramen of monro was not required in any of the case as it was already dilated due to hydrocephalus. gross total resection was achieved in all cases. postoperative complication in the form of seizure developed in two patients. (figure 2) figure 2. (a) cortical incision around 1.5 cm in right middle frontal gyrus (b) entry into right lateral ventricle and identification of cystic mass (c) excision of cystic mass (d) complete excision of mass. subfrontal translamina terminalis approach we used subfrontal translamina terminalis approach in one patient of craniopharyngioma which was located in antero-inferior part of anterior third ventricle. after passing the planum sphenoidale, the optic nerves, the chiasm, and both internal carotid arteries are visualized. a1 was identified bilaterally and after incising the lamina terminalis above the chiasm up to the anterior commissure, tumor was seen which was internally decompressed initially and the remaining part of tumor was excised later. (figure 3) figure 3. (a) pre-operative contrast mri axial cut showing enhancing mass in third ventricle. (b) identification and excision of the tumor in pre-chiasmatic and (c) optico-carotid cistern (d)opening of lamina terminalis and excision of mass (e) complete excision achieved (f) post-operative scan showing complete excision. 548 deepak kumar singh, kuldeep yadav, rakesh kumar et al. endoscopic approach we used endoscopic approach in 6 patients, diagnosis of all patients were colloid cyst. the colloid cyst of the third ventricle is an ideal tumour for endoscopic removal due to its cystic nature. hydrocephalous was present in all cases which helped us to cannulate the lateral ventricle through planned burr-hole on right side. after reaching the colloid cyst, choroid plexus which was attached to colloid cyst was coagulated. after cauterisation of cyst wall, we opened the cyst wall applying endoscopic micro-scissor and then content was aspirated after that cyst wall was excised with minimal traction.in one patient cyst wall was densely adhered to the choroid plexus which was left in-situ after coagulation to prevent recurrence. (figure 4) figure 4. (a) pre-operative ct scan showing hyperdense mass in third ventricle (b) endoscopic view of mass filling the third ventricle, wall of the tumor cauterized at foramen of monro (c) endoscopic view of the third ventricle after complete excision of mass and third ventriculostomy. basilar artery seen in prepontine cistern ( ) (d) postoperative scan showing complete excision. post-operative complications in our retrospective study of anterior third ventricular mass patients we encountered with two complication. first complication was post op seizure which was seen in three patients of which two were operated with transcortical approach, one patient was intubated due to seizure and was extubated next morning and one was operated with transcallosal approach, concluded that there are less chances of post-operative seizure in transcallosal approach. in our study in 66% of patient of transcortical approach post op seizure developed which is very high, may be due to a smaller number of cases operated with transcortical approach. the incidence of postoperative seizures in the transcortical-transventricular approach in some series ranges from 11 to 13%6,1,16,17. another complication was endocrine dysfunction in the form of diabetes insipidus in 4 patients which was transient and cortisol insufficiency and hypothyroidism in 1 patient due to hypothalamic injury, in these patients hormone replacement was given. all four patients of post op endocrine dysfunction were of craniopharyngioma. in multiple studies hormonal replacement therapy was required in approximately 80% of the children.28,23,25,26,24. conclusion anterior third ventricular tumors are mostly benign and best treatment modality is surgical resection. when we analyzed the results of various approaches, we found that despite their unfavorable location, in all techniques the results were satisfactory for different tumors of different location in anterior third ventricle, when treated with carefully planned microsurgical or endoscopic approach and with proper knowledge of anatomical landmarks with minimal complication. transcallosal approach is a safer route, superior to transcortical approach as it is not dependent on ventricle size, direct and avoids incision over cortex. transcortical approach had more chances of post-operative seizure. endoscopic approach is good if done by an experienced hand but have limitation of wide visualization. tumors originating from the antero-superior part of the third ventricle can be easily approached through a transcallosal transforaminal route, whereas lesions arising from the anteroinferior portion of the third ventricle might be safely and effectively approached through subfrontal translamina terminalis approach. in most of the craniopharyngioma patients, postoperative hormone replacement therapy usually needed. references 1. antunes jl, louis km, ganti sr. colloid cysts of the third ventricle. neurosurgery 1980;7:450-55. 2. apuzzo mlj, amara: thetranscallosalinterforniceal approach, in apuzzo mlj (ed) :surgery of the third 549 comparative analysis of anterior third ventricle approaches ventricle. baltimore, williams & wilkins, 1998,ed 2, pp 421-452. 3. apuzzo mlj, chikovani ok, gott ps, teng el, zee cs, giannotta sl, weiss mh: transcallosal, interfornicial approaches for lesions affecting the third ventricle: surgical considerations and consequences. neurosurgery 1982;10:547–554. 4. apuzzo mlj, giannotta sl: transcallosalinterforniceal approach, in apuzzo mlj (ed): surgery of the third ventricle. baltimore, williams &wilkins, 1987, pp 354– 379. 5. apuzzo mlj, zee c-s, breeze re, dayjd: anterior and mid-third ventricular lesions: a surgical overview, in apuzzo mlj (ed): surgery of third ventricular. baltimore, williams & wilkins, 1998, ed 2, pp 63-68. 6. camacho a, abernathey cd, kelly pj, laws er jr. colloid cyst: experience with the management of 84 cases since the introduction of computed tomography. neurosurgery 1989;24:693-700. 7. chibbaro s, di rocco f, makiese o, et al.: neuroendoscopic management of posterior third ventricle and pineal region tumors: technique, limitation, and possible complication avoidance. neurosurg rev. 2012; 35: 331-40. 8. citow js, macdonald rl, refai d: comprehensive neurosurgery board review. new york, thieme,2020,ed 3,pp 167-185. 9. cossu m, lubinu f, orunesu g, pau a, sehrbundtviale e, sini g, turtas s: subchoroidal approach to the third ventricle: microsurgicalanatomy. surgneurol 1984; 21:325-331. 10. dandy we. benign tumours of the third ventricle of the brain: diagnosisand treatment. springfield, il: charles c thomas,1933: pp214-236. 11. ehni g. interhemispheric and pericallosal (transcallosal) approach to the cingulate gyri, intraventricular shunt tubes, and certain deeply placed brain tumours. neurosurgery 1984;14:99-110. 12. fries g, perneczky a. tumors and cysts of the third ventricle. in: rengachary ss, ellenbogen rg, eds. principles of neurosurgery. edinburgh: elsevier mosby; 2005:647-656. 13. kumar v, behari s, kumar singh r, jain m, jaiswal ak, jain vk. pediatric colloid cysts of the third ventricle: management considerations. actaneurochir (wien) 2010;152:451–61. 14. lavyne mh, patterson rh jr: subchoroidal trans-velum interpositum approach, in apuzzo mlj (ed): surgery of the third ventricle. baltimore, williams & wilkins, 1987, pp 381-397. 15. lavyne mh, patterson rh jr: subchoroidal trans-velum interpositum approach to mid-third ventricular tumors. neurosurgery 1983;12:86–94. 16. little jr, maccarty cs. colloid cysts of the third ventricle. j neurosurg 1974;39:230-5. 17. mckissock w. the surgical treatment of colloid cyst of the third ventricle. brain 1951;74:1-9. 18. morrison g, sobel df, kelley wm, norman d. intraventricular mass lesions. radiology. 1984;153:435442. 19. nagata s, rhoton al jr, barry m: microsurgical anatomy of the choroidal fissure. surgneuro 1988; l30:3–59. 20. nitta m, symon l. colloid cysts of the third ventricle: a review of 36 cases. actaneurochir (wien) 1985;86:99104. 21. patterson rh jr: subfrontaltranssphenoidal and translamina terminalis approach, in apuzzo mlj (ed): surgery of the thirdventricle. baltimore, williams & wilkins, 1987, pp 398-412. 22. shucartw: anteriortranscallosal and transcortical approach in apuzzo mlj(ed):surgery of third ventricle. baltimore, williams & wilkins, 1987,pp303-325 23. sklar ca. craniopharyngioma: endocrine sequelae of treatment. pediatrneurosurg. 1994;21(suppl 1):120– 123. 24. sorva r, heiskanen o, perheentupaj. craniopharyngioma surgery in children: endocrine and visual outcome. childs nerv syst. 1988;4:97–99. 25. stahnke n, grubel g, lagenstein i, et al. long-term follow-up of children with craniopharyngioma. eur j pediatr. 1984;142:179–185. 26. thomsett mj, conte fa, kaplan sl, et al. endocrine and neurologic outcome in childhood craniopharyngioma: review of effect of treatment in 42 patients. j pediatr. 1980;97:728–735. 27. viale gl, turtas s, pau a: surgical removal of striate arteriovenous malformations.surgneurol14:321–324, 1980. 28. weiner hl, wisoff jh, rosenberg me, et al. craniopharyngiomas: clinicopathological analysis of factors predictive of recurrence and functional outcome. neurosurgery. 1994;35:1001–1010. 29. wen ht, rhoton al jr, de oliveira ep: transchoroidal approach to the third ventricle: an anatomic study of the choroidal fissure and its clinical application.neurosurgery 1988; 42:1205–1219. doi: 10.33962/roneuro-2022-001 multimodal treatment of glomus jugular tumours. case series and literature review f. stoica, g. popescu, francesca paslaru, anamaria gheorghiu, a.c. paslaru, m. apostol, m.c. zaharia, r.m. gorgan romanian neurosurgery (2022) xxxvi (1): pp. 9-13 doi: 10.33962/roneuro-2022-001 www.journals.lapub.co.uk/index.php/roneurosurgery multimodal treatment of glomus jugular tumours. case series and literature review f. stoica1, g. popescu1, francesca paslaru1, anamaria gheorghiu1, a.c. paslaru2,3, m. apostol1, m.c. zaharia1, r.m. gorgan1,2 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 department of genetics, “dr. victor gomoiu” children’s clinical hospital, bucharest, romania abstract glomus jugulare tumours are extremely rare, slow-growing, hypervascular tumours that arise within the jugular foramen of the temporal bone and frequently involve the lower cranial nerves. we performed a retrospective study for patients treated between january 2005 and december 2019, reviewing clinical and radiological data for 91 cases of glomus jugulare tumours. data were available for 91 patients presenting with 96 tumours. surgery was 1st intention of treatment for 13 cases, the endovascular approach was 1st intention for 6 cases and gkrs was primarily performed in 72 cases. combined treatment options were used in 19 cases. the median age at the time of treatment was of 57 years. the tumour volume varied between 0.5 and 73.4 cm3 with a median value of 8.3 cm3. for the cases treated with gkrs, the peripheral dose ranged between 8 and 35 gy on the 35% to 65% isodose, with a median of 14 gy on the 45% isodose. the average follow-up was 38 months with a maximum of 94 and consisted of contrast-enhanced mri every six months in the first year after the procedure and every 1 to 2 years afterwards. overall tumour control rate was of 95.6% using multimodal treatment options for glomus jugulare tumours. multimodal treatment for glomus jugulare tumours offers the patient the chance for the best possible outcome and long-term survivability. individual treatment approach for this kind of very rare head and neck tumour (0,6% of all head and neck tumours) is recommended to choose the best risk-versus-benefit treatment option. background glomus jugulare tumor is a benign neuroendocrine tumor that arises from the jugular foramen. this tumor is characterized by a slowgrowing pattern. paragangliomas, also known as chemodectomas represent benign tumors with the origin from neural crest derivates also known as the parangalia [1],[2 ],[3 ]. these tumors are highly vascularised. they can receive blood supply from both from the external carotid artery and internal carotid artery. the localization of keywords multimodal, jugular tumours, glomus corresponding author: g. popescu “carol davila” university of medicine and pharmacy, bucharest, romania george_popescu39@yahoo.com” copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 10 f. stoica, g. popescu, francesca paslaru et al. these tumors can widely vary, from carotid bifurcation to the auricular branch of the vagus nerve. the most frequent localization is the carotid body, accounting for almost half of the tumors [5],[6] whereas glomus jugulare tumors represent 24% of them [6]. even though they are benign tumors, the symptomatology can be the cause of the mass effect [2]. usually, these tumors are diagnosed in the fourth to sixth decade of life, with a moderate female predilection. most of the glomus jugulare tumors are isolated lesions but around 20% of them present hereditary components [4]. the inherited tumors are usually bilateral and the onset of the symptoms is reported to be earlier than the onset symptomatology of the sporadic tumors. the reported malignancy of these tumors is less than 5% [2]. around 25% of the paragangliomas remain silent and are incidentally discovered. the symptoms caused by these tumors depend on their location. lower cranial nerves impairment is reported in more than 10% of patients [8]. the most common neurological deficits reported are tongue deviation, hoarseness, facial palsy, dysphagia, and shoulder weakness [2],[7],[8]. additionally, patterns of cranial nerve palsies were described and these include [12]: • vernet syndrome that represents motor paralysis of cranial nerves ix, x and xi; [9] • colletsicard syndrome described as the palsy of cranial nerves ix,x,xi and xii; [10] • horner syndrome – oculosympathetic palsy. [11] due to its slow-growing pattern and the complex anatomy of the skull base and neck, observation of the patient is considered a good treatment alternative. in more than 60% of the cases, tumor volume remains stable or decrease in size [14]. however, if the tumor tend to be symptomatic, surgical excision or stereotactic radiosurgery will be take into account. case series we performed a retrospective study for patients treated between january 2005 and december 2019, reviewing clinical and radiological data for 91 cases of glomus jugulare tumors. data were available for 91 patients presenting with 96 tumors. surgery was the treatment of choice for 13 cases, endovascular embolization was performed as first intention treatment for 6 cases and gkrs was primarily performed in 72 cases. figure 1. distribution of the treatment option combined treatment options were used in 19 cases (1 surgery with gkrs, 18 endovascular with gkrs). 44 glomus jugulare tumors were identified on the right side, and 47 on the left side. in the study group, we had 23 male patients and 63 female patients. 11 patients were in the 15-39 age group while 80 patients were older than 40 yrs. the median age at the time of treatment was of 57 years. the tumor volume varied between 0.5 and 73.4 cm3 with a median value of 8.3 cm3. figure 2. gender distribution of the patients for the cases treated with gkrs, the peripheral dose ranged between 8 and 20 gy on the 35% to 65% isodose, with a median of 14 gy on the 45% isodose. the average follow-up was 38 months with a maximum of 94 and consisted of contrast-enhanced mri every six months in the first year after the procedure and every 1 to 2 years afterward. overall gender distribution male 25% female 75% treatment approach 3, 14% 6, 7% 72, 79% surgery endovascular gkrs 11 multimodal treatment of glomus jugular tumours reccurence gamma knife radiosurgery 4 7 2 emboliz ation 6 open surgery 7 1 3 0 10 20 30 40 50 60 70 80 reccurence cases tumor control rate was 95.6% using multimodal treatment options for glomus jugulare tumors. figure 3. tumour localisation table 1. most common comorbidities comorbidities were noted in 37 patients (40.6%) and consisted of lower cranial nerves deficits (26.4%), dizziness, tinnitus, partial or complete hearing loss in 21.9% of cases, 2 hemorrhages, 2 secondary hydrocephalus, and 1 hemiparesis. 23 patients (24.3%) presented recurrences: 13 after surgery, 6 after embolization, and 4 after gkrs. however, the mortality rate was 0. figure 4. recurrence cases based on the therapeutical approach case 1 the first case is represented by a female patient of 53 years old, whose symptoms are vertigo, hearing loss, and pulsating tinnitus. soon it is discovered the typical aspect of “salt and pepper” for a glomus tumor with temporal localization, millimetric extracranial extension into jugular vein lumen and damage to the structures of the inner ear. 9 years after gkrs, a cerebral mri was performed, which showed that the irradiated tumor volume has been reduced in circumferential dimensions, with a homogeneous intake of contrast substance ("densified" appearance due to sclerosis and obliteration of intratumoral blood vessels) without adverse reactions due to irradiation. no new neurological deficits were recorded after gkrs. figure 5. preoperative aspect of the tumour figure 6. postoperative aspect after gamma knife radiosurgery comorbidity lower cranial nerves deficits dizziness tinnitus hearing impairment hemorrhages hydrocephalus hemiparesis tumour localisation 52% 48 % right side left side 12 f. stoica, g. popescu, francesca paslaru et al. case 2 the second case is represented by a 62 years old female patient, whose symptoms onset with injury to multiple cranial nerves (vii, viii, ix, xi, xii). the diagnosis was represented by a large glomic tumor with an important intracranial component with a mass effect on the brainstem. a cerebral mri was performed 4 years post gkrs, showing a marked reduction in the size of the irradiated tumor, especially in the intracranial component, with a significant decrease in the mass effect, without perilesional reactive edema. no new neurological deficits were recorded. 18 months after irradiation, a complete remission of facial paresis has been noticed and other cranial nerves neurological status remained stationary. figure 7. preoperative aspect of the tumour figure 8. postoperative aspect after gamma knife radiosurgery case 3 for the third case, we have a 35 years old male patient, who presented with glomic tumor located in the temporal bone, onset with hearing disorders (hearing loss and pulsating tinnitus). 6 years after gkrs, a periodic follow-up mri has been performed. the inferior recurrence in the lumen of the jugular vein was identified outside the irradiation field with a volume of 4.6 cm3, asymptomatic. the decision is made in order to irradiate the recurrence with 14 gy on 47% isodose. figure 9. preoperative aspect before gamma knife radiosurgery figure 10. the reccurence aspect, 6 years afte gkrs discussions the best treatment option for glomus jugulare tumors is yet to be debated. due to their localization, surgical treatment does not represent the gold standard because of the complex anatomy of the region, high rates of morbidity, subtotal resection, and the alternative behavior of the tumors that could be very aggressive in some cases. in 2003, roberto pareschi et al [15] described their experience in the surgical treatment of glomus jugulare tumors. 42 patients with glomus jugulare tumors were identified, 3 of them previously undergone surgery for this pathology, and 3 patients presented bilateral temporal lesions. the otoscopic evaluation revealed in 80% of the patients the typical red middle ear mass. 70% of the cases had no preoperative cranial nerve deficit. 37 seven patients were elected for surgical intervention. in 33 cases, infratemporal fossa approaches were used and in 4 cases, conservative jugulopetrosectomy was performed, in order to preserve the facial nerve. in 20% of the cases, cranial nerves ix and x were injured. no recurrence after total resection was reported. an extensive dissection of the posterolateral skull base is required for surgery of glomus jugulare tumors [15]. even though cranial nerve preservation is an 13 multimodal treatment of glomus jugular tumours extremely important goal in the surgical approach, in 22% of the cases facial nerve is sacrificed [15]. the authors concluded that the focus should drift away from total resection to increasing the quality of life of the patient, a philosophy that our clinic shares. only 14% percent of our cases were surgically treated, in order to avoid the decrease in the quality of patient`s life. endovascular treatment is an alternative treatment approach for patients with glomus jugulare tumors. in 2017, kocur et al [17] presented their experience and the outcome of embolization in 3 cases of glomus jugulare tumors. they described the technical difficulty of achieving complete obliteration of the glomus jugulare tumors and concluded that increased risk of revascularization is not beneficial compared to the diminished clinical symptoms. in our clinic, only 6 endovascular treatments were performed. a promising approach for this pathology is represented by radiosurgery. due to the high degree of accuracy, rapid radiation dose falloff at the periphery of the target tumor, and their high precision, radiosurgery became a popular treatment choice. in their meta-analysis, guss et al [13] included 19 studies, compounding 335 glomus jugulare patients. they reported a reduced or unchanged tumoral volume after radiosurgery, sustained by imagistic findings. clinical control was reported as improved or unchanged after radiosurgery in 95% of the cases. the authors emphasized the effectiveness of this treatment option. in our clinic, 72 patients benefited from radiosurgery. conclusions multimodal treatment for glomus jugulare tumors offers the patient the chance for the best possible outcome and long-term survivability. individual treatment approach for this kind of very rare head and neck tumor (0,6% of all head and neck tumors) is recommended to choose the best risk-versus-benefit treatment option. gkrs in these kind of tumors seems to be the option of choice, considering that in our experience, has the lowest comorbidity, reccurence rate and mortality. references 1. fussey jm, kemeny aa, sankar s, rejali d. successful management of a catecholaminesecreting glomus jugulare tumor with radiosurgery alone. j neurol surg b skull base. 2013 dec;74(6):399-402. 2. ramina r, maniglia jj, fernandes yb, paschoal jr, pfeilsticker ln, neto mc, borges g. jugular foramen tumors: diagnosis and treatment. neurosurg focus. 2004 aug 15;17(2):e5. 3. petropoulos ae, luetje cm, camarata pj, whittaker ck, lee g, baysal be. genetic analysis in the diagnosis of familial paragangliomas. laryngoscope. 2000 jul;110(7):1225-9. 4. semaan mt, megerian ca. current assessment and management of glomus tumors. curr opin otolaryngol head neck surg. 2008 oct;16(5):420-6. 5. tokgöz sa, saylam g, bayır ö, keseroğlu k, toptaş g, çadallı tatar e, akın i̇, korkmaz mh. glomus tumors of the head and neck: thirteen years' institutional experience and management. acta otolaryngol. 2019 oct;139(10):930-933. 6. singh s, madan r, singh mk, thakar a, sharma sc. headand-neck paragangliomas: an overview of 54 cases operated at a tertiary care center. south asian j cancer. 2019 octdec;8(4):237-240. 7. wanna gb, sweeney ad, haynes ds, carlson ml. contemporary management of jugular paragangliomas. otolaryngol clin north am. 2015 apr;48(2):331-41. 8. jackson cg, harris pf, glasscock me, fritsch m, dimitrov e, johnson gd, poe ds. diagnosis and management of paragangliomas of the skull base. am j surg. 1990 apr;159(4):389-93. 9. monteiro, f., oliveira, p., peneda, j. and condé, a., 2019. vernet syndrome: intracranial extension of a slowgrowing mass. bmj case reports cp, 12(5), p.e228039. 10. neo s, lee ke. collet-sicard syndrome: a rare but important presentation of internal jugular vein thrombosis. practical neurology. 2017 feb 1;17(1):63-5. 11. spector gj, druck ns, gado m. neurologic manifestations of glomus tumors in the head and neck. archives of neurology. 1976 apr 1;33(4):270-4. 12. spector gj, gado m, ciralsky r, ogura jh, maisel rh. neurologic implications of glomus tumors in the head and neck. the laryngoscope. 1975 aug;85(8):1387-95. 13. guss zd, batra s, limb cj, li g, sughrue me, redmond k, rigamonti d, parsa at, chang s, kleinberg l, lim m. radiosurgery of glomus jugulare tumors: a metaanalysis. international journal of radiation oncology* biology* physics. 2011 nov 15;81(4):e497-502. 14. prasad sc, mimoune ha, d'orazio f, medina m, bacciu a, mariani-costantini r, piazza p, sanna m. the role of waitand-scan and the efficacy of radiotherapy in the treatment of temporal bone paragangliomas. otol neurotol. 2014 jun;35(5):922-31. 15. pareschi r, righini s, destito d, raucci af, colombo s. surgery of glomus jugulare tumors. skull base. 2003 aug;13(03):149-58. 16. kocur d, ślusarczyk w, przybyłko n, hofman m, jamróz t, suszyński k, baron j, kwiek s. endovascular approach to glomus jugulare tumors. polish journal of radiology. 2017;82:322. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 417-423 doi: 10.33962/roneuro-2019-086 www.journals.lapub.co.uk/index.php/roneurosurgery current applications of 3d printing in neurosurgery a. chiriac1, a. iencean1, georgiana ion1, g. stan2, s. munteanu3, i. poeata1 1 “gr. t. popa” university of medicine and pharmacy, iasi, romania 2 national institute of materials physics, bucharest-magurele, romania 3 transilvania university of brasov, romania abstract medical implications of 3-dimensional (3d) printing technology have progressed with increasingly used especially in surgical fields. 3d printing techniques are practical and anatomically accurate methods of producing patient specific models for medical education, surgical planning, training and simulation, and implants production for the assessment and treatment of neurosurgical diseases. this article presents the main directions of 3d printing models application in neurosurgery. introduction since its initial appearance in the 1980s, three-dimensional (3d) printing has revolutionized the practice of rapid prototyping in many areas, such as design, engineering and medicine. this technique consists in the manufacture of 3d physical models, based on computer models, by depositing successive layers of material in the underlying structure to build 3d objects. [1,3,5] modelling by 3d printing uses either a thermoplastic material that hardens after it has been heated during extrusion, or uses a low power ultraviolet (uv) laser to solidify a liquid photosensitive polymer in the case of stereolithography. the development of this technique has allowed the elimination of intermediate stages of product development allowing a cheap and rapid transition of concepts into prototypes or finished products. the numerous innovations in the field of technology and materials of the last decade have allowed improving the precision level of the printed objects and have increased the range of printable materials. thus, the applications of 3d printing technology have expanded greatly in the medical and biomedical fields. applications in clinical medicine appear especially in maxillofacial reconstructions, neurosurgery and spinal surgery. the ability of 3d printing to produce individualized models, devices and implants has greatly contributed to the development of so-called “personalized medicine”. in addition, the proven utility in surgical planning and simulation, assisting in the consent process and use as an educational tool have significantly marked the role of 3d printing in medicine [2,4,6]. keywords 3d printing, neurosurgery, 3d models corresponding author: a. chiriac “gr. t. popa” university of medicine and pharmacy, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 418 a. chiriac, a. iencean, georgiana ion, et al. 3d printing evolution in neurosurgery in the field of neurosurgery, the 3d printing technique has made substantial progress since 2007 as a result of the development of cranioplasty techniques that required the implementation of implants with increasingly complex anatomical configurations. initially, the evolution of this technique was limited as the commercially available printers were still in the beginning and allowed printing only in one material and density. subsequently, 3d printing has progressed, following the success of making models with as accurate spatial representations of the patient's anatomy. thus, with the development in 2012 of printers with the possibility of printing in several materials and densities (shore value), the technique of 3d printing in neurosurgery has developed in several main directions: development of anatomical models specific to the patient for surgical planning; vocational training and education; design of neurosurgical devices for the evaluation and treatment of neurosurgical diseases; and not least, the development of biological tissue implants. in this article, we will review the achievements of 3d printing in every direction in the neurosurgery field to evaluate the usefulness of final products, the challenges encountered and the progress of the field [1,5,7]. cranioplasty (reconstruction of skull defects) cranioplasty is one of the oldest neurosurgical procedures, practiced since 3000 bc. the most common defects of the skull can appear after trauma, neurosurgical procedures such as decompressive craniotomy, tumor resections with bone invasion, infections and congenital defects. the purpose of the cranial repair is to protect the underlying brain tissue, to reduce the local pain, to restore the patient's psychological balance by improving the cranial aesthetics. the materials used initially in the cranioplasty procedure were pieces of autologous bone, polymeric, ceramic and metallic biomaterials. these autologous bones represented by the autologous calvarial bone removed from the patient during the initial operation had long-term problems, including subsidence, disintegration and infection. thus, in a large number of patients, these plates disintegrated following their re-implantation, creating large defects, often accompanied by pain at the edges of the disintegrated defect. subsequently, autologous bones were excluded and various acrylic or metalbased materials became increasingly used in cranial reconstructions. one of the disadvantages of these materials is the need to model them in situ during the operation, usually manually or with minimal equipment. these had to be cut and bent to fit, often reaching with sharp edges that represented a risk to both the surgeon and the patient's overlapping skin. all of these resulted in an extension of the intervention time and also created a number of problems, including poor match and unsatisfactory cosmetic result. figure 1: pmma reconstruction on 3d printed model with the advent of 3d printing, most of the problems mentioned above have managed to be overcome. initially the 3d printing method was used to create a mould model on which the reconstruction joints are prefabricated. also, another approach consisted in the initial creation of some models in the corrected form, and the titanium plates were subsequently modelled to suit the defect based on reconstruction. implants thus reconstructed were then tested on the 3d printed model of the defect before sterilization and surgery. in addition to titanium, other materials such as acrylic (pmma) and peek (polyether ether ketone) have also been used to create implants using similar techniques (figure 1). the use of these materials allowed the creation of a personalized prosthesis using 3d printing moulds characterized by an excellent cranial contour. using the standard printing method described above, it was possible to avoid the possibility of deterioration of adjacent tissues due to the exothermic reaction during the polymerization process. thus, intraoperative 419 current applications of 3d printing in neurosurgery modelling of the final implant can be performed in just a few minutes [1,6,7,8,9]. the introduction of the 3d printing technique by the continuos multilayer deposition method in obtaining the cranioplasty implants determined the elimination of the intraoperative manipulation through cutting and modeling. as the geometry of the facial bones and skull is extremely complex and most of these defects primarily involve underlying bone structures, the application of this more advanced 3d printing technology has proven ideal. neurosurgical training surgical training is usually a multi-step process by which the trainee acquires knowledge and skills of practicing surgical procedures. thus, as the trainee gains skills, he will be able to progress to more complex steps and be given more autonomy. the effectiveness of this learning model can be influenced by the existence of the teaching material (most often represented by the availability of corpses), the number of cases and the interval of pathology related to a certain surgical unit. 3d printing offers solutions to bypass some of these problems and improve the internship experience. the trainees can practice and master the individual operative steps on the models before practicing with a real patient. this can improve learner confidence (especially in cases involving a difficult or unusual anatomy) and can help speed up the training timeline, as skill acquisition is achieved concomitantly with the actual operating experience of the patient. also, the use of 3d printed models in vocational training helps surgical educators standardize the acquisition of operator skills among trainees. 3d printing thus offers a number of advantages, which allow it to be a useful adjunct to existing surgical simulation methods, such as cadaveric dissection and virtual reality techniques [1,2,4,7,9]. figure 2: 3d printed models for vascular aneurysm and sphenoid wigs tumour intervention training. the main directions of neurosurgical pathology that have benefited from the advantages of 3d printing have been the provocative anatomy lesions, such as cerebral vascular malformations of the aneurysm or mav, brain tumors, and techniques such as ventricular or transnational endoscopy, which involve visualization constraints. one area where learning has generally been limited in the operating room is aneurysmal blinking. with the large-scale introduction of the treatment of aneurysms by coil embolization and the lack of cadaveric tissue, simulation-based training has become an absolute must in the strategy of vascular neurosurgery training. mashiko et al. using hollow elastic replicas of the different aneurysms from their vascular networks in a 3d printed model, they offered young neurosurgeons the opportunity to gain experience in selecting the appropriate clip, understanding the shape of the aneurysm and the direction of the clip [1,3,10]. similar to the field of vascular neurosurgery, the surgical training for excision of brain tumors has included the use of simulators based on anatomical models obtained by 3d printing (figure 2). thus, the use of 3d printers has allowed the development of simulators created from a multitude of materials with different consistencies and densities. this achievement contributed to the improvement of the simulation by replicating the handling characteristics of the different types of tissues [1,2,3,4]. it is very well known the absolute necessity of the surgical training in the case of spinal pathology, especially due to the multitude of types of implants proposed at present by the specialized companies. the continuous evolution of the spinal implants correlated with the development of the 420 a. chiriac, a. iencean, georgiana ion, et al. instrumentation specific to each type made the introduction of 3d printed models inevitable in this area. thus, the need for training for specialists in spinal neurosurgery aimed at acquiring the skills of use for various types of implants and instrumentation has greatly increased the use of these 3d printed models and due to the impossibility of access to such a large number of anatomical biological structures. figure 3: 3d printed models for a meningioma approach training. planning in neurosurgical pathology surgical intervention for intracranial aneurysm requires a complete and clear understanding of the complex 3d structure of the aneurysms and individual relationships with the carrier vessels and adjacent branches, in addition to accurate knowledge of the surrounding anatomical structures. despite the evolution of 3d imaging acquisitions and processing (3d-cta or 3d-dsa), the visualization and analysis of aneurysmal and mav lesions by neurosurgeons are paradoxically deprived of a flat-screen 2d computer, making depth interpretations difficult. with the advent of 3d printing, this approach has become a feasible option, which has allowed faithful 3d physical reproduction of the vascular networks of an individual patient [figure 1]. thus, these physical models that can be viewed from any angle and correctly appreciated dimensionally represent a potentially more advantageous method. studies in the literature comprising both qualitative and quantitative evaluations did not show significant dimensional differences between the imaging acquisitions and the printed model, proving the usefulness of using this printing technique. most of the discrepancies reported were the result of the residual support material from the lumen of the vessels. namba et al. reported for the first time the possibility of using these 3d printed models for endovascular planning (choosing the shape of the microcatheter and the coils occlusion). figure 4: 3d printed models for a calvarial tumour planning approach. surgical planning in the resection of brain tumours mainly involves the use of mri imaging. even with the advantages offered by this imaging technique, the relationships between the tumour formation and the 421 current applications of 3d printing in neurosurgery adjacent anatomical elements are difficult to appreciate especially in the case of infiltrative ones. 3d printing technology has allowed the translation of mri imaging data into patient-specific models that show the associations between tumour, skull, vascularisation and non-pathologic brain tissue [figure 4]. [5] moreover, the use of functional mri imaging allowed a much more precise surgical planning through a clear demarcation of the areas of eloquent cortex that needed to be avoided in microsurgical resection manoeuvres. large complex models of skull and brain tissue based on mri could also be used for surgical planning in the case of transnational or transventricular endoscopic approaches. in addition, these models can be used in the planning and development of new treatments for brain tumours such as noninvasive thermocoagulation [1,10]. the identification and understanding of the anatomy in the case of spinal fractures is a fundamental component for the surgical treatment. ct and mri imaging techniques, although, allow a good visualization of the anatomical elements or proved insufficient as regards the spinal interventional planning. this is reinforced by the development of intraoperative referral procedures used in spinal neurosurgery. numerous specialized studies have shown that 3d printed representations of these pathological situations at the spine level are extremely efficient in choosing fixation and prosthesis systems, but also in exercise in implanting them especially in the case of minimally invasive percutaneous interventions. thus, the detailed visual analysis of these 3d printed models allows a much clearer and more accurate dimensional and conformational assessment of the anatomical situation. this technique will allow neurosurgeons to establish some more precise dimensional parameters of the surgical implant insertion trajectory that can be transferred to the intraoperative guidance systems (figure 5). figure 5: 3d printed models for cervical spine planning approach. assisting in the consent process any medical procedure requires informed consent that involves a direct communication between the doctor, the patient and his family regarding the patient's condition, the treatment possibilities, along with its advantages and disadvantages, the consequences of the non-treatment, as well as the risks and complications of each form of therapy. [1,7]. statistical studies have shown that each step of informed consent can be better explained and understood through the use of a tangible object, in other words by materializing an abstract concept. figure 6: spine 3d printed model for assisting in the consent process. 422 a. chiriac, a. iencean, georgiana ion, et al. the use of 3d printed models proved to be very useful in the patient's consent procedure by considerably improving the discussions with them, due to the much clearer explanations of the proposed pathology and interventions. thus, physicians can use customized physical models with in situ pathology for each individual patient. the stages of the surgery as well as the possible specific complications are much better explained to the nonmedical staff through physical models. also, these 3d printed models help to better understand the disease and the results of the treatment, thus reducing the patient's uncertainty about the medical act, preventing complaints, discontents and accusations of malpractice (figure 6) [7,8]. medical education the use of 3d printed models has proven to be an extremely useful teaching tool for both students in the anatomy discipline, and surgical disciplines as well as for residents in the neurosurgery specialty. 3d printing techniques offer significant advantages in the process of medical education within the university and postgraduate programs, compared to the existing methods of anatomical modelling, which include cadaveric dissection, plastic models and plastinated corpus specimens. although traditionally medical education in the field of anatomy and surgery was provided primarily by cadaveric dissection, this learning mode was associated with difficulties related to the costs of setting up and maintaining an anatomical dissection laboratory, the existence of a sufficient number of bodies for educational programs, safety issues for students and staff, and last but not least ethical issues with the use of cadaveric material. figure 7: 3d printed models for student medical education [10]. the use of plastic models as an adjunct to cadaveric dissection to demonstrate certain organs or skeletal anatomy is limited by their lack of anatomical realism and the lack of representation of the variation or pathology specific to the patient. in contrast, 3d printing techniques allow the production of precise models characterized by a great variability and particular anatomical normality, but also pathological. unlike plastination, which presents the major disadvantage of the resources required to create anatomical models, 3d printing does not limit the amount of 3d printed models produced, depending on the number of original copies (figure 7). studies published in the literature have already shown improvements in the scores of anatomy tests of medical students after using 3d printing in the learning process. thus, 3d printed models offer viable solutions for the vast majority of the difficulties faced by educators using more traditional training methods [1,5,10]. conclusions the technique of 3d printing has undergone a remarkable development and use in the field of neurosurgery in the last decade. the possibility offered by this rapid prototyping technology provides a practical and anatomically precise means of producing patient‑specific and disease‑specific 423 current applications of 3d printing in neurosurgery models. besides applications already known in the fields of education and anatomical modelling, surgical planning, simulation and training, the creation of personalized implants for the treatment of various neurosurgical pathologies represents the real challenge of these technologies. thus, extending this technology in neurosurgery will serve both medical students and interventionist, but especially to patients. this study about 3d printing applications in neurosurgery is the subject of the grant: "new diagnostic and treatment methodologies: current challenges and technological solutions based on nanoparticles and biomaterials", that won the 2017 complex projects completed in consortia cdi, grant number: pn-iii-p1-1.2-pccdi-2017-0062, funded by cncs – uefiscdi romania. references 1. baskaran, v., štrkalj, g., štrkalj, m., & di ieva, a. (2016). current applications and future perspectives of the use of 3d printing in anatomical training and neurosurgery. frontiers in neuroanatomy, 10, 69. 2. klein, g. t., lu, y., & wang, m. y. (2013). 3d printing and neurosurgery--ready for prime time?. world neurosurgery, 80(3-4), 233-235. 3. ploch, c. c., mansi, c. s., jayamohan, j., & kuhl, e. (2016). using 3d printing to create personalized brain models for neurosurgical training and preoperative planning. world neurosurgery, 90, 668-674. 4. pucci, j. u., christophe, b. r., sisti, j. a., & connolly jr, e. s. (2017). three-dimensional printing: technologies, applications, and limitations in neurosurgery. biotechnology advances, 35(5), 521-529. 5. randazzo, m., pisapia, j. m., singh, n., & thawani, j. p. (2016). 3d printing in neurosurgery: a systematic review. surgical neurology international, 7(suppl 33), s801. 6. rybicki, f. j., & grant, g. t. (2017). 3d printing in medicine. cham: springer international publishing. 7. tevanov, l., liciu, e., chirila, m. o., dusca, a., & ulici, a. (2017). the use of 3d printing in improving patient-doctor relationship and malpractice prevention. rom j leg med, 25(3). 8. tomasello, f., conti, a., & la torre, d. (2016). 3d printing in neurosurgery. 9. vakharia, v. n., vakharia, n. n., & hill, c. s. (2016). review of 3-dimensional printing on cranial neurosurgery simulation training. world neurosurgery, 88, 188-198. 10. waran, v., narayanan, v., karrupiah, r., & cham, c. y. (2017). 3d printing in neurosurgery. in 3d printing in medicine (pp. 51-58). springer, cham. 11. https://anatomywarehouse.com/3d-printed-head-neckand-shoulder-with-angiosomes-a-105328. doi: 10.33962/roneuro-2021-034 a solitary case of gliosarcoma an indication for tp53 mutation analysis: a non-concordant finding. case report ebtesam abdulla, nabeel hameed, roopa arora romanian neurosurgery (2021) xxxv (2): pp. 210-214 doi: 10.33962/roneuro-2021-034 www.journals.lapub.co.uk/index.php/roneurosurgery a solitary case of gliosarcoma an indication for tp53 mutation analysis: a non-concordant finding. case report ebtesam abdulla1, nabeel hameed2, roopa arora3 1 b.med.sc, md, neurosurgery resident, department of neurosurgery, salmaniya medical complex, manama, bahrain 2 md, afsa, neurosurgery consultant, department of neurosurgery, salmaniya medical complex, manama, bahrain 3 mbbs, md pathology, histopathology consultant, department of anatomical pathology, manama, bahrain abstract background: li-fraumeni syndrome (lfs) is a hereditary, autosomal dominant malignancy predisposition induced by a mutant tp53. here, we describe a gliosarcoma (gs) case with a clinical family history impressive for an lfs case in the absence of inherited germline tp53 mutations. case description: we present a 44-year-old female with a right high parietal mass. the mass proved pathologically to be gs with an isocitrate dehydrogenase-1 (idh1) mutation. pedigree analysis identified five first-degree and second-degree relatives with lfs spectrum malignancies. the patient tested positive for tp53 mutation; however, her family tested negative. conclusion: of all the tumours, gss are the least described entity with lfs. we are highlighting the need to do a genetic survey in family members of the patient who has been diagnosed to have gliosarcoma and other tumours consistent with lfs. introduction gliosarcoma (gs) is an infrequent malignancy that is made up of glial and sarcomatous components (3). according to the who classification (2016), gs falls under the umbrella of isocitrate dehydrogenase (idh)wild type glioblastoma (gbm) (8). the distinction of primary gs is given to gs tumours that arise without the presence of previous gbm (3). despite being known for over a century, many aspects of gs remain illdefined (7) (13). the median age for gs patients at diagnosis ranges from 55 to 61 years (3) (7). gs has a male predominance and a predilection for the temporal lobe (7). currently, gs tumours are treated in accordance with stupp's trimodal regimen originally designed for gbm; the regimen entails the combination of maximum safe surgical resection, radiation therapy, plus concomitant and adjuvant temozolomide (16). despite the absence of solid evidence to support stupp's regimen for gs, several keywords gliosarcoma, idh-1 mutation, li-fraumeni syndrome, tp53 corresponding author: ebtesam abdulla department of neurosurgery, salmaniya medical complex, manama, bahrain dr.ebtesam@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 211 a solitary case of gliosarcoma an indication for tp53 mutation analysis studies have reported encouraging results (3) (4) (15) (17). even in the era of multimodality therapy, the prognosis of gs tumours remains grim, with the median survival ranging between 8.3 and 16.7 years (5-7) (17). factors impacting gs’s survival include age at presentation, the extent of surgical resection, and adjuvant radiotherapy (7). we aim to describe a case of gs with a clinical family history impressive for a lfs case; however, no inherited germline tp53 mutations have been detected. case description a previously asymptomatic 44-year-old female was introduced to our institution after experiencing a fall. she complained of progressive weakness of her left arm and leg over the course of one month, which had led to a worsening ability to walk and handle items (figure 1). she denied any other limb weakness or paraesthesia, speech or visual disturbances, nausea, vomiting, or headache. throughout this period, she also denied any episodes of seizures or alteration in mental status. figure 1. timeline showing the course of the patient during the follow-up and outcome. keys: op: operative; lll: left lower limb; rx: treatment. the patient was presented with left breast cancer with stage iii (at3n2m0) of invasive ductal carcinoma metastasized to the ipsilateral axillary lymph nodes, for which she had modified radical mastectomy and axillary clearance followed by adjuvant radiation therapy two years back. pathological evaluation was negative for oestrogen receptor, progesterone receptor, and human epidermal growth factor receptor-2 defined by immunohistochemistry and fluorescent in situ hybridization. on physical evaluation, she was grossly intact, aside from left-sided hemiparesis (grade ii medical research council) and left-sided deep tendons hyperreflexia. cranial magnetic resonance imaging (mri) (figure 2) verified the presence of a 3.4×3.3 cm right high parietal mass with surrounding hyperintensity on t2-weighted sequence, representing vasogenic oedema. postcontrast images revealed thick irregular peripheral enhancement with central hypointensity representing central necrosis. right frontoparietal craniotomy and brain tumour debulking with stereotactic computer-aided navigation was performed. histopathology (figure 3) revealed a high-grade glial neoplasm admixed with an area comprising of spindle-shaped cells arranged in fascicles. the glial area of the tumour was positive for glial fibrillary acidic protein (gfap) immune stain and showed poor reticular network. the spindleshaped area was negative for gfap and showed a rich reticular network. the specimen was immunoreactive for idh-1. based on the presence of both glial and sarcomatous areas in the tumour, a diagnosis of gs was established. the patient was offered genetic counseling; her family history revealed that her oldest sister was diagnosed with breast cancer at 39 years old (yo) and synovial sarcoma of the foot at 42 yo. her other sister was diagnosed with primary spinal osteosarcoma at 40 yo and breast cancer at 44 yo. among her maternal uncles, one developed leukaemia at 35 yo, and another one had lymphoma at 55 yo. her paternal uncle was diagnosed with lung cancer at 50 yo. based on the clinical family history in the context of gs, a diagnosis of lfs was highly suspected. genetic testing revealed a presence of a mutated tp53 in our patient with an absence of germline tp53 mutations in her family. the brca1, brca2, and pten mutations were not identified. postoperative mri (figure 4) showed 1.3×1cm residual tumour tissue, for which she received adjuvant temozolomide and radiotherapy. at the one-month follow-up, the patient endorsed focal jerky movements in her left leg. cranial computerized tomography (ct) scan revealed a further progression of the previously seen residual 212 ebtesam abdulla, nabeel hameed, roopa arora tumour tissue with significant midline shift and surrounding vasogenic oedema. surgical extirpation of the brain tumour was done. she had recovered from surgery with persistent left-sided hemiparesis and discharge on dexamethasone. one week later, she endorsed severe headaches and episodes of vomiting. a cranial ct scan (figure 5) revealed marked cerebral oedema. her family refused the decompressive craniectomy option. she was started on mannitol and dexamethasone. however, two-day after, she became unresponsive and developed a right fixed dilated pupil for which she had an emergency decompressive craniectomy. unfortunately, her clinical status progressively deteriorated till she expired. figure 2. brain mri demonstrates a right high parietal lesion with surrounding vasogenic oedema. the mass shows isointensity on the sagittal t1-weighted sequence (a), heterogeneous hyperintensity on the sagittal t2-weighted sequence(b), and thick irregular peripheral enhancement in the postcontrast t1-weighted sequence (c). figure 3. the histopathology revealed a brain tumour tissue comprising two cells types. area of neoplasmic glial cells depicting moderate nuclear pleomorphism and frequent mitosis (a) admixed with area comprising of spindle shaped cells arranged in fascicles (b). glial area of tumour was positive for gfap immunostain and showed a poor reticular network (c&d). spindle shaped area were negative for gfap and showed a rich reticulin network (e&f). 213 a solitary case of gliosarcoma an indication for tp53 mutation analysis figure 4. postoperative brain mri demonstrates a 2.8×1.7×2.7 cm fluid filled cystic cavity at the operative bed with 1×1.3cm peripherally irregular enhancing lesion at its anterior-inferior border suggestive of residual tumour tissue. figure 5. cranial ct scan revealed mark cerebral oedema. discussion lfs is an inherited autosomal dominant cancer predisposition triggered by a mutant tp53 (9). tp53 is a transcription factor located on chromosome 17 (17p13.1), which normally controls the cell cycle, genomic stability, and cell death (2) (14). accumulation of secondary mutations over and above the mutated tp53 attributes to the fact that lfs is characterized by unusual patterns of cancer incidence (11). the chompret criteria allows the clinical identification of lfs. the three clinical presentations are taken into consideration: 1. family presentation of lfs cancers such as breast cancer, soft tissue sarcoma, central nervous system cancer, adrenocortical carcinoma, leukaemia, and bronchoalveolar lung cancer under the age of 46 and one first or second degree relative with an lfs cancer under the age of 56. 2. multiple primary tumours related to the lfs spectrum with the first diagnosis before the age of 46. 3. rare cancers such as adrenocortical carcinoma or choroid plexus carcinoma irrespective of family history (1) (12). full-body mri is the currently used screening modality for lfs patients with high sensitivity and specificity in detecting various tumours (10). 18ffluorodeoxyglucose positron emission tomography and full-body ct scan as screening modalities are not recommended as they increase the risk of radiationinduced tumours (10). genetic testing and counseling should be offered to the lfs patient's family. using basic mendelian genetics, the probability of inheritance can be determined, assuming that the mutant allele is inherited in an autosomal dominant fashion. siblings of an affected patient have a 50% chance of having lfs. if neither parent has lfs, the mutation is assumed to be de novo, and the risk to siblings is lower. however, the risk to siblings is higher than the general population due to the possibility of germline mosaicism (10). in this specific instance, the clinical family history was impressive for a lfs case according to chompret criteria; however, no inherited tp53 alterations have been found except for the patient. we believe that this lack of an absolute phenotype-genotype concordance could be ascribed to other, as yet unidentified mutations involved in the pathogenesis of lfs. further genetic studies involved in cell growth regulation and proliferation may be efficient in deciphering such aggregations and addressing the genetic events involved in cancer predisposition in families suspected to have lfs. conclusion the description of this case highlights the importance of genetic family counseling of patients diagnosed to have gs and other tumors consistent with lfs. early identification of high-risk subjects will provide appropriate lifelong monitoring within clinical and psychological programs. importantly, sporadic cases should not be dismissed. references 1. durbin a, sonia n, adam s, david m. li-fraumeni syndrome. university of toronto medical journal. 2007;84. 214 ebtesam abdulla, nabeel hameed, roopa arora 2. fischer m, steiner l, engeland k. the transcription factor p53: not a repressor, solely an activator. cell cycle. 2014;13(19):3037-58. 3. frandsen s, broholm h, larsen va, grunnet k, møller s, poulsen hs, et al. clinical characteristics of gliosarcoma and outcomes from standardized treatment relative to conventional glioblastoma. frontiers in oncology. 2019;9(1425). 4. galanis e, buckner jc, dinapoli rp, scheithauer bw, jenkins rb, wang ch, et al. clinical outcome of gliosarcoma compared with glioblastoma multiforme: north central cancer treatment group results. j neurosurg. 1998;89(3):425-30. 5. han sj, yang i, tihan t, prados md, parsa at. primary gliosarcoma: key clinical and pathologic distinctions from glioblastoma with implications as a unique oncologic entity. j neurooncol. 2010;96(3):313-20. 6. kang s-h, park k-j, kim c-y, yu mo, park c-k, park s-h, et al. o6-methylguanine dna methyltransferase status determined by promoter methylation and immunohistochemistry in gliosarcoma and their clinical implications. j neurooncol. 2011;101(3):477-86. 7. kozak kr, mahadevan a, moody js. adult gliosarcoma: epidemiology, natural history, and factors associated with outcome. neuro oncol. 2009;11(2):183-91. 8. louis dn, perry a, reifenberger g, von deimling a, figarella-branger d, cavenee wk, et al. the 2016 world health organization classification of tumors of the central nervous system: a summary. acta neuropathol. 2016;131(6):803-20. 9. mai pl, malkin d, garber je, schiffman jd, weitzel jn, strong lc, et al. li-fraumeni syndrome: report of a clinical research workshop and creation of a research consortium. cancer genet. 2012;205(10):479-87. 10. paixao d, guimaraes md, de andrade kc, nobrega af, chojniak r, achatz mi. whole-body magnetic resonance imaging of li-fraumeni syndrome patients: observations from a two rounds screening of brazilian patients. cancer imaging. 2018;18. 11. pantziarka p. li fraumeni syndrome : a new hypothesis. oncology news. 2013;8:88-9. 12. penkert j, schmidt g, hofmann w, schubert s, schieck m, auber b, et al. breast cancer patients suggestive of lifraumeni syndrome: mutational spectrum, candidate genes, and unexplained heredity. breast cancer research. 2018;20. 13. salvati m, caroli e, raco a, giangaspero f, delfini r, ferrante l. gliosarcomas: analysis of 11 cases do two subtypes exist? j neurooncol. 2005;74(1):59-63. 14. shlien a, baskin b, achatz miw, stavropoulos dj, nichols ke, hudgins l, et al. a common molecular mechanism underlies two phenotypically distinct 17p13.1 microdeletion syndromes. am j hum genet. 2010;87(5):631-42. 15. smith dr, wu c-c, saadatmand hj, isaacson sr, cheng sk, sisti mb, et al. clinical and molecular characteristics of gliosarcoma and modern prognostic significance relative to conventional glioblastoma. j neurooncol. 2018;137(2):303-11. 16. stupp r, mason wp, van den bent mj, weller m, fisher b, taphoorn mjb, et al. radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. n engl j med. 2005;352(10):987-96. 17. walker gv, gilbert mr, prabhu ss, brown pd, mcaleer mf. temozolomide use in adult patients with gliosarcoma: an evolving clinical practice. j neurooncol. 2013;112(1):83-9. doi: 10.33962/roneuro-2021-019 ossified longitudinal ligament causing same level cord contusion in a case of klippel-feil syndrome amit agrawal romanian neurosurgery (2021) xxxv (1): pp. 114-116 doi: 10.33962/roneuro-2021-019 www.journals.lapub.co.uk/index.php/roneurosurgery ossified longitudinal ligament causing same level cord contusion in a case of klippel-feil syndrome amit agrawal professor of neurosurgery, department of neurosurgery, narayna medical college hospital, nellore, (ap), india abstract klippel-feil syndrome (kfs) is a congenital fusion of two or more cervical vertebrae due to faulty segmentation of the vertebral axis during gestation. (1-5) these patients present with a constellation of manifes­tations and are typically prone to cervical cord injury after a minor fall or a major traumatic episode. (2, 5-8) 34 years old gentlemen, a plumber by profession presented with a history of slipped and fall about two stairs height while he was working. letter to the editor dear sir, klippel-feil syndrome (kfs) is a congenital fusion of two or more cervical vertebrae due to faulty segmentation of the vertebral axis during gestation. (1-5) these patients present with a constellation of manifestations and are typically prone to cervical cord injury after a minor fall or a major traumatic episode. (2, 5-8) 34 years old gentlemen, a plumber by profession presented with history of slipped and fall about two stairs height while he was working. following that he had transient loss of consciousness when he regained the consciousness, he realized that he was not able to move his all four limbs. he also could not pass urine. there was no history of vomiting, ent bleed or convulsion. at the time of admission, he was conscious, oriented to time place and person. his general examination was normal. he had breathing difficulty and the respiration was of diaphragmatic type. chest wall expansion was absent. single breath count was 5. neurologically he was conscious, alert and oriented. cranial nerves were normal. motor system examination revealed quadriparesis with muscle power grade 3/5 in shoulders, 2/5 at elbow, 1/5 at wrist and absent grip in both upper limbs. all the deep tendon jerks were sluggish. the patient was catheterized as he was not able to pass urine. all the sensations were reduced below d8 level. bilateral planters were extensor. the gag and palate reflexes were normal. x-ray films of the keywords klippel-feil, cervical, spinal cord, cord contusion corresponding author: amit agrawal department of neurosurgery, narayna medical college hospital, nellore, (ap), india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 115 ossified longitudinal ligament causing same level cord contusion in a case of klippel-feil syndrome cervical spine showed fusion of the spinous processes of cervical vertebrae at c2 and c3 vertebrae with ossification of posterior longitudinal ligament at the same level (figure-1). magnetic resonance imaging (mri) of the cervical spine showed congenital fusion of the same vertebral spinous processes and in addition there was ossified posterior longitudinal ligament with canal stenosis and cord contusion (figure-2). the patient received injection methylprednisolone as per the standard protocol and planned for surgical decompression at the earliest. the patient underwent posterior approach and c2 and c3 laminectomy to relive the compression of the cord. the patient made gradual recovery. at follow-up the power in all four limbs was improved to grade 4/5. figure 1. a lateral x-rays of the cervical spine showing fusion of the spinous processes of c2-3 vertebral body, also note the ossified posterior longitudinal ligament bridging the posterior border of the c2-3 vertebral bodies. figure 2. mri cervical t1, t2 and flair sagittal images showing calcified posterior longitudinal ligament behind c2-3-disc space with cord compression and cord signal changes. in cases of klippel-feil syndrome fusion of one segment of the spinal column causes hypermobility of the non-fused adjoining segments thus cervical spine is unable to compensate for excessive flexion, extension, rotation and lateral bending and predisposing disc prolapse at adjacent levels and neurological deterioration following even minor trauma. (2, 4, 7-13) central cord syndrome typically described in the elderly patients with preexisting cervical spine spondylosis, only few reports discuss in patients with klippel-feil syndrome with cord compression at adjacent level. (9, 11, 14, 15) in contrary to many other cases where the patients with klippel-feil anomaly presented with adjacent level disc prolapsed and instability, the present case was unique as he developed spinal cord injury due to canal compromise at the level of used segment because of ossified posterior longitudinal ligament leading to canal stenosis. x-ray cervical spine is useful to understand the bony anomalies, however as in present case the mri will better delineate the normal as well pathological spinal cord anatomy including disc prolapsed and cord contusion. (6, 9) treatment regimens depend on the severity of symptoms and the segmental instability or cord compression and vary from modification of activities to extensive spinal surgery including microsurgical removal of the herniated disc with instrumentation. (6, 10, 16-19) however, in presented case the extensive ossification in the posterior ligament was cause of canal compromise and cord compression and, as there was no instability, we opted for posterior decompression alone. references 1. ulmer jl, elster ad, ginsberg le, williams dw, 3rd. klippel-feil syndrome: ct and mr of acquired and congenital abnormalities of cervical spine and cord. j comput assist tomogr. 1993 mar-apr;17(2):215-24. 2. guille jt, miller a, bowen jr, forlin e, caro pa. the natural history of klippel-feil syndrome: clinical, roentgenographic, and magnetic resonance imaging findings at adulthood. journal of pediatric orthopedics. 1995;15(5):617. 3. klippel m, feil a. un cas d’absence des vertebres cervicales. avec cage thoracique remontant jusqu’a la base du crane (cage thoracique cervicale). nouv iconog salpetriere. 1912;25:223-50. 4. vaidyanathan s, hughes pl, soni bm, singh g, sett p. klippel-feil syndrome the risk of cervical spinal cord injury: a case report. bmc fam pract. 2002 apr 11;3:6. 5. samartzis d, kalluri p, herman j, lubicky jp, shen fh. 116 amit agrawal superior odontoid migration in the klippel-feil patient. eur spine j. 2007 sep;16(9):1489-97. 6. agrawal a, badve am, swarnkar n, sarda k. disc prolapse and cord contusion in a case of klippel-feil syndrome following minor trauma. indian j orthop. 2009 apr;43(2):210-2. 7. karasick d, schweitzer me, vaccaro ar. the traumatized cervical spine in klippel-feil syndrome: imaging features. ajr am j roentgenol. 1998 jan;170(1):85-8. 8. pizzutillo pd, woods m, nicholson l, macewen gd. risk factors in klippel-feil syndrome. spine (phila pa 1976). 1994 sep 15;19(18):2110-6. 9. adeleye ao, akinyemi ro. cervical klippel-feil syndrome predisposing an elderly african man to central cord myelopathy following minor trauma. afr health sci. 2010 sep;10(3):302-4. 10. samartzis d, lubicky jp, herman j, kalluri p, shen fh. symptomatic cervical disc herniation in a pediatric klippel-feil patient: the risk of neural injury associated with extensive congenitally fused vertebrae and a hypermobile segment. spine (phila pa 1976). 2006 may 15;31(11):e335-8. 11. strax te, baran e. traumatic quadriplegia associated with klippel-feil syndrome: discussion and case reports. arch phys med rehabil. 1975 aug;56(8):363-5. 12. elster ad. quadriplegia after minor trauma in the klippelfeil syndrome. a case report and review of the literature. j bone joint surg am. 1984 dec;66(9):1473-4. 13. o'donnel dp, seupaul ra. klippel-feil syndrome. am j emerg med. 2008 feb;26(2):252 e1-2. 14. matsumoto k, wakahara k, sumi h, shimizu k. central cord syndrome in patients with klippel-feil syndrome resulting from winter sports: report of 3 cases. am j sports med. 2006 oct;34(10):1685-9. 15. shirasaki n, okada k, oka s. cervical myelopathy in patients with congenital cervical block vertebrae. eur spine j. 1993 jun;2(1):46-50. 16. tracy mr, dormans jp, kusumi k. klippel-feil syndrome: clinical features and current understanding of etiology. clin orthop relat res. 2004 jul(424):183-90. 17. neroni m, gazzeri r, galarza m, alfieri a. intradural cervical disc herniation in a klippel-feil patient. spine (phila pa 1976). 2007 oct 1;32(21):e608-10. 18. leung ch, ma wk, poon ws. bryan artificial cervical disc arthroplasty in a patient with klippel-feil syndrome. hong kong med j. 2007 oct;13(5):399-402. 19. yi s, kim sh, shin hc, kim kn, yoon dh. cervical arthroplasty in a patient with klippel-feil syndrome. acta neurochir (wien). 2007 aug;149(8):805-9; discussion 9. doi: 10.33962/roneuro-2022-012 primary intracranial malignant melanoma. a case report and review of literature deepak kumar singh, diwakar shankar, vipin chand, mohammad kaif romanian neurosurgery (2022) xxxvi (1): pp. 70-72 doi: 10.33962/roneuro-2022-012 www.journals.lapub.co.uk/index.php/roneurosurgery primary intracranial malignant melanoma. a case report and review of literature deepak kumar singh, diwakar shankar, vipin chand, mohammad kaif dr. ram manohar lohia institute of medical sciences, lucknow, india abstract primary intracranial malignant melanoma (pimm) is a very rare neoplasm and accounts for 1% of all melanomas and 0.1% of all intracranial tumours. it carries a poor prognosis with overall poor survival. diagnosis on mere imaging findings of an intracranial melanoma is a daunting task. multimodality treatment with surgery followed by chemotherapy and radiotherapy have proved to be effective in improving clinical outcome in these patients. introduction primary intracranial malignant melanoma (pimm) is a very rare neoplasm and accounts for 1% of all melanomas [5]. it accounts for 0.1% of all intracranial tumours [5]. pimms are derived from melanocytes that are normally present in the leptomeninges. it is more common in males and has a poor survival rate overall. pathologically it is of two types, diffuse type which infiltrates pia-mater and the subarachnoid space (sas); and the solitary type which is present as nodular mass. treatment of choice is complete resection followed by radiotherapy and chemotherapy. we here present a case of pimm in a 35-year-old male presenting with signs and symptoms of a left cerebellar hemisphere malignant melanoma with leptomeningeal spread. case discussion a 35-year-old male presented to our institute with a complaint of headache, decreased hearing in the left ear, difficulty in walking, and diminished vision bilaterally for the past 2 years. non-contrast computer tomography (ct) head revealed a hyperdense lesion in the left cerebellar hemisphere with associated perilesional edema (figure 1, a). contrast-enhanced mri brain revealed a 4.5cm x 5cm x 3.5cm homogenous mass lesion in the left cerebellar hemisphere which was hyperintense on t1 and hypointense on t2 with mass effect and perilesional edema (figure 1, b, c, d). radiographic features were suggestive of meningioma. no evidence of hemorrhage on the gre sequence was seen. keywords melanoma, primary intracranial malignant melanoma, pimm, intracranial melanoma case report, intracranial melanoma literature review corresponding author: diwakar shankar dr. ram manohar lohia institute of medical sciences, lucknow, india dev123diwakar@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 71 primary intracranial malignant melanoma the patient was taken for surgery and complete excision was done through the left retro-mastoid suboccipital approach. meningeal spread of the tumor was evident from the dark-colored dural after removal of the bone flap (figure 2, a). intraoperative observation revealed a firm, well-demarcated, highly vascular, dark brown, 5cm x 4cm sized lesion with dural attachment (figure 2, b, c). histopathological examination confirmed melanocytes on h and e stains. the tumor consisted of polygonal to spindle-shaped cells disposed of in sheets with abundant dark melanin pigment deposits in the cytoplasm. these cells stained positively with human melanin black-45 (hmb-45) antibody, s-100, and melan a. it was reported as malignant melanoma. the patient was evaluated for the alternative site of melanoma but no such sites were found. the postoperative period was uneventful and the patient was discharged on the tenth postoperative day. figure 1. preoperative ct non-contrast (ct) and contrastenhanced mri images. (a) ct images revealed a hyperdense lesion in the left cerebellar hemisphere with associated perilesional edema. (b) axial view, contrast-enhanced t1wi mri. (c) sagittal view, contrast-enhanced t1wi mri. (d) coronal view, contrast-enhanced t1wi mri. contrast-enhanced mri brain revealed a 4.5cm x 5cm x 3.5cm intra-axial heterogeneous mass lesion in the left cerebellar hemisphere which was hyperintense on t1 and hypointense on t2 with mass effect and perilesional edema. figure 2. intraoperative images showing gross total resection of the dark-colored lesion with leptomeningeal involvement and dural attachment. discussion primary intracranial malignant melanoma (pimm) is a very rare neoplasm and accounts for 1% of all melanomas [5]. it accounts for 0.1% of all intracranial tumors [5]. pimms are derived from melanocytes that are normally present in the leptomeninges. it is more common in males and has a poor survival rate overall [4]. in humans, melanocytes are found in skin, mucous membrane, uvea, etc. there are many theories for the origin of primary intracranial melanomas. the endodermal theory states that some aberrant embryonic ectodermal cells in the central nervous system produce melanin pigment. the neurogenic theory states that the neural crest gives rise to pigment cells. neural crest later develops into mesodermal and neural elements. the mesodermal theory proposes that the mesodermal pigment cells reach the central nervous system through pial vessels. hayward proposed a few features of a primary intracranial melanoma[3]. he suggested that for a pimm, there should be no malignant melanoma outside the cns, evidence of leptomeningeal involvement, hydrocephalus, intramedullary spinal lesions, tumor located in the pituitary, or pineal region, and a single intracerebral lesion. gibson et al divided intracranial melanomas into 72 deepak kumar singh, diwakar shankar, vipin chand, mohammad kaif two pathological types [1]. the diffuse type which infiltrates pia-mater and the subarachnoid space (sas); and the solitary (discrete) type which is present as nodular mass. the diffuse type was more prevalent in younger patients (mean age 26-years). it presented with clinical features of intracranial hypertension, cranial nerve deficit, or meningism. solitary type is more common in adults (mean age 44-years). most of the solitary tumors are supratentorial. leptomeningeal involvement is frequently seen in solitary melanoma. our patient has a solitary lesion. symptoms included headache, vomiting (especially due to raised intracranial pressure), hydrocephalus (43%), focal neurological deficit (due to mass effect, 35%), and convulsion or subarachnoid hemorrhage (16%). headache and focal neurological deficit were present in our case. intracranial hypertension and hydrocephalus are more commonly seen in diffuse types. the presence of congenital melanocytic nevus increases the risk of malignant melanoma. 25% of patients with primary intracranial melanomas have congenital nevus. this was not the case with our patient. extracranial metastasis of pimm is rare. it is difficult to differentiate primary central nervous system (cns) melanomas from metastatic melanomas based on imaging alone. melanin cells in cerebrospinal fluid (csf) analysis helps in the diagnosis. 86-97% melanocyte tumors are positive for hmb-45 antigen. other commonly used tumor markers are s100 and melan a. all three were positive in our patient. treatment of choice for the intraparenchymal melanocytic tumor is complete resection and postoperative chemoradiotherapy. survival in adults can be up to 17 years and 8 months in pediatric patients[2]. mean survival was found to be better (19.6 months) in patients in whom complete resection was done as compared with those where partial resection was done (9.3 months). also, the prognosis of secondary melanoma was poorer than pimm. there is 95% mortality in secondary intracranial melanomas. initially, radiotherapy (rt) was not offered to patients of pimm as melanomas were radioresistant tumors but recent studies showed that it was effective in controlling tumor growth. stereotactic radiosurgery (srs) along with whole-brain radiotherapy (wbrt) has been shown to reduce recurrence and improve survival. a high dose of 5000 centigray as srs in small lesions (size less than 3cm) gave better tumor control in almost 80% of cases. hydrocephalus caused by the leptomeningeal spread of the disease has been shown to respond well to wbrt. dacarbazine is commonly used in the treatment of pimms after surgery or radiotherapy. it has 1620% effectiveness. other agents are temozolomide and dimethyl-triazeno-imidazole-carboxamide which is common in use. despite optimum treatment, median survival is less than a year. the leptomeningeal spread has a median survival of 10 weeks. conclusion primary intracranial malignant melanoma (pimm) is a very rare neoplasm and accounts for 1% of all melanomas and 0.1% of all intracranial tumors. it carries a poor prognosis with overall poor survival. diagnosis on mere imaging findings of an intracranial melanoma is a daunting task. it is best diagnosed intraoperatively due to its characteristic appearance as well as during preoperative clinical examination. postoperative chemoradiotherapy plays an important role in preventing recurrence as well as improving overall survival. collaboration of large-scale data from many such small case series from centers all over the world can confirm findings suggested in this paper and formulate guidelines to improve clinical outcomes. references 1. gibson jb, burrows d, weir wp: primary melanoma of the meninges. j pathol bacteriol 74:419–438, 1957. 2. greco crasto s, soffietti r, bradac gb, et al. primitive cerebral melanoma: case report and review of the literature. surg neurol 2001;55:163–8. 3. hayward rd. malignant melanoma and the central nervous system. a guide for classification based on the clinical findings. j neurol neurosurg psychiatry 1976;39:526‑30. 4. ma y, gui q, lang s. intracranial malignant melanoma: a report of 7 cases. oncol lett 2015;10:2171–5. 5. sloan ae, nock cj, einstein db. diagnosis and treatment of melanoma brain metastasis: a literature review. cancer control. 2009;16:248e255. doi: 10.33962/roneuro-2022-048 notes on the history of walter edward dandy one of the outstanding fathers of neurosurgery maria paz bolaño-romero, angie juliana aguilar -ramírez, maría camila hernández -cañas, maría daniela gutiérrez -ortega, valentina gonzález-patiño, michael gregorio ortega-sierra, alfonso pacheco-hernández romanian neurosurgery (2022) xxxvi (3): pp. 279-288 doi: 10.33962/roneuro-2022-048 www.journals.lapub.co.uk/index.php/roneurosurgery notes on the history of walter edward dandy one of the outstanding fathers of neurosurgery maria paz bolaño-romero1,2, angie juliana aguilar-ramírez3, maría camila hernández-cañas3, maría daniela gutiérrez-ortega3, valentina gonzález-patiño4, michael gregorio ortega-sierra5, alfonso pacheco-hernández2 1 grupo prometheus y biomedicina aplicada a las ciencias clínicas, school of medicine, universidad de cartagena, cartagena, colombia 2 grupo colombiano de investigación clínica en neurointensivismo, consejo latinoamericano de neurointensivismo, cartagena, colombia 3 school of medicine, universidad autónoma de bucaramanga, bucaramanga, colombia 4 school of medicine, universidad tecnológica de pereira, pereira, colombia 5 department of neurosurgery, universidad centroccidental lisandro alvarado hospital central antonio maría pineda, barquisimeto, venezuela abstract walter dandy was born in 1886 in missouri into an immigrant family. from an early age, he stood out as a good and curious student, which led him to study initially at the university of missouri and later at the john hopkins school of medicine where he had the opportunity to develop his potential as a researcher in the hunterian surgical laboratory, under the tutelage of the prestigious dr harvey cushing. his contributions to medicine as a surgical resident and later neurosurgeon marked a before and after in the history of the modernization of neurosurgery and enriched the knowledge of the anatomical structures of the central nervous system, considering his discovery of ventriculography as "the greatest single contribution to brain surgery", also being the first to successfully perform various surgical procedures, such as the clipping of aneurysms and the resection of tumours of the cerebellopontine and hypophysial angle. introduction walter edward dandy was born on april 6, 1886 in sedalia, missouri as the only child of immigrants john and rachel dandy (1,2). throughout his life he served as a neurosurgeon and scientist, being considered one keywords biographies as topic, history, walter edward dandy, neurosurgery corresponding author: maria paz bolaño-romero grupo prometheus y biomedicina aplicada a las ciencias clínicas, school of medicine, universidad de cartagena, colombia mbolanor1@unicartagena.edu.co copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 280 maria paz bolaño-romero, angie juliana aguilar-ramírez, maría camila hernández-cañas et al. of the founders of neurosurgery and contributing innovative ideas in multiple fields of medicine, among which are ventriculography, the description of the circulation of cerebrospinal fluid, acoustic neurinomas, the function of the pituitary and pineal glands, pneumocephalus, méniére's disease, glossopharyngeal neuralgia, intraventricular tumors, intracranial aneurysms, ruptured intervertebral discs and neuroradiology. he was also credited with the title of "father of neuroendoscopy", which made him the most famous and influential neurosurgeon in the world for 25 years (2-7). dandy was associated with the john hopkins school of medicine, as it was the place where he obtained his medical training, and later with the hospital of the same name, entering as an intern and remaining there throughout his career as a surgeon, and was associated with other great neurosurgeons even before his graduation as a physician, such as harvey cushing, with whom the differences in personalities and ideas that led to their separation and rivalry throughout their careers were very clearly highlighted (1,8,9,10,11). the importance of his contributions to neurosurgery and medicine in general have allowed the evolution of neurosurgery to what is known today, for this reason it is of great importance to remember and commemorate his work. early age and medical training born and raised in sedalia, missouri in 1886, walter dandy was the only child of the marriage between john and rachel dandy, who were immigrants from england and ireland respectively, socialist supporters and ardent members of the religious sect called "plymouth brethren". john dandy, his father, immigrated with his wife to the united states two years before walter was born, in order to work in the railroad industry, where he worked initially as a fireman and later as a locomotive engineer on the missouri-kansas-texas railroad (1,2,12,13,14,15,16). as an only child, walter was instilled with competitiveness and excellence from a very early age, and established a strong and close relationship with his parents, who always supported his decisions and accompanied his greatest achievements, which is why dandy considered family relationships to be "the best thing in life (7,14,15). dandy's childhood was no different from that of other children, he played with his classmates and frequently had disputes with children much older than him (1). he inherited from his father a taste for trains and from a very young age he showed his fascination for baseball, achieving a balance between his studies and baseball games, so much so that one of his roommates referred to him as a "tough student and a tough player" (12,14,17). dandy attended public school in sedalia in a "1room schoolhouse" along with other immigrant children, from which he graduated in 1903 as the valedictorian of his class and was awarded the title of valedictorian, thus having the duty of giving the final valedictory address in which he spoke of the importance of education (1,2,7,14,15). encouraged by his teachers, he entered the university of missouri in 1903, where, motivated by his interest in learning biology and medicine, he did his laboratory work with winterton c. curtis, phd of johns hopkins university, as an assistant in his zoology laboratory at the university of missouri. this man motivated dandy to continue his medical training at the johns hopkins school of medicine (1,2,7,14,15). in 1907 dandy participated as a candidate for a rhodes scholarship to study at oxford, passing the exams and winning the scholarship. however, he turned it down because in communication with sir william osler, professor of medicine in england, he suggested that he finish medicine at hopkins and later do postgraduate studies abroad (1,2,7,14,16). in the same year, following the suggestions of osler and curtis, he entered the second year of medical school at hopkins, because they recognized part of what he had studied at the university of missouri, and it was not until 1910 that he received his degree from the john hopkins school of medicine (1,2,7,14,15,16). medical training while studying at johns hopkins school of medicine, walter dandy was strongly attracted to anatomy and went to work as a trainee in the laboratory of franklin p. mall, professor of anatomy at johns hopkins and founder of embryology, who upon seeing dandy's skills in drawing and dissection, assigned him as his work the representation of the youngest human embryo he preserved, this work of dandy was published shortly before finishing medical school and for which he was awarded a master's degree, the embryo is still known as the "dandy embryo" (2,14). 281 notes on the history of walter edward dandy after being awarded his medical degree in 1910, dandy was assigned by the famous surgeon dr. william halsted to begin his surgical training by doing research work under harvey cushing at the hunterian surgical laboratory, an experimental laboratory for surgical procedures on animals, because halsted was impressed by dandy's skills and relentless performance in his final year of medical school. a year after his assignment, walter moved up to become cushing's clinical assistant until 1916 (1,2,4,7,12,14,16,18). at the time of dandy's arrival at the hunterian laboratory, cushing was conducting research on the function of the pituitary gland and it is at this time that, guided by cushing, dandy made studies on the irrigation and innervation of the pituitary glands of animals such as dogs and cats, such work earned him his second and third publications, in company with emil goetsch "the blood supply of the pituitary body" in 1911 and alone "the nervous supply of the pituitary body" in 1913 (1,2,7,14). at the beginning of 1911, a great conflict began between the teacher harvey cushing and the trainee walter dandy, generated in the first instance by a controversy that was maintained in the results of a work that consisted in producing glucosuria by stimulation of the sympathetic nerves, in which dandy affirmed that the stimulation produced a great glycosuria, something that made cushing irritable, later dandy corrected that by inhibiting the sympathetic stimulation the glycosuria continued to be produced, so cushing commented "dandy, nobody could think of something like that, except you" (1,2). despite this altercation, dandy was appointed months later as cushing's clinical assistant, ensuring his tenure at the laboratory and interested in investigating hydrocephalus using canines for his experiments, however, the conflict developed a tense and discordant atmosphere between the master and his apprentice, which lasted until the end of cushing's life (1,12,14). in 1912, an assistant resident in pediatrics, kenneth d. blackfan, collaborated with dandy in his research on hydrocephalus, this work led in 1914 to excellent results where they showed the physiology of cerebrospinal fluid and classified hydrocephalus into two types: obstructive and communicating (1,4,7). in late 1912, dr. harvey cushing leaves johns hopkins hospital with the goal of going to boston to give the chair of surgery at harvard university. with this news, walter assumed that, like all the other clinical assistants, cushing would take him and he would have to move to harvard, however, cushing clearly stated that dandy would not be going with him (1,2,7,12). dandy was angered by cushing's manner and, even more so, by the fact that he had previously turned down the position to join dr. halsted's surgical staff at johns hopkins, so he thought his career was totally over (1,4,7). however, walter was rescued by the hospital administrator at the time, dr. winford smith, who provided him with a room to occupy while dr. halsted returned from a trip and could decide on his situation, who did not hesitate to reinstate dandy in his position as assistant resident in general surgery, after looking at his research on hydrocephalus (1,7). after his reinstatement in 1914, halstead encouraged him to investigate the pineal gland, and it was not until 1915 that he published the results of complete pinealectomies performed on dogs, with no effects on the physical well-being of the animals used (1). dandy continued to work as an intern and assistant resident until 1916, when he finally adopted the title of surgical resident, which he held for approximately two years, until 1918, when he was appointed general surgeon. from that time on, all neurological patients at johns hopkins hospital were attended by dr. dandy because of his great skill and surgical technique (1,2,7,14,18). in 1921 he was appointed associate professor of surgery at johns hopkins hospital and ten years later he was clinical professor of neurosurgery (14). until the year of his death, he devoted himself to establishing a neurosurgical residency program at the hospital as a continuation of the strong neurosurgical department that harvey cushing had left behind (18). clinical and scientific contributions ventriculography and neuroradiology among the many contributions made by dandy, the procedure called ventriculography (2) is considered to be the most important. his studies in this area began in 1916, in which, together with his associate george heuer md, he showed the usefulness of xrays for the diagnosis of pituitary tumors and calcified intracranial masses, such as aneurysms with calcification (4,7,18). however, this new finding was of no use to them because diagnosis of tumors by 282 maria paz bolaño-romero, angie juliana aguilar-ramírez, maría camila hernández-cañas et al. this means was late, so they agreed that another method for early detection of these intracranial entities was going to be necessary, and this method was likely to be more than plain radiography because the neurological lesions had densities similar to those of normal brain (4,7,18). subsequently, they had 3 cases of patients with non-calcified tumors that were visualized with x-rays because they were located inside the paranasal sinuses, they then noticed that it was possible to visualize them because they were delineated with air, which contrasted with the tumor tissue (4,7). from this originated the idea that it was going to be possible to locate tumors by x-ray if the ventricles were filled with exogenously administered materials, so dandy tested the injection of various radioopaque dyes into animals, in his words "various solutions and suspensions used in pyelography: thorium, potassium, iodide, collargol, argirol, bismuth subnitrate and subcarbonate", finding that this gave excellent delineation. unfortunately, however, he discovered that these substances were harmful to nerve tissue, as the animals that were injected always had fatal outcomes, producing "marked edema, serosanguinous exudate and petechial hemorrhages" (4,8,18,19,20). from this research dandy concluded that it was unlikely to find a substance that would be so harmless as to warrant injection into the nervous system, and that ventriculography might therefore be possible using only "the substitution of a gas for cerebrospinal fluid” (7,19). in 1917 dandy, having already heard from dr. halsted about the ability of intestinal gas to detail abdominal x-rays, had the opportunity to be in contact with a patient with an intestinal perforation and consequent pneumoperitoneum, who had an abdominal x-ray in which the separation of the liver and diaphragm by a collection of air was seen in detail (4,7,8,18). this finding was surprising to dandy, who published an article on this radiographic phenomenon ("pneumoperitoneum"), which had a major influence on his inventiveness and led him to suggest the injection of air into the ventricles, i.e., pneumoventriculography (18,21). to perform the procedure, a small hole was made in the calvaria, subjecting the patient to local anesthesia, then a needle was inserted into the lateral ventricle and cerebrospinal fluid was extracted, replacing the same volume that was extracted with air. once the air was injected, the patient was taken to the x-ray room and several frontal and lateral x-rays were taken (7,20). by 1919, dandy had already performed his innovative technique in several patients, being able to demonstrate not only intraventricular lesions, but also lesions of the cerebral subarachnoid spaces, as well as the localization of spinal tumors (7). thus, dandy was the first to perform pneumomyelography (22). acceptance of radiographic studies of the nervous system was slow and there were many conservatives who were slow to accept this new technique, and dr. harvey cushing disapproved of the procedure, commenting that he was reluctant to accept the new technique as he felt it might discourage neurosurgeons from training sufficiently and performing the thorough neurological examination, once again highlighting the rivalry between the two (7,18). however, dandy's introduction of pneumoventriculography, fluroscopy of the ventricles, air encephalography and pneumomyelography revolutionized the radiological diagnosis of diseases of the nervous system (4,19,20,22,23). hydrocephalus and cerebrospinal fluid drainage after graduating from john hopkins school of medicine in 1910, dandy dedicated himself to researching hydrocephalus, in this process he associated with dr. kenneth blackfan, pediatrician, who published in 1914 the first extensive study on the subject, from this and during the next 8 years approximately (1914-1922) published about 17 articles on this disease (1,24,25,26). in the initial study, he detailed for the first time the subtypes of hydrocephalus, classifying it as non-communicating (obstructive) and communicating, as well as proposed the surgical technique of removing the choroid plexus for the treatment of this type of hydrocephalus (24,27). dandy emphasized the etiology, objecting that although it could be idiopathic in nature, they recognized that the condition could be the result of blockage at several sites and it was this that they documented in their paper (24). as for the description of cerebrospinal fluid circulation, dandy was the first to do so in his research on hydrocephalus. he developed a study that he published with his associate, dr. blackfan, in 283 notes on the history of walter edward dandy december 1913, which was the first to describe the circulation and absorption of csf in noncommunicative hydrocephalus (24,27). this was achieved using canine models, to which he obstructed silvio's aqueduct and subsequently evaluated their behavior and the possible symptoms that appeared, observing lethargy and vomiting as the first symptoms. additionally, they observed the trajectory of the cerebrospinal fluid and its absorption when stained with phenolsulfonphthalein, a test used to verify whether the obstruction was in the aqueduct of sylvius or in the foramina of luschka and magendie, he was able to visualize a suspension of granules injected into the subarachnoid space that did not pass freely into the blood, and with this dandy became the first to observe that the problem was the lack of csf absorption in the lateral ventricles (1,2,24,25,27,28,29). as for treatment, dandy worked on surgical procedures based on three principles: reducing csf formation at its source, relieving the obstruction in the ventricular system and diverting the fluid to another location in the body where it can be absorbed or excreted. the first procedure for obstructive hydrocephalus was first observed on january 21, 1915, while for communicating hydrocephalus it was on february 6, 1918, three years later (2,24,25,27,29). in 1918 dandy published the technique of choroid plexectomy to communicate hydrocephalus, "based on simple, fundamental, physiological and surgical principles", this procedure involved the removal of the choroid plexuses of the lateral ventricles, the main site of csf formation (24,30). the surgery proposed by dandy was performed through a frontal approach, cutting a window in the anterior wall of the third ventricle, thus releasing retained csf directly into the ventricles while creating an opening for fluid into the chiasmatic cistern (25,26,30,31). by 1920, using ventriculography to determine the precise location of the obstruction, if found to be in the aqueduct of sylvius, dandy was forcing a small tube through the aqueduct to assist in reforming the canal, which would be removed two or three weeks later in a second operation (25,26,30,31). the striking feature of these early publications is the high mortality rate. there was more than 50% operative/immediate postoperative mortality, and few patients survived beyond a few months (24). neuroendoscopy another area of interest that dandy researched was neuroendoscopy, and he was extremely curious about how things could be improved, which is why he strove to improve the instruments available to neurosurgeons (5). by the 1920s, he began to try to use cystoscopes in his operations to remove the choroid plexus, noting that he could visualize the lateral ventricles, the foramen of monro, the choroid plexus and even vascular structures of the ventricle walls, results that greatly excited the researcher, giving rise to the concept of "ventriculoscopy" (5,32,33). then, in 1922, dandy attempted to replace his routine dilator with a cystoscope and a small ventriculoscope; however, the results of these early interventions fell short of his expectations because he was unable to properly remove the choroid plexuses using these tools, so he had to return to the standard nasal dilator and forceps. in the face of this disappointment, he stated that "the instruments, in their relatively primitive construction, were not completely adaptable" for use in a neurointervention (5,32,33). however, dandy continued his research by consulting gynecologist howard kelly, the "father of cystoscopy," for assistance, who lent him one of his small cystoscopes for use in intraventricular surgery (5). this tool proved to be superior to any he had used before, so, making certain modifications to the original, in 1923 he asked the wappler electric co. to help him design his reinvented version of the ventriculoscope (5,33). 10 years later, in 1932, the neurosurgeon had overcome the obstacles he had encountered in his first attempt with the ventriculoscope, and was able to perform choroid plexus resection surgeries with this instrument as routine procedures (5,33). two years later, tracy putnam adapted a urethroscope for endoscopic electrocautery and successfully removed the choroid plexus without resection, so dandy adopted putnam's use of coagulation instead of clipping in his own endoscopic choroid plexectomies, using a probe similar to putnam's that could pass through the endoscope (5). finally, dandy felt that neuroendoscopic procedures were limited by instrumentation and illumination, noting in his book surgery of the brain, published in 1945, that their usefulness was restricted to young children and infants, as well as for 284 maria paz bolaño-romero, angie juliana aguilar-ramírez, maría camila hernández-cañas et al. tumors found incidentally during plexectomies (5,33). aneurysms and neurovascular surgery dandy had a fascination with anomalies of the cerebral vascular tree, which is why this was one of his focuses (2). his research in this area began with his work with dr. heuer on the localization of intracranial tumors, as well as other research of the same era, such as frontotemporal craniotomy for optic chiasm lesions and pituitary tumors, which gave him the opportunity to visualize the cerebral vascular anatomy and provided him with the means he needed to approach and cut intracranial aneurysms (2,26,34). in 1928 he published an article dealing with venous anomalies and angiomas of the brain, and in the same year he recorded 8 cases of congenital arteriovenous aneurysms, and in 1929 he operated on middle cerebral aneurysms, but his first results were poor (2,35). dandy's first isolation of a carotid cavernous fistula resulted in 1934, proving a valuable treatment option for carotid ligation lesions and introducing his work on aneurysms of the circle of willis (2). he maintained that the only hope for the patient with an aneurysm would be treatment that would clip or trap the neck of the anomaly, so 3 years later, on march 23, 1937, he succeeded in applying a silver clip to an internal carotid aneurysm, a procedure he successfully completed, marking a milestone in neurosurgery (2,34,35,36,37). dandy's work on aneurysms ended in 1944 when he published his book entitled "intracranial arterial aneurysms" (34). other contributions we cannot overlook dandy's contributions to the physiology of the pituitary gland, as well as his research on the resection of its tumors. his research on animal models in which he resected the pituitary gland showed that these animals suffered from growth retardation and diabetes insipidus (2,14). dandy performed his first pituitary surgery on july 13, 1912, still during his residency and in the absence of dr. cushing, his mentor, and in his lifetime he performed four times as many pituitary surgeries as cushing, despite cushing being his predecessor (14). he was also the first to use a transcranial approach to this gland, with better results than the traditional approach (2,14). similarly, his contribution to the resection of vestibular schwannomas, following his discovery of ventriculography, which he used as a diagnostic method for these tumors; dandy thought to improve the technique described by cushing in order to reduce the mortality rate, so in 1922 he published a preliminary report on his first successful operation in which he obtained a total resection margin for this tumor, the case had occurred 5 years earlier (38,39). in this report, he described his new method of approach, by means of a bilateral suboccipital flap, first removing the inner portion of the growth, as described by cushing, but then meticulously cutting the veins and arteries surrounding the capsule, and finally separating the capsule carefully from the brainstem (38). however, dandy did not cite cushing's 1917 monograph on acoustic neurinomas, so the latter was offended and refused to accept the new technique (38,39). finally, in 1934 dandy described a more refined technique for the resection of tumors of the cerebellopontine angle with a less invasive unilateral unilateral suboccipital approach (38,40). and as well as these we can mention the resection of pineal gland tumors and their physiology, the resection of tumors of the orbit, his intervention in brain trauma by devising a helmet for baseball players to protect them from blows to the head by balls, herniated discs, douloureux tic and trigeminal neuralgia, tumors of the third ventricle and meniere's disease (1,2,11,17,28,41–46). personal life physically, dandy used to be described as a man a little short in stature, with large hands, small feet, a high-pitched voice and somewhat stocky, but as time went by, the one characteristic that people who interacted with him never forgot was his piercing blue eyes (1). his classmates in medical school remember him as a guy with remarkable skill and determination when it came to work, also commenting that dandy took very little time to spend with his friends on saturday nights (2). while in residency, in the operating room he was described as bold with very confident hand movements, in addition, he liked to maintain a very strict protocol that consisted in that only the resident could talk to him, in case the resident assistant or the intern had any concerns they should communicate first with the resident, this behavior of dandy could fluctuate 285 notes on the history of walter edward dandy depending on the situation, if everything went well he was very easy to work with, in case something went wrong he would yell or throw the surgical instruments (1,13,15). most of the time dandy appeared distant and cold, however, he was always kind to those doctors, residents, interns or patients who had financial problems, always with a great willingness to help them financially (1). dandy's daughter, kathleen louise, related that her father's personality could be confusing for many people, however, the secret was in understanding the personalities of walter dandy's parents. kathleen refers that he inherited the kindness and gentleness of his father, but at the same time the frankness and bad temper of his mother, therefore these opposite traits were in conflict and people usually ended up seeing only one side of the coin, but those who delved a little deeper could find the good side of his father (15). that loving side of walter dandy can be seen in his interaction with his family. he always proved to be a loving father, a good husband and son (13). his relationship with his parents was very close. throughout medical school and the years of his residency at hopkins hospital, he communicated weekly through letters, many of which recount dandy's rivalry with dr. harvey cushing (16). dandy said that most of his neurosurgeon colleagues did not like him and apparently he was very suspicious of harvey cushing, because besides cushing, walter had controversies with different surgeons such as charles frazier, temple fay and loyel davis (1). as a child, dandy was a big baseball fan and player, during his years at the university of missouri he would escape from his dorm to play night games, even while in residency with dr. cushing he managed to play three times a week, being so good that he became captain of the johns hopkins baseball team (17). dandy wrote to his parents, giving merit to baseball, saying that thanks to this game he was able to refine his surgical technique and his skill with his hands became much greater (17). in addition to baseball, dandy was attracted to trains, a taste instilled in him by his father since he was very young. in his spare time he would travel to new york by train to watch baseball games and on the way he would take advantage of the silence and comfort of the train to write his articles (15,17). in dandy's surgical career, one of his most significant early cases was related to the dangerous "beanballs", which consisted of a baseball player being hit in the head with a baseball, the patient suffering from a large cyst on the skull as a result of the traumatic impact, therefore, when dandy was asked thirty years later to work on a protective cover for baseball players' heads, he did not hesitate for a second to accept it, enthusiastic about his love of baseball and his professional attitude (15,17). marriage and family in 1923, walter was already known for his farreaching research in the field of neurosurgery and his position at the hospital was that of associate professor of surgery; that same year, days before an academic trip to europe to study with european doctors, dandy met sadie, a 22-year-old dietetic social worker from the same johns hopkins hospital, at the entrance of an elevator (1,15). sadie and her friends had already seen the hopkins surgeons play tennis on the hospital courts and considered walter a "good catch." some time later, sadie and walter began dating and meeting in places away from the hospital in order to avoid any kind of rumor (15). when walter dandy returned from his trip to europe, he and sadie were married and a year later they had their first child, walter jr.; later in 1927, a second child, mary ellen, was born; in 1928 kathleen louise and finally in 1935 the last daughter, margaret, was born (15). dandy's stress at work was reduced when he played baseball, tennis or golf, and sometimes his great passion for trains meant that he could only relax by sitting and watching the cars go by on the tracks at union station or by riding them and writing articles in his roomette, in order to be relaxed and away from the noise of the hospital (15,17). although he was a somewhat strict father, he never stopped being loving to his children, his home was a refuge in which he isolated himself from his busy work to live a home life with his children and wife (15). dinnertime at dandy's house consisted of the children being at the table by 6 p.m. to receive dinner promptly, properly cleaned and with good manners at mealtime. the topic of conversation was led by dandy, talking excitedly about some tumor removed from one of his surgeries of the day or how stressful neurosurgery can be for the patient's family members (15). after being listened to at dinner, walter always listened eagerly to his children's experiences throughout the day, which is why he was 286 maria paz bolaño-romero, angie juliana aguilar-ramírez, maría camila hernández-cañas et al. always remembered as a warm and playful father. he often invented games to amuse the children, for example, on certain occasions they would sit on the sofa and try to spit plum seeds into the fireplace (15). at the end of dinner, he would go into his room to change his clothes and the moment he would shake out his pants, coins would fall out of his pockets and the children would rush to pick them up and put them in their pockets. at other times he would simply lie down on the sofa and ask little mary ellen to lie in his arms for most of the night (15). in his home office, walter kept a photo of himself and another man in tennis clothes, however, sudie suggested to his children not to ask questions about the man in the photo and that they should only know that his name was harvey cushing (15). dandy often took walter jr. to the hospital to see him operate, perhaps these acts influenced the boy to follow in his father's footsteps, as he later became a great anesthesiologist (15). hobbies and pastimes dr. walter dandy spent his free time playing golf and bridge, most of the time with his family (47). also from a very young age he was taken by his father to play baseball, so he became a fan of this sport, so that after his studies, dr. dandy, identified a natural association between baseball and medical practice for the reduction of brain injuries related to the incline. this history further supports the unique position of neurosurgeons to leverage clinical knowledge, inform innovation, and expand service to society (48). many claim he was an expert in history and had a particular fascination with the american civil war (47). death in april 1946, dandy was with his young daughter margaret, in his backyard garden, when a pain in his chest caused him to stop the work he was doing, when dandy's doctor was called, he diagnosed a "heart attack", he recovered, went home and 17 days later could not resist a second event and died on april 18, 1946 at johns hopkins hospital (1,15). dandy walter's story demonstrates that research in surgery and neurosurgery quickly changed the management and prognosis of certain diseases, which naturally have a chaotic course and are fatal. today, these initiatives in the field of surgical sciences need to be highlighted in order to continue contributing to human development and the field of medicine (49-55). above all, the fact that this author began his career in research from the beginning of his career in medicine, enhancing his skills as a physician and resident (52,53,55); skills that must be replicated today, to advance rapidly in the problems that afflict global health. references 1. alper mg. three pioneers in the early history of neuroradiology: the snyder lecture. doc ophthalmol. 1999; 98(1):29–49. 2. campbell e. walter e. dandy-surgeon, 1886-1946. j neurosurg. 1951; 8(3):249-62. 3. long dm. a century of change in neurosurgery at johns hopkins: 1889-1989. j neurosurg. 1989; 71(5 i):635–8. 4. gutierrez c. the birth and growth of neuroradiology in the usa. neuroradiology. 1981; 21:227–37. 5. hsu w, li kw, bookland m, jallo gi. keyhole to the brain: walter dandy and neuroendoscopy historical vignette. j neurosurg pediatr. 2009; 3(5):439–42. 6. sherman ij, kretzer rm, tamargo rj. personal recollections of walter e. dandy and his brain team. j neurosurg. 2006; 105(3):487–93. 7. erik kilgore ae. walter dandy and the history of ventriculography. 1995; 194:657–60. 8. sampath p, long dm, brem h, yasui t. the hunterian neurosurgical laboratory: the first 100 years of neurosurgical research. neurosurgery. 2000; 46(1):184– 95. 9. woodhall b. walter dandy, m.d.: personal reminiscences. neurosurgery. 1979; 4(1):3-6. 10. tait j. the cushing-dandy conflict two powerful personalities that were best not to collide! world neurosurg. 2015; 83(1):11–2. 11. pearce jms. walter edward dandy (1886–1946). j med biogr. 2006; 14(3):127–8. 12. kelly pj. dandy of johns hopkins. mayo clin proc. 1985; 60(3):215–6. 13. olch pd. book reviews. journal of the history of medicine and allied sciences. 1985; 40(3):366-367. 14. corsello a, di dalmazi g, pani f, chalan p, salvatori r, caturegli p. walter e. dandy: his contributions to pituitary surgery in the context of the overall johns hopkins hospital experience. pituitary. 2017; 20(6):683–91. 15. dandy marmaduke me lle. walter dandy (1886-1946): a personal retrospective. neurosurgery. 2015; 77(4):501– 8. 16. patz md, laws er, thomas aj. the cushing-dandy conflict the dandy family perception of the discord. world neurosurg. 2015; 83(1):69–73 17. brewster r, bi wl, smith tr, gormley wb, dunn if, laws er. the neurosurgeon as baseball fan and inventor: walter dandy and the batter’s helmet. neurosurg focus. 2015; 39(1):e9. 287 notes on the history of walter edward dandy 18. da mota gomes m. from the wax cast of brain ventricles (1508-9) by leonardo da vinci to air cast ventriculography (1918) by walter e. dandy. rev neurol (paris). 2020; 1918:9–12. 19. dandy we. ventriculography following the injection of air into the cerebral ventricles. ann surg. 1918; 68(1):511. 20. dandy we. localization or elimination of cerebral tumors by ventriculography. surg gynecol obstet. 1920; 30:329-342. 21. dandy we. pneumoperitoneum: a method of detecting intestinal perforation-an aid in abdominal diagnosis. ann surg. 1919; 70(3):378-83. 22. dandy we. röntgenography of the brain after the injection of air into the spinal canal. ann surg. 1919; 70(4):397–403. 23. lutters b, koehler pj. cerebral pneumography and the 20th century localization of brain tumours. brain. 2018; 141(3):927–33. 24. rachel ra. surgical treatment of hydrocephalus: a historical perspective. pediatr neurosurg. 1999; 30(6):296–304. 25. dandy w, kenneth b. internal hydrocephalus an experimental, clincal and pathological study. am j dis child. 1914; 8:406–482. 26. dandy we, blacfan kd. internal hydrocephalus: second paper. am j dis child. 1917; 14(6):424–443 27. blitz am, ahmed ak, rigamonti d. founder of modern hydrocephalus diagnosis and therapy: walter dandy at the johns hopkins hospital. j neurosurg. 2019; 131(4):1046–51. 28. rizzoli h. dandy’s contributions to the foundation of neurological surgery. pediatr neurosurg. 1988; 13:316– 22. 29. walter e dandy kb. an experimental and clinical study of internal hydrocephalus. south med j. 1913; 6(12):791–4. 30. dandy we. extirpation of the choroid plexus of the lateral ventricles in communicating hydrocephalus. ann surg. 1918; 68(6):569-79. 31. davidoff lm. treatment of hydrocephalus: historical review and description of a new method. arch surg. 1929; 18(4):1737–1762. 32. demerdash a, rocque bg, johnston j, rozzelle cj, yalcin b, oskouian r, et al. endoscopic third ventriculostomy: a historical review. br j neurosurg. 2017; 31(1):28-32. 33. zada g, liu c, apuzzo mlj. “through the looking glass”: optical physics, issues, and the evolution of neuroendoscopy. world neurosurg. 2013; 79(s-2):s3–13. 34. kretzer rm, coon al, tamargo rj. walter e. dandy’s contributions to vascular neurosurgery: historical vignette. j neurosurg. 2010; 112(6):1182–91. 35. horwitz nh. walter edward dandy (1886-1946). neurosurgery. 1997; 40(1):211-5. 36. louw df, asfora wt, sutherland gr. a brief history of aneurysm clips. neurosurg focus. 2001; 11(2):1–4. 37. lai lt, o’neill ah. history, evolution, and continuing innovations of intracranial aneurysm surgery. world neurosurg. 2017; 102:673–81. 38. akard w, tubbs rs, seymour za, hitselberger we, cohengadol aa. evolution of techniques for the resection of vestibular schwannomas: from saving life to saving function historical vignette. j neurosurg. 2009; 110(4):642–7. 39. flamm e. new observations of the dandy-cushing controversy. neurosurgery. 1994; 35(4):737–40. 40. dandy we. removal of cerebellopontile (acoustic) tumors through a unilateral approach. arch surg. 1934; 29(3):337. 41. black pm, black ct. history of neurosurgery for intracranial mass lesions. neurosurg clin n am. 2001; 12(1):1-9, 42. pinkus rl. innovation in neurosurgery: walter dandy in his day. neurosurgery. 1984; 14(5):623-31. 43. weinstein js, burchiel kj. dandy’s disc. neurosurgery. 2009; 65(1):201–5. 44. cohen-gadol aa, geryk b, binder dk, tubbs rs. conquering the third ventricular chamber: historical vignette. j neurosurg. 2009; 111(3):590–9. 45. patel sk, liu jk. overview and history of trigeminal neuralgia. neurosurg clin n am. 2016; 27(3):265–76. 46. morone pj, dewan mc, zuckerman sl, tubbs rs, singer rj. craniometrics and ventricular access: a review of kocher’s, kaufman’s, paine’s, menovksy’s, tubbs’, keen’s, frazier’s, dandy’s, and sanchez’s points. oper neurosurg. 2019; 0(0):1–9. 47. bhattacharyya kb. walter edward dandy (1886-1946): the epitome of adroitness and dexterity in neurosurgery. neurol india 2018; 66:304-307 48. jusue-torres i, prabhu vc, jones ga. dandy's hemispherectomies: historical vignette. j neurosurg. 2021; online ahead of print. 49. pérez-fontalvo nm, de arco-aragón ma, jimenez-garcía jdc, lozada-martinez id. molecular and computational research in lowand middle-income countries: development is close at hand. j taibah univ med sci. 2021; 16(6):948-949. 50. lozada-martinez id, ortega-sierra mg, hernándezmorales ey, gonzales-méndez r, mejias-riverón k, argüello-manrique m, et al. letter to the editor. latin american collaboration in international neurotrauma registries: a strategy from the academy. j neurosurg. 2022 mar 11:1-2. 51. nuñez-gamez ja, medina-bravo pa, piñeros-lópez nf, contreras ga, rosero-burgos me, lozada-martínez id, et al. global outcomes, surgical teams and covid-19 pandemic: will the same objectives of global surgery persist? ann med surg (lond). 2021; 71:103002. 52. lozada-martinez id, carvajal-bautista j, picón-jaimes ya, dominguez-alvarado g, cabrera-vargas lf, torregrosaalmonacid l, et al. surgical research in colombia part 1: scientific and academic productivity of the colombian research groups in surgery. ann med surg (lond). 2022; 77:103667. 53. mass-hernández lm, acevedo-aguilar lm, lozada 288 maria paz bolaño-romero, angie juliana aguilar-ramírez, maría camila hernández-cañas et al. martínez id, osorio-agudelo ls, maya-betancourth jgem, paz-echeverry oa, et al. undergraduate research in medicine: a summary of the evidence on problems, solutions and outcomes. ann med surg (lond). 2022; 74:103280. 54. silva-rued ml, ramírez-romero a, guerra-maestre lr, forero-hollmann ám, lozada-martínez id. the need to develop specialized surgical centers: the evidence that surgical diseases cannot wait. int j surg. 2021; 92:106036. 55. llamas-nieves a, maiguel-lapeira j, lozada-martinez i, torres-llinas d, moscote-salazar l. the desire to publish a scientific article and the difficulties of publishing it in a high-quality neurosurgery scientific journal. j neurosurg sci. 2022; 66(2):163-164. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0065 article contralateral subdural haematoma as remote secondary lesion in head injury saurabh jain india      502 | saurabh jain contralateral subdural haematoma as remote secondary lesion in head injury             doi: 10.2478/romneu-2018-0065 contralateral subdural haematoma as remote secondary lesion in head injury saurabh jain department of neurosurgery, gbh american hospital, udaipur, rajasthan, india abstract: contalateral extra axial hemorrhage after cranial surgery is uncommon but known phenomenon. most of these hemorrhage are epidural (4) or intraparenchymal (6). the subdural being the rarest with only nine cases reported till date. we are presenting a case of development of contralateral subdural hematoma after decompressive craniectomy for traumatic sdh. introduction traumatic brain injury is a modern epidemic involving the most productive age group. the burden of traumatic brain injury (tbi), is significant in any society. the early intervention is required for better outcome. the tbi is usually limited to any one particular region when it comes to hematoma. early evacuation of hematoma (within four hours) usually associated with favorable outcome. remote secondary lesions are known as lesions which occur at site different than the primary site and spaced well in time. the remote secondary lesions are usually in the form of extradural hematoma or parenchymal contusions. (4, 6) here we are discussing the subdural hematoma as remote secondary lesions. case a 40 year old male brought by paramedics with road traffic accident with head injury. on examination he was unconscious, intubated, pulse 74/min, blood pressure 130/80 mm of hg with glasgow coma scale of e1vtm4. pupils were reacting 3mm bilaterally. on imaging the ncct (figure 1) is suggestive of left frontotemporoparietal subdural hematoma with mass effect and midline shift with diffuse cerebral edema. there are evidence of bilateral subarachnoid hemorrhage. in view of large subdural hematoma with mass effect, patient was subjected to immediate decompressive craniectomy with evacuation of subdural hematoma with lax duroplasty. patient kept ventilated in immediate postoperative period. romanian neurosurgery (2018) xxxii 3: 502 504 | 503             after about five hours patient developed bradycardia with hypertension. he was imaged by ncct scan (figure 2) which suggest craniotomy defect on left side with remote secondary lesion in the form of subdural hematoma in right side. there is midline shift of about 8 mm towards left side in contrast to 4 mm midline shift towards right in pre-operative scan. patient was immediately subjected to opposite side craniectomy with sdh evacuation and lax duroplasty. patient kept ventilated in post-operative period but the patient keep on deteriorating and succumbed after about three hours of second surgery. figure 1 figure 2 figure 3 figure 4 discussion remote secondary lesions are defined as lesions which are developed at a later stage of previous imaging at a site other than previous lesion. the most common lesion is being the parenchymal hemorrhage followed by extra dural hematoma subdural hematoma is the rarest. there are only nine case report are there in world english literature of sdh being the remote secondary lesion, (1-3, 5) we are presenting the tenth. 504 | saurabh jain contralateral subdural haematoma as remote secondary lesion in head injury             the exact cause of remote secondary lesion is not known but it is assumed that the remote secondary lesions are nothing but lesions under development of primary impact which left unrecognized due to its very small size in early imaging that increases later on. another hypothesis that is more relevant in post-operative cases is that decompression of one side causes the opening of small bleeders that were stopped due to compression of edematous brain. though the second hypothesis is more relevant in secondary edh wile the first is for sdh and parenchymal bleed. irrespective of theory of development of remote secondary lesion the lesion should be suspected in every patient and tackled earliest once detected. correspondence dr. saurabh jain drsaurabh_jain@rediffmail.com references 1. ban m, agawa m, fukami t: delayed evolution of posttraumatic contralateral extracerebral hematoma after evacuation of initial hematoma. neurol med chir (tokyo) 31:927-930, 1991 2. fridley j, thomas j, kitagawa r, chern j, omeis i: immediate development of a contralateral acute subdural hematoma following acute subdural hematoma evacuation. j clin neurosci 18:422-423, 2011 3. panourias ig, skandalakis pn: contralateral acute epidural haematoma following evacuation of a chronic subdural haematoma with burr-hole craniostomy and continuous closed system drainage: a rare complication. clin neurol neurosurg 108:396-399, 2006 4. matsuno a, katayama h, wada h, morikawa k, tanaka k, tanaka h, murakami m, fuke n, nagashima t: significance of consecutive bilateral surgeries for patients with acute subdural hematoma who develop contralateral acute epior subdural hematoma. surg neurol 60:23-30, 2003 5. panourias ig, skandalakis pn: contralateral acute epidural haematoma following evacuation of a chronic subdural haematoma with burr-hole craniostomy and continuous closed system drainage: a rare complication. clin neurol neurosurg 108:396-399, 2006 6. tomycz nd, germanwala av, walter ka: contralateral acute subdural hematoma after surgical evacuation of acute subdural hematoma. j trauma 68:e11-12, 2010 6. yonezawa k, kim s, tanaka m: acute epidural hematoma following evacuation of chronic subdural hematoma with continuous closed system drainage. neurol surg (tokyo) 20:1013-1016, 1992 doi: 10.33962/roneuro-2022-071 therapeutic advances in treatment of patients with neurofibromatosis type 1 and type 2. 7 years clinical experience of a single centre and literature review g. popescu, francesca paslaru, m.c. zaharia, m. popescu, r.m. gorgan romanian neurosurgery (2022) xxxvi (4): pp. 389-392 doi: 10.33962/roneuro-2022-071 www.journals.lapub.co.uk/index.php/roneurosurgery therapeutic advances in treatment of patients with neurofibromatosis type 1 and type 2. 7 years clinical experience of a single centre and literature review g. popescu1, francesca paslaru1, m.c. zaharia1, m. popescu3, r.m. gorgan1,2 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 professor. “carol davila” university of medicine and pharmacy, bucharest, romania 3 department of neurosurgery, pitesti emergency hospital, university of pitesti, romania abstract background: neurofibromatosis type 1 (nf1) and neurofibromatosis type 2 (nf2) are rare tumoral suppressor syndromes, triggered by an abnormal mutation in a tumour suppressor gene (tsg) (1). each of these syndromes represents an orphan disease (by itself), but the tumours encountered in these patients are the most frequent lesions of the nervous system. between the two of these diseases, nf1 presents a greater risk of malignancy, hence the importance of an accurate diagnosis and distinction between the two pathological entities. the purpose of this paper is to describe our department's practice protocol with neurofibromatosis and review the current literature regarding clinical diagnosis and management of these complex diseases. methods: our paper is a retrospective study that comprehends 25 patients with neurofibromatosis treated in our clinic between 2011 and 2018. results: our study included 16 female patients (64%) and 9 male patients (36%). the mean age at presentation was 48,7 (range 14-72 years). there were 7 cases (28%) of nf1 and 18 cases (72%) of nf2. seven cases (28%) had a positive family history and 18 patients did not (72%). the most common symptoms at presentation were hearing loss, vertigo, and headache. conclusions: neurofibromatosis is a very complex disease in which the tumours may have an unforeseeable growth pattern. new tumours can grow over the years and the symptoms are unpredictable. surgical treatment is best to be reserved for symptomatic tumours. non-surgical procedures are also an important step of the treatment, but further studies are required to decide their effectiveness. keywords neurofibromatosis, tumoral suppressor syndromes, lesions of the nervous system corresponding author: g. popescu 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 390 g. popescu, francesca paslaru, m.c. zaharia et al. background neurofibromatosis type 1 (nf1) and neurofibromatosis type 2 (nf2) are rare tumoral suppressor syndromes, triggered by an abdormal mutation in a tumor suppressor gene (tsg) (1). each of these syndromes represents an orphan disease (by itself) (2) (3), but the tumors encountered in these patients are most frequent lesions of the nervous system (1). between the two of these diseases, nf1 presents a greater risk of malignancy (4), hence the importance of an accurate diagnosis and distinction between the two pathological entities. the purpouse of this paper is to describe our department`s practice`s protocol with neurofibromatosis and review the current literature regarding clinical diagnosis and management of these complex diseases. materials and methods we performed a retrospective study that comprehends cases from 4th neurosurgical department of the “bagdasar-arseni” clinical emergency hospital. we retrospectively reviewed the charts of 25 patients with neurofibromatosis treated in our clinic between 2011 and 2018. we only included patients who fulfilled the known clinical indicators for of nf1 or nf2. eleven patients, who didn’t fulfill all the other criteria for nf1 or nf2, were therefore excluded from our study. results our study comprehends 16 female patients (64%) and nine male patients (36%). the average age at admission was 48,7 (range 14-72 years). the distribution of the patient sample based on the age group is shown in figure 1. there were 7 cases (28%) of nf1 and 18 cases (72%) of nf2. seven cases (28%) had a positive family history and 18 patients did not (72%). the most common symptoms at presentation were hearing loss, vertigo, and headache (figure 2). other signs and symptoms were seizures, lumbar pain, frontal lobe syndrome, or intracranial hypertension syndrome. figure 1. age groups distribution. figure 2. most frequent symptoms at diagnosis. in 6 cases (24%) gamma knife radiosurgery was chosen as the first treatment option. the distribution of the tumors based on their location is illustrated in fig. 3. figure 3. distribution of the tumours based on their location in the neuroaxis. the distribution of the patients based on whether they did, or did not, undergo surgical procedures is illustrated in fig. 4. figure 4. the distribution of the patients based on whether they did, or did not, undergo surgical procedures. case presentation we present you the case of a 14 years-old child diagnosed type ii neurofibromatosis was referred to our clinic with a 1-year history of cervical and brachial 24% 20% 56% 17-30 years 30-50 >50 distribution of the patients based on the age group 0 2 4 6 headache vertigo hearing loss most frequent symptoms at diagnosis 391 therapeutic advances in treatment of patients with neurofibromatosis type 1 and type 2 neuralgia, hypoesthesia, and mild weakness in her left hand, as well as numbness of the fingers and left foot hypoesthesia. her spinal cord function was evaluated to grade d on the frankel scale. neurological examination revealed an increased patellar reflex, no tricipital reflexes bilaterally, left ankle clonus, and bilateral positive babinski sign. other clinical signs were soft subcutaneous masses (neurofibromas) on the nose, frontal and temporoparietal regions and left hand, and also axillary and thoracal café-au-lait spots. cervical mri investigation revealed on the left side a massive gadolinium-enhancing extramedullary spinal tumor starting at the level of c6-c7 vertebrae, expanding into the mediastinum, displacing the vertebral artery. the tumor was also in contact with the left common carotid artery, without compression. it had a scalloping effect on the left lateral wall of the c6 and c7 vertebral bodies, entered the superior thoracic aperture and extended to the t2-t3 vertebral level (fig. 5). figure 5. gadolinium-enhanced cervical mri, coronal and sagittal section, showing a large extramedullary spinal tumor at the level of c6-c7 vertebrae. the patient underwent for first surgical intervention in order to excise the left medullary compressive portion of the tumor through posterior cervical approach. six weeks later, using an anterior cervical dartevelle approach, the extracapsular excision of the left laterocervical tumoral portion was performed. postoperative, the patient was in good medical state, without any neurological deficit. the third intervention took place 4 weeks after and the previous one. the extracapsular excision of the tumoral process located between the right thyroid lobe, the carotid artery and the transverse processes of c2-c5. for the vestibular schwannoma, gamma knife radiosurgery was the elective treatment. eventually, surgical excision of the subcutaneous neurofibromas was performed. two years later she was referred again to our clinic with complaints of dizziness, gait instability associated with visual dysfunction, more severely right side. the cerebral mri images revealed an expansive process of the sellar and parasellar region with temporal lobe extension (fig. 6). surgical intervention for total removal of the lesion was the therapeutic attitude opted by the patient. under general anesthesia, total removal of the lesion was performed, through a right pterional approach. the histopathological examination concluded a who grade ii meningioma. postoperative, the symptoms from the admission were improved, without dizziness or gait instability. visual dysfunction did not improve but the patient did not accuse the worsening of the visual dysfunction. figure 6. cerebral gadolinium-enhanced mri scan showing an expansive process of the sellar and parasellar region with temporal lobe extension. the patient was strictly followed-up for early detection of new brain tumors because of their unforeseeable growth pattern. the last follow up was in february 2018 and the cerebral ct scan did not revealed any new tumour or progression of the disease. discussion surgical resection represents the gold standard of treatment for plexiform neurofibromas, but the recurrence rates are significantly high (8). targeted therapies, such as anti-ras therapy, seem to have promising effects (9) (10). in 2020, usa food and drug administration has approved the use of selumetinib for treating inoperable plexiform 392 g. popescu, francesca paslaru, m.c. zaharia et al. neurofibromas in pediatric nf1 patients (11). regarding treatment strategies for nf2 patients, currently there is no consensus on the effectiveness of different approaches, because of the high regrowth rate after resection (12). surgical resection is usually guided by the clinical symptoms and the approachability of the lesion. a close clinical and imagistic follow-up is necessary in both nf1 and nf2 syndromes. conclusion neurofibromatosis is a very complex disease in which the tumors may have an unforeseeable growth pattern. new tumors can grow over the years and the symptoms are unpredictable. surgical treatment is best to be reserved for symptomatic tumors. non-surgical procedures are also an important step of the treatment, but further studies are needed in order to determine their effectiveness. references 1. therapeutic advances for the tumors associated with neurofibromatosis type 1, type 2, and schwannomatosis. blakeley jo, plotkin sr. 5, 2016, neuro oncol., vol. 18, pp. 624-38. 2. von recklinghausen neurofibromatosis. a clinical and population study in south-east wales. huson sm, harper ps, compston da. 6, s.l. : brain., 1988, vol. 111, pp. 1355581. 3. incidence of vestibular schwannoma and neurofibromatosis 2 in the north west of england over a 10-year period: higher incidence than previously thought. evans dg, moran a, king a, saeed s, gurusinghe n, ramsden r. 1, s.l. : otol neurotol., 2005, vol. 26, pp. 93-7. 4. distinctive cancer associations in patients with neurofibromatosis type 1. uusitalo e, rantanen m, kallionpää ra, pöyhönen m, leppävirta j, ylä-outinen h, riccardi vm, pukkala e, pitkäniemi j, peltonen s, peltonen j. 17, s.l. : j clin oncol., 2016, vol. 34, pp. 1978-86. 5. the diagnostic evaluation and multidisciplinary management of neurofibromatosis 1 and neurofibromatosis 2. gutmann dh, aylsworth a, carey jc, korf b, marks j, pyeritz re, rubenstein a, viskochil d. 1, s.l. : jama., 1997, vol. 278, pp. 51-7. 6. national institutes of health consensus development conference statement: neurofibromatosis. bethesda, md., usa : s.n., 1987. 7. the diagnosis and management of neurofibromatosis type 1. ly ki, blakeley jo. 6, s.l. : med clin north am., 2019, vol. 103, pp. 1035-1054. 8. current understanding of neurofibromatosis type 1, 2, and schwannomatosis. r., tamura. 22, s.l. : int j mol sci., 2021, vol. 29, p. 5850. 9. malignant peripheral nerve sheath tumour (mpnst): the clinical implications of cellular signalling pathways. katz d, lazar a, lev d. s.l. : expert rev mol med., 2009, vol. 11. 10. neurofibromin: a general outlook. trovó-marqui ab, tajara eh. 1, s.l. : clin genet., 2006, vol. 70, pp. 1-13. 11. selumetinib: the first ever approved drug for neurofibromatosis-1 related inoperable plexiform neurofibroma. mukhopadhyay s, maitra a, choudhury s. 5, s.l. : curr med res opin., 2021, vol. 37, pp. 789-794. 12. management of the patient and family with neurofibromatosis 2: a consensus conference statement. evans dg, baser me, o'reilly b, rowe j, gleeson m, saeed s, king a, huson sm, kerr r, thomas n, irving r, macfarlane r, ferner r, mcleod r, moffat d, ramsden r. 1, s.l. : br j neurosurg., 2005, vol. 19. doi: 10.33962/roneuro-2022-007 spontaneous acute spinal subdural hematoma in patient on oral anticoagulant therapy. a rare case report svetlana kocić, vuk aleksić, milenko stanić, aleksandra živković, radiša vojinović, igor popović romanian neurosurgery (2022) xxxvi (1): pp. 39-42 doi: 10.33962/roneuro-2022-007 www.journals.lapub.co.uk/index.php/roneurosurgery spontaneous acute spinal subdural hematoma in patient on oral anticoagulant therapy. a rare case report svetlana kocić1, vuk aleksić2, milenko stanić2, aleksandra živković3, radiša vojinović4, igor popović2 1 department of radiology, clinical hospital center zemun, belgrade, serbia 2 department of neurosurgery, clinical hospital center zemun, belgrade, serbia 3 department of anaesthesiology, clinical hospital center zemun, belgrade, serbia 4 department of radiology, clinical center of kragujevac, kragujevac, serbia abstract introduction: spontaneous spinal subdural hematoma as a result of coagulation deficit is a very rare and serious condition, with an overall incidence of less than 1%. symptoms can vary according to the level of the bleed. prompt recognition of the presence of spinal subdural hematoma is crucial for treatment. mri is the investigation of choice for diagnosis as well as for planning the surgery. the differential diagnosis includes abscess, lipomatosis, significant discal hernia and tumours. there are no definite guidelines for the management of spinal subdural hematomas. in cases with serious neurological deficits, prompt surgical evacuation may lead to the resolution of symptoms and complete neurological recovery. case report: we present a case of a 75-years-old man with bilateral lower limb radiculopathy, paresthesias, and spinal claudications for four days, progressing to bilateral paraplegia with urine incontinency. the patient was diagnosed with cauda equina syndrome due to spontaneous spinal subdural hematoma in the region from th12 to l2. he was immediately operated and the subdural hematoma was evacuated. minimal recovery was achieved and the patient was referred for further rehabilitation with severe paraparesis and urine incontinence. conclusion: early diagnosis of spinal subdural hematoma is essential for treatment. any delay of correct diagnosis can lead to a devastating neurological deficit. spontaneous spinal subdural hematoma is one of the rare conditions where an emergency mri is indicated and crucial for diagnosis. introduction spinal subdural hematoma (ssdh) is exceedingly uncommon condition with incidence lower than 1%. even rarer finding is spontaneous ssdh. spinal subdural hematomas are usually associated with trauma, keywords spinal subdural hematoma, spontaneous spinal subdural hematoma, magnetic resonance imaging corresponding author: vuk aleksić department of neurosurgery, clinical hospital center zemun, serbia aleksicvuk@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 40 svetlana kocić, vuk aleksić, milenko stanić et al. lumbar puncture, anticoagulant therapy (cause of spontaneous ssdh) or spinal surgery. the prevalence of subdural hematoma in the thoracic and lumbar region as a result of coagulation deficit is a rare cause of spinal cord compression. symptoms can vary according to the level of the hematoma including pain, lower limb weakness, radiculopathy, paresthesias, paraplegia, and urine incontinency. prompt recognition of the presence of ssdh is essential for successful treatment (1, 2). mri is the diagnostic modality of choice for diagnosis as well as for planning the surgical procedure. the differential diagnosis includes severe discus hernia, lipomatosis, abscess, and tumors (1). we present the case of 75-years-old man with bilateral lower limb radiculopathy and paresthesias lasting for four days and progressing to cauda equina syndrome due to spontaneous subdural hematoma at thoracolumbar junction level. case report a 75-years-old man presented with progressive bilateral lower limb radiculopathy, paresthesias and lower back pain progressing to paraplegia and urine incontinency in 4 days, after which he was admitted to our institution with complete cauda equina syndrome. there was no history of trauma. however, the patient had aortic valve prosthesis inserted 5 years prior to admission to our institution and was on anticoagulant therapy (figure 1). his initial international normalized ratio (inr) was 6.020. an initial thoraco-lumbar computed tomography (ct) was performed in another institution two days after the onset of symptoms, and except for l1 vertebral body compression fracture without signs of dislocation, no other pathological finding was described (figure 2). after neurological deterioration to cauda equina syndrome, patient was referred to our institution. upon admission mri of thoracolumbar junction as well as lumbosacral spine was performed and revealed a subdural lesion at the thoraco-lumbar junction level which was hyperintense on t1w imaging and hypointense to spinal cord on t2w image. the stir sequence showed hyperintensity to spinal cord, so presumptive diagnosis of subdural hematoma was made (figure 3). patient was immediately operated and th12, l1 and l2 laminectomies were performed. the underlining dura was blue, tense, and without pulsations. upon opening the dura with linear incision semi-liquid, dark blood clot came out under high pressure (figure 4). the subdural space was irrigated after which flow of liquor was obtained. the dura was sutured watertight and the operation was finished in usual fashion. postoperatively the patient was painless with minimal improvement of lower extremities strength. no improvement of urine incontinence was obtained. patient was referred for further rehabilitation 7 days after the operation. unfortunately, no significant improvement was achieved 2 months after the operation. figure 1. chest x ray showing condition after heart valve replacement as indirect evidence that the patient is on anticoagulant therapy (arrow is pointing at artificial heart valve). figure 2. spine ct scan. arrow is pointing at l1 vertebral body compression fracture without signs of dislocation. no other pathological finding was found. 41 spontaneous acute spinal subdural hematoma in patient on oral anticoagulant therapy figure 3. spine mri perofrmed 4 days after the onset of symptoms. (a) sagittal t1w image showing th12-l2 isointense subdural hematoma; (b) sagittal t2w image showing th12-l2 hyperintense subdural hematoma; (c) sagittal stir sequence showing hyperintense signal of ssdh; (d) axial t2w showing the “y” shaped sign of the ssdh at the level of l1; (e) axial t2w showing ssdh at the level th12 causing absolute spinal stenosis. figure 4. intraoperative finding of ssdh discussion ssdh is a rare condition, and most often these hematomas are associated with trauma, lumbar puncture or spine surgery (1). spontaneous ssdh is exceedingly uncommon finding. de beer et al. give classification of ssdh into: (1) posttraumatic, (2) iatrogenic (following spinal surgery or lumbar puncture), and (3) spontaneous (associated with underlying vascular malformations or coagulation deficits) (3). we presented a case of spontaneous ssdh due to coagulation deficit with inr 6.020, since the patient was on anticoagulant therapy because of heart valve replacement. clinical presentation of spinal subdural hematoma is not specific (1). severe back pain with a radicular component is often the first complaint. the pain followed by the development of weakness and numbness progressing to a complete sensorimotor paraplegia over a few hours to days is typical clinical finding since most of ssdh are located in thoracic or lumbar region (3). according to study of dampeer, spontaneous ssdh are most often located in the thoracic region and presenting with paraparesis or paraplegia, sensory level and pain, and more than 40% are due to coagulation deficit (3, 4). in our case patient had typical clinical picture for lesion located in thoraco-lumbar junction level (th12-l2) with complete cauda equina syndrome. mri is the imaging modality of choice for diagnosis ssdh. the most important factor to distinguish ssdh from other spinal lesions is identification of blood products on mri. also, mri gives better visualization of the longitudinal extent and size of the hematoma. subdural hematoma can be divided into hyperacute, acute and chronic. the hyperacute bleed is iso/hypointense on t1w sequence and hyperintense on t2w sequence. the acute hematoma is hypo-/isointense on t1w images and hypointense on t2w images. in early subacute hematoma the t1w image is hyperintense and hypointense on t2w images. the late subacute hematoma is hyperintense on tland t2weighted images. the chronic hematoma is usually hypointense on t1w and t2w images (5, 6). our patient had acute ssdh from th12 to l2 spinal segment. ct is the workhorse for emergency cases and is usually done before. unfortunately, ssdh can easily be missed in the acute setting. after having identified a subdural hematoma on mri, it is good practice to revise the ct scan in an attempt to identify the ssdh (7). in our case initial ct scan was performed in another institution, and except for l1 42 svetlana kocić, vuk aleksić, milenko stanić et al. vertebral body compression fracture, no other pathological finding was described. we revised ct scan after obtaining mri finding that was suggestive of ssdh, however, no consensus has been reached among 9 neurosurgeons in our department. ssdh is one of the rare conditions where emergency mri is indicated and crucial for diagnosis. it is important to distinguish between ssdh and other spinal subdural space occupying lesions such as empyema, hygroma, lipomatosis, tumors, and arachnoiditis. the “y” shaped sign we noted, is similar to the “inverted mercedes benz” sign described by kasliwal et al. this sign is a result of the encasement of blood around arachnoid lined neural structure. this helps to differentiate between an epidural and subdural location of the hematoma (8). there are no definite guidelines for management ssdh. the location and symptoms are the most important factors for treatment decision. treatment involves conservative management in cases with preserved neurology or laminectomy and drainage in cases with serious neurological deficit. cervical and thoracic ssdh mostly require surgical treatment, while ssdh below the conus medullaris can be treated conservatively. in general ssdh at the cervical or thoracic level are associated with poor outcome. apart from the location, the duration of symptoms is one of important prognostic factors (9). in cases of spontaneous ssdh due to coagulation deficit, anticoagulant therapy should be stopped immediately (10). our patient had complete cauda equina syndrome, so laminectomy and evacuation of ssdh was performed immediately after obtaining the diagnosis with mri. however, due to long duration of symptoms, functional recovery was minimal. in our case we can modify famous neurological maxima “the time is brain” into “the time is spine”. conclusion early diagnosis of ssdh is essential for treatment. so, in patients with cauda equina syndrome and severe back pain, and especially if there is information and evidence of anticoagulant therapy, spine mri should be performed. if ssdh is confirmed in patient with any neurological deficit we suggest prompt surgical decompression and hematoma evacuation, although there are no definite guidelines for management ssdh and personalized medical approach is always reasonable. patient’s clinical symptoms, the location of the ssdh, the amount of spinal canal narrowing, and duration of symptoms are the most important factors which should be taken into account when choosing the most appropriate treatment. references 1. braun p, kazmi k, nogués-meléndez p, mas-estellés f, aparici-robles f. mri findings in spinal subdural and epidural hematomas. eur j radiol. 2007;64(1):119–25. 2. schwartz ft, sarrawi ma, fox jl. unusual hematomas outside the spinal cord. report of two cases.j neurosurg. 1973;39:249–245. 3. de beer mh, eysink smeets mm, koppen h. spontaneous spinal subdural hematoma. neurologist. 2017;22(1):3439. 4. dampeer ra. spontaneous spinal subdural hematoma: case study. am j crit care. 2010;19(2):191-193. 5. mattle h, sieb jp, rohner m, mumenthaler m. nontraumatic spinal epidural and subdural hematomas. neurology. 1987;37(8):1351-1356. 6. konitsiotis s, glantzouni a, argyropoulou mi, tsapoga t, elisaf m, efremidis sc. acute spontaneous spinal subdural haematomas in a patient with essential thrombocythaemia. j neurol. 2003;250(9):1109-1111. 7. pierce jl, donahue jh, nacey nc, quirk cr, perry mt, faulconer n, falkowski ga, maldonado md, shaeffer ca, shen fh. spinal hematomas: what a radiologist needs to know. radiographics. 2018;38(5):1516-1535. 8. kasliwal mk, shannon lr, o'toole je, byrne rw. inverted mercedes benz sign in lumbar spinal subdural hematoma. the journal of emergency medicine. 2014;47(6):692-693. 9. thiex r, thron a, gilsbach jm, rohde v. functional outcome after surgical treatment of spontaneous and nonspontaneous spinal subdural hematomas. j neurosurg spine. 2005;3(1):12–16. 10. toledo e, shalit mn, segal r. spinal subdural hematoma associated with anticoagulant therapy in a patient with spinal meningioma. neurosurgery. 1981;8(5):600-603. doi: 10.33962/roneuro-2020-056 the efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury yasar karatas, mehmet fatih erdi, bulent kaya, fatih keskin, i̇brahim kılınç, mehmet uyar, sabiha serpil kalkan, emir kaan izci, erdal kalkan romanian neurosurgery (2020) xxxiv (2): pp. 254-260 doi: 10.33962/roneuro-2020-056 www.journals.lapub.co.uk/index.php/roneurosurgery the efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury yasar karatas1, mehmet fatih erdi2, bulent kaya1, fatih keskin2, i̇brahim kılınç2, mehmet uyar2, sabiha serpil kalkan2, emir kaan izci3, erdal kalkan1 1 medova hospital, konya, turkey 2 necmettin erbakan university, meram medical faculty, konya, turkey 3 meram training and research hospital, department of neurosurgery, turkey abstract objective: paraplegia is a dangerous complication of thoracoabdominal aortic surgery. various studies have been conducted on the prevention of this complication and some spinal cord protection methods have been proposed. however, there is not any modality that prevent the development of paraplegia certainly. in the i / r period, primary injury triggers secondary injury due to increased inflammation, apoptosis and free radical formation. in this study, we evaluated that the neuroprotective effect of adalimumab in spinal cord ischemia-reperfusion injury. materials and methods: in total, 24 adult new zealand rabbits were divided into three groups: group 1, control; group 2, ischemia-reperfusion by infrarenal aortic clamping; group 3, adalimumab treated followed by ischemia. tissue and plasma tumor necrosis factor alpha, interleukin 6, interleukin 10, thiobarbituric acid reactive substance, total oxidant status and total antioxidant status levels were analyzed as a marker of inflammation and oxidation. histopathological evaluation of the tissues was performed, and apoptosis was evaluated by tunnel method. results: i/r injury significantly increases plasma and spinal cord tissue at tnf alpha, tos, tbars, il6 levels and reduces plasma and spinal cord tissue to tas and il10 levels. adalimumab treatment significantly reduces plasma and spinal cord tissue to tnf alpha, tos, tbars, il6 and increases plasma and tissue to tas and il10 levels. conclusion: adalimumab treatment significantly reduces the spinal cord neuronal damage score and the number of apoptotic cells. this paper aims to demonstrate the important neuroprotective effects of adalimumab on rabbit spinal cord i/r injury. 1. introduction spinal cord reperfusion injury is described as cell death of neurons although improvement of blood supply of spinal cord after ischemia. it usually occurs because of oxygen free radical-induced lipid peroxida keywords spinal, ischemia-reperfusion, neuroprotection, inflammation, adalimumab corresponding author: yasar karatas medova hospital, department of neurosurgery, konya, turkey yasarkrts@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 255 the effect of adalimumab on spinal cord ischemia reperfusion injury tio, leukocyte activation, inflammation and neuronal apoptosis. although many clinical treatments of spinal cord injury have been provided in recent years, the results are far from satisfactory [1]. paraplegia is a serious complication that can occur in a patient undergoing thoracoabdominal aortic surgery and has been seen in 2.4-40% of the patients [2]. factors that cause this complication are: impaired arterial blood flow and i/r injury of the spinal cord due to collateral supplier damage, perfusion insufficiency, prolonged aortic crossclamping time, intraoperative proximal hypertension, high cerebrospinal fluid (csf) pressure and postoperative hypotension [3]. neurological injury that occurs after impact is called primary injury. primary injury triggers secondary injury with increased inflammation, apoptosis and the formation of free radicals that have serious effects on outcome. various pharmacological agents have been used to prevent secondary damage at different success rates [4]. however, there is no complete treatment of secondary injuries. tumor necrosis factor is an important immunoregulator molecule that act important role in central nervous system events such as stroke [5]. there are two type of tnf molecule. first type of tnf molecule is transmembrane tnf which acts through cell-to-cell contact to initiate juxtracrine signaling and is important not only for cellular transmission in the natural immune system but also for functional improvement and axonal preservation [6,7]. the second type of tnf molecule is soluble tnf that acts in a paracrine manner and is a substantial mediator of both acute and chronic inflammation [8]. adalimumab is a potent tnf alpha blocker. it suppresses tnf-α and il-6, initiate to reduction or inhibition of the inflammatory process [9]. many studies have shown that tnf-α and il-6 are elevated during i/r and that they are responsible for activation of the cell death by apoptosis [10]. recently, the neuroprotective impacts of anti-tnf treatment have been studied in a model of focal cerebral ischemia and beneficial effects have been stated [11]. the aim of this study was to investigate the neuroprotective impacts of adalimumab on rabbit spinal cord i/r injury model. 2. materials and methods this research was carried out in the experimental medicine application and research center of necmettin erbakan university. the experimental protocol was assessed and confirmed by the ethics review committee of necmettin erbakan university. the animals were kept at a room temperature (18– 21 ºc) and fed on a standard diet. a 12 -h light–dark cycle (08:00 –20:00 hours light/20:01–07:59 hours dark) was preserved. the animals were able to get as much food and water as they wanted. 2.1 groups twenty-four adult new zealand rabbits were randomly separated into three groups: group 1, control group (n=8); group 2, ischemia-reperfusion (i/r) group and group 3 (n=8), i/r injury+ adalimumab (40 mg/kg, ip, single dose) treatment group. all rabbits were anesthetized by intramuscular (i. m.) injection of ketamine (50 mg/kg) (ketalar, parkedavis, eczacıbaşı, istanbul, turkey) and xylazine (10 mg/kg) (rompun, bayer, istanbul, turkey) and permitted to breathe during the procedure. an intravenous catheter was placed in the auricular vein of the animals and preoperative cefazolin 10 mg/kg (cefamezin, eczacıbası, istanbul, turkey) was given as a single dose. as maintenance, 0.9% nacl (20 ml/h) was given throughout the experiment. all rabbits underwent laparotomy in supine position. aortic cross-clamp was not applied to group 1. in group 2 and 3 the abdominal aorta was detected and dissected carefully from the beginning of the left renal artery by transperitoneal approach. five minutes before occlusion, 100 iu/ kg heparin was given intravenously. the aorta was then crossclamped using an aneurysm clip with a closing force of 70 grams (yasargil fe 721, aesculap). the clipping site was just below the origin of the left renal artery. pulsation of the femoral artery disappeared after occlusion. the aneurysm clip was removed 30 minutes later, and aortic pulsation was restored. neither aortic nor caval hemorrhage were observed during surgery. before closure, rabbits of group 3 received single dose intraperitoneal 40 mg/kg adalimumab treatment. after the closure of laparotomy all rabbits awoke and returned to their cages. the animals were followed neurologically, and motor inefficiency and recovery rates were recorded. seventy-two hours later, all rabbits were reanesthetized by intramuscular (i. m.) injection of ketamine (50 mg/kg) (ketalar, parke-davis, eczacıbaşı, istanbul, turkey) and xylazine (10 mg/kg) 256 yasar karatas, mehmet fatih erdi, bulent kaya et al. (rompun, bayer, istanbul, turkey). blood samples were taken from auricular veins for biochemical examination. for histopathological examination spinal cord samples were taken from lumbar spinal cord segments between l4-l6 by laminectomies and the rabbits were sacrificed. 2.2 biochemical analysis venous blood samples were collected by centrifugation at 4° c and 1,000 g for 10 minutes to remove plasma. plasma samples were kept at -80 ° c until the parameters were studied. spinal cord tissue samples were provided in ph 7.4 50 mm phosphate buffer and kept at -80 ° c until they were analyzed. the thawed tissue samples were weighed and homogenized in ice using a mechanical homogenizer and an ultrasonic homogenizer in a 10fold (w / v) cold phosphate buffer (50 mm, ph: 7.4). the supernatants were separated by centrifuging the homogenates for 10 min at 4 ° c and 10.000 g. pierce bicinchoninic acid-bca (thermo scientific, illinois, usa) was used to measure spectrophotometrically plasma and spinal cord tissue total oxidant (tos) and antioxidant status (tas) (rel assay diagnostics, gaziantep, turkey), thiobarbituric acid reactive substances (tbars) (oxford biomedical research, missouri, usa) and tissue protein levels. plasma and spinal cord tissue il-6, il-10 and tnf alpha levels were examined by using elisa antigens that were intrinsic to rabbits (elabscience biotechnology co., wuhan, china). 2.3 histopathological studies spinal cord samples were stabilized by 10% formaldehyde for two days and then embedded in paraffin blocks. after dehydration, coronal sections of the spinal cord segment were severed at a thickness of 4 μm and stained with hematoxylin and eosin (he) in order to examine the structural changes. gray matter was checked in five different areas in each section. depending on the degree of inflammation, hemorrhage, axonal swelling, congestion, neuronal degeneration and vacuolization of the spinal cord, the light microscopic findings were graded on a scale ranging from 0 to 3, corresponding to “no change”, “mild”, “moderate” and “severe” changes, respectively. the histopathological score was calculated for each spinal cord sample [12]. apoptotic cells were labeled using an apoptag in situ apoptosis detection kit (millipore). dna fragments in spinal cord regions were altered by the action of terminal deoxynucleotidyl transferase. the manufacturer’s instructions were followed during procedures. in each section five dark visual fields were randomly chosen, and the tunel-positive neurons and the total number of neurons in the selective visual fields was counted. tunel-positive index (the tunel-positive to whole neurons ratio) was computed. eight sections from each group were used for measurement, and five high-powered visuals were indiscriminately picked from every section to carry out measurement of the tunelpositive indices [13]. 2.4 statistical analysis data were analyzed using spss (version 24.0, spss inc.) and expressed as mean ± sd. comparisons were made by the kruskal-wallis test. differences among the groups were evaluated by the mannwhitney u test. a p < 0.05 was considered statistically significant. histopathological score and tunel positive cell count were contrasted using a one-way analysis of variance (anova) with tukey test. 3. results 3.1 histopathological evaluation i/r injury significantly increased the spinal cord neuronal damage score and apoptotic cell count. adalimumab treatment statistically substantially decreased spinal cord neuronal injury score and apoptotic cell count (p=0). large motor cells were observed in anterior horn of the spinal cord in the control group (figure 1a). no changes were observed in the neurons. the most serious injury was seen in ischemia-reperfusion group in spinal cord in he sections (figure 1b, c, d). necrosis, hemorrhage and congestion were noticed in ischemia-reperfusion group. nissl substances disappeared in necrotic neurons. in addition, neuropil vacuolization and tissue loss were observed in the gray matter (figure 1e, f, g). compared with control group, it was noticed that histopathological score rose in ischemiareperfusion group. histopathological alterations and score significantly reduced in adalimumab treatment group (fig 1h). myelin swelling determined in white matter in ischemia group and the adalimumab group had less myelin swelling compared to the ischemia group. (figure 2a, b, c). tunel positive cells count 257 the effect of adalimumab on spinal cord ischemia reperfusion injury increased in i/r group when compared with control group (figure 3a, b). adalimumab treatment decreased tunel positive cells count (figure 3c). figure 3d showed differences among groups. figure 1. histopathological photomicrographs of spinal cord tissue stained he a: control group : neurons in grey matter and white matter b: necrotic neurons in ischemia-reperfusion group (black arrow), haemorrhage ve (arrows), *:vacuoles. c: chromatolyses in ischemia-reperfusion group (arrow head), *:vacuoles. d: pyknosis in ischemia-reperfusion group (arrows), necrotic neurons (arrows). e: normal neurons in adalimumab treatment group f: haemorrhage in adalimumab treatment group (arrow). g: congetion in adalimumab treatment group (arows). h: histopathological assessment of spinal cord, (* p < 0.05, compared to group 1; &p < 0.05, compared to group 2). 258 yasar karatas, mehmet fatih erdi, bulent kaya et al. figure 2. histopathological photomicrographs of white matter stained he a: control group. b: ischemia-reperfusion group c: adalimumab treatment group. figure 3. representative spinal cord sections stained in the tunel assay. a: control group, b:i̇schemia-reperfusion group c: adalimumab treatment group .d: comparison of groups according to tunel-positive cells in spinal cord, (* p < 0.05, compared to group 1; &p < 0.05, compared to group 2). 3.2 biochemical evaluation i/r injury significantly increased the plasma and spinal cord tissue tnf alpha, tos, tbars, il6 levels and reduced the plasma and spinal cord tissue tas and il10 levels. adalimumab treatment significantly decreased the plasma and spinal cord tissue tnf alpha, tos, tbars, il6 levels and raised plasma and tissue tas and il10 levels (figure 4, figure 5). 259 the effect of adalimumab on spinal cord ischemia reperfusion injury figure 4. the effects of adalimumab on plasma levels of tas,tos,tbars,tnf alpha,il6,il10. figure 5. the effects of adalimumab on tissue levels of tas,tos,tbars,tnf alpha,il6,il10. 4. discussion neural tissues can be said to be very sensitive to ischemia. i / r damage of the spinal cord during thoracoabdominal vascular surgery can cause serious discomfort such as paraplegia. primary injury triggers secondary injury with increased inflammation, apoptosis and free radical formation during the i / r period [14]. secondary injury may result in endothelial dysfunction and increase vascular permeability that promotes migration and activation of immune cells. these activated immune cells infiltrates the related area and secrete some proinflammatory cytokines. enhanced inflammation causes reactive oxygen species produce and induces lipid peroxidation which causes injury in the ultrastructure of neural cell membranes and hinders their critical functions [15]. the spinal cord is very sensitive to ischemia because it has its own anatomical features. “the infrarenal aortic cross-clamp” method used in this study leads to severe spinal cord injury. it was first described by liang et al. as an experimental method [16,17]. rabbits have segmental blood supply in their lumbosacral spinal cord. thus, rabbit model of spinal cord i/r injury is commonly used. it is clear that there are many causes of paraplegia. long-term ischemia, interruption of critical intercostal and lumbar arteries, decrease in spinal cord perfusion pressure and postoperative reperfusion injury are some of these reasons [18]. therefore, this method is thought to be appropriate to imitate the complications of aortic surgery. high levels of plasma and spinal cord tissue tnf alpha, tos, tbars and il6 in i/r group signifies 260 yasar karatas, mehmet fatih erdi, bulent kaya et al. increased inflammation and oxidative stress. neuronal damage score and apoptotic cell count increase after i/r injury. adalimumab treatment significantly improves biochemical and histopathological adverse impacts of i/r injury. 5. conclusion in this study, it was found that adalimumab had significant neuroprotective effects on rabbit spinal cord i/r injury. after i / r injury, high inflammation and oxidative stress were successfully reversed by adalimumab, and the worse effects of biochemical, histopathological and neurological i / r damage were mitigated. further studies are needed to carry out this treatment in clinical practices. references 1. kieffer e, chiche l, cormier e, guegan e. recurrent spinal cord ischemia after endovascular stent grafting for chronic traumatic aneurysm of the aortic isthmus. journal of vascular surgery 2007; 45: 831–833. 2. coselli js, lemaire sa, conklin ld, koksoy c, schmittling zc. morbidity and mortality after extent ii thoracoabdominal aortic aneurysm repair. ann thorac surg. 2002; 73(4):1107-15, http://dx.doi. org/10.1016/s0003-4975(02)03370-2. 3. kocogullari cu, becit n, erkut b, keleş ms, ceviz m, ates a, gündogdu c, kaygın ma, kocak h. prevention of reperfusion injury of the spinal cord in aortic surgery: an experimental study. surg today 2008; 38(3): 237–44. 4. junk ak, mammis a, savitz si, singh m, roth s, malhotra s, rosenbaum ps, cerami a, brines m, rosenbaum dm. erythropoietin administration protects retinal neurons from acute ischemia-reperfusion injury. proc natl acad sci usa 2002; 99: 10659– 10664. 5. lambertsen kl, biber k, finsen b. inflammatory cytokines in experimental and human stroke. j cereb blood flow metab 2012; 32: 1677–1698. 6. alexopoulou l, kranidioti k, xanthoulea s, denis m, kotanidou a, douni e, blackshear pj, kontoyiannis dl, kollias g. transmembrane tnf protects mutant mice against intracellular bacterial infections, chronic inflammation and autoimmunity. eur j immunol 2006; 36: 2768–2780. 7. brambilla r, ashbaugh jj, magliozzi r, dellarole a, karmally s, szymkowski de, bethea jr. inhibition of soluble tumour necrosis factor is therapeutic in experimental autoimmune encephalomyelitis and promotes axon preservation and remyelination. brain 2011; 134: 2736–2754. 8. ruuls sr, hoek rm, ngo vn, mcneil t, lucian la, janatpour mj, korner h, scheerens h, hessel em, cyster jg, mcevoy lm, sedgwick jd. membrane-bound tnf supports secondary lymphoid organ structure but is subservient to secreted tnf in driving autoimmune inflammation. immunity 2001; 15:5 33–543. 9. mcgovern jl, nguyen dx, notley ca, mauri c, isenberg da, ehrenstein mr. th17 cells are restrained by treg cells via the inhibition of interleukin-6 in patients with rheumatoid arthritis responding to anti-tumor necrosis factor antibody therapy. arthritis rheum 2012; 64: 3129– 3138. 10. xu yf, liu m, peng b, che jp, zhang hm, yan y, wang gc, wu yc, zheng jh. protective effects of sp600125 on renal ischemia-reperfusion injury in rats. j surg res 2011; 169: 77–84. 11. clausen bh, degn m, martin na, couch y, karimi l, ormhøj m, mortensen ml. systemically administered anti-tnf therapy ameliorates functional outcomes after focal cerebral ischemia. j neuroinflammation. 2014; 12: 11:203. doi: 10.1186/s12974-014-0203-6. 12. kishimoto t, akira s, narazaki m, taga t. interleukin-6 family of cytokines and gp130. 1995; 86:1243-54. 13. gürer b, kertmen h, kasim e, yilmaz er, kanat bh, sargon mf, arikok at, ergüder bi, sekerci z. neuroprotective effects of testosterone on ischemia/reperfusion injury of the rabbit spinal cord. injury. 2015; 46(2): 240-8. 14. klune jr, tsung a. molecular biology of liver ischemia/reperfusion injury: established mechanisms and recent advancements. surg clin north am 2001; 90: 665-77. 15. chan ph. role of oxidants in ischemic brain damage. stroke. 1996; 27(6): 1124-9. 16. liang y, yang q-h, yu x-d, jiang d-m. addictive effect of tetramethlpyrazine and deferoxamine in the treatment of spinal cord injury caused by aortic crossclamping in rats. spinal cord 2011; 49: 302-306; doi: 10.1038/sc.2010.113; published online 14 september 2010. 17. shechter r, london a, varol c, raposo c, cusimano m, yovel g, rolls a, mack m, pluchino s, martino g, jung s, schwartz m. infiltrating blood-derived macrophages are vital cells playing an antiinflammatory role in recovery from spinal cord injury in mice. plos med 2009; 6(7): e1000113. doi:10.1371/journal.pmed.1000113. 18. sahin ma, onan b, guler a, oztas e, uysal b, arslan s, demirkilic u, tatar h. cilostazol, a type iii phosphodiesterase inhibitor, reduces ischemia/ reperfusion-induced spinal cord injury. heart surg forum 2011; 14: 171-177. doi: 10.33962/roneuro-2020-029 assessment of malpractice litigation following spine surgery gabriel iacob, alexandru vlad ciurea romanian neurosurgery (2020) xxxiv (1): pp. 179-188 doi: 10.33962/roneuro-2020-029 www.journals.lapub.co.uk/index.php/roneurosurgery assessment of malpractice litigation following spine surgery gabriel iacob1,2, alexandru vlad ciurea1,3 1 professor of neurosurgery, “carol davila” university of medicine and pharmacy bucharest, romania 2 chief of neurosurgery clinic, bucharest emergency hospital, bucharest, romania 3 chief of neurosurgery clinic, sanador hospital bucharest, romania abstract medical litigation in spine surgery is a serious concern today, with a high volume of clinical negligence claims, substantial financial cost and significant burden, who is threatening the future of this surgery. classical spinal surgery should be performed with very well documented indication, in order to improve the expected results, with clear aims: decompression of the neural elements of the spine from tightness, stabilizing the spine to protect the nerves, eliminate the pain resulting from abnormal loading from the different movements. spinal surgery today means a wide analysis, understanding and realization of spinal decompression, also osteosynthesis and fusions, using high-performance gestures, with increased addressability especially in the elderly, for a varied pathology, which involves anaesthetic-surgical risks, complications. in such a context, surgical damage does not necessarily result from an error or from surgical misconduct and the surgeon is not always responsible for the damage in the absence of a proven fault in the legal sense. the paper aims to briefly review the main problems, but also useful recommendations to meet various challenges, expectations, maintaining the quality of life of each patient, reducing risks of getting sued, also to increase the odds of a successful defence. in conclusion: education, vigilance, improved patient-safety strategies, investigation, implementation and sharing of lessons learned from litigation claims remain important components of spinal surgeons training, to reduce future cases of negligence and improve patient care, quality of life, as many of the cases of successful litigation had a preventable cause. seneca: errare humanum est, sed perseverare diabolicum murphy's law: if anything can go wrong, it will! introduction why spine surgery medico-legal aspects? spinal surgery, made classic or minim invasive, means frequent, demanding high risks procedures, required for many people, especially for old people, performed for: trauma, degenerative, infectious, vascular, instability, functional procedures, especially for pain, as a condition: to improve the patients status, to avoid neurologic threatening of neurologic spine function. keywords spine surgery, complications, malpractice, medical litigation in spine surgery, informed consent, medical malpractice stress syndrome, practical advices to avoid spinal litigation corresponding author: gabriel iacob prof. md. phd, “carol davila” university of medicine and pharmacy bucharest, romania gbrl_ cb@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 180 gabriel iacob, alexandru vlad ciurea spinal surgeons, whether of orthopaedic or neurosurgical backgrounds, encountered several adverse events, despite skills, patients compliance and expectations (1). discussion medical litigation in spine surgery a high-risk malpractice specialty is particularly influenced by the current litigation climate and it means (1): • medical error a consequence of a failure of a planned action to be completed as intended or the use of a wrong plan to achieve an aim: special technologies to fulfil decompression, stabilization with motion respect, using standard or minim invasive procedures, not always available in a hospital; a physician fails to act under the same circumstances to respect a standard of judgment, skill, diligence as any reasonable physician (2-4).this standard will be ascertained by appointed experts who will contrast the liable medical conduct to existing practice guidelines, statements of professional organizations and societies, use of leading books, scientific treaties and published articles; • a breach of standard of care, negligence a doctor’s failure to meet this standard, does not necessarily result in liability. bad outcomes may result even with the best of medical care; also technically unsuccessful surgery does not automatically mean a breach of standard of care. it’s important to explain that bad results don’t equate with malpractice and good results don’t means that the patient has had the best of care! (4); • causation covered a high range of causes pre, intra, postoperatively, to prove causal connection, the direct link between the negligence and damage; • damage: proof of damage, directly resulted from the breach of the alleged standard of medical care in 2005 alone, in the usa, 3,229 active certified neurosurgeons paid a total of $28 million in malpractice claims, with the highest average payment per specialist surgeon $465,000 (5). 1. negligence claims in spinal surgery means more than 20,000 spinal operations/year in uk are the highest among other operations, more frequent and expensive: +10% last 2 years (6). spinal epidural abscess generates significantly higher plaintiff verdicts in cases with delay in diagnosis or treatment, in cases with paraplegic or quadriplegic patient (7). 2. in 2013 hellsten et al. (8) mentioned adverse spinal events 17.4%, to a cost of $21,000 per case, $2.1 m per year, 1,171 bed days every year, more than 50% due to ‘minor’ events. 3. in 2019 for plaintiff verdicts, the mean indemnity payment was median $753,057; for settlements, the mean indemnity payment was median $547,935. a neurological deficit was associated with a significantly greater likelihood of a favorable outcome for the plaintiff 52.8% versus 32.1% for plaintiffs without neurological deficit (9). the average time to a decision for defendant verdicts was 5.1 years; for plaintiff rulings, 5.0 years; for settlements, 3.4 years. poor consent, misdiagnosis, delays in the diagnosis and the treatment of a surgical complication predict legal case outcomes favoring the plaintiff (6), also catastrophic complications are linked to large sums awarded to the plaintiff and are predictive of rulings against the physician. 4. for physician defendants, the costs of settlements are significantly less than those of losing in court (1). incidence of spinal malpractice claims is increasing: 56% compared to 39% head and/or brain, 5% miscellaneous, with a multifactorial possible claim, many of them avoidable (10). malpractice spinal claims are influenced by: the number and selection of patients, purpose of the procedure performed classic or minim invasive also by the social systems: compensation claims increasing the incidence rate, with a less patients intention to return to work as assurance payments are bigger (4). in order for the doctor to be liable, the complaining patient must prove four things in the legal sense (6)(7): • duty did a physician-patient relationship exist? • breach of duty did the physician fail to meet the required standard of care whether a body of responsible surgeons would have treated that patient the same way (bolam test) the burden of the proof is on the plaintiff; 181 assessment of malpractice litigation following spine surgery • causation did the physician’s breach cause the patient’s injury? • damages did the patient incur medical expenses, pain, suffering, loss of wages as a result of the breach? there are several causes to litigations: a. inappropriate decisions means: • poor communication despite patient’s compliance, realistic expectation after surgery and the surgeon’s skills lack of respect for patient and relatives, for the surgical team, the institution prestige linked to: misdiagnosis, bad indications, “unindicated surgery” it is often referring to the lack of concordance between clinical, radiological ± neuro-physiological investigations, absence of marked psychosocial economic problems, failure of well conducted medical conservative treatment (1)(6); • poor documentation: imaging’s (mainly mri) must be relatively recent (less than 3 months). in case of clinical changes or new clinical signs, mri needs to be repeated before proceeding with the surgery (13); • inappropriate preoperative patient assessment: comorbid conditions + the aging of the population a growing concern for spine care in the 21st century (10). there are three major problems in elderly patients: 1. failure due to wrong indication: poly-morbid patient, multi-operated patient (also other than spine surgery), diabetic patient with neuropathy, severe osteoporosis: 700,000 of these occur in the spine more than in the hip and wrist combined !, obese patient, parkinson, depressed patient, physically nonactive/active patient, patient in insurance battle waiting compensation. for elderly patients there are a very large pathology: metastatic and infectious diseases, degenerative spine: spinal stenosis, degenerative instability +/-adjacent segment problem (natural or iatrogenic), discogenic, cervical myelopathy, spondylolisthesis, arthritis, adult degenerative scoliosis, muscular insufficiency (fatty degeneration); difficult recovery (12); 2. failure due to wrong biology mostly patient and /or surgeon’s judgement related; sometimes spinal surgery for geriatic patients unnecessary, too much, or too little; 3. failure due to wrong biomechanics mostly patient and also its biology and /or surgeon’s judgement related (11). • surgeons’ expertise: a check list could be established and the steps are followed regularly before starting and during the surgery technique (sign in prior to induction, time out prior to skin incision, sign out prior to drape removal), wrong judgement of own capabilities and skills, lack of expertise, wrong choices of technology (implants, instrumentation, surgical technique) + risks unexplained, failure to recognize the clinical signs and symptoms of complications, inappropriate delegation of procedures to junior doctors(13). legal finding: the majority claims are from patients with no medical negligence, only 3% of patients who suffered negligence filed a claim. (6) b. failure to obtain consent (6): consent should be done by the consultant; to be legally valid for examination or operation should met three conditions: must be given knowingly, freely and voluntarily, the patient or legal entities must be capable of giving legal consent, the patient should be sufficiently informed to make a considered decision. it’s mandatory to discuss immediately after surgical indication is sustained: surgery risks against conservative options; especially to avoid complications, expectations for patients with old, severe neurologic deficits, to patients with low resources to recuperate; ex: lumbar disc or stenosis surgery is for leg pain not back pain, surgical fusion as last resort is not wise,10% are worse after fusion. c. wrong patient (14): • patient biology – age, hypertension and cardio vascular disease, diabetes, patient over 60 years with hemorrhagic risks especially after aspirin, plavix, smoking and pulmonary disease; also asa grad 1 9.1%, asa grade 4 31.3%. in cases of elderly patients with spinal cord tumours (15) age increase in significant morbidity for more than 64, 5 fold; in cases with elderly patients with cervical discs and myelopathy, an operation performed to a patient aged > 65 yrs may increase mortality 14 fold, if the patient aged > 84 yrs mortality increase 44 fold. 182 gabriel iacob, alexandru vlad ciurea • adequate conservative treatment? mri if considering malignancy, sciatica/cauda equina syndr, infection, fracture, ankyl. spond., inflammatory disorders, referral for surgery (13), avoid operation delay (6) • planning operation: think always to do it right the first time! d. wrong/stupid surgeon (14): • wrong-level surgery, wrong side: always perform fluoroscopy before skin incision, before entering the canal; wrong positioning rate is estimated at 4.2%, but is found to be 15.7% on control ct; • wrong procedure: poor surgical performance: inadequate decompression, wrong technology despite right procedure and patient • wise selection of radiation exposures in spinal surgery, safe operating procedure achieving a good balance between patient care and radiation safety, minimize the high fluoro technique, always use alara concept: as low as reasonably achievable (16)(17) • think to the best patient position: each position carries some degree of risk for haemodynamic and physiologic changes; also complications, risks magnified in anaesthetised patient due to loss of ability to compensate or communicate (18); prone position during spinal surgery should be made with the patient’s head raised, in order to minimize facial and per orbital edema, avoiding eyeball compression especially after prolonged position, which may generate peri-operative blindness and litigation both for surgeon and anesthesiologist, ex: 0.03% after spinal fusion (19); all possible compression and traction points on the face, protecting neck position, trunk and limbs using protection pads to cover pressure points avoiding: o ulnar nerve compression at the elbow the most common; o peroneal nerve injuryat the fibular neck is possible in any patient positioning, inducing paresthesia or severe motor impairment with drop foot; o uni or bilateral femoral cutaneous nerve involvement results in meralgia paresthetica o brachial plexus stretch injury. • general anesthesia (18) with care especially during intubation to elderly patients with myelopathy or severe cervical stenosis, hyper flexion or extension, using the philadelphia collar with fiber optics intubation, even under intra operative monitoring; maintaining a stable hemodynamic, avoiding ischemia by hypo perfusion with medullary insults, compensating rapidly any blood loss during hemorrhagic procedures e. possible complications: • general causes which can evolve to death (20-22): deep venous thrombosis, pulmonary embolism, cardio-respiratory failures, abdominal vessel injury if sudden unexplained drop in blood pressure, abnormal bleed coming from the disc space, ileus, sepsis with chest/urinary infections, operating room fires (19) in usa 50-100 events/yr, 1–2/yr fatal, fire triad, location: 34% airway, 28% head or face, 38% on/or inside patient, heat/ignition source: cautery/laser/fiber optic light cord, fuel: drapes/et tube/alcohol prep/hair/o2 build up under impervious drape, especially for cervical spine, oxidizer: oxygen/nitrous oxide/air. • acute or delayed neurologic deficits related to surgery (23)(24): direct iatrogenic medullary and radicular insults in procedures performed without spinal cord monitoring: meps, sseps, nim eclipse, or by hypo perfusion arterial pressure < 80 mm hg, especially in cases with myelopathy, medullary atrophy or ossification of the posterior longitudinal ligament estimated at 0.2 to 0.9%. • cervical disk surgery with medullary decompression for myelopathy entails elevated risk, affecting the c5 root with deltoid impairment in 2.3 to 6.7% of cases (short sheat, subject to traction by medullary mobilization after decompression, inducing spinal cord retractionin surgical interventions restoring lordosis). • complex surgical procedures for spinal deformity of the thoracic and lumbar spine, to correct: sagittal deformity see three-column resection osteotomies with pedicle subtraction osteotomies and vertebral column resections may generate paraplegia 0,55% 1,78%. • high grade lumbar spondylolisthesis may generate 11,8% with neurologic complications especially to the l5 root; cauda equina syndrome 183 assessment of malpractice litigation following spine surgery following decompression for lumbar spinal stenosis, disc herniation: incidence of 2.8%. • iatrogenic medullary and radicular insults could appear after poor positioning estimated at 4.2%, but is found to be 15.7% on control ct or peror postoperative implant mobilization: screws, inter body cages, a.s.o. subsequent stoke: estimated at 3.8% on the left and 1.8% on the right side after iatrogenic surgical trauma to the vertebral artery 0,3%; recurrent laryngeal nerve injury with dysphonia, as the most common postoperative complaint in anterior cervical approaches; horner syndrome due to injury to the cervical sympathetic trunk is a very rare complication of anterior cervical decompression and fusion, the incidence rate is between 0, 2 to 4% mainly after revision surgery; retrograde ejaculation from damage to the hypo gastric plexus during anterior approach of the lumbar spineis estimated between 0, 42 to 4, 1%. • local complications: implant related dysphagia in cervical disc herniation; lymphocele after anterior lumbar interbody fusion; dural tear (25-27) are very frequent during spine surgery (1-15%), versus 7,7% in cases with neurological complications, three-fold higher in revision surgery, may generate csf collections (pseudomeningocele), also intracranial hypotension, acute subdural hematoma, tonsillary herniation; leak must be treated seriously and rapidly! primary repair suturing using microtechnique, if larger than 3 mm, 6/0 suture, cover with: grafts (fat, muscle, fascia, blood patch), tissue sealents, fibrin glue, synthetic membrane; hermetic closure of the various planes, antibiotherapy are necessary, postoperative drainage after dural tear is controversial; radiculopathy: recurrent disc prolapse, ectopic bone/stenosis, fragments end plate prep, symptomatic epidural adhesions, tlif retraction, multiple surgeries, inflammatory bmp reaction, bmp ectopic bone (28)(29) in spinal fusion 92.8%, off label 85%, 16.6% alif, 30.0% plif/tlif, 20.4% postlat,13.6% cervical, 3.9% t/l; no statistical correlation ectopic bone vs. increased leg pain, few cases of neurologic impairment of from ectopic bone; bleeding (17)(28)(30) it can occur damaging the arterial feeder in a rich vascularized vertebral tumor, through epidural varices, rarely by damage to an arterial vessel – see during discectomy. postoperative bleeding could be: residual, discovered incidental or even symptomatic with different topography: epidural, paravertebral, even intradural. main causes are: bad hemostasis, uncontrolled high blood pressure during operation, coagulopathy, drugs; ex. in cervical area is rare 0.2%-1.9%, may cause airways obstruction, requiring evacuation 0.10.4%; in lumbar area is about 5,6%. best solutions are: meticulous dissecting and hemostasis, drain use, pay close attention to the patient's supervision even in icu, quick evacuation; local seroma; instability (13)(17)(31-33) – avoid thinning the pars and aggressive facetectomy, junctional degeneration/instability (fusion disease); improper use of instrumentation (31-33): misplaced instrumentation most frequent are lateral, may generate pedicle breaches 6.7% of screws; percutaneous fluoroscopically or navigation guided pedicle screw placement is safe and accurate, revision is rarely required; may increase the rate of csf leakage, than without instrumentation 16% versus 3,5%, nonunion of the fusion or pseudoarthrosis, hardware malpositioning; infections (19)(28): especially in immunocompromise patients: diabetic, renal failure, hiv, etc, consider prophylactic antibiotherapy. more frequent infections appear as a complication of csf leakage cases in nearly 1/4th of cases. there are several clinic entities: wound infection with postoperative abscess, spondylodiscitis, osteomyelitis, epidural collections, fungal meningitis: exserohilum rostratum, aspergillis fumigatus, cladosporium from csf after epidural steroid injection, 19 days post injection: fever, stiff neck; neuropathic pain, chronic pain corticalization, failed back surgery syndrome (13)(34)(35). such entities can be generated by all previously mentioned complications. patient selection is more important than most of the technical problems in fbss (correct assessment is needed to get an accurate diagnosis, recurrent disc herniation or instability should be treated, no treatable cause, spinal cord stimulation may help improving patient’s pain and functions; vertebroplasty may generate complications 3.7% of cases, kyphoplasty 0.3% of cases (17)(36): severe pulmonary embolism of pmma: 184 gabriel iacob, alexandru vlad ciurea hypertension, hypercapnia, loss of responsiveness, asymptomatic diffuse pulmonary embolism, neural and vascular complications after cement leakage inside the vertebral canal, silent leaks 30% 70% of patients, most are undetected by the surgeon. f. what kind of operation: classic or minim invasive spine surgery. "miss" is an acronym for the term: minimally invasive spine surgery, synonym: "liss" less invasive spine surgery, endoscopic spine surgery = efficient surgery with minimum of iatrogenic trauma, but not minimal surgery: minimal access & techniques spine surgery, percutaneous, even using microscope as a part of a less invasive technology (37-39). the current focus on "miss" refer to several “trendy” procedures, in the early phase of a “concept shift” (39), still met with skepticism, disbelief, hostility by many neurosurgeons for safety reasons, but more accurate. such procedures are using advances in access technology: optical systems (endoscopes, microscopes), navigation guided surgery, specialized retractor systems, hybrids, robotics, new generation of implants suitable for minimal access by anterior/posterior surgery, new solutions for fusion: cages, bone harvesting tools, bone substitutes, 3-d prosthesis; designed to solve a pathological process as using standard open procedures for less pain, morbidity, disability, facilitates faster recovery, improves back muscle function. what does "miss" mean today? advantages (40,44): small incisionsmore aesthetics, appealing -some procedures can be performed as outpatient surgery; accurate fluoroscopic images with x ray exposure or by navigation-guidance; theoretical better quality of life: shorter hospital stay, structure-sparing, or perhaps structurepreserving, a "miss" by products are operative time, reduced tissular distruction, less pressure on muscles using minimally invasive spinal retractors compared to open retractors and reduced scar (periradicular & skin), less blood loss, infection, disability; faster recovery, functional ability to return to normal activity, to work; long term pain control, minimal requirements for narcotic pain medications; may reduce or perhaps eliminate the development of adjacent segment disease; high expectations even to elderly, obese people with a complex spinal problem, such as deformity or trauma; drawbacks and limitations (45)(46): technically more demanding, longer operative time; less working space, extension and quality of direct spinal decompression, placing cross-links, long rods, less surface area of bone exposed for fusion cases -limitations by pathology: possible spinal injuries associated with neurological deficits, see: spondyloptosis, severe multi-level stenosis, en-bloc removal of tumour masses, severe deformities; acute complications 10%, 12% reoperations: bleeding, 5.3% dural tear with csf fistula, 2.6% fracture of an inferior facet for lumbar spinal stenosis, tlif may result in poor fusion without bmp, 10.5% transient neurological complications (47); radiation exposure with fluoroscopy (48) with poor radiological support esp ap; education long steep learning curve, the intraoperative complication rate is highest between the 3rd and the 6th year of training; availability; cost: expensive hardware, hospital stay it could be economic (49)(50); "maximal intra-operative surgical stress" (51). "miss" recent evidence: more frequent miss indications (12): degenerative disc disease herniated disc, lumbar spinal stenosis, spinal deformities such as scoliosis, spinal infections, spinal instability including spondylolisthesis, vertebral compression fractures, reconstruction with internal fixation, resection of spinal or paraspinal tumours. performed with microscope or endoscope there are several miss procedures (12)(52)(53), ex: cervical procedures: posterior foraminotomy, transarticular c1c2 screw fixation; thoracic procedures: foraminal discectomies, percutaneous pedicle screw fixation; lumbar procedures: discectomies, posterolateral interbody fusion plif, midline lumbar interbdy fusion midlf, transforaminal lumbar interbody fusion tlif, extreme lateral lumbar 185 assessment of malpractice litigation following spine surgery interbody fusion dlif (xlif), anterior lumbar interbody fusion alif. for discectomy: micro discectomy (md) vs tubular(52) : no difference (the mean duration of surgery was 34 min shorter for conventional md; the incidence of dural tear was 6.5% in md group and 10.4% in early td and decreased to 7.4% in late td group, possible more leg pain, low-back pain, at 2 years with tubular) (53). for lumbar spinal stenosis: bilateral micro decompressive laminotomy, as minimally invasive endoscopic bilateral decompression with a unilateral approach (endo-bidua) for elderly patients (54)(55). for posterior lumbar fusion: significant advantages over traditional open procedures in the obese population, smaller incisions, less tissue trauma and quicker recovery, higher radiation exposure 84 s vs 37 s, may reduce or perhaps eliminate the development of adjacent segment disease (56-58). revision tlif identical results: less blood loss, less postoperative back pain at the second day postoperatively, same surgical time, higher radiation exposure 79 s vs 39 s (58). adult spinal deformity correction with circumferential minimally invasive surgery and hybrid techniques result in overall reoperation rates of 27.9% and 33.8%, respectively, at minimum 2-year follow-up. junctional failures are more common after hybrid approaches, while pseudarthrosis/fixation failures happen more often with circumferential minimally invasive surgery techniques. early reoperations were less common than later returns to the operating room in both groups, but circumferential minimally invasive surgery demonstrated less risk of infection and early reoperation when compared with the hybrid group (60). practicing a good spinal surgery is not a guarantee to being hit with a medical malpractice lawsuit; nobody is immune from medical malpractice. most spinal surgeons are not well prepared to deal with bad consequences of medical malpractice, they are perceived as a “wound to the heart”, that may lead to frustrated, dissatisfied patients; also to several consequences: loss of reputation and significant supporters, lack of knowledge about the potential process and outcomes, loss of livelihood, control, assets. such situations may lead to “medical malpractice stress syndrome”, expressed by psychological symptoms: anxiety, irritability, tiredness, restlessness, difficulty in concentration, excessive worry, may occupy more than 50% of working hours, tense muscles, insomnia, depression and by physical illness, at work and at home; dissatisfaction, to burnout of the medical practice, early retirement or even may generate extreme reaction, deep depression leading to suicide (1)(4)(59)(61). fear of lawsuits encourages defensive medicine, a defensive attitude, affecting patients (61):to restrict practice, not only to demanding procedures, also for emergency or trauma, to move their practice to a state with "better" malpractice conditions, in detriment of patients losing chances to receive the accurate treatment in the needed time; negatively influence any investment from the medical community, to consider retirement, rather than continue to practice in the face of increasing insurance costs, especially in that states with high malpractice claims and insurance premiums so called "crisis" states. conclusions and practical advices medical malpractice litigation in spinal surgery is one of the most stressful events of the life of any physician, but also a survivable and surmountable event to made you a stronger and better doctor, indeed, as churchill said “there is only one answer to defeat, the victory”. as a general remark, many claims in spinal surgery are avoidable (62-65); however, to reduce medical malpractice stress, vulnerability to potential litigation, negligence, some advices should be retained: good documentation and patient selection is required; the technique must be adapted both to the patient, to resources and facilities in your hospital; limit your activity, avoiding doing something outside of your expertise; to reduce risk of getting sued it is necessary: never regret to lose effort and time to improve communication skills, communicating openly, explaining the patient to complete carefully the informed consent exposing clearly expectations, desired outcome, also possible complications. in more than 70% of litigations to improve situation, if a complication occurs, it's mandatory to justify in the record, explaining how, why it appeared; 186 gabriel iacob, alexandru vlad ciurea discuss non-surgical option, if necessary, thinking twice and choose without delay a procedure with a lower complication rat; achieve a safe and efficient operation . to increase the odds of a successful defence: keep a good communication with the patients, their relatives; don’t avoid the patients or hide the factsall hidden information it will be found; most patients simply want to know what happened and most important knows you care (4), always remember: “the court is after the proof and not the truth”; demonstrate that what occurred was a complication rather than a deviation from the medical standard; visit the patient more often! – convey empathy, welcome the patient, maintain eye contact, let them tell their story, work to help the patient recover, making him a very strong defendant no attorney wants to put time and money necessary to pursue litigation into a case involving unavoidable complications, rather than negligence; try to keep the patient away from the attorney’s office to pursue the claim against you; in difficult cases, always think to an ancient romanian saying: “it’s better to accept a mutual agreement, instead of a fair judgment”; avoid doing something new that you are not adequately trained for, operating in careless way, also possible conflicts of interest with the insurer; temperate young surgeon’s enthusiasm not a head of their surgical skill; be actively involved in the defense team, discuss your ideas and suggestions with your lawyer but follow their instructions; knowledge is power: support education, training or new techniques at any level & any age, professional support, local medical societies and associations, look for supportive 2-nd opinion from international professional medico-legal committees, seek advice from experienced colleagues, consultants, qualified malpractice lawyers experts, attend supportive educational meetings, enrol in risk management seminars, read available materials on litigation stress support, seek support education, training or new techniques at any level & any age, professional support, local medical societies and associations, look for supportive 2-nd opinion from international professional medico-legal committees. demonstrate that what occurred was a complication rather than a deviation from the medical standard. conflicts of interest the authors of this paper state that they have no conflict of interests to disclosure. abbreviations ct: computer tomography mri magnetic resonance imaging asa; american society of anaesthesiologists’ classification of physical health alara concept: as low as reasonably achievable tep: pulmonary troboembolism et tube: endotracheal tube meps: motor evoked potentials sseps: somatosensory evoked potential nimeclipse: a spinal and cranial neuro monitoring system (medtronic) bmp: human bone morphogenetic protein alif: anterior lumbar interbody fusion plif/tlif: posterior lumbar interbody fusion/thoracolumbar interbody fusion fbss: failed back surgery syndrome pmma: poly methyl methacrylate miss: minimally invasive spine surgery liss: less invasive spine surgery md: micro discectomy tb: tubular discectomy endo-bidua: endoscopic bilateral decompression with a unilateral approach references 1. daniels a.h., ruttiman r. et al. malpractice litigation following spine surgery, journal of neurosurgery spine 2017, 27(4):1-6. 2. eloy ja, svider pf, et al. comparison of plaintiff and defendant expert witness qualification in malpractice litigation in neurological surgery. j neurosurg 2014, 120:185 –190. 3. daniels a.h., ruttima r. et al. -malpractice litigation following spine surgery, journal of neurosurgery spine 2017, 27(4):1-6. 4. iacob g, majer c. – reflections on medical malpractice stress disorders in neurosurgery, romanian neurosurgery 2012, xix 4: 247–250. 5. betsy van die study analyzes how the malpractice environment impacts practicing neurosurgeons, aans communications department, 2008 28, (312) 949-3205. 6. ameen a.a. negligence claims in spinal surgery, 5 years experience – 14th dubai spine conference 2013. 7. depasse j.m., ruttiman r et al. assessment of malpractice claims due to spinal epidural abscess, j. neurosurg. spine 2017, 27(4), 476-480. 187 assessment of malpractice litigation following spine surgery 8. hellesten e.k., handbidge m.e. an economic evaluation of perioperative adverse events associated with spinal surgery, spine j. 2013, 13(1):44-53. 9. ahmed s.a., defroda s. f. , et al. – malpractice litigation following traumatic fracture, j.bone joint surg. am 2019, 3;101(7):e27. 10. rovit r.l., simon a.s. et al. neurosurgical experience with malpractice litigation: an analysis of closed claims against neurosurgeons in new york state, 1999 through 2003, neurosurgery 2007 106(6):1108-1114. 11. hamdan t.a. – perils and pitfalls in cervical spine surgery, 14th dubai spine conference 2013. 12. aebi m. complex spine surgery in the elderly and its pitfalls and complcations, 14th dubai spine conference 2013. 13. msaddi a.k., majer c – minimizing side effects in microdiscectomy, 14th dubai spine conference. 14. bolger c. when things go wrong in spinal surgery, the spectre of the problem, 14th dubai spine conference 2013. 15. patil c., patil t., et al. complications and outcomes after spinal cord tumor resection in the united states from 1993 to 2002, spinal cord 2008, 46, 375–379. 16. samaraeea.al radiation safety in spine surgery, 14th dubai spine conference 2013. 17. zerbi a. radiation exposure in spine surgery (surgeons and patients), 14th dubai spine conference 2013. 18. raoof n. – anesthesia and positioning complications, 14th dubai spine conference 2013. 19. wong d. patient safety in spine surgery, 14th dubai spine conference 2013. 20. devivo m.j., black k.j. causes of death during the first 12 years after spinal cord injury, arch.phys. med. rehabil. 1993, 74 (3); 248-254. 21. soden r.j., walsh j. et al. causes of death after spinal cord injury, spinal cord 2000, 38(10): 604-610. 22. connely n, silverman d.g. – review of clinical anesthesia, lippincott williams & wilkins 2013, ch.4., 17-18. 23. nanda a. complications in neurosurgery, elsevier 2019, 30, e-book. 24. roccamo g., haydon j.h. medicine in the litigation process, carswell, 1999, 395. 25. andrews et al. -. cerebellar herniation and infarction as a complication of an occult postoperative lumbar dural defect, ajnr 1995. 26. sciubba,et al. acute intracranial subdural hematoma following a lumbar csf leak caused by spine surgery, spine (phila pa 1976). 2005 dec 15;30(24):e730-2. 27. wong et al. dural tears secondary to operations on the lumbar spine: management and results, j bone joint surgery1998, 1728-1732. 28. stadler j.a., wong a.p. et al. complications associated with posterior approaches in minimally invasive spine decompression, neurosurg. clin n.am 2014, 25(2):233245. 29. haid r, branch c posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. spine j 2004;4:527-539. 30. sokolowski m.j., garvey t.a, et al. – prospective study of postoperative lumbar epidural hematoma, incidence and risk factors, spine 2008, 33,108-113. 31. abumi k. et al. complication of pedicle screws fixation in reconstructive surgery of cervical spine, spine 2000, 25(8), 962-969. 32. fessler r. et al. breach rate of percutaneous lumbar pedicle screws using fluoroscopic guidance, 14th dubai spine conference 2013. 33. alfawareh m. safety and complication avoidance in cervical spine tumors surgery, 14th dubai spine conference 2013. 34. iacob g. the failed back surgery syndrome archives of the balkan medical union, march 2009, vol. 44, 1, 51-55 35. iacob g. the failed back surgery syndrome, conferinta nationala a asociatiei romane pentru studiul durerii, bucuresti, 26-27 octombrie 2017. 36. sagi h.c., yuan a.y. – vertebroplasty and kyphoplasty in the treatment of osteoporotic vertebral compression fractures, in haher t.r, merola a.a.surgical techniques for the spine, thieme, 2003, ch.16, 79-85. 37. szpalski m. does size matter ? what is the evidence for miss, 14th dubai spine conference 2013. 38. jaikumar, s. et al. minimally invasive surgery of the spine: history of minimally invasive spine surgery, neurosurgery 2002, 51, 5, s2,1-s2-14. 39. fessler r. g. – mininally invasive spine surgery, neurosurgery, 2002, 51,2, s2-iv. 40. rosen ds, ferguson sd, et al. obesity and self-reported outcome after minimally invasive lumbapinal fusion surgery. neurosurgery 2008, 63, 956–960. 41. knight rq et al. direct lateral lumbar interbody fusion for degenerative conditions: early complication profile. j spinal disord tech 2009, 22,34–37. 42. gorek et al. minimally invasive surgery of the spine: less is more. semin spine surg 2013:23:2-8. 43. bolger c – minimally invasive spinal surgery, is it worth the effort ? 14th dubai spine conference2013. 44. smith z.a., fessler r.g. paradigm changes in spine surgery—evolution of minimally invasive techniques, nature reviews neurology 2012, 8, 443-450. 45. park y et al. the effect of a radiographic solid fusion on clinical outcomes after minimally invasive transforaminal lumbar interbody fusion. spine j. 2011,11(3),:205-212. 46. raco a. – miss procedures, advantages and limitations, 13th dubai spine conference 2013. 47. ikuta k., tono o. surgical complications of microendoscopic procedures for lumbar spinal stenosis, minim invasive neurosurg. 2007, 50(3), 145-149. 48. bindal rk et al.surgeon and patient radiation exposure in minimally invasive transforaminal lumbar interbody fusion. j neurosurg spine, 2008 ,9(6),570-573. 49. ritz jp. mis and the econimics of it. can mis be cost efficent from a bussiness point of view?, chirurg. 2007, 78(6), 501-504, 506-510. 50. van den akker me et al. – tubular diskectomy vs 188 gabriel iacob, alexandru vlad ciurea conventional micro diskectomy for the treatment of lumbar disk-related sciatica: cost utility analysis along side a double-blind randomized controlled trial, neurosurgery 2011;69:829-35. 51. hamid n. a. safety and limitations of mis in lumbar spine surgery 14th dubai spine conference 2013. 52. bhatia p.s., chhabra h.s. et al. microdiscectomy or tubular discectomy: is any of them a better option for management of lumbar disc prolapse, j craniovertebr junction spine 2016, jul-sep; 7(3): 146–152. 53. arts m.p., brand r. et al. tubular diskectomy vs conventional microdiskectomy for the treatment of lumbar disk herniation: 2-year results of a double-blind randomized controlled trial, neurosurgery 2011 jul;69(1):135-144. 54. celik s.e. et al. – microdecompressive laminotomy with a 5-year follow-up period for severe lumbar spinal stenosis j spinal disord tech, 2010. 55. komatsu j., muta t. et al. tubular surgery with the assistance of endoscopic surgery via a paramedian or midline approach for lumbar spinal canal stenosis at the l4/5 level, journal of orthopaedic surgery 2018, 26(2), 1– 8. 56. rosen d.s., ferguson s.d. et al. obesity and selfreported outcome after minimally invasive lumbapinal fusion surgery, neurosurgery 2008, 63, 956–960. 57. knight r.q. et al direct lateral lumbar interbody fusion for degenerative conditions: early complication profile, j spinal disord tech 2009, 22, 34–37. 58. wang j zhou y. et al. comparison of one-level minimally invasive and open transforaminal lumbar interbody fusion in degenerative and isthmic spondylolisthesis grades 1 and 2, eur spine j 2010, 19, 1780-1784. 59. makhni m.c., park p.j.et al. the medico-legal landscape of spine surgery: how do surgeons fare?, spine j.2018, feb;18(2), 209-215. 60. eastlack rk, srinivas r, et al. early and late reoperation rates with various mis techniques for adult spinal deformity correction, global spine j., 2019;9(1):41-47. 61. lekovic g.p., harrington t.r. – litigation of missed cervical spine injuries in patients presenting with blunt traumatic injury, neurosurgery 2007, 60:516–523. 62. fager c.a. malpractice issues in neurological surgery, surgical neurology 2006, 65(4): 416-421. 63. steele l., mukherjee s. et al. extent of medicolegal burden in neurosurgery an analysis of the national health service litigation authority database, br j neurosurg, 2015;29(5):622-629. 64. hamdan a, strachan rd et al. counting the cost of negligence in neurosurgery: lessons to be learned from 10 years of claims in the nhs, br j neurosurg, 2015; 29(2):169-177. 65. banna se, catano a. complications of spine surgery and litigations – managing malpractice risk. j clinexporthop. 2015, 1:3. doi: 10.4172/2471-8416.100003. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 492-497 doi: 10.33962/roneuro-2019-079 www.journals.lapub.co.uk/index.php/roneurosurgery transzygomatic anterior infratemporal fossa approach and high cervical approach for resection of infra temporal fossa and parapharyngeal space solitary fibrous tumours. report of 2 cases and review of literature kazumi ohmori1, shiduka kamiyoshi1, taku takeuchi1, takanori fukushima2, takashi tsuduki3, toshika arita3 1 nishinomiya watanabe cardiovascular center, japan 2 duke university, usa 3 yao municipal hospital, japan abstract the infratemporal fossa (itf) is the region under the floor of the middle fossa giving passage to most major cerebral vessels and cranial nerves.(1) it is closely related to important adjacent regions such as the middle fossa, pterygopalatine fossa, orbit, and nasopharynx.(2) due to the anatomical complexity in the itf, surgical removal of the lesions in or around it is still challenging.(3) since the 1960s, many surgeons have reported various surgical approaches. the preauricular transzygomatic approach via a transcranial route was reported to be used for exposure of the antero-superior portion of the itf (2,3). solitary fibrous tumours (sfts) were first described by klempere and rabin in 1931 as spindle-cell tumours originating from the pleura.(4) with the exception of myopericytoma, infantile myofibromatosis and hpc-like lesions of the sinonasal tract showing myoid differentiation, all other hpc like lesions are best considered as subtypes of sft.(5) only a few cases of sft have been described in the literature involving the skull base and parapharyngeal space.(6–8) the purpose of this article is to show anatomical dissections involving this surgical approach and to evaluate our surgical experience using it. first case 45 yr old female presented with swelling over left cheek without any neurological deficit. mri revealed left middle cranial fossa base lesion extending into infratemporal fossa. patient underwent surgery by left anterior infratemporal fossa approach and gross total excision of lesion. postoperatively patient developed left v3 dysesthesia, which improved over a period of one month. biopsysolitary fibrous tumor keywords transzygomatic, anterior infratemporal fossa, resection, parapharyngeal space, solitary fibrous tumours corresponding author: ahmed ansari nishinomiya watanabe cardiovascular center, japan ahmed.ansari2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 493 transzygomatic anterior infratemporal fossa approach and high cervical approach figure 1: mri images showing infratemporal fossa tumor with extension into middle cranial fossa. 494 kazumi ohmori, shiduka kamiyoshi, takanori fukushima et al. figure 2: (a-f). a) frontotemporal craniotomy with elevation of zygomatic arch. 495 transzygomatic anterior infratemporal fossa approach and high cervical approach second case 38-year-old male presented with left infra auricular swelling without any neurological deficit. mri revealed left parapharyngeal space tumor. patient underwent surgery by high cervical approach and gross total excision of tumor. biopsy – solitary fibrous tumor. 496 kazumi ohmori, shiduka kamiyoshi, takanori fukushima et al. discussion most cases of soft tissue sfts occur in the early fifth decade of life.(9). its occurrence is less than 2% of all soft tissue tumours.(9) a study conducted by demicco et al of 110 cases found about 32% to be in the abdomen/pelvis, 32% to be pleural, 16% in the extremities, 12% in the trunk, and 12% in the head and neck.(10) skull base sfts may include a wide variety of symptoms, although they are usually asymptomatic 497 transzygomatic anterior infratemporal fossa approach and high cervical approach on presentation.(11) the symptoms manifest most frequently as a slowly expanding painless mass. sfts from any site are usually benign and surgical resection alone is curative.(12,13) the presence of infiltrative margins with surrounding tissues, high mitotic count (≥4 mitoses per 10 high-power high fields) of cellular pleomorphism and tumour necrosis also suggests malignancy.(9,12) the main treatment is surgical for benign and malignant sfts. but when histopathology suggests malignancy or when there are positive surgical resection margins, radiotherapy must be discussed, as for other sarcomas.(9,14) parapharyngeal space tumours are a rare neoplasm, comprising less than 0.5–1% of tumours of the head and neck. sft is very uncommon but should be part of the differential diagnosis in patients with a skull base lesion. diagnosis is difficult but pathologists should be aware of the classical finding of this disease consisting of spindled cells in a disorganized pattern, with alternating hypocellular and hypercellular areas separated by hyalinized collagen. immunophenotyping staining positive for the presence of cd34 and bcl-2 can be useful. most important prognostic factor in patients with solitary fibrous tumour is completeness of resection. the pioneers of the itf were conley [6] and barbosa [3]. a variety of surgical approaches to the itf have been developed. variations include anterior (transfacial, transmaxillary, transoral, and transpalatal), lateral (transzygomatic and lateral infratemporal), or inferior (transmandibular and transcervical) approaches. fukushima et al. developed a classification of itf approaches into three types: anterior, middle, and posterior itf approaches. transcervical approach for parapharyngeal space is the easiest approach for resection of these tumors.(15). references 1. bejjani gk, sullivan b, salas-lopez e, abello j, wright dc, jurjus a, et al. surgical anatomy of the infratemporal fossa: the styloid diaphragm revisited. neurosurgery. 1998 oct;43(4):842–52; discussion 852-853. 2. fukushima t, nonaka y. fukushima manual of skull base dissection. raleigh, nc: af-neuro video; 2010. 3. yoshida k, kawase t, tomita t, ogawa k, kawana h, yago k, et al. surgical strategy for tumors located in or extending from the intracranial space to the infratemporal fossaadvantages of the transcranial approach (zygomatic infratemporal fossa approach) and the indications for a combined transcranial and transcervical approach-. neurol med chir (tokyo). 2009 dec;49(12):580–6. 4. klemperer p, coleman br. primary neoplasms of the pleura. a report of five cases. am j ind med. 1992;22(1):1– 31. 5. gengler c, guillou l. solitary fibrous tumour and haemangiopericytoma: evolution of a concept. histopathology. 2006 jan;48(1):63–74. 6. ransom er, judy kd, bigelow dc. concurrent cochlear implantation with resection of skull base hemangiopericytoma following sudden deafness in an only hearing ear. skull base off j north am skull base soc al. 2010 jul;20(4):279–84. 7. zeitler dm, kanowitz sj, har-el g. malignant solitary fibrous tumor of the nasal cavity. skull base. 2007 jul;17(4):239– 46. 8. lee je, hong hs, chang k-h, kim hk, park j. solitary fibrous tumor of the post-styloid parapharyngeal space. acta radiol short rep [internet]. 2014 jul 26 [cited 2019 aug 18];3(6). available from: https://www.ncbi.nlm.nih.gov/pmc/articles/pmc4184415/ 9. penel n, amela ey, decanter g, robin y-m, marec-berard p. solitary fibrous tumors and so-called hemangiopericytoma. sarcoma. 2012;2012:690251. 10. demicco eg, park ms, araujo dm, fox ps, bassett rl, pollock re, et al. solitary fibrous tumor: a clinicopathological study of 110 cases and proposed risk assessment model. mod pathol off j u s can acad pathol inc. 2012 sep;25(9):1298–306. 11. wignall oj, moskovic ec, thway k, thomas jm. solitary fibrous tumors of the soft tissues: review of the imaging and clinical features with histopathologic correlation. ajr am j roentgenol. 2010 jul;195(1):w55-62. 12. gold js, antonescu cr, hajdu c, ferrone cr, hussain m, lewis jj, et al. clinicopathologic correlates of solitary fibrous tumors. cancer. 2002 feb 15;94(4):1057–68. 13. suster s, nascimento ag, miettinen m, sickel jz, moran ca. solitary fibrous tumors of soft tissue. a clinicopathologic and immunohistochemical study of 12 cases. am j surg pathol. 1995 nov;19(11):1257–66. 14. bowe sn, wakely pe, ozer e. head and neck solitary fibrous tumors: diagnostic and therapeutic challenges. the laryngoscope. 2012 aug;122(8):1748–55. 15. khafif v, segev y, kaplan dm, gil z, fliss dm. urgical management of parapharyngeal space tumors : 10-year review. in. romanian neurosurgery (2019) xxxiii (3): pp. 277-282 doi: 10.33962/roneuro-2019-046 www.journals.lapub.co.uk/index.php/roneurosurgery 3d patient specific implants for cranioplasty. a multicentre study a. ladaru1, h. moisa2, a.v. ciurea3 1 “carol davila” university of medicine and pharmacy, bucharest, romania 2 department of neurosurgery, university emergency clinical hospital, bucharest, romania 3 department of neurosurgery, sanador clinic hospital, bucharest, romania abstract this article presents a multi-centre study cohort study on 50 patients with cranial defects of multiple etiologies (trauma, decompression, tumour surgery, etc.) operated in 10 hospitals. in all patients the neurosurgeon repaired the cranial defect using 3d printed and cnc milling and drilling grafts or patient specific implants, from two world known manufacturers, custom made in accordance with the data obtained from the patient’s 3d ct reconstruction. introduction cranioplasty is defined as the surgical intervention performed to repair cranial defects following trauma, surgical decompression, tumour surgery, congenital anomalies or growing skull fractures. the implications of cranioplasty are psychological, aesthetic and functional. the history of cranioplasty dates back to 7000 bc. with archeologic evidence ( 1, 2) supporting the use of both inorganic and organic materials. although many methods have been described there is little consensus regarding the optimal solution for such cases. materials and methods we started a multicentre cohort study on patients with cranial defects of multiple etiologies (trauma, decompression, tumour surgery, etc.) operated in 10 hospitals having enrolled in study a total of 50 patient from which 16 were female 34 were male, 22 from urban , 28 from rural area of romania, age between 5-68 years old. regarding etiologies: 31 were trauma, 16 were decompression and 3 were tumour. in all patients during the surgery were repaired the cranial defects using patient specific implants made by 3d printing and cad cam manufacturing (cnc milling and drilling) methods using specific data obtained from the patient’s 3d ct reconstruction using a very clear scanning protocol. keywords 3d printing, cnc milling and drilling, cranioplasty, peek, titanium, bioverit, trauma, tumour, decompression, neurosurgery, reconstruction, patient specific implant corresponding author: a. ladaru “carol davila” university of medicine and pharmacy, bucharest, romania alin.ladaru@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 278 a. ladaru, h. moisa, a.v. ciurea figure 1. ct scan protocol used to create specific data to be converted in a 3d dynamic precise model. centres and hospitals involved in this study were as follows: 1. sanador clinic hospital, 2. emergency hospital “ bagdasar arseni” , 3. emergency clinical hospital “ floreasca”, 4. university emergency clinical hospital, 5. “ m.s. curie” clinical emergency hospital for children, 6. “grigore alexandrescu“ emergency hospital for children ,7. medlife metropolitan hospital, 8. elias emergency university hospital, 9. “sf.pantelimon” emergency hospital, bucharest, romania and “prof. dr. nicolae oblu” emergency clinic hospital, iasi, romania. the follow up varies from 1 to 9 years. materials used for implants: peek, titanium alloy and bioverit (ceramic glass). distribution of implant materials from our study was: 45 cases with peek, 4 cases with titanium alloy, 1 case with bioverit. procedure: in almost all cases, the procedure is the same. dicom data files are collected and archived into a zip file and sent encrypted, through a secure transfer platform, with a dynamic password, that has to be communicated each time, to recipients and that is internet safe and keeps all info strictly confidential. files are extracted, verified if scanning protocol was respected and if they are qualified to be transformed in “.stl” extension files or other software extension used to see bone defect, compare it with standard anatomic models, with contra-lateral side of the same patient and create a 3d dynamic model of cranium with all defects and of patient specific implant that has to fit perfectly into that defect. the 3d model (pdf file with 3d media option activated) is sent and presented by manufacturer directly to the surgeon with several comments regarding: surrounding soft tissue, sizes, distances, thickness and a lot of other parameters, including material together with an approval letter that has to be stamped and signed by the surgeon. the surgeon will reply (in written) to the manufacturer with its comments regarding all of the above and in some steps will conclude if he agrees or not, on the proposed 3d model. if the response is affirmative and all legal and financial issues are agreed upon by all parts, the manufacturer will start to produce the implant, respecting all safety and regulations of eu, regarding patient specific implants. that will be delivered in the country of the surgeon, directly to its hospital or during a period of 5-15 days. in some emergency cases, the implant can be delivered within 48 hours, with a set of legal documents and a passport for the implant; the passport contains all of the important info that patient has to have, after surgery. if the implant came unsterile and very well packaged, it will be sterilized to 134 °, 1-2 cicles 20 minutes, 24-48 hours prior the day of surgery. depending on the size of bone defect, anatomical area, position on cranium and risk of infection (frontal, sinus, zygomatic area) the surgeon will decide upon the best material for the implant (titanium alloy, peek or ceramic glass) and what fixation systems are best for the implant. the most common and used materials are: non-resorbable 279 3d patient specific implants for cranioplasty suture 2.0, titanium, peek or bio-resorbable craniofix type implants that use a special tool for anchoring and fixation, titanium 2-4-6 holes plate 1.3/1.6/2.0 mm and 1.3/1.6/2.0 mm, different designs (straight, double-y plate, adjustable mesh or pre-contoured) screws locking or non-locking 3-5 mm length. a b c figure 2. (a) suture; (b) titanium or resorbable craniofix fixation type system; (c) plates; mesh different designs and screws (11) case report female, 23 years old. event that caused trauma: car accident 28.11.2018; at the time of the arrival at the clinical emergency hospital, the patient had intracranial pressure with a peak of 80 mmhg (standard values: 20 mmhg) glasgow score 3 (gcs) state of coma; procedure: the surgeon opted for cranial resection with dural plasty (optional: can be done with artificial dura); observation: cerebral edema post-trauma malign, with progressive values 32-46-62-80 mmhg in spite of conservative treatment; secondary, a large craniectomy ftpo (fontaltemporal-parietal-occipital) and dural plasty with temporal muscle and periosteum is performed. the craniectomy was performed in the 3rd day after the car accident; the cranioplasty surgery was performed in 14.01.2019 (47 days after car accident and 44 days after craniectomy), that means a short term cranioplasty. a b c figure 3. (a, b, c): ct scan images done respecting above scanning protocol. ct dicom files are sent, analysed by the manufacturer and result is a 3d model that is sent directly to the surgeon for discussion and legal approval. there are cases when ct dicom files are rejected, because they are not done as required by the protocol and they are not accurate enough and cannot be used for 3d model and also for implant construction. 280 a. ladaru, h. moisa, a.v. ciurea a b c d e f g h figure 4. presentation for surgeon of a 3d model proposed by manufacturer using adobe acrobat 3d pdf. file where model can be visualized dynamic, 3d in motion. are presented screenshots as follows: (a) right view with implant; (b) proposed model of implant; (c) left view; (d) frontal view with implant into defect; (e) right view without implant; (f) below view; (g) rear view with implant; (h) above view with implant in place. 281 3d patient specific implants for cranioplasty a team of specialists in cranial reconstruction communicate to the surgeon (in writing): any possible complications, details regarding sizes of implants, remaining bone, distances and surrounding soft tissues, options for manufacturing materials, fixation systems (titanium alloy, peek, bioverit – ceramic glass) (9,10) to help him take the most efficient decision. (figure 4) a b figure 5. observation of small islands of ossification are sent in attention of surgeon. (a) large right view; (b) right detailed view. the surgeon requested that the implant had to be made from peek –optima®( polyether-ether –ketone) as being optimal (weight, strength, hardness) in case he needs to make small adjustments intra-op; he also requested suture holes, each 1 cm on implant margin, assuming that the fixation systems could be suture and craniofix type systems. (figure 3, 4) a b figure 6. above view of patient specific implant made from peek in protective case; (b) inferior image of implant the method of implant manufacturing: cad cam manufacturing (cnc milling and drilling) from an initial reclangular block of peek. the final volume of implant was 548 cm3. in the case presented above, for fixation of the implant, non-resorbable sutures were used and small drills of 1-2 mm on perimeter of cranial defect at equal distances were performed, in order to allow the insertion of titanium craniofix type fixation system ( with a 20mm diameter). the patient received its own passport of implant (with all the important details in it: data of production and surgery, surgeon details, sizes in mm ad weight & material of implant). (figure 6) 282 a. ladaru, h. moisa, a.v. ciurea results and discussion in the presented case, the cranioplasty surgery was performed with a patient specific implant from peek, respecting all sizes and anatomy of the patient; the implant fitted perfect into the defect and the surgery was shorter (with about 1-2 hours) because the cranioplasty solution was already created beforehand for that specific patient and implemented in only 1 step; there were no complications after the surgery and a visible aesthetic result for a female patient. regarding the general study: there were a total of 50 patients treated with patient specific implant that proved significant aesthetic, functional and psychological improvements after the cranioplasty surgery. minor complications occurred in several cases, that were related to cranioplasty fixation systems and scalp complications (related to initial trauma), and two cases of wound infection (one related to the type of suture used and the other wound contamination without suture defect). there were no fatalities and no long-term complications. conclusion • custom 3d implants for cranial reconstruction are a safe and viable solution that has been available for some time; • superior aesthetics and good functional outcomes can be achieved with a 3d patient specific implant (where other common methods fail: cement, pmma broken implants, etc.); • a patient specific implant is made 1 time for 1 single patient and involves multiple parties, each with their own responsibilities: the patient ant his family, the surgeon, the hospital, the manufacturer, the project manager; • our study proves the fact that this method can be safely implemented even in surgical centres with no prior experience, using 3d custom made implants; • nevertheless, the financial aspect of using such an implant is the main factor that negatively influences the addressability of such a technique to the general public. at this time patient specific implants in romania are paid by patients and are expensive, but very reliable and effective at the same time; • we can appreciate that the number of cranioplasty cases done with psi (patient specific implants) would be 10 times more in romania , if a national program for neurosurgery would cover the costs of such implants; • this method would also increase the economy of the ministry of health’s budgets, due to a reduced period of post-op recovery and minimal rate of reinterventions and complications. references 1. shah am, jung h, skirboll s. materials used in cranioplasty: a history and analysis. neurosurg focus 2014;36(4):e19. 2. aciduman a, belen d: the earliest document regarding the history of cranioplasty from the ottoman era. surg neurol 68:349–353, 2007. 3. mohammed e. elsalanty, david g. genecov, bone grafts in craniofacial surgery, craniomaxillofac trauma reconstr. 2009 oct; 2(3): 125–134. republicat 2009 apr 14. doi: 10.1055/s-0029-1215875. 4. aydin s, kucukyuruk b, abuzayed b, aydin s, sanus gz: cranioplasty: review of materials and techniques. j neurosci rural pract 2:162–167, 2011. 5. oliveira amp. efeitos da cranioplastia em doentes submetidos à craniectomia descompressiva: avaliação anatômica, neurológica e da hemodinâmica encefálica [thesis]. são paulo: faculdade de medicina da universidade de são paulo; 2015. 6. j. jonkergouw, s.e.c.m. van de vijfeijken, e. nout, t. theys, e. van de casteele, h. folkersma, p.r.a.m. depauw, a.g. becking, outcome in patient-specific peek cranioplasty: a two-center cohort study of 40 implants, journal of craniomaxillofacial surgery 44(9) ·july 2016 doi: 10.1016/j.jcms.2016.07.005. 7. haug rh, adams jm, conforti pj, et al., cranial fractures associated with facial fractures, j oral maxillofac surg, 1994; 52(7):729-33. 8. rish bl, dillon jd, meirowsky am, caveness wf, mohr jp, kistler jp, et al. cranioplasty: a review of 1030 cases of penetrating head injury. neurosurgery. 1979;4:381–5. 9. blake dp. the use of synthetics in cranioplasty: a clinical review. mil med. 1994;159:466–9. 10. grant fc, norcross nc. repair of cranial defects by cranioplasty. ann surg110:488-512, 1939. 11. aesculap (brochure no. c08802 0714/0.5/3), aesculap craniofix® 2, cranial fixation system. doi: 10.33962/roneuro-2022-084 deep motor cortex cavernoma resection supported by navigational intraoperative monitoring. a case report alkawthar m. abdulsada, zahraa m. kareem, haneen a. salih, hagar a. algburi, mustafa ismail, samer s. hoz romanian neurosurgery (2022) xxxvi (4): pp. 465-469 doi: 10.33962/roneuro-2022-084 www.journals.lapub.co.uk/index.php/roneurosurgery deep motor cortex cavernoma resection supported by navigational intraoperative monitoring. a case report alkawthar m. abdulsada1, zahraa m. kareem2, haneen a. salih3, hagar a. algburi2, mustafa ismail2, samer s. hoz4 1 azerbaijan medical university. baku, azerbaijan 2 college of medicine, university of baghdad. baghdad, iraq 3 biology department, college of science, university of mustansiriyah, baghdad, iraq 4 department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa abstract introduction: cavernomas are benign hamartomas of cerebral and spinal vessels, accounting for less than 1% of all arteriovenous malformations. in general, surgical resection is the treatment of choice for enlarging cavernomas or those associated with medically refractory seizures. herein, we report a case of an enlarged deep precentral gyrus cavernoma, with a discussion of the surgical approach and the impact of intra-operative neurophysiological monitoring on the preservation of motor function. case description: a 30-year-old male was referred to our hospital due to 2-month history of focal seizures. initial magnetic resonance imaging revealed right precentral cavernoma with minimal right parietal subarachnoid haemorrhage. revealed the location of the cavernoma deep in the right primary motor cortex. surgery was performed, trans-sulcal dissection was done with the aid of intraoperative ultrasonography neuro-navigation. the cortical motor map was localized by functional mapping with intra-operative neurophysiological monitoring, including somatosensory evoked potentials (sep) and motor evoked potentials (mep). postoperatively, the left side weakness grade was 4/5, and the glasgow coma scale was 15. postoperative imaging confirmed successful resection of the cavernoma and associated hemosiderin ring with no sah. conclusion: the use of preoperative mri and intraoperative ultrasonography supplemented by neurophysiological monitoring utilizing sep, mep, and cortical mapping is essential for the safe resection of paracentral cavernomas. introduction cavernomas are benign hamartoma of cerebral and spinal vessels. its prevalence ranges from 0.1% to 0.8% in the recent literature, ac c o u n tin g fo r 8 15% o f c er e br al an d s pin a l a rte rio v en o u s keywords trans-sulcal approach, ultrasonography neuronavigation, intra-operative neurophysiological monitoring, cortical motor map, motor cortex cavernoma corresponding author: samer s. hoz department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 466 alkawthar m. abdulsada, zahraa m. kareem, haneen a. salih et al. malformations. their formation is related to gene mutations such as ccm1, ccm2, and ccm3, which can occur in hereditary and sporadic forms [5]. they commonly comprise different presentation hemorrhages and calcifications according to age [6]. intracerebral hemorrhage occurs in 30% of cases as the initial complication, leading to the frequently encountered presentation, seizures, and other neurological deficits [2,9]. cavernomas can be managed conservatively; surgical resection is the treatment of choice for enlarging cavernomas or those associated with medically refractory seizures [7]. paracentral cavernomas are quite challenging cerebrovascular pathological entities owing to the prospects of their surgical resection without adversely affecting the eloquent areas around the central sulcus. particularly in deep and subcortical cavernomas, wherein it is demanding to localize and excise. following dissection, immediate impairment in sensory and motor activity may ensue. as such, direct electrical cortical stimulation (des) for cortical somatosensory and motor mapping is an integral part of surgeries with such lesions to preserve function [12,13]. herein, we report a case of a 30-year-old male who suffered from a 2-month history of focal seizures caused by an enlarged deep precentral gyrus cavernoma. we discuss the surgical approach and the impact of intra-operative neurophysiological monitoring on the preservation of motor function. case scenario a 30-year-old male was referred to our hospital due to 2-month history of focal seizures. initial magnetic resonance imaging (mri) revealed right precentral cavernoma with minimal right parietal subarachnoid haemorrhage (sah). the patient was advised to take a single session of stereotactic radiosurgery, but the lesion increased in size in spite. figure 1. a: preoperative sagittal t2weighted mri, reveals the location of the cavernoma deep to the precentral gyrus (primary motor cortex). b: pre-operative axial mra, views the relation between the cavernoma and the cerebral vasculature pre-operative mri (fig.1) revealed the location of the cavernoma deep in the right primary motor cortex. surgery was performed, trans-sulcal dissection was done with the aid of intraoperative ultrasonography neuro-navigation (fig.2). the cortical motor map was localized by functional mapping with intra-operative neurophysiological monitoring (ionm), including somatosensory evoked potentials (sep) and motor evoked potentials (mep). as the lesion was deep to the precentral gyrus, des – bipolar mode (fig.3) identified the face motor area. the area with the lesser corresponding facial motor activity was chosen to start trans-sulcal dissection. complete resection of the cavernoma with the surrounding epileptogenic hemosiderin ring was achieved with preservation of the eloquent motor area. figure 2. intra-operative ultrasonography neuro-navigation showing the exact localization of deep motor cortex cavernoma. post-operatively, the patient had a seizure due to des during neuro-navigation and left side weakness grade 4/5, which improved gradually 3 hours later. glasgow coma scale was 15 (e4v5m6. a postoperative ct scan (fig.4) confirmed successful 467 deep motor cortex cavernoma resection supported by navigational intraoperative monitoring resection of the cavernoma and associated hemosiderin ring with no sah. figure 3. intra-operative image through the right parietal approach, supine position, direct cortical stimulation – (penfield method) bipolar mode for motor mapping. figure 4. postoperative axial ct scan, showing the complete resection of the cavernoma discussion paracentral cavernomas signify a significant challenge to the neurosurgeon, owing to the high risk of complications following its excision, especially in deep and small subcortical lesions, as it involves eloquent areas. microsurgical operation for symptomatic cavernoma is the management of choice to reduce the frequency of seizures and alleviate the mass effect. but the risk of bleeding, and severe neurological deficits, make this decision difficult. surgical removal can result in abrupt cortical damage and consequent sensory and motor function deterioration. therefore, it is crucial to precisely recognize the anatomical landmarks preoperatively and intraoperatively to preserve vital structures, which can be achieved by the appropriate application of neurophysiological monitoring. in this report, successful removal of precentral cavernoma was accomplished through four vital components; meticulous identification of the lesion, accurate evaluation of motor function, minimally invasive trans-sulcal dissection, and optimal removal of the lesion with the surrounding hemosiderin tissue. epileptic seizures represent the most periodic symptom of patients with cavernoma. deep cavernomas have a higher risk of hemorrhage than superficial ones, the blood by-products like iron precipitate in the vicinity of the lesion as hemosiderin stain ring with high epileptogenic latency. this makes the complete removal of the lesion insufficient for patients with epileptic seizures unless the stained tissue is excised. however, the intraoperative surgical decision depends on accounting for all possible complications and postoperative outcomes considering the eloquent area preservation a priority [8]. the trans-sulcal dissection is a harmless and applicable approach to target deep-seated cerebral lesions. it provides pursuing the natural aisles of the brain, the sulci, to obtain better exposure to the lesion and enough dissection depth. dispensing brain retraction by dissecting the normal brain pathways is safer for gyral layers and confers motor function preservation. no serious complications of the trans-sulcal approach are reported especially with pre-operative mri, ionm, intraoperative neuronavigation, and brain mapping [3]. pre-operative ct scan demonstrates a typical hyperdense lesion in the right motor cortex and precentral gyrus around the omega sign of the central sulcus. mri revealed a focal heterogeneous hyperintensity area deep in the right parietal lobe with a low signal intensity peripheral ring indicating a bleeding episode. intraoperatively, exact localization was confirmed by intraoperative ultrasonography neuro-navigation; this assisted image guidance is believed to decrease morbidity. it can overcome intraoperative cerebrospinal fluid loss and cortical shifting, improving the neuro-navigation accuracy [10,11]. proposed direct cortical stimulation by a bipolar handheld probe (penfield method) with 468 alkawthar m. abdulsada, zahraa m. kareem, haneen a. salih et al. a setting of 50 hz frequency, 5-10 ma current intensity, and 0.3-1 msec pulse duration. cortical motor mapping was achieved by defining the central sulcus, stimulating the precentral gyrus, and localization of the primary motor cortex (brodmann area 4) [1]. the area with the lowest face motor function was chosen to start the dissection. pavia et al. reported that the complementary use of cortical motor mapping by des and neuronavigation are the gold standards in deep lesions resection [8]. after using intraoperative ultrasonography neuro-navigation to visualize the position of the cavernoma, trans-sulcal dissection started by separating cortical vessels and dissecting through the central sulcus – peri omega sign of the right frontal lobe reaching 3 cm trans-sulcal depth (fig. 5) [4]. gross excision of the cavernoma with the associated epileptogenic hemosiderin ring was achieved. ionm confirmed intact limb movement after recording multiple responses from abductor pollicis brevis in the upper limbs and abductor hallucis in the lower limbs. postoperative assessment of functional impairment was calculated by the karnofsky performance status scale (100 scores). postoperative observation at the intensive care unit for 24 hours and routine postoperative ct with regular follow-up was done. figure 5. intra-operative image shows the depth of the transsulcal dissection the supplementary use of preoperative mri and intraoperative ultrasonography and ionm using sep, mep, and cortical mapping is crucial to ensure safe excision of the lesion with preservation of the eloquent area. a trans-sulcal approach based on anatomical and neurophysiological data can provide safe and minimally invasive dissection for removing deep paracentral lesions with the surrounding hemosiderin tissue. conclusion in this report, complimentary preoperative mri and intraoperative ultrasonography supplemented by neurophysiological monitoring using sep, mep, and cortical mapping is essential for precise identification of paracentral cavernomas, to discern ominous signs, and to avoid traumatizing the eloquent area. references 1. al-shahi salman r, berg mj, morrison l, awad ia. hemorrhage from cavernous malformations of the brain: definition and reporting standards. stroke. 2008 dec 1;39(12):3222-30. 2. awad i, jabbour p. cerebral cavernous malformations and epilepsy. neurosurgical focus. 2006 jul 1;21(1):1-9. 3. farid am, elkholy ar, shamhoot ea. trans-sulcal or fissure approach for supratentorial brain lesions: evaluation. egyptian journal of neurosurgery. 2019 dec;34(1):1-6. 4. jahangiri fr, dobariya a, kruse a, kalyta o, moorman jd. mapping of the motor cortex. cureus. 2020 sep;12(9). 5. jain d, broduhn m, rosahl s, rosahl sk. de novo cavernoma in the sensory cortex causing cervicobrachialgia. 6. kunz u, goldmann a, bader c, oldenkott p. stereotactic and ultrasound guided minimal invasive surgery of subcortical cavernomas. min-minimally invasive neurosurgery. 1994 sep;37(01):17-20. 7. menzler k, chen x, thiel p, iwinska-zelder j, miller d, reuss a, hamer hm, reis j, pagenstecher a, knake s, bertalanffy h. epileptogenicity of cavernomas depends on (archi-) cortical localization. neurosurgery. 2010 oct 1;67(4):918-24. 8. paiva ws, fonoff et, marcolin ma, bor-seng-shu e, figueiredo eg, teixeira mj. navigated transcranial magnetic stimulation in preoperative planning for the treatment of motor area cavernous angiomas. neuropsychiatric disease and treatment. 2013;9:1885. 9. robinson jr, awad ia, barrow dl. clinical spectrum and natural course. cavernous malformations: american association of neurological surgeons, publications committee. 1993:25-36. 10. spetzger u, laborde g, gilsbach jm. frameless 469 deep motor cortex cavernoma resection supported by navigational intraoperative monitoring neuronavigation in modern neurosurgery. minminimally invasive neurosurgery. 1995 dec;38(04):163-6. 11. willems pw, van der sprenkel jb, tulleken ca, viergever ma, taphoorn mj. neuronavigation and surgery of intracerebral tumours. journal of neurology. 2006 sep;253(9):1123-36. 12. yeole u, gohil d, shukla d, bhardawaj s. removal of perirolandic cavernoma with direct cortical stimulation and neuronavigation with dti. neurology india. 2021 mar 1;69(2):304. 13. zhou h, miller d, schulte dm, benes l, rosenow f, bertalanffy h, sure u. transsulcal approach supported by navigation-guided neurophysiological monitoring for resection of paracentral cavernomas. clinical neurology and neurosurgery. 2009 jan 1;111(1):69-78. doi: 10.33962/roneuro-2021-008 spontaneous intracerebral haemorrhage as an initial presentation of a choriocarcinoma. a case report maher khashea mustafa, wamedh e. matti, hussain j. kadhum, zahraa a. alsubaihawi, zahraa m. kareem, zahraa f. al-sharshahi, samer s. hoz romanian neurosurgery (2021) xxxv (1): pp. 48-51 doi: 10.33962/roneuro-2021-008 www.journals.lapub.co.uk/index.php/roneurosurgery spontaneous intracerebral haemorrhage as an initial presentation of a choriocarcinoma. a case report maher khashea mustafa1, wamedh e. matti2, hussain j. kadhum2, zahraa a. alsubaihawi3, zahraa m. kareem3, zahraa f. al-sharshahi2, samer s. hoz2 1 department of neurosurgery, fallujah teaching hospital, anbar, iraq 2 department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 3 medical student, college of medicine, baghdad university, iraq abstract introduction: choriocarcinoma is a rare gestational trophoblastic neoplasm with a high risk of pulmonary, hepatic, and, rarely, cerebral metastasis. we report a rare case of intracerebral haemorrhage as an initial manifestation of metastatic choriocarcinoma. case presentation: a 33-year-old female with a history of multiple abortions, ectopic pregnancy, and complete hydatidiform mole presented with a disturbed level of consciousness. emergency brain computed tomography (ct) scan revealed an intraventricular haemorrhage (ivh) and a left frontoparietal, non-traumatic intracerebral haemorrhage (ich) with a significant midline shift. the patient underwent emergency evacuation of the hematoma and histological evaluation revealed choriocarcinoma. later investigations revealed evidence of systemic metastasis. the patient underwent chemoradiotherapy and recovered well. conclusion: metastatic choriocarcinoma should always be in the differential of nontraumatic intracerebral haemorrhage in a female child-bearing age. also, the pathological diagnosis should always be performed in cases of ich of an unknown source. introduction choriocarcinoma is a gestational trophoblastic disease; it is a rare, malignant tumor of human chorionic tissue (1). choriocarcinomas have an incidence ranging between 3 and 21.4% with a higher incidence in southeast asia. choriocarcinomas may complicate any type of pregnancy, with more than 50% of cases arising from hydatidiform moles (2, 3). choriocarcinoma is an aggressive tumor that frequently metastasizes to the lung, liver, and to a lesser extent to the brain (4,5). cerebral choriocarcinoma typically presents as single or multiple lesions, manifesting as infarction, subarachnoid hemorrhage, oncotic, keywords ich, brain metastasis, choriocarcinoma corresponding author: zahraa f. al-sharshahi neurosurgery teaching hospital, baghdad, iraq zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 49 spontaneous intracerebral haemorrhage as an initial presentation of a choriocarcinoma or pseudoaneurysms (6, 7). intracerebral hemorrhage (ich) as the initial manifestation of choriocarcinoma is an exceptionally rare presentation and signifies poor prognosis (8). the initial appearance of choriocarcinoma in patients with intracranial hemorrhage (ich) is extremely rare and is considered a poor prognosis factor (8). in this paper, we detail the case of an adult female with ich that later led to a diagnosis of metastatic choriocarcinoma. case report a 33-yearold female presented with a disturbed level of consciousness and a history of repeated episodes of vaginal bleeding lasting 3 days on average. upon neurological examination, her glasgow coma scale was 5/15 with fixed dilation of the left pupil. this lady is a gravida, with a history of recent ectopic pregnancy and two abortions, one of them being a complete hydatidiform mole (g4p1a2). initial brain computed tomography (ct) scan revealed an intraventricular hemorrhage (ivh) and a left frontoparietal, non-traumatic intracerebral hemorrhage (ich) with a significant midline shift (figure 1). the patient underwent surgery to evacuate the hematoma and resect the lesion (figure 2). histopathological examination showed the lesion to be metastatic choriocarcinoma. postoperative gcs was 10/15, and the patient had persistent aphasia with a right-sided hemiparesis (medical research council grade 3/5). figure 1. a non-contrast ct scan axial section showing a left lateral ventricular haemorrhage (ivh, left fronto-parietal intracranial hemorrhage (ich), with significant midline shift and ventricular compression. figure 2. a non-contrast post-operative axial ct scan showing complete evacuation of the intracranial and intraventricular haemorrhages with a significant decrease in the midline shift. the serum level of human chorionic gonadotropin hormone serotype beta (b-hcg) was significantly elevated (78800 miu/ml). abdominal ct scan showed right, a pleural-based, well-defined lesion with a significant post-contrast enhancement. the ct also showed an ill-defined heterogeneously enhancing soft tissue lesion in the left kidney that suggesting a metastatic deposit. the uterus was normal in size. a well-defined mass was detected anterior to the uterus. pelvic mri showed a right ovarian mass that was complex, multiloculated, and had cystic components. the mass invaded the right posterolateral wall of the urinary bladder and uterus. the patient was referred to oncology for further assessment and chemoradiotherapy. she later underwent a total abdominal hysterectomy, bilateral salpingo-oophorectomy, radical left nephrectomy, and excision of the small intestinal metastasis. on follow-up, her b-hcg levels started to normalize. her subsequent follow-up head cts revealed no residual or new lesions or recurrence. 50 maher khashea mustafa, wamedh e. matti, hussain j. kadhum et al. discussion the clinical picture of tumoral ich often overlaps that of cerebral vascular malformations, necessitating the exclusion of these more common pathologies (9, 10). in neurosurgical practice, the primary presentation of non-traumatic ich suggests a local cerebral cause, mostly vascular malformations, rather than tumor metastasis (11). however, choriocarcinoma should be suspected in every female of reproductive age with an unexplained nontraumatic ich and considerable perilesional edema and mass effect. significant elevation of beta-hcg raises the suspicion of choriocarcinoma. serum: csf ratio of beta-hcg is usually used as a confirmatory test for diagnosis, as well as an important follow-up test to measure disease remission and detect recurrence (10-13). the mechanism under which choriocarcinoma is disseminated explains its propensity to manifest as mass hemorrhage, vascular malformations, such as aneurysms or pseudoaneurysms. choriocarcinoma progresses by blood-borne metastases at an early stage. trophoblastic tumors are associated with fragile vessels, by their innate capacity to erode vessel wall after tumor embolization, causing weakening and destruction of the vessel wall, leading to the manifestation of intracranial hemorrhage, aneurysmal dilatation, or infraction if the emboli closed the vessel lumen (14,15). cerebral metastasis is most often seen in patients with advanced stages of choriocarcinoma and is considered to be a poor prognosis indicator. the treatment of choriocarcinoma with cerebral metastases includes chemoradiotherapy with or without surgery. surgery is associated with a high risk of hemorrhagic complications and should thus only be performed in patients with life-threatening ich or focal recurrent lesions resistant to chemoirradiation (5,11,13,16) conclusion metastatic choriocarcinoma should always be in the differential of non-traumatic intracerebral haemorrhage in a female child-bearing age. also, the pathological diagnosis should always be performed in cases of ich of an unknown source. abbreviations dloc disturbed level of consciousness; gcs glasgow coma scale; ich intracerebral hemorrhage; ivh intraventricular hemorrhage; avm – arteriovenous malformation. references 1. weir b, macdonald n, mielke b. intracranial vascular complications of choriocarcinoma. neurosurgery. 1978 mar 1;2(2):138-42. 2. wang d, shu h, zhang q, zhang h, qing c, wang h. brain metastasis of choriocarcinoma presenting as multiple intracranial hematomas: a case report. medicine. 2018 sep;97(37). 3. sierra-bergua b, sánchez-marteles m, cabrerizo-garcía jl, sanjoaquin-conde i. choriocarcinoma with pulmonary and cerebral metastases. singapore med j. 2008 oct 1;49(10):e286-8. 4. xiao c, yang j, zhao j, ren t, feng f, wan x, xiang y. management and prognosis of patients with brain metastasis from gestational trophoblastic neoplasia: a 24-year experience in peking union medical college hospital. bmc cancer. 2015 dec;15(1):1-9. 5. frost as, sherman jh, rezaei k, aron a, lopez-acevedo m. choriocarcinoma with brain, lung and vaginal metastases successfully treated without brain radiation or intrathecal chemotherapy: a case report. gynecologic oncology reports. 2017 may;20:97. 6. singhal m, kudesia s, bhat k, arora p, sharma a. spontaneous intracerebral haemorrhage as initial presentation of gestational choriocarcinoma in a young woman: a case report and review of literature. internet j pathol. 2009;10:2 7. kalafut m, vinuela f, saver jl, martin n, vespa p, verity ma. multiple cerebral pseudoaneurysms and hemorrhages: the expanding spectrum of metastatic cerebral choriocarcinoma. journal of neuroimaging. 1998 jan;8(1):44-7. 8. kidd d, plant gt, scaravilli f, mccartney ac, stanford m, graham em. metastatic choriocarcinoma presenting as multiple intracerebral haemorrhages: the role of imaging in the elucidation of the pathology. journal of neurology, neurosurgery & psychiatry. 1998 dec 1;65(6):939-41. 9. agarwal n, jain sk, sharma v, singhvi s, gandhi s. intracranial hemorrhage in a young woman: an unusual initial presentation of undiagnosed choriocarcinoma. journal of neurosciences in rural practice. 2019 apr;10(2):371. 10. balagopal pg, pandey m, chandramohan k, somanathan t, kumar a. unusual presentation of choriocarcinoma. world journal of surgical oncology. 2003 dec 1;1(1):4. 11. rocque bg, başkaya mk. spontaneous acute subdural hematoma as an initial presentation of choriocarcinoma: a case report. journal of medical case reports. 2008 dec 1;2(1):211. 12. kidd d, plant gt, scaravilli f, mccartney ac, stanford m, graham em. metastatic choriocarcinoma presenting as multiple intracerebral haemorrhages: the role of imaging 51 spontaneous intracerebral haemorrhage as an initial presentation of a choriocarcinoma in the elucidation of the pathology. journal of neurology, neurosurgery & psychiatry. 1998 dec 1;65(6):939-41. 13. suresh tn, santosh v, shastry kolluri vr, jayakumar pn, yasha tc, mahadevan a, shankar sk. intracranial haemorrhage resulting from unsuspected choriocarcinoma metastasis. neurology india. 2001 jul 1;49(3):231. 14. pullar m, blumbergs pc, phillips ge, carney pg. neoplastic cerebral aneurysm from metastatic gestational choriocarcinoma: case report. journal of neurosurgery. 1985 oct 1;63(4):644-7. 15. jones wb, wagner-reiss km, lewis jr jl. intracerebral choriocarcinoma. gynecologic oncology. 1990 aug 1;38(2):234-43. 16. huang cy, chen ca, hsieh cy, cheng wf. intracerebral hemorrhage as initial presentation of gestational choriocarcinoma: a case report and literature review. international journal of gynecologic cancer. 2007 sep 1;17(5). doi: 10.33962/roneuro-2023-033 similarities and differences between two coincidently gravitational bullet cases. a case report from iraq ali adnan dolachee, hagar a. algburi, salima b. alsaad, mustafa ismail, samer s. hoz romanian neurosurgery (2023) xxxvii (2): pp. 185-189 doi: 10.33962/roneuro-2023-033 www.journals.lapub.co.uk/index.php/roneurosurgery similarities and differences between two coincidently gravitational bullet cases. a case report from iraq ali adnan dolachee1, hagar a. algburi2, salima b. alsaad3, mustafa ismail2, samer s. hoz4 1 department of surgery, al-kindy college of medicine, university of baghdad, baghdad, iraq 2 department of neurosurgery, college of medicine, university of baghdad, baghdad, iraq 3 department of radiology, neurosurgical teaching hospital, baghdad, iraq 4 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract many cases of gravitational bullets are reported in developed and non-developed countries. however, few papers highlighted these cases in the literature. in our study, we present two cases of gravitational bullets that have an unusual coincidence in the injury characteristics through their ages, and gender, the site of the inlet. introduction traumatic brain injury (tbi) is young people's most common cause of death and disability. represented by disruption of the brain function when physical force is applied to the brain, in case an object hits the head violently and suddenly or when an item pierces the skull and enters the brain (1). the annual incidence of tbi is estimated at 50 million cases worldwide; this means that half of the international population has occasion of tbi in their life (2). higher mortality and morbidity rates in tbi were found in lowand middle-income countries, making this a global health problem (2). a concussion is among the most common form of tbi; the other types might be in the form of a bullet. in aerial firing or celebratory firing, when the bullets are shot into the sky for celebration or anger expression in some countries, the bullet will firstly move under the effect of explosive acceleration, this velocity will decrease according to the gravity force, and finally, its velocity will reach zero, at this moment the bullet will move downward. its velocity will be increased by the gravity force until reaching the final steady velocity when the air resistance drag equalizes the effect of gravity. the bullets injury caused by this mechanism is called gravitational bullets or keywords traumatic brain injury, craniocerebral falling bullet, aerial firing, advanced trauma life support corresponding author: ali adnan dolachee department of surgery, al-kindy college of medicine, university of baghdad, baghdad, iraq ali.adnan@kmc.uobaghdad.edu.iq copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 186 ali adnan dolachee, hagar a. algburi, salima b. alsaad et al. falling bullets (3). as the minor victims do not go for medical care and death at the scene is not recorded in the hospital, the incidence and outcome of the gravitational bullet are complex and challenging. however, high numbers of falling bullets are announced in the news media, and this number is increasing as firearms are more accessible and available (4). in this paper, we present two cases of randomly gravitational bullets with the characteristic of coincidence in their names, age, site of the inlet, and most site of the bullet inside the brain; no previous study highlighted such discussion about this issue. the cases scenarios the two incidental cases were urgently admitted to the neurosurgical emergency department on the same day, complaining that an unknown object had struck their child’s head, resulting in minor bleeding (figure 1a) (figure 2a); both families and children were not sure of what had hit the dome. both patients had the same name and gender, and both were in six years old; the site of inlet injury was in the midline parietal area (figure 1c) (figure 2c). a. b. c. figure 1. (a) superior view of scalp showing site of wound, (b) computed tomography (ct) scan of the brain showing an axial view in which a metallic artefact is seen near left petrous bone, (c) ct scan bone window sagittal view showing site of bullet entrance of the first patient. a complete neurological examination revealed that both patients were unconscious, glasgow coma scale (gcs) was 11, 12, with right-sided weakness grade 4 in both. a skull x-ray was ordered, surprisingly revealing a bullet inside the skull. a noncontrast brain computed tomography (ct) scan revealed no significant hemorrhage or soft tissue edema and the location of the bullet was confirmed to be near the left petrous bone in the first patient (figure 1b) and left cerebellar hemisphere in the second patient (figure 2b). in the emergency room, the wound was cleaned and redressed; after that, both of them were given amoxicillin and carbamazepine for protection against infection and convulsions. conservative treatment was chosen, and the parietals were neurologically intact on a 6month follow-up. a. b. c. figure 2. (a) superior view of scalp showing site of wound, (b) computed tomography (ct) scan of the brain showing an axial view in which a metallic artefact is seen in left cerebellar hemisphere, (c) ct scan bone window sagittal view showing site of bullet location of the second patient. 187 similarities and differences between two coincidently gravitational bullet cases. discussion tbi is an important cause of morbidity and mortality in developed and industrialized countries. the estimated incidence of hospitalized patients with one or more tbis is 57 million cases worldwide (5). in the united states, the annual average of patients with tbi is 1.4 million, 1.1 million recorded from emergency department visits, 235,000 were hospitalized, and 50,000 were dead. regarding gender and age variability, the occurrence of tbi in males is twice as females. for emergency visits, hospitalizations, and deaths combined, children aged 0-4 years and 15-19 years are more likely to suffer from tbi than other ages; for hospitalizations the adults aged 75 years and older have the highest incidence (6). the important causes of tbi are falls, vehicle crashes, blasts, and bullets; sports and recreation activities are also important causes of tbi, including concussions (6). of patients who die from tbi, 90% of them die within 48 hours of injury, frequently because of uncontrolled raised intracranial pressure that leads to brain stem herniation and death (7). craniocerebral gunshot wounds by areal firing are one of the tbi categories that involve bullets injury falling vertically onto the head after being shot into the sky; the primary cause of this situation is the gravity force that pulls the bullet downward when its muzzle force decreases until reaching the zero. this situation mostly occurs in celebrating events, military and civilian conflicts, or in cases of anger expression in some regions like north africa, south america, the middle east, and the middle of asia. iraq has been involved in many conventional and unconventional wars in the last three decades, becoming one of the most heavily armed nations. these injuries are frequently non-intentional, and the bullet escapes the sociodemographic space or perimeter customarily organized by the circumstances surrounding the firing. so, the source of firing is apart from the scene of injury (9). although the terminal velocity of the bullet is lower than its muzzle, the bullet shot upward may not come back downward. however, it may still cause severe brain injury with a high mortality rate (10). only bullets that travel at 150 feet/second (46 m/s) to 170 feet/sec (52 m/s) can pierce the skin, while at less than 200 feet/sec (60 m/sec) can pierce the human skull and get entrance to the brain (11,12). in general, the mortality rate of falling bullets, about 32%, is more significant than non-falling bullets, with a 2-6% mortality rate. the death cases of falling bullets may sometimes mimic the sudden death without apparent cause, specifically in those with prior medical history (3). managing patients with acute life-threatening traumatic injuries are sometimes challenging and anxious, even for experienced clinicians. to provide an effective and easy approach to management, the american college of surgeons developed the advanced trauma life support (atls) program for initial assessment, stabilization, and management of such injuries starting from brief history. then assessment of (airway, breathing, circulation, disability, and exposure) focused history with a physical exam to the injured area (such as gcs, scalp laceration, avulsions, and open skull fractures) after that recognize the specific problem, for such injury should refer to radiology including ct scan and finally start with the specific treatment (12). for craniocerebral wounds, the management may be just conservative. at the same time, if there is any serious indication, the surgery should be done urgently through bullet ablation, debridement of injured tissue, and evacuation of the hematoma. the outcome of patients with falling bullets is based mainly on the age, gcs of admission, pupil reactivity, the course of bullet through the brain, presence of injured structures, and patency of basal cisterns (13). it is important to highlight the relation between psychological reaction toward the gravitational bullet and its prognosis; the magnitude of psychological trauma is frequently disproportionate to the prognosis, which means that whenever the traumatic reaction is strong, the prognostic management outcome will be more than better. the gravitational bullet is completely different from the cases of homicidal or suicide because the occurrence of the first one is always unexpected, and its prognosis or outcome is better than the other two cases. regarding traumatic psychological reaction of the family and patients, there is also a difference between them; in the event of a gravitational bullet, they react fearfully more than in other situations because the occurrence is unexpected and unknown. many cases of gravitational bullets are reported in developed and non-developed countries. however, few papers highlighted these cases in the literature. in our study, we present two cases of gravitational bullets that have an unusual 188 ali adnan dolachee, hagar a. algburi, salima b. alsaad et al. coincidence in the injury characteristics through their ages, and gender, the site of the inlet was in the midline parietal area. patients were unconscious on their examination, the glasgow coma scale (gcs) was 11, 12, with right sided weakness grade of 4. the location of the bullet inside the brain was confirmed by non-contrast ct scan, which was revealed to be near the left petrous bone and left cerebellar hemisphere for the first and second case, respectively; there was no significant hemorrhage or soft tissue edema. the initial management for both cases in the emergency room was cleaning, redressing, and drug coverage by amoxicillin to prevent wound complication by infection and carbamazepine to prevent epileptic attacks. conservative treatment was chosen and the parietal were neurologically intact on 6-month follow-up. the similarities and differences of both patients were recorded and documented in table 1. table 1. similarities and differences between two gravitational bullet cases similarities differences name site of inlet: midline parietal area age: both were 6 years old. the gcs: was 11 in the first case and 12 in the second one. gender: both were male. location of bullet inside the brain: was near left petrous bone in the first case while left cerebellar hemisphere in the second one. time of admission: same day knowledge about the injury: patients and families of both cases were unknown about their child’s cause of injury. neurological deficit: both had right side grade 4 weakness. pathology in brain ct scan: both patients had not significant hemorrhage or soft tissue edema. initial management in the emergency room by giving amoxicillin and carbamazepine to prevent wound complication and epileptic attacks. the occurrence of same injury at different location in different patients with same age, gender, site of inlet and time of admission was incredible that may base on scientific cause or not. such situation was challenging to be resuscitated and managed at the same time and this circumstance had occurred once till now in our center. in iraq, there is unstable security situation and huge numbers of traumatic cases can be seen, at the same time the neurosurgical teaching hospital is considered to be one from three centers in baghdad that receive and manage such urgent cases which represent a further challenge to the health care professionals. so, welltrained team with the appropriate skills for the particular cases are needed to prevent the occurrence of complication in such urgent admission. the problem caused by this coincidence should be addressed from training perspective and there is no previous study highlighted such discussion about this issue before. conclusions the prevalence of aerial firing that result in gravitational bullet injuries is alarming on rise especially in countries of unstable security, the occurrence of this injury may happen in more than one patient at the same time coincidently. so, this issue should be addressed for any department treating such urgent injuries to be trained and prepared in order to prevent or decrease the occurrence of complication and death. abbreviations tbi traumatic brain injury, gcs glasgow coma scale, ct computed tomography, atls advanced trauma life support. references 1. khellaf a, khan dz, helmy a. recent advances in traumatic brain injury. journal of neurology. 2019 nov;266(11):2878-89. 2. timofeev i, santarius t, kolias ag, hutchinson pj. decompressive craniectomy—operative technique and perioperative care. inadvances and technical standards in neurosurgery 2012 (pp. 115-136). springer, vienna 3. wani aa, ramzan au, shoib y, malik nk, nizami fa, dhar a, alam s. stray bullet: an accidental killer during riot control. surgical neurology international. 2011;2. 4. ali sa, tahir sm, makhdoom a, shaikh ar, siddique aj. 189 similarities and differences between two coincidently gravitational bullet cases. aerial firing and stray bullet injuries: a rising tide. iranian red crescent medical journal. 2015 apr;17(4). 5. murray cj, lopez ad. global health statistics: a compendium of incidence, prevalence and mortality estimates for over 200 conditions. inglobal health statistics: a compendium of incidence, prevalence and mortality estimates for over 200 conditions 1996 (pp. 906-906). 6. langlois ja, rutland-brown w, thomas ke. traumatic brain injury in the united states; emergency department visits, hospitalizations, and deaths. 7. hukkelhoven cw, steyerberg ew, rampen aj, farace e, habbema jd, marshall lf, murray gd, maas ai. patient age and outcome following severe traumatic brain injury: an analysis of 5600 patients. journal of neurosurgery. 2003 oct 1;99(4):666-73. 8. park e, bell jd, baker aj. traumatic brain injury: can the consequences be stopped? cmaj. 2008 apr 22;178(9):1163-70. 9. wintemute gj, claire b, mchenry v, wright ma. stray bullet shootings in the united states. jama. 2011 aug 3;306(5):491-2. 10. abdali ha, hoz ss, moscote-salazar lr. cranial gravitational (falling) bullet injuries: point of view. journal of neurosciences in rural practice. 2018 apr;9(02):278-80. 11. kadhim ah, neamah mj, nema is. cranial falling bullet injuries, a series of 30 cases in iraq. british journal of neurosurgery. 2020 mar 3;34(2):135-41. 12. galvagno sm, nahmias jt, young da. advanced trauma life support® update 2019: management and applications for adults and special populations. anesthesiology clinics. 2019 mar 1;37(1):13-32. 13. gressot lv, chamoun rb, patel aj, valadka ab, suki d, robertson cs, gopinath sp. predictors of outcome in civilians with gunshot wounds to the head upon presentation. journal of neurosurgery. 2014 sep 1;121(3):645-52. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-012 the extended pterional approach for midline anterior skull base meningiomas. technical considerations and clinical outcome ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed romanian neurosurgery (2020) xxxiv (1): pp. 92-100 doi: 10.33962/roneuro-2020-012 www.journals.lapub.co.uk/index.php/roneurosurgery the extended pterional approach for midline anterior skull base meningiomas. technical considerations and clinical outcome ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed neurosurgery department, mansoura collage of medicine, mansoura university, egypt abstract background: various surgical approaches for the management of midline anterior skull base meningiomas exist in the literature. the main surgeon target is proper selection the appropriate approach that achieves total removal of the lesion without causing morbidity or mortality and facilitates safe effective removal of the tumour. objectives: to evaluate the role of the extended pterional approach for excision of midline anterior skull base meningiomas as regarding the effectiveness, extent of resection and surgical outcome. patients and methods: this retrospective study involved 23 cases with midline anterior skull base meningiomas resected through the extended pterional approach. patients' clinical data, operative notes, imaging studies and clinical followup data were analyzed and evaluated. results: tumors studied were 9 olfactory groove meningiomas, 8 tuberculum sellae meningiomas, 4 planum sphenoidale meningiomas and 2 diaphragma sellae meningiomas. gross total resection tumour excision in 15 cases (64.5%), subtotal excision in 5 cases (21.5%) and partial excision in 3 cases (14%). complications were diabetes insipidus (2 cases 8.6%), csf rhinorrhea (3 cases 12.9%) and visual deterioration (3 cases 12.9%). we had two cases of mortality. conclusion: the extended pterional approach allows safe and effective removal of midline anterior skull base meningiomas. it expands the exposure offered by the classic pterional approach and minimizing the necessity for applying fixed brain retraction with good cosmetic outcome and less approach-related morbidities in comparison with the extensive skull base approaches. introduction meningiomas are benign slowly growing tumors originating from arachnoid cap cells and represent almost 20% of primary intracranial tumors. although it's benign nature; the existence of meningiomas in certain location is challenging for neurosurgeons. menin giomas occurring in the midline anterior skull base are among those challenging cases. depending on the site of origin; midlineanterior skull base meningiomas are classified into: olfactory groove menin keywords extended pterional, meningioma, skull base, extent of resection corresponding author: mahmoud saad mohamed neurosurgery department, mansoura collage of medicine, mansoura university, egypt dr_ mhmodsaad@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 93 the extended pterional approach for midline anterior skull base meningiomas giomas planum sphenoidale meningiomas, tuberculum sellae meningiomas, diaphragma sellae meningiomas and dorsum sellae meningiomas. the clinical presentation is variable and varies according to site or origin and size of the tumor but commonly present with frontal manifestations, headache, visual impairment and occasionally manifestation of hypothalamic dysfunction. the surgical challenge of these tumors is how to achieve radical tumor resection without endangering the important neurovascular structures in the vicinity of these tumors. one important step to achieve such goal is choosing the proper approach to achieve adequate tumor resection with minimal morbidities including the approach related complications (2,5,7,9,13,18,22,26). the surgical approaches utilized to remove midline anterior skull base meningiomas include the pterional, the cranio-orbito-zygomatic, the subfrontal, and the anterior interhemispheric approaches. each approach has its advantage and its limitations. the appropriate approach should allow adequate tumor exposure, easily dissection from the surrounding important structures without the need for applying excessive brain retraction. the goal is usually achieved with approaches including the cranio-orbito-zygomatic approach and despite it provide the surgeon with adequate exposure he needs but the approach has its potential functional and cosmetic morbidities (1,4,7,10, 14,18,20,28). in this study; we reported our experience with extended pterional approach as it allow safe and adequate exposure to most of the midline anterior skull base meningiomas and discussing our surgical results for such challenging meningiomas. patients and methods retrospective study including twenty-three patients with midline anterior fossa meningiomas were operated up on via the extended pterional approach in the neurosurgery department, mansoura university during the period from february 2015 till july 2019. patients' demographic, clinical, radiological and operative data are collected and retrospectively analyzed. duration of clinical presentation varied from 6 to 72 months. origin of the meningiomas was assessed from preoperative magnetic resonance imaging studies and confirmed from the surgeon operative data. the extent of tumor resection was evaluated via the operative notes and postoperative magnetic resonance imaging studies done 3 months after surgery. patients were operated up on via the extended pterional approach that include the yasergil standard pterional approach with modifications including extension of the craniotomy to the frontal bone to allow access via the sub-frontal corridor and adding osteotomy along the lateral sphenoid wing toexpose the superior orbital fissure and drilling the orbital roof to flatten its surface and expand the exposure via the sub-frontal corridor. the dura is opened in a curvilinear fashion over the sylvian fissure and the incision is directed toward the falciform ligamentproviding unobstructed working angles for the para-sellar and sub-frontal corridor. we routinely do a post contrast computed tomography scans in the first day after surgery to check for any approach related problems. all patients were then followed up by doing magnetic resonance imaging study 3 months after surgery and then yearly. the mean follow-up period was 26 months, range (6-50 months). results retrospective analysis of 23 patients with midline anterior fossa meningiomas underwent surgery through the extended pterional trans-sylvian approach.the range of patients' age in our study from22 years to 63 years (the mean age was 51.96+10.81 standard deviation. there was a significant female predominance (n=18, 78.3%) females and males were (n= 5, 21.7%). duration of symptoms ranged from 5 to 108 months (mean: 10 months). visual diminution was the most common clinical presentation in our patients in 18 cases (78.2%), followed by headache in 16 cases (69.5%) then frontal manifestations in 8 cases (34.8%) and anosmia occurred in 4 cases (17.4%), fundoscopic examination: bilateral papilledema was detected in 15 cases (65.2%). unilateral optic atrophy was in 4 cases (17.4%), bilateral optic atrophyin 3 cases (13.1%). unilateral papilledema with optic atrophy in the other side (foster-kennedy syndrome) occurred in 2 cases (8.7%) (table 1). the origin of the meningioma was the olfactory groove in 9 cases, thetuberculum sellae in 8 cases, the planum sphenoidale in 4 cases and the diaphragma sellae in 2 cases. histopathological diagnosis of the meningiomas were; meningothelial 94 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed type in 10 cases, transitional type in 6 cases, psammomatous type in 4 cases, fibrous type in 2 cases and atypical type in only one case. we had 12 cases of medium sized meningiomas, 9 cases of large sized meningiomas and 2 cases of giant meningiomas (table 2). gross total resection (simpson grades i) wasachieved in 15 patients (65.3%). subtotal resection (simpson grades ii &iii) was achieved in 5 cases (21.7%). partial resection (simpson grades iv) was achieved in 3 cases (13.1%). table (3) demonstrate the extent of resection in correlation to meningioma location and tumor size. total resection was more feasible for olfactory groove meningiomas (in eight of the nine cases in our study). also, the extent of total resection was achieved more in small sized meningiomas compared to medium and large sized ones. regarding the visual outcome (table 7); 13 patients (56.5%) out of the 18 cases presented with visual disturbances showed post-operative visual improvement, 5 patients (21.7%) remained stable while 2 patients (8.6%) had post-operative visual deterioration which was transient in one of them. no major post-operative morbidities occurred in our operated cases (table 4). no post-operative morbidities happened in 12 cases (52.2%). frontal manifestations were the most common morbidities and occurred in 4 cases (17.4%). 3 cases experienced postoperative diabetes insipidus (12.9%) (transient in 2 cases). post-operative seizures occurred in 2 cases. 2 cases (8.6%) had post-operative visual deterioration that was transient in one of them. one case (4.3%) of tuberculum sellae meningioma developed transient csf rhinorrhea that was managed conservatively with transient lumbar drain. the average duration for follow-up in our study was 25 months, ranged from 6 to 50 monthswith no tumor recurrences reported in the follow-up period. four cases were offered post-operative adjuvant treatment (17.3%) in the form of gamma knife radiosurgery in three cases and conformal 3dimensional radiotherapy in one patient. we had two mortalities (8.6%) in our study (table 4). one mortality happened from intraoperative vascular injury; resulted in massive infarction of both frontal lobes and the 2nd case died from severe hypothalamic dysfunction. illustrated cases case 1: 64 years old female patient with suprasellar meningioma (fig. 1 a & b); subtotal resection was achieved leaving a small part of tumor attached to the pituitary stalk (fig. 1 c & d). case 2: 39 years old male patient with large suprasellar meningioma extending superiorly to 3rd ventricle (fig. 2 a & b) that totally removed via extended pterional approach (fig. 2 c&d). case 3: 50 years old female patient with suprasellar meningioma (fig. 3 a & b) that totally excised (fig. 3 c & d). fig. 1 (a) fig. 1 (b) 95 the extended pterional approach for midline anterior skull base meningiomas fig. 1 (c) fig. 1 (d) figure 1. preoperative mri image of suprasellar tumor sagittal view (a), coronal view (b), postoperative follow-up mri images sagittal view (c), coronal view (d). fig. 2 (a) fig. 2 (b) fig. 2 (c) fig. 2 (d) figure 2. preoperative mri image of suprasellar tumor sagittal view (a), coronal view (b), postoperative follow-up mri images sagittal view (c), coronal view (d). 96 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed fig. 3 (a) fig. 3 (b) fig. 3 (c) fig. 3 (d) figure 3. preoperative mri image of suprasellar tumorcoronal view (a), sagittal view (b), postoperative follow-up mri images coronal view (c),s agittal view (d).. table 1. clinical presentation of our case series. clinical number percentage visual manifestations 18 78.2% headache 16 69.6% behavior changes 8 34.8% anosmia 4 17.4% seizure 3 13.1% hormonal disturbance 1 4.3% fundoscopy ● bilateral papilledema ● unilateral optic atrophy ● bilateral optic atrophy ● foster-kennedy syndrome 15 4 3 2 65.2% 17.4% 13.1 8.7 table 2. classification of tumor types according to origin, histopathological examinationand tumor size (distribution, average). tumor origin numb er percentage average size in cm3 (range of size) olfactory groove 9 (39.1%) 5.14 (3.7 – 6.5) tuberculum sellae 8 (34.8%), 3.95 (3.6 4.2) planum sphenoidale 4 (17.4%) 3.80 (3.5 – 4.3) diaphragma sellae 2 (8.7%) 3.65 (3.5 – 3.8) histopathological types meningothelial type 10 (43.5%) transitional type 6 (26.1%) psammomatou s type 4 (17.4%) fibrous type 2 (8.7%) atypical meningioma (who grade ii) 1 (4.3%) tumor size 97 the extended pterional approach for midline anterior skull base meningiomas medium24cm3 12 52.2% large 4-6 9 39.2% giant >6 2 8.6% table 3. correlation between eor and location of meningioma and tumor size. gtr grade i str grade ii & iii partia l grade iv total meningioma location olfactory groove 8 (34.4%) 1(4.3%) 0 9 planum sphenoid ale 4 (17.2%) 2 (8.6%) 2 (8.6%) 8 tuberculu m sellae 2 (8.6%) 1 (4.3%) 1 (4.3%) 4 diaphrag ma sellae 1 (4.3%) 1 (4.3%) 0 2 meningioma size 2cm 3.9 cm. 9 (39%) 2 (8.6%) 1 (4.3%) 12 4cm 5.9 cm. 4 (17.2%) 3 (13%) 2 (8.6%) 9 >6cm 2 (8.6%) 0 0 2 table 4. visual and surgical outcome and complication of extended pterional approach in anterior skull base meningiomas. number percentag e surgical outcome gtr 15 64.5% str 5 21.5% partial 3 14% mortality 2 8.6% complications frontal manifestations 4 17.4% seizures 2 8.6% diabetes insipidus 3 12.9% transient csf rhinorrhea 1 4.3% visual deterioration 2 8.6% visual outcome improved vision 14 60.7% stable vision 5 21.7% visual deterioration (one is transient) 2 8.6% table 5. review of literature of case series of microsurgical management of anterior skull base meningiomas case series year no. patients gtr (%) visual improvemen t (%) recurrence (%) mortality (%) years of f/u recent series 2019 23 64.5 78.1 n/a 8.6 4.6 lynch et al. 2015 38 86 89.4 5.2 2.6 5.7 romani et al. 2009 65 91 21.4 9 0 3.7 bassioni et al. 2007 55 100 83.3 8.9 0 n/a colli et al. 2007 17 94.1 n/a 0 11.8 4.2 hentsche ls and demonte 2003 13 85 92.3 0 0 2 goel et al. 2002 70 84 n/a 1.4 2.8 n/a jallo&be njamim 2002 23 86.9 55 4.5 8.6 93 fahlbusc h& schott 2002 47 98 80 4.2 0 n/a zeugaridi s et al. 2001 62 n/a 65 n/a 3.2 5.2 98 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed turazzi et al. 1999 37 100 100 0 2.7 4 al-mefty 1993 35 91 25 n/a 8.6 n/a ojemann 1991 14 71 73 n/a 0 n/a solero et al. 1983 55 78 60 3 2.3 n/a symon &rosent ein 1977 33 82 n/a 3.1 3 n/a discussion midline anterior skull base meningiomas have only and exclusively treated through direct microsurgical excision. the main neurosurgical challenge is to achieve total surgical excision with no or minimal postoperative morbidities. however, the surgical difficulties are facilitated by improved microsurgical facilities, more understanding of the microsurgical anatomy through adequate neurosurgical training and progressive learning curve and feasibility of variable surgical approaches. effective reaching the surgical target with minimal normal anatomical disruption is the cornerstone of the surgeon focus (1,3,4,6,8,11,14,16,25). a wide range of surgical approaches have been described in the literature totreat midline anterior skull base meningiomas, including the pterional approach with its modifications and the sub-frontal approach with unilateral or bilateral sub-frontal exposure. each of these approaches has its advantages as well as its limitations. approach selection is dependent on the tumor size, location, and pattern of extension, tumor relation to the important neurovascular structures and the surgeon’s experience and familiarity with the approach (2,3,9,12,15,17,19,25,27). many authors advocated the bilateral subfrontal craniotomy for large symmetrical midline lesions with its advantage of wide exposure of the anterior cranial base and excellent view for dissection of the both anterior cerebral arteries and the optic pathways. other authors prefer to use the unilateral sub-frontal corridor which can allow tumor resection without the increased risk encountered in the bilateral sub-frontal exposure. in many other cases series; the fronto-lateral approaches including the pterional approach, the cranio-orbito-zygomatic approach and the extended pterional approach were preferred by the neurosurgeons to remove midline anterior skull base meningiomas (1, 3,7,15,20,21,23,24,25,27). the extended pterional approach provides certain advantages compared to the bi-frontal craniotomy. it provides the shortest distance to the tuberculum sellae. it allows early exposure to the basal cisterns for csf release to have good brain relaxation to minimize frontal lobe retraction. also, sylvian fissure dissection provided by the approach allow untethering of the frontal lobe from temporal lobe facilitating full exposure of the neurovascular structures with minimal or no frontal lobe retraction which is difficult to achieve from the bilateral or unilateral sub-frontal exposure. moreover, the extended pterional approach provides the surgeon with more working angles for tumor exposure and dissection that cannot be achieved from the subfrontal approach. the extended pterional approach can replace bi-frontal craniotomy for resection of giant midline intradural anterior skull base tumors except for extradural skull base tumors extending to the intradural space (3.4,6,10,15,20,24,25,26,27). pterional craniotomy is a highly flexible skull base approach that gives excellent exposure of the anterior cranial fossa, the circle of willis, and the interpeduncular region. because of its simplicity, flexibility, efficiency; this approach is most utilized for pathologies along the anterior skull base. the major limitation for this exposure is the need for more frontal lobe retraction for lesion with more superior extension reaching the third ventricle and when the tumor extends inferolateral in skull base. the cranioorbito-zygomatic approach can expand the exposure for the hidden areas for the classic pterional approach involving the orbital apex, the paraclinoid and parasellar areas, the cavernous sinus and the interpeduncular fossa. tumors with significant superior extension can be addressed well with expanded inferior-to-superior and medial to lateral operative working angles provided by the cranioorbito-zygomatic approach. the cranio-orbitozygomatic approach is a more complex approach and technically demanding with the concern regarding the cosmetic problems due to the 99 the extended pterional approach for midline anterior skull base meningiomas extensive osteotomes necessary for the exposure (2,3,8,9,13,15,22,24,25,26,28). the extended pterional approach is a modification of the classic pterional approach that obviates the limitation of the classic approach for skull base exposure and minimizes the necessity for the more extensive cranio-orbito-zygomatic approach. the additional osteotomes at the sphenoid wing and orbital roof expands the subfrontal trajectory to the midline anterior skull base without necessity for more frontal lobe retraction. the osteotomy of the orbital roof gives most of the advantages of that provided by the cranio-orbitozygomatic approach with less chance for cosmetic deformities (2,3,15,24,25,26). in our study; the mean age of the cases in our study was 51.96 years. most of our cases were in their 5th and 6th decades and 78.3% of our cases were females. visual manifestations were the most presenting symptoms followed by headache, frontal manifestation then anosmia and behavioral changes. the demographic data and the clinical manifestations of our cases were like other reports in the literatures discussing this pathological entity (1,5,6,11,12,21,27). the onset of clinical presentation for midline anterior skull base meningiomas corelated the origin of the meningiomas. more anteriorly located tumors like olfactory groove meningiomas may reach large size before being symptomatic. earlier clinical presentation in smaller sized meningiomas originating in a close proximity to the optic nerves and the chiasm. in our study, the average size for the ogms was 5.14 cm for the tsms was 3.95 cm while the average size of the psms was 3.80 cm (2,4,5,9,11,15,27). gross total resection (gtr) was achieved in 15 (65.3%) patients and subtotal resection in 5 (21.7%). the highest percentage of gross total tumor excision was in ogm cases (8 tumors out of 9), followed by psms (4 tumors out of 8), and then tsms (2 tumors out of 4) .the extent of tumor resection of midline anterior skull base meningiomas was addressed in many case series with variation in results depending on what is defined as total or near total resection in each series. several studies have advocated that attempting gross total resection should not be with the price of endangering the vision or the hypothalamic function. the extent of gross total tumor resection of such meningiomas varied from 35% to 100% (table 5). the appropriate approach selection is crucial to improve the extent of resection as reported in many series. skull base approaches including the cranio-orbito-zygomatic and cranioorbital approach facilitated adequate tumor exposure and better achievement of tumor resection but with increasing cosmetic morbidities. the extended pterional approach used in our case series facilitated more adequate exposure of the tumor with minimal cosmetic sequalae (2,4,5,8,9,13,15,18, 19,23,24,25,26,27). the preservation of vision is one of the cardinaltargets of surgical management. some case series concluded that better visual outcomes are associated with tumors smaller than 3 cm than tumors larger than 3 cm in diameter(2,8,16). in our series, improvement of vision occurred in 60.7% of patients and preserved vision with no further deterioration in 21.7%. surgery for midline anterior skull base tumors still carry the risk for postoperative morbidities despite the improvement achieved in the modern neurosurgical facilities. in our study, the highest complication rate was frontal manifestations; behavior changes (n=4, 17.4%), diabetes insipidus (n=3, 12.9%), csf rhinorrhea (n=1, 4.3%) then visual deterioration (n=1, 4.3%). cushing reported an operative mortality of 27.5%. as a result of the refinements of microsurgical techniques, death rates had declined in subsequent series. al-mefty(15) and solero et al.(27) observed higher mortality rates in patients with tumors exceeding 3 cm in diameter, compared with mortality rates in patients with smaller tumors. in our study there were only 2 mortalities (8.6%). in our series, 11patients (47.8%) harbored large or giant tumors, but we noticed that there was no increase in mortality in this group of patients (2,7,9,15,18,19,22,25). several series have been published on midline anterior skull base tumors (table 5) with long term follow up for recurrences beyond 10 years following simpson 1 or 2 grade resections. in current study, no tumor recurrences recorded during the follow up period which extended up to 54 months. a longer follow up period is crucial for better assessment of the actual recurrence rate (3,6,7,8,15,23,27). conclusion the extended pterional approach allows safe and effective removal of midline anterior skull base meningiomas. it expands the exposure offered by 100 ahmed nageeb mohamed taha, hosam shata mohamed, mahmoud saad mohamed the classic pterional approach and minimizing the necessity for applying brain retraction with good cosmetic outcome and less approach related morbidities related to the more extensive skull base approaches. abbreviations eor= extent of resection, coz= cranio-orbito-zygomatic, ict= intracranial tension, csf= cerebrospinal fluid, ogm= olfactory groove meningioma, gtr= gross total resection, str= subtotal resection, tsm= tuberculum sellae meningioma, psm= planum sphenoidale meningioma. references 1. colli bo, carlotti cg jr, assirati ja jr et al. olfactory groove meningiomas: surgical technique and follow-up review. arq neuropsquiatr 65 (3b):795-9, 2007. 2. fahlbusch r and schott w. pterional surgery of meningiomas of the tuberculum sellae and planum sphenoidale: surgical results with special consideration of ophthalmological and endocrinological outcomes. j neurosurg 96 (2):235-43, 2002. 3. yasargil mg. general operative techniques. in: yasargil mg, editor.microneurosurgery, vol. 1: microsurgical anatomy of the basal cisterns and vessels of the brain, diagnostic studies, general operative techniques and pathological considerations of the intracranial aneurysms. new york: georg thieme/thieme-stratton p. 208-33, 1984. 4. romani r, laakso a, kangasniemi m et al. lateral supraorbital approach applied to tuberculum sellae meningiomas: experience with 52 consecutive patients. neurosurgery 70 (6):1504-19, 2012. 5. zivgaridis d, medele rj, muller a et al. meningiomas of the sellar region presenting with visual impairment: impact of various prognostic factors on surgical outcome in 62 patients. acta neurochir 143: 471-476, 2001. 6. jallo gi and benjamin v. tuberculum sellae meningiomas: microsurgical anatomy and surgical technique. neurosurgery 51 (6):1432-40, 2002. 7. mcdermott mw, rootman j, durity fa. subperiosteal, subperiorbital dissection and division of the anterior and posterior ethmoid arteries for meningiomas of the cribriform plate and planum sphenoidale: technical note. neurosurgery 36 (6):1215-9, 1995. 8. nakamura m, struck m, roser f et al. olfactory groove meningiomas: clinical outcome and recurrence rates after tumor removal through the frontolateral and bifrontal approach. neurosurgery 62 (6 suppl 3):1224-32, 2008. 9. aguiar ph, tahara a, almeida an et al. olfactory groove meningiomas: approaches and complications. j clin neurosci 16 (9):1168-73, 2009. 10. symon l. olfactory groove and suprasellar meningiomas. in: krayonbühl h, editor. advances and technical standards in neurosurgery. springer p. 67-91, 1977. 11. goel a, muzumdar d, desai ki. tuberculum sellae meningioma: a report on management on the basis of a surgical experience with 70 patients. neurosurgery 51 (6):1358-64, 2002. 12. goel a andmuzumdar d. surgical strategy for tuberculum sellae meningiomas. neurosurg q 15: 25-32, 2005. 13. simpson d. the recurrence of intracranial meningiomas after surgical treatment. j neurol neurosurg psychiatry 20:22-39, 1957. 14. spektor s, valarezo j, fliss dm, gil z, cohen j, goldman j et al. olfactory groove meningiomas from neurosurgical and ear, nose, and throat perspectives: approaches, techniques, and outcomes. neurosurgery 57 (4 suppl): 268-80. 2005. 15. al-mefty o. tuberculum sellae and olfactory groove meningiomas. in: sekhar ln, janecka ip, editors. surgery of cranial base tumors. new york: raven; 1993. p. 507-19. 16. bassiouni h, asgari s, stolke d. olfactory groove meningiomas: functional outcome in a series treated microsurgically. acta neurochir 149 (2):109-21, 2007. 17. bassiouni h, asgari s, stolke d. tuberculum sellae meningiomas: functional outcome in a consecutive series treated microsurgically. surg neurol 66: 37-45, 2006. 18. de monte f. surgical treatment of anterior basal meningiomas. j neuro-oncol 29:239-248, 1996. 19. el gindi s. olfactory groove meningioma: surgical techniques and pitfalls. surg neurol 54:415–417, 2000. 20. park ck, jung hw, yang sy et al. surgically treated tuberculum sellae and diaphragm sellae meningiomas: the importance of short-term visual outcome. neurosurgery 59 (2):238-43, 2006. 21. refaat mi, eissa em, ali mh. surgical management of midline anterior skull base meningiomas: experience of 30 cases. turk neurosurg 25 (3):432-7, 2015. 22. mathiesen t and kihlstrom l. visual outcome of tuberculum sellae meningiomas after extradural optic nerve decompression. neurosurgery 59:570-576, 2006. 23. obeid f and al-mefty o: recurrence of olfactory groove meningiomas. neurosurgery 53: 534-543, 2003. 24. turazzi s, cristofori l, gambin r. the pterional approach for the microsurgical removal of olfactory groove meningiomas. neurosurgery 45:821-826, 1999. 25. lynch, jose carlos, gonçalves et al. the extended pterional approach allows excellent results for removal of anterior cranial fossa meningiomas. arquivos de neuro-psiquiatria 74 (5): 382-387, 2016. 26. hendricks bk and cohen ga.the extended pterional craniotomy: a contemporary and balanced approach operative neurosurgery opz117, vol.0, 2019. 27. solero cl, giombini s, morello g. suprasellar and olfactory meningiomas: report on a series of 153 personal cases. acta neurochir 67 (3-4):181-94, 1983. 28. romani r, lehecka m, gaal e, et al. lateral supraorbital approach applied to olfactory groove meningiomas: experience with 66 consecutive patients. neurosurgery 65 (1): 39-53, 2009. doi: 10.33962/roneuro-2021-067 unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar – 75 years from his passing to eternity horia berceanu, stanislav groppa, horia pleș romanian neurosurgery (2021) xxxv (4): pp. 389-402 doi: 10.33962/roneuro-2021-067 www.journals.lapub.co.uk/index.php/roneurosurgery unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar – 75 years from his passing to eternity horia berceanu1, stanislav groppa2, horia pleș3,4,5 1 md, department of neurosurgery, clinical emergency hospital “elias”, bucharest & “romanian society of medicine history”, romania 2 academician, prof. hab. head of neurology clinic 2 of usmf “nicolae testemițanu”, chișinău, rep. of moldova. vice-rector of usmf „nicolae testemițanu”, chișinău, republic of moldavia 3 assoc. prof. hab. md, phd, university of medicine and pharmacy “victor babeș” timișoara, romania 4 head of neurosurgical department, emergency clinical county hospital “pius brînzeu” timișoara, romania 5 centre for cognitive research in neuropsychiatric pathology (neuropsy-cog), “victor babeș” university of medicine and pharmacy, timișoara, romania abstract dumitru bagdasar, who is indisputably considered as the founder of neurosurgery on the romanian territory during the interwar period, was born in roșiești, the former fălciu county, in 1893. in 1913, after having completed his primary and secondary education, he enrolled at the faculty of medicine of bucharest and, in the summer of 1916, at the end of his third university year, he transferred to the medical military institute. from 1916 to 1918, d. bagdasar dealt with the whole array of illnesses arising from the world conflict, including firearm-related injuries to the nervous system. after the war, he was transferred to the neurology clinic of the colentina hospital where, under the supervision of professor gheorghe marinescu, he elaborated and completed his doctoral dissertation entitled: contribuțiuni la studiul sindromului parkinsonian-postencefalitic (contributions to the study of postencephalitic parkinsonism), which he defended in 1922. from 1922 to 1926, at the military hospital of bucharest, he completed his neurology internship under the guidance of the eminent neurologist dumitru noica and his initiation to surgery under professor mihail butoianu. in 1927, after giving up his military contract, he was transferred to the jimbolia hospital by the ministry of health to work as an attending neuropsychiatrist. at the end of the same year, with a recommendation from professor nicolae paulescu, he earned a neurosurgery specialisation scholarship under professor harvey cushing in boston. there, under the guidance of professor cushing and doctor bailey, he wrote two papers: le traitement chirurgical des gommes cérébrales and intracranial chordoblastoma, which were published in presti keywords education and training in neurology (gh. marinescu, d. noica), surgery and neurosurgery (m. butoianu, w. cushing), reports of the first neurosurgical procedures, connections with leading medical experts (n. paulescu, i. t. niculescu, p. bailey, ch. frazier, j. f. fulton, th. de martel, w. freeman etc.), the first professor of neurosurgery in romania (1945) corresponding author: horia berceanu clinical emergency hospital “elias”, bucharest & “romanian society of medicine history” horiaberceanu@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 390 horia berceanu, stanislav groppa, horia pleș gious medical journals. in 1929, he returned to the jimbolia hospital where, in 1930, he performed his first neurosurgical procedures. at the end of 1931, he transferred to the cernăuți hospital, again as a neuropsychiatrist, and in the following two years he performed a number of 149 operations on the central nervous system, which are described in the surgical reports written by doctor bagdasar himself. in 1934, he transferred to bucharest, where he performed neurosurgical procedures in two hospitals (emergency hospital and central hospital) and, at the end of the same year, he was tenured as an attending neurosurgeon at the central hospital, following a contest organised by the ministry of health. from 1935, he worked primarily in the aforementioned hospital but he also performed operations in other hospitals (emergency, colțea, military etc.). alongside his surgical activity, he was also interested in the histopathology of the operated tumours, he wrote scientific papers based on his own case reports, participated in medical congresses (bucharest, bern, chisinau etc.) and became interested in the social-political issues of the time..., joining the communist party in 1943. in 1940, just before the outburst of world war ii, he wrote acute craniocerebral trauma and published it in probleme de medicină de războiu (war medicine issues). during the war, due to his over a decade long experience in neurosurgical procedures, he assisted the injured (both militaries and civilians), while also managing common neurosurgical cases in romania and the adjacent countries and even in palestine, as a member of the so-called “golden team” (c. arseni, i. ionescu, irina ogrezeanu-ionescu). in 1945, he was appointed minister of health and at the end of the same year, he became the first professor of neurosurgery in romania. unfortunately, his life came to an abrupt end on 16 july 1946 because of a metastatic brain tumour probably caused by primary lung cancer. dumitru bagdasar (1893-1946) was born in roșiești, the former fălciu county, currently vaslui county, on 17 december 1893, in a family of peasants of armenian origin1, being the fourth of twelve children. he attended primary school in the nearby town of indricii de sus, having an exceptional schoolteacher, gh. balaur and completing all five primary school years as best pupil of his class. then, he enrolled to the renowned secondary school „gheorghe roșca codreanu” of bârlad, where he graduated from the humanities program in 1913. given the difficult financial situation of his family, which had been economically destabilized by his mother’s death (while giving birth to her thirteenth child, during her son’s high school years), when he enrolled at the faculty of medicine of bucharest, dumitru bagdasar also took a position as an educator at the sfântul sava high school, thus having free meals and accommodation. he managed to pay his university fees and other expenses (books, lectures and so on) through tutoring. this complex situation (being concomitantly a student, an employee and a tutor) went on for his first two university years – from 1913 to 1915 – without negative consequences on his university exam results. during his 3rd year of medical school, he gave up his educator job and started to work at the zerlendi sanatorium (a tuberculosis sanatorium) as an intern – according to a. kreindler – probably a voluntary intern whose job was to perform the patients’ sputum tests2 from 7:30 pm to 10:30 pm, against meals, accommodation and the monthly wage of 5 lei. at the end of his 3rd year of studies, as romania was preparing to enter into world war i, due to the tempting conditions offered by the medical military institute, he accepted to be transferred to that institution, where he was given the rank of sublieutenant and a corresponding salary which enabled him to continue his medical education without the financial concerns he had previously had. at the same time, he was enlisted in the 41st regiment of infantry (cf. dr. v. lavrov, oameni și fapte din istoria medicinei militare românești, vol. i, editura pro transilvania, 2005, p. 401, where it is stated that he was enlisted in the 66th regiment of infantry, the 17th division, as an ambulance military doctor), which gave him the opportunity to become familiar with the whole array of illnesses arising from the world conflict, in particular, injuries caused by firearms, chemical substances or infective diseases, including disorders of the central and peripheral nervous systems. except for a period when he suffered from exanthematous typhus and a period of reformation of the regiment in 1917, sublieutenant dumitru bagdasar participated in all the military war campaigns, from august 1916 until his demobilisation in november 1918 (cf. dr. v. lavrov, ibidem, “for his devotion and self-sacrifice proven during the war, he was decorated with the 19161918 commemorative cross, the romanian crown order as a knight and the cross of medical merit 2nd class”). it should be noted that, in june 1918, during his military leave, he took all his 4th year examinations at the faculty of medicine of iași, with excellent results3. after the war, in 1921, he wrote two papers in cooperation with doctor dem paulian, entitled a propos du traitement du parkinsonisme (considerație asupra tratamentului în parkinsonism) (on parkinsonism treatment) published in the revue 391 unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar neurologique, june 1921, 7034 and chist hidatic al creierului (hydatid brain cyst), published in spitalul, july 1921, 555. from 1921 to 1922, he attended the neurology clinic run by professor gheorghe marinescu, where he was transferred from the medical military institute for specialisation6. in 1922, he was awarded the doctor of medicine and surgery degree, upon completion of his dissertation entitled: contribuțiuni la studiul sindromului parkinsonianpostencefalitic (contributions to the study of postencephalitic parkinsonism), coordinated by professor gheorghe marinescu4. after defending his doctoral dissertation in 1922, doctor bagdasar did his internship in neurology and psychiatry at the regina elisabeta military hospital of bucharest, where his mentor was the renowned physician dr dumitru noica. under his guidance, from 1922 to 1927, he wrote 12 scientific papers on neurology (which are listed and commented in his work titluri, lucrări științifice, bucharest 19347). at the same time, during his neurology internship, the professional collaboration between the two doctors, d. noica and d. bagdasar, doubled by a personal/spiritual bond between master and disciple, was decisive for dr bagdasar’s path in neurosurgery. at that time, dr bagdasar was interested in gathering sound knowledge on the histopathology of the nervous system, working in the laboratory of pathologic anatomy led by professor șt. beznea, alongside the latter’s assistant, dr i. t. niculescu, who was back from his specialisation in histology in paris; their fellowship soon turned into a strong friendship. after discovering his vocation for neurosurgery that he later developed into a profession, dr dumitru bagdasar started to work on growing his education in surgery (which had started during the war, from 1916 to 1918) at the military hospital, under the guidance of general mihail butoianu8. alongside his activity in neurology, from 1923 to 1926 he worked in the surgery unit of the same hospital, which was led by professor butoianu, and where he was initiated to general surgery. this surgical practice was, undoubtedly, the foundation of his training in neurosurgery, knowing that professor butoianu was one of the pioneers of neurological surgery in romania9. the year 1927 has a triple importance for doctor dumitru bagdasar, being the year when he married florica ciumetti (of armenian origin), was assigned the position of attending neuropsychiatrist at the hospital for mental and nervous diseases of jimbolia (after he resigned from the army) and, following the recommendation of professor nicolae paulescu, he earned a 2-year scholarship from the ministry to health to specialise in neurosurgery at professor harvey cushing’s clinic within the peter bent brigham hospital of boston. it should also be noted that a beautiful professional and personal relationship developed between professor paulescu and doctor dumitru bagdasar, which grew closer and closer in time, from the period of bagdasar’s medical studies and until the premature end of professor paulescu (see the correspondence between master and disciple)10. regarding this beautiful friendship in the romanian medical environment of the early 20th century, it should also be noted that the same kind of relationship existed between two great medical scientists born in the same year (1869) and, though living on two different continents (north america and europe), connected by mutual esteem due to the experimental research on the subtemporal removal of the hypophysis in dogs, which had been successfully performed by nicolae paulescu ever since 11 march 1903 when, with the help of doctor ion bălăcescu, he performed the first hypophysectomy with temporal access. the procedure involved the following sequence: temporal drilling, opening the dura mater, gently lifting the temporal lobe to expose the sella turcica, from which the surgeon: „could pick the hypophysis like a fruit from a tree” (cf. nicolae paulescu). this technique was first described in the journal de physiologie et de pathologie générale of 190711 and then it was detailed in the monography of hypophysis physiology, also published in paris in 190812. the method was superior to all the other existing methods and its advantage was that it allowed to avoid the dreaded complications of the previous attempts (trauma, haemorrhage and meningitis), since it was accompanied by histological checks for the absence of residual gland tissue in the sella turcica and provided all certainties for its application in humans. that is why harvey cushing, when talking about the romanian physiologist’s method in 1910, stated that it was “...by far the most important contribution to the subject matter”13 and adopted “the method in his ground-breaking neurosurgical work that made him famous”14. the correspondence between cushing and paulescu regarding bagdasar goes back to 1926, following a letter written in german from 392 horia berceanu, stanislav groppa, horia pleș bagdasar to the illustrious american neurosurgeon. in cushing’s positive response to bagdasar on 21 august 1926 send to the address of the military hospital of bucharest, the former promised he would give the applicant “an arbeit” and would have him work in the clinic; at the same time, he thought he could arrange for him to have his meals at the hospital but he did not have funds to provide him with accommodation at the clinic. professor cushing concluded his letter as follows: “i wrote to professor paulescu to see if you might want to apply for a rockefeller scholarship. in case you do, it would be better if you asked him to write to mr clifford wells, the scholarship advisor, rockefeller foundation, 61 broadway, new york city, stating that he wants you to come here to work with me for a year and they will probably accept you as one of their itinerant fellows”15. though the two leading medical experts of those times communicated their thoughts to each other through mutual correspondence or through their mutual connection, d. bagdasar, never managed to meet because of the geographic distance or the romanian professor’s illness... the last but one attempt was at the international congress of physiology in boston, 1929, when nicolae paulescu could have met both harvey cushing and ivan petrovici pavlov, the renowned russian physiologist, a recipient of the nobel prize for medicine and physiology in 1904. the last possibility would have been at the international congress of neurology in bern (switzerland), 31 august – 3 september 1931 but unfortunately the romanian professor had died the previous month (17 july 1931). the recommendation letter written by professor nicolae paulescu to professor harvey cushing, alongside the deep knowledge of neurology, the determination and diligence of the young doctor dumitru bagdasar, were the main advantages that gained the latter the appreciation he benefited from throughout his professional specialisation in the united states. professor cushing stated that, “my door is always open for paulescu’s students”16. since professor cushing’s reputation at the peak of his career attracted disciples from all over the world (europeans: h. olivecrona, h. cairns, n. dott, s. obrador; americans: e. cutler, g. horax, l. davidoff, w. wagener), his clinic had become a point of maximum interest and pilgrimage for those who wanted to specialise in neurosurgery. in 1928, professor harvey cushing’s secretary, madeline stanton, stated that, “...we’re toiling to receive 200 visiting surgeons”17! but let us see what the daily schedule of the romanian doctor d. bagdasar at the clinic of the renowned american neurosurgeon h. cushing looked like: i get up at 5:30 am every day and i read in english until 9:00 am, when i leave for the hospital. i go into the operating room every day to see one or two procedures which end at about 2:00 or 3:00 pm. after the operating schedule is over, i go to the laboratory where the extracted pieces are analysed and discussed until about 7:00 pm. i spend 9 to 10 hours at the hospital every day. when i get home, i read in english until 11:00 pm18. in professor cushing’s clinic, the master placed bagdasar under the wing of one of his closest collaborators, the renowned anatomopathologist, neurologist, neurosurgeon and psychiatrist percival bailey, who introduced him to the standard procedures of the main neurosurgical operations performed in the clinic, alongside the techniques for the preparation and anatomopathological analysis of the intraoperatively extracted pieces19. during his training in neurosurgery under professor harvey cushing of the peter bent brigham hospital of boston – as a voluntary assistant – doctor bagdasar wrote two significant papers on neurosurgery: le traitement chirurgical des gommes cérébrales (tratamentul chirurgical al gomelor cerebrale) published in rev. neurologie, 1929, 2 (1), 1-30 and intracranial chondroblastoma (cordoblastoamele intracraniene) published in amer j path., 1929, 5 (5), 429. the first paper had a single author, while the second one had two authors (the second being the renowned p. bailey), both papers having the approval of the scientific mentor in neurosurgery of those times, the great harvey cushing20: after a continuous working schedule of 14 hours a day, of which 9 to 10 hours were in the neurosurgery clinic, added to the fact that bagdasar was a heavy smoker (like his mentor at that time), after 14 months of activity, both bagdasar and his wife florica bagdasar fall ill of tuberculosis. due to cushing’s network of friends, the bagdasars are treated in two of the best american pneumology sanatoriums: the sarnac sanatorium in the anderadaks mountains and then the troudeau sanatorium21. 393 unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar the appreciative characterisation made by the intransigent and authoritative h. cushing regarding dumitru bagdasar remains remarkable – in one of the annual reports of the surgery clinic (report of the surgeon-in-chief of the peter bent brigham hospital, reprinted from the fifteenth annual report 1928, p. 102): “dr dumitru bagdasar from bucharest fell ill and had to temporarily suspend his stay with us. we deeply feel his absence, not only for personal reasons but also for his sharp understanding of neurological matters and his unusual working capacity”22. it has to be mentioned that during the antituberculosis therapy in the abovementioned clinics, the family-like connection – one might say – between cushing and bagdasar continued through an amiable correspondence (found in the personal archives of the two families), where the bagdasars talked about the favourable outcome of their illness and cushing encouraged them or replied affirmatively to their polite requests23. we shall conclude this very important chapter in the training of the romanian doctor dumitru bagdasar in neurosurgery at the american professor harvey cushing’s clinic by mentioning the correspondence that bagdasar had throughout that period with his friends in romania, namely: professor n. paulescu, doctor i. t. niculescu, his colleague, a distinguished neurologist and close friend d. noica (head of the neurology unit of the military hospital in bucharest), as well as the renowned physiologist j. fulton, with whom he had become friends in the usa. in the autumn of 1929, doctor bagdasar was relatively stabilised from a pneumological point of view and returned to work in the jimbolia hospital where, with the help of his wife (who had a degree in medicine and had joined him in the usa where, with professor cushing’s support, earned a fulbrait scholarship which enabled her to specialise in social medicine), performed the first 27 neurosurgical procedures in romania in 1930: 15 ventricular punctions, 9 frontal parietal flaps, two subtemporal decompressions, one cerebellar decompression, as well as 18 procedures not involving the central nervous system: 12 vasectomies, four femoral sympathectomies and two frenectomies24. in 1930, doctor dumitru bagdasar reports all the cases of medullary tumours published and operated in romania up to that date: four had been operated by professor amza jianu upon recommendation from doctor state drăgănescu (information from the doctoral dissertation of l. dragomirescu), two had been operated by professor i. iacobovici and three by the associated professor iancu jianu25. in late august-early september 1931 (31 august 3 september), doctor dumitru bagdasar attended the first international congress of neurology in bern, switzerland, where professor harvey cushing presented his memorable paper based on a personal statistic on 2,023 operated brain tumours. the presentation remained famous in the medical world because, for the first time, none of the participants (of which 25 were cushing’s disciples) was left outside the presentation room. during the congress, the american professor organised a festive dinner at the bellevue hotel, where he invited some of the leading experts in neurosurgery that were present. the disposition of the 29 seats at the table was prepared by the very host. the image below shows the honourable spot occupied by bagdasar, at cushing’s left, facing the head of french neurosurgery, professor thierry de martel and near doctor percival bailey, his second mentor in neurosurgery during his american traineeship26, 27. from june 1931 to december 1933, he worked as an attending psychiatrist at the hospital for mental and nervous diseases “carol al ii-lea” of cernăuți. here, assisted by his wife, florica bagdasar, by miss brenner and others, dumitru bagdasar performed 28 neurosurgical procedures in his first year and 31 in his second year28,29. the procedures performed in 1932 were as follows: the first two procedures were performed on patient karl a. (the age is not specified), the surgeon was doctor bagdasar, the name of the assistant is not mentioned and under “anaesthesia” the first procedure mentions: local with novocaine, and the second one: local with novocaine 5%. the diagnosis for the first procedure of 11 january 1932 was: 394 horia berceanu, stanislav groppa, horia pleș cerebellar tumour and for the second one: tumour of the left cerebellar hemisphere and vermis. under “procedure”, the following is stated for the first operation: right ventriculography, and for the second operation: tumour ablation. description of the first procedure30: classical incision. drilling. a ventricular needle is inserted into the right lateral ventricle on the first attempt; the fluid streams out at first, then drips rapidly. after draining about 65 to 70 cc, filtered air in the amount of 20 cc is introduced. the needle is removed gently (the patient reports slight headaches after receiving the first 15 cc of air). the wound is closed in two layers. dressing with mastisol”. description of the second procedure31: “the procedure begins at 9:30 am and carries on until 8:00 pm; heart beat 120-130, does not answer any questions. the procedure is suspended for 15 minutes (2 cc of caffeine and 10 cc of camphor oil are given). the patient starts to recover, answers questions, the procedure is resumed without further incidents until the end. crossbow (cushing-style) incision. at the level of decompression, the dura is covered with a very think fibrous layer and cannot be separated through cleavage. the dura is opened with the help of a crochet on the left side, the entire left half of the bone breach is under heavy pressure and painful at the slightest movements. after opening the dura for a 2-cm length, a brown neoplastic tissue comes out. the incision is widened beyond the median line. after lifting several bone residues that were forming a bridge on the median line, the neoplastic tissue having a surface equal to the thenar eminence is dissected with a blunt instrument after having delimited the tumour; two stitches are applied on its most convex part and the dissection is continued while applying slight traction on the silk threads. several haemorrhages are stopped with muscle tissue taken from another patient and silver staples. the tumour slightly exceeds the median line to the right side. after lifting the central part of the tumour (the size of a plum), smaller tumour pieces are lifted with a clip, continuing to dissect with blunt instruments. healthy cerebellar tissue becomes visible on the lower side. when several tractions were performed on the lower side of the capsule, the patient felt pain in the left eye and had a strong shake (felt as if electrocuted), probably because of the irritation of the pyramidal fascia. some capsule residue remains on the bottom and becomes heavily excavated, like half of an egg shell. during the procedure, the wound was flooded twice by an enormous quantity of cerebrospinal fluid which probably had drained from the ventricles through the cerebral aqueduct. after the first part of the tumour was lifted, the whole left hemisphere of the cerebellum remained depressed and stayed that way until the end of the procedure. the neoplastic tissue was placed on a pad that absorbed most of the liquids and, at the end of the procedure (several hours after it had been removed – 2 or 3), the tumour weighed 15 g. the dura was closed using the regular method. dressing with gold sheets and mastisol. saline 400 cc is delivered subcutaneously on the surgical table. after the procedure, the patient feels well, no longer reports headaches, is slightly pale. the heartbeat is 130, normal, regular breathing. on 15 february 1932, doctor d. bagdasar, assisted by his wife, florica bagdasar, performed a procedure under local anaesthesia with novocaine in a patient suffering from jacksonian epilepsy, through a left temporal parietal flap. description of the procedure: after cutting the flap, the dura appeared to be under tension, without pulses. an incision was performed on the dura parallelly to the bone and 1 (one) cm inside the bone, leaving an upper pedicle. clips were applied on the smaller veins of the dura. when cutting the dura, adherences were seen between the dura and the cortex at the upward parietal level. the adherences were very thin and broke easily. the arachnoid mater appeared in the upper-front half of the infiltrated breach as superplastic, with several whitish nodules the size of a pin head and a spermaceti-like appearance. at the level of the adherence, that is at the upward parietal level, in the centre of the hand, there is a yellowish, well-delimited nodule near two large veins. the nodule is the size of a bean. two clips are placed on the veins and then the nodule is detached through blunt dissection, also lifting part of the healthy substance in the brain. the bleeding is stopped with muscle tissue. a cotton pad immersed in formalin 10% is pressed on the cavity remaining after the nodule extraction (cushing style). several separated stitches are applied on the dura. then, the bleeding is stopped with several pieces of temporal muscle – haemorrhagic on one half. the flap is put back in place and sutured the regular way32. one month later, on 15 march 1932, doctor bagdasar, again assisted by florica bagdasar, performed a procedure under local anaesthesia with novocaine in a patient suffering from spinal arachnoiditis, through an explorative laminectomy of the 2nd, 3rd and 4th lumbar vertebrae. description of the procedure: the muscle tissues are separated with great difficulty because of the contraction. after lifting the spinal apophyses, drilling is carefully performed and the breach is widened at the level of the 2nd, 3rd and 4th lumbar vertebrae. an incision is performed on the dura which has some adherences to the arachnoid, along a 3–4 cm distance. the arachnoid is very much thickened and slightly translucid. there is nothing else of notice. the spinal cord is normal. the wound is closed with a continuous suture on the dura and 4 additional layers. dressing with mastisol”33. 395 unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar of the 28 surgical procedures performed by doctor dumitru bagdasar in 1932, we shall also stop on the one performed on 1 june. this involved a female patient (gertrude t.) operated by the same operating family team, under general anaesthesia with avertin 2 g 3% sol. + local anaesthesia with novocaine 2%. the patient diagnosed with a right cerebellar cystic tumour (pontopeduncular) was subjected to cerebellar exploration. description of the procedure: crossbow incision. craniotomy under the occipital protuberance, the dura appeared to be destroyed, without pulses. the vld is punctured, the fluid flows with a slight pressure but stops flowing after 5–6 cc of fluid. an incision is performed on the dura and the right cerebellar hemisphere comes out through the breach; the vermis is punctured with the same result. region v iv is examined but nothing is found. given the appearance of the cerebellum, we suspect the presence of a deep tumour, probably located on the front side of the right cerebellum which is inaccessible for our surgical methods. the musculocutaneous flap is closed without suturing the dura (500 cc of saline is given on the table). the surgery lasted from 9:30 am to 1:40 pa. autopsy: a cystic tumour was found under the right cerebellum, between the cerebellum and the pontopeduncular area; it was the size of a large walnut, containing haemorrhagic brown fluid whose appearance was identical to that of the fluid drained through the suboccipital puncture (15 may 1932). the cystic cavity was covered with gliomatosis tissue from which several pieces were collected for anatomopathological examination34. summing up the surgical procedures performed by doctor dumitru bagdasar in cernăuți in 1932, based on the protocols of the 28 procedures, one can conclude that 21 procedures were for brain diseases and the remaining (7) were for spine disorders (ct=1; t=3; l=3, of which one was a medullary tumour). the experience acquired in the boston clinic, in the jimbolia hospital and the cernăuți hospital materialises in 1932 with the publication of three scientific papers and the presentation of two communications on neurosurgery35. from 10 to 18 september 1932, doctor bagdasar participated in the 9th international congress on the history of medicine in bucharest, whose main topic was “the evolutions of medicine in the balkan countries”. among the 137 personalities coming from 23 different countries and representing 48 universities (cf. răzvan constantinescu, carol al ii-lea și congresul din 1932, viața medicală din 18 iulie 2014), there was also doctor john fulton, a friend of bagdasar’s since they had both trained in neurosurgery in the clinic led by professor cushing; the congress was an occasion for them to meet and reconnect. an important aspect of the neurosurgical activity carried out by doctor bagdasar in cernăuți from 1931 to 1932 was his application to the healthcare inspectorate where he requested that a psychiatry unit be converted into a neurosurgery unit. through its official communication no 4429 of 2 november 1932, the inspectorate expressed its approval and thus the first official neurosurgery unit in the country was founded; doctor herbert urban of the surgical clinic of the vienna university asked to be informed on how this unit had been organised so that the same model could be implemented in vienna36. in 1933, 31 neurosurgical procedures were performed by doctor dumitru bagdasar assisted by his wife, doctor florica bagdasar, as well as by ms. stofer, sava, sorodoc, pokai (nurse). these procedures included: cerebral decompressions, explorative or decompressive drillings, cerebellar explorations, abscess opening through the cerebellum, trigeminal neurotomies, laminectomies, cordotomies and decompressions or sutures of the peripheral (median/cubital) nerve traumas29. summing up the activity carried out at the hospital for mental and nervous diseases of cernăuți, doctor bagdasar states that, from 1931 to 1933 he admitted 639 patients to the neurology unit, many of which required neurosurgical treatment: 24 ventricular punctions, 33 subtemporal decompressions, 17 rolandic decompressions, 28 fp flaps, 5 f flaps, 18 cerebellar explorations, 4 retrogasserian neurotomies, 20 laminectomies (tumours, arachnoidites, rhizotomies and cordotomies). besides the aforementioned procedures on the central nervous system, he also performed procedures on the peripheral nervous system: two pericarotidal sympathectomies and a suturing of the median nerve. he also performed 16 vasectomies in patients with mental disorders37. the four scientific papers published in 1933 reflected the neurosurgical issues bagdasar had faced during that year, beginning with cerebro et ventriculoscopie, continuing with two papers on trigeminal procedures and concluding with one paper on a cystic cerebellar tumour38. in 1934, doctor bagdasar returned to bucharest, with the support of professors iacob iacobovici and 396 horia berceanu, stanislav groppa, horia pleș nicolae minovici, where he carried out his neurosurgical activity in two hospitals: the emergency hospital founded by professors minovici and iacobovici within the ambulance station39 on independence street and the central sanatorium40. in 1934, he performed 41 neurosurgical procedures at the emergency hospital41 and 23 procedures at the central sanatorium. the neurosurgical pathology he dealt with during that year led doctor bagdasar to write and publish six scientific papers42. at the end of 1934, doctor dumitru bagdasar published the paper entitled: titluri, lucrări științifice și activitate (titles, scientific papers and activity) including 28 pages, which we mentioned in the bibliographic references. in the chapter surgical activity, he underlines the fact that, alongside his activity in neurology, he also worked in the surgery unit of the same hospital, led by professor mihail butoianu, where, for three years, says the author: “i was given the freedom to operate and i performed a relatively significant number of procedures”, “this surgical traineeship which lasted for three years was useful in my approach to neurosurgery and is the foundation of my training in that field”19. the chapter neurosurgical activity is divided into four parts: the united states, the jimbolia hospital (27), the hospital for mental and nervous diseases of cernăuți (149), the emergency hospital and the central sanatorium of bucharest (60), and mentions the types and number of procedures (236) performed in the hospitals of greater romania from 1930 to 1934. he also makes brief notes on the surgical techniques used and the difficulties he faced in the preoperative radiological exploration of patients43. we previously stated that the surgical report archive of the two hospitals in bucharest (the emergency hospital and the central sanatorium) where doctor bagdasar performed procedures in 1934 contains 64 reports, representing – most certainly – the correct number of procedures performed (the four additional procedures were performed by doctor bagdasar after the publication of that volume). the activity carried out by doctor bagdasar at the emergency hospital of bucharest, since returning to bucharest and until early autumn was described by one of the hospital leaders, professor iacobovici in a certificate of activity, probably required for the enrolment in a contest for an attending neurosurgeon position at the central sanatorium which was approaching. dr bagdasar has been working in the emergency hospital since its founding. he took on 38 cases of non-traumatic injuries and led the treatment of all the skull fractures and all the traumatic nervous injuries. [...] anyone who has experience in nervous surgery would see in mr bagdasar the maximum level of knowledge in this special branch of surgery, an impeccable technique and rare operating dexterity. humble, hard-working, absolutely unbiased, mr bagdasar works with his own personnel, trains other practitioners of the emergency hospital and he brings all his own instruments every time. after surgeries, he attends to each patient day by day with extreme care until the end. [...] i have seldom had a collaborator with such exquisite education, such deep scientific insight and who worked with more self-sacrifice for science and the ill44. in late 1934, from 30 november to 2 december, the first contest in romania for the position of attending neurosurgeon at the central hospital for mental and nervous diseases took place in bucharest. the three practitioners who enrolled in this contest, doctors bagdasar, moruzi and vasiliu had completed their specialisation in important centres of the united states or europe. details about this contest are provided by dumitru bagdasar in a so-called diary45 that we had access to thanks to the efforts of professor ștefan i. niculescu (son of i. t. niculescu). the author of the diary concludes the description as follows: “the ranking was decided as follows: since moruzi and i had equal grades, i was ranked first because the rules set forth that seniority in the ministry was decisive in case of equal grades”. since 1935, doctor dumitru bagdasar’s surgical activity was carried out predominantly in one hospital, the central hospital for mental and nervous diseases of bucharest, where he earned his position following the contest for attending neurosurgeon. in that hospital, he performed 17 neurosurgical procedures in 193546. the working conditions in the operating unit of this hospital that was under refurbishment from the second half of 1934 are described in a very plastic but truthful way by the one who assisted him in a large number of neurosurgical procedures throughout 7 years of activity (1934-1940) – doctor maria i. niculescu. she describes the shocking working conditions of d. bagdasar and his team in those early days of neurosurgery in bucharest: “the patients were naked, 397 unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar kept behind bars and, in that eerie atmosphere, outstanding surgical procedures were performed on an improvised wooden table, using a vacuum cleaner for home use adapted for surgeries and most instruments bought or made based on bagdasar’s instructions, thus following cushing’s example but without comparable financial resources”47. at the same time, he continued to perform procedures at the emergency hospital48 or even other hospitals in bucharest, such as the colțea hospital49 as well as the military hospital50 and the french sanatorium or paul vincent hospital51, using a portable surgical instrument case that he sterilised in the hospital unit where he performed the procedure. alongside his surgical activity in the abovementioned hospitals, doctor bagdasar would attend the histology laboratory of the medical school led by professor ștefan besnea and then by ion t. niculescu each week: “every week, the microscopic sections of all the operated tumours brought in in countless cups and containers were discussed in depth by brătianu, ion bazgan, later c. arseni and occasionally emil crăciun and maria niculescu, drawing up reports including the macroscopic description, size, weight, microscopic description, diagnosis and synthesis of the discussions”52. throughout the years, he participated in various congresses, scientific meetings on neurology (the 1931 bern congress), the history of medicine (the 1932 world congress of bucharest), neurology, psychiatry and endocrinology (chisinau, 1935), surgery (the national congress of surgery, bucharest, 1939) etc. in 1936, doctor dumitru bagdasar wrote a report mentioning all the cases of primordial medullary tumours published and operated in romania up to that date: 12 cases operated by professor amza jianu at the recommendation of dem paulian, two cases operated by doctor constantin leonte at the recommendation of the same doctor and 13 cases operated by doctor alexandru moruzi under the supervision of professor leon ballif. (apud ștefan balmez, tumori medulare – studiu anatomo-clinic și terapeutic (medullary tumours – anatomic, clinical and therapeutic study) (doctoral dissertation)53. from 1931 to 1941, summing up his activity in a report, dumitru bagdasar stated: during the years before the current war (1941), besides the domestic patients, i also received patients from hungary, bulgaria and palestine. from 1931 to date – therefore during a time span of 10 years – i performed 1,800 surgical procedures on the nervous system, divided as follows: 473 ventriculograms having the purpose to diagnose the existence and location of neoplasms, 988 large craniocerebral procedures, 259 laminectomies, 83 procedures on the peripheral nerves54. from 1939 to 1940, after the death of professor marinescu, with his successor, professor nicolae ionescu-sisești and with the approval of the council of the faculty of medicine and the civil hospital board, a plan was drawn up to oversee the fitting of a modern neurosurgery ward with a capacity of at least 80 patients near the neurology clinic of the colentina hospital that could rival similar services abroad... in a report from 1941, after the beginning of the war, doctor bagdasar stated with disappointment: “[...] in february this year, however, i found out that, for reasons unknown to me, the ward had been given a different destination. the war caught me by surprise in a totally insalubrious building and the available personnel that had been trained for these procedures was made up of doctor arseni c. with a 5-year experience in the speciality and 3 nurses who had trained in the neurosurgery unit for the previous years. doctor arseni was mobilized and kept on the battlefront since the beginning of the war, although i had made countless attempts through the ministry of health and the military authorities to have him brought back to the hospital, where he would have been incomparably more useful to the army than on the battlefront. such reasons have not been understood and my requests remained unanswered. [...] during the months of july and august, the injured started to come in as neurological patients with much more serious injuries than those in the general surgery units: complete irreversible palsies of the lower limbs through sectioning of the spinal cord, half-body palsies through brain injuries, brain abscesses, meningitis etc.”55 from 1942 to 1946, according to the reports of doctor sofia ionescu-ogrezeanu56: doctor dimitrie bagdasar would come to the hospital from the cotroceni neighbourhood before 5 am. doctor constantin arseni would walk several kilometres on calea văcărești on any weather to be in the hospital at 5 am. the family ionel and sofia ionescu lived at the hospital. professor bagdasar was renowned for his incredible work capacity. a handful of people had to cater to all the needs of the patients occupying the 80 beds the ward had at that 398 horia berceanu, stanislav groppa, horia pleș time. an ambulance would bring in a war injured or a neurosurgical emergency every minute. professor bagdasar started his day by visiting the patients in the injured ward. then he visited everybody else. once he entered the operating room only god knew when he would come out. he would keep his cool even in the most difficult circumstances in the operating room. he had the lightest hand when operating. at the end of each procedure, he filled in the surgical report for the operating register very meticulously. his notes were a priceless study material for anyone who read them. his writing was easily readable, clear, accompanied by drawings, sometimes using colours. he would describe the key moments of each procedure with extreme meticulosity for his collaborators. any patient in a deep coma was cared for by bagdasar’s team until the very last moment. in doctor bagdasar’s ward, no patient passed away without a doctor by their side. inoperable cases and inane complications caught his interest. he had real talent as a researcher. every case was a lesson learned. in 1946, the neurology professor ionescu sisești, speaking about the activity in his ward, said: it was not only a hospital where surgical procedures were performed, it was a centre of relentless scientific research”57. his left-wing political orientation was a characteristic of his views throughout the years, being materialised through his membership of the romanian communist party since 1943, by signing the memorandum of april 1944 through which the intellectuals demanded the exit of romania from the war, through his activity in the board of “apărarea patriotică” and his tenure as ministry of health in the petru groza government since 6 march 1945. this orientation was analysed, accepted and classified – after o period of 60-70 years – by his daughter, a world-renowned mathematician, professor alexandra (bagdasar) (bellow) calderon58 and by doctor mihail mihailide59. my father’s life was a continuous struggle. he had nothing «for free». extreme poverty marked his childhood and adolescence years. when he thought he had overcome the «money issue», world war i broke out and he was sent to the battle front as a military doctor; there he fell ill of typhus and struggled to survive. his desire to learn and his prodigious work capacity were to a great extent also fed by his strong desire to contribute to the fight against poverty and human suffering which he had personally faced since a young age”. [...] “of course, my parents were not «professional revolutionaries». they were not made for a political career, power games and political scheming. the fight for privileges and benefits had nothing to do with them. but my father grew up seeing a lot of poverty and human suffering in the rural areas. in a country where the majority of people were peasants, he was acutely aware of the situation in the rural environment: illiteracy was spread to a shocking extent, the lack of hygiene and medical care, the huge rate of child mortality were all issues he felt deeply and first-hand. humanistic ideas attracted him instinctively, because social injustice and racism, chauvinistic and exclusivist nationalism revolted him (see his diary from 1934 to 1935). he was, by his nature, on the side of the needy, so his left-wing orientation was natural. my mother, who was devoted to him and passionately believe in him, embraced his ideas”60. being well informed and endowed with the scientific rigour of his profession, doctor mihail mihailide managed to extract – from a history of communism in romania – the parts that refer to doctor bagdasar, drawing up his own motivated presentation after what alexandra bagdasar59, 61 had written before him, in two substantial articles of medical history published in the weekly paper “viața medicală” which he ran at that time and of which we shall quote a small part49: [...] “for his unconditional support to the new government, dumitru bagdasar was appointed minister on 6 march 1945. he travelled across the country, becoming, according to the existing documents, an excellent propagandist, due to his increasing medical prestige and rhetoric qualities. several speeches he held on various occasions have been preserved in his own writing: agitator messages, some of which used a wooden language that was quickly adopted by the speaker, including reverences to the great eastern friend, filled with slogans and concluded with the invariable “long live...!” regarding the awarding of his professor title, reader dumitru bagdasar, who had been recently appointed ministry of health in the petru groza government, there are memorial documents that are considered unique in romanian higher education, where a reader refuses the title of professor on the first proposal and accepts it unwillingly on the second nomination. i shall quote those testimonies left for posterity for the elegant expression and argumentation of the two parties at the dawn of the new democracy through: the request sent to the dean of the faculty of medicine, professor gr. t. popa by bagdasar and the reply that the latter received: “mr dean, please be my interpreter with the faculty professors, to whom i thank with all my heart for the care they show to our higher education or for the efforts they make to accomplish something in our 399 unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar field. the political position i hold at the moment does not allow me to accept this honour. during the dictatorship, i heavily criticised the tendency of certain high dignitaries to secure benefits for themselves or their friends in higher education. the professors and the public opinion of the time shared this view”; professors c. i. parhon, c. i. urechia replied to this request on 1 november 1945: “we, the members of the advisory commission for position holders, have been aware for several months of your refusal to accept this title [...] however, considering the need to have a neurosurgery department in our institution, we and all our colleagues are asking you to please not deny our faculty the honour to have the first department in our country for this branch of medicine and to accept our recommendation”!62 he died on 16 july 1946 after an illness that lasted several months and forced him to give up his ministerial assignment on 24 april 1946, as well as the nomination for ambassador of romania in the united states61. before that date, following a medical examination in vienna, he had found out his primary diagnosis (inoperable lung/digestive cancer)62 and he established his secondary diagnosis on his own (brain metastasis) once apraxia settled in... “with his extraordinary common sense, professor bagdasar did not tell the truth to anyone. he retired to the town of breaza to await his end. on his deathbed, in his very last moments, he called his collaborators: dr constantin arseni, dr ionel ionescu, dr sofia ogrezeanu ionescu. what were his last words? do everything in your power for this speciality to evolve. be as one. continue what you started with the same energy, the same passion and, especially, with the highest ethics. he also wanted doctor constantin arseni to be appointed manager of the ward”63. he became a post-mortem member of the academy of the popular republic of romania in 194864. after he won the contest for the position as attending neurosurgeon, during one decade (19351944), he published 28 scientific papers in medical journals and he presented three reports at specialist congresses. two other papers to which he had contributed substantially were published post mortem: d. bagdasar, gh. pasăre, sindromul senzitivomotor de tip periferic după traumatismele parietale, spitalul, 1947, an. 67, nr. 5-8/mai-august, p. 10610865. d. bagdasar, c. arseni, traité de neurochirurgie, introducere de c. i. parhon, editura academiei r. p. r., bucurești, 1951, 601 [603] p., cu 1 [4] f. (translated in french by doctor maria niculescu)64. for the 10-year anniversary from the death of professor dumitru bagdasar, professor i. t. niculescu, a correspondent member of the academy of the popular republic of romania, made a magnificent description of bagdasar starting from their first encounter in 1914, continuing with the time spent in professor marinescu’s clinic and up to the time in doctor noica’s ward at the military hospital of bucharest where lifelong friendships had been built between co-workers who shared the same spiritual values...: in 1914, i first met a young man with smiling and kind eyes but at the same time endowed with a subtle irony. it was mitică bagdasar. he was the pride of the people of bârlad who had joined him at medical school. his wide general knowledge, his kindness and loyalty had immediately earned him the high esteem and fondness of his colleagues. an original note was his travel wear, with a wide hat and floating lavaliere that completed his appearance as a young man with a mind full of verses and good reading, which had always been his spiritual delight. [...] bagdasar’s first years as a student were impacted by the war of 1916-1918, when he did his duty as a doctor. after the war, i had the privilege to get to know bagdasar better when we worked together in professor marinescu’s clinic in colentina, as well as later, when he worked with the great clinician, doctor noica. mitică bagdasar approached this distinguished person, follower of dejerine, babinski and pierre marie, with fondness and attachment, learning everything from doctor noica’s experience in the admirable french clinic. the intellectual respect for noica was doubled by a rare lifetime friendship between the two. thus, through his long and diligent work alongside noica and marinescu, bagdasar set the foundation of a deeply eradicated neurologic culture which later turned him into one of the most erudite neurologists in romania. since bagdasar knew very early that he was going to become a neurosurgeon, he integrated his activity with extensive work in surgery within professor butoianu’s unit at the military hospital. [...] bagdasar was the founder of modern neurosurgery in romania. romanian science owes him a lot. he transplanted a difficult but very useful science into our country. he brought in all the scientific and technical knowledge in neurosurgery of the great harvey cushing, he applied all the novel scientific breakthroughs in this field 400 horia berceanu, stanislav groppa, horia pleș with discernment and seriousness, bringing important personal contributions and showing at all times the utmost respect for the ill whom he helped with love, delicacy and a sense of humanity. he was a gentle and understanding master for his followers. throughout his tragically ended life, bagdasar was a great doctor and a good man, whom all good people should remember with love and kindness”66. the disciple and successor of professor dumitru bagdasar as leader of the neurosurgery school in bucharest, professor constantin arseni, on the occasion of the 30-year anniversary from his master’s death, wrote in a prestigious journal of the time: doctor bagdasar lived in a golden era of the romanian medical school. that was for him an advantage because he had examples to emulate but also a disadvantage because it is obviously more difficult to shine in the light than in the shade. but – though it was more difficult – ha managed to shine in the light. [...] doctor bagdasar’s personality as a doctor was necessarily and harmoniously doubled by the finest personality as a person. he was a good and generous man, showing endless understanding towards human suffering, he had an unusual sense of justice and therefore of revolt in front of injustice. he was a deeply honest person, having a real cult for honesty, human values and respect for people, for the liberties of the individual and society. he was harsh on himself and would not accept any moral compromise. these ethical principles developed his activist side. it is known that he was one of the initiators and signatories of the 1944 memorandum through which intellectuals requested the exit of romania from the war and after 23 august 1944, as doctor bagdasar was continuing his activity as a neurosurgeon, he found new resources to participate in the leadership of “apărarea patriotică” and in 1945 he was appointed minister of health in unimaginably difficult circumstances of neediness, hunger, epidemics, destruction and disorganisation. with the same perseverance and selflessness, doctor bagdasar did all his duty and gave his whole self. in 1946, he died knowing he had completely honoured his duty67. notes 1. simion tavitian, armeni de seamă din românia, vol. i, p. 55, in: www.ziuaconstanta.ro, 2. acad. prof. dr. a. kreindler, viața și opera profesorului dr. dumitru bagdasar, societatea pentru răspîndirea științei și culturii, bucurești, 1960, p. 4. 3. dumitru bagdasar, muncă și caracter, scrisori-jurnalportrete-discursuri-evocări. introducere, selecție, prezentare și aparat critic de ștefan i. niculescu, editura eminescu, bucurești, 1987, mărturii de nicolae bagdasar, p. 351-353. 4. dr. d. bagdasar, titluri, lucrări științifice și activitate, bucurești, 1934, p. 4. 5. dr. d. bagdasar, op. cit., p. 4-5. 6. dr. d. bagdasar, op. cit., p. 3: “from 1921 to 1922, i attended the neurologic clinic of professor marinescu, being transferred there by the medical military institute for specialisation”. 7. dr. d. bagdasar, titluri, lucrări științifice și activitate, bucurești, 1934, p. 5-11. 8. dr. d. bagdasar, op. cit., p. 12. 9. m. butoianu, i. gilorteanu, cranioplastie tardivă cu placă metalică pentru pierderi mari de substanță craniană, spitalul, 1922, p. 310. 10. ștefan i. niculescu, contribuții la biografia lui d. bagdasar, în: trecut și viitor în medicină, studii și note, sub redacția dr. g. brătescu, editura medicală, bucurești, 1981, p. 618-619. there are three letters that professor nicolae paulescu wrote to doctor dumitru bagdasar in reply to the latter’s own letters to his master, which i shall reproduce here to show their narrative beauty after nearly one century since they were written... the first letter is dated 15 april 1928: “my dear friend, i am delighted by what you found in boston and that it is everything you wished for. please be so kind as to send my greetings to professor cushing, along with my gratitude for the kind welcome he has shown you. yours truthfully, paulescu”. it should be noted that the letter was written in french so that bagdasar could show professor cushing the gratitude that professor paulescu had expressed towards him. the second letter, dated 18 december 1928: “my dear friend, thank you so much for the kind wishes for my onomastic. how long will you be in america? we are anxious to have you back. the other day, i saw a still young gentleman from the higher class (mr bărdescu) with signs of tumour localised on the lower right peri-rolandic region, with jacksonian seizures. since you were not here, i had to send him to paris to be operated by a specialist”. the next part of the letter is written in french, probably for the same reasons we suspected for the first letter: “please remind your eminent and illustrious master, professor harvey cushing, of me and give him my best regards”. at the end, he adds in romanian: “and please accept, my dear friend, my affectionate and devoted greetings, paulescu – p. s. i should be delighted if you sent me a photograph of master cushing”. paulescu’s last letter is dated 11 february 1929: “my dear friend, your incomparable master informed me of the accident that forced you to suspend your training. do not worry too much because such inconveniences have often happened before in many young people, for instance a professor of iași, who is now big and fat and perfectly healthy. i do believe though it would be safer if you returned to our country as soon as your health allows you to travel. please give 401 unpublished data on the founder of romanian neurosurgery – professor dumitru bagdasar my best regards to mrs bagdasar and receive my affectionate and devoted greetings, paulescu”. 11. n. c. paulesco, recherches sur la physiologie de l’hypophyse du cerveau, journal de physiologie et de pathologie générale, no. 1, paris, 1907. 12. n. paulesco, l’hypophyse du cerveau. i. physiologie. recherches expérimentales, paris, 1908. 13. s. j. crowe, harvey cushing and john homas, experimental hypophysectomy, johns hopkins bull, 1910, 21, p. 130. 14. ian murray, paulesco and the isolation of insulin, jl. of the history of medicine and allied sciences, 1971, 26, p. 152. 15. ștefan niculescu, op. cit., p. 617. 16. prof. dr. radu iftimovici, osmoza paulescu – cushing, viața medicală, vineri 21 oct. 2016. 17. hortensiu aldea, istoria modernă și contemporană a neurochirurgiei românești, editura pim, iași, 2017, p. 12 18. dumitru bagdasar, muncă și caracter, scrisori-jurnalportrete-discursuri-evocări. introducere, selecție, prezentare și aparat critic de ștefan i. niculescu, editura eminescu, bucurești, 1987, 413 p., p... 19. hortensiu aldea, op. cit., p. 13. 20. dr. d. bagdasar, op. cit., p. 13-14: in his first paper, tratamentul chirurgical al gomelor cerebrale, the author states that from a statistic of 1,500 brain tumour operated in professor h. cushing’s neurosurgery unit, only 8 (0,5%) were anatomopathologically verified brain gummas. conclusion: surgery is useful because 7 of the operated patients were cured and the specific treatment was more efficient after decompression or removal of the sclero-gummatous lesion. in the second paper, cordoblastoamele intracraniene, the authors reported two cases operated by professor harvey cushing: the first one involved a single procedure following which the patient was cured, while the second one involved two procedures distanced by six months (the second one was fatal). conclusion of the study: total removal of these tumours is not possible and relapses are frequent. 21. h. aldea, op. cit, p. 13. 22. ștefan i. niculescu, op. cit., p. 619-620. 23. ștefan i. niculescu, op. cit., p. 619. in a letter dated 9 march 1929, cushing wrote: “dear bagdasar, i have just received a letter from paulescu who asked me to give you a letter directed to you. from what he writes, i suppose he heard about your illness and the temporary suspension of your work which saddens us all enormously. but i hope you and your wife are both on your way to recovery. please sent him my warmest regards. yours sincerely, harvey cushing”. 24. dr. d. bagdasar, op. cit., p. 14: “in 1930, i performed the first neurosurgical procedures in our country. influenced by dufour’s ideas that in case of neurosyphilis resistant to medical treatment cranial decompression can be beneficial, i performed procedures on four syphilis patients whom i followed up for several months. the patients did not improve. my conclusions were that decompression is only beneficial in case of brain gummas and i abandoned this methos. overall, at the jimbolia hospital, i performed 27 procedures on the central nervous system, divided as follows: 15 ventricular punctures, 2 subtentorial decompressions, 1 cerebellar decompression, 9 frontal parietal flaps. besides these, i performed: 4 femoral periarterial sympathectomies, 2 frenectomies, 12 vasectomies”. 25. h. aldea, op. cit., p. 27. 26. h. aldea, op. cit., p. 15. 27. horia pleș, horia berceanu, eliza berceanu, 150 de ani de la nașterea părintelui neurochirurgiei mondiale, harvey williams cushing (1869-1938), a ix-a ediție a congresului național de istoria medicinei, vaslui, 23-25 mai 2019, volum de lucrări (ediție coordonată și îngrijită de dr. valeriu lupu), editura pim, iași, 2019, p. 314. 28. dumitru bagdasar, surgical reports – 1-28 – procedures performed at the hospital for mental and nervous diseases of cernăuți in 1932. operating register, archives of the clinical emergency hospital bagdasar-arseni, bucharest. the surgical reports are written by doctor dumitru bagdasar in a clear, calligraphic handwriting. 29. dumitru bagdasar, surgical reports – 1-31 – procedures performed at the hospital for mental and nervous diseases of cernăuți in 1933. operating register, archives of the clinical emergency hospital bagdasar-arseni, bucharest. the surgical reports are written by doctor dumitru bagdasar in a clear, calligraphic handwriting 30. dumitru bagdasar, ibidem, surgical report for the first procedure performed in cernăuți in 1932. 31. dumitru bagdasar, ibidem, surgical report for the second procedure performed in cernăuți in 1932. 32. dumitru bagdasar, ibidem, surgical report for the procedure performed on 15 february 1932. 33. dumitru bagdasar, ibidem, surgical report for the procedure performed on 15 march 1932. 34. dumitru bagdasar, ibidem, surgical report for the procedure performed on 1 june 1932. 35. dr. d. bagdasar, op. cit., p. 15-17. 36. dr. s. lavrov, oameni și fapte din istoria medicinei militare românești, vol. i, coordonat de general de brigadă (r) dr. mircea diaconescu, editura pro transilvania, bucurești, 2005, p. 405. 37. dr. d. bagdasar, op. cit., p. 15. 38. dr. d. bagdasar, ibidem, p. 17-20. 39. the emergency hospital of bucharest was founded in 1933 (through decision no 68920 of the ministry of labour, health and social security, published in the official gazette no 251 of 31 october 1933), creating a unified emergency care system, with a sole management for all activities (first aid, transportation – ambulance, specialistic care – emergency hospital). i. iacobovici had been appointed medical manager of the hospital and n. minovici managed administrative matters. after the management had been appointed and approved by the administrative and technical healthcare authority of the ministry in september-october 1933, on 6 november 1933, the ambulance society committee acknowledged 402 horia berceanu, stanislav groppa, horia pleș all the action taken up to that point and gave its approval for the fitting of an emergency surgery hospital within the head office of the ambulance society on splaiul independenței. unofficially but partially, the hospital starts to operate immediately, thus preceding the official opening of the 50-bed hospital on the 5th of may 1934 (apud, mircea beuran, benone duțescu, rodica duțescuzăvoianu, asistența urgențelor chirurgicale din bucurești, certitudini și speranțe, editura academiei române, bucurești, 2014, p. 30-31). 40. the central hospital for mental and nervous diseases was a ward hospital assigned in 1923 where professor alexandru obregia relocated the psychiatry clinic that had been run un until that point at the mărcuța hospice. 41. dumitru bagdasar, ibidem, surgical reports of the emergency hospital of bucharest, 1934. 42. dr. d. bagdasar, op. cit., p. 21-25. 43. idem, p. 25. summing up his neurosurgical activity carried out in the romanian hospitals from early 1930 to november 1934, doctor bagdasar stated that the following procedures had been performed: 49=ventriculograms, 12=t flaps, t-p flaps, 27=cerebellar explorations, 42=subtemporal decompressions, 17=rolandic decompressions, 5=metal plate plastic surgeries of the skull, 4=retrogasserian neurotomies, 32=laminectomies 44. national archives of romania, bucharest, bagdasar family fund, file 20, 21 september 1934. information confirmed in mircea beuran, benone duțescu, rodica duțescu-zăvoianu, asistența urgențelor chirurgicale din bucurești, editura academiei române, bucurești, p. 32). 45. dumitru bagdasar, muncă și caracter, scrisori-jurnalportrete-discursuri-evocări. introducere, selecție, prezentare și aparat critic de ștefan i. niculescu, editura eminescu, bucurești, 1987, 413 p., p. 243-246. the diary includes bagdasar’s daily notes from two time periods: 3 september 1934 – 10 september 1935 and 12 october 1935 – 10 july 1936, the missing time span being due to the author’s illness. these notes by doctor dumitru bagdasar had been originally published by professor șt. i. niculescu in the volume: apărarea sănătății ieri și azi, editura medicală, 1984, p. 399-424. 46. dumitru bagdasar, ibidem, surgical reports from the central hospital, 1935. 47. dumitru bagdasar, muncă și caracter, p. 11. 48. dumitru bagdasar, ibidem, surgical reports from the emergency hospital, 1935. 49. dumitru bagdasar, ibidem, surgical reports from the colțea hospital, 1935. 50. dr. mihail mihailide, d. bagdasar, un exponent al „stângii naive” (1), viața medicală, miercuri 1 mai 2013, or at: https://www.viata-medicala-ro//istoria-medicinei/dbagdasar-un-exponent-al-stângii-naive 51. maria i. niculescu, operații neurochirurgicale la care l-am ajutat eu, manuscript, kept at the library of medical history of the national public health institute, bucharest, p. 63, with the mention that it is currently being printed. 52. dumitru bagdasar, muncă și caracter, p. 12. 53. h. aldea, op. cit. p. 17. 54. rodica simionescu, neodihna binelui, neurochirurg sofia ionescu, editura atlas, bucurești, 1998, p. 86. 55. dumitru bagdasar, muncă și caracter, p. 207-208. 56. tatiana roșca, horia berceanu, antoaneta marinesculucasciuc, maria-gabriela suliman, doctor sofia ionescu (1920-2008) prima femeie neurochirurg din lume, a 47-a reuniune națională de istoria medicinei, roman, 17-19 mai 2018. 57. rodica simionescu, op. cit., p. 81-82. 58. alexandra bagdasar (called “gugu” by her parents) was born on 30 august 1935 in bucharest where she attended primary and secondary school and the faculty of mathematics of the university of bucharest, graduating in 1957. married since 1956 to her first-year mathematics professor, cassius ionescu-tulcea, whom she joined in 1957 to the usa, at the yale university, where he had been invited for a research project. after two years, alexandra defends her doctoral dissertation – ergodic theory of random series (teoria ergodică a seriei aleatorii) at that university (dissertation supervisor: professor shizuo kakutani). she was considered as an elite expert of ergodic theory, probability and mathematical analysis. since 1967, alexandra ionescu was a mathematics professor at the northwestern university and since 1996 she was professor emeritus of the same university. she was married three times: the first marriage lasted from 1956 to 1969, the second marriage to the american writer, recipient of the 1976 nobel prize for literature, saul bellow, lasted from 1974 to 1985 and the third marriage to the renowned mathematician alberto calderon lasted from 1989 to 1998 (when the husband died). 59. https://ro.wikipedia.org/wiki/mihail_mihailide 60. alexandra bellow, asclepios versus hades în românia (i), revista 22 din 25.08.2004. 61. alexandra bellow, asclepios versus hades în românia (ii), revista 22 din 01.09.2004. 62. dr. mihail mihailide, d. bagdasar, un exponent al „stângii naive” (2), viața medicală, vineri 10 mai 2013, or at: https://www.viata-medicala-ro//istoria-medicinei/dbagdasar-un-exponent-al-stângii-naive 63. rodica simionescu, op. cit., p. 84-85. 64. https://ro.wikipedia.org/wiki/lista_membrilor_academie i_române 65. dumitru bagdasar și florica bagdasar, lucrări, p. 10 66. ion t. niculescu, în amintirea doctorului d. bagdasar, analele academiei republicii populare române, 1956, vol. vi, p. 401-404. 67. c. arseni, sentimentul datoriei împlinite, flacăra, nr. 22, 3 iunie 1976, p. 14. doi: 10.33962/roneuro-2020-066 spinal cord injury without radiologic abnormalities in a 4-years old boy. a case report sani madjiri laminou, ibrahim assoumane, adamou harissou, sanoussi samuila, abarchi habibou, smida mahmoud romanian neurosurgery (2020) xxxiv (1): pp. 421-423 doi: 10.33962/roneuro-2020-066 www.journals.lapub.co.uk/index.php/roneurosurgery spinal cord injury without radiologic abnormalities in a 4-years old boy. a case report sani madjiri laminou1, ibrahim assoumane2, adamou harissou3, sanoussi samuila4, abarchi habibou5, smida mahmoud1 1 department of paediatric surgery, tunis, tunisia 2 department of neurosurgery, reference hospital maradi, niger republic 3 department of general surgery, zinder national hospital, niger republic 4 department of neurosurgery, niamey national hospital, niger republic 5 department of paediatric surgery, lamordé national hospital, niger republic abstract in this study, we describe a 4-year-old boy with a head, cervical, and left shoulder injury following the reception of a heavy metallic door on his left side that resulted in sciwora. scwora is defined as spinal cord injury without x rays or ct scans lesions but can be detectable on rmi scans. sciwora follows trauma, sometimes trivial. the management consists of immobilization and nursing. the clinician should be aware of this entity. we are reporting the management of a four years old boy. introduction the term sciwora (spinal cord injury without radiographic abnormality) was coined by pang and wilberger in 1982 [1]. it is defined as objective signs and symptoms of myelopathy with no evidence of fracture or ligamentous instability on plain spine radiographs and tomography. this definition excluded all mri findings and any injuries from open or penetrating trauma, electric shock and all related to congenital spinal anomalies. ergun et al [2] highlighted the patho-physiological basis of sciworas. the anterior spinal artery receives its main blood supply from vertebral arteries. hyper motion effect of the spinal cord during trauma may provoke a temporary occlusion or spasm of the vertebral arteries, the anterior spinal artery keywords trauma, spinal cord, children corresponding author: ibrahim assoumane department of neurosurgery, reference hospital maradi, niger republic as_ ibrah2006@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 422 sani madjiri laminou, ibrahim assoumane, adamou harissou et al. or the distal branches of the central sulcus arteries leading to a spinal cord infarction. other anatomic factors considered by ergun include the vertebral alignments of cervical spine; the planes of the facet joint which are more horizontal, the anterior portions of vertebral bodies are weighed forward, the uncinate processes are flat, the under developed musculature of children’s neck and the heavy head. these above predispose the cervical column of children to flexion, extension or longitudinal distraction injuries. trigylidas et al [3] conclude that the innate ligamentous laxity of the pediatric spine may protects it from injury in minor trauma, but these same protective features expose them to permanent injuries in high intensity trauma. here we are reporting a case of sciwora in a 4years old boy. observation a 4 years old boy polytraumatism referred from poudriere general hospital with head injury with initial loss of consciousness, cervical trauma and left shoulder trauma. the patient was stamped by a heavy metallic door on the head, neck and the left shoulder. at admission the glasgow scale was normal, left mydriasis, bilateral palpebral oedema. he was tetraplegic spontaneous mobilization of the cervical spine, lost of sensation of the right hemi body and reduced sensation of the left side. the rot are absents in the 4 limbs, no babinski sign, cremasteric sign is abolished and the anal sphincter was not tonic. the lesionnel level was the mammary line. the standard radiograph of the head, the cervical spine was normal [fig1]; the left shoulder x ray revealed a mid-shaft clavicle fracture. a cerebrospinal ct scan was performed, but was normal. figure 1. lateral x ray of the cervical spine, no lesion observed. we requested a neurologic view. the patient returned to us with same examination findings. the diagnosis of sciwora was made the patient placed in icu, nursing and resting was consigned and a cerebrospinal rmi was performed. it revealed no cerebral lesion but there was thickening of the spinal cord from c3 to c7 with narrowing of the perimedullar space [fig 2]. figure 2. cervical spine rmi showing cord thickening from c3 to c7; no other lesion was recorded. a: sagital t1; b: sagital t2. discussion sciwora accounts for 1-10% of the spinal cord injury in children. gregory et al [5] reported 0.08%cases in a multicentric study on about 34069 patients., sciwora is more common in children than adult with literature reports of 13 to 19% and 10 to 12% of children and adult spinal cord injuries respectively [6, 8, 9] the trauma causing sciworas may not be of high intensity only, it may be trivial also. this is widely illustrated in the literature. trigylidas [3] found 51% cases of sport related injuries, 36% of rta and 13% of falls. ergun et al reported a 12-year-old girl who slipped on her way home from a volley ball match and developed sciwora. our patient was stamped by a heavy door. injury to the cervical spine is much more common than the thoracic and lumbar spine. the upper cervical spine (c2, c3) is more prone to flexion injuries. snoek [4] reported that traction injuries may be common in thoracic and lumbar spine. clinical features classically include neurological deficit (decrease reflexes and power, reduced sensations below the level of the lesion, reduced anal tone and loss of bladder control), torticolis [4]. these findings correlate with our patient. the irm findings ranged from spinal cord contusion [2], central disc a b 423 spinal cord injury without radiologic abnormalities in a 4-years old boy herniation [2, 5], paramedian disc herniation [5], spinal cord stenosis [5], ligamentous injury spinal cord edema [4] and hemorrhage [4]. the corresponding standard radiographs and ct scans were all normal. we found cord edema in irm reports, lammertse et al [7] coined irm as the gold standard in diagnosis of spinal cord injuries. the outcome of sciwora may be good or devastating to the patients and their families’. the patient in our report sustained permanent injury. snoek reported a good prognosis in a child who sustained bifocal sciwora following rta. the outcome is independent the intensity of the trauma. it would rather be influenced by the patient age and the level of the lesion. the development of the cervical spinal musculator reaches it fulcrum by the age of 8. lesions below 8 years of age may have poor prognosis especially associated with upper cervical injuries [2]. above 8 years the spinal architecture is approaching that adult, thus lesions occur in lower spine under high velocity trauma. conclusion sciwora is a disease entity of children and adult. following injury, a high index of suspicion is necessary in injured patients in whom movement of all limbs is not seen. mri is standard diagnosis and the outcome depends on the spinal injury. references 1. d. pang and j. e. wilberger, “spinal cord injury without radiographic abnormalities in children,” journal of neurosurgery1982, vol.57, no. 1, pp. 114–129. 2. ergun and w. oder, “pediatric care report of spinal cord injury without radiologic anomalies: case report and a review of literature, «spinal cord 2003, vol 41, pp .249253. 3. trigylidas.t, yuh.s.j, vassilyadi.m, matzinger.m.a, mikrogianakis.a, “spinal cord injuries without radiologic anomalies at two pediatric trauma centers in ontario “, pediatric neurosurgery 2010; 43:283-289. 4. snoek .k.g, jacobson .m. a.b.vanas,”bifocal spinal cord injuries without radiographic anomalies in a 5years old boy: case report “case reports in pediatrics 2012. 5. gregory.whendey, allan.bwolfson, william.r mower, jerome. r hoffman «spinal cord injury without radiologic abnormality: result of the national emergency xradiographic utilization study», the journal of trauma, injury and critical care 2002; 53, 1-4. 6. kivanc atesok, nobuhiro tanaka, andrew o’brien, yohan robinson, dachling pang, donald deinlein, sakthivel rajaram manoharan, jason pittman, and steven theiss.< <posttraumatic spinal cord injury without radiographic abnormality>>. hindawi advances in orthopedics volume 2018, article id 7060654, 10 pages. 7. d.lammertse,d.dungan,j.dreisbachetal.,“neuroimagin traumatic spinal cord injury: an evidence-based review for clinical practice and research,” the journal of spinal cord medicine,vol.30,no.3,pp.205–214,2007. 8. m.g.hamiltonands.t.myles,“pediatricspinalinjury:review of174hospitaladmissions,”journalofneurosurgery,vol.77, no.5,pp.700–704,1992. 9. s.sharma,m.singh,i.h.wanietal.,“adultspinalcordinjuryw ithoutradiographicabnormalities(sciwora):clinicaland radiological correlations,” journal of clinical medicine research,vol.1,no.3,pp.165–172,2009. romanian neurosurgery (2019) xxxiii (3): pp. 310-315 doi: 10.33962/roneuro-2019-052 www.journals.lapub.co.uk/index.php/roneurosurgery bilateral traumatic basal ganglia haemorrhage, a rare entity. experience at single institute with review of literature vibhu shankar parashar, vivek kumar kankane, gaurav jaiswal, tarun kumar gupta * department of neurosurgery, r.n.t. medical college & m.b. groups of hospital udaipur (rajasthan), india abstract aims. traumatic basal ganglia haemorrhage is rare entity but post traumatic bilateral basal ganglia hematoma is even extremely rare and was earlier presented as case reports. its incidence is about 3% after a closed head injury however, the incidence is higher in post mortem studies. material & methods. out of 1485 head injury patients admitted to our institute from january 2012 to january 2019, there were 9 cases of traumatic bilateral basal ganglia haemorrhage. the incidence of traumatic bilateral basal ganglia haemorrhage in our series is 0.61% which is very less compared to previous literature. results. there were 6 males and 3 females; age ranging from 19 to 50 years (average 32 years). patients with hypertension, history of drugs abuse, history of coagulopathy, with doubtful history of trauma or unknown mode of injury were excluded from the study. the mode of injury in all the patients was road traffic accidents. average follow up was 9.54 months. outcome was assessed by glasgow outcome score. in 8 out of 9 patients, outcome was good. one patient died. all the nine cases were managed conservatively. conclusion. we report nine cases from a single institute which to the best of our knowledge is the largest series in world literature. prognosis is variable and dependent on many factors. the prognosis of tbgh is favourable if not associated with other disorders like hypertension, diabetes mellitus, and coagulation disorders or diffuse axonal injury. introduction traumatic basal ganglia haemorrhage (tbgh), are a rare entity and reported in only 3% of closed head injuries. [1] however autopsy series indicate a higher incidence ranging between 10%to 12%.[2,3] it is defined as a haemorrhagic lesion located in the basal ganglia or neighbouring structures, such as the internal capsule and the thalamus, it can be classified as “large,” if it is more than 2cm in diameter or as “small” if it measures <2 cm in diameter.[2] bilateral basal ganglia hematoma after trauma is extremely rare and is limited to case reports. the mechanism of tbgh is unclear but is thought to be due to shearing keywords basal ganglia, trauma, bilateral, haemorrhage corresponding author: vivek kumar kankane r.n.t. medical college & m.b.groups of hospital udaipur, rajasthan, india vivekkankane9@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 311 bilateral traumatic basal ganglia haemorrhage of lenticulostriate or anterior choroidal blood vessels due to the violent acceleration deceleration brought about by a high velocity injury. [2,4] since basal ganglia hematoma can be due to trauma and thus takes importance in the medico legal cases where bleeding may be attributed to a non-traumatic cause. thus, the identification of tbgh is of prime relevance. material and methods out of the 1485 traumatic head injury patients, the study group comprised of nine patients of tbgh identified on the basis of initial noncontrast ct (ncct) head, admitted from january 2012 to january 2019 in the department of neurosurgery at r.n.t. medical college and m.b. hospital, udaipur, rajasthan. a written informed consent was taken from all patients, as applicable. hypertensive patients, drugs abuse history, history of coagulopathy with doubtful history of trauma or unknown mode of injury was excluded from the study. the diagnosis of tbgh was made on the basis on ncct head and outcome was assessed by glasgow outcome score. results total head injury patients admitted to the hospital were1485 among which nine patients of traumatic bilateral basal ganglia hemorrhage were identified and thus incidence of bilateral tbgh in our series is 0.61% (nine patients) which is very less as compared to previous literature. there were 6 males and 3 females; age ranging from 19 to 50 years (average 32 years (table1). all patients had sustained road traffic accidents. ncct head was done in all the patients [figure -1, 2, 3, 4 & 5] after initial resuscitation. gcs at admission were 7 to 12 (mean 10.0). (table 1)all the patients were managed conservatively .outcome was assessed by glasgow outcome score (table 2). outcome were labeled as good (gos-5, 4) and poor (gos1-3).the average follow up was 9.54 months. in 8 out of 9 patients the outcome was good. one patient had poor outcome and died. table 1. demographic analysis, management and outcome of all patients s.no age (yr) gender mode of injury gcs at admisson focal neurological deficit management outcome measured by gos 1 19 male rta 12 no conservative 5 2 45 female rta 9 left sided hemiparesis conservative 4 3 24 male rta 10 left sided hemiparesis conservative 5 4 50 male rta 7 left sided hemiparesis conservative 1 5 20 male rta 9 right sided hemiparesis conservative 5 6 40 male rta 9 left sided hemiparesis conservative 5 7 35 female rta 10 no conservative 5 8 25 female rta 12 no conservative 5 9 30 male rta 12 no conservative 5 312 vibhu shankar parashar, vivek kumar kankane, gaurav jaiswal, tarun kumar gupta image 1. ncct head shows hemorrhage in bilateral basal ganglia region, with involvement of right anterior limb of internal capsule. image 2. ncct head shows hemorrhage in bilateral basal ganglia, with left frontal depressed fracture with underlying small left frontal contusion. image 4 & 5. ncct head shows hemorrhage in bilateral basal ganglia region with subdural hemorrhage in right frontotemporoparietal region and subarachnoid hemorrhage along right frontal and temporal sulci and gyri. image 3. ncct head shows hemorrhage in bilateral basal ganglia region with fracture of outer table of right frontal sinus. table 2: glasgow outcome score (gos) gos score functional status 5 resumption of normal life, there may be minor neurological and or psychological deficit 4 able to work in a shattered environment and travel by public transportation 3 dependent for daily support by reason of mental or physical disability or both 313 bilateral traumatic basal ganglia haemorrhage 2 unresponsive for weeks or months or until death 1 death discussion the tbgh is a rare entity with an incidence rate of about 3% in closed head injuries. the exact pathogenesis of basal ganglia hematoma is unclear; however, it is suggested that a strong impact over the vertex, forehead, or occipital region, then shearing force causes the brain to be displaced through the tentorial notch. this results in stretching and tearing of the vessels resulting in hematoma. [2] the sudden acceleration/deceleration forces at the time of injury result in shearing strain over the lenticulostriate and anterior choroidal vessels leading to bleeding. mosberg and lindenberg, in an autopsy of fatal head injury patient, demonstrated massive hematoma in the pallidium and ruptured twig of the anterior choroidal artery. [4] since basal ganglia region is predisposed to hypertensive bleed, at times, it becomes difficult to distinguish between hypertensive and traumatic hemorrhage. it has been suggested that the tbghs are small, multiple, rarely bilateral, located in the zone of lentiform nucleus and external capsule, whereas spontaneous hemorrhages are large, solitary, and located mainly in the region of thalamus and internal capsule. [5, 6] in a known hypertensive patient with head injury and findings of basal ganglia bleed, it is imperative to ascertain the sequence of events. this may be a medico legal issue; as to whether the patient had spontaneous basal ganglia bleed leading to the subsequent head injury or it was the head injury, which caused the basal ganglia hematoma. in all our patients, there was a definite history of trauma with no antecedent history of preexisting medical illnesses and bleeding diathesis, thus the bilateral basal ganglia bleed seen on ct/mri scans was traumatic in nature. as our patients had small bilateral tbgh with volume <25 ml and showed gradual improvement of gcs with medical management, they were managed conservatively. treatment is based on protocol as for intracranial hematoma taking into account the neurological status, presence of mass effect and response to other means of controlling intracranial pressure. treatment options for tbgh include conservative, open surgery, ct guided stereotactic or ultrasound guided aspiration. katz et al [1], bhargava et al [6], jang et al [7] and kimura et al,[8] have reported favorable outcomes for tbgh with conservative management. boto et al advised surgical evacuation of all lesions with volume >25 ml; however, poor outcome was noted in most of these patients. [3] boto et al noted that 84% of surgically managed patients had an unfavorable outcome. surgical evacuation entails approach to the hematoma via the thalamo-ganglionic region, leading to further damage of the eloquent areas resulting in possible poor outcome. surgical management was done in patient described in case report by yanaka etal.[9] craniotomy was performed in patients reported by pandey et al [10],jain et al[11] and calderon et al [12]. the outcome of tbgh has been found to be variable. amongst 37 patients studied by boto et al.59%died, 5% were vegetative, 19% experienced severe disabilities, and 16% made a favorable recovery.[3] katz et al.[1], bhargava et al [6], kaushal et al [13] and zhang et al [14] have also reported good prognosis for tbgh. kankane et al reported bilateral traumatic basal ganglia bleed and both the patient managed conservatively and outcome was good and no focal neurological deficit. [15] zhang yx, et al reported single case of 45year female of traumatic bilateral traumatic basal ganglia bleed and patient managed conservatively and outcome was good. [14]in our study, all the patients were managed conservatively and in 8 out of 9 patients the outcome was good. one patient had poor outcome and died. large size, associated coagulation disorders, dai, presence of other bleeds like intraventricular of brain stem hemorrhage, age >60, abnormal pupillary response, abnormal motor response to pain, and severe head injury are reported to be indicators for poor prognosis.[1,2,5,16,17] this rare entity has been previously reported in literature by yanaka et al (2 cases), jang et al (1 case), kaushal et al (1 case), bhargava et al. 1 (1 case), jain et al (1 case), pandey et al (1 case), calderon et al (1 case), kankane et al (2 cases) and zhang et al (1 case). (table 3) 314 vibhu shankar parashar, vivek kumar kankane, gaurav jaiswal, tarun kumar gupta table 3. review of literature with previously reported cases no author year totalc ase age gender diagnosis management out come 1 yanaka et al 1991 2 17 75 male male tbbgh tbbgh surgical good 2 jang et al 2007 1 50 male tbbgh with sah conservative good 3 kaushal et al 2011 1 42 male tbbgh conservative good 4 bhargava et al 2012 2 25 50 male male tbbgh tbbgh conservative good 5 jain et al 2013 1 38 male tbbgh with epidural hematoma craniotomy good 6 pandey et al 2014 1 37 male tbbgh with subdural hematoma craniotomy poor 7 calderon et al 2014 1 28 male tbbgh with epidural hematoma craniotomy death 8 kankane et al 2016 2 20 40 male male tbbgh with hemiparesis conservative good 9 zhang et al 2016 1 45 female tbbgh conservative good 10 present study 2019 9 19-50 (range) 6-males 3-females 4-tbbgh 5tbbgh with hemiparesis 9--conservative 8-good 1-death conclusion traumatic bgh is uncommon, and bilateral bgh is very rare entity with only few cases reported in world’s literature. we report nine cases from a single institute which to the best of our knowledge is the largest series in world literature. prognosis is variable and dependent on many factors. the prognosis of tbgh is favorable if not associated with other disorders like hypertension, diabetes mellitus, and coagulation disorders or diffuse axonal injury. tbghs are compatible with a favorable recovery if present in isolation and not associated with damage to other cortical and sub cortical structures. patients with isolated tbgh do well with conservative management. references 1. katz di, alexander mp, seliger gm, bellas dn. traumatic basal ganglia hemorrhage: clinicopathologic features and outcome. neurology. 1989;39:897–904. 2. adams jh, doyle d, graham di, lawrence ae, mclellan dr. 315 bilateral traumatic basal ganglia haemorrhage deep intracerebral (basal ganglia) haematomas in fatal non­missile head injury in man. j neurol neurosurg psychiatry. 1986;49:1039–43. 3. boto gr, lobato rd, rivas jj, gomez pa, de la lama a, lagares a. basal ganglia hematomas in severely head injured patients: clinicoradiological analysis of 37 cases. j neurosurg. 2001;94:224–32. 4. mosberg wh, lindenberg r. traumatic hemorrhage from the anterior choroidal artery. j neurosurg 1959 mar;16(2):209-221. 5. kumar s, jha d, abbey p, mishra v, handa a. outcome of traumatic basal ganglia hemorrhage. internet j neurosurg. 2009:61 6. bhargava p, grewal ss, gupta b, jain v, sobti h. traumatic bilateral basal ganglia hematoma: a report of two cases. asian j neurosurg 2012 jul;7(3):147-150. 7. jang kj, jwa cs, kim kh, kang jk. bilateral traumatic hemorrhage of the basal ganglia. j korean neurosurg soc 2007 apr;41(4):272-274. 8. kimura m, sobata e, suzuki s, nonogaki y, iwabuchi t. traumatic hematoma in the basal ganglia (caudate) with favorable prognosis: report of two cases. no shinkeigeka 1994 feb;22(2):155-158. 9. yanaka k, egashira t, maki y, takano s, okazaki m, matsumaru y, kamezaki t, ono y, nose t. bilateral traumatic hemorrhage in the basal ganglia: report of two cases. no shinkeigeka 1991 apr;19(4):369-373. 10. pandey n, mahapatra a, singh pk. bilateral large traumatic hemorrhage of the basal ganglion. asian j neurosurg 2014 oct-dec;9(4):240. 11. jain sk, sundar iv, sharma v, prasanna kl, kulwal g, tiwari rn. bilateral large traumatic basal ganglia haemorrhage in a conscious adult: a rare case report. brain inj 2013;27(4):500-503. 12. calderon-miranda wg, alvis-miranda hr, alcala-cerra g, rubiano am, moscote-salazar lr. bilateral traumatic basal ganglia hemorrhage associated with epidural hematoma: case report and literature review. bull emerg trauma. 2014;2(3):130-132. 13. kaushal r, kataria r, gupta a, sinha v. traumatic bilateral (mirror image) basal ganglia bleed. indian j neurotrauma 2011 dec;8(2):109-110. 14. zhang yx, wei sq, xing yy, liu q, he wj bilateral traumatic hemorrhage of the basal ganglia.chin j traumatol. 2016 aug 1;19(4):247-8. 15. kankane vk, gupta tk, jaiswal g. traumatic bilateral basal ganglia bleed: a report of rare two cases and review of the literature. asian j neurosurg2016;11:457. 16. fujioka m, maeda y, okuchi k, kagoshima t, taoka t. secondary change in the substantia niagra induced by incomplete infarct and minor hemorrhage in the basal ganglia due to traumatic middle cerebral arterial dissection. stroke 1999 sep;30(9):1975-1977. 17. lee jp, wang ad : post-traumatic basal ganglia hemorrhage: analysis of 52 patients with emphasis on the final outcome. j trauma 31 : 376380, 1991.-2. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-022 glioblastoma of septum pellucidum rajneesh misra, sushil kumar, kundan kumar romanian neurosurgery (2020) xxxiv (1): pp. 147-149 doi: 10.33962/roneuro-2020-022 www.journals.lapub.co.uk/index.php/roneurosurgery glioblastoma of septum pellucidum rajneesh misra, sushil kumar, kundan kumar dept. of neurosurgery, st. stephens hospital, tis hazari, delhi, india abstract a rare case of glioblastoma multiforme (gbm) of septum pellucidum is being reported. there were symptoms of altered behaviour, memory and changes in sensorium. the mri was suggestive of a tumour arising from the septum pellucidum. glioblastomas arising from septum pellucidum are rare. while even a partial endoscopic excision of the more common pathology viz. colloid cyst is acceptable, only, a safe maximal excision of a highly malignant pathology like glioblastoma is an acceptable goal in order to give any benefit of surgical exploration to the patient. introduction glioblastoma multiforme (gbm) is a common primary brain tumor accounting for nearly 15-20 % of all intracranial tumors. (1) lee and manzano enumerated the most common tumors in the intraventricular tumors and the gbm doesn’t find a mention in the first fourteen. (2) the table 1 below summarizes all such tumors in the intraventricular location. usually it involves frontal or temporal lobe and involvement of septum pellucidum is very rare. hence the present case is being reported. case report a 70-year-old male was admitted with inappropriate behavior and talking of 20 days duration and impaired memory with progressive drowsiness of 4 days duration. on higher mental function testing, he talked irrelevantly, and did not recognize relatives. on physical examination, the tone was increased in all the four limbs and the gcs was e2v3m5. the deep tendon reflexes were brisk. mri revealed a mass lesion in relation to septum pellucidum and bulging into right lateral ventricle (fig 1). a right frontal craniotomy and a trans-cortical entry into the ventricle revealed tumor arising from septum pellucidum postero-superior to the foramen of monroe. the tumor was soft, suckable and moderately vascular. it was infiltrative in nature. he did not improve neurologically after surgery. post-operative radiotherapy was suggested but the family members were not willing for the same. histo-pathology was suggestive of diagnosis of grade iv glioma (glioblastoma multiforme). keywords glioblastoma multiforme, septum pellucidum, transcortical approach corresponding author: rajneesh misra dept. of neurosurgery, st. stephens hospital, tis hazari, delhi, india misra_ rajneesh@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 148 rajneesh misra, sushil kumar, kundan kumar figure 1. (1a) axial t1 plain mri showing isoto hypo-intense lesion occupying the lower margin of septum pellucidum; (1b) the same lesion on t2 shows hyper-intensity; (1c) post-operative ct brain showing pneumocephalus and residual lesion. discussion gbm is one of the most common tumors encountered in neurosurgical practice. it usually involves the region of centrum semiovale with preference for frontal and temporal lobes. involvement of the septum pellucidum by a tumor is a rare occurrence as it usually gets involved by a spread from the surrounding structures in the lateral ventricles, thalamus or fornices. septum pellucidum is a part of limbic system and forms a relay between corpus callosum and fornix. this is classically known to have functions involving emotions, consciousness and memory. structurally, it contains glial cells, neurons and veins connecting to choroid plexus. (4) multiple theories have been proposed regarding the origin of gbm in this region. the most often quoted origin is that from ependyma which separated early during differentiation and later migrated towards ventricular cavity. a less commonly mentioned hypothesis states that the tumor originates elsewhere in the cns and spreads to septum pellucidum and third ventricle through the csf. (5) however, in our case, there was no evidence of tumor elsewhere. galli et al. in their paper in 2004 proposed another interesting mechanism invoking the progenitor neural stem cells from the subventricular zone. (6) they observed that the subventricular progenitor stem cells are known to migrate to fimbrial fornix in injury. (7) a similar mechanism could work for spread of the tumour. only two of the nine cases of gbm reported in the lateral ventricles were seen to be arising from the septum pellucidum (8).majority of the cases of gbm of septum reported have been from autopsy series. (9, 10, 11) choi et al reported gbm of pellucidum on autopsy in a 41 year old woman. (11) gbm of septum pellucidum arises from the neuroglial cells of the septum and lateral ventricles. (2) there is no pathognomonic feature of the gbm of septum pellucidum gbm. headache, visual deficits, signs of raised intracranial pressure, memory disturbances and personality changes are the features that can occur with any lesion causing slowly progressive rise in icp. patient’s impaired memory could be explained by involvement of the limbic system pathways. (12) therefore, diagnosing a high grade lesion of septum pellucidum on clinical grounds is extremely unlikely. on imaging, gbm is known exhibit aggressive features including evidence of vasogenic edema, necrosis and mass effect. none of these features were present in our case. it is possible that, due to strategic location of the lesion, it became symptomatic due to obstructive hydrocephalus before it could attain enough size to show evidence of its own mass effect or have undergo necrosis. computed tomography of such septal lesions shows irregular hypo-density with widening of the septum. mri usually shows enhancing ring with central hypointense area, although we did not find such appearance in our case. (8) epstein and epstein reported a widened septum pellucidum on pneumoventriculogram and gbm of septum pellucidum and corpus pellucidum on necropsy. (10) mri can 149 glioblastoma of septum pellucidum diagnose the cases with indentation of septum and unilateral or bilateral mass arising from septum as demonstrated in our case. reasonable differentials to be considered due to location of the lesion include central neurocytoma, subependymal giant cell astrocytoma and intraventricular meningioma. surgical de-bulking followed by radiotherapy is the standard treatment. however, attendants of the patient were not keen on radiotherapy when educated about the prognosis of the gbm. conclusions the standard treatment for glioblastoma is safe maximal decompression followed by chemoradiotherapy. however, glioblastoma arising from septum pellucidum is distinctly rare occurrence. it offers an opportunity for a more thorough decompression. however, this is possible if the clinician holds reasonable suspicion about the nature of the lesion and opts for intraoperative frozen section to guide the surgical decision making. the authors declare no conflict of interests. no funding was obtained for producing this work. references 1. lopes mbs, vandenberg sr, scheithauer bw: histopathology, immunochemistry and ultrastructure of brain tumors. in kaye ah, laws er jr, editirs. brain tumors. 1st ed. newyork: churchill livingstone; 1995.pp 125-162. 2. lee tt, manzano gr: third ventricular glioblastoma multiforme; case report. neurosurg rev 1997; 20: 291294. 3. wen py, kesari s. malignant gliomas in adults. n engl j med 2008; 359(5):492–507. 4. sarnat hb, netskymg. evolution of the nervous system. new york,ny: oxford university press; 1974. 5. prieto r, pascual jm, roda jm. third ventricle glioblastoma. case report and review of literature. clin neurol neurosurg 2006;108(2):199–204. 6. galli r, binda e, orfanelli u, et al. isolation and characterization oftumorigenic, stem-like neural precursors from human glioblastoma.cancer res 2004;64(19):7011–7021. 7. steffenhagen c, dechant fx, oberbauer e, et al. mesenchymal stem cells prime proliferating adult neural progenitors toward an oligodendrocyte fate. stem cells dev 2012;21(11):1838–1851. 8. secer hi, dinc c, anik i, duz b, gonule :glioblastoma of multiforme of lateral ventricle: report of nine cases. br j neurosurg 2008;22(3):398-401. 9. chusid jg, and gutierrez-mahoney c: glioblastomamultiforme of of septum pellucidum. j neurosurg 1954;11(3):251-257. 10. epstein ja and epstein bs: glioblastomamultiforme of bith the septum pellucidum and the corpus callosum. j neurosurg1957;14(6):688-692. 11. choisk,byun bj, lee is and chi jg: glioblastomamultiforme of the septum pellucidum: an autopsy case report. j korean neurosurg soc. 1980;9(2):497-504. 12. mckean-cowdin r, razavi p, barrington-trimis j, et al. trends in childhood brain tumor incidence: 1973–2009. j neurooncol 2013;115(2):153–160. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-099 giant dorsal sacral meningocele in a child amit agrawal romanian neurosurgery (2020) xxxiv (4): pp. 577-579 doi: 10.33962/roneuro-2020-099 www.journals.lapub.co.uk/index.php/roneurosurgery giant dorsal sacral meningocele in a child amit agrawal professor of neurosurgery. department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract sacral meningoceles are uncommon congenital lesions, usually described in the anterior or lateral position, and they typically are asymptomatic [1,7]. a nine-years male child presented with a progressively increasing swelling over the lumbosacral region since birth. sacral meningoceles are uncommon congenital lesions, usually described in anterior or lateral position and are typically asymptomatic.1-7 a nine year male child presented with a progressively increasing swelling over lumbo-sacral region since birth. there was no history of any bowel or bladder dysfunctions. motor and sensory examination was normal. planters were flexor. rectal tone was normal. gait was normal. results of her sensory, rectal tone and lower limbs motor exams were within normal limits. there were no abnormal skin lesions, skeletal deformities, abnormal sinus or swellings. a physical examination of the patient showed a soft, 4 x 4-cm fluctuant and nonpulsatile mass over sacral region, completely with normal skin without any stigmata. the transillumination test was positive. routine blood investigations were normal. magnetic resonance imaging (mri) of the lumbo-sacral spine showed a large, well-defined cystic over sacrum without any no evidence of internal echoes, solid component or septae (figure-1 and 2). there was evidence of communication between the cyst and the spinal canal. the patient underwent surgical excision of the swelling and repair of the sac. the large cyst was entered and found to contain clear csf in a terminal continuation of the spinal subarachnoid space. there was no neural tissue in the sac. and there was no evidence of tethering. postoperatively, the child had normal neurological and urological function. ct of the brain did not show any evidence of hydrocephalus. he developed csf leak in post-operative and the defect was repaired with pedicel graft. a meningocele a developmental defect in the dura resulting in an outpouching of leptomeninges through defect covered with only a layer of skin. 4 most of the sacral meningoceles are asymptomatic with a soft tissue mass; they produce clinical symptoms depending on their keywords sacral meningocele, lipomyelomeningocele. mri, meningocele, sacral mass corresponding author: amit agrawal department of neurosurgery, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india dramit_in@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 578 amit agrawal proximity to the spinal cord and nerve roots (e.g. unexplained radiating or low back pain, or sensory or motor deficits, atypical bowel dysfunction 1-4, 8, 9 the differential diagnosis for the mass lesions in children in sacro-coccygeal area includes meningocele, myelomeningocele, myelocystocele, teratoma, lipoma, hamartoma, lymphangioma, hemangioma, chordoma, and ependymoma. 10-15 mri is the investigation of choice as it will better delineate the details of the sac and its contents. also it will help to know the extent of the spinal cord and position of the nerve roots. 3 radiographs may reveal erosion and widening in the sacral bone, 9 scalloping of the pedicles, laminae and vertebral bodies adjacent to the meningocele resulting in an enlargement of the spinal canal. 16, 17 18indications for surgical repair include clinically symptomatic patients 1-3, 8, 19 or if the lesions located in an area where it has greater risk of mechanical trauma or rupture (as in the present case). figure 1. mri of the lumbo-sacral spine t1w, flair and t2w sagittal images showing large, well-defined cystic lesion over sacrum (signal intensity similar to cerebrospinal fluid) without any no evidence of internal echoes, solid component or septae. figure 2. mri of the lumbo-sacral spine t2w axial images showing large, well-defined cystic lesion over sacrum (signal intensity similar to cerebrospinal fluid). figure 3. intraoperative images showing excision and repair of the meningocele. references 1. nishio y, hamada h, kurimoto m, hayashi n, hirashima y, endo s. a case of occult intrasacral meningocele presented with atypical bowel symptoms. child's nervous system : chns : official journal of the international society for pediatric neurosurgery 2004;20:65-67. 2. turgut m, akyüz o, unsal a. occult intrasacral meningocele: case report and review of the literature. zentralblatt fur neurochirurgie 2007;68:34-37. 3. naoumis d, gkiatas k, kararizos g, mitsonis c, kararizou e. sacral meningocele in a military pilot, presenting during flight. aviation, space, and environmental medicine 2010;81:141-143. 4. shetty d, lakhkar b. lateral sacral lipomyelomeningocele: a rare anomaly. neurology india 2002;50:204. 5. lee ks, gower dj, mcwhorter jm, albertson da. the role of mr imaging in the diagnosis and treatment of anterior sacral meningocele. report of two cases. journal of neurosurgery 1988;69:628-631. 6. erkulvrawatr s, el gammal t, hawkins j, green jb, srinivasan g. intrathoracic meningoceles and neurofibromatosis. archives of neurology 1979;36:557559. 7. seddighi a, seddighi as. lateral sacral meningocele presenting as a gluteal mass: a case report. journal of medical case reports 2010;4:81. 8. shiau jsc, raden m, juliano je. sacral intraspinal meningocele in a patient presenting with abdominal pain. case report. journal of neurosurgery 2007;107:5356. 9. kiliçkesmez o, barut y, tasdemiroglu e. expanding occult intrasacral meningocele associated with diastematomyelia and multiple vertebral anomalies. case report. journal of neurosurgery 2004;101:108-111. 10. altman rp, randolph jg, lilly jr. sacrococcygeal teratoma: american academy of pediatrics surgical section survey-1973. journal of pediatric surgery 1974;9:389-398. 579 giant dorsal sacral meningocele in a child 11. gupta dk, mahapatra ak. terminal myelocystoceles: a series of 17 cases. journal of neurosurgery 2005;103:344-352. 12. yu ja, sohaey r, kennedy am, selden nr. terminal myelocystocele and sacrococcygeal teratoma: a comparison of fetal ultrasound presentation and perinatal risk. ajnr american journal of neuroradiology 2007;28:1058-1060. 13. ein sh, adeyemi sd, mancer k. benign sacrococcygeal teratomas in infants and children: a 25 year review. annals of surgery 1980;191:382-384. 14. güvenç bh, etus v, muezzinoglu b. lumbar teratoma presenting intradural and extramedullary extension in a neonate. the spine journal 2006;6:90-93. 15. gross sj, benzie rj, sermer m, skidmore mb, wilson sr. sacrococcygeal teratoma: prenatal diagnosis and management. american journal of obstetrics and gynecology 1987;156:393-396. 16. dubowitz v, lorber j, zachary rb. lipoma of the cauda equina. archives of disease in childhood 1965;40:207213. 17. heckly a, carsin-nicol b, poulain p, hamlat a. diagnosisrelated pitfall of a lateral sacral cyst. case report. journal of neurosurgery spine 2005;2:72-74. 18. philip n, andrac l, moncla a, et al. multiple lateral meningoceles, distinctive facies and skeletal anomalies: a new case of lehman syndrome. clinical dysmorphology 1995;4:347-351. 19. rengachary ss, o'boynick p, karlin ca, batnitzky s, price h. intrasacral extradural communicating arachnoid cyst: cases report. neurosurgery 1981;8:236-240. doi: 10.33962/roneuro-2022-021 paediatric traumatic chronic subdural hematoma – a very rare entity. single institution study of 5 cases vivek kumar kankane, avadhesh shukala, s.n. iyenger romanian neurosurgery (2022) xxxvi (1): pp. 122-126 doi: 10.33962/roneuro-2022-021 www.journals.lapub.co.uk/index.php/roneurosurgery paediatric traumatic chronic subdural hematoma – a very rare entity. single institution study of 5 cases vivek kumar kankane, avadhesh shukala, s.n. iyenger department of neurosurgery, g.r. medical college; jah groups of hospital gwalior (m.p.), india abstract objectives: to study the prevalence of traumatic chronic subdural hematoma in children. material and methods: this is a prospective study conducted at a tertiary care centre at gwalior, from november 2020 to november 2021. we encountered 5 patients admitted for signs of raised intracranial tension due to head trauma, showing chronic subdural haematoma (csdh) in plain ct head or mri brain. all patients had no history of loss of consciousness, no history of vomiting, no history of seizures, no history of nasal or ear bleed and gcs was 15/15. all blood investigation and coagulation profiles are normal. frontal and parietal 2.5 cm trephine craniotomy with evacuation of subdural hematoma was done. patients were followed up at 1 month and 6 months result: all children are male. age ranging from 7 years to 14 years, mean age of presentation was 10 years. all patients had a history of head trauma and mode of injury road traffic accidents (rta) and glasgow coma scale (gcs) at admission was 15 and duration of developed csdh was 20 days to 42 days’(mean30.40 days). all patients had good outcomes and the average follow-up was 6.5 months. all patients went on surgical intervention. and outcome assessed by glasgow outcome score. 3 out of 5 patients had brownish fluid as a collection in subdural space while the other 2 patients had fluid that has motor oil like consistency in subdural space. all the patients were subjected to a similar procedure. the postoperative course was uneventful. mean hospital stay was 7 days. a postoperative scan was done on the 7th day. conclusion: chronic subdural hematoma is a disease reported in infants and the elderly population. it is uncommon in the age group of 2-14 years. most of the children present with symptoms of raised intracranial tension due to head injury, with no reported history of repeated head trauma, child abuse & coagulopathy. traumatic chronic subdural collection should be considered as one of the diagnoses as the prognosis of this disease is better. however, due to the scarcity of reports in the literature, established guidelines are not available. introduction subdural hematoma is the collection of blood on the cortical surface beneath the dura with bleeding from bridging veins or cortical arteries. the term chronic subdural haematoma (csdh) is often applied to keywords traumatic, subdural hematoma, paediatric corresponding author: vivek kumar kankane g.r. medical college, india vivekkankane9@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 123 paediatric traumatic chronic subdural hematoma – a very rare entity these collections, although the content of the accumulation may vary from thin, watery fluid resembling cerebrospinal fluid to thick “motor oil” often associated with adult csdh. the pathophysiology and clinical outcomes of head trauma differ between children and adults. blood vessels are absent in the normal duraarachnoid interface. neo-vasculature is abundant, but just in the outer csdh membrane. abnormal dilated sinusoids measuring as large as 1000 micrometer, with an incomplete basement membrane and attenuated endothelial cells, share the outer membrane with rapidly growing microcapillaries. both vessel types are composed of endothelial cells with irregular surface because of numerous pseudopod-like structures extending into vascular lumen. erythrocyte and platelets in various stages of degeneration are frequently found deposited in the perivascular space. these sinusoids contain gap junction as large as 8 micrometer, sufficient to allow leakage of plasma and even red blood cells into the hematoma cavity. inflammatory mediators present in csdh fluid may potentiate chronic rebleeding of the fragile neovasculature. kallikrein, bradykinin, and plateletactivating factor (paf) have all been identified at significant level in csdh fluid. these inflammatory mediators stimulate vasodilation, increase vascular permeability, prolong the clotting time, and release tissue plasminogen activator (t-pa) from endothelial cells. other work has focused on disturbances of the prostaglandin system as possible components in the pathophysiology [1]. eosinophil degranulation in the outer membrane may be the source of fibrinolytic factors and inflammatory mediators causing local coagulopathy and cell destruction in the csdh [2] the traumatic mass lesions such as subdural and epidural hematomas occur less frequently in children and when present, are associated with lower mortality. common manifestations of csdh are altered mental state and focal neurological deficits [3]. subdural hematomas (sdh) are associated with an increased morbidity and mortality and generally occur as chronic sdh among older patients [4]. the most frequent signs and symptoms like headache, alteration of consciousness, gait impairment and hemiparesis are also seen among other cns diseases, so they have to be considered during evaluation. in the case of symptomatic patients with focal neurological deficits surgical intervention should be considered, where as in case of asymptomatic patients or patients with only slight headaches conservative treatment with clinical and radiological follow-up might be a possibility. also after surgical intervention, the recurrence rate is between 5 and 33% [4]. csdh are much more common in infants because of associated traumatic deliveries and frequently exist as a single entity. it is rare for chronic subdural fluid accumulations to occur after one year of age and they are more frequent during adolescence [5,6]. specific traumatic events are usually unrecognized figure 1. ncct head revealed chronic subdural haematoma in left fronto-temporo-parietal convexity with midline shift toward right side with cisternal effacement. materials and methods this is prospective study conducted at a tertiary care centre at gwalior, from november 2020 to november 2021. we encountered 5 patients admitted for signs of raised intracranial tension who on radiological examination were found to have hemispheric subdural collection. all patients had no history of loss of consciousness, no history of vomiting, no history of seizures, no history of nasal or ear bleed and gcs was 15/15. all blood 124 vivek kumar kankane, avadhesh shukala, s.n. iyenger investigation and coagulation profile normal. frontal and parietal 2.5 cm trephine craniotomy with evacuation of subdural hematoma was done. patients were followed up at 1 month and 6 months. figure 2. ncct head revealed chronic subdural haematoma in left fronto-temporo-parietal convexity with midline shift toward right side with cisternal effacement. figure 3. mri brain revealed chronic subdural haematoma in right fronto-temporo-parietal convexity with midline shift toward right side with cisternal effacement. results all children are male. age ranging from 7 years to 14 years, mean age of presentation was 10 years. all patients had history of head trauma and mode of injury road traffic accidents (rta) and glasgow coma scale (gcs) at admission was 15 and duration of developed csdh was 20 days to 42 days’(mean30.40 days).. all patients had good outcome and average follow-up was 6.5 months. all patients went on surgical intervention [table-1] and outcome assessed by glasgow outcome score [table-2]. table 1. demographic data, management and outcome of patients age (year) sex mode of injury gcs at the time of admission management outcome measure by gos 14 male road traffic accident (rta) 15/15 surgery good 11 male rta 15/15 surgery good 10 male rta 15/15 surgery good 8 male rta 15/15 surgery good 7 male rta 15/15 surgery good table 2. glasgow outcome scale gos functional status 5 resumption of normal life; there may be minor neurological and psychological deficit 4 able to work in a shattered environment and travel by public transportation 3 depend on daily support by reason of mental and physical disability or both 2 unresponsive for weeks or month or until death 1 death table 3. description of previous reported case of traumatic pediatric chronic sdh author year no. of case age/sex of patient description of patient osaka h et al. 1993 1 10 month/male gluteric aciduria type-1 narsinghani et.al 2002 1 5 year/male strikingly large calcified csdh in a 5year-old child with increased intracranial pressure and subfalcine herniation mori et al. 2002 12 all patients are paediatric age group chronic subdural haematoma with arachnoid cyst acakapo satchivi et al. 2007 1 4 month/male macrocrania with chronic subdural haematoma 125 paediatric traumatic chronic subdural hematoma – a very rare entity kumar et al. 2008 20 range 1 month – 2year chronic subdural haematoma following minor head injury wang et al. 2010 1 1 year/male chronic subdural haematoma due to repeated minor dodgeball head injury vivek kankane et.al. 2015 1 7 year/male chronic subdural haematoma due fall from bed 3 month ago discussion wang, et al. reported a rare case of csdh in a 9-yearold child due to repeated minor dodgeball head injuries in 2010 [table-3]. although such a case has never been reported in sport. no altered mental state or focal neurological deficits were observed; the child presented with intermittent severe headache with nausea and vomiting. there was also no evidence of child abuse; however, the history of repeated minor head injuries during playing was significant [3]. kumar et al. reported twenty cases of traumatic subdural empyema (sdes) following minor head injury or unreported. in rare instances, sdh may indicate an underlying bleeding disorder, hematological malignancy or benign expansion of subarachnoid in 2008. the age of these children ranged from 1 month to 2 years. 70% children presented with subtle findings, 30% children presented with overt neurological signs and symptoms. seizures were the most common mode of presentation. bilaterality and ventriculomegaly were more common in the subtle group, each with an incidence of 43%. 35% cases required operative management of traumatic sdes. recurrence was seen in 10% cases who had been conservatively managed previously. only one child showed conversion of traumatic subdural hygroma to csdh on conservative management [7] narsinghani et al. reported a case the dramatic presentation of a strikingly large calcified csdh in a 5-year-old child with increased intracranial pressure and subfalcine herniation in 2002 [5]. mori et al. reported that 12 patients with csdh and arachnoids cyst were significantly younger than the patients with csdh without arachnoid cyst in 2002. the most frequent symptom was headache followed by vomiting in the patients with arachnoid cyst, while gait disturbance and hemiparesis predominated in patients without arachnoid cyst. csdh formation may be preceded by subdural hygroma caused by the rupture of arachnoid cyst [8]. in 2007, acakapo satchivi et al. reported an unusual case of cortical herniation into a csdh. a 4month-old boy with a history of macrocrania and very large bilateral chronic sdhs underwent subduro-peritoneal shunt treatment shortly after presentation. to the authors’ knowledge, this is only the fourth report in the medical literature of cortical herniation through a chronic subdural membrane and the first in which successful treatment with a good outcome is described [9]. csdh in infant after abusive head trauma is a serious form of child abuse that can lead to severe neuropsychological sequelae or death in infants [10]. osaka h, et al. reported a 10-month-old male with glutaric aciduria type-1 (ga-1) in 1993. this patient showed frequent partial motor seizures, irritability, and involuntary movements, including oral dyskinesia at the age of 3 months. on admission, magnetic resonance (mr) scanning revealed a chronic subdural hematoma and widening of the bilateral insular cisterns. urine organic acid analysis showed marked excretion of glutaric acid, 3-hydroxy glutaric acid and glutaconic acid, suggesting ga-1 [11]. new pathophysiologic aspect might have an impact on conservative treatment in future. in particular, detection of the angiogenic cytokines responsible for development of the well-known leaky vessels within the outer membrane of a hematoma might offer new and promising targets to be blocked by pharmacologic agents. recently, it was shown that the angiogenic properties of angiotensin converting enzyme inhibitors could reduce the rate of recurrence in csdh, as well as level of vascular endothelial growth factor within the hematoma [12,13]. 126 vivek kumar kankane, avadhesh shukala, s.n. iyenger subsequent studies have identified lower levels of all coagulation factors in csdh fluid than plasma. factor ii, v, vii, viii, and x are disproportionately depleted. these findings reflected a phase of accelerated fibrinolytic activity after the rapid and defective clot formation. the end result is a milieu of anticoagulant protein (chiefly fdps) and depleted coagulation factors. other author have suggested that the paf derived from lysis of red blood cells may stimulate the synthesis and release of tpa, as well as induce chemotaxis of inflammatory cells to the csdh fluid and elevated plasma level of paf in patient with csdh versus healthy volunteers. the latter observation may suggest a systemic predilection to the development of csdh. conclusions chronic subdural hematoma is disease reported in infants and elderly population. it is uncommon in the age group of 2-14 years. most of the children present with symptoms of raised intracranial tension due to head injury, with no reported history of repeated head trauma, child abuse & coagulopathy. chronic subdural collection should be considered as one of the diagnoses as prognosis of this disease is better. however due to scarcity of reports in literature, established guidelines are not available. references 1. hirashima y, endo s, kato r, ohmori t, nagahori t, et al. (1994) plateletactivating factor and development of chronic subdural haematoma. acta neurochir 129: 20-25. 2. muller w, firsching r (1990) significance of eosinophilic granulocyte in chronic subdural hematomas. neurosurge rev13: 305-308. 3. wang hk, chen hj, lu k, liliang pc, liang cl et al. (2010) a pediatric chronic subdural hematoma after dodgeball head injury. pediatr emerg care. 26: 667-668. 4. 4. gautschi op, gallay mn, kress tt, korte wc, hildebrandt g (2010) chronic subdural hematoma -assessment and management. praxis (bern 1994). 5. narsinghani u, burson g, schmidt mb, anand ks (2002) case of the month. symptomatic chronic calcified subdural hematoma in a 5-year-old child. j ark med soc 98: 300-303. 6. per h, gümüş h, tucer b, akgün h, kurtsoy a, kumandaş s (2006) calcified chronic subdural hematoma mimicking calvarial mass: a case report. brain dev 28: 607. 7. kumar r, singhal n, mahapatra ak (2008) traumatic subdural effusions in children following minor head injury. childs nerv syst. 24: 1391-1396. 8. mori k, yamamoto t, horinaka n, maeda m (2002) arachnoid cyst is a risk factor for chronic subdural hematoma in juveniles: twelve cases of chronic subdural hematoma associated with arachnoid cyst. j neurotrauma 19: 1017-1027. 9. acakpo-satchivi l, luerssen t (2007) brain herniation through an internal subdural membrane: a rare complication seen with chronic subdural hematomas in children. case report. j neurosurg 107: 485-488. 10. wuerfel nee tysiak e, petersen d, gottschalk s, gerling i, gliemroth j, et al. (2012) progression of chronic subdural haematomas in an infant boy after abusive head trauma. eur j paediatr neurol 16:736-739. 11. osaka h, kimura s, nezu a, yamazaki s, saitoh k, et al. (1993) chronic subdural hematoma, as an initial manifestation of glutaric aciduria type-1. brain dev 15: 125-127. 12. weighel r, hohenstein a, schlickum l, weiss c, schilling l (2007) angiotensin converting enzyme inhibition for arterial hypertension reduces the risk of recurrence in patients with chronic subdural hematoma probably by an angiogenic mechanism. neurosurgery 61: 788-792 13. kankane vivek, jaiswal gaurav and gupta tarun, a pediatric traumatic chronic subdural hematoma: rare case report and review of literature. j spine neurosurg 2015, 4:3. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-005 microsurgical clipping of paraclinoid aneurysms. a single centre experience mugurel radoi, ram vakilnejad, suditu stefan, florin stefanescu romanian neurosurgery (2020) xxxiv (1): pp. 31-40 doi: 10.33962/roneuro-2020-005 www.journals.lapub.co.uk/index.php/roneurosurgery microsurgical clipping of paraclinoid aneurysms. a single centre experience mugurel radoi1,2, ram vakilnejad2, suditu stefan2, florin stefanescu2 1 faculty of general medicine, “carol davila” university of medicine and pharmacy, bucharest, romania 2 neurosurgical department of the national institute of neurology and neurovascular diseases, bucharest, romania abstract background. paraclinoid aneurysm is a nonspecific term that includes ophthalmic segment aneurysms and distal cavernous internal carotid artery (ica) aneurysms. the literature mostly described the frequency to be in the range of 1.3-5%. and a high incidence of being multiple or having a large size. methods. a retrospective review of 18 consecutive patients surgically treated for paraclinoid aneurysm was performed. the data of all our consecutive patients were searched to obtain patient and aneurysm characteristics, treatment details, complications and follow up. clinical outcome was graded according to the modified rankin scale. the follow-up period varied widely from 3 to 62 months (mean 26 months). results. surgical clipping was performed for 15 ruptured paraclinoid aneurysms; only in 3 cases the aneurysm was unruptured. post-operative control angiography was performed in 10 patients (55.56%), from which we reported a full occlusion of the aneurysm in 9 patients (90%). best results were obtained in patients who preoperatively were included in 1st and 2nd grade of hunt & hess scale. two months postoperative follow-up was complete for all but one patient who died 12 days after surgery, from cerebral ischemia resulting from severe cerebral vasospasm. there were excellent and good results (mrs 0–2) in 88% of the cases (15 out of 17 patients) at two months follow-up, and 94% (16 out of 17 patients) at six months follow-up. three patients with slight disabilities, ranked mrs 1-2 at two months follow-up, improved to mrs 0, with no symptoms at all, at 6 months postoperative control. all 3 patients with a surgically treated non-ruptured paraclinoid aneurysm had an excellent outcome (mrs 0). conclusions. most appropriate treatment is to occlude aneurysms without compromising patency of the parent artery. anterior clinoidectomy and microsurgical clipping can still be a standard treatment despite of recent development of endovascular coiling procedures. introduction paraclinoid aneurysms is a nonspecific term that includes ophthalmic segment aneurysms and distal cavernous internal carotid artery (ica) keywords paraclinoid aneurysm, surgical clipping, endovascular treatment, postoperative results corresponding author: mugurel radoi university of medicine and pharmacy “carol davilaˮ, bucharest, romania muguradoi@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 32 mugurel radoi, ram vakilnejad, suditu stefan, florin stefanescu aneurysms. these aneurysms arise near the anterior clinoid process and represent a considerable surgical challenge owing to their anatomic features, their proximity to the optic nerves and chiasm, and their relationship to complicate dural structures. paraclinoid aneurysms are classified according to the ica segments from which they arise. there are clinoidal segment aneurysms and ophthalmic segment aneurysms. each variant can be differentiated according to the site of origin, the direction of projection, and relationship with arterial branches, cranial nerves and adjacent dural and osseous structures within the segment (4). clinoidal segment aneurysms have two variants: (a) anterolateral variant and (b) medial variant. ophthalmic segment aneurysms are intradural and include: (a) ophthalmic artery aneurysms, (b) superior hypophyseal artery aneurysms and (c) rare variants of dorsal ica aneurysms (21). this article summarizes the results of microsurgical treatment of 18 paraclinoid aneurysms operated in our department, by two senior neurosurgeons, and discusses treatment strategy and potential complication, comparing them with the results reported in the neurosurgical literature. methods this article presents the results of a retrospective study of paraclinoid aneurysms, surgically treated in the department of neurosurgery of institute of neurology and neurovascular diseases, bucharest. in the period from january 2014 until june 2019, 18 consecutive patients with paraclinoid aneurysms, from a total of 296 patients with carotid system aneurysms, were operated on by two senior neurosurgeons. admission data, operative reports and imaging studies were reviewed to obtain information on patient’s age, gender, aneurysm size and orientation, treatment details, complication and follow-up. from this series of 18 patients, two harboured another middle cerebral aneurysm, both on ipsilateral side. most of the patients (15 patients 83.34%) presented with acute subarachnoid haemorrhage and only 3 presented an unruptured paraclinoid aneurysm. however, in a patient with multiple aneurysms, the source of the haemorrhage was clearly defined to be a middle cerebral artery aneurysm. digital subtraction angiography with 3d reconstruction or computerized tomography (ct) angiography were used to image the intracranial circulation and to achieve proper orientation and visualization of the paraclinoid aneurysm. at admission, the clinical condition of all patients was classified according to the hunt and hess scale. clinical outcome was assessed according the modified rankin scale. an ipsilateral pterional approach was used in all patients and medial sphenoid wing was resected extradurally to the level of the lateral clinoid process. proximal control was achieved by neck dissection and temporary clipping of either internal carotid artery (ica) or common carotid artery (cca). after a standard dural opening, the anterior limb of the sylvian fissure is split to gain access to the ica, anterior clinoid process, and optic nerve. the arachnoid layers were cut form distal to proximal, identifying the distal ica and posterior communicating artery. we continued the microdissection proximally until the neck of the aneurysm on the ica was identified. the optic nerve partially blocked the origin of most ophthalmic artery aneurysms, and it was untethered and gently mobilized by sectioning the falciform ligament. visualization of the entire aneurysm neck during clip application was often impossible, so clip deployment proceeded with visualization of one blade and inspection of the other only after the clip was applied. table 1. distribution of carotid system aneurysms in a series of 296 patients. distribution of carotid system aneurysms aneurysm location number of patients anterior communicating artery aneurysm 126 (42.5%) posterior communicating artery aneurysm 55 (18.5%) medial cerebral artery aneurysms 86 (29,33%) anterior cerebral artery aneurysm 2 (0.67%) anterior choroidal artery aneurysm 3 (1%) pericallosal artery aneurysm 6 (2%) paraclinoid aneurysms 18 (6%) total 296 (100%) 33 microsurgical clipping of paraclinoid aneurysms characteristic no of patients (%) female 12 (66.67%) male 6 (33.33%) hunt &hess scale grade 0 3 (16.67%) grade 1 and 2 10 (55.55%) grade 3 4 (22.33%) grade 4 1 (5.45%) grade 5 0 modified fischer grading scale no sah present 3 (16.67%) focal or diffuse thin sah 12 (66.67%) focal or diffuse thick sah 2 (11.21%) intraventricular haemorrhage 1 (5.45%) table 2. characteristics of patient with paraclinoid aneurysms in our series. charactersitic no of patients (%) left paraclinoid aneurysms 10 (55.55%) right paraclinoid aneurysms 8 (44.45%) location ophthalmic artery aneurysms 16 (94%) superior hypophyseal artery aneurysms 1 (4.3%) clinoidal segment aneurysms (medial variant) 1 (1.7%) size ≤ 5 mm 3 (16.67%) 5-10 mm 10 (55.55%) ≥ 10 mm 5 (27.78%) table 3. aneurysm characteristics. results eighteen patients with paraclinoid aneurysms were operated on in our department between january 2014 and june 2019. of these, two were asymptomatic, two presented with visual symptoms of decreased visual acuity of the relevant eye, and there were 14 ruptured aneurysms without eye involvement. the patient characteristics at admission are presented in table 2. most of the patients were women (66.67%). at the time of surgery, 13 patients were with no subarachnoid haemorrhage or in grade 1 or 2 on hunt&hess scale. the aneurysms characteristics are summarized in table 3. paraclinoid aneurysms had usually larger diameter than aneurysms in other location. in our series, there were 5 (27.78%) aneurysms with a maximum size more than 10 mm. the patients with ruptured aneurysms, except one, who was in poor neurological status, were operated on in the first 5 days following the symptoms onset. in only one case we delayed the surgical treatment of the aneurysm, due to severe vasospasm, and important secondary neurological deterioration of the patient. two patients harboured a coincidental non-ruptured middle cerebral artery aneurysm, which was clipped in the same surgical procedure. post-operative control angiography was performed in 10 patients (55.56%), from which we reported a full occlusion of the aneurysm in 9 patients (90%). preoperative vasospasm was demonstrated on cerebral angiography in 3 patients (16.67%) and clinically was manifested in 1 patient (5.56%). on control angiography, cerebral vasospasm was detected on near half of the patients (40%), but, as postoperative event, 2 patients, including the one with preoperative neurological signs, presented clinical symptoms of vasospasm, with decreased level of consciousness, affected speech and motor deficits. the follow-up period varied widely from 3 to 62 months (mean 26 months). best results were obtained in patients who preoperatively were included in 1st and 2nd grade of hunt & hess scale. two months postoperative follow-up was complete for all but one patient who died 12 days after surgery, from cerebral ischemia resulting from severe cerebral vasospasm. the mean follow-up was 26 months, obtained in 89% of the patients. the outcome was evaluated using modified rankin scale. overall outcome was assessed at first (two months after surgery) and respectively, second (six months after surgery) postoperative controls. there were excellent and good results (mrs 0–2) in 88% of the cases (15 out of 17 patients) at two months followup, and 94% (16 out of 17 patients) at six months follow-up. the most important improvement was recorded for patients graded mrs 1-2 at the first postoperative follow-up. three patients with slight disabilities, ranked mrs 1-2 at two months follow-up, improved to mrs 0, with no symptoms at all, at 6 months postoperative control. all 3 patients with a surgically treated non-ruptured paraclinoid aneurysm had an excellent outcome (mrs 0). complications no of cases intraoperative rupture 2 (11.12%) re-ruptured before surgery (waiting) 0 34 mugurel radoi, ram vakilnejad, suditu stefan, florin stefanescu post-operative rupture 0 pre-operative vasospasm angiography 3 (16.67%) clinic 1 (5.56%) post-operative vasospasm angiography 4/10 (40%) clinic 2 (11.12%) post-operative subdural hematoma 0 meningitis 0 hydrocephalus 1 (5.56%) vp shunt (within 30 days from surgery) 1 (5,56%) complications no of cases intraoperative rupture 2 (11.12%) re-ruptured before surgery (waiting) 0 post-operative rupture 0 pre-operative vasospasm angiography 3 (16.67%) clinic 1 (5.56%) post-operative vasospasm angiography 4/10 (40%) clinic 2 (11.12%) post-operative subdural hematoma 0 meningitis 0 hydrocephalus 1 (5.56%) vp shunt (within 30 days from surgery) 1 (5,56%) table 4. procedural and perioperative complications. outcome of the surgically treated paraclinoid aneurysms after 2, and respectively, 6 months follow-up (17 patients; one died at 12 days after surgery). excellent= mrankin 0, good=mrankin 1–2, fair= mrankin 3. figure 1: (1a,1b) preoperative four vessels cerebral angiography showed a large, 14 mm length, ruptured, left ophthalmic artery aneurysm; (1c,1d) postoperative control cerebral angiography showed the correct clipping of the aneurysm. 0 2 4 6 8 10 12 mrs 0 mrs 1-2 mrs 3 n u m b e r o f p a ti e n ts follow-up and outcome 2 months after surgery 35 microsurgical clipping of paraclinoid aneurysms figure 2: (2a) preoperative cerebral computed tomography (ct) showed subarachnoid haemorrhage; computed tomography angiography (cta) demonstrated a large rightsided paraclinoid aneurysm and the relation with the anterior clinoid process; (2b,2c) preoperative four vessels cerebral angiography showed a 16 mm length right superior hypophyseal artery aneurysm; (2d,2e) postoperative control cerebral angiography showed the correct obliteration of the aneurysm with a straight 11 yasargil clip. discussion paraclinoid aneurysms are classified in clinoidal segment (c5) aneurysms and ophthalmic segment 36 mugurel radoi, ram vakilnejad, suditu stefan, florin stefanescu (c6) aneurysms. this classification system offers prognostic information about lesion’s propensity for subarachnoid haemorrhage (sah) or cranial nerve deficits as well as the anatomic knowledge required for successful low-risk operative management of these lesions (28). paraclinoid aneurysms have a female preponderance (female:male ratio 9:1) and a high incidence of being multiple (4,12). small (<5 mm) asymptomatic clinoidal segment aneurysms carry a very low risk of sah, and isolated lesions should generally be treated with a conservative management plan including periodic follow-up imaging. small symptomatic lesions (visual deficits or focal, unrelenting headache) and a lesion, whose protective anterior clinoidal process roof has been removed for treatment of another pathology in the same region, should be treated. the most frequent paraclinoid aneurysms are ophthalmic aneurysms. the literature mostly described the frequency to be in the range of 1.3-5% (8,30). although ruptured ophthalmic aneurysms require treatment, unruptured small asymptomatic aneurysms can undergo observation with serial imaging. up to half of patients with ophthalmic segment aneurysms have additional intracranial aneurysms elsewhere (6,22). most small aneurysms in the ophthalmic segment have a lower rupture risk than those at other intracranial locations. in this situation and for middle age or older adults, observation is a very reasonable option. in the past, unless symptomatic, these aneurysms were usually not treated due to higher mortality and morbidity rates compared with other intracranial aneurysms (3). with the development of microsurgical technique, most of these aneurysms became operable, with lower mortality and morbidity (12). potential management options for paraclinoid aneurysms include observation, endovascular treatment, microsurgical clip ligation, and carotid occlusion with or without bypass. treatment is indicated for virtually all symptomatic aneurysms and for those larger than 1 cm. the patient presenting with visual loss should be treated urgently, ideally with surgery if the patient’s risk factors and the experience of the operating team are reasonable. endovascular technique is a viable option for the treatment of many aneurysms. the development of endoluminal flow-diverting devices applied to large or giant lesions has become a very good alternative to surgery for very complex paraclinoid lesions. we considered that with all paraclinoid aneurysms, the patient’s neck should be sterilely prepared and marked for dissection if proximal control becomes necessary. some authors consider proximal control (4,6,27) is often unnecessary for small unruptured aneurysms, but often prudent for aneurysms that are ruptured or large. proximal control can be achieved by temporary clipping of either the internal carotid artery (ica) or common carotid artery (cca). clamping the cca avoids potential injury to the ica. despite proximal ica occlusion in the neck, back bleeding from the posterior communicating and ophthalmic arteries can be brisk if intraoperative rupture occurs. the classic pterional craniotomy is used for adequate exposure of almost all ophthalmic artery aneurysms. an orbital osteotomy can be performed to provide additional exposure for larger aneurysms. the lesser wing is removed extradurally down to the base of the anterior clinoid process. the supraorbital craniotomy through the eyebrow incision is reasonable route for uncomplicated aneurysms. the patient’s head position during surgery for these medially situated aneurysms demands less neck rotation (15-20 degrees) to allow the surgeon to look under the optic nerve after the clinoidectomy. slightly less head extension lessens the steep viewing trajectory under the anterior clinoid process. anterior clinoidectomy has great value in surgical exposure and treatment for most paraclinoid aneurysms. it can be completed both extradurally (dolenc approach) or intradurally (8). in our opinion, intradural removal is preferred because it allows simultaneous visualization of the optic nerve and aneurysm during the entire dissection and enables immediate bleeding control if the aneurysm ruptures prematurely. extradural removal of the anterior clinoidal process is performed by extension of the medial dissection of lesser sphenoid wing (8). it uses of a high-speed diamond drill to hollow out the process until it is disconnected at its points of bony fixation. it is then extracted from its dural attachments, and cavernous sinus bleeding can be controlled with packing. this procedure should be avoided if a clinoidal segment aneurysm is suspected, because such aneurysm can 37 microsurgical clipping of paraclinoid aneurysms erode into and through the anterior clinoidal process (4,21). with intradural anterior clinoid process removal, the dura is opened in a curvilinear fashion based on the sphenoid ridge, and the sylvian fissure is widely split, allowing the aneurysm, ica, and visual system to be partially visualized (9). two incision are made: first, a 3to 4-cm longitudinal incision along the lesser sphenoid wing, starting from the tip of the anterior clinoid process and a second dural incision made perpendicular to the first, extending to and including sectioning of the falciform ligament (20). the dura is stripped free from the underlying bone and clinoid process is removed as in extradural way but with better visualization of the optic apparatus and the aneurysm. after anterior clinoidectomy is complete, the optic canal is unroofed, and the optic strut is drilled down to the base of the sphenoid bone. the optic nerve sheath is then sectioned laterally to allow further access to the medial portion of the ica and mobilization of the optic nerve. aneurysm dissection and clip application small ophthalmic artery aneurysms are technically easy to clip. after extradural or intradural removal of the anterior clinoid process, opening of the falciform ligament and mobilization of the ica, the origin of the ophthalmic artery and the neck of the small aneurysm should be readily visible. at the moment of clip application, it is advisable to gently retract the ica laterally rather the optic nerve medially (2). we consider that temporary clipping of the cervical ica greatly aids in the dissection maneuver by softening the aneurysmal sac. ophthalmic artery aneurysms can be ligated with a strait, curved or side-angled clip, depending on their size, complexity and surgeon preference. cohen-gadol considered that side-angled clips orient the blades parallel to the long axis of the parent ica and allow efficient neck closure without causing accordion-like shortening of the carotid trunk. especially in broad neck aneurysms he underlined that a perpendicular clipping technique across the ica leads to partial neck closure, hemodynamic turbulence within the sac, and potentially intraoperative rupture (4). there is a distinct difference in the technical complexity of ligation for superiorly projecting and anteromedially projecting ophthalmic aneurysms. although the former is relatively straightforward, the latter are hidden under the optic nerve and often require a tandem clipping technique: a fenestrated clip around the ica can often be used to close a remnant (18). whereas ophthalmic artery aneurysms are often well visualized, superior hypophyseal aneurysms project medially away from the surgeon, with the ica blocking any substantial view of the neck (14,16). these aneurysms usually require an angled fenestrated clip with the ica within the fenestration and the clip blades pointing toward the distal dural ring. because the superior hypophyseal arteries are often very proximal, the tips of the clip blades must extend up to or past the distal dural ring to completely close the neck. if the ring is not circumferentially dissected, the clip blades will remain partially splayed open and the aneurysm sac will continue to fill (14,27). in paraclinoid aneurysms, usually in large ones, visualization of the entire aneurysm neck during clip application is often impossible, and clip deployment proceeds with visualization of one blade and often inspection of the other, only after the clip is applied. inspection should reveal no perforator injury. depending on the anatomy, one or several angled or right angled fenestrated clips may be necessary (14). large and giant aneurysms present technical challenges, especially if their neck is extending into the carotid cave (4,14). they require the use of complete flow arrest (aneurysm trapping) or suctiondecompression technique for their decompression, manipulation and clip placement. the purpose is not only to prevent intraoperative rupture, but also to obtain adequate neck visualization and reliable neck closure. with large to giant aneurysms, aneurysmal decompression using the retrograde suctiondecompression technique can be lifesaving. with this technique, endovascular inflation of a balloon in the cervical ica is followed by temporary clip occlusion of the distal ica within the operative field. retrograde suction of the blood using a balloon catheter in the neck provides dramatic deflation and clip reconstruction of the patent ica (4). in our cohort, surgical clipping of 18 paraclinoid aneurysms was performed. overall, one patient got worse and died after surgery (5.5%; cerebral ischemia resulting from severe cerebral vasospasm), one patient (5.5%) did not improve and the 38 mugurel radoi, ram vakilnejad, suditu stefan, florin stefanescu remainder (88.8%) improved in terms of mrs, at six months follow-up. no new visual field deficits or eye movement defects were recorded postoperatively. comparing the results in the literature, kothandaram et al (19) in 1971, reported two deaths (20%) and two hemiplegic patients (20%) out of ten operated on with ophthalmic aneurysms. fox (11), reported in 1988, that two of eight patients (25%) with paraclinoid ophthalmic aneurysms showed a transient reduction in visual acuity or ipsilateral blindness. kobayashi et al (17), in 1989, operated on seven patients with the carotid cave subtype of ophthalmic aneurysms, two (29%) of which presented with visual disturbance postoperatively. in 1990, on a series of 54 patients operated for paraclinoid aneurysms, day et al (6) reported a morbidity rate of 7% and a mortality rate of 6%. in a very large study by hoh et al (13), presented in 2000, on 238 patients with carotid-ophthalmic aneurysms from which 180 where clipped, he reported a 6% morbidity rate and only a 0.4% mortality. on a series of 81 patients operated for paraclinoid aneurysms, published in 2005, yonekawa et al (15), reported a surgery-related permanent morbidity in 6 patients (13%), and a surgery-related mortality rate of 0%. the more recent publication of sames et al. (2014), on a series of 37 carotid-ophthalmic clipped aneurysms, reported two patients got worse after surgery (5.4%, one unruptured), three patients (8.1%) did not improve and the remainder (86.5%) improved in the terms of gos (25). microsurgery with clip ligation, including skull base approaches, is a proven effective and durable means to permanently securing paraclinoid aneurysms with good outcomes (1,6,26). complications generally revolve around the anatomic structures encountered within the region—the ica, arterial perforators, and neighboring cranial nerves. even though intraoperative angiography may demonstrate initial ica patency, delayed stenosis or thrombosis can still occur. any evidence of focal neurological deficits after surgery should be immediately addressed with ct and angiography, and the patient returned to the operating room for emergency re-exploration and clip adjustment if obstruction is identified. postoperative visual deterioration, a potential complication in all paraclinoid aneurysm operations, is usually attributable to excessive optic nerve manipulation or perforator compromise during the exposure or clip placement. the clip should not compress or rotate the optic nerve that is especially intolerant of torsion. delayed visual worsening indicates a need for re-exploration to assure the clip is not displaced, causing compression (4). the first series to define the microsurgical anatomy of the ophthalmic segment and meticulously analyze operative results reported excellent outcomes, defined as no postoperative neurological deficit, in 87% of the patients (6). ischemic injury and/or increased visual deficits occurred in 11% of patients, almost all of whom had had very large or giant aneurysms of the superior hypophyseal artery (6). in a later study, nanda and javalkar (23) observed an 8.7% rate of visual deterioration after surgery. no statistically significant difference in outcome was noted between giant and non-giant aneurysms (23). de oliveira and colleagues (24) reported that most patients had improved visual function after surgery. dehdashti and colleagues (7) found an overall surgery-related visual complication rate of 14%. a far as the recovery of visual dysfunction is concerned, the results reported in the literature suggest first few months (10,29) or three months (5) for an operation to be done from the onset of symptoms. furthermore, results in the literature suggest that symptomatic unruptured c6 aneurysms should preferably be treated surgically as the actual cause of the symptoms is eliminated in that way. coiling or flow diverter implantation can exclude the aneurysm from the circulation by inducing thrombosis in the sac, but will not eliminate its expansive behaviour. postoperative oculomotor, trochlear, and abducens palsies, as well as ptosis and miosis secondary to sympathetic fiber disruption, are generally the result of surgical trauma during acp removal, clip blade advancement, excessive cranial nerve manipulation, or cavernous sinus packing. these deficits are usually partial and transient in nature and are best avoided through careful dissection of the cranial nerves and their blood supply. conclusion paraclinoid aneurysms are known to demand special therapeutic considerations due to their special location of close vicinity to bony structures and important neural and vascular structures. size and 39 microsurgical clipping of paraclinoid aneurysms location of the aneurysm, and the fact that it is ruptured or not, are main determinants in the decision to perform surgery. large and giant aneurysms are daunting the handle without generating new visual deficits. even it is a small series, the mortality and morbidity of paraclinoid aneurysm surgically treated in our department, both ruptured and unruptured, are relatively low and comparable with the results presented in the literature. for an experienced neurovascular team, microsurgical aneurysm clipping can currently be a good therapeutic option for paraclinoid aneurysms. references 1. 1. baccin ce, krings t, alvarez h, et al.: multiple mirror-like intracranial aneurysms. report of a case and review of the literature. acta neurochir (wien). 148:1091,2006 2. batjer hh, kopitnik ta, giller ca, samson ds. surgery for paraclinoidal carotid artery aneurysms. j neurosurg.;80(4): 650–658,1994 3. bohm e, hugosson r, wolgast m. carotid ligation for the treatment of carotid artery aneurysms: where we are? j neuroradiol ;38:40-6, 2011 4. cohen-gadol a. paraclinoid aneurysm in the neurosurgical atlas. doi: https://doi.org/10.18791/nsatlas.v3.ch01.9 5. date i, asari s, ohmoto t. cerebral aneurysms causing visual symptoms: their features and surgical outcome. clin neurol neurosurg;100: 259-267, 1998. 6. day al. aneurysm of the ophthalmic segment. a clinical and anatomical analysis. j neurosurg; 72: 677– 691, 1990. 7. dehdashti ar, le roux a, bacigaluppi s, et al.: longterm visual outcome and aneurysm obliteration rate for very large and giant ophthalmic segment aneurysms: assessment of surgical treatment. acta neurochir (wien), 154:43, 2011. 8. dolenc vv. a combined epiand subdural direct approach to carotid-ophthalmic artery aneurysms. j neurosurg ;62:667-72, 1995 9. du r, al day: microsurgery of paraclinoid aneurysms. 6th ed jr youmans neurological surgery, saunders philadelphia ,vol. 4:3824, 2011 10. ferguson cg, drake cg. carotid-ophthalmic aneurysms: the surgical management of those cases presenting with compression of the optic nerves and chiasm alone. clin neurosurg ;27:263-307, 1980 11. fox jl. microsurgical treatment of ventral (paraclinoid) internal carotid artery aneurysms. neurosurgery 22:32-9, 1988 12. guidetti b, la torre e. carotid-ophthalmic aneurysms. a series of 16 cases treated by direct approach. acta neurochir (wien) 22:289-304,1970 13. hoh bl, carter bs, budzik rf, putman cm, ogilvy cs. results after surgical and endovascular treatment of paraclinoid aneurysms by a combined neurovascular team. neurosurgery 48: 78–90,2001 14. joo w, funaki t, yoshioka f, rhoton al. microsurgical anatomy of the carotid cave. neurosurgery.; 70(2 suppl operative):300–311; discussion 311–312, 2012 15. khan n, yoshimura s, roth p, cesnulis e, imhof h, yonekawa y. conventional microsurgical treatment of paraclinoid aneurysms: state of art with the use of the selective extradural anterior clinoidectomy seac. acta neurochir, (suppl) 94:23-29, 2005 16. kim jm, romano a, sanan a, van loveren hr, keller jt. microsurgical anatomic features and nomenclature of the paraclinoid region. neurosurgery; 46(3): 670–680; discussion 680–682, 2000 17. kobayashi s, kyoshima k, gibo h et al. carotid cave aneurysms of the internal carotid artery. j neurosurg ;70:216-21, 1989 18. korosue k, heros rc. “subclinoid” carotid aneurysm with erosion of the anterior clinoid process and fatal intraoperative rupture. neurosurgery 31(2): 356-359; discussion 359-360, 1992 19. kothandaram p, dawson bh, kruyt rc. carotidophthalmic aneurysms. a study of 19 patients. j neurosurg 34:544-8, 1971 20. k kyoshima, s oikawa, s kobayashi: interdural origin of the ophthalmic artery at the dural ring of the internal carotid artery. report of two cases. j neurosurg 92:488, 2000 21. lawton mt. ophthalmic artery aneurysms in seven aneurysms: tenets and techniques for clipping. ed thieme, 2011. 22. n al-rodhan: aneurysms within the cavernous sinus and transitional cavernous aneurysms. r wilkins s rengachary neurosurgery. 3rd. ed 1996 mcgraw-hill new york 2283, 1996 23. nanda a, javalkar v: microneurosurgical management of ophthalmic segment of the internal carotid artery aneurysms: single-surgeon operative experience from louisiana state university, shreveport. neurosurgery pp 68:355, 2011 24. de oliveira jg, borba la, rassi-neto a, et al.: intracranial aneurysms presenting with mass effect over the anterior optic pathway:neurosurgical management and outcomes. neurosurg focus 26: e3, 2009 25. orlicky m,sames m, hejcl a, vachata p. carotidophthalmic aneurysms – our results and treatment strategy. british journal of neurosurgery, early online 1-6, 2014 26. raco a, frati a,santoro a, et al.: long-term surgical results with aneurysms involving the ophthalmic segment of the carotid artery. j neurosurg. pp 108:1200, 2008 27. samson ds, batjer hh. aneurysms of the anterior carotid wall (ophthalmic). chapter 4 in: intracranial 40 mugurel radoi, ram vakilnejad, suditu stefan, florin stefanescu aneurysm surgery:techniques. futura publishing 1990. 28. turkmani ha, day al. microsurgery of paraclinoid aneurysms. in youmans&winn neurological surgery 7th edition vol 4, pp.3298-3306, 2017 29. vargas me, kupersmith mj, setton a, nelson k, berenstein a. endovascular treatment of giant aneurysms which cause visual loss. ophthalmology 101:1091-8, 1994 30. yasargil mg. microneurosurgery: in 4 volumes. new york:thieme medical pub, 1984. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 517-520 doi: 10.33962/roneuro-2019-087 www.journals.lapub.co.uk/index.php/roneurosurgery communicating spinal epidural thoracic arachnoid cyst en-bloc resection. a case report m. al-zekri, f. aichaoui, i. assoumane, a. khelifa, w. bennabi, a. morsli department of neurosurgery, chu bab el oued, algiers, algeria abstract background: spinal extradural arachnoid cyst is an uncommon, expanding lesion which may communicate with the subarachnoid space, the etiology still remains unclear, but the most accepted explanation is the existence of areas of weakness in the spinal dura , spinal arachnoid cysts are usually in the thoracic spine, and they may cause symptoms due to spinal cord compression. case presentation: patient is a 54-years-old female who presented with progressive back pain and motor deficit, magnetic resonance imaging (mri) study revealed an extradural cyst extending from t2 to t4 isointense with the cerebrospinal fluid (csf) on all sequences and did not enhance on t1-weighted post-contrast mri. patient underwent t2-t4 laminectomy, en-bloc resection of the lesion was achieved and the histopathological examination objectified an arachnoid cyst. conclusion: spinal extradural arachnoid cyst can cause neurologic deficit and the mainstay of treatment in patients with neurological symptoms is surgical removal of the cyst together with ligation of the communicating pedicle and closure of the dural defect. introduction arachnoid cysts are benign lesions located in the brain or spinal cord; usually found incidentally during radiological exploration (1), spinal arachnoid cysts result in a collection of cerebrospinal fluid that can occur in a perineural, extradural, intradural, or intra-extradural site (2). spinal arachnoid cysts are a rare cause of spinal cord compression. spinal arachnoid cysts may be associated with other neural tube defects such as spina bifida occulta and diastematomyelia (2). mri is the diagnostic procedure of choice as it is noninvasive and can demonstrate the nature of cyst, size, and the anatomic relationship with the spinal cord. surgical treatment is required when neurological symptoms develop due to cyst induced spinal cord or nerve root compression (4). here we reported our experience on the management of a 54 years old female who presented a communicating spinal epidural thoracic arachnoid cyst. keywords spinal cord, arachnoid cyst, laminectomy, resection corresponding author: m. al-zekri department of neurosurgery, chu bab el oued, algiers, algeria muneeralzekri30@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 530 m. al-zekri, f. aichaoui, i. assoumane et al. case report we reported here a case of a 54 years old female without past medical or surgical history complaining with progressive back pain, and paresthesia in lower limbs which has been initiated from9 years worsening in the last 3months with weakness of lower extremities. clinical examination at admission revealed a paraparesia 4/5. there was no history of recent traumatism. the spinal mri showed a thoracic extradural arachnoid cyst from lower edge of t2 to lower edge of t4 and cervical spinal canal stenosis,the cyst is hyper intense signal in t2-weighted, hypo intense signal in t1-weighted and did not enhance on t1weighted post-contrast (figure 1 and figure 2). figure 1. pre-operative spinal mri shows a cystic lesion extending from lower edge of t2 to lower edge of t4 with hyper intense signal on t2-weighted mri accompanied by a central hypo intense signal (a), hypo intense signal on t1-weighted mri(b). figure 2. t2-weighted mr imaging sequences showing arachnoid cyst with high signal intensity at t2 to t4 level. we operated the patient under general anesthesia in prone position. we performed a midline incision followed by laminectomy (t2-t3-t4), after exposure of the lesion and identification of its superior and inferior poles, we began the soft dissection of the lower pole lesion towards the superior pole, then we identified the communication between the cyst and the subarachnoid spaces through a dural defect, after total excision en bloc we close the dural defect with a muscular patche (figure 3). postoperative histologic findings were compatible with the presence of an arachnoid cyst with fibrous cyst wall-like tissue. back pain in the patient and paraparesis were gradually improved. figure 3. intra-operative view. (a): following laminectomy and visualization of the cyst (yellow star); (b): en-bloc resection of the lesion and visualization of the dura (blue star); (c) ligation of the communicating pedicle and closure of the dural defect (yellow arrow). discussion arachnoid cysts are benign developmental cysts that occur in the craniospinal axis in relation to the arachnoid membrane. we report a case of extra dural arachnoid cyst, for many authors the spinal arachnoid cysts may be intradural or extradural and are composed of normal or slightly thickened arachnoid (6) a spinal extradural arachnoid cyst is a rare disease, accounting for approximately 1% to 3% of spinal tumors (5, 8). they can be idiopathic or acquired, usually intradural, but can also rarely be extradural, primary spinal arachnoid cysts present in the thoracic spine in 80%, secondary arachnoid cysts are usually due to trauma, hemorrhage, inflammation, surgery, or lumbar puncture (8). spinal extradural arachnoid cysts are most commonly found in the middle or lower thoracic spine, and less frequently found in the lumbar region, although they can be detected at any lesion of the spine (1, 3, 4, and 5). the case we report is in the most frequent site. these lesions are more common in men (sex ratio 2/1) and occurs in the 531 communicating spinal epidural thoracic arachnoid cyst en-bloc resection second decade of life. these lesions may be associated with vertebral anomalies, neural tube defects and syringomyelia (1, 2, 3, 5, and 6). various hypotheses have been proposed to explain why spinal arachnoid cysts form: 1 proliferation or loculation of arachnoid trabeculae in the septum posticum; 2a fault in the expansion of the arachnoid trabecula and 3the formation of arachnoid diverticuli in weak areas of the spinal dura mater (5). spinal extradural arachnoid cysts are usually asymptomatic; they can compress the spinal cord and give a neurological deficit; the medullary compression mechanism is still unclear but many authors have speculated that these cysts act as a unidirectional valve that let fluid in but not out.(1,3). the most common presenting symptoms are pain, paresthesia, intermittent claudication, and variable degrees of spastic weakness (3,4,6 ) like our patient who experiment back pain, paresthesia and paraparesia. the differential diagnoses include: tarlov or perineural cyst,ganglion cyst, synovial cyst,epidermoid cysts, cystic neoplasms, parasitic cysts meningeal diverticula next to the nerve roots, meningocele, dermoid cyst,cysticercosis and hydatid cysts (1,5). we use the spinal mri to get the diagnosis , this investigation showed a thoracic extradural arachnoid cyst from lower edge of t2 to lower edge of t4 and cervical spinal canal stenosis, the cyst is hyper intense signal in t2-weighted, hypo intense signal in t1-weighted and did not enhance on t1weighted post-contrast. many authors reported signs of that lesion on other investigations tools. radiographs of the spine usually show bone erosion with widening of the canal, erosion ofpedicles, foraminal enlargement, and scalloping ofthe vertebral bodies or the sacrum (3). ct can be helpful to identify a cyst complicated by internal hemorrhage as the quickest and most readily available neuroimaging test. however,an mri is the most useful tool to diagnose a spinal extradural arachnoid cyst. radiological studies report that a spinal extradural arachnoid cyst appears with low signal intensity on a t1-weighted image and with high signal intensity on a t2-wi, similar to cerebro-spinal fluid. fluid attenuated inversion recovery sequences (flair) sequences are also useful to confirm the similarity of the cyst fluid to csf. diffusion weighted imaging is essential to differentiate arachnoid cysts, inparticular from epidermoid cysts which can sometimes have a similar appearance (7). the management of these cysts can vary according to the patient’s symptoms.there are many surgical options reported in the literature: bone decompression, subtotal or total resection of the cyst, drainage and marsupialisation of the cyst. in asymptomatic patients, conservative management with subsequentclinical observation is recommended(4, 5).the goal of surgical treatment is not only neural decompression but also the prevention of cyst refilling.for symptomatic extradural spinal arachnoid cysts the preferred treatment is surgical removal of the cyst together with ligation of the communicating pedicle and closure of the dual defect (3, 4). in the reported case we achieved the identification of the communication between the cyst and the subarachnoid spaces through a dural defect and after total excision en bloc we close the dural defect with a muscular patch. conclusion spinal extradural arachnoid cyst is rare lesion, it is typically asymptomatic but sometimes can cause spinal cord or nerve root compression and may present with myelopathy. the etiology, pathogenesis and treatment of the spinal extradural arachnoid cysts have not been well established. to treat a spinal extradural arachnoid cyst, diverse surgical techniques have been introduced. however, there is no consensus regarding the most reasonable treatment. references 1. afsounseddighi, amir nikouei, amir saied seddighi, mohammad asadpour, noushin masoudian, afshin samaei, shohada tajrish: a case report extradural thoracic arachnoid cyst en-bloc resection and follow-up comprehensive neurosurgical center of excellence, shahid beheshti university of medical sciences, tehran, iran. 2. dahlgren, ryan m.; baron, eli m.; and vaccaro, alexander r., "pathophysiology, diagnosis, andtreatment of spinal meningoceles and arachnoid cysts" (2007). department of orthopaedic surgery faculty papers. paper 4.https://jdc.jefferson.edu/orthofp/4 3. ertan ergun; alp özgün börcek; berker cemil; fikret dogulu; m. kemali baykaner should we operate all 532 m. al-zekri, f. aichaoui, i. assoumane et al. extradural spinal arachnoid cysts? report of a case turkish neurosurgery 2008, vol: 18, no: 1, 52-55. 4. james k. liu, m.d.chad d. cole, m.d.,peter kan, m.d.,and meic h. schmidt, m.d.s pinal extradural arachnoid cysts: clinical, radiological, and surgical features department of neurological surgery, oregon health & science university, portland, oregon; and department of neurosurgery, university of utah school of medicine, salt lake city, utah neurosurg focus 22 (2):e6, 2007. 5. quillo-olvera j, quillo-reséndiz j, gutiérrez-partida c-f, rodríguez-garcía m.quiste aracnoideo extradurale spinal: reporte de un caso y revisión de la literatura. cir cir. 2017;85:544---548. 6. guru raj aithala, md, laszlo sztriha, md, iradj amirlak, md, kunjupanicker devadas, md, andingrid ohlsson, md: spinal arachnoid cyst with weakness in the limbs and abdominal pain. 7. logan c, asadi h, kok hk, looby s, o’hare a, et al. 2016. arachnoid cysts common and uncommon clinical presentations and radiological features. j neuroimaging psychiatry neurol 1(2): 79-84. 8. lim k, nouri m, haffar a and mazagri r.an unusual, acute presentation of thoracic spinal arachnoid cyst .sm j neuroldisord stroke. 2018; 4(1): 1016. doi: 10.33962/roneuro-2023-041 electroencephalographic findings in autistic non-epileptic children arwa k. ibrahem, hula shareef, kanar k. shaker, dhay mohammed, farqad bader hamdan romanian neurosurgery (2020) xxxiv (1): pp. 229-232 doi: 10.33962/roneuro-2020-041 www.journals.lapub.co.uk/index.php/roneurosurgery electroencephalographic findings in autistic non-epileptic children arwa k. ibrahem1, hula shareef2, kanar k. shaker3, dhay mohammed3, farqad bader hamdan4 1 department of neurophysiology, neurosurgery teaching hospital, baghdad, iraq 2 paediatric neurologist, paediatric neurology department, children welfare hospital, the medical city, baghdad, iraq 3 department of neurophysiology, baghdad teaching hospital, medical city, baghdad, iraq 4 department of physiology, college of medicine, al-nahrain university, baghdad, iraq abstract despite the well-acknowledged link between autism spectrum disorders (asds) and epilepsy, the prevalence and significance of electroencephalogram (eeg) changes in epileptic children in the absence of clinical seizures remains underdetermined. aim. the primary goal of this study is to report the prevalence of eeg abnormalities in non-epileptic or pre-epileptic autistic children, investigate their association with a set of pre-determined risk factors, speculate on their significance, and direct future research efforts. methods. a case-based sampling for children diagnosed with autism was done. only patients without a history of epilepsy and those under the age of 15 were included. all patients underwent an eeg study. children with abnormal eeg findings (case group) were compared to age-matched controls with normal eeg findings using a set of pre-determined factors. results. a total of 38 patients were enrolled in our study, of whom 31.6% (n=12) had abnormal eeg readings. of those, the presence of the following eeg abnormalities were noted – each being present in two patients: frontal sharp waves, frontal slowing, temporal slowing, bitemporal slowing, frontal sharp waves, and generalized sharp waves, frontal intermittent rhythmic delta activity (firda). patients with abnormal eeg findings were more likely to have a positive family history of epilepsy and/or autism, with odd ratios of 28.05, and 12.62, accordingly. conclusion. aberrant brain connectivity patterns have been observed in nonepileptic asd patients, and our findings support these findings. furthermore, we believe that gender, mother's age, mode of delivery, and speech abnormalities could all have an impact on the eeg results. however, more research is needed to expand on these findings. introduction autism spectrum disorders (asds) are a broad category of complex neurodevelopmental disorders. asds are distinguished by impaired social interaction, deterioration of language skills, and a limited keywords autism spectrum disorders, eeg corresponding author: arwa k. ibrahem department of neurophysiology, neurosurgery teaching hospital, baghdad, iraq drarwakhalidibrahem2015@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 230 arwa k. ibrahem, hula shareef, kanar k. shaker et al. repertoire of interests. individuals appear to differ in terms of cognitive function decline, the presence of intellectual disability, behavioral changes, and symptom severity and onset. despite extensive research, the biological factors that govern autism development remain unknown. the first report on the possible neuronal links of asd was published in 1943; kanner examined 11 children with asd in this report; three of them had seizures, three were mute, and five were macrocephalic (5). however, it was not until 1970 when gubbay et al. published the first report on eeg abnormalities in children with asd (3). since then, there has been extensive research into the evidence of neurological involvement in asd subjects. despite the fact that epilepsy is associated with an increased morbidity rates, the clinical significance of eeg abnormalities in the absence of seizures has not been established. nonetheless, the majority of the evidence points to the presence of hyperexcitable brain regions, which may contribute to aberrant connectivity within the brain, resulting in faulty functioning of neural circuits in the brain responsible for basic information processing (1,4). as a result, the primary goal of this study is to report the prevalence of eeg abnormalities in nonepileptic or pre-epileptic autistic children, investigate their association with a set of pre-determined risk factors, speculate on their significance, and direct future research efforts. methods setting the study was conducted at baghdad teaching hospital (bth), medical city, spanning the period september 2018 to march 2019. patient sampling a case-based sampling for children diagnosed with autism was done. only patients without a history of epilepsy and those under the age of 15 were included. patients with medications that might affect eeg readings were excluded. all patients underwent an eeg study. written informed consent was obtained from the parents for participation in the study. eeg findings were interpreted by two consultant neurophysiologists. the study was approved by the ethics committee of baghdad medical city. study design this is a case-control study. children with abnormal eeg findings (case group) were compared to agematched controls with normal eeg findings. both groups had a definite diagnosis of autism and no clinical history of epilepsy. study aim the study was conducted to examine the association between the patient’s age, gender, mode of delivery, maternal age at delivery, family history of epilepsy or autism, socioeconomic status, and speech difficulties. statistical methods the odds ratio (or) was calculated to determine the association of each of the abovementioned factors with the presence of abnormal eeg findings. fisher exact test was used to determine the significance of association. the significance level was set at a pvalue of < 0.05. results a total of 38 patients were enrolled in our study, of whom 31.6% (n=12) had abnormal eeg readings. of those, the presence of the following eeg abnormalities were noted – each being present in two patients : frontal sharp waves, frontal slowing, temporal slowing, bitemporal slowing, frontal sharp waves, and generalized sharp waves, frontal intermittent rhythmic delta activity (firda). the age range was (3-10) years with a mean of 6.1 years. the male-to-female ratio was 32.6. as for the mother age, 26.3% (n=10) were 35 years or older. the percentage of patients that were delivered by cesarean section was 47.4% (n=18). a family history of epilepsy and autism was documented for 10.5% (n=4), and 5.3% (n=2) of the patients, respectively. speech difficulty was present in 47.4 (n=18) of the participants, and 10.5% (n=4) of them belonged to high socioeconomic group. (table 1). patients with abnormal eeg findings were more likely to have a positive family history of epilepsy and/or autism, with odd ratios of 28.05, and 12.62, accordingly. the other parameters understudy, including patient and mother age, gender, mode of delivery, socioeconomic status, and the presence of speech difficulties failed to achieve statistical significance in this study. (table 2). 231 electroencephalographic findings in autistic non-epileptic children table 1. patients’ characteristics. characteristic % (n) age range 3-10 yrs age mean 6.1 yrs m:f 32:6 mother age of 35 + 26.30% (10) c/s delivery 47.40% (18) fhx epilepsy 10.50% (4) fhx autism 5.30% (2) high ses 10.50% (4) speech difficulty 47.40% (18) eeg + 31.60% (12) table 2. odds ratios, 95% confidence intervals, and p-values for the association of abnormal eeg readings with the parameters understudy. or 95% ci p-value gender (m) 0.9 0.14 5.81 1 maternal age (35+ years) 0.45 0.08 2.5 0.5 delivery (cs) 3.2 0.76 13.5 0.2 fhx of epilepsy 28.05 1.37 576.2 0.002 fhx of autism 12.62 0.56 285.6 0.03 ses (high) 0.2 0.01 4.03 0.3 speech difficulties 1.4 0.35 – 5.4 0.73 discussion the high rate of co-existence of epilepsy and asd is well recognized, pointing to a possible shared pathophysiology. however, the prevalence, nature, and clinical implications of abnormal eeg findings in the absence of clinical seizure activity in asd children have received less attention. the existence and potential value of such abnormalities are indicated by data from scattered reports, but their exact nature and clinical significance remain unknown. in our cohort of 38 non-epileptic asd patients, 31.6 percent (n=12) had abnormal eeg findings, which is consistent with the published literature. having a positive family history of epilepsy and/or autism showed a significant association with the presence of abnormal eeg findings among the factors studied. the non-significance of the other factors may be due to the fact that the study is underpowered, and expanding the scope of the study to include more participants or a control group such as children with asd and epilepsy may reveal statistically significant associations. follow-up is also required to determine the persistence or absence of the observed eeg abnormalities. aside from the abovementioned, well-designed longitudinal studies are also required to determine the role, if any, of these bioelectrical abnormalities in the development and natural course of autistic symptoms, language, and cognitive decline. the presence of epileptic discharges in patients with nonepileptic asd may represent an endophenotype with treatment and prognostic implications, and it aids in the precise characterization of study samples. the results of this study as well as the available literature over the span of the previous four decades highlights a set of key questions to be addressed. first, is the cost-effectiveness of extensive initial eeg, and/or follow-up eeg in non-epileptic asd patients justified? currently, there is no data on the costeffectiveness of eeg testing in children exhibiting asd symptoms. however, if early intervention can prevent or ameliorate a life-long disorder, even a low yield may be justified not only economically, but also in terms of avoided suffering for patients and their families. the second question is whether the lack of an epileptic discharge detected by eeg or magnetoencephalography (meg) technology indicates the absence of such an abnormality. according to data published by small (6) and frye et al. (2) different study designs that used alternate detection protocols, such as eeg monitoring units, will result in higher yield. furthermore, comparing electroencephalography (eeg) and magnetoencephalography (meg) readings reveals that the latter is superior, with detection rates of 68 percent and 82 percent, respectively. this means that while an eeg test may produce "negative results," this does not imply that there is no abnormality, and it also highlights the significant false negative problem, which is especially common in eeg studies. another unanswered question is whether the nature of eeg abnormalities influences the course of clinical symptomatology and whether the location of the eeg abnormality is causal. hashimoto et al. found that the coexistence of frontal and temporal lobe abnormalities had a significant impact on the rate of emergence of autistic features in their study. unraveling the clinical significance of these findings in terms of how they might inform treatment decisions is critical, and it is the starting point for answering the questions raised above. 232 arwa k. ibrahem, hula shareef, kanar k. shaker et al. conclusion aberrant brain connectivity patterns have been observed in non-epileptic asd patients, and our findings support these findings. furthermore, we believe that gender, mother age, mode of delivery, and speech abnormalities could all have an impact on the eeg results. however, more research is needed to expand on these findings. abbreviations asds: autism spectrum disorders; eeg: electroencephalogram; firda: frontal intermittent rhythmic delta activity; meg: magnetoencephalography. references 1. filipek pa, accardo pj, ashwal s, baranek gt, cook eh, et al. (2000) practice parameter: screening and diagnosis of autism: report of the quality standards subcommittee of the american academy of neurology and the child neurology society. neurology 55: 468-479. 2. frye re, butler i, strickland d, castillo e, papanicolaou a (2010) electroencephalogram discharges in atypical cognitive development. j child neurol 25(5):556–566. 3. gubbay ss, lobascher m, kingerlee p (1970) a neurologic appraisal of autistic children: results of a western australian survey. dev med child neurol 12:422–429. 4. kagan-kushnir t, roberts sw, snead oc (2005) screening electroencephalograms in autism spectrum disorders: evidence-based guideline. j child neurol 20: 197-206. 5. kanner l (1943) autistic disturbances of affective contact. nervous child 10:217–250. 6. small jg (1975) eeg and neurophysiological studies of early infantile autism. biol psychiatry 10:385–397. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0057 article a rare complication of chronic subdural hematoma evacuation: brain stem hemorrhage: a case report ghassen gader, mouna rkhami, maher ben salem, mohamed badri, kamel bahri, ihsèn zammel tunisia      462 | gader et al complication in chronic subdural hematoma             doi: 10.2478/romneu-2018-0057 a rare complication of chronic subdural hematoma evacuation: brain stem hemorrhage: a case report ghassen gader, mouna rkhami, maher ben salem, mohamed badri, kamel bahri, ihsèn zammel department of neurosurgery, trauma and burns center, ben arous, tunisia abstract: chronic subdural hematoma (csdh), which commonly affects the elderly, is one of the most frequent, but also benign neurosurgical pathologies. burr hole drainage is the standard surgical modality for evacuation of a csdh. this technique is known to be safe, with low morbidity and mortality rates. however, postoperative complications have occasionally been reported. we report the case of a 70-year-old man who presented a fatal brain stem hemorrhage after burr-hole drainage for unilateral chronic subdural hematoma. asymmetrical and rapid decompression were thought to be leading to vascular disruption or sudden increase in cerebral blood flow, was probably responsible for the secondary brain stem bleeding. therefore, a slow rate of evacuation of chronic subdural hematomas, as well as rigorous postoperative reanimation, are recommended in order to prevent serious complications. introduction chronic subdural hematoma is considered among the most benign pathologies to be treated in neurosurgery, with a mortality rate ranging from 0.5 to 4% (5,14). burr hole drainage is the most commonly used modality for surgical evacuation of csdh. this technique is known as safe, easy to perform, with a low morbidity rate ranging from 0 to 9% (14). however, postoperative complications, including cerebral edema, hematoma recurrence, subdural empyema, tension pneumocephalus, and intracranial haemorrhage in other sites, have been reported with variable frequencies (13,17). intracranial hematomas occurring as a result of evacuation of haematomas may be located more or less distant from the site of the csdh. brainstem bleeding secondary to this surgery is extremely rare, as only 3 cases have been reported in the literature (1,6). we report the case of a 70-year old man who suffered brain stem hemorrhage after unilateral csdh evacuation, and discuss the physiopathology of this complication.   romanian neurosurgery (2018) xxxii 3: 462 465 | 463             case presentation a 70-year-old man with a history of ischemic stroke of which he kept no sequelae, presented with progressive alteration of the state of consciousness lasting for 5 days. family reported a minor head trauma following a domestic incident. this trauma occurred 3 weeks before admission. neurological examination found a comatose patient with a gcs of 8. pupils were intermediate, reflective and symmetric. brain ct scan (figure 1) showed a left frontotemporal subdural hematoma with stigmata of recent bleeding. the heamatoma had a maximum thickness of 1.3 cm with a midline shift of 0.8 cm. laboratory studies, including clotting profiles, did not reveal any abnormalities. emergency evacuation of the hematoma was performed. after burr holes were made, the dural surfaces were exposed and coagulated. the dura and outer membrane on the anterior hole were opened first, followed by the posterior hole a few seconds later later. opening of the outer membranes allowed dark brown hematoma to gush out via the openings. we tried to evacuate the hematoma gradually, but rapid decompression occurred during the initial period of the procedure due to the high pressure. thereafter, a subdural drainage system was inserted through the posterior burr hole. the patient's vital signs were stable during the operation, and no elevation of arterial blood pressure was observed. postoperative, there was no signs of awake. pupils were in bilateral myosis. control ct scan made day one postoperative demonstrated regression of the subdural haematoma and of the midline shift, but also detected brain stem hemorrhage that was not present on the preoperative images (figure 2). the patient remained comtose. he had a respiratory infection on 4th postoperative day managed with antibiotics. he presented bilateral mydriasis on the 7th day postoperative, and died the day after. figure 1 figure 2 464 | gader et al complication in chronic subdural hematoma             discussion to the best of our knowledge, only four cases of brain stem hemorrhage as a complication of surgery for csdh have been reported (8,10–12). two cases were diagnosed at autopsy, two at postoperative control ct scan. only one patient survived. brainstem hematoma was diagnosed in the surviving patient as he presented gait disturbance with mild lower limb weakness. two of these patients were managed for bilateral chronic subdural hemorrhage, whereas two were operated for a unilateral hematoma. the principal mechanism causing postoperative intracerebral hemorrhage is thought to be a sudden increase in cerebral blood flow combined with defective vascular autoregulation (9). but, the pathophysiology of brain stem hemorrhage following intracranial hematoma decompression is still not clear, since brain stem hemorrhage is often the cause of sudden death, so hemodynamic changes are difficult to study. it is suggested that the brain stem hemorrhage was likely due to damaged vessels caused by increased intracranial pressure (icp) (4). rapid alleviation of increased icp, under conditions of elevated blood pressure, could disrupt the small injured vessels, invariably resulting in brain stem hemorrhage. in the present case, preoperative ct showed transtentorial herniation, indicating that the blood vessels near the brain stem might be stretched and distorted (7). the decompression was performed with a short time lag between the opening of the anterior and posterior holes. this decompression was brutal due to the high intracranial pressure, associated to a quick blood draft. consequently, the vessels surrounding the brain stem may have torn, precipitating the hemorrhage into the brain stem. vascular disruption could occur easily since the transtentorial herniation was already present, and the vessels surrounding the brain stem had already been maximally stretched. in fact, cranial nerve paresis and brain stem dysfunction have been reported after the removal of csdhs suggesting that the complications may be due to rapid unilateral decompression, which leads to sudden distortion of the midline structures. single photon emission computed tomography has demonstrated that cerebral blood flow in patients with csdhs is diminished, particularly in the ipsilateral basal ganglia and thalamus (2,3), followed postoperatively by progressive normalization of blood flow. physiological aging of the cerebral vascular tree is associated with poor tolerance of sudden variations in cerebral blood flow (15). considering that the present patient was elderly, the increased fragility of the small blood vessels might not have been able to sustain the rapid changes in the brain stem blood flow during decompression of the subdural hematoma. consequently, the brain stem hemorrhage in the present case was likely due to the mechanical disruption of small fragile vessels, and accentuated by an increase in blood flow caused by breakthrough-like dysregulation triggered by the abrupt supratentorial decompression. other factors responsible for brain stem hemorrhage, such as vascular malformations, bleeding tendency, and perioperative hypertension are also evolved (16). gradual decompression avoiding rapid changes in blood flow may be accomplished by primary drainage through a frontal burr hole romanian neurosurgery (2018) xxxii 3: 462 465 | 465             and then applying cotton to the burr hole immediately after opening the outer membrane. continuous closed-system catheter drainage has been proposed for the treatment of csdh, as it allows the brain to reexpand slowly (10). conclusions brainstem hematomas are very rare complications of chronic subdural hematomas evacuation. slow decompression, control of clotting disorders and maintenance of a correct blood pressure perioperatively may prevent the occurrence of these complications. the present case illustrates that asymmetrical and rapid decompression, which leads to vascular disruption and sudden increase in cerebral blood flow, which may cause brainstem hematoma. therefore, decompression with a slow rate of evacuation is recommended for the removal of csdhs, to avoid serious complications such as secondary intracranial hematoma. correspondence ghassen gader resident, gastghagad@yahoo.fr, 0021698604749 references 1. hyam j, turner j, peterson d. cerebellar haemorrhage after repeated burr hole evacuation for chronic subdural haematoma. j clin neurosci. 2007;14:83‑6. 2. ishikawa t, kawamura s, hadeishi h, suzuki a, yasui n, uemura k. cerebral blood flow and oxygen metabolism in hemiparetic patients with chronic subdural hematoma. quantitative evaluation using positron emission tomography. surg neurol. 1995;43:130‑7. 3. kim jk, kim sw, kim sh. intracerebral hemorrhage following evacuation of a chronic subdural hematoma. j korean neurosurg soc. 2013;53(2):108. 4. klintworth g. the pathogenesis of secondary brainstem hemorrhages as studied in an experimental model. am j pathol. 1965;47:525‑36. 5. kotwica z, brzezinski j. chronic subdural haematoma treated by burr holes and closed system drainage: personal experience in 131 patients. br j neurosurg. 1991;5:461‑5. 6. liang c, rau c, lu k, chen h. contralateral acute subdural haematoma after burr-hole for chronic subdural haematoma. injury. 2001;32:499‑500. 7. marupaka s, sood b. atypical duret haemorrhages seen on computed tomography. emerg med australas. 2008;20:180‑2. 8. mckissock w, bloom w. subdural haematoma. a review of 389 cases. lancet. 1960;1:1365‑9. 9. modesti l, hodge c, barnwell m. intracerebral hematoma after evacuation of chronic extracerebral fluid collections. neurosurgery. 1982;10:689‑93. 10. park k-j, kang s-h, lee h-k, chung y-g. brain stem hemorrhage following burr hole drainage for chronic subdural hematoma. neurol med chir (tokyo). 2009;49(12):594–597. 11. patibandla m, thotakura a, shukla d, purohit a, addagada g, nukavarapu m. postoperative hematoma involving brainstem, peduncles, cerebellum, deep subcortical white matter, cerebral hemispheres following chronic subdural hematoma evacuation. asian j neurosurg. 2014;0(0):0. 12. robinson r. chronic subdural hematoma: surgical management in 133 patients. j neurosurg. 1984;61:263‑8. 13. rohde v, graf g, hassler w. complications of burrhole craniostomy and closed-system drainage for chronic subdural hematomas: a retrospective analysis of 376 patients. neurosurg rev. 2002;25:89‑94. 14. sambasivan m. an overview of chronic subdural hematoma: experience with 2300 cases. surg neurol. 1997;47:418‑22. 15. sato m, nakano m, asari j, watanabe k. intracerebral haemorrhage during surgery for chronic subdural haematoma. j clin neurosci. 2007;14:81‑3. 16. sousa j, golash a, vaz j, chaudhary h. spontaneous intracerebral haemorrhage following evacuation of chronic subdural hematomas. j clin neurosci. 2004;11:794‑6. 17. weigl r, schmiedek p, krauss j. outcome of contemporary surgery for chronic subdural haematoma: evidence based review. j neurol neurosurg psychiatry. 2003;74:937‑43. doi: 10.33962/roneuro-2021-077 outcome of patients undergoing posterior spine fixation and decompression for posttraumatic thoracolumbar spine fractures and the factors predicting it geo paul k. jose, tinu ravi abraham, p.k. balakrishnan, irphan muhammed p.s., haris t.p., vala parth prakashbhai romanian neurosurgery (2021) xxxv (4): pp. 457-467 doi: 10.33962/roneuro-2021-077 www.journals.lapub.co.uk/index.php/roneurosurgery outcome of patients undergoing posterior spine fixation and decompression for posttraumatic thoracolumbar spine fractures and the factors predicting it geo paul k. jose, tinu ravi abraham, p.k. balakrishnan, irphan muhammed p.s., haris t.p., vala parth prakashbhai department of neurosurgery, government medical college kottayam, kerala, india abstract background: posterior spine fixation and decompression for thoracic and lumbar spine fractures have the advantage of stabilization of the fracture, decompression of neural canal, early mobilization and rehabilitation of the patient. the study aimed to find out the postoperative outcome and complications following posterior spine surgery and the factors affecting the outcome. methods: a retrospective study was carried out among 44 patients who underwent posterior spine decompression and fusion for thoracic and lumbar spine fracture. the data regarding patient presenting symptoms, comorbidity, associated injuries and imaging finding in ct and mri were collected. the postoperative outcome of patients after surgery was assessed using asia impairment scale, kps, vas scale for pain are noted at the preoperative and postoperative period. other factors like improvement of bowel and bladder symptoms, back stiffness and return to the job after surgery were also found out. results: there was a significant improvement in asia impairment scale (mean =0.74 grade), kps score (mean = 40) and vas pain scale (mean = 6.7) at 6 months follow up after surgery. improvement in asia impairment scale was more in the patient with severe canal compromise (mean = 1.62 grade), patients with translational/ distraction injuries (mean= 1.01grade) and patients with paraparesis (mean=1.06). only onethird of patients with bowel and bladder involvement improved after surgery. around 56.8% of patients were able to return to jobs at 6 months follow up. patients who were paraplegic at the initial presentation were mostly not able to return to jobs. the most common reported complication in the study was intraoperative pedicle breakage. conclusion: decompression of the spinal cord plus posterior spine fixation is a safe, reliable and effective method in the management of thoracic and lumbar fractures with significant improvement in outcome in terms of motor power, pain and quality of life. background thoracic and lumbar spine fractures occurring as a result of trauma can lead to pain, neural compromise and deformity. the appropriate keywords asia impairment scale, vas, kps, thoracolumbar spine fractures corresponding author: tinu ravi abraham department of neurosurgery, government medical college kottayam, kerala, india drtinu@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published october 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 458 geo paul k. jose, tinu ravi abraham, p.k. balakrishnan et al. treatment for these fractures ranges from conservative management with thoracic lumbar corset to surgical management with anterior/posterior instrumentation for fixation plus decompression1,2. surgical management for these fractures has the advantage of stabilization of fracture with fixation, decompression of neural canal, early mobilization and rehabilitation of the patient3. though there are both anterior and posterior approaches for thoracolumbar spine fractures most spine surgeons advocate posterior fusion and decompression as the treatment of choice for unstable fractures as the approach is less extensive1,4,5. various posterior stabilization procedures are there which include hooks, wires, transpedicular screw and rod fixation, of which transpedicular screw and rod fixation is the preferred technique now6. in traumatic spine fractures the outcome following posterior spine decompression and fusion depends on various factors which includes timing of surgery, patient comorbidities, general condition of the patient, associated injuries. the outcome following the surgery is measured based on the extend of pain relief, to be able to mobilize the patient early, return to work, neurological recovery and development of any postoperative complications. this study was done to find out the factors affecting the post-operative outcome following posterior spine decompression and fusion surgery in patients with traumatic thoracolumbar spine fractures. the study also aimed to find out the postoperative outcome and complications following posterior spine surgery. methodology a retrospective observational study was carried out among 44 patients admitted with thoracic and lumbar spine fracture who had underwent posterior spine decompression and fusion in the department of neurosurgery, in a tertiary care center in central kerala, india during the period from 1st january 2019 to 31st december 2020. study involved collecting data regarding those patients who were admitted and operated for traumatic thoracic and lumbar spine fracture using the standard surgical protocol followed in the department. this involved laminectomy and decompression of the spinal cord +/neural foraminal decompression and posterior spine fixation two levels above and below using polyaxial screws and rods. the data regarding presenting symptoms, comorbidities, associated injuries and imaging finding in ct and mri was collected (like type of fracture, canal compromise and level of injury). type of fractures were divided into posterior element only fractures, anterior wedge compression fracture, burst fracture and translation/ distraction injury. canal compromise was divided into no/ mild (obliteration in csf space is <50%), moderate (>/=50% obliteration in csf space, but not deforming the cord), severe (compressing and deforming the cord). level of injury was divided into upper dorsal(d1-d6), mid dorsal (d7-d9), dorso-lumbar junction (d10-l2) and lower lumbar(l3-l5). other details like interval between trauma and surgery, and complications following surgery were also recorded. the post-operative outcome of patients after surgery was assessed using asia (american spine injury association scale) impairment scale (table.1b), kps (karnofsky performance status) scale (table.1a) and vas (visual analog scale) of pain (from 0-10), all of which were noted at the preoperative and postoperative (immediate,1 month and 6 months) periods from the data available in the department. other factors like improvement in bowel and bladder symptoms, back stiffness and return to job after surgery were also found out. a) karnofsky performance status scale7 b) asia scale8 score findings grade findings 100 normal no complaints; no evidence of disease. a (complete) no sensory or motor function is preserved 90 able to carry on normal activity; minor signs or symptoms of disease. b (sensory incomplete) sensory but not motor function is preserved below the neurological level and no motor function is preserved more than three levels below the motor level on either side of the body 80 normal activity with effort; some signs or symptoms of disease. 70 cares for self; unable to carry on normal activity or to do active work. 60 requires occasional c (motor incomplete) motor function is preserved below the 459 outcome of patients undergoing posterior spine fixation and decompression assistance, but is able to care for most of his personal needs. neurological level and more than half of key muscle functions below the neurological level of injury have a muscle grade less than 3 (grades 0-2) 50 requires considerable assistance and frequent medical care. 40 disabled; requires special care and assistance. 30 severely disabled; hospital admission is indicated although death not imminent. d (motor incomplete) motor function is preserved below the neurological level and at least half (half or more) of key muscle functions below the nli have a muscle grade ≥ 3 20 very sick; hospital admission necessary; active supportive treatment necessary. 10 moribund; fatal processes progressing rapidly. e (normal) if sensation and motor function as tested are graded as normal in all segments 0 dead table 1. showing a) karnofsky performance score b) asia impairment scale7,8 in the end of the study the post-operative clinical, radiological and functional outcome in patients undergoing thoraco-lumbar posterior spine fixation and decompression was determined. the factors affecting post-operative outcome in patients undergoing thoraco-lumbar posterior spine fixation and decompression were also determined. the common complications following thoraco-lumbar spine fixation and decompression were also found out. data management and statistical analysis: the data collected was entered in microsoft excel sheet. percentage were calculated for categorical data, whereas numerical data represented as mean+/-sd. statistical analysis was done to determine significant relationship between clinical and radiological factors to post-operative outcome. paired ttest was used to compare preoperative and postoperative outcomes. probability </=0.05 (p</=0.05) was considered significant. inclusion criteria: diagnosed cases of post traumatic thoracic and lumbar spine fracture who had undergone posterior spine decompression and fusion exclusion criteria: i) cases without proper history and clinical examination ii) cases without proper imaging iii) cases without follow up iv) children below 13years of age results mean age affected by traumatic thoraco-lumbar spine fracture is 44.30 +/11.87yrs. most common age group affected was between 30-50 yrs – (26 patients,59.1%) (table.2, fig.1). the age of the study population ranged from 21yrs to 69yrs. figure 1. showing age distribution. age grou ps 10 to 20 20 to 30 30 to 40 40 to 50 50 to 60 60 to 70 70 to 80 no. patie nts (%) 0 / 0.0 % 5/ 11.3 % 14 / 31.8 % 12 / 27.3 % 10 / 22.7 % 3 / 6.8 % 0 / 0.0 % table 2. showing age distribution figure 2. showing gender distribution 0 5 14 12 10 3 0 0 5 10 15 age group age distribution 10 to 20 20 to30 30 to 40 40 to 50 50 to 60 60 to 70 70 above 39(89 %) 5 (11%) gender distribution male famle 460 geo paul k. jose, tinu ravi abraham, p.k. balakrishnan et al. traumatic thoracolumbar spine fractures mainly affect males (39 patients ,88.6%). male to female ratio is 7.8:1 (fig.2). table 3. showing distribution of patients according to a) fracture type, b) canal compromise, c) level of fracture and d)interval between injury and surgery. a) fracture no. of patients b) level no. of patients only pars #/ posterior element 0 (0.0%) d1d6 7 (15.9%) anterior wedge compression 11 (25.0%) d7-d9 6 (13.6%) burst 19 (43.2%) d10-l2 25 (56.8%) translational injury/subluxation / burst # + plc injury 14 (31.8%) l3-l5 2 (4.5%) total 44 (100.0%) multiple levels 4 (9.1%) c) canal compromise no. of patients d) interval between injury and surgery no. of patients no / mild 8 (18.2%) (</=2weeks 16 (36.4%) moderate 23 (52.3%) 2-4weeks 14 (31.8%) severe 13 (29.5%) 1-3months 14 (31.8%) total 44 (100.0%) > 3months 0 (0.0%) most common fracture type involved in the study was burst fractures (19 patients, 43.2%) (table.3a). most of the patients (23patients, 52.3%) in the study had moderate canal compromise (more than 50% obliteration of subarachnoid space, but not deforming the spinal cord) (table .3c). most common level involved was d10 to l2 level (thoraco-lumbar junction) 25 patients (56.8%) (table.3b). for most of the patients in the study surgery was done within 4weeks duration, (30 patients, 68.2%). for 14 patient surgery was done between 1-3 months duration (table.3d). patients who underwent surgery for traumatic thoracolumbar spine fractures showed a mean improvement in grade of 0.43 and 0.76 in asia impairment scale postoperatively at 1month and 6 months respectively compared to preoperative status. these findings were found to be statistically significant (table.4a). patients with paraparesis and paraplegia showed an improvement asia impairment scale of 1.06 and 1.25 grade respectively compared to preoperative scale, which was statistically significant ttable.4b). a) parameter mean n std. deviation difference t p value pre asia 3.27 44 1.633 +0.43 5.25 .000 post asia1* 3.70 44 1.579 pre asia 3.33 43 1.614 +0.76 6.22 .000 post asia6* 4.09 43 1.306 b) symptom parameters mean n std. deviation mean difference t p value paraparesis preasia 3.60 15 .632 +1.06 6.95 .000 post asia6 4.67 15 .488 paraplegia preasia 1.00 12 .000 +1.25 4.48 .001 post asia6 2.25 12 .965 c) parameter canal compromise n mean std. deviation f p value pre asia no/ mild 8 4.38 .744 17.278 .000 moderate 23 3.83 1.370 severe 13 1.62 1.193 post asia6 no/ mild 8 4.75 .463 .463 .001 moderate 23 4.43 1.080 severe 12 3.00 1.477 d) parameter level n mean std. deviation f p value pre asia d1d6 7 3.14 1.676 2.255 .081 d7-d9 6 1.67 1.633 d10-l2 25 3.48 1.584 l3-l5 2 4.00 .000 multiple levels 4 4.25 .957 461 outcome of patients undergoing posterior spine fixation and decompression post asia d1d6 7 3.86 1.676 1.449 .237 d7-d9 6 3.17 1.169 d10-l2 24 4.21 1.285 l3-l5 2 4.50 .707 multiple levels 4 5.00 .000 e) parameters fracture type n mean std. deviation f p value pre asia anterior wedge compression 11 4.27 1.009 7.29 .002 burst 19 3.53 1.467 translational injury/subluxation / burst # + plc injury 14 2.14 1.657 post asia6 anterior wedge compression 11 4.73 .467 6.38 .004 burst 19 4.37 .955 translational injury/subluxation / burst # + plc injury 13 3.15 1.725 table 4. showing a)preoperative and post operative asia impairment scale, . (i 1*-post operative at 1month, 6*post operative at 6month), b))preoperative and postoperative asia impairment scale among paraparesis and paraplegic patients c) relationship of canal compromise with preoperative asia (preasia) , and postoperative asia at 6month (post asia6), d)relationship of level of injury with pre asia and post asia score at 6month, e)relationship of fracture type to pre operative asia (preasia) ,post operative asia at 6months (post asia6). table 6. showing a)pre operative and post operative kps score (i*-immediate post operative, 1*-post operative at 1month, 6*post operative at 6months), b) relationship of fracture type to post operative kps at 6months (postkps6) , c)relationship of canal compromise with preoperative kps (prekps) and postoperative kps at 6months (post kps6). a) parameter mean n std. deviation difference (improvement) t p value pre kps 39.8 44 11.91 +5.7 6.03 .000 post kps i* 45.5 44 11.30 pre kps 39.8 44 11.91 +25 13.09 .000 post kps1* 64.8 44 15.77 pre kps 40.0 43 11.95 +39.8 15.76 .000 post kps6* 79.8 43 18.32 b) parameters fracture type n mean std. deviation f p value post kps6 anterior wedge compression 11 90.9 13.75 7.73 .001 burst 19 82.6 15.93 translational injury/subluxation / burst # + plc injury 13 66.2 17.58 c) parameter canal compromise n mean std. deviation f p value pre kps no /mild 8 46.3 10.61 7.136 .002 moderate 23 42.6 12.51 severe 13 30.8 4.94 post kps6 no/ mild 8 92.5 13.89 10.766 .000 moderate 23 83.9 14.06 severe 12 63.3 17.75 table 8. a) showing distribution of all patients return to job after surgery, b ) showing distribution of patients having weakness returning to job after surgery. a) job no modification old same job total no. of patients 19 (43.2) 17 (38.6) 8 (18.2) 44 (100.0) b) weakness job total no modification old same job ᵡ2 p value 462 geo paul k. jose, tinu ravi abraham, p.k. balakrishnan et al. no weakness 4 (26.7%) 4 (26.7%) 7 (46.7%) 15 (100.0%) 30.755 .000 monoparesis 0 (0.0%) 1 (100.0%) 0 (0.0%) 1 (100.0%) paraparsis 3 (20.0%) 11 (73.3%) 1 (6.7%) 15 (100.0%) paraplegia 12 (92.3%) 1 (7.7%) 0 (0.0%) 13 (100.0%) total 19 (43.2%) 17 (38.6%) 8 (18.2%) 44 (100.0%) pre asia post asia6 a b c d e total a 3 4 4 1 0 12 b 0 0 0 1 0 1 c 0 0 0 2 2 4 d 0 0 0 3 10 13 e 0 0 0 0 13 13 total 3 4 4 7 25 43 table 5. showing comparison of preoperative asia score (pre asia) to postoperative asia score at 6 months (post asia6). none of the operated patients had deterioration in asia score at 6month follow up. of the total of 12 patients operated with preasia grade a, only 3 patients remained at grade a, whereas 4 patients each had improved to asia grade b and c (table 5) on post-operative follow up at 6months. preoperative asia impairment score showed significant relation to fracture type, with patients suffering from translational /distraction injury having a poorer grade (mean asia score of 2.14 = grade b to c) whereas anterior wedge compression fracture having better grades (mean asia score of 4.27= grade d to e). post operatively asia impairment scale at 6 months showed significant relations to fracture type, with patients having anterior wedge compression fracture (mean asia score of 4.73= grade d to e) having better scores than patient with translational injury (mean asia score of 3.15= grade c to d) (table.4e). considering canal compromise, patients with severe canal compromise were having poor asia score both preoperatively and postoperatively when compared with patients having mild / moderate canal compromise (table.4c). regarding the level of involvement, patient with d7-d9 involvement were having lowest preoperative asia score (mean asia score was 1.67= a to b), but these finding didn’t have and statistical significance (table. 4d). interval between injury and surgery failed to find any statistically significant relation in terms of outcome. when compared to preoperative kps there was significant improvement in mean postoperative kps score at 1month and 6 months as 25 and 39.8 respectively. (table.6a). though preoperatively kps failed to show any significant relation to fracture type, post operatively kps at 6 months showed significant relation to fracture type, with patients having anterior wedge compression fracture (kps=90.9) having better scores than patient with translational injury (kps= 66.2) (table.6b). considering canal compromise, patients with severe canal compromise were having poor kps score both pre-operatively (mean=30.8) as well as post operatively (mean=63.3) when compared with patients having mild (mean prekps =46.3, mean post kps6 =92.5)/ moderate (mean prekps =42.6, mean post kps6 = 83.9) canal compromise (table.6c). kps score didn’t have any significant relation with the level of injury. considering the vas pain scale, there was again significant decrease vas pain scale in post-operative period (immediately, at 1month and at 6 month scores being 1.65, 4.88 and 6.7 respectively-table.7). however, vas pain scale didn’t show any significant relations to fracture type, canal compromise or the level of injury. parameter mean n std. deviation difference (decrease in pain) t p value prevas 7.70 44 .851 -1.65 7.975 .000 postvas i* 6.05 44 1.613 prevas 7.70 44 .851 -4.88 26.899 .000 postvas1* 2.82 44 .995 prevas 7.70 43 .860 -6.7 36.423 .000 . postvas6* 1.00 43 1.024 table 7. showing preoperative and postoperative vas pain score. (i*-immediate post operative, 1*-post operative at 1month, 6*post operative at 6 months). of the 44 patients operated, 25 patients (56.8%) were able to return to job. 8 patients (18.2%) were able to return to their old job (table.8a). among the 13 patient operated with paraplegia only 1 patient (7.7%) was able to return to work with job 463 outcome of patients undergoing posterior spine fixation and decompression modification and none of them were able to return to old job. but among 15 patients with paraparesis 12 (80%) were able to return to job (1 patient returned to the same job, rest 11 had to modify their job) (table. 8b). bowel was involved in only 12 patients, of which 4 patients improved after surgery (33.3%) and in the rest 8 patients symptom remained same. bladder was involved in 14 patients of which 4 patients improved (28.6%) and rest 10 patients remained symptomatically same. there was no worsening of bowel or bladder symptom following surgery (table 9). symptom outcome after surgery not involved worsen same improved bowel 32 0 8 4 bladder 30 0 10 4 table 9. showing ouctome of bowel and bladder symptom following surgery. no significant relationship was found out between associated injuries or comorbidities to postoperative outcome. intraoperative complication like pedicle breakage was seen in 3 patients. other intraoperative complications like nerve root injuries were not observed. postoperative complications like surgical site infection was seen in only 2 patients, discitis/ abscess and dvt was observed in 1 patient each. other postoperative complications like implant failure were not observed. post-operative complaint most commonly observed was stiffness in back at the operative site and was present in 25 patients (56.8%). discussion this retrospective study was done during the study period from 1st january 2019 to 31st december 2020, including 44 patients admitted for thoracic and lumbar spine fracture who had underwent posterior spine decompression and fixation. the study had 39 male patients (88.6%), with male to female ratio 7.8:1. the mean age of presentation was 44.30+/ 11.87yrs and most common age group of presentation was 30-50 yrs (59% patients) this again point to the fact that traumatic fractures mainly affects physically active age group and population (males). in a similar study done by hariri o r et al between 2005 to 2015 among 46 patients, 93% patients were male and mean age of presentation was 36.8 years 9. another comparative study done by petr v et al in thoraco-lumbar spine fractures among 35 patients, again had 28 male patients and mean age of presentation as 42.4years10. as the study included only patients undergoing surgery for thoracic and lumbar fractures most common fracture type included in the study was burst fracture 43% (even though posterior element fracture and anterior compression fractures are far more common, as they are commonly managed conservatively, they are lesser in number in this study). in the study population thoraco-lumbar junction (d10-l2) was the most commonly involved fracture level (56.8%), probably due to the relative instability of transition zone. in the study of 66 patients by roop singh et al from 2007 to 2011 had reported similar results with about 57.6% (38 patients) thoracolumbar fracture occurring at d12, l1 levels11. petr vet al again had reported 80% of thoracolumbar fractures from d12, l1 levels10. regarding the postoperative outcome the study showed improvement in asia impairment scale of 0.74 grade at 6 months postoperatively when compared with preoperative status. among 43 patients followed up at 6 months (1patient lost in follow-up at 6month) no patients had deterioration in asia score. on post-operative follow up of 12 patients operated with preoperative asia grade a at 6 months only 3 patients remained at grade a , 4 patients each had improved to asia grade b and c, 1 patient to grade d and non to grade e (table.5). among patients with paraparesis and paraplegic mean preoperative asia were 3.6 (asia grade c to d) and 1 (asia grade a). their post-operative grade improved to 4.67 (asia grade d to e) and 2.25 (asia grade ~b) (table.4b). although there was postoperative improvement in paraplegic patients, it was not up to functional levels. so, we can infer from the study that both paraplegic and paraparesis patient can have significant improvement in asia scale, but chance of paraplegic patients able to walk after surgery is rare. the study by roop singh et al among 66 patients also had similar observations with an improvement of average 1.03 grades in neurological status as per asia impairment scale from the preoperative to final follow-up at one year11. among 34 patients having preasia grade a, 14 patients improved to grade b , 2 patients to grade d and non 464 geo paul k. jose, tinu ravi abraham, p.k. balakrishnan et al. to grade e. the study also showed that the patients having incomplete lesions of the spinal cord showed more neurological improvement (mean, 1.5 grade) than the complete lesion of the spinal cord (mean, 0.53 grade). similar observations were reported in another study by butt et al 12. when asia score was assessed in terms of fracture type, as expected patients with anterior wedge compression fracture had better preasia score (mean preasia=4.27, asia d to e) compared to patient with translational /distraction injury (mean preasia=2.14, asia b to c). this may be due to severe canal compromise / spinal cord injury associated with translation/ distraction injury. but postoperatively there was significant improvement in asia score at 6months for translation/distraction injury (post asia6=3.15, asia c to d) (mean improvement=1.01 grade) and burst fracture (post asia6= 4.37,asia d to e) (mean improvement = 0.84 grade). so we can expect a significant neurological improvement even in patients with translational / distraction injury on doing decompression + fixation. patients with severe canal compromise were having preasia score 1.62 (asia a to b) and with no/mild canal compromise were having preasia score 4.38 (asia d to e). here also post operatively patients with severe canal compromise were having significant improvement at 6month (post asia6= 3.00, asia c) (mean improvement =1.38 grade). similar improvement was seen in moderate canal compromise patients. so, we can expect a significant neurological improvement in patients with moderate to severe canal compromise, on doing decompression + fixation. there was no significant relation between level of injury and asia score but patients with d7-d9 level injury tend to have preasia score very low (mean pre-asia =1.67, asia a to b) and 6month postsurgery there was significant improvement (mean post asia6= 3.17, asia c to d). alessandro l et al in their study have reported poor asia score common for thoracic level vertebra fracture13. in our study, most of the patients underwent surgery within 4weeks of injury, (30 patients, 68.2%). for 14 patient surgery was done between 1-3 months duration (table.3d). surprisingly there was no significant difference in improvement between early surgery group and late surgery group in terms of asia impairment scale. this is primarily because even in early surgery group most of the surgery were done after 1 week (partly because of lack of facilities for emergency stabilization of the spine and due to patient reporting late because of ignorance on the part of the patient or due to late referral from other centers). but study done on 27 patients between 2004 to 2006 by sahika l c et al have reported surgical decompression and stabilization within 8 hours of spinal cord injury had better outcome than when operated between 3 and 15 days14. in the study by roop singh et al the patients of early surgery group showed slightly better improvement in mean asia score (1.2 grade) than the patients who had underwent surgery late (0.95 grade), which was not a statistically significant difference11. chadha et al and butt et al.had also reported a fair neurological recovery in cases were surgery was done late12,15. compared to preoperative kps score (mean prekps=39.8) there was significant improvement in mean post-operative kps score at 1month (mean postkps1=64.8) and 6 months (mean post kps6= 79.8) as 25 and 40 respectively. so, at 6months follow up on an average the patient in the study were able to carry out normal activity with signs and symptoms of disease (kps=80). similar results were seen in a study done by mohsen k et al who compared the outcome after surgery and conservative management among 25 patients. in this study joabpeq (joa back pain evaluation questionnaire) was used to assess the functionality in five domains including walking ability, lumbar function, low back pain, social life function and mental health at admission and at the interval of 3, 6, 12 months after treatment. in both surgery and conservatively managed patients there was improvement in outcome, but faster and better recovery was among post-surgery group16. in our study fracture type and kps score didn’t have significant relation in preoperative period. postoperatively at 6months kps showed significant relation to fracture type with patients with anterior compression fracture having mean kps score as 90.9, and those with translation / distraction injury having mean kps as 66.2. so, even though there was improvement in kps score in all types of fractures, anterior wedge compression fracture followed by burst fracture tend to have best improvement in terms of kps score after 6months of surgery. in terms of canal compromise, pre-operative kps for no/mild, moderate and severe were 46.3, 42.6 and 30.8 respectively which improved to 92.5, 83.9 and 465 outcome of patients undergoing posterior spine fixation and decompression 63.3 at 6month post operatively. so, improvement in kps score in no/ mild, moderate, severe canal compromise were 46.2, 41.3 and 32.5 respectively. so, there was better improvement in kps score in mild and moderate canal compromise patients compared to severe canal compromise patients. these findings may be partly due to absolute bed rest advised for all patients prior to surgery, hence irrespective of fracture type and canal compromise preoperative kps will be low for all, whereas postoperatively patients with less severe injury have far better improvement in kps score. compared to preoperative status, postoperatively there was significant decrease in vas pain scale immediately post op, at 1month post op and at 6-month post op as 1.65, 4.88 and 6.7 respectively (table.4). vas pain scale didn’t find any significant relation in terms of fracture type, canal compromise both preoperatively as well as post operatively. study by rajdeep s b et al on 30 patients conservatively managed had mean vas score of 9.77 ± 0.43, which decreased to 2.03 ± 0.90 at the end of 2 years17. study by roop singh et al had quantified pain using denis pain scale and found out 48.48% patient had mild to no pain, and 42.42% patient had moderate pain at 1 year follow up11. regarding outcome in terms of job, postoperatively at 6months follow up 19 patients (43.2%) were not having job, of which 12 were paraplegic initially itself. among 13 patient having paraplegia initially, only 1 returned to job (7.7%) with job modification, none of them were able to returned to same job. whereas, of the 15 patients having paraparesis 12 (80%) of them returned to job, but 11 of them had to modify their job. in patients having no weakness, 11 patients (73.3%) were able to return to job, of which 7 patients (46.7%) were able to return to old job itself. so, paraplegia in initial presentation implies a very poor outcome in terms of job. patients with no weakness or paraparesis in initial presentation tend to return to same job or to a modified job. study by roop singh et al had reported 63.4% patients not returning to job (most of them were initially paraplegic) and 36.6% patients returning to work (half of them with job modification)11. leferink et al. had reported, 50% of patients changed the intensity of their work or the kind of work they did, after thoracolumbar spine injury and treatment18. study by briem d et al also had reported a low work capacity after thoracolumbar spine fractures19. was involved in only 12 patients, of which 4 improved after surgery (33.3%) and rest 8 symptom remained same. bladder was involved in 14 patients, of which 4 patients improved (28.6%) and for rest 10, symptoms remained same. there was no worsening of bowel or bladder symptom following surgery (table.7). so, there is around one third chance of improvement by surgical decompression when bowel and bladder is involved in thoracolumbar spine fracture. in literature review a study by pingyeh chiu et al among 8 patients from 2005 to 2012 with pure conus medullaris syndrome with thoracolumbar burst fracture, 5 patients regained self-voiding function20. in our study no significant relationship was found out between associated injury or comorbidity to post-operative outcome. complications observed in the study were intraoperative pedicle breakage in 3 patients, postoperative surgical site infection in 2 patients, discitis/ abscess and dvt was observed in 1 patient each. other complications like nerve root injury and implant failure were not seen. though there was no implant failure reported in 6-month follow up (which may be an advantage of fixation of 2 levels above and below the spine fracture), most of the patients (56.8%) complaint of stiffness in back at operative site. in transpedicular screw fixation it is recommended to include two spinal levels above the fracture level and one or two levels caudal to the fracture level21. such long segment spinal fixation might result in significant loss of mobility and increased risk for adjacent level morbidity. in an attempt to lessen the problem arising due to decreased mobility, short segment instrumentation has been introduced, fusing only two motion segments. but it also has come up with mixed results and complications22,23. on literature review the study by butt mf et al.says more than 50% of patients had one or more complications, including 18 cases of hardware failures, involving 20 pedicle screws12. complications reported in study by roop singh et al were single level above and below the fracture site was fused had only one implant failure such as nut loosening (asymptomatic), 4misplaced screws (in 3 patients -asymptomatic)11. chadha et al had reported misplacement of the screw in 3 cases, one case of screw loosening and one screw pullout15. 466 geo paul k. jose, tinu ravi abraham, p.k. balakrishnan et al. conclusion from this retrospective study, we can conclude that laminectomy and decompression of the spinal cord and posterior spine fixation 2 levels above and below, using polyaxial screws and rods is safe, reliable and effective method in the management of thoraco-lumbar fractures. there was significant improvement in asia impairment scale (mean improvement at 6months=0.74 grade) , kps score (mean improvement at 6months= 40) and vas pain scale (mean improvement at 6months= 6.7) at 6 months follow up after surgery. study was able to find out that the improvement in asia impairment scale was more in patient with severe canal compromise (mean improvement at 6months=1.62 grade), patients with translational/ distraction injuries (mean improvement at 6months= 1.01grade) and patients with paraparesis /paraplegia (mean improvement at 6months= 1.06/1.25 grade respectively). only one third patients with bowel and bladder involvement improved after decompressive surgery. around 56.8% patients were able to return to job (either same job or with some modification) at 6 months follow up. patients who were paraplegic at initial presentation, were mostly not able to return to job. most common reported complication in the study was intraoperative pedicle breakage. abbreviations asia american spine injury association scale kps karnofsky performance status scale vas visual analog scale mri magnetic resonance imaging ct computed tomography declarations funding: self conflict of interest: none declared ethical approval: obtained (irb no.-61/2021) acknowledgements dr. shaju mathew, associate professor, department of neurosurgery dr. vinu v. gopal, associate professor, department of neurosurgery dr. philip issac, assistant professor, department of neurosurgery dr. ajax john, senior resident, department of neurosurgery dr. tom jose, senior resident, department of neurosurgery dr. ahammed shameel p, senior resident, department of neurosurgery dr. amritha subramonian, senior resident, department of neurosurgery. references 1. yue jj, sossan a, selgrath c, et al. the treatment of unstable thoracic spine fractures with transpedicular screw instrumentation: a 3-year consecutive series. spine (phila pa 1976) 2002; 27:2782-7. 2. modi hn, chung kj, seo iw, et al. two levels above and one level below pedicle screw fixation for the treatment of unstable thoracolumbar fracture with partial or intact neurology. j orthop surg res 2009; 4:28. 3. alexandra c, william s, dean c, murat p, vedat d, sigurd b. pathologic fractures. in: frank p, isador l, david p, editors. minimally invasive spine surgery: surgical techniques and disease management. new york, ny: springer; 2014: 377–393. 4. shin ts, kim hw, park ks, kim jm, jung ck. short segment pedicle instrumentation of thoracolumbar burstcompression fractures: short term follow-up results. j korean neurosurg soc 2007; 42:265-70. 5. kothe r, panjabi mm, liu w. multidirectional instability of the thoracic spine due to iatrogenic pedicle injuries during transpedicular fixation. a biomechanical investigation. spine (phila pa 1976) 1997; 22:1836-42. 6. korovessis p, baikousis a, koureas g, et al. correlative analysis of the results of surgical treatment of thoracolumbar injuries with long texas scottish rite hospital construct: is the use of pedicle screws versus hooks advantageous in the lumbar spine? j spinal disord tech. 2004;17(3):195-205. 7. asia and iscos international standards committee. the 2019 revision of the international standards for neurological classification of spinal cord injury (isncsci)-what's new? spinal cord. 2019 oct;57(10):815817. 8. schag cc, heinrich rl, ganz pa. karnofsky performance status revisited: reliability, validity, and guidelines. j clin oncology. 1984; 2:187-193. 9. hariri o r, kashyap s, takayanagi a, et al. (march 09, 2018) posterior-only stabilization for traumatic thoracolumbar burst fractures. cureus 10(3): e2296. doi 10.7759/cureus.2296 10. petr vanek, ondrej bradac, renata konopkova, patricia de lacy, jiri lacman, vladimir benes. treatment of thoracolumbar trauma by short-segment percutaneous transpedicular screw instrumentation: prospective comparative study with a minimum 2-year follow-up, j neurosurg: spine / volume 20 / february 2014 (pg 150156). 11. roop s , rajesh kr , kulbhushan k , narender km , kiranpreet k. outcome of pedicle screw fixation and monosegmental fusion in patients with fresh 467 outcome of patients undergoing posterior spine fixation and decompression thoracolumbar fractures .asian spine j 2014;8(3):298308. 12. butt mf, farooq m, mir b, dhar as, hussain a, mumtaz m. management of unstable thoracolumbar spinal injuries by posterior short segment spinal fixation. int orthop 2007; 31:259-64. 13. alessandro landi, nicola marotta, angela ambrosone, emiliano prizio, cristina mancarella, fabrizio gregori, giuseppe la torre, antonio santoro, roberto delfini. correlation between timing of surgery and outcome in thoracolumbar fractures: does early surgery influence neurological recovery and functional restoration? a multivariate analysis of results in our experience.trends in reconstructive neurosurgery pp 231-238. 14. sahika liva cengiz , erdal kalkan, aysegul bayir, kemal ilik, alper basefer.timing of thoracolomber spine stabilization in trauma patients; impact on neurological outcome and clinical course. a real prospective (rct) randomized controlled study. arch orthop trauma surg. 2008 sep;128(9):959-66. 15. chadha m, bahadur r. steffee variable screw placement system in the management of unstable thoracolumbar fractures: a third world experience. injury 1998; 29:73742. 16. mohsen koosha, hossein nayeb aghaei, hamid reza khayat kashani, sepideh paybast. functional outcome of surgical versus conservative therapy in patients with traumatic thoracolumbar fractures and thoracolumbar injury classification and severity score of 4. a nonrandomized clinical trial, bull emerg trauma 2020;8(2):89-97. 17. rajdeep singh bagga, arvind b goregaonkar, aditya anand dahapute, saurabh r muni, sandeep gokhale, jitesh manghwani. functional and radiological outcomes of thoracolumbar traumatic spine fractures managed conservatively according to thoracolumbar injury severity score,j craniovertebr junction spine. 2017 octdec; 8(4): 369–373 18. leferink vj, keizer hj, oosterhuis jk, van der sluis ck, ten duis hj. functional outcome in patients with thoracolumbar burst fractures treated with dorsal instrumentation and transpedicular cancellous bone grafting. eur spine j 2003; 12:261-7. 19. briem d, behechtnejad a, ouchmaev a, et al. pain regulation and health-related quality of life after thoracolumbar fractures of the spine. eur spine j 2007; 16:1925-33. 20. ping-yeh chiu, jen-chung liao. surgical outcomes in thoracolumbar fractures with pure conus medullaris syndrome. biomed j. 2019 aug; 42(4): 277–284 21. cengiz sl, kalkan e, bayir a, et al. timing of thoracolumbar spine stabilization in trauma patients; impact on neurological outcome and clinical course. a real prospective randomized controlled study. arch orthop trauma surg. 2008;128(9):959-966. 22. mahar a, kim c, wedemeyer m, et al. short-segment fixation of lumbar burst fractures using pedicle fixation at the level of the fracture. spine. 2007;32(14):1503-1507. 23. mclain rf, sparling e, benson dr. early failure of shortsegment pedicle instrumentation for thoracolumbar fractures. a preliminary report. j bone joint surg am. 1993;75(2):162-167. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-021 lumbar unilateral laminotomy for bilateral decompression in lumbar spinal stenosis amin sabry, wael zakarya, amr farid khalil romanian neurosurgery (2020) xxxiv (1): pp. 141-146 doi: 10.33962/roneuro-2020-021 www.journals.lapub.co.uk/index.php/roneurosurgery lumbar unilateral laminotomy for bilateral decompression in lumbar spinal stenosis amin sabry, wael zakarya, amr farid khalil neurosurgery department, mansoura university, egypt abstract background: multiple surgical approaches are existing for the management of lumbar canal stenosis. objective: this study was conducted to assess the outcomes of unilateral laminotomy with bilateral decompression in such cases. patients and methods: this prospective study was conducted at mansoura university hospitals, and we included a total of 12 cases with lumbar canal stenosis. all cases underwent unilateral laminotomy with bilateral canal decompression during the period between july 2017 and july 2018. post-operative outcomes included odi, and vas score for both leg and back pain. results: the age of the cases ranged between 38 and 62 years. we included 7 males and 5 females. odi, lower extremity, and back pain showed a significant decrease after the operation (p < 0.05). conclusion: unilateral laminotomy with bilateral canal decompression is a safe and feasible approach to managing lss. excellent outcomes are expected regarding leg pain and quality of life, while slight improvement is anticipated regarding low back pain. introduction lumbar spine stenosis (lss) is one of the commonest spinal pathologies, that present with buttock or lower limb pain associated with decreased neurovascular space in the lumbar spine region. low back pain may be present or not [2]. degenerative lss usually starts in the 5th or 6th decades of life. it is characterized by hypertrophy of ligamentum flavum, intervertebral disc bulging, thickening of the facet joint, and arthropathy. these changes lead to inevitable canal narrowing [2, 15]. cases may express intermittent neurological claudications, and the quality of life is markedly decreased [13]. although conservative treatment can provide a temporary symptom relief, surgical decompression will be eventually needed. nowadays, multiple surgical approaches are existing for management of such disorder. there is no definite data favoring one technique over another one [8]. conventional laminectomy is the commonest approach performed for degenerative lss [5]. however, the integrity of posterior spine keywords lumbar stenosis, lumbar decompression, lumbar laminectomy, unilateral laminotomy, bilateral decompression, lumbar spine, spinal stenosis corresponding author: amr farid khalil neurosurgery department, mansoura university, egypt dr_ amr77@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 142 amin sabry, wael zakarya, amr farid khalil complex is negatively affected. furthermore, elevation of paravertebral muscles from the spinous process leads to spinal muscle atrophy and weakness in the trunk extensors [2]. as most of lss patients are of old age, multiple comorbidities are usually present. thus, the invasiveness of surgery must be kept into consideration since more invasive procedures are associated with higher morbidity and mortality rates along with increased health costs [13]. unilateral laminotomy with bilateral decompression provides the advantage of preserving neural arch and facet joint of the other side. hence, stability is more preserved, and neural tissue are protected against posterior scarring. besides, it offers shorter operative time, less blood loss, and less post-operative morbidity when compared to the conventional approach [3, 10, 12]. the success rate of unilateral approach in patients with bilateral canal decompression ranges between 68 and 94% [2]. this study was conducted at mansoura university hospitals aiming to evaluate the outcome of unilateral laminotomy with bilateral canal dilatation in lss. patient and methods study design this is a prospective study that was conducted during the period between july 2017 and july 2018. study cases a total of 12 cases with degenerative lss were included in the study. all cases experienced failure of medical treatment or physiotherapy for at least 3 months. cases with neurological claudication or radiculopathy, and radiological features of lss were included. cases with previous spine surgery, spinal tumours, instability, or spondylolisthesis were excluded. patient consent a pre-operative written informed consent was obtained from all cases after the explanation of advantages and drawbacks of the surgical approach. moreover, the study was approved by the local ethical committee. patient preparation all cases were subjected to complete history taking, thorough physical examination, and routine laboratory investigations. besides, an mri of the lumbosacral spine was ordered for all cases. in addition, plain x ray was also performed to exclude instability. pain was assessed via visual analogue score (vas), while functional status was evaluated by oswestry disability index (odi). surgical procedure the operation was performed when the patient was in prone position. a midline incision was created over the stenotic area as localized in pre-operative mri. by the aid of microscope or vascular loupe, a unilateral laminotomy was carried out, whereas the inferior aspect of cranial hemilamina and the superior aspect of the caudal hemilamina were partially resected. the spinous process base was undercut after ipsilateral decompression. then, bilateral flavectomy with contralateral neural foramen decompression was done. following bilateral decompression, the nerve roots were visualized easily and at that point, the operation was ended. post-operative care and follow up all cases were transferred to the recovery room, them to the internal ward. mobilization was encouraged on the 1st post-operative day. postoperative vas and odi were recorded at 6-and 12 month visits. post-operative radiological evaluation of stability was not routinely performed unless the patient is still complaining of back pain or claudication is still existing. statistical analysis the collected data were coded, processed and analyzed using the spss (statistical package for social sciences) version 22 for windows® (ibm, spss inc, chicago, il, usa). data were tested for normal distribution using the shapiro walk test. qualitative data were represented as frequencies and relative percentages. quantitative data were expressed as median (range). kruskal wallis test (kw) was used to test the significance between values at more than two time points (preoperative, at 6 months and at 12 months). wilcoxon signed rank test was used to test significance between two different time points. for all tests, p value (< 0.05) was considered significant. 143 lumbar unilateral laminotomy for bilateral decompression in lumbar spinal stenosis figure 1. sagittal t2 pre-operative mri shows severe spinal canal stenosis with multiple disc bulge and ligamentum flavum thickening. figure 2. axial t2 pre-operative mri shows severe spinal canal stenosis with a disc bulge and ligamentum flavum thickening. figure 3. axial ct scans l4 spine after the patient underwent a left l4 unilateral laminotomy. figure 4. axial t2 post-operative mri shows marked widening of the spinal canal after left unilateral laminotomy. figure 5. sagittal t2 post-operative mri after double level (l3l4 and l4-l5 decompression) via unilateral laminotomy. 144 amin sabry, wael zakarya, amr farid khalil figure 6. post-operative ct 3d lumber spine after double level (l3-l4 and l4-5 unilateral laminotomy). results the age of the included cases ranged between 38 and 62 years (median = 56). we included 7 males (58.33%) and 5 females (41.66%). these data are shown at table (1). preoperative odi ranged between 22 and 36 (median = 28). it decreased significantly after operation down to 7 and 6 scores at 6-month and 1years follow up visits (p < 0.001). after operation vas score decreased down to 1 at the scheduled follow up visits. it has a median value of 9 before operation. table (3) illustrates these data. back pain also significantly decreased after operation from score 6 preoperatively down to 3 and 2 scores after 6 and 12 months respectively. these data are illustrated at table (4). table 1. patient criteria. variable data age 56 (38 – 62) sex -male -female 7 (58.33%) 5 (41.66%) table 2. odi before and after surgery. preoperatively after 6 months after 1 year 28 (22-36) 7 (3-11) 6 (3-10) p1 < 0.001* < 0.001* p2 0.145 p < 0.001* p: significance between different durations p1: significance in relation to preoperative value. p2: significance in relation to 6 months value. *: statistically significant (p<0.05) table 3. vas score for limb pain before and after surgery. preoperatively after 6 months after 1 year 9 (7-10) 1 (1-3) 1 (0-2) p1 0.001* < 0.001* p2 0.124 p < 0.001* p: significance between different durations p1: significance in relation to preoperative value. p2: significance in relation to 6 months value. *: statistically significant (p<0.05) table 4. vas score for back pain before and after surgery. preoperatively after 6 months after 1 year 6 (4-7) 3 (2-4) 2(1-4) p1 0.009* 0.001* p2 0.108 p 0.005* p: significance between different durations p1: significance in relation to preoperative value. p2: significance in relation to 6 months value. *: statistically significant (p<0.05) discussion multiple surgical approaches have been proposed for the surgical management of lss. the main surgical goal is to decompress the lumbar canal. however, anatomy should be preserved to maintain the biomechanical function of the lumbar spine [2]. on using the conventional decompression technique, some authors reported paraspinal muscle atrophy on ct scan [7], and others showed electromyographic abnormalities following that approach [14]. these changes can lead to spinal instability and increase the need for spinal fusion surgery [6]. conversely, the unilateral approach decrease the incidence of these complications after surgery [13]. 145 lumbar unilateral laminotomy for bilateral decompression in lumbar spinal stenosis this study was conducted at mansoura university hospitals aiming to evaluate the surgical outcomes of unilateral laminotomy with bilateral decompression for lss. a total of 12 cases were included with a median age of 56 (range, 38-62). we included 7 males (58.33%) and 5 females (41.66%). another egyptian study handled the same perspective included 21 cases in the unilateral approach group, with a mean age of 47.2 years (range, 33 – 69). the presence of young age groups is due to the presence of cases with disco-ligamentous causes of lss, which is more common in young age due to sedentary life and overweight (like in egyptian population), compared to the bony type which is common in the older population [1]. in the current study, the operation successfully decreased odi score from 28 preoperatively down to 7 and 6 scores 6 and 12 months after operation (p <0.001). regarding odi in other studies, it decreased from 28.7 preoperatively down to 5.55 and 6.5 at 1-month and 1-year follow-up visits respectively. however, that change was not significantly different from the conventional approach group [1]. another study used both japanese orthopedic association score (joa) and neurogenic claudication outcome score (ncos) to evaluate the outcomes in unilateral laminectomy patients. there was a significant increase in both parameters form 4.35 and 26.9 up to 10.2 and 61.15 after operation respectively. this improvement was also better than the conventional approach group. that study reported that excellent and good outcomes were achieved in 14 cases in the unilateral hemilaminectomy group (70%) [13]. on assessment of leg pain in the current study, it decreased from 9 preoperatively (range, 7 – 10), down to 1 at the scheduled follow up visits (p < 0.001). in the previously mentioned egyptian study, the pre-operative vas score for lower extremity pain was 9.04, and it decreased significantly down to 1.38 and 1.46 at 1-month and 12-month follow-up visits (p = 0.001) [1]. this comes in line with the findings of çavuşoğlu and his colleagues who stated that most vas changes occur between operation and early follow up [4]. when it comes to back pain in our study, it was also assessed via vas score which decreased significantly from 6 (range, 4 – 7) before operation, to 3 (range, 2 – 4) after 6 months (p = 0.009), and 2 (range, 1 – 4) after 1 year (p = 0.001). in another study, the mean value of preoperative vas score for back pain was 5.42. it decreased slightly down to 2.82 and 1.96 at 1-month and 1-year follow-up visits respectively [1]. another study has also published that vas score for back pain has decreased from 7.6 pre-operatively down to 2.95 after operation. this decrease was also more significant when compared to the conventional approach [13]. another recent study also stated that detailed lower back pain vas score before surgery was 51.5 in motion, 63.0 while standing, and 37.8 while sitting; and showed lbp while standing was significantly greater than lbp while sitting (p < 0.01). after surgery, lbp while standing was significantly improved relative to that while sitting (p < 0.05), and levels of lbp in the three postures became almost the same with odi improvement. bilateral vas scores showed significant improvement equally on both sides (p < 0.01) [16]. regarding complications encountered in the current study, durotomy was encountered in only one case (8.33%), who was managed conservatively. other authors reported that unintended durotomy occurred in 4.5 % of their cases [11]. another study reported that that complication occurred in about 5 – 15% of cases [4]. in addition, ng and his colleagues also reported that the incidence of that complication was 14% [9]. this comes in line with our results. in the study conducted by abbas and his associates, early post-operative complications were encountered in 2 cases (18.2%); one had csf leak, and the other had a wound hematoma [1]. the main disadvantage with our study is the relatively small sample size. so, more studies with larger sample size should be conducted in the near future. conclusion unilateral laminotomy with bilateral canal decompression is a safe and feasible approach in managing lss. excellent outcomes are expected regarding leg pain and quality of life, while slight improvement is anticipated regarding low back pain. 146 amin sabry, wael zakarya, amr farid khalil references 1. abbas m, elwany a, and farag r: efficacy and safety of using unilateral approach for bilateral neural decompression in lumbar spinal stenosis. egyptian spine journal 2017, 24(1),42-9. 2. amir s, qadir m, pasha i f, and qureshi m a: to determine the efficacy of unilateral approach for bilateral decompression in lumbar spinal stenosis. journal of saidu medical college 2018, 7(2). 3. aydin y: efficacy of unilateral laminectomy for bilateral decompression in lumbar spinal stenosis. turkish neurosurgery 2007, 17(2),100-8. 4. çavuşoğlu h, kaya r a, türkmenoglu o n, tuncer c, colak i, and aydın y: midterm outcome after unilateral approach for bilateral decompression of lumbar spinal stenosis: 5-year prospective study. european spine journal 2007, 16(12),2133-42. 5. galiano k, obwegeser a a, gabl m v, bauer r, and twerdy k: long-term outcome of laminectomy for spinal stenosis in octogenarians. spine 2005, 30(3),332-5. 6. lipson s j: spinal-fusion surgery—advances and concerns. new england journal of medicine 2004, 350(7),643-4. 7. mayer t g, vanharanta h, gatchel r j, mooney v, barnes d, judge l, smith s, and terry a: comparison of ct scan muscle measurements and isokinetic trunk strength in postoperative patients. spine 1989, 14(1),33-6. 8. moisi m, fisahn c, tkachenko l, tubbs r s, ginat d, grunert p, jeyamohan s, reintjes s, ajayi o, and page j: unilateral laminotomy with bilateral spinal canal decompression for lumbar stenosis: a technical note. cureus 2016, 8(5). 9. ng l c, tafazal s, and sell p: the effect of duration of symptoms on standard outcome measures in the surgical treatment of spinal stenosis. european spine journal 2007, 16(2),199-206. 10. oertel m f, ryang y-m, korinth m c, gilsbach j m, and rohde v: long-term results of microsurgical treatment of lumbar spinal stenosis by unilateral laminotomy for bilateral decompression. neurosurgery 2006, 59(6),126470. 11. podichetty v k, spears j, isaacs r e, booher j, and biscup r s: complications associated with minimally invasive decompression for lumbar spinal stenosis. clinical spine surgery 2006, 19(3),161-6. 12. rahman m, summers l, richter b, mimran r, and jacob r: comparison of techniques for decompressive lumbar laminectomy: the minimally invasive versus the “classic” open approach. min-minimally invasive neurosurgery 2008, 51(02),100-5. 13. ramesh k, and vimalan g: comparative study between functional outcome of lumbar canal stenosis treated with surgical decompression by laminectomy and unilateral partial hemi laminectomy approaches. international journal of research in orthopaedics 2018, 4(4),610. 14. see d, and kraft g: electromyography in paraspinal muscles following surgery for root compression. archives of physical medicine and rehabilitation 1975, 56(2),80-3. 15. steurer j, nydegger a, held u, brunner f, hodler j, porchet f, min k, mannion a f, michel b, and collaboration l r: lumbsten: the lumbar spinal stenosis outcome study. bmc musculoskeletal disorders 2010, 11(1),254. 16. takahashi h, aoki y, saito j, nakajima a, sonobe m, akatsu y, inoue m, taniguchi s, yamada m, and koyama k: unilateral laminectomy for bilateral decompression improves low back pain while standing equally on both sides in patients with lumbar canal stenosis: analysis using a detailed visual analogue scale. bmc musculoskeletal disorders 2019, 20(1),100. doi: 10.33962/roneuro-2023-008 conservative management of intraventricular migrating intracranial bullet. a case report amjed hassan saheb, rania h. al-taie, ibrahim a. farooq, abbas musaab taha, hawraa sadeq naser, zahraa mohammed yaseen, mustafa ismail, samer s. hoz romanian neurosurgery (2023) xxxvii (1): pp. 59-63 doi: 10.33962/roneuro-2023-008 www.journals.lapub.co.uk/index.php/roneurosurgery conservative management of intraventricular migrating intracranial bullet. a case report amjed hassan saheb1, rania h. al-taie2, ibrahim a. farooq3, abbas musaab taha3, hawraa sadeq naser4, zahraa mohammed yaseen5, mustafa ismail3, samer s. hoz6 1 department of neurosurgery, al husain teaching hospital, dhi qar, iraq 2 college of medicine, university of mustansiriyah. baghdad, iraq 3 college of medicine, university of baghdad, iraq 4 college of medicine, university of al-ameed. karbala, iraq 5 college of medicine, university of diyala. diyala, iraq 6 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract background. the high mortality rate of a cranial bullet injury, the catastrophic damage of vital tissue, and the frequency of gunshot accidents made managing such cases highly effortful in neurosurgical trauma centres. one category of these injuries is the gravitational bullet injury, in which the bullet's movement depends on gravity after losing its kinetic energy. this paper aims to describe the conservative treatment plan we applied for a patient who suffered an intracranial gravitational bullet injury. case description. the patient presented with a cranial bullet injury that migrated caudally to his lateral ventricle. this unapproachable location of the bullet made the surgical intervention undoable. therefore, after the implication of resuscitative management, the patient went under heavy observation with a suitable follow-up plan. the patient's short-term outcome was excellent, and his glasgow coma scale was 15 at the discharge. conclusion. conservative management in a gravitational bullet is one of the possible methods to reach the best outcome in non-operable patients. such measures are highlighted in this case, even when a complication like a bullet migration may occur. introduction cranial bullet injuries constitute a frequent clinical challenge for neurosurgeons in trauma centers. the impact of such injury includes damage to vital tissue and subsequent complications. a missile bullet injury is considered to have a high mortality rate that ranges from 51% to 84% (10). on the other hand, gravitational bullet injury, also known keywords gravitational bullet injury, conservative management, migrating intracranial bullet injury corresponding author: mustafa ismail univeristy of baghdad / collge of medicine, iraq mostafa.ismail1700d@ comed.uobaghdad.edu.iq copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 60 amjed hassan saheb, rania h. al-taie, ibrahim a. farooq et al. as falling bullet injury, occurs when the bullet loses its acceleration and kinetic energy; therefore, its movement will depend only on gravity. in this situation, the bullet does not have a cavitary effect, and the damage will be less dramatic than the missile bullet injury (2). it is noteworthy that there is inadequate mention of the indications of conservative management regarding gravitational bullet injury in the literature, especially the rare phenomena of bullet migration. the aim of this article is to discuss the conservative management steps of gravitational bullet injury and the remarkable outcome of the patient despite the critical location of the bullet and its consequent craniocaudal migration. case description thirty-three years old male with unremarkable past medical history was admitted to the neurosurgical emergency department due to a bullet head injury. his transfer to the hospital was delayed more than one hour because he lives in a rural area. the initial assessment revealed that one entry wound was positioned on the upper part of the frontal bone, slightly right to the bregma area; neither an exit wound nor other concomitant injury has been found. gcs was 14 (e4m5v5) at the admission. he presented with a severe headache with no motor deficit. his vitals were stable, and pupils were equally round and reactive to the light and accommodation. initial skull x-ray was performed, which documented an intracranial bullet (fig 1, 2). computed tomography (ct) scan was done, which revealed a foreign body with moderate volume subarachnoid hemorrhage (sah) (fig 3. e). figure 1. head x-ray in coronal view, a: before bullet migration, b: after bullet migration. resuscitative measures were performed with conservative management, including wound debridement with intravenous effusion of antibiotics, including ampicillin-sulbactam, metronidazole, and cefotaxime for one week in addition to paracetamol, anticonvulsant (phenytoin) and ranitidine. the next day's follow-up ct revealed the migration of the bullet to the occipital horn of the right lateral ventricle (fig 4. h). no surgery was done for him, and he went under heavy observation. the patient was discharged from the hospital after one week of observation. the patient's gcs was 15 at the discharge, with blood pressure 150/65. the follow-up strategy includes repeated imaging that will be conducted every three months to monitor the site of the bullet and the subsequent complications. figure 2. head x-ray in sagittal view, d: before bullet migration, c: after bullet migration. figure 3. head ct in cross-sectional view, e: before bullet migration, f: after bullet migration. figure 4. head ct in sagittal view, g: before bullet migration, h: after bullet migration. 61 conservative management of intraventricular migrating intracranial bullet discussion avoiding invasive measures through a conservative management strategy to preserve vital anatomical structures constitutes a relatively infrequent approach in cranial bullet injuries. one of the compelling situations in which a neurosurgeon will implement conservative management is when a migrating intracranial bullet is positioned in an inaccessible site. bullet fragment migration has been reported in 0.06-4.2% of bullet injury cases (13). since the additional neurological deficit could result from the removal of the bullet, managing such cases is challenging (2,10). additionally, several studies revealed no remarkable association between retained bullet fragments and infection and no associated seizure occurrence (9,14), favoring conservative management for such critical cases. this paper aims to observe the effectiveness of conservative management regarding inaccessible cranial bullets and the patient's short-term outcome. regarding the gravitational bullet effect mechanism, there are three velocity phases (2). the first one is the explosive acceleration after the gun's firing, the second phase represents the velocity's deceleration due to gravity's effect, and the third phase starts when the bullet movement changes in a downward direction with accelerated velocity. after these phases, the bullet reaches the terminal velocity, which depends on multiple factors, including the bullet material, angle of firing, and flight characteristics (7,11). the action of gravitational force on the bullet, the flow of cerebrospinal fluid (csf), the vessels pulsation, and finally, the local tissue damage and the consequent edema with tissue softening are all considered factors that would enable the bullet's movement inside the cranial cavity. the migration will stop by gliosis and the formation of fibrotic scar tissue in a healing process that can take several weeks to years to be completed (3,6). the availability of firearms and the rise of terrorist-related aggressiveness have increased the incidence of missile injuries. indeed, one of the frequent events in which there is a traditional aerial firing is the marriage ceremony which led to an increased incidence of gravitational bullet injuries (3). the ventricular system is one of the most vulnerable sites in craniocerebral bullet injuries. the main reasons for this are the fragility of its structures and its critical site with proximity to vital vascular and neural structures as for the circle of willis, which are located below the frontal horn and the body of the lateral ventricles. moreover, the choroidal arteries have a close correlation with the lateral ventricles. another crucial relation to the ventricles represents the course of the venous channels that drain the deep white and gray matter surrounding the lateral and third ventricles and the basal cisterns into the brain's deep venous system, which include the internal cerebral vein, basal vein, and great vein of galen. these channels pass subependymally through the walls of the lateral ventricles (5). regarding the conventional management of head bullet injury, resuscitative stabilization must be done according to international trauma life support guidelines. then, accurate identification of wound entry sites, monitoring the intracranial pressure, and administering prophylactic anticonvulsants and tetanus toxoids (1,15). it is essential to mention that the leading cause of mortality in falling bullet injuries is a cerebral hernia resulting from increased intracranial pressure (12). after that, individualbased assessment must be applied before making surgical decisions. to illustrate the previous statement, many studies advocated removing the bullet if it is accessible and the removal procedure will not cause severe morbidity. these studies include özkan study (16) and the study of kumar et al. (8). in contrast, there were two reported cases by zafonte et al. (16) of spontaneous migration that caused a neurological collapse in which the two conditions were improved after applying surgical management. the severity of complications associated with the migration of intracranial projectiles often contributes to poor prognostic consequences (8). these complications are divided into two categories; the first one will include bullet lethality with the entering of shattered bone fragments and bleeding. the second category represents the development of seizure foci, neural tissue necrosis, pressure effect of the foreign body, and different types of intracranial infections. this category also includes hydrocephalus, a predicted complication of an intraventricular bullet (13). in our case, after adequate resuscitation of the patient according to advanced trauma life support (atls) protocol by the well-trained neurosurgical team in the emergency department, he was admitted to the operating room for meticulous wound debridement. ct imaging demonstrated that 62 amjed hassan saheb, rania h. al-taie, ibrahim a. farooq et al. bullet removal is more dangerous than leaving it inside the ventricle. thus, surgical intervention was not considered an option. the initial gcs of the patient is one of the most important predictors of outcome (12). as for our case, gcs was 14 (e4m5v5). the patient received an intravenous fluid and antibiotics, including ampicillin-sulbactam, metronidazole, and cefotaxime. palliative measures were performed to relieve his pain using analgesia. anticonvulsant drugs, including phenytoin, were given to avoid the complication of the development of seizure foci in addition to ranitidine. the next day, a follow-up ct was performed to guide further management, revealing the bullet's migration to the occipital horn of the right lateral ventricle. the migration of the bullet made it even more unapproachable; hence, no operation was conducted, and he went under heavy observation. the patient was discharged from the hospital after one week of careful surveillance. at the discharge, the patient's gcs was 15. his blood pressure was 150/65. his follow-up strategy involves repeated imaging every three months to monitor the site of the bullet in addition to regular neurological examination to manage the predicted complications. the follow-up plan has further significance because the bullet might migrate again and give rise to more damage. for instance, in 2010, castillorangel et al. reported the case of a 9-year-old female who had an intracranial bullet injury. no surgical intervention had been performed, and she was discharged after being conservatively managed by a healthcare team. later and after twenty-seven years, she suffered several symptoms, including thoracic pain, bladder/bowel habitus changes, and bilateral lower extremity weakness. the imaging revealed that the bullet had migrated and is now at the t4 level. thus, it was surgically removed (4). to sum up, everything has been stated so far, removing deep-seated bullets could raise the potential for morbidity and mortality. nevertheless, leaving the bullet inside the brain tissue may result in its migration, and a correspondingly significant neurological deficit will occur. this fact decided whether to apply surgical treatment or convey conservative management, a severe challenge in neurosurgical departments. finally, implementing efficient guidelines and the documentation of similar cases would ensure better patient care in such compelling circumstances. conclusion it is essential to acknowledge that gravitational bullet injury cases need more documentation in the literature to be oriented with manageable complications like bullet migration and individualized treatment plans. regarding our case, the bullet settled in the lateral ventricle, which made it inaccessible. the excellent recovery of the patient and the critical location of the bullet encouraged to go with conservative management. abbreviations glasco coma scale = gcs; computed tomography = ct; subarachnoid hemorrhage = sah. references 1. aarabi b, mossop c, aarabi ja. surgical management of civilian gunshot wounds to the head. handbook of clinical neurology. 2015 jan 1;127:181-93. 2. abdali ha, hoz ss, moscote-salazar lr. cranial gravitational (falling) bullet injuries: point of view. journal of neurosciences in rural practice. 2018 apr;9(02):278-80. 3. ali sa, tahir sm, makhdoom a, shaikh ar, siddique aj. aerial firing and stray bullet injuries: a rising tide. iranian red crescent medical journal. 2015 apr;17(4). 4. castillo-rangel c, reyes-soto g, mendizábal-guerra r. cranio-thoracic bullet migration over a period of 27 years: case report. neurocirugía. 2010 jan 1;21(4):326-9. 5. erdogan e, izci y, gonul e, timurkaynak e. ventricular injury following cranial gunshot wounds: clinical study. military medicine. 2004 sep 1;169(9):691-5. 6. fujimoto y, cabrera ht, pahl fh, de andrade af, marino jr r. spontaneous migration of a bullet in the cerebellum—case report—. neurologia medicochirurgica. 2001;41(10):499-501 7. incorvaia an, poulos dm, jones rn, tschirhart jm. can a falling bullet be lethal at terminal velocity? cardiac injury caused by a celebratory bullet. the annals of thoracic surgery. 2007 jan 1;83(1):283-4. 8. kumar r, garg p, maurya v, sahu rn, mahapatra ak. spontaneous bullet migration-uncommon sequelae of firearm injury to the brain. indian journal of neurotrauma. 2008 dec;5(02):119-21. 9. mancuso p, chiaramonte i, passanisi m, guarnera f, augello g, tropea r. craniocerebral gunshot wounds in civilians. report on 40 cases. journal of neurosurgical sciences. 1988 oct 1;32(4):189-94. 10. negrotto, matías, ramon figueroa, and katherine sotomayor. "neurosurgery-cases and reviews." (2019). 63 conservative management of intraventricular migrating intracranial bullet 11. ordog gj, wasserberger j, balasubramanium s. wound ballistics: theory and practice. annals of emergency medicine. 1984 dec 1;13(12):1113-22. 12. özdemir m, ağahan ün. gunshot injuries due to celebratory gun shootings. turkish neurosurgery. 2009 jan 1;19(1). 13. rapp lg, arce ca, mckenzie r, darmody wr, guyot dr, et al. (1999) incidence of intracranial bullet fragment migration. neurol res 21: 475-480. 14. rish bl, caveness wf, dillon jd, kistler pj, mohr jp, weiss gh. analysis of brain abscess after penetrating craniocerebral injuries in vietnam. neurosurgery. 1981 nov 1;9(5):535-41. 15. yue jk, chang d, han kj, wang as, oh t, sun pp. management of migrating intracranial bullet fragments in a 13-year-old female after firearm brain injury: technical and surgical nuances. brain injury. 2022 jan 31:1-8. 16. zafonte rd, watanabe t, mann nr. moving bullet syndrome: a complication of penetrating head injury. archives of physical medicine and rehabilitation. 1998 nov 1;79(11):1469-72. romanian neurosurgery (2019) xxxiii (3): pp. 283-286 doi: 10.33962/roneuro-2019-047 www.journals.lapub.co.uk/index.php/roneurosurgery our experience with a single stage bilateral approach for treatment of bilateral middle cerebral artery aneurysms a. chiriac1,2, georgiana ion1, z. faiyad1, i. poeata1,2 1 “gr. t. popa” university of medicine and pharmacy, iasi, romania 2 “prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract surgical management of bilateral middle cerebral artery (mca) aneurysms is particular challenging clinical situation. for these patients various options of surgical treatment are available as unilateral approach, single stage bilateral craniotomy or two stage bilateral craniotomy. we report our experience with a case of bilateral mca aneurysm which was managed by single stage bilateral pterional craniotomy. introduction surgical management of bilateral intracranial aneurysms is still difficult especially when it involves bilateral middle cerebral artery aneurysms. even though endovascular treatment is widely accepted as the first option in the treatment of intracranial aneurysms, the middle cerebral artery aneurysms remained with quite high addressability for microsurgical clipping due to its special predisposition to have a broad neck that incorporate the parent vessels and frequent association with massive intracranial haemorrhages. depending on some anatomical features, experience and preference of the neurosurgeon, these lesions can be operated in single or two separate sessions by unilateral or bilateral approach. therefore, direct clipping of both ruptured and unruptured aneurysm in a single-stage operation, is more preferred today, if technically possible. the risk and worry about rupture of an untreated associated aneurysm is not insignificant during the early or late postoperative period when aggressive management against vasospasm is fundamental. we report upon our experience with a single stage bilateral craniotomy approach for clipping the bilateral middle cerebral artery aneurysms. case report a 49-year-old woman addressed to the emergency room with spontaneous severe headache, photophobia and few episodes of vomiting form one day. at clinical examination she was conscious with no motor deficits only slight nuchal rigidity. the cerebral ct-scan showed features of acute subarachnoid haemorrhage at basal cisterns keywords middle cerebral artery aneurysm, single stage, bilateral approach corresponding author: a. chiriac “gr. t. popa” university of medicine and pharmacy, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 284 a. chiriac, georgiana ion, z. faiyad, i. poeata e and both sylvain fissure. the patient was classified as fisher grade iii and hunt and hess grade 1. ct angiography was performed and revealed bilateral mca bifurcation aneurysms (figure 1). the presence of a nipple on aneurysmal sac and the slight prevalent sah in left sylvian fissure suggested that the left was the ruptured aneurysm. because the unruptured aneurysms at the contralateral mca were not negligible and concerning represented by necessity of an aggressive triple h therapy a singlestage operation was decided. single stage bilateral craniotomy and microsurgical clipping of the aneurysms was done in the same day of admission. the procedure was performed with the patient under the general anaesthesia. a bilateral small sized pterional approach was performed in consecutive steps. the rupture side was approached first. the head is positioned on the operating table without being fixed in the frame with pins. the head is slightly rotated to the contralateral side and extended enough to minimize the frontal lobe retraction. a curvilinear skin incision was made inside the hairline starting in front of the tragus (5 mm approx.) to the level of the midline. the incision on the attachment of the muscle to the superior temporal line is made with monopolar cut in order to detachment and retraction of the muscle posteriorly and inferiorly with hooks. a classic pterional craniotomy by tow blur holes is performed. by bone flap removal pterion bone and a prominent sphenoid wing are smoothed using a high-speed drill. dura is c-like shape incised and reflected toward the cranial base. after minimal opening of the sylvian fissure, the optic, chiasmatic, and lamina terminalis cisterns are opened with gradually cerebrospinal fluid aspiration to obtain a slack brain and avoiding excessive retraction. with the highlighting of the internal carotid artery and its terminal bifurcation, microdissection is continued with widely opening of the sylvian fissure. a good exposure of the m1 segment is obtained. this segment is followed up to the bifurcation with careful microdissection of the aneurysmal neck to prevent the aneurysm rupture. after the clear exposure of the neck and the origins of the m2 branches a clip is applied with aneurysm exclusion. after carefully haemostasis and dura closure, the bone was fixed in two or three points. finally the wound is closed as the usual fashion. figure 1. a diagnostic ct-scan with left sylvian fissure haemorrhage; b 3d mra; c dsa showing right mca aneurysm; d dsa showing left ruptured mca aneurysm; e – postoperative ct control. 285 our experience with a single stage bilateral approach for treatment of bilateral middle cerebral artery aneurysms a total of three clips were used with two on the right side to preserve the bifurcation anatomy. the total time for surgery was four and a half hours. there was no intraoperative complication. triple-h therapy was started immediately postoperatively. control ct scan was performed 24 hours later. the patient evolution was favourable accompanied only by mild episode of headache. she was discharged home on the 21th day. discussion the clinical status regarding the incidence of bilateral aneurysm of mca was mentioned in the literature around 1.18%. for bilateral mca aneurysms, several surgical treatment options such as unilateral approach, single-stage bilateral craniotomy, or twosided bilateral craniotomy have been reported. for each type of approach it is extremely important to pay attention to several preconditions in order to perform them safely and effectively.[3,4,6,7] single stage surgery has the advantages of removing a new risk of bleeding, curative treatment with one-time risk of general anaesthesia, shorter hospital stay and reduced cost in terms of bed charge, investigations and operative expenditure.[3,4,6,7] the most important reason for single stage surgery by bilateral approach is to eliminate the risk of bleeding from unruptured aneurysm in the early or late postoperative period. two important large studies have showed that associated aneurysm in patients with sah due to another ruptured aneurysm presents a higher risk for future bleeding than makes aneurysms of similar size with no sah history [3,4,6]. furthermore, the necessity of an aggressive hypertensive treatment for fighting with cerebral vasospasm may carry a potential risk of rupturing for associated untreated aneurysm in the postoperative period. [4,6] optimal selection of the patient with bilateral mca aneurysm for a single stage surgery by unilateral or bilateral approach is dependent on a number of parameters such as severity of brain edema, the length of contralateral m1 segment, configuration and projection of the contralateral aneurysm. presence of an important brain swelling, correlated with recent severe sah is usually associated with very difficult microdisection and an excessive brain retraction that leads to a single stage bilateral approach choice. longer contralateral m1 segment and a complex or large associated unruptured aneurysm are also condition this type of approach. if the anterior projection of the associated contralateral aneurysm is an indication for a unilateral single stage approach, the posterior or along the axis of the mca projections are condition more favourable for a bilateral single stage approach. another important factor in bilateral mca aneurysms surgery is represented by correct determining the side of ruptured aneurysm, because surgery should always be started from the ruptured side. in case of the misdiagnosed of ruptured bilateral mca aneurysm with first clipping of unruptured one, the contralateral (ruptured) mca aneurysm should always be clipped via a second contralateral craniotomy. a good clinical grade presentation can also be a factor favourable for a single stage bilateral surgery. conclusions challenging for a single stage bilateral approach should be considered in suitable cases of bilateral mca aneurysm in all centres with experienced vascular neurosurgeons. a careful analysis based on clearly defined parameters will help the neurosurgeon in patient selection for this particular type of approach. this particular approach is more indicated in a patient with bilateral middle cerebral artery aneurysms presenting with bleeding and the ruptured side is not easily identifiable. references 1. acik, v., cavus, g., bilgin, e., arslan, a., gezercan, y., & okten, a. i̇. (2017). surgical treatment of mirror middle cerebral artery aneurysms: bilateral and unilateral approach. world neurosurgery, 108, 774-782. 2. andrade-barazarte, h., kivelev, j., goehre, f., jahromi, b. r., noda, k., ibrahim, t. f. & hernesniemi, j. a. (2015). contralateral approach to bilateral middle cerebral artery aneurysms: comparative study, angiographic analysis, and surgical results. neurosurgery, 77(6), 916-926. 3. inci, s., akbay, a., & ozgen, t. (2012). bilateral middle cerebral artery aneurysms: a comparative study of unilateral and bilateral approaches. neurosurgical review, 35(4), 505-518. 4. maruyama, keisuke & kurita, hiroki & yamaguchi, ryuichi & noguchi, akio & shiokawa, yoshiaki. (2013). one-stage clipping of bilateral middle cerebral artery aneurysms via 286 a. chiriac, georgiana ion, z. faiyad, i. poeata the bilateral pterional keyhole approach. neurologia medico-chirurgica. 53. 148-52. 10.2176/nmc.53.148. 5. rajagopal, n., balaji, a., yamada, y., kawase, t., & kato, y. (2019). etiopathogenesis, clinical presentation and management options of mirror aneurysms: a comparative analysis with non-mirror multiple aneurysms. interdisciplinary neurosurgery, 18, 100535. 6. shin bg, kim js, hong sc. (2005). single-stage operation for bilateral middle cerebral artery aneurysms. acta neurochir (wien). 2005 jan;147(1):33-8; discussion 38. 7. yam b roka, manzil shrestha. (2013). single stage clipping of bilateral middle cerebral aneurysms. nepal journal of neuroscience vol 2, 10:86-87. doi: 10.33962/roneuro-2021-002 navigated transcranial magnetic stimulation mapping in patients with language-eloquent brain lesions george e. d. petrescu, roxana radu, andrei giovani, cristina gorgan, felix m. brehar, radu m. gorgan romanian neurosurgery (2021) xxxv (1): pp. 14-19 doi: 10.33962/roneuro-2021-002 www.journals.lapub.co.uk/index.php/roneurosurgery navigated transcranial magnetic stimulation mapping in patients with language-eloquent brain lesions george e. d. petrescu1,2, roxana radu1,2, andrei giovani1, cristina gorgan3, felix m. brehar1,4, radu m. gorgan1,4 1 neurosurgery department, “bagdasar-arseni” emergency hospital, bucharest, romania 2 phd student, “carol davila” university of medicine and pharmacy, romania 3 neurology department, “bagdasar-arseni” emergency hospital, bucharest, romania 4 neurosurgery department, “carol davila” university of medicine and pharmacy, romania abstract introduction: the surgical resection of brain lesions located in language-eloquent areas harbours a great risk for determining new functional deficits. navigated transcranial magnetic stimulation represents a novel non-invasive cortical mapping method that can be used preoperative to determine language-eloquent areas. materials and methods: we retrospectively reviewed a prospectively maintained database of patients that underwent preoperative cortical mapping using ntms between march 2017 and june 2020. patients older than 18 years old with brain lesions situated in a presumed language eloquent area, that underwent surgical resection of the brain lesion were included in the study. various parameters such as error rate, number of language-negative sites were assessed. results: fourteen patients were included in the study. there were 10 males and 4 females in total. most of the tumours were in the temporal and frontal lobes (five and four cases, respectively). the histopathological diagnosis was glioblastoma in seven cases, in one case there was an anaplastic astrocytoma and there were two cases of low-grade gliomas. there were three cases of brain metastasis and one cavernoma. the median (range) tumor volume was 25.01 cm3 (0.89 – 86.55 cm3). gross-total resection (gtr) was achieved in seven cases. the error rate was significantly higher in patients that continued to have an impaired language function after surgical resection (p = 0.016), while the perilesional error rate was higher in patients with preoperative aphasia (p = 0.019). conclusion: our findings suggest that a lower tumour volume to perilesional negative stimuli ratio is associated with an extended surgical resection of brain tumours located in language-eloquent areas and that patients that presented with aphasia and have a high error rate have a worse functional prognosis. through ntms preoperative cortical mapping of language-eloquent areas, the neurosurgeon has more insight regarding the cortical function and can maximize the surgical resection, while avoiding the onset of new functional deficits. keywords navigated transcranial magnetic stimulation, language areas cortical mapping, brain tumours corresponding author: george e. d. petrescu “carol davila” university of medicine and pharmacy, romania gedpetrescu@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 15 navigated transcranial magnetic stimulation mapping in patients with language-eloquent brain lesions introduction the surgical resection of brain lesions located in language-eloquent areas harbors a great risk for determining new functional deficits. since a complex network is involved in speech and language processing, and there is a high individual variability regarding the cortical representation of language areas, cortical mapping of eloquent areas should be performed in order to decrease this risk (1). moreover, brain tumors can disrupt and reorganize the normal functional areas (2, 3). the ”goldstandard” method for the mapping of language areas is direct cortical stimulation (dcs) under awake surgery (4). however, not all patients can tolerate or have contraindications for an awake craniotomy (5). navigated transcranial magnetic stimulation (ntms) represents a preoperative, non-invasive method used for cortical mapping of motor and language eloquent areas (6, 7). by using navigated repetitive tms (nrtms) pulses, language areas can be mapped in patients with brain tumors, as well as in healthy individuals, without adverse events (3). in this study we present our experience with ntms cortical mapping for language-eloquent brain lesions. materials and methods patient cohort we retrospectively reviewed a prospectively maintained database of patients that underwent preoperative cortical mapping using ntms between march 2017 and june 2020. the inclusion criteria were: (1) patients with brain lesions situated in a presumed language eloquent area; (2) patients that underwent surgical resection of the brain lesion; (3) age > 18 years old. patients that had ntms contraindications (e.g.: frequent generalized epileptic seizures, cranial implants) or did not undergo surgical resection or underwent only a stereotactic biopsy procedure were excluded from the study. ntms language mapping cortical mapping was performed by using the nexstim navigated brain stimulation system 5 (nexstim oy, helsinki, finland) according to the established protocol (8), as previously described (9). briefly, the brain mri and the patients’ head were coregistered, and a motor mapping was performed to determine the resting motor threshold (rmt). afterwards, using the nexspeech software (nexstim oy, helsinki, finland) the patients performed a baseline object-naming task without tms stimuli, in order to evaluate each patients’ vocabulary and misidentified pictures were removed. the baseline procedure was repeated twice. the remaining pictures were used for the object-naming task performed with nrtms pulses. the following parameters were used for the language mapping: picture display time (pdt): 700 ms, interpicture interval (ipi): 2500 ms and picture-to-trigger (ptt) interval: 0 ms. the navigated repetitive tms (nrtms) pulses were applied in bursts of 5 pulses with 5 hz frequency, with an intensity of 100% of the rmt. individual adjustments were performed, when needed, based on the preexisting neurological deficits. every site was stimulated three times. the results were analyzed blinded to the location of the tms stimuli and compared with the baseline. the language errors were defined in the following categories: no response, performance error, semantic error and other. errors due to muscle stimulation were discarded. surgical planning the brain mri scans with the annotated language errors were included in the intraoperative neuronavigation system (sonowand invite sonowand as, trondheim, norway, or medtronic stealth s8 – medtronic, minneapolis, usa). the surgical planning took into account the results from the brain mapping, in order to select the optimal entry point and trajectory, with the goal of avoiding postoperative neurological deficits and maximizing the surgical resection. brain lesion evaluation the brain mri used for the mapping procedure was used the calculate to volume of the brain lesion with the aid of the 3d slicer 4.10.0 software (10, 11). based on the histopathological diagnosis, the tumors were classified in two categories: (1) tumors with slow growth rate (low grade gliomas) and tumors with fast growth rate (high grade gliomas, metastases). language mapping analysis in order to better evaluate the language function and the mapping results, a series of variables were assessed: number of language errors, number of noresponse errors, number of language-negative sites, 16 george e. d. petrescu, roxana radu, andrei giovani et al. error rate (er) = language errors/total stimuli * 100, perilesional error rate (per) = perilesional language errors/perilesional stimuli * 100. the tumor volume to language-negative sites ratio was calculated. statistical analysis statistical analysis was performed using the ibm spss statistics, version 25 (ibm corp., armonk, n.y., usa). the t-test was used for continuous variables with parametric distribution and the mann-whitney u test for the non-parametric ones. p < 0.05 was considered statistically significant. results patient cohort fourteen patients met the inclusion criteria with a mean (sd) age of 51.5 (13.9) years. there were 10 males and 4 females in total. all patients were righthanded, with the left hemisphere being considered the dominant one. most of the tumors were located in the temporal and frontal lobes (five and four cases, respectively). two tumors were in the frontotemporal lobes and one in each of the following: parietal lobe, fronto-parietal and temporo-parietal. the histopathological diagnosis was glioblastoma in seven cases, in one case there was an anaplastic astrocytoma and there were two cases of low-grade gliomas. there were three cases of brain metastasis and one cavernoma. according to the growth rate classification, there were 11 fast-growing tumors and 2 slow-growing tumors (the cavernoma case was excluded from this classification). gross-total resection (gtr) was achieved in seven cases, while in the others a subtotal resection (str) was performed. the median (range) tumor volume was 25.01 cm3 (0.89 – 86.55 cm3). cohort characteristics are summarized in table 1. table 1. cohort characteristics no. age – mean (sd) 51.5 (13.9) tumor location temporal frontal fronto-temporal fronto-parietal parietal temporo-parietal 5 4 2 1 1 1 histopathology high-grade glioma metastasis low-grade glioma cavernoma 8 3 2 1 extent of resection gtr str 7 7 table 1 summarizes the characteristics of the patient cohort. gtr = gross-total resection; str = subtotal resection. language function analysis and cortical mapping results preoperatively, seven patients presented with aphasia. short-term following the surgical resection, there was an improvement of function in four cases. none of the patients had new language functional deficits following surgery. no adverse events were encountered during the preoperative mapping procedure. figure 1 illustrates the results of a language mapping procedure using ntms. the error rate was significantly higher in patients that continued to have an impaired language function after surgical resection (p = 0.016), while the perilesional error rate was higher in patients with preoperative aphasia (p = 0.019). although, the perilesional error rate was increased in tumors with fast-growing rate compared to those with slowgrowing rate, the result was not statistically significant (p = 0.058). the results of the language mapping analysis are depicted in table 2 and table 3. regarding the extent of resection, a lower ratio between tumor volume and number of perilesional negative stimuli (cm3/stimuli) was associated with an extended resection (p = 0.004). table 2. patient characteristics and language mapping results pt. no. age sex tumor location pathology preoperative aphasia er perilesional er eor 1 65 ma tp gbm yes 12% 25% gtr 2 18 ma f cav. no 8% 17% gtr 3 70 fe p met. no 8% 16% gtr 4 62 ma t gbm yes 8% 21% str 17 navigated transcranial magnetic stimulation mapping in patients with language-eloquent brain lesions 5 46 ma fp gbm no 13% 19% gtr 6 54 ma f gbm yes 26% 33% str 7 61 fe t gbm yes 6% 16% str 8 59 ma t met. yes 17% 22% gtr 9 43 ma t lgg no 4% 8% str 10 59 ma t aa no 9% 14% gtr 11 32 fe ft lgg no 13% 12% str 12 45 ma f met. no 8% 22% gtr 13 58 ma ft gbm yes 16% 22% str 14 49 fe f gbm yes 37% 42% str table 2 presents the patients’ characteristics and results of language mapping analysis. aa = anaplastic astrocytoma; cav. = cavernoma; eor = extent of resection; er = error rate; f = frontal; fe= female; fp = fronto-parietal; ft = fronto-temporal; gbm = glioblastoma; lgg = low-grade glioma; ma = male; met. = metastasis; p = parietal; t = temporal; tp = temporo-parietal. table 3. language mapping analysis mean (sd) / median (range) p value persistent aphasia yes no error rate 23.39% (11.82) 10.55% (5.92) 0.016 preoperative aphasia yes no perilesional error rate 25.72% (8.63) 15.40% (4.64) 0.019 tumor type (n = 13) fast growth rate slow growth rate perilesional error rate 22.75% (8.12) 10.10% (2.68) 0.058 extent of resection gtr str vol/ perilesional neg. stim. 0.97 (0.22-5.28) 10.10 (2.39-28.85) 0.004 table 3 depicts the results of the language mapping analysis. gtr = gross-total resection; str = subtotal resection; vol/ perilesional neg. stim. = ratio between tumor volume and number of perilesional negative stimuli (cm3/stimuli). figure 1 illustrates the results of the ntms language mapping in a patient with a left temporal glioblastoma. white dots – no response error, blue dots – semantic error, green dots – performance error, orange dots – muscle stimulation, gray dots – negative stimuli. color figure available only online. discussion numerous objections have been addressed to the classical localizationist theory of speech and language processing, that relies on modular, static structures (such as broca’s and wernicke’s areas) and instead a dynamic model consisting of networks between cortical and subcortical structures has been proposed (12-14). this concept supports the idea that brain has the ability to reorganize following brain injury, if the connection between axons is spared (13). although dcs remains the current “goldstandard” for language mapping, nrtms can aid the surgeon in the preoperative surgical planning and has similar results to dcs regarding languagenegative sites (5, 15-17). in our study, although the gtr group had a higher number of negative stimuli than the str group, the difference was not statistically significant (p = 0.21). therefore, we took into account the tumor volume and the negative stimuli that were situated perilesional. the tumor volume to perilesional negative stimuli ratio (cm3/ stimuli) was significantly lower in the gtr group, meaning that a higher number of negative stimuli were attributed per tumor volume, and thus creating a clearer and more reliable map of the languagenegative areas, which consequently lead to a greater extent of resection. even though ntms is not as reliable as dcs, compared to functional mri (fmri) it has a greater sensitivity, but it is less specific (15, 16, 18). one of the advantages of ntms over fmri in language mapping is represented by the fact that 18 george e. d. petrescu, roxana radu, andrei giovani et al. fmri relies on task-induced metabolic changes and it well known that brain tumors, and especially highgrade gliomas, have the tendency to alter the local metabolic activity and vasculature (15, 19, 20). in our cohort, even though there was no statistically significant difference, the error rate and the perilesional error rate were higher in patients with fast-growing brain tumors. the lack of significance might be due to the fact, that in our study there were few patients with lesions with slow growth rate. in their study, schwarzer et al. had an increased er in fast-growing lesions but, again, there was no statistically significant difference (1). however, the authors found a statistically significant difference regarding the baseline error rate between patients with lesions with fast growth rate and patients with vascular malformations (1). this could be explained through the plasticity of the brain, in reaction to the displacement caused by the brain lesion (2). nevertheless, contradictory data regarding which lesion type (slow or fast-growing) induces an extensive reorganization exist (1, 21). the perilesional error rate was significantly higher in patients that presented with aphasia (25.72% vs. 15.40%, p = 0.019) and the er was increased in patients that had mild or no improvement of aphasia following surgery (23.39% vs. 10.55%, p = 0.016). schwarzer et al. also reported an increased error rate in patients with severe aphasia and altered cognition and proposed a baseline error rate lower than 28% as more probable to correctly determine the true language-positive sites (1). the current study is limited by a relatively small cohort size and the histological heterogeneity of the lesions included in the study. conclusions our findings suggest that a lower tumor volume to perilesional negative stimuli ratio is associated with an extended surgical resection of brain tumors located in language-eloquent areas and that patients that presented with aphasia and have a high error rate have a worse functional prognosis. through ntms preoperative cortical mapping of languageeloquent areas the neurosurgeon has more insight regarding the cortical function and is able to maximize the surgical resection, while avoiding the onset of new functional deficits. conflicts of interest the authors declare no potential conflict of interest. references 1. schwarzer v, bährend i, rosenstock t, dreyer fr, vajkoczy p, picht t. aphasia and cognitive impairment decrease the reliability of rntms language mapping. acta neurochirurgica. 2018;160(2):343-56. 2. kosla k, pfajfer l, bryszewski b, jaskolski d, stefanczyk l, majos a. functional rearrangement of language areas in patients with tumors of the central nervous system using functional magnetic resonance imaging. pol j radiol. 2012;77(3):39-45. 3. rösler j, niraula b, strack v, zdunczyk a, schilt s, savolainen p, et al. language mapping in healthy volunteers and brain tumor patients with a novel navigated tms system: evidence of tumor-induced plasticity. clinical neurophysiology. 2014;125(3):526-36. 4. duffau h, lopes m, arthuis f, bitar a, sichez jp, van effenterre r, et al. contribution of intraoperative electrical stimulations in surgery of low-grade gliomas: a comparative study between two series without (1985–96) and with (1996–2003) functional mapping in the same institution. journal of neurology, neurosurgery & psychiatry. 2005;76(6):845. 5. picht t, krieg sm, sollmann n, rosler j, niraula b, neuvonen t, et al. a comparison of language mapping by preoperative navigated transcranial magnetic stimulation and direct cortical stimulation during awake surgery. neurosurgery. 2013;72(5):808-19. 6. picht t. current and potential utility of transcranial magnetic stimulation in the diagnostics before brain tumor surgery. cns oncology. 2014;3(4):299-310. 7. lefaucheur j-p, picht t. the value of preoperative functional cortical mapping using navigated tms. neurophysiologie clinique/clinical neurophysiology. 2016;46(2):125-33. 8. krieg sm, lioumis p, makela jp, wilenius j, karhu j, hannula h, et al. protocol for motor and language mapping by navigated tms in patients and healthy volunteers; workshop report. acta neurochir (wien). 2017;159(7):1187-95. 9. petrescu g, gorgan c, giovani a, brehar fm, gorgan rm. preoperative mapping of the eloquent cortical areas using navigated transcranial magnetic stimulation combined with intraoperative neuronavigation for intracerebral lesions. romanian neurosurgery. 2018;32(1):16-24. 10. 3d slicer [available from: https://www.slicer.org/]. 11. fedorov a, beichel r, kalpathy-cramer j, finet j, fillionrobin j-c, pujol s, et al. 3d slicer as an image computing platform for the quantitative imaging network. magnetic resonance imaging. 2012;30(9):1323-41. 12. de benedictis a, duffau h. brain hodotopy: from esoteric concept to practical surgical applications. neurosurgery. 2011;68(6):1703-23. 19 navigated transcranial magnetic stimulation mapping in patients with language-eloquent brain lesions 13. duffau h. the error of broca: from the traditional localizationist concept to a connectomal anatomy of human brain. journal of chemical neuroanatomy. 2018;89:73-81. 14. duffau h, moritz-gasser s, mandonnet e. a reexamination of neural basis of language processing: proposal of a dynamic hodotopical model from data provided by brain stimulation mapping during picture naming. brain and language. 2014;131:1-10. 15. sebastian i, nico s, theresa h, stefanie m, noriko t, thomas o, et al. impairment of preoperative language mapping by lesion location: a functional magnetic resonance imaging, navigated transcranial magnetic stimulation, and direct cortical stimulation study. journal of neurosurgery jns. 2015;123(2):314-24. 16. jeltema h-r, ohlerth a-k, de wit a, wagemakers m, rofes a, bastiaanse r, et al. comparing navigated transcranial magnetic stimulation mapping and “gold standard” direct cortical stimulation mapping in neurosurgery: a systematic review. neurosurgical review. 2020. 17. motomura k, takeuchi h, nojima i, aoki k, chalise l, iijima k, et al. navigated repetitive transcranial magnetic stimulation as preoperative assessment in patients with brain tumors. scientific reports. 2020;10(1):9044. 18. babajani-feremi a, narayana s, rezaie r, choudhri af, fulton sp, boop fa, et al. language mapping using high gamma electrocorticography, fmri, and tms versus electrocortical stimulation. clinical neurophysiology. 2016;127(3):1822-36. 19. holodny ai, schulder m, liu w-c, wolko j, maldjian ja, kalnin aj. the effect of brain tumors on bold functional mr imaging activation in the adjacent motor cortex: implications for image-guided neurosurgery. american journal of neuroradiology. 2000;21(8):1415. 20. ulmer jl, krouwer hg, mueller wm, ugurel ms, kocak m, mark lp. pseudo-reorganization of language cortical function at fmr imaging: a consequence of tumorinduced neurovascular uncoupling. american journal of neuroradiology. 2003;24(2):213. 21. desmurget m, bonnetblanc f, duffau h. contrasting acute and slow-growing lesions: a new door to brain plasticity. brain. 2007;130(4):898-914. romanian neurosurgery (2019) xxxiii (4): pp. 363-369 doi: 10.33962/roneuro-2019-060 www.journals.lapub.co.uk/index.php/roneurosurgery cardiac dysfunction evoked by ecg and echocardiography changes and release of cardiac biomarkers in patients with aneurysmal subarachnoid haemorrhage. case presentation and literature review raluca ungureanu1, mihai dumitru2, gabriel iacob3 1 anaesthesia and intensive care department, coltea clinical hospital, bucharest, romania 2 anatomy department, carol davila university of medicine and pharmacy, bucharest, romania 3 neurosurgery department, emergency university hospital, bucharest, romania abstract the invisible brain-heart link has been observed and described for centuries now, although a greater interest in the matter has been manifested over the past several decades, especially in patients with aneurysmal subarachnoid haemorrhage (asah). we present the case of a patient with asah and signs of cardiac injury evoked by ecg changes and elevated cardiac enzymes. furthermore, we reviewed current medical literature by searching the international database pubmed for recent articles on the subject of cardiac biomarkers, ecg and echocardiography changes in the setting of sah. our analysis of the selected articles, published between 2012 and 2018, revealed that 22 are patient population studies, 16 are case studies and 6 are reviews of the literature. the most common ecg changes were prolonged qtc andnonspecific st/t-wave changes. echocardiography changes included regional wall-motion abnormalities, typically involving the base of the heart (neurogenic stunned myocardium), yet there was also the scenario of takotsubo cardiomyopathy (stress cardiomyopathy), which affects the apex of the heart. there is a significant statistical association of elevated levels of troponin and nt-probnp with a bad outcome after sah, and we should always keep in mind the dramatic scenario of misdiagnosing the cerebral haemorrhage and treating for a coronary syndrome instead. therefore, the management of asah requires a close cooperation between neurosurgeons, intensivists, cardiologists and radiologists in high volume centres. introduction cardiac dysfunction in patients with an intracranial pathology represents a well-known complication and a pressing problem for both neurosurgeons and intensivists treating such a patient. the matter is keywords subarachnoid haemorrhage – sah, cardiac dysfunction, electrocardiogram – ecg, cardiac enzymes, troponin, nt-probnp, echocardiography corresponding author: gabriel iacob neurosurgery department, emergency university hospital, bucharest, romania gbrl_cb@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 364 raluca ungureanu, mihai dumitru, gabriel iacob probably best described for cases of subarachnoid hemorrhage (sah), which account for approximately 10% of all strokes. most sahs are caused by ruptured saccular (berry) aneurysms. this is a devastating clinical event, with a high mortality rate average case fatality of 51%, as well as substantial neurologic morbidity in survivors (1-7). the complex interactions between the affected brain and the heart are responsible for unique cardiovascular morbidity and mortality up to 23% of deaths caused by cardiovascular and pulmonary complications (1)(8)(9). a number of cardiac changes occur in the acute phase of sah, including ecg changes, structural changes on echocardiography, and acute troponin and nt-probnp elevations (3)(1016). case presentation a 47-year-old man, with a medical history of hypertension, was brought to the emergency department in pitesti for repetitive generalized seizures. upon presentation, he had a glasgow coma scale of 5 (e1, v1, m3), therefore he was sedated and intubated. his wife told the doctors that a few hours earlier he had complained of a severe headache, followed by a reduction in visual acuity for the left eye. moreover, 2 weeks back, he had presented another severe headache and vomiting. the head ct revealed an interhemispheric hemorrhage and a right-sided fronto-temporo-parietal subdural hematoma. the patient was then transferred to the university emergency hospital in bucharest. upon admission, he was sedated, with a gcs of 3, anisocoria (mydriasis of the right eye) and left hemiplegia; he was intubated and mechanically ventilated and cardiovascularly stable, with a normal ecg (fig. 1). an emergency angiography revealed a ruptured aneurysm on the anterior communicating artery, which was embolized. the subdural hematoma was also evacuated. figure 1. normal ecg upon admission figure 2. st segment depression in the anterolateral territory (v2-v6) 365 cardiac dysfunction evoked by ecg and echocardiography changes and release of cardiac biomarkers figure 3. atrial flutter, with variable atrio-ventricular block, and antero-lateral st depression figure 4. t wave flattening in dii, diii, avf, v1-v2 and v6 on the third day, the patient was neurologically better – a cgs of 8 (e2, v1, m5), maintaining left hemiplegia, yet still intubated and mechanically ventilated, with an arterial pressure of 105/65 mmhg, tachycardic 108 bpm. his ecg started changing, at first with st segment depression in v2v6 (antero-lateral territory), followed by atrial flutter, with variable atrioventricular block, and anterolateral st depression (fig. 2,3). cardiac enzymes were also high – ck 807 u/l, ckmb 105 u/l, troponin i 1,5 ng/ml and nt-probnp 173 pg/ml, with normal creatinine clearance and electrolytes. on echocardiography, there was a normal left ventricular ejection fraction and no wall-motion anomaly, thus the scenario was interpreted by the cardiologist as neurologically mediated. ck (1262 u/l) and ckmb (203 u/l) reached their peak value 8 hours later, while troponin had a maximum value of 8,26 ng/ml approximately 20 hours later. a repeated head ct on day 5 revealed a frontal intraparenchymal hemorrhage of 55/14 mm in axial plane and 27 mm cranio-caudal and a bilateral frontal cortico-subcortical ischemic area in the vascularisation territory of the anterior cerebral artery. the vasospasm was confirmed by 2 subsequent angiographies performed on day 5 and 7, when nimotop (nimodipine) was also locally injected. ck and ckmb normalized on day 5, while troponin i normalized on day 7. on day 36, the patient was conscious, with a cgs of 13-14 (e 4 v 3-4, m 6) and a residual left hemiparesis, spontaneously 366 raluca ungureanu, mihai dumitru, gabriel iacob breathing, cardiovascularly stable and a relatively normal ecg (t wave flattening in dii, diii, avf, v1-v2 and v6) (fig. 4). material ad method for the literature review we queried the international database pubmed for recent articles using the syntax: subarachnoid [title/abstract], hemorrhage [title/abstract], cardiac [title/abstract], restricted with filters: publication date from 2012/01/01 to 2018/04/01; humans. afterwards we selected 44 articles tackling the aspects of raised levels of troponin and nt-probnp and ecg and echocardiography changes in patients with sah. results our analysis of the selected articles revealed that 22 are patient population studies, 16 are case series and 6 are reviews of the medical literature. ecg abnormalities jeong et al., in a study of 122 patients with sah and no previous heart disease (62% women) [17] aimed to determine the frequency, influencing factors and impact on outcome of cardiac arrhythmias after asah. 50% of their population had a clinically significant ecg change, the most common type being nonspecific st-t changes. a multivariate analysis showed no significant association of various factors (age, sex, hunt-hess grade, fisher grade, hypertension, symptomatic vasospasm and icu length of stay) with clinically significant arrhythmia. yet, the presence of ecg changes wasindependently predictive of death and poor outcome. on the other hand, july et al. (18) managed to demonstrate that ecg abnormalities were significantly associated with total cortisol an day 4 and free cortisol on day 2, while amin et al. (19) observed a statistically significant association between sah and qtc prolongation. prolonged qt was the most prevalent ecg change in 413 patients from conscious-1, a prospective randomized trial of clazosentran for the prevention of angiographic vasospasm (10). in this group of patients, the authors tried to identify ecg changes associated with angiographic vasospasm following sah and concluded that, on multivariate analysis, qt prolongation and tachycardia are both associated with this complication. moreover, tachycardia and st changes were associated with worse clinical outcome. in another large prospective study 447 sah patients, schmidt et al. (20) confirmed that uncontrolled prolonged heart rate elevation (pehr) is associated with an increased risk of major cardiopulmonary events: hypertension and hypotension requiring vasoactive therapy, pulmonary edema, myocardial injury evidenced by troponin i elevation and poor outcome. 39% of their patients developed pehr (heart rate of at least 95 beats/minute, for more than 12 hours), with 68% of them having late-onset pehr (more than 72 hours after sah onset), which was correlated with an increased risk of delayed cerebral ischemia from cerebral vasospasm. multifactorial logistic regression revealed the factors associated with pehr: nonwhite race, hunt-hess score of at least 4 at admission, high admission apache-2 score and modified fisher score. in this study, pre-hospital beta-blocker use was protective against pehr. by contrast, in a retrospective review of 254 patients with sah, crago et al. found (21) no relationship between the pre-hospital use of ace inhibitors and/or beta-blockers and the development of pulmonary congestion, elevation in troponin or ckmb, heart rate, ecg changes or echocardiography findings. moreover, a relationship was described between the use of these drugs and arrhythmias (ventricular or supraventricular) recorded by holter monitoring, with patients taking beta-blockers. a study from japan (22) draws attention on the clinical scenario of comatose patients resuscitated from sah-associated out-of-hospital cardiac arrest (ohca) (sah-ohca) who often have clinical signs that mimic acute coronary syndrome-associated ohca (acs-ohca) patients. as the management of sah is totally different from that for acs, doctors should be able to differentiate between the two as quickly as possible. yamashina et al.analysed the retrospective data of 1259 consecutive ohca and included in their study 23 resuscitated comatose acs-ohca patients and 20 resuscitated comatose sah-ohca patients. st-t abnormalities on the ecg suggesting myocardial damage were noted in most patients in both groups (95% in the acs-ohca and 85% in sah-ohca), yet reciprocal st depression was significantly more often absent in the sah-ohca group. moreover, pulseless electrical activity (pea) or asystole as the initial cardiac rhythm, female gender, and preserved left ventricular ejection fraction were 367 cardiac dysfunction evoked by ecg and echocardiography changes and release of cardiac biomarkers significantly more common in the sah-ohca group. in their group, initial pea/asystole and presence of 1 other factor was sufficient to differentiate between sah and acs-ohca patients (100% sensitivity, 91% specificity, 95% accuracy). almost all the 16 case reports also point to the possibility of sah masquerading as an acs (23-36). one of them presents the scenario of sah with the pattern of sinus node dysfunction on the ecg (37), while elsharkawy et al., on a cohort of 20 sah patients observed that patients with fluctuating ecg changes had a poor outcome compared with patients with fixed abnormalities (38). troponin and nt-probnp elevation in a retrospective review of 617 patients with asah conducted by ahmadian et al. (13), 14.1% (87 patients) required a cardiac evaluation: 63% had arrhythmia, 47% suffered a myocardial infarction and 31% developed heart failure. the majority of cases with a myocardial infarction (90.2%) were nonst elevation mi, while atrial fibrillation was the most common form of tachyarrhythmia described. among the patients who had a cardiac event at the time of a sah, those with myocardial infarction, and in particular those with a troponin level greater than 1 mcg/l had a 10 times higher risk of death. oras et al. (11), in a single-centre prospective observational study including 126 sah patients, managed to conclude that both peak levels of troponin (hstnt in their study) and nt-probnp are independently associated with cerebral infarction due to delayed cerebral ischemia. hstnt had its peak level at admission followed by a daily decline; by contrast, nt-probnp had lowest levels on day 1 after sah and increased on days 2 to 4. moreover, age, poor neurological status upon admission, cerebral infarction and peak hstnt were independently associated with poor late outcome. the area under the curve (auc) for the first 4 days was used by nyberg et al. (39) to quantitatively measure the bnp load during the first critical part of the disease in 138 patients with a sah. a more severe sah defined by a higher fisher and world of neurosurgical societies grade, neurological deficits, an aneurysm, infections or higher levels of troponin i at admission had a larger auc for nt-probnp. women, older people and those with poor outcomes also had larger auc for nt-probnp. terao et al. (40) investigated the relationship between urinary albumin/creatinine ratio (acr), ntprobnp level and neurological outcome after sah in 61 patients. nt-probnp highest levels were above normal limits in 93% patients, while 85% of them developed microalbuminuria. the study demonstrated on the one hand that the peak value of nt-probnp was significantly associated with peak troponini value and highest acr. on the other hand, peak acr and hunt-hess grade were independent predictors of poor neurological outcome. neurogenic myocardial stunning prunet et al (3)(41) evaluated cardiac glucose metabolism and myocardial perfusion and assessed the duration and reversibility of cardiac sympathetic impairment after sah in 30 hemodynamically stable acute phase sah patients, by using ffluorodesoxyglucose positron emission tomography (18f-fdgpet), 99mtc-tetrofosmin and 123i-metaiodobenzylguanidine (123i-mibg). 83% revealed initial impairment of cardiac glucose metabolism and the defect pattern could not be explained by a single coronary artery distribution, while 90% exhibited initial impairment of cardiac sympathetic innervation. all patients had normal myocardial perfusion and normal left ventricular systolic function. there was a concordance of 123i-mibg and 18f-fdg uptake abnormalities, as well as a common temporal evolution, which suggests the close relationship between myocardial sympathetic function and glucose metabolism; yet neither of them produced left ventricular systolic or diastolic dysfunction in this group of patients (41). in a group of 300 ash patients, malik et al. (42) tried to determine the risk factors for the occurrence of neurogenic stress cardiomyopathy (nsc), which they defined as having at least one of the following: ecg changes (long oq, t wave inversions), troponin level higher than 0.1 or decreased ejection fraction and wall motion abnormalities on the echocardiogram. after a multivariate analysis, they concluded that higher hunt-hess grade on admission, smoking, older age and lack of hypertension were the strongest predictors of nsc. in a larger group of 715 sah patients, bihorac et al. (43), aimed to compare shortand long-term outcomes in patients with different patterns of regional left ventricular dysfunction (rlvd) as a manifestation of stress-induced cardiomyopathy 368 raluca ungureanu, mihai dumitru, gabriel iacob after sah. 28% (200 patients) of these patients had an echocardiogram for clinical evidence of cardiac dysfunction, 30% of whom (59 patients) had rlvd. the observation was that the risk of death was significantly higher in patients who need an echocardiogram in the first place, regardless of the presence or absence of rlvd on that echocardiogram. conclusion sah should probably be the most feared type of stroke event among clinicians. on the one hand, it affects younger adults and individuals in their prime, therefore the individual disability burden and consequential social impact is devastating. on the other hand, sah is a multisystem disease, and medical complications have been identified as factors that can contribute to worse outcomes, thereby awareness of this fact is warranted. cardiac abnormalities are common after sah, even in non coronary-disease patients. clinically significant arrhythmias after sah are associated with a high mortality rate, as well as serious cardiac and neurological comorbidities[17]. these patients should be submitted to a close cardiac monitoring. some patients (20-30%) present with acute cardiac enzyme elevation, and an increase in troponin i, which occurs in more severe patients, correlates with poor long-term outcome. increased levels of troponin, but also nt-probnp, upon admission are both independently associated with delayed cerebral ischemia (11)(12). troponin i and nt-probnp elevation should therefore be early detected and closely monitored and those patients timely managed by a multidisciplinary team of doctors (44). we should also bear in mind the fact that cardiac alterations associated with sah include both systolic and diastolic dysfunction of the left ventricle, and that, in order to prevent pulmonary and other organ congestion due to heart dysfunction, it is strongly advised to perform echocardiography on admission of a sah patient, and to repeatedly monitor this way a patient with sah and rlvd during the triple h therapy (2)(14)(34)(36). for comatose ohca resuscitated patients, initial ed evaluation might be sufficient to differentiate between an acs or a sah as the cause of the cardiac arrest, prior to further, time consuming tests (22). references 1. okabe et al. cardiovascular protection to improve clinical outcomes after subarachnoid hemorrhage: is there a proven role?, neurocrit care 2013, 18, 271-284 2. salem r. et al. subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study, critical care 2014, 18, 558 3. prunet et al. impairment of cardiac metabolism and sympathetic innervation after aneurysmal subarachnoid hemorrhage: a nuclear medicine imaging study, critical care 2014, 18, r131 4. macdonald et al. understanding the disease: aneurysmal subarachnoid hemorrhage. intensive care med 2014, 40, 1940-1943 5. inamasu et al. effect of insular injury on autonomic functions in patients with ruptured middle cerebral artery aneurysms, stroke 2013, 44, 3550-3552 6. huang et al. comparison of cerebral-cardiac syndrome caused by nonaneurysmal or aneurysmal hemorrhage, eur rev med pharmacol sci, 2014; 18, 3737-3742 7. kim et al. sudden neurological death masquerading as out-of-hospital sudden cardiac death, neurology, 2016; 87, 1669-1673 8. krishnamoorthy et al. cardiac dysfunction after neurologic injury. what do we know and where are we going? chest 2016; 149(5), 1325-1331 9. manea et al. brain-heart axis – review article. journal of medicine and life, 2015; 8, 266-271 10. ibrahim et al. electrocardiographic changes predict angiographic vasospasm after aneurysmal subarachnoid hemorrhage, stroke, 2012; 43, 2102-2107 11. oras et al. elevated high-sensitive troponin t on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study, critical care, 2016; 20:11 12. oras et al. high-sensitive troponin t and n-terminal pro b-type natriuretic peptide for early detection of stressinduced cardiomyopathy in patients with subarachnoid hemorrhage, neurocrit care, 2015: 23, 233-242 13. ahmadian et al. cardiac manifestations of subarachnoid hemorrhage, heart, lung and vessels, 2013; 5(3), 168-178 14. kumai et al. differences between takotsubo cardiomyopathy and reverse takotsubo cardiomyopathy associated with subarachnoid hemorrhage, ijc heart & vasculature, 2016; 11, 99-103 15. huang et al. the 12-lead electrocardiogram in patients with subarachnoid hemorrhage: early risk prognostication, american journal of emergency medicine, 2012; 30,732736 16. juntilla et al. repolarization abnormalities in patients with subarachnoid and intracerebral hemorrhage: predisposing factors and association with outcome, anesth analg., 2013; 116, 190-197 17. jeong et al. clinically significant cardiac arrhythmia in patients with aneurysmal subarachnoid hemorrhage, j cerebrovasc endovasc neurosurg, 2012; 14(2), 90-94 369 cardiac dysfunction evoked by ecg and echocardiography changes and release of cardiac biomarkers 18. july et al. cortisol dynamics are associated with electrocardiographic abnormalities following the aneurysmal subarachnoid hemorrhage, j cardiovasc dis res., 2012; 3(4), 315-318 19. amin et al. qtc interval prolongation and hemorrhagic stroke: any difference between acute spontaneous intracerebral hemorrhage and acute non-traumatic subarachnoid hemorrhage?, med arch, 2017; 71(3), 193197 20. schmidt et al. prolonged elevated heart rate is a risk factor for adverse cardiac events and poor outcome after subarachnoid hemorrhage, neurocrit care, 2014; 20(3), 390-398 21. crago et al. cardiac abnormalities after aneurysmal subarachnoid hemorrhage: effects of β-blockers and angiotesin-converting enzyme inhibitors, am j crit care, 2014; 23(1), 30-39 22. yamashina et al. differentiating between comatose patients resuscitated from acute coronary syndromeassociated and subarachnoid hemorrhage-associated outof-hospital cardiac arrest, journal of cardiology, 2015; 65, 508-513 23. tan et al. concurrent subarachnoid haemorrhage and st elevation myocardial infarction, jrsm open, 2017; 8(2), 1-3 24. lewandowski p. subarachnoid haemorrhage imitating acute coronary syndrome as a cause of out-of-hospital cardiac arrest – case report, anaesthesiol intensive ther, 2014; 46(4), 289-292 25. al-zaiti et al. ecg changes during neurologic injury, am j crit care, 2015; 24, 453-454 26. delelis et al. subarachnoid haemorrhage mimicking acute myocardial infarction, bmj case reports, 2012 27. patel et al. the ischaemic ecg: is it all in the head?, bmj case rep, 2013 28. king c. listening to the head and not to the heart: subarachnoid haemorrhage associated with severe acute left ventricular failure, bmj case rep, 2013 29. park et al. subarachnoid hemorrhage mimicking stsegment elevation myocardial infarction after return of spontaneous circulation, clin exp med, 2015; 2(4), 260-263 30. chen h. angiographic coronary spasm in a case of spontaneous subarachnoid hemorrhage mimicking acute myocardial infarction, cardiol resp, 2013; 4(2), 74-77 31. pothiawala s. spontaneous subarachnoid hemorrhage as a differential diagnosis of pre-hospital cardiac arrest, indian j crit care med, 2012; 16, 216-218 32. heo et al. subarachnoid hemorrhage misdiagnosed as an acute st elevation myocardial infarction, korean circ j, 2012; 42(3), 216-219 33. hatim et al. a case of subarachnoid hemorrhage revealed by an acute coronary syndrome, pan afr med j, 2015; 20, 426 34. shimada et al. takotsubo cardiomyopathy secondary to intracranial hemorrhage. int j emerg med, 2014; 7, 33 35. koklu et al. subarachnoid hemorrhage that electrocardiographically mimics acute coronary syndrome: a case report, turk kardiyol dern ars, 2015; 43(8), 730-733 36. shoukat et al. cardiomyopathy with inverted tako-tsubo pattern in a series of subarachnoid hemorrhage: a series of four cases, neurocrit care, 2013; 18, 257-260 37. bisht et al. warning leak of intracranial aneurysm masquerading as sinus node dysfunction: a case report, sage open med case rep, 2015 38. elsharkawy et al. fluctuating electrocardiographic changes predict poor outcomes after acute subarachnoid hemorrhage, ochsner journal, 2016; 16, 225-229 39. nyberg et al. predictors of increased cumulative serum levels of the n-terminal prohormone of brain natriuretic peptide 4 days after acute spontaneous subarachnoid hemorrhage, j neurosurg, 2014; 120, 599-604 40. terao et al. an observational study of the association between microalbuminuria and increased n-terminal prob-type natriuretic peptide in patients with subarachnoid hemorrhage, journal of intensive care, 2015; 3, 42 41. papanikolaou et al. the role of nuclear cardiac imaging in redefining neurogenic stunned myocardium in subarachnoid hemorrhage: a deeper look into the heart, critical care, 2014; 18, 490 42. malik et al. neurogenic stress cardiomyopathy after aneurysmal subarachnoid hemorrhage, world neurosurg, 2015; 83(6), 880-885 43. bihorac et al. long-term outcomes for different forms of stress cardiomyopathy after surgical treatment for subarachnoid hemorrhage, anesth analg, 2016; 122(5), 1594-1602 44. mavridis et al. troponin elevation in subarachnoid hemorrhage, journal of acute disease, 2015; 4(1), 7-11. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0066 article when the disease is known but the patient is not. outcome of 118 such patients at a tertiary care centre gaurav jaiswal, praveen kumar tripathi, vardan kulshreshtha, tarun kumar gupta india      romanian neurosurgery (2018) xxxii 3: 505 512 | 505             doi: 10.2478/romneu-2018-0066 when the disease is known but the patient is not. outcome of 118 such patients at a tertiary care centre gaurav jaiswal, praveen kumar tripathi, vardan kulshreshtha, tarun kumar gupta department of neurosurgery, r.n.t medical college, udaipur, rajasthan, india abstract: this is a prospective study, carried out at the department of neurosurgery at m.b.g hospital, r.n.t medical college, udaipur, rajasthan (india). many patients with history of trauma with head injury, whose identity cannot be ascertained, are admitted in our hospital. the management of these unattended patients from pre-hospital till discharge, rehabilitation or death is full of difficulties especially when surgical intervention has to be done. from march 16, 2015, until march 30, 2016, 118 consecutive patients unattended patients admitted in our department with history of head injury were enrolled in the study. out of 118 patients, 107 (91%) were male, most were in the age group of 30-39 years. in majority of patients, 115 (97%) principal cause of head injury was road traffic accident. majority of the patients 49 (41%) had glasgow coma scale >13 on admission. twenty three patients 23 (20%) died in hospital, 71 (60%) patients had good recovery. during the course of treatment identity of 115 patients was established and 92 (78%) patients, who survived were discharged to home. three (3%) patients were shifted to destitute home. all discharged patients were followed at 1 month and 6 month interval. 78 (82%) & 76 (80%) patients showed good recovery (gos) at 1 month & 6 month respectively. one patient expired at home within one month of discharge and 6 patients lost to follow up at 6 months. key words: anonymous patient; head injury; nameless patient; outcome; unknown patients; unidentified patient introduction the total number of deaths in road accidents in india was 169107 during 2014 (1). the incidence of road traffic accident in rajasthan in 2014 was 24639 and out of which the total number of deaths in road accidents in rajasthan was 10287 during 2014 (1), which was 6.08% of the total number of deaths in road accidents in india during the year1. in india, the incidence of head injury is steadily increasing with urbanization and increasing number of vehicular population (2). among 506 | jaiswal et al when the disease is known but the patient is not             the road traffic accidents 70% have head injury, among road accident deaths 70% are due to head injury. majority of deaths occur during first 72 hours. recently, number of fatal accidents has increased in india. every minute there is an accident and every eight minute there is a death (3). attempts to systematize care of patients with severe tbi have culminated in evidence-based guidelines issued by the joint task force between the brain trauma foundation and the american association of neurological surgeons (4,5). our institute which is a tertiary care centre of a developing country and a lot of severe head injury patients are being referred to us. many such patients are often brought by policemen and bystanders and their identities are not known at the time of admission. these patients present a unique challenge in management. in this backdrop we prospectively studied demography, mode of injury, presentation, treatment, outcome and factors affecting outcome in this group of patients. methodology this was a prospective study, conducted at department of neurosurgery, maharana bhupal government hospital, rnt medical college, udaipur, rajasthan. from march 16, 2015, until march 30, 2016, 118 consecutive patients unattended patients admitted in our department with history of head injury were enrolled in the study. note was made regarding demography, mode of injury, clinical presentation, and condition at admission, treatment given, hospital stay and outcome of the patients. all patients were clinically evaluated by a team comprising of doctors from surgical, medical and orthopaedics specialties in the emergency department and subsequently admitted and treated in neurosurgery unit. plain ct scan head along with other imaging (if needed) like x-rays, ct scan of spine, usg abdomen, mri spine or contrast ct (abdomen chest) were carried out to rule out other injuries. results out of 118 patients, 107 (91%) were male, and 11 (09%) were female (table 1). only one patient was less than 20 yrs of age, while the most patients 46 (39%) were in the age group of 30-39 years. 12 (10%) patients were > 60 years of age group (table 2). road traffic accident was the major cause of injury in 115 (97%) cases. at the time of admission glasgow coma scale (gcs) score of less than 8 was seen in 33 (28%) cases. gcs of 8-12 was seen in 36 (31%) cases. plain ct scan of head revealed edh in 12 (10%) patients, 28 (24 %) had sdh, 20 (17%) had cerebral contusions, 09 (08%) had sah, 04 (03%) had diffuse axonal injury, 01 (01%) patient had depressed fracture while in 44 (37%) patients no abnormality was found on imaging (table 3). associated injuries were seen in total 64 (54%) patients. 30 patients (25%) had chest injury, 12 (10%) had limb fractures, 20 (17%) had maxillofacial injuries and only two had abdominal injuries. only 11 patients needed neurosurgical intervention where decompressive craniectomy was carried out in 6 (5%), craniotomy was in 4 patients (3%), 1 patient (1%) underwent depressed facture elevation romanian neurosurgery (2018) xxxii 3: 505 512 | 507             (table 4). during treatment, 20 patients (17%) had chest complications, 9 (8%) had wound infection, 4 patients developed meningitis (table 5). at the time of discharge, 81 patients (68%) had gcs of 13-15 and eight (07 %) had gcs score 12-8, only 4 patients had gcs less than 8 at time of discharge. according to glasgow outcome scale (gos) of these patients, 71 (60%) had good recovery, 11 (09%) had moderate disability, 8 (07%) had severe disability, 05 (04%) remained vegetative and 23 (20%) died during treatment. during the course of treatment identity of 110 (93%) patients could be identified and 92 (78%) patients who survived were sent home with relatives, 3 (03%) patients who remained unidentified were sent to destitute home. all patients who were discharged followed at 1 month and 6 month intervals. 78 (82%) & 76 (81%) patients showed good recovery (gos) at 1 month & 6 month respectively, 1 patient died at home. 6 of the discharged patients lost to follow up at 6 months. table 1 demography (gender wise) of head injury in unknown patients admitted in neurosurgery: (n=118) demography (gender) no. of patients(n-118) percentage male female 107 11 91 9 total 118 100 table 2 demography of head injury in unknown patients admitted in neurosurgery: (n=118) demography no. of patients(n-118) percentage mean age(years) age group <20 1 1 20-29 28 23 30-39 46 39 40-49 22 19 50-59 9 8 >60 12 10 total 118 100   508 | jaiswal et al when the disease is known but the patient is not             table 3 clinical characteristic and type of lesions in head injury of unknown patients: (n=118) cause of head injury number of patients (118) percentage road traffic accident other (fall from train) 115 3 97 3 glasgow coma scale at admission 13-15 12-8 <8 49 36 33 41 31 28 type of brain injury (major component) extradural haematoma (edh) subdural haematoma(sdh) cerebral contusion depressed fracture diffuse axonal injury(dai) subarachnoid haemorrhage(sah) no observable abnormality on imaging 12 28 20 01 04 09 44 10 24 17 01 03 08 37 other injuries chest injury abdominal injury limb fracture maxillofacial 30 02 12 20 25 02 10 17 other emergency surgical speciality procedure icd insertion in 20 patients 17 table 4 surgical procedures performed (n=11) types of treatment/ surgery no. of patients (11 of 118) percentage decompressive craniectomy craniotomy depressed fracture elevation burr hole evacuation 6 4 1 05 03 01 total 11 09   romanian neurosurgery (2018) xxxii 3: 505 512 | 509             table 5 complications during treatment of the patients (n-118) complications no. of patients percentage pneumonia meningitis septicemia wound infection csf leak hydrocephalus 20 04 09 17 03 08 total 33 28 table 6 outcome and destination of patients during discharge (n=118) outcome no. of patients (118) percentage glasgow outcome scale good recovery moderate disability severe disability vegetative state death 71 11 08 05 23 60 09 07 04 20 glasgow coma scale at discharge 13-15 8-12 < 8 81 08 04 68 07 03 discharged location home destitute home 92 03 78 03 table 7 outcome during follow up of patients after discharge (n-95) outcome (glasgow outcome scale) after 1 month n=95 after 6 month n=94 good recovery moderate disability severe disability vegetative state death 78 05 07 04 01 76 04 04 04 00 lost to follow 0 06 510 | jaiswal et al when the disease is known but the patient is not             discussion in a study by ahmad et al (6), out of 325 unidentified patients, there were 9 (3%) patients in the paediatric age group and 16 (5%) patients were above 60 years of age. of these, 193 (65%) could be identified during the hospital stay. an additional 40 (13%) patients were sent home after they regained memory of their addresses. forty seven patients (15%) died without their identities being established. seventeen (6%) patients remained unknown and were sent to rehabilitation/poor homes with the help medical social worker: all pediatric patients were identified (6). in study of wanger et al, they reported approximately one third of patients with moderate head injury and half of patients with severe head injury were operated, most of them being for cerebral contusions and/or subdural hematomas7. mortality following head injury has been reported to be in the range of 39-51% (8, 9). study by liew bs et al. showed both known and unknown head injury patients, among 72 patients of head injury eleven patients (15%) died during hospitalization. there were only sixty one (85%) patients were discharged from hospital, where by twenty nine (40%) with good outcome (gos 4 and 5) while the remaining thirty two (44%) patients were with either severe disability or vegetative state. only one patient continued to suffer severe disability, while the rest had moderate or good recovery (10). in another study there were twelve patients (17%) under the age of twenty years, only 5 patients (7%) were above 60 years. twenty patients (29%) were treated by surgery, most often for cerebral contusion (33 patients, 47%) (11). till date no prospective study has been conducted to assess outcome of such unidentified patients who underwent neurosurgical procedures. in our study 118 patients were treated of which 11 patients needed surgical intervention where decompressive craniectomy was carried out in 6 (54%), craniotomy was in 4 (37%), one patient (9%) underwent depressed fracture elevation. remaining107 (91%) patients were treated conservatively. among these patients, 71 patients (60%) had good recovery, 11 patients (09%) had moderate disability, 8 patients (07%) had severe disability, 5 patients (04%) remained vegetative and 23 patients (20%) died during treatment. during the course of treatment identity of 110 (93%) patients could be identified and 92 (78%) patients who survived were sent home with relatives, 3 (03%) patients who remained unidentified were sent to destitute home. these unidentified patients with unknown identities present considerable challenges in their management. they are usually found lying on road in unconscious state and brought to hospital by policemen or bypassers who are ill equipped and often ignorant in handling patients with severe injuries. their prehospital management is usually improper and lack of proper transfer facilities, in ambulances, further aggravates their condition. we receive many such patients from peripheral hospitals, because of lack of proper facilities there. very often such patients are destitute and their injuries are compounded by presence of debility because romanian neurosurgery (2018) xxxii 3: 505 512 | 511             of poor nutrition, other medical conditions like diabetes, hypertension, substance abuse and mental illnesses. therefore, it is imperative that these patients be evaluated with a very high index of suspicion for above conditions. during their hospital stay, the role of paramedical staff is of paramount importance; their daily nursing care in absence of a relative is a challenging task. it needs a team of trained and empathetic nursing staff along with a physiotherapist, dietician, psychologist, and social worker who can help and rehabilitate them. performing neurosurgical procedures in such patients is not devoid of difficulties ranging from consent to rehabilitation. existing infrastructure and much trained staff, enthusiastic multidisciplinary team, social workers and media personnel help many unidentified patients with severe head injury in rehabilitation. it is highly gratifying for the treating team to see such patients return back to our outpatient department with their relatives. we believe that there is an urgent need to sensitize the general public and police about the transportation and prehospital management of such severe head injury patients. our peripheral hospitals need to be well equipped for treatment of such patients. treatment of such unknown patients can entail a huge expenditure and therefore, every hospital should allocate funds for the above purpose and only those patients who are in need of higher medical care should be referred to higher centre. the role of social media and general media also has a capacitive role in spreading awareness and rehabilitating unidentified patients. conclusion management of unidentified head injury patients are posed with challenges. like other patients initial management is of vital importance. outcome of these patients is comparable to patients who are accompanied by their relatives. their management from prehospital to treatment and discharge from hospital is quite challenging especially, when patient requires operative interventions, in icu and meeting nutritional standards. there mean hospital stay and icu stay is sometimes longer in comparison to similar patients as they may remain unidentified. they need special care for which staff should be well trained and hospital must have economic resources. hospital should have a protocol system to deal with such patients especially when they require neurosurgical interventions. a good network of social workers and active involvement of media helps in identification and rehabilitation of these patients. correspondence dr. gaurav jaiswal, associate professor, department of neurosurgery, rnt medical college, udaipur (rajasthan) e-mail: drgauravjaiswal@gmail.com references 1.http://ncrb.gov.in/statpublications/adsi/adsi2014/c hapter-1a%20traffic%20accidents.pdf 2.report of road safety cell: ministry of transport govt of india, january 1993. 3.head injuries: a neglected field in india. national medical journal 1991; 4:53-44. 4.guidelines for the management of severe head injury. the brain trauma foundation. the american association of neurological surgeons, the joint section 512 | jaiswal et al when the disease is known but the patient is not             on neurotrauma and critical care. j neurotrauma. 1996;11:641–734. 5.the brain trauma foundation. the american association of neurosurgical surgeons. the joint section on neurotraumaand critical care. trauma systems. j neurotrauma. 2000;17:457–627. 6.ahmad fu, mahapatra ak, mehta vs. outcome of unknown head injury patients at a tertiary care neurosurgical centre: neurology india 2006; 54:73-4. 7.wanger ak, sessere hc, hammond fm, et al. international traumatic brain injury: epidemiology and risk factors associated with severity and mortality. j trauma 2000; 49:404-10. 8.lannoo e, van rietvelde f, colardyn f, et al. early predictors of mortality and morbidity after severe closed head injury. j neurotrauma 2000;17:403-14. 9.bulger em, nathens ab, rivara fp, et al. brain trauma foundation: management of severe head injury: institutional variations in care and effect on outcome. crit care med 2002; 30:1870-6. 10.liew bs, johari sa, nasser aw, abdullah j. severe traumatic brain injury: outcome in patients with diffuse axonal injury managed conservatively in hospital sultanah aminah, johor bahruan observational study. med j malaysia 2009; 64: 280-8. 11.outcome of head injury in unknown patients at level1 apex trauma centre nath, haradhan deb et al. the indian journal of neurotrauma , volume 8 , issue 1 , 11 – 15. doi: 10.33962/roneuro-2022-049 factors associated with success of trial spinal cord stimulation in patients with chronic pain. preliminary data on the prognostic value of standardized healthrelated scales in a clinical practice setting eleonora grande, marco ciavarro, beatrice cioni, tommaso tufo romanian neurosurgery (2022) xxxvi (3): pp. 289-295 doi: 10.33962/roneuro-2022-049 www.journals.lapub.co.uk/index.php/roneurosurgery factors associated with success of trial spinal cord stimulation in patients with chronic pain. preliminary data on the prognostic value of standardized healthrelated scales in a clinical practice setting eleonora grande1, marco ciavarro2, beatrice cioni1┼, tommaso tufo1,3 1 neurosurgery institute, department of neuroscience, policlinico a. gemelli foundation university hospital i.r.c.c.s., catholic university, rome, italy 2 i.r.c.c.s. neuromed– pozzilli (is), italy 3 neurosurgery unit, fakeeh university hospital, dubai, uae abstract objective: spinal cord stimulation (scs) is a widely employed technique in treating chronic pain, however, it still fails in significantly reducing pain in one-out-of-three cases. poor consensus exists on the most predictive factors of scs outcomes. although psychological criteria such as emotional stability are recommended for this treatment, it is not well understood if the perception of patients’ own health may impact the scs success. therefore, we retrospectively examine factors associated with the patient's subjective conditions, to investigate their relationship with scs success. methods: before the implantation of an scs trial per routine clinical decision-making, and independently from the implanted devices, patients treated in our clinical practice underwent an extensive evaluation of pain, disability, depression and the overall quality of life. in those patients with successful scs trials, the pain level was also evaluated at the end of the trial period. regression analyses were performed to investigate factors predicting successful trial stimulation. results: successful trial stimulation was effective in 15 patients (75%). perceived disability, pain and general health resulted as independent predictive factors on scs trial outcome. further investigation showed perceived disability (i.e. oswestry disability index) as a crucial factor, and roc curve analysis identifies a cut-off of 38 as a predictive score of success. conclusions: although preliminary, these findings suggest that standardized scales examining the overall patients’ perceived health status, particularly the disability index may help shed light on predicting scs trial success. thus, it is argued the potential application of self-administered scales in scs patients’ selection in routine clinical practice. keywords pain, psychological assessment, questionnaire, spinal cord stimulation corresponding author: marco ciavarro i.r.c.c.s. neuromed, pozzilli (is), italy marcociavarro.nch@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 290 eleonora grande, marco ciavarro, beatrice cioni, tommaso tufo introduction chronic pain is a debilitating condition that has a significant impact on patients’ quality of life (qol). the treatment of chronic pain is still challenging, involving many disciplines, including physical and psychological therapies, as well as pharmacological and surgical treatments [1]. since its introduction in the last half-century [2], spinal cord stimulation (scs) has been a reliable treatment for chronic pain conditions, with no pharmacological assumption. although scs can reduce pain symptoms up to 70% with a significant improvement in qol, some clinical features expose at the risk of scs failure [3]. for example, psychiatric comorbidities, older age, longer pain duration prior to intervention, are all predictive of poorer outcome [4]. interestingly, psychological factors are assumed to be essential for the efficacy of scs. in the light of this consideration, it is worth noting that there is a strong association between pain and depression, and the latter has often been suggested as a possible impacting factor on scs efficacy [5,6]. moreover, pain catastrophizing has been described to adversely affect pain-coping behavior and the overall prognosis in susceptible individuals when challenging with painful conditions [7,8]. those evidences have been confirmed in a research examining whether carefully screening patients could predict pain-related and functional outcomes, highlighting that presurgical psychological factors including somatization, depression, anxiety, and poor coping were most predictive of poor response to scs [9]. in this scenario, it appears crucial to better understand those features that may lead to poor scs outcomes. often, the disease-specific scale might not reflect the patient’s functional outcome [10], not capturing the patients’ self-perception of disability, as well as more general aspect of wellbeing and mental health. at the same time, there is to date no “gold standard” in psychological or health-quality related tests for the assessment of scs outcome. based on the aforementioned theoretical hypothesis, the study aim was to investigate the influence of patients’ self-perception of pain and disability, health related qol and depression on the success of scs trial stimulation in a representative case series, to identify those factors that may be more prone to play a role in shaping negative outcomes after scs trial and, therefore, to drive clinical decision-making on scs permanent placement. methods participants to investigate factors associated with successful trial stimulation, the medical records of 20 patients were reviewed. each of the patients underwent to the implantation of scs electrodes at our institution (from march 2017 to november 2019) to treat different chronic pain conditions. review of clinical variables, duration of pain and the score of standardized, self-administered questionnaires were investigated. the entire sample gave informed consent at the time of the hospitalization, and the appraisal was managed in accordance with the clinical practice. participation in the study is completely voluntary and patients could withdraw from the study at any moment, for any reason, without providing any justification. the whole procedures were conducted according to the principles expressed in the helsinki declaration. the mean age of patients (14 f) was 60.00±15.0 (mean ± standard deviation). the sample’s demographic data are summarized in table 1. features total trial group n=20 success group n=15 failure group n=5 gender f:m (%) 14 (70%): 6 (30%) 12 (80%): 3 (20%) 2 (40%): 3 (60%) age, years (mean ± sd) 60 15 5915 6215 years since diagnosis (mean ± sd) 6.30 5.71 6.93 6.40 4.40  2.30 fbss/radiculopathy/forami nal stenosis 13 11 2 lower limbs neuropathy 3 3 chronic pelvic pain 2 1 1 herpetic neuralgia 1 1 ulnar neuropathy 1 1 baseline vas, cm (mean±sd) 8.3  0.9 8.6  0.8 7.7  1.2 table 1. demographic and clinical data demographic and clinical data of patients who underwent scs trial, including pain data etiology and vas evaluation. the inclusion criteria involved eligibility to scs trial, independently from stimulation frequencies and surgical management. patients must be refractory to previous medical treatments, including analgesics, opioid analgesics, physical therapy, and pain blocks. the exclusion criteria were to not complete the 291 factors associated with success of trial spinal cord stimulation questionnaires or reporting a vas score measured at baseline lower than 6/10. patients were randomly assigned to four different stimulation paradigms during the trial period: i) traditional tonic stimulation, intellis scs trial (medtronic inc, minneapolis, mn, usa); ii) burst stimulation, burstdr, (abbott, texas, tx usa); iii) high-density (hd) stimulation, the st. jude medical invisible trial system (abbott, texas, tx usa); iv) high frequency (hf) stimulation, senza system (nevro corp., california, ca, usa). questionnaire as part of the assessment, an extended preoperative evaluation of health related qol was collected using self-administered, standardized questionnaires to investigate pain, disability, global qol and depression. we acquired pain measures through vas [11,12] before the surgery and at the end of the trial period on those patients who reached scs trial success. the test battery includes: pain catastrophizing scale (pcs), an instrument derived from the definitions of catastrophizing described in the literature [13] and items from the catastrophizing subscale of the coping strategies questionnaire (csq) [14]. it allows the evaluation of the patients’ mentalization of pain through three subscales, helplessness, magnification and rumination; the oswestry disability index (odi) was included in the battery [15], it is a tool able to assess the level of pain interference with various activities of daily living. indeed, it has been recommended to measure painrelated disability when considering areas other than and including low back pain [16,17]; a generic healthrelated qol assessment, euroqol five-dimensional questionnaire (eq-5d-3l), was administered, to better understand how pain impacts everyday life globally. the questionnaire evaluates the five dimensions of mobility, self-care, pain, anxiety, and activities of daily living [18]; the 36-item short form survey (sf-36) [19] was collected: an overall healthrelated qol measure extensively used to discriminate, evaluate, and predict outcomes in several health and pathologic conditions [20]; the hamilton rating scale for depression (ham-d) was included in the survey [21], due to the relevance of depressive symptoms on pain perception and on the scs success rate. stimulation management a percutaneous lead with eight contacts was placed under direct fluoroscopic guidance in the epidural space. the correct position was determined using intra-operative stimulation and was deemed successful if the induced paraesthesia had an adequate overlap with the painful area. after the surgery, the patients were randomly assigned to one of the four arms (in a 1:1:1:1: ratio), where they received a one-month combination of tonic, hd, hf and burst stimulation including one treatment modality per week and varying the order of the modality received within the four possible combinations. we used different types of adapters to connect the same provisory lead extension with the various trial stimulators. the length of the trial period was 39±18 days. at the end of the trial, patients were classified into two groups, success and failure group. each patient in the success group decided to proceed to the permanent implantation of the device that showed the highest delta vas score, calculated as the difference between baseline vas and vas with any of the four devices tested. statistical analysis we analysed the following factors: age, sex, duration of pain and the validated scales scores. the significant difference between vas scores was evaluated through the friedman test. univariate analysis was performed to investigate the presence and the strength of any predictor factor on the trial outcome to identify those factors to be included in the logistic regression analysis. then, the generalised linear model (glm) was developed. receiver operating characteristic (roc) curve analysis was performed to identify the best cut-off of the most significant predictor variable specified with the previous analysis. all statistical analysis has been completed with r core team 2020 software (r foundation for statistical computing, vienna, austria. url https://www.r-project.org/). results successful trial stimulation was reached in 15 out of 20 patients (75%). no significant differences at vas score were registered among the four devices, whereas a significant reduction (p<0.05) in the vas score compared to baseline vas was observed in the whole success group, fig. 1. 292 eleonora grande, marco ciavarro, beatrice cioni, tommaso tufo figure 1. preoperative vas (baseline) and vas distribution for each device tested to investigate those factors associated with the success of trial stimulation, data were fit into a logistic regression model to verify whether any of the scores of the variables collected preoperatively correlated with the trial stimulation outcome. all the data are summarized in table 2. significan ce beta p-value sse vas baseline borderlin e 0.0811 85% degree of pain duration (years) no 0.401 eq-5d-3l no 0.915 ham-d no 0.8087 odi borderlin e -0.1772 0.08 44.3% pcs no 0.914 pcs subscale pain helplessness no 0.970 pcs subscale pain rumination no 0.287 pcs subscale pain magnification yes -0.7292 0.0308 69.1% sf-36 physical functioning no 0.2620 sf-36 physical role limitations no 0.1734 sf-36 bodily pain no 0.4491 sf-36 general health perceptions borderlin e 0.0567 0.0598 74% sf-36 energy/vitality no 0.573 sf-36 social functioning no 0.589 sf-36 emotional role limitation no 0.2420 sf-36 mental health no 0.804 table 2. logistic regression logistic regression analysis on independent variables collected at baseline as predictor variables of trial outcome. sse: summary squares error. univariate analysis revealed that four of the analyzed independent factors were associated with the trial stimulation outcome. therefore, we developed a glm named “comprehensive model”, which included odi, pain magnification subscale, general health subscale of sf-36 and preoperative vas (model sse 34.77%). however, the anova test on the comprehensive model revealed that the deviance explained by general health and preoperative vas were not statistically significant (p=0.959 and p=0.299, respectively). therefore, we removed these two variables from the model and generated a simpler model, named pmo model, which included only two variables, i.e., the pain magnification and odi (model sse 39.9%). the equation of the pmo model is as follows with β1 = -0.49853 as estimated parameter of the pain magnification predictor variable and β2= -0.14349 as the estimated parameter of the odi predictor variable and α =6.27127: 𝜂 = 𝛼 + 𝛽1 × (𝑃𝑎𝑖𝑛 𝑀𝑎𝑔𝑛𝑖𝑓𝑖𝑐𝑎𝑡𝑖𝑜𝑛 𝑆𝑐𝑜𝑟𝑒) + 𝛽2 × (𝑂𝐷𝐼 𝑆𝑐𝑜𝑟𝑒) 𝑃(𝑇𝑟𝑖𝑎𝑙 𝑓𝑎𝑖𝑙𝑢𝑟𝑒) = 𝑒𝜂 1 + 𝑒𝜂 to further reduce the complexity of the model, we developed a univariate parsimonious predictive model based only on the odi variable (model sse 44.3%). the equation of the odi model is as follows with 𝛽1 = -0.1772 as estimated parameter of odi predictor variable and 𝛼 = 5.4513: 𝜂 = 𝛼 + 𝛽1 × (𝑂𝐷𝐼) 𝑃(𝑇𝑟𝑖𝑎𝑙 𝑓𝑎𝑖𝑙𝑢𝑟𝑒) = 𝑒𝜂 1 + 𝑒𝜂 = 𝑒𝛼+𝛽1×(𝑂𝐷𝐼) 1 + 𝑒𝛼+𝛽1×(𝑂𝐷𝐼) 𝑃(𝑇𝑟𝑖𝑎𝑙 𝑓𝑎𝑖𝑙𝑢𝑟𝑒) = 𝑒5.4513−0.1772×(𝑂𝐷𝐼) 1 + 𝑒5.4513−0.1772×(𝑂𝐷𝐼) the predicted probability of trial failure based on the univariate odi model is reported in table 3. in the “minimal disability” category (odi ≤20), the predicted probability of the trial failure increases drastically, while in the “severe disability” category (odi ≥60) it is strongly avoided. therefore, to confirm the correlation estimated by the odi model and identify the odi best cut-off that shows the greatest correlation with the trial outcome, we developed a roc curve analysis that 293 factors associated with success of trial spinal cord stimulation revealed that a odi score of 38 is the best cut-off with the highest accuracy or optimal sensitivity (100%) and specificity (85.7%) in our case series. hence, highest odi scores (i.e., worse disability perception) are associated with higher scs trial success. odi 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 p (failure) .996 .99 .975 .942 .871 .735 .534 .321 .163 .074 .032 .013 .006 .002 .001 0 table 3. odi score predicted efficacy on scs trial predicted probability of trial failure based on the univariate odi model. discussion scs is a reliable technique in treating chronic pain, improving patients qol and with a low rate of complications [6]. nevertheless, the heterogeneity of patients and their symptomatology makes it often difficult to establish which patients are eligible for this treatment. indeed, many conditions may expose to the risk of no scs success in reducing pain [22]. psychosocial factors such as dysfunctional coping, poor daily activity level and psychological distress are considered relevant for scs selection [23]. to this purpose, when patients are determined to be eligible and potential candidates for scs, a psychological assessment, including subjective pain intensity, mood and personality, daily activity interference, pain beliefs and coping, is required to help identify the ideal patient to achieve maximum benefit from an implanted device [24-26]. however, the interaction of clinical and psychosocial factors in determining the eligibility of patients with chronic pain to scs implantation has led to a lack of clarity in selection criteria, and often poor consistency among surgical centers [23]. patients typically undergo a trial stimulation to determine scs efficacy and drive clinical judgment regarding appropriateness for permanent implantation. overall, many factors are likely to play a role in shaping pain outcomes of scs, nevertheless, no consensus exists on what factors are most consistently predictive of these outcomes. reliable data are still missing and the available guidelines [2729], due to the great heterogeneity of patients, are quite clear in their recommendations [30-34]. beyond non-modifiable risk-factor of nonsuccess, such as older age or long pain duration [32], it is crucial to better understand how psychological conditions may play a role in the scs efficacy in pain reduction, to maximize patients’ qol [35]. to identify any predictive factors associated with the success of scs trial stimulation, we evaluate, in a cohort of patients treated at our institution, the preoperative patients’ self-perception of pain and disability, as well as more global aspect of wellbeing, including qol and mental health scale. in line with the literature data [32], the 75% of the sample reached a successful scs trial, with a significant postoperative reduction in the pain level measured through vas. therefore, based on the preoperative data on the self-administered questionnaire, we design a predictive model on scs trial outcome. it came out that the degree of perceived pain (vas) and the general health score of sf36 questionnaire, both measured at baseline, seem to play a marginally significant role in the scs trial success in our representative case series. interestingly, the analysis also identifies the pain magnification scale as a predictor of scs success. this result is not surprising, due to the role of pain catastrophizing in negatively affecting pain-coping behavior [7,8]. however, considering that pain mentalization may have divergent impact on other dimension of qol, and depressed mood [36], investigating the unique contributions of each pcs subscales could be crucial to predict the therapies success rate. here emerged that the idea “that something serious may happen”, associated to pain magnification, mainly could lead to a poor efficacy of scs trial. furthermore, the patients’ self-perception of disability, measured through odi scale, results to be the strongest predictor of scs trial success in our model. this result shows the role of patients’ daily abilities level in affecting scs outcome and identify the odi score of 38 as the best cut-off in predicting scs success, with optimal sensitivity and high specificity. that is, moderate or severe disability is related to grater scs success. in other words, scs may be more efficient on those patients with a worse 294 eleonora grande, marco ciavarro, beatrice cioni, tommaso tufo perception of their functional status related to the pain. this result could be seen in term of greater reward with respect to pain relief in those patients with a higher degree of perceived disability compared to those with a preserved functional status, in which the degree of pain reduction could be weaker. although the patients’ mental health, such as depression or psychological distress, is thought to have a major influence on the scs success, our results suggest the importance to take into account even the patients’ own perception of their functional status in the routinely scs eligibility evaluation. not secondarily, the odi scale is a self-administered scale, fast and easy to collect, that do not require clinical judgment and may be easily implemented in the clinical practice. taken together these evidences suggests the crucial importance of an extensive evaluation on patients’ candidates for scs with a multidisciplinary model of care and aims at proposing the adoption of self-administered scales in the routine clinical assessment as a good tool in investigating the patients’ perception of health quality, overcoming the more disease-specific aspects of clinical evaluations. although further research is needed to clarify the role of self-reported scales in a larger cohort of patients and though the impact of several subjective determinants on scs outcome is still unclear and these factors are still rarely studied, our preliminary data highlight that pain and disability perception may become routinely measures when evaluating consensus to scs implantation. beyond the undoubtful limitation of our study is the reduced sample size, the main advantage is the heterogeneity of the sample, being representative of patients’ profiles in a clinical setting, so it is considered to be the environment best suited for developing a predictive model, taking into account the great heterogeneity in scs treatments. our preliminary data suggest that pain and disability perception may become routinely measures when evaluating consensus to scs implantation. the self-administered scale, fast and easy to collect, may help predicting scs trial success and may drive clinicians’ consensus to permanent implantation. references 1. ashburn ma, staats ps. management of chronic pain. lancet. may 29;353(9167):1865-9, 1999. 2. jensen mp, brownstone rm. mechanisms of spinal cord stimulation for the treatment of pain: still in the dark after 50 years. european journal of pain. 23(4), 652–659, 2019. 3. bernstein ca. spinal cord stimulation for chronic pain, 2006. 4. taylor rs, desai mj, rigoard p. predictors of pain relief following spinal cord stimulation in chronic back and leg pain and failed back surgery syndrome: a systematic review and meta-regression analysis. pain pract.14:489– 505, 2014. 5. whitehurst dgt, engel l, bryan s. short form health surveys and related variants in spinal cord injury research: a systematic review. j spinal cord med. 37: 128138, 2014. 6. burchiel kj, anderson vc, wilson bj, denison db, olson ka, shatin d. prognostic factors of spinal cord stimulation for chronic back and leg pain. neurosurgery. 36:1101– 1110, 1995. 7. ruchinskas r, o’grady t. psychological variables predict decisions regarding implantation of a spinal cord stimulator. neuromodulation. 3:183–189, 2000. 8. dansie e j, turk dc. assessment of patients with chronic pain. br j anaesth. 111:19-25, 2013. 9. celestin j, edwards rr, jamison rn. pretreatment psychosocial variables as predictors of outcomes following lumbar surgery and spinal cord stimulation: a systematic review and literature synthesis. pain med. 10:639–653, 2009. 10. guirado vm, taricco ma, nobre mr, couto eb jr, ribas es, meluzzi a, brock rs, dias mr, rodrigues r, teixeira mj. quality of life in adult intradural primary spinal tumors: 36-item short form health survey correlation with mccormick and aminoff-logue scales. j neurosurg spine. 19(6):721-35, 2013. 11. lee ck, hansen ht, weiss ab. developmental lumbar spinal stenosis. pathology and surgical treatment. spine (phila pa 1976). 3:246–55, 1978. 12. mccormack hm, horne dj, sheather s. clinical applications of visual analogue scales: a critical review. psychol med. 18:1007-1019, 1988. 13. sullivan mjl, bishop sr. the pain catastrophizing scale: development and validation. psychological assessment. 7:524-532, 1995. 14. hirsh at, george sz, riley jl, robinson me. an evaluation of the measurement of pain catastrophizing by the coping strategies questionnaire. eur j pain. 11:75-8, 2007. 15. fairbank jc, pynsent pb. the oswestry disability index. spine (phila pa 1976). 25:2940-2952, 2000. 16. mcdowell i. measuring health: a guide to rating scales and questionnaires. oxford university press, new york, 1996. 295 factors associated with success of trial spinal cord stimulation 17. davidson m, keating jl. a comparison of five low back disability questionnaires: reliability and responsiveness. phys ther. 82:8-24, 2002. 18. balestroni g, bertolotti g. l'euroqol-5d (eq-5d): uno strumento per la misura della qualità della vita (euroqol5d (eq-5d): an instrument for measuring quality of life). monaldi arch chest dis. sep;78(3):155-9, 2012. 19. apolone g, mosconi p. the italian sf-36 health survey: translation, validation and norming. j clin epidemiol. nov;51(11):1025-36, 1998. 20. whitehurst d.g.t., engel l, bryan s. short form health surveys and related variants in spinal cord injury research: a systematic review. j spinal cord med. 37: 128138, 2014. 21. carrozzino d, patierno c, fava ga, guidi j. the hamilton rating scales for depression: a critical review of clinimetric properties of different versions. psychother psychosom. 89: 133-150, 2020. 22. sparkes e, raphael jh, duarte rv, lemarchand k, jackson c, ashford rl. a systematic literature review of psychological characteristics as determinants of outcome for spinal cord stimulation therapy. pain. 150:284-289, 2010. 23. thomson s, huygen f, prangnell s, de andrés j, baranidharan g, belaïd h, berry n, billet b, cooil j, de carolis g, demartini l, eldabe s, gatzinsky k, kallewaard jw, meier k, paroli m, stark a, winkelmüller m, stoevelaar h. . appropriate referral and selection of patients with chronic pain for spinal cord stimulation: european consensus recommendations and e-health tool. eur j pain. 24(6):1169-1181, 2020. 24. sullivan mj, rodgers wm, kirsch i. catastrophizing, depression and expectancies for pain and emotional distress. pain. 91:147-154, 2001. 25. ruchinskas r, o’grady t. psychological variables predict decisions regarding implantation of a spinal cord stimulator. neuromodulation. 3:183–189, 2000. 26. schocket kg, gatchel rj, stowell aw, deschner m, robinson r, lou l, whitworth t, bernstein d. a demonstration of a presurgical behavioural medicine evaluation for categorizing patients for implantable therapies: a preliminary study. neuromodulation. 11:237–248, 2008. 27. cruccu g, garcia-larrea l, hansson p, keindl m, lefaucheur jp, paulus w, taylor r, tronnier v, truini a, attal n. ean guidelines on neurostimulation therapy in chronic pain conditions. european journal of neurology, 23(10), 1489–1499, 2016. 28. dworkin, r. h., o’connor, a. b., kent, j., et al. interventional management of neuropathic pain: neupsig recommendations. pain, 154(11), 2249–2261, 2013. 29. national institute for health and clinical excellence. spinal cord stimulation for chronic pain of neuropathic or ischaemic origin. 2008. 30. sparkes e, raphael jh, duarte rv, lemarchand k, jackson c, ashford rl. a systematic literature review of psychological characteristics as determinants of outcome for spinal cord stimulation therapy. pain. 150:284-289, 2010. 31. sparkes e, duarte rv, mann s, lawrence tr, raphael jh. analysis of psychological characteristics impacting spinal cord stimulation treatment outcomes: a prospective assessment. pain physician. 18:e369-377, 2015. 32. de la cruz p, fama c, roth s, haller j, wilock m, lange s, pilitsis j. predictors of spinal cord stimulation success. neuromodulation. 18(7):599-602; discussion 602, 2015. 33. atkinson l, sundaraj sr, brooker c, o'callaghan j, teddy p, salmon j, semple t, majedi pm. recommendations for patient selection in spinal cord stimulation. j clin neurosci. 18:1295–1302, 2011. 34. sparkes e, duarte rv, raphael jh, denny e, ashford rl. qualitative exploration of psychological factors associated with spinal cord stimulation outcome. chronic illn. 8:239-251, 2012. 35. duarte rv, soliday n, leitner a, taylor rs. health-related qol associated with pain health states in spinal cord stimulation for chronic neuropathic pain. neuromodulation. 24: 142-149, 2021. 36. craner jr, gilliam wp, sperry ja. rumination, magnification, and helplessness: how do different aspects of pain catastrophizing relate to pain severity and functioning? clin j pain. 32(12):1028-1035, 2016. doi: 10.33962/roneuro-2021-027 visual outcome analysis in patients with posterior fossa tumours undergoing surgical treatment deepak kumar singh, vrihaspati kumar agrahari, mohd. kaif, rakesh kumar, kuldeep yadav romanian neurosurgery (2021) xxxv (2): pp. 174-179 doi: 10.33962/roneuro-2021-027 www.journals.lapub.co.uk/index.php/roneurosurgery visual outcome analysis in patients with posterior fossa tumours undergoing surgical treatment deepak kumar singh, vrihaspati kumar agrahari, mohd. kaif, rakesh kumar, kuldeep yadav department of neurosurgery, dr ram manohar lohia, institute of medical sciences, lucknow, india abstract background: in the past, there were studies done to assess visual outcomes like visual acuity, fundoscopic findings and visual field mainly in pediatric patients with posterior fossa tumours (pft). we assessed the above parameters preand postoperatively in all age group patients including both extra and intra-axial pft. we also assessed visual outcome in patients with or without hydrocephalus. objectives: to analyze “visual outcomes in patients with posterior fossa tumours undergoing surgical treatment”. the effect of hydrocephalus on the visual outcome was also analyzed. materials and methods: this prospective study including 107 patients with pft undergoing definitive surgery was conducted in the department of neurosurgery at dr rmlims, lucknow. pre-op and post-op (six weeks after tumour resection) visual examinations were done and compared. results: a shifting trend towards normalization of visual acuity (va) was seen postsurgery in all age groups. overall improvement was seen in the majority of cases having pupil normal size sluggish reactive (nssr) after surgery. papilledema improved in the majority of patients in all age groups and patients having hydrocephalus. colour vision and night vision also improved in the majority. the field of vision cut was not improved postoperatively in the majority. conclusion: visual parameters like visual acuity, pupil size and reactivity to light; colour vision and night vision were improved significantly after surgery whereas cut field of vision did not improve. all fundoscopic findings like papilledema, retinal venous dilation and retinal splinters haemorrhage disappeared in a significant number of patients post-operatively. in cases with obstructive hydrocephalus, these parameters also improved significantly after ventriculo-peritoneal shunt/ etv or definitive surgery. introduction posterior fossa tumors (pft) cause symptoms due to compression over brainstem, cerebellum and raised intracranial pressure (icp).[1,2,3,4] . this can lead to obstructive hydrocephalus and papilledema leading to secondary optic nerve atrophy and permanent vision loss. [5 ] hydrocephalus may cause abducens palsy leading esotropia, and keywords posterior fossa tumors, hydrocephalus, visual acuity, papilledema corresponding author: vrihaspati kumar agrahari department of neurosurgery, dr ram manohar lohia, institute of medical sciences, lucknow, india drvkagrahari2012@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 175 visual outcome analysis in patients with posterior fossa tumours undergoing surgical treatment horizontal diplopia. trochlear nerve palsy may cause vertical/oblique diplopia, with hypertropia. these tumors may disrupt visual fixation and vestibular and/or gaze-stabilization mechanisms, resulting nystagmus, skew deviation, and complex gaze palsies vth and viith nerve palsy may lead to corneal damage.[6] in children, cerebellar mutism may result after surgery.[7] specially pediatric pft with ophthalmic complications need more attention.[8] this study was done to prospectively analyze visual outcome after surgery in pft (extra-axial/intraaxial) patients in all age group. aims to analyze “visual outcomes in patients with posterior fossa tumors undergoing surgical treatment” and also to analyze the effect of hydrocephalus on the visual outcome. materials and methods this prospective study included 107 patients was conducted in the department of neurosurgery dr.rmlims lucknow. those patients presenting with symptoms of hydrocephalus underwent cerebrospinal fluid (csf) diversion procedure e.g. ventriculo-peritonial (vp) shunt/endoscopic third ventriculostomy (etv) as emergency procedure. inclusion criteria were pfts with or without hydrocephalus. exclusion criteria were patients with recurrent pft, visual and ocular motor dysfunction unrelated to their tumor, patients undergoing primary radiotherapy treatment, non-co-operative and not following commands. most common procedures performed for definitive surgery were retro-sigmoid sub-occipital craniotomy/craniectomy or midline suboccipital craniotomy/craniectomy with gross total resection or subtotal resection of tumor. pre-op and post-op (after six weeks of tumor resection) visual acuity on snellen chart, pupillary function (size, reactivity), color vision on ishihara test (present/absent), night vision (present /absent), visual field by confrontation test, fundoscopy, papilledema grade (modified frisen scale), retinal findings (venous dilatation and splinter hemorrhage present/absent) were examined. hydrocephalus (present/absent), csf diversion procedure in the form of vp shunt/etv done or not, were also examined. visual acuity outcomes of various age groups, extra-axial and intra-axial posterior fossa tumors and patients with or without hydrocephalus compared with wilcoxon signed-rank test. analysis was performed on stata software. results sample size was 107, out of which 3 patients died due to brainstem injury, infarction and edema. four cases lost follow up due to unknown reasons. total 100 patients were followed up to 6 months. 46 (46%) patients were found to be having extra-axial tumors and 54 (54%) intra-axial tumors (figure 1). total 20 (20%) patients having pfts were found in pediatric age (<20years) group, 70 (70%) patients in middle (20-50 years) age group and remaining 10 (10%) in old age group (>50 years). out of 100, 74 (74%) with obstructive hydrocephalus underwent vp shunt/etv in emergency. 28% 22% 12% 10% 8% 6% 6% 4% 2% 2% figure 1: pathological diagnosis cp angle vestibular schwannoma cerebellar pilocytic astrocytoma 4th ventricular ependymoma cp angle meningioma cerebellar medulloblastoma cerebellar hemangioblasto ma cp angle epidermoid tumours metastatic tumours posterior fossa arachnoid cyst brain stem glioma 176 deepak kumar singh, vrihaspati kumar agrahari, mohd. kaif et al. visual acuity was categorized arbitrarily as normal (6/6), good (6/9 to 6/12 in both eyes), moderate (6/18 to 6/60 in at least one eye), and poor (<6/60 in at least one eye) (table 1). using wilkoxan signed-rank test assessed va outcomes in patients with extra-axial, intra-axial tumor, with/without hydrocephalus and in different age group. s. no. visual acuity category pre-op post-op no. of cases % no. of cases % 1. normal vision (6/6) 48 48 66 66 2. good vision (6/9 to 6/12) 22 22 10 10 3. moderate vision (6/18 to 6/60) 12 12 10 10 4. poor vision (<6/60) 18 18 14 14 total 100 100 100 100 table 1. pre-op and post-op comparison of visual acuity. pupil size and reactivity measured as normal size of pupil and normal reactivity (nsnr), normal size sluggish reactive (nssr), normal size nonreactive (nsnor) and dialated pupil (figure.2) and outcome analysed. overall improvement was seen in majority of cases having pupil nssr post-surgery. out of 100, 26(26%) patients had impaired color vision on pre-op examination, which decreased to 10(10%) after surgery. total number of cases having normal color vision was increased to 90(90%) after surgery but remain impaired or absent in 10(10%) cases. (figure.3) total 72 (72%) patients were found to have normal night vision pre-operatively. patients having normal night vision were increased to 88(88%), after surgery. remaining 12(12%) patients did not improve even after surgery (figure 4). vision field by confrontation outcome is given in table 2. s. no. vision field pre-op post-op no. of cases percentage no. of cases percentage 1. intact 96 96 96 96 2. impaired 4 4 4 4 total 100 100 100 100 table 2. pre-op and post-op comparison of vision field by confrontation. nsnr nssr ns nonr dilated pupil non reactive pre-op (%) 78 18 4 0 post-op (%) 92 2 4 2 0 10 20 30 40 50 60 70 80 90 100 figure 2: pre-op and post-op comparison of pupil size & reactivity 0 20 40 60 80 100 intact impaired figure 3: pre-op and post-op comparison of color vision pre-op (%) post-op (%) 0 10 20 30 40 50 60 70 80 90 100 intact impaired figure 4: pre-op and post-op comparison of night vision pre-op (%) post-op (%) 177 visual outcome analysis in patients with posterior fossa tumours undergoing surgical treatment out of 100 patients, 30(30%) patients were found to have normal fundoscopic findings ( grade 0), which increased to 52(52%) on post op examination. grade iv papilledema was found in 14(14%) patients on preop examination which decreased to 8(8%) after surgery. total no of patients having grade iii papilledema was 28(28%) on pre-op examination which decreased to one after surgery(figure.5). likewise total number of patients with grade ii papilledema decreased post operatively. however in 12(12%) patients, either in one or in both eye, optic atrophy was seen on follow up examination. retinal venous dilation and splinter hemorrhage examined on fundoscopy and outcome given in figure 6 and 7 respectively. after surgery one case was complicated with iiird nerve palsy. discussion clinical profile and presentation: total 100 patients were followed up in this study out of which 20 (20%) patients having pfts were found in pediatric age (<20years) group, 70(70%) patients were in middle (20-50 years) age group and remaining 10(10%) patients were in the age group of >50 years. most common extra-axial tumor was cerebellopontine angle vestibular schwannoma whereas most common intraaxial tumor was cerebellar pilocytic astrocytoma. extra-axial tumors were diagnosed pathologically as cerebellopontine angle vestibular nerve schwannoma (28%) patients, cerebellopontine angle meningioma (10%) patients, cerebellopontine epidermoid tumors (6%) patients and posterior fossa arachnoid cyst (2%) patients. intra-axial tumors were diagnosed pathologically as cerebellar pilocytic astrocytoma (22%) and fourth ventricular ependymoma (12%) cerebellar medulloblastoma (8%) cerebellar hemangioblastoma (6%) cerebellar metastatic tumors (4%) and brainstem glioma in one patient (figure 1). most common symptoms were headache (80%), nausea or vomiting (69%), ataxia (61%), ophthalmologic symptoms (31%) hearing loss (28%) and other cranial nerve involvement. visual and oculomotor disturbance was the fourth most common symptoms (27%), which is similar to a study done by nisha gadgilet al. [8] patients with hydrocephalus (75%) underwent csf diversion procedure, either vp shunt or etv in emergency followed by definitive surgery. patients with persistent ophthalmological complications were consulted 6 weeks post-surgery. 0 10 20 30 40 50 60 grad e 0 grad e i grad e ii grad e iii grad e iv grad e v pre-op (%) 30 8 20 28 14 0 post-op (%) 52 24 14 2 8 0 figure 5: pre-op and post-op comparison of papilledema present absent pre-op(%) 62 38 post-op (%) 18 82 0 10 20 30 40 50 60 70 80 90 a x is t it le figure 6: pre-op and post-op comparison of retinal venous dilatation 62 38 18 82 present absent figure 7: pre-op and post-op comparison of splinter haemorrhage pre-op (%) post-op (%) 178 deepak kumar singh, vrihaspati kumar agrahari, mohd. kaif et al. visual acuity outcome: in our study 48% cases had normal vision (6/6) in both eyes pre-operatively which increased to 66% post surgery. poor visual acuity (<6/60) was observed in 18% patients in pre op examination, which decreased post-operatively to 14%. good visual (6/9 to 6/12) acuity was found in 22% patients pre-operatively, which decreased to 10% after surgery. the sum total of patients having normal visual acuity and good visual acuity was found to be 76% after surgery. likewise, total no of cases having moderate visual acuity (6/18 to 6/60) was also decreased from 12% to 10% post-surgery. over all shifting trend towards normalization of visual acuity was seen in majority, post-surgery. according to peeler et al (2017) va was good in 82.8%, fair in 9.8%, and poor in 7.4%. 9.4% cases had optic atrophy on follow up.[9] however, this study was done only in pediatric patients having pft. recently nisha gadgil et al (2018) concluded that 88% had good visual acuity; 5% had moderate and 5% had poor visual acuity. optic atrophy due to prior hydrocephalus was noted in 13% cases but this resulted in persistent loss of visual acuity only in 2% cases. [8] in those patients presenting with obstructive hydrocephalus, urgent neurosurgical intervention was needed to decrease intracranial pressure for saving vision. patients with poor visual acuity preoperatively, having long duration of raised icp improved little or none after surgery. the median pre-op visual acuity in patients with extra-axial tumors (6/9; iqr 6/6 – 6/12) was better than patients with intra-axial tumors (6/12; iqr 6/6 – fc at 1 mt), but statistically non-significant difference was observed with kw test (p=0.376). similarly, no statistical difference (p=0.182) was observed in the median post-op visual acuity in patients with extraaxial tumors (6/6; iqr 6/6 – 6/9) and patients with intra-axial tumors (6/6; iqr 6/6 – 6/36). wilcoxon signed-rank test revealed statistically significant improvement in visual acuity after surgery in extraaxial tumors (p=0.001) and intra-axial tumors (p=0.005). the median pre-op va in patients without pre-op hydrocephalus (6/6; iqr 6/6 – 6/6) was better than patients with pre-op hydrocephalus (6/12; iqr 6/6 – 6/60), and this difference in visual acuity was found to be statistically significant with kw test (p=0.000). similarly, statistically significant difference (p=0.004) was observed in the median post-op visual acuity in patients without pre-op hydrocephalus (6/6; iqr 6/6 – 6/6) and patients with pre-op hydrocephalus (6/6; iqr 6/6 – 6/24). wilcoxon signed-rank test revealed statistically significant improvement in visual acuity after surgery in patients with pre-op hydrocephalus (p=0.000) and patients without hydrocephalus already had normal median visual acuity. the median pre-op visual acuity in patients aged <20 yrs.’, 20 to <50 yrs.’ and ≥50 yrs.’ was 6/6 (iqr 6/6 – 6/12), 6/9 (iqr 6/6 – 6/60) and 6/24 (iqr 6/36 – 6/12), but this difference in visual acuity by age was found to be statistically nonsignificant with kw test (p=0.153). similarly, the median post-op visual acuity in patients aged <20 yrs.’, 20 to <50 yrs.’ and ≥50 yrs.’ was 6/6 (iqr 6/6 – 6/6), 6/6 (iqr 6/6 – 6/24) and 6/12 (iqr 6/6 – 6/12), and this difference in visual acuities by age too was found to be statistically nonsignificant with kw test (p=0.200). wilcoxon signedrank test revealed statistically significant improvement in visual acuity after surgery in patients of all age groups (‘p’ values for <20 yrs.’, 20 to <50 yrs.’ and ≥50 yrs.’ are 0.047, 0.001 and 0.046 respectively). pupil size and reactivity to light: on pre-op examination nsnr to light was found in 78% cases, which increased to 92% after surgery. nssr was seen in 18% cases pre-operatively, which decreased to 4% post surgery. however, 4% cases having nsnor did not improve even after surgery. one case with nsnor, complicated with third nerve palsy with dilated pupil (figure 2). color vision: 26% patients were found to be having impaired color vision on pre-op examination, which decreased to 10% after surgery. total no. of cases having normal color vision increased to 90% after surgery. in remaining 10% cases color vision was either impaired or absent even after surgery (figure 3). night vision: 72% patients were found to have normal night vision pre-operatively. after surgery, total number of patients having normal night vision increased to 88%. improvement was observed in majority of cases with impaired night vision (figure 4). vision field by confrontation: on pre-op examination 4% patients were found to have field vision cut, which did not improve even after surgery. 179 visual outcome analysis in patients with posterior fossa tumours undergoing surgical treatment all patients with field vision cut had visual acuity plve preoperatively. similarly field cut was observed in 2.7% patients in study done by nisha gadgil et al.[8] in our study defect in field vision was due to optic atrophy. the limitation of this study was inability to report on visual field outcomes in all pediatric patients, because quantitative subjective visual field testing could not consistently performed and better method of measurement of vision field like perimetery could not be done. papilledema: according to study done by m.s. girwan et al papilledema was observed in 94.2% in their experience. [10] in our study, on pre-op examination 30% patients were found to have normal fundoscopic findings (grade 0) while 70% patients were having papilledema (modified frisen scale). the number of patients having normal fundoscopic findings increased to 52% on post op examination. grade iv papilledema was found in 14% patients on pre-op examination which decreased to 8% on post op examination. total no of patients having grade iii papilledema was 28 (28%) on pre-op examination, which decreased to two after surgery. likewise total number of patients with grade ii papilledema decreased post operatively. the trends toward normalization were seen in majority of patients. however in 12(12%) patients, either in one or both eyes, optic atrophy was seen on follow up examinations (figure5). retinal venous dilation: on pre-op fundoscopic examination retinal venous dilation was seen in 62% cases, which decreased to 18% after surgery (figure 6). better outcome was observed in patients who underwent earlier neurosurgical intervention. splinter hemorrhage: total number of patients having retinal splinter hemorrhage was 62(62%), which decreased to 18(18%) after surgery. splinter hemorrhage disappeared in 44% patients after neurosurgical intervention (figure 7) conclusion conclusively, visual parameters like visual acuity, pupil size and reactivity to light; color vision and night vision were improved significantly after surgery whereas cut field of vision did not improve. significant improvement in the visual acuity and papilledema in patients with pre-op hydrocephalus, irrespective of extra or intra axial location of tumor, age group, were observed after surgery. other fundoscopic findings like retinal venous dilation and retinal splinters hemorrhage disappeared in significant number of patients post-operatively. references 1. badhe pb, chauhan pp, mehta nk. brainstem gliomas--a clinicopathological study of 45 cases with p53 immunohistochemistry. indian j cancer. 2004 octdec. 41(4): 170-4. 2. zhou lf, du g, mao y, zhang r. diagnosis and surgical treatment of brainstem hemangioblastomas. surg neurol. 2005 apr. 63(4):307-15; discussion 315-6. 3. wilne s, collier j, kennedy c, koller k, grundy r, walker d. presentation of childhood cns tumours: a systematic review and meta-analysis. lancet oncol. 2007 aug. 8(8): 685-95. 4. zabek m. primary posterior fossa tumours in adult patients. folia neuropathol. 2003. 41(4): 231-6. 5. ostrom qt, gittleman h, fulop j, et al. cbtrus statistical report: primary brain and central nervous system tumors diagnosed in theunited states in 2008-2012. neurooncol 2015; 17(suppl4): iv1-62. 6. miller nr, et.al. eds. walsh and hoyt's clinical neuroophthalmology, 6th ed. lippincott williams and wilkins 2005. pp 237-291 7. gadgil n, hansen d, barry j, chang r, lam s. posterior fossa syndrome in children following tumor resection: knowledge update. surgneurolint 2016; 7:s179–83; 2152-7806. 8. gadgil n, edmond j, stormes k, lam s, shah v. ocular outcomes in pediatric posterior fossa tumors pediatric neurology, 2018. s0887-8994 (18): 30815-4. 9. peeler ce. a review of visual and oculomotor outcomes in children with posterior fossa tumors. seminpediatrneurol 2017; 24:100–3. 10. griwas ms, sharma bs, mahajan rk, kak vk. value of precraniotomy shunts in children with posterior fossa tumours. child’s nervsyst 1993; 9:4626. 11. cassidy l, stirling r, may k, picton s, doran r. ophthalmic complications of childhood medulloblastoma. med pediatroncol 2000; 34:43–7. doi: 10.33962/roneuro-2023-034 role of extent of resection on the survival of glioblastoma multiforme. a monocentric retrospective study dipak chaulagain, volodymyr smolanka, andriy smolanka, taras havryliv romanian neurosurgery (2023) xxxvii (2): pp. 190-197 doi: 10.33962/roneuro-2023-034 www.journals.lapub.co.uk/index.php/roneurosurgery role of extent of resection on the survival of glioblastoma multiforme. a monocentric retrospective study dipak chaulagain, volodymyr smolanka, andriy smolanka, taras havryliv regional clinical centre of neurosurgery and neurology, uzhhord national university, uzhhorod, ukraine abstract background. glioblastoma multiforme (gbm) is the most prevalent form of brain cancer. the effect of extent of resection (eor) on gbm survival is controversial. eor degree, preand postoperative tumour volume estimation, and significance to residual tumour volume are still challenged. gbm has a 14-month overall survival (os) rate. there is no evidence of a link between eor and os survival. we wish to determine whether gbm tumour removal increases survival. methods. at the regional center for neurosurgery and neurology in uzhhorod, ukraine, we conducted a retrospective evaluation of 86 consecutive patients diagnosed with glioblastoma who underwent surgery between january 1, 2010, and december 31, 2020, and who are being followed until january 1, 2022. patients were selected if they met the following criteria: they were at least 18 years old, they had a diagnosis of glioblastoma (primary, secondary, or recurrent), they were either idh mutants or wild types, they had an mri within 2 weeks before surgery, and they had another mri within 72 hours after surgery. before and after surgery, we did a volumetric analysis of gadolinium-enhanced t1 mri scans of the tumour to figure out eor. partial resection (pr) is <70%, sub-total resection (str) is 70-90%, near-total resection (ntr) is 91-99%, and gross total resection (gtr) is >99%. by comparing pre and post-operative volumes with the eor, the kaplan-meier survival curve and cox's regression analysis determined the impact of the eor on survival rates. many researchers considered a p value of 0.05 or below to be significant. results. a total of 86 patients were included in the analysis after being subjected to the criteria used to narrow the pool of potential participants. the average length of time people lived was 15 months. for pr patients, the median survival time was 3 months, for str patients it was 10 months, and for ntr patients it was 16 months. patients receiving gtr, on the other hand, had a considerably better outcome, with a median survival time of 36 months. this data demonstrate a direct correlation between eor and survival rates. it was discovered that eor improvement affected post-op survival. high eor patients have a better prognosis for survival. adjuvant therapy, preand post-operative kps score, preand post-operative tumour volume, and gender also contributed significantly to enhanced survival. conclusion. patients with glioblastoma appear to benefit from a more aggressive treatment strategy that combines maximal safe resection with the use of salvage adjuvant therapy. there was a correlation between complete resection (gross total resection) of intracranial gbm and improved survival. whenever feasible, complete surgical removal of the tumour is recommended. keywords glioma, gbm, extent of resection, glioblastoma multiforme corresponding author: dipak chaulagain regional clinical centre of neurosurgery and neurology, uzhhord national university, uzhhorod, ukraine neurodipak@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 191 role of extent of resection on the survival of glioblastoma multiforme introduction glioblastoma multiforme (gbm) is the most common malignant primary brain tumor in adults [1]. there is currently no agreed-upon drug, surgery, or radiation therapy regimen for treating gbm [2]. the surgical component of treatment may consist of anything from a craniotomy to a minimally invasive biopsy (gtr). however, not all patients have a radical resection [3], despite improvements in 5-aminolevulinic acidguided intraoperative procedures that increase the eor that can be achieved during surgery. large retrospective cohort studies in the field of neurooncology have shown better survival with greater eor in patients with a newly diagnosed gbm, and mathematical modeling of retrospective data implies incremental gains in survival with eors ranging from 78% to 98% [4,5]. the current set of known predictive markers for glioblastoma includes age, preoperative health performance status, tumor resection, and postoperative adjuvant therapy [6-9]. it is challenging to achieve entire excision of tumors despite evidence that it can improve overall survival (os) [10,11,12] because to the risk of neurologic function deficiencies such as paralysis, aphasia, and others, which can reduce quality of life and finally limit longevity. however, reaching this goal of gtr can be challenging due to the peculiarities of brain anatomy and the fear of damaging expressive structures, lowering life quality. pathologic and radiologic investigations show that gbm often invades multiple lobes and both hemispheres at diagnosis [13-16]. age, [17] preoperative performance status according to the kps,[18] tumor location,[19] and preoperative mr imaging characteristics of the tumor,[20] and whether radiation therapy or chemotherapy is delivered affect a patient's prognosis after being diagnosed with gbm. due to the interconnectedness of these characteristics, a multivariate analysis is required to identify the influence of surgical resection on survival and the subset of patients for whom extensive resection is most advantageous. we wanted to establish if surgical resection, as assessed by preoperative and postoperative tumor volumes, has predictive significance and to examine survival durations in defined patient subpopulations in relation to tumor resection. finding out what aspects of life are connected to eor was the driving force behind this research. time-to-event analysis is a useful tool for studying gbm patients, but it should only be used when the confounders have been properly addressed. patients and methods materials and methods: the uzhhorod regional center of neurosurgery and neurology cared for 120 patients diagnosed with gbm between 2010 and 2020. for this statistical analysis, we did not include 86 individuals who had been lost to follow-up, had insufficient information, or were younger than 18 years old. eighty-six patients' medical records were examined in retrospect. the patients who participated in our study broke down as follows: 55 men (63.95 percent), with a mean age of 52.76, and 31 women (36.05 percent), with a mean age of 50.32. our inclusion criteria meant that these patients' records met our minimum standards for inclusion, thus we used them in our analysis. we performed surgery on adults diagnosed with gbm (astrocytoma, grade iv, as determined by histopathology). results were tracked until january 2022. patients were enrolled if a full clinical dossier was available, including information about the patient's background, current condition, previous medical history, radiographic results, surgical specifics, tumor features, and pathology reports. diagnosis and follow-up all patients were judged to have the potential for headache and other regional neurological abnormalities. all patients who met these criteria underwent a preoperative mri with and without gadolinium. no surgical patient was allowed to wait longer than 72 hours before undergoing an mri scan. patients were followed for a median of 36 months (range: 2-144 months) after hospital discharge. all patients were followed up with serial mri scans. moreover, data on postoperative quality of life and recurrence was gathered via telephone interviews, clinical examinations, and imaging. the aberrant mass was initially revealed by a t1weighted magnetic resonance imaging scan, and a resection biopsy was used to confirm the diagnosis, as previously described in the medical literature. independent neuroradiologists evaluated preoperative t1 contrast-enhanced mri sequences 192 dipak chaulagain, volodymyr smolanka, andriy smolanka et al. to quantify tumor volume. using t1 contrastenhanced images in the axial (a), sagittal (b), and coronal planes, the tumor's maximum diameters were measured, and the tumor's volume was then computed using the volumetric approach, as v = (axbxc/2) cm3. within 72 hours of the procedure, we took a second mri scan (post-operative) and used the same volumetric method as before to determine the post-operative volume. patients who underwent follow-up mri were monitored for recurrence, clinical symptoms, and mortality through january 2022. family members, phone calls, and messages were used to verify all deaths. data management and analysis the size of the tumor before surgery (x) was divided into four groups: 1) less than 20 cm3, 2) between 20 and 50 cm3, 3) between 51 and 100 cm3, and 4) greater than 100 cm3, while the size of the tumor after surgery (y) was divided into groups ranging from 1 to 10 cm3, 20 to 50 cm3, and 51 to 100 cm3. the eor was calculated using the volume before and after surgery (x-y/x*100%). after obtaining eor% once more, we categorized our data as follows: 1) gross total resection (gtr), 2) near complete resection (ntr), 3) sub-total resection (str), 4) partial resection (pr), and 5) biopsy for outcomes with eor% of 70% or lower. our study focused primarily on how long patients lived after surgery. the data allowed us to conduct a kaplan-meier analysis of survival for gbm patients, with survival time measured in months post-op and separated into groups based on the percentage of endotracheal intubation used (eor). we used a log-rank test to determine the effect of eor percentage on survival, and we used cox regression analysis models to determine the effect of preand post-op volumes on median survival time. results when strict inclusion criteria were applied, only 86 patients were considered for further study. for the population as a whole, the median survival time was 15 months. those diagnosed with pr lived an average of 3 months longer than those diagnosed with str or ntr, while those diagnosed with ntr lived 16 months longer than those diagnosed with pr. but patients who had gtr had a much better outcome, with a median survival time of 36 months. it reveals that there is a linear link between survival and eor. longevity post-operation was observed to be affected by an increase in eor. high eor predicts a higher life expectancy for patients. survival outcomes kaplan-meier analysis with eor the kaplan-meier test was used to compare the median post-operative survival times of patients in each eor group. the significance level for the log rank test was high (x2 (4) = 118.03, p .001). (table 1). it demonstrates that there is a statistically significant variation in death rates among eor categories. patients who had biopsy had a median survival time of 12 months after surgery. patients with an eor of 70% or lower had a median survival duration of 3 months. with an eor of 70-90%, patients had a median survival period of 10 months after surgery. patients with 91-99% eor levels have a median survival time of 16 months following surgery. however, for those with an eor of >99%, the median time to death is 36 months (table 2). it shows that there is a linear relationship between survival and eor. increase in eor was found to have an influence on the time of survival since operation (fig 1). patients with high eor are more likely to survive longer. figure 1. kaplan-meier survival graph with eor as factor variable for gbm table 1. log rank test for eor and survival for gbm overall comparisons chi-square df sig. log rank (mantel-cox) 118.032 4 .000 test of equality of survival distributions for the different levels of eor %. 193 role of extent of resection on the survival of glioblastoma multiforme table 2. median survival time based on eor levels for gbm eor % median estimate std. error 95% confidence interval lower bound upper bound biopsy 12.000 . . . <70 3.000 .359 2.297 3.703 70-90 10.000 .926 8.185 11.815 91-99 16.000 1.583 12.897 19.103 >99 36.000 2.416 31.265 40.735 overall 15.000 1.274 12.503 17.497 cox regression with pre-op tumour cox regression indicated that there is a significant impact of pre-op tumor volume on survival time of patients as omnibus test was significant (χ2 (3) = 20.444, p < .001) (table 3). the results also indicated that patients with pre-op tumor volume of >100 were approximately 7.7 times more likely to die compared to those having pre-op tumor volume of <20 (b = 2.041, se = .536, wald (1) = 14.502, odds ratio = 7.699, p < .001) (table 4) (fig 2-3). table 3. omnibus test for pre-op volume and survival for gbm omnibus tests of model coefficientsb step -2 log likelihood overall (score) change from previous step change from previous block chi-square df sig. chisquare df sig. chisquare df sig. 1a 479.921 20.444 3 .000 10.861 3 .013 10.861 3 .013 a. variable(s) entered at step number 1: pre-op volume b. beginning block number 1. method = forward stepwise (conditional lr) table 4. coefficients for pre-op volume and survival for gbm sheet variables in the equation b se wald df sig. exp(b) 95.0% ci for exp(b) lower upper step 1 pre-op volume 15.522 3 .001 pre-op volume(1) .081 .300 .073 1 .787 1.084 .602 1.954 pre-op volume(2) .330 .316 1.088 1 .297 1.391 .748 2.584 pre-op volume(3) 2.041 .536 14.502 1 .000 7.699 2.693 22.012 cox regression with post-op tumor the results indicated that there is a significant impact of post-op tumor volume on survival of patients as omnibus test was significant (χ2 (3) = 41.181, p < .001) (table 5). patients with post-op tumor volume of 10.1-50 are 6.7 times more likely to die than those with post-op tumor volume of 0 (b = 1.908, se = .564, wald (1) = 11.456, odds ratio = 6.737, p < .001) (table 6). similarly, patients with post-op tumor volume of 50.1-100 are approximately 36 times more likely to die compared to those who had 0 post-op tumor (b = 3.579, se = .926, wald (1) = 14.946, odds ratio = 35.841, p < .001) (fig 4-5). figure 2. survival graph for pre-op volume for gbm figure 3. hazard graph for pre-op volume for gbm table 5. omnibus test for post-op volume and survival for gbm omnibus tests of model coefficientsb step -2 log likeliho od overall (score) change from previous step change from previous block chisquare df sig. chisquare df sig. chisquare df sig. 1a 470.384 41.181 3 .000 20.398 3 .000 20.398 3 .000 a. variable(s) entered at step number 1: post-op volume b. beginning block number 1. method = forward stepwise (conditional lr) table 6. coefficients for post-op volume and survival for gbm variables in the equation b se wald df sig. exp(b) 95.0% ci for exp(b) lower upper step 1 post-op volume 27.508 3 .000 post-op volume(1) .521 .470 1.229 1 .268 1.684 .670 4.232 194 dipak chaulagain, volodymyr smolanka, andriy smolanka et al. post-op volume(2) 1.908 .564 11.456 1 .001 6.737 2.232 20.332 post-op volume(3) 3.579 .926 14.946 1 .000 35.841 5.839 220.003 figure 4. survival graph for post-op volume for gbm figure 5. hazard graph for post-op volume for gbm) discussion in our study, we reported the median survival time following excision of a glioblastoma multiforme. our analysis also shows that the size of the surgical resection affects post-operative survival rates. surprisingly, both the preand post-tumor volume were linked to the median survival time following surgery. the eor has been demonstrated to be a significant survival predictor [23-27]. total tumor resection rates for gbm, an infiltrative tumor, have been reported to be between 17.4% and 40% [27, 28]. multiple variables affect eor in practice, although no proof has been documented in the literature. most studies relying on volumetric evaluation conclude that extensive surgical resection is linked to increased survival rates for high-grade gliomas [28,29]. total resection was also substantially correlated with a tumor volume of 30 ml in gbm. tumors that are less massive are easier to operate on [29,30]. brain edema and midline displacement were found to be substantially linked with the size of the gbm, and both adversely affected the extent to which the tumor could be removed. in addition, the prognostic factor most strongly linked to complete resection in gbm was a tumor volume of 30 ml or less. surgery is easier to do on smaller tumors than on larger ones [31,32]. brain edema and midline displacement were found to be strongly linked with the size of the gbm and to have a direct impact on the extent to which the tumor could be resected in this investigation [33]. in our data, we found that patients with post-op tumor volume of 10.1-50 cm3 are 6.7 times more likely to die than those with post-op tumor volume of 0 cm3. similarly, patients with post-op tumor volume of 50.1-100 cm3 are approximately 36 times more likely to die compared to those who had 0 cm3 postop tumor we discovered that a substantially higher likelihood of survival was associated with an eor of 98%. this agrees with the findings of a comprehensive study on the volumetric tumor assessment of 416 gbm patients, conducted by lacroix et al. at md anderson cancer center in 2001 [34]. in a study of 92 patients with gbm, keles et al. [35] analyzed how eor affected survival. among the 5 "percent of resection" groups studied, those with a 100% eor had a median survival time of 93 weeks, whereas those with a 75%-99% eor had a median survival time of 88.5 weeks. the median survival time is just 62.9 weeks, based on an eor of 50-74%. in a review of the literature, sanai and berger (2008) contrasted studies that did and did not measure tumor volume (highand low-grade gliomas). a total of 25 trials supported the idea of maximum eor, while 13 did not show a clear preference for either resection group [36]. mcgirt et al. [37] did a retrospective analysis with a large group of 1215 patients who had malignant glioma. in this study, resections were put into one of three groups based on mris taken soon after surgery: near-total resection (ntr), subtotal resection (str), or gross-total resection (gtr). after a gbm primary tumor was removed, the average survival time was 11 months for gtr, 9 months for ntr, and 5 months for str. this was linked to gtr vs. ntr and ntr vs. str. but in our data, 86 patients 195 role of extent of resection on the survival of glioblastoma multiforme were considered for further study. for the population as a whole, the median survival time was 15 months. those diagnosed with pr lived an average of 3 months longer than those diagnosed with str or ntr, while those diagnosed with ntr lived 16 months longer than those diagnosed with pr. but patients who had gtr had a much better outcome, with a median survival time of 36 months. it reveals that there is a linear link between survival and eor. adjuvant therapies, such as chemotherapy and radiation, have a significant impact on patient survival, progression-free survival, and overall survival [38-41], and should be included in the standard of care for gbm patients alongside surgical treatment modalities. with a focus on the svz and high-dose proton beam treatment, matsuda et al. [42] found that patients with newly diagnosed gbm who had gtr had a median overall survival of 36.9 months, compared to 26.2 months for patients who got standard radiation therapy. kaplan-meier estimates from our sample agree with those from the literature that link eor and survival. according to sanai et al. [43], we saw survival improve linearly with eor. full resection should be pursued whenever possible because of the survival data reported here and the evidence supporting the need of optimizing eor to prolong survival in glioblastoma patients. these promising findings highlight the need to maximize resection with cutting-edge techniques; future study should focus on gbm microenvironment and, if needed, surgery and despite the difficulty of treating gbm, the latter should not be ignored. conclusions removing 99% or more of a glioblastoma multiforme (gbm) tumor is associated with improved survival, according to volumetric analyses. we advise a grosstotal resection for these patients whenever possible, but never at the expense of their ability to think and move normally. the primary objective of surgical treatment for gbm should be gtr with an emphasis on cerebral function preservation, as an eor 99% has been found to greatly enhance patient survival. small preand post-operative tumor volume considerably increases survival, as does an eor of 99%. patients with glioblastomas now use eor as a prediction of survival, therefore it's important to learn what factors influence surgical success. references 1. stupp r, mason wp, van den bent mj, et al.; european organisation for research and treatment of cancer brain tumor and radiotherapy groups; national cancer institute of canada clinical trials group. radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. n engl j med 2005;352(10):987–996. 2. sanai n, polley m-y, mcdermott mw, parsa at, berger ms. an extent of resection threshold for newly diagnosed glioblastomas. j neurosurg 2011; 115(1):3–8. 3. aldave g, tejada s, pay e, et al. prognostic value of residual fluorescent tissue in glioblastoma patients after gross total resection in 5-aminolevulinic acid–guided surgery. neurosurgery 2013;72(6):915–920. 4. lacroix m, abi-said d, fourney dr, et al. a multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. j neurosurg 2001;95(2): 190–198. 5. sanai n, mirzadeh z, polley m-y, berger ms. the value of glioblastoma extent of resection: a volumetric analysis of 500 patients. j neurosurg 2010;113(2):a433 6. chaichana kl, jusue-torres i, navarroramirez r, raza sm, pascual-gallego m, ibrahim a, et al. establishing percent resection and residual volume thresholds affecting survival and recurrence for patients with newly diagnosed intracranial glioblastoma. neuro oncol. 2014;16: 113-122. 7. pang bc, wan wh, lee ck, khu kj, ng wh. the role of surgery in high-grade glioma: is surgical resection justified? a review of the current knowledge. ann acad med singapore. 2007;36: 358-363. 8. stupp r, mason wp, van den bent mj, weller m, fisher b, taphoorn mj, et al. radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. n engl j med. 2005;352:987-996. 9. stupp r, hegi me, mason wp, van den bent mj, taphoorn mj, janzer rc, et al. effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase iii study: 5year analysis of the eortc-ncic trial. lancet oncol. 2009;10:459-466. 10. d’amico rs, englander zk, canoll p, bruce jn. extent of resection in glioma: a review of the cutting edge. world neurosurg. 2017;103:538-549. 11. yan jl, van der hoorn a, larkin tj, boonzaier nr, matys t, price sj. extent of resection of peritumoral diffusion tensor imaging-detected abnormality as a predictor of survival in adult glioblastoma patients. j neurosurg. 2017;126: 234-241. 12. mcgirt mj, mukherjee d, chaichana kl, than kd, weingart jd, quinones-hinojosa a. association of surgically acquired motor and language deficits on overall survival after resection of glioblastoma multiforme. neurosurgery. 2009;65: 463-469 [discussion: 469-470]. 13. burger pc, dubois pj, schold sc jr, et al. computerized tomographic and pathologic studies of the untreated, 196 dipak chaulagain, volodymyr smolanka, andriy smolanka et al. quiescent, and recurrent glioblastoma multiforme. j neurosurg 1983;58(2): 159–169. 14. burger pc, heinz er, shibata t, kleihues p. topographic anatomy and ct correlations in the untreated glioblastoma multiforme. j neurosurg 1988;68(5):698– 704. 15. kelly pj, daumas-duport c, kispert db, kall ba, scheithauer bw, illig jj. imaging-based stereotaxic serial biopsies in untreated intracranial glial neoplasms. j neurosurg 1987;66(6):865–874. 16. earnest f iv, kelly pj, scheithauer bw, et al. cerebral astrocytomas: histopathologic correlation of mr and ct contrast enhancement with stereotactic biopsy. radiology 1988;166(3):823–827. 17. burger pc, green sb: patient age, histological features, and length of survival in patients with glioblastoma multiforme. cancer 59:1617–1625, 1987 18. gilbert h, kagan ar, cassidy f, et al: glioblastoma multiforme is not a uniform disease. cancer clin trials 4:87–89, 1981 19. gehan ea, walker md: prognostic factors for patients with brain tumors. natl cancer inst monogr 46:189–195, 1977 20. hammoud ma, sawaya r, shi w, et al: prognostic significance of preoperative mri scans in glioblastoma multiforme. j neurooncol 27:65–73, 1996 21. ammirati m, galicich jh, arbit e, et al: reoperation in the treatment of recurrent intracranial malignant gliomas. neurosurgery 21:607–614, 1987 22. harsh gr iv, levin va, gutin ph, et al: reoperation for recurrent glioblastoma and anaplastic astrocytoma. neurosurgery 21:615–621, 1987 23. lacroix m, abi-said d, fourney dr, et al. a multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. j neurosurg 2001;95:190-8. 24. sanai n, mirzadeh z, polley my, et al. the value of glioblastoma extent of resection: a volumetric analysis of 500 patients. j neurosurg 2010;113:a433. 25. trifiletti dm, alonso c, grover s, et al. prognostic implications of extent of resection in glioblastoma: analysis from a large database. world neurosurg 2017;103:330-40. 26. chaichana kl, jusue-torres i, navarro-ramirez r, et al. establishing percent resection and residual volume thresholds affecting survival and recurrence for patients with newly diagnosed intracranial glioblastoma. neuro oncol 2014;16:113-22. 27. brown tj, brennan mc, li m, et al. association of the extent of resection with survival in glioblastoma a systematic review and meta-analysis. jama oncol 2016;2:1460-9. 28. stupp r, hegi me, mason wp, et al. effects of radiotherapy with concomitant and adjuvant temozolomid versus radiotherapy alone on survival in glioblastoma multiforme in a randomised phase iii study: 5 -years analysis of the eortc-ncic trial. lancet oncol 2009;10:459-66. 29. awad aw, karsy m, sanai n, et al. impact of removed tumor volume and location on patient outcome in glioblastoma. j neurooncol 2017;135:161-71. 30. tunthanathip t, kanjanapradit k, ratanalert s, et al. multiple, primary brain tumors with diverse origins and different localizations: case series and review of the literature. j neurosci rural pract 2018;9:593-607. 31. liu q, liu y, li w, et al. genetic, epigenetic, and molecular landscapes of multifocal and multicentric glioblastoma. acta neuropathol 2015;130(04):587–597 32. thomas rp, xu lw, lober rm, li g, nagpal s. the incidence and significance of multiple lesions in glioblastoma. j neurooncol 2013;112(01):91–97 33. tunthanathip t, sangkhathat s, tanvejsilp p, kanjanapradit k. the clinical characteristics and prognostic factors of multiple lesions in glioblastomas. clin neurol neurosurg 2020;195:105891 34. lacroix m, abi-said d, fourney dr, et al. a multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. j neurosurg. 2001;95(2):190–198 35. keles ge, anderson b, berger ms. the effect of extent of resection on time to tumor progression and survival in patients with glioblastoma multiforme of the cerebral hemisphere. surg neurol. 1999;52(4):371–379. 36. sanai n, berger ms. glioma extent of resection and its impact on patient outcome. neurosurgery. 2008;62(4):753–764; discussion 264–756. 37. mcgirt mj, chaichana kl, gathinji m, et al. independent association of extent of resection with survival in patients with malignant brain astrocytoma. j neurosurg. 2009;110(1):156–162. 38. stupp r, mason wp, van den bent mj, weller m, fisher b, taphoorn mj, et al. r. european organisation for, t. treatment of cancer brain, g. radiotherapy, and g. national cancer institute of canada clinical trials, radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. n engl j med. 2005;352(10):987–96 39. stupp r, taillibert s, kanner a, read w, steinberg d, lhermitte b, et al. effect of tumor-treating fields plus maintenance temozolomide vs maintenance temozolomide alone on survival in patients with glioblastoma: a randomized clinical trial. jama. 2017;318(23):2306–16 40. akiyama y, kimura y, enatsu r, mikami t, wanibuchi m, mikuni n. advantages and disadvantages of combined chemotherapy with carmustine wafer and bevacizumab in patients with newly diagnosed glioblastoma: a singleinstitutional experience. world neurosurg. 2018;113:e508–14 41. yang dy, bu xy, zhou zl, yan zy, ma cx, qu mq, zhao yw, kong lf, wang yw, luo jc. enhanced antitumor effects of radiotherapy combined local nimustine delivery rendezvousing with oral temozolomide 197 role of extent of resection on the survival of glioblastoma multiforme chemotherapy in glioblastoma patients. j cancer res ther. 2018;14(1):78–83 42. matsuda m, kohzuki h, ishikawa e, yamamoto t, akutsu h, takano s, et al. prognostic analysis of patients who underwent gross total resection of newly diagnosed glioblastoma. j clin neurosci. 2018;50:172–6. microsoft word 5cucuai_mirror romanian neurosurgery (2018) xxxii 4: 563 | 563             doi: 10.2478/romneu-2018-0072 mirror, mirror on the wall, who’s the fairest of them all? atypical meningioma associated with multiple meningiomas a.i. cucu1, claudia florida costea1,2, mihaela dana turliuc1,2, gabriela florenta dumitrescu1, anca sava1,2, i. poeata1,2 1“prof. dr. n. oblu” emergency clinical hospital, iaşi, romania 2“grigore t. popa” university of medicine and pharmacy, iaşi, romania abstract: the incidence of multiple meningiomas (mms) without stigmata of neurofibromatosis or family history of meningiomatosis is rare. mms with atypical histology are even rarer, since most of them have benign histology. the authors report three cases of mms, of which the symptomatic meningioma removed was an atypical meningioma (am). we also review their possible pathogenesis and histopathology. although there has not been established any mms management and therapy strategy so far, our recommendation is to treat symptomatic and accessible lesions or growing tumours and also to prefer a conservative approach consisting of the imaging follow-up of asymptomatic lesions. key words: atypical meningioma, multiple meningiomas, meningiomatosis, who grade ii meningiomas introduction the first description of a multiple intracranial meningiomas dates back to 1889 and was made by anfimov and blumenau, who had found one large and four small tumours on an autopsy that they performed (1). later on, in 1938, harvey cushing and louise eisenhardt explained the pathology of this entity and used the term “multiple meningiomas” to refer to the case of a patient who had “more than one meningioma and less than a diffusion of them” (7). meningiomas represent about one third of all primary brain tumours in adults (8, 11), with an incidence that has increased in recent years (10, 35). majority of meningiomas are solitary (33), and mms are defined as the presence of ≥ 2 spatially separated metachronous or synchronous meningiomas and represents up to 10% of all meningiomas (18, 20). they may be sporadic, radiation induced or familial, when they occur as type 2 neurofibromatosis or familial meningiomatosis (33). nowadays, the term mms is used to 564 | cucu et al atypical meningioma associated with multiple meningiomas             describe a condition in which a patient has the simultaneous or sequential appearance of two or more independent meningiomas, whether the tumours have the same pathologic subtypes or not (13). nonetheless, borovich et al. considers that mms might be truly multiple when tumours from the same patient have different histological subtypes and multicentric when tumours have the same histology (3). the pathophysiologic mechanisms underlying the occurrence of mms have not yet been fully understood and thus two different hypotheses have been suggested so far (16, 34, 37). according to the first theory, multiple lesions originate from multicentric neoplastic foci and grow independently under the stimulation of a supposed tumourproducing factor. the second theory argues that a signal transforming event occurs and an original clone of neoplastic meningothelial cells spreads throughout the meninges or along the cerebrospinal fluid, leading to the formation of multiple clonally tumours (13, 16, 34, 37). nevertheless, the tumour histology and dynamics of histopathological changes undergone by these multiple lesions in time have not been fully understood. mms also give rise to special treatment problems, the most important of which are as follows: which lesion is symptomatic, which lesion needs to be treated and what is the best therapeutic approach, what is the best treatment option and how should incidental mms be managed? due to these aspects, and also to their relative rarity, unclear aetiology and issues related to management strategy (29), mms have raised the specialists' interest and they should constitute a priority in meningiomas treatment. methods we followed the 3 years evolution of three patients with mms who underwent surgery in the “profesor dr. nicolae oblu” emergency clinical hospital of iasi in 2010, 2012 and 2013, respectively. the inclusion criteria were adult patients (>18 years) with diagnosis of ≥ 2 separate meningiomas on mri examination, one of which removed by surgery and diagnosed with am (who grade ii). the exclusion criteria were patients with type 2 neurofibromatosis, history of radiotherapy or familial types. results the 3 cases of mms with am are shown in table 1. case 1. a 64-year-old male patient has had slowly progressing vision disorders for about 2 years, which were examined by several ophthalmologists. he had decreased visual acuity in both eyes. the mri examination reveals three mms: one diaphragm sellae meningioma with a right parietal meningioma and a left parietal meningioma (figure 1). through a left fronto-temporal approach the meningioma of the diaphragm sellae was completely resected with good optic chiasma and pituitary stalk decompression (figure 1). postoperative ophthalmologic exam reveald that visual acuity of right eye was 6/6 and left eye 1/500 bcva. also, the fundus examination revealed normally coloured and regular edges of the optic disc, c/d ratio 0.3 for right eye and 0.4 for left eye. case 2. a 65-year-old female patient is hospitalized for intracranial hypertension syndrome with cerebellar syndrome. the mri romanian neurosurgery (2018) xxxii 4: 563 | 565             scan reveals the presence of a left transverse sinus meningioma (figure 2. a) with an associated left parasagittal meningioma (figure 3). the left transverse sinus meningioma was resected through a paramedian suboccipital approach (figure 2. b.). total 0.9 gy irradiation is also performed, both for the remaining tumour on the left transverse sinus and for the left frontal parasagittal meningioma. case 3. a 73-year-old female patient was admitted for gait disorders that have set in 2 years before and have progressively worsened and for 1-month-old intracranial hypertension syndrome. the mri scan reveals superior sagittal sinus meningiomatosis. the surgical procedure, performed through a parieto-occipital approach, consists of intracapsular tumour resection and partial sinus and infiltrated falx cerebri resection (figure 4). in all three patients, both the meningiomas resected and the other meningiomas were followed by yearly mri scan. the follow-up revealed that, 3 years later, the mms had not increased in size. as concerns am recurrence, a 0.1 cm increase of left transverse sinus meningioma was noted in case 2 after one year. table i clinical data of patients with multiple meningiomas, of which one was atypical meningioma case 1 case 2 case 3 location (am) diaphragm sellae meningioma left transverse sinus meningioma parieto-occipital meningioma location of the other meningiomas right parietal left parietal left parasagittal superior sagittal sinus meningiomatosis age, sex m, 64 years f, 65 years f, 73 years symptoms visual acuity decreased visual acuity in both eyes intracranial hypertension syndrome, cerebellar syndrome spastic paraparesis, intracranial hypertension syndrome ki 67 4% 4.7%, with 7.59% on a field 6% discussion demography. as concerns the patients' demographic data, our findings are in accordance with other research shown in literature, which proves that the mean age of presentation with mms is the 6th decade of life and it is the same as for patients with solitary meningioma (12, 13, 26, 27, 33). mms occur much more frequently in females than in males, and their predilection for the female gender is considerably higher than for the male gender, studies showing a significantly higher f: m ratio of 3.5:1 in mms 566 | cucu et al atypical meningioma associated with multiple meningiomas             (12, 13, 27). however, it is still unclear why female preponderance is much higher in mms than in solitary meningiomas, yet according to a recent hypothesis, hormonal dependency may be higher, which may be accounted for by the stronger progesterone expression in these tumours compared with their solitary counterparts (13, 32, 33). moreover, tsermoulas et al. argue that genetic factors may enhance the potential for tumorigenesis in women (33). our case series also exhibited a female predilection, as two of the three patients were women. figure 1 (case 1) preoperative (a) and postoperative (b) sagittal t1-weighted images with contrast. multiple meningiomas with one right parietal meningioma (c) and one left parietal meningioma (e) romanian neurosurgery (2018) xxxii 4: 563 | 567             figure 2 (case 2) preoperative (a) and postoperative (b) axial t1-weighted images with contrast of a left transverse sinus meningioma figure 3 (case 2) axial t1-weighted images with contrast showing a left parasagittal meningioma. no increase in size of meningioma was observed at 3 years of follow-up 568 | cucu et al atypical meningioma associated with multiple meningiomas             figure 4 (case 3) t1-weighted images with contrast showing a superior sagittal sinus meningiomatosis figure 5 (case 2) t1-weighted images with contrast showing local recurrence of a left transverse sinus meningioma at 2 years follow-up symptomatology the frequency of symptoms in mms was proportional to the size of the tumours, the largest meningiomas being more asymptomatic, which was to be expected, since the mode of presentation of meningiomas is due to their mass effect. skull base and midline meningiomas are more symptomatic than convexity meningiomas (33), and the most common location for meningiomas in asymptomatic patients has proven to be the convexity (22). in our case series, the symptoms were due to the mass effect on optic romanian neurosurgery (2018) xxxii 4: 563 | 569             chiasm and optic nerves (case 1), cerebellum (case 2) and motor cortex (case 3). mms distribution in the intracranial space. according to the literature, in mms most patients have a major meningioma accompanied by one or several smaller meningiomas (12, 13), which was also true for two of our patients: the two large skull base meningiomas (the diaphragm sellae meningioma and the transverse sinus meningioma) were accompanied by convexity meningiomas (figure 1. c and e) and parasagittal meningiomas (figure 3). as concerns this association, in a study that included 39 patients with mms, huang et al. noted that in mms a major meningioma is often accompanied by one or more smaller meningiomas (13). this was also reported by domenicucci et al. that found that 11 of the 14 cases of mms were composed of small and large meningiomas (12). thus, huang et al. argue that several different-sized tumours in the same mms case would be an indication of the fact that meningiomas may develop at different times and that it is possible that an original major meningioma may disseminate to form multiple foci through the subarachnoid or subdural space (13). in the same study, they noted that the main location of mms is the cerebral convexity (12, 13). huang et al. think that this predilection may be accounted for by the assumption that mms develop from the major meningioma through the subarachnoid space, since disseminated meningioma cell tend to grow at the cerebral convexity by the circulation of the cerebrospinal fluid (13). this theory is also supported by the location of most of the mms in the hemicranial space in some studies (4, 34). histopathology. in mms, most meningiomas are benign (who grade i) and have uniform histology, the atypical or anaplastic subtypes being rare (15). nevertheless, most meningiomas are benign on presentation. thus, turgot et al. removed 28 meningiomas from 8 patients, of which 14 were meningothelial (50%) (34). the predominance of the meningothelial subtype is also supported by domenicucci et al.'s patient series (12). other authors also reported predominantly benign histologies, yet different, like the fibrous and transitional subtypes (21) or the psammomatous type (27). as concerns meningioma histology in the same patient, some studies have shown that the same patient may have meningiomas of different grade and different histological features (13, 19, 21). in a study that they recently published in 2017, tsermoulas et al. also found that among patients who had more than 2 meningiomas removed, about 1 in 5 had tumours of different grades and most of them had different histological subtypes. from this point of view, some authors argue that these findings are evidence of the different origins of tumours from multiple foci and that their multiplicity is not the consequence of cell migration through the subarachnoid space (4, 19, 21). on the other hand, other authors have supported the theory of clonal spread from a single tumour (13, 16, 17, 24, 27, 30, 37). some authors are of the opinion that both theories may apply in different cases and that further research on the genetics of mms would clarify 570 | cucu et al atypical meningioma associated with multiple meningiomas             the controversial standpoints on the histology and pathogenesis of these lesions (33). atypical meningiomas. as we have said before, most of the published series concluded that the vast majority of mms cases described in literature have benign histology (27, 34), the atypical or anaplastic subtypes being rare (15). as far as the simultaneous occurrence of benign and atypical histological grades in sporadic mms is concerned, mocker et al. consider that this is extremely rare (19), as literature contains only few reports of benign histological types mixed with atypical types (4, 19, 23, 31). tumour recurrence is one of the main problems that have to be dealt with in am management (8). thus, huang et al. found that four meningiomas in three patients were am and all of these three patients had recurrence after the operation (13). in our three-patient series, only one am exhibited tumour recurrence after 2 years (case 2). as concerns the other meningiomas, on which no surgery was performed, they did not grow in size during our 3 year follow-up (figures 1 and 3). our findings are in line with wong et al., who did not note the tumour growth rates in patients with mms to be higher than the growth rates of incidentally found solitary meningiomas (36). genetics of meningiomas. the most significant genetic abnormality in sporadic solitary meningiomas is the loss of heterozygosity on chromosome 22, which occurs in about 50% of patients. an early event of tumorigenesis in one third of these cases was found to be the somatic mutation of the nf2 gene (22q12.2) (5). on the other hand, familial mms do not show mutation or loss of nf2 (28). some authors have described genetic alterations associated with meningioma progression and initiation, yet it is not yet possible to predict the rate of tumour growth or the probability of tumour recurrence (6). thus, the genetics of tumour nodules for the appearance of mms not yet fully known (19). management. not all patients with mms require treatment, and a challenge in the management of mms may be the identification of the responsible tumour. in this algorithm, surgical removal remains the main form of treatment. since the neurological deficits are usually caused by major tumours and peritumoral oedema, the size of the meningioma is an important factor in determining which of the meningiomas need to be removed (9, 13). radiosurgery seems to be an attractive and interesting option for mms up to 3 cm in diameter or residual tumours, but further research is required to establish its effectiveness and determine whether it is safe or not (33). therefore, the authors' opinions are controversial: some of them support the treatment of asymptomatic meningiomas with prophylactic radiosurgery, even without documented growth (14, 25), whereas others are more reserved on that point and they report a complication rate of radiosurgery of 10% (26). as far as mms prognosis is concerned, it depends on the grade of the tumour, on the histological types and on the resection degree of the tumour (2, 8). romanian neurosurgery (2018) xxxii 4: 563 | 571             conclusions there has not been established any mms management and therapy strategy so far. our recommendation is to treat the symptomatic or the potentially symptomatic tumours and to avoid useless procedures and complications. the form of treatment is surgical removal, but radiotherapy may also be considered and may also play an important role, especially for am. nevertheless, even in mms only some of the lesions require treatment, since most of them are small and asymptomatic and they only require clinical and imaging follow-up. our philosophy is to treat symptomatic and accessible lesions or growing tumours and to apply the conservative approach, consisting of imaging follow-up for the asymptomatic lesions. correspondence claudia florida costea “prof. dr. n. oblu” emergency clinical hospital, iasi, romania e-mail: costea10@yahoo.com references 1.anfimow j, blumenau l. ein fall multipler geschwülste in der schadel¬höle. neurol zetralbl. 1889; 8:585. 2.black pm. meningiomas. neurosurgery. 1993; 32:643657. 3.borovich b, doron y. recurrence of intracranial meningiomas: the role played by regional multicentricity. j neurosurg. 1986; 64(1):58-63. 4.butti g, assietti r, casalone r, et al. multiple meningiomas: a clinical, surgical, and cytogenetic analysis. surg neurol. 1989; 31:255-260. 5.campbell ba, jhamb a, maguire ja, et al. meningiomas in 2009: controversies and future challenges. am j clin oncol. 2009; 32(1):73-85. 6.carvalho lh, smirnov i, baia gs, et al. molecular signatures define two main classes of meningiomas. mol cancer. 2007; 6:64. 7.cushing h, eisenhardt l. meningiomas: their classification, regional behavior, life history, and surgical end results. c. thomas, springfield iii, 1938. 8.cucu ai, costea cf, poeata i, et al. prognostic factors in atypical meningioma. rom neurosurg. 2017; 31 (2):165-171. 9.cucu ai, turliuc md, carauleanu a, et al. chemical aspects of peritumoral cerebral edema in atypical meningiomas. rev chim (bucharest). 2018; 69:28042807. 10.cucu ai, costea cf, carauleanu et al. meningiomas related to the chernobyl irradiation disaster in northeastern romania between 1990-2015. rev chim (bucharest). 2018; 69:1562-1565. 11.dolecek ta, propp jm, stroup ne, kruchko c. cbtrus statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2005–2009. neuro oncol. 2012; 14(5): 1-49. 12.domenicucci m, santoro a, d’osvaldo dh, et al. multiple intracranial meningiomas. j neurosurg. 1989; 70:41-44. 13.huang h, buhl r, hugo hh, et al. clinical and histological features of multiple meningiomas compared with solitary meningiomas. neurol res. 2005; 27:324-332. 14.iwai y, yamanaka k, morikawa t, et al. the treatment for asymptomatic meningiomas in the era of radiosurgery. no shinkei geka. 2003; 31:891-897. 15.koh yc, yoo h, whang gc, et al. multiple meningiomas of different pathological features: case report. j clin neurosci. 2001; 1(8 suppl.):40-43. 16.larson jj, tew jm jr, simon m, et al. evidence for clonal spread in the development of multiple meningiomas. j neurosurg. 1995; 83:705-709. 17.lomas j, bello mj, alonso me, et al. loss of chromosome 22 and absence of nf2 gene mutation in a case of multiple meningiomas. hum pathol. 2002; 33:375378. 18.lusins jo, nakagawa h. multiple meningiomas evaluated by computed tomography. neurosurgery. 1981; 9:137-141. 19.mocker k, holland h, ahnert p, et al. multiple meningioma with different grades of malignancy: case report with genetic analysis applying single-nucleotide polymorphism array and classical cytogenetics. pathol res pract. 2011; 207:67-72. 20.nahser hc, grote w, löhr e, et al. multiple meningiomas. clinical and computer tomographic observations. neuroradiology. 1981; 21:259-263. 572 | cucu et al atypical meningioma associated with multiple meningiomas             21.neuss m, westphal m, hansel m, et al. clinical and laboratory findings in patients with multiple meningiomas. br j neurosurg. 1988; 2:249-256. 22.olivero wc, lister jr, elwood pw. the natural history and growth rate of asymptomatic meningiomas: a review of 60 patients. j neurosurg. 1995; 83:222-224. 23.oshita j, sogabe t, maeda h, et al. a case of multiple meningiomas: two lesions have different clinicopathological features, respectively. no shinkei geka. 2007; 35: 929-934. 24.petrella r, levine s, wilmot pl, et al. multiple meningiomas in a patient with constitutional ring chromosome 22. am j med genet. 1993; 47:184-186. 25.salvetti dj, nagaraja tg, levy c, et al. gamma knife surgery for the treatment of patients with asymptomatic meningiomas. j neurosurg. 2013; 119:487-493. 26.samblas j, luis lopez guerra j, bustos j, et al. stereotactic radiosurgery in patients with multiple intracranial meningiomas. j buon. 2014; 19:250-255. 27.sheehy jp, crockard ha. multiple meningiomas: a long-term review. j neurosurg. 1983; 59:1-5. 28.shen y, nunes f, stemmer-rachamimov a, et al. genomic profiling distinguishes familial multiple and sporadic multiple meningiomas. bmc med genomics. 2009; 2:42. 29.spallone a, neroni m, giuffre r. multiple skull base meningiomas: case report. surg neurol. 1999; 51:274-280. 30.stangl ap, wellenreuther r, lenartz d, et al. clonality of multiple meningiomas. j neurosurg. 1997; 86:853-858. 31.tomita t, kurimoto m, yamatani k, et al. multiple meningiomas consisting of fibrous meningioma and anaplastic meningioma, j clin neurosci. 2003; 10:622624. 32.touat m, lombardi g, farina p, et al. successful treatment of multiple intracranial meningiomas with the antiprogesterone receptor agent mifepristone (ru486). acta neurochir (wien). 2014; 156:1831-1835. 33.tsermoulas g, turel mk, wilcox jt, et al. management of multiple meningiomas. j neurosurg. 2018; 128(5):1403-1409. 34.turgut m, palaoğlu s, ozcan oe, et al. multiple meningiomas of the central nervous system without the stigmata of neurofibromatosis. clinical and therapeutic study. neurosurg rev. 1997; 20(2):117-123. 35.willis j, smith c, ironside jw, et al. the accuracy of meningioma grading: a 10-year retrospective audit. neuropathol appl neurobiol. 2005; 31: 141-149. 36.wong rh, wong ak, vick n, et al.natural history of multiple meningiomas. surg neurol int. 2013; 4:71. 37.zhu jj, maruyama t, jacoby lb, et al. clonal analysis of a case of multiple meningiomas using multiple molecular genetic approaches: pathology case report. neurosurgery. 1999; 45:409-416.   doi: 10.33962/roneuro-2020-074 enlarged anterior communicating artery masquerading as intracranial aneurysm. case report saja a. albanaa, zahraa f. al-sharshahi, noor a. hummadi, noor k. al-waely, rasha a. alshakarchy, ali m. neamah, aktham o. alkhafaji, samer s. hoz romanian neurosurgery (2020) xxxiv (1): pp. 455-458 doi: 10.33962/roneuro-2020-074 www.journals.lapub.co.uk/index.php/roneurosurgery enlarged anterior communicating artery masquerading as intracranial aneurysm. case report saja a. albanaa1, zahraa f. al-sharshahi2, noor a. hummadi3, noor k. al-waely4, rasha a. alshakarchy2, ali m. neamah1, aktham o. alkhafaji1, samer s. hoz2 1 medical student. college of medicine, university of baghdad, iraq 2 department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 3 radiologist. c.a.b.h.s-diagnostic radiology, al-imamain alkadhmain medical city, iraq 4 fibms-diagnostic radiology, al-nahrain university, college of medicine, department of surgery, iraq abstract background. the anterior communicating artery (acoa) complex consists of the acoa, the pre-and post-communicating segments of the anterior cerebral artery, and the recurrent artery of heubner. it is the most common site for anatomical variations in the circle of willis. such variations can mimic intracranial aneurysms. case description. a 30-year-old female presented with recurrent episodes of extreme headache and bilateral tinnitus. a brain computed tomography (ct) scan showed no significant lesions, while her ct-angiography (cta) showed an enlarged vascular lesion at the acoa, raising the suspicion for an acoa aneurysm. a repeated cta revealed a rare anatomical variation with a pattern of cross dominance in the acoa complex; the left a1 and right a2 were dominant-enlarged, resulting in an enlargement of the acoa. the presence of an acoa aneurysm was hence excluded and the patient was managed conservatively. at 6-month follow-up, cta showed no new findings. conclusion. acoa enlargement can result from unequal hemodynamics around the acoa complex, which may be mistaken for an aneurysm. a thorough study of the imaging data is of pivotal importance and may change the management strategy. introduction the anterior communicating artery (acoa) connects the two anterior cerebral arteries, dividing them into pre-communicating (a1) and postcommunicating (a2) segments. acoa, a1, a2 segments, and the recurrent artery of heubner are collectively known as the acoa complex [1]. anatomical variations in this complex are common and are detected keywords a1 hypoplasia, acoa complex, anatomic variations, enlarged acoa corresponding author: saja a. albanaa college of medicine, university of baghdad, iraq sajaalbanaa@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 456 saja a. albanaa, zahraa f. al-sharshahi, noor a. hummadi et al. in 58-85% of all patients with acoa aneurysms [2]. a range of different arterial variations was indexed, including fenestration, duplication, trifurcation, hypoplasia, and aplasia [3]. several efforts have been made to classify the acoa complex variations as they may influence the surgical approach of any coexisting vascular disease [1]. also, these anatomical variations can mimic intracranial aneurysms by the superimposition of a duplicated or a fenestrated vessel [2]. furthermore, the net-result of the hemodynamic changes in these variations plays a considerable role in the development of several vascular pathologies, such as aneurysms and ischemic strokes [3]. moreover, acoa complex is the most common site for intracranial aneurysms, constituting up to 40% of all aneurysms, which can further ambiguate identifying these variations [4]. in this report, we present a case report of an enlarged acoa masquerading initially as an acoa aneurysm. to our knowledge, this is the first such case report of its kind in the literature. case scenario an otherwise healthy, 30-year-old, female typist was referred by her general physician with a suspension of an unruptured acoa aneurysm. she had a history of recurrent attacks of severe non-localized headaches associated with episodes of bilateral tinnitus, more on the left side, for two weeks. each attack lasts for more than one hour with no exacerbating factors. the headache was rated as 8/10 by the patient, and it impacted her daily activities. the patient had an intact neurological examination. her brain computed tomography (ct) scan revealed no significant lesions apart from a suspicious anterior interhemispheric lesion. the ctangiography showed a pouched-out vascular lesion at the acoa, raising suspicion for an acoa aneurysm (fig. 1a). as we had no endovascular facility at our institute, we opted to perform another cta, aiming to obtain better-qualified images and more clear views. the new cta showed a dominant left a1 and a hypoplastic right a1 (0.4 mm) segments of the anterior cerebral artery, which is a common variation especially encountered with acoa aneurysms. besides, a noticeable enlargement of the acoa at its junction with the right anterior cerebral artery was found, most probably resulting from the inverted hemodynamics between the two sides of acoa. the left a2 was normal, while the right a2 was enlarged. no intracranial aneurysms were detected (fig. 1b-d). the patient was informed that she had a normal variation in the circulation rather than an acoa aneurysm. simple analgesics were prescribed, which helped the headache. the patient continued to have tinnitus. therefore, a brain magnetic resonance imaging (mri) was done to exclude the possibility of an arteriovenous fistula, which then came back negative. the patient was referred to an otolaryngologist, who diagnosed her with mild otitis media. at her 6-month follow-up visit, the patient’s headache and tinnitus had resolved, and she had resumed her daily activities. the follow-up cta and mri studies revealed no new findings. figure 1. imaging of an acoa variation mimicking an aneurysm. (a): a cerebral ct angiography, 3d reconstructed image showing a suspected acoa aneurysm. (b, c) different views of a second cta, confirming the absence of an intracranial aneurysm. instead, an enlarged acoa was noted accompanied by an enlargement of both the left a1 and right a2. (d) an artistic depiction of the acoa arterial complex demonstrating the inverted hemodynamics. the vascular configuration showing an enlarged acoa (*), la1, and ra2 with a hypoplastic ra1 and a normal-sized la2 with no evidence of aneurysm formation. acoa; anterior communicating artery, ica; internal carotid artery, mca: middle cerebral artery, r; right, l; left. m1: sphenoidal or horizontal segment of the mca. a1: precommunicating segment of the anterior cerebral artery. a2: post-communicating segment of the anterior cerebral artery. a. b. 457 enlarged anterior communicating artery masquerading as intracranial aneurysm c. d. discussion the anterior cerebral artery plays a vital role in the blood supply to the anterior collateral circulation as it gives off penetrating striatal arteries that supply the anterior hypothalamus, septum pellucidum, and parts of the corpus striatum [5]. vascular anomalies of the acoa complex are not uncommon and are mostly encountered in the a1 segment [6]. a unilateral hypoplastic a1 segment is one of the most common anomalies in the circle of willis with an incidence of 3% [3,7]. marinković et al. described two types of a1 hypoplasia based on carotid angiogram namely, mild and extreme hypoplasia [8]. mild hypoplasia is diagnosed when the diameter of the a1 segment is more than 1 mm, whereas extreme hypoplasia is defined by an a2 segment diameter of less than 1 mm [8]. hypoplasia of one a1 segment is compensated by the dominance of the contralateral a1 segment [6]. these variations are often asymptomatic or found incidentally, chronic headache is, however, a possible presentation in patients with arterial hypoplasia [9]. the a1 segment is a rare site for ischemic strokes, representing only 0.6-3% of all stroke etiologies [10]. the risk for ischemic stroke is further aggravated by the presence of such hypoplasia [5,10]. furthermore, the presence of a1 hypoplasia increases the risk of aneurysm formation; a phenomenon that can be explained, in part, by alteration in acoa complex hemodynamics [1]. in this case, the extreme hypoplastic right a1 segment was compensated by the dominance of the left a1 segment, which supplied the right a2 segment through the acoa. these variations manifested radiologically as an enlarged acoa with a pouched-out appearance leading to a suspicion of an acoa aneurysm. moreover, the presence of such inverted hemodynamics around the acoa complex may render the distal circulation more prone to ischemic stroke or aneurysm formation [7]. thereafter, followup by annual imaging is important in determining patient’s prognosis and could confirm or exclude the stability of such anomaly [10]. knowing such variations is also essential in planning surgical and endovascular approaches, as these variations can require a different management strategy [3]. the purpose behind presenting this case is to highlight their propensity to pose a diagnostic dilemma, especially when catheter angiography is not feasible. moreover, our case demonstrates how cautious the surgeon should be in reviewing the patient’s radiology while planning the appropriate management. conclusion anterior communicating artery enlargement can result from unequal hemodynamics around the anterior communicating complex, which may be mistaken for an aneurysm. a thorough study of the imaging data is of pivotal importance and may change the management strategy. abbreviations acoa anterior communicating artery ct computed tomography cta computed tomography angiography mri magnetic resonance imaging. references 1. krzyżewski rm, tomaszewski ka, kochana m, kopeć m, klimek-piotrowska w, walocha ja. anatomical variations of the anterior communicating artery complex: gender relationship. surgical and radiologic anatomy. 2015 jan 1;37(1):81-6. 2. weil ag, bojanowski mw, scholtes f, darsaut te, 458 saja a. albanaa, zahraa f. al-sharshahi, noor a. hummadi et al. signorelli f, weill a. angiographic pitfall: duplicated tapered a1 segment of the anterior cerebral artery mimicking an anterior communicating artery aneurysm. interventional neuroradiology. 2011 jun;17(2):179-82. 3. orakdogen m, emon st, somay h, engin t, is m, hakan t. vascular variations associated with intracranial aneurysms. turk neurosurg. 2017 jan 1;27(6):853-62. 4. ureña fm, ureña jg, almeida s, rabelo nn, mandel m, teixeira mj, figueiredo eg. anterior communicating artery duplication associated with a triplication of anterior cerebral artery–a rare anatomical variation. surgical neurology international. 2020;11(36):1. 5. chuang ym, liu cy, pan pj, lin cp. anterior cerebral artery a1 segment hypoplasia may contribute to a1 hypoplasia syndrome. european neurology. 2007;57(4):208-11. 6. samala n, tallapaneni s. the radio-anatomical study of incidence of aplasia and hypoplasia of anterior cerebral artery in the region of telangana. 2019. 7. vidyasagar k, bai sl, venkataswamy p, chandrasekhar s, sameeraja v, reddy r. bilateral stroke: unpaired anterior cerebral artery infarct rare presentation. international journal of research in medical sciences. 2015 jan;3(1):331. 8. marinković s, kovacević m, milisavljević m. hypoplasia of the proximal segment of the anterior cerebral artery. anatomischer anzeiger. 1989;168(2):145-54. 9. han yk, kim s, yoon cs, lee ym, kang hc, lee js, kim hd. a1 segment hypoplasia/aplasia detected by magnetic resonance angiography in neuropediatric patients. 10. lakhotia m, pahadiya hr, prajapati gr, choudhary a, gandhi r, jangid h. a case of anterior cerebral artery a1 segment hypoplasia syndrome presenting with right lower limb monoplegia, abulia, and urinary incontinence. journal of neurosciences in rural practice. 2016 jan;7(01):189-91. doi: 10.33962/roneuro-2023-016 spontaneous complete resolution of a giant cavernous carotid aneurysm in the setting of ipsilateral ica occlusion sura h. talib, mayur sharma, vishan p. ramanathan, yara alfawares, muntadher h. almufadhal, mustafa ismail, samer s. hoz romanian neurosurgery (2023) xxxvii (1): pp. 101-106 doi: 10.33962/roneuro-2023-016 www.journals.lapub.co.uk/index.php/roneurosurgery spontaneous complete resolution of a giant cavernous carotid aneurysm in the setting of ipsilateral ica occlusion sura h. talib1, mayur sharma2, vishan p. ramanathan3, yara alfawares3, muntadher h. almufadhal4, mustafa ismail4, samer s. hoz5 1 college of medicine, university of al-mustansiriyah, baghdad, iraq 2 department of neurosurgery, university of louisville, ky, usa 3 university of cincinnati college of medicine, cincinnati, oh, usa 4 college of medicine, university of baghdad, baghdad, iraq 5 department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa abstract background. cavernous carotid aneurysms (cca) are rare aneurysms with a relatively benign natural history. the association between cca aneurysm and ipsilateral internal carotid artery (ica) thrombosis or occlusion has not been described previously. the management of patients with these dual lesions is a challenging problem. case description. in this report, we describe an 18-year-old man who presented with left abducent nerve palsy of 3 weeks duration, and imaging revealed left cca with left ica occlusion. the patient was managed conservatively with clinical and imaging follow-up. the patient recovered well with complete resolution of clinical symptoms and disappearance of left cca. conclusions. the association of giant cca and ica occlusion on the same side is a rare phenomenon with no current consensus on the appropriate follow-up and management strategy. in this report, we described the first case of spontaneous complete disappearance of a giant cca in the setting of ipsilateral ica occlusion with complete resolution of symptoms at nine months of follow-up. introduction cavernous carotid aneurysms (cca) are rare with a relatively benign natural history and a lower risk of morbidity and mortality compared to size-matched equivalent aneurysms at other locations [6]. when ccas are asymptomatic or have mild tolerable symptoms, then conservative treatment can be justified with long-term clinic-radiological follow-up. other forms of presentations may require a multidisciplinary team of neuroendovascular and micro-neurosurgeons with catheter-based therapy as the treatment of choice [10]. although partial thrombosis of intracranial aneurysms is reported in keywords cavernous carotid aneurysm, internal carotid artery, spontaneous resolution corresponding author: samer s. hoz department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 102 sura h. talib, mayur sharma, vishan p. ramanathan et al. large and giant aneurysms, a complete thrombosis is a rare phenomenon [2]. an interesting association is reported between large cca thrombosis and parent vessel occlusion with many suggested theories [2]. with extreme rarity, a decrease in the size of the thrombosed aneurysm represents a regression in the hemodynamic pressure and indicates a better prognosis [3]. here we describe the first report on the spontaneous total disappearance of a giant cca in the setting of ipsilateral internal carotid artery (ica) occlusion with complete resolution of symptoms. case scenario an 18-year-old male patient presented to us with left abducent nerve palsy and recurrent attacks of a severe headache of nonspecific localization and character. apart from the palsy, the patient was neurologically intact and had no remarkable medical history. brain magnetic resonance imaging (mri) and magnetic resonance angiography (mra) at presentation showed a giant (28mm x 24mm x 21mm) left cavernous ica aneurysm with mass effect on the left temporal lobe with a striking shadow of the thrombosed aneurysm and absence of the left ica proximal to the clinoidal segment on mra (figure 1 a-d). the patient couldn’t afford the catheter angiography at that time. we opted to treat him conservatively with regular clinico-radiological follow-up. a 3-month follow-up mri showed a reduction in the size of the aneurysm, loss of flow void signal intensity, and his symptoms improved. at the 9-month follow-up, the patient was neurologically intact and did not experience headaches over the last three months. his brain mri and mra cerebral revealed a complete resolution of the cavernous aneurysm, no mass effect on the temporal lobe with the disappearance of the aneurysmal shadow, and the absence of the left ica on mra (figure 1 e-h). a 9-month follow-up digital subtraction angiography (dsa) showed complete occlusion of the left ica just distal to its origin with sufficient collateral circulation from the right ica. no aneurysmal filling was detected (figure 2). the patient remained asymptomatic at the last follow-up. no further investigations were planned, and annual clinical assessment follow-up visits were scheduled. discussion ccas are rare and constitute approximately 2-9% of all intracranial aneurysms [5]. they are predominantly asymptomatic, are discovered incidentally, and have a benign natural history with a low risk of rupture and complications. however, they may become symptomatic due to mass effects from an enlarged aneurysmal mass [6,14]. it is known that ccas rarely cause rupture and subarachnoid hemorrhage (sah) since the cavernous sinus is composed of thick double-dural membranes, which lay over the sphenoid body [16]. the optimal management strategy for cca aneurysms remains controversial. since ccas are known to have a low propensity for a life-threatening sequela, conservative management with serial follow-up imaging seems to be a reasonable strategy. however, there are several compelling reasons to treat this entity, including a rupture with the formation of carotid-cavernous fistula, an increase in the size of the aneurysm on follow-up imaging, progressively worsening headache, and erosions of the sphenoid sinus. these signs and symptoms should be analyzed by a multidisciplinary team (neuro-endovascular and microsurgical) to choose the optimal treatment plan [1,6,14]. aneurysms arising from the circle of willis are likely to cause spontaneous sah leading to a devastating neurological condition. on rare occasions, these aneurysms may undergo spontaneous thrombosis causing symptoms related to a local mass effect and or distal thromboembolism of the parent artery. complete thrombosis of aneurysms occurs at a lower incidence in comparison to partial thrombosis (1320% vs. 60%); generally, it tends to occur in large (>15mm) and giant (>25mm) aneurysms [2]. the association of ipsilateral ica occlusion with giant cca is rare, with only 18 reported cases in the literature [1]. theories addressing the coexistence of these two pathologies and their progression is a matter of contentious debate due to a limited number of reported cases and the variability in the characteristics, progression, and management strategies. one explanation is that the large thrombosed cca tends to compress on the ica against the anterior clinoid process and causes stenosis of the parent artery [8,15]. other proposed theories include direct stretch and compression of the parent artery by the giant aneurysm and proximal propagation of an intramural thrombus [12]. on the other hand, thrombosis of the parent artery can be initially formed in association with giant 103 spontaneous complete resolution of a giant cavernous carotid aneurysm in the setting of ipsilateral ica occlusion cca due to the presence of tough dural folds, bony structures along with the natural bend of the artery at this location, which facilitate parent artery deformity, blood flow stasis and eventually thrombosis. the resultant decreased flow into the aneurysm leads to intra-aneurysmal clot formation [2]. in our case, the treatment decision was challenging because the patient was young and had an acute presentation with abducent palsy of 3 weeks duration. however, the absence of ica ipsilateral to the giant cca led us to choose conservative management with regular follow-up imaging in the absence of a defined management strategy for these lesions. then the patient did well with complete resolution of symptoms at nine months follow-up. table 1. characteristics and follow-up of patients with cca aneurysm and ipsilateral ica occlusion that were treated conservatively authors ageyear/ sex side clinical presentation imaging at presentation (mri and dsa) imaging at f/u (mri and dsa) clinical outcome treatment gautier, 1986. (14) 65/f left cn iii, iv, vi palsies cca: (23mm) thrombosed ica: occluded opthalmo paresis persisted the patient refused treatment sato et al. 1990 (15) 49/m left headache, cn iii, vi, v1 palsies cca: (3cm) partial thrombosed (mri flow void) ica: occluded improved kuroka wa et al. 2001. (10) 50/f right headache, cn iii, vi, and v1 palsies. cca: (25 mm) not thrombosed. ica: intact. cca: has heterogenous thrombus on mri but has no flow in dsa. ica: occlusion of petrous segment. (time from diagnosis: 2 years). only cn iii palsy resolved. the patient refused treatment. tsutsu mi al., et 2002 (11) 74/m right cavernous sinus syndrome cca: complete thrombosis (no flow on dsa) ica: occluded na dehdas hti et al. 2003 (4) 31/f right headache, cn iii, and vi palsies. cca: (30 mm) has heterogenous thrombus on mri but has no flow in dsa. ica: intact. cca: partial resolution (aneurysm decrease in size). ica: occlusion at the origin. (time from diagnosis: 18 months). neurologi cally intact. the patient refused treatment. perrini al., et 2005(16 ) 47/m right headache, cn v1, v2 palsies. cca: (28mm), complete thrombosis ica: mild stenosis ica: occlusion at the origin. (time from diagnosis: 6 weeks cn v palsy persist headache and diplopia resolved treated conservativ ely with anti-platelet vasconc ellos al., et 2009 (7) 47/f right headache, cn iii, iv, v1, v2, vi palsies. cca: giant ica: occlusion (time from diagnosis: 6 months) cn v palsy persist headache and diplopia resolved 104 sura h. talib, mayur sharma, vishan p. ramanathan et al. 44/f left headache, cn iii, iv, vi, v 1, v2 palsies. cca: giant ica: occlusion (time from diagnosis: 6 months) cn vi palsy persist headache and diplopia resolved 65/f right headache, cn iii, iv, vi, v1 palsies. cca: giant, partial thrombosis ica: partial occlusion ica: occlusion (time from diagnosis: 5 years) cn palsies persist , headache and diplopia resolved 84/f left headache, cn iii, iv, vi, v 1, v2 palsies. cca: giant, partial thrombosis (heterogenous thrombus on mri but has no flow in dsa). ica: occlusion at the origin. cn iii, vi palsies persist, cn iv, v partially improved, headache and diplopia resolved sastri al. et 2013 (9) 65/f left cn iii, iv, vi, v 1, v2 palsies. cca: giant, partial thrombosis. ica: occlusion at the origin. ophalmo paresis improved, cn v persist treated conservativ ely on aspirin 55/f left seizure, decrease vision, cn iii, iv, vi, v1, v2 palsies. cca: (28mm) partial thrombosis ica: occlusion at the origin. ophalmo paresis improved, decrease d vision persist treated conservativ ely on aspirin das al.,et 2018(3) 45/m left headache, transient unconsciou sness cca: (23mm) partial thrombosis ica: occlusion at the origin. neurologi cally intact treated conservativ ely on aspirin present cases 2022 18/m left headache, cn vi palsy. cca: (28 mm) has heterogenous thrombus on mri but has no flow in dsa. ica: occlusion. cca: complete resolution (no aneurysm detected). ica: occlusion at the origin. (time from diagnosis: 9 months). neurologi cally intact. treated conservativ ely on aspirin shaded rows represent the patients with complete follow-up imaging. ica internal carotid artery, dsa digital subtraction angiogram, mri magnetic resonance imaging, cca cavernous carotid aneurysm. in our case, a total of fourteen patients with concurrent ica occlusion and ccas have been treated conservatively, highlighting the natural history of this unusual association [2, 3, 4, 8, 16, 11 13, 15] (table 1). unfortunately, follow-up imaging was reported only in 7 patients, and, more specifically, concurrent follow-up mri and dsa were available only in 3. hence, only these 3 cases can be used to assess the actual progression of this disease with a high degree of certainty (table 1-shaded rows) [3,8]. lawton et al. proposed a new classification of thrombotic aneurysms based on anatomic relationships between the aneurysm, thrombus, and 105 spontaneous complete resolution of a giant cavernous carotid aneurysm in the setting of ipsilateral ica occlusion lumen [9]. they defined the completely thrombosed aneurysm as one with the classic signals of thrombus on the brain, computed tomography (ct) scan/mri, and the dsa showing no filling of the lumen [9]. of the abovementioned three cases, two cases had a complete thrombosis at presentation, and they end with varying degrees of aneurysmal regression on follow-up [3]. the other patient had a nonthrombosed aneurysm at the initial imaging, which progressed to complete thrombosis at the 2-year follow-up [8]. the association between the cca-ica occlusion, degree of thrombosis, and outcome cannot be inferred due to the limited number of cases and limited follow-up. the timeline for the occurrence of the two pathologies (i.e., cca and ica occlusion) and which one is present at the presentation, and which one progress with the patient's symptoms is to be answered. for the fourteen cases that have been treated conservatively, eight patients had complete occlusion of the ica at the presentation. the other six patients have either intact ica at the initial investigation (2/14) or partially stenosed ica at the presentation (2/14), with the initial occlusion status of the remaining two patients not mentioned. all the six cases of initially not occluded ica end with complete occlusion but with variable duration and extension of occlusion. those cases with delayed occlusion of ica in the association of ipsilateral cca (6/14) had a reported time for the occlusion to occur to be from 6 weeks to 5 years with a mean of 18.9 months. the location of the occlusion is at the origin of the ica from the common carotid artery, with only one patient having a localized occlusion of the petrous and cavernous ica [2, 3, 4, 8, 16, 11 -13, 15] (table 1). obviously, the limited number of cases produces this heterogenicity in the reported findings, and future studies are recommended to continue recruiting more patients and equally important that the patients should have a full radiological follow-up. this will have a profound impact on understanding this unique association, its related pathophysiology, and, most importantly, how to optimize treatment and prevention. figure 1. brain mri and mra at presentation (a-d) showed a giant left cavernous ica aneurysm with mass effect on the left temporal lobe (a, b) with a striking shadow of the thrombosed aneurysm and absence of the left ica proximal to the clinoidal segment in mra (c, d). at 9-month follow-up (e-h) there is complete resolution of the aneurysm, no mass effect on the temporal lobe (e, f) with the disappearance of the aneurysmal shadow, and the same absence of the left ica mra (g, h). conclusion the association of giant cca and ica occlusion on the same side is a rare phenomenon with no current consensus on the appropriate follow -up and management strategy. in this report, we described the first case of spontaneous complete disappearance of a giant cca in the setting of ipsilateral ica occlusion with complete resolution of symptoms at nine months of follow-up. 106 sura h. talib, mayur sharma, vishan p. ramanathan et al. figure 2. a 9-month follow-up dsa showed complete occlusion of the left ica just distal to its origin with sufficient collateral circulation from the right ica. no aneurysmal filling was detected in both (a) and (b). references 1. ambekar, s., madhugiri, v., sharma, m., cuellar, h., & nanda, a. (2014). evolution of management strategies for cavernous carotid aneurysms: a review. world neurosurgery, 82(6), 1077–1085. 2. das kk, singh g, pandey s, bhaisora ks, jaiswal a, behari s, completely thrombosed giant intracranial aneurysm with spontaneous thrombosis of the parent artery: is it the nature’s divine intervention and a self-cure? world neurosurgery (2018), doi: 10.1016/ j.wneu.2018.07.072. 3. dehdashti ar, de tribolet n. giant intracavernous aneurysm thrombosis by spontaneous carotid occlusion. cerebrovasc dis 2003; 15:301‐2. 4. gautier jc, awada a, majdalani a. ophthalmoplegia with contralateral hemiplegia. occlusion of the internal carotid artery due to thrombosis of an intracavernous aneurysm. stroke. 1986 nov;17(6):1321-2. 5. hans, f.j., krings, t., reinges, m.h.t. et al. spontaneous regression of two supraophthalmic internal cerebral artery aneurysms following flow pattern alteration. neuroradiology 46, 469–473 (2004). 6. jefferson rosi junior, leonardo c. welling, lin tchia yeng. cavernous carotid artery aneurysms: epidemiology, natural history, diagnostic and treatment. an experience of a single institution, clinical neurology, and neurosurgery. 7. krings t, alvarez h, reinacher p, ozanne a, baccin ce, gandolfo c, zhao wy, reinges mh, lasjaunias p. growth and rupture mechanism of partially thrombosed aneurysms. interventional neuroradiology. 2007 jun;13(2):117-26. 8. kurokawa r, kuroshima y, yoshida k, kawase t. spontaneous thrombosis of intracavernous internal carotid artery aneurysm and parent artery occlusion in patients with positive balloon test occlusion: two case reports. neurol med chir (tokyo) 2001; 41:436 41. 9. lawton mt, quiñones-hinojosa a, chang ef, yu t. thrombotic intracranial aneurysms: classification scheme and management strategies in 68 patients. neurosurgery. 2005 mar 1;56(3):441-54. 10. ohtaki s, mikami t, iihoshi s, et al. [strategy for the treatment of large-giant aneurysms in the cavernous portion of the internal carotid artery]. no shinkei geka. neurological surgery. 2013 feb;41(2):107-115. 11. perrini p, bortolotti c, wang h, fraser k, lanzino g. thrombosed giant intracavernous aneurysm with subsequent spontaneous ipsilateral carotid artery occlusion. acta neurochir (wien) 2005;147:215‐7. 12. sastri sb, sadasiva n, pandey p. giant cavernous carotid aneurysm with spontaneous ipsilateral ica occlusion: report of 2 cases and review of literature. j neurosci rural pract. 2013;4(suppl 1): s113-s116. 13. sato k, fujiwara s, yoshimoto t, onuma t. two cases of spontaneous internal carotid artery occlusion due to giant intracranial carotid artery aneurysm. stroke 1990;21:1506‐9. 14. sudha menon, r. girish menon. cavernous carotid aneurysms: to do or not to do? thieme. 15. tsutsumi m, kazekawa k, tanaka a, ueno y, nomoto y: spontaneous thrombosis of a giant intracavernous internal carotid artery aneurysm and ipsilateral internal carotid artery occlusion: radiat med 20:261-263, 2002 16. vasconcellos lp, flores ja, conti ml, veiga jc, lancellotti cl: spontaneous thrombosis of internal carotid artery: a natural history of giant carotid cavernous aneurysms: arq neuropsiquiatr 67:278-283, 2009. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-013 computed tomography-based morphometric measurements of the atlas (c1) posterior arc yasar karatas, bulent kaya, mehmet fatih erdi, fatih keskin, densel arac, emir kaan izci, mehmet uyar, ali sami kıvrak, erdal kalkan romanian neurosurgery (2020) xxxiv (1): pp. 101-105 doi: 10.33962/roneuro-2020-013 www.journals.lapub.co.uk/index.php/roneurosurgery computed tomography-based morphometric measurements of the atlas (c1) posterior arc yasar karatas1, bulent kaya1, mehmet fatih erdi2, fatih keskin2, densel arac2, emir kaan izci3, mehmet uyar2, ali sami kıvrak1, erdal kalkan1 1 medova hospital, turkey 2 necmettin erbakan university, meram medical faculty, turkey 3 meram training and research hospital, department of neurosurgery, turkey abstract study design: single-center retrospective study objectives: this study is performed to determine the anatomic feasibility of the c1 posterior arc screw and help select an optimal screw trajectory in treating patients with craniovertebral junction pathologies. material and methods: we reported a single-centre retrospective study. forty patients (20 male and 20 female) who underwent cervical computed tomography (ct) were chosen from the hospital records. based on ct images, we measured left laminar length (lll), right laminar length (rll), left laminar angle (lla), right laminar angle (rla), left laminar axial thickness (llat), right laminar axial thickness (rlat), left laminar coronal thickness (llct), right laminar coronal thickness (rlct), and craniocaudal angle (cca) of the c1 posterior arc. results: the mean values and standard deviations (sd) for nine parameters at the c1 posterior arc were determined. lll, rll, llct, and rlct were statistically longer in men than women. rlat was bigger in men but there was no statistical difference. rla was statistically wider in women than men. lla and cca were wider in women but there was no statistical difference, llat was bigger in women but there was no statistical difference. there was no statistical difference in measurements by age. conclusion: the results of this study are important to avoid neurovascular injury and pedicle breakage because of choosing large screw while performing c1 laminar screw fixation. introduction the first cervical vertebra is also referred to the atlas1. posterior wiring2,3, transarticular screws4, and pedicle or lateral mass screws5 methods largely used for c1 posterior fixation. recently, the screw fixation has been preferred instead of wiring or hooks because of providing rapid stability and great fusion rate6. however, screw fixation is associated with an increased risk of vertebral artery (va), spinal cord, and root injury. missing to identify va anomalies can cause iatrogenic keywords computed tomography, morphometric measurements, atlas (c1) posterior arc corresponding author: yasar karatas medova hospital, turkey yasarkrts@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 102 yasar karatas, bulent kaya, mehmet fatih erdi et al. va injury and cerebrovascular accidents in cervical spine surgery7. the most dangerous level is the c1-2 level for a posterior approach and c7 for an anterior approach. therefore, an excellent assessment for the variations in the course of the va is vital for surgeons working from a posterior approach in the upper cervical spine8. in this study, we measured c1 posterior arc parameters to create an alternative surgical way to lateral mass screws and pedicular screws. materials and methods fourty patients (20 male and 20 female) who underwent cervical computed tomography (ct) between 2017 and 2019 in our hospital were chosen from the hospital’s picture archiving and communication system (pacs). none of the patients included in the study had cervical spine or craniovertebral junction trauma. siemens somatom perspective 128 slices ct was used to perform ct examinations and measurements on patients. ct scans were performed by the same team. heads of all patients were fixed in the same position on computed tomography. we assessed axial, sagittal, and coronal ct cuts and measured nine parameters on the c1 posterior arc. left and right laminar lengths (lll, rll) were calculated by measuring the line from posterior tubercle to transverse foramen (figure 1). left and right lamina angles (lla, rla), which also mean mediolateral angle, were calculated as the angle of the lamina with the line passing through the anterior and posterior tubercle (figure 2). left and right axial laminar thicknesses (llat, rlat) were measured from the middle of the lamina (figure 3). left and right coronal laminar thicknesses (llct, rlct) were measured from the middle of the lamina (figure 4). craniocaudal angle (cca) was measured as the angle of the lamina with the line that parallel to the earth (figure 5). we investigated the difference between men and women and patients under fifty and patients over fifty years. data were analyzed by spss (version 24.0, spss inc.) and expressed as mean ± sd. comparisons were made using the t-test. differences among the groups were assessed using the independent samples test. a p value < 0.05 was considered statistically significant. figure 1. laminar length was defined as linear measurement from posterior tubercle to transverse foramen both right and left side. figure 2. laminar angles were defined as the angle of the lamina with the line passing through the anterior and posterior tubercle. 103 computed tomography-based morphometric measurements of the atlas (c1) posterior arc figure 3. axial laminar thickness was defined as the mediolateral diameter of the lamina at its middle point. figure 4. coronal laminar thickness was defined superior-inferior diameter of the lamina. 104 yasar karatas, bulent kaya, mehmet fatih erdi et al. figure 5. cranio-caudal angle (cca) was measured as the angle of the lamina with the line that parallel to the earth. results a total of 40 patients and their lamina were analyzed. measurements belong to men and women are presented in table 1. there were 20 men and 20 women in the study. the mean lll was 350,8500±26,12374 mm in male and 315,0000±26,24380 mm in female. there was a statistical difference between male and female by lll( p=.000). the average laminar length in right side (rll) in men was significantly longer (342,0500±22,48854 mm) than that in women (314,5000±24,15411 mm) (p=0.001). rla was statistically wider in women (48,2650±3,49666 mm) than men (40,5650±15,85308 mm). lla was measured 45,1800±10,04084 mm in men and 48,3200±2,94379 mm in women. these results revealed that no statistical significance was detected in the lla along with men and women (p > 0.050). llat was measured 60,9000±9,74355 mm in men and 61,1000±10,70121 mm in women. there were no statistical differences between the groups. rlat was measured 63,6000±10,89858 mm in men and 61,2500±11,77363 mm in women. there were no statistical differences between the groups. rlct were statistically longer in men (57,1000±11,87611 mm) than women (44,9500±12,06768 mm). llct was measured 55,5500±10,56048 mm in men and 46,0000±12,13520 mm in women. there were no statistical differences between the groups. the mean cca was 10,0250±5,07459 mm in male and 10,3700±5,19535 mm in female. there were no statistical differences between the groups.there were 25 patients (62.5%) under 50 years and 15 patients (37.5%) upper 50 years. measurements belong to age are presented in table 2. there was no statistical difference in any measurements by age. discussion craniovertebral junction (cvj) is osteoligamentous membranous complex composed between brain and spinal cord. layers of muscles, ligaments, and membranes promote bony complex of occiput, atlas, and axis from all around which helps in providing motion as well as stability to this field. cvj can be affected by congenital, developmental, degenerative, traumatic, and neoplastic pathologies9, 10. it is very hard to diagnose instability of the cvj and treat due to their complex anatomical composition and biomechanical characteristics. cvj injuries may lead to sudden fatality or delayed impairment of neurological function11. especially c1–2 fixation techniques have been improved to overcome those troubles. c1 lateral mass c2 pedicle screw fixation using has been raised since it was presented in 1994 by goel and laheri5 and modified in 2001 by harms and melcher6. the patients that have anomalies on the bone or va anatomy are under injury risk while performing these techniques. the authors reported c1 posterior arch screw to reduce the risk of va injury12. the coexistence of a small pedicle and high riding vertebral artery is a risk factor for vertebral artery injury13. interlaminar screw placement is safe in patient that have unilateral vertebral artery occlusion, patients have large paravertebral venous 105 computed tomography-based morphometric measurements of the atlas (c1) posterior arc plexus, patients with fracture near lateral mass or pedicle screw placement site14, 15. studying near the fracture site can cause much bleeding. while interlaminar screw placement, surgeons don’t study around large venous plexus. this situation provides to avoid much bleeding. zarro et al compared the pullout strength of c1 lateral mass screw with unicortical c1 posterior arc screw. they found that unicortical c1 posterior arc screw is stronger than the c1 lateral mass screw in the axial direction16. jin et al. showed that there is no statistical difference between unilateral c1 posterior arc screwc2 laminar screw combined with unilateral c1-2 pedicular screw and whole pedicular screw insertion as performing acute stability in cadaver study17. as a result, the c1 interlaminar screw placement is safe salvage technique for craniovertebral junction stabilization and provides strong fusion. conclusion the appropriate laminar screw sizes in the left side in men are 350 mm length, 60 mm axial thickness and 55 mm coronal thickness. the appropriate laminar screw trajectories in the left side in men angles were 45’ medio-lateral angle and 10’ craniocaudal angle. the appropriate laminar screw sizes in right side in men are 342 mm length, 40 mm axial thicknes and 57 mm coronal thickness. the appropriate laminar screw trajectories in the right side in men angles were 40’ mediolateral angle and 10’ craniocaudal angle. the appropriate laminar screw sizes in left side in women are 315 mm lenght, 61 mm axial thickness and 46 mm coronal thickness. the appropriate laminar screw trajectories in the left side in men angles were 48’ mediolateral angle and 10’ craniocaudal angle. the appropriate laminar screw sizes in the right side in women are 314 mm length, 61 mm axial thickness and 44 mm coronal thickness. the appropriate laminar screw trajectories in the left side in men angles were 48’ mediolateral angle and 10’ craniocaudal angle. references 1. arslan sg, dildes n, kama jd. cephalometric investigation of first cervical vertebrae morphology and hyoid position in young adults with different sagittal skeletal patterns. sci world j. 2014;2014:159784. 2. gallie we. fractures and dislocations of the cervical spine. am j surg. 1936;46:495-9. 3. brooks al, jenkins eb. atlanto-axial arthrodesis by the wedge compression method. j bone joint surg am. 1978;60:279-84. 4. grob d, magerl f. surgical stabilization of c1 and c2 fractures. orthopade. 1987;16:46-54. 5. goel a, laheri v. plate and screw fixation for atlantoaxial subluxation. acta neurochir (wien). 1994;129: 47-53. 6. harms j, melcher rp. posterior c1-c2 fusion with polyaxial screw and rod fixation. spine (phila pa 1976). 2001;26:2467-71. 7. burke jp,gerszten pc,welchwc. iatrogenic vertebral artery injury during anterior cervical spine surgery. spine j. 2005;5(5):508-514. 8. smith md, emery se, dudley a, murray kj, leventhal m. vertebral artery injury during anterior decompression of the cervical spine. a retrospective review of ten patients. j bone joint surg br. 1993;75-b(3):410-415. 9. rhoton al., jr the foramen magnum. neurosurgery. 2000;47(suppl 1):s155–93. [pubmed] 10. kawashima m, tanriover n, rhoton al, jr, ulm aj, matsushima t. comparison of the far lateral and extreme lateral variants of the atlanto-occipital transarticular approach to anterior extradural lesions of the craniovertebral junction. neurosurgery. 2003;53:662–74. 11. dickman ca, papadopoulos sm, sonntag vk, spetzler rf, rekate hl, drabier j : traumatic occipitoatlantal dislocations. j spinal disor. 1993;6 : 300-313. 12. jin gx, wang h, li l, et al. c1 posterior arch crossing screw fixation for atlantoaxial joint instability. spine (phila pa 1976). 2013; 38(22): e1397–e1404. 13. yeom js, buchowski jm, kim hj, chang bs, lee ck, riew kd. risk of vertebral artery injury: comparison between c1-c2 transarticular and c2 pedicle screws. spine j. 2013;13:775–785. 14. matsubara t, mizutani j, fukuoka m, et al. safe atlantoaxial fixation using a laminar screw (intralaminar screw) in a patient with unilateral occlusion of vertebral artery: case report. spine (phila pa 1976). 2007; 32(1): e30–e33. 15. ma xy, yin qs, wu zh, et al. c1 pedicle screws versus c1 lateral mass screws: comparisons of pullout strengths and biomechanical stabilities. spine (phila pa 1976). 2009; 34(4): 371–377. 16. zarro cm, ludwig sc, hsieh ah, et al. biomechanical comparison of the pullout strengths of c1 lateral mass screws and c1 posterior arch screws. spine j. 2013; 13(12): 1892–1896. 17. jin gx and huan w. unilateral c-1 posterior arch screws and c-2 laminar screws combined with a 1-side c1–2 pedicle screw system as salvage fixation for atlantoaxial instability. j neurosurg spine. 2015; 24: 315–320. doi: 10.33962/roneuro-2023-005 anterior approach arthrodesis alif with use of a titanium cage for treatment of postoperative spondylodiscitis after lumbar microdiscectomy sofia r. soares, júlia r.g.b. cavalcanti, alexandre l.c.l.r. silva, thiago g. martins, giacomo f. souza, jim u. c. neto romanian neurosurgery (2023) xxxvii (1): pp. 41-45 doi: 10.33962/roneuro-2023-005 www.journals.lapub.co.uk/index.php/roneurosurgery anterior approach arthrodesis alif with use of a titanium cage for treatment of postoperative spondylodiscitis after lumbar microdiscectomy sofia r. soares1, júlia r.g.b. cavalcanti1, alexandre l.c.l.r. silva1, thiago g. martins2, giacomo f. souza2, jim u. c. neto3 1 centro de ciências médicas, universidade federal da paraíba, joão pessoa, paraíba, brazil 2 clínica da coluna, joão pessoa, paraíba, brazil 3 medical hospital dia, joão pessoa, paraíba, brazil abstract introduction. infectious spondylodiscitis has an incidence of 0.21-3.6%. the best intervention should be individualized, using antibiotics only or combining them with stabilizing surgeries. case presentation. a 38-year-old man presented with lumbosciatalgia, severe pain and inability to ambulate. magnetic resonance imaging (mri) of the lumbar spine showed l5-s1 extruded disc herniation and the patient underwent endoscopic microdiscectomy with complete remission of symptoms. after two weeks, he reported severe low back pain and a return of difficulty to walk. laboratory tests showed an increase in crp and esr. mri showed signs of lumbar spondylodiscitis. the patient started on broad-spectrum intravenous antibiotic therapy. he evolved with improvement in laboratory parameters and maintenance of low back pain. due to the failure of conservative treatment, anterior approach arthrodesis (alif) was chosen, with the complete improvement of the low back pain and the return of the ability to walk. discussion. postoperative spondylodiscitis’ frequency depends on the invasiveness of the operation and the type of surgery performed. the most likely source of infection is direct inoculation by virulent pathogens during surgery. a diagnosis delay of more than two months is considered a risk factor for generating adverse results. a conservative approach is indicated for the patient who is neurologically intact and with minimal bone destruction. surgical indications are the presence of neurological deficits, intraspinal abscesses, extensive bone destruction, and failure of conservative management. alif is supported in the literature because it allows wide exposure of the entire disc space through efficient access to the spine with the complete evacuation of the disc, avoiding dissection of perineural scar tissue and preserving the articular facets. conclusion. early diagnosis and treatment are crucial, although there is still no consensus about the best treatment approach. the use of a titanium cage with a bioglass graft had a good response in pain and infection control in our case. keywords arthrodesis, discitis, discectomy, postoperative period corresponding author: sofia ramos soares centro de ciências médicas, universidade federal da paraíba, joão pessoa, paraíba, brazil sofiaramossoares9@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 42 sofia r. soares, júlia r.g.b. cavalcanti, alexandre l.c.l.r. silva et al. introduction infectious spondylodiscitis is an infection of the intervertebral disc and adjacent vertebral bodies, with an postoperative incidence of 0.21-3.6%[1]. the most recommended diagnostic method is magnetic resonance imaging (mri), due to the early identification of the disease made by this exam[2,3]. the appropriate intervention should be individualized, using either conservative methods alone, such as antibiotic therapy, or combined with stabilizing surgery [2,4]. the purpose of this paper is to report and discuss the case of a patient who underwent an anterior approach arthrodesis (alif) using a titanium cage after presenting postoperative spondylodiscitis from a lumbar microdiscectomy. case presentation male patient, 38 years old, attended the first medical appointment with lumbosciatalgia on the right side. he reported severe pain with progressive worsening and inability to ambulate. neurological examination revealed distal paresis of the right lower limb with achilles hyporeflexia and pain in s1 root territory. magnetic resonance imaging (mri) of the lumbar spine showed l5-s1 extruded disc herniation with radicular compression on the right side. patient underwent endoscopic microdiscectomy with complete remission of symptoms. after two weeks, the patient reported severe mechanical low back pain, unresponsive to the use of opioids. moreover, there was a return of difficulty in walking and the need for intravenous analgesia for pain control. laboratory tests showed an increase in c-reactive protein (crp) and erythrocyte sedimentation rate. control mri showed signs of contrast-enhanced l5-s1 lumbar spondylodiscitis, such as diffuse hyposignal on t1 between the l5 and s1 vertebral bodies, with irregularity and loss of definition of the terminal plateaus and compression of the ventral surface of the dural sac and nerve roots (figure 1). in view of the diagnosis, the patient was hospitalized and started on broad-spectrum intravenous antibiotic therapy with vancomycin hydrochloride and meropenem for eight weeks. he evolved with improvement in laboratory parameters, but there was maintenance of intense low back pain. due to the failure of conservative treatment, anterior approach arthrodesis (alif) using a titanium cage and bioglass graft was chosen (figure 2). figure 1. mri with contrast uptake exposing spondylodiscitis of the l5 and s1 vertebral bodies. figure 2. postoperative x-ray presence of the titanium cage and graft. three months after the procedure, the patient presented complete improvement of the low back pain, return of the ability to walk, and undergoing rehabilitation for muscle strengthening. 43 anterior approach arthrodesis alif with use of a titanium cage discussion spinal infections are relatively uncommon, but the incidence is significantly increasing due to the growing number of spinal interventions, which often require long operation times and deployment of significant amounts of instrumentation [3,5]. postoperative spondylodiscitis is a rare primary infection of the nucleus pulposus, with secondary involvement of the cartilaginous endplate and vertebral bone, mainly affecting single segments in the lumbar region [1,6]. the frequency depends on the invasiveness of the operation and is between 0.1% and 0.6% for microsurgical operations, as in the reported case, and between 1.4% and 3% for macrosurgical operations [7]. the incidence also varies with the type of surgery performed, and usually occurs after minimally invasive spinal procedures, including laminectomy, discectomy, discography, myelography, paravertebral injection, lumbar puncture, and spinal fusion, with or without instrumentation [1, 6, 8]. in the presented case, the patient had spondylodiscitis after a microdiscectomy to treat a herniated disc. the most likely source of infection for postoperative spondylodiscitis is direct inoculation by virulent pathogens during surgery, the most common being staphylococcus aureus and streptococcus epidermidis bacteria, but hematogenous contamination, although uncommon, is also a possible cause [6]. among the risk factors, malnutrition, neoplasms, obesity, alcoholism, smoking, chemotherapy, immunosuppression, advanced age, diabetes mellitus, and spinal trauma have been reported in the literature to predispose patients to postsurgical discitis [1, 6]. in addition, several studies report a bimodal age distribution among patients with spondylodiscitis, with peaks in the under 20 age group and the 50 to 70-year-old group, although all ages can be affected [9]. spondylodiscitis also has a male preponderance, with a female/male ratio of 1.5-2:1.9 [9]. the main symptom is low back pain [2, 10, 11]. the pain is not always severe, but tends to be persistent, often preceded by a febrile episode [10, 11]. in the patient, the febrile episode was not reported, but there was intense low back pain. among the diagnostic procedures described in the literature, mri, in particular, is able to show the expansion of inflammatory processes into the spinal canal and soft tissues. esr, crp and the white blood cell count are key parameters for monitoring disease activity and the suspicion of associated infection [2, 11, 12]. early diagnosis including assessment of the extent of infection is crucial [2, 3]. a delay of more than two months is considered a risk factor for generating adverse results [9]. the treatment possibilities consist of conservative or surgical management. a conservative approach is indicated for the patient who is neurologically intact and with minimal bone destruction. therapeutic options are based on the culture and use of antibiotics, immobilization, analgesics and orthoses [3]. despite having a good outcome in most cases, the prolonged period of immobilization and the long duration of antibiotic regimens in the conservative approach can lead to medical such as renal failure and allergic reactions and psychosocial consequences [2]. surgical indications are the presence of neurological deficits, intraspinal abscesses, extensive bone destruction, and failure of conservative management [3, 9, 13, 14]. the objectives of surgical treatment are root decompression, debridement, eradication of the focus of infection, identification of pathogens, correction of deformity, and restoration of the physiologic profile of the spine [3, 14]. based on the treatment of 75 postoperative discitis, ahsan et al. reported that the success rate of surgical treatment was 90% and, compared to conservative treatment, required a shorter hospital stay, shorter immobilization period and administration of antibiotics and greater symptom relief with lower complication rates, similar to other studies [2]. however, there is still no consensus about the decision between proceeding conservatively or surgically and, like the procedure of choice, these are topics still under discussion [3]. the technique chosen in this case was anterior lumbar (interbody) fusion (alif), which is supported in the literature because it allows wide exposure of the entire disc space through efficient access to the spine with complete evacuation of the disc, avoiding dissection of perineural scar tissue and preserving the articular facets. this facilitates the insertion of the cage -correcting the overload of the structure and relieving pain and the restoration of the disc height, which increases the foraminal volume, indirectly decompressing the nerve roots and relieving radicular symptoms [9, 15, 16, 17]. however, the longer surgery time and the 44 sofia r. soares, júlia r.g.b. cavalcanti, alexandre l.c.l.r. silva et al. consequent increased risk of infection were also exposed as negative points of alif [17]. jägersberg et al. reported, in a german retrospective study in which 83 patients with post-discectomy lumbar complications between 2005 and 2011 were analyzed, that from 2008, due to the previously mentioned advantages, the alif technique was applied in preference to the others except in patients with risk factors that complicated the previous approach, such as extreme overweight and men who spoke out against this approach due to the risk, although low, of retrograde ejaculation [17]. the recorded mortality of spondylodiscitis is less than 5% [11]. although uncommon, postoperative spondylodiscitis can be associated with severe longterm sequelae, such as neurological deficit and severe pain resulting in disability, which occurs in about 30% of cases [1, 5, 9]. in addition, it has complex diagnosis and treatment, usually resulting in prolonged hospital stays and recovery time [14]. however, most cases reported in the literature, especially those undergoing surgical treatment and without delay in diagnosis, had good outcomes with significant but partial reduction of symptoms, especially low back pain. the studies by chang et al., ahsan et al. and jägersberg et. al. reported positive results in 80%, 90% and 76% of patients, respectively [2, 8, 17]. for conservative treatments, on the other hand, the overall prognosis is successful in about 7083% of cases [2]. finally, in the literature, the only factor found to prevent infection was preand intraoperative antibiotic prophylaxis. brown et al. recommend first or second generation cephalosporin. vancomycin associated with gentamicin is advised in patients allergic to cephalosporins or colonized by methicillinresistant staphylococcus aureus and in long operative procedures, and for this last group, the use of frequent saline irrigation, with or without povidone-iodine to reduce wound contamination, is also recommended [1]. conclusion in our report, a patient who underwent an arthrodesis for the treatment of postoperative spondylodiscitis was presented. early diagnosis and treatment are crucial, although there is still no consensus about the best treatment approach. the use of titanium cage with bioglass graft had a good response in pain and infection control in our case. references 1. gerometta a, bittan f, rodriguez olaverri jc. postoperative spondilodiscitis. international orthopaedics. 2012;36(2):433-438. doi:10.1007/s00264011-1442-0 2. ahsan mk, hasan ms, khan msi, sakeb n. management of post-operative discitis following discectomy in a tertiary-level hospital. journal of orthopaedic surgery. 2021;29(1). doi:10.1177/2309499020988213 3. weckbach s, lutz b, wölfle-roos j v., reichel h. infections of the spine: therapeutic strategies. chirurg. 2016;87(10):839-846. doi:10.1007/s00104-016-0247-5 4. akgul t, bayram s, korkmaz m, karalar s, dikici f, sar c. surgical approach algorithm in the treatment of lumbar and thoracolumbar pyogenic spondylodiscitis. turkish neurosurgery. 2022;32(1):83-90. doi:10.5137/10195149.jtn.33784-21.2 5. fang a, hu ss, endres n, bradford ds. risk factors for infection after spinal surgery. spine. 2005;30(12):14601465. 6. zou mx, peng ab, dai zh, et al. postoperative initial single fungal discitis progressively spreading to adjacent multiple segments after lumbar discectomy. clinical neurology and neurosurgery. 2015;128:101-106. doi:10.1016/j.clineuro.2014.11.012 7. dulani r, shrivastava s, singh p. a rare case report: tubercular spondylodiscitis following lumbar disc surgery. asian pacific journal of tropical medicine. 2010;3(6):496-498. doi:10.1016/s1995-7645(10)60120-4 8. chang cw, tsai tt, niu cc, et al. transforaminal interbody debridement and fusion to manage postdiscectomy discitis in lumbar spine. world neurosurgery. 2019;121:e755-e760. doi:10.1016/j.wneu. 2018.09.211 9. gouliouris t, aliyu sh, brown nm. spondylodiscitis: update on diagnosis and management. journal of antimicrobial chemotherapy. 2010;65(suppl. 3). doi:10.1093/jac/dkq303 10. digby j, kersley j. pyogenic non-tuberculous spinal infection: an analysis of thirty case. the journal of bone and joint surgery. 1979;61(1):47-55. doi:10.1302/0301620x.61b1.370121 11. mcdermott h, bolger c, humphreys h. postprocedural discitis of the vertebral spine: challenges in diagnosis, treatment and prevention. journal of hospital infection. 2012;82(3):152-157. doi:10.1016/j.jhin.2012.07.009 12. haaker rg, senkal m, kielich i", kr j, kielich t, kr~imer • j. percutaneous lumbar discectomy in the treatment of lumbar discitis. eur spine j. 1997;6:98-99. 13. korinth mc. treatment of cervical degenerative disc disease current status and trends. zentralblatt fur neurochirurgie. 2008;69(3):113-124. doi:10.1055/s-20081081201 14. gasbarrini a, borlani l, zamparinp e, et al. spinal infection multidisciplinary management project (simp): from diagnosis to treatment guideline. international 45 anterior approach arthrodesis alif with use of a titanium cage journal of immunopathology and pharmacology. 2011;24(i):95-100. 15. linhardt o, matussek j, refior hj, krödel a. long-term results of ventro-dorsal versus ventral instrumentation fusion in the treatment of spondylitis. international orthopaedics. 2007;31(1):113-119. doi:10.1007/s00264006-0140-9 16. teng i, han j, phan k, mobbs r. a meta-analysis comparing alif, plif, tlif and llif. journal of clinical neuroscience. 2017;44:11-17. doi:10.1016/j.jocn.2017.06 .013 17. jägersberg m, schneider k, schaller c, richter m. alif versus tlif for post-discectomy syndrome. journal of neurological surgery, part a: central european neurosurgery. 2014;75(5):329-335. doi:10.1055/s-00341372432 doi: 10.33962/roneuro-2021-068 tconfiguration stent assisted coiling treatment of a complex wide-necked basilar tip aneurysm a. chiriac, n. dobrin, georgiana ion, z. faiyad, a. iencean, i. poeata romanian neurosurgery (2021) xxxv (4): pp. 403-407 doi: 10.33962/roneuro-2021-068 www.journals.lapub.co.uk/index.php/roneurosurgery tconfiguration stent assisted coiling treatment of a complex wide-necked basilar tip aneurysm a. chiriac, n. dobrin, georgiana ion, z. faiyad, a. iencean, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi, romania “prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract the advancement of intracranial stent technology and techniques has extended the applications of endovascular coiling methods for complex intracranial aneurysms. coiling of wide-necked and complex bifurcation aneurysms usually requires double stent implantation. different configurations for double stent-assisted coil embolization have been described. the t-configuration stent-assisted coiling procedure was recently described as a feasible, effective, and relatively safe endovascular technique used to treat wide-necked complex bifurcation aneurysms. in this article, we present the successful management of a complex wide-neck basilar tip aneurysm using a slightly modified t-configuration stent-assisted coiling technique introduction stent-assisted coiling is an increasingly used technique for the treatment of wide-necked intracranial aneurysms. stents offers technical stability and durability of coil placement to prevent coil prolapse into the parent artery. however, a single-stent technique it can still be a challenge for the treatment of complex wide-necked aneurysms especially those in which the base of the aneurysm directly involves both bifurcation branches. thus, in the case of these particular anatomical situations, endovascular treatment in optimal conditions requires the use of a double stent technique. the efficacy and safety of various configurations, such as x and y stenting have been reported in the endovascular treatment of the complex intracranial aneurysm. in this study we describe the use of a particular t-configured double stent–assisted coiling technique for the treatment of wide-necked and complex basilar tip aneurysm. the efficacy and safety of this technique were also discussed referring to the few cases already presented in the literature [1,2]. keywords t-configuration, double stent assisted coiling technique, intracranial aneurysm corresponding author: a. chiriac “gr. t. popa” university of medicine and pharmacy, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 404 a. chiriac, n. dobrin, georgiana ion et al. case presentation a female patient of 44-year-old was addressed to our emergency department for a subarachnoid haemorrhage revealed on cranio-cerebral ct scan. at admission she was in unconscious status with mild nuchal rigidity. the family declare severe headache suddenly installed a day ago. her past medical history included hypertension with no regular treatment. the brain ct and ct angiography demonstrated a mild hydrocephalus and a complex basilar tip aneurysm as source of haemorrhage. the patient was intubated and immediately transferred to neurosurgery department for an external ventricular drain implantation. the patient was proposed for an endovascular aneurysm occlusion for the next day. a written informed consent was signed by patient family after discussions with the operating team. figure 1. a, b brain ct diagnosis highlighting sah and the aneurysm lesion; c post interventional barin ct control; d,e – vascular 3d reconstruction showing the bilobate basilar tip aneurysm; f – schematic image of the t-configuration double stent arrangement; g-n – intraprocedural dsa images. 405 tconfiguration stent assisted coiling treatment of a complex wide-necked basilar tip aneurysm the procedure was performed on a biplane angiography system (infinix, toshiba, canon medical system) and started with evaluation of both carotid and vertebral artery. the left ica was founded obliterated and a total compensation of this vascular territory provided by the posterior circulation via a large left posterior communicating artery. the 3d dsa reconstruction image showed a large complex basilar tip aneurysm with two lobes in an hourglass anatomical configuration, a very wide neck involving both posterior cerebral artery junctions, originating from an asymmetric relation with the aneurysm sac. a dual stent support technique was deemed necessary for a safe endosaccular coiling and both pca preservation (fig 1). the patient was premedicated with 150 mg aspirin before procedure and 5000 ui heparin after 6f femoral sheath (merit medical) placement. with the patient under general anaesthesia, the distal cervical part of left vertebral artery was catheterized with 6f chaperon guiding catheter (microvention) carefully advanced over 0.035 glidewire. a bolus dose of 2 mg of nimodipine (nimotop, bayer health care ag) diluted in 140 ml of 0.9% nacl solution was infused through the guiding sheath for 10 minutes to prevent the development of vasospasm during the procedure. 3d angiographic imaging working projection was used for the guidance on roadmap images. we slightly modified the already reported tconfiguration stent–assisted coiling technique by step-by-step catheterizing of the daughter branches and the aneurysm sac to avoid multiple catheter manoeuvring through the basilar trunk. a prowler select plus microcatheter (codman j&j) was then very carefully advanced over a 0.014 transed microwire (boston scientific) and positioned into the left posterior cerebral artery. at that point, the proximal end of the first stent, forming the short arm of the t configuration, was placed at the aneurysm neck, incorporating the corresponding daughter vessel. this branch was chosen for detachment of the first stent due to its closest relationship to the aneurysm neck and the tip of the basilar artery. thus, the circumference of the distal end of this stent will be positioned so as not to overlapping (be under) the orifice of the second vascular branch of the bifurcation. to place the second stent, the right posterior cerebral artery was achieved carefully passing between the proximal end of the first deployed stent and the uncovered/unprotected aneurysmal neck of the prowler select plus microcatheter over .014-inch microwire. the longer second stent was then fully deployed in the other daughter vessel, extending proximally into the basilar artery trunk. after the full deployment of the stents, a prowler 10 microcatheter is placed into the aneurysm the anterior lobe of the aneurysm. after its complete angiographic occlusion, the microcatheter is positioned to the posterior lobe and the coiling of the aneurysm was continued until no further coils could be safely deployed within the aneurysm sac. ffinal dsa images demonstrated a “raymond class i” complete aneurysm occlusion with no neck remnant, coil herniation, clot formation or branch occlusion, and with no perioperative or perspective complications. the patient's evolution was slowly progressive, with suprimation of endotracheal intubation at 2 days postoperatively, and of the external drainage at 7 days. she was transferred to neurological recovery unit at three weeks presenting gait difficulties, dizziness and nystagmus. discussion the endovascular treatment of wide-necked and complex bifurcation aneurysms which incorporates both vascular branches is still a challenge for endovascular neurosurgeons. despite the progressive development of the new techniques for wide-necked aneurysm like double-balloon remodeling method or double-stent–assisted coiling technique, there are still complex anatomical situations that require continuous adjustment of them. in 2005 chow et al. were among the first to describe the y-stent–assisted coiling technique that greatly improved the ability to treat the wide-necked basilar bifurcation aneurysms. with this, the doublestent–assisted coiling procedures began to be used for wide-necked bifurcation aneurysms with various locations. however, subsequent studies have shown that y-stenting may be associated with some technical risks and difficulties, especially when using 2 closed-cell stents. thus, the need for catheterization of the second daughter vessel and passage of the second stent through the interstices of the first deployed stent may cause migration, dislocation, or deformation of the first stent. the occurrence of an hourglass-like deformation or stent narrowing at the point of intersection of the two 406 a. chiriac, n. dobrin, georgiana ion et al. stents may induce thromboembolic events. also, the intersection of the two stents at the level of the aneurysm neck may create technical difficulty for a possible subsequent catheterization of the aneurysm. moreover, studies have shown that intraluminal crossing struts of 2 stents in a y configuration are less susceptible to the progression of the endothelialization phenomenon, and may constitute a source of delayed thromboembolic complications [1,2,3]. cho et al. reported for the first time the use of the t-configuration in the double stenting technique for the endovascular coiling treatment of wide-necked basilar bifurcation aneurysms. inspired by the tstent configuration used to treat coronary atherosclerotic bifurcation lesions, they attempted to resolve the safety issues associated with y stenting. thus, one of the main technical advantages of t stenting is represented by the elimination of risk of dislocation for the initial stent during the second stent passaging and deployment. also, the t-stenting technique does not require any attempt of microcatheterization through the interstices of a crossing stents for coils placement in to the aneurysm. furthermore, the presence of a total conformability with vascular anatomy and complete wall apposition of the stents increase proliferation of the endothelialization phenomenon on the entire surface of the implants, decreasing the risk of structural stenosis over time [2,5,6]. generally, the technique of placing stents in tconfiguration, means the deployment of a stent from one bifurcation branch to the wide aneurysmal neck and the second stent from the other opposite branch of the bifurcation into the parent trunk vessel. however, the technique of double t-stenting is a technical challenge, sometimes difficult or impossible to achieve, as in the case of large complex aneurysms with unfavorable anatomical configurations (sharp angles in the relationship between bifurcation vessels-carrier vessels wide neck) as so called “arrow configuration”. the "anatomical t-shaped configurations" of the bifurcation aneurysms are the most accessible to use the double t-stenting technique even in the case of an asymmetry between the two origins of the bifurcation vessels towards the neck and the parent trunk vessel. however, of course, the placement of the stent in t-configuration should be reserved for patients with well-sized p1 vascular segments. otherwise, placing a single stent in the large p1 is the option for patients with p1 hypoplasia / aplasia on one side. the simultaneous use of multiple microcatheters in the double stenting procedures may create a potential risk of thromboembolism. the possibility of application of a staged stenting by using a single microcatheter in the case of tconfiguration stenting followed by the placement of coils only through the passage of the microcatheter through the interstices of a single stent can reduce this potential complication risk [2,3,4,6]. there are limited data in the literature regarding the safety and efficacy of the t-stent–assisted coiling technique. aydin et all published in 2019 the largest series of patient treated by double t-stent–assisted coiling technique. they also present the successful applicability of t-stent–assisted coiling for the treatment of anterior circulation aneurysms. the immediate complete aneurysm occlusion rates reported was relatively high 83.3% compared with ystent–assisted coiling and close to the results of conventional single-stent–assisted coiling studies. at the last follow-up examinations, the complete occlusion was documented in 90.0% of patients. regarding periprocedural complications, these were highlighted in 13.7% of cases, while delayed complications, generally represented by thromboembolic phenomena, were reported in only 3.9% of cases. of these, only 1.9% led to permanent morbidity, and the death being registered in only 1% [1,2]. conclusions the t-configuration double stent–assisted coiling technique is a feasible and relatively safe endovascular procedure for the treatment of complex wide-neck cerebral aneurysms located at different bifurcation sites. however, a few aspects like the anatomy, angulation and take-off of the vessels may play a role in which technique to choose. through this case report we showed that tconfiguration stent-assisted coiling is an alternative successfully treatment for selected cases with favourable clinical outcomes and satisfactory midterm results. references 1. aydin, k., sencer, s., barburoglu, m., berdikhojayev, m., aras, y., sencer, a., & i̇zgi, n. (2017). midterm results of tstent–assisted coiling of wide-necked and complex 407 tconfiguration stent assisted coiling treatment of a complex wide-necked basilar tip aneurysm intracranial bifurcation aneurysms using low-profile stents. journal of neurosurgery, 127(6), 1288-1296. 2. aydin, k., stracke, c. p., barburoglu, m., yamac, e., berdikhojayev, m., sencer, s., & chapot, r. (2019). longterm outcomes of wide-necked intracranial bifurcation aneurysms treated with t-stent–assisted coiling. journal of neurosurgery, 134(1), 39-48. 3. cheung, n. k., chiu, a. h., cheung, a., & wenderoth, j. d. (2018). long term follow-up of bifurcation aneurysms treated with braided stent assisted coiling and complex t-and y-stent constructs. journal of neurointerventional surgery, 10(6), 560-565. 4. chiriac, a., ion, g., dobrin, n., & poeata, i. (2018). stent assisted coiling technique for anterior communicating artery aneurysms treatment. romanian neurosurgery, 593-601. 5. lazzaro, m. a., & zaidat, o. o. (2011). x-configuration intersecting enterprise stents for vascular remodeling and assisted coil embolization of a wide neck anterior communicating artery aneurysm. journal of neurointerventional surgery, 3(4), 348-351. 6. zhao, k. j., yang, p. f., huang, q. h., li, q., zhao, w. y., liu, j. m., & hong, b. (2012). y-configuration stent placement (crossing and kissing) for endovascular treatment of wide-neck cerebral aneurysms located at 4 different bifurcation sites. american journal of neuroradiology, 33(7), 1310-1316. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-023 efficacy of c-arm scopy-guided erector spinae plane block (espb) in postoperative pain control and reduction of opioid side effects in spinal instrumentation surgery yasar karatas, fatih keskin, mehmet fatih erdi, bulent kaya, ibrahim kosemen, mehmet kenan, erdal kalkan romanian neurosurgery (2020) xxxiv (1): pp. 150-153 doi: 10.33962/roneuro-2020-023 www.journals.lapub.co.uk/index.php/roneurosurgery efficacy of c-arm scopy-guided erector spinae plane block (espb) in postoperative pain control and reduction of opioid side effects in spinal instrumentation surgery yasar karatas1, fatih keskin2, mehmet fatih erdi2, bulent kaya1, ibrahim kosemen1, mehmet kenan2, erdal kalkan1 1 medova hospital, konya, turkey 2 necmettin erbakan university, meram medical faculty, department of neurosurgery, konya, turkey abstract background: spinal instrumentation surgery causes significant pain in patients. as a result, patients are exposed to excessive opioid use and the associated side effects, as well as prolonged hospital stay, resulting in economic burden. local anaesthetics can help both reduce postoperative pain and minimize the side effects associated with systemically administered opioid analgesics. objective: the aim of this retrospective study was to investigate the effect of erector spinae plane block on analgesia in spinal instrumentation surgery and to reduce the side effects of excessive opioid use. materials and methods: we reported a retrospective study. thirty patients, who underwent spinal instrumentation surgery from 2017 to 2018, were chosen from the hospital records. we performed spinal instrumentation and decompression by laminectomy to all patients under general anaesthesia. while 15 of these patients underwent erector spinae plane block, these patients received patient-controlled analgesia postoperative period. the other 15 patients received only patientcontrolled analgesia postoperative period. we analyzed patients' data for differences in preoperative and postoperative visual analogue scores, nausea vomiting scores, constipation life quality scale, patient-controlled analgesia shot count and mean opioid consumption of patients. results: the data of 30 patients undergoing lumbar spinal instrumentation surgery were retrospectively analyzed. there was no significant difference in the age, preoperative vas, preoperative odi and sex between the two groups (p˃0,05). in addition, there were statistically significant differences in postoperative vas, postoperative odi, nausea vomiting score, constipation life quality score (clqs), petidin consumption and pca shot count (p <0.05). in all variables with significant differences, the values in the block group were lower than the non-block group. conclusion: espb provides effective analgesia and reduces side effects due to excessive opioid usage. keywords lumbar, instrumentation, surgery, pain, erector spinae plane, block corresponding author: yasar karatas medova hospital, department of neurosurgery, konya, turkey yasarkrts@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 151 efficacy of carm scopy-guided erector spinae plane block in spinal instrumentation surgery introduction open lumbar spine instrumentation surgery causes significant soft tissue damage because of large dissection and stripping the muscles. as a result, patients complain of nociceptive, neuropathic and inflammatory pain. [1]. in recent years, pain control after spinal surgery has been targeted with minimal opiate use. the use of gabapentinoids, acetaminophen, neural blockages and long-term local anesthetics is supported by scientific evidence [2,3]. erector spinae plane block (espb) was defined for thoracic and abdominal pain previously [4,5]. there are various articles about postoperative pain control of erector spinae plane block. however, for the first time, we present a study showing that the amount of excessive opioid use is reduced and the associated side effects are reduced. materials and methods we reported a retrospective study. this retrospective study included the data of thirty patients, who underwent spinal instrumentation surgery from 2017 to 2018. preoperative and postoperative data such as age, sex, vas, odi, constipation quality life score, nausea vomiting score, petidine use, number of pca shot were collected. each patient’s outcome was noted by the same surgeon. postoperative vas, clqs, nausea vomiting score measured in postoperative day 1 and postoperative odi measured in postoperative day 30. 1. surgery and postoperative protocol the same surgeon performed all operations. instrumentation and decompression by laminectomies were performed for all patient through a midline incision followed by stripping of paraspinal musculature. the patients underwent the same level surgical procedure. the participants had access to intravenous patient-controlled analgesia that comprised 1 mg/h continuous pethidine administration and 20 mg pethidine bolus infusion when requested by the participants. the bolus was permitted three times in a hour for all participants. 2. erector spinae plane block technique c-arm-scopy guided erector spinae plane block was performed just before surgıcal incision by the same surgeon. espb was made bilaterally at the level of instrumentation and decompression. after the patient was placed in prone position and sterile isolation was achieved, transverse process was determined by scopy. with a 20-g needle, the bottom of the transverse process was reached. the bilateral espb were performed by injecting 5% bupivacaine (20 ml into each side) for each level into the deep surface of the erector spinae muscle and the transverse processes of the lumbar vertebrae 3.statistical analysis statistical analysis of the study was performed in r 3.1.2 package program. descriptive measures of the quantitative variables in the study are shown with their median, minimum and maximum values. the suitability of the variables to normal distribution was examined by shapiro wilk test. mann whitney u test was used to compare two independent variables. intragroup changes of variables were examined by wilcoxon test. fisher exact chi-square test was used for group comparison of qualitative variables. in all statistical analyzes in the study, p values less than 0.05 were considered statistically significant. results there was no statistically significant difference between the groups in terms of age, preop vas and preop odi (p> 0.05). in addition, there were statistically significant differences in postop vas, postop odi, nausea vomiting score, clqs, petidine consumption and pca shot count (p <0.05). in all variables with significant differences, the values in the non-block group were higher than the block group (table 1). the change in vas and odi values in the block group was statistically significant (p <0.001). similarly, the change in vas and odi values were significant in the non-block group (p <0.001). both vas and odi variables were significantly reduced in both groups (figure 1). on the other hand, the mean decrease in vas values in the block group was 79.0%, whereas the mean decrease in vas values in the non-block group was 67.1% and there was a statistically significant difference between the groups in terms of vas values (p <0.001). in other words, there has been much more decline in the block group. (figure 2) the mean decrease in odi values in the block group was 55.4% and the mean decrease in odi values in the non-block group was 48.3% and there was no statistically significant difference between the groups in terms of the decrease in odi values (p = 0.202). decreases in odi values were similar in both groups (figure 3). there 152 yasar karatas, fatih keskin, mehmet fatih erdi et al. was no statistically significant difference between the groups in terms of gender (p = 1,000). in both groups, the ratio of men and women is 80% to 20% (table 2). figure 1. both preoperative and postoperative vas and odi variables in the groups. figure 2. the mean decrease in vas values in the groups. figure 3. the mean decrease in odi values in the groups. table 1. mean age of groups, preoperative vas, postoperative vas, preoperative odi, postoperative odi, nausea vomiting score, clqs, petidine consumption and pca shot count are shown in table. espb with bupivacain espb without bupivacain p age 61,13 ± 18,28 66 (14-81) 64,20 ± 13,72 69 (38-85) 0,870 vas preop 8,20 ± 1,21 8 (6-10) 8,73 ± 0,88 9 (7-10) 0,250 vas postop 1,73 ± 0,70 2 (0-3) 2,87 ± 0,64 3 (2-4) <0,001 odi preop 54,47 ± 14,70 60 (26-80) 55,53 ± 14,03 60 (32-80) 0,806 odi postop 22,13 ± 6,83 20 (13-35) 26,80 ± 4,81 27 (16-36) 0,023 nausea vomiting score 1,27 ± 1,22 1 (0-4) 3,07 ± 1,71 3 (1-8) 0,002 clqs 14,47 ± 7,76 15 (4-30) 26,93 ± 8,67 27 (16-42) <0,001 petidin comsumption 42,53 ± 22,96 35 (12-91,6) 146,25 ± 29,83 149,3 (85-200) <0,001 pca shot count 1,80 ± 1,37 2 (0-5) 7,40 ± 1,60 8 (5-10) <0,001 #mann whitney u test table 2. the ratio of men and women in the groups. #mann whitney u test espb with bupivacain espb without bupivacain p male 3 (%20,0) 3 (%20,0) 1,000 female 12 (%80,0) 12 (%80,0) #fisher exact chi-square test discussion posterior spine surgery is a very painful procedure for patients on the first postoperative day [6]. although opioids are an important pillar of postoperative analgesia treatment, high doses given for severe pain control have important side effects such as cognitive impairment, respiratory depression, addiction, constipation, nausea and vomiting [7]. the risk of cardiac and respiratory complications increases in patients without effective pain control. in addition, delay in mobilization due to pain is a separate problem in these patients. hospital stay is prolonged and chronic pain may occur [8]. the paravertebral muscles and the posterior elements of the spine are innervated by the dorsal roots of the 153 efficacy of carm scopy-guided erector spinae plane block in spinal instrumentation surgery spinal nerves. dorsal roots are separated from the root immediately after the exit of the spinal nerve from the foramen and are distributed in the superficial soft tissue. in the erector spinae plane block, the local anesthetic diffuses in the musculofascial plane and affects the dorsal roots of the spinal nerve at several levels [9]. in addition to systemic analgesic therapies, regional methods also play an important role in multimodal analgesic therapy. neuraxial blocks, including patient-controlled bolus or continuous infusion of epidural and spinal blocks, are some of the regional methods. it is an important advantage that the espb only blocks sensory fibers compared to other peripheral nerve blocks [10, 11]. espb have been successfully used in abdominal surgery, neuropathic pain, pneumothorax and breast implant surgery [4, 12, 13]. in this study we used espb for postoperative pain relief after spinal instrumentation surgery. chin kj et al. demonstrated that interfacial blocks provide long-term postoperative pain control and reduce opioid use. 20 ml of local anesthetic injection has been shown to extend from the infiltration site to 3 or 4 levels caudal [14]. we used 20 ml bupivacaine injections for each side. al-alami et al. conducted a study describing the ultrasound-guided dorsal root block at the t12 and l5 level, but did not present a report containing patient outcome data [15]. we described a c-arm scopy-guided espb and reported the outcomes of patients about postoperative pain score, opioid use and its side effects. conclusion in conclusion, on the basis of this retrospective study, it appears that c-arm scopy-guided esp block, is a safe and effective technique for postoperative pain management, can reduce opioid use and its side effects references 1. mathiesen o, dahl b, thomsen ba, et al. a comprehensive multimodal pain treatment reduces opioid consumption after multilevel spine surgery. eur spine j 2013;22:2089-96. 2. devin cj, mcgirt mj. best evidence in multimodal pain management in spine surgery and means of assessing postoperative pain and functional outcomes. j clin neurosci 2015;22:930-8. 3. bajwa sj, haldar r. pain management following spinal surgeries: an appraisal of the available options. j craniovertebr junction spine 2015;6:105-10. 4. forero m, adhikary sd, lopez h, tsui c, chin kj. the erector spinae plane block: a novel analgesic technique in thoracic neuropathic pain. reg anesth pain med 2016; 41: 621-7. 5. chin kj, adhikary s, sarwani n, forero m. the analgesic efficacy of pre-operative bilateral erector spinae plane (esp) blocks in patients having ventral hernia repair. anaesthesia 2017; 72: 452-60. 6. gerbershagen hj, aduckathil s, van wijck aj, peelen lm, kalkman cj, meissner w. pain intensity on the first day after surgery: a prospective cohort study comparing 179 surgical procedures. anesthesiology 2013; 118: 934-44. 7. savarese jj, tabler ng jr. multimodal analgesia as an alternative to the risks of opioid monotherapy in surgical pain management. j healthc risk manag 2017; 37: 24-30. 8. thepsoparn m, sereeyotin j, pannangpetch p: effects of combined lower thoracic epidural/general anesthesia on pain control in patients undergoing elective lumbar spine surgery: a randomized controlled trial. spine (phila pa 1976). 2018, 43:1381-85. 9. saito t, steinke h, miyaki t, et al. analysis of the posterior ramus of the lumbar spinal nerve: the structure of the posterior ramus of the spinal nerve. anesthesiology 2013; 118: 88-94. 10. sinatra rs, torres j, bustos am: pain management after major orthopaedic surgery: current strategies and new concepts. j am acad orthop surg. 2002, 10:117-29. 11. andreae mh, andreae da. regional anaesthesia to prevent chronic pain after surgery: a cochrane systematic review and meta-analysis. br j anaesth 2013;111:711-20. 12. bonvicini d, giacomazzi a, pizzirani e. use of the ultrasound-guided erector spinae plane block in breast surgery. minerva anestesiol 2017; 83: 1111-2. 13. ueshima h, otake h. erector spinae plane block provides effective pain management during pneumothorax surgery. j clin anesth 2017; 40: 74. [crossref] 14. chin kj, mcdonnell jg, carvalho b, sharkey a, pawa a, gadsden j: essentials our current understanding: abdominal wall blocks. reg anesth pain med. 2017, 42:133-83. 10.1097/aap.0000000000000545 15. al-alami a, abou el ezz a, kassab f. ultrasound guideddorsal ramus nerve block for reduction of postoperative pain in patients undergoing lumbar spine surgery: a case series imaging study. middle east j anaesthesiol 2015;23:251-6. doi: 10.33962/roneuro-2023-027 penetrating thoracic spine injury causing haemothorax. a case report injam ibrahim s. rowndzy, hoshanc sdeeq rashid, mustafa ismail, saleh abdulkareem saleh, noor mohammed shaker, ahmed muthana, mohammed mohsen ahmed, najat hassan rahem, samer s. hoz romanian neurosurgery (2023) xxxvii (2): pp. 155-158 doi: 10.33962/roneuro-2023-027 www.journals.lapub.co.uk/index.php/roneurosurgery penetrating thoracic spine injury causing haemothorax. a case report injam ibrahim s. rowndzy1, hoshanc sdeeq rashid2, mustafa ismail3, saleh abdulkareem saleh3, noor mohammed shaker4, ahmed muthana3, mohammed mohsen ahmed3, najat hassan rahem3, samer s. hoz5 1 department of surgery, college of medicine, hawler medical university, erbil, iraq 2 department of neurosurgery, west emergency hospital, erbil, iraq 3 department of neurosurgery college of medicine, university of baghdad, baghdad, iraq 4 department of neurosurgery, al ameed university, karbala, iraq 5 neurosurgeon, postdoctoral research fellow, department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract background. penetrating spine injuries can cause catastrophic complications to the patient, and it demands immense medical care to minimize the insult. mainly, it occurs in the military field; however, it has become more prevalent among civilians due to gun availability. the thoracic spine is the most affected part, followed by the cervical and lumbar spine. case report. a 15-year-old teenage boy had a penetrating injury to the thoracic (t10) vertebrae due to a missile bullet that resulted in bilateral lower limb weakness and required him to undergo decompressive laminectomy. during surgery, a missed hemothorax was discovered incidentally. conclusion. to the best of the author's knowledge, this case of penetrating thoracic spine injury due to a missile bullet associated with missed hemothorax has not been previously reported. this paper discusses the importance of early detection and treatment of injuries associated with penetrating spine trauma to improve patient survival and disability. introduction penetrating spine injuries can lead to devastating effects on the patient, representing a significant challenge to the patient and the treating surgeon. although most penetrating spine injuries occur in the military field, the ubiquity of guns in our society makes them more prevalent among the civilian population. these injuries can be due to any cause, such as a knife, nail, or sharp object but missile bullet injuries due to gunshots represent an important cause. it accounts for about 17-21% of all traumatic spine injuries. it is regarded as the third most common keywords penetrating spine injury, thoracic spine injury, haemothorax, missile injury corresponding author: mustafa ismail department of neurosurgery college of medicine, university of baghdad, baghdad, iraq mustafalorance2233@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 156 injam ibrahim s. rowndzy, hoshanc sdeeq rashid, mustafa ismail et al. cause of spine injuries in the civilian population after falls from height and motor vehicle accidents [4]. the thoracic spine represents the most affected part, followed by the cervical and lumbar spine [9]. the complications due to penetrating thoracic spine injuries can extend beyond the trauma to involve neural elements, supporting structures, and other organs, such as neurological compromise, vascular damage, spine instability, and cerebrospinal fluid (csf) leakage [6]. hemothorax is also a significant complication associated with spine injuries and may occur due to damage to pulmonary parenchyma, heart, intercostal vessels, and major intrathoracic vessels [3]. however, associated missed hemothorax due to penetrating spine injury has rarely been reported. in this paper, the authors report a case of a teenage boy who was presented with a missile bullet injury to the back and then discovered to have a missed hemothorax intraoperatively that required further surgical care and postoperative management. case report a 15-year-old teenage male presented to the emergency department with a missile injury to his back; during the physical examination, he was conscious and alert, and there was bilateral lower limb weakness with grade 1 power. moreover, there were two entry points in the mid-back region at the thoracic 10 (t10) vertebrae level but without an exit site. after the appropriate management and stabilization, a spine x-ray was ordered (fig.1), which revealed two large foreign bodies (metallic fragments) about 2.5-3 cm in size located at the level of t10. figure 1. spine x-ray of both anteroposterior (a) and lateral (b) views showing two metallic fragments at the level of t10. also, (c) shows the extracted foreign bodies. computed tomography (ct) scan (fig.2) has been done and revealed two fragments of foreign bodies at the level of t10 that cross the transverse process and extend to the left pleural cavity. the patient had incomplete spinal cord injury and csf leakage, which renders in performing decompressive laminectomy surgery with foreign bodies (bullet) extraction. figure 2. a plain axial ct scan of the spine showing foreign bodies that crosses the transverse process and extends to the left pleural space. figure 3. artistic depiction shows the site of the penetrating bullet to the spinal cord and extending to the parietal pleura. during surgery, total t10 laminectomy and partial t11 laminectomy were done with midline bullet extraction, then removal of stacked shell from pedicle area. after extraction, a gush of dark-tinged bleeding swung with each ventilation. in the beginning, the source of blood was suspected to be from the fractured bone in the lateral part of the vertebral ring, which stopped using bone wax and 157 penetrating thoracic spine injury causing haemothorax direct compression. however, the gush of blood still came with each ventilation, so there was also a suspicion of associated missed hemothorax that required further cardiovascular care. after chest tube insertion, the collecting system is filled with blood, and the suspicion of hemothorax is confirmed (fig.3). a few days after the laminectomy surgery, the patient underwent another surgery for partial lobectomy due to a collapsed left lung. on the followup, the patient was stable, had normal respiration, and the chest tube was removed. upon discharge, his paraparesis improved to grade 4. discussion penetrating spine injuries represent a significant cause of morbidity and mortality in the military field; however, nowadays, it has also become more prevalent among the general population due to the availability of firearms. male victims are disproportionately affected higher (78-91%) than females, with high incidence during the third decade of life [4,8]. however, in this case, the victim was a male in a child age group who had a penetrating spine injury due to a missile bullet. thoracic spine penetrating injuries cause complications such as myelopathy, central nervous system infections, csf leak following dural tear, spinal instability, and delayed neurological deficits [6,7]. of these complications, our patient had csf leakage with partial neurological compromise. furthermore, according to manzone et al., early removal of a foreign body in penetrating spinal injury may reduce myelopathy, infection, and delayed neurological deficits. hence, the patient underwent laminectomy surgery for correction and bullet and shell extraction [5]. thoracic spine fractures are associated with pleural collection; for example, in a study of 72 patients with thoracic spine fractures, 24% were found to have hemothorax [1]. usually, the hemothorax results from bleeding from the edge of the bone at the unstable fracture site; hence the stabilization of the thoracic spine controls the bleeding [2]. however, in this patient, a gush of blood after extraction of the foreign bodies fluctuated with each ventilation, even after stabilizing the fractured bone with bone wax and direct compression. the bleeding did not stop; therefore, a suspicion of missed hemothorax was confirmed after tube thoracotomy insertion, which resulted in patient stabilization. this hemothorax occurs due to the bullet's penetration of the parietal pleura. hemothorax is usually detected and treated at admission during advanced trauma life support (atls) protocol due to the significant risk of late complications [10]. however, this patient had no signs of respiratory compromise before surgery, and the imaging did not show any signs of pleural effusion, so the diagnosis was missed and firstly present during surgery. to the best of the authors’ knowledge, this presentation of penetrating thoracic spine injury due to a missile bullet associated with missed hemothorax has not been previously reported. this paper refers to the importance of early detection and treatment of injuries associated with penetrating spine trauma, especially hemothorax, as it can raise the mortality and morbidity of the patient. conclusion penetrating spine injuries due to missile bullets are increasing nowadays. it can lead to many complications that increase mortality and morbidity. in this case, we present a patient who had missed hemothorax that was discovered and treated intraoperatively. references 1. dalvie ss, burwell m, noordeen mh. haemothorax and thoracic spinal fracture: a case for early stabilization. injury. 2000 may 1;31(4):269-70. 2. freysz m, adamon o, wilkening m, sautreaux jl. hemothorax and fractures of the dorsal spine. la semaine des hopitaux: organe fonde par l'association d'enseignement medical des hopitaux de paris. 1983 sep 1;59(32):2229-31. 3. hagiwara a, iwamoto s. usefulness of transcatheter arterial embolization for intercostal arterial bleeding in a patient with burst fractures of the thoracic vertebrae. emergency radiology. 2009 nov;16(6):489-91. 4. jakoi a, iorio j, howell r, zampini jm. gunshot injuries of the spine. the spine journal. 2015 sep 1;15(9):2077-85. 5. manzone p, domenech v, forlino d. stab injury of the spinal cord surgically treated. clinical spine surgery. 2001 jun 1;14(3):264-7. 6. nasser r, nakhla j, sharif s, kinon m, yassari r. penetrating thoracic spinal cord injury with ice pick extending into the aorta. a technical note and review of the literature. surgical neurology international. 2016;7(suppl 28):s763. 7. sarkar b, ahuja k, choudhury ak, jain r. penetrating spine injury bisecting thoracic spinal canal with no 158 injam ibrahim s. rowndzy, hoshanc sdeeq rashid, mustafa ismail et al. significant neurological deficits—the midline cord syndrome. spinal cord series and cases. 2018 nov 13;4(1):1-5. 8. schoenfeld aj, newcomb rl, pallis mp, cleveland iii aw, serrano ja, bader jo, waterman br, belmont jr pj. characterization of spinal injuries sustained by american service members killed in iraq and afghanistan: a study of 2,089 instances of spine trauma. journal of trauma and acute care surgery. 2013 apr 1;74(4):1112-8. 9. sidhu gs, ghag a, prokuski v, vaccaro ar, radcliff ke. civilian gunshot injuries of the spinal cord: a systematic review of the current literature. clinical orthopaedics and related research®. 2013 dec;471(12):3945-55. 10. zeiler j, idell s, norwood s, cook a. hemothorax: a review of the literature. clinical pulmonary medicine. 2020 jan;27(1):1. doi: 10.33962/roneuro-2020-030 concomitant orbital and intracranial abscess. a rare complication of sinusitis nae andreea, farrell stephen, sweeney kieron, hoare siobhan, colreavy michael romanian neurosurgery (2020) xxxiv (1): pp. 189-194 doi: 10.33962/roneuro-2020-030 www.journals.lapub.co.uk/index.php/roneurosurgery concomitant orbital and intracranial abscess. a rare complication of sinusitis nae andreea1, farrell stephen2, sweeney kieron3, hoare siobhan4, colreavy michael5 1 md mrcsi(ent). orl department, temple street hospital, dublin, ireland 2 lrcp & si mb bch nui. ophthalmology department, temple street hospital, dublin, ireland 3 mb bch nui bao md frcsi (sn). neurosurgery department, temple street hospital, dublin, ireland 4 lrcp & si mb bch nui. radiology department, temple street hospital, dublin, ireland 5 mb bch nui frcsi. orl department, temple street hospital, dublin, ireland abstract background: intracranial and orbital abscesses in combination together are rare complications of sinusitis. they can be life-threatening and can result in multiple sequelae. case presentation: a 9-year-old female presented with left periorbital swelling, gaze restriction and headache. following scans, she underwent emergency endoscopic sinus surgery, evacuation of the intraorbital empyema and stereotactic minicraniectomy with the evacuation of the extradural empyema as a joint case. the patient recovered well and was discharged to complete intravenous antibiotics for 6 weeks. conclusion: in the pediatric population intracranial complications of acute sinusitis can have more devastating consequences. therefore, prompt recognition and management are essential within a multidisciplinary team setting. we also highlight the rarity of concomitant multi-site abscess formation and the need to be vigilant for same. introduction acute or chronic sinusitis complications can range from minor (headaches, flu symptoms) to loss of organ function (loss of vision) or can be life threatening (brain abscess). early diagnosis and treatment is essential to prevent sequelae. a high index of suspicion is needed when assessing and treating the paediatric population in this setting. in the paediatric setting paranasal sinuses have not completely developed until sometimes early in the teenage years . this is particularly the case particularly with frontal sinus development in the keywords brain abscess, craniectomy, endoscopic sinus surgery, infectious disease, rhinosinusitis, orbital abscess, streptococcus intermedius corresponding author: andreea nae orl department, temple street hospital, temple street, rotunda, dublin, ireland andreea.nae007@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 190 nae andreea, farrell stephen, sweeney kieron, hoare siobhan, colreavy michael paediatric population. indeed, in this population group, frontal sinuses are the commonest to cause significant complications, especially after the age of 10 (10,16). this is mainly due to their vicinity with the orbit and the orbital content but also with the brain and meninges. the lamina papyracea (a thin bony plate that separates the orbital content from the nasal cavity) is very thin and often dehiscent, allowing for direct infection spread between the two anatomical regions. orbital complications alone are more common in patients younger than 5 years of age (16). so preseptal and orbital cellulitis, followed by subperiosteal and orbital abscess are the most common complications secondary to acute or chronic sinusitis. this can lead to compromised vision. cavernous sinus thrombosis is the most serious of all, with intracranial spread of infection and possible contralateral orbital symptoms. in the paediatric population, periorbital swelling is the most common sign that brings the patient to hospital or their family doctor’s attention. this is usually associated with upper respiratory upset, fever and headache as the most common but nonspecific symptoms (16). typical nasal symptoms seen in the adult population (nasal blockage or discharge, postnasal drip and pain over the checks or frontal headache) are sometimes lacking. also a history of previous nasal complaints is absent in most cases (14). extension of the abscess to the intracranial cavity is usually gained through the valveless venous system, direct extension through a previous dehiscent or eroded skull base, or due to septic emboli. subdural empyema is the most common intracranial but extra axial complication, followed by subdural and brain abscess. all are severe complications and can be life threatening or have major sequelae (hemiparesis, aphasia or epilepsy). in the paediatric population the consequences of such complications can effect patients for the rest of their life and can be debilitating and life changing for their families too. simultaneous intraorbital and intracranial complications secondary to acute sinusitis is very rare. this was reported as 9.3% of their patients over the age of 7 with intraorbital complications by hermann (12). a high index of suspicion for intracranial complications needs to be maintained and regular assessment of the child is mandatory to check for any deterioration in their symptoms and signs or failure to improve. hermann et al (12) found that children with intraorbital complications of sinusitis benefit from performing a mri brain early due to a higher association with intracranial infection in: children older than age 7, males, those with neurological status changes, frontal sinus opacification on ct, superior or lateral position of orbital abscess, intraorbital abscess needing drainage. sinus infection may progress to intracranial infection even after appropriate empiric antibiotic therapy has been initiated (14,17,19). lack of early recognition and urgent treatment can be fatal. empirical antibiotic treatment is generally broad-spectrum and started under local microbiological guidelines and supervision. timing of surgical intervention is a controversial subject, with multiple studies being in favour of early rather than late surgical intervention (14,17). intraorbital abscess formation needs to be drained in conjunction with an otorhinolaryngologist (orl) performing endoscopic sinus surgery and intracranial abscess formation needs prompt neurosurgical input and craniotomy with drainage of the infection. case presentation a 9-year-old female patient presented to the emergency department with a 2 week history of flu symptoms and headaches. she complained of right upper eyelid oedema prior to presentation that subsided followed by persistent left periorbital oedema and ophthalmoplegia. prior to her hospital presentation, our patient has been already on 5 days of oral antibiotics started by her family. her medical history was non-contributory with no history of nasal symptoms or allergic rhinitis, nor any history of atopy. the child lived with her family in america and was on holiday visiting her relatives. an initial assessment showed pain on eye movement with no focal neurological signs with a glasgow coma scale (gcs) of 15 out of 15. the patient had neither neck stiffness nor photophobia. she was afebrile with stable vital signs. intravenous access 191 concomitant orbital and intracranial abscess. a rare complication of sinusitis was obtained and routine bloods were sent to the laboratory. she was admitted with a diagnosis of preseptal cellulitis for intravenous antibiotics as per our local guidelines. on admission her inflammatory markers were elevated. white cell count was 18.2 [normal 6.018.0(x10^9/l)], with neutrophelia of 13.9 [normal 1.08.5(x10^9/l)]. her c-reactive protein (crp) was 162 (normal 0-10mg/l). despite 24 hours of intravenous cefotaxime, she developed restriction of eye movement on elevation and downward gaze combined with drowsiness. otorhinolaryngology was consulted and flexible nasal endoscopy did not reveal any intranasal pathology. an urgent ophthalmology consult was requested and vision was found normal in both eyes. our patient underwent urgent computer tomography (ct) of sinuses without contrast. the scan showed pansinusitis on the right side (maxillary, ethmoid and frontal sinuses) with left sided sinuses free of mucosal disease. also she had a small left extraconal fluid collection (measuring 7x 15 x 25mm). pictures 1 and 2 shows the above findings on a coronal and axial ct cut: picture 1. coronal ct sinuses. picture 2. axial ct sinuses. due to the high clinical suspicion of intracranial pathology and increased drowsiness an urgent magnetic resonance imaging (mri) of brain with contrast was performed. this revealed the left orbital extraconal abscess with extension through the posterolateral orbital wall into the extradural space anterior to the left temporal lobe. the bone demonstrated osteomyelitis. there was also a small extracranial component adjacent to the pterion, with inflammatory changes in the left temporalis muscle. all these findings are visible in the pictures 3 and 4: picture 3. coronar mri showing left external orbital abscess. picture 4. coronar mri with contrast showing left extradural empyema. 192 nae andreea, farrell stephen, sweeney kieron, hoare siobhan, colreavy michael after an urgent neurosurgical consult emergency surgery was planned as soon as possible. endoscopic sinus surgery followed by left orbit abscess drainage and stereotactic mini-craniectomy with empyema evacuation was performed. after the patient was prepped as per endoscopic sinus surgery protocol a left maxillary antrostomy was performed where frank pus was found. similar findings were found in the left anterior ethmoidal sinus. on exploring the left posterior ethmoid only mucosa disease was found. sinus surgery found normal sinuses on the right side despite the abnormal findings (pansinusitis) on the ct on this side. the left external orbital abscess was drained via an external approach and a drain was left in situ. a stereotactic mini-craniectomy was performed via a left curved pterional incision, followed by evacuation of the empyema and again a drain was placed. pus for culture and sensitivity was sent from all 3 locations. the patient tolerated the procedure well and no perioperative complications were encountered. no intensive care unit monitoring was needed postoperatively for our patient. she was commenced on intravenous ceftriaxone and metronidazole. the approach to this case was a multidisciplinary one with paediatricians, orl, neurosurgery, ophthalmology, infection disease, microbiology and physiotherapy involved in this child’s care. our patient recovered well from a neurosurgical and orl point of view but was quite slow from an eye perspective. the intraorbital drain was removed after 12 hours and the intracranial drain after 24 hours. no temperature spikes were recorded postoperatively. a repeated mri brain was performed on day 2 postoperatively due to slow intraorbital progress and this revealed a small collection at the site of previous orbital abscess. close ophthalmology review followed until resolution of the collection, 2 and half weeks after the surgery. culture from all sites grew streptococcus intermedius. inflammatory markers returned to normal values. a repeat mri scan at 18 days postoperatively showed near complete resolution of the remaining collection. the patient was hospitalized for 4 weeks duration and further intravenous antibiotics were arranged for 6 more weeks at home. during this period, our patient was reviewed in multiple speciality clinics. she improved totally, with no neurological sequelae. a repeat mri scan at 2 months postoperatively showed complete resolution of the collection and osteomyelitis. due to the fact that our patient lived in another country, further follow up was not possible but all images, documentation and advice on follow up were given to organise orl follow up in her home country. discussion simultaneous intraorbital and intracranial complications secondary to sinus disease are extremely rare. the incidence is unknown with only few cases in the literature (8,9,12,18,22) and a handful of case presentations from paediatric population (4,25). yeh presented the case of 17 years old male with longstanding orbital symptoms (1 month) treated with sinus surgery who developed 1 month after the treatment an inflammatory frontal mass needed excision with no neurological sequels (25). constantin et al (4) reported the case of a 12 years old male patient with sinusitis complicated later by orbital cellulitis ending developing frontal brain abscess. sinus surgery and adenoidectomy was followed at 24 hours by neurosurgical intervention with collection excision. four retrospective studies presented the presented symptoms and management of their patients. hermann et al (12) found a rate of 10% (4 patients) in his study of paediatric patients with simultaneous intraorbital and intracranial complications. all were males and the youngest was 14 years of age. they were treated surgically and all of the abscesses were found to be polymicrobial. he found that mri helped identifying the intracranial complications after they were missed on ct. as a significant finding, in this study all patients had either a superior or lateral intraorbital located complication. in his study germiller et al (8) presented 7 cases of concomitant orbital and intracranial complications treated surgically with a focus on intracranial complications and outcome. in her retrospective review of 10 patients younger than 18 years, raynolds et al (18) found the youngest to be 7 years old and predominantly males. also she 193 concomitant orbital and intracranial abscess. a rare complication of sinusitis found that frontal lobe was involved in 8 out of 10 patients. goyita et al (9) found 14 paediatric patients to have intraorbital and intracranial complications, with a predominant male distribution in this group. our patient (age 9) was amongst the youngest ones from the previously reported cases. an age greater than 7 was found to be associated with the development of sinogenic intracranial complication rather than intraorbital ones alone (5,14,17) but also with dual orbital and intracranial abscesses (11). our patient was a young female, although male adolescents were found to be more prone to intracranial complications alone and in association with intraorbital ones for reasons not yet elucidated (8,9,13,17,19 ,25). if there is a hormonal rather than an anatomical component it is to be discovered. crp, an inflammatory marker was found to be higher in children with brain empyema complicating rhinosinusitis than in uncomplicated rhinosinusitis, with a mean of 18.1mg/dl (17). while ct scan of the paranasal sinuses is the gold standard imaging modality in acute or chronic rhinosinusitis, used by surgeons worldwide to assess sinus disease, mri brain with contrast remains the gold standard in identification of brain abscesses (9,12,21). this should be requested for patients with increased risk factors of intracranial disease or if any suspicion of intracranial complication exists. it should be performed early rather than later in the course of the disease. our patient’s ct sinuses failed to show the true extent of the sinus disease. the scan revealed right sided pansinusitis and during endoscopic sinus surgery all these sinuses were free of disease. the left maxillary sinus seemed free of disease on the scan but frank pus was seen during surgery. why there was such a non concordant finding it is not clear. the subsequent mri brain showed clearly the presence and extent of the intracranial collection. as demonstrated by multiple studies, ct sinuses findings are not absolutely accurate when compared with the endoscopic sinus surgery findings (2,20). another unique aspect of the case was the bacteria grown which was streptococcus intermedius. the most common bacteria in uncomplicated sinusitis in children is haemophilus influenzae followed by streptococcus pneumoniae, staphylococcus aureus, staphylococcus epidermidis, and streptococcus pyogenes (13,23). mixed aerobic and anaerobic cultures are comonly seen also (12,23). streptococcus intermedius is a subspecies of streptococcus milleri. it is highly pathogenic via multiple mechanisms. it is associated with deep, complicated abscesses including cerebral abscess as a complication of sinusitis (5,6,23). this could explain the aggresive course of this case. prompt recognition and aggressive medical and surgical treatment was the key to a complication free and smooth recovery. the role of early multidisciplinary surgical intervention was most useful in this case with all 3 specialities involved. usually a third-generation cephalosporin plus metronidazole is most effective in fighting these types of complicated infections (7,24), but needs to be guided by local microbiology guidelines. the role of surgery, although vital in some cases, still needs to be explored in finding the best technique and timing. the evidence in the literature is mainly based on retrospective reviews and case series. there is a lack of significant evidence in favour of one surgical treatment modality over the other (burr hole drainage, excision or stereotactic surgery) when analyzing their outcomes (1,15). the role and timing of endoscopic sinus surgery needs to be explored more, on larger samples to assess the full benefit these patients can gain. there seems to be some benefit in avoiding neurosurgical intervention if sinus surgery is performed first (3) but this was not reflected in all studies. we advocate that the focus of infection needs to be addressed first and at the same time as sinuitisis being the „driver” of the multicompartmental infection. while very small intracranial infections can be manged conservatively, any large intracranial collection needs to be evacuated or reduced due to the risk of spread, thromosis and poor blood-brain barrier penetration of a lot of antibiotics. each case has to be individually evaluated and judged as no one procedure fits all. multidisciplinary input is common in paediatric practice but proved essential in this patient’s care. conflicts of interest authors have no financial or other conflicts of interest to declare. authors have not received any financial souses of any kind and form. 194 nae andreea, farrell stephen, sweeney kieron, hoare siobhan, colreavy michael references 1. arlotti m, et al. consensus document on controversial issues for the treatment of infections of the central nervous system: bacterial brain abscesses. int j infect dis. 2010;14:s79–92. 2. bair-merritt m.h, shah s.s, zaoutis t.e, bell l.m, feudtner c, suppurative intracranial complications of sinusitis in previously healthy children the pediatric infectious disease journal: 2005, 24 (4):384-386. 3. berdouk s, pinto n, fatal orbital cellulitis with intracranial complications: a case report, int j emerg med, 2018, 11 (1), 51. 4. constantin f, niculescu pa, petre o, et al. orbital cellulitis and brain abscess rare complications of maxillospheno-ethmoidal rhinosinusitis. rom j ophthalmol, 2017, 61 (2), 133-136. 5. fabian j. s. van der velden, alexandra battersby, lucia pareja-cebrian, nicholas ross, stephen l. ball, and marieke emonts, paediatric focal intracranial suppurative. 6. faden, howard s, infections associated with streptococcus intermedius in children, the pediatric infectious disease journal, 2016, 35(9):1047–1048. 7. felsenstein s, williams b, shingadia d, coxon l, riordan a, demetriades ak, chandler cl, bassi s, koutoumanou e, stapleton s, sharland m, bryant pa (2013) clinical and microbiologic features guiding treatment recommendations for brain abscesses in children. pediatr infect dis j 32(2):129–135. 8. germiller j.a., monin d.l, sparano a.m, lawrence w. c. t, intracranial complications of sinusitis in children and adolescents and their outcomes, arch otolaryngol head neck surg. 2006; 132(9):969-976. 9. goytia v.k, giannoni c.m, edwards m.s, intraorbital and intracranial extension of sinusitis: comparative morbidity, j pediatr, 2011, 158 (3), 486-91. 10. hamdy el-hakim, anita c.malik, keitharonyk, edmundledi, ravibhargava, the prevalence of intracranial complications in pediatric frontal sinusitis, int j pediatr otorhinolaryngol. 70(8) (2006) 1383-1387. 11. hartstein me, steinvurzel md, cohen cp.intracranial abscess as a complication of subperiosteal abscess of the orbit. ophthalmic plast reconstr surg. 2001 nov;17(6):398-403. 12. herrmann b.w, forsen j.w, simultaneous intracranial and orbital complications of acute rhinosinusitis in children, int j pediatr otorhinolaryngol.68 (5) (2004) 619625. 13. jiannetto df, prett mf, correlation between preoperative computed tomography and operative findings in functional endoscopic sinus surgery, laryngoscope.1995;105(9): 924–927. 14. johnson dl, markle bm, wiedermann bl, hanahan l.treatment of intracranial abscesses associated with sinusitis in children and adolescents. j pediatr. 1988 jul;113(1 pt 1):15-23. 15. leys d, et al. management of focal intracranial infections: is medical treatment better than surgery? j neurol neurosurg psychiatry, 1990; 53:472–5. 16. kou y.f, killeen d, whittemore b, farzal z, booth t, swift d, berg e, mitchell r, shah g, intracranial complications of acute sinusitis in children: the role of endoscopic sinus surgery, int j pediatr otorhinolaryngol 2018, 110(7):147-151. 17. patel n.a, garber d, hu s, kamat a, systematic review and case report: intracranial complications of pediatric sinusitis, int j pediatr otorhinolaryngol, 2016 jul; 86:20012. 18. reynolds d.j, kodsi s.r, rubin s.e, rodgers i.r, intracranial infection associated with preseptal and orbital cellulitis in the pediatric patient j aapos, 2003, 7 (6), 413-7. 19. rosenfeld ea, rowley ah, infectious intracranial complications of sinusitis, other than meningitis, in children: 12-year review. clin infect dis. 1994 may;18(5):750-4. 20. singhal p, sonkhya n, mishra p, srivastava sp. impact of anatomical and radiological findings for consideration of functional endoscopic sinus surgery. indian j otolaryngol head neck surg. 2012;64(4):382–385. doi:10.1007/s12070-011-0351-2. 21. skelton r, maixner w, isaacs d, sinusitis-induced subdural empyema, arch dis child 1992; 67:1478-80. 22. traficante d, riss a, hochman s. bifrontal brain abscesses secondary to orbital cellulitis and sinusitis extension. int j emerg med. 2016;9(1):23. 23. van der velden fjs, battersby a, pareja-cebrian l, ross n, ball sl, emonts m. paediatric focal intracranial suppurative infection: a uk single-centre retrospective cohort study. bmc pediatr. 2019;19(1):130. published 2019 apr 25. doi:10.1186/s12887-019-1486-7. 24. widdrington jd, bond h, schwab u, price da, schmid ml, mccarron b, chadwick dr, narayanan m, williams j, ong e, pyogenic brain abscess and subdural empyema: presentation, management, and factors predicting outcome, infection. 2018 dec;46(6):785-792. doi: 10.1007/s15010-018-1182-9. 25. yeh ch, chen wc, lin ms, et al. intracranial brain abscess preceded by orbital cellulitis and sinusitis. j craniofac surg. 2010;21(3):934–6. doi: 10.33962/roneuro-2020-098 global neurosurgery, bangladesh and covid-19 era. a perspective from a lowincome country robert ahmed khan, moshiur rahman, amit agrawal, ezequiel garcia-ballestas, luis rafael moscote -salazar romanian neurosurgery (2020) xxxiv (4): pp. 574-576 doi: 10.33962/roneuro-2020-098 www.journals.lapub.co.uk/index.php/roneurosurgery global neurosurgery, bangladesh and covid-19 era. a perspective from a lowincome country robert ahmed khan1, moshiur rahman2, amit agrawal3, ezequiel garcia-ballestas4, luis rafael moscote-salazar4 1 neurosurgery department, bsmmu, dhaka, bangladesh 2 neurosurgery department, holy family red crescent medical college, dhaka, bangladesh 3 department of neurosurgery, all india institute of medical sciences, bhopal, india 4 center for biomedical research (cib), faculty of medicine, university of cartagena, cartagena, colombia abstract background. covid-19 has become an alarming pandemic for our earth. it has created panic not only in china but also in developing countries like bangladesh. bangladesh has adequate confinements to constrain the spread of the infection and in this circumstance, overall healthcare workers including neurosurgeons are confronting a ton of difficulties. the purpose of this paper is to depict the proficiency of global neurosurgery in this covid-19 time. method. global neurosurgery offers the chance of fusing the best proof-based guidelines of care. this paper demonstrated that, in low to middle-income countries, global medical procedure has been received to address the issues of residents who lack critical surgical care. results. inappropriate and insufficient asset allotment has been a significant obstacle for the health system for decently giving security to the patients. the fundamental training process has been genuinely hampered in the current circumstance. worldwide health activities have set to an alternate centre and global neurosurgery as an assurance is slowed down. conclusion. this paper recommended that global neurosurgical activities need to come forward and increase the workforce to emphasize surgical service. covid-19 pandemic has brought terrible impacts and vigorously affected medicinal services including the neurosurgical field.2, 3 this pandemic has represented a challenge for all nations. the entire world is confronting this challenge which requires the engagement of all physicians, including neurosurgeons, to manage covid-19 outcomes.4, 5 although neurosurgery constitutes a small portion of this but still, its impact is significant in those requiring intervention. thus, the concept keywords global neurosurgery, covid-19, low-income country corresponding author: moshiur rahman neurosurgery department, holy family red crescent medical college, dhaka, bangladesh dr.tutul@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 575 global neurosurgery, bangladesh and covid-19 era of global neurosurgery was conceded to address the difference around the world in neurosurgical caregiving. but at present, the world is facing unprecedented effects of covid-19. even though pandemics have a worldwide extension, their impacts on the population are unbalanced. 1 the unequal distribution of health care services amongst different countries is the challenging world facing in the 21st century. surgery has been identified as a major modifiable factor in saving millions of lives. global surgery was thus introduced to address the issue of people who lack essential surgical care especially in low to middle-income countries (lmic). global surgery is defined as an area of study, research, practice, and advocacy that aims to improve health outcomes and achieve health equity for all people in need of surgical and anesthetic treatment, with particular emphasis on underserved populations and populations in crisis. 7 in this context global neurosurgery encompass those who suffer from neurosurgical conditions or those who need neurosurgical care. 8 global neurosurgery as a new paradigm in care offers the possibility of incorporating the best evidence-based standards of care. development of research projects and policies. in the bogota declaration of global neurosurgery, 2016 recommendation for amplification of access, alignment of all neurosurgical activity, the advancement of relevant research, assimilation of neurosurgical capacity, and advocacy of universal coverage was made. 9 it has been estimated that 44% of the world’s neurosurgeons reside in high-income countries whereas more than 80% of the disease arises in lmics. 6 to mitigate this a global neurosurgical collaboration is required to increase the workforce and strengthen the surgical service. there has been less consideration coordinated toward the effect of covid-19 in lmics. according to a report, nine-in-ten spine cases are in lmics, and the spine cases make up 39% of the operative cases in lmics. 6 allowing access to surgical procedures to all patients who require them is not a privilege, it is an obligation of the nations. bangladesh is a country located in southeast asia with a population of 164,689,383 people according to un data. but with around 170 neurosurgeons working in 13 government and few military and private hospitals, it falls way short of providing essential neurosurgical care. making things worse the current pandemic is making essential neurosurgical care more inaccessible and backlogging of chronic neurosurgical conditions. during the time of covid-19 pandemic prioritizing neurosurgical patients has been a major challenge in bangladesh like many other affected countries of the world. inappropriate and inadequate resource allocation has been a major obstacle for the health system to function fairly providing safety to the patients. neurosurgeons are being redeployed to help their colleagues in the hospitals where there was a shortage of personnel. although this task-sharing and task-shifting are very much necessary in the pandemic situation it resulted in curtailing of neurosurgical service in some instances. 10 there has been an enormous abatement in operative cases which has altogether affected the training of neurosurgical residents as they rely upon elective careful volume to sharpen their clinical and operative skills. 11 one of the key elements of providing standard neurosurgical service worldwide is the training of capable and competent neurosurgeons. the country offers postgraduation in neurosurgery in 4 centers. also, as a part of the commitment for global neurosurgery, bangladesh offers post-graduation to neighboring countries. during recent times many neurosurgeons of nepal have done their post-graduation from bangladesh. this systemic and rigorous training process has been seriously hampered in the current situation. although many international conferences and courses were canceled, these were replaced by numerous webinars arranged by different societies where world-renowned neurosurgeons shared their experience and gave their insight. but these opportunities certainly do not make up for the actual training with the first-hand experience. like most other lmic countries bangladesh lack behind in keeping and managing patient data. in any efficient health system, patient data is the key to efficient management. this lack of centralized record-keeping and patient safety disrupts the accountability of service to the patients. 12 apart from the cessation of certain academic activities, the current pandemic has also taken its toll on the country’s research activities. the absence of local research on local needs impedes evidence-based practice. 7 it is estimated that approximately 13.8 million new operative cases exist worldwide each year. of these, nearly 5.2 million cases will require additional 23,300 neurosurgeons from lmics to address them6. 576 robert ahmed khan, moshiur rahman, amit agrawal et al. as global health activities have set to a different focus, the global surgery’s niche part global neurosurgery as a certainty is slowed down. the huge burden on the health care system for the disease as well as the action required to prevent it’s spread has significantly affected the neurosurgical service of lmic like bangladesh. the already loaded of neurosurgical service in an lmic like bangladesh is being overburdened by this pandemic. like any other low-income country bangladesh is facing difficult challenges in carrying out evidence-based surgical procedures, insufficient research activity as a part of the residency, the economic crisis affecting the country’s health sector leading to an indirect impact on neurosurgical patient’s budget allocation in health only 5.15% (tk 292 billion), health insurance not here, lack of health coverage and difficulty in following up the patients. it is during this time of global crises the need for global neurosurgical initiatives to come forward and rise to cause of essential and equal neurosurgical care. abbreviations lmic: low to middle-income countries declarations ethics approval and consent to participate not applicable consent for publication not applicable availability of data and materials the data used in this study are available from the corresponding author on a feasible request. competing interests the authors declare that they have no competing interests. funding no funding. author’s contributions rak, mmr, aa, egb and lrms collected data, wrote and reviewed the manuscript. all authors read and approved the final manuscript. acknowledgments the authors would like to thank all the members who were part of this paper. references 1. quinn sc, kumar s. health inequalities and infectious disease epidemics: a challenge for global health security. biosecur bioterror 2014;12:263-273. 2. burke jf, chan ak, mummaneni v, et al. letter: the coronavirus disease 2019 global pandemic: a neurosurgical treatment algorithm. neurosurgery 2020;87:e50-e56. 3. jean wc, ironside nt, sack kd, felbaum dr, syed hr. the impact of covid-19 on neurosurgeons and the strategy for triaging non-emergent operations: a global neurosurgery study. acta neurochirurgica 2020;162:1229-1240. 4. kondziolka d, couldwell wt, rutka jt. introduction. on pandemics: the impact of covid-19 on the practice of neurosurgery. journal of neurosurgery 2020:1-2. 5. pesce a, palmieri m, armocida d, frati a, santoro a. letter: neurosurgery and coronavirus (covid-19) epidemic: doing our part. neurosurgery 2020;87:e48e49. 6. dewan mc, rattani a, fieggen g, et al. global neurosurgery: the current capacity and deficit in the provision of essential neurosurgical care. executive summary of the global neurosurgery initiative at the program in global surgery and social change. journal of neurosurgery 2018:1-10. 7. meara jg, leather aj, hagander l, et al. global surgery 2030: evidence and solutions for achieving health, welfare, and economic development. lancet (london, england) 2015;386:569-624. 8. haglund mm, fuller at. global neurosurgery: innovators, strategies, and the way forward. 2019;131:993. 9. wfns. global action framework. global neurosurgery committee 2019. 10. tsermoulas g, zisakis a, flint g, belli a. challenges to neurosurgery during the coronavirus disease 2019 (covid-19) pandemic. world neurosurg 2020;139:519525. 11. weber ac, henderson f, santos jm, spiotta am. letter: for whom the bell tolls: overcoming the challenges of the covid pandemic as a residency program. neurosurgery 2020. 12. agrawal a, kumar a, agrawal cs, pratap a. one year of neurosurgery in the eastern region of nepal. surgical neurology 2008;69:652-656; discussion 656. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0058 article biomarkers of glioblastoma multiforme: current update guru dutta satyarthee, luis rafael moscote-salazar, amit agrawal india, colombia      466 | satyarthee et al biomarkers of glioblastoma multiforme             doi: 10.2478/romneu-2018-0058 biomarkers of glioblastoma multiforme: current update guru dutta satyarthee1, luis rafael moscote-salazar2, amit agrawal3 1department of neurosurgery, neurosciences centre, aiims new delhi, india 2neurosurgeon-critical care, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia 3neurosurgery department, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: glioblastoma multiforme (g.b.m.) represents one of the commonest intracranial tumor associated with very poor prognosis. despite recent advances in genomics and microneurosurgical techniques, chemotherapy regimens, radiation technology but despite of these mortality and morbidity still remains unacceptable very high. various markers are utilized to stratify into different category in a desperate attempt to find out suitable therapeutic regimen to promote improved neurological outcome. authors briefly reviews various biomarkers and utility in management of gbm key words: glioblastoma multiforme, prognostic factor, biomarkers, outcome, management introduction glioblastoma multiforme originates from astrocytes.1-5 the different types are markers are expressed differently in different types and molecular subtypes of gbm.6-14 however, with the emergence of new molecular biomarkers and its regulation such as epidermal growth factor receptor viii, o6-methylguanine-dna methyltransferase, isocitrate dehydrogenase mutation.1-6 further, glioblastoma specific micrornas like mir-10b and mir-21 is labelled as promising prognostic values. as gbm represent highly malignant potential is associated with widespread genetic alterations and protein expression, which is utilize to categorize into various types and may have prognostic significance. various molecular biomarkers of glioblastoma multiforme includes: 1. o6-methylguanine-dna methyltransferase (mgmt): it is located on the chromosome number 10q26, the mgmt gene encodes proteins, which are consumed in dna repair. the methylation of this gene increases the efficacy of an alkylating agent like temozolamide after chemoradiotherapy. 2. epidermal growth factor receptor (egfr): amplification of epidermal growth factor receptor and the genetic rearrangement of egfr (egfrviii) are considered as romanian neurosurgery (2018) xxxii 3: 466 468 | 467             common hallmarks of gbm. gbm has highly proliferative nature controlled by the presence of key growth factors and receptors; it can activate pathways essential for gbm tumor cells to proliferate and its activation causes decreased integrity of g1 to s checkpoint in the cell cycle, leading to excessive proliferation. often presenting itself in patients with amplified wild-type egfr, patients with egfrviii mutation have significantly lower survival as compared to those without the mutation (1.4 years).2 3. platelet-derived growth factor alpha receptor: it represents a receptor for specific growth factors whose over expression would lead to abnormal and uncontrolled cellular growth. in, gbm may have either a or b types.3 4. isocitrate dehydrogenase: is a protein enzyme coded by genes in chromosome number 2, whose primary function is catalyze the oxidative decarboxylation process within the krebs cycle.3 5. tumor protein 53: it codes for a widely known tumor suppressor protein, p53. it serves various roles in suppressing tumorigenesis. it is observed at a much higher rate in secondary gbm (90%) compared to cases in primary gbm (30%), and may even remain absent in few primary gbm.4. 5 ii. microrna as biomarkers (mirna): these short rna non-coding molecules which are often correlated with progression and proliferation of gbm cells. the micron plays a major role in the development and progression of tumor based on its pathway modulatory abilities in oncogenic and tumor suppressor genes. the utilization of mirna as molecular biomarkers is being reported to yield >90% specificity in detection of gbm itself mirna is thought to be an useful biomarker in oncology for cancer detection due to its less-invasive approach, mainly from samples collected from various body fluid and it also allows patient stratification over the usual prognostications.6,7 1. mir-21: it is expressed in gbm as well as malignancy of ovary, cervix and lungs. modulatory ability of mir-21 lead to affect tumor suppressor genes such as pten, reck, fasl and pdcd4.8,9 it is up regulated in gbm source sample is csf, blood and urine. it is considered as prognostic marker 2. mir-10b: it is considered as prognostic and predictive marker of gbm. source sample is csf, blood and urine. it is considered as prognostic marker 3. mir-15b: these are is down regulated in gbm, and also represents as one of the prognostic and predictive marker. 4. mir-137: these are usually down regulated in gbm and presents another predictive and prognostic gbm marker.10, 11 the molecular biomarkers and micro rna biomarker were originally were designed and routinely utilized as drug targets to develop recent updared therapies. authors strongly hope biomarker development and advances in therapy in near future may protect humanity against atrocities of the gbm.12-14 conclusion the aggressiveness nurture of gbm, dictate the urgent need of development of biomarkers for accurate and early diagnosis and to precisely categorization for 468 | satyarthee et al biomarkers of glioblastoma multiforme             responsiveness to various therapeutic chemotherapy and other supportive regimen. the molecular biomarkers and micro rna biomarker were utilized as drug targets to develop therapies. authors strongly hope biomarker development and advances in therapy in near future may protect humanity against atrocities of the gbm. correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: drguruduttaaiims@gmail.com references 1. sasmita ao , wong yp , ling apk . biomarkers and therapeutic advances in glioblastoma multiforme. asia pac j clin oncol. 2017 aug 25. doi: 10.1111/ajco.12756.a 2. shinojima n, tada k, shiraishi s, et al. prognostic value of epidermal growth factor receptor in patients with glioblastoma multiforme. cancer res. 2003; 63(20):6962– 6970. 3. motomura k, mittelbronn m, paulus w, et al. pdgfra gain in low-grade diffuse gliomas. j neuropathol exp neurol. 2013; 72(1):61–66 4. furnari fb, fenton t, bachoo rm, et al. malignant astrocytic glioma: genetics, biology, and paths to treatment. genes dev. 2007; 21:2683–2710. 5. laezza c, d'alessandro a, croce ld, et al. p53 regulates the mevalonate pathway in human glioblastoma multiforme. cell death dis. 2015;6:e1909 6. akers jc, ramakrishnan v, kim r, skog j, nakano i, pingle s. mir-21 in the extracellular vesicles (evs) of cerebrospinal fluid (csf): a platform for glioblastoma biomarker development. plos one. 2013;8:c78115. 7. mishra pj. micrornas as promising biomarkers in cancer diagnostics. biomarker res. 2014;2:19 8. niyazi m, pitea a, mittelbronn m, et al. a 4-mirna signature predicts the therapeutic outcome of glioblastoma. oncotarget. 2016;7(29):45764–45775. 9. si ml, zhu s, wu h, lu z, wu f, mo yy. mir-21mediated tumor growth. oncogene. 2007; 26(19):2799– 2803. 10. shah my, calin ga. the mix of two worlds: noncoding rnas and hormones. nucleic acid ther. 2013;23:2–8. 11. griveau a, bejaud j, anthiya s, avril s, autret d, garcion e. silencing of mir-21 by locked nucleic acidlipid nanocapsule complexes sensitize human glioblastoma cells to radiation-induced cell death. int j pharmacol. 2013;454:765–774. 12. satyarthee gd, mahapatra a. kgiant pediatric glioblastoma multiforme causing primary calvarial erosion and sutural diastasis presenting with enlarged head. j pediatr neurosci. 2015 jul-sep; 10(3): 290–293. 13, rajeshwari m, kakkar a, nalwa a, suri v, sarkar c, satyarthee gd, garg a, sharma mc.wnt-activated medulloblastoma with melanotic and myogenic differentiation: report of a rare case. neuropathology. 2016 aug;36(4):372-5 14. satyarthee gd, sudhan md, mehta vs. pilocytic midbrain astrocytoma presenting with fresh bleed after twenty-one-years survival following first surgery: a unique case of longest brainstem glioma survival. j neurosci rural pract. 2016 (suppl 1):s88-s90. doi: 10.33962/roneuro-2021-083 schwannoma of the digital nerve. a rare case report vuk aleksić, jovana prelić, matija radojević, radmila ćulafić romanian neurosurgery (2021) xxxv (4): pp. 490-492 doi: 10.33962/roneuro-2021-083 www.journals.lapub.co.uk/index.php/roneurosurgery schwannoma of the digital nerve. a rare case report vuk aleksić, jovana prelić, matija radojević, radmila ćulafić department of neurosurgery. clinical hospital centre zemun, belgrade, serbia abstract schwannomas are the most common benign tumours affecting the peripheral nervous system. they represent a benign proliferation of schwann cells. schwannomas and other peripheral nerve sheath tumours are common in the head and neck, spine, thorax, abdominal wall, and retroperitoneum. however, localization in hand is exceptional. we present a 22-years-old female patient diagnosed and operated on for schwannoma of the digital nerve (dorsal cutaneous branch originating from the palmar cutaneous branch of ulnar nerve). in the case of a palpable hand mass, one of the possible diagnoses is schwannoma, and since the operative technique is somewhat specific with tumour enucleation and internal neurolysis, it is necessary to preoperatively keep in mind schwannoma in the differential diagnosis. introduction schwannomas are the most common benign tumors affecting the peripheral nervous system (1). they represent a benign proliferation of schwann cells. schwannomas and other peripheral nerve sheath tumors are common in the head and neck, thorax, abdominal wall, and retroperitoneum. these tumors are rarely found in the hands, particularly the fingers (2). they are most frequent in adults between the ages of 30 and 60, and they affect both men and women equally (3, 4). most schwannomas are asymptomatic however they can cause functional deficits and pain depending on which nerve is affected (5). we present a 22-years-old female patient diagnosed and operated on because of left hand digital nerve schwannoma. case report the 22-year-old female patient was admitted to the neurosurgery department for surgical treatment of a tumor in the dorsal region of the left hand, which was described as a scwannoma on ultrasound (figure 1). due to the suspicion of a ganglion cyst the tumor was punctured in another institution and aspiration was tried, however, no content was obtained, and subsequently reddening of the skin above tumor appeared few days later. the tumor has been present for several years and has begun to grow during the last year. phisical examination keywords schwannoma, digital nerve, hand schwannoma corresponding author: vuk aleksić department of neurosurgery. clinical hospital centre zemun, belgrade, serbia aleksicvuk@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 491 schwannoma of the digital nerve revealed small tumor between the third and fourth finger of the left hand on the dorsal side, messuring about 3 x 2 cm, mobile, painless, and percussion in the tumor region gave a positive tinel sign. based on the clinical picture and ultrasound findings, an indication for surgical removal of the tumor was set. the patient was operated under the conditions of local anesthesia and the tumor of the digital nerve in the region of the ulnar nerve branch was microsurgically removed. the change was irregular in shape, pearly white in color in cross section with significant adhesions for the surrounding tissues, so external and internal neurolysis were performed and all shown fascicles were preserved exept the fasciculus from which the tumor grew (figure 2). the operation went smoothly, the patient was transferred to the ward. the postoperative period was uneventful, the patient was neurologicaly intact and was discharged on second postoeprative day. histopathological examination confirmed suspected diagnosis of schwannoma (who grade i) (figure 3). after 3 months, the patient is without symptoms, neurological deficit and with no signs of tumor recurrence. figure 1. ultrasound finding of the mass located in the dorsal region of the hand resembling schwannoma or ganglion cyst. discussion schwannomas are typically benign slow growing tumors of the peripheral nerve. despite its low overall incidence, benign schwannoma is one of the most common peripheral nerve tumors. they are usually find in the head, neck and spine (3, 4). the hands, particularly the fingers, are rarely affected by these tumors (2). we present a rare case of the digital nerve (dorsal cutaneous branch originating from palmar cutaneus branch of ulnar nerve) schwannoma located on the dorsal side of hand. schwannomas are typically described as nonpainful swellings that go unnoticed for years, making clinical identification and therapy more challenging (6). in the differential diagnosis neurofibroma, perineurinoma, ganglion cyst, giant cell tumors of the tendon sheath, fibroma of the tendon sheath, lipoma, extraosseous chrondroma and other softtissue masses should be considered (5). in our case ultrasound finding was described as ganglion cyst or schwannoma. local finding was more suggestive of schwannoma, especialy since the lesion was punctured and no content was obtained. positive tinel's sign also indicated nerve (sheath) tumor. figure 2. intraoeprative findings: (a) preoperative aperance; (b) finding after skin incision; (c) local finding after tumor removal; (d) macroscopic apperance of the tumor after removal; (e) cros section fo tumor. wide spectrum of clinical symptoms such as parasthesias, hypoesthesia, tingling, motor defict, and positive tinel's sign contribute to almost impossible clinical distinction between schwannomas and other peripheral nerve tumors or other soft-tissue tumors. the most common clinical scenario represents a patient with swelling that starts to hurt and grows a bit more after a few years of beeing an asymptomatic lesion. the appearance of pain and the fast growth of a tumor might signal a malignant transformation (7, 8). our patient had 492 vuk aleksić, jovana prelić, matija radojević, radmila ćulafić tumor for several years, but it started to grow during one last year. figure 3. pathohistological diagnosis confirmed schwannoma with typical verocay bodies (rounded). additional diagnostic procedures are usualy required such as ultrasound and magnetic resonance imaging. on ultrasonography, a schwannoma is a homogeneous, hypoechoic mass with enhanced through transmission, target appearance, and pseudocystic appearance, similar to ganglion cysts. as a result, it's difficult to tell the difference between a schwannoma of the hand and a cystic lesion (9). in our case due to suspicion of ganglion cyst patient was first referred to another institution where puncture and aspiration were performed, however, no content was isolated. during the operation in our institution, the intraoperative finding was indicative of schwannoma, which was confirmed with histopathological analysis. treatment for schwannoma is determined by the location of the tumor, if it is causing pain, and how rapidly it grows. sometimes observation is indicated, but surgery is essential if symptoms occur. main goal is enucleating the tumor while avoiding nerve damage with internal neurolysis, so usage of operative microscope is strongly recommended (10). after performed operation our patient didnt have any postoperative complication nor neurological deficit. conclusion schwannomas are benign tumors that are rarely encountered in clinical practice. ultrasound, mri, and finally histological analysis of the tumor verify them. the tumors are normally benign, and the condition is rarely life-threatening, but depending on where they are located, they might cause a variety of symptoms. one of the possible diagnoses in the case of a palpable hand mass is schwannoma, which requires a special microsurgical approach in order to completely remove the tumor while preserving nerve function. therefore, because operative technique is somewhat specific, it is essential to keep schwannoma as a possible diagnosis. references 1. jiang s, shen h, lu h. multiple schwannomas of the digital nerves and common palmar digital nerves: an unusual case report of multiple schwannomas in one hand. medicine (baltimore). 2019;98(10):e14605. 2. balan jr, john jr. digital schwannomas: a diagnosis in retrospect. ip int jaesthet health rejuvenation. 2020;3(3):77-9. 3. fodor l, samuila s, bodog f. a rare case of schwannomatosis of the extremities. j int med res. 2020;48(9):300060520952278. 4. galbiatti ja, milhomens grds, bertozzo lg, escames l, milhomens neto pa, galbiatti mgp. retrospective analysis of 20 patients affected by schwannomas in the upper and lower limbs. rev bras ortop (sao paulo). 2020;55(5):629-636. 5. troy j, barnes c, gaviria a, payne w. schwannoma in digital nerve: a rare case report. eplasty. 2015;15:ic56. 6. kütahya h, güleç a,güzel y, kacira b, toker s. schwannoma of the median nerve at the wrist and palmar regions of the hand: a rare case report. orthopedics. 2013; 2013: 2013950106. 7. mackinnon se. nerve surgery. new york: thieme; 2015. 8. hirai t, kobayashi h, akiyama t, okuma t, oka h, shinoda y, ikegami m, et al.predictive factors for complications after surgical treatment for schwannomas of the extremities. bmc musculoskelet disord. 2019;20(1):166. 9. lee sj, yoon st. ultrasonographic and clinical characteristics of schwannoma of the hand. clin orthop surg. 2017;9(1):91-95. 10. mayoclinic.org [homepage on the internet]. arizona: peripheral nerve tumors; available from: https://www.mayoclinic.org/diseases-conditions/schwan noma/cdc-20352974. doi: 10.33962/roneuro -2020-057 the impact of vertebral osteomyelitis on spinal stability and principles of surgical stabilization. medical literature review vlad catana, radu mircea gorgan romanian neurosurgery (2020) xxxiv (2): pp. 201-208 doi: 10.33962/roneuro-2020-057 www.journals.lapub.co.uk/index.php/roneurosurgery the impact of vertebral osteomyelitis on spinal stability and principles of surgical stabilization. medical literature review vlad catana1,2, radu mircea gorgan1,3 1 university of medicine and pharmacy “carol davila”, bucharest, romania 2 “foisor” clinical hospital of orthopedic and traumatology, bucharest, romania 3 “bagdasar arseni” clinical emergency hospital bucharest, romania abstract vertebral osteomyelitis (vo) is a disease that responds well to conservative treatment and antibiotherapy if diagnosed in an early stage. due to the prolonged onset of this pathology, many cases are diagnosed in mid or late stages and require surgery. the surgical treatment is not yet standardized and may only mean decompression of the infectious outbreak without stabilization, or surgical decompression associated with stabilization. using only bone grafts for surgery or stabilizing the spine through segmental posterior and/or anterior instrumentation is accompanied by many controversies. in this review, we focus on demonstrating that combining a well-conducted antibiotherapy with thorough debridement of the necrotic areas and using metal implants for spinal stabilization lowers the infection rates, provides an early pain-free mobilization of the patient and reduces hospitalization costs. 1. introduction vertebral osteomyelitis (also called osteodiscitis) is an acute or chronic infection of the spine with direct iatrogenic or indirect (hematogenous) inoculation. it is a rare infection concentrated in the spine, the cases being so rare that only 2-4% of all bone infections are attributed to this disease. vertebral osteomyelitis attacks the intervertebral disc and the two adjacent vertebrae, causing the destruction of the intervertebral space. the prognosis of the disease depends on several factors: the place where the infection is concentrated in the spine, the time elapsed between the initial onset and the treatment used, but also the approach used to treat the disease (1,5). historically we will cover the treatments applied to vertebral osteomyelitis over the years. the first measures taken were bed rest and symptomatic medication. laminectomy was the first attempt at surgical treatment, but it brought poor results in the approach to the anterior spine, and the keywords c-reactive protein, osteodiscitis, spinal instrumentation, spine surgery, vertebral osteomyelitis corresponding author: vlad catana md. phd student. university of medicine and pharmacy “carol davila”, bucharest, romania catana.vlad@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 202 vlad catana, radu mircea gorgan main complication was postoperative instability (2, 11). in 1911, albee introduced a posterior bone fusion technique, but this was abandoned due to postoperative kyphosis (6). hodgson and stock introduced the approach technique of the infectious outbreak, which directly resolves the infection and preserves the integrity of the anterior spine, preventing postoperative kyphosis (10). after the introduction in the 1970s by roy camille of the vertebral fixation technique with transpedicular screws and rods, it became a standard in the surgical treatment of vertebral osteomyelitis (5, 8). materials and methods for accomplishing this review, we enlisted a throughout research of database from “pubmed”, “scopus”, “web of science” using key words as “vertebral osteomyelitis”, “spinal infection”, “osteodiscitis”, “spinal stabilization” and “spine surgery”. of the many existing studies, we reviewed 35 studies independent of time and date and from which we concluded this review, comparing different methods of treatment in vertebral osteomyelitis. results etiology and pathophysiology the source of the infection was found in only 40% of cases and was represented by urinary tract infections, soft tissue, respiratory, intestinal, dental infections, endocarditis and penetrating trauma. the etiology of vertebral osteomyelitis consists of infections with staphylococcus aureus, streptococcus, mycobacterium tuberculosis, etc. the study by nolla jm et al shows that acute vo affects mostly elderly patients with associated comorbidities. (27) most cases of osteodiscitis occur due to the inoculation of bacteria by hematogenous at the level of the intervertebral disc. dermal inoculation is also present. the most common bacterial cause is staphylococcus aureus (32-67%). occasionally, coagulase-negative staphylococci may be a cause with or without epidural involvement. gram-negative organisms, such as escherichia coli (21%), often from a urinary tract source are the second most commonly identified cause of infection. pseudomonas sp. are associated with approximately 6% of cases and should indicate a history of environmental water exposure or intravenous drug use (20). in their study, patzakis and coworkers included a 78 % of the patients as intravenous drug users and found s. aureus at a low prevalence as the main bacteria (17%), while pseudomonas aeruginosa was the predominant etiologic agent (38%) (29). spinal infections lead to a spectrum of diseases with a varied clinical presentation. vertebral infection usually results from bacterial insemination of the vertebral disc, which then spreads to adjacent vertebrae (vertebral osteomyelitis). a muscular abscess is frequently present in the paravertebral muscles. in 17% of cases, the infection at the disc level migrates into the epidural space, resulting in the epidural abscess. its timely identification is essential, as 1 in 4 patients with this condition quickly develop paralysis (26). several studies describe the vertebral level involved and describe the following incidence of affection: lumbar spine (58%), thoracic spine (30%) and cervical spine (11%) (34, 28, 2, 26, 17). vertebral defects were found in multiple levels, 6% were reported with continuous character and 3% reported with skipping multifocal involvement. a large number of multifocal involvement was reported in iv drug abusers (29). symptoms. clinical evaluation a detailed neurological examination is essential for any patient suspected of having vertebral osteomyelitis. objective neurological signs are rare, but when present can range from mild (radicular pain corresponding to a nerve root injury), moderate (motor weakness, sensory loss, urinary or intestinal dysfunction), to severe (paralysis). in the presence of an abnormal neurological examination, the presence of a possible epidural abscess should be investigated, because the delay of the diagnosis can lead to the permanence of the deficit. the accentuation of the neurological signs indicates the progression of the infection in the epidural space and the damage of the nerve roots or the compression of the spinal cord. according to numerous studies, many patients present an insidious onset and unspecific symptomatology (neck or back pain, fever, painful 203 the impact of vertebral osteomyelitis on spinal stability and principles of surgical stabilization flexion/extension of the back and/or neurological deficits). early diagnosis of this disease is important, but not always possible as 30-70% of the patients do not show signs of prior infection (5) and a delay of 2 to 6 months from the starting symptomatology to the diagnosis of this disease has been reported. (1, 11) local clinical examination, represented by the point of sensitivity to palpation can differentiate vertebral osteomyelitis from other differential diagnoses. there are no pathognomonic signs or symptoms to indicate the presence of this condition. a normal clinical examination does not rule out presence diagnosis of vertebral osteomyelitis. the classic triad consisting of fever, back pain and neurological deficit is specific to this condition. the potential consequences of undiagnosed vertebral osteomyelitis are devastating, so when referring to a differential diagnosis, laboratory and imaging tests are mandatory. thus, according to the studies of butler et al and frangen et al, the diagnosis should be supported by clinical, laboratory, and imaging findings (1, 11) laboratory tests usual blood tests that help diagnose patients with suspected epidural abscess or vertebral osteomyelitis include: hemoleukogram, erythrocyte sedimentation rate (esr), c-reactive protein (crp). these tests are not completely reliable indicators for the presence of the disease and must be correlated with: clinical suspicion, patient history and imaging study. leukocytosis is variable and does not indicate the severity of the disease. increased esr is important in the early diagnosis of patients with osteomyelitis. crp has a sensitivity of 84-100% in the case of the presence of epidural abscess and is a necessary analysis for the initial diagnosis. however, according to curry and coworkers, esr and crp are more useful than the white blood cell count (wbc), because a normal wbc does not exclude the presence of a spinal infection. (3) also, the positivity of blood cultures indicates the presence of a generalized infection, the most often isolated germ in most cases being staphylococcus aureus. as some studies show, up to 59% of positive blood cultures identify the etiological microorganism in patients with monomicrobial pyogenic spondylodiscitis (24) imaging radiological evaluation of a patient with vertebral osteomyelitis reveals changes only after a few weeks. the first obvious changes after a few days are local edema and loss of the psoas shadow. in the next 710 days, the reduction of the vertebral space and the erosion of the adjacent vertebral plates ("mirror image") are observed. sclerosis at this level generally appears on the radiological image at 10-21 days and it may take 3 to 6 weeks from the onset of the symptoms for bony destruction of the vertebrae to become evident according to jevtic v’s study (20) (figure 1). this results in a delay of the diagnosis. figure 1. preoperative thoracic spine radiograph: major narrowing of t7-t8 disc space (personal collection). the gold standard for imaging diagnosis is mri, which distinguishes hypointensity in t1, hyperintensity in t2 and capture of gadolinium in the t1-weighted sequence. this investigation has a sensitivity of 96% and a specificity of 93% and is also used in the differential diagnosis of this pathology. (12, 13) in case of an mri contraindication, a ct scan is performed, which distinguishes bone abnormalities, abscess formation and the degree of bone damage. another investigation that can be performed in the case of mri contraindication is tc99m technetium bone scintigraphy, but it has a sensitivity of 90% and a much lower specificity than mri. (17) (figures 2,3) according to hadjipavlou and coworkers, positive blood cultures and other paraclinical investigations 204 vlad catana, radu mircea gorgan in association with clinical symptoms do not confirm the diagnosis of a spinal infection. the definitive diagnosis can be obtained by histopathological examination thorough a surgical or ct-guided biopsy. an exact diagnosis of this disease should be achieved in order to ensure a well-conducted management. (16, 17) figure 2. thoracic mri with intravenous contrast t2 sagittal plane: t7-t8 osteomyelitis with intraspinal abscess (personal collection). figure 3. thoracic mri with intravenous contrast t2 transverse plane: t7-t8 osteomyelitis with intraspinal abscess (personal collection). differential diagnosis the main pathologies with which the differential diagnosis can be made are: vertebral tumors, vertebral fracture and degenerative diseases of the spine (disc herniation, spinal canal stenosis, vertebral spondylosis). in a study conducted by tyrell pn et al, it is demonstrated that a destructive bone lesion of the vertebrae associated with a preserved disc space with sharp endplates guides the diagnosis to a neoplastic infiltration, while a destructive bone lesion associated with an undefined vertebral body with loss of definition of the vertebral endplate with or without modification of disc height suggests an infection, which has a better prognosis than cancer. (35) conservative and medicamentous treatment conservative treatment of vertebral osteomyelitis consists of prolonged bed rest and antibiotic therapy for 6 to 12 weeks. during immobilization, the patient is placed in a corset or cervico-thoracic or thoraco-lumbar orthosis depending on the location of the lesion. according to the studies of fleege c et al and skaf gs et al, the first line of treatment is a conservative approach. this choice is made especially for the patients with minor or no neurologic deficits and in case of severe associated comorbidities that limit surgery. antibiotics with a large spectrum are used initially (clindamycin + ciprofloxacin or cefotaxim + flucloxacillin) in order to cover a wider area of potential pathogens. afterwards, the antibiotic treatment is switched to an appropriate medication guided by the antibiogram. these last antibiotics are applied iv for 2-4 weeks or until the crp is markedly dropped. in the final step of the treatment oral antibiotic is continued for a total of 6 to 12 weeks. this treatment is accompanied by prolonged bed rest and pain medication with or without orthosis for at least 6 weeks. (10, 33) medicamentous treatment is a symptomatic as well as an etiological treatment. symptomatic treatment addresses mainly pain, febrile syndrome and includes various types of analgesics and anti-inflammatory drugs. the etiological treatment is addressed to the germ in question and is represented by third generation cephalosporins and / or vancomycin for bacterial and tuberculostatic treatment in cases with mycobacterium tuberculosis (20). medicamentous treatment must also take into account the biological balance of each patient and in 205 the impact of vertebral osteomyelitis on spinal stability and principles of surgical stabilization this context, we refer to parenteral hydration with various osmolar solutions, parenteral nutrition in cases of severe sepsis, combating anemia in cases of severe sepsis through blood transfusions, hypoproteinemia and balancing the metabolic rate of the patient (17). if conservative treatment fails and proper mobilization of the patients is not achieved surgery is then performed as many complications due to immobilization are critical to patients, especially to the elderly. surgical treatment several studies suggest that the main indications for surgical treatment are represented by the following: severe lesional changes in vertebral endplates, formation of abcesses, biomechanical instability due to chronic osteomyelitis, appearance of neurological deficits, decompensated kyphosis, septic pseudarthrosis, pain that does not respond to pharmaceutic treatment, and non-responsive patients to conservative treatment. ( 4, 14, 30) the surgical treatment has the following important objectives: evacuation of infection and debridement, decompression of the dural sac and spinal roots and vertebral fixation / fusion. the main principle of the surgical treatment of this disease is radical and aggressive debridement of all unviable tissues and material according to a study conducted by fayazi ah and coworkers. this study states that all necrotic and infected tissues are mandatory to be removed and all abscesses evacuated for a good management of the disease. (9) the choice of surgical approach depends on the location of the lesion in the spine. thus, the anterior cervical approach, the lateral cavitary approach and costotransversectomy for the thoracic spine, laminectomy, hemilaminectomy and foraminotomy for the lumbar spine are described. choosing between an anterior or posterior approach is debatable. the studies of emery se, fang d and fukuoka m show that due to affection of the vertebral bodies and disc spaces the majority of surgeons incline to an anterior approach for direct access to the infection site and better reconstructive stabilization. (6, 7, 12) fayazi et al and korovessis et al reveal that a posterior approach is used in order to drain the abscesses and for posterior stabilization of the spine and that a combined approach needs to be chosen in relation to the surgical goals that are aimed to be achieved. (9, 22) several studies show that a combined approach results in a lower incidence of postoperative infection and revision surgery and a higher mortality rate with an isolated anterior approach for cervical spine lesions. the increased mortality rate of an anterior approach is also explained by a higher incidence of associated comorbidities of patients with cervical spine lesions. (4, 8, 13, 15, 23) the vertebral fixation is performed using transpedicular screws and rods, but also the reconstruction techniques of the anterior column, with the help of fixed or expandable titanium cages. a relatively new method of treating this disease is represented by minimally invasive surgery. muckley t and coworkers demonstrated in their study that treating vo through video-assisted thoracoscopic surgery has advantages and disadvantages. the main advantages are debridement and surgical instrumentation of multiple levels can be achieved with minimal dissection of the surrounding soft tissues. the disadvantages of this technique are represented by a technically demanding procedure in which special instrumentation and experience of the surgeon are required. (25) hadjipavlou et al revealed in their study of 34 cases an immediate pain relief of 26 patients and stated that the most common long-term complications of the use of minimally invasive surgery are implant failure with axial pain and instability or severe kyphotic deformities. (16) a controversial debate is between the use of single-stage surgery versus two-stage surgery. safran et al revealed in his study of 10 patients with osteodiscitis operated through single-stage surgery that it is a secure and efficient method of controlling the infection and reconstruction of the spine, shortening the hospitalization and mobilization time of the patient and also reducing hospitalization costs for the patient and the institute. the surgery is performed based on the experience of the surgeon and the overall condition of the patient, taking into consideration that medically unstable patients may not be able to withstand a second anesthesia, surgery or increased period of immobilization. (31) increased surgical debridement of a 206 vlad catana, radu mircea gorgan compromised anterior column of the spine results in massive loss of bone tissue and increased axial instability, therefore it is mandatory to perform surgical reconstruction in order to prevent residual instability. bone grafting is required for the reconstruction of the anterior column either with autogenous bone graft or allograft. a study by emery se et al demonstrated that 19 patients operated for vertebral osteomyelitis through aggressive debridement and the use iliac bone grafting in the presence of an active infection had immediate pain relief and no septic complications 2 years after surgery. (6) many surgeons suggest that allografting can be used instead of autogenous grafting. schuster et al conducted a study of 47 patients operated using allografts consecutive to surgical debridement, posterior instrumentation and iv antibiotics and demonstrated that it is a secure method of treating vertebral osteomyelitis. the main advantages of using allografts are lowering the operation time and morbidity associated with harvesting of the graft and the main disadvantages are the host’s immune response and an increased risk of pathological transmission of diseases. (32) hodgson demonstrated in 1956 through his work on the treatment of pott’s paraplegia that anterior debridement and vertebral fusion with autogenous bone grafting rapidly correct axial alignment, however, long-term results show spinal instability with the collapse of the vertebral column, correction malalignment and formation of pseudarthrosis. (19) therefore, the use of spinal instrumentation is mandatory in most cases associated with spinal instability. (figures 4,5) in their studies hee el al. and fayazi et al. reported that the use of a titanium mesh cage with posterior instrumentation for the reconstruction of the spine is an excellent method in improving the mobilization of the patient and a rapid fusion in patients that underwent surgery for active vertebral osteomyelitis. therefore, they demonstrated that the patients had less postoperative complications, lower infection recurrence rates and improved spinal alignment and stability. the loss of kyphosis correction was noted due to collapse of the cage into the adjacent vertebrae, but overall the cases had a good prognosis because of the lower infection rates and early and pain free mobilization. (18, 9) figure 4. intraoperative view showing spinal fixation using 8 transpedicular screws and rods after radical debridation (personal collection), figure 5. postoperative radiographic control: stabilization with 8 transpedicular screws and 2 titanium rods (personal collection). conclusion most cases of vertebral osteomyelitis respond well to conservative treatment if diagnosed in an early stage. in cases that are unmanageable by conservative treatment, surgery is mandatory. aggressive debridement of all necrotic tissues is needed along with surgical stabilization of the spine to ensure a good management of the disease. vertebral fixation and fusion ensure immediate vertebral stability, which allows the patient to 207 the impact of vertebral osteomyelitis on spinal stability and principles of surgical stabilization mobilize quickly in the first days after surgery. this is beneficial for neurological recovery, starting physical therapy and preventing complications associated with prolonged bed rest. the patient can be discharged from the surgery department in the first week after the operation after wound healing and thread extraction, which allows rapid transfer to the infectious diseases department where prolonged and targeted antibiotic treatment will be continued. this reduces hospital stay and costs per patient. this paper will demonstrate that the combination of surgical treatment represented by decompression and fixation-fusion vertebral with targeted antibiotic treatment eliminates local recurrence and allows the patient to quickly return to a normal socioprofessional life. references 1. butler js, shelly mj, timlin m, powderly wg, o’byrne jm. nontuberculous pyogenic spinal infection in adults: a 12year experience from a tertiary referral center. spine. 2006 nov 1;31(23):2695-700. 2. chelsom j, solberg co. vertebral osteomyelitis at a norwegian university hospital 1987-97: clinical features, laboratory findings and outcome. scandinavian journal of infectious diseases. 1998 jan 1;30(2):147-51. 3. curry jr wt, hoh bl, amin-hanjani s, eskandar en. spinal epidural abscess: clinical presentation, management, and outcome. surgical neurology. 2005 apr 1;63(4):36471. 4. dimar jr, carreon ly, glassman sd, campbell mj, hartman mj, johnson jr. treatment of pyogenic vertebral osteomyelitis with anterior debridement and fusion followed by delayed posterior spinal fusion. spine. 2004 feb 1;29(3):326-32. 5. duarte rm, vaccaro ar. spinal infection: state of the art and management algorithm. european spine journal. 2013 dec 1;22(12):2787-99. 6. emery se, chan dp, woodward hr. treatment of hematogenous pyogenic vertebral osteomyelitis with anterior debridement and primary bone grafting. spine. 1989 mar;14(3):284-91. 7. fang d, cheung km, dos ir, lee yk, leong jc. pyogenic vertebral osteomyelitis: treatment by anterior spinal debridement and fusion. journal of spinal disorders. 1994 apr;7(2):173-80. 8. faraj aa, webb jk. spinal instrumentation for primary pyogenic infection. report of 31 patients. acta orthopaedica belgica. 2000 jun;66(3):242-7. 9. fayazi ah, ludwig sc, dabbah m, butler rb, gelb de. preliminary results of staged anterior debridement and reconstruction using titanium mesh cages in the treatment of thoracolumbar vertebral osteomyelitis. the spine journal. 2004 jul 1;4(4):388-95. 10. fleege c, wichelhaus ta, rauschmann m. systemic and local antibiotic therapy of conservative and operative treatment of spondylodiscitis. der orthopade. 2012 sep;41(9):727-35. 11. frangen tm, kälicke t, gottwald m, andereya s, andress hj, russe oj, müller ej, muhr g, schinkel c. surgical management of spondylodiscitis. an analysis of 78 cases. der unfallchirurg. 2006 sep;109(9):743-53. 12. fukuoka m, aoki y, hayashi s, nagasawa k, aita k, hotokebuchi t, satoh t. pyogenic vertebral osteomyelitis caused by prevotella intermedia. journal of infection and chemotherapy. 2002 jan 1;8(2):182-4. 13. fukuta s, miyamoto k, masuda t, hosoe h, kodama h, nishimoto h, sakaeda h, shimizu k. two-stage (posterior and anterior) surgical treatment using posterior spinal instrumentation for pyogenic and tuberculotic spondylitis. spine. 2003 aug 1;28(15):e302-8. 14. gasbarrini al, bertoldi e, mazzetti m, fini l, terzi s, gonella f, mirabile l, barbanti brodano g, furno a, gasbarrini a, boriani s. clinical features, diagnostic and therapeutic approaches to haematogenous vertebral osteomyelitis. eur rev med pharmacol sci. 2005 jan;9(1):53-66. 15. graziano gp, sidhu ks. salvage reconstruction in acute and late sequelae from pyogenic thoracolumbar infection. journal of spinal disorders. 1993 jun;6(3):199207. 16. hadjipavlou ag, katonis pk, gaitanis in, muffoletto aj, tzermiadianos mn, crow w. percutaneous transpedicular discectomy and drainage in pyogenic spondylodiscitis. european spine journal. 2004 dec 1;13(8):707-13. 17. hadjipavlou ag, mader jt, necessary jt, muffoletto aj. hematogenous pyogenic spinal infections and their surgical management. spine. 2000 jul 1;25(13):1668-79. 18. hee ht, majd me, holt rt, pienkowski d. better treatment of vertebral osteomyelitis using posterior stabilization and titanium mesh cages. clinical spine surgery. 2002 apr 1;15(2):149-56. 19. hodgson ar, stock fe. anterior spinal fusion a preliminary communication on the radical treatment of pott's disease and pott's paraplegia. british journal of surgery. 1956 nov;44(185):266-75. 20. jevtic v. vertebral infection. european radiology supplements. 2004 mar 1;14(3):e43-52. 21. karadimas ej, bunger c, lindblad be, hansen es, høy k, helmig p, kannerup as, niedermann b. spondylodiscitis. a retrospective study of 163 patients. acta orthopaedica. 2008 jan 1;79(5):650-9. 22. korovessis p, sidiropoulos p, piperos g, karagiannis a. spinal epidural abscess complicated closed vertebral fracture: a case report and review of literature. spine. 1993 apr 1;18(5):671-4. 23. lee mc, wang my, fessler rg, liauw j, kim dh. instrumentation in patients with spinal infection. neurosurgical focus. 2004 dec 1;17(6):1-6. 24. lener s, hartmann s, barbagallo gm, certo f, thomé c, 208 vlad catana, radu mircea gorgan tschugg a. management of spinal infection: a review of the literature. acta neurochirurgica. 2018 mar 1;160(3):487-96. 25. mückley t, schütz t, schmidt mh, potulski m, bühren v, beisse r. the role of thoracoscopic spinal surgery in the management of pyogenic vertebral osteomyelitis. spine. 2004 jun 1;29(11):e227-33. 26. nather a, david v, hee ht, thambiah j. pyogenic vertebral osteomyelitis: a review of 14 cases. journal of orthopaedic surgery. 2005 dec;13(3):240-4. 27. nolla jm, ariza j, gómez-vaquero c, fiter j, bermejo j, valverde j, et al. spontaneous pyogenic vertebral osteomyelitis in nondrug users. semin arthritis rheum 2002;31:271-8. 28. osenbach rk, hitchon pw, menezes ah. diagnosis and management of pyogenic vertebral osteomyelitis in adults. surgical neurology. 1990 apr 1;33(4):266-75. 29. patzakis mj, rao sa, wilkins je, moore tm, harvey pj. analysis of 61 cases of vertebral osteomyelitis. clinical orthopaedics and related research. 1991 mar(264):17883. 30. priest dh, peacock je. hematogenous vertebral osteomyelitis due to staphylococcus aureus in the adult: clinical features and therapeutic outcomes. southern medical journal. 2005 sep 1;98(9):854-63. 31. safran o, rand n, kaplan l, sagiv s, floman y. sequential or simultaneous, same-day anterior decompression and posterior stabilization in the management of vertebral osteomyelitis of the lumbar spine. spine. 1998 sep 1;23(17):1885-90. 32. schuster jm, avellino am, mann fa, girouard aa, grady ms, newell dw, winn hr, chapman jr, mirza sk. use of structural allografts in spinal osteomyelitis: a review of 47 cases. journal of neurosurgery: spine. 2000 jul 1;93(1):814. 33. skaf gs, domloj nt, fehlings mg, bouclaous ch, sabbagh as, kanafani za, kanj ss. pyogenic spondylodiscitis: an overview. journal of infection and public health. 2010 jan 1;3(1):5-16. 34. torda aj, gottlieb t, bradbury r. pyogenic vertebral osteomyelitis: analysis of 20 cases and review. clinical infectious diseases. 1995 feb 1;20(2):320-8. 35. tyrrell pn, cassar-pullicino vn, mccall iw. spinal infection. european radiology. 1999 jul 1;9(6):1066-77. romanian neurosurgery (2019) xxxiii (3): pp. 316-321 doi: 10.33962/roneuro-2019-053 www.journals.lapub.co.uk/index.php/roneurosurgery risk factors for preoperative and postoperative late seizure in supratentorial meningiomas. a retrospective analysis of 63 patients rahsan kemerdere, mehmet yigit akgun, orkhan alizada, sureyya toklu, burak tahmazoglu, taner tanriverdi department of neurosurgery, cerrahpasa medical faculty, istanbul university-cerrahpasa, istanbul, turkey abstract introduction. seizure following meningioma surgery is common and management may be challenging. identifying risk factors may help physicians to initiate optimal medical management. the aim of this study is to report seizure outcome and risk factors for perioperative seizure. materials and methods. sixty-three adult patients who underwent supratentorial meningioma resection were included, and perioperative data and long-term followup were provided in this retrospective study. binary logistic regression analysis was used to identify the risk factors for perioperative seizure and postoperative late seizure. results. the results showed that 20 (37.1 %) patients had preoperative seizure and 10 (50 %) patients were seizure free at the long-term follow-up. absence of headache was associated with preoperative seizure (p=0.002) while presence of early seizure was significant predictor for postoperative late seizure (p=0.03). although not significant, occurrence of surgical complications (p=0.08) and non-skull base location (p=0.06) tended toward being a significant risk factor for postoperative late seizure. conclusion. presence of early seizures, surgical complications and locations out of skull base may direct postoperative anti-epileptic treatment to decrease seizure incidence which, indeed, increases quality of life for patients with meningioma. introduction meningioma is the most common form of benign intracranial neoplasms and surgery is the first-line treatment. epileptic seizure, as the first symptom, is one of the most common manifestations of supratentorial meningiomas, occurring up to 60% (5, 14). surgical resection results in complete cessation of seizure in the majority of patients, but new-onset seizures can develop following surgery in the patients who are seizure free preoperatively. leaving a proportion of patients with seizure even after total tumor removal significantly decreases quality of life and patients have to use keywords epilepsy, meningioma, postoperative, preoperative, seizure corresponding author: rahsan kemerdere department of neurosurgery, cerrahpasa medical faculty, istanbul university-cerrahpasa, istanbul, turkey rakemerdere@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 317 supratentorial meningioma and seizure anti-epileptic drugs (aed) for long-term, which also affects patients’ life adversely (8). predicting preoperative and postoperative risk factors for seizures in patients with meningioma have become the focus of recent studies and accumulating evidence showed that younger age, presence of preoperative peritumoral edema, and tumour location are the strongest predictors for either preoperative or postoperative seizure (3, 9, 10, 13). prediction of risk factors is of utmost importance which guides physicians to decide whether or not aed should be started (1, 4, 12, 15, 16). more importantly, informing patients or next of their kin about seizure outcome makes the follow-up period easier for both patients and treating physicians. in this paper, we aimed to share our experience related to preoperative and postoperative seizures in patients who underwent meningioma resection and to find out which patients are under risk of seizure after surgery. material and methods patient selection this retrospective study included the patients operated on supratentorial meningiomas between 2010 and 2017. patients who had infratentorial meningioma, multiple meningioma, and previous intracranial meningioma surgery were excluded from the study. to provide a homogeneous population, patients who were younger than 18 were excluded from the study. the remaining 63 patients were enrolled in this study. the research was conducted in accordance with the principles of helsinki declaration. data retrieval perioperative clinical, radiological, and pathological data were retrieved from the patients’ files. all patients were followed-up clinically and radiologically at regular intervals. clinical, radiological, seizure and aed outcomes were noted. statistical analysis statistical analysis was performed by using spss, version 22.0 (ibm, chicago, il). independent sample t test and chi-square test were used in appropriate comparisons. binary logistic regression analysis was used for multivariate testing of factors associated with preoperative and postoperative seizures. the differences were accepted significant if p value was < 0.05. results demographic and clinical characteristics 45 (71.4%) females and 18 (28.6%) males were enrolled in the study with a mean age of 51.9±14.2 years (range: 20-76 years). headache was found in 35 (55.6%) patients at admission and 20 patients (31.7%) suffered from preoperative seizure. of the 20 patients with preoperative seizure, 10 had single (50%) and the other 10 had multiple seizures. the majority of seizure type was generalized tonic-clonic (n=12; 60%), followed by focal motor (n=5; 25%) and focal sensory (n=3; 15%) seizures. neurological examination demonstrated that 22 patients (34.9%) had neurological deficit ranging from cranial nerve dysfunction to paresis. before surgery, 24 patients (38.1%) were on aed monotherapy. nineteen patients with preoperative seizure (19/20; 95 %) and 5 patients with no seizure (5/43; 11.6%) were on aed. the difference regarding use of aed between patients with and without preoperative seizure was significant (p=0.00001). demographic features of the patients are presented in table 1. table 1. demographic and radiological characteristics. gtc: generalized tonic-clonic, r: right, l: left, m: male, f: female. patient number (%) sex (m/f) 18/45 28.6%/71.4% age 51.9±14.2 years preoperative seizure 20 31.7% gtc 12 60% focal motor 5 25% focal sensory 3 15% preoperative aed therapy with seizure 19/20 95% without seizure 5/43 11.6% tumour side (r/l/midline) 24/36/3 38/57.1/4.7 tumour location 318 rahsan kemerdere, mehmet yigit akgun, orkhan alizada et al. skull-base 15 23.8% non-skull base 48 76.2% radiological characteristics all patients were evaluated by cranial magnetic resonance imaging (mri). peritumoral edema (pte) was determined on t2-weighted images. anteriorposterior diameter was measured on post-contrast axial mr images. the location was divided into 2 groups: skull base and non-skull base. non-skull base group included tumors located on convexity or parasagittal/falx region. mri showed that 36 patients (57.1%) had tumor on the left side, followed by the right side (n=24; 38.1%) and midline (n=3; 4.8%). the difference with respect to the side of location was significant (p=0.00001). but side was not significant between the patients with and without preoperative seizure (p=0.41). skull base and non-skull base location were noted in 15 (23.8%) and 48 (76.2%) patients respectively. the difference was significant (p=0.00001). however, the difference did not reach a significant level between patients with and without preoperative seizure related to skull base and nonskull base location (p=0.62). convexity was significantly the most common location (30 patients; 47.6%) (p=0.00001). second common location was the parasagittal/falx region (18; 28.6%). six patients (9.5%) had anterior clinoid and 4 patients (6.3%) had sphenoid wing meningiomas. two olfactory groove, 2 tuberculum sellae, and 1 petroclival meningioma were observed. comparing patients with and without preoperative seizures, no significant difference was found regarding the site (p=0.60). pte on preoperative mri was present in 37 (58.7%) patients. the difference between presence or absence of pte was insignificant in the whole group (p=0.16). fifteen out of 20 patients (75%) with preoperative seizures and 22 of 43 patients (51.16%) without preoperative seizure had pte on preoperative mri and the difference was not significant (p=0.07). none of the 12 patients diagnosed with atypical meningioma showed pte. the mean anterior-posterior (a-p) diameter was found to be 37.6 ± 14.4 mm (range: 10-72 mm). twenty patients with and 38 patients without preoperative seizure had a mean a-p diameter of 40.8 ± 10.5 mm and 36.2 ± 15.7 mm, respectively. the difference was not significant (p=0.17). figure 1. a left temporal grade 1 secretory meningioma presenting with seizure shows homogeneous contrast enhancement (a and b) and pte on t2 weighted (c) mr images. a grade 1 fibrous meningioma which also shows contrast enhancement with cyst formation (d and e) and pte on t2 weighted images (f) without preoperative epileptic seizure. pte: peritumoral edema. 319 supratentorial meningioma and seizure surgical and histopathological characteristics informed consent form was obtained from all patients undergoing surgical resection. extent of surgery was categorized as gross total resection (gtr) and subtotal resection (str) depending on the findings on postoperative mri. gtr was defined as absence of contrast enhancement on postoperative mri. gtr was achieved in 54 (85.7%) patients and str in 9 (14.3%) patients. histopathological diagnosis was grade-i in 51 (81%) and grade-ii (atypical) in 12 (16.9%) patients. gtr was achieved in all grade-i meningiomas, and all strs were noted in the atypical group. considering grade-i meningiomas, transitional type was the most common subtype (n=24; 38.1%). follow-up the mean follow-up period was 46.87 ± 29.4 months (range: 12-96 months). no new neurological deficit was noted early after surgery. nonetheless, 16 patients (25.4%) in the whole group continued to have neurological deficits. of the 22 patients with preoperative neurological deficit, 6 patients recovered after surgery (27.2%). postoperative seizures were divided into two groups: 1) early seizure and 2) late seizure were defined as a seizure occurring within 7 days and after 7 days following surgery respectively. five (7.9%) patients in the whole group showed early seizures and 10 (15.9%) exhibited late seizures. two (4.65%) and 5 patients (11.62%) without seizure before surgery had early and late seizures respectively. three patients who showed early seizure had late seizure at the last follow-up. of the 10 patients with late seizure, 5 (50%) had single and the rest had multiple seizures. focal motor, generalized tonic-clonic, and focal sensory seizures were seen in 5 (50%), 3 (30%), and 2 (20%) patients, respectively. eight patients (8/10; 80%) with persistent seizure at the last follow-up had convexity meningiomas. interestingly most of the patients with late seizure (8/10) had gtr. although the number of patients with seizure decreased from 20 (31.7%) to 10 (15.9%) at the last follow-up, the difference was not significant (p=0.26). overall, seizure free rate of patients with preoperative seizure was 50% at the last follow-up. five patients (7.9%) showed surgery-related complications. two had hematoma within the resection cavity. two other patients developed hydrocephalus which required ventriculo-peritoneal shunting. all patients were put on aed therapy after surgery. at the last follow-up, 10 patients (15.9%) with late seizure were still using aed monotherapy. comparing the number of patients who were on aed before surgery (n=24; 38.1%) and at the last followup showed no significant difference although there was a trend to decrease in the number of patients using aed (p=0.48). the continuation of aed in these 10 patients depended on the clinical and electrophysiological findings. early mri was obtained from all patients during their stay in the hospital. the first follow-up mri was obtained at the 3rd month of surgery. patients with atypical meningioma had mri every 3 months. in contrast, it was performed in patients with grade-1 meningiomas at the 1st year, then every 2 years until 5 years after surgery. no patient showed new tumor formation or progression of residual tumor on the follow-up mris. predictors of preoperative seizure in this study, 6 categorical risk factors were introduced in logistic regression analysis to find out predictors for preoperative seizure. the risk factors included gender (female/male), edema on mri (present/absent), headache (present/absent), neurological deficit (present/absent), location (skull base/non-skull base), and side (right/left/midline). binary logistic regression analysis (log likelihood=60.697; chi square=18.045; p=0.012) showed that among the 6 risk factors, only absence of headache (or 8.295, 95% ci 2.105-32.68, p=0.002)) was found to be a significant and strong predictor for preoperative seizure. predictors of postoperative late seizure for identification of risk factors for late seizure, 10 categorical variables were analyzed. the factors included gender (female/male), preoperative seizure (yes/no), use of preoperative aed (yes/no), postoperative early seizure (yes/no), side (right/left/midline), edema on preoperative mri (present/absent), location (skull base/non-skull base), extent of resection (gross total/subtotal), surgical complication (present/absent), pathological grade (grade-i/grade-ii). binary logistic regression analysis (log likelihood = 36.571; chi square = 18.561; p=0.06) showed that among the variables above, presence of postoperative early seizure (or 0.045; 95% ci 0.0090.864; p=0.03) was a risk factor for postoperative late seizures. although regression analysis did not show non-skull base location (p=0.06) and occurrence of 320 rahsan kemerdere, mehmet yigit akgun, orkhan alizada et al. surgical complication (p=0.08) to be a significant risk factor postoperative late seizure, they tended toward. discussion seizure is a common symptom adversely affecting the quality of life after intracranial tumor surgery (8). in case of meningiomas, seizure even after total removal of the tumor may require collaboration of epileptologists to figure out the epileptogenic area. preoperative and postoperative seizure outcomes after glioma surgery have been studied extensively and risk factors have been defined (6, 11). however, this issue has not been well-studied for meningioma. depending on the limited number of studies, it was shown that nearly 30% of patients present with seizure in supratentorial meningioma (1, 3, 4, 9, 10, 12, 13, 15, 16). however, type of seizure differs among the papers so that either generalized tonicclonic seizures (gtc) or focal tonic seizures can be encountered as the most common type (1, 4, 13, 16). in fact, gtc seizure is expected to be more common given that meningioma generally presents with seizure after reaching a certain size compressing larger cortical zone. following surgery, about 50 to 70% of patients become seizure free but new seizures can be seen in almost 12% (9, 14). previous studies suggested that prophylactic aeds should be used depending on the risk factors which are associated with seizures (8, 12, 15). the rate with respect to prophylactic aed use in the present paper is comparable to previous studies which do not support routine use of prophylaxis without seizure despite of peritumoral edema (5, 14). almost all previous studies showed that the left side was more commonly involved similar to our findings (1, 4, 9,13, 15). different from other series, non-skull base location was more common in the present paper which may be due to smaller number of patients (3, 10, 13). convexity region is noted as the most common site besides the other frequent locations such as tuberculum sellae, sphenoid wing or parasagittal/falx region (3, 4, 10, 12, 13, 16). in the current literature, convexity meningiomas have been shown to be more epileptogenic (3, 9), nevertheless some authors found that parasagittal/falx meningiomas present with seizure more common than other locations (1). side and site of locations were not different between the patients with and without preoperative/postoperative seizures in our study. atypical and malignant meningiomas are generally associated with pte which may explain higher occurrence of seizure in these types. glutamate, an amino acid which decreases electrical threshold of surrounding cortex and aggravate seizure, has been found to be higher in peritumoral edematous tissue (2). furthermore, pte is shown to be related to angiogenesis, increased pial blood supply, and increased vascular endothelial growth factor (7). all these factors give pte an epileptogenic potential and aed is preferred to start upon detection of edema on mri. we found pte in 58.7% of the patients. however, no difference was found regarding presence of pte and preoperative seizure. interestingly, no pte was detected on mri in 12 patients with atypical meningioma. concerning the size of tumor, >3-3.5 cm diameter was associated with either preoperative or postoperative seizure (3, 13). mean diameter did not show difference between the patients with and without preoperative seizure in our study suggesting that location and/or size of pte may be more important than size of meningioma itself. our overall seizure free rate at the last follow-up was 50% similar to previous reports (50-70%; 5, 14). besides, our early and late seizure rates are comparable with the current literature (3, 10, 16) so that 50% of patients with preoperative seizure have become seizure free after surgery. complex-partial seizure is the seizure type that responds to surgery well. almost 80% of patients with late seizure had surgery on convexity meningiomas and again majority had gtr. concerning these results, we support the notion that gtr may result in seizure more commonly due to increased damage to surrounding cortex. predictors of preoperative and postoperative late seizures when the limited number of retrospective studies are reviewed, only the number of variables included in statistical analysis differs while the negative and/or positive predictors before and after surgery are almost similar (5, 14). male gender, convexity or falx location, absence of headache, tumor diameter >3-3.5 cm, presence of peritumoral edema, younger age were found to be predictors of preoperative seizures. on the other hand, male gender, convexity or falx location, tumor size >33.5 cm diameter, 321 supratentorial meningioma and seizure presence of edema, presence of preoperative seizure, use of postoperative aed, location of the left side and higher grade were associated with postoperative seizure (4, 12, 15, 16). the present study demonstrated that among the variables which we introduced into regression analysis, occurrence of postoperative early seizure was a significant risk factor for postoperative seizure. existence of postoperative surgical complications and non-skull base location showed a tendency to be postoperative late risk factor. study limitations the small patient group and retrospective nature of our study are two major limitations. conclusion depending on our results, absence of headache in the preoperative period and presence of postoperative early seizure are associated with seizure outcome. occurrence of surgical complication(s) and non-skull base locations tend toward to be a predictor for postoperative late seizure. identifying risk factors in the perioperative period may lead treating physician to start timely aed and decrease seizure incidence which, indeed, improves quality of life in patients with meningiomas. conflicts of interest the authors inform that there is no conflict of interest in this study. references 1. chaichana kl, pendleton c, zaidi h, olivi a, weingart jd, gallia gl, lim m, brem h, quiñones-hinojosa a, seizure control for patients undergoing meningioma surgery, world neurosurg 79:515-524, 2013. 2. chan ph, fishman ra, lee jl, candelise l, effects of exitatory neurotransmitter amino acids on edema induction in rat brain cortical slices, j neurochem 33:13091315, 1979. 3. chen wc, magill st, englot dj, baal jd, wagle s, rick jw, mcdermott mw, factors associated with preand postoperative seizures in 1033 patients undergoing supratentorial meningioma resection, neurosurgery 81:297-306, 2017. 4. chozick bs, reinert se, greenblatt sh, incidence of seizures after surgery for supratentorial meningiomas: a modern analysis, j neurosurg 84:382-386, 1996. 5. englot dj, magill st, han sj, chang ef, berger ms, mcdermott mw, seizures in supratentorial meningioma: a systematic review and meta-analysis, j neurosurg 124:1552-1561, 2016. 6. kemerdere r, yuksel o, kacira t, yeni n, ozkara c, tanriverdi t, uzan m, ozyurt e, low-grade temporal gliomas: surgical strategy and long-term seizure outcome, clin neurol neurosurg 126: 196-200, 2014. 7. pistolesi s, fontanini g, camacci t, de ieso k, boldrini l, lupi g, padolecchia r, pingitore r, parenti g, meningiomaassociated brain edema: the role of angiogenic factors and pial blood supply, j neurooncol 60:159-164, 2002. 8. ruda r, trevisan e, soffietti r, epilepsy and brain tumors, curr opin oncol 22:611-620, 2010. 9. seyedi jf, pedersen cb, poulsen fr, risk of seizures before and after neurosurgical treatment of intracranial meningioma, clin neurol neurosurg 165:60-66, 2018. 10. skardelly m, rother c, noell s, behling f, wuttke tv, schittenhelm j, bisdas s, meisner c, rona s, tabatabai g, roser f, tatagiba ms, risk factors of preoperative and early postoperative seizures in patients with meningioma. a retrospective single-center cohort study, world neurosurg 97:538-546, 2017. 11. tanriverdi t, kemerdere r, baran o, sayyahmelli s, ozlen f, isler c, uzan m, ozyurt e, long-term surgical and seizure outcomes of frontal low-grade gliomas, int j surg 33:60-64, 2016. 12. wirsching hg, morel c, gmür c, neidert mc, baumann cr, valavanis a, rushing ej, krayenbühl n, weller m, predicting outcome of epilepsy after meningioma resection, neurooncology 18:1002-1010, 2016. 13. xue h, sveinsson o, bartek j jr, förander p, skyrman s, kihlström l, shafiei r, mathiesen t, tomson t, long-term control and predictors of seizures in intracranial meningioma surgery: a population-based study, acta neurochir 160:589-596, 2018. 14. xue h, sveinsson o, tomson t, mathieson t, intracranial meningiomas and seizures: a review of the literature, acta neurochir 157:1541-1548, 2015. 15. zhang b, zhao g, yang hf, wang d, yu jl, huang hy, assessment of risk factors for early seizures following surgery for meningiomas using logistic regression analysis, j int med res 39:1728-1735, 2011. 16. zheng z, chen p, fu w, zhu j, zhang h, shi j, zhang j, early and late postoperative seizure outcome in 97 patients with supratentorial meningioma and preoperative seizure: a retrospective study, j neurooncol 114:101-109, 2013. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-006 management of facial paralysis following treatment of neurosurgical tumours costan v. v., ciofu m. l., sava f., boisteanu o., dabija m. romanian neurosurgery (2020) xxxiv (1): pp. 41-45 doi: 10.33962/roneuro-2020-006 www.journals.lapub.co.uk/index.php/roneurosurgery management of facial paralysis following treatment of neurosurgical tumours costan v.v.1, ciofu m.l.1, sava f.1, boisteanu o.2, dabija m.3 1 faculty of dental medicine, department of surgery, oral and maxillofacial surgery, “grigore t. popa” university of medicine and pharmacy, iasi, romania 2 faculty of dental medicine, department of surgery, anaesthesiology, “grigore t. popa” university of medicine and pharmacy, iasi, romania 3 faculty of medicine, department of surgery ii, neurosurgery, “grigore t. popa” university of medicine and pharmacy, iasi, romania abstract the purpose of this study is to present our experience on improving the quality of life of patients with facial paralysis due to an operated intracranial tumour, by performing minimally invasive static reanimation procedures. we reviewed the clinical information pertaining to neurosurgical patients with facial paralysis that underwent static reanimation. the study included 11 patients with complete facial nerve paralysis of all nerve branches, that reported different primary complaints upon presentation. the performed procedures consisted of gold plate insertion into the superior eyelid, inferior eyelid ectropion correction or suture suspension. the functional results were favourable in all cases and the resulting appearance was acceptable. the choice of the different techniques used is discussed. good outcomes are possible using static reanimation with an adequate adaptation of the techniques to the main patient complaint. introduction definitive facial nerve injury during neurosurgical procedures for benign or malignant tumors of the posterior and middle cranial fossae, cerebellopontine angle and lateral skull base, is often unavoidable, either due to existing preoperative tumor invasion or compression, or due to the proximity of the nerve, since the most important desiderate is avoiding tumor recurrence (1, 2). sequelae associated with facial nerve paralysis lead to important functional impairment as well as aesthetic changes comprising of a ptotic appearance of the involved hemiface with consequences regarding the emotional wellbeing of the patient and social integration. these factors cause a significant decline in the life quality of the patient (3, 4). static reanimation procedures aim to restore facial symmetry, improve deglutition, mastication and phonation disturbances, while also decreasing complications that endanger vision (5, 6). keywords facial nerve, paralysis, static reanimation, lagophthalmos, intracranial tumour corresponding author: ciofu m.l. faculty of dental medicine, department of surgery, oral and maxillofacial surgery, grigore t. popa” university of medicine and pharmacy, iasi, romania ciofu_ mihai@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 42 costan v.v.1, ciofu m.l.1, sava f. et al. the particularity of patients with operated tumors involving the neurosurgical territory is that the nerve is injured along its intracranial route, making functional rehabilitation by nerve graft interposition practically impossible (1). additionally, using the contralateral facial nerve branches carries the risk for bilateral injury. therefore, the minimally invasive static reanimation procedures are highly indicated and can provide an increase in the quality of life of those patients without the need to perform major surgery. in this manuscript we aim to present the benefits of different static facial reanimation procedures that we used in patients operated for neurosurgical tumors, in relation to the main complaints of the patients. material and methods we reviewed the medical charts of patients that presented for facial nerve paralysis following surgery for the removal of tumors in the neurosurgical territory. only patients that underwent static reanimation procedures were included in the study. the minimum follow-up period was 6 months. the general information, the main complaints of the patients, the time passed from the onset of facial paralysis, the type of static reanimation procedure and the postoperative outcomes were all documented. results in total, 11 patients were included in the study, consisting of 6 men and 5 women, aged 46 to 72 years old. all patients had complete nerve paralysis of all facial nerve branches, showing all known signs of nerve paralysis in different degrees, including facial asymmetry, lagophthalmos, lower eyelid ectropion, brow ptosis, ptosis of the oral commissure with sialorrhea, deglutition, mastication and phonation disturbances. still, the most bothersome complaint upon presentation was lagophthalmos in 6 patients, sialorrhea and difficulties eating in 3 patients, and facial asymmetry in 2 patients. the time interval between the onset of facial paralysis and performing the static reanimation procedure was minimum 3 months and maximum 1 year. surgery was performed under local anesthesia in all cases. 7 patients had multiple procedures, performed either at the same time or in separate sessions. one patient had gold plate insertion into the superior eyelid, lower eyelid ectropion correction and suture suspension of the affected hemiface. another patient had gold plate insertion into the superior eyelid and inferior eyelid ectropion correction. five patients had gold plate insertion into the superior eyelid and suture suspension. two patients had only gold plate insertion into the superior eyelid and another two patients had only suture suspension. for the patients in which multiple staged procedures were performed, it was considered that the functional results could be improved after the initial facial reanimation surgery, therefore scheduling for another procedure to complete the previous results. after the completion of all procedures, the functional outcomes were optimal, and the aesthetic results were acceptable. facial asymmetry was ameliorated for all patients that underwent facial suture suspension in all facial segments, while only the upper face was improved in the three patients undergoing only periorbital surgery. lagophthalmos was improved in all patients with a decrease in the subjective complaints. sialorrhea and eating difficulties were improved in all patients undergoing suture suspension. there were no infectious complications or hematoma formation postoperatively. minor ecchymosis and postoperative edema were frequent encounters. the favorable outcomes are presented through images of a facial nerve paralysis patient that underwent static reanimation by simultaneous gold plate insertion into the superior eyelid and suture suspension (fig. 1-5). figure 1. preoperative aspect of the patient during eye closure, demonstrating left lagophthalmos and facial asymmetry. figure 2. preoperative aspect of the patient during cheek inflation, showing decreased tonus in the left cheek. 43 management of facial paralysis following treatment of neurosurgical tumours figure 3. immediate postoperative aspect following insertion of a gold plate into the left superior eyelid and suture suspension of the left hemiface. figure 4. post-operative aspect 10 days after surgery during eye closure, demonstrating complete left eye closure and ameliorated facial asymmetry with lifting of the left oral commissure, definition of the nasogenian sulcus and lifting of the cheek with improved position of the inferior eyelid. figure 5. postoperative aspect 10 days after surgery showing increased tonus of the left cheek and lifted position of the left oral commissure during cheek inflation. discussions dynamic facial reanimation involves complex, time consuming procedures performed under general anesthesia, that are not without risks. in patients operated for intracranial tumors in which the injured proximal facial nerve cannot be used for primary reconstruction using interposition nerve grafts, a dynamic reanimation may necessitate the scarification of another cranial nerve, including the trigeminal, accessory, hypoglossal or contralateral facial nerve (1, 2). the indication for such an invasive procedure should carefully consider the general condition of the patient, the existing associated disorders as well as the long-term prognosis. for older patients with multiple comorbidities, oncologic patients, for patients reluctant to undergo another major procedure or for patients with long-standing facial paralysis, static reanimation offers good outcomes with minimal risks, since it involves local anesthesia and short duration of surgery (7, 8). the goal of static reanimation procedures is to improve the functional and esthetic disturbances associated with facial nerve paralysis. multiple types of procedures exist, targeting different sequelae of facial paralysis. often, several procedures are necessary in order to address all issues and achieve best outcomes (9). the good results achieved in our study were due to the careful tailoring of the procedures performed, considering the most bothersome complaint reported by each patient. by addressing the main expressed issue, all patients perceived an improvement after the static reanimation intervention. the periorbital changes resulting from incomplete eyelid closure and inferior eyelid ectropion are frequently the main focus of reanimation surgery due to the distressing complaints of patients including foreign body sensation and pain, but also due to the serious complications regarding vision that can eventually develop (10, 11). in our study, improving eyelid closure was the main goal in the patients primarily having this complaint. in this regard, we achieved optimal outcomes by inserting a gold plate into the superior eyelid, for added weight. plate positioning was important in order to achieve maximal eyelid closure and avoid plate exposure over time, similarly to the reports of other authors (12). other existing procedures that can improve lagophthalmos are levator lengthening and palpebral spring insertion (13). however, superior eyelid loading is the preferred method for many surgeons (14, 15). lagophthalmos is known as the condition that can cause the most functional damage in facial nerve paralysis patients, due to the increased corneal exposure and drying with subsequent ulcerations and infections that can eventually cause blindness or even the loss of the affected eye (13, 16). it is frequently the first facial nerve sequelae that is addressed during reanimation procedures. in our study it was also the most prevalent complaint, but in some cases, issues related to difficulties during eating and sialorrhea were reported as more distressing, mainly due to the struggling to eat adequately, but also due to social concerns. eating difficulties for facial paralysis patients are mostly caused by the food remaining trapped during mastication in the inferior vestibule that resembles a bag, due to the lack of tonus of the cheek. the associated sialorrhea only worsens the symptoms 44 costan v.v.1, ciofu m.l.1, sava f. et al. due to mucosa dryness, difficulty in forming the food bolus, but also causing frustration during social encounters. suspension of the oral commissure and genian region using usual sutures or barbed threads, lifts the tissues, preventing saliva leakage, but also improves the tonus of the cheek, therefore decreasing food retaining (17, 18). in addition, lagophthalmos is also improved, since the heavy genian region that pulls down on the inferior eyelid, aggravating ectropion and lagophthalmos, is repositioned superiorly, rendering support to the inferior eyelid (6, 18). in our study, in the patients with this main complaint, suture suspension was first performed, since it allowed the initial alleviation of the most distressing symptoms. ectropion correction was mainly indicated in addition to gold plate insertion, for the patients exhibiting significant laxity and length of the inferior eyelid. for the patients that were most bothered by the facial asymmetry, suture suspension was also the best initial choice of static reanimation, since it allowed addressing the upper, middle and lower face simultaneously, and therefore ensured better cosmetic results. good outcomes regarding the restoration of facial symmetry using suspension techniques have also been reported by other studies (19, 20). refinements of particular areas can always be made using barbed sutures, due to the minimally invasive character of the procedure, even when plain suture suspension was initially performed (18). conclusion static reanimation procedures render favorable results when the type of intervention is tailored to fit the most pressing patient complaint. particularly for neurosurgical patients with intracranial injury of the facial nerve, these procedures ensure a noninvasive modality of increasing the quality of life of the patients with minimal complications. references 1. rozen sm, harrison bl, isaacson b, kutz jw jr, roland ps, blau pa, barnett sl, mickey be. intracranial facial nerve grafting in the setting of skull base tumors: global and regional facial function analysis and possible implications for facial reanimation surgery. plast reconstr surg. 2016; 137(1):267-78. 2. panossian a. facial paralysis reconstruction in children and adolescents with central nervous system tumors. j pediatr rehabil med. 2014; 7(4):295-305. 3. nellis jc, ishii m, byrne pj, boahene kdo, dey jk, ishii le. association among facial paralysis, depression, and quality of life in facial plastic surgery patients. jama facial plast surg. 2017; 19(3):190-196. 4. ishii le, nellis jc, boahene kd, byrne p, ishii m. the importance and psychology of facial expression. otolaryngol clin north am. 2018; 51(6):1011-1017. 5. robinson mw, baiungo j. facial rehabilitation: evaluation and treatment strategies for the patient with facial palsy. otolaryngol clin north am. 2018; 51(6):1151-1167. 6. costan vv. management of extended parotid tumors. editura springer, 2016; isbn 978-3-319-26543-8. 7. white h, rosenthal e. static and dynamic repairs of facial nerve injuries. oral maxillofac surg clin north am. 2013; 25(2):303-12. 8. kim l, byrne pj. controversies in contemporary facial reanimation. facial plast surg clin north am. 2016; 24(3):275-97. 9. lafer mp, o tm. management of long-standing flaccid facial palsy: static approaches to the brow, midface, and lower lip. otolaryngol clin north am. 2018; 51(6):11411150. 10. joseph ss, joseph aw, douglas rs, massry gg. periocular reconstruction in patients with facial paralysis. otolaryngol clin north am. 2016; 49(2):475-87. 11. homer n, fay a. management of long-standing flaccid facial palsy: periocular considerations. otolaryngol clin north am. 2018; 51(6):1107-1118. 12. oh ts, min k, song sy, choi jw, koh ks. upper eyelid platinum weight placement for the treatment of paralytic lagophthalmos: a new plane between the inner septum and the levator aponeurosis. arch plast surg. 2018; 45(3):222-228. 13. leckenby ji, ghali s, butler dp, grobbelaar ao. reanimation of the brow and eye in facial paralysis: review of the literature and personal algorithmic approach. j plast reconstr aesthet surg. 2015; 68(5):60314. 14. rofagha s, seiff sr. long-term results for the use of gold eyelid load weights in the management of facial paralysis. plast reconstr surg 2010;125(1):142e9. 15. rozen s, lehrman c. upper eyelid postseptal weight placement for treatment of paralytic lagophthalmos. plast reconstr surg 2013;131(6):1253e65. 16. costan vv, doscas a, ciofu ml, boişteanu o, popescu e. on the management of paralytic lagophthalmos. international journal of medical dentistry 2018, 22(4):433-436. 17. biglioli f. facial reanimations: part ii--long-standing paralyses. br j oral maxillofac surg. 2015; 53(10):907-12. 18. costan vv, popescu e, sulea d, stratulat is. a new indication for barbed threads: static reanimation of the paralyzed face. j oral maxillofac surg. 2018; 76(3):639645. 19. langille m, singh p. static facial slings: approaches to 45 management of facial paralysis following treatment of neurosurgical tumours rehabilitation of the paralyzed face. facial plast surg clin north am. 2016; 24(1):29-35. 20. leach g, kurnik n, joganic j, joganic e. multivectored superficial muscular aponeurotic system suspension for facial paralysis. j craniofac surg. 2017; 28(4):882-887. doi: 10.33962/roneuro-2022-054 surgical outcome of endoscopic third ventriculostomy compared to ventriculoperitoneal shunt in non communicating or obstructive hydrocephalus: a study from tertiary care centre of a low-middle-income country bushra tariq ali, ahtesham khizar, pradhumna kumar yadav, hammad mehtab, madeha amjad, umer farooq raina romanian neurosurgery (2022) xxxvi (3): pp. 315-324 doi: 10.33962/roneuro-2022-054 www.journals.lapub.co.uk/index.php/roneurosurgery surgical outcome of endoscopic third ventriculostomy compared to ventriculoperitoneal shunt in noncommunicating or obstructive hydrocephalus: a study from tertiary care centre of a low-middle-income country bushra tariq ali1,2, ahtesham khizar1, pradhumna kumar yadav1,2, hammad mehtab1, madeha amjad1,2, umer farooq raina3 1 pakistan institute of medical sciences, islamabad (pims), pakistan 2 shaheed zulfiqar ali bhutto medical university (szabmu), islamabad, pakistan 3 district headquarters (dhq) teaching hospital, dera ismail khan, pakistan abstract objectives: to assess and compare the effectiveness of endoscopic third ventriculostomy over ventriculoperitoneal shunt in terms of rate of revision in noncommunicating or obstructive hydrocephalus at a tertiary care centre in a lowmiddle-income country. materials and methods: a prospective cohort study was conducted from january 2019 to december 2020 at pims/szabmu, islamabad, pakistan. a total of 104 patients of either gender under the age of 12 years diagnosed with noncommunicating/obstructive hydrocephalus were enrolled in this study. they were allocated into two equal groups of 52 by the lottery method. one group underwent ventriculoperitoneal shunt (group i) and another group underwent endoscopic third ventriculostomy (group ii). they received routine treatment of one-week postoperative prophylactic broad-spectrum antibiotics. they were discharged on the third postoperative day and were instructed for follow-up on the 4th, 12th and 24th postoperative week. clinically, successful outcomes were defined as no event occurring during or after the surgery that could result in reoperation or any significant postoperative complication. results: there were 55.8% males and 44.2% females in group i while 50.0% males and 50.0% females were in group ii. the mean age of group i was 0.89 years ± 1.5 sd while 2.3 years ± 2.8 sd in group ii. during the procedure, the overall complication rate was 0% in group i and 4.1% in group ii. in the 4th postoperative week, the overall complication rate was 5.9% in group i and 4.1% in group ii. at the 12th postoperative keywords hydrocephalus, endoscopic third ventriculostomy, ventriculoperitoneal shunt, low-middle-income country corresponding author: ahtesham khizar pakistan institute of medical sciences, islamabad, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 316 bushra tariq ali, ahtesham khizar, pradhumna kumar yadav et al. week, the overall complication rate was 17.6% in group i and 2.0% in group ii. on the 24th postoperative week, the overall complication rate was 9.8% in group i and none in group ii. during the procedure, reoperation was needed in 0% in group i and 4.1% in group ii. in the 4th postoperative week, reoperation was needed in 5.9% of patients in group i and 2.0% in group ii. in the 12th postoperative week, reoperation was needed in 17.6% of patients in group i and 2.0% in group ii. at the 24th postoperative week, reoperation was needed in 9.8% of patients in group i and none in group ii. the overall mortality rate was 5.9% in group i and 4.1% in group ii. conclusion: endoscopic third ventriculostomy procedure was found to be better than the ventriculoperitoneal shunt in terms of reoperation and complication rate at the 4th, 12th and 24th week after the procedure in infants and children with noncommunicating/obstructive hydrocephalus. introduction hydrocephalus is an abnormal ventricular dilatation secondary to excessive buildup of cerebrospinal fluid (csf) in the cranial cavity. normal csf production is mostly by choroid plexus and to a lesser extent by interstitial space and ependymal lining of the ventricles and the nerve sleeve dura. it is absorbed into the venous circulation by arachnoid granulations.1 causes of hydrocephalus are congenital or acquired. congenital causes include neural tube defects and those causing aqueductal stenosis. post-traumatic, post-hemorrhagic and posterior fossa tumors (fig. 1) are some of the acquired causes.1,2 figure 1. a: preoperative ct brain plain of an 11-year-old boy with hydrocephalus secondary to posterior fossa tumor. b: postoperative ct brain plain following etv. there are four types of hydrocephalus including communicating, non-communicating, ex vacuo and normal pressure hydrocephalus. impedance of csf flow after it exits the ventricles causes communicating hydrocephalus. obstruction of csf flow within the ventricular chain causes noncommunicating also called obstructive hydrocephalus. hydrocephalus ex vacuo occurs after stroke or traumatic brain injury. normal pressure hydrocephalus is a chronic type usually present in adults and is mostly idiopathic.1 usual presentations of hydrocephalus in children include progressively enlarging head size, drowsiness, vomiting, seizures and sunsetting of eyes. in adults, it may present with headache, visual impairment, poor balance, urinary incontinence, personality changes or mental impairments. diagnosis is by clinical examination and neuroimaging techniques like; ultrasonography, computed tomography (ct), magnetic resonance imaging (mri) and intracranial pressure monitoring techniques.1,3 various treatments for this condition include surgical and non-surgical management. conservative measures work with variable success and often these measures serve only to temporize hydrocephalus until shunt placement. approaches include head wrapping, pharmacological treatment and intermittent csf removal.4 surgical management includes non-shunting and shunting procedures. non-shunting procedures include endoscopic third ventriculostomy (etv), resection of obstructing lesions when possible and choroid plexus coagulation. shunt involves placement of a ventricular catheter into the cerebral ventricles in order to bypass flow obstruction/malfunctioning arachnoid granulations and drain the excess fluid into other body cavities where it is absorbed. most shunts drain fluid into peritoneal cavity therefore called ventriculoperitoneal shunts.4,5 shunts generally work well but they have inherent complications such as disconnection, blockade, infection, overdrainage or underdrainage. all these complications lead to multiple shunt revisions in a patient’s lifetime. it is of particular importance that shunt systems are generally very expensive and cost about all of a month’s income of a family in a developing country like ours.6-10 alternative treatment for obstructive hydrocephalus is etv. surgeon makes a burr hole just anterior to the coronal suture about three centimeters lateral to midline and inserts an endoscope through it inside the ventricles. endoscope assisted opening is made in the floor of third ventricle, which allows the csf to flow directly to basal cisterns thereby shortcutting any obstruction as in aqueductal stenosis.6-10,11,12 317 surgical outcome of endoscopic third ventriculostomy complications of etv include hemorrhage, injury to neural structures and late sudden deterioration. infection, hematoma and csf leak may present in the postoperative period. failure of etv may occur due to occlusion of ventriculostomy that may need revision.12,13 a huge advantage of etv over implantation of shunt is the absence of foreign body. this technique is cost effective but if made with correct surgical expertise it does not need revisions and overall patient morbidity is lower than that caused by multiple shunt issues. multiple studies have shown that etv treated patients have better neurological outcome.2,3,6-13 in this study, we compared the surgical outcome of etv to vp shunt in terms of rate of reoperation and the complications of primary procedure. materials and methods study design: descriptive observational study setting: department of neurosurgery, pakistan institute of medical sciences (pims)/shaheed zulfiqar ali bhutto medical university ( szabmu), islamabad, pakistan. duration of study: 2 years (january, 2019 to december, 2020). sample size: a sample size of 104 patients was included in this study according to who sample size calculator, using the following parameters: ● level of significance: 5% ● power of test: 80% ● anticipated population proportion of unfavorable outcome with etv, p1: 4% ● anticipated population proportion of unfavorable outcome with vp shunt, p2: 18% sampling technique: non-probability based consecutive sampling. sample selection: a. inclusion criteria: ● all the patients of any gender under the age of 12 diagnosed with non-communicating/obstructive hydrocephalus by radiology (ct/mri), clinical correlation and advised for surgical treatment were included. b. exclusion criteria: ● patients already treated (vp shunt or etv) ● active intracranial infection ● patients with communicating hydrocephalus data collection procedure: permission from ethical review board was taken for this study. after obtaining informed consent, patients of any gender under the age of 12 years diagnosed with noncommunicating/obstructive hydrocephalus on ct/mri brain, with clinical correlation and advised for surgical treatment were included in this study. the sample size for this study was 104 patients. informed consent for surgery and inclusion in the study was taken from the parents or their closest available relative. patients were randomly allocated into two equal groups of 52 by lottery method. group i patients underwent ventriculoperitoneal shunt while group ii patients underwent endoscopic third ventriculostomy. all included patients had their history taken and relevant physical examination done preoperatively. they also had routine baseline investigations done preoperatively including chest xray, full blood counts, liver and renal function tests, serum electrolytes, coagulation profiles and hepatitis b and c screening. patients received routine treatment of one-week postoperative prophylactic broad-spectrum antibiotics to avoid infection and analgesia according to who pain ladder for pain control. they were discharged on the third postoperative day or later depending on their clinical condition and recovery. trainee residents recorded data on proforma as per-op, at 4th, 12th and 24th postoperative week of follow-up. ct/mri brain was done preoperatively for diagnosis. follow-up ct/mri brain scans were done as required. clinically, successful outcomes were defined as no event occurring during or after the surgery that would result in an alternate surgical procedure or significant postoperative complication. all complications related to the procedures were analyzed. the time to complication was noted as well as the type of complication (infection, mechanical failure of the shunt or non-functioning etv). the diagnosis of a non-functioning etv/shunt was made according to clinical criteria in patients with signs of raised intracranial pressure or growing head circumference and increase in ventricular size on imaging (ct/mri brain). complications of surgical 318 bushra tariq ali, ahtesham khizar, pradhumna kumar yadav et al. treatment and need for re-operations were recorded during the study period. data analysis procedure: data was analyzed using spss version 23. mean and standard deviation was calculated for quantitative variables like age. frequency and percentages were presented for qualitative variables like gender, presenting complaints, need for reoperation and complications. chi-square test was applied to compare outcome and complications between both the groups. p-value < 0.05 was considered significant. results demography of the selected population: there were 55.8% (n=29/52) males and 44.2% (n=23/52) females in group i while 50.0% (n=26/52) males and 50.0% (n=26/52) females in group ii (table 1). age distribution was also comparable in both groups. mean age of group i patients was 0.89 years ± 1.5 sd while it was 2.3 years ± 2.8 sd in group ii patients (table 2). table 1. gender distribution in both the study groups gender groups total vp shunt etv males 29 (55.8%) 26 (50%) 55 (52.9%) females 23 (44.2%) 26 (50%) 49 (47.1%) total 52 (100%) 52 (100%) 104 (100) table 2. age distribution in both the study groups groups n mean age (years) ± sd (years) vp shunt 52 0.89 1.5 etv 52 2.3 2.8 excluded patients: we enrolled 104 patients and a total of four patients were excluded from the study (3 from etv group and 1 from vp shunt group). two patients from etv and one patient from vp shunt group were excluded as lost to follow up. one patient from the etv group was excluded as procedure aborted due to opaque 3rd ventricular floor. figure 2. a: surgical site swelling in a child with shunt blockade. b: ct brain plain of the same child with shunt blockade. outcome analysis of treatment in both groups: complications: during the procedure, overall complication rate was 0% (n=0/51) in group i and 4.1% (n=2/49) in group ii (p=0.145, table 3). at 4th postoperative week, the overall complication rate was 5.9% (n=3/51) in group i and 4.1% (n=2/49) in group ii (p=0.680, table 3). at 12th postoperative week, overall complication rate was 17.6% (n=9/51) in group i and 2.0% (n=1/49) in group ii (p=0.009, table 3). at 24th postoperative week, overall complication rate was 9.8% (n=5/51) in group i and none in group ii (p=0.025, table 3). overall complication rate was higher in patients who underwent vp shunt procedure as compared to those who underwent endoscopic third ventriculostomy at 4th, 12th and 24th week after the procedure. the difference was not significant at 4th week (p>0.05), however, it was significant at 12th (p=0.009) and at 24th postoperative week (p=0.025). table 3. complications rate per-op, at week 4, 12 and 24 in both study groups complications groups total p-value chisquare vp shunt etv perop present 0 (0%) 2 (4.1%) 2 (2%) 0.145 absent 51 (100%) 47 (95.9%) 98 (98%) week 4 present 3 (5.9%) 2 (4.1%) 5 (5%) 0.680 absent 48 (94.1%) 47 (95.9%) 95 (95%) present 9 (17.6%) 1 (2%) 10 (10%) 0.009 319 surgical outcome of endoscopic third ventriculostomy week 12 absent 42 (82.4%) 48 (98%) 90 (90%) week 24 present 5 (9.8%) 0 (0%) 5 (5%) 0.025 absent 46 (90.2%) 49 (100%) 95 (95%) table 4. reoperation rate per-op, at week 4, 12 and 24 in both study groups reoperation groups total p-value chisquare vp shunt etv perop present 0 (0%) 2 (4.1%) 2 (2%) 0.145 absent 51 (100%) 47 (95.9 %) 98 (98%) week 4 present 3 (5.9%) 1 (2%) 4 (4%) 0.327 absent 48 (94.1%) 48 (98%) 96 (96%) week 12 present 9 (17.6%) 1 (2%) 10 (10%) 0.009 absent 42 (82.4) 48 (98%) 90 (90%) week 24 present 5 (9.8%) 0 (0%) 5 (5%) 0.025 absent 46 (90.2%) 49 (100%) 95 (95%) reoperation: during the procedure, reoperation was needed in 0% (n=0/51) patients in group i and 4.1% (n=2/49) in group ii (p=0.145, table 4). at 4th postoperative week, reoperation was needed in 5.9% (n=3/51) patients in group i and 2.0% (n=1/49) in group ii (p=0.327, table 4). at 12th postoperative week, reoperation was needed in 17.6% (n=9/51) patients in group i and 2.0% (n=1/49) in group ii (p=0.009, table 4). at 24th postoperative week, reoperation was needed in 9.8% (n=5/51) patients in group i and none in group ii (p=0.025, table 4). reoperation rate was higher in patients who underwent vp shunt procedure as compared to those who underwent endoscopic third ventriculostomy at 4th, 12th and 24th week after the procedure. the difference was not significant at 4th week (p>0.05), however, it was significant at 12th (p=0.009) and at 24th postoperative week (p=0.025). figure 3. ventriculoperitoneal shunt hardware exposure. details of complications and reoperations: details of complications and reoperations are mentioned in table 5. ● hardware exposure (fig. 3) was the most frequent complication noted in vp shunt group followed by shunt blockage/breakage/malposition (fig. 2), meningitis and intestinal obstruction. vp shunt revision was the most frequent reoperation procedure followed by shunt removal and external ventricular drain (evd) placement (table 5). ● in the etv group, intraventricular hemorrhage was the most frequent complication followed by csf leak and subdural hygroma. evd placement was the most frequent reoperation procedure (table 5). table 5. complications and reoperation details per-op, at week 4, 12 and 24 in both study groups time complications and reoperation details vp shunt etv perop intraventricular hemorrhage 0 2 evd placement week 4 increased head size 1 shunt revision 0 shunt malposition 1 shunt revision 0 320 bushra tariq ali, ahtesham khizar, pradhumna kumar yadav et al. csf leak 1 shunt distal end revision 1 conservative management csf hygroma 0 1 b/l subdural shunt placement week 12 csf leak 0 1 vp shunt hardware exposure 4 shunt removal 0 meningitis 3 shunt removal + evd 0 intestinal obstruction 2 distal end of shunt exteriorized 0 week 24 shunt blockade 3 shunt revision 0 shunt breakage 1 shunt revision 0 meningitis 1 shunt removal + evd 0 mortality: overall mortality rate was 5.9% (n=3/51) patients in group i and 4.1% (n=2/49) patients in group ii. the difference was not statistically significant (p=0.680, table 6). in the vp shunt group, two patients died due to meningitis and one patient died of a burst abdomen due to intestinal obstruction. in the etv group, one patient died due to intraventricular hemorrhage and one due to subdural hygroma. table 6. overall mortality rate in both the study groups mortality groups total p-value chisquare vp shunt etv present 3 (5.9%) 2 (4.1%) 5 (5%) 0.680 absent 48 (94.1%) 47 (95.9%) 95 (95%) total 51(100%) 49 (100%) 100 (100%) discussion csf shunts have long been the standard treatment for hydrocephalus in children.14,15,16 etv is an alternative approach that has several advantages over csf shunting in that it is relatively low-cost, durable, and potentially avoids the long-term complications that frequently occur with vp shunts.17 in the present study, we aimed to compare both the techniques in terms of rate of reoperation and the complications of primary procedure. in our study, the overall complication rate was higher in patients who underwent vp shunt procedure as compared to those who underwent endoscopic third ventriculostomy. hardware exposure was the most frequent complication noted in the vp shunt group followed by shunt blockage/breakage/malposition, meningitis and intestinal obstruction. delayed presentation of hydrocephalus in low-middleincome countries like pakistan is a reason that patients present with very large head size and thin scalp, which may be the cause of hardware exposure. we suggest that paediatric shunts with small reservoirs should be used in such patients. hardware exposure leads to csf leak from cranial end. if present, csf leak can become a drastic complication. increased operative time or contact of shunt hardware with skin of patient is the most common cause of shunt infection.18,19 in etv group, intraventricular hemorrhage was the most frequent complication followed by csf leak and subdural hygroma. intraoperative hemorrhage is the most dreadful and major complication of etv. although severe hemorrhages are rare, the neurosurgeon needs to be aware of them and has to establish strategies for their management. most hemorrhages can be stopped by constant irrigation and coagulation. in the other rare cases, the dry field technique is a safe and reliable technique and can be easily incorporated into endoscopic surgery. a 2o basilar artery hemorrhage will inevitably lead to evd placement per-operatively and later death. and to avoid it beforehand mri brain sagittal cuts are done to know the thickness of third ventricular floor and relation of basilar artery.20 patients having thin cortical mantle who underwent etv had poor outcome (chances of subdural hygroma formation). kamel et al proposed that the prolonged ventricular dilatation leads to the compression of the thin cortical mantle, causing an alteration in the cerebral viscoelastic properties. thus, there would not be adequate spacing in the cortical mantle following the etv, favoring the collection formation in the increased subdural space.21,22 after piercing floor of 321 surgical outcome of endoscopic third ventriculostomy third ventricle, membrane of liliequist needs to be cut effectively in order to establish a pathway between ventricle and basal cisterns. it is known that its fenestration in microsurgeries for ruptured cerebral aneurysm clipping reduces the risk of the occurrence of postoperative hydrocephalus, however, it increases the formation of subdural collections. cartimill and vloeberghs attributed the occurrence of spinal subdural hematoma in a 9-yearold child to the very same mechanism.23,24 our findings are comparable with other similar studies cited in the literature. lu l conducted a metaanalysis to compare etv and vps in patients with obstructive hydrocephalus. they included 4 trials involving 250 patients. their pooled results showed that etv was associated with lower incidence of postoperative infection (risk ratio [rr] 0.09, 95% confidence interval [ci]: 0.02-0.32, p=0.0002); postoperative hematoma (rr 0.26, 95% ci: 0.08-0.88, p=0.03); and blockage (rr 0.28, 95% ci: 0.13-0.60, p=0.001) compared with vps.25 jiang l et al in their meta-analysis demonstrated that etv was associated with lower incidence of infection (rr: 0.20; 95% ci: 0.06-0.69; p =0 .010). they further highlighted that patients who received etv had shorter duration of surgery (smd: -1.71; 95% ci: -3.16 to -0.27; p = 0.020) and hospital stay (smd: -0.91; 95% ci: -1.45 to -0.38; p = 0.001).23 in our study, we did not take into account duration of procedure and hospital stay as our outcome variables. complications of etv were described in a 2012 systematic review of 24 case series reporting outcomes of >2500 etv procedures in children and adults with hydrocephalus due to a variety of etiologies. the overall complication rate was 8.8 percent, including intraoperative hemorrhage (3.9%), infection (1.8%), csf leak (1.7%), and other surgical complications.26 the analysis was on etv only and no comparison with vp shunting was performed. jiang l et al compared etv and vp shunting for patients with non-communicating hydrocephalus in 10 observational studies. their pooled analysis revealed that etv was associated with lower incidence of major complications when compared with vps (rr: 0.31; 95% ci: 0.17-0.56; p < .001). etv was also associated with lower incidence of infection (rr: 0.20; 95% ci: 0.06-0.69; p = 0.010).27 our results further showed that reoperation rate was higher in patients who underwent vp shunt as compared to those who underwent etv. during operation (0% vs 3.8%, p=0.145), at 4th week (5.9% vs 2.0%, p=0.327), 12th week (17.6% vs 2.0%; p=0.009) and 24th week (9.8% vs 0%, p=0.025). the difference was statistically significant at 12th and 24th postoperative week. vp shunt revision was the most frequent reoperation in vp shunt group followed by shunt removal and evd placement. evd placement was the most frequent reoperation procedure in the etv group. kulkarni av et al compared etv and shunt in infants (<24 months old) with symptomatic triventricular hydrocephalus from aqueductal stenosis. they reported that actual success rates for etv vs shunt at 3, 6, and 12 months were: 68 vs 95 %, 66 vs 88 %, and 66 vs 83.6 the trend appeared in both studies is comparable with higher success rate for etv at 6 months (24 weeks). we, however, did not follow our patients till 12 months. in our opinion, etv success is almost always dependent on surgeon expertise with endoscope. we believe for etv procedure to be successful, the learning curve is steep and good outcome of etv depends on surgical expertise. casual attitude of surgeons towards placement of shunt is a factor which leads to increased rates of infection and causes shunt failure.28 some authors advocate that the etv success score can be used to estimate the likelihood of early success. the score was developed and validated using a dataset of 618 consecutive etv procedures performed at 12 international institutions.8 older age at the time of the procedure (i.e, >1 year old) is the strongest predictor of success; other important predictors include non-infectious hydrocephalus etiology (e.g, aqueductal stenosis, tectal tumor, myelomeningocele, intraventricular hemorrhage), and lack of previous shunt.29 in one study, investigators compared outcomes of etv and shunting using etv scoring in a cohort of children with newly diagnosed hydrocephalus.30 among patients with high predicted etv success (i.e, etv success score ≥80), cumulative reoperation-free survival at 36 months was greater with etv compared with shunting (72% vs 54%). however, among patients with moderate and low etv success scores, outcomes were similar with the two procedures. for patients with moderate etv success scores (i.e, 50 to 70), reoperation-free survival at 36 months was approximately 50% in both groups; and for those with low etv success scores (i.e, ≤40), reoperation-free survival at 36 months was 322 bushra tariq ali, ahtesham khizar, pradhumna kumar yadav et al. approximately 38% in both groups. in the present study, we did not use such scores. other studies compared etv and vp shunting in other causes of hydrocephalus. aranha a et al compared etv and vp shunt in the treatment of hydrocephalus in tuberculous meningitis and reported the success rate for etv 65.4% compared to the 61.54% success rate in vp shunt group.31 gonda dd et al treated patients with hydrocephalus related to cerebral metastases by either etv or vp shunting and analyzed the clinical outcomes. the overall efficacy of symptomatic palliation was comparable in the etv and vps patients (etv=69%, vps=75%). the overall complication rate for the two groups was comparable (etv=12.6%, vps=19.4%), although the spectrum of complications differed.32 the results of both studies are comparable to our study results. there are some ongoing clinical trials as well, which are evaluating outcomes with etv compared with shunting in children with communicating33 and noncommunicating hydrocephalus7. long term followup results are awaited. in summary, both etv and vp shunting are practical treatment options for noncommunicating/obstructive hydrocephalus. criteria for selection of patients for etv versus shunting are not standardized and practice varies considerably. the 2014 evidence-based guidelines of aans and the cns concluded that outcomes of the two procedures are generally equivalent and they did not advocate for one approach over the other. etv is generally not performed for treatment of obstructive hydrocephalus in infants <3 months old due to low success rates in this age group. for children in whom etv is unsuccessful, a shunting procedure is generally performed, because repeating the etv acutely is not likely to be successful. present study results and several other studies cited in the literature showed that etv when performed in a carefully selected group of patients is more effective and associated with lesser complication rates. etv technique is cost effective and if made with correct surgical expertise it does not need revisions and overall patient morbidity is lower than that caused by multiple shunt issues. our study design is the major strength of the study as we used stringent inclusion and exclusion criteria, though this study has some limitations as well. firstly, the sample was relatively smaller, yet sufficient enough for interpretation. secondly, our duration of follow up was relatively shorter and we did not follow the patients beyond 6 months, while studies in the literature showed longer duration of follow up even up to 5 years after the procedure. thirdly, we didn't do etv success scoring, which is an established score predicting the success of etv and finally we did not take into account the duration of procedure, length of hospital stay and neurological outcome as our outcome measures. conclusion endoscopic third ventriculostomy was found to be better than ventriculoperitoneal shunt in terms of reoperation and complication rate at 4th, 12th and 24th week after the procedure in infants and children with non-communicating or obstructive hydrocephalus. we suggest future studies taking larger sample sizes, with longer duration of follow up and taking into account other outcome variables like duration of procedure, length of hospital stay and neurological outcome. list of abbreviations csf: cerebrospinal fluid ct: computed tomography evd: external ventricular drain etv: endoscopic third ventriculostomy mri: magnetic resonance imaging vp: ventriculoperitoneal vps: ventriculoperitoneal shunt sd: standard deviation rr: risk ratio ci: conference interval smd: standardized mean difference p: p-value references 1. rekate hl. the definition and classification of hydrocephalus: a personal recommendation to stimulate debate. cerebrospinal fluid research. 2008 dec;5(1):1-7. 2. warf bc. hydrocephalus associated with neural tube defects: characteristics, management, and outcome in sub-saharan africa. child's nervous system. 2011 oct;27(10):1589-94. 3. sufianov aa, sufianova gz, iakimov ia. endoscopic third ventriculostomy in patients younger than 2 years: outcome analysis of 41 hydrocephalus cases. journal of neurosurgery: pediatrics. 2010 apr 1;5(4):392-401. 4. lifshutz ji, johnson wd. history of hydrocephalus and its treatments. neurosurgical focus. 2001 aug 1;11(2):1-5. 5. idowu oe, falope lo, idowu at. outcome of endoscopic third ventriculostomy and chhabra shunt system in 323 surgical outcome of endoscopic third ventriculostomy noncommunicating non-tumor childhood hydrocephalus. journal of pediatric neurosciences. 2009 jul;4(2):66. 6. kulkarni av, sgouros s, constantini s. international infant hydrocephalus study: initial results of a prospective, multicenter comparison of endoscopic third ventriculostomy (etv) and shunt for infant hydrocephalus. child's nervous system. 2016 jun;32(6):1039-48. 7. kulkarni av, schiff sj, mbabazi-kabachelor e, mugamba j, ssenyonga p, donnelly r, levenbach j, monga v, peterson m, macdonald m, cherukuri v. endoscopic treatment versus shunting for infant hydrocephalus in uganda. new england journal of medicine. 2017 dec 21;377(25):2456-64. 8. kulkarni av, drake jm, kestle jr, mallucci cl, sgouros s, constantini s. predicting who will benefit from endoscopic third ventriculostomy compared with shunt insertion in childhood hydrocephalus using the etv success score. journal of neurosurgery: pediatrics. 2010 oct 1;6(4):310-5. 9. kulkarni av, drake jm, kestle jr, mallucci cl, sgouros s, constantini s. endoscopic third ventriculostomy vs cerebrospinal fluid shunt in the treatment of hydrocephalus in children: a propensity score-adjusted analysis. neurosurgery. 2010 sep 1;67(3):588-93. 10. limbrick dd, baird lc, klimo p, riva-cambrin j, flannery am. pediatric hydrocephalus: systematic literature review and evidence-based guidelines. part 4: cerebrospinal fluid shunt or endoscopic third ventriculostomy for the treatment of hydrocephalus in children. journal of neurosurgery: pediatrics. 2014 nov 1;14(supplement_1):30-4. 11. gorayeb rp, cavalheiro s, zymberg st. endoscopic third ventriculostomy in children younger than 1 year of age. journal of neurosurgery: pediatrics. 2004 may 1;100(5):427-9. 12. uche eo, okorie c, iloabachie i, amuta ds, uche nj. endoscopic third ventriculostomy (etv) and ventriculoperitoneal shunt (vps) in non-communicating hydrocephalus (nch): comparison of outcome profiles in nigerian children. child's nervous system. 2018 sep;34(9):1683-9. 13. gangemi m, mascari c, maiuri f, godano u, donati p, longatti pl. long-term outcome of endoscopic third ventriculostomy in obstructive hydrocephalus. minminimally invasive neurosurgery. 2007 oct;50(05):265-9. 14. demerdash a, rocque bg, johnston j, rozzelle cj, yalcin b, oskouian r, delashaw j, tubbs rs. endoscopic third ventriculostomy: a historical review. british journal of neurosurgery. 2017 jan 2;31(1):28-32. 15. siomin v, cinalli g, grotenhuis a, golash a, oi s, kothbauer k, weiner h, roth j, beni-adani l, pierre-kahn a, takahashi y. endoscopic third ventriculostomy in patients with cerebrospinal fluid infection and/or hemorrhage. journal of neurosurgery. 2002 sep 1;97(3):519-24. 16. bauer df, baird lc, klimo jr p, mazzola ca, nikas dc, tamber ms, flannery am. congress of neurological surgeons systematic review and evidence-based guidelines on the treatment of pediatric hydrocephalus: update of the 2014 guidelines. neurosurgery. 2020 dec;87(6):1071-5. 17. ogiwara h, dipatri aj, alden td, bowman rm, tomita t. endoscopic third ventriculostomy for obstructive hydrocephalus in children younger than 6 months of age. child's nervous system. 2010 mar;26(3):343-7. 18. zervos, t., & walters, b. c. (2019). diagnosis of ventricular shunt infection in children: a systematic review. world neurosurgery, 129, 34–44. 19. white md, mcdowell mm, agarwal n, greene s. shunt infection and malfunction in patients with myelomeningocele. journal of neurosurgery: pediatrics. 2021 feb 26;27(5):518-24. 20. oertel j, linsler s, csokonay a, schroeder hw, senger s. management of severe intraoperative hemorrhage during intraventricular neuroendoscopic procedures: the dry field technique. journal of neurosurgery. 2018 sep 21;131(3):931-5. 21. kamel mh, murphy m, aquilina k, marks c. subdural haemorrhage following endoscopic third ventriculostomy. a rare complication. acta neurochirurgica. 2006 may;148(5):591-3. 22. de almeida silva jm, veiga jc, de aguiar gb. physiopathology of subdural higroma following endoscopic third-ventriculostomy-a review. rev. chil. neurocirugía. 2013 oct 1;39:157-9. 23. cartmill m, vloeberghs m. the fate of the cerebrospinal fluid after neuroendoscopic third ventriculostomy. child's nervous system. 2000 dec;16(12):879-81. 24. fushimi y, miki y, ueba t, kanagaki m, takahashi t, yamamoto a, haque tl, konishi j, takahashi ja, hashimoto n, konishi j. liliequist membrane: threedimensional constructive interference in steady state mr imaging. radiology. 2003;229(2):360-5. 25. lu l, chen h, weng s, xu y. endoscopic third ventriculostomy versus ventriculoperitoneal shunt in patients with obstructive hydrocephalus: meta-analysis of randomized controlled trials. world neurosurgery. 2019 sep 1;129:334-40. 26. kulkarni av, riva-cambrin j, rozzelle cj, naftel rp, alvey js, reeder rw, holubkov r, browd sr, cochrane dd, limbrick dd, simon td. endoscopic third ventriculostomy and choroid plexus cauterization in infant hydrocephalus: a prospective study by the hydrocephalus clinical research network. journal of neurosurgery: pediatrics. 2018 mar 1;21(3):214-23. 27. jiang l, gao g, zhou y. endoscopic third ventriculostomy and ventriculoperitoneal shunt for patients with noncommunicating hydrocephalus: a prisma-compliant meta-analysis. medicine. 2018 oct;97(42). 28. deopujari ce, karmarkar vs, shaikh st. endoscopic third ventriculostomy: success and failure. journal of korean neurosurgical society. 2017 may 1;60(3):306-14. 324 bushra tariq ali, ahtesham khizar, pradhumna kumar yadav et al. 29. kulkarni av, riva-cambrin j, holubkov r, browd sr, cochrane dd, drake jm, limbrick dd, rozzelle cj, simon td, tamber ms, wellons jc. endoscopic third ventriculostomy in children: prospective, multicenter results from the hydrocephalus clinical research network. journal of neurosurgery: pediatrics. 2016 oct 1;18(4):423-9. 30. kulkarni, a. v., sgouros, s., leitner, y., constantini, s., & international infant hydrocephalus study investigators (2018). international infant hydrocephalus study (iihs): 5-year health outcome results of a prospective, multicenter comparison of endoscopic third ventriculostomy (etv) and shunt for infant hydrocephalus. child's nervous system : chns : official journal of the international society for pediatric neurosurgery, 34(12), 2391–2397. 31. weil ag, fallah a, chamiraju p, ragheb j, bhatia s. endoscopic third ventriculostomy and choroid plexus cauterization with a rigid neuroendoscope in infants with hydrocephalus. journal of neurosurgery: pediatrics. 2016 feb 1;17(2):163-73. 32. gonda dd, kim te, warnke pc, kasper em, carter bs, chen cc. ventriculoperitoneal shunting versus endoscopic third ventriculostomy in the treatment of patients with hydrocephalus related to metastasis. surgical neurology international. 2012;3. 33. aranha a, choudhary a, bhaskar s, gupta ln. a randomized study comparing endoscopic third ventriculostomy versus ventriculoperitoneal shunt in the management of hydrocephalus due to tuberculous meningitis. asian journal of neurosurgery. 2018 oct;13(4):1140. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii: pp. 498-507 doi: 10.33962/roneuro-2019-080 www.journals.lapub.co.uk/index.php/roneurosurgery radiological, biomechanical and histopathological characteristics of rat brain in kaolin-induced hydrocephalus m. yavuz samanci, md1, suat erol celik, assoc. prof.2, zafer unsal coskun, prof.3, deniz ozcan, md4 1 department of neurosurgery, istanbul health research and application centre, baskent university, istanbul, turkey 2 department of neurosurgery, okmeydani training and research hospital, university of health sciences, istanbul, turkey 3 department of radiology, okmeydani training and research hospital, university of health sciences, istanbul, turkey 4 department of pathology, okmeydani training and research hospital, university of health sciences, istanbul, turkey abstract objective: a better understanding of the pathophysiology and underlying mechanisms of brain damage in hydrocephalus is vital in developing diagnostic, observational and treatment tools that will have an impact on hydrocephalus outcomes. in this study, we aimed to demonstrate the radiological, biomechanical and histopathological characteristics of rat brain tissue in an experimental hydrocephalus model. materials and methods: thirty-six male sprague-dawley rats (21 days old, weighing between 150 and 200 grams) were used in this study. animals were randomly assigned to control (n = 6), 1-week hydrocephalus (n = 10), 2-week hydrocephalus (n = 10) and 3-week hydrocephalus (n = 10) groups. hydrocephalus was induced with cisternal kaolin injection and controls received sham injection. magnetic resonance imaging was used to measure ventricle size and cortical thickness. vital signs, cerebral blood flow (cbf), mechanical tests and brain histology were assessed. results: three rats in the hydrocephalus group died during the follow-up, yielding an overall mortality of 10% among animals from hydrocephalus groups. ventricular width, cross-sectional area of the lateral ventricles, ventricular index and ventricle / brain area ratio progressively increased and cortical thickness progressively decreased following kaolin injection. cbf was significantly lower at baseline than at 1st, 2nd and 3rd week (p < 0.05, for all). icp was significantly elevated in all hydrocephalic groups in comparison with controls. eit that was calculated from the first load-unload indentation test showed a significant increase at 2nd week postinjection (p=0.0001), indicating increased intracranial stiffness. however, this significant difference disappeared at 3rd week (p=0.956). quantitative immunohistochemistry showed that hydrocephalic brains demonstrated significantly less neun-positive cells and significantly higher iba-1-positive microglia and glial fibrillary acidic protein positive astrocytes cells in the cortex. discussion and conclusion: cisternal kaolin injection causes varying degrees of keywords brain, hydrocephalus, kaolin, mechanical properties, viscoelasticity corresponding author: m. yavuz samanci istanbul health research and application center, baskent university, turkey mysamanci@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published october 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 499 characteristics of rat brain in kaolin-induced hydrocephalus ventricular enlargement in a rat model and hydrocephalus might contribute to neuronal and axonal damage and alter brain stiffness through axonal stretching or local hypoperfusion progressively over a period of days to months. as shown in this study, irreversible changes in viscoelastic behaviour and cellular structure develop in the late stages of hydrocephalus, suggesting the importance of early intervention in the treatment of hydrocephalus. introduction the basic definition of hydrocephalus is “an abnormal accumulation of cerebrospinal fluid (csf) within the ventricles of the brain” [13]. the estimated prevalence is 1–1.5% and the incidence of congenital hydrocephalus is approximately 0.9–1.8/1000 births [17,23]. early onset hydrocephalus often results in the poorest neurological outcomes, with approximately 80% of patients suffering with residual neurological deficits [21]. experimental animal models have been developed using various methods and agents to induce hydrocephalus or through genetic mutations in rodents. although none of these models can fully mimic human condition, they can provide basic information that contributes to better understanding the pathogenesis of hydrocephalus and underlying causes. although ventriculomegaly occurs naturally in congenital rat models, they are not ideal for long-term studies unless hydrocephalus is surgically intervened. thus, the most common method of inducing experimental hydrocephalus without genetic mutation is the cisternal kaolin injection model that was introduced in the 1930s [19]. kaolin is injected into the cisterna magna and spreads in the subarachnoid space, where it induces an inflammatory reaction and leads to an obstruction in the csf pathways [8]. it is a simple, inexpensive and consistent way of inducing hydrocephalus in experimental animals [15]. both clinical hydrocephalus and experimental hydrocephalus are often associated with symptoms of increased intracranial pressure (icp) with ventricular dilatation. understanding the biomechanical properties of the hydrocephalic brain can help in predicting mechanisms, simulating the disease and creating a treatment protocol. however, due to the complexity of the brain and the surrounding structures, data on the mechanical properties of living neural tissue is limited and variable [10,22]. in this study, it was aimed to demonstrate the radiological, biomechanical and histopathological features of rat brain tissue in kaolin-induced hydrocephalus model. materials and methods all animal experiments were conducted in accordance with the institutional animal care and use committee of istanbul university guide for the care and use of laboratory animals in consultation with institutional veterinarians. specific protocols used in this study were approved by istanbul university laboratory animals local ethics committee (2013/47). anaesthesia, preoperative animal preparation, anaesthesia delivery, perioperative analgesia practices, and surgical protocols were optimized to minimize trauma to the animals. thirty-six male pathogen-free sprague-dawley rats (age, 21 days; weight, 150-200 g) were maintained on a 12-hour light/dark cycle and had free access to water and pellet food. animals were randomly assigned to control group (n=6), one-week hydrocephalus group (n=10), two-week hydrocephalus group (n=10) and three-week hydrocephalus group (n=10). all hydrocephalus groups underwent cisternal 0.02 ml sterile kaolin (200 mg / ml kaolin in 0.9% saline solution) injections, whereas controls received sham injection. all groups underwent magnetic resonance imaging (mri), mechanical tests and histopathological examination. induction of experimental hydrocephalus rats were anesthetized with ketamine hcl (ketalar, parke davis-eczacıbaşı, istanbul) and xylazine (rompun, bayer, istanbul) before surgical procedures. the head was secured in a stereotactic frame and a small vertical incision was made over the back of the neck from the top of the occiput to c1. the nuchal muscle layers were divided in the midline and retracted laterally to expose the atlantooccipital membrane (figure 1). in all rats in the hydrocephalus groups, 0.02 ml kaolin suspension was injected slowly into the cisterna magna through a 27-gauge needle. control rats were subjected to sterile saline injection. the muscle layers and skin were sutured and rats were allowed to recover. after recovery from anaesthesia, rats were kept at room temperature and provided with standard chow and water ad libitum. they were examined daily for clinical signs of illness. rats were weighed daily and monitored for neurological deficits. 500 m. yavuz samanci, suat erol celik, zafer unsal coskun, deniz ozcan figure 1. basic demonstration of animal preparation. custom custom-made stereotactic frame (upper left), atlanto-occipital membrane (upper right), preparation of cranial windows (lower left), and cerebral blood flow measurement with laser speckle microcirculation imager and pressure transmitter probe in the cisterna magna for monitoring intracranial pressure (lower right) can be seen. 501 characteristics of rat brain in kaolin-induced hydrocephalus magnetic resonance imaging mri studies were performed under general anaesthesia by the use of a human mr scanner equipped with a 48-cm bore magnet operating at a field of 1.5 t (brivo mr355, ge healthcare, waukesha, us) with a custom coil to obtain t2weighted images of the brain in the coronal plane. the total area of the lateral ventricles and the brain area were evaluated by a radiologist using the pacs workstation (neorad®, teleradiology & 3d, serman medical information, istanbul, turkey) on the coronal brain section that includes the anterior wall of the third ventricle. the frontal ventricle-to-brain area ratio, ventricle width index and cortical thickness measurements were performed as described by shulyakov et al. [26]. animal preparation after mri, spontaneously breathing rats were induced with 4% isoflurane gas delivered by 100% oxygen. the rats were placed in the supine position on a homoeothermic blanket system and instrumented with a rectal temperature probe and foot pulse oximeter to continuously monitor body temperature, blood oxygen saturation, and heart rate. under the operating microscope, the trachea was intubated with a 16g tube through a tracheostomy. the rats were then maintained with mechanical ventilation at fixed tidal volume (7 ml/kg) and inspired oxygen (40%). the left common carotid artery was dissected and cannulated for continuous blood pressure monitoring, serial blood gas analysis and fluid replacement. isoflurane was titrated to maintain a mean arterial pressure of 80-120 mm hg and oxygen saturation >90%. the rats were then positioned prone, fixed in a custom-made stereotactic frame and previous midline incision was used to expose the skull. the periosteum was incised and dissected. the skull was bilaterally thinned using a high-speed drill equipped with a 1.8-mm diamond burr bit to create bilateral penetrating cranial windows, leaving the dura-arachnoid membranes intact. a pressure transmitter probe was inserted into the cisterna magna for monitoring icp. for cerebral blood flow (cbf) measurement, laser speckle microcirculation imager was positioned over the rat with the desired cranial window aligned in the camera field of view. speckle images within a 1.2-cm x 1.6-cm region were acquired at a frequency of 50 hz with a resolution of 100 mm/pixel, with 18.526k points/perfusion unit value. baseline images were recorded and cbf in arbitrary perfusion units was obtained throughout the procedure. physiological data were recorded continuously during the procedure. baseline and hourly blood gas levels were analysed in all animals. the core temperature was measured via rectal probes and used as a reference for brain temperature. mechanical tests a custom-made indentation instrument with a halfspherical indenter was used. the indenter was fastened to the custom-made stereotactic frame and it was positioned over the centre of craniectomy to achieve a planar initial contact. with the use of previously described mechanical force parameters [27,31], a standard sequence of indentation tests including loading-unloading test, load and hold test, and multicycle loading-unloading test was performed. indentation modulus (eit), viscous deformation and viscous nature of the material were assessed. recovery periods of approximately 15 minutes were allowed between tests. histological examination animals were overdosed with pentobarbital after mechanical testing, and transcardially perfused with saline and then 4% paraformaldehyde. brains were post-fixed and subsequently immersed in the same fixative solution overnight at 4 °c and then washed in phosphate-buffered saline and stored in ethanol until processing. coronal slices were sectioned and embedded in paraffin. the paraffinized tissue slices were sectioned at 5 mm thickness. to assess neuronal integrity, activated microglia, and activated astrocytes, the following primary antibodies were used: anti-fox3 (neun) 1:2000, anti-iba-1 1:1000, and anti-glial fibrillary acidic protein (gfap) 1:500. images from the cortex were taken at 200x magnification. using image j, neun, iba-1, and gfap stained cells were counted. statistical analysis statistical analysis was performed using spss 18 (ibm corp., armonk, ny, usa). all data are expressed as mean ± standard error of the mean. comparison across the groups was made by using analysis of variance. statistical significance was accepted at p < 0.05. 502 m. yavuz samanci, suat erol celik, zafer unsal coskun, deniz ozcan results in total, thirty rats underwent induction of hydrocephalus. none of the rats in the hydrocephalus groups experienced major neurological deficits. three rats in the 3-week hydrocephalus group died during the study, yielding an overall mortality of 10% among animals from hydrocephalus groups. two rats died during the 3rd week of hydrocephalus and no cause could be identified. one rat died during indentation testing, probably due to anesthesia overdose. therefore, the assessments were performed with a total of 33 rats. during the study, all animals, regardless of group, showed an increase in body weight (p < 0.0001). hydrocephalic rats lost weight after kaolin injection, typically for 2–3 days. by 1-week post-injection, the rats started gaining weight. nonetheless, rats in the hydrocephalus groups weighed less than controls regardless of hydrocephalus week (p=0.0014 for one-week hydrocephalus; p<0.0001 for two-week hydrocephalus and p<0.0001 for three-week hydrocephalus). mri imaging showed that the ventricular width, cross-sectional area of the lateral ventricles, ventricular index and ventricle / brain area ratio progressively increased and cortical thickness progressively decreased following kaolin injection (table 1) (figure 2) table 1. statistical evaluation of mri parameters in hydrocephalic and control rats. figure 2. magnetic resonance image demonstrating increase in ventricular size in a hydrocephalic rat at 3rd week (right) compared to a control rat (left). in control rats, cbf was significantly lower at baseline than at 1st, 2nd and 3rd week (p < 0.05, for all). hydrocephalic rats also showed an increase in cbf with time, but this was not significant (p=0.2429). hydrocephalic rats at 1st week had a lower cbf than controls; however, the difference was not significant mri parameters ventricular width cross-sectional area of the lateral ventricles ventricular index ventricle / brain area ratio cortical thickness hydrocephalic rats 1st week vs. 2nd week <0.0001 <0.0001 <0.0001 0.0005 0.0142 1st week vs. 3rd week <0.0001 <0.0001 <0.0001 <0.0001 <0.0001 control rats 1st week vs. 2nd week 0.99 0.99 0.96 0.86 0.87 1st week vs. 3rd week 0.79 0.72 0.68 0.61 0.50 503 characteristics of rat brain in kaolin-induced hydrocephalus (p=0.3134). at 2nd and 3rd weeks, hydrocephalic rats had a significantly lower cbf than controls with a highest percentage reduction of 59% (p<0.0001) (table 2). mechanical parameters cbf icp heart rate eit strain during load-hold strain during multi-cycle hydrocephalic rats 1st week vs. 2nd week 0.48 <0.0001 <0.0001 <0.0001 <0.0001 0.0214 1st week vs. 3rd week 0.1865 0.4255 0.0145 0.9443 <0.0001 0.1340 control rats vs. hydrocephalic rats control vs. 1st week 0.0004 <0.0001 <0.0001 0.8842 0.0002 0.0555 control vs. 2nd week <0.0001 <0.0001 <0.0001 <0.0001 0.0001 0.0176 control vs. 3rd week <0.0001 <0.0001 <0.0001 0.956 <0.0001 0.0082 table 2. statistical evaluation of physiological and mechanical parameters in hydrocephalic and control rats cbf: cerebral blood flow; icp: intracranial pressure; eit: indentation modulus figure 3. representative histomicrographs showing significantly decreased neun-positive cells in the cortex of rats in the hydrocephalus group at 3rd week (b) compared to controls (a), and significantly increased iba-1-positive microglia (red) and gfappositive astrocyte cells (gray) in the cortex of rats in the hydrocephalus group at 3rd week (d) compared to controls (c). 504 m. yavuz samanci, suat erol celik, zafer unsal coskun, deniz ozcan for the control and hydrocephalic groups, the indentation tests were associated with an icp increase up to 20%. eit that was calculated from the first load-unload indentation test showed a significant increase at 2nd week post-injection (148 kpa vs. 278 kpa, p=0.0001), indicating increased intracranial stiffness. however, this significant difference disappeared at 3rd week (p=0.956). in the load-hold indentation test, control and hydrocephalic brains exhibited gradual deformation and the associated intracranial strain was significantly greater at each time points in the hydrocephalus groups (p=0.0002 at 1st week, p=0.0001 at 2nd week and p<0.0001 at 3rd week). the multi-cycle indentation test also caused gradual deformation of the intracranial contents in all groups, but there was no significant difference between groups (p=0.0555 at 1st week, p=0.082 at 2nd week and p=0.176 at 3rd week) (table 2). systemic blood pressure and mean arterial pressure were stable during mechanical tests; however, due to increased icp, cerebral perfusion pressure and cbf decreased. after withdrawal of the indenter, blood flow returned immediately to baseline values i all groups. baseline core temperatures were not statistically different between all groups and changes were not significant during indentation (table 2). icp in controls was 6.5 ± 0.86 mmhg. compared to controls, icp was significantly elevated in all hydrocephalic groups, with the pressure being highest at 2nd week (p<0.0001 at all-time points). icp showed a rapid pressure rise during indentation and returned immediately to baseline values after withdrawal in all groups. during indentation, bradycardia was identified at the point of maximal icp (table 2). quantitative analyses of neun-positive, iba-1positive, and gfap-positive cells in the cortex of animals with hydrocephalus demonstrated significantly less neun-positive cells that reflects altered neuronal integrity, and significantly more iba1-positive microglia and gfap-positive astrocyte cells that indicate higher inflammatory signals (figure 3). discussion to investigate the radiological, biomechanical and histopathological changes in experimental hydrocephalus, we analyzed the impact of kaolininduced hydrocephalus in rats. the present data indicate that kaolin-induced hydrocephalus created a reproducible hydrocephalus model with altered brain morphology along with disturbed mechanical properties and neuronal integrity. besides genetic mutations, experimental animal models have been developed using numerous agents to induce hydrocephalus [8,15]. all of these models provide important information to understand the causes and potential treatments of hydrocephalus. the most commonly used method is the injection of kaolin into the cisterna magna [9] and it is an inexpensive, simple and reliable method that has been previously studied in rats [6,7,11,12,18]. in our study, the experimental rats were particularly 21day old rats, as it corresponds to the first 6-month period of human brain development in which cerebral myelination is rapid [24,30]. the rats in our study tolerated the kaolin injection fairly well with acceptable levels of mortality (10% died during 3 weeks, one possibly due to anesthesia overdose) and no evidence of hemorrhage was observed following removal of the brain. compared to higher rates of mortality in the literature, it was thought that the difference might be due to post-operative animal care, animal breed used and the chemical properties of kaolin [5,20]. however, it should be noted that none of these models, including kaolin-induction method, is perfect in imitating human conditions. although kaolin-induced hydrocephalus model offers dose-dependent responses to some extent, there is variable dispersion of kaolin in the subarachnoid space, and this may account for the relatively unpredictable rate and magnitude of ventricular dilatation [8]. consistent with the literature, in our study, kaolin presumably caused a moderate to severe hydrocephalus with a ventricle/brain area ratio of 0.105 ± 0.02 at 3 weeks, compared to 0.018 ± 0.002 at baseline. kaolin causes an inflammatory response, thus causing blockage of the fourth ventricle and mimicking hydrocephalus caused by meningitis. although this model has been criticized for its inflammatory effects such as evident macrophages, cd4and cd8lymphocytes in the subarachnoid space and in surrounding brain parenchyma, and reactive microglia in the white matter surrounding the ventricles [7,16,25], it was reported that kaolin had clearly been ingested by macrophages and there were minimal neutrophils and eosinophils at 10th day post-injection with histologically unaltered brainstem and cerebellum 505 characteristics of rat brain in kaolin-induced hydrocephalus adjacent to kaolin collections [29]. brain injury in hydrocephalus is a multifactorial process marked by ventricular enlargement leading to stretching of axons with concomitant cortical compression. however, these histologically evident progressive destructive changes can be difficult to quantify due to profound tissue distortions [16]. in our study, quantitative analyses of neun-positive, iba-1positive, and gfap-positive cells in the cortex of animals with hydrocephalus demonstrated significantly less neun-positive cells and significantly more iba-1-positive microglia and gfap-positive astrocyte cells. due to the complexity of the brain and the surrounding meningeal structure, information about the mechanical properties of living neural tissue is insufficient [10,22]. to learn about the mechanical changes and to better understand the physical mechanisms involved in hydrocephalus, it is necessary to learn about the mechanical properties of the brain in vivo [1]. the main advantage of in vivo testing is that the tissue structure remains largely intact, as close to its natural state as possible [4]. it is widely known that the mechanical properties of neural tissues are associated with their microstructure [2]. thus, changes in tissue microstructure can be reflected as an altered stiffness. in our study, the live brain mechanical properties reflected a combination of several different anatomical and physiological systems including the dura mater, the intact csf system, and the brain itself. the stiffness of cortical gray matter increased despite the differences in tissue microstructure at 2nd week, similar to the study by shulyakov et al. [26]. however, juge et al. [14] did not find such an increase in the same hydrocephalus rat model. the main difference of their study was that they used mr elastography to measure brain stiffness and the contribution of hydrostatic pressure to mechanical properties was eliminated by elastography analysis method [28]. despite the increase at 2nd week, the difference between controls and hydrocephalic group disappeared at 3rd week. regarding this, it can be suggested that microstructural rearrangement occurs in brain during chronic phase of hydrocephalus possibly through neuronal damage. this damage was also demonstrated in our study by significantly less neun-positive cells in the hydrocephalic group at 3rd week. the absence of permanent change in viscoelastic behaviour in the brain in the early stages of hydrocephalus in our study shows the importance of early intervention in the treatment of hydrocephalus. the main limitation of our study was that we could not use an animal mri equipped with a higher magnetic field strength. however, in a previous study, 1.0t mri was shown to be a reliable equipment to assess mri features in experimental hydrocephalus [3]. conclusion cisternal kaolin injection causes varying degrees of ventricular enlargement in a rat model and reflects the hydrocephalus pathology seen in foetuses and premature infants in some aspects. hydrocephalus might contribute to neuronal and axonal damage and alter brain stiffness through axonal stretching or local hypoperfusion progressively over a period of days to months. the absence of permanent change in viscoelastic behaviour in the brain in the early stages of hydrocephalus necessitates early intervention. references 1. azzi gm, canady ai, ham s, mitchell ja (1999) kaolininduced hydrocephalus in the hamster: temporal sequence of changes in intracranial pressure, ventriculomegaly and whole-brain specific gravity. acta neuropathologica 98 (3):245-250. doi:10.1007/s00401005 1076 2. bilston le (2011) neural tissue biomechanics. studies in mechanobiology, tissue engineering and biomaterials, vol 3. springer-verlag berlin heidelberg. doi:10.1007/978-3642-13890-4 3. castro sc, machado hr, catalao ch, siqueira ba, simoes al, lachat jj, lopes lda s (2012) 0.1t magnetic resonance image in the study of experimental hydrocephalus in rats. accuracy of the method in the measurements of the ventricular size. acta cirurgica brasileira 27 (11):768-772 4. cheng s, clarke ec, bilston le (2008) rheological properties of the tissues of the central nervous system: a review. medical engineering & physics 30 (10):1318-1337. doi:10.1016/j.medengphy.2008.06.003 5. davis gb, kohandel m, sivaloganathan s, tenti g (2006) the constitutive properties of the brain paraenchyma part 2. fractional derivative approach. medical engineering & physics 28 (5):455-459. doi:10.1016/j.medengphy.2005.07. 023 6. del bigio mr, crook cr, buist r (1997) magnetic resonance imaging and behavioral analysis of immature rats with 506 m. yavuz samanci, suat erol celik, zafer unsal coskun, deniz ozcan kaolin-induced hydrocephalus: preand postshunting observations. experimental neurology 148 (1):256-264. doi:10.1006/exnr.1997.6644 7. del bigio mr, zhang yw (1998) cell death, axonal damage, and cell birth in the immature rat brain following induction of hydrocephalus. experimental neurology 154 (1):157-169. doi:10.1006/exnr.1998.6922 8. di curzio dl (2018) animal models of hydrocephalus. open journal of modern neurosurgery 8:57-71. doi:https:// doi.org/10.4236/ojmn.2018.81004 9. dixon we hh (1932) experimentelle hypertonie durch eröhung des intrakaniellen druckes. arch exp pathol pharmakol 166:265-275 10. goldsmith w (2001) the state of head injury biomechanics: past, present, and future: part 1. critical reviews in biomedical engineering 29 (5-6):441-600 11. hochwald gm, boal rd, marlin ae, kumar aj (1975) changes in regional blood-flow and water content of brain and spinal cord in acute and chronic experimental hydrocephalus. developmental medicine and child neurology supplement (35):42-50 12. hochwald gm, nakamura s, camins mb (1981) the rat in experimental obstructive hydrocephalus. zeitschrift fur kinderchirurgie: organ der deutschen, der schweizerischen und der osterreichischen gesellschaft fur kinderchirurgie = surgery in infancy and childhood 34 (4):403-410. doi:10.1055/s-2008-1063383 13. johnston i, teo c (2000) disorders of csf hydrodynamics. child's nervous system: chns: official journal of the international society for pediatric neurosurgery 16 (1011):776-799. doi:10.1007/s003810000383 14. juge l, pong ac, bongers a, sinkus r, bilston le, cheng s (2016) changes in rat brain tissue microstructure and stiffness during the development of experimental obstructive hydrocephalus. plos one 11 (2):e0148652. doi:10.1371/journal.pone.0148652 15. khan oh, del bigio mr (2006) experimental models of hydrocephalus. in: tatlisumak taf, m., (ed) handbook of experimental neurology: methods and techniques in animal research. cambridge university press, pp 457-471. doi:https://doi.org/10.1017/cbo9780511541742.026 16. khan oh, enno tl, del bigio mr (2006) brain damage in neonatal rats following kaolin induction of hydrocephalus. experimental neurology 200 (2):311-320. doi:10.1016/j. expneurol.2006.02.113 17. lemire rj (1988) neural tube defects. jama 259 (4):558-562 18. li j, mcallister jp, 2nd, shen y, wagshul me, miller jm, egnor mr, johnston mg, haacke em, walker ml (2008) communicating hydrocephalus in adult rats with kaolin obstruction of the basal cisterns or the cortical subarachnoid space. experimental neurology 211 (2):351361. doi:10.1016/j.expneurol.2007.12.030 19. lindauer ma, griffith, j.q. (1938) cerebrospinal pressure, hydrocephalus and blood pressure in cat following intracisternal injection of colloidal kaolin. proceedings of the society for experimental biology and medicine 39:547549. 20. mchedlishvili g, nikolaishvili l, itkis m (1979) pathophysiological mechanisms of brain edema development: role of tissue factors. stroke 10 (1):52-57. doi:10.1161/01.str.10.1.52 21. moritake k, nagai h, miyazaki t, nagasako n, yamasaki m, sakamoto h, miyajima m, tamakoshi a (2007) analysis of a nationwide survey on treatment and outcomes of congenital hydrocephalus in japan. neurologia medicochirurgica 47 (10):453-460; discussion 460-451. doi:10.2176/nmc.47.453 22. ommaya ak (1968) mechanical properties of tissues of the nervous system. journal of biomechanics 1 (2):127-138. doi:10.1016/0021-9290(68)90015-8 23. persson ek, hagberg g, uvebrant p (2005) hydrocephalus prevalence and outcome in a population-based cohort of children born in 1989-1998. acta paediatrica 94 (6):726732. doi:10.1111/j.1651-2227.2005.tb01972.x 24. segawa w (1961) rheological equations of generalized maxwell model and voigt model in three-dimensional, non-linear deformation. journal of the physical society of japan 16:320-323. doi:10.1143/jpsj.16.320 25. shinoda m, olson l (1997) immunological aspects of kaolininduced hydrocephalus. the international journal of neuroscience 92 (1-2):9-28. doi:10.3109/00207459708 986386 26. shulyakov av, buist rj, del bigio mr (2012) intracranial biomechanics of acute experimental hydrocephalus in live rats. neurosurgery 71 (5):1032-1040. doi:10.1227/neu. 0b013e3182690a0c 27. shulyakov av, fernando f, cenkowski ss, del bigio mr (2009) simultaneous determination of mechanical properties and physiologic parameters in living rat brain. biomechanics and modeling in mechanobiology 8 (5):415425. doi:10.1007/s10237-008-0147-9 28. sinkus r, tanter m, xydeas t, catheline s, bercoff j, fink m (2005) viscoelastic shear properties of in vivo breast lesions measured by mr elastography. magnetic resonance imaging 23 (2):159-165. doi:10.1016/j.mri.2004.11.060 29. slobodian i, krassioukov-enns d, del bigio mr (2007) protein and synthetic polymer injection for induction of obstructive hydrocephalus in rats. cerebrospinal fluid research 4:9. doi:10.1186/1743-8454-4-9 30. yamamoto y, moritake k, nagai h, sato m (2004) quantitative estimation of brain stiffness measured using a tactile biosensor in animal models. neurological research 26 (6):622-627. doi:10.1179/016164104225016326 31. zhang m, zheng yp, mak af (1997) estimating the effective young's modulus of soft tissues from indentation tests- 507 characteristics of rat brain in kaolin-induced hydrocephalus nonlinear finite element analysis of effects of friction and large deformation. medical engineering & physics 19 (6):512-517. doi: 10.33962/roneuro-2022-042 risk factors for preoperative seizures in meningiomas base versus non-bases of supratentorial. single centre retrospective study in a series of 244 cases abdalrahman nassar, volodymyr smolanka, stydinyk taras, andriy smolanka, dipak chaulagain, mariana pryima, marina yuryk romanian neurosurgery (2022) xxxvi (2): pp. 237-246 doi: 10.33962/roneuro-2022-042 www.journals.lapub.co.uk/index.php/roneurosurgery risk factors for preoperative seizures in meningiomas base versus non-bases of supratentorial. single centre retrospective study in a series of 244 cases abdalrahman nassar, volodymyr smolanka, stydinyk taras, andriy smolanka, dipak chaulagain, mariana pryima, marina yuryk uzhhorod regional neurosurgical centre, uzhhorod national university, uzhhorod, ukraine abstract background: meningiomas are the most frequent benign intracranial lesions. the literature review reported that 19-63% of the patients with meningioma suffer from preoperative seizures, and 35% experience epileptic seizures as the initial symptom. the present study attempted to establish the risk factors for seizures before surgery of supratentorial meningiomas. objective: to compare predictive factors for preoperative seizures for skull base meningiomas (sbms), with non-skull base meningiomas (nsbms). materials and methods: the clinical data of 244 patients with supratentorial meningiomas treated microsurgically between 2007 and 2018 were analyzed retrospectively. there were two groups; group “a” with (nsbms) and group “b” with (sbms). demographic, clinical, imaging, histopathological, and electroencephalographic data were assessed. univariate statistical analyses were performed among factors that might correlate with preoperative seizures. results: a total of 244 patients with a diagnosis of intracranial meningioma were retrospectively evaluated. the mean age was 54.34 years (range 1684), females 165, meals 79. of these 154 patients for the non-skull base, seizures in 65 (42.2%), whereas, 90 patients for skull base, with 32 (35.5%) patients with seizures. the groups had similar preoperative seizure occurrence in relation to age (p=0.154, p=0.819), gender (p=0.396, p=0.445) tumor size (p=0.318, p=0.244), tumor side (p0.836, p=0.702) for group a and b respectively. the pre-op seizure was the third presentation in both groups after non-focal symptoms and (fnd) respectively. for group “a” seizure as the initial symptom was in 49.2% of patients versus 50.8% for others, while in group “b” was in 37.5% vs 62.5%. the both groups had statistically significance between ptbe and pre op seizure, for group “a”, ptbe was in 93(60.4%) patients, (seizure in 51patients 78.5%) vs (42 patients 47.2% for non-seizure), (?2=,15.356, p=0.000). for group “b”, ptbe was in 43(47.8%) patients, (seizure in 25 patients 78.1%) vs(18 patients 31% for nonseizure),(?2=,18.328, p=0.000). the most frequently seizure for group “b” was in ogm (seizure 25% vs 13.8 without seizure) and swm (seizure 71.8% vs 65.5% non-seizure), while lesser overall in planum/tuberculum (seizure3.2% vs 20.7% non-seizure). there was a statistically keywords seizure, skull base meningioma, supratentorial meningioma, oedema corresponding author: abdalrahman nassar uzhhorod regional neurosurgical centre, uzhhorod national university, uzhhorod, ukraine dr.abed.r.nassar@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 238 abdalrahman nassar, volodymyr smolanka, stydinyk taras et al. significant relationship between tumour location and preoperative seizure for (sbm), (?2=5.985, p=0.050) while absent in group “a”. (?2=1.373, p=0.503). there were no differences between the two groups with who grade and preop seizure. the unexpected finding in this study is that the presence of preoperative neurologic deficits has been less frequently associated with preoperative seizures in both groups. careful analysis and further investigation are needed. conclusion: we identified that the major risk factor for pre-op seizure in both group studies is ptbe, and location for skull base meningiomas, where the planum/tuberculum lesser overall risk for pre-op seizure. while other radiological and histopathological factors are statistically non-significant. interestingly, the factors associated with preoperative seizures were the absence of preoperative neurologic deficits for both groups. introduction meningioma is the most common benign intracranial tumor, accounting for approximately one-third of all cns tumors [32]. in the literature review; it was reported that 19-63% of the patients with meningioma are suffered from preoperative seizures, and 35% of them experience epileptic seizures as the initial symptom [19]. interestingly, patients with meningioma experience seizures even more frequently than patients with primary glioblastoma or brain metastasis. this is in particular a high rate taking into account that meningiomas are extra-axial tumors [31]. recurrent seizures in patients with brain tumors lead to significant morbidity, cognitive problems, inability to drive, and diminished quality of life [11,25,29]. for patients with meningioma, surgery is the main treatment modality and offers the possibility of a cure. however, complications and morbidity from meningioma surgery are common [3, 23, 26,27]. the mechanisms of tumor-induced seizures are poorly understood. the causative neoplasm may act as a generator to produce an epileptogenic focus in the peri-tumoral brain. the mechanisms of epileptogenesis pre and postoperative are not sufficiently known. distortion of the cortical structures may be the generator areas for focal seizure [6,12,17,30,34] the following retrospective study summarizes the most important identified risk factors for preoperative seizure in a series of 244patients who underwent surgery for supratentorial meningioma, and subsequently, compares between the skull base and non-skull base. materials and methods general information. between 2007 and 2018, a total 244 of patients with supratentorial meningiomas were treated in uzhhorod neurosurgical center. pediatric(<16 years), recurrent and multiple meningioma patients, also posterior fossa meningiomas included; (clival,petro clival, foramen magnum, tentorial and cerebellopontine angle) were excluded from statistical analysis in this study. they were 244 patients divided into two groups: group “a” (nsbms) included 154 patients with preoperative seizure (65 patients) versus nonseizure (89 patients), and group “b” (sbms) included 90 patients, with preoperative seizure (32 patients) versus non-seizure (58 patients). clinical data collection. the medical records of all the patients were checked for history and initially preoperative seizures. all the patients had been diagnosed by head contrast-enhanced magnetic resonance imaging and/or computed tomography scans, and the maximum tumor size, tumor site and any peritumoral brain edema (ptbe), by employing high signal intensity changes on t2-weighted images, were preliminarily determined. we classified tumor size into 4 categories according to mri findings; small (3cm and less), medium (3cm and less5cm), large (5cm-6cm), and giant (more 6 cm). all patients with preoperative seizures had been diagnosed by interictal 19 channel scalp electroencephalography (eeg). craniotomy for meningioma resection was performed microscopically for all 244 patients. after the resection of the tumor histopathological and immune histochemical analysis, were performed, according to who classification of tumors of the central nervous system, we have analyzed the articles and summarized all risk factors investigated and subdivided risk factors for preoperative seizures into nsbms and sbms. results are summarized in (table 1) nsbms group “a” and in (table 2) for sbms. group “b” statistical analysis; statistical analysis was performed using chi-square test, t-test, and fisher's exact test. p <0.05 was considered statistically significant. comparison between the two groups in relation to age, sex, tumor location, tumor site, tumor side, tumor size, histopathology, and clinical presentation was performed to identify predictive factors for preoperative seizure. pearson chi-square 239 risk factors for preoperative seizures in meningiomas statistics were used to examine the association between categorical variables (seizure and ptbe). there is a significant association at 5% significance level between seizure and ptbe of respondents (x2 =15.356, df=1, p=0.000) for group “a”, and (χ2=,18.328, df=1, p=0.000) for group b.(seizure and locationfor skull base). there was a significant association at 5% significance level between seizure and location of tumor of respondents (x2 = 5.985, df = 2, p = 0.050). results demographic data this study showed that meningioma in females had a higher tendency of 96 as compared to male 58, the ratio f/m was 1.6:1, and mean age 54.29 in group “a”. like that in group “b”, the ratio f/m was 3.2:1.(female 69 vs 21 male), with a mean age of 54.49. the patients’ age ranged from 16 to 84 years old, the mean age for patients with seizures was 53.01 years (range 22 to 75), and 55.68 years (range 16-84) for non-seizure (χ2=3.737, p=0.154). the seizure vs non-seizure for group “a” female 58.4% vs 65.1%, while in male was 41.5% vs 34.8%. (χ2=0.720, p=0.396). there is a weak association was found between the male gender and pre-op seizure, however, the difference not reached statistically significant. for group “b”, the seizure vs non-seizure in females was 81.5% vs 74.1% while in males was 18.5% vs 25.9%. (χ2=0.583, p=0.445). there is a weak association was found between female gender and pre-op seizure in group “b”. however, there was no statistically significant relationship between age or gender and preoperative seizure in both groups. table 1. factors associated with pre-op seizures in patients with nsbm group “a” factor no of cases n=154 (%) seizure n=65 no seizure n=89 p valu e sex female male 96 (62.4%) 58 (37.6%) 38 (58.4%) 27 (41.5%) 58 (65.1%) 31 (34.8%) 0.39 6 age/years < 40 40-60 >60 20(13%) 76(49.4 %) 7 (10.7%) 13 (14.6%) 0.15 4 58(37.6 %) 38 (58.4%) 20 (30.7%) 38 (42.7%) 38 (42.7%) tumor size/ cm small <3 medium >3<5 large 5-6 giant >6 37(24%) 59(38.3 %) 28(18.2 %) 30(19.5 %) 17 (26.2%) 28(43%) 8 (12.3%) 12 (18.5%) 20 (22.5%) 31 (34.8%) 20 (22.4%) 18 (20.3%) 0.31 8 side lt rt both/median 74(48%) 73(47.4 %) 7(4.6%) 33(50.8 %) 29(44.7 %) 3(4.5%) 41(46%) 44 (49.4%) 4 (4.6%) 0.83 6 location convex parasaital/paraf alx intraventricular site frontal fronto temporal fronto parietal temporal tempo paraital parietal paraito occipital occipital 98(63.6 %) 51(33.1 %) 5(3.3%) 49(31.8) 17(11) 47(30.5) 7(4.5) 9(5.8) 12(7.8) 10(6.5) 3 (2) 39(60%) 25(38.5 %) 1 (1.5%) 23(35.4 %) 6 (9.3%) 19 (29.2%) 4 (6.2%) 3 (4.6%) 6 (9.3%) 3 (4.6%) 1(1.5%) 59(66.3 %) 26 (29.2%) 4 (4.5%) 26 (29.2%) 11 (12.3%) 28 (31.4%) 3 (3.3%) 6 (6.7%) 6 (6.7%) 7 (7.9%) 2 (2.3%) 0.50 3 0.68 3 ptbe present absent 93(60.4 %) 61(39.6 %) 51 (78.5%) 14 (21.5%) 42 (47.2%) 47 (52.8%) 0.00 0 imaging finding relation to location in group “a”; convex in 63.6% patients (seizure 60% vs 66.3% non-seizure), parasaital/ parafalx 33.1% patients (seizure 38.5% vs 29.2% non-seizure) and intraventricular 3.3% patients (seizure 1.5% vs 4.5% non-seizure), parasagittal/ parafalcine location had higher occurrence of seizure in this group, however, there was no statistically significant relation between 240 abdalrahman nassar, volodymyr smolanka, stydinyk taras et al. tumor location and preoperative epilepsy, (χ2=1.373, p=0.503). in group “b” (table 3.a, b); swm in 67.8% patients (71.9% seizure vs 65.5% non-seizure), ogm in 17.8% patients, (25% seizure vs 13.8% non-seizure), and planum/tubeerculum in14.4% patients (3.1% seizure vs 20.7% non-seizure). preoperative seizure was more incidence in ogm and swm, respectively, while, lesser in planum and tuberculum meningiomas, (χ2=5.985, p=0.05). there was statistically significant relation between tumor location and preoperative seizure for (sbm) group“b”, while absent in group “a”. table 2. factors associated with pre op seizures in patients with sbm group” b” 90 factor no of cases n=90 / % seizure n=32 (35.6%) no seizure n=58 (64.4%) p sex female male 69(76.7 %) 21(23.3 %) 26 (81.2%) 6 (18.8%) 43(74.1 %) 15 (25.9%) 0.44 5 age/years < 40 40-60 >60 11(12.2 %) 58(64.4 %) 21(23.4 %) 3(9.3%) 21(65.6 %) 8(25%) 8(13.8% ) 37(63.8 %) 13(22.4 %) 0.81 9 tumor size/ cm small 3 and <3 medium >3<5 large 5-6 giant >6 27(30%) 28(31.1 %) 29(32.2 %) 6(6.7%) 12(37.5 %) 12(37.5 %) 7(21.9% ) 1(3.2%) 15(25.8 %) 16(27.6 %) 22(38%) 5(8.6%) 0.24 4 side lt rt both/median 29(32.2 %) 32(35.6 %) 29(32.2 %) 12(37.5 %) 11(34.4 %) 9(28.1% ) 17(29.3 %) 21(36.2 %) 20(34.5 %) 0.70 2 location swm/cs ogm planum/tubercul um 61(67.8 %) 16(17.8 %) 23(71.9 %) 8 (25%) 1 (3.1%) 38 (65.5%) 8 (13.8%) 0.05 0 13(14.4 %) 12 (20.7%) ptbe present absent 43(47.8 %) 47(52.2 %) 25 (78.1%) 7 (21.9%) 18 (31%) 40 (69%) 0.00 0 relation to brain lobes and tumour side preoperative seizure for (nsbm) occurred in all sites of brain lobes, moreover, there was a higher incidence of frontal (seizure 35.4% vs 29.1% nonseizure). however, there was no statistically significant relation between brain lobes lesion and preoperative seizure. (χ2=,0.288, p=0.687). according, to side of meningioma location in group “a”, right in 47.4% patients, (seizure 44.7% vs 49.4% non-seizure), left side in 48% patients (seizure 50.8% vs 46% non-seizure), and medline both side in 6.4% patients, (seizure 4.5% vs 4.6 non seizure). there was no statistically significant relationship between the side of the lesion and preoperative seizure. (χ2=,0.358, p=0.836). while in group “b” left side in 35.6% patients, (seizure 37.5% vs 29.3 non seizure), right side in 48% patients, (seizure 34.4% vs 36.2 non seizure), and medline both side in 32.2% patients, (seizure 28.1% vs 34.5% non-seizure). despite the weak relationship was found between the left side and pre-op seizure, however, there was no statistically significant relationship between the side of the lesion and preoperative seizure. (χ2=,0.707, p=0.702). table 3a. location * seizure. cross tabulation for group b seizure total no yes locati on swm count 38 23 61 expected count 39.3 21.7 61.0 % within location 62.3 % 37.7 % 100. 0% % within seizure 65.5 % 71.9 % 67.8 % ogm count 8 8 16 expected count 10.3 5.7 16.0 % within location 50.0 % 50.0 % 100. 0% % within seizure 13.8 % 25.0 % 17.8 % count 12 1 13 241 risk factors for preoperative seizures in meningiomas pla/tu bercu lum expected count 8.4 4.6 13.0 % within location 92.3 % 7.7% 100. 0% % within seizure 20.7 % 3.1% 14.4 % total count 58 32 90 expected count 58.0 32.0 90.0 % within location 64.4 % 35.6 % 100. 0% % within seizure 100. 0% 100. 0% 100. 0% table 3b. chi-square tests value df asymptotic significance (2-sided) pearson chi-square 5.985a 2 .050 likelihood ratio 7.078 2 .029 linear-by-linear association 2.170 1 .141 n of valid cases 90 chi-square statistics were used to examine the association between categorical variables (seizure and locationskull base). there is a significant association at 5% significance level between seizure and location of tumor of respondents (x2 = 5.985, df = 2, p = 0.050). relation to tumor size preoperative seizure was occurs in all different tumor size, for group “a” small size was in 24% patients,(seizure 26.2% vs 22.5% non-seizure), medium 38.2% patients (seizure 43%vs 34.8% nonseizure), and large/giant in 37.7% patients (seizure 30.8% vs 42.7% non-seizure).the difference is statistically insignificant, (χ2=,3.073, p=0.381). while for group” b”, small size 30% patients,(seizure 37.5% vs 25.8%), medium 31.1% patients (seizure 37.5% vs 27.6%) and large/giant 38.8% patients (seizure 25% vs 46.5%). the difference is statistically insignificant(χ2=,4.167, p=0.244).despite the weak relation was found between small/medium size and pre op seizure, however, distribution of tumor size in both groups showed that there was no statistically significant relation between tumor size and occurrence of pre-op seizure. relation to ptbe there was a higher incidence of peri-tumoral edema in seizure in both groups; for group “a” (table 4.a,b), ptbe was in 93(60.4%) patients,(seizure in 51patients 78.5%) vs (42 patients 47.2% for non-seizure). there was a statistically significant relation between peritumoral edema and pre-op seizure, (χ2=,15.356, p=0.000).for group “b”,(table5.a,b) ptbe was in 43(47.8%) patients,(seizure in 25 patients 78.1%) vs(18 patients 31% for non-seizure). there was a statistically significant relation between peri-tumoral edema and pre-op seizure, (χ2=,18.328, p=0.000).the incidence of ptbe was higher in nsbm, however, distribution of ptbe in both groups showed that there was statistically significant relation between ptbe and occurrence of pre-op seizure . table 4a. seizure * ptbe cross tabulation for group a ptbe total no yes seiz ure no count 47 42 89 expected count 35.3 53.7 89.0 % within seizure 52.8 % 47.2 % 100. 0% % within ptbe 77.0 % 45.2 % 57.8 % yes count 14 51 65 expected count 25.7 39.3 65.0 % within seizure 21.5 % 78.5 % 100. 0% % within ptbe 23.0 % 54.8 % 42.2 % total count 61 93 154 expected count 61.0 93.0 154. 0 % within seizure 39.6 % 60.4 % 100. 0% % within ptbe 100. 0% 100. 0% 100. 0% table 4b. chi-square tests value df asymptotic significance (2-sided) exact sig. (2sided) exact sig. (1sided) pearson chisquare 15.356a 1 .000 continuity correctionb 14.077 1 .000 likelihood ratio 15.962 1 .000 fisher's exact test .000 .000 linear-bylinear association 15.256 1 .000 n of valid cases 154 242 abdalrahman nassar, volodymyr smolanka, stydinyk taras et al. chi-square statistics were used to examine association between categorical variables (seizure and ptbe). there is a significant association at 5% significance level between seizure and ptbe of respondents (x2 =15.356, df=1, p=0.000). table 5a. ptbe * seizure crosstabulation for group b seizure total no yes ptbe 0 count 40 7 47 expected count 30.3 16.7 47.0 % within ptbe 85.1% 14.9% 100.0% % within seizure 69.0% 21.9% 52.2% 1 count 18 25 43 expected count 27.7 15.3 43.0 % within ptbe 41.9% 58.1% 100.0% % within seizure 31.0% 78.1% 47.8% total count 58 32 90 expected count 58.0 32.0 90.0 % within ptbe 64.4% 35.6% 100.0% % within seizure 100.0% 100.0% 100.0% table 5b. chi-square tests value df asymptotic significance (2-sided) exact sig. (2sided) exact sig. (1sided) pearson chi-square 18.328a 1 .000 continuity correctionb 16.489 1 .000 likelihood ratio 19.120 1 .000 fisher's exact test .000 .000 linear-bylinear association 18.125 1 .000 n of valid cases 90 chi-square statistics were used to examine association between categorical variables (seizure and ptbe). there is a significant association at 5% significance level between seizure and ptbe of respondents (χ2=,18.328, df=1, p=0.000). clinical data the preoperative clinical symptoms and signs (nonfocal) like;, headache, vomiting, mental change, memory disorder and cognitive decline, were found in most cases 92(59.7%) patients for group a”, while second presentation was focal neurological deficit (fnd), include; motor weakness, sensory , cranial nerves dysfunction, aphasia, were found in 78(50.6%). in this study, pre op seizure was the third presentation 65(42.2%), of these 32 patients were seizure was single presentation. for group b”, non-focal was first presentation and occurs in 59(65.5%) patients, followed; focal symptoms 36(40%) patients, then seizure was the third presentation 32(35.5%) patients of these 12(37.5%) patients were seizure was single presentation. clinical types of seizure in both groups was; complex partial in (158 patient, 64.8%), generalized tonic clonic (43 patients, 17.6%). simple partial (23 patients, 9.5%) and combined (20 patients, 8.1%). (figure1,2). focal neurological deficit were associated with reduced incidence of pre-op seizure, in both groups for group a,16 (24,6%) patients with seizure compared to 62(69.7%) patients without seizure, and group b, (7patients, 21.8% seizure vs, 29 patients, 50% without seizure). moreover, pre-op seizure was in 49.2% as a first presentation of disease compared to 50.2% for others in group a, and 37.5% vs 62.5 for group b”. a. 243 risk factors for preoperative seizures in meningiomas b. c. figure 1. a female patient aged 48 years, presented with fits, mental changes, and headache. (a) axial and (b) coronal t1 with contrast showing left middle falx meningioma type i, hemispheroid tumor invagination deeply into one hemisphere. (c) preoperative electroencephalography showing focal epileptiform activity in left parietal lobe. a. b. c. figure 2. (a) a female patient aged 65 years, presented with fits, headache, and vision impairment on right side (a) axial and (b) coronal t1 with contrast showing right medial sphenoid wing meningioma. (c) preoperative electroencephalography showingfocal epileptiform activity in right hemisphere. histopathological finding in our groups study (table 6), pathological finding was found; grade i were included 121 (78.6% ) cases,(seizure 80% vs 77.5% non-seizure), grade ii in 24(15.6%) cases, (seizure 13.8% vs 16.8% nonseizure) and grade iii in 9(5.8%) cases, (seizure 6.2% vs 5.7%% non-seizure) for group a. while for group b”, gr.i in 75(83.3%)cases, (seizure 87.5% vs 81% nonseizure), gradeii in 13(14.4%) cases, (seizure 12.5% vs15.5% non-seizure), grade iii in 2(2.3%) cases ,(seizure 0% vs 3.6% non-seizure). for both groups, meningothelial meningioma was the most common histopathological type, and angiomatous subtype had slightly higher occurrence of seizure 10(15.4%) cases compared to 5(5.6%) cases without seizure four group a. table 6. who grade grou pa group b no of case s 154 seiz ure 65 non seizu re89 no of case s90 seizu re 32 non seiz ure 58 who i meningi othelial 121 (78.6 %) 53 52(8 0%) 21 69(77 .5%) 32 75(83 .3%) 44 28(87 .5%) 15 47(8 1%) 29 fibroblas t 33 14 19 11 3 8 transitio nal 10 3 7 6 3 3 angioma tous 15 10 5 8 4 4 psammo matous 9 3 6 5 3 2 244 abdalrahman nassar, volodymyr smolanka, stydinyk taras et al. microcys t 1 1 1 1 who ii 24(15 .6%) 9(13 .8%) 15(16 .8%) 13(14 .4%) 4(12. 5%) 9(15 .5%) who iii 9(5.8 %) 4(6. 2%) 5 (5.7% ) 2(2.3 %) 2(3. 6%) discussion seizures are one of the three most common clinical symptoms besides (and after) headache and focal neurological deficit of patients with meningioma [33]. in the present study, we report the risk factors associated with preoperative seizures in different locations of supratentorial meningiomas. the occurrence of preop seizure for (nsbm) group “a” was slightly higher (42.2% patients) as compared to (sbm) group “b” (35.5% patients). gender distribution in our study in both groups showed that was no statistically significant relationship between gender and preoperative seizure. p=0.396 and p=0.445 respectively. similar results were reported by islim al et al [14] and chozick et al. [9]. the epileptic patients in group “a” have their tumor location mostly in frontal and temporal regions, however, there was no statistically significant relation between tumor related to brain lobes (site) and occurrence of a seizure, p=0638, also we could not find the difference between convexity and parasagittal/parafalcine for the occurrence of a seizure, p=0.503. while we observed an increase of seizure in swm and ogm compared to planum/tuberclum meningiomas and the relation was significant p=0.050 according to most studies addressing this question were reported different results,lieu et al. and das et al. [10,17] identified temporal. islimet al. [14] identified parietal meningiomas to be significantly associated with preoperative seizures. skardelly et al. [28] further identified parafalcine meningiomas to be significantly associated with preoperative seizures. kawaguchi et al.[15] who studied convexity meningioma found that there was a significant relationship between the seizure occurrence and tumor location. however, our result corresponds with other studies that were reported lacking significant relation between the seizure occurrence and tumor location and site. liigant et al.[18] found that a higher incidence of seizures was in tumors involving the frontoparietal (58%), frontotemporal (44%), and temporal (40%) regions but no significant association with tumor location. riva [24] and hess k, et al., [13] found no statistically significant relation between tumor site and occurrence of seizure. in our study, the distribution of tumor side in both groups showed that the left side was slightly higher than the right side, however, there was no statistically significant relationship between the side of the lesion and preoperative seizure, for both groups, (gr. “a”, p=0.836 and gr.” b”, p=0.702. our results were similar to what was reported by, lieu and howng [17]. moreover, tumor side and a number of lesions had no significant influence on preoperative seizure rate [9,14]. the distribution of tumor size in both groups showed that there was no statistically significant relation between tumor size and the occurrence of seizures. similar results were reported in three studies. [6,14,18]. in contrary to what was reported by other studies, were shown a positive correlation between tumor size and preoperative seizure rate [7,15,20,33]. here, we showed that ptbe may be the factor most strongly related to preoperative seizures for both groups: a” and” b”. (χ2=,15.356, p=0.000) and (χ2=,18.328, p=0.000), respectively. various studies in the past have reported a correlation between vasogenic edema and seizure occurrences. [6,11,15,33]. furthermore, lieu and howng[17], and kawaguchiet al.[15]reported that most patients with evident or severe edema, had preoperative and postoperative epilepsy with a significant correlation. despite primarily extra-axial locations, slow progression rates, and usually benign histological characteristics, meningiomas frequently are associated with ptbe [4]. ptbe, as assessed on ct scan, has been found to be associated with more than half of the cases [16]. though the exact mechanism involved in the development of ptbe is not known, several factors have been previously studied like tumour location and tumour volume, interleukin-6, sex hormone receptors and several others [1,2,21]. moreover, peritumoral edema fluid contains a high concentration of glutamate, which may trigger hyperexcitability and epileptogenesis [34]. the preoperative seizure was the third clinical symptom after non-focal and focal symptoms in both groups of patients respectively. moreover, the 245 risk factors for preoperative seizures in meningiomas pre-op seizure was in 49.2% as the first presentation of disease compared to 50.2% for focal and non-focal symptoms for the non-skull base, and 37.5% vs 62.5 for skull base meningiomas. in the literature review; it was reported that 19-63% of the patients with meningioma are suffered from preoperative seizures, and 35% of them experience epileptic seizures as the initial symptom [19]. in our data presence of preoperative neurologic deficits has been less frequently associated with preoperative seizures in both groups: group “a” patients,(seizure in 16 cases 24.6% vs 62 cases 69.7% non-seizure), group “b” patients, (seizure 7 cases, 21.8% vs 29 cases 50% without seizure). this is an unexpected finding. however, considering the increase in meningioma detection and widespread availability of neuroimaging [22], this may be explained by the diagnosis of the tumor prior to the occurrence of neurological deficits or just after a seizure attack. furthermore, by riva study (among seizure in intrinsic brain tumors), he reported that patients with seizures showed a significantly lower incidence of neurological deficit, headache, and mental disturbances compared with nonepileptic patients [24]. otherwise, careful analysis and further investigation are needed. the distribution of tumor histopathology in both groups showed that meningothelial meningioma was the most common histopathological type. while high grade (grii-iii) was higher in non-skull base (21.4%) than skull base (16.7%). despite the increased occurrence of pre-op seizure among angiomatous type, however, there was no relation between the different histopathological types and occurrence of seizure. kawaguchiet al. [15] believed that fibroblastic meningiomas were significantly correlated with preoperative seizures. skardelly et al. demonstrated an increase of preoperative seizures from who gr. ii and gr.iii [28] chowet al.[8]showed that the histologic types were not significantly correlated with preoperative seizure. moreover, in other studies did not have a significant influence on pre-or postoperative seizure rate [5,9]. conclusion we identified that the major risk factor for pre-op seizure in both groups study is ptbe, and location for skull base meningiomas, where the planum/tuberculum lesser overall risk for pre-op seizure. there was a trend for the occurrence of preoperative seizure among (male gender in skull base and female gender in non-skull base), frontal, temporal, left side, and size <5 cm and angiomatous subtype, however, these predictors were statistically insignificant. the factor associated with preoperative seizures were the absence of preoperative neurologic deficit for both groups. careful analysis and further investigation are needed. abbreviations swm: sphenoid wing meningiomas; ogm: olfactory groove meningioma; ct: computer tomography; mri: magnetic resonance imaging; ptbe: peritumoral brain oedema; fnd: focal neurological deficit; who: world health organization; cns: central nervous system; sbm: skull base meningioma; nsbm: non-skull base meningioma; eeg: electro encephalo graphy; cs: cavernous sinus. references 1. benzel ec, gelder fb. correlation between sex hormone binding and peritumoral edema in intracranial meningiomas. neurosurgy. 1988; 23:169–74. 2. bitzer m, opitz h, popp j, morgalla m, gruber a, heiss e, voigt k. angiogenesis and brain oedema in intracranial meningiomas: influence of vascular endothelial growth factor. acta neurochir (wien).1998;140:333–40. 3. black pm (1993) meningiomas. neurosurgery 32:643–657 4. bradac gb, ferszt r, bender a, schorner w. peritumoral edema in meningiomas : a radiological and histological study. neuroradiology.1986; 28: 304-312. 5. brennan cw, verhaak rgw, mckenna a, campos b, noushmehr h, salama sr, et al. the somatic genomic landscape of glioblastoma. cell 2013;155:462–77. https://doi. 6. chaichana kl, pendleton c, zaidi h, olivi a, weingart jd, gallia gl, et al. seizure control for patients undergoing meningioma surgery. world neurosurg 2013;79:515-524. 7. chen wc, magill st, englot dj, baal jd, wagle s, rick jw, et al. factors associated with preand postoperative seizures in 1033 patients undergoing supratentorial meningioma resection. neurosurgery 2017;81:297–306. https://doi.org/10.1093/ neuros/nyx001. 8. chow sy, hsi ms, tang lm, fong vh. epilepsy and intracranial meningiomas. zhonghua yi xue za zhi (taipei) 1995;55:151-5. 9. chozick bs, reinert se, greenblatt sh. incidence of seizures after surgery for supratentorial meningiomas: a 246 abdalrahman nassar, volodymyr smolanka, stydinyk taras et al. modern analysis. j neurosurg 1996;84:382–6.https:// doi.org/10.3171/jns.1996.84.3.0382. 10. das rr, artsy e, hurwitz s, wen py, black p, golby a, et al. outcomes after discontinuation of antiepileptic drugs after surgery in patients with low grade brain tumors and meningiomas. j neurooncol 2012;107:565–70. 11. englot dj, berger ms, chang ef, garcia pa: characteristics and treatment of seizures in patients with high-grade glioma: a review. neurosurg clin n am 23:227–235, vii– viii, 2012 12. fang s, zhan y, xie yf, shi q, dan w. predictive value of electrocorticography for postoperative epilepsy in patients with supratentorial meningioma. j clin neurosci 2013; 20:112-6. 13. hess k, spille dc, adeli a, sporns pb, brokinkel c, grauer o, et al. brain invasion and the risk of seizures in patients with meningioma. j neurosurg 2018:1–8.https:// doi.org/10.3171/2017.11.jns172265. 14. islim ai, ali a, bagchi a, ahmad mu, mills sj, chavredakis e, et al. postoperative seizures in meningioma patients: improving patient selection for antiepileptic drug therapy. j neurooncol 2018;0:0. https://doi.org/10.1007/s11060-018-2941-2. 15. kawaguchi t, kameyama s, tanaka r. peritumoral edema and seizure in patients with cerebral convexity and parasagittal meningiomas. neurol med chir (tokyo) 1995;36:564–8. 16. kim is, kim hd, kim ku, shin hc, choin hj, kim kh. factors influencing the development of peritumoral brain edema in menigiomas. j korean neurosurg soc.1997;26:940-5. 17. lieu as, howng sl. intracranial meningiomas and epilepsy: incidence, prognosis and influencing factors. epilepsy res 2000;38:45-52. 18. liigant a, haldre s, oun a, linnamägi u, saar a, asser t, et al. seizure disorders in patients with brain tumors. eur neurol 2001;45:46-51. 19. longstreth wt jr, dennis lk, mcguire vm, drangsholt mt, koepsell td. epidemiology of intracranial meningioma. cancer1993;72(3):639-48. 20. odebode to, akang ee, shokunbi mt, malamo ao, ogunseyinde ao. factors influencing visual and clinical outcome in nigerian patients with cranial meningioma. j clinneurosci2006;13:649–54. https://doi.org/10.1016/j.jocn.2005.07.023org/10.1016/j. cell.2013.09.034. 21. park kj, kang sh, chae ys, yu mo, cho th, suh jk, et al. influence of interleukin-6 on the development of peritumoral brain edema in meningiomas. j neurosurg. 2010;112:73–80. 22. porter kr, mccarthy bj, freels s, et al: prevalence estimates for primary brain tumors in the united states by age, gender, behavior, and histology. neuro oncol 12:520-7, 2010 23. reinert m, babey m, curschmann j, vajtai i, seiler rw, mariani l. morbidity in 201 patients with small sized meningioma treated by microsurgery. acta neurochir. 2006;148(12):1257–1265; discussion 1266. 24. riva m. brain tumoral epilepsy: a review. neurol sci 2005;26 suppl 1:s40-2. 25. rudà r, trevisan e, soffietti r: epilepsy and brain tumors. curr opin oncol 22 :611–620, 2010 26. sanai n, polley my, berger ms. insular glioma resection: assessment of patient morbidity, survival, and tumor progression. j neurosurg. 2010;112(1):1–9. 27. sanai n, sughrue me, shangari g, chung k, berger ms, mcdermott mw. risk profile associated with convexity meningioma resection in the modern neurosurgical era. j neurosurg. 2010;112(5): 913–919. 28. skardelly m, rother c, noell s, behling f, wuttke tv, schittenhelm j, et al. risk factors of preoperative and early postoperative seizures in patients with meningioma: a retrospective single-center cohort study. world neurosurg 2017;97:538–46. https:// doi.org/10.1016/j.wneu.2016.10.062. 29. taphoorn mj, klein m: cognitive deficits in adult patients with brain tumours. lancet neurol 3:159–168, 2004 30. tomasello f. meningiomas and postoperative epilepsy: it is time for a randomized controlled clinical trial. world neurosurg 2013;79:431-2. 31. vanbreemen msm,wilms eb, vecht cj. epilepsy in patients with brain tumours: epidemiology, mechanisms, and management. lancet neurol 2007;6:421–30. https:// 32. wiemels j, wrensch m, claus eb: epidemiology and etiology of meningioma. j neurooncol 99:307–314, 2010 33. xue h, sveinsson o, bartek j, förander p, skyrman s, kihlström l, et al. long-term control and predictors of seizures in intracranial meningioma surgery: a population-based study. acta neurochir 2018;160:589– 96. https://doi.org/10.1007/s00701-017-3434-3. 34. zheng z, chen p, fu w, zhu j, zhang h, shi j, et al. early and late postoperative seizure outcome in 97 patients with supratentorial meningioma and preoperative seizures:a retrospective study. j neurooncol 2013;114:101-9. doi: 10.33962/roneuro-2020-070 craniopharyngioma and arteriovenous malformation operated using the same craniotomy. an unusual case burak eren, feyza karagöz güzey, i̇lker gülec romanian neurosurgery (2020) xxxiv (1): pp. 437-440 doi: 10.33962/roneuro-2020-070 www.journals.lapub.co.uk/index.php/roneurosurgery craniopharyngioma and arteriovenous malformation operated using the same craniotomy. an unusual case burak eren, feyza karagöz güzey, i̇lker gülec health sciences university, bagcilar training and research hospital, department of neurosurgery, istanbul, turkey abstract craniopharyngiomas (cps) are rare benign epithelial tumours. brain arteriovenous malformations (avms) are also rare lesions occurring in young adults. the appearance of both these lesions in the same patient is rare. a 42-year-old patient presented with headaches for 3 months and a progressive decrease in his visual acuity. bitemporal hemianopsia was detected in the visual field. magnetic resonance imaging (mri) revealed a tumour with cystic and solid components located in the suprasellar region and avm in the right temporal lobe. avm (martin–spetzler grade iii) was visualised using digital subtract angiography (dsa), which was fed from the right middle cerebral artery and drained through the sigmoid sinus via the inferior petrosal sinus. the patient was operated with enlarged right frontotemporal craniotomy. avm nidus was totally removed at the first operation. embolisation was not preferred before the avm surgery. after 3 days, sylvian dissection was performed using the same craniotomy. the tumour was completely removed via the carotid cistern by making sharp dissection from the infundibulum. post-operatively, the patient showed normal neurological examination and significant improvement in his visual field examination. there was no residual/recurrent tumour or avm on contrast-enhanced mri and dsa at post-operative 6 months. histopathological examination revealed avm in the first operative material and papillary-type cp in the second. the coexistence of these two rare pathologies has previously been reported in only one patient. this is the first case of surgical resection of cp and avm using the same craniotomy. introduction craniopharyngiomas (cps) are rare benign epithelial tumours with slow growth. they account for 2%–5% of intracranial tumour primers, with an incidence of 0.5–2.0 billion per year.7 the bimodal age distribution peaks between 0 and 19 and 40 and 79 years of age.20 while complete improvement can be achieved with radical resection of cp, high recurrence rates have been reported for partial resection.1 brain arteriovenous malformations (avms) are also rare lesions that usually occur in young adults. the prevalence of avms in the population is 10–18 per 100,000 adults.11 morphologically, in avm, a vascular mass can be observed, with direct blood flow between the arterial and venous keywords arteriovenous malformation, avm, craniopharyngioma corresponding author: burak eren health sciences university, bagcilar training and research hospital, department of neurosurgery, istanbul, turkey drburakeren@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 438 burak eren, feyza karagöz güzey, i̇lker gülec circulation without a true capillary bed. generally, the high current feeder consists of the arteries, nidus and drainage veins.3 the coexistence of these two rare pathologies has previously been detected using radiology in only one patient. however, we presented the first case of simultaneous occurrence of cp and avm in the same patient who was then treated with surgical resection. case report a 42-year-old patient was referred to our clinic with persistent headache for 3 months and a time-lapse decrease in visual acuity. on magnetic resonance imaging (mri), a 32 × 26 × 24-mm tumour with cystic and solid components extending from the supracellular region to the third ventricle was detected. at the same time, avm of size 36 × 28 × 24 mm was observed in the right temporal lobe. avm (martin–spetzler grade iii) was seen in the patient’s brain digital subtract angiography (dsa), which was fed from the right mild cerebral artery (mca), with no aneurysm in the nidus, and sigmoid sinus was drained via the inferior petrosal sinus (figure 1). bitemporal hemianopsia was detected in the visual field of the patient. the patient then underwent an enlarged right frontotemporal craniotomy. the avm nidus on the temporal basal was totally removed. embolisation was not preferred before the surgery. as the duration of the first operation was relatively long, it was decided to perform cp surgery in the next session. after 3 days, sylvian dissection was performed using the same craniotomy. the cyst was aspirated by passing through the carotid cistern. the tumour was totally removed by making a sharp dissection from the infundibulum. after the surgeries, the patient was placed in intensive care for 1 day. his general condition was good, and his neurological examination was normal. however, diabetes insipidus developed after cp surgery. nasal desmopressin therapy was therefore started but was discontinued after 1 month. the patient showed normal levels of pituitary hormones and no hypothalamic obesity. an improvement was noted in his visual field examination. there was no evidence of residual/recurrent tumour or avm on contrastenhanced mri and dsa during the early postoperative period and at 6-month follow-up (figure 2). histopathological examination the resected tissue was fixed in 10% formalin, embedded in paraffin and stained with haematoxylin–eosin (h&e). in the first surgical material, vessels of different sizes and a lesion composed of the gliotic brain tissue was detected. some of the existing vessels consisted of small-sized, thick-walled arteries, whereas others included larger lumens surrounded by hyalinised veins. these findings were compatible with those of avm. the second operative material showed a welldifferentiated, non-keratinised squamous epithelium papillary-type cp (pcp) around a partially oedematous fibrovascular stroma. calcification was not observed (figure 3). figure 1. (a) axial, (b) coronary contrast t1 and (c) sagittal t2 mri sections showing cystic tumour in the midline, extending to the third ventricle, and a right temporal avm. (d) a-p, (e) lateral (f) and oblique right internal carotid artery dsa images showing avm from the right mca, with no aneurysm in the nidus, and draining of the sigmoid sinus via the inferior petrosal sinus. avm, arteriovenous malformation; dsa, digital subtract angiography; mca, mild cerebral artery; mri, magnetic resonance imaging. figure 2. post-operative (a) a-p, (b) lateral (c) and oblique right internal carotid dsa images. no avm can be seen. postoperative (a) axial, (b) coronary (c) and sagittal contrast t1 mr images showing total resection of both the tumour and avm. 439 craniopharyngioma and avm avm, arteriovenous malformation; dsa, digital subtract angiography. figure 3. (a) malformed, randomly distributed vessels, both in the veins and arteries, separated by variable amounts of intervening brain parenchyma (h&e, ×40). (b) h&e, ×100.and (c) papillary, cauliflower-like appearance, with surface epithelium covering the fibrovascular cores (h&e, ×20). (d) nonkeratinising, well-differentiated squamous epithelium surrounding the fibrovascular stromal cores (h&e, ×100). h&e, haematoxylin and eosin staining. discussion vascular malformations of the abnormal arteries and veins are usually congenital. they can appear at any age but are often diagnosed between 20 and 40 years of age. the clinical symptoms of avm depend on its location. the most common symptoms include headache and seizures, but at least 15% of patients are asymptomatic. every year, more than half of avm cases are referenced with intracranial haemorrhages, constituting to approximately 2% of the total haemorrhagic stroke cases.2,6,8 the methods used for the specific treatment of avm include endovascular embolisation and surgery or gamma knife treatment.4 in this study, we preferred to employ only surgical resection as the treatment approach. it is assumed that cps are histologically of two subtypes: adamantinomatous (acp) and papillary (pcp). acp is the more common type and is characterised by necrotic debris, cystic and/or solid components, fibrous tissues and calcification (more frequent in children). infiltration is also common in the neighbouring brain tissue. pcp mostly occurs in adults, with 14%–50% of adult cases and only 2% of paediatric cases. pcp is characterised by the presence of a solid component or a combination of solid and cystic components. the cystic content is usually yellow and viscous, with rare calcification. pcp is generally well-defined, and infiltration into the neoplastic epithelium of the neighbouring brain tissue is minimal or even absent.10, 13 the patient’s pathological findings indicated pcp, and its dissection from the surrounding tissues was easy during the surgery. the clinical symptoms of cps are related to hypothalamic/pituitary deficiencies, visual impairment and increased intracranial pressure. the preferred treatment is complete resection which is carefully performed so as to preserve the optic and hypothalamic functions.15 post-operatively, in our patient, visual impairment decreased and hypothalamic dysfunction was not observed. in their meta-analysis, dandurand et al.7 compared the gross total resection of cps with subtotal resection followed by adjuvant radiotherapy and found that the lowest recurrence rate was achieved with gross total resection. in our patient, gross total resection of cp was performed, and no recurrence was observed at the first 6-month follow-up. endoscopic trans-sphenoidal approach is the most preferred method for cp surgeries, which involves a pterional approach.18 we prefer endoscopic trans-sphenoidal approach only if the patient is a candidate for cp surgery. however, an extended pterional approach was preferred in this case, considering that both the lesions could be resected using a single craniotomy flap. whether there exists any association between the formation of vascular malformations and development of intracranial meningiomas needs to be discussed. rare cases of vascular malformations with primary brain tumours have been previously reported. in the literature, avm has been reported mostly in association with oligodendrogliomas and astrocytomas.12,17,19pleomorphic xanthoastrocytoma 16, meningioma9 and ganglioneuroma5 have also been reported with avm. mori et al.14 were the first to report avm and cp in patients, which were detected radiologically. however, these patients had only cp resections and were following avm. our patient is the first case in whom both the lesions were completely excised. the occurrence of primary brain tumour in association with cerebral avm has been reported. 440 burak eren, feyza karagöz güzey, i̇lker gülec however, the simultaneous occurrence of cp and avm in a patient is extremely rare. references 1. al-mefty o, ayoubi s, kadri pa. the petrosal approach for the total removal of giant retrochiasmatic craniopharyngiomas in children. j neurosurg. 2007;106(2 suppl):87-92. 2. al-shahi r, warlow c. a systematic review of the frequency and prognosis of arteriovenous malformations of the brain in adults. brain 2001;124:1900-1926. 3. arteriovenous malformation study group. arteriovenous malformations of the brain in adults. n engl j med 1999;340:1812–1818. 4. bradac o, charvat f, benes v. treatment for brain arteriovenous malformation in the 1998-2011 period and review of the literature. acta neurochir (wien) 2013;155:199-209. 5. chovanes gi, truex rc jr. association of a ganglioneuroma with an arteriovenous malformation: case report. neurosurgery. 1987;21(2):241-243. 6. da costa l, wallace mc, ter brugge kg, o’kelly c, willinsky ra, tymianski m. the natural history and predictive features of hemorrhage from brain arteriovenous malformations. stroke 2009;40:100-105. 7. dandurand c, sepehry aa, asadi lari mh, akagami r, gooderham p. adult craniopharyngioma: case series, systematic review, and meta-analysis. neurosurgery. 2017. doi: 10.1093/neuros/nyx570. 8. hernesniemi ja, dashti r, juvela s, vaart k, niemela m, laakso a. natural history of brain arteriovenous malformations: a long-term follow-up study of risk of hemorrhage in 238 patients. neurosurgery 2008; 63:823829; discussion 829-831. 9. honeybul s. coexistence of an intracranial meningioma and an arteriovenous malformation. j surg case rep. 2015. doi: 10.1093/jscr/rjv061. 10. karavitaki n, cudlip s, adams cb, wass ja.: craniopharyngiomas. endocr rev. 2006;27(4):371–97. 11. kim h, marchuk da, pawlikowska l, chen y, su h, yang gy, young wl. genetic considerations relevant to intracranial hemorrhage and brainarteriovenous malformations. acta neurochir suppl. 2008;105:199-206. 12. lai g, muller ka, carter bs, chen cc. arteriovenous malformation within an isocitrate dehydrogenase 1 mutated anaplastic oligodendroglioma. surg neurol int. 2015;6(suppl 9):295-299. 13. larkin sj, ansorge o: pathology and pathogenesis of craniopharyngiomas. pituitary. 2013;16(1):9–17. 14. mori k, handa h, murata t, ishikawa m, takeuchi j, osaka k. craniopharyngiomas with unusual topography and associated with vascular pathology. acta neurochir (wien). 1980;53(1-2):53-68. 15. muller hl. craniopharyngioma. endocr rev. 2014, 35(3):513–543. 16. nagańska e, matyjae, puckoe, ząbekm. the coexistence of pleomorphic xanthoastrocytoma and arteriovenous malformation. a case report. folia neuropathol. 2013;51(3):269-74. 17. nazek m, mandybur ti, kashiwagi s. oligodendroglial proliferative abnormality associated with arteriovenous malformation: report of three cases with review of the literature. neurosurgery. 1988;23(6):781-785. 18. prieto r, pascual jm, rosdolsky m, barrios l. preoperative assessment of craniopharyngioma adherence: magnetic resonance imaging findings correlated with the severity of tumor attachment to the hypothalamus. world neurosurg. 2018;110:e404-e426. doi: 10.1016/j.wneu.2017.11.012. 19. yano, h. , nakayama, n. , ohe, n. , takagi, t. , shinoda, j. and iwama, t. surgical strategy in case with co-existence of malignant oligodendroglioma and arteriovenous malformation: a case report. case reports in clinical medicine 2013;2:473-478. doi: 10.4236/crcm.2013.28125. 20. zacharia be, bruce ss, goldstein h, malone hr, neugut ai, bruce jn. incidence, treatment and survival of patients with craniopharyngioma in the surveillance, epidemiology and end results program. neuro oncol. 2012;14:1070-1078. doi: 10.33962/roneuro-2022-032 practical concepts in the identification of bilateral chronic subdural hematoma c.d. diaz-arroyo, a.e. diaz-arroyo, t.y. carrero-barragán, m.c. gamboa-perdomo, j.a. boada-garnica, a. correa-molina, j.a. trigos-garcía, g. dominguez-alvarado, m.g. ortega-sierra, m.p. bolaño-romero, a. pacheco-hernandez romanian neurosurgery (2022) xxxvi (2): pp. 175-180 doi: 10.33962/roneuro-2022-032 www.journals.lapub.co.uk/index.php/roneurosurgery practical concepts in the identification of bilateral chronic subdural hematoma c.d. diaz-arroyo1, a.e. diaz-arroyo1, t.y. carrero-barragán2, m.c. gamboa-perdomo2, j.a. boada-garnica3, a. correa-molina4, j.a. trigos-garcía5, g. dominguez-alvarado6, m.g. ortega-sierra7, m.p. bolaño-romero8, a. pacheco-hernandez9 1 cirugia y endoscopia research group, school of medicine, university of cartagena, cartagena, colombia 2 grupo de innovación e investigación en cirugía, school of medicine, universidad industrial de santander, bucaramanga, colombia 3 department of medicine, hospital santa ana de muzo, muzo, boyacá, colombia 4 department of medicine, universidad cooperativa de colombia, colombia 5 department of medicine, hospital de san francisco de gachetá, colombia 6 grupo de innovación e investigación en cirugía, semillero de innovación e investigación quirúrgica, bucaramanga, colombia 7 department of neurosurgery, universidad centroccidental lisandro alvarado hospital central antonio maría pineda, barquisimeto, venezuela 8 grupo prometheus y biomedicina aplicada a las ciencias clínicas, school of medicine, universidad de cartagena, cartagena, colombia 9 colombian clinical research group in neurocritical care, latin american council of neurocritical care, cartagena, colombia abstract bilateral chronic subdural hematoma is a neurosurgical pathology whose incidence in older adults has been increasing, as a consequence of the ageing of the population, added to the factors that are linked to it. neurosurgical diseases with chronic evolution generate a high burden of disease due to morbidity, disability, mortality and health costs associated with reinterventions and rehabilitation. for this reason, the interest in this disease has been increasing, also justified by the little information there is about it, unlike unilateral chronic subdural hematomas, although it has been described that both may have pathophysiological similarities that help to understand them. keywords chronic subdural hematoma, trauma, central nervous system diseases, narrative review corresponding author: michael gregorio ortega-sierra department of neurosurgery, universidad centroccidental lisandro alvarado hospital central antonio maría pineda, barquisimeto, venezuela mortegas2021@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 176 c.d. diaz-arroyo, a.e. diaz-arroyo, t.y. carrero-barragán et al. introduction the average age of the population has been increasing and with it are associated several pathologies to which the elderly population is exposed, as well as environmental factors [1]. chronic subdural hematomas (csdh) are one of the most frequent conditions seen in the population over 65 years of age, however, there are several factors that may predispose to this disease [2,3]. bilateral csdh are collections of blood degradation products located between the dura mater and arachnoid, and the denomination of chronicity is given by the amount of time elapsed, which is between 2 or 3 weeks [2,4,5,6,7,8]. it has been described as a pathology that differs from unilateral hematomas in the form of clinical presentation and the rapidity with which it can progress and lead patients to marked deterioration if timely treatment is not carried out [9]. pathophysiologically, bilateral csdhs have no clear difference from their unilateral counterparts [9]. the treatment of choice is surgical and ranges from craniotomies and endoscopic treatment to yl-1 type hematoma needle aspiration [4]. based on the above, the objective of this review is to present practical concepts on the identification and approach to chronic bilateral subdural hematoma. epidemiological focus of the disease the incidence rate of bilateral csdh ranges from 1-5 cases per 100,000 person-years to 7.4 per 100,000 in the elderly population [10–13]. the most frequent location of csdh is supratentorial, as opposed to the posterior fossa, whose diagnosis and pathogenesis are poorly understood [14]. likewise, the average age of patients diagnosed with csdh has been found to range from approximately 62 to 74 years, and, in the case of bilateral csdh, a study by cheng et al found that the average age of patients was 79 years [2]. predisposing factors of csdh unlike acute subdural hematomas (acute-sdh), csdh are poorly associated with head trauma [2,15]. despite this, trauma is considered to be the primary cause, as it has been reported to be associated with csdh in 50-80% of cases [2]. on the other hand, antiplatelet and anticoagulant therapies, in addition to alcohol abuse, liver disease, renal disease in hemodialysis patients, and intracranial hypotension associated with ventricular shunt valves have been linked to the development of hematoma [2,3,5]. pathophysiology of csdh in contrast to unilateral csdh, the pathophysiology of bilateral csdh is still unknown [9]. however, hypotheses and premises have been established as to what may be occurring, such as the involvement of the bridging veins [9,10]. when bilateral csdh is present in the posterior cerebral region, blood deposition may be involved with the occipital, sigmoid and transverse sinuses [14]. the development and progression of the hematoma is gradual and slow, initially constituting a thick outer membrane around the hematoma that eventually results in a complete capsule about two weeks later [15], which requires cell proliferation for the formation of a collagen-rich granular tissue [5]. on the other hand, the increase in hematoma size may be related to the increased permeability of capillaries in the outer membrane of the hematoma, which consequently lead to high blood extravasation and plasma exudation [11]. in addition, there is localized inflammation characterized by increased fibrinolysis, release of tissue plasminogen activator and elaboration of angiogenic factors that promote neovascularization [5]. clinical presentation of csdh and its diagnosis the form in which csdh manifests itself is very variable and can even be confused with other more frequent entities such as stroke, parkinson's disease, dementia, among others [3,5]. in general, cognitive impairment, headache, and motor deficits are the most common presenting symptoms [3,5,13], although patients have also been shown to manifest nausea, vomiting, mental changes, and convulsions. in a study by huang y. et al. in which 25 of the 98 people evaluated had bilateral csdh, it was observed that headache and mental changes were the most common presenting symptoms, followed by nausea and finally seizures [16]. however, because csdhs present in most cases with unilateral convexity [16], many studies have relied on the comparison of several clinical features between the two presentations in order to analyze the point differences in the frequency of presentation of a symptom, or other feature, between unilateral and bilateral csdhs [13,16,17]. in a study by agawa et al. it was observed that 177 practical concepts in the identification of bilateral chronic subdural hematoma symptoms such as headache, pupil abnormalities, and acute impairment of consciousness occurred more frequently in patients with bilateral csdh, while hemiparesis occurred more frequently in patients with unilateral csdh [13]. likewise, in the study by huang y. et al. it was observed that hemiparesis is more frequently seen in patients with unilateral csdh since, in the case of patients with bilateral csdh, there is a lower possibility of the central brain structures being deflected due to the counterbalance of the mass effect on both sides, which is reflected in the radiological findings that showed a lower incidence of midline changes with respect to unilateral [16]. on the other hand, as mentioned above, csdh are often confused with other diseases, so it is of utmost importance to be really informed about the symptomatology of pathologies with similar clinical presentation to csdh, in order to be able to make the differential diagnosis together with other complementary diagnostic tests [5,16]. over the years, cases have been reported in the literature on patients with bilateral csdh presenting with isolated oculomotor nerve palsy, which is a rare symptom in the atypical clinical presentation of this pathology, as it is commonly associated with vascular disorders, posterior circulation aneurysms or with traumatic, inflammatory or neoplastic diseases [7,18]. corrivetti et al, by 2016, published two case reports, one of them was about an 81-year-old patient with diabetes and on anticoagulant management who was referred to the hospital with headache and left palpebral ptosis, on physical examination he showed complete oculomotor nerve palsy and mydriasis, and his computed tomography (ct) scan showed bilateral csdh. he subsequently underwent bilateral surgical evacuation and then, 24 hours after surgery, the ptosis had disappeared and the mydriasis gradually improved [7]. based on the above, the authors refer that having at least one predisposing factor (diabetes mellitus, hypertension, among others) generates a nervous vulnerability, which is necessary but not sufficient to develop this symptom, in this way, it is suggested that the bilateral pressure exerted on both cerebral hemispheres causes a displacement of the posterior part of the brain causing a compression of the encephalic trunk and this, added to the cisternal compression and the narrow vascular corridor through which the oculomotor nerve passes, stretches and flattens the nerve leading to a nervous alteration [7,18]. on the other hand, guppy et al, by 2017, reported a rare case of a patient with an abnormal gait, where it was initially thought to be cervical myelopathy due to stenosis, however, he also presented parkinson'slike symptoms (decreased facial expression, random gait and stooped posture) so a ct scan was requested which subsequently showed bilateral csdh. after drainage of the csdhs the symptoms improved, with bilateral csdh and cervical stenosis being the final diagnosis [19]. finally, in order to confirm csdh and to make the definitive diagnosis, patients usually undergo ct or mri [10,11]. therapeutic approach because bilateral csdh usually occur in the elderly population with other comorbidities such as coagulation disorders, and because of their rapid clinical evolution compared to unilateral csdh, it is of vital importance that they are detected early in order to be treated as efficiently and promptly as possible [3,5]. therefore, two types of treatments have been proposed, which are classified into nonsurgical procedures, such as the use of steroids or mannitol, which require a longer recovery time for symptoms and a prolonged hospital stay [3], and surgical procedures (surgical drainage), the latter being the best therapeutic alternative due to its wide range of procedures and the low morbimortality it represents [3,11]. to evaluate the patient's neurological status, the clinical severity of csdh and the post-surgical evolution, the markwalder classification system is used, with a scale ranging from grade 0 to 4, the higher the grade, the worse the patient's clinical situation [3,20]. the decision to surgically treat a bilateral csdh, should be subject to two circumstances which are the clinical manifestations and the radiological findings which include the presence of a mass effect or a midline shift [5,16]. it is generally accepted that symptomatic patients should undergo surgery because surgical evacuation produces an immediate recovery and a favorable evolution in a high percentage of patients [5]. for surgery, neurosurgeons have proposed several surgical techniques such as small craniotomy with endoscopic removal, burr craniotomy with or without continuous drainage of the closed system, large craniotomy followed by hematoma removal 178 c.d. diaz-arroyo, a.e. diaz-arroyo, t.y. carrero-barragán et al. with membranectomy, cranial drilling (twist-drill), and others [5,11,21]. indications for craniotomy include the presence of any clot causing symptomatology with or without failed conservative or less invasive management, evidence of radiographic progression during a time of conservative observation, and, in addition, craniotomy should be considered in cases of recurrence despite previous surgery or when there are clots with evidence of membranes that may inhibit evacuation [20]. on the other hand, it has been shown that some patients are treated surgically by auger punctures on the side of the subdural hematoma along with irrigation of the subdural space with normal saline, in addition to performing drainage of the closed system by silicone tubes that are removed after the drainage has slowed or stopped, or removal of the hematoma has been confirmed by postoperative ct scanning [10,11,16]. in addition, some patients with coagulation disorders who use anticoagulants as therapy have been shown to have vitamin k, fresh frozen plasma or prothrombin complex administered prior to surgery as a preoperative indication [5,13]. complications recurrence is the most common complication of csdh with an incidence that can vary from 0% to 31.6% depending on the surgical technique [22,23]. recurrence is defined as re-accumulation of the hematoma with progressive neurological deficit and represents the main problem after initial trephination because about 20% of patients require at least one re-intervention [22]. a higher recurrence rate has been reported in patients with bilateral csdh compared to patients with unilateral csdh [23]. in some cases of bilateral csdh, when the contralateral hematoma is asymptomatic and thin, trephination surgery is only performed in one side [24]. up to 20% of these cases may require evacuation of the contralateral hematoma due to subsequent enlargement and appearance of symptoms after a certain period of time [24,25]. the pathophysiology of this complication is not fully understood [22], but in conjunction with bilateral hematoma, many factors have been proposed as predictive of postsurgical recurrence of csdh [24], such as use and reinitiation of antiplatelet or anticoagulant therapy [22], postoperative midline shift, preoperative hematoma size, mean hematoma density, diabetes mellitus, and postoperative air harvesting [24]. hematomas that are hypointense or isointense on preoperative mri on the t1 sequence correlate with a high recurrence rate, because it may reflect intracellular deoxyhemoglobin, signifying relatively recent bleeding [24]. craniostomy with trephination is a simple surgical procedure; however, postoperative bleeding is another well-known and devastating complication. in a study of 303 patients with csdh, the incidence of acute postoperative intracranial hemorrhage was estimated to be approximately 4.57% [23]. it was initially attributed to hypertension and anticoagulation therapy in some patients, but later other mechanisms were discussed [22]. it was mainly attributed to a loss of autoregulation of blood vessels with subsequent hypertension and cortical hyperaemia following rapid brain shift after surgery with excessive drainage of the subdural space and hypoperfusion syndrome [22,23]. more studies are needed to be certain about the treatment of acute postoperative bleeding, but many authors recommend slow brain decompression to prevent rapid intracranial changes [22]. infections are a rare complication of csdh that can lead to subdural empyema [22,26]. a preexisting subdural hematoma can become infected through hematogenous infection, although the actual incidence rate of this complication is less than 1% of cases [26]. if suspected, it should be investigated with computed tomography as first-line imaging and as treatment, trephination lavage and craniotomy with complete evacuation of the hematoma have been proposed as surgical adjuncts to systemic antibiotic therapy [22,26]. the development of seizures or status epilepticus following csdh evacuation is a complication with an overall incidence ranging from 1% to 23% [22,27]. risk factors associated with the development of chronic hematomas are alcohol abuse, change of mental status, previous stroke, and hematoma density on ct scan [27,28]. in this order of ideas, it is necessary to produce more evidence of better quality on the global epidemiology, pathophysiology and management of bilateral chronic subdural hematoma, considering that it is a pathological condition that generates neurological disease burden. similarly, training in their suspicion and identification, to promote 179 practical concepts in the identification of bilateral chronic subdural hematoma professionalism and practice in neurosurgery at the different levels of care. it is necessary to know data from lowand middle-income countries, where there are difficulties in the management of pathologies such as these, due to the absence of specialized centers in rural regions [29,34]. especially in the pandemic and post-pandemic period where funding for research in lines other than emerging infectious diseases has been lost [35-37]. conclusions it is important to recognize the differences in presentation between unilateral and bilateral csdh, as well as with other pathologies of similar presentation that do not require urgent imaging methods, as this may confuse the diagnosis and delay treatment. bilateral hematoma tends to involve greater mass displacement than unilateral hematoma and reduces the autonomic capacity to buffer increased intracranial pressure, making it even more important to implement early surgical decompression of bilateral mass lesions in order to prevent rapid neurological deterioration. healthcare professionals should be aware of the higher incidence of recurrence in patients with bilateral treatment, the risk factors and signs for early detection of recurrence, as well as other complications that, although of lower incidence, represent a risk for patient survival. references 1. castro-rodríguez c, román-pena p, arán-echabe e, gelabert-gonzález m. hematoma subdural crónico en pacientes muy ancianos. rev esp geriatr gerontol. 2016; 51(6):309–16. 2. hsieh c, su i, hsu s, huang c, lian f, chang c. chronic subdural hematoma: differences between unilateral and bilateral occurrence. j clin neurosci. 2016; 34(2016):252– 8. 3. gelabert-gonzález m, arán-echabe e, bandín-diéguez fj, santín-amo jm, serramito-garcía r, prieto-gonzález á, et al. hematoma subdural crónico bilateral: análisis de una serie de 190 pacientes. neurocirugia. 2016; 27(3):103–11. 4. chen l, dong l, wang xd, zhang hz, wei m, she l. bilateral chronic subdural hematoma treated by yl-1 type hematoma aspiration needle complicated by hemorrhage of the basal ganglia and brainstem. world neurosurg. 2017; 97:761.e11-761.e13. 5. gelabert-gonzález m, rico-cotelo m, arán-echabe e. chronic subdural hematoma. med clínica (english ed). 2015; 144(11):514–9. 6. daniel r, servadei f. 45 complications after surgery for chronic subdural hematomas. complications in neurosurgery. elsevier inc; 2018. 274–279. 7. corrivetti f, moschettoni l, lunardi p. isolated oculomotor nerve palsy as presenting symptom of bilateral chronic subdural hematomas: two consecutive case report and review of the literature. world neurosurg. 2016; 88:686.e9-686.e12. 8. goodman jc. 338 neuropathology of traumatic brain injury. seventh edition. youmans and winn neurological surgery, 4-volume set. elsevier inc.; 2018. 2765-2777.e2. 9. huang y, yang k, lee t, liao c. bilateral chronic subdural hematoma: what is the clinical significance? int j surg. 2013; 11(7):544–8. 10. park hs, park es, park jb, kwon sc, lyo iu, kim m, et al. chronic subdural hematomas: comparison between unilateral and bilateral involvement. korean j neurotrauma. 2014; 10(2):55. 11. lee j, park jh. clinical characteristics of bilateral versus unilateral chronic subdural hematoma. korean j neurotrauma. 2014;10(2):49. 12. luongo m, grassi m, godano u. bilateral chronic subdural nontraumatic hematoma in a woman affected by al amyloidosis. j neurol surg reports. 2015 jun 26;76(01):e164–6. 13. agawa y, mineharu y, tani s, adachi h, imamura h, sakai n. bilateral chronic subdural hematoma is associated with rapid progression and poor clinical outcome. neurol med chir (tokyo). 2016; 56(4):198–203. 14. takemoto y, matsumoto j, ohta k, hasegawa s, miura m, kuratsu j. bilateral posterior fossa chronic subdural hematoma treated with craniectomy: case report and review of the literature. surg neurol int. 2016; 7(11):255. 15. herath hmmtb, matthias at, kulatunga a. acute on chronic bilateral subdural hematoma presenting with acute complete flaccid paraplegia and urinary retention mimicking an acute spinal cord injury: a case report. bmc res notes. 2017; 10(1):627. 16. huang yh, yang ky, lee tc, liao cc. bilateral chronic subdural hematoma: what is the clinical significance? int j surg. 2013; 11(7):544–8. 17. jukovic m, petrovic k, till v. the question is whether hemiparesis is more common in unilateral than bilateral chronic subdural hematoma. med pregl. 2014; 67(9– 10):277–81. 18. matsuda r, hironaka y, kawai h, park y-s, taoka t, nakase h. unilateral oculomotor nerve palsy as an initial presentation of bilateral chronic subdural hematoma: case report. neurol med chir (tokyo). 2013; 53(9):616–9. 19. guppy kh, khandhar sm, ochi c. reversible parkinsonlike symptoms in patient with bilateral chronic subdural hematomas and cervical spinal stenosis. world neurosurg. 2018; 109:285–90. 20. abecassis ij, kim lj. craniotomy for treatment of chronic subdural hematoma. neurosurg clin n am. 2017; 28(2):229–37. 21. xu m, yu b, wang c, zhu x, lu x, chen p, et al. minimally invasive approach in bilateral chronic subdural 180 c.d. diaz-arroyo, a.e. diaz-arroyo, t.y. carrero-barragán et al. hematomas: surgical selection and outcome in 74 cases. turk neurosurg. 2016; 27(3):380–5. 22. viaroli e, iaccarino c, maduri r, daniel rt, servadei f. 45 complications after surgery for chronic subdural hematomas. complications in neurosurgery. elsevier inc.; 2018. 274–279 p. 23. hsieh c-t, su i-c, hsu s-k, huang c-t, lian f-j, chang c-j. chronic subdural hematoma: differences between unilateral and bilateral occurrence. j clin neurosci. 2016; 34(2016):252–8. 24. fujitani s, ishikawa o, miura k, takeda y, goto h, maeda k. factors predicting contralateral hematoma growth after unilateral drainage of bilateral chronic subdural hematoma. j neurosurg. 2017; 126(3):755–9. 25. motiei-langroudi r, thomas aj, ascanio l, alturki a, papavassiliou e, kasper em, et al. factors predicting the need for surgery of the opposite side after unilateral evacuation of bilateral chronic subdural hematomas. neurosurgery. 2018; 1–8. 26. dabdoub cb, adorno jo, urbano j, silveira en, orlandi bmm. review of the management of infected subdural hematoma. world neurosurg. 2016; 87:663.e1-8. 27. won sy, konczalla j, dubinski d, cattani a, cuca c, seifert v, et al. a systematic review of epileptic seizures in adults with subdural haematomas. seizure. 2017; 45:28–35. 28. kumar m, yadav k, verma s, maheshwari v. idiopathic bilateral chronic subdural hematoma with left internal carotid artery infarct in a 3 months infant: a rare case report. j pediatr neurosci. 2016; 11(4):364. 29. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. 30. herrera-martinez mp, garcía-ballestas e, lozadamartinez i, torres-llinás d, moscote-salazar l. letter to the editor. creating the conditions for gender equality to end sexual harassment in neurosurgery. j neurosurg. 2021 feb 5:1-2. 31. gaitan-herrera g, lozada-martínez i, acevedo-aguilar l, bohorquez-caballero a, moscote-salazar l. simulation as a tool to educate the patient about neurosurgical pathology. j neurosurg sci. 2021 jan 22 32. ortega-sierra mg, durán-daza rm, carrera-patiño sa, rojas-nuñez ax, charry-caicedo ji, lozada-martínez id. neuroeducation and neurorehabilitation in the neurosurgical patient: programs to be developed in latin america and the caribbean. j neurosurg sci. 2021 jun 10. 33. blanco-teherán c, quintana-pájaro l, narvaez-rojas a, martínez-pérez r, garcía-ballestas e, moscote salazar l, et al. evidence-based medicine in neurosurgery: why and how? j neurosurg sci. 2021 aug 3. 34. ortega-sierra mg, prado-grajales v, martinez-imbett r, unás-perea k, lozada martinez id. research career in neurosurgery: a challenge for future neurosurgeons. j neurosurg sci. 2021 aug 3. 35. zuluaga-ramírez p, lozada-martínez i, moscote-salazar l, cabrera-vargas l. sexual harassment and racism in surgery: a latent problem. int j surg. 2021; 86:13-14. 36. gonzález-herazo ma, silva-muñoz dc, guevara-martínez pa, lozada-martinez id. post-covid 19 neurological syndrome: a fresh challenge in neurological management. neurol neurochir pol. 2021;55(4):413-414 37. llamas-nieves a, maiguel-lapeira j, lozada-martinez i, torres llinas d, moscote-salazar l. the desire to publish a scientific article and the difficulties of publishing it in a highquality neurosurgery scientific journal. j neurosurg sci. 2021 mar 11. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-014 intraventricular arachnoid cyst of lateral ventricle in an elderly patient rajneesh misra, sushil kumar, sandeep sharma, pankaj bharadva romanian neurosurgery (2020) xxxiv (1): pp. 106-109 doi: 10.33962/roneuro-2020-014 www.journals.lapub.co.uk/index.php/roneurosurgery intraventricular arachnoid cyst of lateral ventricle in an elderly patient rajneesh misra, sushil kumar, sandeep sharma, pankaj bharadva st. stephens hospital, tis hazari, delhi, india abstract arachnoid cysts are usually located in relation to the arachnoid cisterns. intraventricular location is rare and its embryological emergence in this site is controversial. we report a large intra-ventricular cyst in a 61-year-old female who presented with decreased vision, headache and right hemiparesis. mri was suggestive of cystic lesion in the lateral ventricle and was excised completely through a craniotomy. introduction arachnoid cyst comprises about 1% of intracranial space occupying lesions and are located in relation to arachnoid cisterns, most common locations being sylvian, chiasmatic, suprasellar, quadrigeminal and cerebellopontine cisterns. symptomatic presentation of an intraventricular arachnoid cyst is very rare especially in the seventh decade of life and hence it being reported. case report a 61-year-old lady presented with decreased vision and headache of about one-year duration and weakness in the right side of the body for the preceding two and half months. on examination: she was conscious; visual acuity was limited to perception of light in the right eye and finger counting at a distance of 2ft in left eye. there was increased tone in all limbs and right hemiparesis with a power grade iii. a retinal hole had been detected in the right eye in another hospital. investigations: routine blood investigations, urinalysis, kidney function, liver function, ecg were reported to be normal. mri of the brain revealed a large lesion, hypo-intense on t1wi and hyper-intense on t2wi suggestive of cystic mass in the lateral ventricle (fig 1). keywords intra-ventricular arachnoid cyst, magnetic resonance imaging, lateral ventricle corresponding author: rajneesh misra st. stephens hospital, tis hazari, delhi, india misra_ rajneesh@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 107 intraventricular arachnoid cyst of lateral ventricle in an elderly patient craniotomy revealed large ventricle containing well defined thin walled cyst which could be easily separated from the ependyma. it was excised in-toto after coagulation of its attachment to the vessels. histopathology of the cyst wall confirmed it to be arachnoid cyst. postoperatively her vision improved to finger counting at 6ft and regained full power in the right sided limbs. her vision continued to improve over the period of observation to 6/16 and 6/24 which could be improved to 6/9 with glasses. figure 1. showing imaging characteristics of the intraventricular arachnoid cyst. on contrast ct (1a) , it shows no enhancement of the cyst wall. the cyst is hypointense on t1 (1b), hyperintense on t2 (1d) with no wall enhancement on t1 contrast (1c). discussion most of the arachnoid cysts are asymptomatic and are discovered incidentally on imaging for other indications (1). when they are symptomatic, the presenting features most often include headache, vomiting and seizures. park et al collected 22 cases of arachnoid cyst of lateral ventricle from the literature and added one of their own (2). of these, 15 108 rajneesh misra, sushil kumar, sandeep sharma, pankaj bharadva were adults and 8 were children. headache was the most common presenting feature in this series. wong et al in 1993 reported a case which presented with positional psychosis due to intermittent blockage of temporal horn that occurred when the patient had been recumbent for 2 -3 hours (3). focal neurological deficits like hemiparesis as seen in our patient are rare at presentation. these lesions are seen usually in children or in the 4th decade of life. recently, relatively large series of pediatric patients treated endoscopically have been published (4). however; our patient seems to have been the oldest in the 7th decade of life. what process had altered the status quo between the cyst and the patient is debatable as she had been apparently living with it for almost all of her life. there are primarily two theories about the embryological origins of the arachnoid cysts. the first is the ‘arachnoid splitting theory’ (5). as the name suggests, it proposes that these cyst s arise as a result of congenital splitting of the arachnoid layer wherein, the csf accumulates gradually. the other theory is in specific context of middle cranial fossa arachnoid cysts and suggests that these arise as a result of temporal lobe agenesis as the primary event. however, it is named as ‘subarachnoid cyst theory’ (6). there are various mechanism proposed for expansion of the arachnoid cysts. these include, but are not limited to, fluid secretion by cyst wall, presence of osmotic gradient and ball valve mechanism (7). as mentioned previously, arachnoid cysts are purported to arise by a congenital splitting of the arachnoid membrane and subsequent accumulation of csf in this ‘potential space’. however, normally, there is no arachnoid tissue in the ventricle. thus, the origin of an arachnoid cyst in intraventricular location is controversial. according to yeates and enzmann, intraventricular arachnoid cysts arise from the vascular mesenchyme by invagination into adjacent brain, picking up an outer covering of adjacent glial tissue (8). nakase et al. postulate that cyst arises from the arachnoid layer brought with vascular mesenchyme which it invaginates via the choroidal fissure (9). usually, the cysts are located in the occipital horn and/or trigonal region and cause dilatation of the temporal horn and/ or occipital horn. in our patient, the cyst pathogenesis seems to mirror the mechanism proposed by nakase et al. as it had an attachment to the choroidal fissure. imaging characteristics are those of any csf containing cavity viz. hypo-intense on t1, hyperintense on t2 and without any contrast enhancement. symptomatic cysts require surgical intervention. the options available include endoscopic fenestration, cyst de-roofing, partial or complete removal and cysto-peritoneal shunt. our patient was treated by complete removal of cyst wall through a craniotomy. endoscopic fenestration was the safer and less invasive option. in park’s series, there were various combinations and permutations of procedures applied for management of adult as well as pediatric intraventricular arachnoid cystsopen removal, open fenestration or partial cyst removal and endoscopic fenestration and shunt (2) . kurokawa et al recommended cyst resection rather than shunt because he found that the size of the ventricle was not reduced after the shunt procedure and the shunt malfunctioned due to wrapping of the shunt by the collapse cyst (10). park et al had case of large arachnoid cyst of the lateral ventricle extending from the suprasellar cistern. the cyst wall could be easily separated from the ventricular ependymal after coagulation and transection of the attachments. cysto-peritoneal shunt or complete removal of the cyst wall are necessary to prevent recurrence, whereas cyst opening alone is insufficient. our patient was treated by complete removal of the cyst wall through a craniotomy to avoid recurrence. conclusions the embryological origin of intraventricular arachnoid cysts is controversial and the jury is still out. our intraoperative observation during the cyst excision had shown the cyst to have an attachment to choroid fissure of the left lateral ventricle. this is in agreement with nakase et al.’s propounded theory that intraventricular arachnoid cyst arises from the arachnoid layer brought with vascular mesenchyme which it invaginates via the choroidal fissure. references 1. al-holou wn, yew ay, boomsaad ze, garton hj, muraszko km, maher co. prevalence and natural history of arachnoid cysts in children. j neurosurg pediatrics 2010; 5:578–585. 109 intraventricular arachnoid cyst of lateral ventricle in an elderly patient 2. park sw, yoon sh, cho kh, shin ys. a large arachnoid cyst of the lateral ventricle extending from the supracerebellar cistern-case report. surg neurol. 2006 jun;65(6):611-4. 3. cheuk-wah wong, sheung-fat ko, yau-yau wai, arachnoid cyst of the lateral ventricle manifesting positional psychosis, neurosurgery, volume 32, issue 5, may 1993, pages 841–843. 4. copley, p., kirkman, m.a., thompson, d. james g, aquilina k. endoscopic surgery for intraventricular arachnoid cysts in children: clinical presentation, radiological features, management, and outcomes over a 12-year period. childs nerv syst (2018) 34: 257. 5. starkman sp, brown tc, linell ea: cerebral arachnoid cyst. j neuropathol exp neurol 17:484-500, 1958. 6. robinson rg: congenital cysts of the brain: arachnoid malformations. prog neurol surg 4:133-174, 1971. 7. basaldella l, orvieto e, dei tos ap, della barbera m, valente m, longatti p. causes of arachnoid cyst development and expansion. neurosurg focus. 2007;22(2): e4. 8. yates a, enzman d. an intraventricular arachnoid cyst. j comp assist tomogr 1979; 3:697-700. 9. nakase h, hisanaga m, hashimoto s, imanishi m, utsumi s. intraventricular arachnoid cyst. report of two cases. j neurosurg 1988; 68:482-6. 10. kurokawa y1, sohma t, tsuchita h, kitami k, suzuki s, ishikawa a. a case of intraventricular arachnoid cyst. how should it be treated? childs nerv syst. 1990 sep;6(6):3657. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0067 article  elizabethkingia meningoseptica causing meningitis after decompressive craniectomy for traumatic brain injury in a immunocompetent adult: serious neurocritical care concern guru dutta satyarthee, mayank garg, deepak agarwal india      romanian neurosurgery (2018) xxxii 3: 513 517 | 513             doi: 10.2478/romneu-2018-0067 elizabethkingia meningoseptica causing meningitis after decompressive craniectomy for traumatic brain injury in a immunocompetent adult: serious neurocritical care concern guru dutta satyarthee, mayank garg, deepak agarwal department of neurosurgery, all india institute of medical sciences, new delhi, india abstract: elizabethkingia is aerobic gram negative bacteria is widely distributed in soil, food and food. it is very rarely pathogenic for human and especially those who are immunocompromised and various risk factors includes intravenous catheter, ventilatory support. we report a case, who had undergone decompressive craniectomy for traumatic brain injury, developed meningitis, csf culture showed growth of elizabethkingia and treated successfully with antibiotics therapy. this study reminds that rare pathogen should also be considered as causative organism for meningitis especially in postoperative cases and it responds well to antimicrobial therapy. key words: meningitis, post-decompressive surgery, immunocompetent host, treatment introduction elizabethkingia meningoseptica, previously termed as flavobacterium meningosepticum or chryseobacterium meningosepticum is an aerobic gramnegative, rod-shaped bacterium (15). it is a rare human pathogen, widely distributed in soil, plants, food and potable water and wet surface in the hospital environment. it can cause serious infections in immunosupressed and intubated patients with prolonged mechanical ventilation. intravascular devices such as intravenous catheter, urinary catheter, intravascular implant are important risk factors. historically, it was associated with neonatal meningitis and sepsis, first identified by king elizabeth in 1959 (7). subsequently, outbreaks of neonatal meningitis, septicaemia and pneumonia in severely immunocompromised and prolonged ventilated individuals were reported. e. meningoseptica is considered inherently resistant to the usual empiric therapy aimed at gram-negative bacilli. authors report a rare case of meningitis caused by e. meningoseptica in an adult operated for severe head injury, managed at tertiary care trauma centre. 514 | satyarthee et al elizabethkingia meningoseptica: meningitis in brain injury             case illustration a 26year-old patient was admitted with acute subdural haemorrhage following road traffic accident with glasgow coma scale of e1vtm2 and underwent decompressive craniectomy and discharged from hospital with gcs of e1vtm3 status. two months following discharge, he was readmitted with high grade fever. on admission vitals were stable with tense bulging flap on decompressive craniectomy site and neck rigidity. routine urinary examination, haematological and biochemistry tests were carried out. repeat computed cranial tomography scan revealed presence of presence of hydrocephalus associated with gross dilatation of ventricles. an emergency csf diversionary procedure, external ventricular drain placement was performed. csf sample sent for bacterial cultures identified the isolated bacterium as gram negative bacilli, e. meningoseptica. csf sugar level was 30 mg/dl and csf protein was 240mg/dl. the isolate was sensitive to piperacillin-tazobactam, cotrimoxazole, tigecycline and vancomycin. patient was treated with intravenous antibiotics according to culture sensitivity for three weeks, to which he responded favourably. discussion e. meningoseptica, is a non-fermentor gram-negative bacillus, widely found in water, soil and wet surfaces of the hospital environment. environmental studies have indicated that this organism can survive even in chlorine-treated water, colonizes in sink basins and taps and ventilator tubing (15). most of the reported cases are of neonatal meningitis (7). isolation of this organism in adults cases of pneumonia, endocarditis and meningitis are reported but none in a case of severe head injury (3). bloch et al (2) reported in 1997 a series of 15 immunocompromised patients with e. meningosepticum infections. 80% of the patients had nosoconmial-acquired infections while 20 % were colonized with e. meningosepticum without evidence of infection. the incidence of e. meningoseptica may be under-reported as identification is difficult without an automated system. environmental samples should be taken to identify the source of infection. treatment of e. meningoseptica infection is challenging because of organism’s multidrug resistance. quinolones, vancomycin, trimethoprim‐sulfamethoxazole, and rifampicin have been documented as potential therapies (5). e. meningoseptica is usually resistant to colistin and carbapenems which are used to treat extended-spectrum beta-lactamase-producing klebsiella pneumoniae and acinetobacter baumannii, and these characteristics give it a survival advantage. the role of tigecycline is not defined, but our patient had a clinical response after treatment with tigecyclin, as the culture showed sensitivity to it. shailja et al (12) showed that e. meningoseptica isolates were resistant to cephalosporins, aminoglycosides, trimethoprim-sulfamethoxazole, beta -lactam combinations, carbapenems while only one romanian neurosurgery (2018) xxxii 3: 513 517 | 515             isolate was susceptible to ciprofloxacin. all the isolates were susceptible to vancomycin, still six of nine neonates died even after using vancomycin. though the organism is susceptible to vancomycin in vitro, its efficacy in vivo is questionable. about ten cases of adult meningitis are reported in literature (1, 3, 4, 8-11, 13-15) but only two cases after neurosurgical procedure (table 1). this is probably the first case report of e.meningoseptica causing meningitis in trauma patients. severe head injury leads to prolonged hospital stay of these predominantly young adult patients who otherwise have no other co-morbidities. high degree of suspicion with rapid diagnosis and prompt institution of appropriate therapy for prolonged period (about 3-4 weeks) are essential in the management of such infections. table 1 review of important cases developing meningitis following neurosurgical procedure s. no. author/ reference year preceding neurosurgical procedure interval of meningitis onset outcome 1 wang et al (14) 2014 aneurysm clipping in 73-year old male 10 days favourable 2 chan et al (3) 1983 transsphenoidal hypophysectomy not reported favourable 3 current case 2017 decompressive craniectomy twomonths excellent about 90% of reported cases of adult meningitis have debilitating predisposing conditions ie. hematological disorders, immunosuppressive state, neoplasms and diabetes mellitus. the common manifestations included fever, disturbances of consciousness, seizure, hydrocephalus and stroke. the initial csf cultures and gram stains were inconclusive in 50% cases. despite treatment, about 50% died during the course of treatment (9). lu et al. observed the clinical and laboratory manifestations in the adult is similar to bacterial meningitis caused by other bacterium. so, clinical diagnosis may be confirmed by isolating positive csf culture, for which repeated csf cultures may be needed (9). lu et al. reported a 21 year old diabetic patient with meningitis, confirmed by a positive csf culture. she presented with fever, headache, consciousness disturbance, and seizure. csf analysis revealed a purulent inflammatory reaction. she was discharged after 21-day course of intravenous antibiotics therapy (9). wang et al. (14) reported a 73-year-old male patient of ruptured middle cerebral artery aneurysm which was clipped followed by lumbar external drainage for acute hydrocephalus. ten days later, csf culture showed growth of e. meningoseptica which responded favourably. 516 | satyarthee et al elizabethkingia meningoseptica: meningitis in brain injury             chan et al (3) in 1983 reviewed literature of flavobacterium meningosepticum causing adult meningitis and could find only five cases. chan et al reported a female developing meningitis following transsphenoidal hypophysectomy surgery. she recovered completely with oral rifampicin and intravenous chloramphenicol and cefoperazone. jean et al. (6) observed elizabethkingia meningoseptica as a potential threat to patients in critical care unit because of multidrug resistance which may produce e. meningoseptica outbreaks and create an important health issue. control of such outbreak requires strictly following standard infection control measures, isolation of contact, identification of the source and very important is cleaning of equipment. conclusion elizabethkingia meningoseptica possess a potentially important threat to patients in neurosurgical critical care unit due to existence of multidrug resistance causing e. meningoseptica outbreaks. it is highly important laboratories should have the facilities to identify the organism. awareness about this organism and sensitivity testing is required to reduce morbidity and control outbreaks. authors presented case of elizabethkingia meningoseptica causing meningitis in an operated case of decompressive craniectomy for traumatic brain injury with successful treatment. correspondence dr. guru dutta satyarthee associate professor department of neurosurgery cnc building, aiims ansari nagar, new delhi, india 110029 email: duttaguru2002@yahoo.com phone no. : +919868398243 references 1.bagely dhj, alexander jcj, gill vj, dolin r, ketcham as. late flavobacterium species meningitis after craniofacial exenteration. arch intern med. 1976 feb; 136(2): p. 229-31. 2.bloch kc, nadarajah r, jacobs r. chryseobacterium meningosepticum: an emerging pathogen among immunocompromised adults. report of 6 cases and literature review. medicine (baltimore). 1997 jan; 76(1): p. 30-41. 3.chan kh, chau py, wang ry, huang cy. meningitis caused by flavobacterium meningosepticum after transsphenoidal hypophysectomy with recovery. surg neurol. 1983 oct; 20(4): p. 294-6. 4.harrington sp, perlino ca. flavobacterium meningosepticum sepsis: disease due to bacteria with unusual antibiotic susceptibility. south med j. 1981 jun; 74(6): p. 764-6. 5.hung pp, lin yh, lin cf, liu mf, shi zy. chryseobacterium meningosepticum infection: antibiotic susceptibility and risk factors for mortality. j microbiol immunol infect. 2008 apr; 41(2): p. 137-44. 6.jean ss, lee ws, chen fl, ou ty, hsueh pr. elizabethkingia meningoseptica: an important emerging pathogen causing healthcare-associated infections. j hosp infect. 2014 apr; 86(4): p. 244-9. doi: 10.1016/j.jhin.2014.01.009. epub 2014 feb 25. 7.king eo. studies on a group of previously unclassified bacteria associated with meningitis in infants. am j clin pathol. 1959 mar; 31(3): p. 241-7. 8.lim lc, low ja, chan km. chryseobacterium meningosepticum (flavobacterium meningosepticum)-a report of five cases in a local hospital. ann acad med singapore. 1999 nov; 28(6): p. 858-60. 9.lu ch, huang cr, tsai nw, chang cs, chuang yc, lee py, et al. an adult case of chryseobacterium meningosepticum meningitis. jpn j infect dis. 2004 oct; 57(5): p. 214-5. 10.madruga m, zanon u, pereira gm, galvão ac. meningitis caused by flavobacterium meningosepticum. romanian neurosurgery (2018) xxxii 3: 513 517 | 517             the first epidemic outbreak of meningitis in the newborn in south america. j infect dis. 1970 mar; 121(3): p. 32830. 11.rios i, klimek jj, maderazo e, quintiliani r. flavobacterium meningosepticum meningitis: report of selected aspects. antimicrob agents chemother. 1978 sep; 14(3): p. 444-7. 12.shailaja vv, reddy ak, alimelu m, sadanand ln. neonatal meningitis by multidrug resistant elizabethkingia meningosepticum identified by 16s ribosomal rna gene sequencing. int j pediatr. 2014. 2014;: p. 918907. doi: 10.1155/2014/918907. epub 2014 feb 9. 13.uchihara t, yokota t, watabiki s, ueki m, miyake s, tsukagoshi h. flavobacterium meningosepticum meningitis in an adult. am j med. 1988 nov; 85(5): p. 738-9. 14.wang x, hu z, fan y, wang h. chryseobacterium indologenes catheter-related meningitis in an elderly patient after intracranial aneurysm clipping surgery. neurol sci. 2014 jan; 35(1): p. 113-5. doi: 10.1007/s10072013-1500-z. epub 2013 jul 17. 15.weaver kn, jones rc, albright r, thomas y, zambrano ch, costello m, et al. acute emergence of elizabethkingia meningoseptica infection among mechanically ventilated patients in a long-term acute care facility. infect control hosp epidemiol. 2010 jan; 31(1): p. 54-8. doi: 10.1086/649223. doi: 10.33962/roneuro -2020-050 headache, seizures and loss of consciousness in an elderly male following groin hernia surgery amit agrawal romanian neurosurgery (2020) xxxiv (1): pp. 333-335 doi: 10.33962/roneuro-2020-050 www.journals.lapub.co.uk/index.php/roneurosurgery headache, seizures and loss of consciousness in an elderly male following groin hernia surgery amit agrawal dr. mch. professor of neurosurgery. department of neurosurgery, mm institute of medical sciences & research, mullana (ambala), india abstract headache after lumbar puncture is a common occurrence and have a benign course in the majority. in rare cases, it can be a mani-festation of rare but potentially lifethreatening intracranial complications. we discuss a case of 65 years male patient who was operated for left inguinal hernia under spinal anaesthesia, had persistent headache partial response to conservative measures developed one episode of seizures and lapsed into altered sensorium. imaging findings were suggestive of extensive left frontal-temporoparietal acute sdh with mass effect and midline shift. the hematoma was evacuated and the patient recovered well. prolonged and persistent post-dural puncture headache complicated by atypical neurological deterioration following spinal anaesthesia should prompt the physician to consider the possibility of intracranial complications and to seek immediate radiological investigations. introduction headache after lumbar puncture [post-dural puncture headache (pdph)] is a common occurrence in most cases after lumbar puncture and most of post-lp headaches are not severe and have a benign course (1-4) but in rare cases pdph can also be a manifestation of a rare but potentially life-threatening complication such as acute subdural hematoma (sdh). (3, 5-16). case report a 65-years old male patient was operated for left inguinal hernia one week back under spinal anaesthesia. he was complaining of persistent headache and with the diagnosis of pdph he was given analgesics, oral hydration, and bed-rest without much improvement. on 7th day he had multiple episodes of vomiting, one episode of generalized tonicclonic seizures and lapsed into altered sensorium. his general and systemic examination was normal. per abdomen examination was normal. bowel sounds were normal. neurologically he was in altered keywords postdural puncture headache, subdural hematoma, headache, seizure, lumbar puncture corresponding author: amit agrawal mm institute of medical sciences & research, mullana (ambala), india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 334 amit agrawal sensorium. glasgow coma scale was 4. pupils were bilateral 3 mm and reacting to light. plantars were bilateral extensor. there was no history of hypertension or diabetes. there was no history suggestive of bleeding disorders, using tobacco, or alcohol. complete blood count including platelets and white blood cells and coagulation tests were within normal range. a plain computed tomography (ct) of brain revealed an extensive left frontal temporoparietal acute sdh with mass effect and midline shift (figure-1). the patient underwent emergency craniotomy and evacuation of hematoma. he was electively ventilated and could be weaned off from ventilator and recovered well. figure 1. plain computed tomography scan brain showing large acute left frontal-temporo-parietal subdural hematoma with mass effect and midline shift. discussion dural puncture with subsequent postdural puncture headache (pdph) is a recognized complication of spinal anesthesia. (13, 17) the possible mechanism for pdph is the leakage of cerebrospinal fluid depletes the cushion of csf supporting the brain and its sensitive meningeal vascular coverings, resulting in gravitational traction on the pain-sensitive intracranial structures causing classical headache. (2, 18) post-dural puncture headache (pdph) is classically postural and responds within 48 h to increased fluid intake and bed rest (5, 19, 20) and more frequently seen in the younger patients and in women. (4, 21, 22) severe and prolonged post-dural puncture headache with or without new neurological signs or deficits should be regarded as a warning sign of an intracranial complications (i.e. subdural haematoma or intracerebral haemorrhage). (3, 5-11, 14, 15, 23-27) in contrast to adults, the dura is adherent to skull and may be less stretchable duramater due to either atherosclerosis or agerelated mechanical changes in the epidural space explaining the lower incidence of pdph. (28) the mechanism responsible for pdph i.e. the leakage of csf and subsequent lowering of the intracranial pressure following dural puncture and caudal movement of the spinal cord and brain stretching and tearing dural veins, results in subdural bleeding in the elderly. (2, 5, 7, 13, 18, 27, 29, 30) the management of acute sdh depends on size of the hematoma as smaller lesions in conscious patients can be managed conservatively under close supervision, (5, 7, 9, 31, 32)however the larger lesions with neurological deficits require neurosurgical intervention and evacuation of hematoma. (7, 8) while considering the patient of pdph for conservative management, particularly a lumbar autologous extradural blood patch as a possible means to stop the csf leakage one should be cautious and has low threshold for cranial imaging as the procedure can worsen the patient and neurological deterioration if there is intracranial hematoma. (7) conclusion in summary, prolonged and persistent post dural puncture headache complicated by atypical neurological deterioration following spinal anesthesia should prompt the physician to consider the possibility of intracranial complications and to seek immediate radiological investigations to avoid a potential negative outcome. references 1. evans rw, armon c, frohman em, goodin ds. assessment: prevention of post–lumbar puncture headaches. neurology. 2000;55(7):909-14. 2. ahmed s, jayawarna c, jude e. post lumbar puncture headache: diagnosis and management. postgraduate medical journal. 2006;82(973):713. 3. kim hj, cho yj, cho jy, lee dh, hong ks. acute subdural hematoma following spinal cerebrospinal fluid drainage in a patient with freezing of gait. journal of clinical neurology (seoul, korea). 2009;5(2):95. 4. kuntz k, stevens j, offord k, ho m. post―lumbar puncture headaches. neurology. 1992;42(10):1884-. 5. acharya r, chhabra s, ratra m, sehgal a. cranial subdural haematoma after spinal anaesthesia. british journal of anaesthesia. 2001;86(6):893. 335 headache, seizures and loss of consciousness in an elderly male following groin hernia surgery 6. macon me, armstrong l, brown e. subdural hematoma following spinal anesthesia. obstetric anesthesia digest. 1990;10(2):108. 7. verda m, martã-nez-lage j, alonso b, sã¡nchez-ortega j, garcia-candel a. non-surgical management of intracranial subdural hematoma complicating spinal anesthesia manejo no quirãºrgico de hematoma subdural intracraneal tras anestesia espinal complicada. neurocirugã-a. 2007;18(1). 8. pavlin dj, mcdonald js, child b, rusch v. acute subdural hematoma-an unusual sequela to lumbar puncture. anesthesiology. 1979;51(4):338. 9. mantia am. clinical report of the occurrence of an intracerebral hemorrhage following post-lumbar puncture headache. anesthesiology. 1981;55(6):684. 10. duarte wl, geber dg. hematoma subdural apã³s punã§ã£o inadvertida da dura-mã¡ter. relato de caso. revista brasileira de anestesiologia. 2008;58(4):387-90. 11. chiravuri s, wasserman r, chawla a, haider n. subdural hematoma following spinal cord stimulator implant. pain physician. 2008;11(1):97-101. 12. lee acw, lau y, li ch, wong yc, chiang aks. intraspinal and intracranial hemorrhage after lumbar puncture. pediatric blood & cancer. 2007;48(2):233-7. 13. cantais e, behnamou d, petit d, palmier b. acute subdural hematoma following spinal anesthesia with a very small spinal needle. anesthesiology. 2000;93(5):1354-5. 14. komplikasyonu ea, hematom s. intracranial chronic subdural haematoma as a complication of epidural anesthesia. turkish neurosurgery. 2009;19(3):285-7. 15. suess o, stendel r, baur s, schilling a, brock m. intracranial haemorrhage following lumbar myelography: case report and review of the literature. neuroradiology. 2000;42(3):211-4. 16. newrick p, read d. subdural haematoma as a complication of spinal anaesthetic. british medical journal (clinical research ed). 1982;285(6347):1047-8. 17. berger cw, crosby et, grodecki w. north american survey of the management of durai puncture occurring during labour epidural analgesia. canadian journal of anesthesia/journal canadien d'anesthã©sie. 1998;45(2):110-4. 18. hatfalvi bi. postulated mechanisms for postdural puncture headache and review of laboratory models: clinical experience. regional anesthesia and pain medicine. 1995;20(4):329. 19. nolte c, lehmann tn. postpartum headache resulting from bilateral chronic subdural hematoma after dural puncture. american journal of emergency medicine, the. 2004;22(3):241-2. 20. skoldefors e, olofsson ci. intracranial subdural haematoma complicates accidental dural tap during labour. european journal of obstetrics and gynecology and reproductive biology. 1998;81(1):119-21. 21. bridenbaugh po, greene nm, brull sj. spinal (subarachnoid) neural blockade. neural blockade in clinical anaesthesia and management of pain 3rd edition philadelphia: lippincott-raven. 1998:203-42. 22. leibold ra, yealy dm, coppola m, cantees kk. post-duralpuncture headache: characteristics, management, and prevention. annals of emergency medicine. 1993;22(12):1863-70. 23. stocks g, wooller d, young j, fernando r. postpartum headache after epidural blood patch: investigation and diagnosis. british journal of anaesthesia. 2000;84(3):407. 24. vaughan d, stirrup c, robinson p. cranial subdural haematoma associated with dural puncture in labour. british journal of anaesthesia. 2000;84(4):518. 25. kayacan n, arä±cä± g, karslä± b, erman m. acute subdural haematoma after accidental dural puncture during epidural anaesthesia. international journal of obstetric anesthesia. 2004;13(1):47-9. 26. ozdemir o, calisaneller t, yildirim e, caner h, altinors n. acute spontaneous spinal subdural hematoma in a patient with bilateral incarcerated inguinal hernia. joint bone spine. 2008 may;75(3):345-7. 27. hung c, tan s. acute-on-chronic subdural haematoma, a rare complication after spinal anaesthesia. hong kong med j. 2003;9(5):384-6. 28. vandam ld, dripps rd. long-term follow-up of patients who received 10,098 spinal anesthetics. journal of the american medical association. 1956;161(7):586. 29. thorsã©n g. neurological complications after spinal anaesthesia: and results from 2493 follow-up cases: kungl. boktrykeriet pa norstedt & soner; 1947. 30. lee k. the pathogenesis and clinical significance of traumatic subdural hygroma. brain injury. 1998;12(7):595-603. 31. scavone bm, wong ca, sullivan jt, yaghmour e, sherwani ss, mccarthy rj. efficacy of a prophylactic epidural blood patch in preventing post dural puncture headache in parturients after inadvertent dural puncture. anesthesiology. 2004;101(6):1422. 32. 32. blake d, donnan g, jensen d. intracranial subdural haematoma after spinal anaesthesia. anaesthesia and intensive care. 1987;15(3):341-2. doi: 10.33962/roneuro-2022-055 comparison of levels of toxic trace elements in two most common spinal pathologies in three different tissues hakan a.k., soner yaycioglu, iskender samet daltaban, mehmet selim gel, ihsan canbek romanian neurosurgery (2022) xxxvi (3): pp. 325-333 doi: 10.33962/roneuro-2022-055 www.journals.lapub.co.uk/index.php/roneurosurgery comparison of levels of toxic trace elements in two most common spinal pathologies in three different tissues hakan a.k.1, soner yaycioglu2, iskender samet daltaban3, mehmet selim gel3, ihsan canbek4 1 kırşehir ahi evran university school of medicine department of neurosurgery kırşehir, turkey 2 aydın adnan menderes university, school of medicine of department of neurosurgery aydın, turkey 3 trabzon sbu kanuni training and reasearch hospital department of neurosurgery trabzon, turkey 4 afyonkarahisar health sciences university of medicine, department of neurosurgery, afyonkarahisar, turkey abstract aim: the toxic trace element levels in serum, bone (lamina), and intervertebral disc tissues of patients with lumbar spinal stenosis and lumbar herniated nucleus pulposus (hnp) which are the two most common spinal pathologies were determined, and it was investigated whether they have a role in the pathophysiology of these pathologies. materials and methods: cadmium (cd), aluminium (al), arsenic (as), mercury (hg), and lead (pb) levels in serum, intervertebral disc, and bone (lamina) tissue of patients with hnp (=20) and 30 with lumbar spinal stenosis (lss) (n=30) were determined by inductively coupled plasma mass spectrometry technique. results: ldh group cd serum level was found to be significantly higher than lss group cd serum level (p=0.024). al disc level in the hnp group was found to be significantly higher than the al disc level in the lss group (p=0.038). while as serum level increased in ldh group, it was determined that as bone level increased very significantly (r= 0.699, p=0.001). in the lss group, it was determined that the hg disc level increased significantly as the hg serum level increased (r=0.608, p<0.01). on the other hand, as the hg serum level increased in the ldh group, the hg disc level also decreased significantly (r= -0.579, p<0.01). conclusion: the difference in toxic trace element levels seen in these pathologies has been discussed in terms of possible causes in light of current literature. the findings of our study support the hypothesis that toxic trace elements may be effective in lumbar disc degeneration. introduction it is known that some environmental factors and especially toxic trace elements that are not essential for human health pass into the human body with contamination and cause physiological and pathological keywords trace element, lumbar spinal stenosis, lumbar disc herniation, inductively coupled plasma mass spectrometry corresponding author: iskender samet daltaban trabzon sbu kanuni training and reasearch hospital trabzon, turkey isamet79@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 326 hakan a.k., soner yaycioglu, iskender samet daltaban et al. negative effects (1). however, there is not adequate and satisfactory information about the effects of presence of these toxic elements in the human body in acceptable amounts or what kind of effects they have on the organism in the amounts below the permissible levels in food, drinking water or air. moreover, the accumulation of these toxic elements in the body and the possibility that they may play a role in the pathophysiology of some different diseases that occur in chronic degenerative processes or may appear as predisposing factors should not be forgotten. in this study, it was investigated whether five toxic substances (aluminum, arsenic, mercury, lead, cadmium) have an effect on lumbar herniated nucleus pulposus and chronic intervertebral disc degeneration. for this reason, two patient groups with lumbar hnp and lss thought to be caused by intervertebral disc degeneration but with different pathogenesis were compared (2). in the hnp, disc degeneration generally develops in a shorter time due to axial loading and annulus fibrosis tears. however, in lss degenerative changes are thought to be due to a more chronic inflammatory process which affects ligaments, bones, discs and facet joints (3,4). in lss, it is predicted that the process occurs mostly with biomechanical effects as a result of instability developing on the basis of degenerative changes due to the aging process of the spine (5). although intervertebral disc degeneration is a common feature in both diseases, it is assumed that they have different pathophysiological basis due to their histopathological differences (6). in this way, toxic trace elements in both groups of diseases were determined in serum, bone and disc tissue, and the effects of these substances on the degenerative process were investigated. material and method after receiving the approval of the yozgat bozok university clinical research ethics committee (12.10.2016 / 68 dated 12.10.2016), the blood, bone (lamina) and intervertebral disc samples were collected from the patients who had undergone lumbar spine pathology operation in the department of neurosurgery of yozgat bozok university faculty of medicine between 2016-2017. trace element levels in the samples were measured by icp-ms (inductively coupled plasma mass spectrometry). the patients were divided into two groups as lumbar spinal stenosis (lss) and lumbar disc herniation (ldh) by preoperative magnetic resonance imaging (mri). patients with rheumatic diseases such as rheumatoid arthritis and ankylosing spondylitis, under the age of 18, with missing file information or missing radiological images, and who underwent surgery due to trauma were excluded from the study. patients with the possibility of prolonged or intense exposure to the trace elements mentioned in the study were excluded from the study. the diagnosis of lss or hnp was made according to clinical and radiological findings. 20 out of 50 patients were diagnosed with l-hnp and 30 with lss. patients who underwent discectomy in addition to total laminectomy in the lss group were included. in lss group, patients who underwent only laminectomy and did not undergo discectomy were excluded from the study. patients who use cigarettes and alcohol, and patients with diseases that require continuous drug use such as hypertension, diabetes, and goiter were excluded from the study. statistical analysis: these measured levels were grouped according to radiological findings. three replicates were obtained for each sample analyzed and their mean value was taken into account for the concluded assessment. if the required statistics are given, it is evaluated by spss 20.0 statistical program. a normality test was used to determine whether sample data of groups a normally distributed. the correlations between toxicological variables among groups were assessed with pearson correlation test. the parametric and nonparametric tests were carried out to determine the association of main parameters concerning among groups. all tests were considered significant at p <0.05. results median age was 53 years old (mean:53.84, std: ±12,55, min: 25, and max: 76). in l-hnp (n=20) median age was 35 and 9 of them were female and 11 were male. in lss group (n=30), mean age was 54 and 18 of them were female and 22 were male. mean, median, standard deviation, minimum, and maximum levels of 5 toxic trace elements were showed in three different tissue presented in table 1. 327 comparison of levels of toxic trace elements in two most common spinal pathologies table 1. general descriptive values of the study n=50 unit [µg/l] age cd al as hg pb bone serum disc bone serum disc bone serum disc bone serum disc bone serum disc mean 53.84 0.31 0.49 0.54 27.13 30.57 2.47 0.82 0.53 1.16 0.26 0.21 0.03 14.76 5.93 6.34 median 53.00 0.32 0.51 0.45 26.32 31.00 2.22 0.65 0.49 0.37 0.02 0.17 0.03 12.91 2.93 3.09 std. deviation 12.55 0.11 0.06 0.43 18.14 2.01 1.40 0.66 0.59 2.10 0.41 0.14 0.03 8.59 12.54 8.76 minimum 28.00 0.02 0.26 0.07 8.64 21.15 0.39 0.03 0.00 0.02 0.00 0.00 0.00 1.75 0.06 0.34 maximum 76.00 0.48 0.58 1.81 149.01 33.67 5.73 3.77 3.89 12.30 2.28 0.53 0.12 47.72 81.65 41.41 table 2. the comparison of the toxic trace elements in between lss and l-hnp groups lss (n=30) ldh (n=20) p mean sd mean sd cd bone 0.30 0.10 0.32 0.12 p>0.05 serum 0.47 0.07 0.51 0.04 0.024* disc 0.57 0.47 0.50 0.35 p>0.05 al bone 28.20 23.24 25.54 4.44 p>0.05 serum 30.39 2.25 30.85 1.58 p>0.05 disc 2.14 1.25 2.97 1.50 0.038* as bone 0.79 0.58 0.88 0.77 p>0.05 serum 0.44 0.28 0.66 0.86 p>0.05 disc 1.54 2.62 0.57 0.53 p>0.05 hg bone 0.30 0.46 0.19 0.33 p>0.05 serum 0.22 0.16 0.18 0.11 p>0.05 disc 0.03 0.03 0.03 0.02 p>0.05 pb bone 15.76 9.81 13.26 6.28 p>0.05 serum 7.84 15.97 3.06 1.29 p>0.05 disc 6.82 9.88 5.61 6.93 p>0.05 lss-lumbar spinal stenosis; hnp-herniated nucleus pulposus; sdstandard deviation; *significant cadmium (cd) evaluation: the lowest cd level was observed in bone tissue in both lss and hnp groups (0.30±0.10 µg/l and 0.32±0.12 µg/l, respectively). while the cd serum level in the l-hnp group was found to be significantly higher than the cd serum level in the lss group (0.51±0.04 µg/l and 0.47±0.07 µg/l, p=0.024, respectively), the cd bone level was also found to be higher, although not significantly, in the hnp group (p>0.05). on the other hand, cd disc level was higher in the lss group (p>0.05). however, for both groups, it was observed that cd accumulated more in disc tissue rather than bone. in addition, while cd serum and bone levels were inversely proportional in the lss group, this was directly proportional in the hnp group. table 3. correlations of cd levels in bone, serum and disc tissues in both groups groups cd_bone [µg/l] cd_serum [µg/l] cd_disc [µg/l] lss (n=30) cd_bone [µg/l] 1 -,119 -,036 cd_serum [µg/l] -,119 1 ,106 cd_disc [µg/l] -,036 ,106 1 hnp (n=20) cd_bone [µg/l] 1 ,182 ,284 cd_serum [µg/l] ,182 1 ,319 cd_disc [µg/l] ,284 ,319 1 graphic 1. graphical view of mean cd levels in bone, serum and disc tissues 328 hakan a.k., soner yaycioglu, iskender samet daltaban et al. aluminum (al) evaluation: the lowest al level was observed in the disc tissue in both lss and hnp groups (respectively, 2.14±1.25 µg/l and 2.97±1.50 µg/l). al disc level in the hnp group was found to be significantly higher than the al disc level in the lss group (respectively, 2.97±1.50 µg/l and 2.14±1.25 µg/l, p=0.038). in both groups, the means were close to each other for each matrix. however, al was found to accumulate in the bone tissue for both groups. table 4. correlations of al levels in bone, serum, and disc tissues in both groups groups al_bone [µg/l] al_serum [µg/l] al_disc [µg/l] lss (n=30) al_bone [µg/l] 1 ,062 ,269 al_serum [µg/l] ,062 1 -,001 al_disc [µg/l] ,269 -,001 1 hnp (n=20) al_bone [µg/l] 1 -,053 -,205 al_serum [µg/l] -,053 1 ,202 al_disc [µg/l] -,205 ,202 1 graphic 2. graphical view of mean al levels in bone, serum, and disc tissues arsenic (as) evaluation: in lss group, when as serum level increased, as bone level decrease was detected (r= 0154, p=0.416). whereas in l-hnp group, as serum level increased in hnp group, as bone level increased significantly (r= 0.699, p=0.001). lss group as mean levels were found to be approximately 3 times higher than hnp group as mean levels. table 5. correlations of as levels in bone, serum and disc tissues in both groups groups as_bone [µg/l] as_serum [µg/l] as_disc [µg/l] lss (n=30) as_bone [µg/l] 1 -,154 -,200 as_serum [µg/l] -,154 1 ,320 as_disc [µg/l] -,200 ,320 1 hnp (n=20) as_bone [µg/l] 1 ,699** ,288 as_serum [µg/l] ,699** 1 ,156 as_disc [µg/l] ,288 ,156 1 graphic 3. graphical view of mean as levels in bone, serum and disc tissues mercury (hg) evaluation: the lowest hg levels were observed in the disc tissue in both the lss and hnp groups (0.03±0.03 µg/l and 0.03±0.02 µg/l, respectively). the highest hg levels in all tissues were detected in bone tissue in both groups (0.30±0.45 µg/l and 0.19±0.33 µg/l, respectively). although not statistically significant, the hg level in the lss group was found to be higher in all three tissues than in the hnp group (p>0.05). in the lss group, as the hg serum level increased, the hg disc level increased significantly (r=0.608, p<0.01). on the other hand, as the hg serum level increased in the hnp group, the hg disc level decreased significantly (r= -0.579, p<0.01). again, an increase in hg bone level was detected with the increase in hg disc level in both groups (p>0.05). table 6. correlations of hg levels in bone, serum and disc tissues in both groups groups hg_bone [µg/l] hg_serum [µg/l] hg_disc [µg/l] lss (n=30) hg_bone [µg/l] 1 ,190 ,053 329 comparison of levels of toxic trace elements in two most common spinal pathologies hg_serum [µg/l] ,190 1 ,608** hg_disc [µg/l] ,053 ,608** 1 hnp (n=20) hg_bone [µg/l] 1 -,579** ,023 hg_serum [µg/l] -,579** 1 ,348 hg_disc [µg/l] ,023 ,348 1 graphic 4. graphical view of mean hg levels in bone, serum and disc tissues lead (pb) evaluation: it was detected that the pb bone level was approximately 2 times the pb disc level for both the lss and hnp groups (15.76±9.81 µg/l and 6.82±9.88 µg/l for lss, respectively; 13.26±6.28 µg/l and 5.61±6.93 µg/l for hnp). the highest pb level in all tissues was detected in bone tissue in both groups (15.76±9.81 µg/l and 13.26±6.28 µg/l, respectively). although not statistically significant, it was observed that as pb serum level increased in both groups, pb bone and pb disc levels decreased (p>0.05). again, an increase in pb bone level was detected with the increase in pb disc level in both groups (p>0.05). while the lowest pb level was observed in the disc tissue in the lss group, it was found in the serum in the hnp group. table 7. correlations of pb levels in bone, serum and disc tissues in both groups groups pb_bone [µg/l] pb_serum [µg/l] pb_disc [µg/l] lss (n=30) pb_bone [µg/l] 1 -,302 ,341 pb_serum [µg/l] -,302 1 -,148 pb_disc [µg/l] ,341 -,148 1 hnp (n=20) pb_bone [µg/l] 1 -,189 ,109 pb_serum [µg/l] -,189 1 -,060 pb_disc [µg/l] ,109 -,060 1 graphic 5. graphical view of mean pb levels in bone, serum and disc tissues discussion mechanical effects, aging, genetic, systemic and toxic factors are held responsible for the pathophysiology of intervertebral disc degeneration (7). however, the accumulation of toxic trace elements in intervertebral discs and the effects they may create have been little studied in the literature. kubaszewsk et al. compared a number of trace element levels in intervertebral disc and bone tissue and concluded that disc tissue provides a more stable environment for elemental analysis (8). in another study, nowakowski et al. determined the trace element in the degenerative intervertebral disc and pointed out that the levels are very different from the levels in other tissues and the existence of positive and negative correlations between the elements (9). although several trace element level determinations and comparisons have been made in the literature in the form of human and animal studies, especially for bone, in this study, which we have done for the first time, the amount of toxic trace elements in intervertebral disc degeneration, which is thought to develop with different pathophysiological mechanisms in two different diseases, has been compared (10-12). the effects of essential and non-essential trace elements on human bone and their toxic threshold limits are stated in plasma, blood, and urine, and it is said that no toxic side effects are observed below 330 hakan a.k., soner yaycioglu, iskender samet daltaban et al. these amounts (13). however, the effects of these trace elements on body metabolism at under the toxic levels and their relationship with some chronic diseases have not been clearly demonstrated yet. in our study, the serum, bone and intervertebral disc levels of five toxic trace elements (cd, al, pb, hg, and as) were compared and the results were tested to see if they were statistically significant. cd element was found to be lowest in bone in both lss and hnp groups (0.30±0.10 µg/l and 0.32±0.12 µg/l, respectively). on the other hand, it was found that it accumulated more in the intervertebral disc tissue than in the bone in both groups and was slightly higher in the lss group. the serum level of cd in the hnp group was significantly higher than the serum level of the lss group. in addition, while cd serum and bone levels were inversely proportional in the lss group, this situation was found to be directly proportional in the hnp group. it is known that the cd can have toxic effects in many organs in humans (14). osteotoxic and osteoporotic effects were observed especially in the male and female groups made on bone (15,16). experimental cell culture studies have shown that the cd element triggers the apoptosis effect on rat osteoblasts with its mechanisms (17). again, in experimental studies, it was determined that the cd element decreases the bone collagen content and increases the collagen solubility (18). in another experimental study performed on male rats, it was concluded that the compact bone microstructure was changed, the bone weight was affected due to decreased the vascular structure which resulted in secondary osteoporosis and decreased potential bone mechanical properties (19). the higher cd element in the intervertebral disc in our study suggests its relationship with degenerative processes. studies have shown that cd element increases osteoclastic differentiation and turns the process in favor of degeneration (20). disc degeneration is a multifactorial process, and effects such as the initiation of disc degeneration by one or more of these factors and the insufficiency of the regeneration process, especially in hnp cases developing as a result of axial loading with acute process, by preventing regeneration with the negative effect of the cd element, rapidly expanding the annulus tear and as a result suggesting the hypothesis that the disc may be mechanically protruding. the high level of serum cd in the hnp group in our study supports this hypothesis. in addition, it has been determined that the cd element has a vasoconstrictor effect on the vascular system (21). for this reason, it was thought that the nutrition of the intervertebral disc may be impaired secondarily and accelerate the degenerative process. since the osmotic supply of the intervertebral disc would be disrupted, it has been hypothesized that the cd element may continue to accumulate in the disc space and increase the degenerative process. as a result, it is predicted that the cd element may directly initiate the degenerative process, either as a cofactor or as a predisposing factor in this process. aluminum (al), another toxic trace element, was found to be higher in the intervertebral disc of the hnp group than in the lss group in our study (2.97±1.50 µg/l and 2.14±1.25 µg/l, respectively, p=0.038). al element is known to cause dementia, osteomalacia and microcytic anemia especially in dialysis patients at toxic doses (22). however, the effects on the human body in amounts below toxic limits and in chronic processes have not been clearly determined yet, and the perception of a safe metal with little effect on human health continues (23). al element is found in almost all human body organs and tissues. the highest concentration was found in the bones after the lungs, and it was reported that nearly half of the body al element was in the skeletal system (24). although these rates change in patients exposed to excessive al, such as dialysis patients, the amount of al may also change with osteoporosis that develops with aging, and the increase in osteoclast cell activity and resorption. there are also studies showing that it is not associated with the development of osteoporosis in elderly patients exposed to normal amounts of al (25). in our study, bone al element levels in both groups were found to be higher than other tissues, which is consistent with the literature. however, the fact that al element, which was found significantly in our results, was at higher levels in the intervertebral discs belonging to the hnp group, again suggests that it may cause a degenerative event in the formation of disc herniation in the acute period, as well as the fact that the intervertebral disc, which has degenerated for some reasons and lost its normal osmotic nutrition feature, may have accumulated more al element. 331 comparison of levels of toxic trace elements in two most common spinal pathologies the second possibility seems more logical since there was no significant difference in bone and serum levels of al element. another toxic trace element, arsenic (as), can have a toxic effect on almost all body organs and tissues (26). although the effect of the as element, which can be stored in the bone, on the bone has not been clearly demonstrated clinically, it has been shown to cause osteoporosis by inhibiting osteoblastic activity in a few experimental studies (27,28). in our study, while there was no significant difference between the element levels between the two patient groups, it was found that while the serum level of as increased in the hnp group, the bone level also increased in direct proportion. as mentioned before, the degenerative event in the lss group is not limited to the intervertebral disc, but develops as a result of an osteoporotic degenerative process that also affects the facet joints and the spine. on the other hand, the hnp group is a group that causes intervertebral disc degeneration and protrusion of the nucleus in a shorter time, but no osteoporotic degeneration of the bones is observed. therefore, as toxic element forms apatite arsenate and possibly other calcium arsenate crystals by competing with the phosphate groups in hydroxyapatite crystals via alkaline phosphatase in the hnp group where bone turnover continues (29,30). in the lss group formed on an osteoporotic background, it will not be possible for the as element to form crystals in the bone as a result of loss of mineralization and the shift of metabolism to catabolism. for this reason, it was thought that the increase of as element in bone tissue of hnp group along with the increase in serum level may be due to the increase in arsenate crystals in the bone. in support of this assumption, in the literature, in an elderly female patient who was chronically exposed to as element, with the dissolution of calcium arsenate crystals as a result of increased bone resorption during and after menopause, as blood levels increased to toxic levels and gave clinical symptoms and signs as a result of many organ damage (31). the other toxic trace element mercury (hg), which we investigated in our study, was found to be the lowest at the disc level for both groups. in the literature, there is no clear data or many studies on the effects of hg element on human bone, and bone toxicity is not mentioned. in a study conducted on men, no correlation was found between the increase in hg level in the blood and lumbar bone mineral density, and even as in some studies, it was observed that the incidence of bone fracture development decreased with the increase of the hg element level in the blood (32,33,34). another data we obtained is that as hg serum level increases in the lss group, the hg disc distance level also increases, and it decreases inversely with the serum level in the hnp group. although these data suggest that the bone density is tried to be preserved with hg increase in the lss group, which is an osteoporotic group, this would be a weak assumption that needs proof. our last toxic trace element lead (pb) was found in the bone and in the intervertebral disc distance in both groups, approximately twice its levels. it is known that pb element has many systemic effects and is stored more in the bone in adults (35). in a study on growing rats, it was found to impair bone development (36,37). the result we found is that the pb element is mostly found and stored in the bone tissue. as a result, today toxic elements pose a great threat to the environment and human life (38,39). determining the standard amounts of toxic trace elements in different organs and tissues in the human body presents difficulties. in the literature, toxic trace element amounts have been detected in some tissues obtained from cadaver studies (40,41). however, within the framework of ethical rules, it is obvious that toxic trace element research can be done and a connection with diseases can be made in materials such as biopsies taken in some diseases that require surgery. supporting meaningful results from clinical studies with experimental studies will accelerate research on toxic elements. acknowledgment thanks are giving to vugar ali türksoy for performing icp-ms. references 1. balali-mood m, naseri k, tahergorabi z, khazdair mr, sadeghi m. toxic mechanisms of five heavy metals: mercury, lead, chromium, cadmium, and arsenic. front pharmacol. 2021;12:643972. published 2021 apr 13. doi:10.3389/fphar.2021.643972. 2. lama p, le maitre cl, dolan p, tarlton jf, harding ij, adams ma. do intervertebral discs degenerate before 332 hakan a.k., soner yaycioglu, iskender samet daltaban et al. they herniate, or after? bone joint j. 2013 aug;95b(8):1127-33. doi: 10.1302/0301-620x.95b8.31660. 3. martin md, boxell cm, malone dg. pathophysiology of lumbar disc degeneration: a review of the literature. neurosurg focus. 2002 aug 15;13(2):e1. doi: 10.3171/foc.2002.13.2.2. 4. lee bh, moon sh, suk ks, kim hs, yang jh, lee hm. lumbar spinal stenosis: pathophysiology and treatment principle: a narrative review. asian spine j. 2020 oct;14(5):682-693. doi: 10.31616/asj.2020.0472. 5. singh k, phillips fm. the biomechanics and biology of the spinal degenerative cascade. seminars in spine surgery. volume 17, issue 3, september 2005, pages 128-136. 6. fruth i, greskötter k, luther w, vıenerıus t, vvıttenberg r. histopathology of herniated lumbar intervertebral discs compared wıth non-herniated lumbar intervertebral discs. j turk spinal surg 1994;5:59-64. 7. hadjipavlou ag, tzermiadianos mn, bogduk n, zindrick mr. the pathophysiology of disc degeneration: a critical review. j bone joint surg br. 2008 oct;90(10):1261-70. doi: 10.1302/0301-620x.90b10.20910. 8. kubaszewski, ł.; zioła-frankowska, a.; frankowski, m.; rogala, p.; gasik, z.; kaczmarczyk, j.; nowakowski, a.; dabrowski, m.; labedz, w.; mi ˛ekisiak, g.; et al. comparison of trace element concentration in bone and intervertebral disc tissue by atomic absorption spectrometry techniques. j. orthop. surg. res. 2014, 9, 99. 9. nowakowski a, kubaszewski ł, frankowski m, wilkfrańczuk m, zioła-frankowska a, czabak-garbacz r, kaczmarczyk j, gasik r. analysis of trace element in intervertebral disc by atomic absorption spectrometry techniques in degenerative disc disease in the polish population. ann agric environ med. 2015;22(2):362-7. doi: 10.5604/12321966.1152096. 10. ericson je, smith dr, flegal ar (1991) skeletal concentrations of lead, cadmium, zinc, and silver in ancient north american pecos indians. environ health perspect 93:217–224. 11. kuo hw, kuo sm, chou ch, lee tc. determination of 14 elements in taiwanese bones. sci total environ. 2000 jun 8;255(1-3):45-54. doi: 10.1016/s0048-9697(00)00448-4. 12. lanocha n, kalisinska e, kosik-bogacka di, budis h, sokolowski s, bohatyrewicz a. comparison of metal concentrations in bones of long-living mammals. biol trace elem res. 2013;152(2):195-203. doi:10.1007/s12011-013-9615-x 13. rodríguez j, mandalunis pm. a review of metal exposure and its effects on bone health. j toxicol. 2018 dec 23;2018:4854152. doi: 10.1155/2018/4854152. 14. genchi g, sinicropi ms, lauria g, carocci a, catalano a. the effects of cadmium toxicity. int j environ res public health. 2020 may 26;17(11):3782. doi: 10.3390/ijerph17113782. 15. nawrot t, geusens p, nulens ts, nemery b. occupational cadmium exposure and calcium excretion, bone density, and osteoporosis in men. j bone miner res. 2010 jun;25(6):1441-5. doi: 10.1002/jbmr.22. 16. akesson a, bjellerup p, lundh t, lidfeldt j, nerbrand c, samsioe g, skerfving s, vahter m. cadmium-induced effects on bone in a population-based study of women. environ health perspect. 2006 jun;114(6):830-4. doi: 10.1289/ehp.8763. 17. zhao h, liu w, wang y, dai n, gu j, yuan y, liu x, bian j, liu zp. cadmium induces apoptosis in primary rat osteoblasts through caspase and mitogen-activated protein kinase pathways. j vet sci. 2015;16(3):297-306. doi: 10.4142/jvs.2015.16.3.297. 18. galicka a, brzóska mm, sredzińska k, gindzienski a. effect of cadmium on collagen content and solubility in rat bone. acta biochim pol. 2004;51(3):825-9. 19. duranova h, martiniakova m, omelka r, grosskopf b, bobonova i, toman r. changes in compact bone microstructure of rats subchronically exposed to cadmium. acta vet scand. 2014 sep 24;56(1):64. doi: 10.1186/s13028-014-0064-0. 20. chen x, zhu g, jin t, zhou z, gu s, qiu j, xiao h. cadmium stimulates the osteoclastic differentiation of raw264.7 cells in presence of osteoblasts. biol trace elem res. 2012 jun;146(3):349-53. doi: 10.1007/s12011-011-9256-x. 21. angeli jk, cruz pereira ca, de oliveira faria t, stefanon i, padilha as, vassallo dv. cadmium exposure induces vascular injury due to endothelial oxidative stress: the role of local angiotensin ii and cox-2. free radic biol med. 2013 dec;65:838-848. doi: 10.1016/j.freeradbio med.2013.08.167. 22. crisponi g, fanni d, gerosa c, nemolato s, nurchi vm, crespo-alonso m, lachowicz ji, faa g. the meaning of aluminium exposure on human health and aluminiumrelated diseases. biomol concepts. 2013 feb;4(1):77-87. doi: 10.1515/bmc-2012-0045. 23. exley c. human exposure to aluminium. environ. sci.: processes impacts, 2013, 15, 1807-1816. doi: 10.1039/c3em00374d 24. ganrot po. metabolism and possible health effects of aluminum. environ health perspect. 1986;65:363-441. doi:10.1289/ehp.8665363. 25. hellström, ho., mjöberg, b., mallmin, h. et al. no association between the aluminium content of trabecular bone and bone density, mass or size of the proximal femur in elderly men and women. bmc musculoskelet disord 7, 69 (2006). https://doi.org/10.1186/1471-2474-7-69. 26. abdul ks, jayasinghe ss, chandana ep, jayasumana c, de silva pm. arsenic and human health effects: a review. environ toxicol pharmacol. 2015 nov;40(3):828-46. doi: 10.1016/j.etap.2015.09.016. 27. wu ct, lu ty, chan dc, tsai ks, yang rs, liu sh. effects of arsenic on osteoblast differentiation in vitro and on bone mineral density and microstructure in rats. environ health perspect. 2014 jun;122(6):559-65. doi: 10.1289/ehp.1307832. epub 2014 feb 14. 333 comparison of levels of toxic trace elements in two most common spinal pathologies 28. tang ch, chiu yc, huang cf, chen yw, chen pc. arsenic induces cell apoptosis in cultured osteoblasts through endoplasmic reticulum stress. toxicol appl pharmacol. 2009 dec 1;241(2):173-81. doi: 10.1016/j.taap.2009.08.011. 29. rodríguez j, mandalunis pm. a review of metal exposure and its effects on bone health. j toxicol. 2018 dec 23;2018:4854152. doi: 10.1155/2018/4854152. 30. maly ip, eppler e, müller-gerbl m. high metabolic activity of tissue-nonspecific alkaline phosphatase not only in young but also in adult bone as demonstrated using a new histochemical detection protocol. gen. comp. endocrinol. (2017), http://dx.doi.org/10.1016/j.ygcen.2017.05.008 31. dani su. osteoresorptive arsenic intoxication. bone. 2013 apr;53(2):541-5. doi: 10.1016/j.bone.2013.01.017. epub 2013 jan 19. 32. kim yh, shim jy, seo ms, yim hj, cho mr. relationship between blood mercury concentration and bone mineral density in korean men in the 2008-2010 korean national health and nutrition examination survey. korean j fam med. 2016 sep;37(5):273-8. doi: 10.4082/kjfm.2016.37.5.273. 33. pollack az, mumford sl, wactawski-wende j, et al. bone mineral density and blood metals in premenopausal women. environ res. 2013;120:76-81. doi:10.1016/j.envres.2012.06.001. 34. cho gj, park ht, shin jh, hur jy, kim sh, lee kw, kim t. the relationship between blood mercury level and osteoporosis in postmenopausal women. menopause. 2012 may;19(5):576-81. doi: 10.1097/gme.0b013e3 182377294. 35. assi ma, hezmee mnm, haron aw, sabri my, rajion ma (2016) the detrimental effects of lead on human and animal health, veterinary world, 9(6): 660-671. 36. bhardwaj p, rai dv. effect of lead toxicity on bone calcium content and morphometric parameters. int j res med sci. 2016 jan;4(1):177-180. 37. conti mi, terrizzi ar, lee cm, mandalunis pm, bozzini c, piñeiro ae, martínez mdel p. effects of lead exposure on growth and bone biology in growing rats exposed to simulated high altitude. bull environ contam toxicol. 2012 jun;88(6):1033-7. doi: 10.1007/s00128-012-0602-2. 38. mahurpawar m. effects of heavy metals on human health. social issues and environmental problems: september, 2015. 39. jain j, gauba p. heavy metal toxicity-implications on metabolism and health. int j pharma bio sci 2017 october; 8(4): (b) 452-460. 40. yoo yc, lee sk, yang jk, sang wi, kim kw, chung kh, chung mg,choung sy. 2002. organ dis-tribution of heavy metals in autopsy materials from normal korean. j. health sci. 48(2):186–194. 41. masae yukawa m.s. , masashi suzuki-yasumoto m.d. , kazuhide amano m.s. & minoru terai ph.d. (1980) distribution of trace elements in the human body determined by neutron activation analysis, archives of environmental health: an international journal, 35:1, 3644. microsoft word 14canazgokhan_giant romanian neurosurgery (2018) xxxii 4: 625 631 | 625             doi: 10.2478/romneu-2018-0081 giant facial schwannoma with intracranial extension: a case report gokhan canaz1, izzet durmusalioglu1, mustafa ali akcetin2, nur topyalin3, cemile ozdemir4, ali osman akdemir2 1bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery, istanbul, turkey 2haseki training and research hospital, department of neurosurgery, istanbul, turkey 3van yuzuncu yil university, department of neurosurgery, van, turkey 4haseki training and research hospital, department of pathology, istanbul, turkey abstract: introduction: facial nerve schwannoma is a rare benign tumor which may originate from any segment of the facial nerve. we present a case of a giant cystic facial nerve schwannoma that showed extension to the middle cerebral fossa, together with its clinical and radiological characteristics, and a short review of the related literature. case report: a 52-year old female patient attended with complaints of numbness in the right half of her face, and mild hearing loss. examinations revealed house-brackmann grade 3 peripheral facial paralysis, sensorineural hearing loss of 30% in her right ear. she described three episodes of facial paralysis in the last six years. cranial mri and ct scan revealed a round cystic lesion of about 40x44x38 mm, located centrally and medially in the right temporal area. the surgical operation was performed and the lesion was totally extracted. the histopathological investigation reported the lesion as a schwannoma. conclusion: facial nerve schwannoma is a rare, benign tumor that occurs in different localizations. it may commonly be mistaken in prediagnosis and may be confused with other clinical states due to its clinical characteristics. it has to be kept in mind in the prediagnosis of patients with facial paresis and hearing loss. key words: schwannoma, facial palsy, tinnitus, hearing impairment introduction facial nerve schwannoma (fns) is a benign tumor that is rarely seen, and is generally difficult to diagnose before surgery. it may originate from any segment of the facial nerve through its extension from its origin in the cerebellopontine angle, to the parotid gland. schwannomas account for 8% of all intracranial tumors. of these, fnss account for about 1.9%. fnss that extend to the middle cerebral fossa are rare, as they commonly 626 | canaz et al giant facial schwannoma with intracranial extension             originate from the geniculate fossa (9, 10). here, we present a case of a giant cystic facial nerve schwannoma that showed extension to the middle cerebral fossa, together with its clinical and radiological characteristics, and a review of the related literature. case a 52-year old female patient attended with complaints of numbness in the right half of her face, and mild hearing loss. her physical examination revealed house-brackmann grade 3 peripheral facial paralysis, and hearing loss. the audiometric evaluation revealed a sensorineural hearing loss of 30% in her right ear. in her anamnesis, the patient described three episodes of facial paralysis: the first one occurred six years previously, the second four years, and the most recent one 15 days previously; a radiological investigation had not been performed. cranial contrast enhanced magnetic resonance imaging (mri), revealed a round cystic lesion of about 40x44x38 mm with regular margin, and with a peripheral capsule of about 8 mm maximal thickness, located centrally and medially in the right temporal area (figure 1). in the computerized tomography (ct), we observed erosion of the petrous bone and widening in the facial hiatus on the right side (figure 2). the patient was operated with a pre-diagnosis of meningioma, metastasis or schwannoma. the tumor was accessed using a right pterional craniotomy and sylvian dissection. the tumor was grey-yellow colored and it has hemorrhages in some areas. the tumor was easily dissected from the surrounding tissue. a tissue specimen was transferred for frozen section investigation. the pathological examination excluded malignancy. the mass was totally extracted following internal decompression. the optic nerve, carotid cisterns, and anterior communicating artery and its segments were intact. it was established that the petrous bone and dura were eroded in the area where the mass was adjacent to the temporal bone; therefore the dura was repaired in this region using a galeal graft, and the operation was completed. the histopathological investigation reported a schwannoma from the palisading pattern with s-100 protein positive, glial fibrillary acidic protein (gfap) and epithelial membrane antigen (ema) negative (figures 3a,b). a post-operative physical examination of the patient revealed progression of right facial paralysis to house brackmann grade 4 level; her hearing loss was also determined to progress. an investigation of the facial nerve electromyography (emg) revealed severe axonal damage in the facial nerve. a control emg was recommended one month later. almost complete hearing loss was determined on the right side in her audiometric evaluation. in the post-operative contrast enhanced cranial mri, it was determined that the mass has been totally excised (figure 4). the patient was discharged from hospital on the postoperative 14th day. the second control emg was administered about two months later, and the result was compatible with a lesion causing complete axonal damage to the right facial nerve segments that branches off from the orbicularis oculi and frontal muscles, and severe axonal damage in the segment that branches off from the orbicularis oris muscle. romanian neurosurgery (2018) xxxii 4: 625 631 | 627             figure 1 contrast enhanced cranial mri: a round cystic lesion of 40x44x38 mm in size with a regular margin, and with a peripheral capsule of 8 mm in maximal thickness, located centrally and medially in the right temporal lobe. a: axial section. b: coronal section figure 2 a: widening and erosion in the facial hiatus in axial section, in the temporal ct. b: erosion in the right temporal bone petrous segment, in the coronal section 628 | canaz et al giant facial schwannoma with intracranial extension             figure 3 a: bundles of fusiform cells by hematoxylin staining, magnified 100 times. b: diffuse positive reaction by s-100 immunohistochemical staining figure 4 postoperative changes in the postoperative contrast enhanced cranial mri romanian neurosurgery (2018) xxxii 4: 625 631 | 629             discussion schwannomas are simply benign tumors that originate from the schwann sheaths of the peripheral neural cells (cranial and spinal). giant size described as > 4.0 cm in maximal extrameatal diameter by samii et al. (7). they arise from sensory nerves, and are also known as neuromas. schwannomas that originate from cranial nerves account for 8% of intracranial tumors, and they occur at a relatively high frequency. fns accounts for 1.9% of all intracranial tumors. a fns generally extends intracranially to the cerebellopontine angle, and to a lesser extent, to the middle cerebral fossa (11). its rare occurrence in middle cerebral fossa, and the presence of more frequently seen lesions in this area that have similar appearances radiologically, make the differential diagnosis and accurate pre-diagnosis difficult. fns occurs clinically as a facial nerve paresis or paralysis with a long-lasting, fluctuating and progressive course. it has to be kept in mind that hearing loss (sensorineural or conductive type) occurs as frequently as facial paralysis. it has found to occur even more frequently in some studies, including large case series (4). this clinical feature often leads to false pre-diagnosis of vestibular schwannoma. symptoms are often found to be associated within the region of the facial nerve in which the lesion is located. the symptoms are generally characterized with various distributions of the facial, otologic, and mass effect signs; however this is not a clinically pathognomonic sign for the diagnosis of fns. a high correlation has been detected between the degree of facial nerve dysfunction and intratemporal location; otologic complaints like sensorineural hearing loss, tinnitus, and vertigo have been reported most frequently in patients with intracranial tumors (2). because the differential diagnosis of acoustic neuroma and fns is difficult, diagnosis of fns is almost always ascertained perioperatively or postoperatively. there are different studies and classifications related to the localization and frequency of fnss on the facial nerve. in many studies, it has been reported that fns most frequently occurs in the geniculate ganglion along the course of the facial nerve (4). in a study comprising 24 patients with a histopathological diagnosis of fns, the facial nerve has been investigated in eight separated segments, as follows: cerebellopontine angle, internal acoustic canal, labyrinth, geniculate fossa, nervus petrosus major, tympanic, mastoid, and intracranial. in this study, the geniculate fossa was established to be the most frequent location (83%); of these tumors located in the geniculate fossa, 60% occurred with extension to the labyrinth, and 30% were with petrosal nerve involvement. only two cases were determined with intracranial extension (8.3%), and both of these originated from the geniculate fossa. facial neuropathy was identified in these two cases with intracranial extension, and one case with sensorineural hearing loss (11). in a study, the location of fns was classified as intratemporal, extratemporal and intracranial, and the most frequent location was in the intratemporal region (61%); tumors with extratemporal (parotid area) and intracranial 630 | canaz et al giant facial schwannoma with intracranial extension             (cerebellopontine angle) locations, were reported in equal frequencies. in this study, extension to the middle cerebral fossa was not included in the intracranial location, and one tumor was reported with intracranial extension occurred in the intratemporal location (2). high-resolution enhanced ct and mri, are the most important visualization methods in the radiological diagnosis of fns. ct may not be considered absolutely essential; however it is important in the visualization of the changes in the temporal bone, to determine the origin of the tumor, and when planning surgery. erosion of the petrous bone, internal acoustic canal and a widened facial hiatus can easily be visualized using ct, which also helps in the preoperative differential diagnosis (8). an contrast enhanced mri is the preferential diagnosis for fns, independent of the size and location of the tumor. these tumors classically occur in mr imaging as hypo-hyperintense in the t1 weighted sequences, hyperintense in the t2 weighted sequences, and with contrast enhancement (3). large tumors commonly show cystic differentiation, and peripheral contrast enhancement. fnss with extension to the middle cerebral fossa, are benign tumors, and they frequently cause mass effect; the first choice of treatment is therefore surgery. different studies make different recommendations regarding the surgical indication and approach; however the most common suggestion for tumors beyond house-brackmann stage 3, is surgery (4). fnss are tumors that grow very slowly (0.02 cm3 /year); however surgery must not be delayed when there is involvement of the middle fossa (6). taking into consideration the sense of hearing, and location of the tumor in the facial nerve segment, suboccipital, infratemporal, frontotemporal, transpetrosal, and retrosigmoid approaches may be undertaken by neurosurgeons, with the participation of nose-ear-throat specialists, if needed. fnss are tumors of the nerve sheath, and it is theoretically possible to extract them without damaging the nerve; however following middle fossa surgery, this segment of the facial nerve is almost always extracted together with the tumor. this results in permanent facial paralysis. there are studies in the literature using different methods of reconstruction; however nerve function better than that of house-brackmann stage 3 cannot be maintained (2, 5). the general methods applied include the interposition of the nervus auricularis major, and hypoglossal nerve anastomosis by grafts from the sural nerve or vestibular nerve. additional techniques including sutures and fibrin tissue adhesives without sutures are also used. facial nerve conduction can be maintained in some of these studies; however clinical improvement does not occur, due to atrophy developing in the muscles that it innervates. in cases with unimpaired hearing occurring with tumors extending to the middle cerebral fossa, transmastoidmiddle fossa combined surgery is recommended. hearing may be maintained to some extent following surgery, in small or moderate tumors (3-15 mm); in large tumors (>18 mm), but it has also been reported that it’s not possible to protect the sense of hearing (1). romanian neurosurgery (2018) xxxii 4: 625 631 | 631             conclusion facial nerve schwannoma is a rare, benign tumor that occurs in different localizations. it may commonly be mistaken in prediagnosis, and may be confused with other clinical states due to its clinical characteristics. it is possible to protect the sense of hearing, and the facial nerve functions in cases diagnosed at an early stage; therefore it has to be kept in mind in the differential diagnosis of patients with facial paresis and hearing loss. correspondence gokhan canaz, bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery, bakirkoy / istanbul, turkey. phone: +90 212 409 15 15 mail:gokhancanaz@gmail.com references 1. arts ha, telian sa, el-kashlan h, thompson bg. hearing preservation and facial nerve outcomes in vestibular schwannoma surgery: results using the middle cranial fossa approach. otology & neurotology : official publication of the american otological society, american neurotology society [and] european academy of otology and neurotology 2006;27:234-241. 2. dort jc, fisch u. facial nerve schwannomas. skull base surgery 1991;1:51-56. 3. lane ji. facial nerve disorders. neuroimaging clin n am 1993;3:129–151. 4. mcmonagle b, al-sanosi a, croxson g, fagan p. facial schwannoma: results of a large case series and review. the journal of laryngology and otology 2008;122:1139-1150. 5. nadeau dp, sataloff rt. fascicle preservation surgery for facial nerve neuromas involving the posterior cranial fossa. otology & neurotology : official publication of the american otological society, american neurotology society [and] european academy of otology and neurotology 2003;24:317-325. 6. o'reilly bf, mehanna h, kishore a, crowther ja. growth rate of non-vestibular intracranial schwannomas. clinical otolaryngology and allied sciences 2004;29:94-97. 7. samii m, gerganov vm, samii a. functional outcome after complete surgical removal of giant vestibular schwannomas. journal of neurosurgery 2010;112:860867. 8. shankar l, hawke m, leekam rn, rutka j. computed tomographic analysis of the intratemporal facial nerve and facial nerve neuromas. canadian association of radiologists journal = journal l'association canadienne des radiologistes 1989;40:150-155. 9. srinivas r, krupashankar d, shasi v. intracerebral schwannoma in a 16-year-old girl: a case report and review of the literature. case reports in neurological medicine 2013;2013:171494. 10. symon l, cheesman ad, kawauchi m, bordi l. neuromas of the facial nerve: a report of 12 cases. british journal of neurosurgery 1993;7:13-22. 11. wiggins rh, 3rd, harnsberger hr, salzman kl, shelton c, kertesz tr, glastonbury cm. the many faces of facial nerve schwannoma. ajnr american journal of neuroradiology 2006;27:694-699. doi: 10.33962/roneuro-2021-073 imaging characteristics, histopathological features and surgical considerations regarding aggressive meningiomas. case series and review of the literature g. popescu, francesca paslaru, a.c. paslaru, m. apostol, m.c. zaharia, t. corneliu, m. mitrica, m. popescu, r.m. gorgan romanian neurosurgery (2021) xxxv (4): pp. 428-433 doi: 10.33962/roneuro-2021-073 www.journals.lapub.co.uk/index.php/roneurosurgery imaging characteristics, histopathological features and surgical considerations regarding aggressive meningiomas. case series and review of the literature g. popescu1,2, francesca paslaru1, a.c. paslaru3,4, m. apostol1, m.c. zaharia1, t. corneliu3,5, m. mitrica6, m. popescu7, r.m. gorgan1,3 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 phd student, “carol davila” university of medicine and pharmacy, bucharest, romania 3 “carol davila” university of medicine and pharmacy, bucharest, romania 4 department of genetics,“dr. victor gomoiu” children’s clinical hospital, bucharest, romania 5 department of neurosurgery, national institute of neurology and neurovascular diseases, bucharest, romania 6 department of neurosurgery, "dr. carol davila" central military emergency hospital, bucharest, romania 7 department of neurosurgery, pitesti emergency hospital, university of pitesti, romania abstract meningiomas are tumors of the meninges that arise primarily from arachnoidal cap cells, but they can also occur rarely as primary tumors in other localizations, such as within the ventricles. they stand for 24-30% of primary intracranial tumors and affect mostly women in their middle age or later adult life [1, 2]. meningiomas can be classified, according to world health organization (who) classification of central nervous system (cns) tumors, as benign (grade i, most frequently encountered type), atypical (grade ii) or anaplastic (grade iii), based mostly on histopathological criteria known to be associated with tumor progression, recurrence risk and survival. since meningioma grading based on the who classification is the most important factor determining therapeutic management and tumor prognosis, there has been an increasing interest in adding new criteria for better characterization of these tumors. thus, the 2016 edition of who classification recognized brain invasion as an independent criterion for atypical (grade ii) meningioma diagnosis [3]. however, meningiomas that display aggressive features such as rapid growth and higher recurrence rate, can also involve blood vessels and bone. hence, the authors aim to describe a different entity, aggressive meningiomas, not previously listed as a tumor keywords aggressive meningiomas, clinicopathological features, imaging characteristics, surgical management corresponding author: c. toader “carol davila” university of medicine and pharmacy, bucharest, romania corneliu.toader@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 429 aggressive meningiomas. case series and review of the literature phenotype in the who classification of meningothelial-cell tumors, with regard to pre-, intra and postoperative methods for diagnosis and explore the implications on surgical strategies and adjuvant therapy. materials and methods we performed a single-center retrospective study. we reviewed the files of all patients diagnosed with primary intracranial meningioma at the 4th clinical department of neurosurgery, bagdasar-arseni clinical emergency hospital, between january 2013 and december 2018 and identified the cases of aggressive meningiomas, characterized by either: invasion into the brain parenchyma, involvement of the major blood vessels, cranial vault bone lysis without involvement of the outer table of the skull or complete bone destruction and aesthetic deformity, as showed by preoperative imaging and confirmed by histopathological examination. results we identified 291 patients with tumors meeting the required imagistic/histopathological criteria, from which we selected 2 representative cases for the current articles, aiming to better describe this tumor entity regarding pre-, intraand postoperative aspect and therapeutic strategy. first case a 65-year-old male was admitted to our department complaining of refractory headache ongoing for more than 3 months. his past history consisted of high blood pressure, permanent atrial fibrillation, type 2 diabetes mellitus, grade ii obesity and chronic anticoagulant treatment. he denied any episodes of seizures or loss of consciousness, limb weakness, paresthesia, visual deficits, speech disturbances or vomiting. clinical examination showed a small swelling in the right frontal region. neurological examination showed no deficits. contrast-enhanced ct scan revealed a large hyperdense extra-axial lesion in the right frontal region, measuring 64/46 mm in cranio-caudal diameter, with a small area of important contrast uptake and associated bone lysis, producing mass effect on midline structures that appear displaced 6 mm to the left side. image 1. contrast-enhanced ct scan, axial section, showing a large hyperdense extra-axial lesion in the right frontal region, with a small area of important contrast uptake, bone lysis, and mass effect displacing midline structures. gadolinium-enhanced mri scan revealed a large right fronto-basal extra-axial lesion displaying central necrosis and displacing the right lateral ventricle, anterior cerebral artery, falx cerebri and the superior sagittal sinus. image 2. gadolinium-enhanced t1-weighted mri scan, sagittal section, showing a large fronto-basal extra-axial lesion eroding into the adjacent bone. 430 g. popescu, francesca paslaru, a.c. paslaru et al. image 3. non-enhanced t2-weighted mri scan, coronal section, showing a right frontal lesion with extensive perilesional edema and displacement of the midline structures. image 4. gadolinium-enhanced t1-weighted mri scan, axial section, showing a large frontal extra-axial lesion eroding into the adjacent bone. the lesion produced erosion of right frontal bone and showed homogenous gadolinium uptake. angiography was performed in order to better describe the vascular supply of the tumor. image 5. digital-substraction angiography showing prolonged vascular blush. the surgical approach was aimed at gross total resection, as well as obtaining enough tissue sample for an accurate histopathological diagnosis with subsequent appropriate adjuvant therapy. a right fronto-temporal craniotomy was performed, revealing a reddish, well vascularized, firm tumor. postoperative ct-scan (image 6) showed gross total resection of the right fronto-basal meningioma. image 6. non-enhanced ct scan showing a right frontotemporal craniotomy and no tumoral remnant. 431 aggressive meningiomas. case series and review of the literature image 7. optic microscopy view of the intraoperative tumor sample, showing meningioma cells with atypical features and invasion into the adjacent parenchima and bone. postoperative evolution was favorable and the patient was discharged 7 days later second case a 7 4 y ea r s o l d f em al e w as a dm it t e d to o u r department for progressive right upper and lower limb weakness. her past history consisted of high blood pressure, ischemic heart disease, grade ii obesity and bilateral lower limb venous insufficiency. she denied any episodes of seizures or loss of consciousness, visual deficits, speech disturbances or vomiting. neurological examination showed right hemipharesis. contrast-enhanced ct scan revealed a left parasagittal parietal extra-axial lesion, partially calcified and displaying homogeneous contrast uptake, measuring 56/33 mm in diameter, with perilesional edema that displaced median structures 6,65 mm towards the right side. the lesion seemed to be inserted on the meninges and determining osteosclerosis of the surrounding bone (image 8). image 8. ct scan showing a left parietal extra-axial lesion, partially calcified, with perilesional edema and displacement of the midline structures towards the right side. mri scan revealed a large left parietal lesion extending towards the right side, with perilesional edema, left lateral ventricle displacement and adjacent bone invasion (image 9). 432 g. popescu, francesca paslaru, a.c. paslaru et al. image 9. t2-weighted mri scan, axial section, showing a large left parietal lesion extending towards the right side, with perilesional edema, left lateral ventricle displacement and adjacent bone invasion. histopathological examination showed atypical meningioma cells, with invasion into the nervous and destructive infiltration of adjacent bone tissue (image 10). image 10. optic microscopy view of the intraoperative tumour sample, showing meningioma cells with atypical features and direct invasion into the adjacent brain parenchima and bone. postoperative evolution was favorable and the patient was discharged 7 days later. discussion meningiomas are a heterogenous group of lesions that can be classified, based mostly on histopathological criteria, as benign (grade i, most frequently encountered type), atypical (grade ii) or anaplastic (grade iii), according to who classification of cns tumors. however, other characteristics have started to be recognized as independent criteria for diagnosing higher-grade meningiomas. nazem et al. studied the genomic alterations supposed to be encountered in many meningiomas patients, such as losses on chromosome 22 (who grade i), losses on chromosomes 1p and 14q (who grade ii) or modifications on chromosome 9p and 17q (who grade iii), but these changes have yet to be listed as independent diagnostic criteria (4). the 2016 edition of who classification stated that brain invasion can be considered an independent criterion for atypical (grade ii) meningioma diagnosis (3). meningiomas that display aggressive features such as rapid growth and higher recurrence rate, can also involve adjacent blood vessels and bone. karabagli et al. reported that no distinct histopathological feature could be used to predict the recurrence rate of meningiomas (5). behling et al reported that intraoperative detection and histopathological assessment of cns invasion can be an independent prognostic factor for recurrence, giving a better risk-adapted tumor classification (6). however, aggressive meningiomas, a tumor phenotype, characterized by rapid growth and involvement of adjacent brain tissue, blood vessels and bone, was not previously recognized as a separate entity in the who classification of cns tumors of the meninges. the involvement of so many important adjacent structures makes it more difficult to achieve a gross total resection, thus 433 aggressive meningiomas. case series and review of the literature making this type of tumors more prone to recurrence. conclusions aggressive meningioma, a different phenotype of tumor, characterised by rapid growth and involvement of adjacent brain tissue, blood vessels and bone, although not previously mentioned in the who classification, has a distinct pattern of evolution and postoperative recurrence rate. surgical procedures are challenging due to the implication of various tissues and the outcome depends on the location, size, grade of invasion and associated pathology. correspondence a.c. paslaru & c. toader (corneliu.toader@gmail.com) author with equal contribution: dr. m. popescu references 1. hanft s, canoll p, bruce jn. a review of malignant meningiomas: diagnosis, characteristics, and treatment. j neurooncol, 2010, 99(3):433-443. doi: 10.1007/s11060010-0348-9. pmid: 20730473. 2. rockhill j, mrugala m, chamberlain mc. intracranial meningiomas: an overview of diagnosis and treatment. neurosurg focus, 2007, 23(4):e1. doi: 10.3171/foc07/10/e1. pmid: 17961033. 3. brokinkel b, hess k, mawrin c. brain invasion in meningiomas-clinical considerations and impact of neuropathological evaluation: a systematic review. neuro oncol, 2017, 19(10):1298-1307. doi: 10.1093/neuonc/nox071. pmid: 28419308; pmcid: pmc5596167. 4. advances in meningioma genomics, proteomics and epigenetics: insights into biomarker identification and targeted therapies. nazem, a. , ruzevick, j. and ferreira, m.j. . 49, s.l. : oncotarget, 2020, vol. 11, pp. 4544-4553. 5. histopatholofical and clinical features as prognostic factors of atypical meningioma. karabagli, p., et al. s.l. : turkish neurosurgery, 2020. 6. cns invasion in meningioma how the intraoperative assessment can improve the prognostic evaluation of tumor recurrence. behling , f. , et al. 12, s.l. : cancers, 2020, vol. 12, p. 3620. microsoft word 6jitaruioana_thoraco romanian neurosurgery (2018) xxxii 4: 573 582 | 573             doi: 10.2478/romneu-2018-0073 thoraco-lumbar spine injuries – a retrospective study on 651 cases ioana viorela jitaru, al. stan, antonia nita, c.e. popescu emergency clinical hospital “prof. dr. n. oblu”, neurosurgery, iasi, romania abstract: introduction: thoracolumbar spine fractures are common injuries that can result in significant disability, deformity and neurological deficit. there are standard classification systems that have been described based on fracture morphology, injury mechanism, neurological deficit and injury to posterior ligamentous complex. the thoracolumbar junction (t10-l2) is uniquely positioned in between the rigid thoracic spine and the mobile lumbar spine. this transition from the less mobile thoracic spine with its associated ribs and sternum to the more dynamic lumbar spine subjects the thoracolumbar region to significant biomechanical stress. hence, fractures of the thoracolumbar region are the most common injuries of the vertebral column. material and methods: this retrospective study was conducted on 651 cases with thoracolumbar spine fractures admitted in emergency clinical hospital “prof. dr. n. oblu”, neurosurgery, iasi, romania between ian 2014dec 2017. conclusions: trauma to the thoraco-lumbar spine and spinal cord is potentially devastating injury an it can be accompanied by significant neurologic damage , including paraplegia . patients with incomplete neurologic deficits may regain a large amount of useful function with early or rapid surgical treatment.imaging studies are essential to confirm the exact location of lesion, to assess the stability of the spine. key words: thoracolumbar spine fractures introduction the thoracolumbar junction (t10-l2) is a biomechanical transition zone prone to injury because of an inherent susceptibility to the kinetic energy transfer from the stiff, rostral thoracic spine to the relatively more flexible, caudal lumbar spine(1). the most common mechanisms of injury are those of a highvelocity pattern; these include motor vehicle collisions, falls, occupational injuries, and sport injuries.(2) high-velocity bony injuries carry an additional 25% risk for accompanying spinal cord injury (sci) and 30% risk for intraabdominal injury. further complicating this problem is the estimated rate of 50% of concomitant neurological injury that is associated with these fractures.(3). estimates of the north american incidence of 574 | jitaru et al thoraco-lumbar spine injuries             thoracolumbar traumatic injury ranges from 12 to 50 million patients annually, mostly occurring in the adolescent to young adult population aged 15 to 29 years. with the aforementioned 50% rate of neurological injury, 6 to 25 million new cases of neurological injury per year can be expected in a demographic whose subsequent lifelong disability results in a huge societal cost from an injury that occurred during their chief productive years.(1-5) classification of thoraco-lumbar spinal injuries with the variety of fracture morphologies that can be seen at the thoracolumbar junction, multidisciplinary teams caring for the trauma population have sought for a simplified classification scheme for determining spinal stability and recommended management. the initial classification schemes have focused on fracture types. because of the highly controversial status of the preferred management of thoracolumbar burst fractures, classifying thoracic and lumbar injuries has been a modern topic of research interest. one reason for the lack of consensus among health care providers is the presence of level i evidence supporting the management of stable thoracolumbar burst pattern fractures in patients without neurological deficit with the use of an orthosis. in this study, equivalent outcomes were found between bracing and arthrodesis. with the considerable number of fracture morphologies, a simplified algorithm for evaluating and organizing fractures gave birth to early thoracolumbar classification systems (1). modern classification systems not only evaluate the fracture pattern but also have evolved with our understanding of the likelihood of a patient’s need for surgery through our knowledge of factors that contribute to spinal instability. the extent of canal compromise and morphology of the thoracolumbar fracture type, presence of a neurological deficit, and radiographic findings that constitute a stable thoracolumbar spine are three major areas of confusion that play a major role in the newest classification system in use, the thoracolumbar injury classification and severity score (tlics), a classification system put forward by the spinal trauma study group (stsg).(1, 3, 6, 7, 8) aospine thoracolumbar spine injury classification system in 2013, the tlics was further expanded and developed into a newer aospine thoracolumbar spine injury classification system. this classification system was developed by an international panel of members evaluating three basic parameters: morphologic classification of the fracture, neurological status, and clinical modifiers. the morphologic classification is based on three main injury patterns: type a compression (including wedge impaction, split pincer, incomplete burst, or complete burst, type b tension band disruption (divided between osseous and osseoligamentous disruptions), and type c displacement-translation (hyperextension, translation, or separation) injuries. eight subtypes were proposed (five in the a group, three in the b group, and one in the c group). additionally, clinical modifiers were incorporated to address indeterminate injuries and patient-specific comorbidities such as ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis. unlike the tlics, the updated aospine classification is based on ct scan, an imaging tool widely romanian neurosurgery (2018) xxxii 4: 573 582 | 575             available at trauma centers worldwide. this classification adds clinical aspects that can better guide fracture management when combined with a severity score in the future. however, clinical validation requires large prospective observational studies. thoracolumbar injury classification and severity score proposed by the stsg, the tlics set out to standardize the decision-making process for operative versus nonoperative management of thoracolumbar spine fractures. for this classification, the stsg evaluates the integrity of the plc, the injury mechanism, and the presence of a neurological deficit..disruption of the plc is given special attention, creating conditions of near instability as detected by mri. hence, plc injury provides enough points alone to warrant surgical correction.(6) 576 | jitaru et al thoraco-lumbar spine injuries             material and methods this retrospective study was conducted on 651 cases with thoracolumbar spine fractures admitted in emergency clinical hospital “prof. dr. n. oblu”, neurosurgery, iasi, romania between 2014-2017. romanian neurosurgery (2018) xxxii 4: 573 582 | 577             inclusion criteria: patients diagnosted with t-l injuries, recent injuries(<30 days) regarding the neurological status. exclusion criteria: minor injuries, pathological fractures. sex distribution in all 3 studies we can see that the majority of the patients were males (60%). age distribution the average age was 52.26, between 8 and 86 years old with 2 peaks between 41-50 in men and 61-70 in women. mechanism regarding the mechanism the most frequent are falls from a height (41%), followed by car accidents (14%). other mechanism implicated are falls form the same level (9%), from cart (6%), aggressions (7%) and unknown (23%). lesion level   8.53% 14.73% 13.18% 25.39% 38.18% 8.14% 5.04% t11 t12 l1 l2 contigue etajate m u lt is e g m e n ta le (44) (131) (197) (76) (42) (26) (68) 578 | jitaru et al thoraco-lumbar spine injuries             ao classification neurological deficit treatament options there are 2 options for treatament: conservative and surgical. we used a conservative treatment in 65% cases (stable lesions a-type). indication for surgery: patients with neurological deficit, unstable lesions, tlics >5. regarding surgical treatment we use a posterior approach with a short or long instrumentation, an anterior approach or in selected cases a combined one (9). romanian neurosurgery (2018) xxxii 4: 573 582 | 579             posterior approach with short instrumentation posterior approach with long instrumentation burst fracture combined anterior-posterior approach results overall the results for surgical treatment have a good outcome for patients with a3, b1, b2 fractures because in this cases we use short instrumentation, one level above and one level below the lesion. for patients with a4 fractures the results were less satisfying with short instrumentation due to the degree of comminution (load-sharing >6 points).in this cases we recommend anterior reconstruction and posterior fixation. postop patients were clinical evaluated at 45 days, 3, 6, 12 months. for the evaluation of pain we used the visual analog scale (vas) (fig 1), odi, kyphosis angle (ka) and vertebral body height (vbh).   580 | jitaru et al thoraco-lumbar spine injuries             moment of evaluation conservative treatment surgical treatment admission 9,1 ( 8 – 10) 9,2 (8 – 10) at 3 months 5,3 (4 – 7) 4,1 (3 – 6) at 6 months 4,4 (3 – 6) 2,4 ( 1 – 3) at 12 months 3,4 ( 2 – 4) 1,8 (1 – 3) it is seen an important decreasing pain at 3 months after the injury regardless of the type of treatment. though patiens who underwent surgery had less pain at 12 months. ka and the reduction of the vbh in the anterior segment of the vertebral body for the patients treated conservately are represented in the next table: admission at 6 months at 12 months ka 13,80 16,53 17,42 vbh % 73,8 65,4 63,7 for this patients we can see an increase in local kyphosis with aprox 4 degrees and a reduction of vbh with 10% at 1 year after the injury. surgical treatment admission at 6 months at 12 months ka 14,22 11,2 13,8 vbh % 67,4 63,5 62,7 for the patients treated surgically the local kyphosis decreased with 0,4 degrees and the vbh decreased with 5% at 1 year after surgery. statistically the ka decreased significant in the group of patients treated surgically (p<0,01). odi evaluation moment odi conservative odi surgical admission 82,5 (73 – 88) 84,3 (69 – 92) at 3 months 48,4 (33 – 53) 39 (28 – 47) at 6 months 30 (21 – 38) 21 (16 – 28) at 12 months 23 (17 – 32) 18 (9 – 28) we can see an important decrease with 50% of the disability at 3 months after the treatment but at the final evaluation we can’t see any significant difference between this 2 groups. discussion in spine surgery, there is an ongoing effort to increase the knowledge of spinal surgery with the generation of well-designed, prospective, randomized trials. wood and colleagues, in a randomized prospective trial comparing operative and nonoperative treatment of thoracolumbar burst fractures, found no clinically significant advantage of surgery. in the surgical arm, the choice of an anterior, posterior, or combined approach was left to the discretion of the surgeon (3,10). siebenga and associates in a multicenter prospective randomized study of operative versus nonoperative treatment of thoracolumbar burst fractures, concluded that surgery resulted in fewer deformities at the mean 4-year follow-up but in superior functional and pain outcome scores (11). gnanenthiran and colleagues in a metaanalysis comparing operative and romanian neurosurgery (2018) xxxii 4: 573 582 | 581             nonoperative outcomes for thoracolumbar burst fractures, found four prospective studies, only two of which were randomized. they concluded that patients who underwent surgery tended have lower rates of kyphosis, but these patients did not statistically differ in terms of functional and pain outcomes at 4 years. however, because thoracolumbar burst fractures are not all the same with regard to their likelihood of developing kyphosis or instability, future prospective studies should incorporate the tlics system into the inclusion and exclusion criteria.(12) operative planning is a multifactorial decision-making process. arguably, the most important factor for determining anterior or posterior approach is the location of the pathology. the most common pathologies at the thoracolumbar junction are anterior and middle column (axial compression mechanisms, e.g., compression or burst). one other pitfall in prospective studies is the heterogeneity of treatment plans with regard to combining anterior, posterior, or combined approaches. . however, modern techniques allow for all three columns to be addressed by the posterior approach (14). also, less invasive techniques such as percutaneous pedicle screw instrumentation and lateral interbody placement allow for stabilization as needed, with minimal disruption. for specific pathology, such as retropulsed fragments into the canal, some authors argue that an anterior, retroperitoneal approach allows for the greatest ease of neural decompression. however, many advocate for the benefits of a posterolateral approach in the ability to access all three columns, decompress retropulsed anterior pathology, and provide three-column stabilization through an anteriorly placed graft as well as a pedicle screw-rod construct. lin and colleagues compared anteroposterior with posterolateral decompression and instrumented fusion, finding no statistically significant difference between the two groups with respect to all functional and radiographic outcomes scores.(13) one systematic review of posterior versus anteroposterior decompression and fusion for thoracolumbar burst fractures found a greater degree of restoration of the sagittal anatomic alignment at the higher cost of blood loss, extended hospital stay, longer intraoperative durations, higher morbidity, and higher monetary costs for anterior – posterior approach. in our cases we had less satisfying results in patients with a4 fractures who had a short fixation due to the degree of comminution in comparison with the other spine units. conclusion the management of thoracolumbar junction pathology remains controversial. the tlics represents the latest advancement in classification, providing a standardized guide for possible surgical management of thoracolumbar junction fractures. using both ao spine revised classification and tlics score we can establish more accurately the surgical indication. the conservative treatment is a reliable solution for patients with simple stable fractures and no neurological deficit. surgical treatment is the best solution for patients with 582 | jitaru et al thoraco-lumbar spine injuries             unstable fractures, complex fractures and neurological deficit. trauma to the thoraco-lumbar spine and spinal cord is potentially devastating injury and it can be accompanied by significant neurologic damage. patients with incomplete neurologic deficits may regain a large amount of useful function with early or rapid surgical treatment. correspondence alexandru stan – alexandrustan21@yahoo.com references 1.youmans and winn neurological surgery, seventh edition, vol 3:2482 – 2564 2.liu yj, chang mc, wang st et al. flexion-distraction injury of the thoraco-lumbar spine.injury 2003;34 920923 3.wood kb, li w, lebl ds, ploumis a. management of thoracolumbar spine fractures. spine j. 2014;14:145–64. [pubmed] 4.inamasu j, guiot bh. vascular injury and complication in neurosurgical spine surgery. acta neurochir (wien) 2006;148:375–87. [pubmed] 5.looby s, flanders a. spine trauma. radiol clin north am 2011;49:129–163 6.rihn ja, anderson dt, harris e, et al. a review of the tlics system: a novel, user-friendly thoracolumbar trauma classification system. acta orthop 2008;79:461– 466 7.sethi mk, schoenfeld aj, bono cm, harris mb. the evolution of thoracolumbar injury classification systems. spine j 2009;9:780–788 8.vaccaro ar, lehman ra jr, hurlbert rj, et al. a new classification of thoracolumbar injuries: the importance of injury morphology, the integrity of the posterior ligamentous complex, and neurologic status. spine 2005;30:2325–2333 9.schmidek and sweet operative neurological techniques indication, methods and results, 6th edition, vol 2, alfredo quifnoneshinojosa 2030 – 2033. 10.wood kb et al management of thoracolumbar spine fractures. spine 2014;14: 145-164 11.siebenga j et al treatment of traumatic thoracolumbar spine fractures:a multicenter prospective randomized study of operative versus non surgical treatment. spine 2006;31:2881-2890 12.gnanenthiran sr et al non operative versus operative treatment for thoracolumbar burst fractures without neurological deficit: a methanalysis . clean orthop relat res 2012; 470:567-577 13.lin b et al anterior aprroapch versus posterior approach with subtotal corpectomy, decompression and reconstruction of the spine in the treatment of thoracolumbar burst fractures: a prospective randomize controlled study.spinal disort tech 2011 14.popescu ce tratamentul fracturilor toraco-lombare. teza de doctorat. 2007 romanian neurosurgery (2019) xxxiii (2): pp. 156-159 doi: 10.33962/roneuro-2019-029 www.journals.lapub.co.uk/index.php/roneurosurgery cerebral pilocytic astrocytoma with spontaneous intratumoral haemorrhage in the elderly a rare entity. a case report and review of the literature amit narang, varun aggarwal, divya kavita, chandni maheshwari, prajjwal bansal * baba farid university of health sciences. faridkot. punjab, india abstract pilocytic astrocytomas (pa) are histologically are low-grade tumours, commonly found in the paediatric and young adult population. although cases of adult and elderly pilocytic astrocytomas are described in the literature, they are quite uncommon. the rate of pas with spontaneous bleeding is very less, with a high occurrence in children than in adults, moreover, that is in cerebellar pas. cerebral pas with intratumoral haemorrhage in the older age group is extremely rare. we present a case of a 60-year female presenting with acute neurological compromise resulting from an acutely haemorrhagic left temporal pilocytic astrocytoma. she was managed surgically with evacuation of tumoral haemorrhages, as well as resection of the tumour. postoperatively the patient made a remarkable recovery. introduction pilocytic astrocytoma (pa) is commonly a paediatric central nervous system glial tumour. adult occurrence is rare, especially in elderly population. [6,2] the most common sites of pas origin are cerebellum, optic chiasma, hypothalamus, and to a lesser exte nt, cerebral hemispheres, brain stem and spinal cord.[6] reports of tumours with intratumoral haemorrhage in elderly population are extremely rare. here we present a 60 years old female who presented with left temporal intratumoral bleed mimicing intracerebral haemorrhage. case summary ours is a 60-year-old female who was a known case of hypertension and was poorly compliant to anti-hypertensive medications. she had complaint of sudden onset of altered sensorium and slurring of speech. there was no history suggestive of trauma. patient was taken to a nearest clinic and was managed conservatively on the line of intra cerebral hemorhage (ich), and was discharched after seven days. three days after the discharge patients attendants brought the patient keywords astrocytoma, cerebral pilocytic astrocytoma, elderly population, intratumoral hemorrhage, tumor excision corresponding author: varun aggarwal guru gobind singh medical college and hospital faridkot, punjab, india drvarunaggarwal86@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 157 cerebral pilocytic astrocytoma with spontaneous intratumoral haemorrhage in the elderly a rare entity to our hospital for second opinion. on presentation her gcs was e3v3m5. contrast mri brain was done which was suggestive 48 x 34 mm altered signal intensity lesion in left temporoparietal cortex with vasogenic edema and with mass effect in the form of midline shift of 6.4 mm towards right. the lesion was hypointens on t2, t1 with marginal t1 hyperintensities, hyperintens on flair and intens blooming in gradient images. in post contrast studies subtle marginal enhancement noted. by enlarge, radiological features were suggestive of left temporal ich with mass effect. [fig-1]. patient was taken up for surgery. left frontotemporal craniotomy and evacuation of intracereberal hematoma was done. intraoperatively brain was bulging and there was large hematoma in rt temporal lobe, brain tissue all around the hematoma was greyish, soft and suckable this tissue was excised all around and was sent for biopsy. post operatively ncct was done suggestive of complete evacuation of ich with reduced mass effect [fig-2]. histopathology was suggestive of pilocytic astrocytoma (who grade i). patient improved significantly and discharged on 5th post op day with gcs e4v4m6. figure 1. a -t1, b -t2, cdw, dpost contrast mri showing lesion in left temporal lobe 158 amit narang, varun aggarwal, divya kavita et al. figure 2. first post op day ncct head showing complete evacuation of hematoma and reduced mass effect figure 3. histopathology was suggestive of low grade astrocytic tumor with abundant eosinophilic granular bodiespilocytic astrocytoma (who grade i) discussion pa is a histological subtype of astrocytomas, which accounted for approximately 15% of central nervous system (cns) tumours. pas are considered world health organization (who) grade i tumours, which have relatively distinct histological appearance and well demarcated boundaries. [1,5]. this tumour has much higher occurrence among children and adolescents than elderly. common age group for pas is 5 to 14 years, followed by 0 to 4 years and 15 to 19 years, however, pilocytic astrocytoma rarely occur over the age of 60. [2] patients having a pilocytic astrocytoma may present with sensory motor deficit, gait disturbance, headaches, cranial nerve deficits and hydrocephalus, depending on the exact location. the most common sites of these tumour origin are cerebellum, optic chiasma, hypothalamus, and to a lesser extent cerebral hemispheres, brain stem and spinal cord. [1] most of glial tumours, such as high-grade astrocytomas, oligodendrocytes, and mixed astrocytomas, have propensity for intratumoral bleeding. however, intratumoral hemorrhage is very rare among patients with pa. [6] the rate of pas with spontaneous bleeding is approximately 8%, with a high occurrence in children than in adults, which is mostly in cerebellar pa [6]. 159 cerebral pilocytic astrocytoma with spontaneous intratumoral haemorrhage in the elderly a rare entity relatively limited amount of literature is available on pas with intratumoral haemorrhage in older age group. although vascular necrosis and tumour invasion are the primary causes of bleeding in highgrade gliomas, the mechanisms underlying lowgrade gliomas remains unclear. [3] previous literature have demonstrated that spontaneous bleeding in pas is due to interaction of various factors, which includes specific pathological changes in vascular structures of tumour, such as proliferation of vascular endothelial cells, hyaline degeneration and interstitial degeneration. sun s. et al [6] suggested in their study, the vascular histology of bleeding tumour reveals a poorly developed capillary bed and thin vessel walls. bleeding tumour blood vessels, although rich in collagen have fewer elastic fibres and poor compliance, which can escalates the chances of tumour rupture. as reported previously the reticular vessels are more prone to rupture, which suggests an association between tumour capillary type and bleeding tendency.[4] in addition, intratumoral bleeding is associated with tumour growth, intratumoral vascular invasion, rupture of an encased aneurysm and coagulopathies. notably, higher arterial pressure and acute intracranial hypertension are also the predisposing factors. previous studies also suggest that calcification may contribute to intratumoral bleeding. [6,4]. it has been found that the spontaneous bleeding of pas is also associated with tumour vegf expression.[7] the patient in our case report developed spontaneous intratumoral hemorrhage, but the cause of bleeding is still not clear. therefore, we speculate that intratumoral bleeding may be attributed to tumour vascular abnormalities and hypertension. pas patients with intratumoral bleed leading to raised intracranial tension requirs emergency neurosurgical care. surgery is the preferred the treatment for pas with hemorrhage, which permits simultaneous removal of tumor and hematoma. tumors that occurred in the brain stem or visual pathway usually cannot be completely removed by surgery, though the residual tumors may cease to grow, or grow slowly, or even regress. therefore, a long-term follow-up is required for patients with complete and partial resection. the patients treated with subtotal resection may require post op chemotherapy and radiotherapy, but it is still a matter of debate. the prognosis of patients with pas is generally good. the location of the tumour and the extent of the resection can play an important role in the prognosis of pas patients. reoperation may be considered for most patients with recurrent pas. patients with partial resection of tumour can have a higher risk of recurrence. [8] literature suggests that a longer follow-up period is required for pas patients with intratumoral haemorrhage. conclusion based on the collective results from the present clinical experience and other related studies, we suggest that cerebral pas with spontaneous intratumoral haemorrhage is extremely rare, especially in elderly patients over the age of 60 years. we agree with the literature that to completely remove the tumour and hematoma; surgery is probably the most effective treatment option. longterm follow-up after surgical treatment of pas with intratumoral haemorrhage is crucial to identify and treat the recurrence if any. references 1. bornhorst m, frappaz d, packer rj. pilocytic astrocytomas. handbook clin neurol 2016;134:329–44. 2. cyrine s, sonia z, mounir t, et al. pilocytic astrocytoma: a retrospective study of 32 cases. clin neurol neurosurg 2013;115:1220–5. 3. kapoor a, savardekar a, tewari mk, et al. spontaneous hemorrhages in pediatric supratentorial pilocytic astrocytomas. malignant presentation of a benign entity. childs nerv syst 2015;31:1617–20. 4. kim ms, kim sw, chang ch, et al. cerebellar pilocytic astrocytomas with spontaneous intratumoral hemorrhage in adult. korean neurosurg 2011;49:363–6. 5. ostrom qt, gittleman h, liao p, et al. cbtrus statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2007–2011. neuro oncol2014;16:1–63. 6. sun s, zhou h, ding zz, shi h.cerebellar pilocytic astrocytomas with spontaneous intratumoral hemorrhage in the elderly: a case report and review of the literature. medicine (baltimore). 2018 aug;97(31). 7. wilson mp, johnson es, hawkins c, et al. hemorrhagic presentations of cerebellar pilocytic astrocytomas in children resulting in death: report of 2 cases. neurosurg pediatr2016;17:446–52. 8. ye jm, ye mj, kranz s, et al. a 10 year retrospective study of surgical outcomes of adult intracranial pilocytic astrocytoma. j clin neurosci 2014;21:2160–4. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-024 the role of strict patient-positioning during nursing in the management of intracerebral migration of gravitational bullet injury samir h. aldelfi, salima b. alsaadi, mohammed maan abdulazeez, mukarram n. musarhad, mohammed d. khudhair, samer s. hoz romanian neurosurgery (2020) xxxiv (1): pp. 154-157 doi: 10.33962/roneuro-2020-024 www.journals.lapub.co.uk/index.php/roneurosurgery the role of strict patient-positioning during nursing in the management of intracerebral migration of gravitational bullet injury samir h. aldelfi1, salima b. alsaadi2, mohammed maan abdulazeez3, mukarram n. musarhad1, mohammed d. khudhair1, samer s. hoz1 1 neurosurgeon, department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 radiologist, department of neuroradiology, neurosurgery teaching hospital, baghdad, iraq 3 medical student, college of medicine, baghdad university, baghdad, iraq abstract the intracranial migration of bullet was described in literature since cushing time and the first world war [1]. the literature is still away from delivering a clear guideline and constitutes more of case reports rather than comprehensive well-designed studies [2-13], this mostly due to the variability and diversity in the presentation and management of such cases. the migration of bullet can be a sequel of any type of penetrating injury to the skull [14]. intracranial migration after gravitational (falling) bullet injury is a unique type of injury that constitutes of significant human and material losses with differences in biomechanics and structural brain changes after the insult especially regarding the velocity of impact and the degree of yaw for the intracranially settled bullet [15]. the gravitational bullets injuries are considered by the international disease classification system as celebratory firing, that is quite common and is part of the traditional happy (marriage) or funeral event in the middle east in general and in rural areas of iraq in particular, and also reported in some areas around the world (south america, north africa, and middle of asia) [15,16]. introduction in the available articles [17-28], the accepted management options for the retained intracranial bullet with possible migration, include: • observation, activity restriction and follow-up: for bullets with minimal risk of migration, those include small irregular bullet fragment with pure intraparanchymal location. here, it is critical to know that the migration of bullet is rarely expected three months keywords patient-positioning, intracerebral migration, gravitational bullet injury corresponding author: mohammed maan abdulazeez college of medicine, baghdad university, baghdad, iraq mohammed.wwt@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 155 the role of strict patient-positioning in the management of intracerebral migration of gravitational bullet injury from the insult as the gliosis (encapsulated within tough scar) will surrounds the bullet and render it extremely resistant for migration [22,28]. • early surgery: for bullets that retained within the ventrciles that have a high risk for obstructive hydrocephalus and those just close to a hematoma cavity [22-26]. • delayed surgery: for migrating (moving) bullet that cause new neurological symptoms, large bullets with smooth (intact) contour, resides near the ventricles, moves toward an eloquent area, migrates for a significant distance (2.5 cm), moves freely in the cistern with risk of neurovascular compression or injury, and those resides in accesible and safe location. still some authors consider surgical removal of the bullet once migrated based on their personal experience [27]. theories on spontaneous bullet migration although the exact mechanism is not always known or being multifactorial [21], theories suggest different explanations for the mechanism, the trajectory and the final destination of the intracranially migrated bullet. the gravidity, the pulsating intracranial contents and softening of the surrounding tissues are the mechanism that is commonly mentioned [26]. the common expected trajectory is usually posteriorly either toward the sella turcica for bullets in the anterior cranial fossa or toward the torchula herophili for those in the posterior parietal, posterior temporal and occipital lobes. otherwise, the trajectory will be back along the initial bullet tract (the damaged brain). in rare occasions, the bullet may take out of the above suggested directions, here, surgeons should consider abscess development as a possibility [17-20,27]. patient positioning after admission for cases with retained intracranial bullet after gravitational (falling) bullet head injury, where the initial decision is close clinical follow-up (nonsurgical), the patient positioning during admission is critical. although activity restriction is part of the general practice during this observation period, some surgeons suggest a more strict head positioning during the nursing period and consider it as pivotal part of the management of such instances [14,28]. both rapp et al. [14] and taarnhoj [28] describe in their reports that they use the strict patient positioning during nursing in few cases, the aim of this positioning is an attempt to change or control the direction of bullet migration in migrationpossible cases. in our practice, we routinely implement this strict-positioning technique to render a deep bullet with possible migration to an accessible and easy to remove one. although rapp et al. [14] and taarnhoj [28] document using this positioning technique for penetrating bullet injury in general, our clinical experience suggests using this technique in gravitiational (falling) bullet injury will be more fruitful taking in consideration multiple factors that are unique for the falling bullets. the gravitiational (falling) bullets are usually non-fragmented, not very small nor too large, smooth outer contour and with less adhesive surrounding brain tissue (less cavitation and necrosis as compared to other types of penetrating bullet injuries), these factors make this falling bullets are more liable for migration and also more amenable to be affected and guided by the patient positioning during the early observation period (figure 1 shows an illustrative case scenario for the mentioned technique). thus, in cases of gravitational cranial bullet injury with a retained bullet that not mandate early surgery, we recommend a patient-specific activity restrictions and strict head positioning taking in consideration the possible trajectories of migration and well-designed for dragging and controlling the bullet movement into an accessible and a safe to remove destination. figure 1. an illustrative case for the use of strict patientpositioning during nursing in the management of intracerebral migration of gravitational bullet injury. a twelve-years-old male, a victim of gravitational bullet injury, presented to the emergency department of the neurosurgery teaching hospital. baghdad. iraq with disturbed consciousness (glasgow coma scale 14), left side weakness (grade 4 both upper and lower limbs), pai in the sky (contralateral upper quadrantanopia) visual field defect, with a small wound (1 cm) in the right frontal area (inlet). initial lateral skull x-ray showed the frontal inlet and the posterior temporal location of the bullet (a), that is confirmed by an urgent brain ct scan (c). the initial decision was to observe the patient as there were not significant wound or hematoma. the patient was put in strict supine position except for bathroom times with physiotherapy to his left side. 156 samir h. aldelfi, salima b. alsaadi, mohammed maan abdulazeez et al. three days later, with the patient still having a severe headache, we did a follow-up skull x-ray then new brain ct scan that showed the migration of the bullet posteriorly (b and d respectively). here, the decision was to remove the bullet as it moved to a surgically accessible location. the surgery went uneventful and the post-operative brain ct scan showed no hematoma at the site of surgery (e). the patient discharged 4 days later, fully conscious with only the same initial visual field defect. on next visits his vision improved, he returned back to school and having good marks too. references 1. cushing h. a study of a series of wounds involving the brain and its enveloping structures. british journal of surgery. 1917;5(20):558-684. 2. duman h, ziyal im, canpolat a: spontaneous subfalcial transcallosal migration of a missile to the contralateral hemisphere causing deterioration in neurological status— case report. neurol med chir (tokyo) 42:332333, 2002. 157 the role of strict patient-positioning in the management of intracerebral migration of gravitational bullet injury 3. fujimoto y, cabrera ht, pahl fh, de andrade af, marino jr: spontaneous migration of a bullet in the cerebellum— case report. neurol med chir (tokyo) 41:499-501, 2001. 4. hughes bd, vender jr: delayed lead pulmonary emboli after a gunshot wound to the head. case report. j neurosurg 105(3 suppl):233-234, 2006. 5. kamenski rs, emch tm, dastur kj, altschuler em: short interval spontaneous migration of an intracranial bullet fragment. j trauma 65:e13-5, 2008. 6. karabagli h: spontaneous movement of bullets in the interhemispheric region. pediatr neurosurg 41: 148-150, 2005. 7. ozkan u, ozate ̧s m, kemalog ̆lu s, güzel a: spontaneous migration of a bullet into the brain. clin neurol neurosurg 108:573-575, 2006. 8. hussain, m., bari, m. (2011). intracerebral migration of stray bullet leading to sudden and fatal worsening. journal of the college of physicians and surgeons pakistan, 21(3), 182-183. 9. kumar r, garg p, maurya v, sahu rn, mahapatra ak. spontaneous bullet migration-uncommon sequelae of firearm injury to the brain. the indian journal of neurotrauma. 2008 dec 1;5(2):119-21. 10. abdulazeez mm, dolachee aa, huber pz, romario mf, obaid ha, arakwazi ah, altaweel mm, hoz ss. intracranial ricocheted-bullet injuries: an overview and illustrative case. journal of acute disease. 2018 sep 1;7(5):186. 11. zafonte rd, watanabe t, mann nr. moving bullet syndrome: a complication of penetrating head injury. archives of physical medicine and rehabilitation. 1998 nov 1;79(11):1469-72. 12. abdulrahman al, shudifat, kefah taha, et al. migrated intracranial falling bullet, crossed midline twice in a conscious pa ent. med case rep. 2016, 2:2. 13. rapp lg, arce ca, mckenzie r, darmody wr, guyot dr, michael db. incidence of intracranial bullet fragment migration. neurological research. 1999 jul 1;21(5):475-80. 14. abdali ha, hoz ss, moscote-salazar lr. cranial gravitational (falling) bullet injuries: point of view. journal of neurosciences in rural practice. 2018 apr;9(2):278. 15. organisation mondiale de la santé, world health organization, who staff, who. the icd-10 classification of mental and behavioural disorders: clinical descriptions and diagnostic guidelines. world health organization; 1992. 16. rengachary ss, carey m, templer j. the sinking bullet. neurosurgery. 1992;30:291–295. 17. milhorat th, elowitz eh, johnson rw,etal. spontaneous movement of bullets in the brain. neurosurgery. 1993;32:140–143. 18. wasserman sm, cohen ja. spontaneous migration of an intracranial bullet fragment. mt sinai j med. 1979;46:512– 515. 19. leibeskind al, anderson rd, schechter mm. spontaneous movement of an intracranial missile. neuroradiology. 1973;5:129 –132. 20. grant ga. migrating intracranial bullets: a rare occurrence. world neurosurgery. 2012 mar 1;77(3):47980. 21. moores le. practical considerations for the management of migrating intracranial bullets. world neurosurgery. 2012 mar 1;77(3):481-3. 22. campbell e, howard wp, weary wb. gunshot wound of the brain: report of two unusual complications: bifrontal pneumocephalus and loose bullet in the lateral ventricle. arch surg. 1942;44:789–798. 23. furlow lt, bender mb, teuber hl. moveable foreign body within the cerebral ventricle: a case report. j neurosurg. 1947;4:380–386. 24. lang ek. acute hydrocephalus secondary to occlusion of the aqueduct by a bullet. j la med soc. 1969;121:167– 168. 25. masoudi ms, ghafarpasand f, yousefi s. a migrating retained intracranial bullet presenting with hydrocephalus and alterations of consciousness: a case report and literature review. journal of archives in military medicine. 2017;5(3). 26. raimondi aj, samuelson gh. craniocerebral gunshot wounds in civilian practice. journal of neurosurgery. 1970 jun;32(6):647-53. 27. taarnhoj p. gravity instrumental in removing an intracerebral missile: case report. journal of neurosurgery. 1962 apr 1;19(4):351-2. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0059 article  intra-cranial malignant peripheral nerve sheath tumor of olfactory nerve: a case report and review of literature varun aggarwal, amit narang, chandni maheshwari, divya kavita india      romanian neurosurgery (2018) xxxii 3: 469 472 | 469             doi: 10.2478/romneu-2018-0059 intra-cranial malignant peripheral nerve sheath tumor of olfactory nerve: a case report and review of literature varun aggarwal, amit narang, chandni maheshwari, divya kavita baba farid university of health sciences. faridkot. punjab, india abstract: malignant peripheral nerve sheath tumors (mpnsts) are one of the very rare high grade malignancies usually affecting extremities or trunk. incidence is 1/lac. intracranial mpnsts are even rarer, schwannomatous and commonly affecting cranial nerves viii &vii). intra-cranial mpnsts are usually sporadic, arising de novo. the second most common mode of origin is from malignant transformation from pre-existing schwannomas or neurofibroma. we present an extremely rare and probably the first case of intra-cranial malignant peripheral nerve sheath tumor of the olfactory nerve in a non neurofibrosis patient with no prior history of irradiation. key words: intra-cranial malignant peripheral nerve sheath tumor, olfactory nerve tumor, mpnst introduction malignant peripheral nerve sheath tumor mpnsts usually arise from peripheral nerves or shows differentiation towards nerve sheath cells. [9] mpnst of cranial nerves is very rare. the incidence of mpnst in the general population is 0.001% [8]. they constitute 5-10 % of all soft tissue sarcomas and 50-70% are associated with neurofibromatosis type 1 (nf1).[3,10] mpnsts involving the head and neck region comprise only 04-08 % of all mpnsts.[1] mpnst arising from olfactory nerve without any features of neurofibromatosis type 1 or type 2 as has been noted in our case. in the background of extensive literature search and with the best of our knowledge, probably this is the first case report of mpnst arising from olfactory nerve. case history a 45 years old male presented to us with history of headache and bilateral loss of smell since six months and altered sensorium since seven days. on examination he had frontal lobe signs and features of foster kennedy syndrome. his pre-operative mri, t1 and t2 weighted images had 8x7x5 cm heterogeneous lesion originating from the anterior cranial fossa. on cemri (figure 1) lesion was heterogeneously enhancing. his metastatic work up was negative. patient was planned for 470 | aggarwal et al intra-cranial malignant peripheral nerve sheath tumor of olfactory nerve             surgery with diagnosis of atypical olfactory groove meningioma. he underwent bifrontal craniotomy and gross total excision of the tumor (figure 2). histopathology was suggestive of malignant peripheral nerve sheath tumor of the olfactory nerve. post operatively patient was discharged on 7th post op day with no fresh deficit. patient underwent post op radiotherapy and is recurrence free since last six months. discussion mpnsts of the cranial nerves are rare tumors, and the literature is limited to isolated case reports and small case series. [9] in general population, the incidence of mpnst is 1/lac population per year. [1] mpnsts generally occur typically between ages 20-50 years whereas 10-20% of cases have been reported in the first 2 decades.[4,8] the common sites of origin include the extremities and trunk, usually sciatic nerve, brachial plexus and the sacral plexus mpnsts of head and neck region comprise 04-08% of all mpnsts and especially the cranial nerves involvement is extremely rare with only few cases or short case series found in the literature.[9] most common intracranial mpnsts are found in viii & v cranial nerves.[7] in retrospective analysis of intra cranial mpnsts by le’hereux and saliba which included 31 case reports and short case series comprising 60 cases, the incidence of cranial nerve mnsts were: viii cn-60%; v cn-27%, vii cn-10%; iii cn-6.7 %; iv cn1.7% &vi cn-1.7 %.[7] etiologically, mpnst may occur infrequently when they arise denovo, occur in association with neurofibromatosis (nf) [5,7], may be consequent to radiation (conventional or srs) or arise as malignant transformation of schwannoma or neurofibroma.[7] mpnsts are highly malignant tumors that grow rapidly along nerves, infiltrate surrounding tissues and develop hematogenous metastasis. mpnsts may develop hematogenous distant metastases (most commonly to lungs; other sites being bones and liver.[5] mri study does not allow confident distinction between benign and malignant nerve sheath tumors. a size more than 5 cm, infiltrative margins and marked signal heterogeneity, adjacent structure compression and local invasion are features which favor mpnsts. the diagnosis of mpnsts necessitates biopsy and remains controversial due to its lack of specific morphological criteria and immunohistochemical or molecular tests.[6] treatment of mpst is primarily surgical. gross total excision of intracranial mpnsts significantly influences overall survival rates and relates inversely with local recurrence. complete surgical tumor resection with preservation of neurological function should be the goal of the treatment. however, critical location and stubborn nature of tumor, complete surgical resection can be challenging and is not always feasible.[1,7] the role of adjuvant radiotherapy remains controversial.[7] numerous chemotherapy regimens have been used against mpnsts but results have been unconvincing even when combined with surgery and radiotherapy.[3,7] in early stages of mnst surgical resection of romanian neurosurgery (2018) xxxii 3: 469 472 | 471             the tumor provides survival benefits. whereas radiotherapy is useful in improving survival in metastatic mpnst. combined therapy with surgery and radiotherapy are prognostically important in patient with tumors >5 cm. [2] conclusion intra-cranial olfactory mpnst is extremely rare. this is the probably first such reported case. complete excision should be the goal of surgery which is the mainstay of treatment. however, due to the stubborn nature of tumor and intimate relation with critical neurovascular structures, this may not always be feasible. combined therapy surgery with post op radiotherapy has some survival benefits in metastatic mpnst. figure 1 pre op contrast enhance mri brain (axial, sagittal and coronal view) showing anterior cranial fossa sol figure 2 post op ncct head axial and (sagittal view) showing complete excision of the tumor 472 | aggarwal et al intra-cranial malignant peripheral nerve sheath tumor of olfactory nerve             correspondence dr. amit narang email: drnarangamit@gmail.com assistant professor, neurosurgery, guru gobind singh medical college and hospital faridkot, punjab. india. 151203. phone 703836244 references 1.anghileri m, miceli r, fiore m, mariani l, ferrari a, mussi c, lozza l, collini p, olmi p, casali pg, pilotti s, gronchi a. malignant peripheral nerve sheath tumors: prognostic factors and survival in a series of patients treated at a single institution. cancer. 2006 sep 1;107(5):1065-74. 2.arshi a, tajudeen ba, st john m. malignant peripheral nerve sheath tumors of the head and neck: demographics, clinicopathologic features, management, and treatment outcomes. oral oncol. 2015 dec;51(12):1088-94. 3.aydin md, yildirim u, gundogdu c, dursun o, uysal hh, ozdikici m. malignant peripheral nerve sheath tumor of the orbit: case report and literature review. skull base. 2004 may;14(2):109-13; discussion 113-4. 4.ducatman bs, scheithauer bw, piepgras dg, reiman hm. malignant peripheral nerve sheath tumors in childhood. j neurooncol. 1984;2(3):241-8. 5.ferner re, gutmann dh. international consensus statement on malignant peripheral nerve sheath tumors in neurofibromatosis . cancer res. 2002 mar 1;62(5):1573-7. 6.kar m, deo sv, shukla nk, malik a, dattagupta s, mohanti bk, thulkar s. malignant peripheral nerve sheath tumors (mpnst)--clinicopathological study and treatment outcome of twenty-four cases. world j surg oncol. 2006 aug 22;4:55. 7.l'heureux-lebeau b, saliba i. updates on the diagnosis and treatment of intracranial nerve malignant peripheral nerve sheath tumors. onco targets ther. 2013 apr 26;6:459-70. 8.panigrahi s, mishra ss, mishra s, das s. malignant peripheral nerve sheath tumor presenting as orbito temporal lump: case report and review of literature. asian j neurosurg. 2016 apr-jun;11(2):170-1. doi: 10.4103/1793-5482.145065. 9.scheithauer bw, erdogan s, rodriguez fj, burger pc, woodruff jm, kros jm, gokden m, spinner rj. malignant peripheral nerve sheath tumors of cranial nerves and intracranial contents: a clinicopathologic study of 17 cases. am j surg pathol. 2009 mar;33(3):32538 10.wanebo je, malik jm, vandenberg sr, wanebo hj, driesen n, persing ja. malignant peripheral nerve sheath tumors. a clinicopathologic study of 28 cases. cancer. 1993 feb 15;71(4):1247-53. doi: 10.33962/roneuro-2022-053 cerebello pontine angle hemangiopericytoma an aggressive tumour needs aggressive management. a case report abhijit verma, vijay kumar gupta, sanjeev attry, qamar siddiqi, shashi singhavi romanian neurosurgery (2022) xxxvi (3): pp. 311-314 doi: 10.33962/roneuro-2022-053 www.journals.lapub.co.uk/index.php/roneurosurgery cerebello pontine angle hemangiopericytoma an aggressive tumour needs aggressive management. a case report abhijit verma1, vijay kumar gupta1, sanjeev attry1, qamar siddiqi1, shashi singhavi2 1 department of neurosurgery. nims university, jaipur, india 2 department of pathology. sms medical college, jaipur, india abstract background: cp angle hemangiopericytoma are rare tumors. pre-operative suspicion and gross total excision are key for better management due to their aggressive nature. case presentation: 18-year-old male presented with signs of progressive brainstem compression. contrast mri showed a polycystic enhancing sol in the right cp angle region compressing the brain stem and cerebellar lobe. operated with histopathology and ihc indicating it to be a hemangiopericytoma. conclusions: hemangiopericytoma being an aggressive tumour with a high rate of recurrence compared to other common tumours at cp angle, complete resection with definitive pathological diagnosis and radiotherapy are needed for a better outcome. background hemangiopericytomas (hpcs) constitutes <1% of primary brain tumors. mostly supra tentorial and dural based. rare in cerebello pontine angle (cpa), mimics meningioma radiologically, but because most are grade 2 or grade 3, this aggressive nature makes their pathological differentiation important. [2,3,4,5,6,7,8,9] we describe here an unusual case of cpa hemangiopericytoma presenting with brainstem and cerebellar signs case presentation an 18-year-old male presented with chief complaints of disequilibrium, progressive weakness all 4 limbs (left>right), slurring of speech, and dysphagia for liquid for 2 months. on admission, his neurological examination revealed a left facial paresis(hunt & hess grade 3) with weak gag reflex and uvula deviated to right and asymmetrical palatal arches(left 9th and 10th cranial nerve paresis), and left side weakness keywords hemangiopericytoma, cerebello pontine angle, cystic enhancing tumor, cp angle meningioma, ihc corresponding author: abhijit v. nims university, jaipur, india draverma09@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 312 abhijit verma, vijay kumar gupta, sanjeev attry et al. more than right with increased tone with left cerebellar signs present, suggesting the presence of the millard-gubler syndrome. head ct scan and an mri of the brain demonstrated a solid cystic enhancing 2.8×3.5 cm sized right cpa lesion compressing brain stem with no internal acoustic meatus extension (fig. 1). figure 1. (a)post-contrast magnetic resonance imaging of the brain in coronal views showing a cystic right cerebellopontine angle tumor with dural enhancement (dural tail sign); (b) t2 weighted image showing peritumoral csf cleft; (c) t1 weighted image showing hyperintese nodule with septations in tumor. as tumor was solid cystic with enhancement a diagnosis of cystic schwannoma was made with differential being pilocytic astrocytoma and hemangioblastoma, cystic meningioma. a suboccipital retrosigmoid approach was attempted. during surgery, the tumor was solid and cystic, soft to firm, greyish pink, was suckable highly vascular, capsule was attached to cranial nerves passing in left cp angle with dural attachment superiorly . tumor was not extending to or coming out from internal auditory canal . it was removed in parts by cavitron ultrasonic surgical aspirator (cusa). somatosensory evoked potentials, brainstem auditory evoked responses, and intraoperative facial nerve monitoring were used to minimise the damage intraoperatively. figure 2. post operative ct of patient showing decompression of cystic part and a small residual attached to the brain stem. the patient had csf discharge from tissue drain more than 100ml on 3rd post op day for which lumbar drain was inserted and tissue drain removed on following day. surgical wound healed and lumbar drain removed on day 5. no leak or pseudomenigocoele formation. patient discharged on 8th post op day without fresh neurological deficit and improved cerebellar and brain stem signs. the histopathology sections revealed moderately cellular neoplasm with closely opposed cells with round nuclei arranged in a haphazard pattern with limited intervening stroma. nuclei are oval to spindle with dense chromatin and scanty cytoplasm. there was mild nuclear atypia with mitotic activity (<5/hpf). cyst formation also seen. there was numerous slit like vascular spaces. vimentin cd34 and cd99 are positive with stat-6 strongly nuclear positive. ki-67 is less than 5%. immunomarkers favoured a grade 2 hemangiopericytoma. while negative for ematle, sox10. (fig. 3, fig. 4, fig.5, fig.6). figure 3. photomicrographs of the tumor specimens showing. a: diffuse sheets of relatively uniform population of cells interspersed by staghorn vascular channels (h&e, original magnification, ×10). b: round to oval cells with finely dispersed nuclear chromatin and moderate cytoplasm and no signs of anaplasia (h&e, original magnification, ×20). h&e, haematoxylin and eosin. figure 4. immunohistochemical staining showing diffuse positivity with cd34 (original magnification, ×100). 313 cerebello pontine angle hemangiopericytoma figure 5. cd 99 staining (oil immersion; original magnification ×1000). figure 6. stat 6 staining (original magnification ×100) metastatic workup including ct of the chest/abdomen/pelvis did not reveal any evidence of extracranial hpc. adjunctive radiation therapy was advised but he was lost to follow up since a month post-surgery. discussion hpcs are rare, and are aggressive neoplasms that arise from the pericytes of zimmerman, which are contractile spindle cells surrounding capillaries and post capillary venules [4]; and most often involve the musculoskeletal system and skin [1].intracranial hpcs constitute just 0.4% of all intracranial tumors [10] and approximately 2% to 4% of all meningeal tumors [5]. immunohistochemistry has major role in diagnosis of hpc. it also helps in differentiation between meningioma and hpc, where hpc is positive with cd34, cd99 and stat-6 [5]. in the present case, the morphological features were distinctive enough to place the lesion in the category of an hpc. fairly uniform cellularity of the tumor and the high mitotic activity was more supportive of this lesion being labelled as grade ii hpc instead of a cellular sft the similarity between meningioma and hpc is limited to radiology and gross morphology. in fact, with a mean survival of 84 months from the time of initial diagnosis [5], a local recurrence rate as high as 91% and a 15-year risk of distant metastasis approaching 70%; intracranial hpcs harbour one of the most aggressive biological/clinical behaviours [16]. in present scenario gross total resection followed by radiotherapy is standard of care. radiation therapy has in fact extended the mean time of local recurrence from 34 to 75 months, and the survival from 62 to 92 months [1]. conclusions in conclusion, hpc being aggressive tumor with high rate of recurrence and metastasis, it should be included as a differential diagnosis in dural based extra axial cpa tumors in age-appropriate cases. a high index of suspicion on radiology imaging is essential to plan for complete excision, and role accurate histopathological diagnosis can’t be overemphasised. as postoperative recurrence seems unavoidable, long-term follow-up with serial imaging should be considered in all cases. references 1. kumar n, kumar r, kapoor r, et al. intracranial meningeal hemangiopericytoma: 10 years experience of a tertiary care institute. acta neurochir (wien) 2012;154:1647–1651. [pubmed] [google scholar] 2. molnar p, nemes z. hemangiopericytoma of the cerebello-pontine angle. diagnostic pitfalls and the diagnostic value of the subunit a of factor xiii as a tumor marker. clin neuropathol. 1995;14:19–24. [pubmed] [google scholar] 3. mallucci cl, ward v, carney as, o'donoghue gm, robertson i. clinical features and outcomes in patients with non-acoustic cerebellopontine angle tumours. j neurol neurosurg psychiatry. 1999;66:768–771. [pmc free article] [pubmed] [google scholar] 4. alén jf, lobato rd, gómez pa, et al. intracranial hemangiopericytoma: study of 12 cases. acta neurochir 314 abhijit verma, vijay kumar gupta, sanjeev attry et al. (wien) 2001;143:575–586. [pubmed] [google scholar] 5. tashjian vs, khanlou n, vinters hv, canalis rf, becker dp. hemangiopericytoma of the cerebellopontine angle: a case report and review of the literature. surg neurol. 2009;72:290–295. [pubmed] [google scholar] 6. cho jm, kim sh, kim sh, lee ks, chang jh. recurred cerebellopontine angle haemangiopericytoma 5 years after stereotactic radiosurgery. clin neurol neurosurg. 2011;113:931–933. [pubmed] [google scholar] 7. zeng j, ogera p, benardete ea, nicastri ad, rao c. cellular solitary fibrous tumor (hemangiopericytoma) with anaplasia at cerebellopontine angle--a case report. pathol res pract. 2012;208:493–496. [pubmed] [google scholar] 8. salunke p, futane s, gupta k, vasishta rk. cerebellopontine angle hemangiopericytoma: an orphan differential diagnosis. clin neurol neurosurg. 2013;115:1184–1186. [pubmed] [google scholar] 9. teoh jw, goh bs, shahizon azura mm, siti aishah ma, nor hafliza ms. an unexpected lesion in cerebellopontine angle: hemangiopericytoma. med j malaysia. 2014;69:146–147. [pubmed] [google scholar] 10. melone ag, d'elia a, santoro f, et al. intracranial hemangiopericytoma--our experience in 30 years: a series of 43 cases and review of the literature. world neurosurg. 2014;81:556–562. [pubmed] [google scholar] 11. soyuer s, chang el, selek u, mccutcheon ie, maor mh. intracranial meningeal hemangiopericytoma: the role of radiotherapy: report of 29 cases and review of the literature. cancer. 2004;100:1491–1497. [pubmed] [google scholar] 12. zhou jl, liu jl, zhang j, zhang m. thirty-nine cases of intracranial hemangiopericytoma and anaplastic hemangiopericytoma: a retrospective review of mri features and pathological findings. eur j radiol. 2012;81:3504–3510. [pubmed] [google scholar] 13. liu l, yin b, geng dy, li y, zhang by, peng wj. comparison of adc values of intracranial hemangiopericytomas and angiomatous and anaplastic meningiomas. j neuroradiol. 2014;41:188–194. [pubmed] [google scholar] 14. chen h, zeng xw, wu js, et al. solitary fibrous tumor of the central nervous system: a clinicopathologic study of 24 cases. acta neurochir (wien) 2012;154:237–248. discussion 248. [pubmed] [google scholar] 15. louis dn, ohgaki h, wiestler od, et al. the 2007 who classification of tumours of the central nervous system. acta neuropathol. 2007;114:97–109. [pmc free article] [pubmed] [google scholar] 16. erdag g, qureshi hs, patterson jw, wick mr. solitary fibrous tumors of the skin: a clinicopathologic study of 10 cases and review of the literature. j cutan pathol. 2007;34:844–850. [pubmed] [google scholar] 17. chamberlain mc, glantz mj. sequential salvage chemotherapy for recurrent intracranial hemangiopericytoma. neurosurgery. 2008;63:720–726. author reply 726-7. [pubmed] [google scholar] 18. angelina graziella melone et al. intracranial hemangiopericytoma--our experience in 30 years: a series of 43 cases and review of the literature. world neurosurg. mar-apr 2014;81(3-4):556-62. romanian neurosurgery (2019) xxxiii (4): pp. 370-378 doi: 10.33962/roneuro-2019-061 www.journals.lapub.co.uk/index.php/roneurosurgery finite element method to study cervical postoperative stability andrei st. iencean1, stefan c. castravete2, ion poeata1,3 1 neurosurgery, “prof. dr. nicolae oblu” hospital iasi, romania 2 caelynx europe, craiova, romania 3 neurosurgery, “gr. t. popa” university of medicine and pharmacy iasi, romania abstract a cervical spine model built by means of the finite element method was used to determine the risk of postoperative cervical instability in relation to the type of discectomy, in cervical disc herniation. furthermore, this model was employed to check whether, at the adjacent levels of the fusion discectomy, the intervertebral translation during cervical movements will maintain the normal amplitude [normal rom] or its amplitude will decrease. the intervertebral displacement and the tension arising from motion and weight in the cervical vertebral structure were thus determined through computer modelling using the above-mentioned method and the software abaqus. it resulted in a cervical spine model consisting of 739666 finite elements interacting through 210530 nodes, with biomechanical properties following the vertebral anatomical structures modelled. two movement situations were studied to determine the behaviour of this model. firstly, the moment of force for flexion and extension of 1 nm. secondly, we aimed to establish the maximum flexion and extension for a normal cervical spine model in order to determine the momentum value of moving forces for each of them. it was showed that both anterior cervical microdiscectomy without fusion and cervical discectomy with cage fusion (used for the surgical treatment of cervical disc herniation at one level), ensure postoperative vertebral stability when performed properly. both types of surgery reduce the mobility of the cervical spine, although more in the case of fusion discectomy. the intradiscal tension increases in movement in both models, with a higher intensification in the fusion discectomy model. the practical conclusion is that microdiscectomy without fusion is preferable in the case of a single-level cervical disc herniation occurred to a cervical spine without instability. introduction cervical spine stability after discectomy is evaluated biomechanically by determining the intervertebral displacement, tensions and stresses in the cervical spine. the finite element method is based on dividing complex structures into smaller ones, called finite elements, with simple geometric forms and easily to be included within the simulation of the process to be studied while tracking their parameters in situations close keywords cervical discectomy, cervical postoperative stability, finite element method, microdiscectomy without fusion corresponding author: stefan c. castravete caelynx europe, craiova, romania scastravete@caelynx.ro copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 371 finite element method to study cervical postoperative stability to real conditions. these finite elements are interconnected with each other at points called nodes, which define the requests as unknown parameters, respectively the movement or displacement and the load or stresses. we used a cervical spine model built through this method to determine the risk of postoperative cervical instability in relation to the type of discectomy. materials and methods we worked with computer programs for image processing, for modelling finite elements of the cervical spine and simulating cervical motion and load. more precisely, we used the mimics software, which creates 3d models from 2d dicom images. thus, the images in dicom format obtained from the ct scan of a normal cervical spine were introduced in mimics, transformed into points with 3d spatial coordinates, then exported to a special format (.stl). mimics software transposes images scanned by ct into a point cloud with spatial coordinates, creating a 3d model. moreover, it can recreate the model of bone structures. the vertebrae model was obtained this way, whilst the other tissues, the intervertebral disc and ligaments were added manually. the cervical vertebral model made in mimics in the form of coarse discretization was further processed to be used through the finite element analysis model. the vertebrae were imported into abaqus cae and the cervical spine model was recreated. to build a model of the cervical spine with finite elements as closest to the real one, we assigned to each modelled structure the specific biomechanical properties of the column (elasticity, rigidity /deformability, resistance to deformation represented by young’s module, and poisson’s coefficient) for each finite element corresponding to the modelled anatomical structures (table 1). table 1. characteristics in terms of elasticity and strength attributed to the corresponding finite element of the modelled anatomical structures. anatomical structure finite element type modulus of elasticity (mpa) coefficient of poisson vertebra the bony cortex first-order tetrahedral element:4 nodes 10.000 0.29 vertebra cancellous bone first-order tetrahedral element:4 nodes 100 0.29 anterior longitudinal ligament bar with 2 nodes 30 0.3 posterior longitudinal ligament bar with 2 nodes 20 0.3 c1-c2 joint capsule 2nd order tetrahedral element:10 nodes 7.7 0.39 c1-c2 supraspinous ligament bar with 2 nodes 10 0.3 yellow ligament c1-c2 bar with 2 nodes 10 0.3 c2-c3 joint capsule 2nd order tetrahedral element, hybrid:10 nodes 10 0.3 c3-c7 levels joint capsule 2nd order tetrahedral element, hybrid:10 nodes 20 0.3 yellow ligament levels c2-c7 bar with 2 nodes 1.5 0.3 interspinous, supraspinous ligament, levels c2-c7 bar with 2 nodes 1.5 0.3 thus, a cervical spine model consisting of 739666 finite elements that interact through 210,530 nodes resulted, with biomechanical properties according to the modelled vertebral anatomical structures (figure 1). once this model with finite elements was settled, we were able to determine its behaviour at load and movement. in this purpose, we appreciated that the head weighs approximately 4.5 5.5 kg and exerts an average force of 50 n applied to the vertebra c1, in the vertical direction lower oriented. movements in the cervical spine are complex, but instability is evident especially in those of flexion and extension. 372 andrei st iencean, stefan c. castravete, ion poeata figure 1. cervical spine model obtained using the finite element method. to study cervical instability during the flexion-extension movement, we considered the c7 vertebra as a fixed point. then, we applied a force of displacement to the upper extremity of the cervical spine, respectively at the level of the c1 vertebra. figure 2. cervical spine model obtained using the finite element method three models of the cervical spine were studied using this method: • a normal cervical spine, • a cervical spine with microdiscectomy without fusionat the level c6-c7 • a cervical spine with discectomy and cage stabilization at the level c6-c7 373 finite element method to study cervical postoperative stability a. b. c. figure 3. cervical spine model built by using the finite elements method (a), with the moment of the displacement force for the flexion (b) and extension movements (c). for each model, movements of flexion and extension were simulated starting from the cervical intermediate position by applying a displacement force for flexion and extension, respectively by considering a moment of force applied to the movement. a. b. a. b. figure 4. flexion movement by applying the force of 1 nm a. the model with microdiscectomy c6-c7 b. the model with discectomy and cage c6-c7 figure 5. extension movement by applying the force of 1 nm a. the model with c6-c7 microdiscectomy b. the model with discectomy and c6-c7 cage two movement situations were studied to determine the behaviour of these three models, as follows: the moment of force for flexion and extension of 1 nm, establishing the maximum flexion and extension for the normal cervical spine model and determining the 374 andrei st iencean, stefan c. castravete, ion poeata value of the momentum of the movement force for these movements. these values are: the moment of force for maximum flexion is 7.3 nm and the moment of force for the maximum extension is 2 nm. figure 6. flexion movement for the moment of force of 7.3 nm, with cervical displacement at a. normal column, b. c6-c7 microdiscectomy and c. c6-c7 discectomy and cage model. figure 7. extension movement by applying the force of 2 nm, in the three models: anormal column, bmodel with microdiscectomy c6-c7 and cmodel with discectomy and cage c6-c7. 375 finite element method to study cervical postoperative stability a. b. c. figure 8. cervical models with discectomy and cage fixation at the c6-c7 level, at which mobility is studied: a. extension, compared with b. intermediate position and c. flexion movement model 1 model 2 model 3 mm mm % of model 1 mm % of model 1 extension 12.37 11.91 3.72% 11.12 10.11% flexion 11.65 10.63 8.76% 8.57 26.44% table 2. cervical mobility in the sagittal plane when applying a moment of force of 1 nm results we obtained the following results based on the finite element model with movement in flexion and extension by applying a moment of force of 1 nm (table 2). figure 9. cervical spine model with the extension of vertebrae in the cervical spine model operated for c6-c7 disc herniation by microdiscectomy without fusion, it was found that the height of the c6-c7 disc space decreased to 50% off the initial disc height although it still allows a degree of intervertebral mobility without the occurrence of vertebral instability. 376 andrei st iencean, stefan c. castravete, ion poeata in the cervical spine model operated by discectomy and fusion using c6-c7 intervertebral cage, the operated disc space is blocked, there is no instability and the cervical movements of flexion and extension are performed by moving the upper vertebrae of the c6 vertebra. the c6 and c7 vertebrae form a fixed block and vertebral mobility is missing. it was found that surgery reduces the mobility of the flexion movement and blocks the c6-c7 disc space with a cage that reduces mobility with 26% in flexion. in the case of microdiscectomy without fusion, the overall cervical mobility decreases by 8.76% compared to the unoperated model. when applying the moment of force corresponding to the maximum movement to the model of not operated cervical spine, respectively the moment of the force for flexion of 7.3 nm and the moment of the force for extension of 2 nm on the other two models, we obtained the results presented in table 3. the flexion and extension movement for all three models is much wider and the differences of mobility per the ensemble movement are 7.63% for microdiscectomy without fusion and 16.05% for discectomy with fusion. table 3. cervical mobility at the moment of application of 7.3 nm in flexion and 2 nm in extension movement model 1 model 2 model 3 mm mm % of model 1 mm % of model 1 % of model 2 extension 18.9 17 10.05% 15.08 20.21% 11.29% flexion 43.23 39.93 7.63% 36.29 16.05% 9.12% a b figure 10. flexion movement for the same model of the cervical spine with finite elements under the action of different moments of force: a. moderate flexion at the moment of force of 1 nm and b. maximum flexion at the moment of force of 7.3 nm. discussions cervical disc herniation is a common degenerative pathology of the cervical spine and surgical treatment is the optimal solution in cases with surgery indication. a cervical discectomy removes from the anterior column an important component for resistance and the axial transmission of movement and weight and, consequently, may affect the stability of the cervical spine. the prospect of postoperative cervical instability has led us to this study, aiming to bring improvements to the operative techniques used so far or replace some of them in order to prevent or correct it. we intended to determine the conditions in which post cervical discectomy instability may occur in relation to the surgical procedure used and to 377 finite element method to study cervical postoperative stability show which technique is appropriate to prevent it. after microdiscectomy without fusion, postoperative healing is based on the formation of an intradiscal fibrous scar to ensures the stability of the cervical spine at the level operated. the postoperative intradiscal scar allows a minimum degree of mobility without overloading the adjacent levels. in the case of discectomy with fusion, a block is formed between the vertebrae adjacent to the operated disc, with the advantage of keeping the normal foramina, but with the loss of the intervertebral mobility at the level operated. we used the normal cervical spine model, not operate, to apply a moment of force of 1 nm in flexion, respectively extension, from the middle position. it determined a small amplitude displacement, namely of 11.65 mm in flexion and 12.37 mm in extension compared to the initial position. the simulation of maximum flexion and extension on this model allowed us to determine the maximum value of the moment of force of displacement for the maximum amplitude of these movements, respectively for 7.3 nm maximum flexion and 2 nm maximum extension. the maximum values of displacement in flexion and extension for the normal model were 43.23 mm flexion, and 18.9 mm extension, starting from the initial intermediate position. the cervical model of microdiscectomy without fusion at the level c6 c7 had the following values of amplitude for the moment of force of 1 nm applied on flexion and extension in movement: 10.63 mm in flexion and 11.91 mm in extension. this means a decrease in the amplitude of the cervical movement of 8.76% in flexion and 3.72% in extension. these values are not significantly lower compared to the amplitude of the normal movement in ordinary situations. a moment of force of maximum amplitude resulted in 39.93 mm in flexion and 17 mm in extension. in this case, the decrease with respect to the amplitude of the normal maximum movement was of 7.63% in flexion and 10.05% in extension. it was found that the decrease in flexion in the patient operated for disc herniation at the c6 c7 level by fusion without microdiscectomy is between 7.63% and 8.76% for maximum flexion, respectively for current flexion. in contrast to flexion, the extension movement decreased slightly, only with 3.72% for the current extension, but the amplitude of the extension decreases by 10%, determined by the moment of maximum force compared to these movements in the case of the cervical spine. in the third model, discectomy with fusion performed at the level c6 c7, 1 nm force produced a stronger decrease in the amplitude of movement: 8.57 mm in flexion, which means a decrease of 26.44% off the value of normal flexion, and 11.12 mm in extension, so with 10.11% less than the normal value. this decrease in amplitude of both movements of flexion and extension is significant and it is explained by the obstruction of the c6 c7 disc space due to the fusion. practically, the movement is produced by having as a fixed point the c6 vertebra. when a moment of force of maximum amplitude is applied on this model, it produces a flexion movement with the amplitude of 36.29 mm (meaning a decrease of 16.05% off the normal movement) and an extension of 15.08 mm, i.e. a decrease of 20.21% off the normal extension. the simulation of flexion-extension movements on this third model established the marked decrease in cervical mobility as a whole, both for the current movement performed at a moderate request (moment of force = 1 nm) and for the maximum movement, namely for a moment of force of 7.3 nm in flexion and 2 nm in extension. this decrease in amplitude in both flexion and extension is explained by the diminished length of the vertebral segment that executes the movement. the study thus showed that limiting the moderate amplitude of the cervical movements is more important in the case of cage fusion discectomy compared to non-fusion microdiscectomy. the ration of amplitude decrease in movement between these two models is 3:1. for a maximum movement, respectively for applying a moment of force of 7.3 nm in flexion and 2 nm in extension, the comparison between the biomechanical behaviour of the two cervical models showed that the decrease in the amplitude of movement is double in the case of discectomy with fusion than in the non-fusion model, both related to the normal, unoperated, cervical model. conclusions the cervical spine model obtained through the finite element method (739666 finite elements and 210530 nodes), in which the vertebral mobility was simulated 378 andrei st iencean, stefan c. castravete, ion poeata for usual and maximum movements, showed that both models of cervical spine operated ensure postoperative stability at the level of the operated intervertebral disc. both types of surgery reduce the mobility of the cervical spine, most notably the model with fusion discectomy. the practical conclusion is that microdiscectomy without fusion is preferable in the case of a singlelevel cervical disc herniation in a cervical spine without instability because, by comparing the two operative models, it appeared that microdiscectomy without fusion at one level does not significantly decrease the mobility of the cervical spine, nor does it tensile the overload intervertebral discs adjacent to the operated disc level. references 1. aarabi b, walters bc, dhall sset al. subaxial cervical spine injury classification systems.neurosurgery. 2013; 72 suppl 2:170-86. 2. abrishamkar s, karimi y, safavi m, tavakoli p. single level cervical disc herniation: a questionnaire-based study on current surgical practices. indian journal of orthopaedics. 2009;43(3):240-244. 3. adam, c. pearcy, m. mccombe, p. stress analysis of interbody fusion – finite element modeling of intervertebral implant and vertebral body. clinical biomechanics 2003;18, 265-272. 4. anderst w in vivo cervical spine kinematics, arthrokinematics and disc loading în asymptomatic control subjects and anterior fusion patients. doctoral dissertation, university of pittsburgh, 2014. 5. anderst wj, donaldson wf 3rd, lee jy, kang jd. cervical motion segment contributions to head motion during flexion\extension, lateral bending and axial rotation. spine j. 2015: 15(12): 2538-43. 6. angevine pd, arons rr, mccormick pc. national and regional rates and variation of cervical discectomy with and without anterior fusion, 1990-1999.spine (phila pa 1976).2003;28(9): 931-9. 7. aydin y, kaya ra, can sm et al. minimally invasive anterior contralateral approach for the treatment of cervical disc herniation. surg neurol. 2005;63(3):210-8. 8. bailey rw, badgley ce: stabilization of the cervical spine by anterior fusion. j bone joint surg 1960; 42-a (4): 56594. 9. bärlocher cb, barth a, krauss jk et al. comparative evaluation of microdiscectomy only, autograft fusion, polymethylmethacrylate interposition, and threaded titanium cage fusion for treatment of single-level cervical disc disease: a prospective randomized study în 125 patients. neurosurg focus. 2002 15;12(1): e4. 10. barsa p, suchomel p. factors affecting sagittal malalignment due to cage subsidence în standalone cage assisted anterior cervical fusion. eur spine j. 2007;16(9):1395-400. 11. bertalanffy h, eggert hr complications of anterior cervical discectomy without fusion în 450 consecutive patients. acta neurochir (wien). 1989; 99(1-2):41-50. 12. bible je, biswas d, miller cp et al. normal functional range of motion of the cervical spine during 15 activities of daily living. j spinal dis tech.2010;23(1): 15-21. 13. iencean a st. the cervical spine postoperative stability. comparative study of the different surgical techniques. phd thesis, grt popa umf iasi, 2018 14. kumaresan, s., yoganandan, n., pintarh, f. a. finite element analysis of the cervical spine: a material property sensitivity study. cl biomech, 1999, 14, 41-53. 15. lee mj, dettori jr, standaert cj et al. indication for spinal fusion and the risk of adjacent segment pathology: does reason for fusion affect risk? a systematic review. spine (phila pa 1976). 2012; 37(22 suppl): s40-51. 16. skovrlj b, qureshi sa. minimally invasive cervical spine surgery. j neurosurg sci. 2017; 61(3):325-334. 17. wang y, wang l, du c, mo z, fan y.a comparative study on dynamic stiffness în typical finite element model and multibody model of c6–c7 cervical spine segment, int. j. numer. meth. biomed. engng. 2016; e02750: 1-13. 18. zafarparandeh i, erbuiut d, lazoglu i, ozer af. development of a finite element model of the human cervical spine, turk neurosurg 2014; 24:3,312-318. 19. vleggeert-lankamp c.l.a., janssen t.m.h., van zwet e., goedmakers c.m.w., bosscher l., peul w., arts m.p. the neck trial: effectiveness of anterior cervical discectomy with or without interbody fusion and arthroplasty in the treatment of cervical disc herniation; a double-blinded randomized controlled trial. spine journal, 2019; 19 (6) , pp. 965-975. doi: 10.33962/roneuro-2023-011 common peroneal neuroma in continuity with complete foot drop secondary to a bullet fragment injury. a case report demonstrating end-to-end nerve repair adnan khaliq, ahtesham khizar romanian neurosurgery (2023) xxxvii (1): pp. 71-74 doi: 10.33962/roneuro-2023-011 www.journals.lapub.co.uk/index.php/roneurosurgery common peroneal neuroma in continuity with complete foot drop secondary to a bullet fragment injury. a case report demonstrating end-to-end nerve repair adnan khaliq1, ahtesham khizar2 1 saidu teaching hospital, swat, pakistan 2 punjab institute of neurosciences, lahore, pakistan abstract background. common peroneal nerve (cpn) injuries are generally common but they are uncommon due to gunshot injuries and are associated with poor motor outcomes. managing neuroma-in-continuity is still challenging because there are currently no accepted standards for deciding on the most effective course of treatment or estimating the time needed for repair. treatment options for a neuroma-in-continuity include neurolysis, neuroma resection with interposition, endto-side nerve grafting, and bypass grafting. case presentation. a 40-year-old man presented with findings of complete right foot drop due to an 8-month-old firearm injury to his right distal thigh. following baseline investigations, imaging, and anaesthesia fitness, he underwent surgical exploration under general anaesthesia. a neuroma-in-continuity was found in the cpn, resected, and an end-to-end nerve repair was performed. along with the neuroma-incontinuity, a bullet fragment was also removed. the neurological status remained unchanged postoperatively. conclusion. regardless of the cause of the lesion, patients should be urged to seek surgical therapy if there is no spontaneous recovery within four months after the cpn injury. sharp injuries and knee dislocations have a better chance of recovery than crush injuries and gunshot wounds. introduction sciatic nerve splits into common peroneal nerve (cpn) and tibial nerve in the mid to distal third of the thigh. from the apex of the popliteal fossa to the lateral popliteal fossa, the cpn descends obliquely across the plantaris muscle and curves around the proximal peroneus longus muscle. it then makes its way to the anterior lower leg, where it splits into deep and superficial branches.1 cpn injuries are generally common but they are uncommon due to gunshot injuries and they are associated with poor motor outcomes. so far, it is believed that nerve reconstruction is a reasonable option and it is recommended up to 6 months after the primary injury.2 managing neuroma-in-continuity is still challenging because there keywords peripheral nerves, peripheral nerve injuries, peroneal neuropathies, neuroma, foot drop, firearms corresponding author: ahtesham khizar punjab institute of neurosciences, lahore, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 72 adnan khaliq, ahtesham khizar are currently no accepted standards for deciding on the most effective course of treatment or estimating the time needed for repair. neurolysis, neuroma resection with interposition, end-to-side nerve grafting, and bypass grafting are all treatment options for a neuroma-in-continuity. the issue with complete neuroma resection is that it separates and sections not only the disorganised fibro-neural tissue mass that forms the neuroma, but also all potentially still viable nerve fibers passing through the damaged nerve part, removing the possibility of spontaneous recovery. simultaneously, there is a limited time frame for axonal regrowth before motor endplates degenerate and muscles are irreversibly paralyzed. it is possible that with a neuroma-in-continuity, enough trophic factors have been transported to the motor endplates to preserve some mechanisms, such as enhanced synchronization of motor unit actuating, muscle fiber hypertrophy, and distal motor fiber sprouting, resulting in doubly innervated muscle fibers and allowing functional recovery. this may allow recovery to extend beyond the traditional one year limit after injury.2 the following case report demonstrates neuroma-in-continuity resection and end-to-end nerve repair in a patient with a cpn neuroma-incontinuity secondary to a bullet fragment injury. case presentation a 40-year-old man presented to us as an outpatient with findings of complete right foot drop due to an 8month-old firearm injury to his right distal thigh. on examination, he had plegia of the ankle dorsiflexors and extensors of the great toe, as well as hypesthesia in the right peroneal nerve supply area. he underwent surgical exploration under general anaesthesia after baseline investigations, imaging, and anaesthesia fitness. nerve conduction study was not performed because the patient was very poor and non-affording. anteroposterior (ap) and lateral x-rays of his right distal thigh and knee revealed a bullet fragment (figure. 1). the patient was positioned prone, with padding beneath the knee and ankle. a vertical s-shaped incision was made in the lower thigh, medial to the short head of the biceps femoris muscle, after cleaning and draping. dissection was carried out. the sciatic nerve bifurcation, the tibial nerve, and the common peroneal nerve were discovered (figure. 2a). a neuroma-in-continuity of the cpn was identified, resected, and an end-to-end nerve repair was performed using ethicon prolene 10.0 suture (figure. 2b). exploration also turned up the bullet fragment, which was also removed along with the neuroma-incontinuity (figure. 3a&b). the surgical wound was thoroughly washed with saline before being closed. the postoperative neurological status remained unchanged. hematoxylin and eosin (he) stains revealed a random and convoluted arrangement of nerve bundles within a fibrous connective tissue stroma (figure. 4). figure 1. x-rays right distal thigh and knee ap and lateral views showing a bullet fragment (marked by white arrows). figure 2. a; 1 (black arrow) sciatic nerve bifurcation, 2 (yellow arrow) tibial nerve, 3 (blue arrow) common peroneal nerve, 4 (white arrow) neuroma-in-continuity. b; 1 (black arrow) sciatic nerve bifurcation, 2 (yellow arrow) tibial nerve, 3 (blue arrow) common peroneal nerve, 4 (white arrow) end-to-end nerve repair after neuroma in-continuity resection. discussion the cpn has been shown to be the most vulnerable and frequently injured nerve of the lower extremity3 due to its superficial anatomical location1,4 and 73 common peroneal neuroma in continuity with complete foot drop secondary to a bullet fragment injury fixation at the sciatic notch and the peroneus longus muscle, as opposed to the less vulnerable location of the tibial nerve.1,2,4,5 at the same time, cpn injuries have a poorer recovery rate when compared to other lower extremity nerve injuries. the reasons for this are a poorer neural blood supply, a "lower forceabsorbing fascicle or connective tissue count," and a greater demand for innervation of peroneal nerve supplied muscles.2,4 aside from the injured nerve, factors influencing the outcome after nerve reconstruction include the trauma mechanism such as laceration, compression, traction, and focal ischemia, the graft length, and the time between grafting and intervention. sharp trauma, shorter grafts, and early reconstruction or neurolysis have all been linked to a better prognosis.6,7 the main limiting factor in the optimal treatment of peroneal nerve lesions associated with foot drop is time. it is well known that nerve regeneration occurs at a rate of 1 mm per day,7,8 that motor endplates die 12-16 months after denervation,7 and that innervated muscles remain viable 18-24 months after the injury.9 when the rate of regeneration and the distance to cover are disproportionate, it leads to irreversible degeneration and fibrosis, as well as permanent paralysis of the denervated muscles.10 the cpn nerve transfer or reconstruction has been said to be reasonable for motor recovery up to 6 months, by no means later than 12 months after denervation, and denervation longer than 12 months has been said to be an absolute contraindication.8,11,12 on the other hand, in patients grafted 13 and 18 months after the injury, simultaneous cpn reconstruction and tibialis posterior tendon transfer results in satisfactory functional recovery, indicating the importance of rebalancing ankle movement forces to enhance neural regeneration.13 neurolysis has been shown to be an effective method for improving nerve function in the context of neuroma-in-continuity,4,14,15 for up to 8 months after the injury.6 however, this method has been linked to microvascular damage and the formation of intraneural scars.16 a few months after the injury, intraoperative nerve action potentials have been proposed as a crucial tool for reevaluating the reason for resection and nerve grafting against neurolysis in the cpn lesions.1 cpn injuries in open wounds should undergo exploration in an emergency room. patients should be urged to seek surgical treatment if a close injury fails to recover on its own within four months of the damage, regardless of the cause of the lesion. sharp injuries and knee dislocations have got a good recovery compared to crush injuries and gunshot wounds which have a poor recovery. figure 3. a: removed bullet fragment. b: resected neuroma. figure 4. hematoxylin and eosin (he) stains reveal a random and convoluted arrangement of nerve bundles inside a fibrous connective tissue stroma. conclusion cpn is the most vulnerable and frequently injured nerve in the lower extremity but gunshot injuries are a less common cause. time is the most important limiting factor in the optimal treatment of peroneal nerve lesions associated with foot drop. cpn injuries in open wounds should be explored in the emergency room. patients should be advised to seek surgical treatment if there is no spontaneous recovery within four months of the injury, regardless of the causative mechanism of the lesion. sharp injuries and knee dislocations have a better chance of recovery than crush injuries and gunshot wounds. 74 adnan khaliq, ahtesham khizar list of abbreviations cpn: common peroneal nerve ap: anteroposterior references 1. kim dh, murovic ja, tiel rl, kline dg. management and outcomes in 318 operative common peroneal nerve lesions at the louisiana state university health sciences center. neurosurgery. 2004;54(6):1421-1429. 2. reichl h, ensat f, dellon al, wechselberger g. successful delayed reconstruction of common peroneal neuromain-continuity using sural nerve graft. microsurgery. 2013;33(2):160-163. 3. noble j, munro ca, prasad vs, midha r. analysis of upper and lower extremity peripheral nerve injuries in a population of patients with multiple injuries. j trauma. 1998;45(1):116-122. 4. murovic ja. lower-extremity peripheral nerve injuries: a louisiana state university health sciences center literature review with comparison of the operative outcomes of 806 louisiana state university health sciences center sciatic, common peroneal, and tibial nerve lesions. neurosurgery. 2009;65(4 suppl):a18-a23. 5. schmalzried tp, noordin s, amstutz hc. update on nerve palsy associated with total hip replacement. clin orthop relat res. 1997;(344):188-206. 6. gosk j, rutowski r, rabczyński j. the lower extremity nerve injuries own experience in surgical treatment. folia neuropathol. 2005;43(3):148-152. 7. trumble te, vanderhooft e, khan u. sural nerve grafting for lower extremity nerve injuries. j orthop trauma. 1995;9(2):158-163. 8. nath rk, lyons ab, paizi m. successful management of foot drop by nerve transfers to the deep peroneal nerve. j reconstr microsurg. 2008;24(6):419-427. 9. robinson lr. traumatic injury to peripheral nerves. muscle nerve. 2000;23(6):863-873. 10. sunderland s, mcarthur ra, nam da. repair of a transected sciatic nerve. a study of nerve regeneration and functional recovery: report of a case. j bone joint surg am. 1993;75(6):911-914. 11. birch r, bonney g, wynn parry cb. traumatic lesions of the brachial plexus. surgical disorders of the peripheral nerves. 1998;1998:157-207. 12. terzis jk, kostopoulos vk. vascularized nerve grafts for lower extremity nerve reconstruction. ann plast surg. 2010;64(2):169-176. 13. ferraresi s, garozzo d, buffatti p. common peroneal nerve injuries: results with one-stage nerve repair and tendon transfer. neurosurg rev. 2003;26(3):175-179. 14. brown ba. internal neurolysis in traumatic peripheral nerve lesions in continuity. surg clin north am. 1972;52(5):1167-1175. 15. kline dg, nulsen fe. the neuroma in continuity. its preoperative and operative management. surg clin north am. 1972;52(5):1189-1209. 16. goth d. animal experiment studies of neurolysis of peripheral nerves. handchir mikrochir plast chir 1987;19:212–216. doi: 10.33962/roneuro-2023-035 delayed intraoperative rupture of clipped aneurysm during the awaking from anaesthesia mustafa ismail, bandar mohammed al-hadeethi, amir ibrahim moushib, hagar a. algburi, aktham o. al-khafaji, hosam al-jehani, samer s. hoz romanian neurosurgery (2023) xxxvii (2): pp. 198-201 doi: 10.33962/roneuro-2023-035 www.journals.lapub.co.uk/index.php/roneurosurgery delayed intraoperative rupture of clipped aneurysm during the awaking from anaesthesia mustafa ismail1, bandar mohammed al-hadeethi1, amir ibrahim moushib2, hagar a. algburi1, aktham o. al-khafaji1, hosam al-jehani3, samer s. hoz4 1 department of neurosurgery, college of medicine, university of baghdad, baghdad, iraq 2 department of anaesthesia, neurosurgery teaching hospital, baghdad, iraq 3 department of neurosurgery, king fahad hospital of the university, imam abdulrahman alfaisal university, dammam, saudi arabia 4 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract introduction. intraoperative rupture (ior) of an aneurysm is a frightful complication that causes significant morbidity and mortality worldwide. ior can be attributed to various parameters, including hypertension, increased intracranial pressure (icp), fragility of the vessels, and inadequate anaesthesia. ior due to insufficient anaesthesia is scarcely reported in the literature. here, we describe a re-ruptured anterior communicating artery (acoa) after incomplete clipping of the neck during craniotomy closure due to unintended early wake-up from anaesthesia with a discussion about the management. case description. a 38-year-old male suddenly developed a severe headache, a brief loss of consciousness, and vomiting. computed tomography (ct) scan showed a subarachnoid haemorrhage in the basal cistern. ct angiography showed a bilobed right acoa aneurysm with a wide neck and murphy's teat. the patient was considered for surgery. clipping of the aneurysm neck was done through two curved clips. during craniotomy closure, the patient started coughing and gagging then a huge ior was encountered. these events can be mainly attributed to unintended inadequate anaesthesia, particularly muscle relaxants. the bleeding ceased after two suction catheters were inserted, temporary clips were applied, and the readjustment of permanent clips. after surgery, the patient showed a left-sided weakness. his postoperative ct scan showed a right distal anterior cerebral artery (aca) territory infarction. the weakness improved in the follow-up period. conclusion. delayed ior due to early awaking from anaesthesia should be considered a potential source of complications and bad outcomes in aneurysm surgery. keywords microsurgical clipping, intraoperative rupture, inadequate anaesthesia corresponding author: samer hoz department of neurosurgery, university of cincinnati, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 199 delayed intraoperative rupture of clipped aneurysm during the awaking from anaesthesia introduction intraoperative rupture (ior) of aneurysm is a dreadful complication that causes significant morbidity and mortality worldwide [2]. the overall incidences of ior are 6.7 percent per aneurysm and 7.9 percent per surgery [10]. ior can be classified according to specific times within the surgery into pre-dissecting, dissecting, clipping, and post-clipping [10]. regarding its causes, ior can be attributed to a variety of parameters, including hypertension, increased intracranial pressure (icp), the fragility of the vessels due to comorbidities, procedural related, and inadequate anesthesia [4,5]. in surgery, rerupture of the aneurysm intraoperatively due to insufficient anesthesia is scarcely reported. here, we described a case of a re-ruptured anterior communicating artery (acoa) aneurysm after incomplete clipping of the aneurysmal neck during craniotomy closure due to unintended early wake-up from anesthesia. case description an otherwise healthy 38-year-old male suddenly developed a severe headache, brief loss of consciousness, and vomiting. the patient presented no weakness and uncontrollable hypertension, and he is a heavy smoker. his initial computed tomography (ct) scan showed subarachnoid hemorrhage (sah) in the basal cistern. ct angiography exhibiting a bilobed right inferiorly directed acoa aneurysm (9 mm) with a wide neck and murphy's teat. the patient was considered for surgery. the endovascular option is usually not applicable in iraq due to its high cost and absence of proper health insurance. following the typical operative steps of the right supra-orbital approach, the aneurysm was identified. the application of a temporary clip was performed on the ipsilateral a1 for proximal control. clipping of the aneurysm neck was done through two curved clips. however, severe arachnoid adhesions due to sah renders the confirmation of complete clipping, which is not feasible. next, muscle wrapping is applied around the aneurysmal neck to enforce the clipping construct, followed by hemostasis. during the closure, the patient suddenly moved his head and started coughing (resisting the endotracheal tube). concretely, a huge ior has been encountered, and bleeding fills the operative field. these events can be mainly attributed to unintended inadequate anesthesia, particularly muscle relaxants. here, two suction catheters were used to control the bleeding with the application of temporary clips under a microscope. to be noticed, the permanent clips were moved after the ior. eventually, the clips were adjusted to include the whole aneurysmal neck, and the ior stopped. this takes around seventeen minutes from the moment of rupture. postoperatively, the patient showed a left-sided weakness grade of 0 on the medical research council of canada (mrc) scale. his postoperative ct scan showed a right distal anterior cerebral artery (aca) territory infarction (figure 1). the weakness improved to grade 4 over the next three weeks. at a 3-month follow-up, the patient was neurologically intact with the imaging showed no aneurysm. figure 1. (a) (pre-operative) 3d constructed imaging of cerebral catheter angiography showing a right bilobed inferiorly directing anterior communicating artery aneurysm (red arrow) with a superiorly directing murphy's teat. (b) (post-operative) ct scan (axial view) showing ipsilateral anterior communicating artery (aca) distal territory infarction. 200 mustafa ismail, bandar mohammed al-hadeethi, amir ibrahim moushib et al. discussion the incidence of overall ior has recently varied between 15 and 50 % [7]. leipzig tj et al, reported that the ruptured aneurysms rate is significantly higher than the unruptured (10.7 versus 1.2 %, p <0.0001). among the 970 ruptured aneurysms treated surgically, 104 of the cases have iors, and its rate in the ruptured aneurysms constitutes 92 % of all iors [10]. they also reported that ior in the ruptured aneurysms during clipping occurred in 49 cases (47.1%) while occurred in 42 cases (40.4%) during the dissection [10]. however, pinpointing the exact cause of ior is quite challenging. the location of the aneurysm is a major risk factor for ior. the acoa and posterior communicating artery aneurysms and the posteroinferior cerebellar artery aneurysm were more likely to rupture intraoperatively [4,10]. however, sundt et al, discovered no association between aneurysm site and ior [13]. aneurysms originating from the acoa and anterior cerebral artery had a greater incidence of ior, with a rate of 36.9%, according to schramm and cedzich [12]. in contrast, neither giannotta et al nor houkin et al found evidence that acoa aneurysms had greater ior rates [7,9]. middle cerebral artery aneurysms were found to have lower ior rates in various studies [7]. in our report, the site was inferiorly directed acoa aneurysm. other factors predisposing to ior can be categorized into preprocedural and intraprocedural [4]. preprocedural rupture of cerebral aneurysms, though uncommon, can result in devastating consequences with a high fatality rate. this phase of ior is influenced by factors associated with anesthesia. there is a delicate balance between mean arterial pressure, icp, and transmural pressure (tmp). acute changes in hemodynamics during the induction, surgical incision, and skull pin fixation may raise transmural pressure and may predispose ior [8]. sudden coughing or gagging at this stage can cause an abrupt increase in blood pressure and icp, resulting in a premature rupture [15]. on the other hand, intraprocedural-related factors are primarily determined by arterial wall fragility, which can be influenced by various comorbidities such as a history of coronary artery disease, hyperlipidemia, copd, and race [6]. ior can be encountered during different phases of surgery, such as in the pre-dissection phase, dural and arachnoid opening, clipping, hematoma evacuation, or during brain retraction [4,6]. on the other hand, brain swelling is a significant factor for ior during the dissection phase [9]. during the clipping phase, ior may occur due to 1) increased turgor in the aneurysm's dome due to pressure transmitted from the neck while applying the clip, 2) detachment of an adherent dome as the clip closure slightly moves the aneurysm, 3) tearing of the neck due to clip misapplication, or 4) shearing of the aneurysmal neck from the parent arterial wall [10]. in our case, the ior occurred during craniotomy closure (post clipping) which is a very rare phenomenon and an equally challenging situation. the main factor that contributed to the ior during the closure, in this case, is the unintended inadequate anesthesia resulting in the patient awakening during the craniotomy closure, where he experiences recurrent coughing and gagging. this was attributed to insufficient muscle relaxant dosing or quality that resulted in a sudden increase in the icp and eventually the ior. despite the patient history of heavy smoking and uncontrollable hypertension, these risk factors may lead to early rupture rather than delayed (post clipping) rupture. the confirmation of complete clipping is usually difficult due to the challenging anatomy of the acoa complex and thick adhesions from the sah, which led to constructing the clipping with muscle wrapping. this step is usually sufficient to protect the aneurysm from rupture. however, in our case, the early waking from anesthesia made the clipping construct fails and resulted in ior. the management of ior has surgical and nonsurgical aspects. surgery-wise, the use of temporary clipping aid in accurate aneurysm clipping and reduce the risk of ior [1,3,14]. factors that influence the success of temporary clipping may include aneurysm location, duration of application, and age [11]. the non-surgical aspects of ior management may consist of cerebral protection, temperature regulation (hypothermia), hemodynamic set points adjustment, and neurophysiological monitoring. these treatment options may all have an impact on temporary occlusion results. however, the current evidence on the usage and benefit of each option is debatable [16]. the prevention of ior will depend on identifying all potential factors and treating them accordingly. thus, ensuring ior-related complication 201 delayed intraoperative rupture of clipped aneurysm during the awaking from anaesthesia avoidance and improving the overall patient outcome. the current literature is mixed regarding the outcome of ior and its long-term neurological outcomes in the form of stroke. some studies have found that intraoperative rupture has a negative impact on the outcome; however, these findings should be interpreted in light of a variety of parameters, including size, location, treatment (clipping vs. coiling), age, management strategies, and the surgeon expertise. the outcome of ior with its re-rupture in our case is an ischemic stroke in the distal circulation territory of ipsilateral (right) aca due to prolong application of the temporary clip after re-rupture. however, our patient is fortunate enough that the deficit is eventually resolved with rehabilitation. in summary, patients with delayed ior during the post-clipping phase can be managed with the typical steps of treating intraoperative bleeding with a relatively higher risk of complications. prevention of the delayed ior can be achieved with adequate anesthesia toward the end of surgery. when construction of the clipping is not straightforward, it may become vulnerable to external circumstances. conclusions intraoperative rupture during aneurysm surgery closure due to early wakeup from anesthesia should be highlighted as a potential source of complications and poor outcomes. sufficient anesthesia is necessary to prevent delayed intraoperative rupture. references 1. ausman j, diaz f. intraoperative aneurysmal rupture: incidence, outcome, and suggestions for surgical management. neurosurgery. 1986;18:706-7. 2. bederson jb, connolly es jr, batjer hh, dacey rg, dion je, diringer mn, duldner je jr, harbaugh re, patel ab, rosenwasser rh; american heart association. guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the stroke council, american heart association. stroke. 2009 mar;40(3):994-1025. 3. bellotti c, oliveri g, allegra g, et al. temporary clipping in the surgery of endocranial aneurysms. journal of neurosurgical sciences. 1998;42(1):77–79. 4. chowdhury t, cappellani rb, sandu n, schaller b, daya j. perioperative variables contributing to the rupture of intracranial aneurysm: an update. the scientific world journal. 2013 jan 1;2013. 5. chowdhury t, petropolis a, wilkinson m, schaller b, sandu n, cappellani rb. controversies in the anesthetic management of intraoperative rupture of intracranial aneurysm. anesthesiology research and practice. 2014 mar 3;2014. 6. elijovich l, higashida rt, lawton mt, et al. predictors and outcomes of intraprocedural rupture in patients treated for ruptured intracranial aneurysms: the carat study. stroke. 2008;39(5):1501–1506. 7. giannotta sl, oppenheimer jh, levy ml, zelman v. management of intraoperative rupture of aneurysm without hypotension. neurosurgery. 1991 apr 1;28(4):531-6. 8. guy j, mcgrath bj, borel co, friedman ah, warner ds. perioperative management of aneurysmal subarachnoid hemorrhage: part 1. operative management. anesthesia & analgesia. 1995 nov 1;81(5):1060-72. 9. houkin k, kuroda s, takahashi a, et al. intra-operative premature rupture of the cerebral aneurysms. analysis of the causes and management. acta neurochirurgica. 1999;141(12):1255–1263. 10. leipzig tj, morgan j, horner tg, payner t, redelman k, johnson cs. analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. neurosurgery. 2005 mar 1;56(3):455-68. 11. ogilvy cs, carter bs, kaplan s, rich c, crowell rm. temporary vessel occlusion for aneurysm surgery: risk factors for stroke in patients protected by induced hypothermia and hypertension and intravenous mannitol administration. journal of neurosurgery. 1996;84(5):785–791. 12. schramm j, cedzich cc. outcome and management of intraoperative aneurysm rupture. surgical neurology. 1993 jul 1;40(1):26-30. 13. sundt tm, kobayashi s, fode nc, whisnant jp. results and complications of surgical management of 809 intracranial aneurysms in 722 cases: related and unrelated to grade of patient, type of aneurysm, and timing of surgery. journal of neurosurgery. 1982 jun 1;56(6):753-65. 14. taylor cl, selman wr, kiefer sp, ratcheson ra. temporary vessel occlusion during intracranial aneurysm repair. neurosurgery. 1996;39(5):893–906. 15. tsementzis sa, hitchcock er. outcome from “rescue clipping” of ruptured intracranial aneurysms during induction anaesthesia and endotracheal intubation. journal of neurology neurosurgery & psychiatry. 1985;48(2):160–163. 16. zhou lf, li sq, yang ml. temporary arterial occlusion during intracranial aneurysm surgery. chinese medical journal. 1993;106(11):803–808. doi: 10.33962/roneuro-2020-038 experience, challenges and lessons learnt from microsurgical clipping of intracranial aneurysms at an emerging neurosurgical centre varun aggarwal, chandni maheshwari, divya kavita, amit narang romanian neurosurgery (2020) xxxiv (1): pp. 261-268 doi: 10.33962/roneuro-2020-038 www.journals.lapub.co.uk/index.php/roneurosurgery experience, challenges and lessons learnt from microsurgical clipping of intracranial aneurysms at an emerging neurosurgical centre varun aggarwal, chandni maheshwari, divya kavita, amit narang baba farid university of health sciences, faridkot, punjab, india abstract objectives: to share our experience, challenges faced, lessons learnt and analyze the results of surgical management by microsurgical clipping of intracranial aneurysms at an emerging neurosurgical centre at guru gobind singh medical college and hospital (ggsmc&h) faridkot, punjab. india. material and methods: this study includes all the patients who presented with the diagnosis of intracranial aneurysm on ct angiography and were treated with the microsurgical clipping, between march 2017 to april 2019. results: there was a total of 23 patients 11f female and 12 male. age range 32 to 85years. on admission 22 patients had sah on ct scan and one was admitted after incidental detection of the aneurysm without sah. the time interval between ictus and admission was 0-3 days in 13 patients, 3-14 days in 8 patients and more than 14 days in 1 patient. wfns grade (gd) i-15 patients, gd ii-2, gd iii-2, gd iv-3 patients. fisher gd i-nil, gd ii-9, gd iii-4, gd iv-9 patients. in 23 patients 27 aneurysms were clipped. distribution of location was anterior communicating-12, distal anterior cerebral artery4, middle cerebral artery (mca) bifurcation-3, mca trifurcation-1, anterior choroidal-1, posterior communicating (p-com) -1, ophthalmic internal carotid artery (oica)-4 and three patients had associated multiple aneurysms. size of aneurysms varied from < 02mm diameter in 2 patients, 2-25mm 23 and, more than 25mm-2 aneurysms. there was intra op rupture in 2 cases. post-operatively 2 patients developed hemiparesis, which recovered, nine patients developed vasospasm. two patients developed chest related complications. one patient developed renal failure. there were 8 deaths. patients are on follow up since march 2017 till date. conclusions: intracranial aneurysms are challenging to manage due to their proximity to vital intracranial structures, and difficulty in securing intracranial proximal control. thorough knowledge of intracranial anatomy of adjacent relations, arachnoid planes and skilful dissection is a key element for a successful outcome. data collected from ggsmc & hospital may not be representative of the entire state or country’s population. therefore, a large-scale data collection is necessary to create our own database to ascertain the risk factors and preventive measures that are exclusive to our state and nation. introduction in simple words an aneurysm is an abnormal dilatation of an artery wall keywords intracranial aneurysm, microsurgical clipping, pterional craniotomy, subarachnoid haemorrhage, vasospasm corresponding author: amit narang assistant professor, neurosurgery, guru gobind singh medical college and hospital faridkot, punjab. india drnarangamit@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 262 varun aggarwal, chandni maheshwari, divya kavita, amit narang and in the brain commonly arises at branching points on a parent artery. intracranial aneurysms (ias) are usually revealed after they rupture, leading to subarachnoid hemorrhage (sah). usually the sentinel headache is the earliest warning sign of incipient rupture. less frequently, they manifest themselves as a result of mass effect or are noticed incidentally during neuro-radiologic examinations performed for other diagnostic purposes.(6,9) subarachnoid hemorrhage (sah) due to the rupture of an intracranial aneurysm is a devastating event associated with high rates of mortality (40%–50%) and morbidity.(10, 20, 23, 13) the risk of intracranial aneurysm for human beings is 1 to 2% . (5) the prime motive of intracranial aneurysm treatment is to exclude the aneurysm from the circulation; this can be achieved through two ways, microsurgical treatment or endovascular obliteration. since ours is an emerging neurosurgical center where we have basic neurosurgical facilities, but lack digital subtraction angiography (dsa) and coiling facility. we are managing intracranial aneurysms with microsurgical clipping. the objective of this article is to share our experience acquired with the use of microsurgical obliteration of intracranial aneurysms at guru gobind singh medical college and hospital faridkot, punjab, india. material and methods this study includes all the patients admitted to the neurosurgery department who presented with diagnosis of intracranial aneurysm and were treated with the microsurgical clipping, in the period between march 2017 and april 2019. patients who presented with poor neurological status, with fixed dilated pupils and who did not give consent for surgery were excluded. on their arrival at the emergency department, all the patients were treated according to the defined protocol for the treatment of subarachnoid hemorrhage in the hospital and were admitted to neurosurgical intensive care units and managed depending on their neurologic state at the moment of admission, determined by using gcs, the word federation of neurologic surgeons (wfns) scale and fisher grades of sah on non contrast computed tomography (ncct) scan of brain. all the patients suspected with intra cranial aneurysm were subjected to cerebral ct angiography. presence of aneurysm on ct angiogram was considered an essentiality to proceed for surgical treatment. the aneurysmal sacs were labeled according to their number in single or multiple aneurysms, and distributed according to their location in the anterior segment or posterior segment of the circle of willis’, the projection and whether unilateral or bilateral. outcome was evaluated using the modified rankin scale (mrs). patients are under follow-up since march 2017 till date. results there were a total 23 patients out of which 11 (47.82%) were female and 12 (52.17%) were male. age range was 32 to 85 years. at the time of admission 22 patients had sah on ct scan and one patient was admitted after incidental detection of aneurysm without sah. time of admission from time of ictus 0-3 days in 13 (59.09%) patients, 3-14 days in 8(36.36%) patients and more than 14 days in 1(04.54%) patient. wfns gd i-15(68.18%), gd ii-2 (09.09%), gd iii-2 (09.09%), gd iv-3(13.36%) patients. fisher gd i-nil, gd ii-9 (40.90%), gd iii-4 (18.18%), gd iv9 (40.90%) patients. there were 31 aneurysms in total out of which 27 were clipped in 23 patients. location wise anterior communicating artery (acom)12 , distal anterior cerebral artery daca4, middle cerebral artery (mca) bifurcation-3, mca trifurcation-1, anterior choroidal-1, posterior communicating (pcom)-1, ophthalmic internal carotid artery (ica)-4 and three patients had associated multiple aneurysms. size of aneurysms varied from < 02mm diameter in 2 patients, 2-25mm in 23 and, more than 25m in 2 patients (table 1). sixteen 69.5% patients had comorbidities out of which 11 (68.75%) hypertension, one (06.25%) diabetes, one (06.25%) asthma, one (06.25%) had chronic liver disease and in 1 patient (06.25%) chronic kidney disease was diagnosed post operatively. there was intra op rupture in 2 (07.07%) cases. post operatively 2 (8.69%) patients developed hemiparesis, which recovered over a period of time, nine (39.13%) patients developed vasospasm after surgery. two (08.69%) patients developed chest related complications. in the study there were 8(34.78%) deaths. follow up has ranged since march 2017 to till date. 263 experience, challenges and lessons learnt from microsurgical clipping of intracranial aneurysms variable no % aneurysm number single 18 78.26 multiple 5 21.73 aneurysm side unilateral 21 91.30 bilateral 2 08.70 size of the sac <2mm 2 7.40 2-25 mm 23 85.18 >25 mm 2 7.40 morphology of the sac secular 21 77.77 fusiform nil 0 multilobulated 6 22.23 condition of the sac ruptured 22 81.48 unruptured 5 18.52 a com aneurysms 12 44.44 superiorly projecting 4 33.33 anteriorly projecting 2 16.66 antero-superior 1 08.33 inferior 3 25 antero-inferior 2 16.66 daca aneurysms 4 14.81 anterior 1 25 anterior superior 2 50 anterior toward opp side 1 25 superior nil 0 mca bifurcation aneurysm 3 11.11 mca trifurcation aneurysms 1 03.70 anterior choroidal aneurysm 1 03.70 ophthalmic seg aneurysm 4 14.81 communicating segment aneurysm 1 03.70 p-com aneurysm 1 03.70 discussion intracranial aneurysms (ias) are localized dilations of the cerebral arteries wall and are prone to rupture, resulting in bleeding. the overall prevalence of unruptured ias is between 2% and 3.2% in the general population with a male to female ratio of 1:2.(19) ruptured aneurysm is responsible for 85% of sah which is one of the leading causes of haemorrhagic stroke. (18) 264 varun aggarwal, chandni maheshwari, divya kavita, amit narang junjie zhao et al have described 4 basic types of intra cranial aneurysms (ias).(25) (a)secular are the most common type of ias. they resemble a round out pouching with well-defined aneurysmal domes and necks connecting to the parent vessel. commonly they occur at bifurcation locations e.g. between the mca and the posterior cerebral artery (pca), between the anterior cerebral artery (aca) and the anterior communicating artery (a com) and between the bifurcations of mca branches. (4) (b)micro aneurysms are ias with diameters smaller than 2 mm.(11) (c)-giant ias are with diameters over 25 mm. the latter account for merely 5% of all ias, but their prognosis is relatively dismal. (7, 17) untreated giant ias have over 50% risk in rupturing and 88% to 100% in mortality at 2-year follow-up. (2,12) we encountered two giant aneurysms. due to their large size the mass effect alone can cause intracranial hypertension and neurological dysfunctions one of our patient with giant aneurysm presented with decreasing vision. (d)-fusiform ia is widened and thinning segment of artery. according to yahia et al, this dilatation must affect at least 270o of the lumen’s circumference to be classified as fusiform.(24) their surgical treatment is challenging due to the vital perforators located within the affected segment. we did not encounter any fusiform aneurysm. in our study the majority of patients were from the state of punjab, (52.17%) male and (47.82%) female. a study conducted by ab ghani et al showed the mean age of affected patients as 48.9 years old, with 56.7% males and 43.3 % females.(1) a study by rinkel et al., suggests that the incidence of intracranial aneurysm increases with age, and the most of the cases occur among patients in fifth decade of their life. (15) in our study the mean age of the patient was 50.3years. male patients were more frequent than females, which is in contrast to the usual pattern of females being affected more than males. (16) however, this ratio does not seem to be applicable in all populations and may vary from state to state and country to country. (8) in our study 69.5% patients had comorbidities out of which 68.75% hypertension, 06.25% diabetes, 06.25% asthma, 06.25% had chronic liver disease and in 1 patient (06.25%) chronic kidney disease was diagnosed post operatively. in the study population of ab ghani et al, 85.7% had hypertension. (1) variation of blood pressure and hypertension are known risk factors for the development of intracranial aneurysm. (21) intracranial arteries are comprised of the outer layer of the adventitia, a muscular media that maintains most of the vessel wall integrity and the inner layer of intima. as compare to other vessels in the body they do not have external elastic lamina, which is located between the adventitia and media leading to less elasticity of the media. they also have thinner adventitia compared to the extra cranial artery wall. these vessels exist in the subarachnoid space, which lack surrounding connective tissue to support the vessels. (1) these features predispose intracranial arteries to the formation of saccular aneurysms, commonly in hypertensive patients as the thin and less elastic vessel wall is subject to increased pressures, as well as in patients with congenital conditions which predispose to defects in the muscular layer of the arterial wall, such as autosomal dominant polycystic kidney disease, ehlerdanlos syndrome fibromuscular dysplasia, and marfan syndrome. (1, 15, 3) patients without history of hypertension in our study but having hypertension on presentation might have been undiagnosed with hypertension previously or it could be due to raised icp. common history among our patients was that they rarely go to the physician for routine checkup and those who do so, many of them had history of poor compliance of antihypertensive medication and no regular follow up. these facts accentuate the importance of hypertension screening and control. among the 23 patients who underwent microsurgical clipping, the majority were fisher ii, iii or fisher iv indicating that most patients only presented post intracranial aneurysm rupture with an added risk of vasospasm. it also reflects that incidental finding of intracranial aneurysm is still rare despite the improvement of our health services and increasing amount of imaging being done for other neurologic symptoms. post operatively two patients developed hemiparesis, which recovered, one patients developed chest related complication because of underlying bronchial asthma despite an improvement in gcs. however, based on the outcome in our observational study , within a span of three months after surgery, 8 (34.78%) had the mrs score of 0 with no symptoms at all, and 8 (34.78%) had the mrs score of 6 or had died. the cause of 265 experience, challenges and lessons learnt from microsurgical clipping of intracranial aneurysms death was post operative vasospasm in 4 (50%) patients. one (12.5%) of them had anaemia secondary to upper gastrointestinal bleed due to stress ulcer which was diagnosed on upper gi endoscopy. postoperative chest infection in one (12.5%), chronic renal failure in one (12.5%) and pulmonary embolism in one (12.5%) patient. literature says maximum risk of vasospasm is 3-14 days of ictus.(22,14) three of our patients who died, developed vasospasm in first two weeks after ictus. after three months of discharge, four patients with mrs scores of 1 and 2 improved to the mrs score of 0, and after 6 months of discharge total 12 (52.17%) patient improve to mrs score 0. others three are still on rehabilitation. this improvement was mainly due to the after care of patients, which comprises intensive rehabilitation and physiotherapy. our interesting cases giant aneurysm case 1: 45 year old female presented with right basal ganglia bleed ct angio revealed giant multi lobulated ophthalmic segment aneurysm. patient underwent right pterional craniotomy with right neck control for proximal ica. because of its large size proximal and distal ica was not visible. so, aneurysmal sac was punctured, with controlled suction aneurysmal sac was deflated that led to visualization of proximal, distal ica and neck of the aneurysm, as a result we were able to apply permanent clip over the neck of the aneurysm. post operatively patient was discharged without any deficit. figure 1. figure 1. computed tomography angiography of right ophthalmic aneurysm, axial view (a) showing multilobulated large aneurysm. coronal view (b) showing the superiorly projecting aneurysm. sagittal view (c) aneurysm with narrow neck. three dimensional ct (d) showing large superiorly projecting ophthalmic aneurysms. post op computed tomography angiography (e and f) complete occlusion of aneurysm. (g) patient is fine with no deficit. multiple aneurysms case 2: 32 years old male patient presented with left anterior choroidal artery aneurysm and right mca bifurcation aneurysm. it was a challenge to manage both side aneurysms in a single surgery. we planed for two stage surgery based on sah picture on ncct brain and ct angio findings, we first clipped left anterior choroidal artery aneurysm. after dissection of the aneurysm the surgeon got engaged in selecting appropriate clip for few seconds, surgical field was out of his sight, aneurysm got ruptured and visible anatomy got distorted that led to difficult management of the ruptured aneurysm. the learning point for us was, if possible never let the aneurysm out of your vision after aneurysmal neck dissection from its surroundings and try to select the appropriate clip prior to final dissection. we clipped right mca bifurcation aneurysm second stage successfully and patient was discharged with no deficit. case 3: 45 years male patient was presented with right mca aneurysm and ophthalmic segment bleb. mca aneurysm was clipped first and we faced difficulty in clip application over bleb, the clip slipped multiple times over bleb. we realized that we had limited number of small aneurysmal clips. although in a small center like ours there are limited resources, surgeon should try to have back up of all sizes and shapes of clips before surgery. figure 2. figure 2. computed tomography angiography of patient with multiple intracranial aneurysm (right middle cerebral artery bifurcation and right ophthalmic aneurysm), axial view (a) showing laterally projecting aneurysm right middle cerebral artery bifurcation aneurysm. coronal view (b) and three dimensional ct (c) showing the inferiorly projecting right mca bifurcation and medially projecting right ophthalmic aneurysm. post op computed tomography angiography, coronal view (d), axial( f and g) showing complete occlusion of both aneurysms. (g) patient is fine with no deficit. a b c g d e f b a cc d g e f 266 varun aggarwal, chandni maheshwari, divya kavita, amit narang case 4: a 65 years old female patient was presented with left pcom (bled), left ophthalmic segment, acom and right mca bifurcation aneurysm. all left sided aneurysms were clipped in the first surgery. right mca bifurcation aneurysm was planned for second stage elective surgery but patient developed thrombocytopenia and surgery was deferred. figure 3 a&b. patient is asymptomatic and on regular follow up and is being worked up for intractable thrombocytopenia. figure 3. axial view (a) showing the laterally projecting left pcom , medially projecting left ophthalmic segment, acom and laterally projecting right mca bifurcation aneurysm and (b) post op computed tomography angiography left pcom,left ophthalmic segment and acom aneurysms t1 contrast mri axial view (c) showing gaint atherosclerotic right communicating segment aneurysm and non-contrast computed tomography, axial view (d) showing post op clip artefact with occlusion of neck. missed aneurysm case 5: a 52 years old male patient was presented with sah in left sylvian fissure and inter hemispheric fissure ct angiogram suggested left daca aneurysm. in view of sah location the aneurysm was approached through left inter hemispheric approach but we could not find aneurysm on the left side. we found aneurysm on right daca after cutting the falx. aneurysm was clipped and patient remained stable for one week and was planned for discharge but the night before discharge patient had a sudden fall in gcs, immediate ncct with ct angio head was done, it showed diffuse sah and suggested right mca aneurysm which was not visualized on the first ct angiogram. we learnt that when ever there is discrepancy in the location of the aneurysm and the location of sah on ct angiogram, dsa should be done. unfortunately, in our setup dsa facility is not available. aneurysms, which required ica ligation. case 6: a 35 years old male patient was presented with left ophthalmic segment aneurysm, neck control was taken before starting surgery, during dissection of sylvian fissure aneurysm neck got avulsed probably due to traction during sylvian fissure dissection and brain started bulging, and patient became hypotensive. we could not control the bleeding with neck control, urgent left temporal and frontal lobe were removed and ica just proximal to its bifurcation was clipped, i our opinion that was the best possible thing we could do in such a condition. post op patient developed aphasia and right-side hemiplegia and is still on follow up and under rehabilitation. again, we realized the importance of dsa in which we could appreciate the collateral supply and prepare our self for bypass. reconstruction of ica at the site of aneurysm with multiple clips and wrapping of it with muscle graft was our back up plan but, patient’s deteriorating conditions did not allow us to attempt that. giant atherosclerotic communicating segment aneurysm which required ica reconstruction case 7: a 55 years female presented with right eye vision loss having giant atherosclerotic right communicating segment aneurysm involving inferior half circumference of ica. aneurysmal sac mediallyextending into the sella with compression on optic chiasma, laterally-adherent to the tent with compression of third nerve, posteriorly-adherent to basilar artery into the interpeduncular fossa. proximal temporary clip was applied. incision was given on aneurysmal neck both medial and lateral to ica leaving 1cm of neck on each side contiguous to wall of ica to reconstruct the inferior vessel wall. major part of the neck and sac were atherosclerosed with calcification. permanent fenestrated rightangled clip applied to reconstruct the ica, which kept on slipping due of atherosclerosis of neck. so, atherosclerotic plaques were removed with penfield 267 experience, challenges and lessons learnt from microsurgical clipping of intracranial aneurysms dissector and ica was reconstructed with three permanent fenestrated right-angled clips. medial and lateral part of sac was excised but part in the interpeduncular fossa couldn’t be removed keeping in mind the risk of injury to basilar artery. post operatively patient had right anterior choroidal artery infarct with medical research council (mrc) gd 3 power in left side. patient was discharged on 7th post op day. patient was put on anti-platelets and after three weeks she started with hematuria in view of which anti-platelets were stopped and patient developed massive pulmonary embolism and expired. figure 3 c&d, figure 4. figure 4. sequential artistic view of reconstruction of ica in giant atherosclerotic communicating segment ica aneurysm. conclusions intracranial aneurysms are challenging to manage due to their proximity to vital intracranial structures, the skull base, visual apparatus and difficulty in securing proximal control intra-cranially. they can be successfully clipped if the intimate anatomical relations of the aneurysm like the optic nerve, anterior clinoid process; optic strut, the dural ring and adjacent vessels are anatomically defined properly during surgery. thorough knowledge of intracranial anatomy, adjacent relations, arachnoid planes and skillful dissection is a key element to successful outcome. data collected from ggsmc & hospital may not be representative of the entire state or country’s population. therefore, a largerscale data collection is necessary to create our own database to ascertain the risk factors and preventive measures that are exclusive to our state and nation. references 1. ailani ag, saiful azli mn, regunath k, et al. characteristics and outcomes of patients with anterior circulation intracranial aneurysm managed with clipping in hospital sungai buloh. malaysian j med sci 2016 nov;23(6):113117. 2. barrow dl, alleyne c. natural history of giant intracranial aneurysms and indications for intervention. clin neurosurg 1995;42:214-244. 3. batjer hh, chandler jp, getch cc, et al. intracranial aneurysm. in: rengachary ss, ellenbogen rg, eds. principles of neurosurgery. edinburgh: elsevier mosby publishing; 2005:215-239. 4. bharatha a, yeung r, durant d, et al. comparison of computed tomography angiography with digital subtraction angiography in the assessment of clipped intracranial aneurysms. j comput assist tomogr 2010;34(3):440-445. 5. brown rd jr, broderick jp. unruptured intracranial aneurysms: epidemiology, natural history, management options, and familial screening. lancet neurol 2014;13:393-404. 6. gasparotti r, liserre r. intracranial aneurysms. eur radiol 2005 mar;15(3):441-447. 7. gobble rm, hoang h, jafar j, et al. extracranialintracranial bypass: resurrection of a nearly extinct operation. j vasc surg 2012;56(5):1303-1307. 8. ingall t, asplund k, mahonen m, et al. a multinational comparison of subarachnoid hemorrhage epidemiology in the who monica stroke study. stroke 2000;31(5):1054-1061. 9. juvela s. natural history of unruptured intracranial aneurysms: risks for aneurysm formation, growth, and rupture. acta neurochir suppl 2002;82:27-30. 10. juvela s, prehemorrhage risk factors for fatal intracranial aneurysm rupture. stroke 2003;34:1852-1858. 11. karasawa h, matsumoto h, naito h, et al. angiographically unrecognized microaneurysms: intraoperative observation and operative technique. acta neurochir (wien) 1997;139(5):416-419. 12. lonjon m, pennes f, sedat j, et al. epidemiology, genetic, natural history and clinical presentation of giant cerebral aneurysms. neurochirurgie 2015;61(6):361-365. 13. millán rd, dempere-marco l, pozo jm, et al. morphological characterization of intracranial aneurysms using 3-d moment invariants. ieee trans med imaging 2007;26(9):1270-1282. 14. pasqualin a. epidemiology and pathophysiology of cerebral vasospasm following subarachnoid hemorrhage. j neurosurg sci 1998;42:15-2. 15. rinkel gj, djibuti m, algra a, et al. prevalence and risk of rupture of intracranial aneurysms: a systematic review. stroke 1998;29(1):251-256. 16. samandouras g. the neurosurgeon’s handbook. oxford university press; 2010. 17. sekhar ln, duff jm, kalavakonda c, et al. cerebral revascularization using radial artery grafts for the treatment of complex intracranial aneurysms: a d c b 268 varun aggarwal, chandni maheshwari, divya kavita, amit narang techniques and outcomes for 17 patients. neurosurgery 2001;49(3):646-658. 18. van gijn j, kerr rs, rinkel gj. subarachnoid haemorrhage. lancet 2007;369(9558):306-318. 19. vlak mh, algra a, brandenburg r, et al. prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: systematic review and meta-analysis. lancet neurol 2011;10(7):626-636. 20. w. schievink. intracranial aneurysms. new eng. j. med 1997;336:28-41. 21. wardlaw jm, white pm. the detection and management of unruptured intracranial aneurysms. brain 2000;123:205-221. 22. weir b, grace m, hansen j, et al. time course of vasospasm in man . j neurosurg 1978;48:173-178. 23. woo d, broderick j. genetics of intracranial aneurysm. j stroke cerebrovascular dis 2002;11(5):230-240. 24. yahia am, gordon v, whapham j, et al. complications of neuroform stent in endovascular treatment of intracranial aneurysms. neurocrit care 2008;8(1):19-30. 25. zhao j, lin h, summers r, yang m, et al. current treatment strategies for intracranial aneurysms: an overview. angiology 2018;69(1):17-30. doi: 10.33962/roneuro-2021-069 clinicopathological features, imaging characteristics and surgical management in a novel tumour entity aggressive meningiomas g. popescu, francesca paslaru, a.c. paslaru, m. apostol, m.c. zaharia, t. corneliu, m. mitrica, m. popescu, r.m. gorgan romanian neurosurgery (2021) xxxv (4): pp. 408-411 doi: 10.33962/roneuro-2021-069 www.journals.lapub.co.uk/index.php/roneurosurgery clinicopathological features, imaging characteristics and surgical management in a novel tumour entity aggressive meningiomas g. popescu1,2, francesca paslaru1, a.c. paslaru3,4, m. apostol1, m.c. zaharia1, t. corneliu3,5, m. mitrica6, m. popescu7, r.m. gorgan1,3 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 phd student, “carol davila” university of medicine and pharmacy, bucharest, romania 3 “carol davila” university of medicine and pharmacy, bucharest, romania 4 department of genetics,“dr. victor gomoiu” children’s clinical hospital, bucharest, romania 5 department of neurosurgery, national institute of neurology and neurovascular diseases, bucharest, romania 6 department of neurosurgery, "dr. carol davila" central military emergency hospital, bucharest, romania 7 department of neurosurgery, pitesti emergency hospital, university of pitesti, romania abstract meningiomas are common neoplasms of the central nervous system, comprising between 24 and 30% of primary intracranial tumors, most commonly affecting females in their middle age or later adult life [1] [2]. meningiomas are classified as benign, atypical or anaplastic meningiomas depending mostly on histopathological criteria known to be associated with worse prognosis in terms of tumor progression, recurrence risk after surgery and overall survival. the 2016 edition of world health organization (who) classification of central nervous system (cns) tumors recognizes brain invasion as an independent criterion for diagnosing an atypical grade ii meningioma [3]. meningioma grading based on the who classification of cns tumors thoroughly impacts therapeutic management and tumor prognosis. aggressive meningiomas, a different phenotype of tumors, characterized by rapid growth and involvement of adjacent brain tissue, blood vessels and bone, was not previously listed as an independent entity in the who classification of meningothelial-cell tumors. regarding the increasing importance of tumor grading in meningioma treatment keywords aggressive meningiomas, clinicopathological features, imaging characteristics, surgical management corresponding author: g. popescu “carol davila” university of medicine and pharmacy, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 409 aggressive meningiomas strategies, the authors here provide an overview of clinicopathological and radiographic features, surgical management and long-term prognosis of this novel meningothelial tumor entity, the aggressive meningioma. in particular, we aimed to describe pre-, intraand postoperative methods for recognizing aggressive meningiomas and explore the implications of this diagnosis on both surgical strategies and adjuvant therapy. patients and methods we performed a single-center retrospective study. we reviewed the files of all patients diagnosed with primary intracranial meningioma at the 4th clinical department of neurosurgery, bagdasar-arseni clinical emergency hospital, between january 2013 and december 2018. inclusion criteria, primary based on preoperative imaging and confirmed by histopathological examination, consisted of either: invasion into the brain parenchima, involvement of the major blood vessels, cranial vault bone lysis without involvement of the outer table of the skull or complete bone destruction and aesththic diformity. results a total of 25 patients, 16 female and 9 male patiens, with a gender female:male ratio of 1.7:1, met the required imagistic/histopathological criteria and were included in the present study. age at diagnosis ranged from 29 to 74 year old, with a median of 53.8 years. figure 1 shows the distribution based on the tumor location. we found 11 frontal meningioma, 6 skull base tumors, 5 parietal meningiomas and one of each: temporal, occipital and posterior fossa (comprised in figure 1 as ”others”). figure 1. distribution of the patients based on tumour location most frequent symptoms at diagnosis were: headache, progressive motor weakness and seizures. regarding the tumor size, based on the largest diameter as measured on preoperative imaging, tumors ranged from 30 mm to 80 mm diameter. figure 2 shows the distribution based on the involvement of the neighbouring structures. bone lysis (image 1, image 2) was observed in 9 cases (36%), major blood vessels involvement in 8 cases (32%), invasion into the brain parenchima in 8 cases (32 %) and complete bone destruction with cosmetic diformity (image 2) in 6 cases (24%). image 1. contrast enhanced computed tomography scan showing a large extraaxial lesion with frontal bone involvement and peritumoral edema image 2. non-enhanced magnetic resonance imaging scan, t2 sequence, axial section, showing a left parietal tumor extending into the corpus callosum, with perilesional edema and bone invasion 11 6 5 3 distribution of the patients based on tumor location. frontal skull base parietal other 410 g. popescu, francesca paslaru, a.c. paslaru et al. figure 3 shows the distribution of the patients based on the extent of resection. all but one patient were operated on, achieving a gross total resection in 16 cases (64%) and a subtotal resection in 8 cases (32%). in the single case where conserative management was chosen, it was because of the patient`s associated diseases. image 3. contrast enhanced cmputed tomography scan showing a large extraaxial lesion with complete parietal bone destruction and cosmetic diformity figure 4 shows the patients distribution based on the histopathological variants, using the current who classification of tumors of the meninges. we found 13 atypical (who grade ii) and 12 who grade i tumors: 5 transitional (mixed), 4 meningothelial, one psamomatous, one fibrous (fibroblastic) and one angiomatous meningioma. postoperative recurrence rate was 16% (4 cases). perioperative mortality rate was 4% (1 case). figure 2. adjacent structures involvement figure 3. distribution of the patients based on the extent of surgical resection figure 4. distribution of the patients based histopathological variant discussion intracranial tumors can be divided into primary and secondary lesions, intra-axial or extra-axial. most common origin structures for extra-axial tumors are cranial nerves and meninges [4]. meningiomas, tumors arising from arachnoidal cap cells, comprise between 24 and 30% of primary intracranial tumors and most commonly affect females in their middle age or later adult life [1] [2]. these tumors are a heterogenous group, commonly defined by histopathological classification based on the who grading scale. however, it has been reported that the clinical aggressiveness of intracranial meningioma does not always correlate with who grading, some tumors displaying early recurrence and invasion, despite maximal surgical resection with of without 9 8 8 6 0 2 4 6 8 10 adjacent structures involvement. 16 8 1 distribution of the patients based on the extent of surgical resection. gtr str wo 13 5 4 1 1 3 distribution of the patients based histopathological variant. atypical transitional (mixed) meningothelial psamomatous 411 aggressive meningiomas adjuvant radiotherapy [5]. the 2016 edition of world health organization (who) classification of central nervous system (cns) tumors has integrated infiltrative growth of meningioma into the adjacent brain parenchima as a stand-alone criterion for diagnosing and atypical meningioma [3]. behling et al. studied the prognostic significance of intraoperative detection of infiltrative growth of primary meningioma and reported that the combination of intraoperative detection and histopathological assesment of central nervous system invasion is an independent prognostic factor for recurrence and gives a better risk-adapted tumor classification [6]. brain invasion could also be predicted based on preoperative mri scans. ong et al. reported that large peritumoral edema was significantly higher in invasive meningioma and enlarged pial feeding arteries, a rare finding, was only seen in brain-invasive meningiomas, while a complete cerebrospinal fluid cleft was only found in non-invasive meningiomas [7]. joo et al. published an imaging-based model that combines interface radiomics and peritumoral edema, in order to predict brain invasion by meningioma [8]. in our study, we found brain parenchima invasion in 8 out of the 25 patients with aggressive meningioma (32%). the primary treatment of intracranial meningioma remains safe maximal surgical resection, being an independent prognostic factor for tumor recurrence [9]. diagnosis of meningioma is based on histopathological examination of the surgical or biopsy sample. however, karabagli et al. studied the prognostic significance of histopathological features of aggressive meningioma regarding the recurrence rate and found that no feature could be used to predict the recurrence rate [10]. conclusions aggressive meningiomas, characterised by rapid growth and involvement of adjacent brain tissue, blood vessels and bone, can be considered a different phenotype of tumors, not previously mentioned in the who classification, with a distinct pattern of evolution and postoperative recurrence. further studies are needed to better asses the criteria for diagnosing this type of tumors. correspondence a.c. paslaru & c. toader (corneliu.toader@gmail.com) author with equal contribution: dr. m. popescu references 1. s. hanft, p. canoll and j. bruce, "a review of malignant meningiomas: diagnosis, characteristics, and treatment," jeorunal of neurooncology, vol. 99, no. 3, pp. 433-443, 2010. 2. j. rockhill, m. mrugala and m. chamberlain, "intracranial meningiomas: an overview of diagnosis and treatment," neurosurgical focus, vol. 23, no. 4, 2007. 3. b. brokinkel, k. hess and c. mawrin, "brain invasion in meningiomas clinical considerations and impact of evaluation: a systemativ review.," neuro-oncology, vol. 19, no. 10, pp. 1298-1307, 2017. 4. w. hou, y. ma, h. xing and y. yin, "imaging characteristics and surgical treatment of invasive meningioma," oncology letters, vol. 13, pp. 2965-2970, 2017. 5. a. nazem , j. ruzevick and m. j. ferreira , "advances in meningioma genomics, proteomics, and epigenetics: insights into biomarker identification and targeted therapies," oncotarget, vol. 11, no. 49, pp. 4544-4553, 2020. 6. f. behling, c. fodi, i. gepfner-tuma, k. machetanz, m. renovanz, m. skardelly, a. bornemann, j. honegger, g. tabatabai, m. tatagiba and j. schittenhelm, "cns invasion in meningioma-how the intraoperative assessment can improve the prognostic evaluation of tumor recurrence," cancers, vol. 12, no. 12, p. 3620, 2020. 7. t. ong, a. bharatha, r. alsufayan, s. das and a. wei lin, "mri predictors for brain invasion in meningiomas," neuroradiology journal, 2020. 8. l. joo, j. eun park, s. young park, s. jung nam, k. younghoon, k. jeong hoon and k. ho sung , "extensive peritumoral edema and brain-to-tumor interface mr imaging features enable prediction of brain invasion in meningioma: development and validation," neurooncology, 2020. 9. f. behling, c. fodi, e. hoffmann, m. renovanz, m. skardelly, g. tabatabai, j. schittenhelm, j. honegger and m. tatagiba , "the role of simpson grading in meningiomas after integration of the updated who classification and adjuvant radiotherapy.," neurosurgical reviews, 2020. 10. p. karabagli, h. karabagli, z. mavi, f. demir and e. ygmur ozekeles, "histopathological and clinical features as prognostic factors of atypical meningiomas," turkish neurosurgery, 2020. doi: 10.33962/roneuro-2022-025 troponin and non-traumatic subarachnoid haemorrhage. results from a study of 243 consecutive patients raluca stoica, diana-gabriela iacob, gabriel iacob romanian neurosurgery (2022) xxxvi (2): pp. 139-144 doi: 10.33962/roneuro-2022-025 www.journals.lapub.co.uk/index.php/roneurosurgery troponin and non-traumatic subarachnoid haemorrhage. results from a study of 243 consecutive patients raluca stoica1, diana-gabriela iacob2, gabriel iacob3 1 anaesthesia and intensive care department, colțea clinical hospital, bucharest, romania 2 infectious disease department, emergency university hospital, bucharest, romania 3 neurosurgery department, emergency university hospital, bucharest, romania abstract introduction: subarachnoid haemorrhage (sah) is a devastating event, with a mortality of up to 50%. acute cardiac dysfunction is common after such an event, and it is known to have a negative impact on the outcome of these patients. cardiac troponin release occurs frequently after sah and represents an early biomarker for neurogenic cardiac dysfunction. objective: the present study aimed to evaluate the impact of a raised troponin value on the outcome of sah patients. methods: this is a prospective observational study held between 2014-2017 at the university emergency hospital, bucharest. data on clinical admission status, highsensitivity troponin i, ecg and echocardiographic evaluation results, icu length of stay and in-hospital mortality rate. statistical analysis was performed using nonparametrical mann-whitney and chi-square tests. the results were considered significant at p<0.05. results: a total of 335 consecutive patients with non-traumatic sah were admitted during the study period. 92 of them were excluded and 243 were analyzed, 203 with aneurysmal sah and 40 with non-aneurysmal, non-traumatic sah. high-sensitivity troponin i reached its peak level 48 to 72 hours after sah and was higher in patients with aneurysmal sah. for all sah patients, its median and peak values on days 1 and 2 were correlated with the icu length of stay and inversely correlated with in-hospital length of stay. for the first 3 days, the median and maximum troponin values are higher in patients who died compared with those who survived and were discharged home (p-value < 0.001). predictors of an elevated troponin on day 1 are loss of consciousness at ictus, a high hunt and hess and fisher scale grade, intraventricular haemorrhage and cerebral midline shift. conclusions: the release of cardiac troponin is a valuable marker of neurogenic cardiac dysfunction in the first 3 days after sah. the study replicates other data in the literature and highlights the association between sah severity, early troponin elevation and in-hospital death. keywords aneurysmal subarachnoid haemorrhage, non-aneurysmal, non-traumatic subarachnoid haemorrhage, cardiac troponin, cardiac markers, neurogenic cardiac dysfunction, stress cardiomyopathy corresponding author: gabriel iacob neurosurgery department, emergency university hospital, bucharest, romania gbrl_cb@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 140 raluca stoica, diana-gabriela iacob, gabriel iacob introduction subarachnoid hemorrhage (sah) is a medical emergency, still associated with a high morbidity and mortality, despite the recent advancement in its treatment. the fact that it affects people in the prime of their lives makes it an important public health concern. it is a well-known fact that subarachnoid hemorrhage is associated with neurogenic myocardial dysfunction, of which cardiac troponin is a reliable marker. up to 63% of aneurysmal sah patients have a cardiopulmonary involvement and 23% of them die as a result of such a complication (13). the cardiac dysfunction becomes a sign of the severity of sah, as well as a marker of bad outcome. it is associated with neurologic complications, such as vasospasm and delayed cerebral ischemia, and with a high in-hospital mortality (4-6). the diagnosis of such a myocardial dysfunction is made taking into consideration the early electrocardiographic changes, the release of cardiac troponin and ntprobnp and the echocardiographic wall motion anomalies. moreover, this stress cardiomyopathy is encountered early in the clinical evolution of aneurysmal sah, as the majority of patients who are diagnosed with such a complication have a lower arterial blood pressure and thus a higher need for vasopressors, more st-t anomalies and even a high value of the cardiac troponin at the moment of their hospital admission (7). troponin has a high sensibility for detecting the cardiopulmonary stress encountered in sah, with up to 70% of patients having a rising troponin value in the first two days from the aneurysmal rupture. furthermore, a high troponin value is corelated with a prolonged corrected qt interval on the electrocardiography and echocardiographic anomallies (3)(4)(7-12). materials and method we conducted a prospective observational study. all consecutive adult patients admitted to the neurosurgical or the intensive care unit of the university emergency hospital, bucharest, between december 2014 and december 2017 were included. their identity was anonymized and all of them were treated by their attending doctors according to national and international protocols for sah, without any interference from the lead author of this paper, who collected the data. a series of data were collected, among them preexisting pathologies and known sah risk factors, clinical status on admission (neurological and cardiovascular parameters, such as glasgow coma scale grade, arterial pressure and heart rate) vasopressor requirement, oxygenation index, sah extension on ct (fisher scale grade, intracerebral and intraventricular hemorrhage extension), ecg and echocardiographic evaluation results, high-sensitivity troponin i value, icu length of stay and in-hospital mortality. exclusion criteria were represented by: traumatic sah, preexisting cardiac disease (ischemic heart disease, congestive heart failure, cardiac pacing, atrial fibrillation or atrial flutter), chronic renal failure, fluid balance and electrolytic anomalies or treatment with drugs that might affect the ecg or a period longer than 24 hours between the debut of symptoms and the transfer to the university emergency hospital. statistical analysis was performed using spss v27.01.0 (spss inc., chicago, ill., usa). data was represented using means or medians and non-parametric mannwhitney tests were performed to analyze the difference between groups. categorical data was assessed using chi-square tests. a p value <0.05 was considered statistically significant. results between december 2014 and december 2017, there were 335 adult patients with sah admitted to the university emergency hospital in bucharest. we excluded 92 of them due to criteria mentioned above, so 243 of them were studied – 203 with aneurysmal sah and 40 with non-aneurysmal, nontraumatic sah. aneurysmal sah of the 203 patients with aneurysmal sah, the majority were women (55.17%) and lived in an urban area (61.58%). the mean age was 51.4±12.1 years old, with the youngest patient being 20, and the oldest 79 years old. the mean age was 52 years old for women and 49 years old for men. the mean body mass index was 28 (interquartile range iqr 26, 31), 102 patients (50,2%) were smokers and 42 (20.7%) were using alcohol. 45 patients (22%) were dyslipidemic, 48 (23.6%) were hypertensive, 11 (5.4%) had a history of stroke and 20 patients (9.9%) had diabetes. the mean duration from symptom debut to hospital admission was 2.67 hours for people coming from rural areas, and 1.64 hours for people coming from urban areas. the median for the 141 troponin and non-traumatic subarachnoid haemorrhage admission glasgow coma scale score was 7.5 (iqr 5, 14). most of the patients with a ruptured aneurysm (135 or 66.5%) were admitted to the intensive care unit, with a median icu stay of 1 day (iqr 0, 4) and a median hospital stay of 9 days (iqr 1, 19). more than half of them (113 or 55.7%) died during their hospital stay. table 1. data for day 1 parameter all patients (n=243) non-aneurysmal sah (n=40) aneurysmal sah patients (n=203) median for systolic arterial pressure (iqr) 135 (125,155) 140 (135,150) 135 (125,155) median for mean arterial pressure (iqr) 101.67 (88.34,11) 105.83 (94.6,113) 101.67 (85,115) no. and percentage of patients with vasopressor treatment 42 (17.3%) 1 (2.5%) 41 (20.2%) median for heart rate (iqr) 85 (70, 95) 80 (71.25, 90) 85 (70, 95) median for oxygenation index (iqr) 300 (263.5, 327) 371.5 (321.5, 448.5) 290 (260, 321.75) mechanically ventilated 145 (59.7%) 20 (50%) 125 (61.6%) median for troponin level (iqr) 0. 62 (0.02,1.24) 0.36 (0.17,0.59) 0.63 (0.09,1.24) no. and percentage of patients with high troponin value 113 (74.8%) 6 / 9 (66.7%1) 107 / 142 (75.4%1) median for corrected qt interval (iqr) 410 (378, 448) 386 (372, 418) 416 (380, 452) no. and percentage of patients with prolonged corrected qt interval 47 (19.3%) 0 47 (23.2%) 1 percentage based on total number of patients with available troponin value for day 1 other data collected for day 1 are shown in table 1. the median for the maximum high-sensitivity cardiac troponin i level was 1.02 ng/ml, with an interquartile range of 0.26 to 1.96 ng/ml. for those patients in whom high-sensitivity cardiac troponin i level was measured, its value increased from day 1, reaching a peak value on day 3 (48 to 72 hours from the rupture of the aneurysm). table 2 shows data regarding the high-sensitivity cardiac troponin i values for patients with aneurysmal sah. table 2. high-sensitivity cardiac troponin i level day 1 day2 day 3 median for troponin level (iqr) 0.63 ng/ml (0.09,1.24) 0.98 ng/ml (0.29,1.91) 1.7 ng/ml (0.85,2.63) no. and percentage of patients with high troponin value 107 / 142 patients (75.4%1) 67 / 84 patients (79.8%1) 41 / 41 patients (100%1) 1 percentage of the patients with available troponin value for day figure 1. distribution of troponin value during the first 3 days after sah versus death rate for all patients (aneurysmal and non-aneurysmal, non-traumatic sah), both maximum troponin value (p<0.001) and troponin value from day 1 (p<0.028) and day 2 (p<0.001) were correlated with their icu stay, and inversely correlated with their in-hospital stay (p<0.001 for all). moreover, for patients with aneurysmal sah, these values were correlated with 142 raluca stoica, diana-gabriela iacob, gabriel iacob their in-hospital stay (p<0.001) and not with their icu stay. furthermore, the maximum troponin value and the troponin level during the first 3 days were significantly higher in patients who died during their hospital stay compared with those who were discharged (p<0.001 for all) (figure 1). table 3. predictors of elevated troponin (troponin ˃ 0.03 ng/dl) on day 1 variable no of patients with elevated troponin on day 1 n=107 (%) or (95%ci) p value loss of consciousness at ictus 68 (63.6%) 5.03 (2.14, 11.83) <0.001 hunt&hess grade iv or v 86 (80.4%) 4.86 (2.14, 11.02) <0.001 fisher scale grade iii or iv 84 (80%) 10 (4.16, 24) <0.001 intraventricular hemorrhage 51 (47.7%) 5.46 (1.97, 15.15) <0.001 midline shift 51 (47.7%) 4.4 (1.69, 11.46) 0.001 admission clinical and radiographic variables (ct) predictive of increased day 1 high-sensitivity cardiac troponin i levels included: loss of consciousness at ictus, higher hunt and hess grade (iv and v), higher fisher scale grade (iii and iv), intraventricular hemorrhage and midline shift on admission ct. non-aneurysmal, non-traumatic sah this group consists of 40 patients, with 57.5% originating from urban areas and 42.5% of them being women. the mean age was also 51.48±11.87 years old, with the youngest being 28, and the oldest 71 years old, in both men and women. the mean body mass index was also 28 (iqr 26, 31), 15 patients (37.5%) were smokers and 6 (15%) were using alcohol. 14 patients (35%) were dyslipidemic, 9 (22.5%) were hypertensive, and 13 patients (32.5%) had diabetes. none had a history of stroke. the mean duration from symptom debut to hospital admission was 4.4 hours for both rural and urban areas, but with a median value of 2 hours for people coming from rural areas, compared with 5 hours for people coming from urban areas. the median for the admission glasgow coma scale score was 11.5 (iqr 5.25,15). just like patients with aneurysmal sah, more than half of the people in this subgroup were admitted to the intensive care unit (21 or 52.5%), with a median icu stay of 1 day (iqr 0, 4) and a median hospital stay of 18.5 days (iqr 5.25, 26).less than half of them (17 or 42.7%) died during their hospital stay. discussion and conclusions our data correlate well with those found in the literature when it comes to the general characteristics of the people in the 2 subgroups: women are more affected by sah caused by aneurysm rupture, while more men are affected by non-aneurysmal, non-traumatic sah. both subgroups are represented by people in their prime (about 51 years old), coming from urban areas (13)(14). as expected, smoking was the most prevalent risk factor encountered in our cohort, in half of the patients. a series of studies cites smoking as the most important modifiable risk factor for aneurysmal rupture (15-20). the fact that alcohol consumption was declared by only about a quarter of the patients may be so because of the social stigma associated with it, or because of the underreporting bias – people tend to underestimate their alcohol intake. a high alcohol consumption represents an important risk factor for aneurysm rupture (15)(17)(21)(22). in contrast to the literature (15)(17)(21-23), not finding hypertension as a main risk factor for sah may be explained by the general lack of preventive medicine in our country, with a certain number of people believing that you should visit a doctor only when you are “sick”, without realizing that a lot of diseases are, in fact, “silent killers”. it was important to study all of these risk factors, as all of them are also risk factors for cardiac disease, where troponin plays a key role. on the one hand, for aneurysmal sah, the more rapid hospital admission for people coming from urban areas compared to those from rural areas could be easily explained by their proximity to a hospital. on the other hand, viceversa was observed for non-aneurysmal, nontraumatic sah. this seems to represent a paradox – lighter symptoms compared to those produced by the rupture of an aneurysm make people living in an urban area ignore them for a longer period of time, precisely because they can access medical support at any time they feel they finally need to. nevertheless, the time frame between symptom debut to hospital 143 troponin and non-traumatic subarachnoid haemorrhage admission remains short in terms of troponin release and detection. this is important as it did not interfere with the trend of our troponin results. a lower median value of the glasgow coma scale score, a higher percentage of icu admission and a higher death rate for patients with aneurysmal sah versus non-aneurysmal, non-traumatic sah was observed, as expected, due to its more severe evolution, with a known high mortality (1)(24)(25). the cardiac dysfunction in patients with sah was readily apparent when analyzing general data, like mean arterial pressure, need of vasopressors, heart rate, and even oxygenation index and need of mechanical ventilation, or specific parameters like, troponin level and corrected qt interval on the electrocardiogram. the subgroup of aneurysmal sah patients had a lower mean arterial pressure and a higher need of vasopressor treatment, a lower oxygenation index and a higher percentage of mechanically ventilated people, all of which are markers of a cardiac involvement. moreover, a higher percentage of aneurysmal sah patients had an abnormal troponin level, with a median troponin value almost double the one observed in nonaneurysmal, non-traumatic sah. the fact that troponin elevation is detected early in the evolution of sah is very useful in order to detect the incidence of cardiac dysfunction immediately after sah. for the first day of hospital admission, our study revealed a high frequency of high-sensitivity cardiac troponin i elevation 74.8% out of the 151 patients who were tested in the entire sah group, with a higher percentage in the aneurysmal sah subgroup (75.4% out of the 142 patients who were tested) compared to the non-aneurysmal, non-traumatic subgroup (66.7% out of the 9 patients who were tested). we may have overestimated the true incidence of an elevated troponin i value, due to the fact that not all patients included in the study were tested. on the one hand, other studies (8)(26-28) revealed that only 20% to 40% of the patients with aneurysmal sah had a detectable troponin i release. on the other hand, all these other cited studies used cardiac troponin i assays, whereas we investigated the dynamics of high-sensitivity cardiac troponin i, which, as its name suggests, has much lower limits of detection (29). therefore, new studies may be needed in order to describe de dynamics of highsensitivity cardiac troponin i assays in patients with sah. troponin reaching a peak on day 3, that is 48 to 72 hours after aneurysmal rupture in our study, is also well correlated with other literature references (30). we found that high-sensitivity cardiac troponin i measurements after sah have prognostic significance. a raised value on day 1 and 2 (which represent the first 48 hours after sah) is significantly correlated with the icu stay, and inversely correlated with in-hospital stay. this suggests a more severe clinical evolution for patients with a high troponin value and supports the idea that cardiac dysfunction associated with sah may be involved in their poor outcome. moreover, the fact that maximum troponin level, as well as troponin values during the first 3 days after sah are significantly higher in patients who died, versus patients who were discharged home suggests that cardiac troponin should be routinely measured in sah patients, in order to be able to offer a more intensive management for these patients. furthermore, these results reinforce the general recommendation of a thorough cardiac monitoring, including serial troponin measurements, especially during the first 3 days in all sah patients. patients with more severe sah grades should be primarily monitored closely for cardiac dysfunction, as they demonstrated to be more likely to develop an elevated level of serum cardiac troponin i. there was a strong correlation between the extent of cardiac troponin i elevation and various parameters of sah severity, such as loss of consciousness at ictus, a high hunt and hess grade, intraventricular hemorrhage, midline shift and a high fisher scale grade. these results demonstrate the neurogenic origin of heart injury in aneurysmal sah patients. further research is needed to investigate whether certain measures to optimize cardiac treatment after sah improve outcome. references 1. okabe t, kanzaria m, et al. cardiovascular protection to improve clinical outcomes after subarachnoid hemorrhage: is there a proven role? neurocrit care 2013, 18(2), 271-284. 2. chen wl, huang ch, et al. ecg abnormalities predict neurogenic pulmonary edema in patients with subarachnoid hemorrhage. am j emerg med, 2016, 34(1), 79-82. 3. zahid t, eskander n, et al. cardiac troponin elevation and outcome in subarachnoid hemorrhage. cureus 2020, 12(8), e9792. 4. mavridis i, meliou m, et al. troponin elevation in 144 raluca stoica, diana-gabriela iacob, gabriel iacob subarachnoid hemorrhage, journal of acute disease 2015, 21, 10, 1016/s2221-6189(14)60074-3. 5. oras j, grivans c, et al. lodding h. elevated highsensitive troponin t on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study. crit care, 2016, 20, 11. 6. mcateer a, hravnak m, et al. the relationships between bnp and neurocardiac injury severity, noninvasive cardiac output, and outcomes after aneurysmal subarachnoid hemorrhage, biol res nurs. 2017, 19(5), 531-537. 7. oras j, grivans c, et al. high-sensitive troponin t and nterminal pro b-type natriuretic peptide for early detection of stress-induced cardiomyopathy in patients with subarachnoid hemorrhage, neurocrit care 2015, 23(2), 233-242. 8. parekh n, venkatesh b, et al. cardiac troponin i predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage, j am coll cardiol. 2000, 36(4), 1328-1335. 9. naval ns, stevens rd, et al. controversies in the management of aneurysmal subarachnoid hemorrhage, crit care med.2006, 34(2), 511-524. 10. stevens rd, nyquist pa. the systemic implications of aneurysmal subarachnoid hemorrhage, j neurol sci. 2007, 261(1-2),143-156. 11. ripoll jg, blackshear jl, et al. acute cardiac complications in critical brain disease, neurol clin.2017, 35(4), 761-783. 12. kagiyama n, sugahara m, et al. neurocardiac injury assessed by strain imaging is associated with in hospital mortality in patients with subarachnoid hemorrhage, jacc cardiovasc imaging, 2020, 13(2 pt 2), 535-546. 13. sarti c, tuomilehto j, et al. epidemiology of subarachnoid hemorrhage in finland from 1983 to 1985, stroke 1991, 22(7), 848-853. 1991. 14. vlak mh, algra a, et al. prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis, lancet neurol. 2011, 10(7), 626-636. 15. van gijn j, rinkel gj. subarachnoid haemorrhage: diagnosis, causes and management. brain 2001, 124(pt 2), 249-278. 16. anderson cs, feigin v, et al. australasian cooperative research on subarachnoid hemorrhage study (across) group. active and passive smoking and the risk of subarachnoid hemorrhage: an international populationbased case-control study, stroke 2004, 35(3), 633-637. 17. feigin vl, rinkel gj, et al. risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies, stroke 2005, 36(12), 2773-2780. 18. feigin v, parag v, et al. asia pacific cohort studies collaboration. smoking and elevated blood pressure are the most important risk factors for subarachnoid hemorrhage in the asia-pacific region: an overview of 26 cohorts involving 306,620 participants, stroke 2005, 36(7), 1360-1365. 19. sandvei ms, romundstad pr, et al. risk factors for aneurysmal subarachnoid hemorrhage in a prospective population study: the hunt study in norway, stroke 2009, 40(6), 1958-1962. 20. korja m, kivisaari r, et al. size of ruptured intracranial aneurysms is decreasing: twenty year long consecutive series of hospitalized patients, stroke 2018, 49(3),746749. 21. andreasen th, bartek j jr, et al. modifiable risk factors for aneurysmal subarachnoid hemorrhage, stroke 2013, 44(12), 3607-3612. 22. vlak mh, rinkel gj, et al. lifetime risks for aneurysmal subarachnoid haemorrhage: multivariable risk stratification, j neurol neurosurg psychiatry 2013, 84(6),619-623. 23. ruigrok ym, buskens e, et al. attributable risk of common and rare determinants of subarachnoid hemorrhage, stroke 2001, 32(5), 1173-1175. 24. anderson t. current and evolving management of subarachnoid hemorrhage, crit care nurs clin north am.2009, 21(4), 529-539. 25. carpenter cr, hussain am, et al. spontaneous subarachnoid hemorrhage: a systematic review and meta-analysis describing the diagnostic accuracy of history, physical examination, imaging, and lumbar puncture with an exploration of test thresholds, acad emerg med. 2016, 23(9), 963-1003. 26. deibert e, barzilai b, et al. clinical significance of elevated troponin i levels in patients with nontraumatic subarachnoid hemorrhage, j neurosurg. 2003, 98(4):741746. 27. tung p, kopelnik a, et al. predictors of neuro cardiogenic injury after subarachnoid hemorrhage, stroke 2004, 35(2), 548-551. 28. naidech am, kreiter kt, et al. cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage, circulation 2005, 112(18), 2851-2856. 29. reichlin t, hochholzer w, et al. early diagnosis of myocardial infarction with sensitive cardiac troponin assays, n engl j med. 2009, 361(9), 858-867. 30. macrea lm, tramèr mr, et al. spontaneous subarachnoid hemorrhage and serious cardiopulmonary dysfunction a systematic review, resuscitation 2005, 65(2), 139-148. romanian neurosurgery (2019) xxxiii (3): pp. 322-325 doi: 10.33962/roneuro-2019-054 www.journals.lapub.co.uk/index.php/roneurosurgery a case report of retrograde suction decompression of a large paraclinoid aneurysm ahmed mohamed khalil1, yashuhiro yamada2, katsumi takizawa3, yoko kato2, ahmed ansari2 1 department of neurosurgery, faculty of medicine, alexandria university, egypt 2 department of neurosurgery, bantane hospital, fujita health university, nagoya, japan 3 department of neurosurgery, asahikawa redcross hospital, hokkaido, japan abstract surgical clipping of large paraclinoidal ic (internal carotid) aneurysm pose a great challenge as there are adhesions hindering exposure of aneurysm dome and parent artery . obtaining adequate visualization of the aneurysm neck is very difficult in these aneurysms, also in the access of proximal control. there are many methods to obtain a proximal control in these aneurysms. retrograde suction decompression provides adequate visualization of the aneurysm neck and its relation with the optic apparatus. retrograde suction decompression can be done by many methods. the technique done via open catheterization of superior thyroid artery is readily accessible and provides adequate relaxation of the aneurysm dome enabling complete dissection of the aneurysm from the surrounding important neurovascular structures. in this report of a case of left paraclinoidal ica aneurysm which was clipped applying this method, we elaborate on the technique and discuss other methods available for proximal control in these difficult aneurysms. introduction microsurgical treatment for paraclinoid aneurysms continue to pose severe challenges to vascular neurosurgeons because of attaining difficulty in proximal control of the parent artery and obtaining adequate visualization of the aneurysm neck. (1) microsurgical treatment of large paraclinoid aneurysms often requires the use of the one or the other methods of attaining proximal control. these can vary from exposure of internal carotid artery in the neck, adenosine induced cardiac arrest, rapid ventricular pacing (rvp), and retrograde suction decompression (rsd). these, in addition to anterior clinoidectomy facilitate safe and complete clipping in these difficult aneurysms. (2,3) rsd can be in the form of both open as well as endovascular approach. in both variants it provides adequate relaxation of the keywords paraclinoidal, proximal aneurysm control, retrograde suction decompression (rsd) corresponding author: ahmed ansari department of neurosurgery, bantane hospital, fujita health university, nagoya, japan ahmed.ansari2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 323 a case report of retrograde suction decompression of a large paraclinoid aneurysm aneurysm dome, enabling the surgeon to dissect the aneurysmal complex from the surrounding structures such as optic apparatus and dural ring allowing adequate visualization of the aneurysm neck and reconstruction of the parent artery. (1, 4, 5, 6) we present a case and discuss the surgical nuances of retrograde suction decompression of a large left paraclinoidal ic aneurysm in banbuntane hotokukai hospital, fujita health university, japan. haemorrhages or eponymously duret haemorrhages are a feared consequence of a transtentorial brain herniation or of a decompression of the intracranial space by means of craniectomy or by removal of an intracranial mass lesions. (16, 21, 22). case report a 49-year-old woman was admitted to our hospital with incidentally detected, no history of headache, dizziness or blurring of vision. magnetic resonance angiography showed a left paraclinoidal aneurysm. three-dimensional computed tomography (ct) angiography (3d-cta) and digital subtraction angiography revealed a left paraclinoidal aneurysm with a fundus height 8.2 mm in size, neck width 8.5mm (figure 1) .we also performed computational fluid dynamics (cfd) which showed wall pressure to be high, wall shear stress was low and vectors were divergent at the base of neck as it impend rupture (figure 2). figure 1. 3d-cta show left paraclinoidal aneurysm with fundus height 8.2 mm, neck width 8.5 mm figure 2: cfd of our left paraclinoidal aneurysmthese operative procedure the patient was placed in supine position with head rotated 30 degrees and neck slightly extended to facilitate cervical incision. intraoperative monitoring mep was used. a curvilinear incision of about 10 cm was made in the neck. deeper layers were exposed in succession to dissect out the common carotid, external and internal carotid artery. the superior thyroid artery was dissected and secured with a loop. a standard left pterional craniotomy in addition to anterior clinoidectomy (extradural) was done. the sylvian fissure was widely split for minimal retraction of the frontal lobe to expose the internal carotid artery and the optic nerve. the large aneurysm arising from the medial wall of the carotid was visualized. the posterior communicating artery, anterior choroid artery (ach), and their branches were also defined. the common carotid, external carotid distal to superior thyroid artery and internal carotid artery distal to the aneurysm were clamped. the superior thyroid artery was opened and a 5f feeding tube was introduced in the direction of the internal carotid artery. retrograde suction decompression (rsd) was performed with the help of 10cc syringe. the aneurysm was effectively deflated following which a definitive clipping of aneurysm was performed with two permanent clips (figure 3). post clipping dual injection video angiography (diva) showed complete occlusion of the aneurysm (figure 4). the postoperative was uneventful and patient recovered well without any deficits. 324 ahmed mohamed khalil, yashuhiro yamada, katsumi takizawa, yoko kato, ahmed ansari figure 3: show defensive clipping of left paraclinoidal aneurysm with 2 permanent clips figure 4. diva showed complete occlusion of aneurysm discussion paraclinoidal aneurysms are surrounded by many important osseous and neurovascular structures, which continue to present great difficulties in achieving proximal control of the parent artery and obtaining adequate visualization of the aneurysm neck because of adhesion to surrounding anatomical components (7, 8). therefore, anterior clinoidectomy and dissection of the neurovascular components from the aneurysm dome are the key steps to safe and successful clipping surgery for these aneurysms. in this scenario, the importance of proximal control of the aneurysm becomes indispensable. among the several options for this rsd technique provides adequate relaxation of the aneurysm dome enabling complete dissection of the aneurysm from the surrounding important neurovascular structures (1, 4, and 6) retrograde suction aspiration was first described by bather and samson, who inserted an angiocatheter into the cervical ica and treated over 40 cases with giant paraclinoid aneurysms using this technique. carotid artery dissection developed in a case in their series, which required emergency endarterectomy. (7) tamaki, et al reported the use of the rsd technique under the name of ‘trapping 325 a case report of retrograde suction decompression of a large paraclinoid aneurysm evacuation.’ they deflated aneurysms by aspirating intra-aneurysmal blood through the ica via the superior thyroid artery (8). in our case, we use rsd via catheterization of superior thyroid artery with clamping common carotid artery, external carotid distal to it and internal carotid artery distal to paraclinoidal aneurysm. so, it allowed dissection, definitive clipping and reconstruction of internal carotid artery. this measure can be done using endovascular balloon but it had a risk of embolization and dissection of internal carotid artery. it has its advantages in that, it avoid neck incision and also allows performing intra-operative angiography (9, 10). other measures described for the proximal control of aneurysms are adenosine assisted cardiac arrest, rapid ventricular pacing. adenosine induced arrest allows temporary flow arrest into the parent vessel, facilitating the circumferential exposure of the aneurysm and decreasing the risk of premature rupture during the dissection, and finally safe clip placement but it had drawbacks like causing atrial fibrillation ,bronchospasm and can be perilous in medically ill patient(11,12).also, rapid ventricular placing (rvp) was to induce hypotension in the face of sudden intraoperative hemorrhage which could not be controlled with conventional means during intracranial aneurysm surgery. unlike adenosine, the consideration to use rvp is not affected by patient factors including allergies or medical conditions such as asthma and heart blocks (13). conclusion the rsd technique viacatheterization of superior thyroid artery provides adequate relaxation of the aneurysm dome enabling complete dissection of the aneurysm from the surrounding important neurovascular structures and also avoids dissection of internal carotid artery and frequent embolization, so it is an important surgical tool in the surgery for large paraclinoid aneurysms. references 1. fulkerson dh, horner tg, payne td, leipzig tj, scott ja, leonardo aj, et al. results, outcomes, and follow-up of remnants in the treatment of ophthalmic aneurysms: a 16year experience of a combined neurosurgical and endovascular team. neurosurgery. 2009; 64:218–29. 2. day jd, gannett sl, fukushima t. extradural temporopolar approach to lesions of the upper basilar artery and infrachiasmatic region. j neurosurg. 1994; 81:230–5. 3. day jd, fukushima t, gannett sl. cranial base approaches to posterior circulation aneurysms. j neurosurg. 1997; 87:544–54. 4. bather hh, samson ds. retrograde suction decompression of giant paraclinoidal aneurysms. technical note. j neurosurg. 1990; 73:305–6. 5. fan yw, chan kh, luis wm, and hung kn. retrograde suction decompression of paraclinoid aneurysm – a revised technique. surge neurol. 1999; 51:129–31. 6. miso k, takahashi a, yoshimoto t, fujiwara s, kosher k. combined endovascular and neurosurgical approach for paraclinoid internal carotid artery aneurysms. neurosurgery. 1993; 33:986–92. 7. bather hh, samson ds. retrograde suction decompression of giant paraclinoidal aneurysms. technical note. j neurosurg 1990; 73:305-6. 8. tamaki n, kim s, hear k, asada m, fujita k, tomato k, et al. giant carotid-ophthalmic artery aneurysms: direct clipping utilizing the “trapping-evacuation” technique. j neurosurg 1991;74:567-72 9. hoh dj, larsen dw, elder jb, kim pe, gannett sl, liu cy. novel use of an endovascular embolectomy device for retrograde suction decompression-assisted clip ligation of a large paraclinoid aneurysm: technical case report. neurosurgery 2008;62(5 suppl 2): onse412-3. 10. fulkerson dh, horner tg, payne td, leipzig tj, scott ja, edgardo aj, et al. endovascular retrograde suction decompression as an adjunct to surgical treatment of ophthalmic aneurysms: analysis of risks and clinical outcomes. neurosurgery 2009; 64(3 suppl):ons107-11. 11. beady jf, gupta dk, benda br, hemmer lb, zen c, aram mj, et al. adenosine-induced flow arrest to facilitate intracranial aneurysm clip ligation: dose-response data and safety profile. anesth analg 2010;110:1406-11. 12. guinn nr, mcdonagh dl, borel co, wright dr, zomorodi ar, powers cj, et al. adenosine-induced transient asystole for intracranial aneurysm surgery: a retrospective review. j neurosurg anesthesiol 2011;23:35-40. 13. davidavicius g, chieffo a, shannon j, arioli f, ielasi a, mussardo m, et al. a high dose of adenosine to induce transient asystole for valvuloplasty in patients undergoing transcatheter aortic valve implantation (tavi): is it a valid alternative to rapid pacing? a prospective pilot study. j invasive cardiol. 2011;23:467–71. doi: 10.33962/roneuro-2023-014 the efficacy of endoscopic endonasal duraplasty compared to transcranial duraplasty for post-traumatic csf rhinorrhea in terms of csf rhinorrhea recurrence and other complications. a prospective cohort study from a lowmiddle-income country pranab regmi, ahtesham khizar, pradhumna kumar yadav romanian neurosurgery (2023) xxxvii (1): pp. 85-94 doi: 10.33962/roneuro-2023-014 www.journals.lapub.co.uk/index.php/roneurosurgery the efficacy of endoscopic endonasal duraplasty compared to transcranial duraplasty for post-traumatic csf rhinorrhea in terms of csf rhinorrhea recurrence and other complications. a prospective cohort study from a low-middle-income country pranab regmi, ahtesham khizar, pradhumna kumar yadav pakistan institute of medical sciences, islamabad, pakistan abstract objectives. to determine the efficacy of endoscopic endonasal dura repair versus transcranial dura repair for post-traumatic csf rhinorrhoea in terms of csf rhinorrhea recurrence and other complications. materials and methods. a total of 92 patients (age 15-50 years, both genders) with an established diagnosis of csf rhinorrhea following traumatic brain injury were enrolled in this prospective cohort study. group a and group b were formed from the patients. group a received endoscopic endonasal duraplasty, while group b received transcranial duraplasty. recurrence of csf rhinorrhea, as well as any other complications (meningitis, anosmia, hydrocephalus, and abscess), were noted and compared between the two groups one week, two weeks, and four weeks after the procedure. results. in group a, the mean age was 28.6 ± 9.9 sd years and in group b it was 29.9 ± 8.6 sd years. in group a, there were 63% (n=29/46) patients who had age between 15-30 years and 37% (n=17/46) had age between 31-50 years. in group b, 52.2% (n=24/46) patients had age between 15-30 years and 47.8% (n=22/46) had age between 31-50 years. in group a, there were 82.6% (n=38/46) males and 17.4% (n=8/46) were females and in group b there were 87% (n=40/46) males and 13% (n=6/46) females. at one month follow-up, overall recurrence of rhinorrhea was observed in 17.4% (n=8/46) patients in group a, while it was 41.3% (n=19/46) patients in group b (p=0.012). on the other hand, overall complications were 8.7% (n=21/46) in group a patients, while they were 45.7% (n=21/46) in group b patients (p=0.001). conclusions. during a one-month follow-up, patients who received endoscopic repair experienced fewer recurrences and other complications overall than patients who underwent transcranial duraplasty, and the difference was statistically significant. we advise conducting studies with a larger sample size and longer followup periods. keywords traumatic brain injury, csf rhinorrhoea, dura mater, endoscopy, craniotomy, developing countries corresponding author: ahtesham khizar pakistan institute of medical sciences, islamabad, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 86 pranab regmi, ahtesham khizar, pradhumna kumar yadav introduction cerebrospinal fluid (csf) rhinorrhea is defined as the leakage of csf from the nose as a result of communication with the subarachnoid space.1 it entails removing all of the barriers that separate the subarachnoid space from the upper aerodigestive tract, including the nasal cavity or paranasal sinus mucosa, skull base (i.e., bone), dura mater, and subarachnoid membrane.2 accidental trauma is responsible for 70-80% of csf rhinorrhea.3 more than half of the leaks are discovered within the first two days, 70% within the first week, and nearly all within the first three months.4 the most commonly presenting sign is unilateral watery nasal discharge following skull base trauma.5 patients may also present with altered mental status, seizures, or meningitis, necessitating a high level of suspicion for an accurate diagnosis.6 the treatment can be either conservative or surgical. early surgical repair is critical to avoid the risk of ascending infection.7 early surgical repair (within 7 days) appears to reduce the risk of meningitis.8 neurosurgeons have traditionally repaired these lesions via a transcranial approach.1 according to reports, the endoscopic endonasal approach is much safer than the transcranial approach and is well tolerated.4 it has gained widespread acceptance as the preferred technique due to its superior visualisation, exact graft placement, minimal harm to the surrounding tissue, preservation of olfactory function in the event of a fistula leak through the cribriform plate, shortened operating time, and quicker recovery time.1 according to published data, the endoscopic endonasal approach results in significantly less recurrence of csf rhinorrhea. given the high morbidity rate associated with open craniotomy, such as brain retraction, olfactory nerve injury, anosmia, abscess/wound infection, sepsis, and recurrence, an endoscopic endonasal approach is preferable. furthermore, the shorter hospital stay and return of functional independence associated with endoscopic endonasal surgery have made it the method of choice for csf rhinorrhea repair. in our study, patients who had endoscopic repair had fewer overall recurrences and other complications than patients who underwent transcranial duraplasty during a one-month follow-up. materials and methods study design: a prospective cohort study setting: department of neurosurgery, pakistan institute of medical sciences, islamabad, pakistan. study duration: 3 years (30-07-2017 to 29-07-2020) sample size: it was calculated by world health organization (who) sample size calculator while keeping the parameters as: 5% level of significance and 80% power of test. the sample size turned out to be 46 patients in each group and a total of 92 patients were included in the study. sampling technique: non-probability based consecutive sampling technique. sample selection a) inclusion criteria ● csf rhinorrhea following traumatic brain injury ● age: 15-50 years b) exclusion criteria ● csf rhinorrhea with concomitant otorrhea ● redo surgeries ● acute infections ● severe deviated nasal septum (dns) ● pregnant woman data collection procedure following approval from the hospital's ethical committee, the study was launched. the study included patients admitted to the neurosurgery ward who had csf rhinorrhea as a result of traumatic brain injury as evidenced by clinical examination, computed tomography (ct) scan skull with 3d reconstruction, and magnetic resonance imaging (mri) brain t2 weighted images with coronal cuts. each study participant provided written informed consent. on pre-designed performa, initial data such as age, gender, contact number, and date of admission were recorded. group a and group b were formed from the patients. group a received endoscopic endonasal duraplasty, while group b received transcranial duraplasty. any complications with any of the procedures were documented. surgical technique for endoscopic duraplasty after baseline investigations, imaging, necessary blood products, and pre-anaesthetic evaluation, the patient was shifted to the operating room with informed written consent. preoperative nasal 87 the efficacy of endoscopic endonasal duraplasty preparation was performed to clean the nasal cavity and prevent perioperative nasal bleeding. eight hours before surgery, cotton gauze soaked in a 2% adrenaline/lignocaine/antibiotic mixture was placed inside each nostril. the surgical field was cleaned and draped after the patient was put under general anaesthesia. the procedure began with locating the source of the leak. a partial middle turbinectomy was performed to widen the surgical corridor and to use the bone as a graft in multilayer repair. to prepare the area for grafting, the mucoperiosteum around the defect was removed. depending on the size, location, and aetiology of the defect, a multilayer (sandwich grafting) reconstruction was performed using some or all of the following 5 layers. the first layer is a fat plug harvested from the anterior aspect of the thigh, the second layer is a fascia layer with fascia lata tucked beneath the bony edge, the third layer is bone harvested from the middle turbinate or nasal septum, the fourth layer is fascia lata overlay graft over defect, and the fifth layer is free mucoperiosteal fat or vascularized nasoseptal flap or middle turbinate flap. the nose was then packed with a water-filled catheter and left for 3-4 days after surgery. at one week, two weeks, and four weeks, csf rhinorrhea was noted if it occurred at all. surgical technique for transcranial duraplasty bicoronal or unilateral subfrontal approaches were used to accomplish transcranial intradural repairs. all patients underwent preoperative standard investigations to get them ready for surgery, and their general anaesthesia readiness was assessed. the patient was moved to the operating room and placed in the supine position. after making the appropriate hairline incisions, the patients who required a wide exposure underwent a bicoronal approach, while the remaining patients underwent a unilateral approach. both techniques used the same remaining steps, which included drilling burr holes and elevating the bone flap bilaterally or unilaterally depending on the situation. if necessary, frontal sinuses were cranialized. a linear dural incision was made, the brain was retracted, the csf was sucked, a cribriform plate defect was found, and a fascia lata graft was applied to cover the defect. dura was sealed up watertight. the dural hitch stitches were applied, and the bone flap was replaced and secured. skin was closed in the usual manner and an antiseptic dressing was applied. data analysis procedure statistical package for social sciences (spss) version 23.0 was used to enter and analyse the collected data. for numerical variables such as age, mean and standard deviation were calculated. for categorical variables such as gender and complications, frequency and percentages were presented in both groups. the chi-square test was used to compare the complication rate between the two groups. pvalues of 0.05 were deemed significant. results 1. demography of the selected population a total of 92 patients (age 15-50 years, both genders) with an established diagnosis of csf rhinorrhea following traumatic brain injury were enrolled in the study. group a and group b were formed from the patients. group a received endoscopic endonasal duraplasty, while group b received transcranial duraplasty. recurrence of csf rhinorrhea, as well as any other complications, was recorded and compared in both groups one week, two weeks, and four weeks after the procedure. there were 82.6% (n=38/46) males and 14.4% (n=8/46) females in group a, and 87% (n=40/46) males and 13% (n=6/46) females in group b. (figure. 1 & table. 1). the mean age in group a was 28.6 (± 9.9 sd) years, while it was 29.9 (± 8.6 sd) years in group b (table. 1). in group a, 63% (n=29/46) of the patients were between the ages of 15 and 30, while 37% (n=17/46) were between the ages of 31 and 50. in group b, 52.2% (n=24/46) of the patients were between the ages of 15 and 30, and 47.8% (n=22/46) were between the ages of 31 and 50 (figure. 2 & table. 1). figure 1. gender distribution in both the study groups 88 pranab regmi, ahtesham khizar, pradhumna kumar yadav figure 2. different age groups in both the study groups 2. outcomes of therapy: a. at one week recurrence of rhinorrhea was observed in 10.9% (n=5/46) patients in group a, while it was 19.6% (n=9/46) in group b patients. although the recurrence rate was lower in patients who underwent endoscopic repair, yet the difference was not statistically significant (p=0.246) (table. 2). overall complications were observed in 6.5% % (n=3/46) patients in group a, while they were observed in 32.6% (n=15/46) patients in group b. the complication rate was lower in patients who underwent endoscopic repair and the difference was statistically significant (p=0.006). the most frequent complication was hydrocephalus (4.3%) followed by meningitis (2.2%) in group a, while the most frequent one in group b was anosmia (8.7%) followed by meningitis (6.5%) (table. 2). b. at two weeks recurrence of rhinorrhea was observed in 13% (n=6/46) patients in group a, while it was 6.5% (n=3/46) in group b patients (p=0.292) (table. 3). overall complications were observed in 2.2% (n=1/46) patients in group a, while they were observed in 6.5% (n=3/46) patients in group b. although the complication rate was lower in patients who underwent endoscopic repair, yet the difference was not statistically significant (p=0.360). the most frequent complication was meningitis (2.2%) in group a, while in group b it was hydrocephalus (4.3%) and meningitis (2.2%) (table. 3). c. at four weeks recurrence of rhinorrhea was observed in 0% (n=0/46) patients in group a, while it was 4.5% (n=4/46) in group b (p=0.041) (table. 4). overall complications were 0% (n=0/46) in group a, while they were 6.5% (n=3/46) in group b (p=0.060) (table. 4). the most frequent complication was abscess (6.5%) in group b at four weeks. d. overall recurrence and other complications rate during one-month follow-up during one month follow-up, recurrence of rhinorrhea was observed in 17.4% (n=8/46) patients in group a, while it was observed in 41.3% (n=19/46) patients in group b. the recurrence rate was lower in patients who underwent endoscopic repair and the difference was statistically significant (p=0.012) (table. 5). during one month of follow-up, complications were observed in 8.7% (n=4/46) patients in group a, while they were observed in 45.7% (n=21/46) patients in group b. the complication rate was lower in patients who underwent endoscopic repair and the difference was statistically significant (p=0.001) (table. 5). stratification results with reference to gender and age groups for overall recurrence and other complications during one-month follow-up are given in table. 6 and table. 7, respectively. discussion csf leaks can be injurious to brain blood supply and function, as well as increase the risk of direct trauma to the brain parenchyma due to fluid cushion loss. furthermore, the presence of csf leak indicates the need for additional evaluation and management to find out the cause. the open communication of the subarachnoid space with csf leak presents a path for life-threatening central nervous system (cns) infection, including meningitis. both intracranial and endoscopic transnasal approaches have been used to treat csf rhinorrhea with high success rates of 70100%. when compared to the endoscopic transnasal approach, the morbidity associated with the intracranial approach has been reported to be significantly higher.8,9,10 we intended to compare the efficacy of endoscopic endonasal dural repair versus transcranial dural repair in this study. a total of 92 adult patients (age 15-50 years, both genders) with a confirmed diagnosis of csf rhinorrhea after traumatic brain injury were included. the recurrence of csf rhinorrhea, as well as any other complications, was recorded at one, two, and four weeks after the 89 the efficacy of endoscopic endonasal duraplasty procedure and compared between the two groups. according to published data, the endoscopic endonasal approach results in significantly less recurrence of csf rhinorrhea. given the high morbidity rate associated with open craniotomy, such as brain retraction, olfactory nerve injury, anosmia, abscess/wound infection, sepsis, and recurrence, an endonasal endoscopic approach is preferable. moreover, decreased time of hospital stay, return of functional independence associated with endoscopic endonasal surgery has established itself as the procedure of choice for csf rhinorrhea repair.8,9,10 we found similar findings in our study. during one month follow-up, the recurrence (17.4% versus 41.3%, p=0.012) and other complications rate (8.7% versus 45.7%, p=0.001) was significantly lower in patients who underwent endoscopic duraplasty compared to those who underwent transcranial duraplasty. bhatti sn et al.9 examined the outcomes of transnasal endoscopic repair for csf rhinorrhea in a previous study. twenty-one patients with csf rhinorrhea who had failed to respond to conservative treatment were included in the study and were operated on transnasally with a rigid endoscope. over a 9-month follow-up period, the overall success rate was 95% (n=20/21 cases). one patient died as a result of csf leak and meningitis one month after surgery. the authors concluded that transnasal endoscopic treatment of csf rhinorrhea was highly effective and safe. tahir mz et al.10 presented 11-year data on the management of csf rhinorrhea at a tertiary care hospital in karachi in another study from the local population. the medical records of 43 patients were scrutinised. eleven of the 43 patients were treated conservatively, 22 had intracranial repairs, and 10 had transnasal endoscopic repairs. they found that the transnasal endoscopic approach has comparable success rates to the intracranial approach while causing significantly less morbidity. furthermore, a summary of different studies performed in pakistan regarding the surgical management of csf rhinorrhea is given in table. 8. a total of 460 patients including 273 with traumatic cause for csf rhinorrhoea had been operated on. endoscopic repair was performed in 223 (49.6%) patients compared to transcranial repair performed in other 232 (50.4%) patients. recurrence was 7% in the endoscopic cases compared to 7.8% for the transcranial ones. other complications were 0.44% in the endoscopic cases compared to 20.3% for the transcranial cases. christoforidou et al.11 conducted a prospective study on 18 consecutive patients with csf leaks who underwent endonasal repair and compared outcomes to a previous cohort of 25 patients who had csf leaks treated with a craniotomy. the endoscopic group had similar success rates with a significantly lower rate of complications and a shorter length of hospital stay than the craniotomy group. endoscopic technique was also associated with significantly lower costs and higher patient satisfaction. the authors concluded that an endoscopic approach is the best way to treat csf leaks in the anterior and middle skull base that are not associated with complex intracranial pathology. however, we did not use cost or patient satisfaction as outcome variables in our study. komotar rj et al.12 assessed the role of endoscopy in the management of csf rhinorrhea due to traumatic injury in a large systematic review that included 71 studies and 1178 patients. their combined findings showed that the rate of successful repair was comparable (90%) between the open and endoscopic cohorts. however, when compared to open approaches, the endoscopic group had a significantly lower rate of complications. meningitis (3.9% versus 1.1%, p=0.034), abscess/wound infection (6.8% versus 0.7%, p=0.001), and sepsis (3.8% versus 0%, p=0.003) were observed as complications. in summary, the current study's findings and evidence from the literature suggest that an endoscopic endonasal approach is a safe and effective treatment for csf rhinorrhea caused by traumatic injury. endoscopic endonasal approach has a success rate comparable to transcranial duraplasty, but with significantly lower recurrence and complication rates. due to the difficulty of randomization and ethical concerns, there are not many studies comparing the two techniques in the literature. the current study's main strength is its prospective design. there are several limitations to the current study. firstly, we feel the sample size was relatively smaller yet sufficient to draw the inference. secondly, the follow-up period (four weeks) was relatively shorter as several studies reported recurrence of csf rhinorrhea even a year after the surgery. furthermore, we did not account for other variables such as procedure duration and hospital stay duration in both groups. the other variables that we did not investigate in this study were patient 90 pranab regmi, ahtesham khizar, pradhumna kumar yadav satisfaction and the overall cost of both procedures. we recommend larger sample size studies with longer follow-up periods. we also propose future studies that take into account other variables such as procedure duration, length of hospital stay, overall cost incurred, and patient satisfaction. several studies have been conducted using various graft materials for endoscopic repair; we believe this is an area for future research. conclusions during a one-month follow-up, patients who underwent endoscopic repair had a lower recurrence and other complications rate than those who underwent transcranial duraplasty, and the difference was statistically significant. we recommend studies with larger sample sizes and longer follow-up periods. we also propose future studies that take into account other variables such as procedure duration, length of hospital stay, overall cost incurred, and patient satisfaction. table. 1. different parameters in both the study groups parameters groups total a b gender male 38 (82.6%) 40 (87%) 78 (84.8%) female 8 (14.4%) 6 (13%) 14 (15.2%) total no. of patients 46 (100%) 46 (100%) 92 (100%) mean age ± sd (years) 28.6 ± 9.9 29.9 ± 8.6 age groups (years) 15-30 29 (63%) 24 (52.2%) 53 (57.6%) 31-50 17 (37%) 22 (47.8%) 39 (42.4%) table. 2. recurrence and complications at one week in both the study groups at one week groups total p-value chi-square a b recurrence present 5 (10.9%) 9 (19.6%) 14 (15.2%) 0.246 absent 41 (89.1%) 37 (80.4%) 78 (84.8%) total 46 (100%) 46 (100%) 92 (100%) complications meningitis 1 (2.2%) 5 (10.9%) 6 (6.5%) 0.006 anosmia 0 (0%) 8 (17.4%) 8 (8.7%) hydrocephalus 2 (4.3%) 2 (4.3%) 4 (4.4%) none 43 (93.5%) 31 (67.4%) 74 (80.4%) total 46 (100%) 46 (100%) 92 (100%) 91 the efficacy of endoscopic endonasal duraplasty table. 3. recurrence and complications at two weeks in both the study groups table. 4. recurrence and complications at four weeks in both the study groups at four weeks groups total p-value chi-square a b recurrence present 0 (0%) 4 (8.7%) 4 (4.3%) 0.041 absent 46 (100%) 42 (91.3%) 88 (95.7%) total 46 (100%) 46 (100%) 92 (100%) complications abscess 0 (0%) 3 (6.5%) 3 (3.3%) 0.06 none 46 (100%) 43 (93.5%) 89 (96.7%) total 46 (100%) 46 (100%) 92 (100%) table. 5. overall recurrence and complications during one month follow-up during one month follow-up groups total p-value chi-square a b overall recurrence present 8 (17.4%) 19 (41.3%) 27 (29.3%) 0.012 absent 38 (82.6%) 27 (58.7%) 65 (70.7%) total 46 (100%) 46 (100%) 92 (100%) overall complications present 4 (8.7%) 21 (45.7%) 25 (27.2%) 0.001 absent 42 (91.3%) 25 (54.3%) 67 (72.8%) total 46 (100%) 46 (100%) 92 (100%) at two weeks groups total p-value chi-square a b recurrence present 3 (6.5%) 6 (13%) 9 (9.8%) 0.292 absent 43 (93.5) 40 (87%) 83 (90.2%) total 46 (100%) 46 (100%) 92 (100%) complications meningitis 1 (2.2%) 1 (2.2%) 2 (2.2%) 0.360 hydrocephalus 0 (0%) 2 (4.3%) 2 (2.2%) none 45 (97.8%) 43 (93.5%) 88 (95.6%) total 46 (100%) 46 (100%) 92 (100%) 92 pranab regmi, ahtesham khizar, pradhumna kumar yadav table. 6. overall recurrence rate during one month follow-up (stratification with reference to gender and age groups) variables overall recurrence during one month follow-up groups total p-value chi-square a b male present 6 (15.8%) 15 (37.5%) 21 (26.9%) 0.031 absent 32 (84.2%) 25 (62.5%) 57 (73.1%) female present 2 (25%) 4 (66.7%) 6 (42.9%) 0.119 absent 6 (75%) 2 (33.3%) 8 (57.1%) 15-30 years present 5 (17.2%) 9 (37.5%) 14 (26.4%) 0.096 absent 24 (82.8%) 15 (62.5%) 39 (73.6%) 31-50 years present 3 (17.6%) 10 (45.5%) 13 (33.3%) 0.041 absent 14 (82.4%) 12 (54.5%) 26 (66.7%) table. 7. overall complication rate during one month follow-up (stratification with reference to gender and age groups) variables overall complications during one month follow-up groups total p-value chi-square a b male present 4 (10.5%) 21 (52.5%) 25 (32.1%) 0.001 absent 34 (89.5%) 19 (47.5%) 53 (67.9) female present 0 (0%) 0 (0%) 0 (0%) 1.0 absent 8 (100%) 6 (100%) 14 (100%) 15-30 years present 3 (10.3%) 11 (45.8%) 14 (26.4%) 0.004 absent 26 (89.7%) 13 (54.2%) 39 (73.6%) 31-50 years present 1 (5.9%) 10 (45.5%) 11 (28.2%) 0.006 absent 16 (94.1%) 12 (54.5%) 28 (71.8%) table. 8. summary of different studies performed in pakistan regarding surgical management of csf rhinorrhea s. no. authors year total no. of patient s traum a endoscopic duraplasty a transcranial duraplasty b recurrence complications a b a b 1 amin mu and ghaffar a13 2006 1 1 1 0 0 93 the efficacy of endoscopic endonasal duraplasty 2 bhatti sn et al.9 2011 21 16 21 2 0 3 tahir mz et al.10 2011 32 11 10 22 3 3 na na 4 farooq mu and ansar ma14 2011 23 17 23 1 0 5 akhter s et al.15 2012 5 1 5 0 0 6 aurangzeb a et al.16 2012 27 23 27 1 5 7 khaleeq s et al.17 2015 48 48 48 5 10 8 sheikh f et al.18 2015 20 4 20 2 0 9 amir s et al.19 2017 30 30 30 3 10 10 rahman zu and khan mm20 2018 60 60 60 6 20 11 abbas t et al.21 2019 40 27 40 4 0 12 satti sa et al.22 2021 14 14 14 na na na na 13 saleem s et al.23 2021 27 11 27 2 0 14 mahmood k et al.24 2021 62 na 62 na na 15 simair ia et al.25 2021 40 na 20 20 2 0 1 1 16 samija s et al.26 2022 10 10 10 na 1 total 460 273 228 (49.6%) 232 (50.4%) 16 (7.0%) 18 (7.8%) 1 (0.44%) 47 (20.3%) *na: not available list of abbreviations csf: cerebrospinal fluid dns: deviated nasal septum ct: computed tomography mri: magnetic resonance imaging who: world health organization spss: statistical package for social sciences 94 pranab regmi, ahtesham khizar, pradhumna kumar yadav acknowledgements we are thankful to professor dr. sajid nazir bhatti for his guidance and supervision during this study. references 1. kljajić v, vuleković p, vlaški l, savović s, dragičević d, papić v. endoscopic repair of cerebrospinal fluid rhinorrhea☆. brazilian journal of otorhinolaryngology. 2017 jul;83:388-93. 2. hegazy hm, carrau rl, snyderman ch, kassam a, zweig j. transnasal endoscopic repair of cerebrospinal fluid rhinorrhea: a meta‐analysis. the laryngoscope. 2000;110(7):1166-72. 3. kerr jt, chu fw, bayles sw. cerebrospinal fluid rhinorrhea: diagnosis and management. otolaryngologic clinics of north america. 2005 aug 1;38(4):597-611. 4. ibrahim aa, okasha m, elwany s. endoscopic endonasal multilayer repair of traumatic csf rhinorrhea. european archives of oto-rhino-laryngology. 2016 apr;273(4):9216. 5. prosser jd, vender jr, solares ca. traumatic cerebrospinal fluid leaks. otolaryngologic clinics of north america. 2011 aug 1;44(4):857-73. 6. mathias t, levy j, fatakia a, mccoul ed. contemporary approach to the diagnosis and management of cerebrospinal fluid rhinorrhea. ochsner journal. 2016 jun 20;16(2):136-42. 7. ibrahim aa, magdy ea, eid m. endoscopic endonasal multilayer repair of traumatic ethmoidal roof cerebrospinal fluid rhinorrhea in children. international journal of pediatric otorhinolaryngology. 2012 apr 1;76(4):523-9. 8. komotar rj, starke rm, raper dm, anand vk, schwartz th. endoscopic endonasal versus open repair of anterior skull base csf leak, meningocele, and encephalocele: a systematic review of outcomes. journal of neurological surgery part a: central european neurosurgery. 2013 jul;74(04):239-50. 9. bhatti sn, khan sa, shah r, aurangzeb a, ahmed e, rizvi f, zadran kk, alvi n. transnasal endosocpic repair of cerebrospinal fluid rhinorrhoea. journal of ayub medical college abbottabad. 2011 jun 1;23(2):15-7. 10. tahir mz, khan mb, bashir mu, akhtar s, bari e. cerebrospinal fluid rhinorrhea: an institutional perspective from pakistan. surgical neurology international. 2011;2. 11. christoforidou a, tsitsopoulos pp, selviaridis p, vital v, constantinidis j. endonasal endoscopic repair of cerebrospinal fluid leaks versus craniotomy: comparison of the outcomes. hippokratia. 2016 oct;20(4):299. 12. fabbri a, servadei f, marchesini g, stein sc, vandelli a. early predictors of unfavourable outcome in subjects with moderate head injury in the emergency department. journal of neurology, neurosurgery & psychiatry. 2008 may 1;79(5):567-73. 13. amin mu, ghaffar a. delayed appearance of posttraumatic cerebrospinal fluid fistula. journal of the college of physicians and surgeons--pakistan: jcpsp. 2006 may 1;16(5):378-80. 14. farooq mu, ansari ma. cerebrospinal fluid rhinorrhea: etiology, site of leakage and endoscopic management. j coll physicians surg pak. 2011 aug 1;21(8):460-3. 15. akhter s, zia s, zafar r. endoscopic repair of cerebrospinal fluid rhinorrhoea in a developing country. jpma. the journal of the pakistan medical association. 2012 sep 1;62(9):972-4. 16. aurangzeb a, ahmed e, khan sa, ali a, ihsan a, mehmood s. outcome of transcranial repair of traumatic csf rhinorrhea. journal of ayub medical college abbottabad. 2012 jun 1;24(2):47-9. 17. khaleeq s, khalid m, zaman k. surgical outcome of transcranial intradural repair in post traumatic cerebrospinal fluid leak. ann. pak. inst. med. sci. 2015;11(2):67-71. 18. sheikh f, ahmed z, aziz a, ishaque k. endonasal endoscopic repair of cerebrospinal fluid leaks. pakistan journal of neurological surgery. 2015 dec 25;19(4):2169. 19. amir s, qadir m, usman m. transcranial dural repair;: efficacy in the management of early traumatic cerebrospinal fluid rhinorrhea. the professional medical journal. 2017 aug 8;24(08):1232-6. 20. rahman zu, khan mm. effectiveness of transcranial dural repair for early post-traumatic cerebrospinal fluid leaks. jpmi: journal of postgraduate medical institute. 2018 apr 1;32(2). 21. abbas t, akmal m, choudhry n, ul hassan a, afzal o, siddiqui i, mahmood k. outcome of endoscopic repair of csf rhinorrhea with endonasal endoscopic approach in terms of success of repair. pakistan journal of neurological surgery. 2019 dec 28;23(4):257-63. 22. satti sa, ramooz k, malik mu, akhtar n, shahzad y. post traumatic csf fistulas–a solved problem?. the professional medical journal. 2021 may 10;28(05):630-4. 23. saleem m, ur rehman n, khan r, alamgir a, bibi s, ahmad h. transnasal endoscopic surgical repair of cerebrospinal fluid (csf) rhinorrhea by inferior turbinate grafts. journal of rawalpindi medical college. 2021 sep 30;25(3):409-13. 24. mahmood k, shabbir z, ishfaq m, irfan m. efficacy and role of intrathecal fluorescein for detection of defect site for treatment of cerebrospinal fluid rhinorrhea. pakistan journal of neurological surgery. 2021;25(4):51927. 25. simair ia, ali j, khattak a, qureshi a, salah-ud-din t. outcome comparison of endoscopic (endonasal transsphenoidal) repairs of css leak vs. transcranial approach. pakistan journal of neurological surgery. 2021 apr 15;25(1):18-28. 26. smaija s, fatima n, shahid l, shahid a. the management options for post traumatic csf rhinorrhea: a case series study. pakistan journal of neurological surgery. 2022 apr 1;26(1):76-82. doi: 10.33962/roneuro-2022-081 epidemio-clinical and therapeutic profile of non-traumatic medullary-radicular compressions at the university hospital of kinshasa israël maoneo, antoine beltchika, teddy ketani, glennie ntsambi romanian neurosurgery (2022) xxxvi (4): pp. 446-455 doi: 10.33962/roneuro-2022-081 www.journals.lapub.co.uk/index.php/roneurosurgery epidemio-clinical and therapeutic profile of non-traumatic medullary-radicular compressions at the university hospital of kinshasa israël maoneo1,2, antoine beltchika1, teddy ketani1, glennie ntsambi1 1 neurosurgery department of the hospital university of kinshasa, university of kinshasa, drc 2 department of surgery, hospital university of kisangani, university of kisangani, drc abstract context and objectives. as the world's population ages, non-traumatic medullaryradicular compressions are becoming more common. this work aims to describe their epidemio-clinical and therapeutic aspects at the university hospital of kinshasa. methods. it is a descriptive cross-sectional study from 2016 to 2022 concerning 61 cases. variables of interest included: sex, age, cause, level of lesion, asia score, treatment, complications, and destination. data were analyzed using spss 26 and stata 16 software. results. one hundred and twenty patients were operated on for medullary-radicular compression, including 61 non-traumatic (50.8%) and 59 traumatic (49.2%). among the non-traumatic, 31 patients were male (50.8%) and 30 females (49.2%). the average age was 51.51 ± 14.21 years. patients between the ages of 40 and 69 accounted for 68.8%. the annual curve was increasing. on admission, the clinical presentation was dominated by an incomplete neurological deficit (67.2%). the mean time to diagnosis was 188.57 days. degenerative pathologies (63.9%) including 31 herniated discs (79.4%) and 8 cases of canal narrowing (20.6%) predominated, followed by tumors 14 (22.9%) half of which included metastases. the most performed surgical procedures included decompression laminectomy (26.2%), laminectomy-discectomy (24.5%) and laminectomy-arthrodesis (32.7%). the postoperative course was unremarkable in 67.2%, except for 15 cases of surgical site infection (24.6%) and 3 deaths (4.9%). asia score on dischached improved in 62.7% (p<0.001). only 2 patients (9.8%) continued their treatment in a rehabilitation centre. conclusion. non-traumatic medullary-radicular compressions are frequent in the service, more caused by herniated discs and tumours. both sexes are equally affected and the age group is ranging from 40 to 69 years. the neurological deficit is often incomplete cord injury. laminectomy, discectomy and arthrodesis are commonly performed. the postoperative outcome is generally better. introduction medullary-radicular compression is a constriction of the spinal cord an d n erv e ro o ts du e to trau m atic o r n o n -t rau m atic c au s es keywords myelopathies, non-traumatic spinal cord compression, spine surgery, traumatic spinal cord injuries, vertebro-spinal lesions corresponding author: israël maoneo neurosurgery department. hospital university of kinshasa, university of kinshasa, drc maoneo@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 447 epidemio-clinical and therapeutic profile of non-traumatic medullary-radicular compressions (degenerative, tumoral, infectious, vascular) involving bony structures and/or disco-ligamentous complex of the spine. the spinal cord and nerve roots may be compressed by expansion of blood, tumoral processes, infectious collections, protrusion of bone or nucleus pulposus into the epidural space or meninges [1]. this lesion is a diagnostic and therapeutic emergency. if not treated early, it can lead to disabling neurological deficits in the short to medium term [2]. medullary-radicular compression is much more common than other mechanisms: compromised blood flow, inflammatory processes, metabolic disorders or exposure to toxins [3]. the worldwide incidence rate of nontraumatic medullary radicular injuries (ntmri) increases with age and ranges from 4 to 80 cases per million people per year [4]. the global prevalence rate ranges from 367.2 to 2,310 per million populations per year [5]. only the study conducted in malawi was able to give an idea of the incidence of ntmri in africa through a survey of all admissions across the country. according to this study, the incidence is 77 new cases per 1,000,000 inhabitants [6]. the prevalence of ntmri should increase steadily with the aging of the population and exceed that of traumatic injuries [4]. ntmris pose various problems such as the low rate of publications compared to those of traumatic origin, devastating physical and functional damage for the patient and his family [7]. we can also mention the difficulty in establishing the diagnosis early for better care. indeed, this diagnosis requires specific laboratory and medical imaging examinations, in this case ct-scan and mri, which are often unavailable and inaccessible in several african regions [7]. the delay in diagnosis and the presence of comorbidities in elderly patients increase the mortality rate of ntmri, which varies between 27,7% and 41 % [7,8]. another challenge lies in the fact that the causes aforementioned of the ntmri vary considerably between countries and regions. in developed countries, degenerative (16.4 to 50.9%), tumoral (15.5 to 30.5%) and vascular (12.5 to 40%) pathologies come first [9, 10, 11]. whereas, in developing countries, infections such as tuberculosis (51 to 56%) and hiv/aids infection (18 to 50%) predominate [12,13,14]. nevertheless, some african countries present the predominance of degenerative and tumoral causes. gaddour et al [15], in tunisia, kassegne et al [16], in togo, ekouele mbaki et al [17], in congo-brazzaville, observed a high frequency of degenerative and tumoral causes. the drc has cosmopolitan and crowded cities such as the city of kinshasa where tuberculosis and hiv/aids continue to be spreading [18]. several congolese hospitals are not equipped with ct scan and mri machines. however, there is no publication on ntmri in general, and nontraumatic medullaryradicular compression (ntmrc), in particular. do infectious ntmrc’s predominate as widely described in the medical literature? what is the average consultation time? what is the result of their treatment? these questions prompted us to conduct this study with the aim of drawing up the epidemiological, clinical and therapeutic picture of non-traumatic medullary-radicular compression. the specific objectives pursued are: determine the hospital prevalence and the distribution of ntmrc across gender and age groups. present the clinical picture and paraclinical explorations. give the different causes of ntmrc. describe the treatment, the operative outcome, the complications and the destination upon discharge from the hospital. materials and methods study design this is a cross-sectional and descriptive study, conducted at the university hospital of kinshasa, from 01 january 2016 to 31 august 2022. the data were collected retrospectively and prospectively. during this 6-year period, 84 patients with nontraumatic radiculo-medullary compression lesions were hospitalised. only the records of 61 patients were retained, as they met the selection criteria. inclusion and exclusion criteria all patients aged 10 years and older, admitted and operated in the spinal cord injury unit for nontraumatic medullar-radicular compression, with radicular medullary compression syndrome, from 1 january 2016 to 31 august 2022, were included. patients with incomplete records were excluded. data collection technique. we collected data in two ways, retrospectively and prospectively, from hospitalization and operating room records. to 448 israël maoneo, antoine beltchika, teddy ketani, glennie ntsambi complete certain information, we contacted the patients and/or their direct family members. variables of interest were sex, age, cause, level of injury, neurological deficit according to the american spinal injury association (asia) score [19,20], treatment, complications and destination after discharge. statistical analysis data were recorded and analysed using spss version 26 and stata version 16 software. descriptive analysis was performed for the main variables included in the study. we determined the possible associations between the different variables considered using pearson's chi-square or fisher's exact tests. since the distribution was normal, we used student's t-test to judge the effectiveness of the surgical treatment by comparing the mean asia scores at admission and discharge. the odds ratio and binary logistic regression model were used to estimate the risk of surgical site infection. a result was considered statistically significant when the pvalue was less than 0.05. results 1. prevalence of non-traumatic medullaryradicular compression one hundred and twenty patients were operated on for medullary-radicular compression, 61 of whom were non-traumatic (50.8%) and 59 traumatic (49.2%). 2. socio-demographic features the average age was 51.51±14.21 years. we counted 50.8% male patients and 49.2% female, sex ratio was 1. patients aged between 40 and 69 years accounted for 42 cases (68.8%). there were 67.2% of married patients, 34.4% of housewives and 29.5% of patients whose occupations were not reported (table 1). table 1. socio-demographic features parameters frequency n=61 percentage age (years) ▪ 10 19 1 1,6 ▪ 20 29 4 6,6 ▪ 30 39 8 13,1 ▪ 40 49 13 21,3 ▪ 50 59 15 24,6 ▪ 60 69 14 23,0 ▪ 70+ 6 9,8 sex ▪ female 30 49,2 ▪ male 31 50,8 marital status ▪ married 41 67,2 ▪ single 12 19,6 ▪ widow 4 6,6 ▪ not reported 4 6,6 profession ▪ households 21 34,4 ▪ not reported 18 29,5 ▪ public officials 6 9,8 ▪ health care workers 6 9,8 ▪ students and pupils 3 4,9 ▪ teachers 3 4,9 ▪ drivers and mechanics 2 3,3 ▪ soldiers 2 3,3 3. annual incidence of non-traumatic medullaryradicular compression we observed an increase in the number of cases in the years 2021 (16 cases) and 2022 (12 cases) (fig. 1) while the annual average of cases during the 7-year period was 8.7 cases. figure 1. annual frequency of ntmrc 4. etiological and clinical data the patients complained of low back pain in 47.5%, sometimes accompanied by bladder and bowel disorders (4.9%) and motor deficits, usually paraparesis (26.2%) or paraplegia (27.9%). most patients had an incomplete spinal cord injury (67.2%: asia score b-d). asia e and d patients accounted for 32.8% and 29.5% of cases respectively compared to (16.4%) asia c and (21.3%) asia b on admission. among the compressive causes, there were 39 (63.9%) cases of degenerative origin including 29 (74.3%) disc herniation and 10 (25.7%) narrow channel, 7 (11.5%) benign tumors, 7 (11.5%) 449 epidemio-clinical and therapeutic profile of non-traumatic medullary-radicular compressions malignant tumors and 8 (13.1%) pott’s disease. on histopathological analysis, all benign tumors were meningiomas. in relation to the dura mater, they were intradural and extramedullary. all malignant tumors were metastases. the underlying primary malignant tumors were: 2 cases of breast cancer, 2 cases of hemangioma and 3 cases of prostate cancer. patients aged 50 years and over suffered more from degenerative compression (p=0.013) and those under 50 years from infectious medullaryradicular compression, mainly tuberculosis (p=0.047). tumoral (benign tumor) radicular spinal cord compression was much more common in women (p=0.040) (table 2). table 2. etiological and clinical data parameters total n=61 sex p-value* age (years) p-value male female <50 ≥50 etiology compressive ▪ degenerative 39 20 19 0,923 12 27 0,013 disc herniation 31 16 15 11 20 canal stenosis 8 4 4 1 7 ▪ tumoral 14 4 10 0,058 8 6 0,211 benign 7 1 6 0,040 4 3 intradural et extramedullary 7 1 6 4 3 malignant 7 3 4 0.654 4 3 ▪ infectious 8 7 1 0,026 6 2 0,047 tbc 8 7 1 complaints 0,070 ▪ neck pain 2 2 0 1 1 ▪ neck +low back pains 4 4 0 3 1 ▪ back pain 11 4 7 6 5 ▪ low back pain 29 14 15 9 20 ▪ low back pain + sensory-motor deficit 12 7 5 5 7 ▪ low back + bladder disorders. 3 0 3 2 1 neurological deficit 0,463 0,980 ▪ monoparesia 3 2 1 1 2 ▪ tétraparesia 3 3 0 1 2 ▪ paraplegia 17 8 9 8 9 ▪ paraparesia 16 8 10 8 10 ▪ no deficit 20 8 12 8 12 asia 0,466 0,663 ▪ b 13 7 6 7 6 ▪ c 10 7 3 5 5 ▪ d 18 7 11 6 12 ▪ e 20 10 10 8 12 table 3. association between causes of non-traumatic medullary-radicular compression and asia score on admission causes total n=61 asia in admission p-value b c d e ▪ herniation disc 31 0 5 10 16 <0,001 ▪ canal stenosis 8 2 0 2 4 450 israël maoneo, antoine beltchika, teddy ketani, glennie ntsambi ▪ benign tumor 7 3 2 2 0 ▪ malignant tumor 7 3 1 3 0 ▪ pott’s desease 8 5 2 1 0 total 61 13 10 18 20 table 4. surgical site infection according to age, causes, duration of surgery, and surgical procedures surgical procedures iso-/iso+ univariate analysis or ic p-value ▪ laminectomy 1,03 (0,27-3,85) 0,965 ▪ laminectomy + discectomy 1,15 (0,30-4,37) 0,830 ▪ laminectomy + arthrodesis 2,22 (0,66-7,37) 0,187 ▪ corporectomy + arthrodesis 1,34 (1,15-1,55) 0,412 ▪ laminectomy + excision 1,38 (1,17-1,63) 0,108 ▪ laminectomy+ excision + arthrodesis 1,33 (1,15-1,54) 0,565 5. association causes of non-traumatic medullaryradicular compression and asia score on admission all 20 asia e patients had degenerative pathologies, of which 16 (80%) were cases of disc herniation and 4 (20%) cases of canal narrowing. thirteen asia b cases were of tumoral (46.1%), infectious (38.5%) and degenerative (15.4%) origin. ten asia c patients had degenerative (50%), tumoral (30%) and infectious (20%) pathologies. of the 18 asia d cases, 66.7% were degenerative, 27.8% tumoral and 5.5% infectious. tumoral and infectious causes were more associated with asia b-c (72.7%) and degenerative causes with asia d-e (82.05%). the relationship between the different causes and asia scores on admission was statistically significant (p= <0.001) (table 3). 6. paraclinical diagnosis the average time to diagnosis of ntmrc was 188.57 days. the diagnoses of tumoral and degenerative pathologies were established by mri in 63.9% of cases, followed by ct scan in 24.6%. all tumor cases were confirmed and differentiated by histopathological analysis. the laboratory examinations helped to determine the specific causes of all infectious pathologies represented in our work by tuberculous spondylodiscitis. 7. location of the injury six (9.8%) lesions were located on the cervical spine. we counted 10 lesions (16.3%) located on the thoracic segment, of which 8 (80%) were of tumoral origin. the lumbar spine was the site of 42 cases (68.9%). thirty-three cases (83.1%) of the lumbar pathologies were degenerative and consisted of disc herniations and canal narrowing. the relationships between the different causes and their respective locations on the spine (p <0.001) and on the different vertebrae (p <0.001) were statistically significant. 8. medical treatment all patients received medical treatment including analgesics, anti-inflammatory drugs, gastric antisecretory drugs, postoperative corticosteroids, neurotropes and anticoagulants, and postoperative antibiotics. anti-tuberculosis drugs were administered to patients with tuberculous spondylodiscitis. 9. surgical treatment the cervical segment was approached by both anterior (2 cases) and posterior (4 cases) routes. all cases in the thoracic, thoracolumbar and lumbar segments were approached via the posterior route. the surgical procedures performed were simple decompression laminectomy 16 cases (26.2%), laminectomy + arthrodesis 20 cases (32.8%) and laminectomy + discectomy 15 cases (24.8%). there were 2 cases (3.3%) of corporectomy and arthrodesis at cervical level. laminectomy and excision were performed for tumoral conditions 10. association of surgical procedures and postoperative complications after the surgical treatment, we recorded 41 (67.2%) 451 epidemio-clinical and therapeutic profile of non-traumatic medullary-radicular compressions patients with unremarkable postoperative courses and 20 cases of complications (32.8%) including 15 cases (24.6%) of surgical site infections (ssi), 2 cases (3.3%) of fistulas and 3 (4.9%) deaths. the 3 deaths were due to complications of comorbidities. the infection of the site of operation was not significantly related to the different surgical treatments. patients who received osteosynthesis implants were twice as likely to develop a surgical site infection as those who did not. but the difference was not statistically significant (table 4). 11. assessment of asia score before and after surgical treatment. among 13 asia b patients at admission, 8 (61.5%) kept the same score and 5 (38.5%) improved their asia score at discharge, of which 2 (40%) by one grade, 2 (40%) by two grades and 1 (20%) by three grades. eight (63.6%) asia c patients at admission improved their discharge score of which 4 (57.1%) by one grade and 4 (57.1%) by two grades. one asia c patient (9.1%) moved back one grade and 3 asia c patients (27.3%) maintained their admission score. out of 16 asia d patients at admission, 5 (31.2%) kept the same score, 8 (50%) improved the exit asia score by one grade and 3 (18.8%) cases moved back in admission score of which 1 (33.3%) by one grade and 2 (66.7%) by two grades. eighteen (85%) asia e patients before surgery kept their score and 3 (15%) moved back, of which 2 (66.7%) by one grade and 1 (33.3%) by three grades. overall, 40 (67.2%) patients improved their initial asia score at discharge and 21 (32.8%) patients either kept their initial asia or worsened. the difference in mean asia scores before and after surgery was statistically significant (p=<0.001) (table 5). table 5. asia score assessment before and after surgery asia admission total asia discharge p-value b c d e b 13 8 2 2 1 <0,001* c 12 1 3 4 2 d 18 2 1 3 12 e 20 1 0 1 18 total 61 12 6 13 30 * we used the t-test for paired samples 12. physiotherapy all patients benefited from rehabilitation sessions by the physical medicine team. this rehabilitation should continue at home or in a rehabilitation centre. physiotherapy improved the results of the surgical treatment and accelerated the functional recovery. 13. discharge destination patients discharged to home accounted for 90.2% of cases. two (3.3%) patients continued care in a rehabilitation centre. three cases of death (4.9%) were recorded and only one patient was transferred to another specialist hospital outside the country. discussion ntmrcs are known as pathologies of the elderly. they are increasing exponentially with the ageing of the world's population and may overtake traumatic spinal cord injuries [4,7]. according to the united nations, the global population of people aged 65 years or older will triple by 2050 [21]. the average age varies from 48.5 to 67 years, depending on the different study series [4,14]. our results support these data from the literature. the hospital prevalence of ntmrc (61 cases or 50.8%) was higher than that of traumatic origin (59 cases or 49.2%). the average age was 51±14.21 years. the curve of our series is increasing with a peak of 16 cases in 2021. non-traumatic medullary-radicular injuries affect both sexes almost equally [22]. for some authors, men are more affected than women [23,24,25] and, for others, it is rather women who suffer more than men [15,26]. in this study, we observed a slight male predominance (51.8%), a sex ratio of 1. twenty-five (67.2%) patients were married. mckinley et al recorded 57% married [27]. in people aged over 50, the incidence of degenerative and tumoral pathologies increases exponentially [28]. with regard to disc herniations, ageing favours dehydration of the intervertebral discs, disorganisation of the collagen architecture (iv, ii, ix) and of the glycosaminoglycans of the nucleus pulposus and the annulus fibrosus. the annulus fibrosus becomes dry, fragile and causes the exit of the nucleus pulposus which compresses the intracanal nerve structures [29]. the increase in degenerative lesions of the spine in elderly women is linked not only to ageing but also to the fall in oestrogenic hormones at the menopause. the intervertebral disc is hormone-sensitive. estrogens ensure the maintenance of the intervertebral disc 452 israël maoneo, antoine beltchika, teddy ketani, glennie ntsambi phenotype. menopause is thought to accelerate the degeneration of intervertebral discs with the loss of their anatomical structure [30,31]. in addition, certain intrarachid tumours, such as meningiomas, are thought to be hormone-dependent in relation to the female sex hormones (oestrogen and progesterone) [32]. tumors, especially metastases [17], and degenerative pathologies (herniated disc, narrow spinal canal) [9,10,15,33] are among the most frequent causes of ntmrc according to several studies. our results show a predominance of degenerative diseases (herniated discs and narrow spinal canal, 63.9%) and tumoral diseases (meningiomas and metastases, 22.9%). this differs from previous series published by other researchers that give precedence to infectious pathologies, in particular tuberculosis and hiv/aids infection, in sub-saharan africa [12,13,14, 34]. changing lifestyles, cultural mixing and increasing efforts to control the above-mentioned infectious diseases may justify this paradigm shift regarding the causes of ntrmrc in sub-saharan africa. ones et al [35] pointed out that differences in the causes of ntmrc are dependent on social, cultural and genetic differences. neurologically, most patients (63.9%) had an incomplete neurological deficit (asia: b-d). mullerjansen et al [36] and mckinley et al [37] found similar results with all asia c-d patients. on further analysis, tumoral and infectious causes (pott's disease) of ntmri had a low asia score (b and c, 72.7%) and degenerative pathologies a high asia score (d-e, 82.05%). new et al [21] reported a similar admission outcome for degenerative diseases, a high asia score (d-e: 65%) and for infections a low asia score (a-c: 62.1%). the neurological manifestation of ntmrc is generally an incomplete neurological deficit [22,23, 37]. this would depend on the non-traumatic pathology itself and the stage of the spinal cord compression. spinal cord compression of infectious origin and, to a certain extent, that of a tumour are often early and of acute deficits, with an asia score that is lower than that of a degenerative origin [38]. in the acute phase, pott's disease can damage vertebral bodies, discs, and paraspinal soft tissues, resulting in the formation of caseous necrotic tissue, pus, and dead bone, which can enter the spinal canal and rapidly cause mechanical compression of the spinal cord resulting in early low asia score paraplegia [39, 40, 41]. spinal cord compression in tumoral pathologies is usually caused by the collapse of a metastasised vertebral body but can also result from direct extension of the tumour into the spinal canal, mechanically compressing the cord and rapidly deteriorating its function [42]. degenerative pathologies are much more insidious than the two previous ones, the asia score remains high for a long time [37]. simple laminectomy, laminectomy-discectomy and laminectomy-arthrodesis by posterior approach were the most performed surgical procedures in our department with 26.2%, 24.5% and 32.8% of cases respectively. similar results were observed by gaddour et al [15], 39.5% of laminectomy and arthrodesis (16.6%), dios et al, [43] 57.4% of laminectomy and 42.6% of laminectomy + arthrodesis. the predominance of degenerative pathologies in this study would justify these results. a simple decompression laminectomy, well performed, a laminectomy-discectomy or a laminectomy-arthrodesis, following the importance of laminectomy levels, constitute sufficient surgical acts in case of radiculo-medullary compression. furthermore, some studies have not found a significant difference between simple laminectomy and laminectomy-arthrodesis [43]. in general, the rate of surgical site infection for spinal surgery varies from 0.5 to 18.8% [44]. in our series, this rate is high (24.6%). surgical site infection is not an uncommon complication after spinal surgery, but it remains a serious problem [45]. the important thing is to identify the risk factor and try to eliminate it. in our study, no factor was found to be significantly at risk, although the infection rate was high. hence the need for a targeted study to identify risk factors for post-spinal surgery ssi. in relation to the three deaths due to comorbidities, it should be noted that comorbidities are described in the medical literature as significant risk factors for mortality after spinal surgery [4,46,47]. forty-one (67.2%) patients were discharged with an improved asia score compared to 22.8% of cases with a stationary asia score. when comparing the mean asia scores before and after surgery, the relationship was statistically significant (p=<0.001). other authors have also described the effectiveness of well-conducted surgery in improving the asia 453 epidemio-clinical and therapeutic profile of non-traumatic medullary-radicular compressions score. with compressive pathologies, the surgical procedure removes compression and frees the nerve structures, thus favouring the progressive restoration of spinal cord function [38,48]. at the end of the hospital stay, 90.2% of patients went home. halvorsen et al [49] recorded 73% and new et al 80.5% [22] of patients who returned home after hospital discharge. once discharged from hospital, many patients prefer to continue outpatient rehabilitation in the family environment. the family atmosphere is said to provide comfort and speed up their recovery. in addition, patients mention the additional care costs of revalidation centres as well as the continuity of hospital isolation. nevertheless, according to the work of choi et al [50], the continuation of post-hospital physiotherapy exercises in a rehabilitation centre offers more benefits (e.g. early return to work) than those performed at home. strengths and limitations this study is the first one to provide a general overview of the management of ntmrc in the city of kinshasa in particular and in the democratic republic of the congo in general. despite some discrepancies, this work reveals many points of similarity with studies carried out in other countries. the limitations of this study concern the data collection technique, which was largely retrospective. some records were missing such as bmi, types of surgical site infections, occupations of some patients, some laboratory tests. the small sample size does not allow us to generalise our conclusions. some epidemiological aspects are missing because the study was not conducted in the general population, it was based only on data from the neurosurgery department. conclusion ntmrcs managed in hospitals are increasing. they are caused more by herniated discs and tumors and affect both sexes indiscriminately. on admission, the majority of patients present an incomplete neurological deficit. patients with tumours and pott's disease have a low asia score (b-c) while those with degenerative pathology have an asia score of d-e. decompression laminectomy, discectomy and laminectomy-arthrodesis are the most commonly performed surgical procedures. many patients have a simple postoperative outcome. surgical site infection remains the major complication and opens new research perspectives to identify a reliable predictive factor. much work remains to be done to bring patients to revalidation centres. references 1. singleton jm, hefner m. spinal cord compression. statpearls publishing llc. island ; 2022. 2. lim rj, mekary ra, rattani a, dewan mc, sharif sy, et al. traumatic spinal injury : global epidemiology and worldwide volume. world neurosurg. 2018 ;113 : e345 63. 3. bennett j, das j, emmady pd. spinal cord injuries. statpearls publishing llc. island ; 2022. 4. new pw, farry a, baxter d, noonan vk. prevalence of non-traumatic spinal cord injury in victoria, australia spinal cord. 2013 ;51(2) :99 102. 5. brown kge. non-traumatic paraplegia in sub-saharan africa. east afr med j. 1979 ; 56: 300–310. 6. noonan vk, fingas m, farry a, baxter d, singh a, fehlings mg, et al. incidence and prevalence of spinal cord injury in canada : a national perspective. neuroepidemiology. 2012 ;38(4):219 26. 7. musubire ak, meya db, bohjanen pr, katabira et, barasukana p, boulware dr, et al. a systematic review of non-traumatic spinal cord injuries in sub-saharan africa and a proposed diagnostic algorithm for resourcelimited settings. front neurol. 2017 ;8:618. 8. ge l, aroul k, ikpeze t, baldwin a, nickels jl, mesfin a. traumayic and nontraumayic spinal cord injuries. world neurosurgery. 2018 ;111 : 142-148. 9. niemi-nikkola v, koskinen e, väärälä e, kauppila a-m, kallinen m, vainionpää a. incidence of acquired nontraumatic spinal cord injury in finland : a 4-year prospective multicenter study. archives of physical medicine and rehabilitation. 2021 ;102(1) :44‑9. 10. smith e, fitzpatrick p, murtagh j, lyons f, morris s, synnott k. epidemiology of non-traumatic spinal cord injury in ireland. a prospective population-based study. the journal of spinal cord medecine. 2020 ;51(1‑2) :19‑24. 11. new pw, cripps ra, bonne lee b. global maps of nontraumatic spinal cord injury epidemiology : towards a living data repository. spinal cord. 2014 ;52(2):97‑109. 12. modi g, ranchhod j, hari k, mochan a, modi m. nontraumatic myelopathy at the chris hani baragwanath hospital, south africa—the influence of hiv. qjm: an international journal of medicine. 2011 ;104(8) :697‑703. 13. owolabi lf, ibrahim a, samaila aa. profile and outcome of non-traumatic paraplegia in kano, northwestern nigeria. annals of african medicine. 2011 ;10(2) : 86-90. 14. scrimgeour em. non-traumatic paraplegia in northern tanzania. br med j (clin res ed). 1981 ;283(6297) :975‑8. 15. gaddour m, ouannes w, samia f, salah s, khachnaoui f, jemni s. traumatic versus non traumatic spinal cord 454 israël maoneo, antoine beltchika, teddy ketani, glennie ntsambi injury : characteristics and functional outcome in a tunisian rehabilitation center. journal of yoga, physical therapy and rehabilitation. 2018 ; yptr-160. 16. kassegne i, sakiye k, kanassoua k, beketi ak, badiane sb, balogou k a. a. management of spinal cord compression in togo. med sante trop. 2013 ;23(2) :206‑10. 17. ekouele mbaki hb, boukassa l, sounga bandzouzi peg, diatewa j, mpandzou ga, ossou-nguiet pm. tiolgies et traitement des compressions radiculo-médullaires non traumatiques en milieu neurochirurgical à brazzaville. health sci. dis. 2020 ; 21(1) : 76-79. 18. shah gh, ewetola r , etheredge g , maluantesa l , waterfield k , engetele e et al. facteurs de risque de la coinfection tb/vih et conséquences sur les résultats pour les patients : données probantes de 241 cliniques en république démocratique du congo. int j environ res public health. 2021; 18(10) : 5165 19. roberts tt, leonard gr, cepela dj. classifications in brief : american spinal injury association (asia) impairment scale. clin orthop relat res. 2017 ; 475 :1499–1504. 20. van middendorp jj, goss b, urquhart s, atresh s, williams rp, schuetz m. diagnosis and prognosis of traumatic spinal cord injury. global spine j. 2011 ;1(1) :1 8. 21. doeasa un world population ageing 2009. new york: united nations publication; 2010 22. new pw, reeves rk, smith e, eriks-hoogland i, gupta a, scivoletto g, et al. international retrospective comparison of inpatient rehabilitation for patients with spinal cord dysfunction: differences according to etiology. archives of physical medicine and rehabilitation. 2016; 96 (6):1080-1087. 23. gedde mh, lilleberg hs, aßmus j, gilhus ne, rekand t. traumatic vs non-traumatic spinal cord injury : a comparison of primary rehabilitation outcomes and complications during hospitalization. the journal of spinal cord medicine. 2019;42(6):695 701. 24. cosar sns, yemisci ou, oztop p, cetin n, sarifakioglu b, yalbuzdag sa, et al. demographic characteristics after traumatic and non-traumatic spinal cord injury: a retrospective comparison study. spinal cord. 2010;48(12):862 6. 25. zárate-kalfópulos b, jiménez-gonzález a, reyes-sánchez a, robles-ortiz r, cabrera-aldana ee, rosales-olivarez lm. demographic and clinical characteristics of patients with spinal cord injury: a single hospital-based study. spinal cord. 2016;54(11):1016 9. 26. gupta a, taly ab, srivastava a, vishal s, murali t. traumatic vs non-traumatic spinal cord lesions: comparison of neurological and functional outcome after in-patient rehabilitation. spinal cord. 2008;46(7):482 7. 27. mckinley wo, seel rt, hardman jt. nontraumatic spinal cord injury: incidence, epidemiology, and functional outcome. archives of physical medicine and rehabilitation. 1999;80(6):619 23. 28. wong ay, karppinen j, samartzis d. low back pain in older adults: risk factors, management options and future directions. scoliosis spinal disord. 2017;12:14. 29. siemionow k, an h, masuda k, andersson g, cs-szabo g. the effects of age, gender, ethnicity, and spinal level on the rate of intervertebral disc degeneration. a review of 1712 intervertebral discs. spine (phila pa 1976). 2011;36(17):1333 9. 30. parenteau cs, lau ec, campbell ic, courtney a. prevalence of spine degeneration diagnosis by type, age, gender, and obesity using medicare data. sci rep. déc 2021;11(1):5389. 31. lou c, chen h, mei l, yu w, zhu k, liu f et al. association between menopause and lumbar disc degeneration: an mri study of 1,566 women and 1,382 men menopause: the journal of the north american menopause society. 2017; 24 (10): pp. 000-000 32. pravdenkova s, al-mefty o, sawyer j, husain m. progesterone and estrogen receptors: opposing prognostic indicators in meningiomas. j neurosurg. 2006;105(2):163 73. 33. new pw. secondary conditions in a community sample of people with spinal cord damage. the journal of spinal cord medicine. 2016;39(6):665 70. 34. draulans n, kiekens c, roels e and peers e. etiology of spinal cord injuries in sub-saharan africa. spinal cord. 2011; 49, 1148–1154 35. ones k, yilmaz e, beydogan a, gultekin o, caglar n. comparison of functional results in non-traumatic and traumatic spinal cord injury. disability and rehabilitation. 2007;29(15):1185 91. 36. müller-jensen l, ploner cj, kroneberg d, schmidt wu. clinical presentation and causes of non-traumatic spinal cord injury : an observational study in emergency patients. frontiers in neurology. 2021 ; 1386. 37. mckinley wo, michael a. tewksbury ma , mujteba nm. spinal stenosis vs traumatic spinal cord injury: a rehabilitation outcome comparison. spinal cord med. 2002;25:28-35. 38. wang h, yang x, shi y, zhou y, li c, chen y et al. early predictive factors for lower-extremity motor or sebsory deficits and surgical results of patients with spinal tuberculosis. medecine (baltimore). 2016; 95 (34): e 4523. 39. li w, liu z, xiao x, xu z, sun z, zhang z et al. early surgical intervention for active thoracic spinal tuberculosis patients with paraparesis and paraplegia. bmc musculoskeletal disorders. 2021; 22:213 40. hodgson ar, yau a. pott’s paraplegia: a classification based upon the living pathology. paraplegia 1967;5(1):1– 16 41. garg rk, somvanshi ds. spinal tuberculosis: a review. the journal of spinal cord medicine. 2011; 34 (5):440-454 42. robson p. metastatic spinal cord compression: a rare but important complication of cancer. clinical medicine. 2014; 14 (5:): 542–5 43. de dios e, heary rf, lindhagen l, macdowall a. laminectomy alone versus laminectomy with fusion for degenerative cervical myelopathy: a long-term study of a national cohort. eur spine j. 2022;31(2): 334-345. 44. chahoud j, kanafani z, kanj ss. surgical site infections 455 epidemio-clinical and therapeutic profile of non-traumatic medullary-radicular compressions following spine surgery: eliminating the controversies in the diagnosis. frontiers in medecine. 2014;1(7). 1-10 45. eshra m a. experience in the management of postoperative spinal infection. the egyptian journal of neurology, psychiatry and neurosurgery. (2019) 55 :9. 46. guilcher sjt, munce sep, couris cm, fung k, craven bc, verrier m, et al. health care utilization in non-traumatic and traumatic spinal cord injury: a population-based study. spinal cord. 2010 ;48(1) :45 50. 47. van den berg mel, castellote jm,pedro-cuesta j, mahillofernandez i. survival after spinal cord injury: a systematic review. journal of neurotrauma. 2010; 27:1517–1528 48. barzilai o, versteeg al; goodwin cr, sahgal a, rhines ld, sciubba dm, et al. association of neurologic deficits with surgical outcomes and health-related quality of life after treatment for metastatic epidural spinal cord compression. cancer. 2019;0:1-8 49. halvorsen a, pettersen al, nilsen sm, halle kk, schaanning ee, rekand t. epidemiology of traumatic spinal cord injury in norway in 2012–2016 : a registrybased cross-sectional study. spinal cord. avr 2019;57(4):331 8. 50. choi g, raiturker pp, kim mj, jin cd, chae ys, lee sh. the effect of early isolated lumbar extension exercise program for patients with herniated disc undergoing lumbar discectomy. neurosurgery. 2005; 57:764-772. doi: 10.33962/roneuro-2023-012 bilateral clinoidal rosai dorfman disease mimicking meningioma – a rare cause of bilateral blindness mayuresh hinduja, hrushikesh kharosekar, vernon velho, laxmikant bhople romanian neurosurgery (2023) xxxvii (1): pp. 75-79 doi: 10.33962/roneuro-2023-012 www.journals.lapub.co.uk/index.php/roneurosurgery bilateral clinoidal rosai dorfman disease mimicking meningioma – a rare cause of bilateral blindness mayuresh hinduja, hrushikesh kharosekar, vernon velho, laxmikant bhople dept. of neurosurgery, sir j.j. group of hospitals and grant medical college, mumbai, india, india abstract rosai dorfman disease is a self-limiting disease usually affecting the lymph nodes. intracranial lesions are seen in less than 5% of cases. isolated intracranial rdd without nodal involvement is rare, only 70 cases have been reported to date. skull base lesions are seen in only 7 cases, petro clival rdd. clionoidal lesions of rdd have not been reported in the literature, we report a rare case of bilateral clionoidal lesions of rdd presenting with bilateral blindness in a young male. introduction rosai dorfman disease was first described in 1969 by juan rosai and ronald dorfman as sinus histiocytosis with lymphadenopathy in young male. it commonly presents as painless massive cervical lymphadenopathy and symptoms of fever, malaise and / or anemia. although all age groups have been effected with the disease, rosai dorfman disease commonly effects young males, usually less than 20 years of age group. the disease is extra nodal in up to 43% of patients with or without lymphadenopathy at any point of time in disease. common extra nodal sites being skin, nose & paranasal sinus, eyelid, orbit & central nervous system. intracranial involvement in rosai dorfman disease is seen in <5 % of cases of extra nodal disease & in most of these cases leptomeninges are affected. isolated cranial involvement without nodal involvement is rare and only 70 such cases are reported in literature till date. to our knowledge bilateral lesions involving the clionoid are not reported in literature, so we report first such case of rosai dorfman disease involving bilateral clionoid process. case report a 21 year male patient presented to us with complaints of decreased vision in both eyes since 1-month, intermittent headache since 15 days more in morning hours. patient had one episode of generalized tonic keywords bilateral, clionoidal, rosai dorfman disease, blindness corresponding author: hrushikesh kharosekar dept of neurosurgery, sir j.j. group of hospitals and grant medical college, mumbai, india hkharosekar@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 76 mayuresh hinduja, hrushikesh kharosekar, vernon velho, laxmikant bhople clonic seizure 2 days back and then he was referred to our hospital. on neurological examination patient only had visual deficits, his vision was 6/12(snellen chart) on right side and only perception of hand movements on left side. patient was investigated further with radilogical examination. mri brain with contrast (fig 2-4) was done which showed two large well circumscribed lobulated extra axial mass lesion seen along both planum sphenoidale region extending upto both anterior clinoid processes of size 5.2 x 3.2 x 1.2 cm on left side and 1.4 x 2.7 x 3 cm on right side with extension to bilateral anterior temporal lobe and inferior frontal lobe. the lesion was isointense on t1 image and hypointense on t2 image with intense post contrast enhancement. the mass was abutting the cavernous sinus bilaterally without any obvious infiltration. and the lesions were compressing optic chiasma from both sides. patient was planned for staged surgery for both sideds considering the lesions as meningioma. left sided lesion was approached in first stage as he was developing optic atrophy on that side. figure 1. preoperative mri brain with contrast showing bilateral clinoidal lesion ( axial images). intraoperatively lesion was reddish grey in color, firm and moderately vascular. complete excision was achieved. to our surprise histopathological examination was showing fibro-collagenous tissue with dense chronic inflammatory infiltrate comprising plasma cells, lymphocytes at places showed large histiocytes with phagocytosis of intact lymphocytes and plasma cells (emperipolesis). russell bodies also noted. cd1a marker was absent suggestive of rosai dorfman disease. (fig 5) as the disease is self limiting with good prognosis after complete excision, patient underwent second stage surgery immediately after 15 days on right side. complete excision was achieved, patient was discharged with minimal improvement in vision on right side. histopathology of the lesion on right side was also suggestive of rosai dorfman disease. post operative mri brain with contrast after 1 month was suggestive of complete removal of both lesions, no residual lesion. patient was planned for radiotherapy. figure 2. preoperative mri brain with contrast showing bilateral clinoidal lesion ( saggital & coronal images). figure 3. preoperative ct brain with contrast showing bilateral clinoidal lesion. discussion rdd is a benign, self-limiting histiocytic disease with 77 bilateral clinoidal rosai dorfman disease mimicking meningioma poorly understood etiopathogenesis. intracranial manifestations are seen n only 5% of cases. there is no age preponderance, th male predomiance seen. the clinical symptoms depend on the location of the lesion, and includes headache, nausea and vomiting, seizures, cranial nerve deficits, and weakness. figure 4. preoperative mri brain with contrast showing bilateral clinoidal lesion (coronal images, t2 weighted images). figure 5. histopathological slide. figure 6. preoperative images ct brain with contrast before second stage surgery. in literature only 70 cases have been reported of isolated cranial manifestations in rdd. no case is been reported of clinoidal rdd. so this first case so far presenting with bilateral lesions of rdd involving the clinoid process on both sides. 7 cases of petroclival lesions have been reported in literature. a previous study found intracranial lesions re growth or recurrence of symptoms in 14% of 29 patients with a mean follow-up period of 10.1 years. radio logically lesions are typically dural based, extra-axial, well-circumscribed mimicking meningioma.[16–19] on ct, they are homogeneous hyperdense or isodense masses. mri is gold standard investigation for evaluating lesions of intracranial rdd. on t1-weighted images, the lesions appear as iso to hyperintense masses with clear margins. on t2-weighted images, the lesions usually appear as isointense masses. on contrast images, the lesions demonstrate homogeneously enhancement, and the dural tail can commonly be seen. in our case, ct demonstrated bilateral welldefined, homogenous, hyperdense masses bed clionoid process; mri showed dural based welldefined, homogenous lesions based on clinoid process left more than right with cavernous sinus extension on both sides. the lesions were isointense on t1 weighted images, hypointense on t2-weighted images, and homogeneously enhanced. so our working diagnosis was meningioma preoperatively.[12,20] preoperative radiological findings using the current mri sequences are difficult to distinguish rdd from meningiomas, but the absence of hyperostosis, bony erosion, or calcification should suggest rdd as a differential diagnosis of meningiomas.[17] radiologically the lesions in rdd are similar to meningioma on t1 post contrast enhancement, but they have low signal intensity in t2 weighted images, which is very unlikely with meningioma. other intracranial lesions with t2 image low signal are melanoma, malignant lymphoma, markedly fibrous or calcified meningioma. the reason of low signal in t2 weighted image in this disease is presence of free radicals released by macrophages during phagocytosis. nisopropyl p-[123i] iodoamphetamine ([123i]imp) single-photon emission computerized tomography (spect) reveals a hot lesion on early and delayed images which is unlikely in cases of meningioma. final diagnosis of rdd can only be confirmed by histopathological and immunohistochemical examinations. on histopathology rosai dorfman disease shows 78 mayuresh hinduja, hrushikesh kharosekar, vernon velho, laxmikant bhople fibrosis, histiocytes and lymphoplasmacytic cells. russell bodies also seen. histopathological examination is definitive for diagnosis of rdd, especially visualization of emperipolesis and s100, and absence of cd1a ( a marker of langhens cell histiocytosis) . histopathological differential diagnosis includes lymphoplasmacytic meningioma,langerhans histiocytosis, lymphoma, plasmacytoma and sarcoidosis. lymphoplasmacytic meningioma can be differentiated by presence of typical meningioma picture with epithelial membrane antigen positivity. langerhans histiocytosis can be differentiated by presence of eosinophils, both s100 and cd1a.lymphoma can be differentiated by presence of cd15 and cd30 along with reed stenberg cells. plasmacytoma also gives similar picture but the lineage of plasma cells is not polyclonal as in rosai dorfman disease. sarcoidosis can be ruled out by presence of granulomatous inflammation. in cases of chronic inflammatory back ground in histology with prominent histiocytes and an absence of infectious agent should alert to proceed with immunohistochemistry staining for s-100. s-100 positivity suggests either rosai dorfman disease or langerhans cell histiocytosis. lch the histiocytes typically show reniform or indented nucleus, contain birbeck granules and cd1a positivity which differentiated it from rosai dorfman disease. surgery with complete resection of the lesion is the goal. use of steroids has shown some promising results in some cases. the lesion is radiosensitive and radiotherapy is a good option for residual or recurrent lesions. figure 7. preoperative images mri brain with contrast before second stage surgery. figure 8. post operative mri brain with contrast after second surgery at 1 month follow up. conclusion rosai dorfman disease mimics intracranial dural based lesions causing mass effect. it may or may not be associated with extranodal disease. it should be included in differential diagnosis in cases with low intensity t2 image lesion and histologically fibrotic chronic inflammatory lesions of cns with predominant histiocytic component. resection of the intracranial lesion is the most effective treatment. in case of subtotal resection, the application of adjunctive radiotherapy and/or steroid agents should be advised. references 1. rosai j, dorfman rf. sinus histiocytosis with massive lymphadenopathy: a newly recognized benign clinicopathological entity. arch pathol1969;87:63-70. 2. foucar e, rosai j, dorfman rf. sinus histiocytosis with massive lymphadenopathy (rosai-dorfman disease): review of the entity. semin diagn pathol1990;7:19-73. 3. vemuganti gk, naik mn, honavar sg. rosai dorfman disease of the orbit. j hematol oncol 2008;1:7. 4. walid ms, grigorian aa. ethmo-spheno-intracranial rosaidorfman disease. indian j cancer 2010;47:80-1. 5. kattner ka, stroink ar, roth tc, lee jm. rosai-dorfman disease mimicking parasagittal meningioma: case presentation and review of the literature. surgneurol2000;53:452-7; discussion 457. 6. udono h, fukuyama k, okamoto h, tabuchi k. rosaidorfman disease presenting multiple intracranial lesion with unique findings on magnetic resonance imaging. j neurosurg 1999;91:335–339. 7. sze g, zimmerman rd: the magnetic resonance imaging of infections and inflammatory diseases. radiol clin north am 26:839–859, 1988. 79 bilateral clinoidal rosai dorfman disease mimicking meningioma 8. prayson ra, rowe jj. dural-based rosai-dorfman disease: differential diagnostic considerations. j clin neurosci. 2014 nov;21(11):1872-3. doi: 10.1016/j.jocn.2014.07.011. epub 2014 sep 30. pmid: 25281034. 9. krishnamoorthy v, parmar cf, panikar d. isolated intracranial rosai dorfman disease. neurol india. 2011;59:443–6. romanian neurosurgery (2019) xxxiii (3): pp. 232-238 doi: 10.33962/roneuro-2019-039 www.journals.lapub.co.uk/index.php/roneurosurgery anatomical localization of intracranial grade ii meningiomas in north-eastern romania. our 25-years experience a.i. cucu1, claudia florida costea1,2, mihaela dana turliuc1,2, cristina mihaela ghiciuc2, b.costachescu1,2, roxana popescu1,2, gabriela florenta dumitrescu1, anca sava1,2, daniela maria tanase2, r. arbore-sorete1, i. poeata1,2 1 "prof. dr. n. oblu" emergency clinical hospital iași, romania 2 "grigore t. popa" university of medicine and pharmacy iași, romania abstract objective. our research aims to assess a possible connection between tumour localization and histological subtypes of grade ii meningiomas. material and methods. 143 patients with grade ii who meningiomas underwent surgical resection in "prof. dr. n. oblu" emergency clinical hospital iași between 1990 and 2015. the collected data included: patient age, gender, tumour localization and histopathological diagnosis (atypical, clear cells and chordoid meningioma). results. 135 (94.4%) of all 143 patients with grade ii meningiomas were atypical meningiomas, 6 (4.2%) were cell clear meningiomas and only 2 (1.4%) were chordoid meningiomas. as concerns their distribution by gender, 79 (55.2%) were female and 64 (44.8%) were male. grade ii meningiomas were most commonly located at convexity 49.7% (n=71), followed by skull base in 30.8% (n=44) of the cases and parasagittal/falcine in 14.7% (n=21) of the patients. conclusions. the most common localization of grade ii meningiomas was convexity, followed by skull base, parasagittal/falcine and intraventricular areas. we have also noticed that convexity meningiomas are more frequent in women, unlike the other anatomical localizations in which the male-female ratio is almost equal. therefore, further research is necessary to determine the role of embryological, anatomopathological and genetic factors in underlying the connection between meningioma grade and anatomical localization. introduction meningiomas makes up about one third of all primary central nervous system tumours, being the most common brain tumour in adults over the age of 35 (1), with an incidence that has increased in recent years (2, 3). as far as romania is concerned, an increase in the number of intracranial meningiomas was noted in its north-eastern region (where this research was conducted) over the 1990-2015 period (4). although meningiomas are usually benign slow-growing tumours, their keywords atypical meningioma, grade ii who meningioma, meningiomas localization corresponding author: claudia florida costea "grigore t. popa" university of medicine and pharmacy iași, romania costea10@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 233 anatomical localization of intracranial grade ii meningiomas in north-eastern romania histological aggressiveness may classify them in grade ii or iii tumours, according to the who classification (5, 6). whereas grade ii meningiomas only made up 5-7% of all types of meningiomas before the 2007 who classification (7), they currently make up more that 20% of all meningiomas (7, 8, 9). grade ii meningiomas include three histological subtypes: atypical, the most common, and also chordoid and clear cell meningiomas, the occurrence rate of which is considerably lower (10). among the multiple prognostic factors that can predict meningioma grade prior to tissue diagnosis (11, 12), several studies also found the anatomical localization (13, 14). thus, several authors noticed the predisposition of grade ii meningiomas for cerebral convexity (13, 15, 16) (figure 1). figure 1. preoperative and postoperative axial t1-weighted images with contrast of an atypical meningioma (professor poeata’s personal collection) the goal of our research was to analyze grade ii meningiomas distribution in north-eastern romania over a 25-year period (1990-2015). the patients underwent surgery in "prof. dr. n. oblu" emergency clinical hospital of iasi, the advantage of this hospital being the fact that it services the whole of northeastern romania, a region with a population of about 4 million inhabitants (17) (figure 2). figure 2. preoperative coronal (a) and axial (b) t1-weighted images with contrast showing a left falcine meningioma. postoperative images showing tumour bed after gross total resection (c) (assoc. professor turliuc’s personal collection) material and methods we have evaluated 143 patients hospitalized in "prof. dr. n. oblu" emergency clinical hospital of iași between 1990 and 2015, with histologically proven grade ii meningiomas (atypical, clear cells and chordoid). also, the histological samples have been reviewed according to the current who 2016 criteria (18). we have excluded all patients with type 2 neurofibromatosis (2 patients) and those for whom we were unable to collect full information about tumors (16 patients). the collected data included: gender, age, anatomical localization and histopatho logical diagnosis (table i). in order to confirm the anatomical localization of grade ii meningiomas, the surgeon’s operative notes were taken into consideration. as concerns the intracranial localization of meningiomas, they were divided into four main categories: (1) convexity, (2) parasagittal/falcine, (3) skull base and (4) intraventricular. results of all 143 patients with meningiomas, 79 (55.2%) were female patients and 64 (44.8%) were male 234 a.i. cucu, claudia florida costea, mihaela dana turliuc et al. patients. the male: female ratio was 1:1.2. as concerns patients distribution on demographic groups, more than half of them were in the 50-69 year age group (58.1%, n=83). as for the distribution of meningiomas according to anatomical localization, they occurred mostly: 49.7% (n=71) at convex ity, 30.8% (n=44) at skull base, 14.7% (n=21) in the p a r a s a g i t t a l / f a l c i n e a r e a a n d 4 . 9 % ( n = 7 ) intraventricular. most meningiomas were atypical (94.4%, n=135), followed by clear cell meningiomas (4.2%, n=6) and only 1.4% (n=2) were chordoid. all patient charac teristics are s ho wn in table i. characteristics grade ii n (%) no. of patients 143 gender female male 79 (55.2) 64 (44.8) age groups (years) 20-29 30-39 40-49 50-59 60-69 70-79 80-89 3 (2.1) 9 (6.3) 23 (16.1) 42 (29.4) 41 (28.7) 22 (15.4) 3 (2.1) tumor localization convexity skull base parasagittal/falcine intraventricular 71 (49.7) 44 (30.8) 21 (14.7) 7 (4.9) histological subtypes atypical meningioma clear cell meningioma chordoid meningioma 135 (94.4) 6 (4.2) 2 (1.4) table 1. characteristics of 143 patients with grade ii meningioma discussion our research revealed a predilection of grade ii meningiomas for the convexity, as 49.7% (n=71) of them occurred in this area, which is consistent with similar studies (10, 14, 19, 20, 21, 22). skull base meningiomas ranked second 30.8% (n=44), followed by the parasagittal/falcine and intraventricular localization (table 1, figure 3). the distribution of the anatomical localization of tumors on age groups was similar in both women and men. figure 3. incidence of grade ii meningiomas according to anatomical localization 235 anatomical localization of intracranial grade ii meningiomas in north-eastern romania although previous studies have demonstrated a predilection of grade ii meningiomas for cerebral convexity (13, 15, 16), a clear etiological connection between a particular meningioma grade and its anatomical localization could not be established. however, some authors consider that the histological grade of the tumor may be related to the meninges’ complex embryological origin, which has a variable neoplastic potential (23, 24, 25, 26). among the first studies that demonstrated the predilection of grade ii meningiomas for cerebral convexity were those conducted by mahmood et al. and maier et al. (27, 28). also, kane et al. later demonstrated that non-skull base tumors would have an increased risk for grade ii meningiomas compared to skull base tumors (13). on the other hand, zhou et al. noted that meningiomas located at the median line of the skull base are the least likely to be grade ii or iii (6), similar to other studies that have revealed that skull base meningiomas are more frequently meningothelial (29, 30) and are also lower grade at initial resection (15). this predilection of meningiomas for various anatomical localizations in the intracranial space could be explained by the distinct embryological origins of non-skull and skullbase dura (14, 15, 30, 31). in this respect, various authors have demonstrated that meninges around the brainstem would arise from cephalic mesoderm, whereas telencephalic meninges arise from neural crest cells (25, 29, 32, 33). this differential meningeal embryogenesis resulted in the predominance of one arachnoid cell type over the other location, which accounts for the aggressive behavior of some meningiomas as compared to others in some anatomical localizations (15). however, genomic studies have shed light on intracranial locations and mutational patterns, as well as on the potential embryonic cancer stem cell-like origin (34). in a study on 110 patients with incidentally discovered meningiomas, hashimoto et al. also noticed that non-skull base meningiomas have a more aggressive behavior and that skull base meningiomas do not tend to grow when compared to non-skull base meningiomas (35). moreover, even when these tumors grow, the growth rate was significantly lower in terms of annual growth rate and percentage (35). also, the same authors demonstrated that 60% of the skull base incidental meningiomas had an exponential pattern of growth, unlike non-skull base incidental meningiomas characterized by a 33% growth percentage (35). in conclusion, the authors recommend non-skull base meningioma follow-up by magnetic resonance imaging at shorter intervals. the authors mention that the results must be interpreted as most meningiomas fit both exponential and linear patterns statistically (35). in 2003, the same authors suggested that a loss of 1p was shown to be significantly correlated with malignant progression of meningiomas, analyzing 72 grade ii and iii meningiomas, with fluorescence in situ hybridization and loss of heterozygosity analyses (35, 36). the authors also pointed out that skull base meningiomas had a significantly lower percentage of cells with 1p loss (20.31%) compared to non-skull base meningiomas (37.87%), suggesting that skull base tumors would have fewer genetic alterations and consequently would have less aggressive biological behavior (35). similarly, murphy et al. showed in their study that meningiomas originating at the convexity had more chromosomal abnormalities than those arise from skull base (37). in terms of histopathology, there have been studies that have shown its importance in the prediction of some types of meningiomas for certain intracranial localizations. thus, mcgovern et al., in a study of 216 patients with grade i, ii and iii meningiomas, claimed that grade i non-skull base meningiomas had a higher mib-1 labeling index than grade i skull base meningiomas, suggesting that nonskull base tumors may have a more aggressive biology (16). as concerns their recurrence, the same author noted that non-skull base meningiomas, when they recur, have a higher who grades than skull base meningiomas (16). also, in 2018, turk et al. concluded in a study of 40 grade i and ii meningiomas that the skull base group had significantly higher cd34 levels than the non-skull base group, suggesting that skull base meningiomas tend to have higher microvascular density and are better vascularized than non-skull base tumors (38). as regards the distribution of meningiomas on genders in the overall number of patients, we revealed a male: female ratio of 1:1.2, with a slight predominance in females, in agreement with other literature studies (14, 19, 39). on the other hand, whereas in the skull base, intraventricular and parasagittal/falcine localizations the male: female ratio was approximately 1:1, location at convexity level was dominated by women, with a male: female 236 a.i. cucu, claudia florida costea, mihaela dana turliuc et al. ratio of 1:1.5 (43/28) (figure 4). in order to justify this predominance of women, research has shown that grade i meningiomas have a high level of progesterone receptor expression relative to grade ii and iii meningiomas, which seem to have a lower frequency of estrogen and androgen receptors (13, 40, 41, 42), which means close male-female ratios. on the other hand, morokoff et al. in a study of 163 convexity meningiomas (grades i, ii and iii) noted a prevalence of the female sex, with a male: female ratio of 1:2.7 (43). in higher-grade meningiomas, morokoff et al. found a male: female ratio of 1:1, much lower than our ratio of 1:1.5. figure 4. incidence of grade ii meningioma according to gender with regard to the distribution of histological subtypes of grade ii meningiomas, atypical meningiomas prevailed in our research (94.4%), followed by clear cell and chordoid meningiomas in a much lower percentage, as there are rare types of tumors (table 1). of all grade ii meningiomas, atypical meningiomas are the most common, their percentage increasing to 20-30% of all meningiomas after the introduction of the who classification in 2000 and 2007 (2, 8, 9). like grade i or iii meningiomas, atypical meningiomas may develop anywhere in the intracranial space, with some studies reporting a higher frequency of atypical meningiomas at the level of cerebral convexity (8, 27, 44, 45). clear cell meningioma is a rare disorder, as it makes up less than 1% of all meningiomas, and english-language literature reports 218 intracranial tumors (46). this percentage is also low in our research, with an incidence rate of this type of meningioma only 4.2% (n=6) over the 25-year period (table i). whereas previous studies revealed that the most common localization for clear cell meningioma was the cerebellopontine angle (47, 48, 49), all clear cell meningiomas in our group were located in the parasagittal/falcine area (n = 6). from this point of view, the results of the studies differ from each other: some studies show that the most affected location is convexity (46), whereas others point to skull base (50), particularly cerebellopontine angle, parasagittal tumors having lower occurrence rates (47). chordoid meningiomas are also rare types of meningiomas, as only a little more than 100 cases are reported in literature (51, 52, 53, 54, 55, 56). rare neoplasia with a unique chordoid appearance, chordoid meningioma has a predilection for the supratentorial localization (1, 57), similar to our study in which the two chordoid meningiomas had parasagittal/falcine localization. conclusions our study has shown a predominance of grade ii meningiomas for cerebral convexity, which is the most common location in the intracranial space, followed by the skull base, parasagittal/falcine and intraventricular locations. we also noticed that convexity meningiomas predominate especially in women. further research is needed to highlight the role of genetic, embryological and anatomopathological factors in highlighting the 237 anatomical localization of intracranial grade ii meningiomas in north-eastern romania connection between meningioma grade and anatomical localization references 1. louis dn, scheitauer bw, budka h, von deimling a, kepes jj. meningiomas. in: kleihues p, cavenee wk (eds). pathology and genetics of tumors of the nervous system. lyon: iarc press, 2000. 2. willis j, smith c, ironside jw, et al. the accuracy of meningioma grading: a 10-year retrospective audit. neuropathol appl neurobiol. 2005; 31:141-149. 3. cucu ai, turliuc dm, costea cf, et al. pathways of metastatic spread in meningiomas. romanian neurosurgery. 2019; 33(1):12-16. 4. cucu ai, costea cf, carauleanu a, et al. meningiomas related to the chernobyl irradiation disaster in northeastern romania between 1990 and 2015. revista de chimie bucharest. 2018; 69:1562-1565. 5. aboukais r, baroncini m, zairi f, et al. early postoperative radiotherapy improves progression free survival in patients with grade 2 meningioma. acta neurochir (wien). 2013; 155(8):1385-1390; discussion 1390. 6. zhou p, ma w, yin s, et al. three risk factors for who grade ii and iii meningiomas: a study of 1737 cases from a single center. neurol india. 2013; 61:40-44. 7. perry a, louis dn, scheithauer bw, et al. meningiomas. in: louis dn, ohgaki h, wiestler od, cavenee wk (eds) who classification of tumours of the central nervous system. lyon: iarc press, 2007. 8. pasquier d, bijmolt s, veninga t, et al. atypical and malignant meningioma: outcome and prognostic factors in 119 irradiated patients a multicenter, retrospective study of the rare cancer network. int j radiat oncol biol phys. 2008; 71:1388-1393. 9. pearson be, markert jm, fisher ws, et al. hitting a moving target: evolution of a treatment paradigm for atypical meningiomas amid changing diagnostic criteria. neurosurg focus. 2008; 24:e3. 10. durand a, labrousse f, jouvet a, et al. who grade ii and iii meningiomas: a study of prognostic factors. j neurooncol. 2009; 95(3):367-375. 11. cucu ai, costea cf, poeata i, et al. prognostic factors in atypical meningioma. rom neurosurg. 2017; 31(2):165171. 12. cucu ai, turliuc md, carauleanu a, et al. chemical aspects of peritumoral cerebral edema in atypical meningiomas. rev chim (bucharest). 2018; 69:2804-2807. 13. kane aj, sughrue me, rutkowski mj, et al. anatomic location is a risk factor for atypical and malignant meningiomas. cancer. 2011; 117(6):1272-1278. 14. cucu ai, costea cf, poeata i, et al. anatomical localization of atypical meningiomas: our experience on 81 patients. rev med chir soc med nat iasi. 2018; 122:744-752. 15. sade b, chahlavi a, krishnaney a, et al. world health organization grades ii and iii meningiomas are rare in the cranial base and spine. neurosurgery. 2007; 61(6):11941198. 16. mcgovern sl, aldape kd, munsell mf, et al. a comparison of world health organization tumor grades at recurrence in patients with non-skull base and skull base meningiomas. j neurosurg. 2010; 112(5):925-933. 17. www.recensamantromania.ro – the official site of the romanian national institute of statistics. 18. louis dn, perry a, reifenberger g, et al. the 2016 world health organization classification of tumors of the central nervous system: a summary. acta neuropathol. 2016; 131(6):803-820. 19. zaher a, abdelbari mattar m, et al. atypical meningioma: a study of prognostic factors. world neurosurg. 2013; 80(5):549-553. 20. nanda a, bir sc, konar s, et al. outcome of resection of who grade ii menin-gioma and correlation of pathological and radiological predictive factors for recurrence. j clin neuro-sci. 2016; 31:112-121. 21. budohoski kp, clerkin j, millward cp, et al. predictors of early progression of surgically treated atypical meningiomas. acta neurochir (wien). 2018; 160(9):18131822. 22. champeaux c, houston d, dunn l. atypical meningioma. a study on recurrence and disease-specific survival. neurochirurgie. 2017; 63(4):273-281. 23. backer-grøndahl t, moen bh, torp sh. the histopathological spectrum of human meningiomas. int j clin exp pathol. 2012; 5(3):231-242. 24. o'rahilly r, muller f. the meninges in human development. j neuropathol exp neurol. 1986; 45:588-608. 25. catala m. embryonic and fetal development of structures associated with the cerebro-spinal fluid in man and other species. part i: the ventricular system, meninges and choroid plexuses. arch anat cy-tol pathol. 1998; 46:153169. 26. rutkowski mj, jian bj, bloch o, et al. intracranial hemangiopericytoma: clinical experience and treatment considerations in a modern series of 40 adult patients. cancer. 2012; 118(6):1628-1636. 27. mahmood a, caccamo dv, tomecek fj, et al. atypical and malignant meningiomas: a clini-copathological review. neurosurgery. 1993; 33:955-963. 28. maier h, ofner d, hittmair a, et al. classic, atypical, and anaplastic meningioma: three histopathological subtypes of clinical relevance. j neurosurg. 1992; 77(4):616-623. 238 a.i. cucu, claudia florida costea, mihaela dana turliuc et al. 29. kros j, de greve k, van tilborg a, et al. nf2 status of meningiomas is associated with tumor localization and histology. j pathol. 2001; 194:367-372. 30. lee jh, sade b, choi e, et al. meningothelioma as the predominant histological subtype of midline skull base and spinal meningioma. j neurosurg. 2006; 105(1):60-64. 31. kepes jj. presidential address: the histopathology of meningiomas. a reflection of origins and ex-pected behavior? j neuropathol exp neurol. 1986; 45(2):95-107. 32. russell d, rubenstein l. pathology of tumours of the central nervous system. baltimore: williams and wilkins, 1989. 33. perry a, gutmann dh, reifenberger g. molecular pathogenesis of meningiomas. j neurooncol. 2004; 70(2):183-202. 34. karsy m, azab ma, abou-al-shaar h, et al. clinical potential of meningioma genomic insights: a practical review for neurosurgeons. neurosurg focus. 2018; 44(6):e10. 35. hashimoto n, rabo cs, okita y, et al. slower growth of skull base meningiomas compared with non-skull base meningiomas based on volumetric and biological studies. j neurosurg. 2012; 116(3):574-580. 36. murakami m, hashimoto n, takahashi y, et al. a consistent region of deletion on 1p36 in meningiomas: identification and relation to malignant progression. cancer genet cytogenet. 2003; 140:99-106. 37. murphy m, pykett mj, harnish p, et al. identification and characterization of genes differentially expressed in meningiomas. cell growth differ. 1993; 4:715-722. 38. turk o, asik m, batur s, et al. correlation of preoperative radiological evaluation of skull and non-skull base meningiomas with clinical and surgical data. turk neurosurg. 2018; in press. 39. barthélemy e, loewenstern j, konuthula n, et al. primary management of atypical meningioma: treatment patterns and survival outcomes by patient age. j cancer res clin oncol. 2018; 144(5):969-978. 40. korhonen k, salminen t, raitanen j, et al. female predominance in meningiomas can not be explained by differences in progesterone, estrogen, or androgen receptor expression. j neurooncol. 2006; 80:1-7. 41. whittle ir, foo ms, besser m, et al. progesterone and oestrogen receptors in meningiomas: biochemical and clinicopathological considerations. aust n z j surg. 1984; 54:325-330. 42. wolfsberger s, doostkam s, boecher-schwarz hg, et al. progesterone-receptor index in meningiomas: correlation with clinico-pathological parameters and review of the literature. neurosurg rev. 2004; 27:238-245. 43. morokoff ap, zauberman j, black pm. surgery for convexity meningiomas. neurosurgery. 2008; 63(3):427-33; discussion 433-434. 44. modha a, gutin ph. diagnosis and treatment of atypical and anaplastic meningiomas: a review. neurosurgery. 2005; 57(3):538-550. 45. hammouche s, clark s, wong ah, et al. long-term survival analysis of atypical meningiomas: survival rates, prognostic factors, operative and radiotherapy treatment. acta neurochir (wien). 2014; 156(8):1475-1481. 46. li p, yang z, wang z, et al. clinical features of clear cell meningioma: a retrospective study of 36 cases among 10,529 patients in a single institution. acta neurochir (wien). 2016; 158(1):67-76. 47. tao x, dong j, hou z, et al. clinical features, treatment, and prognostic factors of 56 intracranial and intraspinal clear cell meningiomas. world neurosurg. 2018; 111:e880-e887. 48. chen h, li xm, chen yc, et al. intracranial clear cell meningioma: a clinicopathologic study of 15 cases. acta neurochir (wien). 2011; 153 (9):1769–1780. 49. wang xq, huang mz, zhang h, et al. clear cell meningioma: clinical features, ct, and mr imaging findings in 23 patients. j. comput assist tomo. 2014; 38(2):200-208. 50. zhang h, ma l, wang yb, et al. intracranial clear cell meningiomas: study on clinical features and predictors of recurrence. world neurosurg. 2017; 97:693-700. 51. kozler p, benes v, netuka d, et al. chordoid meningioma: presentation of two case reports, review of the literature, and plea for data standardisation. j neurooncol. 2008; 88:115-120. 52. kepes jj, chen wy, connors mh, et al. “chordoid” meningeal tumors in young individuals with peritumoral lymphoplasmacellular infiltrates causing systemic manifestations of the castleman syndrome. a report of seven cases. cancer. 1988; 62:391-406. 53. lin jw, ho jt, lin yj, et al. chordoid meningioma: a clinicopathologic study of 11 cases at a single institution. j neurooncol. 2010; 100:465-473. 54. epari s, sharma mc, sarkar c, et al. chordoid meningioma, an uncommonvariant of meningioma: a clinicopathologic study of 12 cases. j neurooncol. 2006; 78:263-269. 55. couce me, aker fv, scheithauer bw. chordoid meningioma: a clinicopathologic study of 42 cases. am j surg pathol. 2000; 24:899-905. 56. zhu hd, chen h, xie q, et al. chordoid meningioma: a retrospective study of 17 cases at a single institution. chin med j. 2013; 126:789-791. 57. tena-suck ml, collado-ortìz ma, salinas-lara c, et al. chordoid meningioma: a report of ten cases. j neurooncol. 2010; 99(1):41-48. doi: 10.33962/roneuro-2022-073 brain abscess – a still high mortality medical condition. our clinic experience and literature review george popescu, marius c. zaharia, ana-maria georghiu, bogdan-ionuț david, ana-maria ioniță, cezar vijlanescu, radu m. gorgan romanian neurosurgery (2022) xxxvi (4): pp. 399-406 doi: 10.33962/roneuro-2022-073 www.journals.lapub.co.uk/index.php/roneurosurgery brain abscess – a still high mortality medical condition. our clinic experience and literature review george popescu1, marius c. zaharia1, ana-maria georghiu1, bogdan-ionuț david1, ana-maria ioniță1, cezar vijlanescu1, radu m. gorgan1,2 1 bagdasar-arseni clinical emergency hospital, department of neurosurgery, bucharest, romania 2 carol davila university of medicine and pharmacy, department of neurosurgery, bucharest, romania abstract background. even in the 21st century, infections of the central nervous system and their secondary damage still represents a high mortality condition. furthermore, brain abscesses (ba) are huge public health issues due to their high mortality and morbidity with high financial implications for the health care system. material and methods. in this article, we want to present our clinic`s experience in the management of brain abscesses between 2012 and 2021. a 10 years retrospective study was performed in the 4th neurosurgery department of “bagdasar-arseni” clinical emergency hospital in bucharest results. in the last 10 years, our clinic admitted 46 patients, 10 women and 36 men. the mean age was 47 years old. the most common symptom was headache (42 cases). in 39 cases, patients had solitary abscesses while seven patients presented multiple abscesses. the therapeutic approach was classic surgery in 37 cases. in four cases abscess drainage was performed and in five cases conservative treatment was used. at discharge, 31 patients were healed and seven patients died. discussions. in ba management, antimicrobial therapy is crucial. thus, identifying the pathogen is crucial for accurate antimicrobial treatment. unfortunately, in too many cases, the agent remains unknown and empiric treatment is required. aspiration of the abscesses proved to be safe and with similar results compared to classic surgery. conclusions. brain abscesses remain a high challenge to manage even in the 21st century. broad-spectrum antibiotic treatment should be applied as soon as possible until the pathogen is identified and specific treatment will be used. background even though trepanation of the skull is one of the first medical procedure performed [10], the first documented surgical intervention of a brain abscess was performed by the s.f morand in 1952 for a temporoethmoidal abscess [11]. despite the evolution of techniques keywords brain abscess, stereotactic biopsy, ribosomal dna amplification corresponding author: g. popescu 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 400 george popescu, marius c. zaharia, ana-maria georghiu et al. and technology such as marsupialization proposed by king [12], aspiration tried by dandy [13] or enucleation of the encapsulated abscess tried by vincent [14], the first case reported to be successfully treated my medical management was in 1971, by heineman [15]. however, vincent [16] proved the efectivness of complete excision of the brain abscess back in 1936. even in the 21st century, infections of central nervous system and their secondary damage still represents a high mortality condition [1]. furthermore, brain abscesses (ba) are a huge public health issue due to its high mortality and morbidity with high financial implication for health care system [2], [3]. brain abscess represents a puss collections located in the brain parenchyma and a lifethreatening emergency. the incidence of ba may widely vary between countries. it is known that developed countries have a lower incidence (about 1-2%) while developing countries may reach an incidence of 8% [4], [5], [6]. the most affected ages are young pediatric population and the elderly with an increased predisposition to male patients. brain abscesses are dynamic focal forms of intracranial lesions. their formation is a long and elaborate process that can be divided in four stages [7], described in table 1. stage duration early cerebritis 1-4 days late cerebritis 4-10 days early capsule development 11-14 days late capsule development >14 days table 1. formation of cerebral abscess. the study of the brain abscess was achieved using ct and mri scans. the first stage, early cerebritis is characterized by the increase of neutrophil, edema and tissue necrosis. in this stage, the microglias and astrocytes activates. they usually remain activated through whole abscess development [8]. the cytokines tnf-alpha and il-1 have key roles in the establishment of antibacterial response in the central nervous system [8]. few studies sugested high level of necrosis factor-alpha, interleukin 1beta and macrophage inflammatory protein-2 are detected from the third week of infection with staphylococcus aureus [9]. the late cerebritis phase is characterized by a lymphocyte and macrophage infiltrate. between 11 to 14 days, the development of the capsule begins. in this stage, a highlyvascularized abscess wall is form, limiting the expansion of the infective process, thus preserving the brain function and structure. in almost half of the cases (40%), the origin of ba remains unidentified. in the developed countries, brain abscesses are usually a surgical intervention complication [17]. before the discovery of antibiotics, the most common isolated pathogen was staphylococcus aureus [18]. sometimes, fungal infections and intracranial tuberculosis may present as an abscess [19], [20], [21]. very often, the pathogenic source is polymicrobial. even though there is a wide range of pathogens responsible for ba, the most isolated pathogens are staphylococcus aureus and streptococcus viridans in about 40% of the cases. there were described three types of sources for pathogens to reach the cerebral parenchyma. the first way is due to spread of infection from pericranial contagious focus, in almost half of the cases (25-50%) such as middle ear, dental infections or sinusitis. dental infections and frontal or ethmoidal sinusitis tend to spread in the frontal lobe, while mastoiditis and chronic otitis media tend to spread through temporal lobe or cerebellum [21]. hematogenous spread is the second mechanism of pathogenic spread from a distal focus of infections. the most common source is the bacterial endocarditis, but other foci such as lung abscess, skin infections or intraabdominal infections were reported [22]. hematogenus spread was encountered in 15% to 30% of the cases [23]. the third mechanism is the direct inoculation through head trauma, implantable devices or neurosurgical interventions. this mechanism is the most frequent in the developed countries, having an increased number of road accidents that can lead to head trauma and therefore to brain abscesses [24]. clinical features of the patients is non-specific and may vary depending on the location of the abscess. the most frequent presentation symptoms are headache and vomiting, due to high intracranial pressure. in more than half of the cases, seizures were reported in literature. the patients may accuse focal neurological deficit and altered states of consciousness. the most common symptoms are displayed in table 2. 401 brain abscess – a still high mortality medical condition symptoms frequency (%) fever 54.5-60 hemiparesis 20.2 headache 72-92.8 cranial nerve 39.8 meingism 52.2 altered level of consciousness 10-100 seizure 21-25.3 nausea 31-40 papilloedema 4,1-50 gcs at admission 3-8 10.3 9-12 28.0 13-15 61.7 table 2. most common symptoms [27]. both mri and ct can be used to emphasize ba, similar features being available for both investigation. however, magnetic resonance imiging has a better ability to differential diagnose the cerebral abscess from other ring-enhancing lesions. a typical ct scan of a brain abscess describe a ring of isodense or hyperdense tissue with uniform thickness and central low attenuation and surrounded by vasogenic edema. ventriculitis may be present as well and confirmed by the enhancement of the ependyma [27], however, mri offers better resolution images compared to ct scan. the specific image of peripheral enhance of contrast substance is emphasized. differential diagnosis can be performed using diffusion-weighted sequences or spectroscopy, showing central diffusion restriction, a typical aspect of brain abscess [27], [28]. there is no well-defined treatment guidelines for brain abscesses and each case should benefit of tailored treatment strategy. regardless of chosen therapeutically approach, a rapid broad spectrum antibiotic treatment should be initiated. the most important characteristic of the chosen antibiotic is the penetration of csf barrier in adequate concentration [29]. despite de symptomatic treatment, anticonvulsant medication should be initiated as soon as possible for patients with ba [30]. the anticonvulsant treatment must be sustained for at least two years of no seizures for patient and no epileptic activity emphasized on eeg. surgical approach of brain abscesses must be taken into consideration when patients present lesions bigger than three cm. a bigger than 5 mm midline shift or brain herniation should be emergency signs for surgical treatment. moreover, surgical excision of the ba should me the elective treatment when the lesion is located close to the ventricular system. in the last decade, stereotactic ct-guided aspiration became widely used for ba drainage. it is a less invasive maneuver that permits the microbiological analysis of the abscess content, a key factor for a proper antimicrobial therapy. furthermore, stereotactic ct-guided aspiration is considered as effective as classic surgical intervention [31]. materials and methods in this article we want to present our clinic`s experience of management of brain abscesses between 2012 and 2021. a 10 years retrospective study was performed in the 4th neurosurgery department of “bagdasararseni” clinical emergency hospital from bucharest. it included 46 patients with brain abscesses who benefited of either medical or surgical treatment of brain abscess. results in the last 10 years, in our clinic were admitted 46 patients with brain abscesses, 10 women and 36 men. the mean age was 47 years old, ranging between 16 to 69 years old. a detailed chart of patient`s age is available in fig.1. figure 1. distribution of patients` age. 0 20 40 60 80 1 4 7 10 13 16 19 22 25 28 31 34 37 40 43 46 age distribution 402 george popescu, marius c. zaharia, ana-maria georghiu et al. the most common symptoms accused by patients at admission were headache (42 cases) and motor deficits (32 patients). moreover, 24 patients had seizures prior to admission. in 20 cases, aphasia was identified and 14 patients had sings of elevated intracranial pressure such as vomiting. furthermore, 14 patients had fever over 39 degrees celsius. figure 2. the most frequent symptoms of patients. figure 3. comorbidities of patients. figure 4. main foci of infection in terms of comorbidities, 23 patients presented infectious diseases prior to occurrence of the brain abscess. autoimmune diseases were reported in nine cases and seven patients presented diabetes. moreover, six cases had a history of cancer with radio/chemotherapy. the main sources of the infections disease that led to formation of cerebral abscesses are detailed in the fig. 4. in the most of cases, osteomastoiditis was the main focus of infection. only eight patients affirmed a traumatic history. the rest of them reported no traumatic history or surgeries. in 39 cases, patients had solitary abscess while seven patients presented multiple abscesses. the mean diameter of the abscesses was about 36 mm, ranging between 10 to 63 mm. one third of the lesions were located in the frontal lobe. in 11 cases, the abscess was present in the temporal lobe and in nine patients in the parietal lobe. the distribution of brain abscesses is available in fig. 5. figure 5. distribution of brain abscesses. when the abscesses exceed the size of 3 centimeters and cause a mass effect, the same surgical approach as an expansive intracranial process is required, and total resection is the gold standard, especially in the case of encapsulated abscesses. therapeutical approach was classic surgery in 37 cases. in four cases abscess drainage was performed and in five cases conservative treatment was used (fig. 6). even though only five patients received a conservative treatment, no pathogen grew on the culture in 25 cases. detailed chart of pathogens identified is available in fig. 7. in terms of postoperative complications: two cases had bone flap osteitis. two patients had extradural hematoma and in four cases abscess recurrence was noted. at discharge, 31 patients were healed and seven patients died. the clinical and neurological state was improved in six cases. 42 33 32 24 20 15 14 0 10 20 30 40 50 headache confusional syndrome motor deficit seizures aphasia vomiting fever 23 9 7 6 0 5 10 15 20 25 infectious diseases autoimmune diseases diabetes cancer 2 6 9 2 4 0 2 4 6 8 10 infectios diseases 403 brain abscess – a still high mortality medical condition figure 6. treatment options of our patients. figure 7. the pathogens identified after culture examination. case 1 – surgical approach first case is a 65-year-old patient, hospitalized for motor aphasia and right hemiparesis, without other medical history. a cerebral mri scan was performed and revealed high left fronto-parietal space replacement process with imaging appearance suggestive of a brain abscess (fig. 8). figure 8. a fronto-parietal left lesion with suggestive aspect of brain abscess. important perilesional edema. integrating the clinical examination (motor aphasia; right hemiparesis) with the paraclinical investigations (cerebral mri with contrast substance frontoparietal left lesion with suggestive aspect of brain abscess and important perilesional edema), the patient presents a neurosurgical indication. the patient underwent surgery and the total ablation of the abscess is performed (fig. 9). cultures are taken for the antibiogram and tissue for the histopathological examination. postoperative brain ct scan confirmed the total removal of the lesion without any signs of hemorrhage. postoperatively, the patient shows a slow favorable evolution under antibiotic treatment (cefepime 6g with vancomycin 2g), daily intake of anticoagulants, antiedematous treatment, depletives, anti-inflammatory treatment. the smear detects gram negative bacilli. in the antibiogram culture, no germs developed after 5 days of incubation. the skin threads are suppressed seven days postoperatively. the patient is then sent to an infectious disease department for further treatment. at discharge, the patient is in good condition, conscious, cooperative, with partially remitted aphasia and almost completely remitted right hemiparesis. figure 9. postoperative cerebral ct scan that shows the complete removal of the abscess. case 2 – conservative approach the 35-year-old patient is hospitalized in the 4th neurosurgery service of “bagdasar arseni” emergency hosptial for visual field disorders and balance disorders with sudden onset approximately 24 hours ago. the cerebral mri scan performed by the patient revealed multiple intracranial expansive processes in etiological observation. based on the investigations carried out, the associated pathology (infective endocarditis with klebsiella and streptococcus), the clinical and neurological 404 george popescu, marius c. zaharia, ana-maria georghiu et al. consultation, the diagnosis of multiple cerebral abscesses is established. figure 10. expansive intracerebral processes, mostly supratentorial, one millimeter infratentorial, with an mri appearance suggesting an infectious substrate brain abscesses. a whole-body ct-scan was performed and showed liver abscess as well. figure 11. liver lesion with a ct appearance suggestive of an infectious inflammatory substrate (abscess). the condition and its therapeutical options are presented to patient and her relatives (surgical for the right occipital lesion, conservative according to the antibiotic scheme recommended on the "wait and see" principle) and they opt for conservative treatment, in full knowledge of the possible risks/benefits. under maximum antibiotic treatment (meropenem 6g/day, vancomycin 2fl/day, gentamicin 80mg 2fl/day) associated with symptomatic treatment (corticosteroid with dexamethasone), the patient's evolution is slowly favorable, with quasi-total remission of symptoms at the time of discharge. imaging investigations (repeated head ct, repeated cerebral mri) show the dimensional decrease of infectious processes from the liver and brain. figure 12. mri 4 weeks after conservative treatment. regression of the lesions. she was discharged almost four weeks later, afebrile, conscious, cooperative, without neurological deficits and referred to cardiovascular department for the surgical intervention in the field of cardiovascular surgery. she will return for clinical and imaging follow-up according to the schedule. figure 13. comparison of the lesions at admission (right) vs discharge (left). at two months follow-up check, patient’s clinical and neurological state were improved. mri performed showed an important downsize of the main two foci (right occipital lesion and left parietal lesion) and the complete remission of other lesions (fig. 14). figure 14. 2 months after discharge mri. important shrink of the main foci (right occipital lesion and left parietal lesion) and complete remission of the other lesions. no edema was emphasized. 405 brain abscess – a still high mortality medical condition discussion in ba therapy, antimicrobial therapy is crucial. thus, identifying the pathogen is crucial for an accurate antimicrobial treatment. unfortunately, in too many cases, the agent remains unknown and empiric treatment is required. in our clinic, the pathogen was not identified in 65% of cases (25 cultures were sterile and in five cases patients chose the conservative treatment). therefore, seven patients lost their lives in the process, despite the maximal therapy. m al masalma et al [32] the authors used ribosomal dna amplification and achieved pathogen identification in 9 of 21 culture‑negative ba, identified 44 distinct bacterial species not previously described in ba, and determined polymicrobial infections at a significantly higher rate than by culture. this way more targeted treatments could be used for a better outcome of the patients. even though brain abscesses are more frequently identified in low/middle-income countries, they did not completely disappear from developed countries. in developed countries, most cases of ba occurred at immunocompetent patients after surgical interventions such as neurosurgical interventions or after professional tooth cleaning procedures, as lp pallesen et al described in their article [25]. however, brain abscesses remain one of the most feared neurosurgical intervention complication. in the last decades, the number of ba increased in developed countries due to a higher number of neurosurgical intervention. the surgical approach evolved as well in the last decades. aspiration of the abscesses proved to be safe and with similar results compared to classic surgery. furthermore, stereotactic guided aspiration of the ba proved to be superior to classic surgery in the hardly accessible areas such as infratentorial space. k. elango et al [26] presented in their paper the stereotactic ct-guided aspiration of a brainstem abscess of a 38 years old female. the patient clinical and neurological state were improved after surgical intervention and aggressive antibiotic therapy. furthermore, the authors consider ct-guided aspiration the best approach for deep lesions such as a brainstem abscess due to its minimally invasiveness and minimal morbidity and mortality [33], [34]. conclusion brain abscesses remain a high challenge to manage even in the 21st century. rapid broad spectrum antibiotic treatment should be applied as soon as possible until the pathogen is identified and specific treatment will be used. signs of intracranial pressure, midline shift >5 mm or abscesses >3 cm should be strong arguments for an invasive approach of the lesion. even though less invasive surgical approaches were developed in the last decades (such as stereotactic ct-guided aspiration) the evolution of the patients is hard to predict due to their primary foci and their comorbidities. conservative treatment is worth trying in cases with multiple lesions, located deep or in eloquent areas, with dimensions smaller than 3 centimeters, in cases where we know the pathogen and the starting point and the patient's neurological condition allows this. references 1. muzumdar d. central nervous system infections and the neurosurgeon: a perspective. international journal of surgery (london, england). 2011;9(2):113-6. 2. mathisen ge, johnson jp. brain abscess. clinical infectious diseases. 1997 oct 1:763-79. 3. menon s, bharadwaj r, chowdhary a, kaundinya dv, palande da. current epidemiology of intracranial abscesses: a prospective 5 year study. journal of medical microbiology. 2008 oct 1;57(10):1259-68. 4. bernardini gl. diagnosis and management of brain abscess and subdural empyema. current neurology and neuroscience reports. 2004 dec;4(6):448-56. 5. moorthy rk, rajshekhar v. management of brain abscess: an overview. neurosurgical focus. 2008 jun 1;24(6):e3. 6. sharma bs, gupta sk, khosla vk. current concepts in the management of pyogenic brain abscess. neurology india. 2000 apr 1;48(2):105. 7. ersin e, tufan c. pyogenic brain abscess. neurosurg focus 2008;24(e2):1e10. 8. kielian t, esen n, liu s, phulwani nk, syed mm, phillips n, nishina k, cheung al, schwartzman jd, ruhe jj. minocycline modulates neuroinflammation independently of its antimicrobial activity in staphylococcus aureus-induced brain abscess. the american journal of pathology. 2007 oct 1;171(4):1199214. 9. salzman c, tuazon cu. value of the ring-enhancing sign in differentiating intracerebral hematomas and brain abscesses. archives of internal medicine. 1987 may 1;147(5):951-2. 10. chauvet d, sainte-rose c, boch al. the mystery of prehistoric trepanations: is neurosurgery the world eldest profession?. neuro-chirurgie. 2010 oct 1;56(5):420-5. 11. canale dj. william macewen and the treatment of brain 406 george popescu, marius c. zaharia, ana-maria georghiu et al. abscesses: revisited after one hundred years. journal of neurosurgery. 1996 jan 1;84(1):133-42. 12. king jej. the treatment of the brain abscess by unroofing and temporary herniation of abscess cavity with avoidance of usual drainage methods, with notes on the management of hernia cerebri general. surg gynecol obstet 1924;39:554e68. 13. dandy we. treatment of chronic abscess of the brain by tapping: preliminary note. journal of the american medical association. 1926 oct 30;87(18):1477-8. 14. sargent p. remarks on drainage of brain abscess. british medical journal. 1928 dec 12;2(3543):971. 15. heineman hs, braude ai, osterholm jl. intracranial suppurative disease: early presumptive diagnosis and successful treatment without surgery. jama. 1971 dec 6;218(10):1542-7. 16. vincent c. sur une méthode de traitement des abcès subaigus des hémisphères cérébraux: large décompression, puis ablation en masse sans drainage. gaz méd de fr. 1936 feb 1;43:93-6. 17. moorthy rk, rajshekhar v. management of brain abscess: an overview. neurosurgical focus. 2008 jun 1;24(6):e3. 18. yang sy. brain abscess: a review of 400 cases. journal of neurosurgery. 1981 nov 1;55(5):794-9. 19. hanamsagar r, hanke ml, kielian t. toll-like receptor (tlr) and inflammasome actions in the central nervous system. trends in immunology. 2012 jul 1;33(7):333-42. 20. konat gw, kielian t, marriott i. the role of toll‑like receptors in cns response to microbial challenge. journal of neurochemistry. 2006 oct;99(1):1-2. 21. mathisen ge, johnson jp. brain abscess. clinical infectious diseases. 1997 oct 1:763-79. 22. kawamata t, takeshita m. patent foramen ovale as a possible risk factor for cryptogenic brain abscess: report of two cases. neurosurgery. 2002 mar 1;50(3):674-5. 23. horiuchi y, kato y, dembo t, takeda h, fukuoka t, tanahashi n. patent foramen ovale as a risk factor for cryptogenic brain abscess: case report and review of the literature. internal medicine. 2012;51(9):1111-4. 24. pallesen lp, schaefer j, reuner u, leonhardt h, engellandt k, schneider h, reichmann h, puetz v. multiple brain abscesses in an immunocompetent patient after undergoing professional tooth cleaning. the journal of the american dental association. 2014 jun 1;145(6):564-8. 25. mace se. central nervous system infections as a cause of an altered mental status? what is the pathogen growing in your central nervous system?. emergency medicine clinics. 2010 aug 1;28(3):535-70. 26. calfee dp. wispelwey (2000). inbrain abscess. seminars in neurology (vol. 20, pp. 353-60). 27. campioli cc, almeida ne, o'horo jc, garrigos ze, wilson wr, cano e, desimone dc, baddour lm, van gompel jj, sohail mr. bacterial brain abscess: an outline for diagnosis and management. the american journal of medicine. 2021 oct 1;134(10):1210-7. 28. lai ph, ho jt, chen wl, hsu ss, wang js, pan hb, yang cf. brain abscess and necrotic brain tumor: discrimination with proton mr spectroscopy and diffusion-weighted imaging. american journal of neuroradiology. 2002 sep 1;23(8):1369-77. 29. de louvois j. bacteriological examination of pus from abscesses of the central nervous system. journal of clinical pathology. 1980 jan 1;33(1):66-71. 30. legg nj, gupta pc, scott df. epilepsy following cerebral abscess a clinical and eeg study of 70 patients. brain. 1973 jun 1;96(2):259-68. 31. hirata s, kobayashi m, ujihara m, takabatake k, wakiya k, fujimaki t. aspiration surgery with appropriate antibiotic treatment yields favorable outcomes for bacterial brain abscess. world neurosurgery. 2022 sep 1;165:e317-24. 32. al masalma m, lonjon m, richet h, dufour h, roche ph, drancourt m, raoult d, fournier pe. metagenomic analysis of brain abscesses identifies specific bacterial associations. clinical infectious diseases. 2012 jan 15;54(2):202-10. 33. patel k, clifford db. bacterial brain abscess. the neurohospitalist. 2014 oct;4(4):196-204. 34. chen mh, kao hw, cheng ca. complete resolution of a solitary pontine abscess in a patient with dental caries. the american journal of emergency medicine. 2013 may 1;31(5):892-e3. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/ roneuro-2019-081 a lateral meningocele in a 48 years lady revealed by a csf fistula. exceptional case ibrahim assoumane,nadhim benmedakhene, adakal ousseini, bachir sabrina, nadia lagha, sidi said abderahmanne, abdelhalim morsli romanian neurosurgery (2020) xxxiv (1): pp. 85-88 10.33962/roneuro-2019-081 www.journals.lapub.co.uk/index.php/roneurosurgery a lateral meningocele in a 48 years lady revealed by a csf fistula. exceptional case ibrahim assoumane1,2, nadhim benmedakhene1, adakal ousseini3, bachir sabrina1, nadia lagha1, sidi said abderahmanne1, abdelhalim morsli1 1 department of neurosurgery chu bab el oued, algiers, algeria 2 department of neurosurgery maradi reference hospital, niger 3 department of general surgery, faculty of health sciences, university of maradi, niger abstract background: lateral meningocele is defined by the presence of protrusions of the arachnoid and the dura matter extending laterally through interor intravertebral foramina. it is an extremely rare condition; to the best of our knowledge, only a few cases are reported in the literature and most of them in childhood. case presentation: authors reported a case of a 48 years old lady who consulted for a lombo-sacral mass right-sided with a csf fistula. the spinal mri objectified a meningocele lateralized in the right side associated with multiples malformations. the patient underwent surgery and the meningocele was closed after excision of the associated subcutaneous lipoma. the long-term outcome was favourable and the follow up was assured by clinical examination monthly in the first year. conclusion: lateral meningocele is very rarely reported, it is usually associated with multiples malformations. surgical treatment is a good option for treatment for avoiding complications. the prognostic depends on the preoperative status and the associated malformations. introduction lateral meningocele is defined by the presence of protrusions of the arachnoid and the dura matter extending laterally through interor intravertebral foramina. these often occur in the setting of marfan syndrome, neurofibromatosis type 1or lateral meningocele syndrome but may also be seen as isolated anomalies. it is extremely rare condition, and only few cases are reported in the literature and most of them in childhood. the most reported cases are in thoracic and cervical regions. the localization at the sacral spine is very infrequent [1] here we report the management of a fistulized lumbo sacral lateral meningocele in a 48 years old lady in the department of neurosurgery of bab el oued teaching hospital of algiers algeria. keywords lateral, meningocele, spinal sacral corresponding author: ibrahim assoumane department of neurosurgery chu bab el oued, algiers, algeria assoubrahim18@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 86 ibrahim assoumane, nadhim benmedakhene, adakal ousseini et al. case presentation madame b n aged of 48 years with past medical history of surgical intervention for a right foot deformation consulted in the emergency unit of our department for cerebro spinal fluid (csf) leaking in the lumbosacral region through a small mass. the patient reported that she was born with a small mass in the lumbo sacral region but any investigation was performed and she never consulted for. one year before, she was victim of a traffic accident and since date the volume of the mass grows progressively with the extension toward the right side. at the admission the clinical exam found conscious patient in good general health, temperature 37 degre celcius, complaining of back pain and a paraparesia coted 4/5, a right clubfoot with stigmas of previous surgical interventions. there was no sensory or sphincter disturbance and no <<café au lait˃˃ lesions. in the lumbo sacral region right sided there was a mass of 15 cm of size, well epidermised with large implantation base (figure 1). through the masse there was a fistula of cerebro spinal fluid (csf). the biological investigations are normal; spinal mri (figure 2) objectified a spinal cord extension up to s1 and a subcutaneous liquid mass extending to the right sacral region as a meningocele. this investigation revealed other malformations; a tethered spinal cord at s1 level, a subcutaneous lipoma, a malformative l2-l3 fusion. we operated the patient under general anesthesia, on prone position. we performed an “ogive fashion” skin incision, after the excision of the subcutaneous lipoma, we dissected the meningocele and found a fibrous stalk attached in the wall of the meningocele, this fibrous element was detached before the closure of the meningocele using silk 3/0. (figure 3) the post-operative outcome was marqued by the relief of back pain and improvement of paraparesia. the patient exited from the hospital seven days after surgery with appointment in three days for total removal of sutures. after 3 days the patient came back for the appointment but we discover a liquid collection, we use a needle gauge to carry out a puncture of 125 cc of serum bloody. the bacteriological study revealed a staphylococcus a coagulase negative. we put her under acetazolamide 250mg twice daily, oxacillin 1g bid daily. the evolution was uneventful and the patient was discharged from the hospital after 7 days of treatment with appointment in one month. she was followed up monthly and after 2 years there is no complaint. she recovered the motor disturbance with the help of physiotherapy. figure 1. pre-operative image of the mass in the lumbo sacral region right sided. figure 2. spine mri showed a spinal cord extension up to s1 and a subcutaneous liquid mass extending to the right sacral region as a meningocele. figure 3. per operative image showing the walls of the meningocele. 87 a lateral meningocele in a 48 years lady revealed by a csf fistula discussion meningomyelocele are the most common forms of neural tube defects. lateral presentations are extremely rare [2, 5], the incidence of lateral meningoceles was reported to be 0.3% [4] these lateral presentations often occur in the setting of marfan syndrome or neurofibromatosis type 1but our patient did not present any café au lait lesions. lateral meningocele is also seen in lateral meningocele syndrome. this syndrome is a rare disorder, originally described by lehman et al. in 1977 [3]; patients with lateral meningocele syndrome present widened spinal canal with scalloping of the posterior surfaces of the vertebral bodies and multiple lateral meningoceles, frequently associated with distinctive craniofacial features such as downslanting palpebral fissures, ptosis, mandibular hypoplasia, a high palate, and skeletal abnormalities such as hypoplasia of the posterior arch of the atlas, short stature, scoliosis, and kyphosis [3], our patient did not present any distinctive craniofacial features. to the best of our knowledge lateral meningocele in adult not associated with marfan syndrome or neurofibromatosis type 1or lateral meningocele syndrome has not been published earlier. many meningomyelocele often are associated with tethered cord [2]. some authors reported that lateral meningoceles are usually associated with vertebral defects such as hemivertebrae, scoliosis, absence of neural arches on the affected side, and widening of the spinal canal and intervertebral foramina. scalloping of the pedicles, laminae and vertebral bodies that are adjacent to the meningocele result in an enlarged spinal canal. butterfly vertebra and segmental anomalies of the vertebral bodies may be found in as many as 43% of affected patients. sacral anomalies, such as confluent sacral foramina and partial sacral agenesis, occur in up to 50% of reported cases [6,7]. our patient presented many associated malformations, a tethered spinal cord at s1 level, a subcutaneous lipoma, and a malformative l2-l3 fusion. a patient with lateral meningoceles may remain asymptomatic or may suffer from paraparesis or back pain [8]. chronic symptoms in lateral meningoceles usually arise when meningeal protrusions compress against or deform the adjacent structures such as vertebral bodies, nerves, and viscera. the index patient presented a mass since birth but the clinical sign were back pain and paraparesia. the consultation was motivated by the csf fistula upon the right sacral mass. patient leaving in some regions did not come to consultation early because of ignorance or poverty. surgical closure is the treatment of choice, because the lateral meningocele does not have spontaneous regression and generally progresses its enlargement with a corresponding increase in the risk of complications like bladder or bowel dysfunction or neurological deficits. surgical excision may be indicated in cases where giant and symptomatic cysts are present and they are causing bladder or bowel dysfunction or neurological deficits [9]. conclusion lateral meningocele is a very rarely reported entity and only few published cases are reported in the literature. surgical treatment is a good option of treatment avoiding complications. the prognostic depends on pre-operative status and the associated malformations. conflict of interests none references 1. erkulvrawtr s, el gammal t, hawkins j: intrathoracic meningoceles and neurofibromatosis. arch neurol 1979, 36:557-559. 2. g raghavendra prasad, tm rashmi, lateral meningomyelocele in a neonate: a case report, journal of neonatal surgery 2016; 5(1):4. 3. alves d, sampaio m, figueiredo r, lea˜o m. 2013. lateral meningocele syndrome: additional report and further evidence supporting a connective tissue basis. am j med genet part a 161a:1768–1772. 4. gripp kw, scott ci jr, hughes he, wallerstein r, nicholson l, states l, bason ld, kaplan p, zderic sa, duhaime ac, miller f, magnusson mr, zackai eh: lateral meningocele syndrome: three new patients and review of the literature. am j med genet 1997, 70:229-239. 5. shetty ds, lakhkar bn: lateral sacral lipomeningomyelocele: a rare anomaly. neurol india 2002, 50:204-206. 6. philip n, andrac l, moncla a, sigaudy s, zanon n, lena g, choux m: multiple lateral meningoceles, distinctive facies 88 ibrahim assoumane, nadhim benmedakhene, adakal ousseini et al. and skeletal anomalies: a new case of lehman syndrome. clin dysmorph 1995, 4:347-351. 7. heckly a, carsin b, poulain p: diagnosis-related pitfall of a lateral sacral cyst. j neurosurg spine 2005, 2:72-74. 8. mizuno, j, nakagawa h, yamada t, watabe t, 2002. intrathoracic giant meningocele developing hydrothorax: a case report. j. spinal disord. tech. 15, 529–532. 9. gohar mushtaq a,b, iqbal hussain c, jalaluddin a, khan a, mohammad a, kamal. lateral meningocele with asymmetric canal stenosis: a case study. saudi journal of biological sciences (2015) 22, 102–105. doi: 10.33962/roneuro-2020-069 an uncommon intracranial malign tumour which was misdiagnosed as glioblastoma multiforme: hemangiopericytoma serdar ercan, turan kandemir, zeki serdar ataizi romanian neurosurgery (2020) xxxiv (1): pp. 434-436 doi: 10.33962/roneuro-2020-069 www.journals.lapub.co.uk/index.php/roneurosurgery an uncommon intracranial malign tumour which was misdiagnosed as glioblastoma multiforme: hemangiopericytoma serdar ercan1, turan kandemir2, zeki serdar ataizi2 1 eskisehir city hospital, department of neurosurgery, eskisehir, turkey 2 yunus emre state hospital, department of neurosurgery, eskisehir, turkey abstract background. hemangiopericytoma (hpc) which is mostly located at the lower extremity and visceral organs was found extremely rare in the central nervous system. radiological images are not enough to differentiate hpc from other cns tumours. the case was analyzed to determine presurgical features for diagnosis and the challenges during surgery. case. a 65-year-old male patient with headache was diagnosed as glioblastoma multiforme (gbm) considering the image findings. however, the intraoperative macroscopic shape and tendency to bleeding were not relevant to the gbm. the mass was reported as hemangiopericytoma which is a malign tumour, originates from pericapillary bodies of veins, and commonly locates out of the cns. conclusion. even in advanced age and radiologically considered high-grade glial tumours, hpc should be considered in the differential diagnosis for preoperative preparation. introduction hemangiopericytoma (hpc), which is mostly located in the musculoskeletal system and the skin, is rarely seen in the central nervous system. it mostly locates in the lower extremities, retroperitoneum and pelvis 1,2. it accounts for 2% of meningeal tumors, less than 1% of all central nervous system (cns) tumors1,3. hpc, first reported by begg 4, originates from the zimmerman pericytes around the capillary and postcapillary veins 1. it is a highly malignant tumor with a tendency to local and distant metastases. it is very difficult to distinguish radiologically from the glial and meningeal tumors observed in the central nervous system 5. our aim is to present the difficulties encountered during intraoperative treatment of hpc, which is rarely located in the cns and radiologically mixed with high grade glial tumor. keywords hemangiopericytoma, diagnosis, central nervous system, surgery corresponding author: serdar ercan eskisehir city hospital, department of neurosurgery, eskisehir, turkey srdrercn@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 435 an uncommon intracranial malign tumour: hemangiopericytoma case report a 65-year-old male patient had a headache and dizziness for about 1 month. he was diagnosed with benign positional vertigo and received medical treatment, but did not recover. the patient, who started complaining of weakness and nausea 3 days ago, worsened gradually and started to vomit and prone to sleep for 1 day. he was admitted to the emergency room with unconsciousness and the occipital mass was detected in the ct scan (figure 1). the patient underwent contrast mr imaging in intensive care unit and a preliminary diagnosis of glioblastoma multiforme (gbm) was made radiologically, which was presented with edema, peripheral contrast, necrotic areas in the center (figure 2). when the mass of the patient was reached during the operation performed under general anesthesia, it was observed that the mass was very smooth and shiny surface, rather fragile, bleeding tendency, but easily dissected in the surrounding tissues. when frozen sample was sent to pathology, it was reported that the mass was extremely malignant, but the diagnosis could not be made before immunohistochemical staining. mass excision was performed by performing difficult bleeding control. it was observed that the mass was removed close to total by postoperative imaging. hpc was diagnosed after further pathological examination of the removed mass. after histopathological diagnosis, radiotherapy was planned and the patient was discharged in good condition. the patient who presented with the same complaints after 3 months showed that the mass recurred as large as the preoperative volume. the patient was missing while preparing for reoperation. discussion intracranial hpc is a malignant tumor that makes up less than 1% of all cns tumors. the location in cns is extremely rare. it tends to locate in the lower limbs and intra-abdominal visceral organs 3. unlike other meningiomas, it is more common in young men (3844 years) and tends to be supratentorial 6. it is very difficult to differentiate hpc with benign meningioma before surgery 5. differential diagnosis can be made by observing multilobulate mass and dural connection in ct and mri imaging. in addition, osteolytic areas can be observed in x-ray and ct imaging. however, in our patient, there was no multilobulate mass and osteolytic area images in preoperative imaging (figure 1 and 2). there was an edematous mass image with peripheral contrast, necrotic areas in the center. considering the current imaging findings and the patient's age, primarily gbm was considered and surgical planning was done accordingly. however, it was understood that the character of the tumor was different due to its intraoperative macroscopic shape and the mass tending to bleed. since meningeal artery bleeding is common during hpc surgery, preoperative arterial embolization is recommended to prevent bleeding 7. tumor embolization also reduces the operationrelated mortality and morbidity rate 3. hpc tends to recur, especially in primer surgical localization. distant organ metastases are frequently observed 8. 5-year life after postoperative adjuvant radiotherapy has been reported as 57% 9. however, despite our patient's radiotherapy, relapse was observed after 3 months and was mortal. figure 1. there was no osteolytic bone lesion in ct images. figure 2. due to the peripheral contrast enhancing and the central necrosis, the preliminary diagnose was glioblastoma multiforme. 436 serdar ercan, turan kandemir, zeki serdar ataizi conclusion hpc is a highly malignant tumor, which is more common in young men and rarely seen in cns. it is quite difficult to make a preoperative diagnosis. multilobulence in ct and mri imaging and osteolytic bone lesions are valuable for preliminary diagnosis. even in advanced age and radiologically considered high grade glial tumors, hpc should be considered in differential diagnosis for preoperative preparation. unlike other glial tumors, preoperative tumor embolization should be planned since hpc tends to bleed more. in addition, since the distant metastasis of hpc is common, the whole-body scan must be performed. declaration of interest: none submission declaration: we confirm that this study is an original contribution, has not been published before and is not currently being considered for publication elsewhere. consent for publication: science the patient died, the family were given detailed information of the procedure and informed written consent was obtained from them. references 1. horten bc, urich h, rubinstein lj, montague sr. the angioblastic meningioma: a reappraisal of a nosological problem: light-, electron-microscopic, tissue, and organ culture observations. j neurol sci. 1977;31(3):387–410. 2. stout ap, murray mr. hemangiopericytoma: a vascular tumor featuring zimmermann’s pericytes. ann surg. 1942;116(1):26. 3. alen jf, lobato rd, gomez pa, boto gr, lagares a, ramos a, et al. intracranial hemangiopericytoma: study of 12 cases. acta neurochir (wien). 2001;143(6):575–86. 4. begg cf, garret r. hemangiopericytoma occurring in the meninges. case report. cancer. 1954;7(3):602–6. 5. chiechi m v, smirniotopoulos jg, mena h. intracranial hemangiopericytomas: mr and ct features. am j neuroradiol. 1996;17(7):1365–71. 6. schröder r, firsching r, kochanek s. hemangiopericytoma of meninges. ii. general and clinical data. zentralbl neurochir. 1986;47(3):191–9. 7. matsushige t, nakaoka m, yahara k, shinagawa k, ohnuma h, shibukawa m, et al. single-stage operation for a giant haemangiopericytoma following intracranial feeder embolization. j clin neurosci. 2007;14(2):162–7. 8. galanis e, buckner jc, scheithauer bw, kimmel dw, schomberg pj, piepgras dg. management of recurrent meningeal hemangiopericytoma. cancer interdiscip int j am cancer soc. 1998;82(10):1915–20. 9. stessin am, sison c, nieto j, raifu m, li b. the role of postoperative radiation therapy in the treatment of meningeal hemangiopericytoma—experience from the seer database. int j radiat oncol biol phys. 2013;85(3):784–90. doi: 10.33962/roneuro-2020-046 cerebral revascularization by ec-ic bypass in ischemic conditions of different etiologies forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi, maliha hakim, sharif uddin khan, mainul haque sarker romanian neurosurgery (2020) xxxiv (1): pp. 308-320 doi: 10.33962/roneuro-2020-046 www.journals.lapub.co.uk/index.php/roneurosurgery cerebral revascularization by ec-ic bypass in ischemic conditions of different etiologies forhad h. chowdhury1, mohammod raziul haque2, jalal uddin mohammod rumi1, maliha hakim1, sharif uddin khan1, mainul haque sarker2 1 national institute of neurosciences and hospital, shere-e-bangla nagar, dhaka, bangladesh 2 dhaka medical college and hospital, dhaka, bangladesh abstract background: even after the failure of ec-ic bypass trial, ecic bypass can help many patients in preventing future stroke. here we present a case series of patients with cerebral ischemia from different etiological modes who underwent ec-ic bypass with positive end results. methods: patients in these cases series with tia/stroke/recurrent stroke were evaluated clinically for the history of tia or recurrent/hemodynamic tia (in rest or during work) or progressive hemiparesis/aphasia/visual disturbances or sudden hemiplegia/hemiparesis/aphasia with subsequent significant (days to a week) recovery. mri of the brain was done in ischemic protocol in all cases. to see the arterial pathology dynamic cta was also done in all cases except one case. dsa was done in 03 cases. when clinical features, cerebral ischemia on mri and arterial stenosis/occlusion on angiogram were concordant with each other, only then cerebral revascularization was done. after bypass, all patients were followed up regularly. all recorded data were reviewed retrospectively. results: total no. of cases were 08. the most common presentation was hemiparesis. etiologies were infective thrombosis of ica, orbital cellulitis, thrombosed giant ica aneurysm, single & multiple vessel occlusion and mca stenosis. high flow ec-ic bypass was done in one case. stamca bypass was done in rest of the cases. all patient were ambulant with static neuro-status without new stroke till last follow up. all bypasses were patent and functioning till last follow up (clinical, doppler/imaging). conclusion: in carefully selected cases cerebral revascularization in ischemic conditions can result positive outcome. introduction after introduction by yasargil in 1967, cerebral revascularization by ecic bypass has become an indispensable tool for managing patients with hemodynamic ischemia, or for managing patients with complex aneurysms or skull base tumors; that are not amenable to radical resection; because of major vascular involvement. [2,14] patients with keywords cerebral revascularization, ec-ic bypass, ischemic conditions, different etiologies corresponding author: forhad hossain chowdhury assistant professor. neurosurgery. national institute of neurosciences and hospital, shere-e-bangla nagar, dhaka, bangladesh forhadchowdhury74@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 309 cerebral revascularization in ischemic conditions hemodynamic ischemia have an annual stroke rate of 25%, which increases by 2% every year.[14] they can develop a fatal stroke. this category also includes moya moya disease. [14,18] after failure of ec-ic bypass trial, neurosurgeons were in search of cases where ecic bypass would help the patients in preventing future stroke and neurological improvement. here we present a case series of patients with cerebral ischemia from different etiological modes underwent ec-ic bypass with positive end results. methods patients in these cases series with tia/stroke/recurrent stroke were evaluated clinically for history of tia or recurrent/hemodynamic tia (in rest or during work) or progressive hemiparesis / aphasia / visual disturbances or sudden hemiplegia / hemiparesis / aphasia with subsequent significant (days to week) recovery. permanent hemiplegia cases were not included in this case series. then the cases were evaluated neuro-radiologically for cerebral ischemia with or without infarct/s and possible cerebral revascularization by ec-ic bypass. ct scan of head was done to exclude hemorrhage and other pathology such as tumor. mri of brain was done in ischemic protocol (all images including dw, adc, pw, dti and mra&mrv including neck vessels) to see cerebral ischemic zone/s (dw& pw mismatch), cortico-spinal tract & other major tracts and intracranial or extracranial arterial stenosis. to see the arterial pathology dynamic cta was also done in all cases except one case. dsa was done in 03 cases. when clinical features, cerebral ischemia on mri and arterial stenosis/occlusion on angiogram were concordant with each other, only then cerebral revascularization by ec-ic bypass was done. after bypass all patient were followed up regularly (clinically and radiologically). all recorded data were reviewed retrospectively. all bypass operation was done from january 2015 to march 2018 representative cases case 1 (table 1, 2; figure 1 a, b, c) a 38 years old male presented with headache, vomiting, dropping of left eyelid and visual disturbance. left sided visual acuity reduced to finger count with left sided complete opthalmoplegia. ct scan of head showed pansinusitis with skull base osteitis. mri of head showed pan-sinusitis with both cavernous sinus involvement and right parietal infarct (figure 1a-a,b&c). he under went diagnostic endoscopic rhino-sinuscopy, which showed rhino-sinusitis involving all sinuses & nose with pseudo-membranes. biopsy reported inflammatory sinusitis. fungal and tubercular cultures were negative. routine bacterial culture revealed methicillin resistances staphylococcus aureus (mrsa). then he was put on high dose injectable antibiotic for three week that resulted significant radiological improvement (figure 1ad,e&f) and then patient was discharged with oral antibiotic for three month. three weeks after discharge he again presented with altered level of consciousness and right sided hemiplegia (ue>le, muscle power in right ue mrc grade1/5 and in lower limb 2/5) and motor aphasia. mri of head showed resolving rhino-sinusitis with patchy infarcts and ischemic zone involving frontoparieto-occipital zones especially on left side and old infarct on right parietal area (figure 1b). mra showed bilateral complete occlusion of ica and whole brain was perfused by basilar artery (figure1c-a&b). on urgent basis the patient underwent left-sided stamca bypass. figure 1. operation under ga the patient was positioned typically supine 310 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. with the head turned more than 60°. at this point, we used digital palpation technique and a handhold doppler probe to map out the course of the sta both frontal and parietal branches. the incision was started at the level of the zygoma and carried up to near midline behind the hairline. both branches were procured up to superior temporal line very carefully to avoid thermal damage or avulsion injury for branches. papaverine solution and plain local anesthetic agent (2% lidocaine) was used to irrigate the sta for prevention of vasospasm. a mini pterional craniotomy was done very carefully (not to damage the procured sta). after durotomy a small posterior sylvian split was done to find out a suitable m3 as a recipient vessel for bypass. among the frontal and parietal branch the suitable and larger frontal branch was used to make a sta-mca anastomosis. after bypass patency was check clinically and with micro-doppler. dura was loosely closed around the sta (not water tight). along the temporal margin of bone flap a portion was removed so that the sta would not be kinked or compressed by the bone. mini plates and screws were used to fix the bone flap. rest of the wound was closed accordingly without drain. postoperative course patient recovered well from anesthesia. in postoperative days the patient recovered hemiparesis quickly. by the end of 7th pod patient became ambulant. by the end of 04 weeks after operation he returned to his professional work and muscle power on right side body improved at the level of mrc grade 4+/5. post-operative ct scan showed no hematoma or new infarct. cta showed patent sta-mca bypass on left side (figure 1c-c&d). case 2 (table 1, 2; figure 2 a, b, c) a 55 years old policeman presented with recurrent occasional episode of fall during walking without loss of consciousness or convulsion and unable to move right side of body with aphasia lasting for 7-10 minutes. the frequency of events increases last few months and reached 3-5 times/day for last few days before presented to us. he was on adequate anti platelet therapy. he was a smoker but non-diabetic and non-hypertensive. ct scan of head showed multiple infarcts especially in left cerebral hemisphere. cta showed absent both va and left ica (figure 1a) with scarcity of left. mca, pca and posterior fossa vessels. mri of brain showed multiple old infarcts with ischemic areas especially in left hemisphere and ischemic zone in left pica area. he was advised for urgent cerebral revascularization. but the patient developed left pica infarct 06 hours before the scheduled ‘urgent ‘operation (figure 2ba&b). in this situation we proceeded for cerebral revascularization by left-sided cca-ra-mca high flow bypass by keeping in mind that posterior fossa decompression might be needed at any time. figure 2a. figure 2b. figure 2c. operation under general anesthesia with endotracheal intubation patient was placed in supine position. head was fixed with 3-pin head holder with neck extension and head turning to the opposite (right) side (300). head end of the table was elevated (200). 311 cerebral revascularization in ischemic conditions eye, ear, pressure points and nerves areas were protected. left upper limb placed on a side ‘limb rest’ in extended elbow, 300 abducted from the trunk in supine for radial artery procurement. after preparation, left front of the forearm, right side of the neck and left pterional areas were draped properly. with longitudinal incision, radial artery was harvested from brachial bifurcation at elbow to wrist (20 cm). the artery was distended with intraluminal injection of heparin and papaverine mixed normal saline. then the artery was kept in heparin and papaverine mixed normal saline. the forearm wound was closed with a drain. a curve incision on the left side of the neck was made from the tip of mastoid and extended downward & medially 2cm posterior to the angle of mandible to the mid line. after cutting platysma and investing deep fascia sternocleidomastoid muscle was retracted laterally. with further dissection posterior belly of digastric muscle, hypoglossal nerve, internal jugular vein, common carotid, internal carotid and external carotid artery with its branches were identified. a left-sided pre-coronal post hairline curvilinear incision was made and superficial temporal artery (sta) and its parietal branch was procured and prepared for sta-mca insurance bypass as donor artery. a temporally extended pterional craniotomy was done. temporal bone was removed down to the middle fossa floor. in the cervical wound, a blunt index finger dissection was made in between the digastric muscle and hypoglossal nerve upward and superiorly to styloid process and then finger dissection was continued upward, medially & anteriorly to lateral pterigoid plate. a curved medium sized artery forceps was passed from middle fossa floor to the fingertip and with finger guidance the arterial tip was brought out into the cervical wound and then a 26fr thoracostomy tube was passed from cervical wound to the middle fossa floor. radial artery (ra) graft was passed from middle fossa floor to cervical wound through the tube. with stabilization of both ends of ra graft thoracostomy tube removed. ra graft was made twist free by injecting heparinized solution into the lumen. after durotomy a sta –mca (temporal m4) ‘insurance bypass’ was done with 10/0 nylon and checked for patency and function with micro doppler (figure 2b-c). after sylvian dissection temporal m2 was identified and prepared for bypass. cranial end of ra graft was also prepared for bypass and the ra graft and temporal m2 bypass was made after systemic heparinization with 3000 unit of injection heparin (figure 2b-d). the patency of anastomosis was checked by retrograde flow of blood through the caudal end of ra graft in cervical wound. with the control of common carotid artery (cca) an anastomosis was made between caudal end of ra graft and cca (figure 2b-e&f). the patency and flow through the anastomoses and ra graft were checked with micro doppler. cervical wound and craniotomy wound were closed with drains. postoperative course postoperatively, he was on tab. aspirin and inj. heparin. ct scan on 1st postoperative day (pod) showed no infarct or any gross hematoma (figure). ct angiogram on second pod showed left eca-ragm2 bypass with pre-operative pica infarct without further swelling. post operatively he became noncommunicable and he used shout with inappropriate & slang words especially at night and did not want to take food. gradually these symptoms improved within three weeks and became communicable but improvement of intellectual functions was slow and incomplete. he became continent by three weeks. within one week he could stand and walk though there was some instability. he became fully ambulant without any cerebellar dysfunction by three months. by the end of one year after operation his intellectual and cognitive function returned to near preoperative level and he returned to his job without any further hemodynamic tia. ct scan and cta after one year showed patent bypass without any new infarct. results total no. of cases were 08. six were male and 02 were female. age range was 25-57 (average 38 years). follow up period was12-48 months. details of all cases were shown in table 1 &2 (figure 1-7). most common presentation was hemiparesis. infection was the etiology of thrombosis of cavernous ica in two cases. in one case orbital cellulitis spread in cs and ica with aneurysm was thrombosed (figure 6-a,b&c). in the other cases pan rhino-sinusitis (of mrsa) spread to both cavernous sinus and both ica was occluded. in one interesting case giant partially thrombosed ica bifurcation 312 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. aneurysm thrombosed totally with distal ica, a1 and m1 (figure 7). acute thrombosis of ica with aneurysm in cs occurred in two female cases where both developed hemiparesis and one was 3 months pregnant. in one case there was intractable tia with impending major stroke where whole brain was supplied by only right sided ica and he developed pica infarct 12 hours before the ‘scheduled urgent” revascularization operation; only high flow ec-ic bypass was done in this case (figure 2a,b&c). post operatively he developed ‘behavioral, intellectual and? psychogenic’ symptoms that recovered slowly. stamca bypass was done in rest of the cases. mca stenosis was the etiology in two cases; one was of 27 years of age (figure 3). average ischemic time was 28 minutes (range 25-35 minutes). there was no clamp related infarction. in one case patient developed postoperative insulo-frontal infarct that not related to temporary clamping (figure 6-c, d & f). all patient improved neurologically. all patient were ambulant with static neuro-status without new stroke/tia till last follow up. all bypass were patent till last follow up (clinical, doppler/imaging). table 1. particulars of cases (age, sex, clinical presentations, investigations and image finding/s). no age/ sex presentation/s investigation/ s image finding/s 1. (figure1) 38/m headache, vomiting, dropping of left eyelid, visual disturbance. left sided visual acuity reduced to finger count with left sided complete opthalmoplegia, three weeks later (on antibiotics): presented with altered level of consciousness and right sided hemiplegia (ue>le, muscle power in right ue mrc grade1/5 and in lower limb 2/5) and motor aphasia ct mri diagnostic sino-nasal endoscopy mri mra pansinusitis with skull base osteitis pansinusitis with both cavernous sinus involvement and right parietal infarct rhino-sinusitis involving all sinuses with pseudomembranes *biopsy-inflammatory sinusitis *culture:fungal-negative, tubercular-negative, routine bacterial culturemultiple antibiotic resistance staphylococcus areus resolving rhino-sinusitis with patchy infarcts and ischemic zone involving fronto-parietooccipital zones especially on left side. old infarct on rt. parietal area. bilateral complete ica block (whole brain is perfused by basilar artery) 2. (figure2) 55/m recurrent episode of fall during walking and unable to move lt. side of body with aphasia,58 times/day before presentation even with ct scan cta multiple infarcts specially in lt. hemisphere absent both va and lt. ica. scarcity of lt. mca, pca and posterior fossa vessels 313 cerebral revascularization in ischemic conditions adequate anti platelet therapy mri mra multiple old infarcts with ischemic areas especially in lt hemisphere. ischemic lt pica area. the pt. developed lt. pica infarct 12 hours before the scheduled ‘urgent ‘operation. 3. (figure3) 27/m h/o tia (recurrent hemiparesis and aphasia), sudden rt. hemiplegia (mrc grade-2/5), and global aphasia mri ct & cta dsa cerebral infarcts and ischemic zones in left hemisphere especially parieto-occipital lobe. ct-cerebral infarcts and ischemic zones in left hemisphere. ctaleft m1 bifurcation stenosis. scarcity of lt. mca vessels left m1 bifurcation stenosis/occlusion with delayed filling of mca territory. 4. (figure4) 45/m headache, left hemiparesis (ue>le, grade1/5) and motor aphasia. h/o tia. oneweek later motor power on left side 2/5. ct cta mri mra right parieto-occipital and right periventricular (corona radiata) infarcts. complete occlusion of right-sided ica from neck to ica bifurcation with decrease vasculatures on right mca zone. right parieto-occipital and right periventricular (corona radiata) infarcts/ischemia with diffusion –perfusion mismatch. tractography showed intact major tracts. complete occlusion of right sided ica from neck to ica bifurcation with decrease vasculatures on right mca zone 5. (figure 5) 27/f sudden headache, eyeache, vomiting, rt. ptosis with complete opthalmoplegia, lt. hemiparesis, 2nd trimester pregnancy mri &mra dsa mri-right cavernous sinus thrombosis with ‘target’ sign. mra-occlusion of rt. ica with giant cs ica aneurysm (thrombosed). scarcity of rt. mca vessels rt. ica occlusion with scarcity of blood flow in rt. mca 6. (figure 6) 25/f fever, lt. proptosis, headache, eyeache, vomiting, lt. ptosis with complete opthalmoplegia, rt. hemiparesis ct scan mri & mra ct-lt eye proptosed otherwise normal mri-lt cavernous sinus thrombosis with ‘target’ sign. lt eye was proptosed. 314 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. mra-occlusion of lt. ica with cs ica aneurysm (thrombosed). scarcity of lt. mca vessels with m1 narrowing 7. 57/m h/o tia with motor dysphasia and hemiparesis. rt. hemiparesis (3/5) and global aphasia ct scan & cta mri mra ct-left gangliocapsular, periventricular, parietal and frontal small infarct/ischemias. ctaleft m2 (upper trunk occlusion) and m2(lower trunk stenosis) left gangliocapsular, periventricular, parietal and frontal small infarst/ischemias. left m2 (upper trunk occlusion) and m2(lower trunk stenosis) 8. (figure7) 35/m initially headache, visual disturbance. later visual problem improved with progressive left. spasticity and hemiparesis (3/5) ct &cta mri ct & cta (4month later) dsa right ica bifurcation giant partially thrombosed aneurysm right sided giant partially thrombosed aneurysm aneurysm size decreased to less than half. anterior corona radiata infarct. no aneurysm on cta with occlusion of rt. ica bifurcation. scarcity of rt. mca vessels non-visualization of right ica bifurcation, a1 and m1 with aneurysm. delayed filling of right mca territory through cortical anastomoses. right ica only supplied the right pca through pcom [m-male,f-female, h/o-history of, rt/rt-right, lt/lt-left, ue-upper extremity, le-lower extremity, tia-transient ischemic attack, mrcmedical research council, ct-computed tomography, cta-ct angiogram, mri-magnetic resonance imaging, mramr angiogram, dsa-digital subtraction angiogram, ica-internal carotid artery, mca-middle cerebral artery, pca-posterior cerebral artery, pcomposterior communicating artery, cs-cavernous sinus, pica-posterior inferior cerebellar artery, va-vertebral artery] table 2. etiology of infarct/ischemia, indication of operation, surgical treatment, complication/s and outcome of bypass. no etiology indication/s surgical treatment complication outcome 1. (figure 1) bilateral complete occlusion of ica due infective inflammatory involvement of cavernous sinus acute on chronic hemodynamic ischemia of whole brain specially icas territory. left sta-mca bypass none opthalmoplegia, hemiparesis and aphasia recovered completely. rhinopansinusitis resolved completely 315 cerebral revascularization in ischemic conditions 2. (figure 2) chronic occlusion of three out of 04 intracranial arteries caused hemodynamic stroke and ischemia chronic and hemodynamic ischemia specially left hemisphere and cerebellum radial graft high flow ec-ic (cca-ra-m1) bypass with insurance stamca bypass early post operative periodbehavioral changes behavioral changes recovered. no hemodynamic tia. 3. (figure 3) acute occlusion of m1 bifurcation on chronic mca stenosis acute on chronic ischemia left sta-mca bypass (parietal) none almost near total recovery of neurodeficit. 4. (figure 4) complete occlusion of right ica from neck. ischemic right cerebral hemisphere (with infarcts) specially mca territory right stamca bypass none hemiparesis improved (mrc grade-4-/5). aphasia improved to dysphasia 5. (figure 5) sudden ica occlusion with occlusion of giant aneurysm in cs ica ischemic hemiparesis (with cs thrombosis) sta-mca bypass with decompression of cs none hemiparesis and opthalmoplegia recovered completely. normal delivery of healthy baby 6. (figure 6) sudden ica occlusion with occlusion of aneurysm in cs ica due to orbital cellulitis spread in to lt. cs ischemic hemiparesis (with infective cs thrombosis) sta-mca bypass with decompression of cs. c/s of cs purulent content injectable antibiotic (long term) anterior insular cortex and broca’s area infarctmotor dysphasia hemiparesis, dysphasia, opthalmoplegia recovered completely 7. acute occlusion of m2 on chronic stenosis acute on chronic ischemia left double sta –mca bypass (parietal and temporal) none motor recovery-near normal, global aphasia converted to sensory aphasia 8. (figure 7) thrombosis of giant aneurysm with progressive occlusion of ica bifurcation right mca territory ischemia right stamca bypass none hemiparesis improved (mrc grade-4/5). 316 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. figure 3a. figure 3b. figure 4a. figure 4b. 317 cerebral revascularization in ischemic conditions figure 5a. figure 5b. figure 6. figure 7. discussion in 1961, pool and potts [2,9] first attempted cerebral revascularization with a synthetic graft using a plastic tube to create a superficial temporal artery (sta) to anterior cerebral artery shunt but angiography showed thrombosed tube though patient recovered and survived. in 1963, woringer and kunlin [11] performed the first extracranial to intracranial (ec-ic) bypass of the common carotid artery cca – intracranial (ic) internal carotid artery (ica) using a saphenous vein (sv) graft but patient did not survive, while the graft was patent on autopsy. in 1967, yaşargil performed the first ec-ic bypass in a patient with an occluded ica.[10] in 1972 yaşargil also started sta-middle cerebral artery (mca) bypass for moyamoya disease. in 1971 lougheed did the first ec-ic bypass using an sv graft, while in 1978 ausman performed ec-ic bypass using a radial artery graft. in the 1970s, sundt et al.[3] and others performed posterior circulation revascularization to treat steno-occlusive disease, vertebrobasilar insufficiency, and unclippable complex aneurysms. ec-ic bypass study (1977-1985) [15] evaluated the result of ec-ic bypass as a means to decrease the subsequent stroke rate for the treatment of “symptomatic atherosclerotic lesions of the ica and/or mca.” but the study failed to show significant difference between the ec-ic bypass group and medically treated group. the study identified two important subgroups that appeared to do ec-ic bypass; 1. patients with severe mca stenosis and 2.those with the persistence of ischemic symptoms in known ica occlusion. ic or mca atherosclerosis results to an ischemic cerebrovascular event through: (1) hypo-perfusion, (2) thrombosis at the site of stenosis, (3) thromboembolism, and (4) direct occlusion of small perforating vessels. [9,16] the clinical presentation may vary from an acute ischemic deficit to intermittent neurological symptoms. the pathophysiologic changes of chronic hypo-perfusion/ischemia have been categorized into three stages stage 0: normal hemodynamics; stage 1: reflex vasodilation in response to inadequate collaterals and a falling perfusion pressure with resultant increases in cerebral blood volume and prolongation of mean transit time, but with preservation of cerebral blood flow (cbf) and normal oxygen extraction fraction (oef); stage 2: misery perfusion in 318 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. response to cerebral perfusion pressure falling below the range of auto-regulatory capability exemplified by falling cbf and increasing oef and maintenance of the cerebral metabolic rate of oxygen (cmro2). [9] progressive mca stenosis, severe stenosis (>70% stenosis), female gender, national institutes of health stroke scale score >1, concurrent diabetes, borderline body mass index values, hyperlipidemia, white ethnicity, and the presence of hemodynamic stenosis increases the risk for stroke. [9] the beginning assessment of transient ischemic attack (tia) or ischemic stroke should include computed tomography (ct) of head to exclude the possibility of ic hemorrhage (and rarely other pathologies such as cavernous sinus mass, giant thrombotic aneurysm etc.) and estimate the extent of ischemic change in consideration of thrombolysis. diffusion-weighted (dw) magnetic resonance imaging (mri) with magnetic resonance angiography (mra) including neck vessels, and perfusion studies can be subsequently obtained to better delineate the extent of infarct and/ ischemia as well as provide more information for further management strategies. [16] tcd, angiography, mra, and computed tomographic angiography [cta]) or parenchymal perfusion (ct perfusion, positron emission tomography [pet], single-photon emission computed tomography [spect], and magnetic resonance perfusion studies are the main neuro radiological evaluations to see the intra cranial flow related pathology. mra and cta both provide excellent detail regarding the caliber of vessels; although, mra has been shown to overestimate the degree of stenosis in some cases. these noninvasive techniques were sufficiently accurate to exclude more than 50% stenosis, but further confirmatory studies were needed to characterize the stenosis and digital subtraction angiography (dsa) is the gold standard. perfusion studies [16] (include pet scans, spect scans, xenon ct perfusion studies, ct perfusion, and perfusion mris) permit the extrapolation of cmro2, oef, and cbf and provide information on the perfusion of the brain. the carotid occlusion surgery study [17] employs measuring oef by pet. since the first sta-mca procedure was described by yasargil, [2,18] many variations have been reported but sta –mca bypass remains the main workhorse of a vascular neurosurgeon. many of these variations have been developed in dealing with complex intracranial aneurysms and skull base tumors. these variations include anastomoses between the bilateral anterior cerebral arteries; occipital artery-to-posterior, inferior cerebral artery (pica), anterior and inferior cerebral artery (aica). others includes pica to pica, vertebral artery to pica, sta to sca or pca, subclavian artery to pca, pca to sca, and even a tandem occipital artery to aica and pica anastomoses. [9] complications in sta-mca bypass are limited and include early postoperative tia, delayed stroke, development of a pseudo-aneurysm, and wound dehiscence. high-flow bypass grafts is more prone to develop complications than low-flow sta-mca bypass. radial artery grafts may suffer vasospasm or intimal hyperplasia and eventually occlude. proatherogenic changes can occur in sv grafts, which eventually leads to occlusion. after parent vessel occlusion thromboembolic complications are common after high flow bypass mainly due to the change in intracranial hemodynamics. preoperative antiplatelet medications, as well as intraoperative anticoagulation, can prevent these thromboembolic events. in patients without vascular reserve, prolonged temporary occlusion times can lead to territory infarcts without changes in the neuromonitoring. so it is important to minimize occlusion times in these patients. in longstanding perfusion deficiency, reperfusion hemorrhage may be problematic after revascularization, though the incidence is low. other complications involve the site of graft harvests such as infection, ischemic hand, or hematoma. [9] here in representative case 1(high flow bypass), there were postoperative behavioral, intellectual and cognitive dysfunctions that recovered slowly. there may be hyper-perfusion of chronically ischemic brain tissue but postoperative radiology did not show any hyper-perfusion signs. retrogradely we thought, could we avoid such complication by giving low flow bypass. most of the ica and other intracranial arterial stenosis or occlusion (acute or chronic) leading to cerebral infarct/ischemia is caused by atherosclerosis predisposing and precipitating by many factors. other causes include dissection, vasculitis, vasospasm and moyamoya disease. [5,13] in this series most of the cases are unique from of etiological point. spontaneous occlusion of 319 cerebral revascularization in ischemic conditions cavernous ica was reported in the literature but such occlusion associated with cerebral ischemia was not reported.[8] infection from paranasal sinuses or orbit usually spread into cavernous sinus but usually does not occlude the ica; in case of fungal infection , fungus may erode the arterial wall and can cause mycotic aneurysm with distal embolism or occlusion of ica.[4,12] giant partially thrombosed ica bifurcation aneurysm case, at initial presentation patient refused operation for aneurysm then he returned with left hemiparesis with complete occlusion aneurysm as well as occlusion of parent ica with a1 and m1 (proximally up to pcom). ica was only supplying right pca through pcom. young patient with mca stenosis recovered near to normal neurology. in our series, in a few cases, we did revascularization on urgent basis. nussbaum es et al [6] did emergency ec-ic bypass in patients with acute ischemic injury, which was seemed to be safe and effective where patients were relatively young. they found bypass was successful in arresting progression of stroke, and in some cases resulted in rapid neurological improvement. although the study on ec-ic bypass failed to show a benefit from the bypass procedure nussbaum es et al [7] continued to perform the operation in selected cases. carefully selected individuals with occlusive cerebrovascular disease and persistent ischemic symptoms, despite maximal medical therapy, seem to obtain demonstrable and durable benefit from cerebral revascularization. conclusion in this small series, cases with concordant clinical features, mri findings and angiographic finding underwent bypass surgical procedure and we found such concordances ended up with positive result (though short term) with cerebral revascularization. abbreviations adc-afferent diffusion co-efficient aica-anterior inferior cerebellar artery cbf-cerebral blood flow cca-common carotid artery ctcomputed tomography ctact angiography cs –cavernous sinus dw-diffusion weighted dsa-digital subtraction angiography ecaexternal carotid artery ec-ic extraranial-intracranial ga-general anesthesia ica-internal carotid artery ic-intracranial hemorrhage le-lower extremity mca-middle cerebral artery mri-magnetic resonance imaging mra-magnetic resonance angiography mrsa-mithicillin resistance staplylococcus areus oef-oxygen extraction fraction pca-posterior cerebral artery pcom-posterior communicating pod-post operative day pica-posterior inferior cerebellar artery pw-perfusion weighted pet-positron emission tomography ra-radial artery rag-radial artery graft sca-superior cerebellar artery spect-single photon emission computed tomography sta-superficial temporal artery sv-shapenous vein tcd-transcranial doppler tia-transient ischemic attack ue-upper extremity va-vertebral artery declaration ethics approval and consent to participate – not applicable (na) consent for publication taken from the patients/patient’s party availability of data and materials na competing interests none funding none authors' contributions all author involved in data collection, re-viewing, interpretation and manuscript preparation and its edition acknowledgements none disclosure there is no conflict of interest and nothing to disclose. references 1. baldawa ss, pendharkar h, menon gr, and nair sr. thrombosed giant cavernous carotid artery aneurysm secondary to cervical internal carotid artery dissection: an unusual entity. indian j radiol imaging. 2011 jul-sep; 21(3): 225–227. doi: 10.4103/0971-3026.85373. 2. biswas a, samadoni a e, elbassiouny a, sobh k, and hegazy a. extracranial to intracranial by-pass anastomosis: review of our preliminary experience from a low volume center in egypt. asian j neurosurg. 2015 oct-dec; 10(4): 303–309. doi: 10.4103/1793-5482.162711. 3. eric s. nussbaum, m.d. donald l. erickson, m.d.extracranial-intracranial bypass for ischemic 320 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. cerebrovascular disease refractory to maximal medical therapy neurosurgery, volume 46, issue 1, 1 january 2000, pages 37–43, https://doi.org/10.1093/neurosur gery/46.1.37. 4. failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic stroke. results of an international randomized trial. the ec/ic bypass study group. n engl j med. 1985;313:1191–200. [pubmed: 2865674]. 5. fiedler j, pribán v, skoda o, schenk i, schenková v, poláková s. cognitive outcome after ec-ic bypass surgery in hemodynamic cerebral ischemia. acta neurochir (wien) 2011;153:1303–11. 6. grubb rl, jr, powers wj, clarke wr, videen to, adams hp, jr, derdeyn cp carotid occlusion surgery study investigators. surgical results of the carotid occlusion surgery study. j neurosurg. 2013;118:25–33. [pmcid: pmc4246998] [pubmed: 23101451]. 7. hwang sw, lee sk, david ca. youmans neurological surgery. 6th ed. ch. 355. vol. 4. philadelphia, pa: saunders, an imprint of elsevier inc; 2011. intracranial occlusive disease. 8. kalani my, zabramski jm, hu yc, spetzler rf. extracranialintracranial bypass and vessel occlusion for the treatment of unclippable giant middle cerebral artery aneurysms. neurosurgery. 2013;72:428–35. 9. lee b, kim c, carrasco j. intracranial infectious aneurysm in orbital cellulitis. orbit. 2015; 34(4):175-8. doi: 10.3109/01676830.2015.1014515. epub 2015 may 8. 10. neil ja, r. orlandi rr, and couldwell wt (2016) malignant fungal infection of the cavernous sinus: case report. j neurosurg 124:861–865. doi:10.3171/2015.2.jns142 668]. 11. nussbaum es, janjua tm, defillo a, lowary jl, nussbaum la. emergency extracranial-intracranial bypass surgery for acute ischemic stroke. j neurosurg. 2010 mar;112(3):666-73. doi: 10.3171/2009.5.jns081556]. 12. obusez ec, hui f, hajj-ali ra, cerejo r, calabrese lh, hammad t, et al.. high-resolution mri vessel wall imaging: spatial and temporal patterns of reversible cerebral vasoconstriction syndrome and central nervous system vasculitis.ajnr am j neuroradiol. 2014; 35:1527– 1532. doi: 10.3174/ajnr.a3909. 13. pool dp, potts dg. aneurysms and arteriovenous anomalies of the brain: diagnosis and treatment. new york: harper & row; 1965. 14. sundt tm, jr, whisnant jp, piepgras dg, campbell jk, holman cb. intracranial bypass grafts for vertebralbasilar ischemia. mayo clin proc. 1978;53:12–8. [pubmed: 625139]. 15. swartz rh, bhuta ss, farb ri, agid r, willinsky ra, terbrugge kg, et al.. intracranial arterial wall imaging using high-resolution 3-tesla contrast-enhanced mri.neurology. 2009; 72:627–634. doi: 10.1212/01.wnl.0000342470.69739.b3.crossrefmedline google scholar. 16. thanapal s, duvuru s, sae-ngow t, kato y, and takizawa k. direct cerebral revascularization: extracranialintracranial bypass. asian j neurosurg. 2018 jan-mar; 13(1): 9–17. doi: 10.4103/ajns.ajns_76_17. 17. woringer e, kunlin j. anastomosis between the common carotid and the intracranial carotid or the sylvian artery by a graft, using the suspended suture technic. neurochirurgie. 1963;9:181–8. [pubmed: 14076765]. 18. yaşargil mg. microsurgery applied to neurosurgery. stuttgart: georg thieme verlag, academic press; 1969. diagnosis and indications for operations in cerebrovascular occlusive disease; pp. 95–118. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-007 mechanical thrombectomy techniques for acute ischemic stroke a. chiriac, georgiana ion, n. dobrin, dana turliuc, i. poeata romanian neurosurgery (2020) xxxiv (1): pp. 46-51 doi: 10.33962/roneuro-2020-007 www.journals.lapub.co.uk/index.php/roneurosurgery mechanical thrombectomy techniques for acute ischemic stroke a. chiriac, georgiana ion1, n. dobrin1, dana turliuc, i. poeata 1 “gr. t. popa” university of medicine and pharmacy, iasi, romania 2 “prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract mechanical thrombectomy technique was introduced as an effective and secure method in acute ischemic stroke patients suffering from intracranial large vessel occlusion (lvo). in this article, we will review the main mechanical thrombectomy techniques and current trends in this type of treatment for acute ischemic stroke. introduction the large global studies have shown that stroke is the second most common cause of death and third commonest cause of disability in the world. the proven limitations of intravenous and intra-arterial thrombolysis for performing large vascular occlusion recanalization resulted in the introduction of mechanical thrombectomy (mt). this was also favoured by technological advances in endovascular neurosurgery with better catheters, to allow more distal access and more effective devices for efficient intravascular thrombus penetration and capture. starting with 2015, the role of mechanical thrombectomy for the occlusion of large vessels in acute ischemic stroke has been scientifically proven with the publication of seven randomized controlled trials that demonstrated better outcomes compared to medical management alone. mechanical thrombectomy evolved from the first generation of thrombus penetration devices, to the direct thrombus-aspiration systems and then to the second generation of devices represented by stent retrievers. in this article we will review the main mechanical thrombectomy techniques and current trends in this type of treatment for acute ischemic stroke [1,2]. the limitations of intravenous thrombolysis have led to the exploration of alternative or complementary treatment approaches for acute ischemic stroke (ais). endovascular mechanical thrombectomy has developed over the past years as a safe and efficient intervention for ais treatment. the fast advancement in catheter and endovascular device technology has led to an increasing number of techniques used in mechanical thrombectomy in patients suffering from an emergent large vessel occlusion. keywords mechanical thrombectomy, acute ischemic stroke corresponding author: a. chiriac “prof. dr. n. oblu” clinic emergency hospital, iasi, romania chiriac_ a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 47 mechanical thrombectomy techniques for acute ischemic stroke clot retriever technique the need to improve the vascular recanalization technique correlated with reducing the risk of cerebral haemorrhage by limiting thrombolytic administration has led to the development of the first mechanical thrombectomy devices. the first steps in the appearance of mechanical thrombectomy devices were performed by dr. y. pierre gobin of the university of california, los angeles, who patented an endovascular device similar to a crib for the recovery of an accidentally released foreign body (usually coils) in the cerebral vasculature. due to its limited use the device was subsequently taken over and licensed by concentric medical, inc. and called the mechanical embolus removal in cerebral ischemia (merci) retriever. the merci retriever is a corkscrew shape device with helical nitinol loops specifically designed and tested for distal placement and enbloc removal of the thrombus for first time approved by fda in 2004. this technique involves physical extraction of the thrombus through a catheter (figure 1). even though this device has benefited from considerable redesigning in time, all versions were preferably used in conjunction with an 8or 9-f balloon guiding catheter to reduce the risk of distal emboli [4,10]. the target vessels were the proximal segments of major cerebral arteries, predominantly m1 segments of the middle cerebral and vertebrobasilar arteries. merci and multi-merci trials were prospective, nonrandomized, multicenter, and single-arm trials that reported the safety and efficacy of merci device in patients presenting with moderate to severe stroke (national institutes of health stroke scale niha score ≥8) from a large-vessel occlusion and treated within 8 hours of symptom onset[2,4,10]. figure 1: clot retriever technique self-expanding stents technique based of development of the retrieval clot technique, attempts to use self-expanding stents for the purpose of assisting and restoring cerebral revascularization have been reported. intracranial angioplasty with self-expanding stents was described for the treatment of acute ischemic stroke due to intraarterial atherosclerotic lesions. even if high rates of stent placement success were achieved immediate and delayed complications were brought into discussion (figure 2). figure 2: self-expanding stents technique distal emboli due to stent detachment, intra-stent thrombosis or re-stenosis as well as potential haemorrhagic risk of concurrent prophylactic antiplatelet and anticoagulation therapy are just a few of the limitations of the frequent use of this technique. initial evaluation of the wingspan stent stent in the saris pilot study (ischemic stroke assisted recanalization) in patients with contraindicated or not available intravenous thrombolysis showed a 100% recanalization rate and a 45% favorable clinic evolution at 90 days. a 10% stent related complications was also reported[3,5]. thrombus aspiration technique the first attempts of thrombectomy by manual suction were described by the use of catheters 48 a. chiriac, georgiana ion, n. dobrin et al. placed in front of the thrombus and by the manual generation of suction through syringes connected to the hub of the catheter, with excellent results [5,11]. in december 2007, the penumbra (ps) system for aspiration of clots (penumbra, inc., alameda, ca) was the second fda approved device in the treatment of acute ischemic stroke. this technique involves the use of a large lumen catheter device that is advanced through a guide catheter to a point near occlusion, in contact with the clot. in the case of non-adherent clots, with easy mobilization, after capturing them at the top of the suction catheter, it is withdrawn slowly, maintaining the continuous aspiration at a vacuum pump. simultaneous aspiration is also applied to the lateral port of the intracranial access system (sheath or guide catheter) to prevent thrombus displacement from the tip of the suction catheter, because it is retracted into the sheath. in the case of adherent clots, a microwire called separator is repeatedly passed through the thrombus to disconnect / fragment the clot, and the constant suction is applied to the ps catheter to aspirate the thrombus fragments. figure 3: direct aspiration first pass technique the introduction of large and flexible suction catheters has led to the development of a new technique called a direct aspiration first pass technique (adapt), which can be used as the primary way for revascularization. kang et al. first reported the use of direct aspiration thrombectomy [2,5,11]. in their report, tici 2b-3 revascularization was performed in 81.9% of cases. in this technique, the largest possible aspiration catheter is advanced over a microcatheter and microwire (which are used to pass the thrombus and provide stable support for catheter advancement) and positioned immediately adjacent to the occlusion site (figure 3). once the suction catheter is in contact with the thrombus, the microcatheter and microwire are removed, and the suction catheter with the clot is withdrawn into the guiding catheter, while continuous negative pressure is applied. particular attention is given to the moment when the clot is captured, the aspiration forces in the lumen of the vessel are lost and the flow around the intermediate catheter can lead to fragmentation and distal migration during retrieval. this shortcoming can usually be eliminated by using alternating and intermittent aspiration by connecting the continuous aspiration pump tubing into one end of a three-way valve and a 60 cc vacuum syringe. if an optimal control of the catheter advancement exists the aspiration turned on upon contact will be allowed. thus, the suction force on the thrombus becomes appreciable when the catheter is very close to the thrombus (below 1 mm) and may increase until it comes into contact with the thrombus [2,3,4,5]. another important element that needs to be carefully analyzed is the direction of the suction catheter in relation to the vessel / thrombus to minimize the number of passes and several procedures. in situation of unfavorable angles, a microcatheter over microwire can be used to direct the tip of the aspiration catheter when positioned across the occlusion. the microcatheter/microwire can be kept inside the system during aspiration. the continuous technological advances allowed the manufacture of last generation of aspiration catheter systems with larger inner-size, excellent navigability, efficacy, and safety profile. reperfusion catheters such as ace68, ace64 and, more recently, jet7 with a suction lumen of 0.072 ″ (penumbra) are the best examples. a prospective study initiated by the european registry on the ace reperfusion catheters and the penumbra system in the treatment of acute ischemic stroke (promise, nct02678169) showed a mtici 2b-3 revascularization rate of 93.1%, 90-day mrs 0–2 rate of 61% and a 2.9% of sich complication, with 7.5% mortality at 90-days[13]. heit jj, et al. described in 2018 a so called “snake” technique witch is a technical variation of adapt. a sofia catheter (microvention) is advanced into the intracranial circulation without using a guiding wire, microcatheter, or microwire. because the distal end of the sofia catheter is extremely soft and pliable it allows a safe “push” of the catheter into different parts of the circle of willis. when the tip of the sofia 49 mechanical thrombectomy techniques for acute ischemic stroke is successfully reaches the proximal end of the clot, a manual aspiration with a large syringe can be performed, and the sofia catheter is slowly withdrawn into the guide catheter. [1,2,5]. also, the use of smaller thrombo-aspiration catheters such as the penumbra 3 max has been reported to be safe and leading to good reperfusion rates especially for distal locations. stent retriever technique the stent retrievers represent the second generation of mechanical thrombectomy devices with has derived from nondetachable neurovascular stents used for aneurism coiling support. the introduction of these devices was an important advantage for endovascular treatment of ais, offering the advantage of navigability and rapid recanalisation of a stent without the potential long-term complications. the detachable solitaire intracranial stent (covidien/ev3; plymouth, mn) turned into a primary clot retriever. the tehchnique utilize a retrievable stent that is advanced within a microcatheter through the thrombus until a few millimeters distal to the clot. thus, the stent is deployed capturing the thrombus into the stent struts and displacing it peripherally to the vessel wall thus restoring blood flow. after 3-5 minutes, the microcatheter and stent retriever are simultaneous removed under continuous proximal aspiration with a syringe (figure 4). figure 4: stent retriever technique some improved variants of this technique have also been described in the literature. haussen et all described an alternative to the conventional unsheathing technique of the stent retriever called push and fluff technique or “active deployment”. this particular deployment maneuver consists in positioning the stent retriever across the clot and unsheathing the distal end of the device until good wall apposition (anchoring) is achieved (brief unsheathing step). then, forward force is applied to the device delivery wire, leading to spontaneous retraction of the microcatheter (pushing step). at the main clot area, additional forward tension is applied to the microcatheter while the delivery wire continues to be pushed to maximize the device struts expansion into embolus (fluffing step). the major concern related to this technique was the potential association with adverse events related to the addition of radial force or forward movement of the device especially in curved vessels. the reports a higher first-pass reperfusion success (modified tici 2b-3 with the first pass), 58% of final full reperfusion and a lower number of overall passes compared to conventional unsheting technique[6]. dual stent retriever technique was proposed as alternative thrombectomy technique in case of “saddle” bifurcation occlusion. this technique involves the use of two different or identical types of stents retriever that are inserted in parallel or in a y configuration, with both tips ending in separate bifurcation limbs. the both stent delivery microcatheters require to be placed across the two targeted branches, and then one after another the stent retrievers are deployed at one point. both stents are gradually retrieved out of the guiding catheter to optimize clot dislodgement. klisch and colleagues, reports an increased median total recanalization time of 60 minutes (interquartile range 45 to 87 minutes) compared with standard mechanical thrombectomy using single-stent retrieval (range 20 to 48 minutes). complete recanalization (tici 2b/3) was achieved in 8 out of 10 cases, with good clinical outcomes (m rankin scale score of 2 or less) in 5 patients[2,7,8]. figure 5: dual stent retriever technique 50 a. chiriac, georgiana ion, n. dobrin et al. combined treatment aspiration-retriever technique also sometime called “solumbra” due to combination of solitaire stent retrieval and a penumbra aspiration catheter. the technique use a triaxial system which includes an aspiration catheter, a microcatheter and s microwire. the microcatheter over microwire is advanced through the thrombus and the stent retrieval is deployed across the embolus. then, the aspiration distal access catheter is advanced close to the proximal end of the stent retrieval in close contact with the thrombus. if necessary the microcatheter can be retracted further to clear the tip of the aspiration catheter optimizing the integration with the thrombus. at the end, the stent retrieval is retracted while continuous negative suction is applied through a pump or manually with an aspiration syringe (figure 6) [8,10]. figure 6: aspiration-retriever technique the prospect technique (proximal balloon occlusion together with direct thrombus aspiration during stent retriever thrombectomy) is combining the use of bgc with large bore distal aspiration catheters that are navigated to the face of the thrombus before retrieving the clot with a stent retriever device. the series of cases published in the literature regarding the use of the prospect technique in the treatment of acute ischemic stroke have shown that the rate of thrombus fragmentations can even be further reduced and the rate of complete and particularly complete first-pass reperfusions can be further increased (figure 7) [5,9]. the late version of this technique, called protectplus is characterized by the fact that the stent retriever loaded with the clot is not primarily retracted into the aspiration catheter but drawn into the bgc as a unit while aspiration is applied to both the aspiration catheter and the bgc. maegerlein et all have published in 2018 a study showing that using the protectplus resulted in a higher rate of first pass complete reperfusions (59.4% vs. 27.7%, p< 0.001) as compared with protect. the protectplus also led to shorter procedure times (21min vs. 37min, p= 0.001) and higher rates of overall complete reperfusion (73.5% vs. 49.5%, p= 0.014)[5,9,12]. figure 7: prospect technique conclusions mechanical thrombectomy approach in large vessel occlusion appears to be a promising method of endovascular stroke treatment, due to a significant increase in the rate of complete first-pass reperfusions and good clinical recovering. mechanical thrombectomy using the combined techniques seems to be effective, fast and safe with high rates of near-complete and complete reperfusion. references 1. alvarez mc., mccarthy dj., samir sur, snelling bm., starke m. (2017) comparing mechanical thrombectomy techniques in the treatment of large vessel occlusion for acute ischemic stroke, world neurosurg. apr;100:681-682. 2. al-bayati, a. r., nogueira, r. g., samaniego, e. a., & haussen, d. c. (2019). mechanical thrombectomy: techniques and hybrid approaches for recanalization. in acute stroke management in the era of thrombectomy (pp. 87-103). springer, cham. 3. asadi h, dowling r, yan b, wong s, mitchell p. advances in endovascular treatment of acute ischaemic stroke. intern med j. 2015;45:798–805. 4. becker, k. j., & brott, t. g. (2005). approval of the merci clot retriever: a critical view. stroke, 36(2), 400-403. 5. chueh, j. y., kang, d. h., kim, b. m., & gounis, m. j. (2020). role of balloon guide catheter in modern endovascular thrombectomy. journal of korean neurosurgical society, 63(1), 14–25. https://doi.org/10.3340/jkns.2019.0114 51 mechanical thrombectomy techniques for acute ischemic stroke 6. haussen, d. c., rebello, l. c., & nogueira, r. g. (2015). optimizating clot retrieval in acute stroke: the push and fluff technique for closed-cell stentrievers. stroke, 46(10), 2838-2842. 7. klisch j, sychra v, strasilla c, et al. double solitaire mechanical thrombectomy in acute stroke: effective rescue strategy for refractory artery occlusions? ajnr am j neuroradiol 2015;36:552–6. 8. lapergue, b., labreuche, j., blanc, r., marnat, g., consoli, a., rodesch, g., ... & duhamel, a. (2020). combined use of contact aspiration and the stent retriever technique versus stent retriever alone for recanalization in acute cerebral infarction: the randomized aster 2 study protocol. journal of neurointerventional surgery. 9. maegerlein, c., berndt, m. t., mönch, s., kreiser, k., boeckh-behrens, t., lehm, m., ... & friedrich, b. (2018). further development of combined techniques using stent retrievers, aspiration catheters and bgc. clinical neuroradiology, 1-7. 10. massari, f., henninger, n., lozano, j. d., patel, a., kuhn, a. l., howk, m., ... & wakhloo, a. k. (2016). arts (aspiration– retriever technique for stroke): initial clinical experience. interventional neuroradiology, 22(3), 325-332. 11. munich, s. a., vakharia, k., & levy, e. i. (2019). overview of mechanical thrombectomy techniques. neurosurgery, 85(suppl_1), s60-s67. 12. puri, a. s., & parthasarathy, r. (2019). aspiration retriever technique in stroke (arts). in 100 interesting case studies in neurointervention: tips and tricks (pp. 359362). springer, singapore. 13. schramm, p., navia, p., papa, r., zamarro, j., tomasello, a., weber, w., ... & gralla, j. (2019). adapt technique with ace68 and ace64 reperfusion catheters in ischemic stroke treatment: results from the promise study. journal of neurointerventional surgery, 11(3), 226-231. doi: 10.33962/roneuro-2021-009 rcbv and adc based grading of gliomas with glimpse into radiogenomics seema rohilla, ambresh r. deodurg, pritviraj s. kanakavvanavar, ishwar singh, veena gupta, dhara b. dhaulakhandi romanian neurosurgery (2021) xxxv (1): pp. 52-65 doi: 10.33962/roneuro-2021-009 www.journals.lapub.co.uk/index.php/roneurosurgery rcbv and adc based grading of gliomas with glimpse into radiogenomics seema rohilla1, ambresh r. deodurg1, pritviraj s. kanakavvanavar1, ishwar singh2, veena gupta3, dhara b. dhaulakhandi4 1 department of radiodiagnosis & imaging. post graduate institute of medical sciences, pt. b.d. sharma university of health sciences, rohtak, india 2 department of neurosurgery. post graduate institute of medical sciences, pt. b.d. sharma university of health sciences, rohtak, india 3 department of pathology. post graduate institute of medical sciences, pt. b.d. sharma university of health sciences, rohtak, india 4 department of biotechnology & molecular medicine. regional cancer centre. post graduate institute of medical sciences, pt. b.d. sharma university of health sciences, rohtak, india abstract purpose. the present study was carried out to study the role of relative cerebral blood volume (rcbv), apparent diffusion coefficient (adc) and mr spectroscopy in grading gliomas to help the surgeon plan the approach and extent of surgery as well as judge the need for any adjuvant radio/chemotherapy. methods. 65 patients with glioma were prospectively studied with mri. basic mr sequences (t1w, t2w, t2w/flair) were followed by diffusion-weighted (dw) imaging with b value of 1000 (minimum adc values used for analysis). then the patients were administered gadobenate dimeglumine/ meglumine gadoterate in a dose of 0.1mmol/kg at a rate of 4ml/sec after which 20ml of saline was flushed at a rate of 4ml/sec and t2*w/ffe dynamic images were acquired; dynamics showing maximum fall in the intensity were used for creating rcbv and rcbf maps and calculating rcbv. single voxel spectroscopy (svc) was done using the press sequence with intermediate te of 144ms. naa/cr, cho/cr, cho/naa, cho+cr/naa and naa/crn ratios (naa from the tumour, crn from the normal side) were calculated. results. grade i gliomas showed minimum adc>0.84x10-3mm2/s and maximum rcbv<1.9ml/100gm, grade ii gliomas showed min adc 0.75-0.84x10-3mm2/s and max rcbv of 1.9-2.6ml/100gm, grade iii had min adc of 0.70-0.75x10-3mm2/s and max rcbv of 2.7-3.0ml/100gm, while grade iv tumours showed min adc<0.70x10-3mm2/s and max rcbv>3.0ml/100gm. rcbv values were better than adc values in differentiating grade i from ii and grade ii from iii. the adc values were better than rcbv values in differentiating grade iii from grade iv. conclusions. both minimum adc and maximum rcbv within the tumour were significant but these parameters within peritumoural oedema were not significant in grading gliomas. though lipid and lactate (especially lipid) peaks were found more frequently in higher-grade tumours, various spectroscopy parameters were not significant in grading gliomas. preoperative grading of gliomas with the help of keywords glioma, relative cerebral blood volume, apparent diffusion coefficient, mr spectroscopy, radio-genomics, proteomics, radiomic corresponding author: seema rohilla post graduate institute of medical sciences, sharma university of health sciences, rohtak, india seemarohilla@yahoo.co.in copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 53 rcbv and adc based grading of gliomas with glimpse into radiogenomics advanced mr parameters like adc and rcbv can help the surgeon plan the approach and extent of surgery as well as judge the need for any adjuvant radio/chemotherapy. advancing radio-genomic and radiomic technologies can supplement the current radiologic methods of diagnosis and prognosis. introduction the majority of primary brain tumours are gliomas which may be low (grade i and ii) or high (grade iii and iv) grade [1]. the inherent heterogeneity of gliomas makes it difficult to grade them with conventional mri. however, advanced mri techniques such as perfusion, diffusion, spectroscopy and largely experimental molecular imaging can aid in such grading. dynamic susceptibility contrast magnetic resonance (dsc-mr) imaging helps in assessing tumour vascularity and angiogenesis non-invasively by way of decrease in signal intensity with time during the first pass of a bolus of paramagnetic contrast agent. the maximum tumour rcbv tends to increase as the grade of astrocytoma increases. increased cell density reduces brownian motion leading to restricted diffusion and reduced adc. thus, higher the tumour grade, lower the adc. in a tumour, the increase in cell turnover leads to an increase in choline concentration, along with a depression of the naa peak due to loss of healthy glioneural structures. lactate peak suggests hypoxia while lipid peak is suggestive of necrosis, an indicator of malignancy. preoperative grading of gliomas with the help of advanced mr parameters like adc and rcbv (specially in hospital settings which lack stereotactic biopsy facility) can help surgeon plan the approach and extent of surgery as well as judge the need of any adjuvant radio/chemo therapy. relationship between imaging features and genetic/molecular features of tumours can be addressed using radiogenomic methods. continuously evolving “omics” procedures and modalities coupled with advances in basic tumour biology, histopathology, computational and molecular tools can complement imaging as well as genetic analysis. integration of imaging markers derived from clinical images and genomic markers such as egfr, mgmt, idh1, 1p/19q codeletion can be explored in a non-invasive manner [2]. for example, a direct association is found in egfr amplification and contrast enhancement in gbm; illdefined tumour margins and tumour heterogeneity can potentially be used as imaging biomarkers for 1p/19q codeletion in gliomas [3]. application of radiogenomic markers is particularly useful when taking biopsy is not possible. to have a deeper insight into tumour makeup, a wide array of quantitative and qualitative imaging features may be utilized to record distinct imaging phenotypes and link them to genomic profiles. whereas staging signifies the tumour spread, grading signifies the general tumour aggressiveness. hybrid of imaging and genomic techniques have not only led to improved tumour grading assessment by capturing heterogeneity more precisely but have also added refinement to staging. various radiological features like location, lateralization, enhancement characteristics, perfusion parameters, adc, etc. can help assess genetic/molecular make-up to some extent which further help in predicting prognosis and effectiveness of therapy. current and evolving radiogenomic, proteomic and spectroscopic technologies can supplement the current radiologic methods and procedures to help clinicians better equip for making accurate diagnosis and precisely grade gliomas. material and methods 65 patients with glioma were evaluated. basic mri sequences i.e. t1w(te-15 ms, tr-596 ms, field of view(fov)-230 mm, matrix size-(186x256), flip angle69o and nsa-1), t2w(te-100 ms, tr-4431 ms, fov230 mm, matrix size-(236x512), flip angle-90o and nsa-2) and t2w/flair(te-120 ms, tr-6000 ms, fov230 mm, matrix size-(172x256), flip angle-100o ti(time to inversion)=2000 ms and nsa-1) were done in axial, sagittal and coronal plains as per requirement on gyroscan intera nova gradient 1.5 tesla philips imaging system, best, netherlands using a sense head coil (6 channel phased array coil). informed consent was taken from the participants. approval of the dean, faculty of medicine and allied sciences was taken for the study which was conducted in accordance to provisions of institutional ethics committee. diffusion weighted imaging (dwi) was carried out with a single shot echo planar imaging (epi) sequence with a te-89 ms, tr-2609 ms, fov 230 mm, matrix size89x256, flip angle-90o and nsa-3, with a b value of 1000. adc map was calculated by automated software on workstation (view forum version 5.1) and minimum adc values used for analysis. the adc 54 seema rohilla, ambresh r. deodurg, pritviraj s. kanakavvanavar et al. values were calculated in tumours in all 65 cases and in peritumoural edema 56 cases. perfusion weighted imaging (pwi). the patients were given gadobenate dimeglumine/ meglumine gadoterate in a dose of 0.1 mmol/kg at a rate of 4 ml/s followed by saline flush of 20 ml at a rate of 4 ml/s using pressure injector medrad spectrosolaris version 008.001-sa. t2*w/ffe dynamic sequence (te-30 ms, tr-627 ms, fov-230, matrix size-128x128, flip angle-40o and nsa -2) was acquired. rcbv and cbf maps were created on the dynamic showing maximum fall in signal intensity on first pass of contrast bolus. maximum rcbv was calculated with the help of automated software on view forum 5.1. the values were calculated in tumour in all 65 cases and in perirumoral edema in 35 cases. spectroscopy. single voxel spectroscopy (svc) was performed using press sequence with intermediate te of 144 ms. the voxel was placed at most dark area in adc map/maximum enhancing area on contrast mri (scalp and skull bones were excluded from the voxel). two spectroscopy data sets were obtained one from the most malignant appearing area of tumour and another from the corresponding normal white matter. naa/cr, cho/cr, cho/naa, cho+cr/naa and naa/crn ratiosnaa from tumour, crn from normal side were calculated. two sample wilcoxon ranksum (mann-whitney) test, kruskal-wallis equality-of-populations rank test and roc analysis were the statistical tests applied with stata software version 11.2. surgery/biopsy were used as gold standard for final diagnosis. results 65 patients with glioma (4-76 years old with mean age of 41 year) with 49 males and 16 females were studied. basic mr sequences showed tumour appearance on t1w, t2w, flair, and contrast enhanced t1w images (figures 1-3). most of the tumours were hypointense on t1w and hyperintense on t2w images. high grade tumours were more heterogeneous and showed contrast enhancement. haemorrhage and necrosis were more common in grade iv tumours. they were seen less frequently in grade ii and grade iii tumours, were almost equally frequent in grade ii and grade iii tumours and were not seen in grade i tumour. mild enhancement could be seen in some low-grade gliomas also. figure 1. 40yr old female patient with oligodendroglioma in left frontotemporal region (grade ii): (a) axial t1w image showing illdefined hypointense lesion in left frontotemporal region showing area of hemorrhage as hyperintense signal and necrosis as hypointense signal. (b) axial t1w contrast image showing mild heterogenous contrast enhancement. (c) axial t2w image showing illdefined hyperintense lesion with minimal peitumoral edema. (d) coronal t2w/flair image showing the lesion causing mass effect on surrounding parenchyma with midline shift towards right side. 55 rcbv and adc based grading of gliomas with glimpse into radiogenomics (e) axial t2*w first pass perfusion image showing color coded rcbv maps along with time-signal intensity curve and various parameters [ rcbv (negative integral), rcbf (index map),mtt and ttp ],rcbv being 1.9ml/100gm. even though the lesion appeared high grade on morphological features the parameters showed low grade and was proved to be grade ii oligodendroglioma. figure 2. 52 yr old female patient with anaplastic astrocytoma in right frontal lobe (grade iii): (a) axial t1w image showingilldefinedhypointense lesion with hemorrhagic areas seen as hyperintense signal seen in right frontal lobe. (b) axial t1w contrast image showing mild heterogenous contrast enhancement. (c) axial t2w image showing the lesion as heterogeneously hyperintense and peritumoral edema as hyperintense signal. (d) coronal t2w/flair image showing the hyperintense mass in right frontal lobe no significantmass effect noted. (e) axial diffusion weighted image showing patchy areas of diffusion restriction seen as hyperintense signal, corresponding area is seen as hypointense signal in adc map. minimum adc value calculated was 0.614x10-3mm2/ sec. (f) dwi and adc maps showing minimum adc value calculated from the peritumoraledema which was 1.621x103mm2/sec. (g) axial t2*w first pass perfusion image showing color coded rcbv maps along with timesignal intensity curve and various parameters [ rcbv (negative integral), rcbf (index map),mtt and ttp ],rcbv being 3.6ml/100gm. 56 seema rohilla, ambresh r. deodurg, pritviraj s. kanakavvanavar et al. dwi tumour areas which showed diffusion restriction appeared hyperintense on dw images and hypointense on adc maps. the adc values obtained for different tumour grades were analysed. dwi in tumour population rank test for adc values in tumour according to different grades showed a probability of 0.0001(highly significant). box plot showing distribution of adc values with respect to grades is shown in figure 4(a). roc curve analysis is shown in figure 4(b-d). the summary statistics [sensitivity, specificity, accuracy, area under the curve (auc), standard error and 95% confidence interval for differentiating various grades based on different cut off values of adc] are shown in table 1. the range of adc values for different tumour grades is as shown in table 2. dwi in peritumoural edema population rank test for adc values in edema according to different tumour grades showed a p value of 0.4386. since p value is more than 0.05 this parameter is not significant in assessing tumour grades. figure 4. a. box plot showing distribution of adc vaues; b. roc curves showing adc values forgrade i v/s grade ii; c. roc curves showing adc values for grade ii v/s grade iii; d. roc curves showing adc values for grade iii v/s grade iv. pwi pwi in tumour population rank test for maximum rcbv values in tumour according to different grades showed a p value of 0.0002. since p value is well below 0.05, the parameter was highly significant in grading tumours. box plot showing distribution of maximum rcbv values in tumour with respect to various grades is shown in figure 5(a). roc curve analysis for this data is shown in figure 5(b-d). the summary statistics [sensitivity, specificity, accuracy, auc, standard error and 95% confidence interval for differentiating various grades based on different cut off values of rcbv] are shown in table 1. the range of rcbv values in various grades is shown in table 2. figure 5. a. box plot showing distribution of rcbv values; b. roc curves showing rcbv values forgrade i v/s grade ii; c. roc curves showing rcbv values forgrade for ii v/s grade iii; d. roc curve showing rcbv values for grade iii v/s grade iv. pwi in periumoural edema population rank test for maximum rcbv values in edema according to different grades showed a p value of 0.1362. since the p value is well above 0.05, the parameter is not significant in grading tumours. percentage signal (%) drop in tumour another parameter obtained on perfusion studies is % drop in intensity. kruskal-wallis equality-ofpopulations rank test for %drop showed a p value of 0.0004. since the p value is less than 0.05, %drop significantly co-related with tumour grade. box plot 57 rcbv and adc based grading of gliomas with glimpse into radiogenomics showing distribution of % drop values with respect to grades is shown in figure 6(a). roc curve analysis is shown in figure 6(b-d). the summary statistics [sensitivity, specificity, accuracy, auc, standard error and 95% confidence interval for differentiating various grades based on different cut off values of percentage drop] are shown in table 1. the range of % drop values with respect to various grades is as shown in table 2. parameter cut off value sensitivity (%) specificity (%) accuracy (%) area under the curve standard error 95% confidence interval grade i vs ii adc value 0.84x10-3 mm2/s 66.67 67.86 67.69 0.8145 0.0684 0.680420.94855 rcbv 1.9 ml/100 g 75 75 75 0.8538 0.0708 0.715000.99359 percentage drop 9 % 88.24 100% 89.29 0.9255 0.0367 0.853540.99744 grade ii vs iii adc value (x10-3 mm2/s 0.75x10-3 mm2/s 71.43 70 70.77 0.7905 0.0593 0.674340.90667 rcbv 2.6 ml/100 g 76.67 76.47 76.56 0.8475 0.0493 0.750940.94415 percentage drop 18 % 70.37 68.97 69.64 0.7618 0.0651 0.634250.88938 grade iii vs iv adc value 0.70x10-3 mm2/s 78.72 77.78 78.46 0.8706 0.0470 0.778530.96260 rcbv 3 ml/100 g 72.22 71.74 71.87 0.7947 0.0584 0.680260.90911 percentage drop 22 % 75 75 75 0.7937 0.0700 0.656650.93085 table 1. table showing summary statistics for different values of adc, rcbv and percentage drop in relation to tumor grades. tumor grade adc value (x10-3 mm2/s) rcbv value (ml/100 g) % drop grade i >0.84 <1.9 <9 % grade ii 0.75-0.84 1.9-2.6 9-18 % grade iii 0.70-0.75 2.7-3.0 19-22 % grade iv <0.70 >3.0 >22 % table 2. table showing range of adc, rcbv and % drop values in various tumor grades figure 6. a. box plot showing distribution of percentage (%) drop values; b. roc curves showing % drop values for grade i v/s grade ii; c. roc curves showing % drop values for grade ii v/s grade iii; d. roc curves showing % drop values for grade iii v/s grade iv. comparision of adc values and rcbv values for grading the rcbv values were better than adc values in differentiating grade i from grade ii and grade ii from grade iii. the adc values were better than rcbv values in differentiating grade iii from grade iv as shown by comparison of auc of adc and maximum rcbv for different grades (table 3). grades auc for adc auc for rcbv i vs ii 0.8145 0.8538 ii vs iii 0.7905 0.8475 iii vs iv 0.8706 0.7947 table 3. table showing auc for adc vs rcbv for different grades 58 seema rohilla, ambresh r. deodurg, pritviraj s. kanakavvanavar et al. spectroscopy kruskal-wallis equality-of-populations rank test showed a p value of 0.505 for naa/cr, 0.2058 for cho/cr, 0.6782 for cho/naa, 0.1275 for cho+cr/naa and 0.5660 for naa/crn. since the p value of all spectroscopy parameters were more than 0.05, these parameters were not significant in grading tumours. hence the further statistical analysis was not done. discussion therapeutic strategies, prognosis, and monitoring response to therapy depend on accurate grading of gliomas [4]. gliomas, specially gbm exhibit both spatial and temporal heterogeneity which allows them to adapt quickly. spatial heterogeneity leads to inadequate sampling of tumour at biopsy which may lead to error in classification. in two of our patients, temporal heterogeneity was evident as radiologically they were grade iii while pathologically, they were grade ii. both the patients deteriorated within six months of diagnosis, hence pointing towards higher grade. this may have been due to sampling error during biopsy. temporal heterogeneity leads to treatment failure and disease progression. one of our patients had grade i tumour transformed to grade iii in which adc dropped from 1.2 to 0.8 x103mm2/s and rcbv increased from 1.1 to 3.2ml/100g. patient remained stable for 4 years, after which there was increased frequency of seizures, refractory to drugs at which stage, mri showed it to be grade iii. the patient died after 1 year. mr imaging can be used to grade astrocytomas into low-grade astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme [5] and may help in management when the clinical course appears to be at odds with the neuropathologic diagnosis. crossing midline, edema, signal heterogeneity, haemorrhage, border definition, cyst formation or necrosis and mass effect are some of the mri features which can aid in predicting grade [6]. necrosis was seen in 83.3% of glioblastoma multiforme (gbm) and 50% of anaplastic astrocytomas, irregular margins in 100% of gbm and anaplastic astrocytomas and haemorrhage in 55% of gbms in our study. gbm most commonly showed edema (100%). corpus callosum involvement was an indicator of higher grade. conventional mr imaging, which depends on contrast enhancement, mass effect, edema, and necrosis for grading, is not always accurate for grading of gliomas. contrast enhancement may be seen in some low grade gliomas while some highgrade tumours do not show enhancement. advanced mr imaging techniques such as diffusion and perfusion imaging can help in such grading [5]. who formulated new guidelines in 2016 which emphasized integration of genetic makeup in classifying tumours. after conception of radiogenomics consortium in 2009, it is well known that distinct sub regions of tumours identifiable by mr imaging have distinct gene expression patterns [7,8]. radiogenomics improved the diagnostic capability of even conventional mr imaging. deep machine learning has increased the amount and accuracy of data by picking up subtle features that could not be picked up by even experienced radiologists. age, gender, location, lateralization, signal intensity, enhancement pattern, surrounding edema and morphology of the tumour tell a lot about molecular subtypes and genetic profiling, based on which treatment selection, prognosis and follow-up can be decided. ring like enhancement, large size with significant necrosis and temporal lobe (posterior subventricular, to be more precise) location suggest primary gbm, while frontal lobe location, homogeneous enhancement and young age suggest secondary gbm which has better prognosis [9]. the molecular subtypes of gbm are best predicted by edematous/tumour infiltrated volume and total tumour volume [10]. idh-mutated gliomas can be differentiated from idh wild type with 98% accuracy based on single lobe confinement, significant nonenhancing tumour, frontal lobe localization, large tumour size and presence of cysts and satellite lesions. mgmt methylated tumours show mixed nodular enhancement, small amount of edema, moderately elevated rcbv, and increased ktrans [11]. ring enhancement with necrosis suggest unmethylated mgmt-promoter region [12]. frontal tumours are commoner in younger patients (<55 years) while elderly mostly have more posterior tumours [13]. this was clearly seen in our 40 year old patient with frontal tumour (fig.1) and 58 year old patient with parietal tumour (fig.3). lower necrosis volume is seen in gbm in female patients. higher necrosis volume in females predicted poor outcome [12]. gbms in temporal lobe are likely to show egfr amplification and egfrv viii mutation and show good effect of chemoradiation [12]. mgmtmethylated gbms have predilection for left 59 rcbv and adc based grading of gliomas with glimpse into radiogenomics hemisphere and mgmtnonmethylated ones for right hemisphere [12]. in childhood brainstem gliomas, pontine involvement suggests high grade glioma (h3 k27 m mutant). pilocytic astrocytoma, medulloblastoma {mainly sonic hedgehog (shh) subtype or type 3} and atypical teratoid rhabdoid tumour (in less than 3 years of age) are the possibilities in posterolateral cerebellum [14]. literature provides evidence that mgmt-methylated tumours show a lower volume of t2 abnormalities; a lower volume ratio of t2 abnormalities to contrast enhancement and central necrosis suggest a mesenchymal glioblastoma subtype and a sharp border makes a 1p19q-intact tumour more likely [11]. a multi institutional study of the cancer genome atlas (tcga) gbm dataset by gutman et al [15] demonstrated that proneural subtype showed low levels of contrast enhancement (reviewed in [9]). zinn et al [16] performed first comprehensive radiogenomic analysis using mri volumetrics and gene and micro rna expression profiling in gbm. they suggested that flair is an imaging marker for edema and invasion and high flair radiophenotypes may have a unique molecular tumour composition that leads to cellular migration and invasion [16]. by combining neuroimaging and dna microarray analysis, multidimensional maps of gene-expression patterns in gbm were created. diehn et al [17] hypothesized that underlying inter and intratumoural gene-expression differences lead to phenotypic diversity of gbm which can be seen on neuroimaging. unique imaging strategies could identify most of the gene expression signatures and hence radiophenotypes could be assessed more specifically by combining gene expression and mri. there was significant complex and simple microvascular hyperplasia within contrastenhancing regions which corresponded to a significant increase in rcbv and relative peak height (rph) measurements. it was hypothesized that the enhancing and nonenhancing regions showed different gene expression patterns which was confirmed when 359 genes significantly overexpressed within contrast-enhancing samples were found to be associated with regulation of angiogenesis, proptosis and mitosis. genes associated with cellular proliferative or infiltrative processes, hypoxia, and angiogenesis were upregulated in contrast enhancing tissues. jain et al [18] showed that cbv and percentage signal (ps) estimates in gbms correlate positively with proangiogenic genes and inversely with anti angiogenic genes. rao et al [19], combining transcriptional, post-transcriptional and signal transduction correlates of relative cerebral blood volume, revealed 326 genes, 76 mirna and 8 proteins expressed between two phenotype classescell proliferation and angiogenesis associated pathways. molecular examination of hemodynamic characteristics other than rcbv may shed further light on useful aspects and enhanced application of the technique for grading gliomas. it would be interesting to investigate if there could be a way to find radioproteomic phenotypes functionally correlating with tumour imaging features in gliomas. hobbs et al [20] studied correlation between gadolinium contrastenhancement patterns on t1-weighted magnetic resonance (mr) images and spatial changes in protein expression profiles in gbm. tissue samples from nonenhancing (ne) and contrast enhancing (ce) regions within a given tumour were compared. proteins common to all individuals studied in both ce and ne regions were used as internal controls. the ce regions were extremely heterogeneous not only across the patients, but also within same patient while ne regions were comparably homogeneous. ce regions also contained more protein species than the ne region. the extracellular matrix in contrastenhancing regions was likely to contain factors that presented increased permeability or microvessel density in neoplastic disease state. this shows that ce-mri can guide proteomic analysis with seldi-tofms in gbm. dwi assesses cellularity of tumours and adc gives quantitative information about the restriction of water movement. brain neoplasms with higher cellularity or with a higher grade show significantly low adc values [21]. in our study, difference in the minimum adc values for different grades of tumour was significant (p<0 .001), finding similar to those of lee et al [22] and kono et al [23] that high-grade gliomas show significantly low adc values and increased signal intensity on dwi. hilario et al [24] found that at a cut off adc value of 1.185x10-3 mm2/s high and low grade gliomas could be differentiated with a sensitivity of 97.6% and specificity of 53.1%. comparison between hilario et al and our study is shown in table 4. a lower cut off 60 seema rohilla, ambresh r. deodurg, pritviraj s. kanakavvanavar et al. value in our study has reduced the sensitivity but improved the specificity. study cut off adc value (for low v/s high grade) sensitivity specificity hilario et al (2012) 1.185x10-3 mm2/s 97.6 % 53.1 % our present study 0.75x10-3 mm2/s 71.43 % 70 % table 4. table comparing adc values in differentiation of high and low-grade gliomas in various studies. fan et al [25] have demonstrated that adc values in peritumoural regions were decreased compared to the contralateral normal white matter, but no significant difference was found as p value was more than 0.05. in our study also p value was more than 0.05 and hence was not a significant parameter for grading gliomas. moreover the edema surrounding the glioma is vasogenic edema [6] which normally does not show diffusion restriction this may also be the reason that adc in peritumoural edema is not very reliable in grading the tumours. dti, a method of visualizing the anisotropy of proton motion, may eliminate the partial volume effect of peritumoural edema, and may highlight the difference between high-grade and low-grade gliomas [26]. zinn et al [27] described diffusion weighted magnetic resonance imaging radiophenotypes and associated molecular pathways in glioblastoma. given that dmri and adc reflect tumour cellularity and a high n:c ratio in niches of restricted diffusion, authors hypothesized that dmri signal intensity beyond the region of enhancement could identify gbms that were highly infiltrative within nonenhancing peritumoural flair area. gene expression profiles associated with restricted diffusion in the peritumoural dmri-flair niche in gbm was examined which showed consistent upregulation of bmi1, a known regulator of stemlike states in cancer cells and is associated with migration, invasion and poor prognosis. likewise, significant negative correlation has been shown between adc and 2-hydroxyglutarate (2-hg) levels, a metabolite found in idh mutated tumours [9], which suggests that adc may be decreased in idh-mutated tumours. methylated tumours display features of lower cellularity (high minimum adc ratio and low minimum fa ratio) [11]. heiland et al [28] found that in enhancing tumour region, fa directly correlated with activation of epithelial-tomesenchymal transition pathway. hence high fa predicted worse prognosis in gbm, while higher md predicted good prognosis. tumour growth depends largely on new blood vessel growth. simple diffusion of oxygen, nutrients and other essential materials can support tumour growth only upto a size of 1-2mm3 beyond which neoangiogenesis is necessary. metastasis also cannot occur without growth of new blood vessels [29]. contrast enhancement occurs due to leakage of contrast and thus ce-mri highlights only the blood brain barrier (bbb) disruption. on the other hand, perfusion study is based upon blood flow at capillary level. it tells about the capillary network and hence shows the degree of neoangiogenesis [30]. as the tumour growth and hence its grade depends on neoangiogenesis rather than on leakage of bbb, perfusion mri is an earlier and better predictor of grade than contrast enhancement. moreover, due to its ability to pick up areas of angiogenesis, pwi imaging has capacity to direct stereotactic biopsy to such areas (which have a higher grade) in an otherwise heterogeneous tumour, thus avoiding understaging of the tumour, specially in cases of non-enhancing gliomas which have comparatively intact bbb [31]. the drawback is that in cases of high grade enhancing gliomas, there is significant bbb breakdown leading to leakage of contrast in extravascular space during first pass of contrast and reduced susceptibility effects between intra and extravascular compartments in this area leading to underestimation of tumour vascularity and hence grade [32]. peritumoural areas in anaplastic tumours show altered capillary morphology as well as tumour cells along newly formed or preexisting dilated vessels while low grade gliomas have less infiltrating tumour cells. this is reflected in elevated blood volume before enhancement. vascularity related heterogeneity of peritumoural region as shown on pwi can be helpful in better estimation of true brain tumour size pre-operatively [33]. although preoperative grading of gliomas is mainly done by dwi and pwi, there are only few studies validating the usefulness of diffusion and perfusion mri solely in non-enhancing gliomas. fan et al [25] hypothesized that dwi/pwi could provide additional useful information in the assessment and tumour grading of supratentorial glial neoplasms, 61 rcbv and adc based grading of gliomas with glimpse into radiogenomics which lacked contrast enhancement on preoperative neuroimaging and therefore evaluated the usefulness of diffusion/perfusion-weighted mri in patients with non-enhancing supratentorial brain gliomas. both solid portions as well as peritumoural regions of anaplastic gliomas showed high rcbv ratios but low grade gliomas did not [25]. so it was concluded that higher rcbv ratios in both solid portions and peritumoural regions correlate significantly with anaplasia. in our study rcbv in peritumoural edema was not significant (p = 0.13). comparison of cut off rcbv values within the tumour between various studies is shown in table 5. spampinato et al [32] demonstrated best sensitivity and specificity for differentiating low and high grades, at a cut off of 2.14 ml/100 g. we also found best sensitivity and specificity at a cut off of 2.6 ml/100 g which is quite close to 2.1 ml/100 g though our sensitivity and specificity were less than that of spampinato. this difference may be explained on the basis of different number of cases in two studies and because our study contained mix of astrocytoma and oligodendroglioma while spampinato’s study had only oligodendroglioma. sensitivity of all the studies is comparable. the difference in specificity arises due to different cut off values of rcbv for low v/s high grade tumours. near cut off of 1.75 ml/100 g, both law et al [34] and hilario et al [24] had a specifity of 50-60%. at a cut off of 3.3 ml/100 g, roy et al [35] showed specificity of 88%. at a cut off of 2.6ml/100mg our specificity was 76.47% which is in between the above values (cut off is also in between the two) and hence in sync with previous studies. study cut off rcbvvalue (ml/100 g) sensitivity (%) specificity (%) law et al(2003) 1.75 95.0 57.5 weber et al(2006) 1.6 94 78 aprile et al(2012) 3.5 79.4 95.8 hilario et al(2012) 1.74 94.4 50.0 roy et al(2013) 3.34 100 88 spampinato et al(2007) 2.14 100 86 shin et al 3.57 72.7 100 our present study 2.6 76.67 76.47 table 5. table comparing rcbv values within the tumor in differentiation of high and low grade gliomas in various studies. ellingson [13] based on his decades of work examined association between radiological and histological features in glioblastoma. he comprehensively reviewed anatomical imaging pathology associations, association between tumour size, location and molecular characteristics, diffusion and perfusion mri pathology correlation and quantification of intuitive radiographic features. maximum rcbv is considered to be a significant predictor of mean vessel diameter. smits and bent [11] found that methylated tumours show less perfusion and increased volume transfer constant (ktrans) than unmethylated tumours. though pseudoprogression is seen commonly, but progression time is significantly longer in patients with mgmt-promoter methylation compared with the unmethylated group, both of which may be due to increased ktrans, i.e., permeability in methylated group which leads to contrast leakage (seen as pseudoprogression) and better drug delivery (prolonging progression) [10]. thus increase in enhancement within three months after completion of radiotherapy in patients with mgmt methylated tumours should be suspected as pseudoprogression rather than progressive disease. this shows how amalgamation of imaging and genomics can reinforce each other. imaging can help in predicting tumour genetics, while genetic profile helps in cautious interpretation of post-treatment enhancement in terms of progression vs pseudoprogression. oligodendroglioma have comparatively higher rcbv regardless of grade on histology [13]. pwi can differentiate pilocytic astrocytoma (rcbvmax = 1.19±0.71)from hemangioblastoma (rcbvmax = 9.37±2.37) [14]. vajepeyam et al have shown that adc histogram metrics combined with permeability metrics differentiate low and high-grade pedistric brain tumours with high accuracy [14]. bulakbasi et al [33, 36] studied usefulness of mr spectroscopy and adc calculation for tumour grading. they found that though mr spectroscopy could not be of much help in grading malignant tumours, it could help to differentiate benign from malignant tumours [36]. in our study also spectroscopy was not helpful in grading of gliomas. hsu et al [37] correlated metabolite ratios with histopathologic grading in 27 patients with cerebral gliomas. they concluded that there was no significant metabolite difference between grade iii and grade iv tumours (p>0.1), or significant difference in lactate occurrence rates among 62 seema rohilla, ambresh r. deodurg, pritviraj s. kanakavvanavar et al. different grades (p = 0.26). though the metabolite ratios in our study were not helpful quantitatively in grading of gliomas, presence of some peaks like lipid and lactate did help in grading. poptani et al [38] and hsu et al [37] stated that lactate peak can be found in all grades of tumours. in our study also lactate peak was found in almost all the grades though with more frequency in higher grades. radiogenomics focused on spectroscopic parameters may also aid in predicting molecular profiling of tumours. gbm harboring idh1 mutation show 2-hydroxyglutarate (2-hg) on mr spectroscppy [9]. so 2-hg level can be a predictor of idh1 mutation, but is not universally available in standard mr equipments at present, but is definitely a way forward. likewise, oligodendrocytic tumours correlated with n-acetylaspartate metabolite, high creatine metabolite (ncr) was seen in proneural gbm subtype, and low ncr predicted mesenchymal subtype; low nglx predicted neural subtype, and its high value suggested classical subtype [10]. a high peak of choline can help differentiate atypical laminated medulloblastoma from lhermitte-duclos disease which are difficult to differentiate on morphology alone [14]. brain shift during surgery often leads to incongruence in tumour borders assessed by preoperative and operative mri. some tumours show false-positive contrast enhancement and small molecule gd-agents may also spread from the initial area of tumour enhancement into the peritumoural zone of edema over time. this leads to inaccuracies in assessment of tumour extent. multimodality approach has been suggested to overcome this shortcoming and to assess true tumour extent. the focus in recent past has been on exploring optical methods which may be based on either intrinsic tissue properties or by using exogenous contrast agents. nevertheless, small field of view, decreased specificity due to auto fluorescence, and rapid photobleaching pose challenges in using these optical procedures. some other useful methods for defining tumour margins include fluorescenceguided resection of malignant gliomas using 5aminolevulinic acid (body’s own metabolite in heme biosynthesis pathway and metabolic marker of malignant cells which is converted into fluorescent porphyrins in cells) as marker [39] and desorption electrospray ionization mass spectrometry (desims) imaging based on lipid patterns for intra operative molecular characterization of brain tumours [40]. using mouse model of glioblastoma, huang et al have reported integrin –targeted serrs nanoparticles to depict the true tumour extent. method bears fairly high potential for clinical translation for glioma grading in humans [41]. various radiological parameters can also predict prognosis with fair degree of accuracy. while performing an integrative network-based analysis of magnetic resonance spectroscopy and genome wide expression in glioblastoma multiforme, heiland et al [42] found that patients with higher nnaa (n-acetyl aspartate) showed longer progression free survival (reviewed in [10]). patients with highly perfused low grade tumours fared worse than patients with lowly perfused high grade tumours. idh-mutated tumours fare much better than idh wild type of same grade. limited peritumoural edema predicted better prognosis in patients with methylated glioblastoma specifically [11]. mutations in the promoter for telomerase reverse transcriptase (tert), an enzyme that elongates telomeres, have been associated with a worse prognosis in both idh mutant and idh wildtype gbms. increased amounts of ki-67, a cellular protein associated with proliferation and present in many tumours, is also associated with a worse prognosis [43]. even choice of chemotherapy can be improved with radiogenomics approach. gbm with proneural signature had better outcome when bevacizumab was given from initiation of therapy. mesenchymal phenotype responded better when bevacizumab was given at recurrence, but not when given as first line along with radiation and temozolomide [13]. the mgmt unmethylated group responded only to radiotherapy [10]. sirna can transduce previously tmz-resistant glioma-initiating cells, enhancing their chemosensitivity against tmz [12]. co-deletion of chromosomal arms 1p and 19q predict favorable outcome and sensitivity to chemotherapy respectively. there are some major issues with universal application of conventional radiogenomics at present. these are overlap of mri features between different mutations, several mutations like idh, mgmt, and tp53, occuring in tandem, intratumoural heterogeneity with different portions of the tumour having different genetic and imaging features. machine learning is better as it does objective quantitative evaluation and can detect subtle voxel 63 rcbv and adc based grading of gliomas with glimpse into radiogenomics level patterns [43]. so a combination of conventional and machine learning based radiogenomics has huge potential towards accurate diagnosis, classification, grading, prognosticating, selecting adequate therapy, monitoring therapy, identifying early therapy failure and modifying therapy accordingly in cases of glioma, i.e., it is the way forward in theranostics and has the potential to replace invasive and non-representative biopsies as it gives the total overview of the tumour. our study has some limitations. stereotactic biopsies were not targeted according to rcbv or adc maps. so there is possibility of histopathologic misdiagnosis attributable to sampling error in the pathologic examination because of the histologic heterogeneity of tumour tissues. only elementary radiogenomics based approach could be followed as the facility for mr based stereotactic biopsies and advanced machine learning facilities do not exist at our place. ongoing radiological, molecular profiling and proteomic studies in our laboratories are focused on providing additional translational tools to decipher mr, genomic and proteomic characteristics of gliomas to better grade them. conclusion both maximum rcbv and minimum adc values within the tumour were useful in grading gliomas, but both these values in peritumoural edema were not significant in grading gliomas. rcbv values were better than adc values in differentiating grade i from ii and grade ii from iii. the adc values were better than rcbv values in differentiating grade iii from grade iv. the metabolite ratios were not helpful in grading of gliomas, but presence of some peaks like lipid and lactate did help in grading. lactate peak was found in almost all the grades (except grade i) though with more frequency in higher grades. presence of lipids suggested a higher grade of malignancy. radiogenomics coupled with multimodality radiomic procedures can further improve the accuracy of grading. acknowledgement authors are thankful to pt. b. d. sharma post graduate institute of medical sciences, rohtak, haryana, (india) for providing the resources needed for the study. authors also thank professor r. m. pandey and mr. ashish dutt upadhyaya of department of biostatistics, all india institute of medical sciences, new delhi, india for help with statistical analysis. ethical considerations the study was carried out in accordance to standards of the institutional ethics committee and with the 1964 helsinki declaration. references 1. okaili, r. n., krejza, j., wang, s., woo, j. h., melhem, e. r. (2006). advanced mr imaging techniques in the diagnosis of intraaxial brain tumors. radiographics, 26, s173-89. 2. jansen, r. w., van amstel, p., martens, r. m., kooi, i. e., wesseling, p., de langen, a. j., van oordt, c. w. m. v. h., jansen, b. h. e., moll, a. c., dorsman, j. c., castelijns, j. a., de graaf, p., de jong, m. c. (2018). non-invasive tumor genotyping using radiogenomic biomarkers, a systematic review and oncology-wide pathway analysis. oncotarget, 9(28), 20134‐20155. 3. seow, p., wong, j. h. d., ahmad-annuar, a., mahajan, a., abdullah, n. a., ramli, n. (2018). quantitative magnetic resonance imaging and radiogenomic biomarkers for glioma characterisation: a systematic review. br j radiol, 91(1092), 20170930. 4. schwartzbaum, j. a., fisher, j. l., aldape, k. d., wrensch, m. (2006). epidemiology and molecular pathology of glioma. nat clin pract neurol, 2(9), 494-503. 5. kernohan, j. w., mabon, r. f., svien, h. j. et al (1995). neuroepithelial tumors of the adult brain. in: youmans. neurological surgery. 4th edition. philadelphia: w.b. saunders co, 2612-84. 6. chishty, i. a., rafique, m. z., hussain, m., akhtar, w., ahmed, m. n., sajjad, z., ali, s. z. (2010). mri characterization and histopathological correlation of primary intra -axial brain glioma. jlumhs, 9(2), 64-69. 7. van meter, t., dumur, c., hafez, n., garrett, c., fillmore, h., broaddus, w. c. (2006). microarray analysis of mridefined tissue samples in glioblastoma reveals differences in regional expression of therapeutic targets. diagn mol pathol, 15(4), 195–205. 8. kuo, m. d., & jamshidi, n. (2014). behind the numbers: decoding molecular phenotypes with radiogenomicsguiding principles and technical considerations. radiology, 270(2), 320-5. 9. elbanan, m. g., amer, a. m., zinn, p. o., colen, r. r. (2015). imaging genomics of glioblastoma: state of the art bridge between genomics and neuroradiology. neuroimaging clin n am, 25(1), 141-53. 10. kazerooni, f. a., bakas, s., rad, h. s., davatzikos, c. (2020). imaging signatures of glioblastoma molecular characteristics: a radiogenomics review. j magn reson imaging, 52(1):54-69. 11. smits, m., & van den bent, m. j. (2017). imaging correlates of adult glioma genotypes. radiology, 284(2), 316-31. 12. moton, s., elbanan, m., zinn, p. o., colen, r. r. (2015). imaging genomics of glioblastoma: biology, biomarkers, and breakthroughs. top magn reson imaging, 24(3), 15563. 13. ellingson, b. m. (2015). radiogenomics and imaging 64 seema rohilla, ambresh r. deodurg, pritviraj s. kanakavvanavar et al. phenotypes in glioblastoma: novel observations and correlation with molecular characteristics. curr neurol neurosci rep, 15(1), 506. 14. kerleroux, b., cottier, j. p., janot, k., listrat, a., sirinelli, d., morel, b. (2020). posterior fossa tumors in children: radiological tips & tricks in the age of genomic tumor classification and advance mr technology. j neuroradiol, 47(1), 46-53. 15. gutman, d. a., cooper, l. a., hwang, s. n., holder, c. a., gao, j., aurora, t. d., dunn, w. d. jr,scarpace, l., mikkelsen, t., jain, r., wintermark, m., jilwan, m., raghavan, p., huang, e., clifford, r. j., mongkolwat, p., kleper, v., freymann, j., kirby, j., zinn, p. o., moreno, c. s., jaffe, c., colen, r., rubin, d. l., saltz, j., flanders, a., brat, d. j. (2013). mr imaging predictors of molecular profile and survival: multi-institutional study of the tcga glioblastoma data set. radiology, 267(2), 560-9. 16. zinn, p. o., majadan, b., sathyan, p., singh, s. k., majumder, s., jolesz, f. a., colen, r. r. (2011). radiogenomic mapping of edema/cellular invasion mriphenotypes in glioblastomamultiforme. plos one, 6(10), e25451. 17. diehn, m., nardini, c., wang, d. s., mcgovern, s., jayaraman, m., liang, y., aldape, k., cha, s., kuo, m. d. (2008). identification of noninvasive imaging surrogates for brain tumor gene-expression modules. proc natl acad sci, 105(13), 5213-8. 18. jain, r., poisson, l., narang, j., scarpace, l., rosenblum, m. l., rempel, s., mikkelsen, t. (2012). correlation of perfusion parameters with genes related to angiogenesis regulation in glioblastoma: a feasibility study. am j neuroradiol, 33(7), 1343-8. 19. rao, a., manyam, g., rao, g., jain, r. (2016). integrative analysis of mrna, microrna, and protein correlates of relative cerebral blood volume values in gbm reveals the role for modulators of angiogenesis and tumor proliferation. cancer inform, 15, 29-33. 20. hobbs, s. k., shi, g., homer, r., harsh, g., atlas, s. w., bednarski, m. d. (2003). magnetic resonance imageguided proteomics of human glioblastoma multiforme. j magn reson imaging, 18(5), 530-6. 21. louis, d. n., ohgaki, h., wiestler, o. d., cavenee, w. k., burger, p. c., jouvet, a., scheithauer, b., w., kleihues, p. (2007). the 2007 who classification of tumours of the central nervous system. acta neuropathol, 114(2), 97109. 22. lee, e. j., lee, s. k., agid, r., bae, j. m., keller, a., terbrugge, k. (2008). preoperative grading of presumptive low-grade astrocytomas on mr imaging: diagnostic value of minimum apparent diffusion coefficient. am j neuroradiol, 29(10), 1872-7. 23. kono, k., inoue, y., nakayama, k., shakudo, m., morino, m., ohata, k., wakasa, k., yamada, r. (2001). the role of diffusion-weighted imaging in patients with brain tumors. am j neuroradiol, 22(6), 1081-8 24. hilario, a., ramos, a., perez, n., salvador, e., millan, j. m., lagares, a., sepulveda, j. m., leon, g., lain, h., ricoy, j. r. (2012). the added value of apparent diffusion coefficient to cerebral blood volume in the preoperative grading of diffuse gliomas. am j neuroradiol, 33(4), 7017. 25. fan, g. g., deng, q. l., wu, z. h., guo, q. y. (2006). usefulness of diffusion/perfusion-weighted mri in patients with non-enhancing supratentorial brain gliomas: a valuable tool to predict tumor grading. british j radiology, 79, 652–8. 26. lu, s., ahn, d., johnson, g., law, m., zagzag, d., grossman, r. i. (2004). diffusion-tensor mr imaging of intracranial neoplasia and associated peritumoral edema: introduction of the tumor infiltration index. british j radiology, 232, 221–8. 27. zinn, p. o., hatami, m., youssef, e., thomas, g. a., luedi, m. m., singh, s. k., colen, r. r. (2016). diffusion weighted magnetic resonance imaging radiophenotypes and associated molecular pathways in glioblastoma. neurosurgery, 63(suppl 1), 127-35. 28. heiland, d. h., simon-gabriel, c. p., demerath, t., haaker, g., pfeifer, d., kellner, e., kiselev, v. g., staszewski, o., urbach, h., weyerbrock, a., mader, i. (2017). integrative diffusion-weighted imaging and radiogenomic network analysis of glioblastoma multiforme. sci rep, 7, 43523. 29. bello, l., giussani, c., carrabba, g., pluderi, m., costa, f., bikfalvi, a. (2004). angiogenesis and invasion in gliomas. cancer treat res, 117, 263–84. 30. batra, a., tripathi, r. p., singh, a. k. (2004). perfusion magnetic resonance imaging and magnetic resonance spectroscopy of cerebral gliomas showing imperceptible contrast enhancement on conventional magnetic resonance imaging. australas radiol, 48(3), 324–32. 31. maia, a. c. m., malheiros, s. m. f., da rocha, a. j., da silva, c. j., gabbai, a. a., ferraz, f. a. p., stavale, j. n. (2005). mr cerebral blood volume maps correlated with vascular endothelial growth factor expression and tumor grade in non enhancing gliomas. am j neuroradiol, 26, 777-83. 32. spampinato, m. v., smith, j. k., kwock, l., ewend, m., grimme, j. d., camacho, d. l. a., castillo, m. (2007). cerebral blood volume measurements and proton mr spectroscopy in grading of oligodendroglial tumors. am j neuroradiol, 188, 204–12. 33. bulakbasi, n., kocaoglu, m., farzaliyev, a., tayfun, c., ucoz, t., somuncu, i. (2005). assessment of diagnostic accuracy of perfusion mr imaging in primary and metastatic solitary malignant brain tumors. am j neuroradiol, 26(9), 2187–99. 34. law, m., yang, s., wang, h., babb, j. s., johnson, g., cha, s., knopp, e. a., zagzag, d. (2003). glioma grading: sensitivity, specificity andpredictive values of perfusion mr imaging and proton mr spectroscopic imaging compared with conventional mr imaging. am j neuroradiol, 24(10), 1989-98. 35. roy, b., gupta, r. k., maudsley, a. a. et al (2013). utility of multiparametric 3-t mri for glioma characterisation. neuroradiology, 55, 603 -13. 36. bulakbasi, n., kocaoglu, m., ors, f., tayfun, c., ucoz, t. 65 rcbv and adc based grading of gliomas with glimpse into radiogenomics (2003). combination of single-voxel proton mr spectroscopy and apparent diffusion coefficient calculation in the evaluation of common brain tumors. am j neurodiol, 24(2), 225-33. 37. hsu, y. y., chang, c. n., wie, k. j., lim, k. e., hsu, w. c., jung, s. m. (2004). proton magnetic resonance spectroscopic imaging of cerebral gliomas: correlation of metabolite ratios with histopathologic grading. chang gung med j, 27(6), 399-407. 38. poptani, h., gupta, r. k., roy, r., pandey, r., jain, v. k., chhabra, d. k. (1995). characterization of intracranial mass lesions with in vivo proton mr spectroscopy. am j neuroradiol, 16, 1593-603. 39. tonn, j. c., & stummer, w. (2008). fluorescence-guided resection of malignant gliomas using 5-aminolevulinic acid: practical use, risks, and pitfalls. clin neurosurg, 55, 20-6. 40. eberlin, l. s., norton, i., orringer, d., dunn, i. f., liu, x., ide, j. l., jarmusch, a. k., ligon, k. l., jolesz, f. a., golby, a. j., santagata, s., agar, n. y. r., cooks, r. g. (2013). ambient mass spectrometry for the intraoperative molecular diagnosis of human brain tumors. proc natl acad sci, 110(5), 1611-6. 41. huang, r., harmsen, s., samii, j. m., karabeber, h., pitter, k. l., holland, e. c., kircher, m. f. (2016). high precision imaging of microscopic spread of glioblastoma with a targeted ultrasensitive serrs molecular imaging probe. theranostics, 6(8), 1075-84. 42. heiland, d. h., mader, i., schlosser, p., pfeifer, d., carro, m. s., lange, t., schwarzwald, r., vasilikos, i, urbach, h., weyerbrock, a. (2016). integrative network-based analysis of magnetic resonance spectroscopy and genome wide expression in glioblastoma multiforme. sci rep, 6, 29052. 43. chow, d., chang, p., weinberg, b. d., bota, d. a., grinband, j., filippi, c. g. (2018). imaging genetic heterogeneity in glioblastoma and other glial tumors: review of current methods and future directions. am j roentgenol, 210(1), 30-38. doi: 10.33962/roneuro -2020-058 incidence of vertebral osteomyelitis and benefits of spinal stabilization in infection. retrospective analysis of 94 cases in 5 years vlad catana, radu mircea gorgan romanian neurosurgery (2020) xxxiv (2): pp. 213-219 doi: 10.33962/roneuro-2020-058 www.journals.lapub.co.uk/index.php/roneurosurgery incidence of vertebral osteomyelitis and benefits of spinal stabilization in infection. retrospective analysis of 94 cases in 5 years vlad catana1,2, radu mircea gorgan1,3 1 university of medicine and pharmacy “carol davila”, bucharest, romania 2 “foisor” clinical hospital of orthopedic and traumatology, bucharest, romania 3 “bagdasar arseni” clinical emergency hospital bucharest, romania abstract in order to evaluate the etiology, characteristics and outcome of the surgical treatment of vertebral osteomyelitis cases in our hospital, patients with vertebral osteomyelitis between january 2014 and december 2018 were included in the study. clinical and paraclinical data of the patients were collected from the medical records of the patients. of the 164 patients diagnosed with vertebral osteomyelitis in our clinic 94 underwent surgery and only these last ones were included in the study. of these 94 patients, 18 cases were diagnosed with tuberculous osteomyelitis and 76 with nontuberculous osteomyelitis. the age of the majority of patients ranged from 40 to 80 years with a peak of incidence between 61-70 years. all of the patients had back pain and regional tenderness of the affected area and many cases presented neurological deficits. the most common involved area affected in our cases was the thoracic spine. magnetic resonance imaging is the examination that reveals the degree of involvement and excludes other pathologies from the differential diagnosis. the majority of patients had several comorbidities which we included in the study. from all the patients included 76 % underwent surgery with decompression and spinal stabilization using titanium instrumentation and 24 % underwent surgery with only spinal decompression. we also evaluated number hospitalization days of the operated cases. an early diagnosis seems crucial for a fast recovery, lowering the hospitalization costs of both the patient and the hospital and preventing sequelae development. introduction the inflammation of the intervertebral disk and the surrounding vertebra is defined as vertebral osteomyelitis (vo) or spondylodiscitis. etiologically it has been divided into 2 groups: tuberculous and nontuberculous osteomyelitis. adults are the most affected in the general population, most patients diagnosed with this disease being over 50 years old. the clinical signs and symptoms are unspecific and this results in a late diagnose of this pathology. (1, 4, 12 ) keywords decompression, osteodiscitis, spinal fixation surgery, tuberculous infection, vertebral osteomyelitis corresponding author: vlad catana md. phd student. university of medicine and pharmacy “carol davila”, bucharest, romania catana.vlad@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 214 vlad catana, radu mircea gorgan the lumbar vertebral bodies of the spine are the most often affected according to literature, being followed by the thoracic and cervical (rare) areas. the clinical presentation of vo is consisted of: acute, subacute or chronic. tenderness and local regional pain are the most common symptoms in 90% of the patients. fever is an inconstant sign, being present in 50% of the cases. neurological deficits may exist when the spinal cord or nerve roots are affected through compression. (6) the most isolated organism that causes vertebral osteomyelitis is staphylococcus aureus (skin, invasive maneuvers and various percutaneous catheters may be an entry portal), being followed by escherichia coli, coagulase-negative staphylococci, propionibacterium acnes. gram-negative aerobic bacteria and candida spp are common microorganisms are discovered in iv drug abusers and immunosuppressed patients. these represent various etiologies for nontuberculous osteomyelitis, while mycobacterium tuberculous is the main factor for developing tuberculous (tb) vertebral osteomyelitis. (1, 7, 10, 13, 16) biopsy of the tissue has a high diagnostic accuracy. leukocytosis is found in 50 % of cases and has a low diagnostic sensitivity. a raised erythrocyte sedimentation rate (esr) and c-reactive protein (crp) levels are highly sensitive. a good clinical response to treatment is noted by lowering of the crp levels. (1, 4, 9, 16) imaging studies used for the diagnosis of vo are represented by radiography, scintigraphy, ct scan and mri. the mri has high diagnostic sensitivity and specificity. for obtaining an anatomopathological and microbiological based diagnostic ct-guided fineneedle aspiration biopsy (fnab) is used and has a sensitivity of 50%. (1) the aim of the treatment is to eradicate the infection, relieve the pain and restore the neurological status of the patient. (1) our purpose of the study was to describe a series of vertebral osteomyelitis cases in our hospital, to differentiate de factors that cause or predispose to the formation of this infection and show the benefits of a surgical stabilization treatment for axial stability and early mobilization. methods type of study we conducted a retrospective descriptive study, in which we included patients operated for osteomyelitis / primary vertebral osteodiscitis in the neurosurgery clinic of the emergency clinical hospital bagdasar arseni for a period of 5 years (january 1, 2014 – december 31, 2018). the study is based on the experience of the neurosurgery ii and iv departments of the hospital. it is the only study conducted in our country over a longer period of time and on a large number of patients, with the theme of multimodal treatment of vertebral osteomyelitis. we had the method of retrospective revision of the electronic observation sheets, of the patients' files taken from the hospital archive and the operative protocols of the patients with osteomyelitis / primary vertebral osteodiscitis operated in the previously mentioned period. based on the information obtained, we created a database using the microsoft office excel 2007 program. the statistical analysis was performed using the ibm spss statistics 20 program. we created a database that can be taken as a starting point in establishing medical and surgical treatment protocols for patients with vertebral osteomyelitis. on a national level, there is no evidence of reported cases of vertebral osteomyelitis and there are no protocols for unitary treatment of this condition. as inclusion criteria, only patients with osteomyelitis/osteodiscitis operated between january 1, 2014 december 31, 2018 were included in the study. patients with vertebral osteomyelitis who received only conservative treatment without surgery or patients with osteodiscitis secondary to operated disc herniation were excluded from our study. the variables introduced in the statistical analysis were nominal, dichotomous (binary, bimodal), ordinal and quantitative (measurable) discontinuous (discrete). depending on the variables studied, we performed uni, bi and multivariate statistical analyzes. results between january 1, 2014 and december 31, 2018, 164 patients were hospitalized and diagnosed with vertebral osteodiscitis in the neurosurgery clinic of the bagdasar-arseni emergency clinical hospital. of 215 incidence of vertebral osteomyelitis and benefits of spinal stabilization in infection these, 94 patients (57.31%) underwent surgery for vertebral osteomyelitis. sexual distribution the distribution by sex was slightly in favor of males, 52 patients being male, representing 55% were operated for vertebral osteomyelitis, compared to 42 female patients, representing 42% operated for the same pathology. the sex ratio of m / f was 1.23 (figure 1). figure 1. sexual distribution of the patients. age distribution in the studied group we distributed the patients by decades of age between 40 and 80 years. the vast majority of patients were in the age range of 51-70 years, respectively 27 patients (29% of cases) in the range of 51-60 years and 32 patients (35% of cases) in the range of 61-70 years. this is justified by the fact that these age groups include relatively active patients, who also perform physical exertion, but who have a personal history that may promote the occurrence of vertebral osteomyelitis. the rest of the patients are distributed in lower percentages in the interval under 40 years old being 7 patients (8% of cases), and between 41-50 years old and over 70 years old 14 patients (15% of cases) in each group (figure 2). figure 2. age distribution of the patients. duration of hospitalization of patients in the study group on the studied group, the hospitalization period varied between 0-10 days, 11-20 days, 21-30 days and respectively hospitalized patients for a period of over 30 days. among the patients studied, the highest percentage was represented by those hospitalized for less than 20 days, who opted for vertebral fixation with titanium instrumentation, in 55 cases (70%), followed by those hospitalized between 21-30 days, in a number of 20 cases (21%) and respectively those hospitalized for a period longer than 30 days, in a number of 4 patients (4%), in which only the vertebral decompression was practiced (figure 3). figure 3. number of hospitalization days of the patients. secondary diagnostics from the point of view of the pathology associated with patients operated for vertebral osteomyelitis, a number of 25 cases (26.6%) had diabetes, 10 cases had a personal history of pulmonary tb (10.6%), 8 cases had had hepatitis b or c virus infection (8.5%). out of the total number of patients, 43 cases (45.7%) were diagnosed and operated for vertebral osteomyelitis on the background of an immunosuppression already present due to the pathologies mentioned above (figure 4). figure 4. associated pathologies of the patients. 15 55 20 4 94 0-10 11-20 21-30 mai mult de 30 total 216 vlad catana, radu mircea gorgan clinical examination lumbar back pain that translates to vertebral instability syndrome is present in all patients with vertebral osteomyelitis. the neurological syndrome occurs in 57 of patients with vertebral osteomyelitis in the study group (60.6%). of these, frankel c and d type paraparesis dominates the clinical picture, frankel c 25 cases (26.5%) and frankel d 24 cases (25.5%). 5 patients from the studied group were frankel type a (5.3%), and 3 patients type frankel b (3.2%) (figure 5). figure 5. preoperative status of the patients according to frankel grading system. localization of the vertebral lesion in the studied group, the vertebral seat of the inflammatory lesion predominates in the thoracic and lumbar region, thoracic osteomyelitis is found in 42 patients (45% of cases), lumbar localization in 40 patients (42% of cases) and cervical in the remaining 12 patients. (13% of cases). (figure 6) this is important in choosing the surgical approach and considering the importance of spinal fixation during surgery. figure 6. incidence of the affected spinal region in the patients studied. surgical treatment the surgical treatment has as important objectives: evacuation of infection and debridement, decompression of the dural sac and spinal roots and vertebral fixation / fusion. surgical decompression involves debridement of the inflammatory focus and evacuation of pus from the intervertebral disc space, curettage of cartilaginous and bony necrotic-inflammatory tissue, evacuation of intraand paraspinal abscesses, and decompression of the dural sac and spinal nerves. the vertebral fixation at the level of the thoracic and lumbar spine is performed using transpedicular screws and titanium rods, but also the reconstruction techniques of the anterior spine, with the help of fixed or expandable titanium cages. the use of titanium instrumentation in vertebral osteomyelitis is a method in continuous debate, but recent studies show the advantages of vertebral stabilization and the compatibility of titanium with infection. the group we studied includes patients operated on 2 neurosurgery departments in the bagdasar arseni emergency clinical hospital by several surgical teams. some surgeons have chosen only surgical decompression alone as a method. in addition to decompression, others also opted for spinal fixation with titanium instrumentation. thus, in the studied group, 72 patients (24%) benefited from internal fixation with titanium instrumentation, while in the remaining 22 cases (76%) only the evacuation of the infectious outbreak and the decompression of the nervous elements were performed, without metal fixation. (figure 7) the aim of this study is to perform a comparative analysis of postoperative results in patients operated for vertebral osteomyelitis in which metal fixation was performed compared to those without metal fixation. figure 7. type of surgical intervention performed on the studied patients. 217 incidence of vertebral osteomyelitis and benefits of spinal stabilization in infection postoperative mobilization due to the improvement of the implantation techniques of the titanium fixing systems (stronger screws, more elastic rods), the period of postoperative immobilization of the patient decreased significantly. this refers to the degree of vertebral stability obtained after surgery, the degree of preoperative neurological injury and the general pathology associated with vertebral osteomyelitis (diabetes, chronic hepatitis, heart failure, copd). the period in which the postoperative mobilization took place varied between 5 and 14 days, this being possible in 75 of (80% of cases). in 19 patients (20% of cases) early mobilization was not possible, requiring postoperative bed rest, which ranged from 6 to 8 weeks. (figure 8) early mobilization of patients was corroborated in particular with the achievement of spinal fixation at the same time as spinal decompression. figure 8. early postoperative mobilization of the patients within 5 to 14 days. histopathological results in absolutely all patients, biopsy was collected from the intervertebral disc, adjacent bone plateaus and evacuated spinal abscesses. the goal was to establish the etiology of the infectious outbreak for proper antibiotic therapy. therefore, the diagnosis of specific granulomatous osteomyelitis (tb) was found in 18 patients (19% of cases), and that of nonspecific osteomyelitis in 76 patients (81% of cases) (figure 9). figure 9. incidence of tuberculous osteomyelitis in the studied cases. discussion vertebral osteomyelitis is a rare disease with an incidence of 5.3 cases per million in one year (3,11). the incidence is growing because of the increasing number of elderly patients with severe comorbidities. the invasive options used for the diagnosis and treatment of this disease (3,16). the diagnosis is in most of the cases delayed due to the prolonged onset of this disease (11). tuberculous osteomyelitis is a disease that can rapidly alter the patient’s prognosis, especially if it becomes infected and coexists with pyogenic osteomyelitis (14,15). non-granulomatous vo has a higher incidence than tb vo and this is concluded in our study as well. specific granulomatous osteomyelitis was detected in 19% of cases, the rest having a nonspecific anatomopathological result (81% of cases). men are more affected than women by vo (1,11). the disease may be diagnosed at any age, but it has a higher incidence in elderly patients (14). in our study the sex ratio between males and females was 1.23. we showed that the average age was between 61-70 years. age groups were dominated by the following percentages: patients between 61-70 years (35%), 51-60 years (29%), 71-80 years (15%), 41-50 years (14% ) and under 40 (14%). this demonstrates the increased frequency of vertebral osteomyelitis in elderly patients. in terms of patient characteristics, it is described in previous papers that diabetes mellitus and chronic 218 vlad catana, radu mircea gorgan renal insufficiency are the most frequent comorbidities in patients with hematogenous related vertebral osteomyelitis (2, 5, 8). in our study, the most common personal pathologies were diabetes mellitus (26.6%), pulmonary tb (10.6%) and hepatic viral infections with hbv and hcv (8%). it has been shown in the study group that patients with a deficient immune system are prone to the appearance of vertebral osteomyelitis. the lumbar spine is the most common affected level (45-50%), followed by the thoracic, cervical and sacral region. in our study we revealed that the location of the lesion is predominantly thoracic (45%), followed by the lumbar location (42%) and then the cervical location (13%). the thoracic spine is the most common site of vertebral osteomyelitis in the patients studied. back pain and muscle spasm of the paravertebral muscles are the most common symptoms of the patients. fever is present in 10-45 % of the cases (3, 11). other clinical findings are represented by: decreased spine motion, paresthesia, anorexia, alteration of the patient’s general state, swelling of the affected region and tenderness at palpation. if the infection spreads into the epidural space this results in the manifestation of neurological deficits (11). in our study, the vast majority of patients have lumbar back pain and spinal instability in the clinical picture. neurological syndrome occurs in 60.6% of all cases studied, this is due to the late presentation at hospital. in the study we conducted, decompression of the dural sac and nerve elements, followed by spinal fixation with titanium instrumentation in the same surgery (76% of cases) shows a rapid postoperative mobilization and a shortening of the hospitalization period, compared to patients who underwent only for surgical decompression (24% of cases). postoperative mobilization was possible in 80% of patients being done from the first 5-14 days after surgery, which demonstrates the effectiveness of using titanium instrumentation for spinal fixation after spinal decompression. the average length of hospitalization of patients was less than 20 days. out of the total of 94 cases studied, a number of 70 cases had a hospitalization time of less than 20 days, 20 cases with hospitalization between 21-30 days and respectively 4 patients with a hospitalization duration of over 30 of days. in the study group, patients treated with spinal fixation with titanium instrumentation had a shorter hospitalization time than those operated without titanium instrumentation. following the study we conducted, we can relate that titanium instrumentation vertebral fixation for instability caused by osteomyelitis allows early mobilization of patients, faster healing of the inflammatory outbreak, reduction of postoperative complications and decreased hospitalization days. conclusion vertebral osteomyelitis occurs in both men and women, with a predisposition for the male population. in addition to old age, other diseases, such as diabetes, chronic kidney failure with dialysis pose a risk for increased incidence. although vertebral osteomyelitis is found in elderly patients, the infection is frequently reported, especially in patients over 60, who are associated with various diseases, such as diabetes, hepatitis or pulmonary tb. the symptoms can be diverse, the dominant symptom is back pain. this translates the pain given by the infection / inflammation but also the spinal pain of vertebral instability. neurological symptoms may range from radiculopathy to spinal cord or ponytail syndrome. the site of the vertebral lesion can be anywhere on the spine, but the thoracic location predominates, then the lumbar one. the surgical treatment aims at the debridement of the inflammatory focus and the evacuation of the pus, the decompression of the dural sac and of the nervous elements. the treatment of spinal instability using fixation-fusion and vertebral reconstruction techniques is a controversial topic, but studies in the literature show the compatibility of instrumentation with infection. the choice of surgical approach depends on the location of the lesion in the spine. early mobilization after surgery is an important goal that can be achieved in patients with metal fixation with titanium instrumentation, without postoperative vertebral instability. early mobilization, especially in elderly patients with various associated pathologies, can significantly reduce the rate of complications associated with prolonged immobilization. 219 incidence of vertebral osteomyelitis and benefits of spinal stabilization in infection references 1. berbari ef, steckelberg jm, osmon dr (2005) osteomyelitis. in: mandell gl, bennett je, dolin r (eds) principles and practice of infectious diseases, vol 1, 6th edn. churchill livingstone, philadelphia, pp 1322–1332. 2. carragee ej: pyogenic vertebral osteomyelitis. j bone joint surg am 1997, 79:874-80. 3. colmenero jd, jime ́ nez-mejias me, sa ́ nchez-lora fj, reguera jm, palomino nicas j, martos f et al (1997) pyogenic, tuberculous, and brucellar vertebral osteomyelitis: a descriptive and comparative study of 219 cases. ann rheum dis 56:709–715. 4. currier bl, eismont fj (1992) infections of the spine. in: rothman rhu ̈ simeone fa (eds) the spine, 3rd edn, vol 2. w.b saunders company, philadelphia, pp 1319–1380. 5. hadjipavlou ag, mader jt, necessary jt, muffoletto aj: hematogenous pyogenic spinal infections and their surgical management. spine (phila pa 1976) 2000, 25:1668-79. 6. jaramillo-de la torre jj, bohinski rj, kuntz c (2006) vertebral osteomyelitis. neurosurg clin n am 17:339– 351. 7. jensen ag, espersen f, skinhoj p, frimodt-moeller n (1998) bacteremic staphylococcus aureus spondylitis. arch intern med 158:509–517. 8. krogsgaard mr, wagn p, bengtsson j: epidemiology of acute vertebral osteomyelitis in denmark: 137 cases in denmark 1978-1982, compared to cases reported to the national patient register 1991-1993. acta orthop scand 1998, 69:513-7. 9. lew dp, waldvogel fa (2004) osteomyelitis. lancet 364:369– 379. 10. mc henry mc, easley ka, locker ga (2002) vertebral osteomyelitis: long-term outcome for 253 patients from 7 clevelandarea hospitals. cid 34:1342–1350. 11. modic mt, feiglin dh, piraino dw, boumphrey fr, weinstein ma, duchesneau pm, rehm su. vertebral osteomyelitis: assessment using mr. radiology. 1985 oct;157(1):157-66. 12. mylona e, samarkos m, kakalou e, fanourgiakis f, skoutelis a (2009) pyogenic vertebral osteomyelitis: a systematic review of clinical characteristics. sem arthritis rheum 39:10–17. 13. pirest dh, peacock je (2005) hematogenous vertebral osteomyelitis due to staphylococcus aureus in the adult: clinical features and therapeutic outcomes. south med j 98:854–862. 14. tsiodras s, falagas me (2006) clinical assessment and medical treatment of spinal infections. clin orthop relat res 444:38–50. 15. weisz rd, errico tj (2000) spinal infections diagnosis and treatment. bull hosp joint dis 59:40–46 16. zimmerli w (2010) vertebral osteomyelitis. n engl j med 362:1022–1029. microsoft word 8negruancuta_penetrating romanian neurosurgery (2018) xxxii 4: 589 592 | 589             doi: 10.2478/romneu-2018-0075 penetrating brain injury with 2 nails as an attempt of suicide ancuța negru, m. angelescu department of neurosurgery emergency county hospital, timişoara, romania abstract: we report the case of a 47-year-old man that was admitted to our hospital secondary to a penetrating brain injury with 2 nails as an attempt of suicide. emergency head ct scan revealed the presence of 2 nails intracranially. the patient underwent surgical removal of the nails by minimal craniectomy. the particularity of the case is the minimal invasiveness of the approach completed by specific follow-up imagistic studies to maximise the outcome. history we present the case of a 47 years old man with no medical or psychiatric history who tried to commit suicide by shooting a nail gun in his temple. patient was referred to the closest hospital where the ct scan of the brain revealed the presence of 2 nails intracranially. he was then transferred to our facility for definitive neurosurgical management. examination at presentation, it was noted that the patient was in remarkably good condition with a glasgow coma scale score of 14 (motor 6, verbal 5, eye 3). a close examination of the scalp revealed 2 small (approx. 5mm) penetrating wounds over right temporal fossae. no portion of any of the nails was visible on the external examination of the head as the wounds where sutured at the previous hospital. the neurological examination demonstrated an incomplete abducens palsy of the right eye, trochlear palsy of the right eye, with diplopia and a slight right-sided hemiparesis. admission laboratory results were within reference limits. the psychiatric evaluation confirmed acute predominantly delusional psychotic disorder. the thorough examination of the ct scan of the brain revealed 2 linear radiopacities with a linear thickness of 0,4 cm and a length of 6,2 cm in the form of nails with a right temporal bone point of entry with comminuted fracture and slight depression at this level. they pass the right temporal lobe and pass beyond the median line, the tip of one being located at the petrous part of the left temporal bone and the other's tip next the fourth ventricle (figure 1). the foreign bodies produce artefacts at the level of the brain, which does not allow the visualization of possible brain damage in their vicinity (figure 2). 590 | negru et al penetrating brain injury with 2 nails as an attempt of suicide             figure 1 figure 2 preoperative management brain ct angiography was performed preoperatively to assess the circulation and demonstrated no evidence of arterial trauma (figure 3). operation under general anesthesia, minimal right temporal craniectomy was performed (figure 4) by the means of carefully raising the comminuted bone fragments right adjacent to the nails with the help of kerrison rongeurs. both nails were extracted by gentle traction and the musculocutaneous incision was rapidly sutured. postoperative course following the neurosurgical procedure, the patient directly underwent brain ct scan for assessing the cerebral parenchyma lesions (figure 5). antibiotics (meropenem and vancomycin) and anticonvulsants were prophylactically administered. romanian neurosurgery (2018) xxxii 4: 589 592 | 591             figure 3 figure 4 infection control was done by the aid of contrast-enhanced ct scan of the brain 6 days postoperatively and a brain magnetic resonance 10 days after surgery, both ruling out any signs of infection. furthermore, a cerebral angiography dsa revealed intact anterior and posterior circulation on both sides without any vascular abnormalities. clinically, without fever, biologically, laboratory results within reference limits and neurologically, gcs 15p with a slight improvement of palsies. given the patient's possible admission that all injuries were self-inflicted, he was transferred to a psychiatric service. figure 5 no abnormal findings except a low-density lesion along the path of the nail and small pneumocephalus 592 | negru et al penetrating brain injury with 2 nails as an attempt of suicide             discussions and literature review in 40% of cases, penetrating skull injuries are fatal because of damage to critical structures, vascular disruption, concussion blast injury, or meningitis. (1, 2, 3, 4, 5, 6, 7). regarding the operation technique there are 2 main options: either by emergency craniotomy under general anesthesia or in an awaked fashion with only local agents (8, 9). the decision is ultimately the choice of the neurosurgeon. as for the infection control there are several measurements to consider: as large as possible debridement of the surrounding tissue, drain catheters inserted in the remaining cavity, and of course broadspectrum antibiotics. in our case we choose to be as minimally invasive as possible. conclusions preoperative cerebral angiography and ct scan are highly recommended to precisely evaluate the brain tissue and vascular damage. we don’t find it mandatory for a wide surgical exposure, but brain ct scans should be repeated as soon as possible. careful neurological examination of the patient as well as late contrast-enhanced images are essential to reveal any potential complications. correspondence ancuța negru department of neurosurgery, emergency county hospital, timişoara, romania, bld. iosif bulbuca no. 10, tel: +40 356 433 422. e-mail address: ancuta.negru@hosptm.ro references 1. litvack zn, hunt ma, weinstein js, west ga. self inflicted nail-gun injury with 12 cranial penetrations and associated cerebral trauma. case report and review of the literature. j neurosurg 2006; 104 (05) 828-834 2. beaveraccheathamml: life-threatening nail gun injuries. am surg65:1113–11161999 3. musa bssimpson bahatfield rh: recurrent self inflicted craniocerebral injury: case report and review of the literature. br j neurosurg 11:564–5691997 4. rezai arlee mkite csmyth djafar jj: traumatic posterior cerebral artery aneurysm secondary to an intracranial nail: case report. surg neurol 42:312– 3151994 5. sakuta yarai s: [penetrating brain injury and traumatic aneurysm caused by a nail gun.]. no shinkei geka 25:357–3621997. (jpn) 6. shibuya tkushi hmiyagi amiyagami mtsubokawa t: [a case of penetrating head injury caused by nail-gun.]. no shinkei geka 21:373–3771993. (jpn) 7. viswanathan rmacarthur dcwhittle ir: nail gun injury to the brain: an unusual case of suicide. scott med j 39:831994 8. rahman nujamjoom ajamjoom zaabu el-asrar a: orbito-cranial injury caused by penetrating metallic foreign bodies: report of two cases. int ophthalmol 21:13–171997 9. sakuta yarai s: [penetrating brain injury and traumatic aneurysm caused by a nail gun.]. no shinkei geka 25:357–3621997. (jpn) a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-015 intraneural synovial sarcoma of median nerve. a rare case report with review of literature sandeep bhardwaj, anil kansal, rohit bansal, rakesh sharma, akangsha sharma romanian neurosurgery (2020) xxxiv (1): pp. 110-115 doi: 10.33962/roneuro-2020-015 www.journals.lapub.co.uk/index.php/roneurosurgery intraneural synovial sarcoma of median nerve. a rare case report with review of literature sandeep bhardwaj, anil kansal, rohit bansal, rakesh sharma, akangsha sharma blk superspeciality hospital, new delhi, india abstract synovial sarcomas are highly aggressive soft tissue tumour with a poor and dismal prognosis. these tumours have a high propensity for distant metastasis and local recurrence. although originally believed to arise from synovium, these tumours have been found to occur anywhere in body1,2. we report here, a case of median nerve sarcoma in a 15-year female. this is a rare tumour, which is diagnosed only after histopathological examination with only a few cases reported in the literature (table 1). although preoperatively tumour was thought to be a nerve sheath tumour, on histopathology analysis was found to be synovial sarcoma. despite aggressive behaviour, wide local excision is recommended even in smaller lesions. so, the diagnosis should always be kept in differentials of nerve sheath tumour, as what may be a synovial sarcoma. introduction synovial sarcomas may arise from different and unusual sites with distinctive morphological genetic features3. they are mostly seen in extremities in young adolescents with male preponderence4. it has been found in unusual locations in heart, lung, small intestine, soft palate and peripheral nerves. only a few cases have been reported in peripheral nerve. prognosis is poor despite radical surgery, radiation and chemotherapy with 50-60 % survival5. these sarcomas have origin in synovium because of periarticular location, but less than 5% are continuous with synovium4. sarcomas have their origin from primitive mesenchymal undifferentiated cells6. synovial sarcoma is diagnosed on immunohistochemical basis because most of them present as lump or swelling with no clinical or diagnostic features7. translocation (x;18) is diagnostic in 90% of cases8.case presented here is a rare sarcoma arising from median nerve in upper arm. we have described here clinical, radiological features and its management. keywords intraneural synovial sarcoma, median nerve, arm, soft tissue tumour corresponding author: sandeep bhardwaj blk superspeciality hospital, new delhi, india sandeep74699@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 111 intraneural synovial sarcoma of median nerve case presentation a 15-year female presented with swelling in left arm for last 6 months with swelling of size of 5*4 cm in left arm which has gradually increased in size. she also complained of pain in left arm radiating along medial aspect of forearm up to left hand. the pain was sharp, and more during night. she also complained of tingling sensation in left upper limb, palm, index and thumb and had history of dropping objects from left hand. on examination, there was decreased sensation along radial three digits with no neurovascular deficit. the patient was evaluated with magnetic resonance imaging (figure 1) which revealed a well encapsulated oval lesion in left upper arm medially burrowing in left biceps and coracobrachialis muscle. the lesion minimally indented the left brachial artery. the lesion was in continuity with median nerve which showed mild enhancement in early and late arterial phase with heterogenous enhancement with non enhancing / cystic areas in venous and delayed phase. overall findings were in favour of neurogenic tumor. electrodiagnostic studies and nerve conduction studies of median nerve were within normal limits. ultrasound color doppler peripheral venous single upper limb was suggestive of hetero-echoic lesion with internal cystic components measuring 43*23 mm causing compression of underlying axillary artery medially at its lower margin. the patient was taken up for surgical resection with preservation of nerve fascicles. the mass found to be associated intimately associated with nerve, soft in consistency and moderately vascular in nature. microvsacular excision of mass was done with preservation of nerve fascicles (figure 2). on histopathological analysis, tumor was greyish tan made up of spindle cells with sheets of cells with vesicular nuclei and ill-defined cell margins suggestive of mild epitheloid morphology (figure 3). focal areas showed perivascular arrangement with cells separated by blood vessels with occasional mitosis and areas of hemorrhage. collagen and osseous tissue was seen adjacent to tumor. on immunohistochemistry cd 99 was positive, ck negative, synaptophysin negative, s-100 negative, hmb-45 negative, bcl2 positive and ki-67 was 15-20 % in cellular areas (figure 4). the histopathological and immunohistochemical analysis were in favour of synovial sarcoma. post operatively, whole body pet/cect scan was done for any metastasis and restaging. this was suggestive of small minimally metabolic active solid soft tissue thickening in proximal left biceps muscle indenting left brachial artery probably? residual lesion. post excision, patient received radiotherapy. 112 sandeep bhardwaj, anil kansal, rohit bansal et al. discussion synovial sarcomas arising from median nerve are very rare and rarest tumors published in literature. other sarcomas arising from various nerves reported in literature are from radial, common digital, posterior tibialis, peroneal, facial nerve, s1 root, c7 root and brachial plexus. there are three basic histology features of synovial sarcoma. the most common pattern is biphasic followed by monophasic and poorly differentiated synovial sarcomas. synovial sarcoma with biphasic type consisted of epithelial cells with fibroblast like spindle cell in various proportions. monophasic type consists of spindle cells only and are difficult to differentiate from other soft tissue and nerve tumors but now can be differentiated on the basis of immunohistochemical analysis4. third pattern of poorly differentiated synovial sarcomas that has worse prognosis and has also been described6. prognosis of biphasic versus monophasic is still under debate9,10,11,12. the present case in our study was biphasic synovial sarcoma having both epithelial and spindle cells in various proportions. it was immunohistochemical positive for cd99 and bcl2. the neoplastic proliferation with characteristic ss18-ssx1 with chromosomal fusion at molecular level is a feature consistent with diagnosis with synovial sarcoma4. patient was advised for chromosomal analysis, but due to financial constraints patient refused for same. published cases of median nerve synovial sarcoma with review of literature is summarised in table 1 and table 2 respectively. chromosomal translocation is the most efficient way to establish the diagnosis of synovial sarcoma. a gene translocation between chromosomes 18 and x t(x;18) (p11.2; q11.2) occurs in over 90% of synovial sarcomas4. this leads to fusion of one of two variants of the ssx gene with the syt gene, resulting in either the syt/ssx1 or syt/ssx2 chimeric fusion proteins4,6. nearly all biphasic tumors express syt/ssx1, while monophasic tumors express syt/ssx1 in approximately half of the cases and syt/ssx2 in the remainder13. patients with syt/ssx2 expressing tumors have a significantly better prognosis when compared to those with syt/ssx1 tumors in terms of rates of metastasis and overall survival13,14,15,16. factors associated with poor prognosis includes old age, tumor size more than 5 cm, bone, nerve and vascular invasion and poor differentiation with higher mitotic index 12,17,18,19.management of synovial sarcoma is wide surgical excision, radiation therapy, and adjuvant chemotherapy which has been found to be correlated to be associated with better prognosis2,20 surgical management followed by radiation and chemotherapy is associated with good prognosis2,20. 5-year survival rates of synovial sarcomas have been around 50-60%, inspite of advances in treatment2,21,22. mortality in synovial sarcoma results from distant metastasis, most frequently to lung23. radical surgical incision followed by radiation allowed for potential decrease in local recurrence but systemic metastasis remained high even with adjunct chemotherapy24. 113 intraneural synovial sarcoma of median nerve conclusion synovial sarcoma involving median nerve is a rare and aggressive tumor and is one of the few cases already published in literature. synovial sarcoma can occur anywhere in our body and should be kept in differentials involving peripheral nerves as in our case. as diagnosis is always made post-operative on histo-patholoical analysis with immunohistochemistry, resulting in change in treatment strategy and final outcome of patient. as in our 114 sandeep bhardwaj, anil kansal, rohit bansal et al. patient, preoperative diagnosis was a benign neurofibroma/schwannoma, we must be aware of aggressive tumor which overall changes the complete treatment and should be always be kept in differentials and managed accordingly. references 1. sandberg aa, bridge ja. updates on the cytogenetics and molecular genetics of bone and soft tissue tumors. synovial sarcoma. cancer genet cytogenet.2002:133:123. 2. guadangnolo ba, zagars gk, ballo mt, et al. long term outcomes for synovial sarcoma treated with conservation surgery and radiotherapy . int j radiat oncol biol phy. 2007;69:1173-80. 3. weiss sw, goldblum jr: enzinger’s and weiss’s soft tissue tumors. 5th ed., philadelphia, mosby elsevier, 2008, 11611182. 4. fischer c. synovial sarcoma .ann diagn pathol. 1998;2(2)401-21. 5. zeren h, moran ca, suster s, fishback nf, koss mn: primary pulmonary sarcomas with features of monophasic synovial sarcomas. a clinicopathological, immunohistochemical and ultrasturctural study of 25 cases. hum pathol; 26:474-480. 6. enzinger fm, weiss sw. soft tissue tumors. st. louis: mosby;1993.synovial sarcoma;pp.757-86. 7. kransdorf mj. malignant soft tissue tumors in a large referral population: distribution of diagnosis by age,sex and location.am j roentgenol.1995;164:129-34. 8. palmerini e, staals el, alberghini m, zanella l, ferrari c, benassi ms, et al. synovial sarcoma: retrospective analysis of 250 patients treated at a single institution. cancer. 2009;115:2988–98. 9. chu pg benhattar j, weiss lm, et al. intraneural synovial sarcoma: two cases. mod pathol. 2004;17:258-63. 10. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 11. kawai a, woodruff j, healey jh, et al. syt-ssx gene fusion as a determinant of morphology and prognosis in synovial sarcoma. n engl j med. 1998;338:153–60. 12. trassard m, le doussal v, hacène k, et al. prognostic factors in localized primary synovial sarcoma: a multicenter study of 128 adult patients. j clin oncol. 2001;19:525–34. 13. kawai a, woodruff j, healey jh, et al. syt-ssx gene fusion as a determinant of morphology and prognosis in synovial sarcoma. n engl j med. 1998;338:153–60. 14. ladanyi m, antonescu cr, leung dh, et al. impact of sytssx fusion type on the clinical behavior of synovial sarcoma: a multiinstitutional retrospective study of 243 patients. cancer res. 2002;62:135–40. 15. inagaki h, nagasaka t, otsuka t, et al. association of sytssx fusion types with proliferative activity and prognosis in synovial sarcoma. mod pathol. 2000;13:482–8. 16. nilsson g, skytting b, xie y, et al. the syt-ssx1 variant of synovial sarcoma is associated with a high rate of tumor cell proliferation and poor clinical outcome. cancer res. 1999;59:3180–4. 17. o'connell jx, browne wl, gropper pt, et al. intraneural biphasic synovial sarcoma: an alternative “glandular” tumor of peripheral nerve. mod pathol. 1996;9:738–41. 18. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 19. bergh p, meis-kindblom jm, gherlinzoni f, et al. synovial sarcoma: identification of low and high risk groups. cancer. 1999;85:2596–607. 20. choong pfm, pritchard dj, sim fh, et al. long-term survival in high grade soft tissue sarcoma: prognostic factors in synovial sarcoma. int j oncol. 1995;7:161–9. 21. spillane aj, a'hern r, judson ir, et al. synovial sarcoma: a clinicopathologic, staging, and prognostic assessment. j clin oncol. 2000;18:3794–803. 22. krsková l, kalinová m, brízová h, et al. molecular and immunohistochemical analyses of bcl2, ki-67, and cyclin d1 expression in synovial sarcoma. cancer genet cytogenet. 2009;193:1–8. 23. enzinger fm, weiss sw. soft tissue tumors. st. louis: mosby; 1993. synovial sarcoma; pp. 757–86. 24. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 25. cugola l, pisa r. synovial sarcoma: with radial nerve involvement. j hand surg (br) 1985;10:243-4. 26. rinehart gc, mustoe ta, weeks pm. management of synovial sarcoma of the median nerve at the elbow. plast reconstr surg 1989;528-32. 27. tacconi l, thom m, thomas dg. primary monophasic synovial sarcoma of the brachial plexus: report of case and review of literature. clin neurol neurosurg 1996;98:249-52. 28. spielmann a, janzen dl, o’connell jx, munk pl. intraneural synovial sarcoma. skeltal radiol 1997;26:67781. 29. chesser tj, geraghty jm, clarke am. intraneural synovial sarcoma of median nerve. j hand surg(br) 1999;24:3735. 30. zenmyo m, komiya s, hamada t, et al. intraneural monophasic synovial sarcoma: a case report. spine 2001;26:310-3. 31. lestou vs, o’connell jx, robinchaud m,et al. cryptic t(x;18), ins(6;18), and syt-ssx2 gene fusion in a case of intraneural monophasic synovial sarcoma. cancer genet cytogenet 2002;138:153-6. 32. weinreb i, perez-ordonez b, guha a, kiehl tr. mucinous gland predominant synovial sarcoma of a large 115 intraneural synovial sarcoma of median nerve peripheral nerve : a rare case closely mimicking metastatic mucinous carcinoma. j clinical pathol 2008;61:672-6. 33. uehara h, yamasaki k, fukushima t, et al. intraneural synovial sarcoma originating from median nerve. neurol med chir 2008;48:77-82. doi: 10.33962/roneuro-2022-019 full endoscopic lumbar decompression of spinal stenosis through uniportal approach. technique and preliminary results talat cem ovalioglu, salih aydin romanian neurosurgery (2022) xxxvi (1): pp. 110-115 doi: 10.33962/roneuro-2022-019 www.journals.lapub.co.uk/index.php/roneurosurgery full endoscopic lumbar decompression of spinal stenosis through uniportal approach. technique and preliminary results talat cem ovalioglu1, salih aydin2 1 bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery, istanbul, turkey 2 uskudar university faculty of medicine, department of neurosurgery, istanbul, turkey abstract introduction: to investigate the certain advantages of full endoscopic lumbar decompression (feld) surgery over conservative techniques in lumbar spinal stenosis (lss). minimal invasive techniques have been introduced recently to treat lumbar spinal stenosis and gained popularity over conservative techniques because of the minimal tissue damage along with the satisfactory postoperative outcome. in our study, the feld technique using a uniportal approach is described and investigated in accordance with the preliminary clinical results of patients who had degenerative spinal stenosis. methods: 55 patients who underwent feld were retrospectively reviewed. general demographics and parameters including operation time, length of hospital stay, mean time to return to work, complications were recorded. clinical outcomes were evaluated using the visual analogue scale (vas) for low back and leg pain, oswestry disability index (odi) for functional assessment. results: the mean follow-up time was 36 months. there was no measurable intraoperative blood loss. the mean operating time was 97,4 minutes. the length of hospital stay after the operation was 27 hours on average. the difference between preoperative and postoperative vas scores was statistically significant (p<0.001). no surgery-related complication was noted. conclusions: amongst other standard techniques, feld has the technical advantages of less paraspinal muscle dissection, less tissue trauma, less risk of spinal instability, minimal blood loss, quicker postoperative recovery and shorter length of hospital stay. introduction degenerative lumbar stenosis is caused by the hyperthrophy of the surrounding bone structures and disco-ligamentous complex and it is more prevalent in the elderly. the compression may cause clinical symptoms of neurogenic claudication with radicular signs. back pain is more likely attributable to the degenerative process, such as segmental instabilities or deformities. keywords endoscopic, lumbar decompression, spinal stenosis, uniportal approach corresponding author: talat cem ovalioglu bakirkoy research and training hospital for neurology, turkey talatovalioglu@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 111 full endoscopic lumbar decompression of spinal stenosis through uniportal approach as minimal invasive techniques, biportal endoscopic decompression technique and uniportal full endoscopic lumbar decompression technique have been introduced recently and it has been reported to have favorable clinical results and less muscle damage for lumbar spinal stenosis and has begun to attract attention. since then, several studies were reported satisfactory results with a follow-up of more than two years after unilateral biportal endoscopic lumbar decompression 8, 9, 13. thus, feld has been suggested as an alternative to open laminectomy. this study evaluates the short-term outcome of unilateral uniportal endoscopic spinal surgery for degenerative spinal stenosis instead of biportal approach. material and methods in this study, 55 patients with symptomatic degenerative lumbar stenosis, who underwent feld operation between 2014 and 2015 were evaluated retrospectively. the indication for surgery was defined according to present-day standards based on radiographic images, radicular pain symptoms or neurogenic claudication unresponsive to conservative treatment and progressive neurological deficits3. ethical approval was obtained from the ethical committee and a written informed consent was obtained from participants in the study prior to surgery. preoperative and postoperative imaging data, including magnetic resonance imaging (mri) and computed tomography (ct) images were collected. follow-up visits were conducted on 3rd, 12th and 36th month as the final follow up. clinical examination was made during the follow-up visits. in addition to general parameters, pain related information was obtained using these questionnaires: vas for back and leg pain and odi for functional assessment. clinical inclusion criteria was neurogenic claudication with unilateral or bilateral leg pain with or without paresis. exclusion criterias were predominant back pain, mono segmental recess stenosis, foraminal stenosis in the lower level, coexisting disc herniation, degenerative spondylolisthesis with maximum meyerding grade i, multidirectional rotation slide,, scoliosis (maximum curvature 20°), prior surgery of the same segment. full-endoscopic instruments the working sheath has an outer diameter of 10 mm and an opening with an oblique tip that enables enhanced visualization. insertion of the working sheath is made bluntly using a dilator. an optic with an outer diameter of 9.5mm is inserted through the working sheath. the optic contains an intraendoscopic, excentric working canal with a diameter of 5.7 mm, a light conductor system, a canal for continuous irrigation and a rod lens system. the angle of vision is 25 degrees. various instruments including drills up to 5.5 mm in diameter can be used through the working canal. all of the operating instruments and optic products were supplied by the wolf company (richard wolf gmbh, knittlingen, germany). operative technique the full-endoscopic interlaminar operation technique was described previously in the literature.17-19 under general anesthesia, patients are positioned in prone position under radiographic control (figure 1). a dilator is inserted bluntly to the lateral edge of the interlaminar window and an operating sheath with an oblique opening is directed toward the ligamentum flavum under constant irrigation. the identification of the medial edge of the ascending facet is made, normal anatomy is recognized (figure 2). then ipsilateral decompression is achieved by cranial and caudal laminectomy, partial facetectomy, and ligamantum flavum resection. then on the contralateral side of the dorsal dura, the ligamentum flavum is initially left intact in order to protect the dura and craniocaudal laminectomy, partial facetectomy is performed (figure 3). subsequently, the ligamentum flavum is completely resected. the decompression is concluded when the dura and the spinal nerves are adequately decompressed on both sides (figure 4). none of the patients had intradiscal nucleotomy along with the fenestration of the annulus. statistical analysis numerical variables expressed by mean, standard deviation. statistical analysis was calculated using the spss (statistical package for social sciences) version 21.0 for windows (spss inc., chicago, il, usa). paired t-test were applied to compare the 112 talat cem ovalioglu, salih aydin preoperative and postoperative vas, odi parameters. p<0.05 was considered significant. results study group there were 21 female and 34 male patients aged between 44 and 84 years (mean 58,2 years). the duration of symptoms ranged from 2 to 78 months (mean 19 months). preoperative average walking distance of the patients was 30 meters. 45 interventions were performed at the l4–l5 level, l3–l4 level was operated on five patients; l5s1 level was operated on two patients; l1-l2 level was operated on two patients; l2–l3 level was operated on one patient. throughout 12 patients who were under the age of 50, 9 patients were operated on the l4-5 level, one patient on the l1-2, one patient on the l3-4 and one patient on the l5-s1 level. no recurrence or complication was noted. throughout the rest of the patients who were over 50 years old, 37 patients were operated on the l4-5 level, four patients on the l3-4, one patient on the l1-2, one patient on the l2-3 level. same as the young age group, no recurrence and complications were noted. perioperative and postoperative outcome the mean operating time was 97,4 minutes (65 to 120min). there was no measurable blood loss. adequate bleeding control was achieved via continuous irrigation and the use of radiofrequency bipolar coagulation. the patients were mobilized five hours after the operation depending on the effects of the anesthesia. overall hospital stay was 27 hours on average and mean time to return to work was 14 days. there were 3 cases of back pain in which the patient recovered well following physical therapy and 5 cases of paresthesia that gradually improved following 2 – 3 weeks of rehabilitation. there were no other complications such as dural tear, hematoma, delayed wound healing, softtissue infection, spondylodiscitis, cauda-equina syndrome or thrombosis. all procedures were successfully completed via endoscopic approach, there was no need to convert to an open approach. clinical outcome significant reduction of radicular pain was noted postoperatively, along with the statistically significant results of vas and odi questionnaires. preoperative vas leg score on the affected side was 7.9±1.1 and the postoperative vas leg score improved to 1.1±0.7 early postoperatively. the improvement was statistically significant (p< 0.001). significant improvement of vas leg scores was achieved on 3rd month, 12th month and 36th month follow-up visits, 0.3 ± 0.5, 0.2 ± 0.5 and 0.1 ± 0.3 respectively (p< 0.001). significant improvement of vas back scores was noted on 3rd month, 12th month and 36th month follow-up visits, 1.6 ± 0.7, 1.01 ± 0.8 and 0.9 ± 0.9, respectively (p< 0.001). odi scores changed from 48.2 ± 21.9 preoperatively to 26.6 ± 7.9 early postoperatively (p< 0.001). significant improvement was noted on 3rd month, 12th month and 36th month follow-up visits, 20.4 ± 5.6, 14.5 ± 5.5 and 12.8 ± 5.4 (p< 0.001) respectively. furthermore, significant development in the walking distance of the patients was observed statistically. walking distance increased from 30.7 ± 14.4 meters to 124.3 ± 38.8 meters early postoperatively (p< 0.001). significant improvement in walking distance was noted on 3rd month,12th month and 36th month final follow-up visits; 301.2 ± 81.1 meters, 682 ± 86.2 and 703.6 ± 202.2 meters respectively (p< 0.001). discussion lumbar spinal stenosis is the result of a dejenerative process, including facet joint hypertrophy, loss of intervertebral disc height, disc bulging, osteophyte formation, and hypertrophy of the ligamentum flavum 1. the hallmark of spinal stenosis is neurogenic claudication, consisting of lower limb pain and neurological symptoms exacerbated by walking 19. nonetheless, people with lss often avoid walking and have reduced walking capacity because of the pain and discomfort in the lower extremities during walking 10, 21. the lss patients also suffer from physical impairments including poor balance, sensory loss (numbness or tingling), and muscle weakness in the lower extremities10, 11. symptoms are generally intermittent and posture-dependent. mostly they appear with standing for a long time and lumbar extension. the symptoms usually worsen by walking and they are relieved by rest in a flexed or seated position. radicular pain may be due to a combination of mechanical compression, inflammatory irritation of neural elements, vascular congestion and segmental instability 1. 113 full endoscopic lumbar decompression of spinal stenosis through uniportal approach depending on the severity of stenosis, various kinds of treatments are available, from surgical procedures to conservative methods. open microscopic laminectomy procedure has been the common standard surgical treatment method for various types of lumbar spinal stenosis. the standard surgery procedure requires, followed by laminectomy and excision of hypertrophic ligamentum flavum for decompression. the multifidus muscle injury and muscle atrophy occur frequently after posterior lumbar spine surgery, and they are associated with lower back pain and functional disability7. postoperative iatrogenic instability following microscopic laminectomy procedure, is a possible postoperative outcome of this technique. however, it has been reported to occur rarely following these procedures. silvers et al. reported that lumbar instability rarely occur after open laminectomy procedure 20. since several studies have reported favorable long-term results, the technique is currently considered the standard technique 2, 6. nowadays, the main goal is to preserve normal anatomical spinal alignement without causing postoperative spinal instability. it has been shown that standard microsurgical lumbar decompression may lead to iatrogenic muscle injury and spinal instability, requiring additional surgical intervention for stabilization 5. regarding these complications, minimal invasive techniques have been introduced recently. on 2015, komp et al. reported bilateral fullendoscopic decompression with equivalent clinical results and less complication rate, less operation time when compared to standard microsurgical laminectomy 14. minimal invasive techniques include bilateral decompression using biportal unilateral approach and uniportal unilateral approach for patients with lumbar stenosis 9, 13, 16. the difference between uniportal and biportal technique is the number of the portals in use during the operation. biportal technique requires two portals whereas uniportal technique requires only one portal for the endoscope and the remaining endoscopic instruments. there isn’t adequte proof of one’s superiority, since it depends on the surgeon’s experience with the technique 9. via uniportal endoscopic technique, there may be no need to make a large facet resection intraoperatively, except when there is hypertrophy of the superior facet that compresses the spinal cord through lateral recess. with the novel endoscopic instruments providing better visual control, stability of the facet joint is not violated significantly while resecting bone elements and this prevents lateral wedging motion of the vertebral segment which maintains stability even after decompression. this technique also allows an extended view of the foramen and lateral recess, especially of the contralateral side, adequately. an enhanced visualization may lead to less neural injury, with adequate decompression of lateral recess and neural foramen on both ipsilateral and contralateral sides. the procedure is performed under general anesthesia with a 1cm vertical incision for each level. this minimal invasive technique with minimal incision site thus leads to less infection rate and it provides an opportunity for even elderly patients who have preexisting comorbidities prior to the procedure. the benefits of feld approaches include decreased blood loss, shorter operation time, shorter hospital stay, decreased postoperative narcotic requirement, decreased rate of infection and cerebrospinal fluid leak and a decrease in time to return to work. lee et al. reported mean time of 2.4 days of hospital stay after uniportal endoscopic laminotomy for spinal stenosis 15. in our study, despite the lack of comparison with lumbar microsurgery patients, mean time to return to work and total hospital stay is significantly short such as 14 days and 24 hours respectively. this result was consistent with the recent literature 15. as for complications, dural tear incidence is the most common complication noted during feld surgery. in 2017, kim et al. reported 6.25% cerebrospinal fluid leakage rate in 48 patients who had endoscopic lumbar decompression procedure 12. since our clinic has fair number of endoscopic cases, there hasn’t been any serious complication perioperatively. we have encountered low infection rate and no cerebrospinal fluid leakage was noted. however, it is important to emphasize that the learning curve is steep for endoscopic operations and complications like cerebrospinal fluid leakage may occur at the beginning phase of this process. as shown in the study of bresnahan et al., preservation of the posterior elements via endoscopic techniques is associated with better 114 talat cem ovalioglu, salih aydin outcomes regarding lumbar spinal stability. main conclusions of these studies are less tissue trauma, shortened rehabilitation period and less postoperative complications 4, 14. since our study is a case series study, a comparison could not be stated, however, our results were consistent with the literature. along with these advantages, there are some certain disadvantages of the procedure, such as; the limited possibility of extending the approach in a case of possible neural injury or cerebrospinal fluid leakage and the steep learning curve of the procedure which may lead to higher complication rate at the beginning of the practice. conclusions the feld operation through uniportal approach for lumbar degenerative stenosis is a sufficient and safe supplementation and alternative to the conventional microsurgical procedure. in our experience, the advantages of the procedure are; facilitation of the procedure via excellent visualization, good illumination, and expanded field of vision with 25 degrees optics; short operating time, adequate pain relief, reduced tissue trauma and rapid rehabilitation. references 1. atlas sj, delitto a. spinal stenosis: surgical versus nonsurgical treatment. clin orthop relat res. 2006;443: 198-207. https://doi.org/10.1097/01.blo.0000198722.70138.96. 2. atlas sj, keller rb, robson d, deyo ra, singer de. surgical and nonsurgical management of lumbar spinal stenosis: four-year outcomes from the maine lumbar spine study. spine (phila pa 1976). 2000;25(5): 556-562. https://doi.org/10.1097/00007632-200003010-00005. 3. binder dk, schmidt mh, weinstein pr. lumbar spinal stenosis. semin neurol. 2002;22(2): 157-166. https://doi.org/10.1055/s-2002-36539. 4. bresnahan l, ogden at, natarajan rn, fessler rg. a biomechanical evaluation of graded posterior element removal for treatment of lumbar stenosis: comparison of a minimally invasive approach with two standard laminectomy techniques. spine (phila pa 1976). 2009;34(1): 17-23. https://doi.org/10.1097/brs.0 b013e318191438b. 5. bresnahan le, smith js, ogden at, et al. assessment of paraspinal muscle cross-sectional area after lumbar decompression: minimally invasive versus open approaches. clin spine surg. 2017;30(3): e162-e168. https://doi.org/10.1097/bsd.0000000000000038. 6. caputy aj, luessenhop aj. long-term evaluation of decompressive surgery for degenerative lumbar stenosis. j neurosurg. 1992;77(5): 669-676. https://doi.org/10.3171/jns.1992.77.5.0669. 7. fan s, hu z, zhao f, zhao x, huang y, fang x. multifidus muscle changes and clinical effects of one-level posterior lumbar interbody fusion: minimally invasive procedure versus conventional open approach. eur spine j. 2010;19(2): 316-324. https://doi.org/10.1007/s00586009-1191-6. 8. huang yh, lien fc, chao ly, lin ch, chen sh. full endoscopic uniportal unilateral laminotomy for bilateral decompression in degenerative lumbar spinal stenosis: highlight of ligamentum flavum detachment and survey of efficacy and safety in 2 years of follow-up. world neurosurg. 2020;134: e672-e681. https://doi.org/10.1016/j.wneu.2019.10.162. 9. hwa eum j, hwa heo d, son sk, park ck. percutaneous biportal endoscopic decompression for lumbar spinal stenosis: a technical note and preliminary clinical results. j neurosurg spine. 2016;24(4): 602-607. https://doi.org/10.3171/2015.7.spine15304. 10. iversen md, katz jn. examination findings and selfreported walking capacity in patients with lumbar spinal stenosis. phys ther. 2001;81(7): 1296-1306. 11. johnsson ke, rosen i, uden a. neurophysiologic investigation of patients with spinal stenosis. spine (phila pa 1976). 1987;12(5): 483-487. https://doi.org/10.1097/00007632-198706000-00012. 12. kim hs, paudel b, jang js, et al. percutaneous full endoscopic bilateral lumbar decompression of spinal stenosis through uniportal-contralateral approach: techniques and preliminary results. world neurosurg. 2017;103: 201-209. https://doi.org/10.1016/j.wneu.2017.03.130. 13. kim sk, kang ss, hong yh, park sw, lee sc. clinical comparison of unilateral biportal endoscopic technique versus open microdiscectomy for single-level lumbar discectomy: a multicenter, retrospective analysis. j orthop surg res. 2018;13(1): 22. https://doi.org/10.1186/s13018-018-0725-1. 14. komp m, hahn p, oezdemir s, et al. bilateral spinal decompression of lumbar central stenosis with the fullendoscopic interlaminar versus microsurgical laminotomy technique: a prospective, randomized, controlled study. pain physician. 2015;18(1): 61-70. 15. lee cw, yoon kj, jun jh. percutaneous endoscopic laminotomy with flavectomy by uniportal, unilateral approach for the lumbar canal or lateral recess stenosis. world neurosurg. 2018;113: e129-e137. https://doi.org/10.1016/j.wneu.2018.01.195. 115 full endoscopic lumbar decompression of spinal stenosis through uniportal approach 16. ruetten s, komp m, godolias g. an extreme lateral access for the surgery of lumbar disc herniations inside the spinal canal using the full-endoscopic uniportal transforaminal approach-technique and prospective results of 463 patients. spine (phila pa 1976). 2005;30(22): 2570-2578. https://doi.org/10.1097/01.brs.0000186327.21435.cc. 17. ruetten s, komp m, godolias g. a new full-endoscopic technique for the interlaminar operation of lumbar disc herniations using 6-mm endoscopes: prospective 2-year results of 331 patients. minim invasive neurosurg. 2006;49(2): 80-87. https://doi.org/10.1055/s-2006932172. 18. ruetten s, komp m, merk h, godolias g. full-endoscopic interlaminar and transforaminal lumbar discectomy versus conventional microsurgical technique: a prospective, randomized, controlled study. spine (phila pa 1976). 2008;33(9): 931-939. https://doi.org/10.1 097/br s.0b013e31816c8af7. 19. ruetten s, komp m, merk h, godolias g. use of newly developed instruments and endoscopes: full-endoscopic resection of lumbar disc herniations via the interlaminar and lateral transforaminal approach. j neurosurg spine. 2007;6(6): 521-530. https://doi.org/10.3171/spi.20 07.6.6.2. 20. silvers hr, lewis pj, asch hl. decompressive lumbar laminectomy for spinal stenosis. j neurosurg. 1993;78(5): 695-701. https://doi.org/10.3171/jns.1993.78.5.0695. 21. tomkins-lane cc, holz sc, yamakawa ks, et al. predictors of walking performance and walking capacity in people with lumbar spinal stenosis, low back pain, and asymptomatic controls. arch phys med rehabil. 2012;93(4): 647-653. https://doi.org/10.1016/j.ap mr.2011.09.023. doi: 10.33962/roneuro-2022-036 flail bone flap in decompressive craniotomy for infants. a case series of five patients mohammad fekry elshirbiny, m.m. amen, assem ahmed romanian neurosurgery (2022) xxxvi (2): pp. 203-208 doi: 10.33962/roneuro-2022-036 www.journals.lapub.co.uk/index.php/roneurosurgery flail bone flap in decompressive craniotomy for infants. a case series of five patients mohammad fekry elshirbiny, m.m. amen, assem ahmed mansoura faculty of medicine, egypt abstract background: subdural hematoma in infants is a challenging condition. acute subdural hematomas can cause intracranial hypertension and a midline shift, but decompressive craniotomies in young patients have shown promising results with specific complications in this age group. hinge craniotomy is an old technique used in many neurosurgical procedures associated with elevated intracranial pressure. the objective of this study is to report the usage of flail bone flap in the management of acute subdural hematoma in infants, its outcome, advantages, disadvantages and related complications. methods: this is a review of the medical records of 5 infants younger than one-yearold who underwent decompressive craniotomy as management of acute subdural hematoma at mansoura university hospital. results: in this series, five babies were included. operative time for decompressive craniotomy (dc) ranged from 1 h and 40 min to 3 h. four infants survived. three infants recovered with good outcomes and one infant developed hemiparesis. conclusion: the use of flail bone flap technique in decompressive craniotomy is associated with a high success rate and low incidence of complications. large-based studies are still required for a better assessment of the results. introduction although acute subdural haematoma is considered uncommon in infants with an incidence of about 20-25 per 100000 cases but its management is a challenging condition. the most common cause in this age group is child abuse especially the shaken baby syndrome. [1]. infantile subdural hematomas cause convulsive seizures, consciousness disorders, retinal haemorrhage, or apnea, which can progress to coma with hemiplegia or death [2]. if it is accompanied by intracranial hypertension, it will result in diffuse edoema, which will then lead to cerebral ischemia [3]. when treating infantile asdh surgically, one must take into consideration how to best regulate intracranial pressure while minimising the risk of complications [4]. decompressive craniectomy (dc) has been successfully used to alleviate (icp) and massive brain swelling following infarction or keywords subdural hematoma, flail bone flap, decompressive craniotomy corresponding author: mohammad fekry elshirbiny mansoura faculty of medicine, egypt mohammad.fekry@mans.edu.eg copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 204 mohammad fekry elshirbiny, m.m. amen, assem ahmed bleeding [5-7]. improved cerebrovascular compliance, cerebral oxygenation, and cerebral perfusion can be achieved through reductions in icp [8]. after a dc, a cranioplasty procedure is required [9] utilising either one's own autologous skull or more expensive synthetic materials [10]. cranioplasty has been associated with some complications including surgical site infection (ssi) [11-13] and bone graft resorption (bgr) in pediatric populations [12-15]. during a decompressive craniotomy, a bone flap will be elevated followed by opening of the dura and evacuation of the hematoma. finally, the bone flap will be repositioned loosely without fixation. the replacement of the bone flap eliminates the need of a second operation lead to avoidance of decompressive craniectomy and subsequent cranioplasty related complications. [16]. there is no clear guidelines for management of ash using craniotomy, so we reported our experience with hinge craniotomy in 5 infants in our tertiary care centre. patients and methods this retrospective case series that was conducted at mansoura university neurosurgery department after obtaining approval from the local ethical committee and institutional review board of mansour faculty of medicine. we included five pediatric cases along one year duration. all patients were subjected to standard history taking, general and detailed neurological examination. initial gcs and presence of other intracranial pathologies were also assessed. on admission, a ct scan of the patient's brain was analyzed to determine the hematoma's thickness as well as the amount of midline shift. the glasgow outcome scale (gos) was used to evaluate the results, and the follow-up period was increased to six months. in addition, routine preoperative laboratory and radiological investigations were ordered. after deciding on surgical intervention, it was completely explained to the patients' guardians with its indications and complications and following that, informed written consent was obtained. all of the procedures were carried out under general anesthesia. a large frontotemproparital question mark skin incision was done on the affected side followed by preservation of pericranial graft to be utilized in duroplasty.after that a small burrhole was done in the temporal region as fast as possible with small opening to the dura to help in relieve of the increase intracranial pressure followed by dissection of the dura from the skull bone. due to very thin bone we used a scissor to complete the craniotomy with continuous dissection and separation of the dura from the bone flap. at the level of coronal suture, the dissection was difficult due to tight adhesion of the dura to the bone so we utilized this limb to hinge the bone flap without doing complete bone elevation. the squamous temporal bone was rongeured to the temporal fossa floor, ensuring that no edge of bone remained that could prevent the swollen temporal lobe from being displaced laterally. the dura was opened in cruciate shape manner followed by evacuation of the haematoma and ensuring haemostasis. then the pericranial graft was used to do duroplasty and the craniotomy flap was left hinged without fixation followed by anatomical closure in layers. all patients received standard post-operative care, with frequent assessment throughout the day. any post-operative complications were noted and then recorded. regular follow up visits were scheduled for these cases. early follow up c.t scan was done to all patients to document evacuation of the hematoma, improvement of the midline shift and to detect any complications that need further management. during the follow up serial follow up c.t scans was ordered to evaluate the brain and the fate of the bone flap. statistical analysis microsoft excel was used to enter and analyse the data. this was followed by data being imported into the statistical package for social sciences (spss 27, ibm/spss inc., chicago, il) for windows. according to kolmogorov-smirnov and shapiro-tests, wilk's the baseline characteristics of the study population were presented in the form of frequencies and percentages (percent) or mean values and standard deviations (sd) or median and range. results the study included 5 infants, 3 boys (60%) and 2 girls (40%). their age ranged from 25 days to 180 days with mean age of 81.5 days. 205 flail bone flap in decompressive craniotomy for infants the cause of sdh was spontaneous in four cases (80%) and traumatic in one case only (20%). the hematoma located in the left side in 3 cases (60%) and on the right side in 2 cases (40%). the sdh was associated with ich in one case only. the lowest preoperative gcs was 5/15 (in one case) and the highest score was 11/15 (in two cases) while the other two cases had gcs of 8/15 and 10/15 respectively. coagulopathy was detected in 4 cases (80%). the mean operative time was 136 minutes with range between 100 minutes and 180 minutes. regarding the outcome in our study, 3 cases (60%) showed favourable outcome in the form of full recovery while 1 case survived with rt. sided weakness g 3. one case died thar represented 20% mortality rate. table 1. detailed literature gender age diagnosis preop gcs coagulopathy operative time (min) outcome boy 25 days lt. acute sdh (spontaneous) 8/15 yes 100 fully recovered girl 2 months rt. acute sdh (spontaneous) 10/15 yes 130 fully recovered boy 4 months lt. acute ich + sdh (spontaneous) 11/15 yes 180 survived with rt. sided weakness g 3 boy 3 months 14 days lt. acute sdh (spontaneous) 5/15 yes 150 died girl 6 months rt. acute sdh (trauma, fall) 11/15 no 120 fully recovered figure 1. 25 days old male child with left acute sdh 206 mohammad fekry elshirbiny, m.m. amen, assem ahmed figure 2. first day post operative after hematoma evacuation and flail bone flap position. figure 3. 2 months postoperative with disappearance of midline shift and bone flap return to normal position 207 flail bone flap in decompressive craniotomy for infants discussion there are numerous surgical and non-surgical treatments for asdhs, including burr holes, craniectomies, osteoplastic flaps, subtemporary decompressions, temporal lobectomy, dural openings, dural augmentation, and dural snips [1720] . in spite of everyone's best efforts, the reported mortality rate has remained somewhere between 80 and 90 percent, and the morbidity rate among the population that has managed to survive has been extremely high [18, 19, 21, 22]. in addition to being less invasive surgically, the technique for hinged bone grafts leaves only one scar, eliminates the need for a second surgery to replace the bone graft, and is more anaesthetically preferred. our results showed full recovery in 3 cases (60%), 1 case died that represented 20% and 1 case survived with right sided weakness represented 20% morbidity. in a study involving 30 adult patients diagnosed with asdhs and undergoing craniectomy, subcutaneous placement of a hinged flail was used, according to the findings of abd el-wahed and ahmed, 17 patients passed away while being treated at the hospital, accounting for 66.7 percent of the total; 13.3 percent of the patients who survived did so in a vegetative state, while 9 patients made a full recovery (30 percent ) [23]. the variation could be explained due to different age groups. the dc group had a worse preoperative gcs, younger age, more extracranial injuries, and a more severe ct, according to a study by li et al., indicating that dc may be more effective than cr based on the actual outcomes, which were comparable in the two groups despite the predicted outcomes being worse for the dc group [24]. tsermoulas et al. evaluated a total of 99 patients, 69 of whom had dc, 17 of whom had cr with a "riding flap," and 13 of whom had cr with a "fixed retained flap.". despite the fact that patients in the dc group had worse outcomes, the baseline characteristics of the two groups were very different; those with dc had significantly more severe mechanisms, lower gcs, more extracranial injuries, and higher rotterdam ct scores than those in the control group [25]. more herniation (pupillary changes) was found in the dc group, which was found by woertgen et al., who looked at 180 patients (111 cr and 69 dc) and found a higher mortality rate in the dc group. there was no significant difference in the outcomes of cr and dc for patients who did not exhibit signs of herniation; however, there was a significant difference in the outcomes of cr and dc for patients who did exhibit signs of herniation [26]. kwon et al. found that while patients with unfavourable features (age >70, anticoagulation or antiplatelet use, time to surgery > 4 hours, gcs < 8, nonreactive pupils, and major extracranial injury) had more poor outcomes those with less unfavourable features. [27]. the cr group and the dc group were compared by kim and his colleagues in terms of age, gender, gcs score, hematoma volume, midline shift, ich score, and the amount of time that passed between the ictus and the surgery. during the course of the study, cr was carried out on a total of 139 patients, while dc was carried out on 125 patients. the mortality rate at 30 days was the same for both the cr group and the dc group (13.7 percent vs. 15.2 percent, p = 0.729). on the other hand, the cr group had a functional survival rate of 46.0 percent after 12 months, which was significantly (p = 0.014) higher than the dc group's survival rate (32.0 percent) [28]. our study has some limitations; it is a singlecentre study that included a relatively small sample size. it also lacks long-term follow up for the included patients. these drawbacks must be handled in the upcoming studies. conclusion using a flail bone flap to perform a decompressive craniotomy may be beneficial, especially in infant cases, because of a high rate of complications associated with dc and subsequent cranioplasty in children and infants. the efficacy of this technique in terms of clinical outcomes and the reduction of complications necessitates further large-scale studies. references 1. el hadji cheikh ndiaye s, cisse y, nzisabira jm, donzo a, ndiaye ps, boubakar badiane s. acute subdural hematoma post ventricular puncture in infants: a case report and review of the literature. international journal of surgery case reports. 2021:105913. 2. elliott ca, ramaswamy v, jacob fd, sankar t, mehta v. early diffusion restriction of white matter in infants with small subdural hematomas is associated with delayed atrophy. child's nervous system. 2017;33(2):289-95. 208 mohammad fekry elshirbiny, m.m. amen, assem ahmed 3. karibe h, kameyama m, hayashi t, narisawa a, tominaga t. acute subdural hematoma in infants with abusive head trauma: a literature review. neurologia medico-chirurgica. 2016:ra. 2015-0308. 4. yokota h, sugimoto t, nishiguchi m, hashimoto h. greenstick fracture-hinge decompressive craniotomy in infants: illustrative case and literature review of techniques for decompressive craniotomy without bone removal. child's nervous system. 2019;35(9):1491-7. 5. honeybul s, ho k. the current role of decompressive craniectomy in the management of neurological emergencies. brain injury. 2013;27(9):979-91. 6. honeybul s, ho k, gillett g. reconsidering the role of decompressive craniectomy for neurological emergencies. journal of critical care. 2017;39:185-9. 7. rahme r, zuccarello m, kleindorfer d, adeoye om, ringer aj. decompressive hemicraniectomy for malignant middle cerebral artery territory infarction: is life worth living? journal of neurosurgery. 2012;117(4):749-54. 8. hossain-ibrahim mk, wasserberg j. decompressive craniectomy--time for a change? british journal of neurosurgery. 2011;25(4):538-9. 9. kolias ag, kirkpatrick pj, hutchinson pj. decompressive craniectomy: past, present and future. nature reviews neurology. 2013;9(7):405-15. 10. shah am, jung h, skirboll s. materials used in cranioplasty: a history and analysis. neurosurgical focus. 2014;36(4):e19. 11. frassanito p, fraschetti f, bianchi f, giovannenze f, caldarelli m, scoppettuolo g. management and prevention of cranioplasty infections. child's nervous system. 2019;35(9):1499-506. 12. rocque bg, amancherla k, lew sm, lam s. outcomes of cranioplasty following decompressive craniectomy in the pediatric population: a systematic review. journal of neurosurgery: pediatrics. 2013;12(2):120-5. 13. rocque bg, agee bs, thompson em, piedra m, baird lc, selden nr, et al. complications following pediatric cranioplasty after decompressive craniectomy: a multicenter retrospective study. journal of neurosurgery: pediatrics. 2018;22(3):225-32. 14. bowers ca, riva-cambrin j, hertzler da, walker ml. risk factors and rates of bone flap resorption in pediatric patients after decompressive craniectomy for traumatic brain injury. journal of neurosurgery: pediatrics. 2013;11(5):526-32. 15. brommeland t, rydning pn, pripp ah, helseth e. cranioplasty complications and risk factors associated with bone flap resorption. scandinavian journal of trauma, resuscitation and emergency medicine. 2015;23(1):1-7. 16. phan k, moore jm, griessenauer c, dmytriw aa, scherman db, sheik-ali s, et al. craniotomy versus decompressive craniectomy for acute subdural hematoma: systematic review and meta-analysis. world neurosurgery. 2017;101:677-85. e2. 17. aarabi b, hesdorffer dc, ahn es, aresco c, scalea tm, eisenberg hm. outcome following decompressive craniectomy for malignant swelling due to severe head injury. journal of neurosurgery. 2006;104(4):469-79. 18. beck j, raabe a, lanfermann h, berkefeld j, de rochemont rdm, zanella f, et al. effects of balloon angioplasty on perfusion-and diffusion-weighted magnetic resonance imaging results and outcome in patients with cerebral vasospasm. journal of neurosurgery. 2006;105(2):220-7. 19. buschmann u, yonekawa y, fortunati m, cesnulis e, keller e. decompressive hemicraniectomy in patients with subarachnoid hemorrhage and intractable intracranial hypertension. acta neurochirurgica. 2007;149(1):59-65. 20. malliti m, page p, gury c, chomette e, nataf f, roux f-x. comparison of deep wound infection rates using a synthetic dural substitute (neuro-patch) or pericranium graft for dural closure: a clinical review of 1 year. neurosurgery. 2004;54(3):599-604. 21. bullock mr, chesnut r, ghajar j, gordon d, hartl r, newell dw, et al. surgical management of acute subdural hematomas. neurosurgery. 2006;58(suppl_3):s2-16-s224. 22. güresir e, beck j, vatter h, setzer m, gerlach r, seifert v, et al. subarachnoid hemorrhage and intracerebral hematoma: incidence, prognostic factors, and outcome. neurosurgery. 2008;63(6):1088-94. 23. abd el-wahed m, ahmed s. comparative study between bone flap insertion in abdominal wall versus flail replacement in decompressive craniectomy of acute subdural hematoma. the medical journal of cairo university. 2018;86(december):3825-32. 24. li lm, kolias ag, guilfoyle mr, timofeev i, corteen ea, pickard jd, et al. outcome following evacuation of acute subdural haematomas: a comparison of craniotomy with decompressive craniectomy. acta neurochirurgica. 2012;154(9):1555-61. 25. tsermoulas g, shah o, wijesinghe he, silva ahd, ramalingam sk, belli a. surgery for acute subdural hematoma: replace or remove the bone flap? world neurosurgery. 2016;88:569-75. 26. woertgen c, rothoerl rd, schebesch km, albert r. comparison of craniotomy and craniectomy in patients with acute subdural haematoma. journal of clinical neuroscience. 2006;13(7):718-21. 27. kwon ys, yang kh, lee yh. craniotomy or decompressive craniectomy for acute subdural hematomas: surgical selection and clinical outcome. korean journal of neurotrauma. 2016;12(1):22-7. 28. kim db, park sk, moon bh, cho br, jang dk, jang ks. comparison of craniotomy and decompressive craniectomy in large supratentorial intracerebral hemorrhage. journal of clinical neuroscience. 2018;50:208-13. doi: 10.33962/roneuro-2022-037 diagnostic and prognostic role of magnetic resonance imaging in cases of moderate to severe traumatic brain injury sanjeev pattankar, nishanth sadashiva, priyadarshi dikshit, ved prakash maurya, dhaval p. shukla, umamaheswara reddy v., rakesh mishra, amit agrawal romanian neurosurgery (2022) xxxvi (2): pp. 209-215 doi: 10.33962/roneuro-2022-037 www.journals.lapub.co.uk/index.php/roneurosurgery diagnostic and prognostic role of magnetic resonance imaging in cases of moderate to severe traumatic brain injury sanjeev pattankar1, nishanth sadashiva2, priyadarshi dikshit1, ved prakash maurya1, dhaval p. shukla2, umamaheswara reddy v.3, rakesh mishra4, amit agrawal5 1 department of neurosurgery. sanjay gandhi post graduate institute of medical sciences, india 2 national institute of mental health and neurosciences [nimhans], bangalore, india 3 department of radiology, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india 4 department of neurosurgery. institute of medical sciences, banaras hindu university, varanasi, india 5 department of neurosurgery. all india institute of medical sciences, saket nagar, bhopal, madhya pradesh, india abstract moderate to severe traumatic brain injury (tbi) remains a leading cause of death and disability worldwide. timely diagnosis and accurate prognostication play a key role in informed clinical decision-making. though magnetic resonance imaging (mri) is a superior anatomical scan compared to computerized tomography (ct), the latter remains the current investigation of choice in the clinical setting of tbi due to some of the former’s inherent deficiencies in imaging bone/blood, limited access, cost, etc. nevertheless, the fact that mri is a valuable adjunct in evaluating the tbi patients with clinical findings disproportionate to the ct scan substantiates its possible complementary/supplementary diagnostic and prognostic role in tbi. mri scan is ideally placed on demonstrating the shear/diffuse axonal injury (dai), nonhaemorrhagic intraparenchymal lesions, and brain stem lesions poorly delineated by a ct scan. the currently available literature demonstrates that dai and caudal brainstem lesions are indicators of poorer outcomes. however, the prognostic value of mri, in addition to that of ct, remains an area of active investigation. we have tried to present the evidence-based use of mri in moderate to severe tbi. advances in newer mri sequences like susceptibility-weighted imaging (swi), diffusion tensor imaging (dti), functional mri (fmri), and magnetic encephalography (meg) have the potential to revolutionize the current role of mri in tbi. introduction though computerized tomography (ct) scan of the head remains the investigation of choice for evaluation of a victim of acute traumatic keywords diffusion axonal injury, haemorrhagic, magnetic resonance imaging, non-haemorrhagic, prognostication, traumatic brain injury corresponding author: ved prakash maurya department of neurosurgery. sanjay gandhi post graduate institute of medical sciences, lucknow, india vpmsurgery@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 210 sanjeev pattankar, nishanth sadashiva, priyadarshi dikshit et al. brain injury (tbi), magnetic resonance imaging (mri) can play a valuable complementary diagnostic/ prognostic role in the same [1]. mri is a superior anatomical scan to ct in all clinical settings, except in the acute moderate to severe tbi, due to its inherent deficiencies in imaging bone/blood. with everincreasing accessibility seen to mri scanners worldwide, there is an accompanying increase in the interest, among clinicians and radiologists alike, regarding the utility of mri in diagnosing and prognosticating a variety of traumatic pathological conditions [2]. the role of mri scanning in identifying and characterizing specific sequelae of tbi is well documented [3]. particularly in evaluating patients whose clinical findings are disproportionate to the ct findings, mri represents a valuable adjunct even in the acute phase. in such cases, mri demonstrates the shear/diffuse axonal injury (dai), nonhemorrhagic intraparenchymal lesions, and brain stem lesions poorly delineated by a ct scan. in subacute or chronic head injury, mri is superior to ct and should be the primary imaging technique whenever possible [3]. despite its unparalleled sensitiveness to deep intraparenchymal tbi lesions and shear injuries, the broad clinical adaptation of mri in the trauma setting is limited, partly due to its higher costs, finite access, and more prolonged time consumption. early prognostication of moderate to severe tbi facilitates appropriate counseling of patients/families, aiding in sound clinical decisions. these informed clinical decisions are essential, as >50% of such patients end up with a permanent disability. widely used ct prognostication scoring systems like rotterdam/marshall/stockholm predict mortality better than tbis' morbidity/permanent disability [1,4]. the 'centripetal model' of tbi, based on animal and postmortem studies, was proposed to better understand the role of shearing injury in clinical outcomes, and add to the existing ct prognostication [5]. it stated that the severity of grading of tbi should be directly proportional to the most caudal cerebral structure affected by the shearing injury. mri is an ideal imaging modality to achieve the same. nevertheless, the prognostic value of mri, in addition to that of ct, remains an area of active investigation. we have tried to present the evidence-based use of mri in moderate to severe tbi. protocol of mri for tbi the national institute of neurological disorders and stroke (ninds) and several co-sponsoring federal agencies have proposed common data elements (cde) for developing data standards for clinical research. the following table shows the cde for tier 1 evaluation of tbi using 1.5t mri. other advanced protocols are available at the ninds website (table 1). diagnostic role of mri in tbi mri appearance of traumatic lesions though ct is highly sensitive for detecting large intracranial hematomas, gradient echo (gre) and t2-weighted mri are equally sensitive. t2 flair (fluid attenuated inversion recovery) is more sensitive than ct to detect minor cerebral contusions. t2 flair and gre are as sensitive as ct for traumatic subarachnoid haemorrhage (sah). t2 flair and dwi (diffusion-weighted imaging) are more sensitive for non-hemorrhagic dai, and gre and swi (susceptibility weighted imaging) for hemorrhagic dai. susceptibility weighted imaging (swi) is a highresolution three-dimensional imaging sequence. it is roughly six times more sensitive than the t2weighted sequence for detecting traumatic microhemorrhages [6]. dwi is the sequence of choice for ischemia. it is essential to differentiate between hemorrhagic and non-hemorrhagic lesions as the hemorrhagic lesions are associated with a worse prognosis. the gre and t2-weighted mri sequences also detect signal dropout caused by ironcontaining heme groups in slow-moving blood. distributions of the microhemorrhages in areas associated with axonal injury such as the corpus callosum, brainstem, and other white matter tracts strongly suggest an imaging diagnosis of dai. dai microhemorrhages typically appear as punctate signal-free lesions in the white matter that ‘bloom’. consequently, signal loss caused by punctate haemorrhages from dai can be visualized years after injury though lesions fade over time. the density of t2-weighted lesions is associated with the severity of tbi in terms of admission glasgow coma scale (gcs) and maximum intracranial pressure (icp) during admission 3-month glasgow outcome score. another factor that needs consideration is the magnetic field strength used, as a 3 tesla mri demonstrates practically twice the sensitivity of a 1.5 tesla device for microhemorrhages. 211 diagnostic and prognostic role of magnetic resonance imaging in moderate to severe traumatic brain injury table 1. common data element (cde) protocol for imaging parameters for mri in tbi1. 1 source-https://www.commondataelements.ninds.nih.gov/traumatic%20brain%20injury#pane-162 *recommend angle to ac-pc line; ** use 800 sec/mm2 for infants <1 year old; ***to reduce acquisition time, use parallel imaging, if possible, af/cl of 2/24-32; † can use swan on ge systems. abbreviations: ir-fspgr inversion recovery, fast spoiled gradient recalled echo; mprage magnetization prepared-rapid gradient echo; ffe fast field echo; fse – fast spin echo; sespin echo; flair – fluid attenuated inversion recovery; epi echo-planar imaging; swisusceptibility-weighted imaging; gregradient echo; te echo delay time; tr repetition time; tiinversion time; fa fractional anisotropy; fov field of view; nex number of acquisitions; bw – bandwidth; etlecho train length; a to p – anterior to posterior; r to l – right to left. sequence 3d t1w (mprage, 3d irfspgr, 3d ffe) t1w se (opt if no 3d t1w) t2w fse t2w flair dwi epi 3d swi† 2d gre (ffe) (opt if no 3d swi) orient sagittal sagittal axial* axial* axial* axial* axial* tr (ms) 9-30 500-600 >3500 >9500 >5000 50 >500 te(ms) 3-5 15-20 >90 >110 >100 40 >20 ti (ms) 1000 >2000 fa (degrees) 8-10 90 90 150 90 15 15-20 freq fov mm (phase fov) 256(100%) 230(87.5%) 230(87.5%) 230(87.5%) 256(100%) 230(87.5%) 230(87.5%) matrix size 256x256 256x192 256x192 256x192 128x128 512x192 256x192 # slices/ thickness (mm) 120/2 32/4 32/4 32/4 32/4 94/2 32/4 gap 0 0-20% 0-20% 0-20% 0-20% 0 0-20% voxel size(mm) 1x1x2 1x1x4 1x1x4 1x1x4 2x2x4 0.5x1x2 1x1x4 nex 1 2 1-2 2 1-3 1 1-2 phase enc. dir a to p a to p r to l r to l a to p r to l r to l fat suppress no no no yes yes no no bw(hz/px) 160 120 130 200 1200 80 80-100 flow comp no slice no no no slice slice etl 15-20 30 128 b-values (sec/mm2) (directions) 0/1000** (3) time*** 8:00 3:00 3:00 3:00 2:00 8:00 3:00 212 sanjeev pattankar, nishanth sadashiva, priyadarshi dikshit et al. classification of severity of dai grading of dai has been described histologically according to the anatomic distribution of injury, which correlated with the clinical outcome. the classification was proposed first by adams in 1989 and divided dai into three grades [5]. this is the commonly applied grading system for classifying dai lesions seen on mri. • grade i: involves grey-white matter interfaces (figure 1). most commonly: parasagittal regions of frontal lobes, periventricular temporal lobes, parietal and occipital lobes, internal and external capsules, and cerebellum. • grade ii: involves corpus callosum in addition to grade i locations (figure 2). most commonly: posterior body and splenium but advance anteriorly with increasing injury severity. most frequently seen unilateral. it may be seen on the swi sequence. • grade iii: involves brainstem in addition to grade i and ii locations (figure 3). most commonly: rostral midbrain, superior cerebellar peduncles, medial lemnisci, and corticospinal tracts. grading of brainstem lesions was proposed by firsching et al. and has been validated by others [7– 10] • grade i: no brainstem involvement; lesions of only hemispheres. • grade ii: unilateral brainstem lesions at any level with or without supratentorial lesions. • grade iii: bilateral lesions of the mesencephalon with or without supratentorial lesions. • grade iv: bilateral lesions of the pons with or without lesions of lesser grades. brainstem injury can be categorized as anterior or posterior, hemorrhagic or non-hemorrhagic, and unilateral or bilateral [11]. other alternative classification of brainstem injury is primary or secondary due to herniation. the primary injury can be due to a direct impact against the tentorial free edge or as a part of dai [12,13]. the brainstem lesions are also classified as superficial or deep [13]. the grading assigned by both the systems is determined by the most caudal brain lesion present, though their definitions vary. figure 1. computerized tomography (ct) scan (a) and magnetic resonance imaging (mri) – susceptibility-weighted imaging (swi) sequence (b) showing multiple haemorrhages in left parasagittal grey-white junction (yellow arrows). the presence of such lesions in absence of corpus callosal or brainstem involvement indicates grade 1 diffuse axonal injury (dai). figure 2. magnetic resonance imaging (mri) – diffusionweighted imaging (dwi) sequence (a) and apparent diffusion coefficient (adc) sequence (b) showing restricted diffusion (yellow arrows) in the splenium of corpus callosum indicating grade 2 diffuse axonal injury (dai). figure 3. computerized tomography (ct) scan (a) and magnetic resonance imaging (mri) susceptibility-weighted imaging (swi) sequence (b) showing hemorrhages (yellow arrows) in right paramedian brainstem and cerebellum indicating grade 3 diffuse axonal injury (dai). 213 diagnostic and prognostic role of magnetic resonance imaging in moderate to severe traumatic brain injury newer mri sequences for tbi diffusion tensor imaging (dti) is a newer mri sequence increasingly used to diagnose dai [14,15]. dti is based on the principle of calculating the directional asymmetry of water diffusion, called anisotropy, in mapping white matter tracts. the injured axons in white matter tracts have lower anisotropy than normal ones. some studies had found it extremely sensitive to axonal injuries following tbi of any severity, even when the ct and conventional mri sequences showed no abnormalities [15,16]. dti comes with its fair share of limitations, like its relative insensitivity to axonal injuries in complex white matter regions, due to the absence of one predominant direction of the axons and lack of spatial resolution to detect injuries in small white matter tracts. other described unique mri sequences for tbi include magnetic resonance spectroscopy (mrs), functional mri (fmri) and magnetic encephalography (meg). mrs can map changes in the brain metabolic processes and resulting metabolite concentration changes after tbi [17]. fmri can also reveal areas of either reduced or increased activation and altered connectivity via its bold (blood oxygenation level-dependent) imaging technique [18]. some authors have reported the usefulness of meg in detecting tbi induced abnormalities that were not identified with dti or conventional mri and correlated with clinical outcome [19]. prognostic role of mri in tbi there is no consensus about the optimal timing for mri after tbi for predicting outcome. however, it should preferably be performed within the firstweek post-injury for reliable prognostication [20]. the presence of brainstem involvement is correlated with outcome. mortality increases gradually from 14% with grade i brainstem lesions to 100% with grade iv lesions [10]. bilateral brainstem involvement is strongly associated with poor outcomes. posterior location is associated with disability. the non-haemorrhagic, anterior lesions or unilateral injuries are associated with better outcome [11]. superficial lesions are associated with better outcomes than deeper lesions [13]. swi lesions in the midbrain corresponding to substantia nigra and tegmentum are independently related to poor outcomes [20]. the grading is also used as a prognostic indicator for recovery of consciousness. park et al. reported that 14.3% of patients with cerebral white matter lesions (grade 1) did not recover their consciousness, and 50% of patients with corpus callosum lesions (grade 2), 51.6% of patients with brain stem lesion (grade 3) did not recover their consciousness [21]. the grading of dai is well correlated with time to regain consciousness after tbi. patients with grade 1 injury become conscious within a week after injury, while grade 2 take two weeks to recover, and patients with grade 3 take two months to regain consciousness [21]. besides grading, the lesion volume also bears the outcome. the volume of visible dai lesions in the corpus callosum, brainstem, and thalamus, in dwi and t2 flair sequences, are independent prognostic factors in patients with severe tbi. an essential predictive mri variable is dwi lesion volume in the corpus callosum. however, in moderate tbi cases, the number of cortical contusions is more critical for prognosis [22]. a systematic review published by haghbayan et al. (2017), reviewing the prognostic value of mri in moderate to severe tbi, concluded that the brainstem lesions were associated with higher mortality and unfavourable functional outcome (glasgow outcome scale 1-3) at ≥ 6 months [23]. and that dai patterns were associated with an increased risk of unfavourable functional outcomes, with depth-based mri scores demonstrating an increased risk of unfavourable outcomes as more caudal structures were affected. along the same lines, a recent meta-analysis by m. m. van eijck et al. (2018), studying the prognostic value of dai in tbi, reported that the presence of dai resulted in three times higher risk of an unfavourable outcome, and this risk further increased three times with each increasing grade of dai [24]. this meta-analysis reviewed data from 32 selected articles, deducing an overall unfavourable (glasgow outcome score 1-3) functional outcome of 38% in patients with dai in tbi. conclusion mri following tbi provides valuable assistance, either complementary or supplementary to ct scan, in determining diagnosis and prognosis in individual cases. the presence of dai and caudal brainstem lesions lead to a poorer outcome. advances in newer mri sequences like swi, dti, fmri, meg. have the 214 sanjeev pattankar, nishanth sadashiva, priyadarshi dikshit et al. potential to revolutionize the current role of mri in tbi. abbreviations: adc apparent diffusion coefficient ct computed tomography dai diffuse axonal injury dwi – diffusion-weighted imaging gcs glasgow coma scale gre gradient recalled echo icp intracranial pressure mri magnetic resonance imaging ninds national institute of neurological disorders and stroke sah subarachnoid hemorrhage sdh subdural hematoma swi – susceptibility-weighted imaging t2 flair t2-weighted fluid attenuated inversion recovery tbi traumatic brain injury fmri – functional magnetic resonance imaging bold – blood oxygen level-dependent mrs – magnetic resonance spectroscopy dti – diffusion tensor imaging meg magnetic encephalography references 1 schweitzer ad, niogi sn, whitlow ct, et al. traumatic brain injury: imaging patterns and complications. radiographics 2019;39:1571–95. doi:10.1148/rg.20 19190076 2 blennow k, brody dl, kochanek pm, et al. traumatic brain injuries. nat rev dis prim 2016;2:1–19. doi:10.1038/nrdp.2016.84 3 kelly ab, zimmerman rd, snow rb, et al. head trauma: comparison of mr and ct--experience in 100 patients. ajnr am j neuroradiol;9:699–708.http://www.ncbi.nlm. nih.gov/pubmed/3135716 4 mata-mbemba d, mugikura s, nakagawa a, et al. early ct findings to predict early death in patients with traumatic brain injury: marshall and rotterdam ct scoring systems compared in the major academic tertiary care hospital in northeastern japan. acad radiol 2014;21:605–11. doi:10.1016/j.acra.2014.01.017 5 adams jh, doyle d, ford i, et al. diffuse axonal injury in head injury: definition, diagnosis and grading. histopathology 1989;15:49–59. doi:10.1111/j.13652559.1989.tb03040.x 6 su e, bell m. diffuse axonal injury. in: laskowitz d, gran g, eds. translation research in traumatic brain injury. boca raton (fl): crc press/taylor and francis group 2016. 7 wedekind c, hesselmann v, lippert-grüner m, et al. trauma to the pontomesencephalic brainstem--a major clue to the prognosis of severe traumatic brain injury. br j neurosurg 2002;16:256–60. doi:10.1080/026886902201 48842 8 kampfl a, schmutzhard e, franz g, et al. prediction of recovery from post-traumatic vegetative state with cerebral magnetic-resonance imaging. lancet 1998;351:1763–7. doi:10.1016/s0140-6736(97)10301-4 9 weiss n, galanaud d, carpentier a, et al. clinical review: prognostic value of magnetic resonance imaging in acute brain injury and coma. crit care 2007;11:230. doi:10.1186/cc6107 10 firsching r, woischneck d, klein s, et al. classification of severe head injury based on magnetic resonance imaging. acta neurochir (wien) 2001;143:263–71. doi:10.1007/s007010170106 11 hilario a, ramos a, millan jm, et al. severe traumatic head injury: prognostic value of brain stem injuries detected at mri. am j neuroradiol 2012;33:1925–31. doi:10.3174/ajnr.a3092 12 shukla d, mahadevan a, sastry kvr, et al. pathology of post traumatic brainstem and hypothalamic injuries. clin neuropathol 2007;26:197–209. doi:10.5414/npp26197 13 shibata y, matsumura a, meguro k, et al. differentiation of mechanism and prognosis of traumatic brain stem lesions detected by magnetic resonance imaging in the acute stage. clin neurol neurosurg 2000;102:124–8. doi:10.1016/s0303-8467(00)00095-0 14 niogi sn, mukherjee p. diffusion tensor imaging of mild traumatic brain injury. j head trauma rehabil 2010;25:241–55. doi:10.1097/htr.0b013e3181e52c2a 15 hulkower mb, poliak db, rosenbaum sb, et al. a decade of dti in traumatic brain injury: 10 years and 100 articles later. am j neuroradiol 2013;34:2064–74. doi:10.3174/ ajnr.a3395 16 mac donald cl, johnson am, cooper d, et al. detection of blast-related traumatic brain injury in u.s. military personnel. n engl j med 2011;364:2091–100. doi:10.1056/nejmoa1008069 17 maudsley aa, govind v, levin b, et al. distributions of magnetic resonance diffusion and spectroscopy measures with traumatic brain injury. j neurotrauma 2015;32:1056–63. doi:10.1089/neu.2014.3505 18 irimia a, van horn jd. functional neuroimaging of traumatic brain injury: advances and clinical utility. neuropsychiatr dis treat 2015;11:2355–65. doi:10.21 47/ndt.s79174 19 huang m-x, theilmann rj, robb a, et al. integrated imaging approach with meg and dti to detect mild traumatic brain injury in military and civilian patients. j neurotrauma 2009;26:1213–26. doi:10.1089/neu.2008.0 672 20 abu hamdeh s, marklund n, lannsjö m, et al. extended anatomical grading in diffuse axonal injury using mri: hemorrhagic lesions in the substantia nigra and mesencephalic tegmentum indicate poor long-term outcome. j neurotrauma 2017;34:341–52. doi:10.1089/n eu.2016.4426 21 park sj, hur jw, kwon ky, et al. time to recover 215 diagnostic and prognostic role of magnetic resonance imaging in moderate to severe traumatic brain injury consciousness in patients with diffuse axonal injury : assessment with reference to magnetic resonance grading. j korean neurosurg soc 2009;46:205. doi:10.3340/jkns.2009.46.3.205 22 moen kg, brezova v, skandsen t, et al. traumatic axonal injury: the prognostic value of lesion load in corpus callosum, brain stem, and thalamus in different magnetic resonance imaging sequences. j neurotrauma 2014;31:1486–96. doi:10.1089/neu.2013.3258 23 haghbayan h, boutin a, laflamme m, et al. the prognostic value of mri in moderate and severe traumatic brain injury: a systematic review and metaanalysis. crit care med 2017;45:e1280–8. doi:10.1097/ ccm.0000000000002731 24 van eijck mm, schoonman gg, van der naalt j, et al. diffuse axonal injury after traumatic brain injury is a prognostic factor for functional outcome: a systematic review and meta-analysis. brain inj 2018;32:395–402. doi:10.1080/02699052.2018.1429018 doi: 10.33962/roneuro-2022-017 utilization of anticoagulant and antiplatelet medications among geriatric patients with neurosurgical diseases abdulrahman al-mirza, omar al-taei, hatem al-saadi, tariq al-saadi romanian neurosurgery (2022) xxxvi (1): pp. 98-106 doi: 10.33962/roneuro-2022-017 www.journals.lapub.co.uk/index.php/roneurosurgery utilization of anticoagulant and antiplatelet medications among geriatric patients with neurosurgical diseases abdulrahman al-mirza1, omar al-taei1, hatem al-saadi1, tariq al-saadi2 1 sultan qaboos university college of medicine. sultanate of omanmuscat, al-khoudh, oman 2 department of neurology and neurosurgery. montreal neurological institute, faculty of medicine, mcgill university, qc, canada and department of neurosurgery, khoula hospital, muscat, sultanate of oman, oman abstract aim: to study the utilization patterns of anticoagulant and antiplatelet medications among geriatric patients with neurosurgical conditions in the neurosurgical department at khoula hospital, muscat, sultanate of oman. introduction: anticoagulant and antiplatelet presumption is a worry in neurosurgical patients, that suggests a subtle balance between the risk of thromboembolism against the risk of periand postoperative haemorrhage. patients taking those medications were found to have an increased risk of bleeding from traumatic and traumatic events. materials and methods: a retrospective study of geriatric cases admitted to the neurosurgery department in khoula hospital (kh) as an example of a neurosurgical center in sultanate of oman, from january 2016 to 31st december 2019. patients demographics, diagnosis, length of hospital stay (los), glasgow coma scale (gcs), length of icu admission, and treatment proposed were recorded. results: the most common diagnostic category was trauma (35.4%). 16.0 % of the patients were taking anticoagulant medications. patients with traumatic brain injury (tbi) were found to have a higher rate of using anticoagulant medications (36.6%). there was a significant difference between the los, type of intervention, icu admission, and the usage of anticoagulant and antiplatelet drugs (p<0.05). enoxaparin was the most commonly used anticoagulant agent. 19.6 % of the patients were taking antiplatelet medications. this study was showed that aspirin is the most commonly used antiplatelet agent among different neurosurgical pathologies. conclusion: patients with tbi were found to have a higher rate of using anticoagulant medications. decisions regarding prescription and resumption of anticoagulants and antiplatelet medications should be taken on a case-by-case basis involves multidisciplinary and holistic approaches. introduction anticoagulant presumption is a worry in neurosurgical patient that keywords anticoagulants, geriatric, elderly, bleeding, trauma, neurosurgery, antiplatelet corresponding author: tariq al-saadi faculty of medicine, mcgill university, qc, canada t.dhiyab@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 99 utilization of anticoagulant and antiplatelet medications among geriatric patients with neurosurgical diseases suggests a subtle balance among the risk of thromboembolism against the risk of perioperative and postoperative hemorrhage (1). the ageing populace has resulted in an alteration in the demographics of trauma (2). numerous of these patients are undergoing anticoagulation therapy and are also at high risk of falls and sustaining injury with possibly serious hemorrhagic complications (2). the main risk of systemic anticoagulation is bleeding, including intracranial hemorrhage, which must be well-adjusted against the recommended chronic anticoagulation for at least the duration of active cancer (3). clinicians often face a patient with a brain tumor who requires anticoagulation for a deep venous thromboembolism (dvt) or pulmonary embolism (pe) or for cardiac reasons, such as atrial fibrillation or peripheral vascular disease. (3). head injury `embodies one of the most important and recurrent traumatic pathology in the emergency department (4). among the diverse risk factors, preinjury use of warfarin has received considerable attention in trauma literature. several studies were undertaken to elucidate the effect of warfarin anticoagulation on the mortality rate and risk of development of intracranial hemorrhage (ich) in adult patients with minor head injuries (4). the risk of mortality in a patient anti-coagulated on warfarin with an ich after head injury ranges in the literature from 16-80% (5). the food and drug administration -usaprojected that 2 millions of people each year start using vitamin k antagonist. the use of anticoagulants is predicted to continue growing in the near future (1). warfarin is a vitamin k antagonist, and works by inhibiting the enzyme vitamin k epoxide reductase. this is essential for calcium binding, allowing the linking to phospholipids surfaces to promote clotting (5). platelets are small, irregularly shaped subcellular fragments that are derived from megakaryocytes and play a major role in the maintenance of haemostasis (6). antiplatelet agents are frequently being used in the management or prevention of cardiovascular disease (7) such as; deep venous thrombosis, atrial fibrillation, pulmonary embolism and coronary artery disease. they are also given postoperatively for prosthetic heart valves or stent placement (8). patients taking these medications found to have an increased risk of bleeding from traumatic and traumatic events (7). therapeutic mechanisms of antiplatelet agents include inhibition of platelet aggregation, so normal haemostasis is impaired, which may lead to an increased incidence of ich and enlargement of hematomas in tbi, potentially increasing mortality and morbidity (9). for instance, patients taking an antiplatelet agent, with ich occurring in approximately 3.6%–67.3% of patients on antiplatelet therapy and 1.6%–50.5% of patients not on this therapy (7). also, posttraumatic ich is associated with a mortality rate of 21% in patients on antiplatelet therapy. (6). antiplatelet agents are necessary for patients undergoing neuroendovascular procedures, due to it is preventative effect against thromboembolic consequences (9). aspirin is the most common used drug while undergoing neuroendovascular procedures. aspirin is typically initiated at least 3–5 days prior to some vascular procedures such as carotid or intracranial stenting (9). clopidogrel is the other most common antiplatelet drug used while undergoing neuroendovascular procedures. variation in individual response to clopidogrel has sparked a great deal of research and controversy in the cardiovascular and neuroendovascular areas. the incidence of clopidogrel hyporesponsiveness has varied from 21% to 53.1% in patients undergoing neuroendovascular procedures (9). this study is conducted to investigate the prevalence of therapeutic antiplatelet and anticoagulant medications among geriatric patients admitted in neurosurgical department at khoula hospital, muscat, sultanate of oman, which is the first of its kind in the region, to the best of our knowledge. the health care services in oman are considered as having one of the best health care systems in the world according to world health organization reports (10,11). the department of neurosurgery in our hospital is the main neurosurgical center in the country with an average annual admission of 1600 patients (12,13) in this study, we chose a cut of 65 years and older according to the local definition, taking into account the increase in life span throughout the last decades as well as the improvement in the quality of life. methods study group this is a retrospective study conducted at khoula hospital located in muscat, sultanate of oman. the study was approved by the research ethical 100 abdulrahman al-mirza, omar al-taei, hatem al-saadi, tariq al-saadi committee at khoula hospital/ ministry of health (pro122020072). medical records of 696 patients who are above the age of 65 and admitted to the neurosurgical ward january 2016 to 31st december 2019 were included. the study includes both omani and non-omani patients. patients with the following features are excluded: non elderly patient (below 65 years), non-neurosurgical conditions, outside the study period (from 1st january 2016 to 31th december 2019), patients with missing or incomplete data. data collection data was obtained from the health information system included: patient demographics. diagnosis, length of hospital stay (los), glasgow coma scale (gcs), length of icu admission and treatment proposed. then the information classified into continues and categorized variables and analysed accordingly. data analysis research database was analysed and processed using the statistical package for the social sciences (spss) software (version23). the categorized variables were cross-tabulated using frequency tables. chi-square test was used to obtain the significance of the association between categorized variables, using a p value of ≤ 0.05 as the cut-off for significance. results the demographic characteristics of the included cases in the present study is represented in table 1. we have total of 669 patients with mean age of 73.3 admitted in the neurosurgical department at kh in muscat the capital city of sultanate of oman in four years ’period (from 2016 to 2019). 2019 accounted for the highest number of admitted patients (30%).61.9% of the study cohort were more than 75year-old. male to female ratio was (1.63:1). most of the patient were having gcs score of 14-15 (72.3%). the most common diagnostic category was trauma, accounted for 35.4% of the study cohort followed by oncology and vascular equally (16.3%).16.0 % of the patients received anticoagulant medications.19.6% of the patients received antiplatelet medications. most of the patients underwent surgical intervention (73.1%). majority of the patients stayed in the hospital less than 15 days (77%). table 1. demographic characteristics of the patients number of patients (%) category number of patients admitted each year 202 (30.0%) 2019 172 (25.7%) 2018 154 (23%) 2017 141 (21.3%) 2016 669 total age 414 (61.9%) >=75 255 (38.1%) < 75 gender 255 (38.1%) female 414 (61.9%) male gcs on arrival 484 (72.3%) 15-14 49 (7.3%) 13-12 36 (5.3%) 11-9 100 (15%) <8 diagnostic category 109 (16.3%) oncology 237 (35.4%) trauma 109 (16.3%) vascular 176 (26.3%) spine and peripheral nerve diseases 13 (2%) infection and functional 25 (3.7%) hydrocephalus anticoagulant drugs 107 (16.0) yes 562 (84.0) no type of interventions 489 (73.1%) surgical 180 (26.9%) observational length of stay (los) 515 (77%) <= 15 days 154 (23%) >15 days utilisation of anticoagulant medications figure 1 illustrates the utilization of anticoagulant medications among different diagnoses (131 patients out of 669 patients). patients with tbi found to have higher rate of using anticoagulant medications (36.6%) followed by patients with spinal diseases and vascular pathologies, respectively (25.9%, 18.3%). there was no significant relationship between the utilization of anticoagulant medications among different neurological diseases investigated 101 utilization of anticoagulant and antiplatelet medications among geriatric patients with neurosurgical diseases (p=0.920). the association between usage of anticoagulant medications among patients and other variables (type of injury, loc, type of intervention, age, and icu admission) is shown in table 2. it demonstrates that there was no significant difference between the utilization of anticoagulant medications the type of injury, as both traumatic and non-traumatic patients were using anticoagulant medications in a similar way (p=0.674). also, it is showing that there was a significant difference in the los and the usage of anticoagulant drugs, in which patients who were not using anticoagulant medications found to stay shorter in the hospital (p<0.05). additionally, patients who were undergone surgical intervention were using anticoagulant medications much less than patients who were on conservative management (p=0.001). added to that the significant relationship that found to be between the icu admission and the utilization of anticoagulant medications, in which majority of the patients who were not on anticoagulant therapy were not admitted to the icu (p<0.05). also, there was no association between the usage of anticoagulant medications and the age of patients (above and below 75 years) (p=0.198). figure 2 illustrates the utilization of anticoagulant agents among different diagnoses. it is showing that enoxaparin was the most commonly used anticoagulant agent among different neurosurgical pathologies in the present study (n=93), followed by warfarin (n=15). heparin was only used by 3 patients in this study. figure 1. the utilization of anticoagulant medications among different diagnoses. utilization of antiplatelet medications the utilization of antiplatelet medications among different diagnoses (n=107) is illustrated in figure 3. patients with tbi found to have higher rate of using antiplatelet medications (33.6%) followed by patients with oncological and vascular pathologies, respectively (26.1%, 21.4%). figure 2. utilization of anticoagulant agents among different diagnoses. figure 3. the utilization of antiplatelet medications among different diagnoses. figure 4. utilization of antiplatelet agents among different diagnoses there was a significant difference in the utilization pattern of antiplatelet medications among different neurological diseases investigated (p<0.05). table 3 is representing the relationship between utilization of antiplatelet agents among patients and other variables. it demonstrates that there was no 102 abdulrahman al-mirza, omar al-taei, hatem al-saadi, tariq al-saadi significant relationship between the usage of antiplatelet medications and the type of injury (traumatic vs non-traumatic) (p=0.746). additionally, there was a significant difference in the los and the usage of antiplatelet medications (p=0.034). patients who were undergone surgical intervention were using antiplatelet medications in a much lesser rate compared with patients who were on non-surgical conservative management (p=0.032). added to that, there was a significant difference between the icu admission and the utilization of antiplatelet medications (p=0.02). also, there was no association between the usage of antiplatelet drugs and the age of patients (above and below 75 years) (p=0.906). figure 4 showed the utilization of antiplatelet agents among different pathologies. aspirin was the most commonly used agent in the present study (n=112), followed by clopidogrel (n=10). dual antiplatelet therapy (aspirin with clopidogrel) was only used by 9 patients in this research. table 2. the relationship between the usage of anticoagulant medications and type of injury (trauma vs. non trauma), length of stay, type of intervention (surgical vs. observation), age group, and icu admission. category type of injury length of stay intervention age icu admission trauma 36 more than 15 days 51 surgical 92 more than 75 years 56 admitted to icu 40 non trauma 71 less than 15 days 56 observation 15 less than 75 years 51 not admitted to icu 67 p-value p= 0.674 p<0.005 p=0.001 p= 0.198 p<0.005 table 3. the relationship between the usage of antiplatelet medications and type of injury (trauma vs non trauma), length of stay, type of intervention (surgical or observation), age group, and icu admission. category (pvalue) type of injury length of stay intervention age icu admission trauma 48 more than 15 days 21 surgical 86 more than 75 years 84 admitted to icu 12 non trauma 83 less than 15 days 110 observation 45 less than 75 years 47 not admitted to icu 119 p-value p= 0.746 p= 0.034 p= 0.032 p=0.906 p=0.002 discussion utilization of anticoagulant medications anticoagulants are important treatments for numerous medical conditions including dvt, pulmonary embolism, and non-valvular af. importantly; the triad of anticoagulation, age above 65 years, and minor head injury was considered lethal by karni et al. on a retrospective review of 278 patients with minor head injuries and ctdocumented ich (14). patients with tbi found to have higher rate of using anticoagulant medications followed by patients with spinal diseases and vascular pathologies, respectively. in comparison, claudia et al reported that 75 patients out of 1410 included in the study was on anticoagulants at the time of tbi (4) an important issue to be raised in elderly patients with higher risk of thromboembolic events, is weighing up the balance between thrombotic risk and falls or bleeding risk which can often be challenging and compounded by the presence of lower number of evidences to guide decisions regarding reinstitution of anticoagulants. (15,16). there was no significant relationship between the utilization of anticoagulant medications among different neurological diseases investigated it the current study (p=0.920). in contrast to our study, pieracci et al. conducted a study to evaluate the effect of anticoagulants on elderly patients and concluded that patients on warfarin had increased severity of head injury, had more chances of ich (17). another study investigated the effect of anticoagulants among patients with glioblastoma stated that anticoagulants was associated with inferior overall survival compared to no use on multivariate analysis (p=0.001) (18). in comparison to this study; another study stated that patients with primary and metastatic brain tumours, can safely use anticoagulants under careful monitoring, except 103 utilization of anticoagulant and antiplatelet medications among geriatric patients with neurosurgical diseases for patients with untreated tumours with a high rate of intracranial haemorrhage (i.e., metastases from melanoma, choriocarcinoma, thyroid carcinoma, hepatocellular carcinoma, and renal cell carcinoma). in patients with cerebrovascular pathologies such as cerebral aneurysm, it has been showed that oral anticoagulants in safer than parental ones. our study ddemonstrates that there was no significant difference between the utilization of anticoagulant medications and the type of injury, as both traumatic and non-traumatic patients were using anticoagulant medications in a similar way. in contrast, another study found that there was an exponential correlation between the intensity of anticoagulation the risk of ich from traumatic events (19). additionally, patients who were undergone surgical intervention were using anticoagulant medications much less then patients on conservative management. kawamata et al addressed postcraniotomy usage of anticoagulants in retrospective review of 27 patients. seventeen of those patients (63%) underwent craniotomy for evacuation of intracerebral of subdural hematomas. also, there was no association between the usage of anticoagulant drugs and the age of patients (above and below 75 years) (p=0.198). another study by sharma et al reported that warfarin consumption is independently associated with higher mortality among a cohort of 384 tbi elderly patients (20) enoxaparin was the most commonly used anticoagulant agent among different neurosurgical pathologies in the present study followed by warfarin. another study by calvin et al found that almost one fifth of elderly patients older than 65 years old admitted to an american level one trauma centre with head injury were on warfarin, reflecting the importance of impact of warfarin on management and outcome of head injuries (21). this can be explained by the co-existence of other comorbidities that requires anticoagulation therapy such as warfarin more than other anticoagulants (21). an observational study on a cohort of 114 patients with severe blunt trauma (severe tbi excluded) showed that use of oral anticoagulants was associated with significantly lower mortality group 8.3% vs. warfarin group 29.5%, p < 0.015) (15). yet; some physicians may be hesitated to prescribe anticoagulants, especially for the very old or frailest patients, as they are perceived to be at higher risk for the consequences of traumatic events (tbi) (20) utilization of anticoagulant medications patients with tbi found to have higher rate of using antiplatelet medications in our study. in comparison to our study; another study showed that 40.7% who sustained blunt head trauma were taking antiplatelet medications and having consequent acute ich following the head trauma (2). posttraumatic ich was associated with significantly increased mortality rate in patients on antiplatelet therapy when compared to controls in previous studies (9,10). these findings are supported by a study by major et al who found evidence that posttraumatic ich is associated with a mortality rate of 21% in patients on antiplatelet therapy (11). the risk for ich appears to be dose dependent with aspirin, the most studied agent, but exists with other antiplatelet agents as well (12). the utilization of those medications was correlated with increased ich volume growth at 12 hours, volume of intraventricular haemorrhage increased chance of death at 14 days, and poor outcome at 3 months (13,14,15). yet, the decision to stop all antiplatelet medication needs to be carefully considered, weighing the size and morbidity of the ich against the reason the agents were initiated. in another hand, platelet function testing appears advisable prior to neurovascular procedures, particularly in patients with risk factors for variable response to antiplatelet medications (16). another important issue to be considered is that in all studies the assessment of pre-injury use of antiplatelet agents was based on the patient’s history and not on assessment of platelet activity through laboratory examinations, thus, incompliance of patients regarding the intake of prescribed medications as well as ineffectiveness of antiplatelet agents in some will affect the overall effect of antiplatelet medications in the body system (4). this study also showed that there was a significant relationship between the utilization of antiplatelet medications among different neurological diseases investigated. correspondingly, a previous study conducted to evaluate the effect of antiplatelet medications on neurosurgical conditions showed that pre-injury antiplatelet agents were associated with three times higher mortality among elderly patients where it was due to a functional rather than quantitative factors (2). our study demonstrates that there was no significant difference between the utilization of antiplatelet medications the type of injury. in 104 abdulrahman al-mirza, omar al-taei, hatem al-saadi, tariq al-saadi comparison to our study, mina et. al found a statistically significant mortality rate (47%) in those who had tbi and taking aspirin compared with controls (8%). this may be attributed to the severity of tbi or the dose of aspirin consumed by the patients as low aspirin doses showed to has a lower risk of bleeding compared with higher doses (12,17) also the present study demonstrated that there is a significant difference in the los and the usage of antiplatelet drugs, in which patients who were not using antiplatelet medications found to stay shorter in the hospital. in comparable results, scott et al reported that patients who were using antiplatelet medications were three times more likely to be discharged to long-term inpatient facilities and 14 times higher mortality rate as compared with those not on antiplatelet additionally, patients who were undergone surgical intervention were using antiplatelet medications much less then patients on conservative management. in contrast to our research; bachelani et al found that neither history of aspirin intake nor platelet inhibition measured by a specific coagulation tests were associated with an increased risk of incidence or progression of ich and consequent need to an operative intervention such as craniotomy (18). added to that the significant relationship that found to be between the icu admission and the utilization in which majority of the patients who were not on antiplatelet therapy were not admitted to the icu. in comparison to a study conducted by sharma et al which stated that antiplatelet therapy with aspirin and clopidogrel did not increase rate of mortality and did not affect length of hospital icu stay (19). also, there was no association between the usage of antiplatelet drugs and the age of patients (above and below 75 years). prior research has shown that the geriatric population suffers from a higher rate of acute ich. as the brain ages, there is volume loss in the brain parenchyma, making bridging cerebral vein more vulnerable to bleeding along with a significant decline in the elasticity of those veins. moreover, the increase in aging population due to improvement of health care services in high income developing countries – like sultanate of oman has led to increased utilization of antiplatelet medications, likely contributing to the increased incidence of bleeds (2). aspirin is the most commonly used antiplatelet agent among different neurosurgical pathologies in the present study followed by clopidogrel. in the same line to our study, a previous study showed that aspirin is the most common utilized antiplatelet drug. this can be attributed to the fact that it is widely available, well tolerated, and has extensive clinical evidence supporting it is use in the cardiovascular protective properties. yet, currently, the combination of aspirin and clopidogrel is recommended prior to some neuroendovascular surgeries such as stent deployment (4). limitations there were some limiting factors in the present study. it was a retrospective, single-centered study over a period of four-years which limit is our ability to investigate whether there is a prior use of anticoagulants and antiplatelet medications especially in patients with chronic diseases that carry a high thromboembolic risk. analysis of coagulation profile was not routinely performed, so it is unclear if patients were compliant with their anticoagulant medications. moreover, the study was conducted in tertiary health care facility so it doesn’t include prescription patterns of medications from other health care facilities. finally, the outcome of using anticoagulant and antiplatelet medications was not illustrated in the present study due to the lack of comprehensive data regarding mortality in the health information system used to collect the data. conclusion patients with tbi found to have higher rate of using antiplatelet and anticoagulant medications. aspirin and enoxaparin were the most commonly used antiplatelet and anticoagulant agents among different neurosurgical pathologies in the present study physiological changes and comorbidities are main contributors to the challenges faced in managing bleeding in geriatric age group which has to be considered essentially. there is a need for further work to explore the balance of thrombotic and antithrombotic factors in elderly patients with neurosurgical diseases and to investigate whether the laboratory measures of thrombotic potential can help identify those at highest risk of thrombosis. decisions regarding prescription and resumption of anticoagulants and antiplatelet medications should be taken on a case-by-case basis involve a multidisciplinary and holistic approaches. the preventative benefit is of antiplatelet and 105 utilization of anticoagulant and antiplatelet medications among geriatric patients with neurosurgical diseases anticoagulant therapy from thromboembolic events of stroke or myocardial infarction have to be weighed against the risk of haemorrhage and death in those patients due to decreases ability of their body to with stand high energy traumatic accidents and their increased risk of frequent falls. it’s worth mentioning that this study is the first of its kind in the region, to the best of our knowledge. abbreviations dvt: deep venous thromboembolism, gcs: glasgow coma scale, ich: intracerebral haemorrhage, icu: intensive care unit, los: length of hospital stays, pe: pulmonary embolism. disclosures nothing to disclose. funding no funding required conflict(s) of interest no conflict of interest. references 1. prior, alessandro, pietro fiaschi, corrado iaccarino, roberto stefini, denise battaglini, alberto balestrino, pasquale anania, enrico prior, and gianluigi zona. 2021. “how do you manage anticoagulant therapy in neurosurgery? the antico survey of the italian society of neurosurgery (sinch).” bmc neurology 21(1):1–14. doi: 10.1186/s12883-021-02126-7. 2. anon. 2018. “typhi strain ty21a carrying a plasmid encoding vascular endothelial growth factor receptor 2 (vegfr2). the bacterium serves as a vector to deliver the plasmid into the peyer’s patches.” (september):2018. 3. ho, sandra, vismay thakkar, and jack jallo. 2013. “outcomes in traumatic brain injury patients on preinjury anticoagulation and antiplatelet agents.” jhn journal 8(1):1–5. doi: 10.29046/jhnj.008.1.002. 4. alter, scott m., benjamin a. mazer, joshua j. solano, richard d. shih, mary j. hughes, lisa m. clayton, spencer w. greaves, nhat q. trinh, and patrick g. hughes. 2020. “antiplatelet therapy is associated with a high rate of intracranial hemorrhage in patients with head injuries.” trauma surgery and acute care open 5(1):1–5. doi: 10.1136/tsaco-2020-000520. 5. claudia, casula, ranalli claudia, ognibene agostino, magazzini simone, and grifoni stefano. 2011. “minor head injury in warfarinized patients: indicators of risk for intracranial hemorrhage.” journal of trauma injury, infection and critical care 70(4):906–9. doi: 10.1097/ta.0b013e3182031ab7. 6. james, robert f., viktoras palys, jason r. lomboy, j. richard lamm, and scott d. simon. 2013. “the role of anticoagulants, antiplatelet agents, and their reversal strategies in the management of intracerebral hemorrhage.” neurosurgical focus 34(5):1–11. doi: 10.3171/2013.2.focus1328. 7. kim, keri s., justin f. fraser, stephen grupke, and aaron m. cook. 2018. “management of antiplatelet therapy in patients undergoing neuroendovascular procedures.” journal of neurosurgery 129(4):890–905. doi: 10.3171/2017.5.jns162307. 8. roth, p., a. pace, e. le rhun, m. weller, c. ay, e. cohenjonathan moyal, m. coomans, r. giusti, k. jordan, r. nishikawa, f. winkler, j. t. hong, r. ruda, s. villà, m. j. b. taphoorn, w. wick, and m. preusser. 2021. “neurological and vascular complications of primary and secondary brain tumours: eano-esmo clinical practice guidelines for prophylaxis, diagnosis, treatment and follow-up †.” annals of oncology 32(2):171–82. doi: 10.1016/j.annonc.2020.11.003. 9. beynon, christopher, daniel n. hertle, andreas w. unterberg, and oliver w. sakowitz. 2012. “clinical review: traumatic brain injury in patients receiving antiplatelet medication.” critical care 16(4). doi: 10.1186/cc11292. 10. the world health report 2000 (health systems: improving performance). who geneva. available at: https://www.who.int/whr/2000/en/. 11. al-kalbani, h., al-saadi, t., al-kumzari, a., & al-bahrani, h. (2020). public’s perception and satisfaction on the health care system in sultanate of oman: a cross-sectional study. annals of the national academy of medical sciences (india), 56(04), 214-219. doi:10.1055/s-00401721554 12. g p mishra, tariq al saadi, neeraj salhotra, samit biniwale, mohammad hadad, mohammad hashim, ali al mashani, qassim al hinai and sharad samson rajmani. brain and spinal tumors incidence annual audit 2017 of dept of neurosurgery khoula hospital muscat oman: a review. american journal of medical case reports. 2018; 6(7):128-131. doi: 10.12691/ajmcr-6-7-2 13. al-saadi t, al sharqi a, alsharqi j, alblushi k, alrasbi a, al-farsi m, al-ghafri s, al-abri s, al-saadi h. leaving against medical advice among patients with brain tumours in the middle east: khoula hospital experience. int clin neurosci j [internet]. 2020sep.28 [cited 2021mar.20];7(4):179-84. available from: https://journals.sbmu.ac.ir/neuroscience/article/view/30 700https://www.ncbi.nlm.nih.gov/books/nbk189784/ta ble/appc.t1/ 14. karni a, holtzman r, bass t, et al. traumatic head injury in the anticoagulated elderly patient: a lethal combination. am surg. 2001;67: 1098–1100 15. anon. 2018. “typhi strain ty21a carrying a plasmid encoding vascular endothelial growth factor receptor 2 106 abdulrahman al-mirza, omar al-taei, hatem al-saadi, tariq al-saadi (vegfr2). the bacterium serves as a vector to deliver the plasmid into the peyer’s patches.” (september):2018. 16. view, point o. f. 2019. “geriatric traumatic brain injury : an old challenge traumatismo craneoencefálico en el anciano : un viejo reto.” 43(1):44–46. 17. chowdhury, subhankar, and partha pratim chakraborty. 2017. “universal health coverage ‑ there is more to it than meets the eye.” journal of family medicine and primary care 6(2):169–70. doi: 10.4103/jfmpc.jfmpc. 18. wong, henna, nicola lovett, nicola curry, ku shah, and simon j. stanworth. 2017. “antithrombotics in trauma: management strategies in the older patients.” journal of blood medicine 8:165–74. doi: 10.2147/jbm.s125209. 19. angelozzi, andrea, giulia renda, and michele mercuri. 2015. “the risk of intracranial hemorrhage with anticoagulation in the elderly estimates of prevalence and therapeutic strategies.” american college of cardiology 1–9. 20. rao lv, pendurthi ur. tissue factor-factor viia signaling. arterioscler thromb vasc biol. 2005;25(1):47-56. doi:10.1161/01.atv.0000151624.45775.13 21. mak, calvin h. k., stephen k. h. wong, george k. wong, stephanie ng, kevin k. w. wang, ping kuen lam, and wai sang poon. 2012. “traumatic brain injury in the elderly: is it as bad as we think?” current translational geriatrics and experimental gerontology reports 1(3):171–78. doi: 10.1007/s13670-012-0017-2. 22. mina aa, knipfer jf, park dy, bair ha, howells ga, bendick pj: intracranial complications of preinjury anticoagulation in trauma patients with head injury. j trauma 2002, 53:668-672. 23. ohm c, mina a, howells g, bair h, bendick p: effects of antiplatelet agents on outcomes for elderly patients with traumatic intracranial hemorrhage. j trauma 2005, 58:518-522. 24. major j, reed mj: a retrospective review of patients with head injury with coexistent anticoagulant and antiplatelet use admitted from a uk emergency department. emerg med j 2009, 26:871-876. 25. naidech am, bendok br, garg rk, bernstein ra, alberts mj, bleck tp, et al: reduced platelet activity is associated with more intraventricular hemorrhage. neurosurgery 65: 684–688, 2009 26. naidech am, bernstein ra, levasseur k, bassin sl, bendok br, batjer hh, et al: platelet activity and outcome after intracerebral hemorrhage. ann neurol 65:352–356, 2009 27. naidech am, jovanovic b, liebling s, garg rk, bassin sl, bendok br, et al: reduced platelet activity is associated with early clot growth and worse 3-month outcome after intracerebral hemorrhage. stroke 40:2398–2401, 2009 hemorrhage. world neurosurg 76:100–104, 2011 28. feeney jm, santone e, difiori m, kis l, jayaraman v, montgomery sc.1 compared to warfarin, direct oral anticoagulants are associated with lower mortality in patients with blunt traumatic intracranial hemorrhage: a tqip study. j trauma acute care surg. 2016;81(5):843– 848. 29. alter, scott m., benjamin a. mazer, joshua j. solano, richard d. shih, mary j. hughes, lisa m. clayton, spencer w. greaves, nhat q. trinh, and patrick g. hughes. 2020. “antiplatelet therapy is associated with a high rate of intracranial hemorrhage in patients with head injuries.” trauma surgery and acute care open 5(1):1–5. doi: 10.1136/tsaco-2020-000520. 30. ho, sandra, vismay thakkar, and jack jallo. 2013. “outcomes in traumatic brain injury patients on preinjury anticoagulation and antiplatelet agents.” jhn journal 8(1):1–5. doi: 10.29046/jhnj.008.1.002. 31. bachelani am, bautz jt, sperry jl, corcos a, zenati m, billiar tr, peitzman ab, marshall gt: assessment of platelet transfusion for reversal of aspirin after traumatic brain injury. surgery 2011, 150:836-843 32. chowdhury, subhankar, and partha pratim chakraborty. 2017. “universal health coverage ‑ there is more to it than meets the eye.” journal of family medicine and primary care 6(2):169–70. doi: 10.4103/jfmpc.jfmpc. romanian neurosurgery (2019) xxxiii (3): pp. 326-328 doi: 10.33962/roneuro-2019-055 www.journals.lapub.co.uk/index.php/roneurosurgery spinal epidural angiolipoma causing spinal cord compression. a case report a. khelifa1, i. assoumane2, s. bachir3, l. berchiche1, a. morsli1 1 neurosurgical department of beo university hospital, algiers, algeria 2 national hospital of niamey, niger 3 neurosurgical department of laghouat hospital, laghouat, algeria abstract background. spinal angiolipoma (sal) is a rare tumour with double component mature adipose tissue and proliferating abnormal blood vessels, which result in spinal cord compression requiring an urgent surgical removal. we report a case of woman with spinal angiolipoma. case presentation. the patient is a 26 years old woman with past medical history of a low grade urothelial bladder carcinoma removed 4 months before she consults at our department, 2 months later the patient presented a lower limbs weakness. the clinical exam at the admission found a patient with paraparesis, hypoesthesia at the level of th4 and urinary urgency. the spinal mri objectified a spinal cord compression by a lesion located at the epidural space from th2 to th4. the patient was operated and a fatty well vascularized tumour distinct from the epidural fat was removed through a th2 to th4 laminectomy. the pathology study was in favour of an angiolipoma. days after the operation the patient recovered totally, the weakness and the urinary urgency disappeared. the patient is flowed since 24 months she got pregnant. conclusion. spinal angiolipoma is a rare tumour with a clinic of spinal cord compression, mri is the gold standard in diagnosis it shows a fatty lesion with a large enhancement, surgery is the perfect treatment with good outcome and exceptional recurrence. introduction spinal angiolipoma (sal) is a rare tumour with double component mature adipose tissue and proliferating abnormal blood vessels, which result in spinal cord compression requiring an urgent surgical removal. we report a case of woman with spinal angiolipoma. case presentation the patient is a 26 years old woman with past medical history of a low grade urothelial bladder carcinoma removed 4 months before she consults at our department, 2 months later the patient presented a lower limbs weakness. the clinical exam at the admission found a patient with paraparesis, hypoesthesia at the level of th4 and urinary urgency. the spinal mri objectified a spinal cord compression by a lesion located at the epidural space from th2 to th4 fusiform measuring 83 x 12 keywords angiolipoma, epidural tumour, spinal cord compression corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 327 spinal epidural angiolipoma causing spinal cord compression mm, hyper intense on t1 and t2 weighted images (figure 1) there was a homogenous enhancement after gadolinium injection with persistence of the signal on t1 spir injected and in stir sequences (figure 2). the patient was operated and a fatty well vascularized tumour distinct from the epidural fat was removed through a th2 to th4 laminectomy. the pathology study was in favour of an angiolipoma. days after the operation the patient recovered totally, the weakness and the urinary urgency disappeared. the patient is flowed since 24 months she got pregnant. figure 1. spinal mri. a: sagittal t1 weighted image; b: sagittal t2 weighted image; c: axial t2 weighted image; showing hyperintense t1 and t2 lesion (arrows and the star) causing spinal cord compression (head of the arrow). figure 2. spinal mri. a: sagittal injected sequence; b: sagittal stir sequence; c: stir injected sequence; showing a homogenous enhancement of the lesion after gadolinium injection with persistence of the signal after the suppression of the fat signal (the arrows). the head of the arrow shows the situation of the spinal cord. 328 a. khelifa, i. assoumane, s. bachir, l. berchiche, a. morsli discussion sal are tumours with double component mature adipose tissue and proliferating abnormal blood vessels (1,2,3,4,5,6,7,8), they are rare, 177cases are found in the literature from 1890 where the first case was reported by berenbruchto to june 2015 (2). some studies suggest that it represent 0.04% to 1.2% of spinal tumours, 2% to 3% of epidural spinal tumors (1,3,5,6,8) and 16 % to 35 % of spinal lipomas (5,8). it has a female predominance (1,2,3,4,5,7,8) with a sex ratio of 3/2 (8), with an average age between 40 and 60 years(2,3,4,7) and mostly located in thoracic spine (1,2,3,4,5,6,7,8) in 78 % of cases (8), mostly between th2 and th5 (6), other location are less common, it occurs in 10 % in the lumbar spine and in 1 % in the cervical spine (8).sal can be infiltrating or non-infiltrating, in the majority of cases it is non infiltrating encapsulated and limited in the epidural space(3,7,8).the clinical presentation include back pain and signs of spinal cord compression (1,2,3,4,5,6,7,8), although the symptoms evolves slowly some cases of acute paraplegia were described (4).mri is the imaging of choice for sal diagnosis(1,2,3,4,5,6,7,8) ,commonly the tumour has a fusiform shape located in the posterior epidural space (2,4,5), the signal of the lesion is the reflect of its two components: lipomatose and angiomatose, so sal is usually hyperintense in t1 and t2 weighted images with loss of the signal in fat suppression sequences which could be regained after injection of gadolinium (1,2,3,6,8).surgery is the reasonable treatment modality (1,2,3,4,6,7,8), usually the lesion is reached by a posterior approach through a suitable laminectomy, total resection is possible for the noninfiltrating lesions with good outcome and exceptional cases of recurrence are reported (1,2,3,4,5,8,7). conclusion spinal angiolipoma is a rare tumour with a clinical presentation of spinal cord compression, mri is the gold standard in diagnosis it shows a fatty lesion with a large enhancement, surgery is the perfect treatment with good outcome and exceptional recurrence. references 1. carrasco moro r, gutiérrez cierco ja, martínez san millán js, pian h, martínez rodrigo ma. 2. spinal extraduralangiolipomas: 7 new cases and review of the literature. neurología. 2019;34:98—104. 3. feifei wang, song wang, wen huaxue and jing liang cheng. 4. epidural spinal angiolipoma: a case series. wang et al. bmc res notes (2017) 10:128. 5. doi 10.1186/s13104-017-2432-0. 6. yang x, richard sa, lei c, liu j, huang s. 7. spinal extradural angiolipoma: a report of two cases and review of literature. j spinesurg 2018;4(2):490-495. 8. doi: 10.21037/ jss.2018.06.11. 9. enrique gonzalo bovier, emilianogardino, lucas nicoláschemes, federico nogueira, verónica diana romero. 10. acute paraplegia by spinal angiolipoma. case report and literature review. coluna/columna. 2014; 13(2):147-9. doi.org/10.1590/s1808-18512014130200403. 11. marcel hungs, md, phd1; laura s. pare´, md, frcsc. 12. spinal angiolipoma: case report and literaturereview. j spinal cord med. 2008;31:315–318. 13. shweikeh f, sangtani a, steinmetz mp, zahos p, chopko b. 14. spinal angiolipomas: a puzzling case and review of a rare entity. j craniovert jun spine 2017;8:91-6. 15. doi: 10.4103/jcvjs.jcvjs_23_17. 16. rajesh k ghanta,kalyan koti, and srinivas dandamudi. 17. spinal epidural angiolipoma: a rare cause of spinal cord compression.j neurosci rural pract. 2012 sep-dec; 3(3): 341–343. 18. doi: 10.4103/0976-3147.102617. 19. mouna rkhamia, mohamed ali kedousb, samehachourac, alia zehanid, kamelbahria,ihsenzammelaa. 20. epidural angiolipoma: a rare cause of spinal cord compression. international journal of surgery case reports 45 (2018) 72–76. doi.org/10.1016/j.ijscr.2018. 03.005 romanian neurosurgery (2019) xxxiii (2): pp. 160-165 doi: 10.33962/roneuro-2019-030 www.journals.lapub.co.uk/index.php/roneurosurgery traumatic posterior fossa extradural hematoma. a comprehensive analysis of cases from a tertiary care centre in southwestern rajasthan vibhu shankar parashar, vivek kumar kankane, gaurav jaiswal, tarun kumar gupta * department of neurosurgery, rabindra nath tagore medical college & m.b. groups of hospital, udaipur, rajasthan, india abstract background. extradural hematoma of posterior fossa (pfedh) is less common and there are not many articles about pfedh. these patients can deteriorate very rapidly due to compression over brainstem. thus, early identification and immediate intervention can save the lives of these patients. objective. this study aims to conduct a comprehensive analysis of patients with pfedh and evaluate the postoperative outcome which may be of help to make further preventive strategies. methods and materials. the study included 16 patients admitted with traumatic pfedh from july 2016 to july 2018 at r.n.t. medical college & m.b. groups of hospital udaipur, southwestern rajasthan, india. we have retrospectively reviewed the data. analysed factors were gender, age, glasgow coma scale (gcs), noncontrast ct scan findings, associated brain injury, type of intervention, glasgow outcome scale (gos). gos was assessed at discharge, at 3 months and 6 months follow-up. results. out of a total of 16 patients, 11 were male and 5 were female with age ranging from 05-46 years. 12 patients had gcs 13 -15 at admission and only one of them had gcs < 8. 15 patients underwent surgical intervention. at 6 months followup, 12 patients had good recovery gos is 5. conclusion. early detection and immediate evacuation of pfedhs should be done if causing fourth ventricle, basal cistern or brain stem compression. it may be rapidly fatal due to the expansion of hematoma leading to brainstem compression, tonsillar herniation, and/or obstructive hydrocephalus. early detection and immediate evacuation lead to a better outcome in these patients. introduction pfedh is an uncommon trauma sequel accounting for only 4% to 12.9% of all edhs [1,2]. in pfedh clinical progress may be silent and slow, but sudden deterioration may occur without significant warning signs. because of limited space in posterior fossa, comparatively small volume can cause clinical deterioration. the patient may deteriorate very rapidly due to compression over the brainstem usually without keywords posterior fossa, extradural hematoma, traumatic, glasgow outcome scale corresponding author: vivek kumar kankane rabindra nath tagore medical college & m.b. groups of hospital, udaipur, rajasthan, india drvarunaggarwal86@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 161 traumatic posterior fossa extradural hematoma any prior warning sign. thus, early intervention before progression to herniation is lifesaving. early diagnosis by cranial computed tomography and emergent evacuation is vital for a good outcome [3]. material and methods in our study, we have retrospectively reviewed the data from july 2016 to july 2018 at tertiary care hospital in r.n.t. medical college & m.b. groups of hospital udaipur, southwestern rajasthan. we found 16 cases of traumatic extradural hematoma (edh) which were located in the posterior fossa. the data was analysed for clinical presentation, glasgow coma scale (gcs) at admission, mode of injury, radiological findings, any other associated intracranial traumatic lesion, type of intervention and postoperative outcome. postoperative scans, within 6-12 hour of surgery were acquired in all cases. outcomes were assessed on the basis of glasgow outcome score (gos) divided into good (normal, moderate disability) and poor (severe, vegetative, dead) outcome at 3 months, 6 months of follow-up. we also assessed the prognosis of posterior fossa edh depending on the compression over the fourth ventricle, basal cistern and brain stem. all patients were divided in two groups. group a were those who showed isolated pfedh and in group b were those patients who showed pfedh associated with brain injury. figure 1. ncct head revealed left posterior fossa extradural hematoma with supratentorial extension figure 2. ncct head revealed left posterior fossa extradural hematoma with bilateral frontal intracerebral hematoma 162 vibhu shankar parashar, vivek kumar kankane, gaurav jaiswal et al. results a total of 16 cases of pfedhs were admitted to our tertiary care centre during 24 months from july2016 july 2018.the mean age of patients was 28.6 years (range 5-46years). 3 (18.75%) of them were below 18 years. 5(31.25%) of them were females (table 1). outcome was better in paediatric patients. most common mode of injury was road traffic accident (n= 11, 68.75%), rest were either fall from height (n = 04, 25%) or assault (n =1, 6.25%) (table 2). most common associated radiological finding is occipital bone fracture followed by supratentorial extension of edh and frontal contusions (table 3). 15 patients underwent surgical evacuation. at 6 months follow-up, 12 (75%) patients had good recovery and one patient died (6.25%) (table 4). patients with pfedh with associated brain injury had lesser gcs score on admission with increased volume of edh, increased hospital stay. outcome was poor in pfedh patients with associated intracranial injury as compared to those with isolated pfedh. (table 5) table 1. correlation of gender and age and outcome analysis total cases number. of patients (n=16) age<18 yrs age>18 yrs percentage (%) good outcome (gos 3-5) poor outcome (gos1-2) gender male 11 03 08 68.75% 10 01 female 05 00 05 31.25% 03 02 age pediatric patients (<18) 03 18.75 % 03 00 adults 13 81.25% 10 03 total 16 100% 13 03 table 2. correlation of mode of injury, gcs at admission and outcome analysis no. of patients percentage good outcome (gos 3-5) poor outcome (gos 1-2) mode of injury road traffic accident 11 68.75% 09 02 fall from height 04 25% 03 01 assault 01 6.25% 01 00 gcs at admission 13-15 12 75% 12 00 9-12 03 18.75% 01 02 3-8 01 6.25% 00 01 total 16 100% 13 03 163 traumatic posterior fossa extradural hematoma table 3. analysis of clinical presentation and radiological findings number of patients percentage clinical presentation headache 10 62.5% altered sensorium 06 37.5% vomiting 08 50% radiological findings occipital bone fracture 12 75% frontal contusions 01 6.25% supratentorial extension of edh 02 12.5% hydrocephalus 01 6.25% intraventricular hemorrhage 01 6.25% table 4. outcome based on gos (glasgow outcome score) outcome based on gos discharge at 3 months at 6 months gos 5 11 12 (75%) 12 (81.25%) gos 4 03 01 (6.25%) no follow up gos 3 00 01 (6.25%) 01 (6.25%) gos 2 01 01 (6.25%) 01 (6.25%) gos 1 01 table 5. analysis of patients with isolated pfedh and those with associated brain injuries parameters isolated pfedh (group a) pfedh and associated brain injury (group b) total patients 13(81.25%) 03(18.75%) radiological findings occipital bone fracture 10(76.9%) 02(66.7%) frontal contusions 01(33.3%) supratentorial extension of edh 02(66.7%) hydrocephalus 01(33.3%) intraventricular hemorrhage 01(33.3%) gcs (admission) 15-13 11 01 12-9 02 01 8-3 00 01 management surgical evacuation 11 03 conservative 02 00 failed conservative and operated 01 00 gcs (discharge) 164 vibhu shankar parashar, vivek kumar kankane, gaurav jaiswal et al. 15-13 13 01 12-9 00 01 8-3 00 01 good outcome (gos 3,4,5) 12 01 poor outcome (gos1,2) 01 02 discussion traumatic brain injury is emerging as the most common cause of morbidity and mortality in both developed and developing countries. pfedhs are reported to constitute 0.1–0.3% of all cranial traumatic conditions. loss of consciousness and vomiting are the most frequent presenting features of pfedh which comprises around 10% of edh. a history of occipital bone fracture combined with these symptoms should raise suspicion of pfedh. lucid interval is classically seen in edh; however, it is uncommon in pfedh and in children. a rapid deterioration is a feature of these lesions. thus, all patients need to undergo imaging promptly in order to diagnose the lesions. unlike supratentorial edhs where the source of bleeding is usually the middle meningeal artery in temporo-parietal edhs and the anterior ethmoidal artery in frontal edhs.[4] pfedhs have a venous origin in 85% of the cases and develop as a result of injury to the transverse or sigmoid sinuses secondary to occipital bone fracture.[5] however, an extradural hematoma can develop without fracture. since most of the pfedhs are of venous origin and expand slowly, it takes longer for the clinical picture to develop in pfedh and it is of vital importance to use imaging methods for early diagnosis. currently, ncct scan is the imaging of choice in brain trauma. in the literature it has been reported that pfedhs are most commonly encountered in the first decade. [6,7] in our study, 03 (18.75%) cases were paediatric patients. male gender dominated in our group, which is in line with data in the literature. this fact is explained by greater liability to trauma at work, road accidents and alcoholism in men. a leading cause of pfedhs in our series were road traffic accidents, although in paediatric patients the most common mode of injury was falls. in all the female patients, the reason for traumatic pfedh was attributed to sitting on vehicles as pillion riders and indicating the lack of support in the vehicles. the majority of pfedhs were unilateral with prevalence on the left side (93.75%). in one patient (6.25 %) the pfedh was bilateral and similar observation was reported by karasu et al. fracture of occipital bone is a common feature (in 58-95% of pfedh) even though not all of them are visible on plain x-rays of the skull .75% of our patients had fracture of occipital bone, or parietal bones in occipital region on the side of extradural hematoma. whereas some authors reported the occurrence of coexisting lesions in 23 50% of cases. we also observed them in three of our patients. the most common associated intradural lesion was supratentorial extension of edh, brain contusion followed by a subdural collectionand acute hydrocephalus. bozbuga et al. reported 73 cases in 1999, the largest series on pfedh till now. out of 73, they operated 53 cases [6]. 89% of operated patients had a good recovery, and 5.4% died. malik et al. published another series of 61 patients in 2007[8]. of these 48 were managed surgically, 36 (59%) had a good recovery and 15% died. roka et al [9]. reported 43 patients in 2008, of these 33 were operated and were followed up for 79 months with 81.8% good recovery in the operated patients and 3% overall mortality [9]. in our study 15 patients underwent surgical evacuation. during 6 months follow­ up, 12(75%) patients had good recovery and one patient died (6.25%). this was similar to study by jang et al [10] and balik et al. [11]. jang et al., in 2011, published the review of 34 patients with 96 months follow-up [10]. nineteen patients underwent surgical evacuation with 73.7% having a good recovery and 5.3% mortality. three series comprised paediatric cases only., gupta et al.in 2002[12], sencer et al., in 2012[13] prasad et al. in 2015[14], and published paediatric series with 18,40 and 18 cases, respectively. sencer reported good recovery in all cases. prasad's series had 94.4% patients with good recovery. both these series showed better outcomes in paediatric age group. outcome was better in paediatric patients in our study. admission gcs is the single most important 165 traumatic posterior fossa extradural hematoma factor that determined the immediate and long-term outcomes. patients with additional intracranial findings had relatively poor gcs at admission and categorically much poor outcomes. patients with mass effect over brainstem had lesser gcs score on admission with increased volume of edh, increased hospital stay and increased mortality [15]. nonsurgical management is a viable option in select patients with low edh volumes, but option should be kept for surgical evacuation in such patients for better outcome. conclusion pfedh is a rare entity and posterior fossa is an unfavorable location. they are usually associated with occipital bone fractures. early diagnosis and emergent evacuation lead to good outcome. pfedh may be rapidly fatal due to the expansion of hematoma and compromise of the posterior cranial fossa space leading to brainstem compression, tonsillar herniation, and/or obstructive hydrocephalus which are associated with worse outcome. references 1. ammirati m, tomita t. posterior fossa epidural hematoma during childhood. neurosurgery 1984; 14: 541–44. 2. asanin b. traumatic epidural hematomas in posterior cranial fossa. acta clin croat. 2009;48:27–30. 3. berker m, cataltepe o, ozcan oe. traumatic epidural haematoma of the posterior fossa in childhood: 16 new cases and a review of the literature. br j neurosurg.2003;17:226–9. 4. samudrala s, cooper pr. traumatic intracranial hematomas. in: wilkins rh, rengachary ss, editorsneurosurgery. 2nd ed. new york: mcgraw­hill; 1996. pp. 2797–807. 5. garza­mercado r. extradural hematoma of the posterior cranial fossa. report of seven cases with survival. j neurosurg. 1983;59:664–72. 6. bozbuga m, izgi n, polat g, gürel i. posterior fossa epidural hematomas: observations on a series of73 cases. neurosurg rev.1999;22:34-40 7. peter jc, domingo z. subacute traumatic extradural haematomas of the posterior fossa: a clinicopathological entity of the 5­ to 10­year­old child. childs nerv syst. 1990;6:135–8. 8. malik nk, makhdoomi r, indira b, shankar s, sastry k. posterior fossa extradural hematoma: our experience and review of the literature. surg neurol. 2007;68:155–8. 9. roka yb, kumar p, bista p, sharma gr, adhikari p. traumatic posterior fossa extradural hematoma. jnma j nepal med assoc. 2008;47:174–8. 10. jang jw, lee jk, seo br, kim sh. traumatic epidural haematoma of the posterior cranial fossa. br j neurosurg. 2011;25:55–61 11. balik v, lehto h, hoza d, sulla i, hernesniemi j. posterior fossa extradural haematomas. cent eurneurosurg. 2010;71:167-72. 12. gupta pk, mahapatra ak, lad sd. posterior fossa extradural hematoma. indian j pediatr.2002;69:489–94. 13. sencer a, aras y, akcakaya mo, goker b, kiris t, canbolat at. posterior fossa epidural hematomas in children: clinical experience with 40 cases. j neurosurgpediatr. 2012;9:139–43. 14. prasad gl, gupta dk, sharma bs, mahapatra ak. traumatic pediatric posterior fossa extradural hematomas: a tertiary­care trauma center experience from india. pediatrneurosurg. 2015;50:250–6. 15. pateriya a, bansal r, mittal r. factors affecting outcome in posterior fossa edh: an analytical study at tertiary referral hospital. romanian neurosurgery .2016; xxx 2: 267-71. doi: 10.33962/roneuro-2023-038 intracranial lipoma associated with a subcutaneous lipoma. a rare entity toyin ayofe oyemolade, james ayokunle balogun romanian neurosurgery (2020) xxxiv (1): pp. 215-217 doi: 10.33962/roneuro-2020-038 www.journals.lapub.co.uk/index.php/roneurosurgery intracranial lipoma associated with a subcutaneous lipoma. a rare entity toyin ayofe oyemolade1, james ayokunle balogun2 1 division of neurosurgery, department of surgery, federal medical centre, pmb 1053, owo, nigeria 2 division of neurosurgery, department of surgery, college of medicine, university of ibadan and department of neurological surgery, university college hospital, ibadan, nigeria abstract intracranial lipomas are rare, frequently asymptomatic, congenital malformations. they are most commonly located in the pericallosal region and are often detected incidentally during neuroimaging studies or postmortem examinations. while other associated brain malformations, most notably callosal agenesis, are frequently reported, association with a subcutaneous scalp lipoma is extremely rare. we present a case of pericallosal lipoma associated with callosal agenesis and subcutaneous lipoma over the anterior fontanelle in a 6-month-old female infant who had excision of only the extracranial mass and has remained asymptomatic from the intracranial mass for the 3 years of follow up. introduction intracranial lipomas are rare benign congenital lesions1. they are most commonly located in the deep interhemispheric fissure especially in the pericallosal region2. intracranial lipomas are frequently asymptomatic and are therefore usually detected incidentally during neuroimaging studies or postmortem examinations3, 4. they are often managed conservatively because the surgical risks outweigh the benefits1, 5, 6, 7. they are frequently associated with other brain malformations, agenesis or dysgenesis of corpus callosum being the most common7. extremely rare however is the association of intracranial lipoma with a subcutaneous lipoma8, 9. we present a case of an asymptomatic giant intracranial lipoma associated with corpus callosal agenesis and a midline frontoparietal subcutaneous lipoma. case presentation a 6-month old female infant was referred to us with a midline frontoparietal subcutaneous mass. the mass was noticed at birth and was increasing in size progressively. the child was otherwise well; the developmental milestones were within normal limits. the neurological examination findings were also essentially normal. the mass measured keywords intracranial, lipoma, subcutaneous corresponding author: toyin ayofe oyemolade department of surgery, federal medical centre, owo, nigeria toyinmolade@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 216 toyin ayofe oyemolade, james ayokunle balogun 8cm by 6cm by 5cm with the anterior half over the anterior fontanelle (fig. 1). other systemic examination findings were normal. brain mri showed a large inter-hemispheric pericallosal and a fronto-parietal subcutaneous mass, hyper intense on t1 (fig. 2) and t2 weighted images but hypointense on t2* and fat suppression sequences (fig 3) consistent with lipoma. there was no connection between the intra and extra-cranial masses. the extracranial mass was excised completely. no cranial defect was found at surgery, confirming no connection between the extra-cranial and intra-cranial masses. the excised subcutaneous mass was confirmed to be a lipoma on histology. she is currently being followed up at the outpatient clinic. she remains asymptomatic 3 years after surgery and her developmental milestones are within normal limits. figure 1. clinical photograph showing the frontoparietal subcutaneous lipoma. figure 2. a sagittal (a) and axial (b) t1weighted mri showing hyperintense frontoparietal subcutaneous and an interhemispheric pericallosal masses. figure 3. sagittal t1 fat suppressed (a) and axial t2* weighted mri images showing hpyointense lesion consistent with lipoma. discussion intracranial lipomas are rare benign congenital lesions accounting for 0.06% to 0.46% of all intracranial tumours1. they result from abnormal persistence and mal-differentiation of the meninx primitive during the development of the subarachnoid cisterns and hence are congenital anomalies rather than true neoplasms10. about 45% of cases occur in the pericallosal region, 25% in the quadrigerminal cistern and 15% in the suprasellar cistern. other locations include cerebellopontine angle cisten (9%), sylvian cistern (5%) and rarely on the surface of the cerebral hemispheres8, 11, 12, 13. the callosal lipomas can be divided into two types: a bulky tubulonodular anterior variety which is associated with forebrain and rostral callosal anomalies and a ribbon-like curvilinear posterior lipoma with a normal or nearly normal corpus callosum14. more than half of intracranial lipomas are associated with other malformations of the central nervous system including callosal agenesis or hypogenesis (the most common), encephalocele, spinal bifida, vermian hypoplasia, absent septum pellucidum and cortical malformation1, 13. interhemispheric lipoma associated with a subcutaneous lipoma as in our patient is however extremely rare8. in these cases, the intra and extracranial masses may have no connection with each other, may be connected by a fibrous lipomatous stalk or may be continuous with each other through cranium bifidum6, 15, 16, 17. intracranial lipomas are usually asymptomatic, often discovered only incidentally on neuroimaging3, 4. when symptomatic, symptoms depend on the location of the lipoma and may include epilepsy, persistent headache, ataxia, psychomotor retardation and cranial nerves deficits7, 18, 19, 20. the imaging findings in intracranial lipomas are characteristic. on cranial ct scan, lipomas are markedly hypodense (density of -50 to -100 hu) with frequent areas of calcifications, the latter being more common in the pericallosal lipomas4, 7. on mri, they have high intensity on t1 and t2 weighted images and low intensity on t2* weighted and fat suppression images without contrast enhancement21, 22. 217 intracranial lipoma associated with a subcutaneous lipoma radical surgical excision is usually contraindicated because of attendant high morbidity and mortality due to high vascularity and strong adherence to surrounding tissues6, 7. stable or asymptomatic lesions are managed conservatively1, 5. in patients with epileptic seizures, anticonvulsant therapy is the treatment of choice23. our patient had excision of only the subcutaneous fat and is being followed up at the outpatient clinic. conclusion intracranial lipomas are rare congenital malformations and are often asymptomatic. intracranial lipoma associated with subcutaneous lipoma is extremely rare. children with subcutaneous scalp lipoma should have brain imaging to look for possible associated intracranial lipoma and other associated anomalies. references 1. truwit cl, barkovich aj. pathogenesis of intracranial lipoma: an mr study in 42 patients. ajr am j roentgenol. 1990;155:855-864. 2. dean b, drayer bp, beresini dc, et al. mr imaging of pericallosal lipoma. ajnr am j neuroradiol 1988;9:929– 933 3. bilir o, yavasi o, ersunan g, kayayurt k, durakoglugil t. incidental finding in a headache patient: intracranial lipoma. west j emerg med 2014;15(4):361-362 4. chaubey v, kulkarni g, chhabra l: ruptured intracranial lipoma--a fatty outburst in the brain. perm j 2015;19:e103-104. 5. eghwrudjakpor po, kurisaka m, fukuoka m, mori k. intracranial lipomas: current perspectives in their diagnosis and treatment. br j neurosurg. 1992;6(2):139144. doi:10.3109/02688699209002916 6. given ca, fields tm, pittman t. interhemispheric lipoma connected to subcutaneous lipoma via lipomatous stalk. pediatr radiol 2005;35:1110–1112 7. yildiz h, hakyemez b, koroglu m, yesildag a, baykal b. intracranial lipomas: importance of localization. neuroradiology. 2006;48(1):1-7. doi:10.1007/s00234005-0001-z 8. ahmetoglu a, kul s, kuzeyli k, ozturk mh, sari a. intracranial and subcutaneous lipoma associated with sagittal sinus fenestration and falcine sinus. ajnr am j neuroradiol 2007;28:1034-1035. 9. reddy s r, panigrahi m, varma r. intracranial lipoma with subgaleal extension: an interesting case report with review of literature. neurol india 2012;60:444-446 10. wallace d. lipoma of the corpus callosum. j neurol neurosurg psychiatry. 1976;39(12):1179-1185. doi:10.1136/jnnp.39.12.1179. 11. gómez-gosálvez fa, menor-serrano f, sala-sánchez ag, rubio-soriano a, carbonell-nadal j, mulas f. intracranial lipomas in paediatrics: a retrospective study of 20 patients. revista de neurologia. 2003;37(6):515-521. 12. fandiño j, bermúdez j, arán e. lipoma de la cisterna cuadrigémina y cisura calcarina: caso clínico y revisión de la literatura [quadrigeminal cistern and calcarine fissure lipoma: case report and review of the literature]. neurocirugia (astur). 2005;16(2):173-176. 13. jabot g, stoquart-elsankari s, saliou g, toussaint p, deramond h, lehmann p. intracranial lipomas: clinical appearances on neuroimaging and clinical significance. j neurol. 2009;256(6):851-855. doi:10.1007/s00415-0095087-5 14. upadhyaya v, upadhyaya d n, sarkar s. sincipital encephalocele with corpus callosum agenesis and intracranial lipoma : a case report. indian j radiol imaging 2005;15:507-510 15. de villiers jc, cluver pf, peter jc. lipoma of the corpus callosum associated with frontal and facial anomalies. actaneurochir suppl (wien).1991;53:1–6. doi:10.1007/978-3-7091-9183-5_1 16. sari a, dinch, gumele hr. interhemisphericlipomaassociatedwithsubcutaneouslip oma. eur radiol 1998;8:628–630 17. yamashita s, kunishio k, tamiya t, nakamura t, ogawa d, igawa hh, et al. parietal lipomeningocele: case report. neurol med chir (tokyo). 2005;45:112–115. doi:10.2176/nmc.45.112 18. gastaut h, regis h, gastaut jl, yermenos e, low md. lipomas of the corpus callosum and epilepsy. neurology. 1980;30(2):132-138. doi:10.1212/wnl.30.2.132 19. guye m, gastaut jl, bartolomei f. epilepsy and perisylvian lipoma/cortical dysplasia complex. epileptic disord. 1999;1(1):69-73 20. loddenkemper t, morris hh 3rd, diehl b, lachhwani dk. intracranial lipomas and epilepsy. j neurol. 2006;253(5):590-593. doi:10.1007/s00415-006-0065-7 21. hua cl. agenesis and lipoma of the corpus callosum: mr findings. ajr am j roentgenol. 1990;154(6):1348. doi:10.2214/ajr.154.6.2110770 22. osborn a, blaser s, salzman k, provenzale j, castillo m, hed-lund gl, et al (eds): diagnostic imaging: brain. salt lake city: amirsys, inc, 2004, pp 12–15, 17 23. venkatesh b p, malik g, bora mk, narasingam ap. multiple intracranial lipoma. j health spec 2014;2:78-81. doi: 10.33962/roneuro-2022-086 mobilization of the temporal pole as integrated step in microsurgical clipping of pure posteriorly directed posterior communicating artery aneurysm mustafa ismail, salima b. alsaadi, muslim mousa badr, mohammed al-dhahir, aanab o. abdulameer, alkawthar m. abdulsada, aktham o. al-khafaji, samer s. hoz romanian neurosurgery (2022) xxxvi (4): pp. 476-478 doi: 10.33962/roneuro-2022-086 www.journals.lapub.co.uk/index.php/roneurosurgery mobilization of the temporal pole as integrated step in microsurgical clipping of pure posteriorly directed posterior communicating artery aneurysm mustafa ismail1, salima b. alsaadi2,muslim mousa badr2, mohammed al-dhahir3, aanab o. abdulameer1, alkawthar m. abdulsada4, aktham o. al-khafaji1, samer s. hoz5 1 department of neurosurgery, college of medicine, university of baghdad, baghdad, iraq 2 department of neuroradiology, neurosurgery teaching hospital, baghdad, iraq 3 department of neuroscience, university of florida, usa 4 azerbaijan medical university. baku, azerbaijan 5 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract a pure posteriorly posterior communicating artery (pcoa) aneurysm represents a surgical challenge. this is mainly when there is a need for good exposure of the aneurysmal neck, sac, pcoa, and anterior choroidal arteries. ruptured pure posteriorly directed pcoa aneurysm imposes significantly extra challenge as the surgeon undergoes dissection through a tight brain. even with measures commonly used to attain brain relaxation like the lumbar drain and cisternal fenestration. here, we describe a technique for posterior temporal pole mobilization (tpm) as an integrated part of microsurgical clipping of ruptured pure posteriorly directed pcoa aneurysms. this technique is implicated in twenty-three successive cases of ruptured pcoa aneurysms in the neurosurgery teaching hospital in baghdad, iraq, with no reported complications. pertinent anatomy the temporal pole is usually connected by bridging veins with the spheno-parietal sinus anteriorly and the cavernous sinus medially. these bridging veins are also known as the pre-uncal veins. these veins are neither described in the literature as a critical contributor to any of the essential surrounding veins (basal vein of rosenthal and deep middle cerebral vein) nor described as a vital drainage pathway for the temporal parenchyma [3]. keywords internal carotid artery, posterior communicating artery aneurysm, temporal lobe corresponding author: samer s. hoz department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 477 mobilization of the temporal pole as integrated step in microsurgical clipping technique following the steps of the pterional approach, which include,1) opening of the carotid cistern,2) dissection of the proximal sylvian fissure then,3) identifying the pre-uncal veins, and,4) cutting the bridging veins between the spheno-parietal and the cavernous sinuses (pre-uncal veins) then,5) releasing of the temporal pole followed by,6) widening of the surgical corridor (at least 2 cm of free space posterior to the sphenoid ridge) [3,4]. to illustrate this technique, two cases of pcoa aneurysms approaches were described in the images below (figure 1 and figure 2). a. b. figure 1. intraoperative images of case 1, through the left pterional approach (a) shows cutting and releasing by cauterization of the anterior temporal veins before temporal pole mobilization. (b) is showing the superficial retraction of the temporal lobe with tpm and now we can more appreciate the space lateral to the supracliniold internal carotid artery which widens the surgical field for safe and easy microsurgical clipping of the pcoa aneurysm. cnii: optic nerve, pcoa a: posterior communicating artery aneurysm, ica: internal carotid artery. advantage the requirement for temporal lobe traction is minimized or even absent (the retractor will hold the released temporal pole), which leads to easy identification of the pcoa aneurysm, wide exposure to the retro-carotid space, and may provide more dissection and clipping angles. the mobilization will render the temporal pole free as it does not disturb the medial (mesial) temporal cortex that usually adheres to the aneurysm. it is technically an easy and time-preserving technique. figure 2. intraoperative view of case 2, through right pterional approach, showing more appreciated and widen surgical space lateral to supra clinoid ica after tpm was performed (balck arrows). cnii: optic nerve, ica: internal carotid artery. limitations generally, the temporal lobe mobilization (usually it used to be retracted) should not be encouraged for all ruptured pcoa aneurysm cases. however, tpm has a peculiar advantage in pure posteriorly directed pcoa aneurysm cases. here, we describe mobilization of the temporal pole only, and no distribution of the mesial temporal cortex is required. also, the tpm technique includes the sacrifice of the bridging veins connecting the temporal tip. thus, there is at least a theoretical risk of venous congestion and subsequent infarction [1]. here, our technique depends on the size of the bridging veins and knowing the pattern of drainage, including a physiological principle that governs the venous drainage in the brain. if the vein is small, its counterpart or alternative pathway will be large and dominate venous drainage. this will lessen the possibility of the development of consequences. when the scarification of the temporal veins is not possible, which may be due to the larger in size, it’s critical to dissect enough of the superficial sylvian vein from the temporal lobe, especially around the temporal tip, to retain temporal veins [2,3]. our patients had not developed such complications, and 478 mustafa ismail, salima b. alsaadi, muslim mousa badr et al. the literature showed no report of venous complications after sacrificing the temporal veins. however, a larger series is required before approving this additive surgical step. references 1. andrews rj, bringas jr. a review of brain retraction and recommendations for minimizing intraoperative brain injury. neurosurgery 1993;33:1052-64. 2. heros rc, lee sh. the combined pterional/anterior temporal approach for aneurysms of the upper basilar complex: technical report. neurosurgery 1993. 3. katsuno m, tanikawa r, izumi n, hashimoto m. a modified anterior temporal approach for low-position aneurysms of the upper basilar complex. surg neurol int 2015;6:10. 4. post n, russell sm, jafar jj. role of uncal resection in optimizing transsylvian access to the basilar apex: cadaveric investigation and preliminary clinical experience in eight patients. operative neurosurgery. 2005 apr 1;56(suppl_4):ons-274. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0060 article a single institute five-year surgical experience with chronic subdural hematoma: analysis of 270 consecutive patients at a tertiary care centre gaurav jaiswal, vivek kankane, ashok kumar, pavan kumar, tarun kumar gupta india      romanian neurosurgery (2018) xxxii 3: 473 482 | 473             doi: 10.2478/romneu-2018-0060 a single institute five-year surgical experience with chronic subdural hematoma: analysis of 270 consecutive patients at a tertiary care centre gaurav jaiswal, vivek kankane, ashok kumar, pavan kumar, tarun kumar gupta department of neurosurgery, rabindra nath tagore medical college, udaipur, rajasthan, india abstract: chronic subdural hematoma (csdh) is one of the very common surgically treatable neurosurgical entities. still there is lack of uniformity in the management of csdh amongst surgeons in terms of various treatment strategies and protocols. burrhole drainage is the treatment modality of choice for an uncomplicated csdh. some recent trials support the use of drain to lessen the rate of recurrence. twist drill craniostomy and craniotomy do also play a role in the management of csdh. the current study is a retrospective analysis of 270 surgically treated patients with chronic subdural hematoma at a tertiary care center over a span of five years. the present study highlighted on rate of recurrence, re-surgery, mortality and morbidity. key words: burr hole, chronic subdural hematoma, csdh, subdural hematoma introduction the annual incidence of chronic subdural hematoma is about 1-5.3 cases per 100,000 populations. the incidence is increasing due to rise in the life expectancy, associated medical diseases in elderly patients such as hemodialysis, use of antiplatelet drugs and anticoagulant therapy. [1,2] closed head injury has been frequently contemplated for the development of csdh, especially in the elderly patients, which primarily seems trivial, may be the trigger for the genesis of csdh. [3] most of patients with csdh, presenting with clinical symptoms and signs, should be intervened for the removal of csdh. the techniques can be performed with an array starting from twist drill craniostomy to craniotomy and membranectomy. [4] burr-hole drainage is one of the easier and very efficient surgical procedures, which can be done for removal of uncomplicated csdh. [5] however, it has been stated that the recurrence rate range from 9.2% to 26.5% when this procedure is contemplated for surgical evacuation. [6] however, there are few other studies that have reported recurrence rates, which vary from 2.3% to 37%. [3] this particular study at our center 474 | jaiswal et al surgical experience with chronic subdural hematoma             retrospectively analyzed the results a single burr hole in consecutive 270 patients with csdh. materials and methods this is a retrospective study of 270 patients with chronic subdural hematoma treated in department of neurosurgery, rnt medical college, udaipur, rajasthan, india from july 2012 to july 2017. either computed tomography (ct) scan or magnetic resonance (mr) of brain was performed to diagnose the condition in all the patients. a surgical evacuation was done depending upon clinical status and thickness of hematoma. the patients, who were neurologically preserved and were on anticoagulant therapy for their medical condition, anticoagulants were withheld, till the control of international normalized ratio (inr). patients on anticoagulants or with coagulopathies who came in emergency with altered sensorium, vitamin-k injections were given for reversal of anticoagulant status with and they were taken up for surgery under the cover of fresh frozen plasma. all the patients were operated by single burr hole technique. the burr-hole was planned at the site of the maximal hematoma thickness in these patients. the patients were analyzed for age, gender, symptomology, glasgow coma scale (gcs), laterality, duration of hospitalization, glasgow outcome scale (gos) at discharge, recurrence rate and mortality. result a total of 270 consecutive patients were included in this retrospective study over a three-year duration. the mean age of the patients with csdh was 63.5 years whereas the range distribution was from 7 to 91 years. among these 270 patients, chronic subdural hematoma was predominant in males with 213 cases (78.9%) whereas 57 patients were female (21.1%), and male to female ratio was 3.7:1 (table 1). hematoma was located on the right side in 113 patients (41.8 %), on the left side in 105 patients (38.9%), whereas bilateral hematomas were present in 52 patients (19.3%) (table 2). clear history of trauma was evident in 181 patients (67 %) while 89 patients (33%) didn’t reveal specific history of trauma to head (table 3). there were various presenting symptoms and signs of patients with csdh. headache was the widespread symptom occurring in 176 patients (65.2%), followed by contralateral hemiparesis in 140 patients (51.8%), speech disturbance in 71 patients (26.3%), and altered behavior in 62 patients (23%). other symptoms include urinary incontinence (6.3%), parapareis (4.1%) and seizure (3.7%) (table 4). the diagnosis of chronic subdural hematoma was confirmed on computed tomography (ct head) in 229 (84.8%) patients, while 41 (15.2%) patients were confirmed under magnetic resonance imaging (mri brain). mean operative time was 44 minutes. the length of hospitalization ranged from 1 to 35 days, with a mean stay of 4.7 days. the mean gcs (glasgow coma score) at admission was 13.3. out of 270 patients, 172 patients (63.7%) had gcs of 15-14, 68 patients (25.2%) had gcs of 13-9 and remaining 30 patients (11.1%) had gcs of 8-3 points (table 5). romanian neurosurgery (2018) xxxii 3: 473 482 | 475             at the time of discharge, general outcome were assessed using gos (glasgow outcome scale) with range of 1-5. out of 270 patients, 225 (83.3%) had favorable outcome (gos 4-5), 38 patients (14.1%) (gos 3-2) had poor outcome. death occurred in seven patients (2.6%) (table 6). a recurrence rate of 11.1% (30 patients) was seen in this study. all the patients with symptomatic recurrences were taken-up for surgery again. ((re-exploration of same burr hole, expansion of same burr hole, making another burr hole, craniotomy and craniectomy were the procedure for the recurrence). table 1 demography (gender wise) of patients of chronic subdural hematoma: (n=270) gender no. of patients(n-270) percentage male female 213 57 78.9 21.1 total 270 100 table 2 location of chronic subdural hematoma: (n=270) location no. of patients(n-270) percentage right left bilateral 113 105 52 41.8 38.9 19.3 total 270 100 table 3 etiology of chronic subdural hematoma: (n=270) etiology no. of patients(n-270) percentage history of head trauma without any history of head trauma 181 89 67 33 total 270 100 table 4 symptomatology of patients of chronic subdural hematoma symptomatology no. of patients (n-270) percentage headache 176 65.2 hemiparesis 140 51.8 476 | jaiswal et al surgical experience with chronic subdural hematoma             speech disturbance 71 26.3 altered behavior 62 23 urinary incontinence 17 6.3 parapareis 11 4.1 seizure 10 3.7 table 5 gcs at presentation (n=270) symptomatology no. of patients (n-270) percentage gcs 15-14 172 63.7 gcs 13-9 68 25.2 gcs 8-3 30 11.1 total 270 100 table 6 gos (glasgow outcome scale) at the time of discharge (n=270) symptomatology no. of patients (n-270) percentage favorable outcome (gos 4-5) 225 83.3 poor outcome (gos 3-2) 38 14.1 death 7 2.6 total 270 100 romanian neurosurgery (2018) xxxii 3: 473 482 | 477             figure 1 left sided hemispheric iso to hypodense lesion (chronic subdural hematoma) producing mass effect, midline shift to the right, dilatation of contralateral temporal horn 478 | jaiswal et al surgical experience with chronic subdural hematoma             figure 2 mri of patient showing extra-axial collection on left side, hyperintense on t2wi as well on t1wi representing free met-hb which further is suggestive of late subacute/ chronic subdural hematoma romanian neurosurgery (2018) xxxii 3: 473 482 | 479             figure 3 ncct head of a patient with mixed density bilateral lesions suggestive of bilateral chronic subdural hematoma with acute component within 480 | jaiswal et al surgical experience with chronic subdural hematoma             figure 4 post-operative ncct head of the same patient (as in figure 3) bilateral pneumocephalus with bilateral burr hole in parietal region romanian neurosurgery (2018) xxxii 3: 473 482 | 481             discussion chronic subdural hematoma is quite routine in neurosurgical practice, [7] with a lot of etiological factors; foremost among them are numerous traumatic factors. however, the etiology of csdh is not completely understood until now. [8] as per literature, csdh is pathologic condition, which is mostly present in older people from 50 to 70 years. the average age of our patients (63.5 years) in this study was comparable to the series by agon et al (62.85 years) [9] but much younger than the average age stated by authors gastone et al. (76.4 years). [10] the ratio of male to female in our patients is 3.7:1 is much higher than the ratio found by gastone et al. and gelabert-gonzales et al. 1.68:1[7], [10]. other authors also found the higher frequency of csdh in males in comparison to females. [11], [12], [13] as per our results, head trauma was the most frequent cause for csdh in 181 patients (67%), while 89 patients (33%) didn’t have certain history of head trauma. our results about the incidence of head trauma (67%) as a causative factor for csdh are comparable to those of other authors, which report that head trauma is accountable for csdh in 35-75% of patients. [13], [14], [15] clinically, csdh is presented with a lot of symptoms. in our study the foremost symptom was headache (65.2%), followed by contralateral hemiparesis (51.8%) and speech disturbances (26.3%). the likewise symptoms and with comparable frequency were narrated by gelabert-gonzαlez et al., mori and maeda, and sousa et al. [7], [8], [16] we have found csdh on the right side in (41.8%), on the left side (38.9%), and bilateral csdh in (19.3%) of the cases. other authors have described the higher frequency of the csdh on the left side though not much of difference was seen. [17], [18] all the patients were treated surgically with single burr hole evacuation primarily. some authors approve that the optimal surgical treatment of patients with csdh can be accomplished with one burr-hole trepanation with a closed drainage system. [11], [19] we have used single burr hole as a primary procedure in all of our 270 patients. although the view of the other authors is dissimilar, they consider that extended craniotomy allows better exposure of csdh with thicker components. [20], [21] the data from literature show that irrespective of surgical procedures, the procedure is accompanied by recurrence rates of 4% to 26%. [7], [8], [22] the recurrence rate in our series was 11.1% and is comparable to the series of the other authors. [4], [11], [19] seven patients (2.6%) of our series have died in the post-operative period, in comparison to 2.7% mortality reported in few other studies. [8], [19] however, some authors state mortality rate ranging from 0% to 13%. [23] conclusion chronic sdh is mainly disease of elderly. single burr hole evacuation is one of the most effective methods of treating uncomplicated csdh. 482 | jaiswal et al surgical experience with chronic subdural hematoma             correspondence dr. gaurav jaiswal address for correspondence: dr. gaurav jaiswal, department of neurosurgery rnt, medical college, udaipur, rajasthan, india email: drgauravjaiswal@gmail.com references 1.karibe h, kameyama m, kawase m, hirano t, kawaguchi t, tominaga t. epidemiology of chronic subdural hematoma. no shinkei geka. 2011;39:1149–53. 2.krupa m. chronic subdural hematoma: a review of the literature. part 1. ann acad med stetin. 2009;55:47–52. 3.soto-granados m. treatment of chronic subdural hematoma through a burr hole. cir cir 2010;78:203-7 4.hamilton mg, frizell jb, tranmer bi. chronic subdural hematoma: the role for craniotomy reevaluated. neurosurgery 1993;33:67-72 5.yadav yr, yadav s, parihar vs. modified twist drill technique in the management of chronic subdural hematoma. turk neurosurg 2013;23:50-4. 6.krupp wf, jans pj. treatment of chronic subdural hematoma with burr-hole craniostomy and closed drainage. br j neurosurg 1995;9:619-27. 7.gelabert-gonzález m, iglesias-pais m, garcía-allut a, martínez-rumbo r. chronic subdural hematoma: surgical treatment and outcome in 1000 cases. clin nurol neurosurg 2005;107:223-9. 8.mori k, maeda m. surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. neurol med chir (tokyo) 2001;41:371-81. 9.mekaj ay, morina aa, mekaj yh, manxhuka-kerliu s, miftari ei, duci sb, hamza ar, gashi mm, gjelaj mr, kelmendi fm, sh. morina q. surgical treatment of 137 cases with chronic subdural hematoma at the university clinical center of kosovo during the period 2008-2012. j neurosci rural pract 2015;6:186-90. 10.gastone p, fabrizia c, homere m, cacciola f, alberto m, nicola dl. chronic subdural hematoma: results of a homogeneous series of 159 patients operated on by residents. neurol india 2004;52:475-7. 11.ernestus ri, beldzinski p, lanfermann h, klug n. chronic subdural hematoma: surgical treatment and outcome in 104 patients. surg neurol 1997;48:220-5. 12.nakaguchi h, tanishima t, yoshimasu n. factors in the natural history of chronic subdural hematomas that influence their post-operative recurrence. j neurosurg 2001;95:256-62. 13.robinson rg. chronic subdural hematoma: surgical management in 133 patients. j neurosurg 1984;61:263-8. 14.mckissock w, richardson a, bloom wh. subdural hematoma: a review of 389 cases. lancet 1960;1:1365-9. 15.ei-kadi h, miele vj, kaufman hh. prognosis of chronic subdural hematomas. neurosurg clin n am 2000;11:553-67. 16.sousa eb, brandão lf, tavares cb, borges ib, neto ng, kessler im. epidemiological characteristics of 778 patients who underwent surgical drainage of chronic subdural hematomas in brasilia, brazil. bmc surgery 2013;13:5. 17.de araújo silva do, matis gk, costa lf, kitamura ma, de carvalho junior ev, de moura silva m, et al. chronic subdural hematomas and the elderly: surgical results from series of 125 cases: old "horses" are not to be shot! surg neurol int 2012;3:150. 18.macfarlane mr, weerakkody y, kathiravel y. chronic subdural hematomas are more common on the left on the right. j clin neurosci 2009;16:642-4 19.kotvica z, brezeniski j. chronic subdural hematoma treated by burr holes and closed system drainage: personal experience in 131 patients. br j neurosurg 1991;5:461-5. 20.putnam ij, cushing h. chronic subdural hematoma: its pathology, its relation to pachymeningitis hemorrhagica, and its surgical treatment. arch surg 1925;11:329-93. 21.tyson g, strachan we, newman p, winn hr, butler a, jane j. the role of craniectomy in the treatment chronic subdural hematomas. j neurosurg 1980;52:776-81. 22.baechli h, nordmann a, bucher hc, gratzl o. demographics and prevalent risk factors of chronic subdural hematoma: result of a large single-center cohort study. neurosurg rev 2004;27:263-6. 23.santarius t, lawton r, kirkpatrick pj, hutchinson pj. the management of primary chronic subdural hematoma: a questionnaire survey of practice in the united kingdom and the republic of ireland. br j neurosurg 2008;22:529-34.   doi: 10.33962/roneuro -2020-051 safety and efficacy of mini doppler in recurrent pituitary tumours. report of 12 cases moshiur rahman, ezequiel garcia-ballestas, luis rafael moscote-salazar romanian neurosurgery (2020) xxxiv (1): pp. 336-342 doi: 10.33962/roneuro-2020-051 www.journals.lapub.co.uk/index.php/roneurosurgery safety and efficacy of mini doppler in recurrent pituitary tumours. report of 12 cases moshiur rahman1, ezequiel garcia-ballestas2, luis rafael moscote-salazar2 1 neurosurgery department, holy family red crescent medical college, dhaka, bangladesh 2 centre for biomedical research (cib), faculty of medicine, university of cartagena, cartagena, colombia abstract background: pituitary surgery is the most common surgery used to remove pituitary tumours. the use of mini doppler in surgical removal of an endonasal pituitary tumour has shown good short-term clinical outcomes and few complications in patients. cavernous sinus invasion limits the surgical excision and still a challenge of gross total resection. objective: the main objective of this study is to evaluate the outcome of surgical removal of an endonasal pituitary tumour using mini doppler. method: a total of 12 patients were studied retrospectively from 2012 to 2018 in a single institution (private hospital) in dhaka, bangladesh. the male and female ratio was 7:5. results: 92% of cases of the total number of patients had satisfactory removal/ neurological improvement/hormonal improvement. among 12 cases, 8 cases had transient diabetes insipidus and one patient had csf leak. conclusion: the intraoperative doppler is a useful tool to localize the carotids, which provides safer resection of endonasal pituitary tumours. thus, it is very safe and effective for laterosellar resection of recurrent pituitary tumours and for cavernous sinus invasions. introduction pituitary tumours are unusual growths that occur in your pituitary gland. recurring pituitary adenomas can cause visual problems to reemerge, as well as the loss of pituitary function. it is generally divided into three categories depending upon their biological functioning: benign adenoma, invasive adenoma, and carcinomas. most adenomas or tumours are benign, about 35% are invasive and just 0.1% to 0.2% are carcinomas.1 since the initial description of a transnasal method for pituitary tumour care in 1907, transsphenoidal surgery has undergone continuous development, marked by close collaboration between neurosurgeons and otolaryngologists. painful excentric muscle training keywords mini doppler, pituitary, endonasal, tumour corresponding author: moshiur rahman md. holy family red crescent medical college, dhaka, bangladesh dr.tutul@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 337 safety and efficacy of mini doppler in recurrent pituitary tumours and ultrasound (us) and doppler-guided sclerosing injections of polidocanol have shown good clinical results, and the traditional surgical approaches have been less necessary.1-3 in 1910, oskar hirsch developed a lateral endonasal approach which he initially conducted as a five-step procedure over several weeks before simplifying the procedure with a single step submucosal transseptal approach.4 for many years, the conventional surgical treatment of mid-stage achilles tendinosis consisted of a dorsal approach with central longitudinal tenotomy and tea excision.5-7 a pilot study using an us and dopplerguided scraping technique combined with a short rehabilitation period showed promising results.8 the scraping technique is based on the same findings that started the sclerosing polidocanol injection treatment, where gray-scale us and doppler showed a relationship between vessels and nerves on the ventral side of the achilles and chronic tendon pain. 9-11 endoscopic endonasal pituitary surgery for the treatment of recurrent pituitary tumours is becoming increasingly common. the endoscopic endonasal transsphenoidal approach (etss) allows for more panoramic viewing and wider access to the base of the skull.12 pituitary adenomas are most often classified as functional or non-functional, depending on their pattern of hormonal secretion. we addressed the safety and effectiveness of mini doppler in recurrent pituitary in this study and this doppler is commonly used in neurosurgical practice at present. it is a safe and non-invasive testing tool for cerebrovascular diseases. it is used to examine parameters of the blood flow, to diagnose stenosis, occlusion, and deformity of major head and neck arteries. doppler ultrasound in carotid and measures both qualitative and quantitative blood flow parameters vertebral arteries, and other forms of care. 13-14 nowadays the application of doppler ultrasonography is becoming increasingly important in endoscopic transsphenoidal surgery. and that is indeed a safe and effective strategy. this study aims to evaluate the outcome of surgical removal of an endonasal pituitary tumour using mini doppler. methods a retrospective chart review was performed on 12 patients who underwent surgical removal of an endonasal pituitary tumour using mini doppler between 2012 and 2018 in a single institution (private hospital) dhaka, bangladesh. informed consent from the patients to archive and process personal data in anonymous form was obtained. inclusion criteria were, namely: patients developed recurrence of the tumour with symptoms like headache, vomiting, visual disturbances or hormonal imbalances. exclusion criteria were, namely: asymptomatic recurrence of the tumour. follow up was carried out with routinely mri of the brain with contrast performed in 1, 6 and 12 months. then yearly for all patients. minimum follow up in this study was 2 years. the hormonal study was assessed by an endocrinologist for functional tumours monthly for the first few months and then every 6 months and according to clinical manifestations. operative procedure for all 12 patients, the same procedure was carried out as follows. the endonasal transsphenoidal approach was done using the binostril technique. anatomical landmarks are posterior choana on both sides, from there 1.5 cm above the mucosal flap with scar tissue were separated and in the midline part of the keel of the sphenoid and the sphenoidal bony defects were identified. a high-speed drill to enlarge the defect and to localize the internal carotid arteries mini doppler was used. for recurrent tumours it’s difficult to localize particularly in the cavernous sinus and with the help of mini doppler medial opticocarotid recess (mocr) can be identified and hence the tumour removal became safer. in some cases, where the tumour extended beyond the carotid, the whole of the artery was exposed by drilling and the tumour was removed from the lateral side. cavernous sinus invasions were removed by localisation of carotid through mini doppler and opening up of cavernous sinus and through two suckers in two hands, along the longitudinal axis of artery tumour was removed to avoid injury to the cranial nerves. bleeding from cavernous sinus was stopped by using fibrillar surgicel. a fascia was taken from the thigh and fibrin glue was used for dural closure. postoperative complications and management diabetes insipidus (di) ● if the consecutive three hours the urine output ≥ 250 ml then injection vasopressin 5 iu intramuscular was given. 338 moshiur rahman, ezequiel garcia-ballestas, luis rafael moscote-salazar ● after 48 hours when the nasal pack was removed desmopressin nasal spray was used 2 puff in one nostril and according to urine output. ● half strength normal saline iv was used to reduce the sodium level. ● avoidance of hydrocortisone iv to minimize the di except for those cases where the cortisol level was low. ● in all cases the di was transient and over one to two weeks the urine output became normal. for the csf leak, the patient was managed with lumbar drainage with bed rest which was failed and re-exploration was done through an endoscopic approach to seal the leak with dural substitute and glue. patient with little residual tumour was followed up with contrasted-mri of the brain every 6 months and found no recurrence of size nor symptoms for the last 3 years. results characteristics of patients are summarized in table 1. it was reported that 8.33% of patients had a residual tumour and 91.67% total removal of tumours among all patients. among 12 cases, 8 cases had transient diabetes insipidus and one had csf leak (figure 1). table 1. characteristics of patients. pt sex, age surgery year clinical presentation type of tumour complication follow-up 1 male,45 2012 headache, visual disturbance non-functional transient di adenoma no residual 2 male,38 2013 weight loss, tachycardia, irritability tsh secreting tumour transient di no residual normal level of hormone 3 male,28 2014 headache, vomiting, visual loss non-functional tumour apoplexy transient di no residual 4 male,32 2015 abnormal growth of hands and feet growth hormone-secreti ng tumour transient di no residual normal level of hormone 5 male,52 2016 headache non-functional tumour csf leak vith nerve palsy no residual 6 male,36 2017 headache, visual disturbance non-functional tumour transient di no residual 7 male,26 2017 headache, vomiting non-functional tumour apoplexy transient di small residual 339 safety and efficacy of mini doppler in recurrent pituitary tumours 8 female,25 2012 amenorrhoea prolactinoma none no residual normal level of hormone 9 female,30 2013 infertility prolactinoma none no residual normal level of hormone 10 female,42 2017 headache non-functional tumour transient di no residual 11 female,24 2018 headache cortisol secreting tumour none no residual 12 female,43 2018 headache non-functional adenoma transient di no residual table 2. complication rates in male and female patients. gender di postoperative hormonal deficiency residual tumour male 6 none 1 female 2 none 0 table 3. tumour resection types. tumour type cavernous sinus invasion gross total removal cranial nerve injury non functional 4 3 1(vith nerve) functional none all none *incomplete removal of one non-functional tumour was due to adherence of tumour with cranial nerve inside the cavernous sinus. 340 moshiur rahman, ezequiel garcia-ballestas, luis rafael moscote-salazar complications the total number of patients was 12 in this study and among them, 8 patients had diabetes insipidus and 1 patient had csf leak. there were 6 male patients and 2 female patients having di. figure 1. bar charts showing the number of patients having diabetes insipidus. in the figure (2a), intraoperative image showing the safe incision line in the midline and the probe, blue arrow touched is the safe incision line. and in figure (2b), contrast mri brain t1 weighted image in sagital section is showing recurrent pituitary tumour. figure 2 (a, b). intraoperative image and mri image of recurrent pituitary tumour. discussion the mini doppler controlled surgical removal of an endonasal pituitary tumour has shown good shortterm clinical outcomes and few complications in patients at varying levels of activity. with this treatment method, rapid pain relief and a return to even high-level sporting activity are feasible. the technique provides the greatest degree of freedom and efficiency at specific anatomical goals for sagittal surgery. this method is one step better for the treatment of recurrent pituitary tumours for improved quality and hospital stay time. more quantitative and qualitative data are required for calculating better results. in reaction to the procedure, athletes back in full pain-free training and competition are found to have a good result. the follow-up period after surgery was also not long, and with time, further failures could occur. ongoing 341 safety and efficacy of mini doppler in recurrent pituitary tumours research will concentrate on longer-term clinical outcomes and impacts on the thickness and function of the tendons. by using this strategy, since these lesions typically displace the optical apparatus away from the surgeon, tumour removal will begin craniopharyngioma and preexisting growth hormone and gonadal deficiencies experienced a complete failure of anterior pituitary function and di following surgery immediately after opening the dura mater, resulting in prompt chiasm decompression. the early decompression probably allows the removal of any tumour adherent to the optical apparatus and/or its arachnoidal and vascular connections with less chance of visual degradation. this approach requires minimal nasal mucosal dissection, resulting in fewer sinonasal complications and a quicker and less painful rhinological recovery.15-16there are a variety of vascular problems associated with an approach through the nose and sublabial route use. the major drawback to the direct endonasal route is the fairly narrow and slightly off-midline direction of operation.17 this issue was largely solved by several technical innovations, including the use of low-profile micro-dissection instruments and cutting blades and the use of mini-dopplers, the use of angled endoscopes for more panoramic cephalad and lateral visualization beyond the microscope's tunnel vision, and the use of intraoperative surgical navigation to validate surgical trajectory and main land making. 18 unfortunately, the complete removal by any method in the three other patients was not a realistic goal given the size and invasiveness of the tumours. some of the patients in this series encountered new permanent endocrinological abnormalities, with the new di occurring in 8 cases. preservation of pituitary function in such patients is challenging particularly those in whom the anterior pituitary function has already failed.19 in our series of 12 patients, the complication rate was low. a common clinical complication in our series was a postoperative csf leak that occurs in 1 patient who had neurological defcits, including new cranial nerve palsy. skin incision or brain retraction is also no longer required. these benefits lead to a decrease in complications, faster patient recovery, minimal postoperative discomfort and a decrease in overall costs. the cavernous sinus extension limits the excision of tumour and adjuvant radiotherapy is the alternate choice of treatment.20 conclusion the intraoperative doppler is a useful tool to localize the carotids, which provides safer resection of endonasal pituitary tumours. thus, it is very safe and effective for laterosellar as well as removal of intracavernous portions of tumour by two hand technique. conflict of interest there is no potential conflict of interest relevant to this research. financial disclosure no specific funding was provided for this research. patient consent this study obtained patient consent directly from the patient. ethical approval as the authors, we hereby declare that all experiments have been examined and approved by the appropriate ethics committee and have therefore been performed by the ethical standards laid down in the 1964 declaration of helsinki. author’s contributions the author’s contributions include manuscript preparation and editing. the manuscript has been prepared and approved by all the authors to be submitted and published. references 1. laws er. transsphenoidal tumours surgery for intrasellar pathology. clin. neurosurgery. 1979; 26: 391.397. 2. foppiani l, ruelle a, cavazzani p, del monte p. hyperthyroidism unmasked several years after the medical and radiosurgical treatment of an invasive macroprolactinoma inducing hypopituitarism: a case report. cases j. 2009; 2:6449. published 2009 jul 29. doi: 10.4076/1757-1626-2-6449. 3. elhadi, ali m., douglas a. hardesty, hasan a. zaidi, m. yashar s. kalani, peter nakaji, william l. white, mark c. preul, and andrew s. little. "evaluation of surgical freedom for microscopic and endoscopic transsphenoidal approaches to the sella." operative neurosurgery 11, no. 1 (2015): 69-79. 4. lanzino g, laws er. pioneers in the development of transsphenoidal surgery: theodor kocher, oskar hirsch, and norman dott. j neurosurg. 2001 dec; 95(6):1097– 103. 5. leadbetter wb, mooar pa, lane gj, et al. the surgical treatment of tendinitis. clinical rationale and biologic basis. clin sports med 1992; 11: 679– 712. 6. nelen g, martens m, burssens a. surgical treatment of chronic achilles tendinitis. am j sports med 1989; 17: 754 – 9. 342 moshiur rahman, ezequiel garcia-ballestas, luis rafael moscote-salazar 7. åström m. on the nature and etiology of chronic achilles tendinopathy [dissertation]. lund, sweden: university of lund, 1997. 8. alfredson h, ohberg l, zeisig e, et al. treatment of midportion achilles tendinosis: similar clinical results with us and cd-guided surgery outside the tendon and sclerosing polidocanol injections. knee surg sports traumatol arthrosc 2007; 15: 1504 – 9. 9. andersson g, danielson p, alfredson h, et al. nerverelated characteristics of ventral paratendinous tissue in chronic achilles tendinosis. knee surg sports traumatol arthrosc 2007; 15: 1272 – 9. 10. aström m, gentz cf, nilsson p, et al. imaging in chronic achilles tendinopathy: a comparison of ultrasonography, magnetic resonance imaging and surgical findings in 27 histologically veri ed cases. skeletal radiol 1996; 25: 615 – 20. 11. weinberg ep, adams mj, hollenberg gm. color doppler sonography of patellar tendinosis. am j roentgenol 1998; 171: 743 – 4. 12. rahman m m, khan r a, et al. surgical outcome of endoscopic endonasal surgery for nonfunctional pituitary adenoma; int j med res prof. sep 2018; 4(5):16872. [googl e scholar] 13. krylov v, ed. surgery of cerebral aneurysms. m: author’s issue; 2011; 1: 126165 (in russ.). 14. nikitin yu. doppler ultrasound in diagnostics of disorders of the major arteries of head and base of brain. uchebnoe posobie. m: institute of neurology, rams, spectromed; 1995. (in russ.). 15. badie b, nguyen p, preston jk: endoscopic-guided direct endonasal approach for pituitary surgery. surg neurol 53:168–173, 2000. 16. zada g, kelly df, cohan p, wang c, swerdloff r: endonasal transsphenoidal approach for pituitary adenomas and other sellar lesions: an assessment of efficacy, safety, and patient impressions. j neurosurg 98:350–358, 2003. 17. das k, spencer w, nwagwu ci, schaeffer s, wenk e, weiss nh, et al. approaches to the sellar and parasellar region: anatomic comparison of endonasal-transsphenoidal, sublabial-transsphenoidal, and transethmoidal approaches. neurol res 23:51–54, 2001. 18. cook sw, smith z, kelly df: endonasal transsphenoidal removal of tuberculum sellae meningiomas: technical note. neurosurgery 55:239–246, 2004. 19. konig a, ludecke dk, herrmann hd: transnasal surgery in the treatment of craniopharyngiomas. acta neurochir 83:1–7, 1986. 20. juyoung hwang, ho jun seol, do-hyun et all: therapeutic strategy for cavernous sinusinvading non-functioning pituitary adenomas based on the modified knosp grading syste . brain tumour res treat 2016; 4(2):63-69. microsoft word 15singhpr_aprospective 632 | singh et al study of operated patients of intradural extramedullary spinal cord tumor             doi: 10.2478/romneu-2018-0082 a prospective observational study of clinical outcome of operated patients of intradural extramedullary spinal cord tumor in our tertiary care center p.r. singh1, t.k. pandey2, f. ahmad3, d.k. chhabra4 department of neurosurgery, vivekananda polyclinic and institute of medical sciences, lucknow, india abstract: aim: this prospective observational study aimed at finding out the efficient clinical and functional factors which affect the surgical outcome on the basis of location of the intradural extramedullary spinal cord tumors (iescts) and in follow up period of 1 year post surgery, treated at a single tertiary institution (vivekananda polyclinic and institute of medical sciences, lucknow). material and methods: we prospectively analyzed 44 consecutive cases of iescts diagnosed on radiology and operated at our center from 2014 to 2016. the demographic data, clinical presentation, tumor radiological parameters (axial and saggital location and tumor occupancy ratio), treatment modality, and follow up outcome of these patients are reviewed. we have excluded patients with neurofibromatosis, recurrent tumors and intradural cauda equina and conus lesions. result: a clinical series of 44 patients with iescts, underwent surgery (standard laminectomy) and excision of tumor have been followed for 1 year. the most commonly involved spinal level was dorsal (65.91%) followed by cervical (20.45%) and lumbar (18.18%) spine. the axial location of tumor was dorsal/posterior (6.82%), ventral/anterior (13.64%) while most common axial location of tumor was lateral (79.55%). we have found that the gait disability score and frankel score shows significant improvement within 1 week after surgery and after 1 year of follow up, 90.91 % patients have gait disability score of > 2 while frankel scale has shown, 81.82 % were ambulatory and only 18.18 % were non-ambulatory. conclusion: analysis of the mri findings should be undertaken in a routine, standardized fashion to insure the accurate evaluation of the location of the tumor for planning the surgical interventions. as a surgeon we should be more cautious while operating on the purely ventrally located tumors through the posterior approach and we may prefer anterior approach in them. similarly in saggital location, we should be cautious to operate the thoracic locating tumors to prevent the post-op complications. key words: intradural extramedullary tumors, meningioma, schwannoma, neurofibroma romanian neurosurgery (2018) xxxii 4: 632 640 | 633             introduction intradural extramedullary spinal cord tumor (iescts) constitute approximately two third of these tumors.1,3,5,9 the most common primary iescts are derived from sheath cells covering the spinal nerve roots (schwannoma and neurofibroma) or meningeal cells located along the spinal cord surface (meningioma)1. spinal nerve sheath tumors account for approximately 40% of all spinal tumors (0.30.4 cases annually per 100,000 people).1,30 while spinal meningioma accounts for about 30% of the iescts. most of the indian studies have shown male preponderance in iescts except in meningioma which has more female preponderance. 1,9 the female preponderance is thought to arise from the sex hormone or other type receptor common in women.10 more than 50 % of the iescts are located in the thoracic spine, and they occur in the cervical and lumbosacral spine at a similar rate, 22 % and 18 %, respectively.1,4,9,16 most nerve sheath tumors are frequently observed in thoracic spine (39%), lumbar spine (32%), and cervical spine (23 %).7,15,16 spinal schwannoma arise from dorsal root1 (hence posterior, lateral or posterolateral in position ) and < 5% originating at the anterior (ventral) root16,18, however as much as 23 % of the cervical nerve sheath tumor have an anterolateral component consistent with ventral root origin.6,7 spinal meningioma is nearly 80 % found in thoracic region, in cervical region it is about 14-27 % and of lumbar is about 2-14 % while sacral meningioma are very rare.1,8,28 surgical approach is determined primarily depending on the location of tumors in spinal canal. however tumor consistency and pathology should also be considered.15 standard posterior approach through bilateral or unilateral laminectomy provides adequate exposure to safely remove the vast majority of these lesions, without the need for potentially destabilizing facet or pedicle resection.6,11 now, modified approaches are used which are minimally invasive and may be routinely used to remove iescts.14,17,22,25 posterior exposures with varying degree of lateral bone resection, dentate ligament division, and gentle cord rotation may also provide adequate exposure for safe removal of non midline ventro-lateral superficial pial presenting spinal cord lesions.26,29 solid ventral midline schwannoma are optimally managed by anterior and anterolateral approaches6,13,19, although soft consistency tumors can be approached from postero-lateral approach with satisfactory outcome.15,18 radiosurgery in intradural spinal tumors is evolving and seems to be an effective tool for the patients, who are not suitable for open surgery, as well as with multiple lesions, recurrences or tumor remnants after microsurgery.1,32 patients and methods a prospective review was performed between june, 2014 and june, 2016 of all the consecutive 44 operated patients of iescts at our institutions. the study was approved by the ethical committee of the hospital and all the patients involved in this study signed the informed consent. a detailed clinical history elucidated, followed by careful clinical examination, which was recorded as per the performa. clinical disability was assessed by 634 | singh et al study of operated patients of intradural extramedullary spinal cord tumor             the gait disability scale and frankel scale in both pre-op, at the time of discharge, 3 months and 12 months follow up. diagnostic evaluations included mri (spine) with or without contrast with an axial slice demonstrating the tumor and the respective spinal column (saggital and axial) location of the lesion. the axial location of the tumor were categorized as anterior, posterior, or lateral with respect to the spinal cord and were described to correlate with a clock face. the tumors that were predominately between “10 and 2 o’ clock ” were considered anterior while if tumor predominately occupied “4 to 8 o’ clock” then they were considered posterior and those that were either “2 to 4 o’ clock” of “8 to 10 o’ clock” were considered “lateral”. tumor occupancy ratio27 was also studied in axial mri (spine). surgery was done in all cases as standard posterior laminectomies26,29 and unilateral medial facetectomy was done in anteriorly located tumor. dura was opened in median or paramedian manner and in few ventrally located tumors or with extra dural extension; we opened dura in t shaped manner and may require for cutting the dentate ligament to retract the cord for removal of the tumor. after dural opening, a plane was developed between arachnoid membrane and tumor surface. the tumor was removed en bloc or piecemeal. the involved nerve roots were coagulated and cut in case of schwannoma while in case of meningioma dural origin coagulated using bipolar cauterization in most of cases (simpson grade ii). gross total excision of tumor done in all cases. in immediate post-op, complications were noted and neurological status was again assessed at the time of discharge by gait disability score and frankel score and then patient was followed up in next 3 months and after 1 year. results the age of all patients ranged from 1675 yrs with mean (±sd): 42.6 (±17.25) yrs. most of the patients were in 40-60 yrs age group (31.2%) followed by 20-30 yrs (27.27%), > 60 yrs (15.91%) and <20 yrs the least (11.36%). most patients were male (70.45%) while only (29.55%) were female. the mean age of presentation in male was 38.5 yrs while in female; it was 46.83 yrs. mean duration of illness was 11 months (male 12.08±12.18, female 9.91±10.60) and it showed no significant difference between the genders. around 38.64% patients were of ≤ 5 months duration while only 18.18% were of > 20 months duration. further, all (100%) patients had back pain, 97.73 % had sensory complaints while 68.18% had myelopathy, 56.85% had motor deficit and 50% had sphincter dysfunction while only 25% had radiculopathy. the most commonly involved spinal level was dorsal (65.91%) followed by cervical (20.45%) and lumbar (18.18%) spine. it has been found that most common location of tumor was d5-d9 in meningioma (56.25%) and in schwannoma most common location is lower dorsallumbar group (39.29%). i have also divided the axial location of tumor into dorsal (6.82%), ventral (13.64%) while most common axial location of tumor was lateral romanian neurosurgery (2018) xxxii 4: 632 640 | 635             (79.55%) which is approximately similar in both the tumor types. we have analyzed the saggital location of the tumor with the clinical outcome in all the clinical outcome groups (on discharge/3 months/12 months) and found that patient with thoracic location has more improvement (> 2 grades) in clinical outcome than with other tumor location while least change in disability score was noticed in lumbar group. the tumor occupancy ratio was divided into 3 groups (70-80, 80-90 and > 90) and found that found that only 6.81 % have tumor occupancy > 90 % while 70-80 and 80-90 % tumor occupancy was approximately equally divided in 2 groups. i have also analyzed the tumor occupancy ratio with the disability score and found that once the tumor occupancy increased, the disability also increased (r0.66, p< .001). according to gait disability score, most of the patients at pre-op were at grade 4 (38.64%), followed by grade 2 (25%), grade 5 (18.18%), grade 1 (15.91 %) and grade 3 only 2.27%. the χ2 test revealed significant improvement in grade of patients in immediate post-op (7 days after surgery) and then over the periods (12 months) of follow up after surgery. frankel scale also has shown similar results as most of patients at pre-op were at grade d (45.45%), grade c (34.09%), grade e (13.64%) and grade b in only 6.82%. similarly the χ2 test revealed significant improvement in frankel score in immediate post op and then over the periods of follow up after surgery. 636 | singh et al study of operated patients of intradural extramedullary spinal cord tumor             bar diagram of frankel score in follow up at final evaluation (i.e. after 12 months), the outcome was that patient was that 90.91% patients have gait disability score >2 while in frankel scale it was shown that after 12 months follow up 81.82 % were ambulatory while only 18.18% were non-ambulatory. bar diagram of final outcome discussion most patients were male (70.45%) while only (29.55%) were female and no significant difference was found between the clinical presentation and duration of illness between the genders. the literature shows the female preponderance in western countries while asian studies1,9,21 favors male preponderance although our study reflects more male ratio which may be because of social stigma or delayed follow up of female patients in eastern u.p of indian population. the female preponderance of meningioma is a well – known entity and our study supports it. we found that meningioma favors the elderly female population while schwannoma are more in young male population similar to the previous literature.13,15,24 the mean age of presentation in our study was 38 years in male and 46 years in female which is same as compared to that of western world along with other asian studies as arora et al, 20151, mondle et al, 201621, govind m et al, 20169, iacob g, 201412. the mean duration of illness was 12 months in male patients and 9 months in female patients in our study. it was found that meningioma groups have more myelopathy in upper thoracic spine as reviewed on other studies. early presentation of the patients are more in upper thoracic spine group which is romanian neurosurgery (2018) xxxii 4: 632 640 | 637             explained by the higher cord-to-canal ratio, as well as the tenuous vascular supply to that region of the spinal cord. the lesser mean duration of illness in female may be found due to higher incidence of thoracic locating tumor in female. no association between the axial location (dorsaldorsolateral/ventralventrolateral) and the clinical outcome was found in our study (p < 0.26) supported by mehta et al, 201320, riad et al, 201323, rinaldo et al, 201624 . the extradural component was noted in 6 (14%) of our all patients of nerve sheath tumors which is similar to other studies22 in literature which is 10 %. our study gives the similar results to mehta et al 20 as the ventrally located tumors trended toward development of neurological deficit as occurred in our 2 patients, although trend not significant (p= 0.45). this can also be explained by the difficult approach to purely ventral locating tumor. mehta et al, 2013 had done the first systemic study to assess the association between axial/saggital tumor location and outcomes and post-operative complication19. however, a saggital spinal column level was significantly associated with the development of a neurological deficit, as patients with iescts tumors located in upper thoracic spine were more likely to have a postoperative neurological deficit. i have also analyzed the tumor occupancy ratio with the disability score and found that once the tumor occupancy increased, the disability also increased (r0.66, p< .001). song et al, 200927 and haq el at, 201510 has included this tumor occupancy ratio in their study but has not shown any co relation with the clinical outcome similar to our study. in our study, only 6 (18.18%) has 2 level of column of tumor while majority of the patients 38 (81.1%) has only 1 level of involvement. stawicki et al, 200728 has considered level of tumor as a prognostic factor but our study did not support it. in case of meningioma we had done gross total excision of tumor with simpson grade ii resection in all of the cases and found no recurrence in the follow-up period as favored by other studies also which consider simpson grade i and grade ii equally effective in complete surgical resection.2,31 however our follow up was of very short duration to comment on the recurrence. we have done coagulation and cutting of involved rootlet in nerve sheath tumor similar to many of the studies 20 and found no functional neurological deficit even in ventrally located tumors except sensory deficits in few cases in the involved region. in post-op we have seen that within 7 days after surgery approx 60 % of the patient walking either with minimal support or independently (grade 4 and 5) within 7 days after surgery similar to frankel score. majority (90%) of clinical improvement noted within 3 months of the operative intervention.24,2 at final evaluation (i.e. after 12 months), the outcome was that patient was that 90.91% patients have gait disability score >2 while in frankel scale it was shown that after 12 months follow up 81.82 % were ambulatory while only 18.18% were non-ambulatory. 638 | singh et al study of operated patients of intradural extramedullary spinal cord tumor             conclusion location of the tumor was important to understand the nature and course of the disease in these tumors. we have found deterioration in 2 ventrally located tumors hence we should be careful in operating purely ventral located tumors through posterior/ posterolateral approach and we may prefer anterior approach for purely ventral tumors. in thoracic locating tumors due to higher cord-to-canal ratio, we should always be more cautious and purely ventral and thoracic tumor has higher chances of post-op complication. mri findings should be undertaken in a routine, standardized fashion to insure that important details are not missed for more accurate evaluation of location of the tumor along with the measurement of tumor occupancy ratio in all the patients. radiological finding as tumor occupancy ratio has an impact on the early presentation of the symptoms and thereby defining the role of location of the tumor. tumor type on the basis of pathology has also not shown any significant association with the clinical outcome in our study.. we have found that disability score (gait disability score and frankel score) both are good clinical outcome predictors in these patients. we have found that approx 60 % of the patient walking either with minimal support or independently within 7 days after surgery while majority (90%) of clinical improvement noted within 3 months of the operative intervention34,6,. at final evaluation (i.e. after 12 months), the outcome was that patient was that 90.91% patients have gait disability score >2 while in frankel scale it was shown that after 12 months follow up 81.82 % were ambulatory while only 18.18% were nonambulatory. thus we should consider that early excision of the tumor for better outcome and recovery. i have not commented on the recurrence of the tumor because of the limited duration of the study as we know the usual period of recurrence is 3 years and follow up radiology should be done after 5 years after surgery. finally the skill of an individual surgeon always be a factor affecting our results and hence can never be ruled out. correspondence dr. p.r singh, senior resident, department of neurosurgery, vivekananda polyclinic and institute of medical sciences, nirala nagar, lucknow. email:prashantsingh2010@yahoo.com references 1.arora r k, rajkumar. spinal tumors: trends from northen india. asian j neurosurg. 2015;10(4):291-297. 2.aydnlar e i, dikmen p y, silav g, berkman m z, elmaci i, ozgen s. intraoperative neurophysiological monitoring to prevent new neurological deficits in spinal tumor cases. turkish journal of neurology 2014; 20:45-48. 3.beall d p, googe d j, emery r l, thimpson d b, campbell s e, ly j q, delone d, smirniotopoulos j, lisanti c, currie t j. extramedullary intradural spinal tumors: a pictorial review. currpronldiagn radio, septoct 2007; 36: 185-198. 4.bokhari i, rehman l, farooq g, qureshi a. postoperative functional outcome of intradural extrameduallry spinal tumors through posterior approach. journal of the college of physician and surgeons, 2016; 26(2):117-120. romanian neurosurgery (2018) xxxii 4: 632 640 | 639             5.chamberlain m c, tredway t l, adult primary intradural spinal cord tumors: a review. current neurolneurosci rep 2011; 11: 320-328. 6.cherqui a, kim d h, kim s, park h, kline d g. surgical approaches to paraspinal nerve sheath tumors. neurosurgery focus 2007; 22 (6): e9. 7.chowdhury f h, haque m r, sarker m h. high cervical spinal schwannoma; microneurosurgical management: an experience of 15 cases. actaneurol taiwan 2013; 22:59-66. 8.galgano m a, beutler t, brooking a, deshaies e m. spinal meningiomas: a review. j spine 2014; 3(1). 9.govind m, mittal r, sharma a, gandhi a. intradural extramedullary spinal cord tumors: a retrospective study at tertiary hospital. romanian neurosurgery jan-march 2016; xxx (1)106-112. 10.haq n u, shah r, khan h m, usman m, ali m. outcome of surgical management is spinal meningioma: a study of 48 cases. gomal j med sci 2015; 13: 49-53. 11.iwatsuki k, ohnishi yu-ichiro, ninomiya k, ohkawa t, yoshimie t. feasibility of the posterior approach for removal of ventrolateral extended intradural tumors. paripex-indian journal of research march 2016; 5(3): 74-77. 12.iacob g. spinal meningiomas. personal experience and review of literature: romanian neurosurgery 2014 xxi 2; 146-160. 13.joaquin a f, almeida j p, santos m j d, ghizoni e, olivieira e d, tedeschi h. surgical management of intradural extramedullary tumors located anteriorly to the spinal cord. journal of clinical neuroscience 2012; 19: 1150-1153. 14.kaya r a. surgical excision of spinal intradural meningioma through a single-sided minimally invasive approach: key-hole laminectomy. asian spine journal 2015;9(2)-225-231. 15.15. kasliwal m k, kale s s, sharma b s, suri v. totally cystic intradural extramedullary schwannoma. turkish neurosurgery 2008; 18(4): 404-406. 16.klekamp j, samii. surgery of spinal tumor. 2007; isbn 978-3-540-44714-6 springer berlin heidelberg new york. 17.lacongeli m, gladi m, rienzoa d, dobran m, alvaro l, nocchi n, maria g l, somma d, colasanti r, scerrati m. minimally invasive surgery for benign intradural extramedullary spinal meningiomas: experience of a single institute in a cohort of elderly patients and review of literature. clinical intervention in aging 2012; 7: 557564. 18.mahore a, muzumdar d, chagla a, goel a, pure ventral midline long segment schwannoma of the cervicodorsal spine: a case report. turkish neurosurgery 2009; 19(3): 302-305. 19.mazel ch, grunenwald d, laudrin p, marmorat j l. radical excision in the management of thoracic and cervicothoracic tumors involving the spine: results in a series of 36 cases. spine nov 2003; 8: 782-792. 20.mehta a i, adogwa o, karikari i o, thompson p, verla t, null u t, friedman a h, cheng j s, bagley c a, issacs r e. anatomical location dictating major surgical complications for intradural extramedullary spinal tumors: a 10year single-institutional experience. j neurosurgery spine dec 2013.19:701-707. 21.mondle s, islam j, rashid h, ashadullah a t m, elahi f, rahman b, uddin k h, yusuf a. surgical outcomes of spinal tumor: experiences of 48 cases at referral neurosurgery hospital in bangladesh. open journal of modern neurosurgery 2016: 6; 98-104. 22.naganawa t, miyamoto k, hideo h, suzuki n, shimizu k. hemilaminectomy for removal of extramedullary or extradural spinal cord tumors: medium to long –term clinical outcomes. yonsei med j jan 2011; 52(1): 121-129. 23.riad h, knafo s, segnarbieux f, lonjon n. spinal meningiomas: surgical outcome and literature review. neurochirugie 2013;59: 30-34. 24.rinaldo l, brandon a, mccutcheon, kerezoudis p, shin j h, mehta a i, clarke m j, oyelese a a, krauss w e, bydon m. outcome after surgical treatment of intraduralextramedullary spinal cord tumors: a review. wsc j 2016; 2: 121-128. 25.sciubba d m, chaichana k l, graeme f w, mcgirt m j, gokaslan z l, jallo g i. factors associated with cervical instability requiring fusion after cervical laminectomy for intradural tumor resection. j neurosurgery spine 2008; 8: 413-419. 26.slin’ko e i, alqashqish i i. intradural ventral and ventrolateral tumors of the spinal cord: surgical treatment and results. neurosurg focus july 2004. 17(1). 27.song w k, shin s, lee j y, kim g l, hyun y s, park y d. surgical results of intradural extramedullary tumors. clinics in orthopedic surgery 2009; 1: 74-80. 28.stawicki s p, guarnaschelli j j: intradural extramedullary spinal cord tumors: a retrospective study 640 | singh et al study of operated patients of intradural extramedullary spinal cord tumor             of tumor types, locations, and surgical outcomes. the internet journal of neurosurgery. 2007 4(2) doi: 10.5580/ae8. 29.takami t, naito k, yamagat t, yoshimura m, arima h, ohata k. posterolateral approach for spinal intradural meningioma with ventral attachment. j craniovertebr junction spine; octdec 2015; 6(4): 173-178. 30.yamahata h, yamaguchi s, mori m, kubo f, tokimura h, arita k. ventral schwannoma of the thoracolumbar spine. asian spine j 2013; 7(4):339-344. 31.yoon s h, chung c k, jahng t a. surgical outcome of spinal canal meningiomas. j korean neurosurgsoc oct 2007; 42:300-304. 32.zong s, zeng g, xiong c, wei b, treatment result in the differential surgery of intradural extramedullary schwannoma of 110 cases. plos one may 2013 8(5): e63867. doi: 10.33962/roneuro-2022-064 madjid samii: omagium when hard work, excellence, and love for patients collide ștefan-octavian grădinaru, andrei alexandru marinescu, cristiana-ștefania gheorghe, dan bentia, alexandru-vlad ciurea romanian neurosurgery (2022) xxxvi (3): pp. 372-375 doi: 10.33962/roneuro-2022-064 www.journals.lapub.co.uk/index.php/roneurosurgery madjid samii: omagium when hard work, excellence, and love for patients collide ștefan-octavian grădinaru1, andrei alexandru marinescu2, cristiana-ștefania gheorghe3, dan bentia4, alexandru-vlad ciurea4,5,6 1 faculty of medicine. "lucian blaga" university of sibiu, romania 2 department of neurosurgery. national institute of neurology and neurovascular diseases, bucharest, romania 3 faculty of medicine. "carol davila" university of medicine and pharmacy, bucharest, romania 4 emeritus professor of neurosurgery. faculty of medicine "carol davila". university of medicine and pharmacy, bucharest, romania 5 department of neurosurgery. "sanador" clinical hospital, bucharest, romania 6 honorary member of the romanian academy abstract prof. madjid samii is an internationally recognized neurosurgeon who has conquered the highest levels of 21st-century neurosurgery. born in iran, he decided to take medical courses at the university of mainz, hanover, germany. he earned his medical degree in 1963, marking the highest achievable score, and started his residency, guided by emeritus professor dr kurt schurmann. numerous various surgeries and studies that reshaped the field of neurosurgery describe his career. starting with a publication regarding a new technique, pneumencephalotomography, he has steadily been ascending, studying and writing about cranial nerves, developing the surgery of the skull base and proving that the transnasal approach is preferred in clivus chondromas. prof. madjid samii founded, 1990, the foundation of national and continental skull base societies and, and since 2001, he has been the honorary president of the world federation of neurosurgery societies (wfns). not only was he successful in his scientific path, but he also gave an example for the future generation of what astonishing results can be obtained with hard work, commitment, and a leader's spirit. he wanted to take worldwide neurosurgery to a whole new level, so he came up with an idea, the concept of an international neuro-excellence centre, which quickly became the reality of the international neuroscience institute of hanover. brief presentation of the evolution of neurosurgery taking a trip down memory lane, neurosurgery is a surgical specialty that set about to develop at the beginning of the 20th century. since keywords madjid samii, neurosurgery, worldwide, pneumencephalotomography, cranial nerves, skull-base, wfns, president, future corresponding author: andrei alexandru marinescu national institute of neurology and neurovascular diseases, bucharest, romania marinescu.andrei.alex@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 373 madjid samii: omagium then, it has been in a progressive evolution, swayed by the contributions of grand names such as harvey cushing (1869-1939) and gazi yasargil (1925). harvey cushing (figure 1), remembered as the father of modern neurosurgery, was an american pioneer of modern operative techniques in brain surgery. his significant contributions have made neurosurgery more approachable and understandable for future generations. gazi yasargil (figure 1) is a turkish neurosurgeon who managed to revolutionize brain surgery by introducing micro-neurosurgery. he was the founder of micro-neurosurgery and trained countless surgeons in the micro-neurosurgical anatomical laboratory in zürich, switzerland. figure 1. harvey cushing, gazi yasargil, madjid samii (golden triangle of neurosurgery) we considered reminiscing these two names as a glimpse of recognition for their scientific and spiritual influences that push neurosurgery to reach new horizons nowadays. certainly, the highest level of 21st century global neurosurgery has been conquered by prof. madjid samii (born in 1937, teheran), not only through his surgical activity but also through his innovative and societal actions. madjid samii life, career and achievements prof. madjid samii (figure 2) is a neurosurgeon who dedicated his career to solving the hardest and most complicated cases, to educating future neurosurgeons, and to publishing an astonishing number of statistics. he was born on the 19th of june 1937 in tehran, iran. after graduating high school in iran, he moved to germany, where he studied medicine at the university of mainz. earning his medical degree from the university of mainz in 1963 by marking the highest achievable score in the final medical examination made him the recipient of the prize of the iranian science ministry for the best iranian student in europe. figure 2. prof. dr med. madjid samii (wfns-president) prof. madjid samii finished his neurosurgical residency at the same university, learning from the emeritus professor dr. kurt schurmann, who provided him with de cushing's motto: "through valor and divine aid" and receiving his board of neurosurgery in 1970. being inspired by what was known at that time: pneumoencephalography-walter dandy (18861946) and cerebral angiography-egas moniz (19272017), prof. madjid samii thought about a new technique and published his first paper, named "pneumencephalotomography", together with prof. schurmann in 1965. three years later, his innovative thinking was brought back to light. he used the previous technique, developing a more advanced one"combined ventriculo-lumbar puncture" and, by 374 ștefan-octavian grădinaru, andrei alexandru marinescu, cristiana-ștefania gheorghe et al. using it, he realized the first radiologic diagnosis of hydrocephalus occlusus. furthermore, this technique was performed by him in the treatment of a case of dorsum sallar chiasma compression syndrome (1972). prof. madjid samii was one of the first to use a microscope in the operating room, back in 1969. afterwards, he dedicated his time to the study of peripheral and cranial nerves, focusing on nerve grafting and nerve transfer operative techniques. two years later, he achieved the success of a hand reimplantation surgery. during the same year, he published "the cranial nerves" book. he also developed the surgery of the skull base. in 1970, he built the first interdisciplinary team in hanover, consisting of neurosurgery, ear, nose and throat (ent) and maxillofacial surgery doctors. as a result of his hard work, in 1989, he published "surgery of the skull base-an interdisciplinary approach" book. regarding the skull base surgery, prof. madjid samii founded in 1990 the foundation of national and continental skull base societies and the foundation of german skull base society (of which he is president). his statement is, "the only real treasures a neurosurgeon can have in his life are his patients". it may explain his commitment to studying, innovating, and discovering during his entire career. thus, he studied all the approaches for clivus and proved that the transnasal approach is preferred in clivus chondromas (using an endoscope and microscope). in 2013, he published the "surgery of cerebellopontine lesions" book, in view of presenting his professional experience between 1968 and 2013 (more than 6000 surgeries). his work and discipline encourage surgeons from all around the world to manage the most difficult cases with extreme precision and determination. he gave lectures that represented a major contribution to the progress of neurosurgery, while publishing numerous papers and statistics. in 1977, prof. madjid samii became chairman of the neurosurgical department at nordstadt krankenhaus, in hanover, germany. he also accepted the chair of neurosurgery at hanover school of medicine. between 1997-2001, he was elected president of the world federation of neurosurgery societies (wfns) according to his societal and humanitarian contributions worldwide through his work. since 2001, he has been the honorary president of wfns and the honorary president of the wfns foundation. the international neuroscience institute of hanover prof. madjid samii's considerable capacity for leadership gives hanover, germany, one of the most recognized centers of excellence in neurosurgery in the world, raising european neurosurgery to a more advanced level. he managed to fulfill his idea of creating a comprehensive neurosurgical center, the international neuroscience institute of hanover. in 2000, at the world expo event, the international neuroscience institute of hanover was officially inaugurated, becoming rapidly the best center for treating neurosurgical conditions. although the project was realized by the "siemens" company, the ideas of prof. madjid samii were vigorously taken into consideration, the interior and exterior designs of the building being decisively influenced by his suggestions. shaped as a "futuristic" human brain, the international neuroscience institute of hanover (figure 3) is a unique architectural landmark, enhancing the suggestion that any pathology of the nervous system can be cured. figure 3. international neuroscience institute of hanover (open in 2000) the main areas of the institute consist of three separate but synergetic departments: neurology, neurosurgery, and interventional neuroradiology. for an elitist final result, it was mandatory to build a team formed by the most competent neurosurgeons. in this matter, prof. madjid samii's imposing personality helped the institute to quickly have the brightest neurosurgeons for each neurosurgical subspecialty practicable. 375 madjid samii: omagium the institute is also focused on skill-improvement specialized training as well as on clinical research, having various laboratories for scientific experiments with successful results spread worldwide. compared to developing countries, the international neuroscience institute of hanover uses highly technological devices for paraclinical analysis, such as: 3 tesla mri,functional mri, a 128-slice ct scanner, and a biplane angiography system. the international neuroscience institute of hanover was soon followed by the international neuroscience institute of china (beijing) and the international neuroscience institute of iran (teheran). romanian neurosurgery at the international neuroscience institute of hanover last but not least, we have to mention that prof. madjid samii is a real friend of the romanian neurosurgical society, as he answers positively to the many congress invitations. he built a strong relationship with the greatest romanian neurosurgeons. a special bond was created in 2014, when prof. madjid samii invited prof. alexandru vlad ciurea to the international neuroscience institute of hanover (figure 4). prof. alexandru vlad ciurea presented a truly complex medical study regarding the embriology and development of the human brain, afterwards being awarded by prof. madjid samii with the title of ''visiting professor''. figure 4. prof. a.v. ciurea & prof madjid samii as prof. madjid samii reaches the age of 85, we would like to pay tribute to his major innovative, scientific, and humanitarian contributions to the field of international neurosurgery references 1. yasargil g.m: my reflections on professor madjid samii, world neurosurgery, 2013, 80(5):475. 2. ciurea a.v: madjid samii a life in the service of neurosurgery; a life in the service of mankind, world neurosurgery, 2013, 80(5):468-469. 3. morcos jacques: the man with the midas touch, world neurosurgery, 2013, volume 80(5):470. 4. konovalov a. porapov a: madjid samii: neurosurgeon of the year, 2013, world neurosurgery, 80(5):470. 5. ramina r: madjid samii, neurosurgeon of the year, 2013, world neurosurgery, 80(5):472. 6. nica d.a, copaciu r., ciurea a.v.: international neuroscience institute (ini) center hanovra. a new step in neurosurgery, 2012, romanian neurosurgery, 19(1), 112-115. romanian neurosurgery (2019) xxxiii (4): pp. 379-384 doi: 10.33962/roneuro-2019-062 www.journals.lapub.co.uk/index.php/roneurosurgery extradural autologous temporal muscle graft mimicking a meningioma. case report mihaela dana turliuc1,2, claudia florida costea1,2, irina elena balan1, b. costachescu1,2, b. dobrovat1,2, s. turliuc2, cristina mihaela ghiciuc2, r. arbore-sorete1, v. hartie1, f. sima1, a. i. cucu1 1 “prof. dr. nicolae oblu” emergency clinical hospital iasi, romania 2 “grigore t. popa” university of medicine and pharmacy iasi, romania abstract meningiomas are the most common dural tumour, but there are also many other dural masses which mimic their appearances, such as neoplastic and non-neoplastic lesions. in this paper we report another mass which may mimic a dural lesion, namely a muscle graft harvested from the temporal site and left in situ, used to achieve haemostasis in a posttraumatic temporal extradural hematoma in a young male patient. solid knowledge of differentiating neuroimaging characteristics of dural masses, as well as its corroboration with the patient’s medical history are extremely helpful in establishing an accurate diagnostic. introduction meningiomas are intracranial tumours and make up about one third of all primary central nervous system tumours, with an incidence rate that has increased in recent years (1, 2, 3, 4, 5), at the same time being the most common dural tumours. however, there may be a variety of other dural lesions (neoplastic and non-neoplastic lesions) mimicking their imagining appearance (6) (table 1). unfortunately, the information about the prevalence of these dural lesions is limited, and most of the examples in literature are small case series and case reports. many of these dural lesions share similar computed tomographic, magnetic resonance imaging and angiographic characteristics with meningiomas such as increased vascularity, avid enhancement, a dural tail and similar signal characteristics (7). in addition to these multiple dural lesions mimicking meningiomas, we report in this paper the existence of a muscle graft harvested from the temporal site and left in situ, used to achieve haemostasis in a case of left temporal extradural hematoma (figure 1). keywords temporal muscle graft, dural lesions, meningioma, computed-tomography corresponding author: claudia florida costea associate professor, md, phd. “grigore t. popa” university of medicine and pharmacy, iași, romania costea10@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 380 mihaela dana turliuc, claudia florida costea, irina elena balan et al. case report we report the case of a 40-year-old male patient, victim of a road accident (bicyclist knocked over by a car), who was brought to the emergency room of our hospital with a gcs of 3 and anisocoria (pupil in the left eye > right eye). the cranial ct scan carried out on his admission revealed a left temporal extradural hematoma with left temporal fracture (figure 1). a surgical procedure was performed immediately to remove the hematoma and the patient’s subsequent evolution was excellent, with no post-operative neurological deficiencies. during surgery, the source of bleeding was identified as being the middle meningeal artery and in order to achieve better haemostasis, a piece of the temporal muscle was left in situ, which was later revealed by the cranial postoperative follow-up ct scan (figure 1. d, white arrow). also, during surgery, in order to reach the skull base and stop the bleeding, the bone flap was complemented by temporal craniectomy, for which a cranioplasty with titanium mesh was later performed (figure 2). during periodic imaging followup, we noticed that the piece of temporal muscle left in situ for haemostasis purposes had become vascularized and a native cranial ct scan revealed its homogeneous appearance (figure 3). also, the electroencephalogram did not reveal any pathological changes. figure 1. preoperative cranial ct scan with left temporal extradural hematoma (*) (a, b, c). postoperative cranial ct scan showing temporal muscle left in situ (white arrow) (d) figure 2. intraoperative photo showing the bone flap (white arrow) and cranioplasty with titanium mesh (a). postoperative ct scan showing the cranioplasty (b) figure 3. the follow-up cranial ct scan performed after 1, 2 and 3 years (b, c, d) revealed the hypervascular muscle graft mimicking a meningioma or other hypervascular lesions 381 extradural autologous temporal muscle graft mimicking a meningioma discussions in neurosurgery, just like in all the other surgical fields, proper haemostasis is a sine qua non requirement when it comes to preventing dramatic postoperative bleedings the consequences of which are not negligible. among the various local haemostatic agents used in neurosurgery (8, 9, 10), fresh muscle harvested from the temporal muscle or thigh is still commonly used to achieve haemostasis (8). before the 1950’s, neurosurgeons used fresh chicken breast as topical haemostatic agents, which were delivered before the surgical procedure. the muscle grafts were applied on the brain during ten minutes, while washing the surgical field with warm serum, and they were removed before closing the dura (8). the first reports on the use of muscle grafts in haemostasis belong to cushing and horsley (11, 12). later, clute also reported the efficient use of both free and viable muscle grafts in achieving haemostasis in different organs (13). the idea of fresh muscle harvested from the temporal site or thigh, which may be left in situ, appeared later. the technique is still used sometimes. in addition to muscle grafts, neurosurgeons have also used other autologous human tissues for haemostasis, such as clots, fascia, dura or fat, yet these have not proven better (12, 14). moreover, autologous human muscle grafts have proven their efficiency and superiority in the management of significant haemorrhage not only in brain surgery, but also in all the other surgical fields which they were used in (15, 16, 17, 18, 19, 20). the use of muscle grafts for haemostasis during neurosurgery has reemerged these last few years (21), and fresh muscle graft is also used in neurosurgery in case of cerebrospinal fluid leak (20) or to repair the internal carotid artery during endoscopic surgery (22). thus, extensive research has proven muscle tissue efficiency in controlling carotid artery bleeding, both in animal and in human models (16, 18, 23, 24). moreover, research on animal and patients undergoing endoscopic sinus surgery has shown that muscle tissue may efficiently control high-flow and high-pressure carotid artery bleeding (16, 18, 23). in a study on human muscle extracts, in which rajiv et al. investigated the haemostatic potential of muscle tissue through various coagulation and platelet aggregation tests, the authors concluded that platelet aggregation plays an important role in the haemostatic efficiency of muscle grafts and the muscle grafts adhere well to blood vessels (21). jukes et al. also showed in a study conducted on autologous but crushed muscle, that this caused a consistently increased ratio of platelet activation when compared with uncrushed muscle (25). in order to understand the imaging appearance of muscle graft left in situ better, the knowledge about dura mater vascularization and about the encephalo-duro-myo-synangiosis mechanism is the key (26, 27). the dura mater is a thick non-elastic membrane made up of fibrous and elastic connective tissue, which surrounds the brain and spinal cord. the cranial dura mater consists of two layers: an external periosteal layer and an inner meningeal layer which are generally fused except when they separate to allow the passage of the dural venous sinuses. of the two layers, the external periosteal layer adheres closely to the skull bone and is highly vascular and innervated and contains blood vessels that supply the bone, exhibits greater angiogenic activity and is like an internal periosteum for the cranium (7, 28, 29). the inner meningeal layer of the dura is smooth and avascular and is lined on its inner surface by mesothelium (7, 28). the neovascularization in the outer layer cannot extend to the inner layer to the cortical surface, so that it is safe to say that the meningeal layer is a natural barrier between the circulation of the external and internal carotid arteries (30, 31). practically, in the case of our patient, the existing vessels in the scalp tissue and temporal muscle passed through the titanium mesh and recruited the vessels in the muscle graft. this vascularization of the external periosteal layer of dura mater has also contributed to the repermeabilization and neovascularization of the muscle graft left in situ to achieve haemostasis. the various vascularized tissues communicate through the titanium mesh (32) and this was also considered by badie et al. who used a reconstruction technique involving the placing of a titanium mesh between two layers of continuous vascularized pericranium in patients with large anterior skull defects. the technique has been proven safe and effective (33). this revascularization mechanism is essential for the effectiveness of burr holes for indirect revascularization in patients with moyamoya disease (34). it seems that new vessels are formed by two distinct phenomena: angiogenesis and 382 mihaela dana turliuc, claudia florida costea, irina elena balan et al. arteriogenesis (34, 35). angiogenesis is the formation of new vascular segments altering the preexistent vascular network, whereas arteriogenesis is the formation of blood vessels from endothelial precursors (35). whether these processes occur simultaneously or sequentially is still to be determined (36, 37). in our patient, the muscle graft became hypervascularized by the double contribution of the meningeal arteries irrigating the dura and the superficial temporal artery vascularizing the scalp tissue, a model which was also taken into consideration by other authors (38). the follow-up ct scan performed after 1, 2 and 3 years, respectively (figure 3) revealed that the muscle graft became hypervascular and had higher perfusion values, mimicking a meningioma or other hypervascular lesions (e. g. renal tumour metastases), compared with most other extra-axial lesions (6). for the treatment of moyamoya disease, houkin et al. showed that collateral circulation develops within 3-4 months after surgery (39) and is directly related to the size of the bone flap (40, 41). this explains the good vascularization of the muscle graft revealed by the periodic cranial ct scans (figure 3). the medical imaging examination of the muscle graft perfectly mimics a dural lesion, therefore the differential diagnosis with the other dural lesions is required (table 1). also, the patient’s clinical examination and personal medical history may be extremely helpful in guiding the diagnosis setting process. table 1. dural lesions (after 6 and 42 ref) neoplastic: • meningioma • metastasis (colon, breast, lung, prostate, leiomyosarcoma) • glioblastoma • lymphoma • hemangiopericytoma • solitary fibrous tumor • hodgkin’s disease • carcinomatosis • plasmocytoma • ewing sarcoma • epstein-barr virus-associated smooth muscle tumors granulomatous: • tuberculosis • neurosarcoidosis • granulomatosis with polyangiitis • plasma cell granulomas lymphoproliferative: • rosai-dorfman disease • erdheim-chester disease autoimmune: • igg4-related disease other: • extramedullary hematopoiesis conclusion in neurosurgery, there are many pathologies affecting the dura and mimicking meningiomas. they include primary and secondary neoplastic lesions, inflammatory and infectious lesions, which may be mistaken for one another because of their similar imaging characteristics. in addition to all these dural lesions, in this case report we mention the existence of autologous muscle graft left in situ mimicking a dural lesion. solid knowledge of differentiating neuroimaging characteristics, as well as its corroboration with the patient’s medical history may help set the right diagnosis and find new optimal therapeutic approaches. references 1. louis dn, scheitauer bw, budka h, von deimling a, kepes jj. meningiomas. in: kleihues p, cavenee wk (eds). pathology and genetics of tumors of the nervous system. lyon: iarc press, 2000. 2. cucu ai, costea cf, poeata i, turliuc dm. prognostic factors in atypical meningioma. romanian neurosurgery. 2017; 31(2):165-171. 3. cucu ai, costea cf, poeata i, costachescu b, dumitrescu gf, et al. anatomical localization of atypical meningiomas: our experience on 81 patients. rev med chir soc med nat iasi. 2018; 122:744-752. 4. cucu ai, costea cf, carauleanu a, dumitrescu gf, sava a, et al. meningiomas related to the chernobyl irradiation disaster in north-eastern romania between 1990 and 2015. rev chimie (bucharest). 2018; 69:1562-1565. 5. cucu ai, turliuc md, carauleanu a, poeata i, costea c, et al. chemical aspects of peritumoral cerebral edema in atypical meningiomas. rev chim (bucharest). 2018; 69:2804-2807. 6. lyndon d, lansley ja, evanson j, krishnan as. dural masses: meningiomas and their mimics. insights imaging. 2019; 10(1):11. 7. smith ab, horkanyne-szakaly i, schroeder jw, rushing ej. from the radiologic pathology archives: mass lesions of the dura: beyond meningioma radiologic pathologic correlation. radiographics. 2014; 34(2):295-312. 8. lapierre f, d’houtaud s, wager m. haemostatic agents in neurosurgery. in: signorelli f (ed). explicative cases of controversial issues in neurosurgery. rijeka: intech, 2012. 383 extradural autologous temporal muscle graft mimicking a meningioma 9. turliuc md, cucu ai, carauleanu a, costea cf. efficiency and safety of microporous polysaccharide hemispheres from potato starch in brain surgery. cellulose chem technol. 2018; 52: 505-513. 10. gazzeri r, galarza m, callovini g, alfieri a. biosurgical haemostatic agents in neurosurgical intracranial procedures. surg technol int. 2017; 30:468-476. 11. cushing hi. the control of bleeding in operations for brain tumors: with the description of silver “clips” for the occlusion of vessels inaccessible to the ligature. ann surg. 1911; 54:1-19. 12. horsley v. note on haemostasis by application of living tissue. br med j. 1914; 2:8. 13. clute hm. muscle grafts for haemostasis in general surgery. n engl j med. 1935; 213:746-748. 14. risley eh. haemostasis by interposition of muscle, fat and fascia in parenchymatous organs. surg gynecol obstet. 1917; 24:85. 15. james ag, zollinger rw sr. an autologous haemostatic agent. surg gynecol obstet. 1984; 159:381-382. 16. valentine r, boase s, jervis-bardy j, dones cabral jd, robinson s, et al. the efficacy of haemostatic techniques in the sheep model of carotid artery injury. int forum allergy rhinol. 2011; 1:118-122. 17. reece ij, al tareif h. muscle tamponade to control venous bleeding around grafts to deeply intramyocardial coronary arteries. j card surg. 1995; 10:703-705. 18. weidenbecher m, huk wj, iro h. internal carotid artery injury during functional endoscopic sinus surgery and its management. eur arch otorhinolaryngol. 2005; 262:640645. 19. losanoff je, richman bw, jones jw. muscle tamponade to control presacral venous bleeding. dis colon rectum. 2003; 46:688-689; author reply 689. 20. hardt n, kuttenberger. craniofacial trauma: diagnosis and management. berlin: springer, 2010. 21. rajiv s, rodgers s, bassiouni a, vreugde s, wormald pj. role of crushed skeletal muscle extract in haemostasis. int forum allergy rhinol. 2015; 5(5):431-434. 22. duek i, sviri ge, amit m, gil z. endoscopic endonasal repair of internal carotid artery injury during endoscopic endonasal surgery. j neurol surg rep. 2017; 78(4):e125e128. 23. fehm np, vatankhah b, dittmar ms, tevetoglu y, retzl g, et al. closing microvascular lesions with fibrin sealantattached muscle pads. microsurgery. 2005; 25:570-574. 24. padhye v, valentine r, paramasivan s, jardeleza c, bassiouni a, et al. early and late complications of endoscopic haemostatic techniques following different carotid artery injury characteristics. int forum allergy rhinol. 2014; 4:651-657. 25. jukes a, miljkovic d, wormald pj, psaltis aj. platelet activation by crushed and uncrushed muscle: a flow cytometry analysis. int forum allergy rhinol. 2017; 7(9):916-919. 26. shen w, xu b, li h, gao x, liao y, et al. enlarged encephaloduro-myo-synangiosis treatment for moyamoya disease in young children. world neurosurg. 2017; 106:9-16. 27. endo m, kawano n, miyaska y, yada k. cranial burr hole for revascularization in moyamoya disease. j neurosurg. 1989; 71(2):180-185. 28. siegel a, sapru hn. essential neuroscience, baltimore/philadelphia: lippincott williams & wilkins, 2006. 29. zhao x, wang c, ji y, han c, wang m. therapeutic effect of multiple burr hole operation combined with dural inversion and periosteal synangiosis for moyamoya disease. br j neurosurg. 2015; 29(6):811-817. 30. kashiwagi s, kato s, yasuhara s, wakuta y, yamashita t, et al. use of a split dura for revascularization of ischemic hemispheres in moyamoya disease. j neurosurg. 1996; 85:380-383. 31. kashiwagi s, kato s, yamashita k, takasago t, akimura t, et al. revascularization with split duro-encephalo-synangiosis in the pediatric moyamoya disease – surgical result and clinical outcome. clin neurol neurosurg. 1997; 99 suppl 2: s115-117. 32. costan vv, sulea d, nicolau a, drochioi ci, luchian s, et al. the use of titanium mesh in facial contour reconstruction. rev med chir soc med nat iasi. 2018; 122:167-175. 33. badie b, preston jk, hartig gk. use of titanium mesh for reconstruction of large anterior cranial base defects. j neurosurg. 2000; 93(4):711-714. 34. mclaughlin n, martin na. effectiveness of burr holes for indirect revascularization in patients with moyamoya disease-a review of the literature. world neurosurg. 2014; 81(1):91-98. 35. zadeh g, guha a. angiogenesis in nervous system disorders. neurosurgery. 2003; 53(6):1362-1374; discussion 1374-1376. 36. nakamura m, imai h, konno k, kubota c, seki k, et al. experimental investigation of encephalomyosynangiosis using gyrencephalic brain of the miniature pig: histopathological evaluation of dynamic reconstruction of vessels for functional anastomosis. laboratory investigation. j neurosurg pediatr. 2009; 3:488-495. 37. saito n, imai h. insights on the revascularization mechanism for treatment of moyamoya disease based on the histopathologic concept of angiogenesis and arteriogenesis. world neurosurg. 2011; 75:204-205. 38. dusick jr, gonzalez nr, martin na. clinical and angiographic outcomes from indirect revascularization surgery for moyamoya disease in adults and children: a review of 63 procedures. neurosurgery. 2011; 68(1):34-43; discussion 43. 39. houkin k, nakayama n, kuroda s, ishikawa t, nonaka t. how does angiogenesis develop in pediatric moyamoya disease after surgery? a prospective study with mr angiography. childs nerv syst. 2004; 20:734-741. 40. matsushima t, inoue t, katsuta t, natori y, et al. an indirect revascularization method in the surgical treatment of moyamoya disease-various kinds of indirect procedures and a multiple combined indirect procedure. neurol med chir. 1998; 38:297-302. 384 mihaela dana turliuc, claudia florida costea, irina elena balan et al. 41. takahashi a, kamiyama h, houkin k, abe h. surgical treatment of childhood moyamoya disease-comparison of reconstructive surgery centered on the frontal region and the parietal region. neurol med chir. 1995; 35:231-237. 42. aggarwal a, patra dp, gupta k, sodhi hb. dural tuberculoma mimicking meningioma: a clinico-radiologic review of dural en-plaque lesions. world neurosurg. 2016; 88:686.e1-7. doi: 10.33962/roneuro-2022-052 haemorrhagic progression of contusions after traumatic brain injury in orally anticoagulated patient. the rule of (6i’s) tariq janjua, ebtesam abdulla, amit agrawal, moshiur rahman, ivan lozada, yelson alejandro picon luis rafael moscote-salazar romanian neurosurgery (2022) xxxvi (3): pp. 306-310 doi: 10.33962/roneuro-2022-052 www.journals.lapub.co.uk/index.php/roneurosurgery haemorrhagic progression of contusions after traumatic brain injury in orally anticoagulated patient. the rule of (6i’s) tariq janjua1, ebtesam abdulla2, amit agrawal3, moshiur rahman4, ivan lozada5, yelson alejandro picon5, luis rafael moscote-salazar5 1 department of critical care medicine, physician regional medical centre, naples, fl 2 department of neurosurgery, salmaniya medical complex, manama, bahrain 3 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india 4 department of neurosurgery, holy family red crescent medical college hospital, dhaka, bangladesh 5 colombian clinical research group in neurocritical care, bogota, colombia abstract traumatic brain injury carries a high risk of neurological disability and fatality1-8. the extent of the injury to the neuronal tissue following a head impact defines the primary injury. the acceleration energy delivered at the time of impact provokes this injury. there are numerous secondary responses to the injury that mostly intensify the primary injury. when a head impact causes a contusion, the hemorrhagic injury frequently progresses over the first few hours after impact, either growing or developing new, non-contiguous hemorrhagic lesions, a condition known as the hemorrhagic progression of a contusion1,2,4,7,9-14. illustrated case an 88-year-old woman was admitted with a severe headache, multiple emetic episodes, and a brief loss of consciousness after falling while doing housework. her past medical history included anticoagulation with warfarin for atrial fibrillation (international normalized ratio (inr): 3.75). she had normal vital signs and a grossly intact neurological examination on admission. a cranial computed tomography (ct) scan was performed 45 minutes after arrival to the emergency department, which revealed small bifrontal contusions (fig 1). it was decided to transfer her to the intermediate care unit with non -invasive hemodynamic monitoring, analgesia, continuous neurological evaluation, and neurosurgical evaluation. at 18 hours, she started keywords intracerebral hemorrhage, contusion, traumatic brain injury corresponding author: ebtesam abdulla department of neurosurgery, salmaniya medical complex, manama, bahrain dr.ebtesam@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 307 haemorrhagic progression of contusions after traumatic brain injury in orally anticoagulated patient having emetic episodes and drowsiness. an emergent follow-up cranial ct scan showed extensive bifrontal and bitemporal contusions with intraventricular bleeding (fig 2). due to rapid deterioration of the respiratory pattern, the airway was protected with a sequence of rapid intubation, sedation, protective mechanical ventilation, osmotherapy, fresh frozen plasma, and prothrombin complex concentrate. the patient progressed to coma and expired 36 hours after her presentation. figure 1. ct scan head on admission figure 2. follow-up ct scan showing marked changes with extensive intracerebral bleeding anticoagulant-associated ich anticoagulated patients represent a major neurocritical care burden, as anticoagulation is one of the leading risk factors for intracranial hemorrhage (ich) after a head impact.15 the risk of developing ich after a head injury is 42.2 times higher in patients on oral anticoagulants than in control patients.16 aggravating factors associated with anticoagulant-induced bleeding complications include older age, alcohol abuse, renal and hepatic insufficiency, uncontrolled anticoagulant, the targeted intensity of anticoagulant, prior stroke, concomitant anti-platelet therapy, and hypertension.6,8,9-13 as a result, prompt screening strategies, and interventions that promote better neurological outcomes in the anticoagulated population after head impact are critical. warfarin versus direct oral anticoagulants (doacs) recent randomized trials on orally anticoagulated participants for atrial fibrillation have demonstrated a 50% reduction in the incidence of ich with doacs compared to warfarin.17-20 nevertheless, given the high prescription rates of doacs and unavailability of the specific reversal agents, ich development with doacs has become an important issue and can result in permanent disability and fatality, as with warfarin.18-21 in a randomized clinical trial by hankey et al22 (2014), the fatality rate from anticoagulantassociated ich was 49% (85/172), and among 85 participants who experienced fatality due to anticoagulant-associated ich, 50% (54/85) were assigned with warfarin and 48% were assigned with rivaroxaban (31/85). given the fact that there is an insignificant difference in fatality rate between doac and warfarin, the natural history of doac-associated ich should be broadly investigated, and prospective studies on hematoma expansion in this specific group are warranted. european federation of neurological societies (efns) guidelines in 2002, efns set guidelines targeting all anticoagulated participants with normal initial ct scans after sustaining a minor head impact.4-6 the efns guidelines entailed one-day admission for close neurological observation, and a second head ct scan before discharge to rule out delayed ich.4-6 however, the growing body of research showed heterogenicity 308 tariq janjua, ebtesam abdulla, amit agrawal et al. to support efns recommendations for anticoagulated patients after minor head impacts. a recently published meta-analysis by puzio et al7 (2021) estimated 2.43% (95% ci, 1.31-3.88%) and 2.31% (95% ci, 1.26-3.66%) for delayed ich on doacs and warfarin, respectively. only a minority of 0.6% (2/1263) and 0.48%(8/1788) of those on doacs and warfarin, respectively, reported fatalities, while the majority 86% (59/69) had no clinical complications. the authors concluded that screening for delayed ich for those on oral anticoagulants is not warranted based on their estimated overall crude risk of fatality 0.36% (11/3051).7 in contrast, in a published study by menditto et al1 (2012) on the delayed ich in orally anticoagulated participants, it was found that 6% (5/87) of participants with normal initial scans, developed delayed ich, which was evident in a ct scan performed 24 hours after the trauma. the estimated relative risk of delayed ich with an initial inr greater than 3.0 was 14 (95% ci, 4-49).1 in a meta-analysis by betchelor et al14 (2012) the estimated higher odd ratio of fatalities in patients on warfarin with the head impact was 2.0008 (95% ci, 1.634-2.467). accordingly, the authors supported the advisability of a second head ct scan as advocated by efns guidelines. confounding factors of haemorrhagic progression the challenges in defining the confounding factors of hemorrhagic progression in specific patients on oral anticoagulants include a paucity of relevant clinical data. however, various predictors have been reported in the literature concerning post-traumatic hematomas associated with trauma in general participants. i. increased age in a published study by melamed et al23 (1980) and purkayastha et al24 (2014), increased age has been associated with contusion progression through several mechanisms. increased age induces structural weakness in the cerebral microvasculature, endothelium loss, and reduced resting cerebral blood flow, which can consequently contribute to contusion progression.23,24 ii. intractable headache and emesis the most common symptoms of a cerebral contusion are headache, emesis, concentration problems, and memory loss.25 patients struggling with continued symptoms despite proper medical management should warrant a second screening with a ct scan as the progression of contusion is highly expected. iii. increased systemic blood pressure (bp) at admission in a retrospective study by wan et al8 (2017), hypertensive participants had 4.5 times the incidence of ich progression compared to normotensive participants, which can be ascribed to increased baseline blood-brain barrier permeability. iv. inclined glasgow coma score (gcs) at admission the initial gcs has been a predictor for contusion progression. the contusion progression was reported with gcs <14 by white et al9 (2009), gcs ≤5 by qureshi et al10 (2015), and gcs <8 by carnevale et al11 (2018). v. inr level >1.2, platelet count <100 × 109 /l regarding laboratory parameters, white et al9 (2009) and wan et al8 (2017) demonstrated contusion progression three times in participants whose initial inr was>1.2 compared to participants whose initial inr was ≤1.2. it has been shown by sharma et al12 (2016) that contusion progression increases seven times for each unit increase in inr. additionally, juratli et al13 (2014) showed a strong association between contusion progression and platelet count <100 × 109/l, about six times the increased risk. vi. intoxication by alcohol several studies have shown a higher frequency of contusion progression with alcohol intoxication.11,13, 26.27 alcohol intoxication contributes to coagulopathy through several mechanisms, including impairment of platelet function and reduction of vascular tone; both counteract each other on contusion progression.27 although the association has been reported, the causality remains unknown. 6i’s rule 1. increased age 2. intractable headache and emesis 3. increased systemic bp at admission 4. inclined gcs at admission 5. inr level >1.2, plt < 100 × 109 /l 6. intoxication by alcohol 309 haemorrhagic progression of contusions after traumatic brain injury in orally anticoagulated patient as a goal to prevent deaths in patients with head impact and oral anticoagulants, we proposed the 6 is rule (table 1). the presence of any of the (i) in context with the history of current oral anticoagulant use indicates admission and performance of serial ct scans after 24 hours or according to neurosurgeon criteria. applying and spreading the rule of the (6is) will facilitate the identification of high-risk individuals and thus early recognition of possible delayed ich or contusion progression. this can be a potentially useful, and reliable objective screening tool for emergency physicians, nurses, and nursing assistants. references 1. menditto v, lucci m, polonara s, et al. management of minor head injury in patients receiving oral anticoagulant therapy: a prospective study of a 24hour observation protocol. annals of emergency medicine.2012: 59 (6): 451455. 2. nishijima d, offerman s, ballard d, et al. risk of traumatic intracranial haemorrhage in patients with head injury and preinjury warfarin or clopidogrel use. academic emergency medicine.2013: 20: 140-145. 3. sharif-alhoseini m, khodadadi h, chardoli m, et al. indications for brain computed tomography scan after minor head injury. journal of emergencies, trauma and shock.2011: 4 (4): 472-476. 4. leiblich a, mason s. emergency management of minor head injury in anticoagulated patients. emerg med j. 2011;28:115118. 5. lavoie a, ratte s, clas d, et al. preinjury warfarin use among elderly patients with closed head injuries in a trauma center. j trauma. 2004;56:802-807. 6. karni a, holtzman r, bass t, et al. traumatic head injury in the anticoagulated elderly patient: a lethal combination. am surg. 2001;67:1098-1100. 7. puzio tj, murphy pb, kregel hr, et al. delayed intracranial hemorrhage after blunt head trauma while on direct oral anticoagulant: systematic review and metaanalysis. j am coll surg. 2021;232(6):1007-1016.e5. 8. wan x, fan t, wang s, et al. progressive hemorrhagic injury in patients with traumatic intracerebral hemorrhage: characteristics, risk factors and impact on management. acta neurochir. 2017;159(2):227–35. 9. white cl, griffith s, caron j-l. early progression of traumatic cerebral contusions: characterization and risk factors. j trauma inj infect crit care. 2009;67(3):508–15. 10. qureshi ai, malik aa, adil mm, defillo a, sherr gt, suri mfk. hematoma enlargement among patients with traumatic brain injury: analysis of a prospective multicenter clinical trial. j vasc interv neurol. 2015;8(3):42–9. 11. carnevale ja, segar dj, powers ay, et al. blossoming contusions: identifying factors contributing to the expansion of traumatic intracerebral hemorrhage. j neurosurg. 2018;129(5):1305–16. 12. sharma m, mittal r, sharma a, gandhi a. posttraumatic contusion: clinical and radiologic factors for progression in early postinjury period. indian j neurotrauma. 2016;13(1):1–6. 13. juratli ta, zang b, litz rj, et al. early hemorrhagic progression of traumatic brain contusions: frequency, correlation with coagulation disorders, and patient outcome: a prospective study. j neurotrauma. 2014;31(17):1521–7. 14. batchelor js, grayson a. a meta-analysis to determine the effect of anticoagulation on mortality in patients with blunt head trauma. br j neurosurg. 2012;26(4):525-530. 15. dowlatshahi d, butcher ks, asdaghi n, nahirniak s, bernbaum ml, giulivi a, et al. poor prognosis in warfarinassociated intracranial hemorrhage despite anticoagulation reversal. stroke 2012;43:1812–7. 16. brown jd, shewale ar, dherange p et al. a comparison of oral anticoagulant use for atrial fibrillation in the pre and post-doac eras. drugs aging.2016: 33, 427–436 . 17. ruff ct, giugliano rp, braunwald e, et al. comparison of the efficacy and safety of new oral anticoagulants with warfarin in patients with atrial fibrillation: a meta-analysis of randomised trials. the lancet. 2014: 383(9921), 955– 962. 18. katsanos ah, mavridis d, parissis j, deftereos s, frogoudaki a, vrettou ar, et al. novel oral anticoagulants for the secondary prevention of cerebral ischemia: a network meta-analysis. ther adv neurol disord 2016;9:359–68. 19. caldeira d, barra m, pinto fj, ferreira jj, costa j. intracranial hemorrhage risk with the new oral anticoagulants: a systematic review and meta-analysis. j neurol 2015;262:516–22. 20. boulouis g, morotti a, pasi m, goldstein jn, gurol me, charidimou a. outcome of intracerebral haemorrhage related to non-vitamin k antagonists oral anticoagulants versus vitamin k antagonists: a comprehensive systematic review and meta-analysis. j neurol neurosurg psychiatry 2018;89:263–70. 21. kasliwal mk, panos ng, munoz lf, moftakhar r, lopes dk, byrne rw. outcome following intracranial hemorrhage associated with novel oral anticoagulants. j clin neurosci 2015;22:212–5. 22. hankey gj, stevens sr, piccini jp, et al; rocket af steering committee and investigators. intracranial hemorrhage among patients with atrial fibrillation anticoagulated with warfarin or rivaroxaban: the rivaroxaban once daily, oral, direct factor xa inhibition compared with vitamin k antagonism for prevention of stroke and embolism trial in atrial fibrillation. stroke. 2014;45(5):1304-1312. 23. melamed e, lavy s, bentin s, cooper g, rinot y. reduction in regional cerebral blood flow during normal aging in man. stroke. 1980;11(1):31–5. 310 tariq janjua, ebtesam abdulla, amit agrawal et al. 24. purkayastha s, sorond fa. cerebral hemodynamics and the aging brain. int j clin neurosci ment heal. 2014;1(suppl. 1):s07. 25. kushner d. mild traumatic brain injury toward understanding manifestations and treatment. arch intern med. 1998;158:1617–1624 26. mehta p, mehta j, lawson d, patel s. ethanol stimulates prostacyclin biosynthesis by human neutrophils and potentiates anti-platelet aggregatory effects of prostacyclin. thromb res. 1987;48(6):653–61. 27. zink bj, walsh rf, feustel pj. effects of ethanol in traumatic brain injury. j neurotrauma. 1993;10(3):275– 86. romanian neurosurgery (2019) xxxiii (3): pp. 239-242 doi: 10.33962/roneuro-2019-040 www.journals.lapub.co.uk/index.php/roneurosurgery syringobulbia and syringomyelia in a case with chiari 0 malformation successfully treated by posterior fossa reconstruction. case presentation and literature review r.b. sandu1, m.i. pantiru1, m. cosman2, i. poeata1,2 1 “prof dr. n. oblu” clinic emergency hospital, iasi, romania 2 “grigore t. popa” university of medicine and pharmacy, iasi, romania abstract “chiari zero malformation” is a rare and a relatively new described condition which associates syringohydromyelia without caudal displacement of the cerebellar tonsils through the foramen magnum. we present a case of a 40 years old woman with chiari zero malformation with both syringomyelia and syringobulbia and a good clinical and radiological outcome after posterior fossa decompression. the presence of associated syringomyelia and syringobulbia in this condition is less frequent and it usually occurs in younger patients. in our case we considered syringobulbia as being an extension of syringomyelia. introduction the chiari malformations were first described by hans chiari in terms of the cerebellar tonsils herniating out of the skull and he identified four different types, of which the type i and ii are more common (4). nowadays, most people define chiari i as tonsillar herniation of greater than 3-5 mm, measured as the distance below the foramen magnum and the condition is often associated with syryngomyelia (1). but patients with syringohydromyelia without hindbrain herniation that respond to posterior fossa decompression have been described and the condition was named “chiari zero malformation” (7). conversely, many patients can have herniations greater than 3-5 mm, but with no symptoms, so tonsillar herniation identified radiographically is of limited prognostic value and requires clinical correlation (5). the association with syringobulbia is even a rarer situation, with only a few cases in the literature and especially in children (19,20). hereby we present a case of a women with chiari zero malformation and the presence of both syringomyelia and syringobulbia who was treated surgically in our department. keywords chiari zero malformation, syryngomyelia, syringobulbia, cerebellar tonsils corresponding author: pantiru mihail-ionut “prof dr. n.oblu” clinic emergency hospital, iasi, romania ionut.mihail26@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 240 r.b. sandu, m.i. pantiru, m. cosman, i. poeata case report a 40-year-old woman was admitted to our hospital with a 2-years history of progressive proximal leftsided upper limb weakness. at admission she had a decreased sensitivity to painful stimuli associated with decreased temperature sensation as well in the upper limbs and swallowing difficulties. she also presented kypho-scoliosis developed during the childhood. the patient was investigated with a head computed tomography (ct) and a 1.5t irm of the cranio-cervical junction, cervical and thoracic spine. on the preoperative images, we made some linear measurements for posterior fossa dimensions: the length of the clivus defined as the distance from the top of the dorsum sellae to the basion, and the length of the supraocciput measured between the internal occipital protuberance and the opisthion. we also calculated the spheroidal posterior fossa volume (pfv) based on the spheroidal formula (6): pfv=4/3 x π x (x/2 x y/2 x z/2), where: x is the anteroposterior measurement from the posterior clinoid process to the torcula; y is the height of the posterior fossa measured from the basion to the peak of the tentorium cerebelli; and z is the maximum width of the posterior fossa. (6) to assess the syrinx characteristics, we noted the cranial and caudal extent and we measured on the pre and postoperative images the ratio between the syrinx and the spinal cord diameter at the level of the maximum expansion. in addition, we calculated the ratio of the surface area of syrinx to spinal cord using the formula πr² for surface area, with r being the radius (7). the clival length of our patient was 4,2 cm and the length of the supraocciput was 4,5 cm. the width of the posterior cranial fossa was 9,9 cm (z=9,9 cm), and the anterior-posterior dimension was 8,3 cm (x=8,3 cm). the height from the basion to tentorium cerebelli was 5,3 cm (y=5,3 cm). the calculated spheroidal posterior fossa volume was 227,9 cm³. these measurements are consistent with a small posterior fosa. figure 1. posterior fossa measurements figure 2. pre and post-operatively mri images 241 syringobulbia and syringomyelia in a case with chiari 0 malformation the cranial extent of the syrinx was at the level of the medulla oblongata and the caudal extent was at the level of t4 vertebral body. we measured the maximum expansion of the syrinx cavity at the level of the t1 vertebral body and compared the pre and 3 months postop values. the ratio of the preoperative syrinx/spinal cord diameter at the level of greatest expansion (t1 vertebral body) was 0.81 (9mm/11mm). the ratio of the postoperative syrinx/spinal cord diameter at the same vertebral level was 0.37 (3mm/8mm). the ratio of the preoperative syrinx/spinal cord surface at the level of greatest expansion (t1 vertebral body) was 0.67, and 3 months postoperatively was 0.14 the patient was surgically treated by performing a craniocervical decompression which consisted of a suboccipital craniectomy, c1 laminectomy, intradural lysis of the arachnoidal adhesions that occluded the foramen of magendie and duraplasty. she had a good post-operative evolution with the progressive remission of the symptoms. discussion chiari 0 malformation is a rare and a relatively new described condition which associates syringohydromyelia without caudal displacement of the cerebellar tonsils through the foramen magnum, of which clinical symptoms and radiological aspect can be ameliorated after posterior fossa decompression. (7,18). while chiari ii and iii malformations can be explained by a maldevelopment of the posterior fossa neural structures, more and more evidence point to an underdevelopment of the bony structures of posterior fossa, leading to a smaller pfossa that contain a normal developed neural tissue as an explanation for chiari i and chiari 0 malformations (2,8,10,11,12,13,14,15,16). syringomyelia may be associated with many conditions such as chiari malformations, spinal trauma, spinal tumours, tethered cord or spinal dysraphism. in a study of strahle et al, the authors identified a number of 271 patients with a syrinx out of 14118 patients who undergone brain or spine imaging during a period of 11 years. the chiari malformation type i was the most common associated condition with syringomyelia and the syrinx was more likely to have the cranial extent in the cervical spine and to have a width greater than 5 mm compared with other conditions. they found only 4 patients with chiari 0 malformation but the syrinx in these cases had the big-gest width and length, bigger than syrinx associated with chiari type i and ii malformations. al-so the chiari type 0 patients had a more superior cranial extent of their syrinx. (17). we considered that the characteristics of our patient are consistent with the chiari 0 malformation. the measurements corresponded with a small posterior fossa and the mri revealed syringomyelobulbia without tonsillar herniation. three months postoperatively, the symptomatology improved, the algesthesia and temperature sensation in the upper limbs were better than preoperatively, the swallowing difficulties disappeared and the abduction of both upper limbs obviously improved. the mri performed 3 months postop showed that syringomyelia diminished semnificatively compared with that before surgery. conclusion the presence of associated syringobulbia with syringomyelia in the chiari zero malformation is a condition rarely described in the literature and in the most of the cases the patients are younger. (19,20). in our case we considered syringobulbia as being an extension of syringomyelia. references 1. aboullez ao, sartor k, geyer ca, gado mh. position of cerebellar tonsils in the normal popu-lation and in patients with chiari malformation: a quantitative approach with mr imaging. j comput assist tomogr. 1985; 9: 1033-1036 2. arnold h. menezes, md,1,2 jeremy d. w. greenlee, md,1– 3 and brian j. dlouhy, md1–4 syringobulbia in pediatric patients with chiari malformation type i j neurosurg pediatr. 2018 jul;22(1):52-60. doi: 10.3171/2018.1.peds 17472. 3. badie b, mendoza d, batzdorf u: posterior fossa volume and response to suboccipital decom-pression in patients with chiari i malformation. neurosurgery 1995, 37(2):214218. 4. chiari h: uber veranderungen des kleinhirns, des pons und der medulla oblongata in folge von congenitaler hydrocephalie des grosshirns. denkschr akad wiss 63:71–116, 1895 5. elster ad, chen my: chiari i malformations: clinical and radiologic reappraisal. radiology 1992, 183(2):347-353. 6. furtado sv, reddy k, hegde as: a posterior fossa morphometry in symptomatic pediatric and adult chiari i malformation. clinical study. journal of clinical neuroscience 16:1449-1454, 2009 242 r.b. sandu, m.i. pantiru, m. cosman, i. poeata 7. iskandar bj, hedlund gl, grabb pa, oakes wj: the resolution of syringohydromyelia with-out hindbrain herniation after posterior fossa decompression. j neurosurg 89:212–216, 1998 8. karagoz f, izgi n, kapijcijoglu sencer s: morphometric measurements of the cranium in pa-tients with chiari type i malformation and comparison with the normal population. acta neuro-chir (wien) 2002, 144(2):165-71; 9. marin-padilla m, marin-padilla tm: morphogenesis of experimentally induced arnold--chiari malformation. j neurol sci 1981, 50(1):29-55. 10. marin-padilla m: notochordal-basichondrocranium relationships: abnormalities in experi-mental axial skeletal (dysraphic) disorders. j embryol exp morphol 1979, 53:15-38. 11. meadows j, kraut m, guarnieri m, haroun ri, carson bs: asymptomatic chiari type i mal-formations identified on magnetic resonance imaging. j neurosurg 92:920–926, 2000. 12. milhorat th, chou mw, trinidad em, kula rw, mandell m, wolpert c, speer mc: chiari i malformation redefined: clinical and radiographic findings for 364 symptomatic patients. neurosurgery 1999, 44(5):1005-1017. 13. nishikawa m, sakamoto h, hakuba a, nakanishi n, inoue y: pathogenesis of chiari mal-formation: a morphometric study of the posterior cranial fossa. j neurosurg 1997,86(1):40 47. 14. nyland h, krogness kg: size of posterior fossa in chiari type 1 malformation in adults. acta neurochir (wien) 1978, 40(34):233-242. 15. sekula rf jr, jannetta pj, casey kf, marchan em, sekula lk, mccrady cs: dimensions of the posterior fossa in patients symptomatic for chiari i malformation but without cerebellar ton-sillar descent. cerebrospinal fluid res. 2(1):11, 2005. 16. stovner lj, bergan u, nilsen g, sjaastad o: posterior cranial fossa dimensions in the chiari i malformation: relation to pathogenesis and clinical presentation. neuroradiology 1993, 35(2):113-118. 17. strahle j, muraszko km, garton hj et al, syrinx location and size according to etiology: iden-tification of chiariassociated syrinx. j neurosurg pediatr. 2015 jul;16(1):21-9. 18. tubbs rs, elton s, grabb p, dockery se, bartolucci aa, oakes wj: analysis of the posteri-or fossa in children with the chiari 0 malformation. neurosurgery 48:1050–1055, 2001 19. tubbs rs1, bailey m, barrow wc, loukas m, shoja mm, oakes wj. morphomet-ric analysis of the craniocervical juncture in children with chiari i malfor-mation and concomitant syringobulbia childs nerv syst. 2009 jun;25(6):689-92. doi: 10.1007/s00381-009-0810-1. 20. yuan zhou a, handong wang a, ning li chiari 0 malformation with syringomyelia sy-ringobulbia and syrinx cavity in pons interdisciplinary neurosurgery: advanced techniques and case management 6 (2016) 35– 37. doi: 10.33962/roneuro-2023-019 the curious case of commitment to religion and prayer in extreme long term survival anaplastic astrocytoma patient goran tasić, igor nikolić, lukas rasulić, aleksandar janićijević, vuk aleksić romanian neurosurgery (2023) xxxvii (1): pp. 115-119 doi: 10.33962/roneuro-2023-019 www.journals.lapub.co.uk/index.php/roneurosurgery the curious case of commitment to religion and prayer in extreme long term survival anaplastic astrocytoma patient goran tasić1,2, igor nikolić1,2, lukas rasulić1,2, aleksandar janićijević1,2, vuk aleksić3 1 clinic for neurosurgery, clinical centre of serbia, belgrade, serbia 2 medical faculty, university of belgrade, serbia 3 department of neurosurgery, clinical hospital centre zemun, belgrade, serbia abstract anaplastic astrocytoma who (world health organization) grade 3 represents about 7% of all primary brain tumours in the adult population. the standard treatment protocol involves safe surgical resection, chemotherapy and radiotherapy. advances in therapeutic protocols have been noted over the past few decades, but the prognoses are still poor with a median survival of 31 months. we present a case of a male patient who is alive 25 years after the initial diagnosis and treatment of anaplastic astrocytoma who grade 3. the patient was operated and reoperated two times due to local tumour recurrence in the first two years after the initial diagnosis. after the last operation, the patient abandoned medical therapy and started praying. the patient is still alive without any clinical or radiological signs of tumour recurrence. introduction anaplastic astrocytoma who (world health organization) grade 3 represents about 7% of all primary brain tumors in adults. the standard protocol for its treatment involves safe surgical resection, chemotherapy and radiotherapy. advances in therapeutic protocols have been noted over the past few decades, but the prognoses are still poor [1]. median survival is 31 months, and relative 5-year survival is about 23.6% and 10-year survival is only about 15.1% [2, 3]. however, it has been observed in clinical practice that some patients live longer than expected. we present a case report of a patient who is alive even 25 years after the initial diagnosis and treatment of anaplastic astrocytoma who grade 3, without any symptoms. and neurological deficits. case report we present a case of a mail patient who was examined for the first time in our institution when he was 23 years old. patient present with keywords anaplastic astrocytoma, long-term survival, prayer, religion corresponding author: vuk aleksić department of neurosurgery, clinical hospital centre zemun, belgrade, serbia aleksicvuk@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 116 goran tasić, igor nikolić, lukas rasulić et al epileptic seizure and headache, in early spring 1998. after a few seizures, brain computer tomography (ct) was performed and it showed infiltrative expansive lesion in the right temporal lobe and basal ganglia (figure 1). patients had left homonymous hemianopsia. after standard preoperative preparation, the patient was operated on in 1998, and maximal tumor reduction was achieved. the histopathological finding showed anaplastic astrocytoma who grade iii (figure 2). a few weeks after the operation he was on chemotherapy with lomustine (ccnu), 200 mg/m2, and radiotherapy with 60 gy in 30 fractions, which was well tolerated. patient had excellent recovery. figure 1. initial brain computed tomography (ct) performed right before first operation in 1998 showing expansive lesion of the right temporal lobe with perifocal edema. figure 2. histopathological finding of anaplastic astrocytoma who grade 3 (after first operation). figure 3. magnetic resonance imaging (mri) before third and last operation in 1999 showing tumor recurrence. however, five months after the first operation, patient was reoperated due tumor recurrence with a significant compressive effect and clinical and radiological signs of the brain herniation. after this operation, the patient was in good condition for another 5 months, after which he was again hospitalized because of the exacerbation of epileptic seizures with poor seizure control. the magnetic resonance imaging (mri) was immediately performed, and showed a tumor recurrence in the frontal part of the right temporal lobe with significant perifocal edema (figure 3). patient was reoperated once again with maximal tumor reduction. the histopathological finding again showed anaplastic astrocytoma who grade 3 without signs of further malignant progression. the oncologist prescribed carmustine (bcnu), 100 mg/m2, but patient rejected any further therapy. his neurological status improved significantly, with only residual left sided homonymous upper quadrant-anopsia at hospital discharge. instead of any other therapy, the patient turned to prayer, and agreed only to further clinical controls. during the next few months, the patient only had occasional headaches, and control mri in 1999 indicated small residual tumor with 1 cm in diameter. next year, the control mri showed a stationary finding without tumor progression. 117 the case of commitment to religion and prayer in extreme long term survival anaplastic astrocytoma patient patient was symptom free, without epileptic seizures. patient also abandoned antiepileptic therapy, and continued only praying. he went to a monastery and soon became an orthodox christian monk within the serbian orthodox church. in 2014, i.e. 14 years after the last control, patient visited our hospital due to symptoms of sciatica, and brain and spine mri was performed, and there were no signs of tumor presence (figure 4). spine mri showed degenerative changes without significant duroradicular compression, so the patient received conservative treatment, which led to a complete resolution of symptoms, and after a year, the patient was without any complaints, with completely normal neurological finding. figure 4. control magnetic resonance imaging (mri) from 2014 without signs of tumor presence. today, almost 25 years after the initial treatment, the patient lives at the chilandar monastery on the mount athos in greece (figure 5a). he spends about 8 hours per day in a prayer, and every day he drinks two drops of oil from a cresset placed in front of the icon of virgin mary (greek: panagia tricherousa, meaning “threehanded theotokos”), one of the most revered icons of the serbian orthodox church (figure 5b). figure 4. picture a is showing the chilandar monastery on the mount athos in greece. picture b is showing the icon of virgin mary. pictures are downloaded from the open-access internet. discussion our patient’s survival period after the treatment of anaplastic astrocytoma who grade iii is significantly longer than the median survival time. furthermore, he has been living without any symptoms for more than a 2 decades. what makes this case particularly noteworthy is the role of religiousness in the patient’s recovery. patient started praying following the third operation. subsequently he started practicing prayer for several hours per day. after the initial period of living as a novice in a monastery, he became a serbian orthodox church monk. religion, medicine, and healthcare have been interrelated in all population groups since the beginning of history [4, 5]. over the past 50 years, different studies have found aspects of religiousness to be positively associated with well-being, considered in a nonclinical sense as life satisfaction or happiness. feelings of optimism and hope have been speculated to be potential mediators of the influence of religiousness on well-being. the positive aspect of religiousness is characterized by “a secure relationship with god, a belief that there is meaning to be found in life, and a sense of spiritual connectedness with others” [6]. numerous studies discuss the influence of religion and spirituality not only on mental health, but also on health behavior. besides, there is growing evidence that reducing stress and negative emotions paired with the involvement of religiousness and spirituality should have a favorable impact on a host of physical diseases and on the response of those diseases to treatment [7-9]. until recently, religiousness and spirituality were set aside in clinical practice. but in the last two decades some of articles on the relationship of religiousness and health have been published in academic literature [10]. it has been shown that religiousness and spirituality are significantly related to positive physiological functions. a positive effect of prayer has been shown on cardiovascular functions in the population with a high risk for cardiovascular disease. it has also been found that those who are more religious have a lower blood pressure [5]. also, despite the difficulty in defining and measuring spirituality, a growing literature describes its importance in cancer patients and is connectivity with survivorship. religious beliefs influence patients' decision-making with respect to both aggressive care at the end of life as well as complementary therapies during treatment 118 goran tasić, igor nikolić, lukas rasulić et al [11]. in our case, the patient refused all therapy and turned exclusively to religion, and he grew stronger in his faith, so that today he spends more than 8 hours a day in prayer. furthermore, given the fact that the intact immune function is critical for health maintenance and disease prevention, including the control of malignant disease, particularly significant are the findings of a positive relationship between religiousness/spirituality and immune functions [12, 13]. high religiousness and spirituality has been related to significantly higher white blood cell count, total lymphocyte count, total t cells, and cytotoxic t cell activity [5]. in light of such findings, we can presume that in the case of our patient his intense prayer, as an aspect of religiousness and spirituality, contributed significantly to maintaining a good condition of his immune functions. also, to our knowledge, this is the first case of spontaneous regression of anaplastic astrocytoma who grade 3 tumor recurrence. although extremely rare, similar scenarios are described in literature as isolated case reports, such as significant regression of grade iv astrocytoma or glioblastoma multiforme (gbm). in this case authors hypothesized a plausible antineoplastic role of levetiracetam and dexamethasone [14]. although a similar explanation could be given in our case, since our patient was also treated with similar combination of drugs. however, our patient stopped all his drug therapy, including antiepileptic drugs while the tumor was still radiologically present. therefore, the clear temporal association between this therapy and the absence of tumor in our patient cannot be fully explained in this way. kumar and koshy described a case of a middle age women with a high-grade glioma of corpus callosum, e.g. a grade 3 anaplastic oligodendroglioma, who was operated and treated with chemotherapy and radiotherapy. the patient presented with tumor recurrence 5 years after the first operation. after another surgery the patient refused radiation therapy, and was given temozolomide and dexamethasone intermittently, with continuation of levetiracetam therapy. mri performed at 10-month follow-up showed significant remission [15]. although in this case a significantly longer survival than expected was achieved, a complete remission of the disease was not achieved, and the patient receives therapy all the time, which is assumed to have an antineoplastic effect as well, while in our patient any form of medical therapy is completely ruled out, and most importantly, there are no signs of tumor recurrence, neither clinical nor radiological. cancer is usually considered to be the worst of all illnesses and most people equate cancer with death [16]. numerous studies have examined relationships between religiousness and spirituality and either the onset or the outcome of cancer, including cancer mortality. most of these studies have found that those who are more engaged in religion, spirituality, and pray have a lower risk of developing cancer or have a better prognosis [5]. for example, one study exploring the influence of religiousness on breast cancer survival has shown an association between the lack of religiousness and poor breast cancer survival among african american women [17]. another study revealed an association between low levels of religious involvement and the risk of colon cancer [18]. in our case patient’s overall health, and especially length of survival is far beyond those expected for the given disease, since he is in good condition, without any signs or symptoms of tumor presence. however, the most impressive research on the relationship between religiousness/ spirituality and physical health is in the area of mortality. namely, it has been found that religiousness/spirituality is a predictive factor of greater longevity in 75% of all cases [5]. it has also been shown that prayer is one of the most frequently used forms of complementary and alternative medicine [11]. prayer can be defined as “the raising up of one’s mind to god”. also, prayer may be considered as the conscious act of opening oneself or activating a connection to a higher being. several types of prayer have been described, including: a) petitioner prayer, which is considered to be some specific request either for oneself or for others; b) colloquial prayer, i.e. a conversational type of prayer in which someone may ask for personal guidance, forgiveness, or general blessings; c) ritual prayer, which includes prayers from books; and d) meditative prayer, which includes reflection upon and adoration of the divine. specifically, it has been shown that one of the most frequent prayers is disease-centered prayer, which is directly related to patients’ illness [11]. based on the account of our patient, we can observe that his prayer comprises aspects of all the abovementioned types. 119 the case of commitment to religion and prayer in extreme long term survival anaplastic astrocytoma patient our patient’s case shows that prayer, as an additional way of positive personal attitude to one’s illness, could be considered as a possible supplementary suggested method, parallel to conventional medical treatment. based on this particular case and on the previous studies on the relationship between religiousness/spirituality and health, we can presume that prayer may have positive influence on the overall physical and psychological health state in cases of brain malignancies as well as in other cases of malignant diseases. references 1. sayegh et, oh t, fakurnejad s, oyon de, bloch o, parsa at. principles of surgery for malignant astrocytomas. semin oncol 2014; 41(4):523-31. 2. barker ca, chang m, beal k, chan ta. survival of patients treated with radiation therapy for anaplastic astrocytoma. radiol oncol 2014; 48(4):381-6. 3. smoll nr, hamilton b. incidence and relative survival of anaplastic astrocytomas. neuro oncol 2014; 16(10):14007. 4. koenig hg, king de, carson vb. a history of religion, medicine, and healthcare, in handbook of religion and health. oxford university press: new york, ny, usa. 2012:15-34. 5. koenig hg. religion, spirituality, and health: the research and clinical implications. isrn psychiatry 2012; 2012:278730. 6. van ness ph, larson d., religion, senescence, and mental health: the end of life is not the end of hope. am j geriatr psychiatry 2002; 10(4):386-97. 7. segerstrom sc, miller ge. psychological stress and the human immune system: a meta-analytic study of 30 years of inquiry. psychol bull. 2004; 130(4):601-30. 8. brown kw, levy ar, rosberger z, edgar l. psychological distress and cancer survival: a follow-up 10 years after diagnosis. psychosom med 2003; 65(4): 636-43. 9. russ tc, stamatakis e, hamer m, starr jm, kivimäki m, batty gd. association between psychological distress and mortality: individual participant pooled analysis of 10 prospective cohort studies. bmj 2012; 345:e4933. 10. fortin ah 6th, barnett kg. studentjama. medical school curricula in spirituality and medicine. jama 2004; 291(23):2883. 11. peteet jr, balboni mj. spirituality and religion in oncology. ca cancer j clin. 2013;63(4):280-289. 12. jors k, büssing a, hvidt nc, baumann k. personal prayer in patients dealing with chronic illness: a review of the research literature. evid based complement alternat med 2015; 2015:927973. 13. pace tw, n.l., adame dd, cole sp, sivilli ti, brown td, issa mj, raison cl. effect of compassion meditation on neuroendocrine, innate immune and behavioral responses to psychosocial stress. psychoneuroendocrinology 2009; 34(1):87-98. 14. peddi p, ajit ne, burton gv, el-osta h. regression of a glioblastoma multiforme: spontaneous versus a potential antineoplastic effect of dexamethasone and levetiracetam. bmj case rep. 2016;2016:bcr2016217393. 15. kumar aa, abraham koshy a. regression of recurrent high-grade glioma with temozolomide, dexamethasone, and levetiracetam: case report and review of the literature. world neurosurg. 2017;108:990.e11-990.e16. 16. ringdal gi. religiosity, quality of life, and survival in cancer patients. soc indic res 1996; 38(2):193-211. 17. van ness ph, kasl sv, jones ba. religion, race, and breast cancer survival. int j psychiatry med 2003; 33(4):357-75. 18. kinney ay, b.l., dudley wn, millikan rc, marshall e, martin c, sandler rs. roles of religious involvement and social support in the risk of colon cancer among blacks and whites. am j epidemiol 2003; 158(11):1097-107. doi: 10.33962/roneuro-2020-068 mri spectrum and prevalence of lumbar spinal degenerative disease in patients with non-traumatic low back pain neha singh, deepak kumar singh romanian neurosurgery (2020) xxxiv (1): pp. 427-433 doi: 10.33962/roneuro-2020-068 www.journals.lapub.co.uk/index.php/roneurosurgery mri spectrum and prevalence of lumbar spinal degenerative disease in patients with non-traumatic low back pain neha singh1, deepak kumar singh2 1 department of radiodiagnosis and imaging, dr. ram manohar, lohia institute of medical sciences, lucknow, india 2 department of neurosurgery, dr. ram manohar, lohia institute of medical sciences, lucknow, india abstract background. low back pain (lbp) is a frequent cause of global disability and activity limitation. in the majority of cases, lbp is nonspecific, yet diagnostic confirmation is required to rule out serious underlying pathologies such as infection, tumour, fracture or degenerative disease. it can be done by a number of imaging techniques. of all available techniques, mri is currently the imaging modality of choice owing to lack of radiation, multiplanar reformation capabilities and high contrast resolution. objectives. to determine various mri patterns and the common sites of spinal degenerative lesions among patients with lbp. method. this study was conducted on 622 patients suffering from non-traumatic lbp, referred for mri of the lumbar spine. mri database of the study population were analysed using axial t2-weighted, sagittal stir, t1and t2-weighted and coronal stir images. after excluding patients with h/o prior surgery and mr findings suggesting infective or neoplastic etiologies, 598 patients constituted the sample size of our study. results. a review of 598 patients with lbp revealed that degenerative changes in intervertebral disc were the most common abnormality detected. among these, disc bulge was the most common abnormality followed by disc desiccation, protrusion, extrusion, hiz/annular tear, reduced ivd space and schmorl’s nodes. other nondisc degenerative findings were modic endplate changes, facet joint arthropathy, osteophytes, spinal canal stenosis and ligamentum flavum hypertrophy. conclusions. results reported the common occurrence of lumbar disc degenerative disease in patients with low backache. research efforts should attempt to trim down risk factors and perk up the quality of life. introduction low back pain (lbp) is one of the most common causes of hospital visits and is the leading cause of activity limitations and work absences in many parts of the world.[1,25,9]in the 2016 global burden of disease study, musculoskeletal conditions were the second highest contributor to global disability, and lower back pain remained the single leading cause of disability.[32] lbp poses a considerable monetary menace to keywords degenerative changes, disc bulge, facet hypertrophy, intervertebral disc, low back pain, sciatica corresponding author: neha singh department of radiodiagnosis and imaging, dr. ram manohar, lohia institute of medical sciences, lucknow, india neha.singh.dr@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 428 neha singh, deepak kumar singh the individual, family, workplace and society. patients presenting with lbp frequently need imaging investigations to determine the cause. standard radiography isusually the first investigation to perform, with mri or ct only usedfor further workup [10]. despite technical advancements inimaging, the specificcause of the pain can only be determined in less than 50% of cases [7]. this study was conductedto determine various mri patterns and the common sites of spinal degenerative lesions among patients with lbp. materials and methods this study was conducted on patients with lbp referred to radiology department of dr ram manohar lohia institute of medical sciences, lucknow for mri of lumbosacral spine. it was a cross sectional observational study conducted from june 2017 to may 2018. permission for study was taken from the ethics committee of our institute. consent from all patients was taken before their enrolment in the study. patients name, age, sex and detailed history were obtained. mri of the lumbar spine was performed with a 3 t (ge) mr imager using spine phased array coils. the scans consisted of axial t2weighted, sagittal stir, t1and t2-weighted and coronal stir images with slice thickness of 4.0mm for each plane. a field of view of 30x30mm for sagittal and coronal images and 18x18mm for axial images were used. the images were stored directly as dicom files in the workstation. inclusion criteria: all patients with non-traumatic lbp referred for mri lumbosacral spine. exclusion criteria: patients with history of recent trauma; prior lumbar spine surgery; metallic implants and pacemakers; and cases with mr findings s/o infective or neoplastic etiology. statistical analysis -statistical analysis was done using spss 15 software. percentages were calculated for the various categories. results there were 622 patients of lbp referred for mri to radiodiagnosis department. out of these 24 were excluded from the study as 18 had radiological diagnosis of infective pathology and 6 had neoplastic etiology. a total of 598 patients constituted the sample size of the study. out of the total patients there were 278 males (46.49%) and 320 (53.51%) females. the age of the patients ranged from 18 years to 80 years. most common age group was between 31 to 40 years (33.76%). distribution of various degenerative spinal abnormalities detected on mri is shown in table 1. type of abnormality frequency (%) disc bulge 72 disc dessication 69.56 disc protrusion 27.42 disc extrusion 4.34 disc sequestration 0.83 hiz /annular tear 28.12 schmorl’s nodes 12.67 osteophytes 51.83 facetal arthropathy 30.43 modic changes 23.21 flaval hypertrophy 13.04 spinal stenosis 53.54 vertebral collapse 6.5 transitional vertebra 6.8 spinal listhesis 5.2 table 1. distribution of various degenerative spinal abnormalities detected on mri. degenerative changes in intervertebral disc were the most common abnormality detected. among these, disc bulge was most common abnormality, constituting 72% of the total study population. it was followed by disc dessication (in 69.56%), disc protrusion (in 27.42%), disc extrusion (in 4.34%) (fig1), hiz/annular tear (in 28.12%), reduced ivd space (in 20.54%) and schmorl’s nodes in 12.67% of the patients (fig-2). figure 1. t2w sagittal and axial images of ls spine show disc bulge (a, b), disc protrusion (c, d), disc extrusion (e, f) and sequestration (g, h) marked by arrows. 429 mri spectrum and prevalence of lumbar spinal degenerative disease in patients with non-traumatic low back pain figure 2. t2w sagittal images show multiple level disc desiccation with grade 5 changes at l5/s1 level (arrow in fig a), multiple schmorl nodes (b) and posterior high intensity zone at l3/4 level (c, d). other nondisc degenerative findings were modic end plate changes (in 23.21%), facet joint arthropathy (in 30.43%), osteophytes (in 51.83%), (fig-3). spinal canal stenosis in 53.54% and ligamentum flavum hypertrophy (in 13.04%) of patients (fig-4). other less commonlyseen but important findings included: vertebral collapse (in 9.1%), transitional vertebral complex (in 6.8%) and spinal listhesis (in 5.2% of the population) (fig-5). in our study, disc bulge was the most common abnormality (72%) seen in patients with low back ache. it was most commonly seen at l4-l5 (in 39.30%) followed by l5-s1 (in 28.14%) and l3/4 (in 24.18%) levels. single level bulge was seen in less than a quarter of patients, (in 24.18%) while multiple level involvement was a more frequent finding (in 75.82%). posterocentral disc bulge was most commonly seen followed by paracentral, forminal and extraforaminal types. figure 3. a) sagittal t1wi shows modic 2 end plate changes. b) sagittal t2wi shows marginal osteophytes. axial t2wi show ligamentumflavum hypertrophy (c) and facet joint hypertrophy (d). figure 4. axial t2wi show central canal stenosis (a), lateral recess stenosis (b) and neural foramina stenosis (c). disc dessication was the 2nd most common abnormality detected in 69.56% of total study population. grade 3 degenerative changes were the most common pattern followed by grade 4 and 5 changes. all these changes were most commonly involving l4/5 and l5/s1 levels. 430 neha singh, deepak kumar singh figure 5. sagittal t2wi show vertebral collapse (a), spondylolisthesis (b) and transitional vertebral complex (c). no sex predilection was noted in cases of disc prolapse. most common age of presentation for both protruded and extruded disc was 31-40 years. disc protrusion was seen in 27.42% of total sample size, most commonly identified at l4-l5 (48%) and l5-s1 (29%) levels. posterocentral disc protrusion (68.2%) was most common type followed by paracentral and forminal protrusions. disc extrusion was demonstrated in 4.34% of the population, most common level being l4/5 followed by l5/s1.posterocentral type extrusion was most frequently seen. disc sequestration was seen in only 5 patients constituting 0.83% of total study population. annular tear is characterised by t2w focal hyperintensity, described as high intensity zone (hiz) in posterior annulus of the disc. it was noted in 28.12% of the total study population and was most prevalent at l4/5 and l5/s1 levels. these changes were most commonly seen between 60-80-year age group. schmorl’s nodes were seen in 12.67% of the cases and were most commonly involving 21-40yr age group males. lumbar canal stenosis was noted in 53.54% of the study population without any sex predilection. multilevel involvement and bi-laterality was the most common presentation in this study. bilateral lateral recess stenosis was most common pattern (in 58.68%) followed by bilateral foraminal stenosis in 23.24% and central stenosis in 18.08%. these patterns can be seen unaccompanied or in amalgamation. spondylolisthesis was demonstrated in 5.2% of population. most common level involved was l4 over l5 and l5 over s1. vertebral collapse was noted in 6.5% of the cases with anterior wedge collapsebeing the most common type. lumbosacral transitional vertebral complex (lstv) was detected in 6.8% of the population. majority of the cases were showing sacralization of l5 vertebra with occasional occurrence of lumbarization of s1. our study demonstrated vertebral end plate changes in 23.21% of cases. modic type i and type ii changes were seen in 3.16% and 20.05% of the population respectively. these changes were most commonly seen after age of 50 years. marginal osteophytes were reported in 51.83% of our study population. facetal arthropathy was seen in 30.43% of cases and was more common in elderly patients. most common vertebral level involved was l4/5 followed by l5/s1. ligamentumflavum hypertrophy was noted in 13.04 % of the study population. discussion low back pain (lbp) is an important public health problem with many possible etiologies and uneven distribution. as a result, the existingenormous literature on lbp is not only heterogeneous but also conflicting. according to a global review published in 2012, point prevalence of lbp was 11.9%+2.0%, overall mean prevalence was 31.0%+ 0.6%, and the lifetime prevalence was 39.9% +24.3%.[12] studies on indian population have shown the prevalence ranging between 6.2% in general population to 92% in heavy physical workers. such great variation can be attributed to the heterogeneity of the population.[4] the diagnostic accuracy of mri for degenerative conditions of spine is high. mri is 75% sensitive and 77% specific in diagnosing nucleus pulposus herniation, resulting in a positive predictive value of 84% and a negative predictive value of 64%.[30] similar studies have shown high sensitivity of 96% coupled with lower specificity of 75% in the identificationof spinal stenosis[2] and sensitivity of 92% tied with higher specificity of 100% in evaluation of nerve root compression [6]. our study demonstrated female predilection for lbp seen in 53.51% females and 46.49% males. it was in accordance with systematic review of the global prevalence of low back pain [12]and studies conducted on indian population [23,26]. most common age group who presented with lbp was 31-40 years (33.76%), an age group that is usually involved in strenuous physical activity. these 431 mri spectrum and prevalence of lumbar spinal degenerative disease in patients with non-traumatic low back pain results were in accordance with those found by kopec [17]. in our study, disc bulge was the most common pathology seen in 72% of cases which correlated well with previous studies [34]. it was seen most commonly at l4-5 level followed by l5-s1 and l3-4 levels respectively. these findings correlated well with study by ma d et al [20]. in our study, single level bulge was seen in less than a quarter of patients with multiple level involvements being a more frequent finding. this finding was in accordance with studies by pokhraj suthar et al [28] and osman et al [24]. posterocentral disc bulge was most common type followed by paracentral and forminal bulge. these findings were well supported by pintu et al [5]. disc desiccation was the 2nd most common abnormality detected in 69.56% of total study population with the last two lumbar levels clearly predominating.these findings were supported by study done by jarvik jg et al [15].while the gradesof disc degeneration are not much taken into account in the literature, so-called ‘discreet or grade 3’ changes seem to be more common than ‘moderate to severe (grade 4/5)’ changes [31]. disc protrusion was next most common abnormality detected in 27.42% of population. this is unlike the findings of pokhraj et al [28] who found disc protrusions in 62.24% and disc bulges in 27.39% of population. this discrepancy could be owing to preponderance of younger individuals in our study. study by pintu biswas demonstrated high incidence of disc bulge (71.59%) as compared to protrusions (8.8%). [5) disc protrusions were mostly seen in 6080-year-old individuals, most common level being l4-l5 (48%) and l5-s1 (29%). disc extrusion was seen in 4.34% of the population, most common level being l4/5 followed by l5/s1. these findings correlated well with study by jacob et al [13]. disc sequestration was seen in only 5 patients constituting 0.83% of total study population. annular tear was noted in 28.12% of the total study population. it corresponds to a previous study by aprill and bogduk, which reported 28% prevalence of annular tear in patients with back pain. this study also concluded that hiz was highly specific and strongly predictive of a painful disc. [3] schmorl’s nodes were seen in 12.67% of the cases and were most commonly involving 21-40yr age group males. these findings correlated well with study by jagannath d et al who reported the prevalence of 9.2% and these features being most common in 4th decade. [14] lumbar canal stenosis was noted in 53.54% of the study population whereas study by shobeiri e et al revealed lower number of cases seen only in 37% of the cases.[27] bilateralism and multilevel involvementwas mostcommon presentation in our study. spinal stenosis can be central, lateral recess or foraminal. central stenosis is a result of hypertrophy of the inferior facet articular process of cephalic vertebra. lateral recess and foraminal stenosis occurs due to hypertrophy of the superior facet articular process of caudal vertebra.[19] bilateral lateral recess stenosis was most common pattern (in 58.68%) followed by bilateral foraminal stenosis in 23.24% and central stenosis in 18.08%. these patterns can be seen unaccompanied or in amalgamation. spondylolisthesis was found in 5.2% of study population, with obvious female predilection. in a study performed by frennered et al. the prevalence of spondylolisthesis in patients with lbp was estimated to be 2.5% which is less than that in present study. [8] recent studies like he et al. and layegh m, hejazian e. estimated higher prevalence [13%] than what was approved in our study [11,18]. most common level involved was l4 over l5 followed by l5 over s1which correlated well with previous studies. [18] vertebral collapse was noted in 6.5% of the cases with anterior wedge collapse being the most common type seen in approximately 80% cases. it was higher as compared to the study bymustapha et al who found wedge collapse in just 1.97% of the cases. it can be explained by higher number of female patients in our study whereas the previous study was a male predominant study [22]. lumbosacral transitional vertebral complex was seen in 6.8% of the population. majority of the cases had sacralized l5 vertebra and only few cases had lumbarized s1. study by layegh on iranian population found the prevalence of lstv to be 9.8%. of all patients, 8.2% had sacralisation of l5 and 1.6% had lumbarisation of s1 [18]. our study demonstrated vertebral end plate changes in 23.21% of cases. systemic review by tue secher documented that median prevalence of end plate changes is 43% in patients with non-specific lbp [29]. type i and type ii changes were seen in 432 neha singh, deepak kumar singh 3.16% and 20.05% of the population respectively. these findings correlated well with the original study of modic et al which demonstrated that type 2 changes were the most frequent and may account for up to 90% of modic changes.[21] marginal osteophytes were reported in 51.83% of our study population. nemoto found osteophytes in 46% of patients and there was no difference between patients with and without back pain. [24] facetal arthropathy was seen in 30.43% of cases and was more common in elderly patients. although study done by p y yong et al was correlating with our study as the prevalence was 29.8%. [33] study by a.k. kohat et al had shown very high prevalence (75%) of facet joint arthropathy in chronic low backache patients. [16] most common vertebral level involved was l4/5 followed by l5/s1which is supported by both the previously mentioned studies. ligamentum flavum hypertrophy was noted in 13.04 % of our study population. it was in accordance with study by py yong et al (prevalence 14.0%) but very low as compared to study by kohat (prevalence 70.8%). it was predominantly seen at lower lumbar levels (l4/l5 and l5/s1). conclusion degenerative disease of the lumbar spine is a common condition that radiologists will come across frequently. role of diagnostic imaging in patients with low back pain is to provide precise anatomic information which in turn affects the management. mri is a mainstay in the evaluation of low back pain and degenerative disease of the lumbar spine. this paper highlights a variety of degenerative patterns affecting the vertebral bodies, intervertebral discs, facet joints, and ligamentum flava, as well as the collective effects of these changes on the spinal canal and neural foramina. references 1. andersson gb. epidemiological features of chronic lowback pain. lancet. 354:581–585,1999. 2. aota y, niwa t, yoshikawa k et al. magnetic resonance imaging and magnetic resonance myelography in the presurgical diagnosis of lumbar foraminal stenosis. spine 32(8):896-903,2007. 3. aprill c, bogduk n. high-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. br j radiol 65:361-369,1992. 4. bindra s, sinha a.g.k., benjamin a.i. epidemiology of low back pain in indian population: a review. international journal of basic and applied medical sciences .5 (1):166179,2015. 5. biswas p, de a. evaluation of degenerative disease of lumbosacral spine by 3 tesla mri. j. evolution med. dent. sci. 7(3): 384-390,2018. 6. chawalparit o, churojana a, chiewvit p et al. the limited protocol mri in diagnosis of lumbar disc herniation.j medassoc thai. 89:182–189,2006. 7. finch p. technology insight: imaging of low back pain. nat clinpractrheumatol 2(10):554—61,2006. 8. frennered k. isthmic spondylolisthesis among patients receiving disability pension under the diagnosis of chronic low back pain syndromes. spine (phila pa 1976).19(24):2766-9, 1994. 9. hart lg, deyo ra, cherkin dc. physician office visits for low back pain: frequency, clinical evaluation, and treatment patterns from a u.s. national survey. spine (phila pa 1976) 20:11–19,1995. 10. has-sante.fr. [homepage on the internet]. diagnostic, prise encharge et suivi des maladesatteints de lombalgiechronique.inc.; © 2000—01. available from: http://www.has-sante.fr/(access in december 2000). 11. he lc, wang yx, gong js et al. prevalence and risk factors of lumbar spondylolisthesis in elderly chinese men and women.eurradiol. 24(2):441-8,2014. 12. hoy d, bain c, williams g et al. a systematic review of the global prevalence of low back pain.arthritis rheum 64:2028–2037,2012. 13. jacob m, akoko lo, kazema rr. lumbar disc degenerative disease: magnetic resonance imaging findings in patients with low back pain in dar es salaam. east & central african journal of surgery. 20(1):122131,2015. 14. jagannathan d, indiran v, hithaya f.prevalence and clinical relevance of schmorl's nodes on magnetic resonance imaging in a tertiary hospital in southern india. j clindiagn res.10(5):06-9,2016. 15. jarvik jg, deyo ra. diagnostic evaluation of low back pain with emphasis on imaging. ann intern med 137(7):586— 97,2002. 16. kohat ak, kalita j, ramanivas s, misra uk, phadke rv. clinical significance of magnetic resonance imaging findings in chronic low backache. indian j med res 145:796-803,2017. 17. kopec ja, sayre ec, esdaile jm. predictors of back pain in a general population cohort. spine. 29(1):70-7, 2004. 18. layegh m, hejazian e. prevalence of spondylolysis and spondylolisthesis in patients afflicted with chronic back pain in babol city, iran, during 2012 and 2013. iran j neurosurg. 3(1):8-14,2017. 19. lee sy, kim th, oh jk, lee sj, park ms. lumbar stenosis: a recent update by review of literature. asian spine journal .9(5):818-828, 2015. 20. ma d, liang y, wang d et al. trend of the incidence of lumbar disc herniation: decreasing with aging in the elderly. clininterv aging. 8:1047-50, 2013. 21. modic mt, steinberg pm, ross js, et al. degenerative disk 433 mri spectrum and prevalence of lumbar spinal degenerative disease in patients with non-traumatic low back pain disease: assessment of changes in vertebral body marrow with mr imaging. radiology 166:193–99,1988. 22. mustapha z, ahmadu ms, abbas aa, ibrahim k & okedayo m. patterns of requests and findings in magnetic resonance imaging (mri) of the lumbosacral spine at university of maiduguri teaching hospital, northeastern nigeria. iosr journal of dental and medical sciences 11(4):18-24,2013. 23. nazeer m, rao sm, soni s, ravinder m, ramakranthi t, bhupathi s. low back pain in south indians: causative factors and preventive measures. sch. j. app. med. sci. 234-243,2015. 24. nemoto o, kitada a, naitou s et al. a longitudinal study for incidence of low back pain and radiological changes of lumbar spine in asymptomatic japanese military young adults. eur spine j 22:453-8,2013. 25. osman nm, fawzy fm, lateef hm.mri evaluation of lumbar disc degenerative disease. the egyptian journal of hospital medicine 68(2):1202-1207 ,2017. 26. papageorgiou ac, croft pr, ferry s, jayson mi, silman aj. estimating the prevalence of low back pain in the general population: evidence from the south manchester back pain survey. spine (phila pa 1976) 20:1889–1894, 1995. 27. ramdas j, jella v. international journal of advances in medicine. 5(5):1120-112, 2018. 28. shobeiri e, khalatbari mr, taheri ms, tofighirad n, moharamzad y. magnetic resonance imaging characteristics of patients with low back pain and those with sciatica singapore med j. 50(1):87-93,2009. 29. suthar p, patel r, mehta c, patel n.mri evaluation of lumbar disc degenerative disease. j clindiagn res. 9(4): tc04–tc09,2015. 30. tue sj, jaro k, joan ss, jaakko n, charlotte ly. vertebral endplate signal changes (modic change): a systematic literature review of prevalence and association with nonspecific low back pain. eur spine j. 17:1407–1422,2008. 31. wassenaar m, van rijn rm, van tulder mw et al. magnetic resonance imaging for diagnosing lumbar spinal pathology in adult patients with low back pain or sciatica: a diagnostic systematic review. eur spine j 21:220– 227,2012. 32. weishaupt d, zanetti m, hodler j, boos n. mr imaging of thelumbar spine: prevalence of intervertebral disk extrusion andsequestration, nerve root compression, end plate abnormalities, and osteoarthritis of the facet joints in asymptomaticvolunteers. radiology 209(3):661—6,1998. 33. who fact sheet february : musculskeletal disorders,2016. 34. yong py, alias naa, shuaib il. correlation of clinical presentation, radiography, and magnetic resonance imaging for low back pain — a preliminary survey. j hk coll radiol 6:144-151,2003. 35. younis f, shahzad r, rasool f. correlation of magnetic resonance patterns of lumbar disc disease with clinical symptomatology of patients. annals of king edward medical university. 17(1):41-47, 2011. romanian neurosurgery (2019) xxxiii, 1: 31-33 doi: 10.33962/roneuro-2019-005 www.journals.lapub.co.uk/index.php/roneurosurgery neuromodulation devices nowadays r.e. rizea1,2, karina lidia gheorghita2, gh. david3, a.v. ciurea4 1 neurosurgery department, “bagdasar-arseni” emergency neurosurgery hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 neurosurgery department, “regina maria” military hospital, brasov, romania 4 neurosurgery department, sanador hospital, bucharest, romania abstract introduction. neuromodulation devices have known a great progress in the past years being used in treatment of drug resistant neurological diseases such as epilepsies and migraines. a neuromodulation device can stimulate profound or superficial neural pathways in order to balance chronic drug-resistant disorders that involve disturbances of cellular electrical potentials. material. cranial neuromodulation devices implants used until now usually determined skull irregularities, implant site infection, resorption of the bone flap or osteomyelitis. in order to solve these problems, it was needed a customized cranial implant that integrates the neuromodulation device. we report the first description of a fully integrated neuromodulation device within a customized cranial implant, publicised in 2018 by gordon et al., that demonstrates the utility of a computerized neurostimulation device combined with clear customdesigned cranial implant. conclusion. the new approach of neurotechnology confines a better solution for neuroimplants devices with less follow-up complications and great patient’s satisfaction. introduction neuromodulation devices stimulate profound or superficial neural pathways in order to balance chronic drug-resistant disorders that involve disturbances of cellular electrical potentials, such as epilepsies and migraines. most of the cranial neuromodulation device implants used until now had adverse reactions like skull irregularities, implant site infection, resorption of the bone flap or osteomyelitis [1-5]. material we report the first description of a fully integrated neuromodulation device within a customized cranial implant, publicised in 2018 by gordon et al., that demonstrates the utility of a computerized neurostimulation device combined with clear custom-designed cranial implant. keywords neuromodulation devices, neurostimulation, drug resistant epilepsy, customized cranial implant corresponding author: a.v. ciurea neurosurgery department, sanador hospital, bucharest, romania avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 32 r.e. rizea, karina lidia gheorghita, gr. david, a.v. ciurea modern day treatment for drug resistant neurological diseases has known a great progress during past years. in 2018, gordon et al. from johns hopkins hospital, maryland, usa, reported first in-human experience using a neuromodulation device within a cranial implant. the neuromodulation was used before in drug resistant epilepsies and migraines [1,2]. it is well known that one in three patients with focal seizures develops a drug resistant form of epilepsy. patients with focal seizures who have failed multiple drug associated treatment that do not fit neurosurgical approach need vagus nerve stimulation or responsive neurostimulation [1,3,4,5]. the responsive neurostimulation system, approved by the fda in 2013, is used for patients that have drug resistant epilepsy with less than 2 epileptogenic foci and it has a cortical stimulator that detects and respond to the electroencephalographic events [1,6]. even though it has a great efficacy, there has been reported a lot of complications about the montage of the device, such as: scalp dehiscence, device exposure, contamination of hardware, infections, contour irregularities, bone flap osteomyelitis, visual deformities that affect quality of patient’s life [1,7,8]. in order to solve all these problems and to reduce the number of re-interventions that increases the risk of infections, gordon et al. started to plan a new improved implant design. they changed the opaque material used before with a transparent one for a better visibility and accuracy of the positioning to avoid the electrocorticographic signal interference. all the components of the device were integrated below the implant as an incorporated piece, fact that prevents the obvious deformities of the skull and scalp and the migration of the device into the scalp [1, 9-11]. discussion gordon et al. used a 54 years old drug resistant epilepsy patient who needed responsive neurostimulation device with cranioplasty. a multidisciplinary team formed by neurosurgeons and plastic surgeons produced a perfect size 3d printed mold of the patient’s skull that was computer-laser modified with a 5-axis robot laser cutter and after that presterilised [1,12,13]. the responsive neurostimulation device with the leads were placed under the clear cranial implant making possible a perfect visualization of the connections and possible inadvertent device interference. the patient was fully recovered with no complications. this was the first description of a fully integrated neuromodulation device within a customized cranial implant [1,13,14]. the method allows the avoidance of visible irregularities, scalp dehiscence, device extrusion and lead migration identified as complications of standard procedures above skull. the technology of cranial implants is expected to develop and treat other brain pathologies such as tumours and movement disorders and maybe it can be implicated more in intelligent cognition devices for memory diseases [1]. conclusion we can make a conclusion that the new approach of neurotechnology confines a better solution for neuroimplants devices with less follow-up complications and great patient’s satisfaction. it is a great demonstration that can inspire new research in other brain pathologies that can use computerized neurostimulation device combined with clear custom-designed cranial implant [1, 15, 16]. references 1. gordon cr, santiago gf, huang j, bergey gk, liu s., armand m, brem h, anderson ws; first in-human experience with complete integration of neuromodulation device within a customized cranial implant, operative neurosurgery, volume 15, issue 1, 1 july 2018, pages 39–45, https://doi.org/10.1093/ons/opx210 2. kwan p, brodie mj. early identification of refractory epilepsy. n engl j med. 2000;342(5):314-319. 3. morris gl 3rd, gloss d, buchhalter j, mack kj, nickels k, harden c. evidence-based guideline update: vagus nerve stimulation for the treatment of epilepsy: report of the guideline development subcommittee of the american academy of neurology. neurology. 2013;81(16):1453-1459. 4. collins kl, lehmann em, patil pg. deep brain stimulation for movement disorders. neurobiol dis. 2010;38(3):338-345. 5. fisher rs, velasco al. electrical brain stimulation for epilepsy. nat rev neurol. 2014;10(5):261-270. 6. rns system in epilepsy study groupmorrell mj. responsive cortical stimulation for the treatment of medically intractable partial epilepsy. neurology. 2011;77(13):1295-1304. 7. lopez j, zhong ss, sankey ew, et al. time interval reduction for delayed implant-based cranioplasty 33 neuromodulation devices nowadays reconstruction in the setting of previous bone flap osteomyelitis. plast reconstr surg. 2016; 137(2): 394e-404e. 8. berli ju, thomaier l, zhong s, et al. immediate single-stage cranioplasty following calvarial resection for benign and malignant skull neoplasms using customized craniofacial implants. j craniofac surg. 2015;26(5):1456-1462. 9. wei z, gordon cr, bergey gk, sacks jm, anderson ws. implant site infection and bone flap osteomyelitis associated with the neuropace responsive neurostimulation system. world neurosurg. 2016;88(687): e1-e6. 10. heck cn, king-stephens d, massey ad, et al. twoyear seizure reduction in adults with medically intractable partial onset epilepsy treated with responsive neurostimulation: final results of the rns system pivotal trial. epilepsia. 2014;55(3):432-441. 11. bergey gk, morrell mj, mizrahi em, et al. long-term treatment with responsive brain stimulation in adults with refractory partial seizures. neurology. 2015;84(8):810-817. 12. zhong s,huang gj, susarla sm, swanson ew,huang j, gordon cr. quantitative analysis of dual-purpose, patient-specific craniofacial implants for correction of temporal deformity. neurosurgery. 2015;11(suppl 2):220-229; discussion 229. 13. liu j, fang j, murphy r, gordon cr, armand m. design and development of 5-axis cranial implant laser cutting system. in: proceedings of the asme 2017 international design engineering technical conferences & computers and information in engineering conference. idetc/cie; 2017. 14. alambeigi f, sefati s, murphy r, armand m, gordon cr, liu s. a cutting machine for resizing raw implants during surgery. wo 2016 086049. u.s. international patent application number pct/us2015/062516. published february 6, 2016. 15. anderson ws, kossoff eh, bergey gk, jallo gi. implantation of a responsive neurostimulator device in patients with refractory epilepsy. neurosurg focus. 2008;25(3): e12. 16. gordon c, bryndza jr, basic t. patient-specific craniofacial implants. issued patent 20160081805. published march 24, 2016. doi: 10.33962/roneuro-2023-029 management of brain aneurysm neck avulsion during clipping surgery. illustrative case and literature review teeba a. al-ageely, mustafa ismail, salima b. alsaadi, fatima f. salim, zahraa m. kareem, sura h. talib, huda jaafer, samer hoz romanian neurosurgery (2023) xxxvii (2): pp. 164-169 doi: 10.33962/roneuro-2023-029 www.journals.lapub.co.uk/index.php/roneurosurgery management of brain aneurysm neckavulsion during clipping surgery. illustrative case and literature review teeba a. al-ageely1, mustafa ismail1, salima b. alsaadi2, fatima f. salim1, zahraa m. kareem1, sura h. talib3, huda jaafer1, samer hoz4 1 college of medicine, university of baghdad, baghdad, iraq 2 department of radiology, al-hadi university college, baghdad, iraq 3 college of medicine, al-mustansiriyah university, baghdad, iraq 4 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract background. intra-operative rupture (ior) of intracranial aneurysms is a critical event affecting the operation course and the patient’s outcome. however, a rupture induced by an avulsion in the aneurysmal neck is exceedingly challenging, as sealing the neck tear by clip application might result in ischemic injury due to parent vessel occlusion. here we reviewed the literature regarding the intraoperative avulsion of the aneurysmal neck with an illustrative case to provide explanations of its surgical management intricacies. methods. a midline pubmed literature review was performed using the following keywords; (aneurysm) and (neck) and (surgery or clipping) and (tear or avulsion). fifty-three results were found initially. after excluding non-human subject studies, and non-english studies, two independent researchers examined the title and the abstract for the cases of neck tear or avulsion with its management. results. fourteen articles were found to be included in this study. the average age of the cases is around 57 years. the percentages of females in the review were 62% (8/13), and among the males, 38% (5/13). regarding the locations, pcoma and acoma were both 23% (3/13) of the cases; other locations include aca, 15%, and mca, 15%. the surgical techniques that opted from the literature include the cotton clip method, clip wrapping, parallel clipping and micro-suturing conclusion. ior due to aneurysmal neck avulsion is a devastating surgical complication, and its management may differ according to the extent of the rupture. choosing the most convenient technique depends on the surgeon’s knowledge and experience. introduction intra-operative rupture (ior) of intracranial aneurysms is a catastrophic event that can adversely affect the course of the operation and the patient’s outcome (3). although there is a continuous decrease in the ior due to microscope introduction in the neurosurgical field, the keywords aneurysmal neck tear, aneurysmal neck avulsion, intraoperative aneurysmal rupture corresponding author: samer hoz department of neurosurgery, university of cincinnati, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 165 management of brain aneurysm neck-avulsion during clipping surgery incidence of aneurysmal ior has reached approximately 20%, ranging from 5.5 to 40 % (7, 9, 16). it is commonly encountered in anterior communicating artery (acoma) aneurysms which are estimated by 40 % of all ior (20), and the risk is significantly increased in ruptured versus unruptured acoma aneurysms (8). the dome of an aneurysm is the most common site for ior, reaching up to 29% of the cases (20). in surgery, a clip application to the neck of the aneurysm may cease the ior of an aneurysmal dome origin (1). however, a rupture induced by a tear in the aneurysmal neck is far more challenging (10), as sealing the neck tear by clip application might result in ischemic injury due to parent vessel occlusion. ior due to aneurysmal neck tear has been well stated in the literature, yet, there is scarcity regarding its operative management (1,4,10,11). here we reviewed the literature regarding the intraoperative avulsion of the aneurysmal neck with an illustrative case, to provide explanations of its surgical management intricacies. case scenario a 44-year-old female presented with behavioral changes, aphasia, headache, and right-sided weakness of grade 3 on the medical research council of canada (mrc) scale. preoperative computed tomography (ct) scan (figure.1) findings included left sylvian subarachnoid hemorrhage (sah) along with interhemispheric hemorrhage. preoperative ct angiography (cta) (figure. 2) showed a right saccular superiorly-directing anterior communicating artery (acoma) aneurysm. figure 1. preoperative ct scan, axial section revealing the left sylvain sah along with interhemispheric haemorrhage. intraoperatively, the right lateral supraorbital approach was performed following the typical steps of surgery. after meticulous dissection, ior was encountered during the initial clip application. it is caused by a tear (avulsion) in the aneurysmal neck; two suction devices were applied in the surgical field alongside attempts for micro-suturing of the rupture site were carried out but weren’t successful as the neck tear was extending to the acoma. figure 2. pre-operative cta showing a superiorly directed saccular aneurysm from the acoma. figure 3. postoperative ct scan, axial section, showing the location of acoma clips as a metallic artifact. temporary clips were placed to regain haemostasis. intra-operative neurophysiological monitoring (ionm), including somatosensory evoked potential (sep) and motor evoked potential (mep), revealed intact motor function in the right lower limbs and no findings of paresis that can be induced by the expected ischemia caused by the temporary clips. a final decision for permanently clipping the acoma 166 teeba a. al-ageely, mustafa ismail, salima b. alsaadi et al. aneurysm was made. a postoperative ct scan (figure. 3) showed no complication of sah or interventricular haemorrhage (ivh). postoperatively, the patient’s glasgow coma scale (gcs) was 13 with the same preoperative weakness. the gcs improved over the next two weeks with the resolution of the right-sided weakness. discussion ior is considered one of the most challenging complications of the surgical management of cerebral aneurysms, with a major influence on patient morbidity and mortality (2,3). similar to other surgical complications, numerous measures are taken to prevent the occurrence of ior; this includes sufficient exposure to the aneurysm, sharp dissection, and the use of temporary clips (1, 6). despite the advances in neurosurgical approaches, techniques, and instruments, aneurysmal ior is still a well-known surgical complication that can impact the surgical procedure and the patient’s prognosis (12). the classification of ior depends on the specific times within the surgery, which include: predissection, initial microdissection, definitive microdissection, clipping, and post-clipping. (12) predissection ior happens between induction of anesthesia and opening of the dura mater. ior during initial microdissection is an aneurysmal rupture that happens while the parent vessels or branches are being defined. ior during definitive microdissection is a rupture happening during exploration of the base or wall of the aneurysm or while the attempt to detach a branch vessel away from the aneurysm. ior during clipping was an aneurysm rupture when the clip was applied to the neck, or it may occur when the clip is manipulated. any change of the clip after its initial application is considered a “clip manipulation” (12). if bleeding occurs after the reopening, moving, or reapplying to the initial clip, the ior is defined as occurring during a clip manipulation. post-clipping ior is defined as any ior that occurs after placement of a permanent aneurysm clip (such as ior caused by intentional puncture of an aneurysm that was incompletely clipped or placement of an additional permanent clip on the aneurysm) (12). in our case, ior happened while the clip was being applied and caused a tear in the neck of the aneurysm, even though the tear extended to the parent artery. there are generally two main obstacles surgeons encounter in the presence of ior; the first is the continuous hemorrhage, which results in a limited field of vision, and the second is difficulty in localizing the aneurysm for clipping, which might endanger the parent vessel (20). several variables might contribute to aneurysmal ruptures intraoperatively; this includes; the aneurysmal site, size, and configuration. fundal adherence to the surrounding structures is also an essential factor associated with ior (2). in previous studies for analyzing the ior rates according to the aneurysmal location, rupture rates in acoma aneurysms reached approximately (48%) which was the highest rate among different aneurysmal sites. the surgical outcome of ior is significantly affected by the bleeding position; although the neck is the least common site constituting approximately 16% of all aneurysmal ruptures (20), ior of the neck is one of the most severe and challenging complications encountered (1). multiple methods have been suggested and applied in managing different types of ior. if the technique is accurately executed, the surgical outcome will mostly improve (20). large-bore suction over the site of aneurysmal rupture (one in the surgeon’s non-dominant hand and the other controlled by an assistant) helps reduce the bleeding and clear the visual field. temporary clipping of the parent vessel is another form of proximal control to prevent blood loss but can be associated with ischemic complications (1,4). clipping of the distal sac of the aneurysm can be applied in cases of ior without neck involvement (3); the cotton-clip method is a widely suggested technique that can be useful for neck avulsion induced ior, it is performed by a cotton placement over the bleeding site to prevent further blood extravasation, and after clearing the field, the neck of the aneurysm can be clipped. when performing this technique, it is considered that the clip and cotton must not compromise and affect the parent vessel (1, 10, 15). numerous other practices and methods are reporting good results in neck tear ior, such as micro-suturing of the ruptured neck, which has variable results, wrapping options, encircling clips placement, bypass, and endovascular trapping techniques (1, 17). although there are many methods for managing ior, they cannot be considered standard 167 management of brain aneurysm neck-avulsion during clipping surgery management of all types of aneurysmal neck tears. the cotton-clip method reported good outcomes in many cases of neck tear ior when the tear is deemed to be minor and can be controlled by adding pressure and cotton placement (1,10, 15). however, this method is not always applicable for a neck tear that extends to the parent vessel, as there cannot be enough pressure applied over the avulsed segment and the bleeding is more profuse than in slight neck tears (20). unconditional neck tears, larger avulsions arising at the aneurysmal neck with an extension to the parent vessel, are far more complex to manage. this is highly dependent on the neck tear degree, as well as the size, location, and shape of the aneurysm. such as the longitudinal finger-like appearance of aneurysms can make them more liable for neck avulsions. the cotton-clip method can be applied successfully for partial neck tear ruptures (10). in our case, initial clip placement over the aneurysmal neck induced ior. further dissection revealed a tear in the neck of the aneurysm extending to the acoma. the modification of surgical steps while repairing the ior due to an aneurysmal neck tear with extension to the parent vessel can be summarized in two points, 1) micro-suturing of the aneurysmal neck to seal the tear, which eventually didn’t work in our case, 2) temporary clip placement over the acoma to reestablish hemostasis with ionm which did not reveal any changes indicating hypoperfusion. as a result, a 3) final decision for permanently clipping the acoma was made. the choice not to use the cottonoid clip is that the tear was extending to the parent artery, and there was no space to put the cottonoid patty around the parent artery. the forced decision to clipping the acoma was the only choice left to cease the hemorrhage encountered intraoperatively. a midline pubmed literature review was conducted using the combinations of the following keywords; (aneurysm) and (neck) and (surgery or clipping) and (tear or avulsion). fifty-three results were found initially. after excluding non-human subject studies, and non-english studies, two independent researchers examined the title and the abstract for the cases of neck tear or avulsion with its management. fourteen articles were found to be included in this study. the average age of the cases is around 57 years. the percentages of females in the review were 62% (8/13) and among the males 38% (5/13). regarding the locations, pcoma and acoma were both 23% (3/13) of the cases, other locations include aca 15%, and mca 15%. the primary aim of our review is to deliver a comparative synopsis of the reported management techniques and outcomes for aneurysmal neck avulsions. the first case was reported in 1997 by yasui et al. (19), who described two cases of intraoperative complications due to neck tears, both managed by the parallel clipping method. since then, several similar cases have been identified in the literature. in 2002, yanaka et al. (18) reported a thinwalled aneurysm on the c1 segment of the right ica, which ruptured at the neck tear during dissection and was further fully separated from the parent vessel. this was managed by temporarily clipping the ica proximally and distally to the avulsion, micro suturing the tear in the arterial wall, and then using an encircling clip on the rupture site. despite postoperative hemiparesis, the outcome and recovery of the patient were good upon follow-up. in 2003, lanzio et al. (10) reported using the clip wrapping method, which consisted of neck clipping preceded by wrapping a cotton swath around the avulsed aneurysmal neck in an acoma aneurysm. the outcome was good during 1-year postoperative follow-up. the cotton-clip method was reported in 2011 by barrow et al. (1) in three different cases of intracranial aneurysms in which clip placement induced a slight tear in the aneurysmal neck managed by the cotton clip method, which was preceded by temporary clipping in the second case (table 1). although it is difficult to draw conclusions from this small number of cases, a few observations can be made. first, the scarcity of cases reported can be partially attributed to the inconsistency and different management methods of intraoperative neck tears, which are not always suitable due to multiple variables. the second observation is the lack of the post-operative outcome for a few of the management methods reported. the main focus of neurosurgeons during microsurgical procedures should be the prevention of intraoperative complications. various measurements for the management of ior are reported; they differ according to the rupture site and the extent of the tear. provisional knowledge of the suggested strategies with awareness of the convenience of each type of ior can drastically improve the surgical procedure and outcome. 168 teeba a. al-ageely, mustafa ismail, salima b. alsaadi et al. table 1. the reviewed cases of aneurysmal neck tear n authors age (years), gender aneurysm location surgical technique outc ome 1 yasui et al. 1997 (9) 50, female aca (a1) parallel clipping yasui et al. 1997 (9) 57, female ic-pc parallel clipping 2 yanaka et al. 2002 (16) 46, female ica suturing and encircling clip good 3 lanzio et al. 2003 (10) 60, female acoma clip wrapping good 4 vashu r et al. (17) 14, female pcoma micro-suturing good 5 park j et al 2009 (14) 73, female aca pericallos al occlusion of pericallosal artery along with a4-a5 in situ bypass with micro-suturing. good 6 barrow et al. 2011 (71) 51, male acoma cotton-clip method 7 barrow et al. 2011 (1) 62, female mca cotton-clip method 8 barrow et al. 2011 (1) 52, female pcoma cotton-clip method 9 feng yg et al 2013 (5) 40, male pcoma dural wrapping with clipping good 1 0 feng yg et al. 2013 (5) 43, female anterom edial wall of ica dural wrapping with clipping good 1 1 feng yg et al. 2013 (5) 41, male anterom edial wall of ica dural wrapping with clipping good 1 2 safaviabbasi s et al. 2015 (15) cotton-clip method 1 3 jiangang liu et al. 2019 (13) 52, male ophthal mic artery cotton-clip method good 1 4 jiangang liu et al. 2019 (13) 45, male mca cotton-clip method good 1 5 al ageely et al. 2022 44, female acoma parent artery clipping good . *all the patients are presented with sah conclusion ior due to aneurysmal neck tears is a devastating surgical complication requiring prevention and management approaches, which can be unique to each case. its management may differ according to the extent of the rupture. several methods have been suggested to treat such cases and the choice of the most convenient technique depends on the surgeon’s knowledge and experience for the best outcome possible. references 1. barrow dl, spetzler rf. cotton-clipping technique to repair intraoperative aneurysm neck tear: a technical note. operative neurosurgery. 2011 jun 1;68(suppl_2):ons294-9. 2. barrow dl. intraoperative misadventures: complication avoidance and management in aneurysm surgery. neurosurgery. 2011 sep 1;58(cn_suppl_1):93-109. 3. batjer h, samson d. intraoperative aneurysmal rupture: incidence, outcome, and suggestions for surgical management. neurosurgery. 1986 jun 1;18(6):701-7. 4. deluca j, diamond bj. aneurysm of the anterior communicating artery: a review of neuroanatomical and neuropsychological sequelae. journal of clinical and experimental neuropsychology. 1995 feb 1;17(1):100-21. 5. feng yg, li sf, zhang pn, xin t, meng qh, tang wz, li ht. clip-on-wrapping with dura mater to treat intracranial aneurysm neck avulsion: case reports and review of the literature. clinical neurology and neurosurgery. 2013 oct;115(10):2284-7. 6. hernesniemi j, dashti r, lehecka m, niemelä m, rinne j, lehto h, ronkainen a, koivisto t, jääskeläinen je. microneurosurgical management of anterior communicating artery aneurysms. surgical neurology. 2008 jul 1;70(1):8-28. 7. jomin m, lesoin f, lozes g. prognosis with 500 ruptured and operated intracranial arterial aneurysms. surgical neurology. 1984 jan 1;21(1):13-8. 8. kheĭreddin as, ium f, belousova ob, iuv p, zolotukhin sp, sazonov ia, khkh z. intraoperative rupture of cerebral aneurysm--incidence and risk factors. zhurnal voprosy neirokhirurgii imeni nn burdenko. 2007 oct 1(4):33-8. 9. kopitnik ta, horowitz mb, samson ds. surgical management of intraoperative aneurysm rupture. operative neurosurgical techniques. 2000;2:1275-81. 10. lanzino g, spetzler rf. clip wrapping for partial avulsion of the aneurysm neck. journal of neurosurgery. 2003 nov 1;99(5):931-2. 11. lawton mt, du r. effect of the neurosurgeon's surgical experience on outcomes from intraoperative aneurysmal rupture. neurosurgery. 2005 jul 1;57(1):9-15. 12. leipzig tj, morgan j, horner tg, payner t, redelman k, johnson cs. analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. neurosurgery. 2005 mar 1;56(3):455-68. 13. liu j, gao g, zhang s, huang y, wu j, hu x, lu j, zhang q, zhou l, huang y. cotton-assisted surgical clipping of very small aneurysms: a two-center study. world neurosurgery. 2019 jul 1;127:e242-50. 14. park j, kang dh. in situ rescue bypass for iatrogenic avulsion of parent artery during clipping large pericallosal artery aneurysm. journal of korean neurosurgical society. 2009 jul;46(1):68. 15. safavi-abbasi s, sun h, oppenlander me, nakaji p, kalani my, zabramski jm, spetzler rf. repair of intraoperative aneurysm neck tear utilizing the cotton-clipping 169 management of brain aneurysm neck-avulsion during clipping surgery technique. neurosurgical focus. 2015 jan 1;38(videosuppl1):video14. 16. sandalcioglu ie, schoch b, regel jp, wanke i, gasser t, forsting m, stolke d, wiedemayer h. does intraoperative aneurysm rupture influence outcome? analysis of 169 patients. clinical neurology and neurosurgery. 2004 mar 1;106(2):88-92. 17. vashu r, tan s, wong as. microsuture repair of intraoperative ruptures of cerebral aneurysms of the internal carotid artery. journal of clinical neuroscience. 2009 jul 1;16(7):960-2. 18. yanaka k, meguro k, nose t. repair of a tear at the base of a blister-like aneurysm with suturing and an encircling clip. neurosurgery. 2002 jan 1;50(1):218-21. 19. yasui t, sakamoto h, kishi h, komiyama m, iwai y, yamanaka k, nishikawa m, nakajima h. intraoperative aneurysmal rupture at the neck. no shinkei geka. neurological surgery. 1997 mar 1;25(3):271-6. 20. zhen y, yan k, zhang h, zhao s, xu y, zhang h, he l, shen l. analysis of the relationship between different bleeding positions on intraoperative rupture anterior circulation aneurysm and surgical treatment outcome. acta neurochirurgica. 2014 mar;156(3):481-91. doi: 10.33962/roneuro-2022-080 evaluation of the benefit of placing a drain in the epidural space in patients undergoing craniotomy emre çavuşoğlu, ümit kocaman romanian neurosurgery (2022) xxxvi (4): pp. 441-445 doi: 10.33962/roneuro-2022-080 www.journals.lapub.co.uk/index.php/roneurosurgery evaluation of the benefit of placing a drain in the epidural space in patients undergoing craniotomy emre çavuşoğlu, ümit kocaman i̇zmir bakırçay university çiğli training and research hospital, department of neurosurgery, i̇zmir, turkey abstract background. placing a drain in each of the intracerebral, subdural, epidural, and subgaleal spaces during craniotomy may be a result of the traditional approach. it may be more appropriate to identify the locations of the drains individually for each case and avoid certain behaviours. we, therefore, planned a study on the necessity of epidural drains, which are commonly used. methods. the study was conducted by screening the charts of the patients who had undergone surgery at i̇zmir bakırçay university çiğli training and research hospital’s neurosurgery department between june 1st 2021 and september 1st 2022. the study was of the retrospective cohort type. there were two groups in the study. twenty cases where only a subgaleal drain was used formed the first group (sg group). twenty cases where subgaleal and epidural drains were used together formed the second group (sg+e group). a total of three parameters were evaluated between these groups. the first parameter was the myocutaneous tissue thickness on the first postoperative day. the second one was epidural collection thickness on the first postoperative day. the third parameter was the rate of wound site infection development in the two groups. the results of the two groups were compared with the wilcoxon rank sum test. a two-way p-value below 0.05 was considered statistically significant. results. a statistically significant difference was present between the two groups in terms of myocutaneous tissue thickness (p=0.035). the mean myocutaneous tissue thickness was 15.8±3.24 mm in the sg+e group and 12.4±5.98 mm in the sg group. the mean epidural collection thickness in the sg+e group was higher than in the sg group and the difference was significant (10.3±3.29 mm and 6.30±3.13 mm, respectively, p<0.001). no infection developed in any of the patients in either group. conclusion. in patients undergoing craniotomy, placing a drain in the epidural space may be an ineffective intervention. the basic principle should be to complete the operation in the least invasive manner and the shortest time possible. introduction manuals play a very important role in neurosurgery operating procedures. it is also common to be influenced by a senior in the form of a master-apprentice relationship and to maintain this influence over the years. there may sometimes be problems with this arrangement but appropriate surgical behavior is usually observed. placing a drain in keywords epidural, drain, craniotomy, benefit corresponding author: ümit kocaman i̇zmir bakırçay university çiğli training and research hospital, department of neurosurgery, i̇zmir, turkey umitkocaman80@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 442 emre çavuşoğlu, ümit kocaman each of the intracerebral, subdural, epidural, and subgaleal spaces during craniotomy may be a result of this traditional approach. it may be more appropriate to identify the locations of the drains individually for each case and avoid certain behaviors. we therefore planned a study on the necessity of epidural drains, which are commonly used. materials and method the study was conducted by screening the charts of the patients who had undergone surgery at i̇zmir bakırçay university çiğli training and research hospital’s neurosurgery department between june 1st 2021 and september 1st 2022. the study was of the retrospective cohort type. the inclusion and exclusion criteria were as follows. inclusion criteria: 1. supratentorial pathology 2. cranial tumors, cranial vascular surgery cases, cranial compression fractures, and cranial epidural hematomas 3. those with a subgaleal drain among the above cases 4. those with a subgaleal and epidural drain among the above cases exclusion criteria: 1. infratentorial pathologies 2. subdural hematomas 3. cases with a subdural drain 4. cases without any drain 5. patients with uncontrolled or untreated comorbidities that could facilitate the development of wound site infection 6. patients with a coagulation disorder there were two groups in the study. twenty cases where only a subgaleal drain was used formed the first group (sg group). twenty cases where subgaleal and epidural drains were used together formed the second group (sg+e group). a total of three parameters were evaluated between these groups. the first parameter was the myocutaneous tissue thickness on the first postoperative day. the second one was epidural collection thickness on the first postoperative day. while performing the calculations, the thickest part of the relevant area was measured in coronal sections of cranial tomography. the distance from the highest point of the scalp to the bone was measured when calculating the second parameter. the third parameter was the rate of wound site infection development in the two groups. in order to evaluate the third parameter, the patients were followed-up for local infectious changes in the wound for 15 days. descriptive statistics were expressed as numbers and percentages for categorical variables and as mean±standard deviation for constant variables. the results of the two groups were compared with the wilcoxon rank sum test. a two-way p value below 0.05 was considered statistically significant. the analyses were performed with the r software, version 4.0.0. results there were 12 females (60%) and 8 males (40%) in group 1. the mean age was 56.3 years. group 2 included 9 females (45%) and 11 males (55%). the mean age was 63.4 years. myocutaneous tissue thickness and epidural collection thickness measurements of all patients are shown in table 1 and table 2. table 1. myocutaneous tissue thickness measurements in the tomography of the patients in group 1 (subgaleal drain) and group 2 (subgaleal+epidural drain) on the 1st postoperative day (mm). patient group 1 (sg) group 2 (sg+e) 1 15 13 2 14 16 3 7 9 4 7 18 5 14 14 6 15 15 7 18 16 8 16 18 9 7 12 10 10 15 11 6 15 12 7 16 13 22 21 14 15 24 15 25 18 16 20 13 17 3 16 18 6 18 19 11 15 20 10 14 443 evaluation of the benefit of placing a drain in the epidural space in patients undergoing craniotomy table 2. epidural collection tissue thickness measurements in the tomography of the patients in group 1 (subgaleal drain) and group 2 (subgaleal+epidural drain) on the 1st postoperative day (mm). patient group 1 (sg) group 2 (sg+e) 1 11 8 2 10 11 3 3 5 4 5 12 5 5 9 6 12 8 7 13 10 8 7 10 9 6 9 10 5 8 11 4 12 12 6 16 13 3 9 14 8 19 15 3 12 16 5 15 17 3 8 18 6 9 19 3 8 20 8 8 a statistically significant difference was present between the two groups in terms of myocutaneous tissue thickness (p=0.035, table 3, figure 1). the mean myocutaneous tissue thickness was 15.8±3.24 mm in the sg+e group and 12.4±5.98 mm in the sg group. the mean epidural collection thickness in sg+e group was higher than in the sg group and the difference was significant (10.3±3.29 mm and 6.30±3.13 mm, respectively, p<0.001, table 3, figure 2). table 3. the comparison of myocutaneous tissue and epidural collection thickness between group 1 (subgaleal drain) and group 2 (subgaleal+epidural drain). all patients, n=40 group 1 (sg), n=20 group 2 (sg+e), n=20 p myocutaneous tissue thickness (mm) 14.1±5.05 12.4±5.98 15.8±3.24 0.035 epidural collection thickness (mm) 8.30±3.76 6.30±3.13 10.3±3.29 <0.001 group 1 and group 2 were also compared in terms of infection development. no infection developed in any of the patients in either group. these results were not suitable for statistical analysis. figure 1. the comparison of myocutaneous tissue thickness between group 1 (subgaleal drain) and group 2 (subgaleal+epidural drain). figure 2. the comparison of epidural collection thickness between group 1 (subgaleal drain) and group 2 (subgaleal+epidural drain). discussion neurosurgeons place a drain in the epidural space on the assumption that it will decrease hematoma development and related complications at the surgical site. this practice is sometimes maintained as a habit or because the physician has learned this from a senior (1). we evaluated whether epidural drain placement is beneficial in the current study. we also wanted to see how a catheter placed in the epidural area changes infection rates. historically, subgaleal drains were first used by ames et al. (6). the number of studies evaluating the effect of placing subgaleal plus epidural drains or only subgaleal drains after craniotomy on the infection 444 emre çavuşoğlu, ümit kocaman and other complication rates is low. the number of studies comparing the relative benefits of drain location is also low. we believed that a simple and conclusive study was required. this study was planned to understand the necessity, advantages, and disadvantages of epidural drain placement and to evaluate the adequacy of using a subgaleal drain only. the results indicated that the epidural hematoma thickness on the first postoperative day in patients with both subgaleal and epidural drains (s+e) was statistically significantly higher than those with a subgaleal drain only (s). these results demonstrate that the current approaches are incorrect. the reason for the current results may be the accumulation of blood oozing from the bone in the epidural area while opening the epidural catheter site and the widening of the burr hole for the drain. another possibility is the insufficiency of the suspending sutures where the drain is placed in the epidural space. although it is difficult to reach a clear conclusion, these are the primary factors to consider. the current results make epidural catheter use controversial. drain placement in group 2 (s+e) patients actually prolongs the duration of surgery. at this stage, the surgeon places the drain in the epidural space, fixes it, and widens the burr-hole to prevent compression in the area where the drain will pass in the craniotomy flap and calvarium. all these cause loss of time and prolongation of the surgery. we observed this procedure to take 7 minutes on average in our cases. although not on a case-by-case basis, this would indicate a serious collective waste of time considering the high number of cranial surgeries performed. at the same time, widening the burr-hole where the epidural drain will pass creates an additional defect. this makes the procedure more invasive. another important point is that large amounts of csf drainage can occur when watertight suturing cannot be achieved in the dura and the epidural drain is directed below the ear level. complications such as subdural hematoma, decreased intracranial pressure, headache, brain edema, intracerebral hematoma, herniation, coma, and death may occur (2,3). a case where large amounts of cerebrospinal fluid drainage and low intracranial pressure following subdural hematoma surgery caused cerebellar hematoma (the zebra sign) is present in the literature. the hydrocephalus that developed later was reported to cause serious prolongation of hospitalization and decrease the glasgow outcome score of the patient (9). the point we want to emphasize by providing this example is that an epidural catheter can also increase morbidity due to excessive csf drainage. blood accumulation in the epidural space remains limited when the epidural space is reduced by suspending the dura with suspension sutures. the reason may be the prevention of potential bleeding with pressure as the space is reduced. besides, the blood may have passed from the bone defects at the craniotomy borders to the subgaleal area and then drained from there with the subgaleal drain. we believe that both these factors played a role. placing a drain in the epidural space to decrease epidural hematoma may therefore be useless. an epidural hematoma quickly solidifies once it develops and cannot enter the drain. the main approach to decrease an epidural hematoma should be to suspend the dura at appropriate intervals in order to reduce the epidural dead space. an epidural drain has been reported to be effective in preventing subgaleal collection when the dura cannot be closed watertight during craniotomy in the parietal region in a study by xin li et al. however, a drain was not used in the control group in that study. we believe that similar results could also be observed if a subgaleal drain had been used in the control group. subgaleal drainage is also a less invasive and more practical method than epidural drainage (10). philip a boney et al. have reported that the location of the drain used in epidural hematoma was associated with repeat surgery and the length of the hospital stay due to residual or recurrent hematoma. they reviewed 52 cases, with a subgaleal drain in 25, epidural drain in 8, and both in 13 patients, no drain was used in 6 cases. the location of the drain was not found to be statistically significant as regards repeat surgery, but the length of hospitalization decreased as the use of drains decreased. these results are similar to ours (11). the issue also needs to be evaluated in terms of susceptibility to infection. no statistically significant difference in terms of infection was found between the two groups in our study. placing a second drain could increase the chance of skin bacteria being carried in. the procedure is also more invasive. the 445 evaluation of the benefit of placing a drain in the epidural space in patients undergoing craniotomy increased duration of the surgery could increase the risk of infection (4). the two groups in the current study were evaluated in terms of myocutaneous tissue thickness on the first postoperative day. the value was statistically significantly lower in group 1 (sg). the reason could be the blood leaking from the bone tissue, muscle, and skin-subcutaneous tissue during epidural drain placement. an increased myocutaneous tissue thickness could impair wound healing. any collection must be removed. the hospital stay of the patient will then be prolonged. from this point of view, placement of an epidural catheter may do more harm than good. prophylactic drain placement has been discontinued over the years in many surgical procedures other than neurosurgery. schietroma m et al. have reported routine drain use after thyroidectomy to be unnecessary and postoperative drain placement to increase pain (7). besides, the use of a drain after lumbar surgery did not change the epidural hematoma or infection rate but increased the patient's pain-related symptoms (8). however, the number of neurosurgical studies on this issue is inadequate. a subgaleal collection could prolong wound healing. a scalp hemorrhage can develop into a chronic cavity and cause serous fluid accumulation when a subgaleal drain is not placed, as this is a very vascular area. it can also impair wound healing and predispose to wound infection. therefore, we think that a subgaleal drain is necessary. however, the subgaleal space is tighter close to the vertex and a subgaleal drain is not used with limited incisions close to the vertex in practice. the basic principle should be to complete the operation in the least invasive manner and the shortest time possible. references 1. li x, li j, sui j, niyazi t, yalikun n, wang s. advantages of using a prophylactic epidural closed drain and nonwatertight dura suture in a craniotomy near the "parietal site". chin neurosurg j. 2020;6:34. published 2020 oct 5. doi:10.1186/s41016-020-00212-2 2. toshniwal gr, bhagat h, rath gp. bradycardia following negative pressure suction of subgaleal drain during craniotomy closure. acta neurochir (wien). 2007 oct;149(10):1077-9; discussion 1079. doi: 10.1007/s00701-007-1246-6. epub 2007 jul 9. pmid: 17616841. 3. roth, jonathan md*; galeano, eduardo md†; milla, sarah md‡; hartmannsgruber, maximilian w md†; weiner, howard l md* multiple epidural hematomas and hemodynamic collapse caused by a subgaleal drain and suction-induced intracranial hypotension: case report, neurosurgery: january 2011 volume 68 issue 1 p e271-e276 doi: 10.1227/neu.0b013e3181fe6165 4. cheng h, chen bp, soleas im, ferko nc, cameron cg, hinoul p. prolonged operative duration increases risk of surgical site infections: a systematic review. surg infect (larchmt). 2017 aug/sep;18(6):722-735. doi: 10.1089/sur.2017.089. pmid: 28832271; pmcid: pmc56 85201. 5. hamou, h.a., kotliar, k., tan, s.k. et al. surgical nuances and placement of subgaleal drains for supratentorial procedures—a prospective analysis of efficacy and outcome in 150 craniotomies. acta neurochir 162, 729– 736 (2020). https://doi.org/10.1007/s00701-019-04196-6 6. ames rh. ventriculo-peritoneal shunts in the management of hydrocephalus. j neurosurg. 1967 dec;27(6):525-9. doi: 10.3171/jns.1967.27.6.0525. pmid: 6065126. 7. schietroma m, pessia b, bianchi z, de vita f, carlei f, guadagni s, amicucci g, clementi m. thyroid surgery: to drain or not to drain, that is the problem a randomized clinical trial. orl j otorhinolaryngol relat spec. 2017;79(4):202-211. doi: 10.1159/000464137. epub 2017 jul 15. pmid: 28715809. 8. davidoff cl, rogers jm, simons m, davidson as. a systematic review and meta-analysis of wound drains in non-instrumented lumbar decompression surgery. j clin neurosci. 2018 jul;53:55-61. doi: 10.1016/j.jocn.201 8.04.038. epub 2018 apr 19. pmid: 29680443. 9. taieb, mohamed amine hadj et al. “remote cerebellar hemorrhage after the evacuation of a subdural hematoma: a case report.” the pan african medical journal vol. 41 24. 11 jan. 2022, doi:10.11604/pam j.2022.41.24.32799 10. xin li, jing li, jianfei sui, tuerdialimu niyazi, naibijiang yalikun, shuo wang. advantages of using a prophylactic epidural closed drain and non-watertight dura suture in a craniotomy near the ‘parietal site’. chinese neurosurgical journal 6, article number:34 (2020). 11. phillip a bonney et al. surgical closed suction drain use after craniotomy for evacuation of supratentorial epidural hematomas: a case series of radiographic and clinical outcomes. world neurosurgery. volume 134, february 2020, pages e460-e468. doi: 10.33962/roneuro-2023-013 secondary optic neuropathy due to sphenoid-ethmoidal sinus mucocele khabibullo khasanov, gulnarakhon alikhodjayeva, jakhongir yakubov, ilkhom khujanazarov romanian neurosurgery (2023) xxxvii (1): pp. 80-84 doi: 10.33962/roneuro-2023-013 www.journals.lapub.co.uk/index.php/roneurosurgery secondary optic neuropathy due to sphenoid-ethmoidal sinus mucocele khabibullo khasanov1, gulnarakhon alikhodjayeva1, jakhongir yakubov2, ilkhom khujanazarov1 1 department of traumatology, orthopaedics, military-field surgery, and neurosurgery, tashkent medical academy. tashkent, uzbekistan 2 department of skull base surgery, republican specialized scientificpractical medical center of neurosurgery. tashkent, uzbekistan abstract secondary visual impairment induced by sinusitis is a rare condition that cannot be recognized in all cases. a steady decline in visual acuity and visual field together or alone is the main symptom patients may complain of on admission. this might be hard for general practitioners in uzbekistan, as possible causes are either intracranial or ophthalmic abnormalities. hence, it is frequently misdiagnosed or leads to late diagnosis once visual impairment becomes severe. in this paper, we discuss the case of a 9-year-old boy with impaired vision on the left side that was detected almost too late and could have led to complete vision loss. ineffective conservative therapy was provided for four months. ct and mri confirmed a lesion in the left sphenoethmoidal sinus. the patient then underwent endoscopic sphenoiethmodotomy with drainage of the left sphenoethmoidal sinus. in the early postoperative phase, as early as the next day after the surgical procedure, the patient experienced visual improvement. forty days following surgery, in combination with postoperative conservative care in an eye hospital, there was a noticeable improvement in vision. in conclusion, it is crucial for ophthalmologists, neurologists, and ent surgeons to focus on inflammation in the sphenoethmoidal sinus in children even with mild vision impairment. introduction visual disturbances in optic neuropathies may be produced by numerous etiologic events such as toxic, nutritional, and other ophthalmological as well as intracranial disorders[1,2]. the most prevalent intracranial pathologies that can lead to optic neuropathies are lesions in the sellar and parasellar areas such as pituitary tumors, meningiomas, craniopharyngiomas, and intracerebral lesions affecting the visual pathways, as well as primary or secondary hydrocephalus. in addition to numerous main ophthalmologic illnesses [3], rhinogenic optic neuritis may also be induced by sphenoid sinus mucocele with sinusitis, ethmoiditis, and onodi cell inflammation [4-7]. in some selected circumstances, it is difficult to make a differential diagnosis. when children with good musculoskeletal development keywords optic neuropathy endonasal surgery, sphenoid sinus mucocele corresponding author: khabibullo khasanov tashkent medical academy. tashkent, uzbekistan xasanovneuro@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 81 secondary optic neuropathy due to sphenoid-ethmoidal sinus mucocele show evidence of gigantism and complain of vision difficulties, they contact multiple physicians such as endocrinologists, neurologists, and even neurosurgeons for probable pituitary tumors. in such particular conditions, mri and ct can be valuable diagnostic tools to detect lesions in the pituitary region that compress the optic nerve and produce vision abnormalities. mri is the best choice to evaluate optic nerves except for its intraocular portion and it is fairly difficult to visualize the retina with high-resolution mr imaging. if a lesion is diagnosed in the sphenoidal and ethmoidal sinuses, notably inflammation of the onodi cells, the physician should think of secondary optic neuritis resulting from this inflammatory process. case report a 9-year-old kid first visited the outpatient clinic of the republican specialized scientific practical medical center of neurosurgery in tashkent, uzbekistan. his major complaints were acute progressive headache and moderate visual problems when his mother initially consulted his brother, a young neurosurgeon. the patient was tall and had strong musculoskeletal development. he complained of headache and slight visual disruption in the left eye that had continued for a week. the patient had no fever or other symptoms; yet, he experienced rhinogenous sinusitis and tonsillitis multiple times in early childhood. in addition, the boy's family history was negative for neurologic or autoimmune disorders. because of his appearance, which was suggestive of a pituitary lesion, he was advised for an mri scan. an ophthalmologic examination yielded normal results, but mri showed a lesion in the left sphenoethmoidal sinus but did not discover any abnormalities in the sellar region (figure 1). on visual evoked potential (vep) (table 1), there was extending latency of the p100mc component by 104,2 mc on the left eye and 100,1 mc on the right eye. ophthalmological examination: visual field: od-mild stage of myopia and os-myopic astigmatism, left temporal hemianopsia, visual acuity was as follows: od-0.9; 0s-0,1. the patient was then advised to consult an ophthalmologist and an otolaryngologist (ear, nose, and throat specialist) in the region where he lived for additional assessment and treatment. after 4 months of conservative outpatient treatment by an ophthalmologist and an otolaryngologist with antibiotics and steroids, the patient's mother called his brother, who was a neurosurgeon, complaining of his son's progressive worsening of visual acuity in his left eye. ophthalmologic and fundus investigations revealed alterations in the vascular anatomy and optic nerve. ct indicated a left sphenoethmoidal lesion (sinusitis) with no mass effect on the left optic canal; no bone erosion was seen with an inferior-medial wall of the left optic canal (figure 1). collegial consultation with experts in endoscopic neurosurgery, and several ent surgeons and ophthalmologists, as well as literature searches, led to the conclusion that optic neuropathy was diagnosed to be induced by sphenoethmoidal sinusitis. table 1. neuroophthalmological examination visual acuity visual field visual evoked potential p100mc component rig ht le ft right left rig ht left preoperati ve o,9 0,1 norm al hemiano psia 100, 1 104, 2 postopera tive 1,0 0. 9 norm al normal 100, 1 101, 7 as a result, in case of probable bone involvement and any intraoperative intracranial findings, along with neurosurgeons, endoscopic sphenoethmoidotomy with the excision of the lesion and draining of the left sphenoid sinus and ethmoidal sinus was performed. during surgery, no direct intracranial invasion and no direct 82 khabibullo khasanov, gulnarakhon alikhodjayeva, jakhongir yakubov, ilkhom khujanazarov compression of the optic nerve were identified. in the early postoperative phase, as early as the next day after the surgical treatment, the patient reported visual improvement. then the patient was taken to the eye hospital where he got postoperative conservative outpatient treatment with antibiotics and steroids. forty days after surgical therapy in combination with postoperative conservative treatment in an eye hospital, there was a considerable improvement in vision. 40 days followup ophthalmologic examination (table 1) showed significant positive changes such as p100mc component latency decreased and was almost similar in both eyes and, on ct (figure 2) near total removal of mucocele in the left sphenoid sinus and there was a small residual one within the left ethmoidal sinus respectively. discussion mucoceles are encapsulated fluid-filled lesions, that can represent in paranasal sinus cavities and there is rarely involvement of sphenoid sinus (up to 3% of all cases) as they are often present in individuals aged over 40 [7]. since the optic canal and the optic nerve have a closer relationship with the posterior part of the sphenoethmoidal sinus, the onodi cells which are usually found in that part can cause serious retrobulbar optic neuropathy and in association with cholesterol granuloma, it causes bone destruction and compression [8,10,11]. the most typical symptoms are headache or facial pain, and occasionally, even if this happens seldom, there are the optic and other iii, iv, and vi cranial nerves become involved. cheng et al. described the case in the pediatric population, where they documented a big sphenoid sinus mucocele of a 10-year-old boy who exhibited right eyelid droop and double vision. even though there was compression and cerebral involvement, following surgery, the patient reported full clearance of mucocele and excellent visual outcome and they argue that the literature reveals cranial neuropathy due to sphenoid sinus mucocele is highly unusual. prompt diagnosis and care may lead to improved clinical results and the avoidance of permanent neuropathy. however, postoperative care also plays a significant role as there is usually secondary optic neuritis that needs to be handled carefully. otsuka et.al. [9] concur with their perspective on the importance of preoperative visual acuity as the prognostic factor for postoperative vision in patients with rhinogenic optic nerve neuropathy, however, poor preoperative vision may be improved by surgical therapy. in addition to this, younger patients are likely to have comparably better results than older people. steroid pulse treatment occasionally might be utilized for visual acuity improvement following surgery. even in their research, there was not any significant difference in the prognosis of vision based on the presence or absence of steroid pulse therapy, in our experience, we consider that both preventative preoperative and postoperative use of steroids may enhance surgical results. numbers of studies have shown that the origin of visual impairment related to mucoceles involves direct mechanical compression, local ischemia, and inflammation. they indicate distinct prognoses. while the slow manifestation of clinical symptoms and a better prognosis typically occur in mechanic compression, the latter two, ischemia and inflammation generate an early start of symptoms that may have a bad prognosis [12-15]. carefully preoperative screening may indicate various causes of optic neuropathy. however, it is difficult to identify a normal optic nerve and an optic nerve lesion. the disc component may be analyzed by utilizing fundoscopy and high-resolution optical coherence tomography, whereas the other three parts are less accessible and require imaging procedures like mr imaging, sonography, and ct. mr imaging is preferred to the other tests described above thanks to several features such as exceptional soft tissue resolution, the absence of ionizing radiation, and high diagnostic accuracy. mr imaging has a 83 secondary optic neuropathy due to sphenoid-ethmoidal sinus mucocele sensitivity of 60-75% and a specificity of up to 90% for identifying abnormalities in the optic nerve [16,17]. in typical circumstances, the intraorbital portion of the optic nerve has a mean diameter ranging from 2.2 to 5.2 mm. the diameter of the optic nerves normally grows throughout the first two years of life. however, for children aged 6 to 12, whereas the diameter of the optic nerves on axial cut mr images on the retrobulbar level is 2.26 0.38 mm, it is 2.27 0.41 mm on coronal plane mri on the retrobulbar space. as a consequence, on both axial and coronal incisions, the midaspect part of the optic nerve should be thinner than the retrobulbar region [18]. in our case, we assume that the visual impairment that the patient experienced was secondary owing to inflammation of the sphenoethmoidal sinus, specifically the posterior region which normally has a tighter relationship with intracanalicular optic nerves. even though there is no direct compression on the optic nerves, this inflammation and toxins are thought to irritate the optic nerve creating a circulatory disturbance and nerve trophic dysfunction. as a consequence, this might lead to a deterioration in vision. our findings on radiological exams such as mri (figure 3a and 3b) and ct (figure 3c), measuring diameters of the optic nerves in retrobulbar space might identify probable alterations in circulation and optic nerves` an or/and hypotrophy that commonly leads in visual difficulties. in early observation days, when the patient first came to admission because of headache and mild impaired vision, an early mri showed a mass lesion within the left sphenoid and ethmoidal sinus. we measured the diameters of both optic nerve and it was almost similar in distal part of the retrobulbar optic nerve in both eyes (figure 3a), however, in its proximal part, close to mass lesion there was a gap between the diameters of the retrobulbar left and right optic nerves on a t2 axial cut mr scan( 3.6 mm and 4.2 mm, respectively). the diameters of both optic nerves should be almost the same in principle, but in the present patient, there was a gap between the diameters of the right and left optic nerves as seen on t2 mri images, and the difference was around 1.2mm, suggesting hypotrophy of the left optic nerve. the diameters of the right and left optic nerves, as well as their difference, remained stable in early preoperative computed tomography (figure 3c right); however, due to the resolution of ct compared to mr imaging, those numbers were slightly different; 4,9mm and 3,6mm in retrobulbar space, respectively. the gap between the right and left optic nerves was about 1.3mm. even after 4 months of conservative therapy by otolaryngologists and ophthalmologists, the patient's visual acuity had deteriorated, and they have referred to us again. because of these alterations and decreasing visual acuity, conservative therapy was proven ineffective, and the patient needed surgical intervention. the patient was checked again 40 days following endonasal surgery and postoperative conservative therapy with antibiotics and steroids. his vision dramatically improved, and he recovered rapidly. there was also no headache. the diameter of the left optic nerve was 5,4 mm on ct, which was approximately identical to the diameters of the right optic nerve we measured before the surgery. as a consequence, the diameter of the left optic nerve expanded from 3,6mm to 5,4mm (figure 3c left). however, owing to a lack of precision and resolution quality, ct may not be a viable technique for assessing the diameter of the optic nerve, which we feel is a drawback of our research. conclusion secondary optic neuropathy, due to sphenoid sinus mucocele is common in the pediatric population. pricey exams such as mri and ct are required for a correct diagnosis and treatment selection. minimally invasive surgical therapy is the major therapeutic objective to conquer even such basic and infrequent instances. if inflammatory illnesses become chronic in youngsters. rhinogen sinusitis may occasionally produce visual difficulties since sinusitis is prevalent in both children and adults. references 1. margolin e, blair k, shemesh a. toxic and nutritional optic neuropathy. 2022 may 20. in: statpearls [internet]. treasure island (fl): statpearls publishing; 2022 jan–. pmid: 29763154. 2. behbehani r. clinical approach to optic neuropathies. clin ophthalmol. 2007 sep;1(3):233-46. pmid: 19668477; pmcid: pmc2701125. 3. rodriguez-beato fy, de jesus o. compressive optic neuropathy. [updated 2022 jul 12]. in: statpearls [internet]. treasure island (fl): statpearls publishing; 2022 jan-. available from: https://www.ncbi.nlm.nih.gov/ books/nbk560583/. 4. deb ak, neena a, sarkar s, devraj a, panicker g, stephen 84 khabibullo khasanov, gulnarakhon alikhodjayeva, jakhongir yakubov, ilkhom khujanazarov am. bilateral compressive optic neuropathy secondary to sphenoid sinus mucocele mimicking bilateral retrobulbar neuritis. saudi j ophthalmol. 2022 jun 13;35(4):368-370. doi: 10.4103/1319-4534.347312. pmid: 35814987; pmcid: pmc9266473. 5. lee sm, lee ki. recurred sphenoethmoidal mucocele after treated with simple endoscopic marsupialization. j craniofac surg. 2021 oct 1;32(7):e661-e663. doi: 10.1097/scs.0000000000007825. pmid: 34191777. 6. ting myl, shan m, gantz o, zhang-nunes s, wrobel b. optic neuropathy due to an ethmoid mucocele: a case report and literature review. case rep ophthalmol. 2019 aug 6;10(2):227-234. doi: 10.1159/000501898. pmid: 31692625; pmcid: pmc6760354. 7. chang h, silva m, weng j, reilly e, levine c, mccrea hj. large sphenoid mucocele presenting with cranial neuropathies in a 10-year-old boy: case report and literature review. childs nerv syst. 2022 may;38(5):10351039. doi: 10.1007/s00381-021-05314-5. epub 2021 aug 4. pmid: 34347143. 8. tzamalis a, diafas a, riga p, konstantinidis i, ziakas n. onodi cell mucocele-associated optic neuropathy: a rare case report and review of the literature. j curr ophthalmol. 2020 mar 23;32(1):107-113. doi: 10.1016/j.joco.2019.08.006. pmid: 32510023; pmcid: pmc7265265. 9. otsuka m, yunoki t, ozaki h, tachino h, takakura h, shojaku h, hayashi a. prognostic factors for postoperative visual acuity in patients with rhinogenic optic neuropathy. j ophthalmol. 2019 oct 3;2019:3417425. doi: 10.1155/2019/3417425. pmid: 31687196; pmcid: pmc6794975. 10. geng c, tong q, wang y, huang s, wang m, xing z, sun k. onodi cell mucocele with cholesterol granuloma is more likely to cause serious optic neuropathy, compared with simple onodi cell mucocele. ear nose throat j. 2022 feb 25:1455613221080069. doi: 10.1177/0145561322 1080069. epub ahead of print. pmid: 35213237. 11. morino t, yanagihara t, kuroyanagi h, ohto h. optic neuropathy caused by expanded onodi cell mucocele. bmj case rep. 2020 jun 2;13(6):e235311. doi: 10.1136/bcr-2020-235311. pmid: 32487523; pmcid: pmc7269546. 12. nickerson jp, lane ap, subramanian ps, izbudak i. onodi cell mucocele causing acute vision loss: radiological and surgical correlation. clin neuroradiol. 2011;21:245-248. 13. tseng cc, ho cy, kao sc. ophthalmic manifestations of paranasal sinus mucoceles. j chin med assoc. 2005;68: 260-264. 14. fukuda y, chikamatsu k, ninomiya h, yasuoka y, miyashita m, furuya n. mucocele in an onodi cell with simultaneous bilateral visual disturbance. auris nasus larynx. 2006;33: 199-202. 15. kim ys, kim k, lee jg, yoon jh, kim ch. paranasal sinus mucoceles with ophthalmologic manifestations: a 17year review of 96 cases. am j rhinol allergy. 2011;25: 272275. 16. chawla b, sharma s, sen s, et al. correlation between clinical features, magnetic resonance imaging, and histopathologic findings in retinoblastoma: a prospective study. ophthalmology 2012; 119:850 –56 crossref medline 17. schueler a, hosten n, bechrakis n, et al. high resolution magnetic resonance imaging of retinoblastoma. br j ophthalmol 2003;87: 330 –35 crossref medline 18. al-haddad ce, sebaaly mg, tutunji rn, mehanna cj, saaybi sr, khamis am, hourani rg. optic nerve measurement on mri in the pediatric population: normative values and correlations. ajnr am j neuroradiol. 2018 feb;39(2):369-374. doi: 10.3174/ajnr.a5456. epub 2017 dec 7. pmid: 29217740; pmcid: pmc7410600. doi: 10.33962/roneuro -2020-040 intraneural synovial sarcoma of median nerve. a rare case report with review of literature sandeep bhardwaj, anil kansal, rohit bansil, rakesh singh, akangsha sharma romanian neurosurgery (2020) xxxiv (1): pp. 275-279 doi: 10.33962/roneuro-2020-040 www.journals.lapub.co.uk/index.php/roneurosurgery intraneural synovial sarcoma of median nerve. a rare case report with review of literature sandeep bhardwaj, anil kansal, rohit bansil, rakesh singh, akangsha sharma blk superspeciality hospital new delhi, india abstract synovial sarcomas are highly aggressive soft tissue tumour with a poor and dismal prognosis. these tumours have a high propensity for distant metastasis and local recurrence. although originally believed to arise from synovium, these tumours have been found to occur anywhere in body [1],[2]. we report here, a case of median nerve sarcoma in a 15-year female. this is a rare tumour, which is diagnosed only after histopathological examination with only a few cases reported in the literature (table 1). although preoperatively tumour was thought to be a nerve sheath tumour, on histopathology analysis was found to be synovial sarcoma. despite aggressive behaviour, wide local excision is recommended even in smaller lesions. so, the diagnosis should always be kept in differentials of nerve sheath tumour, as what may be a synovial sarcoma. introduction synovial sarcomas may arise from different and unusual sites with distinctive morphological genetic features [3]. they are mostly seen in extremities in young adolescents with male preponderance [4]. it has been found in unusual locations in heart, lung, small intestine, soft palate and peripheral nerves. only a few cases have been reported in peripheral nerve. prognosis is poor despite radical surgery, radiation and chemotherapy with 50-60 % survival [5]. these sarcomas have origin in synovium because of periarticular location, but less than 5% are continuous with synovium4. sarcomas have their origin from primitive mesenchymal undifferentiated cells6. synovial sarcoma is diagnosed on immunohistochemical basis because most of them present as lump or swelling with no clinical or diagnostic features [7]. translocation (x;18) is diagnostic in 90% of cases [8]. the case presented here is a rare sarcoma arising from median nerve in upper arm. we have described here clinical, radiological features and its management. case presentation a 15 years old female presented with swelling in left arm for last 6 keywords intraneural synovial sarcoma, median nerve, arm, soft tissue tumour corresponding author: sandeep bhardwaj dr. mbbs. ms. mch. neurosurgery department of neurosurgery, blk superspeciality hospital, new delhi, india. sandeep74699@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 276 hassan z.a. dixon, yasir m. hamandi, ammar m.a. mahmmoud et al. months with swelling of size of 5*4 cm in left arm which has gradually increased in size. she also complained of pain in left arm radiating along medial aspect of forearm up to left hand. the pain was sharp, and more during night. she also complained of tingling sensation in left upper limb, palm, index and thumb and had history of dropping objects from left hand. on examination, there was decreased sensation along radial three digits with no neurovascular deficit. the patient was evaluated with magnetic resonance imaging (figure 1) which revealed a well encapsulated oval lesion in left upper arm medially burrowing in left biceps and coracobrachialis muscle. the lesion minimally indented the left brachial artery. the lesion was in continuity with median nerve which showed mild enhancement in early and late arterial phase with heterogenous enhancement with non-enhancing / cystic areas in venous and delayed phase. overall findings were in favour of neurogenic tumour. figure 1. electrodiagnostic studies and nerve conduction studies of median nerve were within normal limits. ultrasound colour doppler peripheral venous single upper limb was suggestive of hetero-echoic lesion with internal cystic components measuring 43*23 mm causing compression of underlying axillary artery medially at its lower margin. the patient was taken up for surgical resection with preservation of nerve fascicles. the mass found to be associated intimately associated with nerve, soft in consistency and moderately vascular in nature. microvsacular excision of mass was done with preservation of nerve fascicles (figure 2). on histopathological analysis, tumour was greyish tan made up of spindle cells with sheets of cells with vesicular nuclei and ill-defined cell margins suggestive of mild epitheloid morphology (figure 3). focal areas showed perivascular arrangement with cells separated by blood vessels with occasional mitosis and areas of haemorrhage. collagen and osseous tissue was seen adjacent to tumour. on immunohistochemistry cd 99 was positive, ck negative, synaptophysin negative, s-100 negative, hmb-45 negative, bcl2 positive and ki-67 was 15-20 % in cellular areas (figure 4). the histopathological and immunohistochemical analysis were in favour of synovial sarcoma. post operatively, whole body pet/cect scan was done for any metastasis and restaging. this was suggestive of small minimally metabolic active solid soft tissue thickening in proximal left biceps muscle indenting left brachial artery probably? residual lesion. post excision, patient received radiotherapy. figure 2. figure 3. 277 intraneural synovial sarcoma of median nerve figure 4. discussion synovial sarcomas arising from median nerve are very rare and rarest tumours published in literature. other sarcomas arising from various nerves reported in literature are from radial, common digital, posterior tibialis, peroneal, facial nerve, s1 root, c7 root and brachial plexus. there are three basic histology features of synovial sarcoma. the most common pattern is biphasic followed by monophasic and poorly differentiated synovial sarcomas. synovial sarcoma with biphasic type consisted of epithelial cells with fibroblast like spindle cell in various proportions. monophasic type consists of spindle cells only and are difficult to differentiate from other soft tissue and nerve tumours but now can be differentiated on the basis of immunohistochemical analysis4. third pattern of poorly differentiated synovial sarcomas that has worse prognosis and has also been described6. prognosis of biphasic versus monophasic is still under debate9,10,11,12. the present case in our study was biphasic synovial sarcoma having both epithelial and spindle cells in various proportions. it was immunohistochemical positive for cd99 and bcl2. the neoplastic proliferation with characteristic ss18ssx1 with chromosomal fusion at molecular level is a feature consistent with diagnosis with synovial sarcoma4. patient was advised for chromosomal analysis, but due to financial constraints patient refused for same. published cases of median nerve synovial sarcoma with review of literature is summarised in table 1 and table 2 respectively. chromosomal translocation is the most efficient way to establish the diagnosis of synovial sarcoma. a gene translocation between chromosomes 18 and x t(x;18) (p11.2; q11.2) occurs in over 90% of synovial sarcomas4. this leads to fusion of one of two variants of the ssx gene with the syt gene, resulting in either the syt/ssx1 or syt/ssx2 chimeric fusion proteins4,6. nearly all biphasic tumours express syt/ssx1, while monophasic tumours express syt/ssx1 in approximately half of the cases and syt/ssx2 in the remainder13. patients with syt/ssx2 expressing tumours have a significantly better prognosis when compared to those with syt/ssx1 tumours in terms of rates of metastasis and overall survival13,14,15,16. factors associated with poor prognosis includes old age, tumour size more than 5 cm, bone, nerve and vascular invasion and poor differentiation with higher mitotic index 12,17,18,19.management of synovial sarcoma is wide surgical excision, radiation therapy, and adjuvant chemotherapy which has been found to be correlated to be associated with better prognosis2,20 surgical management followed by radiation and chemotherapy is associated with good prognosis2,20. 5-year survival rates of synovial sarcomas have been around 50-60%, in spite of advances in treatment2,21,22. mortality in synovial sarcoma results 278 hassan z.a. dixon, yasir m. hamandi, ammar m.a. mahmmoud et al. from distant metastasis, most frequently to lung23. radical surgical incision followed by radiation allowed for potential decrease in local recurrence but systemic metastasis remained high even with adjunct chemotherapy24. conclusion synovial sarcoma involving median nerve is a rare and aggressive tumour and is one of the few cases already published in literature. synovial sarcoma can occur anywhere in our body and should be kept in differentials involving peripheral nerves as in our case. as diagnosis is always made post operative on histo-patholoical analysis with immunohistochemistry, resulting in change in treatment strategy and final outcome of patient. as in our patient, preoperative diagnosis was a benign neurofibroma/schwannoma, we must be aware of aggressive tumour which overall changes the complete treatment and should be always be kept in differentials and managed accordingly. references 1. sandberg aa, bridge ja. updates on the cytogenetics and molecular genetics of bone and soft tissue tumors. synovial sarcoma. cancer genet cytogenet.2002:133:123. 2. guadangnolo ba, zagars gk, ballo mt, et al. long term outcomes for synovial sarcoma treated with conservation surgery and radiotherapy . int j radiat oncol biol phy. 2007;69:1173-80. 3. weiss sw, goldblum jr: enzinger’s and weiss’s soft tissue tumors. 5th ed., philadelphia, mosby elsevier, 2008, 11611182. 4. fischer c. synovial sarcoma .ann diagn pathol. 1998;2(2)401-21. 5. zeren h, moran ca, suster s, fishback nf, koss mn: primary pulmonary sarcomas with features of monophasic synovial sarcomas. a clinicopathological, immunohistochemical and ultrasturctural study of 25 cases. hum pathol; 26:474-480. 6. enzinger fm, weiss sw. soft tissue tumors. st. louis: mosby;1993.synovial sarcoma;pp.757-86. 7. kransdorf mj. malignant soft tissue tumors in a large referral population: distribution of diagnosis by age,sex and location.am j roentgenol.1995;164:129-34. 8. palmerini e, staals el, alberghini m, zanella l, ferrari c, benassi ms, et al. synovial sarcoma: retrospective analysis of 250 patients treated at a single institution. cancer. 2009;115:2988–98. 9. chu pg benhattar j, weiss lm, et al. intraneural synovial sarcoma: two cases. mod pathol. 2004;17:258-63. 10. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 11. kawai a, woodruff j, healey jh, et al. syt-ssx gene fusion as a determinant of morphology and prognosis in synovial sarcoma. n engl j med. 1998;338:153–60. 12. trassard m, le doussal v, hacène k, et al. prognostic factors in localized primary synovial sarcoma: a multicenter study of 128 adult patients. j clin oncol. 2001;19:525–34. 13. kawai a, woodruff j, healey jh, et al. syt-ssx gene fusion as a determinant of morphology and prognosis in synovial sarcoma. n engl j med. 1998;338:153–60. 14. ladanyi m, antonescu cr, leung dh, et al. impact of sytssx fusion type on the clinical behavior of synovial sarcoma: a multiinstitutional retrospective study of 243 patients. cancer res. 2002;62:135–40. 15. inagaki h, nagasaka t, otsuka t, et al. association of sytssx fusion types with proliferative activity and prognosis in synovial sarcoma. mod pathol. 2000;13:482–8. 16. nilsson g, skytting b, xie y, et al. the syt-ssx1 variant of synovial sarcoma is associated with a high rate of tumor cell proliferation and poor clinical outcome. cancer res. 1999;59:3180–4. 17. o'connell jx, browne wl, gropper pt, et al. intraneural biphasic synovial sarcoma: an alternative “glandular” tumor of peripheral nerve. mod pathol. 1996;9:738–41. 18. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 19. bergh p, meis-kindblom jm, gherlinzoni f, et al. synovial sarcoma: identification of low and high risk groups. cancer. 1999;85:2596–607. 20. choong pfm, pritchard dj, sim fh, et al. long-term survival in high grade soft tissue sarcoma: prognostic factors in synovial sarcoma. int j oncol. 1995;7:161–9. 21. spillane aj, a'hern r, judson ir, et al. synovial sarcoma: a clinicopathologic, staging, and prognostic assessment. j clin oncol. 2000;18:3794–803. 22. krsková l, kalinová m, brízová h, et al. molecular and immunohistochemical analyses of bcl2, ki-67, and cyclin d1 expression in synovial sarcoma. cancer genet cytogenet. 2009;193:1–8. 23. enzinger fm, weiss sw. soft tissue tumors. st. louis: mosby; 1993. synovial sarcoma; pp. 757–86. 24. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 25. cugola l, pisa r. synovial sarcoma: with radial nerve involvement. j hand surg (br) 1985;10:243-4. 26. rinehart gc, mustoe ta, weeks pm. management of synovial sarcoma of the median nerve at the elbow. plast reconstr surg 1989;528-32. 27. tacconi l, thom m, thomas dg. primary monophasic synovial sarcoma of the brachial plexus: report of case 279 intraneural synovial sarcoma of median nerve and review of literature. clin neurol neurosurg 1996;98:249-52. 28. spielmann a, janzen dl, o’connell jx, munk pl. intraneural synovial sarcoma. skeltal radiol 1997;26:67781. 29. chesser tj, geraghty jm, clarke am. intraneural synovial sarcoma of median nerve. j hand surg(br) 1999;24:3735. 30. zenmyo m, komiya s, hamada t, et al. intraneural monophasic synovial sarcoma: a case report. spine 2001;26:310-3. 31. lestou vs, o’connell jx, robinchaud m,et al. cryptic t(x;18), ins(6;18), and syt-ssx2 gene fusion in a case of intraneural monophasic synovial sarcoma. cancer genet cytogenet 2002;138:153-6. 32. weinreb i, perez-ordonez b, guha a, kiehl tr. mucinous gland predominant synovial sarcoma of a large peripheral nerve : a rare case closely mimicking metastatic mucinous carcinoma. j clinical pathol 2008;61:672-6. 33. uehara h, yamasaki k, fukushima t, et al. intraneural synovial sarcoma originating from median nerve. neurol med chir 2008;48:77-82. doi: 10.33962/roneuro-2023-031 west syndrome and multiple sclerosis association. about a case si ahmed hakim, megherbi lilia, daoudi smail romanian neurosurgery (2023) xxxvii (2): pp. 175-177 doi: 10.33962/roneuro-2023-031 www.journals.lapub.co.uk/index.php/roneurosurgery west syndrome and multiple sclerosis association. about a case si ahmed hakim, megherbi lilia, daoudi smail neurology department, university hospital of tizi-ouzou, algeria abstract introduction. west syndrome is a rare and severe infantile epileptic encephalopathy, beginning around the age of six months, characterized by a classic electro-clinical triad. this is a pathology totally different from multiple sclerosis (ms) which is a demyelinating disease of the central nervous system caused, affecting young adults, especially females. the association of these two pathologies has never been described. observation. we report here an exceptional presentation of ms in a 14-year-old girl with a history of west syndrome. she had normal development until the age of six months, when she began to have flexion spasms. the diagnosis of west syndrome was made with a normal mri. the infantile spasms disappeared after treatment with vigabatrin and adrenocorticotropic hormone (acth). it had generally progressed to lennox gastaut encephalopathy, with delayed psychomotor development and epileptic sequelae. at 14, she presented with left hemiparesis within a few days. a cerebral mri showed multiple nodular hyperintensities of the supra and infratentorial white matter, with the presence of an active lesion, fulfilling the diagnostic criteria for multiple sclerosis. csf analysis was normal. anti-aqp4, antimog, anti-nmda and anti-gaba (ab) antibodies were absent in the blood. antibodies against hiv and viral hepatitis were. biotinidase activity and autoimmunity tests were correct. the patient received high doses of methylprednisolone iv (1g/day) for three days with remarkable clinical improvement after 15 days. discussion. ms is a complex and heterogeneous central nervous system (cns) demyelinating disease. it is not uncommon for epilepsy to be the first symptom of multiple sclerosis. seizures, on the other hand, are more common after disease progression. although the disease is characterized by inflammatory lesions of the white matter, various neuropathological and radiological studies have shown that the disease also affects the grey matter. several studies have shown that seizures are three to six times more common in ms patients than in the general population. even though ms can start with epilepsy and a seizure may be the only symptom of a relapse of ms, it is still not known whether the two diseases coexist or whether ms predisposes to seizures. conclusion. the association of these two totally different pathologies can lead us to say that the mechanism of multiple sclerosis may begin in childhood and that the clinical signs appear in adulthood. introduction w e s t s y n d r o m e i s a r a r e a n d s e v e r e a g e r e l a t e d e p i l e p t i c encephalopathy of infancy comprising a triad of infantile spasms, hypsarrhythmia and psychomotor delay. 50% to 90% of patient evolve keywords west syndrome, multiple sclerosis, inflammation corresponding author: si ahmed hakim neurology department, university hospital of tizi-ouzou, algeria siahmed-hakim@hotmail.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 176 si ahmed hakim, megherbi lilia, daoudi smail to other syndromes mostly lennox gastaut syndrome, whereas multiple sclerosis (ms) is a central nervous system demyelinating disease caused by an autoimmune process. it is highly prevalence among young female adults. their presence with a single patient has never been described. we herein report an exceptional presentation of ms in a 14-year-old girl child with a childhood history of west syndrome. observation a 14-year-old_female child presented with rapidly onset left hemiparesis. concerning her past medical history, she was born into a second-degree consanguineous marriage. she had a history of intrauterine growth restriction (iugr) and low birthweight in a normal delivery. nevertheless, she had normal development until the age of six months, when she started having flexion and extension spasms occurring in clusters, usually shortly after waking up. the diagnosis of west syndrome was established. the infantile spasms disappeared after three years of treatment with vigabatrin and adrenocorticotropic hormone (acth). it had typically progressed to lennox gastaut encephalopathy, with psychomotor developmental delay and epileptic sequelae. at the age of four, she presented stereotyped behaviours, most commonly involving hands. therefore, the diagnosis of rett syndrome has been suspected, and it was ruled out by a negative genetic study. a brain mri at this age was without abnormalities. her epilepsy was relatively stable under lamotrigine and sodium valproate with motor and cognitive sequelae. interestingly, she was able to walk at the age of 8 years after intensive motor rehabilitation and was relatively autonomous in dayto-day tasks. at the age of 14, she presented a left hemiparesis worsening over few days. on examination, we found a conscious, very agitated and irritable child with incessant cries and tears, retrognathism, microcrania, low hair implantation, stereotyped hand rubbing movements, generalized hypotonia and left hemiparesis. a brain mri showed multiple nodular and bilateral t2/flair hyper signals and t1 hyposignals in the supra and subtentorial white matter, with the presence of one active lesion in the left oval centre (figure 1). csf analysis with iso-electro-focalisation showed a proteinorachia at 0.33mg/l with the absence of the oligoclonal band (ocb). the anti aqp4, anti-mog, anti nmda, and anti-gaba antibodies (ab) were absent in the blood. antibodies to hiv and viral hepatitis were negative. the biotinidase activity and autoimmunity tests were correct. the patient received high doses of iv methylprednisolone (1g/day) for three days with a remarkable clinical improvement after 15 days. five months later, her motor symptoms had worsened with the recurrence of her left hemiparesis. a brain and spinal cord mri showed a significant increase in lesion load with the presence of at least eight active lesions as well as multiple spinal cord lesions (figure 2). consequently, treatment was initiated, including an iv infusion of methylprednisolone (1 g/d for five days), followed by an iv ig course (25mg/d for three days) with a favourable response. another iv ig course was given after one month, and the girl was remarkably stable. six months after that, the patient had another relapse, which was made of left arm weakness with an exacerbation of her seizures. a brain mri was performed, showing the presence of multiple active lesions (figure 3). she was then admitted for an iv infusion of methylprednisolone (1g/d for three days) followed by monthly repeated courses of iv ig as the diagnosis of mogopathy was highly suspected. under this treatment, the patient's evolution was favourable, and he has been free of relapses ever since. figure 1. brain mri showing multiple flair hypersignals in sub and supra tentorial white matter. 177 west syndrome and multiple sclerosis association. figure 2. brain and spinal cord mri after 2 months, showing an increase in the number and volume of the lesions. figure 3. brain mri after 11 months from the first relapse. discussion multiple sclerosis (ms) is a central nervous system (cns) demyelinating disease that is both complex and heterogeneous. it is not rare for epilepsy to be the first symptom of multiple sclerosis. seizures, on the other hand, are more common after the start of the condition (1). although the disease is characterized by inflammatory lesions in the white matter, various neuropathological and radiological studies have shown that the disease also affects the grey matter. several studies have showed that seizures are three to six times more common among ms patients than in the general population (2) (3). even though ms can start with epilepsy (4) and that a seizure may be the only symptom of an ms relapse (5), it's still unclear whether the two diseases coexist or whether ms predisposes to seizures (6). on the other hand, infantile spasms initially discovered by william james west in his own son in 1841. the term infantile spasms syndrome (iss) now refers to an epileptic syndrome that affects children under the age of one year (rarely older than two years), with clinical spasms that usually occur in clusters, with hypsarrhythmia as the most common eeg finding. the spasms that are frequently associated with developmental arrest or regression. the name west syndrome (ws) refers to a subset of iss marked by clustered spasms and hypsarrhythmia on an eeg, as well as delayed brain development or regression. the pathophysiology of infantile spasms isn't completely understood. it is well-known that partial seizures can progress to spasms, as evidenced by invasive and surface eeg recordings, as well as the peculiar pet (positron emission tomography) finding of hypometabolism of deep grey structures and the brain stem in children with spasms, all support the cortical-subcortical interaction hypothesis (7). the therapeutic response to hormonal therapy, on the other hand, has shown a role for the hypothalamicpituitary axis and immunological systems. the developmental desynchronization model better explains the narrow age of onset as well as the developmental effects (7). conclusion the association of west syndrome and multiple sclerosis has never been described, and the common point is neuroinflammation, which can open perspectives on the understanding of the physiopathological mechanisms of these two pathologies, and can be an argument that the substance gray is not spared from multiple sclerosis. references 1. gasparini, s., ferlazzo, e., ascoli, m. et al. risk factors for unprovoked epileptic seizures in multiple sclerosis: a systematic review and meta-analysis. neurol sci 38, 399– 406 (2017). https://doi.org/10.1007/s10072-016-2803-7 2. spatt j, chaix r, mamoli b (2001) epileptic and non epileptic seizures in multiple sclerosis. j neurol 248:2 –9 2. 3. ghezzi a, montanini r, basso pf, et al. (1990) epilepsy in multiple sclerosis. eur neurol 30:218 –223 4. kinnunen e, wikstrom j. prevalence and prognosis of epilepsy in patients with multiple sclerosis.epilepsia. 1986 nov -dec;27(6):729 -33. 5. spatt j, goldenberg g, mamoli b. simple dysphasic seizures as the sole manifestation of relapse in multiple sclerosis.epilepsia. 1994 nov -dec;35(6):1342 -5. 6. poser cm, brinar vv. epilepsy and multiple sclerosis. epilepsy behav. 2003 feb;4(1):6 -12. review 7. chugani ht. pathophysiology of infantile spasms. adv exp med biol. 2002;497:111–21. microsoft word 1leucesebastian_chronicsubdural romanian neurosurgery (2018) xxxii 4: 523 537 | 523             doi: 10.2478/romneu-2018-0068 chronic subdural haematoma: a retrospective 232 cases review a comparison of a single centre between a population aged under 75 and above 75 years old s. leuce², h.d. bade¹, h. pleș¹,² 1“victor babeș” university of medicine and pharmacy timișoara, romania 2emergency clinical county hospital timișoara, romania abstract: chronic subdural haematoma represents a major problem in the neurosurgical field concerning population both under and above 75 years old. it is not only a matter of prevalence or pure statistics but it embodies true understanding of how the pathology affects older patients, their life expectancy and quality when reliable factors are implied such as comorbidities, relation with the moment of surgery, the existence of anticoagulation therapy, and many more. we target these challenges in a study on 232 cases of treated chronic subdural haematomas with impact on two major categories those under and above 75 years old in the neurosurgery department, county hospital “pius branzeu” timisoara, romania. key words: antithrombotics, chronic subdural haematoma, midline shift, older population introduction at the basis of chronic subdural haematoma (csh) formation stands multiple aetiologies, such as trauma and acute subdural haematoma(ash), spontaneous reasons including hydrocephalus, coagulopathies and chronic anticoagulation therapy, and iatrogenous causes such as a complication of a lumbar puncture (lp). among the risk factors involved are: predisposing of trauma, alcohol consumption, epilepsy, hemorrhage, and other predisposing factors such as coagulopathy, antithrombotics, high blood pressure, brain atrophy, hygroma [2,7,13,22,24] and others. clinical features include: motor deficiency, altering of consciousness, intracranial hypertension (ich) syndrome, pseudotumoral, pseudodementia syndromes, headaches, and progressive speech impairment [11]. differential diagnostics comprise of the following; stroke, dementia, encephalitis, cerebral abscess, tumor, and cerebral parasitosis as showed by standard imagistic 524 | leuce et al chronic subdural haematoma             studies from ct (gold standard) and mri [26,35]. the treatment options for csh are for symptomatic cases, midline shift(mls) with a minimum of 5 mm, mass effect, etc., also, conservative treatment stands for neurologically intact elderly patients on antithrombotics withdrawal of antithrombotic medication 7 days prior to the surgery in the case of eligibility for an operation, perioperative antibiotherapy prophylaxis [5,14,16,17,19,21,33]. in respect of the well-established techniques used for csh evacuation these include; single “burr-hole” or double “burrhole” technique + drainage, craniotomy +/ cranioplasty + drainage, subdural evacuating port system (seps), twist drill craniotomy [23], and endoscopy [10,20,27,30,34]. in the matter of complications and prognostics, the surgical intervention may be grafted by complications such as; haematoma persistency, pressure pneumocephalus, subdural empyema, convulsions, intracerebral hemorrhage, and others [8,35]. recurrence of csh can be early less than 3 months postoperative or late more than 3 months postoperative [3]. postoperative midline-shift over 5 mm, diabetes, preoperative convulsions, over 20 mm in size of the haematoma, intracranian (ic) hypotension, low glasgow coma scale(gcs), mixed density of the haematoma on the ct-scan, antithrombotic therapy, cancer and male population are associated with a higher risk of recurrence [19,29,32]. aim of the study to assess the results of a retrospective comparative study of 232 aged-related subjects over and under 75 years old with csh treated in the neurosurgery dep. timisoara county hospital between 1st of january 2013 and 30th of september 2017. materials and methods a total of 232 enrolled patients diagnosed with csh from which 181 were male and 51 were female. age over 75 yrs.; 70 m and 25 f; under 75 yrs.; 111 m and 26 f. age-related < 75 yrs. old: 0-10 yrs., 9; 11-20 yrs., 2; 21-30 yrs., 1; 31-40 yrs., 2; 41-50 yrs., 17; 51-60 yrs., 28 6174 yrs., 78. age-related >75 yrs. old: 75-80 yrs., 53; 81-85 yrs., 31; 86-90 yrs., 9; 91-95 yrs.:2, comprising a single-centre study of the department of neurosurgery county hospital “pius branzeu” timisoara, romania. chi square test was utilized to predict a statistically significant importance of several findings in the study. romanian neurosurgery (2018) xxxii 4: 523 537 | 525             figure 1 sexes and prevalence of patients in respect to cohort figure 2 age-related no. of patients enrolled under 75 years old regarding the data offered by the study, it shows that the incidence of csh increases with lower ages in the population studied over 75 years old as follows: between 75-80 years old there were 53 patients included; between 81-85 years old, 31 patients; between 86-90 years old, 9 patients and from 91-95 years old, 2 patients. figure 3 age-related no. of patients enrolled above 75 years old total of patients patients over 75 yrs. patients under 75 yrs. total male female rural urban 232 95 137 181 70 111 51 25 26 78 28 50 154 67 87 age number of patients 0-10 9 11-20 2 21-30 1 31-40 2 41-50 17 51-60 28 61-74 78 age number of patients 75-80 81-85 86-90 91-95 53 31 9 2 526 | leuce et al chronic subdural haematoma             overall, fewer people in the segment considering the older than 75 years cohort spent between 1 and 3 weeks in hospital in comparison to the other studied cohort. less than 1 week in hospital includes 26 patients vs. 34 in the same 2 groups; between 1-2 weeks it was 57 vs. 73 patients, and over 3 weeks in hospital there were 7 vs. 8 patients in total. figure 4 cohorts in relation to hospitalization in addition, they were 44 compared to 74 people with left-side csh in the 2 groups, 37 vs. 40 people with right-side csh and 14 vs. 23 having bilateral haematomas. figure 5 cohorts in relation with localization of the csh midline shift is another landmark of the study that shows the following: 61 vs. 83 patients did not have any midline shift; 6 vs.10 patients had 1-5 mm deviation; 15 patients in both groups had mls between 6-10 mm; and 9 vs.18 had a deviation between 11-15 mm and 4 vs.11 patients had mls over 15 mm. figure 6 cohorts in relation with mls time of hospitalization patients over 75 patients under 75 less than 1 week 1-2 weeks 2-3 weeks over 3 weeks 26 34 57 73 5 22 7 8 type of csh patients over 75 patients under 75 left right bilateral 44 74 37 40 14 23 mls (midline-shift) patients over 75 patients under 75 0 mm 1-5 mm 6-10 mm 11-15 mm over 15 mm 61 83 6 10 15 15 9 18 4 11 romanian neurosurgery (2018) xxxii 4: 523 537 | 527             gcs at presentation was recorded for all the patients included in the study: gcs 3p was seen in 2 vs. 4 patients in the 2 groups studied; gcs 4p, 2 vs. 1 patient; gcs 5p, each group had 1 patient; gcs6p, none of the 2 groups; gcs 7p, 1 vs. 2; gcs 8p, 5 vs. 3; gcs 9p, 4 vs. 3; gcs 10p, 3 vs. 2; gcs 11p, 0 vs. 1; gcs 12p, 4 vs. 3; gcs 13p, 10 vs. 7; gcs 14p, 33 vs. 27; gcs 15p, 30 vs. 83 in the cohorts. figure 7 cohorts in correlation with gcs at presentation clinical features of the csh were assessed as being part of the general findings in this study: one-side motor weakness in 61 vs. 73 cases; dysphasia in 31 vs. 37; headaches in 46 vs. 86; convulsions in 6 vs. 15 patients; paraparesis in 1 vs. 4; tetraparesis 1 vs. 0; unilateral babinski signs in 22 vs. 23 and bilateral babinski signs in 12 vs. 7 patients from the over/under 75 groups. gcs at presentation patients over 75 patients under 75 15 30 83 14 33 27 13 10 7 12 4 3 11 0 1 10 3 2 9 4 3 8 5 3 7 1 2 6 0 0 5 1 1 4 2 1 3 2 4 528 | leuce et al chronic subdural haematoma             figure 8 the 2 groups in relation with clinical features figure 9 cohorts in relation to radiological modality of exploration figure 10 relationship between associated haematomas and age-related study groups in the matter of imagistic data, we had 91 patients scanned with ct in the first group and 105 in the second one; 4 had taken an mri scan in the first group vs. 16 in the second one, and both investigations were undergone by 16 of the patients in the second group. clinical features patients over 75 patients under 75 hemiparesis dysphasia headaches convulsions paraparesis tetraparesis unilateral babinski bilateral babinski 61 73 31 37 46 86 6 15 1 4 1 0 22 23 12 7 imagistics patients over 75 patients under 75 ct mri both 91 105 4 16 0 16 associated haematoma patients over 75 patients under 75 extradural parenchymal 3 3 2 1 romanian neurosurgery (2018) xxxii 4: 523 537 | 529             figure 11 associated co-morbidity factors in relation to the 2 populational groups the associated morbidity and mortality factors in the assessment of csh are amongst other important elements in the evaluation of age-related evolution of the pathology, therefore crf (chronic renal failure) was seen in 2 vs. 4; heart failure in 14 vs. 13; stroke in 11 vs. 15; respiratory failure in 12 vs. 9; pneumonia in 7 vs. 9; afib in 17 vs. 12; ischemic cardiopathy in 27 vs. 18; sepsis in equal parts 4:4; cancer in 3 vs. 4; high blood pressure in 53 vs. 62; type ii diabetes in 14 vs. 24 and copd in 1 vs. 5 cases. figure 12 use of antithrombotics in csh regarding cohorts regarding the use of antithrombotics, in the first group of patients we found 10 vs. 9 in the second one who were on antiplatelet therapy and 21 over 75 years old vs. 13 under 75 years old who took anticoagulants. figure 13 time of hospitalization between admission and surgery associated co-morbidity patients over 75 patients under 75 chronic renal failure heart failure stroke respiratory failure pneumonia afib ischaemic cardiopathy sepsis cancer high blood pressure type 2 diabetes copd 2 4 14 13 11 15 12 9 7 9 17 12 27 18 4 4 3 4 53 62 14 24 1 5 basic antithrombotic therapy   patients over 75 patients under 75 antiplatelet anticoagulants 10 9 21 13 patients over 75 patients under 75 median days of hospitalization from admission until surgery   2.30 days 2.99 days 530 | leuce et al chronic subdural haematoma             figure 14 therapy options in respect of the 2 groups figure 15 89 years old patient ct scan in axial plane showing left frontal-parietal csh and a recent ischemic event localized left frontal-pole figure 16 axial ct scan of a 67 years old patient with a 13 cm ap length and a 2.5 cm thick left csh and right midline shift figure 17 a 61 years old patient, axial image showing left fronto-parieto-temporal chronic subdural haematoma therapy options patients over 75 patients under 75 surgery “burr-hole” craniectomy craniotomy minimal craniectomy csh kit seps conservative 85 124 0 2 2 2 83 119 0 1 10 13 romanian neurosurgery (2018) xxxii 4: 523 537 | 531             figure 18 a left isodense csh with several arias of hypodensity showing re-bleeding phenomenon and a 26 mm thickness showing mass effect over the midline shift and almost complete imprinting of the left ventricle results the study shows the mortality in patients older than 75 outnumber those under 75. the difference is statistically significant under the evaluation of the chi square test (0.0001) thus the comatose patient number is higher in the cohort representing patients over 75 in comparison with the second group, this proved not to be statistically significant (chi square score 0.125). from the two groups, those over 75 were treated predominantly in a conservative fashion that meant 10.526% vs. 9.489%, also without importance in the study (value=0.725). the number of those over 75 years old on antithrombotics is significantly higher than younger patients with the same treatment (chi square test 0.007). bilateral chronic subdural haematomas (bcsh) were rarely observed in the over 75 years cohort vs. those under, (14.736% and 16.788%) but this also poses no statistical significance (chi square test 0.943) evenly quoted by song dh et al [28] from the total number of patients, 54% from those under 75 years old, had left hemispheric csh vs 29.1% showing right hemispheric involvement. in the second group regarding the patients over 75 years old, csh was seen more frequently 46.3% affecting the left side vs 38.9% in the right side. in the matter of prevalence of the genderdependent population, 81.1% of males and 18.9% females were under 75 years old in comparison to 73.6% of males and 26.3% females over 75 years also stated in between the values reported in the study by oh j. et al.[24]. the improvement of deficits was more frequently found in the over 75 years old cohort (chi square test 0.010). the medium global hospitalization time was 10.48 days with a standard deviation of 7.233 days with a range from 1-49 days. in the over 75 year old group the study showed that a 532 | leuce et al chronic subdural haematoma             total of 26 patients (25.86%) stayed under 1 week and 7 patients (6.47%) stayed for over 3 weeks. from that, those staying under 1 week comprised 27.37% and those staying over 3 weeks 7.37%, and in the cohort under 75 years old 24.82% under a week and 5.84% over 3 weeks. the second group showed a medium hospitalization time of 10.36 days with a standard deviation of 6.803 days and in those over 75 years old 10.67 days with a 0.839 standard deviation. mortality was seen in 11.4% in the male population and 7.84% in the female population from the total of deaths. in our study, 33.3% were on antithrombotics either antiplatelet or anticoagulation treatment. 38.8% of the deaths registered in the over 75 years old cohort were on antithrombotics, but less than 16.6% was encountered in those under 75. figure 20 outcomes in respect to the clinical features the average value of mls was 4.32 mm with a standard deviation of 5.772 mm. for the first study-group the average mls was 4.68 mm (standard deviation 6.043 mm) and for the second group the study showed a mls of 3.74 mm with a standard deviation of 5.290 mm. a value of 4.45 mm was showed for the patients who overcame the pathology with a median standard deviation of 5.797 mm and in those who died the prevalence translates to a 3.21 mm mls with a median deviation of 5.548 mm, thus there were no significant differences in the two median values concerning the 2 study-groups. clinical features  total  patients over 75 yrs  old  patients under 75 yrs old  hemiparesis  57,758%  64%  53,284%  afazia  29%  32,631%  27,007%  headaches  56,896%  48,421%  62,773%  epilepsy  9,051%  6,315%  10,948%  babinsky sgn.  27,586%  35,789%  21,897%  unilat.babinsky  19,396%  23,157%  16,788%  bilat.babinsky  8,189%  12,631%  5,109%  romanian neurosurgery (2018) xxxii 4: 523 537 | 533             figure 21 outcomes according to gcs in cohorts the average value for gcs was 13.34 with a standard deviation of 2.823. for those under 75 years old, the average gcs was 13.66 with a standard deviation of 2.648 and for those over 75 years old the study showed a value of 12.83 and a mean deviation of 3.027. there is a significant difference regarding the value of gcs between those who survived and those who died. from the conservative-treated patients all of them had an initial gcs of 14 or 15 with 3 exceptions: one patient under 75 with a gcs of 12; one patient over 75 years with a gcs of 3 and one patient over 75 years with a score of 4. overall, neurological improvement was seen in 60% over 75 years old and respectively in 84.61% under 75. without any improvement there were 30% in the first group and 15.38% in the second one. in matter of mortality-csh topography relationship, our study showed statistically higher rates of mortality for the over 75 years group vs. younger ages not only for unilateral csh but also bilateral (chi square test 0.01). the evolution of the disease according to age group can be summarized as follows: average time of hospitalization from admission to surgery was: 2.264 days in the 7580 years old subgroup; 1.580 days in the 81-85 years old subgroup and 1.727 days for those over 85 years old evaluated. the average time of hospitalization was 10.118 days (+/7.913) for the 75-80 years old subgroup; 11.709 days (+/8.327) for the 81-85 years old subgroup and 69.909 days (+/ 6.786) for those over 85 years old. there are no significant differences between the 3 subgroups regarding the average time of hospitalization. as for the topography of the csh in relation with antithrombotics the study found that the prevalence of those over 75 was higher (19.35%) in the anticoagulated group vs. 12.50% in those who did not benefit from the treatment and the same in the under 75 years old group where 22.72% had antithrombotics vs 15.65% without treatment. regarding the prevalence of comorbidity in the study, high blood pressure with a total percentage of 49.568% and in those over 75 years old 55.789% and below 75 years old45.255%; followed by ischemic cardiopathy gcs total patients over 75 patients under 75 13-15 5.263% 9.589% 2.564% 9-12 30% 45.454% 11.111% gcs=8 38% 60% 0% gcs=6-7   0% 0%   0% gcs=4-5   60% 66.666%   50% gcs=3 33.333% 50% 25% 534 | leuce et al chronic subdural haematoma             showing a total of 19.396%, atrial fibrillation comes third in line, followed by stroke, diabetes and others. discussion the study found —that under several aspects— significative differences concerning the evolution of a chronic subdural haematoma in the population under and over 75 years old. the haematomas are frequently encountered in the male population evenly under and over the age of 75, thus the total number of deaths are often seen in those over 75 no matter of gender or topography affected by the pathology. the state of coma was attributed more to those over 75. the administration of antithrombotics was a direct factor of correlation for the apparition and recurrence of the haematoma and presented higher incidence rates of bilateral csh with respect to edlmann e et al. [9] and de bonis p. et al. [7]. the elder patients seemed to have a lower rate of favorable neurological outcomes after the treatment opposite those of younger ages. the mortality is greater in the male population, and the study shows the appearance of motor deficits and aphasia were frequently seen in those under 75 years old in contrast with convulsions and the babinski signs that predominate in those over 75 years old. midline shift as a contributory factor of mortality was on all of its deviations and levels predominantly seen in the over 75 years group and less in those younger, and also independently of the gcs at admission with reference to kim hc et al. [17]. there were no differences in the matter of mortality for those who had bilateral haematomas in respect of the general csh prevalence. those treated conservatively from the group over 75 years old had a lower improvement percentage, higher mortality and stationary neurological outcome than the younger ages [35]. in a 2015 study, aristedis rovlias, spyridon theodoropoulos and dimitrios papoutsaki[26] reported a direct correlation between the csh prognostic and the neurology status at admission, an aspect that is strengthened by this study observing the increasing mortality in parallel with a lower gcs, therefore at a gcs between 13-15, mortality was 5.26%, at a gcs of 9-12 the mortality was 30%, at gcs 8 and 4-5 mortality was 37.5% and 60% respectively. masaaki uno et al. [31] focused in an article over the less favorable outcome of the csh in patients over 75 years old vs. those under 75, as did this study that showed a higher mortality among those over 75 (18.9%) than in those under 75 (4.3%), and lower favorable outcomes for elderly patients (75.7%) vs younger ages (86.8%). antithrombotic usage represents an independent rise factor for the appearance of the csh and it can also influence the prognosis [32,33,27]. in this study, 32.6% of those in the over 75 years old group had antithrombotics in comparison with 16% of those in the younger group. in a study made by agawa et al. [1], he reported a more unfavorable outcome for those with bilateral csh, a fact that this study also confirmed, that mortality from bilateral csh was significantly higher in patients over 75. romanian neurosurgery (2018) xxxii 4: 523 537 | 535             regarding the surgical treatment of the csh, masaaki et al.[31] presented a favorable outcome for those treated by surgery of between 70-90%, also demonstrated by this study in terms of neurological improvement (83.2%), even if the prognostic worsened for those over 80 than under, this aspect determined the making of age-related subgroups and showed that in those over 85 the mortality reduced by half. in-hospital related mortality in this study stands at the limits somewhere at 10.3% in comparison to masaaki with reported limits between 0.21%-27.5%. in a 2012 study on 125 patients made by danilo otavio de araujo silva et al. [6] with csh, headaches showed in 40% of patients and deficits at 44%. this study percentage is nearby those values with 56.8% for the first one and 57.7% for the deficit. i. a. iliescu [11,12], in an article, correlates the higher incidence of the csh in the male population, also demonstrated by this study. from the total of 232 patients,181 were male (78%) and only 51 were female (22%), and apparently the male gender is an independent negative factor for the csh outcome, mortality being significative higher than in the female population (8.6% vs 1.7%). the same study reports a more right cerebral hemisphere dominance of the csh (52%) and only 30% affecting the left side, therefore, in comparison this study found a more left-side prevalence of the csh despite the 2 categories and last but not least between 2-19% of the patients had convulsions in the comparative study, in this study it was found that 9.05% of patients were affected which resemble the study of battaglia et al.[4] who reports incidences of 10.6% and 14.9%. quiang-ping wang et al. [33] exemplified in a study that from their cohort of csh presenting patients, 20.5% had high blood pressure, 16.6% had heart failure and 13.9% had diabetes. in this study the findings were in the order 49.5%,11.6% and 16.3% thus high blood pressure and heart failure were found more often in those over 75 years old. borger v. et al. [5] randomized patients in 3 age-related groups as follows: 65-74 years; 75-84 years and 85-94 years. they concluded that postoperative although all the groups had increased improvement scores, they synchronized with age. our study has similar results, therefore in those treated under 75 the percentage was 86.8% and declining to 75.7% in those over 75. in this study, 3.01% of patients showed a positive diagnosis for cancer, higher for those over 75 years old and it correlates with the study of yuji agawa et al. [1] that stated an unfavorable prognostic for those affected by a tumor. conclusions there are significant differences between the csh outcome in the two study populations, therefore we consider that those differences should be taken into consideration for the in-hospital care of patients in order to maximize the prognostic. patients over 75 years old are posing a higher mortality rate than the younger ages. coma is a complication of the slower rates of improvement, convulsions and deficits in the 536 | leuce et al chronic subdural haematoma             group over 75 do not contraindicate surgery when imposed. those on antithrombotics showed an increased risk of developing bilateral csh at higher ages and a more unfavorable outcome, a fact that is also predicted by the value of the mls or the associated comorbidities, making the approach more complex. the aging process will eventually lead to a higher incidence and prevalence of csh in the population and can also stimulate the necessity of permanent care and evaluation of these kinds of patients. there is a need for supplementary studies and opinions in order to establish a common point of optimum treatment of this vulnerable category of patients. correspondence horia pleș “victor babeș” university of medicine and pharmacy, timișoara ples.horia@umft.ro references 1.agawa y, mineharu y, tani s et al. bilateral chronic subdural haematoma is associated with rapid progression and poor clinical outcome. neurologia medico-chirurgica 2016;56(4):198-203 2.ahn jh, jun hs, kim jh et al. analysis of risk factor for the development of chronic subdural haematoma in patients with traumatic subdural hygroma. journal of korean neurosurgical society. 2016;59(6):622-627. 3.almenawer sa, farrokhyar f, hong c et al. chronic subdural haematoma management: a systematic review and meta-analysis of 34,829 patients. ann surg. 2014 ; 259(3):449-457. 4.battaglia f, lumbrano v, ribeiro-filho t et al. incidence and clinical impact of seizures after surgery for chronic subdural haematoma.neurochirurgie. 2012;58(8):402-409. 5.borger v, vatter h, oszvald a et al. chronic subdural haematoma in elderly patients: a retrospective analysis of 322 patients between the ages 65-94 years. acta neurochir (wien). 2012;154(9):1549-1554. 6.de araujo silva do, matis gk, costa lf, et al. chronic subdural haematomas in the elderly: surgical results from a series of 125 cases: “old horses” are not to be shot! surgical neurology international. 2012; 3:150. 7.de bonis p, trevisi g, de waure c et al. antiplatelet/anticoagulant agents and chronic subdural haematoma in the elderly. ten cate h, ed plos one 2013;8(7): e68732. 8.dinc c, iplikcioglu ac, bikmaz k et al. intracerebral hemorrhage occurring at remote site following evacuation of chronic subdural haematoma. acta neurochir. 2008;150(5): 497-499. 9.edlmann e, giorgi-coll s, whitfield pc et al. pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy. journal of neuroinflammation 2017;14(1):108. 10.guilfoyle mr, hutchinson pja, santarius t. improved long-term survival with subdural drains following evacuation of chronic subdural haematoma. acta neurochirurgica. 2017; 159(5)903-905. 11.iliescu i, constantinescu a. clinical evolutional aspects of chronic subdural haematomas-literature review, journal of medicine and life, 2015;8(spec issue):26-33. 12.iliescu i. current diagnosis and treatment of chronic subdural haematomas, journal of medicine and life 2015;8(3):278-284. 13.ju m-w, kim s-h, kwon h-j, et al. comparison between brain atrophy and subdural volume to predict chronic subdural haematoma: volumetric ct imaging analysis. korean journal of neurotrauma.2015;11(2):8792. 14.kageyama h,toyooka t,tsuzuki n et al.nonsurgical treatment of chronic subdural haematoma with tranexamic acid. journal of neurosurgery 2013;119(2):332-337. 15.kaliaperumal c, khalil a, fenton e et al. a prospective randomize study to compare the utility and outcomes of subdural and subperiosteal drains for the treatment of chronic subdural haematoma. acta neurochir (wien). 2012; 154(11):2083-2089. romanian neurosurgery (2018) xxxii 4: 523 537 | 537             16.kim dh, kim hs, choi hj et al. recurrence of the chronic subdural haematoma after burr-hole drainage with or without intraoperative saline irrigation. korean journal of neurotrauma 2014;10(2):101-105. 17.kim hc, ko jh, yoo ds et al. spontaneous resolution of chronic subdural haematoma: close observation as a treatment strategy. journal of korean neurosurgical society.2016;59(6):628-636. 18.kim j, moon j, kim t, et al. risk factor analysis for the recurrence of chronic subdural haematoma: a review of 368 consecutive surgical cases, korean journal of neurotrauma 2015;11(2):63-69. 19.kim su, lee dh, kim yi et al. predictive factors for recurrence after burr-hole craniostomy of chronic subdural haematoma. journal of korean neurosurgical society. 2017;60(6):701-709. 20.kolias ag, hutchinson pj, santarius t. chronic subdural haematoma: disseminating and implementing best practice. acta neurochirurgica.2017; 159(4):625626. 21.kuwabara m, sadatomo t, yuki k et al. the effect of irrigation solutions on recurrence of chronic subdural haematoma: a consecutive cohort study of 234 patients. neurologia medico-chirurgica 2017;57(5):210-216. 22.lee k-s.chronic subdural haematoma in the aged, trauma or degeneration? journal of korean neurosurgical society. 2016;59(1):1-5. 23.lee s-j, hwang s-c,im sb.twist-drill or burr-hole craniostomy for draining chronic subdural haematomas:how to choose it for chronic subdural haematoma drainage.korean journal of neurotrauma. 2016;12(2)107-111. 24.oh j, shim j-j, yoon s-m et al. influence of gender on occurrence of chronic subdural haematoma; is it an effect of cranial asymmetry? korean journal of neurotrauma. 2014; 10(2):82-85. 25.rovlias a, theodoropoulos s, papoutsakis d. chronic subdural haematoma: surgical management and outcome in 986 cases: a classification and regression tree approach. surgical neurology international. 2015; 6:127. 26.senturk s, guzel a, bilici a et al. ct and mr imaging of chronic subdural haematoma: a comparative study. swiss med wkly. 2010;140(23-24):335-340. 27.shapey j, glancz lj, brennan pm. chronic subdural haematoma in the elderly. is it time for a new paradigm in management? current geriatrics reports. 2016; 5:7177. 28.song dh, kim ys, chun hj, et al. the predicting factors for recurrence of chronic subdural haematoma treated with burr hole and drainage. korean journal of neurotrauma.2014;10(2):41-48. 29.tahsim-oglou y, beseoglu k, hanggi d et al. factors predicting recurrence of chronic subdural haematoma: the influence of intraoperative irrigation and lowmolecular-weight heparin thromboprophylaxis. acta neurochir (wien). 2012; 154(6):1063-1068. 30.tailor j, fernando d, sidhu z et al. clinical audit effectively bridges the evidencepractice gap in chronic subdural haematoma management. acta neurochirurgica 2017; 159(4):627-631. 31.uno m, toi h, hirai s. chronic subdural haematoma in elderly patients: is this disease benign? neurologia medico-chirurgica. 2017;57(8):402-409. 32.wada m, yamakami i, higuchi y et al. influence on antiplatelet therapy on postoperative recurrence of chronic subdural haematoma: a multicenter retrospective study in 719 patients. clin neurol and neurosurg. 2014; 120:49-54. 33.wang q-p, yuan y, guan j-w et al.a comparative study of irrigation versus no irrigation during burr-hole craniotomy to treat chronic subdural haematoma. bmc surgery. 2017;17(1):99 34.yadav yr, parihar v, namdev h et al. chronic subdural haematoma. asian journal of neurosurgery.2016;11(4):330-342 35.you cg, zheng xs. postoperative pneumocephalus increases the recurrence rate of chronic subdural haematoma. clin neurol neurosurg. 2018; 166:56-60. a. chirianc, giorgiana ion, z. faiyad, i. poeata romanian neurosurgery (2019) xxxiii (4): pp. 508-512 doi: 10.33962/roneuro-2019-082 www.journals.lapub.co.uk/index.php/roneurosurgery treatment of chronic pain by spinal cord stimulation f. aichaoui1, a. khelifa1, i. assoumane2, m. al-zekri1, a. morsli1 1 neurosurgical department of beo university hospital, algiers, algeria 2 national hospital of niamey, niger abstract failed back surgery syndrome (fbss) is often used to describe the condition of patients who have experienced continued pain after surgery. it is of multifactorial genesis and may be the consequence of various lumbar spinal diseases; lumbar disc herniation surgery or spinal canal stenosis laminectomy. the presented series included 13 patients affected with chronic pain related to fbss who underwent implantation of spinal cord stimulation. the mean percentage of pain relief was 90 % for all patients. 60% of the patients were in a better psychological status and the intake of analgesic medications has been reduced of more than 70%. more than 50% of the patients could resume professional activities. analysis of the risks and benefits comes in favour of spinal cord stimulation. introduction chronic pain can be seen in 12 to 40% of patients that underwent a spine surgery according to the series (13,14). this persistent pain is known as failed back surgery syndrome (fbss) (8). clinically it appears in the form of lumbar and / or radicular pain. this pain syndrome often appears after multiple surgical procedures for disc herniation or stenotic spinal canal. it can usually be explained by the contribution of several factors including arachnoiditis or periradicular fibrosis (15). the patients have mixed pain syndrome of neuropathic and nociceptive character; the neuropathic component is found in 80 to 96% for lumbosciatic and 8 to 16% for lumbago (5). the fbss is one of the indications of the spinal cord stimulation after failure of conservative treatment (13). this neurostimulation performed for the first time by shealy et al in 1967, consists of placing electrodes in the epidural space in contact with the spinal cord. according to the series, this technique can improve this pain syndrome in 55 to 88% of cases (2). keywords neuromodulation, pain, failed back syndrome, spinal cord stimulation, epidural stimulation corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 521 treatment of chronic pain by spinal cord stimulation materials and methods: patient’s selection we performed a prospective a study of 13 patients with a spinal cord stimulator for persistent chronic pain after spinal surgery. this work was held from may 2013 to december 2017. our serie includes 6 women and 7 men with an average age of 42 years with extreme ages of 21 and 66 years. all patients had a detailed clinical evaluation including their pain characteristics, the intensity of the pain using the visual analogue scale (vas), the drugs intake using mqs (medication quantification scale), and an assessment of the psychological impact of the pain (table 1). imaging investigations and electrophysiology were performed before spinal cord stimulation. imaging, represented by ct and / or spinal mri, eliminated the presence of disc herniations or stenotic spinal canal. implantation concerned patients with severe pain (vas> 5/10), chronic pain (> 6 months) and resistant pain to usual treatment. etiologies the chronic pain that affected our patients was due to herniated disk surgery in 11 cases (84.6%), of narrow lumbar canal surgery in one case (7.7%) of scoliosis surgery also in one case (7.7%). patients who had been implanted for post-traumatic spine pain or for any other condition were excluded from the study (table 1). characteristics of the pain patients suffered from radiculalgia of the lower limbs with or without chronic low back pain. they were of neuropathic type (> 4 at the dn4 score), evolving for more than six months, resisting to several categories of treatments including opioids, anticonvulsants, and tricyclic antidepressants. four patients had previously benefited from transcutaneous stimulation that did not cover the entire pain territory. the delay between the onset of pain and implantation of the spinal cord stimulator was average of 8 years with an interval between 2 and 24 years. implant procedure we use wide and flat electrodes with 16 contacts (penta, saint jude®). their plate configuration allows them to be in contact with the dura over a large area and to generate a 180° stimulation field in the direction of the spinal cord. these types of electrodes are designed to reduce energy consummation by minimizing losses. the wide conformation of the electrode requires an open surgical approach for better visual control of the epidural space. the procedure is performed under general anesthesia in the prone or right lateral position. after minimal skin incision and dissection of the musculo-fascial planes, the electrode is introduced through an inter-spinous approach to have a bilateral effect, at the t9-t10 space (figure.1). a radiological check is performed to confirm the correct positioning (figure.2). then, the wires of this electrode are tunneled to the left subcostal or left subclavian level. a short incision is made at this point to implant the generator after having connected it to the wires of the electrode. figure 1: the electrode is introduced into the epidural space in contact with the spinal cord. figure 2: control x-ray for the good position of the electrode. 522 f. aichaoui, a. khelifa, i. assoumane et al. results the stimulator is started the day after surgery. the parameters used are variable according to the patients with 200 microseconds on average (between 50 and 500 μsec), a frequency of 30 hz (between 30 and 400 hz) and amplitude of 6 ma (between 2 and 20 ma). the settings are refined between 1 and 3 months. the long-term evaluation was performed at 6 months for five patients, at one year for three patients and beyond two years for five patients. the average duration of follow-up is 20 months. all patients reported a relief of more than 50% of the pain intensity at the end of the first settings of the stimulation. statistical analysis showed a significant improvement. the improvement is estimated at 90% with a vas that went from 8.8 to 0.8. the consumption of analgesics has been reduced by 71.8%. this reduction goes hand in hand with improving the quality of life of patients in more than 60% of cases. the professional reintegration concerned more than half of the patients in activity with an arranged post in 60% of the cases. the surgical technique was not accompanied by serious complications. we noted a pain of the surgical site resolving under analgesic, a case of dura tear repaired in per operative and a case of hematoma development around the generator requiring drainage. patients sex age surgery locations initial vas initial mqs lower opioids higher opioids follow-up (months) 1 m 21 dis dif, ll, bil 8.5 32 yes no 54 2 f 37 dis dif, ll, bil 9.5 32 no yes 34 3 f 40 dis ls, uni 9.5 32 yes no 31 4 m 47 dis+lam dif, ll, bil 8.5 32 yes no 26 5 m 52 lam dif, ll, bil 8 32 yes no 26 6 m 66 dis+lam dif, ll, bil 9.5 32 yes no 20 7 f 34 dis+lam ls, uni 10 32 yes no 19 8 m 41 scol dif, ll, uni 10 27 no no 14 9 f 49 dis+lam ls, uni 7 18 yes no 9 10 m 47 dis+lam gu 8.5 30 yes no 8 11 m 47 dis+lam ls, bil 8.5 23 no no 8 12 f 63 dis+lam dif, ll, bil 8.5 24 no no 8 13 f 48 dis+lam dif, ll, bil 8.5 7 no no 6 table 1: summery of the preoperative data and the follow up duration for each patient. dif : diffuse, ls : lombosciatalgia, gu : genitourinary, ll : lower limb, bil : bilateral, uni : unilateral, dis : discectomy, lam : laminectomy, scol : scoliosis correction rods removal, vas (visual analogue scale), mqs (medication quantification scale). discussion persistent pain after spinal surgery or "fbss" is the result of several factors including major and / or prolonged compression of the nerve root during the preoperative period, the occurrence of a surgical complication or nerve damage in peroperative (14,23). the occurrence of arachnoiditis or periradicular fibrosis is a major contributor to pain (10,14), and infection can lead to chronic pain after the appearance of a epidural compressive fibril tissue (23). all our patients presented, prior to implantation of the spinal cord stimulator, a radicular pain at the electromyogram (emg) with scar tissue on the operative site on imaging but without recurrence of herniated disk or residual stenotic spinal canal. the patients suffered from pains of the two lower limbs mainly in lombosciatalgia often extended without precise territory. these pains had a neuropathic character with a dn4 score greater than 4, it is in this context that the indication of spinal cord stimulation was retained. the indication of spinal cord stimulation in neuropathic pain, especially in the "fbss", is widely accepted (4). the control of pain by spinal cord stimulation is based on gate control theory developed by melzack and wall in 1965 (16), in fact, reinforcing the large diameter aβ fibers, increases the inhibitory system of interneurons in lamina ii of the dorsal horn of the spinal cord on the transmission of ascending pain. we implanted our patients with 16 contact electrodes (penta, saint jude®) surgically. the open-air implantation allows a 523 treatment of chronic pain by spinal cord stimulation better visual control of the epidural space. the wide configuration of the electrodes makes it possible a large contact with the convexity of the dura (19).the use of 16-contact electrodes allows a multitude of programming combinations (11). this is interesting in cases of pain with a territory that is very extensive or difficult to recruit (12). the collection of the different evaluation criteria highlights a significant gain on the mqs (medication quantification scale) and vas (visual analogue scale) (16). drug use is reduced by 42.7% at 3 months and by 71.8% at more than 6 months with suppression of opioids. in fact, the mean value of the initial mqs (preoperative) was 27.15 ± 7.58 (95% ci: 22.57-31.74); passed to 15.54 ± 8.08 (95% ci: 10.66-20.42) at 3-month, and to 8 ± 8.90 (95% ci: 2.62-13.38) at more than 6 months (figure 3). the drug reduction has been planned and progressive. it was accompanied by fewer side effects and an improvement in the quality of life. the effectiveness of spinal cord stimulation is defined as obtaining a relief of at least 50% of the intensity of neuropathic pain (14). in the literature, the results of spinal cord stimulation vary, depending on the series, between 47% and 88% (3,6,14). for our part, we obtained a regression of 90% of the pain. the average preoperative vas was 8.81 ± 0.85 (95% ci: 8.29-9.32). average postoperative vas at 3 months increased from 3 ± 1.08 (95% ci: 2.35-3.65) to 0.88 ± 1.04 (95% ci: 0.25-1.52) at more than 6 months (figure. 3). the average duration of follow-up is 20 months with an interval between 6 and 54 months. the gradual improvement of vas beyond the first three months is linked to the optimization of stimulation parameters during successive consultations. patients reported walking facilitation due to improved proprioceptive conduction (1). all this has allowed half of the patients in working age to return to work with an arranged post in 60% of them. these results of spinal cord stimulation in the fbss show a significant gain on both the pain and its repercussions. moreover, the lack of response to the transcutaneous stimulation in the preoperative phase in our patients is not a negative value of spinal cord stimulation. the delay between the onset of pain and implantation of the pacemaker is 8 years on average. this delay is considered relatively long, but it has not acted negatively on the outcome of the results. in the literature, the factors predicting the efficacy of spinal cord stimulation are dependent on several elements, in particular, the neuropathic pain that evolves in uni or bilateral radicular mode (6), and the delay exceeding 3 years after the first surgical intervention. (13,14). the low rate of complications encountered in this series corroborates the results of the literature (11). the phenomenon of tolerance or habituation, synonymous with exacerbation of pain over time, has not been observed in our patients. this phenomenon is not frequently cited by the authors (9). however, it can be overcome by an adaptation of the stimulation parameters. the longterm socio-economic impact is in favor of spinal cord stimulation if we take into account the relief of pain, the reduction or even the stopping of medications and the possibility of reintegration in work (7). figure 3: evolution of the mqs (medication quantification scale): preoperative (mqsi) and postoperative (at 3months and> 6months). figure 4: evolution of the vas (visual analogue scale): preoperative (vasi) and postoperative (at 3months and> 6months). 524 f. aichaoui, a. khelifa, i. assoumane et al. conclusion the benefit / risk ratio is largely in favor of spinal cord stimulation in the management of patients with fbss. the indication is dependent on a good selection of patients. finally, spinal cord stimulation must be part of the therapeutic arsenal of the fbss. declarations of interest: none. funding: this research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. references: references 1. hatzis, g. stranjalis, c. megapanos, p. g. sdrolias, i. g. panourias, and d. e. sakas. the current range of neuromodulatory devices and related technologies. acta neurochir suppl (2007) 97(1): 21–29 2. m. raslan, s. mccartney, and k. j. burchiel. management of chronic severe pain: spinal neuromodulatory and neuroablative approaches. acta neurochir suppl (2007) 97(1): 33–41 3. abeloos l, de witte o, riquet r, et al. (2011) [long6terme outcome of patient treated with spinal cord stimulation for therapeutically refractory failed back surgery syndrome : a retrospective study ], neuro-chirurgie 57 (3 ) : 114-119 4. assaf g, sheng z, yong k , gharibo c (2007) challenges to sitting spinal cord stimulator parameters during intraoperative testing factors affecting càverage of law back and leg pain. neuromodulation : tzchnolgy of the neural interface 10(2) 5. attal n, perrot s, fermanian j, bouhassira d (2011) the neuropathic components of chronic low back pain : a prospective multicenter study using the dn4 questionnaire.j pain off lam pain soc 12 : 1080-1087 6. barolat g, oakley jc, law jd, et al. (2001) epidual spinal cord stimulation with a multiple electrode paddle lead is effective in trating intractable low back pain. neuromodulation 4 (2) : 59-66 7. cameron c (2004) safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20 year literature review. j neurosurg (spine 3) 100l254–100l267 8. cherkin dc, deyo ra, loeser jd, bush t, waddell g (1994) an international comparison of back surgery rates. spine 19: 1201–1206 9. dario a, fortini g, bertollo d, bacuzzi a, grizzetti c, cuffari s (2001) treatment of failed back surgery syndrome. neuromodulation 4: 105–110 10. depalma, michael j, jessica m ketchum, and thomas r saullo. etiology of chronic low back pain in pa tients having undergone lumbar fusion. pain medicine (malden, mass.) (april 11, 2011). 11. frey me, manchikanti l, benyamine rm, et al. (2009) spinal cord stimulation for patients with failed back surgery syndrome : a systematic review. pain physician 12 (2) :379397 12. holsheimer j, wesslink wa (1997) effect of anode-cathode configuration on pararesthesia coverage in spinal cord stimulation. neurosurgery 41 : 654-659 ; discussion 659660 13. hoy d, brroks, blyth f, buchbinder r (2010) the epidemiology of low back pain. best practice and research. clinical rheumatology 24 (6) : 769-781 14. laurence abeloos, cristo chaskis. « fbss » et stimulation médullaire : résultats à long terme dans la littérature.chirurgie de la douleur. springer-verlag paris 2014 (133-147) 15. long dm (1991) failed back surgery syndrome. neurosurg clin nv am 2: 899–919 16. a. levesque · s. raoul · j.-p. nguyen · j. nizard. subcutaneous nerve stimulation for the treatment of refractory low back pain with lumbar neuropathic component. open-label study of 11 patients and review of the literature. douleur analg. (2015) 28:172-178. doi 10.1007/s11724-015-0431-2. 17. north r, shipley j, et al. (2007) ( north rb, kidd d, shipley j, taylor rs (2007) spinal cord stimulation versus reoperation for failed back surgery syndrome : a cost effectiveness and cost utility analysis based on a randomized, controlled trial.neurosurgery 61(2) :361368 ; discussion 368-369 18. north r, shipley j, et al. (2007) practice parameters for the use od spinal cord stimulation in the treatment of chronic neuropathic pain. pain med 8 suppl 4 : s200-75 19. north rb, kidd dh, olin j, et al. (2006) spinal cord stimulation for axial low back pain : a prospective controlled trial comparing 16-contact insulated electrodes with 4-contact percutaneous electrodes : comparison of scs electrodes for low back pai. neuromodulation technol neural interface 9 :56-67 20. national medical management for neuropathic pain : pain 132 (1-2 ) : 179-188 21. rigoard p, jacques l, delmotte a, et al. (2014) an algorithmic programming approach for back pain symptoms in failed back syndrome using spinal cord stimulation with a multicolumn surgically implanted epidural lead : a multicenter international prospective study. pain pract 22. taylor rs, desai mj, rigoard p, taylor rj (2013) predictors of pain relief following spinal cord stimulation in chronic back ans leg pain and failed back surgery syndrome : a systematic review and meta-regression analysis. pain pract doi :10.1111/papr.12095 23. yong h. k. et al. (1980). prevention of nerve root adhesions after laminectomy. spine 5 (1): 59–6. doi: 10.33962/roneuro-2022-002 single stent transverse-configuration in assisted coiling treatment of a double anterior communicating aneurysm a. chiriac, n. dobrin, georgiana ion, z. faiyad, dana turliuc, i. poeata romanian neurosurgery (2022) xxxvi (1): pp. 14-17 doi: 10.33962/roneuro-2022-002 www.journals.lapub.co.uk/index.php/roneurosurgery single stent transverse-configuration in assisted coiling treatment of a double anterior communicating aneurysm a. chiriac, n. dobrin, georgiana ion, z. faiyad, dana turliuc, i. poeata “gr. t. popa” university of medicine and pharmacy, iasi, romania “prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract the stent-assisted coiling technique is more and more used for the anterior communicating aneurysms (acoma) treatment due to the increasing incidence of complex and wide-necked aneurysms at this level. different arrangements of a single stent for assisted coil embolization have been described. the transverseconfiguration from a1-acom-contralateral a1 stent-assisted coiling procedure was previously reported as a feasible, effective, and relatively safe endovascular technique used to treat wide-necked complex acoma aneurysms. in this article, we presented a technique involving transverse stenting through the acoma via the dominant a1 and discuss some particular technical difficulties. introduction the anterior communicating artery (acoma) was reported to be one of the most common location of ruptured aneurysms over the last decades. these lesions are of significant importance due to their higher incidence but also to their complex anatomical features, often associated with a wide neck, difficult vascular angles and a variety of abnormalities. the use of self-expanding stents under various arrangements in coil assisted embolization technique can help to optimally treat aneurysms with this location and to achieve more longterm results. also, due to the numerous disadvantages and technical difficulties specific to double stenting, the single stenting technique seems to be the first option considered in the case of anterior communicating artery aneurysms. in our study we describe the use of a single stent–assisted coiling technique in a transverse configuration for the treatment of double communicating artery aneurysm. the efficacy and limits of this technique were also discussed referring to the few cases already presented in the literature [1,2]. keywords transverse-configuration, stent assisted coiling technique, intracranial aneurysm corresponding author: dana mihaela turliuc “prof. dr. n. oblu” clinic emergency hospital, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 15 single stent transverse-configuration in assisted coiling treatment of a double anterior communicating aneurysm case presentation a 51-year-old male patient was transferred to our neurosurgical department from a local hospital for a subarachnoid haemorrhage revealed on craniocerebral ct scan. at admission he was conscious, confused, agitated, accusing severe headache. the family declare the onset of symptoms four days ago with progressive evolution and a history of medication-treated hypertension. the brain ct angiography demonstrated a double sac complex acoma aneurysm as source of hemorrhage. the patient was proposed for an immediately endovascular aneurysm occlusion. a written informed consent was signed by patient family after discussions with the operating team. the procedure was performed on a biplane angiography system (infinix, toshiba, canon medical system) with the patient under general anesthesia. both carotid arteries were evaluated and a large complex double acoma aneurysm was angiographicaly documented. a slight right side a1 dominance with a better contrast enhancement of the two aneurysmal sac was noticed. the 3d dsa reconstruction image showed wide-neck involving the entire anterior communicating artery segment. a single stent support technique in a transversal configuration was deemed necessary for a safe endosaccular coiling with all anterior communicating artery complex branches preservation (fig 1). a b c d data for 91 cases e f g h i j figure 1. a,b brain ct diagnosis highlighting sah and post interventional brain ct control; c,d,e ; d,e –dsa from the right and left ica showing the double acoma aneurysm; f,g,h,i,j– intraprocedural dsa images and the final dsa control from both ica injection. the patient received 150 mg aspirin before procedure and 5000 iu bolus dose of intravenous heparin was administered after 6f femoral sheath (merit medical) placement. a 6-fr chaperon guiding catheter was placed at the proximal cervical internal carotid artery carefully advanced over 0.035 glidewire. 3d angiographic imaging working projection was used for the guidance on roadmap images. we use a transvers-configuration stent– assisted coiling technique with step by step transstent catheterizing of both aneurysmal sac to avoid 16 a. chiriac, n. dobrin, georgiana ion et al. multiple catheter maneuvering through the right a1 arterial segment. a prowler select plus microcatheter (codman j&j) was then very carefully advanced over a 0.014 transed microwire (boston scientific) via the right a1 through the acoma into the middle part of contralateral a1. a 4/30 mm enterprise 2 stent is then deployed from the middle part of the left a1 over the aneurismal neck through the acoma until the middle part of right a1. after the full deployment of the stents, a prowler 10 microcatheter is placed through the stent into the large sac aneurysm. its complete angiographic coil occlusion was followed by the microcatheter repositioning in to the smaller aneurysm and continued coiling until no further coils could be safely deployed within the aneurysm sac. the control dsa images demonstrated a “raymond class i” complete aneurysm occlusion with no neck remnant, coil herniation, clot formation or branch occlusion, and with no perioperative or postopective complications. a bolus dose of 5 ml of nimodipine (nimotop, bayer health care ag) diluted in 15 ml of 0.9% nacl solution was infused through the microcatheter in to the proximal part of right a1 for 10 minutes to combat procedural vasospasm. the patient evolution was favourable, and he was discarded home after 17 days of hospitalization. discussion the large clinical trial studies showed that acoma is the most common location of ruptured intracranial aneurysm. treatment of wide-neck acoma aneurysms with complex anatomy such as double sac aneurysm usually requires a stent assisted coiling technique for a safety and optimal occlusion. the difficulties and complications described for double stenting techniques as insufficient wall apposition and endothelialisation, and increased risk of acute or chronic thromboembolism have made the single stenting technique to be considered as the first option. however, the most used single stenting configurations through the dominant a1 to the ipsilateral or contralateral a2 may not provide sufficient neck coverage for a double wide-necked acoma aneurysm, resulting in a coil protrusion and normal branches occlusion. for such particular anatomical cases an a1-acoma-contralateral a1 stenting could be performed. this particular transverse stenting configuration may successfully prevent the aforementioned inconveniences with optimal results on long-term aneurysmal occlusion [2,3,4]. the few reports in the literature on the use of single transverse-configuration stent assisted coiling for acoma aneurysms have mentioned beside the success of using this technique, the difficulties encountered in its implementation. the technical challenges with possible related complication such as suboptimal stent deployment, dissection and thrombosis may be increased by difficult navigation through even curved and smaller calibre arteries [3,4,5]. rhoton's publications have shown a higher probability of acoant aneurysm developing as bigger the diameter difference between the bilateral a1 segments. thus, due to hemodynamic influence, most acoma aneurysms appear to arise from the dominant a1 segment of the anterior cerebral artery and form as junction aneurysms between the dominant a1, acoma and a2 ipsilateral. yasargil reports that 81.3% of acoant aneurysms usually occurred at the junction of the dominant a1 and acoma and only 18.7% occurred in the middle of the acoma. this correlate with the fact that only 22% of cases have comparable diameters of a1 segments of the bilateral anterior cerebral arteries, suggesting a relatively low percentage of patients with acoma aneurysms who may benefit from the application of single stent assisted coiling technique with stent in a transverse a1 to a1 configuration [2,3,6]. another aspect of the application of the single stenting technique in the transversal configuration is related to the need for a dual femoral approach with double guidance for a retrograde approach through acoma. even if there are many reports of this type of approach, we believe that the use of a single guide catheter and a single femoral puncture is sufficient in many of these cases for both stent and coils delivery and a clear view of the lesion and surrounding vascular shaft [2,3]. conclusions any of the strategies for placing a stent for the treatment of an acoma aneurysm are dependent on the configuration of the aneurysm, the feasibility of incorporating the neck of the aneurysm into the implant, the difficulty of microcatheter crossing of the acoma channels, and the degree of hypoplasia of one of the a1 segments. the placement of a single transverse-configuration stent via the dominant a1 17 single stent transverse-configuration in assisted coiling treatment of a double anterior communicating aneurysm across the acoma into the contralateral a1 can be a feasible, efficient and relatively safe endovascular technique for the treatment of a wide-necked double acoma aneurysm. this could offer a good long-term occlusion rates with reasonable complication rate. references 1. ahmed, m. e., lum, c., lesiuk, h., iancu, d., & dos santos, m. (2014). navigation of stents across communicating arteries for aneurysm embolization. canadian journal of neurological sciences, 41(2), 193-199. 2. adeeb, n., griessenauer, c. j., patel, a. s., foreman, p. m., baccin, c. e., moore, j. m., ... & thomas, a. j. (2018). the use of single stent-assisted coiling in treatment of bifurcation aneurysms: a multicenter cohort study with proposal of a scoring system to predict complete occlusion. neurosurgery, 82(5), 710-718. 3. ban, s. p., kwon, o. k., & kim, y. d. (2022). long-term outcomes of placement of a single transverse stent through the anterior communicating artery via the nondominant a1 in coil embolization of wide-necked anterior communicating artery aneurysms. journal of korean neurosurgical society, 65(1), 40. 4. choi, h. h., cho, y. d., yoo, d. h., ahn, s. j., cho, w. s., kang, h. s., ... & han, m. h. (2019). stent-assisted coil embolization of anterior communicating artery aneurysms: safety, effectiveness, and risk factors for procedural complications or recanalization. journal of neurointerventional surgery, 11(1), 49-56. 5. kocur, d., zbroszczyk, m., przybyłko, n., hofman, m., jamróz, t., baron, j., ... & kwiek, s. (2016). stent-assisted embolization of wide-neck anterior communicating artery aneurysms: review of consecutive 34 cases. neurologia i neurochirurgia polska, 50(6), 425-431. 6. raslan, a. m., oztaskin, m., thompson, e. m., dogan, a., petersen, b., nesbit, g., ... & barnwell, s. l. (2011). neuroform stent-assisted embolization of incidental anterior communicating artery aneurysms: long-term clinical and angiographic follow-up. neurosurgery, 69(1), 27-37. microsoft word 9chiriaca_stent romanian neurosurgery (2018) xxxii 4: 593 601 | 593             doi: 10.2478/romneu-2018-0076 stent assisted coiling technique for anterior communicating artery aneurysms treatment a. chiriac, giorgiana ion1, n. dobrin1, i. poeata “grigore t. popa” university of medicine and pharmacy, iasi, romania 1“prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract: the anterior communicating artery was reported as the most common location for intracranial aneurysm by most clinical trials in literature. the use of intracranial stent detachment at the anterior communicating artery complex for treatment of wide-neck aneurysms with this location is increasingly reported. in this article we present the various management strategies for stent assisted coiling treatment of the anterior communicating artery aneurysms, their limits and complication. key words: anterior communicating artery, wide-neck aneurysm, stent-assisted technique introduction the anterior communicating artery aneurysm was described in literature as the most common location for intracranial aneurysms responsible for up to 40% of the subarachnoid haemorrhages in adults. microsurgical clipping or endovascular coiling are both techniques alternatives for the treatment of intracranial aneurysm with this location. the inconveniences due to deep lesion location, unfavorable projections or anatomical complexity of anterior communicating artery complex region have made the endovascular treatment the first choice. with the introduction of the stentassisted embolization technique for resolving wide-neck aneurysms, this was also considered for the treatment of complex aneurysms of the anterior communicating artery. the development of new types of intracranial stents allowed the successful use of single or double stent techniques for coil embolization of anterior communicating artery aneurysms. endovascular treatment techniques the low invasiveness, high feasibility and effectiveness of endovascular embolization of anterior communicating aneurysms made this treatment the prime method in most of the neurosurgical centres. the primary technique for endovascular occlusion of acoa is represented by the coil embolization. however, the high rate of small and complex aneurysm for this location and adjacent anomalies of the acoa segment made this 594 | chiriac et al stent assisted coiling technique for artery aneurysms treatment             first option technique more difficult to be applied. it is well known the difficulty of coil embolization of wide-neck aneurysm. for these challenging situations a variety of adjuvant techniques and devices were developed. the remodelling techniques with balloon or microguidewire, and stent assisted technique are the most widespread. detachment of coils in the aneurysmal sac under the protection of a temporarily inflated balloon over the aneurysmal neck has been shown to be associated with lower rate of progression of occlusion and higher rate of retreatment and procedural complication for acoa location. the stent assisted technique consists in deployment of a self-expandable stent in the parent artery over the aneurysm neck. the stent serves as a scaffold to prevent the coil protrusion into the parent artery or the thromboembolic event due to en earlier coil migration into the parent vessel. also, the stents contributes to en earlier thrombosis of the aneurysmal sac by its hemodynamic effects of blood flow redirection and neointimal overgrowth stimulation by its biological properties. there were described various intervention strategies regarding the time of stent deployment in relation with coiling. thus, the stents can be detached before or after the microcatheter is placed into the aneurysm sac. in so called “jailing” technique the microcatheter is introduced into the aneurysm before the stent deployment. by this method, the microcatheter is placed between the vascular wall and the stent, which gives it a good stabilization during coiling. in the “trans-cell” technique, the microcatheter is placed into the aneurysm sac through the mesh of stent [1,2,4,7,8]. in particular cases of aneurysm incorporating both a2 and acoa or in acute angles configuration between the parent and distal arteries, the “waffle-cone” technique is the best alternative. this method consists in deployment of the distal end of the stent into the aneurysm lumen and the proximal end in the afferent vessel. the major advantage of this method is the preservation of the parent artery patency. complex wide-necked acoa aneurysm may also be endovascular treated by the “dual stent” technique. in this method 2 stents are deployed in x or y configuration at the anterior communicating artery (acoa) complex. the dual stent x-configuration is an optimal method in cases of large neck aneurysm involving both a1-a2 junctions, with acoa partially incorporated within the sac and both a2s originating from the aneurysm. in such arrangement the first stent is deployed from the contralateral a2 to the ipsilateral a1 segmeng, crossing through the acoa and the second stent is crossed from the other side. usually, the side with the smaller angle between the a1-acoa and contralateral a2 is stented first. the dual stent xconfiguration could also be applied in two techniques: the “kissing” technique with the stent deployed in a parallel fashion; the “crossing” technique with the second stent is passed through the first stent interstices [1,2,4,7,8,9]. romanian neurosurgery (2018) xxxii 4: 593 601 | 595             “jailing” technique “trans-cell” technique “waffle-cone” technique 596 | chiriac et al stent assisted coiling technique for artery aneurysms treatment             figure 1 single stent possible configurations a – ipsilateral a1 to contralateral a2; b – ipsilateral a1 to a2; c-ipsilateral a1 to contralateral a1; double stent configurations d – y configuration; e – x / kissing configuration; f – x / crossing configuration [8,9] if the x configuration technique is indicated in patients with both normal caliber a1, the dual stent y-configuration is reserved for patients with hypoplasia/aplasia a1 on one side, and the aneurysm neck involving the ipsilateral a2 and acoa. in this technique stents are deployed through the large-sized a1 in the bilateral a2 artery[8,9]. stent assisted coil procedure the procedure is performed with the patient under general anesthesia. the double anti-platelet medication is mandatory initiated before the procedure. the loading dose varies depending on the treatment of a ruptured or unruptured aneurysm. 75 mg of acetylsalicylic acid and additional 75 mg clopidogrel were administrated daily for 7 to 10 days before endovascular procedure in patients harbouring unruptured aneurysm. in case of patients presenting subarachnoid haemorrhage a “shock dose” of 300 mg acetylsalicylic acid administrated 30 minutes before starting the procedure followed by 5000ui heparin after the introducer sheath placement are performed. both conventional and rotational intra-arterial digital subtraction angiography is performed for 3d reconstruction. the planning procedures imply complete evaluation of aneurysmal dome, neck size and anterior communicating complex configuration. a 6f introducer sheath is placed usually into right femoral artery. a 6f impulse guiding catheter (boston scientific) is then navigated into the internal carotid artery to obtain a stable position. the right or left side is chosen depending on the dominant a1 segment, calibre of the anterior communicating artery and predominant side of aneurysm injection. then, a excelsior sl-10  f    a    b    c    d    e   romanian neurosurgery (2018) xxxii 4: 593 601 | 597             microcatheter (stryker neurovascular) with support of transend 0.014 microguidewire (boston scientific) is introduced distally in the ipsilateral or contralateral a2 segment. the microguidewire is retired and a neuroform atlas stent (stryker neurovascular) is advanced into microcatheter and deployed when the precisely targeted location is confirmed. the deployment microcatheter is easy advanced over the stent delivery wire until it reached the neck aneurysm level. at this moment the stent delivery wire is retired and the 0.014 microguidewire is introduced into the microcatheter and navigated until the aneurysm dome. the aneurysm is catheterised via stent mesh and subsequently coiled with gdc-10 coils (stryker neurovascular). at the end control angiography images are performed to confirm the complete aneurysm occlusion. the microcatheter is then carefully retired followed by the guiding catheter and introducer sheath. during the procedure heparinised saline is continuously administrated via a venous line. the patient is transferred to intensive care unit for clinical monitoring. the dual antiplatelet treatment is continued postoperatively for at least 2 month followed my monoantiplatelet therapy. case report a 52-year-old woman presented with sudden onset of worst headache of his life followed by single grand mall seizure. on admission to our emergency room the patient was confuse, agitated and vomiting. there were no focal deficits during neurological examination. initial computed tomography (ct) scan showed thin subarachnoid hemorrhage into the base of the interhemispheric cistern. three-dimensional (3d) ct angiography revealed an acoa aneurysm with a bleb. emergency endovascular coil embolization was decided to be performed. the diagnostic 3d digital subtracted angiography (dsa) showed acoa aneurysm of which maximum diameter was 3.0 mm with broad-neck and a fragile bled on top. the initial coil embolization, was conceive to occlude the ruptured point of the aneurysm, was performed by the simple technique utilizing 1.5/2 mm nano platinum coils. after safety coil deployment the microcatheter is retracted from aneurysmal sac and guided to proximal part of left a2 segment. a 3/2.4 mm neuroform atlas stent was deployed from left a2 over the aneurysm neck and distal part of left a1 segment. using a trans-cell technique the microcatheter is inserted again to aneurysmal sac. the aneurysm was completely angiographic occluded by deployment of two more coils. there were no peri-procedural complications or postoperative sever vasospasm. follow-up ct scan was performed on postoperative day 14, revealing no ischemic or hydrocephaly signs. 598 | chiriac et al stent assisted coiling technique for artery aneurysms treatment             figure 2 a – diagnosis ct scan showing sah; b – 3d reconstruction of cta; cdiagnosis dsa; d – dsa control after first coil deployment; e – fluoroscopy for stent complete deployment control; f – control dsa after complete aneurysm coil occlusion; g – postoperative ct scan control b a  e d c  g f  romanian neurosurgery (2018) xxxii 4: 593 601 | 599             techniques complications the thromboembolic events are the most common cause of morbidity and mortality associated to stent-assisted coiling technique. the literature studies reported values of rates of thromboembolic complications related to stent-assisted coiling technique ranging from 4.2 % to 17.1% [2,8,9]. usually, these events are minor complications clinically silent or causing transient neurological symptoms. they may be diagnosed on later mri investigation as a high-signal intensity lesion on diffusion-weighted image (dwi). however, the correct and careful use of double antiplatelet therapy significantly reduces intra and post procedural thromboembolic risks. the debates are still existing concerning this therapy in patients with subarachnoid haemorrhage and unprotected aneurysm in which an accidental intraprocedural rupture occurs. delayed in-stent stenosis is a rare event that can be clinically silent which may require sometime additional treatment. the rate of instent stenosis was reported between 2.5% (biondi et al) and 29.7% (wingspan) and a percutan transluminal angioplasty was performed in majority of cases[6,8]. stent dislodgement is another complication reported during treatment. this technical problem may be caused by aneurysm catheterization through the stent struts and by retrieving the coiling catheter jailed between the stent and vessel wall. in most of the reported cases the stent still covered the aneurysm neck and procedure was completed successfully. in case of exposure of a portion of aneurysm neck with the possible risk of coil herniation into the parent artery, a secondary stent was deployed across the aneurysm neck.[8] the intraprocedural aneurysm perforation is another important complication reported for stent-assisted coiling technique. disastrous clinical outcome were reported by the most studies in this situation. the coil protrusion between the stent and the parent artery wall with a reduction of distal outflow was also reported as technical complication of this procedure. the long-term aneurysm recanalization was reported by literature studies but with lower rate (13.1%) suggesting that this technique is an effective and durable treatment for complex acoa aneurysms. in this regard, most authors argued that stenting in aneurysms confer a protective effect, stopping especially minor recanalization and thus avoiding the need for additional treatment.[2,10,11] discussions complex anterior communicating artery aneurysms are still challenging lesion for both surgical or endovascular approaches. because most of the studies of anterior circulation aneurysms show for anterior communicating artery aneurysm the higher incidence of postoperative morbidity, the endovascular approaches became the main treatment option. unlike other intracranial aneurysms, the embolization of anterior communicating artery aneurysms are more challenging due to increased incidence of small and complex aneurysm configuration and common anatomical vascular variants. in these 600 | chiriac et al stent assisted coiling technique for artery aneurysms treatment             situations, the endovascular treatment requires application of adjuvant technique like stent-assisted coil embolization. first described by higashida in 1997, as treatment option for wide-necked aneurysm was also applied for complex anterior communicating artery aneurysms[2,8,9]. besides the role of mechanical support for the colis arrangement into aneurysm, hemodynamic and biologic favourable effects of intracranial stenting were highlighted in the literature. the jailing technique and the trans-cell technique are the two type of stent-assisted coiling intervention used by the interventionists. numerous studies have shown the efficiency of using both techniques with the limits and benefits of each [3,4,5]. most of the literature reports showed that stent-assisted coil embolization of intracranial aneurysms lead to a lower rate of immediate complete aneurysm occlusion compared with simple coiling technique. the main cause associated with these results was the more limited manoeuvrability of the coiling microcatheter after the stent deployment due to its fixation between the wall stent and arterial lumen, or passing through the stent struts. the anatomy of the anterior communicating artery complex plays an important role in stent assisted treatment of anterior cerebral circulation aneurysms. the presence of hypoplastic a1 segment, small acoa and difficult angles between a1, acoa and a2 are important factors for stent placement. the double stent placement has been described in some series for the treatment of complex and wide-neck aneurysms. the two stent may be used in x or y configuration. x and y stent-assisted coiling of acoa aneurysms is an effective technique, leading to long-term stability of aneurysm occlusion. nevertheless, a higher rate of technical failures and clinical complications were reported compared with those of other endovascular techniques, such as single stent–assisted coiling or balloon-assisted coiling[9]. references 1. chalouhi, n., jabbour, p., singhal, s., drueding, r., starke, r. m., dalyai, r. t., ... & randazzo, c. g. (2013). stent-assisted coiling of intracranial aneurysms: predictors of complications, recanalization, and outcome in 508 cases. stroke, 44(5), 1348-1353. 2. choi, h. h., cho, y. d., yoo, d. h., ahn, s. j., cho, w. s., kang, h. s., ... & han, m. h. (2018). stent-assisted coil embolization of anterior communicating artery aneurysms: safety, effectiveness, and risk factors for procedural complications or recanalization. journal of neurointerventional surgery, neurintsurg-2018. 3. fang, s., brinjikji, w., murad, m. h., kallmes, d. f., cloft, h. j., & lanzino, g. (2013). endovascular treatment of anterior communicating artery aneurysms: a systematic review and meta-analysis. american journal of neuroradiology. 4. gao, x., liang, g., li, z., wei, x., & hong, q. (2011). complications and adverse events associated with neuroform stent-assisted coiling of wide-neck intracranial aneurysms. neurological research, 33(8), 841-852. 5. huang, q., xu, y., hong, b., zhao, r., zhao, w., & liu, j. (2009). stent-assisted embolization of wide-neck anterior communicating artery aneurysms: review of 21 consecutive cases. american journal of neuroradiology, 30(8), 1502-1506. 6. johnson, a. k., munich, s. a., heiferman, d. m., & lopes, d. k. (2013). stent assisted embolization of 64 romanian neurosurgery (2018) xxxii 4: 593 601 | 601             anterior communicating artery aneurysms. journal of neurointerventional surgery, 5(suppl 3), iii62-iii65. 7. kocur, d., ślusarczyk, w., przybyłko, n., bażowski, p., właszczuk, a., & kwiek, s. (2016). stent-assisted endovascular treatment of anterior communicating artery aneurysms–literature review. polish journal of radiology, 81, 374. 8. ohshima, t., belayev, a., goto, s., yamamoto, t., ishikawa, k., & kato, y. (2017). a case of anterior communicating artery aneurysm successfully treated after a stent migration during stent assisted endovascular coil embolization. nagoya journal of medical science, 79(2), 267. 9. saatci, i., geyik, s., yavuz, k., & cekirge, s. (2011). xconfigured stent-assisted coiling in the endovascular treatment of complex anterior communicating artery aneurysms: a novel reconstructive technique. american journal of neuroradiology, 32(6), e113-e117. 10. santillan, a., schwarz, j., boddu, s., gobin, y. p., knopman, j., & patsalides, a. (2018). stent-assisted coil embolization of anterior communicating artery aneurysms using the lvis jr stent. interventional neuroradiology, 1591019918798144. 11. nishimura, k., ishibashi, t., aoki, k., kan, i., kaku, s., kodama, t., ... & murayama, y. (2018). stent-assisted coiling of acutely ruptured cerebral aneurysms. journal of neuroendovascular therapy, 12(6), 267-272. doi: 10.33962/roneuro-2020-091 traumatic isolated intracerebellar haematoma without any supratentorial lesion. a rare entity. management strategy jain sachin kumar, gupta tarun kumar, jaiswal gaurav, lohar vishnu kumar, prateek patel romanian neurosurgery (2020) xxxiv (4): pp. 533-539 doi: 10.33962/roneuro-2020-091 www.journals.lapub.co.uk/index.php/roneurosurgery traumatic isolated intracerebellar haematoma without any supratentorial lesion. a rare entity. management strategy jain sachin kumar, gupta tarun kumar, jaiswal gaurav, lohar vishnu kumar, prateek patel department of neurosurgery, rnt medical college, udaipur, india abstract purpose. pure isolated cerebellar haematoma of traumatic aetiology, without associated posterior fossa subor epidural haematomas and without supratentorial bleed is a rare entity. we conducted this retrospective study to analyse the management strategy of isolated traumatic intracerebellar haematoma without supratentorial lesion in our institute. methods. we retrospectively reviewed records of more than 15000 head injury patients in our department of neurosurgery between january 2014 and november 2019. in this isolated intracerebellar hematoma patients are 60. patients were divided into two groups assessed by the gcs score at the time of presentation – group a (gcs>13) group b (gcs lesser than or equal to 13). group a treated conservatively and b surgically. group a subdivided according to the size of hematoma into1st (> 3cm) and 2nd (<3 cm). group b subdivided according to gcs into 1st (<8) and 2nd (8-13). results. most group b, subgroup 1st (gcs<8) patients found to be associated with poorer outcome (60 %) and subgroup 2nd (gcs 8-13) had only 10 %. group a subgroup 1st (> 3 cm hematoma) has associated with poor outcome (28.57%) and subgroup 2nd (< 3 cm) has 4.34%. gcs score at the time of admission, hematoma size, hematoma location, the timing of surgery were important factors for outcome. conclusion. we concluded that hematoma size is > 3 cm and gcs > 8 patient should operate within 12 hr. patient of gcs < 8 results of surgery are poor (60%.). if the size of hematoma < 3 cm, lateral hematoma and gcs >13 should be treated conservatively. the factors which may be associated with the poor outcome are low gcs score at the time of admission (<8), the large size of hematoma (>3cm), median location and delay time of surgery(>12hr). introduction haematomas of the posterior fossa are by themselves uncommon and account for only 3.7% of all head injuries. (according to liau)13. approx 0.6-0.82 % cases have cerebellar hematoma without other posterior fossa lesion3,10,14. but isolated intracerebellar hematoma without supratentorial lesion is very rare (approx 40-50% of isolated cerebellar hematoma). as in 9/21-42.85% in bhardwaj et al5 and 8/18 -44.44% in devella et al6. in our study it is 60 (50%). keywords traumatic intracerebellar hematoma, gcs, hematoma size corresponding author: jain sachin kumar department of neurosurgery, rnt medical college, udaipur, india drsachinj6184@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 534 jain sachin kumar, gupta tarun kumar, jaiswal gaurav et al. the clinical presentation of cerebellar haematoma may be readily apparent with classic signs including ataxia, nystagmus and signs of increased icp like headache, lethargy and nausea and vomiting. treatment options for this pathology are still evolving. these hematomas may be totally asymptomatic, with a sudden increase in size can lead to rapid deterioration of neurological status18. previously tested predictive factors in different studies include are size of hematoma, haematoma location (superficial vs. deep), haematoma volume, gcs of patient, degree of fourth ventricle and cistern deformation and assosiated hydrocephalus 9,15,21. previously there was difficulty in diagnose the posterior fossa ich due to lack of ct but with the increasing use of computed tomography (ct) for screening of all head trauma patients, increasing number of cases have been reported to be diagnosed even before the appearance of symptoms and have thus been treated in a timely manner14,22. the cerebellum has four functionally important deep cerebellar nuclei (the dentate, emboliform, globose and fastigial nuclei) embedded in the white matter in its centre8. the locations of the deep cerebellar nuclei span the vermis and the innermost or medially approximately one third of each hemisphere. so it is devided into medial and lateral group / deep and superficial group. we conducted this retrospective study to analyze the management statergy of isolated traumatic intracerebellar haematoma in our institute and study the factors which could be associated with the outcome. (like mode of trauma,gcs,hematoma size,timing of surgery,hematoma location etc). materials and methods we retrospectively screened and (where required) reviewed records of more than 15000 head injury patients who were admitted in our department of neurosurgery between january 2014 and november 2019.in this approx 120 patients ( 0.8%) had intacerebellar hematoma without any other posterior fossa lesion, and in this isolated intracerebellar hematoma without supratentorial lesion are in 60 patients ( approx 50 % of cerebellar ich without posterior lesion). only these 60 patients are included. hematoma volume was assessed by using formula a*b*c/2, where a is maximum transverse diameter of hemorrhage on ct, b is anterioposterior diameter, and c is number of ct slices showing hematoma12.. patients were divided in to two groups based on their level of consciousness assessed by the gcs score at the time of presentation – group a with gcs score greater than 13 and group b with gcs lesser than or equal to 13. group a patients were treated conservatively and group b treated surgically. data on patient age, gender, gcs score, mechanism of injury, timing of surgery, ct scan findings, management strategy and outcome were gathered and analyzed. these all factors detail given in table a. the mode of injury were broadly categorized as road traffic accident (rta), fall from height and assault. table 1. demographics and factors associated with isolated traumatic intracerebellar hematoma s.n factor studied details of factor group a group b total 1 number of patient 30 30 60 2 age (mean age) 860(30) 860(36) 3 male/fe male ratio 3:1 3:1 4 mechani sm of injury rta 15 22 37 fall from height 12 7 19 assault 3 1 4 5 gcs <8 10 10 8-13 20 20 >13 30 30 6 time of surgery <12 hr 22 12-48 hr 5 >48 hr 3 7 cerebell ar hemato ma size >3 cm 7 27 34 2-3cm 10 3 13 <2 cm 13 0 13 8 hemato ma location medial or deep 1/3 and vermis 5 10 15 lateral or superficial 2/3 25 20 45 9 status of fourth ventricle normal 27 6 33 compress ed 3(mild) 24 27 10 surgical treatme nt sub occipital craniecto my 4(after worsen ing ) 27 31 vp shunt 4(after worsen 3 7 535 traumatic isolated intracerebellar haematoma without any supratentorial lesion ct scan findings included clot location, size (largest transverse diameter of clot, categorized as > 3 cm or < 3 cm, or clot volume categorized as > 15 ml or < 15 ml), other associated findings and status of the fourth ventricle (normal vs. compressed) according to all these criteria group a devided into 2 subgroups according to size of hematoma . 1st has >3 cm and 2nd has < 3 cm size of hematoma. group b also devided into 2 subgroups according to gcs . 1st has gcs< 8 and 2nd has gcs 8-13. we also included timimg of surgery after injury in surgical group b and from time of worsen in conservative group a. timing devided into <12 hr, 12-48 hr and > 48 hr. we also asses the location of hematoma and devided patients into medial 1/3rd /deep and superficial /lateral 2/3rd location in cerebellum. surgical treatment (sub-occipital craniectomy ) and insertion of ventriculoperitoneal (vp) shunt was documented. six month follow-up reports of all patients who turned in for the follow-up were also analyzed. outcome was documented as favorable or poor based on the glasgow outcome scale at the time of hospital discharge (gos-hd). gos 5 was counted as favorable whereas gos 1-4 counted as poor response. results there are 7 patients in group a subgroup 1st ( ~ > 3 cm size clot). 5 patients out of 7 ( 71.4%) , worsened and required surgical treatment ( 3 sub occipital craniectomy, 2 vp shunt). in these patients 1 expired due to sudden worsening . 1 patient has poor gos and persist in severe disable stage. both has delayed surgery and ( between 12-48 hr) . rest 3 patients has good outcome because of early diagnosis and early surgery . so poor outcome is 2/728.57%. in group a subgroup 2nd has 23 patients( clot size <3 cm) . in which 3 patient of 2-3 cm clot size ( 30%) has worsened between 4-6 days , repeat scan suggesting of sudden increase in size in one patient and obstructive hydrocephalus in all 3. urgent surgical intervention done ( with in 12 hr) .vp shunt in 2 patient and suboccipital craniectomy in 1 patient. in this 1 patient expired 1 month after sub occipital craniectomy due to chest infection. rest 20 patient has good recovery by conservative treatment. so poor outcome is only 1/234.3%. in group b(surgical group) , subgroup 1st (gcs < 8) has 10 patients , in which 8 patients has hematoma size more than 3 cm ( even 5 patients has hematoma size 4-5cm ) and 2 patient has size < 3 cm but in midline .in these 10 patients 3 expired and 3 has severe morbidity. rest 4 patients survived with favourable results. so 6/10 -60 % has poor outcome inspite of surgery. this result included in table b. table 2. results s . n factor studie d detail of factor outcome mo rta lity poor outco me (gos 1-4) fav our able out com e (go s 5) total 1 group a (gcs > 13) (conse rvative treatm ent) subgroup 1st ( size >3 cm)( 5 /7patient worsens and operated) 2 (28.5 7%) 5 7 1 subgroup 2nd ( size~,< 3 cm) only 3/23 patient worsens and operated) 1(4.3 %) 22 23 1 2 group b (gcs ~<13) ( surgic al treat ment) subgroup 1st ( gcs< 8) 6(60 %) 4 10 3 subgroup 2nd ( gcs-8-13) 2(10 %) 18 20 1 3 timing of surger y <12 hr 3(12 %) 22 25 1 12-48 hr 5(50 %) 5 10 2 >48 hr 3(100 %) 0 3 3 4 locati on of hemat oma deep/medial 1/3rd 7(46. 66%) 8 15 5 superficial/la teral 2/3rd 4(8.8 8%) 41 45 1 gcs 8-13 included 20 patients , in which 19 patients has hematoma size > 3cm and rest 1 has size 2-3 cm near midline. only 1 patient expired and 1 has severe morbidity out of 20 patients .one who expired , operated after 12 hr and one patient who has severe morbidity has associated chest infection. so 2/20 – 10% has poor outcome after surgery . total 38 patient has undergone surgical procedure from which 8 operated in group a after worsening and all 30 operated in surgical group b. 536 jain sachin kumar, gupta tarun kumar, jaiswal gaurav et al. out of 3 patients who operated after 48 hr, all 3 patient expired. ( 3/3 -100 %). between 12 -48 hr 10 patient operated in which 2 expired and 3 patient has severe morbidity ( 5/10-50%). but all 25 patients which are operated before 12 hr had comparable favourable results( 1 expired and two has severe morbidity).( 3/25-12%). patient expired in early surgery had chest infection. vp shunt required only in 3 patients in group b which has hematoma size 2-3 cm, gcs(8-13) and has midline location. vp shunt also done in 2 patient in subgroup 2nd in group a. there is 5 patients in vermis or median ich in group a and 10 patient in group b. rest all are located laterally. the poor outcome in our series at the time of hospital discharge in gcs <8 was 6/1060%. . domenico d’avella7 study shows 58.7% poor outcome in gcs<8 . poor outcome was higher, 60% (6/10) in gcs < 8 in group b as against 10 % (2/20) in gcs 8-13 in group b. mortality was 13.33% (4/30) in group b and only 6.66% (2/30) in group a. poor outcome in group a is 3/30-10% and in group b is 8/3028.6 %. ( in this <8 gcs is 60%, and gcs 8-13 has 10%) so it indicated that gcs is the most important predictor for prognosis in cerebellar ich , either operate or not and second is size. we have added pictures of preoperative cerebellar hematoma and postoperatively ( after suboccipital craniectomy with hematoma evacuation). fig. 1, 2 (1st patient of 40 yr male), fig. 3, 4 (2nd patient of 42 yr male). figure 1. pre-operative ct of a 40 yrs. male figure 2. postoperative ct after sub occipital craniectomy figure 3. preoperative ct of a 42 yrs. male figure 4. post-operative scan after suboccipital craniectomy 537 traumatic isolated intracerebellar haematoma without any supratentorial lesion discussion in our study, rta was the most common 37/60(61.16%) and most damaging mechanism of injury. in this study fall from bike and pillan rider are the most common mechanism of injury. bhardwaj et al has 15/21( 71.14%)5, harsh et al has 15/23 ( 65.21%)23. second most common is fall from tree in this tribal area which are more ( 19/60 -31.66%) in comparision to other studies. bhardwaj et al has 6/21(28.57%), harsh et al 5/23(21.73%).last mode of injury are assault. fall from height was more common amongst children1 while assault was more commonly associated with women and the elderly. but in our study , there are history of fall from tree and height in adult also20. benign course of intracerebellar hematomas may be more frequent than appreciated so not all traumatic hematomas of the cerebellum require surgery17. so it is to be decided in which patient we should operate or not to operate. in accordance with other studies on this topic, ct scan was extremely valuable in predicting patient outcomes20. clots greater than or equal to 3 cm in diameter, gcs<8, deep/meadial 1/3rd hematoma location and timing of surgery were all shown by our study to predict a poor outcome. outcomes were worse for patients has gcs < 8 in subgroup 1st in group b7,15,25. such patients were critically injured and their brain function was already compromised at the time of admission. in accordance with previous studies on this topic our data showed gcs at initial presentation to be the most predictive clinical tool 5,6,7,21,23,25. domenico d’avella et al7 suggest that a gcs score of less than 8 was the most powerful adverse prognostic factor (58.78% probability of poor outcome as sole covariate) . in our study poor outcome is 60% in gcs <8. with supratentorial lesion it is it is 84.61% in harsh et al and 88.78% in d’avella et al. mortility was 3/10 ( 30%) in which 2 patent has median cerebellar hematoma . all 3 had delayed surgery. .rest 3 patient which has poor outcome in which 2 patient has median hematoma and 1 had delayed surgery. outcome is good for gcs 8-13 with surgical treatment. only 1 patient expired in which hematoma was median and one patient has poor outcome had delayed surgery (12-48 hr). delayed surgery after 48 hr had worst outcome (100%), between 12-48 hr had poor outcome (50%). early surgery within 12 hr had poor outcome only 12.0%. so early surgery is good always . it indicated that timing of surgery is one of the most prognostic factor for outcome5,7. 11 patients has poor outcome , in these 7 patient had medial hematoma. so 7/11 (63.63 %) of poor outcome had medial hematoma. bhardwaj et al has ( 62.5%) and s. takeuchi et al21 has 9 patient has medial hematoma in 10 poor outcome patient(9/1090%).so maximum poor outcome occurs in medial and deep hematoma lesion which are also in our study. total medial hematoma is 15 patients in which 7 patients had poor outcome (7/15-46.66%) and superficial hematoma in 45 patients in which only 4 patients has poor outcome (4/45-8.88%). it indicates that medial/deep hematoma has poor outcome5,15,23. in group a subgroup 1st 7 patients has hematoma size > 3 cm and 5 worsened ( 5/771.42%) and then operated .. subgroup 2nd has size < 3 cm only 3 patient worsened (3/2313.04%) , which is also due to midline position. so it is proven that size is important prognostic factor4,5,7. hematoma of > 3 cm size should operate early whether gcs > 13.so size is important factor to take decision of surgery. poor outcome in patient of size> 3 cm in group a is 2/7 -28.57% due to sudden worsening and late surgery . but in < or equal to 3cm poor outcome is only 1/234.3% which is also due to midline hematoma and chest infection. so size is most important factor and equal and less than 3 cm size can treated conservatively4,5,7,15,23. but in group b , all patient operated , so we can not compare size factor for decision of surgery. though trauma is the obvious cause, specific mechanism for this type of injury remains unclear. takeuchi et al.21 created a classification system for the types of trauma causing cerebellar haematomas. their three classes included coup injuries, countercoup injuries and acceleration-deceleration injuries. this classification system proved useful in predicting the site of haematoma, with coup injuries thought to be more common19,24 causing only superficial bleeds while countercoup injuries resulted in deep cerebellar bleeds. in all patients undergoing surgical intracerebellar 538 jain sachin kumar, gupta tarun kumar, jaiswal gaurav et al. clot evacuation sub-occipital craniectomy was done , it is best procedure 2,16 and preferred over suboccipital craniotomy as posterior fossa has less space for accommodation of any post-operative bleeding or post-operative edema. some may note our use of vp shunts over external ventricular drains (evds) for certain patients experiencing hydrocephalus resulting from cerebellar haematoma. vp shunt was chosen over evd placement because in our clinical setting evds have allegedly been found to more frequently result in infections as ventriculitis and meningitis three to four days post-evd placement. however, patients developing acute hydrocephalus need drainage of csf usually for a period of more than two weeks during which the clot resolves and perilesional edema subsides23. hcp can be associated with traumatic intracerebellar clots but not always 17,22. karasawa et al11 mentioned of acute hcp in 20% of intracerebellar hematomas, while in our series it was 16.6%. total poor outcome is in 11 patients so 11/6018.33% which is very less in comparision of other studies because in this study only isolated intracerebellar hematoma taken without supratentorial lesion and 50 patients had gcs > 85,6,7,15,21,23. it also indicates that gcs and associated lesion are important prognostic factor. conclusion in an attempt to study the factors which may be associated with poor outcome in isolated intracerebellar haematoma cases we found that gcs score at the time of admission(<8), large size of hematoma(> 3cm), hematoma location( deep/medial 1/3rd ) and delay time of surgery (>12hr) has poor prognosis. we also concluded that if hematoma size is > 3 cm and gcs > 8 patient should operate, and should operate early within 12 hr. median hematoma should be operated and operated early (whether size is 2-3 cm with ventricle compression) because chances of worsening more. but overall prognosis for deep hematoma was poor. patient of gcs < 8 irrespective to size of ich s results of surgery are poor( 60%.) we also concluded that if size of ich >3 cm and has ataxia and other symptoms and whether the patient is conscious ,but should operate , because chance of worsening is present there or had close observation for 4-5 days and operated immediately after worsening . if gcs > 13 and ich < 3 cm size , patient should treated conservatively and at least 15 days follow up should needed. after 15days there is very less chance of worsening. the overall prognosis is better than other studies because we exclude other supratentorial lesion and 50 patients has gcs > 8. it also conclude that if there is no associated lesion chances of low gcs is less. but the most important thing is that it is the rare study in which only true intracerebellar hematoma without supratentorial lesion included. conflict of interest there is no conflict of interest to disclose. informed consent informed consent was obtained from all individual participants included in this study. references 1. adirim ta, wright jl, lee e, lomax ta, chamberlain jm. injury surveillance in a pediatric emergency department. am j emerg med 1999;17(6):499–503. 2. aghi m, ogilvy cs, carter b, surgical management of intrace-rebellar haemorrhage. in roberts dw, schmeidek hh, eds. schmeidek and sweet’s operative neurosurgical techniques, indications, methods, results. vol. 2, 5th ed. philadelphia: saunders/elsevier2005;1061–1074. 3. arseni c, maretsis m. traumatic cerebellar haematoma associated with posterior cerebral fossa subdural haematoma. psychiatr neurol neurochir 1972;75:113. 4. a. koziarski , e. frankiewicz. medical and surgical treatment of intracerebellar haematomas acta neurochirurgica 1991;110 ;24–28-22. 5. sandeep bhardwaj, vinod sharma, somnath sharma, devendra purohit, sanjeev chopratraumatic posterior fossa hematoma, a rare entity:study of 21 casej neurosci rural pract 2019;10:675–68. 6. d’avella d, cacciola f, angileri ff, et al. traumatic intracerebel-lar hemorrhagic contusions and hematomas. j neurosurg sci 2001;45(1):29–37. 7. d’avella d, servadei f, scerrati met al.traumatic intracerebellar hemorrhage: clinicoradiological analysis of 81 patients neurosurgery 2002;50(1)16– 25.discussion 25–27. 8. deoni sc, catani m. visualization of the deep cerebellar nuclei using quantitative t1 and rho magnetic resonance imaging at 3 tesla. neuroimage 2007;37:1260. 9. ehab ezzat el gamal, ashraf mohamed farid , cerebellar hematomas: management dilemmas, tanta 539 traumatic isolated intracerebellar haematoma without any supratentorial lesion medical journal 2013: 41 ( 4 ) : 358-363. 10. fisher rg, kim jk, sachs e jr. complication in posterior fossa due to occipital trauma; their operability. j am med assoc 1958;167:176–82. 11. karasawa h, furuya h, naito h, sugiyama k, ueno j, kin h. acute hydrocephalus in posterior fossa injury. j neurosurg 1997;86(4):629–632. 12. kothari ru, brott t, broderick jp, et al. the abcs of measuring intracerebral hemorrhage volumes. stroke 1996;27(8):1304–1305. 13. liu k. characteristics of diagnosis and treatment of traumatic intracerebellar hemorrhage [in chinese] zhonghua wai ke za zhi. 1997;35(03):166–167. 14. nagata k, ishikawa t, shigeno t, et al. delayed traumatic intracerebellar hematoma: correlation between the location of the hematoma and the preexisting cerebellar contusion—case report. neurol med chir (tokyo) 1991;31:792–96. 15. patnaik a, mahapatra a k. traumatic cerebellar haematoma: a review. the indian j neurotrauma. 2013;10:24–29. 16. 16.pollak l, rabey jm, gur r, schiffer j. indication to surgical management of cerebellar hemorrhage. clin neurol neurosurg 1998;100(2):99–103 17. pozzati e, grossi c, padovani r. traumatic intracerebellar hematomas. j neurosurg. 1982;56(05):691–694. 18. sokol j h, rowed d w. traumatic intracerebellar haematoma. surg neurol. 1978;10(05):340–341. 19. st john jn, french bn. traumatic hematomas of the posterior fossa. a clinicopathological spectrum. surg neurol 1986;25:457 -66. 20. takeshi satow et al, case report traumatic cerebellar hemorrhage caused by fall ,journal of the japanese association of rural medicine 2015 ; 64 (1) ; 45-49. 21. takeuchi s, takasato y, masaoka h, hayakawa t. traumatic intra-cerebellar haematoma: study of 17 cases. br. j neurosurg. 2011;25(01):62–67. 22. tsai fy, teal js, itabashi hh, huprich je, hieshima gb, segall hd. computed tomography of posterior fossa trauma. j comput assist tomogr 1980;4(3):291–305 23. viraat harsh, anand prakash, james marcellus barry & anil kumar traumatic intracerebellar haematoma: to operate or not to operate? british journal of neurosurgery, 2014-4 24. vrankovic d, splavski b, hecimovic i, kristek b, dmitrovic b,rukovanjski m, blagus g, kovacic d: anatomical cerebellar protection of contrecoup hematoma development: analysis of the mechanism of 30 posterior fossa coup hematomas. neurosury rev 2000:23:156–160. 25. wright rl. traumatic hematomas of the posterior cranial fossa. j neurosurg 1966;25(4):402–409. doi: 10.33962/roneuro -2020-039 endoscopic third ventriculostomy for obstructive hydrocephalus hassan z.a. dixon, yasir m. hamandi, ammar m.a. mahmmoud, samer s. hoz, zahraa f. al-sharshahi romanian neurosurgery (2020) xxxiv (1): pp. 269-274 doi: 10.33962/roneuro-2020-039 www.journals.lapub.co.uk/index.php/roneurosurgery endoscopic third ventriculostomy for obstructive hydrocephalus hassan z.a. dixon1, yasir m. hamandi2, ammar m.a. mahmmoud3, samer s. hoz4, zahraa f. al-sharshahi5 1 neurosurgeon f.i.c.m.s., al-mawanee general hospital, basra, iraq 2 professor of neurosurgery, al-nahrain college of medicine, baghdad, iraq 3 neurosurgeon, neurosurgery teaching hospital, baghdad, iraq 4 neurosurgeon (frcs), department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 5 mb, bch bao (nui, rcsi), lrcp & si, royal college of surgeons in ireland (alumnus), dublin, ireland abstract introduction: obstructive hydrocephalus has long been managed by valveregulated shunts. these shunts are associated with a myriad of short and long-term complications. this has fuelled interest in endoscopic third ventriculostomy (etv) which provides a more physiological pathway for cerebrospinal fluid (csf) diversion while avoiding many shunt-related complications. aim: the objective of this study is to analyse the outcomes of etv at our institution, focusing on the indications, success rates, and short-term complications. methods: between july 2010 and september 2015, 47 patients with obstructive hydrocephalus underwent etv at the neurosurgery teaching hospital in baghdad/ iraq. we retrospectively analysed the data of these patients using hospital health records. simple statistics were performed using spss version 20. a standardized surgical technique was employed in all cases. results: the mean age was 4.4 years (range 40 days 38 years). the male: female ratio was 1.23:1 (55% males and 45% females). the most common cause of obstructive hydrocephalus in patients undergoing etv was aqueductal stenosis (62%; n=29). the second most common cause was posterior fossa tumours (23%; n=11). the overall success rate for etv was 68%. the net post-operative complication rate was 13% (n=6). csf leak and seizures were the only two charted post-operative complications at the rates of 9%(n=4) and 4% (n=2), accordingly. no deaths were recorded. conclusion: etv is a viable alternative to shunt insertion in a select group of patients with obstructive hydrocephalus, with acceptable success rate and safety profile. . introduction hydrocephalus is a condition that results when excess cerebrospinal fluid (csf) accumulates in the cerebral ventricles resulting in ventricular dilatation and raised intracranial pressure (lu, chen, weng, & xu, 2019). hydrocephalus is divided into communicating and non-communicating keywords endoscopic third ventriculostomy, obstructive hydrocephalus, shunts, csf corresponding author: zahraa al-sharshahi mb, bch bao (nui, rcsi), lrcp & si. royal college of surgeons, ireland zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 270 hassan z.a. dixon, yasir m. hamandi, ammar m.a. mahmmoud et al. (aka. obstructive) subtypes, as per dandy's classification (lu et al., 2019). non-physiological csf diversion using valve-regulated ventriculo-peritoneal and ventriculo-atrial shunts has dominated the field of hydrocephalus management over the past 45 years. however, shunts come with many complications including infections, displacement, and hardware failure. failure rates are reported at 25-40 % in the first year then 5-10% per year thereafter (deopujari, karmarkar, & shaikh, 2017). the significant morbidity imposed by these shunts and the need for frequent revisions has warranted the search for novel treatment options (mugamba & stagno, 2013). first introduced by mixter in 1923, endoscopic third ventriculostomy (etv) has regained popularity in the last two decades as an attractive treatment option for hydrocephalus (mixter, 1923). in fact, etv for the treatment of obstructive hydrocephalus is currently the most commonly performed endoscopic neurosurgical procedure (m. gangemi et al., 1999) (hellwig et al., 2005). desirable qualities of etv include 1) its physiological mechanism of csf diversion, 2) its minimally invasive nature and 3) the absence of long-term hardware and all its associated complications (mugamba & stagno, 2013). since it's advent in the early 1990s, etv has shown the highest success rate amongst patients is obstructive hydrocephalus caused by acqueductal stenosis, both congenital and acquired (mugamba & stagno, 2013). nonetheless, both the surgical techniques and indications for etv are constantly being refined. in the last few decades, many authors have been calling to expand the indications for etv and numerous reports have been published to support this notion. (beems & grotenhuis, 2004) (brockmeyer, abtin, carey, & walker, 1998) (choi, kim, & kim, 1999) (cinalli et al., 1999) (feng et al., 2004) (grunert, charalampaki, hopf, & filippi, 2003) (scarrow, levy, pascucci, & albright, 2000) (schroeder, niendorf, & gaab, 2002) (tisell, almström, stephensen, tullberg, & wikkelsö, 2000). in their systematic review and meta-analysis that compared the failure rates of obstructive hydrocephalus vs shunt insertion for patients with non-communicating hydrocephalus, rasul et al concluded that etv has statistically non-significant advantage over shunts; it does, however, appear to provide long-term survival benefit specifically in patients with congenital acqueductal stenosis (rasul, marcus, toma, thorne, & watkins, 2013). in iraq, etv is still a relatively novel modality. in this paper, we aim to report our experience with etv in the management of patients with obstructive hydrocephalus, which is one of the earliest reports in this field from our country. patients and methods we conducted a retrospective analysis of a consecutive sample of 47 patients who underwent etv for obstructive hydrocephalus at the neurosurgery teaching hospital in baghdad (nth) for the period between july 2010 and september 2015. the aim of this study was to determine the success rate of etv at our institution and to identify the main complications. a clinicoradiological criterion was implemented in our study. patients were deemed candidates for etv if they 1) presented with symptoms related to hydrocephalus such as raised icp or enlarging head circumference and 2) had an mri-confirmed diagnosis of obstructive hydrocephalus. patients with communicating hydrocephalus were excluded from the study. the follow-up period ranged between six months and six years (6 months-6 years). the success of etv was defined by a combination of clinical and radiological criteria and ultimately by "shunt-independence". the clinical criteria revolved around the resolution of symptoms and signs caused by the high intracranial pressure by the 3-month follow-up visit. the radiological criteria were defined as the decrease in ventricular size or the arrest of ventriculomegaly as determined by ultrasonography (us) and/or computed tomography (ct), using the evans index or the fronto-occipital horn ratio. all data were obtained from the hospital health records at the nth and statistics were performed using spss version 20. operative technique all operations were performed under general anesthesia. during each surgery, the fowling steps were followed: • the patient was placed in a supine position with the head resting on a doughnut-shaped head rest. • the head and neck were flexed at (15 o). • a longitudinal skin incision was made just in front of coronal suture to the right of the mid-pupillary 271 endoscopic third ventriculostomy for obstructive hydrocephalus line (3 cm off mid line & 1cm anterior to coronal suture). • the skin and periosteum were opened as a single layer with visual identification of coronal suture. • a burr hole was drilled abutting the anterior border of coronal suture. • the dura was coagulated and retracted in a cruciate fashion using a bipolar. • the pia and arachnoid were coagulated and opened sharply in a cruciate fashion. • the articulated arm of the endoscope was installed as close as possible to the patient’s head. • warm ringer lactate solution was connected to the sheath at a height of 15 cm from the patient’s ear. • a rigid sheath (8mm) with its trocar inside was advanced slowly into the brain tissue aiming the tip of the sheath at the inner canthus in mediolateral plane and towards the tragus in antero-posterior plane. • a sudden give up was used as an indication that the ventricle has been punctured. the trochar was then removed. • a telescope with an attached light source and camera (3s) was introduced inside the sheath and locked in the zero position. • the foramen of monro was identified, the arm was released and the sheath was introduced through foramen and placed just above the mammillary body. • the thinned floor of the 3rd ventricle at the region of the tuber cinereum was identified and punctured using the fenestration forceps. • the ringer solutions was allowed to circulate in and out to verify the stoma opening. • the endoscope was then withdrawn slowly while visualising the entry track. • cylindrical pieces of gelfoam were placed in the track and on the burr hole followed by subcutaneous tissue and skin closure. results our sample contained a heterogeneous group of patients in relation to the national geographic distribution, age range, and hydrocephalus etiology. the mean age was 4.4 years (range 40 days -38 years). the male: female ratio was 1.23:1 (55% males and 45% females). the most common cause of obstructive hydrocephalus in patients undergoing etv was acqueductal stenosis (62%; n=29). the second most common cause was posterior fossa tumors (23%; n=11). other aetiologies included third ventricle arachnoid cyst (11%; n=5), choroid plexus tumor of the lateral ventricle (2%; n=1) and thalamic tumors (2%; n=1). the overall success rate for etv was 68%. subgroup analysis showed that success rates were 62% and 78% for patients with acqueductal stenosis and posterior fossa tumors, respectively. regarding the age group, the success rate for the younger population (below 10 years) was (62-65%). in the subset of patients with unclear cerebrospinal fluid (csf), the success rate was 22%. no intraoperative complications were encountered. the net post-operative complication rate was 13% (n=6) and spontaneous closure was charted in 32% (n=15). csf leak and seizure were the only two recorded postoperative complications at the rates of 9%(n=4) and 4% (n=2), accordingly. the mortality rate was 0% (n=0). none of the patients needed redo etv or shunt insertion as per their corresponding last follow-up visits. figure 1. a. nine-year-old female with obstructive hydrocephalus due to 4th ventricular tumor (histopathologically proved who grade 4 ependymoma). a: preetv axial t1-weighted brain mri with contrast showing hydrocephalus with ballooning of the 3rd ventricle and dilatation of both the frontal and temporal horns of lateral ventricles. b: early post-etv brain ct scan (axial section) showing improvement of ventricular dilation with normal shape and size of the 3rd ventricle and the frontal horn of lateral ventricles. 272 hassan z.a. dixon, yasir m. hamandi, ammar m.a. mahmmoud et al. discussion etv is an important treatment option in the management of hydrocephalus. in our cohort of 47 patients with obstructive hydrocephalus, the two most common indications for etv were acqueductal stenosis and posterior fossa tumors; this corresponds to the results published by bouras et.al in their systematic review and meta-analysis (t. bouras & s. sgouros, 2012). recently, etv has replaced extra-cranial shunts as the first-line treatment for occlusive hydrocephalus caused by acqueductal stenosis. although the efficacy of etv has been most established with the congenital forms of acqueductal stenosis, it is still a viable treatment option for other acquired aetiologies including those attributed to inflammatory and neoplastic processes (hellwig et al., 2005). this finding was also reflected in our results, wherein patients with acqueductal stenosis had the highest success rates. etv has also proven effective in the management of occlusive hydrocephalus in patients with posterior fossa tumors (amano et al., 2002) (ruggiero et al., 2004) (cinalli et al., 1999) (schijman, peter, rekate, sgouros, & wong, 2004) (sainte-rose et al., 2001). the incidence of pre-operative hydrocephalus in these patients is estimated at 80%, with 25-30% progressing to persistent post-operative hydrocephalus necessitating surgical intervention (hellwig et al., 2005). in their series of 206, sainterose et al concluded that when performed prior to craniotomy, etv reduced the incidence and progression of post-operative hydrocephalus (sainte-rose et al., 2001). however, there exists no consensus regarding the timing and the definitive treatment modality to be used in the management of these patients (hellwig et al., 2005). since it's advent in the late 1980s and early 1990s, much experience has been gained with etv as a management tool in patients with obstructive hydrocephalus. on the other hand, the efficacy of etv in communicating hydrocephalus has not been scientifically established and is currently under investigation, with some authors reporting encouraging results (hailong et al., 2008) (meier, zeilinger, & schönherr, 2000) (michelangelo gangemi, maiuri, buonamassa, colella, & de divitiis, 2004). at our institution, patients with communicating hydrocephalus are not currently considered candidates for etv. to date, patient selection criteria for etv is a debatable issue in the neurosurgical community; i.e. there is no clear definition of "etv-eligible" patients and patient selection is currently based on local institutional policies, individual surgeon's experience and patient preference. (m. gangemi et al., 1999) (triantafyllos bouras & spyros sgouros, 2012). evaluation of etv outcome has been mainly based on a clinicoradiological criteria. clinical criteria focus on symptomatic improvement and shuntindependence while the radiological criteria centers on the reduction of the ventricular size and/or cessation of its growth (buxton, turner, ramli, & vloeberghs, 2002) (deopujari et al., 2017). however, some recent evidence tells us that the change in ventricular size is an unreliable indicator, especially in the early postoperative period. (schwartz, yoon, cutruzzola, & goodman, 1996) (feng et al., 2004). success rates with etv have been reported to be between 50-90% (hellwig et al., 2005). beams and grotenhius have reported the largest series thus far on patients with etv (339 cases). in the aforementioned series, shunt independence was charted in 258 patients, with a complication rate of 7.7%. (beems & grotenhuis, 2004). regarding factors that predict poor outcomes after etv, a history of shunt infection and postoperative meningitis have been identified as independent risk factors for etv failure (fukuhara, vorster, & luciano, 2000). none of our patients harbored either risk factor. both the immediate and long-term complications associated with etv are currently insufficiently reported in the literature to draw solid conclusions. there exist many inconsistencies in the reported intra-operative, immediate and delayed postoperative complications. in one systematic review, the mortality rate was reported as 0.22% and the permanent morbidity rate was 2.1%. the most common charted complications were csf infections (1.8%) and csf leak (1.7%) (t. bouras & s. sgouros, 2012). further studies have also reported mortality rates below 1% (cohen, 1994; m. gangemi et al., 1999; jones, kwok, stening, & vonau, 1994; teo & jones, 1996). in our study, no deaths were recorded as per the last follow-up visit for each patient. the obvious shortcomings in our study are 1) the short follow-up period and 2) the small cohort size. in fact, these two limitations are shared by the majority of the related reports in the literature, an 273 endoscopic third ventriculostomy for obstructive hydrocephalus observation that highlights the need for multi-center, prospective, long-term studies to elucidate the longterm outcomes of etv. conclusion etv is a promising treatment strategy for patients with obstructive hydrocephalus. however, many questions remain unanswered in relation to its longterm efficacy and safety, calling for further research in this area. references 1. amano, t., inamura, t., nakamizo, a., inoha, s., wu, c.-m., & ikezaki, k. (2002). case management of hydrocephalus associated with the progression of childhood brain stem gliomas. child's nervous system : chns : official journal of the international society for pediatric neurosurgery, 18(11), 599-604. doi:10.1007/s00381-002-0637-5. 2. beems, t., & grotenhuis, j. a. (2004). long-term complications and definition of failure of neuroendoscopic procedures. child's nervous system : chns : official journal of the international society for pediatric neurosurgery, 20(11-12), 868-877. doi:10.1007/s00381-004-0945-z. 3. bouras, t., & sgouros, s. (2012). complications of endoscopic third ventriculostomy: a systematic review. acta neurochirurgica. supplement, 113, 149-153. doi:10.1007/978-3-7091-0923-6_30. 4. bouras, t., & sgouros, s. (2012). complications of endoscopic third ventriculostomy: a systematic review. acta neurochir suppl, 113, 149-153. doi:10.1007/978-37091-0923-6_30. 5. brockmeyer, d., abtin, k., carey, l., & walker, m. l. (1998). endoscopic third ventriculostomy: an outcome analysis. pediatric neurosurgery, 28(5), 236-240. doi:10.1159 /000028657. 6. buxton, n., turner, b., ramli, n., & vloeberghs, m. (2002). changes in third ventricular size with neuroendoscopic third ventriculostomy: a blinded study. journal of neurology, neurosurgery, and psychiatry, 72(3), 385-387. doi:10.1136/jnnp.72.3.385. 7. choi, j. u., kim, d. s., & kim, s. h. (1999). endoscopic surgery for obstructive hydrocephalus. yonsei medical journal, 40(6), 600-607. doi:10.3349/ymj.1999.40.6.600. 8. cinalli, g., sainte-rose, c., chumas, p., zerah, m., brunelle, f., lot, g. renier, d. (1999). failure of third ventriculostomy in the treatment of aqueductal stenosis in children. journal of neurosurgery, 90(3), 448-454. doi:10.3171/jns.1999.90.3.0448. 9. cohen, a. r. (1994). ventriculoscopic surgery. clinical neurosurgery, 41, 546-562. 10. deopujari, c. e., karmarkar, v. s., & shaikh, s. t. (2017). endoscopic third ventriculostomy: success and failure. journal of korean neurosurgical society, 60(3), 306-314. doi:10.3340/jkns.2017.0202.013. 11. feng, h., huang, g., liao, x., fu, k., tan, h., pu, h., . . . zhao, d. (2004). endoscopic third ventriculostomy in the management of obstructive hydrocephalus: an outcome analysis. journal of neurosurgery, 100(4), 626-633. doi:10.3171/jns.2004.100.4.0626. 12. fukuhara, t., vorster, s. j., & luciano, m. g. (2000). risk factors for failure of endoscopic third ventriculostomy for obstructive hydrocephalus. neurosurgery, 46(5), 11001111. doi:10.1097/00006123-200005000-00015. 13. gangemi, m., donati, p., maiuri, f., longatti, p., godano, u., & mascari, c. (1999). endoscopic third ventriculostomy for hydrocephalus. minimally invasive neurosurgery: min, 42(3), 128-132. doi:10.1055/s-2008-1053384. 14. gangemi, m., maiuri, f., buonamassa, s., colella, g., & de divitiis, e. (2004). endoscopic third ventriculostomy in idiopathic normal pressure hydrocephalus. neurosurgery, 55(1), 129-134. doi:10.1227/01.neu.00001 26938.12817.dc. 15. grunert, p., charalampaki, p., hopf, n., & filippi, r. (2003). the role of third ventriculostomy in the management of obstructive hydrocephalus. minimally invasive neurosurgery: min, 46(1), 16-21. doi:10.1055/s-200337957. 16. hailong, f., guangfu, h., haibin, t., hong, p., yong, c., weidong, l., & dongdong, z. (2008). endoscopic third ventriculostomy in the management of communicating hydrocephalus: a preliminary study. j neurosurg, 109(5), 923-930. doi:10.3171/jns/2008/109/11/0923. 17. hellwig, d., grotenhuis, j. a., tirakotai, w., riegel, t., schulte, d. m., bauer, b. l., & bertalanffy, h. (2005). endoscopic third ventriculostomy for obstructive hydrocephalus. neurosurgical review, 28(1), 1-38. doi:10.1007/s10143-004-0365-2. 18. jones, r. f., kwok, b. c., stening, w. a., & vonau, m. (1994). neuroendoscopic third ventriculostomy. a practical alternative to extracranial shunts in non-communicating hydrocephalus. acta neurochirurgica. supplement, 61, 79-83. doi:10.1007/978-3-7091-6908-7_14. 19. lu, l., chen, h., weng, s., & xu, y. (2019). endoscopic third ventriculostomy versus ventriculoperitoneal shunt in patients with obstructive hydrocephalus: meta-analysis of randomized controlled trials. world neurosurgery, 129, 334-340. doi:10.1016/j.wneu.2019.04.255. 20. meier, u., zeilinger, f. s., & schönherr, b. (2000). endoscopic ventriculostomy versus shunt operation in normal pressure hydrocephalus: diagnostics and indication. minimally invasive neurosurgery: min, 43(2), 87-90. doi:10.1055/s-2000-8325. 21. mixter, w. j. (1923). ventriculoscopy and puncture of the floor of the third ventricle. the boston medical and surgical journal, 188(9), 277-278. doi:10.1056/n ejm192303011880909. 22. mugamba, j., & stagno, v. (2013). indication for endoscopic third ventriculostomy. world neurosurgery, 79(2 suppl), s20.e19-s20.e23. doi:10.1016/j.wneu. 2012.02.016. 274 hassan z.a. dixon, yasir m. hamandi, ammar m.a. mahmmoud et al. 23. rasul, f. t., marcus, h. j., toma, a. k., thorne, l., & watkins, l. d. (2013). is endoscopic third ventriculostomy superior to shunts in patients with non-communicating hydrocephalus? a systematic review and meta-analysis of the evidence. acta neurochirurgica, 155(5), 883-889. doi:10.1007/s00701-013-1657-5. 24. ruggiero, c., cinalli, g., spennato, p., aliberti, f., cianciulli, e., trischitta, v., & maggi, g. (2004). endoscopic third ventriculostomy in the treatment of hydrocephalus in posterior fossa tumors in children. child's nervous system : chns : official journal of the international society for pediatric neurosurgery, 20(11-12), 828-833. doi:10.1007/s00381-004-0938-y. 25. sainte-rose, c., cinalli, g., roux, f. e., maixner, r., chumas, p. d., mansour, m., . . . renier, d. (2001). management of hydrocephalus in pediatric patients with posterior fossa tumors: the role of endoscopic third ventriculostomy. journal of neurosurgery, 95(5), 791-797. doi:10.3171/jns.2001.95.5.0791. 26. scarrow, a. m., levy, e. i., pascucci, l., & albright, a. l. (2000). outcome analysis of endoscopic iii ventriculostomy. child's nervous system : chns : official journal of the international society for pediatric neurosurgery, 16(7), 442-445. doi:10.1007/s003810 000307. 27. schijman, e., peter, j. c., rekate, h. l., sgouros, s., & wong, t. t. (2004). management of hydrocephalus in posterior fossa tumors: how, what, when? child's nervous system : chns : official journal of the international society for pediatric neurosurgery, 20(3), 192-194. doi:10.1007 /s00381-003-0900-4. 28. schroeder, h. w. s., niendorf, w.-r., & gaab, m. r. (2002). complications of endoscopic third ventriculostomy. journal of neurosurgery, 96(6), 1032-1040. doi:10.3171/jns.2002.96.6.1032. 29. schwartz, t. h., yoon, s. s., cutruzzola, f. w., & goodman, r. r. (1996). third ventriculostomy: post-operative ventricular size and outcome. minimally invasive neurosurgery: min, 39(4), 122-129. doi:10.1055/s-20081052231. 30. teo, c., & jones, r. (1996). management of hydrocephalus by endoscopic third ventriculostomy in patients with myelomeningocele. pediatric neurosurgery, 25(2), 57-63. doi:10.1159/000121098. 31. tisell, m., almström, o., stephensen, h., tullberg, m., & wikkelsö, c. (2000). how effective is endoscopic third ventriculostomy in treating adult hydrocephalus caused by primary aqueductal stenosis? neurosurgery, 46(1), 104-111. doi: 10.33962/roneuro-2020-089 encephalitic syndrome revealing cerebral gliomatosis in an adolescent si ahmed hakim, daoudi smail romanian neurosurgery (2020) xxxiv (4): pp. 524-527 doi: 10.33962/roneuro-2020-089 www.journals.lapub.co.uk/index.php/roneurosurgery encephalitic syndrome revealing cerebral gliomatosis in an adolescent si ahmed hakim, daoudi smail department of neurology. chu tizi-ouzou. algeria abstract cerebral gliomatosis is a rare glial tumour which is defined by a diffuse and not very destructive infiltration of the encephalon by the glial neoplastic cells in the absence of individualizable tumour mass (sanson et al., 2005). the clinical and radiological presentation is often misleading and not very specific, and the diagnosis is rarely mentioned. histological diagnosis remains difficult. finally, gliomatosis poses a specific therapeutic problem compared to other glial tumours due to the toxicity of panencephalic radiotherapy and the impossibility of achieving surgical reduction of the tumour (sanson et al., 2005). data from the literature show a median overall survival of 14.5 months, a higher frequency of oligodendroglial forms. the prognosis is linked to age, functional status, histological grade, oligodendroglial differentiation (sanson et al., 2005). we report the observation of a gliomatosis occurring in a 14-year-old boy, having presented focal subintral epileptic attacks accompanied by hemiparesis. flair sequence brain mri showed a left fronto-temporo-insular hyper signal. the brain biopsy revealed gliomatosis. the evolution was favourable after radiotherapy. gliomatosis is a diagnosis to be systematically evoked in the presence of a diffuse cerebral affection. its etiopathogenic mechanism is unknown, and evolution is unpredictable (millan. bs et al., 2010). introduction cerebral gliomatosis is a condition initially described by nevin in 1938 (nevin et al., 1938), characterized by diffuse infiltration of glial tumor cells invading a large part of the brain, bilaterally (possibility also of the marrow), with absence of individualizable tumor mass (nevin et al., 1938). it is a rare neurosurgical pathology, since less than 300 cases are reported in the literature (sanson et al., 2005), which can occur at any age, more frequently in adults between 40 and 50 years (millan. bs et al., 2010). the clinical signs are non-specific and the imagery is often misleading, which can simulate a large number of non-neoplastic neurological medical pathologies (inflammatory or infectious encephalitis, angeitis, leukodystrophies) (sanson et al., 2005). its radiological and histological diagnosis is difficult because of the absence of identifiable tumor mass and its diffuse character. (millan. bs et al., 2010). gliomatosis also poses a problem of specific therapeutic keywords encephalitic syndrome, cerebral gliomatosis, adolescent corresponding author: si ahmed hakim department of neurology. chu tiziouzou, algeria siahmed-hakim@hotmail.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 525 encephalitic syndrome revealing cerebral gliomatosis in an adolescent management by comparing them to other glial tumors (its diffuse nature, surgery is excluded, radiotherapy is poorly tolerated since it often involves the entire brain, chemotherapy is possible unlike other gliomas) (sanson et al., 2005). we report a case of gliomatosis in a 14-year-old boy, diagnosed in pre-mortem using mri and brain biopsy data, the clinical and radiological picture of which was misleading, simulating an acute limbic encephalitis picture. observation a 14-year-old boy immediately developed serial, drug-resistant focal seizures with temporal spread, and then developed right hemiparesis. the examination showed right hemiparesis, with no disturbance of consciousness, no signs of intracranial hypertension, or meningeal syndrome. magnetic resonance imaging (mri) revealed a hyper signal on the flair and t2 sequences, without contrast enhancement, unilateral, on the left, touching the fronto-temporo-insular white matter (fig. 1). the ges highlighted left hemispherical brain pain, without paroxysms (figure 2). the cytochemical study of the csf revealed a slight hyperproteinorachia at 0.5 g / l, as well as a lymphocytosis at 30 elements / mm3, and the immunological study did not show a chronic inflammatory process. all serologies were negative (herpes, htlv1, syphillis, hiv, lyme ...), and the autoimunity balance was also negative. the patient received methylprednisolone iv (1g / day for 5 days) with an oral relay (1mg / kg / day), combined with anti-epileptics (levetiracetam 3g / day, lamotrigine 200mg / day). the evolution was marked by a persistence of the epilepsy attacks, an appearance of headache and oculomotor disorders (diplopia, left exophthalmia), see obnubilation. control mri showed an aggravation of the lesions with mass effect and bilateralization of the hyper signal (figure. 3). the brain biopsy was done urgently and returned in favor of a gliomatosis (oligodendrogliale). the child was treated with radiotherapy, with disappearance of disturbances of consciousness and seizures, and persistence of hemiparesis. figure 1. cerebral mri: a: coronal section, flair sequence / b: transverse section, t2 sequence: left fronto-temporo-insular hyper signal. figure 2. eeg. left hemispherical pain (theta delta waves more marked on the left anterior regions). 526 si ahmed hakim, daoudi smail figure 3. control brain mri (flair sequences, cross section): extensive hyper signal affecting the fronto-temporo insular white matter, bilaterally, with mass effect. discussion we report a case of cerebral gliomatosis, the diagnosis of which was based on imaging and brain biopsy data and whose evolution was favorable with disappearance of epilepsy attacks, improvement in disorders of consciousness and hemiparesis. primary gliomatosis often poses diagnostic difficulties because its clinical presentation is not very specific. the most frequent modes of revelation were epilepsy, the occurrence of cognitive disorders, intracranial hypertension (headache), the presence of focal deficits (artigas. j, et al., 1985, sanson et al., 2005). it was in 1986 that the first premortem diagnosis of gliomatosis was made on the combined brain biopsy and mri data (troost d, et al., 1987). the incidence is higher in humans (in fact common to all gliomas) (sanson et al., 2005) and, more specifically in gliomatosis, a younger age of onset in humans (jennings et al., 1995). in mri, the flair and t2 sequences are essential, they show an extended bilateral hyper signal of white matter and gray nuclei, which can extend to the brainstem and the spinal cord (peretti-viton p, et al., 2002 ), and gadolinium intake is generally absent (sanson et al., 2005). it is defined as "an infiltrating process, encompassing at least three lobes, without contrast enhancement or less than 1 cm" (sanson et al., 2004). the brain scan, including with injection, may be normal, but a careful examination may show suggestive abnormalities (discreet ventricular asymmetry, discreet poorly limited hypodensity, appearance of diffuse cerebral edema with small ventricles, and diffuse erasure of the furrows, or, in an elderly patient, the absence of atrophy of the brain scanner) (sanson et al., 2005). the diagnoses most often mentioned were: multiple sclerosis, leukoencephalopathy of unknown cause, encephalitis, progressive multifocal leukoencephalitis, vasculitis, behçet's disease (sanson et al., 2005). although not specific, certain aspects are suggestive of gliomatosis: the presence of a discrete mass effect, the thickening of the corpus callosum, the asymmetrical character of the hypersignal, the heterogeneous and "flaky" character of the hypersignal, better visible in t2 as in flair, the associated impairment of the gray matter, in particular of the thalamus and the loss of the boundaries between the white matter and the gray matter (sanson et al., 2005). the clinical and radiological differential diagnosis includes all diffuse encephalopathies of various causes (infectious, vascular metabolic and tumor) (peretti-viton p, et al., 2002). this is the case of our patient who presented a misleading picture with clinical and para-clinical signs (mri, eeg, csf) of acute limbic encephalitis. the diagnosis by histological study by biopsy is still essential, but often proves difficult, and sometimes non-contributory due to the low cell density, and the preservation of the normal architecture (sanson et al., 2005). the histological grade is sometimes difficult to determine (sanson et 527 encephalitic syndrome revealing cerebral gliomatosis in an adolescent al., 2004). (astrocytic, oligodendroglial, polymorphic aspect…). according to the literature, oligodendroglial gliomatosis is considered rare (balko et al., 1992), unlike some authors where the majority of gliomatosis is of oligodendroglial type (sanson et al., 2005), as was observed in our patient. the extremely diffuse aspect of tumor infiltration could explain the fact that the brain biopsy is sometimes not very contributory. glioma cells do not have the capacity to cross the vascular basement membrane (limiting metastases by hematogenous or lymphatic route) (tonn et al., 2003), but they have the capacity to migrate very far into the neuron (tonn et al., 2003; bellail et al., 2004). spontaneous evolution is extremely variable ranging from less than 1 month to 16 years (artigas, 1985, cervos-navarro, 1987, louis. dn, et al., 2007). survival appears to be linked primarily to clinical factors: gender, age and karnofsky's functional index. the prognosis also appears to be linked to histological characteristics (sanson et al., 2005). our case had a favorable evolution with follow-up for 08 months, marked by a regression of clinical signs (epilepsy attacks, disturbances of consciousness, oculomotor disorders). the criteria which seem in favor of a good evolution are criteria of clinical response (disappearance of convulsions, regression of cognitive disorders and headache) or radiological (reduction of the range of the hyper signal, regression of the mass effect) (sanson et al., 2004, 2005). exeresis is not possible because of the extent of gliomatosis (sanson et al., 2005), and radiotherapy has a major neurotoxicity, since it often involves the entire brain (crossen et al., 1994). this is why some authors have proposed treating these patients with chemotherapy alone as first-line treatment, which has the advantage of better tolerance (sanson et al., 2004). references 1. artigas. j, cervos-navarro. j, iglesias. jr, et al. gliomatosis cerebri: clinical and histological findings. clin neuropathol 1985;4:135—48. 2. balko. mg, blisard. ks, samaha. fj. (1992). oligodendroglial gliomatosis cerebri. hum pathol, 23: 706-707. 3. bellail. ac, hunter. sb, brat. dj, tan. c, van meir. eg. (2004). microregional extracellular matrix heterogeneity in brain modulates glioma cell invasion. int j biochem cell biol, 36: 1046-1069. 4. cairncross. jg, ueki. k, zlatescu. mc et al. (1998). specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. j natl cancer inst, 90: 1473-1479. 5. galanaud. d, chinot. o, nicoli. f et al. (2003). use of proton magnetic resonance spectroscopy of the brain to differentiate gliomatosis cerebri from low-grade glioma. j neurosurg, 98:269-276. 6. hoang-xuan. k, he. j, huguet. s et al. (2001). molecular heterogeneity of oligodendrogliomas suggest alternative pathways in tumoral progression. neurology, 57: 1278-1281. 7. jennings. mt, frenchman. m, shehab. t, johnson. md, creasy. j, laporte. k, dettbarn. wd. (1995). gliomatosis cerebri presenting as intractable epilepsy during early childhood. j child neurol, 10: 37-45. 8. lantos. pl, bruner. jm. (2000). gliomatosis cerebri in tumours of the nervous system. kleihues and cavenee ed, iarc lyon, pp. 92-93. 9. louis. dn, ohgaki. h, wiestler. od, cavenee. wk, editors. gliomatosis cerebri. lyon; 2007, p. 50—2. 10. millan. bs, kaci. r, polivka. m, robert. g, heran. f, gueguen. a, mokhtari. k, gray. f. gliomatose cérébrale diffuse : étude biopsique et autopsique d’un cas. annales de pathologie (2010) 30, 25—29. 11. nevin. s. (1938). gliomatosis cerebri. brain, 61: 170-191. 12. peretti-viton. p, brunel. h, chinot. o, et al. histological and mr correlations in gliomatosis cerebri. j neurooncol 2002;59:249—59. 13. sanson. m, cartalat-carel. s, taillibert. s et al. (2004). initial chemotherapy in gliomatosis cerebri. neurology, 63: 270-275. 14. sanson. m, napolitanon. m, cartalat-carel. s, taillibert. s. la gliomatose cérébrale. rev neurol (paris) 2005; 161: 2, 173-181. 15. tonn. jc, goldbrunner. r. (2003). mechanisms of glioma cell invasion. acta neurochir suppl, 88: 163-167. 16. troost. d, kuiper. h, valk. j, et al. gliomatosis cerebri, report of a clinically diagnosed and histologically confirmed case. clin neurol neurosurg 1987;89:43— 7.1987. doi: 10.33962/roneuro-2021-074 postoperative lumbar spondylodiscitis. a systematic review arsene anamaria-alexandra, iacob gabriel, alexandru vlad ciurea romanian neurosurgery (2021) xxxv (4): pp. 434-443 doi: 10.33962/roneuro-2021-074 www.journals.lapub.co.uk/index.php/roneurosurgery postoperative lumbar spondylodiscitis. a systematic review arsene anamaria-alexandra1, iacob gabriel2, alexandru vlad ciurea2,3 1 department of neurosurgery 2, emergency university hospital, bucharest, romania 2 professor of neurosurgery, ‘‘carol davila’’ university of medicine and pharmacy, bucharest, romania 3 departament of neurosurgery, sanador clinical hospital, neurosurgical department, bucharest, romania abstract background. several causes that can trigger pod can be incriminated: the patient's immune status, surgical technical errors, intra-operative contamination, foreign materials microfilm. extensive analysis is required to eradicate the limited or diffuse infection and manage the optimal therapeutic attitude conservative or by surgery to get: faster recovery time, to improve symptoms, to allow mobilization, to offer a good quality of life and to reduce the average length of hospital stay. objectives. to perform a systematic review of pod outcomes via retrospective analysis of current studies based on the mechanism, the pathogenesis, the management of patient's immunological status, aetiology (microorganism involved, foreign material applied for hemostasis, application of spinal instrumentation, cement, screws, spinal devices), laboratory (tlc, esr, crp), mri/ct-scan, antibiotherapy guidelines and the type of surgery performed: classical or miniminvasive, length of procedure, intraoperative accidents, the experience of the neurosurgeon, post-operative stay in icu, etc. methods. several data were taken into account regarding lumbar infections using a comprehensive review of the literature published studies from 1998 to 2021. demographic data, clinical variables, length of hospital stay, duration of antibiotic treatment, and post-treatment complications were assessed. results. we performed a systematic review concerning 31 studies regarding clinical status, diagnosis and treatment. conclusions. based on our systematic analysis, training and continuous education in spine surgery are necessary to prevent pod. the diagnosis of lumbar pod is based on history and physical examination, biochemical markers, neuroradiologic studies, using appropriate mri imaging. most cases of lumbar pod can be managed by conservative treatment with antibiotics after causative germ isolation and antibiogram. surgery is performed on patients with conservative treatment failure resistant to antibiotic therapy, as those with neurological complications: acute paraplegia, pain resistance to analgetics, acute sepsis, abscesses, spinal instability, severe kyphosis. early surgery with wound irrigation/debridement is more readily able to disrupt biofilm formation and facilitate penetration of systemic antimicrobials to allow for resolution of the infection, vacuum-assisted closure facilitates wound healing and eradicates spinal infections, decrease the rate of complications, permit keywords postoperative lumbar spondylodiscitis, septic and aseptic spondylodiscitis, conservative and surgical treatment, implants, biofilms corresponding author: alexandru vlad ciurea professor. “carol davila” university of medicine and pharmacy, bucharest, romania prof.avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 435 postoperative lumbar spondylodiscitis rapid pain relief while preserving the instrumentation/stability, better clinical outcomes, infection control before extensive destruction of the vertebrae, spinal instability and kyphotic deformity appear. instrumentation can usually be preserved in patients with early infections (e.g., <6 weeks), but instrumentation removal should be considered for infections presenting in a delayed fashion (e.g., >6 weeks to even years) psii. patients should be adequately followed for one postoperative year, to ensure that the infection has been fully eradicated. implant sonication provides cultures for direct identification of active and/or persistent biofilm, while the introduction of enzymes that dissolve the biofilm matrix (e.g., dnase and alginate lyase) and quorum-sensing inhibitors that increase biofilm susceptibility to antibiotics may further help manage postoperative infection (2) (27-31). introduction postoperative lumbar infection, after adult spine surgery may interest the degenerated spinal disc: septic or aseptic spinal disc infections generating post-operative discitis (pod), the adjacent vertebral bodies infections known as osteomyelitis (om), or both osteo-discitis (od). in general these pathologic spinal entities rarely occur separately and are known under the term spondylodiscitis (sd); but also postoperative lumbar infection may extend epidural and/or to facet joint arthropathy, paravertebral spaces. semantically pod a rare complication, representing 3-5% of cases should be differentiated from primary vertebra endplate infection with secondary involvement of the disc; because of this is more accurate to use the term spondylodiscitis (sd) or vertebral osteomyelitis (vo) (1), and surgical site infections (ssis) after adult spine surgery, generated by preoperative, intraoperative, or postoperative factors that contribute to the risk of infection following spinal fusions which varies from 0.7% to 20% (2). the diagnosis of pod must be based on a combination of clinical symptoms, laboratory tests, bacteriological cultures from disc puncture, and radiological findings (36). it’s a severe complication which can lead to severe impairment of quality of life, neurological deficits, deformities, segmental instabilities (4-6). a recent study in denmark showed that the incidence of spondylodiscitis increased from 2.2 to 5.8 per 100.000 people per year between 1995 and 2008, and the incidence of age in germany was estimated at 30 to 250.000 per year based on data provided by the federal statistical office 2015 (7), in the west it is <1%, and in india from 4% to 10% (8). methods 15 studies, published from 2003-2021, are analysed, out of which two: ahsan k. (3) and jain m.(8) publications were referring to postoperative osteodiscitis were considered (table 1).patients were diagnosed clinically, by laboratory investigations such as: complete blood count (cbc) erhrytrocites sedimentation rate (esr), c reactive protein (crp) and coagulation levels, and radiological lumbar studies: x-rays, ct, mri. demographic data, clinical variables, length of hospital stay, duration of antibiotic treatment, and post-treatment complications were assessed. inclusion and exclusion criterias are presented below (table 1). table 1. study of fusion for conservative and interventional treatment of lumbar osteodiscitis, modified after (3)(8). results the patients were followed for 12-24 months by ahshan k. (3). thus, they divided the patients into two groups a and b, respectively in the conservative and operative group and it was found that after primary discectomy, the pain-free interval was 1-6 weeks for the conservative group and 1-8 weeks for the operative group and the duration symptoms before admission were 5-21 days for group a and 721 days for group b. patients experienced moderate to severe pain, radiculopathy, mild fever, paravertebral muscle spasm, positive slr test, and pseudo gower sign. demographic characteristics in both groups showed no significant differences in age, sex, clinical presentation, pain-free interval for the development of disc symptoms, duration, disc level, and associated risk factors. esr and crp values, were elevated in all patients in both groups. after treatment, the values in some patients decreased in one to two weeks, and the values that remained 436 arsene anamaria-alexandra, iacob gabriel, alexandru vlad ciurea elevated returned to the initial preoperative value in 1-3 months. values returned to normal in all patients within six months. biopsy reports showed a mixture of inflammatory cells, including neutrophils, plasma cells and lymphocytes but no granulomatous lesions. simple x-ray imaging investigations in anteroposterior and lateral incidence were recommended in all patients. six to eight weeks later, patients in the first study had localized osteopenia, narrowing of the disc space, erosion of the final plaque, cavitation, and kyphotic deformity. dynamic x-rays were used for patients who experienced pain in the first study, and in the second study no dynamic x-rays were performed due to severe pain on mobilization. ct showed that the final plate erosion had formed 3-6 weeks before the discitis. mri showed hypointensity on t1weighted images and hyperintensity on t2weighted images with improved diffuse and continuous heterogeneous contrast of discs, endplate, and adjacent bone marrow in all patients in both studies. severe pain, after a painless interval, after lumbar discectomy increases the possibility of a recurrent disc herniation but the distinction is made after 6 months after surgery, between a recurrent disc with postoperative changes and scar tissue by mri. ahsan k (3) observed that after treatment with group a (conservative) the condition of patients improved after 4-6 weeks. intravenous antibiotics were given for 4-6 weeks, followed by five weeks of oral administration until the pain improved, esr and crp returned to normal. the administration of antibiotics lasted 69 -92 days. in group b (operated patients) the good condition was found in two to three weeks of intravenous administration of antibiotics and followed by 3-4 weeks of oral administration. the duration of antibiotics was 34-50 days. empirical antibiotics were initially prescribed for all patients (example: ceftriaxone, which was resistant to 40% of cases) and then culture-specific: staphylococcus aureus, s. epidermidis (meropenem, flucoxacillin, linezolid, fusidic acid). ciprofloxacin and tobramycin were administered for the culture in which e. coli, enterobacter, pseudomonas were present. jain m. (7) treated group a (conservative) with antibiotics, analgesics, orthoses and physiotherapy and group b (operated patients) only with debridement surgery; debridement with postero-lateral fusion by autogenous bone graft and stabilization by screw and pedicle stem; inter-body lumbar transforaminal debridement with fusion through titanium cage and autogenous bone graft and stabilization by screw and pediculated stem. serial esr and crp returned to baseline values in about three weeks. the condition of all patients improved in eight weeks. patients were followed by a blood or x-ray test after 1,3,6 and 12 months after discharge and then once a year. the state of fusion was assessed at 6-12 months by x-ray and ct. no patients during the conservative and surgical treatments suffered neurological damage. the satisfaction rate was higher in the operating group than in the conservative group at the end of the one year. the operating group required significantly shorter hospitalization with bed rest and a shorter period of antibiotic administration and reduced discomfort symptoms. the costs of procedures and blood transfusions were higher for the operating group, but the complication rate was also higher. discussion pod is a complication, extremely serious and rare today, after surgery on the intervertebral disc. such entity was first described by frank turnbull in 1953 as a clinical entity (9-11). pod occur more commonly in the lumbar spine: a single level involvement 65%, multiple contiguous levels 20% and multiple noncontiguous levels (10%); appear after about 6-7 weeks mainly after discectomy, see an insufficient operation or a recurrent disc herniation (2-9); may present septic (more frequent as a postoperative complication involving skin flora such as staphylococcus aureus) and aseptic forms (due to disc trauma and vascular compromise during surgery, involving spinal tuberculosis spread along spinal ligament to involve the adjacent anterior vertebral bodies, causing angulation of the ver tebrae with subsequent kyphosis (18). pod may also be caused by hematologic spread from a distant infection site has been identified in almost half of spondylodiscitis patients, as a remote infection (14). common distant infection sites include the genitourinary tract (17%), the heart (endocarditis, 12%), skin and soft tissue (11%), intravascular devices (5%), gastrointestinal tract (5%), respiratory tract (2%) and oral cavity (2%). pod has a male predominance, significant morbidity especially in developing countries it has a high incidence (16) and mortality (17) the most important risk factors (2-12)(15) in the development of pod are: 437 postoperative lumbar spondylodiscitis preoperative: advanced age, male sex, obesity, long-term systemic administration of steroids, organ transplantation, diabetes mellitus, tobacco/alcohol use, malnutrition, coronary and severe vascular diseases, liver cirrhosis, chronic kidney disease, rheumatic disease, also concomitant infections (sepsis, extra-spinal infections of the skin, teeth, lungs, ascending infection, e.g. from urogenital tract), immunocompromised patients especially to aids, intravenous drug abuse, organ transplantation, preoperative hospital stay, prior poly-trauma, tumor/malignancy, high asa score, previous spinal surgery (16), multiple lumbar surgeries, suboptimal timing of prophylactic antibiotic therapy, elevated preoperative serum glucose levels. intraoperative: large blood loss, use of cell savers, operations that last very long > 5 hours, increased wound exposure to air (longer surgical duration), greater soft tissue dissection, and increased mus cle/skin retraction devascularize the para-spinal muscles, increases the potential for blood loss, and results in larger dead spaces, which also contribute to the risk of infection, open interventions, number of levels operated, postoperative incontinence following laminectomy and/or fusion, but also minimally invasive spinal and endoscopic procedures, posterior vs. anterior spinal instrumentation, fu sions, implant material (titanium vs stainless steel), use of allograft, use of microscope/oarm/c-arm, fluoroscopy, intraoperative computed tomography, many people in the operating room (two or more residents on a case), open suction drainage, the failure to drain wounds correlates with a significantly higher risk of delayed spinal infections. the timing of administration of preoperative antibiotics is strongly correlated with an increased risk of pod. ideally, preoperative prophylactic antibiotics should be administered within an hour of surgery (e.g., cephalosporin except in penicillin allergic patients); administration up to 15 minutes prior to the incision may be even more effective, spinal surgery for tumor resection is also independently associated with an increased risk of lumbar pod (2) postoperative urinary/faecal incontinence, poor wound care, postoperative icu stay, elevated postoperative serum glucose levels as an aetiology, pod mono-microbial or polymicrobial infection in 10-50% of cases (2) contiguous infection spread (12)(14): pyogenic bacterial: staphylococcus aureus (60% of cases, methicillin-sensitive staphylococcus aureus mssa, still the predominant aetiologic agent in drug users), streptococcus viridans (vdu, immunocompromised), staphylococcus epidermidis is associated with implantrelated infections, whereas coagulase-negative staphylococci and streptococcus viridans may be a cause of indolent infections, due to their low virulence, gram-negative organisms: enterobacter spp. escherichia coli (11% -25%) is the most common pathogen in this group, followed by proteus, klebsiella and enterobacteriae spp. occur in the elderly, in states of immunosuppression and diabetes, brucella spp.(6-12%) (common in the mediterranean and middle eastern countries) (13), salmonella, pseudomonas aeruginosa in cases associated with intravenous drug abuse enterobacter, and acinetobacter, burkholderia pseudomallei (i.e. melioidosis): diabetic patients from northern australia and parts of southeast asia, brucella spp.; in patients with sickle cell disease salmonella spp... there are also common organisms implicated in pod with spinal instrumentation like s. aureus, coagulase negative staphylococcus and propionibacterium, have a predilection for biofilm formation (after seroma or hematoma who can alter the surface properties of an implant thereby impacting the overall susceptibility of bacterial adherence) with some protection for microbial organisms against antibiotics, phagocytes, and other cellular and humoral immune responses by an altered phenotype with regard to growth rate and gene transcription (both of which can impact diagnostic and management strategies (2). granulomatous: mycobacterium tuberculosis (pott disease) (7)(12)(13) is more frequent in developing countries, accounting for 46% of cases. fungal among immunodeficient people: cryptococcus neoformans, candida spp. histoplasma capsulatum, coccidioides immitis, burkholderia pseudomallei (ie melioidosis) to 438 arsene anamaria-alexandra, iacob gabriel, alexandru vlad ciurea diabetics patients from northern australia and parts of southeast asia parasitic echinococcosis (12)(14) 1/3 of patients the implicated organism may not be isolated (1) in lumbar pod, infection extending to the adjacent disc and vertebra may generate extensive vertebral destruction, deformity, compromise stability, formation of paravertebral abscesses or may spread into the spinal canal causing epidural formation, neurological impairement with spinal cord or cauda equina compression, with high morbidity and mortality rates. there are three main ways of contamination (2) (12): iatrogenic by direct bacterial inoculation, direct open traumas of the spine responsible for 14% to 26% of spinal infections, by biofilm at the surface of the implants where certain bacteria can adhere with altered phenotype with regard to growth rate and gene transcription both of which can impact diagnostic and management strategies (2); hematological dissemination are the most common cause of spondylodiscitis and is mainly arterial, allowing bacteria from distant sites to contaminate the spine in the setting of bacteremia; non-hematological, extension from a contiguous infectious site. clinical pod diagnosis is based on: continuous, deepseated, throbbing low-back back pain the most common symptom (over 90% of patients), located at the site of infection, which worsened at night or gradually increased from mild pain to severe pain, associated with morning stiffness. pod pain appear early within 1-8 weeks of surgery, after an initial postsurgical relief of pain, aggravated by defecation, coughing, and sneezing, also at the slightest touch of the bed. pain is accompanied by severe paravertebral muscle spasm that radiates to the buttocks, thighs, groin, perineum or abdomen; fever (less common under 20% of patients, unreliable parameter, and often absent), fatigue, a general malaise may be seen in 11% 68% of cases. examination revealed severe restriction of movement, loss of lumbar lordosis, a positive pseudo-gower sign, radiculopathy, less common neurologic deficits, wound drainage is common, may be present in up to 90% of patients (1-3)(9). delayed lumbar pod relate to those infections occurring 3-9 months postoperatively (2), especially to those patients with spinal instrumentation typically present several months to years later with chronic pain increased pain at the incision site and tenderness to palpation of the soft tissue under the incision, wound drainage, implant failure, or lack of adequate spinal fusion. delayed infections are more often culture negative vs. early infections because as they are frequently caused by less virulent pathogens (e.g., propionibacterium acnes, coagulase negative staphylococcus epidermidis, bacillus, and micrococcus species), facultative anaerobe pathogens (2), favored by a postoperative sterile inflammatory processes who may create a favorable environment for the growth of low virulence organisms such as propionibacterium. biochemical markers used to diagnose pod are: tlc may be elevated, unsteady (9); esr normal at the time of admission (1)(7), is elevated during the first 2 weeks after lumbar discectomy (10) and slowly returns to baseline between 21-42 days; crp the most important, normal at the time of admission(1)(7), reaches its maximum on the second day after discectomy and returns to normal between within 6 days, if no complication occurs (4), has also high sensitivity compared to cultures if there is only one germ. an elevated crp after the first postoperative week thus indicates a bacterial infection, also higher postoperative crp levels are can be find after instrumented spinal surgery vs. simple decompressions (2). a high crp 2 weeks after surgery should make the neurosurgeon think (1)(3)(7)(16-18); blood culture positive in 17% of cases, in specimens from the intervertebral disc space at surgery and 12% showed a positive culture that came from the operation by microscope itself (6); blood investigations (blood glucose, serum albumin, liver, and renal function tests) (3)(8) aerobic, anaerobic, fungal and mycobacterial liquid and tissue samples, blood and urine cultures, as well as histology (14); biopsy, useful in the diagnosis of polymicrobial infections, if the blood cultures were negative; performed 48 hours after antibiotic treatment only if the patient is stable (6); 439 postoperative lumbar spondylodiscitis ctguided percutaneous biopsy for unidentified pod; technique of vortexing and sonification, followed by generally negative culturing scraped from the implant, in case of biofilm infection in pod with spinal instrumentation (2); neuroradiologic studies were done after hospitalization, before starting empirical treatment with antibiotics (3)(8) they relate to: x-rays performed in the anteroposterior and lateral incidence of the lumbosacral spine to observe in advanced cases, only after 2-4 weeks from the onset of the infection, to notice the extent of bone destruction, but also abnormalities of the infected spine: irregularity or ill definition of the vertebral endplates, cavitation, reduction of disc space, and instability in about 90% of cases, bony sclerosis may begin to appear in 10-12 weeks. in pyogenic pod, the first observation is narrowing of the disc space, followed by blurring and end-plate irregularity. in tb, the integrity of the disc is usually preserved, but after 8-12 weeks, significant bone destruction is evident. lumbar ct scan is more sensitive to plain film but are more sensitive to earlier changes: end-plate destruction, surrounding soft tissue swelling, intervertebral disc enhancement with contrast, collections (paraspinal, psoas muscle abscesses, even epidural abscesses), disc hypodensity. bone necrosis and pathological calcification that occurs in tb are detected. ct is most commonly used for guided biopsy or if mri is contraindicated. ctguided aspiration, was performed using a needle or trocar for microscopy, culture, and biopsy were performed to identify pathogens. the culture from a fine-needle aspiration was positive in 1 patient and negative in 5 (19). serial lumbar mri with gadolinium contrast enhancement, is the investigation of choice in lumbar pod, due to its very high sensitivity and specificity, also to evaluate the response to treatment (21). in the early stage of pod, mr imaging can not differentiate between the septic and aseptic forms (6), vertebral end-plate erosion is found in the majority of cases in both forms of discitis. pod that develops at a disc level with preoperative degenerative type 2 or 3 changes may give some diagnostic problems owing to its variations from typical mr findings (6). signal’s characteristics (1) include: on t1-weighted images irregular intensity with low signal in disc space, in adjacent endplates (bone marrow edema) and in (fluid) pyogenic infections; on t2 (fat saturated or stir especially useful): high signal in disc space (fluid), in adjacent endplates (bone marrow edema), in paravertebral soft tissues, in the psoas muscle (imaging psoas sign): this finding is ~92% sensitive and ~92% specific for spondylodiscitis (fig. 1) (fig. 2) . figure 1. imunocompromised patient with uncontrolled diabetes type 2. after 2 months post-fenestration at l4/l5 level presented with severe low back pain, elevated inflammatory markers. sagittal (a) and coronal mri t2-weighted (b) revealed massive height reduction of l5 vertebral body, edema and t2 hyperintensities at l4/l5 and l5/s1 along disc spaces and adjacent endplates suggestive for pod. note the epidural abcess at the same level (a). after contrast administration (gd) in t1: the enhancement of the disc, the narrowing of the disc space, the development of erosions in the vertebral endplates, peripheral enhancement around fluid collection(s), paravertebral soft tissues, around low-density center indicates abscess formation (hard to distinguish inflammatory phlegmon from abscess without contrast). on dwi sequences: hyperintense in the acute stage, hypointense in the chronic stage. 440 arsene anamaria-alexandra, iacob gabriel, alexandru vlad ciurea positive mr imaging and elevated crp should be followed by disc puncture and optimal antibiotic therapy. figure 2. 55 years old, man, known with a lumbar polidiscopathy and decompensated diabetes presents spastic paraparesis installed one week after lumbar paravertebral infiltrations. examination of lumbar spinal mri (t2-weighted sequences a in the sagittal plane, b and c in the axial plane, d in the coronary plane) revealed a t11-t12 pod, spinal epidural abscess of the posterior vertebral body t11. operated in an emergency, the dural sac and the t11-t12 disc space are decompressed, isolating staphylococcus aureus mrsa +, 1 month postop. the motor deficit remits. if the bacteriological culture is negative, it is appropriate to choose antibiotics against s. aureus, the most frequent cause of pod (21). in the absence of signal increase on t2-weighted images and undetectable or low improvement after the introduction of the contrast substance a fungal infection should be considered, also a diffuse vertebral infection with brucella may be difficult to differentiate with tb (21). in the absence of specific mri characteristics, insignificant values of esr and crp, it suggests a non-infectious aseptic etiology or a malignant tumour, in such case a biopsy is used. the intranuclear cleft sign described by aguila (20), cited by (6) is not relevant indicator for pod (linear enhancement within the disc, seen as two thin bands parallelling the end-plates) appears in 20% of patients without post-operative complications at 3 months after lumbar discectomy, the annular enhancement in the most posterior aspect of the disc at the site of surgical curettage is a normal postoperative finding. if mri is inconclusive or contraindicated, threephase bone scintigraphy with technetium-99m, gallium-67 (2), scintigraphy with single-photon emission ct (spect) and fluorine-18 fluorodeoxyglucose positron (f-18-fdg pet) can be used, which has higher accuracy in pod, but is not widespread (14). if mri is contraindicated or hampered by artifact, dual imaging with pet/ct could become the imaging modality of choice; also promising results in pilot studies/small series has shown non-fdg pet/ct with ga-68 citrate (24). labeled leukocyte imaging less sensitive for processes in which the predominant cellular response is not neutrophilic (e.g., tuberculosis) (2). pod treatment means antibiotics after biopsy, depending on the pathogen involved, cultures, sensitivities; also strict bed rest, nutritional diet, analgetics, orthosis, physiotherapy, reducing the mobility of the affected region, either with a back brace or a plaster cast, recommended about two weeks until the acute pain subsides. many studies have shown that long-term conservative treatment has a success rate of 70% -83% (3)(4)(9)(21-23). antistaphylococcal penicillin or a first-generation cephalosporin is the best choice in the treatment of methicillin-sensitive staphylococci infection. if the germs staphylococcus epidermidis are resistant to methicillin, vancomycin is administered and alternatively linezolid and quinupristin-dalfopristin. penicillin g is of choice in the treatment of infections with streptococcus spp., cephalosporin or a quinolone is administered for gram-negative bacteria and metronidazole or clindamycin is given in cases with anaerobes. the classic regimen in tb includes isoniazid, rifampicin, ethambutol and pyrazinamide because it has a higher resistance. amoxicillin and streptomycin or gentamicin are useful in brucella infection, and amphotericin b or 441 postoperative lumbar spondylodiscitis azole are needed in fungal osteodiscitis (14). if the patient is not stable, antibiotic treatment is performed and the biopsy should be performed approximately 48 hours after the most recent dose of antibiotic (12)(14)(25). the duration of antibiotic therapy varies from case to case, mean time 6-8 weeks of intravenous therapy, others propose 6-8 weeks of intravenous antibiotics followed by 2 months or more of oral therapy, depending on clinical and laboratory responses, up to a year, depending on the complexity of the infection, its resistance to antibiotics, to prevent recurrence and to allow complete healing of pod, especially in immunocompromised patients (3)(12)(14). in cases where treatment begins within 2 weeks of the onset of symptoms, 6 weeks of treatment is considered sufficient. if treatment is delayed 6-7 weeks after the onset of symptoms, then antibiotic therapy for 4-8 weeks is associated with an increased recurrence rate compared to treatment for 12 weeks or more (35)(7)(24). failure of medical treatment should be considered in patients with prolonged back pain, increased inflammatory markers after treatment, important destruction of the vertebral body, damage to the nerve root, progressive kyphosis. it is to avoid prolonged rest leading to skin ulcers, colitis, kidney failure, allergic reactions, deep vein thrombosis, pulmonary embolism, pneumonia, pseudoarthrosis, instability with spinal deformities, chronic pain back, also unwanted psychosocial aspects (11). some authors argue that early surgical debridement, followed by antibiotics, is superior to conservative antibiotic-only treatment. in cases where treatment begins within 2 weeks of the onset of symptoms, 6 weeks of treatment is considered sufficient. if treatment is delayed 6-7 weeks after the onset of symptoms, then antibiotic therapy for 4-8 weeks is associated with an increased recurrence rate compared to treatment for 12 weeks or more (35)(7)(24). surgery is performed to patients with conservative treatment failure resistant to antibiotic therapy, as those with neurological complications: acute paraplegia, pain resistance to analgetics, acute sepsis, anterior abscess larger than 2.5 cm on lumbar mri and epidural abcesses, spinal instability, severe kyphosis. lumbar pod are positively associated with extended hospitalizations, increased morbidity and healthcare costs, poorer long-term outcomes, and greater dissatisfaction with the initial operative procedure (2); for these reasons early surgery permit rapid pain relief, infection control before extensive destruction of the vertebrae, spinal instability and kyphotic deformity appear (3-8)(13)(21-24). especially in piogenic pod exploration by a posterior approach, debridement of all inflammatory tissues, the epidural abscesses are evacuated, the disc space should be irrigated with gentamicin mixed with normal saline (0.9% nacl), betadine irrigation, dispersing powdered vancomycin into the wound just prior to closure (2), followed by interbody fusion with titanium banana cage, autogenous spongy bone grafts or posterolateral fusion by graft bone, posterior instrumentation antimicrobial coated implants, with pedicle screws and rods, vertebral bodies were included above and below the affected segment, then perioperative smears and tissue samples were taken for histological and microbiological evaluation. (3) instrumentation of the spine has a higher success rate after complete debridement and concomitant antibiotic therapy (12). after surgery, patients received 2-3 weeks of broad-spectrum intravenous antibiotics consisting of ceftriaxone/meropenem with flucloxacillin for grampositive and gram-negative organisms and metronidazole for anaerobic coverage.the dose and duration of treatment were based on the patient's weight, kidney, and liver condition, followed by 3 weeks of oral antibiotics or until esr and crp levels improved or back pain decreased significantly (3)(8). pod surgical treatment offer more patient satisfaction because the duration of healing and the administration of antibiotics was shorter than in the case of those treated conservatively, but it can also be risky because there are cases of postoperative recurrence of the infection. the duration of the procedure, which lasts more than five hours, the attempt of a minimally invasive intervention, a more aggressive operation, delayed or incomplete debridement, diabetes, smoking, the advanced age of the patients led to serious postoperative complications (3)(8)(12). surgery at l4 / l5 and l5 / s1 by anterior approach are quite difficult, morbidity being increased and therefore pod was operated by posterior approach. even if there is an active infection, instrumentation after radical debridement will not lead to an increased risk of recurrent infection, as it speeds up the healing process. percutaneous transpediculary discectomy and drainage lead to rapid pain relief (3)(8)(10). 442 arsene anamaria-alexandra, iacob gabriel, alexandru vlad ciurea however, in lumbar pod suited by prosthesesbased biofilm, especially most infectious disease physicians now recommend removal of the underlying spinal instrumentation (2), increasing the chance of eradicating the infection. nevertheless, this potential advantage must be weighed against the risks of prematurely removing spinal instrumentation, essential for maintaining normal spinal alignment and preserving spinal stability. conclusions the diagnosis of lumbar pod is based on history and physical examination, biochemical markers, neuroradiologic studies, using appropriate mri imaging. most cases of lumbar pod can be managed by conservative treatment with antibiotics after causative germ isolation and antibiogram. surgery is performed to patients with conservative treatment failure resistant to antibiotic therapy, as those with neurological complications: acute paraplegia, pain resistance to analgetics, acute sepsis, abscesses, spinal instability, severe kyphosis. early surgery with wound irrigation/debridement are more readily able to disrupt biofilm formation and facilitate penetration of systemic antimicrobials to allow for resolution of the infection, vacuum-assisted closure facilitates wound healing and eradicates spinal infections, decrease the rate of complications, permit rapid pain relief, while preserving the instrumentation/stability, better clinical outcomes, infection control before extensive destruction of the vertebrae, spinal instability and kyphotic deformity appear. instrumentation can usually be preserved in patients with early infections (e.g., <6 weeks), but instrumentation removal should be considered for infections presenting in a delayed fashion (e.g., >6 weeks to even years) psii. patients should be adequately followed for one postoperative year, to ensure that the infection has been fully eradicated. implant sonication provides cultures for direct identification of active and/or persistent biofilm, while the introduction of enzymes that dissolve the biofilm matrix (e.g., dnase and alginate lyase) and quorum-sensing inhibitors that increase biofilm susceptibility to antibiotics may further help manage postoperative infection (2) (27-31). abbreviations pod postoperative discitis om ostemyelitis od osteofyscitis sd spondylodiscitis od vertebral osteomyelitis ssis surgical site infections ivdu intravenous drug users asa american society of anesthesiology score icu intensive care unit tlc total leukocyte count crp c reactive protein esr erhrytrocites sedimentation rate ct tomograph computer mri magnetic nuclear resonance psii postoperative spinal implant infections conflicts of interest there are no conflicts of interest. authors contributions all authors contributed equally. references 1. knipe h. spondylodiscitis radiopaedia, 2021, sept 15. 2. kasliwal m.k., tan l.a. et al. infection with spinal instrumentation: review of pathogenesis, diagnosis, prevention, and management, surg neurol int. 2013; 4(suppl 5): s392–s403. 3. ahsan k., hasan s., et al. conservative versus operative management of postoperative lumbar discitis. journal of craniovertebral junction & spine, 2020, 11(3): 198-209. 4. cornett c. a., vincent s. a. , et al. bacterial spine infections in adults: evaluation and management. journal of the american academy orthopaedic surgeons. 2016; 24(1):11-18. 5. gerometta a., bitan f., et al. postoperative spondilodiscitis. internațional orthopaedics. 2012; 36:433-438.1. 6. grane p., josephsson a., et al. septic and aseptic postoperative discitis in the lumbar spine evaluation by mr imaging. acta radiologica.1998; 39(2):108-115. 7. herren c., jung n., et al. spondylodiscitis: diagnosis and treatment options. deutsches ärzteblatt international. 2017; 114 (51-52): 875-882. 8. jain m., sahu r. n., et al. postoperative lumbar pyogenic spondylodiscitis: an institutional review. journal of neurosciences în rural practice. 2019; 10(3): 511-518. 9. basu s., ghosh j.d.,et al. postoperative discitis following single-level lumbar discectomy: our experience of 17 cases, indian j orthop. 2012; 46(4): 427–433. 10. schinkel c., gottwald m., et al. surgical tratament of spondylodiscitis. surgical infections. 2003, vol. 4, no. 4. 11. singh d. k., singh n., et al. management of postoperative discitis: review of 31 patients, asian journal of neurosurgery 2018; 13(3): 703-706. 12. hera b., sanchez-mariscal f., et al. deep surgical site infection following thoraco-lumbar instrumented spinal surgery. ten years of experience. revista espan᷉ola de cirugίa ortopédica y traumatologίa. 2019; b63(4):b300306. 13. landi a., grasso g., spontaneous spinal discitis and 443 postoperative lumbar spondylodiscitis spondylodiscitis: clinicotherapeutic remarks, journal of neurosciences in rural practice, 2017; 8(4): 642-646. 14. mavrogenis a.f., megaloikonomos p.d. et al. spondylodiscitis revisited, efort open rev. 2017 nov; 2(11): 447– 461. 15. jeong sj, choi sw, youm jy, et al. microbiology and epidemiology of infectious spinal disease. j korean neurosurg soc 2014;56:21-27. 16. yaldiz c., özdemir n., et al. a retrospective study of 39 patients treated with anterior aproach of thoracic and lumbar spondylodiscitis, medicine (baltimore), 2015; 94(47): e2110. 17. nam h. k., song g. s., et al. diagnostic value of biopsy techniques în lumbar spondylodiscitis: percutaneous needle biopsy and open biopsy. korean journal of spine. 2011; 8(4): 267-271. 18. rufener j., schulze c.c. et al. – sterile spondylodiscitis, the lacet 2012, vol. 379., nr. 9828, 1763-1850, may 12, e50-e51. 19. tronnier v., schneider r., et al. postoperative spondylodiscitis: results of a prospective study about the aetiology of spondylodiscitis after operation for lumbar disc herniation, acta neurochir (wien) 1992;117(3-4):149152. 20. aguila l.a., piraino d.w, et al. – the intranuclear cleft of the intervertebral disk: magnetic resonance imaging, radiology 1985;155(1):155-158. 21. katsevman g. a., emery e., et al. secondary discitis masquerading as treatment failure of primary discitis: case report and review of the literature.international journal of spine surgery 2019;13(2): 120-124. 22. kapsalaki e., gatselis n., spontaneous spondylodiscitis: presentation, risk factors, diagnosis, management, and outcome. internațional journal of infectious diseases. 2009; 13(5):564-569. 23. lazzarini l., lipsky b.a., et al. antibiotic treatment of osteomyelitis: what have we learned from 30 years of clinical trials?, international journal of infectious diseases, 2005; 9, 127-138. 24. muscara j. d., blazar e. diskitis. statpearls – ncbi bookshelf. 2020.update 2021 apr 30. in: stat pearls [internet].treasure island (fl): statpearls publishing; 2021. 25. nam h. k., song g. s., et al. diagnostic value of biopsy techniques în lumbar spondylodiscitis: percutaneous needle biopsy and open biopsy. korean journal of spine. 2011; 8(4): 267-271. 26. yaldiz c., özdemir n., et al. a retrospective study of 39 patients treated with anterior aproach of thoracic and lumbar spondylodiscitis, medicine (baltimore), 2015; 94(47): e2110. 27. ahmed r, greenlee jd, et. al. preservation of spinal instrumentation after development of postoperative bacterial infections in patients undergoing spinal arthrodesis. j spinal disord tech. 2012; 25:299–302. 28. mok jm, guillaume tj, et al. clinical outcome of deep wound infection after instrumented posterior spinal fusion: a matched cohort analysis. spine (phila pa 1976) 2009;34:578–583. 29. rayes m, colen cb, et al. safety of instrumentation in patients with spinal infection. j neurosurg spine. 2010; 12:647–659. 30. van rhee ma, de klerk lw, et al. vacuum-assisted wound closure of deep infections after instrumented spinal fusion in six children with neuromuscular scoliosis. spine j. 2007; 7:596–600. 31. prinz v., vajkoczy p. surgical revision strategies for postoperative spinal implant infections (psii), j spine surg. 2020; 6(4):777-784. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-008 puncture site bleeding complications in patients with clopidogrel hyper-response. three case reports nedeljković žarko, vukasinović ivan, majstorović branisalva, milosević medenica svetlana, milićević mihailo, ilić rosanda, aleksić vuk, paunović aleksandra, stanimirovic aleksandar, scepanović vuk, milić marina, todorović marko, milisavljević filip, grujič ić danica romanian neurosurgery (2020) xxxiv (1): pp. 58-65 doi: 10.33962/roneuro-2020-008 www.journals.lapub.co.uk/index.php/roneurosurgery puncture site bleeding complications in patients with clopidogrel hyperresponse. three case reports nedeljković žarko1, vukasinović ivan2, majstorović branisalva3, milosević medenica svetlana2, milićević mihailo1, ilić rosanda1, aleksić vuk1, paunović aleksandra1, stanimirovic aleksandar1, scepanović vuk1, milić marina1, todorović marko1, milisavljević filip1, grujičić danica1 1 clinic for neurosurgery, clinical center of serbia 2 center for radiology and magnetic resonance, clinical center of serbia 3 center for anesthesiology, clinical center of serbia abstract dual antiplatelet therapy (clopidogrel and acetylsalicylic acid) is a standard for the embolization of planned intracranial aneurysms with cns stent due to the possibility of stent thrombus formation. all anti-aggregation drugs, including those listed, have bleeding as a side effect. three patients with aneurysm had an elevated response to antiplatelet therapy with clopidogrel, which was confirmed by a multiplate test on the "verifynow" system. after reducing the dose of clopidogrel or after interrupting it, with the introduction of low molecular weight heparin for the duration of five days, aneurysms were successfully resolved by intracranial implantation of the stent. perioperative angiograms and postoperative ct angiograms have verified hematomas at the place of punction of the femoral artery. bleeding was resolved by the femoral artery suture by a vascular surgeon. all patients were discharged home without further complications and with dual antiplatelet therapy. by measuring the platelet function in vitro, the degree of inhibition of platelet activity achieved by the action of the drug can be assessed. a specific test can identify those patients who are highly responsive to the drug with increased platelet reactivity and the possibility of increased risk of bleeding. our suggestion is to reduce the dosage of clopidogrel or to leave it out for 24 hours with preventive doses of low molecular weight heparin or to change the strategy of treatment of intracranial aneurysm, i.e. avoiding implantation of cns stent. introduction according to statistics, about 5% of the population has intracranial aneurysm, out of which 1 to 2% suffer from aneurysm rupture with a dramatic clinical manifestations and consequences [1,2,3].today, it is keywords intracranial aneurysms, dual antiplatelet therapy, clopidogrel hyper-response corresponding author: vuk aleksic clinic for neurosurgery, clinical center of serbia aleksicvuk@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 59 puncture site bleeding complications in patients with clopidogrel hyper-response believed that endovascular treatment is a better, more modern and less aggressive treatment associated with less complications and lower mortality, shorter length of hospital stay and lower costs of treatment compared to conventional neurosurgical treatment, i.e. microsurgical clipping of aneurysms [4,5,6,7,8]. the current standard of preoperative preparation for stent placement in aneurysms involves dual antiplatelet therapy with acetylsalicylic acid and clopidogrel.antiplatelet drugs inhibit platelet aggregation and thus stop the formation of thrombus. thrombus formation is a complex mechanism of responses to vascular changes, injuries, atherosclerosis and other diseases.the data indicate that in addition to the effect of these drugs, other local and systemic factors (diabetes mellitus, left ventricular hypertrophy, atrial fibrillation) may be the cause of unwanted ischemic events [9,10]. other antiplatelet drugs: prasugrel, dipyridamole, cilostazol, cangrelor and ticagrelor have not been analyzed so far, andtherefore are the subject of recent researches that are yet to define the benefits of their application in therapy. case 1 pre-procedural angiograms showed the condition of 59-year-old patient, after the coiling of aci aneurysms on both sides. from the medical documentation, it is learned that the patient's embolization of aneurysms was done on both internal carotid arteries in 2016. hematological parameters on admision: rbc 4,75x10 12 /l, hgb 138 g/l, hct 0,45 l/l. due to the impaction of the coilling to the right internal carotid artery, placement of the stent was planned, therefore, three days before the intervention, the patient was administered clopidogrel75 mg twice daily and acetylsalicylic acid 100 mg once a day. drug-resistence testing on the „verifynow” device showed an increased sensitivity of platelet activity to the action of clopidogrel. clopidogrel was discontinued for fivedays and acetylsalicylic acid was continued. during this period, a low molecular weight heparin is administered at a dose of 0,3 ml twice a day, and then it was proceeded to the procedure. by accessing the left femoral artery, the flow diverting silc 3x20mm stent is placed over the aneurysm`s neck on the right internal carotid artery, which causes the pathway obstruction of the contrast agent in aneurysm. during puncture there was perforation of the left femoral artery and extravasation of the contrast medium with the expansion pathway caudally. the intervention was interrupted, the puncture site waspressed with longterm compression in groin. the patient complained of pain in the left side of abdomen. physical examination found palpatory pain sensation of the abdomen and drop in blood pressure.ct angiography of the leg and abdomen showed the extravasation of the contrast agent at the level of the left femoral artery with expansion towards the retroperitoneum.[figure 1, figure 2]. figure 1. angiographic presentation of aneurysms and ct angiographic exploration of bleeding at the puncture site. figure 2. angiographic presentation of aneurysms and ct angiographic exploration of bleeding at the puncture site. 60 nedeljković žarko, vukasinović ivan, majstorović branisalva et al. the vascular surgeon was called for consultation. the patient was transferred and operated in the clinic for vascular and endovascular surgery of clincal center of serbia where hematoma was evacuated and suture of left femoral artery was performed. hematological parameters two days after femoral artery puncture: rbc 2,56x10 12 /l, hgb 80 g/l, hct 0,25 l/l. in the postoperative course, the patient received fraxiparine at a dose of 0,3 ml twice daily for the next eight days. after leaving the hospital, dual antiplatelet therapy (clopidogrel and acetylsalicylic acid) was continued for the next three months once a day, followed by acetylsalicylic acid onwards. case 2 a 45-year-old female patient was previously planned for the placementof an intracranial stent due to an aneurysm on anterior communicating artery. she was taking clopidogrel 75 mg twice a day and acetylsalicylic acid 100 mg once a day for three days. hematological parameters on admision: rbc 4,13x10 12 /l, hgb 128 g/l, hct 0,409 l/l. drugresistence testing on the „verifynow” device showed an increased sensitivity of platelets to the action of clopidogrel. administration of clopidogrel was stopped for the next five days, it was continued with the administration of acetylsalicylic acid 100 mg once a day. also, 0,3 ml of fraxiparin was administered twice a day, and then it was proceeded with procedure. through the right femoral artery, the guiding catheter was placed in the left internal carotid artery, the microcatheter was positioned in the aneurysm which was excluded from the circulation by placing the coil. as aneurysm was resolved by a coil, the dual antiaggregation therapy was interrupted in the postoperative course. in the early postprocedural period, hematoma formation in the groin region occured, and therefore changes in the complete blood count: rbc2,87x1012 /l, hgb 91 g/l, hct 0,264 l/l. the patient complained of pain in the lower right quadrant of the abdomen in the area above the right inguinal ligament. a vascular surgeon was consulted, after which a patient was admitted to the clinic for vascular and endovascular surgeryof clinical center of serbia. ct angiography of the leg and abdomen was performed, which showed the presence of a lesion in the area of the transition of the external iliac to the right common femoral artery with extravasation of contrast.[figure3, figure4, figure5] due to active retroperitoneal bleeding, conciliar decision was to undergo emergency surgical treatment. the patient was postoperative hemodynamically stable with palpable pedal pulses. figure 3. ct angiography of the leg and abdomen showing the presence of a lesion in the area of the transition of the external iliac to the right common femoral artery with extravasation of contrast. figure 4. ct angiography of the leg and abdomen showing the presence of a lesion in the area of the transition of the external iliac to the right common femoral artery with extravasation of contrast. figure 5. ct angiography of the leg and abdomen showing the presence of a lesion in the area of the transition of the external 61 puncture site bleeding complications in patients with clopidogrel hyper-response iliac to the right common femoral artery with extravasation of contrast. case 3 a 47-year-old female patient was admitted to perform an endovascular treatment due to the presence of aneurysm on the supraclinoid segment of the left internal carotid artery, which was randomly detected as part of the examination of pituitary microadenoma. the width of aneurysm neck was 6,5 mm. the patient was planned for placing of the flow diverting stent over the aneurysm neck. in the preprocedural period, the patient received dual antiplatelet therapy (clopidogrel 75 mg twice a day and acetylsalicylic acid 100 mg once a day) for three days. drug-resistence testing on the „verifynow” device showed an increased platelet sensitivity to clopidogrel. an aneurysm embolization was attempted on two occasions. during the second intervention, placement of microcatheter was attempted distal from the aneurysm neck in order to place a "flow-diverting" stent, which failed even after several attempts, and as a result, the procedure was interrupted. in the early postprocedural course, the condition of the patient worsened in terms of confusion, paleness, hypotension, and the presence of a larger subcutaneous hematoma in the right groin. ct angiography of the leg and abdomen was performed, which showed extravasation of contrast at the puncture site [figure 6, figure 7, figure 8,figure 9, figure 10]. the patient was transferred to the clinic for vascular and endovascular surgery of clinical center of serbia where the suture of right external iliac artery and evacuation of hematoma were performed. during the third hospitalization, the patient was again prepared for stent placement with dual antiplatelet therapy, and the response to clopidogrel was again too strong. this time, it was also attempted to place the stent through the aneurysm neck, but while the microwirewas passing, further distal from the branch of the left middle cerebral artery, extravasation of contrast occured. protamine sulfate was administered by venous route, which is an antidote for intravenous administration of heparin and the contrast extravasation was no longer shown. it was attempted again to go through with a microcateter distally from the neck of aneurysm, but even after additional attempts, it failed due to extremely unfavorable angioarchitecture.subsequently, the microcatheter was used to access the fundus of aneurysm and to place the "pconus" stent, and then, after placement of several coils, aneurysm was excluded from the circulation with less residual filling and preserved passage of all blood vessels. postprocedurally, the patient was somnolent, slowed down, intubated andwith progressive deterioration of consciousness. there was an acute hydrocephalus occurrence that was taken cared by the external drainage of the cerebrospinal fluid [figure10]. on this occasion, a subdural hematoma was formed, which gradually spontaneously absorbed. ten days after embolization, a permanent drainage system, ventriculoperitoneal shunt, was placed. it was continued with the administration of clopidogrel 75mg and acetylsalicylic acid 100mg once a day for three months, and then only acetylsalicylic acid 100mg going forward. there has been a recovery in the general and neurological condition of the patient with a residual right-sided weakness [figure 11]. figure 6. ct angiography of lower extremities et pelvis showing extravasation of contrast at the puncture site. figure 7. ct angiography of lower extremities et pelvis showing extravasation of contrast at the puncture site. 62 nedeljković žarko, vukasinović ivan, majstorović branisalva et al. figure 8. ct angiography of lower extremities et pelvis showing extravasation of contrast at the puncture site. figure 9. ct angiography of lower extremities et pelvis showing extravasation of contrast at the puncture site. figure 10. head ct scan showing the occurance of acute hydrocephalus. figure 11. control head ct scan 1 month after the embolisation of aneurysm and vp shunt placement. discussion neuroradiological procedures, such as embolization of intracranial aneurysms, have been routinely applied since their implementation in 1990 to the present day. they are performed in general anesthesia for better control of pain and immobility of patients, control of local blood flow at the site of vascular changes via mean arterial pressure, with the use of a continuous or bolus dose of heparin by the venous line. dual antiplatelet therapy is used pre and post-procedually in cases of stent implatantion.in principle, anticoagulant or antiplatelet therapy is widely used in various areas of medicine to prevent the development of occlusive thrombosis. when it comes to drugs, the prevention is achieved by changing the coagulation of the blood. coagulation of the blood, composed of a series of proteolytic reactions, is a complex cascade processof which the ultimate result is the creation of insoluble fibrin. the platelet function is regulated by three types of compounds. the first group consists of compounds that are formed outside of the platelet and act on receptors located on the platelet membrane: catecholamines, collagen, thrombin, prostacyclin. the second group of compounds consists of compounds that form in the platelet itself but act on membrane receptors: adp, prostaglandins d2 and e2, and serotonin. the third group of compounds are produced byplatelet, but they act in the platelet itself: thromboxane a2, cyclic amp and gmp. in clinical practice, acetylsalicylic acid and clopidogrel are generally available. because of the high resistance to clopidogrel antiplatelet activity 63 puncture site bleeding complications in patients with clopidogrel hyper-response (16%) measured by the same in vitro platelet function tests, a full range of drugs is available. current studies evaluate the efficacy of p2y12 receptor inhibitors: prasugrel, ticagrelor, cangrelor, elinogrel; then prothrombin antagonists, glycoprotein inhibitors, phosphodiesterases, and others. a response to antiplatelet therapy with clopidogrel confirmed by drug-resistence testing on the „verifynow” device. verifynow system (accumetrics inc., san diego, california, usa) monitors the platelet aggregation by agglutination of human-fibrinogen-coated granules, which is triggered by activated platelets stimulated by agonists in citrate full blood. this system measures induced platelet aggregation by adp and prostaglandin e1, following an increase in light transmission (p2y12) test. it uses an iso-thrombin receptor activating peptide (iso-trap) that activates platelets regardless of the action of clopidogrel. the results are expressed in the pru (platelet reactivity unit) units showing the degree of aggregation mediated by p2y12 receptors. [11,12,13] acetylsalicylic acid irreversibly inhibits the cox-1 enzyme, then the synthesis of cyclic endoperoxides and all prostaglandins that result therefrom. the cox-1 inhibition inhibits the synthesis of thromboxane, and then prostacyclin and prostaglandin e2. due to irreversible enzyme inhibition, once daily dosing of the drug is sufficient. there are data indicating that at low doses of 100 mg per day, the biosynthesis of thromboxane can be selectively inhibited without any influence on prostacyclyin synthesis. as a result, small doses of acetylsalicylic acid restrict the therapeutic effect of prostaglandins that have a significant role in a large number of physiological and pathophysiological processes in the body (regulation of arterial blood pressure, renal function or interaction with antihypertensive effect of diuretic, and angiotensinconverting enzyme, etc.) [14,15,16] simultaneous administration of analgesic drugs from a group of non-selective cox1 inhibitors, such as ibuprofen and naproxen, can lead to a reduction in acetylsalicylic acid by competing for the same receptor [17,18] in the preoperative and postoperative period. clopidogrel is a drug whose metabolite is a platelet aggregation inhibitor. to switch to an active metabolite that inhibits platelet aggregation, clopidogrel is metabolized by the cyp450 enzyme. the active metabolite of clopidogrel selectively inhibits adenosine-diphosphate adhesion (adp) for its p2y12 receptors on platelets and in this way, via adp-mediated activation of the iib/iiia glycoprotein complex, inhibits platelet aggregation. adp binds to delta granulomas in platelets. adp achieves its effect by binding to its platelet receptors and leads to: inhibition of adenylate cyclase by stimulating gi protein and decreasing the concentration of intracellular camp, the formation of inositol triphosphate (ip3) leading to the mobilization of calcium from cell depots, the release of arachidonic acid leading to the creation of txa2 and activation phospholipase a2. it is believed that adp exhibits its effect by binding to three purinergic receptors: p2y1, p2y12, and p2x1. it is believed that p2y12 plays a key role in the pathogenesis of arterial thrombus, mediating in adp-induced platelet aggregation, potentiating the secretion of granules under the action of agonists and potentiating the inhibition of the antithrombotic effect of natural regulators of the platelet function, prostacyclin. p2y12 is associated with gi2 protein whose stimulation leads to the inhibition of adenylate cyclase and the activation of phosphatidylinositol 3 kinase (pi3k). since this receptor is considered to have a central role in the formation of a coagulum, it is a target molecule for antithrombotic therapy. due to irreversible binding, the effect of inhibition on the affected platelets lasts for the entire duration of their plasma life (about 710 days), and re-establishment of platelet function occurs after plasma exchange time [19]. this drug was approved in 1997 and after showing similar antithrombotic efficacy, but also as a significantly safer medication for patients, it completely replaced ticlopidine. for those patients with a history of stroke, it is known that antithrombotic therapy reduces incidence of re-ischemic events up to 22%. clopidogrel proved superior to aspirin in reducing risk and was recommended for secondary prevention of stroke. due to irreversible inhibition of p2y12 receptor, the effect of clopidogrel is present during the life of platelets (7-10 days). cell recovery is expected in the period of 3 to 5 days, that is, the platelets are fully functional on average for 7 days after taking the last dose of the drug. the maximum inhibition of the p2y12 receptor was achieved after 4-5 days of daily administration of 75 mg of clopidogrel. this interval 64 nedeljković žarko, vukasinović ivan, majstorović branisalva et al. can be reduced to 3-5 hours by taking aloading dose of 300-600mg. thus, in addition to the proven antithrombotic effect, clopidogrel has its disadvantages: its antithrombotic effect is delayed due to the necessary metabolism and activation of the prolapse, as well as interindividual variability in the therapeutic response to the drug. the cyp enzyme system is responsible for 40-80% metabolism of almost all drugs in the active metabolite. since clopidogrel and lipophilic statins are metabolised via the cyp3a4/3a5 enzyme system, the inhibition of the formation of the active metabolite of clopidogrel and unwanted thrombosis can occur [14,15]. observations and randomized clinical studies have shown that the concomitant use of clopidogrel and proton pump inhibitors for preoperative purposes, and due to gastric irritation, can lead to a reduction in the anti-aggregation effect and an increase in the number of repeated thromboses or ischemic events [20]. dual anti-aggregation therapy is used to prevent the formation of thrombus or stent thrombosis. however, antiaggregation drugs can cause bleeding as an adverse drug reaction [21,22]. in the literature there are few studies that investigate increased sensitivity of platelets to the action of clopidogrel as opposed to postprocedural bleeding aneurysms [23]. for this reason, we listed 3 clinical cases with various causes of bleeding at the puncture site. we believe that preprocedural management procedures should be acceptable in order to solve the resulting complication and complete the procedure. we summarized the mechanism of action, the current clinical assessment, and the standards for the use of antiagregating drugs in the pre-procedural, procedural and postprocedural period for the treatment of unruptured aneurysms. n sex age aneurysm n1 f 59 aci bill. n2 f 45 acoa n3 f 47 aci l.sin. table 1. anthropological characteristics of the patients. n clopidogrel bleeding<95208<thrombosis acetylsalicylic acidbleeding<350549<thrombosis n1 3 359 n2 39 525 n3 14 370 table 2. results of the resistance test for clopidogrel and acetylsalicylic acid. references 1. samardžić m, grujičić d, prstojević b. spontanaintrakranijalnakrvarenja, u: samardžić m, ur. hitnastanja u neurohirurgiji. beograd, i.p. obeležja;2010. 2. maud a, lakshminarayan k, suri mf, vazguez g, lanzino g, qureshi a. cost-effectiveness analysis of endovascular versus neurosurgical treatment for ruptured intracranial aneurysms in the united states. j neurosurg 2009;110(5):880 – 6. 3. greving jp, rinkel gj, buskens e, algra a. costeffectiveness of preventive treatment of intracranial aneurysms: new data and uncertainties. neurology 2009;73(4):258 – 65. 4. wolstenholme j, rivero-arias o, gray a. treatmant pathways, resource use, and cost of endovascular coiling versus surgical clipping after sah. stroke 2008;39:111 – 9. 5. higashida rt, lahue bj, torbey mt, hopkings ln, leip e, hanley df. treatment of unruptured intracranial aneurysms: a nationwide assessment of effectiveness. ajnr am j neuroradiol 2007;28(1):146 – 51. 6. varma mk, price k, jayakrishnan v, manickam b, kessell g. anaesthetic considerations for interventational neuroradiology. bja 2007;99(1):75 – 85. 7. labalette c, houdart e, david s. embolization of intracranial aneurysms: reimbursement and perspectives. j radiol 2010;91:895 – 900. 8. majstorović bm, milošević-medenica sb, milakovićbd,naumović ts. new interventional neuroradiological procedures in serbia – the direct costs of classical neurosurgical intervention in relation to the endovascular treatment of intracranial aneurysms. hospital pharmacology. 2015;2(2):272-278. 9. jenningslk.role of platelets in atherothrombosis. am j cardiol2009;103:4a–10a. 10. bhatt dl. role of antiplatelet therapy across the spectrum of patients with coronary artery disease. am j cardiol 2009;103:11a–9a. 11. prinz v, finger t, bayerl s, rosenthal c, wolf s, liman t, vajkoczyp.high prevalence of pharmacologically induced platelet dysfunction in the acute setting of brain injury. acta neurochir (wien) 2016;158(1):117-23. 12. flechtenmacher n, kämmerer f, dittmer r, budde u, michels p, röther j, eckert b. clopidogrel resistance in neurovascular stenting: correlations between light transmission aggregometry, verifynow, and the multiplate. ajnr am j neuroradiol. 2015;36(10):1953-8. 13. jastrzębska m, chełstowski k, wódecka a, siennicka a, clark j, nowackip.factorsinfluencingmultiplate whole blood impedance platelet aggregometry measurements, 65 puncture site bleeding complications in patients with clopidogrel hyper-response during aspirin treatment in acute ischemic stroke: a pilot study. bloodcoagul fibrinolysis 2013;24(8):830-8 14. hall r, mazer cd. antiplatelet drugs: a review of their pharmacology and management in the perioperative period.anesthanalg 2011;112(2):292-318. 15. benedek ih, joshi as, pieniaszek hj, king sy, kornhauser dm. variability in the pharmacokinetics and pharmacodynamics of low dose aspirin in healthy male volunteers. j clinpharmacol 1995;35:1181–6. 16. teo kk, yusuf s, pfeffer m, torp-pedersen c, kober l, hall a, pogue j, latini r, collins r; ace inhibitors collaborative group. effects of long-term treatment with angiotensinconverting-enzyme inhibitors in the presence or absence of aspirin: a systematic review. lancet. 2002;360(9339):1037-43. 17. václavík j, táborským. antiplatelet therapy in the perioperative period. eur j intern med. 2011 feb;22(1):2631. 18. catella-lawson f, reillymp, kapoor sc, cucchiara aj, demarco s, tournier b et al. cyclooxygenase inhibitors and the antiplatelet effects of aspirin. n engl j med 2001;345:1809-15. 19. matula jm, lesiak m, michalak m, kowal j, mączyński m, siniawski a, mularek-kubzdela t, wiśniewski s, grajek s. association between high on-treatment platelet reactivity and occurrence of cerebral ischemic events in patients undergoing percutaneous coronary intervention. thromb res. 2016;138:49-54. 20. saw j, brennan dm, steinhubl sr, bhatt dl, mak kh, fox k. lack of evidence of a clopidogrel-statin interaction in the charisma trial. j am coll cardiol 2007;50:291–5. 21. trenk d, hochholzer w, frundi d, stratz c, valina cm et al. impact of cytochrome p450 3a4-metabolized statins on the antiplatelet effect of a 600-mg loading dose clopidogrel and on clinical outcome in patients undergoing elective coronary stent placement. thromb haemost 2008;99:174–81. 22. ho pm, maddox tm, wang l, fihn sd, jesse rl, peterson ed et al. risk of adverse outcomes associated with concomitant use of clopidogrel and proton pump inhibitors following acute coronary syndrome. jama 2009;301:937–44. 23. kim ms, park es, park jb, lyo iu, sim hb, kwon sc. clopidogrel response variability in unruptured intracranial aneurysm patients treated with stentassisted endovascular coil embolization : is follow-up clopidogrel response test necessary? j korean neurosurg soc. 2018 mar;61(2):201-211. romanian neurosurgery | volume xxxii | number 3 | 2018 | july september  doi: 10.2478/romneu-2018-0061 article magnitude of intracranial pressure changes following rigid external cervical collar immobilization in cases sustaining traumatic brain injury: impact analysis current status guru dutta satyarthee, luis rafael moscote-salazar, amit agrawal india, colombia      romanian neurosurgery (2018) xxxii 3: 483 486 | 483             doi: 10.2478/romneu-2018-0061 magnitude of intracranial pressure changes following rigid external cervical collar immobilization in cases sustaining traumatic brain injury: impact analysis current status guru dutta satyarthee1, luis rafael moscote-salazar2, amit agrawal3 1department of neurosurgery, neurosciences centre, aiims new delhi, india 2department of neurosurgery, critical care unit, red latino, latin american trauma & intensive neuro-care organization, bogota, colombia 3neurosurgery department, narayana medical college & hospital, nellore, india abstract: rigid collars are routinely used to immobilise the cervical spine during early phase of management of trauma cases until cervical clearance is obtained or else diagnosed as case of cervical spine injury following detailed clinical as well as neurological evaluation. spinal injuries commonly coexist in patients sustaining severe head injury. till date, there is no clear cut consensus about effect of application of a rigid collar in cases suffering with traumatic brain injury. however, concern are regularly raised over collar application, such practice may have adverse effect on cerebrovascular regulation and ultimately affecting intracranial pressure and outcome. authors made detailed pubmed, embase, amed, and thomson reuters, medline line search and could find out six articles. according to existing literature, the cervical collar has the potential to influence intracranial pressure in patients suffering with head injury. there are several reports in the literature showing that cervical immobilization may alter intracranial pressure and the changes in icp closely depend on the types of cervical collars used. authors discuss the current status based on review of updated literature on possible effect on the intracranial pressure produced by application of rigid cervical collar and briefly literature is reviewed. key words: utility of cervical collar, head injury, intracranial pressure, concern introduction poly-trauma cases carry high risk of cervical spine injury along with other associated injuries. these patients should be safely evacuated from the site of incident and common protocol includes immobilization of the cervical spine with application of a rigid external cervical collar to further prevent 484 | satyarthee et al rigid external cervical collar immobilization and intracranial pressure             potential exaggeration of unstable cervical spine and associated spinal cord injuries in the prehospital settings (1). placement of a protective cervical collar is common in cases of acute head trauma. hard cervical collar or alternatives like rigid external cervical brace somi is applied and continued till the clearance cervical spine is obtained (1-4). effect on intracranial pressure mobbs et al. observed cases suffering with head trauma carry high risk of having a concomitant cervical spine injury and a rigid cervical collar is usually applied to each patient until spinal stability is confirmed. hard collars application may cause potentially venous outflow obstruction and additionally represents as nocioceptive stimulus, may lead to intracranial pressure rise (5). mobbs et al. in their prospective study involving ten cases suffering with headinjury with a postresuscitation glasgow coma scale score of nine or less underwent measurement of intracranial pressure both the before and following the application of cervical hard collar. authors observed 90% cases had a rise in intracranial pressure following application of the collar and difference in preand post-application intracranial pressure was significant statistically. mobbs et al. concluded early cervical spine assessment and clearance in head-injured patients is recommended to minimize the risk of intracranial hypertension related to prolonged cervical spine immobilization with a hard collar (5). hunt et al. observed significant rise from the baseline intracranial pressure when the collars were applied with the mean rise of 4.6 mmhg, which was statistically significant. further. mean rise was greater in patients with a baseline intracranial pressure greater than 15 mmhg compared to counterpart having less than 15 mmhg. authors observed no significant change in cardio-respiratory parameters during collar application, venous compression in the neck seems to be plausible explanation for intracranial pressure rise. hunt et al. cautioned rigid collars should be removed as soon as cervical spine injury has been excluded in head-injured victims or else an alternative method of spinal stabilisation must be considered. (6) placing a cervical collar is a routine procedure and helps to reduce the risk of secondary spinal injury, however by altering the icp it can lead to intracranial injury. according to these reports, the cervical collar has the potential to influence intracranial pressure in patients with traumatic brain injury. there are several reports in the literature showing that cervical immobilization may alter intracranial pressure and the changes in icp closely depend on the types of cervical collars used. effect of cervical collars on intracranial pressure in patients with head neurotrauma (7). it has been shown that patients with severe head injury particularly those who are unstable, unconscious and intubated may have up to 14% of cervical lesions and up to 7% of these lesions (5, 8). the application of cervical collars has the potential risk to increase intracranial pressure causing obstruction to the venous drainage (8, 9). other adverse effects of cervical immobilization are increased romanian neurosurgery (2018) xxxii 3: 483 486 | 485             respiratory effort, skin ischemia, pain and discomfort kolb et al. prospectively evaluated the change in measured cerebrospinal fluid pressure after the application of a rigid philadelphia collar in 20 adult patients without cervical spine injury undergoing lumbar puncture. the average pressure was 176.8 mm h2o initially and increased to an average of 201.5 mm h2o after collar placement (range 0 to 120) which statistically significant. authors noted even small increment in pressure could be significant in patients who already have an elevated intracranial pressure (11). maissan et al. noted rigid cervical collar immobilization to the cervical spine are known to increase intracranial pressure in severe traumatic brain injury and the cerebral blood flow might decrease according to the kellie monroe doctrine. for this reason, the use of the collar in patients with severe traumatic brain injury has been abandoned from several trauma protocols in the netherlands. maissan et al in a prospective blinded cross-over study evaluated the effect of application of a rigid cervical collar in 45 healthy volunteers by measuring their optical nerve sheath diameter by transocular sonography an indirect non-invasive method to estimate icp and pressure changes. they he studied healthy volunteers including 22 male and 23 female volunteers. they observed application of a collar resulted in a significant increase optic nerve sheath diameter in both side and concluded application of a rigid cervical collar significantly increases the optic nerve sheath diameter in healthy volunteers with intact cerebral autoregulation (12). however, early of diagnosis of cervical spine injury will segregate those cases where cervical immobilization is not required anymore and cervical collar can be safely taken out and can be managed for associated traumatic brain injury (13-16). however, current evidences have several limitations to generalize the findings, as analysis was primarily directed only to determine the effect of intracranial pressure rise on cervical collars and it does not pertain to neurological outcome of patients (7). conclusion the currently available data fail to clearly establishing the impact of cervical collar application always produces rise in the intracranial pressure in those cases, who sustained traumatic head injury; although the rise in intracranially pressure may be of lesser impact than nonapplication might produced devastating consequences in form of worsening of unstable cervical spine injury as well as deterioration of neurological status and associated spinal cord injury. according to recent authors consensus an early evaluation of the cervical spine in patients with head trauma is necessary to reduce the impact of prolonged use of cervical collars and their possible influence on intracranial pressure, multicentric randomized case controlled studies are required to determine and actually quantify the exact and precise magnitude of rise in the intracranial pressure following immobilization of cervical spine with a rigid cervical collar. 486 | satyarthee et al rigid external cervical collar immobilization and intracranial pressure             correspondence dr. guru dutta satyarthee associate professor, department of neurosurgery, room no. 714 neurosciences centre, aiims new delhi e-mail: duttaguru2002@yahoo.com references 1. satyarthee gd. ways to improve outcomes of traumatic acute spinal cord injury: integrated approaches of improved prehospital care, the adoption of synergistic medical and surgical intervention, along with care for associated systemic injury and rehabilitation and social inclusion. world neurosurg. 2017; 101:786-787 2. ho amh, fung ky, joynt gm, karmakar mk, peng z. rigid cervical collar and intracranial pressure of patients with severe head injury. j trauma 2002; 53(6): 1185-8. 3. stone mb, tubridy cm, curran r. the effect of rigid cervical collars on internal jugular vein dimensions. acad emerg med 2010; 17(1): 1002. 4. lemyze m, palud a, favory r, mathieu d. unintentional strangulation by a cervical collar after attempted suicide by hanging. emerg med j 2011; 28(6): 532. 5. mobbs rj, stoodley ma, fuller j. effect of cervical hard collar on intracranial pressure after head injury. anz j surg. 2002 jun; 72(6):389-91. 6. hunt k, hallworth s, smith m. the effects of rigid collar placement on intracranial and cerebral perfusion pressures. anaesthesia. 2001; 56(6):511-3. 7. moscote-salazar lr, godoy da, agrawal a, rubiano am. effect of cervical collars on intracranial pressure in patients with head neurotrauma. journal of emergency practice and trauma 2017 . doi: 10.15171/jept.2017.03. 8. davies g, deakin c, wilson a. the effect of a rigid collar on intracranial pressure. injury 1996; 27(9): 647-9. 9. kuhnigk h, bomke s, sefrin p. effect of external cervical spine immobilization on intracranial pressure. aktuelle traumatol 1993; 23(8): 350-3. [in german]. 10. craig gr, nielsen ms. rigid cervical collars and intracranial pressure. intensive care med 1991; 17(8): 504-5. 11. kolb jc, summers rl, galli rl. cervical collarinduced changes in intracranial pressure. am j emerg med. 1999; 17(2):135-7. 12. maissan im , ketelaars r, vlottes b, hoeks se, den hartog d, stolker rj. increase in intracranial pressure by application of a rigid cervical collar: a pilot study in healthy volunteers. eur j emerg med. 2017 jul 19. doi: 10.1097/mej.0000000000000490 13. verma sk, singh pk, agrawal d, sinha s, gupta d, satyarthee gd, sharma bs. o-arm with navigation versus c-arm: a review of screw placement over 3 years at a major trauma center.br j neurosurg. 2016 dec;30(6):658-661. 14. mishra a, agrawal d, gupta d, sinha s, satyarthee gd, singh pk. traumatic spondyloptosis: a series of 20 patients. j neurosurg spine. 2015 jun;22(6):647-52. 15. sawarkar dp, singh pk, siddique sa, agrawal d, satyarthee gd, gupta dk, sinha s, kale ss, sharma bs. surgical management of odontoid fractures at level one trauma center: a single-center series of 142 cases. neurol india. 2015 jan-feb;63(1):40-8. 16. singh pk, garg k, sawarkar d, agarwal d, satyarthee gd, gupta d, sinha s, kale ss, sharma bs. computed tomography-guided c2 pedicle screw placement for treatment of unstable hangman fractures. spine (phila pa 1976). 2014 aug 15;39(18):e1058-65 doi: 10.33962/roneuro-2022-018 the use of 3d programs in the treatment of glioblastomas 3d angio window. technical note ahmet cemil ergün, fatih demir, metin kaplan romanian neurosurgery (2022) xxxvi (1): pp. 107-109 doi: 10.33962/roneuro-2022-018 www.journals.lapub.co.uk/index.php/roneurosurgery the use of 3d programs in the treatment of glioblastomas 3d angio window. technical note ahmet cemil ergün, fatih demir, metin kaplan firat university faculty of medicine, department of neurosurgery, elazığ, turkey abstract the purpose of this study is to define preand postoperative planning as a new usage area of 3d imaging programs in the follow-up and treatment of glioblastomas. the thin-section mri images of the cases were used in this study. these images were analyzed with the 3d angio window of the radiant dicom viewer © program. in the 3d angio window, it was found that the glioblastoma tumour tissue was revealed in 3d, such as the vascular structures, when calvarium and brain tissue were suppressed. in this examination method, the bleeding in the postoperative surgical area is also suppressed, the contrasting residue tissue is fully visible, and can be monitored in 3d. introduction a good preoperative planning should be made to ensure maximum tumor resection with low surgical complications in glioblastomas. it is very important to make the tumor clear and to define its relationship with environmental structures for a good planning in radiological terms. also, knowing the feeding of the tumor and its relations with vascular structures will facilitate surgery. clearer evaluation of patients in terms of postoperative residue is also very important for treatment and follow-up (1). for this reason, efforts are continuing to develop new radiological imaging techniques and expand their use. for this purpose, 3d imaging programs are widely used in the medical world in this respect. the purpose of this study is to define preand postoperative planning as a new usage area of 3d imaging programs in the follow-up and treatment of glioblastomas. methods for this purpose, 10 cases who were suspected of glioblastoma and were confirmed with diagnosis after surgery were examined. also, the images of 10 cases of intracerebral hematoma with contrasting mri images were included from the archives in the study as the control group to find out if the bleeding was suppressed. the thin-section mri images of the cases were used in this study. these images were keywords brain haemorrhage, glioblastoma, 3d imaging programs corresponding author: ahmet cemil ergün firat university faculty of medicine, department of neurosurgery, elazığ, turkey drahmetcemil@yahoo.com.tr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 108 ahmet cemil ergün, fatih demir, metin kaplan analyzed with 3d angio window of the radiant dicom viewer © (64-bit) program (figure 1). figure 1. radiant dicom viewer ©angio window screenshot discussion there are two basic data in the development of our hypothesis. first of all, calvarium and brain tissue are suppressed in this window of the program, and vascular structures are revealed because of its contrast content. this allows to examine the vascular network in 3d. the second one is that the radiologically environmental-ring contrasting is typical for glioblastoma multiform. this contrasting area also shows the active tumor area where the feeding occurs, and the main target is the complete resection of this area in surgery. this ring-like contrasting of the tumor external wall was our main reference point. in radiant dicom viewer 3d angio window, it was found that the glioblastoma tumor tissue was revealed in 3d, such as the vascular structures, when calvarium and brain tissue were suppressed. also, this situation constitutes an opportunity to examine the relation and feeding of vascular structures as well as to fully reveal tumor size in 3d (figures 2-3). it is important to reveal whether there are postoperative residues in the follow-up and treatment of glioblastomas. sometimes it becomes difficult to evaluate this because of postoperative bleeding areas in control radiological images. it may not be easy to reveal whether it is bleeding or residual tissue, and if it is residual tissue, to determine the exact size of it. in this examination method, the bleeding in the postoperative surgical area is also suppressed, the contrasting residue tissue is fully visible, and can be monitored in 3d (figure 3). these images will contribute to the creation of a roadmap for the follow-up and treatment of glioblastoma multiforme patients after their surgery. also, the bleeding will be suppressed with this examination method in atypical bleedings, and it will be easier to understand the underlying pathology, if any (bleeding into the tumor, vascular malformations) (figure 4-5). figure 2. multiple glioblastoma case; tumors and vascular structures are observed in aaxial contrasted mri, b contrasted sagittal mri, c3d angio window image. figure 3. glioblastoma case; asagittal contrasted mri, b relation with tumors and vascular structures is seen in 3d angio window image, cthe presence of tissue in the postoperative residue in 3d angio window image. figure 4. case of atypical bleeding; asagittal ct, bsagittal t2weighted mri, ccomplete suppression of the bleeding is seen as there is no contrasting in 3d angio window. figure 5. atypical bleeding case; aaxial ct, bcoronalcontrasted mri, cit is seen in 3d angio window that bleeding is suppressed, and the presence of contrasted vascular anomaly is preserved. 109 the use of 3d programs in the treatment of glioblastomas 3d angio window references 1. wang ll, leach jl, breneman jc, mcpherson cm, gaskillshipley mf. critical role of imaging in the neurosurgical and radiotherapeutic management of brain tumors. radio graphics. 2014; 34:702-721. doi: 10.33962/roneuro-2022-026 clinico-pathological features and molecular background of oligodendrogliomas. a single centre retrospective study g. popescu, francesca paslaru, a.c. paslaru, m. apostol, m.c. zaharia, m. popescu, r.m. gorgan romanian neurosurgery (2022) xxxvi (2): pp. 145-149 doi: 10.33962/roneuro-2022-026 www.journals.lapub.co.uk/index.php/roneurosurgery clinico-pathological features and molecular background of oligodendrogliomas. a single centre retrospective study g. popescu1, francesca paslaru1, a. c. paslaru2,3, m. apostol1, m.c. zaharia1, m. popescu4, r. m. gorgan1,2 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 department of genetics, “dr victor gomoiu” children’s clinical hospital, bucharest, romania 4 department of neurosurgery, pitesti emergency hospital, university of pitesti, romania abstract background: diffuse gliomas are the most frequent primary central nervous system (cns) neoplasms, originating from the parenchyma itself, oligodendrogliomas accounting for approximately 10% of cerebral gliomas. for the past 20 years, the study of genetic/molecular mechanisms of glioma genesis and progression has gradually come into focus. however, the biological and clinical significance of these mutations are still to be completely characterized. the purpose of this article is to describe our clinical experience with oligodendrogliomas and to review the current literature, in order to better describe the characteristics of the molecular/genetic oligodendroglioma subgroups. methods: we performed a single-institution retrospective study that included 66 patients with oligodendrogliomas operated in our department between january 2011 and december 2018. results: our study included 26 female patients (39%) and 40 male patients (59%). the mean age at presentation was 39.9year-old (range 26-59year-old). the tumours were located predominantly in the right hemisphere (53%), the majority being situated in the frontal lobe (59%). 64% of the patients had signs of mass effect on the imaging studies, 13% presented with brain herniation syndromes, and 16 % of the surgically treated patients had a relapse with regrowth and malignant transformation of the tumour. the most common complaint that the patients had at admission was a headache. seizures were the second most common symptom that determined the patients to seek medical attention. conclusion: the expanding knowledge regarding the genetic alterations of oligodendroglial tumours could lead to significant changes in treatment strategies. however, the utility of each particular marker in planning the treatment has yet to be keywords oligodendrogliomas, clinico-pathological features, molecular background corresponding author: g. popescu 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 146 g. popescu, francesca paslaru, a.c. paslaru et al. established. emerging data will, most likely, improve outcome prediction and adjuvant therapy strategies by identifying the patients most likely to benefit from a particular treatment. introduction diffuse gliomas are the most frequent primary central nervous system (cns) neoplasms, originating from the parenchyma [1]. about 75% of gliomas in adults are astrocytic, two-thirds being glioblastomas, the most malignant form. oligodendroglial tumors account for than 10% of the gliomas [2]. for the largest part of the last century, the diagnosis of oligodendrogliomas has been based on histopathological aspects alone. for the past 20 years, the study of genetic/molecular mechanisms of glioma genesis and progression has gradually come into focus. the 2021 world health organization (who) classification of tumors of the cns includes molecular features for diagnosis and further classification of oligodendroglioma into idh-mutant and 1p/19q-codeleted [3]. the biological and clinical significance of these mutations are still to be completely characterized. the purpose of this article is to describe our clinical experience with oligodendrogliomas and to review the current literature, in order to better describe the characteristics of the molecular/genetic oligodendroglioma subgroups. materials and methods we performed a single institution retrospective study that included the patients of the 4th clinical department of neurosurgery of the bagdasar-arseni clinical emergency hospital. we retrospectively reviewed the case files of 66 patients with oligodendrogliomas operated in our department between january 2011 and december 2018. we only included patients operated for oligodendrogliomas with a positive anathomopathological examination for a “classical” oligodendroglioma. exclusion criteria were diagnosis of primary glioblastoma, oligoastrocitoma with important oligodendroglial compound or patients with a high suspicion for oligodendroglioma, that refused surgery or biopsy for diagnosis. data were obtained by studying patient files. results our study included 26 female patients (39%) and 40 male patients (59%). the mean age at presentation was 39.9year-old (range 26-59year-old). the tumors were located predominantely in the right hemisphere (53%), the majority being situated in the frontal lobe (59%). 64% of the patients had signs of mass effect on the imaging studies, 13% presenting with brain herniation syndromes (figure 1). figure 1. distribution of patients based on the presence/absence of mass effect on imaging studies. 16 % of the surgical treated patients had a relapse with regrowth and malignant transformation of the tumor (figure 2). figure 2. distribution of the patients based on the presence/absence of relapse with malignant transformation. figure 3. distribution of the patients based on the clinical symptoms at admission. no 84% grade iv glioblastoma 16% no grade iv glioblastoma 0 5 10 15 20 25 30 35 40 51% 36% 13% with without brain herniation syndrome 147 clinico-pathological features and molecular background of oligodendrogliomas the most common complaint that the patients had at admission was headache. seizures were the second most common symptom that determined the patients to seek medical attention (figure 3). illustrative case a 30-year-old male with no significant medical history was referred to our clinic for intense headache, progressively worsened during the month prior to admission. clinical examination showed no neurological deficit. gadolinium-enhanced mri scan revealed a right fronto-temporal tumor, measuring 9.5 cm in diameter, compressing the adjacent structures and producing mass effect on the right lateral ventricle (figure 4). figure 4. gadolinium enhanced mri scan, axial section, showing a right fronto-temporal tumour, measuring 9.5 cm in diameter, compressing the adjacent structures with inhomogenous enhancement. figure 5. intraoperative aspect showing the yellow-grey tumour. figure 6. intraoperative aspect showing the resection cavity. 148 g. popescu, francesca paslaru, a.c. paslaru et al. we performed a gross total resection through a pterional approach (figure 5, figure 6). the patient was discharged 7 days later, with no postoperative neurological deficits. control ct scan showed a gross total resection of the tumor (figure 7). figure 7. postoperative ct scan showing the resection cavity. figure 8. histopathological specimen showing arciform vascularization. histopathological examination showed arciform vascularization (figure 8), “boiled egg cells” (figure 9) and high fibrilarity (figure 10). mlpa analysis of the tumor sample identified a codeletion of 1p19q and a c.395g>a (p.r132h) mutation in the exon 4 of idh1 gene. the analysis was negative for mutations of exons 11 and 15 of braf gene, egfrviii, mgmt promoter methylation and tert promoter mutation. the patient had a favorable evolution, with no neurological deficits and was discharged in the seventh postoperative day. figure 9. histopathological specimen showing “boiled egg cells” aspect. figure 10. histopathological specimen showing high fibrillarity. discussion under the generic term “oligodendroglioma” is a heterogenous group of tumors, with a variable response to adjuvant therapy. this variance highlights the need for markers that can guide the clinical decision-making. codeletion of 1p19q occurs in 50 to 76% of oligodendrogliomas [4] [5]. eortc 26951 and rtog 9402 studies proved that combining radiation therapy with procarbazine, vincristine and lomustine chemotherapy protocol drastically increased overall survival in 1p19q codeleted anaplastic oligodendroglioma patients compared to radiotherapy alone [6] [7]. the eortc 26951 trial investigated the adding of six cycles of standard procarbazine, vincristine and lomustine to 149 clinico-pathological features and molecular background of oligodendrogliomas radiation therapy of 59.4 gy in 33 fractions in anaplastic oligodendroglioma patients and reported a significant difference in overall survival [7] [8]. patients with 1p19q codeleted oligodendrogliomas benefitted more from the addition of chemotherapy to radiotherapy, the risk reduction in patients with non-codeleted tumors being significantly lower [7]. regarding both trials, it is also notable the fact that patients with 1p19q codeleted oligodendrogliomas who were treated with adjuvant radiotherapy alone initially, had a lower survival rate at progression, despite being administered a heightened chemotherapy regimen [4] [7]. the codel trial has been designed to compare administration of adjuvant therapy consisting of either radiotherapy alone, themozolomide alone or radiotherapy combined with themozolomide. the analysis from the initial study design showed that themozolomidealone patients experienced a significantly shorter progression free survival, compared to either one of the radiotherapy arms [9]. the study has been subsequently redesigned to compare radiotherapy combined with procarbazine, lomustine and vincristine to radiotherapy and themozolomide regimens and is still ongoing. mutations of idh1 and idh2 seem to occur in about 70% of oligodendroglioma tumors, mainly affecting amino acid 132 of idh1 or idh2 [10] [11]. idh1 is known to function as a tumor suppressor, its mutational inactivation leading to tumorigenesis, partially through the induction of the hif-1 pathway [12] [13]. idh mutations have been reported in several studies to produce a favorable prognostic impact [7] [10] [14]. however, despite the more favorable prognosis of patients with oligodendrogliomas harboring idh mutations, it hasn’t been proven yet that the treatment strategy should be changed regarding the idh status. conclusion the expanding knowledge regarding the genetic alterations of oligodendroglial tumors could lead to significant changes in treatment strategies. however, the utility of each particular marker in planning the treatment has yet to be established. emerging data will, most likely, improve outcome prediction and adjuvant therapy strategies through identifying the patients most likely to benefit from a particular treatment. doi: 10.33962/roneuro -2020-052 surgical management of intramedullary spinal cord metastasis. report of three cases that revealed unknown malignancies a. khelifa, w. bennabi, l. berchiche, b. yakoubi, f. aichaoui, a. morsli romanian neurosurgery (2020) xxxiv (1): pp. 343-346 doi: 10.33962/roneuro-2020-052 www.journals.lapub.co.uk/index.php/roneurosurgery surgical management of intramedullary spinal cord metastasis. report of three cases that revealed unknown malignancies a. khelifa, w. bennabi, l. berchiche, b. yakoubi, f. aichaoui, a. morsli neurosurgical department of beo university hospital, algiers, algeria abstract intramedullary spinal cord metastasis (imscm) is a rare complication of malignancies still studied by case reports; although surgery is related with the best results, the management is still debated considering the risks and the low life expectancy; in fact, many authors prefer conservative management (radiotherapy, chemotherapy), and so less than 200 cases reported in the literature with patients imscm were treated surgically; reporting such cases will help to understand the pathology and elaborate a clear management protocol. we report three cases of imscm operated at our department; in those patients, the intramedullary lesions revealed the primary tumours. introduction face to patients with intramedullary spinal cord metastasis (imscm) the management is a challenge, because of the low life expectancy and the bad general condition of those patients. we report three patients with imscm managed surgically, in those patients the spinal cord location revealed the primary tumour. case presentation case 1 the first patient is a 57 years old man, with heart disease and smoking history of 30 years. the onset of the troubles dates back to 5 months, with weakness of the left hemibody, and bravais -jacksonian convulsions; a month later, there was the appearance of upper back pain with radiation to the limbs as well as functional impotence which confined the patient to bed. the clinical exam at the admission found: cauda equina syndrome with urinary urgency, saddle anaesthesia, abolition of myotatic reflexes in the two lower limbs, there was a keywords intramedullary, metastases, spinal cord corresponding author: khelifa adel neurosurgical department of beo university hospital, algiers, algeria drkhelifaadel@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 344 a. khelifa, w. bennabi, l. berchiche et al. significant muscular atrophy of the two lower limbs, total deficit of the dorsiflexion and plantar flexion of the foot, sensitive deficit (hypoaesthesia in the path l5-s1), partial deficit in flexion and extension of the leg on the thigh and the thigh on the trunk, and a babinski sign. initially a brain mri objectified right parietal nodular lesion of 2 cm diameter (figure1a). the spinal mri objectified an intramedullary lesion of conus medullaris in heterogeneous hypersignal on t1 wi and t2 wi (figure1b, c, d). the diagnosis of central nervous metastasis was retained and the investigations for the initial tumour was pushed; the thoracic ct objectified a right apical pulmonary neoplasia with parietal extension classified t3 n0 mx (figure 1e). the patient was operated and a gross macroscopic removal of the conus medullaris tumour was performed. in post operative there was a slight recovery on the sensitive and motor functions. the anatomopathological study was in favor of a metastasis of lung adenocarcinoma. the patient was sent then to oncology where a complement of radiotherapy and chemotherapy was performed. there were no complications within 30 days. figure 1. images of patient 1; (arrows: the tumour in different locations). (a): axial t1 injected brain mri, objectifying the right parietal metastasis; (b): sagittal t1 wi injected spinal mri showing the enhancement of conus medullaris nodule; (c): sagittal t2 wi spinal mri; (d): axial t1 wi spinal mri; (e): axial thoracic ct, objectifying right apical pulmonary neoplasia with parietal extension. case 2 the second patient is a 41 years old man, with past medical history of what it was thought to be lung abscess treated with antibiotics without following. the onset of the disorder dates back to two months before admission, marked by the installation of muscle weakness in the lower limbs of rapid progression. the neurological exam at the admission found a total flasco-spasmodic paraplegia, abolishing of osteotendinous reflexes of the two lower limbs and bilateral babinski sign. a spinal mri objectified an expansive intraspinal intramedullary process of the conus medullaris with heterogeneous hypersignal on t1 wi and t2 wi (figure 2a, b). already in the preoperative assessment, a chest x-rays performed for the anesthesia preoperative assessment objectified a suspect inhomogeneous opacity on the lower left lobe (figure 2c). as part of the investigations thoraco-abdomino-pelvic ct objectified a lower left lobe pulmonary excavated mass, and multiple hepatic hypodense lesions (figure 2d, e). the patient underwent a ct-guided transparietal puncture of the lung lesion brought 40 cc of pus, the bacteriological study was negative but the anatomopathological examination was in favor of lung squamous cell carcinoma. the patient was operated; he underwent a partial removal of the tumour of the conus medullaris through th 11, th 12 and l1 laminectomy. in post operative the patient was stable. the pathological examination was in favor of a metastasis of a lung squamous cell carcinoma. the patient was sent then to oncology where a complement of radiotherapy and chemotherapy was performed. there were no complications within 30 days. figure 2. images of patient 2; (arrows: the tumour in different locations). (a): sagittal t1 wi spinal mri, showing the conus medullaris tumour; (b): axial t1 wi spinal mri;(c): chest x-rays 345 surgical management of intramedullary spinal cord metastasis performed in the preoperative assessment showing suspect inhomogeneous opacity on the lower left lobe; (d): axial thoracic ct confirmed the presence of a lower left lobe tumour with necrosis;(e): abdominal ct, showing multiple liver metastasis. case 3 the third patient is 26 years old woman without past medical history; the onset of the disorder dates back to one month before admission with the appearance of a weakness in the four limbs, urinary and fecal urgency. the neurological exam at the admission found neck pain, paresthesia in the four limbs, a total flasco-spasmodic tetraplegia, abolishing of osteotendinous reflexes on the four limbs, right babinski sign, and urinary retention. spinal mri objectified a fusiform enlargement of the cervicodorsal spinal cord with extensive lesions from c4 to th 2, hyposignal t1wi, hyper signal t2 wi, after injection of gadolinium there was an enhancement in form of small heterogeneous eccentric masses extended on 8.5 cm from c4 to th 2, with edematous infiltration of the overlying spinal cord segments up to the bulbomedullary junction as well as underlying segments down to th 7 (figure 3). the patient was operated and the tumour was removed through a c3 to th2 laminectomy. the histological exam found a metastasis from a breast carcinoma; in fact a thoraco-abdominal ct was performed and found a suspect left breast mass (figure 3f); the patient was sent then to oncology for further investigations and management (radio and chemotherapy). in post operative immediately the patient was stable, but three weeks later she presented breathing difficulties for what she was admitted; an urgent spinal ct was performed without abnormalities, but the thoracic ct objectified an atelectasis; the patient was put under oxygenotherapy unfortunately 3 days later she presented sudden hemodynamic instabilities followed by a heart arrest and the resuscitation efforts failed. figure 3. images of patient 3. (a): sagittal t1 wi spinal mri, the tumour appears isointense and hypointense with spinal cord swallowing (arrows);(b): sagittal t2 wi spinal mri, the tumour appears with heterogeneous signal mostly hyperintense with the presence of myelomalacia and a cyst (arrows); (c): sagittal t1 wi injected spinal mri, heterogeneous enhancement of multiple nodules (arrows); (d): mrmyelography, objectifies the amount of swallowing the tumour was creating; (e): axial t2 wi spinal mri, showing spinal cord compression by an intramedullary formation (arrows); (f): thoracic ct, showing the left breast suspect nodule (arrow). table 1: summary of our imscm cases (morbidities and mortalities were evaluated within one month). patients age sex locations primary tumours management other metastasis outcome morbidities & mortalities case 1 57 m conus lung surgery brain improvement none 346 a. khelifa, w. bennabi, l. berchiche et al. case 2 41 m conus lung surgery liver stable none case 3 26 f cervico-dorsal brest surgery none stable death discussion metastasis to the spinal cord are rare [1,2,3,5], and described mostly by case reports [5]. based mostly on sung et al review of the english literature [3], jincai et al performed in 2019 a summary of prior studies about imscm treatment and outcome, they reported also their own series of 61 patients; in their paper, in sum 519 patients have been reported since 1960 of them only 152 were treated surgically [1]. as in our cases, the most common primary locations are the lung and the breast respectively [1, 5]; other locations are less common including colon [6], melanoma [2], and renal [2]; in 10 patients (3.3%) of sung et al series the primary tumour was unknown [2]. one of our three patients had brain location, and in the jincai et al review 206 (40%) of the patients with imscm have brain metastasis [1], so we find it very reasonable to ask systematically for brain mri for those patients even in absence of clinical symptoms. there is no clear protocol for the management of imscm [1, 2, 4, 5]; surgery gave an improvement rate of 77% and a stability of 23 % according to kalayci et al [3], for that it seems to be the optimal management tool if the general condition allows such heavy procedure, and also if the life expectancy is acceptable, in fact the prognosis of imscm is widely depending on the other locations and is frequently poor. for some authors, surgery could be difficult to propose, and they prefer radiotherapy that might assure an acceptable local control, except for radioresistant tumours such as renal cell carcinoma and melanoma [1, 2, 4, 5]. in our cases, the three patients were without past medical history of diagnosed malignancies, and images were not specific; after surgery, the investigations were urged by our pathology laboratory colleagues, even before giving the final histopathological results; so the diagnosis was based on surgical biopsy of the tumours and the invasive management was inevitable [5]. the surgeon should not consider radical removal of the tumour, but rather spinal cord decompressing by debulking [5], keeping in mind the fact that it is about a low life expectancy patient; the surgeon also is warned to not in any case expose the patient to complications that could deteriorate the quality of his short life. conclusion intra spinal cord metastasis are rare complications of some malignant tumours, especially lung and breast cancers; surgery is the treatment of chose if the life expectancy and the general condition of the patient are good; otherwise radiotherapy could in some cases assure relief and local control of the tumour. conflict of interest none. founding none. references 1. jincai lv, bailong liu, xiaoyue quan, cheng li, lihua dong, min liu. intramedullary spinal cord metastasis in malignancies: an institutional analysis and review. oncotargets and therapy 2019:12 4741–4753. 2. wen-shan sung, mei-jo sung, jon ho chan, benjamin manion, jeeuk song, arvind dubey, albert erasmus, andrew hunn. intramedullary spinal cord metastases: a 20-year institutional experience with a comprehensive literature review. world neurosurg. (2013) 79, 3/4:576584.http://dx.doi.org/10.1016/j.wneu.2012.04.005. 3. m. kalayci, f. cagavi, s. gul, s. yenidunya, and b. acikgoz. intramedullary spinal cord metastases: diagnosis and treatment – an illustrated review. acta neurochir (wien) (2004) 146: 1347–1354. doi 10.1007/s00701-004-0386-1. 4. ondrej kalita. current insights into surgery for intramedullary spinal cord metastases: a literature review. international journal of surgical oncology volume 2011, article id 989506, 5 pages doi:10.1155/2011/989506. 5. jörg klekamp, madjid samii. intramedullary tumours. in: jörg klekamp, madjid samii. surgery of spinal tumours, 1st edition; new york: springer berlin heidelberg;2007. p124-127. 6. tai-hsin tsai, i-cheng lin, pei-chen lin, chieh-hsin wu, chih-lung lin, and yu-feng su. intramedullary spinal cord metastasis from colon cancer: analysis of 19 reported cases. spinal cord series and cases (2016) 2, 15026; doi:10.1038/scsandc.2015.26. romanian neurosurgery (2019) xxxiii, 1: 34-36 (2019) doi: 10.33962/roneuro-2019-006 www.journals.lapub.co.uk/index.php/roneurosurgery new technics for removal of intradural spinal tumours r.e. rizea1,2, karina lidia gheorghita2, m.v. salaceanu3, a.v. ciurea4 1 neurosurgery department, “bagdasar-arseni” emergency neurosurgery hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 neurosurgery department, sibiu emergency hospital, sibiu, romania 4 neurosurgery department, sanador hospital, bucharest, romania abstract introduction. neuronavigation is a computer-assisted technology based on preand intraoperative images that permit neurosurgeons to have a better approach of the brain and intradural spinal tumors. the neuronavigation systems have been a significant progress in neurosurgery. these systems allow neurosurgeons to evaluate surgical risks, select the best interventional method, localize better the tumors in order to improve the accuracy of the resection and decide on the optimal trajectory for the surgical procedure, resulting in decreased patient morbidity and mortality. material: spinal cord tumors are rare and uncommon lesions. their growth result in compression of the spinal cord, which can cause severe neurologic deficits such as limb dysfunction, motor and sensation loss with the possibility of leading to death. we present o short report of a study publicated by stefini et al. in 2018 regarding the use of neuronavigation for removal of intradural spinal tumors. conclusion: the benefits of using neuronavigation in resection of the intradural spinal tumors include decreased risk of bad localization of the tumor, minimal invasive surgery technique and reduction of bone removal. introduction neuronavigation is a computer-assisted technology used by neurosurgeons in resection of the tumours to evaluate surgical risks, select the best interventional method, localize better the tumours in order to improve the accuracy of the resection and decide on the optimal trajectory for the surgical procedures. the technique is based on pre and intraoperative images that permit neurosurgeons to have a better approach of the brain and intradural spinal tumours. the neuronavigation systems have been a significant progress in neurosurgery, their use resulted in decreased patient morbidity and mortality [1-4]. material the use of neuronavigation for the removal of spinal tumours has been described since 1990’s, with good detailed notes in 2000 by haberland keywords neuronavigation, intradural spinal tumours corresponding author: a.v. ciurea neurosurgery department, sanador hospital, bucharest, romania avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 35 new technics for removal of intradural spinal tumors et al. [1,2]. nowadays, spinal navigation is used to create 3d images in order to position the pedicle screws. a good microsurgical resection of spinal intradural tumours needs an accurate hemilaminectomy or laminectomy, that sometimes can be more excessive than necessary and leads to chronic pain and acquired deformities of the spine [3,4]. in 2018, stefini et al. described the for first time the possibility to use the merging of the 3d fluoro images obtained intraoperative with spinal navigation with mri preoperative images, in order to make a better approach of the spinal intradural or intramedullary tumours [3,5-7]. stefini et al. published in 2018 a report regarding the use of neuronavigation for removal of intradural spinal tumours. they made a study between january and july 2016 that included 10 navigated procedures for intradural spinal tumours with the technique of merging 3d fluoro images obtained intraoperative with spinal navigation with mri preoperative images. initially, all the patients underwent contrastenhanced mri with volumetric acquisitions and after that there were obtained the 3d fluoro images with neuronavigation. all these images were merged automatically or manually, verified if the association was correctly done on the sagittal, coronal and axial planes and used to perform all the steps of the required procedure using the navigated probes. the studied patients had all completed the fusion procedures, there were no errors detected and the intervention lasted about 20 min for each person [3]. discussion intraoperative navigation, considered an essential tool for cranial surgery, became in the last years an advantageous technique for spinal surgery in degenerative disc disease, spondylolisthesis, tumours and traumatic lesions. it reduces the neurological complications and system failure for the patient and the radiation exposure for the neurosurgical team [3,8]. the idea of merging the 3d fluoro images with the volumetric-enhanced mri images made spinal navigation more accurate. this procedure resolved also problems like the centering of the tumours with a good indication of the precise level of the lesion, length of the skin incision, muscle strip and extent of bone removal, incidence of instability after the surgery, blood loss and postoperative pain [3,9]. the technique was found very useful in case of small and intramedullary tumours, especially for the thoracic lesions because it reduces the need of radiation. the limitation of the procedure is that this it was not studied extensively [3,10]. conclusions in our opinion this technique provides numerous advantages and it is simple to learn by the neurosurgeons. intradural spinal tumours resection using neuronavigation is a minimal invasive technique that has numerous benefits including decreased risk of bad localization of the tumour, minimal invasive surgery technique and reduction of bone removal. the use of neuronavigation is in continuous progress of research that promises to be an excellent neurosurgery tool. references 1. haberland n., ebmeier k., hliscs r. et al., j cancer res clin oncol (2000) 126: 529. https://doi.org/10.1007/s004320000122 2. galloway rl jr, maciunas rj, edwards ca. interactive imageguided neurosurgery. ieeetransbiomedeng. 1992;39(12): 1226-1231. 3. stefini r., peron s., mandelli j., bianchini e., roccucci p.; intraoperative spinal navigation for the removal of intradural tumors: technical notes, operative neurosurgery, volume 15, issue 1, 1 july 2018, pages 54– 59, https://doi.org/10.1093/ons/opx179. 4. bresnahan l, ogden at, natarajan rn, fessler rg. a biomechanical evaluation of graded posterior element removal for treatment of lumbar stenosis: comparison of a minimally invasive approach with two standard laminectomy techniques. spine. 2009;34(1):17-23. 5. ling jm, dinesh sk, pang bc, chen mw, lim hl, louange dt. routine spinal navigation for thoraco-lumbar pedicle screw insertion using the o-arm three-dimensional imaging system improves placement accuracy. j clin neurosci. 2014;21(3):493-498. 6. roccucci p, peron s, minotti mr, stefini r. real-time navigation in spinal surgery: what has it changed in surgical practice? [published online ahead of print may4,2016] jneurosurgsci.2016. 7. vande kelft e, costa f, vander planken d, schils f. a prospective multicenter registry on the accuracy of pedicle screw placement in the thoracic, lumbar, and sacral levels with the use of the o-arm imaging system and stealth station navigation. spine.2012;37(25):1580-1587. 8. gebhard ft, kraus md, schneider e, liener uc, kinzi l, arand m. does computer-assisted spine surgery reduce intraoperative radiation doses? spine. 2006;31(17):20242027. 9. mannion rj, nowitzke am, efendy j, wood mj. safety and efficacy of intradural extramedullary spinal tumor removal 36 r.e. rizea, karina lidia gheorghita, m.v. salaceanu, a.v. ciurea using a minimally invasive approach. neurosurgery.201;68 (1supploperative):208-216. 10. neil w.d. thomas, john sinclair, image-guided neurosurgery: history and current clinical applications, journal of medical imaging and radiation sciences, volume 46, issue 3, 2015, pages 331-342, issn 1939-8654, https://doi.org/10.1016/j.jmir.2015.06.003. (http://www.sciencedirect.com/science/article/pii/s193986 5415001903) doi: 10.33962/roneuro-2022-038 airway management in neurotrauma care. basic considerations indubala maurya, ved prakash maurya, rakesh mishra, luis rafael moscote -salazar, tariq janjua, mohd yunus, amit agrawal romanian neurosurgery (2022) xxxvi (2): pp. 216-219 doi: 10.33962/roneuro-2022-038 www.journals.lapub.co.uk/index.php/roneurosurgery airway management in neurotrauma care. basic considerations indubala maurya1, ved prakash maurya2, rakesh mishra3, luis rafael moscote-salazar4, tariq janjua5, mohd yunus6, amit agrawal7 1 department of anaesthesiology, kalyan singh super specialty cancer institute, cg city, lucknow, india 2 department of neurosurgery, sgpgims, lucknow, india 3 department of neurosurgery, institute of medical sciences, banaras hindu university, varanasi, india 4 latin-american council of neurocritical care (clani), colombia 5 department of critical care medicine, physician regional medical center, naples, fl, usa 6 department of trauma and emergency medicine, all india institute of medical sciences, saket nagar, bhopal, india 7 department of neurosurgery, all india institute of medical sciences, saket nagar, bhopal, india abstract the predictability of the airway compromise affects the decision for tracheal intubation. associated specific injuries, clinical presentation, and expected deterioration are the deciding factors regarding the need for securing the airway. emergent or semi-urgent intubations are straightforward in the majority of patients. airway management in trauma patients aims to improve tissue oxygenation, ensure ventilatory exchange, stabilize other injuries and prevent aspiration. airway management in the trauma and emergency room is challenging as the emergency team has limited time for full airway assessment unlike pre-anaesthesia check-up clinic/operative room. the airway cart must be checked routinely in the emergency room for the working condition of the equipment and its availability. all trauma patients must be considered to have cervical spine injuries unless ruled out. the airway management for trauma patients is best done using a team approach including emergency medicine physicians, anaesthesiologists, surgeons, and trained paramedical staff. regardless of the emergency room setting, airway management of a trauma patient requires effective communication and efficient teamwork. introduction airway management in trauma patients aims to improve tissue oxygenation, ensure ventilatory exchange, stabilize other injury and prevent aspiration. airway management in the trauma and emergency room is challenging as the emergency team has limited time for full keywords neurotrauma, neurocritical care, traumatic brain injury, airway management corresponding author: amit agrawal department of neurosurgery, all india institute of medical sciences, saket nagar, bhopal, india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 217 airway management in neurotrauma care airway assessment unlike pre-anaesthesia check-up clinic/operative room. trauma patients present a varied spectrum of injury from localized to multisystem involvement. the presence of hemodynamic instability, direct airway injury, thoracic injury, combative patient (raised intracranial pressure/intoxication/hypoxemia), etc. can lead to difficult airway situations. availability of trained team, synchronized teamwork, and functional airway equipment are paramount for safe airway management. 1-3 indication for securing the airway associated specific injuries, clinical presentation, and expected deterioration are the deciding factors regarding the need for securing the airway. emergent or semi-urgent intubations are straightforward in the majority of patients. but in some patients, it may be less clear. the eastern association for the surgery of trauma (east) practice management guidelines and the advanced trauma life support (atls) program have given indications for intubation in trauma patients. 1, 4 in general, the indication for emergency tracheal intubation in trauma patients is the failure of oxygenation or ventilation, failure to maintain/protect the airway and anticipated deterioration of the airway. (table 1: indication for tracheal intubation). the trauma patients may have poor oxygenation and ventilation hypoxemia or hypoventilation due to multiple factors and may not respond to simple interventions e.g., oxygen supplementation. adequacy of oxygenation and ventilation can be assessed clinically by pulse oximetry, respiratory effort, and associated injuries. inability to protect the airway could be due to decreased level of consciousness secondary to traumatic brain injury or intoxication. in these cases, early intubation is typically indicated. any patients with penetrating neck injury, inhalation injury (burns from closed space fire), hemorrhagic shock (due to complicated pelvic fracture, liver laceration) may lose airway as natural clinical course, thus they will need intubation in anticipation. the predictability of the airway compromise affects the decision for tracheal intubation. 5, 6 table 1: indication for tracheal intubation eastern association for the surgery of trauma (east) ● hypoventilation ● persistent hypoxemia ● decreased level of consciousness (gcs≤ 8) ● cardiac arrest ● hemorrhagic shock ● airway obstruction ● inhalation injury ● facial injury advanced trauma life support (atls) ● poor respiratory efforts ● hypoxia ● hypercarbia ● cyanosis ● neurological deterioration (gcs≤ 8) ● apnea ● severe facial injury ● direct airway injury ● inhalational injury ● unconscious patients preparedness a preparedness and coordinated approach to airway management is the key step. 7, 8 the airway cart must be checked routinely in the emergency room for the working condition of equipment and its availability. the intuitional/local practice best determines the timing but checking after every shift is recommended. standard airway equipment should be there in the airway cart. 9 the cart should have different sizes/types of facemasks, laryngoscopes, endotracheal tubes, oral airway, nasal airway, bougies, invasive airway equipment, etc. (table 2: difficult airway cart). table 2: difficult airway cart ● manual resuscitator with oxygen reservoir ● oral and nasal airways (various sizes) ● rescue airways device: combi tube, laryngeal mask airway ● endotracheal tube introducer (gum elastic bougie) ● semi-rigid stylet ● endotracheal tubes (range of sizes) ● laryngoscope blades of shorted design and size ● laryngoscope handle with battery (check for functionality) ● syringes, lubricant, tube ties ● video laryngoscope ● cricothyrotomy kit always ensure that oxygen source and suction equipment are available in the functional stage. the emergency drug tray must have induction agents (e.g., etomidate, ketamine, propofol, etc.) and muscle relaxants (e.g., succinylcholine, rocuronium, etc.) 218 indubala maurya, ved prakash maurya, rakesh mishra et al. beside emergency drugs. 2, 3, 10 regardless of the emergency room setting, airway management of a trauma patient requires effective communication and efficient teamwork. the airway management for trauma patients is best done using a team approach including emergency medicine physicians, anaesthesiologist’s, surgeons, and trained paramedical staff. 11-13 emergency intubation in the emergency room requires additional assistance to administer drugs, to ventilate the patient, to give cricoid pressure, and manual in-line stabilization (mils) of the cervical spine if indicated. even extra assistance is needed to control agitated patients due to head injury/intoxication. uncooperative/agitated patients the agitated patients can injure themselves. the trauma patients may be violent or agitated due to various reasons such as alcohol/drugs intoxication, hypoxia, hypercarbia, head injury, hypoglycemia, severe pain, etc. these factors should be addressed along with airway intervention. as per east guidelines, if the severity of agitation hinders assessment and resuscitation, intubation can be considered. 4 craniofacial trauma a significant proportion of individuals with severe maxillofacial injury, more so with pan-facial involvement, have associated traumatic brain and spine injury; therefore, spine stabilization and preventing airway compromise are challenging in these patients. the mechanisms attributed to airway compromise in maxillo-facial trauma are primarily due to tongue fall secondary to bilateral mandible fracture, displacement of the fractured maxilla, hematoma, soft-tissue oedema, foreign body, or direct laryngeal trauma. the patient should be placed in a lateral position for mid-facial trauma with the potential risk of haemorrhage and the mandible pulled forward. this technique would help remove the blood and secretion, and the airway can be easily kept patient. oropharyngeal airway and nasopharyngeal airway devices are used in these cases because traditional manoeuvres of jaw thrust, chin lift, and head tilt may not be possible due to associated oedema or c-spine injury. while intubating, a rigid high suction device may be kept alongside the laryngoscope to prevent soiling of the airway. 14 the available options are orotracheal intubation, nasotracheal intubation, cricothyroidotomy, and tracheostomy. direct airway trauma in patients with direct trauma, the airway is a challenging situation for the emergency team. direct trauma to the airway can be due to blunt or penetrating injury. airway injury can occur at multiple levels and may be associated with a cervical spine injury, injury to the aerodigestive tract, etc. it can result in immediate or delayed airway obstruction. 5, 15, 16 general principles for the management of direct airway trauma include repeated clinical assessment because the airway can compromise due to tissue oedema or hematoma over time. even if the patient appears clinically stable, airway management is required given anticipated deterioration. swallowing of blood from a facial fracture can cause gastric distention and irritation thus it may increase the risk of regurgitation. the emergency team should assess the possibility of difficulty with bag-mask ventilation, endotracheal intubation, supraglottic device placement, and even with the surgical airway. a large-bore catheter suction should be used. if a difficult bmv is anticipated, an awake approach instead of rsii is safer. during bag-mask ventilation, airway obstruction can increase further due to pressure on the mandible and displacement of fractured segments. airway disruption and bleeding make laryngoscopy and intubation challenging. placement of supraglottic airways devices can be difficult due to distorted airway anatomy and limited mouth opening. if initial attempts to laryngoscopy fail, the surgical airway is indicated. in selected patients, the surgical airway may be the most appropriate initial approach to airway intervention. conclusion all trauma patients must be considered to have cervical spine injury unless rules out. the selection of induction drugs should be based on the type/severity of the injury and the patient's hemodynamic status. a variety of effective rescue airway devices are available for use in trauma patients. airway specialists should become familiar with and practice several of them to maximize the options available in case of a failed airway. 219 airway management in neurotrauma care references 1 trauma acosco. advanced trauma life suport atls: student course manual: american college of surgeons, 2012. 2. cranshaw j, nolan j. airway management after major trauma. continuing education in anaesthesia, critical care & pain 2006;6:124-127. 3. louro j, varon aj. airway management in trauma. international anesthesiology clinics 2021;59:10-16. 4. mayglothling j, duane tm, gibbs m, et al. emergency tracheal intubation immediately following traumatic injury: an eastern association for the surgery of trauma practice management guideline. the journal of trauma and acute care surgery 2012;73:s333-340. 5. jain u, mccunn m, smith ce, pittet jf. management of the traumatized airway. anesthesiology 2016;124:199-206. 6. rajandram rk, syed omar sn, rashdi mf, abdul jabar mn. maxillofacial injuries and traumatic brain injury--a pilot study. dental traumatology : official publication of international association for dental traumatology 2014;30:128-132. 7. smith ka, high k, collins sp, self wh. a preprocedural checklist improves the safety of emergency department intubation of trauma patients. academic emergency medicine : official journal of the society for academic emergency medicine 2015;22:989-992. 8. tsai ac, krisciunas gp, brook c, et al. comprehensive emergency airway response team (eart) training and education: impact on team effectiveness, personnel confidence, and protocol knowledge. the annals of otology, rhinology, and laryngology 2016;125:457-463. 9. bjurström mf, bodelsson m, sturesson lw. the difficult airway trolley: a narrative review and practical guide. anesthesiology research and practice 2019;2019:6780254. 10. khan rm, sharma pk, kaul n. airway management in trauma. indian journal of anaesthesia 2011;55:463-469. 11. kovacs g, law ja, ross j, et al. acute airway management in the emergency department by non-anesthesiologists. canadian journal of anaesthesia = journal canadien d'anesthesie 2004;51:174-180. 12. levitan rm, rosenblatt b, meiner em, reilly pm, hollander je. alternating day emergency medicine and anesthesia resident responsibility for management of the trauma airway: a study of laryngoscopy performance and intubation success. annals of emergency medicine 2004;43:48-53. 13. mackersie rc. pitfalls in the evaluation and resuscitation of the trauma patient. emergency medicine clinics of north america 2010;28:1-27, vii. 14. ducanto j, serrano kd, thompson rj. novel airway training tool that simulates vomiting: suction-assisted laryngoscopy assisted decontamination (salad) system. the western journal of emergency medicine 2017;18:117-120. 15. barak m, bahouth h, leiser y, abu el-naaj i. airway management of the patient with maxillofacial trauma: review of the literature and suggested clinical approach. biomed research international 2015;2015:724032. 16. saini s, singhal s, prakash s. airway management in maxillofacial trauma. journal of anaesthesiology, clinical pharmacology 2021;37:319-327. microsoft word 16satyartheegurudutta_ruptured romanian neurosurgery (2018) xxxii 4: 641 646 | 641             doi: 10.2478/romneu-2018-0083 ruptured intracranial internal carotid artery aneurysm causing subarachnoid hemorrhage and opthalmoplegia associated with metastatic carcinoma with unknown primary in sellar-parasellar region: true or coincidental association g.d. satyarthee1, l.r. moscote-salazar2, a. agrawal3 1department of neurosurgery, neurosciences centre, aiims new delhi, india 2red latino. latin american trauma & intensive neuro-care organization, bogota, colombia 3neurosurgery department, narayana medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract: unruptured intracranial aneurysm can be picked up incidentally on cranial angiography screening for other cause. however, with increasing use of neuroimaging led to increasing rate of pickup and many such incidentally detected cases are treated with endovascular treatment, or craniotomy and clipping of aneurysm or uncommonly a very small aneurysm unsuitable for retreatment by currently available modality may be observed as wait and watch policy. extremely uncommonly a patient undergoing investigation for suspected subarachnoid hemorrhage following aneurismal rupture, computed tomography scan revealed presence of subarachnoid hemorrhage associated with sellar mass. such association was previously unreported. in extensive pubmed search by authors could find a case reported by yang et al., a case of known surgically resected gastric carcinoma developing secondary in sella, ct angiography of the intracranial artery revealed an aneurysm of ica located at the inner edge of the siphon segment. authors report an interesting case of 65 year -old male presented with aneurysmal subarachnoid hemorrhage with secondary in sella with unknown primary, ct scan showed presence of sellar mass, underwent digital subtraction angiography at our centre, revealed presence of right supracliniod internal carotid bifurcation aneurysm, underwent craniotomy and successful surgical clipping of aneurysm with gross total decompression of sellar and suprasellar mass to the best knowledge of authors, current case represents first case in western literature, ,who presenting first time 642 | satyarthee et al intracranial internal carotid artery aneurysm with metastatic carcinoma             with aneurysmal subarachnoid hemorrhage and coincidentally associated with incidental sellar mass of metastatic origin pertinent literature is discussed briefly. key words: adenocarcinoma, aneurysm, secondary in sella surgical management, primary lesion, association introduction intracranial aneurysm can be detected after rupture or rarely picked up incidentally. the ruptured intracranial aneurysm present with sudden severe headache may be associated with focal neurological deficit. [1][2][3] imaging study may show presence of subarachnoid hemorrhage, intracerebral hematoma, intraventricular hemorrhage, obstructing hydrocephalus, or in late stage may show developing infarct due to vasospasm. however ruptured intracranial aneurysm associated with parasellar mass is uncommon, although cases of incidental aneurysm with intracranial tumor like pituitary adenoma, meningioma, are reported. however, ruptured internal carotid artery aneurysm with metastatic mass lesion is extremely uncommon. pre-operative knowledge of aneurysms coexisting with sellar mass may help in planning special strategy to deal both lesions simultaneously. case illustration a-65-year old man was admitted to department of neurosurgery at neuroscience centre of all india institute of medical sciences. he experienced sudden onset very severe headache in left frontal and temporal region associated with vomiting. next morning, he noticed diminution of vision involving left eye along with drooping of left eyelid. however, he had persistent headache but intensity has markedly reduced with progressive worsening of drooping of left upper eyelids along with painful progressive ophathalmoplegia. on admission, his supine bp was 130/70. positive neurological findings included with left eye, he was able to count finger at three feet, while, and on right side was 6/6.fundi revealed normal retinal arteries and normal appearance of fundi. his extraocular movement of the left eye -ball was completely absent. routine hemogram and serum biochemistry was normal. endocrine study revealed serum cortisol (8 am ) level 0.8 μ g / dl (n 5 -18 ) tsh1.8 μ iu /dl (n0.44.6 ), t 3 1.3 pg / ml (n 1.6-3.4), t4 – 6.4 ng /dl (n 0.71.8). as serum cortisol level was low, so corticosteroid replacement was started. x-ray chest and electrocardiography were normal. an x-ray skull revealed sellar enlargement with erosion of anterior clinoid process. ct scan of cranium revealed sellar, suprasellar lesion with left parasellar extension, showing enhancement with contrast agent. a 4-vessel digital subtraction angiographic study was done for evaluation, which revealed left internal carotid artery aneurysm which was directed superiorly. through a left pterional osteoplastic flap craniotomy after eighth day of ictus. there was mass filling up left parasellar and suprasellar region, gross decompression was also done, with intra-operative diagnosis of pituitary adenoma was made. in the postoperative romanian neurosurgery (2018) xxxii 4: 641 646 | 643             period, he made good recovery. just prior to discharge from hospital, a repeat angiography was carried out, revealed well clipped aneurysm to look for completeness of aneurysm clipping. he was discharged from hospital on sixth post-operative day. however, the histopathology turns out to be poorly differentiated metastatic adenocarcinoma. discussion the metastatic mass lesion accounts for only 1% of the tumors located in the sellar parasellar regions, for cases, who underwent transsphenoidal surgery [1]. breast and lung cancer are among the most common sites of primary malignant tumors to sellar regions [3] other includes gastrointestinal tract, prostate, kidney, thyroid, and pancreas. the important routes of metastasis to the pituitary gland include hematogenous or direct invasion through the skull base. the hematogenous route is the principal pathway of metastasis and lymphatic system is absent in the brain. the most commonly involved part of the pituitary gland in the order of decreasing frequency is posterior lobe, anterior hypophysis, both the anterior and posterior hypophysis, and the stalk[4] intracranial aneurysms commonly occur in the region of circle of willis, are often saccular or arteriosclerotic in origin. although saccular aneurysms can occur in peripheral branches of the circle of willis, but it is very rare. aetiology of aneurysms ocurring in the peripheral branches includes, in the decreasing order of frequency are mycotic, post-traumatic or secondary to tumour and moya-mmoya diseases. usually the occurrence of intracranial aneurysm association with intracranial brain tumours or secondary’s are extremely uncommon [1][2][3][4][5][6][7][8] very rarely incidental aneurysm can be picked up while investigation of sellar mass and few cases of intracranial aneurysm with associated with pituitary adenoma is reported. such association of intracranial aneurysm with tumor significantly increases the risk of inadvertent rupture during the intraoperative phase; surgery is attempted utilizing either trans-sphenoidal decompression or endoscopic approach. the commonest presenting symptom in patients with sellar metastases is central diabetes insipidus, followed by anterior hypopituitarism, visual loss, [9][10] however, diagnose of sellar metastasis is difficult because symptoms are mostly nonspecific and the radiological differences from primary tumors are nonspecific . [12][13][14][15] imaging study play an important role in the diagnosis of sellar parasellar region, besides clinical examination and hormonal assessment. ct scan head can show presence of subarachnoid hemorrhage, intracerebral hematoma, intraventricular hemorrhage, obstructing hydrocephalus, obstructing hydrocephalus, or in late stage may show developing infarct due to vasospasm. however ruptured intracranial aneurysm associated with parasellar mass further mri better delineates soft tissues and common lesion in sellar region needs exclusions are meningioma, pituitary adenoma and vascular mass. mri shows presence of sellar suprasellar mass, showing 644 | satyarthee et al intracranial internal carotid artery aneurysm with metastatic carcinoma             contrast enhancement, may be associated with areas of hemorrhage or necrosis representing previous pituitary apoplexy. meningiomas are solid, with occasional cyst on the edge or associated with peritumoral arachnoid cap, usually show uniform contrast enhancement, in the coronal section images can show a compressed normal pituitary gland can be seen separately from tumour in cases of meningioma at the bottom of the sella turcica and epicenter of mass lies above the sella a diagnostic mri sign of flow voids is 100% specific for aneurysms as described by teng et al. with the sensitivity of 88%, on t1weighted and t2-weighted imaging sequences[10 ] however olsen et al. reported only 80% giant aneurysms shows sign of blood flow in the aneurysm sac. so mri may fail to detect aneurysm if size of aneurysm being smaller[11] in , mri scan, t 1w image may show evidence of hypointense signal representing flow void caused by as rapidly flow blood in a carotid aneurysm. cases of thrombosed aneurysm, dsa study can be very helpful in arriving at diagnosis, delineating shape, size, direction of fundus, vessel originating from aneurysm, relation with adjoining branches of artery, presence of teat. regarding management of such co-existing aneurysm with secondary is debated is debated and controversial and depends on size of aneurysm, location on anterior or posterior circulation, proximity to sella or , size of sellar mass adenoma, status of adenoma, volume of adenoma, associated neurological manifestation, visual symptom, extension into multiple cranial fossa or multi-compartmental and general status of cases. [16][17] [18 ][19] although differentiating whether a lesion of interest is primary or secondary is very vital in planning treatment modality for such cases and diagnosis mainly rest on histopathological and immunohistochemistry. if a tumor in the pituitary gland is confirmed to be metastatic, local tumor control is planned to relive symptoms, and the overall prognosis depends on the site of the primary malignancy[9][10] yang et al reported a case of known surgically resected gastric carcinoma in a 57year-old woman with internal carotid aneurysm developing secondary in the sella. [2] she presented with oculomotor paralysis, postorbital pain, and hypopituitarism as onset symptoms. she had a history of the surgical removal of gastric cancer ct angiography of the intracranial artery revealed an ica of at the inner edge of the siphon segment. magnetic resonance imaging and singlephoton emission study revealed recurrent sellar mass with intracranial and multiple metastases of bone. he underwent subtotal removal followed by chemotherapy and radiotherapy. [2] with increasing usage of endovascular approach, aneurysm can be coiled and sellar mass can be resected using microsurgical or endoscopic approach separately, however if aneurysm lying in close proximity to mass can be managed in a single setting with clipping of aneurysm and adenoma resection.[20][21][22] however, approach should be individualized and tailor made after analyzing imaging study. however, high degree of suspicion of associated aneurysm is romanian neurosurgery (2018) xxxii 4: 641 646 | 645             must be made, if mri shows some atypical features and dsa must be carried out. conclusion in cases of suspected subarachnoid hemorrhage following aneurysmal rupture, and imaging study showing sellar mass possibility of primary as well as well as metastatic lesion must be considered. ruptured aneurysm co-existing with metastatic sellar mass with unknown primary is previously unreported and constitute a rare but difficult to manage association, which has not received proper attention in the literature. as awareness about coexisting aneurysm can aid in proper planning to deal both associated pathology in safest way. if surgery is attempted. however, precise knowledge can avoid injury, if strategy can be planned to deal both lesion in a single operative session. correspondence g.d. satyarthee department of neurosurgery room no. 714 neurosciences centre, aiims new delhi e-mail: drguruduttaaiims@gmail.com references 1. gsponer j, de tribolet n, déruaz jp, et al. diagnosis, treatment, and outcome of pituitary tumors and other abnormal intrasellar masses: retrospective analysis of 353 patients. medicine. 1999;78(4):236–269. 2.yang c , zhang h, zhang s, liu l, ma b, lou j, sun x, zhang b. oculomotor paralysis, postorbital pain, and hypopituitarism as first presentations of metastatic gastric cancer in the pituitary flourished by internal carotid aneurysm: a case report. medicine (baltimore). 2015 dec;94(50):e2317. 3.. roessmann u, kaufman b, friede rl. metastatic lesions in the sella turcica and pituitary gland. cancer. 1970;25(2):478–480. 4.teears rj, silverman em. clinicopathologic review of 88 cases of carcinoma metastatic to the pituitary gland. cancer. 1975;36:216–220. 5.tancioni f, egitto mg , tartara f, aneurysm occurring within a meningioma: case report. british journal of neurosurg !998,12: 588-591. 6.ho khang-loon . neoplastic aneurysm and intracranial hemorrhage . cancer 1982;50:2935-2940. 7. helmer fa. oncotic aneurysm ,case report. j neurosurg. 1976:45:98-100. 8. leonhardt etg, kullenberg k p-g bilateral atrial myxomas with multiple arterial aneurysms-a syndrome mimicking polyarteritis nodosa. the american journal of medicine .1977:62: 792-794. 9.morita a, meyer fb, laws er., jr symptomatic pituitary metastases. j neurosurg. 1998;89:69–73. 10.sioutos p, yen v, arbit e. pituitary gland metastases. ann surg oncol. 1996;3:94–99. 11.. yi hj, kim ch, bak kh, kim jm, ko y, oh sj. metastatic tumors in the sellar and parasellar regions: clinical review of four cases. j korean med sci. 2000;15:363–367 12.yi hj, kim ch, bak kh, kim jm, ko y, oh sj. metastatic tumors in the sellar and parasellar regions: clinical review of four cases. j korean med sci. 2000;15:363–367 13.housepian em, pool jl, a systematic analysis of intracranial aneurysms from the autopsy files of the preshytereian hospital 1914 to 1956. j neuropathol exp neurol 1958; 17; 409-423. 14.teng mm, nasir qadri sm, luo cb, lirng jf, chen ss, chang cy: mr imaging of giant intracranial aneurysm. j clin neurosci 10: 460-464, 2003 15.olsen wl, brant-zawadzki m, hodes j, norman d, newton th: giant intracranial aneurysms: mr imaging. radiology 163: 431-435, 1987 16.mathuriya sn, vasishta rk, dash rj, kak vk. pituitary adenoma and parasagittal mengioma; an unusual association. neurol india 2000;48:72-74. 17.tripathy rp, gupta a, gupta s, kumaran ss, khusu s, balwant ad, co-existence of dual pathology: clinical relevance of proton mrs. neurol india, 2000;48:365-369. 646 | satyarthee et al intracranial internal carotid artery aneurysm with metastatic carcinoma             18.chen han-jung, liou chiawei, chen l. metastatic atrial myxoma presenting as intracranial aneurysms with hemorrhage: casse report. surg neurol,1993:40: 61-64. 19.kadyrov na, friedman ja, nichools da, cohengadol aa, link mj, pieepgras dg. endovascular treatment of an internal carotid artery pseudoaneurysm following transsphenoidal surgery. case report. j neurosurg 2002. ; 96: 624-627. 20.reina a, seal rb, false cerebral aneurysm associated with metastatic carcinoma of the brain,case report. j neurosurg. 1974:41:380-382. 21.kochi n, tani e, yokota m, nakya y. neoplastic cerebral aneurysm from lung cancer, case report. j neurosurg. 1984:60:640-643. 22.hove b, andersen bb, christiansen tm. intracranial oncotic aneurysm from choriocarcinoma,a case report and review of literature. neuroradiol. !990:32 526-528. pia hw, obrador s, martin jg . association of brain tumours and intracranial aneurysms .acta neurochir (wiem ) 1972; 27:189-204. doi: 10.33962/roneuro-2023-037 sellar hematoma as a new potential radiological clue for superior hypophyseal artery aneurysm rupture. a case report samer s. hoz, hosam al-jehani, waeel o. hamouda, mahmood f. al-zaidy, mustafa ismail, aktham o. al-khafaji romanian neurosurgery (2020) xxxiv (1): pp. 211-214 doi: 10.33962/roneuro-2020-037 www.journals.lapub.co.uk/index.php/roneurosurgery sellar hematoma as a new potential radiological clue for superior hypophyseal artery aneurysm rupture. a case report samer s. hoz1, hosam al-jehani2, waeel o. hamouda3, mahmood f. al-zaidy4, mustafa ismail4, aktham o. al-khafaji4 1 department of neurosurgery, university of cincinnati, ohio, usa 2 department of neurosurgery, king fahad hospital of the university, imam abdulrahman alfaisal university, saudi arabia 3 department of neurosurgery, kasr elainy school of medicine, research and teaching hospitals, cairo university, egypt 4 college of medicine, university of baghdad, baghdad, iraq abstract background. in cases of spontaneous subarachnoid haemorrhage (sah) with multiple intracranial aneurysms (mias) detected on angiography, some radiological clues assist in determining the site of a ruptured aneurysm which is bleeding is quite beneficial for the selection of the best treatment strategy. case description. we report a case of a 60 years old patient who presented with spontaneous sah, sellar hematoma, and three different aneurysms detected in angiography. although the right posterior communicating artery (pcoma) aneurysms showed murphy’s teat on angiography intraoperatively, we discovered that the right superior hypophyseal aneurysm (sha) was the source of the index bleeding. both aneurysms were clipped successfully. conclusion. from the preoperative radiological and intraoperative surgical findings, we propose that sellar hematoma on a non-contrast ct scan is a new potential sign to be correlated with superior hypophyseal artery aneurysm rupture. introduction cranial computed tomography (ct) scan without contrast is the most sensitive imaging choice for the diagnosis of aneurysmal subarachnoid hemorrhage (sah), with a sensitivity of 93% within the first 24 hours of onset [14]. however, the ct scan value for determining the primary source of the hemorrhage (i.e., the site of a ruptured aneurysm) has not been demonstrated with some exceptions. examples of such exceptions include unilateral pure sylvian sah and gyrus rectus hematoma as potential clues for middle cerebral artery (mca) and anterior communicating artery (acoma) aneurysms, respectively [4], propped by an accuracy ratio up to 78% of all cases with challenging multiple intracranial aneurysms (mias) [8]. in cases of spontaneous sah keywords sellar hematoma, superior hypophyseal artery aneurysm, multiple intracranial aneurysms corresponding author: mustafa ismail college of medicine, university of baghdad, baghdad, iraq mustafalorance2233@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 212 samer s. hoz, hosam al-jehani, waeel o. hamouda et al. with mias detected on angiography, these clues are paramount to direct the most appropriate management strategy. in literature, we are the first paper demonstrating the presence of sellar hematoma associated with the typical basal sah on an initial ct scan as a new potential clue for superior hypophyseal artery (sha) aneurysm rupture in a case of mias. case scenario a previously healthy, 60-year-old female was admitted with the complaint of a sudden severe headache, photophobia, and drowsy associated with meningismus, with no weakness. a brain ct scan disclosed acute sah with no specific clue except for an apparent sellar hematoma (figure 1 and 2). the cerebral catheter angiography showed three intracranial aneurysms distributed to (right pcoma, sha, and left pcoma aneurysms) (figure 3). figure 1. noncontrast cranial ct scan axial section showed basal subarachnoid hemorrhage with no predominant clue for the location of the ruptured aneurysm. figure 2. non-contrast cranial ct scan axial sections (the same ct in figure 1) showing a hematoma in the sella turcica. according to the angiography, the right pcoma aneurysm was the most probable site of rupture due to having murphy’s teat (daughter cyst). notably, because our country lacked an endovascular facility, the decision was made to manage the case surgically, using the right pterional approach. the patient was in a supine position with the head tilted to the left side, inverted curvilinear skin incision 1 cm posterior to the hairline, and the craniotomy, osteoplastic bone flap, and durotomy were then performed. following the dissection of the sylvian fissure, the supraclinoid internal carotid artery (ica) and the neck of the right pcoma aneurysm were dissected and clipped. then, intra-operatively, we encountered a huge intraoperative rupture from the right sha aneurysm after dissection of the clipped right pcoma aneurysm. eventually, both aneurysms were clipped with no intraoperative or postoperative complications. figure 3. 3d cerebral catheter angiography. (a and b) right ica anterior and left oblique views respectively, showing pcoma (red arrow) and sha (yellow arrow) aneurysms. the pcoma aneurysm has a daughter cyst. the postoperative course was uneventful. we decided to follow the left pcoma aneurysm due to its size and configuration (small, shallow, and wide neck). at a 6-moth follow-up, the patient is conscious without any neurological deficit, and the left pcoma aneurysm is stable. discussion non-contrast brain ct scan is the most sensitive imaging study in cases with sah. the ct scan has 100% sensitivity and specificity when a ct is performed within 6 hours of headache onset; sensitivity is about 93% during 24 hours of onset, 80% at three days, and 50% in the first week [1,4]. ruptured aneurysms constitute the most common etiology for 80% of nontraumatic (spontaneous) sah, with a 0.4-6% prevalence of intracranial aneurysms in the general population [9,13]. multiple intracranial aneurysms (mias) are evident for 15-33.5% of all patients with aneurysms [5]. detecting the primary source of aneurysmal sah is relatively not straightforward and not without difficulty, and this increases the likelihood of re-bleeding in patients 213 sellar hematoma as a new potential radiological clue for superior hypophyseal artery aneurysm rupture with mias. an observational study reported mortality rates for an aneurysmal sah of 10% to 32% within the first day, 27% to 43% during the first week, and 49% to 56% in the first month after onset [9]. most deaths occur due to re-bleeding from the same aneurysm; if untreated, re-bleeding occurs in 15% of patients on the first day and in 40% of people by one month after sah [9]. in cases with mias, the definite indication of a ruptured aneurysm is the angiographic dye extravasation (smoking gun) sign [10]. however, this is an uncommon sign that denotes a grim prognosis [5]. other high-resolution angiographic findings include the area of focal spasm, irregularity in aneurysm shape (murphy's teat), focal mass effect, and shifts in aneurysm shape upon repeat imaging. if none of the above help, the suspected ruptured one is the largest aneurysm [4,10]. while these signs have a large predictive value for bleeding sources, they are relatively rare [10]. ct scanning can provide suggestions about where the rupture is through potential pivotal clues based on the pattern of a sah that has been proven effective in 78% of all cases with mias, especially for mca and acoma aneurysms [4,8,12]. the most evident clue is the thickness of the clot located within the subarachnoid space. occasionally, an apparent focus clot within the sah area represents the aneurysm responsible for hemorrhage [12]. another clue is the hemorrhage distribution pattern, including sah concentrated in the anterior interhemispheric fissure with or without blood in lateral ventricles or within the gyrus rectus suggests acoma aneurysm rupture [8,12]. while blood mainly concentrated in unilateral sylvian fissures is compatible with pcoma or mca aneurysm on that side [12]. likewise, sah predominantly within the prepontine or peduncular cistern suggests a basilar apex or superior cerebellar artery (sca) aneurysms [8]. also, patterns of blood primarily in the fourth and third ventricle indicate lower posterior fossa source, such as posterior inferior cerebellar artery (pica) aneurysm or vertebral artery (va) dissection [8,12]. then, blood primarily within the third ventricle suggests a basilar apex aneurysm [8]. these potential clues are of critical importance for the surgeon to prevent re-bleeding by determining which aneurysm needs urgent surgery and to assist in deciding optimal surgical strategies and procedures. it has been lucid that the most prevalent cause of late re-bleeding is the ruptured aneurysm misidentified at the time of initial surgery [11]. in our case, the aneurysm suspected of being ruptured was the right pcoma aneurysm, as it contained a murphy’s teat. a cerebral ct scan showed acute sah with none of those mentioned above ct clues. ct revealed a concentrated blood pattern within the sella turcica (sellar hematoma) (figure 1 and 2). patients with sha aneurysms are vulnerable to developing mias, as in our case [7]. these aneurysms are uncommon entities and more likely to be ruptured at a relatively smaller size than other intracranial aneurysms [7]. sha aneurysm originates from the supraclinoid segment, where shas that supply the hypophysis and optic chiasm consistently arise from the ica near the lateral aspect of the sella. mostly sha aneurysms fall into two classifications that are divided into sellar and supraclinoid variants. the sellar variant is directed medially over the diaphragma sellae, while the paraclinoid variant projects inferomedially. these projections are directed by the size of the supraclinoid ica segment and the height of the lateral sellar wall [1,8]. the second classification falls within the sellar variant itself, which has two different varieties: suprasellar or parasellar [6]. the rupture of a parasellar aneurysm typically presents with sah [1]. in our patient, the sha aneurysm was a parasellar variant lying over the sellar area, which was the source of sellar hematoma in the initial ct scan. the sudden massive intraoperative rupture of the right sha aneurysm affirmed that the initial ruptured aneurysm was the same aneurysm, which we did not take seriously despite the clear sign of sellar hematoma. in literature, here, we are the first to report the concentrated blood pattern within the sella turcica (sellar hematoma) in non-contrast brain ct scan, as a new potential radiological clue to be correlated in cases with sha aneurysm rupture. to our knowledge, cranial ct scanning can show sellar hematoma, and sah from an sha aneurysm rupture appears as high-density blood concentrated within the sellar area and suprasellar subarachnoid spaces. with or without typical star shape sah through major cerebral fissures [8,10]. in contrast, pituitary apoplexy (pa) is a rare and potentially severe clinical condition caused by neurologic deterioration as a result of a sudden expansion of a mass within the sella turcica, usually due to an acute 214 samer s. hoz, hosam al-jehani, waeel o. hamouda et al. ischemic infarction or hemorrhage of the pituitary gland [2,10]. on ct scan, it appears an intrasellar mass with hemorrhagic components, seen in 80% of pituitary apoplexy cases as a patchy or hyperdensity in ct scan within a pituitary lesion, leading to sellar enlargement in up to 94 % of cases [2,3]. so these radiological signs of pa, including heterogeneous pituitary mass, are utterly different from clear sellar hematoma with typical basal sah, as in our case. so the pa can be excluded from the differential diagnosis list for patients with sha aneurysms and mias. in summary, the sellar hematoma on the initial ct imaging is a possible milestone sign that hands over a significant indication for sha aneurysm rupture to answer the question of which aneurysm rupture is responsible for this sah in cases with mias. conclusion in cases of spontaneous subarachnoid hemorrhage with imaging showing multiple intracranial aneurysms, the presence of a radiological clue for the source of bleeding in an initial ct scan is quite beneficial for the selection of the best treatment strategy. sellar hematoma on a non-contrast ct scan is a new potential sign to be correlated with superior hypophyseal artery aneurysm rupture. abbreviations ct; computed tomography, sah; subarachnoid hemorrhage, mca; middle cerebral artery, acoma; anterior communicating artery, mias; multiple intracranial aneurysms, pcoma; posterior communicating artery, ica; internal carotid artery, sca; superior cerebellar artery, pica; posterior inferior cerebellar artery, va; vertebral artery, pa; pituitary apoplexy. references 1. day al. aneurysms of the ophthalmic segment. a clinical and anatomical analysis. j neurosurg 1990;72(5):677– 691. 2. dubuisson as, beckers a, stevenaert a (2007) classical pituitary tumour apoplexy: clinical features, management and outcomes in a series of 24 patients. clin neurol neurosurg 109:63–70. 3. flanagan ep, hunderfund al, giannini c, meissner i. addition of magnetic resonance imaging to computed tomography and sensitivity to blood in pituitary apoplexy. arch neurol 2011;68:1336-7. 4. greenberg ms. handbook of neurosurgery. 9th ed: thieme medical publishers; 2020. 5. hadjiathanasiou a, schuss p, brandecker s, welchowski t, schmid m, vatter h, et al. multiple aneurysms in subarachnoid hemorrhage identification of the ruptured aneurysm, when the bleeding pattern is not self-explanatory development of a novel prediction score. bmc neurology 2020;20(1):70. 6. hanak, brian w., et al. "cerebral aneurysms with intrasellar extension: a systematic review of clinical, anatomical, and treatment characteristics: a review." journal of neurosurgery 116.1 (2012): 164-178. 7. hornyak, m., et al. "ruptured intrasellar superior hypophyseal artery aneurysm presenting with pure subdural haematoma: case report." interventional neuroradiology 10.1 (2004): 55-58. 8. karttunen ai, jartti ph, ukkola va, et al. value of the quantity and distribution of subarachnoid haemorrhage on ct in the localization of a ruptured cerebral aneurysm. acta neurochir (wien). 2003; 145:655–61. 9. locksley hb. natural history of subarachnoid hemorrhage, intracranial aneurysms, and arteriovenous malformations. based on 6368 cases in the cooperative study. j neurosurg 1966;25:219–239. 10. nehls dg, flom ra, carter lp, spetzler rf. multiple intracranial aneurysms: determining the site of rupture. j neurosurg 1985;63(3):342-348. 11. perry jj, stiell ig, sivilotti ml, bullard mj, emond m, symington c, et al. sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. bmj. 2011 jul 18. 343:d4277. 12. provenzale, james m., and lotfi hacein-bey. "ct evaluation of subarachnoid hemorrhage: a practical review for the radiologist interpreting emergency room studies." emergency radiology 16.6 (2009): 441-451. 13. rinkel g, djibuti m, algra a, van gijn j (1998) prevalence and risk of rupture of intracranial aneurysms: a systematic review. stroke 29(1):251–256. 14. suarez ji, tarr rw, selman wr. aneurysmal subarachnoid hemorrhage. n engl j med. 2006 jan 26. 354(4):387-96. doi: 10.33962/roneuro-2022-056 cervical chondrosarcoma: a critical review with an illustration of a rare technically challenging case anil kumar sharma, prashant raj singh, satish satpute, nitish nayak, ashish gupta, raghavendra kumar sharma, nitin m nagarkar romanian neurosurgery (2022) xxxvi (3): pp. 334-341 doi: 10.33962/roneuro-2022-056 www.journals.lapub.co.uk/index.php/roneurosurgery cervical chondrosarcoma: a critical review with an illustration of a rare technically challenging case anil kumar sharma2, prashant raj singh2, satish satpute2, nitish nayak2, ashish gupta2, raghavendra kumar sharma1, nitin m nagarkar2 1 a.i.i.m.s. jodhpur, rajasthan, india 2 a.i.i.m.s. raipur, c.g., india abstract chondrosarcoma of the cervical spine is an extremely rare tumour. the indolent course and neglected behaviour of the patient often give enough time for tumour expansion. the surgical management of these types of tumours is challenging. en bloc resection is a proven ideal treatment but it is not always feasible in this region because of the proximity to vital neurovascular structures which explains the recurrence and poor prognosis of this tumour. the role of radiation and chemotherapy in these tumours is limited. we are highlighting unique huge cervical chondrosarcoma which is not mentioned in literature and its management along with a review of 34 cases, published so far. introduction chondrosarcoma (chs) comprises a heterogeneous group of cartilage matrix producing neoplasms.[1] after myeloma and osteosarcoma, chondrosarcoma is the third most common primary malignancy of bone.[2] the majority of these types of tumors are benign and metastasis occurs rarely. incidence of chs of the spine is 7-12% of all primary spine tumor with male predominance and usually presents at the third to fifth decade of life.[3] most commonly it occurs in the thoracic spine (60%) followed by lumbar (20-39%) and less frequently in the cervical spine (19-20%).[4] these slow growing insidious lesions are often voluminous at the time of discovery and diagnosis is usually delayed which pose difficulty in management. surgical treatment is ideal for these types of tumors.[5,6] however, especially in the cervical spine, due to the proximity of tumors with vitals neurovascular structures and the intricate anatomy of this region , these tumors cause great difficulty for a surgeon. we discuss a case of unique huge cervical chondrosarcoma of c3 to c5 and to the best of our knowledge, such a large tumor has not been reported in the literature. successful complete resection of the tumor was achieved using combined posterior to anterior approach with 360 degree stablisation. we also present review of the literature of 34 cases of cervical chondrosarcomas published so far. keywords cervical chondrosarcoma, treatment, recurrence, prognosis corresponding author: raghavendra kumar sharma a.i.i.m.s. jodhpur, rajasthan, india sdr.raghavendra@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 335 cervical chondrosarcoma case description a 50-year-old male patient presented in our department with painless, progressive enlarging right side neck swelling for the last 5 years and weakness of all 4 limbs for the last 4 months. he was unable to walk and wheelchair-bound for the last 2 months. he also had bladder and bowel incontinence. on local examination, he had approx 8x8 cm, nontender, hard, immobile swelling over the right side of the neck,between mastoid and clavicle (figure 1). neurologically he had spastic quadriparesis with exaggerated deep tendon reflexes and ankle clonus . the sensation was otherwise intact. paradoxical respiration was absent and single breath count was 15 and breath-holding time was 17 seconds. his gag reflex was intact and had no other significant neurological deficit. figure 1. (a,b) preoperative photograph of patient which shows a mass on the right side of neck; (c) postoperative photograph shows utility incision by white arrow on right side of neck with no apparent neck mass. figure 2. preoperative magnetic resonance imaging of cervical spine (a) axial; (b,c) sagittal; (d) coronal t2 weighted images showing large hyperintense well defined lobulated predominantly exophytic lesion involving right side of vertebra with significant compressing and pushing the spinal cord on left side; (e) axial gre sequence shows punctuate blooming foci inside the lesion. noncontrast computed tomography (ct) of cervical spine suggestive of the osteolytic lesion filling on the right side of the neck with c3-c5 bony destruction on the side of the tumor with irregularly mottled calcification. the vertebral artery could not be visualized on ct angiography on the right side and the internal carotid artery was pushed anteriorly (figure 3). magnetic resonance imaging (mri) of the neck revealed t1 hypointense, t2 hyperintense and punctuate blooming foci on gre sequence with large well defined lobulated predominantly exophytic lesion arising from the body and right lateral posterior arch of c3 and c4 vertebra (figure 2). large 8x7x7cm exophytic extramural component of the mass on right paravertebral space found which was displacing the adjacent muscles peripherally. there was intraspinal epidural extension of tumor mass through c3-c5 neural foramina into the spinal canal and significant cord compression. a metastatic workup was done to rule out any other primary neoplastic focus or metastasis. f-18 fdg whole-body positron emission tomography with contrastenhanced ct was performed that showed increased uptake of radiotracer on the right side of the neck with no evidence of metastasis. surgical technique because of the huge tumor and multicompartmental involvement, combined approach with ent specialist were planned. due to the destruction of the c3-c4 vertebrae, the posterior cervical approach was used first then it was decided to go from anterior with the help of ent surgeons. the patient was first placed prone and head kept in a 3-pins mayfield fixator with the neck in the neutral position. for prolong spine surgery in a prone position, we avoid horse-shoe fixator because it may cause postoperative vision loss (povl) .[7] a skin incision was made from inion to the c7 vertebrae. soft-tissue dissection was done subperiosteally. posterior vertebral elements were exposed from c1c6 up to the lateral mass laterally but on right side lamina and lateral mass were not identified from c3c4 due to destruction by tumor tissue. the tumor was identified with major bulk on the right side from c3-c4. the tumor was well capsulated, soft, and moderately vascular. the tumor invaded the spinous 336 anil kumar sharma, prashant raj singh, satish satpute et al. process and right side of the lateral masses/laminae/transverse process from c3-c4. tumor tissue which was approached from behind was debulked in piecemeal. en-bloc excision was not possible because the tumor encased the vertebral artery and spinal cord with nerve roots. even tiny pieces of the tumor were excised to prevent a recurrence. the cervical spinal cord which was severely compressed by the tumor was decompressed. all nerve roots were preserved and freed from surround soft tissues. bilateral c1 lateral mass, c2 pedicle screws were inserted. left side c35 and right side c5 lateral mass were placed and all metallic implants were connected with rods. the wound was closed in anatomical layers and position changed from prone to supine after placing the patient’s neck on the hard cervical collar. in supine and neck neutral position, using utility neck incision [8] begins “anteriorly at the level of the cricoid and carried laterally to the posterior border of the sternocleidomastoid, continuing its gradual curve upward to end behind the prominence of mastoid process”.the sternocleidomastoid muscle was divided to ease for tumor excision. ica was identified and separated with the tumor capsule. the major bulk of tumor tissue along with the capsule was excised from the different compartment of the neck to create a large cavity. this anterior tumor cavity joined with the cavity made posteriorly from the previous approach. after dissecting longus colli over the c3 and c4 vertebral body, anterior tubercles were exposed. c2-3, c3-4, and c4-5 d i s c e c t o m y w e r e p e r f o r m e d a n d p o s t e r i o r longitudinal ligament was also excised. partially destroyed vertebral bodies of c3 and c4 were excised in piece-meal fashion with the help of rongeurs. resection was performed carefully to avoid any remnants of the tumor. after preparing endplates of c2 and c5, a corpectomy titanium mesh cage was fixed in between vertebral bodies. artificial bone graft placed in the mesh cage to enhance the fusion. corpectomy screws in c2 and c5 were also inserted to achieve fixation. after careful inspection of tumor residuals and bleeding spots, wound closed in anatomical layers. just after surgery patient was neurologically the same as before, he was advised to wear a hard cervical collar. before discharge on the fifth day, the patient developed signs of recovery in the form of a reduction in spasticity. histopathology his tolo gically this tumo r turn out to be well differentiated conventional chs. pathologically it is characterized by well circumscribed cartilaginous tumor with increased cellularity of chondrocytes with occasional bi to multinucleation. moderate nuclear pleomorphism and cytoplasmic vacuolization within the chondroid matrix (figure 5). follow-up the patient was followed up clinically after 1, 3 and 6 months. the patient showed gradual improvement in his motor power of limbs. after a couple of months, he started walking and became independent after 3 months. now the power in his upper and lower limbs is 4+/5 on mrc grade with improvement in bladder and bowel continence. as per our protocol, noncontrast computed tomography (ncct) scan of the cervical spine was performed postoperatively to know the position of implants (figure 4). table 1. cervical chondrosarcoma: review of 34 cases from literature sn author / year case no age/se x level surgery grade ‡ adjuvant radiotherapy follow up in months outcom e recurrenc e/duration in months 1 arlen/19702 1 1 56y/m c5 str ns rt 36m death y/6m 2 42y/m ns str ns n 60m death y/ns 2 blaylock/ 197622 1 43y/m c2 gtr low grade n 12m alive n 3 wronski/ 197423 1 22y/m c5-6 str well diff rt 2m alive n 4 yang /20125 1 29y/m c7 str low grade n 46m death y/21m 337 cervical chondrosarcoma 2 32y/m c6-7 en bloc resection low grade n 140m alive n 3 42y/m c6 str low grade n 36m death y/24m 4 22y/m c7 gtr high grade rt 92m alive n 5 67y/m c3 gtr low grade rt 37m alive n 5 york / 19996 1 64y/m c4 str average grade n 7m death n 2 54y/m c7 gtr/gtr# average grade rt/n 67.2m alive y/(3.7m/ 1.2m) 3 51y/f c7 str/str# high grade n/rt 10m death y/(4m/n) 4 64y/f c4 str/str/str/st r† low grade rt 3.5m death y/ (9/6/6/n) 6 tessitore/ 200624 1 22y/f c7 str clear cell proton beam therapy 12m alive n 7 ohue/ 199525 1 48y/m c5-6 gtr low grade n 36m alive n 8 simsek/ 200916 1 18y/m c3 gtr ns n 12m alive n 9 foweraker / 200726 1 43y/f c1 str well differ rt 107m alive n 10 dejean / 199827 1 64y/m c7 str average grade n 30m alive y/24m 11 finn / 198428 1 45y/m c7 gtr low grade n 228m alive n 2 64y/m c4 gtr average grade n 8m death chf n 12 merchant / 201429 1 30y/m c5-7 gtr low grade n 12m alive n 13 boriani/ 200015 1 13y/m c7 en bloc resection ns n 236m alive n 2 31y/m c5-7 en bloc resection ns n 40m alive n 14 strike / 201130 1 60y/f c2-4 gtr ns n 24m death due to pul mets ns 2 37y/ f c4c5 str ns proton beam therapy 48m death due to pul mets ns 3 79y/m c5c6 gtr ns n 48m alive n 4 46y/m c1c2 gtr ns n 78m alive n 15 sakayama/ 200431 1 58y/m c2 str average grade n 36m alive y/12m 16 gebhart/ 200832 1 30y/m c4 en bloc resection low grade n 132m alive n 17 camins/ 197833 1 20y/f c5-6 gtr low grade rt 1m alive n 18 shives/ 198910 1 33y/f c4 str average grade rt 14m death due to disease ns 338 anil kumar sharma, prashant raj singh, satish satpute et al. 2 58y/ m c7 str average grade n 60m death due to disease ns 3 35y/ f c7 str low grade rt 233m death due to disease ns 4 59y/m c5 str low grade n 43m death due to disease ns nsnot specified; m-male, f-female; gtrgross total resection, strsubtotal resection; grade: nsnot specified, rt-radiotherpay, n-no radiotherapy, mmonths; recurrence (yyes, n-no recurrence ), nsnot specified; # 2 surgical procedures in the same patient; † 4 surgical procedures in the same patient; ‡ histological grade according to thomson and turner-warwik11 (low, average and high grade). figure 3. preoperative computed tomography angiography (a) sagittal view shows mottled calcification within large osteolytic lesion with anteriorly displaced carotid artery; (b) coronal view shows dominant left vertebral artery without visualization of right vertebral artery with partial destruction of multiple vertebrae. figure 4. postoperative computed tomography of cervical spine (a) coronal view showing metallic construct consist of bilateral c1 lateral mass and c2 pedicle screws, left side c3,5,6 and right side c6 lateral mass screws fixation with rods; (b) sagittal view showing distractable interbody cage in c2-c5 vertebral space with plate/screws. figure 5. h&e stain 100x: shows the well circumscribed cartilaginous tumor with increased cellularity of chondrocytes with occasional bi to multinucleation, moderate nuclear pleomorphism and cytoplasmic vacuolization within the chondroid matrix. discussion spinal chondrosarcoma is a rare entity, out of the vertebral column cervical spine is the least common site affected.[3,5,6] we reviewed 34 cases of cervical chondrosarcomas in literature published by 18 authors so far (table 1). demographically mean age of presentation is 43.5 years and males are more commonly affected than females (25:9). presenting feature of chs patients showed indolent growth pattern and most common presenting symptom is local site pain.[6] neurological features are not uncommon and present as myelopathy or radiculopathy.[9] as the tumor grows further from the vertebral body or posterior elements, it appears as a palpable mass in the neck or back. yang et al reported in his study that the duration between the symptoms and diagnosis ranges from 3-60 339 cervical chondrosarcoma months.[5] our patient had a history of 5 years, the reason for this long-duration presentation was ignorance. the majority of tumors arise from the normal bone without any association of any benign cartilaginous pathology.[10] various allelic losses and nonrandom genetic aberration occur in a majority of tumors (70%), several mutations are associated with malignant degenerations of chondroma which includes amplification of c-myc oncogene and a gain of chromosome 8. the loss of chromosome 6 and the gain of 12q12 also related to high-grade chs. [3,4] yang et al reported that the tumor originated most commonly from the posterior part of the vertebral bodies (73.3%) as compared to posterior elements of the vertebra. extraosseous paravertebral involvement also occurred in the majority of cases in his case series.[5] our case review showed that the c5-7 vertebral region is most commonly affected by the tumor. however, no specific cervical level for common occurrence is mentioned in literature. radiological diagnosis includes characteristics ct findings of bony destruction with irregularly mottled calcification with low attenuation of the mass lesion due to the water content of the cartilage matrix. mri is also very useful to know the extent of soft tissue invasion. t1-weighted images showed hypointense and t2weighted demonstrate hyperintense images of a lesion with heterogeneous or peripheral ring type of enhancement on intravenous gadolinium injection.[3] increased uptake of radiotracer in the region of tumors is often shown in bone scanning. despite the lower proportion of the malignant nature of chs, pet ct is a useful tool to diagnose the extent of disease spread. it helps in the planning of management. pet ct did not demonstrate any secondary deposition or evidence of metastasis in our patient. previously thomson and turner-warwik classified the chs histologically into low, average and high grade.[11] the world health organization (who) described chs as nonmeningothelial, mesenchymal neoplasm.[12] based on histologic features such as tumor cellularity, mitosis nuclear atypia, and stromal content, the grading system is used by who. it ranges from grade i(low grade) to grade iv (high grade). one of the most important prognostic indicators of chs is who grade. in low-grade chs, 10 years survival is 90% where it is 30-40% in high grade.[4] in our review of cases we also found 47% of cases were low grade chs which was the most common histological type among them. chondrosarcomas are also classified into several subtypes based on stereotypic histologic features which include conventional, mesenchymal, clear cell and dedifferentiated types.[13] conventional chs is the most common subtypes (around 80%) and almost all of them are of low grade. malignant degeneration of low-grade conventional chs gives rise to a dedifferentiated type. mesenchymal chs is very much similar to dedifferentiated chs and it has a poor prognosis with a 5-year survival rate of 50%. finally, clear cell chs have a better prognosis than mesenchymal or dedifferentiated subtype (mcloughlin).[3] in tumor management, histopathological diagnosis is required. percutaneous ct guided biopsy can be performed in this type of tumor but it requires careful interpretation. lis et al reported 24% false-negative results in these types of sclerotic lesion.[14] hence it was decided to undergo the excision of the tumor without a biopsy. due to the ineffectiveness of conventional chemotherapy and radiotherapy, surgical management in the form of en-bloc resection is the only ideal method for the treatment of chs.[5,6] out of 34 patients in case review, en bloc resection was achieved in 4 patients. gross total resection was associated with a better outcome as compared to str. gtr performed in 13 and str in 17 patients. local recurrence is reported in 9 patients, out of which 88.9% associated with str. mean follow up was 58.4months. out of 14 deaths, 12 deaths (85.7%) are recorded among those patients who underwent str of the tumor. boriani et al. reported the outcome difference of en-bloc resection and intralesional excision of chs in his study.[15] he found no local recurrence in 9 patients who were treated with en-bloc resection with wide or marginal margin whereas, there was local recurrence in all 13 patients treated with piecemeal or intralesional excision. however, due to the proximity of vital structures and technical obstacles like bleeding or spinal cord injury, it is not always possible to secure en-bloc-resection. many case report also suggests that circumferential excision of cervical chs could provide preserved neurological status with a long recurrence-free survival period.[16,17] preoperative planning with a multidisciplinary approach is very essential in these 340 anil kumar sharma, prashant raj singh, satish satpute et al. types of huge tumors. because of the destruction of long segment vertebral column, postoperatively spinal instability would be expected as experienced by many authors, hence tumor excision along with reconstruction was decided. [16,18] because of huge size of tumor and restriction of neck movements, intubation itself was a challenging task. initially we tried en-bloc resection but due to nonvisualization of vertebral artery in imaging which was untraceable even on intraoperative ultrasound and circumferential involvement of spinal cord and nerve roots, enbloc surgical decision was not feasible, hence piecemeal excision of tumor tissue along with its capsule was performed. we successful preserved all nerve roots without injury to major vessles. follow up radiology is required to detect the local tumor recurrence or distant metastasis and it is decision making in future adjuvant therapy if possible. most studies reported that the adjuvant chemotherapy (ct) and radiotherapy (rt) has only limited role in chs treatment.[5,6,15,19] our case review also supports the limited role of rt as adjuvant therapy. rt received in 13 patients out of which 6 patients did not survive. this ineffectiveness may be due to that chemo or radiotherapy both acts on fast dividing cells and chondrosarcoma are slow growing tumors with low fractions of dividing cells. in addition to slow grade, chondrosarcomas have a rich extracellular matrix and poor vasularity, which produce hindrance of chemotherapy drug penetration.[5] hence adjuvant therapy is not included in standard treatment recommendation.[2] nevertheless, high dose radiotherapy or proton beam therapy may be useful to slow tumor growth and tumor recurrence but the long term results of this therapy are still unknown. gwak et al reported that hypofractionated cyberknife stereotactic radiation therapy can potentially provide promising results in these types of radioresistant tumors.[20] despite the massive size of tumor and involvement of large areas of the neck and cervical spine, we successfully achieved the goal of surgery by doing complete tumor excision and restored the spine integrity by 360-degree spinal fixation. our case is unique from all the cases reported in the literature that no case exists with so much extensive involvement of the cervical spine. conclusion huge cervical chondrosarcoma is rare and usually, these massive tumor presents with neurological deficits. management of neglected cervical chondrosarcoma is technically challenging but adequate anatomical knowledge and detailed surgical planning in the form of a multimodality approach can prevent permanent disability and increase disease-free survival period. references 1. fletcher cd, mertens f, unni kk. world health organization classification of tumours: pathology and genetics tumours of soft tissue and bone. iarc publications; 2002. 2. krol ad, taminiau ah, bovée jv. the clinical approach towards chondrosarcoma. the oncologist 2008;13:320– 329. 3. mcloughlin gs, sciubba dm, wolinsky j-p. chondroma/chondrosarcoma of the spine. neurosurgery clinics of north america 2008;19:57–63. 4. chow wa. update on chondrosarcomas. current opinion in oncology 2007;19:371–376. 5. yang x, wu z, xiao j, feng d, huang q, zheng w, et al. chondrosarcomas of the cervical and cervicothoracic spine: surgical management and long-term clinical outcome. journal of spinal disorders & techniques 2012;25:1–9. 6. york je, berk rh, fuller gn, rao js, abi-said d, wildrick dm, et al. chondrosarcoma of the spine: 1954 to 1997. journal of neurosurgery: spine 1999;90:73–8. 7. kumar a, chaturvedi j, deora h. unilateral visual loss after spine surgery: lesson to be learnt from unexpected devastating complication. interdisciplinary neurosurgery 2019;17:66–68. 8. grandon el, brintnall es. a utility neck incision. archives of otolaryngology head and neck surgery 1960;72:743– 5. 9. yünten n, calli c, zileli m, üstün ee, şener rn. chondrosarcoma causing cervical neural foramen widening. european radiology 1997;7:1028–1030. 10. shives tc, mcleod ra, unni kk, schray mf. chondrosarcoma of the spine. j bone joint surg am 1989;71:1158–65. 11. thomson ad, turner-warwick rt. skeletal sarcomata and giant-cell tumour. j bone joint surg br 1955;37b:266–303. 12. paulus w. mesenchymal, nonmeningiothelial tumours. pathology and genetics tumours of the nervous system 2000; 13. coons s. pathology of tumours of the spinal cord, spine and paraspinous soft tissue. spinal cord and spinal column tumours thieme medical publishers, stuttgart 2006;49–51. 14. lis e, bilsky mh, pisinski l, boland p, healey jh, o’malley 341 cervical chondrosarcoma b, et al. percutaneous ct-guided biopsy of osseous lesion of the spine in patients with known or suspected malignancy. american journal of neuroradiology 2004;25:1583–1588. 15. boriani s, de iure f, bandiera s, campanacci l, biagini r, di fiore m, et al. chondrosarcoma of the mobile spine: report on 22 cases. spine 2000;25:804–812. 16. vertebra çts. circumferential total resection of cervical tumors: report of two consecutive cases and technical note. turkish neurosurgery 2009;19:153–158. 17. alpaslan am, acaroglu re, kis m. three-stage excision of recurrent cervical chondrosarcoma. archives of orthopaedic and trauma surgery 1993;112:245–246. 18. kumar a, nehete l, chaturvedi j, hussain n. large giant cell tumor at dorsal spine with spinal instability. the journal of spinal surgery 2018;5:174–7. 19. fisher cg, versteeg al, dea n, boriani s, varga pp, dekutoski mb, et al. surgical management of spinal chondrosarcomas: spine 2016;41:678–85. 20. gwak h-s, yoo h-j, youn s-m, chang u, lee dh, yoo s-y, et al. hypofractionated stereotactic radiation therapy for skull base and upper cervical chordoma and chondrosarcoma: preliminary results. stereotactic and functional neurosurgery 2005;83:233–243. 21. arlen m, tollefsen hr, huvos g, marcove rc. chondrosarcoma of the head and neck. 1970;120:5. 22. blaylock russl. chondrosarcoma of the cervical spine. j neurosurg 1976;44:4. 23. wronski j, bryc s, kaminski j, chibowski d. chondrosarcoma of cervical spine causing compression of the cord. journal of neurosurgery 1964;21:419–21. 24. tessitore e, burkhardt k, payer m. primary clear-cell chondrosarcoma of the cervical spine: case illustration. spi 2006;4:424. 25. ohue s, sakaki s, kohno k, nakagawa k, kusunoki k, todd h, et al. primary spinal chondrosarcoma localized in the cervical spinal canal and intervertebral foramen. neurologia medico-chirurgica 1995;35:36–39. 26. foweraker kl, burton ke, jena r, jefferies sj. high dose photon radiotherapy in the management of chordoma and chondrosarcoma of the skull base and cervical spine. clinical oncology 2007;19:s28. 27. dejean o, hardy ph, stromboni m, lortat-jacob a, benoit j. chondrosarcoma of the cervical spine: a case report. eur j orthop surg traumatol 1998;8:37–9. 28. finn dg, goepfert h, batsakis jg. chondrosarcoma of the head and neck. the laryngoscope 1984;94:1539–44. 29. merchant s, mohiyuddin sma, rudrappa s, deo rp, a s, menon lr. cervical chondrosarcomarare malignancy: a case report. indian j surg oncol 2014;5:293–6. 30. strike sa, mccarthy ef. chondrosarcoma of the spine: a series of 16 cases and a review of the literature. iowa orthop j 2011;31:154–9. 31. sakayama k, kawatani y, kidani t, sugawara y, miyazaki t, fujibuchi t, et al. dumbbell-shaped chondrosarcoma that primarily developed in the cervical spine: a case report. journal of orthopaedic science 2004;9:166–70. 32. quiriny m, gebhart m. chondrosarcoma of the spine : a report of three cases and literature review. 2008;74:6. 33. camins mb, duncan aw, smith j, marcove rc. chondrosarcoma of the spine. spine 1978;3:202–9. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-016 microbiota gut-brain axis and neurodegenerative disease. a systematic review on alzheimer’s disease, amyotrophic lateral sclerosis and parkinson disease poluyi edward oluwatobi, imaguezegie grace ese, poluyi abigail oluwatumininu, morgan eghosa romanian neurosurgery (2020) xxxiv (1): pp. 116-122 doi: 10.33962/roneuro-2020-016 www.journals.lapub.co.uk/index.php/roneurosurgery microbiota gut-brain axis and neurodegenerative disease. a systematic review on alzheimer’s disease, amyotrophic lateral sclerosis and parkinson disease poluyi edward oluwatobi1, imaguezegie grace ese2, poluyi abigail oluwatumininu3, morgan eghosa4 1 department of life science, clinical neuroscience, university of roehampton, london, united kingdom 2 lagos university teaching hospital, idi-araba, surulere, lagos, nigeria 3 college of medicine, university of lagos, nigeria 4 ambrose alli university, ekpoma, edo, nigeria abstract this review highlights the microbiota gut-brain axis and neurodegenerative diseases excluding studies on animal models. gut microbiota is capable of modulating some brain activities via the microbiota gut-brain axis. a bidirectional communication exists between the gastrointestinal (gi) tract and the central nervous system (cns) in the microbiota gut-brain axis. gut dysbiosis has been linked to neurodegenerative diseases as a result of the imbalance in the composition of its microbiota, which has a damaging effect on the host’s health. the association between the role and mechanism of cns disease and gut microbial is yet to be fully explored. although some studies have shown a positive relationship between a rich diverse microbial community and the brain of the host, and a negative relationship between microbial dysbiosis, intestinal infection and human brain health, our knowledge, however, is limited due to the inability to identify the major players in this heterogeneous microbial community. introduction clinicians and biomedical researchers have shown great interest in the role of gut microbe function and the central nervous system (cns), mainly in the modulation of cholecystokinin. however, this has been extended to a generalized description; the microbiota gut –brain axis especially in its link to neurodegenerative disease.1 the human body and its microbial community such as the skin, vaginal mucosa, oral mucosa and most importantly the gut, co-exist in a symbiotic relation keywords gut dysbiosis, central nervous system, gastrointestinal tract, enteric nervous system, neuroimmune system, neuroendocrine system, autonomic nervous system (ans) corresponding author: poluyi edward department of life science, clinical neuroscience, university of roehampton, london, united kingdom eddiepolz@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 117 microbiota gut-brain axis and neurodegenerative disease ship. this relationship plays a vital role in health and neurodegenerative diseases.2 microbiome is inherited maternally during vaginal delivery through the vaginal fluid enriched with microbiota. this becomes a major player of immune defense and eventually becomes modified to suit the individual’s unique composition.3,4 microbiota concentration is highest in the gut of the human body.5 this can be a source of energy for cells as they provide essential micro nutrients such as thiamine, vitamins a, b, d and k. they also provide nutrients in form of short chain fatty acids (scfas) like acetate, propionate, and butyrate; as the ultimate energy source for colonocytes. when scfas like butyrate, acetate, and propionate are stimulated, it could result in an increased production of immunoglobulin (igg).6 gut microbiota also serves as a barricade between humans and their environment especially in the protection of environmental hazards3 and when it is disease-free, can prolong the lifespan of humans.6 disruptions of gut microbiota barrier can lead to many diseases.7 it was previously considered stable and unique for each individual but has now been reported to have long lasting changes.1 this could be secondary to pathophysiological disruption of short intraluminal regulatory loop that leads to major dysfunction of various cells and microflora, thus, affecting the enteric nervous system(ens) within the submucosal and muscularis layers of the colon.8 gut dysbiosis has been linked to neurodegenerative diseases as a result of the imbalance in its composition which alters and causes damaging effect on the host’s health.9 the aim of this review is to highlight the microbiota gut-brain axis and functional linkages to neurodegenerative diseases such as alzheimer’s disease (ad), amyotrophic lateral sclerosis (als) and parkinson disease (pd), excluding animal models. discussion communication between gut microbiota and the development of the central nervous system (cns) microbiota which consists of bacteria, viruses, fungi and other microorganisms can alter adult hippocampus neurogenesis (ahn), thus affecting the pathogenesis of symptoms of diseases of cns.7,10 it helps in the permeability and maintenance of the blood brain barrier (bbb) and is important in the maturation of glia cells of the cns. the absence of a complex host microbiota could result in an altered glial cells number, a decrease in permeability and could halt the development of the blood brain barrier, thus, causing an impaired immune response resulting in cns disease.11 although, invasive pathogen by microbes is not the only route to the aetiology of neurodegenerative diseases, it has a systemic impact on the microbiota community via the enteric nervous system, immune system, blood stream, intercellular signaling and the vagus nerve.5 the microbiome gut-brain axis the association between the role and mechanism of cns disease and gut microbial have yet to be fully explored.11 a bidirectional communication exists between the gastrointestinal (gi) tract and the central nervous system (cns) in the microbiota gutbrain axis. this is effective under physiological conditions in immune defense, digestive system modulation, perception and sensory response to visceral stimuli, secondary to its incorporation to the cns, neuroendocrine and neuroimmune systems, autonomic nervous system (ans) and enteric nervous system (ens).3 studies have reported four key section to the gut-brain axis, these include: activation of the immune defense, neuroendocrine pathways regulation, autonomic sensorimotor connections and lastly, the interaction between the blood brain barrier and gut microbiota metabolites.2 microbially derived molecules such as short-chain fatty acids (scfas), secondary bile acids, and tryptophan metabolites mediate the communication of microbes and the cns, although cns modulation via neuroimmune and neuroendocrine mechanisms interacts with enterochromaffin cells, mucosal immune system and enteroendocrine cell and sometimes enters the systemic circulation and penetrates the blood-brain barrier, it still remains difficult to ascertain if they induce responses only or get to the brain directly via long-distance neural signaling with vagal and/or afferents from the spinal cord.12 scfa are the main microbial mediators in the gut–brain axis.2 scfa are released from action of microbiota in the gut which are further metabolized by intestinal absorption and finally removed through urination.11 the gut microbiome harbours 150 times more genes than the human genome.2 they are 118 poluyi edward oluwatobi, imaguezegie grace ese, poluyi abigail oluwatumininu et al. heterogeneous group of bacterial species, fungi and viruses found in the gastrointestinal tract having a symbiotic relationship with the human host. the microbiome plays an important function in metabolism, blood-brain barrier integrity, immune defense, secretion, maintaining homeostatic balance of barrier integrity and coordinating the transfers of signals through primary afferent pathway of the vagus nerve to the cns via the gut-brain axis. the vagus nerves serves as the primary afferent pathway for various factors influencing the formation of microbiota, these include: medications, lactation, ingested meal and parturition.11 the use of functional imaging, for example, functional magnetic resonance imaging (fmri) and positron emission tomography (pet) revealed resting brain function alteration in patients with functional gastrointestinal disorders, via the possibility of gutbrain axis dysfunction.13 intriguingly, the concept that microbiome influences the gut-brain axis may seem debatable but it is used routinely by clinician to treat patients. for instance, the use of oral antibiotics medication and laxatives for treatment of patients with altered mental state secondary to hepatic encephalopathy.1 figure 1. bidirectional interactions of four key sections in the gut-brain axis12. the gut microbiota in neurodegenerative disorders the aetiology of most neurodegenerative diseases are multifactorial and speculative, there is possibility that the apotheosis of these mechanism of gut microbiome-host symbiotic relationship contribute to a large extent to the disease pathogenesis in the genetically-predisposed.14 microbiota research on neurodegenerative diseases is still in the infancy stage, interestingly, recent studies have linked the potential role of the gut-microbiota axis on central nervous system (cns) related conditions and its influence on the gut brain axis. 5,7,11 chronic neuroinflammation is a unique feature associated with the pathology of most neurodegenerative diseases (als, pd, ad).6 although, bacterial toxin has been linked to the aetiology of neurodegenerative disease, systemic inflammation and its infectious burden is suggested to be the prime factor that predisposes to neurodegeneration or immune response of the host to gut dysbiosis rather than an isolated single infectious agent. this inflammation is the initial stimulus to the neuropathological cascade seen in neurodegenerative disease that drifts gradually along the sacral autonomic nerves and dorsal motor nucleus of the vagus nerves, to the midbrain cortex through trans-synaptic spread and hence degeneration of the cns.5,14 gut mucosa lymphocytes secrete pro-inflammatory mediators which causes protein misfolding in neighbouring enteric neurons. this is the main cause of pathogenesis seen in neurodegenerative disease such as ad and pd.14 although, bacteria causes misfold of amyloid protein as seen in alzheimer’s disease (ad) and parkinson disease (pd), aggravating oxidative stress, neuroinflammation and progressive neurodegeneration, neurodegeneration could also provide a favourable atmosphere for the growth of microbes via the micro-environmental change 5,6 spirochetes, herpes simplex virus type 1 and chlamydophila pneumoniae infections have been associated with the brain of ad patients and fungal infection in both ad and amyotrophic lateral sclerosis (als).5 prion-like transmission through molecular mimicry pathway suggests that microbiota is vital in prion-like transmission seen in neurodegenerative disease.10 minuit quantities of cyanobacteria which produce β-n-methyl amino-lalanine (bmaa) are reported to be increased in the brain of patients with ad, pd and amyotrophic lateral sclerosis (als). this has been linked to the misfolding of proteins and aggregation seen in neurodegenerative disease.3 119 microbiota gut-brain axis and neurodegenerative disease constipation is a common symptom in pd, this is likely due to neurodegeneration of autonomic centers of the enteric nervous system (ens).9 urinary tract infection is also a common symptom seen in neurodegenerative disease especially in ad and pd. a variety of microbes have been identified in healthy urinary tracts using novel laboratory culture methods, this could be linked to the immune system modulation. interestingly, microbiome found in the skin have been suggested to be linked to microbiological and amyloid axis between the skin and the brain, but no detailed evidence has been reported.14 while research has focused on neural and inflammatory signaling, the future role of circulating metabolites of gut microbe-has been underexplored.2 figure 2. interaction between gut microbiota and neurodegenerative disorders15. gut microbiota and alzheimer’s disease (ad) ad is a progressive degenerative neurological disease with intracellular neurofibrillary tangles, extracellular β-amyloid (aβ) and senile plaques.7 no detailed study on the interaction of gut microbiota and alzheimer’s disease has been reported5, however a study reported the gut microbiota imbalance and the development of ad as a result of inflammation and increasing the permeability of the intestine and endothelium.6,7 high levels of inflammatory markers, total and phosphorylated tau protein have been reported in ad patient with helicobacter pylori (h. pylori) infection.6 studies have also linked the association of serum antibodies and ad and a reduction in brain-derived neutrophilic factor (bdnf).5,7 high levels of inflammatory markers (as shown in figure 3), total and phosphorylated tau protein have been reported in ad patient with helicobacter pylori (h. pylori) infection.6 gut microbial diversity is reduced in patient with alzheimer’s disease (ad). patients with ad show an increase in intestinal bacteria such as bacteroides, bacteroidetes resulting in an exaggerated translocation of lipopolysaccharide (lps) to the cns from the gut. this would in turn cause neuroinflammation and exacerbate ad, while a decrease in bifidobacterium, firmicutes seen in ad patients is associated with a decrease in permeability of the intestine.11 excessive high fat diet, for example corn oil causes an alteration in the composition of gut microbiota thereby increasing intestinal permeability. this is associated with an increased risk of ad, however diet containing n-3 polyunsaturated fatty acids have not been linked to ad. intestinal microbial metabolites of dietary fats for example trimethylamine n-oxide(tmao) can serve as a biomarker for ad, which supports the association of excessive high fat diet meal seen in western diet with ad.6 intriguingly, although gut microbiota such as e. coli, bacillus subtilis, mycobacterium tuberculosis, staphylococcus aureus, salmonella typhimurium, and salmonella enterica, and fungi are capable of secreting amyloid (resulting in a rise of cns amyloid levels distorting the dynamic amyloid protein causing aggregation in the brain and a high risk in ad), they are also able to reduce amyloid of patients with ad via an indirect diet-mediated mechanism. for example bacillus spp and lactobacillus spp produces acetylcholine, a deficient neurotransmitter in ad.6, 7 figure 3. interaction between gut microbiota and inflammatory markers in the pathogenesis of ad6. tumour necrosis factor (tnf), triggering receptor expressed on myeloid cells-2 (trem2,), zonula occludens (zo), interleukins (il), lipopolysaccharide (lps). 120 poluyi edward oluwatobi, imaguezegie grace ese, poluyi abigail oluwatumininu et al. gut microbiota and amyotrophic lateral sclerosis (als) als is a progressive degenerative disorder that affects the brain and spinal cord neurons, it is a multi-system disorder that affects the gastrointestinal tract which could be as a result of the increased permeability of the intestine that would increase circulating lipopolysaccharide (lps).6, 10 chronic neuroinflammation and microglial activation are features of als.6 the pathogenesis of als involves increase circulating lps (derived from gramnegative bacteria cell walls) and innate immune response, suggesting a concept of gut-derived neurotoxins. tight junction proteins (occludin, vecadherin/cd144) and the junction adhesion molecule (jam)) in the lumber spine are reduced leading to the disruption of the blood-spine cord barrier (bscb) and blood brain barrier (bbb) in patients with als thus, facilitating permeability and increased exposed of motor neurons to the toxic substance released from the gut (figure 4).dysfunction of intestinal barrier can lead to the passage of toxins to the blood from the lumen of the intestine.10 constipation is a common symptom in als, however details about the effect of changes in the gut microflora on gastrointestinal motility in als patients seem skeptical.6,10 in a nutshell, research on the dynamics and relationship of gut microbiota and the stages of als is limited.10 figure 4. interaction between gut microbiota and the pathogenesis of als6. tumour necrosis factor (tnf), cyclooxygenase (cox), interleukin (il), vascular endothelial (ve), zonula occludens (zo). gut microbiota and parkinson disease (pd) the loss of dopamine neurons in the substantia nigra, aggregation of misfolded protein (α-synuclein), calcium overload, mitochondrial dysfunction and oxidative stress account for most of the pathogenesis seen in pd.11 although, there is inadequate information on the microbiota-host relationship in pd5, recent studies have shown the role of gut microbiota bi-directional communications between gut and brain in the pathogenesis of pd. studies have reported over expression of protein inclusions (α-synuclein) causing misfolding and aggregation in pd,3 which reaches the brain via the glossopharyngeal and vagus nerves.11 interestingly, misfold and aggregation of α-synuclein is not specific to pd, there is a descending gradient in the frequency of amount of lewy bodies seen in the gi tract. this ranges from submandibular gland with the highest frequency, to lower oesophagus, stomach, small intestine, large intestine and rectum with the lowest frequency. the vagal innervation from the dorsal motor nucleus of the vagus nerve (dmnv) and the enteric nervous system (ens) dopaminergic neurons distribution coincide with the descending gradient of the amount of lewy body’s pathology.9 a clinical staging system of pd (braak stages) proposes that the genesis of neurodegenerative disease is via a dual-hit mechanism in which the neurodegenerative process starts in the olfactory bulb following inhalation and in the ens of the gut secondary to neurotropic pathogen ingestion. this later advances forward to the temporal lobe from the olfactory bulb and backward to the intermediolateral nucleus (iml) cord or dorsal motor nucleus of the vagus (dmnv) and then to the brain stem from the gut through the sympathetic and parasympathetic nerves respectively as illustrated in figure 5. gut microbiota dysbiosis have been linked to patients with pd and increased incidence of small intestinal bacteria overgrowth (sibo) compared to control.3,11over-proliferation of gut microbiota alters intestinal motility.16 constipation is a common and early symptom of pd, and can be as a result of prolong intestinal transit time secondary to impaired colonic motility.9 it is 2 times more prevalent in patients with pd compared to control, and a 2 times probability of individuals with constipation having pd within 10 years.3 intriguingly, a high prevalence of 121 microbiota gut-brain axis and neurodegenerative disease helicobacter pylori (h. pylori) infection has been reported in patient with pd.9 studies have linked changes in intrinsic ratios of gut microbiota fecal specimens with pd.8 the faecal samples of patients with pd shows an increase in bacteria such as lactobacillus and a decrease in prevotella, clostridium coccoides and bacteroides fragilis faecal samples. the decrease prevotella counts is associated with an increase in permeability of the gut and a decrease in synthesis of mucin. although prevotella counts is not unique to the diagnosis of pd alone, the hydrogen sulfide they secrete is reported to have a protective effect on dopaminergic neurons.11 studies have also reported an abundance of enterobacteriaceae count isolated from faecal sample in patients with gait anomaly and postural instability, suggesting a link of microbiota to the pd. further research on the early communication between gut microbiota and pd would give new useful insights in the intervention for diagnosing and treating patients with pd.11 figure 5. genesis of neurodegenerative disease via dual-hit mechanism involving the olfactory bulb and ens9. conclusion gut microbiota is capable of modulating some brain activities via the microbiota gut-brain axis. although, studies have shown a positive relationship between rich diverse microbial community and the brain of the host, and a negative relationship between microbial dysbiosis, intestinal infection and human brain health, our knowledge however, is limited due to the inability to identity the major players in this heterogeneous microbial community. these findings are particularly promising in finding out if microbiota changes precede or succeed the pathogenesis seen in neurodegenerative disease.6 this review excluded literatures on evidence from animal and pharmacological models which some other previous studies focused. although animal models can be controlled experimentally, this microbial community can be easily misrepresented or missed when scanning for total composition of the microbiota composition. besides, reduced diversity in microbiota population is seen more in animal models compared to humans. acknowledgement my sincere gratitude to god almighty for making it possible to complete this module. my utmost appreciation also goes to my supervisor dr costabile for guiding me through this review paper. funding this research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. abbreviations ad: alzhemier’s disease ahn: adult hippocampus neurogenesis als: amyotrophic lateral sclerosis ans: autonomic nervous system bbb: blood brain barrier bdnf: brain derived neurotrophic factor bmaa: β-n-methyl amino-l-alanine bscb: blood-spinal cord barrier cns: central nervous system cox: cyclooxygenase ens: enteric nervous system fmri: functional magnetic resonance imaging gi: gastrointestinal il: interleukin jam:junction adhesion molecule lps: lipopolysaccharide pd: parkinson disease pet: positron emission tomography scfas: short chain fatty acids sibo: small intestinal bacteria overgrowth tmao: trimethylamine n-oxide tnf: tissue necrosis factor trem2: triggering receptor expressed on myeloid cells-2 zo: zonula occludens 122 poluyi edward oluwatobi, imaguezegie grace ese, poluyi abigail oluwatumininu et al. references 1. sandberg aa, bridge ja. updates on the cytogenetics and molecular genetics of bone and soft tissue tumors. synovial sarcoma. cancer genet cytogenet.2002:133:123. 2. guadangnolo ba, zagars gk, ballo mt, et al. long term outcomes for synovial sarcoma treated with conservation surgery and radiotherapy . int j radiat oncol biol phy. 2007;69:1173-80. 3. weiss sw, goldblum jr: enzinger’s and weiss’s soft tissue tumors. 5th ed., philadelphia, mosby elsevier, 2008, 11611182. 4. fischer c. synovial sarcoma .ann diagn pathol. 1998;2(2)401-21. 5. zeren h, moran ca, suster s, fishback nf, koss mn: primary pulmonary sarcomas with features of monophasic synovial sarcomas. a clinicopathological, immunohistochemical and ultrasturctural study of 25 cases. hum pathol; 26:474-480. 6. enzinger fm, weiss sw. soft tissue tumors. st. louis: mosby;1993.synovial sarcoma;pp.757-86. 7. kransdorf mj. malignant soft tissue tumors in a large referral population: distribution of diagnosis by age,sex and location.am j roentgenol.1995;164:129-34. 8. palmerini e, staals el, alberghini m, zanella l, ferrari c, benassi ms, et al. synovial sarcoma: retrospective analysis of 250 patients treated at a single institution. cancer. 2009;115:2988–98. 9. chu pg benhattar j, weiss lm, et al. intraneural synovial sarcoma: two cases. mod pathol. 2004;17:258-63. 10. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 11. kawai a, woodruff j, healey jh, et al. syt-ssx gene fusion as a determinant of morphology and prognosis in synovial sarcoma. n engl j med. 1998;338:153–60. 12. trassard m, le doussal v, hacène k, et al. prognostic factors in localized primary synovial sarcoma: a multicenter study of 128 adult patients. j clin oncol. 2001;19:525–34. 13. kawai a, woodruff j, healey jh, et al. syt-ssx gene fusion as a determinant of morphology and prognosis in synovial sarcoma. n engl j med. 1998;338:153–60. 14. ladanyi m, antonescu cr, leung dh, et al. impact of sytssx fusion type on the clinical behavior of synovial sarcoma: a multiinstitutional retrospective study of 243 patients. cancer res. 2002;62:135–40. 15. inagaki h, nagasaka t, otsuka t, et al. association of sytssx fusion types with proliferative activity and prognosis in synovial sarcoma. mod pathol. 2000;13:482–8. 16. nilsson g, skytting b, xie y, et al. the syt-ssx1 variant of synovial sarcoma is associated with a high rate of tumor cell proliferation and poor clinical outcome. cancer res. 1999;59:3180–4. 17. o'connell jx, browne wl, gropper pt, et al. intraneural biphasic synovial sarcoma: an alternative “glandular” tumor of peripheral nerve. mod pathol. 1996;9:738–41. 18. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 19. bergh p, meis-kindblom jm, gherlinzoni f, et al. synovial sarcoma: identification of low and high risk groups. cancer. 1999;85:2596–607. 20. choong pfm, pritchard dj, sim fh, et al. long-term survival in high grade soft tissue sarcoma: prognostic factors in synovial sarcoma. int j oncol. 1995;7:161–9. 21. spillane aj, a'hern r, judson ir, et al. synovial sarcoma: a clinicopathologic, staging, and prognostic assessment. j clin oncol. 2000;18:3794–803. 22. krsková l, kalinová m, brízová h, et al. molecular and immunohistochemical analyses of bcl2, ki-67, and cyclin d1 expression in synovial sarcoma. cancer genet cytogenet. 2009;193:1–8. 23. enzinger fm, weiss sw. soft tissue tumors. st. louis: mosby; 1993. synovial sarcoma; pp. 757–86. 24. lewis jj, antonescu cr, leung dh, et al. synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. j clin oncol. 2000;18:2087–94. 25. cugola l, pisa r. synovial sarcoma: with radial nerve involvement. j hand surg (br) 1985;10:243-4. 26. rinehart gc, mustoe ta, weeks pm. management of synovial sarcoma of the median nerve at the elbow. plast reconstr surg 1989;528-32. 27. tacconi l, thom m, thomas dg. primary monophasic synovial sarcoma of the brachial plexus: report of case and review of literature. clin neurol neurosurg 1996;98:249-52. 28. spielmann a, janzen dl, o’connell jx, munk pl. intraneural synovial sarcoma. skeltal radiol 1997;26:67781. 29. chesser tj, geraghty jm, clarke am. intraneural synovial sarcoma of median nerve. j hand surg(br) 1999;24:3735. 30. zenmyo m, komiya s, hamada t, et al. intraneural monophasic synovial sarcoma: a case report. spine 2001;26:310-3. 31. lestou vs, o’connell jx, robinchaud m,et al. cryptic t(x;18), ins(6;18), and syt-ssx2 gene fusion in a case of intraneural monophasic synovial sarcoma. cancer genet cytogenet 2002;138:153-6. 32. weinreb i, perez-ordonez b, guha a, kiehl tr. mucinous gland predominant synovial sarcoma of a large peripheral nerve : a rare case closely mimicking metastatic mucinous carcinoma. j clinical pathol 2008;61:672-6. 33. uehara h, yamasaki k, fukushima t, et al. intraneural synovial sarcoma originating from median nerve. neurol med chir 2008;48:77-82. doi: 10.33962/roneuro-2022-087 endoscopic third ventriculostomy. complications and avoidance ammar m. al-smaysim, waleed k. alhayali, salima b. alsaadi, aanab o. abdulameer, mustafa ismail, samer s. hoz romanian neurosurgery (2022) xxxvi (4): pp. 479-482 doi: 10.33962/roneuro-2022-087 www.journals.lapub.co.uk/index.php/roneurosurgery endoscopic third ventriculostomy. complications and avoidance ammar m. al-smaysim1, waleed k. alhayali1, salima b. alsaadi2, aanab o. abdulameer3, mustafa ismail3, samer s. hoz4 1 department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 department of neuroradiology, neurosurgery teaching hospital, baghdad, iraq 3 university of baghdad / college of medicine, baghdad, iraq 4 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract introduction. endoscopic third ventriculostomy (etv) is the treatment of choice in obstructive hydrocephalus. it has become the main standard choice in management since 1962. however, there is scant data regarding the complications from clinical or multi-centre trials. this study highlights the specific complications and prevention methods related to etv in neurosurgical teaching hospital, baghdad, iraq. methods. it is a prospective case series study conducted on cases in the neurosurgical teaching hospital in baghdad, iraq, from january 2014october 2019. we selected ninety patients. the sample selection was convenient as any patients admitted in the study period who met the selection criteria were included. all included patients underwent a computerized tomography scan or magnetic resonance imaging in the periprocedural management. results. ninety cases have 59 (65.5%) females and 31 (34.5%) males. the most common cause of hydrocephalus is congenital causes (51 cases (56.6%), especially within the first decade of life. aqueduct stenosis is the leading cause in 37 cases (72%). etv complications were found in 32 cases (35.5%). the most common cause of complications is congenital cases of 14 (15%). intraoperative complications include bleeding (mild, moderate, and severe) in 18 cases (20%). mild bleeding constitutes 15 cases (16.6%) of all complicated cases. conclusion. etv is a standard procedure in the management of obstructive hydrocephalus. the complication rate is found in around one-third of the cases in our study. surgeons’ selection of indicated patients and better surgical experience decrease the failure rate of etv and complications. introduction endoscopic third ventriculostomy (etv) is considered to be the treatment of choice in obstructive hydrocephalus [1, 16, 17, 19, 21, 25]. since 1962, the first etv procedure was done by gerard guiot, etv has become the primary standard option in obstructed hydrocephalus, but it has specific indications [9]. it is indicated in any patients with keywords endoscopic third ventriculostomy, etv complications, hydrocephalus corresponding author: samer s. hoz department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 480 ammar m. al-smaysim, waleed k. alhayali, salima b. alsaadi et al. obstructed hydrocephalus who exhibit signs and symptoms, and the anatomical features are allowed for procedure success [26]. however, there is scarce data from clinical or multi-centre trials regarding the complications and their efficacy. this study highlights the specific complications and prevention methods related to etv in neurosurgical teaching hospital, baghdad, iraq. methods it is a prospective case series study carried out on cases in the neurosurgical teaching hospital in baghdad, iraq, during the period january 2014 october 2019. we selected ninety patients. the sample selection was convenient as any patients admitted in the study period who met the selection criteria were included. the selection criteria are patients with different etiologies of obstructive hydrocephalus, all had a computerized tomography (ct) scan or magnetic resonance imaging (mri), and all had etv. we used microsoft excel sheets to conduct our data analysis. procedure the endoscope device used is the gaab® system by storz®. it was introduced through a burr hole in the kocher point, but it may need to change laterally and anteriorly when there was a large fontanel to involve the frontal bone. after that, we introduce the endoscope through foramen monro, with fenestration of the floor of the third ventricle by monopolar probe or forceps. then it is easy to direct visualization of the basilar artery. the irrigating wash used was ringer®, and its pressure was controlled through wash-in and wash-out valves. all cases had postoperative day-zero ct scan checking for hemorrhage. follow-up ct scans two months later, checking for the function of the stoma and late complications. we gained consent from all ninety patients (children from the parents or guardians). the patients’ data were put in a password-protected computer. results the total number of patients was 90 cases, with 59 (65.5%) females and 31 (34.5%) males. the most common age group was 70% in the first decade. and all age groups are illustrated in table 1. the most common cause of hydrocephalus is congenital causes (51 cases (56.6%), especially within the first decade of life. aqueduct stenosis is the most common cause within the congenital 37 cases (72%). we found tumors 25 cases (27.7%), arachnoid cyst 8 cases (8.8%), infections 3 cases (3.3%), vascular 2 cases (2.2%), and trauma 1 case (1.1%). table 1. the age groups of the patients and their percentages age group no. percentage 1day-12 months 31 34.4% 2-10 years 31 34.4% 11-50 years 25 27.7% 51-above 3 3.3% total 90 100% etv complications were found in 32 cases (35.5%). eight 8 of them (8.8%) had severe complications, which failed the etv. the most common cause of complications is congenital cases which are 14 (15%), tumor 8(8.8%), arachnoid cyst 6 (6.6%), vascular 2 (2.2%), and infections also 2 (2.2%). intraoperative complications include bleeding (mild, moderate, and severe) in 18 cases (20%). mild bleeding constitutes 15 cases (16.6%) of all complicated cases. it was managed intraoperatively with wash and/or coagulation, stopping the bleeding. on the other hand, severe bleeding, 3 cases (3.3%) which was managed with extraventricular drain (edv), ommaya reservoir, and wash tamponade. the case that was managed with edv ended in death, but the latter two patients survived. other intraoperative complications include bradycardia, the most commonly encountered complication in 20 cases (22.2%). the management stopped the shunt's wash-in and opened the washout. early complications include diabetes insipidus (di) in 11 cases (12.2%), cerebrospinal fluid (csf) leak in 5 cases (5.5%), subdural collection in 1 case (1.1%), hemiparesis in 1 case (1.1%), and fornix injury in 1 case (1.1%). the success rate in our study is 96.6%. there are only three failed cases; one died, and the other two cases, one ends with vds and the other with ommaya. discussion obstructive hydrocephalus management includes different methods, and they have been established as a challenge in various studies [7,12,14]. etv is the 481 endoscopic third ventriculostomy preferred option in managing obstructive hydrocephalus, performed in different neurosurgical centers in the developing world with enough surgical experience [20]. etv has growing popularity in management because it is safe, shunt-free, and treats the condition regardless of the etiology [20]. the overall complication rate is mainly related to the center experience and the surgeon in each procedure [23]. most case series report rates range from 5% to 15% [6,11]. in recent meta-analysis showed that the overall complication rate was 8.5 %. in our study, the complication rate is 35.5%. because we mentioned the significant complications of etv in our research, we may have this lower rate number. as there are case series [5,24] reporting just major complications, their rate is 0%, and with series, even the minor complications, e.g., fever, are reported to be 31.2% [5]. in our study, we have a success rate of 96.6%. in rahman et al. study of 34 cases, they had an overall 79% success rate ([20]. duru et al. reported an 80% success rate in the overall 51 cases of children (<16 years) of all ages and etiologies [10]. regarding specific complications, the rate of bleeding intraoperatively ranges from 0% to 8.5% in the literature [2-4,8,13,22]. the rupture of the basilar artery was reported in <0.2% of the cases [2,4,15,18]. still, in this study, we report 20% of the cases complicated with intraoperative bleeding and 0% of cases of basilar artery rupture. in our study, one patient with medulloblastoma died due to severe bleeding intraoperatively. the counter-effort to stop the bleeding by edv has been established, but he deteriorates postoperatively and ends with death. another complication is csf leak which is the most frequent encounter complication [6,8], and it ranges from 0% to 5.2% of the cases, with an overall complication rate of 1.7% [5]. our csf complication rate is 5.5%. we also had csf leak as early complications, which were severe in 3 cases due to aqueduct stenosis that was managed with ventriculoperitoneal shunt and survived without a sequalae. otherwise, patients who were complicated with di, bradycardia (4 cases due to craniopharyngioma), and hemiparesis had an excellent outcome in our study. the predisposing factors to etv failure include the closure of ventriculostomy stoma by arachnoid granulation tissues, failure of csf absorption, infection, and patients' improper selections [20]. the outcome from etv may include csf, leak, infection, hematoma, and bradycardia. the complications of etv can happen. good surgical experience and early intervention following the surgeon's selection of the patients can ensure the procedure's success and low complication rate. conclusion etv is a standard procedure in the management of obstructive hydrocephalus. but it has complications, including bradycardia, bleeding, csf leakage, and infection. the complication rate is found in around one-third of the cases in our study. surgeons’ selection of indicated patients and better surgical experience decrease the failure rate of etv and complications. abbreviations cerebrospinal fluid (csf), computerized tomography (ct), diabetes insipidus (di), extraventricular drain (edv), endoscopic third ventriculostomy (etv), magnetic resonance imaging (mri). references 1. al-tamimi yz, bhargava d, surash s, ramirez re, novegno f, crimmins dw, et al. endoscopic biopsy during third ventriculostomy in paediatric pineal region tumours. childs nerv syst. 2008;24:1323–6. 2. amini a, schmidt rh: endoscopic third ventriculostomy in a series of 36 adult patients. neurosurg focus 19:e9, 2005. 3. baykan n, isbir o, gercek a, dagcnar a, ozek mm: ten years of experience with pediatric neuroendoscopic third ventriculostomy: features and perioperative complications of 210 cases. j neurosurg anesthesiol 17:33-37, 2005. 4. beems t, grotenhuis ja: i. bilginer b, oguz kk, akalan n: endoscopic third ventriculostomy for malfunction in previously shunted infants. childs nerv syst 25:683-688, 2009. 5. bouras t, sgouros s: complications of endoscopic third ventriculostomy in children. a meta-analysis. j neurosurg pediatr 7:643-649, 2011. (meta-analysis). 6. bouras t, sgouros s. complications of endoscopic third ventriculostomy. world neurosurg. 2013 feb;79(2 suppl):s22.e9-12. doi: 10.1016/j.wneu.2012.02.014. epub 2012 feb 10. pmid: 22381818. 7. brockmeyer d, abtin k, carey l, walker ml. endoscopic third ventriculostomy: an outcome analysis. pediatr neurosurg. 1998;28(5):236–40. 8. de ribaupierre s, rilliet b, vernet o, regli l, villemure jg: third ventriculostomy vs ventriculoperitoneal shunt in 482 ammar m. al-smaysim, waleed k. alhayali, salima b. alsaadi et al. pediatric obstructive hydrocephalus: results from a swiss series and literature review. childs nerv syst 23:527-533, 2007. 9. demerdash a, rocque bg, johnston j, et al. endoscopic third ventriculostomy: a historical review. br j neurosurg. 2017;31(1):28-32. 10. duru s, peiro jl, oria m, et al. successful endoscopic third ventriculostomy in children depends on age and etiology of hydrocephalus: outcome analysis in 51 pediatric patients. childs nerv syst. 2018;34(8):1521–8. 11. ersahin y, arslan d: complications of endoscopic third ventriculostomy. childs nerv syst 24:943-948, 2008. 12. feng h, huang g, liao x, et al. endoscopic third ventriculostomy in the management of obstructive hydrocephalus: an outcome analysis. j neurosurg. 2004;100(4):626–33. 13. gangemi m, maiuri f, buonamassa s, colella g, de divitiis e: endoscopic third ventriculostomy in idiopathic normal pressure hydrocephalus. neurosurgery 55:129-134 [discussion 134], 2004. 14. hoppe-hirsch e, laroussinie f, brunet l, et al. late outcome of the surgical treatment of hydrocephalus. childs nerv syst. 1998;14(3):97–9. 15. kim sk, wang kc, cho bk: surgical outcome of pediatric hydrocephalus treated by endoscopic iii ventriculostomy: prognostic factors and interpretation of postoperative neuroimaging. childs nerv syst 16:161168 [discussion 169], 2000. 16. mohanty a, santosh v, devi bi, satish s, biswas a. efficacy of simultaneous single-trajectory endoscopic tumor biopsy and endoscopic cerebrospinal fluid diversion procedures in intraand paraventricular tumors. neurosurg focus. 2011;30:e4. 17. morgenstern pf, osbun n, schwartz th, greenfield jp, tsiouris aj, souweidane mm. pineal region tumors: an optimal approach for simultaneous endoscopic third ventriculostomy and biopsy. neurosurg focus. 2011;30:e3. 18. ogiwara h, dipatri a jr, alden td, bowman rm, tomita t: endoscopic third ventriculostomy for obstructive hydrocephalus in children younger than 6 months of age. childs nerv syst 26:343-347, 2010. 19. oppido pa, fiorindi a, benvenuti l, cattani f, cipri s, gangemi m, et al. neuroendoscopic biopsy of ventricular tumors: a multicentric experience. neurosurg focus. 2011;30:e2. [ 20. rahman, m., khan, simkn, khan, r.a. et al. endoscopic third ventriculostomy in children: problems and surgical outcome: analysis of 34 cases. chin neurosurg jl 7, 3 (2021). 21. roopesh kumar sv, mohanty a, santosh v, satish s, devi bi, praharaj ss, et al. endoscopic options in management of posterior third ventricular tumors. childs nerv syst. 2007;23:1135–45. 22. ruggiero c, cinalli g, spennato p, aliberti f, cianciulli e, trischitta v, maggi g: endoscopic third ventriculostomy in the treatment of hydrocephalus in posterior fossa tumors in children. childs nerv syst 20:828-833, 2004. 23. santamarta d, diaz alvarez a, goncalves jm, hernandez j: outcome of endoscopic third ventriculostomy. results from an unselected series with noncommunicating hydrocephalus. acta neurochir (wien) 147:377-382 [discussion 382], 2005. 24. scarrow am, levy ei, pascucci l, albright al: outcome analysis of endoscopic iii ventriculostomy. childs nerv syst 16:442-444 [discussion 445], 2000. 25. van beijnum j, hanlo pw, fischer k, majidpour mm, kortekaas mf, verdaasdonk rm, et al. laser-assisted endoscopic third ventriculostomy: long-term results in a series of 202 patients. neurosurgery. 2008;62:437–43. discussion 443-4. 26. yadav yr, parihar v, pande s, namdev h, agarwal m. endoscopic third ventriculostomy. j neurosci rural pract. 2012;3(2):163-173. doi:10.4103/0976-3147.98222. doi: 10.33962/roneuro-2022-074 intracranial aneurysms a battle against time corneliu toader, andrei alexandru marinescu, andrei adrian popa, bogdan gabriel bratu, alexandru vlad ciurea romanian neurosurgery (2022) xxxvi (4): pp. 407-410 doi: 10.33962/roneuro-2022-074 www.journals.lapub.co.uk/index.php/roneurosurgery intracranial aneurysms a battle against time corneliu toader1,2, andrei alexandru marinescu1, andrei adrian popa2, bogdan gabriel bratu2, alexandru vlad ciurea2.3 1 department of neurosurgery, national institute of neurology and neurovascular diseases, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest. romania 3 department of neurosurgery, sanador clinical hospital, bucharest, romania 4 honorary member of romanian academy, medical science section, bucharest, romania abstract introduction: intracranial aneurysms consist in abnormal dilatation of the cerebral arteries, most frequently asymptomatic, with symptoms appearing in the case of aneurysm rupture. from an imaging point of view, a cranial ct scan shows the subarachnoid haemorrhage caused by aneurysm rupture and the “gold standard” for aneurysm diagnosis is cerebral angiography. case presentation: a 49 years-old female, ukrainian refugee, presented with a unique comitial crisis and chronic headache. following an mri performed in kiev, it was decided to perform a bilateral carotid and vertebral angiography in our clinic. clinical and imagistic results showed a giant left middle cerebral artery aneurysm. postoperative, the patient had a favourable neurological recovery, with no neurological deficits. additionally, control angiography and ct scan highlight complete occlusion of the aneurysm and no complications. conclusions: cerebral aneurysms represent a high-risk vascular condition that needs a ct scan and angiography to be precisely diagnosed, surgical clipping should be performed as soon as possible. introduction cerebral aneurysms are abnormal dilatation of the cerebral arteries, which are developing because of pre-existent defects of the arterial wall. usually, cerebral aneurysms are asymptomatic, becoming symptomatic in case of rupture of the aneurysm, leading to clinical signs suggestive for subarachnoid hemorrhage, or in case of excessive aneurysmal volume growth, it can cause a mass effect on the cerebral parenchyma. main signs and symptoms are intense headache (described by patient as being the fastest headache of their life), neck keywords cerebral aneurysm, intracranial haemorrhage, microsurgical clipping, neurosurgery corresponding author: alexandru vlad ciurea professor. “carol davila” university of medicine and pharmacy, bucharest, romania prof.avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 408 corneliu toader, andrei alexandru marinescu, andrei adrian popa et al. pain, vomiting, dizziness, photophobia, motor deficit, focal deficits of cranial nerves etc. an essential aspect is clinical manifestation from subarachnoid hemorrhage which can be caused by rupture of a cerebral aneurysm. for definite diagnosis we need radiological imaging, such as cerebral ct, to accurately identify the subarachnoid hemorrhage. moreover, if subarachnoid hemorrhage diagnosis will be confirmed, a cerebral angiography is indicated for definite identification of the lesion and cause of haemorrhage. neuroimaging diagnosis necessary neuroimaging investigations are: computed tomography (ct) mandatory exam for any subarachnoid hemorrhage. hemorrhage appears hyperdense. a scale that helps us in ct scan examination of the patient is fisher scale (1980). [1] cerebral angiography represents the next step in imaging investigation and stands as the “gold standard” for aneurysms identification. after angiography, we can diagnose the cerebral aneurysm, and also identify the aneurysmal parent artery. a control angiography is necessary after surgery to verify the success of neurosurgical occlusion of the aneurysm. case presentation female patient, 49 years old, ukrainian refugee, was admitted to the national institute of neurology and neurovascular diseases, bucharest, romania for comitial crisis and chronic headache with evolution in last years and increased frequency of crisis in the last months. neurological evaluation revealed grand mal type comitial crisis and elements of expressive aphasia. the patient presented with a native head mri performed in kiev. mri shows a round-oval structure, of 3/2 cm located at middle cerebral artery bifurcation on the left side, hypointense in t1 and hyperintense in t2, in contact with left sylvian artery suggestive for a giant aneurysm of left middle cerebral artery. the rest of mri shows normal aspect of the brain in t1 and t2 sequences. a bilateral carotid and vertebral angiography was performed, which highlighted a giant saccular aneurysm inserted at the medial cerebral artery bifurcation on the left side, with antero-inferior orientation, with a maximum diameter of 1,6 cm and neck of approximately 7 mm. no other abnormal modifications were observed. figure 1. mri t2 sequence figure 2. mri flair sequence figure 3. left carotid angiography, profile incidence. figure 4. left carotid angiography, anteroposterior incidence. surgery was performed and clipping of the giant left middle cerebral artery aneurysm with a maximum diameter of approximative 3,5 cm and neck of approximative 10 mm, was performed. the aneurysm required opening and evacuation of intraluminal thrombus under temporary clipping before fixing the definitive clip. postoperatively, evolution was favorable with no complications. figure 5. incision place – postoperatively. figure 6. standing patient control left carotid angiography highlights clipping of the aneurysm at neck level and preservation of both branches of the left middle cerebral artery. 409 intracranial aneurysms a battle against time figures 7,8. control angiography postoperative native cerebral ct scan, revealed correct positioning of the clip at left sylvian cistern level and a hypodense area with ischemic aspect at left frontal lobe. figure 9. control cerebral ct-scan the patient was discharged 7 days after the surgery, neurological examination at discharge revealed no neurological deficits (normal motor function, normal speech, normal cranial nerve’s function). rankin scale at discharge was 0. discussions intracranial aneurysms are a result of abnormalities to the normal arterial vessel structure, usually from collagen deficiency in the internal elastic lamina, situated between the tunica intima and the tunica media (the muscle middle layer) of the arterial vessel. the most common presentation is subarachnoid hemorrhage, which can be seen from a ct scan, which raises the suspicion of a cerebral aneurysm, angiography showing exactly the aneurysm localization, morphology and dimensions. the surgical management of aneurysm has been debated over time, according to the literature, microsurgical clipping should be used in cases of aneurysm rupture, as in our case, while coil embolization remains recommended in nonruptured aneurysm. choosing between microsurgery or endovascular treatment in cases of unruptured aneurysm, the risk-benefit ratio should be taken into consideration and the final decision will be made together with the patient. [2] pseudotumoral giant aneurysms represent a rare aneurysm presentation and can simulate a neoplasm, as explained in a study from w. wijethunga et al. (2018) of a intracavernous aneurysm that clinically and imaging simulated a pituitary macroadenoma. due to the multilayered and “halo” appearance of the lesion on mri, a ct angiogram was performed, which revealed a large aneurysm from the cavernous portion of the left internal carotid artery. this article shows the necessity of angiography for a correct diagnosis of an aneurysm, since heterogeneity present on an mri can direct the diagnosis to other pathologies, such as tumors. [3] e. kalin-hajdu et al. (2011) presented a unruptured fusiform aneurysm of middle cerebral artery, which underwent spontaneous occlusion and regression. angiography indicates a pseudotumorallike mass, supposedly from inflammation and neovascularization within the aneurysm wall and body. inflammation and neovascularization is associated with giant cerebral aneurysms and intramural hemorrhage. before embolization, 410 corneliu toader, andrei alexandru marinescu, andrei adrian popa et al. angiography revealed complete spontaneous thrombosis of the aneurysm. due to this event, endovascular treatment was not necessary anymore. the patient presented at 11 months follow up and the mri revealed near complete regression. those spontaneous healing mechanisms are currently unknown, but they’re probably explained by theory of inflammation and secondary neovascularization. [4] in another case presentation, o. doron et al. (2016) described a giant partially thrombosed left carotid-ophthalmic aneurysm with a bone erosion of the sphenoid sinus, re-shaping the intracranial micro-environment. bone erosion was correlated with giant aneurysm and has multiple implications regarding pre-surgical planning. clipping was performed due to the optic nerve and chiasm relations and excision of the thrombosed part, as in our aforementioned case. from this case report, multiple theories were proposed for the evolution of a giant thrombosed aneurysm. first of all, repeated endothelial damage caused by turbulent flow and healing can significantly enlarge the aneurysm dimensions through an inflammatory cascade. secondly, a slow growth can be determined from recurrent hemorrhages. so, the understanding of thrombosed aneurysm evolution is becoming more clear in the last years, helping with pre-surgical management and being ready for spontaneous structural modifications. [5] conclusions cerebral aneurysms are vascular lesions which can endanger the patient's life when they rupture. intracranial hemorrhage can significantly affect nervous cells` metabolism and the patient state of consciousness, explaining the clinical presentation. additionally, the hemorrhage can fill the basal cisterns and ventricles, altering the state of conscience. emergency hospitalization is mandatory for a complete clinical and imaging evaluation; surgical intervention needs to be performed as soon as possible. regarding our case of a large, thrombosed aneurysm, due to the aneurysm nature, endovascular embolization cannot be achieved, and the treatment of choice will be surgical approach. before clipping, thrombus evacuation under temporary clipping is necessary for a complete and long-term occlusion of the aneurysm. additionally, the real dimensions of the aneurysm can only be seen intraoperatively, during microscopic inspection, because the contrast agent from angiography will not enter completely into the aneurysm body. in cases of non-ruptured and asymptomatic aneurysm, deciding between microsurgical clipping and endovascular embolization should be made by a well-informed patient. in a few of those cases, conservative treatment will be taken into consideration to avoid surgical interventions and possible postoperative complications. thus, neurosurgeons have the obligation to correctly inform the patient about different surgical procedures and their alternatives. references 1. fisher cm, kistler jp, davis jm (1980) relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. neurosurgery 6:1– 9. 2. keedy a. an overview of intracranial aneurysms. mcgill j med. 2006;9(2):141-6. 3. wijethunga wmua, dissanayake ha, perera s, katulanda p. intra cavernous aneurysm of internal carotid artery masquerading as a pituitary adenoma: a case report. bmc res notes. 2018;11(1):237. 4. kalin-hajdu e, guilbert f. transformation of a cranial fusiform aneurysm into a pseudotumoral-like mass prior to spontaneous occlusion and regression. interv neuroradiol. 2011;17(1):70-3. 5. doron o, cohen je, gomori m, spektor s. extensive bone erosion caused by pseudotumoral aneurysm growth. j clin neurosci. 2017;36:54-56. doi: 10.33962/roneuro-2020-067 fever as an independent prognostic factor in traumatic brain injury srikrishna majhi, sanjeev k. chhabra, sabyasachi saha romanian neurosurgery (2020) xxxiv (1): pp. 424-426 doi: 10.33962/roneuro-2020-067 www.journals.lapub.co.uk/index.php/roneurosurgery fever as an independent prognostic factor in traumatic brain injury srikrishna majhi, sanjeev k. chhabra, sabyasachi saha 1 department of neurosurgery, ipgme&r, bangur institute of neuroscience, kolkata, west bengal, india abstract traumatic brain injury (tbi) patients more often than not develop fever within the first few days of their hospitalization. studies report that causes are variable and according to the pathogenesis, fever may be harmful or protective. the study was conducted to correlate the development of fever with clinical prognosis. throughout the study spanning 6 months, a total of 98 patients of tbi were included. in the first 48 hours, 54 patients did not develop fever (temperature >37℃), 20 patients recorded temperatures between 37℃ and 39℃; and 24 patients developed high fever (39℃). on regular temperature monitoring and follow up, it was found that patients developing fever relatively early during hospitalization were more likely to end up with a poor outcome (glasgow outcome scale 4 to 5). therefore, fever is independently a predictor of poor prognosis in tbi patients and should be managed diligently in the first few days. introduction a major proportion of neurosurgical patients are victims of traumatic brain injury (tbi). tbis are a leading cause of morbidity, mortality, disability and socioeconomic losses in india and other developing countries. road traffic accidents are the leading cause of tbis followed by falls and violence.1 according to indianheadinjuryfoundation.org india has the unfortunate distinction of having highest rate of head injury in the world.2 a large proportion of patients with any type of acute brain injury will develop fever within the first few days of their icu or hospital stay. the causes are variable. often the patient gets non-infectious fever which is a direct consequence of brain injury itself in addition to the high risk of infections in brain-injured patients.3 we aim at studying the effect of hyperthermia in patients admitted with moderate to severe head injury and try to correlate the outcome of these patients with hyperthermia. materials and methods this study was conducted at a tertiary health care centre (ipgmer and bangur institute of neurosciences, kolkata, india) between july 2019 to december 2019. keywords fever, prognostic factor, traumatic brain injury corresponding author: sanjeev k. chhabra department of neurosurgery, ipgme&r, bangur institute of neuroscience, kolkata, west bengal, india dr.sanjeevpremchhabra@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 425 fever as an independent prognostic factor in traumatic brain injury all patients with glasgow coma scale of 12 or below admitted with history of head injury were included. exclusion criteria: • all patients with normal radiological findings (ct scan or mri) • all patients requiring surgical intervention (except minor procedures like repair of open wound, tracheostomy etc). the study was limited to patients managed conservatively. all patients fulfilling the above criteria were included in the study. the temperature was recorded 6 hourly. according to the reading, the patients were divided into three groups upto 37℃, temperature 37℃-39℃ and temp >39℃. all patients were managed for head injury appropriately and patients requiring surgical intervention at a further stage (due to failure of conservative management) were dropped from the study. the outcome of the patients was divided into two: good outcome (glasgow outcome scale score 4 to 5) and poor outcome (glasgow outcome scale score 1 to 3).4 results a total of 98 patients were included in the study. the most common mode of injury was road traffic accidents (66 patients), fall from height (18 patients) and assault (10 patients). (table 1) of these, 62 patients were males and 36 patients were females. the average age of male patients was 39.4 years and that of females was 42.2 years. all these patients were regularly monitored for hyperthermia. as hyperthermia within 48 hours of tbi is more significant, so the patients were divided into three groups at the end of 48 hours. the result are tabulated in table 2. the patients who did not develop hyperthermia within the first 48 hours were followed up for any subsequent development of hyperthermia and were again categorized into three groups. the data obtained was tabulated in table 3. the patients who developed temperature >39℃ in any time period were treated vigorously with antipyretics, sponging and suitable antibiotics. the patient who developed fever >37℃ but less than 39℃ were managed with sponging and antibiotics but no antipyretics. mode of injury male female rta 40 26 fall from height 12 6 assault 7 3 others 3 1 table 1. mode of injury and gender wise distribution. temperature within 48 hours good outcome poor outcome death upto 37℃ 36 12 6 37-39℃ 8 6 6 >39℃ 2 3 19 table 2. proportion of patients developing hyperthermia within first 48 hours and outcome ratio. temperature after first 48 hours good outcome poor outcome death upto 37℃ 18 4 1 37-39℃ 14 7 3 >39℃ 4 1 2 table 3. proportion of patients developing hyperthermia after first 48 hours and outcome ratio. discussion fever occurs with an incidence of up to 70% in neurologically injured patients and typically is not an isolated event but rather a sustained response seen for as long as 2 weeks following injury. only half of the febrile patients are attributable to infection. in one fifth to one third of cases, fever remains unexplained despite extensive diagnostic workup.5 early fever (within 24 hour) has been associated with an increased relative risk of a poor outcome by 2.2 fold with every 1℃ increase and even a 0.5℃ increase may lead to a series of secondary injuries and neuron death.4,6 what adds to the already complicated situation is that after major brain injury, brain temperature is higher than and can vary independently of systemic temperature. in such scenario, the brain is extremely sensitive and vulnerable to small variations in temperature.7 there is growing evidence that elevated body temperature may be detrimental in patients with acute neurological disorder. many work done till date shows that elevated body temperature is associated with increased mortality rate and poor functional outcome.3,8 the epidemiological and etiological spectrum of traumatic brain injury revealed in our study agrees with the already available data.2 our study reveals that temperature >39℃ within first 48 hours of traumatic brain injury after 426 srikrishna majhi, sanjeev k. chhabra, sabyasachi saha admission is significantly associated with higher death rate which concurs with other studies like that of bao l et al.4 the net effect of fever is reduction in internal perfusion pressure with diminished oxygenation of brain tissue resulting in cerebral oedema. the association of early development of fever with poor outcome is probably because already compromised brain tissue is more susceptible to oxygenation deficit.9 in addition, fever causes a generalized increase in metabolic rate ( 7-10% increase per ℃ increase in core temperature), with corresponding increase in minute ventilation and oxygen consumption which can be detrimental.3 our study does not establish a significance to delayed development of hyperthermia and poor outcome. this needs to be evaluated further. according to some studies, the hospital stay is likely to be increased in patients who develop hyperthermia.10 it remains to be studied and should be evaluated further in the backdrop of a developing country like india where resources are limited. targeted temperature management like therapeutic hypothermia has been touted as a valid candidate of neuroprotective treatment but the same has not been proven in larger randomized controlled trials. while overwhelming majority of tbi injury patients may benefit from fever control, the patients with severe infection who need an inflammatory response might not benefit and may even suffer adverse consequences. additionally, in a small subset of patients both conditions may coexist.11 conclusively, fever acts as an independent prognostic factor in patients of tbi in first few hours of admission and is associated with a poor outcome. it should be carefully watched for and vigorously treated. further studies are required to assess the relation between delayed fever development and its impact on outcome. the pathophysiology of hyperthermia (infective or non-infective) also plays an important role in making a clinical decision. references 1. gururaj g. epidemiology of traumatic brain injuries: indian scenario. neurological research, 2002, 24:1, 24-28, doi: 10.1179/016164102101199503. 2. indian head injury foundation.org. 3. polderman kh. an injured brain needs cooling down: yes. intensive care med. 2015; 41:1126-1128. 4. long bao, du chen, li ding, weihua ling and feng xu. fever burden is an independent predictor for prognosis of traumatic brain injury. plos one. 2014; 9(3): e90956, doi 10.371/journal.pone.0090956. 5. neeraj badjatia hyperthermia and fever control in brain injury. critical care medicine 2009, 37(7), s250-257. 6. reith j, jorgensen hs, pedersen p.m., nakayama h, raaschou ho. body temperature in acute stroke: relation to stroke severity, infarct size, mortality and outcome. lancet 1996 347: 422-425. 7. mrozek s, vardon f and geeraerts t. brain temperature: physiology and pathophysiology after brain injury. doi 10.1155/2012/989487. 8. greer d.m., funk s.e., reaven n.l., ouzounelli m., uman g. c. impact of fever on outcome in patients with stroke and neurologic injury a comprehensive meta-analysis. stroke, 200839:3029-3035: originally published online august21, 2008 doi: 10.1161 strokeaha. 108.521583. 9. jiang j.y., gao g.y., li w. p., yu m.k., zhu c. early indicators of prognosis in 846 cases of severe traumatic brain injury. journal of neurotrauma volume 19, number 7, 2002. 10. diringer m. n., reaven n.l., funk s.e., uman g. c. elevated body temperature independently contributes to increased length of stay in neurologic intensive care unit patients. crit care med 2004 vol 32, no. 7. 11. saxena m, young p, pilcher d et al. early temperature and mortality in critically ill patients with acute neurological diseases: trauma and stroke differ from infection. intensive care med.2015 doi: 10.1007/s00134015-3676-6. microsoft word 10iongeorgiana_combined 602 | ion et al combined treatment of a giant anterior skull base meningioma             doi: 10.2478/romneu-2018-0077 combined treatment of a giant anterior skull base meningioma georgiana ion, z. faiyad1, i. poeata, a. chiriac “grigore t. popa” university of medicine and pharmacy, iasi, romania 1“prof. dr. n. oblu” clinic emergency hospital, iasi, romania introduction meningiomas are tumors developed from arachnoid cells, and represent 20% of all intracranial tumors, from which 6% are located at the anterior skull base. incidence is higher in female population, with an age peak in the fifth and sixth decade. regarding anterior skull base meningiomas, 3,6% have the dural attachment at the level of tuberculum sellae and 3% at the olfactory groove. these tumors may invade the surrounding structures, such as dura mater and bone.these tumors are vascularized by ethmoidal arteries and rarely by frontopolar branches. case presentation a 65 years old female, having cardiovascular pathology associated was admitted to our department for memory disorders (in particular short-term memory), urinary incontinence and bilateral anosmia with 1 year onset. for this reason, the patient was initial diagnosed with dementia. for the last 3 months, the condition of the patient is deteriorating, with behavioral changes, headache and visual symptoms (decreased visual acuity, lack of campimetry). non contrast ct scan revealed a well circumscribed low density formation without calcifications located in the frontal cranial fossa that invades the right ethmoidal air cells. the mri with contrast scan, highlighted an anterior skull base meningioma, well vascularized with very little brain edema and erosion of the cribriform plate. tumor insertion is located at the olfactory groove with extension in the planum sphenoidale and tuberculum sellae. figure 1 non-contrast ct scan -giant tumor with right ethmoidal cells infiltration figure 2 mri t1 with contrast 7/7,83/7,49cm size tumor romanian neurosurgery (2018) xxxii 4: 602 606 | 603             figure 3 t2 –mri intratumoral arterial pedicles for better understanding of the tumoral vascular supply, an angiographic exploration has been achieved. righ internal carotid artery contrast injection pointed out a significant posterior shift of the anterior cerebral artery and few small branches from ophthalmic artery that supply the tumor. left carotid artery showed the same anterior cerebral artery displacement, and a major tumoral pedicle from ethmoidal branches of the ophthalmic artery, with important tumoral blush. from the external carotid artery, there were no arterial intake. figure 4 right carotid artery dsa (arterial and venous phase) small pedicles from ophthalmic artery with no important tumoral blush aca displacement figure 5 left internal carotid artery dsa-major ethmoidal artery contribution important tumoral blush we decided that the major arterial contribution from ethmoidal artery should be closed with liquid agents (glue n-butyl-2cyanoacrylate). after embolization patient declared decreased visual acuity until only light perception on the left eye, important headache and confusional periods. comparative ct scan pre and post embolization showed no semnificative modifications. 604 | ion et al combined treatment of a giant anterior skull base meningioma             figure 6 left ica dsa; cra-central retinal artery ophthalmic artery anatomy; pedicular contrast injection figure 7 glue injection figure 8 pre/post glue occlusion of the ethmoidal artery period between embolization and surgical resection was of 6 days. tumor resection has been achieved through a bifrontal approach. intraoperative, the right side of the tumor was relatively well vascularized, while the left side it was almost no bloody, clearly delimited, white colored. subtotal resection of the tumor was achieved with cusa (intraethmoidal part was left in place), with coagulation of the dural insertion at the cribriform plate, wax coating and anterior base reconstruction with vascularized pericranial flap. romanian neurosurgery (2018) xxxii 4: 602 606 | 605             postoperatively, patient develop an involution of the cognitive function (decrease of the mini mental state examination with 5 points) with a good recovery during hospitalization without other complications. postoperative ct scans (immediate and at 7 days) showed a discreet increase in size of the ventricular system. figure 10 postop. contrast ct scan -ethmoidal sinus remaining tumor definitive anatomic-pathology result was of atipic meningioma (who grade ii) discussions embolization of ethmoidal branches from the ophthalmic artery represents a real challenge for the neurointerventional surgeon because of the high risk of ophthalmic artery occlusion and blindness. that's why a superselective catheterization of the distal branches is necessary. the highest risk with liquid agents, is that of reflux into the central retinal artery. a most reliable agent in this situation would be onyx injection because of the low precipitation rate. complications of glue agent use are: hemorrhage, local reflux and distal delivery of emboli. there are not many studies to report mortality rates and complications of internal carotid artery feeding vessels embolization, but the study of rosen et al.demonstrates an overall complication rate of 21% in this cases. in giant meningioma reducing blood supply it's necessary by facilitating tumor resection (simpson i and ii). in skull base meningiomas, control and access of the vascular pedicles are difficult and are accessible only after at least a subtotal resection has been achieved. complications which could appear during or after embolization are: intratumoral hemorrhage (due to intratumoral necrosis or rupture of fragile vessels) , retinal artery occlusion or tumor swelling. figure 9 intraoperative images 606 | ion et al combined treatment of a giant anterior skull base meningioma             in general, the indications for embolization of the tumors are: very vascularized tumors, deep and hardly accessible arterial intake,eloquent area location, tumor with the diameter over 3-4 cm. regarding the optimal period of time necessary for safe resection of the tumor after embolization, studies vary, with a mean period of 7 days. conclusions giant anterior skull base meningiomas represent a challenge for every neurosurgeon, starting from choosing the most advantageous approach, total tumor resection with minimal complications and a long term lower recurrence rate. preoperative embolization decreases surgical mortality and morbidity and increase the probability of total tumor resection. correspondence prof. dr. ion poeata ipoeata@gmail.com references 1.preoperative onyx embolization of meningiomas fed by the ophthalmic artery: a case series; f. trivelatto, g.s. nakiri, m. manisor, r. riva, m. al-khawaldeh, i. kessler and c. mounayer;american journal of neuroradiology october 2011, 32 (9) 1762-1766 2.preoperative embolization of intracranial meningiomas:efficacy, technical considerations, and complications; d.m.s. raper, r.m. starke, f. henderson jr, d. ding, s. simon, a.j. evans, j.a. jane sr, and k.c. liu; am j neuroradiol 35:1798 –804 sep 2014 3.preoperative embolization of meningiomas with pial supply: successful treatment of two cases; kaji t, hama y, iwasaki y, et al; surg.neurol 1999;52:270 –73. 4.necrosis score, surgical time, and transfused blood volume in patients treated with preoperative embolization of intracranial meningioma: analysis of a single-centre experience and a review of literature.; nania a, granata f, vinci s, et al; clin neuroradiol 2014;24:29 –36. 5.embolization of skull base meningiomas and feeding vessels arising from the internal carotid circulation; james s. waldron, md*,michael e. sughrue, md*steven w. hetts, md†,sean p. wilson, ba,steven a. mills, bfa*,michael w. mcdermott, md*,christopher f. dowd, md†,andrew t. parsa, md, phd*; neurosurgery 68:162–169, 2011 6.outcome analysis of preoperative embolization in cranial base surgery. rosen cl, ammerman jm, sekhar ln, bank wo; acta neurochir (wien). 2002;144(11):1157-1164. doi: 10.33962/roneuro-2022-060 impact of dome projection on operative steps during clipping of a ruptured pure posteriorly directed posterior communicating artery aneurysms mustafa ismail, ali k.alshalchi, muslim m.badr, aanab o. abdulameer, hagar a. algburi, rania h. al-taie, saleh al-lami, aktham o. al-khafaj, samer s. hoz romanian neurosurgery (2022) xxxvi (3): pp. 355-358 doi: 10.33962/roneuro-2022-060 www.journals.lapub.co.uk/index.php/roneurosurgery impact of dome projection on operative steps during clipping of a ruptured pure posteriorly directed posterior communicating artery aneurysms mustafa ismail1, ali k. alshalchi2, muslim m. badr3, aanab o. abdulameer1, hagar a. algburi1, rania h. al-taie1, saleh al-lami1, aktham o. al-khafaj1, samer s. hoz4 1 department of neurosurgery, college of medicine, university of baghdad, baghdad, iraq 2 department of neurosurgery, college of medicine, university of baghdad, baghdad, iraq 3 department of radiology, neurosurgical teaching hospital, baghdad, iraq 4 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract background: ruptured posterior communicating artery (pcoa) aneurysms are common; they usually present with subarachnoid haemorrhage (sah) and oculomotor nerve palsy. the aneurysmal dome projection may influence the safety access and aneurysmal neck clipping. here, we discuss additional intraoperative steps that may be required to widen the surgical field to ensure safe surgical clipping of a rupture pure posteriorly directed pcoa aneurysm. case description: a previously healthy 38-year-old male reported sudden severe headache and disturbed level of consciousness with a glasgow coma scale (gcs) of 13. his initial computed tomography (ct) scan of the head showed sah in the basal cistern. 3d-constructed ct angiography (cta) revealed a left pure posteriorly directed pcoa aneurysm. in the surgery, through the left pterional approach, all intraoperative steps were carried out. additional steps were performed as well. three additional intraoperative steps were contemplated because a pure posteriorly directed pcoa aneurysm is not well appreciated and is often hidden behind the supra cliniold internal carotid artery (ica). first, the extension of sylvian fissure dissection to include the distal part and the proximal. second, temporal pole mobilization is performed by cutting small anterior temporal veins. third, a brain retractor is placed on the temporal lobe to gently tract the superficial part of the lobe. all these steps widened the surgical corridor to ensure the aneurysm's safe clipping. conclusion: surgical clipping is influenced by the aneurysmal dome projection. in a ruptured pure posteriorly directed pcoa aneurysm, further intraoperative steps may facilitate complete access and safe clipping of the aneurysm. keywords intracranial aneurysms, posterior communicating artery, microsurgical clipping corresponding author: mustafa ismail department of neurosurgery, university of baghdad / college of medicine. baghdad, iraq mostafa.ismail1700d@comed. uobaghdad.edu.iq copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 356 mustafa ismail, ali k.alshalchi, muslim m.badr et al. introduction posterior communicating artery (pcoa) aneurysms represent 25% of all aneurysms and 50% of the entire internal carotid artery (ica) aneurysms [3]. ruptured pcoa aneurysms frequently present with subarachnoid hemorrhage (sah) and oculomotor nerve palsy [4]. surgical clipping and endovascular coiling are two therapeutic options for ruptured pcoa aneurysms, and the outcome of the endovascular has a slight advantage compared to surgical clipping [8]. in the surgery, intraoperative clipping of pcoa aneurysms is influenced by the dome projection, which includes lateral and posterior directions [9]. pcoa aneurysm’s surgical clipping carries surgery-related nuances [12]. in pure posteriorly direct pcoa aneurysm may render peculiar intraoperative steps [10,12]. here, we discuss the procedure-related surgical steps in a ruptured pure posteriorly directed pcoa aneurysm. case description an otherwise healthy 38-year-old male presented with a sudden onset of severe headache, disturbed level of consciousness (glasgow coma scale (gcs) 13, e3, m6, v4), right-sided weakness grade 2 (medical research council (mrc) scale), left partial oculomotor nerve palsy, and neck stiffness. a noncontrast cranial computed tomography (ct) scan revealed sah in the basal cistern. 3d-reconstructed ct angiogram (cta) revealed a left pure posteriorly directed aneurysm with a wide neck arising from the supracliniod ica in the junction with pcoa (figure 1). the surgery was advised to the patient because of the unavailability of the endovascular choice in iraq and the high cost to the patients. through the left pterional approach with all the steps contemplated to reach the aneurysm, including using a retractor on the frontal lobe and deep part dissection of the sylvian fissure. because the pcoa aneurysm is not well appreciated due to its projection as a pure posteriorly directed and its neck is hidden behind supra cliniod ica. here, additive steps were performed, including first, lengthening the sylvian fissure dissection to encompass the distal part (wide sylvian dissection). second, temporal pole mobilization was carried out by releasing the anterior part of the temporal pole from small bridging veins connecting it to the sphenoparietal and cavernous sinuses. third, using the temporal lobe retractor mainly on the superficial part of the temporal lobe to minimize the risk of early rupture here, the operative field widened, and the surgeon had full access to the aneurysmal neck. the aneurysm was exposed, dissected then clipped safely without incident (figure 2). pcoa patency was checked. the postoperative course was uneventful. on the follow-up, the patient was conscious (gcs 15), with no neurological deficit aside from improving his right-side weakness (mrc grade 4). figure 1. left anterolateral ct angiogram showing left pure posteriorly directed pcoa aneurysm. figure 2. intraoperative images through the left pterional approach show (a) before clipping. (b) after clipping insertion. l.pcoa a: left posterior communicating artery aneurysm. l.ica: left internal carotid artery (supracliniod) l.on: left optic nerve. discussion ruptured pcoa aneurysms represent 13-25% of all intracranial aneurysms, and the unruptured aneurysms are proportionally lower [2]. in a metaanalysis study, clark et al, estimated the risk of rupture of pcoa aneurysm (0.46%) yearly, and it regularly presents with sah [1,4,13]. however, the oculomotor nerve palsy may present with ruptured or unruptured aneurysms in 19-38% of pcoa aneurysm patients, and it may be partial or complete [4,5,7]. in the treatment of pcoa aneurysm, molyneux et al, 2005 trial found endovascular coiling increased the survival rate independently by one year compared to surgical clipping; and the survival benefit extended for seven years with the former 357 impact of dome projection on operative steps option [8]. with limited resources, hospitals such as the status in iraq and the high cost to the patients made endovascular options off the choice in most of the cases as well as in our example here. the intraoperative surgical steps of pcoa aneurysm clipping may be affected by the dome projection [4,5]. the lateral or the posterolateral projection, which is the most common projection of the pcoa aneurysm, is particularly operated with regular steps of 1) pterional craniotomy and dura opening, 2) positioning of the brain retractor on the frontal lobe; however, some surgeons prefer retractor less surgery [6]. obviously, this is not always possible in ruptured aneurysm cases with an expected tense brain, 3) proximal sylvian fissure dissection, 4) identification and dissection of supracliniod ica and its bifurcation, optic nerve, pcoa (proximal to the aneurysmal neck), and anterior choroidal artery (distal to the aneurysmal neck), 5) dissection of the neck of the aneurysm then placement of the aneurysmal clip to exclude the aneurysm from the circulation, 6) oculomotor nerve decompression by opening and shrinking the aneurysmal dome [4,6]. on the other hand, with a pure posteriorly directed pcoa aneurysm, there are further steps required to reach the neck of the aneurysm due to technical difficulties. because first, the major segment of the aneurysm is positioned posterior to the supra clinoid ica, thus it will be hidden from the surgeon’s view during the typical pterional approach [4,5]. second, pcoa is commonly arising proximal to the aneurysm and course posteromedial in addition to the possible presence of perforator branches in the area close to the neck [4]. these reasons may render further steps mandatory for the neurosurgeon to ensure adequate surgical view, thus ensuring complete safe clipping of the aneurysm. in our case, three additional steps were contemplated, which include a) extended dissection of the sylvian fissure to include the distal part in addition to the proximal one to widen the operative corridor. b) the mobilization of the temporal pole is performed carefully by cutting the small anterior temporal veins, thus releasing the temporal lobe and gaining extra space for the operating surgeon. c) placing a retractor on the temporal lobe to enlarge the surgical view in these cases of the tight brain due to ruptured aneurysm and the consequences of sah. although nadar et al, advised not to use a retractor on the temporal lobe, we only retracted the superficial part of the temporal lobe gently to gain a better surgical view and at the same time to prevent early rupture of the aneurysm [9]. in summary, the modification of the pterional approach by these three additional steps intraoperatively allowed better access and safe clipping of pure posteriorly directed pcoa aneurysm’s neck. conclusions ruptured pcoa aneurysm clipping is affected by the dome projection. a ruptured pure posteriorly directed pcoa aneurysm may require additional intraoperative steps to improve the operative view and widen the surgical field, thus ensuring complete and safe clipping. references 1. clarke g, mendelow ad, mitchell p. predicting the risk of rupture of intracranial aneurysms based on anatomical location. acta neurochir. 2005;147:259–63. 2. froelich jj, neilson s, peters-wilke j, dubey a, thani n, erasmus a, et al: size and location of ruptured intracranial aneurysms: a 5-year clinical survey. world neurosurgery 91:260–265, 2016. 3. golshani k, ferrell a, zomorodi a, smith tp, britz gw. a review of the management of posterior communicating artery aneurysms in the modern era. surg neurol int. 2010 dec 22;1:88. 4. hitoshi fukuda, md, kosuke hayashi, md, kumiko yoshino, md, takashi koyama, md, benjamin lo, md, yoshitaka kurosaki, md, sen yamagata, md, impact of aneurysm projection on intraoperative complications during surgical clipping of ruptured posterior communicating artery aneurysms, neurosurgery, volume 78, issue 3, march 2016, pages 381–390, 5. huhtakangas j. aneurysmal subarachnoid hemorrhage: posterior communicating artery aneurysms and longterm excess mortality. 6. july j. (2019) surgery of posterior communicating artery aneurysm. in: july j., wahjoepramono e. (eds) neurovascular surgery. springer, singapore. 7. lee kc, lee ks, shin ys, lee jw, chung sk: surgery for posterior communicating artery aneurysms. surgical neurology 59:107113, 2003. 8. molyneux aj, kerr rs, yu lm, et al; international subarachnoid aneurysm trial (isat) collaborative group. international subarachnoid aneurysm trial (isat) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, 358 mustafa ismail, ali k.alshalchi, muslim m.badr et al. dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. lancet. 2005;366(9488):809-817. 9. nader sanai, md, nolan caldwell, bs, dario j. englot, md, phd, michael t. lawton, md, advanced technical skills are required for microsurgical clipping of posterior communicating artery aneurysms in the endovascular era, neurosurgery, volume 71, issue 2, august 2012, pages 285–295, 10. saeki n, rhoton al jr. microsurgical anatomy of the upper basilar artery and the posterior circle of willis. j neurosurg. 1977;46(5):563-578. 11. soni sr: aneurysms of the posterior communicating artery and oculomotor paresis. j neurol neurosurg psychiatry 37:475484, 1974. 12. thiarawat p, jahromi br, kozyrev da, intarakhao p, teo mk, choque-velasquez j, hernesniemi j. microneurosurgical management of posterior communicating artery aneurysm: a contemporary series from helsinki. world neurosurgery. 2017 may 1;101:37988. 13. yasargil mg, smith rd, young ph, teddy pj: microneurosurgery: ii clinical considerations, surgery of the intracranial aneurysms and results, in thieme(ed). 1984, vol. 2, pp 71–93. romanian neurosurgery (2019) xxxiii (3): pp. 243-248 doi: 10.33962/roneuro-2019-041 www.journals.lapub.co.uk/index.php/roneurosurgery learning curve in rat dissection for experimental sciatic nerve repair marin andrei1, marin georgiana gabriela2, dobrete nicoleta amalia3, enescu dan mircea4 1 plastic surgery department, “bagdasar arseni” emergency hospital, bucharest, romania 2 cardiology department, “cc iliescu” hospital, bucharest, romania 3 haematology department, “fundeni” hospital, bucharest, romania 4 plastic surgery department, “grigore alexandrescu” emergency paediatric hospital, bucharest, romania abstract the baseline for any key research in nerve regeneration is an experimental model and the sciatic nerve in the rat model is the workhorse in this field. although physically resistant to external traumas, a surgical intervention constitutes a major distress even for a rat. in the following presentation, we will analyse the learning curves for different stages in the rat sciatic nerve surgery as well as possible factors which influence these times. introduction every major breakthrough discovery starts from research. in surgery, it is immoral, unethical and sometimes even illegal for experiments which can be performed on animals to be done directly on humans. for this reason, animal experiments in the field of modern medicine are a necessity and they constitute the starting point for most of the innovative techniques in the surgical field. when it comes to nerve regeneration, the preferred choice is the sciatic nerve in the rat model. the reason for this choice is that the sciatic nerve has a reasonable size (1-3mm in diameter), is fairly easily accessible (being located underneath the gluteus maximus, at the intersection between this muscle and the biceps femuri muscle, running its course between the knee joint and the ischial tuberosity) and because it divides towards the knee joint into its 3 main branches (common peroneal nerve, tibial nerve and sural nerve). these 3 branches can be large enough for individual repair, but the sciatic nerve has proximal to this division sufficient length for different types of operations (grafts, nerve conducts), where an artificial gap can be created. keywords learning curve, operation times, sciatic nerve rat, nerve defect corresponding author: marin andrei plastic surgery department, “bagdasar arseni” emergency hospital, bucharest, romania marin_dpt@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 244 marin andrei, marin georgiana gabriela, dobrote nicoleta amalia, enescu dan mircea sciatic nerve and its divisions right leg of a rat: [1], [2] material and method for the experiment 42 wistar male rats were used. all rats weighed between 240g and 310g and were 50-62 days of age at the time of surgery. all conditions regarding the safety and the well-being of the animals have been met. 2 rats were sacrificed to harvest vascular conducts and blood for prp processing and the other 40 rats were divided into 4 batches of 10. the learning curve presented in this article was designed for the first 2 batches (20 rats). the operations were performed under general anaesthesia. the rat was positioned in supine position and an incision on the right posterior gluteal-thigh region was performed, followed by an incision of the biceps femuri muscle with sciatic nerve exposure. in the first batch, a distal section of the nerve was created, followed by nerve repair, proximal section of the sciatic with nerve anastomosis (by doing so, a controlled nerve graft of 0,5cm in size was created in each rat, which was then sutured back into its original place). a 5th grade sunderland lesion – neurotmesis was created at 2 different sites and then repaired. [3] in the 2nd batch, a 0,5cm nerve defect was created and then solved using a vascular conduct. batches 3 and 4 are part of a different study and involve adding prp (platelet rich plasma) or human stem cells from the umbilical cord in the vascular conduct. [4],[5],[6]. [7] rat leg anatomy 245 learning curve in rat dissection for experimental sciatic nerve repair sciatic nerve exposure all interventions were performed in sterile conditions. an assistant was present for the duration of every operation to ensure the sterile conditions. all microsurgical anastomosis were performed using 10.0 nylon suture under the microscope using a 10x magnification. the rats received 3 subcutaneous doses of meloxicam 0,04ml and 3 doses of enroxil 0,02ml (1 immediately after the operation, and one for each of the next 2 days). each rat was marked with circles on the tail and put in a separate cage. every procedure was recorded using a chronometer from the moment of the intraperitoneal injection till the skin suture. we observed the rat preparation times, the nerve exposure times and the anastomosis times. the rat preparation time (t1) represents the time from the first doses of anaesthesia till the moment of incision and involves the time needed to shave the area which will be operated as well as time needed for setting the sterile field and the disinfection time. the nerve exposure time has 2 components: a macroscopic time for skin incision and muscle dissection till the nerve can be visualized (t2) and a microscopic time consisting in proper nerve dissection (t3). the 4rd registered time is the anastomosis time (t4)– the distal anastomosis followed by the proximal anastomosis. once the nerve was completely repaired, muscle repair and skin suture finalized the intervention (t5). tt – total time – represents the sum of t1-t5. the anaesthesia protocol consisted of using a mixture of ketamine 75mg/kg and xylazine 10mg/kg injected intraperitoneal. the anaesthesia normally worked in 5 minutes and one dose lasted between 20 and 50 minutes, when a new dose may have been required. before the nerve dissection, as well as before nerve section, drops of lidocaine were supplementary used at the dissection site. the time for every anaesthesia dose administered was recorded and correlated to one of the 4 above mentioned times. the rats in the 1st batch were operated in 3 separate days during the first week of the experiment (1 rat the first day, 4 rats the second day and 5 rats the 4th day of the week). the rats in the second batch were operated in 4 separate days over the second week of the experiment (2 rats the first day, 2 rats the 4th day, 4 rats the 5th day and 2 rats the 6th day). files for every operation were created in order to record all the data and for the assistant to remember the steps in the operations which they needed to fulfil (preparing the operating area, disinfection, adding lidocaine directly on the nerve once exposed, dropping saline solution in the eyes to prevent eye dryness and noting down all the previously mentioned times). first batch – autograft 2nd batch – vascular conduct 246 marin andrei, marin georgiana gabriela, dobrote nicoleta amalia, enescu dan mircea results there is no statistical meaning between the 2 batches when referring to the median of age (p=0.148) or weight (p=0.264). batch 1 ranged between 50-61 days of age at the time of the operation, while the weight ranged between 246300g. in the second batch, the age varied between 50 and 53 days and the weight between 235-268g. variable batch 1 batch 2 total median (iqr) median (iqr) median (iqr) age (days) 52 (4) 51 (1) 55 (2) weight (gram) 269 (28) 245 (18) 258.5 (25) t1 (min) 43 (17) 23 (9) 35 (21) t2 (min) 5.5 (2) 7 (8) 6 (5) t3 (min) 9 (4) 8 (6) 8.5 (5) t4 (min) 37 (9) 29 (16) 35 (11) tt (min) 93 (43) 71.5 (30) 86 (31) no. anesthesia 2 (1) 2 (1) 2 (1) no. sutures 6.5 (2) 8 (3) 7 (3) there was a statistically significant difference between the preparation times (t1) in the 2 batches p=0.005 (the second batch having shorter preparation times compared to the first one). in the first batch, the t1 times improved from 136 minutes to 26 minutes, while the second batch had t1 times ranging from 37 to 19 minutes. an overview of the variables recorded for the operations in the 2 batches shows: 1. number of doses of anaesthesia administered: batch 1 – median=2 (iqr:1), with minimum 2 and a maximum of 6 doses batch 2 – median=2 (iqr:1), with a minimum of 1 and a maximum of 3 doses 2. number of sutures for both proximal and distal anastomosis batch 1 – median = 6,5 (iqr:2), with a minimum of 4 and a maximum of 9 sutures batch 2 – median = 8 (iqr:3), with a minimum of 7 and a maximum of 12 sutures after the statistical analysis (pearson correlation), 2 positive correlation with statistical meaning were observed: on the one hand between the number of doses of anaesthesia administered and the total time of the operation for the 2 batches (r=0.59, p= 0,007) – diagram a and on the other hand between the number of doses of anaesthesia and the anastomosis time t4 (r=0.65, p=0.002) –diagram b. the t4 times recorded for the 2 batches varied. for the first batch, there was a median of 37 minutes for the 2 anastomosis performed (with a maximum of 63 minutes and a minimum of 29 minutes), while in the second batch the median was at 29 minutes for 2 anastomoses (with a maximum of 60 minutes and a minimum of 13 minutes). diagram a diagram b 247 learning curve in rat dissection for experimental sciatic nerve repair batch 1 batch 2 total (batch1 + batch2) correlation correlation coef (r) p correlation coef (r) p correlation coef (r) p t4 – no. of anaesthesia 0.74 0.014 0.52 0.12 0.65 0.002 t4 – no. of sutures 0.29 0.41 0.68 0.03 0.24 0.31 tt – no. of anaesthesia 0.43 0.21 0.8 0.005 0.59 0.007 tt – no. of suturi 0.19 0.59 0.46 0.18 0.18 0.43 no. of sutures – no. of anaesthesia 0.18 0.6 0.45 0.19 0.12 0.62 no statistically significant correlations were established between the number of sutures and the anastomosis time t4 (r= 0.24, p=0.31), number of doses of anaesthesia administered (r=0,12, p=0.62) or total time (r=0.18, p=0.43). discussions there are no scientific data regarding operation times in sciatic nerve surgery performed in the rat model. the correlation between the number of doses of anaesthesia administered and the total time of the operation is reasonable, taking into consideration that administrating a new dose of anaesthesia requires extra time; this is due to the fact that the rat was placed in supine position, while the anaesthesia was administered intraperitoneal (on the ventral side) by elevating the opposite inferior limb under sterile conditions. the correlation between the number of doses of anaesthesia and the anastomosis time t4 can also be explained by the fact that the 2nd or 3rd dose of anaesthesia administered occurred mostly during t4, thus prolonging the anastomosis time. subjective factors may also influence the t2, t3 and t4 operation times (the overwork of the operator prolong the operating times) and resulted in fewer rats operated in a single day over the second week of the experiment. the assistant who was partially in charge of shaving the rat after anaesthesia was able to considerably reduce the t1 time by improving his technique, as well as the operator who prepared simultaneously the sterile draping and suitable placed pins and retractors for the operation. this is how the rat preparation time was considerably reduced in the second batch. the number of sutures might not have been correlated with the anastomosis time t4 because in the second batch this number was higher compared to the number of sutures performed in the first batch and while having similar or even faster times of execution. therefore, when performing a higher number of sutures in similar times shows that the learning curve improved the timing of these anastomoses. the only longer t4 time in the second batch of 60 minutes was in the case of the first rat, in which a new element was introduced – the bridging of the defect using the aortic conduct. all the other t4 times were under 40 minutes (compared to the first batch were 6/10 t4 times were under 40 minutes). this shows an improvement in the learning curve for the anastomosis, although no statistical difference was found. (p=0,31). conclusions the learning curve improved in the preparation time in the second batch compared to the first one, existing a statistical difference between the 2 batches. t4 – anastomosis times also improved in the second batch compared to the first one but this result wasn’t statistically different. prolonged overall times were observed when a second or 3rd dose of anaesthesia was needed during the intervention. the anastomosis time and total operation time is directly proportional with the number of anaesthesia’s performed for the anastomosis. the learning curve also improved when referring to the anastomoses of the nerves, since a higher number of sutures was performed in similar or even shorter times. however, the number of sutures 248 marin andrei, marin georgiana gabriela, dobrote nicoleta amalia, enescu dan mircea performed does not appear to influence the anastomosis time or the overall time in the given experiment. references 1. prodanov, dimiter & petkov, dimiter. (2006). morphometric analysis of the rat lower limb nerves: anatomical data for neural prosthesis design. 2. https://www.semanticscholar.org/paper/tibial-andfibular-nerves-evaluation-using-in-rats.-nepomucenopolitani/fcf3b6bbf5462ec73be2ee46987cc907abc03715/fi gure/5. 3. andrei, m., ioana, m., & mircea, e. (2019). underlying histopathology of peripheral nerve injury and the classical nerve repair techniques. romanian neurosurgery, 33(1), 17-22. https://doi.org/10.33962/roneuro-2019-003. 4. gärtner a, pereira t, armada-da-silva p, et al. effects of umbilical cord tissue mesenchymal stem cells (ucx®) on rat sciatic nerve regeneration after neurotmesis injuries. j stem cells regen med. 2014;10(1):14–26. published 2014 apr 30. 5. sayad fathi s, zaminy a. stem cell therapy for nerve injury. world j stem cells. 2017;9(9):144–151. doi:10.4252/wjsc. v9.i9.144. 6. casal d, mota-silva e, iria i, et al. reconstruction of a 10mm-long median nerve gap in an ischemic environment using autologous conduits with different patterns of blood supply: a comparative study in the rat. plos one. 2018;13(4):e0195692. published 2018 apr 16. doi:10.1371 /journal.pone.0195692. 7. https://www.biologycorner.com/worksheets/rat_external .html doi: 10.33962/roneuro-2023-001 pitfalls in the diagnosis of glioblastoma bica dorin, poeata ion romanian neurosurgery (2023) xxxvii (1): pp. 9-14 doi: 10.33962/roneuro-2023-001 www.journals.lapub.co.uk/index.php/roneurosurgery pitfalls in the diagnosis of glioblastoma bica dorin1, poeata ion2 1 neurohope, enayati medical city, sisesti 8a, bucharest, romania 2 university of medicine and pharmacy ‘grigore t. popa’, iasi, romania abstract glioblastoma (gbm) is one of the most dreadful human cancers having a literaturereported median of life of 14 months with maximal treatment. the correct diagnosis is of crucial importance for the best chances of treatment. misdiagnosis is uncommon, but seen in daily practice, and leads to important delays for patients. this paper will discuss the delays found in glioblastoma diagnosis in a series of 60 newly diagnosed patients. four out of 60 patients had a delay of more than 6 weeks of treatment initiation, as at first imaging, gbm was not suspected as a diagnosis. introduction glioblastoma is one of the most dreadful human cancers having a literature reported median of life of 14 months with maximal treatment6. the natural history of the disease is a median of two to three months from diagnosis. hence the correct diagnosis is of crucial importance so that these patients have the best chances to treatment. the clinical manifestations of glioblastoma vary from headaches to neurological deficits, epilepsy or, in some instances, psychiatric manifestations are seen21. imaging is normally done for neurological manifestations or persistent symptomatology, starting with mri or ct scan. resection surgery or biopsy is usually the next step in diagnosing and treating a glioblastoma patient. at surgery tumour tissue is taken and analysed in the pathology laboratory. during all these steps, from first symptoms to diagnosis, due to the complexity of cases, difficulties can arise, and these could lead sometimes to misdiagnosis. this paper will discuss the delays found in glioblastoma diagnosis in a series of 60 newly diagnosed patients. clinical material and methods from january 2015 to october 2022, 60 newly diagnosed patients with glioblastoma have been operated by the first author either by resection or stereotactic biopsy. of these patients we have analysed the cases in which the time from first imaging to surgery was more than six weeks. six weeks is an arbitrary number chosen to sort out only the patients where an important delay has been observed. usually, in our clinic it t a k e s a m a x i m u m o f t e n d a y s t o s c h e d u l e a p a t i e n t w i t h keywords glioblastoma misdiagnosis, glioblastoma diagnosis pitfalls, glioblastoma treatment delay corresponding author: bica dorin neurohope, enayati medical city, sisesti 8a, bucharest, romania bicadorin@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 10 bica dorin, poeata ion glioblastoma for surgery, so definitely six weeks sorts out only a patient where gbm was missed as diagnosis. in our standard procedure follow up is not an option when gbm is a suspicion. medical records were reviewed, including all imaging. patient data included age, gender, diagnosis, symptoms, past medical history, karnofsky score, imaging, time from first to secondary imaging, symptoms that led to secondary imaging and then to surgery. results we found five patients out of 60 that had surgery more than 6 weeks after first cerebral imaging was done. of these five patients 1 had an initial image highly suggesting gbm, but the patient refused any form of treatment for 3 months. she showed up to the hospital eventually with a state of confusion and hemiplegia and surgery was done. this patient is excluded from the discussions as the diagnosis was suspected from the first imaging. the other four patients had initial imaging 7, 6, 4 and 2 months respectively after first imaging to surgery for gbm and the considered diagnosis was ischaemia for two patients, haemorrhage, and lowgrade glioma respectively for the other two (table 1). the first patient is a 61-year-old male who presents an episode of intermittent paraesthesia on the right side of the body followed by slurred speech, and simple motor jackson contractions on the right side. a non-contrast mri scanning is done showing left temporal pole t1 hypointensity, and t2 hyperintensity (fig. 1). a. b. figure 1. (case no. 1): a. mri t2 hyperintensity at first imaging; b. contrast enhancing t1 mri showing tumour 7 months later. the past medical history shows hypertension and dyslipidaemia. ischaemia is considered as diagnosis and the patient is sent home with antiepileptics and follow up indication. seven months later the patient presents to hospital with fatigue, headaches and a follow up mri shows a contrast enhancing lesion. stereotactic biopsy is done in the first instance in another clinic confirming the diagnosis of gbm, followed by resection surgery in our clinic one month later. the second patient is a 69-year-old male who presents to the emergency room with an episode of confusion and memory disturbances. an initial ct scan is done, and the patient is considered to have had a stroke. low resolution mri is done during the same hospitalisation, and it does not raise the suspicion of tumour. initial evolution is favourable, and the patient is discharged home. few months later progressive confusion is observed, situation which culminates with a grand-mal convulsion. he is referred to the emergency room where new scanning is done including enhanced mri that shows left frontal enhancing intra axial tumour (fig. 2). the patient is referred to surgery and the glioblastoma diagnosis is confirmed. six months have passed between first head scan and surgery. a. b. a. b. figure 2. (case no. 2): a, b. ct scan and mri scan at first symptoms; c, d. contrast enhanced mri and perfusion mri 6 months later. the third patient is a 47-year-old lady that is referred to our clinic with confusion, aphasia, right side 11 pitfalls in the diagnosis of glioblastoma hemiparesis, having hypertension and epilepsy as past medical history. four months in advance the patient presents to the emergency room with right side hemiplegia. a ct enhanced and non-enhanced scanning shows a left frontoparietal profound ich (fig 3). she is considered to have haemorrhage after hypertensive bleed, and she is discharged to rehabilitation. there is initial good evolution but 3 months later the patient slowly deteriorates presenting again to the emergency room with confusion, aphasia and deteriorated right sided hemiparesis. mri shows a contrast enhancing tumour. the patient is referred to surgery and gbm is confirmed by the pathology report. table 1. medical record details of patients. lgg – low grade glioma no gender age initial imaging initial diagnosis time to surgery initial symptoms karnofsky score before surgery 1 male 61 mri ischemia 8 months epilepsy 90 2 male 69 ct/mri ischemia 6 months confusion 70 3 female 47 ct hemorrhage 4 months hemiplegia 40 4 female 61 mri lgg 2 months slurred speech 90 figure 3. (case no. 3): a. non enhanced ct scan showing ich at first symptoms; b. contrast enhanced ct scan with no obvious tumour; c. contrast enhanced mri 3 months later showing tumor, highly suggestive for gbm. figure 4. (case no. 4): a. t2 hyperintensity 1 at first symptoms; b. contrast enhanced t1 at first symptoms; c. t2 hyperintensity 6 weeks later. very fast growing is to be observed. the fourth patient is a 61-year-old lady that is referred to the neurology department for slurred speech. initial contrast enhanced mri is done showing a left frontal tumour in the vicinity of broca area which is considered as low-grade glioma (fig 4). initial evolution is favourable under corticosteroids and the patient is sent home with mri follow up indication. six weeks later after initial good clinical evolution the slurred speech reappears, and the patient complains also of headaches and fatigue. 12 bica dorin, poeata ion imaging studies show an important augmentation of the tumour which is highly suggestive for glioblastoma at this point. the patient is referred to surgery confirming diagnosis. discussions misdiagnosis can be seen in different phases of the gbm diagnosis. misdiagnosis can be of different sources: symptomatic/clinical origin12,13, 14, 19, of radiological origin, of surgical origin or of pathology origin 5, 9. when considering the radiological origin of misdiagnosis in glioblastomas, the initial image can be interpreted as other diagnostics like lymphoma4, metastasis, meningioma10, ischemia7,17, haemorrhage11, parasites23, abscess1, inflammatory diseases and degenerative processes13. it can even be misdiagnosed as contusion15. other sources of errors can be seen but the discussion is beyond the scope of this article. in this cohort of patients three of the 60 patients have been considered on initial scanning of having other diagnosis than tumour. a fourth one has been diagnosed with tumour, but it has been considered to be a lower grade, whose treatment implied only follow up if the diagnosis were to be correct. the survival of patients with glioblastoma is dismal. with treatment, most of the teams report a 14 months median survival. without treatment the median survival is two to three months6. sometimes patients present as emergency cases and surgical treatment needs to be instituted immediately. this is usually the case of high-volume tumours that have mass effect. in such cases the survival of the patient can be even of days without surgery14. very fast evolution can be seen23 confirming in vitro studies8. in our current practice we have all met patients, in whom despite maximal treatment with surgery, very fast recurrence of tumour is observed. case number four in this article seems to have such an evolution (fig 4). the importance of a correct diagnosis is crucial for patients with glioblastoma because of the speed of evolution of this disease. the longer the delay to diagnosis, the more difficult the surgery. the delay allows the spread of the tumour, by infiltrating farther into the brain. there are several prognostic factors for patients with gbm and one of them is the extent of resection. there are multiple studies showing that the extent of resection is important on the survival of these patients16. the sooner the diagnosis, the better for the patient in terms of surgery complexity and initiation of treatment. the delay makes surgery more complex, resection complexity usually being proportional with the size and location of the tumour. an important part of gbm patients is sent directly to palliative care, in part probably due to the operability of the tumour18, meaning that a late diagnosis can even prevent any initiation of active treatment. two of our patients were considered to have an ischemic stroke. they were discharged home with prophylactic antithrombotic therapy, but with no clear follow up indication of mri, as tumour was not considered as differential diagnosis. there are other case reports in literature with an almost identical trajectory with a percentage of misdiagnosis up to 10% in different series3. in our patients, presentation at the hospital did not imply thrombolysis or thrombectomy, but should they have arrived at the hospital inside the thrombolysis window, the stroke treatment could have harmed them as thrombolytic therapy should not be given to patients with brain tumours17. for the third patient, hypertensive bleed was the diagnosis on the initial enhanced ct scan. the diagnosis of tumour was not suspected. hence, the patient presented three months later with deteriorated symptomatology. a contrast enhanced mri showed tumour (fig 3). other teams report delay of diagnosis in case of haemorrhage20. in the case of the fourth patient, on the initial mri the diagnosis was low grade glioma. four out of 60 patients, 6,66% of patients, in this cohort of gbm patients, have been misdiagnosed in a way or another. as this is a devastating disease time is crucial for these patients. certain teams relate that in the case of misdiagnosis, only initial ct scanning was done3. in our cohort three of the patients had initial mri scanning, situation that could suggest that standard mri scanning or lowresolution mri is not always enough in depicting differential diagnosis between ischemic stroke and gbm or between lgg and gbm. diffusion mri, including dwi and adc, should be standard procedure for every brain pathology. new advanced mri techniques like spectroscopy, perfusion mri, dti should be used in diagnosing and making the differential diagnosis between other brain diseases and gbm22. obviously, advanced mri techniques cannot be made for every ischemic stroke even in highly developed societies because of 13 pitfalls in the diagnosis of glioblastoma cost-effectiveness issues11, as for developing societies advanced mri techniques for every patient is prohibitive. in difficult cases where there is doubt over the diagnosis spect1 and pet ct2 have been proposed as imaging techniques to be able to sort out the diagnosis. there are several possible reasons for fallacies in our cases, as retrospectively, few things could have been done better: better communication between clinician and radiologist, closer follow up, better communication with the rehabilitation clinic, advanced mri techniques when in doubt. these cases leave the impression that the scanning was done at the very beginning of the developing of the tumor. unfortunately, no genetic profile of the tumor has been done to further understand the evolution of these cases. gbm could be misdiagnosed as other pathologies like lymphoma, metastasis, or abscess. in these cases, immediate surgery is the standard treatment so at least there is no harm done by any delay. the correct diagnosis is the target for every single case, the diagnosing methods should be properly used, but this discussion is beyond the aim of this study. conclusions literature suggests that a non-negligible percentage of patients with ‘stroke’ are actually misdiagnosis for an even more devastating disease. other brain pathologies have been rarely considered instead of gbm, so it should be kept in mind that gbm is part of the differential diagnosis in other types of diseases of the brain. the conclusion of our study is in concordance with the reports of other teams. there are permanently updated guidelines for the diagnosis of gbm, but the pattern observed in all our cases is that the diagnosis has not been considered in the first instance. yet, the multitude of teams reporting misdiagnosis shows that this problem is not yet solved. improvements can be done in decreasing the number of misdiagnoses in gbm patients, but the diagnosis is not always straight forward, nor advanced technology is readily available. list of abbreviations ich: intracerebral haematoma; gbm: glioblastoma; mri: magnetic resonance imaging; ct: computed tomography; lgg: low grade glioma. references 1. alexiou ga, tsiouris s, kyritsis ap, polyzoidis ks, voulgaris s, fotopoulos ad. rapidly progressing glioblastoma resembling brain abscess in leukemia. 2008 mar;108(1):24-6. pmid: 18575184. acta neurol belg. published online 2008. 2. alongi p, vetrano ig, fiasconaro e, et al. choline-pet/ct in the differential diagnosis between cystic glioblastoma and intraparenchymal hemorrhage. curr radiopharm. 2018;12(1):88-92. doi:10.2174/187447101166618081712 2427 3. bell d, grant r, collie d, walker m, whittle ir. how well do radiologists diagnose intracerebral tumour histology on ct? findings from a prospective multicentre study. br j neurosurg. 2002;16(6):573-577. doi:10.1080/0268869 021000056179 4. bhatt. near misdiagnosis of glioblastoma as primary central nervous system lymphoma. j clin med res. published online 2014. doi:10.14740/jocmr1846w 5. chand p, amit s, gupta r, agarwal a. errors, limitations, and pitfalls in the diagnosis of central and peripheral nervous system lesions in intraoperative cytology and frozen sections. j cytol. 2016;33(2):93-97. doi:10.4103/0970-9371.182530 6. delgado-lópez pd, corrales-garcía em. survival in glioblastoma: a review on the impact of treatment modalities. clinical and translational oncology. 2016;18(11):1062-1071. doi:10.1007/s12094-016-1497-x 7. farkas a, schlakman b, khan m, joyner d. glioblastoma presenting with acute middle cerebral artery territory infarct. journal of stroke and cerebrovascular diseases. 2018;27(7):e113-e114. doi:10.1016/j.jstrokecerebrovasdi s.2018.01.019 8. furneaux ce, marshall es, yeoh k, et al. cell cycle times of short-term cultures of brain cancers as predictors of survival. br j cancer. 2008;99(10):1678-1683. doi:10.1038 /sj.bjc.6604716 9. gokden m. if it is not a glioblastoma, then what is it? a differential diagnostic review.; 2017. www.anatomicpathology.com 10. huang q ling, cao x, chai x, wang x, xiao c, wang j. the radiological imaging features of easily misdiagnosed epithelioid glioblastoma in seven patients. world neurosurg. 2019;124:e527-e532. doi:10.1016/j.wneu.201 8.12.128 11. inamasu j, kuramae t, nakatsukasa m. glioblastoma masquerading as a hypertensive putaminal hemorrhage: a diagnostic pitfall-case report. vol 49.; 2009. 12. khan f, khan s, masud s, masud n. glioblastoma multiforme misdiagnosed as squint: a case report. j family med prim care. 2020;9(8):4418. doi:10.4103/jfmp c.jfmpc_541_20 13. lakhan se, harle l. difficult diagnosis of brainstem glioblastoma multiforme in a woman: a case report and review of the literature. j med case rep. 2009;3. doi:10.1186/1752-1947-3-87 14 bica dorin, poeata ion 14. leo rj, frodey jn, ruggieri ml. subtle neuropsychiatric symptoms of glioblastoma multiforme misdiagnosed as depression. bmj case rep. 2020;13(3). doi:10.1136/bcr2019-233208 15. li x, wang k, zhang a, et al. glioblastoma mimicking a cerebral contusion: a case report. oncol lett. 2013;6(5):1499-1501. doi:10.3892/ol.2013.1537 16. li ym, suki d, hess k, sawaya r. the influence of maximum safe resection of glioblastoma on survival in 1229 patients: can we do better than gross-total resection? j neurosurg. 2016;124(4):977-988. doi:10.3171 /2015.5.jns142087 17. morgenstern lb, frankowski rf. brain tumor masquerading as stroke. vol 44.; 1999. 18. noorbakhsh a, tang ja, marcus lp, et al. gross-total resection outcomes in an elderly population with glioblastoma: a seer-based analysis. clinical article. j neurosurg. 2014;120(1):31-39. doi:10.3171/2013.9.jns13 877 19. sanli a, turkoglu e, dolgun h, sekerci z. unusual manifestations of primary glioblastoma multiforme: a report of three cases. surg neurol int. 2010;1(1):87. doi:10.4103/2152-7806.74146 20. vetrano ig, ganduscio g, alongi p. letter to the editor regarding “the radiological imaging features of easily misdiagnosed epithelioid glioblastoma in seven patients.” world neurosurg. 2019;125:544-545. doi:10.1 016/j.wneu.2019.01.109 21. wen py, kesari s. medical progress malignant gliomas in adults. vol 359.; 2008. www.nejm.org 22. wen py, macdonald dr, reardon da, et al. updated response assessment criteria for high-grade gliomas: response assessment in neuro-oncology working group. journal of clinical oncology. 2010;28(11):1963-1972. doi:10.1200/jco.2009.26.3541 23. zhang yy, ruan lx, zhang s. rapid progression of glioblastoma multiforme: a case report. oncol lett. 2016;12(6):4803-4806. doi:10.3892/ol.2016.5228. doi: 10.33962/roneuro-2022-088 surgical outcome of pineal region lesions in paediatric population shaam bodeliwala, sharad pandey, pankaj kumar, daljit singh, anita jagetia, hukum singh, a.k. srivastava, anil kumar, rajesh ruttala romanian neurosurgery (2022) xxxvi (4): pp. 483-491 doi: 10.33962/roneuro-2022-088 www.journals.lapub.co.uk/index.php/roneurosurgery surgical outcome of pineal region lesions in paediatric population shaam bodeliwala1, sharad pandey2, pankaj kumar2, daljit singh1, anita jagetia1, hukum singh1, a.k.srivastava1, anil kumar3, rajesh ruttala4 1 govind ballabh pant institute of postgraduate medical education and research (gipmer), india 2 atal bihari vajpayee institute of medical sciences and dr ram manohar lohia hospital, india 3 esic medical college, faridabad, india 4 maulana azad medical college, india abstract introduction. pineal region pathologies are heterogenous, spectrum ranging from benign, infective to malignant in nature such as parenchymal, germ cell, glial, melanomas, metastatic, tubercular, etc. these lesions are commoner in the pediatric age group and have a variable outcome. the goal of this study is to present our experience regarding the surgical outcomes of pineal region lesions in the paediatric population. objective. the objective of this study is to access the surgical outcome of pineal region lesions in the paediatric population methods and material. eighty cases of pineal region lesions in the paediatric population (up to 15 years of age) operated in the neurosurgery department, g.b pant hospital new delhi via either occipital transtentorial or supracerebellar infratentorial approaches were retrospectively analysed. results. there were four main groups of lesions with pineal parenchymal tumours (35 cases) being the commonest. glial tumours were the next most common contributing 29 cases. germ cell tumours comprise 7 and miscellaneous 9 cases. the outcome showed graded improvement with the extent of tumour removal and 57 patients (71.25%) improved following surgery. the clinical status of 20 patients (25%) remained unchanged and 3(3.75%) deteriorated from their pre-operative status. 3 patients (3.75%) died in the immediate post-operative period and 11(13.75%) died due to recurrent disease. conclusion. a graded increase in survival was noted with increasing the degree of resection and postoperative adjuvant therapy in malignant pineal tumours whereas benign pineal lesions can be managed with surgery. pure germinomas are the only tumour for which the survival rate was unrelated to extent of tumour resection. introduction the pineal region lesions are heterogenous in nature such as germ cell tumours, glial tumours, pineal parenchymal tumors, primary melanoma, metastasis,cysts, infective, etc.1,2,3 keywords paediatric population, pineal region lesions, surgical outcome corresponding author: pankaj kumar atal bihari vajpayee institute of medical sciences and dr ram manohar lohia hospital, india aditya.thewinner@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 484 shaam bodeliwala, sharad pandey, pankaj kumar et al. these tumours are common in children comprising of more than 10% of all pediatric tumours with common presentation of raised intracranial pressure secondary to obstructive hydrocephalous due to close relation with posterior third ventricle.4,5,6 with better microsurgical skills, the surgical outcome is associated with less morbidity and mortality, however the long term surgical and functional outcome depends on various factors such as age, extent of resection of tumour, pathological grade, distant seedling at the time of presentation, neurological condition, visual status, possibility of giving adjuvant therapy .8,9,10, 11,12,13,14,15,16. in the present study, we retrospectively analyzed the surgical outcome of pineal region lesion in children treated over last 15 years. material and methods eighty cases of pineal region lesions in children operated via two approaches i.e occipital transtentorial and supracerebellar infratentorial (fig1a,b) in the department of neurosurgery, gipmer, new delhi were retrospectively analyzed. the techniques for both the approaches were as standards described in the literature. postoperatively clinical and radiological outcome was analyzed. postoperative tumour excision was graded as gross total, near total, subtotal or biopsy when >99%, >90%, 51-90% or <50% tumour was resected respectively based on mri study. figure 1. a. occipital transtentorial; b. supracerebellar infratentorial. a-inferior saggital sinus,b-great cerebral vein of galen, ctransverse sinus, d-internal cerebral vein, e-posterior cerebral artery, f-superior cerebellar artery, g-anterior inferior cerebellar artery. results eighty children were followed up for 1-5 years depending upon the pathology. twenty children (25%) were in the age group of 4-6 years and 16 cases (15%) were 8-10 years old; the youngest patient being 2 years and oldest was14 years old with a mean age of 7.5 years. there were 39 males (48.75%) and 41females(51.25%) with the m:f ratio of 0.95:1(table 1) figure 2a. pre-operativet1 saggital & t2 axial images of pineal region teratoma figure 2b. post-operative ct showing complete removal of teratoma histopathologically pineal parenchymal tumors was constituting 43.75%, out of which pinealoblastoma(21.25%) constituted the major portion followed by glial tumours (36.25%), germ cell tumours(8.75%). remaining lesions like meningioma, choroid plexus papilloma, epidermoid cyst and tubercular abscess and cysticercosis were uncommon. (table 2). headache was the most common presenting symptom observed in all cases followed by vomiting in 41.25%, visual disturbance in 41.25%, diplopia in 31.25%, papilloedema 46.25%. parinauds syndrome was present in 38.75%, weakness in upper or lower extremity was common in glial tumors infiltrating surrounding structures, 15% had cerebellar signs, 6.25% hormonal imbalance and 3.75% were in altered sensorium at the time of presentation. eighteen cases underwent hcg or afp level assessment in csf and 3 cases showed elevated levels in germinoma & teratoma. 485 surgical outcome of pineal region lesions in paediatric population out of 80 cases,57 (71.25%) improved, 20 (25%) remained unchanged and 3(3.75%) patients deteriorated in postoperative period. three patients (3.75%) died in immediate post-operative period and 11(13.75%) died in the follow up due to recurrent disease. surgical outcome based on extent of resection is given in table 4.based on extent of resection, total removal led to improvement in 75-100 % cases irrespective of pathology. improvement in pilocytic astrocytomas was 90%, pineocytoma 57%, pineoblastoma 47%, intermediate pineal tumor was 45% and 60% in germinoma cases. improvement was almost 100% in benign lesions such as meningioma, epidermoid cyst, oligodendroglioma, choroid plexus papilloma, infective pathologies (figure 3,5) near total removal showed 47% improvement in pineoblastoma whereas patients with pathologies such as fibrillary astrocytoma, anaplastic astrocytomas, germinomas showed 100% improvement even after near total excision. figure 3a & 3b. preoperative axial & saggital images of pineal region epidermoid. figure 3c & 3d. post-operative axial ct showing excision of pineal region epidermoid. except for germinoma subtotal removal of tumours showed no improvement in postoperative period. in the biopsy group out of 2 patients,50% remained unchanged and 50% deteriorated with one immediate and one delayed mortality. all cases of ependymoma improved after gross and near total resection. out of 5 patients of germinoma, 3 patients improved after gross total removal, near total and subtotal resection and radiotherapy (figure 4), 2 patients underwent biopsy out of which one remained unchanged and one deteriorated and died in post operative period due to disseminated disease. out of 2 cases of immature teratoma (figure 2a,b), 1 patient improved and one remained unchanged after near total excision.(table 3 & 4). a csf diversion procedure as ventriculoperitoneal shunt was needed in 31 patients(38.75%) of pineal tumour patients . figure 4a & 4b. pre-operative saggital mr image in t1 contrast of pineal region germinoma & post operative saggital t1 mr after excision and radiotherapy. figure 5a & b. pre-operative saggital & axial t1 contrast mr images of tubercular abscess. figure 5c & d. post-operative axial ct of tubercular abscess after excision of tubercular abscess. 486 shaam bodeliwala, sharad pandey, pankaj kumar et al. table 1. age and sex distribution sr. no. age group no. of females no. of males total no. of cases 1 0-2 1 0 1 2 2-4 6 7 13 3 4-6 9 11 20 4 6-8 9 5 14 5 8-10 7 9 16 6 10-12 5 3 8 7 12-14 4 4 8 8 14-15 0 0 0 total 41 39 80 51.25% 48.75% table 2. histopathology of 80 cases of pineal region tumours diagnosis no. of cases • pineal parenchymal tumors • pineocytoma • pineal parenchymal tumor of intermediate differentiation • pineoblastoma 35 (43.75%) 7 (8.75%) 11 (13.75%) 17 (21.25%) gliomas • pilocytic astrocytoma • fibrillary astrocytoma • anaplastic astrocytoma • glioblastoma • oligodendroglioma • ependymoma • subependymal giant cell astrocytoma 29 (36.25%) 10 (12.50%) 4 (5%) 3 (3.75%) 1 (1.25%) 3 (3.75%) 6 (7.50%) 2 (2.5%) germ cell tumors • germinoma • immature teratoma 7 (8.75%) 5 (6.25%) 2 (2.5%) miscellaneous • meningioma • choroid plexus papilloma • epidermoid cyst • tubercular abscess • cysticercosis 9 (11.25) 2 (2.25%) 3 (3.75%) 2 (2.25%) 1 (1.25%) 1 (1.25%) total 80 (100%) table 3. surgical outcome according to histopathology diagnosis no. of cases (n) outcome mortality (%) improved (%) unchanged (%) deteriorated (%) pineocytoma 7 4(57.14%) 3(42.85%) 0 0 pineal parenchymal tumor of intermediate differentiation 11 5(45.45%) 6(54.54%) 0 4(36.36%) pineoblastoma 17 8(47.05%) 7(41.17%) 2(11.76%) 8(47.05%) pilocytic astrocytoma 10 9(90%) 1(10%) 0 0 487 surgical outcome of pineal region lesions in paediatric population fibrillary astrocytoma 4 4 0 0 0 anaplastic astrocytoma 3 3 0 0 0 glioblastoma 1 0 1 0 1 oligodendroglioma 3 3 0 0 0 ependymoma 6 6 0 0 0 sega 2 2 0 0 0 germinoma 5 3(60%) 1 1(20%) 1(20%) immature teratoma 2 1 1 0 0 meningioma 2 2 0 0 0 choroid plexus papilloma 3 3 0 0 0 epidermoid cyst 2 2 0 0 0 tubercular abscess 1 1 0 0 0 cysticercosis 1 1 0 0 0 total (%) 80 (100%) 57 (71.25%) 20 (25.00%) 3 (3.75%) 14 (17.5%) table 4. surgical outcome based on extent of tumour removal diagnosis no. of cases extent of tumour removal no of cases outcome mortality improved unchanged deteriorated pineocytoma 7 gt 4 3(75%) 1(25%) 0 0 nt 1 1 0 0 0 st 2 0 2 0 0 pineal parenchymal tumor of intermediate differentiation 11 gt 6 5(83.33%) 1(16.67%) 0 0 nt 2 0 2(100%) 0 1 st 2 0 2(100%) 0 2 biopsy 1 0 1(100%) 0 1 pineoblastoma 17 gt 5 4(80%) 1(20%) 0 0 nt 7 4(57.14%) 3(42.85%) 0 3 st 3 0 2(66.66%) 1(33.33%) 3 biopsy 2 0 1(50%) 1(50%) 2 pilocytic astrocytoma 10 excision 2 2(100%) 0 0 0 gt 6 6(100%) 0 0 0 nt 1 1(100%) 0 0 0 st 1 0 1(100%) 0 0 fibrillary astrocytoma 4 gt 3 3(100%) 0 0 0 nt 1 1(100%) 0 0 0 anaplastic astrocytoma 3 gt 2 2(100%) 0 0 0 nt 1 1(100%) 0 0 0 glioblastoma 1 st 1 0 1(100%) 0 1 oligodendroglioma 3 gt 3 3(100%) 0 0 0 ependymoma 6 gt 5 5(100%) 0 0 0 nt 1 1(100%) 0 0 0 sega 2 excision 1 1(100%) 0 0 0 gt 1 1(100%) 0 0 0 germinoma 5 gt 1 1 0 0 0 nt 1 1 0 0 0 st 1 1 0 0 0 biopsy 2 1(50%) 1(50%) 1 immature teratoma 2 nt 2 1(50%) 1(50%) 0 meningioma 2 simpson’s grade iii excision 2 2(100%) 0 0 0 488 shaam bodeliwala, sharad pandey, pankaj kumar et al. choroid plexus papilloma 3 gt 3 3(100%) 0 0 0 epidermoid cyst 2 excision 2 2(100%) 0 0 0 tubercular abscess 1 excision 1 1(100%) 0 0 0 cysticercosis 1 excision 1 1(100%) 0 0 0 gt, gross total resection; nt, near total resection; sega, subependymal giant cell astrocytoma; st, subtotal resection upgaze palsy was present in 3 which persisted in post-operative period. subdural effusion was present in 4 cases & was self limiting. most severe complication was postoperative haemorrhage in 2 cases due to incomplete resection of tumor. in infratentorial supra-cerebellar approach venous air embolism & hypotension was noted in 8 cases. venous air embolism was treated with rapidly packing the operative field with wet sponges,waxing bony edges, air aspiration from right atrium via cvp catheter, ventilation of patients with 100% o2, use of vasopressor & volume expanders.postoperative hemianopia was the most common complication following suboccipital transtentorial approach and was encountered in 7 cases due to prolonged retraction of occipital lobe. meningoencephalitis was noticed in one case. suitable candidates were referred for adjuvant treatment. five-year survival rate of the patients is shown in table 5. table 5. survival rates for patients with pineal tumours 5 year survival pineocytoma (pc) 71% pineal parenchymal tumour of intermediate differentiation (pid) 63% pineoblastoma(pb) 46% high grade glial tumours 80% germ cell tumours (gcts) 90% discussion transcallosal approach for pineal lesions was first described by dandy18 in 1921, however all patients died initially and first successful excision was performed in 1931. the operative mortality of pineal region lesions was as high as 90% as per reported by russel and sachs 19 in 1943. thereafter with more refined surgical skills and knowledge of anatomy, increasing sophistication of stereotactic surgery and the high morbidity and mortality rates of open operation on the pineal region, neurosurgeons advocated stereotactic biopsy for pineal region masses. however with recent advances, surgery on the pineal region has became increasingly safer & is now the treatment of choice as it allows significant debulking of lesions and adequate specimen to identify the pathology of lesion. we are also in favor of surgery to radically remove the lesion to avoid unnecessary radiation to benign lesions and radiation associated significant morbidity particularly in children. radiation can cause arachnoid thickening, adhesions and which can be troublesome especially for recurrent tumours. hoffman et al.20 also recommended open surgery in order to establish accurate histological diagnosis to guide the adjuvant therapy indications. the median age of presentation in this study was 7.5years (range 1-15) and male to female ratio was 0.95:1 (table 1). in the present study pineal parenchymal tumours(ppt) were most common constituting 43.75% followed by glial tumors comprising 36.25% and germ cell tumours<9%.in indian population ppt is commoner than germ cell tumours(table 2). tatkem et al. reported 42% of tumours to be ppt in indian population.24 in contrast to this, cho bk et al. reported even higher incidence of both ppt and germ cell tumours i.e. 69% and 19% respectively in far east population22. aal-hussaini m et al collected data from 17 seer registries (these data included a total of 5306606 tumors diagnosed from january 1973-december 2005) and reported germ cell tumors as most common histological type followed by pineal parenchymal tumors23. rosenstock17 et al and reported 32% pineal parenchymal tumors and 26% glial tumours respectively in their series. in this study headache was present in all cases followed by vomiting and diplopia in 41.25% and 38.75%respectively. papillodema was observed in 46.25% with parinauds syndrome in 38.75%.various studies by hoffman et al,20, villa et al, 25konovalov and pitskhelauri3 et al , cho b.k et al also found signs and symptoms of raised intracranial pressure in 80 489 surgical outcome of pineal region lesions in paediatric population 90% and parinaud’s syndrome in 25%-50% of cases. al-hussaini m et al collected data from 17 seer registries (these data included a total of 5306606 tumors diagnosed from january 1973-december 2005) and concluded that amoung malignant tumours of pineal region germ cell tumours had best outcome, which was further improved by radiotherapy use but not by total excision23. konovalov an and pitskhelauri di3 et al reported pure germinomas having 95% and 88% 5 year and 10 year survival; high grade glial tumors as 80% and 50%, 5 year and 10 year survival rate; malignant pineal parenchymal tumours as 44% and 0% 5 year and 10 year survival rate; malignant gcts as 20% and 0% 5 year and 10 year survival rates respectively. in our study highest mortality was noted in cases of pineoblastoma(47.05% mortality), which is the most malignant tumour of pineal region followed by pineal parenchymal tumor of intermediate differentiation(36.36%). in our study pineal parenchymal tumor of intermediate differentiation had 70% overall 5 year survival rate; pineoblastoma having 70.58% overall 5 year survival rate; germinoma having 75% overall survival rate. there is 34.28% mortality in pineal parenchymal group followed by 20% mortality in germ cell tumor group and 3.44% mortality in glial tumor group without any mortality in bening lesions of pineal region, correlating mortality with the histopathological diagnosis. konovalov an and pitskhelauri di3 found an association between the extent of tumor removal and survival in patients with all types of malignant tumors except pure germinoma. the 5 year survival rate was 70% for patients who had a total tumor resection and 30% for patients who had a biopsy or partial resection. pure germinomas was the only tumor for which survival rate was not associated with the extent of tumor resection. tatke m et al reported a graded increase in survival with increasing degree of resection (5 year survival rate:84% for gtr vs 53% for str vs 29% for debulking in case of pineoblastomas. (table4,5). konovalov an and pitskhelauri di3 found an association between the extent of tumor removal and survival in patients with all types of malignant tumors except pure germinoma. the 5 year survival rate was 70% who had a total tumor resection and 30% who had a biopsy or partial resection. pure germinomas was the only tumor for which survival rate was not associated with the extent of tumor resection perhaps these are the tumours which responds best to radiotherapy. tatke m24 et al also reported a graded increase in survival with increasing degree of resection in pineoblastomas. clark aj et al suggested that aggressive surgical resection provides a survival benefit over subtotal resection for patients of pineocytomas 26. in our study, 75% of pineocytomas improved after gross total removal , 83.33% of pineal parenchymal tumors improved after gross total removal and 80% of pineoblastomas improved after gross total removal. in cases of pilocytic astrocytoma all cases of gross total and near total removal improved with one case of subtotal removal remained unchanged. all cases of fibrillary astrocytoma, anaplastic astrocytoma, ependymomas and sega showed improvement after gross and near total excision. one case of glioblastoma expired after subtotal removal. all cases of germinomas showed improvement regardless of extent of removal except one case of disseminated germinoma which died in post op period and one case remained in unchanged status. all other miscellaneous lesions improved after excision, gross total or near total removal(table3,4) konovalov an and pitskhelauri di3 described the principles of treatment of the pineal region tumours on the basis of total 287 operations done over a period from 1976 to 1999. it included 161 males and 126 females with a mean age of 20 years at presentation. they used occipital transtentorial approach in 138(54%) and infratentorial supracerebellar approaches in 87(34%) of patients. total removal was achieved in 58% patients, subtotal removal in 29% and partial removal in 13% patients. 58% patients had obstructive hydrocephalus that underwent craniospinal fluid shunting before radiotherapy or with tumour removal. features of raised intracranial pressure and eye movement disorders were among the most common presentation. present study, includes 80 patients with pineal region lesions. a csf diversion procedure as ventriculoperitoneal shunt was needed in 31 patients(38.75%) of pineal tumour patients . two approaches were commonly used: supracerebellar infratentorial approach was used in 62(77.5%) and occipital transtentorial in 18(22.5%) patients of pineal tumours. stein bm 27 reported their experience of 6 cases of pineal lesions, 490 shaam bodeliwala, sharad pandey, pankaj kumar et al. operated using krause’s supracerebellar infratentorial approach. they had no operative mortality. operative morbidity was negligible and except for a varying degree of meningeal reaction managed effectively with steroids, their pateints had uneventfull postoperative courses. suzuki and iwabuchi have reported the largest series of successfully treating lesions of the pineal region using the direct surgical approach. 17 of 19 cases underwent total or near total removal via a supratentorial approach. in our study post operative complications according to surgical approach were as follows; infratentorial supracerebellar approach: ocular abnormality in the form of upgaze palsy was present in 3 which lasted for few weeks in post-operative period. subdural effusion was present in 4 cases & was self limiting. most severe complication was postoperative haemorrhage in 2 cases due to incomplete resection of tumor. occipital transtentorial approach: postoperative hemianopia was the most common complication in this approach encountered in 7 cases due to excessive retraction of occipital lobe. gentle & gradual retraction of occipital lobe is necessary to avoid this complication. meningoencephalitis was noticed in one case. clark aj et al reported that patients receiving subtotal tumor resection (str) versus those undergoing str plus external beam radiotherapy (xrt), the addition of adjuvant radiation does not yield a survival benefit when compared to str alone. in the light of the superiority of gross total resection (gtr) to str, it appeared that pineocytomas are relatively radioresistant and are optimally treated with aggressive surgery rather than xrt. stoiber em et al reported that fractionated local radiotreatment of pineocytomas seems to be safe and effective method with a local recurrence control rate of 100%, intensification of therapy in aggressive variants of intermediate pineocytomas as well as pineoblastomas seemed necessary28. the ccg921(childrens cancer group) report suggested that radiation therapy has a significant impact on survival with a 3-year survival of 61% in paediatric pineoblastoma population. konovalov an and pitskhelauri di et al reported that radiation therapy should be administered to all patients with pineal region tumors other than meningioma, mature teratoma and some rare bening tumors or cysts3.germinoma is chemotherapy & radiosensitive. for intracranially arising germonimas radiation therapy is the primarily curative. radiation therapy is best avoided in young children & many centres advocate few cycles of chemotherapy followed by radiation therapy as well. more aggressive tumors of pineal region like malignant germ cell and pineal parenchymal tumors tend to invade surrounding cerebellar structures and have a high risk of spinal dissemination and commonly cannot be totally resectable, so radiation therapy and chemotherapy play a crucial role in the treatment3. schild s.e et al. reported that pineoblastomas and pineal parenchymal tumor of intermediate differentiation, it is possible to obtain better results with surgical resection and relatively high doses of radiation (50 to 55 gy)29. according to tate m et al the addition of radiotherapy to gross total removal did not improve survival; however, the addition of radiotherapy to subtotal removal did yield a survival benefit in cases of pineoblastoma19. in our study total 30(37.5%) patients received radiotherapy and 12(15%) patients received chemotherapy. in patients with pineoblastomas, pineal parenchymal tumors of intermediate differentiation, germinomas, immature teratomas, anaplastic astrocytomas, patients who received post-operative radiotherapy have better overall and progression free survival. chemotherapy as part of treatment for pineal tumors(cisplatinetoposide combination) was used. many of our patients were in the advanced stage of their illness bearing large tumours which is an additive factor to the morbidity and mortality of our patients. in patients with bening lesions, surgical removal is curative. in malignant tumours, satisfactory decompression of tumour improve response to postoperative adjuvant therapy. conclusion pineoblastoma is the most common histological type among pineal region tumours in children.a graded increase in survival noted with increasing the degree of resection and post-operative adjuvant therapy in malignant pineal tumors.pure germinomas are the only tumor for which survival rate was not associated with the extent of tumor resection. selection of the surgical approach (supra/infra-tentorial) according to the extension of the tumor (above or below the 491 surgical outcome of pineal region lesions in paediatric population tentorium) may give window to the greater surgical resection and reflect the improved outcome. references 1. bruce jn, stein bm. surgical management of pineal region tumors. acta neurochirurgica. 1995 sep;134(3):130-5. 2. hernesniemi j, romani r, albayrak bs, lehto h, dashti r, ramsey iii c, karatas a, cardia a, navratil o, piippo a, fujiki m. microsurgical management of pineal region lesions: personal experience with 119 patients. surgical neurology. 2008 dec 1;70(6):576-83. 3. konovalov an, pitskhelauri di. principles of treatment of the pineal region tumors. surgical neurology. 2003 apr 1;59(4):252-70. 4. abay eo ii, laws er, grand gl, et al. pineal tumors in children and adolescents. j neurosurg1981;55:889–95. 5. fuller bg, kapp ds, cox r. radiation therapy of pineal region tumors: 25 new cases and a review of 208 previously reported cases. international journal of radiation oncology* biology* physics. 1994 jan 1;28(1):229-45. 6. hart mn, earle km. primitive neuroectodermal tumors of the brain in children. cancer. 1973 oct;32(4):890-7. 7. bruce jn, stein bm. supracerebellar approaches in the pineal region. in: apuzzo mlj, ed. brain surgery: complication, avoidance and management. new york: churchill-livingstone, 1993:511–36. 8. jooma r, kendall be. diagnosis and management of pineal tumors. journal of neurosurgery. 1983 may 1;58(5):654-65. 9. neuwelt ea, glasberg m, frenkel e, clark wk. malignant pineal region tumors: a clinico-pathological study. journal of neurosurgery. 1979 nov 1;51(5):597-607. 10. neuwelt ea. an update on the surgical treatment of malignant pineal region tumors. in: clinical neurosurgery: proceedings of the congress of neurological surgeons, volume 32. baltimore: williams & wilkins, 1985:397-428. 11. cumins fm, taveras jm, schlesinger eb. treatment of gliomas of the third ventricle and pinealomas. with special reference to the value of radiotherapy. neurology 1960;10:1031–6. neuwelt ea, glasberg m, frenkel e, clark wk. malignant pineal region tumors: a clinicopathological study. journal of neurosurgery. 1979 nov 1;51(5):597-607. 12. dandy we. operative experience in cases of pineal tumor. archives of surgery. 1936 jul 1;33(1):19-46. 13. davidoff lm. some considerations in the therapy of pineal tumors. bulletin of the new york academy of medicine. 1967 jul;43(7):537. 14. horrax g. treatment of tumors of the pineal body: experience in a series of twenty-two cases. archives of neurology & psychiatry. 1950 aug 1;64(2):227-42. 15. poppen jl, marino r. pinealomas and tumors of the posterior portion of the third ventricle. journal of neurosurgery. 1968 apr 1;28(4):357-64. 16. suzuki j, iwabuchi t. surgical removal of pineal tumors (pinealomas and teratomas): experience in a series of 19 cases. journal of neurosurgery. 1965 dec 1;23(6):565-71. 17. packer rj, sutton ln, rosenstock jg, rorke lb, bilaniuk lt, zimmerman ra, littman pa, bruce da, schut l. pineal region tumors of childhood. pediatrics. 1984 jul;74(1):97102. 18. dandy we. operative experience in cases of pineal tumor. arch surg 1936;33:19–46. 19. russell ow, sachs e. pinealoma. a clinicopathologic study of seven cases with a review of the literature. the journal of nervous and mental disease. 1944 jun 1;99(6):974. 20. hoffman hj, otsubo h, hendrick eb, humphreys rp, drake jm, becker le, greenberg m, jenkin d. intracranial germ-cell tumors in children. journal of neurosurgery. 1991 apr 1;74(4):545-51. 21. tate m, sughrue me, rutkowski mj, kane aj, aranda d, mcclinton l, mcclinton l, barani ij, parsa at. the long‐ term postsurgical prognosis of patients with pineoblastoma. cancer. 2012 jan 1;118(1):173-9. 22. cho bk, wang kc, nam dh, kim dg, jung hw, kim hj, han dh, choi ks. pineal tumors: experience with 48 cases over 10 years. child's nervous system. 1998 mar;14(1):53-8. 23. al-hussaini m, sultan i, abuirmileh n, jaradat i, qaddoumi i. pineal gland tumors: experience from the seer database. journal of neuro-oncology. 2009 sep;94(3):3518. 24. kumar p, tatke m, sharma a, singh d. histological analysis of lesions of the pineal region: a retrospective study of 12 years. pathology-research and practice. 2006 feb 15;202(2):85-92. 25. villà s, miller rc, krengli m, abusaris h, baumert bg, servagi-vernat s, igdem s, lucas a, boluda s, mirimanoff ro. primary pineal tumors: outcome and prognostic factors—a study from the rare cancer network (rcn). clinical and translational oncology. 2012 nov;14(11):827-34. 26. clark aj, sughrue me, ivan me, aranda d, rutkowski mj, kane aj, chang s, parsa at. factors influencing overall survival rates for patients with pineocytoma. journal of neuro-oncology. 2010 nov;100(2):255-60. 27. stein bm. the infratentorial supracerebellar approach to pineal lesions. journal of neurosurgery. 1971 aug 1;35(2):197-202. 28. stoiber em, schaible b, herfarth k, schulz-ertner d, huber pe, debus j, oertel s. long term outcome of adolescent and adult patients with pineal parenchymal tumors treated with fractionated radiotherapy between 1982 and 2003--a single institution's experience. radiation oncology. 2010 dec;5(1):1-7. 29. schild se, scheithauer bw, schomberg pj, hook cc, kelly pj, frick l, robinow js, buskirk sj. pineal parenchymal tumors: clinical, pathologic, and therapeutic aspects. cancer. 1993 aug 1;72(3):870-80. microsoft word 2gorganmr_deontological_for 240 m.r. gorgan et al misdiagnosis of cerebral metastases deontological issues possible misdiagnosis of cerebral metastases m.r. gorgan, narcisa bucur, angela neacsu,v.m. pruna, s. craciunas, aura sandu, adriana dediu, calina nichi, iulia vapor iulia, a. giovani first neurosurgical clinic, fourth neurosurgery department, clinic emergency hospital “bagdasar-arseni” bucharest abstract authors analysed a number of 4588 (52, 24% over 50 years old) patients operated for cerebral tumors in the clinic emergency hospital “bagdasar-arseni” from bucharest, between 2000-2010, with peculiar attention to the concordance between the preoperative and postoperative diagnosis, related to the actual policy to evaluate a neurosurgical patient before surgery. 903 cases were cerebral metastases and 69,5% aged over 50 years old. in 9,7% of cases we recorded a preoperative misdiagnosis of a metastasis due to few main reasons: unavailable information about a present primitive cancer, treacherous mri image with a single confusing appearance of a cerebral lesion, age less than 50 years old, clinical presentation and biological evaluation inconsistent with malignancy. authors point that these situations can have serious consequences related to professional competence, deterioration of the patientdoctor relationship, increasing costs for completion of diagnosis and treatment, and inadequate information about patient’s prognosis. keywords: cerebral metastases, deontological issues, diagnosis, concordance introduction cerebral metastases represent the spread of a neoplasm from a primary site to the brain. the most common primary tumors metastatic to brain include lung cancer (adenosquamous and small cell especially), breast cancer, melanoma, renal cancer and colon cancer. metastases are frequently found at the grey/white junction. they are usually well demarcated from the brain parenchyma. the majority of metastases (greater than 75%) are found supratentorially with the minority (less than 10%) found in the brainstem. the patients present with signs and symptoms referable to either increased intracranial pressure or focal pathology (4). a contrast enhanced mri will give the best view of suspected metastatic cancers. therapy for the metastatic cancer is based upon the therapy that would be or has been given to the primary cancer. in any event corticosteroids can be useful for reduction of patients' symptoms. metastases to the brain is the most feared complication of systemic cancer and the most common intracranial tumor in adults. the incidence of brain metastasis is rising with the increase in survival of cancer patients. currently, cancer patients live longer as a result of important advances in cancer diagnosis and management, and in particular, the romanian neurosurgery (2011) xviii 3: 240 254 241 widespread use of mri to detect small metastases. approximately 40% of intracranial neoplasms are metastatic (9). multiple, large autopsy series suggest that, in order of decreasing frequency, lung, breast, melanoma, renal, and colon cancers are the most common primary tumors to metastasize to the brain. brain metastases are an increasingly important cause of morbidity and mortality in cancer patients. thus, brain metastases presents a therapeutic challenge for the treating physician and is an emotionally and physically debilitating event for the patient. early diagnosis and aggressive treatment of brain metastasis may result in remission of brain symptoms and may enhance the quality of the patient's life and prolong survival (2, 12). the radiologist plays a primary role in the management of cancer patients by helping detect, localize, and diagnose the lesion. the prognosis for patients with brain metastases typically is poor (13). of particular relevance to imaging is the fact that for patients with a solitary brain metastasis who undergo treatment by surgical resection, the survival rate after 1 year is approximately doubled. most available treatment is palliative; however, consideration should be given to prolonging the patient's quality of life through specific therapy to the brain (15). most patients with a known primary tumor undergo imaging studies when neurologic signs and symptoms develop. magnetic resonance imaging (mri) with contrast enhancement currently is the procedure of choice, because mri is more sensitive and specific than other imaging modalities in determining the presence, location, and number of metastases. contrast-enhanced computed tomography (ct) scanning is used widely because of its accessibility and low cost. with regard to screening for intracranial metastases, no consensus has been reached concerning when to use ct or mri for initial staging evaluation of a patient with cancer. however, brain mri for patients with primary cancers that frequently metastasize to the brain (eg, bronchogenic carcinoma) is probably cost effective. numerous studies have shown that contrast-enhanced mri detects 2-3 times as many lesions as contrast-enhanced ct, especially lesions less than 5 mm in diameter. in addition, approximately 20% of patients with solitary metastatic lesions on ct show multiple lesions on mri. the decision to perform imaging for patients with other cancers is made on the basis of the clinical evaluation. in the presence of multiple cerebral metastases from an unknown primary source, a limited search for the primary tumor is of value; such a search includes a chest radiograph, breast examination and mammography, and abdominal ultrasound (us). an extensive search for an occult malignancy is unrewarding. surgery may be required for patients presenting with a solitary intracranial tumor or to search for a possible primary tumor. they occur some limitations of techniques: approximately one third of patients operated on for a single cerebral metastasis diagnosed with contrast-enhanced ct probably have more than one lesion. contrast-enhanced mri is more sensitive than ct in detecting the number of cerebral metastases. the diagnosis of a brain tumor is best made by cranial mri. this should be the first test obtained in a patient with signs or symptoms suggestive of an intracranial mass. mri is superior to ct and should always be obtained with and without contrast material such as gadolinium. a 242 m.r. gorgan et al misdiagnosis of cerebral metastases contrast-enhanced ct scan may be used if mri is unavailable or the patient cannot undergo mri (eg, because of a pacemaker). ct is adequate to exclude brain metastases in most patients, but it can miss low-grade tumors or small lesions located in the posterior fossa. tumor calcification is often better appreciated on ct than on mri. body positron emission tomography (pet) scans performed for staging of systemic malignancies have a sensitivity of only 75% and a specificity of 83% for identification of cerebral metastases. therefore, they are less accurate than mri, which remains the gold standard. on ct or mri, most brain metastases are enhancing lesions surrounded by edema, which extends into the white matter. unlike primary brain tumors, metastatic lesions rarely involve the corpus callosum or cross the midline. the radiographic appearance of brain metastases is nonspecific and may mimic other processes, such as infection. therefore, the ct or mri scan must always be interpreted within the context of the clinical picture of the individual patient, particularly as cancer patients are vulnerable to opportunistic cns infections or may develop second primaries, which can include primary brain tumors. magnetic resonance spectroscopy (mrs) and perfusion imaging can help differentiate low-grade from high-grade brain tumors but cannot distinguish different tumor types of the same grade. material and methods between 2000-2010, 4588 files of patients operated for a brain tumor in the clinic emergency hospital “bagdasararseni” from bucharest, were retrospectively analyzed with peculiar attention to the concordance between the preoperative and postoperative diagnosis. 903 cases (100%) were recorded as cerebral metastases of different etiologies, after pathological examinations of the specimens. we recorded age, sex, symptoms on presentation and their duration, type of investigations and lesions description, clinical and biological profile, and if existed a known primary tumor. actual protocol before operation in a patient with a brain tumor supposes: cerebral ct scan native and contrast, cerebral mri native and contrast, mri angiography when necessary, dsa angiography in specific cases. patient has a standard chest x-ray, skull x-ray, eeg, ekg, cardiologic examination after 45 years old, ophthalmologic evaluation, standard blood test and urine test. patient’s files analyze were done due to electronic patient database from our hospital and statistical data was obtained by microsoft excel ®. concordance analysis was done by assigned key-words, inconsistent data was manually evaluated for excluding/including the cases related to different written expressions. results 773 cases (85,6%) presented initially a single cerebral metastases, and 556 patients (61,5%) were investigated by contrast ct scan and contrast mri scan. 347 patients were operated only after a contrast ct (115 patients-12,7%) or mri (232 patients25,69%). from the 773 cases (100%) operated with a single lesion, in 590 cases the primary tumor was not known before neurosurgical procedure (76,32%). in the time of hospitalization 309 cases (40%) benefitted of other investigations (wholebody contrast ct, bronchoscopy, digestive endoscopy, etc) and the primary cancer was documented. 281 patients (36,35%) romanian neurosurgery (2011) xviii 3: 240 254 243 remained cases with a non-documented primary cancer were referred to the oncology department for other specific investigations and supplementary pathologic histochemistry analysis for identifying the organ of tumor origin.108 patients (13,19%) obtained a diagnose of the primary cancer origin during the oncologic treatment. from a number of 173 cases (22,38%) with an unknown origin of the primary tumor, 123 continued investigations and treatments and a diagnosis was possible in the lifetime and 50 patients (6,46%) deceased without the primary cancer known. in 75 patients (9,70% )operated for a single cerebral lesion, without a known primary tumor, we recorded a misdiagnose of a cerebral metastasis , after analyzing the concordance between the preoperative and postoperative diagnosis. we analyzed the most important criteria for a correct diagnosis: 1) history and symptomshistory was not conclusive for a primary known cancer. the most frequent symptom at presentation was headache, dizziness, and memory disturbances. 2) age: medium age was 51,6 years old, they were 34 females and 41males; 3) diagnose imaging study35 patients were investigated by both ct and mri, 22 had only mri and 18 had only a ct; most of the situations revealed a confusing image with a primary brain tumor or cerebral abscess. 4) clinical and biological standard preoperative evaluation was inconsistent with malignancyabsence of any inflammatory syndrome, no suspicion of cancer on the standard evaluations. in all cases clinical and biological profile was not conclusive for a neoplastic disease. figure 1.1 figure 1.2 figure 1.3 244 m.r. gorgan et al misdiagnosis of cerebral metastases figure 1.4 figure 1 (1.1, 1.2, 1.3, 1.4) contrast mri axial and sagital ,t1-left parietal lesion, well delineated, attached of dura mater, with moderate surrounding edema, suggesting a meningioma. pathological examination after surgery revealed a metastases of a papillary adenocarcinoma. discussion treacherous image on a contrast ct scan or mri, with a confusing appearance of a single cerebral lesion, is, undoubtedly, one of the major source of diagnosis errors. this is the reason for which we will take in review the most important radiologic data related on the degree of confidence of every investigation. ct scan. on noncontrast ct, the density of metastatic lesions may be less than, equal to, or greater than that of adjacent brain parenchyma. most of the patterns are variable and are nondiagnostic. noncontrast ct is performed to detect hemorrhage into metastases. hyperdensity in a metastasis is more likely to be hemorrhage than calcification (see the image below). iv administration of contrast material (30-40 g iodine) increases the diagnostic accuracy of ct. figure 2.1 figure 2.2 figure 2 (2.1, 2.2) contrast ct scan revealing a right parieto-occipital cystic lesion, with a contrast enhancing nodule inside attached from the falx and cerebral mantle, with severe mass effect on the posterior right ventricular horn, and midline shift, suggesting a cystic glioma. pathological evaluation after surgery revealed an undifferentiated carcinoma of pulmonary origin (chest x-ray was inconsistent for tumor). romanian neurosurgery (2011) xviii 3: 240 254 245 figure 3.1 figure 3.2 figure 3.3 figure 3.4 figure 3 (3.1, 3.2, 3.3, 3.4) contrast mri axial and sagital t1, t2right cystic near-round lesion with a fluid content, enhancing contrast peripherally, with mass effect and moderate edema, suggesting a cerebral abscess. pathological examination revealed a metastasis of a breast carcinoma. finally a right breast small nodule was discovered and treated. figure 4.1 246 m.r. gorgan et al misdiagnosis of cerebral metastases figure 4.2 figure 4.3 figure 4.4 figure 4 (4.1, 4.2, 4.3, 4.4) contrast mri, axial and sagital t1,t2-left temporo-occipital mass lesion enhancing contrast marginally, with necrotic content, with mass effect on the ventricular horn and midline shift, with serious peritumoral edema, suggesting a glioblastoma. postoperative pathological evaluation revealed a metastases of colon carcinoma. figure 5.1 figure 5.2 romanian neurosurgery (2011) xviii 3: 240 254 247 figure 5.3 figure 5.4 figure 5 (5.1, 5.2, 5.3, 5.4) contrast mri, axial and sagital t1,t2-left cerebellar cystic mass lesion, enhancing contrast peripherally, with a significant contact with the petrous bone in the area of internal auditory canal, with mass effect on the brain stem and fourth ventricle, suggesting a cerebellar abscess. postoperative pathological examination revealed a metastasis of a clear cell carcinoma. figure 6.1 figure 6.2 figure 6.3 248 m.r. gorgan et al misdiagnosis of cerebral metastases figure 6.4 figure 6 (6.1, 6.2, 6.3, 6.4) contrast mri, axial and sagital t1,t2left solid parietal lesion highly contrast enhancing, attached on the falx in the posterior third, with a severe peritumoral edema, and mass effect with midline shift. content of the lesion in unhomogenous with necrosis and intratumoral vessels. the aspect suggest a atypical falx meningioma. postoperative pathological examination revealed a metastasis of a lung epidermoid carcinoma. figure 7.1 figure 7.2 figure 7.3 romanian neurosurgery (2011) xviii 3: 240 254 249 figure 7.3 figure 7.4 figure 7 (7.1, 7.2, 7.3, 7.4, 7.5) contrast ct scan and contrast mri, t1, t2left solid temporooccipital lesion attached to the dura, enhancing homogenously contrast on the ct and trabecular on the mri, with regional mass effect, invading the brain surface, suggesting a superficial glioma. postoperative pathological examination revealed a metastasis of highly differentiated adenocarcinoma most metastases enhance after a standard dose of iv contrast. use of a higher dose of contrast (80-85 g of iodine) and delaying scanning by 1-3 hours after injection of the contrast agent lead to a further increase in the detection of multiple metastases; such an approach is appropriate if mri is not available. the detection of additional metastases has important diagnostic and therapeutic implications. in cases in which there is no known primary cancer, if a solitary lesion is found on routine enhanced ct, the presence of an additional lesion may suggest a metastatic process, provided the solitary lesion is believed to be a primary lesion. in cases involving a solitary metastatic lesion of the brain, detection of an additional lesion may have a bearing on treatment; with multiple lesions, surgical treatment may be forgone in favor of chemotherapy, radiation therapy, or both. contrast-enhanced ct is effective in detecting major leptomeningeal spread. contrastenhancing subdural or epidural metastases may be seen, usually secondary to calvarial lesions. of breast, lung, prostate, and renal-cell neoplasms, 5% metastasize to the calvarium; of these, 15% extend into the subdural space. degree of confidence. on findings of multiple, enhancing solid lesions at the gray matter–white matter junction and prominent surrounding edema in a patient with known primary cancer, a diagnosis of metastases may be confidently made. approximately 90% of patients with a history of cancer who present with a single supratentorial lesion have brain metastases. patients with multiple lesions are even more likely to have metastatic disease. before undergoing definitive therapy, patients who are found to have a single metastasis on contrast-enhanced ct should undergo a contrast-enhanced mri examination, if facilities for such an examination are available. routine cranial ct is useful in the staging of cancer in the patient with non–small-cell lung cancer; cranial ct has a sensitivity of 92%, a specificity of 99%, and an accuracy of 98% in detecting brain metastases. contrast-enhanced ct is perhaps the best method to identify calvarial metastases. in studies comparing contrastenhanced ct with contrast-enhanced mri, approximately 20% of patients who demonstrated a single lesion on ct demonstrated multiple lesions on mri. mostly, the lesions missed on contrast-enhanced ct were smaller (< 2 cm in diameter) and were located next to the bone in a frontotemporal 250 m.r. gorgan et al misdiagnosis of cerebral metastases location. dural-based metastases may mimic meningioma. (1, 3, 7, 11, 16) magnetic resonance imaging. multiple lesions with marked vasogenic edema and mass effect are typically seen in patients with brain metastases, as shown in the images below. lesions are isointense to mildly hypointense on t1-weighted images; they are hyperintense on t2-weighted images or with fluid attenuation inversion recovery. surrounding edema is relatively hypointense on fluid attenuation inversion recovery and on t1-weighted images; they are hyperintense on t2-weighted images. hemorrhagic metastases or melanoma lesions are hyperintense on t1-weighted images.on t2-weighted images, mucinous adenocarcinoma may be hypointense, owing to calcification; hemorrhagic metastases may be hypointense, owing to the chronic breakdown of blood products. following administration of a contrast agent, solid, nodular (see first image below), or irregular ring patterns of enhancement are seen. nonenhancing lesions (see second image below) are less likely to be metastases. contrast-enhanced mri is the best method for detection of meningeal tumor seeding, which appears as abnormal dural enhancement. this is a nonspecific finding; however, in the correct clinical setting, it correlates with the presence of sheets of tumor cells affecting the meninges. the usefulness of diffusion-weighted and perfusion-weighted imaging and proton-mr spectroscopy in the initial diagnosis of brain metastases has not been established. gadolinium-based contrast agents have been linked to the development of nephrogenic systemic fibrosis (nsf) or nephrogenic fibrosing dermopathy (nfd). nsf/nfd has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance mri or mra scans. nsf/nfd is a debilitating and sometimes fatal disease. characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. degree of confidence. gadolinium-enhanced mri is superior to contrast-enhanced ct in the diagnosis of brain metastases. gadolinium-enhanced mri has the following advantages: useful for detecting smaller lesions, provides better soft tissue contrast, provides relatively stronger enhancement with paramagnetic contrast agents, no bone artifacts in the images, provides less partial-volume effects, particularly for lesions adjacent to bones, provides direct multiplanar imaging. use of magnetization transfer with single-dose gadolinium administration is roughly equivalent to tripledose, postcontrast, spin-echo imaging in detecting lesions and lesion conspicuity. it has been shown that treatment with dexamethasone leads to a reduction in evidence on mri of peritumoral edema and, occasionally, a lessening in the extent of contrast enhancement. if a lesion is found and a definitive diagnosis cannot be established, biopsy should be performed. detection of additional lesions is important when considering surgical treatment of a solitary lesion. magnetization transfer used with routine-dose gadolinium contrast is closely comparable to the high-dose technique. false positives/negatives.on imaging, dural-based metastases may resemble meningioma. leptomeningeal carcinomatosis may resemble chronic meningitis; however, an appropriate history or detection of primary cancer may be sufficient for establishing the diagnosis. leptomeningeal enhancement may occur after the administration of radiation or following extra-axial hemorrhage; it may also occur below a craniotomy site. single or multiple ringenhancing lesions with edema may resemble infectious processes. solitary lesions resemble primary brain tumors (5,8,16). nuclear imaging. currently, nuclear medicine studies are not employed routinely as primary imaging techniques for detecting intracranial metastatic disease. typical findings are multiple intracerebral areas of increased activity. the standard isotope used is technetium-99m (99m tc). on isotope wholebody bone scans, calvarial metastases may appear as multiple focal areas of increased romanian neurosurgery (2011) xviii 3: 240 254 251 activity. with whole-body 18fluorodeoxyglucose (fdg) positron emission tomography (pet) used in cancer staging, intracerebral metastases may appear as areas of increased metabolism. degree of confidence. radionuclide studies are sensitive but are highly nonspecific. in studies involving a small number of patients, fdg-pet demonstrated low sensitivity and low specificity. currently, fdg-pet is not considered superior to ct or mri in the initial evaluation of suspected brain metastases. false positives/negatives. in older reports, radionuclide imaging was reported to detect intracerebral metastases in approximately 90% of patients, but the findings were nonspecific. neoplasm, inflammation, vascularity, or trauma may cause the abnormal uptake. fdg-pet has been reported to detect approximately two thirds of brain metastases resulting from systemic cancer. (6, 10, 14) age is an important factor in judging a cerebral metastasis case, mainly because in the last 10 years, due to the increased accessibility for investigations, an higher number of patients are diagnosed with mass cerebral lesions, and are routinely having a ct or mri. another reason is that we statistically assist to a decrease of age in cancer patients, and to an increase of survival of this patients due to specific treatment improvements. history and symptoms plays an important role: most of our cases with socalled misdiagnosis of cerebral metastases had few neurological signs, had a good clinical and biological status, ignoring maybe a possible neoplastic disease. clinical picture of the individual patient is a reliable factor for the correlation of imaging data, in order to precise, preoperatively a correct diagnosis. table 1 focuses on some of the tumor markers often used today. tests for many other markers are available through commercial testing labs, but these are not commonly used. the list below is limited to those tumor markers that are available to most doctors and have reliable scientific information showing that they are useful. the values listed below are average values, and most labs will list their own "reference ranges". most of the tests are not screening tests, but they are useful instruments to monitor the evolution of a tumor under treatment. a suite of deontological issues appear to act as an infringement situation of the normal relation between the patient and the doctor, and can generate a series of legal consequences: the patient and his family considers being lied, the supposed prognosis presented before surgery will appear wrong, life expectancy changes, the costs for completing the diagnosis and treatment will increase tremendously, and the professional reputation of the doctor and his team will suffer. family may request penalties for malpraxis. in order to avoid such situations, they are three methods to clarify them before surgery: when clinical condition of the patient permits, one can proceed to obtain more data by biological tests (tumor markers), whole body mri or ct, pet scan, etc., or to proceed to a tumor biopsy. when surgical procedure became urgent, and if the lesion is somehow unclear and not correlated entirely with clinical status, it is recommended to avoid a clear-cut information and to maintain a reserve related to the future of the patient, because in about 9-10% of the cases the supposed brain tumor maybe a metastasis, and this is a fact who changes dramatically all situation. if a patient over 50 years old, is admitted for a brain tumor, and radiologist’s interpretation of the data may be unconclusive, we need to clarify first if a primary cancer exists. 252 m.r. gorgan et al misdiagnosis of cerebral metastases table 1 actual used tumor markers and conditions associated with elevated levels (adapted from american cancer society, revised on 03.24.2011). tumor marker normal value primary tumor(s) additional associated malignancies benign conditions level above which benign disease is unlikely sensitivity ca 27.291,2 < 38 units per ml breast cancer colon, gastric, hepatic, lung, pancreatic, ovarian, and prostate cancers breast, liver, and kidney disorders, ovarian cysts > 100 units per ml elevated in about 33% of early-stage breast cancers and about 67% of latestage breast cancers cea < 2.5 ng per ml in nonsmokers < 5 ng per ml in smokers colorectal cancer breast, lung, gastric, pancreatic, bladder, medullary thyroid, head and neck, cervical, and hepatic cancers, lymphoma, melanoma cigarette smoking, peptic ulcer disease, inflammatory bowel disease, pancreatitis, hypothyroidism, cirrhosis, biliary obstruction >10 ng per ml elevated in less than 25% of early-stage colon cancers and 75% of late-stage colon cancers ca 19-9 < 37 units per ml pancreatic cancer, biliary tract cancers colon, esophageal, and hepatic cancers pancreatitis, biliary disease, cirrhosis > 1,000 units per ml elevated in 80% to 90% of pancreatic cancers and 60% to 70% of biliary tract cancers* afp < 5.4 ng per ml hepatocellular carcinoma, nonseminomat ous germ cell tumors gastric, biliary, and pancreatic cancers cirrhosis, viral hepatitis, pregnancy > 500 ng per ml elevated in 80% of hepatocellular carcinomas nonseminomatous germ cell tumors: see β-hcg below β-hcg < 5 miu per ml nonseminomat ous germ cell tumors, gestational trophoblastic disease rarely, gastrointestinal cancers hypogonadal states, marijuana use > 30 miu per ml afp or β-hcg elevated in 85% of nonseminomatous germ cell tumors; elevated in only 20% of early-stage nonseminomatous germ cell tumors ca 125 < 35 units per ml ovarian cancer endometrial, fallopian tube, breast, lung, esophageal, gastric, hepatic, and pancreatic cancers menstruation, pregnancy, fibroids, ovarian cysts, pelvic inflammation, cirrhosis, ascites, pleural and pericardial effusions, endometriosis > 200 units per ml elevated in about 85% of ovarian cancers; elevated in only 50% of earlystage ovarian cancers psa < 4 ng per ml for screening undetectable level after radical prostatectomy prostate cancer none prostatitis, benign prostatic hypertrophy, prostatic trauma, after ejaculation > 10 ng per ml elevated in more than 75 percent of organconfined prostate cancers legend: ca = cancer antigen; cea = carcinoembryonic antigen; afp = alpha-fetoprotein; β-hcg = beta subunit of human chorionic gonadotropin; psa = prostate-specific antigen.*— the greatest possible sensitivity is 95 percent, given that 5% of the population have lewis-null blood type and are unable to produce the antigen. romanian neurosurgery (2011) xviii 3: 240 254 253 thereafter we need to evaluate the case and all radiological and medical information by ourselves, and to avoid the traps resulting from an incorrect correlation of data. if radiologist advocates for a malignant primary brain tumor (high-grade glioma, glioblastoma, etc), we need to inform the patient’s family that the prognosis is poor, but if a metastasis is confirmed after pathological evaluation of the specimen, the future of the patient might be the worst. any time when a systemic cancer is revealed by a brain metastasis, statistically, the total surviving time with or without the treatment attain about 6 to 8 months. when radiologic data suspects a brain abscess, and the patient status does not match with an infectious condition, we need to maintain a serious doubt about patient’s prognosis, until pathologic examination reveals the final result. a number of tumors, mainly in immune suppressed patients (cirrhosis, diabetes mellitus, renal failure, etc ), may exhibit a false pus aspect, as a component of intratumoral necrosis or subacute hemorrhage in different stages of resolution. the neurosurgeon is the most important decision factor and is the one who bears the final responsibility towards neurosurgical indication, neurosurgical procedure and documented information provided to patients and family. conclusions any patient over 50 years old with a unique brain lesion must be suspected for a cerebral metastases. when doubt exists, cerebral biopsy and additional investigations should be done. according to the recent frequency criteria of cerebral metastases versus the total number of cerebral tumors in adult, between 30 and 40 % of cases may have a cerebral metastases. the patient must be evaluated correctly and the diagnosis must be affirmed with caution. in 6 -8% of the patients with cerebral metastases, the primary neoplasm remain unidentified until the decease. neurosurgical operation is certainly the most important step to establish a precocious and clear diagnosis. corresponding author narcisa bucur md, phd narcisabucur@yahoo.com references 1. akeson p, larsson em, kristoffersen dt. brain metastases--comparison of gadodiamide injectionenhanced mr imaging at standard and high dose, contrast-enhanced ct and non-contrast-enhanced mr imaging. acta radiol. may 1995;36(3):300-6. posner jb. management of brain metastases. rev neurol (paris). 1992;148(6-7):477-87. 2. das s. muro k. raizer jj. (2007) “surgery for brain metastases ” cancer treatment & research. 136:75-90. 3. ferrigno d, buccheri g. cranial computed tomography as a part of the initial staging procedures for patients with non-small-cell lung cancer. chest. oct 1994;106(4):1025-9. 4. gavrilovic, i. t. and j. b. posner (2005). "brain metastases: epidemiology and pathophysiology." journal of neuro-oncology 75 (1): 5-14. wen py, loeffler js. management of brain metastases. oncology (huntingt). jul 1999;13(7):941-54, 957-61; discussion 961-2, 9. 5. ginsberg le, lang ff. neuroradiologic screening for brain metastases--can quadruple dose gadolinium be far behind?. ajnr am j neuroradiol. may 1998;19(5):829-30. griffeth lk, rich km, dehdashti f. brain metastases from non-central nervous system tumors: evaluation with pet. radiology. jan 1993;186(1):37-44. 6. hardy j, smith i, cherryman g. the value of computed tomographic (ct) scan surveillance in the detection and management of brain metastases in patients with small cell lung cancer. br j cancer. oct 1990;62(4):684-6. 7. hochstenbag mm, twijnstra a, wilmink jt. asymptomatic brain metastases (bm) in small cell lung cancer (sclc): mrimaging is useful at initial diagnosis. j neurooncol. jul 2000;48(3):243-8. 8. kaal, e. c., m. j. taphoorn, et al. (2005). "symptomatic management and imaging of brain 254 m.r. gorgan et al misdiagnosis of cerebral metastases metastases." journal of neuro-oncology 75 (1): 15-20. 9. kitajima k, nakamoto y, okizuka h, onishi y, senda m, suganuma n, et al. accuracy of whole-body fdg-pet/ct for detecting brain metastases from non-central nervous system tumors. ann nucl med. aug 2008;22(7):595-602. 10. kuhn mj, hammer gm, swenson lc. mri evaluation of "solitary" brain metastases with triple-dose gadoteridol: comparison with contrast-enhanced ct and conventional-dose gadopentetate dimeglumine mri studies in the same patients. comput med imaging graph. sep-oct 1994;18(5):391-9. 11. langer, c. j. and m. p. mehta (2005). "current management of brain metastases, with a focus on systemic options." journal of clinical oncology 23 (25): 6207-19. 12. modha, a., s. r. shepard, et al. (2005). "surgery of brain metastases--is there still a place for it?" journal of neuro-oncology 75 (1): 21-9. 13. nakamura h, taguchi m, kitamura h, nishikawa j. fluorodeoxyglucose positron emission tomography integrated with computed tomography to determine resectability of primary lung cancer. gen thorac cardiovasc surg. aug 2008;56(8):404-9. 14. nguyen, td & deangelis, lm (2007). “brain metastases” neurologic clinics 25(4): 1173-92. 15. schellinger pd, meinck hm, thron a. diagnostic accuracy of mri compared to cct in patients with brain metastases. j neurooncol. 1999;44(3):275-81. microsoft word 2sanduaureliamihaela_primary 538 | sandu et al primary intramedullary spinal cord non-hodgkin lymphoma             doi: 10.2478/romneu-2018-0069 primary intramedullary spinal cord non-hodgkin lymphoma case report and review of the literature aurelia mihaela sandu1, m.a. fürtös1, g. petrescu1, anamaria gheorghiu1, b.i. david1, f.m. brehar1, 2, a. giovani1, m.r. gorgan1,2 1“bagdasar-arseni” department of neurosurgery, emergency clinical hospital, bucharest, romania 2“carol davila” university of medicine and pharmacy, bucharest, romania abstract: introduction: primary intramedullary spinal cord lymphomas are extremely rare, occurring mainly in immune compromised patients. case report: we report a case of a 43 years old patient admitted with spinal cord compression. spinal mri revealed two thoracic intramedullary tumours. the patients underwent surgery and we performed resection of both primary intramedullary tumours, with favourable neurological outcome. the histopathologic exam was non-hodgkin lymphoma. the patient underwent adjuvant radiotherapy. two months later the patient presented thoracic and cerebellar drop metastases, confirmed histopathologically. conclusions: the diagnosis of primary intramedullary spinal lymphoma must be kept in mind in patients with myelopathy. surgery is needed to provide histopathological samples for positive diagnosis and spinal decompression. primary intramedullary spinal lymphomas have a propensity to disseminate along the neuraxis. key words: intramedullary lymphoma, non-hodgkin lymphoma introduction spinal cord lymphomas are rare. spinal lymphomas are usually extradural, occurring in vertebral bodies or in epidural tissue. primary intramedullary spinal cord lymphomas are very rare and accounts for 1% of cns lymphomas.1,2 the majority of intramedullary lymphomas are secondary drop metastases. some studies found them most commonly located in cervical and thoracic spinal segments3, while other considered that conus medullaris and cauda equina are more affected4. they usually occur in the fifth or the sixth decades of life.1,3,4 men are more commonly affected compared with women are white race is more affected.1,4 risk factors for occurrence of lymphomas are immune depression, such as: aids, congenital immune deficiency, cancer, organ transplant related immune romanian neurosurgery (2018) xxxii 4: 538 – 546 | 539             suppression, infection with epstein-barr virus, etc. intramedullary lymphomas usually appear as a solid, homogenously enhancing mass, isointense in t1w and hyperintense in t2w.5 csf cytology shows increased cellularity.3 treatment of spinal lymphomas usually consists of surgical biopsy to establish a positive diagnosis, followed by adjuvant radiotherapy. chemotherapy is controversial. prognosis is poor, 2 years survival rate is 32-36%.1,4 case report a 43 years old man was admitted in our department with spinal cord compression with neurological level t1, frankel c severe right > left and loss of consciousness. the patient was immune competent and had no relevant medical history. neurologic exam showed paraparesis, right l2 asia 2, right l3 asia 2, right l4 asia 1+, right l5 asia 1+, right s1 asia 3-, left l2 asia 3-, left l3 asia 3-, left l4 asia 3-, left l5 asia 3and left s1 asia 3. total motor score on the right side was 34 and on the left was 40. we also found hypoesthesia with level t1, bilateral diminished osteotendinous reflexes, bilateral babinski sign and urinary incontinence. spinal mri revealed two solid intramedullary tumours hyperintense in t1w and isointense in t2w, contrast enhancing. the first intramedullary tumour was located right posterolateral at t1 level, had an important exophytic expansion sizing 27/13/12.5 mm, compressing and pushing the spinal cord to the left. it had an associated syringomyelia extending upwards to c4 and inferiorly to t7. the second tumour was also intramedullary exophytic, located left posterolateral at level t3 and measured 5/4 mm. (figure 1) thoracic spine x-ray showed no radiological changes of vertebral bodies. cerebral mri showed a right temporomesial infiltrative tumour. blood workout, ekg and pulmonary x-ray showed no relevant changes. the patient underwent surgery. we performed a longitudinal midline skin incision, from c5 to t5 and bilateral subperiosteal skeletonization of paravertebral muscle from c7 to t4. we performed t1-t3 laminectomies and midline dural incision. we found two intramedullary infiltrative tumours with exophytic components, one located right paramedian at level t1, measuring 2.5/1.5 cm in diameter and another located left paramedian at level t3, measuring 0.5/0.5 cm. we performed total resection of t1 tumour and near total resection of t3 tumour. haemostasis. dural closure. epidural external drainage. wound closure. histopathological exam from both spinal tumours found malignant non-hodgkin lymphoma. (figure 2) postoperative outcome was favourable, without any additional neurological deficits. 540 | sandu et al primary intramedullary spinal cord non-hodgkin lymphoma             he received dexamethasone 24 mg / d. he began rehabilitation the second day after surgery. he underwent adjuvant radiotherapy. two months later, the patient was readmitted with seizures, headache and diplopia. neurological exam showed paraparesis, right l2 asia 3+, right l3 asia 3+, right l4 asia 3, right l5 asia 3, right s1 asia 4-, left l2 asia 4, left l3 asia 4, left l4 asia 4 and left l5 asia 4. total motor score on the right side was 41 and on the left was 46. he also had pain and temperature hypoesthesia with level t3 and full sphincter control. spinal mri showed dural contrast enhancement from c3 to t8 and numerous micronodular lesions from t2 to t10, suggestive for drop metastases. the largest lesion sizing 7/8 mm was located at t3 level. (figure 3) thoracic spine x-ray showed t1-t3 laminectomies and no radiological changes of vertebral bodies. cerebral mri showed bilateral cerebellar drop metastases, measuring 0.98 cm on the right and 0.92 cm on the left and right temporo-mesial tumour hypointense in t1w and hyperintense in t2w and flair, without contrast enhancement. (figure 4) the patient underwent second surgery and we performed stereotactic biopsy of the right temporo-mesial tumour. histopathological exam revealed diffuse infiltrative astrocytoma grade ii who. for the third surgery, performed under the same general anaesthesia, we performed a minimal left suboccipital craniectomy. dural mater was cut in x. we found a cortical tumour located immediately inferior to the transverse sinus. we performed total resection of a tumour 1 cm in diameter. haemostasis. dural closure. epidural drainage. wound closure. histopathological exam revealed malignant non-hodgkin lymphoma. postoperative outcome was favourable; the patient presented no additional neurological deficits. under antiepileptic therapy (carbamazepin 200 mg x 3 / d) the patient presented no seizures. at 6 months follow-up the patients had paraparesis right l2 asia 4-, right l3 asia 4-, right l4 asia 4, right l5 asia 4, left l2 asia 4+, left l3 asia 4+ and left l4 asia 4+. romanian neurosurgery (2018) xxxii 4: 538 – 546 | 541             figure 1. spinal mri. right posterolateral t1 intramedullary with exophytic mass; polar syringomyelia from c4 to t7; left posterolateral t3 intramedullary tumour with exophytic component figure 2. histopathological exam. malignant b-cell non-hodgkin lymphoma. (he stain, 20x) 542 | sandu et al primary intramedullary spinal cord non-hodgkin lymphoma             figure 3. spinal mri. dural contrast enhancement from c3 to t8; micronodular drop metastases micronodular t2 to t10 figure 4. cerebral mri. right temporo-mesial non-enhancing tumour; cerebellar drop metastases romanian neurosurgery (2018) xxxii 4: 538 – 546 | 543             table i primary intramedullary lymphomas no. author, year of publication no. of cases 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 bruni j et al., 1977 10 mitsumoto h et al, 1980 11 hautzer nw et al., 1983 3 itami j et al., 1986 12 landan i et al., 1987 13 slowik f et al., 1990 14 wong chung me et al., 1991 15 mcdonald ac et al., 1995 16 urasaki e et al., 1996 8 caruso pa et al., 1998 17 bekar a et al., 2001 18 nakamizo t et al, 2002 5 peltier j et al., 2007 19 machiya t et al., 2007 20 matsuyama y et al., 2009 21 flanagan ep et al., 2011 4 lin yy et al., 2012 22 bhushanam tv et al., 2014 23 sivri m et al., 2015 2 guzzetta m et al., 2015 6 yang w et al., 2017 1 our case, 2018 1 1 1 1 1 1 1 1 1 1 1 2 1 1 3 14 1 1 1 1 346 1 discussions primary intramedullary lymphomas are rare. so far, besides the two clinical studies reported by yang et al.1 and flanagan et al.4, only case reports have been described in the literature. (table 1) being so rare, the diagnostic of patients without spinal cord compression syndrome is often delayed4, so we must keep in mind this diagnosis to insure a prompt diagnosis and initiate appropriate therapy. spinal lymphomas must be always suspected in immunocompromised patients. histopathologic diagnosis is made after surgery (tumour resection or biopsy) or at autopsy. according to who classification, the vast majority are b-cell non-hodgkin lymphomas, with subgroups diffuse large bcells and follicular being the most frequent.1 tcell lymphomas are extremely rare, representing only 1.4% of primary intramedullary spinal lymphomas.1,6-8 other histopathological types that can be found are small b-cell, burkitt, precursor cells and unspecified. primary intramedullary hodgkin lymphoma is exceptionally rare.1 nowadays the diagnosis is made on mri. spinal lymphomas are hyperintense in t2w, in contrast with cranial lymphomas which are isointense. multifocal lesions with contrast enhancement are pathognomonic for spinal lymphomas. csf increased cellularity have no specific pattern. even though mri was suggestive for a subdural extramedullary tumour, intraoperative findings showed that the tumour was in fact intramedullary with massive exophytic component. the exophytic mass was contiguous with an intramedullary tumour and presented no other attachment to any structure. differential diagnosis is made with other intramedullary tumours: astrocytomas, ependymomas, epidermoid and dermoid tumours, metastases, hemangioblastomas, spinal embryonal tumours, multiple sclerosis. treatment consists from surgery, for establishing positive diagnosis and spinal cord decompression, concomitant high-dose corticosteroids, followed by adjuvant radiotherapy and chemotherapy. 544 | sandu et al primary intramedullary spinal cord non-hodgkin lymphoma             surgery is the first step in treatment of patients with spinal cord tumours. the goals of surgery are obtaining tissue for histopathological diagnosis, achievement of maximum tumour removal without inducing new neurological deficits and preservation of spinal stability. in lymphomas, if the tumour is small and does not cause spinal cord compression, there is no need to perform total resection, a biopsy being sufficient. if the tumour is large and compresses the spinal cord, surgical cytoreduction immediately reduces compression. tumoral cytoreduction may also be beneficial for adjuvant therapy. surgical decompression improves neurological outcome and survival.9 we performed a posterior approach, through t1, t2, t3 laminectomies. in this way we were able to gain access to both lesions. although the patients had bipolar syringomyelia extending from c4 to t7, there is no need to address it, because it is secondary, and after tumour resection the syrinx will regress. there are several ways to resect an intramedullary tumour. the most used surgical route is posterior midline myelotomy. this is a safe anatomic area. keeping the midline does not induce neurological damage to surrounding structures. this approach is widely used in all intramedullary tumours, especially in those who have no expression on the cord surface. in some cases, when the tumour causes cord distortion keeping within the midline may be challenging. tumours that come in contact with the cord surface and are not infiltrative display normal structures and can be approach through this safe zone. exophytic tumours have an important part situated outside the cord. this part is resected first and then the approach can be done through the area where exophytic part of the tumour exited the cord. intramedullary tumours can be either well-defined or infiltrative. in well-defined tumours the resection is made within the cleavage plane and complete resection is possible, in infiltrative lesions there is no such plane of demarcation and only subtotal or near-total resection is possible. we choose to resect the exophytic component and then enter the cord through this safe area and resect the intramedullary part from inside out. the larger the tumour, and more precisely the larger the area of effraction of the cord, the bigger is the surgical corridor, this is why the bigger tumour could be totally resected and the small one cannot. however, total resection is not needed in lymphomas and the tumour situated at t3 level was not causing compression on the spinal cord. intraoperative somatosensory and motor evoked potentials are very useful to monitor the effects on spinal cord induced by surgical gestures. we did not consider necessary to perform osteosynthesis of the spinal column because the spinal thoracic column is stable and we performed only three laminectomies, with complete preservation of articular facets. lymphomas have a high sensibility to corticosteroids and immediately after initiating the therapy neurological improvement occurs. combined adjuvant oncologic therapy with radio and chemotherapy is more effective than either of romanian neurosurgery (2018) xxxii 4: 538 – 546 | 545             them used alone. chemotherapy consists of cyclophosphamide, vincristine, doxorubicin, methotrexate, cytarabine, rituximab, vincristine. lymphomas of the cns display a highly aggressive behaviour, are prone to disseminate and drop metastases can be found along the neuraxis, intracranial or spinal. two months after surgery, our patient came with two drop metastases in the posterior fossa and numerous at the spinal level. despite radiotherapy and chemotherapy, the prognosis is poor. median survival rate is 6-9 months, and 2 years survival is 32-36%.1,4 young age, early diagnosis, low stage, follicular histologic type are positive prognostic factors.1 conclusions the diagnosis of primary intramedullary spinal lymphoma must be kept in mind in patients with myelopathy. surgery is needed to provide histopathological samples for positive diagnosis and spinal decompression. rapid surgical decompression, corticosteroids and adjuvant radiotherapy improve neurological outcome. primary intramedullary spinal lymphomas have a propensity to disseminate along the neuraxis. correspondence aurelia mihaela sandu address: fourth department of neurosurgery, emergency clinical hospital bagdasar-arseni, no. 10-12, berceni road, district 4, bucharest, romania, postcode 041902 e-mail: aurasandu@gmail.com references 1. yang w, garzon-muvdi t, braileanu m, porras jl, caplan jm, rong x, hunag j, jallo gi. primary intramedullary spinal cord lymphoma: a populationbased study. neuro oncol 2017; 19:414-421. 2. sivri m, erdogan h, allahverdiyev i, koplay m, temizoz o. a rare cause of spinal mass: primary intramedullary spinal cord lymphoma. spine j 2015; 15:e43-e44. 3. hautzer nw, aiyesimoju a, robitaille y. "primary" spinal intramedullary lymphomas: a review. ann neurol 1983; 14:62-66. 4. flanagan ep, o`neil bp, porter ab, lanzino g, haberman tm, keegan bm. primary intramedullary spinal cord lymphoma. neurology 2011; 77:784-791. 5. nakamizo t, inoue h, udaka f, oda m, kawai m, uemura k, takahashi m, nishinaka k, sawada h, kameyama m, koyama t. magnetic resonance imaging of primary spinal intramedullary lymphoma. j neuroimaging 2002; 12:183-186. 6. guzzetta m, drexler s, buonocore b, donovan v. primary cns t-cell lymphoma of the spinal cord: case report and literature review. lab med 2015; 46:159-163. 7. gijtenbeek jm, rosenblum mk, deangelis lm. primary central nervous system t-cell lymphoma. neurology 2001; 57:716-718. 8. urasaki e, yamada h, tokimura t, yokota a. t-cell type primary spinal intramedullary lymphoma associated with human t-cell lymphotropic virus type i after a renal transplant: case report. neurosurgery 1996; 38:10361039. 9. chang cm, chen hc, yang y, wang rc, hwang wl, teng cl. surgical decompression improves recovery from neurological deficit and may provide a survival benefit in patients with diffuse large b-cell lymphomaassociated spinal cord compression: a case-series study. world j surg oncol 2013; 11:90. 10. bruni j, bilbao jm, gray t. primary intramedullary malignant lymphoma of the spinal cord. neurology 1977; 27:896-898. 11. mitsumoto h, breuer ac, lederman rj. malignant lymphoma of the central nervous system: a case of primary spinal intramedullary involvement. cancer 1980; 46:1258-1262. 12. itami j, mori s, arimizu n, inoue s, lee m, uno k. primary intramedullary spinal cord lymphoma: report of a case. jpn j clin oncol 1986; 16:407-412. 546 | sandu et al primary intramedullary spinal cord non-hodgkin lymphoma             13. landan i, gilroy j, wolfe de. syringomyelia affecting the entire spinal cord secondary to primary spinal intramedullary central nervous system lymphoma. j neurol neurosurg psychiatr 1987; 50:1533-1535. 14. slowik f, mayer a, afra d, deak g, havel j. primary spinal intramedullary malignant lymphoma. a case report. surg neurol 1990; 33:132-138. 15. wong chung me, van heesewijk jp, ramos lm. intramedullary non-hodgkin's lymphoma of the spinal cord; a case report. eur j radiol 1991; 12:226-227. 16. mcdonald ac, nicoll ja, rampling r. intramedullary non-hodgkin's lymphoma of the spinal cord: a case report and literature review. j neurooncol 1995; 23:257-263. 17. caruso pa, patel mr, joseph j, rachlin j. primary intramedullary lymphoma of the spinal cord mimicking cervical spondylotic myelopathy. ajr am j roentgenol 1998; 171:526-527. 18. bekar a, cordan t, evrensel t, tolunay s. a case of primary spinal intramedullary lymphoma. surg neurol 2001; 55:261-264. 19. peltier j, cretu i, fichten a, toussaint p, desenclos c, le gars d. primary intramedullary lymphoma. case report. neurochirurgie 2007; 53:375-378. 20. machiya t, yoshita m, iwasa k, yamada m. primary spinal intramedullary lymphoma mimicking ependymoma. neurology. 2007;68(11):872-872. neurology 2007; 68:872. 21. matsuyama y, sakai y, katayama y, imagama s, ito z, wakao n, sato k, kamiya m, yukawa y, kanemura t, yanase m, ishiguro n. surgical results of intramedullary spinal cord tumor with spinal cord monitoring to guide extent of resection. j neurosurg spine 2009; 10:404-413. 22. lin yy, lin cj, ho dmt, guo wy, chang cy. primary intramedullary spinal cord lymphoma. spine j 2012; 12:527-528. 23. bhushanam tv, rajesh a, linga vg, uppin ms, malik m. primary intramedullary non-hodgkin's lymphoma in an immunocompetent child. spinal cord 2014; 52 suppl:s21-s23. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-001 overview of patients with vascular pathology and cost analysis of medical care – research market faor an entrepreneurial project aurelia mihaela sandu, adrian mircea fürtös, radu mircea gorgan romanian neurosurgery (2020) xxxiv (1): pp. 9-16 doi: 10.33962/roneuro-2020-001 www.journals.lapub.co.uk/index.php/roneurosurgery overview of patients with vascular pathology and cost analysis of medical care – research market for an entrepreneurial project aurelia mihaela sandu1,2, adrian mircea fürtös1, radu mircea gorgan1,2 1 department of neurosurgery, emergency clinical hospital bagdasar-arseni, bucharest, romania 2 university of medicine and pharmacy “carol davila”, bucharest, romania abstract introduction: brain vascular pathology, aneurysms, arteriovenous malformations (avms), cavernomas, dural arteriovenous fistulas (davf), venous angiomas and capillary telangiectasia, represents a serious health problem worldwide. aim: the aim of this article is to perform an analysis of patients with brain vascular pathology and to analyze costs of health services, a research market for an entrepreneurial project, in order to design guidelines for patients’ selection and treatment. material and methods: we performed an observational, descriptive study of patients with vascular pathology, from 2018 to 2019. results: a total of 153 patients with brain vascular pathology were admitted in our department. mean age was 49.53 ± 13.997 years. sex ratio was 0.86. mean hospital stay was 11.33 ± 13.724 days. seventy-four patients (48.37%) underwent surgery. seventy-eight patients (50.98%) had cerebral aneurysms. complications were seen in 24 patients (30.77%) and vasospasm in 32 cases (41.03%). thirty-six patients underwent surgery. outcome was favorable, according to mrs(p=0.001) and karnofsky score(p=0.006). thirty-three patients (21.57%) had brain avms. twenty patients underwent surgery. complications were seen in 4 cases (12.12%). the outcome was favourable, according to mrs(p=0.001) and karnofsky score (p=0.002). thirty-nine patients (25.49%) had cavernomas. surgery was performed in 18 cases. the outcome was favourable, according to engel epilepsy surgery outcome scale, mrs (p=0.000) and karnofsky score (p =0.000). costs of health services were correlated with longer hospitalization, higher mrs, lower karnosfsky score, presence of complications and presence of vasospasm. conclusions: proper treatment of brain vascular pathology ensures a favourable outcome. adequate patients’ selection and choosing the best treatment can reduce costs. surgery is the treatment of choice in ruptured aneurysms, avms and cavernomas. early surgery, with specific treatment of the vascular lesion and removal of intracranial blood ensures a better outcome, with lower medical costs. prevention of complications, aggressive treatment of vasospasm reduces medical costs. keywords aneurysm, arteriovenous malformation, cavernoma, dural arteriovenous fistula, health care costs corresponding author: aurelia mihaela sandu university of medicine and pharmacy “carol davila”, bucharest, romania aurasandu@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 10 aurelia mihaela sandu, adrian mircea fürtös, radu mircea gorgan introduction brain vascular pathology is represented by aneurysms and vascular malformations. vascular malformations are arteriovenous malformations (avms), cavernomas, duralarteriovenousfistulas (davf), venous angiomas and capillary telangiectasia.1 brain vascular pathology is a serious health problem world-wide. the incidence of cerebral aneurysms is 0.2-7.9% and the prevalence is 5%.2 the incidence of brain avms is 0.15-3%3,4 and the prevalence is 0.14%5,6. the incidence of cavernomas is 0.15-0.56% and the prevalence is 0.17-0.9%.7 davf, venous angiomas and capillary telangiectasia are rare. unfortunately brain vascular pathology occurs in young, active people and more than half of patients present with intracerebral hemorrhage, with significant morbidity and mortality. peak incidence of aneurysms is 55-60 years2, avms become symptomatic in younger people, mean age is 33 years5,6 and in cavernomas is 42 years8. the most common form of presentation is rupture with subsequent brain hemorrhage. pattern of hemorrhage depends on type of vascular disease. aneurysms usually rupture in the subarachnoid space, while avms and cavernomas cause intraparenchymatal hematoma. regardless the type of intracerebral hemorrhage, all are major aggressive factors to the brain and carry important risks of death or development of serious neurological complications. other forms of presentation are seizures, cranial nerves palsies, motor or sensory deficits, intracranial hyperpressure, ischemia, hydrocephalus, etc. surgery is the treatment of choice for aneurysms, avms and cavernomas.9-11even though a benign pathology, surgery for brain vascular pathology carries significant risks. for cerebral aneurysms embolization can also be tried.11 besides surgery, avms also benefit from stereotactic radiosurgery and embolization. davf is usually treated through embolization and venous angiomas and capillary telangiectasia do not require treatment. the aim of this article is to perform an analysis of patients with brain vascular pathology and to analyze the costs of health services, a research market for an entrepreneurial project, in order to design guidelines for patients’ selection and treatment. material and methods we performed an observational, descriptive study in which we included patients with vascular pathology admitted in the ivth department of neurosurgery, emergency clinical hospital bagdasar-arseni, from january 2018 to december 2019. data were collected in a retrospective manner from january 2018 to august 2019 and prospectively from september 2019 to december 2019. we collected data from hospital medical records and electronic health record hipocrate. statistic analysis of data was done using spss®. results a total of 153 patients with brain vascular pathology were admitted over a period of time of two years in the ivth department of neurosurgery, emergency clinical hospital bagdasar-arseni from bucharest, romania.patients with brain vascular pathology represented 2.09% from the total number of admissions in our department. vascular brain pathology was represented by aneurysms, avms, cavernomas and davf. (figure 1) mean age of all patients with vascular pathology was 49.53 ± 13.997 years. sex ratio (m/f) was 0.86. mean hospital stay was 11.33 ± 13.724 days. a total of 74 patients (48.37%) underwent surgery. the rest of 73 patients either had no indications for surgery, refused surgery or benefit from other nonoperative treatments. figure 1. types of brain vascular pathology. 11 overview of patients with vascular pathology and cost analysis figure 2. sex ratio per each type of vascular pathology. figure 3. basilar tip aneurysm. aneurysms seventy-eight patients (50.98%) were admitted with cerebral aneurysms. mean age of these patients was 53.73 ± 11.146 years. there were 53 women (67.95%) and 25 men (32.05%). sixty-two patients (79.49%) had single aneurysm and 16 patients (20.51%) had multiple aneurysms. the latter 16 patients harbor a total number of 35 aneurysms, varying from 2 to 6 lesions per patient. aneurysms’ locations are shown in table 1. forty-eight (61.54%) had ruptured aneurysms and only 30 people (38.46%) had unruptured ones. from the total number of patients with ruptured aneurysms, according to hunt and hess scale, 22 patients were grade i, 4 grade ii, 3 grade iii, 8 grade iv and 11 grade v. according to fisher scale, 2 patients had grade i, 17 grade ii, 8 grade iii and 21 grade iv. patients with ruptured aneurysms had the following pattern of brain hemorrhage: 45 had subarachnoid hemorrhage, 9 had intraparenchymatal hematoma, 19 intraventricular hemorrhage and 2 had subdural hematoma. complications were seen in 24 patients (30.77%). vasospasm, a fearful complication was seen in 32 patients (41.03%). vasospasmwas more commonly encountered in patients with higher grades on hunt and hess and fisher scales (p=0.000, p=0.000). thirty-six patients underwent surgery (34 patients had their aneurysms clipped and in 2 wrapping was done). outcome was favorable, mrs at discharge were lower than mrsat admission (z=3.426, p=0.001) and final karnofsky scores were higher than initial scores (z=-2.754, p=0.006). avms thirty-three patients (21.57%) were admitted with brain avms. mean age was 40.82± 14.501 years. there were 20 males (60.61%) and 13 females (39.39%). sixteen patients (48.48%) presented with ruptured avms and 13 cases (39.39%) had history of seizures. according to brain hemorrhage pattern 12 patients had intraparenchymatal hematoma, 4 had intraventricular hemorrhage, 3 had subarachnoid hemorrhage and only one had subdural hematoma. motor deficit was encountered in 11 cases. according to spetzler-martin scale, 9 cases (27.27%) were grade i, 8 patients (24.24%) were grade ii, 8 (24.24%) grade iii, 3 patients (9.09%) were grade iv, 3 cases (9.09%) were grade v and 2 cases (6.06%) had grade vi avms. three patients had flow-related associated 12 aurelia mihaela sandu, adrian mircea fürtös, radu mircea gorgan aneurysms. no patient presented cerebral vasospasm. twenty patients underwent surgery, 5 cases underwent stereotactic radiosurgery gamma knife and 2 patients were embolized. five patients refused surgery and 2 cases had grade vi spetzler-martin avms and did not benefit from therapy. complications were seen in 4 cases (12.12%). outcome was favorable, discharge mrswere lower than admission mrs (z=-3.332, p=0.001) and finalkarnofsky scores were higher than initial scores (z=-3.047, p=0.002). figure 4. grade iii spetzler-martin avm. cavernomas thirty-nine patients (25.49%) were admitted with brain cavernomas. mean age for patients with cerebral cavernomas was 48.28 ± 15.788. sex ratio (m/f) was 1.6. thirty-three patients (84.62%) had single cavernomas, but 6 (15.38%) had multiple lesions, the number of cavernomas varying from 3 to 8. ruptured cavernomas were found in 16 patients. according to the pattern of brain hemorrhage, all 16 patients had intraparenchymatal hematoma, one associated intraventricular hemorrhage and one subdural hematoma. nine patients had motor deficit and 10 cases were admitted with seizures.positive diagnosis was done by mri, t2 echo-gradient and flair. only 6 patients underwent dsa, and the angiography was negative in all cases. surgery was performed in 18 cases. deep cavernomas required intraoperative usage of ultrasound-based neuronavigation system sonowand®. from the total of 10 patients with epilepsy, 6 underwent surgery, and 3 were free of disabling seizures (engel ia) postoperative, 2 had worthwhile improvement (engel iiib) and one had no worthwhile improvement (engel ivb). outcome was favorable, according to mrs (z=-4.274, p=0.000) and karnofsky score (z=4.283, p =0.000). figure 5. pontine cavernoma. dural av fistulas there were only 3 patients (1.96%) with davf. mean age was 52.33 ± 4.933. figure 6. davf type iv merland-cognard, injected from middle meningeal artery. 13 overview of patients with vascular pathology and cost analysis total health care costs accounted for 3215558.4658 lei, and they were composed by 2574452.06 lei hospitalization costs, 14067.4 lei food costs, 15993.085 lei medication costs, 18641.038 lei blood work costs, 105797 lei imaging examinations costs. hospital staywas positively correlated with hospitalization costs (p=0.000), food costs (p=0.000), medication costs (p=0.000), medical products costs (p=0.000), blood work costs (p=0.000), imaging examinations costs (0=0.002) and total cost of health care(p=0.000). patients who underwent surgery have higher costs (p=0.000).patients who presented complications and vasospasm have also higher costs (p=0.000, p=0.000). higher mrs and lower karnofsky score at admission were associated with higher costs (p=0.000, p=0.000). another 575 days for postoperative controls were gathered with additional total costs of 638406.916 lei. discussions brain vascular pathology was encountered in young, active patients, meanage for the entire group being under 50 years old, with differences for every pathology. surgery for vascular lesions is challenging. only 50% of patients diagnosed with vascular pathology benefit from surgery. this low rate of patients with surgery is caused by several factors. surgery is indicated when benefits are higher than risks, and we must not forget that we are dealing with high risk surgeries, so there are patients with grade vi avms, deep seated unruptured, asymptomatic cavernomas or unruptured ectatic vessels, in which surgery is not required. more, there are patients, or families who refused surgery after they were informed of the possible risks. and there is another group of patients who are not candidate for surgery. in case of brain aneurysms clipping is the curative treatment.11,12 surgical technique depends on location, type and size of aneurysm and angioarchitecture of parental and efferent vessels.9one or more clips of different sizes can be used to secure the aneurysm (simple clipping, multiple clipping, tandem clipping, fenestration tubes, clip reconstruction).9other surgical techniques are wrapping and trapping. surgery for aneurysm must be performed early, to hinder the risk of rebleeding. found almost exclusively in cerebral aneurysms, vasospasm is causing important morbidity. vasospasm occurs between days 3 and 14 after subarachnoid hemorrhage onset, and it is due to presence of blood in the subarachnoid space, which induces arterial vasoconstriction. vasospasm is associated with higher fisher and hunt and hess grades. many surgeons do not recommend surgery in this period of time because it increases the risk of vasospasm. early intensive treatment for vasospasm, such as triple h therapy (hypertension, hypervolemia and hemodilution), intraoperative washing of all subarachnoid spaces from blood clots, calcium channel blockers (nimodipine) or angioplasty may reduce the incidence of vasospasm and its devastating consequences. so, ideally surgery is done early after rupture, before installation of vasospasm and postoperative medical treatment is initiated. but if patient is not admitted in a specialized center before day 3, timing for surgery is debatable. we recommend operating the patient even in the delicate period from day 3 to 14, because clipping the aneurysm allows intraoperative removal of blood clots and postoperative triple h therapy. in our opinion removal of subarachnoid blood, triple h therapy and nimodipine are the most effective treatments. costs are influences by occurrence of complications, mainly vasospasm, so preventionof vasospasm reduces costs. vasospasm is not found in patients with avms or cavernomas, because they do not bleed in the subarachnoid space, so for this group of patients,specific treatment for vasospasm is not indicated. surgery is the treatment of choice in avms.13,14 complete resection ensures cure of the lesion. stereotactic radiosurgery causes progressive occlusion of vessels, but unfortunately the effect occurs in time, and until 1-2 years the nidus is still active. embolization is recommended only as adjuvant before surgery or in grade vi avms.14the effect of embolization is limited in time, surgery must be performed in the first week after occlusion procedure. after one month the nidus recruits new blood vessels. principles of surgery for avms depend on location, spetzler-martin score and angioarchitecture of the lesion. we recommend surgery for all ruptured avms and in all lesions located in non-eloquent areas.15 conservative treatment and stereotactic radiosurgery can be tried in patients with small, unruptured, located in eloquent areas avms.13 surgical principles are represented by early coagulation of feeding arteries, 14 aurelia mihaela sandu, adrian mircea fürtös, radu mircea gorgan circumferential dissection of the nidus progressing deep and, after complete arterial disconnection of the nidus occlusion of draining veins.10we do not perform preoperative embolization of avms because it carries the risk of intraprocedural nidus rupture and developing normal perfusion pressure breakthrough. but other authors consider it helpful before surgery. the angiography was negative in all cases with cavernomas. they are considered to be occult angiographic lesions, because they have very low flow and do not enhance with contrast. we do not recommend angiography in cases suggestive for cavernomas. the imaging of choice is t2 echogradient and flair mri. we recommend surgery in patients with ruptured cavernomas, with intraparenchymatal hematoma, in symptomatic cavernomas and in superficial accessible lesions. deep, unruptured and asymptomatic cavernomas are kept under surveillance. for brainstem cavernomas, we strongly recommend surgery after the first bleeding, because the second has devastation consequences. in supratentorial cavernomas we recommend resection of hemosiderin ring surrounding the cavernoma. brain surrounding the lesion impregnated with hemosiderin can be responsible for seizure persistence. so resection of hemosiderin ring ensures good outcome, evaluated through engel epilepsy surgery outcome scale. in lesions located in the brainstem we recommend resection of the lesion leaving the hemosiderin ring in place. infratentorial cavernomas do not produce seizure, and aggressive resection in this delicate area full with eloquent structures induces severe neurological deficits. we recommend embolization of davf. total health care costs of patients is composed by hospitalization costs, food costs, medication costs, medical products costs, blood work costs and imaging exams costs. longer hospitalization increases costs. higher costs in the group of patients who underwent surgery compare with patients belonging to the conservative group, even if it is highly significant, it is not relevant because we are a neurosurgical department and we only keep patients for surgery. if a patient has no surgical indication or refuses surgery, we discharge him and he will be treated further in the territorial neurological department. so costs for nonsurgical patients are not adequately evaluated. so, we can conclude that our study illustrates best the surgical group. food costs are bound to hospitalization cost and comorbidities (e.g. diabetes, renal failure, etc.). usually blood work costs are not so high, we only take the minimum set before surgery. vascular pathology does not require special, expensive blood test before surgery. it may increase if patients require repetitive blood analysis (e.g. postoperative anemia, patients in icu, etc.). unfortunately, other costs, such as costs with the medical personnel, cost of surgery or costs for days in the icu, which are included in a bill from the private hospitals, are not included in a state hospital. complications also increased costs. so, adequate patients’ selection and choosing the best treatment for lowering the rate of possible complications can reduce costs. cost analysis is useful as a market research to predict resources needed for patients’ investigation and treatment. such analysis is a useful tool in developing guidelines. the principles of guidelines choosing the best treatment, while optimizing health care services. a limit of the study is represented by the fact that it precisely illustrates the surgical group, but it is not so reliable in characterizing the conservative group. conclusions proper treatment of brain vascular pathology ensures a favorable outcome. adequate patients’ selection and choosing the best treatment to lower the rate of possible complications can reduce costs. surgery is the treatment of choice in ruptured aneurysms, avms or cavernomas. early surgery, with specific treatment of the vascular lesion and removal of intracranial blood ensures a better outcome, with lower medical costs. prevention of complications, aggressive treatment of vasospasm reduces medical costs. further analysis is needed to perfect guidelines for treatment of patients with brain vascular pathology. 15 overview of patients with vascular pathology and cost analysis table 1. aneurysms’ location. aneurysm location single aneurysm multiple aneurysms total no. total % ica segm c4 3 1 4 4.12 ica segm c5 4 4 8 8.25 ica segm c6 10 10 20 20.62 ica segm c7 2 1 3 3.09 acoa 18 1 19 19.59 aca 5 3 8 8.25 mca 9 11 20 20.62 acop 4 3 7 7.22 sca 1 0 1 1.03 basilar artery 4 1 5 5.15 pica 1 0 1 1.03 vertebral artery 1 0 1 1.03 total 62 35 97 100 table 2. avms’ location. avm location total no. total % f 7 21.21 t 4 12.12 p 4 12.12 o 5 15.15 fp 3 9.09 ft 1 3.03 sylvian fissure 1 3.03 tp 3 9.09 tpo 2 6.06 intraventricular 1 3.03 posterior fossa 2 6.06 total 33 100 acknowledgement this paper was co-financed from the human capital operational program 2014-2020, project number pocu / 380/6/13/125245 no. 36482 / 23.05.2019 "excellence in interdisciplinary phd and post-phd research, career alternatives through entrepreneurial initiative (excia)", coordinator the bucharest university of economic studies”. conflict of interests the authors declare no conflict of interests. abbreviations aca anterior cerebral artery acoa anterior communicating artery acop anterior posterior artery avm arteriovenous malformation davf dural arteriovenous fistula ica internal carotid artery mca middle cerebral artery mrs modified rankin score pica posteroinferior cerebellar artery sca superior cerebellar artery references 1. mccormick wf. the pathology of vascular (“arteriovenous”) malformations. j neurosurg 24, 807816. 1966. 2. greenberg ms. sah and aneurysms. in greenberg ms (ed). handbook of neurosurgery. new york: thieme medical publishers; 2010:1055-1097. 3. misra m, aletich v, charbel ft, debrun gm, ausman ji. multidisciplinary approach to arteriovenous malformations. in kaye ah, black pm (eds). operative neurosurgery. london: harcourt publishers limited; 2000:1137-1151. 4. stapf c, mast h, sciacca rr, berenstein a, nelson pk, gobin yp, pile-spellman j, mohr jp. the new york islands avm study: design, study progress, and initial results. stroke 34, e29-34. 2003. 5. altschul d, smith ml, sinson gp. intracranial arteriovenous malformation. medscape emedicine[surgery/neurosurgery/vascular]. 2011. 6. greenberg ms. vascular malformations. in greenberg ms (ed). handbook of neurosurgery. new york: thieme medical publisher; 2010:1098-1142. 16 aurelia mihaela sandu, adrian mircea fürtös, radu mircea gorgan 7. goldstein he, solomon ra. epidemiology of cavernous malformations. handb clin neurol 2017; 143:241-247. 8. gross ba, du r. hemorrhage from cerebral cavernous malformations: a systematic pooled analysis. j neurosurg 2017; 126:1079-1087. 9. lawton mt. seven aneurysms: tenets and techniques for clipping. new york: thieme medical publishers; 2010. 10. lawton mt. seven avms tenets and techniques for resection. new york: thieme medical publishers; 2014. 11. hulsbergen afc, mirzaei l, van der boog atj, smith tr, muskens is, broekman mld, mekary ra, moojen wa. long-term durability of open surgical versus endovascular repair of intracranial aneurysms: a systematic review and meta-analysis. world neurosurg 2019; 132:e820-e833. 12. lindgren a, vergouwen md, van der schaaf i, algra a, wermer m, clarke mj, rinkel gj. endovascular coiling versus neurosurgical clipping for people with aneurysmal subarachnoid haemorrhage. 13. kato y, dong vh, chaddad f, takizawa k, izumo t, fukuda h, hara t, kikuta k, nkai y, endo t, kurita h, xu b, benes v, christian r, pavesi g, hodaie m, sharma rk, agrawal h, mohan k, liew bs. expert consensus on the management of brain arteriovenous malformations. asian j neurosurg 2019; 14:1074-1081. 14. rutledge c, nelson j, lu a, nisson p, jonzzon s, winkler ea, cooke d, abla aa, lawton mt, kim h. cost determinants in management of brain arteriovenous malformations. acta neurochir (wien) 2020; 162:169173. 15. gorgan rm. malformaţiile arteriovenoasecerebrale. in ciurea av (ed). tratat de neurochirurgie. bucuresti: editura medicală; 2011:117-129. romanian neurosurgery (2019) xxxiii (2): pp. 166-173 doi: 10.33962/roneuro-2019-031 www.journals.lapub.co.uk/index.php/roneurosurgery secondary (duret) brainstem haemorrhage may not always represent a fatal event. review of literature and report of four cases martin hanko1, branislav kolarovszki1, kristián varga1, rené opšenák1, pavol snopko1, radoslav hanzel1, kamil zeleňák2 1 clinic of neurosurgery, university hospital in martin, jessenius faculty of medicine in martin, comenius university in bratislava, slovakia 2 clinic of radiology, university hospital in martin, jessenius faculty of medicine in martin, comenius university in bratislava, slovakia abstract background. secondary brainstem haemorrhage (eponymously called duret haemorrhage) is a well-known complication of transtentorial brain herniation or of rapid decompression of intracranial space. it is considered to be a consequence of arterial rupture, venous infarction or ischemia-reperfusion injury and it is regarded as a harbinger of an unfavourable outcome for the patient. despite this, several case reports describing good outcome after duret haemorrhage preceded by evacuation of an expansive traumatic intracranial mass lesion, an episode of intracranial hypotension or lumbar drainage have been published. case description. we present four cases of patients with secondary brainstem haemorrhage linked to an episode of intracranial hypertension due to various reasons who were treated at our clinic. the first patient suffered a small brainstem haemorrhage that was described on his initial ct scan presumably as a result of massive intracranial expansion caused by an acute subdural haematoma and this duret haemorrhage markedly expanded after the subdural haematoma was evacuated by means of a decompressive craniectomy. the next two patients developed duret haemorrhage after the evacuation of intracranial haematomas. the fourth patient presented with posttraumatic cerebral oedema complicated by a subtle duret haemorrhage displayed on his initial ct scan and this bleeding remained stable even after a bilateral decompressive craniectomy. one patient passed away, one remained in a persistent coma and two survived with a light neurological deficit. conclusions. however ominous a newly discovered duret haemorrhage may be, it alone should not discourage us from the further intensive treatment of our patients as their outcome may considerably vary. the extent of this bleeding, type and severity of underlying brain injury and complete clinical status and history of our patients should all be taken into account when deciding about patients’ prognosis. introduction originally described by a french surgeon henri duret[6], secondary keywords duret haemorrhage, intracranial hypertension, prognosis, secondary brainstem haemorrhage corresponding author: branislav kolarovszki jessenius faculty of medicine in martin, comenius university in bratislava, clinic of neurosurgery, university hospital in martin kollárova 2, 036 59 martin, slovakia kolarovszki@jfmed.uniba.sk copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 167 secondary (duret) brainstem haemorrhage may not always represent a fatal event brainstem haemorrhages or eponymously duret haemorrhages are a feared consequence of a transtentorial brain herniation or of a decompression of the intracranial space by means of craniectomy or by removal of an intracranial mass lesions [16,21,22]. they can occur with a delay of only 30 minutes after the initial insult and primarily affect the ventral midline parts of the pons and the mesencephalon, but never the medulla oblongata [7,15,26]. because such haemorrhages often irreversibly destroy the brainstem reticular formation, functional centres and descending pathways, their prognosis is usually very poor with patient either dying or surviving for a limited amount of time with a severe deficit, often unconscious and ventilator-dependent [15,18,26]. however, case reports of patients suffering duret haemorrhage and achieving a highly favourable outcome with a gentle or no persistent neurological deficit are known [1,2,3,8,11,16,20]. currently, the question of whether a diagnosis of duret haemorrhage should discourage us from an aggressive treatment is debated. in this work we review the available knowledge concerning secondary brainstem haemorrhage with attention paid on its pathogenesis and outcome of patients who suffer it. we also present four cases of our patients with duret haemorrhages which resulted in various outcome. case presentations case a a 50 years old man was found unconscious with a right-sided mydriasis. he had a history of chronic alcoholism and ethylic liver disease. the emergency ambulance was called, he was intubated and sedated, then transported to our hospital. after arrival, his gcs score was 4 (1-1-2), he was anisocoric with bilateral absence of pupillary and corneal reflexes and with a decerebrate response to painful stimuli. ct scan verified an acute left-sided subdural haematoma 24 mm thick, descending transtentorial herniation, enlargement of the right lateral ventricle, midline shift of 21 mm and a small interhemispheric haemorrhage. there was also a subtle duret haemorrhage located in the pons (figure 1a). the patient was immediately brought to the operating room and a decompressive craniectomy with an evacuation of the subdural haematoma was performed. he was then kept sedated and ventilated with circulatory support by norepinephrine until a control ct scan was performed 6 hours after the surgery. it revealed a reduction of the midline shift to 3 mm, however remains of the subdural haematoma were present and new bilateral intracerebral haemorrhages occurred together with a bleeding into the third and fourth ventricle. massive enlargement of the pontine haematoma that was now extending into mesencephalon was described. perimesencephalic cisterns were bilaterally compressed (figure 1b). based on these findings the patient’s prognosis was considered highly unfavourable and no other surgical intervention was indicated, we continued in a palliative care. the sedation and mechanical ventilation were discontinued (the patient remained unconscious with gcs 3), oxygen and norepinephrine support was further provided. 14 hours after the surgery our patient died due to failure of cardiorespiratory functions. figure 1. preoperative ct scan (a) revealing a massive acute subdural haematoma 24 mm thick, smaller interhemispheric acute subdural haematoma, enlargement of the right lateral ventricle, midline shift of 21mm, and a subtle duret haemorrhage located in the pons. after a decompressive craniectomy (b) the midline shift had resolved however remains of subdural haematomas are apparent. new intracerebral haemorrhages together with progression of pontine bleeding are visible. 168 martin hanko, branislav kolarovszki, kristián varga et al. case b this 64 years old man with a history of arterial hypertension, liver steatosis, lung resection due to tuberculosis and chronic obstructive pulmonary disease underwent a right-sided decompressive craniectomy with an evacuation of an acute posttraumatic haemorrhage into a chronic subdural haematoma. two months later he was admitted again for a planned cranioplastic surgery usong an autologous bone flap. at that time, he was fully conscious, well-oriented and communicating with a moderate left-sided hemiparesis persistent since the event of his traumatic brain injury. he underwent the cranioplasty without any serious complications and without any changes in his neurological status immediately after surgery. approximately 8 hours later the patient had an epileptic seizure that terminated after a 5 mg intravenous dose of diazepam, he however remained non-responsive, his right-sided pupil was enlarged. the attending neurosurgeon indicated an immediate ct scan which revealed an epidural haematoma 47 mm thick at the site of reimplanted bone flap, midline shift of 19 mm, compression of lateral ventricles and perimesencephalic cisterns and a transtentorial herniation of the right-sided temporal lobe. the patient was transported to the operating room with pupils already bilaterally mydriatic and non-reactive. emergent evacuation of the epidural haematoma was performed and the bone flap was returned with drainage tubes placed into the epidural space. the patient remained sedated and ventilated until the next ct scan 8 hours later which revealed a recent haemorrhage into right-sided basal ganglia, all four ventricles and a duret haemorrhage into the upper pons and mesencephalon. 24 hours later the sedation and mechanical ventilation were discontinued and a tracheostomy was performed. at that time the patient was unconscious with gcs 3, he had irregular pupils with a slight right-sided mydriasis, absent pupillary reflex and present corneal reflex, spontaneously ventilating. he was later transferred to a nursing home and remained in persistent coma with his neurological status unimproved (as reported from his last known clinical check 2 months after the surgery). case c a 63 years old woman pedestrian was struck by a car and subsequently transported to a peripheral hospital, unconscious with gcs 7 (1-1-5), present pupillary reflex, sedated and intubated. ct scan was performed revealing a skull base fracture, pneumocephalus, traumatic subarachnoid haemorrhage, small subdural haematoma over the right hemisphere and a small haemorrhagic contusion in right temporal lobe. she also suffered numerous smaller lung contusions. 24 hours later she was transferred to our institution due to a progressive oedema of the right hemisphere with an enlargement of the haemorrhagic contusion in the right temporal lobe. decompressive craniectomy and evacuation of the haemorrhagic contusion was subsequently performed and the patient remained sedated for following 24 hours. a control ct scan revealed two subtle duret haemorrhages (one located in the pons and one in the mesencephalon) both with a diameter of approximately 1 cm (figure 2). no further surgical intervention was indicated. two months later she underwent autologous bone flap replantation and a ventriculo-peritoneal shunt insertion due to development of a posttraumatic hydrocephalus. after the surgery she remained conscious with gcs 14 (4-4-6), disoriented with signs of organic psychosyndrome slightly bradypsychic, occasionally agitated and verbally aggressive. her only persistent motoric deficit was a right sided ptosis. figure 2. postoperative ct scan verifying basally located remains of haemorrhagic contents and a subtle duret haemorrhage in the pons. 169 secondary (duret) brainstem haemorrhage may not always represent a fatal event case d a 27 years old patient who suffered a motorcycle accident was immediately sedated and transferred to our clinic due to a ct verified posttraumatic cerebral oedema, subarachnoid haemorrhage, nonexpansive right-sided acute subdural haematoma, intracerebral haematomas in both frontal lobes and a small duret haemorrhage located in his ventral mesencephalon. prior to sedation he had gcs 8 (1-25), he was isocoric with pupillary reflex bilaterally preserved. due to a presence of non-expansive haemorrhagic intracranial lesions only an intraparenchymal intracranial pressure sensor was initially inserted but 12 hours later the patient developed a refractory intracranial hypertension with pressure values exceeding 40 mmhg and a bilateral decompressive craniectomy was performed. however, because of a ct verified duret haemorrhage the patient’s prognosis was considered unfavourable. the postoperative ct revealed stabilized intracranial findings with an adequate decompressive effect of the bilateral craniectomy with the brainstem haemorrhage being stable and non-expanding. the sedation was discontinued and the patient was later discharged to a peripheral hospital surprisingly achieving a highly favourable outcome: gcs 15 and a slight right sided hemiparesis and facial nerve palsy. discussion henri duret (1849-1921), a french surgeon and a pioneer of neuroscience focused his aim in neurological research on localising of functional areas in the brain, describing the vascular supply of the central nervous system and investigating pathomechanisms of traumatic brain injuries [27]. in experimental conditions he had described mechanisms of intracranial hypertension by simulating intracranial mass lesions and correctly assumed brainstem (especially medulla oblongata) as a centre of cardiorespiratory functions. he had also noted a disturbance in the cerebral tissue perfusion during periods of increased intracranial pressure and had observed microscopic haemorrhages located in the floor of the fourth ventricle which were associated with episodes of increased intracranial pressure [6,27]. despite of having inaccurately linked these bleedings to an increased cerebrospinal fluid pressure at the moment of primary brain injury and despite a fact that these haemorrhages might not even be true secondary brainstem bleedings, duret haemorrhages have remained an eponymous term for secondary brainstem haemorrhagic lesions caused mostly by intracranial hypertension and following the transtentorial herniation [21,27]. causes of duret haemorrhage duret haemorrhage is typically a result of a descending transtentorial brain herniation. cases of a brainstem haemorrhage preceded by an occurrence of an intracerebral haematoma [19,21], acute subdural haematoma [1,10,17,20,21], cerebral infarction [19] or diffuse cerebral oedema caused by hyponatremia [11] are known. on the other hand, several cases of the duret haemorrhage following an episode of intracranial hypotension which can also provoke a descending transtentorial herniation have been reported. cardinale et al. have published a case of the duret haemorrhage in a patient after a decompressive craniectomy complicated by an episode of intracranial hypotension and a paradoxical brain herniation presenting as the sinking skin flap syndrome [4]. similarly, yuan et al. have described a case of the duret haemorrhage in a patient with lumbar drainage following an operation of a thalamic tumour [28]. there is also a report of a patient who suffered a brainstem haemorrhage caused by a postoperative lumbar pseudomeningocele and associated intracranial hypotension [3]. interestingly, even a rapid decompression of the intracranial space by means of evacuation of an expansive intracranial haemorrhage [2,8,13,22] or by means of a decompressive craniectomy [16,17,25] can result in the duret bleeding. incidence in their autoptic research of haemorrhagic stroke nedergaard et al. have observed an incidence of the duret haemorrhage in 45% of intracerebral haemorrhages, 15% of cerebral infarctions and 36% of aneurysm haemorrhages [19]. in a clinicopathological report of klintworth, duret haemorrhage was typically associated with intracranial lesions complicated by a rapidly expanding intracranial haemorrhage or brain oedema or with a surgical decompression of intracranial space even in slowly growing lesions with overall incidence of 16.5%, specifically 31.5% for 170 martin hanko, branislav kolarovszki, kristián varga et al. intracerebral haemorrhages, 21.5% for subdural haematomas and 11.6% for cerebral infarctions [13]. in a non-missile brain injury, graham et al. have reported an incidence of the duret haemorrhage in 51% of autopsies [9]. however, almost 20% of these haemorrhages could only be discovered during microscopic examination [9] and this fact leads us to expect that radiological examination will underestimate the incidence of secondary brainstem haemorrhages in surviving patients. pathogenesis unlike primary brainstem haemorrhage which could be a result of a spontaneous arterial rupture, direct traumatic injury to the brainstem or of a rupture of vascular malformation, secondary brainstem haemorrhage typically presents with a delay and is mostly a consequence of the descending transtentorial herniation or follows a rapid decompression of the intracranial space [16,21]. there are several main explanations for pathogenesis of the duret haemorrhage. the theory of an arterial origin of the duret haemorrhage assumes that a descending transtentorial herniation causes a displacement and angulation of the brainstem with an elongation and straining of the perforating arteries extending from the basilar artery which is fixed in its upper end by the posterior communicating arteries and the posterior cerebral arteries. this tension results in either vasospasm or rupture of the perforating arteries and causes the duret haemorrhage [12,15,21,26]. the very appearance of the duret haemorrhage is highly dependent on the volume and rate of expansion of the underlying intracranial mass lesions and also on variations of systemic blood pressure and blood inflow into the perforating arteries during the episodes of transtentorial herniation. slowly expanding intracranial mass lesions do not usually cause the duret haemorrhage [7,12]. an extremely rapid descending transtentorial herniation causing acute brainstem ischaemia results in early death of the patient without an episode of the secondary brainstem bleeding (which is prevented by the disturbed blood flow in perforating arteries) [12]. based on experimental research on animal model, klintworth has postulated that the duret haemorrhage arises during two possible scenarios: the transtentorial herniation can extensively displace the perforating branches of the basilar artery. if sufficient blood flow in these vessels is retained, they are prone to rupture and cause secondary brainstem haemorrhage [12]. evacuation of the intracranial mass lesion causing transtentorial herniation and perforating vessel damage (mechanic or ischaemic) can also provoke duret haemorrhage in a situation when the blood flow into these damaged arteries is restored causing them to bleed even more extensively than during transtentorial herniation only, especially in situation of elevated systemic blood pressure [12,14,15,24]. it is possible that all types of blood vessels in the ventral brainstem are damaged in a manner of an ischaemia-reperfusion injury and are later prone to cause a massive secondary brainstem haemorrhage [14]. the theory of reperfusion injury is supported by a report of sim et al. who have observed an enhancement of ventral pontomesencephalic area on ct angiography in a patient with a transtentorial herniation due to bilateral chronic subdural haematoma and acute tentorial subdural haematoma. after a burr-hole drainage of chronic haematomas was performed, a massive duret haemorrhage in the area of previous parenchymal enhancement occurred. the contrast extravasation probably demonstrated damaged perforating arteries [24]. arterial origin of duret haemorrhage is also supposed when based on a report by chew et al. who have performed a postmortem ct angiography on a patient who died due to a middle cerebral artery aneurysm rupture associated with a transtentorial herniation and a secondary brainstem haemorrhage. multiple linear enhancing foci corresponding to ruptured paramedian perforating arteries found in autopsy were detected in the central pons [5]. theory of a venous infarction arises from an observation of venous congestion in the brainstem in patients with a supratentorial mass lesions, perivenous localisation of several duret haemorrhages and a fact that the veins are thin-walled vessels easily compressed by an external pressure, specifically at the site of the tentorial notch. compression can cause the veins to thrombose and result in venous brainstem haemorrhages [12,15,21,23]. this explanation has been however questioned because secondary brainstem haemorrhages often extend anatomical regions of the venous drainage and the evacuation of intracranial mass lesions can rather provoke duret haemorrhage than prevent it [12]. observations of a brainstem ischaemia with no secondary 171 secondary (duret) brainstem haemorrhage may not always represent a fatal event haemorrhage in patients with the transtentorial herniation also challenges this theory of pathogenesis [26]. favourable outcome of patients suffering a duret haemorrhage despite being considered a predictor of infaust prognosis, several reports describing a favourable outcome of patients with the duret haemorrhage caused by various types of intracranial pathologies have been published. dramatic recovery has been reported by ishizaka et al.: a patient with an idiopathic subdural haematoma and preoperatively described duret haemorrhage underwent evacuation of the subdural haematoma and despite of a severe preoperative neurological deficit his status resolved to a persistent oculomotor palsy only [10]. similarly, nguyen et al. have described a patient with an acute subdural haematoma and a duret haemorrhage achieving a favourable outcome (dysarthria and no motor deficit) after an evacuation of a subdural bleeding [20]. stiver et al. have also reported a favourable outcome of a young woman who developed a duret haemorrhage after an evacuation of an epidural haematoma by means of decompressive craniectomy [25] and another case of favourable outcome after an evacuation an epidural haematoma in a patient with a duret haemorrhage has been published by fujimoto et al. [8]. a report by park et al. describes a patient who suffered a duret haemorrhage after a burr-hole drainage of bilateral chronic subdural haematomas and survived with his only persistent deficit being a gentle gait disturbance [22]. lonjaret et al. have published a case report of patient with a duret haemorrhage triggered by a decompressive craniectomy for an acute subdural haematoma resulting in a favourable outcome with no neurological deficit [16]. kamijo et al. have reported a favourable outcome (gentle hemiparesis) in a patient with a severe hyponatremia causing a transtentorial herniation and a duret haemorrhage [11]. a favourable outcome with persistent internuclear ophtalmoplegia only in a patient with a duret haemorrhage due to an intracranial hypotension has been published by bonow et al. [3]. in paediatric patients, beier and dirks have reported a favourable outcome in two patients with duret haemorrhage preceded by a traumatic brain injury [1]. when summarized, most of patients surviving with favourable outcome have suffered a brainstem haemorrhage of a limited extent only [1,2,3,8,20], however exceptions exist [11,16,22]. younger age of these patients could be a factor predicting a favourable outcome [1,11,16,20]. a typically reported persisting neurological deficit in patients with the favourable outcome is often a cranial nerve weakness [1,3,8,10,11,16], or various subtle forms of the organic psychosyndrome and a cognitive deficit [1,25]. analysis of our case series the first three patients (a,b,c) described in our work represent cases of duret haemorrhage provoked or worsened by a rapid decompression of intracranial space combined with a decompressive craniectomy in 2 of 3 patients. the explanation of this phenomenon could be based on the theory of reperfusion into the damaged pontine perforating vessels as initially postulated by klintworth [12,13,14,24]. alleviation of a significant pressure on the brainstem had most likely increased the blood inflow into mechanically and metabolically injured vessels in the pontomesencephalic region and resulted in the secondary brainstem haemorrhage (or its significant expansion in one case). the patient d probably suffered a duret haemorrhage due to a massive cerebral oedema with a mass effect that displaced the brainstem and distorted the mesencephalic perforating arteries thus causing them to rupture because of a combination of metabolic and mechanic damage [12,15,21,26]. it is possible that due to patient’s younger age and absence of complicating diagnoses the perforators remained relatively stable even after the alleviation of the intracranial hypertension by means of decompressive craniectomy and the secondary brainstem haemorrhage did not expand. two of our four patients had achieved a good outcome and this was probably caused by a smaller extent of the pontine haemorrhage and a younger age of patient d. chronic liver disease present in two patients with unfavourable outcome could play a role as a potential negative prognostic factor as it can negatively affect the function of the blood coagulating system, however a definite conclusion can only be made when relating to a larger group of patients. conclusions massive elevation of intracranial pressure, decompression of the intracranial space by means of 172 martin hanko, branislav kolarovszki, kristián varga et al. craniectomy or intracranial bleeding evacuation can make the patient susceptible to the secondary brainstem (duret) haemorrhage. such bleeding, typically localised in the midbrain and pons has been considered a significant predictor of poor prognosis. despite of this, outcome of patients suffering the duret haemorrhage can considerably vary as presented in our report. when deciding about the prognosis of a patient with the duret haemorrhage, attention should be paid to the type and severity of the underlying brain injury, patient’s clinical status and history and at last but not least to the extent of the very brainstem bleeding. abbreviations ct: computed tomography gcs : glasgow coma scale references 1. beier ad, dirks pb. pediatric brainstem hemorrhages after traumatic brain injury. j neurosurg pediatrics. 2014; 14(4), 421-4. 2. bermudéz g, areitio e. duret haemorrhage with full recovery. acta neurochir (wien). 2015; 157(8), 1337-8. 3. bonow r, bales jw, morton rp, levitt mr, zhang f. reversible coma and duret haemorrhage after intracranial hypotension from remote lumbar spine surgery: case report. j neurosurg spine. 2016; 24(3): 389-93. 4. cardinale m, meaudre e, cunqi pq, nguyen c, esnault p, joubert c. duret hemorrhage complicating a sinking skin flap syndrome. br j neurosurg. 2017; sep 8,1-2. 5. chew kl, baber y, iles l, o’donnell c. duret hemorrhage: demonstration of ruptured paramedian pontine branches of the basilar artery of minimally invasive, whole body postmortem ct angiography. forensic sci med pathol. 2012; 8(4), 436-40. 6. duret h. études expérimentales et cliniques sur les traumatismes craniocérébraux. paris: thése; 1878. 7. fields ws, halpert b. pontine hemorrhage in intracranial hypertension. am j pathol. 1953; 29(4), 677-87. 8. fujimoto y, aquiar ph, freitar ab, de andrade af, marino júnior r. recovery from duret hemorrhage: a rare complication after craniotomy. neurol med chir (tokyo). 2000; 40(10), 508-10. 9. graham di, lawrence ae, adams jh, doyle d, mclellan dr. brain damage in non-missile head injury secondary to high intracranial pressure. neuropathol appl neurobiol. 1987; 13(3), 209-17. 10. ishizaka s, shimizu t, ryu n. dramatic recovery after severe descending transtentorial herniation-induced duret haemorrhage: a case report and review of literature. brain inj. 2014; 28(3), 374-7. 11. kamijo y, kishita r, hamanaka s, soma k. duret haemorrhage is not always suggestive of poor prognosis: a case of acute severe hyponatremia. am j emerg med. 2005; 23(7), 908-10. 12. klintworth gk. the pathogenesis of secondary brainstem hemorrhages as studied in an experimental model. am j pathol. 1965; 47(4), 525-36. 13. klintworth gk. evaluation of the role of neurosurgical procedures in the pathogenesis of secondary brain-stem hemorrhages. j neurol neurosurg psychiatry. 1966; 29(5), 423-5. 14. klintworth gk. paratentorial groowing of human brains with particulatr reference to transtentorial herniation and the pathogenesis of secondary brain-stem hemorrhages. am j pathol. 1968; 53(3) 391-408. 15. leestma je. forensic neuropathology. boca raton: taylor&francis; 2014. 16. lonjaret l, ros m, boetto s, fourcade o, geeraerts t. brainstem haemorrhage following decompressive craniectomy. j clin neurosci. 2012; 19(9), 1293-5. 17. martins wa, teixeira ab, frigeri tm, paglioli e. spontaneous subdural hematoma associated to duret haemorrhage. interdisciplinary neurosurgery. 2015; 2(1), 13-15. 18. moore as, mittal mk, rabinstein aa. duret hemorrhage following subdural hematoma evacuation. jama neurol. 2013; 70(4), 518. 19. nedergaard m, klinken l, paulson ob. secondary brain stem hemorrhage in stroke. stroke. 1983; 14(4), 501-5. 20. nguyen hs, doan mb, gelsomino mj, shabani s, mueller wm. good outcomes in a patient with a duret haemorrhage from an acute subdural hematoma. int med case rep j. 2016; 9, 15-18. 21. parizel pm, makkat s, jorens pg, ozsarlak o, cras p, van goethem jw, et al. brainstem hemorrhage in descending transtentorial herniation (duret haemorrhage). intensive care med. 2002; 28(1), 85-8. 22. park kj, kang sh, lee hk, chung yg. brain stem hemorrhage following burr hole drainage for chronic subdural hematoma. neurol med chir (tokyo). 2009; 49(12), 594-7. 23. scheinker im. transtentorial herniation of the brain stem. a characteristic clinicopathologic syndrome; pathogenesis of hemorrhages in the brain stem. arch neurpsych. 1945; 53(4), 289-298. 24. sim kb, na dg, park jk. precedence of parenchymal enhancement on ct to a fatal duret hemorrhage. j korean neurosurg soc. 2013; 53(6), 380-2. 25. stiver si, gean ad, manley gt. survival with good outcome after cerebral herniation and duret hemorrhage caused by traumatic brain injury. j neurosurg. 2009; 110(6): 1242-6. 173 secondary (duret) brainstem haemorrhage may not always represent a fatal event 26. tomliston be, brain-stem lesions after head injury. j clin pathol suppl (r coll pathol). 1970; 4, 154-65. 27. walusinski o, cou.rivaud p. henri duret (1849-1921): a surgeon and forgotten neurologist. eur neurol. 2014; 72(3-4), 193-202. 28. yuan x, zhao h, zhao c, zhao h, xiaho h, sun g, et al. duret hemorrhage after lumbar drainage. j craniofac surg. 2014; 25(4), 1551-2. doi: 10.33962/roneuro-2023-025 the t2flair mismatch novel radiogenomic marker in the newly suspected low-grade gliomas. implications for grading and neurosurgical management in light of the 2021 who classification of tumours of the central nervous system (whocns5) iulia miculescu, daniela l. ivan, aurelia dabu, daniel teleanu, a. v. ciurea romanian neurosurgery (2023) xxxvii (2): pp. 141-149 doi: 10.33962/roneuro-2023-025 www.journals.lapub.co.uk/index.php/roneurosurgery the t2flair mismatch novel radiogenomic marker in the newly suspected low-grade gliomas. implications for grading and neurosurgical management in light of the 2021 who classification of tumours of the central nervous system (whocns5) iulia miculescu1, daniela l. ivan1, aurelia dabu1, daniel teleanu1,2, a. v. ciurea3 1 department of neurosurgery, university emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 “sanador” clinic hospital, bucharest, romania abstract background. the t2-flair (fluid-attenuated inversion recovery) mismatch sign has been defined over the last few years as an important novel radiogenomic marker highly suggestive of isocitrate dehydrogenase mutated (idh-mut) 1p19q noncodeleted gliomas (astrocytomas). existing studies have demonstrated that this has good specificity but limited sensitivity for idh-mut astrocytomas. the new 2021 who classification of tumors of the central nervous system (who cns5) has introduced a layered grading system in which all idh mutant diffuse astrocytic tumours are considered a single type (astrocytoma, idh-mutant) and are graded as cns who grade 2, 3, or 4. because of the growing importance of molecular information in cns tumour classification, diagnoses and diagnostic reports need to combine different data types into a single diagnosis. whether the t2flair mismatch sign is of clinical relevance for the management of low-grade gliomas still needs to be further determined. methods. we included histologically verified supratentorial low-grade gliomas (lgg) who grade 2-3 retrospectively during the period 2013–2018 (n=18). for the period 2019–2023 (n=27), patients with a radiological presumptive diagnosis of low-grade glioma were prospectively included, and we took into consideration the fact that in t h i s g r o u p w e c o u l d e n c o u n t e r o t h e r d i a g n o s e s t h a n g l i o m a . clinical, radiological and histology data were collected. we aimed to examine the association of the t2-flair mismatch sign (where identified) with clinical factors and outcomes. we evaluated the diagnostic reliability of the mismatch sign and its keywords t2flair, low-grade gliomas, whocns5 corresponding author: alexandru vlad ciurea professor. “carol davila” university of medicine and pharmacy, bucharest, romania prof.avciurea@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 142 iulia miculescu, daniela l. ivan, aurelia dabu et al. relation to the definitive histological diagnosis, the co-existence of an mr spectroscopy signature; we have also tried to determine whether the identification of the radiogenomic marker had any impact on the clinical outcome through the decision-making in neurosurgical management. results. out of 45 patients with radiological suspected glioma, 30 had a definitive diagnosis of diffuse astrocytoma grade 2 and 3 (astrocytoma, idh-mutant according to whocns5). 6 patients had a diagnosis of glioblastoma (glioblastoma, idhwildtype according to whocns5). 8 patients have been diagnosed with oligodendroglioma (oligodendroglioma, idhmutant, and 1p/19q-codeleted according to whocns5) and 1 case had a definitive histology of cerebral abscess. out of the 30 patients with idh-mut astrocytoma, 6 (20.0%) showed a mismatch sign. the sensitivity and specificity of the mismatch sign for idh-mut astrocytoma detection were 20% and 98.6%, respectively. there were no differences between patients with an idh-mut astrocytoma with or without t2flair mismatch sign when grouped according to this with related to baseline characteristics, clinical outcome and presenting symptoms. mr spectroscopy sequences were analyzed where available for the retrospective and prospective cohort. there were 7 cases where mr spectroscopy was performed and, for the idh-mut astrocytoma cases (n=4) it showed a persistent high cho/naa ratio without any difference between the patients with or without the t2flair mismatch sign. figure 1 (left). axial t2flair images of 50m with final histology brain abscess. figure 2 (right). axial t2w images of 50m with final histology brain abscess. conclusion. in our relatively small retrospective and prospective cohorts, the t2-flair mismatch sign, where identified, was not correlated with clinical features at presentation, prognosis or outcome. until recently, the grading of cns tumours has been focusing mainly on histology characteristics, but specific molecular markers can now be used for valuable prognostic information. for this reason, molecular-specific information has been added as an essential feature in grading and it is considered very useful for further estimation of prognosis within variable tumor types. we could not determine if the idh-mut astrocytomas with mismatch sign represent a specific subgroup. our study has confirmed that the t2-flair mismatch sign is a reliable and specific marker of idh-mut astrocytomas. background the t2-flair (fluid attenuated inversion recovery) mismatch sign has been defined over the last few years as an important novel radiogenomic marker highly suggestive of isocitrate dehydrogenase mutated (idh-mut) 1p19q non-codeleted gliomas (astrocytomas)[7]. existing studies have demonstrated that this has a good specificity but limited sensitivity for idh-mut astrocytomas. the new 2021 who classification of tumors of the central nervous system (who cns5) has introduced a layered grading system in which all idh mutant diffuse astrocytic tumors are considered a single type (astrocytoma, idh-mutant) and are graded as cns who grade 2, 3, or 4 [10]. because of the growing importance of molecular information in cns tumor classification, diagnoses and diagnostic reports need to combine different data types into a single diagnosis. whether the t2flair mismatch sign is of clinical relevance for the management of low-grade gliomas still needs to be further determined [11]. figure 3 (left). axial t1w non-contrast images of 50m with final histology brain abscess. figure 4 (right). adc map images of 50m with final histology brain abscess. several recent studies have recently demonstrated that the idh mutation and 1p/19q non codeletion status can be predicted by conventional and advanced mri [13]. figure 5. brain mri spectroscopy images of 50m with final histology brain abscess. 143 the t2flair mismatch novel radiogenomic marker in the newly suspected low-grade gliomas mri with gadolinium contrast is the main imaging investigation of election for diagnosis and management [11]. diffuse astrocytoma idh-mut involves the white matter and causes expansion of the surrounding cortex. on conventional mri, the t2flair mismatch sign is an easily identifiable imaging finding that has been studied in extensor recently [11, 12, 13]. few studies in the last couple of years have validated the idea that this radiogenomic marker plays a relevant role in making preoperative diagnosis and treatment planning [6, 7, 8]. figure 6. axialt2w images of 61f with final histology who grade 3 astrocytoma. the t2-flair mismatch sign is defined by a homogenously hyperintense signal on t2weighted imaging and a central hypointensity with peripheral hyperintensity on flair. this constitutes a radiogenomic marker regarded as highly specific for idh-mutant and 1p/19q non-co-deleted gliomas (astrocytomas). there is a strong possibility that it reflects microcystic changes in idhmutant astrocytomas [14]. figure 7 (left). axial non-contrast t1w images of 61f with final histology who grade 3 astrocytoma. figure 8 (right). coronal flair images of 61f with final histology who grade 3 astrocytoma. biomarkers are the essential elements of patientspecific management strategies, but the commonly analyzed histological biomarkers are available only after the surgical procedure [correll et all. (2020)]. therefore, in the neurosurgical management and decision making, radiogenomic biomarkers are of great interest to help identify relevant subgroup of patients. the newly described imaging feature of t2flair (fluid attenuation inversion recovery) mismatch sign has attracted increased interest, since it is a widely available and simple potential imaging marker to predict idhmutated (idh-mut) 1p19q non-codeleted (non-codel) gliomas (astrocytoma) with high specificity [16]. figure 9 (left). axial non-contrast t1w images of 61f with final histology who grade 3 astrocytoma. figure 10 (right). coronal flair images of 61f with final histology who grade 3 astrocytoma. the tumors showing a t2flair mismatch sign on mri are different radiologically from gliomas without the mismatch sign with their distinct features. this raises questions regarding underlying biology. until recently existing studies have not indicated that this radiogenomic marker is reflected by a specific biological feature [17]. we aimed to evaluate demographic, clinical, radiological and histological parameters with regard to mismatch sign and we have tried to redefine the diagnosis in conformity with the new 2021 whocns5 classification of cns tumors. in addition, we analyzed if idh-mut astrocytomas with mismatch sign had similar mr spectroscopy features compared to samples without the mismatch sign. figure 11 (left). axial t2flair images of 61m with final histology who grade 3 astrocytoma. figure 12 (right). axial t1w non contrast images of 61m with final histology who grade 3 astrocytoma. 144 iulia miculescu, daniela l. ivan, aurelia dabu et al. figure 13. coronal t2flair images of 61m with final histology who grade 3 astrocytoma. methods we included histological verified supratentorial lowgrade gliomas (lgg) who grade 2-3 retrospectively during the period 2013–2018 (n=18). for the period 2019–2023 (n=27), patients with a radiological presumptive diagnosis of low grade glioma were prospectively included, and we took into consideration the fact that in this group we could encounter other diagnoses than glioma. clinical, radiological and histology data were collected. we centralized and redefined the perspective on the histological diagnosis of all the patients in both the prospective and retrospective cohorts in line with new 2021 who classification of tumors of the central nervous system (who cns5). we aimed to examine the association of the t2flair mismatch sign (where identified) with clinical factors and outcomes. we evaluated the diagnostic reliability of the mismatch sign and its relation to the definitive histological diagnosis, the co-existence of an mr spectroscopy signature; we have also tried to determine whether the identification of the radiogenomic marker had any impact on the clinical outcome through the decision making in the neurosurgical management. the neurosurgical department at the emergency university hospital in bucharest covers the population of approximately 1 million inhabitants. the patients in the bucharest region in romania with newly diagnosed primary intracranial intraaxial tumors are referred either through the gp (general practitioner) service or by direct presentation in the accident and emergency department. from the moment of clinical and radiological presumptive diagnosis of cns tumor they enter a clinical pathway involving neurosurgery, neuroradiology, oncology, being managed in a multidisciplinary team (mdt) with weekly meetings (“tumor board”) at the emergency university hospital bucharest. our patients groups consisted of two components; one retrospective group (2013-2018) and one prospective (2019-2023). we performed a retrospective analysis of clinical and imaging data between 2013 and 2018, including surgical procedure logs, patients clinical notes and histology results, including all patients with a histology result diagnosis of a supratentorial infiltrating who grade 2 or 3 glioma with available magnetic resonance imaging (mri) (n=18). figure 14 (left). axial t2w images of 37f with final histology who grade 3 oligodendroglioma. figure 15 (right). coronal flair images of 37f with final histology who grade 3 oligodendroglioma. figure 16. mr spectroscopy of 37f with final histology who grade 3 oligodendroglioma. between 2019 and 2023, we worked prospectively on a cohort including patients with a suspected diagnosis of diffuse low grade glioma, referred either through the gp or presenting directly to our emergency department (n=27). this prospective group of patients consisted of intraaxial space-occupying lesions suggestive of primary brain tumor with a hyperintense signal in t2w images, with or without significant contrast enhancement. we took into consideration the fact 145 the t2flair mismatch novel radiogenomic marker in the newly suspected low-grade gliomas that we might encounter other histopathological diagnoses (e.g. cerebral abscess or other tumors). the main reason for including these patients was to enable the evaluation of the mismatch sign in a group with mostly similar mri appearance, but also potential different diagnoses than low grade glioma, as opposed to previous studies that used tissue diagnosis as inclusion criteria [7, 17]. we used mri images from all patients in the both retroand prospective groups to identify the t2 flair mismatch sign (n = 45). we included parameters such as patient age, gender, presenting symptom, localisation of the lesion, eloquence. we separated further the patients with idh-mut astrocytomas (n=30) divided into two subgroups, with and without mismatch sign. figure 17. axial t2w images of 69m with final histology who grade 2 diffuse astrocytoma. mri examinations reviewed in this study were performed in the radiology department of the emergency university hospital bucharest as part of the pre-operative work-up investigation. mri images were analyzed for: main part of the brain involved (frontal, temporal, parietal, occipital, insula), side (right, left, bilateral), eloquence [14], t2-flair mismatch (yes/no) and mr spectroscopy sequences characteristic features (cho/naa high ratio) correlated with the presence or absence of the t2flair mismatch sign. evaluation was performed independently by a neurosurgical specialist, a neurosurgical resident, a senior neurosurgeon and a neuroradiologist [14, 16, 17]. results out of 45 patients with radiological suspected glioma, 30 had a definitive diagnosis of diffuse astrocytoma grade 2 and 3 (astrocytoma, idhmutant according to whocns5). 6 patients had a diagnosis of glioblastoma (glioblastoma, idhwildtype according to whocns5). 8 patients have been diagnosed with oligodendroglioma (oligodendroglioma, idh-mutant, and 1p/19qcodeleted according to whocns5) and 1 case had a definitive histology of cerebral abscess. out of the 30 patients with idh-mut astrocytoma, 6 (20.0%) showed a mismatch sign. the sensitivity and specificity of the mismatch sign for idh-mut astrocytoma detection were 20% and 98.6%, respectively. there were no differences between patients with an idh-mut astrocytoma with or without t2flair mismatch sign when grouped according to this with related to baseline characteristics, clinical outcome and presenting symptoms. mr spectroscopy sequences were analyzed where available for the retrospective and prospective cohort; a number of n=4 mri spectroscopy images were available for the idh-mut astrocytoma group (n=30). in all the cases of mr spectroscopy from the idh-mut astrocytoma group, this showed a persistent high cho/naa ratio without any difference between the patients with or without the t2flair mismatch sign. table 1. demographic, clinical and radiological characteristics of patients diagnosed between 2013 and 2023 with low grade glioma (n = 30), analyzed comparing the t2-flair mismatch sign presence or absence and the mr spectroscopy high cho/naa ratio. t2 flair mismatch sign present n=6 t2 flair mismatch sign absent n=24 high cho/naa ratio on mr spectroscop y n=4 age (median) 51 52 51.5 gender (f) n 4 (66.6%) 16 (67%) 3 location of the tumor (lobe) n frontal 3 (50%) 16 (67%) 2 temporal 0 1 (4%) 0 parietal 2 (33%) 6 (25%) 2 insular 1 (16%) 1 (4.6%) 0 lateralisation and eloquence n right side 2 (33.3%) 13 (54.16%) 3 left side 3 (50%) 8 (33.3%) 1 bilateral 1 (16%) 3 (12.5%) 0 functional area 4 (75%) 11 (45.83%) 1 presenting symptoms n asymptomatic 0 3 (12.5%) 0 motor deficits 3 (50%) 12 (50%) 2 dysphasia 3 (50%) 7 (29.17%) 1 146 iulia miculescu, daniela l. ivan, aurelia dabu et al. visual disturbance 0 2 (8.33%) 0 cognitive impairment 1 (16%) 5 (20.83%) 0 seizures 3 (50%) 14 (58.33%) 3 intracranial hypertension 1 (16%) 3 (12.5%) 0 surgical procedure biopsy only 1 (16%) 4 (16.67%) 1 resection 5 (84%) 20 (83.3%) 3 whocns5 grade 2 2 (33.3%) 11 (45.83%) 1 3 4 (66.6%) 13 (54.17%) 3 our patient cohort included retroand prospectively 45 patients with available mri images. the retrospective part of the cohort included 18 patients with mean age of 47 years and 11 patients (61%) were females. the majority of this group underwent biopsy followed by resection, as opposed to biopsy only (n=15, 83.33%). in the prospective part, we evaluated 27 patients with a suspected diffuse idh-mut astrocytoma. this included both tumor and non-tumor diagnoses, such as an atypical cerebral abscess. in this cohort, 18 patients were female (66.6%) and the mean age was 49.2 years. the most common surgical procedure was resection (83.3%). out of the 45 patients, the majority were diagnosed with who grade 2 or 3diffuse astrocytoma (n = 30), oligodendroglioma (n = 8) and glioblastoma (n = 6). other diagnoses included nonneoplastic lesions such as cerebral abscess (n=1). the mismatch sign was not present in the non-tumor diagnosis. in total there were 30 patients with idh-mut diffuse astrocytoma. these were separated based upon the presence of t2flair mismatch sign (n = 6) or absence (n = 24). in table 1 we elaborate on comparison between these groups in regards to clinical features, imaging variables (including mr spectroscopy) and clinical aspects. there were no differences regarding lobe involvement, presenting symptoms or surgical procedure employed. there was no difference between groups with respect to the extent of resection, with mismatch sign and without mismatch sign) [14]. in six patients (20%) from both groups the t2flair mismatch sign was identified and all of them had idh-mutated diffuse astrocytomas. we have not identified any patient with positive t2flair mismatch sign in the idh-wild type group (glioblastoma). from the retrospective and prospective groups, 7 cases had available mr spectroscopy images. from the total number of mr spectroscopy performed (n=7), 4 patients were diagnosed with idhmut diffuse astrocytoma, 1 patient was diagnosed with idh-mut 1p19q co-deleted glioma (oligodendroglioma), 1 patient was diagnosed with idh-wild type glioblastoma and 1 with cerebral abscess. in all of the cases of mr spectroscopy and idh-mut astrocyoma, a persistent high cho/ naa ratio, without any difference between the patients with or without the t2flair mismatch sign was present. discussion until recently, the grading of cns tumors has been focusing mainly on histology characteristics, but specific molecular markers can now be used for valuable prognostic information. for this reason, molecular specific information has been added as an essential feature in grading and it is considered very useful for further estimation of prognosis within variable tumor types. see tables 2-4 [10] table 2. world health organisation classification of tumors of the central nervous system, fifth edition (who cns5) [10]. 2021 who classification of tumors of the central nervous system gliomas • adult-type diffuse gliomas; • astrocytoma, idh-mutant; • oligodendroglioma, idh-mutant, and 1p/19qcodeleted; • glioblastoma, idh-wildtype. in this relatively small study we found no difference between diffuse idh-mut astrocytomas with or without the mismatch sign with regards to extent of resection or any other clinical variable. we reconfirmed that the t2flair mismatch sign has a good specificity for diffuse idh-mut astrocytomas. 147 the t2flair mismatch novel radiogenomic marker in the newly suspected low-grade gliomas figure 18 (left). cor flair images of 69m with final histology who grade 2 diffuse astrocytoma. figure 19 (right). mr spectroscopy images of 69m with final histology who grade 2 diffuse astrocytoma. as reiterated in many previous studies, it is well known that gliomas may vary in consistency and their macroscopic aspect, and with the radiological image of homogenous signal on t2-weighted sequences and infiltrative tumor border, the question was raised whether the extent of the resection is related to the mismatch sign. this may be of particular importance, since the idh-mut astrocytoma group seems to be the one where extensive surgery is of definite benefit [11, 12, 14]. table 3. key diagnostic genes, molecules, pathways, and/or combinations in major primary cns tumors (who cns5) [10] tumor type genes/molecular profiles characteristically altered astrocytoma, idh-mutant idh1, idh2, atrx, tp53, cdkn2a/b oligodendroglioma, idhmutant, and 1p/19q codeleted idh1, idh2, 1p/19q, tert promoter, cic, fubp1, notch1 glioblastoma, idh-wildtype idh-wildtype, tert promoter, chromosomes 7/10, egfr in our study, the extent of resection was not different between groups, therefore the t2flair mismatch sign should probably not be considered a factor influencing the extent of resection in diffuse idh-mut astrocytomas. patel et all. had evaluated the association between survival and the mismatch sign, with a median follow-up of 65.7 months, and found no differences in overall survival between groups [17]. table 4. cns who grades of selected types, covering entities for which there is a new approach to grading, an updated grade, or a newly recognised tumor that has an accepted grade (who cns5) [10] cns who grades of selected types astrocytoma, idh-mutant 2, 3, 4 oligodendroglioma, idhmutant, and 1p/19q codeleted 2, 3 glioblastoma, idh-wildtype 4 broen et al and patel et al have reported a 100% specificity for idh-mut astrocytomas [6, 17]. more recent studies have found overall specificity in the range of 96.0–100.0% [6, 17, 18]. the t2 flair mismatch sign has been found rarely in idh-mut codel gliomas (oligodendrogliomas), but also in pediatric low-grade brain tumors. until now, the mismatch sign has been reported in pilomyxoid astrocytoma, low grade glioma with myb rearrangement, oligodendroglioma (idhmut co-del) [11]. one previous study (correll et all.) has reported a patient with t2-flair mismatch sign had a diagnosis of idh-mut glioblastoma, suggesting that the mismatch sign is not grade specific [11]. importantly, there were no other differential diagnoses beyond diffuse gliomas that presented with the mismatch sign. although of low sensitivity (27.1–51.0%), the specificity for idh-mut astrocytomas makes the evaluation of mismatch sign useful in a clinical setting for individual cases [6, 11, 17, 18]. adding advanced imaging characteristic sequences like apparent diffusion coefficient (adc) and cerebral blood volume (cbv) to the mismatch sign may further improve the diagnostic capabilities of idhmut astrocytomas[11]. foltyn et all. (2022) have hypothesised that the higher adc value in idh-mutant gliomas with a t2/flair-mismatch sign (as compared to those without) translate into a measurable prognostic effect, although this requires investigation in future studies. the same study affirms that spatial differences in adc values between the core and rim of tumors with a t2/flair-mismatch sign potentially reflect specific distinctions in tumor cellularity and microenvironment [12]. conclusion in our relatively small retrospective and prospective cohorts, the t2-flair mismatch sign, where identified, was not correlated with clinical features at presentation, prognosis or outcome. we could not determine if the idh-mut astrocytomas with mismatch sign represent a specific subgroup. our study has confirmed that the t2-flair mismatch sign is a reliable and specific marker of idh-mut astrocytomas. mr spectroscopy, where available, has proven a very useful imaging investigation with a high value for management of these cns neoplastic tumors. 148 iulia miculescu, daniela l. ivan, aurelia dabu et al. fast progress in identification of more preoperative non-invasive tumor markers represents the way forward in the context of rapid evolution of the complexity and transformation of the whole concept of cancer treatment; advanced imaging characteristic sequences like apparent diffusion coefficient (adc), cerebral blood volume (cbv) and identification of the t2flair mismatch will improve the pre-operative diagnostic possibilities [11]. it is also of crucial importance that the new whocns5 grading system will be integrated into our standard clinical practice, with the main purpose being a more adaptable and reliable, also more practical diagnosis and management tool. references 1. tom mc, cahill dp, buckner jc, dietrich j, parsons mw, yu js. management for different glioma subtypes: are all low-grade gliomas created equal? am soc clin oncol educ book. 2019 jan;39:133-145. doi: 10.1200/edbk_238353. epub 2019 may 17. pmid: 31099638. 2. pallud j, mckhann gm. diffuse low-grade gliomarelated epilepsy. neurosurg clin n am. 2019 jan;30(1):43-54. doi: 10.1016/ j.nec.2018.09.001. epub 2018 nov 1. pmid: 30470404. 3. morshed ra, young js, hervey-jumper sl, berger ms. the management of low-grade gliomas in adults. j neurosurg sci. 2019 aug;63(4):450-457. doi: 10.23736/s03905616.19.04701-5. epub 2019 mar 27. pmid: 30916536. 4. dono a, ballester ly, primdahl d, esquenazi y, bhatia a. idh-mutant low-grade glioma: advances in molecular diagnosis, management, and future directions. curr oncol rep. 2021 jan 25;23(2):20. doi: 10.1007/s11912020-01006-6. pmid: 33492489. 5. slaghour rm, almarshedi ra, alzahrani am, albadr f. t2fluid-attenuated inversion recovery (flair) mismatch as a novel specific mri marker for adult low-grade glioma (lgg): a case report. cureus. 2022 sep 22;14(9):e29457. doi: 10.7759/cureus.29457. pmid: 36299937; pmcid: pmc9587756. 6. broen mpg, smits m, wijnenga mmj, dubbink hj, anten mhme, schijns oemg, beckervordersandforth j, postma aa, van den bent mj. the t2-flair mismatch sign as an imaging marker for non-enhancing idh-mutant, 1p/19qintact lower-grade glioma: a validation study. neuro oncol. 2018 sep 3;20(10):1393-1399. doi: 10.1093/neuonc/noy048. pmid: 29590424; pmcid: pmc6120363. 7. han z, chen q, zhang l, mo x, you j, chen l, fang j, wang f, jin z, zhang s, zhang b. radiogenomic association between the t2-flair mismatch sign and idh mutation status in adult patients with lower-grade gliomas: an updated systematic review and meta-analysis. eur radiol. 2022 aug;32(8):5339-5352. doi: 10.1007/s00330022-08607-8. epub 2022 feb 15. pmid: 35169897. 8. deguchi s, oishi t, mitsuya k, kakuda y, endo m, sugino t, hayashi n. clinicopathological analysis of t2-flair mismatch sign in lower-grade gliomas. sci rep. 2020 jun 22;10(1):10113. doi: 10.1038/s41598-020-67244-7. pmid: 32572107; pmcid: pmc7308392. 9. guo j, yao c, chen h, zhuang d, tang w, ren g, wang y, wu j, huang f, zhou l. the relationship between cho/naa and glioma metabolism: implementation for margin delineation of cerebral gliomas. acta neurochir (wien). 2012 aug;154(8):1361-70; discussion 1370. doi:10.1007/s00701-012-1418-x. epub 2012 jun 23. pmid: 22729482; pmcid: pmc3407558. 10. louis dn, perry a, wesseling p, brat dj, cree ia, figarellabranger d, hawkins c, ng hk, pfister sm, reifenberger g, soffietti r, von deimling a, ellison dw. the 2021 who classification of tumors of the central nervous system: a summary. neuro oncol. 2021 aug 2;23(8):1231-1251. doi: 10.1093/neuonc/noab106. pmid: 34185076; pmcid: pmc8328013. 11. corell a, ferreyra vega s, hoefling n, carstam l, smits a, olsson bontell t, björkman-burtscher im, carén h, jakola as. the clinical significance of the t2-flair mismatch sign in grade ii and iii gliomas: a population-based study. bmc cancer. 2020 may 20;20(1):450. doi: 10.1186/s12885-02006951-w. pmid: 32434559; pmcid: pmc7238512. 12. foltyn m, nieto taborda kn, neuberger u, brugnara g, reinhardt a, stichel d, heiland s, herold-mende c, unterberg a, debus j, von deimling a, wick w, bendszus m, kickingereder p. t2/flair-mismatch sign for noninvasive detection of idh-mutant 1p/19q noncodeleted gliomas: validity and pathophysiology. neurooncol adv. 2020 jan 10;2(1):vdaa004. doi: 10.1093/noajnl/vdaa004. pmid: 32642675; pmcid: pmc7212872. 13. yang x, lin y, xing z, she d, su y, cao d. predicting 1p/19q codeletion status using diffusion-, susceptibility-, perfusion-weighted, and conventional mri in idh-mutant lower-grade gliomas. acta radiol. 2021 dec;62(12):16571665. doi: 10.1177/0284185120973624. epub 2020 nov 22. pmid: 33222488. 14. capper d, jones dtw, sill m, hovestadt v, schrimpf d, sturm d, koelsche c, sahm f, chavez l, reuss de, et al. dna methylation-based classification of central nervous system tumors. nature. 2018;555(7697):469–74. 15. wiestler b, capper d, sill m, jones dt, hovestadt v, sturm d, koelsche c, bertoni a, schweizer l, korshunov a, et al. integrated dna methylation and copy-number profiling identify three clinically and biologically relevant groups of anaplastic glioma. acta neuropathol. 2014;128(4):561– 71. 16. christensen bc, smith aa, zheng s, koestler dc, houseman ea, marsit cj, wiemels jl, nelson hh, karagas mr, wrensch mr, et al. dna methylation, isocitrate dehydrogenase mutation, and survival in glioma. j natl cancer inst. 2011;103(2):143–53. 149 the t2flair mismatch novel radiogenomic marker in the newly suspected low-grade gliomas 17. patel sh, poisson lm, brat dj, zhou y, cooper l, snuderl m, thomas c, franceschi am, griffith b, flanders ae, et al. t2-flair mismatch, an imaging biomarker for idh and 1p/19q status in lower-grade gliomas: a tcga/tcia project. clin cancer res. 2017;23(20):6078–85. 18. lasocki a, gaillard f, gorelik a, gonzales m. mri features can predict 1p/19q status in intracranial gliomas. ajnr am j neuroradiol. 2018;39(4):687–92. doi: 10.33962/roneuro-2023-006 influence of clinical and neurophysiological parameters on the function outcome of the facial nerve after vestibular schwannoma surgery drazen radanovic, rosanda ilic, ivan bogdanovic, bojana zivkovic, srbislav pajic, magdalena nikolic, djurdjina bogosavljevic romanian neurosurgery (2023) xxxvii (1): pp. 46-53 doi: 10.33962/roneuro-2023-006 www.journals.lapub.co.uk/index.php/roneurosurgery influence of clinical and neurophysiological parameters on the function outcome of the facial nerve after vestibular schwannoma surgery dražen radanović1, rosanda ilić1, ivan bogdanović1, bojana živković1, srbislav pajić2, magdalena nikolić3, đurđina bogosavljević4 1 clinic of neurosurgery, university clinical centre of serbia, belgrade, serbia 2 department of neurotraumatology, university clinical centre of serbia, belgrade, serbia 3 general hospital pančevo, serbia 4 department of physical medicine and rehabilitation, university clinical center serbia, belgrade, serbia abstract introduction: vestibular schwannomas are benign neoplasms of the nerve seath, and they represent the third most common endocranial tumour, following the meningioma and the pituitary adenomas. the primary symptoms of vestibular schwannomas are hearing loss, tinnitus as well as a balance disorder. the therapy of vestibular schwannoma consists of observation, surgery and radiosurgery. the majority of patients who are good candidates for surgery are already affected by significant hearing impairment, thus one of the primary goals of the surgery is the preservation of facial nerve function. aim: to analyze the outcome of facial nerve function one-year post-surgery using clinical and neuropsychological parameters. material and methods: this study analyzed the patient's clinical status on admission along with the neuroradiological characteristics of tumours and the neurophysiological intraoperative parameters and their effect on the facial nerve function in the early postoperative period as well as one year after the surgery using the house–brackmann scale. results: a total of 30 patients who underwent surgery from january 1st 2015 to december 31st 2018 at the clinical centre of serbia, neurosurgery clinic for vestibular schwannomas were examined. the median age of the patients was 51 years. hearing loss was present in all patients. sensitivity drop in the innervation region of n. trigeminus was present in 7 (23.3%) patients, as was tinnitus. cerebellar symptomatology (76%) was present in the highest percentage of patients. conclusion: we can conclude that the most important aspects of the facial nerve function are the preoperative state of the facial nerve and the electrophysiological parameters. although the radical procedure of surgery led to an immediate postoperative outcome, it was not significant for the ultimate outcome of treatment. thus, radical surgery may be considered to carry the same risk of definitive impairment of the facial nerve function, just like a combination treatment with subtotal resection and stereotaxic radiosurgery. keywords facial nerve, nerve palsy, paralysis, vestibular schwannoma corresponding author: srbislav pajic university clinical centre of serbia, belgrade, serbia nevus-ng@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 47 facial nerve after vestibular schwannoma surgery introduction vestibular schwannomas, also called acoustic neuromas, are benign intracranial tumors arising from schwann cells of the vestibular portion of the eight cranial nerve. the cause of vestibular schwannomas is usually unknown; however there are evidences that sporadic defects in tumor suppressor genes, including familial and sporadic vestibular schwannomas, have been linked to a mutation in a single gene, the neurofibromin 2 (nf2). the gene is located on the long arm of chromosome 22, band q11-13.1 [1]. vestibular schwannomas represent 85% of intracranial growths arising at the cerebellopontine angle [2]. the size of the tumor is commonly classified via the koos grading scale with respect to extrameatal extension and brainstem compression (table 1) [3]. table 1. koos grading system for vestibular schwannoma koos grade description i intracanalicular ii extension into cerebellopontine angle, <2cm iii occupies cerebellopontine angle, no brainstem displacement, < 3cm iv brainstem displacement, > 3cm vestibular schwannomas represent a risk to varius intracranial structures due to mass effect. symptoms include progressive hearing loss and tinnitus which are reported in over 60% of patients. larger tumor manifestations can cause hydrocephalus and brainstem compression which are followed with symptoms such as facial paraesthesia, vertigo, and headache [4]. approximately around 8% of all intracranial tumors are vestibular schwannomas with an incidence of 10.4 per million per year [5]. in the population at a median age of 50 years, vestibular schwannomas are presented. they are predominantly unilateral in >90% of patients, with an equal incidence on the left and right. patients are more often presented with chronic asymmetric sensorineural hearing loss than tinnitus or unsteadiness. via audiometry and brain stemevoked response audiometry, sensorineural hearing loss can be confirmed in >90%-95% of patients with vestibular schwannomas [6]. from the pathological aspect of the tumor behavior, more than half of all vestibular schwannomas grow at an average of 24mm/year, whereas <10% regress [7]. one study has revealed that extrameatal tumors (28.9%) show a tendency to grow progressively compared with intrameatal tumors (17%), and a larger percentage of tumors grew early on after detection [8]. some studies have also revealed that vestibular schwannomas of >2cm are more likely to grow compared with a smaller size [9], [10]. decreased rates of hearing preservation have been associated with growth rates of>2mm/year, compared with slower growth rates [11]. surgical approaches surgical techniques which are used to approach the tumor are the translabyrinthine approach (tl), retrosigmoid approach (rs), or middle fossa (mf) craniotomy. at the clinical centre of serbia, neurosurgery clinic, the prefered surgical approach is the retrosigmoid approach (rs). the retrosigmoid approach is a posterior approach that which allows the neurosurgeon a panoramic view of the cerebellopontine angle (cpa). this approach also allows the neurosurgeon to have a better view on the facial and vestibulocochlear nerve; hence the facial nerve and hearing preservation has a higher rate. following a suboccipital craniotomy posterior to the sigmoid sinus, the cerebellum is then retracted medially, that allows the exposure of the cerebellopontine angle (cpa) mass and neurovascular structures. the facial nerve can be identified, and the cerebellopontine angle (cpa) component is dissected. with the use of the neurosurgical drill on the posterior meatal lip, the intrameatal component can then be accessed and removed. vestibular schwannoma infiltration of the cochlear nerve, poor preoperative hearing, and larger tumor size, decrease the likelihood of hearing preservation [12]. with the retrosigmoid approach (rs) the neurosurgeon can resect large extrameatal and small medial intrameatal tumors while allowing hearing preservation [13], [14], [15]. the retrosigmoid approach to intrameatal vestibular schwannomas can be limited by a highriding jugular bulb or obstructed by the labyrinth [15]. when the cerebellum is retracted the consequence can be a parenchymal injury. also included are early postoperative headaches which 48 drazen radanovic, rosanda ilic, ivan bogdanovic et al. are more often in the retrosigmoid approach (rs) than in the translabyrinthine approach (tl) [16]. electrophysiological monitoring electrophysiological monitoring is a standard procedure in modern neurosurgery of the vestibular schwannoma. the main goal of the intraoperative monitoring process is the preservation of the facial nerve. in cases with large tumors it is necessary to monitor the brain stem function that includes monitoring the long motor nerve pathways and other cranial nerves. beside the neuromonitoring, the electrophysiological methods can give us also the location of the cranial nerves, which by the presence of the vestibular schwannoma can be dislocated and deformed [17]. materials and methods a retrospective analysis of 30 patients with histologically confirmed vestibular schwannoma was performed. the cohort consisted of adult patinets operated on between january 2015. and december 2018. by a surgical team of neurosurgeons at the department of neuro-oncology of the clinical senter of serbia. this study analyzed the patients clinical status on admission along with the neuroradiological characteristics of tumors and the neurophysiological intraoperative parameters and their effect on the facial nerve function in the early postoperative period as well as one year after the surgery using the house–brackmann scale. this study also analyzed the intraoperative neurophysiological parameters and their influence on the facial nerve function in the early postoperative period, likewise one year after the surgery using the house-brackmann scale (hb scale) (table 2). patient demographics, clinical preoperative features, extent of resection, postoperative treatment modalities, date of progression, or reoperation, salvage chemotherapy, and date of latest follow-up or death were retrieved from an electronic database. table 2. house-brackmann scale grade description measurement function % estimated function% i normal 8/8 100 100 ii slight 7/8 76-99 80 iii moderate 5/8 – 6/8 51-75 60 iv moderately severe 3/8 – 4/8 26-50 40 v severe 1/8 – 2/8 1-25 20 vi total 0/8 0 0 statistical analysis from statistical methods, frequency estimation and relative numbers were used as methods of descriptive statistics. in the analysis of the results, depending on the nature of the variables themselves, the pearson-ov x2 was used in the form of stacking tests and contigency tables to compare the frequency difference in nonparametric features respectively. fisher0s exact probability test was applied twice to the numerical constraints of the table. in the statistical analysis, the p-value <0,005 was taken as a statistically significant. the data are presented in tables and graphs. data were prcoessed using the easy-r system (ezr, version 1.41. 64-bit). results our study consisted of 30 patients with histologically confirmed vestibular schwannoma from the period 01.01.2015. till 31.12.2018 at the department of neuro-oncology of the clinical senter of serbia, where 18 patients were female (60%), and 12 patients were male (40%) (figure 1). mean age was 51 years, the youngest patient was 30 years of age, and the oldest was 76 years old (figure 2). figure 1. gender distribution. the symptoms lasted 3,3±2,1 years at avreage, with maximum od 10 years, and minimum of 2 months. the loss of sensation in the trigeminal nerve region and tinitus was reported in 7 (23,3%) patients. most 49 facial nerve after vestibular schwannoma surgery of the patients had cerebelar simptomatology (76%). preoperative facial nerve palsy was reported in 23,3% patients (figure 3.). figure 2. distribution by age groups. figure 3. frequency of the preoperative facial nerve lesion. figure 4. patient distribution by tumour size. the largest number of patients 22 (73,4%) had tumors in size between 3 to 5cm, in 6 (20%) patients the tumor size was less then 3cm, and in 2 patients (6,6%) a giant tumor, whose dimensions are >5cm in size. the average tumor size was 38±9,4mm. the distribution of patients according to tumor size iz shown in figure 4. the tumor was localized with approximately the same frequency in the left and right internal auditory canal (meatus acusticus internus – mae) (56,7% on the left, and 43,3% on the right). hydrocephalus was noted in 16 patients (53,3%) and a vp shunt was placed in all patients before surgery. optic nerve papillary edema was present in 3 patients (10%). half of the patients, 15 (50%), underwent radical surgery when the mae was opend and part of the tumor was removed, while in the other half of the patients, a smaller part of the tumor was left in the porus of the mantle of the tumor towards the brainstem and the facial nerve. on this occasion, more than 90% of the tumors were removed. patients who had a residual tumor were treated with stereotactic radiosurgery. none of the patients progressed during the follow-up period. postoperative complications occured in 2 patients (6,7%) – hematoma located in the field which required surgical evacuation. also, in 2 patients (6,7%) there were general complications – pneumonia and systemic infection. no postoperative local infection, and csf infection, nor infection of the central nervous system was present. examination of electrophysiological parameters proved the connection of the baseline function of the facial nerve with a clinical presentation, and in 7 patients (23,3%) in whom preoperative facial nerve paresis was reported, neurophysiological damage to the nerve function was detectetd preoperatively. table 3. postoperative facial nerve function house brackman n (%) i 5 (16,7) ii 8 (26,7) iii 8 (26,7) iv 8 (26,7) v 1 (3,3) 7 23 present absent 6 22 2 <3cm 3-5 cm >5cm 50 drazen radanovic, rosanda ilic, ivan bogdanovic et al. the facial nerve was located in the region of the brainstem, and in the porus region, as well as in relation to the localization of the tumor via the direct nerve stimulation. in 3 patients (10%) there was a decrease in the facial nerve potential reported during tumor removal, but the potentials were not completly extinguished in any patient. posteperatively, in most patients there was a deterioration in facial nerve function (table 3.). postoperative physical therapy measures were implemented, and the house brackman scale (hb) was tested at subsequent controls. after a follow-up period of 2 years, the results of the recovery of the facial nerve function were recorded (table 4.). satisfactory results were achieved in 17 patients (56%), their facial nerve function can be considered perserved (hb gradus 1 and 2). in 4 (13%) patients the results were unsatisfactory, there still was severe impairment of the facial nerve function present (hb grade 4 and 5). table 4. facial nerve function 2 years after surgery. house brackman (%) i 12 (40) ii 5 (16) iii 9 (30) iv 3 (10) v 1 (4) in the further course, predictor factors – clinical, and electrophysiological parameters of postoperative facial nerve function were examined, immediately postoperatively, and 2 years after surgery. in relation to the immediate postoperative function of the facial nerve, (table 5) were examined, where no statistical sigificance was detected (p> 0,05). the degree of tumor resection (p=0,025) proved to be a statistically significant parameter, which indicates that in patients who underwent radical surgery, statistically significantly more patients had worse results on the hb scale. the existene of preoperative neurophysiological impairment of the facial nerve function also stood out as a predictor of poor outcome (p=0,015). in relation to the facial nerve function, 2 years after surgery, the factors (table 6) were examined, where the existence of statistical significance was not reported (p>0,05). preoperative facial nerve function (p=0,012) was singled out as a predictor of the facial nerve function after 2 years of surgery, with a worse outcome in patients who had preoperative loss of facial nerve function. preoperative neurophysiological impairment of the facial nerve function (p=0,022) as well as a decrease in potentials during surgery (p=0,018) were also singled out as negative predictors. table 5. presentation of predictor factors for immediate postoperative function of the facial nerve in which the existence of statistigal significance was not detected. examined predictive factor p-value years of age 0,072 gender 0,631 lesion of the trigeminal nerve 0,176 tinitus 0,173 cerebellar symptomatology 0,839 comorbidities 0,092 facial nerve function preoperative 0,247 tumor size 0,336 the side on which the tumor is located 0,855 hydrocephalus 0,360 intraoperative drop of nerve potential of the facial nerve 0,055 table 6. predictive factors for the facial nerve function 2 years after surgery in which the existence of statistical significance was not detected. examined predictive factor p-value years of age 0,620 gender 0,586 lesion of the trigeminal nerve 0,497 51 facial nerve after vestibular schwannoma surgery tinitus 0,497 cerebellar symptomatology 0,942 comorbidities 0,333 tumor size 0,736 the side on which the tumor is located 0,847 hydrocephalus 0,333 degree of tumor resection 0,547 discussion vestibular schwannomas, although they make up a third of all endocranial tumors, still represent an insufficiently researched topic. in most patients who are candidates for surgical treatment, there is already significant hearing impairment, so one of the main goals of surgery is to perserve the facial nerve function. the average age of patients with vestibular schwannoma is 50 years of age and it is unilateral in more than 90% of patients, with equal incidence of left and right side. in the cohort stury of i.taha et al., in 2020. [18], the function of the facial nerve and the function of the sense of hearing after microsurgical removal of sporadic vestibular schwannoma were analyzed. the average age of the patients was 54 years of age. the study consisted of 95 subjects, 37 males, 58 females, compared to our study which contains 30 subjects, 12 males, 18 females. after 1 year of surgery in a study by i. taha et al., 67% of patients had a good outcome (hb 1-2), no intraoperative facial nerve damage, no hydrocephalus, and a 30mm tumor. 16% of patients had a moderate outcome (hb 3-4), while 17% of patients had a poor outcome (hb 5-6). tumor size varied within groups (p<0,05). patients were divided into 3 groups based on the house-brackmann scale, where the third group had the largest tumor diameter 32±15mm, the second group 33±10mm, and the first group 24±12mm. based on the hb scale, the symptomatology was also divided into thre groups, where the most pronounced hydrocephalus (33,3%) was in the third group, as well as facial nerve paresis (20%) and headache (15,3%) in the first group together with dizziness (59,3%), impaired hearing (86,4%), tinnitus (32,2%), loss of trigeminal sensigility (25,4%), and cerebellar symptomatology (8,5%). [18] in the study lawani et al. [19] the data has shown that hb grade 1 or 2 facial nerve function was 100% for tumors ≤30mm but 79% for tumors larger than 30mm in 1 or more years after surgery. the predictive function was further studied by fenton et al. [20], and demonstrated that the long-term facial nerve function was strongly correlated with tumor size by a correlation factor of 0.47. in another study by samii m. et al. [21], a comparsion was made of facial nerve function between tumors larger than 4cm (giant) and tumors smaller than 3.9cm (2.6cm in average). the result indicated that patients with giant tumors were less likely to achieve facial nerve function of hb grade 1. no significant difference was found between two groups with grade 2 to 6. for large vestibular schwannoma resection, one of the primary goals is to maintain facial neve integrity, which is thought to be the key aspect of good facial nerve function [20]. in this study, the facial nerve functions of 98,1% patients were intact after tumor removal. acceptable facial nerve function was achieved in 37,8% of total cases 3–7 days after surgery and 78% remained good facial nerve function after 2 years. the adventage of intraoperative neruomonitoring (inom) is to lessen intraopeative facial nerve damage and to get a higher total resection rate. one inom parameter as prognostic factor for postoperative facial nerve function is a-train activity, which is a distinct emg waveform classified as a sinusoidal symmetric sequence of high-freqzency and low-amplitude signal during intraoperative emg monitoring [22]. the overall appearance of its pattern might vary in different cases. in a study prell et al [23], the time exceeding 10s was correlated with deterioration of post-surfical facial nerve function by two or more grades immediately after surgery. in this study, long train time predicted poor facial function. another key factor for the prediction of the facial nerve function is the facial motor evoked potential (fmep), which was documented to be correlated with postoperative facial nerve function [24, 25]. because of its adventage of less invasivity, fmep monitoring can be performed before and after operation do tedect nerve integrity without direct visualization and its thought to be a useful supplement for facial nerve monitoring [24]. in a study by fakuda et al. [20, 26] and acioly et al. [24], it has been found that a start 52 drazen radanovic, rosanda ilic, ivan bogdanovic et al. to-final baseline fmep amplitude ratio of 50% was a predictive threshold for a poor facial nerve outcome (hb grade 3–6) both in short and long-term followup. tringali et al. observed a good correlation between caloric weakness and tumour size when they tested the preoperative response of 629 tumour patients. in the group of patients with uw > 70%, who had a larger tumour size, postoperative facial palsy was more frequent. postoperative hearing preservation was more frequently observed in the “normal group” with a uw < 20%. they concluded that a normal caloric response can be a good predictive factor for hearing preservation and normal postoperative facial function [27]. in our study the tumor size were between 3 and 5cm in 22 patients ( 73,4%), <3cm in 6 patients (20%), and >5cm in 2 patients (6,6%). based on th hb slace, preoperative facial nerve lesion was reported in 7 patients (23,3%), hearing loss was present in all patients. sensitivity drop in the innervation region of n. trigeminus was present in 7 (23,3%) patients, as was tinnitus. cerebellar symptomatology (76%) was present in the highest percentage of patients. conclusion in the examined series of 30 patients who underwent surgery in the clinic for neurosurgery, the function of the facial nerve after vestibular schwannoma surgery was monitored. the degree of tumor resection as well as the existence of preoperative neurophysiological impairment of the facial nerve function stood out as significant predictors of function immediately after surgery. the preoperative neurophysiological impairment of the facial nerve function as well as nerve potential decrease during surgery were singled out as negative predictors. based on the results we can conclude that for the final outcome of the facial nerve function and the most important aspects for the facial nerve function are the preoperative state of the facial nerve and the electrophysiological parameters. although the radical procedure of surgery led to immediate postoperative outcome, it was not significant for the ultimate outcome of treatment. thus, radical surgery may be considered to carry the same risk of definitive impairment of the facial nerve function, just like a combination treatment with subtotal resection and stereotaxic radiosurgery. in interpreting these results, it should be borne in mind that this is a relatively small series of patients, and the study should be expanded to include a larger number of subjects. it is also clear that for the successful treatment of these patients it is necessary to diagnose the tumor early as possible, so there would be a significant improvement in outcomes. these outcomes are also in correlation with education of the physicians in primary care, as well as education of the general population, so that hearing loss can be understood as a significant symptom of the vestibular schwannoma. with a better education the diagnostic procedures could be carried out early on, and the result would be a more successful treatment. references 1. sughrue me, yeung ah, rutkowski mj, et al. molecular biology of familial and sporadic vestibular schwannomas: implications for novel therapeutics. j neurosurg 2011;114:359–66. 2. singh k, singh mp, thukral c, rao k, singh k, singh a. role of magnetic resonance imaging in evaluation of cerebellopontine angle schwannomas. indian j otolaryngol head neck surg. 2015;67(1):21–7. 3. koos wt, day jd, matula c, levy di. neurotopographic considerations in the microsurgical treatment of small acoustic neurinomas. j neurosurg. 1998;88(3):506–12 4. matthies c, samii m. management of 1000 vestibular schwannomas (acoustic neuromas): clinical presentation. neurosurgery. 1997;40(1):1–9. 5. evans dg, moran a, king a, saeed s, gurusinghe n, ramsden r. incidence of vestibular schwannoma and neurofibromatosis 2 in the north west of england over a 10-year period: higher incidence than previously thought. otol neurotol. 2005;26(1):93–7. 6. doyle kj. is there still a role for auditory brainstem response audiometry in the diagnosis of acoustic neuroma? arch otolaryngol head neck surg 1999;125:232. 7. smouha ee, yoo m, mohr k, et al. conservative management of acoustic neuroma: a meta–analysis and proposed treatment algorithm. laryngoscope 2005;115:450–54. 8. stagerupse, caye–thomasen p, tos m, et al. natural history of vestibular schwannoma. otol neurotol 2006;27:547–52. 9. nikolopopulos tp, fortnum h, o’donoghue g, et al. acoustic neuroma growth: systematic review of the evidence. otol neurotol 2010;31:478–85. 10. fucci mj, buchman ca, brackmann de, et al. acoustic tumor growth: implications for treatment choices. am j otol 1999;20:495–99. 11. sughrue me, yang i, aranda d, et al. the natural history 53 facial nerve after vestibular schwannoma surgery of untreated sporadic vestibular schwannomas: comprehensice review of hearing outcomes. j neurosurg 2010;112:163–67. 12. oghali js, driscoll cl. atlas of neurotologic and lateral skull base surgery, berlin: springer; 2016:19–103. 13. madjid s, cordula m. management of 1000 vestibular schwannomas (acustic neuromas): hearing function in 1000 tumor resections. neurosurgery 1997;40:248–62. 14. samii m, gerganov v, samil a. improved perservation of hearing and facial nerve function in vestibular schwannoma surgery via the retrosigmoid approach in a series of 200 patients. j neurosurg 2006;105:527–35. 15. blevins nh, jackler rk. exposure of the lateral extremity of the internal auditory canal through the retrosigmoid approach: a radioanatomic study. otolaryngol head neck surg 1994;111:81–90. 16. ruckenstein mj, harris jp, cueva ra, et al. pain subsequent to resection of acoustic neuromas via suboccipital and translabyrinthine approaches. am j otol 1996;17:620–24. 17. kircher ml, kartush jm. pitfalls in intraoperative nerve monitoring during vestibular schwannoma surgery. neurosurg focus 2012; 33-35. 18. taha i, hyvärinen a, ranta a, kämäräinen op, huttunen j, mervaala e, löppönen h, rauramaa t, ronkainen a, jääskeläinen je, immonen a, danner n. facial nerve function and hearing after microsurgical removal of sporadic vestibular schwannomas in a population-based cohort. acta neurochir (wien). 2020 jan;162(1):43-54. doi: 10.1007/s00701-019-04055-4. epub 2019 sep 7. pmid: 31494730; pmcid: pmc6942003. 19. lalwani ak, butt fy, jackler rk, pitts lh, yingling cd. facial nerve outcome after acoustic neuroma surgery: a study from the era of cranial nerve monitoring. otolaryngol head neck surg 1994;111:561–70. 20. fenton je, chin ry, shirazi a, fagan pa. prediction of postoperative facial nerve function in acoustic neuroma surgery. clin otolaryngol allied sci 1999;24:483–6. 21. samii m, gerganov vm, samii a. functional outcome after complete surgical removal of giant vestibular schwannomas. j neurosurg 2010;112:860–7. 22. neff ba, ting j, dickinson sl, welling db. facial nerve monitoring parameters as a predictor of postoperative facial nerve outcomes after vestibular schwannoma resection. otol neurotol 2005;26:728–32. 23. prell j, rampp s, romstock j, fahlbusch r, strauss c. train time as a quantitative electromyographic parameter for facial nerve function in patients undergoing surgery for vestibular schwannoma. j neurosurg 2007;106:826–32. 24. acioly ma, gharabaghi a, liebsch m, carvalho ch, aguiar ph, tatagiba m. quantitative parameters of facial motor evoked potential during vestibular schwannoma surgery predict postoperative facial nerve function. acta neurochir (wien) 2011;153:1169–79. 25. lin vy, houlden d, bethune a, nolan m, pirouzmand f, rowed d, et al. a novel method in predicting immediate postoperative facial nerve function post acoustic neuroma excision. otol neurotol 2006;27:1017–22. 26. fukuda m, oishi m, takao t, saitoa, fujii y. facial nerve motor-evoked potential monitoring during skull base surgery predicts facial nerve outcome. j neurol neurosurg psychiatry 2008;79:1066–70. 27. s. tringali, a. charpiot, m. ould, c. dubreuil, and c. ferberviart, “characteristics of 629 vestibular schwannomas according to preoperative caloric responses,” otology and neurotology, vol. 31, no. 3, pp. 467–472, 2010. doi: 10.33962/roneuro-2022-079 double curve linear incision approach in cases of sagittal craniosynostosis muhammet arif ozbek, naci emre aksehirli, alican tahta, nejat akalan romanian neurosurgery (2022) xxxvi (4): pp. 435-440 doi: 10.33962/roneuro-2022-079 www.journals.lapub.co.uk/index.php/roneurosurgery double curve linear incision approach in cases of sagittal craniosynostosis muhammet arif ozbek, naci emre aksehirli, alican tahta, nejat akalan department of neurosurgery, istanbul medipol university, istanbul, turkey abstract craniosynostosis is the premature fusion of one or more sutures in the cranial dome or anterior skull base, resulting in an abnormal head shape. this pathological process is observed less frequently in eastern geography and approximately one in 2000 to 2500 births in western countries. isolated sagittal synostosis accounts for more than half of craniosynostosis cases. in our study, the duration of surgery, duration of anaesthesia, duration of hospital stay, estimated amount of bleeding during surgery and the months of surgery were examined in 16 patients. the performed craniotomy is not different from the four different craniotomies described in the literature. strip craniectomy and barrel osteotomy were performed on each patient. according to the incisions described in the literature, the incision type and location are different. as the described incision provides less skin dissection, less bleeding and less dead space formation allows surgery in earlier months. introduction craniosynostosis is the premature fusion of one or more sutures at the cranial dome or anterior skull base, resulting in an abnormal head shape. reconstruction of craniofacial structure is typically required when physical or mental well-being becomes affected. this pathological process is observed less frequently in the eastern geography, at about 2000 to 2500 births in western countries (1). the first surgical treatment was reported with linear craniectomy to open fused sutures in the 1890s, and this method was used for a long time until the 1960s (2,3). craniofacial surgical techniques were described in the 1960s with the repositioning of the frontal bone to enlarge the cranial volume. since this revolutionary medical event, the surgical procedure for craniosynostosis has been developed in various ways based on various ideas through trial-and-error methods. a recent study found that 84% of the patients had isolated craniosynostosis, 7% had other clinical symptoms, and 9% had suspected syndromic craniosynostosis. this is consistent with a frequency of 0.4 to 1.0 per 1000 live births for nonsyndromic craniosynostosis. keywords sagittal, craniosynostosis, double curve linear incision corresponding author: muhammet arif özbek department of neurosurgery, istanbul medipol university, istanbul, turkey m_a_ozbek@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 436 muhammet arif ozbek, naci emre aksehirli, alican tahta, nejat akalan sagittal and unicoronal synostosis patients are predisposed differently based on their gender, with sagittal synostosis happening more frequently in males at a rate of 4:1 and unicoronal synostosis occurring more frequently in females at a rate of 3:2.2. (4) in a review of 519 subjects, the sagittal suture was affected in 56 percent, the coronal suture in 25 percent, the metopic suture in 4 percent, and the lambdoid suture in 2 percent of cases (5). although many families with craniosynostosis children present to the craniofacial surgeon with the goal of restoring normal head shape for purely cosmetic reasons. the fundamental reason for intervention is to avoid the consequences of intracranial hypertension (defined as more than 15 mm hg). although the exact prevalence of intracranial hypertension is unknown, it can cause neurodevelopmental delay. according to the most recent research, cerebral hypertension affects 15% of the population(6). however, the resulting neurodevelopmental delay is more difficult to predict and is likely multifaceted, with factors such as hydrocephalus, anatomical alterations in the brain, preterm, and family history all playing a role. some studies have shown indications of neurodevelopmental delay in patients with single suture craniosynostosis as high as 37%(7). another much debated question is the timing of surgical intervention. surgery is normally postponed for nonsyndromic children until they are at least 3 months old, which is considered to help the child to better adjust for the physiologic stress of bleeding. although the amount of blood lost after surgery is typically non-substantial, it accounts for a bigger proportion of the baby's growing total blood pool than in older patients. in addition to the effect of brain growth on head shape, proponents of an early surgery for open repair point to the advantages of avoiding further advancement of secondary craniofacial alterations and having more readily shaped bone stock. furthermore, children who get early care are more likely to spontaneously correct any lingering calvaria problems. late intervention supporters point to the greater rate of revision necessary in early intervention children. in practice, most surgeons intervene in between 3 and 12 months of age, and this decision is affected by technique and surgeon bias. in our clinic, we will talk about a method that will shorten the surgical time and reduce the complications and eliminate the deformity. patient and methods patients who underwent craniosynostosis surgery between 2016-2021 were retrospectively reviewed. between these dates, due to sagittal synostosis; 16 patients who underwent the front-to-back doublecurved method were identified in our clinic. the duration of their surgery, duration of anesthesia, amount of bleeding, length of hospital stay and preoperative weights of the patients were examined. patients who will undergo cranial synostosis surgery; it was expected to exceed six kilos in order to reduce the risks of anesthesia and surgery. it was decided to perform a surgical procedure with preoperative physical examination and 3d computed tomography. surgical procedure the same surgical technique was applied to all patients discussed in our study. in cases where the sagittal suture was closed, the patient was positioned in the prone position and the sagittal suture, coronal suture and lambdoid sutures were exposed using a front to back double-curved anterior to posterior incision starting from the front of the coronal suture and progressing until past the lambdoid suture at the back. (figure 1) figure 1. sagittal synostosis and cranium are seen after skin incision. two bilateral burr holes were opened 2 cm in front of the coronal suture, one cm lateral to the midline. two burr holes were opened at the rear, one cm 437 double curve incision of sagittal craniosynostosis lateral to the midline at the lambda level. craniectomy was performed along the 2 cm wide suture centered on the sagittal suture. the suture spacing was expanded by excising the lambdoid suture with a kerrison. barrel osteotomies were performed 2 cm apart on the parietal bone. (figure 2) a drain was placed under the skin and the operation was terminated. (figure 3) figure 2. strip craniectomy parietal and occipital barrel osteotomies. figure 3. postop skin incision. statistical analysis statistical analysis was performed using the turcosa (cloud-based statistical software) program using the student's t test, p-value of less than 0.05 (p <0.05). was considered statistically significant. table 1. demographic information of patients no age closed suture length of stay in hospital amount of bleeding (ml) preop hgb weight (kg) polideks (ml) surgery time (min) anaesthesi a time (min) 1 6 months sagittal posterior 3 20 12 6,1 100 75 145 2 5 months sagittal 2 35 12,3 5 80 100 160 3 5 months sagittal posterior 4 50 10,7 8 140 95 175 4 6 months sagittal 4 60 10,2 8 300 102 175 5 4 months sagittal 3 55 10,7 6,5 160 75 150 6 4 months sagittal 3 20 11 7 85 95 170 7 4 months 11 days sagittal 3 30 12,3 8 200 102 150 8 5 months 7 days sagittal 3 40 11,1 7 80 80 130 9 5 months 8 days sagittal 3 80 11,3 8,5 250 80 145 10 4 months 18 days sagittal 3 30 10,6 7 200 77 143 11 5 months 1 days sagittal 3 20 11,7 7 130 85 138 12 4 months 26 days sagittal 3 30 12,2 8 125 100 160 13 5 months 11 days sagittal 2 30 12,1 6 120 93 140 14 4 month 20 days sagittal 2 30 12,4 7,1 300 72 120 15 4 months sagittal 3 30 9 7 100 78 128 16 6 months sagittal, lambdoid 3 50 10,7 8 150 70 140 438 muhammet arif ozbek, naci emre aksehirli, alican tahta, nejat akalan table 2. statistical results are shown in the table n mean and standard seviation p duration of surgery group a our data 50 16 174.9±400 86.1±11.6 (min) <0,001 duration of surgery group b our data 22 16 136.1±30.4 86.1±11.6 (min) <0,001 amount of bleeding group a our data 50 16 113.3±100.3 38.1±16.7(ml) <0,001 amount of bleeding group b our data 22 16 168.1±50.6 38.1±16.7(ml) 0,004 volume of crystalloid in group b our data 22 16 329.4±70.8 157.5±73.1(ml) <0,001 results of the 16 patients who were operated in the examined date range, 3 were female patients and 13 were male patients. the mean age of the patients was 4.9±0.6 months (min 4 months, max 6 months), preop weight was 7.14±0.9 any developmental delay was observed in any of the patients. no examination finding suggestive of increased intracranial pressure was detected in any of the patients. the mean hospital stay of the patients was 2.94±0.5 days, the mean amount of bleeding was 38.1ml±16.7ml. mean surgery time is 86.1±11.6 mins, mean anesthesia time is 148±16.3 mins. (table 1) as the control group in the study of christopher m. runyan et al. named 'long-term outcomes of spring-assisted surgery for sagittal craniosynostosis'(8) defined as group a and paul j. escher et al.'s 'minimizing transfusion in sagittal craniosynostosis surgery: the children's hospital of minnesota protocol'(9) the craniotomy group in the study was defined as group b. when the means and standard deviation values in articles a and b were compared with the means and standart deviation in our study. (table 2) discussion the main finding in patients with craniosynostosis is premature closure of the cranial sutures; the malformations that occur in the anatomical regions it affects are proportional to the extent of closure of which sutures. malformations are usually prominent in the vertical direction of the affected joint. since the aim of surgery is to prevent head deformity by recreating the closed suture line, the application of surgical intervention in the first six months after birth, when head development is rapid, prevents the occurrence of secondary effects on head shape development. a smoother head shape result can be obtained in surgeries performed in the first six months. in infants, low weight and fragile hemodynamics cause many risks related to anesthesia as well as surgical difficulties. although surgeries for craniosynostosis have been performed since 1890, today the development of anesthesia and the development of surgical techniques allow for a decrease in morbidity, mortality and better surgical results. because of the myriad risks of allogeneic transfusions such as infection, hemolytic reactions, allergic reactions, and transfusion-induced acute lung injury (trali), strategies to reduce the need for transfusions in patients with craniosynostosis are a subject of ongoing research. preoperative epo use and iron replacement therapies have been described in the literature(10–12). although replacement therapy was not applied to our patients, none of the patients required blood transfusion therapy. the aim of the described surgical techniques is to correct the head deformity. the success of the surgery directly affects the success of the surgery. in surgery, it is necessary to perform the procedure to reveal the largest suture line of the cranium. although it is not related to the intracranial area, it should not be forgotten that the superior sagittal sinus is under the suture. since minimal bleeding in the surgical procedure enables early intervention, it indirectly affects the success of the surgery. from the 1960s to the 1990s, the evolution of operative intervention for sagittal craniosynostosis involved increasingly extensive cranial dome reshaping(13). these techniques included wide stripe craniectomy with bilateral parietal wedges, extended vertex craniectomy, and complete calvarial remodeling via the pi procedure(14–16). such operations were associated with long operative time, high blood loss, and prolonged hospital stays(13,17). in the early 1990s, surgical techniques reduced the morbidity of these operations. during this time, surgeons also began to explore the use of force therapy to counter the cranial vault's tendency to relapse after surgery and realized that surgical intervention provides a unique opportunity for cranial molding early in life.(13,18,19) a more minimally invasive approach, jimenez and barone 439 double curve incision of sagittal craniosynostosis 1990 showed that endoscopic strip craniectomy has low morbidity and that the cephalic index can be normalized when combined with postoperative helmet therapy.(18) basically, four different craniotomy have been defined; strip craniectomy alone, strip craniectomy with wedges, strip craniectomy with parietal barrel staves and midline osteotomy with separate burr holes for spring placement. the technique we use is strip craniectomy with parietal barrel staves. although the width of the osteotomy performed in the literature varies inversely with the age at which the surgical intervention was performed(20–22), we used the same width of craniectomy for each patient regardless of age. with the help of barrel osteotomies, it was observed that the head took its normal shape and expanded the craniectomy area. in our surgical procedure, in addition to strip craniectomy with parietal barrel staves, occipital barrel states were added to provide a wider area for remodeling. the most important difference from the literature is our double curved incision, which remains completely at the vertex. considering the area where the scalp is stripped from the calvarium and the area being worked on, the more unnecessary calvarium area in the classically applied bicoronal incision causes more bleeding and a longer operation time. it is not possible to create occipital barrel staves by reaching as far back as we reached with a bicoranal incision. in the study of runyan et al. (8) with 50 patients and in the study of 22 patients by paul j. escher's friends(9), the mean operative time was stated as 174 and 136 minutes, respectively. again, the mean amount of bleeding is indicated as 113 and 168 milliliters. in the study of paul j. escher with his friends, the average use of crystalloids during surgery was found to be 329 milliliters. in our technique, the amount of crystolloid used during surgery was found to be statistically less. in this case, it can be associated with direct bleeding and less volume loss. considering that the same craniotomy model was applied, where our only technical difference with these studies is the incision difference, we can say that our incision statistically reduces the operation time and the amount of bleeding compared to the bicoronal incision. as a result of our study, none of the patients needed intensive care and no complications were encountered, suggesting that our surgical method was successful. in one study(23), 26 pediatric neurosurgeons reported an average hospital stay of 1 to 4 days after surgery. in our patient group, the mean hospital stay was 2.9 days. our study has important limitations. this study is a retrospective study of a single center surgical team. the small sample size is the limitation of this study. for more reliable data, the study should be developed as a multicenter and control group. conclusion the purpose of the incision in sagittal craniosynostosis operations is to reveal the largest line of the cranium. in our study, one of the four different craniotomy methods defined basically was used. in the literature, strip craniectomy and parietal barrel osteotomies, which are generally performed with bicoronal incision, reduce surgical time and surgical damage with a new incision with a smaller and less dead space component. the earliest surgical intervention in surgical surgery had a positive effect on the success of the surgery in terms of results. the benefits of this technique will be more visible with the children of patient visits and follow-up periods. this incision is prominent in sagittal synostosis treatments. references 1. slater bj, lenton ka, kwan md, gupta dm, wan dc, longaker mt. cranial sutures: a brief review. plast reconstr surg. 2008 apr;121(4):170e–8e. 2. lannelongue: de la craniectomie dans la microcephalie google akademik [internet]. [cited 2022 oct 7]. available from: https://scholar.google.com/scholar_lookup?journal=co mpt+rend+seances+acad+sci&title=dela+craniectomie +dans+la+microcephalie&author=m+lannelongue&volu me=50&publication_year=1890&pages=1382-1385& 3. lane lc. pioneer craniectomy for relief of mental imbecility due to premature sutural closure and microcephalus. journal of the american medical association. 1892;18(2):49–50. 4. persing ja. moc-ps(sm) cme article: management considerations in the treatment of craniosynostosis. plast reconstr surg. 2008 apr;121(4 suppl):1–11. 5. shillito j, matson dd. craniosynostosis: a review of 519 surgical patients. pediatrics. 1968 apr;41(4):829–53. 6. thompson dn, harkness w, jones b, gonsalez s, andar u, hayward r. subdural intracranial pressure monitoring in craniosynostosis: its role in surgical management. childs nerv syst. 1995 may;11(5):269–75. 7. kapp-simon ka, speltz ml, cunningham ml, patel pk, 440 muhammet arif ozbek, naci emre aksehirli, alican tahta, nejat akalan tomita t. neurodevelopment of children with single suture craniosynostosis: a review. childs nerv syst. 2007 mar;23(3):269–81. 8. runyan cm, gabrick ks, park jg, massary d, hemal k, owens es, et al. long-term outcomes of spring-assisted surgery for sagittal craniosynostosis. plastic & reconstructive surgery. 2020 oct;146(4):833–41. 9. escher pj, tu a, kearney s, wheelwright m, petronio j, kebriaei m, et al. minimizing transfusion in sagittal craniosynostosis surgery: the children’s hospital of minnesota protocol. childs nerv syst. 2019 aug;35(8):1357–62. 10. velardi f, di chirico a, di rocco c, fundarò c, genovese o, rendeli c, et al. “no allogeneic blood transfusion” protocol for the surgical correction of craniosynostoses. ii. clinical application. childs nerv syst. 1998 dec;14(12):732–9; discussion 740-741. 11. velardi f, di chirico a, di rocco c. blood salvage in craniosynostosis surgery. childs nerv syst. 1999 nov;15(11–12):695–710. 12. white n, bayliss s, moore d. systematic review of interventions for minimizing perioperative blood transfusion for surgery for craniosynostosis. j craniofac surg. 2015 jan;26(1):26–36. 13. mehta va, bettegowda c, jallo gi, ahn es. the evolution of surgical management for craniosynostosis. neurosurgical focus. 2010;29(6):e5. 14. jane ja, edgerton mt, futrell jw, et al. immediate... google akademik [internet]. [cited 2022 oct 8]. available from: https://scholar.google.com/scholar?hl=tr&as_sdt=0%2c5 &q=jane+ja%2c+edgerton+mt%2c+futrell+jw%2c+et+ al.+immediate+correction+of+sagittal+synostosis.+j+ne urosurg+1978%3b49%3a705%e2%80%93710&btng= 15. tessier p. relationship of craniostenoses to craniofacial dysostoses, and to faciostenoses: a study with therapeutic implications. plastic and reconstructive surgery. 1971;48(3):224–37. 16. marchac d, renier d, broumand s. timing of treatment for craniosynostosis and faciocraniosynostosis: a 20-year experience. british journal of plastic surgery. 1994;47(4):211–22. 17. ridgway eb, berry-candelario j, grondin rt, rogers gf, proctor mr. the management of sagittal synostosis using endoscopic suturectomy and postoperative helmet therapy. journal of neurosurgery: pediatrics. 2011;7(6):620–6. 18. jimenez df, barone cm. endoscopic craniectomy for early surgical correction of sagittal craniosynostosis. journal of neurosurgery. 1998;88(1):77–81. 19. lauritzen c, sugawara y, kocabalkan o, olsson r. spring mediated dynamic craniofacial reshaping: case report. scandinavian journal of plastic and reconstructive surgery and hand surgery. 1998;32(3):331–8. 20. dlouhy bj, nguyen dc, patel kb, hoben gm, skolnick gb, naidoo sd, et al. endoscope-assisted management of sagittal synostosis: wide vertex suturectomy and barrel stave osteotomies versus narrow vertex suturectomy. journal of neurosurgery: pediatrics. 2016;18(6):674–8. 21. gociman b, marengo j, ying j, kestle jr, siddiqi f. minimally invasive strip craniectomy for sagittal synostosis. journal of craniofacial surgery. 2012;23(3):825–8. 22. garland cb, camison l, dong sm, mai rs, losee je, goldstein ja. variability in minimally invasive surgery for sagittal craniosynostosis. journal of craniofacial surgery. 2018 jan;29(1):14–20. 23. lee bs, hwang ls, doumit gd, wooley j, papay fa, luciano mg, et al. management options of nonsyndromic sagittal craniosynostosis. journal of clinical neuroscience. 2017 may;39:28–34. doi: 10.33962/roneuro-2020-090 brain radionecrosis after radiation therapy for atypical meningioma. an unexpected treatment outcome. case report ebtesam abdulla, harleen luther, tejal shah, nisha chandran romanian neurosurgery (2020) xxxiv (4): pp. 528-532 doi: 10.33962/roneuro-2020-090 www.journals.lapub.co.uk/index.php/roneurosurgery brain radionecrosis after radiation therapy for atypical meningioma. an unexpected treatment outcome. case report ebtesam abdulla1, harleen luther2, tejal shah3, nisha chandran4 1 bsc, md neurosurgery resident, department of neurosurgery, salmaniya medical complex, manama, bahrain 2 m.s, m.ch, neurosurgery consultant, department of neurosurgery, salmaniya medical complex, bahrain 3 md, radiology consultant, department of radiology, salmaniya medical complex, manama, bahrain 4 md, histopathology specialist, department of anatomical pathology, salmaniya medical complex, manama, bahrain abstract introduction. atypical meningioma (am) is at high risk of local failure. the role of radiation therapy (xrt) as an adjuvant to surgical resection is incompletely defined. the most deleterious consequence of brain-directed xrt is radiation necrosis. brain radionecrosis (brn) after am has been rarely reported. the relevant literature is reviewed, highlighting its diagnostic challenges. case presentation. we report a 25-year-old male with a brn after adjuvant xrt for am, which has been misdiagnosed as a recurrent neoplastic lesion upon magnetic resonance spectroscopy (mrs) examination. surgery and histopathological description were made and yielded a definitive diagnosis of brn. the patient was treated by dexamethasone with concomitant hyperbaric oxygen therapy (hbo2). the patient showed a further progression of the disease. therefore, he was elected to receive bevacizumab. however, the patient finally died for refractory brain edema. conclusion. brn is a relatively rare instance after xrt for am. there is no single modality that can reliably distinguish brn from tumour recurrence. therefore, reaching an early prompt treatment decision is challenging. introduction meningiomas are extra-axial tumors that represent 30% of all primary brain tumors (1). the most common locations are along the cerebral falx and over the cerebral convexity, such in the case reported here (2). am falls under the world health organization (who) grade ii tumors, accounting for 20% of all meningiomas (1-3). the distinction of am is given to the meningeal tumor that exhibits high mitotic rate and brain invasion (1, 3). the median age for am patients at diagnosis is 56 years (3). am has a female predominance and a high predilection for recurrence (1-3). keywords atypical, meningioma, radiation necrosis, radiotherapy, resection, spectroscopy corresponding author: ebtesam abdulla department of neurosurgery, salmaniya medical complex, manama, bahrain dr.ebtesam@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 529 brain radionecrosis after radiation therapy for atypical meningioma currently, am's treatment guideline entails the combination of maximum safe surgical resection and xrt (1-3). despite the absence of solid evidence to support xrt for am, several studies have reported encouraging results (1, 2). xrt has been shown to improve am prognosis with a median 5-year progression-free survival of 54.2% ranging from 38% to 100% after xrt (1). nevertheless, xrt carries a risk of radiation necrosis (1, 4-16). herein, we report a case of brn after adjuvant xrt for am, which has been misdiagnosed as a recurrent neoplastic lesion upon the mrs examination. case presentation a 25-year-old male presented with a nine-month history of intermittent headache, described as 'generalized pressure' and dizziness. the symptoms had become more severe, and weakness on the left side extremities started to progress over the last week. the vital signs were stable, and the patient was fully conscious. neurological examination showed no abnormality aside from mild left hemiparesis (grade 4/5 medical research council). cranial computed tomography (ct) scan revealed an enhancing extra-axial mass in the right frontal region, which contained multiple foci of calcification. there was significant peritumoral edema. cranial magnetic resonance imaging (mri) showed an isointense mass, with an area of low-intensity corresponding to the calcification observed on the ct scan (fig. 1). magnetic resonance arteriogram and magnetic resonance venogram showed multiple feeding arteries mainly from the anterior cerebral arteries and, to a lesser extent, from the distal right middle cerebral arteries with multiple, prominent draining veins. based on the radiographic appearance, a diagnosis of right frontal convexity meningioma was made. the patient underwent a craniotomy with total resection of the mass. the postoperative cranial ct scan reported no residual tumor with a regression of brain edema (fig. 2). the histopathology was am (who grade ii) (fig. 3). this case discussed in the multidisciplinary tumor board. accordingly, the patient was referred for xrt for a total dose of 60-gy (30 fractions of 2-gy) over six weeks duration, all delivered with intensity-modulated technique. the patient reported new-onset of generalized seizures and worsening of left hemiparesis (grade 3/5 medical research council) three months after completion of xrt. an electroencephalogram revealed epileptic discharges over the right frontal derivations. cranial mri reported an iso-signal poorly defined lesion in t1 and t2 sequences compromising the right frontal lobe with extensive central necrosis and peri-lesional edema (fig. 4). additionally, a ring, cut green-paper enhancement, was seen involving the genu of the corpus callosum (fig. 4). a confirmatory mrs study was used. the metabolites studied were choline (cho), which appeared at 1.4ppm, n-acetyl aspartate (naa) at 0.65ppm, creatine (cr) at 0.6ppm, and lipid at 1.3ppm (fig. 5). using multi-voxel mrs, the cho/naa ratio > 2.15 and cho/lipid>1 were favoring a recurrent neoplastic lesion. nonetheless, surgery and histopathological description were made and yielded a definitive diagnosis of pure brn (fig. 6). the lesion was nonvascular and intra-axial involving the right frontal lobe parenchyma and deep, abutting the frontal horn of the lateral ventricle. the patient had improvement of neurologic function after surgical resection. however, the patient was readmitted due to breakthrough seizures and worsening of left hemiparesis. a high dose of dexamethasone was initiated with concomitant hbo2. the patient showed a further progression of the disease. thus, he was elected to receive four cycles of 5mg/kg bevacizumab intravenously every two weeks. however, the patient finally died for refractory brain edema. figure 1. preoperative, mri brain of the lesion showing isointense signal (white arrow) in the t2-weighted sequence. the tumor homogeneously enhanced with areas of central hypointensity (red arrow) in post-contrast, t1-weighted images. 530 ebtesam abdulla, harleen luther, tejal shah, nisha chandran figure 2. sections from atypical meningioma show syncytial pattern along with areas of necrosis,10x(a&b). brain invasion noted in h&; e stain and highlighted by gfap immunostain,10x(c&d). figure 3. a postoperative ct scan of the brain showing total excision of the tumor with regression of brain edema. figure 4. mri brain of the lesion showing an ill-defined, peripheral enhancing lesion (white arrow) with central necrosis in post-contrast, t1-weighted sequence. the genu of the corpus callosum was also enhanced (red arrow)—the lesion iso-intense (black arrow) in the t2-weighted sequence, surrounded by extensive, vasogenic edema. figure 5. magnetic resonant spectroscopy showed a high elevation of cho and depression of naa. figure 6. post rt resection specimen is entirely submitted, and sections show areas of necrosis, mixed inflammation,10x(a&b). 531 brain radionecrosis after radiation therapy for atypical meningioma infiltration by foamy histiocytes,20x(c) and vasculitis, 20x(d). no neoplastic pathology noted. discussion the incidence of brn ranged from 3.4% to 16.7% for am after xrt (1). it peaks at two years after xrt and pursues a regressive course in most cases (5, 6). it regresses 40% at six months and 76% at 18 months from the onset of brn's radiological changes (6). there is a myriad of reasons for this, including total radiation dose, dose per fraction, treatment duration, irradiated volume, and concurrent use of chemotherapy (4-6). wang tm et al. implicated a radiation injury susceptibility gene (cep128) as an underlying mechanism of brn, as it tightly interacts with multiple radiation-resistant genes (7) . the pathophysiology of brn is not well understood. however, two main theories suggested. the first theory postulates that irradiation damages endothelial cells by upregulating ceramide. thus, results in vascular insufficiency and infarction (4, 6, 8, 9). hypoxia caused by endothelial cell damage leads to the liberation of hypoxia-inducible factor 1α and vascular endothelial growth factor (vegf) (4, 6, 8, 9). vegfs induce new vessel formation, but these tend to be leaky capillaries, resulting in perilesional edema (6, 8, 9). the second theory postulates that necrosis arises due to direct injury of the brain parenchyma, especially glial cells. the glial injury causes demyelination and white matter necrosis (4, 6). the clinical features of brn vary depending upon the location and size, including features of increased intracranial pressure. the characteristic findings are seizures, hemiparesis, headache, vomiting, poor concentration, and altered level of consciousness (46, 10). the literature also reported neurocognitive impairment (hippocampus), especially in children, which includes poor academic performance, distorted self-image, and psychological distress (6, 11). mri of the brain will demonstrate some degree of contrast enhancement surrounded by edema (4-6, 9, 10). although, the patterns of enhancement described in the literature as swiss cheese, cut greenpaper or soup bubble, are believed to favor brn, these patterns posse a 88% negative predictive value (12). mrs is used to assess the metabolite composition of the lesion (6, 13, 14). on mrs, the peak of cho and the depression of naa and cr correlated with a neoplastic lesion than brn. anbarloui et al. demonstrated that cho/naa > 1.8 or cho/lipid ratio >1 had increased odds of being a pure neoplastic lesion rather than pure necrosis, with sensitivity and specificity of 73% and 75%, respectively, for cho/naa ratio, and 87% for cho/lipid ratio (13). our patient's mrs failed to differentiate brn from tumor recurrence. the study revealed a neoplastic lesion, and the histopathology was purely brn. why there was such a non-concordant finding, it is not clear. hellstrom j et al. found 51/208 cases of clinically indicated mrs to have false-positive mrs findings (14). as demonstrated by this study, mrs findings are not accurate when compared to the histopathology findings. positron emission tomography (pet) scan uses 18f-fluorodeoxyglucose (fdg) to assess the tissue activity (4, 6, 10). necrotic tissue will demonstrate low fdg uptake (4, 6, 10). however, a pet scan may not distinguish brn when epileptic activity coexists. sasaki m et al. reported the case of 37 years old female with ependymoma treated by surgery and xrt, complicated later by brn, presented with seizures, and the pet scan was showing abnormally high fdg uptake (10). as the viable tumor has an intact vasculature, perfusion mri can predict tumor recurrence (4, 6, 12, 14). sugahara et al. suggested that a relative cerebral blood volume (rcbv) >2.1 favors tumor recurrence, while an rcbv value <0.6 favors radiation necrosis (15). however, we could not be able to spare time for this advanced imaging method. we applied surgical intervention to relieve the mass effects and to obtain a histopathology specimen. brn responds well to conservative management if diagnosed early (4, 6, 9, 12). corticotherpay is the first option to treat these cases (6, 9, 12). other supportive treatments include antiplatelet, anticoagulant, and a high dose of vitamins (6, 9). hbot utilized to improve tissue oxygenation and neovascularization (4, 6). several studies found that bevacizumab, an anti-vegf monoclonal antibody is effective in treating radiation-induced brain edema (4, 6, 8, 9). however, the safety of bevacizumab warrants further validation as the only randomized control trial published by levin va et al. in 2011 involved a limited number of 14 patients (9). if the conservative management fails or significant mass effects exist, then surgical extirpation is mandatory 532 ebtesam abdulla, harleen luther, tejal shah, nisha chandran (4, 6, 9, 12). recently, laser interstitial thermal therapy (litt) has become a treatment option for lesions that are difficult to access or for patients who are not candidates for surgery (16). a review study by katherine g et al. documented a favorable clinical response after litt for brn (16). unfortunately, none of the mentioned treatment approaches utilized halted the progression of brn in this patient. conclusion this case highlights the fact that brn is a potential complication of xrt for am. there is no shadow of a doubt that a diagnosis of brn is a matter of high importance in all settings since misinterpretation can result in delays in treatment and thus noticeable morbidity and mortality. there is no single modality that can reliably distinguish brn from tumor recurrence. thus, multimodality approach is highly recommended. abbreviations am: atypical meningioma; xrt: radiation therapy; brn: brain radionecrosis; mrs: magnetic resonance spectrometry; hbo2: hyperbaric oxygen therapy; who: world health organization; ct: computed tomography; mri: magnetic resonance imaging; cho: choline; naa: n-acetyl aspartate; cr: creatine; vegf: vascular endothelial growth factor; pet: positron emission tomography; fdg: 18f-fluorodeoxyglucose; rcbv: relative cerebral blood volume; litt: laser interstitial thermal therapy. references 1. kaur g, sayegh et, larson a, bloch o, madden m, sun mz, et al. adjuvant radiotherapy for atypical and malignant meningiomas: a systematic review. neurooncology. 2014;16(5):628-36. pubmed 2. kumar n, kumar r, khosla d, salunke p, gupta s, radotra b. survival and failure patterns in atypical and anaplastic meningiomas: a single-center experience of surgery and postoperative radiotherapy. journal of cancer research and therapeutics. 2015;11(4):735-9. pubmed 3. alghamdi m, li h, olivotto i, easaw j, kelly j, nordal r, et al. atypical meningioma: referral patterns, treatment and adherence to guidelines. canadian journal of neurological sciences. 2017;44(3):283-7. pubmed 4. na a, haghigi n, drummond kj. cerebral radiation necrosis. asia‐pacific journal of clinical oncology. 2014;10(1):11-21. pubmed 5. schüttrumpf lh, niyazi m, nachbichler sb, manapov f, jansen n, siefert a, et al. prognostic factors for survival and radiation necrosis after stereotactic radiosurgery alone or in combination with whole brain radiation therapy for 1–3 cerebral metastases. radiation oncology. 2014;9(1):105. pubmed 6. ali fs, arevalo o, zorofchian s, patrizz a, riascos r, tandon n, et al. cerebral radiation necrosis: incidence, pathogenesis, diagnostic challenges, and future opportunities. current oncology reports. 2019;21(8):66. pubmed 7. wang t-m, shen g-p, chen m-y, zhang j-b, sun y, he j, et al. genome-wide association study of susceptibility loci for radiation-induced brain injury. jnci: journal of the national cancer institute. 2019;111(6):620-8. pubmed 8. zhuang h, shi s, yuan z, chang jy. bevacizumab treatment for radiation brain necrosis: mechanism, efficacy and issues. molecular cancer. 2019;18(1):21. pubmed 9. levin va, bidaut l, hou p, kumar aj, wefel js, bekele bn, et al. randomized double-blind placebo-controlled trial of bevacizumab therapy for radiation necrosis of the central nervous system. international journal of radiation oncology* biology* physics. 2011;79(5):148795. pubmed 10. sasadi m, ichiya y, kuwabara y, yoshida t, inoue t, morioka t, et al. hyperperfusion and hypermetabolism in brain radiation necrosis with epileptic activity. journal of nuclear medicine. 1996;37(7):1174-6. pubmed 11. lawrence yr, li xa, el naqa i, hahn ca, marks lb, merchant te, et al. radiation dose–volume effects in the brain. international journal of radiation oncology* biology* physics. 2010;76(3):s20-s7. pubmed 12. dequesada im, quisling rg, yachnis a, friedman wa. can standard magnetic resonance imaging reliably distinguish recurrent tumor from radiation necrosis after radiosurgery for brain metastases? a radiographic-pathological study. neurosurgery. 2008;63(5):898-904. google scholar 13. anbarloui mr, ghodsi sm, khoshnevisan a, khadivi m, abdollahzadeh s, aoude a, et al. accuracy of magnetic resonance spectroscopy in distinction between radiation necrosis and recurrence of brain tumors. iranian journal of neurology. 2015;14(1):29. pubmed 14. hellström j, zapata rr, libard s, wikström j, ortiz-nieto f, alafuzoff i, et al. the value of magnetic resonance spectroscopy as a supplement to mri of the brain in a clinical setting. plos one. 2018;13(11). pubmed 15. sugahara t, korogi y, tomiguchi s, shigematsu y, ikushima i, kira t, et al. posttherapeutic intraaxial brain tumor: the value of perfusion-sensitive contrastenhanced mr imaging for differentiating tumor recurrence from nonneoplastic contrast-enhancing tissue. american journal of neuroradiology. 2000;21(5):901-9. pubmed 16. holste kg, orringer da. laser interstitial thermal therapy. neuro-oncology advances. 2019. google scholar. doi: 10.33962/roneuro-2023-009 wandering intracranial bullet. a case report with review of the literature anand sharma, a. shukla, avinash sharma romanian neurosurgery (2023) xxxvii (1): pp. 64-66 doi: 10.33962/roneuro-2023-009 www.journals.lapub.co.uk/index.php/roneurosurgery wandering intracranial bullet. a case report with review of the literature anand sharma, a. shukla, avinash sharma gajra raja medical college, gwalior, madhya pradesh, india abstract multidirectional migration of bullets has been reported infrequently in the literature. the surgical retrieval of an intracranial migrating bullet is suggested because of its capacity to produce an additional neurological deficit. intraoperative image guidance using the c arm is indicated in all intracranial migrating metallic foreign bodies following gunshot injury. a rare case of migrating bullet fragment in its trajectory with the migration of metallic fragment in both cerebral hemispheres is reported, and relevant literature is reviewed. introduction a bullet generally travels in a straight line after entering the body and following the dissipation of its energy, either exits or lodges. the initial movement of the bullet fragment follows the physical principles and power of moving pieces; the subsequent migrating of the bullet fragment in the intracranial compartment depends upon gravity, pulsatile force, coughing, sneezing and movement of the patient’s head1. we report a case of a bullet injury in which the metallic fragment was moving freely from its initial site in the left parietal to the opposite side and then traversing back to the original position, probably in the initial trajectory created by the force of a bullet. the bullet fragment in the present case migrated along the path of least resistance created at the initial impact. this differs from the other reported case where the fragment moved according to gravity and dependent position. case report a 30-year-old male becomes unconscious after a gunshot injury to the head. glasgow's coma scale on admission was e2v2m5 with left-side hemiparesis. his pupils were equally reactive, and his vitals were stable. the entry wound was situated on the right parietal bone; the exit wound could not be found. cranial non-contrast computerised tomography (ncct) revealed a gunshot wound through the right parietal bone and underlying right parietal lobe, with underlying contusions, intraventricular bleed, and corpus callosum contusions. the single metallic foreign body was found over the left parietal lobe (figure 1). initially, the patient was managed conservatively with debridement and keywords migrating bullet, intracranial corresponding author: anand sharma gajra raja medical college, gwalior, madhya pradesh, india dranandsharma100123@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 65 wandering intracranial bullet primary closure of the cranial wound. repeat ncct head was done after two days to find the status of contusions, brain oedema, and location of metallic foreign body. repeat ncct head revealed resolving contusion. however, the single foreign metallic body was shifted to the right parietal lobe near the entry wound (figure 2), thereby confirming the migration of the bullet fragment in the trajectory. considering the bullet location and the entry wound, the patient was planned for bullet retrieval with wound debridement under image guidance. a fresh ct scan was done before shifting the patient to the operation theatre, and a repeat ncct revealed the remigration of the bullet towards the left parietal lobe (figure 3). right parietal craniotomy was done with wound debridement and primary closure of dura matter using the pericranial patch. intraoperatively bullet position was re-confirmed with the c-arm, and a leftside parietal craniotomy was done with the removal of the bullet. post-operative ct showed resolving intraparenchymal contusion and intraventricular haemorrhage with no foreign body (figure 4). a. b. c figure 1. day 1: initial ncct head showing a) metallic foreign body over left parietal lobe; b) bone widow with foreign body; c) entry wound over right parietal bone. figure 2. day 3: ncct head revealed entry wound over right parietal bone with metallic fragment over right parietal lobe, suggesting migration of bullet towards entry wound. a. b. figure 3. day 4: ncct head revealed remigration of bullet towards left parietal lobe. figure 4. postoperative ncct head revealed post-operative changes with no foreign body with resolving contusions. discussion the bullet migration in the intracranial cavity has been reported previously by several authors. the metallic fragments following gunshot injuries have been reported to migrate in different cranial compartments depending upon the brain's and cerebrospinal fluid's gravity and pulsatile forces. extensive migration of bullet fragments from the intracranial compartment to the spinal subarachnoid space has been reported in the literature 2,3. however, in the present case, the movement of the fragment across the cerebral hemisphere crossing the midline was noted in the direction of the initial trajectory, as pointed out in the first ct scan. the bullet initially impacted the right parietal region, 66 anand sharma, a. shukla, avinash sharma causing a fracture of the right parietal bone and lodging in the left parietal lobe involving injury to the ventricle system, causing an intraventricular bleed. the subsequent ct scan showed the bullet fragment shifted to the right parietal lobe at the original point of impact. at the time of surgery, the bullet fragment was again turned to the left parietal lobe following the same trajectory. this is very clear that the metallic foreign body was moving freely to and fro in the same course. the hemispheric migration of bullet has been earlier reported by umredkar et al. 4yadav yr. et al. have reported supratentorial to infratentorial migration of bullet5. according to rapp, at all. 4.2% of bullet fragments migrate6; other authors have found that less than 0.1% to 10% of bullets migrate inside the head. the mechanism of migration of intra cerebral bullet is influenced by the following factors: 1. cerebral softening, 2. the specific gravity of the bullet compared with brain tissue, 3. pulsatile force of the brain and the cerebral spinal fluid pulsatile waves, 4. the sink function of the cerebral ventricles. hence, it is not only the firearm injury but also any foreign body with a different density than the brain and cerebrospinal fluid that will migrate intracerebrally. (4,7) repeated bullet movement in the same injury tract is rare and makes our case unique. after reviewing the available english literature in detail, we have not found any similar issues. the least resistance can explain the movement of the bullet offered to the bullet fragment in the preformed trajectory. ct is the imaging procedure of choice for evaluating these injuries; however, the migrating fragments require intraoperative image guidance to know the position of the bullet fragment in the operating theatre. the retained bullet complications include infection, haematoma formation, seizures, and abscess formation. spontaneous bullet migration causing additional parenchymal damage because of migrating nature makes surgery difficult. surgical treatment of bullet injury is controversial and represents a dilemma for the neurosurgeon. where feasible, the missile and bone fragments must be removed, but without enhancing the preexisting neurological deficit. kumar at all. reported that removal of bullet should be done in the patients undergoing surgery for the vacation of haematoma if it is easily accessible and removal does not lead to further deterioration of neurological structures8. zofonte et al. reported two cases with neurological deterioration from spontaneous migration of bullet; postoperatively, the patient demonstrated significant functional recovery9; considering the potential of neurological deterioration due to migration of bullet in several compartments, including spinal subarachnoid, the surgery of retrieval of the bullet fragment is advisable, we have removed the bullet. however, few cases reports favour conservative treatment in which the bullet is lodged in safe areas without evidence of migration and additional neurological damage. conclusion spontaneous intratragectory migration of bullet represents a rare complication and makes treatment more challenging. the surgical retrieval of the intracranial migrating bullet is suggested because of its capacity to produce an additional neurological deficit. intraoperative image guidance using the c arm is suggested in all intracranial migrating metallic foreign bodies following gunshot injury. references 1. s gupta, rls senger (2000). wandering intraspinal bullet. british journal of neurosurgery 13(6):606-7. 2. arasil e, tascioglu ao. spontaneous migration of an intracranial bullet to the cervical spinal canal causing lhermitte's sign. j neurosurg 1982;56:158-9. 3. kerin ds, fox r, mehringer cm, grinell v, miller re, hieshima gb. spontaneous migration of bullet in the central nervous system. surg neurol 1983;20[4] :301-4. 4. umredkar aa, mohindra s. intracranial moving bullet syndrome. neurol india 2010;58:151-152. 5. yadav y r, pandey s, tiwari m, agrawal a, nelson a. supratentorial to infratentorial and antigravity migration of intracranial bullet. neurol india 2006;54:453-4. 6. rapp lg, arce ca, mckenzie r, darmody wr, guyot dr, et al. (1999) incidence of intracranial bullet fragment migration. neurol res 21: 475-480. 7. negrotto m, figueroa r, sotomayor k (2019) multidirectional spontaneous migration of intracranial bullet: a case report and literature review. neurosurg cases rev 2:019. 8. mahapatra ak, raj kumar, pallav garg, vijendra maurya, rabi narayan sahu (2008) spontaneous bullet migrationuncommon sequelae of firearm injury to the brain. ijnt 5: 119-121. 9. mann nr, watanabe t, zafonte rd (1998) moving bullet syndrome: a complication of penetrating head injury. arch phys med rehabil 79: 1469-1472. doi: 10.33962/roneuro-2022-039 post ventriculoperitoneal shunting s. maltophilia meningitis. an uncommon case amol mittal, pankaj kumar, sharad pandey, l.n. gupta romanian neurosurgery (2022) xxxvi (2): pp. 220-223 doi: 10.33962/roneuro-2022-039 www.journals.lapub.co.uk/index.php/roneurosurgery post ventriculoperitoneal shunting s. maltophilia meningitis. an uncommon case amol mittal, pankaj kumar, sharad pandey, l.n. gupta department of neurosurgery, a.b.v.i.m.s. and dr ram manohar lohia hospital, new delhi, india abstract background: leptomeningeal inflammation caused by s. maltophilia is rare. it is inextricably linked with prior antimicrobial therapy; prolonged icu stays and antecedent neurosurgical intervention. case description: we describe a case of a 5-year-old male child with posterior fossa medulloblastoma with obstructive hydrocephalus who underwent ventriculoperitoneal shunt followed by suboccipital midline craniotomy and later presented with s. maltophilia meningitis. conclusion: the overall mortality in the cases reviewed was 17 per cent. inherent resistance to a wide array of antimicrobial agents with a simultaneously increasing number of cases poses a therapeutic challenge. trimethoprim/sulfamethoxazole is recommended as empirical and as a definitive treatment in patients with s. maltophilia infection. the optimal duration of therapy for s. maltophilia meningitis is similar to the treatment of gram-negative bacillary meningitis, which is usually 2 weeks after the culture has been negative. introduction after p. aeruginosa. baumannii,s. maltophilia is the third most common isolated non-fermenting aerobic gram-negative bacilli.[1]s. maltophilia rarely causes meningitis.[2]it is particularly common among critically ill / immunosuppressed patients and is inextricably linked with prior antimicrobial therapy, prolonged icu stays, prematurity, intracranial hemorrhages, malignancies, and antecedent neurosurgical intervention. it has recently come into the limelight in the last two decades owing to its increased pathogenicity and also because of marked antibiotic resistance.[3]we describe a case of a 5-year-old male child with posterior fossa medulloblastoma with obstructive hydrocephalus who underwent ventriculoperitonealshunt followed by suboccipital midline craniotomy and later presented with s. maltophilia meningitis. case report a 5-year-old male came to a&e with complaints of headache and vomiting (3-4) episodes since the last five days. there was no history of keywords s. maltophilia meningitis, nosocomial meningitis, neurosurgery corresponding author: sharad pandey department of neurosurgery, a.b.v.i.m.s. and dr ram manohar lohia hospital, new delhi, india drsharad23@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 221 post ventriculoperitoneal shunting s. maltophilia meningitis fever, loss of consciousness, seizures, visual impairment, hearing loss, motor or sensory deficit. on presentation, neurological examination revealed glasgow coma scale of e4v5m6, the pupil were equal and reactive, cranial nerve ix & x were involved (uvula was in the midline but gag reflex was impaired), and cerebellar signs (ataxia and dysdiadochokinesia) on the right side were positive. non-contrast ct scan head showed posterior fossa hyperdense lesion arising from the floor of the fourth ventricle causing upstream dilatation of third and bilateral lateral ventricle causing obstructive hydrocephalus. mri brain showed intra-ventricular solid cystic lesion arising from the floor of the fourth ventricle with no restriction on diffusion weighted sequence and elevated choline peak with reduced nacetyl aspartate suggestive of medulloblastoma.the patient underwent right ventriculoperitoneal shunt via right keen’s point under general anaesthesia in view of obstructive hydrocephalus, papilledema on direct fundoscopy (frisen’s grade ii), and clinical signs of raised intra-cranial pressure. csf analysis revealed no signs of meningitis and csf for malignant cytology revealed no malignant cells. the patient was discharged thereafter. four weeks later, the patient presented to the a&e with complaints of altered sensorium, increased drowsiness, and recurrent episodes of vomiting. the glasgow coma scale was e4v4m6, and pupils were equal and reactive. the shunt chamber was compressible and recoil was good. however, a repeat ct scan showed an increase in the tumour size with peri-lesional edema. the patient underwent suboccipital midline craniotomy with tumor excision under general anesthesia. postoperatively, the patient was shifted on mechanical ventilation. an extubation trial was given but was not successful. tracheostomy was done on post-operative day two in view of anticipated prolonged ventilator requirement, impaired gag reflex and pooling of chest secretions. the glasgow coma scale of the patient was e3vtm6. he developed fever 102.3°f and neck stiffness on post-operative day three. all routine investigations including blood, urine, tracheal, csf cultures, and pro-calcitonin were sent for this patient. the patient’s blood and urine cultures yielded no sign of bacteria. however, analysis of csf revealed sugar 2.1mmol/l, protein 0.23g/l, wbc count 0.53 x 109 cells /l (78% neutrophils, 10% lymphocytes, 10% mononuclear). pro-calcitonin was significantly positive for this patient (>10). csf gram staining showed gram-negative bacilli. antibiotics were upgraded to meropenem and vancomycin from ceftriaxone and amikacin. the patient fever and neck stiffness responded partially to the antibiotics. however, the child later experienced an episode of the seizure (generalized tonic-clonic), and he was shifted on a continuous mode of mechanical ventilation in view of a dip in the glasgow coma score (e2vtm5). clinical examination showed that the shunt chamber was non-compressible and recoil was absent. repeat ct scan revealed dilated ventricles with ventriculoperitoneal shunt in situ. the shunt was removed (in view of meningitis) followed by external ventricular drain insertion and the tip was sent for the culture. tip culture yielded s. maltophilia; which showed sensitivity to trimethoprim/sulfamethoxazole, ciprofloxacin, and amikacin. meropenem and vancomycin were discontinued. the minimum inhibitory concentration interpretive breakpoints of trimethoprim/ sulfamethoxazole were susceptible, ≤2/38 g/ml; and resistant, ≥4/76 g/ml for s. maltophilia. trimethoprim/sulfamethoxazole, 8-12 mg/kg/day administered intravenously every 6 hours was added to the antibiotic regimen. the patient’s fever abated 4 days later and her stiff neck resolved. the next sample analysis of csf from the drainage fourteen days after starting trimethoprim/sulfamethoxazole revealed the following profile: sugar 3.0 mmol/l, protein 0.1g/l, wbc count 0.1 x 109 cells /l (30% neutrophils, 55% lymphocytes, 15% mononuclear). repeat culture was consistent with s. maltophilia; ciprofloxacin (15 mg/kg q12hr) was added to the treatment regime. the external ventricular drain catheter was changed and after 7 days of the combination therapy, csf culture was sterile. antibiotics were continued for fourteen more days, which was followed by a right ventriculoperitoneal shunt insertion. however, the patient later developed bilateral basal pneumonia three weeks after recovering from meningitis, which led to acute respiratory failure. the patient could not be resuscitated and died thereafter. discussion leptomeningeal inflammation caused by s. maltophilia is rare. medline search was conducted with the phrase “s. maltophilia” which revealed 1660 222 amol mittal, pankaj kumar, sharad pandey et al. published articles. of these, only twenty-nine cases including the present case were linked with a prior neurosurgical procedure, whereas the rest accompanied community-acquired meningitis.[4] the incidence of neurosurgery-related meningitis is less, complicating less than 1% of craniotomies.[5] s. maltophilia being a multi-resistant organism, meningitis due to it is often insidious and protracted in course when compared to spontaneously occurring gram-negative meningitis.[6] fever was the most common presenting symptom in these cases. in patients with neurosurgery-related meningitis, the average csf cell count was 0.434 x 109 cells/l (range, 0.014 – 1.77 x 109 cells/l), glucose was 32.94 mg/dl (range, 4.9 – 77 mg/dl) and protein was 916 mg/dl (range, 76 – 3400 mg/dl). the average age was 49.85 years (range, 28 – 73 years) in adults, 4.29 months in infants (range, 2-6 months), and 4.5 years in children (range, 4-5 years). of all the 29 cases, six patients had an intracerebral haemorrhage, five patients had hydrocephalus (out of which two had congenital hydrocephalus), four were diagnosed with the intracranial-extra-axial lesion, four had intraventricular haemorrhage on the ct scan, three cases had extracranial lesion with brain metastasis, three patients had aneurysm as their initial diagnosis, and rest included recurring cholesteatoma, subdural hematoma, subarachnoid haemorrhage, and a posterior fossa tumor with hydrocephalus (current case). out of 29 cases associated with neurosurgeryrelated meningitis, nearly 50 per cent of them were due to ventriculoperitoneal shunt and prior craniotomy respectively. in the remaining, nearly one-third (28 per cent) cases occurred in patients who underwent prior craniectomy and had external ventricular drain in situ. the remaining included three cases that had ommaya reservoir in situ, two were linked with prior endoscopic third ventriculostomy, and one with stereotactic aspiration. our patient also had a similar risk factor profile as reported earlier, i.e. neurosurgical procedures (ventriculoperitoneal shunt and craniotomy), icu stays, exposure to broad-spectrum antimicrobial treatment (ceftriaxone, amikacin, meropenem, and vancomycin). the overall mortality rate in the cases reviewed was 17 per cent. although up to 50 per cent of cases of shunt infections can be treated by using antibiotics alone, many authors recommend removal of the prosthetic device followed by immediate or delayed insertion at a later stage.[7] clinical data are limited regarding optimal therapy for infections caused by s. maltophilia. nicodemo et al. suggested trimethoprim/sulfamethoxazole as the empirical choice for clinically suspected s. maltophilia infections and as the treatment of choice for culture-proven infections by this agent.[3] it has been found that s. maltophilia is generally resistant to quinolones, aminoglycosides, and thirdgeneration cephalosporins. inducible betalactamase activity (a zinc-containing penicillinase [l1] and a cephalosporinase [l2]), efflux mechanism, aminoglycoside-modifying enzyme activity, biofilm formation, and expression of an outer membrane protein (omp54) are responsible for its resistance to multiple antibiotics. contemporary literature shows that resistance to trimethoprim/sulfamethoxazoleis on the rise.[3] tigecycline has demonstrated good in vitro activity against s. maltophilia strains.[3] new fluoroquinolones such as clinafloxacin, levofloxacin, moxifloxacin have shown superior in vitro activity compared to earlier quinolones. gesu et al., in an in vitro study comparing levofloxacin and ciprofloxacin against s. maltophilia 124 strains, confirmed the susceptibility rates of 85.5 and 58.9%, respectively, to levofloxacin and ciprofloxacin.[8]although, ticarcillinclavulanic acid combination demonstrated susceptibility against s. maltophilia above 70%,[3] further in vitro studies showed incomplete growth suppression followed by regrowth, mandating the requirement of additional controlled studies to further establish the true potential of this combination in s.maltophilia infections.[9] as per zelenitsky et al., combination therapy with ceftazidime, gentamicin, tobramycin, and ciprofloxacin showed a significant bactericidal effect when compared with the trimethoprim/sulfamethoxazole monotherapy alone.[10] however, it is difficult to infer the treatment for s. maltophilia due to limitations in the number of strains tested, wide variety of antimicrobial combinations, and different method used in the invitro studies. although the synergistic action between drug combinations is evident, it is difficult to achieve the synergism in clinical drug concentrations.[3]the median duration of antibiotic therapy was 13 days (range 10–28 days). the optimal duration of therapy for s. maltophilia meningitis is 223 post ventriculoperitoneal shunting s. maltophilia meningitis not known but we believe it to be similar to the treatment of gram-negative bacillary meningitis, which is usually 2 weeks after culture have been negative.[11] conclusion s. maltophilia is an evolving gram-negative bacilli with an armamentarium of antimicrobial resistance. inherent resistance with a simultaneously increasing number of cases poses a therapeutic challenge.it is associated with prior neurosurgical procedures, long icu stays, and previous exposure to antibiotic treatment. empirical treatment should consist of vancomycin plus a third-generation cephalosporin (ceftazidime or cefepime) for 48-72 hours. clinicians should be alerted for s. maltophilia in whom empirical therapy fails or in those with the risk factors mentioned earlier. trimethoprim/ sulfamethoxazoleis the treatment of choice for culture-proven infections by this agent. further in vivo studies are necessary to better delineate the efficacy of individual antimicrobial agents, combination therapy, and to establish the therapeutic outcomes for s. maltophilia meningitis. references 1 chang yt, lin cy, chen yh, hsueh pr. update on infections caused by stenotrophomonas maltophilia with particular attention to resistance mechanisms and therapeutic options. front microbiol2015;6. 2. yemisen m, mete b, tunali y, yentur e, ozturk r. a meningitis case due to stenotrophomonas maltophilia and review of the literature. int j infect dis 2008;12. 3. nicodemo ac, paez jig. antimicrobial therapy for stenotrophomonas maltophilia infections. eur j clin microbiol infect dis2007;26:229–37. 4. khanum i, ilyas a, ali f. stenotrophomonas maltophilia meningitis a case series and review of the literature. cureus 2020;12:e11221. 5. mcclelland s, hall wa. postoperative central nervous system infection: incidence and associated factors in 2111 neurosurgical procedures. clin infect dis 2007;45:55–9. 6. papadakis ka, vartivarian se, vassilaki me, anaissie ej. stenotrophomonas maltophilia meningitis. j neurosurg 2009;87:106–8. 7. james he, walsh jw, wilson hd, connor jd, bean jr, tibbs pa. prospective randomized study of therapy in cerebrospinal fluid shunt infection. neurosurgery 1980;7:459–63. 8. gesu g pietro, marchetti f, piccoli l, cavallero a. levofloxacin and ciprofloxacin in vitro activities against 4,003 clinical bacterial isolates collected in 24 italian laboratories. antimicrob agents chemother 2003;47:816–9. 9. garrison mw, anderson de, campbell dm, carroll kc, malone cl, anderson jd, et al. stenotrophomonas maltophilia: emergence of multidrug-resistant strains during therapy and in an in vitro pharmacodynamic chamber model. antimicrob agents chemother 1996;40:2859–64. 10. zelenitsky sa, iacovides h, ariano re, harding gkm. antibiotic combinations significantly more active than monotherapy in an in vitro infection model of stenotrophomonas maltophilia. diagn microbiol infect dis 2005;51:39–43. 11. briggs s, ellis-pegler r, raymond n, thomas m, wilkinson l. gram-negative bacillary meningitis after cranial surgery of trauma in adults. scand j infect dis2004;36:165–73. doi: 10.33962/roneuro -2020-053 malfunction of a ventriculoperitoneal shunt during pregnancy. two clinical cases and literature review haidara a., diallo o., tokpa a., nda h.a., yao k.s. romanian neurosurgery (2020) xxxiv (1): pp. 347-352 doi: 10.33962/roneuro-2020-053 www.journals.lapub.co.uk/index.php/roneurosurgery malfunction of a ventriculoperitoneal shunt during pregnancy. two clinical cases and literature review haidara a.1, diallo o.2, tokpa a.1, nda h.a.3, yao k.s.1 1 department of neurosurgery, teaching hospital of bouaké, bouaké, cote d’ivoire 2 department of neurosurgery, hospital of mali 3 department of neurosurgery, teaching hospital of yopougon, abidjan, cote d’ivoire abstract bringing a pregnancy to term is possible for a woman carrying a ventriculoperitoneal bypass valve, however, pregnancy can be a source of malfunction of the bypass system. we report two cases of malfunction of a vps during the pregnancy's 3rd trimester in two patients aged 25 and 30 years respectively. the valve was examined in both cases and the persistence of the neurological signs required a cesarean section. the diagnostic aspects and management strategies were discussed as regards these two cases and throughout the literature review. introduction since the introduction of derivative csf techniques in the treatment of hydrocephalus, the prognosis for children with this pathology has considerably improved [2,12,15,24,26] bacterial meningitis is a common cause of morbidity in pediatric wards and constitutes the main aetiology of hydrocephalus occurrence [8.23]. with the development of neurosurgery in the past 20 years, many children are operated on from an early age and most often benefit from the establishment of a vps. today, many of these female children are of childbearing age. malfunction can occur in 50% to 70% of women in labour with vps, and doesn't necessarily mean anything in the development of future pregnancies. [18]. treatment may be difficult and requires multidisciplinary collabouration between neurosurgeons, obstetriciangynecologists-, and anaesthetists. clinical cases case 1 a 25-year-old pregnant woman, second gesture and primiparous, was admitted to the gyneco-obstetrics emergency department for seizures keywords malfunction, pregnancy, ventriculoperitoneal shunt corresponding author: tokpa andré teaching hospital of bouaké, bouaké, cote d’ivoire valentin_ tokpa@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 348 haidara a., diallo o., tokpa a., nda h.a., yao k.s. et al. and impaired alertness. there was a record in the case of a vps bypass performed at the age of 5 years for obstructive hydrocephalus. a previous pregnancy 5 years ago had been carried to term without incident. the physical examination revealed a glasgow score of 11 without focal neurological deficit. the diagnosis of a pregnancy toxemia in the 3rd trimester was brought up. however, blood pressure and pulse were normal, blood sugar and proteinuria dosages were also normal. the obstetric examination found a pregnancy of 32 weeks of amenorrhea (wa), a uterine height (uh) at 29 cm in relation to gestational age, and fetal heart sounds (fhs) being normal. the vps examination noted resistance to depression of the valve reservoir and the cranio-cerebral ct scan showed dilation of the ventricular cavities with a ventricular drain in place (figure 1). an evaluation of the vps has been carried out. removal of the peritoneal drain did not reveal any obstruction of the distal catheter, and it was reintroduced into the peritoneal cavity. the postoperative course was marked by a noteworthy improvement in the state of consciousness. the patient was kept under intensive care monitoring observation. a week later moderate signs of intracranial hypertension (icht) reappeared. a caesarean was performed at 34 wa. upon extraction of the newborn, the peritoneal drain was found in the vesico-uterine pouch. after verifying its permeability and extensive washing of the operating site, the drain was replaced in the peritoneal cavity. the post-operative course was satisfactory for the mother and for the child throughout a follow-up of 15 months. figure 1. head ct scan showing ventricular dilation. case 2 a 30-year-old pregnant woman, first gesture, consulted in neurosurgery for headache and visual disturbances having developed for a week during a pregnancy of 34 weeks. there was a record of vps for post-meningitis hydrocephalus at the age of 6 years. a valve revision was performed at the age of 16 following a vps malfunction and the patient had retained neurosensory sequelae with a significant decrease in visual acuity. upon examination, the blood pressure was normal. the obstetrical examination found an uh at 30cm in relation to the gestational age and the fetal heart sounds were normal. the cranioencephalic scanner had shown dilation of the ventricular cavities. given the worsening of neurological disorders with impaired alertness, a revision of the vps was carried out. the peritoneal drain has been repositioned on the other side of the midline. the clinical improvement had been brief and the outcome on day two was marked by the onset of seizures and a new impairment of consciousness. an emergency cesarean was performed with the extraction of a newborn with a good apgar score. the development was marked by an improvement in consciousness but with permanent blindness in the mother. discussion ventriculoperitoneal shunt remains the most widely used method for the treatment of hydrocephalus [18]. its complications, which are most often mechanical and/or infectious, have been widely reported in the literature [1,3,4,7]. in pregnant women with a vps, malfunction can occur in 50% to 70% of cases [2,18,20,26]. furthermore, it is established that vps has a higher incidence of fault during pregnancy than other types of leads [2,5,10,21,24,25,27]. it usually occurs during the pregnancy's 3rd trimester [2,5,18,26]. a summary of the cases reported in the literature is shown in table 1. the mechanism for the occurrence of vps malfunction remains still little understood [11]. the mechanism most often described would be the increase in intra-abdominal pressure due to the presence of the fetus, which would hinder resorption of csf in the peritoneum [5,11,12,13]. the regression of symptoms observed in most series after childbirth is an argument in favor of this mechanism. the second hypothesis would be the compression of the catheter by a large uterus or a neighboring viscera 349 malfunction of a ventriculoperitoneal shunt during pregnancy such as the stomach, bladder or liver [14.15]. in our 1st case, the peritoneal drain was wound in the vesico-uterine pouch. in our 2nd case, the malfunction is linked to a functional obstruction of the peritoneal catheter, probably related to the increase in intra-abdominal pressure. it has been noted by several authors that there is no correlation between the type of valve and the occurrence of the fault. [17, 20,21]. the classic clinical picture is the occurrence of signs of intracranial hypertension (icht) whose intensity is variable. these are usually isolated or associated with persistent headaches to vomiting or visual disturbances [11]. these signs can also be observed in pregnant women without vps malfunction noted. in the series of wishoff et al. [27], 59% of patients with vps had signs of intracranial hypertension. the onset of drowsiness, confusion syndrome, blindness, or altered consciousness is evidence of the severity of intracranial hypertension. the occurrence of inaugural convulsive seizures as in our first case, or intense headache, can mimic the image of pre-eclampsia in the third trimester of pregnancy and mislead the diagnosis of valve malfunction [2,10,15,24]. a malfunction can be suspected through the revision of the vps which sometimes displays resistance to the depression of the valve reservoir. however, the majority of current vps systems are no longer equipped with a flexible csf tank. the scanner and/or mri, in the event of a malfunction, assesses the dilation of the ventricular cavities associated or not with transependymal resorption and erasure of the cortical grooves with a well-positioned ventricular drain. there is however a risk of irradiation of the fetus by x-rays [6.18]. isotopic cisternography can diagnose the malfunction, but also risks fetal exposure to radioactive products [5, 6, 18,27]. mri is the examination of choice because it does not involve any risk of fetal irradiation, and makes it possible to assess the hydrodynamics of the lcs on the flow sequences [2,6,13,18,27]. the problem is the existence of a shunt which is not compatible with mri, and the deregulation of the drainage pressure by the magnetic field [9]. in our two cases, the scanner made it possible to diagnose the malfunction of the vps. the treatment of vps malfunction during pregnancy requires a multidisciplinary collabouration between obstetrician-gynecologist, anesthesiologist-resuscitator, and neurosurgeon. it must take into account gestational age, and especially the mother's neurological state. valve overhaul is sometimes not necessary. liakos et al [17], in their series, had respectively reported a rate of malfunction and valve revision of 13.7% and 5% among 138 pregnancies followed in 70 patients. when the neurological signs are moderate, a conservative treatment is proposed as a first intervention by several authors. [5,11,13,14,27]. the bed rest sometimes associated with a diuretic treatment such as furosemide or acetozolamide and the daily mechanical pumping of the valve reservoir when possible most often allow a regression of the symptoms of icht and allow to carry pregnancy to term. mechanical pumping can be associated with regular suction of the valve reservoir [5, 11, 12]. however, we believe that this method, even if it can be effective in managing icht, carries a high risk of infection. in our 1st case, the change of site of the peritoneal drain allowed us to attain an acceptable period for childbirth. hawg et al 2010, have advocated for the same approach. rees et al made the change to the complete system although obstruction of catheter was not proven. several authors argue for the conversion of vps to vas (ventriculoatrial shunt) in the event of malfunction [11,15,21,22,25]. the arguments proposed are the low rate of malfunction and neurological signs observed in the patients with a vas during pregnancy. sova et al [26] had proposed the externalisation of the peritoneal catheter until delivery, but this approach in our opinion increases the risk of infection. endoscopic ventriculocisternostomy can be performed in case of vps malfunction on obstructive hydrocephalus, and at the same time allows the complete removal of the defective bypass system [9.25]. the obstetric approach also depends on the neurological condition of the patient. in most of the series vaginal delivery is recommended [2,6,9,13,18]. on the other hand, in the event of significant neurological deterioration, a cesarean is necessary. in this case, the revision of the vps can be carried out simultaneously. 350 haidara a., diallo o., tokpa a., nda h.a., yao k.s. et al. table 1. summary of cases from the literature. authors matern al age (years) gestational age (wa) symptoms treatment type of birth anaesthesia outcome mother newborn freo et al [10} 35 36 coma shunt revision caesarean section general good good hwang et al [13] 32 headach e and drowsine ss shunt revision caesarean section general good good cuisimano et al [5] 21 30 headach e and vomiting pumping and suction caesarean section general good good houston et al [12] 26 33 headach e and nausea suction vaginal delivery no anaesthesia good good riffaud et all [25] 33 20 headach e, vomiting and visual disturban ce ventriculocisternosto my and valve removal vaginal delivery epidural anaesthesia good good 26 15 headach e and visual disturban ce ventriculocisternosto my and valve removal vaginal delivery epidural anaesthesia good unspe cified 27 8 headache ventriculocisternosto my and valve removal vaginal delivery epidural anaesthesia good good hanakita et al [11] 25 32 headach e, visual disturban ce and alertness disorder conversion of vps to vas vaginal delivery no anaesthesia good good fletcher et al. [9] 32 36 headach e, amnesia and urination shunt revision caesarean section general good good rees et al [24] 27 20 convulsio ns and alertness disorder change of ventriculop eritoneal bypass device abortion no anaesthesia good bad sova et al [26] 27 27 headach e, diplopia and parinaud external ventricular drain caesarean section general good good 351 malfunction of a ventriculoperitoneal shunt during pregnancy syndrom e murakami et al [21] 20 unspecifi ed headach e and visual disturban ce conversion of vps to vas vaginal delivery epidural anaesthesia good good kleinman et al. [14] 20 29 headach e and vomiting pumping vaginal delivery no anaesthesia good good kurtsoy et al. [15] 34 31 headach e, vomiting and balance disorder conversion of vps to vas unspecified unspecified good good conclusion the treatment of a bypass malfunction during pregnancy is sometimes difficult. it requires close collabouration between neurosurgeons, obstetrician -gynecologists, and anaesthetists. awareness of these different actors is necessary given the number of female children who have reached the reproductive age. the choice of ventriculocisternostomy in the treatment of hydrocephalus in children when it is indicated may allow avoiding the occurrence of this complication. it is also a treatment of choice when hydrocephalus or vps malfunction occurs during pregnancy. in all cases, carrying out a pre, peri and post conceptual survey of patients with vps is necessary. references 1. ahmed a, sandlas g, kothari p, sarda d, gupta a, karkera p, joshi p. outcome analysis of shunt surgery in hydrocephalus. j. indian. assoc. pediatr. surg. 2009, 14 (3): 98-101. 2. bradley nk, liakos am, mcallister jp, magram g, kinsman s, bradley mk. maternal shunt dependency: implications for obstetric care, neurosurgical management, and pregnancy outcomes and a review of selected literature. neurosurgery.1998, 43 (3): 448-60. 3. browd sr, ragel bt, gottfried on, kestle jr. failure of cerebrospinal fluid shunts: part i : obstruction and mechanical failure. pediatr. neurol. 2006, 34 (2),83-92. 4. browd sr, ragel bt, gottfried on, kestle jr. failure of cérébrospinal fluid shunts: part ii: over drainage, loculation, and abdominal complications. pediatr. neurol. 2006,34 (3):171-6. 5. cusimano md, meffe fm, gentili f, sermer m. ventriculoperitoneal shunt malfunction during pregnancy. neurosurgery. 1990,27(6):969-71. 6. cusimano md, meffe fm, gentili f, sermer m. 1991.management of pregnant woman with cerebrospinal fluid shunt. pediatr. neurosurg.1991,92 (17):10-3. 7. drake jm, kestle jr, milner r, cinalli g, boop f, piatt jjr, haines s, schiff sj, cochrane dd, steinbok p, macneil n.1998 randomized trial of cerebrospinal fluid shunt valve design in pediatric hydrocephalus. neurosurgery. 1998,43:294-303. 8. eholier sp, boni b, aoussi e, konan a, orega m, koffi a l, ba zézé v, bissagnene e, kadio a. complications neurochirurgicales des méningites purulentes en zone tropicale. neurochirurgie. 1999,45(3):219-24. 9. fletcher h, crandon iw, webster d. maternal hydrocephalus in pregnancy and delivery: a report of two cases. west. indian. med. j.2007,56(6):558-9. 10. freo u, pitton m, carron m, ori c. 2009.anesthesia for urgent sequential ventriculoperitoneal shunt revision and cesarean delivery. int. j. obstet. anesth. 2009,18(3): 284-7. 11. hanakita j, suzuki t, yamamoto y, kinuta y, nishihara kj. ventriculoperitoneal shunt malfunction during pregnancy. j neurosurg.1985, 63(3):459-60. 12. houston cs, clein lj. ventriculoperitoneal shunt malfunction in a pregnant patient with meningomyelocele. cmaj.1989,141(1):701-2. 13. hwang s.c, tae-hee k, bum-tae k, soo-bin i, won-han s. acute shunt malfunction after cesarean section delivery. j. korean. med. sci.2010,25(4):647-50. 14. kleinman g, sutherling w, martinez m, tabsh k. malfunction of ventriculoperitoneal shunts during pregnancy. obstet gynecol. 1983,61(6):753-4. 15. kurtsoy a, selçuklu a, kemal kr, pasaoglu a, kavuncu ai. management of maternal hydrocephalus. turkish neurosurgery.1994,4:174-5. 352 haidara a., diallo o., tokpa a., nda h.a., yao k.s. et al. 16. landwehr jb, jr, isada nb, pryde pg, johnson mp, evans mi, canady ai. maternal neurosurgical shunts and pregnancy outcome. obstet gynecol. 83(1):134-7. 17. liakos am, bradley nk, magram g, muszynski c. hydrocephalus and the reproductive health of women: the medical implications of maternal shunt dependency in 70 women and 138 pregnancies. neurol res .2000,22(1):69-88. 18. maheut-lourmière j, chu tan s. hydrocephalus during pregnancy with or without neurosurgical history in childhood. practical advice for management neurochirurgie.2000,46 (2):117-21. 19. monafared ah, kee sk, apuzzo mlj, collea jv. obstetric management of pregnant woman with extracranial shunts. can. med. assoc. j. 1979,120(5):562-3. 20. mouelhi c, srasra m, zhioua f, ferchiou m, zine s, meriah s. maternal hydrocephaly and pregnancy. rev. fr. gynecol. obstet. 89(2):88-90. 21. murakami m, morine m, iwasa t, takahashi y, miyamoto t, hon pk, nakagawa y. management of maternal hydrocephalus requires replacement of ventriculoperitoneal shunt with ventriculoatrial shunt: a case report. arch. gynecol.obstet. 2010,282 (3):339-42. 22. okagaki a, hanzaki h, moritake k, mori t.1990. case report: pregnant woman with a ventriculoperitoneal shunt to treat hydrocephalus. asia. oceania. j.obstet. gynaecol. 1990,16: 111-3. 23. orega m, eholier s p, boni n, konan a, koffi a l. méningites purulentes et complications neurochirurgicales chez l’enfant à abidjan. médecine d'afrique noire. 2005,52(4):251-2. 24. rees gj, francis c, sizer a r. convulsions in an undiagnosed pregnancy due to blocked ventriculoperitoneal shunt.j. obstet. gynaecol. 2008,26(5), 533-4. 25. riffaud l, ferre, jc, carsin-nicol b, morandi x. endoscopic third ventriculostomy for the treatment of obstructive hydrocephalus during pregnancy.obstet. gynecol. 2006,108:801-4. 26. sova m, smrcka, m, baudysova o, gogela j management of a shunt malfunction during pregnancy. bratisl lek listy. 2001,102(12):562-3. 27. wishoff jh, kratzert kj, handwerker sm, young bk, epstein f. pregnancy in patients with cerebrospinal fluid shunts: report of a series and review of the literature. neurosurgery. 1991,29(6):827-31. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-041 preoperative evaluation of superficial cortical venous drainage surjeet singh, stuti kumari, abhijeet sachan, shashi kant jain romanian neurosurgery (2020) xxxiv (1): pp. 280-287 doi: 10.33962/roneuro-2020-041 www.journals.lapub.co.uk/index.php/roneurosurgery preoperative evaluation of superficial cortical venous drainage* surjeet singh1, stuti kumari2, abhijeet sachan1, shashi kant jain1 1 sms medical college and hospital, jaipur, rajasthan, india 2 institute of medical sciences bhu varanasi, uttar pradesh, india full title: preoperative evaluation of superficial cortical venous drainage around the lesion and localization of tumour boundaries preoperatively by applying cod liver capsule over the scalp with the help of mri and mrv brain and comparison between 2-dimensional time-of-flight (2dtof) and 3-dimensional contrast-enhanced magnetic resonance venography (3dcemrv) brain in capsule marked cortical lesion and assessment of post-operative neurological outcomes. abstract objectives and methodology: the preoperative exact localization of superficial intracranial lesions and superficial cortical veins is often necessary for making craniotomy and evaluation of cortical veins. we developed a simple and cheap method for such localization using cod liver oil capsule during the preoperative mri and mrv brain examination. with the help of mrv brain, 3dcemrv and 2dtof images were taken and superficial cortical veins studied in the marked area for comparison between both modalities of mrv and planning of surgery for avoiding venous injury. results: most of the cases were in the age group 16-60 years (91.6%). the most common clinical manifestation was headache (85.4%) and meningioma (60.4%) was found to be the most common pathology. clear visualization (grade 3) of the individual superficial cortical vein was observed in 48 cases (100%) in 3dcemrv as compared to 2dtof 22 cases (45.8%) p <0.001s. clear visualization (grade3) of superior sagittal sinus was observed in 48 cases (100%) in 3dcemrv as compared to 2dtof 33 cases (68.6%) p <0.001s. in post-operative ct head, we found 4 (8.3%) cases were having venous infarction. 5 patients (10.4%) developed motor weakness postoperatively. in 3 cases, postoperative mrv were done and found no venous injury. conclusion: this study showed that preoperative localization and evaluation of the tumoral area and cortical veins with the help of cod liver oil in mri and mrv brain was very helpful in planning the surgery, making craniotomy and to avoid injury of the veins. this technique is easy to perform and the capsule is easily constructed and inexpensive. 3dcemrv was found to be better modality than 2dtof for delineation of veins. final neurosurgical outcomes were better. introduction imaging of intracranial cortical venous system anatomy is important in planning neurosurgical operations of midline masses such as colloid cyst, daca aneurysm, corpus callosal gliomas, parasagittal and keywords cod liver oil capsule, 2dtof, 3dcemrv, mr venography, midline lesions, sagittal sinus, superficial cortical vein corresponding author: sandeep bhardwaj dr. mbbs. ms. mch. neurosurgery department of neurosurgery, blk superspeciality hospital, new delhi, india. sandeep74699@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 281 preoperative evaluation of superficial cortical venous drainage parafalcine masses and other midline brain tumors. parafalcine masses may not be as closely related to the sss as parasagittal tumors, but because of their close relation, their growth may also contribute to anatomical changes to the nearby cortical veins. during parasagittal tumors resection, saving the cortical veins is important as it offers normal venous drainage of the brain, as well as important collateral drainage. disruption in venous outflow may result in venous infarction which leads to swelling, hemorrhage, neuronal death and may have catastrophic result [1,2]. mr venography is very helpful to know the anatomic changes in the cortical veins and its relation with respect to tumor position before surgery so that it can be saved intraoperatively. assessment of the patency of sagittal venous sinuses is very important to avoid major sinus injury, air embolism and catastrophic bleeding intraoperatively. moreover, cortical vessels especially the veins are important landmarks in craniotomy. with the help of 3dcemrv, it has become possible to see the intracranial venous structures noninvasively. mr imaging technique with mip method also presents more detailed information of brain surface structure by showing cortical veins [3,4]. the purpose of this study is to assess the usefulness of 3dcemrv for the evaluation of intracranial venous system in preoperative surgical planning of brain tumors. in this study, we have compared the visibility of the intracranial venous system on 3dcemrv with respect to those of 2dtofmrv in surgical planning and compared it with intraoperative findings and also evaluated neurological outcomes postoperatively. in few cases post-operative mrv were done to look for any venous injury. material and methods patient population from may 2017 to feb 2019, 48 patients were included which was admitted in department of neurosurgery sawai man singh medical college and hospital, jaipur. all patients underwent 3dcemrv, as well as 2dtofmrv in axial and sagittal planes. method all the patients with midline supratentorial masses were selected on mri brain images. after this cod liver oil capsules were placed on anterior and posterior ends of medial and lateral border of the tumour at scalp according to location of tumor on mri images and thus, the tumour boundaries were marked with the help of permanent marker. then mrv 2-dtof image were taken in axial and sagittal view. after that, 0.4ml/kg of gadolinium contrast agent was administered in cubital vein over 4 seconds and 3dcemrv images were taken in axial and sagittal plane. all mr examinations were performed with 3-tesla unit. all mr venographic source images were postprocessed with a maximum-intensity projection (mip) algorithm to create projection venograms for both the 2dtof mrv and the 3dcemrv. all images were saved in dicom software. the marked area concerned, superficial cortical veins such as frontopolar vein, anterior frontal vein, middle frontal vein, posterior frontal vein, precentral vein, central vein, post central vein, anterior parietal vein, posterior parietal vein and occipital vein and bridging veins joining the superior sagittal sinus were studied preoperatively. sagittal sinus compression were also evaluated, which was defined as a narrowing and filling defect of the lumen. on the basis of these informations and surgeons preference the surgical corridor was decided. intraoperative findings were compared with that of 3dcemrv images and intraoperative photographs of cortical veins were taken. in few cases post operative mrv were done to look for any venous injury. all patients neurological status were assessed. inclusion criteria conscious, co-operative and stable patients with supratentorial midline brain tumors. exclusion criteria unconscious, uncooperative and unstable stable allergic to gadolinium ferromagnetic cardiac pacemakers, aneurismal clip and defibrillators. claustrophobia image analysis degree of visualization and patency of the intracranial venous system, superficial as well as superior sagittal sinus on 3dcemrv was compared with those of 2dtof in capsule marked tumoral area. the image quality of 8 predefined venous structures was graded as follows: intense and continuous = 3, faint and continuous = 2, noncontinuous = 1, and invisible = 0. in post 282 surjeet singh, stuti kumari, abhijeet sachan, shashi kant jain operative period, in few cases mrv were done to look for any venous injury. ethical consideration the study protocol was approved by ethical committee. all patient gave written informed consent to participate after having received full written information about the study objective and conducts. investigations were done using aseptic precautions. they had right to withdraw from study. protection was given from any kind of harm. full confidentiality of data was maintained. no religious issues involved. all religious customs were respected. study was conducted under supervision. statistical analyses statistical analyses were done using computer software (spss trial version 23 and primer). the qualitative data were expressed in proportion and percentages and the quantitative data expressed as mean and standard deviations. the difference in proportion was analyzed by using chi square test. significance level for tests were determined as 95% (p< 0.05). result in our study, a total of 48 patients were included, in which 25 were males and 23 were females. all patients were conscious, oriented and glasgow coma scale was 15/15 at the time of admission. most of the cases were 16 -60 years (91.6%) of age, followed by elderly (>60 years) (4.4%) (table no.1). chi-square = 0.008 with 2 degrees of freedom; p = 0.996ns. no significant difference was observed according to age groups and gender. no significant difference was observed in age among the male and females (p=0.42ns). among 48 cases, 20 were parafalcine and 28 were parasagittal . majority of the cases were located in frontal lobe. most common clinical manifestation were found to be headache (85.4%) followed by seizure (14.5%) and limb weakness (12.5%). we found 2 patients with diminution of vision and 2 cases of bladder disturbances (table no.2). most common histological diagnosis was found to be meningioma (60.4%) followed by glioma(29.1%) and epidermoid cyst (6.25%) with 1 case of colloid cyst and 1 case of avm (table no.3). all lesions (100%) were circumscribed precisely through small craniotomy. number of veins visualized in capsule marked area were as follows : anterior frontal vein (12), middle frontal vein (20), posterior frontal vein (26), central vein (11), anterior parietal vein (7), posterior parietal vein (2), occipital vein (1) and superior sagittal sinus (48). the mean grading score of imaging of individual superficial cortical veins were superior in 3dcemrv as compared to 2dtof (table no. 4). poor depiction (grade 2, 1, 0) of superficial cortical vein was observed in 26 cases (54.16%) in 2dtof (n=48) as compared to 3dcemrv (n=48)0 (0%). whereas clear depiction (grade 3) of superficial cortical vein was observed in 48 cases (100%) in 3dcemrv (n=48) as compared to 2dtof (n=48) 22 case (45.8%) p<0.001s. (100%) showed in 3dcemrv. in addition to this, we also found extra other small cortical vein drain the superior sagittal group in 7(14.5%) cases in 3dcemrv as compared to 2dtof. poor depiction (grade 2, 1, 0) of superficial sagittal sinus was observed 15 (31.2%) in 2dtof (n=48) as compared to 3dcemrv(n=48)0 (0%).whereas clear depiction (grade 3) of superior sagittal sinus was observed 48 (100%) in 3dcemrv(n=48) as compared to 2dtof (n=48)33 (68.6%) p<0.001s (table no.5). 14 case (29.1%) showed sagittal sinus compression in both study groups. no new vein encountered during surgery. in post operative ct head, we found 4 (8.3%) cases of infarction, 1 (2.0%) post operative site hematoma, and 3 (6.2%) cases of pneumocephalus. no residual mass was present in any cases. in the present study 5 patients (10.4%) developed neurological manifestations post operatively in the form of newly developed motor weakness, 4 patients (8.3%) developed altered sensorium and 1 patient died in post operative period, no patient developed seizure. in 3 cases, post operative mrv were done and these were analysed with respective preoperative images and no venous injury were identified. age group (years) total no. of patient male female ≤ 18 2(4.1%) 1(2.0%) 1 (2.0%) 18-60 44(91.6%) 23(47.9%) 21(43.7%) 283 preoperative evaluation of superficial cortical venous drainage ≥ 60 2(4.1%) 1(2.0%) 1 (2.0%) total 48(100%) 25(52%) 23(47.91%) mean±s d 42.08±12.1 5 40.72±11.7 3 43.57±12.1 5 table 1. age and sex distribution. clinical symptoms no. of cases headache 41 (85.4%) motor deficit 6 (12.5%) seizure 7 (14.5%) diminution of vision 2 (4.1%) bladder disturbances 2 (4.1%) table 2. clinical manifestations of patients. histological diagnosis no. of cases meningioma 29 (60.4%) glioma 14 (29.1%) epidermoid cyst 3 (6.25%) colloid cyst 1 (2.0%) avm 1 (2.0%) total 48 (100%) table 3. distribution of patients based on histological diagnosis. superficial cortical veins total number veins visualisation in capsule marked area in all mean grading score (2dtof /3dcemrv) 2d tof /3dcemrv (superior) patients (n=48) anterior frontal vein 12 2.29/3.0 3dcemrv middle frontal vein 20 2.4/3.0 3dcemrv posterior frontal ein 26 2.3/3.0 3dcemrv central vein 11 2.36/3.0 3dcemrv anterior parietal vein 7 2.51/3.0 3dcemrv posterior parietal vein 2 2.8/3.0 3dcemrv occipital vein 1 3.0/3.0 none superior sagittal sinus 48 (2.6/3.0) 3dcemrv table 4. comparative study of image quality of individual superficial cortical veins in 2dtof and 3dcemrv according to mean grading score. veins poor image ( grade 2,1,0) 2dtof clear image (grade 3) 2d tof poor image ( grade 2,1,0) 3dcemrv clear image (grade 3) 284 surjeet singh, stuti kumari, abhijeet sachan, shashi kant jain 3dcemr v superfi cial cortical veins 26 (54.16%) 22 (45.8%) 0 (0%) 48 (100%) superi or sagittal sinus 15(31.2%) 33 (68.7%) 0(0.0%) 48(100 %) other small cortical vein seen none none 2(4.1%) 5(10.4% ) p value (2dtof /3dce mrv) <0.001s <0.001s <0.001s <0.001s table 5. comparison of the image quality of superficial cortical veins and superior sagittal sinus in 2dtof, 3dcemrv. post operative clinical status of patients no. of patients altered sensorium 4 (8.3%) newly developed motor deficit 5(10.4%) seizure 0(0%) death 1(2.0%) table 6. post-operative neurological manifestations. post-operative ct head no. of patient venous infarction 4 (8.3%) post operative site hematoma 1 (2.0%) residual mass 0(0.0) pneumocephalus 3(6.2%) table 7. post-operative ct head. figure 1. image showing preoperative tumour marking with help of cod liver oil capsule. figure 2. comparison of 2d tof and mr 3d ce mrv venography. thick white arrow denotes superficial cortical veins (anterior and middle frontal vein) and thin arrow denote capsule in the anterior and posterior border of tumoral area. (a: sagittal view; c: axial view) 2d tof mrv, (b: sagittal view; d: axial view) 3d ce mrv, showing clear visualization of anterior and middle frontal vein and entire superior sagittal sinus in 3dcemrv. (e) intraoperative photograph arrow showing 285 preoperative evaluation of superficial cortical venous drainage superficial cortical vein (anterior and middle frontal vein) in defined marked area. figure 3. comparison of preoperative and postoperative superficial cortical vein on mr venography. thin arrow denote capsule in the anterior and posterior border of tumoral area. (a: sagittal view; c: axial view) showing preoperative mrv and (b: sagittal view; d: axial view) showing postoperative mrv, suggests that no superficial cortical venous injury in defined tumoral and peritumoral area. (e); intraoperative photograph showing superficial cortical vein in defined marked area. discussion exact localization of superficial cortical venous system anatomy with respect to midline masses is very important in planning neurosurgical operations. on the basis of the cortical area that they drain, the superficial cortical veins are divided into four groups of bridging veins,:1. superior sagittal group, which drains into the sss; 2. sphenoidal group, which drains into the sphenoparietal and cavernous sinuses;3. tentorial group, which converges on the sinuses in the tentorium; and 4. falcine group, which empties into the inferior sagittal sinus or straight sinus[5]. surgery for midline masses such as colloid cyst, daca aneurysm, corpus callosal gliomas, parasagittal and parafalcine masses are synonymous with dissection of the veins surrounding the tumour, specifically the cortical parasagittal and bridging veins, superior sagittal sinus (sss) and collateral venous channels [6]. these information on intracranial venous system anatomy can be obtained by tof mrv and ce mrv which are noninvasive techniques. generally, mrv is performed without using contrast agent through 2d tof mr venographic techniques [7]. 2d tof mrv has been widely accepted for the imaging of intracranial venous system despite the well known technique associated pitfalls. a major pitfall of tof mrv is the artifactual intravascular signal loss that occurs at predictable points in the intracranial venous anatomy [8]. . images of higher spatial resolution are obtained in 3dce mrv with less scanning time than 2d tof mrv[9]. common flow related artifact seen on 2d tof mrv can be avoided with the use of 3d ce mrv as it is flow insensitive [10]. false-negative results can also occur in 3d ce mrv in patients with enhancing intracranial lesions, such as neoplasms adjacent to dural sinus or veins. [11]. however, various literatures have reported that administration of contrast agent help to highlight these vessels especially small veins and also improve the vascular visualisation [12,13,14,15]. in our study 54.16% and 45.8% cases were having poor (grade 2 ,1 ,0) and clear (grade 3) depiction of superficial cortical vein respectively on 2dtof whereas all cases (100%) showed clear (grade 3) depiction of studied vein in 3dcemrv. also, 68.7% and 100% cases showed clear depiction (grade 3) of superior sagittal sinus in 2dtof and 3dcemrv respectively. the mean grading score of imaging of individual superficial cortical veins were superior in 3dcemrv as compared to 2dtof . thus the results of present study indicate better efficacy of 3dcemrv over 2dtofmrv. study done by leach et al;[16] also showed gadolinium-enhanced mrv to be superior than tof mrv and also suggested the best evaluation using mri. in the present study, the area over the tumor was marked by putting cod liver oil capsules, overlying veins were identified on 2dtof mrv and 3dcemrv image after that the surgical corridor was decided. thus preoperative decision of surgical corridor allowed us to preserve the cortical veins maximally. in the study done by burtscher et al. [17] have shown that 3-d image technique revealed additional information compared with conventional 2-d images and had an influence on neurosurgical planning and strategy, improving neurosurgical performance and patient outcome. in the present study also, additional other small cortical vein were found in 3dcemrv in 7(14.5%) cases as compared to 2dtof. information about tumour and overlying superficial cortical veins and sagittal sinus in the marked area are obviating the need for the surgeon to mentally reconstruct the surgical anatomy from 2d image. thus, orientation would be faster and more comprehensible [18,19,20]. with this information, the surgeon can plan the best approach for surgery. in the study by khu et al; also concluded that 286 surjeet singh, stuti kumari, abhijeet sachan, shashi kant jain knowing the exact location of cortical vein with respect to tumor helps in preserving them during surgery. in our study, 2dtof and 3dcemrv images were taken and found that 2dtof images showed less depiction of superficial cortical veins in the marked area as compared to 3dcemrv, thus suggesting 3dcemrv as preferred modality for locating veins. abnormal radiological findings of intracranial venous structures were confirmed with intraoperative findings. in the study done by r.klingebiela et al.[22];observed that image quality was superior (4.3 ± 0.8; p < 0.001) for 3dcemrv as compared with 2d tof mrv (3.1 ± 0.7). in our study assessment of the evaluated sinus and veins was significantly improved by using 3dcemrv (p < 0.05) as compared with 2d tof mrv. superior depiction of the cerebral venous anatomy on maximum intensity projection images from 3dcemrv [22]. so 3dcemrv is more informative than 2dtof in delineation of superficial cortical and superior sagittal vein for surgical planning. and to avoid the venous injury while operating. all the patients were followed up and 5 (10.4%) patients developed neurological manifestations post operatively in the form of newly developed motor weakness, 4 (8.3%) patients developed altered sensorium and 1 patient died in post operative period. in post operative ct head, we found 4 (8.3%) cases of infarction ,1 (2.0%) post op site hematoma, and 3 (6.2%) cases of pneumocephalus. no residual mass was present in any cases. in 3 cases, post operative mrv were done and these were compared with respective preoperative images and no venous injury were identified. evaluation of preoperative and postoperative mrv can be useful in assessment of venous injury. our study had the following limitations: there was low statistical impact because of a small number of patients. furthermore, cerebral venous thrombosis could not be detected in any of the participants; thus, the drawing of conclusions from these data about the performance of ce mrv and mprage sequences in the detection of venous thrombosis remains difficult conclusions this study showed that preoperative localization and evaluation of tumoral area and cortical veins with the help of cod liver oil in mri and mrv brain was very helpful in planning the surgery, making craniotomy and to avoid injury of the veins. this technique is easy to perform and the capsule is easily constructed and inexpensive. 3dcemrv was found to be better modality than 2dtof for delineation of veins. final neurosurgical outcomes were better. abbreviations 3dcemrv: 3-dimensional contrast enhanced magnetic resonance venography; 2dtof: 2-dimensional time of flight; daca: distal anterior cerebral artery; mrv: magnetic resonance venography; ct: computed tomography; sss: superior sagittal sinus; mip: maximum-intensity projection; sd: standard deviationism: arteriovenous malformation. references 1. sekhar ln, chanda a, morita a (2002) the preservation and reconstruction of cerebral veins and sinuses. j clin neurosci 91(4):391–399. doi:10.1054/jocn.2001.1008 2. andrews bt, dujovny m, mirchandani hg, ausman ji (1989) microsurgical anatomy of the venous drainage into the superior sagittal sinus. neurosurgery 24:514– 520. 3. katada k, anno h, takeshita g. mr images of brain surface anatomy scanning (sas). jpn j magn reson med 1990;9:21525. 4. katada k. mr imaging of brain surface structures: surface anatomy scanning (sas). neuroradiology 1990;32:439 48. 5. oka k, rhoton al, barry m, rodriguez r (1985) microsurgical anatomy of the superficial veins of the cerebrum. neurosurgery 17 (5):711–748. doi:10.1097/00006123-198511000-00003 6. hancq s, baleriaux d, brotchi j (2003) surgical treatment of parasagittal meningiomas. semin neurosurg 14:203– 210.doi:10.1055/s-2004-828923 7. chakeres dw, schmalbrock p, brogan m, yuan c, cohen l. normal venous anatomy of the brain: demonstration with gadopentetate dimeglumine in enhanced threedimensional mr angiography. ajr am j roentgenol 1991;156:161 72. 8. farb ri, scott jn, montanera wj, wright ga, terbrugge kg. intracranial venous system: gadolinium-enhanced three-dimensional mr venography with auto-triggered elliptic centric-ordered sequenceinitial experience. radiology 2002;226:203 – 9 9. ayanzen rh, bird cr, keller pj, mccully fj, theobald mr, heiserman je. cerebral mr venography: normal anatomy and potential diagnostic pitfalls. ajnr am j neuroradiol 2000; 21: 74–78 10. farb ri, scott jn, montanera wj, wright ga, terbrugge kg. intracranial venous system: gadolinium-enhanced three-dimensional mr venography with auto-triggered 287 preoperative evaluation of superficial cortical venous drainage elliptic centric-ordered sequenceinitial experience. radiology 2002;226:203 9. 11. lewin s, masaryk tj, smith as, ruggrieri pm, ross js. time-offlight intracranial mr venography: evaluation of the sequential oblique section technique. ajnr am j neuroradiol 1990;15:1657 64. 12. chakeres dw, schmalbrock p, brogan m, yuan c, cohen l. normal venous anatomy of the brain: demonstration with gadopentetate dimeglumine in enhanced threedimensional mr angiography. ajr am j roentgenol 1991;156:161 72. 13. creasy jl, price rr, presbrey t, goins d, partain cl, kessler rm. gadolinium-enhanced mr angiography. radiology 1990;175:280 – 3 14. ikawa f, sumida m, uozumi t, kiya k, kurisu k, arita k, satoh h. demonstration of venous systems with gadolinium-enhanced threedimensional phase-contrast mr venography. neurosurg rev 1995;18:101 7. 15. stevenson j, knopp ea, litt aw. mp-rage subtraction venography. a new technique. j magn reson image 1995;5:239 41. 16. leach jl, strub wm, gaskill-shipley mf. cerebral venous thrombus signal intensity and susceptibility effects on gradient recalled-echo mr imaging. am j neuroradiol. 2007;28:940–5. 17. burtscher j, kremser c, seiwald m, obwegeser a, wagner m, aichner f et al (1998) three-dimensional computer assisted magnetic resonance imaging for neurosurgical planning in parasagittal and parafalcine central region tumors. comput aided surg 3(1):27–32 18. oka k, rhoton al, barry m, rodriguez r (1985) microsurgical anatomy of the superficial veins of the cerebrum. neurosurgery 17 (5):711–748. doi:10.1097/00006123-198511000-00003 19. rosahl sk, gharabaghi a, shahidi uh, samii m (2006) virtual reality augmentation in skull base surgery. skull base 16(2):59– 66. doi:10.1055/s-2006-931620 20. chua gg, serra l, kockro ra, hern n, nowinski wl, chan c (1998) volume-based tumor neurosurgery planning in the virtual workbench. virtual reality annual international symposium, 1998. proceedings ieee: 167– 173 21. kathleen joy khu & ivan ng & wai hoe ng; the relationship between parasagittal and falcine meningiomas and the superficial cortical veins: a virtual reality study; acta neurochir (2009) 151:1459–1464 doi 10.1007/s00701-009-0379. 22. r. klingebiela, h.c. bauknechta , g. bohnera , r. kirschb , j. bergera and f. masuhrc; comparative evaluation of 2d time-of-flight and 3d elliptic centric contrastenhanced mr venography in patients with presumptive cerebral venous and sinus thrombosis, 2007 efns european journal of neurology 14, 139–143. doi: 10.33962/roneuro-2021-075 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours. speech disorders orest i. palamar, andriy p. huk, dmytro s. teslenko, ruslan v. aksyonov, dmytro i. okonskyi, nazarii v. lazko romanian neurosurgery (2021) xxxv (4): pp. 444-451 doi: 10.33962/roneuro-2021-075 www.journals.lapub.co.uk/index.php/roneurosurgery postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours. speech disorders orest i. palamar1, andriy p. huk1, dmytro s. teslenko1, ruslan v. aksyonov1, dmytro i. okonskyi1, nazarii v. lazko2 1 si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine 2 municipal non-commercial enterprise “kyiv city clinical hospital no. 1”, kyiv, ukraine abstract neurosurgical approaches to lesions of the lateral and the third ventricles are divided into two fundamentally different groups: transcortical neurosurgical approaches, including endoscopic and interhemispheric transcallosal micro-neurosurgical approaches. complications in surgery of lateral and third ventricle tumours are often associated with the specific approach technique and could be transient. we analyzed postoperative neurological complications and the approach criteria on mri or ct scans in the postoperative period such as localization of corticotomy, distance from corticotomy to the coronal suture, “angle of attack” after the frontal transcortical approach to the lateral and third ventricle based on 54 cases and presume transient nature of specific to approach complications and approaches’ factors that have a role in postoperative mutism. introduction neurosurgical approaches to the tumors of the lateral and the third ventricles are divided into two fundamentally different groups: transcortical neurosurgical approaches, including endoscopic and interhemispheric transcallosal microneurosurgical approaches. two different approaches to the ventricular system cause distinct brain injuries: tightly compressed commissural fibers of the corpus callosum are injured by the interhemispheric transcallosal approach, while the transcortical approach damages gray and white matter of the brain on its way [1,2]. complications in surgery of lateral and third ventricle lesions are often associated with the specific approach technique and today is a widely discussed problem [3,4]. when applying the abovementioned approaches, the most common complications are aphasia, mutism, keywords endoscopic, lateral ventricle, mutism, third ventricle, transcortical approach corresponding author: nazarii v. lazko si “romodanov neurosurgery institute” nams of ukraine, kyiv, ukraine naztar02@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 445 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours hemiparesis, seizure, memory impairment, apatheia/abulia, endocrinopathy, subdural hygroma, etc. [1, 16]. manifestations of mutism, which are currently little studied in the context of the use of these neurosurgical approaches, constitute a field of particular scientific interest. mutism is a clinical state, in which a conscious patient is unwilling to or unable to speak, resulting in the absence or marked paucity of verbal output. the patients can be mute while their ability to write or comprehend spoken language is intact [1,11]. mutism can occur as a result of damage to the broca area, premotor cortex, and supplementary motor area of the dominant hemisphere, association fibers of white matter, the anterior part of the cingulate gyrus, commissural fibers of the corpus callosum, damage of the corticalbulbar fibers bilaterally, bilateral thalamotomy and damage of reticular formation of the midbrain [7,5]. materials and methods a retrospective analysis of 54 patients with neoplasms and lesions of lateral (anterior horn, body, atrium) and third ventricles who underwent surgery in the period from october 2015 to may 2021. male – 26 patients, the mean age was 44.5 years (range: 20-71 years), female – 28 patients, the mean age was 42.4 years. (range: 15-74 years). mean preoperative karnofsky performance statuse score (kps) was 76.37. localization of neoplasm: the third ventricle 41 (75.9 %) patients; lateral ventricular tumors 13 (24.1 %) patients. histological distribution depending on the location is given in table 1. figure 1. a-b. tumor in the posterior part of the third ventricle (glioblastoma), preoperative contrast-enhanced, t1w images. histopathological evaluation of these 54 neoplasms and lesions indicated 15 distinct diagnostic entities including brain tumors of glial origin with invasion in the ventricular system (diffuse and anaplastic astrocytoma, glioblastoma, oligodendroglioma, and anaplastic oligoastrocytomas) accounted for 35,2% (fig. 1), subependymoma and ependymomas varying degrees of malignancy – 14,8%, colloid cysts 13%, central neurocytomas 11.1%, craniopharyngiomas 11.1%, germinomas 7.4%, others 7.4% histopathology lateral ventricles (n-13) third ventricle (n-41) pilocytic astrocytoma, who gr i 1 diffuse astrocytoma, who gr ii 2 3 anaplastic astrocytoma, who gr iii 3 glioblastoma, who gr iv 1 5 oligodendroglioma, who gr ii 1 2 anaplastic oligoastrocytomas who gr iii 1 subependymoma, who gr i 1 1 446 orest i. palamar, andriy p. huk, dmytro s. teslenko et al. typical and atypical meningiomas, who gr i та ii 2 central neurocytomas, who gr ii 4 2 pineoblastoma, who gr iv 1 ependymoma, who gr ii, anaplastic ependymoma who gr iii 1 5 craniopharyngioma, who gr i 6 colloid cysts 7 germinomas 4 mature teratoma 1 table 1. histopathology of intraventricular neoplasms. preoperative symptoms include: cephalalgia 49 (90.7 %) patients, sings of elevated icp 32 (59.25 %) patients, neurocognitive disorders and psychoorganic syndrome 10 (18.5%) patients, oculomotor dysfunction 10 (18.5%) patients, motor deficits 9 (16.6%) patients, short term memory loss 8 (14.8%) paients, decreased visual acuity and loss of peripheral vision 7 (12.9%) patients, endocrinopathy 4 (7.4%) patients, seizures 2 (3.7%) patients. preoperative contrast-enhanced magnetic resonance imaging (mri) (fig.2) of the brain and computer tomography (ct) were also used for the preoperative planning of the approach side, optimal for the resection of the neoplasm and minimization of postoperative complications. we analyzed the localization of the neoplasms in the ventricular system, the side with greater distribution, signs of occlusive hydrocephalus, the side with the wider interventricular foramen of monro, localization of estimated corticotomy ("entry point"), and the best "angle of attack ". figure 2. a-b. tumor in the posterior part of the third ventricle (ependymoma), preoperative contrast-enhanced t1w images and t2w images. in surgery of neoplasms of the lateral (anterior horn, body, atrium) and third ventricle, we use endoscopic frontal (craniotomy over the frontal lobe) transcortical (corticotomy through the upper or middle frontal gyrus) approache. we perform an endoscopic frontal transcortical approach via parasagittal craniotomy over the non-dominant hemisphere of the brain (or over the priority hemisphere for approach) with the centration at the kocher’s point. corticotomy up to 2.2 cm. is carried out through the top of the middle or upper frontal gyrus. the next stage is white matter fibers dissection to the front horn of the lateral ventricle and the subsequent introduction of intracerebral retractors. depending on the location of the tumor or lesion in the third ventricle, its size, and available hydrocephalus we used transventricular (through the cavity of the lateral ventricles) approach and further transforaminal (approach to the third ventricle through the interventricular foramen of monro) or extended transforaminal transchoroidal approach (approach to the third ventricle through the interventricular foramen of monro with the anterior choroidal dissection). surgery was performed using an endoscopic stand based on the hdendoscope “image-1hd” (karl storz, germany). 447 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours rigid endoscopes "karl storz" 4 mm in diameter with viewing angles of 0 and 35 degrees were used as the main tool for visualization of the operating field. approach through the right hemisphere has been performed in 38 (70.4 %) cases and through the left one in 16 (29, 6 %) cases. endoscopic frontal transcortical approach to the lateral ventricles was used in 13 (24.1 %) cases; endoscopic frontal transcortical transentricular transforaminal approach to the third ventricle 13 (24.1 %) cases, extended transforaminal transchoroidal approach 28 (52%) cases. in all cases, a 100% endoscopic technique (" fully endoscopic resection ") was performed. in case of clinical and mr signs of occlusive hydrocephalus and with the purpose of preventing the progression of hydrocephalus in 22 (40.7%) cases with simultaneous resection of tumor we performed endoscopic third ventriculostomy. in the early postoperative period, all patients underwent contrast-enhanced ct or mri in order to detect residual component of the tumor, potential postoperative ischemia and bleeding, and evaluations of the ventricular system. the follow-up ranged from 3 to 42 months, at average 12.5 months. during the follow-up examination of patients, which was performed approximately 2-4 months after the surgery, we assessed the overall health status, neurological status, contrast-enhanced mri of the brain (fig. 3). on mri we evaluated the presence of residual component of the tumor or tumor growth, ventricular system (presence of hydrocephalus), expansion/narrowing of the transcortical channel in the matter of the frontal lobe. a. b. c. d. figure 3. a-b. tumor in the right lateral ventricle (ependymoma), preoperative t1w images. c-d. 5-month postoperative contrast-enhanced t1w images depicted gross total resection of the tumor. 448 orest i. palamar, andriy p. huk, dmytro s. teslenko et al. results and discussion extent of resection in our series: gross total resection/near total resection 34 (63 %) patients, subtotal/partial resection 15 (27.7 %) cases, biopsy 5 (9.2 %) cases. 39 (72.2 %) patients had no postoperative complications, 15 (27.7 %) patients had at least one postoperative complication. postoperative complications included: speech disorders such as mutism 6 (11.1 %) patients and apathia/abulia 5 (9.2%) patients. we observed that 4 patients with postoperative manifestations of apathia/abulia also had concomitant mutism. in the postoperative period, at the follow-up examination 2-4 months after the surgery, a complete or partial regression of both mutism and apathia/abulia was observed in all 6 patients; short term, "fixation" memory loss 5 (9.2 %) patients. in all 5 cases the endoscopic transcortical transventricular transforaminal or extended transforaminal transchoroidal approach to the third ventricle was applied. in the postoperative period, at the follow-up examinations during the next 2-6 months after the surgery, a complete or partial regression was observed in 3 patients; oculomotor dysfunction 5 (9.2%) patients. oculomotor dysfunction included paresis of n. oculomotorius and/or parinaud syndrome and in all 5 cases have been associated with tumor resection of the posterior part of the third ventricle. in the postoperative period, complete or partial regression was observed in 1 patient; motor deficits 4 (7, 4%) patients. in our series, we associate the occurrence of this complication either with resection of the glial tumor (originated in close proximity to corticospinal tracts) with the invasion in the third ventricle or with the premotor cortex and supplementary motor area injury. we observed the complete regression in 2 patients during the next 4 months after the surgery; neurocognitive disorders 4 (7.4%) patients which regressed in 1 patient 4 months after the surgery; endocrinopathy 3 (5.5%) patients. we associate this complication with the resection of tumors that have been tightly fused to the hypothalamic area of the bottom of the third ventricle. regression was observed in 1 patient after 3 months; postoperative hemorrhage – 2 (3,7%) patients; postoperative wound infection occurred in 1 (1.85%) patient; postoperative meningitis 1 (1.85%) patient. in our series, seizures, as a postoperative complication, did not occur. postoperative mortality 1 (1.9%) patients due to hypothalamic dysfunction, leading to acute electrolyte shifts, after the resection of craniopharyngioma with the significant spread in the third ventricle. compared with the series brian d. milligan at al in the group transcortical approach, short-term memory loss in the postoperative period was recorded in 6 (12 %) patients, that is 2.8% higher than in our series. motor deficits were recorded in 18 (35%) patients, that is 27.6 % higher than in our series. neurocognitive disorders were 4.6% higher than in our series, and the percentage of patients with endocrinopathy was the same as in the series brian d. milligan at al. [16] the average kps on the day of discharge was 83,35%. in the early postoperative period, all patients underwent contrast-enhanced ct or mri of the brain and, among other things, we evaluated the following approach criteria (table. 2) using radiant dicom viewer software: 1) localization of corticotomy, "entry point" (upper/middle frontal gyrus (upper parts ); 2) the distance from the coronal suture to the corticotomy in front; 3) "angle of attack " (the angle between the sagittal plane and plain "entry point" the point of entry into the frontal horn of the lateral ventricle). (fig. 4) localization of corticotomy right hemisphere n-38 (70,4%) left hemisphere n -16 (29,6%) upper frontal gyrus 12 (31,5 %) 7 (43,7%) middle frontal gyrus, upper part 26 (68,5 %) 9 (56,3%) distance from the coronal suture to 2,8 cm, min 1,2, max3,6 2,8 cm, min0,5, max2,9 449 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours the corticotomy (mean, min-, max). "angle of attack" (mean, min-, max). 27,4○, min17○, max 35○ 26,7○, min-21○, max34○ table 2. approach criteria. figure 4. a. tumor of the third ventricle (craniopharyngioma), preoperative, contrast-enhanced t1w image. b. 4-month postoperative contrast-enhanced t1w images, “angle of attack” calculation using using radiant dicom viewer software. in our series, mutism, as a manifestation of specific speech disorders caused by the frontal transcortical approach to the lateral and third ventricles, was observed in the postoperative period in 6 (11.1 %) patients (approach on the left 6 patients). this clinical condition was transient and regressed within 4 months after the surgery. we indicate that corticotomy in patients who had postoperative mutism was performed in the upper frontal gyrus – 4 patients, in the middle frontal gyrus – 2 patients. we presume that postoperative mutism is related to the following features of the approach: 1) the approach side dominant hemisphere. 2) corticotomy in the upper frontal gyrus and at a distance of less than 2 cm. from the coronal suture. 3) "angle of attack" less than 26.7○. in their series, s. asgari et al reported that when applying the transcortical approach, transient mutism occurred in 11% of patients, while via interhemispheric/transcallosal approach in 18% of patients, that equals and is 8.2% higher compared to our series respectively [7]. r. g. ellenborg concluded that speech disorders are a fairly common complication when applying a transcortical approach through the dominant hemisphere and occur in 1030% of patients [13]. in the article by brian d. milligan et, when comparing transcortical and interhemispheric approaches, mutism is not distinguished as a complication, instead this clinical condition is classified as a separate group of complications aphasia/abulia, which occurs in 31% and 25% of cases, respectively, when applying transcortical and transcallosal approaches [16]. in our series of cases, aphatia/abulia manifested in the postoperative period in 5 (9.2%) patients, in all cases together with mutism. it is uncertain whether there is a direct link between apathy, abulia and mutism. however, there is some evidence that the medial part of the frontal lobes, especially the cortex and fibers of the anterior cingulate gyrus, may play a role in manifestations of aphatia/abulia along with signs of mutism, as well as akinetic mutism [12]. the anterior part of the cingulate gyrus has a complex relationship with the limbic structures, other parts of the frontal cortex and periaqueductal gray matter of 450 orest i. palamar, andriy p. huk, dmytro s. teslenko et al. the midbrain. it is involved in interaction between the decision-making process and the "emotional" world of the limbic system, which is considered crucial for the start of speech and vocalization [6,19]. functionally, the corpus callosum is closely related to speech function [9,20]. mutism often occurs in the postoperative period after the interhemispheric approach with callosotomy [8,18]. jin hong et al suggested that damage to the corpus callosum can lead to speech disorders [15]. ishizaki et al describe that transcallosal diaschisis is a possible mechanism of aphasia [14]. in our opinion, the commissural fibers of the corpus callosum and forceps minor fibers injury while applying the transcortical approach to the ventricular system, may play a role in the development of transient mutism. utilizing magnetic resonance diffusion-tensor tractography and comparing two different localizations of corticotomy (through the middle frontal gyrus and through the upper frontal gyrus) applying transfrontal transcortical access, t. szmuda et al concluded that the application of access through the upper and middle frontal gyrus one way or another leads to trauma, including the upper longitudinal fascicles ii, which is partially responsible for the relationship between the fields of brock and wernicke [21]. although most of the fibers involved in the speech network and connecting the middle and lower frontal gyrus and posterior part of superior temporal gyrus are a part of the so-called upper longitudinal fasciculus iii (anterior fibers of arcuate), they are located more caudally to the potential injury of the white matter via frontal transcortical approach in our cases [17]. injury to the supplementary motor area and the premotor cortex, especially of the dominant hemisphere of the brain, can also cause mutism. penfield and welch used cortical stimulation to identify the boundaries and functions of this area. the connections of this cortex are quite branched and include the upper temporal gyrus, the intraparietal sulcus, the caudate nucleus, the thalamus, and other. [10] conclusions the endoscopic frontal transcortical approach in surgery of neoplasm and lesions of the lateral and third ventricle is effective and minimally invasive approach. the transient nature of postoperative complications is due to the gentle manipulations of anatomical structures when applying this approach. specific surgical approach complications such as mutism, apathia/abulia, motor deficits (due to the injury of the premotor cortex and supplementary motor area) were mostly transient and had a tendency to regress immediately in the postoperative period and most of them completely regressed from 2 to 4 months after the surgery. the nature of mutism as a manifestation of speech complications when applying endoscopic frontal transcortical approach is multifactorial. the development of postoperative speech complications, namely of transient mutism when applying the endoscopic frontal transcortical approach is not a frequent complication and according to our observations regresses within 4 months. in our opinion, in order to reduce the risk of mutism in the postoperative period, endoscopic frontal transcortical approach should be performed via the non-dominant hemisphere (unless otherwise specified during preoperative planning) and in the upper part of the middle frontal gyrus at a distance more than 2 cm from the coronal suture. corticotomy should be gentle and based on our series no more than 2.2 cm in length, "angle of attack" should be no less than 26.7○ which reduces cerebral cortex and white matter injury and the risk of postoperative complications associated with the application of this approach, including manifestations of mutism. references 1. altshuler ll, cummings jl, mills mj (1986) mutism: review, differential diagnosis, and report of 22 cases. amer j psychiatry 143:1409 1414. 2. anderson rc, ghatan s, feldstein na. surgical approaches to tumors of the lateral ventricle. neurosurg clin n am. 2003;14(4):509-525. 3. apuzzo ml, chikovani ok, gott ps, et al. transcallosal, interfornicial approaches for lesions affecting the third ventricle: surgical considerations and consequences. neurosurgery. 1982;10(5):547-554. 4. apuzzo mlj (1987) surgery of the third ventricle. williams & wilkins, baltimore. 5. apuzzo mlj, litofsky ns. surgery in and around the anterior third ventricle. in: apuzzo mlj, ed. brain surgery: complication avoidance and management. new york: churchill-livingstone; 1993:541-579. 6. arnts h, van erp ws, lavrijsen jcm, van gaal s, groenewegen hj, van den munckhof p. on the 451 postoperative complications in endoscopic frontal transcortical surgery of lateral and third ventricle tumours pathophysiology and treatment of akinetic mutism. neurosci biobehav rev. 2020 may;112:270-278. 7. asgari s, engelhorn t, brondics a, sandalcioglu ie, stolke d. transcortical or transcallosal approach to ventricleassociated lesions: a clinical study on the prognostic role of surgical approach. neurosurg rev. 2003 jul;26(3):1927. 8. bogen je (1987) physiologicai consequences of complete or partial commissural section. in: apuzzo mlj (ed) surgery of the third ventricle. williams & wilkins, baltimore london los angeles sydney, pp 175-194. 9. catani m, jones dk, ffytche dh, et al. perisylvian language networks of the human brain. ann neurol 2005;57:8–16. 10. crutchfield js, sawaya r, meyers ca, moore bd 3rd. postoperative mutism in neurosurgery. report of two cases. j neurosurg. 1994 jul;81(1):115-21. 11. cummings jl, benson df, houlihan jp, etal (1983) mutism: loss of neocortical and iimbic vocalization. j nerv ment dis 171:255-259. 12. darby rr, joutsa j, burke mj, fox md. lesion network localization of free will. proc natl acad sci u s a. 2018 oct 16;115(42):10792-10797. 13. ellenbogen rg. transcortical surgery for lateral ventricular tumors. neurosurg focus. 2001 jun 15;10(6):e2. 14. ishizaki m, ueyama h, nishida y, et al. crossed aphasia following an infarction in the right corpus callosum. clin neurol neurosurg 2012;114:161–5. 15. jin hong , song xiaojing , song , et al. clinical analysis of 14 cases of corpus callosum infarction. chin j clin res 2010;23:1016–1016. 16. milligan bd, meyer fb. morbidit y of transcallosal and transcor tical approaches to lesions in and around the lateral and third ventricles: a single-institution experience. neurosurgery. 2010 dec;67(6):1483-96; discussion 1496. 17. nakajima r, kinoshita m, shinohara h, nakada m. the superior longitudinal fascicle: reconsidering the frontoparietal neural network based on anatomy and function. brain imaging behav. 2020 dec;14(6):2817-2830. 18. sass kj, novelly ra, spencer dd, spencer ss. postcallosotomy language impairments in patients with crossed cerebral dominance. j neurosurg. 1990 jan;72(1):85-90. 19. shenhav a, botvinick mm, cohen jd. the expected value of control: an integrative theory of anterior cingulate cortex function. neuron. 2013 jul 24;79(2):217-40. 20. sussman nm, gur rc, gur re, o'connor mj. mutism as a consequence of callosotomy. j neurosurg. 1983 sep;59(3):514-9. doi: 10.3171/jns.1983.59.3.0514. 21. szmuda t, słoniewski p, szmuda m, waszak pm, starzyńska a. quantification of white matter fibre pathways disruption in frontal transcortical approach to the lateral ventricle or the interventricular foramen in diffusion tensor tractography. folia morphol (warsz). 2014 may;73(2):129-38. doi: 10.33962/roneuro-2022-045 brain abcess with nocardia farcinica tracicaru r.v., cucu a.i., curecheriu m. loredana, turliuc dana mihaela romanian neurosurgery (2022) xxxvi (3): pp. 259-263 doi: 10.33962/roneuro-2022-045 www.journals.lapub.co.uk/index.php/roneurosurgery brain abcess with nocardia farcinica tracicaru r.v.2, cucu a.i.2, curecheriu m. loredana2, turliuc dana mihaela1,2 1 "grigore t. popa" university of medicine and pharmacy, iasi, romania 2 department of neurosurgery, "prof. n. oblu" emergency clinical hospital, iasi, romania abstract introduction: brain abscesses caused by nocardia farcinica pathogen are rare and usually present as large abscesses with a thick and irregular wall. we present a case of a patient with signs and symptoms of central nervous system infection and had a fulminant evolution with malign cerebral oedema and death. case report: the 35-year-old patient presented with mild symptoms that appeared 2 weeks prior and became more aggressive in the last 48 hours. after the initial examination and blood tests, the patient was suspected of a systemic infection because of the high white cell count and high level of inflammatory markers. antibiotic therapy was started with ciprofloxacin and amoxicillin/ clavulanic acid. the brain mri showed a multinodular lesion in the right hemisphere, with contrast enhancement and central high diffusion restriction on t1, t2 and flair. during the antibiotic treatment, the patient suddenly became comatose. urgent brain ct scan showed malign cerebral oedema with brain shift. discussion: there are 58 documented cases of nocardia farcinica in the literature, as shown in a recent systematic review. most of the cases are with immunocompromised patients, either through disease or secondary to treatment after organ transplant. in our case, we suspected immunodeficiencies based on the anamnestic data offered by the patient's family. mortality rates are between 19% and 36,7% in all reported cases, but in our presented case the patient had a rapid aggressive evolution with malign brain oedema that resulted in death. conclusions. the management of these cases requires urgent diagnostics and treatment. for our team, the first reported case of nocardia farcinica and the fast aggressive evolution resulted in a negative outcome, even with antibiotics treatment and surgical evacuation of the abscess. introduction nocardial brain abscesses are a serious and quite rare pathology caused by bacteria from the genus nocardia, a group of gram-positive aerobic bacilli falling under the broader umbrella of aerobic actinomycetes (loeffler et al., 2001; prod'hom & bille, 2017). soil-based, these bacteria usually enter the body either by inhalation or local contamination of damaged skin (corsini campioli et al., 2021). of these, n. farcinica is one of the more virulent species due to additional virulence factors (prod'hom & bille, 2017). the manifest infection usually presents as large abscesses with a thick, irregular wall with keywords brain abscess, nocardia farcinica, infection, central nervous system corresponding author: curecheriu m. loredana department of neurosurgery, "prof. n. oblu" emergency clinical hospital, iasi, romania curecheriu.loredana@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 260 tracicaru r.v., cucu a.i., curecheriu m. loredana, turliuc dana mihaela multilocular abscesses not being uncommon. the preferred locations for these are the lungs and the brain (beucler et al., 2022; prod'hom & bille, 2017). in the following report we will analyse the case of a patient who presented with a symptomatic nocardial abscess with n. farcinica leading to malign cerebral oedema and death. case report we present the case of a 35-year-old patient that arrived at the emergency department complaining of an intense headache. the symptoms started two weeks prior to the presentation and intensified in the last 48hours. the patient presented one episode of vomiting which alleviated his symptoms. on initial examination, the patient was alert, responsive but agitated with mild neck stiffness. we observed a generalized skin erythema and multiple tattoos. a cranial ct was performed (figure 1) in which a nodular parenchymal lesion was observed in the right hemisphere. the lesion showed important perilesional digitiform oedema. complementary tests were performed including serologies, hiv and quantiferon test. blood test showed leucocytosis, thrombocytosis with high levels of fibrinogen and esr. tests for syphilis, tuberculosis and hiv were negative. figure 1. initial brain ct scan without contrast showing one nodular lesion in the right hemisphere on sagittal (a), axial (b) and coronal (c) planes. perilesional digitiform oedema shown in the blue circle. the family of the patient noted that he worked for 6 years in barcelona, spain, undocumented and is a frequent user of drugs and alcohol. we performed a thoracic radiograph that showed multiple focal lesions bilaterally. we followed up with a thoracic ct scan that showed multiple cystic lesions with thin wall located in the superior lingula lobe and in the left fowler segment with antero-posterior diameter of 24/15 mm and respectively 17/10mm. on the left inferior pulmonary lobe, it was found a cyst lesion with a 7,5 mm and 1,8 mm diameter (figure 2). figure 2. thoracic ct scan showing multiple pulmonary cystic lesions (illustrated with the blue circle) with thin wall located in the superior lingula lobe and in the left fowler segment with antero-posterior diameter of 24/15 mm and respectively 17/10mm. on the left inferior pulmonary lobe, it was found a cyst lesion with a 7,5 mm and 1,8 mm diameter. empirical antibiotic therapy was started with ciprofloxacin 400mg per day + amoxicillin/ clavulanic acid 6g per day. in the following day he developed a high fever, a cough and became agitated and delirious. the symptoms did not respond to treatment. figure 3. brain mri showing the heterogenous lesion in the right hemisphere, with extension in the right trigone of the lateral ventricle. the lesion shows central high diffusion restriction on t1 (a), t2 (b), flair (c). figure 4. brain mri shows contrast ring enhancement on sagittal (a) and axial (b) plane. at the basal cisterns the contrast enhancement is suggestive for pachymeningitis (shown with blue arrows). a brain mri was performed showing an heterogenous lesion in the right hemisphere, located in the parietal lobe with extension in the right trigone 261 brain abcess with nocardia farcinica of the lateral ventricle without and evident delimitation. the lesion shows central high diffusion restriction on t1, t2 and flair, with a low swi signal (figure 3). on t1 with contrast it presented ring and meningeal enhancement, especially at the basal cisterns. furthermore, brain oedema was perilesional with digitiform aspect. all of these radiological features were suggestive of brain abscess and pachymeningitis (figure 4). on the 4th day of his stay, he suddenly became comatose and underwent urgent brain ct scan, that showed and important perilesional oedema with mass effect. a decompressive craniectomy was performed and the brain abscess was evacuated with ultrasonography guide for microbiological evaluation (figure 5). figure 5. brain ct scan performed on the 4th day of admission showing perilesional oedema with brain (illustrated with red circle in all images) with brain shift. the brain abscess had multiple fibrin cells, pmn and macrophages, with negative bacterioscopy. microbiological cultures revealed a gram-positive bacterium, nocardia farcinica. postoperatively, the patient remained in comatose state, with fixed bilateral dilated pupils and the following day had a heart arrest that did not respond to resuscitation. discussion epidemiology brain abscesses with n. farcinica are a rare pathology, a recent systematic review describing only 58 completely documented cases in literature (beucler et al., 2022). it seems that amongst nocardial infections, n. farcinica is a common pathogen involved in the formation of brain abscesses. there are differences in regions between the united states and switzerland where it is the most common, and france and italy where it was the second most common species.(boiron et al., 1992; corsini campioli et al., 2021; farina et al., 1995; loeffler et al., 2001). in our case, this is the first documented instance of a nocardial brain abscess for our team. the patients are generally immunocompromised. in his review, beucler et al. reported that 74% of cases presented some form immunodeficiency whether through disease or secondary to treatment in case of organ transplant (beucler et al., 2022). in other series immunodeficiencies were present in 83,3%, 70.5%, 90%, 62.5% and 82% of cases respectively (anagnostou et al., 2014; boiron et al., 1992; corsini campioli et al., 2021; farina et al., 1995; loeffler et al., 2001), one of them reporting cases of immunodeficiencies associated with drug abuse (farina et al., 1995). in our case, no apparent immunocompromising factors were identified. the patient had white cell counts concurrent with normal response during infectious pathologies and the tests for syphilis, tuberculosis and hiv were all negative. the only reference we have is anamnestic data from the family about alleged drug abuse (unspecified) and chronic alcohol abuse which are both proven to induce a degree of immunodeficiency (kaushik et al., 2011; pasala et al., 2015), however only circumstantial evidence is available. in our case the patient died 5 days after admission due to malign cerebral oedema combined with the systemic infection diagnosed. mortality rates are high in all reported series ranging between 19% and 36.7% (anagnostou et al., 2014; beucler et al., 2022; boiron et al., 1992; corsini campioli et al., 2021; farina et al., 1995; loeffler et al., 2001). amongst these, higher mortality in nocardial infections with cns determination was observed in immunocompromised patients: 57%, 55%, 64% (corsini campioli et al., 2021; loeffler et al., 2001; mamelak et al., 1994) rather than in immunocompetent hosts: 20%,42% (loeffler et al., 2001; mamelak et al., 1994). n. farcinica was by far the more aggressive species, representing a high proportion of the deaths: 57% (boiron et al., 1992; kumar et al., 2014). we cannot reflect on mortality rates in our area since this is the first documented case we encountered, but we will monitor and report any further cases. being such a rare entity, usually associated with other pathologies like immune deficiencies whether acquired or induced through medication, clinical and paraclinical presentations vary. the presentation in most series is intracranial hypertension (45%, 50%, 262 tracicaru r.v., cucu a.i., curecheriu m. loredana, turliuc dana mihaela 33% (anagnostou et al., 2014; beucler et al., 2022; loeffler et al., 2001)), concurring with the findings for our patient. no neurological deficits were identified for our case although these are also very common (51%, 50% 50% (anagnostou et al., 2014; beucler et al., 2022; loeffler et al., 2001). meningismus is quite frequent, especially when abscesses are in contact with the ventricular walls (9%, 9%, 17% (anagnostou et al., 2014; beucler et al., 2022; loeffler et al., 2001)). fever was not present in our case, and despite the classic triad of fever, elevated icp and focal deficit, is not seen in most cases, probably due to the immunodeficiencies related with this pathology. (anagnostou et al., 2014; beucler et al., 2022; loeffler et al., 2001). when it comes to paraclinical tests, an inflammatory syndrome marked by elevated wbc crp, fibrinogen and platelets levels was present and is a possible, although quite inconsistent finding (beucler et al., 2022). when it comes to intracerebral radiological findings, a single abscess is most common, 59%, 66%, 83% and 57% respectively (beucler et al., 2022; corsini campioli et al., 2021; loeffler et al., 2001; mamelak et al., 1994), mostly supratentorial 52%, 91%, 83%, 57% (beucler et al., 2022; corsini campioli et al., 2021; loeffler et al., 2001; mamelak et al., 1994). described as looking as a grape bunch in most cases it is associated with intense vasogenic oedema (beucler et al., 2022), which was certainly evident in our case since it evolved with malign cerebral oedema. the parietal lobe localisation seems to be the second most common (37.5% (corsini campioli et al., 2021)), and explains the lack of focal neurological deficits. management of these cases is complex and requires both surgical intervention and long-term antibiotic therapy. the surgical approach serves both to reduce the dimensions or completely excise the abscess and to produce pathological material for microbiological identification. however, when microbiological identification is possible from a secondary location, a more conservative approach can be considered. in general, between 45% and 77% of patients benefited from surgical intervention (beucler et al., 2022; corsini campioli et al., 2021; farina et al., 1995; loeffler et al., 2001; mamelak et al., 1994) and this led to a positive outcome for 93% 87% and 65% of them respectively (anagnostou et al., 2014; beucler et al., 2022; mamelak et al., 1994). the preferred strategy was craniotomy an excision as opposed to aspiration and drainage since it led to better results 8% and 24% mortality versus 23% and 50% mortality respectively (beucler et al., 2022; mamelak et al., 1994), with a lower risk of surgical revision 8% vs 31% (beucler et al., 2022), 22% vs 27% (mamelak et al., 1994). antibiotic treatment usually employed trimethoprim-sulfamethoxazole (tmpsmx) in 45%, 41,6%, 90% (beucler et al., 2022; corsini campioli et al., 2021; mamelak et al., 1994) of cases usually associated with other antibiotics such as vancomycin, amikacin, metronidazole, ceftriaxone, minocycline and amoxicillin. (corsini campioli et al., 2021; farina et al., 1995; loeffler et al., 2001; mamelak et al., 1994). in vitro studies showed the most susceptibility to tmp-smx, linezolid, amikacin, imipenem and meropenem, minocycline (beucler et al., 2022; corsini campioli et al., 2021; mamelak et al., 1994). other studies in italy and france showed resistance to tmp-smx, and high susceptibility to amikacin (boiron et al., 1992; farina et al., 1995), but these were not focused on n. farcinica only. most found a high level of resistance to amoxicillin and clavulanic acid. (beucler et al., 2022; boiron et al., 1992; corsini campioli et al., 2021; farina et al., 1995; mamelak et al., 1994). thus, it seems that the best empiric antibiotic treatment would combine amikacin with either tmp-smx or imipenem, meropenem, minocycline depending on region related particularities. conclusions this was the first reported case of a n. farcinica brain abscess in our region and represented a challenge through its particularities. the atypical presentation, the disseminated infection and the choice of treatment all contributed to the high degree of gravity of the case. immunosuppression could not certainly be ruled out in our case. management of these cases require prompt identification of the bacteria, aggressive surgical treatment, and the correct choice of antibiotic treatment. we aim to raise awareness about this pathology, seldom found in our geographical area and to further our standards of practice in these cases. references 1. anagnostou, t., arvanitis, m., kourkoumpetis, t. k., desalermos, a., carneiro, h. a., & mylonakis, e. (2014). nocardiosis of the central nervous system: experience from a general hospital and review of 84 cases from the 263 brain abcess with nocardia farcinica literature. medicine (baltimore), 93(1), 19-32. https://doi.org/10.1097/md.0000000000000012 2. beucler, n., farah, k., choucha, a., meyer, m., fuentes, s., seng, p., & dufour, h. (2022). nocardia farcinica cerebral abscess: a systematic review of treatment strategies. neurochirurgie, 68(1), 94-101. https://doi.org/ https://doi.org/10.1016/j.neuchi.2021.04.022 3. boiron, p., provost, f., chevrier, g., & dupont, b. (1992). review of nocardial infections in france 1987 to 1990. eur j clin microbiol infect dis, 11(8), 709-714. https://doi.org/10.1007/bf01989975 4. corsini campioli, c., castillo almeida, n. e., o’horo, j. c., challener, d., go, j. r., desimone, d. c., & sohail, m. r. (2021). clinical presentation, management, and outcomes of patients with brain abscess due to nocardia species. open forum infectious diseases, 8(4). https://doi.org/10.1093/ofid/ofab067 5. farina, c., boiron, p., goglio, a., & provost, f. (1995). human nocardiosis in northern italy from 1982 to 1992. northern italy collaborative group on nocardiosis. scand j infect dis, 27(1), 23-27. https://doi.org/10.3109/00365549509018968 6. kaushik, k. s., kapila, k., & praharaj, a. k. (2011). shooting up: the interface of microbial infections and drug abuse. journal of medical microbiology, 60(4), 408-422. https://doi.org/https://doi.org/10.1099/jmm.0.027540-0 7. kumar, v. a., augustine, d., panikar, d., nandakumar, a., dinesh, k. r., karim, s., & philip, r. (2014). nocardia farcinica brain abscess: epidemiology, pathophysiology, and literature review. surg infect (larchmt), 15(5), 640646. https://doi.org/10.1089/sur.2012.205 8. loeffler, j. m., bodmer, t., zimmerli, w., & leib, s. l. (2001). nocardial brain abscess: observation of treatment strategies and outcome in switzerland from 1992 to 1999. infection, 29(6), 337-341. https://doi.org/10.1007/s15010-001-1147-1 9. mamelak, a. n., obana, w. g., flaherty, j. f., & rosenblum, m. l. (1994). nocardial brain abscess: treatment strategies and factors influencing outcome. neurosurgery, 35(4), 622-631. https://doi.org/10.1227/00006123-199410000-00007 10. pasala, s., barr, t., & messaoudi, i. (2015). impact of alcohol abuse on the adaptive immune system. alcohol res, 37(2), 185-197. 11. prod'hom, g., & bille, j. (2017). 178 aerobic grampositive bacilli. in j. cohen, w. g. powderly, & s. m. opal (eds.), infectious diseases (fourth edition) (pp. 15371552.e1532). elsevier. https://doi.org/https://doi.org /10.1016/b978-0-7020-6285-8.00178-7 romanian neurosurgery (2019) xxxiii (4): pp. 385-395 doi: 10.33962/roneuro-2019-063 www.journals.lapub.co.uk/index.php/roneurosurgery secondary giant cell glioblastoma in a multiple drug abuser simple association or ethiopathogenic correlation? case presentation and literature review l. eva1, m.s. ples4, m.r. munteanu1, gabriela florenta dumitrescu2, nicoleta dumitrescu3, horia ples4 1 neurosurgery clinic, “prof. dr. n. oblu” emergency clinical hospital, iasi, romania 2 pathology laboratory, “prof. dr. n. oblu” emergency clinical hospital, iasi, romania 3 4th year student, faculty of medicine, “grigore t. popa” university of medicine and pharmacy, iasi, romania 4 department of neurosurgery, “victor babes university of medicine and pharmacy” timisoara, romania abstract experimental investigations have shown that drug abuse initiates a cascade of pathophysiological events including toxic and hypoxic-ischemic injury on neurons, microglia and astrocytes, which finally lead to widespread disturbances in the brain. there are many reports about the psychiatric and neurologic effects of multiple drug abuse, but only a few clinical studies reporting possible correlation between recreational illicit drugs and gliomas. in this paper we present the case of a 40 years-old male patient, with a long history (almost ten years) of multiple drug abuse, including cocaine, heroin, marijuana, ethnobotanical drugs and nicotine, who was diagnosed and surgically treated for a supratentorial secondary giant cell glioblastoma (sgcgb) developed in a diffuse astrocytoma nos. depending on the type of the illicit drug used by the patient and the moment of life he used them, the morphological features identified in the histological samples of our patient confirmed the gliomagenesis effect of chronic multiple drug abuse, but also its inhibitory effects on tumour cells growth. this was due to the fact that although the tumour was large in size and caused brain subfalcine herniation, the patient reported the onset of seizures only late in the evolution. in conclusion, the diagnosis of a brain tumour should take into consideration not only patient's clinical and imaging data, but also his lifestyle, especially his addiction to recreational drugs. introduction the psychostimulants (cocaine, methamphetamine, etc.), opiates and opioids (heroin, methadone, etc.), sedatives (benzodiazepines), and keywords multiple drug abuse, psychiatric symptoms, secondary giant cell glioblastoma, partial tumour resection corresponding author: maria-raluca munteanu neurosurgery clinic, “prof. dr. n. oblu” emergency clinical hospital, iasi, romania raluca13r@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 386 l. eva, m.s. ples, m.r. munteanu et al. some other drugs such as cannabis (marijuana) and nicotine are the most widely consumed recreational drugs in order to obtain a sense of well-being. unfortunately, in the same time, these drugs of abuse have a significant negative impact on public health as they can induce pulmonary (1-4), cardiovascular (5, 6), renal diseases (7), gastrointestinal and endocrine diseases or infections (8). however, psychiatric and neurologic symptoms are the most common manifestations of drug abuse toxicity. along with the psychotic effects of recreational psychostimulants (9, 10), there are also reports of their neurological side effects, such as vasogenic edema formation (11), cerebral and spinal cord infarction, cerebral vasculitis associated with intraparenchymal or subarachnoid haemorrhage (12), hypoxic-ischemic leukoencephalopathy (13), ischemic optic neuropathy as well as partial and generalized seizures (14, 15). some researchers have made systematic histological, immunohistochemical and morphometric investigations in order to identify the morphological alterations in the brains of multiple abusers. there are reports of intramyelinic edema and mitochondrial dysfunction due to cocaine abuse, but also of neurovascular toxicity due to heroin (16). other studies reported a toxic spongiform leukoencephalopathy after intravenous heroin injection or after inhaling heroin vapors (17-19). the morphological substrate of this disease is a spongiform demyelination that develops due to a dysfunction of the oligodendrocyte mitochondria (20, 21). neuropathological features encountered included neuronal loss, neurodegenerative alterations with significant widespread axonal damage (22), specific astroglial reaction patterns (23, 24), with a reduction of glial fibrillary acidic proteinimmunopositive astrocytes, concomitant microglial activation as well as reactive and degenerative changes of the cerebral microvasculature (due to alterations of the endothelial cell and the basal lamina) (25). fredericks et al. reported nonnecrotizing, nonleukocytoclastic small-vessel arteritis associated with cocaine use (26). on the molecular level, alterations in the expression of transcription factors and changes of brain neurotransmitter systems have been reported, too (27). all these results have provided evidence that drugs of abuse initiate a cascade of pathophysiological events including toxic, hypoxicischemic injury, microglial and astrocytic associated cytokine releases, which finally lead to widespread disturbances within the complex network of central nervous system cell-to-cell interactions (25, 28). however, as far as we know, there is a scarcity of literature concerning the correlation of drug abuse with the development of a cerebral glioma. there is only one epidemiological study published in 2004 by efird et al. that found a 2.8-fold increased risk for malignant primary adult-onset glioma for people who had smoked cannabis once or more per month (29). in this paper we present the case of a 40 years male patient, a chronic multiple abuser for ten years, who was diagnosed and treated for a supratentorial secondary giant cell glioblastoma (sgcgb) developed in a diffuse astrocytoma nos. we discuss the possible role of drug of abuse effects on tumour initiation, development and progression taken into consideration patient's history of multiple abuse. case presentation a male patient, 40 years old, heavy smoker (about 20 cigarettes per day for 30 years), was brought by his family to the “socola” institute of psychiatry, iași, romania, for strong headache and altered mental status over the last 24 hours. they considered that patient's status was the effect of his dependence on psychoactive substances as he had a long history (almost ten years) of multiple abuse, including cocaine, heroin, marijuana, and ethnobotanical drugs. firstly, he used cocaine for five years, then he continued with heroin and marijuana for another two years and finally he only consumed ethnobotanical drugs over the most recent three years. the patient's relatives also declared that he had symptoms of anger or euphoria and changes in behaviour over the last twelve months, but also a state of sleepiness in the last month. the patient complained of intermittent diffuse headaches, which developed during the preceding months and improved with the use of ethnobotanical drugs. on physical examination the patient was apparently conscious, cooperative, and partially communicative. he had temporo-spatial orientation 387 secondary giant cell glioblastoma in a multiple drug abuser and only presented a slight attention deficit. he denied any hallucinations and alcohol consumption, referring only to the chronic consumption of psychoactive substances. the general medical examination was unremarkable. his blood pressure was 136/96 mmhg, pulse = 90 beats/minute, temperature = 36.30c, and glycemia = 113 mg/dl. there were no relevant family risk factors for neoplastic disease. one day after his admission in the psychiatric unit, the patient's condition progressively worsened. the vomiting was triggered with a continuous frequency, even from the sitting position. brain computer tomography (ct) scans, carried out in emergency, highlighted a large, irregularly shaped fronto-temporo-parietal expansive mass lesion, being hypoand isointense on native examination, and with evidence of post-contrast heterogeneous enhancement; it was surrounded by an edema and induced an important mass effect. he was transferred to the 2nd neurosurgery clinic, “prof. dr. n. oblu” emergency clinical hospital, iasi, romania, and a surgical intervention was performed the same day after admission with partial tumour resection. the histopathological examination identified an astrocytic tumour of low cellularity, moderate nuclear atypia and focal microcystic degeneration (figure 1, a and b). some tumoural cells demonstrated apoptotic changes (smaller size, dark eosinophilic cytoplasm, condensed and hyperchromatic chromatin) (figure 2, c and d). there were only few thin-wall vessels with near normal morphology (figure 2,e and f). the diagnosis of a secondary anaplastic astrocytoma, who grade iii (30), developed into a diffuse astrocytoma was established. approximately two weeks after his brain tumour surgery, the patient once again presented himself to our neurosurgical department with nausea, vomiting, diffuse headache, vertigo, and an episode of convulsive crisis. blood pressure was 130/70 mmhg, pulse = 88 beats/minute, and temperature = 36,8oc. neurological examination showed left facial paresis, muscular weakness and a slightly loss of sensibility of his left part of the body. some minimal changes of the preoperative laboratory investigation due to previous surgery were identified. there were a slightly increased absolute number of wbc (13.03x103 /mm3) and slightly elevated polymorphonuclear neutrophils (71.3%) on a differential count. in addition, a slightly fibrinogenemia (465 mg/dl) and slight hyperglycemia (120mg/dl) were recorded. brain ct scans revealed a right fronto-temporoparietal enhancing tumour with a digitiform perilesional edema, with larger dimensions than the first tumour and with compression and dislocation of medial cerebral structures to the left (approximately 13.1 mm). the patient underwent surgical therapy with partial resection of the tumour. the microscopical exam of hematoxylin-eosin (h&e) stained histological specimens revealed a highly malignant glial tumour made up of large, grotesque looking multinucleated giant cells, some containing up to 7 nuclei with abnormal shapes (figure 4, a-d). some of the nuclei contained prominent nucleoli and atypical mitotic figures. there were numerous blood vessels of various sizes and shapes, many of them presenting marked endothelial proliferation (figure 4, e and f). both large and small areas of ischemic necrosis were also observed. histological reevaluation of all the available specimens highlighted the fact that the tumour was in fact a secondary giant cell glioblastoma (sgcgb), who grade iv (30), developed in a diffuse astrocytoma nos. one week after surgery the patient had a first check-up brain irm scan that revealed an increase in the size of the lesion. the patient was referred to the regional institute of oncology in order to be treated with adjuvant chemotherapy (with temozolomide) and radiotherapy. it should be mention that the patient didn’t use any psychostimulants in all during this period. 388 l. eva, m.s. ples, m.r. munteanu et al. figure 1. preoperative axial head computed tomography scan (a. native; b. after contrast administration) performed on patient's first admission showed a large irregularly outlined cerebral lesion with central necrosis, peripheral contrast uptake, compression and dislocation of medial cerebral structures to the left. a b b c d a 389 secondary giant cell glioblastoma in a multiple drug abuser figure 2. histological sections of the first excised sample identified a glial tumor with focal microcystic degeneration and moderate cell density, made up of uniform cells resembling mature astrocytes, accompanied by dispersed anaplastic cells [a. (h&e, x10); b. (h&e, x40)]; at higher magnification, some tumoral cells revealed apoptotic changes (smaller size, dark eosinophilic cytoplasm, condensed and hyperchromatic chromatin) [c. (h&e, x40); d. (h&e, x100)]; there were also thin-wall vessels with near normal morphology, but surrounded by anaplastic astrocytic cells [e. (h&e, x100); f. (h&e, x100)]. figure 3. axial head computed tomography scans (a. native, b. after contrast administration) performed on patient's second admission (at two weeks after first tumor resection) identified temporal scalp swelling, temporal craniotomy and increased lesion size with compression and dislocation of medial cerebral structures to the left. e f b a 390 l. eva, m.s. ples, m.r. munteanu et al. figure. 4. histological section of the second excised sample pointed out a glial tumor with moderate cell density, and cellular and nuclear pleomorphism [a. (h&e, x40); b. (h&e, x40); a higher magnification revealed in some other areas a highly cellular tumor tissue made up of bizarre looking, giant glial cells, with rich eosinophilic cytoplasm and one or many hyperchromatic irregular shaped nuclei [c. (h&e, x100); d. (h&e, x100)]; in areas close to the central part of the tumor there were many thickwall vessels with disordered arrangement and moderate endothelial and pericytic proliferation [e. (h&e, x20); f. (h&e, x40)]. a b c d e f 391 secondary giant cell glioblastoma in a multiple drug abuser figure 5. axial mr images (a. flair; b. t1 gadolinium-weighted) performed at one week after the second surgery highlighted a huge heterogeneous infiltrating mass that filled frontal, temporal and parietal lobes, with extensive peripheral edema and midline shift, all these features being indicative of rapid tumor progression. discussion the world health organization (who) defines multiple drug use “as the use of more than one drug or type of drug by an individual, often at the same time or sequentially, and usually with the intention of enhancing, potentiating, or counteracting the effects of another drug” (31). the most common association is with caffeine, nicotine and alcohol. however, the most important is the association of cocaine, with various combinations of heroin, barbiturates, and marijuana. our patient, a multiple drug abuser, who used at least four types of drugs (cocaine, heroin, marijuana, and nicotine) during a period of at least 10 years, presented a glioblastoma that developed in his right fronto-temporo-parietal area, which is known to be affected by alterations due to drug abuse (32). major neuropathological mechanisms underlying chronic abuse of recreational psychostimulants (such as cocaine) or nicotine consist of pronounced levels of oxidative stress and mitochondrial dysfunction in the blood-brain-barrier (bbb) endothelium and perivascular cells, i.e. astrocytes, due to an uncontrolled increase in cellular reactive oxygen and nitrogen species (33, 34). the abuse of drugs also induces neuroinflammatory signals and disrupts glutamate homeostasis through their interaction with microglia and astrocytes (35). the german legist andreas büttner, who extensively investigated the neuropathological changes induced by chronic drug abuse, considered that the alterations of the intracellular messenger pathways, transcription factors and immediate early genes within the brain reward system are the most important factors for the development of addiction (25). in 2016, some american researchers concluded that cocaine determines the proliferation of human astrocytes as this drug increased cyclin a2 (an essential regulator of the cell cycle) expression in human astrocytes. lee et al. used cocaine with various concentrations and applied them to human astrocyte culture. they found that cocaine with increasing concentrations significantly increased human astrocyte proliferation using the jnk map kinase pathway as a driver of cell proliferation (36). a b 392 l. eva, m.s. ples, m.r. munteanu et al. in the same year, certain other american researchers (37) reported the potential of the psychostimulant drugs such as cocaine in inducing astrogliosis through the sequential activation of endoplasmic reticulum stress and autophagy in human astrocytes. it was possible to demonstrate that cocaine could also induce microglial activation via both the endoplasmic reticulum stress and autophagy pathways (38, 39). cocaine potentially modulates the immune response in the cns leading to an neuroinflammatory state that is characterized by enhanced activation of glial cells in the brains of addicts (40) as it seems that cocaine-mediatedincreased upregulation of gfap correlated with increased expression of proinflammatory mediators such as tnf, il1b, and il6 (37). reactive astrocytosis and microgliosis are classical features underlying neuroinflammation observed in drug abusers and in various neurodegenerative diseases. astrogliosis is accompanied by the release of a wide range of neurotoxic mediators consisting of chemokines, complementary factors, cytokines, growth factors and reactive oxygen species (41), which remodel the cellular homeostasis in the cns. recently, it has been reported that reactive astrocytes are prone to develop gliomas. taken into consideration, the older hansemann concept that tumours were derived by dedifferentiation of mature cells, it is possible to consider that astrocytes are able to dedifferentiate into a pluripotent precursor as a critical step in gliomagenesis (42, 43). in 2002, bachoo et al. showed that combined loss of p16(ink4a) and p19(arf), but not of p53, p16(ink4a), or p19(arf), enables astrocyte dedifferentiation in response to egfr activation (44) (https://www.ncb i.nlm.nih.gov/pmc/articles/pmc3033226/ r61) thus suggesting a possibility that an astrocyte, due to some extrinsic factors in its environment, could acquire some mutations necessary for its oncogenic transformation. based on all these scientific facts and the histopathological features of our patient’s tumour that revealed a sgcgb developed in a diffuse astrocytoma, we can presume that during those five years of cocaine use, astrogliosis and then gliomagenesis have been triggered. firstly, a low grade astrocytoma developed as we were able to see in the peripheral areas of the tumour. as he began to use heroin and marijuana, it is more likely that these substances had beneficial effects by reducing edemas, intra tumoural inflammation and the progression of the disease due to tumour cells apoptosis as some other reports have shown (45-46). because our patient wasn’t able to buy cocaine, heroin or marijuana over the last three years (however only ethnobotanical drugs containing at least benzodiazepine) the tumour slowly progressed to an anaplastic astrocytoma and ultimately to secondary glioblastoma as the histopathological features of these two tumours can be seen in the middle portion and in the center of the tumour, respectively. also, the absence of the symptoms induces by glioblastoma could correlate with the inhibitory role of benzodiazepine on glioblastoma proliferation (47). however, when the tumour had grown to considerable size, the patient presented periods of apathy alternating with periods of nervousness and ultimately somnolence, nausea and vomiting, that led him to the psychiatrist. many scientific studies have indicated the potential use of cannabinoids in the fight against cancer. experiments carried out on cell lines in vitro and on animal models in vivo have shown that phytocannabinoids, endocannabinoids, synthetic cannabinoids and their analogues can lead to inhibition of the growth of many tumour types, exerting cytostatic and cytotoxic neoplastic effects on cells thereby negatively influencing neoangiogenesis (48). our patient's glioblastoma showed extensive necrotic areas, however intra tumoural microvasculature was reduced and there was only mild proliferation of the pericytes, demonstrating neoangiogenesis inhibition probably due to the toxic effect of multiple drugs abuse. pokrywka et al. have shown that the main molecular mechanism leading to inhibition of glioma cell by cannabinoids is apoptosis, being a consequence of induction of endoplasmic reticulum stress and autophagy (49). indeed, a detailed examination of our patient's histological samples revealed many apoptotic tumour cells with cell shrinkage, dark eosinophilic cytoplasm, and condensed chromatin. forty years ago, white et al. (50) demonstrated the fact that cannabinoids inhibited tumour growth because delta9-tetrahydrocannabinol (delta9-thc) decreased dna synthesis in transformed cell cultures. more recently, other studies have 393 secondary giant cell glioblastoma in a multiple drug abuser investigated the molecular mechanism of anticancer effect of cannabinoids and have found that these substances inhibited tumour cell growth and induced apoptosis by modulating different cell signaling pathways e.g. via the upregulation of the endoplasmic reticulum stress-related genes atf-4, chop, and trb3 (51). delta (9)-tetrahydrocannabinol (thc), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy, a precursor event of apoptosis (52, 53). the first clinical study with the aim to evaluate cannabinoid anti tumoural action was a pilot study conducted in 2006 in a cohort of terminal patients harbouring recurrent glioblastomas (54). all these patients were administered δ9tetrahydrocannabinol intra tumouraly. inhibition of tumour-cell proliferation in vitro and decreased tumour-cell ki67 immunostaining were observed. literature has shown that giant cell glioblastoma represented a distinct pattern of cytogenetic alterations when compared with small cell glioblastoma and suggested that multinuclear giant cells evolved from a non-giant tumour cell at an early tumour stage (51). routine histological preparations of our patient's surgical specimens showed a variety of characteristic changes in tumour cell and nuclear morphology (prominent formation of giant monstrous cells, with bizarre, irregular, and hyperchromatic nuclei, a decrease in the number of mitoses, and severe cytoplasmic degeneration) indicating inhibition of tumour cell division. these morphological changes, quite similar with those induced by chemotherapy on glioma cells (56, 57), probably represent the effects of drug abuse on glial tumour cells. johnson and weissman also reported an interference of cocaine with cell replication as it produced fine structural nuclear alterations in cultured neuroglioblastoma cells. (58). in 1993, garg et al. exposed c6 glioma cells to cocaine and observed a reduced thymidine and uridine incorporation in these cells after four days of exposure (59). after almost ten years, other experimental studies have shown that various concentrations of cocaine caused a significant downregulation of cyp2c8 and cyp2c9 genes and a decrease in the level of cellular protein in human u373 mg astrocytoma cells (60). more recently, badisa et al. have demonstrated that the dual inhibition of cell cycle phases at g0/g1 and g2/m could appear in c6 glioma cells exposed to cocaine (61). all these articles represent the evidence that cocaine exposure may be the cause for the appearance of monstrous, bizarre looking nuclei identified in our patient's tumoural astrocytes as their cell cycle was affected. the main molecular mechanism leading to inhibition of proliferation of cancer cells by cannabinoids is apoptosis (49) which was also identified in great number in our patient's histological sections. conclusion the effects of illicit psychostimulant drugs exposure are not fully known. the morphological features identified in the histological samples of our patient revealed a sgcgb developed in a diffuse astrocytoma and in this respect, the case we presented in this paper was able to confirm the gliomagenesis effect of chronic multiple drug abuse. on the other hand, the drugs could have had inhibitory effects on tumour cells growth because, although the tumour was large in size and caused brain sub-falcine herniation, the patient only reported the onset of seizures late in the evolution. alongside the toxic effects on healthy organs and systems, these illicit drugs also have the effects of both inducing and inhibiting cancerogenesis, depending on the type of the drug. therefore, the diagnosis of a brain tumour should take into consideration not only patient's clinical and imaging data, but also his lifestyle, especially his addiction to recreational drugs. references 1. ribeiro li, ind pw. effect of cannabis smoking on lung function and respiratory symptoms: a structured literature review. npj prim care respir med. 2016, 26:16071. doi: 10.1038/npjpcrm.2016.71. 2. baldini a, von korff m, lin ehb. a review of potential adverse effects of long-term opioid therapy: a practitioner’s guide. the primary care companion to cns disorders. 2012; 14(3):pcc.11m01326. doi:10.4088/pcc.11m01326. 3. dushay km, evans sk, ghimire s, liu j. cocaine-induced diffuse alveolar hemorrhage: a case report and review of the literature. r i med j. 2016, 99(8):34-6. 4. kempker ja, honig eg, martin gs. the effects of marijuana exposure on expiratory airflow. a study of adults who participated in the u.s. national health and nutrition 394 l. eva, m.s. ples, m.r. munteanu et al. examination study. ann am thorac soc. 2015, 12(2):135-41. 5. zhuo l, liu q, liu l, sun ty, wang rs, qu gq, liu q, liu y, ren l. roles of 3,4-methylenedioxymethamphetamine (mdma)-induced alteration of connexin43 and intracellular ca(2+) oscillation in its cardiotoxicity. toxicol. 2013, 310:6172. 6. pacher p, steffens s, haskó g, schindler th, kunos g. cardiovascular effects of marijuana and synthetic cannabinoids: the good, the bad, and the ugly. nat rev cardiol. 2017 sep 14. doi: 10.1038/nrcardio.2017.130. [epub ahead of print] 7. alfaro r, vasavada n, paueksakon p, hernandez gt, aronoff gr. cocaine-induced acute interstitial nephritis: a case report and review of the literature. j nephropathology. 2013, 2(3): 204-209. 8. treadwell sd, robinson tg. cocaine use and stroke. postgrad med j. 2007, 83(980): 389–394. 9. cherland e, fitzpatrick r. psychotic side effects of psychostimulants: a 5-year review. can j psychiatry. 1999, 44(8):811-3. 10. favrod-coune t, broers b. the health effect of psychostimulants: a literature review. pharmaceuticals. 2010, 3:2333-2361. 11. pérez-hernández m, fernández-valle me, rubio-araiz a, vidal r, gutiérrez-lópez md, o'shea e, colado mi. 3,4methylenedioxymethamphetamine (mdma, ecstasy) produces edema due to bbb disruption induced by mmp-9 activation in rat hippocampus. neuropharm. 2017, 118:157-166. 12. kaye br, fainstat m: cerebral vasculitis associated with cocaine abuse. jama. 1987, 258:2104-2106. 13. solis e jr, cameron-burr kt, shaham y, kiyatkin ea. intravenous heroin induces rapid brain hypoxia and hyperglycemia that precede brain metabolic response. eneuro. 2017 jun 7;4(3). pii: eneuro.0151-17.2017. doi: 10.1523/eneuro.0151-17.2017. ecollection 2017 may-jun. 14. klonoff dc, andrews bt, obana wg. stroke associated with cocaine use. arch neurol. 1989, 46:989-993. 15. krendel da, ditter sm, frankel mr, ross wk: biopsy proven cerebral vasculitis associated with cocaine abuse. neurol. 1990, 40:1092-1094. 16. fitsiori a, nguyen d, karentzos a, delavelle j, vargas mi. the corpus callosum: white matter or terra incognita. br j radiol. 2011, 84(997): 5–18. 17. long h, zhou j, zhou x, xie y, xiao b. acute hydrocephalus following heroin induced leukoencephalopathy. neurol sci. 2013, 34(6):1031-2. 18. villella c, iorio r, conte g, batocchi ap, bria p. toxic leukoencephalopathy after intravenous heroin injection: a case with clinical and radiological reversibility. j neurol. 2010, 257(11):1924-6. 19. weber w, henkes h, möller p, bade k, kühne d. toxic spongiform leucoencephalopathy after inhaling heroin vapour. eur radiol. 1998, 8(5):749-55. 20. bach ag, jordan b, wegener na, rusner c, kornhuber m, abbas j, surov a. heroin spongiform leukoencephalopathy (hsle). clin neuroradiol. 2012, 22(4):345-9. 21. weber w, henkes h, möller p, bade k, kühne d. toxic spongiform leucoencephalopathy after inhaling heroin vapour. eur radiol. 1998, 8(5):749-55. 22. büttner a, rohrmoser k, mall g, penning r, weis s. widespread axonal damage in the brain of drug abusers as evidenced by accumulation of beta-amyloid precursor protein (beta-app): an immunohistochemical investigation. addiction. 2006, 101(9):1339-46. 23. weis s, büttner a. neurotoxicology and drug-related disorders. handb clin neurol. 2017, 145:181-192. 24. büttner a, mall g, penning r, sachs h, weis s. the neuropathology of cocaine abuse. leg med (tokyo). 2003, 5 suppl 1:s240-2. 25. büttner a. review: the neuropathology of drug abuse. neuropathol appl neurobiol. 2011, 37, 118–134. 26. fredericks rk, lefkowitz ds, challa vr, troost bt. cerebral vasculitis associated with cocaine abuse. stroke. 1991, 22(11):1437-1439. 27. büttner a. neuropathological alterations in cocaine abuse. curr med chem. 2012, 19(33):5597-600. 28. ramage sn, anthony ic, carnie fw, busuttil a, robertson r, bell je. hyperphosphorylated tau and amyloid precursor protein deposition is increased in the brains of young drug abusers. neuropathol appl neurobiol. 2005, 31(4):439-48. 29. efird jt, friedman gd, sidney s, klatsky a, habel la, udaltsova nv, van den eeden s, nelson lm. the risk for malignant primary adult-onset glioma in a large, multiethnic, managed-care cohort: cigarette smoking and other lifestyle behaviors. j neurooncol. 2004, 68(1): 5769. 30. louis dn, perry a, reifenberger g, von deimling a, figarella-branger d, cavenee wk, ohgaki h, wiestler od, kleihues p, ellison dw. the 2016 world health organization classification of tumors of the central nervous system: a summary. acta neuropathol. 2016, 131(6):803-20. 31. the world health organization lexicon of alcohol and drug terms, world health organization, geneva, 1994, p. 46. 32. verdejo-garcía a, pérez-garcía m, sánchez-barrera m, rodriguez-fernández a, gómez-río m. neuroimaging and drug addiction: neuroanatomical correlates of cocaine, opiates, cannabis and ecstasy abuse.rev neurol. 2007, 44(7):432-9. 33. walker j, winhusen t, storkson jm, lewis d, pariza mw, somoza e, somoza v. total antioxidant capacity is significantly lower in cocaine-dependent and methamphetamine-dependent patients relative to normal controls: results from a preliminary study. hum psychopharmacol. 2014, 29: 537–543. 34. sajja rk, rahman s, cucullo l. drugs of abuse and bloodbrain barrier endothelial dysfunction: a focus on the role of oxidative stress. j cereb blood flow metab. 2016, 36(3):53954. 35. bachtell rk, jones jd, heinzerling kg, beardsley pm, comer sd. glial and neuroinflammatory targets for treating substance use disorders. drug alcohol depend. 2017, 180:156-170. 36. lee ct, boeshore kl, wu c, becker kg, errico sl, mash dc, 395 secondary giant cell glioblastoma in a multiple drug abuser freed wj. cocaine promotes primary human astrocyte proliferation via jnk-dependent up-regulation of cyclin a2. restor neurol neurosci. 2016, 34(6):965-976. 37. periyasamy p, guo ml, buch s. cocaine induces astrocytosis through er stress-mediated activation of autophagy. autophagy. 2016, 12(8):1310-29. 38. bowers ms, kalivas pw. forebrain astroglial plasticity is induced following withdrawal from repeated cocaine administration. eur j neurosci. 2003, 17:1273–1278. 39. guo ml, liao k, periyasamy p, yang l, cai y, callen se, buch s. cocaine-mediated microglial activation involves the er stress-autophagy axis. autophagy. 2015, 11(7):995-1009. 40. clark kh, wiley ca, bradberry cw. psychostimulant abuse and neuroinflammation: emerging evidence of their interconnection. neurotoxicity res. 2013, 23:174-88. 41. anderson ma, ao y, sofroniew mv. heterogeneity of reactive astrocytes. neurosci letters. 2014, 565:23-9. 42. mclendon re, kleihues p. classification of tumors of the nervous system: an historical annotation. in: roger e. mclendon, marc k. rosenblum & darell d. bigner (edited by), russell & rubinstein's pathology of tumors of the nervous system, 7th edition, london, hodder arnold, 2006, pp. 4. 43. lassman ab, holland ec. molecular biology and genetic models of glioma and medulloblastoma, in: roger e. mclendon, marc k. rosenblum & darell d. bigner (edited by), russell & rubinstein's pathology of tumors of the nervous system, 7th edition, london, hodder arnold, 2006, pp. 1068-1069. 44. bachoo rm, maher ea, ligon kl, sharpless ne, chan ss, you mj, tang y, defrances j, stover e, weissleder r, rowitch dh, louis dn, depinho ra. epidermal growth factor receptor and ink4a/arf: convergent mechanisms governing terminal differentiation and transformation along the neural stem cell to astrocyte axis. cancer cell. 2002, 1:269– 277. 45. zagon is, mclaughlin pj. heroin prolongs survival time and retards tumor growth in mice with neuroblastoma. brain research bulletin. 1981, 7(1):25-32. 46. friesen c, hormann i, roscher m, fichtner i, alt a, hilger r, debatin km, miltner e. opioid receptor activation triggering downregulation of camp improves effectiveness of anticancer drugs in treatment of glioblastoma. cell cycle. 2014, 13(10):1560-70. 47. chen j, ouyang y, cao l, zhu w, zhou y, zhou y, zhang h, yang x, mao l, lin s, lin j, hu j, yan g. diazepam inhibits proliferation of human glioblastoma cells through triggering a g0/g1 cell cycle arrest. j neurosurg anesthesiol. 2013, 25(3):285-91. 48. chakravarti b, ravi j, ganju rk. cannabinoids as therapeutic agents in cancer: current status and future implications. oncotarget. 2014, 5(15): 5852–5872. 49. pokrywka m, góralska j, solnica b. cannabinoids a new weapon against cancer? postepy hig med dosw (online). 2016, 70(0):1309-1320. 50. white ac, munson ja, munson ae, carchman ra. effects of delta9-tetrahydrocannabinol in lewis lung adenocarcinoma cells in tissue culture. j natl cancer inst. 1976, 56(3):655-8. 51. carracedo a, lorente m, egia a, blázquez c, garcía s, giroux v, malicet c, villuendas r, gironella m, gonzález-feria l, piris ma, iovanna jl, guzmán m, velasco g. the stressregulated protein p8 mediates cannabinoid-induced apoptosis of tumor cells. cancer cell. 2006, 9(4):301-12. 52. salazar m, carracedo a, salanueva ij, hernández-tiedra s, lorente m, egia a, vázquez p, blázquez c, torres s, garcía s, nowak j, fimia gm, piacentini m, cecconi f, pandolfi pp, gonzález-feria l, iovanna jl, guzmán m, boya p, velasco g. cannabinoid action induces autophagy-mediated cell death through stimulation of er stress in human glioma cells. j clin invest. 2009, 119(5):1359-72. 53. zogopoulos p, korkolopoulou p, patsouris e, theocharis s. the antitumor action of cannabinoids on glioma tumorigenesis. histol histopathol. 2015, 30(6):629-45. 54. guzmán m, duarte mj, blázquez c, ravina j, rosa mc, galve-roperh i, sánchez c, velasco g, gonzález-feria l. a pilot clinical study of delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. br j cancer. 2006, 95:197–203. 55. martinez r, roggendorf w, baretton g, klein r, toedt g, lichter p, schackert g, joos s. cytogenetic and molecular genetic analyses of giant cell glioblastoma multiforme reveal distinct profiles in giant cell and non-giant cell subpopulations. cancer genet cytogenet. 2007, 175(1):2634. 56. gerstner l, jellinger k, heiss wd, wöber g. morphological changes in anaplastic gliomas treated with radiation and chemotherapy. acta neurochir (wien). 1977, 36(1-2):11738. 57. ogashiwa m, takeuchi k, akai k. [monstrous cell in malignant gliomas--in relation to radiation and chemotherapy (author's transl)]. no to shinkei. 1981, 33(7):733-42. 58. johnson je jr, weissman ad. cocaine produces fine structural nuclear alterations in cultured neuroglioblastoma cells. brain res bull. 1988, 20(1):39-47. 59. garg uc, turndorf h, bansinath m. effect of cocaine on macromolecular syntheses and cell proliferation in cultured glial cells. neurosci. 1993, 57(2):467-72. 60. malaplate-armand c, ferrari l, masson c, visvikis-siest s, lambert h, batt am. down-regulation of astroglial cyp2c, glucocorticoid receptor and constitutive androstane receptor genes in response to cocaine in human u373 mg astrocytoma cells. toxicol lett. 2005, 159(3):203-11. 61. badisa rb, darling-reed sf, goodman cb. cocaine induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat c6 astroglioma cells. neurochem res. 2010, 35(2):288-97. microsoft word 17pandeysharad_isolated romanian neurosurgery (2018) xxxii 4: 647 653 | 647             doi: 10.2478/romneu-2018-0084 isolated dorsal vertebral chondroblastoma: a rare case with review of literature s. pandey, k. kaushik, l.n. gupta, r. varshney, prarthana saxena department of neuro surgery, p.g.i.m.e.r. dr ram manohar lohia hospital, new delhi, india abstract: accounting for approximately 1-2% of all bone tumors, chondroblastoma is a benign bone tumor that is locally aggressive too typically affects the epiphyses or apophyses of long bones. less commonly affected sites include the talus and calcaneus of the foot and flat bones.vertebral involvement by chondroblastoma is very rare, with advance pubmed search we could find only 30 cases, reported in literature of vertebral chondroblastoma.we are presenting one such rare case with review of available literature to evaluate clinical radiological and pathological characteristics of vertebral chondroblastoma. key words: chondroblastoma, bone tumor, vertebral involvement introduction accounting for approximately 1-2% of all bone tumors, chondroblastoma is a benign bone tumor that is locally aggressive too typically affects the epiphyses or apophyses of long bones. it arises from an outgrowth of immature cartilage cells (chondroblasts) from secondary ossification centers, originating from the epiphyseal plate or some remnant of it.1 this tumour is known to be prevalent in children and young adults in the second decade of life18 with predilection towards the male sex (male to female ratio 2:1). it commonly involves the femur, followed by the humerus and tibia with talus and calcaneus of the foot and flat bones being the less affected.1 however, its vertebral involvement is very rare and with advanced pubmed search we could find only 30 cases of vertebral chondroblastoma, which have been so far reported in literature. one such rare case with review of available literature to evaluate clinical radiological and pathological characteristics of vertebral chondroblastoma is discussed below. case report history & clinical examination a 30 year male patient was admitted with chief complaints of backache for two months which was gradually progressive and was 648 | pandey et al isolated dorsal vertebral chondroblastoma             radiating to left subcostal region intermittently with aggravation of pain during walking or lifting any weight by forward bending. patient also developed insidious onset rapidly progressive ascending type of weakness of both lower limbs for last two weeks. however he had no bowel or bladder complaints. there was no history of trauma, recent fever or tuberculosis. on neurological examination: tone of bilateral lower limbs was increased (modified ashworth grade 2). power at hip and knee joints was 4/5 and ankle and below was 3/5(as per mrc grading).there was decreased sensation vibration & proprioceptionbelow 8th thoracic vertebra. the deep tendon reflexes of the lower limbs was exaggerated and babinski sign was present bilaterally. radiological examination plain x-ray shows osteolytic lesion involving right side of d7 vertebrae. m.r.i. thoracic spine revealed bony expansile lesion involving d7 vertebra with involvement of right transverse process, spinous process and right posterior body with involvement of adjacent paraspinal soft tissue, causing compression of spinal cord and signal change in the cord. patient was worked up for unknown primary and on lines of plasmocytoma which was negative. surgery by a posterior approach, he underwent d7 laminectomy and a thorough intralesional excision involving the posterior elements and the vertebral body, with complete decompression of spinal cord. d7 spinous process and right sided lamina and posterior part of body were eroded out by tumor, which was greyish yellow and moderately vascular. it was located in epidural space and there was no breach in dura. after tumor debulking spinal cord returned to normal position and began to pulsate. near total excision of tumor was achieved. a spinal stabilization was performed with a posterior fusion from d6 to d8 with pedicle screws and titanium rods post-operative course postoperatively patient was given thoracolumbar brace and gradually mobilized. there was gradual improvement in lower limb power and patient regained his normal power. there was no postoperative complication. histopathology showed multiple fragments of tumour composed of mononuclear oval to spindle cellsarranged in sheets with collagenised stroma. the cells show mild pleomorphism with nuclear groove and indentation intervening many thick and thin walled blood vessels, with chicken wire calcification andfocal cartilaginous differentiation. scattered osteoclast type of giant cells were also seen. these histopathological findings wereconsistent with chondroblastoma (figure 1). discussion the term chondroblastoma was described by ernest armory codman, in 1931 as an epiphyseal chondromatous giant cell tumor of the proximal humerus, hence the term codman tumor 11. this tumor was described to be benign in nature by henry l.jaffe and louis lichtenstein in 194212. romanian neurosurgery (2018) xxxii 4: 647 653 | 649             figure 1 histopatholgical slide showing cells mild pleomorphism with nuclear groove and indentation intervening many thick and thin walled blood vessels, with chicken wire calcification and focal cartilaginous differentiation.cartilage with chicken wire apparence although chondroblastoma occur most often in the epiphysis of the major tubular bones, this tumor can appear in any secondary ossification center, such as greater trochanter. one of the rare location of this tumor is vertebrae due to presence of a secondary ossification centre. first case of chondroblastoma of the mobile and nonmobile spine was reported in 19575. the incidence of vertebral chondroblastoma is 1.4% of all chondroblastomas, and 30 cases have been reported in the english (28 cases)4 and korean literature (two cases)5,6 (table 1). the most common location in spine is cervical followed by thoracic spine2. the most common presenting complaint is localised pain. the clinical findings are somewhat nonspecific and vary depending on the tumor extent and level of involvement. this tumor has a typical radiological finding of an eccentric osteolytic lesion, frequently accompanied by a thin sclerotic rim. vertebral chondroblastomas may sometimes appear malignant radiologically due to bony destruction and/or soft tissue extension, as compared to chondroblastomas of the extremities, which are usually well demarcated from surrounding bony tissue2,4,7,12,13. however, these findings are nonspecific in vertebral chondroblastomas thus not of much diagnostic help. spinal cord compression and/or neurological deficit occasionally accompany the lesion2,4,14. therefore, the possibility of vertebral chondroblastoma should be kept in mind if vertebral mass imaging findings are reminiscent of a malignancy such as a destructive bony lesion with large soft mass formation or spinal invasion. the differential diagnosis includes both benign and malignant lesions, including tuberculous spondylitis, eosinophilic granuloma, aneurismal bone cyst (abc), giant cell tumor, chondromyxoid fibroma, osteoid osteoma, osteoblastoma, chondrosarcoma, and metastasis. the final diagnosis should be confirmed by histological examination. as far as size is concerned these tumors range from 2.3 cm to 8.2 cm (diameter). with respect to histological findings vertebral chondroblastoma are not different from chondroblastomas at other usual sites. this tumor is defined to be cellular with sheets of uniform roundto polygonal mononuclear cells with well-defined cytoplasmic borders which have clear to slightly eosinophilic cytoplasm with occasional nuclear grooves admixed with scattered giant cells3. importantly, chondroid differentiation and characteristic chicken-wire calcification are needed to confirm the diagnosis admixed with scattered giant cells. approximately 35-50% of chondroblastomas show matrix calcification 4,14 and more than one-third of chondroblastomas contain secondary abc-like changes 3,10. 650 | pandey et al isolated dorsal vertebral chondroblastoma             table i author no. of cases sex/age neurological deficit location extent operation follow-up braczewski et al (1957) [2] 1 m/28 yes t3/t4 ste laminectomy and debulking 24 months symptomfree ehalt et al (1967) [3] 1 m/12 ns cervical spine ns surgical treatment recurrence wisniewski et al (1973) [4] 1 m/17 no c1, c2 ste curettage ns akai et al (1986) [5] 1 m/48 no s1 ste curettage 120 months recurrence and death from renal failure hoeffel et al 1987 [6] 1 m/9 yes c7 ste repeated surgery 72 months recurrence and death from tetraplegia howe et al (1988) [7] 1 m/16 yes c5, c6 st e combined anterior and posterior surgery no information kurth et al (2000) [8] 1 m/62 no t1, t2 st e repeated surgery 4 recurrences malignant transformation shin et al (2001) [9] 1 f/36 no l1 no mass excision 14 months ned leung et al (2001) [10] 1 f/54 yes lower lim weakness l5 sce and ste intracapsular tumor excision, l5 vertebrectomy two recurrences then lost to follow-up nishida et al (2001) [11] 1 m/19 yes tetrapresis c5, c6, c7 sce and ste thorough curettage. combined anterior and 2 years and 3 months ned neurologic deficit fully recovered ned romanian neurosurgery (2018) xxxii 4: 647 653 | 651             posterior approaches attar et al (2001) [12] 1 m/48 no t2 sce thorough curettage. combined anterior and posterior approaches ns shung et al (2003) [13] 1 m/54 yes cauda equine syndrome l5 sce and ste combined anterior and posterior surgery. intralesional excision two recurrences death after 44 months ilaslan et al (2003) [14] 9 mean age 28, 6m & 3f ns c2,t5, l1, s1 sce in 6 cases & ste in all cases ns ns vialle et al (2005) [15] 2 f/55, f/23 no l4/l3 ns vertebrectomy in two cases 6 years ned 3 years ned lee yh et al (2005) [16] 1 m/40 yes lower extremity weakness t7 sce and ste combined anterior and posterior surgery, t7 vertebrectomy ns sohn et al (2009) [17] 1 m/21 no l4 lung metas tasis total laminectomy of l4, thoracic surgery for pulmonary biopsy 3 years ned mohamed et al (2011) [18] 1 m/46 no t12l1 ste total laminectomy t11t12l1 died one day after operation because of bleeding hernández martínez et 1 f/30 no l4 no ns ns 652 | pandey et al isolated dorsal vertebral chondroblastoma             al (2011) [19] kim sa et al (2011) [20] 1 m/25 no l3 sce total tumor resection 18 months ned osman w et al(2014) [21] 1 m/18 yes b/l paraperesis d12 ste total laminectomy t11t12l1 with d10 to l2 fusion 12 years with lacal relapse after 12 years giri p.j et al (2017) [22] 1 m/17 yes b/l paraperesis d8 d6 d7 laminectomy ns ns: non specified, ste: soft tissue extension, sce: spinal canal extension, ned: non evidence of disease treatment modality of this tumor is usually simple curettage with bone grafting. recurrence depends on anatomical location. chondroblastomas of the spine behave more aggressively due adjacent vertebrae destruction and resulting neurological complications 2,7,10,17,18 with a higher rate of relapse and mortality. hence, efforts should be directed towards complete excision which is the recommended treatment modality for vertebral chondroblastomas2,10,11. however, frequent involvement of the spinal canal and paraspinal muscles makes it difficult to completely remove the tumor without neurological deficit. local recurrence occurs in about one-third of patients4,17,18 and is apparently higher than that of extraspinal chondroblastoma, which is 5-18% 3,11,13.this may be attributed to the frequent extension to adjacent soft tissue and the spinal canal, which hinders complete resection 11. high recurrence rate and difficult complete resection necessitates the need for follow up over the long-term post surgery. to summarise this was a case report of chondroblastoma arising in the lumbar spine with a sincere effort to review the relevant literature. for any vertebral mass appearing aggressive on imaging findings chances of it being vertebral chondroblastoma should be kept in mind and a histopathology should be performed to confirm the same. one should not forget that vertebral chondroblastomas may behave differently from those of chondroblastomas of the extremities. lastly, long-term clinical follow-up is required as far as vertebral chondroblastomas are concerned. correspondence sharad pandey department of neurosurgery p.g.i.m.e.r. dr ram manohar lohia hospital, new delhi110001, india previously with department of neuro surgery, sir sunder lal hospital, ims, bhu, romanian neurosurgery (2018) xxxii 4: 647 653 | 653             varanasi, uttar pradesh -221005, india. contact number 9454939067 email address drsharad23@yahoo.com references 1.dahlin, d.c., ivin, j.c., “benign chondroblastoma: a study of 125 cases”. cancer, 30(2), 401-413, aug 1972. 2.buraczewski, j., lysakowska, j., rudowski, w., “chondroblastoma (codman's tumour) of the thoracic spine”. j bone joint surg br, 39-b(4), 705-710, 1957. 3.ehalt, w., ratzenhofer, m., “on the case history of a benign chondroblastoma”. z orthopihregrenzgeb, 102(4), 625-629, 1967. 4. wisniewski, m., toker, c., anderson, p.j., huang, y.p., malis, l.i., “chondroblastoma of the cervical spine. case report”. j neurosurg, 38(6), 763-766, 1973. 5. akai, m., tateishi, a., machinami, r., iwano, k., asao, t., “chondroblastoma of the sacrum. a case report”. actaorthopscand, 57(4), 378-381, 1986. 6. hoeffel, j.c., brasse, f., schmitt, m., plenat, f., vignaud, j.m., czorny, a., montaut, j., marchal, a.l., “about one case of vertebral chondroblastoma”. pediatrradiol, 17(5), 392-396, 1987. 7. howe, j.w., baumgard, s., yochum, t.r., sladich, m.a., “case report 449: chondroblastoma involving c5 and c6”. skeletal radiol, 17(1), 52-55, 1988. 8.kurth, a.a., warzecha, j., rittmeister, m., schmitt, e., hovy, l., “recurrent chondroblastoma of the upper thoracic spine. a case report and review of the literature”. arch orthop trauma surg, 120(9), 544-547, 2000. 9. shin, b.j., yun, t.k., lim, k.c., lee, j.c., kim, k.j., kim, d.w., kim, y.i., “chondroblastoma of the first lumbar vertebra: a case report”. j korean soc spine surg, 8, 90-95, 2001. 10. leung, l.y., shu, s.j., chan, m.k., chan, c.h., “chondroblastoma of the lumbar vertebra”. skeletal radiol, 30(12), 710-713, dec 2001. 11. nishida, j., kato, s., murakami, h., ehara, s., satoh, t., okada, k., shimamura, t., “tetraparesis caused by chondroblastoma of the cervical spine: a case report”. spine (phila pa 1976), 28(9), e173-178, may 2003. 12. attar, a., ugur, h.c., caglar, y.s., erdogan, a., ozdemir, n., “chondroblastoma of the thoracic vertebra”. j clinneurosci, 8(1), 59-60, jan 2001. 13.shung, o.m., yip, s.f., ngan, k.c., ng, w.f., “chondroblastoma of the lumbar spine with cauda equina syndrome”. spinal cord, 41(6), 359-364, jun 2003. 14.ilaslan, h., sundaram, m., unni, k.k., “vertebral chondroblastoma”. skeletal radiol, 32(2), 66-71, feb 2003. 15.vialle, r., feydy, a., rillardon, l., tohme-noun, c., anract, p., colombat, m., de pinieux, g., drapé, j.l., guigui, p., “chondroblastoma of the lumbar spine. report of two cases and review of the literature”. j neurosurg spine, 2(5), 596-600, may 2005. 16. lee, y.h., shin, d.a., kim, k.n., yoon, h., “a case of thoracic vertebral chondroblastoma, treated with 3-d image resection and reconstruction”. j korean neurosurgsoc 37,154-156, 2005. 17.sohn, s.h., koh, s.a., kim, d.g., park, s.w., lee, k.h., kim, m.k., choi, j.h., hyun, m.s., “a case of spine origin chondroblastoma metastasis to lung”. cancer res treat, 41(4), 241-244, dec 2009. 18. mohamed, b., madiha, m., ridha, s., abdelaziz, z., khelil, e., mondher, k., mongi, z., “aggressive spinal chondroblastoma”. tunis med, 88(2),134-136, feb 2010. 19. hernández martínez, s.j., campanúñez, h., ornelas cortinas, g., garza garza, r., “chondroblastoma of the fourth lumbar vertebra diagnosed by aspiration biopsy: case report and review of the literature”. actacytol, 55(5), 473-477, 2011. 20. kim, s.a., cho, k.j., park, y.k., lee, j.s., kwon, h.j., chung, h., kim, m.j., “chondroblastoma of the lumbar spine. a case report and review of the literature”, korean journal of pathology, 45, 532-536, 2011. 21.osman1w, zaouia, abdelkrimsb, hamidarb, ayèche mb, “ chondroblastoma of the lower thoracic spine. a case report and review of the literature.”ajmcr/2/4/2 78-81,2014 22.giri pj, vaibhav. chavans, “chondroblastoma of thoracic vertebra in young adult causing paraparesis” romanian neurosurgery (2017) xxxi 3: 335 338 | 335doi: 10.1515/romneu-2017-0054 doi: 10.33962/roneuro-2022-057 intradiploic meningioma. a series of two cases and literature review neha singh, deepak kumar singh, rakesh kumar romanian neurosurgery (2022) xxxvi (3): pp. 342-345 doi: 10.33962/roneuro-2022-057 www.journals.lapub.co.uk/index.php/roneurosurgery intradiploic meningioma. a series of two cases and literature review neha singh1, deepak kumar singh2, rakesh kumar2 1 department of radiodiagnosis and imaging, dr ram manohar lohia institute of medical sciences, lucknow, india 2 department of neurosurgery, dr ram manohar lohia institute of medical sciences, lucknow, india abstract intradiploic meningioma is a rare subtype of primary intraosseous meningiomas. the convexity and the skull base are the two primary locations for intraosseous meningiomas. they usually present as a painless expansile mass without any neurological findings. intradipoic meningiomas are seldom correctly diagnosed preoperatively and are usually mistaken for primary bone tumours. ct scan head with bone windows and contrast-enhanced mri brain should be done for diagnosis and evaluation. intraosseous meningioma should be considered in the differential diagnosis of patients presenting with osteoblastic or osteolytic skull lesions as the treatment of choice is resection, which is potentially curative. introduction primary intraosseous meningioma is the most uncommon manifestation of meningiomas.1 the extradural or ectopic meningiomas form 1-2 % of all meningiomas, which was first described by winkler, in 1904 [5,8]. most of the intraosseous meningiomas arise from cranial bones, although a few cases in the mandible have been reported [4]. intradiploic meningioma is a term to describe the purely calvarial meningioma. preoperative diagnosis of intradiploic meningioma is very difficult and often diagnosed as bone tumours or metastasis. here we are reporting two cases of intradiploic meningioma presented with painless scalp swelling and surgically treated with good outcome. case report case 1 a 45-year-old man presented with a painless scalp swelling in right fronto-parietal region. the scalp swelling was present for last 6 years and had gradually increased in size. there was no history of trauma. physical examination revealed a swelling in the right fronto-parietal region about 3 cm in diameter. swelling was non tender, immobile and not adhered to the overlying skin. the patient had no neurologic deficit. keywords primary intraosseous meningioma, intraosseous meningioma, intradiploic meningioma corresponding author: neha singh dr ram manohar lohia institute of medical sciences, lucknow, india neha.singh.dr@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 343 intradiploic meningioma the laboratory studies were unremarkable. ct head revealed a right-sided fronto-parietal intradiploic mass expanding the calvaria with marked thinning of both inner and outer tables with areas of cortical breach. the lesion was protruding extra cranially causing focal bulge over the scalp. the intracranial component was causing compression of underlying brain parenchyma. mr imaging showed a solitary calvarial mass lesion of the frontoparietal region that was hyper intense on t2-weighted images, hypo intense on t1-weighted and was showing marked post contrast enhancement. mr imaging also demonstrated intracranial but extradural extension of the lesion. (figure 1) preoperative diagnosis of primary or secondary malignant osteolytic lesion was made. complete workup was done to rule out calvarial metastasis but no primary could be found. per-operatively scalp was easily elevated from tumour and there was destruction of both the inner and outer tables of the claverium with extradural extention. total tumour removal with a wide surgical resection followed by cranial reconstruction was done. final histopathological diagnosis of intradiploic meningioma was made. at one year follow up, patient was doing well without any evidence of recurrence. figure 1. (a) axial image of ncct brain in bone window shows right-sided fronto-parietal intra-diploic mass (*) expanding the calvarium with large intra and extra cranial components causing marked thinning of both inner and outer tables with areas of cortical breach. mri brain shows large intra-diploic expansile lesion (b) hyper-intense on coronal t2wi, (c) hypointense on axial t1wi, and (c) marked enhancement on coronal fat supressed t1wi. displacement of duramater and compression of underlying brain parenchyma by the intracranial component of the lesion is clearly visible (arrow). case 2 a 50-year-old man presented with a painless progressive swelling of scalp the right frontal region and headache for eight years. there was no history of trauma. physical examination revealed a swelling of about four cm diameter in the right frontal region. swelling was non tender, nonmobile and not adhering to the overlying skin. figure 2. (a) axial image of ncct brain in bone window and (b) soft tissue window shows right-sided frontal intra-diploic expansile lesion (*) with intra and extra cranial components causing destruction of both inner and outer tables. mri brain shows large intra-diploic expansile lesion (c) t2wi of mri brain in coronal plane shows hyper-intense lesion causing compression of underlying brain. (d) peroperative image showing extracalvarial component of the lesion. the patient had no signs of neurologic deficit. the laboratory investigations were within normal limits. ct scan of head revealed a right-sided frontal intradiploic mass expanding the calvaria with destruction of both inner and outer tables. the lesion was extending both intraand extra cranially. mr imaging showed a solitary calvarial mass 344 neha singh, deepak kumar singh, rakesh kumar lesion of the frontal region that was hypo intense on t1-weighted and hyper intense on t2-weighted images with post contrast enhancement. the lesion showed intracranial but extradural extension of the lesion. (figure 2) preoperative diagnosis of primary or secondary malignant osteolytic lesion was made. complete workup was done to find out primary lesion anywhere else in the body, however tests were negative. per-operatively scalp was easily elevated from tumour and there was destruction of both the inner and outer tables of the calvarium with extradural extension of the lesion. total tumour removal with a wide surgical resection followed by cranial reconstruction was done. histo-pathological features were suggestive of intradiploic meningioma. on six months follow up patient was well without any evidence of recurrence. discussion primary intraosseous meningioma is a subtype of extradural meningiomas that arise in bone and does not involve the underlying dura [7]. approximately 68% of the primary extradural meningiomas involved the calvaria. intraosseous meningiomas most commonly involve the fronto-parietal and orbital regions. primary extradural meningiomas occur approximately with equal frequency in both sexes. primary intradural and extradural meningiomas occur predominantly during later decades of life with a second peak incidence in younger patients (especially during the second decade) in primary extradural meningiomas [3]. lang et al. classified interosseous meningiomas as type ipurely extracalvarial, type iipurely calvarial and type iiicalvarial with extracalvarial extension. the type ii and iii are further divided as convexity (c) or skull base (b) forms [3]. thus, intraosseous meningiomas could be considered type ii or iii primary extradural meningiomas based on whether extracalvarial extension is observed or not, while intradiploic meningiomas are type ii only [3]. there are three explanations for the origin of primary intraosseous meningioma. first being the trapping of arachnoid cap cells in the cranial sutures during birth and head molding suggested by azarkia, et al. it is thought that the formation of small meningoceles containing arachnoid cells during that period which got entrapped within the cranial sutures and give rise to intraosseous meningiomas later in life [1]. second postulated theory states that lesions are secondary to previous trauma which was first described by cushing and eisenhardt [2]. thirdly it has been postulated that meningiomas may arise from mesenchymal precursors, in reaction to a yet unknown stimulus [9]. usually, the neurological signs and symptoms are absent in the patients. a painless expansile mass without any neurological finding is usually the initial symptom. the symptoms are dependent on tumor location, size, and involvement of the neighbouring structures. meningiomas presenting with scalp swelling and extracranial soft-tissue masses are more aggressive in nature than others [10]. osteolytic meningiomas associated with a soft-tissue component must be considered malignant until proven otherwise [6]. although calvarial meningiomas have been observed to be benign and slow-growing, but they are more prone to develop malignant changes (11%) compared with intracranial meningiomas (2%) [3]. bone remodelling and calvarial thickening at the site of origin of the meningioma are frequent with these tumors. in calvarial meningiomas osteolytic skull lesions are also known to occur. hyperostosis is the most common radiographic finding (reported in 59% of the cases) but osteolysis, as in our case is also reported in 35% of the cases. mixed picture of hyperostosis and osteolysis is reported in 6% of the cases in the literature [2]. scalp swelling with osteolytic skull lesions and extracranial soft-tissue masses suggest the aggressiveness of meningioma. ct scan head with bone windows is necessary to detect the tumor, cortical destruction, and both intraand extraosseous extension. mri brain provides a better anatomic delineation in the evaluation of the soft tissue component and extradural extension of the lesion. although rare, intraosseous malignant meningioma should be excluded in an osteolytic skull lesion associated with soft-tissue component. complete tumour excision with a wide surgical resection followed by cranial reconstruction is the treatment of choice in symptomatic primary intradiploic meningioma. in subtotal resection due to involvement of critical structures within the orbit, paranasal sinuses, or skull base radiological follow up is mandatory [2]. in symptomatic residual lesions and lesion showing evidence of progression adjuvant radiation therapy is recommended [2]. 345 intradiploic meningioma conclusions in the patient having osteolytic calvarial lesions associated with a soft-tissue component, a primary intraosseous meningioma should be considered. osteolytic meningiomas associated with a soft-tissue component must be considered malignant until proven otherwise. ct scan head with bone windows and mri brain should be done for diagnosis and evaluation. by keeping the defferential diagnosis in mind while evaluation, this can be treated with good outcome. complete excision with a wide surgical resection followed by cranial reconstruction should be done. references 1. azar-kia b, sarwar m, marc ja, schechter mm: intraosseous meningioma. neuroradiology 6:246–253, 1974. 2. crawford t s, ette k. kleinschmidt. demasters and kevin. o. lillehei: primary intraosseous meningioma. j neurosurg .83:912–915, 1995. 3. lang ff, macdonald ok, fuller gn, demonte f: primary extradural meningiomas: a report on nine cases and review of literature from the era of computerized tomography scanning. j neurosurg. 93:940–950, 2000. 4. lell m, tudor c, aigner t, kessler p: primary intraosseous meningioma of the mandible: ct and mr imaging features. am j neuroradiol. 28:129–131, 2007. 5. muzumdar dp, vengsarkar us, bhatjiwale mg, goel a: diffuse calvarial meningioma: a case report. j postgrad med. 47:116–118, 2001. 6. partington md, scheithauer bw, piepgras dg:carcinoembryonic antigen production associated with an osteolytic meningioma. case report. j neurosurg 82:489-492,1995. 7. politi m:intraosseous hemangioma of the skull with dural tail sign: radiologic features with pathologic correlation.am j neuroradiol. 26:2049-2052, 2005. 8. pompili a, caroli f, cattani f, iachetti m:intradiploic meningioma of the orbital roof. neurosurgery.12:565568, 1983. 9. willis ra: pathology of tumors, ed 4. london: butterworths, pp 658–662, 736–746, 1967. 10. younis g, sawaya r: intracranial osteolytic malignant meningiomas appearing as soft-tissue masses. neurosurgery .30:932–935,1992. doi: 10.33962/roneuro-2022-027 multimodal treatment of glomus jugular tumours. case series and literatur e review f. stoica, g. popescu, francesca paslaru, anamaria gheorghiu, a.c. paslaru, m. apostol, m.c. zaharia, r.m. gorgan romanian neurosurgery (2022) xxxvi (2): pp. 150-154 doi: 10.33962/roneuro-2022-027 www.journals.lapub.co.uk/index.php/roneurosurgery multimodal treatment of glomus jugular tumours. case series and literature review f. stoica1, g. popescu1, francesca paslaru1, anamaria gheorghiu1, a.c. paslaru2,3, m. apostol1, m.c. zaharia1, r. m. gorgan1,2 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 department of genetics, “dr victor gomoiu” children’s clinical hospital, bucharest, romania abstract glomus jugulare tumours are extremely rare, slow-growing, hypervascular tumours that arise within the jugular foramen of the temporal bone and frequently involve the lower cranial nerves. we performed a retrospective study for patients treated between january 2005 and december 2019, reviewing clinical and radiological data for 91 cases of glomus jugulare tumours. data were available for 91 patients presenting with 96 tumours. surgery was 1st intention of treatment for 13 cases, the endovascular approach was 1st intention for 6 cases and gkrs was primarily performed in 72 cases. combined treatment options were used in 19 cases. the median age at the time of treatment was of 57 years. the tumour volume varied between 0.5 and 73.4 cm3 with a median value of 8.3 cm3. for the cases treated with gkrs, the peripheral dose ranged between 8 and 35 gy on the 35% to 65% isodose, with a median of 14 gy on the 45% isodose. the average follow-up was 38 months with a maximum of 94 and consisted of contrast-enhanced mri every six months in the first year after the procedure and every 1 to 2 years afterwards. the overall tumour control rate was 95.6% using multimodal treatment options for glomus jugulare tumours. multimodal treatment for glomus jugulare tumours offers the patient the chance for the best possible outcome and long-term survivability. an individual treatment approach for this kind of very rare head and neck tumour (0,6% of all head and neck tumours) is recommended to choose the best risk-versus-benefit treatment option. background glomus jugulare tumor is a benign neuroendocrine tumor that arises from the jugular foramen. this tumor characterized by a slow-growing pattern. paragangliomas, also known as chemodectomas represent benign tumors with the origin from neural crest derivates also known as the parangalia [1],[2],[3]. these tumors are highly vascularised. they can receive blood supply from both from the external carotid artery and internal carotid artery. the localization of these tumours can widely keywords tumour, glomus, jugular corresponding author: g. popescu 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 151 multimodal treatment of glomus jugular tumours vary, from carotid bifurcation to the auricular branch of the vagus nerve. the most frequent localization is the carotid body, accounting for almost half of the tumors [5], [6] whereas glomus jugulare tumors represent 24% of them [6]. even though they are benign tumors, the symptomatology can be the cause of the mass effect [2]. usually, these tumors are diagnosed in the fourth to sixth decade of life, with a moderate female predilection. most of the glomus jugulare tumors are isolated lesions but around 20% of them present hereditary components [4]. the inherited tumors are usually bilateral and the onset of the symptoms is reported to be earlier than the onset symptomatology of the sporadic tumors. the reported malignancy of these tumors is less than 5% [2]. around 25% of the paragangliomas remain silent and are incidentally discovered. the symptoms caused by these tumors depend on their location. lower cranial nerves impairment is reported in more than 10% of patients [8]. the most common neurological deficits reported are tongue deviation, hoarseness, facial palsy, dysphagia, and shoulder weakness [2],[7],[8]. additionally, patterns of cranial nerve palsies were described and these include [12]: • vernet syndrome that represents motor paralysis of cranial nerves ix, x and xi; [9] • colletsicard syndrome described as the palsy of cranial nerves ix,x,xi and xii; [10] • horner syndrome – oculosympathetic palsy. [11] due to its slow-growing pattern and the complex anatomy of the skull base and neck, observation of the patient is considered a good treatment alternative. in more than 60% of the cases, tumor volume remains stable or decrease in size [14]. however, if the tumor tends to be symptomatic, surgical excision or stereotactic radiosurgery will be take into account. case series we performed a retrospective study for patients treated between january 2005 and december 2019, reviewing clinical and radiological data for 91 cases of glomus jugulare tumors. data were available for 91 patients presenting with 96 tumors. surgery was the treatment of choice for 13 cases, endovascular embolization was performed as first intention treatment for 6 cases and gkrs was primarily performed in 72 cases. figure 1. distribution of the treatment option combined treatment options were used in 19 cases (1 surgery with gkrs, 18 endovascular with gkrs). 44 glomus jugulare tumors were identified on the right side, and 47 on the left side. in the study group, we had 23 male patients and 63 female patients. 11 patients were in the 15-39 age group while 80 patients were older than 40 yrs. the median age at the time of treatment was of 57 years. the tumor volume varied between 0.5 and 73.4 cm3 with a median value of 8.3 cm. for the cases treated with gkrs, the peripheral dose ranged between 8 and 20 gy on the 35% to 65% isodose, with a median of 14 gy on the 45% isodose. the average follow-up was 38 months with a maximum of 94 and consisted of contrast-enhanced mri every six months in the first year after the procedure and every 1 to 2 years afterward. overall tumor control rate was 95.6% using multimodal treatment options for glomus jugulare tumors. table 1. most common comorbidities comorbidity lower cranial nerves deficits dizziness tinnitus hearing impairment hemorrhages hydrocephalus hemiparesis treatment approach 13, 14% 6, 7% 72, 79% 152 f. stoica, g. popescu, francesca paslaru et al. comorbidities were noted in 37 patients (40.6%) and consisted of lower cranial nerves deficits (26.4%), dizziness, tinnitus, partial or complete hearing loss in 21.9% of cases, 2 hemorrhages, 2 secondary hydrocephalus, and 1 hemiparesis. 23 patients (24.3%) presented recurrences: 13 after surgery, 6 after embolization, and 4 after gkrs. however, the mortality rate was 0. case 1 the first case is represented by a female patient of 53 years old, whose symptoms are vertigo, hearing loss, and pulsating tinnitus. soon it is discovered the typical aspect of “salt and pepper” for a glomus tumor with temporal localization, millimetric extracranial extension into jugular vein lumen and damage to the structures of the inner ear. 9 years after gkrs, a cerebral mri was performed, which showed that the irradiated tumor volume has been reduced in circumferential dimensions, with a homogeneous intake of contrast substance ("densified" appearance due to sclerosis and obliteration of intratumoral blood vessels) without adverse reactions due to irradiation. no new neurological deficits were recorded after gkrs. figure 2. preoperative aspect of the tumour figure 3. postoperative aspect after gamma knife radiosurgery case 2 the second case is represented by a 62 years old female patient, whose symptoms onset with injury to multiple cranial nerves (vii, viii, ix, xi, xii). the diagnosis was represented by a large glomic tumor with an important intracranial component with a mass effect on the brainstem. a cerebral mri was performed 4 years post gkrs, showing a marked reduction in the size of the irradiated tumor, especially in the intracranial component, with a significant decrease in the mass effect, without perilesional reactive edema. no new neurological deficits were recorded. 18 months after irradiation, a complete remission of facial paresis has been noticed and other cranial nerves neurological status remained stationary. figure 4. preoperative aspect of the tumour 153 multimodal treatment of glomus jugular tumours figure 5. postoperative aspect after gamma knife radiosurgery case 3 for the third case, we have a 35 years old male patient, who presented with glomic tumor located in the temporal bone, onset with hearing disorders (hearing loss and pulsating tinnitus). 6 years after gkrs, a periodic follow-up mri has been performed. the inferior recurrence in the lumen of the jugular vein was identified outside the irradiation field with a volume of 4.6 cm3, asymptomatic. the decision is made in order to irradiate the recurrence with 14 gy on 47% isodose. figure 6. preoperative aspect before gamma knife radiosurgery figure 7. the recurrence aspect, 6 years after gkrs discussions the best treatment option for glomus jugulare tumors is yet to be debated. due to their localization, surgical treatment does not represent the gold standard because of the complex anatomy of the region, high rates of morbidity, subtotal resection, and the alternative behavior of the tumors that could be very aggressive in some cases. in 2003, roberto pareschi et al [15] described their experience in the surgical treatment of glomus jugulare tumors. 42 patients with glomus jugulare tumors were identified, 3 of them previously undergone surgery for this pathology, and 3 patients presented bilateral temporal lesions. the otoscopic evaluation revealed in 80% of the patients the typical red middle ear mass. 70% of the cases had no preoperative cranial nerve deficit. 37 seven patients were elected for surgical intervention. in 33 cases, infratemporal fossa approaches were used and in 4 cases, conservative jugulopetrosectomy was performed, in order to preserve the facial nerve. in 20% of the cases, cranial nerves ix and x were injured. no recurrence after total resection was reported. an extensive dissection of the posterolateral skull base is required for surgery of glomus jugulare tumors [15]. even though cranial nerve preservation is an extremely important goal in the surgical approach, in 22% of the cases facial nerve is sacrificed [15]. the authors concluded that the focus should drift away from total resection to increasing the quality of life of the patient, a philosophy that our clinic shares. only 14% percent of our cases were surgically treated, in order to avoid the decrease in the quality of patient`s life. endovascular treatment is an alternative treatment approach for patients with glomus jugulare tumors. in 2017, kocur et al [17] presented their experience and the outcome of embolization in 3 cases of glomus jugulare tumors. they described the technical difficulty of achieving complete obliteration of the glomus jugulare tumors and concluded that increased risk of revascularization is not beneficial compared to the diminished clinical symptoms. in our clinic, only 6 endovascular treatments were performed. a promising approach for this pathology is represented by radiosurgery. due to the high degree of accuracy, rapid radiation dose falloff at the periphery of the target tumor, and their high precision, radiosurgery became a popular treatment 154 f. stoica, g. popescu, francesca paslaru et al. choice. in their meta-analysis, guss et al [13] included 19 studies, compounding 335 glomus jugulare patients. they reported a reduced or unchanged tumoral volume after radiosurgery, sustained by imagistic findings. clinical control was reported as improved or unchanged after radiosurgery in 95% of the cases. the authors emphasized the effectiveness of this treatment option. in our clinic, 72 patients benefited from radiosurgery. conclusions multimodal treatment for glomus jugulare tumors offers the patient the chance for the best possible outcome and long-term survivability. individual treatment approach for this kind of very rare head and neck tumor (0,6% of all head and neck tumors) is recommended to choose the best risk-versus-benefit treatment option. gkrs in these kinds of tumors seems to be the option of choice, considering that in our experience, has the lowest comorbidity, recurrence rate and mortality. references 1. fussey jm, kemeny aa, sankar s, rejali d. successful management of a catecholaminesecreting glomus jugulare tumor with radiosurgery alone. j neurol surg b skull base. 2013 dec;74(6):399-402. 2. ramina r, maniglia jj, fernandes yb, paschoal jr, pfeilsticker ln, neto mc, borges g. jugular foramen tumors: diagnosis and treatment. neurosurg focus. 2004 aug 15;17(2):e5. 3. petropoulos ae, luetje cm, camarata pj, whittaker ck, lee g, baysal be. genetic analysis in the diagnosis of familial paragangliomas. laryngoscope. 2000 jul;110(7):1225-9. 4. semaan mt, megerian ca. current assessment and management of glomus tumors. curr opin otolaryngol head neck surg. 2008 oct;16(5):420-6. 5. tokgöz sa, saylam g, bayır ö, keseroğlu k, toptaş g, çadallı tatar e, akın i̇, korkmaz mh. glomus tumors of the head and neck: thirteen years' institutional experience and management. acta otolaryngol. 2019 oct;139(10):930-933. 6. singh s, madan r, singh mk, thakar a, sharma sc. headand-neck paragangliomas: an overview of 54 cases operated at a tertiary care center. south asian j cancer. 2019 octdec;8(4):237-240. 7. wanna gb, sweeney ad, haynes ds, carlson ml. contemporary management of jugular paragangliomas. otolaryngol clin north am. 2015 apr;48(2):331-41. 8. jackson cg, harris pf, glasscock me, fritsch m, dimitrov e, johnson gd, poe ds. diagnosis and management of paragangliomas of the skull base. am j surg. 1990 apr;159(4):389-93. 9. monteiro, f., oliveira, p., peneda, j. and condé, a., 2019. vernet syndrome: intracranial extension of a slowgrowing mass. bmj case reports cp, 12(5), p.e228039. 10. neo s, lee ke. collet-sicard syndrome: a rare but important presentation of internal jugular vein thrombosis. practical neurology. 2017 feb 1;17(1):63-5. 11. spector gj, druck ns, gado m. neurologic manifestations of glomus tumors in the head and neck. archives of neurology. 1976 apr 1;33(4):270-4. 12. spector gj, gado m, ciralsky r, ogura jh, maisel rh. neurologic implications of glomus tumors in the head and neck. the laryngoscope. 1975 aug;85(8):1387-95. 13. guss zd, batra s, limb cj, li g, sughrue me, redmond k, rigamonti d, parsa at, chang s, kleinberg l, lim m. radiosurgery of glomus jugulare tumors: a metaanalysis. international journal of radiation oncology* biology* physics. 2011 nov 15;81(4):e497-502. 14. prasad sc, mimoune ha, d'orazio f, medina m, bacciu a, mariani-costantini r, piazza p, sanna m. the role of waitand-scan and the efficacy of radiotherapy in the treatment of temporal bone paragangliomas. otol neurotol. 2014 jun;35(5):922-31. 15. pareschi r, righini s, destito d, raucci af, colombo s. surgery of glomus jugulare tumors. skull base. 2003 aug;13(03):149-58. 16. kocur d, ślusarczyk w, przybyłko n, hofman m, jamróz t, suszyński k, baron j, kwiek s. endovascular approach to glomus jugulare tumors. polish journal of radiology. 2017;82:322. doi: 10.33962/roneuro-2022-006 novel technique for intraoperative imaging of the vertebral artery in patients undergoing dorsal osteosynthesis of the cervical spine o. pavlov, n. mirchev, a. ruiz, j. obersheimer, k. kallenberg, r. behr romanian neurosurgery (2022) xxxvi (1): pp. 30-38 doi: 10.33962/roneuro-2022-006 www.journals.lapub.co.uk/index.php/roneurosurgery novel technique for intraoperative imaging of the vertebral artery in patients undergoing dorsal osteosynthesis of the cervical spine o. pavlov1, n. mirchev2, a. ruiz2, j. obersheimer3, k. kallenberg3, r. behr2 1 klinikum krefeld helios, department of neurosurgery, krefeld, germany 2 klinikum fulda, department of neurosurgery, fulda city, germany 3 klinikum fulda, department of neuroradiology, fulda city, germany abstract background: the incidence of fractures in the upper cervical spine is a common entity among elderly patients. the incidence depends on the health care system and the adopted protocols for a computer tomogram in the emergency unit, in order to assure an easier and earlier detection. injuries to the vertebral artery could occur with devastating consequences, due to this type of fracture. the aim of the current surgical strategies is to stabilize the fractures and avoid further injuries to the vertebral arteries. methods: we adopted a previously hypothesized method for intraoperative imaging of the vertebral artery when performing an o-arm navigated cervical osteosynthesis. three patients were included in this group: one patient with dens fracture type ii after anderson and d’alonzo, one patient with a complex c1/c2 fracture and dissection of the vertebral artery on the left side and one patient with a kyphotic deformity due to larynx carcinoma metastasis in c4-c6. after positioning the patients, a 100 ml contrast was applied prior to the primary o-arm scan, thus obtaining real-time imaging of the vertebral artery in the navigational ct series. results: a total of 18 screws were placed. none of the screws bridged the vertebral canal. the average operative time was 174 mins. no new neurological deterioration was observed in the postoperative period. conclusions: with the development of this technique, it is possible to reduce the surgery-related injury of the vertebral artery to 0%. further studies are necessary to assess the feasibility of this technique. this technique could be especially helpful in the cases of distorted anatomical relations. introduction the incidence of fractures in the upper cervical spine in elderly patients (>65 years) after trauma lies between 1,26% and 3% (squarza, uggetti et al. 2019). the precise incidence of those fractures is hard to be determined because it depends on the health care system in every keywords vertebral artery, cervical osteosynthesis, hangman fracture, spinal fractures, spine, cervical vertebrae corresponding author: orlin pavlov klinikum krefeld helios, department of neurosurgery, krefeld, germany orlinpavlov88@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 31 novel technique for intraoperative imaging of the vertebral artery country and the adopted protocols for emergency computer tomogram (ct) in every emergency department. robinson et al. reported an increase in the incidence of c2 fractures from 3 to 6 per 100 000 from 1997 to 2014 (robinson, olerud et al. 2017), which corresponds to the development of strict protocols for emergency ct of cervical spine in the elderly population. ct has turned to be golden standard for detection of fractures of the upper cervical spine with ability to detect up to 99% of the fractures (acheson, livingston et al. 1987). due to the alternations of the in the upper cervical spine, including reduced bone density and increased rigidity, upper cervical spine is more susceptible to flexion, extension, rotation traumas. the incidence of the vertebral artery injuries (vai) after trauma is reported to be between 0, 5% and 88% (willis, greiner et al. 1994, gleizes, jacquot et al. 2000, fassett, dailey et al. 2008, mueller, peters et al. 2011) the majority of those vai remain clinically silent, but this injury could lead to major stroke and neurological deterioration. the mortality rate following vai reported in the literature varies from 8% to 18% (fusco and harrigan 2011). up to 70% of the traumatic vai have an associated cervical spine fracture (miller, fabian et al. 2001). three major diagnostic methods are available for detection of vai, including duplex ultrasonography (sensitivity 38,5%, specificity 100%), magnetic resonance angiography (sensitivity 43%, specificity 97%) and computer tomography angiography (cta) (sensitivity 53%, specificity 99%) (eastman, chason et al. 2006, harshavardhana and dabke 2014), whereas the duplex ultrasonography is not reliable for detection of intimal tears. the treatment options of vai include: 1. observation, 2. anticoagulation, 3. surgery (nizare, abdelali et al. 2013, harshavardhana and dabke 2014). the treatment modalities for upper cervical spine fractures (c-spine) vary from halo-fixation to surgery, including fixation with hooks and rods, wiring, transarticular screws fixation, lateral mass screw fixation or ventral fusion (vergara, bal et al. 2012). for the treatment of c1/c2 fractures, the lateral screw fixation (goel/harms technique) and the transarticular screw fixation (magerl technique) have shown a superior fusion rate, thus gaining more acceptances among the spine surgeons. both of these techniques could be performed free-hands, with c-arm fluoroscopy or with navigation for 3d imaging (o-arm, c-arm with integrated navigation). the postoperative complications rate in goel/harms technique is reported up to 10,6% and in magerl technique up to 21%(neo, sakamoto et al. 2005). the risk for vertebral artery injury, when performing either of both techniques is between 8% and 9,5% (yeom, buchowski et al. 2013, pavlov, mirchev et al. 2020) when using c-arm fluoroscopy. to our knowledge, the incidence of vertebral injury during dorsal stabilization with o-arm navigation or freehands is unknown. we already suggested a possible novel technique for the intraoperative visualization of the vertebral artery using hybrid technique from two visualization modalities: o-arm navigation and ct-angiography (cta) (weller, rossitch et al. 1999). the core of this technique lies in the administration of intravenous contrast (as for a common cta) before the intraoperative ct, which is performed by the o-arm navigation. the aim of this hybrid technique is to bring the intraoperative injuries of the vertebral artery to 0% (pavlov, mirchev et al. 2020). to our knowledge, this technique has not been published up to the date of the submission of this paper and we would present the first three cases, utilizing this method. material and methods in our pilot group, three patients were included: case1, case 2 and case 3. a number of possible contraindications have to be considered: known allergic reaction to contrast, uncooperative patients and pregnant patients. in none of the patients, contraindications for this hybrid technique were found. consent of the patients was obtained prior to surgery. to perform this surgical technique, the following protocol was used(pavlov, mirchev et al. 2020): 1. indications/contra-indications for this technique, careful anamnesis has to be taken for allergies against contrast. 2. prone positioning, patient is positioned in the carbon mayfield clamp, in order to reduce the artifacts from the intraoperative ct 3. o-arm navigational system positioning over the targeted area, the position is saved and the oarm needs to be brought to parking position, in order to ensure a maximal working space for the surgeon. 32 o. pavlov, n. mirchev, a. ruiz et al. 4. surgical approach to the target area (c1/c2 complex or upper cervical spine) 5. re-positioning of the o-arm navigation over the area of interest 6. bolus manual application of contrast-100ml through central line, 5 seconds before the intraoperative scan for optimal visualization of the vertebral artery and eliminating the venous contrast artefacts. 7. ventilation pause and carrying out an intraoperative ct scan, then the data is transferred to the surgeon’s monitor 8. screws insertion under 3d guidance with intraoperative visualization of the vertebral artery 8. ventilation is paused and another intraoperative ct scan is carried out to verify the correct position of the screws. 9. wound closure case 1 diagnosis: dens fracture type ii anderson and d’alonzo surgical strategy: dorsal osteosynthesis in goel/harms technique c1-c2 brief summary of the patient’s history: a 95-years old patient, in a good clinical condition, presents herself in our emergency room after falling from her sofa backwards. she complained pain in the dorsal region of the c-spine without neurological deficits. the anamnesis showed pre-existing strokes in the left and right medial cerebral artery. figure 1 and 2. 3d data with intraoperative imaging of the vertebral artery the trauma scan depicted dens fracture type ii after anderson and d’alonzo classification. the surgery was indicated and after obtaining patient’s consent, the surgery was carried out on the 2nd day after the admission of the patient. the indication for applying contrast, during the surgery, in this patient was based on the pre-existing strokes, suggesting progressive atherosclerosis, and a sufficient kidney function (glomerular filtration rate71ml/min and creatinine 1,3 mg/dl). the application of contrast allowed a good intraoperative imaging of the vertebral artery, optimal length of the screws was chosen without risking a vascular injury (fig 1-3). 33 novel technique for intraoperative imaging of the vertebral artery figure 3. 3d intraoperative navigation with direct imaging of the vertebral artery case 2 diagnosis: complex c1 fracture (jefferson fracture ii)/ c2 fracture (hangmann fracture) and a. vertebralis dissection links surgical strategy: dorsal fusion in goel/harms technique c1/c2 and massa lateralis screws in c3 brief summary of the patient’s history: a 79-year old patient presented at our emergency room after a 6 fall from a roof. the patient complained pain in the dorsal region of the cervical pain without radiculopathy or myelopathy. the neurological examination showed normal neurological status. the anamnesis depicted no pre-existing health issues. the trauma scan depicted a complex c1/c2 fracture, where the consecutive cta showed a dissection of the vertebral artery on the left side. because of the dissection of the vertebral artery, the patient was put on antiplatelet therapy with aspirin. surgery was indicated and after obtaining the patient’s consent, it was carried out on the 7th day. the indication for applying a contrast in this patient was based on the previous traumatic injury of the vertebral injury on the left side and preserved kidney function (glomerular filtration rate69ml/min and creatinine 1,5 mg/dl. during surgery, after the application of contrast and after carrying out the intraoperative ct, the occlusion of the left vertebral artery was still visible (fig. 4). figure 4. intraoperative ct navigation with contrast, performed with o-arm, where dissection of the left vertebral artery is still visible polyaxial screws on both sides in massa lateralis and in the pedicles were placed. the postoperative condition of the patient deteriorated due to postoperative delirium, which was treated with atypical antipsychotic (risperidone) and benzodiazepines (diazepam). the postoperative c-spine ct showed an optimal placement of all screws. case 3 diagnosis: larynx carcinoma metastasis c4-c6, cervical instability and kyphotic deformity c4-c6 surgical strategy: dorsal osteosynthesis (massa lateralis and pedicle screws) c3-d1 brief summary of the patient’s history: the case of the 57-years old patient with larynx carcinoma was discussed at neuro-oncological board due to a new metastasis in the c-spine with progressive deformity. the patient complained pain in the middle cervical spine with irradiation of the pain in shoulders. the neurological examination showed intact neurological status. the patient had tracheostoma because of the larynx carcinoma, making a ventral approach to the c-spine not possible. 34 o. pavlov, n. mirchev, a. ruiz et al. an mri and ct of the c-spine showed destructive process in c4 to c6 with kyphosis, without tumour bridging in the spinal canal. after interdisciplinary discussion of this case, regarding life-expectancy, neurological outcome and patient’s will, surgery was indicated. after obtaining patient’s consent, the surgery was carried out on the 3rd day after admission. the indication for applying intraoperative contrast was based suspicion of tumour infiltration on left vertebral canal c4-c6. the intraoperative ct-navigation with contrast depicted a tumour mass from c4 to c6, infiltrating the left vertebral canal, without pressuring the artery. figure 4. tumour infiltration in the left vertebral canal c5 after the screw insertion, a second scan was carried out. the second scan depicted a perfect positioning of the screws, unfortunately the vertebral artery was not visible any longer (94 minutes after the initial scan) fig.8. postoperatively the patient recovered well and was discharged on the 7th day. results a total of 18 screws were placed (massa lateralis or pedicle screws). none of them breached the walls of vertebral canal. the average operative time was 174 minutes in the three surgeries. using this imaging technique, the vertebral artery was depicted from segment v1 to segment v3, without discontinuity in any of the vertebrae levels. on the second scan, in none of the cases, the vertebral artery was visible any longer. discussion the interest of fusion techniques in intraoperative neuroimaging exists for a long time, especially when vascular structures are involved. leng et al. were the first to describe the fusion between intraoperative three-dimensional rotational angiography and flat panel detector computed tomography for cerebrovascular navigation.(leng, rubin et al. 2013) in this case report, the treatment of a patient harbouring two aneurysms was described, using this fusion/hybrid technique. although, it is not obligatory to use this technique, this method adds to the arsenal of surgical strategies, which could be used for intraoperative support. since both the cspine trauma and the stabilisation technique independently add up to the risk of vai, it is mandatory to utilize all the possible techniques to preserve the functional vertebral artery, in order to avoid further neurological deterioration. in all patients, where vai is suspected, aggressive actions need to be taken, in order to confirm the diagnosis because of its therapeutic significance. the preoperatively obtained ct/ct-angiography is a valid method for intraoperative navigation in trauma cases. fiorenza et al. conducted a retrospective study in a series of 21 patients, who underwent a posterior upper cervical spine fixation using a navigational system with intraoperative single level vertebral registration on preoperative ct/ct-angiography (fiorenza and ascanio 2019). no neurovascular damage occurred in any of the patients. in the treatment of upper cervical trauma cases, however, it is not mandatory to conduct a preoperative ct-angiography (lockwood, smith et al. 2016). the development of strict protocols for ctangiography in trauma patients is still in development. lockwood et al. presented one of the most significant studies for ct-angiography in patients with upper cervical spine, up to date (lockwood, smith et al. 2016). using the denver criteria (biffl, moore et al. 1999, kerwin, bynoe et al. 2001, cothren, moore et al. 2003, parks and croce 2012) for high risk fracture pattern, the authors analysed 1435 patients, where only combined c1-c2 35 novel technique for intraoperative imaging of the vertebral artery fractures, subluxations and transverse foramen involvement were predictive for vai. the odds for developing of vai were 3,8, 4,8 and 6,3 respectively. of the 1435 patients with cervical spine fractures, only 10 (0,7%) suffered from posterior circulation stroke(lockwood, smith et al. 2016). the preoperative ct-angiography gives the surgeons valuable information about the position of the vertebral artery and its position the osseous structures. however, it is interesting to point out, that many studies have shown, that vai shown in preoperative ct-angiography and applying treatment (anticoagulation or antiplatelet therapy) does not prevent stroke (eastman, chason et al. 2006, scott, sharp et al. 2014, lockwood, smith et al. 2016). this data would suggest that the obtained ctangiography would not have any effect on the neurological outcome of the patients after trauma. the use of our suggested technique shows a realtime intraoperative visualization of the vertebral artery. one must consider that the patient’s head is fixated in a rigid collar for the ct-angiography and prior to the operation, the collar is taken off and patient’s head needs to reclined and fixated in mayfield for the posterior fixation. in this manoeuvre, the position of the vertebral artery does not change in respect to the osseous anatomy, however its blood flow could be changed because of kinking due to fractures (george and carpentier 2001, berti, zafar et al. 2018). our suggested technique could provide the surgeon with certainty, that prior to the screw insertion, that both of the vertebral arteries are intact. o-arm navigation has also shown to reduce the operative time, in comparison with the preoperative scans with image guidance (costa, cardia et al. 2011) and to reduce the radiation exposure compared to fluoroscopic guidance(costa, cardia et al. 2011, nottmeier, pirris et al. 2013). performing intraoperative ct at the end of the procedure, reduces the need to return the patients to the operating room.(van de kelft, costa et al. 2012) associated atlas and axis fractures account for 3% of acute cervical spine lesions and 12% of the upper cervical spine lesions (jung, jung et al. 2010), where the normal anatomy of the c1/c2 complex is altered, with possible displacement of the vertebral artery. in those cases, even with conventional o-arm navigation, an injury of the vertebral artery is possible, even with 99,9% accuracy of the screw positioning(bydon, martin ma et al. 2014). tumours of the craniocervical junction (ccj) represent a challenging entity for the neurosurgeon(bydon, martin ma et al. 2014). bydon et al. showed that the rate of vertebral artery involvement significantly effects the rate of radical resections of the tumours, located in the ccj. the patients without involvement of the artery had a total resection, statistically significant to those with involvement of the vertebral artery. pirotte et al. and talacchi et al. showed that aiming for a total resection of the tumors in ccj, which involve the vertebral artery, is related to many postoperative complications, including lateromedullary infarction, respiratory failure, cranial nerve palsy, etc.(pirotte, brotchi et al. 2010, talacchi, biroli et al. 2012). with this technique for intraoperative imaging of the vertebral artery, it could be possible to increase the percentage of tumor resection, extending the lifeexpectancy, tumor-free period. kern et al. were the first to use o-arm navigational system in 2014 for resection of a chordoma in ccj, however no angiography was performed at the time(kern, indro et al. 2014). because of the distortion of the normal bony structures due to the tumor, it is difficult to appreciate intraoperatively many important landmarks. the use of o-arm navigation has proven to be a valuable tool in the tumor resection process. the developed in john hopkins university algorithm by sciubba et al.(sciubba, mavinkurve et al. 2006), proved successful in treatment of hemangioblastomas in the cervical spine. 3d digital subtraction angiography provides high-resolution images of the vascular structures, however often it does not provide reliable anatomical information about the nearby osseous structures, or in the cases, when it does, resolution of the vascular anatomy in the immediate vicinity of bone sacrificed. (sciubba, mavinkurve et al. 2006) the authors used a novel angiographic reconstruction by combining two separate sequences of images of bone and blood vessels in a single 3d fusion imaging series. although, only two case reports were presented by the authors, the need for a better osseous intraoperative imaging is noted. su et al. already used this fusion technique between o-arm and ontable angiography for the resection of the occipitocervical tumor in 12/2020, independently from our published hypothetical usage of this 36 o. pavlov, n. mirchev, a. ruiz et al. method in 02/2020(pavlov, mirchev et al. 2020, su, prezerakos et al. 2020). this facilitates safe resection by mapping the surgical field occult to direct vision. there are two major factors for injury of the vertebral artery, when performing a cervical osteosynthesis: high riding vertebral artery (hrva), as an anatomical variant and narrow pedicle of the c2 vertebrae(wang, xia et al. 2013, wajanavisit, lertudomphonwanit et al. 2016). both of these factors could be present in the setting of spinal trauma or tumor in the ccj. morin et al. demonstrated the close relationship between traumatic brain injury (tbi) and the cervical spine involvement (morin, langevin et al. 2016) and thus the neurological outcome. outcomes from tbi can be temporary or permanent dysfunction of cognition, motor function, physiology, and psychology (blennow, hardy et al. 2012) and post tbi neurological disorders such as posttraumatic epilepsy, chronic traumatic encephalopathy and dementia (papa, mendes et al. 2012, cotter, kelso et al. 2017). the resulting costs for the treatment of these patients are increased exponentially. the patients with extracranial involvement (c-spine fractures, lung contusion, etc.) have worse outcome, compared to the patient without additional injuries(konar, pavlov et al. 2020). the learning curve for a posterior fixation in the upper cervical spine represents a steep due to the complex anatomy of the ccj, subaxial spine and its neurovascular relations (heo, lee et al. 2019). the proposed technique could improve the learning curve, making the posterior fixation easier for the young neurosurgeons. with the better understanding of the anatomic relations of the bones to the neurovascular structures, one would improve the operating time and minimize the blood loss. conclusions with the development of this technique, we do not aim to set it as a “golden standard” for the treatment of pathologies in the c-spine. we would suggest that this technique would be “good to know” in the cases, where it is needed. since we present only a technical note, no statistical analysis is carried out. in the setting of polytrauma or multitrauma, where a cervical dorsal osteosynthesis is required, all measures for reducing the risk for additional injuries need to be considered. the procedure-associated risk for additional neurological deficit, due to injury of the vertebral artery, must be kept as low as possible. this technique offers the possibility for a real-time intraoperative imaging of the vertebral artery and thus protecting it. this is a pilot cohort of patients with very promising results. further studies will be carried out to confirm the diminished rate of vai, to compare the average blood loss, operation time, perioperative mortality and morbidity between the patients undergoing c-spine dorsal osteosynthesis with and without this technique. disclosures no disclosures references 1. acheson, m. b., et al. (1987). "high-resolution ct scanning in the evaluation of cervical spine fractures: comparison with plain film examinations." american journal of roentgenology 148(6): 1179-1185. 2. berti, a. f., et al. (2018). "recurrent posterior circulation infarcts secondary to vertebral artery external compression treated with endovascular deconstruction." interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences 24(2): 178-182. 3. biffl, w. l., et al. (1999). "optimizing screening for blunt cerebrovascular injuries." am j surg 178(6): 517-522. 4. blennow, k., et al. (2012). "the neuropathology and neurobiology of traumatic brain injury." neuron 76(5): 886-899. 5. bydon, m., et al. (2014). "surgical outcomes of craniocervial junction meningiomas: a series of 22 consecutive patients." clinical neurology and neurosurgery 117: 71-79. 6. costa, f., et al. (2011). "spinal navigation: standard preoperative versus intraoperative computed tomography data set acquisition for computer-guidance system: radiological and clinical study in 100 consecutive patients." spine (phila pa 1976) 36: 2094-2098. 7. cothren, c. c., et al. (2003). "cervical spine fracture patterns predictive of blunt vertebral artery injury." j trauma 55(5): 811-813. 8. cotter, d., et al. (2017). "genetic biomarkers of posttraumatic epilepsy: a systematic review." seizure european journal of epilepsy 46: 53-58. 9. eastman, a. l., et al. (2006). "computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime?" j trauma 60(5): 925-929; discussion 929. 37 novel technique for intraoperative imaging of the vertebral artery 10. fassett, d. r., et al. (2008). "vertebral artery injuries associated with cervical spine injuries: a review of the literature." j spinal disord tech 21(4): 252-258. 11. fiorenza, v. and f. ascanio (2019). "safety and efficacy of posterior atlanto-axial stabilization using intraoperative navigation system with preoperative computed tomographic scan." world neurosurg 129: 110-119. 12. fusco, m. r. and m. r. harrigan (2011). "cerebrovascular dissections: a review. part ii: blunt cerebrovascular injury." neurosurgery 68(2): 517-530; discussion 530. 13. george, b. and a. carpentier (2001). "compression of and by the vertebral artery." operative techniques in neurosurgery 4(4): 202-218. 14. gleizes, v., et al. (2000). "combined injuries in the upper cervical spine: clinical and epidemiological data over a 14year period." european spine journal : official publication of the european spine society, the european spinal deformity society, and the european section of the cervical spine research society 9(5): 386-392. 15. harshavardhana, n. s. and h. v. dabke (2014). "risk factors for vertebral artery injuries in cervical spine trauma." orthopedic reviews 6(3): 5429-5429. 16. heo, y., et al. (2019). "the learning curve of subaxial cervical pedicle screw placement: how can we avoid neurovascular complications in the initial period?" oper neurosurg (hagerstown) 17(6): 603-607. 17. jung, s. h., et al. (2010). "tailored surgical approaches for benign craniovertebral junction tumors." j korean neurosurg soc 48(2): 139-144. 18. kern, h. g., et al. (2014). "the use of intraoperative navigation for complex upper cervical spine surgery." neurosurgical focus foc 36(3): e5. 19. kerwin, a. j., et al. (2001). "liberalized screening for blunt carotid and vertebral artery injuries is justified." j trauma 51(2): 308-314. 20. konar, s., et al. (2020). "critical appraisal of traumatic brain injury and its management." indian journal of neurotrauma 17(02): 079-084. 21. leng, l. z., et al. (2013). "fusion of intraoperative threedimensional rotational angiography and flat-panel detector computed tomography for cerebrovascular neuronavigation." world neurosurg 79(3-4): 504-509. 22. lockwood, m. m., et al. (2016). "screening via ct angiogram after traumatic cervical spine fractures: narrowing imaging to improve cost effectiveness. experience of a level i trauma center." journal of neurosurgery. spine 24(3): 490-495. 23. miller, p. r., et al. (2001). "blunt cerebrovascular injuries: diagnosis and treatment." j trauma 51(2): 279-285; discussion 285-276. 24. morin, m., et al. (2016). "cervical spine involvement in mild traumatic brain injury: a review." journal of sports medicine 2016: 1590161. 25. mueller, c.-a., et al. (2011). "vertebral artery injuries following cervical spine trauma: a prospective observational study." european spine journal : official publication of the european spine society, the european spinal deformity society, and the european section of the cervical spine research society 20(12): 2202-2209. 26. neo, m., et al. (2005). "the clinical risk of vertebral artery injury from cervical pedicle screws inserted in degenerative vertebrae." spine (phila pa 1976) 30(24): 2800-2805. 27. nizare, e. f., et al. (2013). "upper cervical spine injuries: a management of a series of 70 cases." the pan african medical journal 15: 57-57. 28. nottmeier, e. w., et al. (2013). "operating room radiation exposure in cone beam computed tomography–based, image-guided spinal surgery." journal of neurosurgery: spine 19(2): 226-231. 29. papa, l., et al. (2012). "mild traumatic brain injury among the geriatric population." current translational geriatrics and experimental gerontology reports 1(3): 135-142. 30. parks, n. a. and m. a. croce (2012). "use of computed tomography in the emergency room to evaluate blunt cerebrovascular injury." adv surg 46: 205-217. 31. pavlov, o., et al. (2020). "a possible novel technique for intraoperative imaging of the vertebral artery during arthrodesis of the upper cervical spine." medical hypotheses 140: 109641. 32. pavlov, o., et al. (2020). "a possible novel technique for intraoperative imaging of the vertebral artery during arthrodesis of the upper cervical spine." medical hypotheses 140: 109641. 33. pirotte, b. j., et al. (2010). "management of anterolateral foramen magnum meningiomas: surgical vs conservative decision making." neurosurgery 67(3 suppl operative): ons58-70; discussion ons70. 34. robinson, a.-l., et al. (2017). "epidemiology of c2 fractures in the 21st century: a national registry cohort study of 6,370 patients from 1997 to 2014." advances in orthopedics 2017: 6516893. 35. sciubba, d. m., et al. (2006). "preoperative imaging of cervical spine hemangioblastomas using threedimensional fusion digital subtraction angiography. report of two cases." journal of neurosurgery. spine 5(1): 96-100. 36. scott, w. w., et al. (2014). "clinical and radiological outcomes following traumatic grade 1 and 2 vertebral artery injuries: a 10-year retrospective analysis from a level 1 trauma center." j neurosurg 121(2): 450-456. 37. squarza, s., et al. (2019). "c1-c2 fractures in asymptomatic elderly patients with minor head trauma: evaluation with a dedicated head ct protocol." radiol bras 52(1): 17-23. 38. su, z., et al. (2020). "novel use of intraoperative conebeam imaging with on-table angiography for excision of an occipitocervical tumour: a technical note and its feasibility." interdisciplinary neurosurgery 22: 100784. 39. talacchi, a., et al. (2012). "surgical management of ventral and ventrolateral foramen magnum meningiomas: report on a 64-case series and review of the literature." neurosurg rev 35(3): 359-367; discussion 367-358. 38 o. pavlov, n. mirchev, a. ruiz et al. 40. van de kelft, e., et al. (2012). "a prospective multicenter registry on the accuracy of pedicle screw placement in the thoracic, lumbar, and sacral levels with the use of the o-arm imaging system and stealthstation navigation." spine (phila pa 1976) 37(25): e1580-e1587. 41. vergara, p., et al. (2012). "c1-c2 posterior fixation: are 4 screws better than 2?" neurosurgery 71(1 suppl operative): 86-95. 42. wajanavisit, w., et al. (2016). "prevalence of high-riding vertebral artery and morphometry of c2 pedicles using a novel computed tomography reconstruction technique." asian spine journal 10(6): 1141-1148. 43. wang, j., et al. (2013). "an anatomic consideration of c2 vertebrae artery groove variation for individual screw implantation in axis." european spine journal : official publication of the european spine society, the european spinal deformity society, and the european section of the cervical spine research society 22(7): 1547-1552. 44. weller, s. j., et al. (1999). "detection of vertebral artery injury after cervical spine trauma using magnetic resonance angiography." j trauma 46(4): 660-666. 45. willis, b. k., et al. (1994). "the incidence of vertebral artery injury after midcervical spine fracture or subluxation." neurosurgery 34(3): 435-441; discussion 441-432. 46. yeom, j. s., et al. (2013). "risk of vertebral artery injury: comparison between c1-c2 transarticular and c2 pedicle screws." spine j 13(7): 775-785. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-017 association of platelet count and platelet indices with cranial meningioma yasar karatas, fatih keskin, mehmet fatih erdi, bulent kaya, densel arac, emir kaan izci, erdal kalkan romanian neurosurgery (2020) xxxiv (1): pp. 123-126 doi: 10.33962/roneuro-2020-017 www.journals.lapub.co.uk/index.php/roneurosurgery association of platelet count and platelet indices with cranial meningioma yasar karatas1, fatih keskin2, mehmet fatih erdi2, bulent kaya1, densel arac2, emir kaan izci3, erdal kalkan1 1 medova hospital, department of neurosurgery, konya, turkey 2 necmettin erbakan university, meram medical faculty, department of neurosurgery, konya, turkey 3 meram training and research hospital, department of neurosurgery, turkey abstract introduction and objectives: in this study, we aimed to investigate whether platelet count (plt) and platelet indices included mean platelet volume (mpv), platecrit (pct), platelet distribution width (pdw) values can be used as diagnostic markers in cranial meningiomas. materials and methods: the study included results of 29 patient and 47 healthy contributors. based on pathologies, the patients were divided into two groups. the first group included meningioma patients and the second one included healthy individuals. healthy contributors named control group. platelet count and platelet indices were determined using sysmex xn 550 haematology analyzer. the preoperative platelet count (plt) and platelet indices included mean platelet volume (mpv), platecrit (pct), platelet distribution width (pdw) values were recorded from the routine laboratory tests. results: there was no statistically significant difference in plt between the meningioma and healthy groups (p = 0.217). there was a statistically significant difference in pct between the meningioma group and the healthy group (p = 0.002). there was a statistically significant difference in pdw between meningioma group and healthy group (p = 0.001). in terms of mpv, there was a statistically significant difference between meningioma group and the healthy group (p = 0.001) conclusion: platelet count and indices are easily available in the routine blood tests. despite the retrospective design and small sample size, our findings suggest that altered mpv, pdw and pct levels might serve as potential biomarkers for the diagnosis of meningiomas. introduction platelets are reproduced from megakaryocytes1. we know that platelets play an important role in the coagulation process. platelets have been studied for many years for their vital role in tumorigenesis. many different mechanisms of the relationship between cancer cells and platelets have been demonstrated. newly, platelets were declared to be associated with the development and progression of malignan keywords platelet, platelet indices, inflammation, meningioma corresponding author: yasar karatas medova hospital, department of neurosurgery, konya, turkey yasarkrts@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 124 yasar karatas, fatih keskin, mehmet fatih erdi et al. cies2.3. the relation between cancer and inflammation was identified in the last century. as known, neutrophils, and lymphocytes are responsible for inflammation. new studies reported that platelets play a major role in inflammation4,5. platelets are the first to accumulate at the site of damage and they secrete proinflammatory and growth factors such as platelet activated factor (paf), vascular endothelial growth factor (vegf), platelet derivate growth factor (pdgf), and thromboxane a2 at the injured area. vegf plays a key role in regulating angiogenesis via increasing vascular permeability and facilitating the branching and formation of new blood vessels in the tumor site 6.meningioma is a central nervous system tumor arising from the arachnoid cells present in the arachnoid mater. it is the most common benign primary tumor of the brain. currently, there is still no consensus for biomarkers that can be used for early diagnosis and prognosis for meningiomas. in this study, we used platelet indices for the search of potential biomarkers for meningiomas. materials and methods the study included results of 29 patient and 47 healthy contributors. the patients underwent surgery. patients’ laboratory and pathology results were retrospectively reviewed from the hospital archive. based on pathologies, the patients were divided into two groups. the first group included meningioma patients and the second one included healthy indivudials. healthy contributors named control group. platelet count and platelet indices were determined using sysmex xn 550 hematology analyzer. the preoperative platelet count (plt) and platelet indices included mean platelet volume (mpv), platecrit (pct), platelet distribution width (pdw) values were recorded from the routine laboratory tests. statistical analysis the r 3.2.1 package program was used to analyze data. descriptive statistics of the quantitative variables included in the study were determined by mean, standard deviation, median, minimum and maximum values; qualitative variables are indicated by frequency and percentage. the suitability of the continuous variables to the normal distribution was examined by the shapiro wilk test. mann whitney u test was used to compare two groups of continuous variables that do not show normal distribution. the relationships between continuous variables were interpreted with the pearson correlation coefficient. pearson chi-square and yates chi-square tests were used to comparing qualitative variables between groups. in all statistical analyzes in the study, p values less than 0.05 were considered statistically significant. results a total of 76 contributors were included in this study. 29 of them meningioma patients, and 47 of them were healthy contributors. there was no statistically significant difference in plt between the meningioma and healthy groups (p = 0.217)(figure 1). there was a statistically significant difference in pct between the meningioma group and the healthy group (p = 0.002)(figure 2). there was a statistically significant difference in pdw between meningioma group and healthy group (p = 0.001)(figure 3). in terms of mpv, there was a statistically significant difference between meningioma group and the healthy group (p = 0.001)(figure 4). figure 1. comparison of plt levels between the patients and the healthy control group. figure 2. comparison of pct levels between the patients and the healthy control group. 125 association of platelet count and platelet indices with cranial meningioma figure 3. comparison of pdw levels between the patients and the healthy control group. figure 4. comparison of mpv levels between the patients and the healthy control group. discussion although it is known that genetic factors are essential in the development of cancer, the host inflammatory response is reported to be very important in the underlying mechanism of carcinogenesis 7. releasing inflammatory cytokines and chemokines in the damaged areas caused platelet activation. platelets facilitate endothelial adhesion of leukocytes. recently, researchers suggest that platelets act an important role in neoplastic disease. they put forward that platelets cause encapsulation of neoplastic cells and provide them to get out of recognition by the host immune system 8,9. meningiomas are the common benign neoplasms of the central nervous system. they appear approximately 20 percent frequently in all of the brain tumors and risk factors for these neoplasms are still little known 10. high level of different cytokines which is multiple pathways of carcinogenesis was found in brain tumor specimens 11. platelets increase megakaryocytes and proinflammatory cytokines released by cancer 12. in this study, we aimed to measure plt and it’s indices in patient with meningioma, and healthy group. pdw values were found significantly lower in meningioma group compared to the healthy control group but pct and mpv values were found significantly higher in meningioma group compared to the healthy control group. numerous study proposes that plt increases in many cancer types also some others propose that no changes in plt. taucher et al showed that platelet count is significantly higher in patients with breast cancer compared with the control group 13. inagaki et al found that platelet count is significantly higher in patients with non-small cell lung cancer 14. ma, ozaksit and okuturlar et al established that there were no statistical changes in plt while compared the groups similarly to our study 15, 16, 17. in our study, we found no statistical changes in plt while comparing the groups. the average platelet volume in the blood mean mpv and heterogeneity in platelet volume mean pdw. mpv is generally used for determining the platelet activity and function in the platelet indices 18. theoretically, reduction in platelet counts causes stimulation of megakaryocytes and they are transformed into large platelets 19. larger platelets are more metabolically and enzymatically active than smaller platelets 20. cho et al. found that patients with hepatocellular carcinoma had higher mpv. in our study, we found statistical higher mpv level in meningioma patients compared to the healthy group. inagaki n and kumagai s et al. showed that the patients had non-small cell lung cancer with poor prognosis had low mpv levels 14, 21. there are different results in pdw in many research. inagaki et al. found lower pdw levels similarly our study in non-small cell lung cancer 14. okuturlar et al. showed no statistical difference between breast cancer patients and the healthy groups in pdw 17. ma et al. found that increase pdw levels in epithelial ovarian cancer 15. xuegong et al. have established that the level of pct is higher in patients with epithelial ovarian cancer compared to the healthy group 22. ozaksit et al. showed that there is no difference between the malignant and benign ovarian masses and the control group in terms of 126 yasar karatas, fatih keskin, mehmet fatih erdi et al. pct values 16. we found statistical lower levels of pct in meningioma patients compared with the healthy group. conclusion we suggest that the usability of plt and indices in the early diagnosis of meningioma patients and should be researched by further studies that have larger populations diagnosed with meningioma and their grades. references 1. george jn. platelets. lancet. 2000;355(9214):1531–1539. 2. franco, a. t. corken, a. & ware, j. platelets at the interface of thrombosis, inflammation, and cancer. blood 126, 582–588, https:// doi.org/10.1182/blood-2014-08-531582 (2015). 3. buergy, d. wenz, f. groden, c. & brockmann, m. a. tumor-platelet interaction in solid tumors. int j cancer 130, 2747–2760, https://doi.org/10.1002/ijc.27441 (2012). 4. balkwill f. & mantovani a. inflammation and cancer: back to virchow? lancet. 2001;357:539-45. 5. tozkoparan e, deniz o, ucar e, et al. changes in platelet count and indices in pulmonary tuberculosis. clin chem lab med. 2007;45:1009-13. 6. cai j, ma h, huang f, et al (2013). correlation of bevacizumab induce hypertension and outcomes of metastatic colorectal cancer patients treated with bevacizumab: a systematic review and meta-analysis. world j surg oncol, 11, 306. 7. coupland la, parish cr (2014). platelets, selectins, and the control of tumor metastasis. semin oncol, 41, 422-34. 8. m. r. barnard, l. a. krueger, a. l. frelinger iii, m. i. furman, and a. d. michelson, “whole blood analysis of leukocyte-platelet aggregates,” current protocols in cytometry, 2003. 9. r. leblanc and o. peyruchaud, “metastasis: new functional implications of platelets and megakaryocytes,” blood, vol. 128, no. 1, pp. 24–31, 2016. 10. sergentanis tn, tsivgoulis g, perlepe c, ntanasisstathopoulos i, tzanninis ig, sergentanis in, psaltopoulou t. obesity and risk for brain/cns tumors, gliomas and meningiomas: a meta-analysis. plos one. 2015;10:e0136974. [pmc free article] [pubmed] [google scholar] 11. albulescu, r.; codrici, e.; popescu, i.d.; mihai, s.; necula, l.g.; petrescu, d.; teodoru, m.; tanase, c.p. cytokine patterns in brain tumor progression. mediat. inflamm. 2013, 2013, 979748. [crossref] [pubmed] 12. mutlu h, artis ta, erden a, akca z. alteration in mean platelet volume and platicrit values in patients with cancer that developed thrombosis. clin appl thromb hemost. 2013;19:331-3. 13. taucher s, salat a, gnant m, kwasny w, mlineritsch b, et al. (2003) impact of pretreatment thrombocytosis on survival in primary breast cancer. thromb haemost 89(6): 1098-1106. 14. inagaki n, kibata k, tamaki t, et al (2014). prognostic impact of the mean platelet volume/platelet count ratio in terms of survival in advanced non-small cell lung cancer. lung cancer, 83, 97-101. 15. ma x, wang y, sheng h, et al (2014). prognostic significance of thrombocytosis, platelet parameters and aggregation rates in epithelial ovarian cancer. j obstet gynaecol res, 40, 178-83. 16. ozaksit g, tokmak a, kalkan h, et al (2015).value of the platelet to lymphocyte ratio in the diagnosis of ovarian neoplasms in adolescents. asian pac j cancer prev, 16, 2037-41. 17. okuturlar y, gunaldi m, tiken ee, et al (2015). utility of peripheral blood parameters in predicting breast cancer risk. asian pac j cancer prev, 16, 2409-12. 18. gasparyan ay, ayvazyan l, mikhailidis dp, kitas gd. mean platelet volume: a link between thrombosis and inflammation? curr pharm des. 2011;17(1):47–58. 19. alsweedan sa, al-shurman a, mahmoud as (2008). diagnostic value of platelet indices in children with leukemia. j pediatr hematol oncol, 30, 953-5. 20. kannar v, raja v, suresh tn (2017) evaluation of platelet indices in oral squamous cell carcinoma. clin cancer investig j 6(1): 40-43. 21. kumagai s, tokuno j, ueda y, marumo s, shoji t, nishimura t, fukui m, huang cl. prognostic significance of preoperative mean platelet volume in resected nonsmall cell lung cancer. mol clin oncol. 2015;3:197-201. 22. xuegong ma, yingmei wang, hongna sheng, wenyan tian, zheng qi, fei teng, fengxia xue. prognostic significance of thrombocytosis, platelet parameters and aggregation rates in epithelial ovarian cancer. journal of obstetrics and gynaecology research 2014, 40 (1): 17883. doi: 10.33962/roneuro-2023-040 total intracranial migration of ventriculoperitoneal shunt. a case report with literature review ahtesham khizar, syed aamir shah, soha zahid, jayant kumar yadav romanian neurosurgery (2020) xxxiv (1): pp. 224-228 doi: 10.33962/roneuro-2020-040 www.journals.lapub.co.uk/index.php/roneurosurgery total intracranial migration of ventriculoperitoneal shunt. a case report with literature review ahtesham khizar1, syed aamir shah1, soha zahid2, jayant kumar yadav3 1 pakistan institute of medical sciences, islamabad, pakistan 2 jinnah medical and dental college, karachi, pakistan 3 tribhuvan university teaching hospital, maharajgunj, kathmandu, nepal abstract background. the ventriculoperitoneal shunt is a common treatment for hydrocephalus. there are several complications associated with it. shunt failure is one of the most frequent complications, but total intracranial shunt migration is quite uncommon. the exact cause of shunt migration is unknown, but several factors are thought to play a role. case presentation. a 10-month-old boy was diagnosed with total intracranial migration of a ventriculoperitoneal shunt (chhabra type). we used neuroendoscopy to remove this intracranially migrated shunt and implanted a new ventriculoperitoneal shunt (medtronic type) on the opposite side. he had a favourable clinical outcome. conclusion. total intracranial shunt migration is an uncommon complication which is most likely caused by increased intraperitoneal pressure, strong head movements, and insufficient shunt fixation. better patient handling combined with appropriate operative technique would be the best way to prevent shunt migration. introduction the ventriculoperitoneal (vp) shunt is one of the most commonly performed procedures in neurosurgery. it is frequently used to treat various types of hydrocephalus, namely obstructive, non-obstructive and normal pressure hydrocephalus. kausch performed the first vp shunt surgery for the treatment of hydrocephalus in 1908.1 shunt failure is the most common complication in 40-70% of cases. shunt blockage, infection, overdrainage, underdrainage, and visual field defects are all possible complications associated with the vp shunt. shunt migration is another complication and it can migrate to various parts of the body such as the thorax, stomach, liver, gallbladder, umbilicus, colon, and urinary bladder but complete intracranial migration of the vp shunt has rarely been reported.2 keywords ventriculoperitoneal shunt, intracranial migration, shunt complications corresponding author: ahtesham khizar pakistan institute of medical sciences, islamabad, pakistan arwain.6n2@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 225 total intracranial migration of ventriculoperitoneal shunt anterior cerebral artery (daca) represents all segments of the anterior cerebral artery (aca) distal , saccular aneurysms of the a4-a5 segments have only been reported once in the literature (4). giant partially thrombosed aneurysms usually have been proposed to result from accumulative intramural bleeding, enlargement, and thrombosis (11). therefore, endovascular treatment can often be ineffective, as it only eliminates the intraluminal portion of the aneurysm, leaving the mural portion liable to more bleeding, enlargement, and even rupture (2). this makes microsurgical management of giant partially thrombosed a4-a5 aneurysms more appealing, and raises several surgical challenges owing to their location posteriorly within the anterior interhemispheric fissure, the configuration of their domes, involvement of proximal and distal vessels within their base, and the mass effect which can significantly alter the anatomy of this region (11-13). all of the aforementioned highlights the importance of this paper, in which we report the second case of an idiopathic, giant, saccular, partially thrombosed a4-a5 daca aneurysm, discussing the treatment nuances of such extremely rare lesions. case description a 10-month-old boy came in with a history of progressive head enlargement, multiple episodes of vomiting, and decreased oral intake for the last three days. he had congenital hydrocephalus and received a medium pressure vp shunt (chhabra type) surgery at another hospital when he was one month old. he recovered well from his vp shunt surgery. on clinical examination, he had an enlarged head, as well as a tense and bulging anterior fontanelle. engorged scalp veins were prominent and there was a sunset sign present. the shunt chamber could not be felt. routine investigations became the norm. an x-ray shunt series revealed abnormal cranially migrated vp shunt assembly (figure. 1, a&b). computed tomography (ct) brain plain revealed grossly dilated ventricles, subdural hygroma, and the assembly of vp shunt within the ventricles (figure. 2 a&b). the previous burrhole site was explored during surgery. the burrhole was approximately 1x1 cm in size. through the burrhole, a rigid paediatric neuro endoscope was inserted, and the entire shunt was seen coiled up within the lateral ventricle. an endoscopic grasper was used to remove it. on the opposite side, a new vp shunt (medtronic type) was implanted. he recovered well postoperatively, improved clinically, and was discharged in the next three days. figure 1. a&b: x-rays skull ap and lateral views showing total intracranial migration of ventriculoperitoneal shunt. figure 2. a&b: ct scan brain plain axial views showing gross hydrocephalus, subdural hygroma and intracranial migration of ventriculoperitoneal shunt. discussion vp shunts may be simple to perform but they are associated with intracranial and intra-abdominal complications. meningitis, ventriculitis, sepsis, and subcutaneous infection are intracranial complications, whereas pseudocyst formation, intestinal volvulus, and spontaneous bowel perforation are intra-abdominal complications. one of the complications of vp shunt is the migration of the shunt. this migration typically occurs distally, into the thorax, diaphragm, heart, pleural cavity, breast, stomach, gallbladder, liver, umbilicus, inguinal canal, hernia sac, scrotum, urinary bladder, urethra, vagina, colon, and rectum, among other places.3 on the other hand, proximally total 226 ahtesham khizar, syed aamir shah, soha zahid et al. intracranial migration of the vp shunt is a very uncommon complication. total upward intracranial migration of vp is estimated to be between 0.1 and 0.5 percent.4 we discovered twenty-eight cases of total intracranial vp shunt migration to date after conducting a thorough literature review (table.1). although the precise cause of this unusual complication is unknown, a number of factors are thought to play a role in proximal shunt migration. paediatric patients are particularly vulnerable to shunt migration due to the shorter distance between the peritoneum and the cranium. this short distance, combined with violent, uncontrolled head movements, could result in mechanical shunt displacement.5 another possibility for proximal shunt migration is insufficient distal shunt fixation or detachment due to rapid growth in the early stages of life.6,7 furthermore, the thin cortical mantle, large ventricles, and wide fontanelles produce intracranial pressure close to atmospheric pressure, whereas abdominal pressure remains positive in comparison to atmospheric pressure. this produces a pressure gradient, which can cause the shunt to suction towards the cranium. this drastic complication can be avoided by tightly securing connector sites of the shunt to the periosteum and by avoiding large dural openings and burrholes.5 it is interesting to note that numerous additional case reports list comparable patient-related characteristics, such as malnutrition, younger age, a thin cortical layer, and severe hydrocephalus, all of which may be connected to upward shunt migration.4,5,6,7 in most vp shunt insertions, a burrhole is made in the occiput to provide a straight path up from the peritoneum because it is the simplest mode of insertion, but as the path is straightforward, it may contribute to cranial shunt migration.8 due to their affordability, chhabra shunt systems are commonly used in our area. this type of shunt system contains a valve and a reservoir, but the valve is cylinder-shaped and it has a diameter that is just a little bit larger than the shunt tube. it appears that this type of shunt system is more vulnerable to migration. in our case, we used a neuro endoscope to remove the shunt assembly through a burrhole to avoid craniotomy-related morbidity. the safe removal of the shunt tube and prevention of unintentional pulling, which could result in choroid plexus bleeding, are additional benefits of using a neuro endoscope. in the future, as an alternative to shunting techniques, the use of endoscopic third ventriculostomy and choroid plexus cauterization should be acknowledged and encouraged in suitable patients. table 1. twenty-eight previously reported cases of intracranial migration of ventriculoperitoneal shunt in literature. s. no. authors' name year reported no. of cases reported 1 mori k et al.6 1975 1 2 gariejo ja9 1979 1 3 villarejo f et al.10 1979 1 4 drigo p et al.11 1983 2 5 young ha et al.7 1983 2 6 eljamel ms et al.12 1995 1 7 ammar a and nasser m8 1995 1 8 abou el nasr ht13 1998 1 9 gupta pk et al.14 1999 1 10 dominguez cj et al.15 2000 1 11 acharya r et al.16 2002 1 12 shimzu et al.17 2002 1 13 umberto pereira c et al.18 2004 1 14 nadkarni td et al.5 2007 1 15 oluwole ke and abiodun aa19 2007 1 16 ali mn et al.20 2008 1 17 agarwal a and kakani a21 2011 1 18 shahsavaran s et al.2 2012 2 19 naik v et al.22 2013 1 20 malhotra a and malhotra m23 2015 1 21 sharma r et al.4 2015 1 227 total intracranial migration of ventriculoperitoneal shunt 22 gundogdu eb et al.24 2017 1 23 shrestha r et al.3 2018 1 24 mehtab h et al.25 2021 1 25 deo rc et al.26 2022 1 conclusions total intracranial migration of the vp shunt in individuals with severe hydrocephalus is an uncommon but significant event. the optimum strategy for limiting shunt migration would involve better shunt attachment to the pericranium and peritoneum, a frontal burrhole instead of an occipital burrhole, and a smaller burrhole opening. additionally, parents should be informed about warning signs and shunt related issues and should receive continuous follow-up. a nationwide analysis of the prevalence as well as incidence of risk variables for vp shunt migration is advised to direct future therapeutic practises. abbreviations vp: ventriculoperitoneal ct: computed tomography references 1. surchev j, georgiev k, enchev y, avramov r. extremely rare complications in cerebrospinal fluid shunt operations. j neurosurg sci. 2002;46(2):100-103. 2. shahsavaran s, kermani hr, keikhosravi e, nejat f, el khashab m. ventriculoperitoneal shunt migration and coiling: a report of two cases. j pediatr neurosci. 2012;7(2):114-116. 3. shrestha r, pradhan r, pradhan mm. intracranial migration of proximal and distal components of ventriculoperitoneal shunt in the child. world j surg surgical res. 2018; 1. 2018;1038. 4. sharma rk, bansal m, agrawal m, gupta a, sinha vd. complete intracranial migration of a ventriculoperitoneal shunt: rare complication of a common procedure. neurol india. 2015;63(1):106-107. 5. nadkarni td, menon rk, dange nn, desai ki, goel a. cranial migration of complete ventriculo-peritoneal shunt assembly. j clin neurosci. 2007;14(1):92-94. 6. mori k, yamashita j, handa h. "missing tube" of peritoneal shunt: migration of the whole system into ventricle. surg neurol. 1975;4(1):57-59. 7. young ha, robb pj, hardy dg. complete migration of ventriculoperitoneal shunt into the ventricle: report of two cases. neurosurgery. 1983;12(4):469-471. 8. ammar a, nasser m. intraventricular migration of vp shunt. neurosurg rev. 1995;18(4):293-295. 9. garijo ja, pecourt jc, de la resurrección m. migration of ventriculo-peritoneal shunt into lateral ventricle of an adult. surg neurol. 1979;11(5):399-400. 10. villarejo f, alvarez-sastre c, gimenez d, gonzalez c. migration of an entire one-piece shunt into the ventricle. neurochirurgia (stuttg). 1979;22(5):196-198. 11. drigo p, casara gl, laverda am, et al. una rara complicanza dell'intervento di shunt ventricoloperitoneale: la migrazione intracranica del sistema derivativo [a rare complication of ventriculo-peritoneal shunt: intracranial migration of the derivative system]. pediatr med chir. 1983;5(6):623-624. 12. eljamel ms, sharif s, pidgeon cn. total intraventricular migration of unisystem ventriculo-peritoneal shunt. acta neurochir (wien). 1995;136(3-4):217-218. 13. abou el nasr ht. modified method for prophylaxis against unishunt system complications with presentation of total intraventricular migration of unisystem ventriculoperitoneal shunt. childs nerv syst. 1988;4(2):116-118. 14. gupta pk, dev ej, lad sd. total migration of a ventriculoperitoneal shunt into the ventricles. br j neurosurg. 1999;13(1):73-74. 15. dominguez cj, tyagi a, hall g, timothy j, chumas pd. sub-galeal coiling of the proximal and distal components of a ventriculo-peritoneal shunt. an unusual complication and proposed mechanism. childs nerv syst. 2000;16(8):493-495. 16. acharya r, bhutani a, saxena h, madan vs. complete migration of ventriculoperitoneal shunt into the ventricle. neurol sci. 2002;23(2):75-77. 17. shimizu s, mochizuki t, nakayama k, fujii k. visual field defects due to a shunt valve migrating into the cranium. acta neurochir (wien). 2002;144(10):1055-1056. 18. umberto pereira c, silva santos ea, silva monteiro jt, araújo dias la. migration of ventriculoperitoneal shunt catheter into the cranium-case report. rev. chil. neurocir. 2004:46-7. 19. oluwole ke, abiodun aa. complete intraventricular migration of a ventriculo-peritoneal shunt-a case report and brief literature review. afr j neurol sci. 2007;26:6974. 20. ali mn, atif sm, khan s. intracranial migration of a ventriculoperitoneal shunt. j coll physicians surg pak. 2008 jun 1;18(6):382-3. 21. agarwal a, kakani a. total migration of a ventriculoperitoneal shunt catheter into the ventricles. j pediatr neurosci. 2011;6(1):88-89. 22. naik v, phalak m, chandra ps. total intracranial shunt migration. j neurosci rural pract. 2013;4(1):95-96. 23. malhotra a, malhotra m. ventricular migration of shunt: chhabra shunt complication. international surgery journal. 2016 dec 14;2(4):706-9. 24. gundogdu eb, ozsoy u, tuzun y. complete intraventricular migration of the ventriculoperitoneal shunt. the european research journal. 2017;3(1):87-9. 228 ahtesham khizar, syed aamir shah, soha zahid et al. 25. mehtab, h., khizar, a., zahid, s. et al. complete intracranial migration of ventriculoperitoneal shunt: a common procedure with a rare complication. egypt j neurosurg 36, 34 (2021). 26. deo rc, acharya a, senapati sb, panigrahi s, mohapatra ak. complete intraventricular migration of ventriculoperitoneal shunt: a rare case report. int j surg case rep. 2022;101:107772. microsoft word 11vukaleksic_familial romanian neurosurgery (2018) xxxii 4: 607 612 | 607             doi: 10.2478/romneu-2018-0078 familial cerebral cavernous malformation syndrome in serbian family aleksić vuk1, mandarić aleksandar2, mihajlović miljan1, aleksić nemanja3, rapaić marko4, jovančević miroljub5, stanić milenko1, samardžić marko1, popović igor1, miladinović vladimir1, spaić milan1 1department of neurosurgery, clinical hospital center zemun, belgrade, serbia 2department of radiology, clinical hospital center zemun, belgrade, serbia 3clinic for cardiac surgery, clinical center of serbia, belgrade, serbia 4faculty for special education and rehabilitation, university of belgrade, serbia 5department of radiology, “euromedik” hospital, belgrade, serbia abstract: cavernomas are benign vascular malformations, and about 50% of all cases are multiple. the hereditary form of brain cavernomas is uncommon, and it is certainly under diagnosed. another entity is familial cerebral cavernous malformation syndrome. it is defined as the occurrence of multiple cavernomas or the occurrence of cavernomas in at least two members of a family or the presence of a mutation in one of the three genes causing familial cerebral cavernous malformation syndrome. we present a serbian family in which three consecutive members of family had brain cavernoma. according to our knowledge, this is second case of hereditary cavernoma described in serbian population. key words: cavernoma; familial cerebral cavernous malformation syndrome; multiple cavernomas introduction cavernomas are a benign vascular malformations (e.g. hamartomas), and about 50% of all cases are multiple (1). they are located in the brain or rarely in the spinal cord. the size of cavernomas ranges from a few millimeters to several centimeters. cavernomas increase or decrease in diameter and increase in number over time. the majority of cavernomas become apparent between the second and fifth decades with presentation such as focal neurological defcit, headache, seizure, or cerebral hemorrhage (2). the hereditary form of cavernomas is relatively rare, and this, usually autosomal dominant pathology generally presents with focal neurological symptoms and seizures, however, many patients remain 608 | vuk et al familial cerebral cavernous malformation syndrome in serbian family             asymptomatic, although, acute hemorrhages sometimes appear over time (3). we present a serbian family in which three consecutive members of family had brain cavernoma. according to our knowledge, this is second case of hereditary cavernoma described in serbian population. case presentation the first patient is a 35 years old female who presented to our emergency department with headache, right sided paresthesis, and persistent singultus (hiccup). she rated the pain as 8 out of 10. a head ct was performed and brain stem bleeding was suspected. the cranial mri revealed a cavernoma with signs of hemorrhage in the region of medulla oblongata and medulla spinalis junction (figure 1). figure 1. cranial mri showing a cavernoma with signs of hemorrhage in the region of medulla oblongata and medulla spinalis junction. (a) swi sequence. (b) t2 sequence corticosteroid therapy was started, and symptoms disappeared. however, she had occasional attacks of right sided body numbness. one year after first onset of symptoms, control mri showed enlargement of cavernoma with signs of hemosiderin deposits, after which she was accepted for stereotactic radio-surgery treatment in another hospital, which was performed about 2 years after the first onset of symptoms. also, she was treated with a total of 1200cgy to 85% isodense line to the cavernoma lesion, using 6d skull igrt system. she didn’t suffer from any side effects, and control mri showed signs of cavernoma regression, without signs of de novo hemorrhage (figure 2). figure 2. control mri with signs of cavernoma regression her neurological finding was normal, and she was without complaints. control mri after two years showed state after radiation therapy, and cavernoma dimensions were unchanged. however, swi mri sequence was performed and multiple brain cavernomas without signs of hemorrhage were found, and further neuro-radiological follow ups were advised. control mri was performed in another hospital, and we couldnt obtainen the images, but only radiological description. also, since multiple cavernomas were found on the last mri, familial form of cerebral cavernous malformation was suspected. mri was performed in patient’s father at the age of 73, and multiple brain cavernomas, without sigs of hemorrhage were found (figure 3). romanian neurosurgery (2018) xxxii 4: 607 612 | 609             patient had normal neurological finding, and also only follow ups were recommended. in further investigation, we performed brain mri in patient’s 15-year old son, and single caveroma located in pons was found (figure 4). figure 3. brain mri showing multiple cavernomas figure 4. brain mri showing caveroma located in pons. (a) swi sequence. (b) dwi sequence this young patient had normal neurological status, and since he is symptom free, only regular brain mri controls are recommended. no other members of family undergo radiological investigations. discussion brain cavernous malformations or cavernous angiomas are vascular malformations in the brain or sometimes in spinal cord. in one third of patients, these cavernous malformations are multiple. the hereditary form of brain cavernomas is uncommon, and it is certainly under diagnosed (3). we present a serbian family in which three consecutive members of family had brain cavernoma, of which in 2 members, 610 | vuk et al familial cerebral cavernous malformation syndrome in serbian family             cavernomas were multiple, and one member had solitary lesion. another entity is familial cerebral cavernous malformation syndrome. it is defined as the occurrence of multiple cavernomas (usually 5 or more) or the occurrence of cavernomas in at least two members of a family or the presence of a mutation in one of the three genes causing familial cerebral cavernous malformation syndrome. three genes are known to cause muta¬tions in familial cerebral cavernous malformation syndrome: krit-1 (ccm-1), ccm-2, and pdcd-10 (ccm-3) (table 1) (3-6). table i diagnostic criteria’s for familial cerebral cavernous malformation syndrome (at least 1 of the following criteria) the presence of multiple brain or spinal cord cavernomas (typically 5 or more) the occurrence of brain or spinal cord cavernomas in at least 2 members of a family the presence of a mutation in one of the three genes causing familial cerebral cavernous malformation syndrome according to presented criteria’s, this is almost typical familial cerebral cavernous malformation syndrome, and to our knowledge, this is second case of hereditary cavernoma described in serbian population, first being described by mitić et al. (7). the disease frequently presents with focal neurological deficit (35-50%), and epileptic seizures (38-55%) (8). a headache, spontaneous paraplegia, or signs of cerebral hemorrhage are less frequently encountered symptoms and signs. also, one quarter to one half of patients with cavernomas remain symptom free during life (9). in presented family, one patient had two frequent symptoms: headache, and focal neurological deficit-parestheis. however, this patient also had prolonged hiccups (singultus), which is defined as singultus lasting more than 2 days. eisenacher and spiske presented a similar case in which patient had persistent hiccups as the presenting symptom of medullary cavernoma. conducting literature review we found two more similar cases of persistent cavernoma due to presence of medullary cavernoma (10). according to described cases, as well as study of musumeci et al, conducted on animals, the region of the medulla oblongata lateral of the obex is probably responsible for the singultus reflex (11). overall, singultus is rarely described in the context of a tumor or vascular malformation (e.g. cavernoma) in the region of the medulla oblongata, but persistent singultus, lasting more than 48 hours should arouse suspicion on this rare cause or some other rare neurological disorder. genetic testing may confirm suspicion on familial cerebral cavernous malformation syndrome. three genes muta¬tions are found in this hereditary syndrome: krit-1 (ccm1), ccm-2, and pdcd-10 (ccm-3) (6). also, this is an autosomal dominant disease, and romanian neurosurgery (2018) xxxii 4: 607 612 | 611             each child of a person with familial cerebral cavernous malformation syndrome has a 50% chance of inheriting the mutation. a higher incidence of this disease is found in hispanoamerican individuals of mexican descent, probably due to a common ancestor with a mutation in the krit-1 gene (12). in presented family, we didn’t perform genetic testing, since family wasn’t motivated. in majority of cases, mri shows multiple focal regions of susceptibility induced signal loss of different size, well seen on gradientecho sequences, or better on susceptibilityweighted imaging (swi sequence). lesion can be multiple (about 30% of patients), and in familiar form, the number of cavernomas is higher, in majority of cases more than 5. number of lesions is increasing with age. however, young patients may already have numerous cavernomas (13). in our case, mri features of all patients were typical, with swi sequence being most valuable. in two out of 3 patients from presented family, cavernomas were multiple, while the youngest patient had only one cavernoma. one patient received stereotactic radio-surgery treatment, after which neuroradiological follow ups were advised. for other two patients only regular follow ups were indicated. microsurgical removal of cavernoma is may be reasonable if patient has epileptic seizures, or focal deficit due to mass effect or recurrent bleeding. stereotactic radiosurgery is a safe therapy for cavernomas located in deep or eloquent sites (3, 14). it is important to find structural and the functional abnormalities with data from eeg, mri, and spect so the spatial relationships may be demonstrated, which can help in the decision making for right therapy approach. in presented family, one patient had to be subjected to stereotactic radiosurgery, since she had cavernoma presented with focal neurological deficit, and radiological signs of repeated bleeding, while other two patients were asymptomatic, and only neuroradiological follow ups were advised. references 1.kayali h, sait s, serdar k, kaan o, ilker s, erdener t. intracranial cavernomas: analysis of 37 cases and literature review. neurol india. 2004;52(4):439-42. 2.morrison l, akers a. cerebral cavernous malformation, familial. 2003 feb 24 [updated 2016 aug 4]. in: adam mp, ardinger hh, pagon ra, wallace se, bean ljh, stephens k, amemiya a, editors. genereviews® [internet]. seattle (wa): university of washington, seattle; 1993-2018. 3.mespreuve m, vanhoenacker f, lemmerling m. familial multiple cavernous malformation syndrome: mr features in this uncommon but silent threat. j belg soc radiol. 2016 mar 21;100(1):51. 4.denier c, labauge p, brunereau l, cavé-riant f, marchelli f, arnoult m cecillon m, maciazek j, joutel a, tournier-lasserve e; sociéte française de neurochirgurgie; sociéte de neurochirurgie de langue française. clinical features of cerebral cavernous malformations patients with krit1 mutations. ann neurol. 2004 feb;55(2):213-20. 5.verlaan dj, davenport wj, stefan h, sure u, siegel am, rouleau ga. cerebral cavernous malformations: mutations in krit1. neurology. 2002 mar 26;58(6):853-7. 6.labauge p, denier c, bergametti f, tournier-lasserve e. genetics of cavernous angiomas. lancet neurol. 2007 mar;6(3):237-44. 7.mitić r, stojanović n, radovanović z, rasulić l. familial cavernous angiomatosis: case report of a family with multiple intracranial lesions. acta chir croat 2016; 13: 43–51. 8.brunereau l, labauge p, tournier-lasserve e, laberge s, levy c, houtteville jp. familial form of intracranial cavernous angioma: mr imaging findings in 51 families. 612 | vuk et al familial cerebral cavernous malformation syndrome in serbian family             french society of neurosurgery. radiology. 2000 jan;214(1):209-16. 9.siegel am, andermann e, badhwar a, rouleau ga, wolford gl, andermann f, hess k. anticipation in familial cavernous angioma: a study of 52 families from international familial cavernous angioma study. ifcas group. lancet. 1998 nov 21;352(9141):1676-7. 10.eisenacher a, spiske j. persistent hiccups (singultus) as the presenting symptom of medullary cavernoma. deutsches ärzteblatt international. 2011;108(48):822826. 11.musumeci a, cristofori l, bricolo a. persistent hiccup as presenting symptom in medulla oblongata cavernoma: a case report and review of the literature. clin neurol neurosurg. 2000;102 12.haasdijk ra, cheng c, maat-kievit aj, duckers hj. cerebral cavernous malformations: from molecular pathogenesis to genetic counselling and clinical management. eur j hum genet. 2012 feb;20(2):134-40. 13.brunereau l, levy c, laberge s, houtteville j, labauge p. de novo lesions in familial form of cerebral cavernous malformations: clinical and mr features in 29 nonhispanic families. surg neurol. 2000 may;53(5):475-82; discussion 482-3. 14.nagy g, razak a, rowe jg, hodgson tj, coley sc, radatz mw, patel uj, kemeny aa. stereotactic radiosurgery for deep-seated cavernous malformations: a move toward more active, early intervention. clinical article. j neurosurg. 2010 oct;113(4):691-9. doi: 10.33962/roneuro-2023-030 chiari 1 malformation with platybasia. a case report abdurrahman mousa, deni nasution, muhammad ari irsyad, fahmi rasyid romanian neurosurgery (2023) xxxvii (2): pp. 170-174 doi: 10.33962/roneuro-2023-030 www.journals.lapub.co.uk/index.php/roneurosurgery chiari 1 malformation with platybasia. a case report abdurrahman mousa, deni nasution, muhammad ari irsyad, fahmi rasyid department of neurosurgery, faculty of medicine, universitas sumatera utara, indonesia abstract background. the incidence of cm-i is estimated to be 1/1,000 births. in rare cases, cm-i is complicated by associations with other malformations of the craniocervical junction, including mainly basilar invagination (bi). chiari malformation (cm) is characterized by a congenital malformation of the posterior cranial fossa with cerebellar tonsils herniation through the foramen magnum, probably due to the underdevelopment of the posterior bony skeleton (exo-occipital and supraoccipital bones). cm may be complicated by a variety of other malformations, including platybasia, basilar invagination and occipitalization, although syringomyelia (sm) is the most commonly observed case report. a girl, 14 years old came with a chief complaint of headache, which is exacerbated whenever the patient coughed or sneezed. the patient also complained about neck pain and a tingling sensation in her hand. a history of vomiting or seizure has not been found. a history of muscle weakness was not found. on physical examination, the patient has a gcs score of 15 on admission, with normal muscle tone and normal reflexes. the patient has a sensory deficit, on the level below c4. the patient underwent ct scan and mri whole spine, chiari 1 malformation and platybasia were diagnosed. the patient underwent posterior fossa decompression, and postoperatively symptoms of chiari and sensory deficit gradually improved. discussion. as an association with this syndrome, there is also basilar invagination as shown by flat basioccipt (platybasia) and upward odontoid projection. hydrocephalus [3]. virchow coined the term ‘platybasia’ to describe an abnormal flattening of the skull base, a defect which he attributed to abnormal bone development. in addition to the flattening of the base of the skull, there was upward displacement (impression) of the basilar and condylar portions of the occipital bone, which caused infolding, or impression of the foramen magnum, reduction of the posterior fossa, and consequent protrusion of the upper cervical spine into the anterior brainstem, with neurological signs. the symptomatology presented by cm-1 patients is diverse, and its severity does not correlate with the degree of th, with some asymptomatic cases presenting with prominent th. the onset of symptoms generally develops gradually, however, trauma, coughing/sneezing or pregnancy can also precipitate the event. the most common treatment for these patients is surgical pcf decompression (alone or with duraplasty), although cerebellar tonsillectomy, cervical laminectomy, and suboccipital cranioplasty are also applied. the goal of these surgical procedures is to decompress the foramen magnum and increase the subarachnoid space in order to avoid the impaction of the cerebellar tonsils, reestablish the csf flow and reverse the symptoms keywords chiari malformation, platybasia, posterior fossa surgery corresponding author: abdurrahman mousa department of neurosurgery, faculty of medicine, universitas sumatera utara, indonesia machiavafabignami@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 171 chiari 1 malformation with platybasia conclusion. this patient was diagnosed with chiari 1 malformation and platybasia, as suggested in the literature, posterior fossa decompression was done and the patient improved clinically. background according to estimates, 1 in 1,000 newborns will result in cm-i. in a small percentage of instances, cmi is complicated by relationships with other craniocervical junction abnormalities, primarily basilar invagination (bi).1a cerebellar tonsil herniation through the foramen magnum is a characteristic of the chiari malformation (cm), which is most likely caused by the posterior bony skeleton's incomplete development (exo-occipital and supraoccipital bones).2 the cerebellar tonsils and the medial sections of the lower cerebellar lobes were pushed >5 mm past the craniospinal transition and into the upper spinal canal, resulting in the disease known as chiari malformation type i. (cm-i).1 syringomyelia (sm) is the most frequently reported abnormality, but cm may be worsened by a number of other deformities, such as platybasia, basilar invagination, and occipitalization.3 basilar invagination, basilar impression, and platybasia are examples of congenital and acquired abnormalities of the craniovertebral junction (cvj), which can manifest as either abrupt or slowly advancing neurologic impairment.4 while basilar invagination refers to the projection of the odontoid process toward the posterior fossa, platybasia refers to flattening of the skull base. basilar impression, platybasia, brainstem kinking, and retroflexed odontoid deformities were present in 7.7% of our chiari malformation type i patients.6 figure 1. ct and mri of patient, chiari i was found. in addition to a reduction in the size of the posterior cerebral fossa (pcf), cm is usually linked to a number of disorders including platybasia, basilar invagination, and clivus concavity. in roughly 20–72% of instances involving csf problem, the cerebrospinal fluid (cfs) flow dynamics can deteriorate in cmi, and syringomyelia can develop most frequently in the cervical area. nearly 20–30% of people will experience cranial-vertebral junction anomalies include basilar invagination, platybasia, a small posterior fossa, concavity of the clivus, occipitalization of the atlas, and spina bifida in the upper cervical area.7 figure 2. mri of spine. figure 3. posterior fossa decompression surgery done on patient. case report a girl, 14 years old came with a chief complaint of headache, which is exacerbated whenever patient 172 abdurrahman mousa, deni nasution, muhammad ari irsyad et al. coughed or sneezed. patient also complain about the neck pain and tingling sensation on hand. history of vomiting or seizure has not been found on patient. history of muscle weakness was not found. on physical examination, patient has gcs score of 15 on admission, with normal muscle tone and normal reflex. patient has sensory deficit, on level below c4. patient underwent ct scan and mri whole spine, chiari 1 malformation and platybasia was diagnosed. patient underwent posterior fossa decompression, and postoperatively symptom of chiari and sensory deficit gradually improving. discussions the most common kind of "chiari malformations," known as chiari malformation type 1 (cm-1), is characterized by a downward herniation of the caudal section of the cerebellum into the upper cervical area through the foramen magnum.8 syringomyelia and a downward tonsillar herniation make up the chiari i malformation. additionally, basilar invagination, as evidenced by a flat basioccipt (platybasia) and an upward odontoid projection, is associated with this disease. the dens should typically extend up to 3 mm above the chamberlain line and 5 mm above the mcgregor line.9 according to bao et al., problems related to chiari i malformation (cmi) included hydrocephalus in 17 patients, 51 patients with basilar impressions, 38 patients with platybasia, 32 patients with occipitalization, 67 patients with scoliosis, and 16 patients with neuropathic arthropathy.3 to characterize an abnormal flattening of the skull base, a deformity he linked to aberrant bone growth, virchow developed the name "platybasia." the occipital bone's basilar and condylar portions were displaced upward, flattening the base of the skull in addition. this upward displacement resulted in reduction of the posterior fossa, infolding of the foramen magnum, and protrusion of the upper cervical spine into the anterior brainstem, along with neurological symptoms.10 it is commonly recognized that platybasia and basilar invagination are related. in his initial investigation, chamberlain referred to both of these things as being the same thing. later, a number of scholars questioned platybasia's clinical value and claimed that it solely had anthropological significance. the more horizontal angulation and shortening of the clivus were related to the superior position of the odontoid process. klaus observed that the tip of the odontoid process almost never reaches the wackenheim clival line in basilar invagination associated with platybasia, whereas in a steeply shelving or normal clivus, the line from the dens frequently reaches or even overshadows it. the presence of platybasia suggests that it played a similar role to odontoid process invagination in producing the front concavity of the brainstem and decreasing the size of the posterior fossa.11 the current diagnosis of chiari malformation type 1 relies on imaging evidence of cerebellar tonsil herniation (th) that extends at least 3-5 mm below the foramen magnum. in other words, the resulting decreased cranial space causes overcrowding in the brain processes and causes the cerebellum to herniate through the foramen magnum. this directly compresses the neural tissue at the craniovertebral junction and frequently causes disruptions in the cerebrospinal fluid (csf) (decreased velocity and increased impedance), which can lead to various related diseases. the symptoms displayed by cm-1 patients are varied, and the severity of the symptoms does not always correspond to the degree of th, with some asymptomatic instances exhibiting substantial th. the onset of symptoms often happens gradually, although it's possible for trauma, coughing/sneezing, or pregnancy to trigger it.8 for more than a century, basilar invagination has been associated with physical characteristics such a short neck, low hairline, web-shaped neck muscles, torticollis, a reduction in the range of neck movements, and several other morphological abnormalities. there have also been reports of other bone fusion abnormalities and platybasia. it is common to experience neck pain, muscle spasms, and restricted neck movement, all of which point to localized instability.11 the most effective diagnostic approach for identifying chiari malformation is mri. mri can reveal precise anatomical details on the structures in the cranial basement. the diameter of the foramen magnum, the volume of the pcf, and the condition of the platybasia were measured using cranial distance and angle measurements. measurements of pcf development and platybasia were made using the slope of the tentorium cerebelli. the patient group showed a considerable reduction in distances measured for the evaluation of platybasia, such as the distance between the chamberlain line and the tip of the dens axis, the klaus index, the clivus length, 173 chiari 1 malformation with platybasia and the distance between the internal occipital protuberance and the opisthion. the measurement of head basis angles reveals a platybasia tendency.7 although cerebellar tonsillectomy, cervical laminectomy, and suboccipital cranioplasty are also used, surgical pcf decompression (either alone or in conjunction with duraplasty) is the most often used treatment for these patients. in order to prevent the impaction of the cerebellar tonsils, restore the csf flow, and treat the symptoms, these surgical treatments aim to widen the foramen magnum and enhance the subarachnoid space.8 to choose the best care and compare surgical results, it is becoming increasingly important to divide all other cases into particular subgroups. chiari malformation type i is the general term for the results of cmi patients who have a platybasia or a hypoplasic posterior cerebral fossa. actually, the same surgical procedure, posterior fossa decompression, with or without dural expansion, might result in a further hindbrain descent in the first case or in “ascent” of the cerebellar tonsils in the second case.12 marinpadilla concluded from their study that the chiari-like deformities reflect the effects of clival and occipital molding, which act mainly anteriorly. platybasia did not directly result in any neurological symptoms, but it participated with basilar invagination in critically reducing the posterior cranial fossa volume.11 conclusion chiari malformation is generally related to occipital bone dysplasia and it is frequently associated with various conditions such as platybasia, basillar invagination and clivus concavity in addition to decrement in posterior cranial fossa (pcf) size. chiari malformation type 1 results in a direct compression of the neural tissue at the craniovertebral junction and, often, cerebrospinal fluid (csf) disturbances (decreased velocity and elevated impedance), that can cause other related conditions and bone fusion deformities such as platybasia. mri method is the best diagnostic tool for detecting chiari malformation. mri provides detailed anatomical information regarding the structures located at the cranial basement. the most common treatment for these patients is surgical pcf decompression (alone or with duraplasty), although cerebellar tonsillectomy, cervical laminectomy, suboccipital cranioplasty are also applied. the goal of these surgical procedures is to decompress the foramen magnum and increase the subarachnoid space in order to avoid the impaction of the cerebellar tonsils, reestablish the csf flow and reverse the symptoms. list of abbreviation cm: chiari malformation csf: cerebrospinal fluid ct: computed tomography cvj: craniovertebral junction gcs: glasgow coma scale mri : magnetic resonance imagin pcf : posterior cranial fossa sm: syringomyelia th: tonsillar herniation references 1. brito jnp; santos ba; nascimento if; martins la; tavares cb. basilar invagination associated with chiari malformation type i: a literature review. clinics 2019;74:653. 2. joaquim af. severe cerebellar degeneration and chiari i malformation – speculative pathophysiology based on a systematic review. rev assoc med bras. 2020; 66(3): 375379. 3. bao c; yang f; liu l; wang b; li d; gu y; et al. surgical treatment of chiari i malformation complicated with syringomyelia. experimental and therapeutic medicine. 2013; 5: 333-337. 4. pinter, n.k., mcvige, j. & mechtler, l. basilar invagination, basilar impression, and platybasia: clinical and imaging aspects. curr pain headache rep 20, 49 (2016). available from: https://link.springer.com/article/10.1007%2fs11916016-0580-x [accessed on 16th september 2021] 5. silva atpb, silva ltpb, vieira aenr, melo cie, nascimento jjc, mello júnior cf, vasconcelos sc, araújo-neto sa. craniometric parameters for the evaluation of platybasia and basilar invagination on magnetic resonance imaging: a reproducibility study. radiol bras. 2020 set/out;53(5):314–319 6. royo-salvador mb; fiallos-rivera m; salca h. caudal traction as a pathogenetic mechanism of chiari malformation type i. intechopen. 2019. available from: https://www.intechopen.com/chapters/70103 [accessed on 16th september 2021] 7. alkoc oa; songur a; eser o; toktas m; gonul y; esi e; et al. stereological and morphometric analysis of mri chiari malformation type-1. journal of korean neurosurgical society 2015; 58(5): 454-461. 8. urbizu a, khan tn, ashley-koch ae. genetic dissection of chiari malformation type 1 using endophenotypes and stratification. j rare dis res treat. (2017) 2(2): 35-42 9. abdrabou, a. chiari 1 malformation with basilar invagination. case study, radiopaedia.org. (accessed on 174 abdurrahman mousa, deni nasution, muhammad ari irsyad et al. 16 sep 2021) https://radiopaedia.org/cases/34375 10. pearce jms. platybasia and basilar invagination. eur neurol 2007;58:62–64 11. goel a. basilar invagination, chiari malformation, syringomyelia: a review. neurol india 2009;57:235-46 12. rocco cd. should we stop using the term “malformation” for chiari type 1?. child's nervous system (2019) 35:1649–1650. romanian neurosurgery (2019) xxxiii (2): pp. 174-177 doi: 10.33962/roneuro-2019-032 www.journals.lapub.co.uk/index.php/roneurosurgery spinal extradural meningioma en plaque with nerve root attachment and extracanal (intrathoracic) extension. review of literature on management and case report morgan e.1, hakkou m.2, mellaoui a.2, poluyi e1, el ouahabi a.2 1 lagos university teaching hospital, idi-araba, lagos, nigeria 2 faculte de medicine et de pharmacie, mohamed v. university, souissi rabat, morocco abstract meningiomas are relatively common primary spinal tumours, being the second most common intraspinal tumours probably after vertebral haemangioma. it constitutes about 25% of all intraspinal tumours; however, in the presence of extradural spinal lesions, the diagnosis of meningioma is uncommon and often not among the first two considerations. purely extradural spinal meningioma, especially of the “en plaque” variety, usually simulate malignant disease (metastatic diseases and lymphoma) and may result in inadequate therapy, however, the presence of nerve root attachment is even rarer. our case report is that of an entirely cervicothoracic extradural en‑plaque meningioma (who grade 1) with a nerve root attachment (right c7) and intrathoracic extension. we highlighted the issues in diagnosis, operative intervention and longterm follow-up. introduction meningiomas account for about a quarter of all intraspinal tumours and literature has shown that it is the second commonest primary intraspinal tumour [1]. the majority of spinal meningiomas are entirely intradural and this is seen in about 10% of cases. there is an extradural spinal extension, but attachment to spinal nerve root and/or intrathoracic extension are not a frequent finding [2]. meningiomas located purely in the extradural space are very rare and, therefore, are not often listed in the differential diagnosis of spinal extradural lesions [2]. we present a case report of purely extradural meningioma “en plaque” of the spine that was noticed to be attached to right c7 nerve root which create a bias for preoperative diagnosis of spinal schwannoma (intradural extramedullary) with extradural extension. keywords spinal extradural meningioma, intrathoracic extension, case report corresponding author morgan eghosa lagos university teaching hospital, idi-araba lagos, nigeria morganeghosa@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 175 spinal extradural meningioma en plaque with nerve root attachment and extracanal (intrathoracic) extension case report we report a case of a 28-year old woman with no previous significant medical history presented with 2-month history of progressive spastic tetraparesis (with muscle power in most muscle groups being 4) associates with right brachio-cervical hyperesthesia involving c6/c7 distribution. cervico -thoracic magnetic resonance imaging (mri) don e was reported as intradural extramedullary tumour (schwannoma) extending from c4-t1 vertebral level by the radiologist with attachment to right c7 nerve root. lesion was iso-hypointense on tiwi and enhances on t2wi as shown in image 1 and image 2 perioperatively, the tumour was accessed via c4 –t1 laminectomy, and it was entirely extradural extending from c4-t1 with right c7 nerve root attachment and extending to the intrathoracic region anteriorly as shown in intra-operative images 1 and 2. the tumour was firm, fibrous, highly vascular and dissectible, tumour resected with coagulation of the attachment to right c7 nerve root but the intrathoracic component left in-situ. both frozen section and definitive histopathological/immunohistochemical analyses confirmed mengioma “en plaque” (who grade 1) as shown in histology slides below. 176 morgan e., hakkou m., mellaoui a et al. post operatively, there was an initial loss of sensory modality of right c7 nerve root distribution which improved subsequently in conjunction with motor functions (preoperative tetraplegia) after six (6) weeks of function education and rehabilitation. follow up is been done regularly using both clinical and radiological tools and there has not been change in improvement achieved postoperatively and also the size of the intrathoracic component. discussion meningioma is one of the commonest central nervous system (cns) tumours which is essentially a benign tumour. majority are intracranial, with about 90% supratentorial, but spinal meningioma account for between 1.2%-12,5% of all meningiomas [3,4,5}. meningioma arises from arachnoid cap ceil (meningiothelial cell in the arachnoid villi just like any meningioma elsewhere). the prevalence of extradural meningioma in literature ranges from 3.3% and 21.4% of all cases of spinal meningioma [6]. tumours occur more in female to male of ratio 4:1 with a peak incidence between 5thand 6th decades of life. almost about 80% occur in the thoracic spinal region [6]. majority of these lesions are intradural extramedullary and are placed ventral or ventrolaterally to the dura, however, about 10% do extend to the extradural space [2]. the presence of a “sole” extradural spine meningioma is entirely rare [2]. common tumours located in the spinal extradural space are metastatic spinal tumour and lymphoma, hence the dilemma in preoperative diagnosis which was also emphasis by saryedekar et al in the two cases reported by them [7]. our patient reported above had purely extradural spinal “en plaque” meningioma with right c7 nerve root attachment and intrathoracic extension. the occurrence of “en plaque” variety of meningioma is rarer. moreso, the presence of nerve root attachment with or without intrathoracic extension is even much more a rarity. only 16 cases in literature have shown extradural spinal meningioma adhering/proximity to spinal nerve root. tuli et al in their case report of a 42-year old lady with t4-t6 extradural spinal meningioma revealed attachment to left t5 spinal nerve root. the presence of extradural meningioma with or without nerve root attachment remain a puzzle and been described as a paradox in view of absence of arachnoid cap cell in the extradural space. several theories have been ascribed to the occurrence of an entirely extradural spinal meningioma and possibility of nerve root adherence. reasons adduced for these in literatures include migration of arachnoid tissue into the extradural space, or extradural spinal meningioma could arise from ectopic or separated arachnoid tissue around the periradicular nerve root sleeve, which is the point of contact of the spinal leptomeninges directly into the dura. this probably explains the attachment to nerve root [2]. another reason alluded to the occurrence of spinal extradural meningioma is that the periradicular dura which is said to be less thick, may have vestigial remnants of the superficial layer of the embryonal arachnoid mater and villi [6] also, it has been suggested that islands of arachnoid tissue that may have migrated into the extradural space can be the source of the meningioma [2,6]. an entirely spinal extradural meningioma especially of the ‘en plaque; variety poses a dilemma in pre-operative diagnosis [2, 7]. in this index case, a pre-operative diagnosis of c4-t1 schwannoma of the spine in view of its location and c7 nerve root attachment. intraoperative frozen section histopathological analysis is a necessity in view of other possibility such as metastatic spine tumour and lymphoma [8]. in this index case, the frozen section was done which showed a meningioma en plaque. this was done for decision making as regards extend of tumour resection. the extradural tumour with its attachment to the right c7 nerve root was resected and point of c7 nerve root adhesion was coagulated. however, the thoracic extension was left in-situ. saryedekar et al in their work shows the importance of intraoperative frozen section with near total resection of spinal extradural meningioma en plaque [7]. this strategy will give the best postoperative outcome, as prognosis depends on the extent of tumour resection [8], another consideration in the operation is to decide whether to open the dura or not. however, in consideration of the pathogenesis of the lesion from the dura nerve root sleeve and not from the external part of the spinal dura. it may be necessary to only 177 spinal extradural meningioma en plaque with nerve root attachment and extracanal (intrathoracic) extension peeled off the tumour from the dura. saryadekar et al in the two cases reported shows that the tumour was stripped off the dura with no durotomy done [7]. though there is essentially no consensus on whether the dura should be excised or not, however, it is necessary that the dura be opened to rule out intradural extension of the meningioma which is seen in literature to account for about 10% of cases [2]. tuli et al. reported 12 cases out of 47 supposedly pure extradural spinal meningioma who had durotomy, three (3) of these 12 patients was noticed to have intradural extension. this buttresses the importance of durotomy in hitherto purely extradural spinal meningioma. we had to open the dura to be very sure that there was not intradural component of the tumour as done in standard procedure [6]. issues relating to long term outcome still remain an item of debate. issues been debated such as gross total resection versus incomplete resection, benign versus malignant meningioma remain an important factor in considering long-term outcome following operation for extradural spinal meningioma. literature has revealed that this tumour may have a local malignant potential despite been a relatively benign tumour. also, worse prognosis is seen with incompletely tumour resection due to bony involvement or paraspinal extension [2, 3, 8]. in the index case been reviewed, all except the thoracic extension was excised. tumour has remained static after a regular follow-up period of over 2 years. conclusion spinal extradural meningioma is a rare tumour, even more with the ‘en plaque’ variety with spinal nerve root attachment. in view of the prevalence of between 3.3% to 21.4%, it is essential that cases of extradural spinal meningioma should be entertained in conjunction with common tumours such as metastatic spine disease and lymphoma and in doubtful cases intraoperative frozen section and durotomy are essential in operative decision making either to do gross total resection or partial. for the incompletely resected tumours, long-term follow-up period using both clinical and radiological monitoring tools is essential. references 1. santiago bm, rodeia p, cunha e sa m. extradural thoracic spinal meningioma. neurol india 2009; 57:98. 2. zevgaridis d, thomé c. purely epidural spinal meningioma mimicking metastatic tumor: case report and review of literature. spine (phila pa 1976) 2002;27: e403‑5. 3. osborn ag: diagnostic neuroradiology. st. louis: mosby; 1994. 4. solero cl, fornari m, giombini s, lasio g, oliveri g, cimino c, pluchino f: spinal meningiomas: review of 174 operated cases. neurosurgery 25:153-160,1989. 5. yamashita j, handa h, iwaki k, abe m: recurrence of intracranial meningiomas, with special reference to radiotherapy. surg neurol 14:33-40, 1980. 6. tuli j, drzymalski dm, lidov h, tuli s. extradural en‑plaque spinal meningioma with intraneural invasion. world neurosurg 2012;77: 202.e5‑13. 7. savardekar a, chatterjee d, chatterjee d, dhandapani s, mohindra s, salunke p. totally extradural spinal en plaque meningiomas diagnostic dilemmas and treatment strategies. surg neurol int 2014;5: s291-4. 8. frank bl, harrop js, hanna a, ratliff j. cervical extradural meningioma: case report and literature review. j spinal cord med 2008; 31:302‑5. doi: 10.33962/roneuro-2020-058 the 3d printed models technology for the management of intracranial aneurysms a. chiriac, georgiana ion, g. stan, s. munteanu, n. dobrin, dana turliuc, i. poeata romanian neurosurgery (2020) xxxiv (1): pp. 373-378 doi: 10.33962/roneuro-2020-058 www.journals.lapub.co.uk/index.php/roneurosurgery the 3d printed models technology for the management of intracranial aneurysms a. chiriac1, georgiana ion1, g. stan2, s. munteanu3, n. dobrin1, dana turliuc1, i. poeata1 1 “gr. t. popa” university of medicine and pharmacy, iasi, romania 2 national institute of materials physics, bucharest magurele, romania 3 transilvania university of brasov, romania abstract management of intracranial aneurysms is still a therapeutic challenge, especially in cases of complex lesions. thus, the improvement of the study and intervention planning possibilities correlated with the access to continuous professional training based on simulation and clinical diversity represent optimal conditions for the efficient solution of this pathology. the development of three-dimensional printing technology offers a new opportunity in the modern treatment of intracranial aneurysms. the aim of this study is to present some aspects related to the materials and methods of manufacturing simulation models of individual 3d printed aneurysms and their influence in the optimal management of these lesions. introduction intracranial aneurysms are increasingly complex vascular lesions, both in terms of their shape and relationships with parent and adjacent vessels. these will require a much more elaborate interventional treatment, based on a much more careful anatomical study and a much clearly interventional planning. the three-dimensional (3d) printing technology is a promising technique with more and more applications in the field of medicine. the development of 3d printing technology provides a new perspective for the treatment of intracranial aneurysm. the intracranial aneurysm 3d printing simulation models created on the basis of 3d angiographic imaging acquisitions offers technical, practical and educational support to both neurointervention specialists and young residents in professional training. the aim of the present study was to presents our experience concerning the materials and methods of producing 3d printed individual aneurysm model and its significance in the treatment of intracranial aneurysm. keywords intracranial aneurysm, 3d printed models corresponding author: a. chiriac “gr. t. popa” university of medicine and pharmacy, iasi, romania chiriac_ a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 374 a. chiriac, georgiana ion, g. stan et al. aneurysm modeling angiographic imaging data generation and postprocessing cta and 3d dsa images data acquisition were used for intracranial aneurism investigation and therapeutically management. dynamic cta images were acquired using a toshiba aquilion 32 ct scanner (canon medical systems usa, inc.). the scanning parameters used are: scan range 16 cm, gantry rotation time 0.75, slice thickness 0.5 mm, field of view (fov) 240 mm, tube potential, 120 kv and tube current 218 ma. a mean total scanning time was 21 s and dlp 930mgy. the 3d dsa images acquisitions were obtained on a clinical biplane carm system toshiba infinix (canon medical systems usa). a 5 s conventional mask and fill run protocol (70 kvp, 0.36mgy/fr, 200° and 133 images were used. the injection parameters were 2.5 ml/s for 7 s with 2 s x-ray delay using 100% contrast concentration. the 3d dsa images acquisitions were obtained on a clinical biplane c-arm system toshiba infinix (canon medical systems usa). a 5 s conventional mask and fill run protocol (70 kvp, 0.36mgy/fr, 200° and 133 images were used. the injection parameters were 2.5 ml/s for 7 s with 2 s x-ray delay using 100% contrast concentration. anatomical 3d computer model reconstruction the original 3d cta or dsa imaging dates, in dicom format, are extracted through the picture archiving and communication system (pacs; erad, china) and imported into mimics (materialise 18, leuven, belgium), a medical reconstruction software suite. mimics allowed the reconstruction of only the intracranial arteries or both arteries and the skull in the case of cta after format conversion and threshold extraction. the image threshold must be carefully adjusted to expose the image of the vessels as clearly as possible. the method of threshold segmentation is combined with manual segmentation to obtain the most important region of interest (roi). also, surrounding tiny branches or interfering bony structures could be removed for a better roi exposure (aneurysm region). then, we used the 3d calculate function to reconstruct the computer model. it is then stored and sent out as stl format files. aneurysm 3d printing model fabrication the stl format file is input into the rapid prototyping 3d printer machine (objet connex350 3d printer objet technologies ltd, rehovot, israel) for virtual model fabrication. if plaster was initially used to make a solid model including the skull, blood vessels and aneurysm, they proved too rigid and fragile to simulate human blood vessels. thus, to create a suitable model of aneurysm it is necessary to use three different materials for the reconstruction of the solid skull, flexible blood vessels and eventually the empty aneurysm. the new types of 3d printers objet connex500, offer the possibility to work with a mixture of rigid and flexible materials. a light-cured resin material for bone reconstruction and a different flexible resin material for vessels and aneurysm modelling were used. both types of 3d models were manufactured with this method. interventional planning all manufactured 3d models were studied by the team of vascular neurosurgeons in order to establish the most appropriate therapeutic approach. the shape, dimensions, orientation and relationships between the aneurysmal sac, its neck, the carrier vessel and the adjacent branches were carefully analyzed to establish the optimal interventional planning for each lesion. a microsurgical clipping or endovascular occlusion was decided. in case of microsurgical clipping the 3d model was used to choose the type of clips, to simulate access and clipping direction, and in more complex lesions to establish the optimal clips arrangement for a complete closing of the aneurysmal neck. for endovascular treatment, the printed 3d models helped both to choose the coils and the proper endovascular technique of aneurysms occlusion. images were exported in standard digital imaging and communication in medicine (dicom) format to the 3d calculation software, soft mimics17.0 (materialise, belgium). soft tissue and brain tissue around the skull was removed. the vascular and bone area was segmented by the software, and the virtual 3d angiogram was generated. the skull, intracranial artery and aneurysm were distinguished by different colors. data from the segmented area was transformed into a stereolithography (stl) format, which was used in the rapid prototyping machine. 375 the 3d printed models technology for the management of intracranial aneurysms case presentation a 43-years-old female patient was addressed to our emergency unit for sudden violent headache followed by a short episode of loss of consciousness 24 hours ago. at the neurological examination the patient was evaluated with gcs of 13 points presenting nuchal rigidity, confusion, somnolence, and no motor deficits. she was immediately investigated by ct scan that showed a subarachoidian hemorrhage in the basal cistern and both sylvian fissures. the patient also presented intraventricular hemorrhage in the fourth and third ventricle (figure 1). after that an angio-ct was performed that revealed an anterior communicating artery aneurysm as a source of bleeding. (figure 2). a 3d printed simulation model that comprised of entire vascular tree of aneurysm and parent artery and its branches was immediately manufactured. the 3d model was carefully studied by the neurovascular team and an endovascular aneurysm occlusion was decided for the next day after admission (figure 3). the patient was placed under general anesthesia by endotracheal intubation. right femoral approach using 6f introducer sheath was performed and the right internal carotid artery catheterization was achieved with a 6f guiding catheter (imager™ ii, boston scientific). different angulations biplane dsa series were obtained for an optimal working position. a road-mapping was used throughout the duration of the procedure for aneurysm occlusion. a microcatheter was then advanced over a microguidewire into the aneurysm dome. if the aneurysm remnant had a wide neck, the balloonassisted neck remodeling technique was used. 6 gdcs were then advanced and detached in the aneurysm until a complete agiographical occlusion was achieved (figure 5). all catheters and the femoral sheaths were then removed from the femoral arteries and hemostasis was obtained by manual compression. control cerebral ct scan was performed 5 days later. anticoagulation was routinely continued 14 days after the procedure. the postoperative course was uneventful, with a progressive improvement of neurological status. after 14 days of hospitalization the patient was transferred to the neurological department to continue the medical treatment. figure 1. diagnostic cerebral ct scan showing a sah figure 2. cerebral angio-ct scan showing an anterior communicating artery aneurysm (arrow) figure 3. 376 a. chiriac, georgiana ion, g. stan et al. figure 3. different view of the acoa aneurysm on 3d-printed simulation models figure 4. dsa images with the acoa aneurysm pre and post coils embolization figure 5. cerebral ct scan control postembolizati discussions the development of materials and manufacturing technology through 3d printing has allowed the realization of vascular anatomical models as accurate as possible, with lower and lower costs. gradually, the limitations of 3d printing technology represented by the creation of flexible vascular models of tubular type (hollow inside) were overcome allowing the production of high-precision anatomical articles with optimal haptic properties. thus, 3d-printed simulation models based on dsa imaging can perfectly replicate the geometries of aneurysms, parent vessels, and adjacent vascular branches. the reconstruction and 3d printing of implants / models specific to each patient were based on the correlations between digital images and finite element analysis. the data of the computer models thus obtained are finally transferred to a 3d printing unit for the realization of the simulation model. the use of modern printers that allow the simultaneous use of various materials, sequential multilayer modeling technique or rotary model printing technique have contributed greatly to the introduction of this technique both in the current practice of treatment of intracranial aneurysms and 377 the 3d printed models technology for the management of intracranial aneurysms in the professional training of vascular neurosurgery specialists[2,3,4,6]. although major advances have been made in the treatment of cerebral aneurysms with or without subarachnoid haemorrhage, therapeutic management remains one of the most challenging decisions, especially in complex anatomical situations. numerous studies have shown that the main determinants in establishing the therapeutic strategy are the angioarchitecture of the lesion (size, location and direction of the aneurysm itself), the anatomy of the pathway and preprocedural clinical status (wfns or fisher's degree of the patient) [8]. ripley et al [9] reported that 3d printed simulation models make a major contribution both to decisionmaking and to the completion and efficiency of traditional techniques for the treatment of intracranial aneurysms. with the development of the 3d printed simulation models that allow realistic reconstruction of the shape of the aneurysm, important changes influence the traditional aneurysm treatment not only on the fields of microsurgical clipping but also on the endovascular coiling. if the microsurgical clipping treatment strategy was in the past exclusively based on an imaging analysis with or without 3d computer reconstruction, at present, the possibility of clip model selection (as shape, size and curvature), the clipping direction and clips successive arrangement for aneurysmal neck reconstruction are favoured by the realization of 3d printed simulation models. in the case of endovascular interventions, the realization of simulation models by 3d printing can be a valuable tool both for the optimal choice of the implant type (whether we are talking about coils or stents) and for predicting possible vascular deformations due to endovascular implant insertion. this can help improve the intervention plan, avoiding possible complications by using inappropriate and unnecessary materials [6, 7]. in the case of difficult interventions such as stent-assisted coil occlusion in the basilar trunk or complex vascular bifurcations, their planning and vascular reconstruction are difficult, accurate mounting and positioning of implants are essential to allow complete aneurysmal occlusion while maintaining permeable its branches [5,6]. a retrospective study on the efficient use of endovascular materials showed an increase in costs of up to 30% when it was necessary to perform immediate emergency interventions compared to cases in which they were performed after a thorough study on 3d imaging and simulation model by 3d printing. the use of oversize or undersized implants, of additional types of devices not initially anticipated compared to those used in a standard procedure, lead to an increase in the average cost of some classic interventions. the authors concluded that an adequate preoperative planning based on an imaging and model study, correlated in certain situations on practical simulation on the model lead both to a minimization of costs and to an improvement and efficiency of the interventions results [1,4]. the cost of producing 3d printed models seems much more reasonable especially compared to the cost of an endovascular material. improving the planning of interventions based on 3d printed simulation models has led to the development of neurovascular training procedures (microsurgical clipping and endovascular embolization) for specialists in their professional training period. the growing limitation of access to cadavers or to a sufficient number of neurovascular intervention procedures was perfectly offset by the development of increasingly high-performance vascular models both as a material and as a design possibility. conclusions 3d printed simulation models offer the possibility of optimal visual exposure of intracranial aneurysms to help neurointerventionists for application of a more appropriate therapeutic strategy. also, creation of anatomi¬cally accurate 3d printed aneurysm models demonstrated its utilities for continues professional training. access to fast-printing 3d machines and materials with advanced properties at lower and lower costs will certainly lead to the increasing use of this technology in the therapeutic management of intracranial aneurysms. acknowledgment this study about intracranial aneurysm 3d printing simulation models applications in vascular neurosurgery is the subject of the grant: "new diagnostic and treatment methodologies: current challenges and technological solutions based on nanoparticles and biomaterials", that won the 2017 complex projects completed in consortia cdi, grant number: pn-iii-p11.2-pccdi-2017-0062, funded by cncs –uefiscdi romania. 378 a. chiriac, georgiana ion, g. stan et al. references 1. abla, a. a., & lawton, m. t. (2015). three-dimensional hollow intracranial aneurysm models and their potential role for teaching, simulation, and training. world neurosurgery, 1(83), 35-36. 2. itagaki, m. w. (2015). using 3d printed models for planning and guidance during endovascular intervention: a technical advance. diagnostic and interventional radiology, 21(4), 338. 3. kang, y., yu, l. h., xu, t., zheng, s. f., yao, p. s., liu, m., ... & kang, d. z. (2016). three-dimensional printing technology for treatment of intracranial aneurysm. chinese neurosurgical journal, 2(1), 24. 4. konno, t., mashiko, t., oguma, h., kaneko, n., otani, k., & watanabe, e. (2016). rapid 3-dimensional models of cerebral aneurysm for emergency surgical clipping. no shinkei geka. neurological surgery, 44(8), 651-660. 5. mashiko, t., otani, k., kawano, r., konno, t., kaneko, n., ito, y., & watanabe, e. (2015). development of threedimensional hollow elastic model for cerebral aneurysm clipping simulation enabling rapid and low cost prototyping. world neurosurgery, 83(3), 351-361. 6. torres, i. o., & de luccia, n. (2017). a simulator for training in endovascular aneurysm repair: the use of three dimensional printers. european journal of vascular and endovascular surgery, 54(2), 247-253. 7. torres, i., & de luccia, n. (2018). artificial vascular models for endovascular training (3d printing). innovative surgical sciences, 3(3), 225-234. 8. wang, l., ye, x., hao, q., chen, y., chen, x., wang, h. & zhao, j. (2017). comparison of two three-dimensional printed models of complex intracranial aneurysms for surgical simulation. world neurosurgery, 103, 671-679. 9. wang, l., ye, x., hao, q., ma, l., chen, x., wang, h., & zhao, y. (2018). three-dimensional intracranial middle cerebral artery aneurysm models for aneurysm surgery and training. journal of clinical neuroscience, 50, 77-82. doi: 10.33962/roneuro-2022-075 surgical management of spinal cord hemangioblastoma. our clinic experience and case report george popescu, marius c. zaharia, andrei giovani, ioana miron, cezar vîjlănescu, radu m. gorgan romanian neurosurgery (2022) xxxvi (4): pp. 411-417 doi: 10.33962/roneuro-2022-075 www.journals.lapub.co.uk/index.php/roneurosurgery surgical management of spinal cord hemangioblastoma. our clinic experience and case report george popescu1, marius c. zaharia1, andrei giovani1, ioana miron1, cezar vîjlănescu1, radu m. gorgan1,2 1 bagdasar-arseni clinical emergency hospital, department of neurosurgery, bucharest, romania 2 carol davila university of medicine and pharmacy, department of neurosurgery, bucharest, romania abstract background. hemangioblastomas are considered rare tumours that are located, in most cases, in the posterior cranial fossa. in most of cases, spinal hemangioblastomas are identified on the thoracic and cervical levels and can be associated in one-third of cases with von hippel lindau syndrome. material and methods. in this paper, we are presenting our clinic`s experience with spinal hemangioblastomas and the follow-up of the patients in the last 10 years. results. in our study, we included six men and three women with a mean age of 45 years, ranging between 36 to 61 years. the mean hospitalization days was 17 days. among nine patients, there were identified 12 tumors. six patients presented cervical spine hemangioblastomas, two of them had thoracic spine lesions and in one case, the tumour was identified at the lumbar level. furthermore, two patients presented multiple lesions. two patients had been associated with von hippel lindau syndrome. in all cases, surgery was the therapeutic approach. discussions. despite the rapid advance of technology and the new alternatives for the treatment of these lesions, surgical resection of hemangioblastomas remains the gold standard treatment. conclusions. hemangiolbastomas are benign tumours that can be associated with von hippel lindau. a whole-body scan is required to confirm or exclude this syndrome. even though the surgical treatment for asymptomatic patients remains debatable, surgical intervention is the only treatment that can lead to the total removal of the tumour. background hemangioblastomas are rare intra-axial tumors that usually occur in the posterior fossa [1]. histologically wise, these are benign, highlyvascularized tumors that can present a muriform nodule. moreover, spinal cord hemangioblastomas are rarely identified and represent one to six procents of all spinal cord tumors and just 1-2,5% of all central nervous system tumors [2]. in most cases, spinal hemangioblastomas keywords hemangioblastoma, von hippel-lindau, stereotactic radiosurgery corresponding author: g. popescu 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 412 george popescu, marius c. zaharia, andrei giovani et al. are identified on the cervical and thoracic segments and are usually described as intramedullary lesions situated at the posterior pole of the spinal cord, due to their development from dorsal root precursors [5], [7]. spinal hemangioblastomas may be sporadic lesions but in up to 30% of the cases, they represent a feature of von hippel lindau syndrome [3]. von hippel-lindau (vhl) disease is a rare autosomal dominant tumor syndrome characterized by the development of benign and malignant tumors in the parenchyma of the various organs and systems, including the central nervous system [4]. it usually affects young adults, and in the vhl context, multiple hemangioblastomas are identified [12]. over 50% of the people with vhl (63%) present central nervous system tumors, and usually the first manifestations of the syndrome are determined by hemangioblastomas [6], [11]. one of the most affected organs by vhl is the kidney. vhl determines renal cell cysts and clear cell carcinoma [8]. other organs usually affected by the syndrome are the pancreas and retina [9], [10]. the most effective tool to identify these lesions is magnetic resonance. the rapid and constant evolution and accessibility of magnetic resonance imaging (mri) raised the discovery rate of hemangioblastomas and more accurate descriptions were obtained [13], [14]. on t1-weighted mr imaging, the tumors have the aspect of bright enhancing lesions, and t2-weighted imaging can be used for a better characterization of the tumor, as well as emphasize any accompanying edema or syringomyelia [14]. however, spinal hemangioblastomas` features are not always well defined and difficult clinical diagnosis may occur. the symptoms of patients with hemangioblastomas may range based on the segment where the lesion is located. despite de rapid advance of technology and the new alternatives for the treatment of these lesions (such as embolization, stereotactic radiosurgery, and even some molecules such as bevacizumab and other inhibitors of angiogenetic signaling pathways), total removal of the hemangioblastomas remains the most appropriate therapy. however, even after the most laborious microsurgical excision, postoperative neurological degradation is not uncommon, being reported in up to 50% of the patients [15], [16]. therefore, the management of asymptomatic lesions is still under debate. furthermore, the longterm outcome of the patients with intramedullary hemangioblastomas is not well defined, due to the small number of cases. materials and methods in this article, our target is to describe our clinic`s experience with spinal hemangioblastomas and the follow-up of patients with spinal hemangioblastomas in the last 10 years. we performed a 10 years retrospective study that included 9 patients who benefited from surgical treatment for intramedullary spinal cord hemangioblastoma at the 4th neurosurgery department of “bagdasar-arseni” clinical emergency hospital from bucharest. results in our study were included three women and six men with a mean age of 45 years, ranging between 36 to 61 years. the mean hospitalization days was 17 days, ranging from 7 to 36 days. detailed hospitalization dates are available in fig. 1. table 1. patient's presentation state. # age/ sex sex signs/ symptoms duration (months) location of tumor no. of tumours 1 42 m headache, gait impairment, right hemiparesis 6 cervical 1 2 43 f headache, dysphagia, dysphonia 4 cervical 1 3 61 m gait impairment, dysphagia, tetraparesis 2 cervical 1 4 41 f paraparesis, sphincter dysfunction 4 lumbar 1 5 45 m headache, ataxia, right hemiparesis 3 cervical 1 6 39 m paraparesis, numbness of lower limbs 5 thoracic 2 7 36 m paraparesis, sphincter dysfunction 6 thoracic 3 8 48 f headache, paraparesis, sphincter dysfunction 3 cervical 1 9 51 m paraparesis, numbness of upper/lower limbs, sphincter dysfunction 4 cervical 1 413 surgical management of spinal cord hemangioblastoma figure 1. hospitalization chart for each patient. the signs and symptoms of the patients at admission vary depending on the level of the lesion and they will be detailed in table 1. karnofsky's performance score and mccormick's functional score for each patient as well as their discharge state and follow-up are presented in fig. 2 and fig. 3. figure 2. karnofsky performance score at admission and discharge. figure 3. mccormick functional score at admission and discharge. the presence of the tumours, localization, distribution and other possible characteristics such as the presence of syringomyelia were evaluated for each patient using mr imaging. among nine patients, there were identified 12 tumors. the mri described seven cases of hemangioblastomas associated with cystic component. six patients presented cervical spine hemangioblastomas, two of them had thoracic spine lesions and in one case, the tumor was identified at the lumbar level. furthermore, two patients presented multiple lesions. it is worth noting that both cases presented thoracic hemangioblastomas. one of them presented two lesions while the other had 3 thoracic spinal hemangioblastomas, located on the posterior edge of the spine. because of the risk of multiple lesions for these patients, they were imagistically checked for vhl syndrome, such as brain tumors, retinal angiomas, pancreatic lesions renal masses and. all of them benefited from ct scans in order to emphasize the other possible tumors. two patients were linked with vhl syndrome, one presented with pancreatic cyst and the second patient had multiple kidney cysts. none of them had a documented family history of the disease. in all cases, surgery was the therapeutic approach. the patients were placed in ventral position. after midline incision was performed, spinal laminectomy and posterior midline approach for the resection of spinal tumors were used. laminectomies were performed at the level of the tumor as well as adjacent levels to ensure better visualization of the tumor and to avoid postoperative compressive edema. complete resection was achieved in all cases, under microscope magnification. one patient had concomitent removal of both hemangioblastomas from the thoracic segment while the second patient with multiple thoracic lesions underwent two surgical interventions in order to completely remove his three tumoral masses. due to preserved articular capsules, none of the patients required instrumentation, and no signs of instability were accused on the follow-up. the postoperative evolution of the patients was heterogeneous. two patients developed hydrocephalus and 3 of them developed. unfortunately, one patient died during hospitalization, due to multiple comorbidities. the follow-up was between 6 to 36 months. four patients were lost after 12 months of follow-up. during this 414 george popescu, marius c. zaharia, andrei giovani et al. time, two patients presented tumoral recurrence which required another surgical intervention. case presentation a 51-year-old male presented to our clinic for headache, progressive numbness of the limbs, and paraparesis high-level frankel c. the onset of the signs and symptoms was 4 months ago. he had no significant pathological history and no traumatism was reported. head and cervical mris were performed. head mri had presented no tumoral masses intra/extra-axial and no other lesions of the brain, dura mater, or bone were identified. on the other hand, the cervical spine mri emphasized an intramedullary subdural tumor at the c2 level with medullary infiltration (fig. 4). figure 4. cervical spine mri intramedullary subdural tumour at the c2 level with medullary infiltration. compelling the clinical and neurological state of the patient with the imagistic finding, the patient had surgical indication. after the written consent of him and his family, the patient underwent surgery. under total anesthesia, he was placed in a ventral position. a c1-c3 midline incision was performed. the paravertebral muscles were detached bilaterally at these levels and laminectomies of c2 and c3 levels were performed in order to ensure better control of the tumor. dura mater was carefully incised on the midline and the tumor was revealed, covered by the arachnoid. after the arachnoid layer was dissected as well, a large muriform highly vascularized tumor with a high caliber feeder vessel in the cranial side of the tumor was exposed. using microscope magnification, circumferential dissection was performed with bipolar forceps and cotton pads. the accurate localization of the main nutrient artery is a crucial step in surgery. the main feeder was carefully dissected at cut using bipolar forceps and surgical scissors after tumor dissection was complete. the tumor was sent to the anatomopathological laboratory. after laborious hemostasis, the dura mater was sutured in a watertight proof fashion and the surgical wound was closed layer by layer, performed respecting the anatomical planes. figure 5. dura mater was opened. the csf exited with high pressure when the arachnoid layer was incised. figure 6. after complete exposure of the tumour, carefully dissection was performed using bipolar forceps. figure 7. complete resection of the lesion was achieved. the tumour is pushed cranially to obtain better exposure to the main feeder. dissection of the main feeder. 415 surgical management of spinal cord hemangioblastoma figure 8. the main feeder was coagulated and sharply cut using a surgical scissor. figure 9. complete dissection of the tumour was achieved. it was sent to histopathological analysis. postoperative, clinical and neurological state of the patient remained stationary. postoperative mri firmly established the total removal of the lesion and some blood that respected the surgical passage without any medullary compression figure 10. postoperative mri. one week after the surgical intervention, the patient started to feel drowsy, he accused headache and nausea as well. a brain ct scan was performed (fig. 11). ct scan showed slight enlargement of the ventricles and periventricular edema, with clear signs of hydrocephalus. moreover, hemorrhage was identified in the right occipital corn. figure 11. discrete enlargement of the ventricles. periventricular edema. intraventricular hemorrhage in the right occipital corn. figure 12. postoperative mri – 2 months after surgical intervention. the spinal cord presents a normal signal, without signs of compression, and no blood signal in the tumoral bed. the patient underwent a new surgical intervention to evacuate the blood clots and to preserve csf drainage in order to preserve the normal csf flow. postoperative, the newly installed symptoms were remitted. the patient was transferred to neuromotory rehabilitation clinic, stationary compared to the admission state. after two months of kinesiotherapy, the patient is able to walk again and take care of himself by performing simple yet critical actions, such as changing his clothes or holding a glass of water. discussions hemangioblastomas are rare, vascularized tumors that usually develop in the posterior cranial fossa. spinal cord hemangioblastomas constitute about 16% of all spinal cord tumoral pathology. therefore, there is a lack of large cohort studies regarding the subject in the specialty literature. the accurate localization of the main nutrient artery is a crucial step in surgery. especially in the cervical region, hemangioblastomas present a rich network of blood 416 george popescu, marius c. zaharia, andrei giovani et al. vessels and the removal of one of them may prove to be difficult and with major consequences for spinal cord vascularization. total resection may be very difficult due to intraoperative hemorrhage that can occur and blur the interface between the spinal cord and the lesion. to prevent intraoperative bleeding, preoperative embolization can be performed. however, preoperative embolization presented multiple complications such as neurological deterioration and intradural hemorrhage and its use remains controversial [17], [18]. histologically wise, hemangioblastomas are benign tumors and the recurrence rate is low. however, it was noted a higher recurrence among the patients with von hippel lindau syndrome [19]. moreover, 20-30% of spinal hemangioblastomas are linked with vhl [20]. in order to avoid intraoperative and postoperative risks, alternative treatments were developed. in recent years, stereotactic radiosurgery was used as a therapeutic adjuvant, optimizing tumor dose while sparing the spinal cord [21], [22]. the biggest downside of stereotactic radiosurgery is the radiation-inducted myelopathy with potential permanent neurological impairment, which has been reported already in some cases [23], [24]. in addition, the overall recurrence rate after stereotactic radiosurgery is higher compared to classic surgery as few articles suggested [25], [26], [27], [28]. conclusions despite the multiple treatment options available today for hemangioblastomas, the surgical approach remains the gold standard therapy. a whole-body scan is required to confirm or exclude von hippel lindau syndrome. even though the surgical treatment for asymptomatic patients remains debatable, surgical intervention is the only treatment that can lead to the total resetion of the lesion. however, the clinical and neurological condition of the patient is not always improved. a multidisciplinary team is required in order to achieve the best results for the victim of this pathology and the best quality of life. references 1. kuharic m, jankovic d, splavski b, boop fa, arnautovic ki. hemangioblastomas of the posterior cranial fossa in adults: demographics, clinical, morphologic, pathologic, surgical features, and outcomes. a systematic review. world neurosurgery. 2018 feb 1;110:e1049-62. 2. aldape kd, plate kh, vortmeyer ao, zagzag d, neumann hp. haemangioblastoma. who classification of tumours of the central nervous system. 2007;4:184-6. 3. pietilä ta, stendel r, schilling a, krznaric i, brock m. surgical treatment of spinal hemangioblastomas. acta neurochirurgica. 2000 aug;142(8):879-86. 4. gläsker s, vergauwen e, koch ca, kutikov a, vortmeyer ao. von hippel-lindau disease: current challenges and future prospects. oncotargets and therapy. 2020;13:5669. 5. mechtler ll, nandigam k. spinal cord tumors: new views and future directions. neurologic clinics. 2013 feb 1;31(1):241-68. 6. neumann hp, eggert hr, weigel k, friedburg h, wiestler od, schollmeyer p. hemangioblastomas of the central nervous system: a 10-year study with special reference to von hippel-lindau syndrome. journal of neurosurgery. 1989 jan 1;70(1):24-30. 7. vortmeyer ao, tran mg, zeng w, gläsker s, riley c, tsokos m, ikejiri b, merrill mj, raffeld m, zhuang z, lonser rr. evolution of vhl tumourigenesis in nerve root tissue. the journal of pathology: a journal of the pathological society of great britain and ireland. 2006 nov;210(3):37482. 8. choyke pl, glenn gm, walther mm, zbar b, weiss gh, alexander rb, hayes ws, long jp, thakore kn, linehan wm. the natural history of renal lesions in von hippellindau disease: a serial ct study in 28 patients. ajr. american journal of roentgenology. 1992 dec;159(6):1229-34. 9. park ty, lee sk, park js, oh d, song tj, park dh, lee ss, seo dw, kim mh. clinical features of pancreatic involvement in von hippel–lindau disease: a retrospective study of 55 cases in a single center. scandinavian journal of gastroenterology. 2015 mar 4;50(3):360-7. 10. gaudric a, krivosic v, duguid g, massin p, giraud s, richard s. vitreoretinal surgery for severe retinal capillary hemangiomas in von hippel–lindau disease. ophthalmology. 2011 jan 1;118(1):142-9. 11. lonser rr, butman ja, huntoon k, asthagiri ar, wu t, bakhtian kd, chew ey, zhuang z, linehan wm, oldfield eh. prospective natural history study of central nervous system hemangioblastomas in von hippel-lindau disease. journal of neurosurgery. 2014 may 1;120(5):1055-62. 12. wanebo je, lonser rr, glenn gm, oldfield eh. the natural history of hemangioblastomas of the central nervous system in patients with von hippel—lindau disease. journal of neurosurgery. 2003 jan 1;98(1):82-94. 13. mccormick pc, post kd, stein bm. intradural 417 surgical management of spinal cord hemangioblastoma extramedullary tumors in adults. neurosurgery clinics of north america. 1990 jul 1;1(3):591-608. 14. rebner m, gebarski ss. magnetic resonance imaging of spinal-cord hemangioblastoma. ajnr: american journal of neuroradiology. 1985 mar;6(2):287. 15. lonser rr, weil rj, wanebo je, devroom hl, oldfield eh. surgical management of spinal cord hemangioblastomas in patients with von hippel—lindau disease. journal of neurosurgery. 2003 jan 1;98(1):106-16. 16. mandigo ce, ogden at, angevine pd, mccormick pc. operative management of spinal hemangioblastoma. neurosurgery. 2009 dec 1;65(6):1166-77. 17. saliou g, giammattei l, ozanne a, messerer m. role of preoperative emboliza-tion of intramedullary hemangioblastoma. neurochirurgie 2017;63(5):372– 5.pubmed pmid: 27236735. 18. sultan a, hassan t, aboul-enein h, mansour o, ibrahim t. the value of preoperative embolization in large and giant solid cerebellar hemangioblastomas. interventional neuroradiology. 2016 aug;22(4):482-8. 19. de la monte sm, horowitz sa. hemangioblastomas: clinical and histopathological factors correlated with recurrence. neurosurgery. 1989 nov 1;25(5):695-8. 20. miller dj, mccutcheon ie. hemangioblastomas and other uncommon intramedullary tumors. journal of neurooncology. 2000 may;47(3):253-70. 21. trost ha, seifert v, stolke d. advances in diagnosis and treatment of spinal hemangioblastomas. neurosurgical review. 1993 sep;16(3):205-9. 22. wang c, zhang j, liu a, sun b. surgical management of medullary hemangioblastoma: report of 47 cases. surgical neurology. 2001 oct 1;56(4):218-26. 23. emami b, lyman j, brown a, cola l, goitein m, munzenrider je, shank b, solin lj, wesson m. tolerance of normal tissue to therapeutic irradiation. international journal of radiation oncology* biology* physics. 1991 may 15;21(1):109-22. 24. schultheiss te. the radiation dose–response of the human spinal cord. international journal of radiation oncology* biology* physics. 2008 aug 1;71(5):1455-9. 25. li x, wang j, niu j, hong j, feng y. diagnosis and microsurgical treatment of spinal hemangioblastoma. neurological sciences. 2016 jun;37(6):899-906. 26. boström a, kanther nc, grote a, boström j. management and outcome in adult intramedullary spinal cord tumours: a 20-year single institution experience. bmc research notes. 2014 dec;7(1):1-8. 27. harati a, satopää j, mahler l, billon-grand r, elsharkawy a, niemelä m, hernesniemi j. early microsurgical treatment for spinal hemangioblastomas improves outcome in patients with von hippel–lindau disease. surgical neurology international. 2012;3. 28. liu a, jain a, sankey ew, jallo gi, bettegowda c. sporadic intramedullary hemangioblastoma of the spine: a single institutional review of 21 cases. neurological research. 2016 mar 3;38(3):205-9. doi: 10.33962/roneuro-2022-003 postero-lateral arterio-venous fistula with particular histological aspects as the main cause of severe spinal thoracal stenosis. case report d. balasa, al. tunas, l. mocanu, m. enescu romanian neurosurgery (2022) xxxvi (1): pp. 18-22 doi: 10.33962/roneuro-2022-003 www.journals.lapub.co.uk/index.php/roneurosurgery postero-lateral arterio-venous fistula with particular histological aspects as the main cause of severe spinal thoracal stenosis. case report d. balasa1, al. tunas1, l. mocanu2, m. enescu3 1 department of neurosurgery, clinical county hospital constanta, romania 2 department of anatomopathology, clinical county hospital constanta, romania 3 department of orthopaedics, private clinic medstar, constanta, romania abstract spinal dural arteriovenous fistulas (avfs) are rare spine vascular malformations. we report a case of avf in the epidural space of t10 and degenerative medial osteophytes leading to clinical symptoms of severe spinal stenosis operated with good evolution. object: our report’s objective is to present a particular, extremely rare case of spinal stenosis at t10-t11 level, mostly on the right side, result of the cumulative effect of a vertebral postero-lateral avf, medial degenerative osteophites and a synovial cyst at the same level. the avf is the main cause of the spine stenosis. case report: a 69 year-old man presented for 5 years’ pain in the thoracal spine, intermitent paresthesias on the right leg. from one week he complains of painful paresthesias on both legs (predominant on the right side), gait with progressive difficulty. on examination we observed incomplete paraplegia (frankel c+/e), sensory examination revealed hypoesthesia with sensitive level t10, knee and ankles reflexes increased bilaterally with predominance on the right side, babinsky sign present bilateral. on mri imaging: thoracal spine stenosis t10-t11, by degenerative osteophites t10-t11 predominant on the right side, synovial cyst in the lateral recess who severelly compresses the dural sac and the spinal cord. the patient was operated (laminectomy t10 and t11 on the right side, microsurgical complete resection of a heterogenous extradural keywords epidural fistula, thoracal spine stenosis corresponding author: mocanu liliana department of anatomopathology, clinical county hospital constanta, romania lilianamcn@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 19 postero-lateral arterio-venous fistula with particular histological aspects lesion (bony and vascular, intensively bleeding), severely compressive over the spinal cord. the postoperative evolution was favorable: the incomplete paraplegia has improved (asia c+ on the right side, d on the left side), hipoesthesia diminished. figure 1. coronal t2.: dorsal spine stenosis t10-t11, by degenerative osteophytes t10-t11 predominant on the right side (blue arrow) who severely compress the spinal cord. figure 2. sagittal t2: severe spine stenosis produced by degenerative osteophytes t10-t11 and synovial cyst (green arrow). figure 3. axial contrast t1: dorsal spine stenosis t10-t11, by medial degenerative osteophytes t10-t11 predominant on the right side (red arrow). the histological exam material and method: the probe was sent fresh with a cold ischemic time of 20 minutes, then it was paraffined embedded. the conventional slides (haematoxylin – eosine stained) revealed a conjunctive tissue with coiled vessels, some dilated, some collapsed, attached on a spinal node immunohystochemical method was done on ventana platforme gx, with antibodies cd34 (clona qbend10); wt1 (clona 6fh2) comments wilms' tumor-1 (wt-1) was originally described as a tumor suppressor gene based on its mutational inactivation in a subset of wilms' tumor. it plays an essential role in haematopoiesis and angiogenesis by regulating vascular endothelial growth factor, angioproteins, nestin, and proliferation of vascular smooth muscle cells1 human skin vasculature shows cytoplasmic wt1 protein expression, detected by an antibody recognizing the c-terminal of the protein (6f-h2). reports have demonstrated that wt-1 protein is expressed in a variety of vascular anomalies. defects in wt1 signalling might underlie the inability of endothelial cells in vascular malformations to undergo physiological apoptosis and remodelling 20 d. balasa, al. tunas, l. mocanu, m. enescu cd34 commonly used marker of hematopoietic progenitor cells and endothelial cells; also called hematopoietic progenitor cell antigen cd34; cd34+ stromal cells are called dendritic interstitial cells; cd34: membranous stain wt1: nuclear stain endothelium of normal vessels acts as a positive internal control in our case, the positive reaction was noted in a greater number of vessels to cd34 than to wt1, so the interpretation, correlated with clinical and imagistic data, was of a vascular spinal fistula with loss of wt1 expression (as in avms). we couldn’t find other reports about wt1 expression in spinal avfs. figure 4. cd34, ob4x figure 5. cd34, ob 10x; positive in endothelial cells and in some interstitial dendritic cells figure 6. wt1 positive in a normal vessel, negative in other vessels postoperative control was favourable figure 7. postoperative ct scan follow up at 6 months discussion: extradural (or epidural) avfs are relatively uncommon malformations characterized by anomalous communication between an extradural branch, usually of a radicular artery, and the epidural venous plexus2. spinal arteriovenous malformations (avms) (constituting 3-4% of all spinal cord space occupying lesions)3. after lim the symptoms of epidural avfs are related to the pattern of venous drainage4. if they are 21 postero-lateral arterio-venous fistula with particular histological aspects exclusively epidural, they may present with local pain or radicular pain or with progressive myelopathy4. spetzler et all5 proposed a modified classification of the spine/spinal cord arteriovenous lesions to arteriovenous malformations (avms) and arteriovenous fistulas (avfs). avfs areclassified according to their location as intradural and extradural. according to geibprastert et all6, dural avfs are classified on anatomical bases in ventral group (most of them) and dorsal epidural group the dorsal group of dural av fistulas is related to veins that normally drain the spinous process and lamina at the spinal level7. patients with dural av fistulas within this space typically present with spontaneous epidural hematomas. these symptomatic lesions are extremely rare7. spinal dural av fistulas are fed by the radicular arteries and/or the surrounding vertebral branches7 after classification of spetzler et al5 there are extradural av fistulas ventral or dorsal, with single or multiple feeders. there is no gender predilection (male 52.9%) of avfs.8 common to unruptured avfs are symptoms of myelopathy and pain, such as lower or upper extremity weakness, abnormal sensory, disturbance of gait, back pain, and bladder and/or bowel incontinence8.most cases of ruptured avfs are manifested as spontaneous epidural hematoma (64.7%)8. typically, initial symptoms of spinal epidural hematoma are rapid development of excruciating back pain, with or without neurological deficit, followed by rapidly progressive severity of myelopathy, such as abnormal sensory, disturbance of gait, bladder and/or bowel incontinence, lower or upper extremity weakness/paralysis due to the location of hematoma9 after steinmetz10 there are two options in the treatment of spinal dural av fistulas; surgical occlusion of the intradural reflux vein, and endovascular therapy employing embolic material into the fistula. surgery is a relatively simple and safe intervention, resulting in long-term shunt occlusion in 98% of cases10. any avfs with progressive myelopathy have to be treated as soon as diagnoses are made. after lim4, surgical disconnection of the intradural radicular vein is the curative method, so is endovascular occlusion of the fistula and proximal part of its venous drainage with liquid embolic material. prompt diagnosis and emergency surgical treatment are crucia11. the best management for avfs is still surgical operation11. our case illustrates a severe compression of the thoracal spinal cord produced by a combination of degenerative lesion (medial degenerative osteophites t10-t11) and posterior extradural avf. we have realized a correct treatment of these lesions with good results. conclusions surgical treatment was the mandatory method of healing of the avf and decompression of the dorsal spinal cord. the delay in diagnosis left residual incomplete paraplegia. references 1. manisha choudhary, ira sharma, manveen kaur, varsha dalal,1 and avninder singh immunohistochemical expression of wt-1 helps to differentiate cutaneous vascular tumors from vascular malformations. indian dermatol online j. 2017 jul-aug; 8(4): 282–284. 2. racchiusa s, cavallaro m, longo m, et al. spinal cord arteriovenous malformations: a practical guide. j neurol stroke. 2018;8(2):113–115. doi: 10.15406/jnsk.2018.08.00292 3. bao yh, ling f. classification and therapeutic modalities of spinal vascular malformations in 80 patients. neurosurgery 1997;40:75 81. 4. lim s.m., choi i.s. spinal epidural arteriovenous fistula:a unique pathwayinto the perimedullary veina case report. interventional neuroradiology 15: 466-469, 2009 5. spetzler r. , detwiler p. w. , riina h., porter, r. w. modified classification of spinal cord vascular lesions, j. neurosurg: spine / volume 96 / march, 2002 6. geibprasert s, pereira v et al: dural arteriovenousshunts: a new classification of craniospinal epidural ve-nous anatomical bases and clinical correlations. stroke39: 2783-2794, 2008 7. krings t., lasjaunias p.l., geibpraswert s., hans fj., thron a.k. , terbrugge k.g., reinges m.h.t. classification of spinal vascular malformations. the neuroradiology journal 22 (suppl. 1): 97-106, 2009 8. yamamoto s. , kim p. spinal arteriovenous fistulasand arteriovenous malformations– complicated vasculature and surgical imaging http://dx.doi.org/10.5772/56367. intech, chapter 5, pag 2-21, 2013 9. strom rg, derdeyn cp, moran cj, et al. frequency of spinal arteriovenous malformations in patients with unexplained myelopathy. neurology 66(6), 928-931, (2006). 10. steinmetz mp, chow mm, krishnaney aa, andrewshinders d, benzel ec, masar‐yk tj, et al. outcome after 22 d. balasa, al. tunas, l. mocanu, m. enescu the treatment of spinal dural arteriovenous fistulae: a con‐temporary single-institution series and metaanalysis. neurosurgery. 2004 jul;55(1):77-87; 11. singh, et al.: spinal arteriovenous malformations: indications for surgery. asian journal of neurosurgeryvol. 11, issue 2, april june 2016. doi: 10.33962/roneuro-2022-051 focal cerebritis with vasculitis mimicking a high-grade glioma. a case report vissa shanthi, nandyala rukmangadha, badiginchala suguna, boagala vijayalakshmi devi, ramesh chandra, ravikumar thenmozhi romanian neurosurgery (2022) xxxvi (3): pp. 302-305 doi: 10.33962/roneuro-2022-051 www.journals.lapub.co.uk/index.php/roneurosurgery focal cerebritis with vasculitis mimicking a high-grade glioma. a case report vissa shanthi1, nandyala rukmangadha1, badiginchala suguna1, boagala vijayalakshmi devi2, ramesh chandra3, ravikumar thenmozhi4 1 department of pathology, sri venkateswara institute of medical sciences, tirupathi, ap, india 2 department of radiology, sri venkateswara institute of medical sciences, tirupathi, ap, india 3 department of neurosurgery, sri venkateswara institute of medical sciences, tirupathi, ap, india 4 department of neurosurgery, sri venkateswara institute of medical sciences, tirupathi, ap, india abstract cerebritis is an inflammatory reaction in the brain which can be localized or diffuse and can be secondary to various etiologies like granulomatous demyelinating infections, vasculitis or neoplastic. identifying the aetiology is very essential for the proper treatment. we report a case of 24 years male patient, who came with a history of headaches for 3 months. ct scan revealed intra-axial hypodense lesion suggesting high-grade glioma, which on histopathological examination revealed reactive gliosis with diffuse lymphocytic infiltrate and perivascular lymphocyte collection. introduction differentiation between tumor like lesions and tumors of central nervous system is very essential for selecting the mode of treatment and prognosis. both have similar features in ultrasound (us), computerized tomography (ct), and magnetic resonance imaging (mri) studies. misinterpretation leads to delay in the treatment of malignant tumors or over-treatment of tumor – like benign lesions. on imageology, tumor presents as focal density or signal alteration displacing or infiltrating adjacent structures surrounded by vasogenic edema and with or without matching contrast enhancement. but many tumor like lesions such as abscess, vascular malformations, resolving hematomas, tumefactive multiple sclerotic (ms) plaques also present with similar features. development of functional mri sequences such as magnetic resonance spectroscopy, diffusion tensor imaging (dti), perfusion weighted imaging, ph weighted mri and susceptibility weighted imaging (swi) helps in differentiating tumor like lesions and tumors.[1] histopathological examination of biopsied tissue can give confirmed diagnosis. keywords cerebritis, vasculitis, tumour like lesion corresponding author: v. shanthi sri venkateswara institute of medical sciences, tirupathi, ap, india santhijp@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 303 focal cerebritis with vasculitis mimicking a high-grade glioma case report a 24-year-old male patient came to neurology op with chief complaints of headache and paresthesia on right side since 3 months. in 2014, he had history of diplopia and headache. in 2018, patient had transient ischemic attack. patient had no history of vomiting, seizures, fever, neck stiffness, photophobia, double vision or jaw deviation. he had no history of hypertension, diabetes, tuberculosis, chronic obstructive pulmonary disease, or chronic kidney disease. on examination patient was conscious coherent, with no pallor, icterus, cyanosis, clubbing or pedal edema. patient was afebrile with pulse rate 85/minute, blood pressure of 110/80mm hg and respiratory rate of 20/minute. cns examination revealed glasgow coma score of 14/15. higher mental functions and cranial nerves were normal. motor examination revealed normal bulk, tone and power. sensory system examination revealed intact cerebellar signs and no meningeal signs. no abnormality was detected in skull and spine. figure 1. pre and post iv contrast mri brain showing well defined peripherally enhancing lesion with perilesional edema in the right temporal region which is hyperintense on t2w image, supressed on flair, hypointense on t1w images with evidence of enhancing pachymeninges adjacent to the lesion. ct scan revealed intra axial hypodense lesion measuring 3.5x2.9cm in the right temporal lobe with adjacent perilesional edema in the surrounding white matter of the right temporal and parietal lobes. mri scan with contrast study revealed ill-defined mixed signal intensity lesion with solid and cystic components. solid component was t2/flair (fluid attenuated inversion recovery) hypointense (figure 1), and isointense on t1 in the right anterior and medial temporal lobe which was showing no evidence of restricted diffusion on dw1 with diffuse contrast enhancement. cystic component was t2/ flair hyperintense and hypointense on t1 with no evidence of restricted diffusion on dwi (diffusion weighted magnetic resonance imaging) with evidence of peripheral contrast enhancement. medially the lesion was invading the cavernous sinus. irregular t2 hyperintensity was not suppressed on flair showing no evidence of contrast enhancement in perilesional region involving right temporal lobe, insular cortex, right external capsule and posterior limb of internal capsule suggesting edema. lesion was causing mass affect in the form of midline shift of 5mm towards left side. imageology suggested the clinical diagnosis of high-grade glioma. figure 2. glial tissue showing diffuse lymphoplasmacytic infiltrate and perivascular lymphocytic cuffing (h&e,x40). all the hematological investigations were with in normal limits except for erythrocyte sedimentation rate which was 82mm/1st hour. figure 3. glial tissue with vessels showing lymphocytic infiltration in the vessel wall (h&e,x100). 304 vissa shanthi, nandyala rukmangadha, badiginchala suguna et al. patient underwent right fronto temporo parietal minicraniotomy and right temporal pole excision. excised tissue was sent for histopathological examination. we received multiple grey, brown soft tissue bits altogether measuring 2x1.5x1cm. sections studied shows glial tissue with diffuse lymphoplasmacytic infiltrate. adjacent foci showed reactive gliosis with gemistocytes. perivascular lymphocytic cuffing was noted (figure 2). some of the vessels showed lymphocytic infiltrate into the vessel wall (figure 3). few vessels showed fibrinoid necrosis of the wall. dense lymphocyte predominant lymphoplasmacytic infiltrate was seen in the meninges. immunohistochemistry showed lca, cd3 and cd20 positivity in the dense inflammatory infiltrate indicating the polyclonal nature of lymphocytes. gfap and s-100 showed positivity in glial tissue. cd 68 was positive in scattered histiocytes. cd138 was positive in plasma cells. ki67 was seen positive in some inflammatory cells. special stains for acid fast tubercle bacilli and fungal elements were negative. due to the above histopathological and immunohistochemical features diagnosis of cerebritis, probably secondary to vasculitis was considered. discussion cerebritis is an inflammatory reaction in the brain which can be due to systemic or local etiologies and can mimic neoplasm. [2] imaging features of various tumor like lesions like resolving hematoma, tumefactive ms plaque, vascular malformation and abscess are similar and are difficult to differentiate. [1] solitary lesion in various demyelinating diseases including acute disseminated encephalomyelitis, progressive multifocal leukoencephalopathy and multiple sclerosis may mimic tumor. histopathological examination is gold standard for diagnosis. idiopathic focal cerebritis could be secondary to infectious disease, vasculitis, granulomatous or demyelinating diseases. tumor like mass lesions are reported in patients having systemic vasculitis such as sle (systemic lupus erythematosus), and primary angiitis of cns. huang et al reported a large temporal mass lesion mimicking tumor in 14-year-old boy with systemic lupus erythematosus.[3] molloy et al described a solitary tumor-like mass lesion in a subset of primary angiitis of cns presenting with edema and contrast enhancement. [4] mohamad ezzeldin at al described idiopathic focal cerebritis, presenting as tumor like lesion in right posterior parietal lobe in 35-year-old male. in this case esr, c reactive protein (crp) and anti-nuclear antibodies (ana) were normal and had no involvement of arteries. in our case, esr was raised, and vessels showed lymphocytic infiltrate indicating possible cause may be vasculitis leading to cerebritis. differential diagnosis for this condition on imageology is focal cortical dysplasia, ganglioglioma, oligodendroglioma, dysembryoplastic neuroepithelial tumor (dnet). [5] focal cortical dysplasia type 1 occurs in adults with changes in the temporal lobe. type 2 occurs in children and presents in frontal lobes with severe clinical symptoms. mri may show focal cortical thinning or thickening with increased signal on t2 and gray and subcortical matter tapering towards ventricles on flair weighted images. [6] gangliogliomas contain cystic, solid and calcified components which gives inhomogeneous appearance to tumor. [7] oligodendrogliomas commonly arise in frontal lobe, has well defined margins and with frequent calcifications. on mri, t1 weighted images of tumor are hypointense and t2 weighted images of tumor are hyperintense. surrounding vasogenic edema is uncommon [5]. dnet shows hypointensity on t1 weighted images and hyperintensity on t2 weighted images, without or with minimal mass effect and with surrounding vasogenic edema. 30% of cases show contrast enhancement. [7] however histopathological examination is gold standard for diagnosis. microscopically focal cortical dysplasia are two types. type i shows cortical architectural abnormality (type ia) with hypertrophic neurons and immature neurons (type ib). type ii shows dysmorphic neurons with dislayering abnormalities (type iia) and with balloon cells (type iib). [6] gangliogliomas are well differentiated benign neuroepithelial tumors. histologically these tumors show combination of glial and neuronal elements exhibiting marked heterogeneity. [8] oligodendroglioma is a low grade gliocytoma (who grade ii) composed of monotonous cells having uniform round nuclei with perinuclear clearing (fried egg appearance) and thin branching vasculature (chicken wire vasculature). [9] dysembryoplastic neuroepithelial tumor is characterized by presence of 305 focal cerebritis with vasculitis mimicking a high-grade glioma abundant mucinous background with small round oligodendroglial like cells without dysplasia.[10] cerebritis secondary to vasculitis can be confused with lymphoma as in both the conditions diffuse lymphocytic infiltrate can be present. [11] immunohistochemistry helps in differentiating polyclonality of lymphocytes which rules out the possibility of lymphoma. conclusion focal cerebritis can present as neoplasm on imageology. focal cerebritis can be idiopathic or can be secondary to infectious disease, vasculitis, granulomatous or demyelinating diseases. correct diagnosis and appropriate treatment are essential for prognosis. proper awareness in neurologist and radiologist is essential regarding the tumor like lesions of brain. histopathology is the gold standard for diagnosis. references 1. huisman ta. tumor-like lesions of the brain. cancer imaging 2009;spec no a:s10-s13. https://doi:org/10. 1102/1470-733.2009.9003 2. mohamad ezzeldin, ahmed yassin, daniel graf, gerald campbell, narges moghini, xiangping li, todd masel and xiang fang. idiopathic focal cerebritis mimicking neoplasm. journal of neurology and experimental neuroscience 2019;5(2):106-109. 3. huang ch, hung ch, chu yt, hua ym. tumor-like cerebral perivasculitis in a pediatric patient with syatemic lupus erythematosus. kaobsiung j med sci 2008;24(4):218-222. 4. malloy es, singhal ab, calabrese lh. tumor like mass lesion: an under-recognized presentation of primary angiitis of the central nervous system. ann rheum dis 2008.67(12):1732-1735 5. koeller kk, henry jm.. from the archives of afip: superficial gliomas: radiologic-pathologic correlation. armed forces institute of pathology. radiographics 2001; 21(6):15331556.https://doi.org/10.1148/radiographicsradiographic s.21.6.g01nv051533 6. kabat j, krol p. focal cortical dysplasia-review. pol j radiol 2012;77(2):35-43.https://doi.org/10.12659/pjr.882968 7. giulioni m, marucci g, martinoni m, marliani af, toni f et al. epilepsy associated tumors: review article. world j clin cases 2014;2(11):623-641.https://doi.org/10.12998/wjcc .v2.i11.623 8. zhang d, henning td, zou lg, hu lb, wen l, feng xy, dai sh, wang wx, sun qr, zhang zg. intracranial ganglioglioma: clinicopathological and mri findings in 16 patients. clin radiol 2008;63(1):80–91. 9. samaan mahmoudzadeh, allison parrill, tiffany tsao, kimberly eaton, kirk sheplay, jessica eisold, sofia nunnelee, and mohamed aziz. oligodendroglioma with anaplastic features, case report and review of the literature.s m j neurol neurosci 2021;7: 5 10. yibirin m, de oliveira d, suarez i, et al. a case of dysembryoplastic neuroepithelial tumor in an adolescent male. cureus 2021.13(3): e13917. doi:10.7759/cureus.13917 11. m.fischer, b.pfausler. intravascular large b cell lymphoma mimicking central nervous system vasculitis. human pathology:case reports 2017;8:3-8. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro -2020-009 risk factors and clinical and neurological consequences of intraoperative rupture of brain aneurysms in microsurgical operations bindu a. v., orlov m. yu., litvak s. o., m. v. yeleynik romanian neurosurgery (2020) xxxiv (1): pp. 66-76 doi: 10.33962/roneuro-2020-009 www.journals.lapub.co.uk/index.php/roneurosurgery risk factors and clinical and neurological consequences of intraoperative rupture of brain aneurysms in microsurgical operations bindu a. v., orlov m. yu., litvak s. o., m. v. yeleynik department of neurosurgical pathology of vessels of the head and neck si "academician a.p." romodanov institute of neurosurgery of nams of ukraine", kyiv, ukraine abstract objective. to assess the frequency, risk factors and clinical and neurological consequences of intraoperative rupture of arterial aneurysm (aa) of the brain (b) in clipping operations of the b aa. materials and approaches. a retrospective analysis of microsurgical operations clipping of cerebral aneurysms in 1449 (100%) patients for the period from 2011 to 2018 was performed, of which 141 (9.73%) cases had intraoperative rupture of the aneurysm (iora). preoperative examination: clinical and neurological examination, ct of the brain, cerebral angiography (cag), duplex scanning of the main vessels of the head and neck. the analyzed criteria are risk factors of iora: aa size, localization, shape, duration of surgery after the primary rupture of aa, the presence of hypertension and the patient's condition before surgery. results. the frequency of iora in clipping operations of b aa was 9.73% (141 patients) in a series of observations 1441 (100%). most often iora-141 (100%) was registered in clipping operations of aa of complex aca-acoma (86 (61%) cases out of 141 (100%)). iora is possible at all stages of the operation with the maximum frequency of contact breaks – 135 (95.74%); the rarest-6 (4.26%) non contact iora (at the stage of craniotomy) was recorded. at the preoperative stage, the vast majority of patients with subsequent iora were diagnosed with cerebral edema, aa of large size, atherosclerotic changes in the aneurysm-affected segment of the artery and cervical areas of the aneurysm, high blood pressure during surgery, adhesive arachnoid changes. at the time of discharge from the hospital, according to the glasgow results scale: 69 (48.94%) full or partial restoration of labor activity, 18 (12.77%) had limited daily activities without the need for outside assistance, 37 (26 24%) deep disability ) deaths were in the group of "contact" iora 17 (12.06%). at 6 ( 4.26%) of "non-contact" iora, a deepening of initial neurological symptoms was recorded with a suppression of the level of consciousness, the addition of pyramidal insufficiency, speech impairment and psycho-organic syndrome, and a deepening of the phenomena of initial cerebral arterial vasospasm. conclusions. iora is predominantly in contact with a frequency of occurrence-9.73 %. the most common risk factors for iora were: cerebral edema, large aa, atherosclerotic changes in the aneurysm-affected artery segment and cervical keywords aa-arterial aneurysm, ioc-intraoperative complications, sah-subarachnoid haemorrhage, iora-intraoperative rupture of aneurysm corresponding author: arthur vasylovych bindu “academician a.p. romodanov” institute of neurosurgery of nams of ukraine artur.bindiu@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 67 risk factors and consequences of intraoperative rupture of brain aneurysms in microsurgical operations aneurysm sites, high blood pressure during surgery, adhesions arachnoid changes. iora leads to deepening of initial neurological symptoms, phenomena of initial vasospasm of cerebral arteries with the level of total mortality-17 (12.06%). introduction. essays on the history of brain aneurysm surgery the first description of cerebral aneurysm belongs to weissmann in may 1676. it took two centuries until hodson (1815) and bramwell (1886) established that the extravasation of blood into the subarachnoid space is a consequence of the rupture of an intracranial aneurysm and called this form of "subarachnoid" hemorrhages (hsa)[22]. the start of brain aneurysm surgery is provided by the scottish neurosurgeon dot, who in 1933 published two cases of microsurgical exclusion of a cerebral aneurysm from the bloodstream by enveloping the aneurysm with a piece of muscle [1]. on march 23, 1937, walter dandy first excluded a sac-shaped aneurysm of the right internal carotid artery from the bloodstream by clipping the neck of the aneurysm with a metal clip to a 43-year-old patient. in 1944 walter dandy published the first monograph devoted to the surgical treatment of brain aneurysms, in which the author publishes the results of surgical treatment of 107 patients with various localisations of aneurysms, thereby demonstrating that patients with such a complex pathology necessarily require surgery [3]. nowadays microsurgical and endovascular approaches are used in aneurysm surgery (konovalov a. n., 1973; oleshkevich f. v., 1973; zozulya yu. a., 1986; romodanov a. p. et al., 1990; shcheglov v. i., 1998; serbinenko f. a., 1971; suzuki j., 1979; yasargil gm, 1984). the first method of surgical treatment of brain aneurysms was carotid artery ligation, which was used by a. pare (1510-1590) as a method of stopping arterial bleeding in victims with neck wounds. for decades, it was the only possible method of surgical treatment of aa, which at the end of the xix century. widely used by the founders of neurosurgery (horsley, 1891; shing, 1911). the latter described aa as random finds of " cysts that pulsate." in 1960, removable clips, which are widely used in aa surgery were proposed. in the 1970s, neurosurgery began to use the operating microscope. given the rapid development of cerebrovascular neurosurgery, in particular microsurgical clipping of brain aneurysms, in the 1980s and 1990s, a large number of publications appeared on the problem of intraoperative complications (ioc), including intraoperative ruptures of aneurysms (iora), with clipping of cerebral aneurysms [1]. but despite the historical development and achievements of modern neurosurgery, cerebral iora remains the most frequent ioc [2,3,4]. there are contact and non-contact iora. contact include iora, which occur during direct mechanical action on the aneurysm: during the retraction of the medulla with a spatula, during arachnoid dissection, clipping the neck of a sacculated aneurysm. iora, which occurs in the early stages of an operation, is considered non-contact, prior to the dissection of the dura mater (dm), when there is no mechanical effect on the aneurysm (when shifting the patient on the operating table, induction of anesthesia, osteoplastic trepanation). according to the literature [9,10] contact iora occur in 91-94% of cases, non-contact iora-2.5-9% of cases. the main criteria and risk factors, which affect the frequency of iora, consider the size of the aneurysm, its location, shape, duration of surgery after the primary rupture of the aneurysm, the presence of hypertension and the severity of the patient's condition before surgery [11,12,13,14,15,16,17,18] the size of the aneurysm. most authors believe that non-contact ioras are more likely to be expected in small aneurysms (5-6 mm), and contact ioras in large aneurysms (more than 15 mm), as they are more difficult to isolate and exclude from the bloodstream [6,14]. localization of aa. the greatest risk for iora is represented by aneurysms of aca-acoma and ica complex [19] through hemodynamic prerequisites and a high frequency of such aneurysms (23.240.3%) [20]. the severity of the patient's condition before surgery. to date, a clear relationship between iora and the severity of the patient before surgery has not been established. some authors indicate that the incidence of iora is higher in patients with severity of iv-v degree according to the hunt–hess scale [18,21]. however, j. schramm and c. cedzich (1993), p. d. le roux et al. (1996), t. inagawa (1999) have not established a clear dependence of the frequency of iora on the severity of patients according to the hunt-hess scale. 68 bindu a. v., orlov m. yu., litvak s. o. et al. time of surgery after a primary aa rupture. surgery in the early stages after the primary rupture of the aneurysm, in the presence of cerebral edema, with difficulty in accessing aa, the need to perform sufficient traction of the cerebral substance is often accompanied by iora [5,7,11,12,15,11]. methods and materials a retrospective analysis of the surgical treatment of 141 patients with intraoperative ruptures in the course of clipping of brain aneurysms, out of the total number of 1449 operated patients in the period from 2011 to 2018, was performed. the age of the patients ranged from 19 to 78 years (average age46.7 + 11.6 years). males-71 (50.35%), females-70 (49.65%). after primary rupture 121 (85,82%) patients were operated, repeated rupture was observed in 20 (14,18%) patients. perioperative examination of patients included clinical and neurological examination, brain ct scan, cerebral angiography (cag), ultrasound (us) duplex scanning with a color doppler mapping of the head and neck vessels mode and transcranial doppler (tcd) was performed in all patients according to the standard methods at admission and in dynamics of perioperative period every 2 days, and in severe cases, daily. the severity of vasospasm (bc) was established by the complex of data of cag and tcd, the following us criteria were used: the severity of distinct degree-systolic linear velocity (syst. linear velocity of blood flow) > 240 cm/s, critical degreesyst. linear velocity of blood flow>300 cm/s. subarachnoid (sah) hemorrhage was detected in 67 (47.52%) patients, subarachnoid parenchymal hemorrhage – in 49 (34.75%) patients; subarachnoid ventricular – in 6 (4.26%) patients; subarachnoid parenchymal-ventricular – in 19 (13.46%) patients; sah complicated by the formation of intracerebral hematoma – in 50 (35.46%) patients. in the acute period of aa rupture (the first 21 days) 127 patients were operated (73 patients-the first 3 days; 35 patients-4-7 days after the rupture; 15 patients-8-14 days; 4 patients-15-21 days, 22 days and later-14 patients (tab.1). the period from the moment of aa rupture prior the operation number of patients n р, % 1-3 days 73 51.77 4-7 days 35 24.82 8-14 days 15 10.64 15-21 days 4 2.84 after 21 days 14 9.93 total 141 100 table 1. term of operation after the last aa rupture before the operation, the severity of the patients' condition was assessed according to the hunt-hess scale (tab.2), the level of consciousness according to the glasgow coma scale. among the patients operated in early terms patients with severity of a condition of iii-iv degree on h-h prevailed. with the increase in the duration of the operation, the proportion of patients in a compensated state (i-ii degree according to h-h) increased. severity of the condition according to the scale of the hunt-hess number of patients n р, % і 34 24.11 іі 61 43.26 iii 37 26.24 iv 5 3.55 v 4 2.84 total number 141 100.00 table 2. consciousness before the operation was clear in 86 (62.41%) patients, moderate stunning-in 32 (22.70%) patients, deep stunning – in 13 (9.22%), sopor-in 3 (2.13%), moderate coma (according to gcs 6-7 points) – in 1 (0.71%) patient, deep coma ( according to gcs 4-5 points) – in 4 (2.84%) patients. focal neurological disorders before surgery were in 40 (28.37%) patients. in 13 (9.42%) patients there were violations of motor functions of the central type, 17 (12.32%) oculomotor disorders, 6 (4.35%) a combination of paresis and oculomotor disorders, 1 – a combination of motor and mental disorders, 2 (1.45%) – a combination of motor and afatic disorders. computer tomography. all patients underwent brain ct before a surgery. intracranial haemorrhage was assessed by ct scan (fig.3) according to the scale of c. м. fisher et al. (1980) (tab. 4). the presence of cerebral edema or cerebral ischemia, 69 risk factors and consequences of intraoperative rupture of brain aneurysms in microsurgical operations lateral or axial displacement were also taken into account. the nature of the hemorrhage number of patients ab. % subarachnoid 67 47,52% subarachnoid parenchymal 49 34,75% subarachnoid ventricular 6 4,26% subarachnoid parenchymal ventricular 19 13,46% total 141 100 table 3. the nature of intracranial hemorrhage. degree of sah number of patients ab. % і blood in the liquor spaces is not visualized 5 3.62 іі diffuse hemorrhage or vertical size in the cistern less than 1 mm 73 52.90 iii the apparent convolution in the cistern or the vertical size of the blood signal in the cistern is more than 1 mm 54 39.13 iv intracerebral or intraventricular hemorrhage 6 4.35 total 138 100 table 4. degree of sah according to the fisher scale. cerebral angiography. all patients underwent cerebral angiography at the planning stage of the operation. according to the results of cag, 135 (95.74%) patients had single aneurysms, 6 (4.26%) had multiple aneurysms (table. 5). localization of aneurysm (rupture) number of patients ab. % aca-acoma on the left 47 33.33 aca-acoma on the right 36 25.53 mca on the left 9 6.38 mca on the right 17 12.06 ica on the left 11 7.80 ics on the right 14 9.93 pica on the left 0 0 pica on the right 1 0.71 multiple aa acaacoma aa rupture 6 3 4.26 2.13 mca aa rupture 1 0.71 ica aa rupture 1 0.71 pica aa rupture 1 0.71 table 5. transcranial doppler. tcd in the perioperative period was carried out in all cases: before surgery 25 (17.73%) patients, after surgery in all cases (100 %). with an increase in the linear velocity of blood flow through the arteries of the base of the brain more than 120 cm/s and the value of the lindegaard index more than 3, vascular spasm was considered moderate, with a blood flow rate exceeding 200 cm/s and the value of the lindegaard index more than 6 expressed. angiospasm was assessed as nonwidespread if it covers 1-2 arteries of the arterial circle of the brain, and was considered common with spasm of 3 or more arteries. among the examined patients before surgery angiospasm was detected in 11 (7.80%) patients (tab.6). the degree of vasospasm number of patients (out of 141) number of patients (out of 11) ab. % ab. % і 10 7.09 10 90.91 іі 1 0.71 1 9.09 iii-iv 0 0 0 0 table 6. surgical interventions. all patients underwent microsurgical interventions. in 107 (75.89%) patients clipping of aneurysm with blood washing from basal cisterns was performed, in 22 (15.60%) patients – clipping of aneurysm was combined with removal of intracerebral hematoma, in 3 (2.13%) patients – clipping of aneurysm of was combined with external ventriculostomy, in 6 (4.26%) patients operated on vital indications due to dislocation syndrome and 70 bindu a. v., orlov m. yu., litvak s. o. et al. volume intracranial hemorrhage clipping of the aneurysm, removal of intracerebral hematoma and decompression trepanation of the skull were performed. intraoperative assessment of the blood flow in the aneurysm-affected arterial segments of cerebral arteries and radicality of clipping was assessed using intraoperative contact dopplerography with a 20 hz sensor. in the postoperative period, msct-angiography and cag were performed. results and discussion treatment results were assessed at hospital discharge according to the glasgow results scale (jennett b., bond m., 1975). this scale includes 5 stages (tab.7). value number of points recovery of the patient without neurological disorders, or with minimal deficiency. complete or partial recovery of labour activities. 5 moderate disability. neurological disorders that limit daily activities, but the patient does not need help. 4 deep disability. the patient needs outside care 3 vegetative state or a deep psycho-organic disorders 2 death 1 table 7. satisfactory results were recorded in most cases – 81 (61.71%) at the time of discharge from the hospital: complete or partial resumption of work – 69 (48.94%), recovery of labour activities without the need for assistance was 18 (12.77%) according to the glasgow results scale (tab.8). number of points (glasgow results scale)) description number of patients ab. % 5 complete recovery recovery of the patient without neurological disorders, or with minimal deficiency. complete or partial recovery of labour activities. 69 48.94 4 moderate disability neurological disorders that 18 12.77 limit daily activities, but the patient does not need help. 3 deep disability. the patient needs outside care 37 26.24 2 vegetative state 0 0 1 death 17 12.05 table 8. glasgow results scale recorded iora dominated on the stages of the isolation and clipping of aa – 126 (89.36%) (tab. 9). the stage of the operation at which the aa rupture occurred number of patients ab. % non-contact (at the stage of craniotomy) 6 4.26 early arachnoid dissection 3 2.13 when the affected aa artery is isolated 6 4.26 when an aneurysm is isolated 119 84.40 at the stage of aneurysm clipping 7 4.96 table 9. the frequency of iora at different stages of surgical interventions. non-contact aa rupture was recorded in 6 (4.26%) patients out of 141 (tab.10), men 4 (2.84%), women 2 (1.42%), age from 40 to 52 years; 5 (3.55%) patients underwent clipping of single aneurysms, in 1 (0.71%) – multiple (aca-acoma on the right and mca on the right); in all cases, the aneurysms were of medium size (from 4.0 mm to 14 mm); 3 (2.13%) patients were operated after primary hemorrhage, 3 (2.13%) – after repeated aa ruptures; 2 (1.42%) patients had sah and 4 (2.84%) subarachnoid parenchymal hemorrhage with the formation of intracerebral hematoma. the frequency of non-contact rupture in our observations was 4.26%. features of the manifestation of non-contact rupture of aa during surgery were: signs of arterial bleeding with basal spread and signs of edema-swelling of the brain, which were associated with spontaneous short-term (up to several minutes) fluctuation of blood pressure (not significant in relation to the systemic hemodynamics). two (1.42%) patients were operated on the first 3 days after sah, 2 (1.42%) – on the 4-6th day after rupture, 1 (0.71%) on the 9th day after the last aa rupture, 1 (0.71%) – on the 16th day. 71 risk factors and consequences of intraoperative rupture of brain aneurysms in microsurgical operations in all cases of non-contact rupture of aa, all further stages of surgery: isolation of the arterial segment affected by the aneurysm, isolation of the initial sections of the perforant arteries, neck and body of aa itself, clipping of the aneurysm, were performed using the technique of gradual temporary blocking of blood flow in the proximal segments of the cerebral arteries in relation to the location of the aneurysm. thus, the gradual blocking of segments of cerebral arteries on the affected side from the proximal segment of the internal carotid artery ( ica) aneurysm to the affected segment ( a1 segment of the aca or the m1 segment of mca) with a stages offset of clips for temporary locking in the distal direction to the arterial segment affected by the aneurysm and reperfuse of pre-blocked (proximal) segment was performed to 3 (2,13%) patients, in 3 (2,13%) cases a temporary blockage of blood flow to highlight the aa and its clipping of an arterial segment directly affected by the aneurysm (a1 segment of the aca or the m1 segment of mca) was technically possible . in the postoperative period, the secondary cerebral ischemia as a result of strengthening of the phenomena of initial cerebral angiospasm in conjunction with the duration of temporary blocking of blood flow, which exceeded 5 minutes, was observed in 2 (1.42%) patients with non contact intraoperative breaks aa mca, according to msct of the brain. table 10. operation for a non-contact rupture of b aa. angiospasm in the early postoperative period was observed in the vast majority-5 (83, 33%) out of 6 (100%) patients with non-contact iora (tab.11). angiospasm number of patients (out of 141) number of cases (out of non-contact ruptures -6) ab. % ab. % i degree 0 0 0 0 ii degree 3 2.13 3 50.00 iii degree 2 1.42 2 33.33 iv degree 0 0 0 0 the absence of vasospasm 1 0.71 1 16.67 table 11. angiospasm after surgery. in all patients with angiospasm in the postoperative period, there was a deepening of the initial neurological symptoms in the form of the operation aa localization aa size (mm) number of chambers the period after a rupture number of patients ab. % ab . % aa clipping. rehabilitation of basal cisterns aca-acoma on the right 4-14 single-chamber after 21 days 1 0.71 2 1.45 mca on the right 4-14 single-chamber on the 8-14th day 1 0.71 aa clipping. sanitation of the basal cisterns. removal of i/m strokehematoma. mca on the right 4-14 single-chamber first 3 days 1 0.71 2 1.45 4-7 days 1 0.71 aa clipping. sanitation of the basal cisterns. removal of i/m strokehematoma. decompressive craniotomy. aca-acoma on the right 9 single-chamber first 3 days 1 0.71 1 0.72 aa clipping. blood washing from the basal cisterns. decompressive craniotomy. aca-acoma on the right 4-14 single-chamber 5th day 1 0.71 1 0.72 72 bindu a. v., orlov m. yu., litvak s. o. et al. appearance or deepening of pyramidal insufficiency, motor, sensory aphasia or mental disorders. in 1 patient operated on for aca-acoma aa on the left, in the postoperative period, right-sided hemiparesis joined; in 1 patient operated on for rupture of sa mca on the right with the formation of intracerebral hematoma in the postoperative period, there were signs of psychoorganic syndrome ( walter-buehl triad) according to the explosive type with psychotic complications; in 3 patients, the symptoms combined paresis (sensorimotor, motor aphasia) and organic psychosyndrome. contact intraoperative aa rupture was observed in 135 (100%): men – 67 (49.6%), women – 68 (50.4%), which was 95.74% of 141 cases (100%). age of patients from 19 to 68 years. the vast majority of patients with contact iora were operated for acaacoma aa (tab. 14). in 4 (2.96%) cases there were multiple aa: aca-acoma (3 cases) and ica. localization of aneurysm number of patients ab. % aca-acoma on the left 47 34.81 on the right 38 28.15 mca on the left 9 6.67 on the right 14 10.37 ica on the left 12 8.89 on the right 14 10.37 pica on the left 0 0 on the right 1 0.74 total 135 100 table 12. localization of b aa complicated by contact iora. the degree of consciousness according to the gcs before surgery in 84 (62.22%) patients was clear, in 30 (22.22 %) was impaired by the type of moderate stunning; in 13 (9.63%) deep stunning; in 3 (2.22%) – sopor; in 1 (0.74%) – moderate coma (according to the gcs 6-7 points); in 4 (2.97%) deep coma (according to the gcs 4-5 points). out of 71 (52.59%) patients operated on in the first 3 days after aa rupture, 32 (23.7%) patients had sah; 22 (16.29%)-subarachnoid parenchymal hemorrhage; 3 (2.22%)-subarachnoid ventricular hemorrhage; 14 (10.37%) subarachnoid parenchymal-ventricular hemorrhage. the overall mortality rate after iora was 17 (12.06%) cases out of 141 (100%) cases, whereat deaths in the contact iora group – 17 (12.6% out of 135 (100%)). although according to the literature, a significant increase in the number of fatal cases is observed after early iora, which occurred at the stages of craniotomy before the opening of tmo and the beginning of arachnodal dissection, when there is no possibility of direct control of bleeding from the aneurysm by temporary or permanent blocking of the neck or body of the aneurysm, or the imposition of a temporary clip on the affected segment of the artery, there was no such trend in the analyzed series of observations. however, there was a significant increase in the number of cases of deepening of the initial neurological symptoms in the group of patients with non-contact iora, which probably, given a larger sample, could be associated with an increase in the number of deaths. table 13. operations on b aa complicated by contact iora. surgical interventions in the first 3 days after aa rupture (81) operation aa localiza tion aa size (mm) number of chambers number of patients ab . % ab. % aa clipping. rehabilitation of basal cisterns acaacoma on the left 4-14 single-chamber 37 26.24 14 9.93 on the right 15-24 multichamber 3 2.13 4-14 single-chamber 8 5.67 up to 3 single-chamber 1 0.71 mca on the right 4-14 single-chamber 3 2.13 15-24 multichamber 1 0.71 ica on the left 4-14 single-chamber 1 0.71 5-24 single-chamber 1 0.71 on the right 4-14 single-chamber 5 3.55 73 risk factors and consequences of intraoperative rupture of brain aneurysms in microsurgical operations aa clipping. sanitation of the basal cisterns. removal of i/m stroke-hematoma. acaacoma on the left 15-24 double chamber 36 25.53 1 0.71 4-14 single-chamber 2 1.42 double chamber 1 0.71 three-chamber 1 0.71 up to 3 single-chamber 2 1.42 on the right 15-24 multichamber 1 0.71 4-14 single-chamber 5 3.55 multichamber 1 0.71 up to 3 single-chamber 1 0.71 mca on the left 4-14 single-chamber 3 2.13 up to 3 single-chamber 1 0.71 on the right 15-24 single-chamber 1 0.71 multichamber 1 0.71 4-14 single-chamber 5 3.55 up to 3 single-chamber 1 0.71 ica on the left 15-24 single-chamber 1 0.71 4-14 single-chamber 1 0.71 on the right giant double chamber 1 0.71 4-14 single-chamber 6 4.26 aa clipping. drainage of the ventricular system. pica on the right 7 single-chamber 1 0.71 1 0.71 aa clipping. removal of i/m hematoma. decompressive craniotomy. acaacoma on the left 4-14 single-chamber 6 4.26 4 4.26 on the right 15-24 multichamber 1 0.71 mca on the left 4-14 single-chamber 1 0.71 aa clipping. blood washing from the basal cisterns. decompressive craniotomy. acaacoma on the right 4-14 single-chamber 1 0.71 1 0.71 surgical interventions for 4-7 days after aa rupture 34 operation aa localiza tion aa size (mm) the presence of diverticula, q-ty of chambers number of patients ab . % ab. % aa clipping. rehabilitation of basal cisterns acaacoma on the left 15-24 single-chamber 24 17.02 1 0.71 multichamber 1 0.71 4-14 single-chamber 5 3.55 up to 3 single-chamber 1 0.71 on the right 15-24 multichamber 2 1.42 4-14 multichamber 1 0.71 single-chamber 4 2.84 up to 3 single-chamber 1 0.71 mca on the left 15-24 multichamber 1 0.71 on the right 4-14 single-chamber 1 0.71 ica on the left giant multichamber 1 0.71 4-14 single-chamber 2 1.42 on the right 15-24 multichamber 1 0.71 4-14 single-chamber 2 1.42 aa clipping. sanitation of the basal cisterns. removal of i/m stroke-hematoma. acaacoma on the left 4-14 single-chamber 9 6.38 2 3.62 on the right up to 3 single-chamber 1 0.71 4-14 single-chamber 1 0.71 mca on the right 4-14 single-chamber 2 1.42 ica on the left 4-14 single-chamber 2 1.42 on the right up to 3 single-chamber 1 0.71 74 bindu a. v., orlov m. yu., litvak s. o. et al. aa clipping. drainage of the ventricular system. mca on the left 4-14 single-chamber 1 0.71 1 0.71 ssurgical interventions on the 8-14th day -14 (9,93%) operation aa localiza tion aa size (mm) the presence of diverticula, q-ty of chambers number of patients ab. % a b. % aa clipping. rehabilitation of basal cisterns acaacoma on the left 4-14 single-chamber 12 8.51 1 0.71 multichamber 1 0.71 on the right 4-14 single-chamber 2 1.42 up to 3 double chamber 1 0.71 mca on the left 4-14 single-chamber 1 0.71 on the right 15-24 multichamber 1 0.71 4-14 multichamber 1 0.71 ica on the left 4-14 multichamber 1 0.71 single-chamber 1 0.71 on the right up to 3 single-chamber 2 1.42 aa clipping. sanitation of the basal cisterns. removal of i/m stroke-hematoma. acaacoma on the left 4-14 double chamber 2 1.42 1 0.71 on the right 15-24 multichamber 1 0.71 s surgical interventions on the 15-21 day -11 ( 7,8% ) operation aa localiza tion aa size (mm) the presence of diverticula, q-ty of chambers number of patients ab. % a b. % aa clipping. rehabilitation of basal cisterns acaacoma on the left 15-24 multichamber 10 7.09 1 0.71 4-14 single-chamber 2 1.42 multichamber 1 0.71 up to 3 single-chamber 1 0.71 on the right 4-14 single-chamber 1 0.71 mca on the right 4-14 single-chamber 1 0.71 ica on the left 4-14 multichamber 1 0.71 on the right 4-14 single-chamber 2 1.42 aa clipping. blood washing from the basal cisterns. decompressive craniotomy. ica on the left 4-14 single-chamber 1 0.71 1 0.71 s surgical interventions after 21 days-13 (9,22%) operation aa localiza tion aa size (mm) the presence of diverticula, q-ty of chambers number of patients ab. % a b. % aa clipping. rehabilitation of basal cisterns acaacoma on the left 15-24 multichamber 13 9.22 1 0.71 4-14 single-chamber 3 2.17 up to 3 single-chamber 1 0.71 on the right 4-14 single-chamber 1 0.71 multichamber 1 0.71 mca on the left 4-14 multichamber 1 0.71 on the right 4-14 single-chamber 1 0.71 ica on the left 4-14 multichamber 1 0.71 single-chamber 1 0.71 on the right 4-14 single-chamber 2 1.42 summary 1. the frequency of iora in b aa clipping operations was 9.73% (141 patients) in a series of observations 1441 (100%). according to our observations, most often iora-141 (100%) was registered in operations pf clipping of aa complex ofaca-acoma (86 (61%) cases out of 141 (100%)). 75 risk factors and consequences of intraoperative rupture of brain aneurysms in microsurgical operations 2. iora is possible at different stages of the aneurysm clipping operation with a maximum frequency of contact breaks -135 (95.74%): at the stage of aa isolation (119 cases-84.40%), with the imposition of a clip on the neck of aa 7 (5.07%), with the isolation of the artery affected by aneurysm 6 (4.26%) and with arachnoid dissection – 3 ( 2.17%). non-contact iora (at the stage of craniotomy) was recorded less often-6 (4.26%). 3. the most common risk factors for iora were: cerebral edema, large aa, atherosclerotic changes in the aneurysm-affected artery segment and cervical aneurysm sites, high blood pressure during surgery, adhesions arachnoid changes. 4. at the time of discharge from the hospital, according to the glasgow results scale: 69 (48.94%) full or partial restoration of labor activity, 18 (12.77%) had limited daily activities without the need for outside assistance, 37 (26 24%) deep disability ) deaths were in the group of "contact" iora 17 (12.06%). at 6 (4.26%) of "non-contact" iora, a deepening of initial neurological symptoms was recorded with a suppression of the level of consciousness, the addition of pyramidal insufficiency, speech impairment and psychoorganic syndrome, and a deepening of the phenomena of initial cerebral arterial vasospasm. abbreviations aa – arterial aneurysm; sa– sacculated aneurysm; ioc – intraoperative complications; sah – subarachnoid hemorrhage; bp – blood pressure; iora– intraoperative aneurysm rupture; tc – temporary clipping; aca-acoma– anterior cerebral anterior communicating artery; mca– middle cerebral artery; ica – internal carotid artery; pica– posterior inferior cerebellar artery; iah – induced arterial hypotension; h-h – hunt-hess scale; gcs – glasgow coma scale; cag – cerebral angiography; msct – multispiral computed tomography. references 1. lai lt, o’neill ah. history, evolution, and continuing innovations of intracranial aneurysm surgery. world neurosurg. 2017 jun;102:673-681. doi: 10.1016/j.wneu.2017.02.006. pubmed pmid: 28189863. 2. acciarri n, toniato g, raabe a, lanzino g. clipping techniques in cerebral aneurysm surgery. j neurosurg sci. 2016 mar;60(1):83-94. pubmed pmid: 26657306. 3. lawton mt, du r. effect of the neurosurgeon’s surgical experience on outcomes from intraoperative aneurysmal rupture. neurosurgery. 2005 jul;57(1):9-15; discussion 9-15. doi: 10.1227/01.neu.0000163082. 20941.ef. pubmed pmid: 15987535. 4. liu q, jiang p, wu j, gao b, wang s. the morphological and hemodynamic characteristics of the intraoperative ruptured aneurysm. front neurosci. 2019 mar 26;13:233. doi: 10.3389/fnins.2019.00233. pubmed pmid: 30971874; pubmed central pmcid: pmc6443834. 5. tian z, zhang y, jing l, liu j, zhang y, yang x. rupture risk assessment for mirror aneurysms with different outcomes in the same patient. front neurol. 2016 dec 5;7:219. doi: 10.3389/fneur.2016.00219. pubmed pmid: 27994571; pubmed central pmcid: pmc5136536. 6. choque-velasquez j, hernesniemi j. microsurgical clipping of a large ruptured anterior communicating artery aneurysm. surg neurol int. 2018 nov 28;9:233. doi: 10.4103/sni.sni_345_18. pubmed pmid: 30595954; pubmed central pmcid: pmc6287331. 7. дзяк л.а., зорин н.а., голик в.а., скребец ю.ю. артериальные аневризмы и артериовенозные мальформации головного мозга. днепропетровск: пороги; 2003. 8. dzyak la, zorin na, golik va, skrabets yu. [arterial aneurysms and arteriovenous malformations of the brain]. dnepropetrovsk: porogi, 2003. russian. 9. крылов в.в., природов а.в. факторы риска хирургического лечения аневризм средней мозговой артерии в остром периоде кровоизлияния. нейрохирургия. 2011;(1):31-41. 10. krylov v.v., prirodov a.v. risk factors of surgical treatment for middle cerebral artery aneurysms in acute period of subarachnoid hemorrhage. the russian journal of neurosurgery. 2011;(1):31-41. russian. available from: https://elibrary.ru/item.asp?id=16449822 11. хейреддин а.с., филатов ю.м., белоусова о.б., пилипенко ю.в., золотухин с.п., сазонов и.а., зарзур x.x. интраоперационный разрыв церебральных аневризм-частота и факторы риска. журнал вопросы нейрохирургии им. н.н. бурденко. 2007;(4):33-8. 12. kheireddin as, filatov ium, belousova ob, pilipenko iuv, zolotukhin sp, sazonov ia, zarzur khkh. [intraoperative rupture of cerebral aneurysm--incidence and risk factors]. zh vopr neirokhir im n n burdenko. 2007 octdec;(4):33-8; discussion 38. russian. pubmed pmid: 18274133. 13. lakićević n, vujotić l, radulović d, cvrkota i, samardžić m. factors influencing intraoperative rupture of intracranial aneurysms. turk neurosurg. 2015;25(6):85885. doi: 10.5137/1019-5149.jtn.12966-14.2. pubmed pmid: 26617133. 14. leipzig tj, morgan j, horner tg, payner t, redelman k, johnson cs. analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. neurosurgery. 2005 mar;56(3):455-68; discussion 455-68. doi: 10.1227/01.neu.0000154697.75300.c2. pubmed pmid: 15730570. 15. nanda a, vannemreddy p. management of intracranial aneurysms: factors that influence clinical grade and 76 bindu a. v., orlov m. yu., litvak s. o. et al. surgical outcome. south med j. 2003 mar;96(3):259-63. doi: 10.1097/01.smj.0000051906.95830.1f. pubmed pmid: 12659357. 16. lin tk, hsieh tc, tsai hc, lu yj, lin cl, huang yc. factors associated with poor outcome in patients with major intraoperative rupture of intracranial aneurysm. acta neurol taiwan. 2013 sep;22(3):106-11. pubmed pmid: 24030089. 17. lawton mt, du r. effect of the neurosurgeon’s surgical experience on outcomes from intraoperative aneurysmal rupture. neurosurgery. 2005 jul;57(1):9-15; discussion 9-15. doi: 10.1227/01.neu.0000163082.20941.ef. pubmed pmid: 15987535. 18. liu q, jiang p, wu j, gao b, wang s. the morphological and hemodynamic characteristics of the intraoperative ruptured aneurysm. front neurosci. 2019 mar 26;13:233. doi: 10.3389/fnins.2019.00233. pubmed pmid: 30971874; pubmed central pmcid: pmc6443834. 19. forget tr jr, benitez r, veznedaroglu e, sharan a, mitchell w, silva m, rosenwasser rh. a review of size and location of ruptured intracranial aneurysms. neurosurgery. 2001 dec;49(6):1322-5; discussion 1325-6. doi: 10.1097/00006123-200112000-00006. pubmed pmid: 11846931 20. kopitnik ta, horowitz mb, samson ds. surgical management of intraoperative aneurysm rupture. in: schmidek hh, sweet wh, editors. schmidek & sweet’s operative neurosurgical techniques: indications, methods, and results. 4th ed. philadelphia: wb saunders co; 2000. p. 1275–1281. 21. chen sf, kato y, kumar a, tan gw, oguri d, oda j, watabe t, imizu s, sano h, wang zx. intraoperative rupture in the surgical treatment of patients with intracranial aneurysms. j clin neurosci. 2016 dec;34:63-69. doi: 10.1016/j.jocn.2016.01.045. pubmed pmid: 27692502. 22. lawton mt, du r. effect of the neurosurgeon’s surgical experience on outcomes from intraoperative aneurysmal rupture. neurosurgery. 2005 jul;57(1):9-15; discussion 9-15. doi: 10.1227/01.neu.0000163082.20941.ef. pubmed pmid: 15987535. 23. weir b, disney l, karrison t. sizes of ruptured and unruptured aneurysms in relation to their sites and the ages of patients. j neurosurg. 2002 jan;96(1):64-70. doi: 10.3171/jns.2002.96.1.0064. pubmed pmid: 11794606. 24. della puppa a, rossetto m, volpin f, rustemi o, grego a, gerardi a, ortolan r, causin f, munari m, scienza r. microsurgical clipping of intracranial aneurysms assisted by neurophysiological monitoring, microvascular flow probe, and icg-va: outcomes and intraoperative data on a multimodal strategy. world neurosurg. 2018 may;113:e336-e344. doi: 10.1016/j.wneu.2018.02.029. pubmed pmid: 29452324. 25. de rooij n. k., linn f. h., van der plas j a, et all. incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends. in: j. neurol. neurosurg. psychiatry 2007,78, p.1365–1372. doi: 10.33962/roneuro-2023-028 bobble head doll syndrome. a series of 3 clinical cases managed at the yalgado ouédraogo university hospital and review of the literature yakouba haro, sylvain d. zabsonre, abdoulaye sanou, inoussa zoungrana, joseph biogo, abel kabre romanian neurosurgery (2023) xxxvii (2): pp. 159-163 doi: 10.33962/roneuro-2023-028 www.journals.lapub.co.uk/index.php/roneurosurgery bobble head doll syndrome. a series of 3 clinical cases managed at the yalgado ouédraogo university hospital and review of the literature yakouba haro1,2, sylvain d. zabsonre1,2, abdoulaye sanou2, inoussa zoungrana2, joseph biogo3, abel kabre1,2 1 “joseph ki zerbo” university of ouagadougou, burkina faso 2 university hospital yalgado ouedraogo (chuyo), burkina faso 3 regional university hospital of ouahigouya, burkina faso abstract introduction. bobble head doll syndrome is a neurological syndrome characterized by abnormal involuntary movements of the head combining repetitive or episodic movements of 2 to 3 hz back and forth in the anterior-posterior direction that can be assimilated to approval movements (yes-yes) and occasionally lateral rotations that can be assimilated to disapproval signs (no-no). it is a rare entity first described by benton[1]. we describe three cases managed at the yalgado ouédraogo university hospital in burkina faso. observations. three children, one girl and two boys, aged respectively 5, 9 and 14 years were seen for involuntary abnormal head movements associating lateral rotations assimilated to signs of disapproval (no-no) in two cases, and back and forth movements of the head in one case. in the 14-year-old adolescent, there was also a picture of intracranial hypertension. clinical examination revealed ataxia and macrocrania in both cases and a syndrome in 1 case. imaging revealed triventricular hydrocephalus on aqueductal stenosis in all cases with an associated supra sellar cyst in 2 cases. the treatment consisted of endoscopic treatment in 2 cases and ventriculoperitoneal shunt in 1 case. surgery allowed a considerable regression of involuntary movements of the head in the immediate postoperative period and a complete recovery in the long term. conclusion. the bobble head doll syndrome is a rare entity related to the consequences of chronic hydrocephalus responsible for abnormal movements whose management done well and early leads to favourable results. introduction bobble head doll syndrome is a rare pediatric neurological syndrome characterized by abnormal involuntary head movements with repetitive or episodic 2-3hz back-and-forth movements in the anteriorposterior direction that can be assimilated to approval movements (yes-yes) and occasional lateral rotations that can be assimilated to keywords bobble-head-dollsyndrome, endoscopy, hydrocephalus corresponding author: yakouba haro “joseph ki zerbo” university of ouagadougou, burkina faso yaksterharo@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 160 yakouba haro, sylvain d. zabsonre, abdoulaye sanou et al. disapproval signs (no-no). this condition was first described in 1966 by benton[1]. it is a complication of chronic hydrocephalus. the intracranial anomalies that are commonly observed are: noncommunicating hydrocephalus, supra sellar arachnoid cyst, septum pellucidum cyst, choroid plexus papilloma, stenosis of the mesencephale aqueduct[5,7,8,10]. we report 03 cases observed and managed at the yalgado ouédraogo university hospital of burkina faso with review of the literature. clinical aspects case report no. 1 a 9-year-old child, attending school, was admitted for abnormal lateral head movements and recent blindness associated with walking disorders evolving since the age of 3 years. the abnormal movements were initially intermittent and later on permanent, causing, with the onset of blindness, an enormous hindrance to the good progress of schooling. moreover, this child had a history of two congenital cataract surgeries without favorable results. the physical examination noted normal consciousness, a cranial perimeter of 56 cm, bilateral blindness, microphthalmia, and permanent lateral movements of the head in the form of lateral rotation, which could be assimilated to signs of disapproval (no-no). encephalic computed tomography (ct) showed triventricular hydrocephalus by stenosis of the mesencephalic aqueduct with major lamination of the cerebral cortex (figure 1), and diffuse parenchymal and subarachnoid calcifications. figure 1. preoperative ct images of case n° 1. a): axial section, b): sagittal reconstruction showing triventricular hydrocephalus with cortical lamination predominating in the parietal and occipital lobes, and intra parenchymal calcifications. an indication for ventriculocisternostomy was given and performed. the postoperative course was initially favorable with considerable regression of the abnormal movements but 4 weeks later, there was a resumption of lateral movements associated with spasms described as electrical discharges and generalized hyperesthesia treated as sensory epilepsy. magnetic resonance imaging (mri) of the brain revealed persistent triventricular hydrocephalus (figure 2). therefore, a new ventriculocisternostomy was performed. figure 2. mri images of case n° 1 performed 4 weeks after the first ventriculocisternostomy at the resumption of abnormal movements. a): t1 axial slice; b): t2 sagittal slice showing the persistence of a significant triventricular hydrocephalus. the clinical evolution was marked by a total regression of the abnormal movements. two months later he was readmitted for a left hemiparesis of progressive onset, associated with moderate headaches. a follow-up ct scan revealed a chronic right hemispheric subdural hematoma with a mass effect on the medial structures. the hematoma was evacuated and drained, and the postoperative course was favorable, marked by a complete recovery of the hemiparesis. three months later he was readmitted again for a resumption of involuntary head movements; after a cranioencephalic ct scan which showed no other abnormality apart from hydrocephalus, we concluded that the ventriculocisternostomy had failed and indicated a ventriculoperitoneal shunt with a medium pressure valve, which was immediately performed. after this bypass, the abnormal movements disappeared completely and definitively. case report no. 2 a 14-year-old boy suffering from chronic headaches 161 bobble head doll syndrome was admitted for involuntary head movements associated with a recent worsening of the headaches with the occurrence of vomiting in an intracranial hypertension picture. the history also revealed episodes of generalized seizures and a notion of running away. on physical examination, we noted a psychomotor slowing down, a head circumference of 58 cm, permanent lateral movements of the head with lateral rotation that could be assimilated to signs of disapproval (no-no). these movements were aggravated by arousal, diminished during voluntary movements and disappeared during sleep. these movements could also be suspended for a few seconds to a few minutes on demand. there was also a spastic right hemiparesis with a motor strength rated at 4/5, a static and locomotor ataxia. brain mri (figure 3) showed tri-ventricular hydrocephalus, a supra sellar cyst exerting a mass effect on v3 and a left temporo-parietal arachnoid cyst. there was also a ptosis of the cerebellar tonsils suggestive of an arnold chiari type i malformation. a ventriculoperitoneal shunt was performed with a medium pressure valve. the immediate postoperative course was favorable, with improvement of the intracranial hypertension syndrome and significant regression of involuntary head movements. at three months postop, the abnormal head movements had completely disappeared. figure 3. brain mri of case n° 2. a): t1 axial slice; b): t2 sagittal slice showing triventricular hydrocephalus with supra sellar cyst (red arrow on axial slice), left temporo-parietal arachnoid cyst (blue arrow on axial slice) and arnold chiari i malformation (arrow on sagittal slice). case report no. 3 a 4-year-old girl operated at the age of 2 years for triventricular hydrocephalus (ventriculoperitoneal shunt) with placement of a medium-pressure valve was admitted for abnormal head movements in the form of "yes-yes" head movements. clinical examination was normal. craniocerebral ct scan noted triventricular hydrocephalus and a cyst extending from the pineal region to the third ventricle, exerting a mass effect on the cerebellum (figure 4). we indicated endoscopic treatment, which consisted of a cysto-ventriculostomy. the postoperative course was favorable, marked by an improvement of the abnormal movements from the first postoperative days. the control made 6 months later noted a complete amendment of the abnormal movements. figure 4. ct images of case n°3 a): axial section, b): sagittal reconstruction showing triventricular hydrocephalus and a cyst of the septum pelucidum extending from the pineal region to the third ventricle and compressing the cerebellum. discussion bobble head doll syndrome is a disorder of children under 10 years of age, rarely seen in adults. it is characterized by a stereotypy of back-and-forth movements of the head of 2-3hz and inconstantly of laterality movements. in some cases the movements may extend to the shoulders, all upper limbs and trunk [9]. these movements are rhythmic, may intensify during stress, but are partially controllable by the patient and disappear during sleep [11]. at least 81 other cases have already been described before our cases [2,3,5,8,14,15,17,20] which have a particular clinical character due to the predominance of ‛‛non-non laterality movements''. since the first description in 1966[1], the consistency of intracerebral cystic abnormalities has been noticed but the direct causal link remains for the moment subject to controversies. the intracranial anomalies commonly observed are non-communicating hydrocephalus, supra sellar arachnoid cyst, septum 162 yakouba haro, sylvain d. zabsonre, abdoulaye sanou et al. pellucidum cyst, choroid plexus papilloma, midbrain aqueduct stenosis and by extension all lesions of topography likely to lead to chronic obstructive hydrocephalus. these cystic lesions constitute valves that close the midbrain aqueduct[11,19,23]. the precise physiopathology remains unknown until now but many authors recognize the involvement of dysfunctions of the interconnections between the frontal lobes, the corpus callosum and the basal ganglia[16,17]. on this subject, several hypotheses have been formulated. in the case of supra sellar cysts, some authors stipulate that the movements of the head would aim at tilting the cyst making the valve backwards in order to allow the opening of the mesencephalic aqueduct. thus, the movements are interpreted as adaptation mechanisms serving to promote the restoration of normal cerebral spinal fluid (csf) circulation in order to lower the intracranial pressure[19,23]. for other authors, the perpetual and rhythmic movements of the intracystic fluid or csf on the diencephalon, the dorso-medial red nucleus and the motor pathways in the upper part of the midbrain would lead to dysfunctions of the extrapyramidal motor pathway[11,17,23]. the patient's ability to control movements and their disappearance during sleep would be arguments that support this hypothesis. in our series we noted 2 cases of supra sellar cysts interfering with the circulation of the csf; in addition we noted diffuse intracerebral calcifications which suggest sequelae of torch ( toxoplasmosis, other agents, rubella, cytomegalovirus, and herpes simplex) infection including cytomegalovirus infection[6,18,22] in the pediatric age. these same infections could also lead to meningitis and hydrocephalus as well as ocular manifestations including cataracts [12,18,21,22]. the symptomatology may be enriched by other signs related to intracranial hypertension. the development of ct and mri scans has improved the diagnostic time. early diagnosis allows to avoid the permanent installation of the consequences of intracranial hypertension[9] such as blindness and endocrine disorders. surgical management combines several techniques depending on the causal lesion: ventriculocisternostomy, cysto-ventriculoperitoneal shunt, cystectomy, endoscopic or open marsupialization [10,11,13]. in our case the indicated techniques were ventriculocistrenostomy, cystoventriculostomy and ventriculo-peritoneal shunt. the postoperative results are generally marked by a significant clinical improvement[10,20]. on the other hand, there is still a residual risk of the usual complications linked to the type of operation and the approach. recurrences are rare[20], estimated at 11%, and may be the consequence of obstruction of the ventriculocisternostomy orifices, dysfunction of the ventriculoperitoneal shunt system or postoperative ectasia of the fourth ventricle[11,4]. in one of the cases in our series (case n° 1) early clinical improvement was observed but shortened due to the probable closure of the ventriculocisternostomy orifices. the occurrence of the chronic subdural hematoma would result from a possible hyper draining following the second ventriculocisternostomy. conclusion bobble head doll syndrome is a rare pediatric clinical entity, responsible for abnormal movements. it is a manifestation of the consequences of chronic hydrocephalus, which, if managed well and early, leads to favorable results. the quality of the clinical improvement depends on the diagnostic delay and the success of the etiological procedure. our series of cases are typical examples that have been effectively managed with favorable results. references 1. benton jw, nelhaus g, huttenlocher pr, ojemann rg, dodge pr. the bobble-head doll syndrome. neurology (minneap). 1966; 16:9. 2. cavalheiro s, da costa mds, valsechi lc, suzuki fs, leite al, dastoli pa, et al. endoscopic laser fenestration to treat a bobble-head doll syndrome caused by suprasellar cyst. world neurosurg. 2021;150:17. https://linkinghub.elsevier.com/retrieve/pii/s187887502 1004058 3. da silva ajf, malta doria al, de oliveira avelino lopes tl. hydrocephalus and bobble-head doll syndrome. j pediatr. 2021 ;233:277. https://linkinghub.elsevier.com/retrieve/pii/s002234762 1002171 4. dell s. further observations on the « bobble-headed doll syndrome ». j neurol neurosurg psychiatry 1981;44(11):1046‑9. http://jnnp.bmj.com/cgi/doi/10.1136/jnnp.44.11.1046 5. doya lj, kadri h, jouni o. bobble-head doll syndrome in an infant with an arachnoid cyst: a case report. j med 163 bobble head doll syndrome case reports 2022;16(1):393. https://jmedicalcasereport s.biomedcentral.com/articles/10.1186/s13256-0220362 3-0 6. eyaid w, al-tassan rs, al-nouri dm. intracranial calcifications, microcephaly, and seizure. neurosciences. 2012;17(3):5. 7. franco i de a, vale tc, freitas lf, barbosa avs, aragão m de m, rodrigues mm. obstructive hydrocephalus presenting with bobble-head doll syndrome. neuropediatrics. 2022;53(1):78‑9. 8. george r, gaxa l, lockhat z, hlahla sk, van der meyden ch, kisten r, et al. suprasellar cyst presenting with bobble-head doll syndrome. world neurosurg. 2020;133:80‑3. https://linkinghub.elsevier.com/retrieve/ pii/s1878875019325756 9. guerreiro h, vlasak a, horinek d, tichy m, lisy j, vanek p, et al. bobble-head doll syndrome: therapeutic outcome and long-term follow-up in four children. acta neurochir (wien). 2012 ;154(11):2043‑9. http://link.springer.com/10. 1007/s00701-012-1458-2 10. gui s-b, wang x-s, zong x-y, zhang y-z, li c-z. suprasellar cysts: clinical presentation, surgical indications, and optimal surgical treatment. bmc neurol. 2011;11:52. https://www.ncbi.nlm.nih.gov/pmc/articles/pmc311916 8/ 11. hahm mh, woo j, kim kh. hypomania in bobble-head doll syndrome: a case report of surgically treated stereotypy and hypomania. psychiatry investig. 2018;15(5):546‑9. http://psychiatryinvestigation.org/jour nal/view.php?doi=10.30773/pi.2017.10.25.2 12. lu y, xiong j, yin b, wen j, liu l, geng d. the role of threedimensional pseudo-continuous arterial spin labelling in grading and differentiating histological subgroups of meningiomas. clin radiol. 2018;73(2):176‑84. http://linkinghub.elsevier.com/retrieve/pii/s0009926017 304397 13. maher co, goumnerova l. the effectiveness of ventriculocystocisternostomy for suprasellar arachnoid cysts. j neurosurg pediatr. 2011;64‑72. https://thejns.org/view/journals/j-neurosurg-pediatr/7/1 /article-p64.xml 14. mahfouf l, tikanouine a, abdennebi b. le syndrome de tête de poupée bobble ou bobble head doll syndrome (bhds). (à propos d’un cas et revue de la littérature). neurochirurgie 2017;63(1):54. https://linkinghub.elsevier.com/retrieve/pii/s002837701 6301990 15. mba se, musara a, kalangu k, nyamapfene b. an unusual presentation of bobble-head doll syndrome in a patient with hydranencephaly and chiari 3 malformation. childs nerv syst. 2019 ;35(5):879‑82. http://link.springer.com/10.1007/s00381-019-04054-x 16. nellhaus g. the bobble-head doll syndrome: « tic » with a neuropathologic basis. pediatrics. 1967;15. 17. olvera-castro jo, morales-briceño h, sandoval-bonilla b, gallardo-ceja d, venegas-cruz ma, estrada-estrada em, et al. bobble-head doll syndrome in an 80-year-old man, associated with a giant arachnoid cyst of the lamina quadrigemina, treated with endoscopic ventriculocystocisternotomy and cystoperitoneal shunt. acta neurochir (wien). 2017 ;159(8):1445‑50. http://link.springer.com/10.1007/s00701-017-3195-z 18. patnaik a, mishra s, das s. extensive intracranial calcification of pseudo-torch syndrome with features of dandy–walker malformation. asian j neurosurg. 2017;12(3):541. http://www.asianjns.org/text.asp?2017/12/3/541/14516 2 19. rana pvs, malhotra a. bobble-head doll syndrome. nepal journal of neurosciences. 2004;1(2):135‑7. 20. renne b, rueckriegel s, ramachandran s, radic j, steinbok p, singhal a. bobble-head doll syndrome: report of 2 cases and a review of the literature, with video documentation of the clinical phenomenon. j neurosurg pediatr. 2018 ;21(3): 236‑46. http://thejns.org/doi/10.3171/2017.9.peds16704 21. roche o, beby f, orssaud c, dupont monod s, dufier jl. cataracte congénitale. j fr ophtalmol. 2006 : 29(4):443‑55. https://linkinghub.elsevier.com/retrieve/pii/s018155120 6777105 22. sanchez tr, datlow md, nidecker ae. diffuse periventricular calcification and brain atrophy: a case of neonatal central nervous system cytomegalovirus infection. neuroradiology journal 2016;29(5):314‑6. http://journals.sagepub.com/doi/10.1177/19714009166 65372 23. wiese ja, gentry lr, menezes ah. bobble-head doll syndrome: review of the pathophysiology and csf dynamics. pediatr neurol. 1985;1(6):361‑6. http://linkinghub.elsevier.com/retrieve/pii/08878994859 00736. doi: 10.33962/roneuro-2021-078 a very rare fact occurring after v/p shunt in the surgical treatment of pseudotumor serebri syndrome. liver subcapsular pseudocysts mehmet akif ambarcioglu, i. burak atci, okan türk, veysel antar, nail demirel, nuriye güzin özdemir, emre eğilmez, a. can karaoğlu, b. özgur baran romanian neurosurgery (2021) xxxv (4): pp. 468-471 doi: 10.33962/roneuro-2021-078 www.journals.lapub.co.uk/index.php/roneurosurgery a very rare fact occurring after v/p shunt in the surgical treatment of pseudotumor serebri syndrome. liver subcapsular pseudocysts mehmet akif ambarcioglu, i. burak atci, okan türk, veysel antar, nail demirel, nuriye güzin özdemir, emre eğilmez, a. can karaoğlu, özgur baran i̇stanbul research and education hospital, neurosurgery department, turkey abstract introduction: in this study, it is aimed to present a very rare liver subcapsular accumulation of a patient after ventriculoperitoneal shunt surgery who was diagnosed with pseudotumor cerebri syndrome with progressive sight loss. case: the patient is a 38-year-old female who was diagnosed with lomber spondylose and later operated with stabilization and fusion surgery. seven days after the operation her headaches became clear and blackout in her left eye was seen and she was observed with medical treatment. csf pressure of her was measured to be 25 cm/ water, so she was diagnosed as pseudotumour cerebri and taken to the operation immediately. on the 3rd day of post-operation, there occurred to be intense stomach ache and abdominal sensitivity of the case. after the scanning of abdominal ct, 7 cm of liquid collection was detected in the shunt distal of liver subcapsular area. discussion: liver pseudocyst should be considered, even if it is a rare complication when back striking abdominal pain and high liver enzymes are seen in patients with shunt dysfunction. usg and abdominal bt tests should be made for these patients. the drainage of the cyst and then the removal of the abdominal catheter should be applied. introduction pseu do tumo r cerebri sydrom e (p tss), is characterized with hydrocefaly intracranial infection in the form of obstructive lesion situated in the brain with the increase of intracranial pressure without radiological findings (1). it is called pseudotumor cerebri or idiopathic intracranial hypertension at the same time. it was first defined by quinke in 1897 and its diagnostic criteria were determined by dandy in 1937 but its patophysiology has not been described completely (2). the biggest risk factors are female sex and o besity. its clinical keywords v/p shunt, surgical treatment, pseudotumor serebri syndrome, liver subcapsular pseudocyst corresponding author: i.burak atci i̇stanbul research and education hospital, neurosurgery department, turkey drburakatci@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published october 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 469 a very rare fact occurring after v/p shunt in the surgical treatment of pseudotumor serebri syndrome symptoms are frequently seen as headache, loss of sight, dizziness, tinnitus and diplopy (3). its most significant finding is papil oedema. however, cases without headache and papil oedema have rarely been found out. treatment is priviliged with the retraction of secondery reasons of weight loss. if there are cases without any recovery then medical and surgical treatment can be used. in this study, it is aimed to present a very rare liver subcapsular accumulation of a patient after ventriculoperitoneal shunt surgery who was diagnosed as pseudotumor cerebri syndrome with progressive sight loss. figure 1. the enhanced ct after operation. (a) axial ct showed water-like hypointense mass in the liver contour. figure 2. the enhanced ct after operation. (a) axial ct showed water-like hypointense mass and catheter image in the liver contour. case the patient is a 38-year-old female who was diagnosed with lomber spondylose and later operated with stabilization and fusion surgery. seven days after the operation her headaches became clear and blackout in her left eye was seen and she was observed with medical treatment. opthalmology consultation was demanded as a result of sight loss in her left eye 15 days after the operation. in her consultation in left eye optical atrophy and in her right eye papil oedema was detected as a result of which she was sent to our clinic straightaway.when the patient was seen in our emergency service her conscious was clear koopere oryante ır +/bmi which was not deficit neurologically. in order to exclude pseudotumour cerebri possibility, firstly cranial mrg, diffusion mrg, and venography were applied to her. as there were not any patological find-outs, csf pressure of her was measured to be 25 cm/ water, so she was diagnosed as pseudotumour cerebri and taken to the operation immediately. lumboperitoneal shunt was set in the surgery. she was discharged on the 4th day of post operation as her oedema in the right eye had drawn back and her headache had soothed.2 months later she came again with serious headache and sight loss in the right eye.csf pressure measured to be 29 cm/ water via lp. she was consulted to opthalmology clinic with the diagnosis of lumboperitoneal shunt dysfunction for the fenestration of optical nerve cover fact. there was not any extra pathology in the following of the operated case. after ‘ years, she applied to emergency service with the increase of sight loss, headache, tinnitus and dıplopy. after neuroimaging, csf was measured to be 28 cm/water, therefore neuronavigation guided ventriküloperitoneal shunt was planned. after the operation, the complaints of the patient decreased. on the 3rd day of post operation, there occurred to be intense stomach ache and abdominal sensitivity of the case. after the scanning of abdominal ct, 7 cm of liquid collection was detected in the shunt distal of liver subcapsular area(fugure 1,2,3,4). when usg performed; dren was placed into the subcapsular area. the liquid not compatible to the csf was discharged for three days. 470 mehmet akif ambarcioglu, i. burak atci, okan türk et al. then shunt distal revision was made with reoperation. figure 3. the enhanced ct after operation. (a) coronal ct showed water-like hypointense mass in the liver contour. figure 4. the enhanced ct after operation. (a) coronal ct showed water-like hypointense mass and catheter image in the liver contour. discussion pseudotumor cerebri is often seen in women, that is; the intensity of pseudotumor cerebri for general population is 0,9/100.000 while it is 19,3/100.000(1,2) for obese women who are at a childbearing age(4,5). it is essential to start treatment without delay as the sydrome causes headache and progressive sight loss. the aim of the treatment is to control headache and to protect seeing. during the treatment, making the obese patients lose weight helps most patients recover without any need of medication. the first option in medical treatment is a carbonic anhidraz inhibitor, asetolozolaid which is used to decrease the production of bos pressure(6). topiramat and furosemid can be started at chosen cases as well(6). optical nerve fenestration, shunt, venos sinüs stent and barıatrıc surgery are applied in surgeric operations.ventriculoperitoneal or lumboperitoneal shunt are applied when the patients utilise from lomber ponction in case of no progress in medical treatment(7). in these operations, especially shunt obstruction, infection, intracranial hypotension, and mechanic complications due to the catheter can be observed. obctruction that is one of the often seen reasons of shunt dysfunction can be a result of pseudocysts growing in abdominal part. the frequency of mentioned complication is between 0,25% and 10 % among all v/p shunt complications in theory(8,9). pseudocysts in liver subcapsular area is rarely seen in literature. 16 cases have been reported in all literature so far.the forming of pseudocysts in liver is defined as two kinds. in the first one, there occurs to be cyst existing in intraaxial in which the shunt dystal is within the liver parenchymal. the second kind happens to be in extraaxial and its catheter dystal is in the glisson capsul. as the capsul is sensitive to the pain, in extraaxial pseudocysts, heavy pain striking to the back in lower right dial and hard breathing due to dıaphragm irritation are seen (10). in the cases there happens to be pseudoscysts, the increase of liver enzymes can be observed. in our case, the increase in sub ast ggt alp parameters as a result of intense cyst formation and the pressure of gallbladder were detected. in diagnosis, first abdominal usg among non invasive verifications and then for some cases the imaging of cyst size by abdominal tomography can be chosen. in the treatment, when the other 15 cases are examined , it is seen that shunt dystal revision is made when there is no infection is found in the content of the cyst after the aspiration of extraaxial cysts. shunt dystal revision is suggested instead of cyst aspiration because of bleeding risk in liver cysts. in our case, shunt revision operation was applied as there were no cells in csf after the drainage of catheter within the cyst for 3 days and the culture was negative. abdominal pseudocyst can repeat after revision surgery. the repetition rate can change from 7,1 % to 62 % in literature. on the other hand, there are no 471 a very rare fact occurring after v/p shunt in the surgical treatment of pseudotumor serebri syndrome reports on the recurrency of liver pseudocysts. conclusion liver pseudocyst should be considered, even if it is a rare complication, when back striking abdominal pain and high liver enzymes are seen at patients with shunt dysfunction. usg and abdominal ct tests should be made to these patients. the drainage of the cyst and then the removal of abdominal catheter should be applied. when the cell is negative in csf and when 3 negative cultures were seen, then catheter should be set with reoperation. in these operations, cooperation with the general surgery staff should be made in order to remove the shunt dystal from the liver to a distant part by open surgery or laparoscopıc methods. references 1. binder dk, horton jc, lawton mt, mcdermott mw. idiopathic intracranial hypertension. neurosurgery 2004;54:538-51. 2. friedman di, liu gt, digre kb. revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. neurology. 2013;81:1159-1165. 3. julayanont p, karukote a, ruthirago d, et al. idiopathic intracranial hypertension: ongoing clinical challenges and future prospects. j pain res. 2016;9:87-99. 4. friedman di, jacobson dm. idiopathic intracranial hypertension. j neuroophthalmol 2004;24:138-45. 5. friedman di. papilledema and pseudotumor cerebri. ophthalmol clin north am 2001; 14:129–147. 6. friedman di. the pseudotumor cerebri syndrome. neurol clin. 2014;32:363396. 7. mollan sp, markey ka, benzimra jd, et al. a practical approach to, diagnosis, assessment and management of idiopathic intracranial hypertension. pract neurol. 2014;14:380-390. 8. dukurah tk, adams f, iddrissu m, wepeba gk, akoto h, bankah p, et al. . management of hydrocephalus with ventriculoperitoneal shunts: review of 109 cases of children. world neurosurg 2016;96:129–35. [pubmed] [google scholar]. 9. joseph fj, bernard j jr, augustin s jr. factors associated with postoperative complications in hydrocephalus infants diagnosed at bernard mevs hospital in port-auprince, haiti, from 2011 to 2013. world neurosurg 2017;103:386–90. 10. huang lt, chen cc, shih tt, ko sf, lui cc. pyogenic liver abscess complicating a ventriculoperitoneal shunt. pediatr surg int 1998;13:6–7. doi: 10.33962/roneuro -2020-044 hypotension intracrânienne spontanée (his). a propos d’un cas leklou h., djellaoui m. romanian neurosurgery (2020) xxxiv (1): pp. 298-302 doi: 10.33962/roneuro-2020-044 www.journals.lapub.co.uk/index.php/roneurosurgery hypotension intracrânienne spontanée (his): a propos d’un cas leklou h., djellaoui m. service de neurologie, chu beo, alger, algeria abstract l’his est une céphalée chronique, liée à une fuite de lcr. son diagnostic est facilité par l’irm et sa prise est essentiellement médicale. nous rapportons le cas d’une jeune femme ayant présenté un tableau clinique et signes irm compatibles avec ce diagnostic et ayant bien évolué sous traitement. introduction l’hypotension intracrânienne spontanée (his) fût décrite par le neurologue allemand schaltenbrand en 1938 (1). en effet, il définit sous le terme d'aliquorrhée une pathologie d'apparition spontanée associant une très basse pression d'ouverture du liquide céphalorachidien (lcr) (inférieure à 60 mm d’eau) et des céphalées orthostatiques (2). le diagnostic de l’his a été considérablement facilité par le développement de l'imagerie par résonance magnétique cérébrale, avec une connaissance plus précise des anomalies caractéristiques de cette affection lors de cette exploration (3,4). observation histoire de la maladie madame n, 38 ans, fonctionnaire, sans antécédents pathologiques notables ni de facteurs de risque cardiovasculaires, a consulté pour céphalées diffuses à type de constriction, fluctuantes, d'aggravation progressive depuis 1 mois et résistantes aux antalgiques du premier palier. les céphalées apparaissaient rapidement lors du passage de la position allongée à la position assise ou debout et s’accompagnait de nausées et de deux épisodes de vomissements. on note la présence d’une phonophobie, d’une hypoacousie avec une sensation d'oreille bouchée et des acouphènes à gauche, mais pas de diplopie ni de flou visuel. ces céphalées s’associaient également à des douleurs de la nuque, tout en augmentant d’intensité au fur et à mesure du maintien de la position debout ou assise et s’amélioraient rapidement lors du passage keywords céphalée chronique, fuite du lcr, hypotension du lcr corresponding author: leklou h. service de neurologie, chu beo, alger, algeria leklou_ hakim@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 299 hypotension intracrânienne spontanée (his) à la position allongée, avant de disparaitre complètement par la suite. examen clinique l'examen neurologique ne retrouvait aucune anomalie. il n’y avait pas de signes d'hypertension intracrânienne ou de syndrome méningé. l'examen général était normal avec une tension artérielle est de 130/85. examens complémentaires scanner cérébral avec injection réalisé en urgence, lors des premiers accès de céphalées et n’avait pas montré d’anomalies. irm cérébrale l'irm cérébrale montrait en séquence flair un épaississement diffus des méninges encéphaliques avec un aspect de petits ventricules (fig. 1). figure 1. il s'y associait de chaque côté une fine lame d'épanchement sous dural fronto-pariétale bilatérale (fig. 2). figure 2. en t1 après injection de gadolinium, on observait un rehaussement de la dure mère au niveau de la convexité sus et sous tentorielle, de la faux et de la tente du cervelet (fig. 3). figure 3. 300 leklou h., djellaoui m. on notait enfin une hypertrophie hypophysaire (fig. 4). figure 4. il n'y avait pas d'anomalie du parenchyme cérébral. irm médullaire collection sous durale d'allure liquidienne, antérieure entre c7 et d3, en hypersignal t2 (fig. 5). figure 5. on observait sur les coupes sagittales cervicales hautes une ptose de l'encéphale et notamment des amygdales cérébelleuses sans anomalies morphologiques associées (fig. 4). prise en charge et évolution devant les céphalées d'aggravation orthostatique, l’absence de notion de traumatisme crânien, de ponction lombaire ou d’intervention neurochirurgicale et les images en irm, le diagnostic d’hypotension intracrânienne spontanée a été retenu. le décubitus prolongé au-delà de 24 h avec hyperhydratation a permis l'amélioration de la symptomatologie. discussion l'hypotension intracrânienne spontanée (his) est une pathologie qui reste rare, dont la prévalence se situe entre 1/50 000 et 5/100 000, avec une prépondérance féminine (sex-ratio à 2/1) et un pic d'incidence vers 40 ans [5]. elle est plus fréquente au cours des maladies du tissu conjonctif (marfan, ehler-danlos) [6]. sa forme classique associe des céphalées postérieures et des cervicalgies à type de constriction, d'intensité modérée à sévère, s'installant dans les 15 minutes suivant l'orthostatisme, soulagée par le décubitus, en l'absence de traumatisme sévère ou de gestes invasifs (chirurgie ou ponction lombaire). l'association à des signes de nature orl est classique, en lien avec des modifications de pression de l'oreille interne. une atteinte de nerfs crâniens, notamment du vi, est plus rarement décrite. toutefois les céphalées deviennent moins caractéristiques avec la chronicisation ; le tableau peut alors évoluer vers des céphalées chroniques quotidiennes, parfois associées à un abus médicamenteux. la physiopathologie supposée repose sur une hypovolémie du liquide céphalo-rachidien (lcr) secondaire à des brèches dure mériennes le plus souvent médullaires, responsable de la traction sur les différentes structures du cerveau et à l'origine des signes irm [7]. ces brèches seraient favorisées par l'association d'un traumatisme parfois mineur et d'une fragilité du tissu méningé spinal. l’hypertrophie hypophysaire, les collections sous-durales à l’étage cérébral et rachidien, l’expansion veineuse au niveau intracrânien et rachidien et l’épaississement de la dure mère sont 301 hypotension intracrânienne spontanée (his) liés à la baisse de pression du lcr qu’ils permettent de compenser (loi de monro-kellie). le rehaussement diffus de la dure mère au niveau de la convexité sus et sous tentorielle, de la faux et de la tente du cervelet est un important signe pour le diagnostic différentiel avec une méningite infectieuse ou carcinomateuse. l'irm cérébrale peut être normale dans environ 20 % des cas [5, 7,8] et n'exclut donc pas le diagnostic en cas de forte présomption clinique. l’irm médullaire avec notamment des séquences t2 et stir doit être toujours réalisée lorsque l'on suspecte une his. en effet, il s'agit de l'examen le plus performant [9] avec une sensibilité proche de 94 % [3], notamment à la phase précoce, montrant dans 88 % des cas des collections épidurales, dans 78 à 94 % des cas une dilatation des veines épidurales cervicales [6]. il a également été observé des prises de contraste au contact de ces collections en lien avec la réaction leptoméningée [11,12]. enfin, il faut penser à une étiologie de l’hic pouvant expliquer la fuite chronique de lcr (brèche durale) qui est rarement retrouvée à l’irm médullaire (pseudoméningocèle, ectasie durale, kystes radiculaires, protrusions disco-ostéophytiques, etc). l'évolution sans traitement peut se faire vers la rémission spontanée, la chronicisation ou des complications (hématome sous-dural, thrombose veineuse cérébrale). ces dernières modifient les caractéristiques de la céphalée, avec notamment l'apparition rapide de tableaux d'hypertension intracrânienne et un engagement amygdalien. toute modification de la céphalée chez un patient souffrant d'une his justifie donc une réévaluation clinique et irm en urgence. la prise en charge thérapeutique repose sur le traitement conservateur (repos en décubitus, hyperhydratation) et le blood-patch (plusieurs tentatives pouvant être nécessaires). lorsque le patient ne s’améliore pas malgré le traitement médical (voir le blood patch), il y a nécessité d’essayer de trouver la fuite, avec un myéloscanner ou une cisternographie, pour apporter un diagnostic complet et guider ainsi la conduite thérapeutique (blood patch au bon endroit et éventuelle chirurgie). les indications chirurgicales sont exceptionnelles et concernent, avant tout, les lésions sévères ou développementales, résistantes au traitement médical [5,13]. les anomalies de signal méningées en irm régressent généralement suite au traitement, avec un décalage par rapport à l'amélioration clinique [5]. conclusion l’his est une céphalée chronique, liée à une fuite de lcr. les conséquences de cette hypovolémie du lcr sont essentiellement la ptôse cérébrale et la compensation veineuse. ces deux conséquences expliquent les manifestations cliniques et irm de cette pathologie. enfin, il faut souligner l’intérêt de l’imagerie médullaire, notamment, le myéloscanner pour rechercher une brèche durale ; ce qui est recommandé en l’absence d’amélioration au traitement médical et au blood patch. references 1. schaltenbrand g. neuere anschauungen zur pathophysiologie der liquorzirkulation. zentrablbl neurochir 193 8;3 :290-300. 2. mokri b. spontaneous intracranial hypotension spontaneous csf leaks. headache currents 2005;2(1): 1 1-22. 3. fishrnan ra, dillon wp. dura1 enhancement and cerebral displacement secondary to intracranial hypotension. neurology 1993;43(3 pt 1):609-6 1 1. 4. sable sg rn. meningial enhancement and low cerebrospinal fluid pressure headache. an mri study. cephalalgia 199 1 ; 1 1 :275-276. 5. schievink wi. spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. jama 2006;295:2286– 96. 6. schievink wi, gordon ok, tourje j. connective tissue disorders with spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension: a prospective study. neurosurgery 2004;54:65–70. 7. watanabe a, horikoshi t, uchida m, koizumi h, yagishita t, kinouchi h. diagnostic value of spinal mr imaging in spontaneous intracranial hypotension syndrome. ajnr am neuroradiol 2009;30(1):147–51. 8. schoffer kl, benstead tj, grant i. spontaneous intracranial hypotension in the absence of magnetic resonance imaging abnormalities. can j neurol sci 2002;29(3):253–7. 9. schievink wi, maya mm, louy c, moser fg, tourje j. diagnostic criteria for spontaneous spinal csf leaks and intracranial hypotension. ajnr am j neuroradiol 2008;29(5):853–6. 10. farb ri, forghani r, lee sk, mikulis dj, agid r. the venous distension sign: a diagnostic sign of intracranial 302 leklou h., djellaoui m. hypotension atmr imaging of the brain. ajnr am j neuroradiol 2007;28(8):1489–93. 11. good dc, ghobrial m. pathologic changes associated with intracranial hypotension and meningeal enhancement on mri. neurology 1993;43:2698–700. 12. mokri b, parisi je, scheithauer bw, et al. meningeal biopsy in intracranial hypotension: meningeal enhancement on mri. neurology 1995;45:1801–6. 13. schievink wi, morreale vm, atkinson jld, et al. surgical treatment of spontaneous spinal cerebrospinal fluid leaks. j neurosurg 1998;88:243–6. doi: 10.33962/roneuro -2020-054 cranium metastasis of hpv positive oropharyngeal squamous cell carcinoma gokhan canaz, huseyin canaz, sabri aydin romanian neurosurgery (2020) xxxiv (1): pp. 353-356 doi: 10.33962/roneuro-2020-054 www.journals.lapub.co.uk/index.php/roneurosurgery cranium metastasis of hpv positive oropharyngeal squamous cell carcinoma gokhan canaz1, huseyin canaz2, sabri aydin2 1 arnavutkoy state hospital, department of neurosurgery, istanbul, turkey 2 florence nightingale hospital, istanbul bilim university, department of neurosurgery, istanbul, turkey abstract head and neck squamous cell carcinomas rarely cause cranial metastases, but hpv related subgroup is known for unusual metastasis sites on the body. despite the good overall treatment responses in this group, intracranial metastases are always accepted as a sign of rapid deterioration. we present a case of cranium metastasis of hpv related oropharyngeal squamous cell carcinoma, which had been very well responded to the treatment for years but deteriorates in a short period after the cranium metastasis. introduction head and neck squamous cell carcinomas (hnscc) are known as rarely causing intracranial metastases. in the last years, hpv related subgroup of hnscc has become a distinct subject of studies. they mostly occur at oropharynx. the incidence of hpv-positive hnscc is increasing. unlike the hpv-negative one, this subgroup does not show a relationship with tobacco and alcohol, which are prominent risk factors of hnscc. more favourable results of chemotherapy and radiotherapy have been reported in comparison to the hpv-negative variant. the more successive local control means better morbidity and survival rates. on hpv-positive cases, a better prognosis was reported even on lung metastasis, which is the most frequent site of distant recurrence. also, a different pattern of metastasis has been mentioned in recent studies (3). on the other hand, the presence of brain metastasis has always been accepted as a bad sign regardless of hpv status. we present a case of a patient who has one of the most extended survival lengths reported in the literature despite unusual multisite metastases but deteriorated rapidly due to very aggressive cranium metastasis. case report sixty-four years old female patient had submitted to hospital with pain on the chest and back in 2013. examinations revealed metastatic keywords metastasis, human papilloma virus, hpv, cranium, squamous cell corresponding author: gokhan canaz arnavutkoy state hospital, department of neurosurgery, istanbul, turkey gokhancanaz@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 354 gokhan canaz, huseyin canaz, sabri aydin lymphadenopathies on mediastinum and metastases on the lung, liver, and vertebra corpus, but the primary tumour had not been found. with consecutive periods of chemotherapy (including carboplatin, capecitabine, and cisplatin-etoposide) and radiotherapy, local control was achieved, and the patient has succeeded five years of survival. in 2018, the patient had multiple enlarged lymph nodes in the cervical area. following the tru-cut biopsy results, the pathology report pointed out cd117 positivity and low metabolic activity despite the clinical features. as a result, pathological examinations could not suggest a diagnosis. the new pet scan revealed multiple mediastinal and intraabdominal lymphadenopathies and improved uptake in various areas in the gastrointestinal system. with chemotherapy and radiotherapy, the local cure was succeeded. other sites also responded to the treatment. in november 2018, in an examination for head-ache, extensive cranium metastasis was spotted. the patient was consulted to neurosurgery, and surgery was offered (fig. 1). during the decision period of patient, right hemiparesis and headache complaints were developed. in concomitant mris within three months period, significant enlargement was discovered, and operation was performed (fig. 2,3). first, question mark skin incision was performed, and the tumour was revealed, extruding from the calvarium. a large frontoparietal craniotomy flap, which was covering the whole tumour and adherent dura, was elevated. because of the cohesiveness, the dura was incised and elevated with the tumour. no invasion to parenchyma was observed but cerebrum was edematous. because of that after bone-tumourdura complex resection, cranioplasty was planned for a further time. pathologic examination revealed that the tumour was hpv positive oropharyngeal squamous cell carcinoma metastasis with strong p16 and neuroendocrine marker positivity. different from the previously pathological examination, ki-67 index was found to be very high (about %80). post-op pet scan also revealed an oropharyngeal mass with improved up-take near the base of the tongue. discussion hpv positive hnscc are characterized by a better therapeutic response and lower recurrence in comparison to hpv negative variant, which means figure 1. overall better clinical outcome in terms of survival and morbidity (2). because of this nature of hpv positive hnscc, even in the presence of metastases, more direct and curative approaches are preferred instead of palliative treatment options. besides the better outcomes, the distant metastasis pattern of hpv positive scc also differs. the longer survival lengths, thank to better therapeutic results, may contribute to increased numbers of distant metastases on hpv positive scc. the most frequent metastasis sites for hnscc are known as lung, liver, and bone (5). in this order, liver and bone metastases were reported as much rarer than the lung. an increased incidence in bone metastases, especially in vertebras, were reported in patients with p16 positive tumours lately. the recent articles are reporting hpv positive scc cases with multisite metastasis, including unusual sites such as long bones, brain, dura, pancreas, and skin (3,4). among the metastasis sites, the brain was accepted to have the worst prognosis and defined as “noncurable”. brain metastasis frequency on hnscc was mentioned in a few articles as 0.43 – 5.7%. the tumour-free episodes in hpv positive scc are reported to be longer than non-hpv variants in several studies (2). when the recurrence or first metastasis was spotted during follow-ups, patients usually have metastasis on more than one site. in both hpv + and – tumours, metastases have much more aggressive behaviors than their primary tumours. independent from the response of these metastases to the treatment, different, unexpected new metastases may occur, and the death of patients is usually caused by these aggressive new tumours. the development time of metastases is 355 cranium metastasis of hpv positive oropharyngeal squamous cell carcinoma approximately two years following the primary tumour treatment (4, 5). in a recent study about brain metastases of hnscc, mean time of interval between diagnosis of primary and brain metastasis was reported as 26 months. among the eleven patients, two longest intervals were 137 and 66 months, and the latter patient had 65.7 months of disease-free time, meaning prognosis of the brain metastasis was the decisive factor in patients’ life (1). besides clinical features, hpv positive scc’s are known to be hard to detect on pet and mri scans. as in our case, this mass had not been detected previous pet and mri scans. conclusion extended patient follow-up times are suggested for hpv positive tumours in many papers as a conclusion (2, 4). under these circumstances, we think that it would not be wrong to define the length of follow-up as "lifelong". considering positive features of hpv-positivity, with further analysis of metastasis pattern of hpv positive hnscc and with the developments of neurosurgical oncology, much longer survivability can be achieved in this patient group. patient consent the patient has consented to the submission of the case report for submission to the journal. declaration of conflict of interest: none acknowledgements we would like to thank “cura canaz medical arts (www.ccmedicalarts.com)” for the illustrations. references 1. ahmed a, sandlas g, kothari p, sarda d, gupta a, karkera p, joshi p. outcome analysis of shunt surgery in hydrocephalus. j. indian. assoc. pediatr. surg. 2009, 14 (3): 98-101. 2. bradley nk, liakos am, mcallister jp, magram g, kinsman s, bradley mk. maternal shunt dependency: implications for obstetric care, neurosurgical management, and pregnancy outcomes and a review of selected literature. neurosurgery.1998, 43 (3): 448-60. 3. browd sr, ragel bt, gottfried on, kestle jr. failure of cerebrospinal fluid shunts: part i : obstruction and mechanical failure. pediatr. neurol. 2006, 34 (2),83-92. 4. browd sr, ragel bt, gottfried on, kestle jr. failure of cérébrospinal fluid shunts: part ii: over drainage, loculation, and abdominal complications. pediatr. neurol. 2006,34 (3):171-6. 5. cusimano md, meffe fm, gentili f, sermer m. ventriculoperitoneal shunt malfunction during pregnancy. neurosurgery. 1990,27(6):969-71. 6. cusimano md, meffe fm, gentili f, sermer m. 1991.management of pregnant woman with cerebrospinal fluid shunt. pediatr. neurosurg.1991,92 (17):10-3. 7. drake jm, kestle jr, milner r, cinalli g, boop f, piatt jjr, haines s, schiff sj, cochrane dd, steinbok p, macneil n.1998 randomized trial of cerebrospinal fluid shunt valve design in pediatric hydrocephalus. neurosurgery. 1998,43:294-303. 8. eholier sp, boni b, aoussi e, konan a, orega m, koffi a l, ba zézé v, bissagnene e, kadio a. complications neurochirurgicales des méningites purulentes en zone tropicale. neurochirurgie. 1999,45(3):219-24. 9. fletcher h, crandon iw, webster d. maternal hydrocephalus in pregnancy and delivery: a report of two cases. west. indian. med. j.2007,56(6):558-9. 10. freo u, pitton m, carron m, ori c. 2009.anesthesia for urgent sequential ventriculoperitoneal shunt revision and cesarean delivery. int. j. obstet. anesth. 2009,18(3): 284-7. 11. hanakita j, suzuki t, yamamoto y, kinuta y, nishihara kj. ventriculoperitoneal shunt malfunction during pregnancy. j neurosurg.1985, 63(3):459-60. 12. houston cs, clein lj. ventriculoperitoneal shunt malfunction in a pregnant patient with meningomyelocele. cmaj.1989,141(1):701-2. 13. hwang s.c, tae-hee k, bum-tae k, soo-bin i, won-han s. acute shunt malfunction after cesarean section delivery. j. korean. med. sci.2010,25(4):647-50. 14. kleinman g, sutherling w, martinez m, tabsh k. malfunction of ventriculoperitoneal shunts during pregnancy. obstet gynecol. 1983,61(6):753-4. 15. kurtsoy a, selçuklu a, kemal kr, pasaoglu a, kavuncu ai. management of maternal hydrocephalus. turkish neurosurgery.1994,4:174-5. 16. landwehr jb, jr, isada nb, pryde pg, johnson mp, evans mi, canady ai. maternal neurosurgical shunts and pregnancy outcome. obstet gynecol. 83(1):134-7. 17. liakos am, bradley nk, magram g, muszynski c. hydrocephalus and the reproductive health of women: the medical implications of maternal shunt dependency in 70 women and 138 pregnancies. neurol res .2000,22(1):69-88. 18. maheut-lourmière j, chu tan s. hydrocephalus during pregnancy with or without neurosurgical history in childhood. practical advice for management neurochirurgie.2000,46 (2):117-21. 19. monafared ah, kee sk, apuzzo mlj, collea jv. obstetric management of pregnant woman with extracranial shunts. can. med. assoc. j. 1979,120(5):562-3. 356 gokhan canaz, huseyin canaz, sabri aydin 20. mouelhi c, srasra m, zhioua f, ferchiou m, zine s, meriah s. maternal hydrocephaly and pregnancy. rev. fr. gynecol. obstet. 89(2):88-90. 21. murakami m, morine m, iwasa t, takahashi y, miyamoto t, hon pk, nakagawa y. management of maternal hydrocephalus requires replacement of ventriculoperitoneal shunt with ventriculoatrial shunt: a case report. arch. gynecol.obstet. 2010,282 (3):339-42. 22. okagaki a, hanzaki h, moritake k, mori t.1990. case report: pregnant woman with a ventriculoperitoneal shunt to treat hydrocephalus. asia. oceania. j.obstet. gynaecol. 1990,16: 111-3. 23. orega m, eholier s p, boni n, konan a, koffi a l. méningites purulentes et complications neurochirurgicales chez l’enfant à abidjan. médecine d'afrique noire. 2005,52(4):251-2. 24. rees gj, francis c, sizer a r. convulsions in an undiagnosed pregnancy due to blocked ventriculoperitoneal shunt.j. obstet. gynaecol. 2008,26(5), 533-4. 25. riffaud l, ferre, jc, carsin-nicol b, morandi x. endoscopic third ventriculostomy for the treatment of obstructive hydrocephalus during pregnancy.obstet. gynecol. 2006,108:801-4. 26. sova m, smrcka, m, baudysova o, gogela j management of a shunt malfunction during pregnancy. bratisl lek listy. 2001,102(12):562-3. 27. wishoff jh, kratzert kj, handwerker sm, young bk, epstein f. pregnancy in patients with cerebrospinal fluid shunts: report of a series and review of the literature. neurosurgery. 1991,29(6):827-31. doi: 10.33962/roneuro-2022-089 letter to editor contusion index a diagnostic and treatment algorithm for neurointensive care ebtesam abdulla, amit agrawal, rafael cincu, tariq janjua, luis rafael moscote -salazar romanian neurosurgery (2022) xxxvi (4): pp. 492-493 doi: 10.33962/roneuro-2022-089 www.journals.lapub.co.uk/index.php/roneurosurgery letter to editor contusion index a diagnostic and treatment algorithm for neurointensive care ebtesam abdulla1, amit agrawal2, rafael cincu3, tariq janjua4, luis rafael moscote-salazar5 1 department of neurosurgery, salmaniya medical complex, manama, bahrain 2 department of neurosurgery, all india institute of medical sciences, saket nagar, madhya pradesh, india 3 department of neurosurgery, general university hospital, valencia, spain 4 department of critical care medicine, physicians regional medical center, naples, fl, usa 5 colombian clinical research group in neurocritical care, bogota, colombia globally, traumatic brain injury is one of the major causes of death in developed countries, with a massive social and economic impact [1]. the majority of these traumatic brain injuries (80%) are considered mild (glasgow 14–15), 10% are moderate (glasgow 9–13), and the rest are severe (glasgow less than 9). these injuries range from mild concussions to extensive bleeding, fractures, and parenchymal injuries. among the primary traumatic brain injuries are contusions, which need close neurological examination, clinical monitoring, serial brain ct scans, and any changes in the glasgow coma score. traumatic cerebral contusion with single or multiple presentations is frequently found in these patients. this type of injury can be found in coexistence with acute intracerebral, extradural, or subdural hematomas [2]. it is important to clarify that brain parenchymal injury with dura mater integrity is defined as a contusion, as opposed to a laceration, where there is a tangential disruption of bone tissue and the meninges [3]. biomechanically, contusions are related to multiple kinetic mechanisms such as acceleration and deceleration, with the subsequent development of cerebral edema that can be local or progressive [2]. the pathobiology of cerebral contusions is heterogeneous in its initial stages , charac terize d by alterations such as punctate keywords contusion index, traumatic brain injury, neurointensive care corresponding author: ebtesam abdulla department of neurosurgery, salmaniya medical complex, manama, bahrain dr.ebtesam@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 493 contusion index a diagnostic and treatment algorithm for neurointensive care hemorrhage, swelling, edema, and areas of necrosis in the initial stages. the pathophysiology of contusions includes changes in cerebral and local blood flow [4]. the pathobiology of cerebral contusions is heterogeneous in its initial stages, characterized by alterations such as punctate hemorrhage, swelling, edema, and areas of necrosis in the initial stages. the pathophysiology of contusions includes changes in cerebral and local blood flow [4]. the term "contusion index (ci)" was first described by adams et al in 1982 [5,6]. these results were obtained in pathological specimens by determining the extent and depth of the lesions. the depth of the contusion was measured based on a 03 scale; 0: no contusion seen, 1: contusion not involving the full thickness of the cortex, 2: contusion involving the full thickness of the cortex, 3: contusion extending to the white matter [6]. the extent of the contusion was measured based on the 0-3 scale: 0: no contusion, 1: localized contusion, 2: moderately extensive contusion, and 3: extensive contusion [6]. the ci score (0–9) equals the depth of contusion multiplied by the extent of contusion. patients with ci with a ci of 0 to 4 were treated conservatively. patients with a ci of 6 were treated surgically, and patients with a ci of 9 were treated conservatively or surgically depending upon the glascow coma score. in the field of neuroradiology, an index of contusions has been used in clinical series in an interesting way [7,8]. a further modification was suggested by postmortem analysis, where a two-tier system is proposed based upon superficial or deeper injury. gray matter injury is assigned a 0-3 scale while parenchymal injury is given a scale of 0-4 based on the extensión and depth of the bleed [9]. we consider that cerebral contusions, due to their dynamic pathogenetic nature and varied evolution process, can hardly be evaluated with the glasgow scale [10,11] alone. many patients with cerebral contusions find themselves in the universe of patients categorized as "moderate head trauma" using the glasgow scale. we believe that patients with cerebral contusions without other structural injuries (hematomas that need to be treated by neurosurgery) need to get a case-based decision making and treatment plan. references 1. quintard h, bouzat p, geeraerts t. towards a new pattern for epidemiology of traumatic brain injury. anaesth crit care pain med. 2021 feb;40(1):100808. 2. alahmadi h, vachhrajani s, cusimano md. the natural history of brain contusion: an analysis of radiological and clinical progression. j neurosurg. 2010;112(5):1139-1145. 3. zhu bl, quan l, ishida k, et al. longitudinal brainstem laceration associated with complex basilar skull fractures due to a fall: an autopsy case. forensic sci int. 2002;126(1):40-42. 4. katz ps, molina pe. a lateral fluid percussion injury model for studying traumatic brain injury in rats. methods mol biol. 2018;1717:27-36. 5. adams jh, doyle d, graham di, et al. the contusion index: a reappraisal in human and experimental non-missile head injury, neuro appl neurobiol, 1985; 11:299-308. 6. adams jh, scott g, parker ls, graham di, doyle d. the contusion index: a quantitative approach to cerebral contusions in head injury. neuropathol appl neurobiol. jul-aug 1980;6(4):319-24. 7. macpherson bc, macpherson p, jennett b. ct evidence of intracranial contusion and haematoma in relation to the presence, site and type of skull fracture. clin radiol 1990;42(5):321–326. 8. khaliq a, ali m, azam f, gul n, chaurasia b. contusion index is an important tool for the management of traumatic intracerebral hematoma. indian j neurotrauma. 9. omalu bi, nnebe-agumadu uh, shakir am, rozin l, wecht ch. postmortem grading of cerebral contusions : a proposed modification of the adams' contusion index with re-definition of anatomic markers. forensic sci med pathol. 2005 jun;1(2):105-12. 10. adatia k, newcombe vfj, menon dk. contusion progression following traumatic brain injury: a review of clinical and radiological predictors, and influence on outcome. neurocrit care. 2021;34(1):312-324. 11. kurland d, hong c, aarabi b, gerzanich v, simard jm. hemorrhagic progression of a contusion after traumatic brain injury: a review. j neurotrauma. 2012;29(1):19-31. doi:10.1089/neu.2011.2122. doi: 10.33962/roneuro-2023-039 a giant a4-a5 distal anterior cerebral artery aneurysm treated with microsurgical clip reconstruction mustafa ismail, ali k. al-shalaji, bahaa s. abdalnaby, aktham o. al-khafaji, ali a. kadhim, rasha a. al-shakarchy, sarmad a. zangana, ahsan a. al-rubaye, samer s. hoz romanian neurosurgery (2020) xxxiv (1): pp. 218-223 doi: 10.33962/roneuro-2020-039 www.journals.lapub.co.uk/index.php/roneurosurgery a giant a4-a5 distal anterior cerebral artery aneurysm treated with microsurgical clip reconstruction mustafa ismail1, ali k. al-shalaji1, bahaa s. abdalnaby2, aktham o. al-khafaji1, ali a. kadhim3, rasha a. al-shakarchy3, sarmad a. zangana3, ahsan a. alrubaye3, samer s. hoz4 1 department of neurosurgery, college of medicine, university of baghdad, baghdad, iraq 2 department of radiology, neurosurgical teaching hospital, baghdad, iraq 3 department of neurosurgery, ghazi al-hariri hospital, baghdad, iraq 4 department of neurosurgery, university of cincinnati college of medicine, cincinnati, oh, usa abstract background. aneurysms of the distal anterior cerebral artery (daca) are uncommon; they often form near the pericallosal-callosomarginal junction and are typically small. to our knowledge, giant daca aneurysms developing from the more distant parts of the anterior cerebral artery (aca), a4-5, have been described only once in the literature. case description. a 66-year-old gentleman reported with a brief loss of consciousness followed by weakness in his right lower leg. the patient was admitted with a glasgow coma score (gcs) of 15. a computed tomography (ct) scan of the head revealed a left hyperdense mass in the frontal parasagittal supracallosal region. contrast mri revealed a heterogeneously enhancing mass measuring 35x30x25 mm. ct angiography (cta) revealed a small saccular aneurysm on the posteromedial aspect of the mass, perpendicular to the vertical plane of the coronal suture, corresponding to the a4-a5 junction of the left aca. through a left paramedian craniotomy, a modified anterior interhemispheric approach that was more posterior than the conventional projection was performed. a giant partially thrombosed was found. the aneurysm was resected, and the neck was reconstructed using four clips placed on top of them to enhance the clipping force over any remaining thrombus. the patient recovered as expected and was neurologically intact three months later. conclusion. giant distal anterior cerebral artery (daca) aneurysms found in the a4a5 segment represent a pathologically uncommon phenomenon. due to the rarity of giant aneurysms at this location, their reporting is important to inform meticulous pre-operative planning. keywords distal anterior cerebral artery aneurysms, giant cerebral aneurysms, microsurgical clip reconstruction corresponding author: samer hoz department of neurosurgery, university of cincinnati, cincinnati, oh, usa hozsamer2055@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 219 a giant a4-a5 distal anterior cerebral artery aneurysm treated with microsurgical clip reconstruction introduction the distal anterior cerebral artery (daca) represents all segments of the anterior cerebral artery (aca) distal to the anterior communicating artery. daca aneurysms constitute up to 6% of all intracranial aneurysms (7, 10, 12, 13, 16, 17, 19, 21, 23, 29, 30, 31). most of these aneurysms arise from relatively “proximal” segments of the aca; mainly the pericallosal-callosomarginal junction (69-82%). daca aneurysms arising from the more distal a4 and a5 segments of aca are very rare; representing less than 0.6% of all intracranial aneurysms (7, 13). figure 1. pre-operative imaging. axial sections of non-contrast head ct scan (a) as well as t1 (b), t2 (c), flair (d), and gadoliniumenhanced t1 (e) mri show a left frontal parasagittal (supracallosal) mass that appears hyperdense on ct and heterogenous on mri, with contrast enhancement of the posteromedial part of the lesion. figure 2. pre-operative ct angiography with (a) axial section, (b) sagittal section, and (c) 3d reconstruction. a superiorly-directing aneurysm (8x4 mm) can be seen at the a4-a5 junction, with 2 distal a5 branches arising from the neck of the aneurysm. the location of this aneurysm corresponds to the posteromedial enhancement of the mass on mri. figure 2. intraoperative images for a pericoronal anterior interhemispheric approach. a: initial exposure showing the large dome of the aneurysm (d), which is opened for internal decompression and thrombectomy. b: the borders of the giant dome of the 220 mustafa ismail, ali k. al-shalaji, bahaa s. abdalnaby et al. aneurysm are outlined in yellow with an incision in the center for internal decompression and thrombectomy. c: following internal decompression of the thrombosed aneurysmal dome, the pericallosal artery (a4) and the distal branches (a5) can be seen, as well as the neck (n) and dome (d) of the intraluminal portion of the aneurysm, prior to the application of clips. hemosiderin staining can be seen deep within the interhemispheric fissure, denoting old hemorrhage from the aneurysm. fc; frontal cortex, d; aneurysmal dome, f; falx cerebri, n; aneurysmal neck, a4, a5; segments of pericallosal artery. giant daca aneurysms (those measuring more than 25 mm in their greatest diameter) are extremely rare and mostly fusiform in nature. to the best of our knowledge, saccular aneurysms of the a4-a5 segments have only been reported once in the literature (4). giant partially thrombosed aneurysms usually have been proposed to result from accumulative intramural bleeding, enlargement, and thrombosis (11). therefore, endovascular treatment can often be ineffective, as it only eliminates the intraluminal portion of the aneurysm, leaving the mural portion liable to more bleeding, enlargement, and even rupture (2). this makes microsurgical management of giant partially thrombosed a4-a5 aneurysms more appealing, and raises several surgical challenges owing to their location posteriorly within the anterior interhemispheric fissure, the configuration of their domes, involvement of proximal and distal vessels within their base, and the mass effect which can significantly alter the anatomy of this region (11-13). all of the aforementioned highlights the importance of this paper, in which we report the second case of an idiopathic, giant, saccular, partially thrombosed a4-a5 daca aneurysm, discussing the treatment nuances of such extremely rare lesions. case description a 66-year-old male with a history of a prior ischemic stroke and infrequent seizures on treatment presented with sudden temporary loss of consciousness, followed by right lower limb weakness. he had complained of a poorly localized headache for the past few months with no other symptoms. on admission, the patient had a glasgow coma score (gcs) of 15 and his neurological examination was normal apart from weakness of the right lower limb, medical research council (mrc) grade 4. head computed tomography (ct) scan revealed a left frontal parasagittal supracallosal hyperdense mass with relative ventriculomegaly (figure 1a). magnetic resonance imaging (mri) of the brain showed a left extra-axial heterogenous lesion measuring 35x30x25 mm, with contrast enhancement of its postero-medial part (figure 1b1e). ct angiography (cta) showed a small (8x4 mm) saccular aneurysm perpendicular to the vertical plane of the coronal suture, corresponding to the a4a5 junction of the left aca (figure 2). digital subtraction angiography was not performed as modalities were not available. this aneurysm corresponds to the contrast-enhancing part of the lesion. a pre-operative list of differentials for the mass was made to help with planning for the procedure, and included cavernous malformation, hematoma, neoplasm, and lastly, or a thrombosed part of an aneurysm. the patient was operated via a left paramedian craniotomy bisected by the coronal suture, and a modified anterior interhemispheric approach that was more posterior than the classic projection, to target the more posterior a4-a5 junction. splitting of the fissure revealed a yellowish, solid wall of a thrombosed part of the aneurysm, corresponding to the giant mass on preoperative imaging (figure 3a). a rupture site on the lateral surface of the dome (the part of the dome facing the cerebral hemisphere). the fissure also showed thick adhesions and hemosiderin staining, indicating previous rupture of the aneurysm. the thrombosed part was opened, the thrombus evacuated and the mass internally decompressed to allow easier exposure of the active part of the aneurysm and identification of proximal and distal vessels (figure 3b). proximal control of the ipsilateral a4 was gained, and the aneurysm was resected, followed by reconstruction of the neck with 2 opposing tandem clips and 2 additional clips stacked over them to reinforce the clipping force over any residual thrombus. patency of proximal and distal vessels was visually confirmed by microdoppler. no intraoperative angiography was available in the facility. postoperatively, the patient was fully conscious with no new neurological deficits. a post-operative cta showed complete occlusion of the aneurysm, with preservation of the distal branches of the aca. the patient was put on antiepileptic medications and discharged 7 days post-operatively, oneand 3month follow-up appointments revealed a 221 a giant a4-a5 distal anterior cerebral artery aneurysm treated with microsurgical clip reconstruction neurologically intact patient, with complete resolution of the headache and no seizure activity. discussion the aca is anatomically divided into 5 segments; a1 through a5. the first “pre-communicating” segment arises at the bifurcation of the internal carotid artery, and ends at the anterior communicating artery. the second segment extends to the region between the rostrum and genu of corpus callosum, and its continuation curving anterior to the genu is the a3 segment, which ends at the rostral part of the body of corpus callosum. a4 and a5 segments comprise the horizontal portion of the aca, and are demarcated by the virtual plane of the coronal suture. a2 to a5 segments are collectively referred to as daca (12, 13). the majority of daca aneurysms (69-82%) are located within the a3 segment, usually around the callosomarginal-pericallosal junction. daca aneurysms of the a4-a5 segments are rare, representing 5-20% of daca aneurysms, and less than 0.6% of all intracranial aneurysms (7, 10, 13, 16, 17, 19, 21, 23, 29, 30, 31). a4-a5 aneurysms arise anywhere along the horizontal portion of the aca back towards the spleneum of the corpus callosum, and the distal cortical branches that arise from the termination of that segment (12). on the other hand, giant cerebral aneurysms are in themselves a rare occurrence, representing about 5-8% percent of all intracranial aneurysms (13). with a predilection for the posterior circulation, they tend to arise in large vessels, such as the basilar tip, and are usually partially or completely thrombosed (15, 27). a possible explanation for this predilection is the increased flow rate at these locations, which increases the shear forces acting on the vessel wall, increasing the risk of damage and microdissection (32). such vascular injuries accumulate damage on the vasa vasorum of the vessel, causing repeated intramural bleeding and progressive swelling of the aneurysm into giant sizes (2). additional factors such as trauma or infection also play a role in the pathogenesis of these giant aneurysms (13). there are less than 40 cases of giant daca aneurysms reported in the literature. the majority of those are fusiform in nature, and none are located at the a4a5 segments (5, 12, 14, 15, 20, 25). a possible explanation of this scarcity would be the decreased flow rate at the distal cerebral circulation, reducing the wall shear stress on the arterial walls and making damage, dissection, and formation of giant aneurysms less likely (8, 18, 32). as such, the finding of an idiopathic, giant saccular aneurysm at this location is surprising, counter-intuitive, and raises questions regarding the possible underlying pathomechanisms of these lesions. the natural history of giant thrombosed aneurysms tends to differ from that of intracranial aneurysms in general. in many cases, they present due to their size as mass lesions compressing adjacent structures and causing subsequent neurological deficits, as was the case in our patient (11, 13). however, according to the international study of unruptured intracranial aneurysms (isuia) trial, 50% of giant intracranial aneurysms tend to rupture within 5 years of presentation (28). it is worthwhile to mention that the isuia does not report on the presence of intramural thrombosis within these giant aneurysms, which might be an important determinant of the risk of rupture (11). the pathomechanism responsible for the formation of giant partially thrombosed aneurysms implies that bleeding from those lesions is often extraluminal (2). this entails that endovascular management of giant partially thrombosed aneurysms can be ineffective (14, 27). endovascular coiling can obliterate the lumen of the aneurysm, but the aneurysm continues to grow despite a patent lumen as their growth is related to intramural hemorrhage from the vasa vasorum (2, 14). moreover, coiling daca aneurysms in general poses a challenge compared to other aneurysms, given the distal location of these lesions (12). as such, resection of these lesions with neck reconstruction or trapping with bypass may provide the best outcomes (15, 22, 31). the scarcity of giant saccular daca aneurysms in general, all the more so of giant a4-a5 aneurysms, makes for little experience in the surgical management of such complex lesions. daca aneurysms are treated via an anterior interhemispheric approach (12). the interhemispheric fissure presents a very narrow and challenging surgical corridor, leaving little room for instrument manipulation and limiting the possible angles for application of clips (12, 13). to complicate things, a4-a5 aneurysms, laying way posterior to the genu of corpus, are difficult to identify in the fissure due to lack of any reliable landmarks at this location 222 mustafa ismail, ali k. al-shalaji, bahaa s. abdalnaby et al. (12). this posterior location also means that the classic anterior interhemispheric approach needs to be modified, to project more posteriorly and reach the lesion. we recommend creating a paramedian craniotomy centered around the coronal suture, to ensure direct access to the a4-a5 junction. additional factors also affect the anatomy of the fissure, such as the presence of a large intracerebral hematoma displacing the structures, subarachnoid hemorrhage causing thick adhesions within the fissure, and the variation in the anatomy of a4-a5 segments and their branches (12, 13, 26). fortunately, internal thrombectomy and decompression of the giant thrombosed part in our case was used reliably to reach the active part of the aneurysm and identify proximal and distal vessels. an alternative would be the use of neuronavigation to help guide the surgeon into the lesion (15). resection of the thrombosed part of the aneurysm ensures the arterial dissection and potential intramural space is treated (2, 11). simple clipping is sometimes difficult in these cases, due to their wide-base and the presence of atherosclerotic plaques at the neck, preventing full closure of the clip (9). this can be overcome with multiclipping techniques like booster clips and tandem clipping, as well as techniques like clip compression and microendarterectomy (3, 9, 24). in our case, clip reconstruction of the neck was possible, due to thorough evacuation of the thrombosis, absence of calcification at the base of the aneurysm, and favorable configuration of the pericallosal artery, which allowed for the application of the clips without impinging proximal and distal vessels. when neck reconstruction is difficult, microsurgical trapping of the parent vessel with intracranial-intracranial bypass can be attempted. this technique ensures cessation of blood flow both into the wall and the lumen of the aneurysm while maintaining blood flow to distal vessels. many bypass techniques for the reconstruction of the aca and its branches have been studied (30). however, these intracranial-intracranial bypass techniques require a high level of surgical dexterity, practice, and experience, and carry a possibility of failure and complications, particularly when dealing with small-caliber vessels such as those of the distal aca (1, 6, 12, 13). giant partially thrombosed aneurysms of the a4a5 segments of the aca are extremely rare lesions. we report the second such case in the literature. the intramural -rather than intraluminalnature of these lesions makes them poor candidates for endovascular therapy. the anatomical disruption they cause within the anterior interhemispheric fissure makes the already difficult task of locating them more daunting. excluding these lesions from the circulation without compromising proximal and distal branches of the pericallosal artery is challenging, and requires a comprehensive knowledge of the pertinent anatomy, as well as experience in microvascular procedures like neck reconstruction and intracranial-intracranial bypass techniques. conclusions giant partially thrombosed a4-a5 aneurysms are an extremely rare disease entity. their pathological mechanisms are likely to be different from small saccular aneurysms, and their location poses unique surgical challenges. surgical management must be adjusted to deal with these challenges and ensure the best outcome. abbreviations daca: distal anterior cerebral artery. ct: computed tomography. mri: magnetic resonance imaging. cta: ct angiography. gcs: glasgow coma score. mrc: medical research council. references 1. abla aa, lawton mt. anterior cerebral artery bypass for complex aneurysms: an experience with intracranialintracranial reconstruction and review of bypass options. journal of neurosurgery. 2014 jun 1;120(6):1364-77. 2. alvarez h. etiology of giant aneurysms and their treatment. american journal of neuroradiology. 2009 jan 1;30(1):e8. 3. bhatia s, sekula rf, quigley mr, williams r, ku a. role of calcification in the outcomes of treated, unruptured, intracerebral aneurysms. acta neurochir (wien). 2011 apr;153(4):905-11. 4. farias jp, trindade am. giant distal anterior cerebral artery aneurysm not visualized on angiography: case report. surgical neurology. 1997 oct 1;48(4):348-51. 5. fathi nq, syahrilfazli aj, azizi ab, redzuan im, sobri m, kumar r. ruptured giant left distal anterior cerebral artery aneurysm in a two-month-old baby. pediatr neurosurg. 2015;50(5):275-80. 6. hafez a, raj r, lawton mt, niemelä m. simple training 223 a giant a4-a5 distal anterior cerebral artery aneurysm treated with microsurgical clip reconstruction tricks for mastering and taming bypass procedures in neurosurgery. surgical neurology international. 2017;8. 7. hernesniemi j, tapaninaho a, vapalahti m, et al. saccular aneurysms of the distal anterior cerebral artery and its branches. neurosurgery 1992; 31(6): 994-9. 8. hoz ss, aljuboori z, albanaa sa, al-sharshahi zf, alrawi ma, neamah am, al-khafaji ao. ruptured giant aneurysm of a cortical middle cerebral artery: a case report. surgical neurology international. 2021;12. 9. inci s, akbay a, orunoglu m. aneurysm clip compression technique in the surgery of aneurysms with hard/calcified neck. world neurosurg. 2015 sep;84(3):688-96. 10. inci s, erbengi a, özgen t. aneurysms of the distal anterior cerebral artery: report of 14 cases and a review of the literature. surg neurol 1998; 50(2): 130-40. 11. krings t, alvarez h, reinacher p, ozanne a, baccin ce, gandolfo c, zhao wy, reinges mh, lasjaunias p. growth and rupture mechanism of partially thrombosed aneurysms. interv neuroradiol. 2007 jun;13(2):117-26. 12. lehecka m, dashti r, hernesniemi j, niemelä m, koivisto t, ronkainen a, rinne j, jääskeläinen j. microneurosurgical management of aneurysms at a4 and a5 segments and distal cortical branches of anterior cerebral artery. surgical neurology. 2008 oct 1;70(4):35267. 13. lehecka m, dashti r, lehto h, kivisaari r, niemelä m, hernesniemi j. distal anterior cerebral artery aneurysms. acta neurochir suppl. 2010;107:15-26. 14. mahajan a, goel g, das b, banga v, narang ks. bizarre growth of partially thrombosed giant aneurysm of distal anterior cerebral artery—the end of the treatment is not the end. neurol india 2021;69:1067-9 15. matsushima k, kawashima m, suzuyama k, takase y, takao t, matsushima t. thrombosed giant aneurysm of the distal anterior cerebral artery treated with aneurysm resection and proximal pericallosal arterycallosomarginal artery end-to-end anastomosis: case report and review of the literature. surg neurol int. 2011;2:135. 16. miyazawa n, nukui h, yagi s, et al. statistical analysis of factors affecting the outcome of patients with ruptured distal anterior cerebral artery aneurysms. acta neurochir (wien) 2000; 142(11): 1241-6. 17. ohno k, monma s, suzuki r, et al. saccular aneurysms of the distal anterior cerebral artery. neurosurgery 1990; 27(6): 90713. 18. penn dl, komotar rj, connolly es. hemodynamic mechanisms underlying cerebral aneurysm pathogenesis. journal of clinical neuroscience. 2011 nov 1;18(11):1435-8. 19. sato y, samii m. a technique for sequential, progressive clipping for a giant thrombosed distal anterior cerebral artery aneurysm. surgical neurology international. 2017;8. 20. senbokuya n, kanemaru k, kinouchi h, horikoshi t. giant serpentine aneurysm of the distal anterior cerebral artery. j stroke cerebrovasc dis. 2012 nov;21(8):910.e711. 21. sindou m, pelissou-guyotat i, mertens p, et al. pericallosal aneurysms. surg neurol 1988; 30(6): 434-40. 22. spetzler rf, riina ha, lemole gm,jr. giant aneurysms. neurosurgery 2001; 49(4): 902-8. 23. steven da, lownie sp,ferguson gg. aneurysms of the distal anterior cerebral artery: results in 59 consecutively managed patients. neurosurgery 2007; 60(2): 227-34. 24. sundt tm jr, piepgras dg, marsh wr. booster clips for giant and thick-based aneurysms. j neurosurg. 1984 apr;60(4):751-62 25. tao t, dai w, li w, hang c. giant serpentine distal anterior cerebral artery aneurysm treated with in situ side-to-side a3-a3 anastomosis and aneurysm resection. world neurosurg. 2019;133:21-24. 26. ugur hc, kahilogullari g, esmer af, et al. a neurosurgical view of anatomical variations of the distal anterior cerebral artery: an anatomical study. j neurosurg 2006; 04(2): 278-84. 27. van rooij wj, sluzewski m. endovascular treatment of large and giant aneurysms. american journal of neuroradiology. 2009 jan 1;30(1):12-8. 28. wiebers do, whisnant jp, huston j 3rd, meissner i, brown rd jr, piepgras dg, forbes gs, thielen k, nichols d, o'fallon wm, peacock j, jaeger l, kassell nf, kongablebeckman gl, torner jc; international study of unruptured intracranial aneurysms investigators. unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. lancet. 2003 jul 12;362(9378):103-10. 29. wisoff jh, flamm es. aneurysms of the distal anterior cerebral artery and associated vascular anomalies. neurosurgery 1987; 20(5): 735-41. 30. yaşargil mg, carter lp. saccular aneurysms of the distal anterior cerebral artery. j neurosurg 1974; 40(2): 218-23. 31. yoshimoto t, uchida k, suzuki j. surgical treatment of distal anterior cerebral artery aneurysms. j neurosurg 1979; 50(1): 40-4. 32. zarrinkoob l, ambarki k, wåhlin a, birgander r, eklund a, malm j. blood flow distribution in cerebral arteries. journal of cerebral blood flow & metabolism. 2015 apr;35(4):648-54. romanian neurosurgery (2019) xxxiii, 1: 37-48 doi: 10.33962/roneuro-2019-007 www.journals.lapub.co.uk/index.php/roneurosurgery the surgical procedure of syringomyelie with chiari i in adults regarding the intrapial aspiration of cerebellar tonsils: does this procedure improve symptoms with less complication? ait bachir mustapha1,2, t. benbouzid1,2 1 department of neurosurgery, nedir mohamed hospital, tizi ouzou, algeria 2 department of neurosurgery, bab el oued hospital, algeria abstract introduction. cranio-vertebral decompression remains the common denominator for the treatment of syringomyelia associated with chiari i. on the other hand, the details of the procedure, remains controversial. the success of the surgery is to restore the circulation of cerebro-spinal fluid at the level of the foramen magnum. how is this circulation restored to the level of foramen is the question? we offer our attitude towards the treatment of syringomyelia with chiari i. material and method. consecutive series of 32/121 patients benefiting from craniovertebral decompression associated with intrapial aspiration of cerebellar tonsils treated for syringomyelia with a chiari i malformation in adults. result. motor deficits were present in 20 / 22 patients, representing 90% of the entire patient group. these motor deficits are improved in 16 out of 22 cases, and remained unchanged in 06cas. no motor aggravation occurred. in our study, bone decompression and intra pial aspiration of cerebellar tonsils (sub arachnoids manipulation) were found to be associated with favourable results on clinical signs and symptoms. however, sub arachnoids manipulation and intra pial aspiration of cerebellar tonsils showed a little more complication compared with bone decompression with dural plasty. conclusion. the bone decompression with dural graft and intradural dissection of adhesions and reduction by intra pial aspiration or resection of the tonsils is indicated on the mri aspect of cerebellar tonsils of considerable size totally obstructing the foramen magnum, the intraoperative finding, through the arachnoid, of the absence of passage of the cerebro-spinal fluid because of the bulging of the cerebellar tonsils. introduction the understanding of the pathophysiology of the development of syringomyelia with chiari malformation formulated in many series [1,12,20,32,34,38,54,60,67,85]. explains the use today more and more of cranio-vertebral decompression technique is therefore the common denominator of syringomyelia treatment associated with chiari i, on the other hand the details of the procedure, the technique of closure of the dura mater, and whether a drainage system should be placed or not in the syringomyelia cavity remains controversial. the maintenance of restored cerebrospinal fluid flow, however, is often problematic. keywords syringomyelia, chiari i, intra pial aspiration of cerebellar tonsils corresponding author: ait bachir mustapha department of neurosurgery, nedir mohamed hospital, tizi ouzou, algeria mustaphaaitbachir@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 38 ait bachir mustapha, t. benbouzid many different surgical techniques are utilized to treat syringomyelia with chiari type i malformation, and there is no consensus. surgical technique may include bony decompression of the posterior fossa with or without duraplasty, arachnoid dissection, or shrinking of the cerebellar tonsils. the goal of any of these operations is to restore adequate cerebro spinal fluid csf flow at the level of the foramen magnum and reconstruction of the cisterna magna. is the reduction of the volume of the cerebellar tonsils by intra pial aspiration or resection of cerebellar tonsils or finally tonsilar shrinking associated with osteo dural decompresionis the best choice of traitment. we will discuss the results of our series of intra pial aspiration of cerebellar tonsils by comparing it with the different publications cited in the literature and propose our opinion. materials and methods preoperative population characteristics in our consecutive series of 32/121 patients with cranio-vertebral decompression associated with intrapial aspiration of the cerebellar tonsils or resection of the cerebellar tonsils treated for syringomyelia associated with a tonsillar herniation (chiari i malformation) in adults, 10 of them were however excluded from the study for lack of fully exploitable files. our series therefore includes 22 patients.the mean age of the patients was 30 years. there were 13 female (59%) and 09 male (40%) patients. preoperative clinical symptoms signs and symptoms are summarized in table i. sensory disturbances were present in the upper limbs in 59%. motor weakness was present together in the upper limbs and in the lower limbs in 90,9% of patients. headaches were noted in 45,4%, lower cranial nerves palsy in 13,6% and balance disorders or gait ataxia in 08 cases. table i. symptoms/signs in 22 patients symptom / sign preoperative status syringomyelie+chiarii (no. of patients) postoperative result (no. of patients) weakness & muscular atrophy 20 15 sensory disturbance 15 13 balance disorders, gait problems or gait ataxia 08 08 pain headache 10 10 cranial nerv dysfonction 03 03 the presence or absence of clinical signs was noted in all of these patients and motor disorders were assessed according to mc cormick's classification (table ii). all our patients were adults. the distribution by sex shows a female preponderance, which corresponds to what has been reported in some series [57,91,3,93,45,28 , 66,79 ,17, 51,49,14]. motor disorders were the main symptom of the majority of patients in this series, followed by the sensory disturbances and headaches. we noted ataxia in 08 cases and cranial nerve deficits in 03 cases. table ii. mc cormick's classification. table iii. summary of preoperative status of motor disorders and postoperative results grade in 22 patients i: motor disorders were assessed according to mc cormick's classification: pré-opérative stading and after surgery. pré-opérative status chiarii+syringomyelie (no. of patients) post opérative status chiarii+syringomyelie (no. of patients) 09 cases grade iii 08 grade ii (improvement) 01 cases (unchanged) 08 cases grade ii 08 grade i (improvement) 03 cases grade iv unchanged 39 the surgical procedure of syringomyelie with chiar i in adults 02 cases grade i unchanged 22 total preoperative imaging all patients underwent magnetic resonance imaging (mri) studies including sagittal and axial spin-echo t1 and t2 sequences. we analyzed the size of the ventricles, studied the anatomy of the occipitovertebral junction, namely the position of the tonsils, the posterior arch of c1, the height extension of the syringomyelia cavity. preoperative mri showed that the syrinx predominantly involved the cervical or the cervicothoracic spinal cord (28% and 50% of the patients respectively) and occupied from 30% to 80% of the spinal canal according to the vaquero's index [81]. septa were present in 30% of patients.all patients showed tonsillar herniation reaching the inferior rim of c1. none showed spinal dysraphism or basilar invagination surgical technique regarding the surgical technique, all patients of our series of 121 cases were operated in the ventral position which allows the easy visualization of the tonsils, since in the sitting position the tonsils are stretched down under the effect of the universal attraction so they will be less visible than ventral, and also the brainstem and cerebellum have a tendency to migrate downward in the sitting position. in this series, the craniocervical decompression procedure was chosen based on the different flow of the cerebro spinal fluid dynamics at the cervico vertebral junction. after a small craniectomy, opening the foramen magnum, removing the small lower part of the posterior fossa, and removing the posterior arch of c1. the extent of bone decompression is also important, if the craniectomy is too wide in height, the patient is at risk of ectopy of the cerebellum and recurrence of symptoms. some authors suggest that the craniectomy should be wide [21] in addition to the craniectomy, isu [47] is satisfied with the removal of the outer layer of the dura as a treatment for syringomyelia occurring with a chiari i malformation for him is enough. and others, like us, prefer a small craniectomy in order to avoid the sagging of the cerebellum (cerebellar ptosis), which is sometimes responsible for the patient's death, as reported after a wide craniectomy [43,83,84]. zhang et al. [92] retrospectively analysed 132 patients in a comparison of small and large craniectomy. as noted above, the success rate was 78.2% in the large craniotomy group, with nearly half of patients developing complications, the most common of which was cerebro spinal fluid fistula (11.5%), whereas in the small craniotomy group, the success rate was 82.5% with only three cases of complications. this study demonstrated the superiority of smaller craniotomies. but according to ellenbogen [29] a limited craniectomy can lead to inadequate decompression and persistence or recurrence of symptoms, i totally agree with ellenbogen if we do not realize an intra pial aspiration of cerebellar tonsils. in 2003, milhorat and bolognese reported a good result in their experience in tailoring the craniectomy based on the extent of the compressed subarachnoid space on pre-operative magnetic resonance imaging. we advocate a suboccipital craniectomy limited to enlarging the occipital foramen and allowing both decompression and maintenance of the cerebellum in the posterior fossa. for some authors occipitovertebral decompression alone is enough di lorenzo n [26]. then the opening of the dura with keeping the arachnoid intact and an intraoperative exploration that will show if there is a good passage of the cerebro spinal fluid by visualization or observation of the bulge of the arachnoid or not (figure1). if there is a bulge of the arachnoid it means that there is a good passage of the cerebro spinal fluid so this procedure is sufficient. according to this finding the decision of the realization of the intrapial aspiration of the cerebellar tonsils will be taken. all of the 21 patients in our series have benefited from the intrapial aspiration of the cerebellar tonsils, the extent of intra pial aspiration or resection was ended when the tonsils were reduced and magendie foramen with the obex of the fourth ventricle are seen. so even in our therapeutic attitude the decision to use either bone decompression or sub arachnoid manipulation was routinely made intraoperatively, before the dural opening was made. at last duraplasty was also done to all patients using fascia lata graft (figure2). during the whole procedure, careful hemostasia isperformed with bipolar forceps under saline irrigationto keep the field bloodless, to prevent adhesions that canbe induced around the spilled blood. 40 ait bachir mustapha, t. benbouzid results immediate postoperative result and complications in our series no mortality was seen, this are similar to those reported by [7,5,16,93] who reported no mortality in their series. but we noted, some cases of postoperative complications, such as cerebro spinal fluid leakage (04/22, 18.1%) who were treated with the use of repeated lumbar puncture with complete closure of the cerebro spinal fluid leakage, three patients 13.6% have intracranial infection who were treated medically. we have noted, hiccups in one case, who was traited only with the use of a synthetic drug as a tranquilizer, sedative, and antiemetic (chlorpromazine). the most serious complication was aseptic meningitis (02/22, 9.09%) with cerebro spinal fluid leakage (04/22, 18.1%). based on the results of this series, headache responds very well to decompression surgery with intra pial aspiration of cerebellar tonsils, on 10 of 22 patients with preoperative headache experienced relief complete immediately after surgery. motor deficits were present in 20 / 22 patients, representing 90,9% of the entire patiens. no motor and sensory aggravation occurred. but the follow-up of the patients shows us that the motor improvement occurs slowly. other symptoms, such as ataxia in 08 cases and cranial nerve deficits in03 cases, are improved in imediat postoperatively in our series, similar with findings reported by other authors. [14,17,30,33,37,16] series, which adopts the same surgery technique of craniovertebral decompression with tonsillectomy used in this study. mri follow-up on the neuro-radiological level, the mri was performed successively at one month, six months and 12 months then every 02 years, found a normalization of the position of the cerebellar tonsils in all cases with a reconstruction of a new large cisterna magna. the syrinx cavity was clearly or markedly regressed in 09 case, and slightly regressed in 13cas. syrinx cavity clearly regressed in 09 casefig2 figure 3. preoperative mri scan reveals syrinx cavity with tonsillar herniation extending below the foramen magnum (chiarii). post op postoperative mri scan reveals the regression of the syrinx cavity and absence of cerebellar tonsil herniation. (a) slightly regressed in 13cas fig3: figure 1. preoperative picture of dural opening with preservation of intact arachnoid (a) showed a bulge of the arachnoid which confirms the good passage of the cerebro spinal fluid (b) shows the large tonsils that occupy a large space and prevent the normal passage of the cerebro spinal fluid 41 the surgical procedure of syringomyelie with chiar i in adults figure 2: preoperative step-by-step photos of the procedure used in osteo dural decompression with intra pial aspiration of cerebellar tonsils: bone decompression and dural opening with preservation of arachnoid, exposure of tonsils which are bulky (a, b), progressive intra pial aspiration of the cerebellar tonsils (c, d, e, f) and duralplasty (g). figure 3. pre-operative (a) syringomyelia cavity with chiari i post-operative(b) clearly regression of the syringomyelia cavity figure 4. syringomyelia cavity pre op with chiari i (a) slight postoperative regression of the syringomyelic cavity (b) 42 ait bachir mustapha, t. benbouzid the reoperation was not performed in our series because the result of long-term follow-up of our patients showed an improvement especially on the motor level. among patients who improved 15.79% remained stable in their initial improvement with an average follow-up over 8 years. these are similar to those in the series of reports on the best prognosis of the literature summarized and reported by nozar aghakhani [2]. literature review a literature review was performed with the pubmed search engine of the national library of medicine of the national institutes of health (http://www.ncbi. nlm.nih.gov/pubmed) and on the research gate site, using the following keywords “chiari malformation,” “chiari malformation type i with syringomyelia,”,” “posterior fossa decompression with or without duraplasty,” and “ craniocervical decompression with duraplasty and cerebellar tonsillectomy.” the search was restricted to english-language publications without date limitations. discussion first, we will say what are the circumstances that led us to opt for this method. secondly, we analyse the various publications through the literature, is this method seen our retreat is effective or not, based on the following parameters: the immediate postoperative and the long-term results. third is that this method can be proposed in some patients. to discuss the first issue, as you know that the key point of surgery in syringomyelia with chiari imalformation is to allow a flow of cerebrospinal fluid at the level of magendie foramen and foramen magnum. for our part, we have opted for the 22 patients a osteo-dural decompression associated with intra pial aspiration of the cerebellar tonsils for several reasons: when the opening of the dura with maintenance of the arachnoid intact and an intraoperative exploration will show us intraoperatively, through the arachnoid, the absence of passage of cerebrospinal fluid due to the large volume of the cerebellar tonsils. as there is no bulge of the arachnoid, this means that there is not a good passage of cerebrospinal fluid in sufficient quantity. it has not been demonstrated that the resection of the cerebellar tonsils does not lead to neurological disorders. the function of which is not yet clearly determined. vvsualization or appearance of large cerebellar tonsils and considerable size completely obstructing the foramen magnum causes neurological disorders.depending on the presence of these 03 parameters, the decision to perform intrapital aspiration of the cerebellar tonsils will be taken. in our experience, the intra pial aspiration or resection of the tonsils does not lead to a noticeable neurological deficit. according to asgari s and al [9] during removal of the cerebellar tonsil, the integrity of the pia mater of the cerebellar tonsil should be preserved to reduce postoperative adhesions, causes aggravation or reappearance of neurological disorders. we take into account the analysis of the literature publication and the study of arnautovic a [6], and aghakhani n [2] ,royo salvador [71] to evaluate of surgical treatment options in the chiarii malformation type i with syringomyelia and concerning the occurrence of complications during the realization or not of the intrapial aspiration of the cerebellar tonsils, we found that the debate still exists as to whether, once the dura mater is open, arachnoid dissection should be performed or not and if the cerebellar tonsils are resected or retracted or not?. for some neurosurgeons the manipulation of the tonsils can lead in the long term to arachnoid adhesions between the cerebellar tonsils and the dura mater which prevents or hinders the subsequent flow of the cerebro spinal fluid at the foramen magnum, with worsening of syringomyelia and symptoms according to asgari s [9]. to avoid this postoperative arachnoiditis sindou et al [76] and others authors such hyun seok l [ 44], lee hs [56], oldfield eh [67], perrini .p[69] advocated or suggested opening of the dura with preservation of the arachnoid membrane and adding duraplasty, and reported favourable results. while in our series on an average of 8 years of follow up , we did not have this type of problem since we did not have any post-operative neurological aggravation in medium and long term (after minimum 1 year of follow-up) which eliminates the eventual arachnoiditis following intra pial aspiration of cerebellar tonsils which is confirmed in the study of junpeng ma1[49]and zuev a.a[93] that the cerebellar 43 the surgical procedure of syringomyelie with chiar i in adults tonsillectomy with suboccipital decompression and duraplasty can provide long-time cure for most chiarii malformation cases, and some authors reported, the good results with this procedure[55, 91]and they have good results. williams also recommended to remove part of the tonsils to ensure that the pathways are maximally opened. many papers have supported arachnoid opening and/or tonsillectomy [5,16,7,93]. however, a successful surgical outcome (100% normalization of hindbrain herniation) was reported without arachnoid opening by heiss et al [39] what was mentioned also by royo salvador [71] in his article. klekamp [52]and lee hs [56] showed that combined arachnoid pathology was a strong risk factor for symptom recurrence, because any operation undertaken to improve a problem related to arachnoid scarring may create new arachnoid scars, the lesser the extent of dissection and the lesser the contamination of the surgical field with blood, the better the chance of achieving good long-term results alden [4] in his article explains that, tonsillar shrinkage or resection has been advocated “as a way to improve the volume mismatch and to increase communication between the fourth ventricle and the spinal compartment”. fisher [30] recommends subpial resection of the cerebellar tonsils, while batzdorf u [16] and others many neurosurgeons recommend tonsil shrinkage by coagulation or other means. and other authors gonçalves da silva j, arruda j am [7], galarza m [30], raftopoulos c [70] have another way to achieve sub arachnoid manipulation, and claim that this technique improves decompression in the region of the foramen magnum. in his article josé alberto gonçalves da silva1and al [22], observed a blockage of the foramen of magendie in 55 (52.8%) patients, mainly caused by the presence of a dense membrane or adhesions between the cerebellar tonsils. in our opinion this is a valid argument for the exploration of the cerebellar tonsil and foramen of magendie. on the other hand, some of the neurosurgeons [63,21, 39. leave them intact, performing especially the opening of the fourth ventricle. on the other side, batzdorf [16] recommends lightly diathermying the pia mater over the surface of the tonsils. for raftopoulos[70] it is enough just to open the arachnoid and then remove the adhesions. secondarily in the past, decompression treatment of the occipito cervical junction has been a dangerous operation, with a significant mortality r a te [d i lo re n z o]. w it h t h e d e ve lo pm en t o f neurosurgery, occipito vertebral decompression has become a relatively low-risk procedure. in our series, there have been no cases of death, or serious infections requiring revision of the wound, badie et al. [10] retrospectively evaluated 20 cases treated via decompression technique with duraplasty and tonsillectomy. the success rate was 85%, with no mortality. complications were not described. the 04/22 cases of cerebro spinal fluid leakage in our series is slightly high but if we take all our series of 121 patients who have benefited from occipito cervical decompression with dural plasty, the leak rate of cerebro spinal fluid is similar to that reported in other series [28,35,40,46,48,49]. the incidences of csf-related complications and hydrocephalus in studies about occipito cervical decompression with dural plasty were 4–10% and 3–4% respectively [79]. no appearance of a a pseudomeningocel in our series because we use a small suboccipital decompression, this makes it possible to avoid the appearance of a a pseudomeningocel. recently, jeffrey s et al [17], performing a small bone decompression report in his article on minimally invasive subpial tonsillectomy for chiari i decompression significantly reduced the risk of pseudo-meningocele formation. the incidence of motor deficits and sensory disorder in our series is higher than in other series [8,10,68]. in our series, these motor deficits are improved in 16 out of 22 cases after functional rehabilitation, and remained unchanged in 06cases, we agree with bălaşa. a, gherasim.d.n[11 ] who believes that preoperatory longtime neurological deficit is a predictor of poorer outcome, making early surgery. this explains why in our series we had 06 patients who remained unchanged postoperatively and this is probably due to late diagnosis in our p a ti en ts w ho o nl y c ons ul t at th e la te st ag e . depreitere et al. [25] retrospectively analysed 22 cases operated used tonsillectomy. on initial followup, 16 patients (76%) were improved. in late followup, the success rate was 68%. alfieri et al, reported that surgical decompression with durotomy, arachnoid opening, tonsillar shrinkage, and recreation of the cisterna magna was a safe and effective procedure. prognosis was excellent, with 44 ait bachir mustapha, t. benbouzid global clinical and radiological improvement in more than 90% and 80% of patients, respectively stanko et al [77] suggested that tonsillar cautery might provide an extra benefit in the resolution of the syrinx compared with bone-only decompression alone or in combination with dural opening. another previous study reported on 22 adult patients, with the conclusion that sub arachnoid manipilutaion may improve the symptoms in chiari i malformation [30],in an older study, seven of eight patients who underwent sub arachnoid manipulation showed very good clinical outcomes [36,37] for some neurosurgeons sub arachnoid manipulation are generally accepted as the effective surgical procedures in the treatment of chiari i malformation [67,70,72], and their effects have been confirmed by clinical practice. in our series postoperative, mri scan reveals clearly regression of the syrinx cavity in 09 case, and slightly regression of the syrinx cavity in 13 cases, based on the vaquero index and absence of cerebellar tonsil herniation in all cases. wetjen [82] and co-authors have estimated the rate of syringomyelia resolution by examining the postoperative images in patients after chiarii malformation decompression. based on the largest anteroposterior diameter of the syringomyelia, the authors concluded that the median time to greater than 50% narrowing of the syringomyelia was 3.6 months postoperatively, whereas the mean time was 6.5 months. in a follow-up study by wu et al. [86], syringomyelia was found to be obviously reduced in all patients examined and completely eliminated in eight patients. in the study of bao and al [14], the reexamination by mri in 44 patients showed successful construction of the cis¬terna magna, with eliminated or obviously reduced syringomyelia in 42 patients. according to de lotbinière acj [58] the tonsillectomy or cerebellar tonsil exeresis proposed by some authors probably adds to the mortality and morbidity rates. it can be an unnecessary and maiming surgical manoeuvre. alden [4] states that “no neurological deficit has been demonstrated as a result of tonsillar resection; however, the exact function of this structure is largely unknown we agree with alden effectively, we have practiced it since 1999 and we have not had neurological disorders following their resection including cognitive disorders. taking into consideration that, the role of the cerebellum in learning and cognition began to be considered. in 1997 and 1998 schmahmann and sherman [75] named dysfunction of the cerebellums contribution to cognition and behavior the cerebellar cognitive affective syndrome. the posterior lobe of the cerebellum and the vermis contribute to verbal fluency, short-term memory, abstract reasoning, and spatial cognition, functions that may underlie the frequent complaint of “brain fog” in patients the chiari i malformation. according to royo salvador mb [71] the tonsillectomy for syringomyelia with chiari i,is not indicated, given that no benefit is obtained and it involves an amputation of a part of the cerebellum that can only contribute to sequelae, situations of permanent instability and vertigo. in our study of clinical presentation in 32 patients with the chiari i malformation with syringomyelia, we did not consider the psychological and or congenital state during the preoperative clinical examination. finally, and generally, the results of this procedure are favourable and differ little between the series. this was confirmed by the present study that the results were good, the complications limited in number .in 2005 we presented our comparative study of 40 patients between bone decompression with dural plasty(20 patients) and bone decompression with dural plasty followed by intrapial aspiration of cerebellar tonsils (20 patients) we found that the clinico-radiological results of bone decompression with dural plasty followed by intrapial aspiration of cerebellar tonsils are comparable and sometimes better than the bone decompression with dural plasty [18]. we believe that one of the advantages of arachnoid dissection, in the context of syringomyelia with chiari i malformation, is that it allows the surgeon to release the adhesions especially at the foramen of magendie which could contribute to the obstruction of the cerebro spinal fluid flow from the fourth ventricle to the spinal canal. whereas the subpial resection of the cerebellar tonsils, especially when they are bulky, we recommend it as a means of improving particularly the passage volume of the cerebro spinal fluid flow and increasing the communication between the fourth ventricle and the spinal cord. our experience that patients treated by tonsils resection had a good outcome with no increased operative risk and no additional surgery required 45 the surgical procedure of syringomyelie with chiar i in adults surgical technique. i totally agree with arruda and al []in his study arruda conclude that craniocervical decompression with tonsillectomy and duramater graft proved an effective method for the treatment o f s y r i ng om y e l ia a n d c hi a r i m a l fo rm a t i o n . limitations first, the present study was a retrospective analysis of 22 patients and the small number may have resulted in a lower statistical power. second a prospective multicentre study with a large and equal n u m be r of p a ti e n ts i n t h e occ i p it o c e rv ic a l decompression and occipito cervical decompression with intra pial aspiration of cerebellar tonsils or tonsillectomy groups might provide sufficient data for an adequate comparison of these 2 techniques to better define the i ndications and benefits. conclusions for the treatment of symptomatic patients, various approaches may be used: bone decompression with dural graft, or bone decompression with dural graft and intradural dissection of adhesions and reduction by intrapial aspiration of the cerebellar tonsils or resection of tonsils because the key point of surgery in syringomyelia with chiarii malformation is to allow a cerebro spinal fluid flow at the level of foramen of magendie and foramen magnum. for our part, we have opted for a certain category of patients for osteo-dural decompression associated with subpial resection of the cerebellar tonsils for several reasons: -no neurological disturbance has been demonstrated to result from the intra pial aspiration resection of ectopic cerebellar tonsils,the function of which is not yet clearly determined the attribution of the neurological disorders, noted in the pre-surgical phase, to the malformation of arnold chiari, the mri appearance of cerebellar tonsils of considerable size totally obstructing the foramen magnum. -the intraoperative finding, through the arachnoid, of the absence of passage of the cerebro spinal fluid due to the bulging of the cerebellar tonsils. according to beecher. j.s[17] the indications for subpial resection of the cerebellar tonsils surgery are the presence of one or more of the following criteria: 1. karnofsky score of 70 or less secondary to chiari malformation stereotypic constellation of symptoms 2. an expanding syringomyelia on consecutive mri scans, syringomyelia cavities in excess of 75 % of the transverse cord diameter on the index mri, or eccentric appearance of the syringomyelia cavity with intraparenchymal blebs 3. severe, rapidly progressive neurological deficit however, it should be acknowledged that this is an observational study and ultimately, we can say that the technique can be used in particular cases. it would be interesting to pay more attention to the effectiveness / inefficiency of the indication of intra pial aspiration of the cerebellar tonsils in the syringimyelie surgery with tonsils herniation (chiari i malformation). for these reasons, i believe long-term follow-up, with periodic measures, is required to really understand the success of surgery. references 1. aboulker j (1979) la syringomyeâlie et les liquides intrarachidiens. neurochirurgie 25: 1±144 2. aghakhani n, parker f, david p, morar s, lacroix c, benoudiba f, tadie m: long-term follow-up of chiarirelated syringomyelia in adults: analysis of 157 surgically treated cases. neurosurgery 64: 308-315; discussion 315, 2009 3. aghakhani n, parker f, tadie m: syringomyelia and chiari abnormality in the adult. analysis of the results of a cooperative series of 285 cases [in french]. neurochirurgie 45:23–36, 1999 4. alden.t.d, ojemann.j.g, and park.t.s, “surgical treatmentof chiari i malformation: indications and approaches,” neurosurgical focus , vol. 11, no. 1, article e2, 2001 5. alfieri a, pinna g: long-term results after posterior fossa decompression in syringomyelia with adult chiari type i malformation. j neurosurg spine 17(5):381387, 2012 6. arnautovic a, splavski b, boop fa, arnautovic ki. pediatric and adult chiari malformation type i surgical series 19652013: a review of demographics, operative treatment, and outcomes. j neurosurg pediatr. 2015; 15:161-77. 7. arruda jam, costa cmc, de tella jr oi. results of the treatment of syringomyelia associated with chiari malformation: analysis of 60 cases. arq neuropsiquiatr 2004; 62:237-244.] 8. ascho¨ a, donauer e, huwel n, urban v, spahn b, lohlen a, adams hp (1993) evaluation of syrinx-surgery. a critical comment on requirements for reliable follow-up-studies. acta neurochir (wien) 123: 224±225 9. asgari s, engelhorn t, bschor m, sandalcioglu ie, stolke d: surgical prognosis in hindbrain related syringomyelia. actaneurol scand 107:12-21, 2003 10. badie b, mendoza d, batzdorf u: posterior fossa volume and response to suboccipital decompression in patients 46 ait bachir mustapha, t. benbouzid with chiari i malformation. neurosurgery 37:214–218, 1995 11. bălaşa.a, gherasim.d.n our experience in surgical treatment of chiari type 1 malformations, romanian neurosurgery (2012) xix 4: 279 – 288 12. ball mj, dayan ad (1972) pathogenesis of syringomyelia. lancet 2: 799±801 13. bao.c.s, liu.l,wang.b, xiax.g, gu.y.j, li.d.j,zhan.s.l, chen. g. l and yang.f.b , craniocervical decompression with duraplasty and cerebellar tonsillectomy as treatment for chiari malformation-i complicated with syringomyelia genetics and molecular research 14 (1): 952-960 (2015) 14. bao cs, yang fb, liu l, wang b, et al. (2011). cerebellar tonsilletomy and reconstruction of the cistern magna for treatment of syringomyelia with chiari malformation. chin. j. neuromed. 10: 993-995. 15. bao c, yang f, liu l, wang b, li d, gu y, et al. surgical treatment of chiari i malformation complicated with syringomyelia. exp ther med. 2013; 5(1):333-7. 16. batzdorf.u, mcarthur.d.l,bentson.j.r, surgical treatment of chiari malformation with and without syringomyelia: experience with 177 adult patients, j. neurosurg. j neurosurg. 2013 feb;118(2):232-42 17. beecher. j.s, liu.y,qi.x,bolognesep.a minimally invasive subpial tonsillectomy for chiari i decompression acta neurochir (2016) 158:1807–1811 18. benbouzid t., ait bachir m., berchiche l., morsli a.yacoubi b., sidi said a. la syringomyélie foraminale. choix de la procédure chirurgicale. à propos de 40 cas revue française de neurochirurgie, 2005,51, n° 5, 523-527. 19. brugieres p, idy-peretti i, iffenecker c, et al: csf flow measurement in syringomyelia. ajnr 21:1785–1792, 2000 20. catala m. reflexions d’un neuro-embryologiste. a propos de la syringomyélie dite malformative. neurochirurgie, ed masson, paris, 1999, 45, suppl.1 :9-22 21. chou yc, sarkar r, osuagwu fc, ja. lazareff . suboccipital craniotomy in the surgical treatment of chiari i malformation childs nerv syst (2009) 25:1111–1114 22. da silvaja g, melo lrs; posterior fossa decompression with tonsillectomy in 104 cases of basilar impression, chiari malformation and/or syringomyelia; arq neuropsiquiatr 2011;69(5):817-823 23. da silva. j.a.g, holanda mma. basilar impression, chiari malformation and syringomyelia. a retrospective study of 53 surgically treated patients. arq neuropsiquiatr 2003; 61:368-375.] 24. deniz b, uygur er, levent g, kazim y; delayed pseudomyelomeningocele: a rare complication after foramen magnum decompression for chiari malformation; surgical neurology 71 (2009) 357–361 25. depreitere b, van calenbergh f, van loon j, et al: posterior fossa decompression in syringomyelia associated with a chiari malformation: a retrospective analysis of 22 patients. clin neurol neurosurg 102:91–96, 2000 26. di lorenzo n, palma l, palatinsky e, et al: "conservative" cranio-cervical decompression in the treatment of syringomyelia-chiari i complex. a prospective study of 20 adult cases. spine 20:2479–2483, 1995 27. duddy mj, williams b. hindbrain migration after decompression for hindbrain hernia: a quantitative assessment using mri. brit j neurosurg 1991 ;5 :141-152 28. dyste gn, menezes ah, vangilder jc: symptomatic chiari malformations. an analysis of presentation, management, and long-term outcome.j neurosurg 71:159–168, 1989 29. ellenbogen rg, armonda ra, shaw dw, et al. toward a rational treatment of chiari i malformation and syringomyelia. neurosurg focus 2000; 8(3): e6. i 30. fischer eg: posterior fossa decompression for chiari i deformity, including resection of the cerebellar tonsils. childs nerv syst 11:625–629, 1995 30. galarza m, gazzeri r, alfieri a, martínez-lage jf (2013) b triple r tonsillar technique for the management of adult chiari i malformation: surgical note. acta neurochir 155:1195–1201. 32. gardner wj, angel j (1959) the mechanism of syringomyelia and its surgical correction. clin neurosurg 6: 131±140 33. goel a, desai k: surgery for syringomyelia: an analysis based on 163 surgical cases. acta neurochir 142:293–302, 2000 34. greitz d. unraveling the riddle of syringomyelia. neurosurg rev 2006; 29:251– 63; discussion 264 crossref medline 35. gurbuz m s, karaaslan.n, calıskan.t, unal. e, erkman m.z. comparison of the surgical results for foramenmagnum decompression with and withoutduraplasty in chiari malformation type 1 turk neurosurg 2015, vol: 25, no: 3, 419-424 36. guyotat j, bret p, mottolese c, jouhanneau e, abdulrahman m, lapras c: chiari i malformation with syringomyelia treated by decompression of the cranio-spinal junction and tonsillectomy. apropos of 8 cases. neurochirurgie 43(3):135-41, 1997. (french). 37. guyotat.j, p. bret, e. jouanneau, a.-c. ricci, and c. lapras: syringomyelia associated with type i chiari malformation. a 21-year retrospective study on 75 cases treated by foramen magnum. decompression with a special emphasis on the value of tonsils resection acta neurochir (wien) (1998) 140: 745±754 38. heiss jd, patronas n, devroom hl, et al: elucidating the pathophysiology of syringomyelia. j neurosurg 91:553– 562, 1999 39. heiss jd, suffredini g, bakhtian kd, sarntinoranont m, oldfield eh. normalization of hindbrain morphology after decompression of chiari malformation type i. j neurosurg. 2012; 117(5):942-6. 40. heckman ke, aliaga l, straus d. et al. positive and negative predictors for good outcome after decompressive surgery for chiari malformation type i as scored on the chicago chiari outcome scale. neurol res. sep; 2012 34(7): 694-700 42. hofmann e, warmuth-metz m, bendszus m, et al: phasecontrast mr imaging of the cervical csf and spinal cord: volumetric motion analysis in patients with chiari i malformation. ajnr 21:151–158, 2000 47 the surgical procedure of syringomyelie with chiar i in adults 43. holly lt, batzdorf u: management of cerebellar ptosis following craniovertebral decompression for chiari i malformation. j neurosurg 94:21–26, 2001 44. hyun seok l, sun-ho l, kim e, kim j, jung-il l, hyung jin s et al surgical results of arachnoid-preserving posterior fossa decompression for chiari i malformation with associated syringomyelia journal of clinical neuroscience 19 (2012) 557–560 45. hurth m, sichez jp (1979) la chirurgie de la charniere craniocervicale. etude critique à propos de 63 cas d'hydrosyringomyelie operes. neurochirurgie 25: 114±128 46. ilyas m, frim d, stine-reyes r et al. effects of posterior fossa decompression with and without duraplasty on chiari malformationassociated hydromyelia. neurosurg, 2000; 46,6 47. isu t, sasaki h, takamura h, et al. foramen magnum decompression with removal of the outer layer of the dura as treatment for syringomyelia occurring with chiari i malformation. neuro surgery 1993; 33:845-50 48. juan c. alzate, m.d., karl f. kothbauer, m.d., george i. jallo, m.d., and fred j. epstein, m.d. treatment of chiari type i malformation in patients with and without syringomyelia: a consecutive series of 66 cases neurosurg focus 11 (1): article 3, 2001 49. junpeng ma, chao you, haifeng chen, siqing huangang , chengcheng ieong ; cerebellar tonsillectomy with suboccipital decompression and duraplasty by small incision for chiari i malformation (with syringomyelia):long term follow-up of 76 surgically treated cases, turkish neurosurgery 2012, vol: 22, no: 3, 274-279 50. kalb.s, luis perez-orribo.p.o, mahan.m, theodore.n, nakaji .p , bristol.r.e. evaluation of operative procedures for symptomatic outcome after decompression surgery for chiari type i malformation. journal of clinical neuroscience 19 (2012) 1268–1272 51. klekamp j, surgical treatment of chiari i malformation— analysis of intraoperative findings, complications, and outcome for 371 foramen magnum decompressions, neurosurgery 71:365–380, 2012 52. klekamp j, iaconettag, batzdorf.u, samii.m. syringomyelia associated with foramen magnum arachnoiditis j neurosurg (spine 3) 97:317–322, 2002 53. klekamp j, samii m. syringomyelia—diagnosis and treatment. heidelberg, germany: springer verlag; 2001 54. koyanagi i, houkin k. pathogenesis of syringomyelia associated with chiari type i malformations: review of evidences and proposal of a new hypothesis. neurosurg rev 2010; 33:271– 84; discussion 284–85 crossref medline 55. lazareff ja, galarza m, gravori t, spinks tj: tonsillectomy without craniectomy for the management of infantile chiari i malformation. j neurosurg 97:1018-1022, 2002 56. lee hs, lee sh, kim es, kim js, lee ji, shin hj, eoh w (2012) surgical results of arachnoid-preserving posterior fossa decompression for chiari i malformation with associated syringomyelia. j clin neurosci 19(4):557–560 57. levy wj, mason l, hahn jf chiari malformation presenting in adults: a surgical experience in 127 cases. neurosurgery, 1983; 12: 377-90 58. lotbinière acj. historical considerations. in anson ja, benzel ec, awad ia (eds). neurosurgical topics: syringomyelia and chiari malformations.illinois: american association of neurologic surgeons, 1997:1-26. 59. menezes ah (2011) current opinions for treatment of symptomatic hindbrain herniation or chiari type i malformation. world neurosurg 75:226–228, 60. milhorat th, capocelli al jr, anzil ap, et al: pathological basis of spinal cord cavitation in syringomyelia: analysis of 105 autopsy cases. j neurosurg 82:802–812, 1995 61. milhorat th, chou mw, trinidad em, et al: chiari i malformation redefined: clinical and radiographic findings for 364 symptomatic patients. neurosurgery 44:1005– 1017, 1999 62. milhorat th, johnson wd, miller ji, et al: surgical treatment of syringomyelia based on magnetic resonance imaging. neurosurgery 31:231–245, 1992 63. milhorat th, bolognese pa (2003) tailored operative technique for chiari type i malformation using intraoperative color doppler ultrasonography. neurosurgery 53:899–905 discussion905-896 64. misao n, hiroaki s, akira h, naruhiko n, yuichi i: pathogenesis of chiari malformation: a morphometric study of the posterior cranial fossa. j neurosurg 16:14491454, 2009 65. momen m almamoun, md., walid k abouzeid, md. efficacy and safety of duraplasty in chiari malformation type-i patients associated with syringomyelia egy spine j volume 17 january 2016. 66. munshi i, frim d, stine-reyes r, et al: effects of posterior fossa decompression with and without duroplasty on chiari malformation-associated hydromyelia. neurosurgery 46: 1384–1390, 2000 67. oldfield eh, muraszko k, shawker th, et al: pathophysiology of syringomyelia associated with chiari i malformation of the cerebellar tonsils. implications for diagnosis and treatment. j neurosurg 80:3–15, 1994 68. paul ks, lye rh, strang fa, et al: arnold–chiari malformation. review of 71 cases. j neurosurg 58:183–187, 1983 69. perrini. p, benedetto.n,tenenbaum.r,di lorenzo.n, extraarachnoidal craniocervical decompression for syringomyelia associated with chiari i malformation inadults: technique assessment, acta neurochir. 149 (2007) 1015–1022, 70. raftopoulos c, sanchez a, matos c, baleriaux d, bank wo, brotchij. hydrosyringomyelia-chiari 1 complex. prospective evaluation of a modified foramen magnum decompression procedure: preliminary results. neurol surg 1993; 39:163-9 71. royo salvador mb. filum system® a brief guide. chiari & scoliosis & syringomyelia foundation. 2017.]. 72. rocque bg, oakes wj (2015) surgical treatment of chiari i malformation. neurosurg clin n am 26:527–531 48 ait bachir mustapha, t. benbouzid 73. sakamoto h, nishikawa m, hakuba a, et al: expansive suboccipital cranioplasty for the treatment of syringomyelia associated with chiari malformation. acta neurochir 141:949–961, 1999 74. santamarta d, kusak me, de campos jm, et al: increased cerebrospinal fluid flow through the foramen of magendie after decompression for chiari i malformation. j neurol neurosurg psychiatry 66:799, 1999 75. schmahmann jd, sherman jc. the cerebellar cognitive affective syndrome. brain 1998; 121 (pt 4): 561-579 76. sindou m, chávez-machuca j, hashish h. craniocervical decompression for chiari type i-malformation, adding extreme lateral foramen magnum opening and expansile duraplasty with arachnoid preservation. technique and long-term functional results in 44 consecutive adult cases—comparison with literature data. acta neurochir (wien). 2002;144(10):1005-1019 77. stanko km, lee ym, rios j et al (2015) improvement of syrinx resolution after tonsillar cautery in pediatric patients with chiari type i malformation. j neurosurg pediatr 30:1–8 78. stovner lj, rinck p: syringomyelia in chiari malformation: relation to extent of cerebellar tissue herniation. neurosurgery 31:913–917, 1992 79. tetsuryu m,, yasuo a, takaomi t, seiichiro e, kentaro c,yoshikazu o, takakazu k reevaluation of foramen magnum decompression with dura left open for chiari i malformation interdisciplinary neurosurgery 10 (2017) 150–154 80. udani v, holly lt, chow d, batzdorf u. posterior fossa reconstruction using titanium plate for the treatment of cerebellar ptosis after decompression for chiari malformation. world neurosurg. 2014; 81(5-6):836-41. 81. vaquero j, martínez r, arias a. syringomyelia-chiari complex: magnetic resonance imaging and clinical evaluation of surgical treatment. j neurosurg. 1990 jul;73(1):64-8. 82. wetjen nm, heiss jd, oldfield eh. time course of syringomyelia resolution following decompression of chiari malformation type i. j neurosurg pediatr. 2008; 1:118–123. 83. williams b. surgery for hindbrain related syringomyelia. in advances and technical standarts in neurosurgery, vol 20, berlin, springer verlag, 1993; 108-164 84. williams, b(chapter in book). management schemes for syringomyelia: surgical indications and nonsurgical management. in: anson j, benzel ec, awad i, eds. syringomyelia and the chiari malformation (neurosurgical topic vol 26), usa: thieme/the american association of neurological surgeons. 1997: pp 125-143 85. williams b: a critical appraisal of posterior fossa surgery for communicating syringomyelia. brain 101:223–250, 1978 86. wu hb, chen j and li am (2010). reconstruction of the cistern magna for treatment of syringomyelia with chiari i malformation. chin. j. pract nerv. dis. 13: 89-90. 87. yamazaki y, tachibana s, takano m, et al: clinical and neuroimaging features of chiari type i malformations with and without associated syringomyelia. neurol med chir 38:541–547, 1998 88. yilmaz a, kanat a, musluman am, et al. when is duraplasty required in the surgical treatment of chiari malformation type i based on tonsillar descending grading scale? world neurosurg. 2011;75(2):307-313. 89. yundt kd, park ts, tantuwaya vs, et al: posterior fossa decompression without duraplasty in infants and young children for treatment of chiari malformation and achondroplasia. pediatr neurosurg 25:221–226, 1996 90. zamel k, galloway g, kosnik ej, et al. intraoperative neurophysiologic monitoring in 80 patients with chiari i malformation: role of duraplasty. j clin neurophysiol 2009; 26:70-5. 91. zhang zq, chen yq, chen ya, wu x, wang yb, li xg. chiari i malformation associated with syringomyelia: a retrospective study of 316 surgically treated patients. spinal cord. 2008;46(5):358-363 92. zhang y, zhang n, qiu h, zhou j, li p, ren m, et al. an efficacy analysis of posterior fossa decompression techniques in the treatment of chiari malfor¬mation with associated syringomyelia. j clin neurosci. 2011; 18(10):1346-9. 93. zuev a.a, pedyash n.v, epifanov d.s, kostenko g.v: results of surgical treatment of syringomyelia associated with chiari 1 malformation. an analysis of 125 cases. pirogov national medical surgical center, moscow, russia. problems of neurosurgery named after n.n. burdenko 1, 2016 doi: 10.33962/roneuro-2022-058 cervical carotid artery vasospasm during cerebral angiography mustafa ismail, muthanna n. abdulqader, fatimah o. ahmed, aktham o. al-khafaj, hosam al-jehani, samer s. hoz romanian neurosurgery (2022) xxxvi (3): pp. 346-349 doi: 10.33962/roneuro-2022-058 www.journals.lapub.co.uk/index.php/roneurosurgery cervical carotid artery vasospasm during cerebral angiography mustafa ismail1, muthanna n. abdulqader2, fatimah o. ahmed1, aktham o. al-khafaj1, hosam al-jehani3, samer s. hoz4 1 department of neurosurgery, college of medicine, university of baghdad, iraq 2 department of neurosurgery, neurosurgical teaching hospital, baghdad, iraq 3 department of neurosurgery, king fahad hospital of the university, imam abdulrahman alfaisal university, dammam, saudi arabia 4 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract background: vasospasm occurs commonly in the intracranial arteries as a complication of subarachnoid haemorrhage. on the other hand, extracranial internal carotid artery (ica) vasospasm is scarce, and it may occur due to mechanical manipulation during cerebral angiography. we report a case of cervical carotid artery vasospasm during diagnostic cerebral angiography, which caused anterior cerebral artery territory hypoperfusion, to discuss potential risk factors. case description: for a 22-year-old female with a ten-year history of epilepsy on multiple drugs, brain magnetic resonance imaging (mri) showed frontal periventricular developmental venous anomaly. diagnostic catheter cerebral angiography was used to better identify the vascular abnormality. in the procedure, extra steps were performed, including instruments being sterilized with cidex® opa solution (phthalaldehyde as the active ingredient), the reuse of the set including the catheters more than twice or triple times, and cold temperature of normal saline that was used in the flushing procedure. under conscious sedation, the procedure went uneventful until the catheterization of the left carotid artery was performed, where severe vasospasm was noticed in the extracranial ica, followed by cessation of flow in the ipsilateral aca. pulling the catheter to a more proximal location in the extracranial ica was performed to alleviate the vasospasm. it took twelve minutes for the circulation to be restored, and that was under continuous irrigation and flushing. the patient did not develop any symptoms throughout the procedure or postprocedural course. conclusion: chemical irritation from the sterilizing agent and reuse of the catheters could cause extracranial ica vasospasm. introduction vasospasm in the intracranial arteries is a common complication of subarachnoid hemorrhage, cerebral vasculitis, and reversible cerebral keywords cerebral angiography, internal carotid artery, vasospasm corresponding author: mustafa ismail department of neurosurgery, university of baghdad / college of medicine. baghdad, iraq mostafa.ismail1700d@comed. uobaghdad.edu.iq copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 347 cervical carotid artery vasospasm during cerebral angiography vasoconstriction syndrome (rcvs) (6,20). extracranial internal carotid artery (ica) vasospasm, on the other hand, is rare, and its potential causes may include ergot poisoning or mechanical manipulation (2,16,8). regarding mechanical irritation, it can attribute either to external manipulation or intraluminal stimulation. intraluminal stimulation can be seen during catheter cerebral angiography, and it may trigger vasospasm in the ica (1,10). however, extracranial vessels vasospasm can occur due to various causes depending on the procedural setting and the patient’s condition. we report a case of cervical carotid artery severe vasospasm that causes anterior cerebral artery (aca) territory hypoperfusion during diagnostic cerebral angiography with a discussion of potential factors. case scenario a 22-year-old female with a ten years history of epilepsy on multiple drugs. brain magnetic resonance imaging (mri) showed frontal periventricular developmental venous anomaly (dva). diagnostic catheter cerebral angiography to better identify the vascular abnormality. the angiography procedure went with the typical steps used in every case in our institution. it is noted that we are obligated to reuse the instruments because of the cost-related issues and the absence of an insurance system in iraq. that is why only the additive step that procedural set was reused more than two times at least after the sterilization with cidex® opa solution (phthalaldehyde as the active ingredient). underwent conscious sedation, the procedure went uneventful until the catheterization of the left carotid artery was performed, where severe vasospasm was noticed in the extracranial ica, followed by cessation of flow in the ipsilateral aca. we tried to pull the catheter to a more proximal position (2 cm below the skull base) in the ica along with irrigation with warm normal saline multiple times was done, and it didn’t work. so, the subsequent trial was to put the catheter in an even more proximal site at the left common carotid artery, and an irrigation procedure was performed again. it took twelve minutes for the aca circulation to be restored, and that was under continuous irrigation and flushing (figure 1). during these events, the patient was assessed clinically because she was under conscious sedation, and fortunately enough, the patient didn’t develop any symptoms throughout the procedure and during the post-procedural course. figure 4. cerebral angiography images. (a) is showing the left ica (anteroposterior view) showing the normal (prevasospasm) ica with its branches. while (b) is showing ica (anteroposterior view) showing spasm in the cervical of the ica with ipsilateral aca flow absence. (c) shows left ica (anteroposterior view) showing partial resolution of the vasospasm in the cervical ica with reestablishment blood flow in the aca. discussion intracranial vasospasm is temporary, focal, or diffuse narrowing in the caliber of intracranial arteries that mainly contribute to the arterial wall’s smooth muscle contraction (17). it can be classified into intracranial or extracranial, depending on the ica segments. intracranial vasculatures are prone to vasospasm compared to extracranial (5,9). however, extracranial vasculatures vasospasm was also reported (2,16). extracranial ica vasospasm can be attributed to many factors that may be proceduralassociated or patient-related. in cerebral angiography, advancing the catheter and wires in the ica may induce mechanical vasospasm. ishihara h et al, examined 147 patients who underwent therapeutic neuro-endovascular procedures; severe vasospasm was noted in up to 40% of the sample (8). individuals with significant anxiety, having a history of vasospasm in diagnostic angiography, and increase vascular tortuosity with a degree ≥ 30° vessel bends were all potential risk factors for severe vasospasm (12). patients with high anxiety have a high probability of developing vasospasm in both general anesthesia and conscious sedation because of the increase in the sympathetic response in the body during the procedure (8,12). the history of diagnostic angiography and the increase in vascular tortuosity may cause vasospasm because of mechanical irritation of the vascular lumen. 348 mustafa ismail, muthanna n. abdulqader, fatimah o. ahmed et al. based on the literature review, the intracranial location of the catheter within the ica is a well-known cause of irritation in the form of pain or vasospasm (2,8,9). however, extracranial ica vasospasm is either not well reported or usually doesn’t affect the distal flow (9). during the procedure, the wire may induce vasospasm if it reaches the skull base. however, in our case and our practice, we localize the wire in the proximal portion of the cervical carotid. here, we describe a case with apparent distal flow affection in the form of ipsilateral aca flow cessation due to cervical carotid vasospasm. vasospasm due to mechanical irritation caused by sterilizing material is not described in the literature. in our case, after exclusion of the above risk factors, we propose the following points as potential causes for severe vasospasm, 1) chemical irritation with the use of cidex® opa solution, which has phthalaldehyde as the active ingredient, the primary tool for the sterilization of the procedure tools 2) re-sterilization of the equipment in the procedure and the set may be used twice or triple times 3) cold temperature of normal saline that was used in the flushing during the procedure. in the procedure, the reuse of the catheters has obvious advantages from a cost perspective and has several disadvantages because catheters are made for single-use (15). the practice of reusing catheters in cerebral angiography is common, and in iraq, the reusage can occur particularly when there is a limitation of resources. the treatment of vasospasm in the setting of subarachnoid hemorrhage is well established by using calcium channel blockers (4,7). mechanical irritation-related-vasospasm treatment needs further studies because it is clinically significant, and it is difficult to pinpoint the cause. there are a few reports on the efficacy of intra-arterial injections of calcium channel blockers, papaverine, and lidocaine in the mechanical irritation-related-vasospasm. still, no comprehensive studies have been conducted on this topic (3,14). reports listed that deep anesthesia or muscle relaxants may effectively reduce vasospasm and others suggested warm compression, especially while using the radial access (11). we propose different steps in the management of vasospasm in the setting of neuro-endovascular procedure, 1) dragging the catheter in a more proximal portion within the affected artery (in our case, the cervical carotid), 2) copious irrigation with normal saline, 3) administration of vasodilators as discussed above, 4) the use of angioplasty. the use of one of these steps or a combination may result in the resolution of the vasospasm. in our case, continuous irrigation with warm normal saline was sufficient to resolve the vasospasm and restore the distal circulation. as for prevention, vasospasm is expected to be relieved by prophylactic treatments in patients with risk factors such as sedative drugs and warm compresses (3,12). also, using the optimum sterilization technique is needed as well as utilizing the tools once only is the preferable setting. while in limited resources setting where re-usage represents the only viable option, sufficient irrigation to ensure clearance of any sterilizing agent is mandatory. flushing and the irrigating fluid’ temperature can be monitored to use the fluid with body temperature as much as possible. clinical assessment of the patient is quite ready if the patient is under conscious sedation, and this fits well for diagnostic cerebral angiography. however, in certain cases, general anesthesia can be applied. sriganesh k et al, proposed that the bispectral index bis might be utilized to detect and monitor substantial changes in regional cerebral blood flow following neuro-endovascular procedures with general anesthesia (19). in our case, the patient was on conscious sedation, the assessment of vasospasm was imminent, and it was carried out radiologically and clinically during the procedure. in summary, vasospasm may occur in diagnostic cerebral angiography due to mechanical manipulation, chemical irritation, equipment usage, and temperature fluctuations in normal saline. the treatment options include the administration of intra-arterial calcium channel blockers or papaverine, or lidocaine. prevention can be achieved by targeting the risk factors. vasospasm as a complication during endovascular management should be highlighted and kept in mind during the explanation of the procedure to the patient, and it should be disclosed as there is a plurality of causes of this condition; we haven’t scratched its surfaces yet. conclusion cervical carotid artery severe vasospasm is a rare complication during diagnostic cerebral angiography. chemical irritation from the sterilizing 349 cervical carotid artery vasospasm during cerebral angiography agent and re-usage of the catheters should be kept in mind as potential causes of vasospasm. references 1. al-jehani h, angle m, marcoux j, teitelbaum j. early abnormal transient hyperemic response test can predict delayed ischemic neurologic deficit in subarachnoid hemorrhage. crit ultrasound j. 2018 jan 4;10(1):1. 2. arning c, schrattenholzer a, lachenmayer l. cervical carotid artery vasospasms causing cerebral ischemia: detection by immediate vascular ultrasonographic investigation. stroke 1998;29:1063–1066. 3. biondi a, ricciardi gk, puybasset l, abdennour l, longo m, chiras j, van effenterre r: intra-arterial nimodipine for the treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results. ajnr am j neuroradiol 25: 1067– 1076, 2004. 4. coon al, colby gp, mack wj, feng l, meyers p, sander connolly e, jr: treatment of mechanically-induced vasospasm of the carotid artery in a primate using intraarterial verapamil: a technical case report. bmc cardiovasc disord 4: 11, 2004. 5. da ros v, scaggiante j, pitocchi f, sallustio f, lattanzi s, umana ge, chaurasia b, di poggio mb, toscano g, bigliani cr, ruggiero m. mechanical thrombectomy in acute ischemic stroke with tandem occlusions: impact of extracranial carotid lesion etiology on endovascular management and outcome. neurosurgical focus. 2021 jul 1;51(1):e6 6. dorsch n: a clinical review of cerebral vasospasm and delayed ischaemia following aneurysm rupture. acta neurochir suppl 2011;110:5-6. 7. eckard da, purdy pd, girson ms, samson d, kopitnik t, batjer h: intraarterial papaverine for relief of catheterinduced intracranial vasospasm. ajr am j roentgenol 158: 883– 884, 1992. 8. ishihara h, ishihara s, niimi j, et al. risk factors and prevention of guiding catheter-induced vasospasm in neuroendovascular treatment. neurol med chir (tokyo). 2015;55(3):261-265. 9. janzarik wg, ringleb pa, reinhard m, rauer s. recurrent extracranial carotid artery vasospasms: report of 2 cases. stroke. 2006 aug 1;37(8):2170-3. 10. miura i, kawashima a, hayashi m, tanda a, ishikawa t, kawamata t. extracranial internal carotid artery vasospasm during thrombectomy. the neuroradiology journal. 2018 jun;31(3):313-6. 11. moeller s, hilz mj, blinzler c, koehn j, doerfler a, schwab s, köhrmann m. extracranial internal carotid artery vasospasm due to sympathetic dysfunction. neurology. 2012 jun 5;78(23):1892-4. 12. muehlschlegel s, rordorf g, bodock m, sims jr: dantrolene mediates vasorelaxation in cerebral vasoconstriction: a case series. neurocrit care 10: 116– 121, 2009. 13. muehlschlegel s, rordorf g, sims j: effects of a single dose of dantrolene in patients with cerebral vasospasm after subarachnoid hemorrhage: a prospective pilot study. stroke 42: 1301– 1306, 2011. 14. oran i, cinar c: continuous intra-arterial infusion of nimodipine during embolization of cerebral aneurysms associated with vasospasm. ajnr am j neuroradiol 29: 291– 295, 2008. 15. ribeiro sm, graziano ku, alfa mm, goveia vr. reuse of cardiac catheters: a review. brazilian journal of cardiovascular surgery. 2006;21:334-42. 16. senter hj, lieverman an, pinto r: cerebral manifestations of ergotism. report of a case and review of the literature. stroke 1976;7:88-92. 17. singh j, wicks rt, wilson ja, wolfe sq, fargen km. radiographic vasospasm and clinical (symptomatic) vasospasm. inintracranial aneurysms 2018 jan 1 (pp. 161-178). academic press. 18. smith pg, killeen te: carotid artery vasospasm complicating extensive skull base surgery: cause, prevention, and management. otolaryngol head neck surg 1987;97:1-7. 19. sriganesh k, chatterjee n, singha s: bispectral index monitoring facilitates early detection of catheter-induced vasospasm during neuro-endovascular procedures. acta anaesthesiol scand 53: 406– 407, 2009. 20. wöpking s, kastrup a, lentschig m, brunner f. recurrent strokes due to transient vasospasms of the extracranial internal carotid artery. case reports in neurology. 2013;5(2):143-8. microsoft word 18chaurasiaid_therapeutic 654 | chaurasia et al palmitoylethanolamide in the management of neuropathic pain             doi: 10.2478/romneu-2018-0085 therapeutic benefit of palmitoylethanolamide in the management of neuropathic pain i.d. chaurasia, kunal vinayak, shashikant tiwari, prateek malpani, sheikh behram, mahim koshariya department of surgery, gandhi medical college & associated hamidia hospital, bhopal, m.p., india abstract: background: neuropathic pain is defined by international association for the study of pain (iasp) as “pain caused by a lesion or disease of the somatosensory nervous system”. elderly patients generally have high incidence of chronic neuropathic pain. the safe and effective treatment for chronic pain is a large public health concern. palmitoylethanolamide (pea) is an endogenously produced amide cannabimimetic compound with tissue protection and anti-inflammatory activity. objectives: the aim & objective of this study is to evaluate the effectiveness and safety of palmitoylethanolamide (pea) in patients suffering from neuropathic/chronic pain. study designed: prospective study. materials and methods: the study was conducted in the neurosurgery unit of surgery department in gandhi medical college & associated hamidia hospital, bhopal. a total no. of 150 patients aged 20-78 years were included in the study and divided into two groups, group i (study group) and the group ii (control group) pea was given to group i to evaluate the effect of pea in neuropathic pain. result: we studied 150 patients with pea for 60 days in a dose of 354 mg orally three times (tds) a day for first 10 days and then two times (bid) a day for 50 days. it is available in india by the name of palmiges. pea was associated with greater pain reduction in the study group compared to the placebo controlled group. the primary outcome measured was the mean pain reduction evaluated by vas scale. conclusion: pea seems to be useful in the treatment of neuropathic / chronic pain and it is well tolerated in patients in study group. palmiges pea reduces the inflammation in neuropathic pain, which results in lowering/reduction of neuropathic pain. controlled trials are further needed to prove efficacy and reliability and also to find out the adverse reaction associated with the drug. key words: pea, palmitoylethanolamide, neuropathic pain, analgesics, vas (visual analogue score) introduction neuropathic pain is a complex condition that has its origin in a primary lesion or dysfunction of any part of the nervous system from the peripheral receptor to the brain. persistent neuropathic pain often interferes with sleep, work, recreational activities and the romanian neurosurgery (2018) xxxii 4: 654 661 | 655             emotional state of the individual who suffers from it, thus affecting quality of life [1]. neuropathic pain is usually described as the perception of strange or unusual painful sensations like burning, stabbing or lancing pains experienced as electrical discharges or other painful sensations [2,3] . neuropathic pain may be evoked by mechanical, thermal or chemical stimuli. the global prevalence: reported in the literature •a review of the epidemiology of chronic pain found that there is still no accurate estimate available for the population prevalence of neuropathic pain (smith et al.2012). [4] •overall, neuropathic pain affects 7-10% of the general population. •in the primary care setting, the prevalence has been reported to be between 2 to 11%. •by neuropathy symptom score (nss) and neuropathy disability score (nds) criteria, the prevalence of dpn was 29.2%. •in cancer patients the prevalence is 19%. in indian scenario: •the prevalence of neuropathic pain in indian scenario is difficult to establish, as there are many confounding factors that may lead to under reporting of neuropathic pain. •the prevalence in males is around 26.1% and females is 33.8%, whereas prevalence of neuropathic pain in cancer patients is 19%. •about 1% to 37% of chronic lower back pain patients may have a neuropathic component related to it. •prevalence of neuropathic pain in low backache-related leg pain (lblp) patients varies from 19% to 80%. •a study done by ind inep study group in indian patients in the year 2008 suggests that painful diabetic neuropathy is the most common cause of neuropathic pain (72%). •ind inep study group also suggests that, about 50% of patients reported co-morbid mood disorders, while 67% reported medication-related adverse event in the preceding week. inflammation: inflammation is the response of living tissue to injury. it involves a well-organized cascade of fluid and cellular changes within living tissue. the inflammatory process is of great significance in the development of neuropathic pain (np) [5]. pea, an endogenously produced amide has been established to work on the inflammatory pathways acting as a pacifier against inflammation. in neuropathic pain, the amount of the amide reduces drastically in the body resulting in aggravated inflammation and furtherance of diseased condition [6] . the endogenously produced faah (fatty acid amide hydrolase) enzyme further degrades the available amide, further reducing its quantity and effectiveness. palmiges (pea) is an endogenously produced amide. pea, genistein and daidzein function to counter the action of faah enzyme, thereby improving the condition of aggravated inflammation, which is the root cause of neuropathic pain [7]. current treatment modalities and their drawbacks: •current treatment drugs such as gabapentin, pregabalin and duloxetine etc. have annoying side effects such as drowsiness, dizziness, blurred vision, somnolence, peripheral edema etc. moreover, using these drugs in the long term causes desensitization 656 | chaurasia et al palmitoylethanolamide in the management of neuropathic pain             of neuron receptors. therefore, the dose of these drugs has to be increased to elicit the desired response and that leads to more number of side effects. in addition, some drugs require dose adjustment in renal impairment. hence, the current treatment paradigms have some gaps and require some new arsenal to fight against neuropathic pain. thus, what is needed at this critical juncture is a solution which corroborates to the core of neuropathic pain with no side effects. palmiges contains the following components: a. palmitoylethanolamide (pea): •pea is considered an endogenous peroxisome proliferator activated receptors (ppar) agonist or activator, interacting with this receptor to inhibit inflammatory pathways & oxidative stress. •during neuropathic pain, pea can modulate the ppar pathway that is able to attenuate nuclear factor kappa b cells (nfkb) induced inflammatory factors or tumor necrosis factor (il-1 or tnf), inhibit infiltration and activation of mc, reduce mesangial matrix proliferation induced by reactive oxidative stress (ros) which then resulted in albuminuria [8] . b. genistein: •genistein is a faah inhibitor that not only prevents the degradation of pea from faah enzyme in the body but also exerts synergistic effect with pea to reduce oxidative stress in the overinflamed neuronal cells. c. daidzein: •daidzein belongs to the class of isoflavones and serves as a potent faah inhibitor in conjunction with genistein. it works as a competitive binder to faah disallowing it to degrade the externally supplemented pea. d. mpfaitech: a technology to ensure the proprietary blend is presented in a form that could be easily absorbed in the human body. palmitoylethanolamide (pea) is a cannabimimetic compound which reduces neuropathic pain. it is a special food for medical purpose in the treatment of chronic pain. material and methods the study includes patients with neuropathic pain and pain due to various causes like chemo-therapy induced neuropathic pain, chronic pain, trigeminal neuralgia, lower back pain and cervical spondylosis pain etc. these patients reported in the outpatient department (opd) of neurosurgery of hamidia hospital bhopal. in a period of four months total 150 patients with neuropathic pain between age group of 20-78 years were studied. male patients were 94 and female patients were 56. they were divided into two groups each consisting of 75 patients. the control group received usual conventional treatment like nsaid’s, antiepileptics (carbamazepine, gabapentein or pregabalin etc.), snris (duloxetine), opioids (acetaminophen, tramadol, tapendol etc.) or tcas (amitriptolene, nortreptolene). the study group patients received pea (palmiges) daily, three times a day for 10 days (tds), and then two times a day (bid) for 50 days. patients were allowed to continue with their usual treatment if they had other comorbidities. pain reduction was more evident in group i (study group) treated with romanian neurosurgery (2018) xxxii 4: 654 661 | 657             pea as compared to controlled group. source of data: 150 patients were examined and treated on opd basis in the neurosurgery opd of hamidia hospital bhopal from oct 2017 to feb 2018 and 14 patients were admitted in the neurosurgery unit of surgery department. discussion neuropathic pain can be treated with neuroepileptics, antidepressants and opioids whereas musculoskeletal pain can be treated with acetaminophen and non-steroidal antiinflammatory (nsaid) drugs. chronic use of analgesics is often limited by side effect, toxicity and diminished patient compliance and is a problem, especially in older patients. neuropathic pain results from damage or disease affecting the somatosensory system. up to 7-8% of the western population is affected and in 5%, it may be severe also. treatment of neuropathic pain is challenging because about 50% of patients with neuropathic pain get partial relief from treatment which currently comprises of opioids, nsaids, and antiepileptics etc. so the choice of treatment for neuropathic pain should always be taken into consideration, besides efficacy, safety and tolerability of the treatment and interaction with other concomitant treatments. the draw backs of current drugs in neuropathic pain and need of new solution: current treatment options for neuropathic pain are mainly focused on neuronal system suppressing gaba or other inhibitory receptors. most of the drugs used for neuropathic pain cause drowsiness, dizziness, blurred vision, somnolence, peripheral edema, psychomotor slowing and paresthesia and many more. moreover, using these drugs on long term basis causes desensitization of receptors. therefore, there is an increase in the dose of these drugs to elicit the desired response and that leads to more number of side effects. in conclusion, the current treatment paradigms have some gaps and require some new arsenal to fight against neuropathic pain. the second described treatment is pea. pea has high affinity to the nuclear peroxisome proliferator activated receptors α (ppar-α) and pea has indeed analgesic and antiinflammatory effects in clinical trials. biosynthesis of pea in tissues, live neurons and glial cells occurs in inflammatory and chronic pain states [9]. when given orally, pea has almost no side effect, though it has clear pain reducing properties in various pain states [10]. it seems that pea reduces pain via the natural modulation pathway and besides modulation of the central nervous system, through the release of endorphins, serotonin, norepinephrine and dopamine. pain reducing effects of acupuncture can also be explained by suppression of activated glial cell [11]. pea may have a synergistic effect in modulating glial cells, mast cells and neurons [12s]. we often observe pain reduction when we add pea to our treatment. pea also enhances the analgesic effect of compounds such as pregabalin and amitriptyline. in 1986, the famous neuroscientist professor erminio costa delivered a key note lecture in washington, bearing the title “to follow where nature leads”. in this speech costa talked with great vision about how 658 | chaurasia et al palmitoylethanolamide in the management of neuropathic pain             nature itself can become our tutor in developing new drugs. pea is one of these molecules entering clinical use and developed according to costa’s vision. that is why pea seems such a good compound to combine with other treatment modalities. result pea (palmitoylethanolamide) generally provided better pain relief than placebo in a comparison that includes three different chronic neuropathic pain conditions (trigeminal neuralgia, diabetic neuropathy and cervical pain). there was some indication of pain improvement, mainly over the short term, but with poorly defined outcome. the mean decrease on the vas was largest in the study group: a reduction from 7.1 to 2.1 which is more than 50% pain reduction. in the control group, the vas score decreased from 6.6 to 4.6. pea resulted in a significant reduction in pain symptoms in neuropathic pain after 7 weeks (49 days). the median values obtained from tss (total symptom score) and nspi (neuropathic pain symptoms inventory) were compared to base level at many observation points until the end of treatment at 60 days confirming a significant attenuation (p<0.001) in the intensity and presence of symptoms. after completion of treatment i.e. after 60 days the same significant reduction (p<0.001) was seen in relation to the frequency and intensity of symptoms like pain, burning, numbness and paresthesia. what we have is an indication that pea can produce good level of pain relief for some patients with distressing chronic painful conditions. figure 1 50% decrease in vas in study and control groups romanian neurosurgery (2018) xxxii 4: 654 661 | 659             figure 2 the mean decrease on the vas was largest in the study group: a reduction from 7.1 to 2.1 which is more than 50% pain reduction. in the control group the vas score decreased from 6.6 to 4.6 figure 3 effect of pea on painful neuropathy evaluated by michigan neuropathy screening instrument (mnsi), neuropathic pain symptoms inventory (npsi) and total symptom score (tss),. analysis of variance shows a significantly decreased pain intensity and symptom scores observed by mnsi, tnpsi and tss (𝑃 < 0.0001) during the treatment period 660 | chaurasia et al palmitoylethanolamide in the management of neuropathic pain             figure 4 effect of micronized pea on each neuropathic pain symptom assessed by total symptom score (tss). the intensity and frequency evaluated by tss, show a significant mitigation (𝑃 < 0.0001) after 60 days of treatment compared to baseline. this effect was persistent even after one month of treatment discontinuation in this study the important observation is that a clinical and statistical difference was found that after 7 weeks (49 days) and onset of pain reduction was at 2 weeks (14 days) but the pain reduction at 7th week was satisfactory. these observations support the recommendation to use pea for at least 2 months before evaluating the result. overall completeness and applicability of evidence available include: •limited size •short duration •inadequate outcome •incomplete outcome assessment in order to be sure that pea works in neuropathic/chronic pain and to be confident of the magnitude of the effect, the ideal would be several large randomized double blind studies comparing pea at sensible doses with placebo over 8 to 12 weeks. conclusion chronic pain management remains a challenge for the clinician. pea induced pain relief is progressive, age and gender independent and not related with the etiopathogenesis of chronic pain. pea also controls the mechanism common to different conditions where neuropathic pain is associated e.g. neuro inflammation. pea is safe and well tolerated treatment for control/reduction of chronic neuropathic pain and can be combined with other standard/routinely used analgesic medications. pea possesses intrinsic efficacy towards syndromes co-morbid with chronic pain e.g. depression and anxiety. pea also lacks acute and chronic toxicity and is not associated with gastric mucosal lesions. that is why it has become possible to include pea in romanian neurosurgery (2018) xxxii 4: 654 661 | 661             new class of therapeutic agent called food for special medical purposes “fsmp”. pea is safe and well tolerated treatment for the reduction of neuropathic pain and can easily be combined as well added to classical medication without fear of negative interactions. correspondence dr. i.d. chaurasia ms, mch, associate professor neurosurgery email: chaurasiaid@gmail.com references 1. raja s. and haythornthwaite j. combination therapy for neuropathic painwhich drugs, which combination, which patients? new england journal of medicine 2005; 352:1373-1375. 2. ropper a. and brown r. and victor’s principles of neurology chapter 8, 8th edition, philadelphia saunders company 2000. 3. woolf cj, mannion rj. neuropathic pain: aetiology, symptoms, mechanisms, and management. the lancet. 1999 jun 5;353(9168):1959-64. 4. smith bh, torrance n, ferguson ja, et al. towards a definition of refractory neuropathic pain for epidemiological research. an international delphi survey of experts. biomed central neurology. 2012;12:29. [pubmed] 5. schomberg d, ahmed m, miranpuri g, olson j, resnick dk. neuropathic pain: role of inflammation, immune response, and ion channel activity in central injury mechanisms. annals of neurosciences. 2012 jul;19(3):125. 6. lunelta r le moli, g grasso aw l. sangiorgiodiabetes research and clinical practice vol 39 pg 165-172 1998. 7. padur c., briane s., jann et al. validation of italian version of the neuropathic pain system inventory in peripheral nervous system disease, neurological sciences vol 30, no 2 pg 99-106, 2009. 8. bouhassira d, attal n, fermanian j, alchaar h, gautron m, masquelier e, rostaing s, lanteri-minet m, collin e, grisart j, boureau f. development and validation of the neuropathic pain symptom inventory. pain. 2004 apr 1;108(3):248-57. 9. petrosino s, iuvone t, di marzo v. n-palmitoylethanolamine: biochemistry and new therapeutic opportunities. biochimie. 2010 jun 1;92(6):724-7. 10. biasiotta, a., la cesa, s., leone, c., di stefano, g., truini, a. and cruccu, g., 2010. 265 efficacy of palmitoylethanolamide in patients with painful neuropathy. a clinical and neurophysiological open study. preliminary results. european journal of pain supplements, 4(s1), pp.77-77. 11. liang ll, yang jl, lü n, gu xy, zhang yq, zhao zq. synergetic analgesia of propentofylline and electroacupuncture by interrupting spinal glial function in rats. neurochemical research. 2010 nov 1;35(11):1780-6. 12. muccioli gg, stella n. microglia produce and hydrolyze palmitoylethanolamide. neuropharmacology. 2008 jan 1;54(1):16-22. romanian neurosurgery (2019) xxxiii (2): pp. 127-134 doi: 10.33962/roneuro-2019-025 www.journals.lapub.co.uk/index.php/roneurosurgery initial single centre experience with barrel vrd stent in large neck aneurisms cristian mihalea1,2, felicia otilia humulescu3,4, hazem abdelkhalek1,5, sorin pescariu6, bogdan valeriu popa7, horia ples1 1 department of neurosurgery, “victor babes” university of medicine and pharmacy, timisoara, romania 2 department of interventional neuroradiology, neuri brain vascular center, bicêtre hospital, le kremlin-bicêtre, france 3 bucharest university of economic studies, faculty of cybernetics, statistics and economic informatics, romania 4 bucharest university of medicine and pharmacy faculty, faculty of dental medicine, romania 5 department of neuropsychiatry, tanta university hospital, tanta, egypt 6 cardiology department, “victor-babes” university of medicine and pharmacy, timisoara, romania 7 department of radiology and medical imaging, “floreasca” clinical emergency hospital, “carol davila” university of medicine and pharmacy, bucharest, romania abstract introduction. despite the use of new techniques, such as y-stenting, the waffle-cone technique and intrasaccular flow disrupters the treatment of wide-neck bifurcation aneurysms is still challenging, especially for those where adjacent branches are arising at the neck level. moreover, the use of flow diverter stents in bifurcation aneurysms has been proposed by several teams, although the results remain controversial. this study is reflecting initial experience in our department with a relatively new device available on the market: barrel vrd stent. the unique design feature of the device is the “belly-like” central part of the stent which protects the adjacent branches. methods. we retrospectively reviewed all patients in whom stenting with braided or laser-cut stents had been performed in our center. three patients were identified and analyzed. technical success, complications, immediate angiographic outcomes, procedural data, are reported here. results. one mca bifurcation and two basilar tip large neck aneurysms with one branch arising from the neck level have been identified. technical success was achieved in all procedures. overall procedure-related morbidity and mortality was 0%. in the immediate post-treatment angiography, adequate occlusion (neck remnant or total occlusion) was observed in all patients. shortand mild-term followup angiography showed adequate occlusion of the aneurysms. conclusions. in this small case series, retrospective single-center analysis we showed keywords cerebral aneurysms, barrel stent, endovascular treatment corresponding author: cristian mihalea department of neurosurgery, “victor babes” university of medicine and pharmacy, timisoara, romania cristianmihalea@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 128 cristian mihalea, felicia otilia humulescu, hazem abdelkhalek that barrel vrd stent assisted coiling is a safe and feasible technique. moreover, it offers an elegant and effective endovascular solution for large neck basilar tip aneurysms on which the neurosurgical clipping remains challenging. introduction endovascular treatment is the standard first-line therapy for both ruptured and unruptured intracranial aneurysms [1-3]. unfavorable anatomy as wide-neck aneurysms also require adjuvant therapy to be treated safety and efficiently [4, 5] knowing the fact that simple coiling or balloonassisted coiling has a high risk of coil protrusion in to the parent vessel. the use of stent-assisted coil embolization for wide-necked intracranial aneurysms has significantly expanded the range of aneurysms that are candidates for endovascular treatment [6-8]. however, single stent-assisted coiling in particular situations does not provide sufficient support when the neck of the aneurysm is centered on the bifurcation branches. in these cases, the use of two stents or y-stenting has been proposed [9-12]. from technical point of view this technique remain challenging but it has high immediate and long-term occlusion rates [11].the waffle-cone technique is a feasible alternative to ystenting and consists of deploying the distal end of a dedicated stent, such as pconus (phenox gmbh, bochum, germany) and pulserider (pulsar vascular, san jose, california, usa), inside the aneurysm sac and the proximal end in the parent artery. coiling is performed through the expanded distal end of the stent. the main advantage of this technique is that both branches of the bifurcation are not involved in endovascular treatment. small retrospective studies have evaluated and reported its safety and efficacy [13-15]. in asymmetric bifurcations where two or even three branches are arising from the neck level those techniques described above offer limited solutions and unpredictable branch protection during coiling. the use of flow diverters in wide-neck bifurcation aneurysms (wnba) remains controversial owing to inconsistent patency of bifurcation branches covered by the stent and poor occlusion of the aneurysm at follow-up angiograms [16]. targeted, large prospective multicenter studies are needed to evaluate the safety and efficacy of this treatment specifically for wnba. intrasaccular flow disruption devices, such as web (woven endobridge; microvention, tustin, california, usa) are presently a feasible and efficient tool of wnba treatment; moreover, retrospective and prospective studies confirmed the high safety level and low morbidity and mortality rates [17,18]. despite the advantages of flow diversion in the case of complex irregular shapes and bi-lobed aneurysms or asymmetrical bifurcations, placing the web device proved to be unfeasible or at least very challenging even in experienced hands. in this context a single stent with “belly-like” central part which protects the adjacent branches in wnba seems to be a promising solution for this type of aneurysms. here, we report our single-center experience with barrel vrd stent assisted coiling, with clinical and angiographic periprocedural results, in order to evaluate the safety and efficiency of this technique. materials and methods population we retrospectively reviewed interventional neuroradiology database records to identify patients in whom stenting with laser-cut or braided stents had been performed. we identified three patients treated with this technique in our institution between april 2015 and august 2018. demographic data, aneurysm location and size are summarized in table 1. all aneurysms were unruptured; all of them were primary endovascular treatments. in all cases, the aneurysm neck was wide, with an average dome to neck ratio of 1.49. the barrel vascular reconstruction device the barrel device (medtronic/covidien, irvine, california, usa) is a nitinol self-expandable, closedcell laser cut micro-stent with electrolytic detachment system. two main characteristics offer two this type of stent the feasibility for wnba’s treatments. main advantage is that due to “barrel” design that is represented by the “belly-like” central part of the stent protects the adjacent branches. secondly due to the property to be re-sheathable up to three times. endovascular technique dual antiplatelet therapy was prescribed 2 days before the procedure as in all stent-assisted coiling treatment. in all patients, endovascular treatment was performed using a monoplane angiography unit with three-dimensional rotational capability (allura monoplan; philips, best, the netherlands) under general anesthesia and systemic heparinization. 129 initial single centre experience with barrel vrd stent in large neck aneurisms after the procedure, dual antiplatelet therapy (ticagrelor 2 × 90 mg/day and aspirin 150 mg/day) was administered for the first 3 months, and aspirin 160 mg/day alone was administered for the following 9 months. in our department clopidogrel (plavix 75 mg) was replaced by ticagrelor (brilique 90 mg) due to multiples advantages of the last one and also knowing that 20-25% of the subjects are naturally resistant to clopidogrel. a baseline activated clotting time (act) was obtained prior to the bolus infusion of heparin (30 to 50 iu/kg body weight), and hourly thereafter. the bolus infusion of heparin was followed by a continuous drip (1000 to 1500 iu/h), with the purpose of doubling the baseline act. from the femoral arterial access, a 6 fr 100 cm distal-access catheter (envoy/codman, usa) was placed into the internal carotid artery or in the dominant vertebral artery. in all procedures, the most challenging branch of the bifurcation was first catheterized in order to place the distal tip of the stent. then the simple deploying by retrieving the 0.021-inch microcatheter (rebar 18, medtronic, irvine, ca, usa) was performed similar to solitaire ab stent. the convenient placement of the “belly-like” central part of the stent was analyzed during the deployment in subtracted and non-subtracted angiograms. in all procedures the barrel stent used was bv 4065 (“belly” diameter was 6,5mm and 4 mm proximal end diameter and 3.5 mm distal diameter) and in case 1 and 3 the satisfactory positioning of the stent was achieved after a first deployment. the precise placement of the “belly-like” central part of the stent is relatively simple to archive by the first attempt (2 out of our 3 cases). in one case the good positioning was achieved after third attempt due to acute angle between left pca basilar trunk and consecutive drop of the microcatheter whine deploying the device. each time the barrel stent was safely re-sheeted inside rebar 18 microcatheter and a new catheterization of the left pca was done. in all three cases the aneurismal sac was microcatheterized easily through barrel interstices after stent placement and detachment (no jailing technique was used). in all procedures, passing through both stents studs with 0.014-inch microguidewire was achieved without any technical incident. finally, the aneurysm was coiled using detachable coils. after coiling in all three cases no collapse of the stent has been noticed neither thromboembolic event was noticed in the protected neck-sided branch. complications no intra-procedural or delayed thromboembolic or hemorrhagic complication were noticed for all three cases treated in our department. follow-up protocol at the end of the procedure, immediate control angiograms were obtained from all patients. modified raymond–roy occlusion classification (rroc) was used for grading the occlusion status of coiled aneurysms. patients underwent angio-mri at 3 months to reassess filling status of the coiled aneurysm, in-stent stenosis, and thrombosis. the modified rankin scale was used for scoring neurologic status at discharge and follow-up. results all three treated aneurysms were un-ruptured. procedural details and follow-up angiographic results are shown in table 1. treatment was successfully performed in all three cases. angiographic results were categorized according to the revised rroc into one of the following groups: complete occlusion (rr1), remnant neck (rr2), or residual aneurysm (rr3) by two senior neuroradiologysts in consensus. there was no evidence of in-stent stenosis or thrombosis during follow-up angio-mri. discussion stent-assisted coiling represents a wide world accepted solution for the treatment of wide-neck cerebral aneurysms over treatment with conventional coiling targeting higher rates of complete occlusion and lower rates of recurrence at long-term follow-up. however, treatment of wnba and fusiform aneurysms is requiring a higher level of interventional neuro-endovascular skills and frequently requires a second stent (that is, a y-, xor waffle-cone-stenting configuration [19–20]) or dedicated endovascular stents such as pconus, pulserider, and barrel stent [21]. there are currently little clinical data on these last three devices available. 130 cristian mihalea, felicia otilia humulescu, hazem abdelkhalek despite the potential benefit of single stent-assisted coiling, complex aneurysms can pose a significant challenge for achieving immediate and durable embolization. specifically, for wide-necked aneurysms located at shallow angle arterial bifurcations, single stent-mediated coiling may provide insufficient support of the coil mass to prevent coil herniation through the aneurysm neck. a special situation is represented by the aneurysms with branches incorporated in the aneurysm base; kim et al. [22] published a study with 68 patients with 78 intracranial aneurysms treated with multiple endovascular techniques: single-catheter coiling, multi-catheter coiling, balloon-assisted coiling, stentassisted coiling, and combined techniques. 5.8% morbidity have been reported in this study and no mortality. 10 out of 55 (18%) intracranial aneurysms had a recanalization from which six were retreated. it represents a significant proportion and, moreover, retreatments are even more challenging in this situation. in 2004, chow et al detailed the y-stent technique [12], whereby double open-cell neuroform stents (boston scientific, fremont, ca, usa) were deployed sequentially — first, proximal to the arterial bifurcation, and then into each arterial branch followed by coiling of the aneurysm sac. this represented an efficient endovascular solution for bifurcation lesions that are too complex for coiling alone, remodeling technique, or single-stent assisted coiling. several authors have evaluated this technique in retrospective single-center studies, mostly including unruptured aneurysms [9-11]. the safety was relatively limited: bartolini et al. reported 10.0% procedure-related permanent neurologic deficits and 1.0% death [10]. however, in other studies, the rate of intra-procedural complications was lower, with 4.2% in the study by limbucci et al. and 2.7% in the study by yavuz et al. with mortality rates of 2.1% and 0.5%, respectively [9,11]. at longterm follow-up, the rate of complete aneurysm occlusion was high with 85.8% in the bartolini study, 95.7% in the yavuz study, and 93.6% in the limbucci study. several types of stents can be used for ystenting; mainly open-cell stents (neuroform, stryker neurovascular, fremont, california, usa) or closedcell stents (enterprise, codman, miami lakes, florida, usa) have been reported. intrasaccular flow disruption devices, such as the web device, are specially designed for the treatment of wnba and have shown a high level of safety, with morbidity and mortality at 1-month post-procedure of 2.7% and 0.0%, respectively [23]. the efficacy of this technique also proved to be higher than single-stent assisted coiling, and adequate occlusion was reported in 82.0% of cases at 12 months follow-up (complete occlusion: 56.0% and neck remnant: 26.0%). despite progressive technological improvements, such as the replacement of dual layer by single layer versions, and progressive decreases in the diameter of the micro-catheter used to deliver the device, there are still bifurcation aneurysms with challenging anatomy which are not suitable for this technique. more recently new web-balloon remodeling techniques have been described by mihalea et al [24] where the web device can be deployed and tilted in the aneurysm sac using so called “balloon remodeling technique” and it may represent a feasible solution for this type of wide neck bifurcation aneurysms. in this category of wide neck aneurysms with branches incorporated at the neck level are technically particular and we strongly believe that barrel stents represents a feasible and efficient solution. moreover, it offers a solution for those anatomies where y-stenting is not a suitable solution as in recurrent branch anatomies like in the cases presented in this report (figure 1, 2 and 3). being a nitinol self-expandable, closed-cell laser cut microstent barrel device is definitely less thrombogenic then braided stents that can be used for y-stenting configuration. in our experience ystenting demands higher technical skills and prolonged duration of treatment and from this point of view the solution to protect the both side branches of an wbna with only one stent is more elegant and particularly less susceptible to peroperative thromboembolic complications. several particular anatomical conditions are feasible for this technique: a dome to neck ratio below 1,5; branches incorporated at the neck level usually with a smaller diameter (not suitable for stent deployment); polylobed bifurcation aneurysms; and asymmetry between the aneurysm plan and the bifurcation plan. from a technical point of view, one of the main advantages over y-stenting is represented by the fact that the stent micro-catheter (0.021-inch internal diameter) rebar 18 in our cases, has to be placed only once at the level of desired branch and no recatheterization of the stent and second stent placement is needed. 131 initial single centre experience with barrel vrd stent in large neck aneurisms figure 1. right mca bifurcation non-ruptured aneurysm with superior division of mca arising from the neck level (yellow arrow). barrel vrd was deployed in the inferior branch of the inferior division, the red arrow on intra op middle row (upper) indicates the radio-opaque markers protruding below the aneurysm neck. post-op pictures are demonstrating total occlusion of the aneurism sac and patency of the superior division of mca. figure 2. basilar tip non-ruptured aneurysm with both pca’s arising from the neck level; barrel vrd was deployed between the p1p2 segment of left pca and the middle third of basilar artery. post-op pictures (3dra and subtracted 2d images) are demonstrating total occlusion of the aneurism sac and patency of the both pca’s and sca’s arteries. 132 cristian mihalea, felicia otilia humulescu, hazem abdelkhalek fig 3. giant basilar tip non-ruptured aneurysm with both pca’s arising from the neck level; barrel vrd was deployed between the p1 segment of right pca and the middle third of basilar artery. red arrow indicating adequate apposition of the “belly” of the stent at the neck level with protection of both origins of pca’s. post-op pictures (3dra and subtracted 2d images) are demonstrating adequate occlusion of the aneurism sac and patency of the both pca’s and sca’s arteries. there is high visibility of the markers and positioning of the “barrel” at the neck level is clearly controlled under road map in conjunction with non-subtracted fluoroscopy (figure 1 and 3; intra-op – middle row, upper image). in the same time the operator has to be aware that in angulated anatomies the stent positioning can be challenging and it requires reshiting of the stent. is always preferable the more distal start of deploying than more proximal one. in this way we adjusted permanently the “barrel” part till the best matching with the neck is achieved. in all cases the stent has been detached once the deployment was proper and in the second time micro-catheterism through the stent struts was done without any technical difficulties with an 0,017 coiling microcatheter (echelon 10/medtronic,usa) . coiling of the aneurysm sac was achieved using coils that were 1 mm smaller than aneurysm maximal diameter. this strategy allowed safe coiling of the sac and also avoided the micro-catheter expulsion from the aneurysm. in the current study, the initial immediate angiographic result was complete occlusion in all cases, and no recanalization occurred during follow-up. we found that this type of technique is useful in cases of asymmetrical wnba, in which a web device is not a feasible solution and is less challenging than y-stenting technique. in the same time, we are aware of the strong limitation of our small number of aneurysms treated by this technique and certainly further prospective studies comparing this technique with y-stenting or web technique is needed in order to quantify the potential complication rates, long term angiographic outcomes. conclusion wnba remains challenging to endovascular treatment, although new devices that are dedicated 133 initial single centre experience with barrel vrd stent in large neck aneurisms to this type of anatomy are available. barrel stent seems to be a promising device and difficult anatomies where y-stenting or web device were only technical solution are now suitable for this technique. main advantage of the device is the possibility to protect complex bifurcations or even trifurcations and branches incorporated at the neck level. however, further study using this technique in a prospective study with a large population and a long follow-up period is warranted. funding statement this research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors. competing interests statement no competing interests to declare. references 1. molyneux a, kerr r, stratton i, et al. international subarachnoid aneurysm trial (isat) of neurosurgical clipping versusendovascular coiling in 2143 patients with ruptured intracranialaneurysms: a randomised trial. lancet 2002;360:1267—74. 2. cognard c, pierot l, anxionnat r, ricolfi f, clarity studygroup. results of embolization used as the first treatmentchoice in a consecutive nonselected population of rupturedaneurysms: clinical results of the clarity gdc study. neuro-surgery 2011;69:837-41. 3. pierot l, spelle l, vitry f, for the atena investigators. clinical outcome of patients harbouring unruptured intracranialaneurysms treated by endovascular approach: results of theatena trial. stroke 2008;39:2497—504. 4. pierot l, cognard c, spelle l, moret j. safety and efficacy ofballoon remodeling technique during endovascular treatmentof intracranial aneurysms: critical review of the literature.ajnr am j neuroradiol 2012;33:12—5. 5. pierot l, spelle l, leclerc x, cognard c, bonafé a, moret j.endovascular treatment of unruptured intracranial aneurysms:comparison of safety of remodeling technique and standardtreatment with coils. radiology 2009;251:846—55. 6. gentric jc, biondi a, piotin m, et al. balloon remodeling mayimprove angiographic results of stent-assisted coiling of unrup-tured intracranial aneurysms. neurosurgery 2015;76:441—5. 7. piotin m, blanc r, spelle l, et al. stent-assisted coiling of intracranial aneurysms: clinical and angiographic results in 216consecutive aneurysms. stroke 2010;41:110—5. 8. hetts sw, turk a, english jd, et al. stent-assisted coiling versus coiling in unruptured intracranial aneurysms in the matrixand platinum science trial: safety, efficacy, and midterm out-comes. ajnr am j neuroradiol 2014;35:698—705. 9. yavuz k, geyik s, cekirge s, saatchi i. double stent-assisted coilembolization treatment for bifurcation aneurysms: immediatetreatment results and long-term angiographic outcome. ajnram j neuroradiol 2013;34:1778—84. 10. bartolini b, blanc r, pistocchi s, redjem h, piotin m. « y » and « x » stent-assisted coiling of complex and wideneckintracranial bifurcation aneurysms. ajnr am j neuroradiol 2014;35:2153—8. 11. limbucci n, renieri l, nappini s, et al. y-stent assisted coiling of bifurcation aneurysms with enterprise stent: longtermfollow-up. j neurointerv surg 2016;8:158—62, 12. chow mm, woo hh, masaryk tj, et al. a novel endovascular treatment of a wide-necked basilar apex aneurysm by using a y-configuration, double-stenttechnique. ajnr am j neuroradiol 2004;25:509–12. 13. aguilar-pérez m, kurre w, fischer s, bäzner h, henkes h. coil occlusion of wide-neck bifurcation aneurysms assistedby a novel intrato extra-aneurysmatic neckbridgingdevice (pconus): initial experience. ajnr am j neuroradiol2014;35:965—71. 14. gory b, aguilar-pérez m, pomero e, et al. pconus devicefor the endovascular treatment of wide-neck middle cerebralartery aneurysms. ajnr am j neuroradiol 2015;36:1735—40,http://dx.doi.org/10.3174/ajnr.a4392. 15. spiotta am, chaudry mi, turk as, turner rd. initial experience with the pulserider for the treatment of bifurcationaneurysms: report of first three cases in the usa. jneurointerv surg 2016;8:186—9, http://dx.doi.org/10.1136/neurintsurg-2014-011531. 16. gawlitza m, januel ac, tall p, bonneville f, cognard c.flow diversion treatment of complex bifurcation aneurysmsbeyond the circle of willis: a single center series with spe-cial emphasis on covered cortical branches and perforatingarteries. j neuro intervent surg 2015, http://dx.doi.org/10.1136/neurintsurg-2015-011682. 17. pierot l, moret j, turjman f, et al. web treatment of intracra-nial aneurysms: clinical and anatomical results in the frenchobservatory. ajnr am j neuroradiol [epub ahead of print]. 18. pierot l, spelle l, molyneux a, byrne j, webcast and frenchobservatory investigators. clinical and anatomical follow-up inpatients with aneurysms treated with the web device: 1-yearfollow-up report in the cumulated population of 2 prospec-tive, multicenter series (webcast and french observatory). neurosurgery 2016;78:133—41 19. bartolini b, blanc r, pistocchi s, et al. “y” and “x” stentassisted coiling of complex and wide-neck intracranial bifurcation aneurysms. ajnr am j neuroradiol2014;35:2153–8. 20. saatci i, geyik s, yavuz k, et al. x-configured stent-assisted coiling in the endovascular treatment of complex anterior 134 cristian mihalea, felicia otilia humulescu, hazem abdelkhalek communicating artery aneurysms: a novel reconstructive technique. ajnr am j neuroradiol 2011;32:e113–17. 21. piotin m, blanc r, berge j, et al. the barrel vrdtm vascular reconstruction device for the treatment of wide-neck bifurcation aneurysms. stroke 2015;46(suppl 1): awp86. 22. kim bm, park si, kim dj et al (2010) endovascular coil embolization of aneurysms with a branch incorporated into the sac. ajnr am j neuroradiol 31:145–151 23. pierot l, spelle l, molyneux a, byrne j, webcast and frenchobservatory investigators. clinical and anatomical follow-up inpatients with aneurysms treated with the web device: 1-yearfollow-up report in the cumulated population of 2 prospective, multicenter series (webcast and french observatory). neurosurgery 2016;78:133—41. 24. cristian mihalea, simon escalard, jildaz caroff, léon ikka, aymeric rouchaud, valerio da ros, igor pagiola, joaquin jose marenco de la torre1, thomas yasuda1, bogdan valeriu popa, horia ples, nidhal benachour, augustin ozanne, jacques moret1, laurent spelle; balloon remodeling-assisted woven endobridge technique: description and feasibility for complex bifurcation aneurysms; j neurointerv surg. 2018 oct 5. pii: neurintsurg2018-014104. doi: 10.1136/neurintsurg-2018-014104. doi: 10.33962/roneuro-2022-040 traumatic brain contusions. key things to know in the emergency room c.d. diaz-arroyo, a.e. diaz-arroyo, l.f. hurtado-quiros, l.a. galindo-ruiz, f. torres-pérez, l.j. cruz-rodríguez, v.a. campos-castillo, j.j. cruz-trujillo, m.a. vargas-riascos, k. serrano-mesa, m.p. bolaño-romero romanian neurosurgery (2022) xxxvi (2): pp. 224-229 doi: 10.33962/roneuro-2022-040 www.journals.lapub.co.uk/index.php/roneurosurgery traumatic brain contusions. key things to know in the emergency room c.d. diaz-arroyo1, a.e. diaz-arroyo1, l.f. hurtado-quiros2, l.a. galindo-ruiz2, f. torres-pérez2, l.j. cruz-rodríguez2, v.a. campos-castillo3, j.j. cruz-trujillo4, m.a. vargas-riascos4, k. serrano-mesa5, m.p. bolaño-romero6 1 cirugia y endoscopia research group, school of medicine, university of cartagena, colombia 2 department of medicine, hospital internacional de colombia, piedecuesta, colombia 3 school of medicine, universidad de santander, bucaramanga, colombia 4 school of medicine, universidad autónoma de bucaramanga, colombia 5 semillero de innovacion e investigacion en cirugia, universidad autónoma de bucaramanga, colombia 6 medical and surgical research centre, future surgeons chapter, colombian surgery association, cartagena, colombia abstract traumatic brain injury is one of the most important causes of morbidity and mortality worldwide. one of its presentations includes traumatic brain contusions. brain contusions are cortical lesions of necrotic tissue and multiple petechial haemorrhages, initially perivascular, that predominantly affect the crests of the convolutions, but that can extend through the cortex and reach the subcortical white matter. these result from a collision of the brain with the adjacent inner table of the skull, without proper treatment these can evolve and cause a rapid deterioration of clinical and neurological status. the classification includes mild, moderate, and severe tbi depending on the nature of the injury and the impact on the patient's clinical status. for the initial evaluation, computed tomography is usually used, although the magnetic resonance has greater sensitivity for the detection in these patients. treatment is guided at preventing the progression of the lesion or the development of a secondary lesion, avoiding hypotension and hypoxia and maintaining adequate cerebral perfusion. surgery is frequently needed in severe cases to remove intracranial hematomas, provide space for the brain to swell, or place monitors to track intracranial pressure and brain oxygenation. the aim of this article is to review the most important aspects to know about brain contusion. introduction traumatic brain injury (tbi) is a complex disease that should be understood as a public issue due to the high rates of mortality and keywords brain contusion, trauma, emergency treatment, neurotrauma, central nervous system diseases, narrative review corresponding author: maria paz bolaño-romero medical and surgical research centre, future surgeons chapter, colombian surgery association, cartagena, colombia mbolanor1@unicartagena.edu.co copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 225 traumatic brain contusions disability attributed to it; being part of the leading causes of death in developed countries [1]. this condition encompasses an interesting spectrum that should not only consider its immediate consequences, rather it is important to assess the long-term impact also, especially those of working age [2]. the classification of the severity of the tbi is based on the clinical status, using the glasgow coma scale (gcs) [3,4], knowing that a patient with mild tbi is (gcs 13-15), moderate (gcs 9-12) or severe (gcs ≤8) [4]. also, according to the radiological characteristics of the lesion in the computed tomography (ct) or magnetic resonance (mr), they can be classified into brain focal injuries or diffuse injury (affecting multiple brain regions); different than diffuse injuries, the focal lesions are localized brain damage that may occur with the presence or absence of cranial opening and also present changes both intra and extra-axial [1,5]. brain contusions are part of the focal injuries [5]. brain contusions are one of the most common findings within the initial studies in patients with tbi, being present in up to 31% of the ct [1,6]. contusions are found in 89% of the brains examined postmortem in patients with tbi [1]. these results from direct loading and often occurs in the absence of a generalized injury [1,7]. the most frequent locations of brain contusions are the brain regions where it collides with the irregular adjacent inner table of the skull [5], such as frontal and temporal poles, the orbitofrontal spin, the perisylvian cortex and temporal lobe cortex inferolaterally [1,8]. this injuries typically encountered with an hemorrhagic component eventually with the bleeding within a contusion which triggers local edema and ischemic changes, which leads to tissue destruction, neuronal necrosis, and ultimately cavitation and reactive gliosis around [3]. epidemiology before discuss about specific numbers that allow us to discern the picture of this disease, we must remember that tbi is strongly related with traffic accidents and falls [4]; these are the most common causes of tbi of any severity which together account for over 50% of all cases [9,10]. knowing this we could focus on prevention programs that reduce the incidence, mortality and cost. in the international frame, it has significant socio-economic implications, in the united states (us) over 1.7 million people suffer from tbi each year [1,2,4,5]. the incidence rate of hospitalizations due to tbi has been estimated in approximately 262 cases per 100,000 people derived from a meta-analysis of 16 european countries [7,9]. for contused brain injuries associated with sports, we have an incidence rate on emergency room visits in the us of 152 cases per 100,000 people, of whom at least two-thirds where children and adults under 19 years old [9,11]. another visibly affected population are military, according to the brain injury center, us defense and veterans, more than 22,000 service members had tbi in 2015 [9]. it is widely described in the literature that actually statistics are underestimated and it is believed that if population continue along this way in the future the numbers will be markedly higher than those of today. pathophysiology because of the complexity of this disease it can be seen that has a very diverse pathophysiology including from biomechanical forces to very specific cellular changes. however, although it has been heavily studied, main mechanism that underlies the brain contusion is not yet fully clarified [1]. when the individual receives an injury, energy transfer beyond the capacity of the brain tissue to absorb it (tensegrity) without develop consequences on the function, thereby an insult or traumatic injury is generated [12]. this insult commonly takes a short time and is known as a dynamic load including loads by direct impact and impulse without physical contact. it is essential to know the speed and the time elapsed for this insult given that these variables play an important role. it is known that an insult at high speed tends to cause more severe damage [1,7]. accordingly, traumatic insult triggers a series of consequences directly related to the cerebral inflammatory response to, forming a contusion zone leading to brain suffering and death of the tissue [1]. traumatic brain inflammation can be summarized in three related but different phases [3,13]. firstly, lipids and proteins of the cell membrane are degraded into smaller molecules which prompt an osmotic gradient. in the central area of the contusion, cells as neurons and glia suffer disintegrative and homogenization processes. all this results in a disbalance in osmolality passing from normally 310 milliosmoles to 370-390 milliosmoles in 226 c.d. diaz-arroyo, a.e. diaz-arroyo, l.f. hurtado-quiros et al. the contusion area [13]. towards 24-48 hours after the insult the second phase predominates, which is mediated by the activation of thrombin as a result of the coagulation cascade [1]. thrombin among other inflammatory mediators act accordingly to stop the cerebral blood flow, resulting in vasogenic edema. the start of the third phase is triggered by lysis of erythrocytes in the intracerebral clot, subsequently hemoglobin breakdown leads to the activation of the complement system, and cytokines and reactive oxygen species contribute to the inflammatory process [1,12,13]. this inflammatory process also has a vascular component that causes a hypoperfusion in the tissue. mass effect in contusion processes results in decreased cerebral blood flow by various causes. the occurrence of increased intracranial pressure due to cerebral vascular failure self-regulatory mechanisms leads to a marked decrease of the perfusion pressure and the develop of secondary injuries [3,13]. neuroimaging usually, for the initial evaluation of a patient with tbi, the imaging modality of choice is usually the ct, due to its availability, cost and sensitivity for acute intracranial hemorrhage and fractures [14]. however, in recent decades there has been increasing use of mr, because this offers improved soft tissue with increased sensitivity for the detection of a wide variety of traumatic pathologies such as diffuse axonal injury and brain contusions. this increased sensitivity for tbi is particularly useful in the context of a traumatic brain contusion where initial ct image may be negative [15]. however, images with ct tracking may become apparent, because these tend to enlarge and become more visible [16]. contusions appear as mixed density lesions on brain ct, often surrounded by areas wedge-shaped, hypodense and are in close contact with the inner surface of the skull, this lack of homogeneity often confer an appearance of "salt and pepper" [1,17]. the mr is more sensitive (93% -98%) than the ct (18% -56%) in the location of hemorrhagic and nonhemorrhagic contusions, which are more explicitly distinguished in t2 weightings, therefore, mr better detects all types and stages of intracranial hemorrhage, including contusions [15,17]. the recovery sequence by fluid attenuated inversion (flair) is superior to t1-weighted sequences and t2 weighted for detecting cerebral edema in the context of a cc [17]. yuh et al. in rack / tbi study (clinical research and knowledge transformation traumatic brain injury) observed that 28% of patients with normal ct, mr showed abnormalities [18]. however, for primary evaluation of acute trauma not using mri unless the patient continues with neurological signs and symptoms and ct proven no initial or follow-up is required no injury apparent recommended [1]. treatment brain contusions become over time in space occupying lesions, as the inflammatory process and the secondary edema can elevate intracranial pressure (icp), which may lead to deterioration of the patient's condition. in this sense, the treatment is guided to prevent progression of the lesion, reduce edema, icp control and maintain good brain perfusion [1,19]. some guidelines have recommended maintaining sbp at ≥ 100 mmhg for patients 50 to 69 years of age or ≥ 110 mmhg for patients aged 15 to 49 or more than 70 years [20,21], start treatment for icp values above 22mmhg [20,21] and maintain cerebral perfusion pressure (cpp) between 60 and 70 mmhg to reduce mortality and improve outcomes [20–23]. oxygenation the guidelines recommend control ventilation and paco2 in patients with severe tbi [23], the paco2 should be maintained between 30 and 35mmhg and the pao2 at 100%, since it optimizes the supply of o2 [13]. hypocapnia induces cerebral vasoconstriction and cerebral ischemia [24]. cerebrospinal fluid drainage a method for reducing the icp is the drainage of cerebrospinal fluid (csf), with external ventricular drainage [13]. brain trauma foundation's (btf) recommends the use of csf drainage to reduce icp in patients with gcs <6 during the first 12 hours after injury [21]. hyperosmolar therapy osmotherapy has been used for a long time for the management of intracranial hypertension (ich) and still remains an important element for the management of tbi [20]. hypertonic saline (hts) and mannitol are commonly used effectively to reduce 227 traumatic brain contusions icp [25], these are able to establish an osmotic gradient between the brain and the cerebral vasculature, resulting in a net loss of water in brain tissue [26–28]. the hts is administered in concentrations of 2% to 23.4% and usually of choice for patients requiring resuscitation volume, mannitol is administered at doses of 0.25 to 1g/kg every 4 to 6 hours [26,29]. until recently the gold standard was considered mannitol, but is now controversial superiority of one agent over another [26], however, rockswold et al showed that hypertonic saline had a more significant effect on icp reduction, increased cerebral perfusion pressure, cardiac output and oxygen tension in the brain tissue that mannitol [30]. consequently, the decision to choose one drug over the other may be based on factors such as drug availability, comfort physician to administer an unknown agent and side effects [26]. anticonvulsant therapy patients with a gcs score ≤10, age <65 years, chronic alcoholism and cortical contusion increased risk of seizures, which can aggravate neurological deficit, therefore these patients should be considered anticonvulsant drugs [1]. btf recommends the use of phenytoin for seizure prevention early posttraumatic (within 7 days after injury) when the overall benefit outweighs the complications associated with treatment, but not recommended for use late seizures posttraumatic [21]. surgical management current indications for surgery for traumatic brain contusions include a lower score on the gcs, location of the contusion, presence of neurological deterioration, increase in the volume of the lesion, appearance of the lesion in ct (increase of the midline and/or compression of the basal cistern) and increase of the icp [31]. decompressive craniectomy the aim of decompressive craniectomy (dc) is to suppress the relationship between pressure and volume of the closed cranial cavity, with a large bone flap is removed and the dura is expanded with the help of autologous or artificial tissue [13]. there is no evidence that dc improves the outcome compared to medical therapy [32]. the decra trial showed that in patients with severe tbi refractory diffuse and ich, early bifrontotemporoparietal dc decreased icp and length of stay in the icu [33]. but, at six months of follow-up, 70% of patients in the craniectomy group had an unfavorable outcome compared to 51% of patients in the standard care group. in general, this trial has shown that dc reduces mortality but at the expense of a greater number of survivors with severe neurological disability and loss of independence [34]. surgical evacuation surgical excision is best performed by brain contusions conservatively with minimal or absent trauma to the surrounding tissue, and ideally is performed through a limited incision and placed cortical optimally [1,13], but it is reported that conservative contusectomies are better combined with a decompressive craniectomy [13]. sinha et al. a recent study showed that contusectomy or right lobectomy is useful in severe tbi with contusions [35]. the benefit of eliminating the contusion zone, include suppression and removal of necrotic and apoptotic process caused by degradation products of blood [13]. outcome a recent study observed that the frontal and temporal location is associated with a better surgical result than parietal and cerebellar contusions. in addition, they reported that age> 30 years, a severe gcs, and a median line displacement of more than 5 mm were the greatest predictors of mortality after surgery [36]. laccarino et al, showed similar results to the previous study, but also observed that the clinical deterioration in the first hours after the trauma and the onset or increase of the midline change in the follow-up ct images were associated with unfavorable clinical results [37]. in this order of ideas, despite what has been described, there are many points that need to be reinforced from the volume and quality of evidence, such as epidemiology, diagnosis and specific treatment in areas where there are barriers to access high-cost technological tools, to contribute to the reduction of the burden of neurological diseases, in addition to reducing the risk of morbidity, mortality and disability [38-44]. it is necessary to carry out prospective multicenter studies that allow us to know the behavior, approach and outcomes of this disease in different contexts and to design a standardized prognostic tool that has an excellent 228 c.d. diaz-arroyo, a.e. diaz-arroyo, l.f. hurtado-quiros et al. performance, accessible and understandable to all health professionals. in the current post-pandemic phase of covid-19, many of the efforts in disciplines other than infectious diseases have waned, so it is necessary to resume research in other areas [45,46]. conclusions brain contusions if not treated in time can have rapid and progressive in the clinical condition of the patient and neurologic effects, not only for their local ripple effects, but also the possible injury of hippocampal and brainstem. in this regard it is important to establish a proper, immediate and effective treatment because it has been shown that this improves clinical outcomes. information about brain contusions is scarce and concepts need to be standardized to provide proper management of patients with tbi. references 1 alvis-miranda h, alcala-cerra g, moscote-salazar lr. traumatic cerebral contusion: pathobiology and critical aspects. rom neurosurg. 2013; 20(2):125–37. 2. davanzo jr, sieg ep, timmons sd. management of traumatic brain injury. surg clin north am. 2017; 97(6):1237–53. 3. mcginn mj, povlishock jt. pathophysiology of traumatic brain injury. neurosurgery clinics of north america. 2016; 27: 397–407. 4. wells aj, hutchinson pj. the management of traumatic brain injury. surg (united kingdom). 2018; 36(11):613–20. 5. pervez m, kitagawa rs, chang tr. definition of traumatic brain injury, neurosurgery, trauma orthopedics, neuroimaging, psychology, and psychiatry in mild traumatic brain injury. neuroimaging clin n am. 2018; 28(1):1–13. 6. soustiel jf, mahamid e, goldsher d, zaaroor m. perfusion-ct for early assessment of traumatic cerebral contusions. neuroradiology. 2008; 50(2):189–96. 7. blyth bj, bazarian jj. traumatic alterations in consciousness: traumatic brain injury. emerg med clin north am. 2010; 28(3):571–94. 8. prins m, greco t, alexander d, giza cc. the pathophysiology of traumatic brain injury at a glance. dis model mech. 2013; 6(6):1307–15. 9. blennow k, brody dl, kochanek pm, levin h, mckee a, ribbers gm, et al. traumatic brain injuries. nat rev dis prim. 2016; 2:1–19. 10. psota m, theadom a, taylor ms, holkovic l, buckova v, synnot a, et al. epidemiology of traumatic brain injury in europe: a living systematic review. j neurotrauma. 2015; 30:1–30. 11. coronado vg, haileyesus t, cheng ta, bell jm, haarbauer-krupa j, lionbarger mr, et al. trends in sportsand recreation-related traumatic brain injuries treated in us emergency departments. j head trauma rehabil. 2015; 30(3):185–97. 12. dixon kj. pathophysiology of traumatic brain injury. phys med rehabil clin n am. 2017; 28(2):215–25. 13. mathai k, sengupta s, shashivadhanan, sudumbrekar s. surgery for cerebral contusions: rationale and practice. indian j neurotrauma. 2012; 6(1):17–20. 14. agarwal r, bergey m, sonnad s, butowsky h, bhargavan m, bleshman mh. inpatient ct and mri utilization: trends in the academic hospital setting. j am coll radiol. 2010; 7(12):949–55. 15. altmeyer w, steven a, gutierrez j. use of magnetic resonance in the evaluation of cranial trauma. magnetic resonance imaging clinics of north america. 2016; 24:305–23. 16. ratnaike te, hastie h, gregson b, mitchell p. the geometry of brain contusion: relationship between site of contusion and direction of injury. br j neurosurg. 2011; 25(3):410–3. 17. useche jn, bermudez s. conventional computed tomography and magnetic resonance in brain concussion. neuroimaging clinics of north america. 2018; 28:15–29. 18. yuh el, mukherjee p, lingsma hf, yue jk, ferguson ar, gordon wa, et al. magnetic resonance imaging improves 3-month outcome prediction in mild traumatic brain injury. ann neurol. 2013; 73(2):224–35. 19. ahmad helmy ak, salmah jalaluddin wm, ab rahman ig. computed tomography perfusion imaging on traumatic cerebral contusion: a preliminary report. malays j med sci. 2010; 17(4):51–6. 20. dash hh, chavali s. management of traumatic brain injury patients. korean j anesthesiol. 2018; 71(1):12–21. 21. carney n, totten am, oʼreilly c, ullman js, hawryluk gwj, bell mj, et al. guidelines for the management of severe traumatic brain injury, fourth edition. neurosurgery. 2016; 80(1):1. 22. vanderkolk we, ott mm, eriksson ea, figueroa be, barletta jf, bonnell bw, et al. cerebral perfusion pressure and intracranial pressure are not surrogates for brain tissue oxygenation in traumatic brain injury. clin neurophysiol. 2011; 123(6):1255–60. 23. geeraerts t, velly l, abdennour l, asehnoune k, audibert g, bouzat p, et al. management of severe traumatic brain injury (first 24 hours). anaesth crit care pain med. 2018; 37(2):171–86. 24. coles jp, fryer td, coleman mr, smielewski p, gupta ak, minhas ps, et al. hyperventilation following head injury: effect on ischemic burden and cerebral oxidative metabolism. crit care med. 2007; 35(2):568–78. 25. battison c, andrews pjd, graham c, petty t. randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. crit care med. 2005; 33(1):196–202. 229 traumatic brain contusions 26. jinadasa s, boone md. controversies in the management of traumatic brain injury. anesthesiol clin. 2016; 34(3):557–75. 27. vella ma, crandall ml, patel mb. acute management of traumatic brain injury. surg clin north am. 2017; 97(5):1015–30. 28. tsang kkt, whitfield pc. traumatic brain injury: review of current management strategies. br j oral maxillofac surg. 2012; 50(4):298–308. 29. freeman n, welbourne j. osmotherapy: science and evidence-based practice. bja educ. 2018; 18(9):284–90. 30. rockswold gl, solid ca, paredes-andrade e, rockswold sb, jancik jt, quickel rr. hypertonic saline and its effect on intracranial pressure, cerebral perfusion pressure, and brain tissue oxygen. neurosurgery. 2009; 65(6):1035–42. 31. bullock mr, chesnut r, ghajar j, gordon d, hartl r, newell dw, et al. surgical management of traumatic parenchymal lesions. neurosurgery. 2006; 58(s-3):s2546. 32. honeybul s, ho km. decompressive craniectomy a narrative review and discussion. aust crit care. 2014; 27(2):85–91. 33. cooper dj, rosenfeld jv, murray l, arabi ym, davies ar, d’urso p, et al. decompressive craniectomy in diffuse traumatic brain injury. n engl j med. 2011; 364(16):1493– 502. 34. honeybul s, ho km, lind crp, gillett gr. the current role of decompressive craniectomy for severe traumatic brain injury. j clin neurosci. 2017; 4. 35. sinha s, rathore ys, mahapatra ak, sharma bs. surgical outcome of brain contusions treated by decompressive craniotomy with or without lobectomy at high volume tertiary care trauma centre. indian j neurotrauma. 2014; 11(1):5–9. 36. akyam l, gudla v, jyothi s. factors affecting the surgical outcome of patients with cerebral contusions. int surg j. 2015; 2(4):665–9. 37. cerasti d, goldoni m, caspani m, schiavi p, iaccarino c, picetti e, et al. patients with brain contusions: predictors of outcome and relationship between radiological and clinical evolution. j neurosurg. 2014; 120(april):908–18. 38. lozada-martínez i, maiguel-lapeira j, torres-llinás d, moscote-salazar l, rahman mm, pacheco-hernández a. letter: need and impact of the development of robotic neurosurgery in latin america. neurosurgery. 2021; 88(6):e580-e581. 39. herrera-martinez mp, garcía-ballestas e, lozadamartinez i, torres-llinás d, moscote-salazar l. letter to the editor. creating the conditions for gender equality to end sexual harassment in neurosurgery. j neurosurg. 2021 feb 5:1-2. 40. gaitan-herrera g, lozada-martínez i, acevedo-aguilar l, bohorquez-caballero a, moscote-salazar l. simulation as a tool to educate the patient about neurosurgical pathology. j neurosurg sci. 2021 jan 22 41. ortega-sierra mg, durán-daza rm, carrera-patiño sa, rojas-nuñez ax, charry-caicedo ji, lozada-martínez id. neuroeducation and neurorehabilitation in the neurosurgical patient: programs to be developed in latin america and the caribbean. j neurosurg sci. 2021 jun 10. 42. blanco-teherán c, quintana-pájaro l, narvaez-rojas a, martínez-pérez r, garcía-ballestas e, moscote salazar l, et al. evidence-based medicine in neurosurgery: why and how? j neurosurg sci. 2021 aug 3. 43. ortega-sierra mg, prado-grajales v, martinez-imbett r, unás-perea k, lozada martinez id. research career in neurosurgery: a challenge for future neurosurgeons. j neurosurg sci. 2021 aug 3. 44. zuluaga-ramírez p, lozada-martínez i, moscote-salazar l, cabrera-vargas l. sexual harassment and racism in surgery: a latent problem. int j surg. 2021; 86:13-14. 45. gonzález-herazo ma, silva-muñoz dc, guevara-martínez pa, lozada-martinez id. post-covid 19 neurological syndrome: a fresh challenge in neurological management. neurol neurochir pol. 2021;55(4):413-414 46. llamas-nieves a, maiguel-lapeira j, lozada-martinez i, torres llinas d, moscote-salazar l. the desire to publish a scientific article and the difficulties of publishing it in a highquality neurosurgery scientific journal. j neurosurg sci. 2021 mar 11. doi: 10.33962/roneuro-2020-018 fast growing recurrent grade i meningioma. a rare case report prashank goel, daljit singh romanian neurosurgery (2020) xxxiv (1): pp. 127-132 doi: 10.33962/roneuro-2020-018 www.journals.lapub.co.uk/index.php/roneurosurgery fast growing recurrent grade i meningioma. a rare case report prashank goel1, daljit singh2 1 senior resident, department of neurosurgery, g. b pant institute of post graduate medical education and research, new delhi, india 2 director, professor and head of department, department of neurosurgery, g. b pantinstitute of post graduate medical education and research, new delhi, india abstract meningiomas are mostly regarded as benign tumours, accounting for 13% to 26% of all primary intracranial tumors1. according to 2016 world health organization (who) classification, meningiomas are classified into grade i (benign), ii (atypical), and iii (anaplastic).2 meningioma are neoplasms derived from arachnoidal (meningothelial) cells. these lesions can occur in people of any age but commonly present in middle age. women are more likely to develop a meningioma, with a female/male ratio of approximately 2:1 intracranially and 10:1 in the spine.3 even after complete removal, meningiomas have been estimated to recur in 10 to 32% of the cases within 10 years. however, recurrences in grade 1 meningiomas are rare and occur after long duration.4 we herein report a case of grade 1 meningioma that recurs very fast, within the duration of 1 yr and the recurrent size of the tumor was approx three times the size of the primary one. to our knowledge, very few cases in the literature have been reported with such a fast-growing grade 1 meningioma. case report a 45 years female, case of right cavernous sinus meningioma (figure 1,2) operated 1 year back, was admitted to o ur department of neurosurgery with altered sensorium for last 20 days. simpson grade iii excision of the tumor was done 1 year back. the histopathology report of first surgery was transitional meningioma grade 1 with mib index 10-12%. after the first surgery post-operative scan (figure 3) reveals gross total excision of tumor and patient went back with no deficits. now after 1 year patient present to us in altered sensorium, right lower motor neuron paresis of facial nerve and paresis of lower cranial nerves over the right side. mri brain plain with contrast was done which reveals a large recurrent mass lesion extending from right keywords grade i meningioma, recurrence, fast-growing corresponding author: prashank goel g. b pant institute of post graduate medical education and research, new delhi, india prashankgoel1@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 128 prashank goel, daljit singh cavernous sinus to ipsilateral cerebellopontine angle attaching to the petrous bone with gross hydrocephalus (figure 4,5). as the patient presented in altered sensorium, patient was intubated, put on ventilator and emergency ventriculoperitoneal shunt was done. subsequently right retromastoid suboccipital craniotomy and tumor decompression was done and a part of tumor inside the cavernous sinus was left behind (figure 6). histopatholgy report again came out to be transitional meningioma. post operatively patient continued on ventilator, tracheostomised and after few days gradually weaned from tracheostomy. at the time of discharge, patient was conscious, oriented, following commands and walking with support. figure 1. contrast ct scan (coronal and saggital images) of patient done preoperatively 1 yr back, showing homogenously contrast enhancing lesion in right cavernous sinus. 129 fast growing recurrent grade i meningioma figure 2. mri brain (axial, coronal and saggital images) of patient done preoperatively 1 yr back, showing homogenously contrast enhancing lesion in right cavernous sinus. 130 prashank goel, daljit singh figure 3. contrast ct (axial and coronal) post-operative images of the patient done 1 year back, showing gross total resection of meningioma. figure 4. contrast ct axial images showing brilliantly homogenous contrast enhancing lesion in cavernous sinus with extension to the right cerebellopontine angle. figure 5. mri brain contrast images showing brilliantly homogenous contrast enhancing lesion in cavernous sinus with extension to the right cerebellopontine angle. 131 fast growing recurrent grade i meningioma figure 6. ct brain palin and contrast post-operative images showing total removal of meningioma in c p angle with residual tumor in cavernous sinus with vp shunt in situ. discussion recurrences in grade 1 meningioma are rare and occur after long duration. in our case patient had recurrent grade i meningioma and that too in just 1 year and now tumor has grown to such a big size that it had extended to right cerebelloopontine angle displacing the midbrain causing mass effect and hydrocephalus. to date very few cases has been reported in literature where the grade 1 meningioma recurs in such a short interval and of such a big size. recurrences in grade 2 and grade 3 are common. in the study by gallagher5, the median time to recurrence /progression was 60 months (range 6 to 134 months) and another study done by ildan4, the mean time to recurrence was 60.5 ±  27.9 months (range, 28 to 114 months) for benign meningiomas and 39 ± 14.5 months (range, 28 to 68 mos) for malignant meningiomas. despite complete total resection, 7-20% of benign (grade i), 29-40% of atypical (grade ii), 50-78% of anaplastic (grade iii) meningiomas recur.6 the factors involved in tumor recurrence, other than tumor grading are extent of surgery, age, gender, location and brain invasion. meningiomas in males and children tend to be aggressive and recur more than in females7,8. however, ildan et al4, and 132 prashank goel, daljit singh adegbite et al9 reported that age and gender has no influence on proliferative activity. location was one of the factors implicated in recurrence. meningiomas of the skull base and tumors close to major sinuses were reported to have a high proliferative index and were associated with recurrence4,8,12. bitzer et al10 and ide et al11 reported that large tumors were more prone for recurrence than smaller tumors, as large sized tumors were associated with a higher incidence of tumor infiltration and adherence to arachnoid membrane and the adjacent brain tissue. nakasu et al12 found that lobulated tumors recurred more often than round tumors. gallagher et al reported that 5-year recurrence / progression free survival (rpfs) for simpson grade 1 was 96.8%, 2: 100%, 4: 82.4% and 5: 0%. simpson grade and gross total/subtotal resection were significant predictors of recurrence with most of the recurrences occurring in the subtotal resection group and only a few occurring in patients who underwent total removal. the overall mortality among recurrent meningiomas was 9.7%, and recurrence-related mortality constituted 75% of all meningioma related mortalities in the series by guarnaschelli et al2. conclusion recurrence in grade 1 meningioma is rare. recurrence is common with subtotal resection of meningiomas. the predicting factors for recurrence in this case were subtotal resection, primay tumor location (cavernous sinus) with high mib index. a regular radiological follow up should be done in these patients, so that recurrence could be identified at an early period without causing more impact on patient’s general condition. references 1. liu y, song dp, wang t. meningiomas with different histological grade in the same patient: case report. medicine (baltimore). 2017;96(50):e9086. 2. guarnaschelli jj, stawicki sp. brief communication: recurrent brain meningiomas. opus 12 scientist 2008;2(2):32-34. 3. commins, d. l., atkinson, r. d., & burnett, m. e. (2007). review of meningioma histopathology, neurosurgical focus foc, 23(4), e3. 4. ildan f, erman t, göçer ai, et al. predicting the probability of meningioma recurrence in the preoperative and early postoperative period: a multivariate analysis in the midterm follow-up. skull base. 2007;17(3):157-71. 5. gallagher mathewj, jenkinson michael d, brodbelt andrew r, mills samantha j, chavredakis emmanuel. who grade 1 meningioma recurrence: are location and simpson grade still relevant?. clinical neurology and neurosurgery http://dx.doi.org/10.1016/j.clineuro.2016. 01.006 6. babu s, uppin sg, uppin ms, panigrahi mk, saradhi v, bhattacharjee s, sahu b p, purohit a k, challa s. meningiomas: correlation of ki67 with histological grade. neurol india 2011;59:204-7 7. darlix a, zouaoui s, rigau v , et al. epidemiology for primary brain tumors: a nationwide population-based study. j neurooncol 2017;131:525–46. 8. kasuya h, kubo o, tanaka m, amano k, kato k, hori t. clinical and radiological features related to the growth potential of meningioma. neurosurg rev 2006;29:293-7. 9. adegbite a b, khan m i, paine k we, tan l k. the recurrence of intracranial meningiomas after surgical treatment. j neurosurg. 1983;58:51–56. 10. bitzer m, wöckel l, morgalla m, et al. peritumoral brain edema in intracranial meningiomas: influence of tumor size, location and histology. acta neurochir (wien) 1997;139:1136–1142. 11. ide m, jimbo m, kubo o, yamamoto m, takeyama e, imanaga h. peritumoral brain edema and cortical damage by meningioma. acta neurochir suppl (wien) 1994;60:369–372. 12. nakasu s, nakasu y , nakajima m. potential doubling time and tumor doubling time in meningiomas and neurinomas. acta neurochir (wien) 1996;138:763–770. doi: 10.33962/roneuro-2023-002 the challenges and opportunities of patient safety culture in neurosurgical departments from the republic of moldova silvia danu romanian neurosurgery (2023) xxxvii (1): pp. 15-23 doi: 10.33962/roneuro-2023-002 www.journals.lapub.co.uk/index.php/roneurosurgery the challenges and opportunities of patient safety culture in neurosurgical departments from the republic of moldova silvia danu state university of medicine and pharmacy “nicolae testemițanu”, republic of moldavia abstract neurosurgery is a high-risk speciality, so the patient safety culture should become a priority to improve patient safety and the quality of medical care. the purpose of the study was to explore the perception of patient safety culture (psc) among the staff in the neurosurgical departments of the republic of moldova. a cross-sectional study was conducted in neurosurgical departments using the hospital survey on patient safety culture (hsopsc). descriptive statistics were carried out, comprising the cronbach "α" coefficient, frequency of positive answers (pprs), and level of minimum and maximum of 95% confidential interval. pprs by question and dimension were analysed overall and classified according to the harrington scale. medical staff from five hospitals voluntarily participated in the study. most of the respondents rated the patient's safety grade as excellent and very good. the value of the frequency of positive responses to the dimensions of the survey varies between 37.3% (nonpunitive response to error) and 85.0% (teamwork within units). the dimensions with the highest score of the pprs stand out: „teamwork within units”, „organizational learningcontinuous improvement” and „supervisor/manager expectations and actions promoting patient safety”. the dimension with a high score of pprs was „feedback and communication about error”. the dimensions with a satisfactory score of the pprs were „handoffs and transitions”, „frequency of events reported”, „management support for patient safety”, „teamwork across units”, „communication openness”, „overall perceptions on patient safety”, „non-punitive response to errors” and „staffing”. for the first time in the republic of moldova, the perception of patient safety culture in neurosurgery departments was studied. the results reflect the positive attitude of the staff towards most dimensions of the patient safety culture. the study made it possible to highlight the strong and vulnerable points of the patient safety culture in neurosurgical departments from moldova. introduction patient safety is a strategic priority for modern health care and is central to countries’ efforts in working towards universal health coverage (1). keywords patient safety culture, neurosurgery, patient safety corresponding author: silvia danu state university of medicine and pharmacy “nicolae testemițanu”, republic of moldavia silviadanu@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 16 silvia danu developing a culture of safety is cardinal to any sustainable efforts towards patient safety improvement (1). according world health organization patient safety is a framework of organized activities that creates cultures, processes and procedures, behaviours, technologies, and environments in health care that consistently and sustainably: lower risks, reduce the occurrence of avoidable harm, make error less likely and reduce its impact when it does occur (2).incident: any deviation from usual medical care that either causes an injury to the patient or poses a risk of harm, including errors, preventable adverse events and hazards (2).adverse event: an incident that results in preventable harm to a patient (2) every year, large number of patients are harmed or die because of unsafe health care, creating a high burden of death and disability worldwide, especially in lowand middle-income countries. on average, an estimated one in 10 patients is subject to an adverse event while receiving hospital care in high-income countries. available evidence suggests that 134 million adverse events due to unsafe care occur in hospitals in lowand middle-income countries, contributing to around 2.6 million deaths every year. the social cost of patient harm can be valued at us$ 1 trillion to 2 trillion a year (1). in neurosurgery, little is known about the frequency of adverse events and the contribution of human error (3)according hanno s. meyer (2021) one in four patients treated at an academic neurosurgical tertiary care centre experiences at least one adverse event. most adverse events occurred during (19.6%) or after (76.3%) surgery (3). more than one in four of the cases with adverse events were associated with human error (25.9%). the most frequent class of human performance deficiency (hpd) was execution (18.3%). another relevant hpd was planning or problem solving (5.6%). rules violation accounted for 1.7% of adverse events cases. (3) mardon re( 2010) explored the relationships between hospital patient safety culture and adverse events and found that hospitals with a more positive patient safety culture scores had lower rates of inhospital complications or adverse events (4). the study supports the idea that a more positive patient safety culture is associated with fewer adverse events in hospitals (4). the global patient safety action plan strives to eliminate avoidable harm in health care with the vision of “a world in which no one is harmed in health care, and every patient receives safe and respectful care, every time, everywhere” (1). according to ahrq patient safety culture is the extent to which an organization's culture supports and promotes patient safety. it refers to the values, beliefs, and norms that are shared by healthcare practitioners and other staff throughout the organization that influence their actions and behaviours. patient safety culture can be measured by determining the values, beliefs, norms, and behaviours related to patient safety that are rewarded, supported, expected, and accepted in an organization (5). it is believed that in order to reduce the number of adverse events, hospitals have to stimulate a more open culture and reflective attitude towards errors and patient safety (6). a strong safety culture is not only core to reducing patient harm, it is also critical for providing a safe working environment for health workers. this includes creating a psychologically safe work environment, whereby health workers can speak up regarding patient safety and other concerns without fear of negative consequences (1). “changing our culture to advance patient safety” served as the theme of the 81st annual meeting of the american association of neurological surgeons (7). the neurosurgeon of the future has to embrace the ideals of individualism and innovation while never giving up the art of medicine, prioritizing the doctor-patient relationship, and changing our culture to practice the science of medicine within systems that help us to understand and prevent errors from occurring (7). leaders should be educated in the importance of safety culture, and they need tools to help create this culture (8). in addition, many organizations now use standard surveys to measure culture, although many struggle with how to improve in low-scoring areas (8). the ahrq surveys on patient safety culture™ (sops®) are surveys of providers and staff that assess the extent to which their organizational culture supports patient safety and safe practices (9). the areas of patient safety culture assessed by the ahrq sops surveys include: communication about error, communication openness, organizational learning—continuous improvement, overall rating on patient safety, response to error, staffing, 17 the challenges and opportunities of patient safety culture supervisor and management support for patient safety, teamwork, work pressure and pace (9). as of september 2022, there are 107 known countries where the ahrq surveys on patient safety culture™ (sops®) have been administered (10). as of september 2022, there are 56 known translations for the ahrq surveys on patient safety culture™ (sops®) (11). the european network for patient safety (eunetpas) has been an important promoter of this tool in europe. one of the aims of the eunetpas project was “promoting a culture of patient safety” (12). the original us hospital survey on patient safety culture (hsops), designed by the american agency for healthcare research and quality (ahrq) in 2004 was translated in romanian and experimented in romania. the study explored the psychometric properties of the romanian version of the us hsops and found that psychometric properties of the romanian version of the hsops tested in romania was acceptable for nine composites with 31 items (13). then a cross-sectional study which measured the patient safety culture was carried out in six hospitals, located in four romanian regions by tereanu c et all (2017)(14).the study shows that staff perceptions of most areas of patient safety were positive although reporting of adverse events was low(14).later a cross-sectional study was conducted in moldovan healthcare settings, using the romanian translation of the us hospital survey on patient safety culture hsopsc (15). the results of the study suggested that staff avoid to openly report adverse events and/or discuss errors, likely because a poor understanding of the potential of these events for learning and because of fear of blame or punitive actions (15). also, the phenomenon of underreporting of adverse events was mentioned in the study by turcanu t. et all in 2010 regarding patient safety, medical errors, and event reporting in moldova (16). currently, the republic of moldova does not have in use any tool to assess patient safety culture in hospital settings (15).therefore, the actuality of the problem was associated with the lack of research on the patient safety culture of neurosurgical patients during hospitalization and the high risks of medical care for patients with neurosurgical diseases. the purpose of the study was to explore the perception of patient safety culture among the staff in neurosurgical departments from republic of moldova. methods a cross sectional study was conducted in neurosurgical departments from moldova using the hospital survey on patient safety culture (hsopsc) romanian version, developed by the us agency for healthcare research and quality, created by sorra j, yount n, famolaro t, et al. (17). the research project was approved by the research ethics committee of state university of medicine and pharmacy “nicolae testemitanu”, republic of moldova on 19.06.2018. the survey was distributed from january till september 2019 in neurosurgical departments in five hospitals from republic of moldova. there was voluntary involved in the survey 345 doctors, residents, and nurses. we distributed paper form questioners to 400 members of medical staff. the questionnaire was anonymously completed. the surveys that did not meet the requirements for completion of the ahrq guide were excluded. overall, 345 completed questioners were returned, which constituted the 86% response rate. completed surveys were collected and digitized. statistical analyses were performed using ibm spss statistics 26. the matrix of results was created. the survey contains forty-two questions and two output indicators: one question asks the respondents to appreciate the patient safety grade and another question asks about the number of events reported during the last 12 months. the survey questions used likert scale of 5-point response options of degree of agreement: 1 point mean strongly disagree, 5 points -strongly agree, and the frequency 1 point mean never, and 5 points mean always. for negatively worded items, percentage of positive responses is the percentage of respondents who answered “strongly disagree” or “disagree,” or “never” or “rarely,” because a negative answer on a negatively worded item indicates a positive response (17). we recoded negatively worded items to calculate an item percent positive score. we averaged the percent of positive scores for each item included in the composite measure, to calculate score on a particular safety culture composite measure as described the ahrq guide (17). descriptive statistics were carried out, comprised the cronbach "α" coefficient, frequency of positive answers pprs, variance, standard error, level 18 silvia danu of minimum and maximum of 95% confidential interval. pprs by question and dimension were analysed overall and classified according to harrington scale (18). results for the first time we explored the staff perception about patient safety culture in neurosurgical departments from five hospitals providing in-patient hospital care. 345 persons voluntarily participated in the study. from 345 respondents there were: doctors 12436.0%, nurses17249.8%, residents 49-14.2%. all of respondents were in direct interaction or contact with patients. most of respondents 173 (50,1%; îi 95% [44,6-55,1]) were worked in neurosurgery units and 172 (49,9%; îi 95% [44,9-55,4]) were worked in anaesthesiology and intensive care units where neurosurgical patients received medical care. the distribution of respondents by intervals of years of work experience in the hospital showed that a third of them have a work experience in the hospital 1-5 years-109 people (31,6%; îi 95% [27,0-36,5]), and another third had 21 and more years of work experience 122 people (35,4%; îi 95% [30,1-40,6]). the distribution of respondents by intervals of years of work experience in the unit showed that: 1-5 years -38.6 % respondents, 6-10 years-18.6% respondents, 11-15 years -10.7% respondents, 16-20 years -9% respondents, > 20 years -23.2 % respondents. the results showed that a half of respondents worked 40-49 hours per week figure 1. figure 1. distribution of respondents according to working hours per week, %. the output indicator -frequency of adverse events reported in the last 12 months by respondents reflects that the most part of staff did not report any adverse events during last year of activity figure 2. figure 2. frequency of adverse event reported in the last 12 months, %. most of the employees rated the patient's safety grade as excellent39,1 % and very good 43,8%. table 1 reflects the staff perception of patient safety grade. table 1. patient safety grade -output indicator. patient safety grade -points frequency of responses patient safety grade abs. % 95% ci 9-10 135 39,1 33,9-44,1 excelent 7-8 151 43,8 38,6-48,0 very good 5-6 44 12,8 9,3-16,5 acceptable 3-4 11 3,2 1,4-5,2 poor 1-2 4 1,2 0,3-2,3 failing table 2 express the item and composite positive scores for the patient safety culture with 95% confidence intervals. table 2. item and composite percent positive scores for the patient safety culture with 95 % confidence intervals. code composites and items abs. % 95% ci d i teamwork within units 1173 85,0 83,186,9 a1 people support one another in this unit 301 87,2 83,890,7 a3 when a lot of work needs to be done quickly, we work together as a team to get the work done 310 89,9 86,792,8 a4 in this unit, people treat each other with respect 292 84,6 80,988,1 a11 when one area in this unit gets really busy, others help out 270 78,3 73,682,9 0.9 20.9 49.9 26.1 2.0 0.3 0 10 20 30 40 50 60 < 20 hours 20-39 hours 40-59 hours 60-79 hours 80-99 hours > 100 hours 90.7 5.8 2.6 0.6 0.3 0 20 40 60 80 100 0 events 1-2 events 3-5 events 6-10 events 11-20 events 19 the challenges and opportunities of patient safety culture d ii supervisor/manager expectations and actions promoting patient safety 1117 80,9 78,983,0 b1 my supervisor/manager says a good word when he/she sees a job done according to established patient safety procedures 311 90,1 87,093,0 b2 my supervisor/manager seriously considers staff suggestions for improving patient safety 285 82,6 78,886,7 b3r whenever pressure builds up, my supervisor/manager wants us to work faster, even if it means taking shortcuts 220 63,8 58,868,7 b4r my supervisor/manager overlooks patient safety problems that happen over and over 301 87,2 83,890,7 d iii organizational learningcontinuous improvement 839 81,1 78,783,4 a6 we are actively doing things to improve patient safety 276 80,0 75,784,3 a9 mistakes have led to positive changes here 288 83,5 79,487,2 a13 after we make changes to improve patient safety, we evaluate their effectiveness 275 79,7 75,783,8 d iv management support for patient safety 613 59,2 56,262,2 f1 hospital management provides a work climate that promotes patient safety 228 66,1 60,971,3 f8 the actions of hospital management show that patient safety is a top priority 228 66,1 60,971,3 f9r hospital management seems interested in patient safety only after an adverse event happens 157 45,5 40,350,8 d v overall perceptions on patient safety 611 44,3 41,746,9 a10r it is just by chance that more serious mistakes 105 30,4 25,835,1 don’t happen around here a15 patient safety is never sacrificed to get more work done 96 27,8 22,932,8 a17r we have patient safety problems in this unit 178 51,6 46,456,8 a18 our procedures and systems are good at preventing errors from happening 232 67,2 62,072,2 d vi feedback and communication about error 792 76,5 73,979,1 c1 we are given feedback about changes put into place based on event reports 300 87,0 83,290,1 c3 we are informed about errors that happen in this unit 220 63,8 58,668,7 c5 in this unit, we discuss ways to prevent errors from happening again 272 78,8 74,282,9 d vii communication openness 491 47,4 44,450,5 c2 staff will freely speak up if they see something that may negatively affect patient care 225 65,2 60,370,4 c4 staff feel free to question the decisions or actions of those with more authority 144 41,7 36,547,0 c6r staff are afraid to ask questions when something does not seem right 122 35,4 30,740,3 d viii frequency of events reported 621 60,0 57,063,0 d1 when a mistake is made, but is caught and corrected before affecting the patient, how often is this reported? 215 62,3 57,167,2 d2 when a mistake is made, but has no potential to harm the patient, how often is this reported? 210 60,9 55,966,1 d3 when a mistake is made that could harm the patient, but does not, how often is this reported? 196 56,8 51,362,0 20 silvia danu d ix teamwork across units 719 52,1 49,554,7 f2r hospital units do not coordinate well with each other 122 35,4 30,440,9 f4 there is good cooperation among hospital units that need to work together 212 61,4 56,266,9 f6r it is often unpleasant to work with staff from other hospital units 140 40,6 35,146,1 f10 hospital units work well together to provide the best care for patients 245 71,0 66,175,9 d x staffing 515 37,3 34,839,9 a2 we have enough staff to handle the workload 135 39,1 33,944,6 a5r staff in this unit work longer hours than is best for patient care 103 29,9 25,535,1 a7r we use more agency/temporary staff than is best for patient care 147 42,6 37,147,8 a14r we work in "crisis mode" trying to do too much, too quickly 130 37,7 32,542,9 d xi handoffs and transitions 854 61,9 59,364,4 f3r things “fall between the cracks” when transferring patients from one unit to another 202 58,6 53,363,2 f5r important patient care information is often lost during shift changes 238 69,0 63,573,9 f7r problems often occur in the exchange of information across hospital units 192 55,7 50,460,9 f11r shift changes are problematic for patients in this hospital 222 64,3 59,469,3 d xii non punitive response to errors 447 43,2 40,246,2 a8r staff feel like their mistakes are held against them 207 60,0 54,865,5 a12r when an event is reported, it feels like the person is being written up, not the problem 150 43,5 38,048,7 a16r staff worry that mistakes they make are kept in their personnel file 90 26,1 21,730,7 table 3. classification of the results of patient safety culture dimensions according to the harrington scale. grade frequency of positive responses % level of harrington scale dimension the total value of dimensi on % i. 80-100% very good (excellent) teamwork within units 85,0 organizational learning-continuous improvement 81,1 supervisor/manager expectations and actions promoting patient safety 80,9 ii. 63-79% good feedback and communication about error 76,5 iii. 37-62% satisfactory handoffs and transitions 61,9 frequency of events reported 60,0 management support for patient safety 59,2 teamwork across units 52,1 communication openness 47,4 overall perceptions on patient safety 44,3 non punitive response to errors 43,2 staffing 37,3 iv. 20-36% bad not identified v. 0-19% very bad (critical) not identified discussions the ultimate goal of the global patient safety action plan is to achieve the maximum possible reduction in unavoidable harm due to unsafe health care globally (1). one from seven guiding principles establish underpinning values to shape the development and implementation of the action plan is instill a safety culture in the design and delivery of health care (1). because of its high level of complexity, neurosurgery is a high-risk specialty, and improving patient outcomes has remained central in its spectrum of academic pursuits (19). for the first time was explored the perception on patient safety culture of staff in neurosurgical departments from republic of moldova. the staff demonstrates openness to participate in this study and the participation rate was high. the results of the study 21 the challenges and opportunities of patient safety culture express the positive attitude of the staff from the neurosurgery departments towards the culture of patient safety. the study reflects the particularities of patient safety culture in neurosurgical departments from republic of moldova with strength and weaknesses. the value of the frequency of positive responses to the dimensions of the survey varies between 37.3% (nonpunitive response to error) and 85.0% (teamwork within units). russell e. mardon et all (2010) reflected similar results in their study where the mean hsops scores ranged from 42% positive response (nonpunitive response to error) to 79% positive response (teamwork within units) (20). the mean value of patient safety grade was 7.8 points (ci 95% [7,6-8,0]) from 10 that correspond to very good level of patient safety grade. 39.1% of respondents appreciated as a “excellent” the grade of patient safety, 43.8% “very good”, 12.8% “acceptable”, 3.2%“poor” and 1.2%“failing”. the results of the study showed that the assessment of patient safety in neurosurgical departments is higher compared to previous studies carried out in the republic of moldova and romania (13) (15). the explanations can be that neurosurgery clinicians have always taken pride in being providers who carry a strong sense of personal responsibility for their patients (19). neurosurgery is far from immune to the errors. the complexity of neurosurgical patients and the interdisciplinary teams required to manage their conditions expose these patients to the same errors found in other medical and surgical specialties, along with errors unique to neurosurgery (21). our study reflects the phenomenon of underreporting of adverse events -about 90 % of respondents did not report any adverse event during the last year. tereanu c. et all find the same phenomenon in their study in moldova68% of respondents did not report any adverse event in the last 12 months (15) and 73 % in romania (14). in comparison with japan “no event reports” was in 34,9 %, taiwan 48.8% and united states 50.8% (22). understanding the frequency and danger posed by medical errors, and offering strategies to prevent them, forms the basis of the modern patient safety movement (21). although voluntary event reporting is often described as an inadequate method to detect patient safety events and is marked by underreporting rates (23). in moldova, there is no centralized system for mandatory anonymous reporting of adverse events. the high level of underreporting of adverse events can be explained by the voluntary reporting system. russell e. mardon mentioned in 2010 that there tends to be considerable underreporting of events in hospitals, which is problematic because potential safety problems may not be recognized or identified and therefore may not be addressed (20).maureen l. falcone mentioned in his study 4 factors accounted for 67.5% of the variance in barriers to reporting medication errors: fear, cultural barriers, lack of knowledge/feedback, and practical barriers. other barriers include workload, interruptions, and lack of knowledge. also, an important barrier is providers not prioritizing problems as reportable if they are easily resolved (24). the item and composite percent positive scores with 95 % confidence intervals represented in table 2 highlight the strengths and the weaknesses of the patient safety culture in neurosurgery departments from republic of moldova. their classification was carried out using the harrington verbal-numerical universal scale, which is used in cases when the answers have a subjective character (18). among the dimensions with the highest score of the frequency of positive answers according to harrington scale, the following dimensions stand out: „teamwork within units”, „organizational learning -continuous improvement” and „supervisor/manager expectations and actions promoting patient safety”. the dimension with a high score of the frequency of positive answers according harrington scale was „feedback and communication about error”. the dimensions with a satisfactory score according harington scale of the frequency of positive answers were „handoffs and transitions”, „frequency of events reported”, „management support for patient safety”, „teamwork across units”, „communication openness”, „overall perceptions on patient safety”, „non punitive response to errors” and „staffing”. in our study, no dimensions with a "bad" or "critical" score according to the harrington scale were identified. the results of our study reflected that the composite "staffing" was rated with the lowest score of the frequency of positive responses. the same results reflected in the ahrq database where this composite was rated with the lowest score of the frequency of positive answers (25). c tartaglia reis explain that the staff felt overloaded by the unsuitability of personnel to their work activities, 22 silvia danu which can prejudice the quality of care provided (26). another reason of low score in moldova could be the insufficient staff of both doctors and nurses, which is why they work more intensively and more hours per week. lower frequency of adverse event reporting, „non punitive response to errors” and “communication openness” are another weakness points of patient safety culture in neurosurgical departments in moldova. maureen l. falcone et all remarked in their study that fear of blame and retaliation are common reasons nurses and physicians do not report errors (24). the item "staff worry that mistakes they make are kept in the personnel file" had the lowest level of positive responses and it influenced the composite score. the results suggest the existence of a so-called blame culture in neurosurgical departments, conclusions for the first time in the republic of moldova, the perception of patient safety culture in neurosurgery departments was studied, using an international instrument. the results reflect the positive attitude of the staff from the neurosurgery departments towards most dimensions of the patient safety culture. the study made it possible to highlight the strong and vulnerable points of the patient safety culture in neurosurgical departments, which require prompt intervention to be improved. the study outlined that the most vulnerable aspect of the patient safety culture is staffing. a particular problem in neurosurgical departments from republic of moldova remains the shortage of personnel and the large number of hours worked per week, which negatively influence patient safety, highlighting the necessity to develop policies and implement measures to motivate and influence health specialists to stay working in the medical system. another weakness points of patient safety culture in neurosurgical departments which need a prompt intervention for improvement are the lower frequency of adverse event reporting, along with „non punitive response to errors” and “communication openness”. to change the situation in this sensitive but very important field, it is necessary to develop and to implement a system for reporting of adverse events associated with the medical care, to encourage and to stimulate the adverse event reporting and to develop the culture of learning from errors. it is important to exclude blaming or punishing those who report or commit errors. to achieve this, it is necessary to organize training courses and constructive discussions to analyse the reported adverse events, so that the staff understand that the goal of this process is to increase patient safety and the quality of medical care. references 1. world health organization. global patient safety action plan 2021–2030:towards eliminating avoidable harm e health care [internet]. world health organization. 2021. 1689–1699 p. available from: https://www.who.int/team s/integrated-health-services/patientsafety/policy/globalpatient-safety-action-plan 2. world health organization. patient safety incident reporting and learning systems [internet]. technical report and guidance. 2020. available from: https://www.who.int/publications/i/item/978924001033 8 3. meyer hs, wagner a, obermueller t, negwer c, wostrack m, krieg s, et al. assessment of the incidence and nature of adverse events and their association with human error in neurosurgery. a prospective observation. brain and spine. 2022;2:100853. 4. mardon re, khanna k, sorra j, dyer n, famolaro t. exploring relationships between hospital patient safety culture and adverse events. j patient saf [internet]. 2010 dec [cited 2022 oct 10];6(4):226–32. available from: https://journals.lww.com/01209203-201012000-00006 5. what is patient safety culture? | agency for healthcare research and quality [internet]. [cited 2022 jun 14]. available from: https://www.ahrq.gov/sops/about/patie nt-safety-culture.html 6. wagner c, smits m, sorra j, huang cc. assessing patient safety culture in hospitals across countries. available from: https://academic.oup.com/intqhc/article/25/3/213 /1815095 7. berger ms, wachter rm, greysen sr, lau cy. changing our culture to advance patient safety: the 2013 aans presidential address. j neurosurg [internet]. 2013 dec 1 [cited 2021 aug 10];119(6):1359–69. available from: https://thejns.org/view/journals/j-neurosurg/119/6/articl e-p1359.xml 8. expert panel convened by the national patient safety foundation. free from harm. 2015;1–45. 9. what is patient safety culture? | agency for healthcare research and quality [internet]. [cited 2022 oct 17]. available from: https://www.ahrq.gov/sops/about/patien t-safety-culture.html 10. sops user network a. international use: countries where sops ® has been administered. 11. sops user network a. international use: languages that sops ® has been translated into. 23 the challenges and opportunities of patient safety culture 12. kirimlioğlu n. patient education and its importance in terms of patient safety. int j res. 2018;6(12):109–20. 13. tereanu c, smith sa, ghelase s, sampietro g, molnar a, moraru d, et al. maedica-a journal of clinical medicine psychometric properties of the romanian version of the hospital survey on patient safety culture (hsops). maedica-a j clin med [internet]. 2018;13(1):34–43. available from: https://doi.org/10.26574/maedica.2018.1 3.1.34 14. tereanu c, ghelase m, ligia furtunescu f, dragoescu a, molnar a, moraru d, et al. original paper measuring patient safety culture in romania using the hospital survey on patient safety culture (hsopsc). curr heal sci j. 2017;43(1). 15. tereanu c, sampietro g, sarnataro f, siscanu d, palaria r, savin v, et al. survey on patient safety culture in the republic of moldova: a baseline study in three healthcare settings. med pharm reports [internet]. 2018 jan 30;91(1):65–74. available from: https://www.medpharma reports.com/index.php/mpr/article/view/869 16. ţurcanu t, buta g, clişcovschi t. siguranţa pacientului: ce este de făcut în republica moldova? sanat publica, econ si manag med [internet]. 2018;75–76(2–2):14. available from: http://www.who.int/ 17. westat j, sorra n, yount t, famolaro mps, gray mbal. ahrq hospital survey on patient safety culture version 2.0: user’s guide. 2021 [cited 2022 oct 24]; available from: http://www.ahrq.gov 18. (pdf) оценка эффективности научных и научно-технических проектов на основе обобщенной функции харрингтона [internet]. [cited 2022 nov 8]. available from: https://www.researchgate.net/publication/338543651_o cenka_effektivnosti_naucnyh_i_naucno-tehniceskih_pro ektov_na_osnove_obobsennoj_funkcii_harringtona 19. han sj, rolston jd, lau cy, berger ms. improving patient safety in neurologic surgery. neurosurg clin n am [internet]. 2015 apr 1 [cited 2020 jul 30];26(2):143–7. available from: https://linkinghub.elsevier.com/retrieve/ pii/s1042368014001429 20. mardon re, khanna k, sorra j, dyer n, famolaro t. exploring relationships between hospital patient safety culture and adverse events. j patient saf. 2010;6(4):226– 32. 21. rolston jd, bernstein m. errors in neurosurgery. neurosurg clin n am [internet]. 2015 apr 1 [cited 2020 sep 10];26(2):149–55. available from: http://dx.doi.org/1 0.1016/j.nec.2014.11.011 22. fujita s, seto k, ito s, wu y, huang cc, hasegawa t. the characteristics of patient safety culture in japan, taiwan and the united states. bmc health serv res. 2013; 23. burlison jd, quillivan rr, kath lm, zhou y, courtney sc, cheng c, et al. a multilevel analysis of u.s. hospital patient safety culture relationships with perceptions of voluntary event reporting hhs public access. j patient saf. 2020;16(3):187–93. 24. falcone ml, van stee sk, tokac u, fish af. adverse event reporting priorities: an integrative review. j patient saf [internet]. 2022 jun 1 [cited 2022 nov 24];18(4):e727–40. available from: https://journals.lww.com/journalpatientsafety/fulltext/2 022/06000/adverse_event_reporting_priorities__an_inte grative.20.aspx 25. sops user network a. patient safety surveys on patient safety culture tm (sops ®) hospital survey 2.0 2022 user database report surveys on patient safety culturetm. 2022 [cited 2023 jan 16]; available from: www.ahrq.gov 26. tartaglia reis c, guerra paiva s, sousa p. the patient safety culture: a systematic review by characteristics of hospital survey on patient safety culture dimensions. int j qual heal care [internet]. 2018 [cited 2020 jul 31];30(9):660–77. available from: https://academic.oup.com/intqhc/article/30/9/660/4998 840 27. draganović š, offermanns g. overview of patient safety culture in bosnia and herzegovina with improvement recommendations for hospitals. j patient saf. 2022;publish ah(february). doi: 10.33962/roneuro-2022-004 clinical-pathological features and molecular background of oligodendrogliomas. a single centre retrospective study g. popescu, francesca paslaru, a.c. paslaru, m. apostol, m.c. zaharia, m. popescu, r.m. gorgan romanian neurosurgery (2022) xxxvi (1): pp. 23-27 doi: 10.33962/roneuro-2022-004 www.journals.lapub.co.uk/index.php/roneurosurgery clinical-pathological features and molecular background of oligodendrogliomas. a single centre retrospective study g. popescu1, francesca paslaru1, a.c. paslaru2,3, m. apostol1, m.c. zaharia1, m. popescu4, r.m. gorgan1,2 1 4th neurosurgical department, “bagdasar arseni” clinical emergency hospital, bucharest, romania 2 “carol davila” university of medicine and pharmacy, bucharest, romania 3 department of genetics, “dr. victor gomoiu” children’s clinical hospital, bucharest, romania 4 department of neurosurgery, pitesti emergency hospital, university of pitesti, romania abstract background: diffuse gliomas are the most frequent primary central nervous system (cns) neoplasms, originating from the parenchyma itself, oligodendrogliomas accounting for approximately 10% of cerebral gliomas. for the past 20 years, the study of genetic/molecular mechanisms of gliomagenesis and progression has gradually come into focus. however, the biological and clinical significance of these mutations is still to be completely characterized. the purpose of this article is to describe our clinical experience with oligodendrogliomas and to review the current literature, in order to better describe the characteristics of the molecular/genetic oligodendroglioma subgroups. methods: we performed a single-institution retrospective study that included 66 patients with oligodendrogliomas operated in our department between january 2011 and december 2018. results: our study included 26 female patients (39%) and 40 male patients (59%). the mean age at presentation was 39.9year-old (range 26-59year-old). the tumours were located predominantly in the right hemisphere (53%), the majority being situated in the frontal lobe (59%). 64% of the patients had signs of mass effect on the imaging studies, 13% presented with brain herniation syndromes, 16 % of the surgically treated patients had a relapse with regrowth and malignant transformation of the tumour. the most common complaint that the patients had at admission was headaches. seizures were the second most common symptom that determined the patients to seek medical attention. conclusion: the expanding knowledge regarding the genetic alterations of oligodendroglial tumours could lead to significant changes in treatment strategies. however, the utility of each particular marker in planning the treatment has yet to be established. emerging data will, most likely, improve outcome prediction and adjuvant therapy strategies through identifying the patients most likely to benefit from a particular treatment. keywords oligodendrogliomas, molecular corresponding author: g. popescu “carol davila” university of medicine and pharmacy, bucharest, romania george_popescu39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 24 g. popescu, francesca paslaru, a.c. paslaru et al. introduction diffuse gliomas are the most frequent primary central nervous system (cns) neoplasms, originating from the parenchyma [1]. about 75% of gliomas in adults are astrocytic, two-thirds being glioblastomas, the most malignant form. oligodendroglial tumors account for than 10% of the gliomas [2]. for the largest part of the last century, the diagnosis of oligodendrogliomas has been based on histopathological aspects alone. for the past 20 years, the study of genetic/molecular mechanisms of glioma genesis and progression has gradually come into focus. the 2021 world health organization (who) classification of tumors of the cns includes molecular features for diagnosis and further classification of oligodendroglioma into idh-mutant and 1p/19q-codeleted [3]. the biological and clinical significance of these mutations are still to be completely characterized. the purpose of this article is to describe our clinical experience with oligodendrogliomas and to review the current literature, in order to better describe the characteristics of the molecular/genetic oligodendroglioma subgroups. materials and methods we performed a single institution retrospective study that included the patients of the 4th clinical department of neurosurgery of the bagdasar-arseni clinical emergency hospital. we retrospectively reviewed the case files of 66 patients with oligodendrogliomas operated in our department between january 2011 and december 2018. we only included patients operated for oligodendrogliomas with a positive anathomopathological examination for a “classical” oligodendroglioma. exclusion criteria were diagnosis of primary glioblastoma, oligoastrocitoma with important oligodendroglial compound or patients with a high suspicion for oligodendroglioma, that refused surgery or biopsy for diagnosis. data were obtained by studying patient files. results our study included 26 female patients (39%) and 40 male patients (59%). the mean age at presentation was 39.9year-old (range 26-59year-old). the tumors were located predominantely in the right hemisphere (53%), the majority being situated in the frontal lobe (59%). 64% of the patients had signs of mass effect on the imaging studies, 13% presenting with brain herniation syndromes (figure 1). figure 1. distribution of patients based on the presence/absence of mass effect on imaging studies 16 % of the surgical treated patients had a relapse with regrowth and malignant transformation of the tumor (figure 2). figure 2. distribution of the patients based on the presence/absence of relapse with malignant transformation the most common complaint that the patients had at admission was headache. seizures were the second most common symptom that determined the patients to seek medical attention (figure 3). figure 3. distribution of the patients based on the clinical symptoms at admission no 84% grade iv glioblastoma 16% no grade iv glioblastoma 0 5 10 15 20 25 30 35 40 51% 36% 13% with without brain herniation syndrome 25 clinical-pathological features and molecular background of oligodendrogliomas illustrative case a 30-year-old male with no significant medical history was referred to our clinic for intense headache, progressively worsened during the month prior to admission. clinical examination showed no neurological deficit. gadolinium-enhanced mri scan revealed a right fronto-temporal tumor, measuring 9.5 cm in diameter, compressing the adjacent structures and producing mass effect on the right lateral ventricle (figure 4). figure 4. gadolinium enhanced mri scan, axial section, showing a right fronto-temporal tumor, measuring 9.5 cm in diameter, compressing the adjacent structures with inhomogenous enhancement we performed a gross total resection through a pterional approach (figure 5, figure 6). figure 5. intraoperative aspect showing the yellow-grey tumour figure 6. intraoperative aspect showing the resection cavity the patient was discharged 7 days later, with no postoperative neurological deficits. control ct scan showed a gross total resection of the tumor (figure 7). figure 7. postoperative ct scan showing the resection cavity 26 g. popescu, francesca paslaru, a.c. paslaru et al. histopathological examination showed arciform vascularization (figure 8), “boiled egg cells” (figure 9) and high fibrilarity (figure 10). figure 8. histopathological specimen showing arciform vascularization figure 9. histopathological specimen showing “boiled egg cells” aspect figure 10. histopathological specimen showing high fibrillarity mlpa analysis of the tumor sample identified a codeletion of 1p19q and a c.395g>a (p.r132h) mutation in the exon 4 of idh1 gene. the analysis was negative for mutations of exons 11 and 15 of braf gene, egfrviii, mgmt promoter methylation and tert promoter mutation. the patient had a favorable evolution, with no neurological deficits and was discharged in the seventh postoperative day. discussion under the generic term “oligodendroglioma” is a heterogenous group of tumors, with a variable response to adjuvant therapy. this variance highlights the need for markers that can guide the clinical decision-making. codeletion of 1p19q occurs in 50 to 76% of oligodendrogliomas [4] [5]. eortc 26951 and rtog 9402 studies proved that combining radiation therapy with procarbazine, vincristine and lomustine chemotherapy protocol drastically increased overall survival in 1p19q codeleted anaplastic oligodendroglioma patients compared to radiotherapy alone [6] [7]. the eortc 26951 trial investigated the adding of six cycles of standard procarbazine, vincristine and lomustine to radiation therapy of 59.4 gy in 33 fractions in anaplastic oligodendroglioma patients and reported a significant difference in overall survival [7] [8]. patients with 1p19q codeleted oligodendrogliomas benefitted more from the addition of chemotherapy to radiotherapy, the risk reduction in patients with non-codeleted tumors being significantly lower [7]. regarding both trials, it is also notable the fact that patients with 1p19q codeleted oligodendrogliomas who were treated with adjuvant radiotherapy alone initially, had a lower survival rate at progression, despite being administered a heightened chemotherapy regimen [4] [7]. the codel trial has been designed to compare administration of adjuvant therapy consisting of either radiotherapy alone, themozolomide alone or radiotherapy combined with themozolomide. the analysis from the initial study design showed that themozolomidealone patients experienced a significantly shorter progression free survival, compared to either one of the radiotherapy arms [9]. the study has been subsequently redesigned to compare radiotherapy combined with procarbazine, lomustine and vincristine to radiotherapy and themozolomide regimens and is still ongoing. mutations of idh1 and idh2 seem to occur in about 70% of oligodendroglioma tumors, mainly 27 clinical-pathological features and molecular background of oligodendrogliomas affecting amino acid 132 of idh1 or idh2 [10] [11]. idh1 is known to function as a tumor suppressor, its mutational inactivation leading to tumorigenesis, partially through the induction of the hif-1 pathway [12] [13]. idh mutations have been reported in several studies to produce a favorable prognostic impact [7] [10] [14]. however, despite the more favorable prognosis of patients with oligodendrogliomas harboring idh mutations, it hasn’t been proven yet that the treatment strategy should be changed regarding the idh status. conclusions the expanding knowledge regarding the genetic alterations of oligodendroglial tumours could lead to significant changes in treatment strategies. however, the utility of each particular marker in planning the treatment has yet to be established. emerging data will, most likely, improve outcome prediction and adjuvant therapy strategies through identifying the patients most likely to benefit from a particular treatment. romanian neurosurgery (2019) xxxiii (2): pp. 178-182 doi: 10.33962/roneuro-2019-033 www.journals.lapub.co.uk/index.php/roneurosurgery the evaluation of long-term screw pull-out rates following posterior thoracolumbar fusion surgery with short and thin pedicle screws umit kocaman1, hakan yilmaz2 1 izmir cigli region education and research hospital, department of neurosurgery, izmir, turkey 2 university of healt sciences izmir bozyaka education and research hospital, department of neurosurgery, izmir, turkey abstract background. the aim of this study was to evaluate screw pull-out rates after fusion operations with short and thin pedicle screws. methods. a total of 200 posterior lumbar and thoracolumbar fusion operations performed at our clinic with short and thin pedicle screws (5.5x35 mm) were retrospectively evaluated. the patients were assessed with computed tomography postoperatively on the day of surgery and at the 6th month. single groove retraction of the transpedicular screw was evaluated as pull-out. the results were evaluated by the 'number of pull-out cases / total number of cases' and also the 'total number of pull-out screws / total number of screws used' ratios. results. there were 112 (56%) female and 88 (44%) male patients with a mean age of 58 years. the total number of screws used in the 200 cases was 1188. there were 88 (7.4%) thoracic pedicle screws, 1056 (88.9%) lumbar pedicle screws and 44 (3.7%) sacral pedicle screws used. no pull-out was found in the control cts taken postoperatively. left side t11 and t12 pull-out was observed in one case and left l4 pull-out was observed in another case in the control cts taken at the postoperative 6th month. pull-out was observed in 2 (1%) of the 200 cases and 3 (0.25%) of the 1188 screws. conclusions. all the short and thin pedicle screws used had passed the pedicle length and neurocentral junction. the use of a 5.5x35 mm screws in fusion operations is less invasive than using longer and thicker screws while the pull-out rates may be similar. introduction posterior lumbar and thoracolumbar fusion operations constitute an important part of neurosurgery practice. the major problems after these operations are screw pull-out, adjacent segment degeneration, deterioration of instrumentation integrity, and fusion insufficiency. various preventive measures such as post-cement screw application and porous coated screw application are rarely used to prevent screw pull-out, while the tendency is to use long and thick screws. the general keywords fusion, instrumentation, pedicle, screw corresponding author hakan yilmaz university of healt sciences izmir bozyaka education and research hospital, department of neurosurgery, izmir, turkey dr_hakanyilmaz@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 179 the evaluation of long-term screw pull-out rates following posterior thoracolumbar fusion surgery preference is to use 6.5x45 mm, 6.5x50 mm, 6.0x45 mm, 6.0x50 mm screws for the lumbar and thoracolumbar junction. screws 7.0 mm thick or 55 mm long are also in use for the lumbar region. although long and thick screw applications increase spine stability, they also create surgical risk [2,4,12]. we investigated the pull-out rates in the cases where we used screws that were shorter and thinner than those generally used in thoracolumbar fusion operations. we would like to share our experiences on surgical safety in posterior lumbar and thoracolumbar fusion surgeries in this regard. methods a total of 200 posterior lumbar and thoracolumbar fusion operations performed with short and thin pedicle screws between 2016 and 2018 at the izmir cigli regional training hospital's neurosurgery department were evaluated retrospectively. this evaluation was performed only in patients who underwent posterior segmental instrumentation and fusion with 5.5×35 mm transpedicular screws. cases where screws of a different size were used as necessary and those that required revision for postoperative screw malposition were not included in the study. an evaluation was made with preoperative ct in all cases and a screw length of 35 mm was used after it was deemed to be adequate to reach the neurocentral junction. the patients were evaluated with computed tomography postoperatively on the day of surgery and at the 6th month. single groove retraction of the transpedicular screw was evaluated as pull-out. the results were evaluated by the 'number of pull-out cases / number of cases' and the 'total number of pull-out screws / total number of screws' ratios. statistical analysis descriptive statistical methods were used in the evaluation of the data. the results were expressed as mean ± standard deviation and frequency (%). results the 200 patients included in the study consisted of 112 (56%) females and 88 (44%) males. the mean age was 58 years and the age range was 22-78 years. the primary pathology was narrow lumbar canal in 100 cases, lumbar spondylolisthesis (grade 1) in 26 cases, degenerative type lumbar spondylolisthesis (grade 1) in 24 cases, post-traumatic burst fracture requiring posterior thoracolumbar fusion in 22 cases, post-traumatic burst fracture requiring posterior lumbar fusion in 6 cases and primary or recurrent lumbar disc hernia with segmental instability in 22 cases (table 1). the number of screws used in the 200 cases was 1188. these consisted of 88 (7.4%) thoracic pedicle screws, 1056 (88.9%) lumbar pedicle screws and 44 (3.7%) sacral pedicle screws (table 2). no pull-out was found in any patient on the control cts taken the same day postoperatively (figure 1,2). left t11 and t12pull-out was observed in control cts performed at the postoperative 6th month in 1 case who had undergone thoracolumbar fusion (figure 3). left l4 pull-out was observed in 1 patient who had undergone surgery due to narrow lumbar canal. both patients underwent revision surgery. pull-out was therefore observed in 2 (1%) of the 200 cases and 3 (%0.25) of the 1188 screws. pathology female male total narrow lumbar canal 59 41 100 isthmic type lumbar spondylolisthesis (grade 1) 13 13 26 degenerative type lumbar spondylolisthesis (grade 1) 13 11 24 burst fracture requiring thoracolumbar fusion 12 10 22 lumbar disc herniation with segmental instability 12 10 22 burst fracture requiring posterior lumbar fusion 3 3 6 total 112 88 200 table 1. the distribution of the cases where short and thin pedicle screws were applied according to the primary pathology and gender. pathology lumbar pedicle screw thoracic pedicle screw sacral pedicle screw narrow lumbar canal 558 0 12 isthmic type lumbar spondylolisthesis (grade 1) 66 4 14 180 umit kocaman, hakan yilmaz degenerative type lumbar spondylolisthesis (grade 1) 206 6 8 burst fracture requiring thoracolumbar fusion 130 78 0 lumbar disc herniation with segmental instability 54 0 6 burst fracture requiring posterior lumbar fusion 42 0 4 total 1056 88 44 table 2. the distribution of the screws used. figure 1,2. spinal ct sagittal and axial images of the posterior lumbar fusion operation where short and thin pedicle screws (5.5 mm-35 mm) was used. figure 3. left side t12 screw pull-out of a patient on the spinal ct axial image who was inserted a short and thin pedicle screw. 181 the evaluation of long-term screw pull-out rates following posterior thoracolumbar fusion surgery discussion the mechanisms preventing pull-out are thought to be large screw outer diameter, low screw inner diameter, short intergroove distance, and a strong bone structure. the most important of these has been shown to a large screw outer diameter. it is believed that a length that goes past the neurocentral junction is sufficient in terms of stability. however, pericortical and even bicortical screw lengths that markedly go past the neurocentral junction are used in practice [2,4]. no significant correlation was found between the screw length and the force needed to create pull-out in the cadaver study of diaremes et al. bone density seemed to be a more important factor in their study [5]. karami et al. compared the force needed to create pull-out in mid-body, pericortical and bicortical screws in their cadaver study. the force needed to create pull-out increased as the screw depth increased. however, a statistically significant difference was only found between mid-body and bicortical screws [7]. there are also studies reporting opposite results in the literature [5]. our study provides the results of the pull-out evaluation of screws with a thickness of 5.5 mm and invasion depth of 35 mm that were used to go past the neurocentral junction. there was no significant difference between our pull-out rates during 6-month follow-up after 5.5x35 mm short and thin pedicle screws were inserted and the results of long and thick pedicle screw use in the literature [4,5,6]. it is possible that long and thick screws will be more effective in terms of spine stability according to denis' three-column theory [3,8]. however, all screws went past the pedicle length and neurocentral junction with short and thin pedicle screw use. the importance of short pedicle screws in terms of surgical safety increases when it is considered that spinal surgery makes up a significant part of neurosurgical practice and a large number of surgeries are performed by surgeons with various levels of experience. the anterior, antero-lateral and lateral areas of the pedicle screw application area are surrounded by arterial and venous structures with very high flow. although rare, damage to these structures during the screw implantation stage carries a high mortality rate [1,9,10,11]. most of these surgeries are elective and concern the spine and any mortality creates a difficult situation. vascular damage can occur at 3 different stages: pedicle probe implantation, tapping, and screw implantation [10,11]. we believe that using a 35 mm screw at the pedicle probe placement stage will improve surgical safety and may decrease the probability of invading the main vascular structures in case of lateral malposition. according to the results of this study, we recommend short pedicle screw use in appropriate cases after considering the risk-benefit balance. every patient needs to evaluated separately. biomechanical studies can evaluate the stability of short pedicle screws more clearly. our results indicate that the pull-out rates of short pedicle screws that reach the neurocentral junction are similar to those of long screws. the critical point here is that each patient should be evaluated according to his/her spine characteristics and the length of the screw to be used should be chosen so as to reach the neurocentral junction during preoperative planning. using a 5.5 mm screw instead of a 6.0 / 6.5 mm screw makes it easier to stay within the pedicle boundaries. it decreases the risk of pedicle burst during screw implantation and allows the use of a thicker screw when revision is required. our results indicate that the pull-out rate for 5.5 mm screws is similar to thicker screws. specific planning may be required for each patient in the presence of comorbid situations such as advanced osteoporosis, scoliotic deformity and rheumatic diseases. conclusion the use of a 5.5x35 mm screw during posterior lumbar and thoracolumbar instrumentation and fusion operations is less invasive than using longer and thicker screws and the pull-out rates may be similar. references 1. akinrinlola a, brinster dr. endovascular treatment of a malpositioned screw in the thoracic aorta after anterior spinal instrumentation: the screwed aorta. vasc endovascular surg. 2013;47:555–557. 2. chatzistergos p. e., magnissalis e. a., kourkoulis s. k. a parametric study of cylindrical pedicle screw design implications on the pullout performance using an experimentally validated finite-element model. medical engineering & physics.2010;32(2):145–154 182 umit kocaman, hakan yilmaz 3. cho w, cho sk, wu c. the biomechanics of pediclescrewbased instrumentation.j bone joint surg br. 2010 aug;92(8):1061-5. 4. daftari tk, horton wc, hutton wc. correlations between screw hole preparation, torque of insertion, and pullout strength for spinal screws. j spinal disord. 1994;7:139–45 5. diaremes p, kokkinakis mc, kurth aa, kafchitsas k. the role of insertion length of pedicle screws on their pullout strength. a cadaveric study.orthopaedic proceedings 201193-b:supp_iii, 366-366 6. galbusera f, volkheimer d, reitmaier s, berger-roscher n, kienle a, wilkehj. pedicle screw loosening: a clinically relevant complication? eur spine j.2015may;24(5):1005-16. doi: 10.1007/s00586-015-3768-6. 7. karami kj, buckenmeyer le, kiapour am, kelkar ps, goelvk, demetropoulosck, soo tm. biomechanical evaluation of the pedicle screw insertion depth effect on screw stability under cyclic loading and subsequent pullout. j spinal disord tech. 2015 apr;28(3):e133-9. 8. mehmanparast h, petit y, mac-thiong jm. comparison of pedicle screw loosening mechanisms and the effect on fixation strength. j biomech eng. 2015;137:121003 9. mirza ak, alvi ma, naylor rm, kerezoudis p, krauss we, clarke mj, shepherd dl, nassr a, demartino rr, bydon m. management of major vascular injury during pedicle screw instrumentation of thoracolumbar spine. clinneurol neurosurg 2017;163:53-59 10. wegener b, birkenmaier c, fottner a, et al. delayed perforation of the aorta by a thoracic pedicle screw. eur spine j. 2008;17:s351–s354. 11. zeiller sc, lee j, lim m, et al. posterior thoracic segmental pedicle screw instrumentation: evolving methods of safe and effective placement. neurol india. 2005;53:458–465. 12. zhang qh, tan sh, chou smm. investigation of fixation screw pull-out strength on human spine. journal of biomechanics. 2004;37(4):479–485. doi: 10.1016/j.jbiomec h.2003.09.005. romanian neurosurgery (2019) xxxiii (3): pp. 249-259 doi: 10.33962/roneuro-2019-042 www.journals.lapub.co.uk/index.php/roneurosurgery neurosurgery in the elderly patient gabriel iacob* * university hospital bucharest, romania motto: “love and respect old age people because you are aging too” aparna verma abstract objective. for government officials and health providers, elderly population aged 65 and over, especially neurosurgical patient, represent a larger concern, an increasing problem not only for socio-economic reasons related to the medical act, but also for additional care requirements which should be done by the family and society, including rehabilitation facilities, occupational & physical therapy, speech therapists, visiting nurses, to insure an effective recuperation after hospital discharge. a retrospective study with 325 "elderly" patients cohort, aged 65 and over, admitted in the neurosurgery department undergoing common neurosurgical procedures, in the last five years offer an evaluation for neurosurgical procedures, outcomes, comorbidities, anaesthetic and analgesic requirements, outcome. material and method. this study was performed on patients aged 65 years or older, with neurosurgical diseases, admitted to the neurosurgery or the intensive care unit of our hospital, between 2014-2019. an analysis was made on variables such as age, pathology, comorbidities, length of hospital stay especially in the icu unit, type of cranio-cerebral or spinal procedures performed, anaesthesia protocols, complications, performance status, re-admissions and mortality. results. patients age were divided into three categories: between 65-70 years old there were 152 patients (46,76%), between 70-85 years old 93 patients (28.61%) and over 85 years old 80 patients (24,61%). 173 patients were females (53,23%), 152 were males (46.76 %). the admission glasgow coma scale (gcs) score to those over 85 years old was between 3-12 in 29 cases (8.02%) with early death in 13 patients. several comorbidities were noticed in 294 patients (90.15%): cardiac, pulmonary, hematologic especially coumarinic overdose, hepatic and renal failures, psychiatric illnesses, concomitant systemic disease or immunosuppressed patients by decompensated diabetes, primitive cancers affecting various organs, infectious diseases, also severe osteoporosis, chronic ethylic intoxication, limiting surgical attitude, also obtaining the informed consent for surgery. there were 154 (47,38%) patients with cerebral pathology and 171 (52,61%) patients with spinal pathology. most common surgical procedures performed were: craniotomies for tumours and hematoma removal, minimal invasive procedures for spine, endovascular and vertebroplasty. the median length of stay for emergency patients was significantly longer than that of elective patients (13 vs. 8 days). for 215 (66.15%) patients general anaesthesia was performed, local anaesthesia in 97 (29.84%) patients, 13 patients (4%) were not operated. good quality of life results appreciated by patients and relatives were recorded in 236 cases (72.61%) in the first and second category; less better results to those over 85 years old; same symptoms especially pain 63 patients (19.38%), complications to 47 patients (14,46%) especially cardiac, renal and keywords geriatric neurosurgical patient, anaesthetic and analgesic requirements to aged people, concomitant diseases, minim invasive neurosurgical procedures, pre-and postoperative care, life quality corresponding author: gabriel iacob university hospital bucharest, romania gbrl_cb@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 250 gabriel iacob respiratory failures, also motor deficits, seizures, csf fistula, mortality in 26 cases (8%), re-admissions in 45 cases (13.84%) less than 1 month after discharge. conclusions. old prejudices that old age is a contraindication for surgery have to be removed. clinical and surgical decisions for neurosurgical procedures in the elderly are decisive for limiting reported morbidity and mortality rates. for life quality, realistic family and society expectations, several aspects should be considered for safe and effective results: careful patient selection on patient status, comorbidities and physiological reserve; neurosurgical pathology, urgency of the surgical procedure, the strategy of neurosurgical management based on advances in imaging and interventional radiology, minimal invasive neurosurgical procedures with significant preoperative and postoperative care. good results could be obtained even in elderly people for chronic subdural hematoma, simple brain or spinal tumour, good grade aneurysm, trigeminal pain, vertebroplasty in spinal vertebral fractures, etc. introduction aging means concomitant a physiological process but also structural degeneration, a graded loss of functional capacity of all organs and tissues (1)(2). the number of elderly patients is increasing worldwide, generating a larger concern (3-7), an increasing problem regarding socio-economic reasons related to the medical act, morbidity and additional care requirements, perioperative adverse events (8-10). it is estimated that between 2000 and 2050, the proportion of the world's population over 60 years will double, and the number of people aged 80 and older will quadruple (7)(11). for neurosurgical patient, beyond the age of 65 years, both chronic or in emergency, all measures should be institute to maintain quality of life, to avoid perioperative mortality and morbidity (10). in romania the share of people over 65 years of age, was 18% of the total population on january 1, 2018, respectively 3,559,957 persons out of 19,523,621. according to the nis data, among the elderly, the men numbered 1,433,412 persons (15% of the total number of men in romania of 9,543,228 persons) and the women 2,117,495 (21% of the total number of women residing in romania of 9,980,393 persons)(12). material and method this retrospective study was performed on 325 patients aged 65 years or older, with neurosurgical diseases, admitted to the neurosurgery or the intensive care unit of our hospital, between 20142019. an analysis was made on variables such as: age, pathology, the admission glasgow coma scale (gcs) score, both chronic or in emergency, comorbidities using charlson comorbidity index (13)(14), length of hospital stay especially in the icu unit, type of cranio-cerebral or spinal procedures performed, anaesthesia protocols, complications, performance status, re-admissions morbidity and mortality. 45.8% of patients had neurosurgical cranial pathology and 54,2% had neurosurgical spinal diseases. patients age were divided into three categories: between 65-70 years old there were 152 patients (46,76%), between 70-85 years old 93 patients (28.61%) and over 85 years old 80 patients (24,61%). 173 patients were females (53,23%), 152 were males (46.76 %). the admission glasgow coma scale (gcs) score was between 3-15, worse: between 3-5 especially to those over 85 years old in 29 cases (8.02%) with early death in 13 patients. a cgs score between 7-14 was recorded to 89 patients (27,38%): 12 cases (3.69%) in the first category, 42 cases (12.95%) cases in the second and 35 cases (10.76%) in the third. several combined comorbidities were encountered in 294 patients (90.15%), limiting surgical attitude, also obtaining the informed consent for surgery: cardiac insufficiency, several cardiac diseases with damage to the ejection fraction (myocardial infarction, arrhythmias, valvular stenosis or insufficiency, untreated hypertension); chronic pulmonary disease, bronchial asthma; previous strokes with hemiplegia; severe haematological diseases (lymphoma, leukemia, myeloma, coagulation disorders with thrombocytopenia or coumarinic overdose); hepatopathy (cirrhosis, portal hypertension with variceal bleeding history, chronic hepatitis); kidney failure patients submitted in the dialysis program; peptic ulcer disease; connective tissue disease; peripheral vascular disease (intermittent claudication, chronic arterial insufficiency with by-pass, untreated thoracic or abdominal aneurysm), psychiatric illnesses (dementia); concomitant systemic disease or immunosuppressed patients by diabetes, primitive and metastatic cancers affecting various organs, chemotherapies, transplant patients, infectious diseases even aids; severe osteoporosis, chronic ethylic intoxication, drug allergies. neurosurgical pathologies varied alone or concurrently: 154 (47,38%) patients with cerebral pathology and 171 (52,61%) patients with spinal pathology: cranio-cerebral and spinal trauma 251 neurosurgery in the elderly patient (hematomas: epidural, subdural, intracerebral, posttraumatic subarachnoid haemorrhage, cerebral and spinal contusions, dai, cerebral lacerations, csf fistula, schneider syndrome, hematomyelia); cerebral tumours: extraaxial meningioma, metastasis, gliomas especially glioblastoma, schwanomas, pituitary and spinal tumours: extradural, intradural, intramedullary, frequent metastasis in lung, breast, prostate cancer; cerebral aneurysm, carotid-cavernous fistula, mav, spinal degenerative myeloradiculopathy, mielopathy with cervical and lumbar canal stenosis, spinal instability with osteoporotic vertebral changes, vertebral fractures; arnold neuralgia, trigeminal, atypical facial pain, spinal neuropathic pain; tremor (parkinson's syndroms & disease, dystonic movements), blepharospasm even meige syndrome, spasmodic torticollis. all patients were carefully neurologic, biologic, neuro-imagistic, multidisciplinary evaluated; neurosurgical surgical indication, anaesthesia protocol, informed consent to be used to each patient were supported with accuracy. several procedures have been performed: craniotomies for tumours and hematoma removal, minimal invasive procedures for spine, endovascular, vertebroplasty, nerve block, neurovascular decompression or gamma-knife for pain procedures have been performed. results the median length of stay for emergency patients was significantly longer than that of elective patients ranged between 13 vs.8 days, and in the icu unit vary from 1 to 63 days. for 215 (66.15%) patients general anaesthesia was performed, local anaesthesia in 97 (29.84%) patients, 13 patients (4%) were not operated. good quality of life results appreciated by patients and relatives were recorded in 236 cases (72.61%) in the first and second category; less better results to those over 85 years old; same symptoms especially pain 63 patients (19.38%), complications to 47 patients (14,46%) especially cardiac, renal and respiratory failures, also motor deficits, seizures, csf fistula, mortality in 26 cases (8%), re-admissions in 45 cases (13.84%) less than 1 month after discharge. for old patients physical therapists may improve strength and balance, safely walk ability, climb stairs before being released from the hospital. occupational therapists may help such patients to be able to do personal hygiene using the bathroom, to get dressed; speech language pathologists could help patients with speech, language or thinking. discussion the elderly patient defined as an individual 65 years of age and over, still represent all around world in general, a fragile population, a great concern, with higher costs of health care, a difficult issue for the health systems struggling with limited resources (37)(9)(10). for each aging person there are a personal rate of degeneration of cns as like as the whole body, in anatomy, in mental and physical activity, also in higher costs of living, lifestyle change, loneliness, possible dependence of specific medication for medical associated illnesses such as diabetes and cardiovascular disease (3)(6). it's also a reality that the elderly population represent the fastest growing segment of the world's population; the world's population over 60 years will double between 2000 and 2050 and the number of people aged 80 and older will quadruple (7). 47,8 million the number of people age 65 and older in the united states on july 1,2015; this group accounted for 14,9 per cent of the total population (15). 98,2 million the projected population of people age 65 and older in 2060; of this number 9,7 million will be age 85 or older (16). such growing proportion affect also the neurosurgical admissions both in emergency surgeries or classical presentations for every group of persons on age “young-old” 65-74, “middle-old” 75-84 and “old-old” > 85 (17). there are several changes involved in different degree with age, with neurosurgical interest too (1)(2)(18-23): -cerebral atrophy affecting especially the frontal and temporal lobes, decline in brain weight, increase in ventricular size, thickening of meninges, decrease in width of gyri, deep sulci, cortical neurons, myelinated axons, the number of synapses per neuron, loss of nissl substance, nuclear atrophy; intracellular deposits, granulation or fragmentation of mitochondria. these aspects are generating tolerance in front of any expansive process, clinical onset delay in case of tumours, intracranial hematoma, facilitates surgical approach, allows intracranial expansive processes removal. -cerebral fragility with decreased cerebral compliance that induces the brain's difficulty to resume its 252 gabriel iacob anterior position, able to generate hematoma recurrence, hydrocephalus, etc. -decreased cerebral blood flow, loss of vascular autoregulation and responsiveness to neuronal demand, hypercapnia, heterogeneous regional variations with decreased cellular oxygen, glucose and oxidative metabolism, altered sodium, potassium and calcium homeostasis with reduced axoplasmatic transport, calcium mediated and synaptic neurotransmitter release. there are also general decrease in excitability, peripheral nerve conduction velocity, altered reflex responses and increased latency of evoked potential, a disorganization of highly coordinated activities, with autonomic and homeostatic changes: reduced temperature regulation, orthostatic hypotension, chronic constipation, slowed hear rate, decreased blood pressure. -leukoaraiosis (gr."leuko-" = white, meaning white matter and the adjective «araios" ="thin."hachinski v. 1987) are typically generated by: lacunar stroke/transient ischemic attack (tia), dementia of both vascular and non-vascular etiologies (hypertension, degenerative, in alzheimer's disease), sporadic cerebral amyloid angiopathy, diabetes; the precise pathogenic mechanisms remain unclear. recent genetic results strongly supported that leukoaraiosis is associated with immune response and neuroinflammation (23). pathologically, leukoaraiosis is characterized by white matter gliosis, axonal and myelin loss, increased perivascular spaces, patchy demyelination, hyaline thickening and arteriosclerosis of small vessels that can evolve to lipohyalinosis, fibrinoid necrosis, and denudation of ependyma. main clinical manifestations are cognitive and executive troubles (memory loss especially short-term memory, visual and hearing loss, declining endurance, verbal intelligence, processing speech dysfunction in learning and language skills, depression), ankle jerks decreased or absent, increased primitive reflexes (glabella, palmomental), slowed forward flexed, altered gait, tremor with loss of fine motor coordination bladder instability. there are hypo-dense areas to cerebral ct scan, diffuse, heterogeneous, imprecisely delimited, primarily interesting the centre of the white substance or the immediate subcortical areas. the mri examination in weighted t1 sequences shows hypointense areas and the weighted t2 sequences show hyperintense areas; sometimes without correlation as number, localization. mri findings are commonly seen to elderly people with prevalence ranging from 50% to 100%. leukoaraiosis may explain poor clinical outcomes and increases the risk of disability, dementia, depression, stroke, and the overall morbidity and mortality. -amyloid angiopathy > 70 years: explains the difficulties of hemostasis, haemorrhagic recurrences, preanesthetic assessment, informed consent, perioperative evaluation, risk issues especially for those people identified with asa physical status of iii or iv. and care are magnified in older patient, anaesthetic management, efficient surgical skills procedures especially functional neurosurgery, radiosurgery, planned postoperative management may contribute to successful outcomes also to ameliorate quality of life related to neurosurgical diseases, also to a specific neurosurgical pathology, especially pain (3)(5)(7)(8)(10)(11)(24-29). there are medical factors affecting anaesthesia: multiple medical comorbidities including sepsis, metabolic disturbances severe obesity or poor nutritional status, alcohol and/or drug abuse, history of cardiac failure or myocardial infarction ≤ 1 year with low ejection fraction (ef) on echocardiography, severe uncontrolled hypertension, severe respiratory dysfunction, hepato-renal failures, neurovascular, psychiatric disease, history of cva or tia, peripheral vascular disease, immuno-compromised patients by diabetes, tuberculosis, etc; severe coagulopathy status with trombocytemia, haemophilia, antiplatelet agents even help syndrome (to old patients even a normal coagulogram may coexist with difficult hemostasis), cognitive function at risk especially at advanced age > 70 years: cognitive impairment, acute confusional state, delirium. there are also surgical factors affecting anaesthesia in all such high-risk geriatric patients which should be discussed in detail for optimizing the outcome with the anaesthesiologist and cardiologist (28)(29): -surgical position: prone, sitting, concorde position have always cardio-respiratory implications, wilson frame or similar with varying degrees of inclination, neck stabilization, spine traction, requirement of elective ventilation, head up to 10 degree and reverse trendelenburg may avoid perioperative blindness by direct/indirect eye pressure, ischemic 253 neurosurgery in the elderly patient optic neuropathy, central retinal artery occlusion (crao), cortical blindness. also a severe spinal trauma or an important scoliosis, osteoporosis, osteomyelitis, severe obesity or undernourished people. -plan of surgical excision, anticipated duration (in general surgery should never exceed 6.5 h in older patient), anticipated blood loss, neurophysiologic monitoring, postoperative ventilation. the anaesthetic regimen has to be tailored according to the physiological reserve: local or general anaesthesia. for general anaesthesia there are several remarks: -before induction the invasive monitoring for arterial blood pressure abp and central venous pressure cvp should be instituted under local anaesthesia. -induction should be performed with fentanyl, etomidate (etomidate requirement beyond the age of 80 years may decrease by 50%,), non depolarisant muscular blockade agents intravenously. propofol produces an exaggerated fall in blood pressure especially to old patients, dehydrated, midazolam has increased duration and potency, neuromuscular blocking agents are unchanged oral intubation. -anaesthesia should be maintained with 50% oxygen, air, sevoflurane in minimum alveolar concentration mac of 0.5 (mac requirement for volatiles also decreases in the elderly, though the onset may be delayed due to decreased cardiac output). monitoring should be performed by pulse oximetry: spo2, arterial blood pressure abp avoiding acidosis, hyper or hypotension 84 mm systolic minimum, hct > 28%/, hb > 9.4 with cardiac index (stroke volume) ↓ 24%; blood loss > 45%, heart rate hr, electrocardiogram ecg, end-tidal carbon dioxide, hourly urine output, temperature. to maintain hemodynamics and to avoid cerebral perfusion pressure crash crystalloids and noradrenaline should be infused intraoperatively. -even in case with normal coagulation test, haemostasis could be laborious in the confined space of the cranial cavity or the spinal canal presenting as the surgical field; in case of bleeding diathesis (due to prescribed medications in the form of clopidogrel, warfarin, etc., alone or more often in combination) especially in emergency this is dangerous. for such situations there are several costly, time consuming, delaying procedures: red blood cell transfusion, donor platelet, frozen plasma, novoseven, pronative, hemocompletan, recombinant factor viia, all of this are costly, time consuming, delay procedures. -postop. slowly awakening, extubated and closely watched in neurosurgical intensive care unit to improve resource utilization, decreased in-hospital mortality (26). the effect of depth of anaesthesia on outcomes is still a grey area. perioperative cardiac maintaining volume status, pulmonary evaluation are reliable predictors of complications, (ex. unoptimized pulmonary diseases, increased closing volumes and decreased expiratory flow rates, tracheostomy, postoperative mechanical ventilation) predispose older patients to complications and death, also renal status avoiding nephrotoxic drugs, prevention of hyperglycemia or hypoglycemia, adequate prophylaxis for deep venous thrombosis even with pneumatic compression devices, multiple medications for other co-morbidities. mental status should be assessed preoperatively because dementia is a predictor of poor outcome perioperatively, increasing mortality by 50% (25). nutritional deficiencies should be corrected because they play a role in wound healing and recovery albumin levels of < 3.2 g/dl in hospitalized elderly patients increased perioperative mortality (28), also pain should be treated. most common geriatric pathology are: -traumatic brain injuries, more common: subdural uni or bilateral hematoma a common pathology (11)(30-35), mainly affecting elderly patients, " not a benign disease" (34) in patients over 80 years old chronic subdural hematoma incidence is reported 127.1/100.000/year, with a mortality of less than 10%, a history of head injury is not always admitted, several cases could be under anticoagulant treatment because of cardiac pathologies or ictus cerebri, arterial hypertension, diabetes mellitus with severe thrombocytopenia, high inr, even with a normal coagulogramm haemostasis may be difficult. the most common clinical presentation include hemiparesis, disphasia/ aphasia, disorientation, hemianopsia. diagnosis is sustained on ct scan. anaesthesia should be local or general, to correct a severe coagulopathy may be necessary: thrombocytes, novoseven-factor vii, pronativ, hemocompletan in case of fibrinolysis. several 254 gabriel iacob surgical techniques could be used: craniotomy centred on the thickest portion of the clot (useful in clots that can't be evacuated through a simple trepan hole, allows brain to resume its anterior position, to evacuate a concomitant intracerebral hematoma, to monitor intracranial pressure in those with cgs <9 bullock et al, allows haemostasis), craniotomy, useful when intracranial pressure is maintained, requiring removal of the bone, trephination or two several trepan holes in the thickest parts of the hematoma (for example, frontal and parietal that may be needed to be incorporated into a fronto-temporoparietal craniotomy in case of relapse, hematoma consistency, thick membranes), the subdural evacuating port system (seps): the minimally invasive technique, a safe method, effective in subacute and chronic subdural hematoma in elderly patients, easy to perform with local or general anaesthesia, it takes less than 10 minutes, without irrigation, aspiration, catheter (36). postop complications are: recurrences, persistence of preop. brain position by decreased cerebral compliance, parenchymal haemorrhages in the same hemisphere or controlateral. outcome are measured with glasgow outcome scale (gos) or markwalder grading system (mgs) to evaluate improvement in neurological function in general a good gos in 86.1% of patients older than 80 years (11), the discharge disposition to return to an independent life, to rehabilitation or nursing home. there are also cerebral contusions and lacerations, rare extradural hematoma with late shift effect of cerebral parenchima, veins ruptures and haemorrhagic events, dimished recovery capacity. -cerebral aneurysm and less frequent cerebral arteriovenos malformation with subarahnoidian haemorrhage, ischemic & haemorrhagic strokes supra and infratentorial, associated with hydrocephalus and occlusive cerebrovascular disease 40% (3)(37). -epilepsy to older patients is are more frequent (the annual incidence is 85.9 per 100,000 for people aged 65-69 years and 135 per 100,000 for those aged over 80 years (38); similar status epilepticus appears to occur more frequently with significantly greater morbidity and mortality in this age group (39). there are focal seizures, automatisms without generalisation or with secondary generalisation, the postictal phase is prolonged with confusion and memory problems corresponding with focal changes on electroencephalograph (eeg) and neuroimaging epileptogenic lesion (40). epilepsy are more common encountered with stroke the risk of epilepsy increases up to 20-fold in the first year after a stroke, hypertensive encephalopathy, cerebral vasculitis, tumours (gliomas, meningiomas and metastases), trauma, dementia, alzheimer's disease are up to 10 times more likely to develop epilepsy than those without the condition (38). to older patients there are: side-effects, toxicity, increased susceptibility to anti-epileptic drug, a mortality rate 2-3 times higher than the general population, a very variable prognosis depending on the epilepsy syndrome, the frequency of seizures, the response to treatment an inadequate seizure control raise the suspicion of poor adherence or progressive neurodegenerative disease; social difficulties, multidisciplinary service requirements in the community (41). -cerebral tumours: meningiomas: are 12.8/100,000 incidence to those of ≥ 65 years of age, increasing with age (42) in the elderly, meningiomas are diagnosed small, slow growing, asymptomatic extraaxial tumours without brain edema, even calcified, occurring more frequently in women than men (43). for such tumours therapeutic attitude are conservative clinical observation and radiologic follow-up (44-46). for clinically symptomatic and fast growing meningioma, especially atypical or malignant, to elderly patients with limited physiological capacities and comorbidities, surgery after a careful consideration should be the mainstay of treatment for local tumour control (47-52), to realise genetic and histological diagnosis (it's possible to the same patient to see meningiomatosis with different genetic and histologic behaviour: benign and malignant meningiomas), but also stereotactic radiotherapy (srt), gamma knife, linac-based stereotactic radiosurgery effective in terms of tumour control and survival, safe with regard to toxicity the overall rates of complications ranged from 2.7% to 29.8%, and the overall incidence of complications 20% (range, 3–61%)(53-59). metastasis are increasing to the majority of cancer patients over the age of 65, not only cerebral or intradural spinal metastasis, but more frequent bone metastasis, involving the spine in approx. 50% (60). elderly survivors of breast cancer, lung cancer, and melanoma face risk of brain metastasis later in life; rates of synchronous brain metastases incidence 255 neurosurgery in the elderly patient proportions in lung, breast, and melanoma cancers were 9.6%, 0.3%, and 1.1%, respectively; such tumours may require extra surveillance in the years following initial cancer treatment. non-small cell lung cancer made up the majority of lung cancer sbm ip, at 13.4%, and small-cell lung cancer made up the majority of lung cancer lifetime brain metastases at 23.1%. the most frequent spinal metastases (60%) are from breast, lung, or prostate cancer (61). the chance that an elderly patient (60–79 years old) is affected by bony metastases is four times higher in men and three times higher in women than a middle-aged patient (40–59 years old). pain, neural compression with motor deficits, pathological fracture, and instability are the most common surgery indication. for cervical area: the occipitocervical junction can generally be treated by posterior resection and stabilization, in the middle and lower cervical spine the anterior approach with anterior decompression and anterior column reconstruction; in the thoraco-lumbar spine a posterior decompression and postero-lateral vertebral body resection through a posterior approach only, with a concomitant reconstruction and stabilization. there are also for paleative cases different treatment modalities—irradiation, chemotherapy, steroids, biphosphonates, morphine pump. since prospective randomized studies comparing different treatment modalities for spinal metastases including surgery are not available and are ethically difficult to achieve, each case remains an interdisciplinary, shared decision-making process for what is considered best for a patient or elderly patient. however, whenever surgery is an option, it should be planned before irradiation since surgery after irradiation has a significant higher complication rate. glioblastoma multiforme are at old age a high incidence, also most significant associated with poor prognosis, even after the introduction of temozolomide (tmz) in 2006, without any clear borderline (62). after published statistics from the japan brain tumour registry from 2001 to 2004 (63), patients aged > 65 years and > 75 years accounting for 42% and 11.4%, respectively; the most frequent age group of patients was 65–69 years, which accounted for 17% of the cases, median overall survival was 15 months. gbms are subdivided according to their molecular phenotype see who classification of central nervous system (cns) tumour 2016 (64), namely, cpg island methylator phenotype (g-cimp) and isocitrate dehydrogenase (idh) mutation: idh wild type and idh mutant absence of idh mutation, is the most predominant gbm in the elderly. also mgmt promoter methylation is independent of age, with 47% in the elderly, epidermal growth factor receptor egfr, p53, cdkn2a, pten were not prognostic factors (65), vascular endothelial growth factor (vegf) was higher in gbm in the elderly than in young patients, also the prognostic value of telomerase reverse transcriptase (tert) promoter mutation in gbm has been debated (66). although age is a poor prognostic factor, old age alone is suggested to have no association with poor prognosis, an aggressive treatment should not be withheld because of old age (67). multimodal treatment in elderly patients with gbm aged > 65 years should include: -surgical resection: achieving maximal tumour cytoreduction within the safety margin, brain decompression, histopathological and genetic diagnosis especially for idh mutation and mgmt methylation status. such aggressive attitude may prolonge survival by 2.8 times than biopsy (median os: 171 days after the craniotomy versus 85 days after the biopsy), also for aged patients ≥75 years may extend survival by 2 months, delayed tumour progression and improved functional prognosis (68-76). -radiotherapy hypofractionated radiotherapy (hypo-rt 40 gy/15 fr) alone can be considered if the tumour has an unmethylated mgmt promoter (7780) -with concurrent and adjuvant tmz in elderly patients with mgmt methylated tumours monotherapy with tmz can expect prolonged survival (78-82); clinical benefits of bevacizumab use in remain unclear (83)(84), also lack of evidence regarding the efficacy of carmustine wafer (85)(86). another cerebral tumor: schwanoma, pituitary adenoma (87) -spinal pathology means for old patients a wide range of neurosurgical procedures to solve: spinal degenerative myeloradiculopathy, mielopathy with cervical canal stenosis, lumbar spinal stenosis (it's important to clarify that surgery will not give 256 gabriel iacob another spine, also surgery is better to be done in a only surgical procedure); spinal tumours: extra/intra dural, intramedullary and more frequent vertebral metastasis in lung, brest or prostate cancers; spinal instability and osteoporotic vertebral changes. -chronic geriatric pain defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage", is a longstanding pain that persists beyond the usual recovery period or occurs along with a chronic health condition, for greater than 3 months is a more frequent neuropathic, persistent, recurrent, underreported; much more difficult to treat especially for those with long-lasting pain compared to young people, justified by pain corticalisation (88). such condition is impairing activities of daily living, ambulation, quality of life; more difficult to be understood especially to those patients with cognitive or language impairments; also may generate polypharmacy with concomitant medication, but also responsive for poor health, accidents, gait abnormalities, cognitive decline, denial, depression, psychosocial concerns, with direct and indirect estimated treatments costs close to $50 billion a year (89). there are several types of chronic pain, complex, multifactorial in older population, very debilitating and painful: trigeminal neuralgia, atypical facial pain, occipital neuralgia, postherpetic neuralgia, headache, stroke and phantom limb pain, failed spinal surgery, referred or pain related to cancer; also pain perception is more difficult to be treated. for such patients a multidisciplinary approach needs to be conceived: pharmacotherapy, psychological support, psychological support, also interventional procedures. a wide range of procedures (88) should be wisely proposed taking into account life expectancy, comorbidities, the patient's desire focusing on neuromodular rather than lesional techniques, also risks for each procedure: microvascular decompression, chemical neurolysis, radiofrequency and glycerol rhizotomy, stereotactic radiation, deep brain & spinal cord stimulation, motor cortex stimulation and neuraxial drug delivery. -tremor (parkinson's syndrome & disease and dystonic movements) treated especially by medication, dbs, motor cortex stimulation (90). -neuro-infections especially to immunocompromise patients: diabetes, tb, hiv, etc. -multiple sclerosis -dementia conclusions this study is a plea argue that in elderly patients, which is likely to continue to grow (6), risk factors should be adequately managed even in emergency (3), with correct preoperative evaluation, appropriate perioperative care (8), titrated anesthetic management, efficient surgical skills. planned postoperative management may improve neurological status (30)(91), outcomes, reduce mortality rates, reduce length of intensive care stay, improved resource utilisation, fiscal benefits (7)(9). further studies in the elderly are mandatory to be performed to improve clinical decisions on risk benefit ratios pending on new technologies. references 1. hickey r., sloan t.b. – physiologic changes with aging in the central nervous system, in albin m.s. text book of neuroanesthesia with nerosrgical and neuroscience perspective, 1997, 37, 1349-1360. 2. arseni c., balaceanu stolnici c., nica i. neurogeriatrie, editura medicala 1984. 3. dujovny m, charbel f geriatric neurosurgery, surg neurol. 1987, 28(1), 10-16. 4. o’brien d.p, nagaria j., et al. neurosurgery for the elderly: facts and figures, gerontology 1996, 42, 1– 6. 5. rha h.k., lee k.j. et al. neurosurgery for the elderly, journal of korean neurosurgical society 1997, 26 (12), 1699-1704. 6. chibbaro s, di rocco f et al. neurosurgery and elderly: analysis through the years, neurosurg rev. 2010, 34(2), 229-234. 7. gonzález-bonet lg, tarazona-santabalbina fj, et al. neurosurgery in the elderly patient: geriatric neurosurgery, neurocirugia (astur). 2016, 27(4), 155-166. 8. jin f, chung f. minimizing perioperative adverse events in the elderly. br j anaesth 2001, 87, 608-24. 9. mcgory ml, kao kk, et al. developing quality indicators for elderly surgical patients. ann surg 2009, 250, 338-347. 10. bhatnagar v., datta s.g.s., et al. the perioperative concerns of emergency neurosurgery in elderly patients: a series of three cases, journal of marine medical society 2017, 9, 1, 58-60. 11. gelabert-gonzález m, fernández-villa jm, et al. chronic subdural hematoma in patients over 80 years of age, neurocirugia (astur). 2001, 12, 325-330. https://www.jkns.or.kr/articles/search_result.php?term=author&f_name=hyung%20kyun&l_name=rha https://www.jkns.or.kr/articles/search_result.php?term=author&f_name=kyung%20jin&l_name=lee http://www.marinemedicalsociety.in/searchresult.asp?search=&author=vidhu+bhatnagar&journal=y&but_search=search&entries=10&pg=1&s=0 http://www.marinemedicalsociety.in/searchresult.asp?search=&author=sgs+datta&journal=y&but_search=search&entries=10&pg=1&s=0 257 neurosurgery in the elderly patient 12. ins romania, ponderea persoanelor varstnice, de peste 65 de ani, mediafax, 30 septembrie 2018, ora 14:19. 13. charlson me, pompei p, et al. a new method of classifying prognostic comorbidity in longitudinal studies: development and validation. j chronic dis 1987;40:373–83. 14. zhang jx, iwashyna tj, et al. the performance of different lookback periods and sources of information for charlson comorbidity adjustment in medicare claims, med care 1999; 37,1128–39. 15. united states census bureau -vintage 2015 population estimates. 16. united states census bureau 2014 national population projections. 17. leppik i antiepileptic drug trials in the elderly. epilepsy res. 2006 jan, 68(1), 45-48. 18. hickey r., sloan t.b. – physiologic changes with aging in the central nervous system, in albin m.s. text book of neuroanesthesia with neurosurgical and neuroscience perspective,1997, 37, 1349-1360. 19. duckett s. the normal aging human brain, in duckett s (ed): the pathology of the aging human nervous system, philadelphia, lea &febiger 1991, 1-19. 20. morris j.c. mcmanus d.q. the neurology of aging: normal versus pathologic change, geriatrics 1991, 46-47. 21. vital c, vital a. peripheral neuropathy, in duckett s (ed): the pathology of the aging human nervous system, philadelphia, lea & febiger 1991, 393-432. 22. berhouma m., salmon p.k.brain and spine surgery in the elderly, neurosurg rev. 2010, 34 (2), 229-234. 23. qing lin, wen-quing huang et al. genetic association of leukoaraiosis indicate pathophysiological mechanisms in white matter lesions etiology, reviews in the neurosciences, 2015-03_11, vol 26, issue 3. 24. audisio ra, ramesh h, et al. preoperative assessment of surgical risk in oncogeriatric patients. oncologist 2005, 10, 262-268. 25. cruickshank g.h, marshall .i neuroanesthesia in the elderly, current anesthesia &critical care 1997, 8,3, 103-107. 26. lang jm, meixensberger j, et al. neurosurgical intensive care unit-essential for good outcomes in neurosurgery? langenbecks arch surg. 2011, 396(4), 447-451. 27. maurice-williams rs, kitchen n. the scope of neurosurgery for elderly people, age ageing. 1993, 22(5), 337-342. 28. ciurea a.v., iacob g. technici neurochirurgicale, cartea universitara 2006, 1-28. 29. wong d. recognizing and controlling preoperative anesthesia and surgical risk factors in the older patient, dubai neurosurgery congress 2015. 30. zoia c, verlotta m, et al. chronic subdural haematoma in patients over 90 years: outcome after surgical treatment, austin neurosurg open access. 2014, 1(5), 1022. 31. lee l, ker j, ng hy et al. outcomes of chronic subdural hematoma drainage in nonagenarians and centenarians: a multicenter study, j neurosurg. 2016, 124(2), 546-551. 32. mulligan p, raore b, liu s, olson jj. neurological and functional outcomes of subdural hematoma evacuation in patients over 70 years of age, j neurosci rural pract. 2013, 4, 250-256. 33. stippler m, ramirez p, et al. chronic subdural hematoma patients aged 90 years and older, neurol res. 2013, 35, 243-246. 34. miranda lb, braxton e, et al. chronic subdural hematoma in the elderly: not a benign disease, j neurosurg. 2011, 114, 72-76. 35. gelabert-gonzález m, fernández-villa jm, et al. chronic subdural hematoma in patients over 80 years of age, neurocirugia (astur). 2001, 12, 325-330. 36. kenning t.j., dalfino j.c.. et al. analysis of the subdural evacuating port system for the treatment of subacute and chronic subdural haematomas, j.neurosurg. 2010, 113(5), 1004-1010. 37. ballotta e, da giau g, et al. early and long-term outcomes of carotid endarterectomy in the very elderly: an 18-year single-center study. j vasc surg 2009, 50, 518-525. 38. johnston a., smith p.e epilepsy in the elderly, expert rev neurother. 2010, 10(12), 1899-1910. 39. cloyd j, hauser w, et al. epidemiological and medical aspects of epilepsy in the elderly, epilepsy res. 2006 suppl 1:s39-48. 40. scottish intercollegiate guidelines network sign 2015: diagnosis and management of epilepsy in adults. 41. elger c.e., schmidt d. modern management of epilepsy: a practical approach. epilepsy behav. 2008, 12(4), 501-39. 42. claus e.b., bondy m.l. et al. epidemiology of intracranial meningioma, neurosurgery 2005, 57, 6, 1088–1095. 43. lee j, sadeb. the novel ‘class’ algorithmic scale for patient selection in meningioma surgery, in meningiomas, lee j., springer london, uk ed.,2009, 217–221. 44. bateman b.t., spellman j.p., et al. meningioma resection in the elderly: nation wide in patient sample, 1998–2002, neurosurgery 2005, 57, 5, 866– 871. 45. cahill k. s, claus e. b. treatment and survival of patients with nonmalignant intracranial meningioma: results from the surveillance, epidemiology, and end results program of the national cancer institute. https://www.ncbi.nlm.nih.gov/pubmed/?term=lang%20jm%5bauthor%5d&cauthor=true&cauthor_uid=21384190 258 gabriel iacob clinical article, journal of neurosurgery 2011, 115, 2, 259–267. 46. dolecek t.a., j. m. propp j.m. et al. cbtrus statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2005–2009, neuro-oncology 2012, 14, suppl. 5, v1– v49. 47. patil c.g., veeravagu a. et al. craniotomy for resection of meningioma in the elderly: a multicentre, prospective analysis from the national surgical quality improvement program,” journal of neurology, neurosurgery and psychiatry 2010, 81, 5, 502–505. 48. schul d. b., wolf s., et al. meningioma surgery in the elderly: outcome and validation of 2 proposed grading score systems, neurosurgery 2012, 70, 3, 555–565. 49. maurice-williams rs, kitchen nd.intracranial tumours in the elderly: the effect of age on the outcome of first time surgery for meningiomas, br j neurosurg. 1992, 6(2), 131-137. 50. tucha o., smely c., lange k. w., effects of surgery on cognitive functioning of elderly patients with intracranial meningioma, british journal of neurosurgery, 2001, 15, 2, 184–188. 51. poon m. t.c., fung l. h.k., et al. outcome of elderly patients undergoing intracranial meningioma resection a systematic review and meta-analysis, british journal of neurosurgery 2014, 28, 3, 303– 309. 52. boviatsis e. j., bouras t.i., et al. impact of age on complications and outcome in meningioma surgery, surgical neurology 2007, 68, 4, 407–411. 53. iwai y., yamanaka k., ikeda h. gamma knife radiosurgery for skull base meningioma: long-term results of low-dose treatment, journal of neurosurgery 2008, 109, 5, 804–810. 54. komotar r.j., lorgulescu j.b., et al. the role of radiotherapy following gross-total resection of atypical meningiomas, journal of neurosurgery 2012, 117, 4, 679–686. 55. kaul d., budach v., et al. “linac-based stereotactic radiotherapy and radiosurgery in patients with meningioma,” radiation oncology, 2014, 9, 1, 78. 56. kaul d., budach v. et al. outcome of elderly patients with meningioma after image-guided stereotactic radiotherapy: a study of 100 cases, biomed research international, 2015, article id 868401. 57. fokas e., henzel m., et al. stereotactic radiotherapy of benign meningioma in the elderly: clinical outcome and toxicity in 121 patients, radiotherapy and oncology 2014, 111, 3, 457–462. 58. pechlivanis i., wawrzyniak s., et al. evidence level in the treatment of meningioma with focus on the comparison between surgery versus radiotherapy: a review, journal of neurosurgical sciences 2011, 55, 4, 319–328. 59. stessin a.m., schwartz a., et al., “does adjuvant external-beam radiotherapy improve outcomes for nonbenign meningiomas? a surveillance, epidemiology, and end results (seer)-based analysis,” journal of neurosurgery, 2012, 117, 4, 669–675. 60. ascha ms, ostrom qt, et al. lifetime occurrence of brain metastases arising from lung, breast, and skin cancers in the elderly: a seer-medicare study, cancer epidemiol biomarkers prev 2019, 28(5), 917-925. 61. aebi m spinal metastasis in the elderly, eur spine j. 2003 oct; 12(suppl 2), s202–s213. 62. okada m., miyake k., tamiya t. glioblastoma treatment in the elderly, neurol med chir (tokyo), 2017, 57(12), 667–676. 63. committee of brain tumor registry of japan : report of the brain tumor registry of japan (2001– 2004), neurol med chir (tokyo)2014, 54, 1–102. 64. louis dn, ohgaki h, wiestler od, et al. who classification of tumours of the central nervous system. who/iarc classification of tumours, 4th edition revised, 2016. 65. bozdag s, li a, riddick g, et al.: age-specific signatures of glioblastoma at the genomic, genetic, and epigenetic levels. plos one 8, 2013, e62982. 66. arita h, yamasaki k, et al. : a combination of tert promoter mutation and mgmt methylation status predicts clinically relevant subgroups of newly diagnosed glioblastomas, acta neuropathol commun 2016, 4, 79. 67. gately l, collins a, murphy m, dowling a: age alone is not a predictor for survival in glioblastoma. j neurooncol 2016, 129, 479–485. 68. sahebjam s., mcnamara mairead, et al. management of glioblastoma in the elderly clinical advances in hematology & oncology 2012, 10, 6, 379-386. 69. iwamoto fm, reiner as, et al. patterns of care in elderly glioblastoma patients. ann neurol. 2008, 64, 628-634. 70. yovino s, grossman sa. treatment of glioblastoma in “elderly” patients. curr.treat options oncol. 2011, 12, 253-262. 71. ewelt c, goeppert m, et al. glioblastoma multiforme of the elderly: the prognostic effect of resection on survival. j.neurooncol. 2011, 103, 611618. 72. chaichana kl, chaichana kk, et al. surgical outcomes for older patients with glioblastoma multiforme: preoperative factors associated with decreased survival. clinical article. j neurosurg. 2011, 114, 587-594. 73. sahebjam s., mcnamara mairead, et al. management of glioblastoma in the elderly clinical 259 neurosurgery in the elderly patient advances in hematology & oncology 2012, 10, 6, 379-386. 74. oszvald a, guresir e, et al. glioblastoma therapy in the elderly and the importance of the extent of resection regardless of age. j neurosurg 2012, 1162, 357-364. 75. noorbakhsh a, tang ja, et al. : gross-total resection outcomes in an elderly population with glioblastoma: a seer-based analysis. j neurosurg 2014, 120: 31– 39. 76. babu r, komisarow jm, et al. glioblastoma in the elderly: the effect of aggressive and modern therapies on survival. j neurosurg 2016, 124, 998–1007. 77. roa w, brasher pm, et al. : abbreviated course of radiation therapy in older patients with glioblastoma multiforme: a prospective randomized clinical trial. j clin oncol 2004, 22: 1583–15880. 78. cao jq, fisher bj et al .hypofractionated radiotherapy with or without concurrent temozolomide in elderly patients with glioblastoma multiforme: a review of ten-year single institutional experience. j neurooncol. 2012, 107, 395-405. 79. zarnett oj, sahgal a, et al. treatment of elderly patients with glioblastoma: a systematic evidencebased analysis, jama neurol 2015, 72, 589–596. 80. yin aa, zhang lh, et al. radiotherapy plus concurrent or sequential temozolomide for glioblastoma in the elderly: a meta-analysis. plos one 2013, 8: e74242. 81. stupp r, hegi me, et al. effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase iii study: 5-year analysis of the eortc-ncic trial. lancet oncol. 2009, 10, 459466. 82. stummer w, nestler u, et al. favorable outcome in the elderly cohort treated by concomitant temozolomide radiochemotherapy in a multicentric phase ii safety study of 5-ala. j neurooncol. 2011, 103, 361-370. 83. chinot ol, wick w, et al. bevacizumab plus radiotherapy-temozolomide for newly diagnosed glioblastoma. n engl j med 2014, 370: 709–722. 84. reyes-botero g, honnorat j, et al. temozolomide plus bevacizumab in elderly patients with newly diagnosed glioblastoma and poor performance status: an anocef phase ii trial. j clin oncol 2013, 30: abstr 2020. 85. westphal m, ram z, et al. executive committee of the gliadel study group : gliadel wafer in initial surgery for malignant glioma: long-term follow-up of a multicenter controlled trial. acta neurochir (wien) 2006, 148: 269–275; discussion 275. 86. chaichana kl, zaidi h, et al. the efficacy of carmustine wafers for older patients with glioblastoma multiforme: prolonging survival. neurol res 2011, 33: 759–764. 87. locatelli m., bertani g., et al. the trans-sphenoidal resection of pituitary adenomas in elderly patients and surgical risk, pituitary 2013, 16, 2, 146–151. 88. ciurea a.v., iacob g. technici neurochirurgicale, cartea universitara 2006, 104-214. 89. american geriatrics society panel on pharmacological management of persistent pain in older persons. pharmacological management of persistent pain in older persons. j am geriatr soc. 2009, 57(8), 1331–1334. 90. ciurea a.v., iacob g. technici neurochirurgicale, cartea universitara 2006, 216-294. 91. whitehouse kj, jeyaretna ds, et al. neurosurgical care in the elderly: increasing demands necessitate future healthcare planning, world neurosurg. 2016, 87, 446-454. doi: 10.33962/roneuro-2020-059 organizing a microsurgery workshop for residents marin andrei, lungu adrian, dobrete nicoleta amalia, marin georgiana gabriela, dima simona olimpia, sîrbu boeţi mirela patricia, popescu irinel romanian neurosurgery (2020) xxxiv (1): pp. 379-385 doi: 10.33962/roneuro-2020-059 www.journals.lapub.co.uk/index.php/roneurosurgery organizing a microsurgery workshop for residents marin andrei1, lungu adrian2, dobrete nicoleta amalia3, marin georgiana gabriela4, dima simona olimpia5, sîrbu boeţi mirela patricia5, popescu irinel5 1 plastic surgery department, “bagdasar arseni” emergency hospital, bucharest, romania 2 rehabilitation department, national institute of rehabilitation, physical medicine and balneoclimatology, bucharest, romania 3 haematology department, county hospital ploiesti, romania 4 cardiology department, “c.c. iliescu” hospital, bucharest, romania 5 general surgery department, fundeni hospital, bucharest, romania abstract microsurgery represents an important branch in plastic and reconstructive surgery. it involves fine skills which doctors need to repair nerves, vessels and thus being able to perform replantation and transplantation of different types of tissue. after traumatic injuries, a plastic surgeon is capable of either coverage of the exposed noble tissue or can perform the replantation of the amputated limb using microsurgery. this field can be very challenging at the beginning, but very rewarding in the end. the utility microsurgery is quite vast; however, the skills to perform such surgery require a lot of training beforehand. before doing any replantation or other tissue transplant in humans, it would be recommended that a surgeon should have a basic microsurgical course completed and afterwards several hours of practice in front of the microscope. last but not least, one should also test the skills acquired in vivo, in order to improve and perform the correct manoeuvres from the beginning. in order to do this, a plastic surgery trainee must therefore have a dedicated laboratory where he/she can practice this art. this place should be quiet, equipped with microscopes and microsurgery instruments and authorized to perform experiments on live animals. introduction a growing interest in the field of microsurgery has led to the development of training facilities, where residents can practice microsurgery. [1] the development in technology has led to new ways of doing microsurgery, such as using a smartphone to use magnification. [2] although it is mainly addressed to the plastic surgery trainees, microsurgical skills are also useful in neurosurgery, ophthalmology, keywords experimental microsurgery, training, laboratory corresponding author: marin andrei “bagdasar arseni” emergency hospital, bucharest, romania marin_ dpt@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 380 marin andrei, lungu adrian, dobrete nicoleta amalia et al. cardiovascular surgery, orthopedic surgery and even general surgery or urology (for liver and kidney transplant).[3],[4],[5]. a formal curriculum of microsurgery in the plastic surgery program proved to be very useful according to mueller et. al. [6] for this reason, there are several microsurgery centers in romania, each having a similar basic program focused mostly on nerve and vessel repair. in time and with experience, these initial programs are developed and divided into more complex courses – involving the dissection of smaller vessels (lymphatic vessel or perforating vessel), with direct applicability in the clinical practice. materials and methods in order to begin organizing such course, a suitable location is required. the location needs to have a veterinary employed in that facility (which is a compulsory condition for the other requirements). it would also be more comfortable for the participants if the location were far from loud noises and distraction, as microsurgery requires attention and calm. due to the legislation, there are several approvals needed for research or medical education involving living animals. every project has to pass the ethics committee and afterwards get the approval from the veterinary department. in romania, this process may take up to 4 months and should be planned carefully before the beginning of the course.[7] every major project which involves a teaching activity should be performed under the supervision of the medical university or a recognized professional association. for the first edition of the microsurgical program, there was collaboration between 3 associations – the romanian multidisciplinary residents association, the romanian plastic surgery association and the romanian aesthetic surgery association. the course took place in 2 distinct locations – the non-living tissue experiments were performed in a private facility (medworkshops), while the second part which involved live animal surgery took place in cemt –the excellence centre in translational medicine, part of the fundeni hospital. the course duration was 4 days (8 hours/day), over 2 consecutive weekends. medworkshops center excellence centre in translational medicine once all the approvals were obtained, a curriculum of the course was sketched and the dates for the course established. the lecturers for the theoretical part of the course were invited with a 2 months’ notice (at least) and asked for the name of their presentation. a number of 10 participants per course was considered to be suitable for a microsurgery course. the selection of the animal to be practiced on was done taking into consideration several criteria – suitable size and type of the tissue (nerves, vessels), affordable costs, easy for manipulation, easy to induce anesthesia, accessible to purchase from special laboratories. for all the previous 381 organizing a microsurgery workshop for residents mentioned reasons, the wistar rat is the ideal candidate. [8] wistar rat the announcement of the course was done with one and a half months in advance. there were 3 channels by which the marketing was done – internet (official web sites of the associations involved, social media pages as well as personal pages), direct speech among colleagues, and posters in the hospitals which prepared residents in plastic surgery. poster a list of all materials needed for the 4-day workshop was created. the list included instruments for the participants and trainer, other materials, logistics for the theoretical part, the material on which the participants train and food and drink supplies for catering. based on the presumed amount of the materials used, a budget was established to support the expenses for renting of the microscopes, the facilities and acquiring all materials needed. sutured silicone tube table 1. list of requirements for organizing the course instruments & sanitary other materials logistic theory practical workshop insulin syringes black bags for waste laptop latex gloves syringes 10/20ml cages projector silicone tubes disinfectants (alcohol) cleaning paper folders & pens cherry tomatoes/grapes gloves first aid kit diplomas leaves and petals tampons/dressing cotton swabs chicken legs yellow cannulas cork plates wistar rats blue dye plastic wrap anesthetics pins and paper clips euthanasia solution rubber band sutures 8.0-10.0 tape sutures 3.0-5.0 electronic scale microsurgical instruments (scissors, needle holder, forceps, dilator, clamps and approximator) yellow bucket for sharp materials macrosurgery instruments (forceps, small scissor) yellow bags for contaminated waste scalpel blades hair clipper serum background material hand sanitizers cups microscopes adjustable chairs 382 marin andrei, lungu adrian, dobrete nicoleta amalia et al. another important aspect which needed to be taken into consideration when organizing such a workshop was the fact that acquiring live animals could be done only in special conditions and from designated institutions. these institutions allow the purchase of these animals only based on the previously approved documentation. being an initiation microsurgery course, it needed to remain at an entry-level, both the theory and especially the practice. the selection of the participants was based on prior experience in the microsurgery training as well as year of residency. taking into consideration the entry-level of the course, the curricula was designed to meet the experience of these participants. the program was thought to have 1,5-2 hours of theory and 6-6,5 hours of practice daily. the level of difficulty of the procedures performed was also designed to increase daily. day 1 day 2 day 3 day 4 theory theory theory theory introduction in microsurgery vascular anastomosis nerve anastomosis clinical experience in peripheral nerve repair microsurgical instruments. surgical technique. free flaps – clinical experience ethics in animal experimentation practical part practical part practical part practical part latex glove sutures silicon tube sutures anastomosis of the femoral artery anastomosis of the femoral vein grape/cherry tomato sutures vascular anastomosis on chicken leg leaves/petals sutures sciatic rat nerve repair anastomosis of the aorta elastic band suture anastomosis of v. cava table 2. basic microsurgery training program another bureaucratic aspect of the workshop consisted of making individual folders for the participants. these folders contained the program, the list of equipment they received and for which they were responsible during the day, a file regarding work safety which they had to sign before the beginning of the course. at the end of the course the participants received a diploma and were requested to complete a feedback file. results after making the formal announcement of the course, 20 plastic surgery residents sent an application for one of the 10 available places. 10 participants were selected based on their microsurgical experience and the other 10 were promised a place in the next course. the residents were in different years of training (from the 1st to the 3rd), all but one having no former experience with microsurgery (one resident having previously participated to a 2-day microsurgery course). all participants attended all 4 days of the course, except one who could not come on the 4th day. there were 4 lecturers who presented their clinical experience in the theoretical part of the workshop and the official organizer of the course who presented and demonstrated the practical experiments. latex tube anastomosis 383 organizing a microsurgery workshop for residents dissection on chicken leg sciatic nerve exposure the theoretical lectures permitted the participants to learn the basics about the structure of a peripheral nerve and vessel [8],[9],[10] and also about the possibilities in the reconstruction of nerve defects, either with nerve grafts or conduits. [11],[12] participants were also taught about the pitfalls in nerve microsurgery [13] as well as the basics in how to perform rat anaesthesia. [14] in the practical part, the residents were also taught some tricks which they could use in order to improve their outcomes. [15] all participants improved their microsurgical technique between the first day and the final day of the course. all participants managed to complete the tasks required in different time-frames. [16] 8/10 participants managed to achieve a patent vascular anastomosis but all participants were able to perform a correct nerve anastomosis by the end of the program. dissection for rat aorta femoral artery in chicken leg (cut open) 384 marin andrei, lungu adrian, dobrete nicoleta amalia et al. anastomosis for femoral artery participants during sciatic nerve repair on wistar rat discussions having little experience, all the participants showed great interest in microsurgery, most of them staying the full 8 hours every day (some wanting to stay even longer). however, working long hours under the microscope was strenuous (some participants complaining about minor problems: back pain or headaches associated to eyesight problems). since the workshop was splint over 2 consecutive weekends, the more zealous participants could also come for an extra 2 days during the week to have more practice outside the formal course. this was a great opportunity to improve their surgical skills (especially in those who had no prior experience). in the formal feedback, some participants mentioned that they would have liked an extra day of practice on live animals, so that they would be able to achieve all perfect results. overall, the feedback was positive and the participants said they feel more confident with their microsurgical skills, thus having no issue in performing these procedures in their clinical practice. furthermore, they mentioned that they would gladly attend a more advanced workshop if this was to be planned. although this was an entry-level course, more elaborated course could be developed in time, depending on the interest of the participants. conclusions both theoretical and practical knowledge is needed when it comes to learning microsurgery skills. these should first be learned in the safe environment of a laboratory, during a microsurgery course and then applied in clinical practice. organizing a microsurgery course requires special equipment, designated facilities and many approvals, but such courses are absolutely needed for the training of the medical residents. references 1. oltean m, sassu p, hellström m, et al. the microsurgical training programme in gothenburg, sweden: early experiences. j plast surg hand surg. 2017;51(3):193–198. doi:10.1080/2000656x.2016.1213735. 2. capkin s, cavit a, kaleli t. microsurgery training with smartphone. mikrochirurgische übungen mit smartphone als vergrößerungshilfe. handchir mikrochir plast chir. 2018;50(6):443–445. doi:10.1055/a-0661-6015. 3. kobayashi e. new trends in translational microsurgery. acta cir bras. 2018;33(9):862–867. doi:10.1590/s0102865020180090000015. 4. pastuszak aw, wenker ep, lipshultz li. the history of microsurgery in urology. urology. 2015;85(5):971–975. doi:10.1016/j.urology.2014.12.059. 5. hinds rm, klifto cs, guss ms, capo jt. microsurgery case volume during orthopedic surgery residency: a 7-year 385 organizing a microsurgery workshop for residents assessment. hand (n y). 2017;12(6):610–613. doi:10.1177/1558944716675128. 6. mueller ma, pourtaheri n, evans grd. microsurgery training resource variation among us integrated plastic surgery residency programs. j reconstr microsurg. 2019;35(3):176–181. doi:10.1055/s-0038-1668160. 7. andrei marin, georgiana gabriela marin, anca patea, dan mircea enescu. timing, logistics and bureaucratic process in planning an experimental in vivo nerve regeneration project from a to z. modern medicine | 2019, vol. 26, no. 2. 8. caillaud m, richard l, vallat jm, desmoulière a, billet f. peripheral nerve regeneration and intraneural revascularization. neural regen res. 2019;14(1):24-33. 9. lastofka, d., manolescu, n., balint, e., costea, r., & ionescu, m. m. (2017). histopathological modifi cations in sciatic nerve allograph in wistar rats. journal of biotechnology, 256, s86. 10. andrei, m., ioana, m., & mircea, e. (2019). underlying histopathology of peripheral nerve injury and the classical nerve repair techniques. romanian neurosurgery, 33(1), 17-22. https://doi. org/10.33962/roneuro-2019-003. 11. ionescu, m. m., costea, r., balint, e., & lastofka, d. (2017). surgery technique models of sciatic nerve allograph in wistar rats. abstracts/journal of biotechnology 256s, 44, s116. 12. mihai mehedintu-ionescu, ovidiu stefanescu, radu cristian jecan. nervous regeneration allograph type of periferic nerv. modern medicine | 2019, vol. 26, no. 2. 13. marin andrei, mihai ruxandra ioana, marin georgiana gabriela. pitfalls and problems encountered in rat model sciatic nerve surgery. romanian neurosurgery (2019) xxxiii (4): pp. 396399doi: 10.33962/roneuro-2019-064. 14. costea ruxandra, daniel lastofka, and mihai mehedinţu. “comparison of ketamine–medetomidine-butorphanol and ketamine – dexmedetomidine butorphanol anesthesia in rats.” agriculture and agricultural science procedia 6 (2015): 305-308. 15. marin andrei, mihai ruxandra ioana, marin georgiana gabriela. tips and tricks in experimental nerve defect surgery. modern medicine | 2020, vol. 27, no. 1. 16. andrei, m., gabriela, m., amalia, d., & mircea, e. (2019). learning curve in rat dissection for experimental sciatic nerve repair. romanian neurosurgery, 33(3), 243-248. https://doi. org/10.33962/roneuro-2019-041. doi: 10.33962/roneuro-2022-020 clinical outcomes and satisfaction in patients after lumbar microdiscectomy. a single centre study dipak chaulagain, volodymyr smolanka, andriy smolanka, taras havryliv, alexandr shecko romanian neurosurgery (2022) xxxvi (1): pp. 116-121 doi: 10.33962/roneuro-2022-020 www.journals.lapub.co.uk/index.php/roneurosurgery clinical outcomes and satisfaction in patients after lumbar microdiscectomy. a single centre study dipak chaulagain, volodymyr smolanka, andriy smolanka, taras havryliv, alexandr shecko regional clinical centre of neurosurgery and neurology, uzhhord national university, uzhhorod, ukraine abstract introduction: lumbar disc herniation is a common cause of low back and radicular pain. microdiscectomy is the recommended surgical technique for herniated lumbar discs at the moment. it has great success rates and little postoperative morbidity. we aimed to assess the clinical result and patient satisfaction of micro-discectomy in lumbar disc herniation patients. methodology: this is prospective observational hospital-based research of 26 patients who had micro-discectomy at the regional clinical center of neurosurgery and neurology in uzhhorod, ukraine, during august and september 2021. the research excluded patients with recurrent prolapsed intervertebral discs, multiple level herniated discs, and disc surgery requiring stability. during surgery, the kind of prolapsed intervertebral disc, its level, and the duration of the procedure were recorded. additionally, we recorded the duration of the patient's hospital stay and any complications. the visual analogue scale (vas), the oswestry disability index (odi), and the macnab score questionnaires were used to measure pain, disability, and patient satisfaction, respectively. result: all procedures were performed on a single level using micro-discectomy. the mean age of the study population was 45.69 years. micro-discectomy surgeries were performed in less than an hour in 69.2% of cases. the most often seen lumbar prolapsed intervertebral disc occurred at the l4-l5 level (57.7%). the most often seen kinds of prolapse were disc extrusion (30.8%) and disc sequestration (26.9%). the mean length of stay in the hospital was 3.96 days. after surgery, 57.7% of patients received an excellent rating on the macnab's scale. there was a statistically significant difference between preand postoperative vas and odi scores (p<0.05). conclusion: overall 65.4% of patients had no postoperative complications. in these instances, a proper surgical technique might help avoid problems. our findings demand additional investigation with bigger sample sizes and longer follow-up periods. introduction low back pain is a prevalent complaint among patients seeking basic care. lumbar disc herniation (ldh) causes low back pain and leg pain [23]. nucleus pulposus or annulus fibrosis displacement beyond keywords disc herniation, lumbar pain, microdiscectomy corresponding author: dipak chaulagain regional clinical centre of neurosurgery and neurology, uzhhord national university, uzhhorod, ukraine neurodipak@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 117 clinical outcomes and satisfaction in patients after lumbar microdiscectomy normal intervertebral disc space is a typical cause for radiculopathy. 95 percent of lower lumbar disc herniation occur at l4-5 and l5-s1 [12, 17]. a lumbar disc herniation may be treated in many ways, but the diagnosis is made based on the patient's history, physical exam, and radiograph patients with persistent lower back pain, with or without leg radiating pain, difficult to manage pain, or acute paresis, including cauda equine syndrome, are frequently given surgery [28]. radiculopathy caused by ldh usually heals without surgery. if nonsurgical treatment fails, micro-discectomy may be explored. lumbar micro-discectomy has good success rates and little postoperative morbidity. the operation has been shown to be successful in treating lumbar radicular pain and sciatica with success rates ranging from 50% to 98% [26]. elective lumbar discectomy is one of the most popular neurosurgical treatments for lumbar disc herniation. if sciatica or neurological impairments remain following a period of conservative therapy, a discectomy is regarded the gold standard [4, 13]. more than 70 years, fenestrated discectomy has been the primary treatment for lumbar disc herniation worldwide [15]. a long midline incision and significant muscle retraction with complete laminectomy were first documented in 1934 by mixter and barr [3]. ldh surgery entered a new era in 1977 when surgeons started using operating microscopes to remove herniated disc material [6]. as early findings showed, micro-discectomy was equally as effective as regular discectomy and had certain benefits over the latter. this was soon after the launch of the aforementioned invention. an advantage of microdiscectomy over traditional open discectomy is the ability to do surgery with fewer incisions and less harm to the skin and fascia [18]. oswestry impairment index (odi) measures the degree of disability caused by low back pain and is based on the oswestry low back pain questionnaire. vas was the last scale to be implemented [5, 8]. following micro-discectomy surgery, we documented the surgical procedures, clinical results, postoperative patient satisfaction (vas and odi), length of stay in the hospital and early problems (macnab score) that we encountered. the study's goal was to evaluate the short-term clinical outcomes after a single-level lumbar micro-discectomy operation. material and methods from august to september 2021 at a regional clinical center of neurosurgery and neurology in uzhhorod, ukraine, we conducted a cross-sectional observational research to evaluate our patients who had had a microlumbar discectomy. patients with a single level lumbar disc herniation were eligible to participate in the trial. cases with repeated disc herniations, several levels of lumbar disc herniation and disc surgery with instrumentation were ruled out. types and levels of ldh, and surgical time were all reported during surgery for ldh (central, lateral extrusion, protrusion, lateral disc bulge, and sequestration). complications that occurred during treatment were also reported. patient’s pain was assessed using vas and odi before and after surgery. this was the main outcome. two questionnaires, the visual analogue scale (vas, 0-10) and the oswestry impairment index (odi, 0-100% disability), were used to evaluate patient’s levels of pain and disability before and after surgery. when it comes to assessing low back function, the odi is the gold standard [19, 25]. the macnab questionnaire was used to measure patient satisfaction and it was rated excellent, good, fair, or bad [16]. early complications like nausea and vomiting, post-operative cerebrospinal fluid leak, wound infection and discitis were recorded. spss version 25 was used for data collection, and the data were then analyzed using the statistical software for social sciences (spss). for example, age and gender, type of ldh and complication. odi and vas were evaluated by the paired samples t-test method. p < 0.05 was assessed as significant. results from august to september 2021, lumbar disc herniation patients who had micro-lumbar discectomy were studied prospectively. the patients were mostly male and average age was 45.69 [table 4]. all surgeries were single level micro-discectomy including l3-l4 (3.8%), l4-l5 (57.7%), and l5-s1 (38.5%) [table 1] .69.2% cases were performed surgically by less than one hour whereas 30.8% cases took more than one hour for micro-discectomy [table 1]. average day of staying in hospital of patients post-operatively was 3.96 days [table 4]. disc extrusion (30.8%) and disc sequestration (26.9%) were the most commonly seen types of prolapse [table 1]. there was statistically significant difference (p<0.05) in pre-operative and post 118 dipak chaulagain, volodymyr smolanka, andriy smolanka et al. operative vas scores and odi [table 5]. after surgery, 57.7% of patients received an excellent rating on the macnab's scale [table 2] and overall 65.4% of patients had no postoperative complications [table 3]. table 1. description of patients involved in the study total number of patients 26 average age (range) 30-58 males 16 (61.5%) females 10 (38.5%) side of pivd right side 15 (57.7%) left side 11 (42.3%) level of prolapse l3-l4 1 (3.8%) l4-l5 15 (57.7%) l5-s1 10 (38.5%) types of pivd central disc bulge 6 (23.1%) lateral disc bulge 8 (30.8%) disc protrusion 3 (11.5%) disc extrusion 7 (26.9%) disc sequestration 2 (7.7%) operation duration less than hour 18 (69.2%) more than hour 8 (30.8%) table 2. description of macnab’s score (post-op) in the study frequency percent valid percent cumulative percent excelle nt 15 57.7 57.7 57.7 fair 3 11.5 11.5 69.2 good 7 26.9 26.9 96.2 poor 1 3.8 3.8 100.0 total 26 100.0 100.0 table 3. description of early post-op complication in the study freq. % valid percent cumulative percent csf leak 1 3.8 3.8 3.8 discitis 1 3.8 3.8 7.7 nausea,vomiting 5 19.2 19.2 26.9 no complication 17 65.4 65.4 92.3 wound infection 2 7.7 7.7 100.0 total 26 100.0 100.0 table 4. descriptive mean statistics of age and duration of hospital stay (post-op) in the study n min. max. mean std. deviation age 26 30 58 45.69 8.966 post-op duration of hospital stay(day) 26 2 6 3.96 1.311 table 5. paired-samples t-test of vas score and odi (pre-op and post-op) in the study t df sig. (2-tailed) mean std. deviation std. error mean 95% confidence interval of the difference lower upper pair 1 vas score (pre-op) vas score (post-op) 6.500 1.105 .217 6.054 6.946 30.007 25 .000 pair 2 odi % (pre-op) odi % (post-op) 30.000 14.213 2.787 24.259 35.741 10.763 25 .000 discussion if the nucleus pulposus and the annulus fibrosus degenerate, ldh is almost always caused by this. lifting accidents or other trauma may also be to blame. people who have lower back pain almost always have their intervertebral discs bulging, especially if they push on a nerve root. numbness and tingling are very common in the lower legs because of the pain caused by this. the l4-l5 and l5s1 segments of the spinal column are the most often affected by disc disease. there are a variety of therapy options available for lumbar discopathy. 90% of individuals will have a conservative improvement in their pain levels [22]. patients with lumbar disc herniation had satisfactory long-term treatment outcomes for their sciatica symptoms, regardless of whether they underwent surgery or received conservative therapy. when compared to conservative therapy, surgical surgery alleviated back pain more quickly; nevertheless, after three months, no difference was seen between any of the treatments [21]. discectomy of the lumbar spine is one of the most frequent surgical procedures performed today. open surgery and endoscopic surgery are both 119 clinical outcomes and satisfaction in patients after lumbar microdiscectomy acceptable methods of doing the procedure. the discectomy process has gone a long way since yasargil conducted the first microscopic surgery in 1968 and schreiber and suezawa conducted the first endoscopic discectomy in 1986, then mayer, brock, and mathews refined the technique in the 1990s [7, 9,14,24]. in this cross-sectional research, we looked at the surgical result and patient satisfaction rate of microlumbar discectomy, which is the most common kind of spine surgery. discectomy of the lumbar spine is one of the most frequent surgical procedures performed today. open surgery and endoscopic surgery are both acceptable methods of doing the procedure. the outcomes of this research corroborate the long-held notion that discectomy is a safe and effective therapeutic option for lumbar discopathy associated with sciatic pain in the lower back. patients have claimed success rates ranging from 88–97% for this treatment; however, more realistic results, as determined by patient-reporting measures, range from 75–80% [1]. because of rising healthcare expenditures and other costs connected with hospitalization, most neurosurgical centers across the globe perform lumbar microdiscectomy as a day care procedure to save costs. one of the most important considerations during a surgery is the duration of the procedure, especially in light of the probability of blood loss and the existence of intraoperative risk factors for surgical site infections. micro-discectomy has a number of advantages, one of which is that the quantity of blood lost during the treatment is significantly decreased, according to the findings of various studies [20, 29, 30]. in our study, 69.2% of cases were completed surgically in less than one hour, while 30.8% of patients required more than one hour for micro-discectomy surgery. according to our study, the median length of hospitalization was 3.96 days, with a range of 2 to 6 days being recorded. differential results in discectomy-related outcomes are primarily influenced by changes in patient selection, follow-up period, and the tools employed to quantify outcome and their interpretation. patients who have had lumbar disc herniation surgery are able to return to work in 76% of cases after one year [2]. the kind of disc herniation has also been shown to have a substantial impact on the functional results of patients [27]. following surgery, 4% of patients report a decrease in their functional condition. prior to surgery, the following factors are associated with deterioration: lengthy duration of pain and low odi (greater function) [11]. according to shriver, michael f et al., the overall complication rate of micro-lumbar discectomy was 12.5%, with 1.3% reporting new or worsening neurological deficit, 2.6% reporting direct nerve root injury, 0.5% hematoma, 2.1% wound complications (infection, dehiscence, seroma), and 4.1% recurrent disc complications [10]. while in our study, 65.4% of patients had no postoperative issues, we discovered that 3.8%, 3.8%, 19.2%, and 7.7% of cases experienced difficulties such as cerebrospinal fluid leak, discitis, nausea and vomiting, and wound infection, respectively [table 3]. while our research had a small number of participants, it was not without its faults. proposed multi-center study on lumbar micro-discectomy with long-term follow-up should be conducted in order to get more universal and reasonable findings. limitations a single-center research has a smaller sample size. prospective research with large sample sizes and long follow-up times are also necessary to correctly extrapolate results to the general population. conclusions a lumbar micro-discectomy is a safe and efficient treatment for disc herniation-related sciatic lumbar pain. it will be necessary to conduct additional multicentric studies with a larger sample size and a longer follow-up period in order to verify our findings. references 1. asch, h. l., lewis, p. j., moreland, d. b., egnatchik, j. g., yu, y. j., clabeaux, d. e., & hyland, a. h. (2002). prospective multiple outcomes study of outpatient lumbar microdiscectomy: should 75 to 80% success rates be the norm?. journal of neurosurgery, 96(1 suppl), 34–44. 2. bailey, c. s., rasoulinejad, p., taylor, d., sequeira, k., miller, t., watson, j., rosedale, r., bailey, s. i., gurr, k. r., siddiqi, f., glennie, a., & urquhart, j. c. (2020). surgery versus conservative care for persistent sciatica lasting 4 to 12 months. the new england journal of medicine, 382(12), 1093–1102. 3. brodke, d. s., goz, v., lawrence, b. d., spiker, w. r., neese, a., & hung, m. (2017). oswestry disability index: a psychometric analysis with 1,610 patients. the spine 120 dipak chaulagain, volodymyr smolanka, andriy smolanka et al. journal : official journal of the north american spine society, 17(3), 321–327. 4. carragee, e. j., han, m. y., suen, p. w., & kim, d. (2003). clinical outcomes after lumbar discectomy for sciatica: the effects of fragment type and anular competence. the journal of bone and joint surgery. american volume, 85(1), 102–108. 5. caspar, w., campbell, b., barbier, d. d., kretschmmer, r., & gotfried, y. (1991). the caspar microsurgical discectomy and comparison with a conventional standard lumbar disc procedure. neurosurgery, 28(1), 78–87. 6. chiarotto, a., maxwell, l. j., ostelo, r. w., boers, m., tugwell, p., & terwee, c. b. (2019). measurement properties of visual analogue scale, numeric rating scale, and pain severity subscale of the brief pain inventory in patients with low back pain: a systematic review. the journal of pain, 20(3), 245–263. 7. deyo, r. a., & mirza, s. k. (2016). clinical practice. herniated lumbar intervertebral disk. the new england journal of medicine, 374(18), 1763–1772. 8. fairbank, j. c., & pynsent, p. b. (2000). the oswestry disability index. spine, 25(22), 2940–2952. 9. fardon, d. f., milette, p. c., & combined task forces of the north american spine society, american society of spine radiology, and american society of neuroradiology (2001). nomenclature and classification of lumbar disc pathology. recommendations of the combined task forces of the north american spine society, american society of spine radiology, and american society of neuroradiology. spine, 26(5), e93– e113. 10. gibson, j. n., & waddell, g. (2007). surgical interventions for lumbar disc prolapse: updated cochrane review. spine, 32(16), 1735–1747. 11. gugliotta, m., da costa, b. r., dabis, e., theiler, r., jüni, p., reichenbach, s., landolt, h., & hasler, p. (2016). surgical versus conservative treatment for lumbar disc herniation: a prospective cohort study. bmj open, 6(12), e012938. 12. hamawandi, s. a., sulaiman, i. i., & al-humairi, a. k. (2020). open fenestration discectomy versus microscopic fenestration discectomy for lumbar disc herniation: a randomized controlled trial. bmc musculoskeletal disorders, 21(1), 384. 13. javedan, s., & sonntag, v. k. (2003). lumbar disc herniation: microsurgical approach. neurosurgery, 52(1), 160–164. 14. kahanovitz, n., viola, k., & muculloch, j. (1989). limited surgical discectomy and microdiscectomy. a clinical comparison. spine, 14(1), 79–81. 15. kulkarni, a. g., bassi, a., & dhruv, a. (2014). microendoscopic lumbar discectomy: technique and results of 188 cases. indian journal of orthopaedics, 48(1), 81–87. 16. macnab i. (1971). negative disc exploration. an analysis of the causes of nerve-root involvement in sixty-eight patients. the journal of bone and joint surgery. american volume, 53(5), 891–903. 17. mathews h. h. (1996). transforaminal endoscopic microdiscectomy. neurosurgery clinics of north america, 7(1), 59–63. 18. mayer, h. m., & brock, m. (1993). percutaneous endoscopic discectomy: surgical technique and preliminary results compared to microsurgical discectomy. journal of neurosurgery, 78(2), 216–225. https://doi.org/10.3171/jns.1993.78.2.0216. 19. mixter wj, barr js. rupture of the intervertebral disc with involvement of the spinal canal. n engl j med. 1934; 5:210-215. 20. peul, w. c., van houwelingen, h. c., van den hout, w. b., brand, r., eekhof, j. a., tans, j. t., thomeer, r. t., koes, b. w., & leiden-the hague spine intervention prognostic study group (2007). surgery versus prolonged conservative treatment for sciatica. the new england journal of medicine, 356(22), 2245–2256. 21. porchet, f., bartanusz, v., kleinstueck, f. s., lattig, f., jeszenszky, d., grob, d., & mannion, a. f. (2009). microdiscectomy compared with standard discectomy: an old problem revisited with new outcome measures within the framework of a spine surgical registry. european spine journal : official publication of the european spine society, the european spinal deformity society, and the european section of the cervical spine research society, 18 suppl 3(suppl 3), 360–366. 22. reed, m. d., & van nostran, w. (2014). assessing pain intensity with the visual analog scale: a plea for uniformity. journal of clinical pharmacology, 54(3), 241– 244. 23. ruan, w., feng, f., liu, z., xie, j., cai, l., & ping, a. (2016). comparison of percutaneous endoscopic lumbar discectomy versus open lumbar microdiscectomy for lumbar disc herniation: a meta-analysis. international journal of surgery (london, england), 31, 86–92. 24. schreiber, a., & suezawa, y. (1986). transdiscoscopic percutaneous nucleotomy in disk herniation. orthopaedic review, 15(1), 35–38. 25. shriver, m. f., xie, j. j., tye, e. y., rosenbaum, b. p., kshettry, v. r., benzel, e. c., & mroz, t. e. (2015). lumbar microdiscectomy complication rates: a systematic review and meta-analysis. neurosurgical focus, 39(4). 26. solberg, t. k., nygaard, o. p., sjaavik, k., hofoss, d., & ingebrigtsen, t. (2005). the risk of "getting worse" after lumbar microdiscectomy. european spine journal : official publication of the european spine society, the european spinal deformity society, and the european 121 clinical outcomes and satisfaction in patients after lumbar microdiscectomy section of the cervical spine research society, 14(1), 49– 54. 27. varlotta, g. p., brown, m. d., kelsey, j. l., & golden, a. l. (1991). familial predisposition for herniation of a lumbar disc in patients who are less than twenty-one years old. the journal of bone and joint surgery. american volume, 73(1), 124–128. 28. weinstein, j. n., lurie, j. d., tosteson, t. d., skinner, j. s., hanscom, b., tosteson, a. n., herkowitz, h., fischgrund, j., cammisa, f. p., albert, t., & deyo, r. a. (2006). surgical vs nonoperative treatment for lumbar disk herniation: the spine patient outcomes research trial (sport) observational cohort. jama, 296(20), 2451–2459. 29. williams r. w. (1978). microlumbar discectomy: a conservative surgical approach to the virgin herniated lumbar disc. spine, 3(2), 175–182. 30. yasargil mg. microsurgical operation for herniated disc. adv neurosurg. 1977;4:81. microsoft word 12kemerdererahsan_diagnostic romanian neurosurgery (2018) xxxii 4: 613 621 | 613             doi: 10.2478/romneu-2018-0079 diagnostic value of preoperative systemic inflammatory markers in patients with intracranial meningiomas rahsan kemerdere1, mehmet yigit akgun1, sureyya toklu1, orkhan alizada1, oguz baran2, taner tanriverdi1 1department of neurosurgery, medical faculty, istanbul university-cerrahpasa, istanbul, turkey 2neurosurgery clinic, istanbul research and training hospital, istanbul, turkey abstract: introduction: the role of inflammation in cancer has been defined, and now, inflammation is accepted as one of the hallmarks of cancer development. the aim of this study was to evaluate the difference regarding preoperative neutrophil to lymphocyte (nlr) and platelet to lymphocyte ratios (plr) in patients with meningioma between patients and healthy controls and between grade-i and grade-ii meningiomas. methods: retrospective analysis of preoperative neutrophil, lymphocyte, monocyte, and platelet counts and nlr, and plr were evaluated in 61 patients underwent meningioma surgery. results: neutrophil count was significantly increased while lymphocyte count significantly decreased patients compared to controls. similar findings were obtained in grade-ii meningiomas compared with grade-i meningiomas. nlr were significantly higher in both grade-i and grade-ii meningiomas than controls. conclusion: we for the first time provided that higher nlr may be associated with grading of meningioma and be a predictive factor for progression of meningiomas. the use of medication against neutrophil-related inflammation may be helpful for patients with higher grade of meningioma decreasing peritumoral edema before and after surgery. key words: inflammation; meningioma; neutrophil-lymphocyte ratio; plateletlymphocyte ratio introduction meningiomas are the most commonly seen intracranial extra-axial tumors, accounting for 25% of all intracranial space-occupying lesions. females are affected more predominantly than males due to estrogen functions (1). although meningiomas are accepted as generally benign in nature, the recurrence rate in some cases is extremely high, even after the total surgical removal of the lesion. thus, in 2007, the world health organization classified meningiomas into three grades. grade i is more commonly encountered when compared to grades ii and iii, and the recurrence rate for grade i tumors 614 | kemerdere et al preoperative systemic inflammatory markers in intracranial meningiomas             is very low. however, in grade ii or iii tumors, a high recurrent rate is common, and radiotherapy is required after surgery (2). meningiomas originate in the arachnoid cap cells, but the exact nature of the development of these common tumors remains unknown. the role of inflammation in cancer has been defined, and now, inflammation is accepted as one of the hallmarks of cancer development (3). with regard to inflammation in brain tumors, meningiomas have been focused on less when compared to gliomas. however, recent evidence has suggested that inflammation plays a pivotal role in the development and progression of brain tumors, including gliomas (4, 5). finding a useful biomarker to predict the progression of brain tumors would be exciting for a neurosurgeons because there has been no such marker used in brain tumors, as opposed to certain other solid tumors such as breast cancer (6). recent studies have shown that the preoperative blood inflammatory markers, such as the neutrophil to lymphocyte ratio (nlr) or platelet to lymphocyte ratio (plr), can be used as indices of glioma progression. for example, it has been reported that a high nlr (increase in the neutrophil count and decrease in the lymphocyte count) has a diagnostic value, and it correlates with the glioma grade (4, 5, 7-10). those studies emphasized the fact that local inflammation around the tumor microenvironment can be reflected systemically, and that the inflammation severity can be tested by using peripheral blood tests that are cheap, reproducible, and effective. surprisingly, there have been no reports focusing on the preoperative blood markers in intracranial meningiomas. therefore, in this retrospective analysis, we wanted to show how the preoperative nlr and plr levels change when compared to the controls. we hypothesized that the nlr and plr would be higher in meningiomas cases (compared to controls), and that the levels would correlate with the meningioma grade, given that the same inflammatory processes take place in both glioma and meningioma cases. materials and methods patients the patient group included here underwent surgeries for intracranialsupratentorial meningiomas by a single surgeon between 2010 and 2017. a total of 100 cases were retrieved from the medical records, but only 61 patients were included, according to the following criteria: 1) the meningioma grade was verified by a histopathological study, 2) no chemotherapy, radiotherapy, and steroids were taken before the surgery, 3) no co-morbidities or extracranial tumors were seen, 4) there was no previous surgery due to any intracranial pathology; 5) there was a complete blood count (cbc) before surgery; and 6) an informed consent form was completed. data collection the demographic, clinical, radiological and histopathological data were retrieved from each patient’s medical records. after hospitalization, blood samples were taken for a cbc and other tests, including hepatic function, serology and the electrolyte level, as a standard preoperative work-up. the neutrophil (103/mm3), lymphocyte romanian neurosurgery (2018) xxxii 4: 613 621 | 615             (103/mm3), and platelet (103/mm3) counts were recorded. additionally, the preoperative nlr (quotient of the absolute number of the neutrophil count to the lymphocyte count) and plr (quotient of the absolute number of the platelet count to the lymphocyte count) were calculated. all of the patients underwent cranial magnetic resonance imaging (mri) with contrast enhancement. the anterior-posterior diameter (cm) was measured by using t1weighted contrast-enhanced axial images, and the presence of peritumoral edema was noted by using t2-weighted and fluid-attenuated inversion recovery (flair) images. controls the control group in this study was composed of 35 subjects who were admitted to our clinic and underwent cbc testing for some other reason, such as a headache. none of the subjects exhibited any abnormalities in their cranial mri scans and no other organ system illnesses were detected. the blood samples were obtained during their admission to our outpatient clinic. statistical analysis the statistical analysis was performed by using ibm spss statistics for windows version 22.0 (ibm corp., armonk, ny, usa). the results were reported here as the mean ± standard deviation. an independent samples t-test and chi-squared test were used in the appropriate comparisons and the correlation analysis was judged using pearson’s correlation coefficient. the area under the curve (auc) for the nlr and plr with a receiver operating characteristics (roc) curve analysis was used for the diagnostic performance. a probability value (p value) < 0.05 was considered to be statistically significant. results demographic characteristics the patient group included 26 males (42.6 %) and 35 females (57. 4 %) with a mean age of 51.91 ± 13.01 years old (range = 23 to 76 years). the control group had 19 males (54.3 %) and 16 females (45.7 %) with a mean age of 32.08 ± 10.09 years old (range = 10 to 51 years). based on the cranial mri scans, there were 26 (42.6 %) and 35 (57.4 %) right and left-sided meningiomas, respectively. peritumoral edema was noted in 37 patients (60.7 %). the histopathological diagnoses revealed grade i meningiomas in 48 patients (78.7 %) and grade ii in 13 patients (21.3 %). all of the patients with grade ii meningiomas had peritumoral edema. the mean of the anterior-posterior diameters of the tumors was 36.73 ± 13.6 cm. inflammatory markers: patients versus controls table i shows a summary of the comparisons between the patients and the controls with regard to the preoperative inflammatory markers studied here. the mean of the neutrophil count levels was significantly higher in the patients when compared to controls (p = 0.001). the lymphocyte and platelet counts were lower in the patients; however, the differences were not significant. as expected, the nlr was significantly higher in the patient group (p = 0.001). moreover, the mean plr level was higher in the patients than the controls, but the difference was not significant. however, there was a trend toward 616 | kemerdere et al preoperative systemic inflammatory markers in intracranial meningiomas             significance in the plr levels of the patients (p = 0.05). inflammatory markers: meningioma grade and edema versus controls given that inflammation has been shown to play an important role in upgrading of tumors and the presence of peritumoral edema, we compared how the preoperative inflammatory marker levels change. table ii shows that the neutrophil count increases, whereas the lymphocyte and platelet counts decrease in grade ii when compared to gradei meningiomas. table i preoperative inflammatory markers in patients and controls marker patients (n = 61) controls (n = 35) p value neutrophils 5.42 ± 2.63 4.20 ± 0.81 0.001* lymphocytes 2.11 ± 1.09 2.39 ± 0.54 0.15 platelets 252.54 ± 76.18 271.57 ± 57.66 0.20 nlr 3.42 ± 3.62 1.83 ± 0.49 0.001* plr 136.46 ± 57.27 118.51 ± 34.24 0.05 nlr: neutrophil-lymphocyte ratio; plr: platelet-lymphocyte ratio. *denotes statistically significant difference. table ii preoperative inflammatory markers according to meningioma grade and controls marker neutrophils lymphocytes platelets nlr plr grade-i 5.14 ± 2.54 2.21 ± 1.13 255.46 ± 61.29 2.75 ± 2.17 128.78 ± 48 grade-ii 6.45 ± 2.81 1.71 ± 0.82 241.73 ± 118.9 5.90 ± 6.28 164.83 ± 79.15 controls 4.20 ± 0.81 2.39 ± 0.54 271.57 ± 67.66 1.83 ± 0.49 118.51 ± 34.24 edema+ 5.84 ± 2.96 2.03 ± 0.87 252.82 ± 85.73 4.0 ± 4.47 141.18 ± 66.95 edema4.77 ± 1.91 2.22 ± 1.37 252.10 ± 60.28 2.52 ± 1.39 129.19 ± 30.07 grade-i versus grade-ii p value 0.11 0.14 0.69 0.09 0.13 grade-i versus controls p value 0.02* 0.4 0.22 0.006* 0.28 grade-ii versus controls p value 0.01* 0.002* 0.4 0.03* 0.06 romanian neurosurgery (2018) xxxii 4: 613 621 | 617             edema present versus absent p value 0.12 0.49 0.96 0.06 0.37 nlr: neutrophil-lymphocyte ratio; plr: platelet-lymphocyte ratio. *denotes statistically significant difference. edema+: presence of peritumoral edema. edema-: absence of peritumoral edema. as expected, the nlr and plr were increased in the grade ii meningiomas but no significant differences were found between these two grades. however, there was a trend toward significance with regard to the nlr. when the grade i meningiomas and the controls were compared, we found that the neutrophil count and nlr increased, while the lymphocyte count, platelet count, and plr decreased in the grade i cases. however, the difference reached significance only regarding the neutrophil count and nlr. findings supporting the role of inflammation in the upgrading of a meningioma were found when a comparison between the grade ii meningiomas and the controls was performed. the neutrophil count, platelet count, nlr, and plr were higher and the lymphocyte count and platelet count were lower in the grade ii cases than in the controls. the differences were significant regarding the neutrophil count and lymphocyte count, and nlr levels. the presence and/or absence of peritumoral edema caused differences in the inflammatory marker levels, but none reached a significant level. here, we must emphasize the fact that the neutrophil and lymphocyte counts increased and decreased, respectively, suggesting that inflammation may play a role in the development of peritumoral edema. although we did not find significant differences between the presence and absence of peritumoral edema with respect to the nlr and plr, both showed elevations in the presence of peritumoral edema. correlations the strong positive correlations were as follows: neutrophil count and nlr (r = 0.65, p = 0.00001), neutrophil count and plr (r = 0.28, p = 0.005), lymphocyte count and platelet count (r = 0.32, p = 0.001), platelet count and plr (r = 0.21, p = 0.03), and nlr and plr (r = 0.61, p = 0.00001). contrarily, the strong negative correlations were as follows: lymphocyte count and nlr (r = 0.47, p = 0.00001), lymphocyte count and plr (r = 0.63, p = 0.00001), and platelet count and nlr (r = 0.26, p = 0.008). diagnostic efficacy when the patients with meningiomas were tested against the controls (figure 1), the aucs were 0.70 [95 % confidence interval (ci) 0.59-0.80, p = 0.001] for the nlr and 0.57 (95 % ci = 0.45-0.69, p = 0.22) for the plr. however, when grade i meningiomas were tested against the grade ii meningiomas (figure 2), the aucs were 0.70 (95 % ci = 0.53-0.86) for the nlr and 0.64 (95 % ci = 0.45-0.83, p = 0.1) for the plr. the findings showed that the nlr exhibited the best 618 | kemerdere et al preoperative systemic inflammatory markers in intracranial meningiomas             accuracy for a meningioma diagnosis and predicting the meningioma grade. figure 1 roc curve analysis showing diagnostic efficacy when patients with meningioma were tested against healthy subjects figure 2 roc curve analysis showing diagnostic efficacy when patients with meningioma were tested against those with grades i and ii discussion the role of chronic inflammation in both the development and progression of cancer has been identified, and it has been strongly suggested that inflammation-related neutrophils and lymphocytes, as well as platelets, participate in angiogenesis and the proliferation of tumor cells (11, 12). meningiomas, especially grade i lesions are slow-growing tumors, and obviously, chronic inflammation may take place in their development and progression. however, the exact mechanism(s) behind the neutrophilia and lymphopenia that are commonly found in cancer is poorly understood. some researchers have suggested that the cytokines and chemokines secreted by tumor cells can cause neutrophil infiltration, thus causing an elevation in their counts in both the tumor microenvironment and the peripheral blood (13, 14). the increased neutrophil levels subsequently inhibit the white blood cells, including lymphocyte activity, and this leads to lymphocyte apoptosis. the studies reported during the last decade showed that higher neutrophil and lower lymphocyte counts are associated with poor prognoses in various cancers, including glial tumors of the brain (4, 5, 7-10, 15, 16). unfortunately, there have been a limited number of studies focusing on brain tumors with regard to the preoperative inflammatory markers, when compared to the other organ system tumors, and there have been no reports focusing on meningiomas. a few studies have reported the preoperative inflammatory markers, such as the nlr, plr, and lymphocyte to monocyte ratio (lmr), in some extra-axial tumors, such as vestibular schwannomas and craniopharyngiomas (15, 16). for example, kontorinis, et al. (15) demonstrated that a very high nlr is a reliable marker for vestibular schwannoma growth romanian neurosurgery (2018) xxxii 4: 613 621 | 619             and that it can predict grooving schwannomas. chen, et al. (16) found that the levels of white blood cells, neutrophils, nlr, and plr were higher in craniopharyngiomas when compared to other sellar tumors, and they emphasized the fact that these markers can be used to differentiate craniopharyngiomas. moreover, zheng et al. (5) provided the first evidence that patients with gliomas have higher nlr levels than patients with nonlesional epilepsy, vestibular schwannomas, meningiomas, and healthy controls. because there have been no previous reports studying preoperative inflammatory markers in meningioma cases, we could not compare our results with those from the current literature. however, we did discuss our results with regard to previous reports including gliomas. first, we would like to emphasize the fact that our results were strongly in line with those of other studies including patients with gliomas (4, 5, 7-10). a significantly higher neutrophil count and nlr were found in our patient group when compared to the healthy controls. although we did not find a statistically significant difference regarding the plr, there was a trend toward significance. the lymphocyte count was also lower in the meningioma patients, but the difference was not significant. these results mentioned above support the previous glioma studies in which a higher neutrophil count, lower lymphocyte count, higher nlr, and, in some studies, a higher plr were found to be strongly associated with the prognosis (5, 8). more importantly, the glioma grade was associated with a higher nlr, and it was stated that the nlr can be used as an index for glioma progression, with an nlr ≥ 4 showing a poor prognosis (5, 8). it is clear that as tumor grade increases, the inflammatory reaction increases and the levels of the inflammatory markers, such as the neutrophil count, nlr, and plr, increase. for the first time, we demonstrated preoperative inflammatory marker levels in different meningioma grades (grade i and ii). we obtained very supportive findings that malignancy increases, the inflammationrelated markers increase. the grade ii patients showed higher and lower levels of neutrophils and lymphocytes, respectively, when compared to the grade i patients, but more importantly, the nlr and plr were higher in the grade ii patients although the differences were not significant. this may be due to the fact that the number of grade ii patients (n = 13) was smaller than that of the grade i patients (n = 48). we believe that if we were able to include an equal number of patients in each grade, the differences would be significant. the neutrophil counts and nlr were also clearly higher in each grade when compared to the healthy subjects but the biggest differences were found when comparing the grade ii and the healthy subjects, suggesting that inflammation may play a role in tumor progression, as in the current literature on glioma patients (4, 5, 7-10). from a clinical standpoint, we know that as the tumor malignancy increases, the peritumoral edema, which can sometimes cause life-threatening conditions, increases. recent studies have shown that inflammatory cells play roles in the formation of peritumoral edema, and they have been found in 620 | kemerdere et al preoperative systemic inflammatory markers in intracranial meningiomas             edematous tissues (17). we hypothesized that because peritumoral edema is associated with inflammation, the levels of the inflammatory markers studied here, would increase in those patients who exhibited peritumoral edema on their cranial mri scans. we note the fact that peritumoral edema was observed in all 13 of the patients who were diagnosed with grade ii meningiomas. the neutrophil count and lymphocyte count were increased and decreased, respectively, in the patients with peritumoral edema when compared to those who had no peritumoral edema, and there were higher nlr and plr levels in those patients with peritumoral edema. these finding supported our hypothesis that inflammation may play an important role in the development of peritumoral edema, and an anti-edematous treatment including a medication inhibiting neutrophil action in addition to steroids would be beneficial. as in the few studies including extra-axial tumors, such as vestibular schwannomas and craniopharyngiomas (15, 16), and the studies including gliomas (4, 5, 7-10), the nlr compared to the plr exhibited the highest diagnostic value in predicting meningiomas. this can differentiate grade i meningiomas from grade ii meningiomas, and it could be used as an index for possible tumor progression after surgery. limitations the authors contributed to this study are aware that there are a few limitations. first, this is a retrospective study that may cause selection bias although we had strict selection criteria. second, our patient sample consisted of a relatively small number of patients with meningioma, in particular, limited number of grade i meningiomas thus the literature needs prospective studies with larger cohort of meningioma patients. third, higher levels of neutrophil count, nlr, and plr can be a reflection of non-specific inflammatory response due to meningioma thus we have a risk of having false-positive results. we underline that until we have enough number of studies including larger cohort of patients, the results obtained from the current literature and from the present study should be evaluated carefully. conclusion apart from the limitations mentioned above, we for the first time provided that higher nlr may be associated with grading of meningioma and a predictive factor for progression of meningiomas. the use of medication against neutrophil-related inflammation may be helpful for patients with higher grade of meningioma for decreasing peritumoral edema before and after surgery. we were not able to compare our results with the current literature due to absence of studies included same type of tumor. thus, further studies are needed. correspondence oguz baran, m.d. istanbul research and training hospital, neurosurgery clinic, istanbul; turkey. e-mail: oguzbaran@gmail.com telephone number: +905325990034 fax : +90 (212) 459 62 30 mailing address: istanbul egitim ve arastirma hastanesi, beyin ve sinir cerrahisi klinigi. kasap romanian neurosurgery (2018) xxxii 4: 613 621 | 621             ilyas mah. org. nafiz gurman cad. 34098 samatya/istanbul references 1. carroll rs, zhang j, black pm. expression of estrogen receptors alpha and beta in human meningiomas. j neurooncol 1999;42:109–16. 2. louis dn, ohgaki h, wiestler od, cavenee wk, burger pc, jouvet a, et al. the 2007 who classification of tumours of the central nervous system. acta neuropathol 2007;114:97-109. 3. hanahan d, weinberg ra. hallmarks of cancer: the next generation. cell 2011;144:646-74. 4. zadora p, dabrowski w, czarko k, smolen a, kotlinska-hasiec e, wiorkowski k, et al. preoperative neutrophil-lymphocyte count ratio helps predict the grade of glial tumora pilot study. neurol neurochir pol 2015;49:41-4. 5. zheng sh, huang jl, chen m, wang bl, ou qs, huang sy. diagnostic value of preoperative inflammatory markers in patients with glioma: a multicenter cohort study. j neurosurg 2017;3:1-10. 6. banin hirata bk, oda jm, lost gr, ariza cb, de oliveira ce, watanave wa. molecular markers for breast cancer: prediction on tumor behavior. dis markers 2014;2014:513158. 7. bambury rm, teo my, power dg, yusuf a, murray s, battley je, et al. the association of pre-treatment neutrophil to lymphocyte ratio with overall survival in patients with glioblastoma multiforme. j neurooncol 2013;114:149-54. 8. han s, yang l, qingchang l, zhonghua l, haipei h, anhua w. pre-treatment neutrophil-to-lymphocyte ratio is associated with neutrophil and t-cell infiltration and predicts clinical outcome in patients with glioblastoma. bmj cancer 2015;15:617-26. 9. wang pf, song hw, cai hq, kong lw, yao k, jiang t, et al. preoperative inflammation markers and idh mutation status predict glioblastoma patient survival. oncotarget 2017;8:50117-23. 10. auezova r, ryskeldiev n, doskaliyev a, kuanyshev y, zhetpisbaev b, aldiyarova n, et al. association of preoperative levels of selected blood inflammatory markers with prognosis in gliomas. onco targets ther 2016;9:6111-7. 11. grivennikov si, greten fr, karin m. immunity, inflammation and cancer. cell 2010;140:883-99. 12. malietzis g, giacometti m, kennedy rh, athanasiou t, aziz o, jenkins jt. the emerging role of neutrophil to lymphocyte ratio in determining colorectal cancer treatment outcomes: a systematic review and metaanalysis. ann surg oncol 2014;21(12):3938-46. 13. del prete a, allavena p, santoro g, fumarulo r, corsi mm, mantovani a. molecular pathways in cancer-related inflammation. biochem med 2011;21:264-75. 14. gregory ad, houghton am. tumor-associated neutrophils: new target for cancer theraphy. cancer res 2011;71:2411-26. 15. kontorinis g, crowther ja, iliodromiti s, taylor was, locke r. neutrophil to lymphocyte ratio as a predictive marker of vestibular schwannoma growth. otol neurotol 2016;37:580-5. 16. chen m, zheng sh, yang m, chen zh, li st. the diagnostic value of preoperative inflammatory markers in craniopharyngioma: a multicenter cohort study. j neurooncol 2018;138:113-22. 17. polyzoidis s, koletsa t, panagiotidou s, ashkan k, theoharides tc. mast cells in meningiomas and brain inflammation. j neuroinflammation 2015;12:170. doi: 10.33962/roneuro-2023-004 preliminary results of minimally invasive stereotaxic surgery of intraparenchymal hematomas at the hospital of mali (23 cases) mahamadou dama, oumar diallo, oumar coulibaly, daouda sissoko, theodore maxim coulibaly, kalba tembine, thomas coulibaly, fengqiang liu, cisse el hassimi mohamed, drissa kanikomo romanian neurosurgery (2023) xxxvii (1): pp. 36-40 doi: 10.33962/roneuro-2023-004 www.journals.lapub.co.uk/index.php/roneurosurgery preliminary results of minimally invasive stereotaxic surgery of intraparenchymal hematomas at the hospital of mali (23 cases) mahamadou dama1, oumar diallo1, oumar coulibaly1, daouda sissoko1, theodore maxim coulibaly1, kalba tembine1, thomas coulibaly1, fengqiang liu1,2, cisse el hassimi mohamed1,3, drissa kanikomo1 1 fmos, usttb, hospital of mali. bamako, mali 2 hospital zhejiang university school of medicine, popular republic of china 3 mother-child hospital of luxembourg, bamako, mali abstract introduction: spontaneous intracerebral haemorrhage (ich) is a rupture of blood vessels in the brain parenchyma, in the absence of any underlying structural vascular lesion. it’s destructive and associated with a high mortality rate. there is a specific threshold of hematoma evacuation to impact mortality or functional outcome in ich even the curative effect of minimally invasive hematoma removal for cerebral haemorrhage has not been fully recognized worldwide. we aim to evaluate surgical performance on hematoma volume and functional outcomes of patients. methods: this study is a retrospective and observational clinical study. a total of 30 ich patients were treated in the department of neurosurgery at the hospital of mali from december 2019 to november 2020. minimal invasive puncture hematoma removal was performed in all the patients. the modified rankin scale (mrs) was used to assess functional outcomes at 6 months and one year of surgery. was considered poor functional outcome mrs >3. the percentages (%) of the count data were assessed by fisher’s exact test by spss 23.0 software was used. results: a total of 23 ich patients met the inclusion criteria, the mean was 47,78 years. among the risk factors, the hta is present in 91,3% of patients. the evacuation was satisfactory in 91.30% of cases. conclusion: this first study of minimally invasive stereotaxic for ich evacuation must be followed up and encouraged. even if the results are satisfactory, a double-blind study is required in the largest sample. introduction spontaneous intracerebral hemorrhage (ich) or primary intracerebral hemorrhage (ich) is a rupture of blood vess els in the brain parenchyma, in the absence of any underlying structural vascular keywords evacuation, haematoma, minimally, stereotactic, surgery corresponding author: mahamadou dama fmos, usttb, hospital of mali damasmaha1@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 37 preliminary results of minimally invasive stereotaxic surgery of intraparenchymal hematomas lesion, can lead to the accumulation of the blood within the brain substance (7). ich is the second most severe type of stroke; it is destructive and associated with a high mortality rate. the current treatment methods are limited, and only a few surviving patients can recover their self-care ability, leading to a heavy economic burden on families and society (12). it is urgent that new therapeutic methods for cerebral hemorrhage are developed. a brain injury caused by cerebral hemorrhage can be considered either a primary brain injury or a secondary brain injury, and the treatment of cerebral hemorrhage focuses on the following two concepts: on the one hand, a mechanical injury, on the other hand, reducing the risk for deterioration of neurological function after cerebral hemorrhage (10). there is a specific thresholds of hematoma evacuation to impact mortality or functional outcome in ich (5) even the curative effect of minimally invasive hematoma removal for cerebral hemorrhage has not been fully recognized worldwide (4,7). in mali there is no study on the intracerebral hemorrhage evacuation, nor in west africa and with the development of minimally invasive techniques we initiated the stereotactic evacuation of ich. we aim to evaluate surgical performance on hematoma volume and functional outcome of patients. methods subject this study is a retrospective and observational clinical study. a total of 30 ich patients treated in the department of neurosurgery at the hospital of mali from december 2019 to november 2020. were included in this study 23 patients with complete clinical and radiological data. the inclusion criteria were: age ≥18 with ich whose surgical volume was location function. lobar≥ 30cc, thalamic and basal ganglia≥ 15cc, brainstem≥5cc, cerebelum≥10cc with blood presure≤160/90 mmhg. glasgow score≥8pts and/or motor deficit≤3/5, presence of symptoms≤72h exclusion criteria were: secondary ich, patient on anticoagulation or antiaggregating or plaletet≤100000. the stereotaxic frame was attached to the patient's head under local anesthesia (lidocaine 2%). all patients were operated on under general anesthesia,10cc plastic syringes were used for hematoma aspiration. evacuation was considered satisfactory for a volume evacuated ≥ 80% of the volume of the hematoma. the cavity was rinsed with isotonic serum, the temperature of which oscillated between 2 and 4 degrees. all patients were awakened in intensive care unit, a brain ct scan at 24h-48h postoperatively was performed. minimally invasive puncture hematoma removal method: surgical procedures brain ct scan was performed after frame fixation. the center of the largest plane of the scanned hematoma was selected as the target point and we used the axial plan for the planification and calculation of coordinates. in the operating room the patient position depended of hematoma location and all coordinates were calculated by manual way as anke formula (11). we disinfected the surgical area with a conventional way and the patient is champed (figure1). a 3cm skin incision is made at the enter point and we drilled through the skull a 5mm hole. after opening the dura, we make a puncture with 4mm canula and the gently aspiration was made a 10cc sterile syringe (figure 2). finally, the hematoma cavity was cleaned with 2–4-degree nacl 0,9%. figure 1. patient champed figure 2. puncture of hematoma 38 mahamadou dama, oumar diallo, oumar coulibaly et al. clinical data collection in this study the variables analyzed were demographic (sex, age), history (hypertension, diabetes mellites,), toxic habits (smoking, alcoholism) mode of transport to hospital (ambulance, personal vehicle, taxi), glasgow scale at admission, the volume of the hematoma was measured by the abc/2 method, presence or absence of intraventricular blood. the time points for minimal invasive surgery were divided into three groups: ≥6h ≤24 h group ⅰ, >24h≤48h group ⅱ and >48h≤72h group ⅲ. modified rankin scale (mrs) was used to assess functional outcome at 6 months and one year of surgery. was considered poor functional outcome mrs >3. the percentages (%) of the count data were assessed by fisher’s exact test. univariate analysis with chi-square test and mann-whitney test by spss 23.0 software was used. results a total of 23 ich patients met the inclusion criteria, including 12 males and 11 females who were aged mean 47,78years. according to the time from onset to minimally invasive surgery, they were divided into three groups: group ⅰ (34,8%), group ⅱ (26,1%), and group ⅲ (39,1%). among the risk factors, the hta is present in 91,3% cases with 100% in the group ⅱ. all patients were transported by personal vehicle. the majority of patient operated were gsc between 9 and 13pts as showed in table 1. 65.14% of patients had deep localization versus 30.43% lobar localization. the less volume operated is 6cc in the brainstem and 70cc in lobar hematoma as maximum volume (figure 3). the evacuation was satisfactory by 91.30% of patients. there was no intraventricular blood in 95.7% of cases. there was no difference between the 6 months and 12 months mortality. figure 3. preoperatory ct scan after frame fixation. discussion the evacuation of intraparenchymal hematomas is a holy grail in management, however, no previous study has correlated the success of the procedure with the residual volume of ich (8,9). the conclusions in an explanatory trial, with rigorous monitoring of the process and results of the surgical intervention, demonstrated that there is a threshold (of ≤15ml eot ich or ≥70% hematoma evacuated) associated with the favorable functional result, after the control of the gravity variables of the disease (5). in this first study of hematoma evacuation in mali, we didn’t used the thrombolytic drogue and for hemostatic effect we used isotonic salt serum from 2-4 degree to clean the hematoma cavity, the relationship between temperature and adrenergic response seems to be one of the pivots of the cold-induced vasospasm process (3). we considered eot if the was absolutely clear. our satisfaction threshold was an evacuation ≥80% of hematoma and it was 91.30% of patient. the mean residual volume was 6,95cc. figure 4. postoperative figure 5. preoperatory ct scan ct scan of brainstem hematoma figure 6. control ct scan there is no consensus on the appropriate timing of minimally invasive surgery. the time at which the surgery is performed may affect the curative effect, 39 preliminary results of minimally invasive stereotaxic surgery of intraparenchymal hematomas table 1. data analysis of the three groups variables group ⅰ (n=8) group ⅱ (n= 6) group ⅲ (n= 9) p value sex(m/f) (5/3) (4/2) (3/6) mean age 39,12 50,16 53,89 hta 87,5% 100% 88,89% dm 0% 16,67% 11,11% smoke 12,5% 50% 0% alcoholism 0% 33,33% 0% mode of transport • ambulance 0% 0% 0% • personal vehicle 100% 100% 100% • taxi 0% 0% 0% hematoma location • lobar 25% 33,33% 33,33% • thalamic and bg 62,5% 66,67% 66,67% • brainstem 12,5% 0% 0% • cerebellum 0% 0% 0% glasgow scale • 8pts 12,5% 33,33% 0% • 9-13pts 75% 50% 100% • 14=15pts 12,5% 16,66% 0% mean vol of hematoma 40,5cc 44,7cc 51,5cc mean residual vol 4,4cc 4,33cc 11cc mrs at 6 months 0.01 • ≤3 75% 83,33% 55,56% • >3 25% 16,67% 44,44% mrs at 1year 0.01 • ≤3 75% 83,33% 55,56% • >3 25% 16,67% 44,44% thus affecting the selection range of patients for this treatment (12). the choice to divided the time point was motived by: the time for hematoma stabilization generally 6 hours after bleeding and 72 hours after ich, delayed perihematomal oedema (phe) is associated with the destruction of the blood–brain barrier (angioedema), massive lysis of red blood cells and neurotoxicity induced by hemoglobin decomposition products (6). about 39% of the patients were in group ⅲ because of the blood pressure which was very high and which had to be checked first. none of our patients has benefited from a pre-hospital resuscitation because all of them came to the hospital in personal vehicle, which is perhaps a worsening factor. the deep location was most frequent in all three groups with a total of 65,13% of patients. the threshold associated we favorable functional outcome maybe applicable to lobar, thalamic and basal ganglia hematoma but not to brainstem hematoma (figure 4 and figure 5) in which despite zero cc eot the patient was mrs at 6 in the first month. one month mortality rates associated with this devastating illness range from 35% to 52%, with half of those deaths occurring in the first 2 days (1,2) and in our sample it was 21,73%. theoretically, removal of hematoma and reduction of cerebral oedema through surgical treatments can reduce intracranial pressure, relieve symptoms of cerebral tissue compression, and reduce inflammatory response and neurotoxic effects. however, the benefits of clinical surgical treatment for deep cerebral hemorrhage are unclear at present. the risks of surgery itself and the damage to brain tissue during the process of entering the hematoma limit the therapeutic effect (13). there was no statistical difference at 6 mouths and one-year functional outcome and mortality between the three groups (p value 0.01). limitations: this is a single department study with limited means. the sample is small and the inclusion criteria are not accepted by many neurosurgeons. 40 mahamadou dama, oumar diallo, oumar coulibaly et al. conclusion this first study of minimally invasive stereotaxic for ich evacuation must be followed up and encouraged. even if the results are satisfactory, a double-blind study is required in largest sample. the result on the hematoma volume was good. abbreviations: ich: intracerebral hemorrhage ct: computed tomography mrs: modified rankin scale cc: centimeter cubic eot: end of treatment phe: perihematomal oedema bg: basal ganglia m: male. f: female. hbp: high blood pressure dm: diabetes mellitus spss: statistical package for the social sciences. anke: name of company. fmos: faculty of medicine and odontostomatology usttb: university of sciences, technics and technologies of bamako references 1. chiewvit p, danchaivijitr n, nilanont y, poungvarin n. (2009) computed tomographic findings in non-traumatic hemorrhagic stroke. j med assoc thai. 92(1):73-86. 2. ehtisham a, taylor s, bayless l, klein mw, janzen jm. (2009) placement of external ventricular drains and intracranial pressure monitors by neurointensivists. neurocrit care. 10(2):241-247. 3. harker c.t., ousley p.j., harris e.j.,edwards j.m., taylor l.m., porter j.m.( 1990)the effects of cooling on human saphenous vein reactivity to adrenergic agonists. j.vasc.surg.12 (1): 45-9. 4. hemphill jr, greenberg sm, anderson cs, et al. (2015) guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for health care professionals from the american heart association/american stroke association. stroke.46:2032–2060. 5. issam a. awad., sean p. polster., julián carrión-penagos., richard e. thompson, ying cao., agnieszka stadnik., et al (2019) surgical performance determines functional outcome benefit in the minimally invasive surgery plus recombinant tissue plasminogen activator for intracerebral hemorrhage evacuation (mistie) procedure. neurosurgery doi:10.1093/neuros/nyz077. 6. lim-hing k, rincon f. (2017) secondary hematoma expansion and perihemorrhagic edema after intracerebral hemorrhage: from bench work to practical aspects. front neurol. 8:74. 7. mahua dey, md., agnieszka stadnik, msc., issam a. awad, md. (2014) spontaneous intracerebral and intraventricular hemorrhage: advances in minimally invasive surgery and thrombolytic evacuation, and lessons learned in recent trials. neurosurgery, https:// doi: 10.1227/neu.0000000000000221. 8. mendelow ad, gregson ba, fernandes hm, et al. (2005) early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the international surgical trial in intracerebral haemorrhage (stich): a randomised trial. lancet north am ed.365(9457):387-397. 9. mendelow ad, gregson ba, rowan en, murray gd, gholkar a, mitchell pm. (2013) early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (stich ii): a randomised trial. lancet north am ed.382(9890):397-408. 10. selim m, norton c. (2018) perihematomal edema: implications for intracerebral hemorrhage research and therapeutic advances. j neurosci res, https://doi.org/10.1002/jnr.24372. 11. shenzhen anke high-tech co., ltd. asa-602s high accurate brain stereotactic system, operation instructions. 2.0 ed. shenzhen, gygx(z) z2001 no.3030237. 12. yang ma., ping zhang., yingxin tang., xiaohua yang., zhouping tang. (2020) effects of the treatment timing of minimally invasive surgery and urokinase dosage on perihematomal oedema in intracerebral hemorrhage evacuation, brain hemorrhages. brain hemorrhages, https://doi.org/10.1016/j.hest.2020.01.003. 13. ziai wc, carhuapoma jr. (2018) intracerebral hemorrhage. continuum (minneap minn).24:1603–1622. doi: 10.33962/roneuro-2022-077 evaluation of surgical characteristics and clinical outcome of 11 patients with thoracic discectomy through transfacet approach talat cem ovalioglu romanian neurosurgery (2022) xxxvi (4): pp. 423-429 doi: 10.33962/roneuro-2022-077 www.journals.lapub.co.uk/index.php/roneurosurgery evaluation of surgical characteristics and clinical outcome of 11 patients with thoracic discectomy through transfacet approach talat cem ovalioglu bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery, istanbul, turkey abstract background: in thoracal disc herniation (tdh) requiring surgery, the size, level, anatomic location, and calcification of the disc are extremely important in the selection of the technique to be applied. since the thoracic region does not allow spinal cord manipulation, the surgery is difficult and requires experience. a consecutive series of patients who underwent thoracic discectomy through a posterior transfacet approach is presented in this study. methods: eleven patients (6 men, and 5 women) underwent surgery at 12 disc levels. the mean age was 53.54 years (range 28-72 years). patients presented with myelopathy (n = 8, 73%), radiculopathy (n = 7, 64%), back pain (n =10, 91%), and urinary dysfunction (n = 6, 55%). seven (58%) lateral, 3 (25%) calcified, and 4 (33%) large disc herniations were revealed by preoperative imaging. the mean follow-up period was 21.02 ± 8.04 months (range 6 – 43 months). results: a posterior transfacet approach was used for all eleven patients with tdh. thoracic discectomy was performed at t1112 (36%) level for 4 patients, and equally at t1011 (36%) level for the other 4 patients. a bilateral approach with laminotomy was performed in one patient, and a two-level discectomy was performed in another patient. unilateral partial laminectomy was added for 3 patients. the average operating time was 146.85 minutes (range 125-220 minutes). the average hospital stay was 4.2 days (range, 213 days) while no neurological functional deterioration was observed in any of the patients after surgery. postoperative 1-month and 6-month odi scores were found significantly different from preoperative odi scores in all patients. conclusions: thoracal discectomy through the posterior transfacet approach route is a safe and effective technique to achieve adequate decompression without requiring instrumented fusion. introduction surgical treatment of symptomatic thoracal disc herniation (tdh) is a major challenge for spine surgeons because the thoracic spine is not suitable for manipulation. the main problem of thoracic disc surgery is the lack of a “gold standard” surgical technique to be applied. total keywords discectomy, herniation, spine, thoracal, transfacet corresponding author: talat cem ovalioglu bakirkoy research and training hospital for neurology, neurosurgery and psychiatry, department of neurosurgery, istanbul, turkey talatcem@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 424 talat cem ovalioglu laminectomy, which was performed for a period, has been abandoned today as a result of severe complications (15, 21, 26). recently, advanced techniques for the treatment of tdh, including the transpedicular, microsurgical pedicle-sparing transfacet, costotransversectomy, lateral extracavitary, transthoracic, and thoracoscopic approaches have been used in different centers (1, 8, 15, 18, 20, 24, 25, 27, 31, 36). each technique has particular disadvantages and potential complications. ultimately, the goal of any of these procedures is to reduce the patients’ pain, improve their quality of life, and improve their neurological status with limited morbidity. this study presents a consecutive series of surgically excised tdh through a posterior transfacet approach. the goal was to assess the outcomes and complications in patients undergoing transfacet discectomy. materials and methods patient characteristics and operative indications eleven patients with symptomatic extradural tdh surgically treated by a single surgeon between january 2010 and january 2016 were analyzed clinically, radiologically, and surgically. ethical approval was obtained from the ethical committee and written informed consent was obtained from participants in the study before surgery. six men and 5 women (mean age; 53.54 years, range 28-72 years) were included, with surgery performed at 12 disc levels (table 1). history and neurologic examination were obtained at the initial presentation and followups. indications for surgery included myelopathy, radiculopathy, and urinary dysfunction. patients with isolated back pain without neurologic symptoms were not considered for surgical intervention. all patients underwent preoperative spinal magnetic resonance (mr) and computed tomographic (ct) imaging. imaging studies were reviewed for assessment of calcification, location relative to midline, and size of disc herniation. the size of disc herniation was classified into three groups: small (010% canal occupation), medium (10-20% canal occupation), and large (>20% canal occupation). operative parameters including surgical time, estimated blood loss, the length of hospital stay, and complications were tabulated from the available record. the standardized oswestry disability index (odi) questionnaire (23) was used to determine the disability of the patients preoperatively and postoperatively 1 month and 6 months. spss 21 (statistical package for social sciences) for windows software was used for the evaluation of the findings. a p-value less than 0.05 was considered statistically significant. the paired t-test was used for the comparison. surgical technique and operative data a posterior transfacet approach was used for all patients. a midline skin incision was used in all of the 11 patients. of those,10 patients underwent a unilateral subperiosteal approach with bony decompression. one patient with a large central tdh and severe cord compression had undergone bilateral exposure with laminectomy before attempting discectomy. patients were positioned prone on the operating table following induction of general anesthesia and endotracheal intubation. intra-operative spinal cord monitoring was utilized in six patients (patients number 4, 7, 8, 9, 10, 11) while the remaining five did not have any spinal cord monitoring during the procedure. the incision was marked using lateral carm fluoroscopy. after a 4-cm midline skin incision centered over the disc space, posterior vertebral elements were exposed in standard fashion out laterally to the transverse processes using a subperiosteal dissection. the surgical level was confirmed intraoperatively with fluoroscopy on the transverse process overlying the disc of interest. the facet complex is partially removed with a high-speed drill under the operative microscope. this proceeded through a limited unilateral laminotomy with medial facetectomy. the foraminal soft tissue is coagulated using bipolar cautery and the lateral annulus is exposed. following exposure of the disc space lateral to the thecal sac, focal posterolateral soft disc herniations were removed, working in a lateral to the medial direction to create a central cavity. for large midline calcified tdh, a small trough was additionally drilled into the adjacent vertebral bodies, and the cavitation was extended medially through the disc space and adjacent endplates to undermine the herniation. the herniated disc material is decompressed into the disc cavity by using angled microrongeurs, nerve hooks, and reverse-angle microcurettes. the microscope is angulated medially and the patient is tilted contralaterally to allow visualization across the midline. the disc fragments 425 thoracal discectomy through transfacet approach were then removed cautiously with curettes and pituitary forceps to achieve adequate decompression. suction drains are not routinely placed. an exercise program is started one week after discharge to strengthen the paravertebral muscles and the patient is advised to return to daily activities. results preoperative findings the mean time from symptom onset to surgical decompression was 22.6 months (range, 1 -54 months). eight (73%) patients presented with myelopathy, 7 (64%) with radiculopathy, 6 (55%) with urinary dysfunction, and 10 (91%) with axial back pain. preoperative magnetic resonance and computed tomographic imaging showed 2 small (17%), 6 medium (50%), and 4 large (33%) discs. the majority of cases were lateral disc prolapses (n = 7, 58%), with 3 centrolateral (25%) and 2 centrally (17%) located. five cases were soft disc prolapses (42%), 3 were calcified (25%), and 4 were partially calcified (33%) (table1). table 1. sex ratio of patients patient age/gender duration of symptoms (months) presenting symptoms level axial location size calcification approach 1 55/m 22 bp, m, r t1011 l medium calcified tf + pl 2 67/m 39 bp, m, r, u t1112 cl large partial bilateral tf + l + fusion 3 52/f 14 bp, r t1112 l small soft tf 4 28/m 6 bp, m, r, u t1011 c large soft tf 5 63/f 45 bp, m, u t8-9 cl medium calcified tf + pl 6 46/f 42 bp, m t1112 l small soft tf 7 72/m 24 bp, m, r, u t9-10 t1011 cl l medium medium calcified partial tf + pl tf 8 49/f 1 bp, u t1112 c large partial tf 9 54/m 18 m, r t1011 l medium soft tf 10 37/m 11 bp, m, r, u t9-10 l large soft tf 11 66/f 27 bp, m t8-9 l medium partial tf surgical findings and functional outcomes eleven patients underwent a total of 12 operated disc levels. figure 1 illustrates preoperative and postoperative imaging for a selection of typical cases from the series. ten patients underwent surgery on a single level, one of those (patient 2) had a large centrolateral tdh with severe cord compression and underwent a bilateral transfacet approach with bilateral laminotomy before attempting discectomy. interbody autograft bone fusion was added to that patient. two-level discectomy was performed in one of the patients (patient 7) while unilateral partial laminectomy was added for 3 patients (patients 1, 5, 7). the average operating time was 146.85 minutes (range, 125-220 minutes). the average blood loss was 580 ml (range, 150-1200 ml) (table 2). neurophysiological status was monitored via ssep and mep testing intraoperatively with no deterioration in signals noted in any of the 6 patients. one patient (patient 9) required a second operation for a tdh at a different level on the contralateral side 25 months after the first surgery. there were no cases of neurological deterioration after surgery, and there were no major complications and no wrong-level surgeries in this series. a dural tear occurred in one patient who had 426 talat cem ovalioglu a calcified centrolateral disc herniation (patient 5). the dural tear was repaired with primary suture and fibrin sealant, and it healed without complication. figure 1. sagittal (a) and axial (b) preoperative t2-weighted mr images of t8-9 disc herniation with cord compression. sagittal (c) and axial (d) postoperative t2-weighted mr images after decompression with discectomy through the unilateral transfacet approach. table 2. operative data of the patients operative data average operating time (minutes) 146.85 (range 125-220) average blood loss (ml) 580 (range 150-1200) average hospital stay (days) 4.2 (range 213) mean follow-up period (months) 21.02 ± 8.04 (range 6 – 43) the average hospital stay was 4.2 days (range 213 days). the mean follow-up period was 21.02 ± 8.04 months (range 6 – 43 months) (table 2). the odi scores decreased significantly in both 1-month and 6-month follow-up evaluations from a mean preoperative score of 42.44 ± 11.38 to 27.46% ± 7.44% (p<0.05) and 24.16% ± 6.48% (p<0.05), respectively. no postoperative instability was developed requiring an instrumentation-assisted secondary fusion. discussion in spine surgeons’ practice, symptomatic thoracic disc herniation is a relatively rare pathology among spinal disc herniations. appropriate surgical management of this rare pathology continues to be a subject of clinical studies. there have been several surgical techniques and various approaches for the treatment of tdh. the features of the herniated material, comorbidities of the patient, and the experience of the surgeon are primarily important factors in selecting an approach. furthermore, severe neurological symptoms and the presence of spinal deformity should be considered while deciding on the technique. in the present series of transfacet approaches for thoracic discectomy, we noted functional improvement with significantly decreased odi scores, relief of radicular pain, and no major complications. a two-level approach was used in one of these cases without difficulty. it was previously reported that in the rare occurrence of multiple disc herniations, multilevel discectomies via the transfacet approach may be performed (10). any further surgery on the operated thoracic region was required by any patients in the series. thoracic discectomy using the transfacet pediclesparing approach was first described by stillerman et al. in 1995, in which the lateral articular process is excised to reach the intervertebral disc (35). this method avoids the risk of neurological injury caused by intraoperative traction of the dural sac. the interference to the dural sac is minimal during exposure and the herniated disc can be well exposed for complete excision. diminished operative time, decreased blood loss, limited bone removal, and limited soft-tissue disruption are the main advantages of this procedure. compared with the transpedicular discectomy, less postoperative localized axial back pain was seen due to the preservation of the pedicle. moreover, shortened hospital stays and earlier return to work give an advantage over the transthoracic and lateral extracavitary approaches. they recommended the transfacet approach for the surgical management of all soft symptomatic herniations, lateral calcified, and selected centrolateral calcified thoracic discs (35). the transfacet approach is comparable with the other posterolateral procedures concerning the surgical trajectory and the relatively small amount of bone removal. one advantage of this approach is that the pedicle and most of the facet joints are preserved. in cases of calcified disc extension caudal to the disc space, the superomedial pedicle cortical wall resection favored greater access (35). the 427 thoracal discectomy through transfacet approach inferomedial cortical wall of the pedicle, the transverse process, and related rib are preserved to protect the nerve root. it is suggested that the incidence of long-term localized pain secondary to loss of mechanical integrity will be reduced with this transfacet approach (35). there is no common consensus on the requirement for instrumented fusion after a thoracic discectomy. some authors claim anterolateral and more extensive posterolateral techniques need instrumented fusion more commonly than the posterior unilateral transfacet approaches (19, 37). patients with an intact unilateral facet, or >50% of facets remaining bilaterally, were considered stable by other clinical reviews reporting that fusion is uncommonly required (20, 22, 24). although some authors have argued for the importance of an intact bilateral facet complex for stability (7, 29), others report relatively minor destabilizing effects of total facetectomy (12, 34). in the current series, evidence of preexisting segmental instability was not seen in any case. interbody autograft bone fusion following discectomy via bilateral transfacet approach with bilateral laminotomy was performed on one patient (patient 2) who had a large centrolateral tdh. we also recognize that the addition of a partial laminectomy without instrumentation in 3 cases does not induce spinal instability at the related segment in the follow-up period. there were several thoracal discectomy reports evaluating blood loss, operating time, the length of hospital stay, and odi scores in the literature (7, 9, 34, 38). in the study of sivakumaran et al., the average operating time was found 125 minutes for 24 patients who had transfacet and transpedicular approaches for thoracic discectomy (34). the mean hospital stay was found to be 3.3 days (2-10 days) when they excluded 3 patients who needed care of sociorehabilitative service because of significant preoperative neurologic dysfunction. bransford et al. reported their experience with thoracic discectomy using a modified transfacet pedicle-sparing decompression and fusion (7). in this 16-case series, the length of postoperative hospital stay ranged from 3–11 days (mean 4.2 days) when they excluded 2 patients because of wound infections that lengthened the hospital stay. the average estimated blood loss was found to be 870 ml (range 150–3000 ml). in the study of carr et al., the average blood loss of thoracic discectomy via posterior unilateral modified transfacet pedicle–sparing decompression with segmental instrumentation and interbody fusion was found at 770 ml (range 25-2000 ml) for 32 operations (9). yüce et al. reported their 23 patients who had thoracic microdiscectomy with bilateral decompression via a unilateral approach. the odi scores of the patients significantly decreased from a mean preoperative score of 43,86 ± 8,73 to 26,52 ± 7,11 in early postoperative and 25,91 ± 6,78 at 12 (late) months (p <0,05) (38). some reports were on the comparison of anterior and posterior approaches (3, 30). oltulu et al. reported significantly improved postoperative odi scores of the patients with thoracic discectomy via posterior approach (p < 0.05) while the anterior group remained stable (p>0.05) (30). they found that the mean blood loss was 390.88 ml (range 50-2000 ml) for the anterior group (68 patients), 602.78 ml (range 25-2550 ml) for the posterior group (18 patients) (p = 0.983). arts et al. compared the results of the anterior approach (56 patients) and the posterior approach (44 patients) (3). the average duration of the surgery through the posterior approach was 98 minutes (no stabilization done), while it was 229 minutes through the anterior approach. blood loss in the anterior procedure was 1157 ml, and in the posterior one, it was 213 ml. the average hospitalization of patients treated through the anterior approach was markedly longer (10.1 days) than the posterior one with an average hospitalization of 4.9 days. in this series, there are no giant thoracal disc herniations as those occupying more than 40% of the spinal canal based on preoperative imaging. these giant thoracic discs have a unique clinical presentation, surgical considerations, and outcomes as compared to smaller size tdhs. a giant calcified central tdh increases the risk of intradural extension due to erosion and progressive thinning of the dura thus making its excision more difficult and more prone to surgical complications (4, 16, 28, 32). generally, a transthoracic approach is preferred to gain excellent exposure to the ventral aspect of the spinal canal without the need for manipulation of the dura. thus, ventral dural access and direct repair of the defect can be possible with this approach (7, 13, 14). thoracoscopic discectomy may be another choice for central disc herniations with the advantage of reducing morbidity (5, 11, 17). the primary disadvantage of the transfacet approach is 428 talat cem ovalioglu that opening the dura for the removal of an intradural disc fragment may not be possible because of inadequate direct ventral visualization (6, 34, 35). there was no obvious intradural penetration found in the present series. results of the newer minimally invasive techniques using tubular or endoscopic systems for thoracic disc resection, such as posterior and posterolateral approaches demonstrate significant improvements in pain relief, neurological outcomes, and postoperative spinal stability (2, 5). in some studies, endoscopy-assisted thoracic discectomy via posterior approaches was found useful for visualizing the ventral dura (20, 33, 35). this study is limited by a few factors. this study has a small series of patients who underwent surgery by a single surgeon at a single institution. another limitation is the analysis of the data in a retrospective manner rather than a prospective one. despite the retrospective nature of this report, the efficacy and safety of the procedure are confirmed by the symptomatic improvement of the patients without concomitant morbidity. further studies should focus on late collapse, mechanical back pain, and reherniation in long-term follow-up of the patients who underwent a transfacet approach for thoracic discectomy. conclusion while deciding on thoracic discectomy, it is necessary to know spinal biomechanics and the surgical techniques very well with their advantages and disadvantages. the study presents a single surgeon’s experience with the thoracic discectomy via the transfacet approach with the results of a significant symptomatic improvement and no major complications. for the treatment of thoracal disc herniated patients with myelopathy, radiculopathy, and back pain, thoracal discectomy through the posterior transfacet approach route is a safe and effective technique to achieve adequate decompression without requiring instrumented fusion. references 1. allan h. the surgical approach to the thoracic intervertebral disc protrusions. j neurol neurosurg psychiatry 1960;23(2):133-137. 2. arnold pm, johnson pl, anderson kk. surgical management of multiple thoracic disc herniations via a transfacet approach: a report of 15 cases. j neurosurg spine 2011;15(1):76-81. 3. arts mp, bartels rh. anterior or posterior approach of thoracic disc herniation? a comparative cohort of minitransthoracic versus transpedicular discectomies. spine j. 2014;14(8):1654-62. 4. barbanera a, serchi e, fiorenza v, nina p, andreoli a. giant calcified thoracic herniated disc: considerations aiming a proper surgical strategy. j neurosurg sci 2009;53(1):19–25. 5. bilsky mh. transpedicular approach for thoracic disc herniations. neurosurg focus 2000;15(4): e3. 6. black p. laminotomy/medial facet approach in the excision of thoracic disc herniation. neurosurg focus 2000;9(4):e6. 7. bransford r, zhang f, bellabarba c, konodi m, chapman jr. early experience treating thoracic disc herniations using a modified transfacet pedicle-sparing decompression and fusion. j neurosurg spine 2010;12:221-231. 8. burke t, caputy a. treatment of thoracic disc herniation: evolution toward the minimally invasive thoracoscopic technique. neurosurg focus 2000;9(4):1-7. 9. carr da, volkov aa, rhoiney dl, setty p, barrett rj, claybrooks r, bono pl, tong d, soo tm. management of thoracic disc herniations via posterior unilateral modified transfacet pedicle-sparing decompression with segmental instrumentation and interbody fusion. global spine j 2017;7(6):506-513. 10. chin ls, black kl, hoff jt. multiple thoracic disc herniations. case report. j neurosurg 1987;66:290–292. 11. connelly cs, manges pa. video-assisted thoracoscopic discectomy and fusion. aorn j 1998;67:940–945. 12. deniz fe, brasiliense lb, lazaro bc, reyes pm, sawa ag, sonntag vk, et al. biomechanical evaluation of posterior thoracic transpedicular discectomy. j neurosurg spine 2010;13:253-259. 13. dickman ca, rosenthal d, regan jj. reoperation for herniated thoracic discs. j neurosurg 1999;91(2 suppl):157–162. 14. dietze dd jr, fessler rg. thoracic disc herniations. neurosurg clin n am 1993;4:75–90. 15. fessler rg, sturgill m. review: complications of surgery for thoracic disc disease. surg neurol 1998; 49:609-618. 16. hott js, feiz-erfan i, kenny k, dickman ca. surgical management of giant herniated thoracic discs: analysis of 20 cases. j neurosurg spine 2005;3(3):191–197. 17. hulme a. the surgical approach to thoracic intervertebral disc protrusions. j neurol neurosurg psychiatry 1960;23:133–137. 18. kasliwal m, deutsch h. minimally invasive retropleural approach for central thoracic disc herniation. minim invasive neurosurg 2011;54(4):167-171. 19. larson sj, holst ra, hemmy dc, sances a jr. lateral extracavitary approach to traumatic lesions of the thoracic and lumbar spine. j neurosurg 1976; 45:628637. 429 thoracal discectomy through transfacet approach 20. le roux pd, haglund mm, harris ab. thoracic disc disease: experience with the transpedicular approach in twenty consecutive patients. neurosurg 1993;33:58–66. 21. lesoin f, rousseaux m, autricque a, reesaul y, villette l, clarisse j, et al. thoracic disc herniations: evolution in the approach and indications. acta neurochir (wien) 1986;80(1-2):30-34. 22. levi n, gjerris f, dons k. thoracic disc herniation. unilateral transpedicular approach in 35 consecutive patients. j neurosurg sci 1999;43:37-42. 23. little dg, macdonald d. the use of the percentage change in oswestry disability index score as an outcome measure in lumbar surgery. spine (phila pa 1976) 1994; 19:2139-2143. 24. mack m, regan j, bobechko w, acuff e. application of thoracoscopy for diseases of the spine. ann thorac surg 1993;56(3):736-738. 25. mccormick p. retropleural approach to the thoracic and thoracolumbar spine. neurosurgery 1995;37(5):908-914. 26. mccormick we, will sf, benzel ec. surgery for thoracic disc disease. complication avoidance: overview and management. neurosurg focus 2000; 9:e13. 27. mixter w, barr j. rupture of the intervertebral disc with involvement of the spinal canal. n engl j med 1934;211(5):210-215. 28. moran c, ali z, mcevoy l, bolger c. mini-open retropleural transthoracic approach for the treatment of giant thoracic disc herniation. spine (phila pa 1976) 2012;37(17): e1079–e1084. 29. oda i, abumi k, cunningham bw, kaneda k, mcafee pc. an in vitro human cadaveric study investigating the biomechanical properties of the thoracic spine. spine (phila pa 1976) 2002;27:e64-e70. 30. oltulu i, cil h, berven s, chou d, clark a, ulu mo, ames c, deviren v. surgical management of thoracic disc herniation: anterior vs posterior approach. turk neurosurg 2019;29(4):584-593. 31. patterson r, arbit e. a surgical approach through the pedicle to protruded thoracic discs. j neurosurg 1978;48(5):768-772. 32. quraishi na, khurana a, tsegaye mm, boszczyk bm, mehdian sm. calcified giant thoracic disc herniations: considerations and treatment strategies. eur spine j 2014;23 (suppl 1):s76-83. 33. rosenthal d, rosenthal r, de simone a. removal of a protruded thoracic disc using microsurgical endoscopy. a new technique. spine 1994;19:1087–1091. 34. sivakumaran r, uschold td, brown mt, patel nr. transfacet and transpedicular posterior approaches to thoracic disc herniations: consecutive case series of 24 patients. world neurosurg 2018;120:e921-e931. 35. stillerman c, chen t, day j, couldwell w, weiss m. the transfacet pedicle-sparing approach for thoracic disc removal: cadaveric morphometric analysis and preliminary clinical experience. j neurosurg 1995;83(6):971-976. 36. tovi d, strang r. thoracic intervertebral disk protrusions. acta chir scan suppl 1960;267:1-41. 37. wakefield ae, steinmetz mp, benzel ec. biomechanics of thoracic discectomy. neurosurg focus 2001;11:e6. 38. yüce i̇, kahyaoğlu o, çavuşoğlu ha, çavuşoğlu h, aydın y. midterm outcome of thoracic disc herniations that were treated by microdiscectomy with bilateral decompression via unilateral approach. j clin neurosci 2018;58:94-99. doi: 10.33962/roneuro-2022-046 personal experience in intramedullary lesions, in adults g. iacob romanian neurosurgery (2022) xxxvi (3): pp. 264-273 doi: 10.33962/roneuro-2022-046 www.journals.lapub.co.uk/index.php/roneurosurgery personal experience in intramedullary lesions, in adults g. iacob professor of neurosurgery, “carol davila” university school of medicine, bucharest, romania abstract background: intramedullary spinal cord lesions (imscl) although they are rare, it generates invasion and destruction of the spinal cord. such lesions must be diagnosed as early as possible, some have histological and genetic aggressiveness, generating severe functional neurological damage. objective: to identify the optimal strategy for diagnosis and treatment in imsc, to improve prognosis. methods: a retrospective clinical study from 2001 to 2021, was performed on 33 adult patients (18 women, 15 men), diagnosed with magnetic resonance imaging with imsct. the most common topography was: thoracic 27 cases disposed between t2t12, cervical 6 cases disposed between c2-c6, lumbar 2 cases at l1-l2. the most frequent symptoms in my cases were: unilateral radicular pain related to the tumour topography or bilateral diffuse burning pain, especially during the night; back and neck stiffness; paresthesia, motor disturbances with an asia score of 2-4, and severe atrophy especially in cervical topography, ataxia, initial retention, impotence and later loss of bowel and bladder function with incontinence. all patients were operated by the same senior neurosurgeon with at least 6 months of follow-up postoperatively. for functional outcome, the most important predictors are the preoperative neurological grade, and the high-grade imsct generating recurrence and reoperations. results: the patients addressed the clinic for pain and neurological deficits; the topography of the intramedullary lesion was confirmed by mri native / with contrast, ultrasonography, and spinal arteriography. several histologic entities were recorded: ependymomas 12 cases, astrocytomas 8 cases, hemangioblastomas 3 cases, cavernomas 6 cases, metastases 2 cases, germ cell tumour 1 case, malignant peripheral nerve sheath tumour 1 case. gross total excision was performed in 25 cases, with no mortality. in eight cases recurrences were recorded requiring the resumption of surgical treatment. in all cases physiotherapy-rehabilitation approach was used, and the outcome was correlated with pre-operatory motor deficits severity, 3 patients with thoracic high-grade astrocytoma underwent stereotactic spine radiosurgery (ssr) with cyberknife abroad, stopping tumour growth one year after. conclusions: intramedullary spinal cord lesions (imscl) are rare conditions, and mri development allows an early diagnosis of these tumours. to adequately counselled patients, with minor preoperative deficits, real expectations concerning the functional outcomes, in benign tumours, and even anatomical healing should be based still on refinements of radical surgical excision. actual radiotherapy techniques should be used in aggressive tumours. keywords intramedullary spinal cord lesions (imscl), radical excision, neurofibromatosis (nf), radiotherapy, stereotactic spine radiosurgery (ssr), chemotherapy, functional outcome corresponding author: g. iacob “carol davila” university school of medicine, bucharest, romania gbrl_cb@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 265 personal experience in intramedullary lesions, in adults introduction intramedullary spinal cord lesions (imscl) are rare neoplasms, with various etiology (1-15). spinal cord compression with mass effect in benign lesions or destruction and invasion of the gray and white matter in aggressive tumors may lead to a variable degree of neurological dysfunction, different symptomatology (2)(3). spinal mri is essential for early diagnosis due to its sensitivity, is the preferred modality to characterize imscl for preoperative planning and early detection of recurrent lesions, even if it does not allow for histological diagnosis (1)(2). the management of imscl is mainly surgical (3-10), despite surgical morbidity; provides the best outcome; adjuvant radiotherapy may be an available alternative in aggressive tumors subtotal excised with ill-defined margins; the role of chemotherapy is still questionable. i present my strategy, during 20 years, for diagnosis and treatment in imscl, to improve prognosis. materials and methods a retrospective clinical study from 2001 to 2021, was performed on 33 adults patients (18 woman, 15 men), diagnosed on magnetic resonance imaging with imscl. the most common topography was: thoracic 27 cases disposed between t2-t12, cervical 6 cases disposed between c2-c6, lumbar 2 cases at l1-l2. most frequent symptoms in my cases were: unilateral radicular pain related to the tumor topography or bilateral diffuse burning pain, especially during night; back and neck stiffness; paresthesia, motor disturbances with asia score of 2-4, severe atrophy especially in cervical topography, ataxia, initial retention, impotence and later loss of bowel and bladder function with incontinence. all patients where operated by the same senior neurosurgeon with at least 6 months follow up postoperatively. for functional outcome the most important predictor are the preoperative neurological grade, and the high grade imsct generating recurrence and reoperations. results the patients addressed the clinic for pain and neurological deficits; the topography of the intramedullary lesion being confirmed by mri native with contrast, ultrasonography, spinal arteriography. several histologic entities were recorded: ependymomas 12 cases, astrocytomas 8 cases, hemangioblastomas 3 cases, cavernomas 6 cases, metastases 2 cases, germ cell tumor 1 case, malignant peripheral nerve sheath tumor 1 case. gross total excision was performed in 25 cases, with no mortality. in eight cases recurrence were recorded requiring the resumption of surgical treatment. in all cases physiotherapy-rehabilitation approach was used, outcome was correlated with pre-operatory motor deficits severity, 3 patients with high-grade thoracic astrocytoma underwent stereotactic spine radiosurgery (ssr) with cyberknife abroad, stopping tumor growth one year after. discussion intramedullary spinal cord lesions (imscl) are rare tumors, located within the spinal cord, occur in both adult and pediatric population, predominantly in the middle decades of life (1-3). their incidence is evaluated at: 4 cases per million inhabitants and per year (9), 2-6 % of all central nervous system tumors, found most frequently in the thoracic cord (1-3). most important historical data in intramedullary lesions (2)(3): -first successful removal of an intramedullary tumor was realized by elsberg in 1907 -greenwald in 1963 has large series of successfully removed tumors published -kurze in 1964 has introduced operating microscope imscl can be linked to genetic diseases (1-9) more common in patients with neurofibromatosis: ependymomas occur more often in patients with an average of 40 years with nf2, hemangioblastomas (associated with von hippel lindau syndrome); astrocytomas occur more often in young adults with an average age of 30 years with nf1 most common imscl (1-15) are: glial neoplasms 90-95% spinal ependymoma: 60% of all glial spinal cord tumors, are found in adults in the third to sixth decades prevalence for the fourth-decade, with a slight male predominance, arise from the cells of the ependymal canal, are soft and encapsulated, grow slowly, their plane of cleavage from the surrounding medullary tissue is clear, are located centrally within the spinal cord leading to symmetric expansion, occupy the whole width of the cord. histologically, ependymomas can be classified into 4 266 g. iacob types: myxopapillary ependymoma (who grade i), subependymoma (who grade i), ependymoma (who grade ii), and anaplastic ependymoma (who grade iii). myxopapillary ependymomas account for up to 50% of ependymoma cases, typically arise from the filum terminale, and are usually located in the cauda equina while the other 3 subtypes follow the normal distribution of imscts and are most often found in the cervical or thoracic spinal cord (90%) extending on average in length across 3 to 5 medullary segments, but also lower cord, in the conus medullaris, and filum, where an exophytic component may be present, rarely metastasize. lesions are characteristically hypo vascular, well circumscribed, and non-infiltrative of the surrounding cord. intramedullary ependymomas are generally low-grade, symptoms are due to compression of the surrounding cord rather than infiltration, complete resection often results in prolonged survival; malignant variants having been reported only very exceptionally, also with intratumoral hemorrhage. in my series i have had 12 ependymomas, 4 cervical and 8 thoracic, from which in only 3 cases i identify aggressive malignant ependymomas, who should be reopererated. in one case of thoracic malignant imsct ependymoma the patient developed a secondary active hydrocephalus and shunt was placed spinal astrocytoma: 33% of all glial spinal cord tumors, are common in the third to fifth decades, are infiltrative, glossy, associated with microcysts or syrinxes. the pilocytic varieties are well differentiated and tend to be indolent, with a definable surgical plane. spinal astrocytoma predominate at the cervical-thoracic level (80%) extending on average over 6 medullary segments, positioned more eccentrically, with a poorly defined surgical resection plane. different histologic aspect could be seen: low-grade astrocytomas papillary type, can degenerate into a malignant subtype and high-grade astrocytomas more polymorphic, aggressive with nuclear abnormalities, areas of necrosis, new vessels, intra tumoral hemorrhage. (7%– 30% of astrocytomas are considered malignant). grade iii and iv astrocytomas carried a poor prognosis the most aggressive and infiltrative, with a mean survival of 15.5 months in my series there were 8 cases in the thoracic level, 5 cases relapsed after 2 years, requiring reoperation. spinal primary glioblastoma multiforme: 7.5% of all intramedullary gliomas and only 1.5% of all spinal cord tumors, locally invasive, rapid growth, may seed the csf, with very poorly defined surgical resection plane spinal oligodendroglioma (3%) unproved responses to chemotherapy as in intracranial type spinal ganglioglioma: 1% of all glial spinal cord tumors, they are very rare tumors from both neuronal and glial origins that are composed of glial and ganglion cells, usually located within the cervical level, larger than other types of imscts and difficult to distinguish on mri. they tend to mostly affect older children and young teenagers, are typically benign, slow-growing tumors (who grade i or ii), although malignant transformation has been shown and is presumed to involve the glial component of the tumor. spinal hemangioblastoma: are the third most common imscl, account for 2 to 15%, are rare, benign tumors of mesenchymal origin that originate from the vascular system within the spinal cord, more common in men, tend to develop in the dorsal portion of the spinal cord and thus present with progressive sensory deficits, particularly proprioceptive deficits; highly vascularized, with risk of hemorrhage: subarachnoid hemorrhage (73%) or intramedullary hemorrhage (27%). tumor consist of small mural nodules with cysts, associated with syringomyelia (occurs in approximately 50% of all intramedullary tumors, but is most frequently associated with hemangioblastomas) rarely extend beyond one or two vertebral bodies. some tumors have a tendency to occur in multiple areas, and imaging the entire neuroaxis may be indicated. removal of the lesion is considered curative. approximately 10%–30% of patients diagnosed with spinal cord hemangioblastoma is strongly associated with von hippel-lindau disease: multiple spinal tumors with abnormalities such as renal cell carcinoma, pheochromocytoma, pancreatic cysts; gene mutation results in the enhanced transcription of several genes, including vascular endothelial growth factor (vegf). i have had 3 hemangioblastomas in thoracic area. spinal cavernomas, are unusual: solitary or multiple vascular malformation with abnormally dilated blood vessels, surrounded by gliotic tissue, often stained with hemosiderin, expression of previous hemorrhage. account to woman in two thirds of cases, during the fourth decade of life, could 267 personal experience in intramedullary lesions, in adults be concomitant discovered both in the brain and spinal cord, also skin, retina, associated with café au lait skin lesions. i have had only spinal cavernoma, disposed 2 cervical and 4 in thoracic areas. developmental tumors (3%) are slow-growing neoplasms with a thoraco-lumbar predominance: teratoma, germ cell tumors of the cns are made up of cells similar to the germinal cells that develop in the gonads. there are 2 types of germ cell tumors: nongerminomatous and germinoma. patients with primary intramedullary germinomas typically present with sensory and motor deficits of the lower extremities that can progress to include gait disturbance and urological dysfunction. intramedullary spinal cord lymphoma is a rare form of primary lymphoma and can occur anywhere in the cns. it can originate in the spinal cord, accompany tumors in other locations throughout the cns, or occur as a part of systemic lymphoma. it is usually an aggressive nonhodgkin lymphoma of bcell origin. spinal paraganglioma intramedullary metastasis from a primary malignancy found in the lung (49%), breast (15%), and lymphoma (9%), are rare, they affect 0.4% of all patients with cancer and represent 1%–3% of intramedullary tumors, only two cases in my series from lung cancer spinal primitive neuroectodermal tumor solitary fibrous tumor intramedullary schwannoma, neurofibroma, malignant peripheral nerve sheath tumor 1 case in my series primary intramedullary melanoma are very rare, account for about 1% of all melanomas, develop with progression of symptoms more rapidly. lipoma (2%) may be associated with cutaneous abnormalities, difficult to perform complete excision due to fibrous adhesions to the spinal cord spinal cysts in 70% of intramedullary tumors: lesional (intratumoral) cysts, contained within the tumor itself, may result from necrosis, fluid secretion, or degeneration of the neoplasm; with peripheral enhancement; need to be resected along with the solid portion of the tumor because there is a high likelihood of neoplastic cells within the cyst wall. such cysts were described in: ganglioglioma 46%, spinal ependymoma 22%, spinal astrocytoma 21%, spinal hemangioblastoma 2-4% non-tumoral (reactive) cysts occur rostral or caudal to the solid portion of the tumor, due to dilatation of the central canal, do not enhance, present in 60% of all intramedullary spinal tumors, may resolve once the neoplasm is resected. clinical signs in imsct lesions (2-16) depends on lesion size and topography, evolve in general slowly; diagnosis is often made late on average after 4 years of evolution. symptoms are in general not specific to spinal cord lesions, may be present in any myelopathic process; vulnerable vascular areas for vascular insult are cervical, t1-t4 and l1 areas. more rapid evolution it is found in intramedullary metastasis (12-14), which are diagnosed within one month of symptom, onset in up to 75% of cases. -pain more than 50% of cases, may be local or radiating; often is the earliest symptom, characteristically occurring at night when the patient is supine. pain could be: spinal type occurring at rest, increasing with exercise, typically dull, deep, tenacious, with stiffness, radicular type cervical, brachial, thoracic, sciatic and posterior cord pains with numbness, paresthesia, sensation of burning, stricture. -cervical stiffness, weakness of an upper limb in particular clumsiness of one hand progressive weakness may occur in the arms or legs. intramedullary thoracic tumors associate pain, motor deficit of the lower limbs with variable limitation of walking, spasticity, abolition of osteotendinous reflexes, paresthesia and localized suspended hypoesthesia, accompanied by sublesional signs brown-sequard syndrome -limping, instability, weakness in walking, poor or loss of balance -sphincter disorders (dysuria, constipation, genital problems even impotence) – see conus medullary involvement. in cavernomas there are 4 clinical patterns (10): -acute headache due to subarachnoid hemorrhage, also complete paralysis due to hemorrhage extension into the spinal cord -mild neurological symptoms with acute onset of gradual decline during weeks to months, events related to small hemorrhage or thrombosis within the lesion, with changes in the microcirculation surrounding the lesions -chronic mild neurological deterioration from months to years with acute episodes lasting for 268 g. iacob hours to days with possible neurological recovery between episodes during weeks to months -gradual slow neurological deterioration over months to years, caused by small hemorrhages, changes in the blood flow surrounding the lesion or to changes in the size of the malformation. imscl diagnosis is difficult, with discreet not specific neurological signs; it is sustained on mri (19)(16-18): -t1 weighted images sequences: spinal cord is increased in volume on one or more levels; hypoor isointense signal for both ependymomas and astrocytomas span multiple vertebral segments, also cavities secondary to trauma, arachnoiditis, anomaly of the cranio-cervical hinge, rostral and caudal cysts, malformative syringomyelia. hypointensity at the tumor margin (17) was found to be a relatively firm pseudocapsule and hypointensity within the tumor corresponded to intratumoral hematoma. when mr imaging shows an intramedullary tumor with hypointensity at the tumor margin, it is suggestive, but not pathognomonic, of an ependymoma (17) -t2 weighted images sequences: hyper signal of the fleshy portion of the tumor both ependymomas and astrocytomas, by the cysts; hyposignals linked sometimes to chronic bleeding (deposits of hemosiderin, etc) -after gadolinium intravenous injection mri exams highlights, a contrast enhancement in the majority of cases, in contrast to intracranial neoplasms, even low-grade intramedullary tumors enhance to some degree; however, the absence of enhancement does not exclude an intramedullary neoplasm in the presence of cord expansion ependymomas often are located centrally within the spinal cord leading to symmetric expansion, occupy the whole width of the cord, and enhance diffusely with a well-defined border. astrocytomas tend to be positioned more eccentrically, can be non-enhancing or have an enhancing nodule or large satellite cysts, usually do not have a well-defined border. intratumoral hemorrhage can be seen in both types but are more common in ependymomas (17). hemangioblastomas have homogeneous contrast enhancement compared to the more heterogeneous pattern found in astrocytomas or ependymomas. they also have mural nodules, are associated with syringomyelia, and can have significant surrounding edema, also several topographies. in cavernomas: mri is the current study of choice both for diagnosis and for surgical planning, with high sensitivity blood oxygenation level. the typical manifestation is that of a webbed core, composed of blood and blood products in various states of evolution “popcorn appearance”, of mixed spinal intensity on both t1 and t2-weighted images, with a moderate occasionally strong absorption of contrast medium after gadolinium. for previous hemorrhage a proof is a black ring of low signal intensity around the cavernoma consistent with hemosiderin deposits both in t1 and t2 indicating disturbances of susceptibility caused by the iron in hemosiderin. if edema is present, the signal outside the hemosiderin rim is increased on the t2-weighted images. small cavernous malformations may appear only as petechial areas of decreased signal density ”black dots”. depending the age of a hemorrhage blood products are isointense to slighty hypointense on t1 weighted images and hypointense on t2-weighted images – susceptibility effect. few days later in the subacute hemorrhage stade, the lesion that contains methemoglobine are hyperintense on t1-weighted images and hypointense on t2-weighted images. after several weeks on the hemosiderin chronic stade old blood products are hypointense on both t1 and t2 weighted images. in cavernomas edema is usually absent in smaller cavernous malformations, different from hemorrhagic neoplasms, even when small, with characteristic surrounding edema. in germinomas: mri typically shows an expanding mass often at the lower thoracic level, contrast enhancement with t1 and t2 weighted mri can vary and focal spinal cord atrophy may be an important sign (one case in my series). these may have a dense capsule, precluding complete removal; although, this may be compatible with prolonged symptom-free survival. when complete removal is unobtainable, debris produced by the tumor may cause an early recurrence of symptoms in lymphomas: t1 weighted mri shows homogeneous contrast enhancement in an enlarged area of the spinal cord, while diffusion-weighted and t2 weighted mri demonstrate hyperintensity melanomas typically display hyperintensity on t1 weighted images due to the presence of melanin, while t2 weighted images are generally hypoor isointense. spinal arteriography is useful in hemangioblastoma (8), to characterize feeding 269 personal experience in intramedullary lesions, in adults vessels and associated dilated pial veins, for preoperative embolization. the study of somatosensory evoked potentials (p.e.s.) and motor evoked potentials (p.e.m.) makes it possible to quantify the neurological impairment, to specify its topography at the medullary level and to monitor postoperative progress. intraoperatively, it is possible to record the p.e.s. but this exploration is complicated and ultimately not very useful because it does not modify the surgical technique (19). surgery is the treatment of choice, it should be performed as soon as possible, observation can lead to further neurologic deficits, some of which are irreversible; outcome it correlate with the preoperative neurologic conditions (2-15) (20-21). in the perioperative period or in a rapid decline in neurologic function occurs, steroids are used. the goals of surgical treatment are: 1. to maximize tumor resection – good predictor of outcome, looking for a clear dissection plane, with preservation of neurologic function, in one stage operation, to avoid adhesions, using operating microscope, micro neurosurgical instrumentation, cusa, electrophysiological monitoring to reduce the incidence of iatrogenic damage: intraoperative somatosensory, motor evoked potentials 2. to obtain a tissue diagnosis, after analysis of the surgical sample 3. to improve neurologic functions minimizing further neurologic deficits, avoiding pain 4. in case of clinical and/or radiological progression, especially in benign lesions 5. adjuvant therapy for those cases where the lesion cannot be completely excised 6. to be suited by physiotherapy-rehabilitation approach to provide better outcomes (21)(22) surgical technique (2-6). after general anesthesia induction, opioids, propofol and low levels of muscle relaxants are used to minimize spontaneous muscle activity, to enable emg, motor evoked potentials. halogenated volatile anesthetics are avoided because these interfere with sensory evoked potentials (ssep). an arterial line is needed to ensure that dips in blood pressure are detected and corrected as quickly as possible because the spinal cord is sensitive to decreased perfusion. the patient is positioned prone on bolsters or a wilson frame, freeing the abdomen and thorax from pressure and taking care to pad all pressure points. for cervical and high thoracic lesions, the head is immobilized using a mayfield head holder or equivalent. the level is confirmed by with carm, o-arm, navigation. a standard dorsal midline approach is used, subperiosteal dissection of the paraspinal musculature expose the lamina and spinous processes a wide laminectomy or laminoplasty next to the fleshy portion of the tumour is performed. meticulous hemostasis is obtained. a closed dura mater ultrasound is performed to confirm the correct exposure of the tumor, the satellite cysts being empty of echo. the dura is wide, bloodless exposed for 2 cm rostral and caudal to the upper and lower lesion margins. the dura is sharply incised on the midline, reflected to expose the lesion, the dural edges, without tension, are tacked to the soft tissues laterally using no. 4-0 silk sutures exposing the arachnoid overlying the swollen spinal cord. the tumor is localized visually with intraoperative ultrasound. under operating microscope, the arachnoid is opened and tacked laterally to the dural edges, a midline longitudinal myelotomy between the dorsal columns, at the thinnest area between the tumor and spinal cord are performed, exposing the entire posterior face of the tumour, cysts adjacent to the tumor poles are open, the fine vascular network on the posterior face of the tumour is preserved also the white matter tracts; for eccentric lesions, incision through the dorsal root entry zone can be performed. the pia is sharply incised, the dorsal columns are dissected apart, traversing blood vessels are cauterized and divided, the tumor is encountered. the spinal cord parenchyma is dissected circumferentially off of the tumor capsule, looking for a clear plane between cord and tumor, sectioning and cauterizing thin vessels. the initial area of approach could be changed if the tumor has an exophytic component. a tumor specimen should be sent for frozen section early on in the dissection. intramedullary benign lesions (10) should optimally be removed en bloc, releasing the lesion poles and the anterior part of the lesion, disconnecting from its major blood supply off of the anterior spinal artery. if lesion are located more ventrally the margins of the myelotomy may be retracted with pial sutures. for very large lesions, for lesions with poor internal integrity and lesions with 270 g. iacob an unclear surgical plane: a micro dissector, cavitron ultrasonic surgical aspirator (cusa) is often useful either to debulk internally to facilitate capsule dissection or to perform an inside-out resection, facilitating complete removal (20) intraoperative electrophysiology, such as somatosensory-evoked potentials and motorevoked potentials may lead to improved outcomes, had a high sensitivity and specificity to prevent neurologic damage, but limited the extent of tumor resection (19) . dura is closed primary using a running stitch, or in case of subtotal resection dural grafting and sealants may be necessary to aid closure water-tight. hemostasis should be careful performed, then the musculo-aponeurotic and cutaneous planes are closed, without drainage. the outcomes of surgery (3)(4)(9)(10)(21-22) are related to: -early intervention -younger age (advancing age > 60 y is a negative prognostic factor) -the extent of preoperative neurologic deficit: mildto-moderate deficits often improve significantly following surgical removal, while those with advanced neurologic compromise generally have no worthwhile improvement -lesion topography: patients with cervical tumors should be considered for continued mechanical ventilation in the immediate postoperative period with corticosteroid usage, upper thoracic and conus lesions induce higher morbidity, tumors spanning several levels requires extensive dissection of the spinal cord in order to expose the tumor. -extent of resection mri the day after surgery gives the best estimate of completeness of resection, quality of surgery -tumor histology: -for grade ii who ependymomas gross total resection is reported in more than 90% of cases, with a distinct tumor and normal spinal cord interface. the rate of recurrence is dependent on the extent of tumor resection, avoiding scarring and cord atrophy -for low-grade astrocytoma, if a plane can be developed between the non-encapsulated tumors tumor and spinal cord, gross total resection is an option -for low-grade astrocytoma with no definable plane of resection, high-grade astrocytoma, biopsy plus limited resection or subtotal resection can be attempted, despite recurrence in 47.6% of patients (4). postoperative radiotherapy can be used for highgrade astrocytomas, but with longer-term consequences several adverse effects, including radiation myelopathy, radiation necrosis, vasculopathy, changes to the normal spine parenchyma and a 25% risk of secondary tumors in 30 years (6). for high-grade lesions, such as anaplastic astrocytoma and glioblastoma (15), the prognosis is clearly poor, aggressive surgical resection having a debatable role in prolonging survival. in hemangioblastomas preoperative embolization can attenuate their rich vascular supply, such tumors exhibit a clear dissection plane, a complete resection is expected in 83% to 92% of patients with clinical improvements, especially for those disposed in the posterior half of the spinal cord. the presence of a syrinx suggests a noninfiltrative lesion and carries a better prognosis. patients with von hippel lindau disease (8) are at risk of developing new lesions and must have their entire neuroaxis imaged periodically. in spinal gangliogliomas, resection is the primary treatment of choice, achieved at a much higher rate (83.3%) even in cervical spinal cord; spinal gangliogliomas have a higher relative risk of recurrence than both cerebral and brainstem topography and have a 10-year survival rate of 83%. in aggressive intramedullary tumors removal of tumor has not been shown to be of value, with survival of less than 2 years see anaplastic astrocytoma, a radical surgical removal can lead to severe neurologic impairment recent studies, however, have shown that surgical intervention for the management of high-grade astrocytoma is associated with higher rates of long-term neurological complications with no derived benefit for patients (4). when a plane of dissection is absent (15), resection is often associated with poor outcomes (despite advances in microsurgical techniques, electrophysiological monitoring during the procedure). fluorescence-guided resection of malignant cerebral gliomas utilizing 5-aminolevulinic acid (5-ala) and protoporphyrin ix (ppix) accumulation in tumors has not been determined in spinal intramedullary tumors (4) in intramedullary lipomas limits between lipoma and medullary tissue are imprecise, limiting surgical technique 271 personal experience in intramedullary lesions, in adults for metastases, neuromas, teratomas, germ cell tumor, malignant peripheral nerve sheath tumor the surgical technique remains unchanged, type of excision depending on the infiltrative nature of the lesion. in cavernomas surgical indication should be reserved to those with symptomatic lesion, causing objective neurological deficit, especially to those lesions that extend to the dorsal surface of the spinal cord with an exophytic component, subtotal removal can generate future hemorrhages. for residual tumor growth or recurrence, imaging the entire neuraxis is warranted to detect seeding. therapeutic alternatives are: observation, repeat resection (reoperation is possible even in high grade lesions, but with high functional results), radiation therapy. for astrocytomas and ependymomas with no clear surgical resection planes, initial irradiation (20) improves neurological deficits. closed follow-up: increasing symptoms or new neurological deficits should lead to a search for tumor growth; in general there is a transiently neurological worsening after surgery deep sensitivity disorders, balance, motor deficits; new-onset urinary retention may require prolonged bladder catheterization, either continual or intermittent, also a bowel stimulation regimen. possible postoperatory complications: spinal hematoma, deep vein thrombosis, pulmonary embolism, atelectasis, arachnoiditis, tumor dissemination, bedsores, infectious or chemical meningitis particularly from epidermoid and dermoid tumors, csf fistula and meningocele, wound infection, sepsis, hydrocephalus. physical therapy, occupational therapy, rehabilitation should be instituted early in the postoperative course. radiotherapy in the management of imscl remains controversial (23-25): no lesion should undergo radiotherapy without a tissue diagnosis in spinal myxopapillary ependymomas more recent studies suggest that radiotherapy is not associated with lower overall recurrence regardless of the extent of resection (24) in radiosensitive germinomas 5-year survival rates of 65%–95% with irradiation alone is possible; for multiple spinal cord germinomas chemotherapy with cisplatin and etoposide might provide an alternate option in the treatment of intramedullary germinomas that could avoid the negative side effects associated with radiation treatment radiotherapy may be primary treatment for local control and survival in case of inoperable tumors and aggressive tumors such as: high grade ependymomas, anaplastic astrocytomas and glioblastomas with modestly improvement. modern treatment planning and imaging allow more accurate target definition and respect for related normal tissue tolerances (23) in cases of residual or recurrent tumor viable options are watchful waiting, reoperation, radiation radiotherapy is responsible for acute and delayed myelopathy, increased difficulty with subsequent surgical tumor removal, diminished skeletal growth in young people. stereotactic spine radiosurgery (ssr)(25) is an alternative treatment option to conventional radiotherapy, effective and safe, using externally generated ionizing radiation to inactivate or eradicate defined targets in the spine, to reach local control by delivering large cumulative doses of rt in fewer fractions (less than 5). the most commonly utilized ssr machines include elekta synergy s, novalis (brainlab) and cyberknife; all systems have excellent accuracy, targeting areas remain accurate to within 1mm. prior reports of stereotactic spine radiosurgery for intramedullary metastases, arteriovenous malformations, ependymomas, and hemangioblastomas demonstrated favorable outcomes (25). chemotherapy (2-15) is considered experimental in the treatment of spinal cord tumors; is knowed the inability of large molecules to bypass the blood– spinal cord barrier (bscb); unlike cerebral topography, intramedullary tumors do not respond to chemotherapy, also the rarity of these types of tumors make it very difficult to evaluate therapeutic options and potential at a statistically significant level the topoisomerase-2 inhibitor, etoposide, temozolomide had modest benefit and had a partial response in 2 of 10 treated patients (20%)(6) also with constipation, fatigue, neutropenia, lymphopenia and thrombocytopenia in several patients; 27% progression-free survival at 2 years with a median survival of 23 months antiangiogenic therapy using the vegf receptor-2 inhibitor su5416 in patients with hemangioblastomas 272 g. iacob and von hippel lindau disease (4)(8) shown to be somewhat effective; in contrast, the use of the monoclonal antibody bevacizumab to inhibit the vegf receptor was shown to be ineffective, resulting in increased tumor invasiveness following antiangiogenic therapy, in conclusion some hemangioblastomas might show responsiveness to angiogenesis inhibitors, while others may not, depending on the level of upregulation of the vegf gene bevacizumab may be beneficial for patients with significant tumor burden that is not amenable to resection spinal cord ependymomas in neurofibromatosis type nf2 (2)(3)(9) epidermal growth factor receptor (egfr) inhibitor gefitinib following radiotherapy and other chemotherapeutic agents in intramedullary metastases from lung adenocarcinoma with mixed results of efficacy: 2 weeks improvements, even complete response; such response warrants continued investigation (13) high-dose methotrexate-based therapy combined with alkylating agents such as temozolomide has been shown to be effective in elderly patients suffering from primary cns intramedullary lymphomas in spinal melanomas intrathecal injections of interferon-b, chemotherapy with dacarbazine following the resection of a primary spinal melanoma while resection is the primary treatment option for intramedullary melanoma, gross total resection is difficult and most patients will require (20) postoperative radiotherapy (a combination of wholebrain and local radiation therapy), intrathecal injections of interferon-b and chemotherapy with dacarbazine following the resection of a primary spinal melanoma and demonstrated the control of progression and prolonged survival. therapeutic perspectives (22)(25) in intramedullary tumors are: -development of neuroprotective agents to be use during surgery -the development of drug delivery systems that allow the precise localization of chemotherapeutic drugs conclusions intramedullary spinal cord lesions (imscl) are rare condition. mri even if it does not allow for histological diagnosis, still is the preferred method of diagnosis due to its sensitivity de detect lesion for preoperative planning: size, location, length, extent of surrounding edema, focal or diffuse spinal cord expansion, the cord lesion interface, associated cysts, also to early detect recurrent lesions. to adequately counseled patients, with minor preoperative deficits, in benign lesion, real anatomical healing should be based on refinements of radical surgical excision. actual radiotherapy techniques should be used in aggressive tumors anaplastic astrocytomas and high-grade ependymomas who are associated with a higher rate of recurrence, where radical excision is not achieved or in inoperable cases. references 1. knipe h. intramedullary spinal tumors, radiopedia 15 mar 2021. 2. kane pj, el-mahdy w, et al. -. spinal intradural tumours: part ii intramedullary. br j neurosurg 1999; 13, 558-63. 3. kumar r, banerjee s. management and functional outcome of intramedullary spinal cord tumors: a prospective clinical study. asian j neurosurg 2014; 9, 177181. 4. babu r, karikari io, et al. spinal cord astrocytomas: a modern 20-year experience at a single institution. spine (phila pa 1976) 2014, 39, 533–540. 5. tobin m.k., geraghty j.r. et al. intramedullary spinal cord tumors: a review of current and future treatment strategies, neurosurg focus 2015, 39, 2, e14, 1-9. 6. chamberlain m.c., tredway t.l. adult primary intradural spinal cord tumors: a review. curr neurol neurosci rep 2011, 11, 320–328. 7. khalid s, kelly r, et al. adult intradural intramedullary astrocytomas: a multicenter analysis, j spine surg. 2019, 5(1), 19-30. 8. wang c., zhang j. et al. – surgical management of medullary hemangioblastoma: report of 47 cases, surg. neurol. 2001, 56, 4, 218-226. 9. malhotra n, bhowmick d, et al. intramedullary spinal cord tumours: diagnosis, treatment, and outcomes. adv clin neurosci rehabil 2010, 10, 21-25. 10. iacob g., olarescu a. spinal intramedullary cavernomas. personal experience reffering to six cases romanian neurosurgery 2014, xxi 4: 407 – 415. 11. navarro fernández jo, monroy sosa a, et al. cervical intramedullary schwannoma: case report and review of the literature, case rep neurol. 2018 jan-apr, 10(1), 1824. 12. o'neill ah, phung tbet al. intramedullary spinal cord metastasis from thyroid carcinoma: case report and a systematic pooled analysis of the literature, j clin neurosci. 2018 mar, 49:7-15. 273 personal experience in intramedullary lesions, in adults 13. goyal a, yolcu y, et al. intramedullary spinal cord metastases: an institutional review of survival and outcomes. j neurooncol. 2019 apr, 142(2), 347-354. 14. weng y, zhan r, intramedullary spinal cord metastasis from renal cell carcinoma: a systematic review of the literature, biomed res int. 2018, 2018, 7485020. 15. chanchotisatien a, xiong j, yu j, chu s. exophytic primary intramedullary spinal cord glioblastoma: case report and critical review of literature. world neurosurg. 2019 feb;122:573-576. 16. goy a.m., pinto r.s., et al. intramedullary spinal cord tumors: mr imaging, with emphasis on associated cysts, https://doi.org/10.1148/radiology.161.2.3763905. 17. nemoto y., inoue y., et al. intramedullary spinal cord tumors: significance of associated hemorrhage at mr imaging. https://doi.org/10.1148/radiology.182.3.1535896 18. benjamin cg, frempong-boadu a, et al. combined use of diffusion tractography and advanced intraoperative imaging for resection of cervical intramedullary spinal cord neoplasms: a case series and technical note. oper neurosurg (hagerstown). 2019, 01, 17(5), 525-530. 19. rijs k, klimek m, et al. intraoperative neuromonitoring in patients with intramedullary spinal cord tumor: a systematic review, meta-analysis, and case series, world neurosurg. 2019 may, 125, 498-510.e2. 20. kopelson g., linggood r.m. et al. management of intramedullary spinal cord tumors, https://doi. org/10.1148 /radiology.135.2.7367644 21. sandalcioglu ie, gasser t, et al. functional outcome after surgical treatment of intramedullary spinal cord tumors: experience with 78 patients. spinal cord 2005, 43, 34-41. 22. garcés-ambrossi gl, mcgirt mj. factors associated with progression-free survival and long-term neurological outcome after resection of intramedullary spinal cord tumors: analysis of 101 consecutive cases, j neurosurg spine 2009, 11, 591-599. 23. isaacson s.r. radiation therapy and the management of intramedullary spinal cord tumors, journal of neurooncology 2000, 47, 231–238. 24. feldman wb, clark aj, et al. tumor control after surgery for spinal myxopapillary ependymomas: distinct outcomes in adults versus children: a systematic review. j neurosurg spine 2013,19,471–476. 25. park h-ki., chang j-c. review of stereotactic radiosurgery for intramedullary spinal lesions, korean j spine. 2013, 10, 1, 1–6. microsoft word 19congress 662 | 44th congress of the romanian society of neurosurgery considerations             44th congress of the romanian society of neurosurgery considerations the 44th congress of the romanian society of neurosurgery (rsn) in association with the 5th danube carpathian region congress took place between the 5th and the 8th of september, in timișoara. the location was the regional business centre (craft), an exquisite academic ambience, with all the possible facilities in use. romanian neurosurgery (2018) xxxii 4: 662 665 | 663             the opening of the congress was the 23d french course in neurosurgery, a major contribution of the french speaking neurosurgeons, who manage each time to present in a very exciting and educational way an entire series of elements of neurosurgical pathology, addressing especially the young neurosurgeons. the francophone course focused mainly on cerebral vascular pathology, but there were many exchanges between the french and romanian teams concerning this very difficult and frequent issue. the congress of neurosurgery was structured in parallel sessions in several halls because of the number of various elements of neurosurgical pathology discussed: sellar and parasellar tumors, neurotrauma, functional neurosurgery, trigeminal neuralgia, tumor pathology and degenerative spine pathology, pediatric neurosurgery, intracerebral and skull base neurosurgery. we mention also the 2 sessions regarding epilepsy surgery, endovascular treatment for vascular cerebral malformations at the centres in timișoara and iași, and the outstanding works of the young neurosurgeons at the „young neurosurgeons corner”. during the congress, the 2nd symposium of nurses in neurosurgery also took place. from the works sustained at the congress, at the category „sellar and parasellar tumors” we mention the contribution of f. tomasello (italy), g. rosseau (united states), i. kannan (saudi arabia). at the „craniocerebral trauma” section we mention w. i. steudel (germany) and s. florian (romania), „functional neurosurgery”. at „functional neurosurgery” section we mention p. mertens and m. sindou (france), a. brînzeu (romania). in the „spine surgery” section worth mentioning are c. popescu (romania), g. zapuhlih (moldova) and m. ivanon (great britain). at the „pediatric neurosurgery” section s. ferraresi (italy) and d. nica (romania) stood out with their works; for „cerebral tumors”, h. pleș (romania), i. solaroglu (turkey) and v. sinha (india); for „skull base tumors”, f. tomasello (italy), m. gorgan, a. v. ciurea, d. teleanu (romania). among the activities was also the presentation of the book „principles of neurological surgery”, the 4th edition (edited by ellenbongen rg, sekhar ln, kitchen nd, elsevier 2018), the first romanian edition is coordinated by prof. dr. ioan stefan florian and published at hipocrate publishing house. at the end of the congress the new president of the general assembly rsn was chosen for the next 2 years: conf. dr. horia pleș, timisoara and vice presidents dr. vicențiu săceleanu, sibiu, chief of lectures, prof. dr. mircea gorgan, bucharest, prof. dr. ion poeata, iasi; conf. dr. constantin costea, timișoara, was appointed general secretary of the general association of neurosurgery. all the above mentioned were voted unanimously. 664 | 44th congress of the romanian society of neurosurgery considerations             the president of romanian society of neurosurgery – conf. dr. horia pleș (timișoara) during the general assembly it was also established that prof. dr. grigore zapuhlih, the representative of the association of neurosurgeons in moldavia, be made a member of the romanian society of neurosurgery. the next congress, the 45th congress of the romanian society of neurosurgery will take place at sibiu, in october 2019. the entire event took place in a special academic and cultural environment, in timișoara, romania. 387 participants were registered. there were 37 lecturers from abroad who represented 17 countries on 4 continents. the scientific schedule was comprised of a total of 20 lectures, 3 sessions of the young neurosurgeons, 2 sessions of the nurses, 144 spoken presentations and 17 poster presentations. for these 3 days, the neurosurgical activity in romania was presented exhaustively, receiving unanimous appreciations and showing that, right now, the romanian neurosurgery is perfectly aligned to the european standards. the congress proceedings were in the english language. romanian neurosurgery (2018) xxxii 4: 662 665 | 665             the administrative-organizational part, as well as the social program, including the opera concert on the 6th of september, were in agreement with the congressional requirements, made by the exceptional team “medevents”. finally, we conclude that the romanian society of neurosurgery is in the european trending of real growth of the quality of the surgical act. this is reflected, on one hand, by the multiple efforts to implement the neuroimaging diagnostic apparatus and, on the other hand, by even extraordinary endowment of the neurosurgical operating' rooms at the university centers. andreea-anamaria idu, md, phd student,“carol davila” university of medicine and pharmacy, neurosurgery resident, emergency university hospital of bucharest, romania prof. alexandru-vlad ciurea, md, phd, msc, dr. h. c. mult., sanador medical center, bucharest, romania doi: 10.33962/roneuro -2020-055 contribution of memory evaluation in temporal epilepsy surgery h. lelklou, m. djellaoui, h. si ahmed, b. yakoubi romanian neurosurgery (2020) xxxiv (1): pp. 357-360 doi: 10.33962/roneuro-2020-055 www.journals.lapub.co.uk/index.php/roneurosurgery contribution of memory evaluation in temporal epilepsy surgery h. lelklou1, m. djellaoui1, h. si ahmed2, b. yakoubi3 1 neurologist, department of neurology, bab el oude university hospital, algiers, algeria 2 neurologist, department of neurology, tizi ouzou university hospital, algeria 3 neurosurgeon, department of neurology, bab el oude university hospital, algiers, algeria abstract memory assessment is a crucial step in the pre-surgical assessment of temporal epilepsy. indeed, it participates to a certain extent in the process of localization of the epileptogenic zone and also makes it possible to anticipate the possible risks of surgical treatment on the memory. we propose to specify the contribution of memory evaluation in 60 patients’ candidates for temporal epilepsy surgery, in terms of localization of the “epileptogenic zone” and in the appreciation of the risk of postoperative memory decline. i. introduction during the preoperative assessment, the neuropsychological results, particularly in terms of memory evaluation, participate to a certain extent in the process of localizing the epileptogenic zone. they also make it possible to anticipate the possible risks of a surgical treatment on memory and language. we propose to specify the contribution of memory evaluation in 60 patients’ candidates for temporal lobe epilepsy surgery, in terms of localization of the “epileptogenic zone” and in the appreciation of the risk of postoperative memory decline. we present a case of a patient who has one of the most extended survival lengths reported in the literature despite unusual multisite metastases but deteriorated rapidly due to very aggressive cranium metastasis. ii. patients and methods 1. population studied we included in our study 60 patients on the following criteria: • severe, drug-resistant temporal lobe epilepsy (at least 03 major antiepileptics at optimal doses have been tried as monotherapy and in association with an evolutionary decline of at least 02 years); keywords memory, pre-surgical assessment of epilepsy, pharmaco-resistant temporal lobe, epilepsy corresponding author: h. lelklou bab el oude university hospital, algiers, algeria leklou_ hakim@yahoo.fr copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 358 h. lelklou, m. djellaoui, h. si ahmed, b. yakoubi • age less than 50 years; • presence of a temporal lesion on brain mri; • patients whose "epileptogenic zone" is clearly defined at the end of the non-invasive pre-surgical exploration. • patients operated on for epilepsy surgery with a regulated temporal lobectomy with broad hippocampal resection. 2. applied methods • we have studied hemispheric dominance in all of our patients. • we specified the anatomical lesions found on brain mri and we separated the patients into two groups (one group with hippocampal sclerosis and another with a lesion of another nature). • we also specified the lateralization of the "epileptogenic zone" and the extent of the surgical procedure (hippocampus resected or not). • an overall intellectual efficiency (mms) and memory (verbal and visual) assessment was performed on all of our patients. the exploration of verbal memory was carried out by the grober and buschke test. as for visual memory, it was assessed by the dms-48 test. the frequency of memory disorders was evaluated pre-operatively in the whole population and was then evaluated according to the associated lesions and the lateralization of the "epileptogenic zone" • the development of postoperative memory disorders was specified in all patients and was then studied according to the preoperative memory status and the nature of the lesions found on mri). 3. place and period of the study the patients were recruited from the epileptology consultation of the department of neurology of bab el oued university hospital over a period from january 2010 to december 2019. iii. results distribution of patients according to manual dominance: 100% of patients are right-handed. distribution of patients according to the nature of the lesion found on mri: 32 patients had hippocampal sclerosis on brain mri (53%) and 28 patients had a lesion of another nature (neuroepithelial dysembryoplastic tumours, gangliogliomas and finally cavernomas) (47%). distribution of patients according to the lateralization of the epileptogenic zone: the lateralization of the epileptogenic zone was on the left (dominant hemisphere for language) in 27 patients (45%) and on the right (minor hemisphere) in 33 patients (55%). number of patients percentage % presence of memory deficit 39 65 absence of memory deficit 21 35 total 60 100 table 1. frequency of preoperative memory disorders in all operated patients. a memory deficit is found preoperatively in 65% of operated patients. epileptogenic zone on the left (dominant hemisphere) epileptogenic zone on the right (minor hemisphere) number of patients percentage % numb er of patient s percentage % deficit of the visual memory 00 00 33 100 deficit of the verbal memory 27 100 00 00 total 27 100 33 100 table 2. nature of memory deficit according to the lateralization of "the epileptogenic zone". all the patients with an epileptogenic zone lateralized on the left (dominant hemisphere) have a deficit in verbal memory and all patients with an epileptogenic zone on the right (minor hemisphere) have a deficit in visual memory. group with hippocampal sclerosis group with another lesion number of patients percenta ge % number of patients percentage % presence of memory deficit 30 94 09 32 359 contribution of memory evaluation in temporal epilepsy surgery absence of memory deficit 02 06 19 68 total 32 100 28 100 table 3. frequency of preoperative memory disorders according to the nature of the lesion. a memory deficit is found in 93% of patients with hippocampal sclerosis and only in 32% of patients with a lesion of another nature. number of patients percentage % post-operative decline 9 15 no effects 51 85 improvement 00 00 occurrence of global amnesia 00 00 total 60 100 table 4. postoperative memory status in all operated patients. postoperative memory decline is noted in 15% of operated patients. no cases of global amnesia have been noted. group with preoperative deficit groupe without preoperative deficit number of patients percentage % number of patients percenta ge % postoperative decline 00 00 09 43 no effects 39 100 12 57 improvem ent 00 00 00 00 total 39 100 21 100 table 5. postoperative memory status based on the presence or absence of a preoperative memory deficit. no patient had a memory decline in the preoperative memory deficit group; whereas a decline is noted in 43% of the cases in the group without preoperative deficit. group with hippocampal sclerosis group with another lesion number of patients percentage % number of patients percentage % postoperative decline 02 06 07 25 no effects 30 94 21 65 improvement 00 00 00 00 total 32 100 28 100 table 6. postoperative memory status depending on the nature of the lesion found on mri. no patient had memory decline in the hippocampal sclerosis group; while a decline is noted in 25% of cases in another lesion group. iv. discussion the high frequency of memory disorders found in our series confirms the data in the literature. indeed, temporal lobe epilepsy is the greatest provider of memory disorders observed in epileptic patients [1]. patients with hippocampal sclerosis were more likely to have a preoperative memory deficit than patients with other lesions. these results agree with the data in the literature; indeed, the presence of hippocampal sclerosis, whether right or left, appears to be a predictive factor for the presence of memory impairment in a patient with temporal lobe epilepsy [2; 3]. in addition, the severity of the memory deficit appears to be correlated with the degree of neuronal loss of the diseased hippocampus [4]. it has also been shown that when temporal lobe epilepsy is linked to a structural lesion of another nature, disorders of verbal memory are correlated with left hippocampal neuronal loss [5]. in our series, the nature of the memory deficit observed in right-handed patients depended on the side on which the epileptogenic zone was lateralized. indeed, the deficit concerned in all cases the verbal memory when the epileptogenic zone was lateralized on the left (dominant hemisphere) and the visual memory when the epileptogenic zone was lateralized on the right (minor hemisphere). this observation is consistent with the data in the literature which recognizes a lateralizing value for the memory deficit [6]. indeed, temporal lob epilepsies concerning the dominant hemisphere are characterized by a deficit in verbal memory [7; 8; 2; 9] and temporal lobe epilepsies concerning the 360 h. lelklou, m. djellaoui, h. si ahmed, b. yakoubi minor hemisphere (the right for right-handers) can be associated with a deficit of non-verbal memory [10; 11; 12]. the risk of a memory deficit after an anterior temporal lobectomy is much greater when the preoperative memory efficiency is normal [13; 14; 15; 16; 17]; this could be explained by the fact that the absence of a preoperative memory deficit suggests that the hippocampus concerned by the excision is still functional. the data from our study confirm this view; indeed, patients who underwent an intervention comprising a large hippocampal resection with a preoperative memory deficit, did not degrade their memory scores postoperatively. this could be explained by the fact that the preoperative deficit suggests a loss of the function of the hippocampus concerned by the resection. this favourable postoperative outcome in terms of memory is also noted in patients with hippocampal sclerosis with a correct preoperative memory score. this recalls the favourable prognostic value, in terms of memory, of the presence of hippocampal sclerosis (see above). indeed, the presence of unilateral hippocampal sclerosis (especially when it is severe) with a correct memory score, is compatible with a loss of hippocampal function compensated by the contralateral side. finally, no global amnesia was noted due to the absence of signs indicating a dysfunction of the contralateral hippocampus, such as the case of simultaneous impairment of verbal and visual memory. this notion underlines the major interest of memory evaluation in the context of the pre-surgical assessment of temporal lobe epilepsy surgery. iv. conclusion during the preoperative assessment of temporal epilepsies, the results of the memory assessment participate to a certain extent in the process of localization and lateralization of the epileptogenic zone. they also make it possible to anticipate the possible risks of a surgical treatment on the memory. references 1. rouleau i. la neuropsychologie de l'épilepsie: 50 ans de progrès. revue de neuropsychologie 2010; 2: 2703 271. 2. hermann bp, seidenberg m, schoenfeld j, davies k. neuropsychological characteristics of the syndrome of mesial temporal lobe epilepsy. arch neurol 1997 ; 54:369-76. 3. marques cm, caboclo losf, da silva ti et al. cognitive decline in temporal lobe epilepsy due to unilateral hippocampal sclerosis. epilepsy behav 2007; 10: 477–85. 4. sallie b. the impact of epilepsy surgery on cognition and behavior. epilepsy behav 2008; 12: 592–9. 5. sass kj, spencer dd, kim jh et al. verbal memory impairment correlates with hippocampal pyramidal cell density. neurology 1990; 40: 1694-1697. 6. henry tr, roman dd. presurgical epilepsy localization with interictal cerebral dysfunction. epilepsy behav 2011; 20: 194–208. 7. delanney r, rosen a, mattson r, novelly r. memory function in focal epilepsy : a comparaison of non surgical, unilateral temporal lobe epilepsy and frontal lobe samples. cortex 2000; 16:103-117. 8. hermann bp, wyler a, richey e, rea jm. memory function and verbal learning ability in patients with complex partial seizures of temporal lobe origin. epilepsia 1987; 28: 547-554. 9. selwa lm, serent s, giordani b et al. serial cognitive testing in temporal lobe epilepsy: longitudinal changes with medical and surgical therapies. epilepsia 1994; 35: 743-749. 10. alessio a, damasceno bp, camargo ch, kobayashi e, guerreiro ca, cendes f. differences in memory performance and other clinical characteristics in patients with mesial temporal lobe epilepsy with and without hippocampal atrophy. epilepsy behav 2004; 5. 11. helmstaedter c, pohl c, hufnager a, elger c. visual learning in non-resected patients with right lobe epilepsy. cortex1991; 27:547-555. 12. jones-gotman m. presurgical neuropsychological evaluation for localization and lateralization of seizure focus. in: lüders h, ed. epilepsy surgery. new york : rven press, 1991: 469-75. 13. baxendale s, thompson p, harkness w, duncan j. predicting memory decline following epilepsy surgery: a multivariate approach. epilepsia 2006; 47: 1887–94. 14. helmsteadter c, kurthen m, lux et al. chronic epilepsy and cognition : a longitudinal study in temporal lobe epilepsy. ann neurol 2003; 54: 425-432. 15. jones-gotman m, smith ml, risse gl, westerveld m, swanson sj, giovagnoli ar, et al. the contribution of neuropsychology to diagnostic assessment in epilepsy. epilepsy behav 2010; 18:3-12. 16. lee tmc, yip jth, jones-gotman m. memory deficits after resection from left or right anterior temporal lobe in humans: a meta-analytic review. epilepsia 2002; 43: 283–91. 17. rausch r, kraemer s, pietras cj et al. early and late cognitive changes following temporal lobe epilepsy. neurology 2003; 60: 951-959. romanian neurosurgery (2019) xxxiii, 1: 49 -51 doi: 10.33962/roneuro-2019-008 www.journals.lapub.co.uk/index.php/roneurosurgery primary cerebellopontine angle glioblastoma in a child. a rare entity kaviraj kaushik1, sharad pandey1, l.n. gupta1, rahul varshney1 1 department of neuro surgery, p.g.i.m.e.r.d.r ram manohar lohia hospital, new delhi, india abstract cerebellopontine angle extraaxial glioblastoma (gbm) is extremely rare at any age but especially in children. we reported a case of 14-year-old girl, who presented with nausea, vomiting and ataxia. she was evaluated with computed tomography (ct) and magnetic resonance imaging (mri). imaging demonstrated irregular ring enhancing right cp angle mass. the atypical findings of irregular ring enhancement, cp angle location and presentation in childhood, combine to make the prospective diagnosis of gbm a difficult one. this combination of findings has been reported very rarely. introduction most lesions involving the cerebellopontine angle (cpa) are located extra-axially. the common differentials at this location include acoustic schwannomas, meningiomas, epidermoid tumours, metastases, and arachnoid cysts. glioblastomas are usually intraxial and mostly in supratentorial compartments and usually in elderly age groups. gbm rarely present in cerebellopontine angle (cpa). most of cases reported are primary intraaxial gbm arising from cerebellar hemisphere or brainstem, with exophytic extension into cpa. pubmed advanced search only single of primary extraaxial gbm in the cpa has been reported, arising from the region of root entry zone of the eighth cranial nerve1. regardless of the site of origin, tumours in the cpa represent with sign and symptoms resulting from compression of fifth, seventh, and eighth cranial nerves and pons and cerebellar peduncle. because these lesions have different treatment modalities, prognosis, and outcome, so it is important to make differential diagnosis of these lesions. appropriate diagnosis is important for the management of these lesion, as clinical manifestations of these are similar. case report a 14-year-old girl, presented to neurosurgery opd with a several week histories of progressively increasing frontal headaches, projectile vomiting and excessive drowsiness and recent onset left sided weakness. neurological examination revealed gcs-e3v2m6 with left keywords glioblastoma, paediatric, cp angle corresponding author: sharad pandey department of neuro surgery, p.g.i.m.e.r.d.r ram manohar lohia hospital, new delhi, india drsharad23@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 50 kaviraj kaushik, sharad pandey, l.n. gupta, rahul varshney sided hemiparesis and right sided 5, 6, 7th and lower cranial nerve palsies. computed tomography (ct) demonstrated right cp angle mass lesion of size 5x3.5 cm with effacement of fourth ventricle with obstructive hydrocephalous, with irregular ring enhancement. magnetic resonance (mr) imaging demonstrated the lesion to be essentially isointense on t1 and hyperintense on t2 weighted sequence (fig.1), and restricted diffusion on dwi. post contrast t1 weighted images demonstrated irregular peripheral enhancement. there were areas of peripheral blooming on swi in periphery of mass lesion in pons area (suggestive of hemorrhage). patient underwent emergent ventriculoperitoneal shunt to relieve hydrocephalus. but patient condition did not improve and further deteriorated after vp shunt and emergency right retromastoid suboccipital craniectomy with tumour decompression was done. intraoperatively the tumour mass was situated extraxially in cp angle, extending across 7, 8th cranial nerves complex to lower cranial nerves and medially extending to brainstem. morphologically it was grayish pink, highly vascular, soft and cusa amenable. pathologic examination was conclusive for glioblastoma multiforme. patient did not improve neurologically even after tumour decompression and finally expired 2 months after surgery. the diagnosis of gbm could be made after histopathological examination. figure 1. (a) axial noncontrast ct showing an iso to hypodense right cp angle mass lesion with obstructive hydrocephalous. (b) t2 weighted mri image showing lesion heterogeneously hyperintense with a linear hypointensity. (c) axial contrast ct image showing lesion enhancing heterogeneously with cystic component. discussion most of the gliomas including gbm occur in the cerebral hemispheres, and posterior fossa glioma is uncommon, estimating as 1.5% in the cerebellum and 4.1% in the brainstem [2]. however primary gbm arising in the cpa is further rare with a few reported cases [1], [3]-[7] depending on the origin of the tumour primary cpa glioblastoma can be divided into two types. the first type of the cpa glioblastoma is an intraaxial tumour originated from brain stem or cerebellum with an exophytic growth into the cpa [4] –[6], [8]. this type of gbm is rare, and especially cerebellar gbm with the exophytic growth pattern is very rare, and up to date, four cases have been reported in the literature [3], [4], [8]. two cases showed exophytic growth into cpa, and the other two cases were in the crural/quadrigeminal cistern and cisterna magna, respectively. the second type is an extraaxial cpa glioblastoma. there has been one case of primary extraaxial gbm in the cpa, arising from the proximal portion of cranial nerve viii [7]. few possible mechanisms were documented regarding the origin of primary extraaxial gbm in the cpa . one is that the tumour arose from cranial nerve system tissue within proximal cranial nerve itself, and the other is that the tumour originated from heterotopic neuroglial cells in the leptomeninges covering the proximal cranial nerve or brainstem [1], [7]. 51 primary cerebellopontine angle glioblastoma in a child. a rare entity in patients with cerebellopontine gbm the clinical features are similar to those of other aggressive fast growing infratentorial tumors. signs and symptoms include headache, nausea, vomiting, and cerebellar dysfunction including ataxia, imbalance and unsteady gait, ipsilateral cranial nerves [9]-[11]. the radiological features of posterior fossa gbm are nonspecific [10]-[12]. lesions occur laterally in the cerebellopontine angle. the lesions are typically infiltrating with indistinct margins. signal characteristics are heterogenous, often with necrotic and cystic components. a thick and irregular wall is commonly seen. irregular peripheral enhancement occurs following contrast administration. edema is usually present and obstructive hydrocephalus is common. other features as histology and biology of cerebellar gbm are similar to that of cerebral gbm.11 this includes malignant tumour cells, mitoses, hypercellularity, pleomorphism and neoangiogenesis. the presence of necrosis helps differentiate gbm from anaplastic astrocytoma or from well-differentiated astrocytoma [9]. cerebellar gbm has poor prognosis as with any gbm and any paediatric malignant brain tumour. this is attributed to rapid tumour progression, locally aggressive behaviour as well as the common findings of csf pathway spread [12]. early intervention has been advocated to increase the disease-free interval and to prolong survival includes, aggressive surgery as well as aggressive radiation and chemotherapy [9], [12]. despite these measures; however, survival of children with cp angle gbm is very poor. however, the optimal management for the cpa glioblastoma is to be defined because of its rarity. conclusions primary glioblastoma arising in the cpa in paediatric age group although very rare and cannot always be differentiated from other usual benign tumours at this site radiologically, we should keep gbm in the differential diagnosis of an atypical lesion of the cerebellopontine angle, when patient presented with rapid clinical deterioration due to fast progression of the lesion. references 1. arnautovic ki, husain mm, linskey me. cranial nerve root entry zone primary cerebellopontine angle gliomas: a rare and poorly recognized subset of extraparenchymal tumors. j neurooncol. 2000; 49:205–212. [pubmed]. 2. larjavaara s, mäntylä r, salminen t, haapasalo h, raitanen j, jääskeläinen j, et al. incidence of gliomas by anatomic location. neuro oncol. 2007; 9:319–325. [pmc free article] [pubmed]. 3. kasliwal mk, gupta dk, mahapatra ak, sharma mc. multicentric cerebellopontine angle glioblastoma multiforme. pediatr neurosurg. 2008; 44:224–228. [pubmed]. 4. matsuda m, onuma k, satomi k, nakai k, yamamoto t, matsumura a. exophytic cerebellar glioblastoma in the cerebellopontine angle: case report and review of the literature. j neurol surg rep. 2014;75: e67–e72. [pmc free article] [pubmed]. 5. salunke p, sura s, tewari mk, gupta k, khandelwal nk. an exophytic brain stem glioblastoma in an elderly presenting as a cerebellopontine angle syndrome. br j neurosurg. 2012; 26:96–98. [pubmed]. 6. swaroop gr, whittle ir. exophytic pontine glioblastoma mimicking acoustic neuroma. j neurosurg sci. 1997; 41:409–411. [pubmed]. 7. wu b, liu w, zhu h, feng h, liu j. primary glioblastoma of the cerebellopontine angle in adults. j neurosurg. 2011; 114:1288–1293. [pubmed]. 8. yamamoto m, fukushima t, sakamoto s, tsugu h, nagasaka s, hirakawa k, et al. cerebellar gliomas with exophytic growth--three case reports. neurol med chir (tokyo) 1997; 37:411–415. [pubmed]. 9. chin hw, maruyama y, tibbs p. cerebellar glioblastoma in childhood. j neuro-oncol. 1984; 2:79–84. [pubmed]. 10. kuroiwa t, numaguchi y, rothman mi, et al. posterior fossa glioblastoma multiforme mr findings. am j neuroradiol. 1995; 16:583–9. [pubmed]. 11. luccarelli g. glioblastoma multiforme of the cerebellum description of three cases. acta neurochir. 1980; 53:107– 16. [pubmed]. 12. katz ds, poe lb, winfield ja, et al. a rare case of cerebellar glioblastoma multiforme in childhood mr imaging. clin imag. 1995; 19:162–4. [pubmed]. doi: 10.33962/roneuro-2022-061 the impact of coagulation profile derangements and their effect on the outcome of head injury patients. a prospective study surendra saini sury, sushil acharya, ramsevak yogi, mohan lal echara, shashin vyas, deepika gehlot romanian neurosurgery (2022) xxxvi (3): pp. 359-364 doi: 10.33962/roneuro-2022-061 www.journals.lapub.co.uk/index.php/roneurosurgery the impact of coagulation profile derangements and their effect on the outcome of head injury patients. a prospective study surendra saini sury, sushil acharya, ramsevak yogi, mohan lal echara, shashin vyas, deepika gehlot sms medical college and hospital, jaipur, india abstract background: in traumatic brain injury patients, coagulation disorder causes secondary brain injury, thereby increasing mortality and morbidity. aim: this study aims to know the impact of coagulation profile derangements and their effect on the outcome of head injury patients. materials and methods: a total of 100 patients admitted with traumatic brain injury were included in the study. samples of complete haemogram (cbc), prothrombin time (pt), partial thromboplastin time (pttk), d-dimers and fibrinogen were obtained. coagulopathy was defined as platelet counts < 100,000 cells/mm2 and pti >15 seconds or a dic (disseminated intravascular coagulation) score of more than 4. the outcome in each group was measured according to the glasgow outcome score. the data were analysed with the chi-square test and independent t-test. results: in patients with severe and moderate traumatic brain injury, there was no significant difference in the haemoglobin, fibrinogen and d-dimer between the patients with and without coagulopathy. but the platelet count was significantly lower in the patients with coagulopathy and the pt and pttk were significantly higher in the patients with coagulopathy in comparison to the patients without coagulopathy (p<0.05). there was no significant difference in the fibrinogen and d-dimer between the expired and discharged patients. but the platelet count was significantly higher in the discharged patients and the dic score, pt and pttk were significantly lower in the discharged patients (p<0.05). conclusion: coagulation profile derangements are seen in patients with traumatic brain injury. early diagnosis and prompt management can make remarkable improvements in the mortality of these patients. introduction traumatic brain injury (tbi) is one of the most important causes of death and long-term disability in young adults (boto et al. 2006). tbi has also been found to be a significant factor behind the deaths occurred in the very first day after trauma (shackford et al. 1993). the incidence of coagulopathy in different types of tbi ranges from 10 to keywords coagulation, head injury corresponding author: settingssurendra saini sury sms medical college and hospital, jaipur, india royaldrsk@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 360 surendra saini sury, sushil acharya, ramsevak yogi et al. 97.3% (lustenberger et al. 2010, harhangi et al. 2008) and in case of acute brain injury, coagulopathy leads to hemorrhagic lesions (oertel et al. 2002, allard et al. 2009, tian et al. 2010) and increased chances of mortality (talving et al. 2009, wafaisade et al. 2009). although the pathophysiology of tbi induced coagulopathy has not been completely understood, the following factors have been proposed to be responsible for the same: release of tissue factors (goodnight et al. 1974, keimowitz et al. 1973, scherer et al. 1998), disseminated intravascular coagulation (stein et al. 2004, stein et al. 2002, hulka et al. 1996), thrombocytopenia or platelets dysfunction (carrick et al. 2005, schnu¨riger et al. 2010, nekludov et al. 2007, engstrom et al. 2005), activation of protein c pathways (cohen et al. 2007, frith et al. 2010). early recognition of coagulopathy is of value in predicting the occurrence of delayed brain injury and may contribute to prevention of bleeding disorders (stein et al. 1992). most studies, however, report a mixture of early and delayed coagulopathy in isolated tbi, and knowledge about the prognostic value of acute, early diagnosed coagulopathy is therefore limited. a recent evaluation of a large german trauma registry revealed that 23% of patients with isolated tbi are presented with acute coagulopathy upon arrival of the emergency department, which was associated with increased morbidity and mortality (wafaisade et al. 2010). although the prevalence of coagulopathy increases in the period after admission to the emergency department, there are only limited data available about the evolvement of hemostatic parameters and the relative number of patients that develop delayed coagulopathy in the first days post-trauma (carrick et al. 2005, zehtabchi et al. 2008). therefore, the aim of the present study was to know the impact of coagulation profile derangements and their effect on the outcome of head injury patients. materials and methods this prospective observational study was carried out on 100 patients of head injury admitted in the neurosurgery department of sms medical college attached hospital, jaipur, rajasthan from june 2020 to september 2021. ethical approval was obtained from the institutional ethical committee and informed consent was taken from the patient attendants. the inclusion criteria for the patients was that they should be within the age range of 1 to 70 years. the exclusion criteria for the patients were: i) patients having other associated injuries such as chest injury, bony injury, abdominal solid and hollow viscus injury etc., ii) patients having known case of hypertension, diabetes or any other chronic disease, iii) patients having pre-existing coagulopathy, taking anticoagulants or drugs which interfere with the laboratory testing and iv) patient have history of chronic alcohol intake, ongoing liver disease; history of of hepatotoxic drug intake and history of long time anti-inflammatory drug intake. all the selected patients were divided based upon their gcs into two groups based on their gcs. there were two subgroups of patient moderate head injury (gcs 9-13) and severe head injury (gcs < 9). initial resuscitation and subsequent management was done as per advanced trauma life support (atls). samples for complete haemogram (cbc), prothrombin time (pti), partial thromboplastin time (ptk), d-dimers and fibrinogen were drawn. the blood was collected by venepuncture in edta vacutainers as well as pt tubes containing anticoagulant sodium citrate and processed immediately. based on results of these blood investigations, dic score was calculated and severity of the dic was graded. dic score was calculated (table 1). after calculating the dic score severity of the dic was graded (table 2). table 1. dic score platele t count (in lac) pt time (in secs) aptt (in secs) d-dimer (μg/dl) fibri nog en (g/l) score awarded normal >1.5 13.5 2634 <1000 >1 0 mild derangem ent 1-1.5 13.515.0 >34 10002000 <1 1 moderate derangem ent 0.601.0 1518 >39 20004000 <1 2 severe derangem ent <0.60 >18 >54 >4000 <1 3 table 2. severity of dic dic score inference 0-3 normal 3-6 mild derangement 7-10 moderate derangement >10 severe derangement 361 the impact of coagulation profile derangements and their effect on the outcome of head injury patients outcome was defined by the gos (glassgow outcome score) and the comparison of presenting gcs was done with the gos and dic score was done. coagulopathycoagulopathy was defined as platelet counts < 100,000 cells/mm2 and pti >15 seconds or a dic score more than 4. the outcome in each group was measured as discharged (gos5) or vegetative state (gos-2) or dead (gos-1). during follow up of the patients gcs, cranial nerve palsy, haematoma formation (surgically operated), local surgical site infection and fever were noted. statistical analysis the data was tabulated in microsoft excel software and analysed with spss v.24 software statistical analysis was done by using chi square method and independent t-test. the p-value of <0.05 was considered as statistically significant. results a total of 100 patients of isolated head injury were included in the study and were further categorized into moderate and severe head injury on the basis of gcs. the patients with gcs 3-8 were categorized as severe head injury (n=54) and patients with gcs 913 were categorized as moderate head injury (n =46). among severe head injury (gcs 3-8) group, 31 (57.4%) patients out of 54 developed coagulopathy and in moderate head injury group 18 (39.1%) patients out of 46 developed coagulopathy. the demographic parameters, hospital stay and in‑house mortality of the patients with severe and moderate tbi are shown in tables 3 & 4. in both the tables, there was no significant difference in the age and gender between the groups. but, total stay, icu stay and outcome (death) were found to be significantly higher in the patients with coagulopathy (p<0.05). the laboratory parameters of the patients with severe tbi was shown in table 5. there was no significant difference in the haemoglobin, fibrinogen and d-dimer between the patients with and without coagulopathy. but, the platelet count was significantly lower in the patients with coagulopathy and the pt and pttk were significantly higher in the patients with coagulopathy in comparison to the patients without coagulopathy (p<0.05). the laboratory parameters of the patients with moderate tbi was shown in table 6. there was no significant difference in the haemoglobin, fibrinogen and d-dimer between the patients with and without coagulopathy. but, the platelet count was significantly lower in the patients with coagulopathy and the pt and pttk were significantly higher in the patients with coagulopathy in comparison to the patients without coagulopathy (p<0.05). table 7 shows the comparison of total dic scores and the laboratory parameters of expired and discharged patients with severe tbi. out of the 54 patients, 34 expired and 20 were discharged. there was no significant difference in the fibrinogen and ddimer between the expired and discharged patients. but, the platelet count was significantly higher in the discharged patients and the dic score, pt and pttk were significantly lower in the discharged patients (p<0.05). table 8 shows the comparison of total dic scores and the laboratory parameters of expired and discharged patients with moderate tbi. out of the 46 patients, 5 expired and 41 were discharged. there was no significant difference in the fibrinogen and ddimer between the expired and discharged patients. but, the platelet count was significantly higher in the discharged patients and the dic score, pt and pttk were significantly lower in the discharged patients (p<0.05). table 9 shows the comparison of total dic scores and the laboratory parameters of expired and discharged patients with coagulopathy. out of the 49 patients who developed coagulopathy, 35 expired and 14 were discharged. there was no significant difference in the platelet count, pt, pttk, fibrinogen and d-dimer between the expired and discharged patients. but, the dic score was significantly higher in the expired patients (p<0.05). table 10 shows the comparison of total dic scores and the laboratory parameters of expired and discharged patients without coagulopathy. out of the 51 patients who did not develop coagulopathy, 4 expired and 47 were discharged. there was no significant difference in the dic score, pt, pttk, fibrinogen and d-dimer between the expired and discharged patients. but, the platelet count was significantly lower in the expired patients (p<0.05). bivariate analysis was carried out to identify the risk factors associated with the development of coagulopathy (table 11). on bivariate analysis, severity of tbi, effaced basal cisterns on ct scan and low haemoglobin level were found to predict the development of coagulopathy (p<0.05). 362 surendra saini sury, sushil acharya, ramsevak yogi et al. table 3. association of demographic parameters, hospital stay and in‑house mortality of severe tbi in presence or absence of coagulopathy parameters patients with coagulopathy (n=31) patients without coagulopathy (n=23) p value age (years) 30.5±7.1 31.8±8.4 >0.05 male:/female 27:4 18:5 >0.05 total stay (days) 13.4±2.7 6.8±1.5 <0.05* icu stay (days) 8.1±2.3 4.9±1.8 <0.05* outcome (deaths) 20 (64.5%) 11 (47.8%) <0.05* table 4. association of demographic parameters, hospital stay and in‑house mortality of moderate tbi in presence or absence of coagulopathy parameters patients with coagulopathy (n=18) patients without coagulopathy (n=28) p value age (years) 33.5±8.6 29.2±6.4 >0.05 male:female 16:2 25:3 >0.05 total stay (days) 12.7±3.5 7.1±2.9 <0.05* icu stay (days) 6.7±2.1 4.4±1.3 <0.05* outcome (deaths) 8 (44.4%) 3 (10.7%) <0.05* table 5. association of laboratory parameters in severe tbi in presence and absence of coagulopathy parameters patients with coagulopathy (n=31) patients without coagulopathy (n=23) p value hb 10.4±2.1 11.9±2.4 >0.05 platelet 1.45±0.3 2.18±0.7 <0.05* pt 20.2±4.4 14.6±4.1 <0.05* pttk 36.1±7.2 26.5±6.3 <0.05* fibrinogen 0.68±0.2 0.37±0.1 >0.05 d-dimer 2761±884 2519±729 >0.05 table 6. association of laboratory parameters in moderate tbi in presence and absence of coagulopathy parameters patients with coagulopathy (n=18) patients without coagulopathy (n=28) p value hb 11.2±2.7 12.9±3.1 >0.05 platelet 1.52±0.4 2.37±0.8 <0.05* pt 20.8±4.5 14.1±3.8 <0.05* pttk 35.7±7.3 25.9±6.9 <0.05* fibrinogen 0.73±0.2 0.42±0.1 >0.05 d-dimer 2837±895 2489±706 >0.05 table 7. comparison of total dic scores and the laboratory parameters of expired and discharged patients with severe tbi parameters expired (n=34) discharged (n=20) p value dic score 5.9±2.2 3.6±1.4 <0.05* platelet 1.72±0.4 2.61±1.3 <0.05* pt 19.6±3.5 15.2±2.8 <0.05* pttk 34.3±7.1 24.1±6.4 <0.05* fibrinogen 0.75±0.2 0.47±0.1 >0.05 d-dimer 2768±831 2504±634 >0.05 table 8. comparison of total dic scores and the laboratory parameters of expired and discharged patients with moderate tbi parameters expired (n=5) discharged (n=41) p value dic score 7.6±3.1 3.4±1.1 <0.05* platelet 1.03±0.2 1.95±1.2 <0.05* pt 18.7±3.2 14.2±2.4 <0.05* pttk 33.8±6.6 25.2±5.8 <0.05* fibrinogen 0.77±0.3 0.51±0.1 >0.05 d-dimer 3015±912 2461±527 >0.05 table 9. comparison of total dic scores and the laboratory parameters of expired and discharged patients with coagulopathy parameters expired (n=35) discharged (n=14) p value dic score 7.6±2.2 4.1±1.3 <0.05* platelet 1.26±0.2 1.57±0.5 >0.05 pt 35.1±7.2 31.7±4.3 >0.05 pttk 36.7±8.4 34.2±7.1 >0.05 fibrinogen 0.77±0.3 0.65±0.2 >0.05 d-dimer 2806±793 2752±785 >0.05 table 10. comparison of total dic scores and the laboratory parameters of expired and discharged patients without coagulopathy parameters expired (n=4) discharged (n=47) p value dic score 2.9±0.8 2.5±0.6 >0.05 platelet 1.28±0.7 1.84±1.1 <0.05* pt 16.5±3.1 14.7±2.2 >0.05 pttk 28.4±6.1 25.7±5.9 >0.05 fibrinogen 0.61±0.4 0.57±0.2 >0.05 d-dimer 2513±844 2422±785 >0.05 363 the impact of coagulation profile derangements and their effect on the outcome of head injury patients table 11. risk factors for development of coagulopathy following isolated tbi parameters unadjusted odds ratio (95% ci) p value adjusted odds ratio (95% ci) p value gcs ≤ 8 3.8 (1.6‑5.9) <0.05* 2.5 (1.4‑4.8) <0.05* effaced basal cisterns 2.1 (1.2‑4.2) <0.05* 2.5 (1.6‑5.5) <0.05* hb ≤10g/dl 2.4 (1.1‑4.9) <0.05* 2.9 (1.2‑5.3) <0.05* *statistically significant difference exists between the groups discussion traumatic brain injury is associated with activation of the coagulation cascade through fulminant cerebral tissue factor release, contributing to disseminated intravascular coagulation and cerebral microthrombi. this process is independent of bleeding. the subsequent disparity between clot formation and fibrinolysis in combination with coagulopathy may increase the risk for secondary bleeding and mortality. the present study showed a male predominance (86%) in the patients with tbi. this is in accordance with the studies done by talving et al. in 2009 (78% males) and affonseca et al. in 2007 (69.1% males). in the present study, mortality was 39% which was at par with affonseca et al. in 2007 and greuters et al. in 2011. coagulopathy was developed in 49% patients in our study which was in concordance with affonseca et al. in 2007, but more than the mortalities reported in the studies by greuters et al. in 2011 where it was 54% and by harhangi et al. in 2008 where it was 33%. the present study showed that the mean platelet count in the severe head injury group patients was lower than in patients of moderate head injury patients in our study. this finding is supported by the results of the study by engstrom et al. in 2000, were they observed thrombocytopenia to be an independent risk factor for traumatic brain injury. in the present study, the mean pt in the severe head injury group was higher in the expired patients than the discharged patients. saggar et al. in 2009 reported similar findings in their study. in the present study, the mean d-dimers value was higher in the patients with severe than the patients with moderate head injury. similar results were reported in the study by scherer et al. in 1998 and kuo et al. in 2007. they also reported that increased d-dimer values was associated with poor prognosis in head injury patients. 35% of the patients in the present study had moderate dic scores. selladurai et al. in 1997, observed that 38% of their patients had moderate to severe dic scores while saggar et al. in 2009 observed 63% of their patients had moderate to severe dic scores. plasma fibrinogen concentration was found to be significantly higher among the patients who developed coagulopathy. jovan et al. in 1998 in their study also reported similar results. in the present study, severity of head injury (gcs ≤ 8), effaced basal cisterns on ct scan and haemoglobin level less than 10 g/dl strongly predicted the development of coagulopathy. talving et al. in 2009 had also reported gcs ≤ 8 and presence of cerebral edema, sah, sbp < 90 mm hg, midline shift as the factors, which independently predicted development of coagulopathy. similar findings were also reported by affonseca et al. in 2007 in their study on pediatric patients where they found severity of head injury, presence of brain swelling, and injuries to chest and abdomen being associated with the development of coagulopathy conclusions the present study concludes that, traumatic brain injury is complicated by the coagulopathy. the mortality of the patients with moderate or severe tbi can be predicted with the presence of coagulopathy and the severity of head injury. early diagnosis and prompt management can make remarkable improvement in the survival rate of these patients. references 1. affonseca ca, carvalho lf, guerra sd, ferreira ar, goulart em (2007). coagulation disorder in children and adolescents with moderate to severe traumatic brain injury. j pediatr (rio j) 83:274‑82. 2. allard cb, scarpelini s, rhind sg, et al. (2009). abnormal coagulation tests are associated with progression of traumatic intracranial hemorrhage. j trauma.67:959–67. 3. boto gr, go´mez pa, de la cruz j, lobato rd (2006). severe head injury and the risk of early death. j neurol neurosurg psychiatry.77:1054–9. 4. carrick mm, tyroch ah, youens ca, handley t (2005). subsequent development of thrombocytopenia and coagulopathy in moderate and severe head injury: support for serial laboratory examination. j trauma 58:725–9. 364 surendra saini sury, sushil acharya, ramsevak yogi et al. 5. cohen mj, brohi k, ganter mt, manley gt, mackersie rc, pittet j-f (2007). early coagulopathy after traumatic brain injury: the role of hypoperfusion and the protein c pathway. j trauma. 63:1254–61. 6. engstrom m, romner b, schalen w, reinstrup p (2000). thrombocytopenia predicts progressive haemorrhage after head trauma. j neurotrauma. 22:291-96. 7. frith d, brohi k (2010). the acute coagulopathy of trauma shock: clinical relevance. surgeon. 8:159–63. 8. goodnight sh, kenoyer g, rapaport si, patch mj, lee ja, kurze t (1974). defibrination after brain-tissue destruction: a serious complication of head injury. n engl j med. 290(19): 1043–7. 9. greuters s, berg annelies van den, franschman g, viersen va, beishuizen a, peerdeman sm, et al. (2011). acute and delayed mild coagulopathy are related to outcome in patients with isolated traumatic brain injury. critical care. 10. harhangi bs, kompanje ejo, leebeek fwg, maas air (2008). coagulation disorders after traumatic brain injury. acta neurochir. 150:165-75. 11. hulka ff, mullins rjr, frank ehe (1996). blunt brain injury activates the coagulation process. arch surg. 131:923–7. 12. jovan a, milorad b, goran i, zoran m, stojanka, d, jovan t, et al. (1998) blood coagulation and fibrinolysis parameter changes after various types of brain damage. med biol 5:44‑9. 13. keimowitz rm, annis bl (1973). disseminated intravascular coagulation associated with massive brain injury. j neurosurg. 39:178–80. 14. kuo jr, lin kc, lu cl, lin hj, wang cc, chang ch (2007). correlation of a high d-dimer level with poor outcome intraumatic intracranial haemorrhage. eur j neurol. 14:1073-76. 15. lustenberger t, talving p, kobayashi l, et al. (2010) early coagulopathy after isolated severe traumatic brain injury: relationship with hypoperfusion challenged. j trauma. 69:1410–4. 16. nekludov m, bellander b-m, blomba¨ck m, wallen hn. (2007) platelet dysfunction in patients with severe traumatic brain injury. j neurotrauma. 24:1699–706. 17. oertel m, kelly df, mcarthur d, et al. (2002) progressive haemorrhage after head trauma: predictors and consequences of the evolving injury. j neurosurg. 96:109–16. 18. saggar v, mittal rs, vyas mc. (2009) haemostatic abnormalities in patents with closed head injuries and their role in predictingearly mortality. j neurotrauma. 26:1665-68. 19. scherer ru, spangenberg p (1998). procoagulant activity in patients with isolated severe head trauma. crit care med. 26: 149–56. 20. schnu¨riger b, inaba k, abdelsayed ga, et al. (2010) the impact of platelets on the progression of traumatic intracranial hemorrhage. j trauma. 68:881–5. 21. selladurai bm, vickneswaran m, duraisamy s, atan m (1997). coagulopathy in acute head injurya study of its role as a prognostic indicator. br j neurosurg. 11:398404. 22. shackford sr, mackersie rc, holbrook tl, et al. (1993). the epidemiology of traumatic death: a populationbased analysis. arch surg. 128:571–5. 23. stein s, young g, talucci r, greenbaum b, ross s (1992). delayed brain injury after head trauma: significance of coagulopathy. neurosurgery 30:160-165. 24. stein sc, chen xh, sinson gp, smith dh (2002). intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury. j neurosurg. 97:1373–7. 25. stein sc, smith dh (2004). coagulopathy in traumatic brain injury. neurocrit care. 1:479–88. 26. talving p, benfield r, hadjizacharia p, inaba k, chan ls, demetriades d (2009). coagulopathy in severe traumatic brain injury: a prospective study. j trauma. 66:55–61. 27. tian h-l, chen h, wu b-s, et al. (2010). d-dimer as a predictor of progressive hemorrhagic injury in patients with traumatic brain injury: analysis of 194 cases. neurosurg rev. 33:359–65. 28. wafaisade a, lefering r, tjardes t, et al. (2009). acute coagulopathy in isolated blunt traumatic brain injury. neurocrit care. 12:211–9. 29. wafaisade a, lefering r, tjardes t, wutzler s, simanski c, paffrath t, fischer p, bouillon b, maegele m, trauma registry of dgu (2010). acute coagulopathy in isolated blunt traumatic brain injury. neurocrit care 12:211-219. 30. zehtabchi s, soghoian s, liu y, carmody k, shah l, whittaker b, sinert r (2008). the association of coagulopathy and traumatic brain injury in patients with isolated head injury. resuscitation 76:52-56. doi: 10.33962/roneuro -2020-045 predictors of severe head injury in tertiary centre rajendra shrestha romanian neurosurgery (2020) xxxiv (1): pp. 303-307 doi: 10.33962/roneuro-2020-045 www.journals.lapub.co.uk/index.php/roneurosurgery predictors of severe head injury in tertiary centre rajendra shrestha department of neurosurgery, national academy of medical sciences, national trauma centre, bir hospital, kathmandu, nepal abstract introduction: severe head injury (shi) is associated with a high mortality and morbidity rate and is one of the leading causes of death in intensive care units. the aim of this study was to identify predictors of hospital outcome and mortality in icu admitted shi patients and to estimate their impact. methods: a retrospective analysis was carried on patients (n=321) with a severe head injury, defined as glasgow coma scale (gcs) ≤ 8 who were admitted to the icu neurosurgical department of national trauma center from 2017 to 2018. both clinical and radiological predictors of hospitalized patients were identified. results: total mortality rate was 5.9%. 243 (75.7%) of the patients were male and 78 (24.3%) were female. 55 % of cases were due to traffic accidents. patients middle ages group was 60%. coexisting injuries, found in 25% of the patients aggravated the prognosis. blood grouping pattern in shi were b+, a+ and o+ 36.1, 28 and 24.3% respectively.45% of the patients had tattoo which was aggravating factors. the outcome is highly correlated with gcs’ values. ct scan findings revealed that patients with subdural hygroma after few days of admission ct scan which was very important prognostic factors in shi. conclusions: shi has high mortality and morbidity in today world as it has a high negative impact on young people, especially men with blood group b+. the age of the patient, presence of tattoo, gcs at admission, the ct scanning at admission and ct scanning after a week of admission were significant predictors of outcome. introduction head injury (hi) is injuries to the scalp, skull, or brain (traumatic brain injury) produced by trauma, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with diminished or altered state of consciousness. severe traumatic brain injury (tbi) is associated with a high mortality and morbidity rate and is one of the leading causes of death in the intensive care units (3, 16). this is a retrospective study to identify predictors of hospital outcome/ mortality in icu admitted severe tbi patients and to estimate their impact. moreover, this study also intends to find the recent trends of head injury. materials and methods a retrospective analysis was done on patients with severe head injury, keywords glasgow coma scale, ct scan, severe head injury, subdural hygroma, tattoo corresponding author: rajendra shrestha national academy of medical sciences, national trauma centre, bir hospital, kathmandu, nepal rajendra39@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 304 rajendra shrestha defined as glasgow coma scale (gcs) ≤ 8, who were admitted to the icu neurosurgical department of national trauma center from june 2017 to july 2018. ct scan brain plain was done as a part of routine evaluation for all patients when presented in emergency department (er). patient’s inpatient files, er and police records were used to retrieve the data. the consciousness level was assessed by the glasgow coma scale (gcs) and the outcome was assessed by the glasgow outcome score (gos). patient characteristics like age, gender distribution, mode of injury, alcohol influence, gcs on admission, pupil reactivity, presence of extra-cranial associated injuries, laboratory tests and ct scan results were evaluated. outcome assessment for survivors was based on data from the medical records of patients during their hospitalization, and that obtained within a 6 month-period after discharge. unfavorable outcome (death or severe disability) at six months was defined with the gos. the scale comprises five categories: death, vegetative state, severe disability, moderate disability, and good recovery. our results are statistically analyzed and discussed. inclusion criteria: all the severe head injury patients who were admitted in intensive care unit under the neurosurgery care during the study period. exclusion criteria: the severe head-injured patients who had polytrauma with cervical injury. results in this study, there were 321 patients with severe head injury. 243 (75.7%) of the patients were male and 78 (24.3%) were female (figure 1). patients middle ages group was 60% (figure 2). the number of patients with severe head injury admitted to the hospital was 321, out of which 174 (54%) patients had a head injury following road traffic accident (rta), 114 (36%) sustained head injury following fall from height, 20 (6%) secondary to physical assault, and 13 (4%) attributed to other modes of injury (figure 3). most of the cases admitted in icu (96%) were intubated and mechanically ventilated. the radiological findings on head injury patients showed contusion in most cases around 29% (figure 4). nonsurgical (conservative) treatment was provided to 225 (70%) patients while 96 (30%) patients required surgical intervention (figure 5). coexisting injuries, found in 25% of the patients, affected the prognosis. two third of the patients admitted with shi were under the influence of alcohol (figure 6). blood grouping pattern in shi were b+, a+ and o+ 36.1, 28 and 24.3% respectively (figure 7). 45% of the rta patients had tattoo which was aggravating factors. ct scan findings revealed that patients with subdural hygroma after few days of admission ct scan which was very important prognostic factors in tbi. outcome highly correlated with gcs score. figure 1. gender distribution of admitted shi. figure 2. age distribution of admitted shi. figure 3. the distribution of causes of injury in admitted shi (n=321) . 76% 24% male(243) female(78) rta 54%fall injury 36% physical assault 6% others 4% rta fall injury physical assault 305 predictors of severe head injury in tertiary centre figure 4. radiological finding of admitted shi patients. figure 5. management of admitted shi patients. figure 6. numbers of patients under alcohol influences. figure 7. blood grouping pattern in severe head injuries. discussion severe head injury (shi) is the most common global cause of morbidity and mortality in people under 45 years of age and possess major public health and socioeconomic challenges, which can negatively impact the daily life activities and possess high risk of readmission to hospital and subsequent death. despite advancements in diagnosis and treatment, there are many queries regarding the diagnosis, prognosis and best possible treatment of shi. there are no acceptable clinical and pathological predictive factors have been recognized for developing clinical trials and promoting effective therapeutic strategies to improve the prognosis. there were a lot of different prognostic factors related to outcome. the most important prognostic factors included: age, glasgow coma scale, pupil size, coexistence of other injuries, a history of previous head injury, alcohol abuse and lower socioeconomic, educational status, hypotension, hypoxia, glucose, coagulopathy, haemoglobin, marshall ct classification and traumatic subarachnoid haemorrhage (1, 2, 9, and 11). this article focuses mainly on the clinically significant aspects of potential interrelationship between potential diagnostic and prognostics tools in severe brain injury. assessing prognosis after traumatic brain injury was both very important and difficult. in this study, the majority of patients were male 76% and only 24% were female (figure 1). patients of both sexes primarily belong to an age group of 15-50 years in the age-distribution curve of shi (figure 2). this could be credited to this group of people predominantly being more active and vulnerable in the community and country. in the present study, rta was established as the most common cause of shi. it contributed to almost 55% of the head injury cases leading to admission (figure 3). this finding can be attributed to more men being drivers and more prone to be involved in rta (5, 6). noticeably, cases of head injuries due to the physical assault appear to be on the rise, compared to zero percent in the study of gongal and devkota (1979) to 6% in the present series (4). in nepal, the zero-tolerance policy against drinking and driving significantly reduced the number of rta in past years. however, two third of the patients with shi, in this study were under the influence of alcohol. patients with shi with gcs ≤ 8 were intubated and mechanically ventilated in icu. nearly all patients in the present study underwent ct imaging of the head immediately after emergency admission. neurosurgical procedures were operative 30% nonoperative 70% 219 102 0 100 200 300 yes no aab+ o.9 28.0 7.5 36.1 3.1 24.3 306 rajendra shrestha performed between admission to the emergency room and transfer to intensive care unit. initial ct examination demonstrated abnormalities in approximately 90% of patients with severe head injury. ct scan plays a vital role in early assessment of patients with severe head injury. repeat ct scan was done within 48-72 hours to exclude conversion of contusion into increase hematoma. our study showed, patients with shi developed subdural hygroma after a week, as seen on their ct scans. subdural hygroma is defined as acute or chronic cerebrospinal fluid accumulation in the subdural space, which is a virtual space between the arachnoid and subdural membranes (17). in our series, bilateral subdural hygroma were located mainly frontoparietal region representing more than 77% of the cases. in the literature, this sort of lesion is usually related with contusions, cerebral atrophy, subdural and epidural hematomas or post operatory complications (12, 15, and 17). although etiology is well documented, pathogenesis of this condition is not well explained. some author proposed that the formation of a one-way valve allowing the passage of csf into the subdural space, caused by a traumatic tear of the arachnoidal mater or rupture of incidental arachnoids cyst (7, 13). in our series, we noticed prognosis of patients could be good once bilateral subdural hygroma in the ct scan. the study also revealed a correlation between tattoo and shi. 45% of rta cases with shi had tattoo. however, present research does not indicate any particular group, age, gender, occupation, personality or a particular level of social status that get tattoos. there are many reasons to why people get tattoo; describing personal tales, expressing individuality, spiritual meaning, fashion, scar hiding, marking new beginnings like birth, adulthood, marriage, divorce, death, etc. and even marking memories as milestone for love or loss (14). another interesting finding of our study, blood grouping pattern in shi were b+, a+ and o+ 36.1, 28 and 24.3% respectively (figure 7). in our country, normal blood grouping distribution are a, o, b and ab at 55.05%, 21.64%, 14.72%, and 8.6% respectively (8). but o, a, b and ab were 46%, 41%, 9% and 4% in the usa respectively (10). these findings can be incidental or crucial. further study needs to be conducted as our study had its limitation; small study group, single center findings and limited follow up to understand its outcome. we strongly recommended that prediction factors should be kept in mind for the best management and outcome of severe head injury patients. head trauma should highly be prevented in order to reduce incidence of tbi related mortality. thus, awareness of the impact of head trauma should be raised through information campaigns. conclusion severe head injury has a high negative impact on young people, especially men and also b+ blood group. the age of the patient, presence of tattoo, gcs at admission, ct scanning at admission and ct scanning after week of admission with hygroma were significant predictors of outcome. references 1. baguley ij, nott mt, howle aa, simpson gk, browne s, et al. late mortality after severe traumatic brain injury in new south wales: a multi center study. med j aust, 2012; 196: 40-45. 2. brazinova a, rehorcikova v, taylor ms, buckova v, majdan m, et al. epidemiology of traumatic brain injury in europe: a living systematic review. journal of neurotrauma 2016; 33:1–30. 3. cesar reis et al. what’s new in traumatic brain injury: update on tracking, monitoring and treatment; international journal of molecular science,2015; 16: 11903-11965 4. gongol dn, devkota up. an analysis of head injuries in children of nepal. journal of nepal medical association (jnma souvenir): 1979;181-9. 5. husson ec, ribbers gm, willemse-van son ah, verhagen ap, stam hj, et al. prognosis of six-month functioning after moderate to severe traumatic brain injury: a systematic review of prospective cohort studies. j rehabil med, 2010; 42: 425-436. 6. kolias ag, guilfoyle mr, helmy a, allanson j, hutchinson pj:traumatic brain injury in adults. pract neurol,2013; 13: 228-235. 7. kusuno, k., yoshida, y., takahashi, a., & ishii, s.: chronic subdural hygroma caused by rupture of arachnoid cyst. as a probable course of chronic subdural hematoma-case report. neurologia medico-chirurgica, 1984; 24(5), 349-354. http://dx.doi.org/10.2176/nmc.24.349. 8. lava shrestha, uzwali malla:abo and rh blood groups and their ethnic distribution in a teaching hospital of kathmandu, nepal ,2013;vol 52 190. doi: https://doi.org/10.31729/jnma.2112 9. maas ai, steyerberg ew, butcher i, dammers r, lu j, marmarou a, et al. prognostic value of computerized tomography scan characteristics in traumatic brain injury: results from the impact study. j neurotrauma. 2007; 24(2): 303–314. 307 predictors of severe head injury in tertiary centre 10. mollison pl, engelfriet cp, conteras m. the rh blood group system. in blood transfusion in clinical medicine, 9th edition. oxford: black well scientific publication.1993; 2008–09. 11. murray gd, butcher i, mchugh gs, lu j, mushkudiani na, maas ai, et al. multivariable prognostic analysis in traumatic brain injury: results from the impact study. j neurotrauma 2007; 24(2): 329–337. 12. park, j., cho, j.-h., goh, d.-h, et al. postoperative subdural hygroma and chronic subdural hematoma after unruptured aneurysm surgery: age, sex, and aneurysm location as independent risk factors. journal of neurosurgery, 2015; 1-8. 13. pillai, p., menon, s. k., manjooran, r. p., kariyattil, r., pillai, a. b., & panikar, d. temporal fossa arachnoid cyst presenting with bilateral subdural hematoma following trauma: two case reports. journal of medical case reports, 2009; 3(1), 53. http://dx.doi.org/10.1186/17521947-3-53. 14. shannon bell;tattooed: a participant observer's exploration of meaning,the journal of american culture,2004; 22(2):53-58:doi: 10.1111/j.1542734x.1999.2202_53.x. 15. sun, h.-l., chang, c.-j., & hsieh, c.-t. contralateral acute subdural hematoma occurring after evacuation of subdural hematoma with coexistent contralateral subdural hygroma. neurosciences (riyadh, saudi arabia), 2014:19(3), 229-232. 16. traumatic brain injury-definition, epidemiology, pathophysiology: segun toyin dawodu, updated aug 16,2017; https://emedicine.medscape.com /article/326510-overview. 17. zanini, m. a., resende, l. a. d. l., faleiros, a. t. d. s., & gabarra, r. c.traumatic subdural hygromas: proposed pathogenesis based classification. the journal of trauma, 2008; 64 (3), 705-713. ttp://dx.doi.org/10.1097/ta.0b013e3180485cfc. doi: 10.33962/roneuro-2021-075 the complementary multimodal treatment of recalcitrant cerebral aneurysms. two centres experience mohamed adel deniwar, mohamed kassem, ashraf ezzeldin, jafar j. jafar romanian neurosurgery (2021) xxxv (4): pp. 452-456 doi: 10.33962/roneuro-2021-076 www.journals.lapub.co.uk/index.php/roneurosurgery the complementary multimodal treatment of recalcitrant cerebral aneurysms. two centres experience mohamed adel deniwar1, mohamed kassem1, ashraf ezzeldin1, jafar j. jafar2 1 mansoura university, faculty of medicine, egypt 2 langone medical center, new york university, usa abstract background: the main treatment of cerebral aneurysms is the direct surgical clipping or endovascular coil embolization. however, some cerebral aneurysms that we reviewed in the literature are still not susceptible to a single treatment approach. these aneurysms can be referred to as complex aneurysms. objective: we aim to report these aneurysms and share our clinical experience with their treatment and diagnosis. methods: all cases of cerebral aneurysms treated in new york university and in mansoura university from 2010-2021 were retrospectively reviewed. results: 18 patients with 21 cerebral aneurysms were treated by combined surgical and endovascular modalities. aneurysms associated with arteriovenous malformations (avms) in 3 patients, associated with vasospasm in 7 patients, and 3 patients had double aneurysms. a total of 18 patients with aneurysms were treated with combined endovascular and microsurgical therapy. early angiogram (< 1 week) reveled; complete obliteration of 19 aneurysms (90%) out of total 21 aneurysms, residual filling was observed in 2 aneurysms (10%). late radiological follow up (> 3 months2 years) reveled; a stable residual filling in one and the other case underwent retreatment. conclusions: the recalcitrant or complex cerebral aneurysms can be better referred to as diseases rather than lesions as many clinical and anatomical factors make their treatment difficult. endovascular and microsurgery could be complementary to each other and create a multimodal approach for treating them. background direct surgical clipping or endovascular coil embolization is the most common treatment for cerebral aneurysms. (4) despite significant advancements in microsurgical techniques and equipment, as well as endovascular devices in a parallel direction, some brain aneurysms that we evaluated in the literature are still not susceptible to a single treatment approach. these aneurysms can be referred to as recalcitrant or complex aneurysms. (6,8,10-12,21) we aim to report these challenging aneurysms and share our clinical experience with their treatment and diagnosis. keywords complex aneurysms, cerebral, multimodal, complementary treatment corresponding author: mohamed adel deniwar mansoura university, faculty of medicine, egypt mohameddeniwar@mans.edu.eg copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published october 2021 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 453 the complementary multimodal treatment of recalcitrant cerebral aneurysms methodology after irb approval for both new york university and mansoura university, all cases of cerebral aneurysms treated in new york university and in mansoura university from 2010-2021 were retrospectively reviewed. inclusion criteria patients proved radiological (ct or mr angiogram or digital subtraction angiography) to harbor cerebral aneurysms that was treated by both endovascular and open surgery with any of the following criteria: 1. ruptured or unruptured 2. single or multiple 3. giant and/or widely necked aneurysms 4. with or without avms 5. with or without vasospasm 6. compressing or involving origin of adjacent arteries. 7. aneurysms were primary managed with surgery or endovascular embolization and showed residual or recurrence on follow-up. exclusion criteria aneurysms that were treated by one modality only (endovascular or open surgery). patient demographics, aneurysm characteristics, procedural details, clinical outcome (glasgow outcome scale) and radiological follow-up were analyzed. the radiological follow-up was achieved using digital subtraction angiography (dsa) and/or magnetic resonance angiography (mra) and/or ct scan angiography (cta). results 18 patients harboring cerebral aneurysms were found to be treated by combined surgical and endovascular modalities. patient demographics there were 11 females and 7 males. the mean age was 58 years (age range, 40–70 year). characteristics of aneurysms in total, there were 21 aneurysms in 18 patients. three patients had aneurysms linked with arteriovenous malformations (avms), seven patients had vasospasm, and three patients had double aneurysms (figure1). figure 1. diagram illustrating the included aneurysm cases. aneurysmal rupture and/or bleeding from associated avms were the commonest presentation, in 14 patients. the admission hunt and hess (hh) grade distribution of this patient group was as follows: grade i, ii 9 patients; and grade iii or more, 5 patients. the other 4 patients with unruptured aneurysms were as follow: incidentally discovered 1 patient during screening for familial aneurysm; 1 patient presented with third cranial palsy; 1 patient presented with agitation and confusion and another patient with aneurysm associated avm was presented by convulsions. the mean aneurysm size was 8.5 millimeters (mm). there were 16 small aneurysms (up to 10 mm diameter), and 5 large aneurysms (15–28 mm in diameter). 9 aneurysms had a wide neck (>3mm in width), 6 were saccular in shape and 4 were lobulated. the most common locations of the aneurysms were the posterior communicating artery (pcomma) and middle cerebral artery (mca) and for the avms associated with the aneurysms were as follows: 2 cerebellar and 1 temporal. (table 1) table 1. aneurysmal location parent artery number (n) pcomm 5 mca 4 acomm 3 ica –bifurcation3 aca 2 pica-aica complex 1 sca 1 anterior choridal 1 ophthalmic 1 pcomm, posterior communicating; acomm, anterior communicating; pica-aica, posterior inferior cerebellar artery anterior inferior cerebellar artery; sca, superior cerebellar artery. 454 mohamed adel deniwar, mohamed kassem, ashraf ezzeldin, jafar j. jafar treatment techniques a total of 18 patients with aneurysms were treated with combined endovascular and open surgery. 1 case with residual aneurysmal neck following surgical clipping underwent coil embolization. 3 cases with recurrent aneurysm following pervious coil embolization underwent surgical clipping. 3 cases of double aneurysms underwent coil embolization and surgical clipping. 4 cases of avm flow related aneurysms underwent partial embolization of the nidus and coil embolization of aneurysm followed by surgical resection. 7 cases developed cerebral vasospasm following surgical clipping underwent balloon and pharmaceutical angioplasty. to facilitate surgical clipping: preoperative balloon occlusion test (bto) and intraoperative dsa was applied in 3 and 7 cases receptively. (figure 2 and 3) figure 2. an intraoperative image showing complementary surgical resection of avm after pervious endovascular onyx embolization of the avm associated with an aneurysm. a white arrow points to onyx in the nidus. figure 3. (a): an intraoperative image showing a pervious coiled aneurysm that developed significant recurrence (white arrow points to the coil in the aneurysmal sac). (b): an intraoperative image showing clipping of the same aneurysm in figure 3a with two clips after removal of the coils. outcome the average radiological and clinical follow-up intervals were 13 and 16 months, respectively. all patients had an early (one week) postoperative radiological follow-up. an early angiography revealed full obliteration of 19 aneurysms (90%) out of a total of 21 aneurysms, with residual filling found in 2 aneurysms (10%), which were followed up on. late radiological follow up (> 3months2 years) was done for the patients on follow-up visits. a stable residual filling in one case and the other underwent retreatment (clipping with intraoperative dsa guidance). (table 2) table 2. summary of the clinical outcome patients clinical outcome prior to discharge (< 1 month) (n)* late outcome (>3 months) neuro logically intact same neurol ogical deficit postmanag ement new neurologi cal deficit post manage ment individual aneurysms 17 0 1** no significant change aneurysms associated with avms 2 0 1*** complete improvement neurological status factors: glasgow coma score, motor, cranial nerve and cognitive functions; other psychological and intellectual assessment were not included. * number of patients. ** 1 patient developed monocular blindness post ophthalmic artery aneurysmal clipping postoperative angiogram revealed patent ophthalmic and orbital branches though ophthalmology consult revealed no optic disc abnormalities, but diagnosis was posterior ischemic neuropathy with poor prognosis. *** 1 patient developed right lower limb weakness grade 4+ and positive romberg, patient had avulsed pica during avm embolization and sacrifice the vertebral artery was done, later developed massive cerebellar infarction later on, however gradual improvement was not noticed during outpatient clinic visits in 6 months. discussion complex and recalcitrant aneurysms many researches had attempted to categorize recalcitrant aneurysms in some way. hacin-bey et al., as a combination of anatomical aneurysm variables and clinical factors describe complex aneurysm characteristics. these characteristics are summarized in a table in his study. (8) (see table 3) 455 the complementary multimodal treatment of recalcitrant cerebral aneurysms table 3. hacin-bey et al. table of features that define recalcitrant or complex aneurysms (7). aneurysm anatomy (best assessed by 3d aneurysm reconstruction from dsa or cta data) clinical features (detailed clinical risk stratification important) size: large or giant, too small for a clip or coil clinical grade at presentation: hh_3. shape: fusiform, serpentine, pseudoaneurysm, dissecting aneurysm. timing: vasospasm at the time of presentation. content: filled with thrombus, calcified wall, dysplastic vessel wall. medical comorbidities: cardiovascular, pulmonary, renal or endocrine comorbidity. neck: difficult surgical access, broad, calcified, involving perforator vessels, and other branching vessels. advanced age. perianeurysmal environmental: aneurysm embedded ineloquent brain tissue, bone, edema, scar from previous surgery. 3d, three dimensional: dsa, digital subtraction angiography: cta, computed tomography angiography; hh, hunt and hess. used table from with permission from wolters kluwer health with modifications. the isat (international subarachnoid aneurysm trial) requires subjective agreement that an aneurysm might be treated by endovascular or open surgery (5). many aneurysms, however, did not fit the requirements, such as: 1patients with lifethreatening intracerebral or subdural hematomas; 2incompatible neck-to-dome ratios; 3-parent artery or branch artery incorporation into the dome; 4 fusiform aneurysms; 5-thrombotic aneurysms; 6 giants; 7-blisters; 8pseudo/traumatic aneurysms; 9those with mass effect; and 10-those that had failed repeated endovascular treatment (16,20). complementary multimodal therapeutic approach choudhri et al described the stanford neurosurgical experience with the combination of endovascular and open surgery in 67 cases. the aneurysms in all of the individuals in the study were completely obliterated, with no mortality. (2) the combination method was used to treat a total of 96 aneurysms, according to lawton et al. the aneurysms were enormous or giant in size in 43% of the cases, and fusiform or dolichoectatic in 34%. in 91 aneurysms, the angiographic obliteration was complete (95%) (15). chen et al. and cockroft et al., both had reported the treatment of recalcitrant cerebral aneurysms by surgical reconstruction of aneurysm neck followed by endovascular coiling on a planned concept. cockroft et al. also reported in his series the initial coil embolization of ruptured basilar tip aneurysm to reduce the risk of rebleeding followed by permanent surgical clipping (1,3). the radiological and clinical out come of this multimodal treatment in these reported studies and our study was favorable. these good results of combing both surgical and endovascular techniques encouraged the evolution of a new treatment modality, which is the hybrid cerebrovascular surgery. hybrid cerebrovascular surgery era in several subspecialties, hybrid surgery is regarded as a cutting-edge technique. the term "hybrid" refers to a combination of standard surgical and endovascular methods. actually, it's a multimodal technique that may be done in one session or over a period of time (scheduled). the use of hybrid surgery in the treatment of cardiovascular disorders has ushered in a new era in disease management.(18,19) in the same direction for the cerebrovascular diseases, hybrid operative theatres have been innovated in the neurosurgical institutes in last few years. between november 2003 and august 2011, muryma et al. and kurtia et al. published two case series of patients with intractable complicated cerebrovascular lesions who were treated with a combination strategy (endovascular and surgical). (14,17) other case reports were documented in the literature too. (5,7,9,13) a furthermore studies are expected be conducted on a larger scale concerning the hybrid cerebrovascular surgery in the nearby future. conclusion the recalcitrant or complex cerebral aneurysms can be better referred to as diseases rather than lesions; of which many clinical factors in add to the anatomical one define their complexity and make their treatment difficult. endovascular and open surgery could be complementary to each other and create a multimodal or combined approach for treating these aneurysms, and that concept has 456 mohamed adel deniwar, mohamed kassem, ashraf ezzeldin, jafar j. jafar evolved to what known nowadays as the hybrid cerebrovascular surgery. contributorship statement mohamed deniwar, mohamed kassem and ashraf ezz eldin designed the study. mohamed deniwar, mohamed kassem, ashraf ezz eldin and jafar j. jafar, participated in data extraction, analysis, writing and drafting of the manuscript, jafar j. jafar critically revised the manuscript and all authors approved the final version. irb approval after irb approval for both new york university (i14-01394) and mansoura university (r.21.03.1240), all cases of cerebral aneurysms treated in new york university and in mansoura university from 2010-2021 were retrospectively reviewed. references 1. chen l, kato y, sano h, watanabe s, yoneda m, hayakawa m, sadato a, irie k, negoro m, karagiozov kl, kanno t. management of complex, surgically intractable intracranial aneurysms: the option for intentional reconstruction of aneurysm neck followed by endovascular coiling. cerebrovascular diseases. 2007 apr 2;23(5-6):381-7. 2. choudhri o, mukerji n, steinberg md, gary k. combined endovascular and microsurgical management of complex cerebral aneurysms. frontiers in neurology. 2013 aug 8;4:108. 3. cockroft km, marks mp, steinberg gk. planned direct dual-modality treatment of complex broad-necked intracranial aneurysms: four technical case reports. neurosurgery. 2000 jan 1;46(1):226-31. 4. colby gp, coon al, tamargo rj. surgical management of aneurysmal subarachnoidal hemorrhage. neurosurgclin n am (2010) 21(2): 247–61. 5. deniwar m, ambekar s, elhammady ms. multimodal management of a complex indirect carotid cavernous fistula. neurology india. 2015 jul 1;63(4):606. 6. greenberg, ms. handbook of neurosurgery: sah and aneurysms. in: 8th ed. greenberg, lakeland; 2016 may. 7. guerrero ca, raja ai, naranjo n, krisht af. obliteration of carotid-cavernous fistulas using direct surgical and coilassisted embolization: technical case report. neurosurgery. 2006 feb 1;58(2):e382. 8. hacein-bey l, connolly jr es, mayer sa, young wl, pilespellman j, solomon ra. complex intracranial aneurysms: combined operative and endovascular approaches. neurosurgery. 1998 dec 1;43(6):1304-12. 9. heiroth hj, turowski b, etminan n, steiger hj, hänggi d. coiling of a carotid cavernous sinus fistula via microsurgical venotomy: recommendation of a combined neurosurgical and endovascular approach. journal of neurointerventional surgery. 2013 mar 1; 5(2):e7. 10. kallmes df, hanel r, lopes d, boccardi e, bonafé a, cekirge s, fiorella d, jabbour p, levy e, mcdougall c, siddiqui a. international retrospective study of the pipeline embolization device: a multicenter aneurysm treatment study. american journal of neuroradiology. 2015 jan 1;36(1):108-15.n. 11. killory bd, nakaji p, gonzales lf, ponce fa, wait sd, spetzler rf. prospective evaluation of surgical microscope–integrated intraoperative near‐infrared indocyanine green angiography during cerebral arteriovenous malformation surgery. neurosurgery. 2009 sep 1;65(3):456-62. 12. kim hk, hwang sk, kim sh. types of thromboembolic complications in coil embolization for intracerebral aneurysms and management. journal of korean neurosurgical society. 2009 sep 1;46(3):226-31. 13. krisht af, burson t. combined pretemporal and endovascular approach to the cavernous sinus for the treatment of carotid-cavernous dural fistulae: technical case report. neurosurgery. 1999 feb 1; 44(2):415-8. 14. kurita h, takeda r, ikeda t, kikkawa y, fushihara g, ooigawa h, ishihara s. hybrid cerebrovascular surgery for complex cerebral aneurysms and arteriovenous malformations. japanese journal of neurosurgery. 2015;24(3):173-9. 15. lawton mt, quinones hinojosa a, sanai n, malek jy, dowd cf. combined microsurgical and endovascular management of complex intracranial aneurysms. neurosurgery (2003) 52(2):263–74. 16. molyneux, andrew j., et al. "international subarachnoid aneurysm trial (isat) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion." the lancet 366.9488 (2005): 809-817. 17. murayama y, arakawa h, ishibashi t, kawamura d, ebara m, irie k, takao h, ikeuchi s, ogawa t, kato m, kajiwara i. combined surgical and endovascular treatment of complex cerebrovascular diseases in the hybrid operating room. journal of neurointerventional surgery. 2013 sep 1;5(5):489-93. 18. nollert g, figel a, bulitta c, altenbeck f, hartkens t, gerhard v. the hybrid operating room. intech open access publisher; 2012. 19. nollert g, wich s, hartkens t, figel a. the cardiovascular hybrid operating room. inatlas of advanced endoaortic surgery 2013 (pp. 1-9). springer london. 20. origitano tc. current options in clipping versus coiling of intracranial aneurysms: to clip, to coil, to wait and watch. neurosurgery clinics of north america. 2008 jul 31;19(3):469-76. 21. terada t, tsuura m, matsumoto h, masuo o, shintani a, ryujin y, itakura t. factors leading to and treatment of aneurysmal perforation during coil embolization analysis of 105 consecutive cases. interventional neuroradiology. 2003 mar 1;9(1):21-9. doi: 10.33962/roneuro-2023-003 autologous versus synthetic cranioplasty. single centre study and literature review arif zafar, samantha strickland, shailendra achawal romanian neurosurgery (2023) xxxvii (1): pp. 24-35 doi: 10.33962/roneuro-2023-003 www.journals.lapub.co.uk/index.php/roneurosurgery autologous versus synthetic cranioplasty. single centre study and literature review arif zafar1, samantha strickland2, shailendra achawal1 1 department of neurosurgery, hull royal infirmary, anlaby road, hull, hu3 2jz, uk 2 hull and york medical school, university rd, heslington, york yo10 5dd, uk abstract background. cranioplasty has been described in history as far back as the 16th century. the use of autologous cranioplasty has been published since 1821 and is still under practice today worldwide. recent evidence however has suggested increased complication and revision rates with the use of autologous bone. we compared our results of autologous cranioplasty versus synthetic material. methods. a retrospective study was carried out of cranioplasty procedures at our unit between august 2009 and march 2018. bone flaps were placed in a sterile sealed plastic container and stored at -81 degrees. swabs and bone chips were used for cultures and bone flap disposed if positive. on re-implantation, the bone was thawed at room temperature and soaked in gentamicin. synthetic cranioplasties were constructed using thin-slice ct to design a custom flap for each patient. results. 144 cranioplasties were studied. 51 own bone and 93 synthetic. the average delay in cranioplasty was 286 days (range 16 – 1264 days). the overall complication rate for all 144 cranioplasties was 20.8%; autologous 31.4% and synthetic 15.1%; p 0.031. bone flap infection rate overall for all 144 cases was 9.7% autologous 11.8% and synthetic 8.6%; p 0.565. the revision rate was found to be 13.2% overall; 23.5% for autologous and 7.5% for synthetic. the difference in revision rate was found to be statistically significant (p 0.01). conclusion. revision rate and overall complication rate were higher in the own bone group with p<0.05. there was no difference in infection. our results mirror recent publications and should be considered when undertaking a cranioplasty. introduction the practice of cranioplasty is well documented in history and records date back to the 16th century when gold plates were used in reconstruction. there is also evidence of the practice of trephination and cranioplasty from as early as 3000 bc. the first reported use of bone for reconstruction was in 1668 when a canine bone was described to have been used to repair a cranial defect in a russian male. walther in 1821 was reported to be the first to practice autograft cranioplasty. this technique was subsequently popularised by macewen in 1885 who began routinely replacing trephined bone plugs back into the defects. wagner in 1889 took this one step further by describing the osteoplastic keywords cranioplasty, autologous cranioplasty, synthetic cranioplasty, bone flap corresponding author: arif zafar hull royal infirmary, anlaby road, hu3 2jz, uk arifzafar86@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 25 autologous versus synthetic cranioplasty craniotomy in which bone was left attached to underlying muscle1,2. the practice of successful delayed cranioplasty in its earliest form was described by sedel in 1889 who used pieces of tibia to repair a parietal defect and later axhausen used this technique successfully for multiple cases1. this technique became popular in early 1900s with multiple authors reporting good results. muller and konig in 18903 described their technique of split local graft of skin, periosteum and outer table to reconstruct defects, and later hacker modified this to include only periosteum and outer table4. subsequent to this, various anatomical sites have been used for autografts including ribs, scapula, ilium and sternum with varying popularity5. cadaver allografts have also been used in the past but were noted to be susceptible to infection and resorption1. aluminium was the first metal in the development of modern cranioplasty but was found to be locally irritant and epileptogenic6. silver and gold7 were also used with good results being reported with gold cranioplasties however this practice was not considered cost efficient. lead has also been used but abandoned due to the obvious risk of toxicity. platinum revealed very little reaction but again abandoned due to cost. use of alloys showed promising results and vitallium (cobalt, chromium and molybdenum)8 and ticonium (cobalt, chromium, nickel, molybdenum)9 became popular 1 abhay s, haines sj. repairing holes in the head: a history of cranioplasty. neurosurgery. 1997 mar 1;40(3):588-603. 2 feroze ah, walmsley gg, choudhri o, lorenz hp, grant ga, edwards ms. evolution of cranioplasty techniques in neurosurgery: historical review, pediatric considerations, and current trends. journal of neurosurgery. 2015 oct;123(4):1098-107. 3 grant fc, norcross nc. repair of cranial defects by cranioplasty. annals of surgery. 1939 oct;110(4):488. 4 roka yb. review of the history of materials used with experience with bone cement cranioplasty. nepal journal of neuroscience.;14(1):7-13. 5 aydin s, kucukyuruk b, abuzayed b, aydin s, sanus gz. cranioplasty: review of materials and techniques. journal of neurosciences in rural practice. 2011 jul;2(2):162. 6 booth ja, curtis bf. i. report of a case of tumor of the left frontal lobe of the cerebrum; operation; recovery. annals of surgery. 1893 feb;17(2):127. 7 mitchell ab. repair of injuries to the skull by perforated plates. british journal of surgery. 1917;5(17):40-1 8 beck cs. repair of defects in skull by ready made vitallium plates. journal of the american medical association. 1942 mar 7;118(10):798-9. prior to the second world war. tantalum, an inert metal with good results in animal models, became popular and used widely to treat combat injuries in the second world war10 but due to the difficulties in acquiring and purifying this, it remained an expensive metal. zirconium was also shown to have minimal tissue reaction in studies11. the use of titanium was first described by simpson in 196512. the author reported that although the material was not perfect and less malleable than tantalum, it was radiolucent when used in an appropriate thickness and cheaper as a material in his experience of 7 cases. non-metallic compounds have also been long explored in a bid to find an ideal cranioplasty material. celluloid was first used in 1890 and subsequently gained popularity due to its elasticity and resilience13. this material lost favour as there was noted to be considerable tissue reaction sometimes causing fistula formation. acrylic gained increasing popularity around 1940 when its use in dental implants was recognised to show no tissue reaction. methyl methacrylate (also known as lucite, vitacrylic, plexiglass, crystallite, craniolast and perspex) was felt to be considerably malleable and radiolucent and could be easily used to reconstruct large defects14. use of other inert compounds such as polyethylene15 and silicon rubber16 have been considered but did not gain popularity due to their soft structure. 9 campbell e, meirowsky a, hyde g. studies on the use of metals in surgery. annals of surgery. 1941 sep;114(3):472. 10 mayfield fh, levitch la. repair of cranial defects with tantalum. the american journal of surgery. 1945 feb 1;67(2):319-32. 11 bates ji, reiners cr. the repair of cranial defects with zirconium: an experimental study. journal of neurosurgery. 1948 jul;5(4):340-8. 12 simpson d. titanium in cranioplasty. journal of neurosurgery. 1965 mar 1;22(3):292-3. 13 pringle jh. remarks on the closure of gaps in the skull, with notes of cases. british medical journal. 1906 feb 3;1(2353):246. 14 gurdjian es, webster je, brown jc. impression technique for reconstruction of large skull defects. surgery. 1943 dec 1;14(6):876-81. 15 ingraham fd, alexander e, matson dd. polyethylene, a new synthetic plastic for use in surgery: experimental applications in neurosurgery. journal of the american medical association. 1947 sep 13;135(2):82-7. 16 courtemanche ad, thompson gb. silastic cranioplasty following cranio-facial injuries. plastic and reconstructive surgery. 1968 feb 1;41(2):165-72. 26 arif zafar, samantha strickland, shailendra achawal it was however noted that the acrylic plates could be prone to fracture and therefore galicich and hovind in 1967 described stainless steel mesh reinforced acrylic cranioplasty17. this was later modified by malis to use a titanium mesh instead of stainless steel due to multiple reasons including the artefact produced on ct and compatibility issues with mri18. hydroxyapatite is a more recent development in cranioplasty materials and is a calcium phosphate compound. this is a natural mineral found in bone but can be synthesised as a hexagonal structure creating a ceramic. the material has shown minimal tissue reaction. it has also shown increased bone repair and osteointegration to its advantage. however if used alone it can be very brittle and prone to fracture. it has been used in oral and maxillofacial surgery for many years19,20 and pompili et al published one of the first series in use of this material for cranioplasty21. a total of 11 cases underwent cranioplasty with a material composed of hydroxyapatite, combined with a gel, and laid on titanium mesh or micronets. post operatively the patients were reported to have good outcomes with impressive levels of osteo-integration according to the authors. polyetheretherketone (peek) is another organic compound which has gained popularity as it is inert and radiolucent. it is a semicrystalline thermoplastic which has been shown to have similar strength to bone and can be used to print accurate 3d reconstructions of the required implant. one main disadvantage is the cost involved as peek implants can often be expensive22. the debate between autologous versus synthetic cranioplasty has been ongoing with various publications and authors arguing advantages and risks of both. in our unit we practice both autologous and synthetic cranioplasty and historically this has been done with surgeon preference in cases where 17 lake pa, morin ma, pitts fw. radiolucent prosthesis of mesh-reinforced acrylic. journal of neurosurgery. 1970 may;32(5):597-602. 18 malis li. titanium mesh and acrylic cranioplasty. neurosurgery. 1989 sep 1;25(3):351-5. 19 beirne or, curtis ta, greenspan js. mandibular augmentation with hydroxyapatite. journal of prosthetic dentistry. 1986 mar 1;55(3):362-7. both options were available. we chose to look at our outcomes for these groups. method a retrospective study was carried out of all cranioplasty procedures at our unit between june 2009 and march 2018. the patients were identified from a combination of electronic theatre records for a cranioplasty coded procedure and from our bone bank register. once patients were identified, information was collected via their electronic patient records, theatre notes and all available imaging. bone flaps sent to the bank were placed in sterile saline solution during the period of operation until a decision was made regarding replacement. once a decision was made, swabs and bone chips were taken prior to the bone being placed in a double sterile sealed plastic container (one sealed container within another). swabs and bone chips were used for cultures and sensitivity. if any positive cultures were found, the bone was disposed. the plastic containers were wrapped in a further plastic bag before being stored in a deep freezer at -81 degrees. prior to reimplantation, the bone was thawed at room temperature and soaked in either gentamicin in sterile saline or aqueous betadine based on surgeon preference and/or patient allergies. this was undertaken while incision and exposure were taking place. decision for material used for synthetic cranioplasty was based on surgeon preference. there are no established protocols within our department for choice of material however in general if a bone flap can be salvaged (i.e. it is not deemed immediately infected or fragmented due to trauma), then an autologous cranioplasty is usually undertaken in the future. there are however exceptions in even these cases whereby a consultant may choose to select synthetic materials out of personal preference or experience. 20 frame jw, brady cl. the versatility of hydroxyapatite blocks in maxillofacial surgery. british journal of oral and maxillofacial surgery. 1987 dec 1;25(6):452-64. 21 pompili a, caroli f, carpanese l, caterino m, raus l, sestili g, occhipinti e. cranioplasty performed with a new osteoconductive, osteoinducing hydroxyapatite-derived material. journal of neurosurgery. 1998 aug;89(2):236-42. 22 shah am, jung h, skirboll s. materials used in cranioplasty: a history and analysis. neurosurgical focus. 2014 apr;36(4):e19. 27 autologous versus synthetic cranioplasty each cranioplasty was custom manufactured using thin slice ct. a combination of titanium, ceramic, acrylic and hydroxyapatite plates were used, all pre-manufactured and delivered in a sterile pack which was opened just prior to surgery. these too were placed in either gentamicin in sterile saline or aqueous betadine prior to placement. all cranioplasties were fixed with 5mm self-tapping titanium screws with mini plates. figure 1 demonstrates the common synthetic materials used within our department. primary outcome was need for revision. information was also collected for other complications including infection, timing of cranioplasty and original diagnosis. fisher 2 tailed tests were conducted at 5% significance level to confirm statistical significance for revision rates and multiple factors. odds ratios were calculated for various factors. results 145 patients were identified. 1 patient with synthetic cranioplasty was exclude as the implant had to be removed due to failure of a complex advancement skin flap one patient had own bone cranioplasty which was complicated by resorption of the bone flap. this complication was included under autologous group. the defect was then repaired using a synthetic implant which was placed overlying the partially absorbed autologous flap. however, this was further complicated by infection and necessitated removal of the partially resorbed bone and synthetic implant. as it was not clear as to what caused the infection, this was excluded from infection rate of both groups. 81 males and 63 females were included in the study with an average age of 51.6 years (range 18.1 – 85.3 years). overall 51 cranioplasties were performed using own bone and 93 synthetic. table 1 details the synthetic cranioplasty materials used. average delay in cranioplasty was 268 days (range 16 – 1264 days). the most common reason for craniectomy was acute subdural haemorrhage (23.6%), post operative infection (19.4%) and intracranial haemorrhage (15.3%). table 2 illustrates patient characteristics for those undergoing cranioplasty. overall complication rate was 20.8% (30 cases) with 16 cases in the own bone group (31.4%) and 14 cases in the synthetic group (15.1%). there were significantly more complications in the autologous group as compared to the synthetic group (p 0.031). bone flap infection rate for all 144 cases was 9.7% (14 cases) with 6 cases in the autologous group (11.8%) and 8 cases in the synthetic group (8.6%). difference 28 arif zafar, samantha strickland, shailendra achawal in infection rate was not found to be statistically significant (p 0.542). other complications are shown in table 3. the only significant difference was found to be in post operative extra-dural haematoma (edh) with 3 cases (5.9%) in autologous group and none in synthetic group (p 0.043). resorption was not included as a comparative complication risk for analysis as this would not apply to synthetic cranioplasty and therefor was analysed as part of revision rates. overall resorption rate for autologous cranioplasty was 27.5%. of these 14 cases, 6 required revision due to significant resorption of the bone flap, however 8 cases only had partial resorption, hence did not need revision. resorption was deemed significant if it resulted in either gross anatomical or aesthetic defect necessitating revision. partial resorption included those patients with evidence of radiological bone resorption without a substantial anatomical deficiency or concerns from the patient. if bone resorption is included in the complication, the complication rate in autologous group becomes 31.4% if only revised flaps were included. the total complication rate for autologous group was 54.9% including all bone flaps which showed any resorption (either partial or near total). revision rate was found to be 13.2% overall with 12 revisions in the autologous group (23.5%) and 7 in the synthetic group (7.5%). all revisions in the synthetic group took place due to infection, including 1 case of subdural empyema. 6 cases within the autologous group were revised due to infection and the remaining 6 cases due to resorption. difference in revision rate was found to be statistically significant (p 0.01). the significant increase in 23 brommeland t, rydning pn, pripp ah, helseth e. cranioplasty complications and risk factors associated with bone flap resorption. scandinavian journal of trauma, resuscitation and emergency medicine. 2015 dec;23(1):75. 24 shoakazemi a, flannery t, mcconnell rs. long-term outcome of subcutaneously preserved autologous cranioplasty. neurosurgery. 2009 sep 1;65(3):505-10. 25 movassaghi k, ver halen j, ganchi p, amin-hanjani s, mesa j, yaremchuk mj. cranioplasty with subcutaneously preserved revision rate was found to be due to bone resorption in the autologous group. risk of requiring revision of cranioplasty in autologous group was 3.5 times (range1.5 – 8.1) that of synthetic group. discussion autologous cranioplasty remains practiced across the world but is losing popularity due to growing belief in increased complication rates and the inherent risk of resorption. one study of 125 patients undergoing autologous cranioplasty estimated complication rate at 9.2% and resorption rate at 19.7%23. there has also been some dispute as to the best solution for storing autologous cranioplasties and some have argued that different techniques can contribute to complication risks. in one study, the infection rate following reimplantation of cranioplasty stored subcutaneously was 5.6% and 2 further bone flaps (2.2%) were removed for resorption. 2 haematomas were noted, one extradural and one within the abdominal pocket. the remaining results were deemed to be acceptable however follow up was only for 1 year at the time of publication24. the authors felt the subcutaneous storage was a viable and acceptable means of storage. another study of 53 patients undergoing cranioplasty following subcutaneous storage reported 3 bone flap infections (6%). one was noted to be infected in the subcutaneous space where it was stored and had to be discarded. two were infected post cranioplasty and needed removal25. the paper does however report that 8 of the cranioplasties (15%) required immediate augmentation with synthetic material but do not specify whether this was for resorption or other reasons. they also do not specify whether infections occurred within the augmented cranioplasties or entirely autologous grafts. morina et al reported only 2 revisions needed out of 75 cases for infection for bone stored in an abdominal subcutaneous pocket26. again, 9 of their cases required autologous bone grafts. plastic and reconstructive surgery. 2006 jan 1;117(1):202-6. 26 morina a, kelmendi f, morina q, dragusha s, ahmeti f, morina d, gashi k. cranioplasty with subcutaneously preserved autologous bone grafts in abdominal wall— experience with 75 cases in a post-war country kosova. surgical neurology international. 2011;2. 29 autologous versus synthetic cranioplasty augmentation with synthetic material and the authors do not comment on whether the infection was in autologous alone or combined cranioplasties. hauptli and segantini report their change in practice after observing frequent osteolysis in their cryopreserved bone flaps, particular at edges, in up to 60%. following changing their method of preservation to subcutaneous pocket, they reported improved bone resorption rates with only 2 bone flaps showing signs of resorption following implantation and one removed for infection27. the paper however does only quote a 2 year follow up. cryopreservation is another method widely employed of storing bone flaps. in a large retrospective study, fan et al reported their experience of cryopreserved bone flaps over a 12year period28. a total of 946 cases of cranioplasties were assessed and re-implantation took place between 67 – 641 days (average 194 days). bone flaps were stored after gentile irrigation with sterile saline, wrapped in 2 layers of sterile plastic and then placed in a storage medium (including dimethyl sulfoxide, dmso) and slowly cooled by various methods to a final temperature of -196 degrees in liquid nitrogen. swabs were sent prior to storage and if any positive growth found, the flaps were discarded. through their storage process the authors reported that microscopically the bone retained features of normal bone including good osteocyte activity as compared to fast freezing or autoclaving. overall infection rate was 4.06% (39 flaps) and resorption rate was 4.28% (42 flaps). all infected bone flaps were removed however the authors do not report their outcomes with resorbed flaps. the use of bioactive materials such as those used by fan et al have been argued to improve bone flap viability during cryopreservation and in a laboratory study of mice femoral tissue, storing in 27 häuptli j, segantini p. new tissue preservation method for bone flaps following decompressive craniotomy. helvetica chirurgica acta. 1980 jun;47(1-2):121-4. 28 fan mc, wang ql, sun p, zhan sh, guo p, deng ws, dong q. cryopreservation of autologous cranial bone flaps for cranioplasty: a large sample retrospective study. world neurosurgery. 2018 jan 1;109:e853-9. 29 leunig m, yuan f, berk da, gerweck le, jain rk. heating or freezing bone: effects on angiogenesis induction and growth potential in mice. acta orthopaedica scandinavica. 1996 jan 1;67(4):383-8. 30 hng d, bhaskar i, khan m, budgeon c, damodaran o, knuckey n, lee g. delayed cranioplasty: outcomes using dmso solution was shown to have improved cell proliferation as compared to a control solution29. hng et al discussed their results of 187 patients with cryopreserved cranioplasty over a 10-year period30. bone was wrapped in a sterile plastic sheath and stored at -30 degrees. prior to reimplantation the bone was thawed at room temperature and soaked in betadine. the authors also recommend against autoclaving due to the higher risk of bone resorption. 64.7% of cranioplasties were undertaken within 90 days (range 10 – 390 days) and overall complication rate was 34.2% (64 cases). bone flap infection requiring removal was noted in 11.2% and revision of bone flap due to resorption occurred in 5.34%. other complications included superficial wound infection (3.21%), hydrocephalus 3(.21%) and seizures (2.67%) iwama et al also reported good outcomes with their experience of cryopreserved bone flaps in 49 patients31. they stored bone in 3 sterile vinyl plastic bags at either -35 or -84 degrees and flaps were washed in sterile saline and tobramycin prior to reimplantation (4 – 168 days, average 50.6 days). only 2 complications were noted (4%), one case of infection and one case of revision needed for bone resorption. grossman et al reported no complications in their 12 cases of cryopreserved cranioplasties32. in their series the bone was irrigated with saline and neomycin antibiotic, wrapped in 2 sterile plastic wraps and stored at -80 degrees. an extended point in this series was the average reimplantation duration was 9.25 months (0.25 to 27 months) however despite this duration, no complications were reported in this, albeit small sample. lu et al published their experience with 16 cases of cryopreserved bone flaps at -80 degrees33. the bone flaps were wrapped in 2 sheets of sterile plastic frozen autologous bone flaps. craniomaxillofacial trauma & reconstruction. 2015 sep;8(3):190. 31 iwama t, yamada j, imai s, shinoda j, funakoshi t, sakai n. the use of frozen autogenous bone flaps in delayed cranioplasty revisited. neurosurgery. 2003 mar 1;52(3):591-6. 32 grossman n, shemesh-jan hs, merkin v, gideon m, cohen a. deep-freeze preservation of cranial bones for future cranioplasty: nine years of experience in soroka university medical center. cell and tissue banking. 2007 sep 1;8(3):2436. 33 lu y, hui g, liu f, wang z, tang y, gao s. survival and regeneration of deep-freeze preserved autologous cranial bones after cranioplasty. british journal of neurosurgery. 2012 apr 1;26(2):216-21. 30 arif zafar, samantha strickland, shailendra achawal before being placed into an “ultra low freezer” at -80 degrees. prior to replacement, they were soaked in providone-iodine for 30 minutes and average delay in cranioplasty was 117 days (range 63 – 289 days). they reported no infection or other complication with their re-implanted bone and conducted post operative spect imaging which the authors reported showing equal radioactive uptake in re-implanted bone as compared to native bone. this is in contrast to some studies that have suggested that bone flap viability becomes limited following a period of storage. a laboratory study by bhaskar et al revealed no cell growth in bone flaps stored at -30 degrees for over 6 months rendering the bone flaps non-viable34. another study however, revealed no effect on the biomechanical properties of human skull bone when comparing fracture loading, tested by bending forces until the sample fractured. the bones were tested following storage at -20 degrees for up to 3 months35. in a paper comparing subcutaneously stored (sc) bone versus cryopreservation (cp) at -70 degrees following betadine soaking, there was no statistical difference in infection rates between the groups. of the 39 cranioplasty stored in subcutaneous pocket and 31 cryopreserved, there were 2 (5.1%) and 5 (16.1%) infections respectively. in the sc group, one infection occurred in the abdomen and one on reimplantation. on infection within the cp group was considered superficial only and treated with intravenous antibiotics. a subgroup analysis however revealed significantly higher infection in cryopreserved bone for those undergoing craniectomy for traumatic brain injury (tbi)36. cheng et al also compared subcutaneous versus cryopreservation of bone flaps of patients undergoing decompression over a 10-year period37. 290 patients were included with 110 preserved 34 bhaskar ip, yusheng l, zheng m, lee gy. autogenous skull flaps stored frozen for more than 6 months: do they remain viable?. journal of clinical neuroscience. 2011 dec 1;18(12):1690-3. 35 torimitsu s, nishida y, takano t, koizumi y, hayakawa m, yajima d, inokuchi g, makino y, motomura a, chiba f, iwase h. effects of the freezing and thawing process on biomechanical properties of the human skull. legal medicine. 2014 mar 1;16(2):102-5. 36 inamasu j, kuramae t, nakatsukasa m. does difference in the storage method of bone flaps after decompressive craniectomy affect the incidence of surgical site infection after cranioplasty? comparison between subcutaneous subcutaneously and 180 cryopreserved. the bones were immersed in betadine for 30 mins and then vancomycin for another 30 mins prior to being stored. microbiology swabs were sent. overall infection rate was 13.8% with 20 cases of infection in each group (11.11% sc, 18.18 cp) with no statistically significant difference. in the subcutaneous pocket group, 12 of these were as a result of cranioplasty and the remainder were within the stored pocket requiring disposal of bone flap. the authors also studied bone resorption by comparing frontal bone thickness and found that there was statistically significant decreased thickness in the cp group, but they do not comment on whether any revisions were needed as a result. another method of bone flap preservation used by some surgeons is subgaleal storage on the opposite side of the craniectomy. goel and deogaonkar reported their outcome of subgaleal bone flap preservation38. 8 cases were included however only 4 of the bone flaps were replaced with very unclear indication within the paper as to the reason for this. the authors concluded that within the replaced bone flaps, there were no complications with bone flaps being stored for anywhere between 3-16 months. krishnan et al described 55 cases of subgaleal preserved bone flap and reported only 2 complications related to wound or skin breakdown from pressure39. korfali and aksoy reported no complication following 27 cases of replacement of bone flaps stored under the galea. both papers felt subgaleal storage was an easy and cost-effective method of storage. a review paper comparing multiple techniques of bone flap storage concluded that there was no statistically significant difference between technique of bone flap preservation and post operative pocket and cryopreservation. journal of trauma and acute care surgery. 2010 jan 1;68(1):183-7. 37 cheng ch, lee hc, chen cc, cho dy, lin hl. cryopreservation versus subcutaneous preservation of autologous bone flaps for cranioplasty: comparison of the surgical site infection and bone resorption rates. clinical neurology and neurosurgery. 2014 sep 1;124:85-9. 38 goel a, deogaonkar m. subgaleal preservation of calvarial flaps. surgical neurology. 1995 aug 1;44(2):181-3. 39 krishnan p, bhattacharyya ak, sil k, de r. bone flap preservation after decompressive craniectomy-experience with 55 cases. neurology india. 2006 jul 1;54(3):291. 31 autologous versus synthetic cranioplasty outcome40. this was however not a systematic review. yadla et al conducted a systemic review on subcutaneous storage versus extracorporeal and found no statistical difference41. many papers have also attempted to compare autologous bone flaps with synthetic materials. piitulainen et al studied their results over a 10-year period with 100 cranioplasties42. 20 were performed using autologous bone and the remainder with various synthetic material. bone flaps were stored at -80 degrees and swabs were taken to ensure no growth prior to re-implantation. overall complication rates were 60% for autografts and 25% for synthetic material. revision rates were 40% for autografts and 14% for synthetic materials. the paper reports there was no significant difference between autologous cranioplasty and synthetic subgroups but do not undertake an overall comparison. from their data a chi squared test reveals a p value of 0.02. serious infection rate was 25% in autologous and 5% in synthetic group with a resorption rate of 15%. there were no specific risk factors shown to be significant including time of implantation. klinger et al also published their experience of 258 cranioplasties over a 10-year period43. autologous bone was stored between -40 to -80 degrees following swabs being undertaken to ensure no growth. synthetic cranioplasty was undertaken with acrylic flaps. a total of 138 (53%) procedures were with autologous bone and 120 (47%) with acrylic. the authors reported an overall 10.9% complication rate and reported no significant difference between the two groups. in their series, 40 joaquim af, mattos jp, neto fc, lopes a, de oliveira e. bone flap management in neurosurgery. revista neurociencias. 2009. 41 yadla s, campbell pg, chitale r, maltenfort mg, jabbour p, sharan ad. effect of early surgery, material, and method of flap preservation on cranioplasty infections: a systematic review. neurosurgery. 2011 apr 1;68(4):1124-30. 42 piitulainen jm, kauko t, aitasalo km, vuorinen v, vallittu pk, posti jp. outcomes of cranioplasty with synthetic materials and autologous bone grafts. world neurosurgery. 2015 may 1;83(5):708-14. 43 klinger dr, madden c, beshay j, white j, gambrell k, rickert k. autologous and acrylic cranioplasty: a review of 10 years and 258 cases. world neurosurgery. 2014 sep 1;82(3-4):e52530. 44 punchak m, chung lk, lagman c, bui tt, lazareff j, rezzadeh k, jarrahy r, yang i. outcomes following polyetheretherketone (peek) cranioplasty: systematic review only 2 (1.4%) bone flaps underwent significant bone resorption. a systemic review looking at impact of cranioplasty material on infection rates concluded that there was no significant difference between autologous and synthetic flaps41. another systemic review and meta-analysis comparing peek cranioplasty to other materials including autologous again did not find any significant difference in complication rates44. however, they analysis only included 2 studies in their review. time of cranioplasty has long been debated as an independent risk factor for revision. a large retrospective study reported that cranioplasty undertaken between 15 to 30 days post craniectomy were associated with a lower infection, seizure and resorption rate45. cranioplasty after 90 days was associated with lower hydrocephalus rates but higher risk of seizures. a recent systemic review found that although early cranioplasty (<90 days) was associated with higher incidence of hydrocephalus, there was no statistical difference between any other complication46. overall infection rate was reported between 0 to 24% with an average of 7.4%. this systemic review echoed a previous study which concluded the same results with no significant difference between early and late groups but a significantly higher hydrocephalus rate in the early group47. although the several systemic reviews have concluded that there is no increase in complication rates, evidence has suggested neurological outcome may be improved with early cranioplasty48. a and meta-analysis. journal of clinical neuroscience. 2017 jul 1;41:30-5. 45 morton rp, abecassis ij, hanson jf, barber jk, chen m, kelly cm, nerva jd, emerson sn, ene ci, levitt mr, chowdhary mm. timing of cranioplasty: a 10.75-year single-center analysis of 754 patients. journal of neurosurgery. 2017 aug 11;128(6):1648-52. 46 malcolm jg, rindler rs, chu jk, grossberg ja, pradilla g, ahmad fu. complications following cranioplasty and relationship to timing: a systematic review and meta-analysis. journal of clinical neuroscience. 2016 nov 1;33:39-51. 47 xu h, niu c, fu x, ding w, ling s, jiang x, ji y. early cranioplasty vs. late cranioplasty for the treatment of cranial defect: a systematic review. clinical neurology and neurosurgery. 2015 sep 1;136:33-40. 48 malcolm jg, rindler rs, chu jk, chokshi f, grossberg ja, pradilla g, ahmad fu. early cranioplasty is associated with greater neurological improvement: a systematic review and meta-analysis. neurosurgery. 2017 apr 17;82(3):278-88. 32 arif zafar, samantha strickland, shailendra achawal cochrane registered article by a german team concluded in their abstract that ultra-early (within 6 weeks) cranioplasty improved neurological outcome49. however, the remaining article is in german and therefore we could not critique their methods. another cochrane registered prospective multinational trial concluded that there was no increase in risks by early cranioplasty (under 12 weeks) but did not establish a significant benefit50. the authors admit that they only recruited 70 patients into their study and potentially was underpowered to obtain statistically significant results. in our study the average delay in cranioplasty was 268 days with a range of 16 to 1264 days with a median of 224 days. there are no specific established protocols within our department to specify the timing of cranioplasty however most surgeons’ preference is to undertake this procedure after 3 to 6 months to judge clinical recovery. with cases of infection, the surgery is usually undertaken after a period of observation on completion of antibiotic therapy, which is usually continued for a minimum of 6 weeks. 31.3% of cranioplasties occurred within 6 months and 69.4% within 1 year. some cases had an unusually long delay mainly due to patient factors with regards to clinical recovery however due to the retrospective nature of our study, in some cases the delay was unclear. in view of paucity of data, a recent randomised control trial has been published comparing autologous flaps with titanium cranioplasty51. 64 patients were recruited and outcomes assessed at 1 year. bone flaps were preserved at -80 degrees in double layer of sterile plastic and on the day of procedure, were thawed in warm saline solution. all patients underwent post operative ct on day 1. the 49 archavlis e, nievas mc. cranioplasty after supratentorial decompressive craniectomy: when is the optimal timing. der nervenarzt. 2012 jun;83(6):751-8. 50 quah bl, low hl, wilson mh, bimpis a, nga vd, lwin s, zainuddin nh, wahab na, salek ma. is there an optimal time for performing cranioplasties? results from a prospective multinational study. world neurosurgery. 2016 oct 1;94:13-7. 51 honeybul s, morrison da, ho km, lind cr, geelhoed e. a randomized controlled trial comparing autologous cranioplasty with custom-made titanium cranioplasty. journal of neurosurgery. 2017 jan;126(1):81-90. 52 honeybul s, morrison da, ho km, lind cr, geelhoed e. a randomised controlled trial comparing autologous authors reported no infection of primary cranioplasty however 1 case of infection in a patient requiring titanium cranioplasty following own bone resorption. complete resorption was reported in 7 (22%) of cases but only 5 of these patients agreed to a revision cranioplasty as the other 2 were still satisfied with overall cosmesis. resorption was observed more commonly in younger patients (32 vs 45, p 0.013 and a further 12 cases were noted to have some degree of resorption. there was no difference between complication rates including post op haematoma requiring surgery which was reported as 5% in own bone and 6% in titanium group. the authors also conducted a cost analysis and found no statistical difference and thus concluded that primary titanium cranioplasty should be considered in all patients, especially young to improve cosmesis and reduce need for revision. a follow up article by this author looking at 24 months outcome reported that the 2 patients who chose for conservative management of their resorbed bone flaps changed their minds due to increasing postural headaches and another patient progressed from moderate to severe resorption needing revision. therefore, over the 24-month period, 25% of own bone cranioplasty required revision versus none in the titanium group (p 0.001)52. a recent systematic review and metaanalysis also reported similar finding of significantly increased revision rate with autologous cranioplasty primarily due to resorption, which was reported as 20% overall53. the article reported no significant difference in other complications including infection. our series reflects the findings of the randomised control trial and recent systematic review in that significantly greater revisions were needed with own bone cranioplasties. there were also greater number of complications overall as compared to the cranioplasty with custom-made titanium cranioplasty: longterm follow-up. acta neurochirurgica. 2018 may 1;160(5):88591. 53 malcolm jg, mahmooth z, rindler rs, allen jw, grossberg ja, pradilla g, ahmad fu. autologous cranioplasty is associated with increased reoperation rate: a systematic review and meta-analysis. world neurosurgery. 2018 aug 1;116:60-8. 33 autologous versus synthetic cranioplasty synthetic group. this raises the question of continuation of own bone cranioplasties and whether all patients should receive synthetic flaps. in our series the only statistically significant complication was extradural haematoma however the significance of this is uncertain. no previous study has highlighted a significant increase in post operative edh and this may be purely artefactual. no factors could be clearly identified in relation to this complication, including placement of drain which is routinely practiced regardless of cranioplasty material. one consideration for choice is cost of cranioplasty. in our unit, the storage cost of bone flaps are negligible and cost of theatre and ward stay are the same regardless of the choice of material. therefore there is a significant cost disparity between the groups and use of synthetic cranioplasty in all patients would increase costs for the unit. a formal cost analysis was not undertaken and when accounting for increased complication rates with autologous cranioplasty, the difference may not be significant. conclusions our study reflects results from previous publications showing increased revision rates with autologous cranioplasty as compared to synthetic materials. although there may be a cost implication, the increased risks should be strongly considered when deciding the best method of cranioplasty for any patient. in keeping with other recent publications, we would recommend synthetic cranioplasty should be favoured over autologous unless patient factors, cost implications or local resources influence otherwise. abbreviations 3d three-dimensional cp cryopreservation ct computed tomography dmso dimethyl sulfoxide edh – extra-dural haematoma mri magnetic resonance imaging peek polyetheretherketone sc subcutaneously stored spect single-photon emission computed tomography tbi traumatic brain injury references 1. abhay s, haines sj. repairing holes in the head: a history of cranioplasty. neurosurgery. 1997 mar 1;40(3):588-603. 2. archavlis e, nievas mc. cranioplasty after supratentorial decompressive craniectomy: when is the optimal timing. der nervenarzt. 2012 jun;83(6):751-8. 3. aydin s, kucukyuruk b, abuzayed b, aydin s, sanus gz. cranioplasty: review of materials and techniques. journal of neurosciences in rural practice. 2011 jul;2(2):162. 4. bates ji, reiners cr. the repair of cranial defects with zirconium: an experimental study. journal of neurosurgery. 1948 jul;5(4):340-8. 5. beck cs. repair of defects in skull by ready made vitallium plates. journal of the american medical association. 1942 mar 7;118(10):798-9. 6. beirne or, curtis ta, greenspan js. mandibular augmentation with hydroxyapatite. journal of prosthetic dentistry. 1986 mar 1;55(3):362-7. 7. bhaskar ip, yusheng l, zheng m, lee gy. autogenous skull flaps stored frozen for more than 6 months: do they remain viable?. journal of clinical neuroscience. 2011 dec 1;18(12):1690-3. 8. booth ja, curtis bf. i. report of a case of tumor of the left frontal lobe of the cerebrum; operation; recovery. annals of surgery. 1893 feb;17(2):127. 9. brommeland t, rydning pn, pripp ah, helseth e. cranioplasty complications and risk factors associated with bone flap resorption. scandinavian journal of trauma, resuscitation and emergency medicine. 2015 dec;23(1):75. 10. campbell e, meirowsky a, hyde g. studies on the use of metals in surgery. annals of surgery. 1941 sep;114(3):472. 11. cheng ch, lee hc, chen cc, cho dy, lin hl. cryopreservation versus subcutaneous preservation of autologous bone flaps for cranioplasty: comparison of the surgical site infection and bone resorption rates. clinical neurology and neurosurgery. 2014 sep 1;124:859. 12. courtemanche ad, thompson gb. silastic cranioplasty following cranio-facial injuries. plastic and reconstructive surgery. 1968 feb 1;41(2):165-72. 13. fan mc, wang ql, sun p, zhan sh, guo p, deng ws, dong q. cryopreservation of autologous cranial bone flaps for cranioplasty: a large sample retrospective study. world neurosurgery. 2018 jan 1;109:e853-9. 14. feroze ah, walmsley gg, choudhri o, lorenz hp, grant ga, edwards ms. evolution of cranioplasty techniques in neurosurgery: historical review, pediatric considerations, and current trends. journal of neurosurgery. 2015 oct;123(4):1098-107. 15. frame jw, brady cl. the versatility of hydroxyapatite blocks in maxillofacial surgery. british journal of oral and maxillofacial surgery. 1987 dec 1;25(6):452-64. 16. goel a, deogaonkar m. subgaleal preservation of calvarial flaps. surgical neurology. 1995 aug 1;44(2):1813. 34 arif zafar, samantha strickland, shailendra achawal 17. grant fc, norcross nc. repair of cranial defects by cranioplasty. annals of surgery. 1939 oct;110(4):488. 18. grossman n, shemesh-jan hs, merkin v, gideon m, cohen a. deep-freeze preservation of cranial bones for future cranioplasty: nine years of experience in soroka university medical center. cell and tissue banking. 2007 sep 1;8(3):243-6. 19. gurdjian es, webster je, brown jc. impression technique for reconstruction of large skull defects. surgery. 1943 dec 1;14(6):876-81. 20. häuptli j, segantini p. new tissue preservation method for bone flaps following decompressive craniotomy. helvetica chirurgica acta. 1980 jun;47(1-2):121-4. 21. hng d, bhaskar i, khan m, budgeon c, damodaran o, knuckey n, lee g. delayed cranioplasty: outcomes using frozen autologous bone flaps. craniomaxillofacial trauma & reconstruction. 2015 sep;8(3):190. 22. honeybul s, morrison da, ho km, lind cr, geelhoed e. a randomised controlled trial comparing autologous cranioplasty with custom-made titanium cranioplasty: long-term follow-up. acta neurochirurgica. 2018 may 1;160(5):885-91. 23. honeybul s, morrison da, ho km, lind cr, geelhoed e. a randomized controlled trial comparing autologous cranioplasty with custom-made titanium cranioplasty. journal of neurosurgery. 2017 jan;126(1):81-90. 24. inamasu j, kuramae t, nakatsukasa m. does difference in the storage method of bone flaps after decompressive craniectomy affect the incidence of surgical site infection after cranioplasty? comparison between subcutaneous pocket and cryopreservation. journal of trauma and acute care surgery. 2010 jan 1;68(1):183-7. 25. ingraham fd, alexander e, matson dd. polyethylene, a new synthetic plastic for use in surgery: experimental applications in neurosurgery. journal of the american medical association. 1947 sep 13;135(2):82-7. 26. iwama t, yamada j, imai s, shinoda j, funakoshi t, sakai n. the use of frozen autogenous bone flaps in delayed cranioplasty revisited. neurosurgery. 2003 mar 1;52(3):591-6. 27. joaquim af, mattos jp, neto fc, lopes a, de oliveira e. bone flap management in neurosurgery. revista neurociencias. 2009. 28. klinger dr, madden c, beshay j, white j, gambrell k, rickert k. autologous and acrylic cranioplasty: a review of 10 years and 258 cases. world neurosurgery. 2014 sep 1;82(3-4):e525-30. 29. krishnan p, bhattacharyya ak, sil k, de r. bone flap preservation after decompressive craniectomyexperience with 55 cases. neurology india. 2006 jul 1;54(3):291. 30. lake pa, morin ma, pitts fw. radiolucent prosthesis of mesh-reinforced acrylic. journal of neurosurgery. 1970 may;32(5):597-602. 31. leunig m, yuan f, berk da, gerweck le, jain rk. heating or freezing bone: effects on angiogenesis induction and growth potential in mice. acta orthopaedica scandinavica. 1996 jan 1;67(4):383-8. 32. lu y, hui g, liu f, wang z, tang y, gao s. survival and regeneration of deep-freeze preserved autologous cranial bones after cranioplasty. british journal of neurosurgery. 2012 apr 1;26(2):216-21. 33. malcolm jg, mahmooth z, rindler rs, allen jw, grossberg ja, pradilla g, ahmad fu. autologous cranioplasty is associated with increased reoperation rate: a systematic review and meta-analysis. world neurosurgery. 2018 aug 1;116:60-8. 34. malcolm jg, rindler rs, chu jk, chokshi f, grossberg ja, pradilla g, ahmad fu. early cranioplasty is associated with greater neurological improvement: a systematic review and meta-analysis. neurosurgery. 2017 apr 17;82(3):278-88. 35. malcolm jg, rindler rs, chu jk, grossberg ja, pradilla g, ahmad fu. complications following cranioplasty and relationship to timing: a systematic review and metaanalysis. journal of clinical neuroscience. 2016 nov 1;33:39-51. 36. malis li. titanium mesh and acrylic cranioplasty. neurosurgery. 1989 sep 1;25(3):351-5. 37. mayfield fh, levitch la. repair of cranial defects with tantalum. the american journal of surgery. 1945 feb 1;67(2):319-32. 38. mitchell ab. repair of injuries to the skull by perforated plates. british journal of surgery. 1917;5(17):40-1 39. morina a, kelmendi f, morina q, dragusha s, ahmeti f, morina d, gashi k. cranioplasty with subcutaneously preserved autologous bone grafts in abdominal wall— experience with 75 cases in a post-war country kosova. surgical neurology international. 2011;2. 40. morton rp, abecassis ij, hanson jf, barber jk, chen m, kelly cm, nerva jd, emerson sn, ene ci, levitt mr, chowdhary mm. timing of cranioplasty: a 10.75-year single-center analysis of 754 patients. journal of neurosurgery. 2017 aug 11;128(6):1648-52. 41. movassaghi k, ver halen j, ganchi p, amin-hanjani s, mesa j, yaremchuk mj. cranioplasty with subcutaneously preserved autologous bone grafts. plastic and reconstructive surgery. 2006 jan 1;117(1):202-6. 42. piitulainen jm, kauko t, aitasalo km, vuorinen v, vallittu pk, posti jp. outcomes of cranioplasty with synthetic materials and autologous bone grafts. world neurosurgery. 2015 may 1;83(5):708-14. 43. pompili a, caroli f, carpanese l, caterino m, raus l, sestili g, occhipinti e. cranioplasty performed with a new osteoconductive, osteoinducing hydroxyapatite-derived material. journal of neurosurgery. 1998 aug;89(2):23642. 44. pringle jh. remarks on the closure of gaps in the skull, with notes of cases. british medical journal. 1906 feb 3;1(2353):246. 45. punchak m, chung lk, lagman c, bui tt, lazareff j, rezzadeh k, jarrahy r, yang i. outcomes following polyetheretherketone (peek) cranioplasty: systematic 35 autologous versus synthetic cranioplasty review and meta-analysis. journal of clinical neuroscience. 2017 jul 1;41:30-5. 46. quah bl, low hl, wilson mh, bimpis a, nga vd, lwin s, zainuddin nh, wahab na, salek ma. is there an optimal time for performing cranioplasties? results from a prospective multinational study. world neurosurgery. 2016 oct 1;94:13-7. 47. roka yb. review of the history of materials used with experience with bone cement cranioplasty. nepal journal of neuroscience.;14(1):7-13. 48. shah am, jung h, skirboll s. materials used in cranioplasty: a history and analysis. neurosurgical focus. 2014 apr;36(4):e19. 49. shoakazemi a, flannery t, mcconnell rs. long-term outcome of subcutaneously preserved autologous cranioplasty. neurosurgery. 2009 sep 1;65(3):505-10. 50. simpson d. titanium in cranioplasty. journal of neurosurgery. 1965 mar 1;22(3):292-3. 51. torimitsu s, nishida y, takano t, koizumi y, hayakawa m, yajima d, inokuchi g, makino y, motomura a, chiba f, iwase h. effects of the freezing and thawing process on biomechanical properties of the human skull. legal medicine. 2014 mar 1;16(2):102-5. 52. xu h, niu c, fu x, ding w, ling s, jiang x, ji y. early cranioplasty vs. late cranioplasty for the treatment of cranial defect: a systematic review. clinical neurology and neurosurgery. 2015 sep 1;136:33-40. 53. yadla s, campbell pg, chitale r, maltenfort mg, jabbour p, sharan ad. effect of early surgery, material, and method of flap preservation on cranioplasty infections: a systematic review. neurosurgery. 2011 apr 1;68(4):112430. a. chirianc, giorgiana ion, z. faiyad, i. poeata doi: 10.33962/roneuro-2020-019 a giant occipital encephalocele. a case report m. al-zekri, f. aichaoui, a. khelifa, a. morsli romanian neurosurgery (2020) xxxiv (1): pp. 133-136 doi: 10.33962/roneuro-2020-019 www.journals.lapub.co.uk/index.php/roneurosurgery a giant occipital encephalocele. a case report m. al-zekri, f. aichaoui, a. khelifa, a. morsli department of neurosurgery, chu bab el oued, algiers, algeria abstract occipital encephalocele is a rare congenital anomaly that is characterized by herniation of brain tissue through a defect in the skull. because of their enormous size, they pose a surgical challenge. occipital encephalocele is the commonest of all encephalocele; the management of encephalocele defects requires immediate surgical closure. the author reports a case of a five months old female baby who presented a progressively increasing swelling over the occipital region. this swelling was present since birth. surgery was planned to reduce the size of the swelling as well as its contents. the sac was excised and reduced sufficiently enough to accommodate the healthy-looking brain tissue. this infant did well postoperatively. introduction an encephalocele is a congenital herniation of intracranial contents throughout a cranial defect. the intracranial contents which extrude to the exterior from the defect, may incorporate cerebrospinal fluid (csf), m e n i n g e a l s t r u c t u r e s , o r / a n d b r a i n t i s s u e ( 2 , 4 ) . o c c i p i t a l encephaloceles constitute 80 to 90% of all encephaloceles and occurs between the lambda and the foramen magnum, predominantly in the midline (1, 4, 5). in giant occipital encephaloceles the size of the swelling is larger than the size of the head from which they arise, and because of their enormous size they pose a surgical challenge (1, 3, 5). meningoencephalocele is diagnosed antenatally using sonography; it can achieve diagnostic accuracy in 80% of cases. other imaging modalities including: ct scan, mri (6) and the management of encephalocele defects requires immediate surgical closure (5). case presentation a five months female baby presented with progressively increasing swelling over the occipital region since birth. the baby was born at term from consanguineous marriage. on neurological examination the patient was conscious; in a general state preserved with a weight of 7 kg. she has a slight psychomotor delay with a closed anterior fontanel. local examination showed: an occipital encephalocele of large size, well epidermised, measuring 28 cm with relatively wide neck (fig.1). keywords encephalocele, dysraphism, spina bifida corresponding author: muneer al-zekri department of neurosurgery, chu bab el oued, algiers, algeria muneeralzekri30@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 134 m. al-zekri, f. aichaoui, a. khelifa, a. morsli magnetic resonance imaging (mri) of the brain showed a giant encephalocele at the occipital region with cerebral hernia and meninges across a large bone defect (fig.2 a, b). surgical treatment consists of the exclusion of the malformation while respecting the healthy brain tissue. the patient was put in lateral position; first, we reduced the volume of the sac by subtracting its cerebrospinal fluid (lcs) content; then, a circumferential incision was placed over the sac, and the neck was dissected out; after that, the sac was opened to expose nervous content. the resection of the sac and non-functional cerebral tissue was performed up to the limit of the healthy tissue visible next to the bone defect. in the end a watertight meningeal closure was done, with cutaneous and subcutaneous closure (fig. 3 a,b,c,d,e,f). the post-operative course was without complications. figure 1. preoperative picture showing massive occipital encephalocele. figure 2. preoperative t1 wi mri; a: sagittal, and b: transversal. figure 3. preoperative views; a: lcs extraction, b: incision over the sac, c: sac was then opened and exposure of its nervous content, d: resection of the sac, e: meningeal closure, f: cutaneous and subcutaneous closure. 135 a giant occipital encephalocele figure 4. postoperative picture. discussion encephaloceles are congenital anomalies of the central nervous system. they are protrusions of brain tissue. the cranial defect lead to the development of a sac with variable contents (2, 4, 7). the content of occipital encephalocele may include meninges, occipital lobes, or ventricles and rarely contain cerebellum, brainstem, or torcula. typically, bony defect may be only confined to only occipital bone or may descend down to involve defect of the posterior lip of foramen magnum and even up to the posterior arch of the atlas and accordingly divided into supra and infra torcular types (4,5). the size of occipital encephalocele may vary from small, large to giant and could be pedunculated or sessile (1). it may be associated with hydrocephalus; or other organs and extremities malformations. cortical dysplasia and corpus callosum agenesis are frequently present (4,5). encephaloceles account for 10 to 20% of all craniospinal dysraphisms and 80% of them are occipital. they are more common in female than male (1, 3, 5). encephalocele is believed to be multifactorial: genetic and environmental. genetic background may increase the risk of developing this condition. also, due to close relationship between encephalocele and neural tube defects, folate deficiency has been believed to play a role in the pathogenesis of encephalocele (6). these lesions are usually covered either with normal skin, dysplastic skin or a thin distorted meningeal membrane (3). the severity of mental retardation is higher and the prognosis is worse in cases neural aberrations asssociation. in a study supported by french et al. 17% of patients with encephaloceles had normal development, whereas severe mental retardation and physical delay were present in 83% of the patients (4). mri could reveal the exact anatomical description of the encephalocele and displaced brain structures; it also reveals the configuration of the brainstem regions. moreover, postnatal follow-up mri confirms the prenatal findings and shows additional morphological information such as vascular anatomy. furthermore, magnetic resonance angiography is the optimal investigation to visualize the relationship of the sac to the venous sinuses; while ct scans are used to detect the extent of cranial defect (6). patients with a large encephalocele are considered complicated cases because of csf leakage or difficulty in repositioning the viable extruded brain tissue inside the cranium without increasing intracranial pressure (4). further, torcula as a content poses a great challenge as its injury may lead to cerebral deep venous system thrombosis (5). surgery is indicated for esthetic goal, to avert the risk of rupture, csf leak, and meningitis. before incision, aspiration of csf may aid in the dissection of the sac, especially in large or giant encephalocele (5). the surgical intervention involves excision of the nonfunctional neural tissues hernia with dural repair. in case of a very large cerebral hernia, surgical treatment may be limited only to wide cranioplasty. intra-operatively, care must be taken to identify the contents of the sac. rarely, the sagittal sinus, torcula and transverse sinus are in the vicinity of the sac. major veins should be spared to prevent any venous infarction (8). in the postoperative period, the possibility of aggravation of hydrocephalus should be kept in mind and its occurring may need shunt surgery; about 60% of posterior encephalocele may develop hydrocephalus requiring surgical management (5). the factors of poor prognosis are microcephaly with neurological disorder and the importance of the nervous elements inside the sac including the brain, the cerebellum and the brainstem. conclusion encephaloceles are rare and complicated defects. it is associated with other congenital anomalies such as hydrocephalus, dandy–walker malformation, and microcephaly. its treatment like excision and repair when done in early age, greatly reduces 136 m. al-zekri, f. aichaoui, a. khelifa, a. morsli complications like csf leak, reduced iq level of the patients and other effects of associated anomalies are controlled in time. closed monitoring postoperatively is essential as the patient may developed hydrocephalus and required ventriculo-peritoneal shunt. references 1. h. d. nath, a. k. mahapatra, s. a. borkar: a giant occipital encephalocele with spontaneous hemorrhage into the sac: a rare case asian journal of neurosurgery vol. 9, issue 3, july-september 2014 doi:10.4103/17935482.142736. 2. lal rehman, ghulam farooq, irum bukhari: neurosurgical interventions for occipital encephalocele, rehman l, farooq g, bukhari i. neurosurgical interventions for occipital encephalocele. asian j neurosurg 2018; 13:233-7. 3. amit agarwal, aruna vijay chandak, anand kakani, shivshankar reddy: a giant occipital encephalocele agarwal a, chandak av, kakani a, reddy s. a giant occipital encephalocele. apsp j case rep 2010; 1:16 4. ashraf el badrya ,azza abdel azeez , ahmed abdelkhalek: microsurgical management results of occipital benha medical journal, vol. 35 no. 2, may-august 2018 5. guru dutta satyarthee, luis rafael moscote-salazar, nidia escobar hernandez, jose aquino-matus, paulo cesar puac-polanco, samer s hoz, willem guillermo calderon-miranda: a giant occipital encephalocele in neonate with spontaneous hemorrhage into the encephalocele sac: surgical management. j pediatr neurosci 2017; 12:268-70. 6. ahmed alwahab, adnan kharsa, alaa nugud and shomous nugud: occipital meningoencephalocele case report and review of current literature alwahab et al chinese neurosurgical journal (2017) 3:40, doi 10.1186/s41016-017-0104-5. 7. ashfaq ul hassan : a giant occipital encephalocele universal journal of applied science 1(1): 8-10, 2013 8. sim sk, theophilus sc, noor azman ar :surgical management of large occipital encephalocoele: a case report the international medical journal malaysia volume 13 number 2, dec 2014. doi: 10.33962/roneuro-2022-005 management of nontraumatic intracranial haemorrhage (subdural hematoma) in immune thrombocytopenia. case report d. balasa, al. tunas, v. stan, t. adam romanian neurosurgery (2022) xxxvi (1): pp. 28-29 doi: 10.33962/roneuro-2022-005 www.journals.lapub.co.uk/index.php/roneurosurgery management of nontraumatic intracranial haemorrhage (subdural hematoma) in immune thrombocytopenia. case report d. balasa1, al. tunas1, v. stan1, t. adam2 1 department of neurosurgery, clinical emergency hospital constanta, romania 2 department of haematology, clinical emergency hospital constanta, romania abstract intracranial haemorrhage is a devastating complication of immune thrombocytopenic purpura [1]. the occurrence of a spontaneous subdural hematoma in immune thrombocytopenia (itp) is rare [2], affecting 1% or less of patients [3]. in itp contrary to traumatic sdh the brain parenchyma is well preserved [3]. we present the case of a patient with immune thrombocytopenia, subdural haemorrhage and asymptomatic parietal parasagittal meningioma. neurological parameters were closely monitored, including the level of consciousness, pupillary size, motor or sensorial deficit. he was managed successfully medically (platelet-rich plasma and steroids) and then surgically (craniotomy, subdural hematoma aspiration). introduction we present tha case of a patient with imune thrombocytopenia intracerebral hemorhage and parietal parasagital meningioma. case report we present the case of a patient who suferred a head trauma in unccleared conditions. he acuse mild left hemiparesis (asia 4/5), intense headache vas 8/10, vomiting and diziness, from 3 days. few purpuric spots were noted on all the four members. medical datas revealed chronical itp, without continous treatment hemoglobine: 14,20 g/dl, tlc 4000/cm3. coagulation tests were normal. clinical exam revealed mild hemiparesis (asia 4/5), osteotendinous reflexes diminished on the left side, babinsky on the left side, purpuric lesions on all the four members. glasgow scale 15. ct scan of the head revealed hyperdensity in the subdural space in the temporo parieto occipital region on the right side, and in the subdural area in right posterior part of the sagital sinus,left parasagital meningioma. keywords hematoma, subdural, subarachnoid haemorrhage, idiopathic thrombocytopenic purpura corresponding author: balasa daniel department of neurosurgery, clinical emergency hospital constanta, romania balasadaniel100@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 29 management of nontraumatic intracranial haemorrhage (subdural hematoma) in immune thrombocytopenia l figure 1. temporoparietooccipital acute subdural hematoma (blue arrow). acute subdural interemispheric (falx cerebri) (pink arrow). parietal parasagital meningioma (orange arrow). the patient was treated with dexametazone 40 mg/day and platelet transfusion. after 4 days her platelet count rose to 130000/mm3 who allowed surgical intervention. clinical status was stationary : intense headache (vas 7/10), left hemiparesis (asia 4/5), vomiting 1-2/day, gcs 15. the patient was operated (frontotemporoparietoociipital craniotomy, complete evacuation of the subdural hematoma). figure 2. complete evacuation of the subdural hematoma clinical postoperative evolution was very good with healing of hemiparesis, of headache, vomiting and diziness. persisted only slight left pyramidal syndrome. discussion essential thrombocitopenia is revealed by constant diminution of the platelets without any cause. (denis, hayem, frank. ) itp was first described by werlhofin 17354 as an aquired disorder which leads to immune mediated destruction of platelets characterised by low platelet count and normal coagulation studies4. intracranial hemorrhage is a devastating complication of itp1,4. the occurence of a spontaneous subdural hematoma in immune thrombocytopenia (itp) is rare2, affecting 1-2% or less of patients3,4,5. the clinical features are mainly headache, hemiparesis, signs of raised intracranial tension, altered consciousness4. usually, subdural hematoma occurs, when are associatecd with itp around the the top and side of the frontal and parietal lobes, in the posterior cranial fossa, near the falx cerebri and tentorium cerebelli4 . conclusions medical treatment enabled us to achieve an adequate hemostasis wich was esential to be able to perform surgery in proper time. combination between medical treatment of imune thrombocitopenia and surgical treatment of acute subdural hematoma was mandatory for a good clininical and neurological evolution. references 1. pavithran k , thomas m management of subdural hematoma in imune thrombocytopenic purpura: report of seven patients and a literature review. clinical neurology and neurosurgery, vol 111, issue 2, february 2009, 189-192 2. mathews m h, yu w, chappell e t. spontaneous subdural hematoma in the setting of imune thrombocytopenia complicated by ischemis infarcts. neuroradiol j, 2007 apr 30 (2): 224-227. epub 2007 apr 30 3. sunitha r, mathew r, thomas m. conservative management of subdural hematoma in idiopathic thrombocytopenic purpura: report of two cases and review of the literature. ann indian acad neurol 2007; 10: 184-6 4. chatterjee s, karmakar ps, ghosh p, ghosh a. subdural hematoma associated with thrombocytopenic purpura in two different settings.the journal of the association of phisicians of india, 2010, vol 58, 504-506 5. meena a k, murthy j m. subdural haematoma in a patient with immune thrombocytopenic purpura. neurol india 1999;47:335. 6. brill n. e., rosenthal n. treatment by splenectomy of essential thrombocytopenia (purpura hemorrhagica). arch intern med (chic). 1923; 32 (6): 939-953. doi: 10.33962/roneuro-2022-059 coil migration during pressure-cooker technique for cerebral avm. a case report mustafa ismail, sura h. talib, sama albairmani, aktham o. al-khafaj, hosam al-jehani, samer s. hoz romanian neurosurgery (2022) xxxvi (3): pp. 350-354 doi: 10.33962/roneuro-2022-059 www.journals.lapub.co.uk/index.php/roneurosurgery coil migration during pressure-cooker technique for cerebral avm. a case report mustafa ismail1, sura h. talib2, sama albairmani3, aktham o. alkhafaj1, hosam al-jehani4, samer s. hoz5 1 department of neurosurgery, college of medicine, university of baghdad, iraq 2 al-mustansiriyah university, college of medicine, baghdad, iraq 3 al_iraqia university, college of medicine, baghdad, iraq 4 department of neurosurgery, king fahad hospital of the university, imam abdulrahman alfaisal university, dammam, saudi arabia 5 department of neurosurgery, university of cincinnati, cincinnati, oh, usa abstract introduction: in recent decades, the endovascular treatment of cerebral arteriovenous malformations (avms) has advanced. however, it still carries risks of unanticipated complications. coil migration is a reported complication of aneurysmal coiling procedures. herein, we report a case of early intraprocedural coil migration during pressure cooker technique embolization of right thalamic avm, discussing the management and potential explanations. the literature showed no report of coil migration after the pressure cooker technique in the form of coil-augmented onyx injection technique (cait). case description: an otherwise healthy 26-year-old female suddenly developed a severe headache with no loss of consciousness. computed tomography (ct) scan of the head illustrated intraventricular haemorrhage. magnetic resonance imaging (mri) showed the bag of worms' sign in the right thalamic area. the size and location of the avm prompted the decision for multistage endovascular embolization using onyx. in the anterior circulation, the right a5 arterial feeder has a high flow which indicates the pressure cooker technique embolization in the form of cait. in the procedure, early detachment and migration of the coil occurred in the medial prefrontal branch through the anterior cerebral artery. no intervention to retrieve the coil was carried out because the detachment piece is small and lodged distally. onyx was injected directly without the coil because of the risk of radiation to the patient. otherwise, the intraprocedural and postprocedural courses went uneventful. conclusion: this is the first report of coil migration during the pressure cooker technique with cait for the right thalamic avm. introduction therapeutic embolization of cerebral arteriovenous malformations (avms) was documented for the first time by luessenhop and spence in 1960 (3). since then, endovascular treatment has advanced keywords arteriovenous malformations, pressure cooker technique, endovascular embolization corresponding author: mustafa ismail department of neurosurgery, university of baghdad / college of medicine. baghdad, iraq mostafa.ismail1700d@comed. uobaghdad.edu.iq copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 351 coil migration during pressure-cooker technique for cerebral avm significantly in recent years, particularly for avms, and it is now utilized as a preoperative adjuvant before microsurgery or radiosurgery and as a curative option (11). however, this treatment still carries the potential for unanticipated complications (5,15). coil migration is a reported complication of aneurysmal coiling procedures with up to 6% of the cases (4). however, the literature showed no report of coil migration after the pressure cooker technique in the form of coil-augmented onyx injection technique (cait) or balloon-assisted embolization of avm. herein, we report a case of early intraprocedural coil migration during cait of right thalamic avm with a discussion about the management and potential explanation. case description an otherwise healthy 26-year-old female suddenly developed a severe headache which made her seek the private clinic. her initial glasgow coma scale (gcs) is 15/15 and muscle power grade 5 bilaterally on the medical research council of canada (mrc) scale. her initial computed tomography (ct) scan of the head illustrated intraventricular hemorrhage in the lateral ventricles. her magnetic resonance imagining (mri) showed the bag of worms’ sign in the right thalamic area. she was advised to undergo diagnostic catheter angiography, which showed right thalamic arteriovenous malformation with multiple arterial feeders from both anterior and posterior circulations (figure 1). the patient doesn’t have other associated abnormalities such as aneurysm, varix, stenosis, and steal phenomenon. figure 1. dsa with anteroposterior right internal carotid artery (ica) and its branches showing right thalamic avm with feeders from ipsilateral aca with onyx from the first embolization procedure. figure 2. dsa with the ap view of the right ica showing (a) the detached coil in the contralateral collosomarginal branch of the right aca (black arrow) with onyx from the previous embolization (red arrow). (b) the detached coil migrated more distally in the contralateral aca (black arrow) in the road map image. figure 3. dsa of ap view of right ica showing the coil migration in a distal branch of aca (back arrow). it also shows complete obliteration of the avm nidus with embolization of the arterial feeder from a5 (yellow arrow). the first stage embolization onyx is also noted (red arrow). note: the cma in this case is a segmented artery with the 2 segments originating separately from the pericallosal artery. the size and the location of the avm prompted the decision for multistage endovascular embolization using onyx. the first stage was performed through embolization of the posterior choroidal artery by passing through the posterior cerebral artery and utilizing onyx as the liquid emblazing agent. two weeks later, the second stage was contemplated. however, in the anterior circulation, the right a5 352 mustafa ismail, sura h. talib, sama albairmani et al arterial feeder has a high flow. right a5 feeder coiling was considered prior to the onyx to raise proximal resistance and facilitate plug formation, leading to improved reflux control and better distal penetration. all these steps are with the pressure cooker technique in the form of cait. balloonassisted embolization was one of the options, but the high cost of this method and lack of medical insurance in iraq make the utilization of this option unlikely. in the procedure, early detachment and migration of the coil occurred in the prefrontal medial branch through the contralateral callosomarginal branch of the anterior cerebral artery (aca) (figure 2). distal migration of the coil happened pre-onyx injection, and no intervention to retrieve the coil was carried out because the detachment piece is small and lodged distally (figure 3). onyx was injected directly without the coil because of the risk of radiation to the patient. postprocedural digital subtraction angiography (dsa) imaging exhibits 90% obliteration of the avm. otherwise, the procedure went uneventful. postprocedural examination showed gcs 15/15 and mrc grade 5 bilaterally. patient follow-up includes antiepileptic drugs, diagnostic catheter angiography three months after the second stage of embolization, and referral for gamma knife radiotherapy. discussion treatment of cerebral avms successfully is a major challenge (14). embolization has become more essential in the therapy of cerebral avms as endovascular materials and experience have improved (1). nidus reduction before surgery or radiosurgery, as well as curative embolization, are the two main goals of avm embolization. the goal of nidus reduction is to reduce operative difficulty and risk during surgical removal (18). curative embolization aims for the entire obliteration of the avms, and in the cases of partial occlusion, embolization can reduce the volume of the nidus, allowing radiosurgery to be attempted (10). similarly, while waiting for the delayed occlusion accomplished by radiosurgery, embolizing the feeding artery can lower the risk of hemorrhage (3,10). the pressure cooker technique as cait of avm and balloonassisted coiling has specific indications, which are highlighted with avm of high flow feeders and large caliber such as in the current report. cait, according to gao x et al has several advantages, including 1), the microcatheter used for coil infusion is far more navigable than the balloon, 2), the coil can provide sufficient proximal resistance to enable plug formation and obtain better distal penetration, allowing more onyx to be injected from a single feeding pedicle while reducing procedure time and radiation exposure (8). in our case, cait was used because, in the anterior circulation, right a5 was a high flow feeder. in addition, balloon-assisted coiling was off the choice because healthcare insurance in iraq is immature, making costs significantly elevated for the patient. the hemodynamics of the avm in the arterial system is working as a suction device in which the majority of the flow is in the direction of the main feeder. when the navigation is performed by microwire, microcatheter, or coiling, it is easy to carry out within the flow of the main feeder as it has negative pressure. in our case, the presence of the microcatheter in the proximal part of the feeder (in our case, right aca) may result in a decrease in the feeder’s flow and a change in the hemodynamics of the avm, which was apparent in the migration of the coil in the contralateral aca. this could be unexpected if the hemodynamics of the avm is unchanged and all pressure is within the nidus direction. avm embolization can result in significant treatment-related morbidity and mortality (6). complication rates associated with avm embolization have been observed to range from 5% to 15% (7). according to a recent meta-analysis by van beijnum et al., complications after avm embolization resulted in irreversible neurological impairments or death in 6.6 percent (range 0–18 percent) of patients (16). after 846 embolizations in 408 individuals, baharvahdat et al. observed an 11 percent procedural complication rate. after embolization, 7.6% and 1.6 percent of patients, respectively, reported persistent, new impairment and mortality due to hemorrhage (2). in addition, coil migration is a potential complication in cait in the avm, which was not reported in the literature yet. in the present report, coil migration occurred pre-onyx injection and migrated distally to the prefrontal medial branch through the contralateral callosomarginal branch of aca. however, the patient was assessed clinically and radiologically 353 coil migration during pressure-cooker technique for cerebral avm intraoperatively, which was unremarkable, and stayed asymptomatic through the follow-up period. our experience in coil migration in terms of classification is based on general principles mainly derived from the studies in aneurysmal coiling. migration can be categorized into acute procedure migration and delayed postprocedural migration depending on the time the migrated coil was identified (1). coil migration found after the coiling technique was completed is referred to as delayed migration (1,12). the period between endovascular coiling and detection of the migrating coil should be noted. the location of the migrated coil is classified as proximal or distal. the mentioned classifications are more related to the endovascular coiling in aneurysms, but the general principle can be applied to the cait of the avm. although, in cait of avm with high caliber and flow feeders, as in the case, the potential migration of the coil after its detachment may occur before or after the onyx injection, and the migration was acute procedural with distal migration. in general, coil migration management differed depending on the timing of migration (acute or delayed), the location of the migrated coil (proximal or distal), the target vessel's patency, and the vascular territory's eloquence (1,4). when a migrated coil relocates intraprocedurally, lodges in a proximal or eloquent position, and/or there is a concomitant accessible vascular obstruction, migrated coil retrieval should be performed endovascularly or by open surgery (9,17). in contrast, distal migration requires conservative treatment (1,13). in the present report, the management of coil migration depends on the principles that were extracted mainly from the literature on aneurysmal coiling. in avm with high vessel caliber and increased flow feeders, as in the current study, distal migration was managed conservatively. otherwise, early assessment of the patient within the procedure and after the procedure, along with early intervention, may lead to better management of the patient’s condition. in summary, endovascular embolization by cait may result in size reduction in avm nidus or complete obliteration, especially for the arterial feeder with the high flow as in our case. we report a case of coil migration in cait of avm. in this report, contralateral aca distal coil migration was managed conservatively. conclusions coil migration is a rare complication in aneurysms. this report is the first case of coil migration during the pressure cooker technique with cait for the right thalamic avm. references 1. abdalkader m, piotin m, chen m, ortega-gutierrez s, samaniego e, weill a, norbash am, nguyen tn. coil migration during or after endovascular coiling of cerebral aneurysms. journal of neurointerventional surgery. 2020 may 1;12(5):505-11. 2. baharvahdat h, blanc r, termechi r, pistocchi s, bartolini b, redjem h et al. hemorrhagic complications after endovascular treatment of cerebral arteriovenous malformations. ajnr am j neuroradiol. 2014 may;35(5):978–83. 3. bruno ca jr, meyers pm. endovascular management of arteriovenous malformations of the brain. interv neurol. 2013;1(3-4):109-123. 4. ding d, liu kc. management strategies for intraprocedural coil migration during endovascular treatment of intracranial aneurysms. j neurointerv surg 2014;6:428–31. 5. duckwiler gr, dion je, viñuela f, reichman a. delayed venous occlusion following embolotherapy of vascular malformations in the brain. ajnr am j neuroradiol. 1992;13:1571–1579. 6. ellis ja, lavine sd. role of embolization for cerebral arteriovenous malformations. methodist debakey cardiovasc j. 2014;10(4):234-239. doi:10.14797/mdcj-104-234 7. friedlander rm. clinical practice. arteriovenous malformations of the brain. new engl j meditor. 2007 jun 28;356(26):2704–12. 8. gao x, liang g, li z, et al. transarterial coil-augmented onyx embolization for brain arteriovenous malformation. technique and experience in 22 consecutive patients. interv neuroradiol. 2014;20(1):8390. 9. gatto la, rocha lb, koppe gl, demartini jr z. late coil migration after embolization of cerebral aneurysms–case series. arquivos brasileiros de neurocirurgia: brazilian neurosurgery. 2018 mar;37(01):71-5. 10. katsaridis v, papagiannaki c, aimar e. curative embolization of cerebral arteriovenous malformations (avms) with onyx in 101 patients. neuroradiology. 2008;50(7):589–597. 11. luessenhop aj, spence wt. artificial embolization of cerebral arteries. report of use in a case of arteriovenous malformation. jama. 1960;172:1153–1155. 12. maeda k, motoie r, karashima s, otsuji r, ren n, nagaoka s, ikai y, uno j, gi h. a case of delayed distal coil migration after coil embolization of an unruptured distal azygos anterior cerebral artery aneurysm: a case report 354 mustafa ismail, sura h. talib, sama albairmani et al and literature review. interv neuroradiol. 2018 dec;24(6):643-649. 13. phatouros cc, mcconachie ns, jaspan t. post-procedure migration of guglielmi detachable coils and mechanical detachable spirals. neuroradiology 1999;41:324–7. 14. richling b, killer m, al-schameri ar, et al. therapy of brain arteriovenous malformations: multimodality treatment from a balanced standpoint. neurosurgery. 2006;59(5) suppl 3:s148–157. 15. sipos ep, kirsch jr, nauta hj, debrun g, ulatowski ja, bell wr. intra-arterial urokinase for treatment of retrograde thrombosis following resection of an arteriovenous malformation. case report. j neurosurg. 1992;76:1004– 1007. 16. van beijnum j, van der worp hb, buis dr, al-shahi salman r, kappelle lj, rinkel gj et al. treatment of brain arteriovenous malformations: a systematic review and meta-analysis. jama. 2011 nov 9;306(18):2011–9. 17. viñuela f, duckwiler g, mawad m. guglielmi detachable coil embolization of acute intracranial aneurysm: perioperative anatomical and clinical outcome in 403 patients. j neurosurg 2008;108:832–9. 18. weber w, kis b, siekmann r, et al. preoperative embolization of intracranial arteriovenous malformations with onyx. neurosurgery. 2007;61(2):252–254. microsoft word 13hozsamer_adoughnut 622 | hoz et al treatment options for intracranial doughnut-shape aneurysm             doi: 10.2478/romneu-2018-0080 a doughnut in the brain: an overview of the pathophysiology and the current treatment options for intracranial doughnut-shape aneurysm s.s. hoz1, l.r. moscote-salazar2 1department of neurosurgery, neurosurgery teaching hospital-baghdad, iraq 2department of neurosurgery, latin-american neurotrauma and neurocritical care (red latino), bogota, colombia key words: doughnut aneurysm, giant aneurysm, outflow occlusion, partially thrombosed aneurysm giant aneurysms, those larger than 25 mm in diameter, are relatively uncommon and are often accompanied by thrombosis (1). doughnut‑shaped aneurysms are giant round‑shaped aneurysms composed of an intraluminal thrombus and marginal parent arteries (2). doughnut-shaped aneurysms are rare subtype of partially thrombosed giant aneurysms and account for ≤1% of large/giant aneurysms (2,3). pathophysiology: the doughnut-shaped aneurysms formed when the aneurysm geometry and flow conditions result in circular laminar flow (4). this type of aneurysm constitutes of 3 parts: the inflow artery, outflow artery and a central thrombosed part which is already excluded from circulation. disruption of flow (slow flow) within the aneurysm results in progressive thrombosis and exclusion from the intracranial circulation (5). horowitz et al. described a mathematical model showing the intraluminal pressure changes that might be expected following outflow occlusion (6). they reported that the resulting variations in pressure should be less than those induced by normal daily activities and concluded that outflow occlusion would not be expected to increase the risk of an aneurysm rupture (1). on imaging, rooij et al describe the ‘donut sign’ on angiography, with the central filling defect which is the doughnut hole represent the intraluminal thrombus and is responsible for the donut-shaped appearance seen at angiography (4). treatment options: optimal management of giant doughnut‑shaped aneurysms has not yet been established. in contrast to the usual saccular aneurysm, giant doughnut‑shaped aneurysms have separate inflow and outflow vessels; therefore, clipping the aneurysmal neck is romanian neurosurgery (2018) xxxii 4: 622 624 | 623             unsuitable (1). given its rarity and unusual appearance, the best treatment approach for this type of aneurysm has not been well established (5). the treatment options include: 1. complete obliteration of the aneurysm lumen with or without resection (7). 2. outflow occlusion with distal revascularization (1). 3. proximal occlusion (8). 4. endovascular coil embolization (5). 5. endovascular flow diversion (5). although complete obliteration of the aneurysm lumen with or without resection is an ideal treatment for such complex aneurysms, for some cases, it is difficult to achieve trapping and distal revascularization during surgery (7). outflow occlusion with distal revascularization could be an effective surgical option for such a unique aneurysm. for some cases, trapping of the involved segment with or without distal bypass is recommended (1,6). bypass surgery to treat distal aca aneurysms can be categorized as intracranial–intracranial (ic–ic) and extracranial–intracranial (ec– ic) types. ic–ic bypasses include in situ bypass, reanastomosis, reimplantation, and bypass with graft placement. ic–ic bypass has several advantages. ic–ic bypass could provide enough hemodynamics to the target region without additional blood flow (1). furthermore, ic–ic bypass do not require secondary incision and graft harvest. however, ic–ic bypass also has disadvantages. this maneuver is technically challenging in the narrow and deep working space in the interhemispheric fissure. in addition, if a bypass fails and occludes, both distal arterial territories could develop serious ischemia (1). proximal occlusion is also considered to be suitable for cases with surgical difficulty of trapping because proximal occlusion for aneurysms is believed to reduce the hemodynamic burden of the aneurysm, promote complete thrombosis in the aneurysm sac, and reduce the size of the aneurysm (8). recently, endovascular treatment has shown good results for large and giant aneurysms. however, the usefulness of coil embolization for partially thrombosed giant aneurysms remains controversial because of coil compaction and/or migration into the thrombus (1). endovascular coil embolization is typical for some cases but the technical difficulty limits its application in most of the circumstances (5). endovascular flow diversion has been shown to be an effective alternative to coil embolization of intracranial aneurysms (5). however, while effective in treating intracranial aneurysms, flow diverter stents are associated with procedurerelated complications (9). partially thrombosed aneurysms in particular have a high recurrence rate of up to 75%, with larger aneurysms having a worse prognosis (10). limited published experience with donut aneurysms suggests they are also prone to recurrence (4). conclusion the treatment of partially thrombosed giant (doughnut) aneurysm is critical and should be individualized case by case putting in mind the above surgical and endovascular options. 624 | hoz et al treatment options for intracranial doughnut-shape aneurysm             references 1.ito h, miyano r, sase t, wakui d, matsumori t, takasuna h et al. outflow occlusion with a3-a3 anastomosis for a doughnut-shaped partially thrombosed giant a2 aneurysm. surgical neurology international. 2016;7(42):1069. 2.rosta l, battaglia r, pasqualin a, beltramello a, italian cooperative study on giant intracranial aneurysms: 2. radiological data. acta neurochir suppl 1998;42:53‑9. 3.ogawa t, okudera t, noguchi k et al (1996) cerebral aneurysms: evaluation with three-dimensional ct angiography. ajnr am j neuroradiol 17:447–454. 4.van rooij sb, bechan rs, markenstein je, et al. the donut sign: a new angiographic sign for partially thrombosed aneurysms with flow-induced intraluminal thrombus. intervent neuroradiol 2014; 20: 55–59. 5.cholet c, mathon b, law-ye b. rare intracranial donut aneurysm. world neurosurgery. 2017;103:950.e1950.e3. 6.horowitz mb, yonas h, jungreis c, hung tk, management of a giant middle cerebral artery fusiform serpentine aneurysm with distal clip application and retrograde thrombosis: case report and review of the literature. surg neurol 1994;41:221‑5. 7.day al, gaposchkin cg, yu cj, rivet dj, dacey rg jr., spontaneous fusiform middle cerebral artery aneurysms: characteristics and a proposed mechanism of formation. j neurosurg 2003;99:228‑40. 8.hoh bl, putman cm, budzik rf, carter bs, oglivy cs, combined surgical and endovascular techniques of flow alteration to treat fusiform and complex wide‑necked intracranial aneurysms that are unsuitable for clipping or coil embolization. j neurosurg 2001;95:24‑35. 9.alderazi y, shastri d, kass-hout t, prestigiacomo c, gandhi c. flow diverters for intracranial aneurysms. stroke research and treatment. 2014;2014:1-12. 10.ferns s, van rooij w, sluzewski m, van den berg r, majoie c. partially thrombosed intracranial aneurysms presenting with mass effect: long-term clinical and imaging follow-up after endovascular treatment. american journal of neuroradiology. 2010;31(7):11971205. doi: 10.33962/roneuro-2020-073 supratentorial pnet in a geriatric patient. a rare differential diagnosis leading to diagnostic dilemma hrushikesh kharosekar, laxmikant bhople, reshma pujara, smita ranveer romanian neurosurgery (2020) xxxiv (1): pp. 452-454 doi: 10.33962/roneuro-2020-073 www.journals.lapub.co.uk/index.php/roneurosurgery supratentorial pnet in a geriatric patient. a rare differential diagnosis leading to diagnostic dilemma hrushikesh kharosekar1, laxmikant bhople2, reshma pujara3, smita ranveer4 1 associate professor, dept of neurosurgery, sir j. j. group of hospitals and grant medical college, mumbai, india 2 assistant professor, dept of neurosurgery, sir j. j. group of hospitals and grant medical college, mumbai, india 3 consultant anaesthesiologist, oscar hospital, thane, india 4 consultant pathologist, radiance pathology laboratory, thane, india abstract supratentorial pnets are most commonly seen in children and rarely seen in adults. pnet show a proliferation of undifferentiated or poorly differentiated neuroepithelial cells and, thus, are histologically similar to medulloblastomas. they account for approximately 2.5% of brain tumours in children and only 0.4% in adults. prognosis is poor in the pediatric age group while it shows favourable prognosis in adults. in literature, less than 100 cases of adult pnet have been reported till date with mean age of 35years. pnet in the geriatric age group is rarely been reported. introduction the term of primitive neuroectodermal tumor (pnet) was coined by hart and earle in 1973 for small round cell tumors with high malignant potential and affecting both the central and peripheral nervous systems. pnets show a proliferation of undifferentiated or poorly differentiated neuroepithelial cells and, thus, are histologically similar to medulloblastomas. world health organization (who) described supratentorial pnets as cerebral or suprasellar embryonal grade iv tumor with capacity to display differentiation along neuronal, astrocytic, ependymal, muscular or melanocytic lines. these tumors are most commonly seen in children and rarely seen in adults. they account for approximately 2.5% of brain tumors in children and only 0.4% in adults. prognosis is poor in pediatric age group while in shows favorable prognosis in adults. (1) in literature less than 100 cases of adult pnet have been reported till date with mean age of 35years. pnet in geriatric age group is rarely been reported. (2) keywords pnet, geriatric, diagnostic corresponding author: hrushikesh u. kharosekar dept of neurosurgery, sir j. j. group of hospitals and grant medical college, mumbai, india hkharosekar@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 453 supratentorial pnet in a geriatric patient case we had a 67-year-old male patient presented to us with sudden onset severe headache and vomiting for 1 day, patient was drowsy on examination. his ct scan of brain with contrast was suggestive of a large ,5*4*3 cm, well circumscribed lesion in right temporal lobe with perilesional edema. lesion was minimally enhancing on contrast with isodense centre. as patient was drowsy, he underwent emergency craniotomy with near total excision of lesion. small part of lesion which was invading the basal ganglia was left behind as seen on postoperative ct scan. post operatively patient improved in consciousness and was discharged on 7th postoperative day without any deficits. histopathology was suggestive of highly cellular lesion with nests, cords and sheets of tumor cells with high n/c ratio. hyperchromatic nuclei, inconspicuous nucleoli and brisk mitoses was seen. on ihc, tumor cells were positive for cd99, cd 56 and vimentin, gfap negative, ki-67 ratio was high (60-70%), suggestive of pnet (intracranial central). patient was advised post-operative radiotherapy and chemotherapy. 454 hrushikesh kharosekar, laxmikant bhople, reshma pujara et al. discussion primitive neuroectodermal tumors (pnets) include a group of tumors, thought to originate from undifferentiated neuroepithelial cells, that are commonly seen in pediatric patients and rare in adults. hart and earle described the term of primitive neuroectodermal tumor – pnet – in 1973 originally for cerebral high-grade undifferentiated neuroepithelial tumor of childhood, rarely demonstrating focal differentiation along glial and neuronal lines. this term was soon generalised for undifferentiated embryonal tumors of all cns sites and all ages by rorke in 1983. pnets may occur in almost any location within or outside the central nervous system. pnets seen outside the cns are termed as peripheral pnets (ppnet). cns pnet and ppnet are two different entities with different immunohistochemical profiles and genetics. clinically both are aggressive tumors, but show different local manifestation and metastatic spread. cns pnets can be further divided into 2 types: infratentorial tumors (medulloblastoma) and supratentorial tumors (spnets). all these tumor types are rare in adults. (1,2) intracranial pnets are uniformly distributed in the frontal lobe, temporal lobe, and parietal lobe and they are more than 6cm in size. intracranial pnets are further divided into central and peripheral according to their location with peripheral variety carrying a better prognosis. accordingly, it is essential to differentiate between the two types. chromosomal translocation of chromosome (11;22) is unique to central and not seen in peripheral pnets. immuno-histochemical assay for cd99 and fluorescence in situ hybridization (fish) assay for the (11;22) translocation are specific for central pnet.(2,3) the exact protocol for treatment of pnet is not clearly defined yet. so as per patient’s clinical status, complete tumor excision, chemotherapy, and radiotherapy are performed as standard procedures like any other intracranial tumors. prognosis of patients with pnet differs according to age. pediatric age group carries poor prognosis with older age appears to be have favorable prognosis. unfortunately, the 5-year survival in case of cns pnet remains to be less than 50% in all age groups. (1,2) conclusion the diagnostics and treatment protocol of primitive neuroectodermal tumors does not differ from other types of the central nervous system tumors. complete tumor excision, chemotherapy, and radiotherapy are performed as a treatment standard with better survival prognosis in old age. so even though very rare in older age group pnet should be kept as one of differential diagnosis as it carries better prognosis in this age group. a cd99 and fish assay for the (11;22) translocation (unique to central and not peripheral pnets) should be conducted in order to distinguish between intracranial peripheral and intracranial central pnets, as peripheral pnet carries better prognosis. references 1. virginija ašmonienė et al. a primary primitive neuroectodermal tumor of the central nervous system in a 51-year-old woman: a case report and literature review. medicina (kaunas) 2011;47(8):440-5. 2. lawandy et al. supratentorial primitive neuroectodermal tumor in an adult: a case report and review of the literature. journal of medical case reports 2012, 6:361. 3. he et al. a primitive neuroectodermal tumor in an adult case report of a unique location and mri characteristics. medicine (2018) 97:7. microsoft word 20tratat 666 | short review of “principiile chirurgiei neurologice”, 4th edition             short review of “principiile chirurgiei neurologice”, 4th edition editors: ellenbongen rg, sekhar ln, kitchen nd, elsevier 2018 first romanian edition, coordinated by prof. ioan ștefan florian m.d., at hipocrate publishing house the three princeps authors, well known in the neurosurgery world, ellenbongen rg, sekhar ln, kitchen nd, have the merit of publishing this monography, comprising the experience of an entire team of neurosurgeons, radiologists, radiotherapists, geneticists, anesthetists, from the united states but also from canada, australia, brazil and great britain. the publishing of a complete monography in any specialisation is not only obligatory, but well necessary. such world wide recognized monographies have appeared everywhere in medical literature, like „harrison's principles of internal medicine” (originally published in 1950) for internal medicine. in neurosurgery, for years, the specialised literature was dominated by the successive publishing of „youman’s neurological surgery” (originally published in 1973). the same happened in pediatric neurosurgery and, even today, a. leland albright and his collaborators` works, especially „principles and practice of pediatric neurosurgery” (originally published in 1999), in various editions, have been the conduite guides in this discipline, detailing some particularities related to pediatric age. the neurosurgery treatise was named in the classic tradition „principles of neurological surgery”, the 4th edition (editors: ellenbongen rg, sekhar ln, kitchen nd, elsevier 2018), first romanian edition coordinated by prof. dr. ioan ștefan florian at hipocrate publishing house. it constitutes a modern, contemporary and novel view on neurosurgical pathology. the first edition of the "principles of neurosurgery" (elsevier publishing house) originally published in 1993 by setti s. rengachary as first author, later joined by robert h. wilkins. the authors framed their work under the precise denomination „principles of neurological surgery”. the material in the 4th edition addresses especially neurosurgery romanian neurosurgery (2018) xxxii 4: 666 668 | 667             residents, practitioners, but also all the medicine students with inclinations for neurosciences. the three authors are renowned both for their extremely precise written works in neurosurgery, but also for their numerous neurosurgical interventions they developed over time, with personal upgrades and procedures. considering all of the above, the president of the romanian society of neurosurgery, with the support of hipocrate publishing house, appreciated that the romanian society of neurosurgery and all the practitioners in this field should possess the principles of neurosurgery in romanian, in order to study in depth the clinical and operative details of the challenging neurosurgical pathology. considering, furthermore, that often the information in english is not perfectly assimilated, the coordinator of this edition in romanian, prof. dr. ioan ștefan florian, made the translation as correct and appropriate as possible. moreover, some chapters were revised by specialised translators so that nothing unclear or interpretable would appear, especially not in the operative procedures. the treatise „principiile chirurgiei neurologice” has 9 parts: part 1 general considerations; part 2 pediatric neurosurgery; part 3 vascular neurosurgery; part 4 cranial-cerebral trauma; part 5 spine and medulla pathology; part 6 intracranial tumors; part 7 radiosurgery and radiotherapy; part 8 functional neurosurgery. pain; part 9 refers to several issues that were not covered in the previous parts, such as the pathology of peripheral nerves. each chapter is structured beginning with several clinical notes, then a framing of the issue, its history, its epidemiology, genetic and etiological factors, anatomical-pathologic observations, clinical diagnostics evaluation and imagery; after that, the surgical procedures are described thoroughly, with operative timing, advantages and disadvantages for every procedure, then results, complications and future progress. the bibliography at the end of each chapter is carefully selected and comes mainly from actual data. as a whole, this monography firstly answers the major challenges of the specialists in this field regarding the correct diagnosis, and secondly it gives the recommended operative procedures of today. the romanian edition „principiile chirurgiei neurologice”, coordinated by prof. dr. ioan ștefan florian, published at hipocrate publishing house (translation of the 4th edition in english edited by ellenbongen rg, sekhar ln, kitchen nd, elsevier 2018), supported by fundația transilvania leaders, is extremely interesting, clear and efficient, with an exceptional scientific and educational quality. the translation of the documents was the result of a collective effort attended by 58 physicians, alongside highly experienced teachers from all traditional university centers, including resident physicians with major inclinations for english language, for whom this approach was an intense educational exercise. 668 | short review of “principiile chirurgiei neurologice”, 4th edition             reading the treatise in detail we see that the main topics in neurosurgery pathology are discussed, but some modern elements as well, such as the endovascular treatment of vascular cerebral malformations. furthermore, radiotherapy and radiosurgery are also thoroughly discussed, with a focus on the recent aspects of proton therapy. the image-guided neurosurgery procedures are detailed and explained very clearly and very educationally, which contributes to a deeper understanding of the value and importance of image-guided surgery by magnetic resonance when diagnosticating neurosurgical traumas, in preor postoperative. the first chapter is extremely interesting and is dedicated entirely to the history of neurosurgery, starting from the first trepanations and leading to more and more sophisticated approaches. the many progresses in this difficult field are all presented in short. furthermore, this monography is also an efficient guide book for extremely difficult cases, complications or malpraxis in neurosurgery, with medical-legal interpretations. the presentation of each chapter is extremely clear, with exceptional illustrations, demonstrating the professionalism and dedication of the 3 authors, exceptional neurosurgical personalities. the monograph is done in nearly 900 pages, with an alphabetical index of pathology at the end. we consider this neurosurgery treatise is edited at an international level by a complex team from the united states and great britain and also other personalities from different parts of the world, and as such it deserves a place on the main shelf of neurosurgical and adjacent specialties education (neurology, psychiatry, anesthesia etc.). the effort of the entire team of neurosurgery residents in romania, coordinated by prof. dr. ioan ștefan florian, in translating this book contributes immensely to the upgrade of the neurosurgical knowledge in this country. most of all, publishing this treatise in romanian represents a great opportunity for the neurosurgery experts in this country to have access to a modern and renowned international neurosurgical treatise. andreea-anamaria idu, md, phd student ,“carol davila” university of medicine and pharmacy, neurosurgery resident, emergency university hospital of bucharest, romania prof. alexandru-vlad ciurea, md, phd, msc, dr. h. c. mult., sanador medical center, bucharest, romania romanian neurosurgery (2019) xxxiii, 1: 52-54 doi: 10.33962/roneuro-2019-009 www.journals.lapub.co.uk/index.php/roneurosurgery ossification of the yellow ligament in thoracic spine: a case report aydin kazempour azar1, javad aghazadeh1, firouz salehpoor1, amir rezakhah1, amir kamalifar1, saber ramezanpour1, samar kamalifar2 1 department of neurosurgery, school of medicine, nazlou campus, urumia university of medical sciences, urumia, iran 2 department of anatomy, school of medicine, arak university of medical sciences, arak, iran abstract ossifications of yellow ligament (oyl) and calcification of yellow ligament are relatively rare clinical entities, and can make sever morbidity surgical evaluation can relived the sign and symptom and improve life quality we present a patient with ossification of yellow ligament in level of t9 and t10 of thoracic spin. case presentation a 54 years old woman with chief complaint of back pain and lower limbs paraesthesia from 9 month ago, past medical history was negative and in drug history only she used pain relief agent like nsaids or acetaminophen in clinical evaluation upper motor neurons sign is positive ( plantar reflex double extensor , deep tendon reflex in knee and achile reflex significantly increased +4 ) and no episode of bladder or anal dysfunction , in mri of thoracic we found stenosis in level of t9t 10 from posterior element compression ,extradural lesion which was isosignal in t1 hypo signal in t2 without enhancement with gadolinium( figure 1) , for future evaluation ct of vertebral column with 3d reconstruction show a tiny ossification in interlamina space which bulged to central canal ( figure 2 ) ,patient admitted to operation room in prone position under general anaesthesia standard laminectomy was done bony yellow ligament was removed thecal sac was decompressed , 2 days after surgery patient discharged back pain and paraesthesia was improved after 3 month lower limbs muscles strong before and after surgery was 5/5 upper motors sign improve immediately a day after surgery discussion a symptomatic oyl usually is located at the lower thoracic spine (38.5%) and the lumbar spine (26.5%) and is rare at the cervical spine (0.9%) (3). the detailed mechanism of oyl is unclear. there are several keywords yellow ligament, thoracic spin, canal stenosis corresponding author: amir kamalifar department of neurosurgery, school of medicine, nazlou campus, urumia university of medical sciences, urumia, iran amirkamalifar@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 53 ossification of the yellow ligament in thoracic spine: a case report there are several reports that support the relationship between the growing factors of these ossification diseases and static and dynamic factors. (4,5) the pathophysiology of oyl is similar to that of yl hypertro¬phy. degeneration of the yl is due to hyper mobility of the poste¬rior column, which results in collagen hyperplasia and hypertro¬phy of the yl (5). subsequent deposition of calcium pyrophosphate dehydrates and calcium hydroxyapatite occurs in the ligament, resulting in oyl (6). the pathology of yl hypertrophy includes fibro cartilaginous changes due to proliferation of type ii collagen, ossification, and calcium crystal deposition, degeneration of collagen and elastic fibers, and chondroid metaplasia of ligament fi¬broblasts .(6,7) ossification of the spinal ligament is characterized by heterotrophic bone formation in the spinal ligaments, which are normally composed of fibrous tissue chondroid metapla¬sia in yl hypertrophy appears to play a pivotal role in ligament ossification, as cartilage differentiation, hypertrophy, and cell death are followed by bone formation in the bone morphogenetic pathway(7). ct and mri are useful tools for diagnosis, surgical planning, and evaluation of surgical prognosis. reconstructed 2dimensional and 3-dimensional ct images visualize the ossified lesion in all directions, which clarifies the actual shape and extent of oyl and opll and contributes to surgical planning surgical treatment for symptomatic oyl and opll is recommended. posterior decompression by partial laminectomy or laminoplasty with removal of oyl is effective for cases. (8,9). in this case posterior decompression of spinal canal with standard laminectomy was done patient pain was improved immediately after the surgery and muscle force was improver after 3 month and tendon reflex and upper motor singe disappeared after surgery, the location of the pathology in lower thoracic similar to usual site of this pathology. ethical considerations compliance with ethical guidelines all steps of this research were reviewed by urmia university of medical sciences, ethical committee, with ethical code of 43256/43269. funding this article was supported by urmia university of medical sciences. figure 1: t 2 sequence of thoracic mri sagital and axial view, hypo signal extradural lesion which compress the thecal sac from posterior 54 a. chirianc, giorgiana ion, z. faiyad, i. poeata references 1. 1. guo jj, luk kd, karppinen j, yang h, cheung km. prevalence, distribution, and morphology of ossification of the ligamentum flavum: a population study of one thousand seven hundred thirty-six magnetic resonance imaging scans. spine phila pa; 35:51-56. 2010. 2. inamasu j, guiot bh. a review of factors predictive of surgical outcome for ossification of the ligamentum flavum of the thoracic spine. j neurosurg spine; 5:133-139. 2006. 3. al-orainy ia, kolawole t: ossification of the ligament flavum. eur j ra¬diol 29: 76-82, 1998. 4. baur st, mai jj, dymecki sm: combinatorial signaling through bmp receptor ib and gdf5: shaping of the distal mouse limb and the genetics of distal limb diversity. development 127: 605-619, 2000. 5. sanghvi av, chhabra hs, mascarenhas aa, mittal vk, sangondimath gm thoracic myelopathy due to ossification of ligamentum flavum: a retrospective analysis of predictors of surgical outcome and factors affecting preoperative neurological status. eur spine j 20(2):205–215, 2011. 6. chen y, lu xh, yang ll, chen dy ossification of ligamentum flavum related to thoracic kyphosis after tuberculosis: case report and review of the literature. spine, phila pa; 34(1): e41–e44 (2009). 7. kang kc, lee cs, shin sk, park sj, chung ch, chung ss: ossification of the ligamentum flavum of the thoracic spine in the korean population. j neurosurg spine 14: 513-519, 2011. 8. kuh su, kim ys, cho ye, jin bh, kim ks, yoon ys, et al.: contributing factors affecting the prognosis surgical outcome for thoracic olf. eur spine j 15: 485-491, 2006. 9. mori k, kasahara t, mimura t, nishizawa k, murakami y, matsusue y, et al.: prevalence, distribution, and morphology of thoracic ossification of the yellow ligament in japanese: results of ct-based cross-sectional study. spine (phila pa 1976) 38: e1216-e1222, 2013. romanian neurosurgery (2019) xxxiii (2): pp. 135-143 doi: 10.33962/roneuro-2019-026 www.journals.lapub.co.uk/index.php/roneurosurgery correlations between clinical, imaging and histological findings in a patient with neurofibromatosis type 1 (von recklinghausen's disease) gabriela florența dumitrescu1, anca sava1,2, ion poeată1,2, danisia haba1,2, bogdan dobrovăț1,2, nicoleta dumitrescu1, camelia margareta bogdănici2,3, claudia florida costea1,2 1 “prof. dr. n. oblu” emergency clinical hospital, iași, romania 2 “grigore t. popa” university of medicine and pharmacy, iași, romania 3 “saint spiridon” emergency county hospital, iași, romania abstract neurofibromatosis type 1 (nf1) or von recklinghausen disease is one of the most common genetic diseases, affecting 1/4,000 individuals. it is transmitted by autosomal dominant inheritance and the gene nf1, which is responsible for the disease, is located on the long arm of chromosome 17. nf1 is characterized by varied expressions of the disease, even within the same family. we present the case of a 22-year-old patient with nf1 admitted in the department of neurosurgery for a two months history of diffuse intercostal nevralgias that did not respond to treatment and discuss the histopathological and immunohistochemical features of her cutaneous and spinal neurofibromas. our case adds new data to the knowledge of the diverse biological behaviour of nf1, highlighting the fact that this condition is a complex disease even in the same individual. we report here a highly variability among neurofibromas in the same patient from a histopathological point of view. our data are also important as they demonstrate the fact that the management of a patient with nf1, due to the various and complex manifestations of the disease, requires a multidisciplinary approach, including neurologist, neurosurgeon, ophthalmologist, plastic surgeon, dermatologist, radiologist and pathologist. introduction neurofibromatosis type i (nf1) is a complex neuro-cutaneous disease with dominant autosomal transmission, whose nfi gene is located on chromosome 17. the definitive diagnosis needs the existence in the same individual of two or more criteria from the following seven main elements: a). six or more café-au-lait spots, larger than 5 mm in puberty and larger than 15 mm after puberty, disseminated on the whole body; keywords neurofibromatosis type 1, cutaneous neurofibroma, spinal neurofibroma, pseudomeissnerian corpuscle, ganglia cell, immunohistochemistry corresponding author anca sava “grigore t. popa” university of medicine and pharmacy, iași, romania dr.anca.sava68@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 136 gabriela florența dumitrescu, anca sava, ion poeată et al. b). axillary and inguinal freckling (crowe sign); c). two or more cutaneous or spinal nerve neurofibromas of any type or at least 1 plexiform neurofibroma; d). optic nerve glioma; e). two or more lisch nodules (iris hamartomas); f). characteristic skeletal dysplasia; g). at least one first-degree relative affected by nf1 (parent, sibling, child) (1). however, nf1 is characterized by varied expressions of the disease, even within the same family. we present the case of a 22-year-old patient with nf1 fulfilling five main criteria of the disease and discuss the histopathological features of her cutaneous and spinal neurofibromas highlighting the fact that nf1 is a complex disease even in the same individual. case presentation a 22-year-old female patient was referred to neurosurgery department, „prof. dr. n. oblu” emergency clinical hospital iaşi, with a two months history of diffuse intercostal nevralgias that did not respond to treatment. the patient had a positive family history for von recklinghausen’s disease. she had an uncle (44 years-old), her father's brother, with nf1, who was diagnosed five months ago with plexiform neurofibromas of the spinal nerves (from d12 nerve roots to the sacral roots), the terminal segments showing the appearance of pelvic "masses". our patient's past medical history revealed a diagnosis of nf1 that was established when she was 8 years old as she has had already café-au-lait spots, disseminated on her limbs and trunk, and cutaneous soft, painless tumours, one of them located in her left retroauricular area. the tumour was incompletely excised when the patient was 12 years old and the diagnosis of a cutaneous diffuse neurofibroma was histopathologically established, thus confirming the diagnosis of von recklinghausen's (nf1) disease. as the tumour slowly increased in size, after 9 years a head magnetic resonance imaging (mri) was performed, identifying the presence of a lesion that developed in the dermis and distorted the left temporo-occipital region (figure 1). the tumour was completely excised and the specimen was sent to the pathology department where it was processed using the standard histological technique. the immunohistochemical stainings were performed using anti-s-100 protein antibody, anti-vimentin antibody, and a two-step staining technique (envision+ dual link system-hrp, dako). on histological examination, an intact epidermis covered a relatively ill-defined dermal tumoural proliferation of schwann cells with hyperchromatic wavy nuclei, few aggregates of pseudomeissnerian corpuscles, associated with fibroblasts and normal appearing nerve bundles. tumour mass infiltrated the hypoderm, entrapping adipocytes and distorting serous gland acini. immunopositivity for vimentin in randomly arranged fibroblasts and intense immunopositivity for s-100 protein in randomly arranged schwann cells, but also in the cells of pseudomeissnerian corpuscles, established the final diagnosis: cutaneous neurofibroma with pseudomeissnerian corpuscles (figures 2, 3, and 4). figure 1. mri t2 se scan revealed a cutaneous tumour in the left temporo-coccipital region. 137 correlations between clinical, imaging and histological findings in a patient with neurofibromatosis type 1 figure 2. cutaneous neurofibroma: a). tumoral proliferation of schwann cells with hyperchromatic wavy nuclei, which were intimately associated with fibroblasts and fine collagen strands. in some areas, there were aggregates of pseudomeissnerian corpuscles (he, x100); b). tactilelike/pseudomeissnerian corpuscles in tumoral mass (he, x200). c). small scattered fascicles of nerve bundles entrapped into the tumour mass (he, x100); d). tumour mass infiltrated the hypoderm, entrapping adipocytes and distorting serous gland (he, 1200). figure 3. intense immunopositivity for s100 protein in randomly arranged schwann cells, but also in all cells located in the pseudomeissnerian corpuscles (anti – s100 protein, x 200). figure 4. immunopositivity for vimentin in randomly arranged fibroblasts (anti vimentin, x 100). one year later, on admission in our hospital due to diffuse intercostals nevralgias, the patient's physical examination revealed: axillary and inguinal freckling, six café-au-lait spots with diameters ranging from 1,5cm to 6 cm, located on the trunk, six cutaneous tumours that were soft, pink, painless, ranging from a few millimeters to 2 centimeters, which were located on the dorsal trunk and right shoulder (figure 5). 138 gabriela florența dumitrescu, anca sava, ion poeată et al. figure 5. a). on the dorsal inferior trunk there were several "café-au-lait" spots, along with red, soft, depressible tumours. b). on the dorsal superior trunk there were three large (ranging from 2 cm to 6 cm in long diameter) "café-au-lait" spots; c). on her right shoulder area there was a cutaneous soft, pink colored tumour, with a diameter of 1.5cm. figure 6. the contrast enhanced ct exam showed an intraforaminal and para-vertebral tumour formation with widening of the vertebral left foramen at d10-d11, with left paravertebral extension, being in contact with the superior pole of the left kidney. the nodular aspect of the lesion, visible in the sagital plane, is associated with the inclusion of the left d10 and d11 spinal roots into the tumoural mass, as seen in the axial image. a). axial section in a parenchymal window; b). axial section in a bone window; c). sagital section. an abdominal ct scan was performed and revealed the existence of a left paravertebral solid tumour, which was developed intraforaminal and paravertebral around the dorsal level d11. the tumour extended upward at the d10 level and downward at the d12 level, encompassing left d10 and d11 spinal 139 correlations between clinical, imaging and histological findings in a patient with neurofibromatosis type 1 roots. the tumoural formation was solid, oval, well defined, with dimensions of 35/16 / 65mm (figure 6). the standard laboratory tests values were in the normal range. surgical intervention was performed by external approach at d11-d12 lateral level, with microsurgical total ablation of the tumour. the surgical specimen was sent to the pathology department of the same hospital for histopathological analysis. the specimen was fixed in formalin, embedded in paraffin, cut at 5 μm and stained with hematoxylineosin (he). on representative sections, immunehistochemical stainings were performed using antis-100 protein antibody, anti-vimentin antibody, and a two-step staining technique (envision+ dual link system-hrp, dako). histological sections stained with he showed a non-encapsulated tumour, consisting of neoplastic wavy schwann cells, entrapped ganglion cells as the tumour extended to associated ganglia, a myxoid stroma, and delicate collagen fibers (figure 7). s100 protein immunestaining highlighted neoplastic schwann cell component and ganglia cells of the spinal root that were entrapped into the tumour (figure 8). vimentin immunostaining revealed numerous fibroblasts (figure 9). the final pathological diagnosis was spinal neurofibroma with tumoural infiltration of the associated ganglia. the ophthalmologic examination revealed myopia in both eyes (best corrected visual acuity in right eye was 1 with -1 d and in the left eye was 1 with – 0,5 d). the ophthalmoscopic examination showed normal appearance of the ocular fundus in both eyes. direct photomotor reflex was bilaterally present. intraocular pressure was within normal range: right eye = 12 mmhg and left eye = 13 mmhg. both eyes presented many small, bright brown, oval, and dome-shaped irian nodules (lisch nodules) (figure 10). figure 7. spinal neurofibroma: a). non-encapsulated tumour made up of neoplastic wavy schwann cells, a myxoid stroma, and delicate collagen (h-e, x100); numerous ganglia cells entrapped into the tumour mass (he, x100). figure 8. immunopositivity for s100 protein in neoplastic schwann cells and ganglia cells (anti – s100 protein, x 100). figure 9. immunopositivity for vimentin in randomly arranged fibroblasts (anti vimentin, x 100). 140 gabriela florența dumitrescu, anca sava, ion poeată et al. figure 10. numerous small lisch nodules at both eyes [a). right eye; b). left eye]. discussion there are suppositions that ebers papyrus case #873 can represent the first mention of a case of neurofibromatosis type 1 (nf1) (2). the important landmarks in the history of the disease are the irish neurosurgeon robert william smith, who, in 1849, realized a systematic review of clinical cases (3), and the german pathologist friedrich daniel von recklinghausen (1833-1910), who fully described this condition in 1882. von recklinghausen introduced the term “neurofibroma” into clinical practice to define the benign tumours that accompany this disease. he was the first who found that these tumours develop from the peripheral nerve sheath, consisting of a mixture of schwann cells and fibroblasts (4). in recognition of his discovery, the disease received his name. however, there are different forms of neurofibromatosis that vm riccardi, the director of the baylor nf program (1978-1990), attempted to classify the disease in 1982 (5). he considered that there were eight types, but later, in 1986, carey et al. proposed a new classification into only five types, as follows: nf1 classical, nf2 acoustic, nf3 segmental, nf4 calm familial and nf5 nfnoonan phenotype (6). nf1 represents 90% of all cases with nf, being characterized mainly by multiple café-au-lait spots and neurofibromas along peripheral nerves. even though nf1 has been recognized as a clinical entity for more than a century, its etiopathogenesis was better understand only in 1990 when the nf1 gene was identified on chromosome 17. nf1 gene is a tumour suppressor gene that encodes a protein named neurofibromin (7), which is a negative regulator of the ‘‘rat sarcoma viral oncogene homologue’’ (ras) (8). approximately 50% of the cases with nf1 disease represent new mutations and the expression of the disease is highly variable, both between and within families (9). the most important hypothesis regarding the neurofibromas was that these tumours can develop only after both nf1 alleles have been lost in the schwann cell lineage. when schwann cells begin to proliferate, they recruit some other cells from their environment (10). as such, neurofibromas are complex tumours, consisting in a mixture of cell types: schwann cells, fibroblasts, perineurial cells, and mast cells (7, 10). it was also hypothesized that these different cellular phenotypes can represent divergent cellular differentiation pathways of multipotent precursor cells (11). it was considered that the development of neurofibromas include the presence of a clonal population of nf1-/schwann cells in a microenvironment harbouring other cell types with an nf1+/genotype. it was also hypothesised that the multipotent nf1+/cells are the major source of different cell types found in the neurofibromas (11). neurofibromas developing in a nf1-affected individual can be classified according to their anatomical location into: cutaneous, subcutaneous, intraneural, and spinal nerve roots tumours (12). cutaneous neurofibromas generally appear during preadolescence. they are soft, pink coloured tumours, sessile or dome-shaped, being most numerous on the trunk and limbs. the tumour diameter usually varies between a few millimetres 141 correlations between clinical, imaging and histological findings in a patient with neurofibromatosis type 1 and approximately 2 centimetres (11). it is considered that these benign tumours developed from small nerve tributaries of the skin (13). histologically, cutaneous neurofibromas are nonencapsulated, loosely textured dermal mixed tumours, consisting of schwann cells, neurons, perineurial cells, fibroblasts, and mast cells, but also adipocytes, epithelial cells, and axonal processes (11). all of these cellular elements are embedded in an abundant collagenous extracellular matrix. megahed (14) described ten histopathological variants of neurofibroma: classic, cellular, myxoid, hyalinized, epithelioid, plexiform, diffuse, pigmented, granular cell, pacinian. subsequently, some other variants such as dendritic cell neurofibroma with pseudorosettes (15), lipomatous neurofibroma (16), and angioneurofibroma (17) have been reported. pseudomeissnerian corpuscles can be seen in cutaneous neurofibromas, but not so frequently. using traditional histological staining as well as immunohistochemical staining (anti-s100 protein antibody and anti-vimentin antibody) can be the proofs that the neoplastic component is made of schwann cell. neurofilament protein immunereactivity (nfp) revealed the occurrence of residual axons within tumour nodules. some authors highlighted the fact that, using factor xiiia as an immunohistochemical marker, the pathologist can differentiate cutaneous neurofibromas from neurotized nevi and cutaneous schwannomas (18.) aggregates of pseudo-meissnerian corpuscles are frequent in diffuse cutaneous neurofibromas (19). as these structures consist entirely of schwann cells, they can be can be highlighted with anti-s100 protein antibody immunostaining (20). our patient presented at least one cutaneous neurofibroma since he was 8 years-old, but the definitive diagnosis of nf1 was realized only after the surgical excision of the tumour (when patient was 12 years-old). histological and immunohistochemical examinations identified diffuse cutaneous neurofibroma with clusters of organoid structures resembling meissner corpuscles (pseudomeissnerian structures), thus being in line with other researchers' findings. the incidence of spinal involvement in nf1 patients varies among authors. mautner et al. reported that spinal neurofibromas are found in up to 38% of nf1 patients but very few of them are symptomatic (21). in a study of patients with nf1 made by thakkar et al., 6% of patients had intramedullary tumours, 57% had intraforaminal tumours (dumbbell), and 33% had extradural tumours (22). at the spinal level, patients with nf1 may have either one or more tumours that can develop in one or more spinal nerve roots. usually, spinal tumours are diffuse or plexiform neurofibromas. some authors found out that more frequently these spinal tumours are solitary neurofibromas (23), but others reported plexiform neurofibromas, which grow involving multiple nerve fascicles, branches and plexuses (24). our patient had a solitary spinal neurofibroma, but her uncle had multiple plexiform spinal neurofibromas. our article prove the fact that neurofibromas developing in a patient with nf1 can have different histological features, each of them displaying microscopical appearances more closely related to the histology of the region in which the tumour occurs, i.e., cutaneous neurofibroma exhibited pseudomeissnerian corpuscle, and spinal neurofibroma revealed schwann cells arranged in bundles, reminding of spinal nerve histology. the age at onset of symptoms caused by spinal neurofibromas can vary from 11 to 49 years (mean 32.8 years), but most cases present symptoms at adult ages (22 to 43 years) (25). spinal neurofibromas cause neurological symptoms in only 2% of nf1 patients, provoking both sensory and motor deficits due to compression of the spinal cord or nerve root (22). in a recent article, mauda-havakuk et al. analyzed the radiological findings of a series of thirty-four patients with nf1 with spinal neurofibromas. they classified spinal involvement into four types according to the anatomic location of the tumours along the spine and to their type of involvement of the spinal canal and foramina: 1. foraminal tumour; 2. “kissing” tumours; 3. paraspinal tumour; 4. intradural tumour (26). these authors reported that most spinal neurofibromas developed in the lumbo-sacral area and fell into group 1 (foraminal). our patient was diagnosed as having a spinal foraminal neurofibroma at the age of 22. as her left d10 and d11 spinal roots were entrapped into the tumour mass, the patient presented a two months history of diffuse intercostal nevralgias that did not respond to the treatment, thus imposing the surgical intervention. 142 gabriela florența dumitrescu, anca sava, ion poeată et al. lisch nodules are hamartomas of the iris that are also characteristic for nf1. they have variable dimensions and dome-shaped configuration. some researchers reported that patients affected by nf1 and older than twenty could have an incidence of lisch nodules of 100% (27). lewis et al. found out that 92% of subjects aged 6 years and older had lisch nodules, but their presence was not correlated to number of café-au-lait spots, number of neurofibromas, or severity of disease (28). our patient, being in her third decade of life, also presented lisch nodules in both her eyes. due to varied and complex manifestations of the disease, the management of a patient with nf1 requires a multidisciplinary approach. once the diagnosis is established, clinical monitoring is needed to identify possible complications. as a result, annual assessment is required to reduce morbidity and improve the quality of life. this assessment should include: a) dermatological examination to analyze the progression of the existing neurofibromas and to identify possible new lesions; b). head and spine mri, chest and abdomen imaging to detect the majority of complications that could be associated with this disease; c). full ophthalmological examination for early detection of optic nerve lesions; d). neurological examination for early detection of paresthesia, radiculopathy, muscle fatigue or muscle atrophy; e). removal of skin tumours for cosmetic or therapeutic purposes; f). education and psychological support for nf1 patient. conclusion the patient described in this article is a very typical case of nf1, having six ”café-au-lait” spots, six neurofibromas, axillary or inguinal freckling, lisch nodules, and a first degree relative (her father's brother) with nf1.our case presents a considerable interest because of a complete description of the natural evolution of nf1, highlighting the histological pictures of her cutaneous and spinal neurofibromas. because the expression of the disease is highly variable, both between and within families, our study data are especially valuable as they also showed a highly variability among neurofibromas in the same patient from a histopathological point of view. these data are also important as they demonstrate the fact that the management of a patient with nf1, due to the various and complex manifestations of the disease, requires a multidisciplinary approach, including neurologist, neurosurgeon, ophthalmologist, plastic surgeon, dermatologist, radiologist and pathologist. references 1. stumpf d, alksne j, annegers j, brown s, conneally p, housman d, leppert m, miller j, moss m, pileggi a, rapin i. strohman r, swanson l, zimmerman a. neurofibromatosis. conference statement. national institutes of health consensus development conference. arch neurol. 1988;45:575–578 2. sanchez gm, siuda t. ebers papyrus case #873: a probable case of neurofibromatosis 1. s d j med. 2002;55(12):529-35 3. kobrin jl, blodi fc, weingeist ta. ocular and orbital manifestations of neurofibromatosis. surv ophthalmol, 1979, 24:45 4. von recklinghausen fd. ueber die multiplen fibrome der haut und ihre beziehung zu den multiplen neuromen. hirschwald, berlin, 1882 5. riccardi vm. neurofibromatosis: clinical heterogeneity. curr probl cancer, 1982, 7:1 6. carey jc, baty bj, johnson jp, morrison t, skolnik m, kivlin j. the genetic aspects of neurofibromatosis. ann ny acad sci. 1986;486:45–46 7. theos a, korf br. pathophysiology of neurofibromatosis type 1. ann intern med. 2006;144:842-849 8. martin ga, viskochil d, bollag g, mccabe pc, crosier wj, haubruck h, conroy l, clark r, o’connell p, cawthon rm, innis ma, mccornick f. the gap-related domain of the neurofibromatosis type 1 gene product interacts with ras p21. cell. 1990;63:843–849 9. huson sm, hughes rac. the neurofibromatoses: a pathogenetic and clinical overview. chapman and hall medical, london, uk, 1994. 10. zhu y, ghosh p, charnay p, burns dk, parada lf. neuroþbromas in nf1: schwann cell origin and role of tumour environment. science. 2002; 296:920-922 11. jouhilahtilow em, peltonen s, heape am, peltonenlow j. the pathoetiology of neurofibromatosis 1. am j pathol. 2011; 178(5):1932-1939 12. evans d, komminoth p, scheihauer b, peltonen j. neurofibromatosis type 1. pathology and genetics of tumours of endocrine organs: world health organization classification of tumours. in: delellis r, lioyd r, heitz p, eng c. (editors). iarc press, lyon, france, 2004, pp. 243– 248 13. jouhilahti em, peltonen s, callens t, jokinen e, heape am, messiaen l, peltonen j. the development of cutaneous neurofibromas. am j pathol. 2011; 178(2): 500–505 14. megahed m. histopathological variants of neurofibroma. a study of 114 lesions. am j dermatopathol. 1994; 16:486– 495 143 correlations between clinical, imaging and histological findings in a patient with neurofibromatosis type 1 15. michal m, fanburg-smith jc, mentzel t, kutzner h, requena l, zamecnik m, miettinen m. dendritic cell neurofibroma with pseudorosettes: a report of 18 cases of a distinct and hitherto unrecognized neurofibroma variant. am j surg pathol. 2001;25:587–594. 16. val-bernal jf, de sa dehesa j, garijo mf, val d. cutaneous lipomatous neurofibroma. am j dermatopathol. 2002;24:246–250 17. saxer-sekulic n, kaya g. cutaneous angioneurofibroma: a new histopathological variant of neurofibroma, dermatopathol. 2014;1:7–10 18. gray mh, smoller br, mcnutt ns, hsu a. immunohistochemical demonstration of factor xiiia expression in neurofibromas. a practical means of differentiating these tumours from neurotized melanocytic nevi and schwannomas. arch dermatol. 1990;126(4):472-6 19. zhang ml, suarez mj, bosley tm, rodriguez fj. clinicopathologic features of peripheral nerve sheath tumours involving the eye and ocular adnexa. hum pathol. 2017; 63:70–78. 20. shiurba ra, eng lf, urich h. the structure of pseudomeissnerian corpuscles. an immunohistochemical study. acta neuropathol. 1984;63(2):174-6. 21. mautner vf, asuagbor fa, dombi e, funsterer c, kluwe l, wenzel r, et al. assessment of benign tumour burden by whole-body mri in patients with neurofibromatosis 1. neurol oncol 2008;10:593-8 22. thakkar sd, feigen u, mautner v-f. spinal tumours in neurofibromatosis type 1: a study of frequency, multiplicity and variety. neuroradiol. 1999; 41: 625-629 23. khong pl, goh whs, wong vcn, fung cw, ooi gc. mr imaging of spinal tumours in children with neurofibromatosis 1, ajr. 2003; 180: 413-417 24. acharya s, shukla s, banode p. multiple spinal neurofibromatosis. astrocyte. 2014;1(3):250-251 25. kluwe l, tatagiba m, fünsterer c, mautner v-f. nf1 mutations and clinical spectrum in patients with spinal neurofibromas. j med genet. 2003;40:368–371 26. mauda-havakuk m, shofty b, ben-shachar s, ben-sira l, constantini s, bokstein f. spinal and paraspinal plexiform neurofibromas in patients with neurofibromatosis type 1: a novel scoring system for radiological-clinical correlation. ajnr am j neuroradiol. 2017. www.ajnr.org 27. lubs me, bauer ms, formas me, djokic b: lisch nodules in neurofibromatosis type 1. n engl j med. 1991; 324:1264. 28. lewis ra, riccardi vm. von recklinghausen neurofibromatosis. incidence of iris hamartomata. ophthalmology. 1981;88(4):348. doi: 10.33962/roneuro-2023-036 prospective study of selective intraarterial cerebral infusion and intra operative local application of carboplatin for recurrent glioblastoma multiformis tareq abdul ghani hamid, abdul wahab mahmoud ibrahim, ibrahim ali awad, talal ahmed youssef amer, wael k. zakaria romanian neurosurgery (2023) xxxvii (2): pp. 202-210 doi: 10.33962/roneuro-2023-036 www.journals.lapub.co.uk/index.php/roneurosurgery prospective study of selective intra-arterial cerebral infusion and intra-operative local application of carboplatin for recurrent glioblastoma multiformis tareq abdul ghani hamid1, abdul wahab mahmoud ibrahim2, ibrahim ali awad3, talal ahmed youssef amer⁴, wael k. zakaria5 1 assistant fellow of neurosurgery, ahmed maher teaching hospitals, cairo, egypt 2 professor of neurosurgery, department of neurosurgery, mansoura university hospital, mansoura, egypt 3 professor of clinical oncology and nuclear medicine, mansoura university hospital, mansoura, egypt 4 professor of diagnostic radiology, faculty of medicine, mansoura university, egypt 5 assistant professor of neurosurgery, department of neurosurgery, mansoura university hospital, mansoura, egypt abstract background. high-grade glioma is the commonest primary malignant brain tumour in adults. intra-arterially selectively infused chemotherapeutic agents into the tumour bulk is being widely trialled recently with promising results. methods. this is a prospective study designed between november 2015 and november 2019. thirty patients were diagnosed with recurrent histo-pathologically proven gbm after one surgery at least and followed by standard radiotherapy and temodal. patients aged between 37-76 years, 18 males and 12 females were subdivided into group a of 21 patients who underwent intra-arterial delivery of carboplatinand group b of 9 patients who underwent re-surgical resection and local application of carboplatin. results. the mean age of the included cases was 55.4 years (range, 37-76 years). selective intra-arterial injection was performed in 21 cases (70%), while the remaining 9 cases (30%) had local application of carboplatin in the tumour bed. post-treatment vomiting was reported in 7 cases (23.3%). significant and partial responses were achieved in 2 cases for each (6.7%). time to tumour progression had a mean of 19.03 weeks (range, 3 – 30 weeks). after receiving carboplatin, the study cases had a mean survival of 26.5 weeks (range, 6 – 70 weeks). intra-arterial injection had significantly better results compared to local tumour bed infiltration (p = 0.01). conclusion. although recurrent glioblastoma multiformis has poor survival, intraarterial delivery of carboplatin may have a slight positive impact on patient survival. the procedure however is relatively safe with manageable complications. keywords gbm, carboplatin, intra-arterial injection, tumoricidal, dsa corresponding author: wael k. zakaria department of neurosurgery, mansoura university hospital, mansoura, egypt drwaelmusa@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 203 local application of carboplatin for recurrent glioblastoma multiformis introduction high grade glioma is the commonest primary malignant brain tumor in adults with an incidence of approximately 5 per 100,000[1]. a published phase iii randomized trial showed only 9.8% 5-year survival rate for patients with high grade glioma treated by standard protocol of surgery plus radiation and temozolomide. intra-arterially selectively infused chemotherapeutic agents into the tumor bulk is being widely trialed recently. some of the trails showed promising results and point to more investment in the field of selective intra-arterial infusion of tumoricidal agents for treatment of malignant glioma[2].glioblastoma multiformis which is the high-grade glioma targeted in our study like most malignant carcinoma, its cells possess replicative immortality. normal cells that undergo dna damage and telomere shortening have the ends of their dna strands bind together to stop replication and apoptosis commences. loss of p53 gene results in over expression of telomerase enzyme that is responsible in maintaining dna strand length, repairing damage and protecting the ends of chromosomes allowing cells to continuously proliferate [3]. the protocol of maximum safe surgery of gbm followed by adjuvant chemo-radiotherapy and adjuvant chemotherapy is established as usual standard management[9]. but local recurrence is expected, with the majority of cases within 6–9 months of 1ry treatment due to resistant stem cells of gbm [10, 11]. molecular factors such as mutation of p53,methylation of o-6-methylguanine-dna methyltransferase (mgmt) and mib-1 labeling index are associated with gbm recurrence [16]. controversy exists regarding diagnosing recurrence, with histo pathological examination of tissue as the ultimate diagnosis .on the other hand, the majority of cases having imaging finding indicative of progression could be unfit for a surgery, hindering diagnosis of recurrence difficult [12,13,17,18]. surgery is still a significant important strategy in management of gbm. on the other hand, only few cases are recognized appropriate for a complete resection. re-irradiation (rert) has improved in the last years [19].. chemotherapy is utilized by variable groups to improve survival. despite this , however , patients of rgbm and gbm still remain fated for poor outcomes[15].the blood–brain barrier (bbb) prevents the deliverance of the majority of the chemotherapeutic drugs [20]. on the other hand, the majority of the regimens of management surfaced via single institute retrospective analysis of phase ii clinical trials, thus, there is no standard treatment for those patients non responsive to tmz [21]. carboplatin is the drug chosen to target recurrent glioblastoma in our study, it is an analogue of cisplatin containing a platinum atom. once inside tumorous cells carboplatin becomes activated to produce reactive platinum complexes that form inter-strand and intra-strand cross linking of dna molecules inhibiting dna synthesis and replication resulting in cellular death. its action can occur during any phase of the cell cycle (cycle non-specific). in the brain only malignant cells will be affected and normal cells are spared because they are normally non dividing stable cells [4]. adverse effects of systemic iv carboplatin use includes; bone marrow depression usually reversible within 30days resulting in anemia 71%, febrile neutropenia18%, thrombocytopenia 25% [5]. nausea (15%) and vomiting (64%)starts within 612 hours after carboplatin injection but can be limited by prior anti-emetics[5].hepatotoxicity may also occur in the form of elevated alkaline phosphatase (24%), elevated ast (15%), elevated bilirubin (5%) [6]. selective intra-arterial cerebral infusion of carboplatin involves its delivery to tumor site via balloon assisted endovascular techniques and prior focal disruption of the blood brain barrier by injecting 10cc of mannitol 20% over 2 mins[7]. pre-infusion studies and post-infusion studies including magnetic resonance imaging with and without gadolinium to detect the effect on tumor size and magnetic resonance spectroscopy to detect the metabolic response are carried out for candidate patients [8]. ia infusion of chemotherapy refers to the regional delivery of chemotherapy to the cns, that results in a major rise in plasma peak concentration and in the auc associated with the 1stpass effect. this leads to a 3– 5.5-fold factor major rise in the concentration of intra-tumoral chemotherapy as theses lesions are vascular in nature[27]. the fischer animal model [29], found that accumulation of platinum in the tumor cells nuclei was elevated by a 20-fold factor (9 ng platinum/g tissue) when infused via an ia route, when put side by side with the iv route (0.5 ng platinum/g tissue) [30]. 204 tareq abdul ghani hamid, abdul wahab mahmoud ibrahim, ibrahim ali awad et al. clinical trials incorporating patients with gbm who received cisplatin monotherapy or combined with others chemotherapeutic drugs as etoposideor tmz documented only modest outcomes [27,28]. patients and methods this is a prospective study designed for patients have recurrent gbm between november 2015 and novemeber2019 in neurosurgery department, mansoura university hospitals, egypt. this study aims to evaluate the efficacy of single dose selective intra-arterial cerebral infusion and tumor bed application of carboplatin for such patients.is. study subject thirty patients were diagnosed with recurrent histo pathologically proven gbm after a one surgery at least and followed by standard radiotherapy and temodal. they were all referred from the outpatient neurosurgery clinic. patients aged between 37-76 years , 18 males and 12 females were subdivided into two groups: group a(21 patients who underwent intra-arterial delivery of carboplatin), group b(9 patients who underwent re-surgical resection and local application of carboplatin). inclusion criteria • age above18 years old • patients with recurrent glioblastoma multiforme • karnofsky performance status scale 40 or above primary outcome measures evaluating response to both ways of chemotherapy delivery using imaging techniques. secondary outcome measure 1. post-treatment complications. 2. survival. patients consent a written informed consent was obtained from all patients before the operation after describing and explaining the details and complications of each approach. procedure patients were admitted for a variable period of time ranging between 3-7 days. all patients were investigated by a baseline pre and post enhanced mri and routine lab most notably serum creatinine and a baseline blood picture (cbc). history taking and baseline neurological examination was established as well for all patients. the patients were then grouped into two groups after assessment of the following: • whether or not they require surgical decompression because of significant radiological mass effect and weather the recurrence is surgically accessible or not • history of complications (csf wound leakage, poor wound healing, poor scalp texture after radiotherapy, deep venous thrombosis ,pulmonary embolism severe chest infection ) related to prior surgery or adjuvant chemoradiotherapy rendering surgery high risk. carboplatin dosage was calculated based upon body surface area calculated using the mostellar formula bsa (m2) = sqrt ([height (cm) * weight (kg)] / 3600) body surface area (m2) = square root ( [height (cm) * weight (kg) ] divided by 3600. the first group (group a) selective intra-arterial cerebral infusion of carboplatin was performed at a dose of 400 mg/m2 bsa. on table, digital subtraction angiography (dsa) was done to identify the tumor vascular bed then endovascular techniques are employed to reach the vascular bed, followed by injection of 10cc mannitol 20% over to 2 minutes, dsa was redone to detect focal hyperemia indicating successful bbb disruption, after that carboplatin infusion was commenced through a marathon flow directed micro-catheter usually within the middle cerebral artery( mca) or anterior cerebral artery(aca) or one of their branches as well as a small dosage at the carotid bifurcation. mostly, this was carried out under local anesthetic with the patient instructed to either report increasing headache, nausea, blurring of vision or increasing tingling or numbness or heaviness of an extremity. the second group (group b) local application of carboplatin during re-surgery at a dose 400mg/m2 bs. after sufficient tumor debulking a cotton pack soaked in carboplatin solution is placed in the tumor cavity before coagulation of the walls of the cavity for 10mins; the pack is then removed and final hemostasis is 205 local application of carboplatin for recurrent glioblastoma multiformis achieved and lastly the cavity is filled with the rest of carboplatin solution. post-procedural follow up mri with ce was carried out at 2 weeks and at one or two months later. response to treatment was then determined as a significant response (sr) if ce tumor size was reduced in any of the following mris. a partial response pr was considered if the tumor exhibited less mass effect and edema without reduction in the size of ce tumor. a stable disease sd if no changes regarding size or mass effect occurred. a progressive disease pd was established if size or mass effect and edema were increased post procedurally. data analysis statistical analysis of the data in this study was performed using spss software, version 20 (chicago, il). descriptive data was expressed as means with standard deviation or medians with ranges according to data distribution. results the mean age of the included cases was 55.4 years (range, 37-76 years). we included a total of 18 males (60%) as well as 12 females (figure 1). figure 1. gender distribution in the study cases. the karnofsky performance score (kps) had a mean of 71.33 in the study cases (range, 50-80) (table1). table 1. analysis of kps in the study cases items study cases n=30 kps mean ± sd 71.33 ± 8.99 median (min-max) 70 (50-80) continuous data expressed as mean ±sd and median (range) all study cases had been commenced on chemo radiotherapy after the first surgery. evidence of mass effect was present in all study cases (table2). table 2 analysis of the history of the disease in the study cases. id hx of radiotherapy hx of chemotherapy previous surgery pre-ttt evidence of mass effect 1 yes temodal yes yes 2 yes temodal yes yes 3 yes temodal yes yes 4 yes temodal yes yes 5 yes temodal yes yes 6 yes temodal yes yes 7 yes temodal yes yes 8 yes temodal yes yes 9 yes temodal yes yes 10 yes temodal yes yes 11 yes temodal yes yes 12 yes temodal yes yes 13 yes temodal yes yes 14 yes temodal yes yes 15 yes temodal yes yes 16 yes temodal yes yes 17 yes temodal yes yes 18 yes temodal yes yes 19 yes temodal yes yes 20 yes temodal yes yes 21 yes temodal yes yes 22 yes temodal yes yes 23 yes temodal yes yes 24 yes temodal yes yes 25 yes temodal yes yes 26 yes temodal yes yes 27 yes temodal yes yes 28 yes temodal yes yes 29 yes temodal yes yes 30 yes temodal yes yes regarding the method of carboplatin delivery, selective intra arterial injection was performed in 21 cases (70%), while the remaining 9 cases (30%) had local application of carboplatin in the tumour bed (figure2). post-treatment vomiting was reported in 7 cases (23.3%), whereas epilepsy was present in 8 cases 0 10 20 male female gender male female 206 tareq abdul ghani hamid, abdul wahab mahmoud ibrahim, ibrahim ali awad et al. (26.7%). additionally, hemiparesis was diagnosed only in 2 cases (6.7%) (figure3). figure 2. method of carboplatin delivery in the study cases. figure 3. treatment complications in the study cases. more than half of the study cases had progressive disease (16 cases – 53.3%), followed by stable disease (10 cases – 33.3%). significant and partial responses were achieved in 2 cases for each (6.7%) time to tumour progression had a mean of 19.03 weeks (range, 3 – 30 weeks).after receiving carboplatin, the study cases had a mean survival of 26.5 weeks (range, 6 – 70 weeks). on dividing our study cases according to the method of carboplatin delivery, no significant difference was detected between the two groups regarding treatment complications (p > 0.05) (figure 4). regarding treatment response, it was evident that intra arterial injection had significantly better results compared to local tumor bed infiltration (p = 0.01). all cases in local bed infiltration had progressive disease after treatment, while 2 cases in the other group had significant response (table3). figure 4. treatment complications in both study groups. table 3. analysis of response in the two study groups groups test of significance group 1 [selective ia] (n=21) group 2 [local in tumor bed] (n=9) significant response 2 (9.5%) 0 (0%) 2= 11.250 p= 0.010* stable disease 10 (47.6%) 0 (0%) progressive disease 7 (33.3%) 9 (100%) partial response 2 (9.5%) 0 (0%) p: probability. categorical data expressed as number (%) x2= chi-square test table 4. analysis of ttp in the two study groups. groups test of significance group 1 [selective ia] (n=21) group 2 [local in tumor bed] (n=9) ttp (weeks) 19 (6.5 -34) 8 (7.5 -11) t= -1.383 p = 0.178 p: probability. continuous data expressed as median (iqr). z= mann whitney u-test 0 5 10 15 20 25 selective intraarterial local in tumour bed carboplatin delivery selective intraarterial local in tumour bed 0 2 4 6 8 10 treatment complications vomiting epilepsy hemiparesis 0 2 4 6 8 vomiting epilepsy neurological deficit treatment complications ia injection local delivery 207 local application of carboplatin for recurrent glioblastoma multiformis there was no significant difference between the two groups regarding time to disease progression (p = 0.178) although the mean ttp was shorter in the tumor bed infiltration group (8 vs. 19 weeks in the ia group) (table4). survival was significantly longer in the ia drug group (35 vs. 14 weeks in the local tumour bed group – p = 0.028) (figure5). figure 3. survival in the study groups. discussion even with respect to all advances in aspects of treatment, patients with gbm still remain of poor prognosis[33]. during progression, salvage treatments provide highly modest efficiency. several agents have been tested concerning this topic, providing low rates of response varying from 5 to 20% and median total survival between 5 and 7.5 months [34]. we included an overall of 30 patients in the current study, having a mean age of 55.4 (range, 37 – 76 years). we included a total of 18 males (60%) as well as 12 females. another study conducting similar perspective included 24 patients with recurrent gbm. the mean age of the included cases was 44.5 years (range, 26 – 67 years). investigators comprised 13 males and 11 females in that study [25]. another study included an overall of 25 patients whose mean age was 37.8 years (range, 22 – 68). a total of 13 males and 12 females were included in that study [26]. in our study, karnofsky performance score (kps) had a mean of 71.33 in the study cases (range, 5080). in a similar study, at the time of initiation of therapy, median kps was eighty. at the time of disease progression, the median kps was sixty [35]. another study reported that the mean kps score was 66.8 (range, 40 – 90) [26]. in the current study, time to tumor progression had a mean of 19.03 weeks (range, 3 – 30 weeks). newton and his associates reported that the overall median ttp was 24.2 weeks, while for responders the median ttp was 32 weeks (range 10–174 weeks) [26]. in the current study, more than half of the study cases had progressive disease (16 cases – 53.3%), followed by stable disease (10 cases – 33.3%). significant and partial responses were achieved in 2 cases for each (6.7%). it was evident that intra-arterial injection had significantly better results compared to local tumor bed infiltration (p = 0.01). all cases in local bed infiltration had progressive disease after treatment, while 2 cases in the other group had significant response. ia injections depend on drug provision throughout capillary networks and finally to the perfused tissue. the tissue concentrations reached by utilizing a selective ia route are significantly greater than those reached following iv administration [36].it is assessed that above 2000 cases were managed with ia chemotherapy for gbm, most of which are parts of phases i and ii trials. there has been small evidence of considerably better results throughout the course of these trials. numerous series state increased survival by only some weeks, with neurotoxicity or ocular toxicity appearing in 7-50% of the patients [22].in another study, volumetric analysis of serial mris revealed decrease in tumor mass in three out of ten cases. a rise in tumor mass in the range of 23% to 230% was detected in the other 7 cases in time extending from 2.3 to 37.7 months after starting of therapy by carboplatin [25]. additionally, 68.29% of cases had tumor progression while the remaining cases had stable disease in another study [24]. in another study, that utilized criteria of macdonald in order to categorize tumor responses radio logically, authors detected three full responses, twenty-two partial responses, fourteen stable disorders and twelve progressions [28]. follézou et al. showed that carboplatin had a partial response in high grade glioma patients using a dose of 400 mg/m2[31, clocchlatti et al. achieved a 208 tareq abdul ghani hamid, abdul wahab mahmoud ibrahim, ibrahim ali awad et al. 74% response rate after 250 mg/m2 ia carboplatin infusion[32], and cloughesy et al. increased carboplatin dose up to 1400 mg/ hemisphere in a dose-escalation study based on cerebral blood flow[37]. other authors reported that 45 out of 57 patients evaluated with gbm (79%) experienced sd or better. authors concluded that along with the use of standard treatment guidelines and protocols, intra-arterial chemotherapy with or without osmotic disruption of the bbb is feasible across several centers with a low incidence of catheter-related complications[23]. after receiving carboplatin, our study cases had a mean survival of 26.5 weeks (range, 6 – 70 weeks). survival was significantly longer in the ia drug group (35 vs. 14 weeks in the local tumor bed group – p = 0.028).in another study, twenty-three patients (out of 46 cases) died after an average of 205 days; 18 were surviving at an average of 324 days from the start of intra-arterial chemotherapy [24]. stewart et al. reported the results of intra-carotid infusion of carboplatin (200–400 mg/m2) in 15 patients with either glioblastoma or metastatic tumors. median survival was 9 weeks [191]. in another study, more than one year survival subsequent to start of ia therapy by carboplatin has been observed in twelve out of the twenty-three cases [25]. furthermore, in another study, the median total survival from time of diagnosis was twenty-three months with a median survival of eleven months from start of study was detected. the progressionfree survival subsequent to therapy was 6.1 months, while a free survival progression of 4.3 months was detected subsequent to the ia therapy [38]. surgery in case of recurrent gbm may involve either biopsy (for diagnostic purposes) or repeat debulking of tumor. only approximately 20 to 30 percent of patients with recurrent glioblastoma are candidates for a second surgery [39]. in a patient with recurrent gbm, the indications for a debulking reoperation are still to be definitely recognized. the median survival for cases submitted to operation for recurrent glioblastoma ranges from 8 to 12 months in most series [40.41] and varies from 12 to 18 months for patients with anaplastic astrocytoma [42,43,44]. there is no evidence to suggest that the results of re-surgery are more useful than could be expected with radiation and/or chemotherapy alone. however, selected patients could benefit from reoperation (eg, those with a bulky tumor exerting symptomatic mass effect). favorable prognostic variables include patients whose age is young, a greater interval from the original operation, and the size of the recurrence as well as extent of the 2nd surgical resection [45,46]. in the current study, post-treatment vomiting was reported in 7 cases (23.3%), whereas epilepsy was present in 8 cases (26.7%). additionally, hemiparesis was diagnosed only in 2 cases (6.7%). on dividing our study cases according to the method of carboplatin delivery, there was no major difference observed among the 2 groups regarding treatment complications (p > 0.05).bone marrow suppression (bms) in the form of thrombocytopenia or leucopenia was not observed in cases in this study and this can be most probably be attributed to the fact that the patients received only a single non incremented dose of carboplatin that the body eliminated too soon before bms sets in. in the study conducted by stewart and his associates, three of four patients who received 400 mg/m2 of carboplatin developed retinal toxicity. three of 9 patients who received 300 mg/m2 had decreased ipsilateral vision and one other developed worsening of a preexisting hemiparesis. focal seizures and transient aphasia occurred in one patient each [38]. follezou et al. described 23 patients with malignant glioma who were treated with an intraarterial infusion of 400 mg/m2 of carboplatin every 4 weeks. one patient developed central neurotoxicity and another developed a reversible decrease in visual acuity [31]. cloughesy et al. reported the use of escalating doses of carboplatin (up to 1400 mg/hemisphere) infused either in the supra clinoid internal carotid artery or basilar artery above the anterior inferior cerebellar artery in 21 patients with recurrent glioma. one patient had permanent neuromotor decline. the predominant complication was hemopoietic toxicity. the median survival was 39 weeks [37]. in another series of 51 cases, authors detected one grade iii anemia, three grades iv and five grade iii thrombocytopenia and three grade iii neutropenia according to criteria of the national cancer institute common toxicity. these toxicities were all manageable easily. 3 cases of carotid spasms were detected and there was a asymptotic. these spasms were elicited by positioning of the catheter, and all 209 local application of carboplatin for recurrent glioblastoma multiformis resolved spontaneously. no cases of neurotoxicity had been detected in this work [28]. conclusion although recurrent glioblastoma multiformis has a poor survival, intra-arterial delivery of carboplatin may have a slight positive impact on patient survival. the procedure however is relatively safe with manageable complications. references 1. burkhardt jk, riina h, shin bj, moliterno j, hofstetter c, boockvar ja. intra-arterial chemotherapy for malignant gliomas: a critical analysis. interventional neuroradiology. 2011;17(3):286-95. 2. khosla d. concurrent therapy to enhance radiotherapeutic outcomes in glioblastoma. annals of translational medicine. 2016;4(3). 3. price sj, bulstrode h, mair r. high-grade gliomas and molecular biology of neurosurgical oncology. oxford textbook of neurological surgery. 2019:89. 4. paldor i, chaichana kl, brem h, tyler bm. targeted local therapy for management of intracranial high-grade gliomas. intracranial gliomas part iii-innovative treatment modalities. 32: karger publishers; 2018. p. 159-71. 5. rajeswaran a, trojan a, burnand b, giannelli m. efficacy and side effects of cisplatin-and carboplatin-based doublet chemotherapeutic regimens versus nonplatinum-based doublet chemotherapeutic regimens as first line treatment of metastatic non-small cell lung carcinoma: a systematic review of randomized controlled trials. lung cancer. 2008;59(1):1-11. 6. thatishetty av, agresti n, o'brien cb. chemotherapyinduced hepatotoxicity. clinics in liver disease. 2013;17(4):671-86. 7. riina h, knopman j, greenfield j, fralin s, gobin y, tsiouris a, et al. balloon-assisted superselective intra-arterial cerebral infusion of bevacizumab for malignant brainstem glioma: a technical note. interventional neuroradiology. 2010;16(1):71-6. 8. jeon j, kovanlikaya i, boockvar j, mao x, shin b, burkhardt j, et al. metabolic response of glioblastoma to superselective intra-arterial cerebral infusion of bevacizumab: a proton mr spectroscopic imaging study. american journal of neuroradiology. 2012;33(11):2095102. 9. stupp r, hegi me, mason wp, van den bent mj, taphoorn mj, janzer rc, et al. effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase iii study: 5-year analysis of the eortcncic trial. the lancet oncology. 2009;10(5):459-66. 10. gupta t, nair v, paul sn, kannan s, moiyadi a, epari s, et al. can irradiation of potential cancer stem-cell niche in the subventricular zone influence survival in patients with newly diagnosed glioblastoma? journal of neurooncology. 2012;109(1):195-203. 11. chen l, chaichana kl, kleinberg l, ye x, quinoneshinojosa a, redmond k. glioblastoma recurrence patterns near neural stem cell regions. radiotherapy and oncology. 2015;116(2):294-300. 12. iagaru a, mosci c, mittra e, zaharchuk g, fischbein n, harsh g, et al. glioblastoma multiforme recurrence: an exploratory study of 18f fpprgd2 pet/ct. radiology. 2015;277(2):497-506. 13. campos b, olsen lr, urup t, poulsen h. a comprehensive profile of recurrent glioblastoma. oncogene. 2016;35(45):5819. 14. noel g, mazeron j. reirradiation in primary or secondary brain tumors. cancer radiotherapie: journal de la societe francaise de radiotherapie oncologique. 2010;14(67):421-37. 15. fokas e, wacker u, gross mw, henzel m, encheva e, engenhart-cabillic r. hypofractionated stereotactic reirradiation of recurrent glioblastomas. strahlentherapie und onkologie. 2009;185(4):235-40. 16. fowler jf, tomé wa, fenwick jd, mehta mp. a challenge to traditional radiation oncology. international journal of radiation oncology* biology* physics. 2004;60(4):124156. 17. archavlis e, tselis n, birn g, ulrich p, baltas d, zamboglou n. survival analysis of hdr brachytherapy versus reoperation versus temozolomide alone: a retrospective cohort analysis of recurrent glioblastoma multiforme. bmj open. 2013;3(3):e002262. 18. niyazi m, ganswindt u, schwarz sb, kreth f-w, tonn j-c, geisler j, et al. irradiation and bevacizumab in high-grade glioma retreatment settings. international journal of radiation oncology* biology* physics. 2012;82(1):67-76. 19. ellis ja, banu m, hossain ss, singh-moon r, lavine sd, bruce jn, et al. reassessing the role of intra-arterial drug delivery for glioblastoma multiforme treatment. journal of drug delivery. 2015;2015. 20. hossain ss, hughes tj, decuzzi p. vascular deposition patterns for nanoparticles in an inflamed patient-specific arterial tree. biomechanics and modeling in mechanobiology. 2014;13(3):585-97. 21. boockvar ja, tsiouris aj, hofstetter cp, kovanlikaya i, fralin s, kesavabhotla k, et al. safety and maximum tolerated dose of superselective intraarterial cerebral infusion of bevacizumab after osmotic blood-brain barrier disruption for recurrent malignant glioma. journal of neurosurgery. 2011;114(3):624-32. 22. newton hb. intra-arterial chemotherapy of primary brain tumors. current treatment options in oncology. 2005;6(6):519-30. 23. doolittle nd, miner me, hall wa, siegal t, hanson ej, osztie e, et al. safety and efficacy of a multicenter study using intraarterial chemotherapy in conjunction with osmotic opening of the blood‐brain barrier for the 210 tareq abdul ghani hamid, abdul wahab mahmoud ibrahim, ibrahim ali awad et al. treatment of patients with malignant brain tumors. cancer. 2000;88(3):637-47. 24. chow kl, gobin yp, cloughesy t, sayre jw, villablanca jp, viñuela f. prognostic factors in recurrent glioblastoma multiforme and anaplastic astrocytoma treated with selective intra-arterial chemotherapy. american journal of neuroradiology. 2000;21(3):471-8. 25. qureshi ai, fareed m, suri k, khan j, sharma m, olson k, et al. superselective intra-arterial carboplatin for treatment of intracranial neoplasms: experience in 100 procedures. journal of neuro-oncology. 2001;51(2):151-8. 26. newton hb, slivka ma, stevens cl, bourekas ec, christoforidis ga, baujan ma, et al. intra-arterial carboplatin and intravenous etoposide for the treatment of recurrent and progressive non-gbm gliomas. journal of neuro-oncology. 2002;56(1):79-86. 27. newton hb, slivka ma, volpi c, bourekas ec, christoforidis ga, baujan ma, et al. intra-arterial carboplatin and intravenous etoposide for the treatment of metastatic brain tumors. journal of neuro-oncology. 2003;61(1):35-44. 28. fortin d, morin p-a, belzile f, mathieu d, paré f-m. intraarterial carboplatin as a salvage strategy in the treatment of recurrent glioblastoma multiforme. journal of neurooncology. 2014;119(2):397-403. 29. mathieu d, lecomte r, tsanaclis am, larouche a, fortin d. standardization and detailed characterization of the syngeneic fischer/f98 glioma model. canadian journal of neurological sciences. 2007;34(3):296-306. 30. charest g, sanche l, fortin d, mathieu d, paquette b. glioblastoma treatment: bypassing the toxicity of platinum compounds by using liposomal formulation and increasing treatment efficiency with concomitant radiotherapy. international journal of radiation oncology* biology* physics. 2012;84(1):244-9. 31. follezou j, fauchon f, chiras j. intraarterial infusion of carboplatin in the treatment of malignant gliomas: a phase ii study. neoplasma. 1989;36(3):349-52. 32. clocchiatti l, cartei g, lavaroni a, vigevani e, fabris g, tommasini g, et al. intra-arterial chemotherapy with carboplatin (cbdca) and vepesid (vp16) in primary malignant brain tumours: preliminary findings. interventional neuroradiology. 1996;2(4):277-81. 33. cloughesy tf, mochizuki ay, orpilla jr, hugo w, lee ah, davidson tb, et al. neoadjuvant anti-pd-1 immunotherapy promotes a survival benefit with intratumoral and systemic immune responses in recurrent glioblastoma. nature medicine. 2019;25(3):477-86. 34. yung wa, albright r, olson j, fredericks r, fink k, prados m, et al. a phase ii study of temozolomide vs. procarbazine in patients with glioblastoma multiforme at first relapse. british journal of cancer. 2000;83(5):588-93. 35. mrugala mm, crew lk, fink jr, spence am. carboplatin and bevacizumab for recurrent malignant glioma. oncology letters. 2012;4(5):1082-6. 36. tyler j, yamamoto y, diksic m, theron j, villemure j, worthington c, et al. pharmacokinetics of superselective intra-arterial and intravenous [11c] bcnu evaluated by pet. j nucl med. 1986;27(6):775-80. 37. cloughesy tf, gobin yp, black kl, viñuela f, taft f, kadkhoda b, et al. intra-arterial carboplatin chemotherapy for brain tumors: a dose escalation study based on cerebral blood flow. journal of neuro-oncology. 1997;35(2):121-32. 38. stewart dj, belanger jg, grahovac z, curuvija s, gionet lr, aitken se, et al. phase i study of intracarotid administration of carboplatin. neurosurgery. 1992;30(4):512-7. 39. weller m, van den bent m, tonn jc, stupp r, preusser m, cohen-jonathan-moyal e, et al. european association for neuro-oncology (eano) guideline on the diagnosis and treatment of adult astrocytic and oligodendroglial gliomas. the lancet oncology. 2017;18(6):e315-e29. 40. ringel f, group ss, pape h, group ss, sabel m, group ss, et al. clinical benefit from resection of recurrent glioblastomas: results of a multicenter study including 503 patients with recurrent glioblastomas undergoing surgical resection. neuro-oncology. 2015;18(1):96-104. 41. van linde me, brahm cg, de witt hamer pc, reijneveld jc, bruynzeel am, vandertop wp, et al. treatment outcome of patients with recurrent glioblastoma multiforme: a retrospective multicenter analysis. journal of neuro-oncology. 2017;135(1):183-92. 42. landy h, feun l, schwade j, snodgrass s, lu y, gutman f. retreatment of intracranial gliomas. southern medical journal. 1994;87(2):211-4. 43. ammirati m, galicich jh, arbit e, liao y. reoperation in the treatment of recurrent intracranial malignant gliomas. neurosurgery. 1987;21(5):607-14. 44. harsh gr, levin va, gutin ph, seager m, silver p, wilson cb. reoperation for recurrent glioblastoma and anaplastic astrocytoma. neurosurgery. 1987;21(5):61521. 45. bloch o, han sj, cha s, sun mz, aghi mk, mcdermott mw, et al. impact of extent of resection for recurrent glioblastoma on overall survival. journal of neurosurgery. 2012;117(6):1032-8. 46. oppenlander me, wolf ab, snyder la, bina r, wilson jr, coons sw, et al. an extent of resection threshold for recurrent glioblastoma and its risk for neurological morbidity. journal of neurosurgery. 2014;120(4):846-53. romanian neurosurgery (2019) xxxiii (2): pp. 183-187 doi: 10.33962/roneuro-2019-034 www.journals.lapub.co.uk/index.php/roneurosurgery traumatic complete transection of dorsal spinal cord un-associated with spinal fracture or subluxation. management review guru dutta satyarthee, satyajit panda * department of neurosurgery, neurosciences centre, aiims new delhi, india abstract complete transection of spinal cord is an extremely rare occurrence, and usually associated with spinal instability, fracture or spondylolisthesis and also have associated systemic polytrauma involving multiple organs injury. however, a complete transaction of spinal cord unassociated with fracture or dislocation or without abnormality on x-ray and ct scan imaging is extremely uncommon. kalfas et al. observed 11.2 % of cases had cord transection in the study of sixty-two cases spinal cord-injured patients, who underwent spinal mri, were additionally had evidence vertebral injury. in 2010, cha et al reported the first case of transection of cord in the cervical region in a 34yearadult male, as the first case in literature, which was not associated with any vertebral body fracture or dislocation. authors report an interesting case, 15-year boy, who had complete transection of the spinal cord associated with polytrauma following a motor vehicle accident, spinal x-ray and ct scan imaging was unremarkable, however spinal mri scan established the diagnosis. briefly, imaging, management and pertinent literature are reviewed. introduction acute spinal injury can present with a spectrum of pathology including vertebral body fracture, dislocation, cord contusion, but spinal cord transection represents very uncommon occurrence. [1-8] however mostly such cord transection is reported with spinal column injury in form of fracture, dislocation or spondyloptosis. however, unassociated with fracture dislocation is uncommon. in 2010, cha et al was first to report a case of cervical cord transection of cord in a 34yearmale, which was not associated with fracture or dislocation. [1,2] however, in a detailed radiological review, kalfas et al. reported his observation of sixty-two spinal cord-injured patients, who underwent spinal mri evaluation within the first thirty six hours of sustaining spinal injury, seven cases had evidence of anatomical cord transection with various types of fracture and dislocations. [3] spinal cord injury is usually associated with severe traumatic injury involving spine and other body keywords complete spinal cord transection, magnetic resonance imaging study, associated injury, management corresponding author guru dutta satyarthee department of neurosurgery, neurosciences centre, aiims new delhi, india duttaguru2002@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 184 guru dutta satyarthee, satyajit panda organs. however, paediatric population can sustain various grades of spinal cord injury without evidence of a radiographic abnormality, and acronym sciwora (spinal cord injury without radiographic abnormality) was coined in the year 1982 by pang and wilberger for describing cases sustaining spinal cord injury and presenting with clinical symptoms of traumatic myelopathy, however, no radiographic or computed tomographic scan shows evidence of spinal fracture or instability. [1] sciwora is considered rare in adults, but relatively commoner in children. in the paediatric cases, sciwora represents about 8 to 19% of all paediatric spinal cord injuries [4]. however, mri can show presence of in cases of sciwora. sciwora lesions have predilection for cervical spine commonly but can affect the thoracic or lumbar spine although much less frequently. sciwora in adults is rare, but is of considerable important because of the potential problems of management inherent in the diagnosis. authors report a case, who sustained complete transaction of spinal cord but without association of vertebral column fracture or dislocation. kalfas et al. reported observation of sixty-two spinal cord-injured patients, who underwent spinal mri evaluation within the first thirty-six hours of sustaining injury, showed presence of anatomical cord transection in 7 cases. [3] case illustration a 15year old male pillion rider presented to emergency services with the complaints of inability to move associate with numbness involving both lower limbs following a high-speed road traffic accident. he wore helmet and received initial first aid was given at primary health centre, evaluation on arrival to our emergency services, he had history of loss of consciousness for ten minutes, when regained consciousness, complained of severe pain in the abdomen. on arrival at hospital his pulse rate was 160 per minute and blood pressure was 70/40/mm hg. immediately resuscitation started with colloid and blood transfusion started, with momentary recovery of blood pressure followed by fall. gcs was e3vtm5 and pupils were normal size briskly reacting to light with motor evaluation showed flaccid paraplegia with absent deep tendon jerks. the x –ray chest and cervical spine was normal. non-contrast computed tomography of cervical spine showed was essentially normal with no evidence of fracture, subluxation or compromise of spinal canal. (figure 1) cranial computed tomography scan head showed presence of multiple contusions with diffuse cerebral edema with absence of midline shift. ultrasound abdomen revealed presence of hemoperitoneum, ct scan abdomen revealed presence of hepatic tear with hemoperitoneum. figure 1. computed tomography scan spine of 15-year male, sagittal section image of spine showing no evidence of fracture or dislocation. he was planned for emergency surgical exploration by trauma surgery team. he suffered cardiac arrest in casualty while shifting to operation theatre, but revived and immediately shifted to operation theatre and underwent emergency laparotomy under general anaesthesia. a midline laparotomy done; two litters of blood mixed collection were drained. intraoperative, solid organs were examined, showed presence of grade -3 liver laceration on anterolateral 185 traumatic complete transection of dorsal spinal cord un-associated with spinal fracture or subluxation surface in the second segment with bile staining with serosal tear found on greater curvature of stomach and associate retroperitoneal hematoma in ascending and descending mesocolon and gastric tear was also repaired, sub hepatic drain was placed and mesh laparostomy was carried out. in the postoperative phase, mri of whole spine was carried out to causes of paraparesis, showed non visualization of the spinal cord from upper border of d3 to lower border of d5 vertebra with retraction of upper and lower cord segment suggestive of complete cord transaction. (figure 2) foci of blooming seen in the retracted upper cord at d3 level suggestive of hemorrhage. in the proximal part of the transacted cord there was a linear t2 hyperintensity at d1-d3 level might be wallerian degeneration. t2/stir hyperintensity seen in the supraspinous and interspinous ligaments from c7 to d10 levels suggestive of sprain in ligaments. figure 2. mri, spine, t2 weighted image, sagittal section image of spine showing discontinuity of dorsal spinal cord at level of d3 to lower border of d5 vertebra with retraction of upper and lower cord segment suggestive of complete cord transaction. foci of blooming seen in the retracted upper cord at d3 level suggestive of haemorrhage. figure 3. magnetic resonance imaging study of dorsal spine, axial section, t2 weighted image of showing absence of spinal cord signal. discussion the incidence of sciwora is considered highest among children below eight years also being predisposed by presence of weaker neck muscles, and relatively heavy head and more horizontal orientation of facet joints and associated greater elasticity of vertebral ligaments. the cervical spinal cord is most commonly involved [5]. sciwora involvement in the thoracic is rare and contributes for about 10 to 13% of all paediatric sciwora cases. [4,5] the commonest cause of thoracic sciwora is high velocity trauma, including motor vehicular highspeed vehicular collisions, severe distraction injuries related to lap belts and crush injuries in slow-moving motor vehicles [5] other includes sports injuries, assault or gunshot injury and falls. in most cases, sciwora occurs as a result of hyperextension forces or from a direct frontal impact to the face and may to occur during sports such as diving, wrestling, and baseball. however, cha et al put forward combined hyperflexion-hyperextension mechanism for cervical cord transection. [2] in children, such movement of the vertebral column allows the musculoskeletal system to move beyond the normal physiological range of motion without the risk of fracture, however injury to the spinal cord is caused contusion or ischemia due to temporary occlusion of vertebral arteries followed by a spontaneous return of vertebrae to their original venous congestion within the compressed spinal cord is also a pathogenic factor. the onset of clinical symptoms is delayed from a few minutes to 48 hours after injury in about 50% of patients. this latency is associated with repeated micro-insults to the spinal cord from striking against the unstable vertebrae. various spinal cord pathology includes, signal cord swelling, contusion or oedema, however cord transaction is uncommon. [5] patients may present with variety of clinical 186 guru dutta satyarthee, satyajit panda presentation depending on severity of injury and location of involvement of spinal cord includes transient weakness, paraesthesia, numbness, paraparesis, quadriplegia, complete cord transection syndrome and brown–sequard syndrome. [17] ct scan spine is best for assessing the associated bony injuries which may need concomitant treatment consideration but does not assess the cord itself. mri is considered as investigation of choice and is often performed acute phase in the context of recent traumatic spinal injury and picks up spinal cord pathology, associated extramural hematoma, or hematomyelia, or ligament injury, which that may or may not be confirmed by trauma ct. the role of acute mri is usually to assess for the presence of acute pathologies treatable such as an epidural haematoma or cord compression, which can be targeted by surgical decompression. the identification of significant cord trans section can potentially contraindicate surgery. kalfas et al analyzed cases had spectrum of lesions including anatomical spinal cord transection in seven cases, other finding were 28 cases had spinal cord deformity secondary to extrinsic compression, 21 had focal cord enlargement/swelling, hyperintensity intramedullary lesions noted in 17 cases, and rest two cases had disc herniations. [3] boese et al. analyzed 114 patients, on admission, neurologic deficit assessed by the american spinal injury association impairment scale was an in 28%, b in 17%, c in 31%, and d in 25%. on basis of mri, they categorize finding. type i noted in 43%cases with no mri abnormalities and 57% exhibited abnormal scan results (type ii): 6% revealed extra neural (type imia), 38% intramural (type ibis) and 13% combined abnormalities (type sic). [15] pang classified mri finding into five common patterns, first type is complete cord disruption represents most severe injury predominantly involving upper cervical and thoracic spine in younger children as a result of flexion injury. second being major cord haemorrhage with axial mri showing haemorrhagic involvement of greater than 50% of cord, next is a minor cord haemorrhage, fourth is isolated cord edema and fifth pattern is groups of patients presenting with acute clinical neurologic deficit consistent with sciwora and with no evidence of injury in the cord on mri study. [17] prognosis depends on spinal cord pathology and associated spinal injury. for isolated spinal cord injury case with only cord oedema have most favorable prognosis but intermediate for cord oedema and contusion and remains worse for cord contusion and associated intramedullary hemorrhage. the prognosis for spinal cord transaction still remains very poor. however, in cases with sciwora, associated extrinsic compression caused by vertebral body fragment and disc must be surgically corrected. in cases with fracture may need spinal fixation and fusion. management of spinal cord transection is still a mystery, and no clear solution seems in the pipeline in near future. [6-9] satyarthee advocated ideally care management acute traumatic spinal cord injury should commence immediately at the moment of traumatic impact, continue during safe evacuation, immediate resuscitation by trained paramedics, adequate immobilization, and proper prehospital care, and emergence transportation to a specialized hospital after prompt resuscitation, a detailed neurologic evaluation, pertinent neuroimaging studies, medical intervention including maintenance of airway and circulation, augmentation and maintenance of target level mean arterial pressure, avoidance of any hypotensive episodes, assessment and appropriate care of associated systemic injury, early surgical spinal decompression as judiciously needed. [8] however, these are effective in minor cord injury, but for complete teransection of spinal cord, situation remains gloomy. [8-10] tabakow et al observed management of cases suffering complete spinal cord injury remains an unsolved clinical problem because of the lack of spontaneous regeneration of injured central axons. [13] exact management is still not available. [10-16] various suggested method are suggested mostly on experimental basis. olfactory ensheathing cells support axon outgrowth in the olfactory system, and transplantaion after spinal cord injury lead to axon regeneration and improvement in recovery. thornton et al. observed rats with mid-thoracic transection and olfactory ensheathing cells transplantation, and for assessing connectivity across the transection, pseudorabies virus injected into muscles of hind-limb and finally noted presence of large number of serotonergic axons crossed the rostral scar border and the area of neurofilamentpositive axons in the injury site. [11] authors concluded olfactory ensheathing cells transplantation can increase axonal growth across 187 traumatic complete transection of dorsal spinal cord un-associated with spinal fracture or subluxation the injury site and may promote recovery of propioception circuit. tabakow et al reported 38-year-old with asia a injury at 21 months. the olfactory bulbs were removed to obtain a culture containing olfactory ensheathing cells and olfactory nerve fibroblasts. the cultured cells were transplanted following resection of the glial scar. he improved to asia c with improved trunk stability, partial recovery of the voluntary movements of the lower extremities, and an increase of the muscle mass in the left thigh. neuroimaging confirmed grafts producing bridge over left side of the spinal cord with majority of the nerve grafts implant, and further neurophysiological examinations confirmed the restitution of the integrity of the corticospinal tracts. [ 13] conclusion every cases with suspected head injury sustaining can presenting with shock and paraplegia, a high index of suspicion for cord transaction should also be considered, although rarer. it is highly imperative that paediatrician, neurosurgeons, orthopaedician and emergency physician should be aware for entity total spinal cord transection. references 1. pang d, wilberger je jr. spinal cord injury without radiographic abnormalities in children. j neurosurg 1982; 57(1):114–129. 2. cha yh , cho th, suh jk. traumatic cervical cord transection without facet dislocations--a proposal of combined hyperflexion-hyperextension mechanism: a case report. j korean med sci. 2010 aug;25(8):1247-50. 3. kalfas i, wilberger j, goldberg a, prostko er. magnetic resonance imaging in acute spinal cord trauma. neurosurgery. 1988 sep;23(3):295-9. 4. carroll t, smith cd, liu x et al spinal cord injuries without radiologic abnormality in children: a systematic review. spinal cord 2015; 53(12):842–848. 5. parizel pm, van der zijden t, gaudino s et al. trauma of the spine and spinal cord: imaging strategies. eur spine j. 2010;19 suppl 1 (s1): s8-17. 6. satyarthee gd, sangani m, sinha s, agrawal d. management and outcome analysis of pediatric unstable thoracolumbar spine injury: large surgical series with literature review. j pediatr neurosci. 2017 jul-sep; 12(3):209-214. doi: 10.4103/jpn 7. farrell ca, hannon m, lee lk. pediatric spinal cord injury without radiographic abnormality in the era of advanced imaging. curr opin pediatr. 2017 ;29(3):286-290. 8. satyarthee gd. ways to improve outcomes of traumatic acute spinal cord injury: integrated approaches of improved prehospital care, the adoption of synergistic medical and surgical intervention, along with care for associated systemic injury and rehabilitation and social inclusion. world neurosurg. 2017;101:786-787 9. lukovic d, moreno-manzano v, lopez-mocholi e, rodriguez-jiménez fj, jendelova p, sykova e, oria m, stojkovic m, complete rat spinal cord transection as a faithful model of spinal cord injury for translational cell transplantation. erceg s. sci rep. 2015 apr 10;5:9640. 10. verma sk, singh pk, agrawal d, sinha s, gupta d, satyarthee gd, sharma bs. o-arm with navigation versus c-arm: a review of screw placement over 3 years at a major trauma center. br j neurosurg. 2016 dec;30(6):658-661. 11. thornton ma , mehta md , morad tt , ingraham kl , khankan rr , griffis kg ,et al. evidence of axon connectivity across a spinal cord transection in rats treated with epidural stimulation and motor training combined with olfactory ensheathing cell transplantation. exp neurol. 2018 jul 26. pii: s0014-4886(18)30263-2. doi: 10.1016/j.expneurol.2018.07.015. 12. ahmann pa, smith sa, schwartz jf, et al. spinal cord infarction due to minor trauma in children. neurology. 1975;25:301–7. 13. tabakow p , raisman g, fortuna w, czyz m, huber j, li d, szewczyk p, et al. functional regeneration of supraspinal connections in a patient with transected spinal cordfollowing transplantation of bulbar olfactory ensheathing cells with peripheral nerve bridging. cell transplant. 2014;23(12):1631-55. 14. chandrashekhara sh, kumar a, gamanagatti s, kapoor k, mukund a, aggarwal d, sinha s. unusual traumatic spondyloptosis causing complete transection of spinal cord. unusual traumatic spondyloptosis causing complete transection of spinal cord. int orthop. 2011 nov;35(11):1671-5. 15. boese ck , oppermann j, siewe j, eysel p, scheyerer mj, lechler p. spinal cord injury without radiologic abnormality in children: a systematic review and meta-analysis. j trauma acute care surg. 2015 apr;78(4):874-82. 16. szwedowski d, walecki j spinal cord injury without radiographic abnormality (sciwora)—clinical and radiological aspects. pol j radiol. 2014; 79:461–464. 17. pang d. spinal cord injury without radiographic abnormality in children, 2 decades later. neurosurgery 2004; 55:1325–1342. doi: 10.33962/roneuro -2020-047 a technical note. the role of liliequist membrane fenestration during the pterional approach for anterior circulation aneurysm clipping samer s. hoz, zaid aljuboori, zahraa f. al-sharshahi romanian neurosurgery (2020) xxxiv (1): pp. 321-325 doi: 10.33962/roneuro-2020-047 www.journals.lapub.co.uk/index.php/roneurosurgery a technical note. the role of liliequist membrane fenestration during the pterional approach for anterior circulation aneurysm clipping samer s. hoz1, zaid aljuboori2, zahraa f. al-sharshahi3 1 mbchb, fabms/neurosurgery, department of neurosurgery, neurosurgery teaching hospital, baghdad, iraq 2 md, neurosurgery, department of neurosurgery, university of louisville, kentucky, usa 3 mb, bch bao (nui, rcsi), lrcp & si, royal college of surgeons in ireland (alumnus), dublin, ireland abstract the liliequist membrane is a critical membrane located at the base of the brain separating the supratentorial from the infratentorial cisterns. the advantages of liliequist membrane fenestration as a critical part of the pterional trans-sylvian approach for ruptured anterior circulation aneurysm clipping is not well established. we demonstrated that the fundamental role of liliequist membrane fenestration is brain relaxation through the egress of csf that is not usually gained from other modalities (e.g., placement of a lumbar drain, fenestration of lamina terminalis) in this specific setting. background dissection through the arachnoid planes and fenestration of the accessible cisterns are the cornerstones of modern microsurgery while dealing with intracranial lesions. the liliequist membrane is a horizontal arachnoid membrane attached to the dorsum sellae anteriorly, the mammillary body superiorly and the basilar artery posteriorly. it is bounded by the oculomotor nerve on each side. embryologically, the liliequist membrane is considered a remnant of the primary tentorium (1). the first recognition of the liliequist membrane was in 1875 by key and retzius (2). eight decades later, it was rediscovered by an eminent swedish radiologist named bengt liliequist (1923-1972) as part of his doctoral thesis titled “the subarachnoid cisterns. an anatomical and roentgenologic study” (3). the liliequist membrane became a universally accepted medical eponym and officially settled through keywords liliequist membrane fenestration, pterional approach, anterior circulation aneurysm corresponding author: zahraa al-sharshahi mb, bch bao (nui, rcsi), lrcp & si, royal college of surgeons in ireland (alumnus), dublin, ireland zahraaalsharshahi@rcsi.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 322 samer s. hoz, zaid aljuboori, zahraa f. al-sharshahi yasargil’s paper “anatomical observations of the subarachnoid cisterns of the brain during surgery” in1976 (34). since that time, the liliequist membrane underwent detailed descriptions in literature based on cadaveric and radiological studies (4-8). in this article, we describe the technique and benefits of liliequist membrane fenestration to achieve brain relaxation during the pterional transsylvian approach for ruptured anterior circulation aneurysm clipping. pertinent anatomy of the liliequist membrane intracranially, the arachnoid membranes can be either outer or inner membranes. the outer membranes include both the convexity and the basal arachnoid membranes, while the inner membranes include the trabecular arachnoid membranes which encase the neurovascular bundle within the cisterns (8). the liliequist membrane is an inner rather than outer arachnoid membrane (9). there is some controversy regarding the number of layers of the liliequist membrane. the early literature published by liliequist and yasargil described a single-layer membrane (5,10-12). later studies by matsuno and rhoton (13,14) assumed the two-layer model (the diencephalic membrane and the mesencephalic membrane). recently, the existence of a third layer was described, but it was questionable as to whether this third layer represents a distinct layer or sparse arachnoid trabeculae (8). from the dorsum sellae, the diencephalic membrane extends superoposteriorly to the mammillary bodies between the chiasmatic and the interpeduncular cisterns and can sometimes be identified radiologically in the sagittal mri view. the mesencephalic membrane is a thin sheet that extends inferoposteriorly to the pontomesencephalic junction, between the interpeduncular and the prepontine cisterns. laterally, the liliequist membrane is attached to the oculomotor nerve and/or the uncus and tentorium. the liliequist membrane is closely related and variably penetrated by the posterior communicating and basilar arteries and their perforating branches (4-8,10-14). the general indications for liliequist membrane fenestration liliequist membrane fenestration plays an important role in multiple procedures related to microscopic or endoscopic cranial surgery: 1. in surgery for tumors in the sellar and parasellar regions such as craniopharyngiomas, meningiomas, basilar tip aneurysms, and arachnoid cysts, liliequist membrane fenestration provides an effective surgical corridor and promotes brain relaxation through csf egress. (1,15,17). 2. liliequist membrane fenestration is one of the most critical steps for endoscopic third ventriculostomy success. 3. some reports consider the microscopic fenestration of the basal subarachnoid cisterns as an effective method to decrease the intracranial pressure in acute intra-operative brain swelling and also in severe traumatic brain injury. these reports advocate the inclusion of liliequist membrane fenestration as a mandatory procedural step to achieve a good surgical outcome (16,18) the technique for liliequist membrane fenestration during the pterional approach for anterior circulation aneurysm clipping the pterional approach is the preferred approach for the clipping of most anterior circulation aneurysms except for the distal anterior cerebral artery aneurysm. using the trans-sylvian route, the liliequist membrane can be approached laterally. opening the liliequist membrane can be achieved through different corridors; namely, the carotidoculomotor triangle, the optico-carotid triangle and even through the interoptic space. fenestration through the carotid-oculomotor space is the most convenient, relatively wide and safe technique. after dural opening, the sylvian fissure is widely opened from inside to outside on the frontal side of the sylvian veins and the proximal segment of the middle cerebral artery until the internal carotid artery bifurcation. frontal and temporal retractors are gently applied; these retractors should “hold” the brain tissue with intermittent retraction to avoid vascular compromise. the frontal lobe is elevated, and the temporal lobe is retracted gently downward and posteriorly. the carotid cistern is opened and the thickened arachnoid fibers over the origins of the anterior and middle cerebral arteries are released. once the 3rd nerve is identified, the carotidoculomotor triangle is dissected and subsequently 323 the role of liliequist membrane fenestration during the pterional approach the deeper membrane of liliequist can be identified. as the exposure is deepened, the surgeon will extend the arachnoid opening laterally over the third nerve. sectioning of the liliequist membrane should be started from its anterior part as there is a large space behind the membrane. then, the interpeduncular cistern is opened through caudal dissection of the liliequist membrane between the oculomotor nerve and the internal carotid artery to release the cerebrospinal fluid. at this point, the posterior communicating and the anterior choroidal arteries may be visualized as they arise from the posterior surface of the internal carotid artery (the posterior communicating artery courses perpendicular to the liliequist membrane whereas the anterior choroidal artery courses obliquely into the crural cistern) (12). the egress of the csf and the identification of the basilar artery within the inter-peduncular cistern is the critical step that ensures the completion of the fenestration process. additional steps were suggested by some reports including irrigation and mechanical cleaning of blood clots beyond the liliequist membrane to minimize the possibility of postoperative vasospasm and hydrocephaly (15,16). sharp dissection is always advised to minimize the risk of uncontrolled bleeding from tearing of the vessel wall. also, the blunt and vigorous dissection may cause disastrous consequences by injuring the hypothalamus either directly or indirectly, by affecting its blood supply. structures at risk during this step include the posterior communicating artery or its perforators, the oculomotor nerve or its blood supply and the proximal part of the superior cerebellar artery. in the case of sah due to a ruptured aneurysm, several studies have described the effectiveness of liliequist membrane fenestration, either alone or in tandem with lamina terminalis fenestration, in reducing the incidence of post-sah hydrocephalus, (9, 12, 15, 19-21). however, none of these studies focused on the effect of liliequist membrane fenestration on brain relaxation specifically, which is crucial in such complex procedures regardless of the presence of hydrocephaly. liliequist membrane fenestration will create a free connection between the supratentorial and infratentorial compartments which represents the crucial advantage of liliequist membrane fenestration over the opening of the cisterns or lamina terminalis; this fact was supported by yaşargil and winkler-lawton et al reports through the “fifth ventricle theory” (12, 19). the fifth ventricle theory can be described as the following; in cases of aneurysmal sah, the liliequist membrane will entrap blood clots and it will be inflamed and thickened, thus the interpeduncular and prepontine cisterns will be isolated and dilated with csf creating a “fifth ventricle”. at this point, liliequist membrane fenestration will result in dramatic csf egress with striking brain relaxation which renders further surgical steps safer and more effective. castro-flores et al have suggested that in several patients, even after the opening of the supratentorial cisterns, the csf pathway will remain constricted until the liliequist membrane is opened (15). an illustrative case a 59-year male presented to the emergency department with an altered level of consciousness (glasgow coma scale:9) of sudden onset. initial resuscitation was done and the patient was transferred to the intensive care unit. a brain ct scan showed left gyrus rectus hemorrhage. contrasted brain ct scan and ct angiography revealed complex ruptured anterior communicating artery aneurysm with a wide neck, and hypoplastic left proximal anterior cerebral artery. the anterior communicating artery was vertically oriented, and the anterior cerebral arteries were connected distally to the anterior communicating artery, with two murphy's teats (figure 1a). surgical clipping through the standard right pterional trans-sylvian approach was chosen. after dural opening, around 20cc of csf was drained through a lumbar drain. a microsurgical arachnoid dissection was performed using an operative microscope; starting with the opening the proximal sylvian fissure and the carotid cisterns; there was minimal egress of csf. the liliequist membrane was identified and opened lateral to the supracliniod internal carotid artery through the carotid-oculomotor space. at this point, there was a striking csf egress that filled the surgical field despite repetitive suctioning. this csf egress had a profound effect on brain relaxation, provided us a wide operative corridor, and rendered the subsequent steps of aneurysm dissection and clipping more feasible. (figure 2). 324 samer s. hoz, zaid aljuboori, zahraa f. al-sharshahi the postoperative course was uneventful and the patient gradually improved and was discharged with no neurological deficits (figure 1b and c). figure 1. illustrative case of a ruptured anterior communicating artery aneurysm. a: contrasted ct scan of the brain showing the left gyrus rectus due to a ruptured anterior communicating artery aneurysm. b: an intraoperative microscopic view showing a twoclip reconstruction for the aneurysmal neck through the right pterional trans-sylvian approach. c: an early postoperative brain ct scan showing the clipping result. figure 2. stages of liliequist membrane fenestration through the right pterional trans-sylvian approach (intraoperative microscopic view). the liliequist membrane identified as a whitish layer lateral to the supracliniod internal carotid artery through the carotidoculomotor space. (a) opening the liliequist membrane resulted in striking csf egress that filled the surgical field several times (b). (+): pointer on the liliequist membrane, f: frontal lobe, t: temporal lobe, c: internal carotid artery, on: optic nerve. conclusion fenestration of the liliequist membrane has a fundamental role during the pterional trans-sylvian approach for ruptured anterior circulation aneurysm clipping as it allows brain relaxation through egress of csf that is not usually achieved through other 325 the role of liliequist membrane fenestration during the pterional approach modalities (e.g, placement of a lumbar drain, fenestration of lamina terminalis). further studies are needed to verify this observation towards making the fenestration of the liliequist membrane a recommended surgical step rather than an optional one. abbreviations mri: magnetic resonance imaging; csf: cerebrospinal fluid, sah: subarachnoid hemorrhage. declaration consent for publication: our local institutional consent was obtained from the patient. competing interests: the authors declare that they have no competing interests. funding: nothing to declare. references 1. froelich sc, aziz km, cohen pd, loveren hr, keller jt. microsurgical and endoscopic anatomy of liliequist's membrane: a complex and variable structure of the basal cisterns. operative neurosurgery. 2008 jul 1;63(suppl_1):ons1-9. 2. retzius mg, key a. studien in der anatomie des nervensystems und des bindegewebes, von axel key und gustaf retzius,... samson und wallin; 1875. 3. connor jr de, nanda a. bengt liliequist: life and accomplishments of a true renaissance man. journal of neurosurgery. 2017 feb;126(2):645-9. 4. matsuno h, rhoton jr al, peace d. microsurgical anatomy of the posterior fossa cisterns. neurosurgery. 1988 jul 1;23(1):58-80. 5. brasil av, schneider fl. anatomy of liliequist membrane. neurosurgery 1993; 32:956 –960. 6. zhang m, an pc. liliequist's membrane is a fold of the arachnoid mater: study using sheet plastination and scanning electron microscopy. neurosurgery. 2000 oct 1;47(4):902-9. 7. vinas fc, panigrahi m. microsurgical anatomy of the liliequist's membrane and surrounding neurovascular territories. min-minimally invasive neurosurgery. 2001 jun;44(02):104-9. 8. lü j, zhu xi. microsurgical anatomy of liliequist's membrane. min-minimally invasive neurosurgery. 2003 jun;46(03):149-54. 9. zhang xa, qi st, huang gl, long h, fan j, peng jx. anatomical and histological study of liliequist’s membrane: with emphasis on its nature and lateral attachments. child's nervous system. 2012 jan 1;28(1):65-72. 10. liliequist b. the anatomy of the subarachnoid cisterns. acta radiologica. 1956 jul(1-2):61-71. 11. epstein bs. the role of a transverse arachnoidal membrane within the interpeduncular cistern in the passage of pantopaque into the cranial cavity. radiology. 1965 nov;85(5):914-20. 12. yasargil mg. microneurosurgery. new york: thieme verlag, 1984; 27: 15±53 13. matsuno h, rhoton jr al, peace d. microsurgical anatomy of the posterior fossa cisterns. neurosurgery. 1988 jul 1;23(1):58-80. 14. rhoton al. the posterior fossa cisterns. neurosurgery 2000; 47 (suppl): 297 ± 297 15. juan antonio castro-flores., et al. “efficacy of the lamina terminalis fenestration associated with the liliequist membrane fenestration in reducing shunt-dependent hydrocephalus following aneurysm surgery in the acute phase of aneurysmal subarachnoid hemorrhage”. ec neurology 2.4 (2015): 162-166. 16. cherian i, grasso g, bernardo a, munakomi s. anatomy and physiology of cisternostomy. chinese journal of traumatology. 2016 feb 1;19(1):7-10. 17. miyajima m, arai h, okuda o, hishii m, nakanishi h, sato k. possible origin of suprasellar arachnoid cysts: neuroimaging and neurosurgical observations in nine cases. journal of neurosurgery. 2000 jul;93(1):62-7. 18. abdulqader mn, al-tameemi ah, salih h, hoz ss, al ramadan ah, salazar lr. acute intra-operative brain swelling managed effectively with emergency basal cisternostomy: a case report. journal of acute disease. 2018 jan 1;7(1):43. 19. winkler ea, burkhardt jk, rutledge wc, rick jw, partow cp, yue jk, birk h, bach am, raygor kp, lawton mt. reduction of shunt dependency rates following aneurysmal subarachnoid hemorrhage by tandem fenestration of the lamina terminalis and membrane of liliequist during microsurgical aneurysm repair. journal of neurosurgery. 2017 dec 15:1-7. 20. ultrastrüktürel hs. ultrastructural changes in the liliequist membrane in the hydrocephalic process and its implications for the endoscopic third ventriculostomy procedure. turkish neurosurgery. 2011;21(3):359-66. 21. wang ss, zheng hp, zhang fh, wang rm. microsurgical anatomy of liliequist’s membrane demonstrating threedimensional configuration. acta neurochirurgica. 2011 jan 1;153(1):191-200. doi: 10.33962/roneuro-2022-072 the assessment of risk factors for brainstem injuries and supratentorial brain injuries in patients with traumatic brain injury iulia-sevastiana pastor, lăcrimioara perju dumbravă, costel siserman, horațiu stan, ioana para, delia lupu, ioan ștefan florian romanian neurosurgery (2022) xxxvi (4): pp. 393-398 doi: 10.33962/roneuro-2022-072 www.journals.lapub.co.uk/index.php/roneurosurgery the assessment of risk factors for brainstem injuries and supratentorial brain injuries in patients with traumatic brain injury iulia-sevastiana pastor1, lăcrimioara perju dumbravă2, costel siserman3, horațiu stan1, ioana para4, delia lupu5, ioan ștefan florian1 1 department of neurosurgery, faculty of medicine, "iuliu hațieganu" university of medicine and pharmacy, cluj-napoca, romania 2 1st department of neurology, faculty of medicine, "iuliu hațieganu" university of medicine and pharmacy, cluj-napoca, romania 3 department of legal medicine, faculty of medicine, "iuliu hațieganu" university of medicine and pharmacy, cluj-napoca, romania 4 4th department of internal medicine, faculty of medicine, "iuliu hațieganu" university of medicine and pharmacy, cluj-napoca, romania 5 2nd department of internal medicine medical clinic ii, faculty of medicine, "iuliu hațieganu" university of medicine and pharmacy, cluj-napoca, romania abstract traumatic brain injury (tbi) is an important cause of death with a significant worldwide percentage. in the united states, there are approximately 2.8 million tbis yearly with 250,000 hospitalized patients and 50,000 tbi-related deaths. every year, there are one million hospitalizations in the european union, resulting in more than 50,000 deaths, most of which occur due to road traffic accidents. needless to say, these estimations varied based on the different sources of data. the patient’s outcome is determined by the context of the trauma, the type of lesion, as well as other factors. the aim of the study was to assess variables associated with brainstem injury and supra-tentorial brain injury in patients with tbi. this cohort included 70 consecutive tbi-related deaths from the institute of legal medicine cluj-napoca. there was a significant difference in brainstem contusion (haemorrhage contusion) in patients younger than 60. according to the computed tomography (ct) data, brain contusion and laceration were observed in association with brainstem contusion in a significant percentage of tbi-related deaths (p=0.016). neither the meningocerebral blood collections nor the intraparenchymal hematomas had a significant occurrence with brainstem contusion. the diffuse axonal injuries were detected on a ct scan in a significant number of cases with brainstem contusion (p=0.011). the mass effect with brain herniation in the posterior fossa was associated with the occurrence of brainstem contusion, possibly as an extensive process (p=0.041). keywords brainstem injury, supratentorial brain injury, severe traumatic brain injury, imagistic data, histopathological data corresponding author: iulia-sevastiana pastor department of neurosurgery, faculty of medicine, "iuliu hațieganu" university of medicine and pharmacy, cluj-napoca, romania iulia.pastor@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published december 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 394 iulia-sevastiana pastor, lăcrimioara perju dumbravă, costel siserman et al. analyzing the histopathological data, we observed the significant presence of intracranial haemorrhage in association with a hemorrhagic contusion in the brainstem (p=0.004), but not with meningeal haemorrhage. the poor neurological assessment evaluated by gcs was not an independent variable in relation with this brainstem lesion. that was probably caused by the complexity of the tbi. we did not include this variable in a multivariate analysis considering the poor outcome for all patients introduction traumatic brain injury (tbi) has an important impact regarding the overall mortality rate and the permanent disability. the brain injuries result from various mechanisms, the most common of which are related to falls (35%) and motor vehicle collisions (17%) (1). also, the head wounds complete the high incidence of death. tbi is clinically divided into mild, moderate and severe; and the lesions are described histologically as primary and secondary brain tissue injuries. in the majority of cases the primary lesions involve the occurrence of secondary mechanisms such as brain edema, elevated intracranial pressure and brain herniation. these secondary lesions are the consequence of impaired cerebral blood flow regulation and brain metabolism alterations with upregulation of inflammatory mediators, oxidative stress, and vasospasm (2). the prognostic of tbi depends on multiple factors, some of which are: the anatomical localization of the primary lesion, the type of injury, the secondary mechanisms, the proportion of damaged brain tissue, and also the accurate management for tbi. an acute hemorrhage or a contusion is clearly detected with an appropriate technique (computer tomography) or during the autopsy as morphopathology aspects. these aspects should explain the prognostic of tbi. diffuse axonal injury (dai) is often observed in extensive brain damage with intracranial hemorrhage, after rapid and sustained deceleration or acceleration of the brain (3). dai occurred in up to 50% of traumatic brain injuries (tbis), detected by magnetic resonance imaging (mri), in the united states (4). the brainstem injury is an important cause of death, related to the anatomical and functional mechanisms of the cardio-respiratory control in the lower brainstem and spinal cord (5). some types of posterior fossa lesions are difficult to detect on the mri and are not completely understood. also, the correlation between the brainstem injury and the outcome is still unclear. of course, the researchers assumed a relationship between the brainstem lesions and other brain lesions, from the supratentorial fossa. these could be explained by secondary lesions that occurred as a consequence of the primary lesions. brain edema is one of the most important secondary lesions that occurs almost in every tbi, including the brainstem injury or the supratentorial brain injury. beside of the common mechanism of brain edema, cytotoxic or vasogenic, there is currently discussed about a new term "csf(cerebrospinal fluid) shift edema" that defined a new mechanism of brain edema occurred in traumatic subarachnoid hemorrhage, as a consequence of rapid shift of csf from the cisterns. (6) there are many instances where the initial cortical contusion develops at the white/gray border with expansion into overlying grey matter (7). contusion progression was found with a frequency of 63%-70% (8)(9). tbi is frecquently associated with coma status, caused by alteration of ascending arousal system, that could be observed in dai with widespread damage white matter or mainly in bilateral brainstem injury.(10) despite the preclinical and clinical management during hospitalization which is mainly focused on preventing the secondary lesion, the outcome of patients with brainstem injury is still discouraging. in this study we assessed the variables associated with brainstem injury and supratentorial brain injury in patients with tbi, and to assess imagery data related to the tbi. methods the study was retrospective, longitudinal, observational, analytical, cohort type. in this study we included 70 tbi-related deaths from the institute of legal medicine cluj-napoca, from january 2017 to december 2021. the data were noted from the reports of eligible patients for this study. this study was approved by the clinical ethics committee of the ˝iuliu haţieganu˝ university of medicine and pharmacy in cluj-napoca. the eligible cases for this study were: the autopsied cases with tbi who were admitted in a department of neurosurgery before death. patients with tbi who died immediately after trauma were excluded from the study, because we considered that they had a fatal brain injury. in the first part of the analysis, we noted the demographical information and the following clinical 395 risk factors for brainstem injuries and supratentorial brain injuries data: the neurological status related to glasgow coma scale (gcs) on initial evaluation, the classification of tbi (mild, moderate and severe), the comorbidities, the type of surgical intervention used, the complications developed during hospitalization, the number of days of hospitalization until death occurred. we recorded the imagistic data detected on the initial ct: the primary cerebral lesions subdural hematoma and its maximal thickness (in millimeters, mm), intraparenchymal hematoma and its maximal thickness (mm), subarachnoid hemorrhage, contusion and laceration, diffuse axonal injuries, cranial fracture; and the secondary brain lesions – brain edema, brain herniation and the midline shift. in the next part we noted the microscopic aspects of the brain lesions from the histopathological reports. we distinguished the cases with brainstem injuries from cases without them and we established two groups on this criterion. we defined the brainstem contusion as the lesion with a hemorrhagic character in the brainstem tissue, as viewed microscopically. we considered that the brainstem contusion would be a primary lesion or a consequence of an expansive process from the other brain lesions. also, we noted the presence of meningeal hemorrhage or intracranial hemorrhage from the histopathological reports. statistical analysis was carried out using the medcalc statistical software version 19.4.1 (medcalc software ltd, ostend, belgium; https://www.medc alc.org; 2020). quantitative data was tested for normality of distribution using the shapiro wilk test and was characterized by median and 25, 75 percentiles. qualitative data were expressed as frequency and percentage. comparisons between groups were performed using the mann-whitney or chi-square tests, whenever appropriate. a p value <0.05 was considered statistically significant. results the demographical and clinical data are described in detail, in table i. in this study there were 36 patients with histopathological brainstem contusion. patients with brainstem contusions were significantly younger than patients without them, but there was no difference noted between males and females. also, we analyzed the impact of the brainstem lesion on the clinical status of patients. we did not observe a correlation between the consciousness state and the patients with brainstem contusion, neither with the severity of the tbi. patients with comorbidities such as chronic consumption of alcohol, arterial hypertension and atrial fibrillation presented a significant occurrence of brainstem contusion. the surgery status was not related with the localization of the lesions. table 1. demographic and clinical data variable non histopathological brainstem contusion (n=34) histopathological brainstem contusion (n=36) p age 65 (56; 82) 59.5(32.5; 73.5) 0.014 sex, n (%) m 21 (61.8%) 27 (75%) 0.3 f 13 (38.2%) 9 (25%) gcs 4 (3.75; 7.25) 3.5 (3; 7) 0.4 tbi, n (%) mild 5 (14.7%) 4 (11.1%) 0.7 moderate 7 (20.6 %) 6 (16.7%) severe 22 (64.7%) 26 (72.2%) comorbidities, n (%) none 7 (20.6%) 22 (61.1%) 0.01 arterial hypertension 7 (20.6%) 6 (16.7%) chronic alcohol composition 4 (11.8%) 5 (13.9%) atrial fibrillation 16 (47.1%) 3 (8.3%) surgery, n (%) no 9 (26.5%) 12 (33.3%) 0.7 applied 25 (73.5%) 24 (66.7%) complications, n (%) none 25 (73.5%) 26 (72.2%) 0.1 hemorrhagic shock 0 (0.0%) 2 (5.6 %) septic shock 3 (8.8%) 0 (0.0%) bronchopneumonia 6 (17.6%) 8 (22.2%) days of hospitalization 8.5 (4.5; 15.25) 6 (3; 10) 0.8 396 iulia-sevastiana pastor, lăcrimioara perju dumbravă, costel siserman et al. table 2. imagistic data variable non histopathological brainstem contusion histopathological brainstem contusion p subdural hematoma, n (%) absent 5 (14.7%) 8 (22.2%) 0.6 present 29 (85.3%) 28 (77.8%) thickness of subdural hematoma, mm 9.5 (6.75; 19.50) 15.50 (11; 24.5) 0.3 intraparenchymal hematoma, n (%) absent 25 (73.5%) 20 (55.6%) 0.1 present 9 (26.5%) 16 (44.4%) thickness of intraparenchymal hematoma, mm 32.5 (11; 71.5) 31 (6.25; 41) 0.9 subarachnoid hemorrhage, n (%) absent 25 (73.5%) 24 (66.7%) 0.7 present 9 (26.5%) 12 (33.3%) brain contusion and laceration, n (%) absent 23 (67.6%) 13 (36.1%) 0.01 present 11 (32.4%) 23 (63.9%) midline shift, mm 10.5 (5.5; 14.5) 7 (4; 9.5) 0.4 diffuse axonal injury, n (%) absent 30 (88.2%) 21 (58.3%) 0.01 present 4 (11.8%) 15 (41.7%) brain edema, n (%) absent 7 (20.6%) 6 (16.7%) 0.9 present 27 (79.4%) 30 (83.3%) brain herniation, n (%) absent 26 (76.5%) 18 (50.0%) 0.04 present 8 (23.5%) 18 (50.0%) cranial fracture, n (%) skull dome 19 (59.9%) 16 (44.4%) 0.5 skull base 9 (26.5%) 8 (22.2%) skull dome and base 4 (11.8%) 7 (19.4%) table 3. histopathological data variable non histopathological brainstem contusion histopathological brainstem contusion p meningeal hemorrhage, n (%) absent 3 (8.8%) 5 (13.9%) 0.7 present 31 (91.2%) 31 (86.1%) intracranial hemorrhage, n (%) absent 19 (55.9%) 7 (19.4%) 0.004 present 15 (44.1%) 29 (80.6%) ct detected all the other brain lesions, beside the brainstem injury. the supratentorial brain lesions were assessed according to the presence or absence of brainstem contusion. the cerebral blood collections did not seem to have a direct relation with the brainstem injury. the meningocerebral collection such as the subdural hematoma (sdh) was an independent factor of tbi. neither the thickness of the subdural hematoma or the midline shift did not describe a causal relation with the posterior fossa lesion. beside this, a direct relation was found between the supratentorial brain laceration and the brainstem contusion. diffuse axonal injuries were detected in a significant number of patients with brainstem contusion (p= 0.011). another diffuse brain injury, namely brain herniation as a consequence of brain edema, was a significant information which showed a correlation with brainstem contusion. all the supratentorial lesions and their comparisons are mentioned in table ii. analyzing the histopathological data, we observed a significant presence of intracranial hemorrhage in patients with brainstem contusion (p=0.004), but this association was not reported for meningeal hemorrhage. the comparisons of these histopathological aspects are described in table iii. discussion in some cases of brain trauma, the exact mechanism which lead to death is difficult to explain. the physiopathological mechanism that follows tbi is not completely known and is still an investigated subject. the fatal head impact was characterized by a depression activity on electrophysiology in both cortex and brainstem and of course, death occurred immediately. (11) in mild and severe tbi, the lesion could be limited at a part of the brain. in terms of its location, it does not always include the vital centers from the brainstem that generate and maintain the cardiac and respiratory rhythm. it is well known that 397 risk factors for brainstem injuries and supratentorial brain injuries the mechanisms of central control are complex, by receiving signals from other sites while also having a nervous, reflex and humoral regulation. it is still challenging to know the mechanism of death in tbi when the primary lesion does not include the vital centers from the brainstem or spinal cord. in this study we were interested to find out the variables associated with the brain lesions from different locations of the brain. we were looking at the supratentorial and the brainstem lesions, focusing on their imagistic and microscopic aspects. in regard to the relation with the supratentorial injuries, mannion et all studied the aspects of the brain lesions, detected mostly on mri. (12) in their study, the brainstem injuries were observed in association with severe diffuse axonal injury or in the context of a significant mass lesion and all of those patients had a poor outcome.(12) only two patients from their study had a good outcome and that was in association with minor supratentorial abnormalities. (12) evaluating the outcome, john r williams showed in their study that the patients with associated brainstem and cerebrum injury had an unfavorable outcome compared with duret hemorrhage alone or brainstem contusion.(13) in contrast, the duret hemorrhage was associated with transtentorial herniation as a consequence of severely elevated intracranial pressure (14) in our study we showed a significant association of brainstem injury with supratentorial lesions, including diffuse axonal injuries and brain herniation. despite worse outcome, moen et all evaluated through mri the traumatic axonal injuries and they demonstrated the reduction of non-hemorrhagic lesions from hemispheres and corpus callosum and the complete absence of brainstem lesions, 3 months after tbi. (15) the hemorrhagic axonal injuries were only attenuated at the 3 months examination. (15) even though, they observed an important evolution of traumatic axonal injury, the number of lesions and their volume on mri predicted a worse clinical prognosis. (15) in the same study, quoted at 4 points, the authors found that isolated traumatic axonal injury or other brainstem lesions with a volume less than 1 ml measured on the ct-scan, predicted a favorable outcome. (4) in contrast, the brainstem lesions (contusion or duret hemorrhage) with a volume larger than 1 ml were against the favorable long-term outcome. (4) isolated tai in brainstem are caused mostly after rotational acceleration mechanism and they tend to have the prospect of recovery. (16) (17) (18) besides, the hemorrhagic brainstem contusion and durret hemorrhage are the result of more complex intracranial mechanisms and they could lead to a more severe brainstem injury. (16) the poor neurological assessment evaluated by gcs was not an independent variable in relation with brainstem lesions in our study. that was probably caused by the complexity of tbi. we did not include this variable in a multivariate analysis considering the poor outcome for all patients. two extensive studies, the international mission on prognosis and analysis of clinical trials in traumatic brain injury database (impact models) and the corticosteroid randomisation after significant head injury trial data (crash models) were performed to predict the mortality and unfavourable outcome and in both the gcs variable predicted it. (19)(20) conclusion the brainstem contusion was reported to the clinical, imagistic and other histopathological aspects of tbi. related to the primary supratentorial lesions, the extensive brain laceration was significantly associated with the brainstem injury. diffuse axonal injuries were detected on ct for a significant number of cases with brainstem contusion (p =0.01). the mass effect with brain herniation in the posterior fossa was associated with the occurrence of brainstem contusion, possibly as an extensive process. the histopathological data showed a significant presence of intracranial hemorrhage with hemorrhage contusion in brainstem, but not with meningeal hemorrhage. the poor neurological assessment evaluated by gcs was not an independent variable in relation with brainstem lesions. that was probably caused by the complexity of tbi. references 1. vella ma, crandall ml, patel mb. acute management of traumatic brain injury. surg clin north am [internet]. surg clin north am; 2017 oct 1 [cited 2022 feb 21];97(5):1015–30. available from: https://pubmed.ncbi.nlm.nih.gov/28958355/ 2. werner c, engelhard k. pathophysiology of traumatic brain injury. br j anaesth [internet]. br j anaesth; 2007 398 iulia-sevastiana pastor, lăcrimioara perju dumbravă, costel siserman et al. [cited 2022 feb 21];99(1):4–9. available from: https://pubmed.ncbi.nlm.nih.gov/17573392/ 3. humble ss, wilson ld, wang l, long da, smith ma, siktberg jc, et al. prognosis of diffuse axonal injury with traumatic brain injury. j trauma acute care surg [internet]. nih public access; 2018 jul 1 [cited 2022 apr 9];85(1):155. available from: /pmc/articles/pmc6026031/ 4. meythaler jm, peduzzi jd, eleftheriou e, novack ta. current concepts: diffuse axonal injury-associated traumatic brain injury. arch phys med rehabil [internet]. arch phys med rehabil; 2001 [cited 2022 apr 9];82(10):1461–71. available from: https://pubmed.ncbi.nlm.nih.gov/11588754/ 5. ikeda k, kawakami k, onimaru h, okada y, yokota s, koshiya n, et al. the respiratory control mechanisms in the brainstem and spinal cord: integrative views of the neuroanatomy and neurophysiology. j physiol sci [internet]. j physiol sci; 2017 jan 1 [cited 2022 feb 20];67(1):45–62. available from: https://pubmed. ncbi.nlm.nih.gov/27535569/ 6. cherian i, beltran m, landi a, alafaci c, torregrossa f, grasso g. introducing the concept of “csf-shift edema” in traumatic brain injury. j neurosci res [internet]. j neurosci res; 2018 apr 1 [cited 2022 jun 13];96(4):744– 52. available from: https://pubmed.ncbi.nlm.nih.gov/ 28836291/ 7. pellot je, jesus o de. cerebral contusion. ned tijdschr geneeskd [internet]. statpearls publishing; 2021 sep 2 [cited 2022 mar 31];126(37):1690–1. available from: https://www.ncbi.nlm.nih.gov/books/nbk562147/ 8. cepeda s, gómez pa, castaño-leon am, martínez-pérez r, munarriz pm, lagares a. traumatic intracerebral hemorrhage: risk factors associated with progression. j neurotrauma [internet]. j neurotrauma; 2015 aug 15 [cited 2022 apr 9];32(16):1246–53. available from: https://pubmed.ncbi.nlm.nih.gov/25752340/ 9. cepeda s, castaño-león am, munarriz pm, paredes i, panero i, eiriz c, et al. effect of decompressive craniectomy in the postoperative expansion of traumatic intracerebral hemorrhage: a propensity score-based analysis. j neurosurg [internet]. j neurosurg; 2019 may 1 [cited 2022 apr 9];132(5):1623–35. available from: https://pubmed.ncbi.nlm.nih.gov/31026834/ 10. rosenblum wi. immediate, irreversible, posttraumatic coma: a review indicating that bilateral brainstem injury rather than widespread hemispheric damage is essential for its production. j neuropathol exp neurol [internet]. j neuropathol exp neurol; 2015 mar 28 [cited 2022 jun 14];74(3):198–202. available from: https://pubmed.nc bi.nlm.nih.gov/25668566/ 11. aboghazleh r, parker e, yang lt, kaufer d, dreier jp, friedman a, et al. brainstem and cortical spreading depolarization in a closed head injury rat model. int j mol sci [internet]. int j mol sci; 2021 nov 1 [cited 2022 mar 19];22(21). available from: https://pubmed.ncbi.nlm. nih.gov/34769073/ 12. mechanism-based mri classification of traumatic brainstem injury and its relationship to outcome pubmed [internet]. [cited 2022 feb 20]. available from: https://pubmed.ncbi.nlm.nih.gov/17263676/ 13. williams jr, nieblas-bedolla e, feroze a, young c, temkin nr, giacino jt, et al. prognostic value of hemorrhagic brainstem injury on early computed tomography: a track-tbi study. neurocrit care. nlm (medline); 2021 oct 1;35(2):335–46. 14. [a rare and little known hemorrhagic syndrome] pubmed [internet]. [cited 2022 mar 19]. available from: https://pubmed.ncbi.nlm.nih.gov/14378705/ 15. moen kg, skandsen t, folvik m, brezova v, kvistad ka, rydland j, et al. a longitudinal mri study of traumatic axonal injury in patients with moderate and severe traumatic brain injury. j neurol neurosurg psychiatry. bmj publishing group; 2012;83(12):1193–200. 16. h. richard winn m. youmans & winn neurological surgery. youmans winn neurol surg. elsevier health sciences; 2017;8256–64. 17. adams jh, doyle d, ford i, gennarelli ta, graham di, mclellan dr. diffuse axonal injury in head injury: definition, diagnosis and grading. histopathology [internet]. histopathology; 1989 [cited 2022 mar 22];15(1):49–59. available from: https://pubmed.ncbi.nlm.nih.gov/2767623/ 18. gennarelli ta, thibault le, adams jh, graham di, thompson cj, marcincin rp. diffuse axonal injury and traumatic coma in the primate. ann neurol [internet]. ann neurol; 1982 [cited 2022 mar 22];12(6):564–74. available from: https://pubmed.ncbi.nlm.nih.gov/7159060/ 19. roozenbeek b, lingsma hf, lecky fe, lu j, weir j, butcher i, et al. prediction of outcome after moderate and severe traumatic brain injury: external validation of the impact and crash prognostic models. crit care med [internet]. nih public access; 2012 may [cited 2022 mar 23];40(5):1609. available from: /pmc/articles/pmc3335746/ 20. lingsma h, andriessen tmjc, haitsema i, horn j, van der naalt j, franschman g, et al. prognosis in moderate and severe traumatic brain injury: external validation of the impact models and the role of extracranial injuries. j trauma acute care surg [internet]. j trauma acute care surg; 2013 feb [cited 2022 mar 23];74(2):639–46. available from: https://pubmed.ncbi.nlm.nih.gov/2335 4263/ doi: 10.33962/roneuro-2022-047 efficiency of 3d simulation models in emergency microsurgical clipping of intracranial aneurysms a. chiriac, n. dobrin, georgiana ion, a. iencean, i. poeata romanian neurosurgery (2022) xxxvi (3): pp. 274-278 doi: 10.33962/roneuro-2022-047 www.journals.lapub.co.uk/index.php/roneurosurgery efficiency of 3d simulation models in emergency microsurgical clipping of intracranial aneurysms a. chiriac1, n. dobrin2, georgiana ion2, a. iencean2, i. poeata1 1 "grigore t. popa" university of medicine and pharmacy, iasi, romania 2 "prof. n. oblu" emergency clinical hospital, iasi, romania abstract the latest developments in three-dimensional printing technology both in terms of equipment and materials offer a new opportunity in the microsurgical treatment of intracranial aneurysms. 3d printed model of the patient’s aneurysms enables optimal anatomical visualization with personalized preoperative planning. this is a retrospective study of a series of 16 patients suffering from ruptured intracranial aneurysms, admitted and microsurgical treated based on rapid 3d printed models to our clinic from september 2016 to march 2018. we analyzed the dates concerning patient demographics, clinical, surgical technique and outcomes correlated with the data of the 3d-printed replica used for planning emergency surgeries. 1. introduction even if according to numerous international specialized studies, the endovascular treatment of intracranial aneurysms remains the first-line treatment, the microsurgical clipping technique is a necessary option, imposed by many particular anatomical-clinical situations. also, an excellent trained vascular microneurosurgical team will definitely put the two intervention techniques on equal terms. it is well known that extremely careful microsurgical planning is absolutely essential for achieving optimal postoperative results. thus, by avoiding excessive manipulation of the parenchyma and intracranial vessels, with a significant reduction in the time of intervention, the main predisposing factors for intraoperative (aneurysmal rupture) and postoperative complications (vasospasm, infections, etc.) are eliminated. with the development of 3d printing technology, 3d simulation models have been adopted b y the field of micro neurosurgery [4.6]. the technology offers the advantage of 3 dimensional views of cerebral vessels and aneurysms from various angles, and of practicing the optimal clips construction for total aneurysm neck occlusion. such 3d simulation models may improve our concepts of aneurysm configuration and approach and clipping keywords intracranial aneurysm, 3d printed models corresponding author: a. chiriac "grigore t. popa" university of medicine and pharmacy, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 275 efficiency of 3d simulation models in emergency microsurgical clipping of intracranial aneurysms technique selection. [2,3.8] therefore, in this paper we aim to present our experience in the manufacture of aneurysmal simulation models by 3d printing technique and to investigate the possible effects of the application and utility of this printing system in emergency microsurgical clipping. 2. materials and methods 2.1. patients information in this study 16 patients with intracranial aneurysms treated in our department from september 2016 to march 2018 were retrospectively selected. these were separated into two groups, 8 cases that benefited from microsurgical clipping after analysis and simulation of this technique on a preoperatively printed 3d model and 8 cases in which microsurgical clipping was performed only on the basis of 3d imaging analysis. a similarity in the location of aneurysms was followed in the selection of the two groups. 2.2. image data generation and post-processing dynamic cta imaging was obtained for all patients using a dynamic volume ct scanner with 32 detectors toshiba aquilion ct (canon medical systems usa, inc.). the scan parameters were as follows: scan interval, 16 cm; portal rotation time, 350 s; slice thickness, 0.5 mm; field of view (fov), 240 mm; tube potential, 120 kv; and tube current, 218 ma. during the scanning process, the reconstruction with layer thickness (0.5 mm) and interval (0.5 mm) was obtained. the images thus obtained were exported in standard digital imaging and medical communication (dicom) format to a computerized unit for 3d image processing and reconstruction. they are imported into mimics17.0 (materialize, leuven, belgium) software. mimics allow the automatic extraction of soft and cerebral tissue around the skull with the highlighting of cerebral vascularisation in 3d reconstruction. the image threshold should be carefully adjusted to display the image of the vessels as clearly as possible. the threshold segmentation method is combined with manual segmentation to obtain the most important region of interest (roi). also, interfering bone structures could be removed for better roi (aneurysm region) exposure (fig 1). the resulting 3d image is stored and sent as stl files. the procedure was performed together by a neurosurgeon and a software expert from our team. figure 1. vascular tree and aneurysmal lesion segmentation on 3d angio ct acquisitions. images 2.3. 3d aneurysm model printing the 3d aneurysm printed models were obtained using an objet connex 350 3d printer (stratasys, eden prairie, mn, usa) or a zortrax inkspire printer (zortrax s.a., olsztyn, poland). the manufacturing process of the 3d-printing machine is based on fused deposition modeling (fdm) technologie. to make the prototype models, two types of semi-rigid and rigid materials were used as pla (polylactic acid) and abs (acrylonitrile–butadiene–styrene) filaments. thus, to form the object, the printer heats the thermoplastic filament cable into liquid form and extrudes it layer by layer (fig. 2). figure 2. 3d angio ct vascular tree and aneurysmal lesion and 3d printed models 276 a. chiriac, n. dobrin, georgiana ion et al. 2.4. preoperative planning all the models thus obtained were analysed by the vascular neurosurgery team in the preoperative period. thus, 3d printed models were used to propose the most optimal approach to reach the target aneurysm. also, a selection of clips regarding their size and shape as well as the configuration of their application on the aneurysmal neck was proposed and practiced. model-based preoperative plans were correlated with cta-based imaging to verify the value of the model in preoperative planning. figure 3. preoperative clipping simulation on 3d printed models and postinterventional 3d angio ct 3. results our study included 16 patients with a total of 16 ruptured intracranial aneurysms. for all these patients, a 3d printed model was created and they benefited from microsurgical clipping of the aneurysm based on a preoperative planning simulated on these models. all surgeries were performed under general anesthesia by the same neurosurgical team. the mean age was 46 ± 7, with a median of 43.5 and a range of 35–65 years. about 62% (n = 10) of our patients were female with a female-to-male ratio of 1.6. regarding the location of the aneurysms, there were 7 at the acom level, 3 at the mca bifurcation, 3 at the posterior com and 2 at the terminal level of the internal carotid artery bifurcation and one at ophthalmic segment. the standard pterional approach for aneurysm clipping was followed in 11 of patients, whereas the other 5 of patients were treated through the fronto-pterional approach. the conformation of the intraoperative clipping of the aneurysms, both in terms of arrangement and number of clips used, was similar in 13 of the cases to that practiced on the 3d printed models in the preoperative planning. in two cases, an additional clip had to be used for the complete and safe occlusion of the aneurysm. in one case, due to an atheromatous plaque at the level of the aneurysmal neck, which required the cutting of the aneurysmal sac and its extraction, and in the other case, as a result of the appearance of a rupture at the aneurysmal neck level during the microsurgical dissection. about 81% (n = 13) of the patients had a gos of 5 and 19% (n = 3) had a gos of 4. the median production time used for the models described in this manuscript was 4.25 h (range: 3.50–5.00 h). the average duration of microsurgical clipping interventions was 3h10, varying between 4 and 5 (table1). 277 efficiency of 3d simulation models in emergency microsurgical clipping of intracranial aneurysms patient age (years) sex lesion size mm clips configuration on model clips used in surgery residual neck 3d model production time surgical procedure time (h) 1 35 f r mca 7/6 slightly curved same no 3.50 3.00 2 65 f acoma 6/5 straight+ slightly curved same no 4.30 3.30 3 43 m pcoma 7//7 angled laterally same no 5.00 2.50 4 51 f acoma 4/3 bayonet+strait same no 4.50 3.10 5 38 m acoma 8/6 straight x 2 same no 4 3.10 6 44 f oft ica 11/ 9 straight x2 +fenest. same no 4.10 3.50 7 56 f r mca 5/6 slightly curved + fenest. same no 4.20 3.20 8 37 m pcoma 6/4 straight same no 4.55 2.30 9 40 f acoma 4/3 angled laterally same no 4.40 3.00 10 55 m ter ica 5/4 angled laterally same no 4.30 3.20 11 37 f pcoma 10/ 7 straight x 2 same no 4.00 4.00 12 40 m acoma 7/6 straight x 2 same no 4.30 3.00 13 35 f l mca 8/7 straight+fenest. same no 4.10 5.00 14 41 m ter ica 4/3 straight same no 4.50 3.15 15 53 f acoma 5/4 straight same no 4 2.50 16 60 f acoma 4/4 slightly curved same no 4 3.10 table 1. patients, aneurysms and interventions dates discussion the technology of printing 3d models has become more and more popular in the field of medical applicability. this was mainly due to the increased availability, ease of use and affordability of 3d printers [1,4,6]. numerous publications have described the increased applicability of 3d printing in intracranial aneurysm modeling and its benefits preoperatively [7,9]. one of the main difficulties during the microsurgical treatment of intracranial aneurysms is the selection of the appropriate clip(s) to be implanted according to anatomical variations. it is well known that surgical planning is essential [1,8], to avoid excessive manipulation of intracranial vessels and prolonged surgical time, which are predisposing factors of mechanical vasospasm and intraoperative aneurysmal rupture [9]. the results of this work describe a simplified and rapid method of manufacturing individualized 3d models and report the effects of its application to the choice and simulation of the pre-surgical approach. the total time used to create a 3d model experienced a spectacular evolution from a week, initially (wurm et al) to 24 hours (faraj et al) and later to 4-6 hours (błaszczyk et all). the average total time required to make the 3d printed model in our study (from cta acquisition to the finished model) was approximately 4.25 hours. this is registered in the direction of rapid protopiping in order to perform emergency surgical interventions. regarding the statistical comparison between the clipping configuration practiced preoperatively on the 3d printed model and the one performed during the microsurgical intervention for aneurysm occlusion, we note that this was not significant. also, the analysis regarding the number, shape and dimensions of the clips used for each intervention compared to those proposed and practiced preoperatively on the 3d models showed a statistically no significant difference. all this demonstrated the relevance of using these 3d printed vascular models in preoperative interventional planning. these results are based on an observational analysis and objective evaluation of the diameter, length and thickness measurements of the aneurysm on the 3d printed model in relation to the computerized radiological image. although 3d printing technology has gained increased popularity in vascular neurosurgery due to its proven safety, feasibility, accuracy, efficacy, reproducibility, and cost-effectiveness, there are still several hurdles to overcome before the technology is fully incorporated into routine neurosurgical practice. as other reports have shown, an important limitation is determined by the lack of a standardized 278 a. chiriac, n. dobrin, georgiana ion et al. production method that governs the assimilation of 3d models. this is due to a great variability in terms of the type of printers used, the 3d printing technology used and, perhaps most importantly, the characteristics of the resin materials used in the reconstruction process. the use of 3d printed aneurysm models will also be a great success in the future, as they have proven to be an excellent tool in practical simulations, specialized educational training, as well as in educating patients and their families. [1,2,5] conclusions the 3d printed model of the aneurysm is a precise, hands-on simulator, which allows neurosurgical specialists to plan and practice microsurgical intervention preoperatively even for emergency cases. they greatly improve their anatomical understanding of aneurysms, define surgical techniques and enhance their skills to choose of suitable clips and optimal clips arrangements. references 1. błaszczyk, m., jabbar, r., szmyd, b., & radek, m. (2021). 3d printing of rapid, low-cost and patient-specific models of brain vasculature for use in preoperative planning in clipping of intracranial aneurysms. journal of clinical medicine, 10(6), 1201. 2. bedo, t., munteanu, s. i., popescu, i., chiriac, a., pop, m. a., milosan, i., & munteanu, d. (2019). method for translating 3d bone defects into personalized implants made by additive manufacturing. materials today: proceedings, 19, 1032-1040. 3. cogswell, p. m., rischall, m. a., alexander, a. e., dickens, h. j., lanzino, g., & morris, j. m. (2020). intracranial vasculature 3d printing: review of techniques and manufacturing processes to inform clinical practice. 3d printing in medicine, 6(1), 1-13. 4. kimura, t., morita, a., nishimura, k., aiyama, h., itoh, h., fukaya, s., ... & ochiai, c. (2009). simulation of and training for cerebral aneurysm clipping with 3dimensional models. neurosurgery, 65(4), 719-726. 5. konno, t., mashiko, t., oguma, h., kaneko, n., otani, k., & watanabe, e. (2016). rapid 3-dimensional models of cerebral aneurysm for emergency surgical clipping. no shinkei geka. neurological surgery, 44(8), 651-660. 6. mashiko, t., otani, k., kawano, r., konno, t., kaneko, n., ito, y., & watanabe, e. (2015). development of threedimensional hollow elastic model for cerebral aneurysm clipping simulation enabling rapid and low cost prototyping. world neurosurgery, 83(3), 351-361. 7. ryan, j. r., almefty, k. k., nakaji, p., & frakes, d. h. (2016). cerebral aneurysm clipping surgery simulation using patient-specific 3d printing and silicone casting. world neurosurgery, 88, 175-181. 8. wang, l., ye, x., hao, q., ma, l., chen, x., wang, h., & zhao, y. (2018). three-dimensional intracranial middle cerebral artery aneurysm models for aneurysm surgery and training. journal of clinical neuroscience, 50, 77-82. 9. wurm, g., lehner, m., tomancok, b., kleiser, r., & nussbaumer, k. (2011). cerebrovascular biomodeling for aneurysm surgery: simulation-based training by means of rapid prototyping technologies. surgical innovation, 18(3), 294-306. romanian neurosurgery (2019) xxxiii, 1: 55-59 doi: 10.33962/roneuro-2019-010 www.journals.lapub.co.uk/index.php/roneurosurgery comparison of the predictive strength of total white blood cell count within 24 hours on the outcome of traumatic brain injury with cranial computed tomography scan in a resource-limited tertiary health centre in sub-saharan africa eghosa morgan1,2, olufemi bankole1, okezie kanu1, omotayo ojo1, edward poluyi1 1 lagos university teaching hospital, idi-araba lagos state, nigeria 2 irrua specialist teaching hospital, edo state, nigeria abstract background: the enormous disease burden of patients with traumatic brain injury (tbi) remains a huge source of concern to the patient and caregivers. computed tomography (cct) scan is a valuable investigative tool in patients with traumatic brain injury which can be used to predict the outcome of tbi. the use of total white blood cell as a predictive parameter in patients with tbi is still at a primordial stage. this study aimed to compare the predictive strength of total wbc count within 24 hours of tbi with cranial computed tomography scan. methods: this research was done over one-year period at the lagos university teaching hospital, lagos. one hundred and fifty-eight patient who met the inclusion criteria were studied and the male to female ratio of 3.6:1. results: the mean total wbc count was 14,279.94 and the area under the curve of total wbc count and cct scan was 0.633 and 0.855 respectively. conclusion: our conclusion was that despite both parameters been a predictor of the outcome of tbi, the total white blood cell is a weaker predictor of outcome compared to cranial computerize tomography scan. background traumatic brain injury (tbi) is likened to an epidemic and it will be the third leading cause of death in the developing world by 20201. it is defined as an alteration of brain function or other evidence of brain pathology caused by an external mechanical force2. it is a time bomb almost happening if left unattended to, with the male productive sector of the population affected1. it causes a huge drain on socioeconomic status of the affected individual, family, and country at large. total white blood cell (wbc) count have been known to be elevated due to varied reasons in traumatic brain injury3,4,5,6,7 and this have been found to correlate with poor outcome. cranial tomography (cct) scan have been known to predict outcome of traumatic brain injury. our aim was to establish if the predictive strength of total wbc count can be compared with another known outcome model such as cct scan. keywords tbi, wbc count, ct scan corresponding author: eghosa morgan lagos university teaching hospital, idi-araba lagos state, nigeria morganeghosa@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 56 eghosa morgan, olufemi bankole1, okezie kanu, omotayo ojo, edward poluyi methodology this is a hospital based prospective study of 158 patients who presented with isolated tbi within 24 hours of injury over a year period ranging from october 2014-september 2015. 5mls of blood sample was obtained in an ethylene diamine tetra acetic acid (edta) bottle and sent for full blood count analysis at a specific reference laboratory in lagos university teaching hospital (luth) during which the total white blood cell count was analysed using autoanalyser (mek-6400 haematology analyser). the patients with traumatic brain injury (tbi) meeting the inclusion criteria were reviewed. cranial computed tomography (cct) scan was performed at the radiological department of luth using toshiba aqillol 128 slice ct scanner. outcome was determined using standard scale such as the gos-e at 6 months post injury. inclusion criteria patients with clinical and radiological features of isolated tbi presenting within 24 hours of injury to the neurosurgical unit of luth after obtaining informed consent. exclusion criteria 1. patients with tbi who present to the hospital after 24 hours of injury. 2. patients with tbi who are diagnosed clinically to be brain dead at presentation. 3. patients with evidence of confirmed/established ongoing infectious processes before injury. 4. patients with confirmed diseases that may alter white blood cell count such as haematological disorders like leukaemia and lymphoma, and uncontrolled diabetes mellitus. 5. patients with open wounds and other systems injuries other than tbi. 6. patients not consenting to be part of the study. data analysis. all statistical analyses were done using descriptive and inferential statistics. p value <0.05 was taken as significant. data collected were collated using statistical package for social science (spss) illinois chicago version 21. receiver operating characteristic (roc) curve was constructed to compare predictive strength of the variables. results age and sex distribution a total of one hundred and ninety-nine patients were recruited into the study. 41 (20.6%) of these patients were excluded from analysis due to incomplete data and lost to follow. altogether 158 patients met the inclusion criteria with complete data and were analysed. age of patients ranged between 5-83 years with a mean age of 37.04 + 18.37 years. most of the patients were in the age range of 31-40 years and 20-29 years representing 21.5% and 20.9% respectively. this is closely followed by those between 40-49years and 60-69years representing 16.5% and 12.7% respectively. one hundred and sixteen (73.4%) of these patients were males, while 42(26.6%) were females, with a male: female ratio of 3.6: 1. table 1 shows the age group distribution and figure 1 shows the gender distribution. table 1: distribution of patients’ age group age group in year(s) frequency (%) 0-9 16(10.1) 10-19 9(5.7) 20-29 33(20.9) 30-39 34(21.5) 40-49 26{16.5) 50-59 15(9.5) 60-69 20(12.7) 70-79 4(2.5) >80 1(0.6) total 158(100) table 1 shows the age distribution of patients with 20.9% and 21.5% between the third and fourth decade respectively. figure 1 showing sex distribution male accounted for 73.4% of the total patients studied as shown in the pie chart in figure 1, while 26.6% were female. 26.60% 73.40% female male 57 comparison of the predictive strength of total white blood cell count table 2: showing the relationship between the mean total wbc count and cct scan findings 24 hours post-injury marshall cct scan grading n (%) mean wbc count standard deviation 1. normal findings 23(14.56) 12,672.61 3,923.81 2. cistern present 63(39.87) 14,552.54 3,773.85 3. cistern present 21(13.29) 13,585.24 4,049.10 4. >5mm midline shift 3(1.90) 13,266.67 5,262.45 5. surgically correctable lesion 27(17.09) 15,064.07 4,786.97 6. non-surgically correctable lesion 21(13.29) 15,053.81 5,531.47 total 158(100) 14,279.94 4,312.06 figure 2 showing the area under the curve of various tbi outcome predictors table 3 showing area under the curve of the predictive strength of both outcome parameters test result variable(s) area under curve sensitivity specificity p value cct scan within 24 hours 0.855 72 97.74 <0.001 total wbcc within 24 hours 0.633 44 83.36 <0.001 table 3 revealed area under the curve of total wbc count as 0.633 with a sensitivity and specificity of 44% and 83.33% respectively. while, cct scan within 24hours has the highest capacity to predict outcome with sensitivity and specificity of 72% and 97.74 % respectively. 58 eghosa morgan, olufemi bankole1, okezie kanu, omotayo ojo, edward poluyi discussion studies have shown that the total white blood cell count increases with severity of traumatic brain injury, several pathophysiological processes have explained these processes responsible for elevated total wbc count3,4,5,6,7. radiological outcome model such as cct scan have been identified to help predict the outcome of tbi, however studies comparing the predictive strength of total wbcc is sketchy. cranial computed tomography (cct) scan is a radiological tool which is useful in predicting the outcome of patients with tbi. it is a reproducible, relatively available, although expensive radiological investigative tool which helps to identify the type and severity of tbi9,10. studies have shown a higher predictive value with cct scan in patients with tbi when compared to pr and gcs score in predicting short-term outcome of tbi. findings on cct scan such as compressed basal cistern and presence of a mass lesion are predictive of poor outcome. studies by van dongen et al11 and teasdale g et al12 confirmed strong association between gcs score, pr and cct scan. these studies showed that predictive strength of cct scan alone was about 48%. the cct scan done within 24 hours has a high area under the curve of 0.855 which was statistically significant p<0.001. sensitivity and specificity of the cct scan (done within 24 hour) predictive strength was 72% and 97.74% respectively. this showed that the cct scan has a strong discriminative capability for outcome prediction in traumatic brain injury. few studies have predicted the strength of total wbcc. gunkalar et al13 showed that predictive value of wbc count exceeding 17.5 x106/l has a predictive value for poor outcome at p < 0.001. in this study the predictive value of total wbcc was weak, evident by area under the curve of 0.633 at statistically significant p<0.001 as shown in figure 2 and table 3. therefore, the predictive strength of these parameters to predictive outcome of tbi is strongest with cct scan findings, and weakest with total wbc counts assessed within 24 hours of tbi. conclusion it can be concluded that the predictive strength of total white cell count in patients with traumatic brain injury is weaker compared to radiological tool (cct) used to predict outcome in tbi. references 1. 1. roozenbeek b, maas al, menon dk. changing patterns in the epidemiology of traumatic brain injury. nat rev neurol. 2013; 9 (4): 231-236. 2. menon dk, schwab k, wright dw, maas ai. demographics and clinical assessment working group of the international and interagency initiative toward common data elements for research on traumatic brain injury and psychological health position statement: definition of traumatic brain injury. arch of phys med rehabil. 2010; 91(11): 1637-1640. 3. keskil s, baykaner mk, ceviker n, aykol s. head trauma and leukocytosis. acta neurochir [wien]. 1994; 131(3-4): 211-214. 4. hortangl h, hammerle af, hackl jm, brucke t, rumpl e, the activity of the sympathetic nervous system following closed head injury. intensive care med. 1980; 6(3): 169 -177. 5. bednar mm, gross ce, howard db, lynn m, neutrophil activation in acute human central nervous injury. neurol res. 1997; 19 (6): 588-599. 6. suval wd, duran wn, boric vip, hobson rv. microvascular transport and endothelial cell alteration preceding skeletal muscle damage in ischemia and reperfusion injury. am j surg 1987; 154(2): 211215. 7. yamakawa t, yamaguchi s, niimi h, sugiyama i. wbc plugging and blood flow maldistribution in the capillary network of cat cerebral cortex in acute hemorrhagic hypotension; an intra-vital microscopic study; circ shock. 1987; 22 (4): 323-322. 8. braakman r, gelpke, gj, habbema jdf, et al.: systematic selection of prognostic features in patients with severe head injury. neurosurg. 1980; 6(4):362-370. 9. hydel mj, preston ca, mills tj, luber s, blaundean e, deblielux mc. indication for computerised tomography in patient with minor head injury. n engl j med 2000; 343(2): 100-105. 10. teasdale g, jennet b. assessment of coma and impaired consciousness: a practical scale. lancet. 1974; 304(7872):81-84. teasdale g, jennett b. assessment of coma and impaired consciousness: a practical scale. the lancet. 1974 jul 13; 304(7872):81-84. 11. van dongen kj, braakman r, gelpke gj: the prognostic value of computerized tomography in comatose head injured patients. j neurosurg. 1983; 59 (6): 951-957. 12. teasdale g, teasdale e, hadley d. computed tomographic and magnetic resonance imaging classification of head injury. j neurotrauma.1992; 1(9): 249-257. 13. gurkanlar d, lakadamyali h, ergun t, yilman c, yucel e, altinor n.; predictive value of leukocytosis in head trauma. turkish neurosurgery, 2009:19(3); 211-215. 14. kaufmann ma, buchmann b, scheidegger d. severe head injury: should expected outcome influence resuscitation and first-day decisions. resuscitation 1992; 23(3):199-206. 15. thatcher rw, cantor ds, mcalaster r.: comprehensive predictions of outcome in closed head-injured patients. the development of prognostic equations. ann n y acad sci. 1991; 620 (1):82-101. romanian neurosurgery (2019) xxxiii (2): pp. 188-190 doi: 10.33962/roneuro-2019-035 www.journals.lapub.co.uk/index.php/roneurosurgery post traumatic isolated ipsilateral oculomotor nerve palsy. an uncommon presentation praveen kumar1, sharad pandey2, kulwant singh1, mukesh sharma1, prarthana saxena2 1 department of neurosurgery, sir sunder lal hospital, ims, bhu, varanasi, uttar pradesh, india 2 department of neurosurgery, p.g.i.m.e.r. dr ram manohar lohia hospital, new delhi, india abstract the common causes of isolated third nerve palsy are microvascular infarction, intracranial aneurysm, diabetes, hypertension and atherosclerosis. here we are presenting a case of 26-year female presenting with a history of head injury two months back. she presented with ptosis on the left side. on computed tomography, a large left-sided chronic subdural hematoma with significant midline shift was found. isolated ipsilateral third nerve palsy is a rare presentation with unilateral chronic subdural hematoma. improvement in ptosis after surgery indicate a good neurological outcome. introduction chronic subdural hematoma is a collection of liquefied old blood between the duramater and arachnoid membrane of brain. it is first described by virchow as “pachymeningitis hemorrhagic interna “in 1857. later trotter put forward the theory of traumatic rupture of bridging veins as a cause of what he named “subdural hemorrhagic cyst” chronic sdh is commonly present in elderly patients after a trivial trauma [1,2]. unilateral chronic sdh is more common in comparison to bilateral sdh [3]. chronic sdh is a common presentation in people taking anticoagulant or antiplatelet drugs. commonly chronic sdh patients present with headache, vomiting, hemiparesis, ataxia, altered consciousness, seizures, urinary incontinence [4]. patients with chronic sdh rarely present with vertigo and nystagmus upward gaze palsy, and isolated third nerve palsy [5,6,7]. isolated third nerve palsy presented with ptosis is rare presentation in post-traumatic chronic sdh patients. case report we are presenting a 26-year-old female patient, non-hypertensive, keywords ptosis, third nerve palsy, chronic subdural hematoma (chronic sdh) corresponding author sharad pandey department of neurosurgery, p.g.i.m.e.r. dr ram manohar lohia hospital, new delhi. india drsharad23@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 189 post traumatic isolated ipsilateral oculomotor nerve palsy non diabetics, not on antiplatlet drugs. she presented with history of head injury two months back. no initial ct head was done at the time of injury. patient was conscious, cooperative and well orientated at the time of admission. patient’s vitals were within normal limit. all hematological investigations were normal. she presented with complaining of headache after one month of head injury, headache was not severe in nature and relieving on taking analgesic. there was no vomiting, hemiparesis, gait disturbance and urinary incontinence. after one and half month of head injury she complaining of dropping of left upper eyelid and patient vision was 6/9 in left eye. left eyeball was placed outward and downward due to loss of adduction and elevation [figure 1]. left side pupil was mid dilated but fundus examination was normal. a ct head was done showing large left side fronto-temporo-parietal chronic subdural hematoma with significant midline shift [figure 2]. patient was taken up for left sided two burr hole drainage of subdural hematoma under general anesthesia. post operatively patient has no significant complaints and patient was put on antiepileptic medications. her neurological and clinical condition improved after surgery. patient left eye ptosis and eyeball position improved same day after the surgery. patient discharge from the hospital after 3 days in a stable condition. improvement in ptosis after surgery indicates good neurological outcome and this was due to brainstem compression and transtentorial (uncal) herniation which cause compression of oculomotor nerve. figure 1. (a) severe ptosis of left eye with outward & downward displacement of eyeball (b) preoperative ct head showing left fronto-temporo-parietal chronic subdural hematoma with significant midline shift and mass effect. figure 2. (a) postoperative improvement in ptosis & position of eyeball (b) postoperative ct showing no residual hematoma. discussion oculomotor nerve supplies all the extaocular muscle of eye except superior oblique and lateral rectus muscle. it also supplies the striated muscle of the levator palpebrae superioris and the smooth muscle concerned with accommodation namely the sphincter papillae and ciliary muscle. in a complete lesion of the nerve the eye movement restricted in upward, downward and inward direction. patient complaining of diplopia. there is drooping of upper eyelid due to paralysis of levator palpebrae superioris. chronic subdural hematoma represents one of the most frequent intracranial hemorrhages encountered in the neurosurgical department, with elderly people being more frequently affected [8]. in an elderly patient brain undergo atrophied leads to 11% increase in extra cerebral space [9]. the other predisposing factors are head injury, alcohol abuse, coagulopathic disorder, antiplatlet drugs [10]. a history of head injury due to trivial trauma is presented in 6080% of the elderly patients [11, 12]. most of the patient presented with complaining of headache, vomiting & hemiparesis. isolated third nerve palsy presented with ptosis is a rare presentation. the most common causes of isolated third nerve palsy are microvascular infarction, intracranial aneurysm, diabetes, hypertension, atherosclerosis. (13, 14) conclusion ipsilateral third nerve palsy in post-traumatic unilateral chronic subdural hematoma is a rare condition. improvement in ptosis after surgery indicates good neurological outcome as in large chronic subdural hematoma brain shift to opposite site leads to brainstem compression and transtentorial (uncal) herniation which cause compression of oculomotor nerve [15] financial support and sponsorship nil conflict of interest there are on conflicts of interest. references 1. adhiyaman v., asghar m., ganeshram k.n., bhowmick b.k. chronic subdural haematoma in the elderly. postgrad med j. 2002 feb;78(916):71–75. 190 praveen kumar, sharad pandey, kulwant singh et al. 2. arpino l., gravina m., basile d., franco a. spontaneous chronic subdural hematoma in a young adult. j neurosurg sci. 2009 jun;53(2):55–57. 3. nayil k, ramzan a, sajad a, zahoor s, wani a, et al. (2012) subdural hematomas: an analysis of 1181 kashmiri patients. world neuro¬surg 77(1): 103-110. 4. mulholland c., knox f.a. subacute subdural haematoma presenting with oculomotor nerve palsy, reduced vision, and hallucinations. eye (lond) 2006 jan;20(1):125–126. 5. ashkenazi e, pomeranz s (1994) nystagmus as the presentation of tentorial incisure subdural haematoma. j neurol neurosurg psychi¬atry 57(7): 830-831. 6. phookan g, cameron m (1994) bilateral chronic subdural haemato¬ma: an unusual presentation with isolated oculomotor nerve palsy (letter). j neurol neurosurg psychiatry 57(9): 1146. 7. sandyk r (1982) isolated failure of upward gaze as a sign of chronic subdural haematoma (letter). s afr med j 61(2): 32. 8. kim j.h., kang d.s., kim j.h., kong m.h., song k.y. chronic subdural hematoma treated by small or large craniotomy with membranectomy as the initial treatment. j korean neurosurg soc. 2011 aug; 50(2):103–108. 9. stanisic m, lund-johnsen m, mahesparan r (2005) treatment of chronic subdural haematoma by burr-hole craniostomy in adults: in¬fluence of some factors on postoperative recurrence. acta neurochir (wien) 147(12): 1249-1256 10. stroobandt g, fransen p, thauvoy c, menard e (1995) pathogenic factors in chronic subdural haematoma and causes of recurrence af¬ter drainage. acta neurochir (wien) 137(1-2): 6-14. 11. markwalder tm, steinsiepe kf, rohner m, reichenbach w, mark¬walder h (1981) the course of chronic subdural haematomas after burr-hole craniostomy and closedsystem drainage. j neurosurg 55(3): 390-396. 12. matsumoto k, akagi k, abekura m, ryujin h, ohkawa m, et al. (1999) recurrence factor for chronic subdural haematoma after burr-hole craniostomy and closed system drainage. neurol res 21(3): 277-280. 13. ortega-martínez m., fernández-portales i., cabezudo j.m., rodríguez-sánchez j.a., gómez-perals l.f., giménez-pando j. isolated oculomotor palsy. an unusual presentation of chronic subural hematoma. neurocirugia (astur) 2003 oct;14(5):423–425. 14. ko j.h., kim y.j. oculomotor nerve palsy caused by posterior communicating artery aneurysm: evaluation of symptoms after endovascular treatment. interv neuroradiol. 2011 dec17(4):415–419. 15. cameron mm (1978) chronic subdural haematoma: a review of 114 cases. j neurol neurosurg psychiatry 41(9): 834-839. microsoft word 4costanvv_multidisciplinary 552 | costan et al multidisciplinary approach to orbital fracture repair             doi: 10.2478/romneu-2018-0071 multidisciplinary approach to orbital fracture repair v.v. costan1, m. dabija2 “grigore t. popa” university of medicine and pharmacy iasi, romania 1faculty of dental medicine, department of surgery, oral and maxillofacial surgery 2faculty of medicine, department of surgery ii, neurosurgery abstract: the orbit is a frequent location for fracture occurrence, often in association with other fractures of the facial skeleton. due to the anatomical situation of the orbit at the crossroads of multiple specialties, including maxillofacial surgery, ophthalmology, neurosurgery and otolaryngology, this territory must be managed by multidisciplinary teams for an accurate diagnosis and treatment. this paper focuses on reviewing the main types of orbital fractures, the indication for surgical repair and the contribution of different specialties in the management of various orbital fracture patterns. key words: orbit, fracture, multidisciplinary, blow-out, blow-in introduction fractures of the orbit are often encountered in the context of facial trauma, either isolated or in association with other fractures of the facial skeleton. over 40% of all facial fractures have an associated orbital involvement (1). the most frequent patterns of fractures including the orbit are orbitozygomatic fractures and naso-orbitoethmoidal fractures. isolated fractures of the orbital walls are reported in between 4-16% of facial fractures cases (2). with such a high occurrence and potential for important functional and morphologic impairment, it is important to accurately diagnose and treat orbital fractures. the orbit pathology is situated at the intersection of multiple medical specialties due to the anatomical location, the neighboring anterior skull base and paranasal sinuses, but also due to its contents consisting of the globe and optic nerve. in a traumatic setting, all the named structures can be damaged to various degrees, necessitating a collaboration between the maxillofacial surgeon, the neurosurgeon, ophthalmologist and otolaryngologist for an accurate diagnosis, treatment and follow-up, aiming for minimal complications. the anatomic characteristics of the orbital region explain the various fracture patterns and the frequent association of fractures involving multiple facial bones. the orbits and the anterior skull base form a guarding ensemble, in the biomechanical context of the naso-ethmoido-maxillo-fronto-orbital complex. the whole architecture of the nose, paranasal sinuses, the orbits and the anterior romanian neurosurgery (2018) xxxii 4: 552 562 | 553             skull base comprises an anterior strength zone (the glabella, the naso-maxillary suture, the nasal process of the frontal bone, the orbital rims) absorbing the impact and a posterior fragile complex (the cribriform plate, the ethmoidal labyrinth, the perpendicular plate of the ethmoid bone, the sinus cavities) dissipating the forces (1, 3). the design of the orbit is well adapted to soften any traumatic impact on its fragile contents. the orbital rims are thickened bone structures forming horizontal and vertical buttresses of the facial skeleton absorbing and resisting the direct force of the impact (4). the orbital fat behaves like a cushion dissipating forces to protect the globe and optic nerve. the thin orbital walls allow for pressure to escape the orbit by fracturing in case of important traumatism, thus avoiding crushing of the intraorbital structures. similarly, the orbital roof also serves as a pressure release for superior traumatisms, impacting the skull and brain. its down-fracture dissipates the crushing force directed on the brain substance. in addition to these protective features, the surrounding paranasal sinuses act as air-bags consuming the strength of the traumatism (5, 6, 7). their role is emphasized by the increased frequency of orbital blow-in fractures in children due to the absence of frontal sinus pneumatization (8). in relation to the anatomical characteristics, the impact point, strength and direction, the fracture trajectory may interest to various degrees the orbital rims, the walls of the orbit, as well as the adjacent bones of the facial skeleton translating into the frequently encountered clinical forms: naso-ethmoidomaxillo-fronto-orbital complex (cnemfo) fractures (3), more commonly named noe complex (naso-orbito-ethmoidal) fractures, orbito-zygomatic fractures, isolated orbital walls fractures including blow-in and blowout types, and combined orbital fractures comprising the orbital frame and walls (1). less frequent, but with a high morbidity, is the association of orbital fractures with skull and skull base fractures in high-velocity traumatisms. the complex shape of the orbit, as well as the anatomical situation in areas of high risk of injury to important structures, make the reconstruction of the orbital cavity a difficult task, often requiring multidisciplinary evaluation, diagnosis and management. multidisciplinary evaluation and management a facial trauma patient is habitually evaluated by a multidisciplinary team in the emergency setting, including maxillofacial, neurosurgical, ophthalmological and otolaryngology consultations together with other necessary consultations for excluding serious injuries in other body parts. common emergency procedures include maintenance of a patent airway, management of epistaxis and hemostasis for bleeding in soft tissue lacerations, drainage of retrobulbar hematoma, management of persistent oculocardiac reflex, and intracranial vascular lesions. the initial consultation is usually determined by the predominant emergency in each case. diagnostic imaging is recommended in hemodynamically stable patients. facial fracture repair is performed after the resolution of acute life-threatening injuries. 554 | costan et al multidisciplinary approach to orbital fracture repair             clinical examination is often indicative of the type of fracture, but a thin slice ct (computer tomography) evaluation is cardinal for the assessment of orbital injuries (9, 10) that may otherwise be missed due to the presence of edema and masked clinical signs and symptoms. even more so, ct is necessary due to the possible presence of skull base fractures, dura tears, posttraumatic intracranial lesions, possible occurrence of orbital apex syndrome, extraocular muscle incarceration, globe injuries. the threedimensional reconstruction of the ct images aids the greater understanding of the fracture characteristics and assists in deciding the treatment plan (11, 12). stereolithic models obtained by mirroring techniques and threedimensional printing are useful for the choice and modelling of the reconstruction material, particularly in cases of comminuted fracture repair (13). there is controversy on the indication for surgery and particularly regarding the most appropriate timing for performing surgical repair in orbital fracture cases. the indications for immediate surgery, performed within 24 hours, are less of a subject for debate. consensus has been achieved regarding emergency interventions in cases of diplopia, incarcerated extraocular muscle and persistent oculo-cardiac reflex (syncope, bradycardia, heart block, nausea, vomiting), emergency intervention for “white-eyed” blowout fracture (patient under 18, minimal clinical signs, superior gaze restriction, muscle entrapment, trap-door mechanism), and also in cases with severe displacement of the globe, orbital apex syndrome, optic nerve compression and high risk of vision loss (14). the debate is ongoing regarding the indications for early (within two weeks) and late surgery (beyond two weeks). consideration is given to the amount of fracture displacement, orbital volume changes, the comminution of the fracture, the degree of functional and esthetic impairment, the presence of priming neurosurgical lesions, and to the existence of important comorbidities as contraindications for surgery. it is most difficult to determine the indication for the surgical repair or conservative management in minimally displaced fractures, in the absence of initial symptoms, since posttraumatic changes in the orbital soft tissues could progress with the apparition of late enophthalmos. most authors agree that in the absence of contraindication, the best functional and cosmetic results are obtained by performing the primary repair of volume modifying orbital fractures, with primary grafting when necessary, or reconstruction using alloplastic materials (15, 16). this is true for the majority of inferior wall, medial and lateral wall orbital fractures. orbital roof fractures, however, are commonly managed conservatively in almost 90% of cases comprising minimally displaced fractures (12). possible complications include the onset of pulsatile exophthalmos and orbital encephalocele that has been reported to also occur late after the conservative management of minimally displaced fractures of the superior orbital wall (12). blowin fractures with severe displacement, as well as orbital roof fractures with a surface greater than 2 cm2 must be closely monitored since there is a high risk of encephalocele development and orbital dystopia (8). for severely and moderately romanian neurosurgery (2018) xxxii 4: 552 562 | 555             displaced orbital roof fractures the surgery indication is maintained. the presence of an orbital encephalocele is a surgical indication for the removal of the herniated tissue with closure of the dura and orbital reconstruction (17). surgery is also performed in the presence of superior orbital wall fractures in association with dural tears and cerebrospinal fluid (csf) leaks (18). other situations in which surgery is necessary encompass the presence of intraorbital foreign bodies, or impingent bone fragments causing the compression and lesion of the optic nerve, or of the extraocular muscles. there is no agreement regarding the best reconstructive material, with some authors advocating for the use of autologous bone grafts (16), while others have obtained good outcomes by titanium mesh reconstruction and thus avoidance of donor site morbidity and associated complications (15, 19). in the absence of treatment due to late presentation, missed diagnosis or delayed surgery due to contraindication, the resulting orbital sequelae can be addressed in late correction procedures, performed after six months from the initial injury, for the maturation of the scar tissue (20, 21). common orbital sequelae include the presence of enophthalmos, exophthalmos, orbital dystopia, hypoglobus, diplopia, orbital contour changes and facial asymmetry, eyelid malpositioning, epiphora, restriction of eye movements and soft tissue contraction. following orbital roof fractures in the pediatric population that were managed nonoperatively, and other skull and skull base fractures, there is concern for the development of “growing skull fractures” with enlargement of existing communications with the intracranial space, dural tears and brain herniation (22, 23). timely diagnosis facilitates early intervention and prevention of complications. maxillofacial surgery contribution fractures of the inferior, medial and lateral orbital walls and rims, in the absence of associated skull and skull base fractures, in conjunction or not with other fractures of the facial skeleton, are managed by the maxillofacial surgeon, after the initial emergency multidisciplinary evaluation. other fractures that comprise neurosurgical lesions, such as orbital roof fractures, or panfacial and skull fractures, are often managed in mixed surgical teams. isolated blow-out fractures of the inferior orbital wall account for 22-47% of orbital injuries (24, 25, 26). orbital floor fractures are often found in association with fractures of the medial orbital wall. most remaining orbital fractures are found in the context of other facial fractures, mainly orbito-zygomatic fractures, or nasoorbito-ethmoid fractures (1, 3) (fig. 1-6). the recognition of emergency situations is key for preserving unaltered visual function. retrobulbar hematomas in the context of orbital fractures is encountered in 0.45–0.6% of cases. the key to avoiding permanent injury to the optic nerve and posttraumatic blindness is the early recognition of the condition, with the help of the ophthalmologist and adequate imaging, followed by the drainage of the hematoma by lateral canthotomy. it is recommended to perform the drainage within one hour from onset, and under 24 hours, since studies showed that function preservation is better when the interval from 556 | costan et al multidisciplinary approach to orbital fracture repair             onset to treatment is shorter (27). careful monitoring for retrobulbar hematomas must also be performed in the postoperative period. compression of the optic nerve by displaced bone fragments or intraorbital foreign bodies are also indications for emergency surgery, just like the un-resolving oculo-cardiac reflex. other lesions indicating the need for immediate surgical treatment are related to the entrapment of the extraocular muscles and orbital fat (trap-door fracture) especially in children, when the thick periosteum causes more pressure on the entrapped tissues (14). the early and late treatment indications vary on the presence of clinical signs, the amount of fracture displacement and orbital volume change, the presence of comorbidities and associated traumatic lesions (19). the maxillofacial surgeon is familiar with several types of access for repairing orbital fractures and complex midfacial fractures, such as the superior eyelid, inferior eyelid, transconjunctival, intraoral approaches, and the coronal flap offering exposure for the frontal skull, temporal regions, the superior, medial and lateral orbit (28, 4). the coronal flap is often used in mixed approaches for repairing skull fractures, frontal sinus fractures, superior orbital rim fractures, noe fractures, and fractures of the orbital roof, particularly the blow-out type. the blow-in type of orbital roof fracture can be adequately accessed and repaired through an upper lid approach, in mixed surgical teams (29). additionally, the closure of large csf fistulas associated with tissue loss may be performed in mixed surgical teams, by using various types of pedicled or free flaps. figure 1 three-dimensional ct reconstruction of a patient with a displaced naso-orbito-ethmoidal fracture managed by a multidisciplinary approach soft tissue frontal view demonstrating facial asymmetry due to left nasal displacement and orbital contour change figure 2 three-dimensional ct reconstruction of the same patient demonstrating the displaced fractures of the nasal bones and right inferior orbital rim, ascending process of the maxilla and anterior wall of the maxillary sinus romanian neurosurgery (2018) xxxii 4: 552 562 | 557             figure 3 inferior view showing the inward and inferior displacement of the right medial fractured maxillary fragment comprising the inferior orbital rim and ascending process of the maxilla with orbital volume change figure 4 transverse ct section showing the displacement of the right medial maxillary fragment with obstruction of the right nasal fossa figure 5 coronal ct section demonstrating right maxillary sinus fracture and hemosinus figure 6 transverse ct section showing the displacement of the nasal fracture neurosurgical contribution orbital roof fractures are encountered in less than 9% of facial fractures in most studies (12, 18, 30). they are reported more often in children under the age of seven, because of the anatomical characteristics with incomplete frontal sinus development and a more prominent frontal region (18, 30, 31). in isolated superior orbital wall fractures, the direction of the impact force determines the type of fracture, with either a “blow-out” mechanism, which is more common and often determining orbital volume enlargement and 558 | costan et al multidisciplinary approach to orbital fracture repair             enophthalmos, or a “blow-in” mechanism seen in high velocity traumatisms, determining the diminution of the orbital volume and the onset of exophthalmos. as previously described, most orbital roof fractures are managed conservatively. still, indications for surgery should be carefully revised and adequate monitoring of the patient must be implemented, for early diagnosis of possible complications. surgical procedures for repairing orbital roof fractures often imply a collaboration between the neurosurgeon and maxillofacial surgeon for achieving adequate access. simple blow-in orbital roof fractures can be surgically approached through an upper blepharoplasty palpebral incision, while blow-out fractures are more challenging, requiring a neurosurgical craniotomy approach via a coronal incision (29). severe neurosurgical lesions and ophthalmologic injuries may be encountered in conjunction with orbital roof fractures, consisting of brain injuries, pneumocephalus, dura tears, csf leaks, pulsatile exophthalmos, orbital meningoencephalocele, entrapment of the extraocular muscles, globe rupture, optic neuropathies, retrobulbar hematoma (18). the morbidity is increased when there is association with other fractures of the orbital rims (fig. 7-10), skull, skull base and facial skeleton. orbital roof fractures, skull and skull base fractures in children require special neurosurgical surveillance, especially in cases where there is evidence of dural tears. this is due to the possibility of developing “growing skull fractures”, needing early diagnosis and management for prevention of complications and sequelae (22, 23). figure 7 three dimensional ct reconstruction of a patient with a displaced fracture of the left superior orbital rim that necessitated a multidisciplinary management including a neurosurgeon and a maxillofacial surgeon figure 8 transverse ct section proving the intraorbital displacement of the left superior orbital rim fragments romanian neurosurgery (2018) xxxii 4: 552 562 | 559             figure 9 coronal ct section demonstrating the displaced left intraorbital fractured fragment impinging on the left globe and the superior rectus muscle figure 10 sagittal ct section showing the presence of the displaced intraorbital fragment causing pressure on the globe and on the superior rectus muscle otolaringology contribution otolaryngology is often the first examination performed in the emergency setting for the management of epistaxis, frequently encountered in facial traumatisms, particularly in association with midface, lateral face and central face fractures. isolated naso-orbito-ethmoid fractures represent approximately 5% of facial fractures in adults, but they have a high incidence in the context of other facial fractures. more than half of all noe fractures are associated to orbito-zygomatic fractures, while 20% are found in the context of panfacial fractures (32). the most challenging part in the treatment of central face fractures is management of the frontal sinus. fractures located here often interest both the anterior and the posterior bone plates, with the possible occurrence of dura tears and brain herniation. multidisciplinary management is important for minimizing the morbidity and achieving good functional and cosmetic outcomes. complications of frontal sinus fractures include the formation of mucocele, sinusitis, osteomyelitis, meningitis, encephalocele, cerebrospinal fluid fistula, central face deformity (33). in the presence of small dural discontinuity and csf leaks, conservative treatment may often lead to the spontaneous closure of the fistula, justifying the observation of these fractures for up to one week before considering surgery. frontal sinus obliteration or cranialization is indicated in cases where the ventilation of the frontal sinus cannot be reestablished (33). the endoscopic management of central face fractures allows for a minimally invasive approach and accurate visualization (32). in skull base fractures with cerebrospinal fluid fistulas, local flaps from the nasal cavity can be utilized for the closure of csf leaks using an endoscopic technique. fractures of the medial and inferior orbit can also be accessed endoscopically, or by a combined approach comprising a transconjunctival and an endoscopic trans 560 | costan et al multidisciplinary approach to orbital fracture repair             nasal access (34, 35). there are some disadvantages to the entirely endoscopic approach consisting of difficult insertion of the reconstruction material, with the orbital contents being supported by the nasal packing, which predisposes to the onset of postoperative enophthalmos. thus, a combined open and endoscopic approach would associate the superior endoscopic visualization of the posterior bone ledges, with the improved access for titanium mesh insertion (34, 35). opthalmology contribution careful observation and interdisciplinary management are mandatory in orbital fractures, frequently requiring multiple ophthalmological examinations. one in four patients with orbital fractures has an associated ocular lesion (36). it is for this purpose that any periorbital trauma patient must be initially evaluated by an ophthalmologist. the eye examination involves determination of ocular lesions in the anterior or posterior segments, diagnosis of a globe rupturing or retrobulbar hematoma. evaluation of eye mobility and the degree of exophthalmos and enophthalmos may not be accurate in the presence of posttraumatic edema and necessitates subsequent examinations. studies have shown that the greatest risk for posttraumatic vision loss in orbital fracture patients is found in the ones presenting with penetrating orbital lesions, in patients with diagnosed fractures of the posterior orbit, involving the orbital apex, patients exhibiting a decrease in visual acuity, or an afferent pupillary defect (36, 37). ophthalmologic examinations are important in the perioperative period to rule out the occurrence of a retrobulbar hematoma, which represents an indication for emergency drainage surgery through lateral canthotomy. the finding of postoperative retrobulbar hematomas has decreased since the implementation of fenestration for reconstructive materials used in orbital surgery (38), but nevertheless the importance of periodic inquiry regarding visual acuity in the postoperative time remains crucial for the timely intervention in case of compressive hematoma development. the ectropion-related ophthalmologic sequelae that are frequently linked to periorbital traumatisms may lead to a decrease in the life quality of the patient and often necessitate repeated correction procedures. conclusion maxillofacial surgeons, neurosurgeons, otolaryngologists and ophthalmologists handling the acute orbital trauma patient should be familiar with the possible complications, the indications for immediate, early and delayed surgery, or for the conservative management in different patterns of orbital fractures. good collaboration between the different specialties increases the chances for early diagnosis, accurate operative or non-operative management with proper follow-up and minimal complications. the surgical approach often requires a multidisciplinary participation for achieving a good exposure, performing a proper anatomical repair, resulting in favorable functional and aesthetic outcomes. romanian neurosurgery (2018) xxxii 4: 552 562 | 561             references 1.kunz c, audigé l, cornelius cp, buitrago-téllez ch, rudderman r, prein j. the comprehensive aocmf classification system: orbital fractures level 3 tutorial. craniomaxillofac trauma reconstr. 2014 dec;7(suppl 1):s092-102. 2.kim hs, jeong ec. orbital floor fracture. arch craniofac surg. 2016; 17(3):111-118. 3.barbrel p, géré é. fractures de l’orbite. encycl méd chir, stomatologie, 22-072-a-10, 2001, 20 p. 4.uzelac a, gean ad. orbital and facial fractures. neuroimaging clin n am. 2014; 24(3):407-24 5.perry m, holmes s. atlas of operative maxillofacial trauma surgeryprimary repair of facial injuries. springer-verlag london 2014. 6.cobzeanu md, bâldea v, bâldea mc, vonica ps, cobzeanu bm. the anatomo-radiological study of unusual extrasinusal pneumatizations: superior and supreme turbinate, crista galli process, uncinate process. rom j morphol embryol. 2014; 55(3 suppl):1099-1104. 7.özkan ö, coşkunfirat ok, özkan ö. midface reconstruction. semin plast surg. 2010; 24(2): 181–187. 8.coon d, yuan n, jones d, howell lk, grant mp, redett rj. defining pediatric orbital roof fractures: patterns, sequelae, and indications for operation. plast reconstr surg. 2014 sep;134(3):442e-448e. 9.righi s, boffano p, guglielmi v, rossi p, martorina m. diagnosis and imaging of orbital roof fractures: a review of the current literature. oral maxillofac surg. 2015; 19(1):1-4. 10.lee hj, jilani m, frohman l, baker s. ct of orbital trauma. emerg radiol. 2004; 10(4):168-72. 11.mici e, calvo a, cicciù m, cervino g, belli e. complex orbital fractures: three-dimensional planning and combined surgical approach. j craniofac surg. 2018; 29(7):1965-1968. 12.ha ay, mangham w, frommer sa, choi d, klinge p, taylor ho, oyelese aa, sullivan sr. interdisciplinary management of minimally displaced orbital roof fractures: delayed pulsatile exophthalmos and orbital encephalocele. craniomaxillofac trauma reconstr. 2017; 10(1):11-15. 13.novelli g, tonellini g, mazzoleni f, bozzetti a, sozzi d. virtual surgery simulation in orbital wall reconstruction: integration of surgical navigation and stereolithographic models. j craniomaxillofac surg. 2014; 42(8):2025-34. 14.dubois l, steenen sa, gooris pj, mourits mp, becking ag. controversies in orbital reconstruction-ii. timing of post-traumatic orbital reconstruction: a systematic review. int j oral maxillofac surg. 2015; 44(4):433-40. 15.palmieri cf jr, ghali ge. late correction of orbital deformities. oral maxillofac surg clin north am. 2012; 24(4):649-63. 16.wolfe sa, ghurani r, podda s, ward j. an examination of posttraumatic, postsurgical orbital deformities: conclusions drawn for improvement of primary treatment. plast reconstr surg. 2008; 122(6):1870-1881. 17.antonelli v, cremonini am, campobassi a, pascarella r, zofrea g, servadei f. traumatic encephalocele related to orbital roof fractures: report of six cases and literature review. surg neurol. 2002; 57(2):117-25. 18.cossman jp, morrison cs, taylor ho, salter ab, klinge pm, sullivan sr. traumatic orbital roof fractures: interdisciplinary evaluation and management. plast reconstr surg 2014 19.liss j, stefko st, chung wl. orbital surgery: state of the art. oral maxillofac surg clin north am. 2010; 22(1):59-71. 20.kellman rm, bersani t. delayed and secondary repair of posttraumatic enophthalmos and orbital deformities. facial plast surg clin north am 2002; 10:311-323. 21.chen ct, huang f, chen yr. management of posttraumatic enophthalmos. chang gung med j. 2006; 29(3):251-261. 22.havlik rj, sutton ln, bartlett sp. growing skull fractures and their craniofacial equivalents. j craniofac surg. 1995;6(2):103-10 23.singh i, rohilla s, siddiqui sa, kumar p. growing skull fractures: guidelines for early diagnosis and surgical management. childs nerv syst. 2016; 32(6):1117-22. 24.antoun js, lee kh. sports­related maxillofacial fractures over an 11­year period. j oral maxillofac surg. 2008; 66:504–508. 25.hwang k, you sh, sohn ia. analysis of orbital bone fractures: a 12­year study of 391 patients. j craniofac surg. 2009; 20:1218–1223. 26.gart ms, gosain ak. evidence-based medicine: orbital floor fractures. plast reconstr surg. 2014; 134(6):1345-55. 562 | costan et al multidisciplinary approach to orbital fracture repair             27.christie b, block l, ma y, wick a, afifi a. retrobulbar hematoma: a systematic review of factors related to outcomes. j plast reconstr aesthet surg. 2018; 71(2):155161. 28.brady sm, mcmann ma, mazzoli ra, bushley dm, ainbinder dj, carroll rb. the diagnosis and management of orbital blowout fractures: update 2001. am j emerg med. 2001; 19(2):147-54. 29.matsuzaki k, enomoto s, aoki t. treatment of orbital roof blow-up fracture using a superior blepharoplasty incision. orbit. 2015; 34(3):166-71. 30.haug rh, van sickels je, jenkins ws. demographics and treatment options for orbital roof fractures. oral surg oral med oral pathol oral radiol endod 2002; 93(3):238–246 31.clauser l, dallera v, sarti e, tieghi r. frontobasilar fractures in children. childs nerv syst. 2004; 20:168–175. 32.baril se, yoon mk. naso-orbito-ethmoidal (noe) fractures: a review. int ophthalmol clin. 2013; 53(4):149-55. 33.pawar ss, rhee js. frontal sinus and naso-orbitalethmoid fractures. jama facial plast surg. 2014; 16(4):284-9. 34.shi w, jia r, li z, he d, fan x. combination of transorbital and endoscopic transnasal approaches to repair orbital medial wall and floor fractures. j craniofac surg. 2012; 23(1):71-4. 35.cheung k, voineskos sh, avram r, sommer dd. a systematic review of the endoscopic management of orbital floor fractures. jama facial plast surg. 2013; 15(2):126-30. 36.andrews bt, jackson as, nazir n, hromas a, sokol ja, thurston te. orbit fractures: identifying patient factors indicating high risk for ocular and periocular injury. laryngoscope. 2016; 126 suppl 4:s5-11. 37.ho tq, jupiter d, tsai jh, czerwinski m. the incidence of ocular injuries in isolated orbital fractures. ann plast surg. 2017; 78(1):59-61. 38.farber sj, yu jl, nguyen dc, woo as. fenestration of solid orbital implants: reducing retrobulbar hematoma rate. j craniofac surg. 2017; 28(1):248-249. romanian neurosurgery (2019) xxxiii (3): pp. 227-231 doi: 10.33962/roneuro-2019-038 www.journals.lapub.co.uk/index.php/roneurosurgery 150 years since the birth of harvey williams cushing h. ples1, h. berceanu2 1 “victor babes” university of medicine and pharmacy, timisoara, romania 2 elias emergency university hospital, bucharest, romania the first practitioner physicians of modern neurosurgery are sir william macewen, (1848-1939) with 21 surgical interventions, and sir victor horsley (1857-1916) who performed 10 skull surgeries in 1886. (1) during this time, the most important character in the development of neurosurgery was harvey cushing. the complex personality of harvey cushing becomes evident after reading the monumental biography written by john fulton. cushing was a genius with exemplary determination, working strength and an extraordinary perseverance. like any genius, he was a difficult person, hard to collaborate with. these difficulties were minor in the light of his great achievements. (2) it seems a sacrilege to criticize a human being who almost by himself abolished the terrible spectre of the “cerebral fungus” which was the common result of surgeries performed in that era. harvey williams was born on april 8, 1869, in cleveland, ohio, and died on october 7, 1939 in new haven, connecticut. between 1887 and 1891 he studied at yale college, and continued his studies and graduated from the harvard medical school in 1895 cum laude. he studied for four years at johns hopkins hospital in baltimore under the famous surgeon w.s. halsted. (1) his collaboration with halsted influenced cushing’s career. halsted used local anaesthesia with cocaine in the vicinity of nerves. after he injected his own hand, he developed a cocaine addiction, which kept him away from his patients and the operating room. this allowed young cushing to take on responsibilities closer to those of a senior surgeon, helping him advance in his career. (7) harvey cushing also trained brain surgery techniques with theodor kocher in bern and charles scott sherrington in liverpool. during his collaboration with kocher, the “cushing reflex” was described, which highlighted the relationship between blood pressure and intracranial pressure. he also studied intracranial pressure with kocher. together with sherrington he had contributions to the cortical localization of brain centres (10). keywords neurosurgery, harvey williams cushing corresponding author: h. ples “victor babes” university of medicine and pharmacy, timisoara, romania horia.ples@neuromed.ro copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 228 h. ples, h. berceanu cushing’s best friend was osler, the famous father of american internal medicine, and one of four professors who founded the johns hopkins hospital. cushing won the pulitzer prize in 1926 with his book “life of sir william osler”. he was a surgeon in the same hospital from 1902 to 1912. (3) in 1903 he obtained the title of associate professor in surgery. (6) cushing managed neurological cases. in 1904 he presented “the special field of neurological surgery” with a great amount of enthusiasm in front of the medical academy in cleveland. (1) he became chief surgeon at peter bent brigham hospital in boston and professor of surgery at harvard medical school. cushing joined yale in 1933. (3) cushing came from two generations of physicians. he married his childhood sweetheart, katharine s. crowell, on june 10, 1902 in cleveland, ohio. they had five children: two boys and three girls. one of his daughters married james roosevelt, the son of the president of the united states in that time (franklin d. roosevelt). (4) in his professional life cushing was a “tough hombre”. nurses were sometimes reduced to tears and residents had nervous breakdowns due to cushing’s withering scorn and sarcasm. he demanded of his team work 98 hours per week. this took a toll on his wife and children. (5) one can see cushing’s character in how he behaved upon the death of his eldest son in a car accident at the age of 22. he received the news early in the morning. he notified his wife, and then he went to the hospital to perform scheduled surgeries. (1) he smoked a lot, drank very little, did not approve of alcohol in the family, disapproved of jazz, movies, fashion, telephones, friends, women in medicine, women 229 150 years since the birth of harvey williams cushing smoking, and young men who did not attend classes. (5) his patients knew another cushing wonderful and elegant manners, absolute dedication and empathy. (5) he was of medium height, elegant, with a depressing smile and pleasant manners. he had charm and charisma, and he was proud of his own attire. he was a good speaker, but a terrible listener, with a tendency to interrogate his interlocutor. he used to follow his scientific ideas even if it meant sacrificing his friends (an example of this is walter dandy). his lack of diplomacy sometimes got him in serious trouble, such as the episode in 1917 in france when he was enrolled in the united states army. only the intervention of general pershing saved him from court martial, following an incident that was rather a stupid verbal exchange. (2) after this episode, between 1917-1919, he was the director of the “us army base hospital no 5”. (6) professional activity when he entered neurosurgery, postoperative mortality was about 50%. his ability and surgical technique were able to decrease it to 10%. as mentioned above, he spearheaded the eradication of “cerebral fungus”. (4) cushing’s major interest was brain tumours. between 1912 and 1938 he published 5 books, and he had a database of 2023 brain tumours. (7) in 1931, in bern, at the first international neurology congress (august 31st september 3rd), harvey cushing presented his memorable paper on 2000 brain tumour surgeries, a presentation which remained famous among neurologists and neurosurgeons. in the room there also were 25 of his pupils and at least 1,000 listeners. (7) during the presentation, no one remained outside the meeting room, says john fulton. during this congress, harvey cushing organized a dinner to which he invited the great personalities who were there. the seating arrangement was personally guided by harvey cushing. from the image you can see that our countryman dumitru bagdasar was placed on the left of the great cushing; this shows the appreciation and friendship felt by the american neurosurgeon for him. dr. dumitru bagdasar, subsequently university professor and minister of health in romania (?)(19451946), specialised in neurosurgery at peter bent brigham hospital from 1927-1929 with his mentors harvey cushing and percival bailey. prof. a. v. ciurea (bucharest) together with dr. pleș horia (timisoara) visited the boston hospital. two articles written by dumitru bagdasar during his work in the united states (treatment of brain gummas and intracranial chordoblastomas) can be found up to this day. there are several letters addressed by harvey cushing to the romanian neurosurgeon mentioned in dr. dumitru bagdasar’s “work and character” (“muncă și caracter”). cushing’s affection for doctor bagdasar is evident from these letters. here is one of the letters: dear bagdasar, i wonder if i have answered you regarding the receiving of the delicious book that you have sent me on the art of romanian peasants. if i did not, it was an omission. we liked it very much. i hope that you and your wife are making satisfying progress. we are often talking about you here. i have seen your countryman researcher, grigore popa, in london, at the university college. he made an excellent paper on the circulation of the pituitary gland and hypothalamus. with warm regards, i remain forever yours, harvey cushing together with louise eisenhardt, he wrote a monography about brain meningiomas, another passion of professor cushing. the most famous meningioma patient of cushing was general leonard wood, from the us army. general wood was chief of military personnel in the usa, himself a military surgeon. in 1899 the general suffered a craniocerebral trauma, apparently without consequences until 1902, when he developed paresthesia in the left lower limb, and then epilepsy. in 1905 he underwent a surgery to remove a tumour mass located at the calvaria and an epidural tumour section. the jacksonian seizures continued. in 1910, professor cushing performed surgery in two steps four days apart to remove an intracranial parasagittal meningioma. general wood had a complete recovery. no doubt that the general’s personal fame helped cushing to obtain the position of chief surgeon in the new peter bent brigham hospital. in 1927 general wood came again to doctor cushing, this time in boston, with spastic 230 h. ples, h. berceanu left hemiparesis and ipsilateral hemianopsia. cushing re-operated the tumour relapse without apparent complications, but the general died unexpectedly a few hours later as a result of a haemorrhage with intraventricular effraction. cushing commented later: “i was never so upset because of the death of a patient. he was so close to success. he was a great man.” (8) between 1896-1912 he performed almost 200 surgeries intervention on children, attempting to establish paediatric neurosurgery as a sub-specialty (9). cushing studied the pituitary gland (1912), adding to his international reputation. he was the first person who described pituitary gland disorders, now called ‘cushing syndrome’ or ‘disease’. (3) he was the first person who associated pituitary adenoma with cushing syndrome. he used the transsphenoidal approach in 227 patients with a mortality of 5.2%. (4) one of cushing’s important contributions is in the area of neuroradiology. he immediately understood the importance of professor roentgen’s discovery, and he managed to bring a crooke tube to the massachusetts general hospital to generate x-rays at approximately five months after the discovery. after he insisted that the boston hospital have a radiology service. after a few months cushing left with the tube to the johns hopkins hospital, to the bewilderment of his colleagues. (4) in november 1896 he used x-rays to investigate a spine after a gunshot. the female patient had brown-secquard syndrome. it was for the first time that a neurologic syndrome to benefit of this investigation. the exposure lasted 35 minutes. cushing was not the first person to appreciate xrays. in 1987 alone, more than 1,000 articles were published on their role in medicine. (4) together with ernest amory codeman, he developed the predecessor of the modern anaesthesia machine, monitoring temperature, heart rate, and blood pressure during surgical interventions. (4) among other innovations initiated by cushing are cortical stimulation, understanding of the natural evolution of the central nervous system, and understanding of increases in intracranial pressure. he collaborated with w.t. bovie in the development of the electrocautery with the same name, leading in 1925 to the resection of a brain tumour, and to widescale use since 1928. (4) cushing’s scientific activities included those of his resident, walter e. dandy, with whom he worked on hydrocephaly. dandy discovered ventriculography, but cushing was upset that he experimented on children with hydrocephaly and not on dogs, as there was a risk of secondary herniation of the amygdalae. (4) on the other hand dandy did not agree with cushing on using metallic clamps in aneurysm surgery. (4) the relationship between cushing and dandy was tense, as dandy was quite aggressive. (4) when they are talking about the competition between harvey cushing and walter dandy, other authors think that the first did not have an elegant behaviour. (7) when the composer george gershwin was discovered with a brain tumour and went into a coma, cushing was sought immediately. as he retired several years before, he recommended dr. walter dandy, who was on the ocean with the governor of the state of maryland. the white house sent a coast guard ship to fetch dandy as quick as possible. he published 13 books and over 300 articles during his career. the best known books are “surgery of the head” (1910), “the pituitary body and its disorders” (1912), and “meningiomas” (1938). at cushing’s suggestion in 1919, the “society of neurological surgery” was formed, and in 1931, with cushing’s permission, a group of young neurosurgeons founded the “harvey cushing society”. (1) he donated his collection of books and magazines to the yale medical library near the end of his career. (1) the destroyer “uss cushing”, named to honour the achievements of harvey cushing, was launched on december 31, 1935. in 1988 he was honoured with a stamp issued as part of the “great americans” series. (1) notes 1. l. f. haas. (2002). neurological stamp. journal of neurology, neurosurgery, and psychiatry, p. 596, http://dx.doi.org/ 10.1136/jnnp.73.5.596. 2. derek denny – brown. (1979). harvey cushing: the man, journal of neurosurgery, vol. 50, ian. 1979, doi: 10.3171/jns.1979.50.1.0017. 231 150 years since the birth of harvey williams cushing 3. https://www.britannica.com/biography/harvey-williamscushing. 4. richard b. gunderman and zachary a. seymour. (2010). 'harvey cushing', american journal of roentgenology. 2010; 194: 296-298. 10.2214/ajr.09.3356. 5. peter farley. (2006). harvey cushing: the man, the surgeon and the father, yale medicine, 2006, https://medicine .yale.edu/news/yale-medicine-magazine/ harvey-cushingthe-man-the-surgeon-and-the.aspx 6. john f. fulton. (1946). harvey cushing—a biography. by. pp. 754. oxford: blackwell 7. michael bliss. harvey cushing: a life in surgery, oxford university press, isbn-13: 978-0195329612 8. joung h. lee. meningiomas, springer, isbn 978-1-84628526-4, doi: 10.1007/978-1-84628-784-8 9. vivek a. mehta, olindi wijesekera, courtney pendleton, alfredo quiñones-hinojosa, george i. jallo and edward s. ahn. harvey cushing and “birth haemorrhage”: early paediatric neurosurgery at the johns hopkins hospital. historical vignette, doi: https://doi.org/10.3171/2011. 9.peds11198 10. chisholm hugh. (1922). "cushing, harvey" . encyclopædia britannica (12th ed.). london & new york. doi: 10.33962/roneuro-2023-042 cerebellopontine angle tumours: clinico radiological features and surgical outcome. single institutional experience vivek kumar kankane, ketan gujral, avinash sharma, aditya shrivastava romanian neurosurgery (2020) xxxiv (1): pp. 233-238 doi: 10.33962/roneuro-2020-042 www.journals.lapub.co.uk/index.php/roneurosurgery cerebellopontine angle tumours: clinicoradiological features and surgical outcome. single institutional experience vivek kumar kankane, ketan gujral, avinash sharma, aditya shrivastava department of neurosurgery, g.r. medical college & jah groups of hospital gwalior (m.p.), india abstract object. our aim is to demonstrate the various aspects of clinical-radiological presentation and surgical outcome with association to the tumour size concerning cerebellopontine angle (cpa) tumours. materials and method. this is a prospective study of 40 patients at the department of neurosurgery, jayarogya group of hospitals, grmc gwalior, m.p. india. all of the patients were pre-operatively evaluated with either non-enhanced and enhanced computerized tomography (ct) or magnetic-resonance (mr) imaging or both.cpa tumours (predominantly acoustic neuroma) that underwent surgical removal using a suboccipital retro sigmoid approach over a 2-year period (june 2019 to may 2021). results. there was a female preponderance. the most common presentation was sensorineural hearing loss (90%) followed by headache (67.5%). the majority of cases of vestibular schwannoma have heterogenous enhancement with cystic component.65% of patients have large (26-40mm) size tumours and facial nerve preservation is 86.4% in medium size tumours (10-25 mm).and incidence of postpostoperative of facial nerve palsy is more in giant size tumour (> 40mm) so positive association between size of lesion and incidence of post-operative facial nerve palsy. csf leak occurs in 6 patients and postoperative hydrocephalus occur in 2 patients and mortality occurs in 3 patients. conclusion. cp angle tumor was common in middle age group, with the incidence in females slightly more than in males. the majority of lesions were of large size (2640mm). most of the patients on admission had a non-serviceable hearing. heterogeneous enhancement with cystic components was found in most of the lesions. gross-total excision was one in the majority of cases and vestibular schwannoma was the most common histopathological lesion obtained. facial nerve palsy was the most complication and as the size of the lesion increased, the possibility of facial nerve palsy also increased post-operatively. overall mortality is 7.5%. introduction cp angle tumors account for 5-10% of intracranial tumors. [1, 2] most cerebello-pontine angle tumors are benign, with over 85% being vestibular schwannomas (acoustic neuromas). primary malignancies or metastatic lesions accounting less than 2% of neoplasm in the cpa. keywords cerebellopontine angle tumours, tumour size, facial nerve, surgical outcome corresponding author: aditya shrivastava department of neurosurgery, g.r. medical college & jah groups of hospital gwalior (m.p.), india vivekkankane9@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 234 vivek kumar kankane, ketan gujral, avinash sharma et al. ct and mri are widely used radiological methods for cerebello-pontine angle imaging. the main radiological diagnostic goal is the description of the relation of the tumor to iam, the brainstem and cerebellar hemispheres. the second line basic information is if the lesion is extra-or intracerebral. the options available for management includes observation, surgery, stereotactic radiosurgery, fractionated radiotherapy. some patients might also be candidates for a combination of these therapies. the ideal treatment is total excision of tumor. several approaches and techniques are available for the resection of cpa tumors, including trans labyrinthine, retro sigmoid, suboccipital, retro labyrinthine, trans cochlear, transotic and middle fossa approaches. surgery improves quality of life in patients but each approach is associated with postoperative complications like mortality, hematoma, pneumocephalus, cranial neuropathies, cerebellar dysfunction, brainstem complications, infections, csf leaks etc. the suboccipital retro sigmoid approach is a popular method of excising cpa tumors. advantages of this approach include a low complication rate, particularly with regard to facial nerve function, and total tumor removal in the vast majority of cases. moreover, the technique is safe and effective, even with the largest of tumors. technical advances in surgery and anesthesia have revolutionized the results of surgery in cerebellopontine angle lesions with reduced mortality and morbidity. use of intra-operative nerve stimulators and intraoperative evoked potentials have made the resection of the lesions possible along with preservation of cranial nerves. material and methods this is a prospective study of 40 patients at the department of neurosurgery jayarogya group of hospitals , g.r.m.c. gwalior, m.p. were carried out and undergoing surgical removal using the suboccipital retro sigmoid approach. all of the patients were pre operatively evaluated with either non-enhanced and enhanced computerized tomography (ct) or magnetic-resonance (mr) imaging or both. computed tomography characteristics reviewed included tumor density and homogeneity, presence and type of contrast enhancement and calcifications. mri examination was performed on different imaging units, using a field strength ranging between 0.5 and 1.5 tesla. the magnetic resonance (mr) image parameters used for this study included signal homogeneity and intensity (t1-,and t2-weighted images), presence and type of contrast enhancement, calcifications, and lesion margins, characteristic of the tumor on diffusion weighted (dwi) and absoluted diffusion coefficient(adc)sequences. hearing assessment was done with the help of puretone audiometry (pta) analysis pre-operatively in all patients and were divided into serviceable and non-serviceable category. gardner robertson hearing classification scale was used. speech discriminations coreless than 50% and pta value>50db were defined as nonserviceable hearing. fundoscopy was done in all patients with the help of direct ophthalmoscope to assess the papilledema pre-operatively and was graded according to modified frisen scale. in all patients, radical excision was attempted. operating microscope was used in every case. the patients were maintained peri-and postoperatively on steroids. operative data, including surgical approach, extent of removal, morbidity, and mortality, were evaluated. the completeness of tumor removal was assessed intraoperatively and with postoperative ct and mr imaging. extent of removal was divided into gross total removal, neartotal removal and sub-total removal. discussion in general cpa tumors are divided in to acoustic and non-acoustic tumors. the main factor under scoring the importance of accurate preoperative diagnosis is the different surgical approach for vestibular schwannomas and the other tumors. there is general agreement that completeness of tumor resection and preservation of the facial nerve are the major neurosurgical goals. an appreciation of the vascular and cranial nerve micro anatomy and the relationships between neurovascular structures and the tumor are essential for achieving optimal surgical results. in our study majority of patients 21-30yr, 32.5% [table-1] females in our study were 57.5% whereas the males were 42.5%. arismendi g, et al. showed a 2:1 female to male ratio with a median age was 48+/12. 7years. faramarz memari, et al. [3]. showed that the mean age was 49 years and there was a slight male predominance of 55%.joarder ma,etal. [4] showed the maximum incidence between 30-50yrs 235 cerebellopontine angle tumours: clinico-radiological features and surgical outcome. with female predominance of 55%. maheswararao y.v.n, et al. [5] showed that the highest incidence of extra axial cerebo-pontine angle tumors’ were found in 5160 years age group with 70% being females. table 1. distribution of case according to age age (yrs) total patients percentage 0-20 2 5 21-30 4 10 31-40 13 32.5 41-50 11 27.5 51-60 8 20 61-70 2 5 table 2. distribution of cases according to clinical presentation clinical findings vestib ular schwa noma menin gioma epider moid cyst abs cess tota l pati ents perce ntage sensori neural hearing loss 30 3 2 1 36 90 cerebel lar signs 20 2 1 0 23 57.5 headac he 22 3 1 1 27 67.5 trigemi nal dysfunc tion 15 2 0 0 18 45 facial dysfunc tion 17 2 1 0 19 47.5 papilloe dema 7 3 0 0 11 27.5 tinnitus 14 2 0 0 16 40 pyrami dal signs 9 1 0 0 10 25 9,10,11 nerve dysfunc tion 5 1 0 0 6 15 in our study sensorineural hearing loss was observed in 90% cases, cerebellar signs were present in 57.5% cases, headache was present in 67.5%,trigeminal dysfunction was present in 45%, facial nerve dysfunction was present in 47.5%, papilledema was present in 27.5%, tinnitus was present in 40%,pyramidal signs was present in 25%, 9,10,11 nerve dysfunction was present in 15% [table2] .our pure tone audiometry results of serviceable hearing were in 22.5% cases and non-serviceable hearing in 77.5% cases[table-3]. faramarz memari, et al,& joarder ma, et al [3,4] showed same results of clinical presentation. table 3. distribution of cases according to pure tone audiometry class vestib ular schwa noma menin gioma epider moid cyst abs cess total pati ents perce ntage i &ii (servic eable) 3 3 2 1 9 22.5 iii & iv (non service able) 28 2 1 0 31 77.5 table 4. distribution of cases according to size of lesion & anatomical preservation of facial nerve size total patients patients with anatomically preserved facial nerve medium (1025mm) 6 6 ( 100%) large( 2640mm) 26 22 (84.6%) giant ( >40 mm) 8 4 (50%) our study depicted medium size (10-25mm) tumors in 15%, large size (26-40 mm) in 65%, giant (>40mm) in 20% [table-4]. faramarz memari, etal [3] showed the mean tumor size was 24mm, ranging from 35 mm. joarder ma, et al [4] showed medium size, tumors in 15%, large size in 58%, giant (>40mm) in 27%. anatomical preservation of facial nerve was achieved in the present study for large size tumors in 84.6% of the cases and for giant size tumors in 50% . joarder ma ,et al.[4]showed that preservation of facial nerve was achieved in 75% for large size tumors and in 55% for giant size tumors. in our study anatomical preservation of facial nerve was achieved in 80.6% of vestibular schwannoma cases overall. in a study on vs by samii and matthias preservation rate was reported to be 93%, independent of tumour size. in a study on vs by vijendra k.jain, et al [6].the preservation of facial nerve was 84.3%. in our study it is observed that there is a positive association between size of tumor and incidence of 236 vivek kumar kankane, ketan gujral, avinash sharma et al. post-operative facial nerve palsy. post operatively 1 patient developed facial palsy in medium tumors (16.6%), 14 patients developed facial palsy in large tumors (53.8%) and 7 patients developed facial palsy in giant tumors (87.5%) [table-5]. as the size increases, possibility of facial nerve palsy also increases post-operatively. joarder ma, et al [3] and faramarz memari,et al [3] also depicted a significant correlation between tumor size and facial nerve outcome, with larger tumors yielding worse outcomes. table 5. distribution of cases according to size of lesion & incidence of post -operative facial nerve palsy size total patients facial nerve palsy medium (10-25mm) 6 1 (16.6%) large ( 26-40 mm) 26 14 (53.8%) giant ( >40mm) 8 7 ( 87.5%) table 6. distribution of cases according to facial nerve functional grading (postoperative) in already involved facial nerve on admission) grade pre-op (19) post-op (19) follow -up (6 month) (16) 2 3 & 4 5 & 6 2 3 & 4 5 & 6 2 16 8 6 2 7 4 2 3 & 4 3 0 0 3 0 1 2 5 & 6 0 0 0 0 0 0 0 our study showed 19 patients have pre-operative facial palsy in which16 have grade 2,and 3 have grade 3 & 4.out of 16 patients of grade 2, 6 patients increase to grade 3& 4and 2 patient increase to grade 5 & 6.out of 3 patients of grade 3&4 , 3patient increase to grade 5 & 6 [ table-6]. samii m,etal. [8] showed postoperative grade1 & 2 facial nerve function in 64% cases, grade 3 & 4 in 21% cases and grade 5 & 6 in15%cases. our study on radiological examinations in vestibular schwannoma showed homogenous enhancement in 2 cases, heterogenous enhancement in 29 cases, cystic component in 29 cases, hyperostosis not found in any radiologiacal imaging. in meningioma,5 cases had homogenous enhancement and 2 cases had hyperostosis, none had cystic component. in epidermoid cyst, none case had heterogenous enhancement and one case had cystic component, where as in abscess the only case had heterogenous enhancement with cystic component [table-7]. in the study of maheswara raoy.v.n,etal [5] . table 7. distribution of cases according to finding on imaging imaging finding ( mri) vestibular schwanno ma ( 31) meningio ma (5) epiderm oid cyst (3) absce ss (1) homogen ous enhancem ent 2 5 0 0 heterogen ous enhancme nt 29 0 1 1 cystic compone nt 29 0 1 1 centered of iam 27 1 0 0 broad base dural tail 0 5 0 0 table 8. distribution of cases according to resectability tumor gross total excision near-total excision sub-total excision vestibular schwannoma (31) 26 (84%) 3 (10%) 2 (6%) meningioma (5) 4 (80%) 1 (20%) 0 (0%) epidermoid (3) 2 (67%) 1 (33%) 0 (0%) abscess (1) 1 (100%) 0 (0%) 0 (0%) we performed vp-shunt followed by definite surgery in 25% cases and direct tumor surgery in 75% cases. in our study, in vestibular schwannoma we did gross total excision in 84% cases, near-total in 10% and sub-total in 6%cases. in meningiomas we had gross total excision in 80%, near-total in 20%. in epidermoid we had 67% gross-total excision and 33% near total excision. where as in abscess we had gross total excision in 100% of cases [table-8]. overall gross total resection done in 33 patients (82.5%) and near-total resection in 5 patients (12.5%) and sub-total resection in 2 patients (5%). in all the 40 cases, operation was done by suboccipital retro-mastoid approach in semi-sitting position and in none of the cases we found any position related clinically apparent complication 237 cerebellopontine angle tumours: clinico-radiological features and surgical outcome. (intra-operative and postoperative). iac drilling was done in all cases of vs (31cases). faramarz memari,et al. [3] in a study on cp-angle lesions, achieved complete gross tumor removal in 92% of patients. in study done by sourabh dixit, et al [10] on vs, the gross total resection was done in 84.61% cases and subtotal done in 15.38% cases. in our study, in histopathology, vestibular schwannoma accounted for 77.5% cases, meningioma for12.5%, epidermoid cyst for 7.5% and abscess for 2.5%. our study showed csf leak in15% cases over all. all were initially managed conservatively with lumbar drain and medication. meningitis occurred in10% cases in which two patients recovered with appropriate antibiotics whereas rest of the two patients who also had simultaneous csf leak, deteriorated and expired. faramarz memari,et al [3].in cp-angle cases had rates of csf leakage for retro-sigmoid approach around 18% and meningitisin10% cases. in our study lower cranial nerves palsy was seen in 20% cases (6 deteriorated cases+2 new onset cases) and they were managed with nasogastric tube feeding. at 6 months follow up 2 patients showed incomplete recovery of lower cranial nerves palsy. we observed, in vs subgroup, facial nerve palsy in 47.5% cases and lower cranial nerve palsy in 22.5% cases. vijendra k.jain,et al [6] in their study on vs had the incidence of lower cranial nerve paresis of 6.8%.sourabh dixit, et al [10] in their study on vs had transient lower cranial nerve paresis in 46.15% patients which gradually improved. the reported incidence of lower cranial nerve paresis in the rest of literature ranges from1.5%to 5.5%. in our study pre-operatively, 77.5% of cerebellopontine angle tumor patients had no useful hearing(>50decibels).out of the 9 patients (3 vestibular schwannomas, 3 meningiomas, 2 epidermoid cyst,1 abscess) who had useful hearing preoperatively, 3 patients (2 epidermoid cyst and1 abscess patient) retained it postoperatively also making our over all hearing preservation upto 33.3%.invs sub-group hearing preservation was 0%.hearing status of all the patients at 6 months follow up remained same as that of post-operative period. samii, et al [8].in their study on vs, reported hearing preservation in 23.6% with large tumors.vijendrak.jain,et al[6]. in their study on vs, reported hearing preservation in 29.6% of their patients who had useful pre-operative hearing. in our study, follow up of 37 patients showed recurrence in two patients (5%) (one vestibular schwannoma and one meningioma) and were managed conservatively as both the patients were not ready for re-operation or srs referral. faramarz memari,etal. [3] in their study on cp angle lesions, had residual tumor in 7% for retro sigmoid approach. in our study, in vs subgroup we had 3.22% recurrence. gormley and sekhar, et al [7] in their study on vs, reported complete tumor resection was accomplished in 99% of the patients, and there was no evidence of recurrence in this group. vijendra k.jain,etal.[6] in their study on vs, had achieved complete tumor excision in 96.5%. in our study overall mortality was seen in 7.5% cases mainly attributable to post-operative csf leak and meningitis. faramarz memari,et al [3] in their study on cp angle lesions, had mortality of 2% for retro-sigmoid approach. mortality in their series of vs. conclusion cp angle sol was common in middle age group, with incidence in females slightly more than males. decreased hearing and cerebellar symptoms were the most common complaints. majority of lesions were of large size(26-40mm). most of the patients on admission had non-serviceable hearing. heterogenous enhancement with cystic component was found in most of the lesions. gross-total excision was done in majority of cases and vestibular schwannoma was the most common histopathological lesion obtained. facial nerve palsy was the most complication and as the size of lesion increased, possibility of facial nerve palsy also increased post-operatively. overall mortality was in 7.5% cases, mainly due to post-operative meningitis and csf leak. references 1. ramamurti and tandon’s textbook of operative neurosurgery 3rd edition pg499-503. 2. youmans neurological surgery by h.richard winn 6th edition pg1460-1475 3. memarif, hassanniaf, abtahis. surgical outcomes of cerebellopontine angle tumors in 50 cases. iranian journal of otorhinolaryngology, 2015;vol.27(1),serialno.78. 4. joarder ma, karim akmb, sujonsietal. surgical outcomes 238 vivek kumar kankane, ketan gujral, avinash sharma et al. of cerebellopontine angletumors in 34 cases.pulse volume 2015;8:8-14. 5. maheswararao yvn, baru r. mri evaluation of extra-axial cerebello-pontine angletumours.international journal of contemporary medicine surgery and radiology. 2018;3(3):c33-c38. 6. jain vk, mehrotra n. surgery of vestibular schwannomas: an institutional experience.neurology india.2005;53:41 7. gormley wb, sekhar ln, wright dcetal. acoustic neuromas. results of current surgical management. neurosurgery 1997; 41:50-60. 8. samii m, matthies c. management of 1000 vestibular schwannomas (acoustic-neuromas): surgical management and results with an emphasis on complications and how to avoid them.neurosurgery 1997;40:11–23. 9. ramamurthi b. the continuing challenge of acoustic neurinomas (1949-1993). brj. neurosurgery. 1995;9:3616. 10. dixit s, banga m, saha setal. a study assessing the post operative outcome in patients of acoustic schwannoma operated through retrosigmoid approach at tertiary care institutions-an experience of one year. asian journal of medical sciences 2017;8(4):44-49. doi: 10.33962/roneuro -2020-048 intraventricular dissemination of the pilocytic astrocytomas in an adult vijay p. joshi, ashwin valsangkar, satish nivargi, anish dekhne, amit agrawal romanian neurosurgery (2020) xxxiv (1): pp. 326-329 doi: 10.33962/roneuro-2020-048 www.journals.lapub.co.uk/index.php/roneurosurgery intraventricular dissemination of the pilocytic astrocytomas in an adult vijay p. joshi1, ashwin valsangkar1, satish nivargi1, anish dekhne1, amit agrawal2 1 s. p. institute of neurosciences, solapur, maharashtra, india 2 narayna medical college hospital, chinthareddypalem, nellore, andhra pradesh, india abstract pilocytic astrocytoma (pa) is a subset of gliomas characterized by a benign course with an excellent prognosis and rarely metastasizing or spreading along the neuraxis. we report a case of a 56-year female with intraventricular dissemination of pilocytic astrocytoma in an adult and discuss the clinical significance diagnosis and management including the peculiar pattern of dissemination of the pilocytic astrocytoma. the course of the disseminated disease may not be as good as that of patients with localized recurrence or totally resected primary disease and can vary from rapid progression to prolonged stabilization. introduction pilocytic astrocytoma (pa) is subset of gliomas characterized by a benign course with an excellent prognosis and rarely metastasizing or spreading along the neuraxis. 1-14 dissemination of a pilocytic astrocytoma is a rare event that occurs in 2-4% of cases particularly in children. 6, 8, 11 we report a case of intraventricular dissemination of pilocytic astrocytoma in an adult and discuss the clinical significance diagnosis and management including the peculiar pattern of dissemination of the pilocytic astrocytoma. case report a 56-year old female patient presented with progressively increasing headache, vomiting and blurring of vision without any focal neurological deficits or seizures. her general and systemic examination was unremarkable. neurologically she was conscious, alert and oriented to time, place and person. higher mental functions were normal. she had bilateral papilloedema and other cranial nerves were normal. motor and sensory examination was normal. her general and systemic examination was normal. the patient underwent mri brain and it showed minimally contrast enhancing bilateral thalamic lesions, with intraventricular spread in third ventricle and the aqueduct causing obstructive hydrocephalus (figure 1, 2 and 3). the patient underwent keywords pilocytic astrocytoma, leptomeningeal dissemination, cerebrospinal fluid, metastasis, hydrocephalus corresponding author: amit agrawal professor of neurosurgery. department of neurosurgery, narayana medical college hospital, chinthareddypalem, andhra pradesh, india dramitagrawal@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 327 intraventricular dissemination of the pilocytic astrocytomas in an adult endoscopic exploration of the third ventricular lesion that could be excised as well as the lesion in the aqueduct also could be excised. part of the lesion in the fourth ventricle was left alone as it was densely adherent to the surrounding structures. intraoperatively external ventricular drainage was (evd) was inserted and was kept in situ for 5 days till the csf was acceptably clear. she later underwent right ventriculo-peritoneal shunt surgery. histopathological examination of the section and additional made serial deeper section showed few fragments bits of cellular neoplasm of astrocytic origin. the tumour composed admixture of compact cellular and oedematous loose-knit tissue showing scattered protoplasmic astrocytes having fairly uniform round to oval or slightly elongated nuclei with delicate open chromawr pattern and barely discernible cytoplasm. the fibrillary background showed few microcytfic spaces and vascular proliferation comprising few ectatic congested blood vessels coupie of foe show doubtful rosenthal fibers (figure-4). no granulomas were seen. histopathological features were consistent with 'pilocytic astrocytoma'. section shows a tumor of moderate cellularity with cells amidst fibrillary background. microcystic change, hyalinized vasculature were seen. no mitosis, necrosis, microvascular proliferation seen. rosenthal fibres and eosinophilic granular bodies were seen. the tumor cells express gfap & p 53 (focal) and were immunonegative for synaptophysin 8i ema. the mib1 labeling index was approximately 1%. low grade astrocytic neoplasm suggestive of pilocytic astrocytoma. in post-operative made she did well as she was conscious, with no focal neurological deficits. figure 1. mri brain t1w, t2w and flair axial images showing bilateral thalamic tumor with blockage of the aqueduct and associated hydrocephalus. figure 2. mri brain t1w sagittal images and t2w coronal image showing the blockage of aqueduct by tumour. figure 3. post-operative mri t2w and flair axial images showing although the tumor could be removed from upper part of the aqueduct but still the lower part is closed. figure 4. histopathological examination of the section and additional made serial deeper section showed few fragments bits of cellular neoplasm of astrocytic origin. the tumour composed admixture of compact cellular and oedematous 328 vijay p. joshi, ashwin valsangkar, satish nivargi et al. loose-knit tissue showing scattered protoplasmic astrocytes having fairly uniform round to oval or slightly elongated nuclei with delicate open chromawr pattern and barely discernible cytoplasm. the fibrillary background showed few microcytfic spaces and vascular proliferation comprising few ectatic congested blood vessels coupie of foe show rosenthal fibers. discussion dissemination of primary central nervous system neoplasms along the neuraxis is commonly associated with high grade lesions i.e. medulloblastoma, germ cell tumors and malign glial tumors. 1-5, 11, 15-18 dissemination of low-grade gliomas has been documented only in few cases. 1-14, 19 usually the site of dissemination is spinal 1, 6, 8, 11, 16, 1923 but in rare cases it can be intraventricular metastasis leading to hydrocephalus. 21 clinically it can occur after a long postoperative period or may be the first sign of disease or of relapse. 1, 6, 8, 11, 16, 19-25 the clinical presentation ranges from asymptomatic cases to hydrocephalus, meningismus, worsening of focal deficits, new onset of neurological deficits and onset of seizures. 8, 11, 19, 24 the tumour spread in these patients is via the csf and it is accepted that low grade astrocytomas in proximity to ventricles or csf cisterns are more likely to spread than deeply located tumors. 21, 26, 27 several mechanisms have been hypothesized to explain the spread of intracranial tumors by csf pathways including malignant transformation, cellular anaplasia, surgical manipulation, natural history, multiplicity and presence of cell adhesion molecules (cd44 adhesion molecule as it may play a role in astrocytic invasion and adhesion). 7, 28 it has been suggested that the tumor mass located in the floor of the third ventricle may breach the ependyma, invading the ventricular cavity and thus resulting in to ependymal or leptomeningeal seeding. 2, 3, 5, 8, 9 pilocytic astrocytoma is a benign tumor that corresponds to histological grade i 13, 29-31 and associated with 20-year survival rates of greater than 90% in patients who undergo total excision of the lesion. 8, 13, 29, 30 presently there is not much known about the optimum treatment and course of disseminated low-grade astrocytomas. 1, 2, 14, 16, 32 probably hydrocephalus, biopsy and partial resection may also be additional favorable factors, although this remains unproven. 8, 14 in has been suggested that the total resection must be performed as often as possible and no adjuvant therapy should be carried out for low grade gliomas, 13, 14 however the treatment of the disseminated tumor, remains controversial. 14, 20, 25 the course of the disseminated disease may not be as good as that of patients with localized recurrence or totally resected primary disease and can vary from rapid progression to prolonged stabilization. 1, 2, 14, 16, 25, 32 11, 20, 21 references 1. civitello la, packer rj, rorke lb, siegel k, sutton ln, schut l. leptomeningeal dissemination of low-grade gliomas in childhood. neurology 1988;38:562-566. 2. gajjar a, bhargava r, jenkins jj, et al. low-grade astrocytoma with neuraxis dissemination at diagnosis. journal of neurosurgery 1995;83:67-71. 3. kellie sj, kovnar eh, kun le, et al. neuraxis dissemination in pediatric brain tumors. response to preirradiation chemotherapy. cancer 1992;69:1061-1066. 4. packer rj, siegel kr, sutton ln, litmann p, bruce da, schut l. leptomeningeal dissemination of primary central nervous system tumors of childhood. annals of neurology 1985;18:217-221. 5. ushio y, arita n, hayakawa t, et al. leptomeningeal dissemination of primary brain tumors in children: clinical and experimental studies. progress in experimental tumor research 1987;30:194-205. 6. mccowage g, tien r, mclendon r, et al. successful treatment of childhood pilocytic astrocytomas metastatic to the leptomeninges with high-dose cyclophosphamide. medical and pediatric oncology 1996;27:32-39. 7. morikawa m, tamaki n, kokunai t, et al. cerebellar pilocytic astrocytoma with leptomeningeal dissemination: case report. surgical neurology 1997;48:49-51; discussion 51. 8. mamelak an, prados md, obana wg, cogen ph, edwards ms. treatment options and prognosis for multicentric juvenile pilocytic astrocytoma. journal of neurosurgery 1994;81:24-30. 9. 9. garcia dm, fulling kh. juvenile pilocytic astrocytoma of the cerebrum in adults. a distinctive neoplasm with favorable prognosis. journal of neurosurgery 1985;63:382-386. 10. gjerris f, klinken l. long-term prognosis in children with benign cerebellar astrocytoma. journal of neurosurgery 1978;49:179-184. 11. shapiro k, shulman k. spinal cord seeding from cerebellar astrocytomas. child's brain 1976;2:177-186. 12. haddad sf, menezes ah, bell we, godersky jc, afifi ak, bale jf. brain tumors occurring before 1 year of age: a retrospective reviews of 22 cases in an 11-year period (1977-1987). neurosurgery 1991;29:8-13. 13. wallner ke, gonzales mf, edwards ms, wara wm, sheline ge. treatment results of juvenile pilocytic astrocytoma. journal of neurosurgery 1988;69:171-176. 329 intraventricular dissemination of the pilocytic astrocytomas in an adult 14. figueiredo eg, matushita h, machado agg, plese jpp, rosemberg s, marino r. leptomeningeal dissemination of pilocytic astrocytoma at diagnosis in childhood: two cases report. arquivos de neuro-psiquiatria 2003;61:842847. 15. pezeshkpour gh, henry jm, armbrustmacher vw. spinal metastases. a rare mode of presentation of brain tumors. cancer 1984;54:353-356. 16. mishima k, nakamura m, nakamura h, nakamura o, funata n, shitara n. leptomeningeal dissemination of cerebellar pilocytic astrocytoma. case report. journal of neurosurgery 1992;77:788-791. 17. arseni c, horvath l, carp n, constantinescu a, ciurea v. spinal dissemination following operation on cerebral oligodendroglioma. acta neurochirurgica 1977;37:125137. 18. bell wo, packer rj, seigel kr, et al. leptomeningeal spread of intramedullary spinal cord tumors. report of three cases. journal of neurosurgery 1988;69:295-300. 19. pollack if, hurtt m, pang d, albright al. dissemination of low grade intracranial astrocytomas in children. cancer 1994;73:2869-2878. 20. auer rn, rice gp, hinton gg, amacher al, gilbert jj. cerebellar astrocytoma with benign histology and malignant clinical course. case report. journal of neurosurgery 1981;54:128-132. 21. jamjoom ab, jamjoom za, al-rayess m. intraventricular and leptomeningeal dissemination of a pilocytic cerebellar astrocytoma in a child with a ventriculoperitoneal shunt: case report. british journal of neurosurgery 1998;12:56-58. 22. tamura m, zama a, kurihara h, et al. management of recurrent pilocytic astrocytoma with leptomeningeal dissemination in childhood. child's nervous system : chns : official journal of the international society for pediatric neurosurgery 1998;14:617-622. 23. versari p, talamonti g, d'aliberti g, fontana r, colombo n, casadei g. leptomeningeal dissemination of juvenile pilocytic astrocytoma: case report. surgical neurology 1994;41:318-321. 24. patt s, haberland n, graupner h, schreiber d, kalff r. may 1999--16 year old male with an unexpected mri finding. brain pathology (zurich, switzerland) 1999;9:743744. 25. kanda m, tanaka h, shinoda s, masuzawa t. leptomeningeal dissemination of pilocytic astrocytoma via hematoma in a child. case report. neurosurgical focus 2002;13:ecp2. 26. prados m, mamelak an. metastasizing low grade gliomas in children. redefining an old disease. cancer 1994;73:2671-2673. 27. obana wg, cogen ph, davis rl, edwards ms. metastatic juvenile pilocytic astrocytoma. case report. journal of neurosurgery 1991;75:972-975. 28. 28. cooper dl, dougherty gj. to metastasize or not? selection of cd44 splice sites. nature medicine 1995;1:635-637. 29. garcia dm, latifi hr, simpson jr, picker s. astrocytomas of the cerebellum in children. journal of neurosurgery 1989;71:661-664. 30. geissinger jd. astrocytomas of the cerebellum in children. long-term study. archives of neurology 1971;24:125-135. 31. kleihues p, cavenee w. tumours of the nervous system: pathology and genetics. world health organization classification of tumours iarc press, lyon 2000:198-203. 32. packer rj, lange b, ater j, et al. carboplatin and vincristine for recurrent and newly diagnosed low-grade gliomas of childhood. journal of clinical oncology : official journal of the american society of clinical oncology 1993;11:850-856.. romanian neurosurgery (2019) xxxiii (2): pp. 144-149 doi: 10.33962/roneuro-2019-027 www.journals.lapub.co.uk/index.php/roneurosurgery experience of choroid plexus papilloma in children at mansoura university hospital hatem badr, ahmad zaher, mohamed state, amr farid khalil * mansoura university, egypt abstract choroid plexus papilloma (cpp) are rare, benign tumours of neuroectodermal origin; they represent 1-3% of central nervous system (cns) tumours in paediatric patients. authors present their experience in the management of such lesion in mansoura university hospitals. methods. for children with choroid plexus papilloma who were treated via microsurgical excision over 4 years from january 2012 to january 2016 in mansoura university hospitals, a retrospective analysis was done for age, sex, clinical manifestations, surgical treatment and follow up. results. twenty-three paediatrics were treated over 4 years. age ranged from (7 months 8 years). there were 13 female and10 males. tumours were located in the lateral ventricle in all cases. features of raised intracranial pressure were the predominant presentation. total microsurgical excision was achieved in all cases. all cases had intraoperative blood loss < 100 ml with mean haematocrit 28%. follow up period (7-53 months). complete relief of all symptoms was reported in all cases with no mortality. one of our patients needs postoperative ventriculoperitoneal shunt for persistent csf leakage and another one required subdural peritoneal shunt for persistent subdural csf collection. conclusion. total excision of choroid plexus papilloma is usually the rule with an excellent outcome. routine external ventricular drainage for at least 3 days is effective in lowering shunt-dependent cases as it allows the release of bloody csf and small tumour residue. with proper microsurgical technique through superior parietal lobule to access lateral ventricle then tumour coagulation at the same time of irrigation that helps the tumour to shrink and thus, decrease the incidence of bleeding. the tumour vascular pedicle should be resected with the last part of the tumour to avoid pedicle retraction that may lead to ventricular haemorrhage. introduction choroid plexus papilloma (cpps) are benign neoplasms of the choroid plexus, a structure made from tufts of villi within the ventricular system that produces cerebrospinal fluid (csf) [13, 24]. lateral ventricle of the brain is the commonest site of cpps in paediatrics, but they can occur in adults too. although the major percent of these tumours are considered benign in nature, a small percent is classified to be malignant [1, 3]. cpps represent about 1% of intracranial neoplasms but this percentage tends to be higher in children (2-4%). the most common keywords choroid plexus papilloma, surgical resection, complications corresponding author: hatem badr mansoura university, egypt hatembadr1@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 145 experience of choroid plexus papilloma in children at mansoura university hospital location is the atrium of the lateral ventricle in paediatric population while 4th ventricle represents the commonest location in adults. cerebellopontine angle (cpa), 3rd ventricle, and parenchyma of the cerebrum are considered rare locations of these tumours [20]. clinically infants and children with cpp presented with; headache, vomiting, progressive head enlargement and excessive crying, as reported by the patients mothers, usually caused by hydrocephalus that results from; csf pathway obstruction, csf overproduction, or arachnoidal fibrosis due to recurrent occult bleeding from tumour [8]. computed tomography (ct) and magnetic resonance imaging (mri) show isoor hyperdense, t1 isointense, and t2 hyperintense masses inside the ventricles that enhance with contrast, generally associated with hydrocephalus [17]. grossly, these tumours arise as wellcircumscribed cauliflower-like exophytic growths from the ventricular wall. histologically, choroid plexus papilloma appears as papillary proliferation with a fibrovascular core lined by a single layer of monotonous cuboidal to columnar epithelium with a basement membrane [5]. gross total excision is considered the main line of treatment of these tumours as it is associated with excellent outcomes after surgery. moreover, adjuvant radiotherapy can be used for progressing tumours that were treated by subtotal resection. a meta-analysis of 566 choroid plexus tumours found no difference in survival when comparing patients with recurrent cpps and those with stable disease [10]. choroid plexus tumours can be distinguished from each other via mouth intestinal bacteria (mib1) labelling, status of p53, and histology into cpp, atypical papilloma, and carcinoma, and this differentiation can direct follow-up and adjuvant treatment plans later on [22]. in management of choroid plexus papilloma, there are two main problems: treatment of associated hydrocephalus, rich tumour vascular supply that is medially located in these young patients, can lead to a hazardous intraoperative blood loss. preoperative embolization, to minimize risk of intraoperative loss, is associated with exposure to radiation and also to vessel injury and stroke [21]. we present our experience in management of such lesions in the neurosurgical department located at mansoura university hospitals. figure 1. a 2-year-old female child with left lateral ventricle choroid plexus papilloma. a: preoperative mri brain with contrast; b: 3-month follow up mri brain with subdural csf effusion and total tumour excision. figure 2. a 6-year-old female child with right lateral ventricle choroid papilloma. a: preoperative mri brain with contrast, b: 1-month follow up ct brain with contrast showing total tumour excision. 146 hatem badr, ahmad zaher, mohamed state et al. figure 3. right lateral ventricle choroid papilloma which was managed by microsurgical resection. a: preoperative mri brain, b: 3-month follow up mri brain showing no residual or tumour recurrence. methods retrospective analysis of children with choroid plexus papilloma who were treated by microsurgical resection over 4 years from january 2012 to january 2016 in mansoura university hospitals. each patient was subjected to complete medical history taking, through physical examination, routine pre-operative laboratory tests, and radiological studies (ct and mri brain). the tumour size was calculated as the maximum diameter of the lesion measured by ct and mri. all research activities were approved by mansoura university local ethical committee. post-operative complications were classified into two categories; major or minor. denovo permanent neurological deficits and functional status worsening were classified as major complications. minor complications included temporary post-operative problems that faded with time like transient cranial neuropathy, temporary postoperative seizures, deep venous thrombosis (dvt), or wound healing problems such as infection, cerebrospinal fluid (csf) leak, and pseudo meningocele. the collected data were coded, processed and analysed using the spss (statistical package for social sciences) version 22 for windows® (spss inc, chicago, il, usa). qualitative data was presented as number (frequency) and percent. quantitative data was expressed as median (range). results table 1: demographic, clinical, operative, and follow up data. variable range or number age (month) 39 (7 – 96) sex male female 10 (43.47%) 13 (56.52%) variable range or number symptoms -headache -vomiting -progressive head enlargement -excessive crying 13 (56.52%) 8 (34.78%) 9 (39.13%) 6 (26.08%) tumour size (cm) 3.1 (2.4 – 4.2) calcification 3 (13.04%) major complications 0 (0%) mortality 0 (0%) minor complications -csf leakage -persistent subdural effusion 2 (8.69%) 1 (4.34%) 1 (4.34%) follow up (month) 20 (7-53) need for shunt 2 (8.69%) residual in follow up ct 0 (0%) twenty-three paediatrics were treated via microsurgical resection over 7 years. age ranged from (7 months 8 years). there were 13 females (56.52%) and 10 males (43.47%). features of increased intracranial pressure were present in all our cases with varying combination like headache, vomiting, excessive crying, and progressive head enlargement. all cases were evaluated preoperatively via ct and mri brain. lateral ventricle of the brain was the site of the ccp in all our paediatric cases. the ct scans showed a mass that was lobulated, globular, and brightly enhancing in the lateral ventricle. median tumour diameter measured by ct or mri was 3.1 cm. calcification was diagnosed radiologically in 3 cases (13.04%), whereas all the cases had varying degrees of hydrocephalus. in all patients, mri showed an enhancing mass in the lateral ventricle that was isointense on t1and hyperintense on t2-weighted images. total microsurgical excision was performed via the transcortical approach through the superior parietal lobule in the all patients who had the tumour located the lateral ventricle trigone. the tumour was identified and then, its surface was coagulated. moreover, it was excised after shrinking its size via combined coagulation and irrigation. coagulation, then division of the vascular tumour pedicle was achieved on removal of the last tumour part. routine closed ventricular drainage was applied in all patients to allow csf drainage for three days post-operatively. that ventricular drain was removed after exclusion of ventricular hematoma by ct scan and absence of red colour in the draining csf fluid. in one case (4.34%), csf leakage from the operative 147 experience of choroid plexus papilloma in children at mansoura university hospital incision occurred and that child needed ventriculoperitoneal shunt for persisting hydrocephalus. another patient (4.34%) needed subduro-peritoneal shunt because of persistent, subdural effusion. the follow-up ranged from 7–53 months (median: 20 months). all patients experienced no symptoms at follow-up as well as the post-operative ct and mri showed no residual lesions. discussion choroid plexus papilloma are considered as who grade i tumours and are among the most common tumours in the paediatric group less than 2 years. they are of neuroectodermal origin representing 13% of central nervous system (cns) tumours in paediatric patients [23]. choroid plexus papilloma has been reported to be associated with aicardi syndrome [4, 25, 28] and li-fraumeni syndrome [6]. leptomeningeal dissemination may occur [7]. usually, cpps occur in the lateral ventricles in paediatric population, while the 4th ventricle is the commonest location in adults; other rare sites included 3rd ventricle and the cerebellopontine angle (cpa). cpps have also been reported in other regions like the suprasellar area, frontal lobe, and cerebellum [17]. in our study, all tumours were located in the lateral ventricle (23 cases). in children, before closure of the sutures and fontanelles, the sequel of raised intracranial pressure such as blindness will be difficult to manifest. seizures or mental changes may be the only presentations of these lesions while tumours involving the 4th ventricle may manifest itself with cerebellar signs. cerebellopontine angle cpps have been reported to cause cranial nerve deficits [8]. the predominant clinical features in our study can all be traced back to raised intracranial pressure that as consistent in all of our patients. clinical picture of cpp in paediatrics includes; headache, vomiting, progressive head enlargement and excessive crying. these are usually caused by hydrocephalus that results from csf pathway obstruction, excessive csf production, and recurrent occult bleeding from the tumour that results in arachnoidal fibrosis and adhesions [8]. in our study, headache was present in 56.52 % of cases while vomiting was experienced in 34.78 % of cases. moreover, progressive head enlargement and excessive crying were reported by the mothers of in 39.13 and 26.08% of our cases respectively. the mean value of maximum tumour diameter in our study was 3.1 cm, while the study conducted by safaee and his colleagues included cases with median diameter of 3 cm in the total resection group [21]. calcification was detected in ct in 13.04% (3 cases) in our study cases. this is consistent with the findings reported in the literature stating that choroid plexus tumours calcification can be detected radiologically in around 4–20% of cases [9, 19]. surgical gross total excision of the tumour should be attempted in all cases of choroid plexus papilloma [2]. as these tumours are highly vascular, great care should be taken during surgery to avoid excessive blood loss that may lead to mortality, as reported in some series, especially in young children. securing the main arterial supply of the tumour, which is usually a branch of choroidal artery, is of crucial importance to avoid hazardous intraoperative bleeding followed by coagulation of the tumour and en bloc or piecemeal removal [15]. regarding surgical excision for paediatric cpps, there is a surgical opinion stating that there is some sort of benefit from delaying surgery till hydrocephalus develops. that is because this delay lessens the length of the corridor to the ventricles and widens the space surrounding the lesion making it more surgically accessible. the drawback to this delay is that hydrocephalus may not be the presenting symptom, leading to more tumour growing that may lead to neurological deficit that may not resolve after surgical resection [11, 16]. in addition, the drawbacks to a watchful waiting on dealing with such tumours are many. initially, repeated general anaesthesia will be needed for mri for follow up which will be burdensome and not devoid of risks. moreover, although ct scan may alleviate the need for mri< but excess radiation exposure will carry risk to the child as well [11]. we reported that blood loss in this study was less than 100 ml in every patient. no major complications or mortality were reported in our study. major complications reported in another series were rare, that may be attributed to the fact that these modern studies were conducted at a tertiary care centres [21]. compared to published series from the modern microsurgical era, our observed morbidity was very minimal, once again confirming that these tutors can 148 hatem badr, ahmad zaher, mohamed state et al. be safely resected in both children and adults [14, 27, 29]. whereas complete surgical excision is the ideal treatment, it could be impossible to accomplish in some cases, due to excessive blood loss or due to tumour infiltration into the surrounding vital structures. if significant residual tumour is left or recurrence is diagnosed, redo-surgery may be an option after sometime. moreover, adjuvant therapy has been reported to be another option [18]. pneumocephalus, pneumoventricle, subdural effusions, persistence of hydrocephalus (in those not previously shunted), and new onset hydrocephalus are the most common reported complications after surgical intervention [21, 26]. total surgical removal of these tumours is associated with excellent survival that reaches 100% at 10-year follow up as reported in the literature [14]. in our series, only two cases required postoperative shunts; one needed ventriculoperitoneal shunt due to persistent csf leakage, and the other needed subduroperitoneal shunt for persistent subdural csf collection. although some studies have described neurocognitive sequelae related to surgery for cpp [12, 16], our study is not large enough to make any significant conclusions with respect to differential outcomes in children compared to adults. safaee and his associates also reported a 22 % incidence of temporary swallowing dysfunction that required percutaneous endoscopic gastrostomy tubes, tracheostomy, or both, with no difference in the incidence when comparing patients who received gross total resection with the subtotal resection group [21]. the prognosis for cpp patients treated with gross total resection (gtr) is excellent, with a report of 100% survival at 5 years after surgical resection in many series including ours, and adjuvant therapy is not indicated in these patients. radiotherapy is not necessary after gtr, and its usefulness should be reserved for recurrent disease. unfortunately, the prognosis for patients with choroid plexus carcinoma cpc is guarded, with an overall 5-year survival rate of 26-50%. gtr is generally considered the most important prognostic factor for cpc as was confirmed in our analysis [14]. several limitations can be noted in this current study. small sample size limits the statistical power of our analysis, but is an unfortunate and inevitable consequence of studying such a rare tumour. moreover, this study is a single centre study that could affect the validity of our results as it serves a localized population. conclusion total excision of choroid plexus papilloma is usually the rule with excellent outcome. routine external ventricular drainage for at least 3 days is effective in lowering shunt dependent cases as it allows release of bloody csf and small tumour residue. with proper microsurgical technique through superior parietal lobule to access lateral ventricle then tumour coagulation at the same time of irrigation that helps the tumour to shrink and thus, decrease the incidence of bleeding. the tumour vascular pedicle should be resected with last part of the tumour to avoid pedicle retraction that may lead to ventricular haemorrhage. authors contributions this work was carried out in collaboration between all authors. author amr farid, designed the study, author mohamed state wrote the protocol, author ahmed zaher managed the literature research, author hatem badr performed the statistical analysis and revised the final manuscript. all surgical procedures were carried out by the same surgical team including the four authors. all authors read and approved the final manuscript. abbreviations cpc choroid plexus carcinoma. cpp choroid plexus papilloma. cpa cerebellopontine angle. gtr gross total resection. mib-1 mouse intestinal bacteria. mri magnetic resonance imaging. references 1. abdulkader m m, mansour n h, van gompel j j, bosh g a, dropcho e j, bonnin j m, and cohen-gadol a a: disseminated choroid plexus papillomas in adults: a case series and review of the literature. journal of clinical neuroscience 2016, 32, 148-154. 2. bettegowda c, adogwa o, mehta v, chaichana k l, weingart j, carson b s, jallo g i, and ahn e s: treatment of choroid plexus tumors: a 20-year single institutional experience. journal of neurosurgery: pediatrics 2012, 10(5), 398-405. 3. dudley r w, torok m r, gallegos d, liu a k, handler m h, and hankinson t c: pediatric choroid plexus tumors: epidemiology, treatments, and outcome analysis on 202 149 experience of choroid plexus papilloma in children at mansoura university hospital children from the seer database. journal of neurooncology 2015, 121(1), 201-207. 4. frye r e, polling j s, and ma l c: choroid plexus papilloma expansion over 7 years in aicardi syndrome. journal of child neurology 2007, 22(4), 484-487. 5. fung k-m, yu z, and petropoulou k; tumors of the central nervous system, in pediatric malignancies: pathology and imaging. 2015, springer. p. 151-201. 6. gozali a e, britt b, shane l, gonzalez i, gilles f, mccomb j g, krieger m d, lavey r s, shlien a, and villablanca j g: choroid plexus tumors; management, outcome, and association with the li–fraumeni syndrome: the children's hospital los angeles (chla) experience, 1991–2010. pediatric blood & cancer 2012, 58(6), 905-909. 7. irsutti m, thorn-kany m, arrue p, richaud j, sol j, delisle m, and manelfe c: suprasellar seeding of a benign choroid plexus papilloma of the fourth ventricle with local recurrence. neuroradiology 2000, 42(9), 657-661. 8. jaiswal a k, jaiswal s, sahu r n, das k, jain v k, and behari s: choroid plexus papilloma in children: diagnostic and surgical considerations. journal of pediatric neurosciences 2009, 4(1), 10. 9. koeller k k and sandberg g d: from the archives of the afip: cerebral intraventricular neoplasms: radiologicpathologic correlation. radiographics 2002, 22(6), 14731505. 10. krishnan s, brown p d, scheithauer b w, ebersold m j, hammack j e, and buckner j c: choroid plexus papillomas: a single institutional experience. journal of neuro-oncology 2004, 68(1), 49-55. 11. laarakker a s, nakhla j, kobets a, and abbott r: incidental choroid plexus papilloma in a child: a difficult decision. surgical neurology international 2017, 8. 12. levy m l, goldfarb a, hyder d j, gonzales-gomez i, nelson m, gilles f h, and mccomb j g: choroid plexus tumors in children: significance of stromal invasion. neurosurgery 2001, 48(2), 303-309. 13. lun m p, monuki e s, and lehtinen m k: development and functions of the choroid plexus–cerebrospinal fluid system. nature reviews neuroscience 2015, 16(8), 445. 14. menon g, nair s n, baldawa s s, rao r b, krishnakumar k, and gopalakrishnan c: choroid plexus tumors: an institutional series of 25 patients. neurology india 2010, 58(3), 429. 15. mishra a, ojha b, chandra a, singh s, chandra n, and srivastava c: choroid plexus papilloma of posterior third ventricle: a case report and review of literature. asian journal of neurosurgery 2014, 9(4), 238. 16. nagib m g and o’fallon m t: lateral ventricle choroid plexus papilloma in childhood: management and complications. surgical neurology 2000, 54(5), 366-372. 17. ogiwara h, dipatri jr a j, alden t d, bowman r m, and tomita t: choroid plexus tumors in pediatric patients. british journal of neurosurgery 2012, 26(1), 32-37. 18. pawar s, sharma r, mahapatra a, lad s, and musa m: choroid plexus papilloma of the posterior third ventricle during infancy & childhood: report of two cases with management morbidities. neurology india 2003, 51(3), 379. 19. pencalet p, sainte-rose c, lellouch-tubiana a, kalifa c, brunelle f, sgouros s, meyer p, cinalli g, zerah m, and pierre-kahn a: papillomas and carcinomas of the choroid plexus in children. journal of neurosurgery 1998, 88(3), 521-528. 20. prasad g l and mahapatra a k: case series of choroid plexus papilloma in children at uncommon locations and review of the literature. surgical neurology international 2015, 6. 21. safaee m, clark a j, bloch o, oh m c, singh a, auguste k i, gupta n, mcdermott m w, aghi m k, and berger m s: surgical outcomes in choroid plexus papillomas: an institutional experience. journal of neuro-oncology 2013, 113(1), 117-125. 22. safaee m, oh m c, bloch o, sun m z, kaur g, auguste k i, tihan t, and parsa a t: choroid plexus papillomas: advances in molecular biology and understanding of tumorigenesis. neuro-oncology 2012, 15(3), 255-267. 23. sethi d, arora r, garg k, and tanwar p: choroid plexus papilloma. asian journal of neurosurgery 2017, 12(1), 139. 24. spector r, keep r f, snodgrass s r, smith q r, and johanson c e: a balanced view of choroid plexus structure and function: focus on adult humans. experimental neurology 2015, 267, 78-86. 25. taggard d a and menezes a h: three choroid plexus papillomas in a patient with aicardi syndrome. pediatric neurosurgery 2000, 33(4), 219-223. 26. talacchi a, de micheli e, lombardo c, turazzi s, and bricolo a: choroid plexus papilloma of the cerebellopontine angle: a twelve patient series. surgical neurology 1999, 51(6), 621629. 27. tena-suck m l, salinas-lara c, rembao-bojórquez d, and castillejos m: clinicopathologic and immunohistochemical study of choroid plexus tumors: single-institution experience in mexican population. journal of neurooncology 2010, 98(3), 357-365. 28. trifiletti r r, incorpora g, polizzi a, cocuzza m d, bolan e a, and parano e: aicardi syndrome with multiple tumors: a case report with literature review. brain and development 1995, 17(4), 283-285. 29. wolff j, sajedi m, brant r, coppes m, and egeler r: choroid plexus tumours. british journal of cancer 2002, 87(10), 1086. doi: 10.33962/roneuro-2022-050 efficacy of neuronavigation guided biopsy in deep seated brain lesions anuj chhabra, deepak kumar singla, deepak kumar singh, surender kumar gupta, mohd kaif, kuldeep yadav, farhan ahmad romanian neurosurgery (2022) xxxvi (3): pp. 296-301 doi: 10.33962/roneuro-2022-050 www.journals.lapub.co.uk/index.php/roneurosurgery efficacy of neuronavigation guided biopsy in deep seated brain lesions anuj chhabra1, deepak kumar singla2, deepak kumar singh3, surender kumar gupta4, mohd kaif5, kuldeep yadav5, farhan ahmad6 1 mbbs, ms, mch (neurosurgery). assistant professor, dept. of neurosurgery, kcgmc, karnal, india 2 mbbs, ms (general surgery). associate professor, dept. of general surgery, kcgmc, karnal, india 3 mbbs, ms,mch (neurosurgery). professor and head, dept. of neurosurgery, dr ram manohar lohia institute of medical sciences, lucknow, india 4 mbbs, ms, mch (neurosurgery). associate professor, dept. of neurosurgery, aiims, raipur, india 5 mbbs, ms, mch (neurosurgery). associate professor, dept. of neurosurgery, dr ram manohar lohia institute of medical sciences, lucknow, india 6 mbbs, ms, mch (neurosurgery). senior resident, dept. of neurosurgery, dr ram manohar lohia institute of medical sciences, lucknow, india abstract localisation of brain lesions and prevention of damage to vital structures are important goals in the operation of brain pathologies, which can be aimed after the development of many techniques (e.g. angiography, mri, sonography, frame base stereotaxy). in spite of current developments in radiological imaging techniques, accurate histological diagnosis is required to determine the appropriate treatment methods for intracranial lesions. the study was conducted in the department of neurosurgery, dr ram manohar lohia institute of medical sciences, over a period of 18 months. descriptive statistics (frequencies and percentages) were used to interpret the collected data. after editing, data was entered into spss free versions for statistical studies. the results from various sites of the biopsy were compared based on sensitivity, specificity, positive and negative predictive values. in this study, 4 patients were found to be below 20 years, 7 patients in the 20 – 40 years age group, 10 patients in the age group of 40 to 60 years and 4 patients were above sixty years. 22 (88%) patients were found to have positive yield when the biopsy was taken from the core area while 3 (12%) patients were not having any positive results from the biopsy. sensitivity, specificity, positive predictive value, and negative predictive value of various sites of the biopsy were calculated sensitivity of the periphery came out to be 68.2 % while specificity was 67.7%. the positive predictive value of the periphery was found to be 93.8 % while the negative predictive value was keywords neuronavigation, stereotactic surgery corresponding author: deepak kumar singla associate professor. dept. of general surgery. kcgmc, karnal, india drdeepak112@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published july 2022 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 297 efficacy of neuronavigation guided biopsy in deep seated brain 22.2%. the sensitivity of the contrast-enhanced area came out to be 72.7 %, with specificity being 67.7%. the positive predictive value of periphery in such cases was found to be 94.1 % and the negative predictive value was 25%. the most common system-related complication was the inability to show choline peak properly, which was present in 7 patients. hence, it can be concluded safely that the use of neuronavigation is beginning to have a vital role in a variety of intracranial procedures with precise localisation of both intracranial as well as spinal lesions and prevention of damage to vital structures intraoperatively thereby significantly reducing procedure-related morbidity and mortality. introduction recently, there has been an increasing trend in most branches of surgery towards a reduction in the morbidity of a procedure by limiting surgical entry. this usually involves the application of technology such as laparoscopic cholecystectomy in general surgery1. a new era of neurosurgery has recently been unveiled with advent of image guided surgery.. nowadays, a lot of of patients suffering from neurological focal deficiency or symptoms of increasing intracranial pressure or even for patients with slighter symptoms are being correctly diagnosed due to advent of technique such as computed tomography (ct) scan and magnetic resonance imaging (mri) ,2,3,. furthermore, advances in the therapeutic methods and increasing number of survival in patients with systematic diseases, resulted in the development of metastasis into the central nervous system or high incidence of cns infections, which are partly due to high confrontation with immune system deficiency (due to acquired immunodeficiency syndrome (aids) or following immunosuppressive treatment in the recipients of transplantation or in patients under chemotherapy for systematic cancer); diversity and the number of cns neuro-pathologies has increased requiring the needs for the more accurate detailed differential diagnosis of histology and cytology of cerebral spaceoccupying lesions (sols)4,5. in most of the patients, it is possible to diagnose the brain lesions accurately through clinical and laboratory findings. examples are multiple sclerosis, secondary infectious and parasite diseases, metastatic tumors and brain involvement of systemic disease. but ,numerous brain lesions that are diagnosed in ct scan or mri are the only provable documents for the disease and their treatment designing depends on the histological diagnosis6,7 materials and method the study was conducted in department of neurosurgery, dr. ram manohar lohia institute of medical sciences, over a period of 18 months.total of 25 patients admitted in neurosurgical wards underwent thorough examination and investigation. the inclusion and exclusion criteria used for study are as follows: inclusion criteria ➢ deep seated lesions situated in basal ganglia, internal capsule, corpus callosum, periventricular areas, brain stem ➢ lesions located in eloquent areas. ➢ lesions refractory to an empirical therapy given previously. ➢ diagnosis could not be ascertained by radiology (e.g., multiple lesions) exclusion criteria ➢ large lesions in non-eloquent and easily accessible areas amenable to surgical excision. ➢ lesions producing mass effect and neurological deterioration ➢ lesions near the surface of brain contrast enhanced ct scans/ mri of the patients was taken in neuronavigation protocol one day prior to surgery. histological examination was performed in the department of pathology. radiological support was provided by department of radio diagnosis at institute. ct and mri were done according to feasibility based on location of tumor, status of stent or metallic stents. the data was stored in cd. dvd in dicom format and transferred to workstation for planning. descriptive statistics (frequencies and percentages) were used to interpret the collected data.. after editing, data were entered into spss free versions for statistical studies and analysis of the data was done by comparing all the details in the form of tables, texts and charts. finally,the results from various sites of biopsy were compared on basis of sensitivity, specificity ,positive and negative predictive value. results and observations table 1. sex ratio of patients sex number of patients male 15 298 anuj chhabra, deepak kumar singla, deepak kumar singh et al. female 10 total 25 table 1 shows the distribution of patients according to gender between. 10 patients were found females and 15 patients were found male. table 2. age distribution of patients sn age distribution number 1 0-20 4 2 20-40 7 3 40-60 10 4 60 and above 4 table 2 showing that 4 patients were below 20 years. 7 patients were found in 20 – 40 years age group, 10 patients were found in the age group of 40 to 60 years and 4 patients were above sixty years. table 3. histological diagnosis sn histology number 1 gbm 6 2 grade 3 astrocytoma 4 3 low grade glioma 3 4 tbm 4 5 abscess 2 6 nhl 2 7 demyelinating disease 1 8 negative 3 table 4. histological diagnosis from various sites of biopsy table 4a. 22 (88%) patients having positive yield when biopsy was taken from core area 3 (12%) patients were not having any positive result of biopsy. out of this 22 patients 13 (52%) were diagnosed to be glioma, 2 (8%) were having abscess, 2 (8%) were diagnosed as nhl, 4 (16%) were heaving tb and 1 (4%) patient was diagnosed as demyelinating disease. table 4b. 16 (64%) patients having positive yield when biopsy was taken from periphery area 9 (36%) patients were not having any positive result of biopsy. out of these 16 patients 9 (36%) were diagnosed to be glioma, 3 (12%) were having abscess, 2 (8%) were diagnosed as nhl and 2 (8%) were having tb. table 4c. 17 (68%) patients having positive yield when biopsy was taken from periphery area 8 (32%) patients were not having any positive result of biopsy. out of these 17 patients 11 (44%) were diagnosed to be glioma, 2 (8%) were having abscess, 2 (8%) were diagnosed as nhl and 2 (8%) were having tb. table 4d. due to registration error and inability to get mri in few patients, only 12 (48%) patients underwent biopsy from choline peak voxals. while in 13 patients study was not possible. out of these 12 patients in 3 (12%) biopsy results came out as glioma, while in 9 (36%) patients having no positive yield. table 5. sensitivity, specificity, positive predictive value, negative predictive value of various sites of biopsy table 5a. sensitivity of periphery came out to be 68.2 % while specificity was 67.7% and positive predictive value was 93.8 % and negative predictive value of periphery was 22.2%. positive negative positive 15 1 negative 7 2 299 efficacy of neuronavigation guided biopsy in deep seated brain table 5b. sensitivity of contrast enhanced area came out to be 72.7 % while specificity was 67.7% and positive predictive value was 94.1 % and negative predictive value of periphery was 25%. positive negative positive 16 1 negative 6 2 table 6. patient related complication sn complication number 1 unintentional ventricular puncture 1 2 intraoperative haemorrhage 0 3 post operative neurological deficit 0 4 post operative seizures 0 5 surgical site infection 0 during this study only one patient had unintentional ventricular rapture while no other complication such as post operative neurological deficit, seizures, intraoperative haemorrhage or surgical site infection was noted. all biopsy were taken in single attempt. table 7. system related complication sn complication number 1 registration error 3 2 system shut down 0 3 inability to show contrast film properly 0 4 inability to show choline peak are properly 7 during this study the most common system related complication was inability to show choline peak properly, which was present in 7 patients while registration error was the second most common system related complication present in 3 patients. discussion image guided neurosurgery (neuro-navigation) or frameless stereotactic surgery has made a tremendous impact in the recent years. it gives a patient specific three-dimensional (3-d) anatomy for preoperative planning and intra-operative navigation thus helping the surgeon to perform complicated procedures with improved accuracy and safety8 stereotactic biopsy for intracranial lesions is a realistic relatively safe procedure and is also a very efficient method especially in patient who need histological confirmation for the treatment. the overall diagnostic accuracy varies from 80-99%9 in this study, out of 25 cases 22 biopsy (88%) came out to be positive and 3 cases (12%) came out to be negative which was comparable to previous studies showing positive yield of 89% and negative yield of 11%10 in deep seated lesions. in one more study a diagnostic yield of 86.16%11was found which was comparable to present study and in two other studies on frameless navigation guided biopsy, positive yield of 99%12,13 was found. there was a study based on frame-based navigation guided biopsy which was showing positive yield of 84.21%, which was comparable to present study with positive yield of 88%14. in previous studies, discrepansy was noted in results of biopsy taken from central hypodense and well contrast enhanced area .so we took biopsy from various sites to look for efficacy from different areas, biopsy from core revealed 22(88%) positive results while 3(12%) were negative.in positive 22 cases, 6 cases of gbm, 4 cases of grade 3 anaplastic or grade 3 giomas, 3 cases of low grade gliomas, 4 cases of tbm,2 cases of nhl, 2 cases of abscess and 1 case of demyeliting disease while 3 having negative biopsy.biopsy taken from periphery sites having 16 (64%) positive results while (36%) were negative in positive results 9 cases were glioma, 3 were abscess, 2 were nhl and 2 were t.b. in contrast enhanced area 17 cases (68%) were positive while 8(32%) were negative, in which 11(44%) were glioma, 2(8%) were nhl ,2 were abscess and 2 (8%) were tb.in mr marked (voxols) there were only 12 cases out of which 3 (25%) were positive and 9(75%) were negative and these are all gliomas. in our study 22 (88%) patients were having positive yield which was taken from core region while on comparing periphery region biopsy from core region biopsy, periphery was having 16(68%) yield with sensitivity of 68.2% specificity of 67.7% positive and negative predictive value of 93.8 and 22.2% in comparision to core while contrast enhanced area having a positive yield of 17(72.5%) with sensitivity of 72.7% specificity of 67.7% positive and negative predictive value of 94.1% and 25% respectively. in comparision to core, only 12 cases underwent biopsy 300 anuj chhabra, deepak kumar singla, deepak kumar singh et al. of mrs with choline peak voxals as few patients were not co-operative so mri was not possible in these cases and also in few patients there was problem in marking choline peak area accurately in neuronavigation system. the complications in this series range from registration error, accurately localizing choline peak area on navigation machine, unintentional ventricular puncture, intra-operative haemorrhage, post operative neurological deficit, post operative seizures, surgical site infection etc. registration error of 2.2 to 6 mm have been reported by roessler et al (1998)15, in our system it provides more accurate localization but a registration error of 1 mm was considered to be acceptable in view of brain shift. in initial cases we also had difficulty in registering choline peak voxals. in our series there was 1(4%) patient associated with unintentional ventricular puncture, 3 patients had problem of registration error and 7 patients had problem of inability to show choline peak area properly. in various other previous studies complication such as symptomatic haemorrhage, morbidity due to neurological deficit, and mortality was observed with rates of 5.1%, 3.7%, 0.6% respectively but in our study, we had no cases of symptomatic haemorrhage, neurological deficit associated morbidity and mortality. study limitations relatively low number of patients and short followup periods are the limitations of our study. conclusion neuronavigation guided biopsy has proved beyond benchmark of technology for various deep seated lesions along with added advantages of safety, cost effectiveness, accuracy, ease of use ,decreaed duration surgery, reduced post surgery complications such as neurological deficit, intracerebral haemorrhage and reduced hospital stay. references 1. apuzzo ml, chandrasoma pt, cohen d, zee cs, zelman v (1987): computed imaging stereotaxy: experience and perspective related to 500 procedures applied to brain masses. neurosurgery 20:930-937. 2. aylin okcu heper, mda,t, esra erden, mda, ali savas, md, phdb, koray ceyhan, mda, ilhan erden, mdc, serdar akyar, mdc, yqcel kanpolat, mdb. an analysis of stereotactic biopsy of brain tumors and nonneoplasticlesions: a prospective clinicopathologic study. a.o. heper et al. / surgical neurology 64 (2005) s2:82– s2:88 3. bilgisayarl› tomografi eflli.inde yap›lan stereotaktik beyin biyopsilerinde histopatolojik tan› verim ve do.rulu.u. turkish neurosurgery 2008, vol: 18, no: 1, 1722. 4. boethius j, et al 1978 collins vp, edner g, lewander r, zajicek j (1978): stereotactic biopsies and computer tomography in gliomas. acta neurochir (wien) 40:223232 5. borbély k. functional imaging in brain tumors. orv hetil. 2004;145:411–23. 6. dammers r, haitsma ik, schouten jw, kros jm, avezaat cj, vincent aj. safety and efficacy of frameless and framebased intracranial biopsy techniques. acta neurochir (wien) 2008;150:23–9. 7. david shooman, m.b.ch.b.,1 antonio belli, m.d.,2 and paul l. grundy, b.m. (hons), m.d.1 image-guided frameless stereotactic biopsy without intraoperative neuropathological examination, j neurosurg 113:170– 178, 2010 8. hu ls, baxter lc, smith ka, feuerstein bg, karis jp, eschbacher jm, et al. relative cerebral blood volume values to differentiate high-grade glioma recurrence from posttreatment radiation effect: direct correlation between image-guided tissue histopathology and localized dynamic susceptibility-weighted contrastenhanced perfusion mr imaging measurements. ajnr am j neuroradiol. 2009;30:552–8 9. jain d, sharma mc, sarkar c, deb p, gupta d, mahapatra ak. correlation of diagnostic yield of stereotactic brain biopsy with number of biopsy bits and site of the lesion. brain tumor pathol. 2006;23:71–5. 10. jain d1, sharma mc, sarkar c, gupta d, singh m, mahapatra ak. comparative analysis of diagnostic accuracy of different brain biopsy procedures. neurol india. 2006 dec;54(4):394-8. 11. jawahar a, weilbaecher c, shorter c, stout n, nanda a. multicentric glioblastoma multiforme determined by positron emission tomography: a case report. clin neurol neurosurg. 2003;106:38–40. 12. laurent j. livermore , ruichong ma , stana bojanic & erlick a. c. pereira, yield and complications of framebased and frameless stereotactic brain biopsy – the value of intra-operative histological analysis british journal of neurosurgery, october 2014; 28(5): 637–644 © 2014 the neurosurgical foundation issn: 0268-8697 print / issn 1360-046x online doi: 10.3109/02688697.2014.887657 13. lucchinetti cf, popescu bf, bunyan rf, moll nm, roemer sf, lassmann h, et al. inflammatory cortical demyelination in early multiple sclerosis. n engl j med. 2011;365:2188–97. 14. mercier l, del maestro rf, petrecca k, et al. new prototype neuronavigation system based on 301 efficacy of neuronavigation guided biopsy in deep seated brain preoperative imaging and intraoperative freehand ultrasound: system description and validation. int j comput assist radiol surg. 2011; 6(4):507–522. [pubmed: 20886304] 15. orringer da, golby a, jolesz f. neuronavigation in the surgical management of brain tumors: current and future trends. expert rev med devices. 2012 sep;9(5):491-500. 16. quinn j, spiro d, schulder m. stereotactic brain biopsy with a low-field intraoperative magnetic resonance imager. neurosurgery. 2011; 68(1 suppl operative):217– 224. discussion 224. [pubmed: 21206306] 17. risholm p, golby aj, wells w 3rd. multimodal image registration for preoperative planning and image-guided neurosurgical procedures. neurosurg clin n am. 2011; 22(2):197–206. viii. [pubmed: 21435571] 18. roessler k, czech t, dietrich w, ungersboeck k, nasel c, hainfellner ja koos wt (1998) frameless stereotacticdirected tissue sampling during surgery of suspected lowgrade gliomas to avoid histological undergrading. minim invasive neurosurg 41:183-186 19. shooman d, belli a, grundy pl. image-guided frameless stereotactic biopsy without intraoperative neuropathological examination. j neurosurg. 2010; 113(2):170–178. [pubmed:20136389] 20. von campe g, moschopulos m, hefti m. 5-aminolevulinic acid-induced protoporphyrin ix fluorescence as immediate intraoperative indicator to improve the safety of malignant or high-grade brain tumor diagnosis in frameless stereotactic biopsies. acta neurochir (wien) 2012;154:585–8. doi: 10.33962/roneuro-2020-072 optic nerve sheath fenestration (onsf). indications, techniques and results forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi, gurudas mondal, mainul haque sarker, quazi deen mohammod romanian neurosurgery (2020) xxxiv (1): pp. 444-451 doi: 10.33962/roneuro-2020-072 www.journals.lapub.co.uk/index.php/roneurosurgery optic nerve sheath fenestration (onsf). indications, techniques and results forhad h chowdhury1, mohammod raziul haque2, jalal uddin mohammod rumi1, gurudas mondal1, mainul haque sarker2, quazi deen mohammod1 1 neurosurgery, national institute of neurosciences and hospital, shere-e-bangla nagar, dhaka, bangladesh 2 neurosurgery, dhaka medical college and hospital, dhaka, bangladesh abstract objectives. optic nerve sheath fenestration (onsf) is commonly used in idiopathic intracranial hypertension (iih). here we will present our experiences of onsf in 26 patients with special attention to indications, surgical techniques and results methods. the recorded data of patient management (with the result) who underwent onsf were reviewed and studied retrospectively. results. the total number of patients who underwent onsf was 26. the male-female ratio was 1:12. indications of onsf were: 1. idiopathic intracranial hypertension (iih)-23 cases; 2. cerebral venous sinus thrombosis (cvst)-02 cases; 3. cns tuberculosis-01case. all patient underwent bilateral onsf with post-operative continues lumbar csf drain for 04 days. after fenestration gush of csf came out with force in all-first operated eyes whereas 13-second operated eyes showed very little csf flow after fenestration. vision improved in different grades in all cases at discharge except in three cases. preoperatively, visual acuity was either pl&pr or hand movement in 40 eyes where 04 eyes were preoperatively total blind (no pl&pr). visual acuity improved in 48 eyes (92.3% eyes) where the patient can do his/her daily life activities including self-care. improvement in iih is 100% (23 cases i.e-46 eyes) whereas 01 case out of 02 cases in cvst. though vision was improved dramatically fundal appearances changes very slowly and very less frequently returned to normal appearance. conclusion. due to the delicate and technically demanding nature of the surgery, safety is a major concern of the onsf. our experience showed onsf is a technically safe operation with very good results where indicated. introduction orbit contains eyeball, optic nerve (on), extraocular muscles, fat, lacrimal gland, vessels and nerves (figure 1). actually, the optic nerve is an optical system projection white matter tract of the cns. it is covered by pia mater, arachnoid mater, and dura mater. on has intracranial, foraminal and orbital part. the subarachnoid space (sas) of the cns is continues with sas of optic nerve. so increased intracranial pressure is transmitted to the optic nerve head and causes papilledema.1 keywords optic nerve sheath fenestration, onsf, iih, cvst, tb, visual impairment corresponding author: forhad hossain chowdhury assistant professor, neurosurgery, national institute of neurosciences and hospital, shere-e-bangla nagar, dhaka-1207, bangladesh forhadchowdhury74@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published september 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 445 optic nerve sheath fenestration optic nerve sheath fenestration (onsf) was first used by de wecker in 1872 as an incision in the dura and arachnoid surrounding the optic nerve in order to relieve increased intracranial pressure. 2,3the technique is commonly applied in idiopathic intracranial hypertension (iih) with rapid and/or progressive vision loss.4 but this technique can also be used in other conditions where csf pressure in optic nerve sas is increased locally, compartmentally or generally i.e. cerebral venous sinus thrombosis, cns infection such as tuberculosis. here we will present our experiences of onsf in 26 patients with special attention to indications, surgical techniques and results. figure 1. schematic hand drawing showing the orbital structures including optic nerve after removal of orbital roof. methods from january 2011 to december 2018, the patients who underwent onsf in national institute of neurosciences & hospital and some other private hospital in dhaka, bangladesh were studied. the recorded data of patient management along with follow up were reviewed retrospectively. clinical pictures, investigations, medical and other failed surgical management/s, onsf procedures and follow up (clinical and investigations) were carefully studied and presented as results. post-operative follow ups were done on 1st pod, 3rd pod, at discharge, after one month, at the end of six month and then 01 yearly. if patient failed to attend for follow up then follow up was achieved through voice or videophone call. perimetry and fundal photograph were done six months after operation. total follow up period was ranging from 06 months to 72 months (average 22.4 months) except one patient where patient recovered vision from pl&pr to hand movement at discharge on 7th pod and then she lost from follow up even over telephone. results the total number of patients who underwent onsf was 26. male female ratio was 1:12. age range was 11 years to 38 years (average22.5years). build of patients was average and no one was obese or morbidly obese patient. two patients were pregnant and were in 2nd trimester. in all cases bilateral onsf was done i.e. total number of eyes were 52. no one was taking any drugs, steroid or contraceptive. indications of onsf were: 4. idiopathic intracranial hypertension (iih)-23 cases; 5. cerebral venous sinus thrombosis-02 cases; 6.cns tuberculosis-01case. clinical profile (table 1) all iih patients were diagnosed as iih in neurology department according to iih diagnostic criteria. all underwent mri of brain and eyeball (figure 2) including mrv where all ventricles were normal with normal mrv. figure 2. a&bmri of brain and orbit (t2w axial and sagittal image) showing elongated & curvy on with increased csf spaces and depression on globe by on head (arrows marked) in iih. when there was severe visual deterioration even after having adequate medical management including serial lumbar puncture and/ continues lumbar csf drainage for three days. opening pressure was measured in all cases where csf pressure was above the normal level ranging from 280 to 330 mm of csf (average 295mm). csf study was normal in all cases except three (one with cns tb, 01 cases with iih where csf protein was just above the normal another case with high csf 446 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. without any known cause) preoperative visual status of patient was shown in table 1. no patient underwent lumbo-peritneal (lp) or ventriculo-peritoneal (vp) shunt procedure. preoperatively (just before onsf) no patient had nausea or vomiting and in 08 patients (30%) there was only mild to moderate (not severe) headache. four patient had diplopia but clinical 6th nerve palsy was found in two cases. pre-operatively fundoscopy and fundal photograph was taken in all cases and perimetry was done in cases where vision is not badly impaired. fundal photographic and perimetric findings are shown in table 1. table 1. particulars of patients with pre and postoperative visual acuity and papilledema outcome. age (years), sex & diagnosis pre operative-va post operative last f/u-va pre operative papilledema (frisén scale ) post operative papilledema (after six month) 22,f,iih rt-pl&pr, left -hm 6/18 bilaterally g-4 g-3 31,f iih pl&pr bilaterally hand movement bilaterally (at discharge) g-4 - 11, m, iih pl&pr-bilaterally 6/6 bilaterally g-4 g-2 35, f, iih finger countbilaterally 6/6 bilaterally g-4 g-2 19, f, iih pl&prbilaterally 6/12 bilaterally (only central field of vision recovered) g-5 g-4 27,f, iih pl&prbilaterally 6/6-rt 6/12-lt g-4 g-3 19,f,iih rt-pl&pr lt-finger count rt-6/24 lt-6/12 g-5 g-4 23,f, iih hand movement-bilaterally 6/18 bilaterally g-4 g-4 26,f, iih hand movement-bilaterally 6/6 rt 6/12 lt g-4 g-4 15,f,iih lefttotal blind, rt-pl&pr rt-6/36 lt-6/24 g-5 g-4 22,f,iih pl&pr-bilaterally 6/36bilaterally g-5 g-5 25, f ,iih hand movement-bilaterally 6/6-bilaterally g-4 g-3 16,f, iih pl&pr-bilaterally 6/6-rt 6/12-lt g-4 g-4 26,f,iih hand movement-bilaterally 6/18 -bilaterally g-4 g-3 33,f, cvst) pl&pr-bilaterally rt-6/18 lt-6/24 g-4 g-4 27, f, iih hand movement-bilaterally 6/6-bilaterally g-4 g-3 26, f ,iih rt-hand movement lt-6/24 rt-6/12 lt-6/6 g-4 g-3 14, f, cvst blind(no pl&pr)-bilaterally blind (no improvement) early optic atrophy optic atrophy 30, f, iih rt-6/60 lt-6/36 rt-6/12 lt-6/6 g-4 g-4 38, f,iih hand movement-bilaterally rt-6/12 lt-6/6 g-4 g-4 26,m, iih hand movement –rt lt6/24 rt-6/12 lt-6/6 g-4 g-3 20, f, iih pl&pr -bilaterally total recovery 6/6-bilaterally g-4 g-2 447 optic nerve sheath fenestration 32, f, iih hand movement-bilaterally 6/18 -bilaterally g-5 g-4 14, f, iih rt-6/18 lt-pl&pr rt-6/6 lt-6/12 g-4 g-3 26, f, iih hand movement-bilaterally 6/6-bilaterally g-4 g-3 30, f, tb, rt eye vision loss (no pl/pr) lt-pl&pr rt-no improvement lt-pl&pr lost (blind) early optic atrophy optic atrophy operation (onsf) all patient underwent bilateral onsf with postoperative continues lumbar csf drain for 04 days. surgical techniques (figure 3 and figure 4) under general anaesthesia with endotracheal intubation patient was positioned in supine position. eyelid and periorbital skin was painted carefully (with protection of cornea and conjunctiva) by diluted povidone iodine solution. then eyelids, corneal and conjunctiva were irrigated with normal solution. keeping both eye exposed patient was draped. more severely affected eye was operated first. universal eye speculum was placed to retract the eyelids. then rest of the procedure was done with operating neurosurgical microscope under high magnification. a perilimbal conjunctival incision was given 12 to 3 o’clock position on right side and 9-12 o’clock position on left side. scleral insertion of superior and medial rectus muscle were identified and a 2-0 silk was passed under the tendons of sr and mr muscles near its insertion to sclera for controlling the movement of eyeball. the eyeball was rotated downward and outward to make the optic nerve superficial and accessible. by dissecting under the bulbar conjunctiva in between sr and mr on was reached. conjunctiva and upper eyelid was retracted upward and medially. on was identified by its position, color and continuity with the posterior eyeball. vortex veins and cilliary nerves also help to identify the on to some extent. if orbital fat prolapse in the field then the situation becomes difficult and more number of spatula’s retraction may be needed. undue pressure on globe was avoided. during globe rotation with mr &sr stay sutures corneal injury was carefully avoided. a linear, parallel to optic nerve incision was given to dural sheath and gush of csf was noted and aspirated. then retractor, mr & sr sutures were removed. conjunctiva was re-sutured with 7-0 vicryl. same procedure was done on the opposite eye and antibiotic eye ointment was given. the patient was positioned lateral to insert lumbar csf drain and 200ml/day csf was drained for the next four days. tab. acetazolamide continued for next six months. figure 3. sequential (a, b, c &d) schematic hand drawings of medial trans-conjunctival onsf on left side. n-nasal side, ttemporal side, er-eyelids retractor, r-retractor, sutures controlling sutures on superior and medial rectus tendon, srsuperior rectus, mr-medial rectus, on-optic nerve. figure 4. a, b, c, d, e & f per operative sequential images showing stages of onsf on right side. a&bconjunctival incision and trans conjunctival dissection (arrow marked). c, d&e-fenestration on sheath (arrow marked). f-conjunctival closure after onsf. 448 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. observations the total operation time was ranging from 45 minutes to 90 minutes (average 55 minutes). peroperative corneal abrasion occurred in 02 cases. single vortex vein injured in one case that needed to be coagulated. peroperative minor venous bleeding occurred in two cases that needed to be coagulated. in six cases peroperative difficulties occurred due to orbital fat prolapse in the targeted zone. after fenestration gush of csf came out with force in allfirst operated eyes whereas 13-second operated eyes showed very little csf flow after fenestration. there was no scleral injury or bulbar perforation or rupture. post-operative transient upper eyelid swelling occurred in three cases. transient anisocoria with abnormal light reflexes occurred in 18 eyes that recovered within three days. there was no proptosis, retrobulbar hematoma or no ocular cranial nerve palsy occurred in any of the cases. headache cured in all cases after the operation. vision improved in different grades in all cases at discharge except in three cases: 1. case with cns tb 2. one cvst case & 3. one case of iih where at discharge there was no visual improvement but by the end of three month her vision recovered to 6/12 bilaterally. case with high csf protein began to improve from 1st pod. by the end of three month all sixth nerve palsy recovered. in one case patient’s vision recovered from hand movement to near normal but at the end of six month she developed left sided sixth nerve palsy without any return of iih symptoms. this abducent nerve palsy recovered with steroid therapy for three weeks. pre-operative and postoperative (last follow up) visual status is shown in table1. in all cases vision were severely affected preoperatively. preoperatively, visual acuity was either pl&pr or hand movement in 40 eyes where 04 eyes were preoperatively total blind (no pl&pr). visual acuity improved in 48 eyes (92.3% eyes) where the patient can do his/her daily life activities including self-care. in one case (two eyes), vision recovered only in central part of visual fields where peripheral part did not recovered even after one year (figure 5). improvement in iih is 100% (23 cases i.e-46 eyes) whereas 01 case out of 02 case in cvst. pre and postoperative fundoscopic findings are also shown in the table 1. though vision improved dramatically fundal appearances changes very slowly and very less frequently returned to normal appearance (figure 6 & 7). in our series, six months after onsf papilledema improved in 23 cases (88.4%). figure 5. visual field analysis (in iih). a-preoperative. b &cconsecutive postoperative visual field analysis 06 and 12 after operation showed only central fields recovery (though patients’ visual acuity was 6/6 bilaterally). figure 6. a-preoperative fundal photograph, b-post operative (03 months after onsf) fundal photograph and cpost operative (06 months after onsf) fundal photograph. 449 optic nerve sheath fenestration figure 7. a-pre operative fundal photograph and b-post onsf fundal photograph (after six month). discussion pathogenesis of raised intracranial pressure includes increased production of csf, reduced drainage to circulation, intracranial space occupying lesions, traumatic brain injury, cerebral venous outflow obstruction, cvst and idiopathic intracranial hypertension (iih).6,7,8 iih is a special pathology, a diagnosis of exclusion, diagnosed by papilledema without any identifiable cns pathology, and usually occurs in obese women of child bearing age.9 iih is also referred to as pseudotumor cerebri. it is a disorder of unknown etiology that must meet the following criteria: • signs and symptoms of increased intracranial pressure (headache, nausea, transient visual obscurations lasting seconds, double vision, dizziness, emesis); • elevated cerebrospinal fluid (csf) pressure (>200 mmhg in nonobese adults and >250 mmhg in obese adults); • normal neuroimaging studies; • normal neurologic examination (with the exception of papilledema and/or cranial nerve palsies); • no other identifiable cause such as medications (including vitamin a, tetracycline, oral contraceptive pills, nalidixic acid, lithium, steroid use, or withdrawal)5. the effects of raised icp are responsible for disruption of the axoplasmic flow, swelling of axons, leakage of water and proteins resulting papilledema.10,11papilledema in its severe form (if left untreated), causes significant and irreversible loss of vision, with visual field (vf) defects and color vision.12 papilledema treatment is primly focused on treating identifiable etiologies of raised icp. iih is treated by medical or surgical options as indicated. medical treatment includes acetazolamide, steroids, topiramate, frousemide whereas surgical options include optic nerve sheath fenestration (onsf) or shunt procedures(lumboperitoneal shunts, ventriculo-peritoneal shunts, or ventriculo-atrial shunt).9,13,14 onsf, first described by dewecker in 1872 for treatment of papilledema.14 hayreh described the blood supply of optic nerve, and thus also described the efficacy of onsf in resolution of papilledema.15 the onsf is principally used for the treatment of iih. the onsf is also used less frequently for the management of other pathological conditions that adversely affect the vision such as progressive nonarteritic ischemic optic neuropathy, and optic disc drusen,16 cryptococcal meningitis,17 cvst, and intracranial masses causing raised icp that causes visual deterioration. the three main surgical approaches for onsf are superior eyelid, lateral orbital, and medial transconjunctival approach. in medial transconjunctival approach scleral insertion of mr is cut and after fenestration it is reattached.1 in our series we used the medial transconjunctival approach but we performed the nerve fenestration without cutting the mr tendon.1 primarily visual acuity (va) is the function of fovea, and does essentially provide the idea into preservation of central or paracentral visual field (vf).18 incresed icp essentially affects the macula, as a result of swelling of retinal nerve fibre layer as well as exudates and subretinal fluid. so resolution of papilledema is expected to improve vision after onsf. analysis the histological features of iih have shown that vision loss from outer retinal layer changes in the macula is more reversible than vision loss from optic neuropathy and inner retinal layer change.19 improvement in va does not depend upon pre-operative papilledema stage and thus explains the macular function is independence of optic disc swelling alone. it also means change in va is independent from pre-operative va, explaining 450 forhad h. chowdhury, mohammod raziul haque, jalal uddin mohammod rumi et al. that poor vision before surgery doesn’t necessarily contra-indicates the performance of onsf. the range of improvement in va after onsf is a debatable and variable subject. studies have shown wide range in improvement in va, from as low as 14% to as high as 100%.20,21in our series improvement in va in 24 cases (92,3%), nonimprovement in 2 cases (7.7%).in iih visual improvement is 100% (23cases out of 23 cases of iih. in one of the largest studies conducted on 578 eyes of 331 patients, improvement or stability was seen in 94.4% and worsening in 5.6% of eyes.16 onsf principally means the improvement of vision. but it has efficacy in improvement of other symptoms also. published data shows wide range in headache improvement, with as low as 13%, and as high as 90% patients with headache.22,23 our series also showed the same. so there is indirect evidence that onsf has role is in controlling chief symptom of iih or raised icp. post onsf improvement of papilledema ranges of 71 to 100%. 24,25it is logical to mention that improvement in papilledema stage does not necessarily mean complete resolution of papilledema. after onsf complete resolution of papilledema is rare. in our series, six month after onsf papilledema improved in 23 cases (88.4%). in the largest meta-analysis done on result of onsf with follow up of 20 months, improvement in headache, visual acuity and papilledema was seen in 26%, 42% and 92% respectively.9 the complication rate of onsf is ranging from 5 to 45% in the literature.26 complications of onsf including visual deterioration (<1%),22 permanent atonic pupil, retrobulbar hemorrhage and sixth nerve palsy have been reported in the literature.27 other less frequently seen complications are transient blindness, choroidal infarction, diplopia and orbital infections.16,28in our series we face no major permanent complication. conclusion due to the delicate and technically demanding nature of the surgery, safety is a major concern of the onsf. our experience showed, onsf is a technically safe operation with very good results where indicated. declaration ethics approval and consent to participate – not applicable (na) consent for publication taken from the patients/patient’s party. availability of data and materials na competing interests none funding none abbreviations cvst-cerebral venous sinus thrombosis cns-central nervous system csf-cerebro spinal fluid icp-intracranial pressure iih-idiopathic intracranial hypertension lp-lumbo-peritoneal mr-medial rectus mrv-magnetic resonance venography on-optic nerve onsf-optic nerve sheath fenestration pod-post operative day pl-perception of light pr-projection of rays sr-superior rectus sas-subarachnoid space tb-tuberculosis va-visual acquity vf-visual fields vp-ventriculo-peritoneal references 1. nisha mukherjee n, a el-dairi, and m tariq bhatti mt. optic nerve sheath fenestration—indications and techniques. us ophthalmic review, 2013;6(2):125–131. doi: 10.17925/usor.2013.06.02.125. 2. de wecker l. on incision of the optic nerve in cases of neuroretinitis. int ophthalmol cong reps. 1872. 4:11-14. 3. moskowitz, b. optic nerve sheath fenestration. r.c. della rocca, edward h. bedrossian, b. p. arthurs. ophthalmic plastic surgery: decision making and techniques. 1. new york: mcgraw-hill; 2002. 291-4. 4. 4alsuhaibani ah, carter kd, nerad ja, lee ag. effect of optic nerve sheath fenestration on papilledema of the operated and the contralateral nonoperated eyes in idiopathic intracranial hypertension. ophthalmology. august/2010. 5. optic nerve sheath fenestration: overview, preparation, technique https://emedicine.medscape.com/article/189 1241-overview?src=soc_tw_share via @medscape. 6. yaqub ma, mehboob ma, islam qu. efficacy and safety of optic nerve sheath fenestration in patients with raised intracranial pressure. pak j med sci. 2017 mar-apr; 33(2): 471–475. doi: 10.12669/pjms.332.11937 7. raoof n, sharrack b, pepper im, hickman sj. the incidence and prevalence of idiopathic intracranial 451 optic nerve sheath fenestration hypertension in sheffield, uk. eur j neurol. 2011;18:1266–1268. doi:10.1111/j.1468-1331.2011.033 72.x. 8. lee ag, wall m. papilledema:are we any nearer to a consensus on pathogenesis and treatment? curr neurol neurosci rep. 2012;12:334–339. doi:10.1007/s11910012-0257-8. 9. julayanont p, karukote a, ruthirago d, panikkath d, panikkath r. idiopathic intracranial hypertension:ongoing clinical challenges and future prospects. j pain res. 2016;9: 87–99. doi:10.2147/jpr. s60633. 10. bidot s, bruce bb, saindane am, newman nj, biousse v. asymmetric papilledema in idiopathic intracranial hypertension. j neuroophthalmol. 2015;35:31–36. doi:10.1097/wno.0000000000000205. 11. zamecki kj, frohman lp, turbin re. severe visual loss associated with idiopathic intracranial hypertension (iih) in pregnancy. clin ophthalmol. 2007;1:99–103. 12. thurtell mj, wall m. idiopathic intracranial hypertension (pseudotumorcerebri):recognition, treatment, and ongoing management. curr treat options neurol. 2013;15:1–12. doi:10.1007/s11940-012-0207-4. 13. spitze a, lam p, al-zubidi n, yalamanchili s, lee ag. controversies:optic nerve sheath fenestration versus shunt placement for the treatment of idiopathic intracranial hypertension. indian j ophthalmol. 2014;62:1015–1021. doi:10.4103/0301-4738.146012. 14. prabhakaran vc, selva d. vertical lid split approach for optic nerve sheath decompression. indian j ophthalmol. 2009;57:305–306. doi:10.4103/0301-4738.53057. 15. hayreh ss. pathogenesis of oedema of the optic disc (papilloedema). a preliminary report. br j ophthalmol. 1964;48:522–543. 16. moreau a, lao kc, farris bk. optic nerve sheath decompression:a surgical technique with minimal operative complications. j neuroophthalmol. 2014;34:34–38. doi:10.1097/wno.0000000000000065. 17. milman t, mirani n, turbin re. optic nerve sheath fenestration in cryptococcal meningitis. clin ophthalmol. 2008;2:637–639. 18. knight rs, fielder ar, firth jl. benign intracranial hypertension:visual loss and optic nerve sheath fenestration. j neurol neurosurg psychiatry. 1986;49:243–250. 19. chen jj, thurtell mj, longmuir ra, garvin mk, wang jk, wall m, et al. causes and prognosis of visual acuity loss at the time of initial presentation in idiopathic intracranial hypertension. invest ophthalmol vis sci. 2015;56:3850–3859. doi:10.1167/iovs.15-16450. 20. goh ky, schatz nj, glaser js. optic nerve sheath fenestration for pseudotumorcerebri. j neuroophthalmol. 1997;17:86–91. 21. sergott rc, savino pj, bosley tm. modified optic nerve sheath decompression provides long-term visual improvement for pseudotumorcerebri. arch ophthalmol. 1988;106:1384–1390. 22. banta jt, farris bk. pseudotumorcerebri and optic nerve sheath decompression. ophthalmology. 2000;107:1907– 1912 23. kelman se, heaps r, wolf a, elman mj. optic nerve decompression surgery improves visual function in patients with pseudotumor cerebri. neurosurgery. 1992;30:391–395. 24. fonseca pl, rigamonti d, miller nr, subramanian ps. visual outcomes of surgical intervention for pseudotumourcerebri:optic nerve sheath fenestrationversus cerebrospinal fluid diversion. br j ophthalmol. 2014;98:1360–1363. doi:10.1136/bjophthalmol-2014-304953. 25. yazici z, yazici b, tuncel e. findings of magnetic resonance imaging after optic nerve sheath decompression in patients with idiopathic intracranial hypertension. am j ophthalmol. 2007;144:429–435.[ 26. uretsky s. surgical interventions for idiopathic intracranial hypertension. curr opin ophthalmol. 2009;20:451–455. doi:10.1097/icu.0b013e3283313c1c. 27. corbett jj, nerad ja, tse dt, anderson rl. results of optic nerve sheath fenestration for pseudotumorcerebri. the lateral orbitotomy approach. arch ophthalmol. 1988;106:1391–1397. 28. flynn wj, westfall ct, weisman js. transient blindness after optic nerve sheath fenestration. am j ophthalmol. 1994;117:678–679. doi: 10.33962/roneuro-2023-018 incomplete currarino triad in an adult woman. a case report rasha a. al-youzbaki, emad hazim mahmoud, zahraa a. alsubaihawi, mohammed a. almeran, saja a. albanaa, samer s. hoz romanian neurosurgery (2023) xxxvii (1): pp. 111-114 doi: 10.33962/roneuro-2023-018 www.journals.lapub.co.uk/index.php/roneurosurgery incomplete currarino triad in an adult woman. a case report rasha a. al-youzbaki1, emad hazim mahmoud1, zahraa a. alsubaihawi2, mohammed a. almeran1, saja a. albanaa2, samer s. hoz3 1 department of neurosurgery, ibn sina teaching hospital, mosul, iraq 2 college of medicine, baghdad university, iraq 3 department of neurosurgery, university of cincinnati, ohio, usa abstract introduction: currarino syndrome (cs) is a rare entity characterized by a triad of sacral agenesis, anorectal malformations, and pre-sacral masses. cs is typically diagnosed during the first decade of life. case description: we present a rare case of incomplete currarino syndrome manifesting in a 36-year-old lady who presented with back pain, urinary retention, anal paresthesia, and lower limb weakness. the patient underwent multiple laminectomies and partial resection of an epidermoid cyst and regained function. conclusion: although rare, the possibility of currarino syndrome should be entertained in adult patients with lower lumbosacral symptoms and a pre-sacral mass. a thorough physical examination and strategic pre-operative planning are mandatory to maximize patient outcomes. introduction currarino syndrome is a rare entity with a set of complex congenital anomalies. it manifests clinically as a triad of sacral bony defects, anorectal malformations, and pre-sacral masses, such as anterior meningocele (1,2). this condition is usually diagnosed during the first decade of life and diagnosis in adults is rare (3,4). both sporadic and inherited cases have been reported, with an estimated incidence of 1 in 100,000 of the population (5,6). here, we report a rare case of an incomplete currarino syndrome (sacral agenesis, epidermoid cyst with no anorectal malformations) manifesting in adulthood. case description a 36-year-old female presented with a two-week history of lower back pain, urinary retention, and anal numbness. she had no history of trauma. her examination was significant for sacral anesthesia and weakness in ankle plantar and dorsiflexion -medical research council (mrc) scale 4/5 -. magnetic resonance imaging (mri) of the lumbosacral keywords currarino syndrome, sacral agenesis, epidermoid cyst corresponding author: saja albanaa university of baghdad, college of medicine, iraq sajaalbanaa@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 112 rasha a. al-youzbaki, emad hazim mahmoud, zahraa a. alsubaihawi et al spine and pelvis revealed sacral agenesis and an intradural cystic lesion extending from the level of the second lumbar vertebrae (l2) to the sacrum with an anterior meningocele (figure 1). multiple laminectomies (from l2 to sacrum) were performed through the posterior approach. . the cystic lesion was identified and durotomy revealed a soft white pearly lesion suggestive of epidermoid tumor which was partially resected as it wrapped most nerve roots with an adherent surrounding capsule. the histopathological analysis revealed flakes of keratinous materials with strips of unremarkable squamous epithelium consistent with epidermoid cyst (figure 2). the patient had an uneventful recovery and was discharged on a course of steroids and referred to a bladder training program. on her one-month followup, her bladder function was back to normal as were her lower limb power and peri-anal sensation. the mri showed a decrease in the size of the epidermoid cysts and anterior meningocele (figure 3). figure 1. a, b mri sagittal view of the lumbosacral spine t1 and t2 showing an intradural mass hypointense in t1 and hyperintense in t2 extending from l2 to the sacrum and turning anteriorly to the. partial agenesis of the sacrum is also evident. c: mri axial view showing cystic cavity in the sacral spine extending anteriorly in the pelvis through a widened sacral foramen. figure 2. pictures of histopathology showing flakes of keratinous materials with strips of unremarkable squamous epithelium consistent with epidermoid cyst. figure 3. post-operative mri t1 and t2 sagittal view showing operative site from l2 to the sacrum and decrease in the size of the intradural lesion and the anterior meningocele. discussion sacral agenesis is a congenital deformity that ranges from partial agenesis of the unilateral sacrum to complete bilateral sacral agenesis (7-9). in a normal pregnancy, the incidence of sacral agenesis is between 0.005 and 0.1%. however, 16-20% of sacral agenesis patients have diabetic mothers. sacral agenesis is associated with an increased incidence of spinal dysraphism, and currarino triad. (10) spinal meningocele is a posterior protrusion of meningeal elements out of the spinal canal, usually seen in the lumbosacral region. an anterior sacral meningocele is a meningeal protrusion into the presacral, retroperitoneal, and intraperitoneal space as a consequence of partial anterior sacral agenesis (11). anterior sacral meningoceles may occur anteriorly through a defect in the body of sacrum or anterolaterally through an enlarged intervertebral foramen or coalesced foramina as in our case (12) such improper development can result from other coexisting abnormalities in the skin, subcutaneous tissues, spine, and internal organs. anterior sacral meningocele occurs sporadically, but familial cases have been reported in literature as part of the currarino triad. (13) 113 incomplete currarino triad in an adult woman the most common presacral masses are teratomas and anterior sacral meningocele, while dermoid tumors, lipomas, pelvic hamartomas, leiomyosarcoma, and carcinoid tumors have all been documented in literature but are very uncommon. our case had an epidermoid cyst which is exceptionally uncommon, with a frequency of 4% among patients with curarrino triad in adulthood. (14) currarino traid is rare in adults and should be diagnosed early to prevent life-threatening complications, such as meningitis, rectal fistulas, and malignant transformation. approximately, 80% of the patients with the classic triad are recognized during the first decade of life. (15) urinary symptoms and chronic constipation are amongst the most common manifestations of currarino triad (16) other clinical presentations include gynecological anomalies, spinal cord tethering, perianal sepsis, and meningitis (17). sacral bony defects are pathognomonic for this triad. pelvic x-ray is the initial imaging modality of choice (18). on mri, epidermoid cysts appear as a well-defined cystic mass generally with no perilesional edema (19). mri can also define the extension of presacral mass and may detect other malformations. prenatal ultrasound and fetal mri could be used to identify the presence of a presacral mass during in-utero and is indicated when a history of maternal currarino triad is present. (20) the variable set of complex anomalies associated with curranio mandates a multi-disciplinary management approach. surgical management involves correction of the anorectal malformations before attending to any existing pre-sacral masses (18,21) . the anterior sacral meningocele is surgically managed through the posterior sagittal approach to provide full perineum exposure by incision from the sacrum to the anus. in our case, the trans-dural pathway was accessed by sacral laminectomy, which permits the excision of the intradural epidermoid cyst (18,21). given the high level of morbidity and mortality associated with this condition, timely diagnosis and precise pre-operative planning are paramount to maximize patient outcomes (22). conclusion although rare, the possibility of currarino syndrome should be entertained in adult patients with lower lumbosacral symptoms and a pre-sacral mass. a thorough physical examination and strategic preoperative planning are mandatory to maximize patient outcomes. abbreviations: cs: currarino syndrome; mrc: medical research council; mri: magnetic resonance imaging; l2: second lumbar vertebrae. references 1. sonek jd, gabbe sg, landon mb, stempel le, foley mr, shubert-moell k (march 1990). "antenatal diagnosis of sacral agenesis syndrome in a pregnancy complicated by diabetes mellitus". am. j. obstet. gynecol. 162 (3): 806–8. doi:10.1016/0002-9378(90)91015-5. pmid 2180307. 2. man climbs mt. kilimanjaro on hands. abc news. 22 june 2012. 3. faith karimi and joe sutton. "'american horror story' actress rose siggins dead at 43 – cnn. 4. osborn ag. diagnostic neuroradiology. mosby inc. (1994) isbn:0801674867. 5. ziv et, gordon mccomb j, krieger md et-al. iatrogenic intraspinal epidermoid tumor: two cases and a review of the literature. spine. 2004;29 (1): e15-8. 6. gonzalvo a, hall n, mcmahon jh et-al. intramedullary spinal epidermoid cyst of the upper thoracic region. j clin neurosci. 2009;16 (1): 142-4. 7. kikuchi k, miki h, nakagawa a. the utility of diffusionweighted imaging with navigator-echo technique for the diagnosis of spinal epidermoid cysts. ajnr am j neuroradiol. 21 (6): 1164-6. 8. diel j, ortiz o, losada ra et-al. the sacrum: pathologic spectrum, multimodality imaging, and subspecialty approach. radiographics. 2001;21 (1): 83-104. 9. currarino g, coln d, votteler t: triad of anorectal, sacral and presacral anomalies. am j roentgenol 137:395-398, 1981. 10. haga y, cho h, shinoda s, masuzawa t: recurrent meningitis associated with complete currarino triad in an adult – case report. neurol med chir (tokyo) 43:505-508, 2003. 11. shamoto h, yoshida y, shirane r, yoshimoto t: anterior sacral meningocele completely occupied by an epidermoid tumor.childs nerv syst 15:209-211, 1999. 12. grossman ri, yousem dm. neuroradiology, the requisites. mosby inc. (2003) isbn:032300508x. 13. beyazal m. an asymptomatic large anterior sacral meningocele in a patient with a history of gestation: a case report with radiological findings. case reports in radiology. 2013 dec 17;2013. 14. kurosaki m, kamitani h, anno y, watanabe t, hori t, yamasaki t. complete familial currarino triad: report of 114 rasha a. al-youzbaki, emad hazim mahmoud, zahraa a. alsubaihawi et al three cases in one family. journal of neurosurgery: spine. 2001 jan 1;94(1):158-61. 15. colombo f, janous p, buxton n. carcinoid transformation of presacral dermoid cyst in patient with currarino syndrome: a case report. british journal of neurosurgery. 2019 may 4;33(3):285-6. 16. yates vd, wilroy rs, whitington gl, simmons jc. anterior sacral defects: an autosomal dominantly inherited condition. the journal of pediatrics. 1983 feb 1;102(2):239-42. 17. chakhalian d, gunasekaran a, gandhi g, bradley l, mizell j, kazemi n. multidisciplinary surgical treatment of presacral meningocele and teratoma in an adult with currarino triad. surgical neurology international. 2017;8. 18. urioste m, del carmen garcia‐andrade m, valle l, robledo m, gonzález‐palacios f, méndez r, ferreirós j, nuño j, benítez j. malignant degeneration of presacral teratoma in the currarino anomaly. american journal of medical genetics part a. 2004 jul 30;128(3):299-304. 19. menenjit cs. epidermoid cyst inside anterior sacral meningocele in an adult patient of currarino syndrome manifesting with meningitis. turkish neurosurgery. 2012;22(5):659-61. 20. shoji m, nojima n, yoshikawa a, fukushima w, kadoya n, hirosawa h, izumi r. currarino syndrome in an adult presenting with a presacral abscess: a case report. journal of medical case reports. 2014 dec 1;8(1):77. 21. isik n, elmacı i, gokben b, balak n, tosyalı n. currarino triad: surgical management and follow-up results of three cases. pediatric neurosurgery. 2010;46(2):110-9. 22. kim ay, yoo sy, kim jh, eo h, jeon ty: currarino syndrome: variable imaging features in three siblings with hlxb9 gene mutation. clin imaging. 2013, 37: 398402. 10.1016/j.clinimag.2012.05.007. doi: 10.33962/roneuro -2020-049 solitary plasmacytoma of occipital bone rajneesh misra, sushil kumar, sandeep sharma, rohan sinha romanian neurosurgery (2020) xxxiv (1): pp. 330-332 doi: 10.33962/roneuro-2020-049 www.journals.lapub.co.uk/index.php/roneurosurgery solitary plasmacytoma of occipital bone rajneesh misra1, sushil kumar1, sandeep sharma1, rohan sinha2 1 dept. of neurosurgery, st. stephens hospital, delhi, india 2 jaypee hospital, noida, up, india abstract we report a case of a 35-year-old male who presented with a pulsatile swelling in the posterior parieto-occipital area. ct and mri revealed an extra-axial mass. gross total resection was performed. histologically it was found to be a plasmacytoma. no recurrence has been noted in the last 48 months of follow up. introduction plasma cell neoplasm is characterized by proliferation of single clone of plasma cells. solitary plasmacytoma of skull bone in a young adult is very rare, it is hence being reported. case report a 35-year-old male presented with headache, vomiting and decreased vision and swelling in the occipital region. the swelling had appeared about 3 days after a fall sustained 6 months back. it had started as a small swelling but had since then gradua lly increased in size. on examination, the patient was conscious, alert and oriented. he had a 6x4 cm sized cystic swelling over the left parieto-occipital region. the swelling had irregular margins and had a smooth surface. its consistency was solid with areas of cystic change. there was no pulsation or tenderness. ct scan revealed an osteolytic solid mass. mri showed hyper-intense lesion on t1 with enhancement on contrast. it had mixed intensity on t2.laboratory investigations showed a hemoglobin of 15.9 g/dl, total wbc count was 8700/microl, differential count p52l35m8e4b1, and platelet count of 2.37 lakhs /dl. there was no evidence of hypercalcemia.no m component was detected in the serum protein electrophoresis. the patient underwent craniotomy under general anesthesia in jan 2016. the tumor was purple in color, nodular, vascular and separable from the underlying dura. margins of the bone were nibbled and cranioplasty with methyl meth-acrylate was done in the same sitting. histopathology revealed the diagnosis of plasma cell tumor. he was given a course of radiotherapy. the patient was planned for bone keywords plasmacytoma, skull, solitary corresponding author: rajneesh misra ms, mch. dept. of neurosurgery, st. stephens hospital, delhi, india misra_ rajneesh@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2020 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 331 solitary plasmacytoma of occipital bone marrow aspiration which he refused. skeletal survey did not reveal any other lesion. there was no evidence of recurrence in the last 45 months. figure 1. figure 2. discussion solitary plasmacytoma of the skull without signs of multiple myeloma is a rare entity and only a few cases have been reported in the literature. (1) it may involve cranial vault, skull base or orbit. symptoms and signs are non-specific and usually lack neurological deficits. the diagnostic characteristics are based on the presence of radiological solitary skull lesion, histological evidence of plasma cells, fewer than 5% plasma cells in the bone marrow aspirate, less than 24mg/dl monoclonal protein in the serum, urine negative for bence-jones proteins and no evidence of hypergammaglobulinemia, hypercalcemia or anemia and no recurrence in 2 years of follow up. (2) usual presentation of the plasmacytoma of skull is as a painless or painful lump without any neurological deficit which depends upon the size and location of the tumor. (3) cosmetic skull deformity is usual reason for referral to neurosurgeon. total surgical resection followed by radiotherapy has been advocated as effective in managing the solitary plasmacytoma. (1) arienta et al. report that if total resection has been achieved, then radiotherapy should be reserved for the case of tumor recurrence. (4) furthermore, there are reports of complete cure after biopsy and radiotherapy because plasma cell neoplasms are exquisitely sensitive to radiation. (5) the lesion can be highly vascular. (6) preoperative embolization has been resorted to in order to reduce vascularity.(7) craniectomy and cranioplasty is recommended because of high recurrence rate from the residual tumor cells on the involved bone surface. (8) computed tomography reveals destructive well demarcated soft tissue mass with peripheral bony fragments. usually, the lesion is isointense on t1wi and t2wi and enhances on contrast administration in both ct and mri. however, in our patient it was slightly hyperdense on ct and slightly hyperintense on t1w1 with mixed attenuation on t2wi. in the absence of early diagnosis of multiple myeloma, the lesion can be misdiagnosed as a meningioma, lymphoma or even myxoma. declarations conflict of interest: none acknowledgements: none references 1. singh ad, chacko ag, chacko g, rajshekhar v. plasma cell tumors of the skull. surg neurol 2005;64:434-8. 332 rajneesh misra, sushil kumar, sandeep sharma, rohan sinha 2. tanaka m, shibui s, nomura k, nakanishi y. solitary plasmacytoma of the skull: a case report. jpn j clin oncol. 1998;28(10):626–630. 3. jacquet g, vuillier j, viennet a, godard j, steimle r. solitary plasmacytoma simulating pituitary adenoma. neurochirurgie 1991;37:67-71. 4. arienta c, caroli m, ceretti l, villani r. solitary plasmacytoma of the calvarium: two cases treated by operation alone. neurosurgery 1987;21:560-3. 5. strojan p, soba e, lamovec j, munda a. extramedullary plasmacytoma: clinical and histopathologic study. int j radiat oncol biol phys 2002;53:692-701. 6. alessandro g, alfonso c, marzia d, et al. plasmacytoma of the skull. eur j haematol 2011;88:369. 7. kuo y, huang w, wu j (november 01, 2018) surgical treatment for a giant solitary plasmacytoma with skull erosion. cureus 10(11): e3535. doi:10.7759/cureus.3535 8. bindal ak, bindal rk, van loveren h, sawaya r. management of intracranial plasmacytoma. j neurosurg 1995 83:218-21. romanian neurosurgery (2019) xxxiii 1: 7-11 doi: 10.33962/roneuro-2019-001 www.journals.lapub.co.uk/index.php/roneurosurgery endovascular management of recurrent anterior communicating aneurysm previously embolized. case presentation a. chiriac1,2, georgiana ion1,2, z. faiyad1,2, i. poeata1,2 1 “grigore t. popa” university of medicine and pharmacy, iasi, romania 2 “prof. dr. n. oblu” clinic emergency hospital, iasi, romania abstract although endovascular coiling treatment has been widely accepted as the method of choice for intracranial aneurysms, concerns about its durability are still discussed. attention was largely focused on aneurysm recurrence after coil occlusion with possible unfavourable evolution to a new bleeding episode. we present our experience of a patient with a ruptured anterior communicating artery aneurysm previously treated by endovascular coil embolization that presented over a 4-year period for aneurysm recurrence. introduction coil embolization for intracranial aneurysms is currently the most accepted modality of treatment for patient with this vascular pathology. this is due to numerous studies which demonstrated its effectiveness in preventing rebleeding after aneurysmal rupture and a better outcome in terms of disability-free survival compared with aneurysmal neck clipping. today, the main concern in endovascular treatment is represented by its durability due to aneurysm recurrence with disastrous potentially for the patient. the purpose of this study was to describe a clinical situation requiring repeat embolization in a patient with a ruptured anterior communicating artery aneurysm previously treated by endovascular coil embolization, and discuss different aspects of aneurysm recurrence. case presentation a 50-year-old woman was referred for evaluation of an embolized anterior communicating aneurysm that demonstrated small coil compaction by fundus migration and aneurysm regrowth on serial angiography control. four years before this referral, she had undergone an endovascular coil occlusion for a ruptured anterior communicating aneurysm. the patient made a good recovery. keywords aneurysm recurrence, rebleeding, coil embolization corresponding author: alexandru chiriac “grigore t. popa” university of medicine and pharmacy, iasi, romania chiriac_a@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ http://www.lapub.co.uk/ 8 a. chiriac, giorgiana ion, z. faiyad, i. poeata d postoperative angiography control at 12 months revealed a small aneurysm neck repermeabilization due to partial coil compaction. the angiography control at 2 and 3 years showed a slow development of the remnant neck portion by aneurysm regrowth. initially, a conservative management by imaging monitoring was decided. the angiography control at 4-year interval revealed a clear aneurysm sac enlargement with a 1:1 ratio of occluded aneurysm versus the permeable portion of aneurysm sac. a new session of coil embolization was decided for complete occlusion of the residual aneurysm (fig.1). figure 1: a-brain ct scan showing the initial sah; b, c-angio-ct diagnosis of acoa aneurysm and initial measurements; d, g-initial dsa diagnostic and aneurysm measurements; e-dsa control postembolization with coils; f, hdsa control 4 years later showing aneurysm regrowth; ipostprocedural dsa control after additional coil embolization; jbrain ct scan control after additional coil embolization. a c b e f g h i j 9 endovascular management of recurrent anterior communicating aneurysm previously embolized endovascular procedure the interventional neurosurosurgeon team performed the endovascular treatment with the patient under general anaesthesia in a monoplane angiosuite. treatment approach was performed through the right femoral access route with a 6f introduction sheath. anticoagulation with 5000 iu heparin was used from the beginning of the procedures according to our centre protocol for unruptured aneurysm. the systemic administration of heparin is continued to entire period of the procedure (perfuzable solution of 1ml heparin/500ml nacl). a 6f guiding catheter (ghider softip 40xf boston scientific) was placed in the left internal carotid artery that provided arterial supply to the aneurysm remnant. multiple dsa series were obtained in different degrees of obliquity. also, a three-dimensional rotational angiography was finally performed to choose the working projection. once an appropriate angle of obliquity was obtained on 3d postprocessing unit that optimally highlight the relationship of neck of the aneurysm remnant and the parent vessel, the position was automatically send it to angiograph c-arm. on this projection a road-mapping acquisition is performed and maintained throughout the duration of the procedure. a microcatheter (excelsior sl-10, stryker) was then advanced over a microguidewire (transend 0.0014, boston scientific) under road-mapping guidance into the aneurysm remnant. two gdcs-10 (stryker) were then advanced and detached in the aneurysm remnant. the attempt to introduce the third gdc was not technically possible due to its distal end protruding into the parent vessel. serial dsas were performed to verify and to monitor the progress of aneurysm remnant occlusion. once the aneurysm remnant was deemed to be satisfactorily occluded, the microcatheter was gently removed. this was followed by the guiding catheter removal through the femoral sheaths after obtaining a final dsa. the femoral sheaths were then removed from the femoral artery and hemostasis was obtained by prolonged compression. the patient was awakened from general anaesthesia and then admitted to the neuro–intensive care unit for 24-hour observation and monitoring. patient was discharged home 48 hours later. antiplatelet medication was maintained for the period of hospitalization. follow-up protocol the imaging control of intracranial aneurysms postembolization was represented by conventional angiography. flow-up angiography was performed during the early years of our endovascular activities, and was completed by mr angiography in the later years. thus, in case of a completely embolized aneurysm conventional cerebral angiography, dynact and magnetic resonance angiography with threedimensional reconstruction (3d mra) were recommended at 1.5, 3, 6, 12 months, post embolization, respectively. when a coil mass compaction, change configuration or migration was suspected in noninvasive studies, conventional angiography was performed immediately to check the exact state of the aneurysm and to decide the necessity of further treatment. if a stable occlusion is documented angiographically, follow-up conventional angiography was recommended after another 12 to 36 months. if stable occlusion was confirmed in post-embolization angiography performed after 1 to 2 years, follow-up was continued by noninvazive imaging studies [1,2]. in cases with unsatisfactory (low grade of coil packing) or incomplete aneurysm occlusion after initial coil embolization, we performed control conventional angiography at 3 months post embolization. the next follow-up protocol depended on the stability of the coil mass and configuration of the embolized aneurysm. if a minor aneurysmal recanalization by minimal coil compaction at the aneurysmal neck occurs during the follow up, another 6-month mra and 1-year angiography is performed. instead, an early additional embolization treatment we performed when a major recanalization, with significant coil loosening, coil compaction or coil mass extrusion beyond the edge of a coil basket, or contrast filling within an aneurysm sac, occurs [2,3]. discussion most of the largest studies from literature demonstrated that in patients treated for ruptured cerebral aneurysm, the risk of recurrence and rebleeding is significantly higher with endovascular coil embolization in comparison with surgery. also, a direct relationship was shown between endovascular treatment and/or aneurysmal rupture, with an increased rate of incomplete occlusion of aneurysms. the aneurismal recurrence was defined in the literature as being residual larger than 20% of the primary aneurysm, unstable progressing neck 10 a. chiriac, giorgiana ion, z. faiyad, i. poeata a remnants, aneurysm regrowth with or without coil compactation, and outgrowth of new aneurysmal sac. the evaluation of aneurysmal recurrence was usually performed by angioarchitecture comparing of angiographic controls with immediate postcoiling angiograms based on aneurysm sac size, neck morphology, dome-to-neck ratio and initial coil packing. dorfer and all showed that 15,2% of the aneurysm smaller than 10mm and 38,2% of the aneurysm larger than 10mm had relevant recurrences and similarly 17,2% of aneurysm with neck <4mm and 27,3% with neck >4mm presented with recurrences. they also reported that a threshold of 25% packing density and 30% volumetric aneurysm filling has been correlated with significantly stable angiographic results [2,5,6]. different mechanisms of aneurysm recurrence after endovascular treatment were described in large series. the most common mechanism of aneurysmal recurrence is residual aneurysm due to coils compaction. this is the most common situation in the cases of large and giant aneurysms with simple coils embolization. lower rates of repermebilisation were reported for those aneurysms when the stentassisted or balloon technique was associated with coil occlusion. coil migration into the intraluminal thrombus was also frequently reported especially in large partial thrombosed aneurysm. if initially this situation was considered by specialists as a separate entity, it is currently included in the category of compaction aneurysms. nevertheless, coil mass compactation was not constantly associated with aneurysm recurrence. there have been many situations where the coil compaction phenomenon has been stable over time without any evolution to an aneurysm recurrence that would impose a type of reintervention [1,2,3]. figure 2: mechanisms of aneurysm recurrence: a-coil complete occlusion; b-coil compactation; c-coil fundal migration; d-coil regrowth. in the situations of aneurysmal enlargement without signs of coil compactation, the mechanisms of aneurysm recurrence were defined as regrowth. the third entity of aneurysmal recurrence mechanism defined by the last publications was fundal migration of the coil package through the wall of the aneurysmal sac. also, some authors have mentioned as an aneurysm recurrence mechanism a combination of regrowth and fundal migration or compactation and fundal migration. all of these situations imposed an additional treatment. aneurysm recurrence could benefit from both endovascular and surgical treatment. the decision, regarding which type of treatment must be used, should be individualized as much as possible for each individual case. most of the studies demonstrate that additional treatment is usually associated with a low complication risk and results in satisfactory stable occlusion in most patients. the main indication for initiating additional treatment was made because of the reported increased risk of further haemorrhage associated with unstable remnants and incompletely occluded aneurysms. the reported rebleed rate after endovascular therapy indicated in isat1 was 0.2% per patient year with a follow-up from 1 to 8 years (mean, 4 years) and 1.3/100 patient years in the carat study, with no haemorrhage occurred after 2 years[..]. the main factors to be considered when deciding on the method of treatment used in the aneurysmal recurrence were represented by the aneurysm size and location, patient age and clinical condition, size of aneurysm remnant and its relation with adjacent vessels, presence of coils in the aneurysm neck, mechanism of recurrence and history of sah manifestation [2,6]. the time interval between aneurysm coil occlusion and angiographic control that demonstrate a clear evolution to aneurysm recurrence which require additional occlusion treatment was named the recurrence latency. it was demonstrated that the first control angiogram often performed at approximately 6 months is not sufficient to detect all aneurysms that may require additional treatment. raymond et al have also reported progressive deterioration with aneurysms recurrences that were angiographically occluded at 6 months. progressive neck remnant enlargement has been demonstrated in 14.8% of aneurysms in the first year after treatment and a major recurrence in b c d 11 endovascular management of recurrent anterior communicating aneurysm previously embolized 20.7% at a mean of 16.48 ± 15.93 months. the other authors detected 46.9% of all recurrences by 6 months and 96.9% by 36 months [1,2,5]. the complication rate following aneurysms retreatment by endovascular retreatment ranged from 0% to 11% in previous reported series. some of these series included patients with multistage treatment. thromboembolic events were the major complication mentioned but only 3.2% of patients had a permanent neurologic deficit as henkes et al described [2]. conclusions the coil mass instability due to compactation, migration or aneurysm regrowth that impose additional retreatment remains a major deficiency of endovascular treatment. the great challenge in managing patients with aneurysm recurrences remain the ability to early recognition of unstable aneurysm residuals with rehemorrhage potential by benign nonprogresive one. in case of relevant aneurysm recurrences both endovascular and surgical techniques could be successfully applied. references 1. boet, r., poon, w. s., & yu, s. c. h. (2001). the management of residual and recurrent intracranial aneurysms after previous endovascular or surgical treatment—a report of eighteen cases. annals of the college of surgeons of hong kong, 5(1), a3-a3. 2. dorfer, c., gruber, a., standhardt, h., bavinzski, g., & knosp, e. (2011). management of residual and recurrent aneurysms after initial endovascular treatment. neurosurgery, 70(3), 537-554. 3. liu, j. j., nielsen, t. h., abhinav, k., lee, j., han, s. s., marks, m. p., ... & steinberg, g. k. (2019). surgical treatment of recurrent previously coiled and/or stent-coiled intracerebral aneurysms: a single-center experience in a series of 75 patients. world neurosurgery. 4. renowden, s. a., koumellis, p., benes, v., mukonoweshuro, w., molyneux, a. j., & mcconachie, n. s. (2008). retreatment of previously embolized cerebral aneurysms: the risk of further coil embolization does not negate the advantage of the initial embolization. american journal of neuroradiology, 29(7), 1401-1404. 5. sedat, j., chau, y., moubarak, k., vargas, j., & lonjon, m. (2012). endovascular treatment of recurrent coiled aneurysms: assessment of complications and rebleeding during a decade in a single center. interventional neuroradiology, 18(1), 14-19. 6. yu, l. b., fang, z. j., yang, x. j., & zhang, d. (2019). management of residual and recurrent aneurysms after clipping or coiling: clinical characteristics, treatments, and follow-up outcomes. world neurosurgery, 122, e838e846. romanian neurosurgery (2019) xxxiii (2): pp. 191-199 doi: 10.33962/roneuro-2019-036 www.journals.lapub.co.uk/index.php/roneurosurgery endoscopic management of intraventricular shunt-related cystic compartment in paediatric patients ahmed zaher, amr farid khalil, mohamed state, hatem badr * department of neurosurgery, faculty of medicine, mansoura university, egypt abstract background. intraventricular uniloculated compartments are relatively seen frequently in children previously treated with ventriculoperitoneal shunts for hydrocephalus. these compartments may present before shunt insertion and even as an end result to the shunt gliosis. although the availability of different surgical modalities for the management of such loculations but till now there is no consensus about a single therapeutic approach for its management. objective: the aim of this study is to assess the role of neuroendoscopy in management of uniloculated compartments, in pediatric cases who underwent shunting for hydrocephalus, to avoid multiple shunt insertion and even to eliminate the need for the preexisting shunt system. patients and methods. we retrospectively studied 44 consecutive previously shunted patients with isolated intraventricular compartment who underwent 58 endoscopic procedures by a single surgeon during the period between february 2015 and february 2018. these procedures included endoscopic cyst fenestration, intraventricular septum pellucidotomy, foraminoplasty and additionally third ventriculostomy in some cases was added to the previous procedures. multiloculated hydrocephalus and cysts related to the tumours were excluded. clinical, radiological and surgical data were assessed. results. the most common cause of a single loculation in those patients was neuroepithelial cyst (20 cases) followed by post shunt isolated compartment (12 cases), meningitis (8 cases) and four cases of intraventricular haemorrhage. the patient's age varied from two months up to seven years (mean = 3.2 years). the follow-up period was ranged from (2-49 months) with the mean of 12.3 months. the overall success of restoration of communication between the uniloculated compartment and the ventricular system was achieved in 36 patients (81.8%), with 28 (63.6%) patient needed only one shunt and eight (18.2%) patients became independent of their previous shunts. fourteen repeated endoscopic procedures were considered necessary in ten patients for either reopening of a closed stoma and/or shunt revision and finally, eight patient (18%) required additional shunt insertion during follow up period. the complications encountered were minor and reversible (csf leak in two cases, infection in two cases, subdural fluid collection in four cases) with no mortality. conclusion. minimal invasive endoscopic technique is a useful operative alternative to control uniloculated compartments in patients with previous ventriculoperitoneal shunts. it does not only simplify the existing shunt system by restoration of the communication between the loculated compartment and the draining shunt but it may eliminate the need for external shunt in some cases as well. keywords loculated hydrocephalus, endoscopy, fenestration corresponding author ahmad zaher department of neurosurgery, faculty of medicine, mansoura university, egypt azaher2005@hotmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 192 ahmed zaher, amr farid khalil, mohamed state et al. introduction intraventricular septation may lead to formation of an isolated csf cystic component which may become enlarged even if the shunt system is functioning. such enlarging intraventricular loculation may be attributed to altered csf dynamics as result of separation between the ventricular catheter tip and the site of csf production [14]. variable anatomical and radiological forms of loculations were described according to the site of obstruction and consequent csf accumulation including either uniloculated or multiloculated. identification and distinction between the two forms is crucial because everyone has a particular different pathogenesis, treatment and prognosis [7]. loculated hydrocephalus usually develops after episodes of neonatal meningitis or germinal matrix hemorrhage. occlusion of the foramen of monro, the aqueduct, and the outlet foramina of the fourth ventricle may result from shunt infection and its consequences like ventriculitis and ventricular septations. however, isolated intraventricular compartment may evolve after insertion of ventriculoperitoneal shunt via other mechanisms rather than shunt infection [11, 14]. direct ependymal trauma during shunt insertion, collapse of shunted ventricular compartment with subsequent obstruction of the catheter tip perforations by proliferating fibrillary astrocytes and over drainage of existing shunt may play important roles that may stimulate the enlargement of an isolated shunt related compartment [14]. the management of such complex condition is challenging to most neurosurgeons. the main goal of treatment is to elevate the manifestation of increased intracranial pressure by creating a free connection between the isolated compartment and the ventricular system cavity via converting them into a solitary component that will be drained by a single ventricular catheter with little morbidity and mortality [8, 19]. multiple treatment strategies for intraventricular loculation are available but the best choice of the proper procedure remains controversial. this group of patients presented with intraventricular compartments related to ventriculoperitoneal shunts often require multiple and repeated operations. these patients usually necessitate either traditional shunt revisions alone or in combination with other procedures like insertion of multiple perforated catheter, craniotomy with transcallosal fenestration, stereotactic aspiration, endoscopic cyst fenestration, septostomy, foraminoplasty or third ventriculostomy [18, 20]. recent advancement of neuroendoscopy and the higher incidence of complication associated with traditional shunt revision or open craniotomy have shifted many neurosurgeons to the different endoscopic techniques as simple and minimal invasive alternatives to solve this complex condition [9]. patients and methods from february 2015 to february 2018, forty-four consecutive paediatric cases presented with shunt related cystic compartments and a preexisting ventriculoperitoneal shunts were operated at “neurosurgical department of mansoura university hospitals” by a single surgeon using neuroendoscopic techniques. our study included 28 boys and 16 girls; their ages ranged from two months to seven years (mean 3.2 years). the follow up period renged from (2-49 months) with the mean of 12.3 months. cases of multiloculated hydrocephalus or uniloculated hydrocephalus without previous shunt insertion were excluded from our study. tumour related cysts were also excluded. we retrospectively reviewed the patient's data retrieved from the patient charts which included: patient history, clinical examination, radiological investigations, operative data, patient outcome, shunt independency, the need for additional shunts and the prerequisites to repeat endoscopic procedures. plain x-ray to the shunt system, ct scan and mri brain with or without gadolinium were done to all patients preoperatively. csf sample was obtained and examined to exclude csf or shunt infection prior to endoscopic procedures. endoscopic surgery was indicated when the patients had clinical deterioration in the form of progressive enlargement of head size, development of manifestations of intracranial hypertension, worsening of the focal neurological deficits, gait disturbance or refractory epilepsy. the previous clinical manifestations had been correlated with radiological signs of the cyst enlargement and/or shunt malfunctioning. cognitive dysfunction was not 193 endoscopic management of intraventricular shunt-related cystic compartment in paediatric patients considered as an indication for surgical management. our aim of endoscopic surgery was to connect the isolated compartment to the ventricular cavity in order to drain both of them by the same shunt in order to simply the pre-existing shunt device and to avoid implanting another device whenever possible. in all patients, surgery was done under general anaesthesia. the entry point was tailored individually in every case according to the cyst location and the location of the previous shunt entry point. a proper burr-hole location and the direct surgical corridor were the most critical points for proper cyst fenestration and shunt revision simultaneously. different angles rigid lens endoscopes (0o, 30o, 70o karl-storz rigid gaab system) were used. the endoscopic sheath has an outer diameter of 6 mm and working channel of 2 mm. after endoscopic introduction, continuous irrigation was essential for clear identification of key anatomical landmarks and proper visualization of cyst wall as well as the proximal end of the pre-existing ventricular catheter. initial cyst fenestration was performed in a thin, translucent and relatively a vascular segment of the cyst wall by the use of bipolar electrocoagulation. dilation and enlargement of the initial stoma was continued by with the aid of fogarty balloon catheter, punches, and sharp scissor to fashion a wide stoma that secure a free csf passage and minimize the incidence of reclosure of the stoma. coagulation and devascularization of the cyst wall were done in order shrink the cyst wall and hold the cyst growth. other endoscopic procedures like endoscopic revision of the shunt, septum pellucidotomy, foramioplasty and third ventriculostomy were done in combination with endoscopic cyst fenestration to advance the communication of csf isolated compartments. any bleeding point was secured with continuous irrigation, bipolar electrocoagulation and tamponading with embolectomy balloon catheter to achieve a non-vascular surgical field as well as the site of fenestration. at the end of the surgery, the endoscopic sheath was retrieved under continuous irrigation to clear out the surgical field from any blood clots or any surgical debris. clinical outcome was defined as improved, unchanged or worsened. developmental delay was not considered in post-operative clinical outcome assessment. epilepsy was defined to be improved if the attacks were controlled after withdrawal or even reduction of the dose of antiepileptic drugs. if the head circumference remained stable or slightly reduced in size, this was considered as a postoperative sign of improvement. routine postoperative ct brain was done to all patients twenty-four hours after surgery. follow up ct and mri brain were done routinely 3 months after surgery. the procedure was considered to be successful when endoscopic procedure was able to restore the continuity between the cyst and the ventricular system cavity without the need to insert additional shunt devices. repeated endoscopic procedures were considered when the patient experienced recurrence or progression of his clinical manifestations that were concomitant with progressive cyst and/or ventricular enlargement on follow up ct and/or mri images. results progressive enlargement of the head size was the most common presenting symptom in our patients (28 cases, 63.6%) followed by seizures (14 cases, 31.8%), headache (10 cases, 22.72%), focal neurological deficits (10 cases, 22.72%) and gait disturbance in 6 patients (13.6%) (table 1). the non-colloidal neuroepithelial cysts were the most prominent underlying cause of intraventricular unilateral compartments with preexisting shunts in our study (twenty cases, 45.5%) while uniloculated cysts related to either previous shunt insertion or shunt infection represented the second most common cause (twelve cases, 27.3%) followed by meningitis (eight cases,18.2%) and neonatal intraventricular haemorrhage (four cases, 9%) (table 2) . endoscopic fenestration of cyst wall was done in all patients. other additional endoscopic procedures that were required to be done simultaneously with the endoscopic cyst fenestration included either endoscopic third ventriculostomy (six patients), septum pellucidotomy (ten patients) or foraminoplasty (six patients). during the previous endoscopic procedures, shunt revisions were indicated in only six patients (33%) who had non-colloidal neuroepithelial cysts whenever 20 out of 24 patients (83%) of shunt related cysts, postmeningitic cysts and post 194 ahmed zaher, amr farid khalil, mohamed state et al. haemorrhagic cysts required endoscopic shunt revisions. throughout the follow up periods, the previous endoscopic procedures were successful to restore the connection between the isolated compartments and the ventricular system cavities in 36 patients (81.8%). simplification of the previous shunt systems were achieved in 28 patients (63.6%) who required only a single device, while eight patients needed additional shunt system, the remaining eight cases (18.2%) became shunt independent after previous endoscopic procedures and shunt removal (table 2). fourteen repeated endoscopic procedure were done in 10 patients for either reopening of the stoma in ten procedures or shunt revisions in the remaining other procedures. (2 cases due to gliosis and 2 due to depris). finally, eight (18.2%) patients required additional shunt insertion after failure of restoration of a proper connection between the isolated compartments and the ventricular system cavities with failure of a single shunt to drain the dilated cavities. as regard clinical outcome, most patients n=28 (63.6%) presented with progressive head enlargement showed either stabilization or slight reduction in their head size. headache was improved in eight patients from 10 patients (80%) with only two patients sustained to complain of headache after successful fenestration. ten from 14 patients (72%) presented with epilepsy achieved clinical improvement by either absence of their epilptogenic attacks after withdrawal of antiepileptic treatment or reduction of the doses of their treatment regimens, whenever two patients (14.2%) remain dependent on the same drug regimen and another two patients required addition of another antiepileptic drug to control his seizures. we had no mortalities among our patients whenever the procedure related morbidities were minimal including two of csf leakage, two cases of superficial wound infection and four cases of subdural fluid collection. table 1. clinical presentation and postoperative clinical outcome. clinical presentation no. (%) clinical outcome improved stable worsening head enlargement 28 (63.6%) 14 (50%) 12 (43%) 2 (7%) seizures 14 (31.8%) 10 (72%) 2 (14%) 2 (14%) headache 10 (22.7%) 8 (80%) 2 (2%) 0 focal neurological deficit 10 (22.7%) 6 (60%) 4 (40%) 0 gait disturbance 6 (13.6%) 4 (66.7%) 2 (33.3%) 0 table 2. number of required shunts and repeated endoscopic procedures in relation to different etiologies. etiology no. of patients no. of required shunt repeated endoscopic procedures no shunt one shunt additional shunt neuroepithelial cyst 20 6 14 0 0 shunt related cysts 12 2 10 0 2 meningitis 8 0 2 6 8 195 endoscopic management of intraventricular shunt-related cystic compartment in paediatric patients table 3. repeated endoscopic procedure in ten patients. type of the procedure no. % closed fenestration 10 71.4 shunt revision 4 28.6 gliosis 2 14.3 obstruction form debris 2 14.3 figure 1. a-l: radiological and intraoperative endoscopic photographs of a case of shunt related cyst. a) preoperative ct. b) ct after insertion of a shunt. c) three months follow up ct after shunt insertion with development of shunt related cyst. d) ct after intraventricular age 4 0 2 2 4 total no. and % 44 (100%) 8 (18%) 28 (64%) 8 (18%) 14 (24%) 196 ahmed zaher, amr farid khalil, mohamed state et al. endoscopic fenestration and shunt revision with improvement of hydrocephalus e) endoscopic view of the cyst wall. f) opening of the cyst. g) coagulation and shrinkage of the wall of the cyst. h) fenestrated cyst with adherent shunt. i) shunt adherent to the inner cyst wall. j) occlusion of the shunt perforations by proliferation of the cyst wall. k) sharp dissection of the shunt from the adherent cyst. l) endoscopic view after shunt revision and cyst perforation. (e) (f) (g) (h) figure 2. a-f: radiological and endoscopic photographs of a case of post-haemorrhagic hydrocephalus. a) preoperative ct. b) ct after insertion of the shunt with early formation of a cyst. c) ct after three months with progressive cyst enlargement. d) t2-mri after cyst fenestration with good communication. e) endoscopic view of thick cyst wall. f) bipolar perforation of the cyst wall. g) sharp dilatation of the stoma. h) endoscopic view of the shunt within the ventricle through the performed stoma. discussion uniloculated intraventricular discrete csf filled compartment has been defined as a particular diagnostic entity by cushing since he reported his first case of intraventricular unilocular compartment [1]. subsequently salmon in 1970 reported five cases of uniloculated hydrocephalus [17]. non-colloidal neuroepithelial cysts are the most common underlying etiological causes for uniloculated hydrocephalus which may lead to obstruction of normal ventricular pathways with subsequent cystic dilation of one segment of the ventricular system, e.g. foramen of monro or aqueduct and formation of uniloculated compartment. excess csf drainage via previously inserted ventricular catheters within a previously communicating ventricular system can cause ventricular morphological changes and possibly leads to isolation of ventricular compartments. moreover, csf over drainage might result in unilateral ventricular collapses or obstruction of foramen of monro or aqueduct [4, 7]. failure of the previous shunt may result from collapse of the isolated compartment around the tip of the catheter with subsequent obliteration of ventricular catheter fenestrations by reactive proliferation of fibrillary astrocytes [12]. although the pathogenesis of univentricular 197 endoscopic management of intraventricular shunt-related cystic compartment in paediatric patients loculation is not well known but the most accepted theory is that the inflammatory reaction related to previous shunt insertion, infection and intraventricular hemorrhage are the triggering factors for subendymal gliosis that may enhance the formation of glial tufts which occlude the holes of the ventricular system and act as a nidus for ventricular septations [11, 18]. regardless of the accurate mechanism, the problem progress steadily toward greater complexity with time and traditional treatment ultimately require repeated surgeries with increasingly complex shunt devices [1]. the synonyms and classification of complex hydrocephalus are still interchangeable and unclear in the literatures. spennato et al. published a classification for variable types of ventricular loculation defined by the location and number of compartments [19]. according to the previous proposed scheme "uniloculated" and "multiloculated" are broadly defined based on anatomical factors only [1]. these categories should be further subdivided into physiologically simple or physiologically complex based on whether csf absorption is normal or impaired [2]. differentiation between the previous entities is of great importence as their pathogenesis, surgical outcome and prognosis are quite different [6]. the clinical features of loculated hydrocephalus are not specific and are difficult to recognize because they often arise in a neurologically compromised infant or child with a previous history of hydrocephalus, neonatal meningitis or intraventricular haemorrhage. in our study the progressive head enlargement was the most common presenting symptom in 28 cases (63.6%) followed by seizures in 14 cases (31.8%) headache in 10 cases (22.7%), focal neurological deficit in 10 cases (22.7%) and gait disturbance in 6 cases (13.6%). intraventricular loculation with previous ventriculoperitoneal shunt is a complex disorder that is difficult to treat. those patients usually require repeated shunt revisions. furthermore, those patients may need division and lysis of intraventricular septations either surgically through transcallosal craniotomy or through endoscopic techniques [13, 16]. the best advantages of the endoscopic procedures over transcallosal craniotomy are limited invasiveness and short postoperative recovery time. nowadays the recent technical improvement in endoscopic techniques and high morbidity associated with multiple shunt revision or transcallosal craniotomy has shifted neurosurgeon toward the minimally invasive endoscopic techniques for lysis of intraventricular septae simultaneously with endoscopic shunt revisions [5]. our objective in management of a single intraventricular loculation in a previously shunted patient was to restore the continuity between the isolated compartment and the ventricular system cavity to create a single cavity with the intent of simplifying or removal of the previous shunt system and reducing the need for repeated procedure. the proposed goal has been achieved in thirty-six patients (81.8%) with simplification of the previous shunts in 28 patients (63.6%); out of them eight patients (18.2%) became shunt independent after endoscopic cyst fenestration and additional endoscopic foraminoplasty, septum pellucidotomy or third ventriculostomy. shunt malfunctioning was found in most cases of our series (34 cases, 77%) due to either collapse and adhesive scarring of the cyst around the catheter tip or occlusion of the catheter perforations by debris or proliferating epithelial tufts. we used bipolar coagulation for safe dissection of the catheter tip from the adherent collapsed cyst wall to avoid catastrophic intraventricular bleeding which may happen in absence of endoscopic control. in his series of 31 pediatric patients with uniloculated hydrocephalus, el-ghandour treated 9 cases of uniloculated hydrocephalus with preexisting shunt system demonstrating reduction of shunt revision rate from 2.7 per year before fenestration to 0.25 per year after fenestration with simplification of four previous complex shunt systems and all patients required single repeated endoscopic procedures [6]. lewis et al. reported 34 cases of both multiloculated and uniloculated hydrocephalus and shunt revision rate dropped from 3.04% prior to endoscopy to 0.25 after the procedure and 50% of the patients shunted prior to endoscopy required repeat endoscopic procedures [12]. in our series 90 revisions were required in 32 patients prior to endoscopy with shunt revision rate was 2.98/year which have been reduced to 0.27 after endoscopic fenestration as only four patients required endoscopic shunt revision. ten patients (22.7%) of our series required fourteen repeated endoscopic procedure for opening of a closed 198 ahmed zaher, amr farid khalil, mohamed state et al. fenestrae or endoscopic shunt revision. the explanation of small percentage of repeated endoscopic procedure, in our cases compared by previously mentioned series is that we have 20 cases of neuroepithelial cysts presented to us with malfunctioning shunts and none of them required to repeat surgery. moreover, we have only 12 cases of post meningitis and post haemorrhagic uniloculated hydrocephalus in which 8 cases required 12 repeated endoscopic surgery and only two patients with shunt related cysts had a single repeated endoscopic surgery during repeated endoscopic procedures, ten cysts required reopening of closed stoma and four ventricular catheters required reopening of the closed stoma either due to gliosis in two cases or obstruction of the catheter openings by a debris in the other cases. ultimately, eight patients (18.2%) "six with post-meningitis loculations and two with post-haemorrhagic loculations" required insertion of additional ventricular catheters after failure of repeated endoscopic procedures to achieve proper communication with persistent undrained intraventricular loculated compartments. in the context with the experience of other endoscopic surgeons, we found that sharp dissection, employment of wide fenestrations of at least one cm and coagulation of the cysts wall ensured the success of the procedure and reduced the chance of recurrence [10, 15]. previous series of endoscopic fenestration of loculated hydrocephalus highlighted the combination of endoscopic procedures to achieve better success and moreover may help shunt independence [6, 20].the obvious advantages of leaving one shunt in complex hydrocephalus are fewer opportunities for obstruction, rupture, infection and gliosis [3]. septum pellucidotomy, foraminoplasty and third ventriculostomy were employed in our cases in combination with endoscopic cyst fenestration and shunt revision that have been succeed to achieve simplification of the previous shunt systems in (63.6%) and elimination of shunt dependency in eight patients (18%). the immaturity and deficient absorptive capabilities of scared subarachnoid space by a previous inflammatory process may be responsible for the lower shunt independent incidence in our study in line with others series [2, 12]. nida and haines who advocate transcallosal craniotomy for division and lysis of intraventricular septation criticized the endoscopic approaches by their limited ability to control intraoperative bleeding which may obscure the operative field [13]. however, intraoperative haemorrhage presented no great problem and did not result in termination of any procedure in this series. haemorrhage was controlled by continuous irrigation with warm lactated ringer solution and occasionally monopolar and bipolar coagulation were helpful to control any bleeding point. moreover, proper coagulation of site of fenestration may help to minimize the incidence of intraoperative bleeding. as regard clinical outcome 28 patients (63.6%) who presented with head enlargement had stabilization or decline in their head circumference. epilepsy was controlled in ten patients (72%) out of fourteen patients presented with seizures. focal neurological deficient was improved in six patients (60%) and gait disturbance was improved in four patients (67%). development delay was excluded from postoperative assessment as developmental improvement is not correlated with the change of the cyst size. our results are going with the previous series which assessed the postoperative clinical outcome, in addition to radiological improvement of hydrocephalus [6]. our morbid complications were minimal and reversible including csf leakage in two cases which stopped within few days after medical therapy, four cases of subdural hygroma that resolved spontaneously during follow up and only two cases of superficial wound infection which improved with antibiotic and repeated dressing. conclusion intraventricular loculations in previously shunted patients is among the most challenging scenarios encountered by a neurosurgeon. this complex disorder has a relatively evolving course in the form of ongoing worsening with time that requires increasingly difficult surgical procedures. the main objective in management of such cases is to reduce the number of surgical procedures more than improving the quality of life of the patient. endoscopic surgical techniques are attractive minimal invasive alternatives that may help to achieve treatment objectives with minimal postoperative morbidity. 199 endoscopic management of intraventricular shunt-related cystic compartment in paediatric patients authors contributions this work was carried out in collaboration between all authors. author amr farid, designed the study, author mohamed state wrote the protocol, author ahmed zaher managed the literature research, author hatem badr revised the final manuscript. all surgical procedures were carried out by single surgeon and assisted by the same surgical team including the four authors. all authors read and approved the final manuscript. references 1. akbari s h a, holekamp t f, murphy t m, mercer d, leonard j r, smyth m d, park t, and limbrick d d: surgical management of complex multiloculated hydrocephalus in infants and children. child's nervous system 2015, 31(2), 243-249. 2. andresen m and juhler m: multiloculated hydrocephalus: a review of current problems in classification and treatment. child's nervous system 2012, 28(3), 357-362. 3. cipri s, gambardella g, and gangemi m: neuroendoscopic approach to complex hydrocephalus: personal experience and preliminary report. journal of neurosurgical sciences 2001, 45(2), 92. 4. cushing h: surgery of the head. surgery: its principles and practice 1908, 3, 255-256. 5. el-ghandour n m: endoscopic cyst fenestration in the treatment of multiloculated hydrocephalus in children. journal of neurosurgery: pediatrics 2008, 1(3), 217-222. 6. el-ghandour n m: endoscopic cyst fenestration in the treatment of uniloculated hydrocephalus in children. journal of neurosurgery: pediatrics 2013, 11(4), 402-409. 7. eller t w and pasternak j f: isolated ventricles following intraventricular hemorrhage. journal of neurosurgery 1985, 62(3), 357-362. 8. gangemi m, maiuri f, donati p, and sigona l: neuroendoscopy: personal experience, indications and limits. journal of neurosurgical sciences 1998, 42(1), 1. 9. greenfield j p and souweidane m m: endoscopic management of intracranial cysts. neurosurgical focus 2005, 19(6), 1-9. 10. heilman c b and cohen a r: endoscopic ventricular fenestration using a “saline torch”. journal of neurosurgery 1991, 74(2), 224-229. 11. jamjoom a, mohammed a, al-boukai a, jamjoom z, rahman n, and jamjoom h: multiloculated hydrocephalus related to cerebrospinal fluid shunt infection. acta neurochirurgica 1996, 138(6), 714-719. 12. lewis a i, keiper g l, and crone k r: endoscopic treatment of loculated hydrocephalus. journal of neurosurgery 1995, 82(5), 780-785. 13. nida t y and haines s j: multiloculated hydrocephalus: craniotomy and fenestration of intraventricular septations. journal of neurosurgery 1993, 78(1), 70-76. 14. oi s and abbott r: loculated ventricles and isolated compartments in hydrocephalus: their pathophysiology and the efficacy of neuroendoscopic surgery. neurosurgery clinics of north america 2004, 15(1), 77-87. 15. oi s, hidaka m, honda y, togo k, shinoda m, shimoda m, tsugane r, and sato o: neuroendoscopic surgery for specific forms of hydrocephalus. child's nervous system 1999, 15(1), 56-68. 16. powers s; fenestration of intraventricular cysts using a flexible, steerable endoscope, in minimally invasive neurosurgery i. 1992, springer. p. 42-46. 17. salmon j h: isolated unilateral hydrocephalus following ventriculoatrial shunt. journal of neurosurgery 1970, 32(2), 219-226. 18. schulz m, bohner g, knaus h, haberl h, and thomale u-w: navigated endoscopic surgery for multiloculated hydrocephalus in children. journal of neurosurgery: pediatrics 2010, 5(5), 434-442. 19. spennato p, cinalli g, ruggiero c, aliberti f, trischitta v, cianciulli e, and maggi g: neuroendoscopic treatment of multiloculated hydrocephalus in children. journal of neurosurgery: pediatrics 2007, 106(1), 29-35. 20. teo c, kadrian d, and hayhurst c: endoscopic management of complex hydrocephalus. world neurosurgery 2013, 79(2), s21. e1-s21. e7. romanian neurosurgery (2019) xxxiii (2): pp. 150-155 doi: 10.33962/roneuro-2019-028 www.journals.lapub.co.uk/index.php/roneurosurgery hydatid cyst of the quadrigeminal cistern. a case report for unusual location with literature review saif saood abdelrazaq1, abdullah h. al ramadan2, ali adnan dolachee3, mohammed maan abdulazeez4, ali saud abdulrazzaq5, amar saeed rashid6, samer s. hoz5 1 neurosurgery department, al sadar teaching hospital, najaf, iraq 2 department of neurosurgery, king faisal specialist hospital and research centre, riyadh, saudi arabia 3 department of neurosurgery, college of medicine, al qadisiyah university, iraq 4 college of medicine, university of baghdad, baghdad, iraq 5 neurosurgery department, neurosurgery teaching hospital, baghdad, iraq 6 department of neurosurgery, college of medicine, kufa university, baghdad, iraq abstract intracranial hydatid cyst involves supratentorial area and mainly affecting the middle cerebral artery territory with the predilection of the partial lobe. it can be single which is the most common or multiple up to 35 cysts. they tend to be huge at the time of symptomatic presentation especially when they are presented as a solitary lesion with a slow growth rate around 1.5 cm/year, however, it is variable and it can be up to 10 cm/year. surgical treatment is mandatory for all patients once the correct diagnosis is made, except for patients with multiple organ involvement in poor general conditions and deep-located cysts. the existence of hydatidosis in the cisternal spaces must not be neglected given the capacity of e. granulosus larvae to disseminate via the csf. in this case report; two and half years’ male child presented with a history of 2 attacks of generalized seizure for the last 72 hours with the head circumference at the upper normal limit for his age. this paper presents the first case report demonstrating a primary single hydatid cyst located in the quadrigeminal cistern in a child. we concluded that in spite of the feasibility of the imaging and the high suspension of cerebral hydatid cyst, still, the reports show more locations which can be described as unusual although for a head to toe suspected distribution of hydatid disease is already understood. an eminent medical and surgical (if indicated) treatment of the primary cerebral hydatid cyst are always effective and recommended. introduction choroid echinococcosis could be characterized as a zoonotic infestation caused by cestode species of the genus echinococcus (1). keywords neurosurgery, hydatid, quadrigeminal cistern, case report corresponding author: mohammed maan abdulazeez college of medicine, university of baghdad, baghdad university, iraq mohammed.wwt@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 151 hydatid cyst of the quadrigeminal cistern it is most commonly involving the liver then lungs. (2) intracranial involvement occurs in 1-2% of echinococcosis and 50-70% of these cases affect the paediatric age group. (3) it showed slightly male preference in most of the case series. (4,5,6,7,8) geographically endemic area of hydatid disease includes some of south america countries like argentina, brazil, chile, peru and uruguay, france, italy and greece in europe, turkey, israel, lebanon, syria and jordan in the middle east, china, iran, and india in southeast asia and tunisia in africa. (9) intracranial hydatid cyst involves supratentorial area and mainly affecting the middle cerebral artery territory with the predilection of the partial lobe. it can be single which is the most common or multiple up to 35 cysts. (10,11,12) they tend to be huge at the time of symptomatic presentation especially when they are presented as a solitary lesion with a slow growth rate around 1.5 cm/year, however, it is variable and it can be up to 10 cm/year. (13) surgical treatment is mandatory for all patients once the correct diagnosis is made, except for patients with multiple organ involvement in poor general conditions and deep-located cysts. (14) the existence of hydatidosis in the cisternal spaces must not be neglected given the capacity of e. granulosus larvae to disseminate via the csf. (15) this paper presents the first case report demonstrating a primary single hydatid cyst located in the quadrigeminal cistern in a child. case scenario two and half years’ male child presented with history of 2 attacks of generalized seizure for the last 72 hours with head circumference at the upper normal limit for his age. initial lab workup was done to exclude metabolic derangements the patient was sent for neuroimaging. the general lab tests were within normal ranges and the brain mri showed a midline rounded cystic lesion, 5x3 cm in size, located in extraaxially in the quadrigeminal cistern and extend infratentorially to compress the cerebellum downward along with bilateral dilated lateral ventricles (figure 1). figure 1. pre-operative brain mri showing a midline rounded cystic lesion, 5x3 cm in size, located in extra-axially in the quadrigeminal cistern and extend infratentorially to compress the cerebellum downward along with bilateral dilated lateral ventricles. the lesion was hypointense and homogenous in t1 with intensity higher than csf, hyper-intense in t2 and showed no enhancement in contrasted image, also there was some vivid inclusions within the upper part of the cyst. figure 2. the delivered intact hydatid cyst. 152 mohammed maan abdulazeez, ali adnan dolachee, saif saood abdelrazaq et al. the lesion was hypo-intense and homogenous in the t1 sequence of the mri with intensity higher than the csf, hyperintense in the t2, and showed no enhancement in the contrasted image, also there were some vivid inclusions within the upper part of the cyst. at that point, the top differential diagnosis included were epidermoid, dermoid and arachnoid cysts only, because that location was an unusual location for a hydatid cyst and the age of the patient was too young for a hydatid cyst. the decision was to do a surgical resection or fenestration according to the intra-operative findings. we planned to delay the csf shunting option as the sulci were not effaced, the young age of the patient and the surgery would remove the cause of the obstruction of the csf pathways. the surgery conducted at the next day, an intratentorial supra-cerebellar approach was done via midline occipital craniotomy. the cyst was a typical hydatid cyst. the cyst resected as one piece via initial dissection and then delivered using dowling’s hydrodissection technique (figure 2,3). the postoperative course went uneventfully. the histopathology confirms the diagnosis, further workup excluded other organs involvement. figure 3. early postoperative axial brain ct scan showing resection cavity table 1. intracranial cisternal hydatid cysts: case report in english literature no. authors age/gender complain diameter location treatment 1 rumboldt et al (27) 50 year/ male headache 30 mm premedullary cisten surgery 2 beskonakli et al (28) 33 year/ male headache and impair vision n/a interpeduncular cistern surgery 3 sanli et al (29) 7 year/ male symptoms of high intracranial pressure 25 x 25 mm ambient cistern surgery 4 kizilca et al (37) 45 year/ female symptoms of high intracranial pressure n/a premedullary cisten surgery 5 the authors of this case report 2.5 year/ male seizure 50 x 30 mm quadrigeminal cistern surgery 153 hydatid cyst of the quadrigeminal cistern discussion variant locations of hydatid cyst were reported in the literature including aqueduct of sylvius (16), frontal lobe associated with massive edema and raise in the intracranial pressure (17), temporal lobe with midbrain herniation. (18) thalamic hydatid cyst was managed surgically through the transcallosal approach in a child who presented with left-sided weakness. (19) an interosseous lesion involving the skull estimated to represent 3-4% of the lesion involving the skeleton which evident in 2% of all hydatid cyst. (20) spinal hydatid cysts are estimated at less than 1%, they are usually extradural and tend to rupture intraoperative more than other location. (21) meckel’s cave can be involved with extension to the cerebellopontine angle and the middle fossa. (22) brainstem hydatid cyst was reported in middle age woman presented with a headache and progressive hemiparesis. (23) both cases of meckel’s cave and brainstem hydatid cysts were treated with decompression first prior to the removal to decrease the chances of intraoperative rupture. (22,23) cerebellar lesion with mass effect causing obstructive hydrocephalus was encountered in a child with a progressive headache followed by signs and symptoms of high intracranial pressure. (24) intraventricular involvement was estimated between 1.3 16.6% of multiple case series for intracranial hydatid disease with overall good outcome after surgical excision. (25) other unusual locations include the seller and the para-sellar regions were reported. (26) cisternal hydatid cysts were reported to involve the pre-medullary, the interpeduncular and the ambient cisterns. (27,28,29) (table 1) an intermittent headache can be the only presenting symptoms even with a huge cyst. (30) in a large series from china, headache and vomiting were the most common symptoms, this finding was supported in the literature as well. seizure attacks, focal neurological deficits, and skull deformities were reported. papilledema was frequent in the ophthalmological examination especially in patients with high intracranial pressure, optic atrophy was seen as well. (4,31,32) the magnetic resonance imaging (mri) thought to be more sensitive than the computed tomography (ct) to identify the pericystic layer and to differentiated the hydatid cyst from the other similar cystic lesions like the epidermoid cyst, however, ct scan is more sensitive to identify the calcified lesions. (33) serious complications related to the rupture of the hydatid cyst include recurrence, cerebral vasospasm and infarction, hydrocephalus, anaphylactic shock, chemical meningitis, and even death. (34) in two series of long-term follow up for cerebral hydatidosis in children, it can be concluded that the improvements of the imaging facilities lead to early recognition and improve the outcome. poor prognostic factors can be identified including delay in the treatment, the rupture of the cyst at the presentation or intraoperatively, and poor control of the systemic disease. single versus multiple cyst and age at the presentation was not identified as prognostic factors, however, some authors consider the multiplicity as a malignant form of the disease. (35,36) review of all the available literature reveals that our case is the first reported case of hydatid cyst located in the quadrigeminal cistern which was removed successfully. conclusion in spite of the feasibility of the imaging and the high suspension of cerebral hydatid cyst, still, the reports show more locations which can be described as unusual although for a head to toe suspected distribution of hydatid disease is already understood. an eminent medical and surgical (if indicated) treatment of the primary cerebral hydatid cyst are always effective and recommended. abbreviations ct: computed tomography mri: magnetic resonance imaging csf: cerebrospinal fluid references 1. eckert j, deplazes p. biological, epidemiological, and clinical aspects of echinococcosis, a zoonosis of increasing concern. clin microbiol rev. 2004 jan;17(1):107-35. review. pubmed pmid: 14726458; pubmed central pmcid: pmc321468. 2. madeo j, zheng x, ahmed s, ramos de oleo r. primary cerebral echinococcosis presenting as long-standing generalized weakness. germs. 2013 jun 1;3(2):63-6. doi: 10.11599/germs.2013.1038. ecollection 2013 jun 1. 154 mohammed maan abdulazeez, ali adnan dolachee, saif saood abdelrazaq et al. pubmed pmid: 24432288; pubmed central pmcid: pmc3882828. 3. erşahin y, mutluer s, güzelbağ e. intracranial hydatid cysts in children. neurosurgery. 1993 aug; 33(2): 219-24; discussion 224-5. pubmed pmid: 8367043. 4. turgut m. intracranial hydatidosis in turkey: its clinical presentation, diagnostic studies, surgical management, and outcome. a review of 276 cases. neurosurg rev. 2001 dec;24(4):200-8. review. pubmed pmid: 11778827. 5. khaldi m, mohamed s, kallel j, khouja n. brain hydatidosis: report on 117 cases. childs nerv syst. 2000 nov;16(1011):765-9. pubmed pmid: 11151730. 6. kocaman s, ersahin y, mutluer s. cerebral hydatid cysts in children. j neurosci nurs. 1999 oct;31(5):270-7. pubmed pmid: 10633303. 7. duishanbai s, jiafu d, guo h, liu c, liu b, aishalong m, mijiti m, wen h. intracranial hydatid cyst in children: report of 30 cases. childs nerv syst. 2010 jun;26(6):821-7. doi: 10.1007/s00381-009-1008-2. epub 2009 dec 16. pubmed pmid: 20013283. 8. limaiem f, bellil s, bellil k, chelly i, mekni a, khaldi m, haouet s, zitouna m, kchir n. primary hydatidosis of the central nervous system: a retrospective study of 39 tunisian cases. clin neurol neurosurg. 2010 jan;112(1):238. doi: 10.1016/j.clineuro.2009.09.001. epub 2009 sep 24. pubmed pmid: 19781849. 9. nourbakhsh a, vannemreddy p, minagar a, toledo eg, palacios e, nanda a. hydatid disease of the central nervous system: a review of literature with an emphasis on latin american countries. neurol res. 2010 apr;32(3):245-51. doi 10.1179/016164110x12644252260673. review. pubmed pmid: 20406602. 10. ali m, mahmood k, khan p. hydatid cysts of the brain. j ayub med coll abbottabad. 2009 jul-sep;21(3):152-4. pubmed pmid: 20929036. 11. sen n, laha d, gangopadhyay pk, mohanty bc. young girl with multiple intracranial hydatid cyst. ann neurosci. 2012 apr;19(2):96-8. doi: 10.5214/ans.0972.7531.12190212. pubmed pmid: 25205976; pubmed central pmcid: pmc4117048. 12. binesh f, mehrabanian m, navabii h. primary brain hydatosis. bmj case rep. 2011 mar 8;2011. pii: bcr0620103099. doi: 10.1136/bcr.06.2010.3099. pubmed pmid: 22707660; pubmed central pmcid: pmc3063272. 13. thakur sh, joshi pc, kelkar ab, seth n. unusual presentation of hydatid cyst ruptured intraventricular hydatid. indian j radiol imaging. 2017 jul-sep;27(3):282-285. doi: 10.4103/ijri.ijri_70_16. pubmed pmid: 29089673; pubmed central pmcid: pmc5644318. 14. yurt a, avci m, selçuki m, ozer f, camlar m, uçar k, taşli f, altinörs n. multiple cerebral hydatid cysts. report of a case with 24 pieces. clin neurol neurosurg. 2007 nov; 109(9): 821-6. epub 2007 aug pubmed pmid: 17765392. 15. andronikou s, welman cj, kader e. classic and unusual appearances of hydatid disease in children. pediatr radiol. 2002 nov;32(11):817-28. epub 2002 aug 16. pubmed pmid: 12389111. 16. gökalp hz, erdoğan a. hydatid cyst of the aqueduct of sylvius. case report.clin neurol neurosurg. 1988;90(1):835. pubmed pmid: 3359737. 17. bahloul k, ouerchefani n, kammoun b, boudouara mz. unusual brain edema caused by an intracranial hydatid cyst: c ase report and literature review. neurochirurgie. 2009 feb;55(1):53-6. doi: 10.1016/j.neuchi.2008.03.008. epub 2008 jun 30. review. pubmed pmid: 18586282. 18. duransoy yk, mete m, barutçuoğlu m, unsal uü, selçuki m. intracranial hydatid cyst is a rare cause of midbrain herniation: a case report and literature review. j pediatr neurosci. 2013 sep 8(3): 224-7. doi: 10.4103/1817-1745. 123683. pubmed pmid: 24470819; pubmed central pmcid: pmc3888042. 19. erşahin y, mutluer s, dermirtaş e, yurtseven t. a case of thalamic hydatid cyst. clin neurol neurosurg. 1995 nov; 97 (4): 321-3. pubmed pmid: 8599900. 20. erman t, tuna m, göçer i, ildan f, zeren m, cetinalp e. intracranial intraosseous hydatid cyst. case report and review of literature. neurosurg focus.2001 jul 15;11(1): ecp1. review. pubmed pmid: 16724818. 21. luo k, luo dh, zhang tr, wen h. primary intracranial and spinal hydatidosis: a retrospective study of 21 cases. pathog glob health. 2013 mar;107(2):47-51. doi: 10.1179/2047773213y.0000000072. pubmed pmid: 23683 329; pubmed central pmcid: pmc4001477. 22. taghipour m, saffarrian a, ghaffarpasand f, azarpira n. dumbbell-shape hydatid cyst of meckel cave extending to cerebellopontine angle and middle fossa; surgical technique and outcome of rare case. world neurosurg. 2017 aug;104 :1049.e7-1049.e10. doi: 10.1016/j.wneu. 2017.05.091. epub 2017 may 25. pubmed pmid: 28552738. 23. muthusubramanian v, pande a, vasudevan mc, ravi r. surgical management of brainstem hydatid cyst--an unusual site. surg neurol. 2009 jan;71(1):103-6; discussion 106. doi: 10.1016/j.surneu.2007.06.077. epub 2008 feb 11. pubmed pmid: 18262629. 24. fakhouri f, ghajar a, mahli n, shoumal n. giant hydatid cyst in the posterior fossa of a child. asian j neurosurg. 2015 oct-dec;10(4):322-4. doi: 10.4103/1793-5482.162719. pubmed pmid: 26425166; pubmed central pmcid: pmc4558813. 25. guzel a, tatli m, maciaczyk j, altinors n. primary cerebral intraventricular hydatid cyst: a case report and review of the literature. j child neurol. 2008 may;23(5):585-8. doi: 10.1177/0883073807309791. epub 2008 jan 11. review. pubmed pmid: 18192651. 26. turgut m. hydatidosis of central nervous system and its coverings in the pediatric and adolescent age groups in turkey during the last century: a critical review of 137 cases. childs nerv syst. 2002 dec;18(12):670-83. epub 2002 oct 25. review. pubmed pmid: 12483350. 27. rumboldt z, jednacak h, talan-hranilović j, rumboldt t, kalousek m. unusual appearance of a cisternal hydatid cyst. ajnr am j neuroradiol. 2003 jan;24(1):112-4. pubmed pmid: 12533337 155 hydatid cyst of the quadrigeminal cistern 28. beskonakli e, solaroglu i, tun k, albayrak l. primary intracranial hydatid cyst in the interpeduncular cistern. acta neurochir (wien). 2005 jul;147(7):781-3; discussion 783. epub 2005 may 20. pubmed pmid: 15900396. 29. sanlı am, türkoğlu e, kertmen h, gürer b. hydatid cyst of the ambient cistern radiologically mimicking an arachnoid cyst. j neurosurg pediatr. 2012 sep;10(3):186-8. doi: 10.3171/2012.6. peds 11562. epub 2012 jul 13. pubmed pmid:22793161. 30. basarslan sk, gocmez c, kamasak k, ceviz a. the gigant primary cerebral hydatid cyst with no marked manifestation: a case report and review of literature. eur rev med pharmacol sci. 2015 apr;19(8): 1327-9. review. pubmed pmid: 25967703. 31. erşahin y, mutluer s, güzelbağ e. intracranial hydatid cysts in children. neurosurgery. 1993 aug;33(2): 219-24; discussion 224-5. pubmed pmid: 8367043. 32. duishanbai s, geng d, liu c, guo hr, hao yj, liu b, wang yx, luo k, zhou k, wen h; research group of hydatid diseases. treatment of intracranial hydatid cysts. chin med j (engl). 2011 sep;124 (18): 2954-8. pubmed pmid: 22040508. 33. tsitouridis j, dimitriadis as, kazana e. mr in cisternal hydatid cysts. ajnram j neuroradiol. 1997 sep;18(8): 15867. pubmed pmid: 9296204. 34. salunke p, patra dp, mukherjee kk. delayed cerebral vasospasm and systemic inflammatory response syndrome following intraoperative rupture of cerebral hydatid cyst. acta neurochir (wien). 2014 mar;156(3):6134. doi: 10.1007/s00701-013-1675-3. epub 2013 mar 10. pubmed pmid: 23474734. 35. lunardi p, missori p, di lorenzo n, fortuna a. cerebral hydatidosis in childhood: a retrospective survey with emphasis on long-term follow-up. neurosurgery. 1991 oct;29(4): 515-7; discussion 517-8. pubmed pmid: 1944831. 36. onal c, unal f, barlas o, izgi n, hepgul k, turantan mi, canbolat a, turker k, bayindir c, gokay hk, kaya u. longterm follow-up and results of thirty paediatric intracranial hydatid cysts: half a century of experience in the department of neurosurgery of the school of medicine at the university of istanbul (1952-2001). pediatr neurosurg. 2001 aug;35(2): 72-81. pubmed pmid: 11549917. 37. kızılca o, altaş m, senol u, oztek ma. hydatid disease located in the cerebellomedullary cistern. case rep med. 2014: 271365. doi: 10.1155/2014/271365. epub 2014 mar 24. pubmed pmid: 24782895; pubmed central pmcid: pmc3982244. doi: 10.33962/roneuro-2023-032 the first and foremost unilateral pallidothalamic tractotomy done in india for parkinson’s disease. an interesting case report sanjiv chamraj, shavan srinivasan romanian neurosurgery (2023) xxxvii (2): pp. 178-184 doi: 10.33962/roneuro-2023-032 www.journals.lapub.co.uk/index.php/roneurosurgery the first and foremost unilateral pallidothalamic tractotomy done in india for parkinson’s disease. an interesting case report sanjiv chamraj, shavan srinivasan department of neurology, jain institute of movement disorder and stereo toxic neurosurgery, bangalore, karnataka, india abstract background. pallidothalamic tractotomy” can be effective in parkinson’s disease by exhibiting anti-parkinsonian effects. case presentation. the patient was a 53 years old gentleman, having parkinson’s disease for the last 14 years. the disease onset was on the left side and slowly moved to the right side. he had tremors, slowness of body movements and stiffness of the movements. the first right pallidotomy was done in january 2019. there was a noticeable improvement in a few weeks. he continued to have symptoms on the right side. the preoperative unified parkinson disease rating scale (updrs) part 3 score in 2019 was 53 while the postoperative score was only 26 showing drastic improvement after right pallidotomy. after 2 years of the first surgery, a new technique called pallido thalamic tractotomy (ptt), an mri-guided stereotactic surgery was done on the left side. tremors reduced gradually by 99% in 3 weeks after surgery. this is the first case of ptt performed on a patient with parkinson’s disease in india. conclusion. ptt is an effective procedure in pd that acts by disconnecting the pallidothalamic tract. unilateral pallidothalamic tractotomy done on the left side improved contralateral side rigidity, tremors and bradykinesia. introduction parkinson's disease (pd) is a progressive neurodegenerative disorder primarily affecting the body's movements [1]. it is characterized by global slowing of body movements, known as bradykinesia, and other symptoms such as resting tremors and rigidity. james parkinson first described parkinson’s disease in 1817 [2,3]. initially, the term shaking palsy was used by medical writers like parkinson for parkinson’s disease [2]. it was further refined, characterized, and expanded by jean-martin charcot in the mid-1800s [3]. it affects, on average, one to two people per 1000 population at any time. pd is a multifactorial disease [4]. the etiology is unknown in the majority of the cases, with genetic and environmental risk factors also playing a role [4,5]. the prevalence increases with age affecting about keywords pallidothalamic tractotomy, pallidotomy, parkinson’s disease, tremor, unilateral corresponding author: sanjiv chamraj department of neurology, jain institute of movement disorder and stereo toxic neurosurgery, bangalore, karnataka, india sanjivchamraj@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2023 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 179 the first and foremost unilateral pallidothalamic tractotomy done in india for parkinson’s disease 1% of the population aged more than 60 years [6]. the prevalence of pd generally increases with an increase in age [7,8]. the incidence is higher in males in all age groups, with a significant difference in incidence between 60-69 and 70-79 years [8]. according to “the parkinson’s foundation prevalence project,” it was estimated that around 930,000 people in the united states would have pd by the year 2020, and it is expected to rise to 1.2 million by 2030 [9]. symptoms start gradually, sometimes starting with a barely noticeable tremor in just one hand. tremors are typical, but the disorder mainly causes stiffness or slowing of movement [1,4,10]. postural instability occurs with the progression of the disease. but, the detailed clinical course has not yet been elucidated [10]. the primary pathophysiology appears to be due to the accumulation of alpha-synuclein in various parts of the brain, primarily the substantia nigra, leading to degeneration and subsequent loss of dopamine in the basal ganglia that control muscle tone and movement [4,11]. parkinson’s disease is typically treated with medication. the medication usually works very well in the first few years of treatment, but it becomes less effective after some time. the best management then usually involves placing a pacemaker inside the brain by inserting electrodes and modulating the pacemaker’s frequency. it produces a result for the patient for the symptoms of the disease. it is known as deep brain stimulation surgery (dbs) [12]. but it is costly, especially considering the cost of the pacemaker. as known, there is no cure for parkinson’s disease at all. parkinson’s is a progressive degenerative disease that can only be treated by medicines to curb rapid growth or sustain tremors. it progresses faster in some and slow in some patients. all parkinson’s patients do not benefit from surgery. the pallidothalamic tract is a part of the basal ganglia. it connects the internal globus pallidus and thalamus (a ventrolateral portion of the thalamus). it is comprised of ansa lenticularis and fasciculus lenticularis [13]. both of them take their origin from the internal part of the pallidum. these tracts merge into the fasciculus thalamicus before entering the thalamus [13]. pallidothalamic fires of the ansa reticularis and fasciculus lenticularis are funneled into the thalamic fasciculus (h1 forel field) before reaching the thalamus. they join two to three millimeters below the intercommissural plane (h2 forel field). hence interruption of the pallidothalamic tract at the h1 level amounts to pallidotomy functionally because the major pallidal outputs go through it and can be achieved with smaller lesion size. ptt can be compared to a pallidotomy that is optimized, as it is capable of extensive liberation of the dynamics of the thalamocortical system by leaving intact thalamus using a very restricted ablation of the tissue. neurosurgical ablation of the pallidothalamic tract is called pallidothalamic tractotomy (ptt). it has been reported as an effective treatment for pd in a few studies by exhibiting anti-parkinsonian effects [14,15]. but there is a lack of literature in india regarding ptt. case presentation case description the patient was a 53 yrs old gentleman, having parkinson's disease for the last 14 yrs. it started with mild tremors in his left hand and progressed to some stiffness and difficulty moving the hand. he had tremors, slowness of body movements, and stiffness. over the next few years, it involved his entire body, with the left side more affected than the right side to the extent of losing his confidence in even walking or performing his daily activities. with this situation, he was unable to do his tailoring, which was his sole source of revenue for him and his family. he approached doctors, took treatment, and was put on regular medications. they were given since the disease started. an increase in the dosage of drugs did not alter the symptoms. it was started with two doses of levodopa and carbidopa and increased gradually. the medication included tablet levodopa and carbidopa 100/25 mg used four times a day, t.ropinorole 6mg per day, and t.trihexyphendyl 4mg per day. the patient was intolerant to drugs for further enhancement. his tremors would subside when he took medicines and aggravate once their effect was over, the medicines' so-called on and off period. he was suggested to undergo deep brain stimulation surgery (dbs). but it was not affordable for him. medical treatment was started at various places for nearly 12 years without full benefit. the patient had developed a side effect called druginduced dyskinesia (levodopa). he presented in 2018 – 2019 to a tertiary care institute with symptoms despite medications. levodopa (400 mg/day) was required to maintain daily activities. the 180 sanjiv chamraj, shavan srinivasan timeline of the clinical presentation and management is shown in figure 1. figure 1. t1 axial mri of the brain showing the first operation pallidotomy scar on the right side. first surgery (2019) the first right pallidotomy was done in january 2019. it was an mri-guided macro stem controlled, stereotactic right pallidotomy [16,17]. it was done on 2 postero ventral pallidum (pvp) tracks with 3 lesions each, using a 1x4 electrode at 70 degrees centigrade for 40 seconds. there was a noticeable improvement in a few weeks. tremors, stiffness, and slowness improved significantly on the left side. he continued to have symptoms on the right side. the preoperative unified parkinson disease rating scale (uprds) part 3 score in 2019 was 53, while the postoperative score was only 26 showing drastic improvement after right pallidotomy. the old pallidotomy scar on the right side can be seen in figure 2. figure 2. surgiplan software post-op mri, showing the precision of targeting with preop planned targets in green and the post-op lesion. green indicates pallidothalamotomy lesion in ptt lesion area. second surgery (2021) after 2 years of the first surgery, a new technique called pallido thalamic tractotomy (ptt), an mriguided stereotactic surgery was done on the left side [14,15,18,19]. on 7th july 2021, he underwent ptt surgery. there is a risk of dysphagia and dysarthria with bilateral pallidotomy, even if it is a staged pallidotomy. hence, we decided to use a white matter target the ptt or the pallido thalamic tract. this tract is just lateral to the mamillothalamic tract. it covers the czi/ psa area (including the fields of forel h1 & h2) [13]. these 2 references were based on the schaltenbrand-wahren atlas [20], and studies reported by aufenberg c et al. (2005) [19], and magara a et al. (2014) [21]. this is located just above the superior border of the stn, seen as low-intensity areas on t2 mri and the location where we usually get the best results in stn dbs. mri-guided, stereotactic, macro stem-controlled lesioning in ptt1 and ptt-2. one lesion each using 1x4 electrode, at 70 degrees centigrade for 40 secs. the pre-op targets fixed for ptt can be seen in figure 3. figure 3. surgiplan software post-op mri, showing the precision of targeting with pre-op planned targets in green and the post-op lesion. stereotactic mri is taken to mark the exact location with the help of special software to locate the target 181 the first and foremost unilateral pallidothalamic tractotomy done in india for parkinson’s disease circuit to be burnt. stereotaxic surgery or stereotactic surgery is a three-dimensional surgery technique [13,18,22]. it enables the detection of deep lesions in the tissues to be located and then treated using heat or cold, or chemicals. the procedure itself is so complicated. it is a procedure that involves fixing a particular frame called a stereotactic frame on the skull by drilling 4 screws [23]. a 14 mm hole is made in the skull. an electrode is inserted inside the brain. the correct location is tested by giving a mild current and burning the circuit at 70 degrees for 40 seconds with a radio frequency lesion generator. this procedure is called an mriguided stereotactic pallidotomy, which goes 9 to 11 cm deep inside the brain [16]. as soon as the lesioning was done, tremors came down gradually, and the hand became loose. rigidity, stiffness of their body both in his hand and leg improved gradually. within a few weeks, there was a decline in tremors, stiffness, and improvement in slowness significantly. tremors reduced gradually and significantly within 3 weeks after surgery as measured by the updrs scale. he had no memory or other intellectual brain issues. he can carry out day-to-day activities without any difficulties. ptt surgery on the left side resulted in a significant fall in the right side updrs off phase score from 25 in the preoperative period to 4 in the postoperative period. unilateral pallidothalamic tractotomy on the left side improved contralateral side rigidity, tremors, and bradykinesia. table 1. comparative table for total score of part 3 updrs (unified parkinson disease rating scale) year surgery done preoperative (or) postoperative updrs score 2019 right pallidotomy pre op 53 post op 26 2021 left pallidothalamic tractotomy pre op off phase 30 post op off phase 10 table 1 describes the updrs (unified parkinson disease rating scale) scores preoperatively and postoperatively after right pallidotomy in 2019 and left pallidothalamic tractotomy in 2021, respectively. the preoperative uprds part 3 score in 2019 was 53, while the postoperative score was only 26 showing drastic improvement after right pallidotomy. the preoperative uprds part 3 score in 2021 was 30, while the postoperative score was 10, thereby demonstrating significant clinical improvement after left pallidotomy tractotomy. there was no alteration in cognitive function before and after surgery. table 2 describes the comparison of right and left updrs scores preoperatively and postoperatively after left pallidothalamic tractotomy in 2021, respectively, in the off phase. the preoperative uprds score was 25 in the off phase in the right, while the postoperative score was only 4 showing drastic improvement after right pallidothalamic tractotomy in 2021. table 2. comparative table for right and left updrs scores before and after left pallidothalamic tractotomy done in 2021 pre-operative (or) post-operative right left pre op 2021 off phase off25 (on11) off-5 (on-4) post op – 2021 off phase off4 off-6 discussion the present case report describes a staged lesioning surgery with pallidotomy and ptt for treating parkinson’s diseases symptoms. it is the first time in india pallidothalamic tractotomy has been done to cure parkinson’s or any other movement related disorder. in other countries like the u.s. and japan, ptt has been used to manage parkinson’s disease and other movement disorders. stereotactic surgery has become popular in treating parkinson’s disease (pd) due to the long-term complications of levodopa therapy, causing significant disability.[24] surgery for parkinson’s disease has evolved from ablation with careful lesion placement in various brain structures to stimulating particular brain targets in the basal ganglia.[25] there has been a better understanding of the physiology and the circuit of basal ganglia in recent decades with the improvement of neuroimaging and surgical techniques. the first surgery we did in 2019 is called the pallidotomy, and the surgery done in the area of the brain is called gpi – globus pallidus interna. the second surgery is called the pallidothalamic tractotomy (ptt), where the surgery was an mriguided stereotactic surgery. 182 sanjiv chamraj, shavan srinivasan ptt is a part of the brain circuit that connects two nucleus globus pallidus and the thalamus deep inside the brain, which plays a vital role in the symptoms of parkinson’s disease. lesioning or burning a circuit inside the brain has been a standard of care treatment and has been there for around several decades [13,26,27]. burning this circuit can alleviate parkinson’s symptoms. the brain circuit connects two prominent nucleus in the brain. alteration of the activity due to the disease process causes parkinson’s symptoms on the opposite side. by burning this circuit pallido-thalamic tract (ptt), the symptoms of parkinson’s disease. this is the first case of ptt performed in a patient with parkinson’s disease in india. it has been reported as an effective treatment for pd in a few descriptive studies worldwide by exhibiting anti-parkinsonian effects [14,15]. our current approach, i.e., targeting the pallidal efferent fibers in the subthalamus as shown in figure 3, was proposed by meyers r [28]. then, pallidothalamic tractotomy was explicitly done for pd by aufenberg c et al.[19], godinho f and magnin m et al.[29] there was a drastic improvement in postoperative score after right pallidotomy in the present case. after 2 years of the first surgery, ptt surgery was done. the uprds off-phase preoperative score (in 2021) was 30, while the postoperative score was only 10 after ptt surgery. there was no alteration in cognitive function before and after surgery. ptt surgery is done on the left side, resulting in a significant fall in the right side updrs off phase score from 25 in the preoperative period to 4 in the postoperative period. horisawa s et al.[14] in 2019 presented the first single case report of ptt performed in a patient with parkinson's disease, with a follow-up of one year. their patient was a 68-year-old woman who had a similar presentation of pd in comparison with the present case. she started to experience the "wearing-off" phenomenon after 14 years of medical management. she also required levodopa (300 mg/day) to maintain daily activities similar to the present case. during the preoperative, she underwent ptt on the left side without any perioperative complications. on follow-up after 1 year, she had daily maintenance levodopa (200 mg) without an "off" condition all day. the 1-year updrs scores showed significant improvement, similar to the present case. they concluded that ptt might be useful in pd subjects who don’t desire device implantation. horisawa set al.[15] in 2021 studied unilateral pallidothalamic tractotomy for akinetic-rigid parkinson's disease in 14 patients. they observed that the total mds-updrs part iii score significantly improved from 45 ± 4.6 at baseline to 32.9 ± 4.8 at 12 months postoperatively (p = 0.005) in the 10 patients available for follow-up. they also observed, similar to our case, that contralateral side rigidity and bradykinesia significantly improved. they also observed no severe permanent neurological deficits similar to our study. horisawa s et al. [14] in 2019 presented the first single case report of ptt performed on a 68-year-old female patient with parkinson's disease, with a follow-up of one year on levodopa (300 mg/day) for maintaining daily activities. her preoperative unified dyskinesia rating scale (udysrs) and parkinson's disease questionnaire-39 (pdq-39) scores were 102 and 46, respectively. she underwent left-sided ptt, and no perioperative complications were observed. her udysrs and pdq-39 scores after one year of surgery were 20 and 20, respectively. ptt might be useful in patients who do not desire device implantation. gallay mn et al.[18] in 2021 did bilateral mr-guided focused ultrasound ptt for 10 patients suffering from chronic and therapyresistant pd. they were followed up for 1 year after the operation of the second side. they observed a reduction in total updrs score off-medication similar to the present case at 1 year after the second ptt by 52% compared to baseline on-medication (p < 0.007). they concluded that bilateral ptt effectively controls pd symptoms compared to medical management at its best. conclusions preliminary case reports across the globe have shown reasonably good outcomes. the present case report, the first of its kind in india, reports this procedure's effectiveness and safety. it was the first time in india, pallidothalamic tractotomy had been done to treat motor symptoms of parkinson’s or any other movement related disorder. it is also the first time in india, bi-lateral lesioning surgery for treating parkinson’s diseases symptoms has been done. this surgery will be a boon for patients with pd as it will improve their quality of life. the cost associated with this surgery is much less than the cost of pacemaker 183 the first and foremost unilateral pallidothalamic tractotomy done in india for parkinson’s disease implantation in the brain. this case report gives substantial evidence to support the need for future studies. larger scale interventional studies with randomization are required to make evidence-based recommendations. limitations being a single case report, the reliability of the present study findings is poor. there was also no control to compare the results. the data available from this study is not enough to advocate the use of ptt and it’s relatively low risk profile. lessons ptt is an effective procedure in pd that acts by disconnecting the pallidothalamic tract. unilateral pallidothalamic tractotomy on the left side improved contralateral side rigidity, tremors, and bradykinesia. it is the first time in india that ptt has been done for treating symptoms of parkinson’s disease. it will enable them to carry out their day-to-day activities without support. the cost associated with this surgery is much less than the cost of pacemaker implantation in the brain. abbreviations ptt – pallidothalamic tractotomy, pd parkinson’s disease, updrs unified parkinson disease rating scale, dbs deep brain stimulation surgery references 1. zafar s, yaddanapudi ss. parkinson disease. [updated 2021 aug 11]. in: statpearls [internet]. treasure island (fl): statpearls publishing; 2021 jan-. available from: https://www.ncbi.nlm.nih.gov/books/nbk470193/. 2. parkinson j. an essay on the shaking palsy. 1817. j neuropsychiatry clin neurosci. 2002;14:223-36. 3. goetz cg. the history of parkinson's disease: early clinical descriptions and neurological therapies. cold spring harb perspect med. 2011;1:a008862-a. 4. kouli a, torsney km, kuan wl. parkinson’s disease: etiology, neuropathology, and pathogenesis. in: stoker tb, greenland jc, editors. parkinson’s disease: pathogenesis and clinical aspects [internet]. brisbane (au): codon publications; 2018 dec 21. chapter 1. available from: https://www.ncbi.nlm.nih.gov/books/nbk536722/1. 5. lees aj, hardy j, revesz t. parkinson's disease. lancet. 2009;373:2055-66. 6. tysnes ob, storstein a. epidemiology of parkinson's disease. j neural transm (vienna). 2017;124:901-5. 7. pringsheim t, jette n, frolkis a, steeves td. the prevalence of parkinson's disease: a systematic review and meta-analysis. mov disord. 2014;29:1583-90. 8. hirsch l, jette n, frolkis a, steeves t, pringsheim t. the incidence of parkinson's disease: a systematic review and meta-analysis. neuroepidemiology. 2016;46:292300. 9. marras c, beck jc, bower et al. prevalence of parkinson's disease across north america. npj parkinsons dis. 2018;4:21-. 10. massano j, bhatia kp. clinical approach to parkinson's disease: features, diagnosis, and principles of management. cold spring harb perspect med. 2012;2:a008870-a. 11. galvan a, wichmann t. pathophysiology of parkinsonism. clin neurophysiol. 2008;119:1459-74. 12. informedhealth.org [internet]. cologne, germany: institute for quality and efficiency in health care (iqwig); 2006-. parkinson’s disease: parkinson’s disease: deep brain stimulation. 2020 jul 30. available from: https://www.ncbi.nlm.nih.gov/books/nbk560202/. 13. gallay mn, jeanmonod d, liu j, morel a. human pallidothalamic and cerebellothalamic tracts: anatomical basis for functional stereotactic neurosurgery. brain struct funct. 2008;212:443-63. 14. horisawa s, nanke m, kawamata t, taira t. pallidothalamic tractotomy for parkinson disease with 1year follow-up: a case report. world neurosurg. 2019;121:193-5. 15. horisawa s, fukui a, yamahata h et al. unilateral pallidothalamic tractotomy for akinetic-rigid parkinson's disease: a prospective open-label study. j neurosurg. 2021:1-7. 16. llumiguano c, dóczi t, baths i. tratamiento de la enfermedad de parkinson con palidotomía y palidotalamotomíaestereotáctica guiada por microelectrodos [microeletrode guided stereotactic pallidotomy and pallido-thalamotomy for treatment of parkinson's disease]. neurocirugia (astur). 2006;17:420-32. 17. jung ny, park ck, kim m, lee ph, sohn yh, chang jw. the efficacy and limits of magnetic resonance-guided focused ultrasound pallidotomy for parkinson's disease: a phase i clinical trial. j neurosurg. 2018:1-9. 18. gallay mn, moser d, magara ae, haufler f, jeanmonod d. bilateral mr-guided focused ultrasound pallidothalamic tractotomy for parkinson's disease with 1-year followup. front neurol. 2021;12:601153. 19. aufenberg c, sarnthein j, morel a, rousson v, gallay m, jeanmonod d. a revival of spiegel's campotomy: long term results of the stereotactic pallidothalamic tractotomy against the parkinsonian thalamocortical dysrhythmia. thalamus relat syst. 2005;3:121–132. 20. nowinski wl. anatomical targeting in functional neurosurgery by the simultaneous use of multiple schaltenbrand-wahren brain atlas microseries. stereotact funct neurosurg. 1998;71:103-16. 21. magara a, bühler r, moser d, kowalski m, pourtehrani p, jeanmonod d. first experience with mr-guided focused ultrasound in the treatment of parkinson's disease. j ther ultrasound. 2014;2:11. 22. gallay mn, moser d, rossi f et al. mrgfus 184 sanjiv chamraj, shavan srinivasan pallidothalamic tractotomy for chronic therapyresistant parkinson's disease in 51 consecutive patients: single center experience. front surg. 2020;6:76. 23. safaee m, burke j, mcdermott mw. techniques for the application of stereotactic head frames based on a 25year experience. cureus. 2016;8:e543. 24. thanvi br, lo tc. long term motor complications of levodopa: clinical features, mechanisms, and management strategies. postgrad med j. 2004;80:452-8. 25. wagle shukla a, okun ms. surgical treatment of parkinson's disease: patients, targets, devices, and approaches. neurotherapeutics. 2014;11:47-59. 26. gallay mn, moser d, federau c, jeanmonod d. anatomical and technical reappraisal of the pallidothalamic tractotomy with the incisionless transcranial mr-guided focused ultrasound. a technical note. front surg. 2019;24;6:2. 27. landi a, grimaldi m, antonini a, parolin m, zincone a marina. mri indirect stereotactic targeting for deep brain stimulation in parkinson's disease. j neurosurg sci. 2003;47:26-32. 28. meyers r. surgical interruption of the pallidofugal fibers. its effect on the syndrome of paralysis agitans and technical considerations in its application. ny state j med. 1942; 42:317–25. 29. godinho f, magnin m, filho pt et al. stereotactic lesion in the forel's field h: a 2-years prospective open-label study on motor and nonmotor symptoms, neuropsychological functions, and quality of life in parkinson disease. neurosurgery. 2019;85:e650-e659. romanian neurosurgery xxxiii (1): 12-16 (2019) doi: 10.33962/roneuro-2019-002 www.journals.lapub.co.uk/index.php/roneurosurgery pathways of metastatic spread in meningiomas a. i. cucu1, dana mihaela turliuc1,2, claudia florida costea1,2, b. costachescu1,2, andreea eliza malaimare3, l. a. blaj1, violeta trandafir1,4, cristina danca1, i. poeata1,2 1 “prof. dr. n. oblu” clinic emergency hospital, iasi, romania 2 “grigore t. popa” university of medicine and pharmacy, iasi, romania 3 individual medical practice, romania 4 “sf. spiridon” emergency clinical hospital iaşi, romania abstract meningioma is a common intracranial neoplasm derived from meningothelial cells, and it is generally associated with a benign clinical course. in spite of this, the malignant behaviour of these tumours as the occurrence of extracranial meningioma metastases in different organs is described in literature: lung and pleura, spine and other bones, abdominal organs, lymph nodes or even skin. the aim of this review is to analyse the pathways of metastatic spread of the intracranial meningioma tumour cells towards different organs. introduction meningiomas are the most common central nervous system tumours in adults, making up approximately 30% of all the intracranial tumours, with an increasing incidence (14, 57). according to the mitotic activity and tumour differentiation, the world health organization (who) grading meningiomas as it follows: grade i, grade ii and grade iii, the last two being characterized by a more aggressive behaviour, a high risk of recurrence (12, 39) and even metastasis. these extracranial meningioma metastases (emm) are more frequently associated with atypical meningiomas (table 1) or anaplastic meningiomas (20, 27, 59). although typical meningiomas are benign solitary intracranial neoplasms, they can cause extracranial metastasis, a rare phenomenon found only in 0.1% of cases (15, 23, 26, 35, 37). according to epidemiological data, about one in 1000 cases of meningiomas metastasize (35, 56). the most frequent sites of emm are: the lung (60%-70%), abdominal viscera (the liver most frequently) (30-40%), pleura (23%), lymph nodes (14-20%) and bones (10%) (3, 6, 21, 38, 42, 50, 60, 66). other rare localizations were identified in the parotid gland (17), skin (32, 51), deep soft tissue (9, 18, 44, 48, 64, 70), kidney, spleen, thyroid and adrenal gland (64). keywords meningioma, metastasis, malignant, who classification corresponding author: dana mihaela turliuc “grigore t. popa” university of medicine and pharmacy, iasi, romania turliuc_dana@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 2 a. i. cucu, dana mihaela turliuc, claudia florida costea et. al. due to the rare nature of emm, this is a challenging diagnosis for physicians and pathologists (25). because the treatment has not yet been standardized and a management protocol has not been developed, the prognosis of these patients remains unknown (3, 42, 50). table 1. review of publications on extracranial metastasis of atypical meningiomas metastatic spread although all types of meningioma, including the grade i meningiomas can metastasize, emm is more common in the atypical (5%) and anaplastic (30%) histopathological subtypes (7). nevertheless, some authors believe that these percentages are overestimated, firstly because some of the reported cases probably are metastatic angioblastic meningiomas and not genuine meningioma metastases. moreover, the angioblastic meningioma is now classified as haemangiopericytoma (25, 28, 34, 46). thus, considering all these modifications, the 5% rate of metastasis in atypical meningiomas does not coincide with the current who classification (25). however, the true prevalence of emm is unknown at present (64).as for the time interval between the initial diagnosis of the meningioma and that of extracranial metastasis, it varies from 3 months to 30 years (40). although throughout time, some authors emphasized tumour necrosis, blood vessel invasion, high cellularity, cellular heterogeneity, high mitosis rate and nuclear pleomorphism in the occurrence of emm (1, 20, 54), these criteria apply to malignant tumours and do not explain metastatic disease in benign meningiomas (64). in spite of this, the exact etiology of metastatic spread in meningioma is still unknown (7, 22). initially, the surgical resection was reported as one of the most important risk factors for iatrogenic metastasis of histologically aggressive meningiomas (2). hence, it was hypothesised that surgery causes the seeding of the lymphatics and vascular channels (including that of the scalp), resulting in extracranial metastatic disease via haematogenous or lymphatic route (31). besides, other studies showed that tumour cells can propagate with no previous surgery (25, 36), considering that the invasion of adjacent venous sinuses can lead to extracranial spread of meningioma, especially when there is no history of surgery (23). lung metastasis. as mentioned before, the lung is the most common site of the emm. in these cases, the seeded tumour cells access dural venous sinuses and cranial veins, then diffuse through the azygos system into pulmonary circulation and then they can reach either the lung or the pleura (21, 32, 40). most emm were found along the jugular vascular drainage, such as in the cervical lymph nodes, parotid and thyroid gland and finally in lung and pleura (64). bone metastasis. bone is one of the least common sites of meningioma metastasis (38, 60). in a review of meningioma metastasis in the bone, khan et al. found out that half of the patients had multiple areas of bone metastatic disease, while the author gender, age intracranial localization metastasis localization andric et al. (5) f 52 parasagittal lung baek et al. (9) m 44 nasal septum chest wall, parietal region drummond et al. (19) m 66 frontal lung doxtader et al. (18) m 8 parasagittal subcutaneous tissue of neck, lymph nodes kim et al. (41) m 68 parietal skull bone lanfranchi et al. (43) m 74 not specified lung, liver pinsker et al. (55) m 76 frontal cervical spine 3 pathways of metastatic spread in meningiomas other half had solitary bone involvement (40). the most common region was the axial skeleton, namely the thoracolumbar spine and sacrum (40), while metastases in the extra-axial bone were rarely identified (22). the most common involvement of the spine can be explained by the connection between the dural venous sinuses and the vertebral venous system (10). this route via the paravertebral venous plexus may also play a role in the metastatic spread across the kidney or adrenal glands (64). of the non-axial skeleton, the femur was the most common long bone site of involvement (40), and this metastasis location is more difficult to explain, even if some authors suggested the extension of the tumour via arterial spread (68). the bone metastatic disease is a lytic bone lesion and may result in pathological fractures or collapse of the vertebral bodies (40). liver metastasis. as far as the dissemination pathways for hepatic metastasis are concerned, some authors believe that this lies in the dissemination through the vertebral venous system connected with the veins of the thoracoabdominal wall or dissemination of tumour cells of the bone metastasis to the liver (24, 25). the liver can be involved whether the metastases pass through the right atrium towards the inferior vena cava and further into the hepatic veins (64). in literature, cases of hepatic metastasis of meningioma via a ventriculoperitoneal shunt through the cerebrospinal fluid route were cited (51). scalp metastasis. surgical seeding of tumour cells in meningioma surgery is a rare entity and it usually involves soft tissues near the craniotomy site (8). in literature, 19 such cases of scalp metastasis of intracranial meningiomas were reported (8). scalp metastasis of meningioma were firstly reported by harvey cushing, with an incidence of 1.21% cases in a cohort of 313 patients, which results in 4 patients suffering from this condition. in all of these cases, scalp metastases were found in surgical scar many years after the first surgery (4, 30, 49, 69). different series reported percentages of 3% in a cohort of 119 patients with who grade ii and iii meningiomas (53) and others of 1.2% (8). the suggested mechanism is intraoperative seeding and it may apply to all histological grades of meningiomas. avecillas-chasin et al. considers that immunosuppression, radiation therapy, csf fistulae and multiple reoperations with subsequent surgical wounds problems (8). nevertheless, the reason for extracranial tissue invasions is still unclear. carrying out multiple interventions can be a risk factor for the extracranial spreading of intracranial tumours, in that surgical bone deteriorates the natural barriers for intracranial tumour dissemination, providing access to the blood vessels and lymphatic system (8, 63). the higher-grade histopathological meningioma also contributes to this in case of tumours which have the tendency to produce greater levels of vascular endothelial growth factor and angiogenesis, thus favouring vascular invasion and metastatic behaviour (29). piecemeal resection was also presented as a risk factor of extracranial dissemination of tumour cells in who grade iii meningiomas (8). although initially, it was suggested that the latency period of meningioma metastasis is influenced by the histological grade (2), the significant variability over this la-tency period proved that this is not related only to the histological grade of meningioma (2, 16, 30, 45, 47, 52, 61, 62, 65, 67, 69). with regard to preventing the spread of tumour cells, some authors recommended: air-tight closure of dura mater, changing the gloves and surgical instruments for wound closure after the intracranial phase, replacing the bone flap and saline irrigation, wound abundance before the closure (4, 33). treatment strategies. the treatment for meningioma metastasis has yet to be set out. in spite of this, metastectomy seems to improve the prognosis, especially when the tumour is a low-grade meningioma. as for the chemotherapy with hydroxyurea, vincristine, cyclophosphamide and doxorubicin, this has a limited efficiency with progression under chemotherapy (25). moreover, some immunotherapies with interferon-α and somatostatin analogue were tested lately, but with limited effects (11, 58). nonetheless, the choice treatment in meningiomas remains the gross total resection and adjuvant radiotherapy (13). conclusions because of the fact that emm were rarely reported, there are no guidelines regarding the staging or treatment of emm. metastatic spread remains a therapeutic challenge and the treatment must be multidisciplinary evaluated. in addition, this data highlights the fact that metastatic dissemination of meningiomas is possible even under conditions of 4 a. i. cucu, dana mihaela turliuc, claudia florida costea et. al. benign histopathological grades and thus organ donation should be considered. references 1. adlakha a, rao k, adlakha h, et al. meningioma metastatic to the lung. mayo clin proc. 1999; 74(11): 1129-1133. 2. akai t, shiraga s, iizuka h, et al. recurrent meningioma with metastasis to the skin incision--case report. neurol med chir (tokyo). 2004; 44(11): 600-602. 3. alexandru d, glantz mj, kim l, et al. pulmonary metastases in patients with recurrent, treatment-resistant meningioma: prognosis and identification by ¹¹¹indiumoctreotide imaging. cancer. 2011; 117(19): 4506-4511. 4. allan rs. scalp metastasis from glioblastoma. j neurol neurosurg psychiatry. 2004; 364 75(4): 559. 5. andric m, dixit s, dubey a, et al. atypical meningiomas–a case series. clin neurol neurosurg. 2012; 114: 699-702. 6. asioli s, senetta r, maldi e, et al. “benign” metastatic meningioma: clinico-pathological analysis of one case metastasising to the lung and overview on the concepts of either primitive or metastatic meningiomas of the lung. virchows arch. 2007; 450: 591-594. 7. ather enam s, abdulrauf s, mehta b, et al. metastasis in meningioma. acta neurochir. 1996; 138: 1172-1178. 8. avecillas-chasin jm, saceda-gutierrez j, alonso-lera p, et al. scalp metastases of recurrent meningiomas: aggressive behavior or surgical seeding? world neurosurg. 2015; 84(1): 121-131. 9. baek bj, shin jm, lee ck, et al. atypical primary meningioma in the nasal septum with malignant transformation and distant metastasis. bmc cancer. 2012; 12:275. 10. batson ov. the function of the vertebral veins and their role in the spread of metastases. ann surg. 1940; 112(1): 138-149. 11. chamberlain mc, barnholtz-sloan js. medical treatment of recurrent meningiomas. expert rev neurother. 2011; 11: 1425-1432. 12. cucu ai, costea cf, poeata i, et al. prognostic factors in atypical meningioma. rom neurosurg. 2017; 31 (2): 165171. 13. cucu ai, turliuc md, costea cf, et al. atypical meningiomas of cerebellopontine angle. a five case series. rev med chir soc med nat iasi. 2018; 122:533-545. 14. cucu ai, costea cf, carauleanu a, et al. meningiomas related to the chernobyl irradiation disaster in northeastern romania between 1990 and 2015. revista de chimie bucharest 2018; 69: 1562-1565 15. d’aiuto m, veronesi g, pelosi g, et al. two-year survival after multiple bilateral lung metastasectomies for cranial meningioma. ann thorac surg. 2005; 80: 1129-1130. 16. darwish b, munro i, boet r, et al. intraventricular meningioma with drop metastases and subgaleal metastatic nodule. j clin neurosci. 2004; 11(7): 787-791. 17. dmytriw aa, gullane p, bartlett e, et al.parotid gland metastasis originating from malignant meningioma. clin imaging. 2013; 37(4): 740-743. 18. doxtader ee, butts sc, holsapple jw, et al. aggressive pediatric meningioma with soft tissue and lymph node metastases: a case report. pediatr dev pathol. 2009; 12(3): 244-248. 19. drummond kj, bittar rg, fearnside mr. metastatic atypical meningioma: case report and review of the literature. j clin neurosci. 2007; 7: 69-72. 20. enam sa, abdulrauf s, mehta b, et al. metastasis in meningioma. acta neurochir (wien). 1996; 138: 1172-1178. 21. erman t, hanta i, haciyakupoglu s, et al. huge bilateral pulmonary and pleural metastasis from intracranial meningioma: a case report and review of the literature. j neurooncol. 2005; 74: 179-181. 22. estanislau es, de carvalho gtc, reis bl, et al. malignant meningioma with extracranial metastases. arq neuropsiquiatr. 2009; 67: 730-732. 23. fabi a, nuzzo c, vidiri a, et al. bone and lung metastases from intracranial meningioma. anticancer res. 2006; 26: 3835-3837. 24. figueroa be, quint dj, mckeever pe, chandler wf. extracranial metastatic meningioma. br j radiol. 1999; 72: 513-516. 25. forest f, berremila sa, gyenes c, et al. metastatic meningiomas: an unusual clinical and pathological diagnosis with highly variable outcome. j neurooncol. 2014; 120(2): 411-421. 26. frydrychowicz c, holland h, hantmann h, et al. two cases of atypical meningioma with pulmonary metastases: a comparative cytogenetic analysis of chromosomes 1p and 22 and a review of the literature. neuropathology. 2015; 35: 175-183. 27. gezen f, kahraman s, canakci z, bedük a. review of 36 cases of spinal cord meningioma. spine (phila pa 1976). 2000; 25: 727-731. 28. gordon a, maloney a. a case of metastasizing meningioma. j neurol neurosurg psychiatry. 1965; 28:159. 29. guevara p, escobar-arriaga e, saavedra-perez d, et al. angiogenesis and expression of estrogen and progesterone receptors as predictive factors for recurrence of meningioma. j neurooncol. 2010; 98(3): 379384. 30. gunes m, tugcu b, gunaldi o et al. seeding metastasis in the scalp after removal of the meningioma: a case report. turkish neurosurg. 2005; 15: 136-139. 31. gyepes mt, d'angio gj. extracranialmetastases fromcentral nervous systemtumors in children and adolescents. radiology. 1966; 87(1): 55-63. 32. hu s, zhang y, sun y, et al. lung metastases from intracranial bleeding meningioma: a case report. medicine (baltimore). 2018; 97(16):e0457. 33. jain n, mirakhur m, flynn p, choudhari k a. cutaneous metastasis from 409 glioblastoma. br j neurosurg. 2005; 19(1): 65-68. 34. kabus d, sidhu gs, wieczorek rl, choi hs. metastatic meningioma. hemangiopericytoma or angioblastic meningioma? am j surg pathol. 1993; 17: 1144-1150. 5 pathways of metastatic spread in meningiomas 35. kaminski jm, movsas b, king e, et al. metastatic meningioma to the lung with multiple pleural metastases. am j clin oncol. 2001; 24(6): 579-582. 36. kamiya k, inagawa t, nagasako r. malignant intraventricular meningioma with spinal metastasis through the cerebrospinal fluid. surg neurol. 1989; 32: 213218. 37. kanzaki r, higashiyama m, fujiwara a, et al. surgical resection of pulmonary metastases from meningioma: report of a case. surg today. 2011; 41: 995-998. 38. karasick jl, mullan sf. a survey of metastatic meningiomas. j neurosurg. 1974; 40(2): 206-212. 39. kessler ra, garzon-muvdi t, yang w, et al. metastatic atypical and anaplastic meningioma: a case series and review of the literature. world neurosurg. 2017; 101:4756. 40. khan i, amary f, khoo mm. meningioma metastasis to the bone review of a rare finding with emphasis on distribution and imaging appearances. clinical imaging. 2015; 6: 1134-1139. 41. kim h, jung t-y, kim i-y, lee j-k. two cases of primary osteolytic intraosseous meningioma of the skull metastasizing to whole skull and the spine. j korean neurosurg soc. 2012; 51: 151-154. 42. koenig ma, geocadin rg, kulesza p, olivi a, brem h. rhabdoid meningioma occurring in an unrelated resection cavity with leptomeningeal carcinomatosis. case report. j neurosurg. 2005; 102: 371-375. 43. lanfranchi m, nikpoor n. detection of meningioma metastasis to liver and lung using somatostatin receptor scintigraphy. clin nucl med. 2013; 38: 668-670. 44. lee gc, choi sw, kim sh, kwon hj. multiple extracranial metastases of atypical menigiomas. j korean neurosurg soc. 2009; 45:107-111. 45. li z, cen y, gu m, wei y. giant malignant meningioma invading the calvarial bone and scalp. j craniofac surg. 2012; 23(2): 599-602. 46. louis d. who classification of tumours of the central nervous system. lyon: iarc press, 2007. 47. lüdemann wo, obler r, tatagiba m, samii m. seeding of malignant meningioma along a surgical trajectory on the scalp. case report and review of the literature. j neurosurg. 2002; 97(3): 683-686. 48. mccarthy c, hofer m,vlychou m, et al. metastatic meningioma presenting as a malignant soft tissue tumour. clin sarcoma res. 2016; 6: 23. 49. mentrikoski m, johnson md, korones dn, scott ga. glioblastoma multiforme in skin: a report of 2 cases and review of the literature. am j dermatopathol. 2008; 30(4): 381-384. 50. merell r. brain tumors. in: bope et, kellerman rd (eds) conn’s current therapy. atlanta: elsevier, 2017. 51. moir ja, haugk b, french jj. hepatic metastasis via a ventriculoperitoneal shunt from an intracranial meningioma: case report and review of the literature. case rep gastroenterol. 2010; 4: 267-272. 52. ozer e, kalemci o, acar ud, canda s. pin site metastasis of meningioma. br j neurosurg. 2007; 21(5): 524-527. 53. pasquier d, bijmolt s, veninga t, et al. atypical and malignant meningioma: outcome and prognostic factors in 119 irradiated patients. a multicenter, retrospective study of the rare cancer network. int j radiat oncol biol phys. 2008; 71(5): 1388-1393. 54. peker s. meningioma metastasis. in: pamir mn, black pm, rahlbusch r (eds) meningiomas. münchen: elsevier, 2010. 55. pinsker mo, buhl r, hugo h–h, mehdorn hm. metastatic meningioma who grade ii of the cervical spine: case report and review of the literature. zentralbl neurochir. 2005; 66: 35-38. 56. pramesh cs, saklani ap, pantvaidya gh, et al. beningn metastasizing meningioma. jpn j clin oncol. 2003; 33(2): 8688. 57. raizer j, sojka sherman wj. meningiomas. in: packer r, schiff d (eds) neuro-oncology. oxford: john wiley, 2012. 58. saraf s, mccarthy bj, villano jl. update on meningiomas. oncologist. 2011; 16: 1604-1613. 59. scognamiglio g, d’antonio a, rossi g, et al. cd90 expression in atypical meningiomas and meningioma metastasis. am j clin pathol. 2014; 141:841-849. 60. shuangshoti s, hongsaprabhas c, netsky mg. metastasizing meningioma. cancer. 1970; 26(4): 832-841. 61. singh sk, ojha bk, chandra a, et al. scalp meningioma. indian j dermatol. 2008; 53(4): 196-198. 62. spagnuolo e, calvo a, erman a, tarigo a, mañana g. recurrent meningiomas with progressive aggressiveness and posterior extracranial extension. neurocirugia (astur). 2003; 14(5): 409-416. 63. subramanian a, harris a, piggott k, shieff c, bradford r. metastasis to and from the central nervous system--the “relatively protected site”. lancet oncol. 2002; 3(8): 498507. 64. surov a, gottschling s, bolz j, et al. distant metastases in meningioma: an underestimated problem. j neurooncol. 2013; 112: 323-327. 65. tahir mz, shamim ms, chishti kn. recurrent atypical meningioma seeding to surgical scar. neurol india. 2009; 57(2): 222-224. 66. teague sd, conces dj jr. metastatic meningioma to the lungs. j thorac imaging. 2005; 20: 58-60. 67. velnar t, bunc g. iatrogenic metastasis of a benign meningioma to the periosteum at the site of previous craniotomy: a case report. wien klin wochenschr. 2008; 120: 766-769. 68. wasserkrug r, peyser e, lichtig c. extracranial bone metastases from intracranial meningiomas. surg neurol. 1979; 12(6): 480-484. 69. waterson kw jr, shapiro l. meningioma cutis: report of a case. int j dermatol. 1970; 9(2): 125-129. 70. williamson be, stanton ca, levine ea. chest wall metastasis from recurrent meningioma. am surg. 2001; 67: 966-968. romanian neurosurgery (2019) xxxiii (2): 200-214 doi: 10.33962/roneuro-2019-037 www.journals.lapub.co.uk/index.php/roneurosurgery the use of folic acid in the prevention of spinal bifida. knowledge, attitude, and practice of women of childbearing age in low income rural communities eghosa morgan1, nosa akpede2, emmanuel friday osagiede2, vivian ajekweneh2, francis erah2, victoria aishetu momoh3, mohammed irumhekhai momoh3, ezemwenghian aikomien morgan1, ese tracy osagiede4 1 department of surgery, ambrose alli university, ekpoma, nigeria 2 department of community medicine, irrua specialist teaching hospital, irrua, nigeria 3 department of community medicine, ambrose alli university, ekpoma, nigeria 4 accident and emergency unit, irrua specialist teaching hospital, irrua, nigeria abstract background. spinal bifida is a congenital malformation of the spine that typified defect of the neural tube with devastating neurological, psychosocial and developmental burden to the growing child with associated huge financial burden to the parents, community and the country. past and present studies have shown strong evidence to indicate that folic acid supplementation during the periconceptional period reduces the occurrence of spinal bifida in children. aim. to assess the knowledge, attitude, and practice of use of folic acid during the periconceptional period among women of childbearing age in two rural communities in edo state, nigeria. materials and methods. a prospective cross-sectional study of 170 women between the ages of 15 and 49 years recruited through a multi-stage sampling technique. the survey instrument was a structured interviewer-administered questionnaire. the data was analysed using statistical package for social sciences (spss) version 21 and presented as charts, tables, and associations tested with chi-square at a statistical level of significance set at p<0.05. results. one hundred and twenty-two (71.8%) of the respondents showed good knowledge, 147(86.5%) had a positive attitude, and 106 (62.4%) had a good practice of use of folic acid. there was a statistically significant association between respondents’ age, marital status, level of education, occupation, and their knowledge of the use of folic acid as well as with their attitude towards the use of folic acid. however, the practice was mainly associated with the socio-demographic variable of each household. conclusion. the use of folic acid during the perinatal period for the prevention of keywords folic acid, spinal bifida, childbearing age, prevention corresponding author eghosa morgan department of surgery, ambrose alli university ekpoma and irrua specialist teaching hospital, irrua, nigeria morganeghosa@gmail.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published june 2019 by london academic publishing www.lapub.co.uk http://www.lapub.co.uk/ 201 the use of folic acid in the prevention of spinal bifida spinal bifida is found to be absent in about two-fifths of the study population, a number found to be alarming despite the high level of good knowledge and attitude towards the use of folic acid. there is, therefore, an urgent need to step up more advocacy and health education to women of childbearing age to increase the uptake of folic acid for effective reduction of the incidence of spinal bifida. introduction spinal bifida is part of a group of birth defects called neural tube defects (ntds) which are caused by the abnormal closure of the embryonic neural tube between 22 and 28 days after conception.1 the neural tube is the embryonic structure that eventually develops into the baby’s brain and spinal cord as well as adjacent tissues. there are two major types of spinal bifida: spinal bifida occulta as seen when the vertebral defect or malformation is covered by skin and hence hidden, and spinal bifida cystic characterized by a cystic protrusion. spinal bifida cystic is further subdivided into meningocele in which the protrusion contains meninges and cerebrospinal fluid, and may or may not be covered by skin or myelomeningocele is the most severe form where the protrusion which contains spinal cord and nerves is exposed to the exterior.2 the worldwide incidence of spinal bifida varies between 0.17 and 6.39 per 1000 live-births.3 in nigeria, however, the general incidence of neural tube defects has been reported at rates of 2.75 to 7 per 1000 livebirths.4,5 past and ongoing studies have shown that the use of folic acid has significantly reduced the occurrence of spinal bifida and other neural tube defects. the relationship between apparent folate deficiency and spinal bifida was hypothesized as early as 1965. this prompted the conduction of randomized control trials by the medical research council where they found that women with the previous history of ntd-related pregnancies reduced the risk of occurrence by 70% by taking 4000 micrograms of folic acid daily. in 1984, hungarian randomized control trial found 100% reduction in risk of having the first occurrence of ntd-affected pregnancy among women who took 800 micrograms of folic acid daily 6,7 although the exact mechanism by which folic acid prevents spina bifida, and other ntds is still not known, its role in the synthesis, repair, and methylation of dna especially in rapidly growing cells is instructive. the world health organization recommends that all women of childbearing age consume 400 micrograms of folic daily and that women with pregnancies previously affected by ntds consume 5000 micrograms of folic acid daily.8 women should consume these amounts in the periconceptional period as it takes eight weeks to reach the optimal serum level of folic acid.9 methodology this is an eight-month (june 2017 to january 2018) prospective cross-sectional study involving 170 women of child bearing age attending the primary health care facility at usugbenu and opoji, edo central senatorial district, edo state, nigeria. this study was carried out by the use of an intervieweradministered questionnaire with emphasis on the following areas: knowledge of use of folic acid in the prevention of spinal bifida among women of child bearing age, compliance to use of folic acid among women of childbearing age, and factors that influence use of folic acid among women of child bearing age. data were analyzed using spss version 21. descriptive and inferential statistics were used to describe and interpret the data with the level of statistical significance set at p<0.05. results majority of the respondents 90 (52.9%) were between age 30-39, while only 5 (2.9%) were less than 20 years. all the respondents 170 (100%) were females. those married were 131 (77.1%) while 4 (2.4%) were cohabiting. a total of 84 (49.4%) respondents had secondary education, while 34 (20%) has primary education. most of the respondents 79(46.5%) were self-employed while 6(3.5%) were students. most of the respondents had been pregnant 70(41.2%) while a total of 19(11.2%) had not been pregnant before. (table 1). majority 127 (74.7%) have not had spinal bifida child, while 43 (25.3%) have had a spinal bifida child in the past (figure 1). seventy-nine (46.5%) said they had had a miscarriage while 91(53.5%) said they had not had any miscarriage (figure 2). in scoring for “knowledge,” 11 points were considered from the questionnaire, and a score of > 7 points was graded as “good,” a score of 5 -7 was graded as “fair,” while a score of < 5 was graded as “poor.” in scoring for “attitude,” 8 points were considered from the questionnaire, and a score of >4 was graded as “positive,” while a score of ≤ 4 was 202 eghosa morgan, nosa akpede, emmanuel friday osagiede et al. graded as “negative.” in scoring for “practice,” 6 points were considered from the questionnaire, and a score of >3 was graded as “good,” a score 2 -3 was graded as “fair” while a score of < 2 was graded as “poor.” in scoring for “determinants,” 5 points were considered from the questionnaire, and if > 2 “no” were ticked, it was graded as “strong” while if ≤ 2 “no” were ticked it was graded as “weak” (table 2). there was a statistically significant relationship between age group, marital status, level of education, occupation, number of pregnancies had and spinal bifida. however, there was no statistically significant relationship with the number of miscarriage (table 3a). there was a statistically significant relationship between, level of education and occupation. however, there was no statistically significant relationship with age group, spinal bifida child, pregnancies had, marital status and miscarriage (table 3b). there was a statistically significant relationship between age-group, marital status, level of education and number of pregnancies had. however, there was no statistically significant relationship with having spinal bifida child (table 5). there was a statistically significant relationship between age group and occupation, but there is no statistically marital status, level of education, number of pregnancies had, spinal bifida child and miscarriages (table 7). table 1. socio-demographic characteristics of respondents. variable frequency (n=170) percent (%) age group(year) < 20 5 2.9 20-29 46 27.1 30-39 90 52.9 40-49 29 17.1 mean ± sd = 28.41±0.73 marital status single 21 12.4 married 131 77.1 widowed 14 8.2 co-habiting 4 2.4 level of education primary 34 20.0 secondary 84 49.4 tertiary 52 30.6 occupation 203 the use of folic acid in the prevention of spinal bifida figure 1. prevalence of spinal bifida. figure 2. prevalence of miscarriages. 43(25.3%) 127( 74.7%) percentage aware not aware 79 (46.5%) 91(53.5%) had miscarriage yes no employed 58 34.1 unemployed 27 15.9 self-employed 79 46.5 student 6 3.5 pregnancies had none 19 11.2 1-3 39 22.9 4-6 70 41.2 7-9 35 20.6 >9 7 4.1 204 eghosa morgan, nosa akpede, emmanuel friday osagiede et al. table 2. respondents knowledge, attitude, practices, and determinants in the use of folic acid in the prevention of spinal bifida. table 3a. association between socio-demographic characteristics of respondents and their knowledge on the use of folic acid in the prevention of spina bifida. variable frequency (n=170) percent (%) knowledge good 122 71.8 fair 36 21.2 poor 12 7.1 attitude positive 147 86.5 negative 23 13.5 practice good 106 62.4 fair 49 28.8 poor 15 8.8 determinants strong 9 5.3 weak 161 94.7 demographic knowledge of respondent variable good (%) fair (%) poor (%) total (%) age group (years) < 20 1(20) 2(40) 2(40) 5(100) 20-29 27(58.7) 14(30.4) 5(10.9) 46(100) 30-39 74(82.2) 12(13.3) 4(4.5) 90(100) 40-49 20(70) 8(27.6) 1(2.4) 29(100) total 122(71.7) 36(21.2) 12(7.1) 170(100) x2 = 20.280 p=0.002 205 the use of folic acid in the prevention of spinal bifida table 3b. socio-demographic characteristics of respondents and knowledge on the use of folic acid in the prevention of spinal bifida. marital status single 8(38.1) 6(28.6) 7(33.3) 21(100) married 98(74.8) 28(21.4) 5(3.8) 131(100) widowed 12(85.7) 2(14.3) 0(0) 14(100) cohabiting 4(100) 0(0) 0(0) 4(100) total 122(71.7) 36(21.2) 12(7.1) 170(100) x2 = 29.775 p<0.001 level of education primary 22(64.6) 4(11.8) 8(23.6) 34(100) secondary 56(66.6) 26(31) 2(2.4) 84(100) tertiary 44(84.7) 6(11.5) 2(3.8) 52(100) total 122(71.7) 36(21.2) 12(7.1) 170(100) x2 = 25.662 p<0.0001 occupation employed 48(82.8) 8(13.8) 2(3.4) 58(100) unemployed 13(48.2) 8(29.6) 6(22.2) 27(100) self-employed 58(73.4) 18(22.8) 3(3.8) 79(100) student 3(50.1) 2(33.3) 1(16.6) 6(100) total 122(71.7) 36(21.2) 12(7.1) 170(100) x2 =18.262 p= 0.006 demographic variables knowledge of respondent pregnancies had good (%) fair (%) poor (%) total (%) none 11(57.9) 3(15.8) 5(26.3) 19(100) 1-3 24(61.5) 11(28.2) 4(10.3) 39(100) 4-6 53(75.7) 15(21.4) 2(2.9) 70(100) 206 eghosa morgan, nosa akpede, emmanuel friday osagiede et al. table 4a. sociodemographic characteristics of respondents and attitude on the use of folic acid in the prevention of spina bifida. 7-9 28(80) 7(20) 0(0) 35(100) >9 6(85.7) 0(0) 1(14.3) 7(100) total 122(71.7) 36(21.2) 12(7.1) 170(100) x2 =19.714 p=0.011 had spinal bifida child yes 39(90.7) 3(7) 1(2.3) 43(100) no 83(65.3) 33(26) 11(8.7) 127(100) total 122(71.7) 36(21.2) 12(7.1) 170(100) x2 =10.182 p =0.006 had a miscarriage yes 61(77.2) 15(19) 3(3.8) 79(100) no 61(67.1) 21(23.1) 9(9.8) 91(100) total 122(71.7) 36(21.2) 12(7.1) 170(100) x2=3.169,p=0.205 demographic variable attitude of respondent age group (years) positive (%) negative (%) total (%) < 20 3(60) 2(40) 5(100) 20-29 38(82.6) 8(17.4) 46(100) 30-39 82(91.1) 8(8.9) 90(100) 40-49 24(82.8) 5(17.2) 29(100) total 147(86.5) 23(13.5) 170(100) x2 = 5.579 p=0.134 marital status single 15(71.4) 6(28.6) 21(100) married 114(87) 17(13) 131(100) 207 the use of folic acid in the prevention of spinal bifida widowed 14(100) 0(0) 14(100) cohabiting 4(100) 0(0) 4(100) total 147(86.5) 23(13.5) 170(100) x2 = 6.912 p=0.075 level of education primary 24(70.6) 10(29.4) 34(100) secondary 73(86.9) 11(13.1) 84(100) tertiary 50(96.2) 2(3.8) 52(100) total 147(86.5) 23(13.5) 170(100) x2 = 11.512 p=0.003 occupation employed 52(89.7) 6(10.3) 58(100) unemployed 17(63) 10(37) 27(100) self-employed 72(91.1) 7(8.9) 79(100) student 6(100) 0(0) 6(100) total 147(86.5) 23(13.5) 170(100) x2 =15.667 p=0.001 pregnancies had none 15(78.9) 4(21.1) 19(100) 1-3 29(74.4) 10(25.6) 39(100) 4-6 64(91.4) 6(8.6) 70(100) 7-9 33(94.3) 2(5.7) 35(100) >9 6(85.7) 1(14.3) 7(100) total 147(86.5) 23(13.5) 170(100) x2 = 9.111 p=0.058 208 eghosa morgan, nosa akpede, emmanuel friday osagiede et al. table 4b. sociodemographic characteristics of respondents and attitude on the use of folic acid in the prevention of spinal bifida. table 5a. socio-demographic characteristics of respondents and practice on the use of folic acid in the prevention of spinal bifida. demographic variable attitude of respondent had spinal bifida child positive (%) negative (%) total (%) yes 38(88.4) 5(11.6) 43(100) no 109(85.8) 18(14.2) 127(100) total 147(86.5) 23(13.5) 170(100) x2 =0.178, p=0.673 had a miscarriage yes 70(88.6) 9(11.4) 79(100) no 77(85.6) 14(15.4) 91(100) total 147(86.5) 23(13.5) 170(100) x2=0.576, p=0.448 demographic variable practice of respondent good (%) fair (%) poor (%) total (%) age group (years) < 20 1(20) 2(40) 2(40) 5(100) 20-29 22(47.8) 16(34.8) 8(17.4) 46(100) 30-39 64(71.1) 22(24.4) 4(4.4) 90(100) 40-49 19(65.6) 9(31) 1(3.4) 29(100) total 106(62.4) 49(28.8) 15(8.8) 170(100) x2 = 17.821 p=0.007 marital status single 8(38.1) 5(23.8) 8(38.1) 21(100) married 82(62.6) 44(33.6) 5(3.8) 131(100) widowed 12(85.7) 0(0) 2(14.3) 14(100) 209 the use of folic acid in the prevention of spinal bifida cohabiting 4(100) 0(0) 0(0) 4(100) total 106(62.4) 49(28.8) 15(8.8) 170(100) x2 = 35.461 p<0.001 level of education primary 13(38.2) 17(50) 4(11.8) 34(100) secondary 53(63) 26(31) 5(6) 84(100) tertiary 40(77) 6(11.5) 6(11.5) 52(100) total 106(62.4) 49(28.8) 15(8.8) 170(100) x2 =17.314, p=0.002 occupation employed 43(74.2) 9(15.5) 6(10.3) 58(100) unemployed 10(37) 15(55.6) 2(7.4) 27(100) self-employed 49(62) 23(29.1) 7(8.9) 79(100) student 4(66.7) 2(33.3) 0(0) 6(100) total 106(62.4) 49(28.8) 15(8.8) 170(100) x2 =15.131 , p=0.019 pregnancies had none 8(42.1) 3(15.8) 8(42.1) 19(100) 1-3 25(64.1) 10(25.6) 4(10.3) 39(100) 4-6 41(58.5) 27(38.6) 2(2.9) 70(100) 7-9 28(80) 7(20) 0(0) 35(100) >9 4(57.1) 2(28.6) 1(14.3) 7(100) total 106(62.4) 49(28.8) 15(8.8) 170(100) x2 = 37.809 p=0.000 210 eghosa morgan, nosa akpede, emmanuel friday osagiede et al. table 5b. socio-demographic characteristics of respondents and practice on the use of folic acid in the prevention of spinal bifida. demographic variable practice of respondent good (%) fair (%) poor (%) total (%) had spinal bifida yes 32(74.4) 10(23.3) 1(2.3) 43(100) no 74(58.3) 39(30.7) 14(11) 127(100) total 106(62.4) 49(28.8) 15(8.8) 170(100) x2 =4.717, p=0.095 had a miscarriage yes 56(70.9) 22(27.8) 1(1.3) 79(100) no 50(54.9) 27(29.7) 14(15.4) 91(100) total 106(62.4) 49(28.8) 15(8.8) 170(100) x2=11.326,p=0.003 table 6a. socio-demographic characteristics of respondents and the determinants on the use of folic acid in the prevention of spinal bifida. demographic variable determinants of respondent strong (%) weak (%) total (%) age group (years) < 20 1(20) 4(80) 5(100) 20-29 6(13) 40(87) 46(100) 30-39 2(2.2) 88(97.8) 90(100) 40-49 0(0) 29(100) 29(100) total 9(5.3) 161(94.7) 170(100) x2 = 10.981 p=0.012 marital status single 3(14.3) 18(85.7) 21(100) married 6(4.6) 125(95.4) 131(100) 211 the use of folic acid in the prevention of spinal bifida table 6b. socio-demographic characteristics of respondents and the determinants on the use of folic acid in the prevention of spinal bifida. widowed 0(0) 14(100) 14(100) cohabiting 0(0) 4(100) 4(100) total 9(5.3) 161(94.7) 170(100) x2 = 4.526, p=0.210 level of education primary 2(5.9) 32(94.1) 34(100) secondary 3(3.6) 81(96.4) 84(100) tertiary 4(7.7) 48(92.3) 52(100) total 9(5.3) 161(94.7) 170(100) x2 =1.117 p= 0.572 occupation employed 2(3.4) 56(96.6) 58(100) unemployed 4(14.8) 23(85.2) 27(100) self-employed 2(2.5) 77(97.5) 79(100) student 1(16.7) 5(83.3) 6(100) total 9(5.3) 161(94.7) 170(100) x2 =80.26 p=0.045 demographic variable determinants of respondent strong (%) weak (%) total (%) pregnancies had none 3(15.8) 16(84.2) 19(100) 1-3 2(5.1) 37(94.9) 39(100) 4-6 4(5.7) 66(94.3) 70(100) 7-9 0(0) 35(100) 35(100) >9 0(0) 7(100) 7(100) 212 eghosa morgan, nosa akpede, emmanuel friday osagiede et al. discussion this research was carried out to assess the knowledge, attitude, and practice of use of folic acid in the prevention of spinal bifida among women of childbearing age in eclga of edo state. the research also assessed the relationship between sociodemographic factors and knowledge and use of folic acid in the prevention of spinal bifida. a total of 170 women, all of childbearing age, were interviewed. the mean age is 32 years with the highest proportion of participants 90(52.9%) consisting of those within the age group 30-39 years. majority of the participants were married 131(77.1%) as compared to singles 21(12.4%), widows 14(8.2%), cohabiting (2.4%). up to 84(49.4%) had secondary education, 52(30.6%) had tertiary education, and 34(20.0%) had primary education. we observed that the majority of the respondents 71.8% had good knowledge about the use of folic acid in the prevention of spinal bifida. this is in sharp contrast to a study done on awareness of mothers about birth defects in ibadan, in which only 15.8% knew that birth defects could be prevented.10 in another study in ibadan, only 11.8% knew that folic acid could prevent birth defects although as much as 98.3% were using folic acid in the current pregnancy.11 64.6% awareness of folic acid was reported in jos.12 in port harcourt, 94.4% knew about folic acid, but only 24.1% knew folic acid could prevent birth defects.13 the high awareness in this study is quite encouraging. it could be explained by the proximity of the respondents to a tertiary health facility (irrua specialist teaching hospital) which gives them access to health education through campaigns or interactions with resident health personnel. also, there is routine education of women during antenatal visits, as most respondents stated. we also observed that certain socio-demographic factors had a demonstrable influence on knowledge of folic acid use in the prevention of spinal bifida. age, marital status, level of education, occupation, previous pregnancy and having babies with spinal bifida in the past were significantly associated with knowledge of the use of folic acid whereas factors like religion and number of miscarriages were not. these observations are by earlier observations.11, 1418 on the aspect of attitude towards the use of folic acid, most of the respondents 86.5%. showed a positive attitude. sociodemographic factors significantly associated with this positive attitude were level of education (p=0.003), occupation (p=0.001). more than half of the respondents 62.4 had a good practice which compares favorably with the total 9(5.3) 161(94.7) 170(100) x2 =6.549, p=0.162 had spinal bifida child yes 0(0) 43(100) 43(100) no 9(7.1) 118(92.9) 127(100) total 9(5.3) 161(94.7) 170(100) x2 =3.218, p=0.073 had miscarriage yes 4(5.1) 75(94.9) 79(100) no 5(5.9) 86(94.1) 91(100) total 9(5.3) 161(94.7) 170(100) x2=0.016, p=0.900 213 the use of folic acid in the prevention of spinal bifida result of the study done in jakarta, indonesia where 64% of respondents claimed to have been compliant with the use of folic acid.33 in another study done in canada, 71% were compliant with the use of folic acid,35 while only 22.3% of the women in a study in denmark showed compliance19. the differences between our observation and between the results in previous reports could be due to the difficulty in measuring the actual practice of use of folic acid by women of childbearing age, for example in the jakarta study20; two parallel results were obtained from the same respondents using qualitative and quantitative tools. there was a statistically significant relationship between age (p=0.007), number of miscarriages (p=0.003), marital status (p=0.000), level of education (p=0.002), number of pregnancies had (0.000). a number of pregnancies had the highest statistical significance. determinants of use of folic acid showed statistically significant relationship with certain sociodemographic factors such as with age group such as women between 30-39 years had strong score while women less than 20 years had weak score reason for which may be due to teenage unplanned pregnancy, ignorance and late antenatal booking which is in keeping with the study done in south-western nigeria.17 in our study, the occupation had the highest statistical significant relationship (p=0.045). this shows that employment empowers these women making them better placed to use folic acid. also, employment is also related to an older age. conclusion we concluded that 1. the knowledge of the use of folic acid among women of childbearing age in eclga is good. furthermore, attitude and practice of use of folic acid match the knowledge and compares unfavourably with the levels reported from other places. 2. the level of knowledge, attitude, and practice on the use of folic acid among women of childbearing age in eclga are dependent on age, marital status, level of education, occupation, number of pregnancies, previous child with spinal bifida. recommendation we recommend that: 1. the government and health institution should work closely with stakeholders in the health sector to create more public enlightenment campaigns to increase awareness about spinal bifida and use of folic acid either in their diet or as medication in its prevention especially among women of childbearing age 2. communities should organize forums where a health worker enlightened member about the benefits of the use of folic acid by women of childbearing age while also answering any questions they may have. references 1. botto ld, et al. neural tube defects n engl j med. 1999 nov. 11; 341 (20): 1509-19 2. molloy, am. the role of folic acid in the prevention of ntds. trends food sci technol. 2005; 16 (6-7): 241-5. 3. bowman rm, boshnjaku v. and mclone dg (2009). the changing incidence of myelomeningocele and its impact on paediatric neurosurgery: a review from the children’s memorial hospital child’s nerv syst july 2009 25 (7): 801-6 4. anyanwu lc, danborno b, hamman w.o. the prevalence of neural tube defects in live born neonates in kano, north-western nigeria. afr j med 2015; 2:105-9 5. airede ki. neural tube defects in the middle belt of nigeria. j trop pediatr 1992; 38:27-30 6. mrc vitamin study research group. prevention of neural tube defects: results of the medical research council vitamin study. lancet 1991; 338:131-7 7. ezeizel ae, dudas i. prevention of the first occurrence of neural tube defects by periconceptional vitamin supplementation, n engl j med 1992; 327: 1832-5 8. who e-library of evidence for nutrition actions (elena). www.who.int/elena/title/folate_periconceptional/en/ last accessed: 9.00pm, 25th july 2017. 9. crider ks, devine o, haoling, dowling nf, lis, molly am et al. population red blood cell folate concentrations for prevention of neural tube defects: a bayesian model. bmj 2014; 349: g4554 10. lawal ta, et al. "knowledge of birth defects among nursing mothers in a developing country" african health science 2015 mar; 15(1):180-187. www.ncbi.nlm.nih.gov/pmc/arti cles /pmc4370152/ 11. adebo oo, et al. "knowledge and uptake of folic acid among pregnant women attending a secondary health facility in nigeria" british journal of midwifery 2017 june; 25(6): 358-364 12. anzaku sa. "assessing folic acid awareness and its usage for the prevention of neural tube defects among pregnant women in jos, nigeria. journal of basic and clinical reproductive science jan-june 2013; 2(1): 13-17 214 eghosa morgan, nosa akpede, emmanuel friday osagiede et al. 13. eghwrudjakpor po, et al. " evaluation of the level of awareness of the role of folic acid in the prevention of neural tube defects amongst women of reproductive age in a tertiary health institution." niger j med 2011 apr-jun. 14. dessie ma, zeleke eg, et al. "folic acid usage and associated factors in the prevention of neural tube defects among pregnant women in ethiopia: a cross-sectional study" bmc pregnancy childbirth v. 17(2017) 15. sadore aa, et al. "compliance with iron-folate supplement and associated factors among antenatal care attendant mothers in misha district, south ethiopia: communitybased cross-sectional study" journal of environmental and public health 2015(2):1-7 16. gathigi ln. "factors influencing utilization of iron and folic acid supplementation services among women attending antenatal clinic at nyeri provincial hospital, kenya" 17. lawal ta and adeleye a. o. "determinants of folic acid intake during preconception and in early pregnancy by mothers in ibadan, nigeria" the pan african medical journal 18. ezegwui hu, et al. "preconception care in south eastern nigeria" japan obstet gynaecol. 2008 19. knudsen vk, oroziva-bekkevold i, rasmussen lb, mikkelsen tb. low compliance with recommendations on folic acid use in relation to pregnancy: is there a need for fortification? doi: 10. 1079?phn2004630. public heal nutrition 2004: 7(7); 843-850 20. schultink well, et al. (1993). "low compliance with an iron supplementation program: a study among pregnant women in jakarta, indonesia." am j clin nutr 57(2):135-139. romanian neurosurgery (2019) xxxiii, 1: 23-30 doi: 10.33962/roneuro-2019-004 www.journals.lapub.co.uk/index.php/roneurosurgery surgical management of middle cerebral artery aneurysms mugurel radoi1,2, florin stefanescu1,2, ram vakilnejad2 1 faculty of general medicine, “carol davila” university of medicine and pharmacy, bucharest, romania 2 neurosurgical department of the national institute of neurology and neurovascular diseases, bucharest, romania abstract background. the middle cerebral artery (mca) harbors approximately 14% to 30% of all ruptured cerebral aneurysms. they can occur at multiple sites throughout the course of the middle cerebral artery, but most often are found at the bifurcation of the first segment (m1). methods. a retrospective review of 116 consecutive patients with an mca aneurysm treated by surgical clipping, by two senior neurosurgeons, was performed. the data of all our consecutive patients were searched to obtain patient characteristics, details of the aneurysm size and orientation, treatment details, complications and follow up. at admission, the clinical condition of all patients was classified according to the hunt and hess scale. clinical outcome was graded according to the modified rankin scale. the follow-up period varied widely from 2 to 72 months (mean 30 months). results. surgical clipping was performed for 113 ruptured mca aneurysms; only in 3 cases the aneurysm was unruptured. fourteen patients presented with significant hematoma which required the evacuation of the clot. post-operative control angiography was performed in 32 patients (27.5%), from which we reported a full occlusion of the aneurysm in 32 patients (93.75%). perioperative mortality was 5.2% (6 patients), due to neurological (4 patients) or systemic causes (2 patients). the outcome was graded mrankin 0–2 in 72.5% of the cases (84 patients) at the end of the first postoperative months, and 78.5% (91 patients) at six months follow-up. the most important improvement was recorded for patients graded mrankin 1-2 at the first month follow-up. all 3 patients with a surgically treated asymptomatic mca aneurysm had an excellent outcome (mrs 0) at both follow-up, 1 months and respectively 6 months. conclusions. for experienced neurovascular team, mca aneurysms currently make microsurgical treatment the preferred treatment modality for most mca aneurysms. introduction the middle cerebral artery (mca) originates at the internal carotid artery (ica) bifurcation and courses laterally within the sylvian cistern. mca aneurysms are common, representing approximately 14% to 20% of all intracranial aneurysms (13,24). they can occur at multiple sites throughout the course of the middle cerebral artery, but most often are found at the bifurcation of the first segment (m1) and projects laterally keywords mca aneurysm, surgical clipping, endovascular treatment, postoperative results corresponding author: mugurel radoi faculty of general medicine, “carol davila” university of medicine and pharmacy, bucharest, romania muguradoi@yahoo.com copyright and usage. this is an open access article, distributed under the terms of the creative commons attribution non–commercial no derivatives license (https://creativecommons .org/licenses/by-nc-nd/4.0/) which permits noncommercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. the written permission of the romanian society of neurosurgery must be obtained for commercial re-use or in order to create a derivative work. issn online 2344-4959 © romanian society of neurosurgery first published march 2019 by london academic publishing www.lapub.co.uk 24 mugurel radoi, florin stefanescu, ram vakilnejad in the plane of the m1 segment (31). because they project into the adjacent brain parenchyma, mca ruptured aneurysms are more likely to present with intraparenchymal rather than subarachnoid haemorrhages. thus, intracerebral haemorrhage rate is 43% versus 11% for aneurysms in other locations (13,24). methods a retrospective review of our neurovascular database was performed for patient diagnosed and surgically treated for mca aneurysm in the period from january 2012 until may 2018, by two senior neurosurgeons. in this period, 116 consecutive patients with an mca aneurysm were treated by surgical clipping, from a total of 384 patients operated for cerebral anterior circulation aneurysms. from this series of 116 patients, 26 patients harboured multiple intracranial aneurysms and at least one mca aneurysm. of our patients with multiple intracranial aneurysms, 12 had bilateral mca aneurysms (mirror aneurysms). table 1 distribution of carotid system aneurysms in a series of 116 patients distribution of carotid system aneurysms aneurysm location number of patients anterior communicating artery aneurysm 168 (44%) posterior communicating artery aneurysm 75 (19.5%) right medial cerebral artery aneurysm 65 (17%) left medial cerebral artery aneurysm 51 (13%) anterior cerebral artery aneurysm 4 (1%) internal carotid artery aneurysm 4 (1%) anterior choroidal artery aneurysm 6 (1,5%) pericallosal artery aneurysm 5 (1.5%) ophthalmic artery aneurysm 6 (1.5%) total 384 (100%) after clinical assessment, each patient performed cerebral computed tomography (ct) scan and conventional cerebral angiography with digital subtraction. if treatment options, clipping or coiling, were considered equal, in mca aneurysm surgery had priority. the data of all our consecutive patients, surgically treated for mca aneurysms, were searched to obtain patient characteristics, details of the aneurysm size and orientation, treatment details, complications and follow up. at admission, the clinical condition of all patients was classified according to the hunt and hess scale. clinical outcome was graded according to the modified rankin scale. only 3 patients with an unruptured mca aneurysm (hunt&hess 0) were included in this series. most of the patients were diagnosed as a cause of haemorrhagic stroke, subarachnoid haemorrhage or intracerebral hematoma. patients with a ruptured aneurysm of a good grade (hunt&hess 1-3) were, as a rule, treated within 48-72 h after the diagnosis of the aneurysm. in a minority of symptomatic patients, the treatment of the ruptured aneurysm was postponed because of comorbidity, late referral or poor clinical condition of the patient (hunt&hess 4-5). in these cases, acute hydrocephalus or clinical vasospasm, were treated before making the final decision about the timing of aneurysm clipping. in case of multiple aneurysms, treatment was at first selectively aimed at the ruptured aneurysm; additional unruptured aneurysms were not treated in the same session, unless in the same surgical field. results the patient characteristics are presented in table 2. table 2 characteristics of patient with mca aneurysms in our series characteristic no of patients (%) male 42 (36.2%) female 74 (63.8%) hunt &hess scale grade 0 5 (4.2%) 25 surgical management of middle cerebral artery aneurysms grade 1 and 2 81 (70%) grade 3 20 (17.3%) grade 4 8 (6,8%) grade 5 2 (1.7%) modified fischer grading scale no sah present 5 (4.3%) focal or diffuse thin sah 62 (53.5%) focal or diffuse thick sah 42 (36.2%) intraventricular haemorrhage 7 (6%) there were 116 patients with mca aneurysms operated in our series. most of the patients were women (63.8%). at the time of surgery, 70% of the patients were in grade 1 or 2 on hunt&hess scale. the aneurysm characteristics are summarized in table 3. most mca aneurysms were larger than 5 mm (70%). table 3 aneurysms characteristics characteristics no of patients (%) left mca 51 (44%) right mca 65 (56%) location mca bifurcation 109 (94%) m1 (pre-bifurcation segment) 5 (4.3%) m2/m3 (post-bifurcation) 2 (1.7%) size ≤ 5 mm 37 (31.9%) 5-10 mm 67 (57.75%) ≥ 10 mm 12 (10.35%) surgical clipping of an mca aneurysm was performed following a subarachnoid haemorrhage in most of the patients, only in 3 cases the aneurysm was unruptured. the majority of the patients, 83 representing 71.5%, was treated within 96 h following the haemorrhage. five patients had postponed clipping of ruptured aneurysm, due to re-bleeding, im po rt ant m edic al co -mo rb id iti es an d acu t e hydrocephalus that needed external drainage. seven patients harboured a coincidental non-ruptured posterior communicating artery aneurysm (3 cases) and anterior communicating artery aneurysm (4 cases), which were clipped in the same surgical procedure. fourteen patients presented with significant hematoma which required the evacuation of the clot. post-operative control angiography was performed in 32 patients (27.5%), from which we reported a full occlusion of the aneurysm in 32 patients (93.75%). table 4procedural and perioperative complication complications no of cases intraoperative rupture 18 (15.5%) re-ruptured before surgery (waiting) 1 (0.85%) post-operative rupture 1 (0.85%) pre-operative vasospasm angiography 14 (12%) clinic 6 (5%) post-operative vasospasm angiography 15/32 (46.85%) clinic 23 (20%) post-operative subdural hematoma 2 (1.7%) meningitis 3 (2.5%) hydrocephalus 8 (7%) 26 mugurel radoi, florin stefanescu, ram vakilnejad vp shunt (within 30 days from surgery) 4 (3.5%) epilepsy 2 (1.7%) preoperative vasospasm was demonstrated on cerebral angiography in 14 patients (12%) and clinically was manifested in 6 patients (5%). as postoperative event, 23 patients, including the ones with preoperative neurological signs, presented clinical symptoms of vasospasm including insidious onset of a decreasing level of consciousness, affected speech and/or motor deficits. on control angiography, cerebral vasospasm was detected on near half of the patients (46.85%). preoperative subarachnoid rebleeding, while waiting surgery, occurred in one patient. postoperative rebleeding of a clipped mca aneurysm occurred once, leading to a poor outcome. outcome of the surgically treated mca aneurysms after 2 months and after 6 months follow-up. excellent and good=mrankin 0–2, fair= mrankin 3, poor=mrankin 4-5, death=mrankin 6 the follow-up period varied widely from 2 to 72 months (mean 30 months). best results were obtained in patients who preoperatively were included in 1st and 2nd grade of hunt & hess scale. follow-up of the surgically treated symptomatic patients at 2 months was complete for all but 6 patients who died of neurologic or systemic causes. perioperative mortality was 5.2% (6 patients), due to neurological (delayed cerebral ischemia-3 patients and meningitis–1 patient) or systemic causes (pulmonary embolism -2 patients). the mean followup was 30 months, obtained in 94.8% of the patients. the outcome was graded mrankin 0–2 in 72.5% of the cases (84 patients) at the end of the first postoperative months, and 78.5% (91 patients) at six months follow-up. the most important improvement was recorded for patients graded mrankin 1-2 at the first month follow-up. all 3 patients with a surgically treated asymptomatic mca aneurysm had an excellent outcome (mrs 0) at both follow-up, 1 months and respectively 6 months. 0 10 20 30 40 50 60 70 80 mrs 0 mrs 1-2 mrs 3 mrs 4-5 mrs 6 nu m be r of p at ie nt s follow-up and outcome 2 months 6 months 27 surgical management of middle cerebral artery aneurysms figure legend: (a) preoperative native cerebral computed tomography (ct) showing subarachnoid haemorrhage, mainly in the left sylvian fissure; (b,c) preoperative four vessels cerebral angiography showed a 8 mm length left middle cerebral artery bifurcation aneurysm; (d,e) postoperative control cerebral angiography showed the correct clipping of the aneurysm and the preservation of both m2 branches. discussions the middle cerebral artery (mca) is the largest of the cerebral arteries. the diameter of the mca at its origin is about 4 mm (range, 2.4–4.6 mm). the mca starts as the larger and the more direct branch at the internal carotid artery bifurcation and courses laterally below the anterior perforated substance within the sylvian fissure, where it gives rise to the lateral lenticulostriate arteries and cortical branches and, then, divides into its main trunks (23,28). the mca is classically subdivided into four segments: the sphenoidal (m1) segment extending from the internal carotid artery bifurcation to the main mca bifurcation where insular trunks (m2) begin and course over the insula until the peri-insular sulcus, where the opercular (m3) segments start and continue until the lateral surface of the brain in the sylvian fissure and, then, continue as cortical (m4) segments (23,31). the middle cerebral artery (mca) harbors approximately 30% of all ruptured cerebral aneurysms and 36% of all unruptured cerebral aneurysms (7,10). mca aneurysms are classically divided into three groups: proximal middle cerebral artery aneurysms (m1 aneurysms), main middle cerebral artery bifurcation aneurysms (bifurcation aneurysms) or distal middle cerebral artery aneurysms (m3 or m4 aneurysms) (7,15). most of them are located at the mca bifurcation and often project laterally in the plane of the m1 segment (11). each location raises different surgical considerations, but the anatomic features of mca aneurysms render them amenable to microsurgical clipping as the primary treatment of choice for most patients. in addition, mca aneurysms are often broad necked and incorporate branches at the neck, which challenges endovascular coiling more than surgical clipping (15,21). around 40% of patients with mca aneurysms have multiple aneurysms, in contradistinction to approximately 20% of those with aneurysms in other locations (25). moreover, mirror aneurysms can be seen in 13% of patients with mca aneurysms (25,29). microsurgical clipping of mca aneurysms is still the preferred treatment modality in most centers due to the relatively straightforward surgical approach to these relatively superficial aneurysms (2,11). surgery provides effective and durable exclusion of mca aneurysms, and, also, allows the reduction of intracranial pressure through evacuation of related intracerebral hematoma. the different locations of mca aneurysms pose distinct challenges to the neurosurgeon and require specific surgical strategies. proximal mca aneurysms (m1 aneurysms) are especially challenging lesions because of their intimate relation to lateral lenticulostriate artery. these perforators arteries may arise from the m1 segment or from the aneurysm neck itself. these branches are quite easily damaged during dissection, included with the aneurysm during clipping or compressed by the clip with subsequent thrombosis (2,12). lateral lenticulostriate arteries irrigate eloquent areas of the brain and, thus, 28 mugurel radoi, florin stefanescu, ram vakilnejad damage to them could result in a poor clinical outcome. the m1 bifurcation is the most common location for aneurysms in the mca. in a large series, 60-83% of middle cerebral artery aneurysms are located at the bifurcation (24,31). the bifurcation of the mca typically lies medial to the junction of the horizontal and anterior portions of the sylvian fissure near the anterior edge of the island of reil or limen insulae. clipping of mca bifurcation aneurysm must be precise with careful attention paid to the origins of the m2 branches. after m1 is exposed the dissection proceeds distally along the anterior and inferior aspects of m1 to reach the aneurysm neck at the mca bifurcation (9). anteriorly pointing aneurysms allow m1 exposure along their posterior pole, and, posteriorly pointing aneurysms allow m1 exposure along their anterior pole. some mobilization of the m2 trunks may be necessary for creating enough space to place a temporary clip on m1 (8,16). temporary clipping is very important, because it softens the aneurysm sac during difficult and risky dissection maneuvers and is particularly helpful for isolating branching and perforating arteries adherent to the dome. anterior temporal artery and both m2 branches should be completely dissected free, before clip application. the aneurysm neck should usually be clipped along the plane of the m2 branches and perpendicular to the m1 (14). after clip application, the tips of the blades should be inspected to ensure the safety of all branching and perforating vessels. care must be taken not to kink the frontal or temporal m2s. “perfect” clip application is dangerous and often leads to stenosis of the m2 outlets (14,16). multilobed aneurysms often require more than one clip and more complex clip reconstruction. they often also have calcified or atheromatous walls, all this requiring higher closing pressure or grater occlusion surfaces for full obliteration. in these situations, tandemclipping techniques applying fenestrated clips with higher closing pressure to the distal neck supplemented by proximal neck occlusion with non-fenestrated clips are useful (6,14). sometimes, in large ruptured mca aneurysms, temporary clipping of the dome will provide sufficient control of the bleeding site to facilitate final dissection of the neck (6,17). the main challenge during surgery for distal mca aneurysm is to localize it, particularly when they are small and distal to the m2–m3 junction or when the sylvian fissure is filled with subarachnoid hemorrhage or intracerebral hematoma (7). localization of distal mca aneurysms requires more experience and careful study of the preoperative angiography. the distance from the mca genu, the location in relation to the associated ich if present, the depth of the aneurysm from the surface of the brain are some of the data that can be obtained from cta and which can help during surgery (2,7). neuronavigation, intraoperative dsa or intraoperative ultrasound might also be considered. giant and fusiform aneurysms of the bifurcation may require bypasses techniques. when performing the craniotomy for a large mca aneurysm, it is important to preserve at least one branch of the superficial temporal artery (sta) in case an unanticipated sta-mca bypass is needed. high-flow extracranial-intracranial bypasses using saphenous vein or radial artery grafts may needed to be considered for fusiform aneurysms involving more than one branch (16). the implementation of adjunctive tools including somatosensory evoked potential (ssep) monitoring, indocyanine green (icg) angiography or intraoperative digital subtraction angiography (dsa) improve surgical outcomes by providing critical information regarding optimal clip placement (5). efficacy of endovascular approach was evaluated in multicenter randomized control trials (rct) as the international subarachnoid aneurysm trial (isat) started in 2002 or the barrow ruptured aneurysm trial (brat) started in 2003 (18,19). in both trials, the early results at 1-year follow-up suggested superiority of coiling compared to clipping. but, longterm follow-up outcomes in both studies, evaluated at more than 3 years, demonstrated an attenuation of the benefit gain achieved by endovascular treatment to the point where no significant difference of neurological outcome was observed between the two treatment modalities (18,27). in the endovascular group, at long term follow-up, higher re-bleeding risk, lower obliteration rate and higher retreatment rate were noticed. but there were no specific randomized control trials to compare safety and efficacy of mca aneurysm treatment between the two modalities. regli et al. (22) described the first series of comparison between endovascular and surgical treatment in a single cohort; the surgical results were excellent with only 3% morbidity, 29 surgical management of middle cerebral artery aneurysms compared with a failure rate of 85% in coiling, with only two patients successfully treated by coiling with a “first coil” policy. a most recent comparison study (2014) was conducted by diaz and co-workers (9) but with the selection criteria bearing a moderate disadvantage towards surgery, where for all ruptured mca aneurysm a “coil first” strategy was implemented and for unruptured mca aneurysms only large ones were recommended to undergo clipping. the authors reported comparable results in poor outcome for coiling (10%) and clipping (5.9%) with a slight advantage toward surgery. they also observed a 14% recanalization of the aneurysm in endovascular group in comparison to none in the surgery group in a 9-months follow-up period (9). all these results were supported by evidence from systematic reviews and meta-analysis of the current literature that showed slight to moderate advantage of surgery over endovascular embolization in treatment of mca aneurysms (1,30). for ruptured mca aneurysms, the outcome after endovascular treatment is reported to be good in 48–100% of cases and poor in up to 52% of cases with a mortality rate of up to 14% (3,4). the outcome after the surgical treatment of ruptured mca aneurysms is recorded to be good in 55–95% of cases and poor in 5–45% with a mortality rate of up to 13% (20,26,27). for unruptured mca aneurysms, the outcome after endovascular treatment is reported to be good in 93–99% of cases and poor in up to 5% of cases with a mortality rate of up to 3% (3,22). the outcome of surgical treatment is recorded to be good in 88–100% of cases and poor in 4–12% of cases with a mortality rate of up to 2% (2,8,26). conclusions a good anatomic understanding of mca branching patterns and sylvian fissure compartments, and experience with standard management strategies are required to effectively treat these, often, complex aneurysms. all attempts to treat mca aneurysms endovascularly, despite ample progress in endovascular techniques and devices has been made, are unjustified in a situation where an excellent surgical solution is at hand. for experienced neurovascular team, mca aneurysms currently make microsurgical treatment the preferred treatment modality for most mca aneurysms. references 1. blackburn sl, abdelazim am, cutler ab, brookins kt, fargen km, hoh bl, et al. endovascular and surgical treatment of unruptured mca aneurysms: meta-analysis and review of the literature. stroke res treat. 2014;34847. 2. bohnstedt, b.n., h.s. nguyen, c.g. kulwin, m.m. shoja, g.m. helbig, t.j. leipzig, t.d. payner, and a.a. cohen-gadol, outcomes for clip ligation and hematoma evacuation associated with 102 patients with ruptured middle cerebral artery aneurysms. world neurosurg, 2013. 80(3-4): p. 33541. 3. bracard, s., a. abdel-kerim, l. thuillier, o. klein, r. anxionnat, s. finitsis, a. lebedinsky, c.m. de freitas, n. pinheiro, g.c. de andrade, and l. picard, endovascular coil occlusion of 152 middle cerebral artery aneurysms: initial and midterm angiographic and clinical results. j neurosurg, 2010. 112(4): p. 703-8. 4. brinjikji, w., g. lanzino, h.j. cloft, a. rabinstein, and d.f. kallmes, endovascular treatment of middle cerebral artery aneurysms: a systematic review and single-center series. neurosurgery, 2011. 68(2): p. 397-402; discussion 402. 5. caplan jm, sankey e, yang w, radvany mg, colby gp, coon al, et al. impact of indocyanine green videoangiography on rate of clip adjustments following intraoperative angiography. neurosurgery. 2014;75(4):437-434. 6. chyatte d, porterfield r. nuances of middle cerebral artery aneurysm microsurgery. neurosurgery. 2001;48:339-346. 7. dashti, r., j. hernesniemi, m. niemela, j. rinne, m. lehecka, h. shen, h. lehto, b.s. albayrak, a. ronkainen, t. koivisto, and j.e. jaaskelainen, microneurosurgical management of distal middle cerebral artery aneurysms. surg neurol, 2007. 67(6): p. 553-63 8. dashti r, hernesniemi j, niemela m, rinne j, porras m, lehecka m, shen h, albayrak bs, lehto h, koroknay-pál p, de oliveira rs, perra g, ronkainen a, koivisto t, jääskeläinen je. microneurosurgical management of middle cerebral artery bifurcation aneurysms. surg neurol. 2007; 67:441-456. 9. diaz om, ranger-castila l, barber s, mayo rc, klucznick r, zhang yj. middle cerebral artery aneurysms: a single-center series comparing endovascular and surgical treatment. world neurosurg. 2014;81(2):322-329. 10. doerfler, a., i. wanke, s.l. goericke, h. wiedemayer, t. engelhorn, e.r. gizewski, d. stolke, and m. forsting, endovascular treatment of middle cerebral artery aneurysms with electrolytically detachable coils. ajnr am j neuroradiol, 2006. 27(3): p. 513-20. 11. elsharkawy, a., m. niemela, m. lehecka, h. lehto, b.r. jahromi, f. goehre, r. kivisaari, and j. hernesniemi, focused opening of the sylvian fissure for microsurgical management of mca aneurysms. acta neurochir (wien), 2014. 156(1): p. 17-25. 12. guresir, e., p. schuss, j. berkefeld, h. vatter, and v. seifert, treatment results for complex middle cerebral artery aneurysms. a prospective single-center series. acta neurochir (wien), 2011. 153(6): p. 1247-52. 30 mugurel radoi, florin stefanescu, ram vakilnejad 13. heros r. aneurysms in the middle cerebral artery. in simon l, thomas dgt, clarke k (eds): rob and smith’s operative surgery: neurosurgery. new york: chapman & hall, 1994, pp 171-179. 14. heros, r.c. and m.j. fritsch. surgical management of middle cerebral artery aneurysms. neurosurgery, 2001. 48(4): p. 780-5; discussion 785-6. 15. hosoda, k., s. fujita, t. kawaguchi, y. shose, and s. hamano, saccular aneurysms of the proximal (m1) segment of the middle cerebral artery. neurosurgery, 1995. 36(3): p. 441-6 16. lawton mt. middle cerebral artery aneurysms, in: seven aneurysms: tenets and techniques for clipping. new york: thieme medical publishers, 2011. 17. madhugiri vs, ambekar s, pandey p, et al. the pterional and suprabrow approaches for aneurysm surgery: a systematic review of intraoperative rupture rates in 9488 aneurysms. world neurosurg. 2013;80:836-844. 18. mcdougall cg, spetzler rf, zabramski jm, partovi s, hills nk, nakaji p, et al. the barrow ruptured aneurysm trial. j neurosurg 2012;116(1):135-44. 19. molyneux a, kerr r, stratton i, sandercock p, clarke m, shrimpton j, et al. international subarachnoid aneurysm trial (isat) of neurological clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized trial. lancet 2002; 360 (9342):1267-74. 20. morgan, m.k., w. mahattanakul, a. davidson, and j. reid, outcome for middle cerebral artery aneurysm surgery. neurosurgery, 2010. 67(3): p. 755-61; discussion 761. 21. quadros, r.s., s. gallas, r. noudel, p. rousseaux, and l. pierot, endovascular treatment of middle cerebral artery aneurysms as first option: a single center experience of 92 aneurysms. ajnr am j neuroradiol, 2007. 28(8): p. 1567-72. 22. regli l, uske a, de tribolet n. endovascular coil placement compared with surgical clipping for the treatment of unruptured middle cerebral artery aneurysms: a consecutive series. j neurosurg 1999;90 (6):1025-30. 23. ring, b.a., middle cerebral artery: anatomical and radiographic study. acta radiologica, 1962. 57: p. 289-300. 24. rinne j, hernesniemi j, niskanen m, et al. analysis of 561 patients with middle cerebral artery aneurysms: anatomic and clinical features as correlated to management outcome. neurosurgery 38:2-11, 1996. 25. rinne, j., j. hernesniemi, m. puranen, and t. saari. multiple intracranial aneurysms in a defined population: prospective angiographic and clinical study. neurosurgery, 1994. 35(5): p. 803-8. 26. rodriguez-hernandez, a., m.e. sughrue, s. akhavan, j. habdank-kolaczkowski, and m.t. lawton, current management of middle cerebral artery aneurysms: surgical results with a “clip first” policy. neurosurgery, 2013. 72(3): p. 415-27. 27. spetzler rf, mcdougall cg, albuquerque fc, zabramski jm, hills nk, partovi s, et al. the barrow ruptured aneurysm trial: 3-year results. j neurosurg. 2013:19(1):146-57. 28. ture, u., m.g. yasargil, o. al-mefty, and d.c. yasargil. arteries of the insula. j neurosurg, 2000. 92(4): p. 676-87. 29. ulm, a.j., g.l. fautheree, n. tanriover, a. russo, e. albanese, a.l. rhoton, jr., r.a. mericle, and s.b. lewis, microsurgical and angiographic anatomy of middle cerebral artery aneurysms: prevalence and significance of early branch aneurysms. neurosurgery, 2008. 62(5 suppl 2): p. ons344-52; discussion ons352-3. 30. zaidat oo, castonguay ac, teleb ms, asif k, gheith a, southwood c, et al. middle cerebral artery aneurysm endovascular and surgical therapies: comprehensive literature review and local experience. neurosurg clin n am. 2014;25(3):455-69. 31. yasargil mg. middle cerebral artery aneurysms. in yasargil mg (ed): microneurosurgery, vol 2. stuttgart: thieme verlag, 1984, pp 124-164.